PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32776829-1 2020 Previously, we have used mathematical modeling to gain mechanistic insights into insulin-stimulated glucose uptake. Glucose 100-107 insulin Homo sapiens 81-88 32516539-6 2020 This review aims to highlight the current evidence for PGC-1alpha-mediated regulation of skeletal muscle mitochondrial function beyond the effects on mitochondrial biogenesis as well as the potential PGC-1alpha-related impact on insulin-stimulated glucose uptake in skeletal muscle. Glucose 248-255 insulin Homo sapiens 229-236 32738964-2 2020 Pancreatic GLUT2 also plays an important role in the mechanism of glucose-stimulated insulin secretion. Glucose 66-73 insulin Homo sapiens 85-92 32933950-0 2020 Comparison of weight-based insulin titration (WIT) and glucose-based insulin titration using basal-bolus algorithm in hospitalized patients with type 2 diabetes: a multicenter, randomized, clinical study. Glucose 55-62 insulin Homo sapiens 69-76 32933950-1 2020 INTRODUCTION: Subcutaneous administration of insulin is the preferred method for achieving glucose control in non-critically ill patients with diabetes. Glucose 91-98 insulin Homo sapiens 45-52 32314521-1 2020 The relationship between baseline fasting C-peptide (FCP) and glucose control was examined in insulin-naive people with type 2 diabetes mellitus (T2DM) inadequately controlled with oral anti-hyperglycaemic drugs commencing basal insulin glargine 300 U/mL (Gla-300) or 100 U/mL (Gla-100) in the absence of sulfonylurea/glinides. Glucose 62-69 insulin Homo sapiens 42-51 32314521-1 2020 The relationship between baseline fasting C-peptide (FCP) and glucose control was examined in insulin-naive people with type 2 diabetes mellitus (T2DM) inadequately controlled with oral anti-hyperglycaemic drugs commencing basal insulin glargine 300 U/mL (Gla-300) or 100 U/mL (Gla-100) in the absence of sulfonylurea/glinides. Glucose 62-69 insulin Homo sapiens 94-101 32436323-4 2020 Although basal insulin (BI) therapy is effective in reducing fasting plasma glucose (FPG), postprandial plasma glucose (PPG) often remains uncontrolled. Glucose 76-83 insulin Homo sapiens 15-22 32518064-6 2020 Our study suggests that a combination of SU and incretin-based treatment may be efficacious in patients with HNF1A diabetes via potentiation of glucose-stimulated insulin secretion. Glucose 144-151 insulin Homo sapiens 163-170 32556615-4 2020 Insulin sensitivity was calculated using a modified insulin sensitivity index that included fasting and 1 h glucose and C-peptide levels after a 75 g glucose load. Glucose 108-115 insulin Homo sapiens 0-7 32556615-5 2020 RESULTS: Per-metabolite and network analyses across the four ancestries identified numerous metabolites associated with maternal insulin sensitivity before and 1 h after a glucose load, ranging from amino acids and carbohydrates to fatty acids and lipids. Glucose 172-179 insulin Homo sapiens 129-136 32586980-7 2020 Conversely, addition of 3-HIB to white and brown adipocyte cultures increases fatty acid uptake and modulated insulin-stimulated glucose uptake in a time-dependent manner. Glucose 129-136 insulin Homo sapiens 110-117 32641374-0 2020 The Association Between HbA1c and Time in Hypoglycemia During CGM and Self-Monitoring of Blood Glucose in People With Type 1 Diabetes and Multiple Daily Insulin Injections: A Randomized Clinical Trial (GOLD-4). Glucose 95-102 insulin Homo sapiens 153-160 32661108-2 2020 We aimed to investigate the effect of Afrezza inhaled insulin with ultrafast-in and -out action profile on improving postprandial blood glucose control during hybrid closed-loop (HCL) treatment in young adults with type 1 diabetes. Glucose 136-143 insulin Homo sapiens 54-61 32683660-7 2020 We provide a comprehensive review on the use of the basal-bolus insulin regimen, including its principles, rationale, indications, prerequisites, initiation, and dose titration, and also suggest targets for blood glucose control and different levels of capillary blood glucose monitoring. Glucose 213-220 insulin Homo sapiens 64-71 32683660-7 2020 We provide a comprehensive review on the use of the basal-bolus insulin regimen, including its principles, rationale, indications, prerequisites, initiation, and dose titration, and also suggest targets for blood glucose control and different levels of capillary blood glucose monitoring. Glucose 269-276 insulin Homo sapiens 64-71 32683660-8 2020 Various case scenarios are used to illustrate how optimal glucose control can be achieved, such as through adjustments in doses of prandial and basal insulin, the use of correctional insulin dosing and changes in the timing and content of major and minor meals. Glucose 58-65 insulin Homo sapiens 150-157 32683660-8 2020 Various case scenarios are used to illustrate how optimal glucose control can be achieved, such as through adjustments in doses of prandial and basal insulin, the use of correctional insulin dosing and changes in the timing and content of major and minor meals. Glucose 58-65 insulin Homo sapiens 183-190 32721233-4 2020 Under high glucose exposure, rs3765467 and rs10305492 impaired beta cell secretion of insulin and beta cell viability in the same way; in other words, GLP1R rs3765467 and rs10305492 exert an effect on pancreatic beta cell glucose-stimulated insulin secretion. Glucose 11-18 insulin Homo sapiens 86-93 32721233-4 2020 Under high glucose exposure, rs3765467 and rs10305492 impaired beta cell secretion of insulin and beta cell viability in the same way; in other words, GLP1R rs3765467 and rs10305492 exert an effect on pancreatic beta cell glucose-stimulated insulin secretion. Glucose 11-18 insulin Homo sapiens 241-248 32721233-4 2020 Under high glucose exposure, rs3765467 and rs10305492 impaired beta cell secretion of insulin and beta cell viability in the same way; in other words, GLP1R rs3765467 and rs10305492 exert an effect on pancreatic beta cell glucose-stimulated insulin secretion. Glucose 222-229 insulin Homo sapiens 86-93 31637465-5 2020 In response to the glucose drink, and in comparison to subjects with normal weight, we observed in subjects with OW/OB a trend towards increased plasma insulin levels (+7445 +- 4858 vs. +4968 +- 1924 mU h L-1; p = 0.08), which was not seen for blood glucose (p = 0.59). Glucose 19-26 insulin Homo sapiens 152-159 31637465-5 2020 In response to the glucose drink, and in comparison to subjects with normal weight, we observed in subjects with OW/OB a trend towards increased plasma insulin levels (+7445 +- 4858 vs. +4968 +- 1924 mU h L-1; p = 0.08), which was not seen for blood glucose (p = 0.59). Glucose 250-257 insulin Homo sapiens 152-159 32561286-0 2020 Insulin exacerbated high glucose-induced epithelial-mesenchymal transition in prostatic epithelial cells BPH-1 and prostate cancer cells PC-3 via MEK/ERK signaling pathway. Glucose 25-32 insulin Homo sapiens 0-7 32561286-4 2020 The in vitro experiment results showed that high glucose (HG) promoted EMT process in a glucose-dependent manner in human prostate hyperplasia cells (BPH-1) and prostate cancer cells (PC-3), and this pathological process was exacerbated by co-culture with insulin. Glucose 49-56 insulin Homo sapiens 256-263 30892232-3 2020 A convex Lasso formulation is used to estimate the glucose fluxes that combines (1) the known patient parameters; (2) a sparse vector space encoding the space of plausible glucose flux profiles; (3) continuous glucose monitor measurements taken during the meal; (4) amount of insulin injected; (5) amount of meal carbohydrates and (6) an estimate of the initial conditions. Glucose 51-58 insulin Homo sapiens 276-283 30892232-4 2020 Three glucose fluxes are estimated: glucose rate of appearance from the intestine; endogenous glucose production from the liver; insulin dependent glucose utilization and other important state variables. Glucose 6-13 insulin Homo sapiens 129-136 32583238-5 2020 Sensitivity study of the system parameters using LHS-PRCC method reveals that some rate parameters, which represent the input of plasma glucose, absorption of glucose by noncardiac cells and insulin production, are sensitive and may cause significant change in the system dynamics. Glucose 136-143 insulin Homo sapiens 191-198 32583238-5 2020 Sensitivity study of the system parameters using LHS-PRCC method reveals that some rate parameters, which represent the input of plasma glucose, absorption of glucose by noncardiac cells and insulin production, are sensitive and may cause significant change in the system dynamics. Glucose 159-166 insulin Homo sapiens 191-198 32174045-10 2020 Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that the major targets of these ncRNAs were associated with insulin resistance and abnormal glucose and lipid metabolism. Glucose 180-187 insulin Homo sapiens 148-155 32267995-1 2020 A 38-year-old woman with type 1 diabetes, whose fasting plasma glucose levels were >500 mg/dL under 176 U/day of subcutaneous insulin injection, was admitted to our hospital. Glucose 63-70 insulin Homo sapiens 126-133 32569679-1 2020 OBJECTIVE: This work aimed to estimate population-level insulin sensitivity (SI) from 2-hour oral glucose tolerance tests (OGTT) with less than 7 samples. Glucose 98-105 insulin Homo sapiens 56-63 32129002-5 2020 The capacity of insulin secretion was assessed by C-peptide immunoreactivity (CPR) index (100xfasting CPR/fasting plasma glucose). Glucose 121-128 insulin Homo sapiens 50-59 32809102-0 2020 Molecular process of glucose uptake and glycogen storage due to hamamelitannin via insulin signalling cascade in glucose metabolism. Glucose 21-28 insulin Homo sapiens 83-90 30374190-4 2020 Injection of long RNA fraction from sperm of males exposed to postnatal trauma recapitulates the effects on food intake, glucose response to insulin and risk-taking in adulthood whereas the small RNA fraction alters body weight and behavioural despair. Glucose 121-128 insulin Homo sapiens 141-148 32999525-5 2020 For example, peripheral nerve contains insulin receptors that transduce the neurotrophic and neurosupportive properties of insulin, independent of systemic glucose regulation, while the detection of neuropathy and neuropathic pain in patients with metabolic syndrome and failure of improved glycemic control to protect against neuropathy in cohorts of type 2 diabetic patients has placed a focus on the pathogenic role of dyslipidemia. Glucose 156-163 insulin Homo sapiens 39-46 32506739-7 2020 SMBs that were associated with blood glucose control across groups were frequency of checking blood glucose at mealtime, missing an insulin dose, and checking blood glucose with a meter. Glucose 37-44 insulin Homo sapiens 132-139 32591906-2 2020 Reduced glucose transport activity results in aberrant use of energy substrates and is associated with insulin resistance and type 2 diabetes. Glucose 8-15 insulin Homo sapiens 103-110 32591906-3 2020 It is well established that GLUT2, the main regulator of hepatic hexose flux, and GLUT4, the workhorse in insulin- and contraction-stimulated glucose uptake in skeletal muscle, are critical contributors in the control of whole-body glycemia. Glucose 142-149 insulin Homo sapiens 106-113 32591906-4 2020 However, the molecular mechanism how insulin controls glucose transport across membranes and its relation to impaired glycemic control in type 2 diabetes remains not sufficiently understood. Glucose 54-61 insulin Homo sapiens 37-44 32732089-0 2020 Triglyceride/glucose index is a reliable predictor of insulin resistance in schizophrenia. Glucose 13-20 insulin Homo sapiens 54-61 32782164-7 2020 Pharmacological management of diabetes is needed in patients with blood glucose levels exceeding 2.16 g/l (12 mmol/l) and insulin therapy can be started when blood glucose levels are higher than 3.6 g/l (20 mmol/l) with clinical symptoms of diabetes. Glucose 164-171 insulin Homo sapiens 122-129 32782164-8 2020 Insulin can then be replaced with oral hypoglycemic compounds when both blood glucose levels and corticosteroid dose have decreased. Glucose 78-85 insulin Homo sapiens 0-7 32996429-3 2020 Closed-loop systems autonomously direct subcutaneous insulin infusion via a control algorithm based on real-time continuous glucose monitoring. Glucose 124-131 insulin Homo sapiens 53-60 32620516-1 2020 Insulin stimulates glucose transport by triggering regulated delivery of intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 32620516-1 2020 Insulin stimulates glucose transport by triggering regulated delivery of intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane. Glucose 117-124 insulin Homo sapiens 0-7 32878048-6 2020 Islet/ADSC sheet (AI sheet) group showed higher viability and glucose-stimulated insulin secretion than islet-only group. Glucose 62-69 insulin Homo sapiens 81-88 33041132-3 2021 The primary objective of this study was to assess the impact of IV regular insulin on glucose reduction and ED length of stay in patients presenting to the ED with non-emergent hyperglycemia. Glucose 86-93 insulin Homo sapiens 75-82 33351357-14 2020 In patients with insulin resistance, an increase in glycated hemoglobin increases the likelihood of detecting short telomeres by 2.4 times, and in diabetes mellitus by 4.26 times, an increase in fasting plasma glucose by 90%, and an increase in HOMA-IR by 35%. Glucose 210-217 insulin Homo sapiens 17-24 32984307-3 2020 The insulin secreted by pancreatic beta cells is the only hormone in the body that lowers blood glucose levels and plays vital roles in maintaining glucose homeostasis. Glucose 96-103 insulin Homo sapiens 4-11 32923633-6 2020 Complete in vivo studies of platforms with multiple, independently controlled release events in live-animal models illustrate capabilities for control of blood glucose levels by timed delivery of insulin. Glucose 160-167 insulin Homo sapiens 196-203 33005504-7 2020 The finding of plasma glucose levels within normal range prompted patients to maintain and sometimes even lower their insulin dose; even their providers were often misled by the euglycemia that resulted in delayed diagnosis and treatment. Glucose 22-29 insulin Homo sapiens 118-125 32678390-3 2020 The exposure of adipocytes to H2O2 (generated by glucose oxidase) resulted in an elevated level of ROS, a reduced content of GSH and an increase in JNK activation, concomitantly with a decrease in insulin-stimulated PI3K, Akt and p70S6K activation and cellular glucose uptake. Glucose 49-56 insulin Homo sapiens 197-204 32678390-3 2020 The exposure of adipocytes to H2O2 (generated by glucose oxidase) resulted in an elevated level of ROS, a reduced content of GSH and an increase in JNK activation, concomitantly with a decrease in insulin-stimulated PI3K, Akt and p70S6K activation and cellular glucose uptake. Glucose 261-268 insulin Homo sapiens 197-204 32875763-11 2020 CONCLUSION: Glucose pretreatment before hip replacement can relieve insulin resistance, improve immunity and change energy storage under fasting, which can be widely used in clinic. Glucose 12-19 insulin Homo sapiens 68-75 32943895-5 2020 In the case of insulin resistance, miR-21-5p knockdown promoted glucose uptake, but no significant effect was found under physiological condition. Glucose 64-71 insulin Homo sapiens 15-22 32381645-3 2020 Here we report that DS, but not dextran, protects human beta-cells against cytokine-mediated cytotoxicity in vitro DS also protects mitochondrial function and glucose-stimulated insulin secretion and reduces chemokine expression in human islets in a pro-inflammatory environment. Glucose 159-166 insulin Homo sapiens 178-185 32560812-5 2020 We found that deletion of miR-143/145 in smooth muscle results in a dramatic upregulation IRS-1 expression and insulin signaling, and an increased insulin-induced glucose uptake. Glucose 163-170 insulin Homo sapiens 147-154 32885091-6 2020 We hypothesized that indexes of insulinemia (primary outcome: postprandial insulin and glucose after standardized breakfast and lunch; secondary outcomes: fasting plasma glucose and insulin, HbA1c, 24-h continuous glucose monitoring) would be improved more with the low-GI versus the high-GI MED-HEP. Glucose 87-94 insulin Homo sapiens 32-39 32885091-6 2020 We hypothesized that indexes of insulinemia (primary outcome: postprandial insulin and glucose after standardized breakfast and lunch; secondary outcomes: fasting plasma glucose and insulin, HbA1c, 24-h continuous glucose monitoring) would be improved more with the low-GI versus the high-GI MED-HEP. Glucose 170-177 insulin Homo sapiens 32-39 32885091-6 2020 We hypothesized that indexes of insulinemia (primary outcome: postprandial insulin and glucose after standardized breakfast and lunch; secondary outcomes: fasting plasma glucose and insulin, HbA1c, 24-h continuous glucose monitoring) would be improved more with the low-GI versus the high-GI MED-HEP. Glucose 170-177 insulin Homo sapiens 32-39 32513541-7 2020 We performed viability tests by confocal microscopy and glucose stimulated insulin secretion (GSIS) test in vitro to assess the functionality of naked and encapsulated islets. Glucose 56-63 insulin Homo sapiens 75-82 32650643-8 2020 In insulin-resistance HepG2 cell, 1 promoted glucose consumption in a dose-dependent manner. Glucose 45-52 insulin Homo sapiens 3-10 32650643-10 2020 In conclusion, geranylated flavonoids in mulberry leaves inhibite PTP1B and increase the glucose consumption in insulin-resistant cells. Glucose 89-96 insulin Homo sapiens 112-119 32270304-2 2020 Of her many accomplishments, she is best known for devising the diabetes and pregnancy protocols of intensive insulin delivery and glucose control that have made it possible for thousands of women with diabetes to deliver healthy babies and for pioneering the use of insulin analogues in pregnancy. Glucose 131-138 insulin Homo sapiens 267-274 32586477-2 2020 Insulin therapy remains a useful regimen for many elderly patients, such as those with moderate to severe hyperglycemia, type 1 diabetes, hyperglycemic emergencies, and those who fail to maintain glucose control on non-insulin agents alone. Glucose 196-203 insulin Homo sapiens 0-7 32182545-1 2020 Insulin-regulated trafficking of the facilitative glucose transporter GLUT4 has been studied in many cell types. Glucose 50-57 insulin Homo sapiens 0-7 32182545-2 2020 The translocation of GLUT4 from intracellular membranes to the cell surface is often described as a highly specialised form of membrane traffic restricted to certain cell types such as fat and muscle, which are the major storage depots for insulin-stimulated glucose uptake. Glucose 259-266 insulin Homo sapiens 240-247 32924003-4 2020 Direct effects of BAIBA on acute glucose-mediated insulin release were probed in INS-1832/3 cells under normal and "diabetes-like" conditions. Glucose 33-40 insulin Homo sapiens 50-57 32819363-7 2020 Hence, there is no general insulin resistance but selective impairment of insulin signaling which causes less glucose uptake from the blood and reduced activation of endothelial NO synthase (eNOS). Glucose 110-117 insulin Homo sapiens 74-81 32839388-2 2020 However, the use of glucose-insulin-potassium (GIK) solution in patients undergoing cardiac surgery does not alleviate ischemia/reperfusion (I/R)-induced energy shortage. Glucose 20-27 insulin Homo sapiens 28-35 32973816-11 2020 After rectification of DKA, he was treated with insulin therapy daily, which has since controlled his plasma glucose well. Glucose 109-116 insulin Homo sapiens 48-55 32973816-14 2020 After plasma glucose is well controlled using insulin therapy, PD-1 inhibitor treatment might be continued, especially when the immunotherapy is effective. Glucose 13-20 insulin Homo sapiens 46-53 32813948-6 2020 Weight loss was associated with increased insulin-stimulated glucose disposal, from 30.5+-15.9 to 61.6+-13.0 mumol per kilogram of fat-free mass per minute in the diet group and from 29.4+-12.6 to 54.5+-10.4 mumol per kilogram of fat-free mass per minute in the surgery group; there was no significant difference between the groups. Glucose 61-68 insulin Homo sapiens 42-49 32891058-4 2020 Insulin stimulated glycolysis by promoting Glut4 activity by enhancing phosphorylation of AS160 at S595, stimulated fatty acid synthesis by promoting Acly activity through allosteric activation by glucose 6-phosphate or fructose 6-phosphate, and stimulated glutamate synthesis by alleviating allosteric inhibition of Gls by glutamate. Glucose 197-204 insulin Homo sapiens 0-7 32820223-6 2020 Insulin sensitivity was measured by glucose clamp technique. Glucose 36-43 insulin Homo sapiens 0-7 32807828-4 2020 Insulin-requiring GDM was defined as no claims for diabetes mellitus and a fasting blood glucose level of < 126 mg/dL before pregnancy, and initiation of insulin treatment during pregnancy. Glucose 89-96 insulin Homo sapiens 0-7 32783464-13 2021 CONCLUSIONS: A simple automated SQIA can be used to titrate insulin to meet the changing metabolic requirements of individuals perioperatively and maintain glucose within the target range for these hospitalized patients. Glucose 156-163 insulin Homo sapiens 60-67 32784178-10 2020 During regular or normal situations, higher insulin and reduced carbohydrate intake usually results in lower blood glucose levels. Glucose 115-122 insulin Homo sapiens 44-51 32785222-7 2020 Fluorescence microscope and flow cytometry were used to detect the glucose uptake capacity of ovarian granulosa cells in PCOS patients under the action of insulin after berberine. Glucose 67-74 insulin Homo sapiens 155-162 32771021-1 2020 BACKGROUND: Triglyceride glucose (TyG) index is a reliable marker of insulin resistance, which is linked to obstructive sleep apnea (OSA). Glucose 25-32 insulin Homo sapiens 69-76 32969484-2 2020 Described here is a patient who, within a few months after the onset of an autoimmune type 1 diabetes, increased her insulin requirements more than 20-fold, and despite this having a considerable difficulty maintaining her P-glucose < 40-60 mmol/L. Glucose 226-233 insulin Homo sapiens 117-124 32874990-12 2020 The patient also showed improved blood glucose control, with reduced levels of fasting insulin (857.84 pmol/L) and HbA1c (7.0%). Glucose 39-46 insulin Homo sapiens 87-94 32774470-13 2020 Interestingly, Ba2+-microencapsulated aggregates respond to high external glucose with insulin secretion. Glucose 74-81 insulin Homo sapiens 87-94 32744083-0 2021 Predictive capacity of triglyceride-glucose (TyG) index for insulin resistance and cardiometabolic risk in children and adolescents: a systematic review. Glucose 36-43 insulin Homo sapiens 60-67 33786271-1 2021 Background: In general, basal insulin targets fasting plasma glucose (FPG) levels, and prandial insulin targets postprandial glucose (PPG) levels. Glucose 125-132 insulin Homo sapiens 96-103 32267356-5 2020 Insulin sensitivity was obtained using the estimated glucose disposal rate (eGDR) formula. Glucose 53-60 insulin Homo sapiens 0-7 32302669-3 2020 In this study, by using live cell imaging and biochemical approaches, we demonstrate that IFN-gamma plus high glucose augment endothelial connexin43 hemichannel activity, resulting in the increase of ATP release, ATP-mediated Ca2+ dynamics and production of nitric oxide and superoxide anion, as well as impaired insulin-mediated uptake and intercellular diffusion of glucose and cell survival. Glucose 110-117 insulin Homo sapiens 313-320 32816872-3 2020 Insulin-stimulated glucose uptake and fasting-free fatty acid uptake in visceral adipose tissue (VAT), abdominal and femoral subcutaneous adipose tissues (SATs) were quantified with positron emission tomography. Glucose 19-26 insulin Homo sapiens 0-7 32283257-1 2020 Glucose-stimulated insulin secretion from pancreatic beta cells is mediated by Ca2+ influx and amplified by stimulation of GLP-1-receptors through cAMP-based signaling pathways. Glucose 0-7 insulin Homo sapiens 19-26 32464760-8 2020 The insulin signal transduction pathway of glucose translocation was analyzed by Western blot analysis. Glucose 43-50 insulin Homo sapiens 4-11 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 83-90 insulin Homo sapiens 0-7 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 83-90 insulin Homo sapiens 112-119 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 83-90 insulin Homo sapiens 174-181 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 237-244 insulin Homo sapiens 0-7 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 237-244 insulin Homo sapiens 174-181 32504189-4 2020 Stronger responses with oral glucose may be related to incretin effects on insulin secretion or from a direct effect on bone turnover. Glucose 29-36 insulin Homo sapiens 75-82 32409493-4 2020 Insulin sensitivity was assessed by oral glucose tolerance test. Glucose 41-48 insulin Homo sapiens 0-7 32439823-5 2020 At 1 year, AUC C-peptide/AUC glucose was significantly higher (p<0.05) in the oral insulin group than in the placebo group in each trial (p=0.057 with age adjustment in the TrialNet trial; p<0.01 for trials combined with or without age adjustment). Glucose 29-36 insulin Homo sapiens 83-90 32457219-7 2020 Moreover, proinsulin misfolding induced by oxidative stress or high glucose was accompanied by sulfonylation of PRDX4, a modification known to inactivate peroxiredoxins. Glucose 68-75 insulin Homo sapiens 10-20 32503838-0 2020 Effects of COVID-19 Lockdown on Glucose Control: Continuous Glucose Monitoring Data From People With Diabetes on Intensive Insulin Therapy. Glucose 60-67 insulin Homo sapiens 123-130 32428240-6 2020 Upon glucose stimulation, DAPA treatment led to lower blood glucose and proportionally lower human insulin, irrespective of treatment duration. Glucose 5-12 insulin Homo sapiens 99-106 32473019-6 2020 However, gefitinib lowered glucose-stimulated insulin secretion only in obese Ripk2-/- mice. Glucose 27-34 insulin Homo sapiens 46-53 32473019-12 2020 However, imatinib increased glucose-stimulated insulin secretion during the glucose challenge. Glucose 28-35 insulin Homo sapiens 47-54 32473019-12 2020 However, imatinib increased glucose-stimulated insulin secretion during the glucose challenge. Glucose 76-83 insulin Homo sapiens 47-54 32744543-5 2020 Moreover, the hypoglycemic activity of PLP-1 was investigated by palmitic acid and high glucose induced insulin resistant HepG2 cells. Glucose 88-95 insulin Homo sapiens 104-111 32013564-6 2020 Insulin sensitivity was assessed by the glucose disposal rate (GDR), determined using the hyperinsulinemic-euglycemic clamp, performed at seven years from diagnosis of diabetes. Glucose 40-47 insulin Homo sapiens 0-7 30557891-1 2020 BACKGROUND: Insulin has to be transported across the capillary endothelium to stimulate muscle glucose uptake. Glucose 95-102 insulin Homo sapiens 12-19 30557891-12 2020 Modulation of insulin extraction from the circulation may be a novel target to improve glucose metabolism in T2D. Glucose 87-94 insulin Homo sapiens 14-21 32744543-6 2020 The results elucidated that PLP-1 could decrease the glucose concentration by up-regulating the expression of PI3K and AKT, and down-regulating the expression of FoxO1, PCK2, and G6Pase in insulin resistant cells. Glucose 53-60 insulin Homo sapiens 189-196 32453489-3 2020 The novelty of the proposed study is to stabilize the glucose level in blood for type 1 diabetic patients by infusion of insulin in reduced time with optimal quantity. Glucose 54-61 insulin Homo sapiens 121-128 32392375-5 2020 However, insulin is a high-risk drug and to patients without previously known diabetes, initiation of insulin therapy requires training in blood glucose measurements and insulin injections. Glucose 145-152 insulin Homo sapiens 9-16 32392375-5 2020 However, insulin is a high-risk drug and to patients without previously known diabetes, initiation of insulin therapy requires training in blood glucose measurements and insulin injections. Glucose 145-152 insulin Homo sapiens 102-109 32392375-5 2020 However, insulin is a high-risk drug and to patients without previously known diabetes, initiation of insulin therapy requires training in blood glucose measurements and insulin injections. Glucose 145-152 insulin Homo sapiens 102-109 32402840-7 2020 However, reducing injectable insulin dosage prior to resistance exercise may blunt its favorable effects on glucose levels. Glucose 108-115 insulin Homo sapiens 29-36 32407514-1 2020 CONTEXT: Glucagon acts reciprocally with insulin to regular blood glucose. Glucose 66-73 insulin Homo sapiens 41-48 32270361-7 2020 Most importantly, resveratrol-treated insulin is nontoxic for HepG2 cells and it effectively maintains low blood glucose in a mouse model. Glucose 113-120 insulin Homo sapiens 38-45 32505477-1 2020 Diabetes is a chronic disease, characterized by hyperglycemia, which refers to the elevated levels of glucose in the blood, due to the inability of the body to produce or use insulin effectively. Glucose 102-109 insulin Homo sapiens 175-182 31782586-8 2020 Of 10 trials that measured mean blood glucose levels and the 11 trials reported HbA1c, the computerized insulin dose adjustment resulted in lower mean blood glucose levels in 70.0% (seven of 10) and 36.4% (four of 11) of RCTs, respectively. Glucose 38-45 insulin Homo sapiens 104-111 31782586-8 2020 Of 10 trials that measured mean blood glucose levels and the 11 trials reported HbA1c, the computerized insulin dose adjustment resulted in lower mean blood glucose levels in 70.0% (seven of 10) and 36.4% (four of 11) of RCTs, respectively. Glucose 157-164 insulin Homo sapiens 104-111 32567161-6 2020 Human islets encapsulated there have a glucose induced insulin response (GIIS) similar to nonencapsulated islets. Glucose 39-46 insulin Homo sapiens 55-62 32649492-1 2020 OBJECTIVE: To examine whether an insulin protocol for intrapartum glucose control among parturients with diabetes was associated with improved outcomes. Glucose 66-73 insulin Homo sapiens 33-40 32649492-14 2020 CONCLUSION: A formal protocol to manage insulin and glucose infusions for parturients with diabetes was associated with improved intrapartum maternal glucose control, but an increased frequency of neonatal hypoglycemia. Glucose 150-157 insulin Homo sapiens 40-47 32751231-13 2020 BaSO4 with loaded Insulin showed an onset of glucose-lowering action within 1 hr, with blood glucose level measured significantly lower compared to the 2nd and 3rd h (p < 0.05). Glucose 45-52 insulin Homo sapiens 18-25 32751231-13 2020 BaSO4 with loaded Insulin showed an onset of glucose-lowering action within 1 hr, with blood glucose level measured significantly lower compared to the 2nd and 3rd h (p < 0.05). Glucose 93-100 insulin Homo sapiens 18-25 32751231-14 2020 Insulin-loaded BaCO3 particles showed a significant decrease in blood glucose level at 1-2 h, although the glucose level started to show a slight rise at 3rd h and by 4th h, it was back to baseline level. Glucose 70-77 insulin Homo sapiens 0-7 32751231-14 2020 Insulin-loaded BaCO3 particles showed a significant decrease in blood glucose level at 1-2 h, although the glucose level started to show a slight rise at 3rd h and by 4th h, it was back to baseline level. Glucose 107-114 insulin Homo sapiens 0-7 32802055-5 2020 Insulin sensitivity was evaluated using the hyperinsulinemic-euglycemic clamp technique (HEC) with glucose disposal rate (GDR, M value). Glucose 99-106 insulin Homo sapiens 0-7 32754417-5 2020 The patient was treated with a low-dose insulin infusion (0.05 unit/kg/hr) with dextrose for six days. Glucose 80-88 insulin Homo sapiens 40-47 32709256-2 2020 Triglyceride-glucose index (TyG index) was made for a marker of insulin resistance. Glucose 13-20 insulin Homo sapiens 64-71 32801814-12 2020 However, anti-diabetic drugs including insulin up-regulate the TNF-alpha gene expression in mild or severe glucose load. Glucose 107-114 insulin Homo sapiens 39-46 32782776-7 2020 During the hospital stay, insulin titration was guided mainly by flash glucose monitoring (FGM). Glucose 71-78 insulin Homo sapiens 26-33 32782776-12 2020 In addition, interstitial glucose-monitoring technologies including continuous glucose monitoring and FGM can facilitate inpatient intensive insulin therapy in diabetic HH by avoiding hypoglycemia. Glucose 26-33 insulin Homo sapiens 141-148 32782776-12 2020 In addition, interstitial glucose-monitoring technologies including continuous glucose monitoring and FGM can facilitate inpatient intensive insulin therapy in diabetic HH by avoiding hypoglycemia. Glucose 79-86 insulin Homo sapiens 141-148 32698837-5 2020 Both insulin and GLP-1RAs have shown optimal glucose-lowering and anti-inflammatory effects in type 2 diabetic patients and may represent a valid therapeutic option to treat asymptomatic and non-critically ill COVID-19 diabetic patients. Glucose 45-52 insulin Homo sapiens 5-12 32707917-7 2020 In females, but not males, insulin sensitivity improved (HOMA%S +35%, p = 0.016, marginally significant) with longer fast duration (16 h vs. 12 h), but paradoxically, postprandial glycaemia was higher (glucose iAUC +37%, p = 0.002). Glucose 202-209 insulin Homo sapiens 27-34 32690029-4 2020 In this case, intravenous insulin infusion with continuous glucose monitoring should be the choice. Glucose 59-66 insulin Homo sapiens 26-33 32693054-1 2020 A major trigger of adult beta-cell insulin secretion is glucose. Glucose 56-63 insulin Homo sapiens 35-42 32683846-2 2020 Glucose appears to play a pivotal role in the regulation of insulin synthesis and secretion, the mechanism known as glucose-stimulated insulin secretion (GSIS). Glucose 0-7 insulin Homo sapiens 60-67 32683846-2 2020 Glucose appears to play a pivotal role in the regulation of insulin synthesis and secretion, the mechanism known as glucose-stimulated insulin secretion (GSIS). Glucose 0-7 insulin Homo sapiens 135-142 32683846-2 2020 Glucose appears to play a pivotal role in the regulation of insulin synthesis and secretion, the mechanism known as glucose-stimulated insulin secretion (GSIS). Glucose 116-123 insulin Homo sapiens 60-67 32683846-2 2020 Glucose appears to play a pivotal role in the regulation of insulin synthesis and secretion, the mechanism known as glucose-stimulated insulin secretion (GSIS). Glucose 116-123 insulin Homo sapiens 135-142 32683846-3 2020 Glucose plays a major role in the expression of insulin gene via the recruitment of transcription factors to the insulin gene and the regulation of its histone modifications, resulting in insulin secretion. Glucose 0-7 insulin Homo sapiens 48-55 32683846-3 2020 Glucose plays a major role in the expression of insulin gene via the recruitment of transcription factors to the insulin gene and the regulation of its histone modifications, resulting in insulin secretion. Glucose 0-7 insulin Homo sapiens 113-120 32683846-3 2020 Glucose plays a major role in the expression of insulin gene via the recruitment of transcription factors to the insulin gene and the regulation of its histone modifications, resulting in insulin secretion. Glucose 0-7 insulin Homo sapiens 113-120 32904711-1 2020 Context: In healthy individuals, glucose-dependent insulinotropic polypeptide (GIP) enhances insulin secretion and reduces bone resorption by up to 25% estimated by absolute placebo-corrected changes in carboxy-terminal type 1 collagen crosslinks (CTX) during GIP and glucose administration. Glucose 33-40 insulin Homo sapiens 51-58 33643468-10 2021 Results: We confirmed the presence of insulin resistance through reduction of Akt phosphorylation, Glut4 expression, Glut4 translocation and glucose uptake. Glucose 141-148 insulin Homo sapiens 38-45 32445468-1 2020 Diabetes mellitus is characterized by chronic high blood glucose levels resulted from deficiency and/or dysfunction of insulin-producing pancreatic beta cells. Glucose 57-64 insulin Homo sapiens 119-126 32283211-6 2020 In vivo, daily administration of marketed long-acting insulin, glargine, resulted in fluctuating blood glucose levels between 91 and 443 mg/dL in type 1 diabetic rats. Glucose 103-110 insulin Homo sapiens 54-61 32283211-8 2020 Sustained release of basal insulin also correlated with efficient glycemic control (blood glucose <120 mg/dL), prevention of diabetic ketoacidosis and absence of cataract development, unlike other treatment groups. Glucose 90-97 insulin Homo sapiens 27-34 32409841-3 2020 Non-insulin-dependent glucose lowering strategies may provide a strategy in improving glycaemic control without hypoglycaemia and weight gain. Glucose 22-29 insulin Homo sapiens 4-11 32664432-2 2020 These sensors provide in real-time, every 1-5 min, the current blood glucose concentration and its rate-of-change, two key pieces of information for improving the determination of exogenous insulin administration and the prediction of forthcoming adverse events, such as hypo-/hyper-glycemia. Glucose 69-76 insulin Homo sapiens 190-197 32695161-11 2020 Postload glucose and insulin levels (as insulin AUC) were progressively higher from the Hp1-1 to Hp2-2 phenotype. Glucose 9-16 insulin Homo sapiens 40-47 32695161-13 2020 We showed that the presence of Hp2 allele is associated with a worse response of glucose load in terms of both glucose and insulin levels. Glucose 81-88 insulin Homo sapiens 123-130 32196765-1 2020 Insulin is a small protein crucial for regulating the blood glucose level in all animals. Glucose 60-67 insulin Homo sapiens 0-7 32574064-6 2020 Meanwhile, the pH/redox dual-responsive FEMI hydrogel achieved a sustained and spatiotemporal controlled release of insulin to regulate the blood glucose. Glucose 146-153 insulin Homo sapiens 116-123 32341128-9 2020 Finally, we separated young and old insulin SGs, revealing that preferential secretion of younger granules occurs in glucose-stimulated insulin secretion. Glucose 117-124 insulin Homo sapiens 36-43 32640511-1 2020 Glucagon-like peptide-1 (GLP-1) has been shown to potentiate glucose-stimulated insulin secretion binding GLP-1 receptor on pancreatic beta cells. Glucose 61-68 insulin Homo sapiens 80-87 33479590-6 2021 Hence, another bolus insulin injection was simultaneously added to the basal insulin dose before breakfast, which, subsequently, decreased his preprandial glucose levels to <= 220 mg/dL before lunch and <= 350 mg/dL before dinner. Glucose 155-162 insulin Homo sapiens 21-28 32620690-1 2020 Insulin is stored in secretory granules to facilitate rapid release in response to rising glucose levels, but the mechanisms by which these granules are identified and prioritized for secretion remains unclear. Glucose 90-97 insulin Homo sapiens 0-7 32619466-3 2020 Hepatic gluconeogenesis is then inhibited synergistically by insulin and IL-10 to facilitate glucose clearance. Glucose 93-100 insulin Homo sapiens 61-68 32544115-1 2020 BACKGROUND: Diabetes impairs the body"s ability to produce or respond to the hormone insulin resulting in abnormal metabolism of carbohydrates and elevated glucose levels in the body. Glucose 156-163 insulin Homo sapiens 85-92 32459523-7 2020 Thus, myostatin inhibition improves muscle insulin-stimulated glucose disposal in obese high fat diet-fed mice independent of muscle hypertrophy, potentially involving previously unidentified pathways. Glucose 62-69 insulin Homo sapiens 43-50 32502373-1 2020 Vasodilatory effects of insulin support the delivery of insulin and glucose to skeletal muscle. Glucose 68-75 insulin Homo sapiens 24-31 33479590-6 2021 Hence, another bolus insulin injection was simultaneously added to the basal insulin dose before breakfast, which, subsequently, decreased his preprandial glucose levels to <= 220 mg/dL before lunch and <= 350 mg/dL before dinner. Glucose 155-162 insulin Homo sapiens 77-84 33019344-2 2020 Hands-on implementation using all these techniques and comparing them towards same system (in our case glucose-insulin regulation) we teach pros and cons of each technique. Glucose 103-110 insulin Homo sapiens 111-118 31893932-10 2020 Patients receiving long-acting insulin had significantly more encounters with diabetes education (10.6 vs 5.1 visits per patient, P = 0.002) and more consistently provided glucose readings at their appointments (8.3 vs 4.8, P = 0.043). Glucose 172-179 insulin Homo sapiens 31-38 33019136-3 2020 A T2D simulator (T2DS), consisting of a model of the glucose-insulin system and an in silico population describing glucose-insulin dynamics in T2D subjects, has been recently developed based on early-stage T2D data, studied with sophisticated experimental techniques. Glucose 53-60 insulin Homo sapiens 61-68 32404008-4 2020 Before, during, and after the hypercaloric diet, and upon return to baseline weight, all participants underwent (1) a hyperinsulinemic-euglycemic clamp to determine insulin-induced glucose uptake and suppression of lipolysis (2) contrast-enhanced ultrasonography to measure insulin-induced microvascular recruitment in skeletal muscle and adipose tissue. Glucose 181-188 insulin Homo sapiens 165-172 32828456-2 2020 Currently, two opposing treatment approaches exist: in formulaic methods, insulin care is calculated by parameter-based computation (i.e., correction factor, insulin-to-carb ratio, and absorption duration), which are fixed by the medical team based on the history of a tested patient blood glucose levels (BGLs). Glucose 290-297 insulin Homo sapiens 74-81 32166852-1 2020 AIMS: To test the effect of energy restriction with maintained protein intake on body composition and the insulin sensitivity of glucose and protein metabolism in adults with type 2 diabetes mellitus (T2D). Glucose 129-136 insulin Homo sapiens 106-113 32828456-4 2020 Unlike the body, both these systems are reactive - chasing insulin dosage based on fluctuating BGL - resulting in significant fluctuations of glucose values, rather than the relatively flat profile normal to the body"s glycemic control. Glucose 142-149 insulin Homo sapiens 59-66 32828456-7 2020 We model patient reaction to insulin treatment as Markov decision process (MDP) thus allowing the system to find a unique, individualized and dynamically updating insulin care policy that would lead to flat blood glucose profiles in target areas. Glucose 213-220 insulin Homo sapiens 29-36 32828456-7 2020 We model patient reaction to insulin treatment as Markov decision process (MDP) thus allowing the system to find a unique, individualized and dynamically updating insulin care policy that would lead to flat blood glucose profiles in target areas. Glucose 213-220 insulin Homo sapiens 163-170 32160329-8 2020 RESULTS: The biomarkers of impaired glucose metabolism showed strong significant difference in HOMA-Index, adiponectin, proinsulin and body mass index (BMI) and Insulin levels in 0 - 60 - 120 minute of glucose tolerance test but also with parameters of ovarian function as AMH, AMH z-score sAMHR2, and sAMHR2/AMH ratio. Glucose 36-43 insulin Homo sapiens 120-130 32699114-2 2020 RESEARCH DESIGN AND METHODS: A model was developed to estimate, with the perspective of the Spanish health system, the annual costs associated with glucose monitoring and hypoglycemic events management in T1DM population, with multiple insulin daily doses (MDI). Glucose 148-155 insulin Homo sapiens 236-243 32160329-8 2020 RESULTS: The biomarkers of impaired glucose metabolism showed strong significant difference in HOMA-Index, adiponectin, proinsulin and body mass index (BMI) and Insulin levels in 0 - 60 - 120 minute of glucose tolerance test but also with parameters of ovarian function as AMH, AMH z-score sAMHR2, and sAMHR2/AMH ratio. Glucose 36-43 insulin Homo sapiens 161-168 32350565-11 2020 GPR44 inhibition antagonised the reduction in glucose-stimulated insulin secretion induced by HG and IL-1beta in human islets. Glucose 46-53 insulin Homo sapiens 65-72 32017362-4 2020 RESULTS: The acute insulin response to glucose potentiation of arginine-induced insulin release was less in non-obese T2D than in controls and associated with impaired beta-cell sensitivity to glucose (PG50 ). Glucose 39-46 insulin Homo sapiens 19-26 32017362-4 2020 RESULTS: The acute insulin response to glucose potentiation of arginine-induced insulin release was less in non-obese T2D than in controls and associated with impaired beta-cell sensitivity to glucose (PG50 ). Glucose 39-46 insulin Homo sapiens 80-87 32017362-4 2020 RESULTS: The acute insulin response to glucose potentiation of arginine-induced insulin release was less in non-obese T2D than in controls and associated with impaired beta-cell sensitivity to glucose (PG50 ). Glucose 193-200 insulin Homo sapiens 19-26 32017362-4 2020 RESULTS: The acute insulin response to glucose potentiation of arginine-induced insulin release was less in non-obese T2D than in controls and associated with impaired beta-cell sensitivity to glucose (PG50 ). Glucose 193-200 insulin Homo sapiens 80-87 32017362-7 2020 CONCLUSIONS: In non-obese T2D, insulin secretory defects predominate with impaired beta-cell sensitivity to glucose and proinsulin processing in the absence of insulin resistance. Glucose 108-115 insulin Homo sapiens 31-38 32381586-0 2020 Instability of Insulin Aspart Diluted in Dextrose. Glucose 41-49 insulin Homo sapiens 15-22 32354857-6 2020 Maternal WSD reduced insulin-stimulated glucose uptake and impaired insulin signaling at the level of Akt phosphorylation in fetal muscle. Glucose 40-47 insulin Homo sapiens 21-28 32354857-7 2020 In juvenile offspring, insulin-stimulated glucose uptake was similarly reduced by both maternal and post-weaning WSD and corresponded to modest reductions in insulin-stimulated Akt phosphorylation relative to controls. Glucose 42-49 insulin Homo sapiens 23-30 32354857-7 2020 In juvenile offspring, insulin-stimulated glucose uptake was similarly reduced by both maternal and post-weaning WSD and corresponded to modest reductions in insulin-stimulated Akt phosphorylation relative to controls. Glucose 42-49 insulin Homo sapiens 158-165 32354857-8 2020 We conclude that maternal WSD leads to a persistent decrease in offspring muscle insulin-stimulated glucose uptake even in the absence of increased offspring adiposity or markers of systemic insulin resistance. Glucose 100-107 insulin Homo sapiens 81-88 32356104-10 2020 We showed that elevated blood glucose in the CC strains was not due to insulin resistance nor obesity but resulted from reduced insulin secretion. Glucose 30-37 insulin Homo sapiens 128-135 32385603-0 2020 Insulin sensitivity depends on the route of glucose administration. Glucose 44-51 insulin Homo sapiens 0-7 32385603-2 2020 Our goal was to study whether routes and dose of glucose administration have an acute impact on insulin sensitivity. Glucose 49-56 insulin Homo sapiens 96-103 32385603-3 2020 The primary endpoint of this proof-of-concept study was the difference in insulin-mediated metabolic clearance rate (MCR/I) of glucose between the oral and intravenous routes of glucose administration. Glucose 127-134 insulin Homo sapiens 74-81 32385603-3 2020 The primary endpoint of this proof-of-concept study was the difference in insulin-mediated metabolic clearance rate (MCR/I) of glucose between the oral and intravenous routes of glucose administration. Glucose 178-185 insulin Homo sapiens 74-81 32385603-15 2020 Insulin clearance was significantly higher when glucose was infused rather than ingested (2.53 +- 0.82 vs 2.16 +- 0.49 l/min in intravenous and oral procedure, respectively, p = 0.006). Glucose 48-55 insulin Homo sapiens 0-7 33534727-5 2020 DATA EXTRACTION: The main outcome of interest was the change in insulin sensitivity, derived from the gold standard hyperinsulinemic-euglycemic clamp or the Matsuda index derived from the oral glucose tolerance test and insulin sensitivity index from intravenous glucose tolerance test. Glucose 193-200 insulin Homo sapiens 64-71 32172486-3 2020 One of diabetic cases is caused by insulin resistance and changing the homeostasis of blood glucose control so glucose concentration stood beyond normal rate (hyperglycemia). Glucose 92-99 insulin Homo sapiens 35-42 32580152-8 2020 Notably, changes in the GIR after SGLT2 inhibitor administration, which indicated improvement in peripheral insulin sensitivity, were negatively correlated with T2DM duration and positively with reduction in fluctuation of daily plasma glucose profiles before and after treatment. Glucose 236-243 insulin Homo sapiens 108-115 32073747-8 2020 Our findings provide a helpful understanding of the toxic effects posed by MC-LR on the glucose metabolism of liver via interference with the INS signaling pathway. Glucose 88-95 insulin Homo sapiens 142-145 32299062-4 2020 Treatment challenges include the opposing effects of insulin and glucocorticoids on glucose homeostasis, and the need to balance and synchronize these two treatments. Glucose 84-91 insulin Homo sapiens 53-60 32568924-1 2020 The glucose transporter GLUT4 is critical for skeletal muscle glucose uptake in response to insulin and muscle contraction/exercise. Glucose 4-11 insulin Homo sapiens 92-99 32568924-1 2020 The glucose transporter GLUT4 is critical for skeletal muscle glucose uptake in response to insulin and muscle contraction/exercise. Glucose 62-69 insulin Homo sapiens 92-99 33107450-1 2020 Background: Omentin is an adipocytokine secreted by visceral adipose tissue cells associated with the action of insulin-increasing, insulin-facilitated glucose uptake. Glucose 152-159 insulin Homo sapiens 132-139 32247531-4 2020 Using insulin-dextrose infusions to induce HE, we conducted four experiments to determine (1) how insulin infusion duration, dose, and presence of insulin resistance affect MBFR response; and (2) the effect of an insulin-dextrose infusion given immediately following revascularization of STEMI on myocardial perfusion. Glucose 14-22 insulin Homo sapiens 6-13 32247531-10 2020 Experiment 3 (insulin resistance): five metabolic syndrome and six type 2 diabetes (T2DM) participants received 1.5 mU/kg/minute of insulin-dextrose for 60 minutes. Glucose 140-148 insulin Homo sapiens 132-139 32247531-14 2020 RESULTS: Experiment 1: MBFR increased with time through to 120 minutes in the insulin-dextrose group and did not change in controls. Glucose 86-94 insulin Homo sapiens 78-85 32311037-12 2020 RESULTS: Insulin enhances glucose uptake in human BMAT. Glucose 26-33 insulin Homo sapiens 9-16 32461034-2 2020 While a reasonable glycemic control prevents complications, inadvertent intramuscular (IM) insulin injection results in hypoglycemia and fluctuations of blood glucose levels. Glucose 159-166 insulin Homo sapiens 91-98 32382759-2 2020 Enhanced beta-cell glucose responsivity contributes to insulin hypersecretion. Glucose 19-26 insulin Homo sapiens 55-62 32382742-0 2020 Adipocyte Insulin Resistance in PCOS: Relationship With GLUT-4 Expression and Whole-Body Glucose Disposal and beta-Cell Function. Glucose 89-96 insulin Homo sapiens 10-17 32020726-0 2020 The Shape of the Glucose Response Curve during an Oral Glucose Tolerance Test Is Associated with Insulin Clearance and Muscle Insulin Sensitivity in Healthy Nonobese Men. Glucose 17-24 insulin Homo sapiens 97-104 31777280-2 2020 In this pilot study we evaluated the use of the glucose telemetry system (GTS) using CGM technology and remote monitoring to prevent inpatient hypoglycemia in high-risk insulin-treated patients with type 2 diabetes (DM2). Glucose 48-55 insulin Homo sapiens 169-176 32020726-0 2020 The Shape of the Glucose Response Curve during an Oral Glucose Tolerance Test Is Associated with Insulin Clearance and Muscle Insulin Sensitivity in Healthy Nonobese Men. Glucose 17-24 insulin Homo sapiens 126-133 32090456-5 2020 RESULTS: We first observed a greater insulin response in islets from obese donors under both basal and high glucose conditions, confirming their hyperresponsiveness to glucose. Glucose 108-115 insulin Homo sapiens 37-44 32090456-5 2020 RESULTS: We first observed a greater insulin response in islets from obese donors under both basal and high glucose conditions, confirming their hyperresponsiveness to glucose. Glucose 168-175 insulin Homo sapiens 37-44 32090456-6 2020 When islets from obese donors were cultured in the presence of moderate or severe glucose concentrations, insulin response to glucose remained unchanged or was slighly reduced, as opposite to that observed in lean subjects. Glucose 82-89 insulin Homo sapiens 106-113 32090456-6 2020 When islets from obese donors were cultured in the presence of moderate or severe glucose concentrations, insulin response to glucose remained unchanged or was slighly reduced, as opposite to that observed in lean subjects. Glucose 126-133 insulin Homo sapiens 106-113 32090456-7 2020 Moreover, culture of islets from obese donors with high palmitate also induced a less reduction in insulin response to glucose than in lean subjects. Glucose 119-126 insulin Homo sapiens 99-106 32691685-10 2020 Multiple linear regression analysis showed that body mass index, glucose at 0 minutes, and SIBO were independently associated with the early-phase and total-phase insulin secretion. Glucose 65-72 insulin Homo sapiens 163-170 32376986-1 2020 The ATP-sensitive potassium channel (KATP channel) couples blood levels of glucose to insulin secretion from pancreatic beta-cells. Glucose 75-82 insulin Homo sapiens 86-93 32028458-3 2020 Insulin sensitivity (ISI) was estimated by oral glucose tolerance test using the Soonthorpun model. Glucose 48-55 insulin Homo sapiens 0-7 32371087-6 2020 Ghrelin exerted a glucose-dependent insulin-suppressing effect in islets from both T2D and non-T2D donors. Glucose 18-25 insulin Homo sapiens 36-43 32314178-2 2020 Insulin resistance or dysfunction of insulin signaling is a universal feature of T2D, the main culprit for altered glucose metabolism and its interdependence on cell death pathways, forming the basis of linking T2D with AD as it may exacerbate Abeta accumulation, tau hyperphosphorylation and devastates glucose transportation, energy metabolism, hippocampal framework and promulgate inflammatory pathways. Glucose 115-122 insulin Homo sapiens 0-7 32314178-2 2020 Insulin resistance or dysfunction of insulin signaling is a universal feature of T2D, the main culprit for altered glucose metabolism and its interdependence on cell death pathways, forming the basis of linking T2D with AD as it may exacerbate Abeta accumulation, tau hyperphosphorylation and devastates glucose transportation, energy metabolism, hippocampal framework and promulgate inflammatory pathways. Glucose 115-122 insulin Homo sapiens 37-44 32483339-1 2020 Human insulin and its current therapeutic analogs all show propensity, albeit varyingly, to self-associate into dimers and hexamers, which delays their onset of action and makes blood glucose management difficult for people with diabetes. Glucose 184-191 insulin Homo sapiens 6-13 32141687-7 2020 Insulin resistance (fasting insulin and HOMA-index of insulin resistance) in early pregnancy was an important predictor for boys" sum of skinfolds, in addition to fasting glucose and maternal adiposity (leptin, BMI and neck circumference) throughout pregnancy. Glucose 171-178 insulin Homo sapiens 0-7 32618430-4 2020 Highly blood perfused islets had superior function and lower glucose threshold for insulin release when compared with other islets. Glucose 61-68 insulin Homo sapiens 83-90 32618430-8 2020 In human subjects, differences in glucose threshold for insulin (C-peptide) secretion was evaluated in individuals recently diagnosed for type 1 diabetes and compared to control subjects. Glucose 34-41 insulin Homo sapiens 56-63 32618430-9 2020 A preferential loss of capacity for insulin release in response to low glucose concentrations was observed at debut of type 1 diabetes. Glucose 71-78 insulin Homo sapiens 36-43 32618430-10 2020 Our study indicates that highly blood perfused islets with direct venous drainage and lower glucose threshold for insulin release are of great importance for normal glucose homeostasis. Glucose 92-99 insulin Homo sapiens 114-121 32618430-10 2020 Our study indicates that highly blood perfused islets with direct venous drainage and lower glucose threshold for insulin release are of great importance for normal glucose homeostasis. Glucose 165-172 insulin Homo sapiens 114-121 31831356-4 2020 Residing in the islets of Langerhans, pancreatic beta cell serves as a central mediator in glucose homeostasis through secreting insulin, the only hormone that could reduce glucose level in the body, into the blood. Glucose 91-98 insulin Homo sapiens 129-136 32134347-6 2020 Insulin sensitivity was measured as the insulin sensitivity index (SI) modelled from IVGTT in cohort I, and in II as total glucose disposal (TGD) estimated from a euglycaemic-hyperinsulinaemic clamp. Glucose 123-130 insulin Homo sapiens 0-7 31831356-4 2020 Residing in the islets of Langerhans, pancreatic beta cell serves as a central mediator in glucose homeostasis through secreting insulin, the only hormone that could reduce glucose level in the body, into the blood. Glucose 173-180 insulin Homo sapiens 129-136 32057664-1 2020 Beta cells assume a fundamental role in maintaining blood glucose homeostasis through the secretion of insulin, which is contingent on both beta cell mass and function, in response to elevated blood glucose levels or secretagogues. Glucose 58-65 insulin Homo sapiens 103-110 32057664-1 2020 Beta cells assume a fundamental role in maintaining blood glucose homeostasis through the secretion of insulin, which is contingent on both beta cell mass and function, in response to elevated blood glucose levels or secretagogues. Glucose 199-206 insulin Homo sapiens 103-110 32417220-1 2020 beta cells uniquely produce and secrete insulin under the control of several, integrated signals, to maintain blood glucose concentrations within a narrow physiological interval. Glucose 116-123 insulin Homo sapiens 40-47 32085965-2 2020 The major physiological insulin secretagogue, glucose, triggers [Ca2+]cyt oscillations in beta cells. Glucose 46-53 insulin Homo sapiens 24-31 32629825-1 2020 A closed-loop system imitating the function of pancreatic cells, connected to microneedles (MNs) that automatically "release" insulin in response to the blood glucose (BG) levels would be highly satisfactory for improving the quality of life and health for diabetes patients. Glucose 159-166 insulin Homo sapiens 126-133 28722947-3 2022 The complex balance of glucose is affected by food, insulin doses, body stresses, exercise, and dozens of other factors. Glucose 23-30 insulin Homo sapiens 52-59 32629825-2 2020 This paper describes an easy, fast and simple technique of coating a porous polymer layer on stainless steel (SS) MNs that release insulin in a glucose-responsive fashion. Glucose 144-151 insulin Homo sapiens 131-138 32629825-7 2020 These MNs demonstrated both in vitro (in porcine skin and PBS) and in vivo (in diabetic rats) glucose-mediated insulin release under hyperglycemic conditions with rapid responsiveness. Glucose 94-101 insulin Homo sapiens 111-118 32629825-8 2020 This study validated that the release of insulin from porous MNs was effectively correlated with glucose concentration. Glucose 97-104 insulin Homo sapiens 41-48 32323986-7 2020 Finally, effect of designed peptides on insulin activity was quantified using a spectrophotometric assay for glucose uptake by HepG2 cells. Glucose 109-116 insulin Homo sapiens 40-47 32622342-6 2020 IPCs differentiated from GDM-iPSCs also had lower total insulin content and a lower capacity for insulin secretion to glucose stimulation compared to their normal-iPSC counterparts. Glucose 118-125 insulin Homo sapiens 97-104 33345051-6 2020 Adipose tissue glucose uptake was assessed by positron emission tomography/computed tomography (PET/CT) by the glucose analog [18F]fluorodeoxyglucose ([18F]FDG) during continuous insulin infusion (40 mU m-2 min-1). Glucose 15-22 insulin Homo sapiens 179-186 32552001-0 2021 Practical Approach to Using Trend Arrows on Real-Time Continuous Glucose Monitoring System in Type 1 Diabetes Adolescents Living Camp Setting Treated With Multiple Daily Injection or Continuous Subcutaneous Insulin Infusion Insulin Therapy. Glucose 65-72 insulin Homo sapiens 224-231 32560352-1 2020 BACKGROUND: Intercellular communication mediated by cationic fluxes through the Connexin family of gap junctions regulates glucose-stimulated insulin secretion and beta cell defense against inflammatory stress. Glucose 123-130 insulin Homo sapiens 142-149 32385603-16 2020 The efficacy of insulin in inhibiting lipolysis and proteolysis was decreased after oral glucose loads. Glucose 89-96 insulin Homo sapiens 16-23 32385603-18 2020 CONCLUSIONS/INTERPRETATION: Our study shows that insulin sensitivity depends on the route of glucose administration, the oral route leading to increased insulin secretion and compensatory insulin resistance compared with the intravenous route. Glucose 93-100 insulin Homo sapiens 49-56 32385603-18 2020 CONCLUSIONS/INTERPRETATION: Our study shows that insulin sensitivity depends on the route of glucose administration, the oral route leading to increased insulin secretion and compensatory insulin resistance compared with the intravenous route. Glucose 93-100 insulin Homo sapiens 153-160 32385603-18 2020 CONCLUSIONS/INTERPRETATION: Our study shows that insulin sensitivity depends on the route of glucose administration, the oral route leading to increased insulin secretion and compensatory insulin resistance compared with the intravenous route. Glucose 93-100 insulin Homo sapiens 153-160 32385603-19 2020 The efficacy of insulin in blocking lipolysis and protein breakdown is lower after oral glucose loads vs the intravenous route. Glucose 88-95 insulin Homo sapiens 16-23 32385603-20 2020 Our findings suggest that, while the glucose-mediated incretin release is followed by an increase in insulin release, the effect of the released insulin is limited by an increase in insulin resistance. Glucose 37-44 insulin Homo sapiens 101-108 32394228-1 2020 AIMS/HYPOTHESIS: Treatment of diabetes secondary to total pancreatectomy remains a challenge and insulin constitutes the only glucose-lowering treatment for these patients. Glucose 126-133 insulin Homo sapiens 97-104 32676581-1 2020 A cascade of highly regulated biochemical processes connects glucose stimulation to insulin secretion in specialized cells of mammalian pancreas, the beta-cells. Glucose 61-68 insulin Homo sapiens 84-91 33345051-10 2020 Insulin-stimulated glucose uptake, assessed by [18F]FDG-uptake during PET/CT, was similar in pre- and post-menopausal women in abdominal, gluteal, and femoral adipose tissue depots, despite skeletal muscle insulin resistance in post- compared to pre-menopausal women in the same cohort. Glucose 19-26 insulin Homo sapiens 0-7 33345051-11 2020 Insulin-stimulated glucose uptake in adipose tissue depots was not changed after 3 months of high-intensity exercise training, but insulin sensitivity was higher in visceral compared to subcutaneous adipose tissue depots (~139%). Glucose 19-26 insulin Homo sapiens 0-7 32508185-6 2020 In endothelial cells from patients with T2DM, normal glucose conditions (24 hours at 5 mmol/L) lowered O-GlcNAc levels and restored insulin-mediated activation of endothelial nitric oxide synthase, whereas high glucose conditions (30 mmol/L) maintained both O-GlcNAc levels and impaired insulin action. Glucose 53-60 insulin Homo sapiens 132-139 32508185-7 2020 Treatment of endothelial cells with Thiamet G, an O-GlcNAcase inhibitor, increased O-GlcNAc levels and blunted the improvement of insulin-mediated endothelial nitric oxide synthase phosphorylation by glucose normalization. Glucose 200-207 insulin Homo sapiens 130-137 32532930-1 2020 Proinsulin, insulin and proinsulin/insulin (P/I) ratio have been reported to be correlated with fasting plasma glucose (FPG) and Hemoglobin A1c (HbA1c) in whole population study therefore sensitive predictors of T2D progression. Glucose 111-118 insulin Homo sapiens 0-10 32546151-4 2020 The index of homeostasis model assessment insulin resistance (HOMA-IR) was calculated from insulin and glucose. Glucose 103-110 insulin Homo sapiens 42-49 32224027-2 2020 Insulin therapy for type 1 DM (DM1) can achieve overall blood glucose control, but glycemic variations can occur during injection intervals, which may contribute to some complications. Glucose 62-69 insulin Homo sapiens 0-7 32534586-1 2020 BACKGROUND: The triglyceride-glucose index (TyG index) has been regarded as a reliable alternative marker of insulin resistance and an independent predictor of cardiovascular outcomes. Glucose 29-36 insulin Homo sapiens 109-116 32587797-11 2020 Moreover, the highest ROS and the lowest insulin secretion were found in FAC combined with IL-1beta and TNF-alpha in the high-glucose condition of human pancreatic beta cell, which could be involved in the mechanism of DM development in beta-thalassemia patients. Glucose 126-133 insulin Homo sapiens 41-48 32532930-1 2020 Proinsulin, insulin and proinsulin/insulin (P/I) ratio have been reported to be correlated with fasting plasma glucose (FPG) and Hemoglobin A1c (HbA1c) in whole population study therefore sensitive predictors of T2D progression. Glucose 111-118 insulin Homo sapiens 3-10 32532930-1 2020 Proinsulin, insulin and proinsulin/insulin (P/I) ratio have been reported to be correlated with fasting plasma glucose (FPG) and Hemoglobin A1c (HbA1c) in whole population study therefore sensitive predictors of T2D progression. Glucose 111-118 insulin Homo sapiens 24-34 32532930-1 2020 Proinsulin, insulin and proinsulin/insulin (P/I) ratio have been reported to be correlated with fasting plasma glucose (FPG) and Hemoglobin A1c (HbA1c) in whole population study therefore sensitive predictors of T2D progression. Glucose 111-118 insulin Homo sapiens 12-19 32587566-1 2020 Background: The triglyceride glucose index (TyG index) has been proposed as a simple and credible surrogate marker of insulin resistance. Glucose 29-36 insulin Homo sapiens 118-125 33479589-2 2021 The patient"s intravenous glucose tolerance test indicated marked reductions in insulin sensitivity and endogenous insulin secretion. Glucose 26-33 insulin Homo sapiens 80-87 33479589-2 2021 The patient"s intravenous glucose tolerance test indicated marked reductions in insulin sensitivity and endogenous insulin secretion. Glucose 26-33 insulin Homo sapiens 115-122 32373901-5 2020 This platform showed good biocompatibility against insulin-secreting cells and presented glucose-dependent insulin release behaviour. Glucose 89-96 insulin Homo sapiens 51-58 32581820-6 2020 Insulin sensitivity was evaluated by measuring insulin-stimulated Akt T308 phosphorylation and glucose uptake. Glucose 95-102 insulin Homo sapiens 0-7 32526875-3 2020 Activation by ABA of AMP-dependent kinase (AMPK), in contrast to the insulin-induced activation of AMPK-inhibiting Akt, is responsible for stimulation of GLUT4-mediated muscle glucose uptake, and for the browning effect on white adipocytes. Glucose 176-183 insulin Homo sapiens 69-76 32373901-5 2020 This platform showed good biocompatibility against insulin-secreting cells and presented glucose-dependent insulin release behaviour. Glucose 89-96 insulin Homo sapiens 107-114 32617449-7 2020 Results: PG levels as well as IRI and Pro levels 60 and 120 minutes after glucose-loading increased incrementally with deteriorating glucose tolerance. Glucose 74-81 insulin Homo sapiens 38-41 32655618-7 2020 Glucose-stimulated insulin secretion was assessed by enzyme-linked immunosorbent assay (ELISA). Glucose 0-7 insulin Homo sapiens 19-26 32655618-12 2020 ELISA analysis confirmed that glucose-stimulated insulin secretion was less efficient after transfection with the three pTFs alone. Glucose 30-37 insulin Homo sapiens 49-56 32248978-1 2020 Glucose mediated insulin biosynthesis is tightly regulated and shared between insulin granule proteins such as its processing enzymes, prohormone convertases, PC1/3 and PC2. Glucose 0-7 insulin Homo sapiens 17-24 32248978-1 2020 Glucose mediated insulin biosynthesis is tightly regulated and shared between insulin granule proteins such as its processing enzymes, prohormone convertases, PC1/3 and PC2. Glucose 0-7 insulin Homo sapiens 78-85 32617449-7 2020 Results: PG levels as well as IRI and Pro levels 60 and 120 minutes after glucose-loading increased incrementally with deteriorating glucose tolerance. Glucose 133-140 insulin Homo sapiens 38-41 32517068-3 2020 Frequent insulin titrations are needed to adequately manage glucose, however, provider adjustments are typically made every several months. Glucose 60-67 insulin Homo sapiens 9-16 33479588-6 2021 His blood glucose level improved with insulin therapy after discontinuation of the ceritinib. Glucose 10-17 insulin Homo sapiens 38-45 31968186-2 2020 Methods: GlucoStabilizer calculates the dose of IV insulin required to reach a prescribed target glucose range. Glucose 97-104 insulin Homo sapiens 51-58 32286881-1 2020 Oral glucose ingestion leads to impaired muscle microvascular blood flow (MBF), which may contribute to acute hyperglycemia-induced insulin resistance. Glucose 5-12 insulin Homo sapiens 132-139 32149451-12 2020 CONCLUSIONS: This pilot study suggested that SZC with insulin and glucose may provide an incremental benefit in the emergency treatment of hyperkalemia over insulin and glucose alone. Glucose 169-176 insulin Homo sapiens 54-61 32031745-7 2020 Both shielded RI and HI show higher viability and increased glucose-stimulated insulin secretion after exposure to hypoxia in vitro compared to control islets. Glucose 60-67 insulin Homo sapiens 79-86 32045699-6 2020 We analyzed the lipid kinetics of palmitic acid (PA) in hepatoma liver cells cultured in vitro in which insulin resistance has been induced by high glucose supplementation. Glucose 148-155 insulin Homo sapiens 104-111 31833019-1 2020 Hemoglobin A1c (HbA1c) is a reliable marker of insulin resistance in normal glucose tolerance patients; however, several physiological, environmental, and genetic factors may affect HbA1c and cause false results. Glucose 76-83 insulin Homo sapiens 47-54 31840936-13 2020 CONCLUSION: Insulin Resistance is significantly associated with BMI and synovitis in RA, suggesting distinct interplay between glucose availability and inflammation in RA. Glucose 127-134 insulin Homo sapiens 12-19 32171728-1 2020 Insulin, produced by pancreatic beta-cells, is responsible for the control of whole-body glucose metabolism. Glucose 89-96 insulin Homo sapiens 0-7 32171728-2 2020 Insulin is secreted by pancreatic beta-cells in a tightly regulated process that is controlled by the serum level of glucose, glucose sensing and glucose oxidative metabolism. Glucose 117-124 insulin Homo sapiens 0-7 32171728-2 2020 Insulin is secreted by pancreatic beta-cells in a tightly regulated process that is controlled by the serum level of glucose, glucose sensing and glucose oxidative metabolism. Glucose 126-133 insulin Homo sapiens 0-7 32171728-2 2020 Insulin is secreted by pancreatic beta-cells in a tightly regulated process that is controlled by the serum level of glucose, glucose sensing and glucose oxidative metabolism. Glucose 126-133 insulin Homo sapiens 0-7 32711830-3 2020 There is consensus regarding the maintenance of intraoperative glucose levels below 10.0 mM through the use of subcutaneous or intravenous insulin, and over the avoidance of aggressive strategies in order to minimize the risk of hypoglycemia. Glucose 63-70 insulin Homo sapiens 139-146 32291276-6 2020 Dimercaptosuccinic acid capsules were prescribed and memory recovered to some extent, which was accompanied by decreased insulin dosage for glucose control by 5 units. Glucose 140-147 insulin Homo sapiens 121-128 32546549-11 2020 Finally, people with T2D on insulin should always be encouraged to have oral glucose and rescue medication immediately available. Glucose 77-84 insulin Homo sapiens 28-35 32017152-7 2020 Among the individuals who received statin therapy, those with and without dyslipidemia showed significantly decreased LDL-C levels (all P < .0001) and significantly increased fasting plasma insulin levels (Delta = +24.1%, P = .0230; Delta = +30.1%, P < .0001); however, their glycated haemoglobin A1c and fasting blood glucose levels did not change (all P > .05). Glucose 319-326 insulin Homo sapiens 190-197 32048396-6 2020 RESULTS: After 12 weeks, a greater reduction in mean CGM glucose from baseline was observed in the vildagliptin-insulin group compared with the insulin-only group, although the between-treatment difference was not statistically significant (mean difference [CI 95%]: -0.96 mmol/L [-2.09; 0.18] vs. -0.29 mmol/L [-1.29; 0.76], P = 0.32). Glucose 57-64 insulin Homo sapiens 112-119 32312867-6 2020 In shATGL pseudoislets, biphasic glucose-stimulated insulin secretion (GSIS), and insulin secretion to 3-isobutyl-1-methylxanthine and KCl were all reduced without altering oxygen consumption rate compared with scramble control. Glucose 33-40 insulin Homo sapiens 52-59 32413380-5 2020 Utilizing intravenous insulin to normalize plasma glucose levels in the acute phase of a stroke does not improve the outcome. Glucose 50-57 insulin Homo sapiens 22-29 32383989-7 2020 Shared glucose data through CGM facilitated frequent insulin dose adjustments, increased fluid and carbohydrate intake, and prevented hospital admissions in both cases. Glucose 7-14 insulin Homo sapiens 53-60 32410184-2 2020 Insulin, the first medication to be discovered for diabetes, is still the safest and most potent glucose-lowering therapy. Glucose 97-104 insulin Homo sapiens 0-7 32484751-7 2020 We evaluated glucose metabolism disorders as a potential modifier by comparing associations between participants with high vs. low average fasting blood glucose (FBG) and homeostasis model assessment insulin resistance (HOMA-IR) levels. Glucose 13-20 insulin Homo sapiens 200-207 32243891-10 2020 Under high glucose stimulation, the overexpression of PDX-1 alone restored the insulin secretion which was inhibited by the simultaneous overexpression of MALAT1 and PDX-1. Glucose 11-18 insulin Homo sapiens 79-86 32243891-11 2020 Under high glucose and IL-1beta stimulation, the simultaneous knockdown of MALAT1 and PDX-1 reduced the enhancement of the insulin secretion which was raised by knocking down MALAT1 alone. Glucose 11-18 insulin Homo sapiens 123-130 32307751-4 2020 Compared to islets cultured on tissue culture plastic (TCP), islets cultured on 3D-ECM exhibited greater attachment, higher survival rate, increased insulin content, and enhanced glucose-stimulated insulin secretion. Glucose 179-186 insulin Homo sapiens 198-205 32140727-7 2020 Insulin sensitivity was derived from oral glucose tolerance testing (ISOGTT). Glucose 42-49 insulin Homo sapiens 0-7 32219330-7 2020 Overall, holoTC neither associated with fasting nor glucose-stimulated beta-cell function and insulin-stimulated glucose disposal. Glucose 113-120 insulin Homo sapiens 94-101 32232327-2 2020 OBJECTIVE: To identify the molecular mechanisms underlying electroacupuncture-induced glucose uptake in skeletal muscle in insulin-resistant overweight/obese women with and without polycystic ovary syndrome (PCOS). Glucose 86-93 insulin Homo sapiens 123-130 32253041-0 2020 Identification of novel peptides from goat milk casein that ameliorate high-glucose-induced insulin resistance in HepG2 cells. Glucose 76-83 insulin Homo sapiens 92-99 32253041-2 2020 From the obtained hydrolysates, we also purified and characterized novel peptides that ameliorated high-glucose-induced insulin resistance in HepG2 cells. Glucose 104-111 insulin Homo sapiens 120-127 32253041-3 2020 The 3-h hydrolysate caused the highest glucose consumption rate in insulin-resistant HepG2 cells. Glucose 39-46 insulin Homo sapiens 67-74 32253041-7 2020 Our findings indicated that specific bioactive peptides from goat milk casein hydrolysates ameliorated insulin resistance in HepG2 cells that had been treated with high glucose. Glucose 169-176 insulin Homo sapiens 103-110 32303406-4 2020 Changes in patient insulin dose were made at clinic visit based on their self-monitored glucose (SMG) data. Glucose 88-95 insulin Homo sapiens 19-26 30189765-10 2020 Frequent monitoring of serum potassium and glucose after administration of insulin is necessary to confirm adequate response and avoidance of hypoglycemia. Glucose 43-50 insulin Homo sapiens 75-82 32285997-6 2020 Compared with HepG2 spheroids, rPH spheroids indicate stronger glucose metabolism abilities in terms of glucose consumption, intracellular glycogen content, gluconeogenesis rate and sensitivity to glucose modulator hormones like insulin and glucagon. Glucose 63-70 insulin Homo sapiens 229-236 32060407-4 2020 Depletion of Wfs1 in vivo and in vitro causes functional defects in glucose-stimulated insulin secretion and insulin content, triggering Chop-mediated apoptotic pathways. Glucose 68-75 insulin Homo sapiens 87-94 32445739-3 2020 Current findings from human research suggest that boosting central insulin action in the brain modulates peripheral metabolism, enhancing whole-body insulin sensitivity and suppressing endogenous glucose production. Glucose 196-203 insulin Homo sapiens 67-74 32087490-1 2020 Diabetes is a metabolic condition associated with hyperglycemia manifested by the elevation of blood glucose levels occurring when the pancreas decreases or stops the production of insulin, in case of insulin resistance or both. Glucose 101-108 insulin Homo sapiens 181-188 32087490-1 2020 Diabetes is a metabolic condition associated with hyperglycemia manifested by the elevation of blood glucose levels occurring when the pancreas decreases or stops the production of insulin, in case of insulin resistance or both. Glucose 101-108 insulin Homo sapiens 201-208 31994004-9 2020 The homeostasis model assessment index of insulin resistance (HOMA-IR) was calculated (plasma glucose (mmol/L) x insulin (muU/mL)/22.5). Glucose 94-101 insulin Homo sapiens 42-49 32439332-7 2020 The serum glucose level (SGL) was used to reflect insulin resistance. Glucose 10-17 insulin Homo sapiens 50-57 32547147-6 2020 Adipsin is one of the adipokines secreted by adipose tissues which is involved in maintaining adipose tissue homeostasis and increasing insulin secretion in response to glucose. Glucose 169-176 insulin Homo sapiens 136-143 32462459-10 2020 The long-term ability to control the blood glucose level might help to reduce the daily frequency of insulin injections. Glucose 43-50 insulin Homo sapiens 101-108 32460030-2 2020 Human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) are differentiated to beta cells (SC-beta cells) and mature to undergo glucose-stimulated insulin secretion, but molecular regulation of this defining beta cell phenotype is unknown. Glucose 156-163 insulin Homo sapiens 175-182 32460030-4 2020 Knockdown (KD) or knockout (KO) of SIX2 in SC-beta cells drastically limits glucose-stimulated insulin secretion in both static and dynamic assays, along with the upstream processes of cytoplasmic calcium flux and mitochondrial respiration. Glucose 76-83 insulin Homo sapiens 95-102 33145563-5 2020 Our patient required a large amount of continuous glucose to maintain euglycemia for persistent intractable hypoglycemia induced by overdose of long-acting insulin. Glucose 50-57 insulin Homo sapiens 156-163 32447335-8 2020 Conclusion As a result, a plasma glucose concentration above or equal to 155 mg/dL at 1 h during an OGTT is associated with a worse clinical phenotype characterized by changes in insulin sensitivity and beta-cell function. Glucose 33-40 insulin Homo sapiens 179-186 32448382-7 2020 On the other hand, patients had lower average blood glucose readings (mg/dl) when they were on thrice daily insulin injections (161.4 +- 62.7) compared to twice daily regimen (166.0 +- 69.5), p < 0.05. Glucose 52-59 insulin Homo sapiens 108-115 32440803-1 2021 Type 1 diabetes (T1D) is a chronic illness that requires intensive lifelong management of blood glucose concentrations by means of external insulin administration. Glucose 96-103 insulin Homo sapiens 140-147 32109481-7 2020 When glucose is elevated above the threshold value, the oxidative fate of glucose in mitochondria is the main source of energy required for effective insulin secretion, i.e. the "aerobic switch". Glucose 5-12 insulin Homo sapiens 150-157 32109481-7 2020 When glucose is elevated above the threshold value, the oxidative fate of glucose in mitochondria is the main source of energy required for effective insulin secretion, i.e. the "aerobic switch". Glucose 74-81 insulin Homo sapiens 150-157 32430053-10 2020 RESULTS: Differentiated hiPSCs were 38.32% +- 3.54% insulin-positive cells and released insulin/C-peptide in response to glucose stimulus in a manner comparable to adult human islets. Glucose 121-128 insulin Homo sapiens 88-95 32429597-7 2020 In parallel, glucose stimulated insulin secretion was measured revealing a diminished insulin response after day 3 of culture. Glucose 13-20 insulin Homo sapiens 32-39 32429597-7 2020 In parallel, glucose stimulated insulin secretion was measured revealing a diminished insulin response after day 3 of culture. Glucose 13-20 insulin Homo sapiens 86-93 32429597-8 2020 Additionally, MEA spiking profiles were similar to the time course of insulin response when glucose concentration is switched from 1.1 to 16.7 mM. Glucose 92-99 insulin Homo sapiens 70-77 32429597-9 2020 Our analyses suggest that extracellular recordings of dissociated islet cells using MEA is an effective approach to rapidly assess islet functionality, and could supplement standard assays such as glucose stimulate insulin response. Glucose 197-204 insulin Homo sapiens 215-222 31399480-3 2020 Insulin sensitivity is notoriously variable in these babies and glucose control is time-consuming, with management requiring frequent changes of dextrose-containing fluids and careful monitoring of insulin treatment. Glucose 145-153 insulin Homo sapiens 0-7 32434238-2 2021 We sought to assess the insulin amount required to normalize glucose levels after a fat- and protein-rich meal (FPRM). Glucose 61-68 insulin Homo sapiens 24-31 32434238-7 2021 RESULTS: Glucose levels (median, mg/dL) 12-hour post-meal with 20% extra insulin vs. 40% vs. insulin dose for SM were 116 vs. 113 vs. 91. Glucose 9-16 insulin Homo sapiens 73-80 32434238-8 2021 Glucose-AUC over 12-hour post-meal with 20% extra insulin vs. 40% vs. insulin dose for SM was 1603 mg/dL/12 h vs. 1527 vs. 1400 (no significance). Glucose 0-7 insulin Homo sapiens 50-57 32434238-9 2021 Glucose levels in the target range with 20% extra insulin vs. 40% were 60% vs. 69% (p=0.1). Glucose 0-7 insulin Homo sapiens 50-57 32375679-9 2020 SLC2A9, that also facilitates glucose transport, has been implicated to enhance insulin secretion, however, the non-synonymous mutations found in SLC2A9 gene of this patient were not dysfunctional variants. Glucose 30-37 insulin Homo sapiens 80-87 32375783-1 2020 BACKGROUND: The triglyceride-glucose (TyG) index is a marker of insulin resistance (IR) and has been associated with various metabolic syndromes, cardiovascular diseases, and cerebrovascular diseases. Glucose 29-36 insulin Homo sapiens 64-71 32459554-6 2020 The insulin content, endocrine cellular composition, and differentiation of beta cells were significantly improved in PPIs cultured in IMM, which subsequently augmented their insulin secretory capacity in response to glucose challenge compared to control islets.Conclusions: Culturing PPIs in IMM increases islet yield, isolation index, viability, insulin content, endocrine cellular composition, differentiation of endocrine progenitor cells toward beta cells, and insulin secretion. Glucose 217-224 insulin Homo sapiens 175-182 32459554-6 2020 The insulin content, endocrine cellular composition, and differentiation of beta cells were significantly improved in PPIs cultured in IMM, which subsequently augmented their insulin secretory capacity in response to glucose challenge compared to control islets.Conclusions: Culturing PPIs in IMM increases islet yield, isolation index, viability, insulin content, endocrine cellular composition, differentiation of endocrine progenitor cells toward beta cells, and insulin secretion. Glucose 217-224 insulin Homo sapiens 175-182 32459554-6 2020 The insulin content, endocrine cellular composition, and differentiation of beta cells were significantly improved in PPIs cultured in IMM, which subsequently augmented their insulin secretory capacity in response to glucose challenge compared to control islets.Conclusions: Culturing PPIs in IMM increases islet yield, isolation index, viability, insulin content, endocrine cellular composition, differentiation of endocrine progenitor cells toward beta cells, and insulin secretion. Glucose 217-224 insulin Homo sapiens 175-182 30450993-3 2020 Insulin Resistance in PCOS patients ranges from 50% to 70% and may encourage OS by production of reactive oxygen species.Objective: Our study determines serum MDA levels along with plasma glucose, serum insulin, and insulin resistance in obese and nonobese PCOS subjects.Materials and methods: A case control study was conducted on diagnosed 100 PCOS patients and 100 controls. Glucose 188-195 insulin Homo sapiens 0-7 32643574-1 2020 Diabetes mellitus is a condition resulting from loss of production of insulin, or insufficient production/insulin resistance leading to high blood glucose levels. Glucose 147-154 insulin Homo sapiens 106-113 32477453-10 2020 So, a new blood glucose regulation system, effective in type 2 diabetes and its prediabetic phase, is based on variations in the acyl composition of phospholipids and operates independent of changes in insulin and glucose concentration. Glucose 16-23 insulin Homo sapiens 202-209 32402282-2 2020 Differentiation of SC-beta cells yields transplantable islets that secrete insulin in response to glucose challenges. Glucose 98-105 insulin Homo sapiens 75-82 32402282-4 2020 Here, we profile metabolism of SC-beta cells and islets to quantify their capacity to sense glucose and identify reduced anaplerotic cycling in the mitochondria as the cause of reduced glucose-stimulated insulin secretion in SC-beta cells. Glucose 185-192 insulin Homo sapiens 204-211 32393179-3 2020 Insulin resistance, the exposure, was defined by quartiles for three indexes: 1) the homeostatic model assessment of insulin resistance (HOMA-IR), 2) the triglyceride and glucose index (TyG), and 3) the triglyceride to high-density lipoprotein cholesterol ratio (TG/HDL-C). Glucose 171-178 insulin Homo sapiens 0-7 32393351-1 2020 BACKGROUND: The triglyceride and glucose index (TyG) has been proposed as a marker of insulin resistance. Glucose 33-40 insulin Homo sapiens 86-93 32397662-0 2020 Association between Frequency of Breakfast Consumption and Insulin Resistance Using Triglyceride-Glucose Index: A Cross-Sectional Study of the Korea National Health and Nutrition Examination Survey (2016-2018). Glucose 97-104 insulin Homo sapiens 59-66 32375022-3 2020 Here, we find that after birth beta cell function shifts from amino acid- to glucose-stimulated insulin secretion in correlation with the change in the nutritional environment. Glucose 77-84 insulin Homo sapiens 96-103 32255552-5 2020 Preweaned porcine islets are encapsulated in peptide-functionalized alginate microcapsules, and those encapsulated in RGD-functionalized alginate displays enhanced viability and glucose-stimulated insulin release. Glucose 178-185 insulin Homo sapiens 197-204 32505428-3 2020 Triglyceride-glucose (TyG) index has been proven useful in clinical studies for quantifying insulin resistance and for the early identification of individuals at T2D risk but still not applied by GPs for diagnostic purposes. Glucose 13-20 insulin Homo sapiens 92-99 32423964-0 2020 Insulin enhances renal glucose excretion: relation to insulin sensitivity and sodium-glucose cotransport. Glucose 23-30 insulin Homo sapiens 0-7 32423964-0 2020 Insulin enhances renal glucose excretion: relation to insulin sensitivity and sodium-glucose cotransport. Glucose 23-30 insulin Homo sapiens 54-61 32423964-7 2020 With insulin, whole-body glucose disposal rose more in controls than T2D (183 (48) vs 101 (48) micromol/kgFFM/min, p<0.0003). Glucose 25-32 insulin Homo sapiens 5-12 32423964-12 2020 Under these conditions, insulin still enhanced both glucose and sodium excretion. Glucose 52-59 insulin Homo sapiens 24-31 31307843-7 2020 Measures of insulin sensitivity by oral glucose tolerance testing were collected at baseline and 22 weeks. Glucose 40-47 insulin Homo sapiens 12-19 31465811-10 2020 Factors associated with regression to normal glucose levels and progression to diabetes were age, body mass index, and insulin resistance. Glucose 45-52 insulin Homo sapiens 119-126 31930670-1 2020 The class of rapid-acting insulin analogues were introduced more than 20 years ago to better control postprandial plasma glucose (PPG) excursions than unmodified regular human insulin (RHI). Glucose 121-128 insulin Homo sapiens 26-33 30114722-1 2020 Diabetes type 1 (T1D) is a common autoimmune disease characterized by permanent destruction of the insulin-secreting beta-cells in pancreatic islets, resulting in a deficiency of the glucose-lowering hormone insulin and persisting high blood glucose levels. Glucose 183-190 insulin Homo sapiens 99-106 32390400-0 2020 Increased Intact Proinsulin in the Oral Glucose Challenge Sample is an Early Indicator for Future Type 2 Diabetes Development - Case Reports and Evidence from the Literature. Glucose 40-47 insulin Homo sapiens 17-27 32390400-3 2020 This has raised the question as to whether a marked increase in intact proinsulin levels after oral glucose load in healthy subjects might be considered as indicative for beta-cell dysfunction and prediabetes. Glucose 100-107 insulin Homo sapiens 71-81 32390400-4 2020 METHODS: A previous study from 2011 examined, inter alia, intact proinsulin levels in blood samples from twenty healthy study participants at baseline and two hours after an oral glucose tolerance test (OGTT) with 75 g glucose. Glucose 179-186 insulin Homo sapiens 65-75 32390400-4 2020 METHODS: A previous study from 2011 examined, inter alia, intact proinsulin levels in blood samples from twenty healthy study participants at baseline and two hours after an oral glucose tolerance test (OGTT) with 75 g glucose. Glucose 219-226 insulin Homo sapiens 65-75 31724878-3 2020 METHODS: Insulin-treated adults with diabetes and an episode of clinically significant biochemical hypoglycemia (blood glucose (BG) <3.0 mmol/L) or symptomatic hypoglycaemia and BG <4.0 mmol/L were randomized to six months of isCGM (intensive group) or SMBG (control group) against a background of usual care. Glucose 119-126 insulin Homo sapiens 9-16 32119099-1 2020 CONTEXT/OBJECTIVE: In insulin resistant subjects, hyperinsulinemia is a key compensatory mechanism, aimed at maintaining glucose homeostasis. Glucose 121-128 insulin Homo sapiens 22-29 31369389-1 2020 Hypoglycemia or low blood glucose is the most feared complication of insulin treatment of diabetes. Glucose 26-33 insulin Homo sapiens 69-76 31536025-5 2020 The proposed approach is able to predict whether overnight blood glucose concentrations are going to remain within or outside the target range, and therefore allows the user to take the appropriate preventive action (snack or change in basal insulin). Glucose 65-72 insulin Homo sapiens 242-249 32027066-2 2020 These genes encode the subunits of the beta-cell ATP sensitive potassium channel, a key component of the glucose-stimulated insulin secretion pathway. Glucose 105-112 insulin Homo sapiens 124-131 31745553-7 2020 MAIN OUTCOME MEASURES: Post-glucose ingestion insulin was determined by peak insulin and area under the insulin curve (iAUC) during a five-sample oral glucose tolerance test. Glucose 28-35 insulin Homo sapiens 46-53 31745553-7 2020 MAIN OUTCOME MEASURES: Post-glucose ingestion insulin was determined by peak insulin and area under the insulin curve (iAUC) during a five-sample oral glucose tolerance test. Glucose 28-35 insulin Homo sapiens 77-84 31745553-7 2020 MAIN OUTCOME MEASURES: Post-glucose ingestion insulin was determined by peak insulin and area under the insulin curve (iAUC) during a five-sample oral glucose tolerance test. Glucose 28-35 insulin Homo sapiens 77-84 31745553-7 2020 MAIN OUTCOME MEASURES: Post-glucose ingestion insulin was determined by peak insulin and area under the insulin curve (iAUC) during a five-sample oral glucose tolerance test. Glucose 151-158 insulin Homo sapiens 46-53 31745553-13 2020 Insulin was only significantly lower 120 minutes following glucose consumption (68.8 +- 34.5 vs. 56.2 +- 31.9 uU/ml, p<0.05), and there was a significant interaction with past/present aromatase inhibitor (AI) use for peak insulin (-11.99 (non-AI) vs +13.91 (AI) uU/mL) and iAUC (-24.03 (non-AI) vs +32.73 (AI) uU/mL). Glucose 59-66 insulin Homo sapiens 0-7 31745553-14 2020 CONCLUSIONS: Exercise training had limited overall benefits on insulin concentrations following glucose ingestion in breast cancer survivors but was strongly influenced by AI use. Glucose 96-103 insulin Homo sapiens 63-70 32432727-5 2020 RESULTS: Both insulin and QNZ stimuli to chondrocytes contributed to the expression of Glut4 and glucose uptake compared to the normal cells. Glucose 97-104 insulin Homo sapiens 14-21 32167208-2 2020 But its role in insulin-mediated suppression of lipolysis, free fatty acids (FFA), and endogenous glucose production (EGP) in humans is unknown. Glucose 98-105 insulin Homo sapiens 16-23 32325487-7 2020 Insulin sensitivity was determined using the Matsuda index following an oral glucose tolerance test. Glucose 77-84 insulin Homo sapiens 0-7 31961826-8 2020 Finally, an intravenous glucose tolerance test revealed higher insulin sensitivity, glucose effectiveness, and insulin secretion.CONCLUSIONThese findings indicate that human BAT metabolic activity can be increased after chronic pharmacological stimulation with mirabegron and support the investigation of beta3-AR agonists as a treatment for metabolic disease.TRIAL REGISTRATIONClinicaltrials.gov NCT03049462.FUNDINGThis work was supported by grants from the Intramural Research Program of the NIDDK, NIH (DK075112, DK075116, DK071013, and DK071014). Glucose 24-31 insulin Homo sapiens 63-70 31961826-8 2020 Finally, an intravenous glucose tolerance test revealed higher insulin sensitivity, glucose effectiveness, and insulin secretion.CONCLUSIONThese findings indicate that human BAT metabolic activity can be increased after chronic pharmacological stimulation with mirabegron and support the investigation of beta3-AR agonists as a treatment for metabolic disease.TRIAL REGISTRATIONClinicaltrials.gov NCT03049462.FUNDINGThis work was supported by grants from the Intramural Research Program of the NIDDK, NIH (DK075112, DK075116, DK071013, and DK071014). Glucose 24-31 insulin Homo sapiens 111-118 32244181-4 2020 METHODS: The effect of injection with recombinant human ApoA-1 (rApoA-1) on glucose tolerance, glucose-stimulated insulin secretion, and glucose uptake into skeletal and heart muscle with and without block of insulin secretion by injection of epinephrine (0.1 mg/kg) and propranolol (5 mg/kg), were investigated in 8 weeks high-fat diet-fed (60E%) wild-type and AMPKalpha2 kinase-dead mice in the overnight-fasted state. Glucose 95-102 insulin Homo sapiens 114-121 31983225-1 2020 When used in hospital settings, glucose meter performance issues involve analytic comparability to lab-based testing, patient and sample variables, and clinical affects such as insulin treatment protocol outcomes and morbidity or outcome risk factors. Glucose 32-39 insulin Homo sapiens 177-184 32452372-2 2020 When circulating glucose reaches a critical threshold, pancreatic beta-cells secrete insulin, which has two major actions: lowering circulating glucose concentrations by facilitating its uptake mainly in skeletal muscles and the liver, and inhibiting glucose production. Glucose 17-24 insulin Homo sapiens 85-92 32452372-2 2020 When circulating glucose reaches a critical threshold, pancreatic beta-cells secrete insulin, which has two major actions: lowering circulating glucose concentrations by facilitating its uptake mainly in skeletal muscles and the liver, and inhibiting glucose production. Glucose 144-151 insulin Homo sapiens 85-92 32452372-2 2020 When circulating glucose reaches a critical threshold, pancreatic beta-cells secrete insulin, which has two major actions: lowering circulating glucose concentrations by facilitating its uptake mainly in skeletal muscles and the liver, and inhibiting glucose production. Glucose 144-151 insulin Homo sapiens 85-92 31770476-0 2020 Elevation of the renal threshold for glucose is associated with insulin resistance and higher glycated hemoglobin levels. Glucose 37-44 insulin Homo sapiens 64-71 32015407-2 2020 However, insulin delivery systems with rapid in vivo glucose-responsive behaviour typically have limited insulin-loading capacities and cannot be manufactured easily. Glucose 53-60 insulin Homo sapiens 9-16 32015407-3 2020 Here, we show that a single removable transdermal patch, bearing microneedles loaded with insulin and a non-degradable glucose-responsive polymeric matrix, and fabricated via in situ photopolymerization, regulated blood glucose in insulin-deficient diabetic mice and minipigs (for minipigs >25 kg, glucose regulation lasted >20 h with patches of ~5 cm2). Glucose 220-227 insulin Homo sapiens 90-97 32244181-4 2020 METHODS: The effect of injection with recombinant human ApoA-1 (rApoA-1) on glucose tolerance, glucose-stimulated insulin secretion, and glucose uptake into skeletal and heart muscle with and without block of insulin secretion by injection of epinephrine (0.1 mg/kg) and propranolol (5 mg/kg), were investigated in 8 weeks high-fat diet-fed (60E%) wild-type and AMPKalpha2 kinase-dead mice in the overnight-fasted state. Glucose 95-102 insulin Homo sapiens 114-121 32244181-9 2020 When insulin secretion was blocked during a GTT, rApoA-1 still enhanced glucose tolerance (AUC lowered by 20% compared to control; p < 0.001) and increased glucose clearance into skeletal (+50%; p < 0.05) and heart muscle (+270%; p < 0.001). Glucose 72-79 insulin Homo sapiens 5-12 32244181-9 2020 When insulin secretion was blocked during a GTT, rApoA-1 still enhanced glucose tolerance (AUC lowered by 20% compared to control; p < 0.001) and increased glucose clearance into skeletal (+50%; p < 0.05) and heart muscle (+270%; p < 0.001). Glucose 156-163 insulin Homo sapiens 5-12 31340878-6 2020 In the present paper, we review the influence of a person"s sex on key aspects of metabolism involved in the cardiometabolic disease process, including insulin action on endogenous glucose production, tissue glucose disposal, and adipose tissue lipolysis, insulin secretion and insulin plasma clearance, postprandial glucose, fatty acid, and triglyceride kinetics, hepatic lipid metabolism and myocardial substrate use. Glucose 181-188 insulin Homo sapiens 152-159 32320145-6 2020 Independent of maternal prepregnancy BMI, one SD score (SDS) higher maternal early-pregnancy glucose and insulin concentrations were associated with higher childhood glucose (0.08 SDS, 95% CI: 0.04-0.11) and insulin concentrations (0.07 SDS, 95% CI: 0.03-0.10), but not with childhood blood pressure, lipids, and fat measures. Glucose 93-100 insulin Homo sapiens 208-215 32320145-6 2020 Independent of maternal prepregnancy BMI, one SD score (SDS) higher maternal early-pregnancy glucose and insulin concentrations were associated with higher childhood glucose (0.08 SDS, 95% CI: 0.04-0.11) and insulin concentrations (0.07 SDS, 95% CI: 0.03-0.10), but not with childhood blood pressure, lipids, and fat measures. Glucose 166-173 insulin Homo sapiens 105-112 32320145-7 2020 CONCLUSIONS: These results suggest that maternal early-pregnancy random glucose and insulin concentrations are associated with childhood glucose and insulin concentrations but not with other childhood cardiometabolic risk factors. Glucose 72-79 insulin Homo sapiens 149-156 32320145-7 2020 CONCLUSIONS: These results suggest that maternal early-pregnancy random glucose and insulin concentrations are associated with childhood glucose and insulin concentrations but not with other childhood cardiometabolic risk factors. Glucose 137-144 insulin Homo sapiens 84-91 32127696-5 2020 When insulin binds to its receptor, it initiates a sequence of phosphorylation events that lead to activation of the catalytic activity of phosphoinositide 3-kinase (PI3K), a lipid kinase that coordinates the intake and utilization of glucose, and mTOR, a kinase downstream of PI3K that stimulates transcription and translation. Glucose 235-242 insulin Homo sapiens 5-12 32374082-9 2020 However, oral glucose tolerance tests revealed improved stimulation of insulin secretion in both strains. Glucose 14-21 insulin Homo sapiens 71-78 32374082-11 2020 Interestingly, glucose-stimulated insulin secretion was blunted in isolated primary NZO islets in perifusion experiments. Glucose 15-22 insulin Homo sapiens 34-41 32305097-1 2020 The failure of insulin to suppress glucose production by the liver is a key aspect of the insulin resistance seen in type 2 diabetes. Glucose 35-42 insulin Homo sapiens 15-22 32305097-1 2020 The failure of insulin to suppress glucose production by the liver is a key aspect of the insulin resistance seen in type 2 diabetes. Glucose 35-42 insulin Homo sapiens 90-97 32812911-7 2020 In conclusion, isoorientin impacts insulin resistance in vitro by improving glucose uptake and mitochondrial function, consistent to modulating the expression of genes involved in energy metabolism and fat browning. Glucose 76-83 insulin Homo sapiens 35-42 32426290-1 2020 Unrestricted tumor growth requires a permanent supply of glucose that can be obtained from cancer-stimulated hepatic glucose production and/or glucose redirecting from host insulin resistant tissues to cancer cells. Glucose 57-64 insulin Homo sapiens 173-180 32478674-2 2020 Described here is a patient who within a few months after the onset of autoimmune type 1 diabetes increased her insulin requirements more than 20-fold; despite this she had considerable difficulty maintaining a plasma glucose value of <40-60 mmol/L (720-1100 mg/dL). Glucose 218-225 insulin Homo sapiens 112-119 32478674-10 2020 We describe here a young patient in whom, a few months after the onset of a regular autoimmune diabetes, insulin requirements in a short time increased more than 20-fold, but despite this, the plasma glucose level could be kept at <40-60 mmol/L only with considerable difficulty. Glucose 200-207 insulin Homo sapiens 105-112 32365859-11 2020 Our findings demonstrate that IL-6 and insulin can phosphorylate AS160 via different signaling pathways (AMPK and PI3K/Akt, respectively) and promote GLUT4 translocation towards the neuronal plasma membrane, resulting in increased neuronal glucose uptake in SH-SY5Y cells. Glucose 240-247 insulin Homo sapiens 39-46 32345350-12 2020 IPCs with LSD1 inhibitor tranylcypromine treatment displayed enhanced insulin secretion in response to glucose stimulation. Glucose 103-110 insulin Homo sapiens 70-77 32341337-11 2020 Further, we identified genetic sharing between peripheral insulin signaling-related traits: type 2 diabetes with "aggressive taboo thoughts", and levels of fasting insulin and 2 h glucose with OCD. Glucose 180-187 insulin Homo sapiens 58-65 32341337-11 2020 Further, we identified genetic sharing between peripheral insulin signaling-related traits: type 2 diabetes with "aggressive taboo thoughts", and levels of fasting insulin and 2 h glucose with OCD. Glucose 180-187 insulin Homo sapiens 164-177 32347070-7 2020 The result shows that adenovirus-mediated overexpression of miR-22 significantly decreased insulin-induced glucose uptake in HepG2 cells. Glucose 107-114 insulin Homo sapiens 91-98 32368538-9 2020 She responded to the administration of calcium gluconate, sodium bicarbonate, and insulin with glucose, and the serum potassium level improved. Glucose 95-102 insulin Homo sapiens 82-89 32332780-4 2020 In muscle, LRP2 is necessary for insulin-dependent IR internalization, an initial trigger for insulin signaling, that is crucial in regulating downstream signaling and glucose uptake. Glucose 168-175 insulin Homo sapiens 33-40 32332780-4 2020 In muscle, LRP2 is necessary for insulin-dependent IR internalization, an initial trigger for insulin signaling, that is crucial in regulating downstream signaling and glucose uptake. Glucose 168-175 insulin Homo sapiens 94-101 32325974-4 2020 Glucose-responsive insulin delivery systems, consisting of a glucose sensor connected to an insulin infusion pump, have improved dosing but they still suffer from inaccurate feedback, biofouling and poor patient compliance. Glucose 61-68 insulin Homo sapiens 19-26 32334629-5 2020 In addition, hyperandrogenism gave rise to negative regulation of BMAL1 expression to nicotinamide phosphoribosyltransferase and sirtuin 1, which further inhibited downstream glucose transporter type 4, leading to insulin resistance in mature adipocytes, which was consistent with our previous results in HepG2 cells. Glucose 175-182 insulin Homo sapiens 214-221 32342025-6 2020 Owing to the altered pharmacology of high-concentration insulin glargine when administered at large doses in cases of intentional overdose, patients are likely to require a much longer period of supplemental dextrose support than may otherwise be expected when these agents are used at therapeutic doses. Glucose 208-216 insulin Homo sapiens 56-63 32321868-4 2020 After differentiation to beta cells with our recent six-stage differentiation strategy, corrected WS SC-beta cells performed robust dynamic insulin secretion in vitro in response to glucose and reversed preexisting streptozocin-induced diabetes after transplantation into mice. Glucose 182-189 insulin Homo sapiens 140-147 32382513-1 2020 Aims: To compare the insulin sensitivity and secretion indices of pregnant Bangladeshi women with GDM and normal glucose tolerance (NGT). Glucose 113-120 insulin Homo sapiens 21-28 32290465-2 2020 Insulin degludec/insulin aspart (IDegAsp), comprising rapid-acting insulin aspart and ultra-long-acting insulin degludec in solution, enables both fasting and post-prandial glucose control, with some advantages over other treatment intensification options. Glucose 173-180 insulin Homo sapiens 17-24 31978443-0 2020 pH-sensitive MOF integrated with glucose oxidase for glucose-responsive insulin delivery. Glucose 33-40 insulin Homo sapiens 72-79 31978443-1 2020 Glucose-responsive insulin delivery system mimicking the function of pancreatic beta-cells to maintain blood glucose homeostasis would effectively alleviate diabetes. Glucose 0-7 insulin Homo sapiens 19-26 31978443-2 2020 Here, a new glucose-responsive delivery (ZIF@Ins&GOx) for self-regulated insulin release was constructed by encapsulating insulin and glucose oxidase (GOx) into pH-sensitive zeolitic imidazole framework-8 (ZIF-8) nanocrystals. Glucose 12-19 insulin Homo sapiens 77-84 31978443-2 2020 Here, a new glucose-responsive delivery (ZIF@Ins&GOx) for self-regulated insulin release was constructed by encapsulating insulin and glucose oxidase (GOx) into pH-sensitive zeolitic imidazole framework-8 (ZIF-8) nanocrystals. Glucose 12-19 insulin Homo sapiens 126-133 31978443-4 2020 Then, ZIF-8 nanocrystals would be degraded under the acidic microenvironment that in turn triggers the release of insulin in a glucose responsive fashion. Glucose 127-134 insulin Homo sapiens 114-121 31978443-5 2020 In vitro studies indicated that the biological activity of insulin could be protected by the rigid structure of ZIF-8 and the release of insulin could be modulated in response to glucose concentrations. Glucose 179-186 insulin Homo sapiens 59-66 31978443-5 2020 In vitro studies indicated that the biological activity of insulin could be protected by the rigid structure of ZIF-8 and the release of insulin could be modulated in response to glucose concentrations. Glucose 179-186 insulin Homo sapiens 137-144 31774682-1 2020 Glucagon counters insulin"s effects on glucose metabolism and serves as a rescue medicine in the treatment of hypoglycemia. Glucose 39-46 insulin Homo sapiens 18-25 32337422-7 2020 Furthermore, the EtOAc fraction increased the glucose consumption of insulin-resistant HepG2 cells at a concentration range of 25-100 mug mL-1. Glucose 46-53 insulin Homo sapiens 69-76 32537414-8 2020 Moreover, they exhibit sensitive glucose-stimulated insulin secretion function, demonstrating the capability of these binary capsules to engineer human organoids from hiPSCs. Glucose 33-40 insulin Homo sapiens 52-59 32200720-4 2020 The profiles of plasma glucose and immunoreactive insulin during oral glucose tolerance tests were assessed using the total area under the curve. Glucose 70-77 insulin Homo sapiens 50-57 32017937-4 2020 Metformin is the most often used oral glucose-lowering agent; its beneficial properties include lowering insulin resistance, weight reduction and cardioprotection. Glucose 38-45 insulin Homo sapiens 105-112 32637004-3 2020 This study set out to determine the serum insulin levels of ill neonates as related to their point-of-admission blood glucose estimation at the Wesley Guild Hospital, Ilesa, Nigeria. Glucose 118-125 insulin Homo sapiens 42-49 32637004-12 2020 There was weak positive correlation between serum insulin and blood glucose levels of the babies (r = 0.197, p = 0.001). Glucose 68-75 insulin Homo sapiens 50-57 32637004-14 2020 Conclusion: Serum insulin level increases with increasing blood glucose in ill Nigerian babies at presentation to the hospital. Glucose 64-71 insulin Homo sapiens 18-25 31423670-1 2020 Type 1 and advanced type 2 diabetes treatment involves daily injections or continuous infusion of exogenous insulin aimed at regulating blood glucose levels in the normoglycemic range. Glucose 142-149 insulin Homo sapiens 108-115 32308645-2 2020 These homones facilitate glucose regulation by stimulating insulin secretion in a glucose dependent manner while suppressing glucagon secretion. Glucose 25-32 insulin Homo sapiens 59-66 32308645-2 2020 These homones facilitate glucose regulation by stimulating insulin secretion in a glucose dependent manner while suppressing glucagon secretion. Glucose 82-89 insulin Homo sapiens 59-66 32256145-2 2020 In later stages of the disease insulin-secreting beta cell degeneration commences and patients require insulin replacement therapy in order to accomplish proper regulation of their blood glucose. Glucose 187-194 insulin Homo sapiens 31-38 31423670-3 2020 Therefore, a range of glucose-responsive components that can undergo changes in conformation or show alterations in intermolecular binding capability in response to glucose stimulation has been studied for ultimate integration into closed-loop insulin delivery or "smart insulin" systems. Glucose 22-29 insulin Homo sapiens 244-251 31423670-3 2020 Therefore, a range of glucose-responsive components that can undergo changes in conformation or show alterations in intermolecular binding capability in response to glucose stimulation has been studied for ultimate integration into closed-loop insulin delivery or "smart insulin" systems. Glucose 22-29 insulin Homo sapiens 271-278 31423670-3 2020 Therefore, a range of glucose-responsive components that can undergo changes in conformation or show alterations in intermolecular binding capability in response to glucose stimulation has been studied for ultimate integration into closed-loop insulin delivery or "smart insulin" systems. Glucose 165-172 insulin Homo sapiens 244-251 32392650-7 2020 In the HbA1c >7% and insulin groups, blood glucose was significantly increased 1 day after injection compared to that in the HbA1c <=7% (p=0.011) and non-insulin (p=0.024) groups, respectively. Glucose 43-50 insulin Homo sapiens 21-28 32130661-1 2020 INTRODUCTION: Many Chinese patients who are uncontrolled by oral antidiabetic drugs (OADs) receive short-term intensive insulin therapy (IIT) in hospital to rapidly relieve glucose-associated toxicity and to preserve/improve beta-cell function. Glucose 173-180 insulin Homo sapiens 120-127 33487832-8 2020 Insulin infusion was started only when blood glucose levels exceeded 200 mg%. Glucose 45-52 insulin Homo sapiens 0-7 31868941-5 2020 This vascular action of insulin is pivotal for glucose disposal in skeletal muscle, as insulin-stimulated vasodilation increases the delivery of both glucose and insulin to the myocyte. Glucose 47-54 insulin Homo sapiens 24-31 32775362-0 2020 Glucosamine potentiates the differentiation of adipose-derived stem cells into glucose-responsive insulin-producing cells. Glucose 79-86 insulin Homo sapiens 98-105 32775362-8 2020 Basal and glucose-stimulated insulin secretion (GSIS) was significantly increased and the expression of insulin and C-peptide was increased in differentiated IPCs as compared with that in differentiated IPCs using the conventional protocol (protocol C). Glucose 10-17 insulin Homo sapiens 29-36 31962378-1 2020 The whole-body insulin sensitivity index (WBISI) is a widely used surrogate of insulin sensitivity estimated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 114-121 insulin Homo sapiens 15-22 31868941-5 2020 This vascular action of insulin is pivotal for glucose disposal in skeletal muscle, as insulin-stimulated vasodilation increases the delivery of both glucose and insulin to the myocyte. Glucose 47-54 insulin Homo sapiens 87-94 31962378-1 2020 The whole-body insulin sensitivity index (WBISI) is a widely used surrogate of insulin sensitivity estimated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 114-121 insulin Homo sapiens 79-86 31962378-1 2020 The whole-body insulin sensitivity index (WBISI) is a widely used surrogate of insulin sensitivity estimated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 114-121 insulin Homo sapiens 79-86 31868941-5 2020 This vascular action of insulin is pivotal for glucose disposal in skeletal muscle, as insulin-stimulated vasodilation increases the delivery of both glucose and insulin to the myocyte. Glucose 47-54 insulin Homo sapiens 87-94 31962378-1 2020 The whole-body insulin sensitivity index (WBISI) is a widely used surrogate of insulin sensitivity estimated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 164-171 insulin Homo sapiens 15-22 31962378-1 2020 The whole-body insulin sensitivity index (WBISI) is a widely used surrogate of insulin sensitivity estimated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 164-171 insulin Homo sapiens 79-86 31962378-1 2020 The whole-body insulin sensitivity index (WBISI) is a widely used surrogate of insulin sensitivity estimated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 164-171 insulin Homo sapiens 79-86 31868941-5 2020 This vascular action of insulin is pivotal for glucose disposal in skeletal muscle, as insulin-stimulated vasodilation increases the delivery of both glucose and insulin to the myocyte. Glucose 150-157 insulin Homo sapiens 24-31 31868941-5 2020 This vascular action of insulin is pivotal for glucose disposal in skeletal muscle, as insulin-stimulated vasodilation increases the delivery of both glucose and insulin to the myocyte. Glucose 150-157 insulin Homo sapiens 87-94 31868941-5 2020 This vascular action of insulin is pivotal for glucose disposal in skeletal muscle, as insulin-stimulated vasodilation increases the delivery of both glucose and insulin to the myocyte. Glucose 150-157 insulin Homo sapiens 87-94 31868941-8 2020 This is in part due to complex variations in glucose and insulin dynamics that occurs postprandially - with changes in humoral concentrations of glucose, insulin, amino acids, gut and pancreatic peptides - compared to the hyperinsulinaemic euglycaemic clamp. Glucose 45-52 insulin Homo sapiens 154-161 31868941-8 2020 This is in part due to complex variations in glucose and insulin dynamics that occurs postprandially - with changes in humoral concentrations of glucose, insulin, amino acids, gut and pancreatic peptides - compared to the hyperinsulinaemic euglycaemic clamp. Glucose 145-152 insulin Homo sapiens 57-64 30585663-3 2020 The main goals of insulin delivery are to try to simulate the physiology of beta-cell insulin secretion as closely as possible and to overcome the challenges of peripheral insulin administration by achieving rapidity of onset with mealtime insulins and stability of the glucose-lowering effects of long-acting insulins. Glucose 270-277 insulin Homo sapiens 18-25 31831339-2 2020 However, insulin receptors are also expressed on a range of cells that are not canonically implicated in glucose homeostasis. Glucose 105-112 insulin Homo sapiens 9-16 31580150-6 2020 Insulin pump target glucose was 5.8 mmol/L. Glucose 20-27 insulin Homo sapiens 0-7 31055056-3 2020 Most studies identify, however, better control of fasting plasma glucose with insulin degludec vs. either insulin glargine U100 or detemir, and all have consistently demonstrated clinically relevant decreases in (nocturnal) hypoglycaemic episodes. Glucose 65-72 insulin Homo sapiens 78-85 31178432-1 2020 Glucagon is historically described as the counterregulatory hormone to insulin, induced by fasting/hypoglycemia to raise blood glucose through action mediated in the liver. Glucose 127-134 insulin Homo sapiens 71-78 31749275-6 2020 The primary outcome was insulin administration for blood glucose above 8 0 mmol/L in the operating theatre. Glucose 57-64 insulin Homo sapiens 24-31 31873789-9 2020 The effect of the 4hD29 nanobody on cell death and glucose-stimulated insulin secretion was measured in EndoC-betaH1 cells and in human islets using Hoechst/propidium iodide staining and an anti-insulin ELISA, respectively. Glucose 51-58 insulin Homo sapiens 70-77 31793165-4 2020 Lixisenatide mainly reduced postprandial glycaemia, while insulin glargine mainly reduced fasting glucose after breakfast (p < 0.05). Glucose 98-105 insulin Homo sapiens 58-65 31793165-13 2020 The combination with insulin glargine enhances the glucose-lowering effect, due to complementary modes of action. Glucose 51-58 insulin Homo sapiens 21-28 32144167-2 2020 In this context, smart bolus calculators that automatically tailor prandial insulin dosing to the metabolic state of a person can improve glucose management in T1D. Glucose 138-145 insulin Homo sapiens 76-83 31802616-7 2020 Similarly, MET+SITA was more effective in increasing OGTT-based glucose sensitivity (55.7+-11.3 to 108+-56.2 pmol x min-1 m-2 x mM-1 ; p=0.04) and insulin sensitivity (M/I: 2.2+-0.5 to 4.6+-1.3 mg/kg/min/muIU/min/ml; p=0.04; Matsuda Index (SI): 3.1+-0.4 to 5.7+-1.1; p=0.03) as compared to either MET or SITA. Glucose 64-71 insulin Homo sapiens 147-154 31974138-4 2020 Whole-body glucose disposal was ~18% lower on the exercise day as compared with the resting day due to decreased (~37%) insulin-stimulated glucose uptake in the nonexercised muscle. Glucose 11-18 insulin Homo sapiens 120-127 31974138-4 2020 Whole-body glucose disposal was ~18% lower on the exercise day as compared with the resting day due to decreased (~37%) insulin-stimulated glucose uptake in the nonexercised muscle. Glucose 139-146 insulin Homo sapiens 120-127 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. Glucose 312-319 insulin Homo sapiens 43-50 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. Glucose 312-319 insulin Homo sapiens 141-148 32012372-9 2020 The improved function manifests primarily through the increased insulin content of the beta cell and its increased ability to secrete insulin in response to a glucose stimulus. Glucose 159-166 insulin Homo sapiens 134-141 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. Glucose 312-319 insulin Homo sapiens 141-148 32058049-2 2020 The present study reported the scaffold hopping of the lead compound to obtain a new isoxazole derivative, C45, which has improved glucose consumption at the nanomolar level (EC50 = 0.8 nM) in insulin resistant (IR) HepG2 cells. Glucose 131-138 insulin Homo sapiens 193-200 32351264-0 2020 Utility of Short-Acting Intravenous Insulin Therapy in Preparation of F-18 Fluorodeoxyglucose Positron Emission Tomography Computed Tomography Scan in Cancer Patients Incidentally Detected with High Blood Glucose Levels on the Day of Test. Glucose 205-212 insulin Homo sapiens 36-43 32154621-2 2020 We hypothesized that small extracellular vesicles (sEVs) isolated from healthy pregnant women promote islet glucose-stimulated insulin secretion (GSIS) and peripheral insulin resistance in nonpregnant mice and that sEVs from GDM women fail to stimulate insulin secretion and cause exacerbated insulin resistance. Glucose 108-115 insulin Homo sapiens 127-134 32044662-2 2020 Glucose-stimulated insulin secretion (GSIS) is regulated by the activity of numerous neurotransmitters, hormones and paracrine factors that act by stimulating specific G protein-coupled receptors expressed by pancreatic beta-cells. Glucose 0-7 insulin Homo sapiens 19-26 32351264-3 2020 Aim and Objectives: To show the utility of short acting IV insulin therapy in preparation of cancer patients incidentally detected with high blood glucose levels for F-18 FDG PET CT scan, (>160mg/dL) and to compare the obtained image quality with patients detected with fasting blood glucose level (FBG) <100mg/dL and <160 mg/dL, using visual and semi quantitative methods. Glucose 147-154 insulin Homo sapiens 59-66 32351264-3 2020 Aim and Objectives: To show the utility of short acting IV insulin therapy in preparation of cancer patients incidentally detected with high blood glucose levels for F-18 FDG PET CT scan, (>160mg/dL) and to compare the obtained image quality with patients detected with fasting blood glucose level (FBG) <100mg/dL and <160 mg/dL, using visual and semi quantitative methods. Glucose 284-291 insulin Homo sapiens 59-66 32351264-9 2020 Conclusion: This short acting I.V insulin protocol is safe and can be used to obtain optimal quality F-18 FDG PET CT scan images by alleviating the need for rescheduling patients though they present with high glucose levels. Glucose 209-216 insulin Homo sapiens 34-41 32934948-4 2020 Mitochondrial metabolism of pancreatic beta cells is a crucial part of glucose-stimulated cascade of insulin secretion. Glucose 71-78 insulin Homo sapiens 101-108 32934948-6 2020 This review enhances our knowledge of factors influencing mitochondrial function as a key mediator of glucose-induced insulin release that accordingly will be helpful to further our understanding of the mechanisms implicated in the progressive beta cell failure that results in diabetes. Glucose 102-109 insulin Homo sapiens 118-125 32052032-1 2020 CONTEXT: Glucagon-like peptide-1 (GLP-1) potently reduces food intake and augments glucose-stimulated insulin secretion. Glucose 83-90 insulin Homo sapiens 102-109 31937469-5 2020 MATERIALS AND METHODS: Over a 2-month period, we prospectively identified non-critically ill cognitively intact hospitalized insulin-requiring patients who were undergoing bedside glucose monitoring. Glucose 180-187 insulin Homo sapiens 125-132 31990657-2 2020 The purpose of these experiments was to characterise glucose uptake, insulin signalling and relevant gene expression in primary human skeletal muscle derived cells (HMDCs), in response to prolonged insulin exposure (PIE) as a model of hyperinsulinemia induced insulin resistance. Glucose 53-60 insulin Homo sapiens 198-205 31990657-2 2020 The purpose of these experiments was to characterise glucose uptake, insulin signalling and relevant gene expression in primary human skeletal muscle derived cells (HMDCs), in response to prolonged insulin exposure (PIE) as a model of hyperinsulinemia induced insulin resistance. Glucose 53-60 insulin Homo sapiens 198-205 31990657-4 2020 HMDC"s exposed to PIE were characterised by impaired insulin stimulated glucose uptake, blunted IRS-1 phosphorylation (Tyr612) and Akt (Ser473) phosphorylation in response to an acute insulin stimulation. Glucose 72-79 insulin Homo sapiens 53-60 32243407-5 2020 The levels of glucagon, proinsulin, C-peptide (CP), and blood glucose were measured at timepoints 0, 30, and 120 minutes during the meal tolerance test.Intensive insulin treatment was associated with a decrease in glucagon levels (at 0, 30, and 120 minutes) and proinsulin/CP, and an increase in the insulin-secretion index DeltaCP30/DeltaG30 and DeltaCP120/DeltaG120, at 12 weeks and 12 months during the follow-up, compared with the corresponding effects of OHAs. Glucose 62-69 insulin Homo sapiens 162-169 32104981-5 2020 An excessive insulin secretion with the oral glucose tolerance test rationalized that she had experienced frequent attacks of paralysis on high-carbohydrate diets. Glucose 45-52 insulin Homo sapiens 13-20 32094658-5 2020 SC-beta cells differentiated from four hPSC lines exhibited first- and second-phase dynamic glucose-stimulated insulin secretion. Glucose 92-99 insulin Homo sapiens 111-118 32180558-1 2020 BACKGROUND: The diminished glucose lowering effect of insulin in obesity, called "insulin resistance," is associated with glucose intolerance, type 2 diabetes, and other serious maladies. Glucose 27-34 insulin Homo sapiens 54-61 32180558-1 2020 BACKGROUND: The diminished glucose lowering effect of insulin in obesity, called "insulin resistance," is associated with glucose intolerance, type 2 diabetes, and other serious maladies. Glucose 27-34 insulin Homo sapiens 82-89 32180558-5 2020 Key aspects of adipose function related to insulin resistance reviewed are: 1) the modes by which specific adipose tissues control hepatic glucose output and systemic glucose disposal, 2) recently acquired understanding of the underlying mechanisms of these modes of regulation, and 3) the steps in these pathways adversely affected by obesity that cause insulin resistance. Glucose 139-146 insulin Homo sapiens 43-50 32180558-8 2020 In contrast, brown/beige adipocytes are very active in directly taking up glucose in response to beta adrenergic signaling and insulin and enhancing energy expenditure. Glucose 74-81 insulin Homo sapiens 127-134 31638084-1 2020 Diabetes is a lifelong disease characterized by glucose metabolic imbalance, in which low insulin levels or impaired insulin signaling lead to hyperglycemic state. Glucose 48-55 insulin Homo sapiens 90-97 31638084-1 2020 Diabetes is a lifelong disease characterized by glucose metabolic imbalance, in which low insulin levels or impaired insulin signaling lead to hyperglycemic state. Glucose 48-55 insulin Homo sapiens 117-124 31802562-7 2020 Therefore, these two phenolic compounds promoted glucose transport through two separate routes, and they had an additive effect on the increase of glucose uptake in insulin-resistant muscle cells. Glucose 147-154 insulin Homo sapiens 165-172 32045621-2 2020 Disruption of this pathway is commonly seen in critical illness such as following severe burn injuries where homeostatic control is lost, leading to "insulin resistance" with poor blood glucose control. Glucose 186-193 insulin Homo sapiens 150-157 32339440-0 2020 Improved glucose tolerance with DPPIV inhibition requires beta-cell SENP1 amplification of glucose-stimulated insulin secretion. Glucose 9-16 insulin Homo sapiens 110-117 32339440-0 2020 Improved glucose tolerance with DPPIV inhibition requires beta-cell SENP1 amplification of glucose-stimulated insulin secretion. Glucose 91-98 insulin Homo sapiens 110-117 32339440-10 2020 Thus, an impaired ability of glucose to amplify insulin exocytosis results in a deficient effect of DPPIV inhibition to improve in vivo insulin responses and glucose tolerance. Glucose 29-36 insulin Homo sapiens 48-55 32339440-10 2020 Thus, an impaired ability of glucose to amplify insulin exocytosis results in a deficient effect of DPPIV inhibition to improve in vivo insulin responses and glucose tolerance. Glucose 158-165 insulin Homo sapiens 48-55 32730451-0 2020 [A program to estimate insulin resistance based on data from the oral glucose tolerance test]. Glucose 70-77 insulin Homo sapiens 23-30 32238837-5 2020 Furthermore, linagliptin improved insulin-induced phosphorylation of insulin receptor substrate 1 (IRS1) and Akt, which was inhibited in high-glucose conditions. Glucose 142-149 insulin Homo sapiens 34-41 31912945-2 2020 Insulin secretion from islet beta-cells is primarily controlled by mitochondrial ATP generation in response to elevations in extracellular glucose. Glucose 139-146 insulin Homo sapiens 0-7 32006524-9 2020 FGL-1 disrupted the gluconeogenic action of insulin in HepG2 cells, and decreased insulin-induced glucose uptake by L6 myotubes. Glucose 98-105 insulin Homo sapiens 82-89 32234723-5 2020 In shATGL pseudoislets, biphasic glucose-stimulated insulin secretion (GSIS) and insulin secretion to IBMX and KCl were all reduced without altering oxygen consumption rate compared with scramble control. Glucose 33-40 insulin Homo sapiens 52-59 32337294-1 2020 Aims: This study is aimed at assessing the association of previously developed indices of glucose homeostasis derived from principal component analysis (PCA) with parameters of insulin action, secretion, and beta cell function during pregnancy. Glucose 90-97 insulin Homo sapiens 177-184 32313609-4 2020 Several randomised controlled and real-world studies have proven the resultant advantages of second-generations insulin analogues in lowering intra-individual variability in plasma insulin levels, flexibility in dosing, a sustained glucose-lowering effect, and decreasing the risk of hypoglycaemia. Glucose 232-239 insulin Homo sapiens 112-119 32258491-6 2020 The results obtained include an encapsulation efficiency of above 70 %; in vitro release was sustained over 10 h and in vivo evaluations in diabetic rat model shows that insulin-loaded microencapsulation effectively reduced blood glucose levels over a period >8 h after oral administration. Glucose 230-237 insulin Homo sapiens 170-177 31931619-6 2020 siRNA-mediated knock-down of NOX5 in human islets cultured in basal glucose concentrations resulted in diminished glucose-induced insulin secretion in vitro. Glucose 68-75 insulin Homo sapiens 130-137 32077280-5 2020 In vivo, GNF2133 demonstrated significant dose-dependent glucose disposal capacity and insulin secretion in response to glucose-potentiated arginine-induced insulin secretion (GPAIS) challenge in rat insulin promoter and diphtheria toxin A (RIP-DTA) mice. Glucose 120-127 insulin Homo sapiens 87-94 32341874-1 2020 Blood glucose measurements help to guide insulin therapy, thus reducing disease severities, secondary complications, and related mortalities. Glucose 6-13 insulin Homo sapiens 41-48 31931619-6 2020 siRNA-mediated knock-down of NOX5 in human islets cultured in basal glucose concentrations resulted in diminished glucose-induced insulin secretion in vitro. Glucose 114-121 insulin Homo sapiens 130-137 31931619-7 2020 However, when islets were preincubated in high (16.7mM) glucose media for 12 hours, NOX5 appeared also in insulin-positive (beta) cells. Glucose 56-63 insulin Homo sapiens 106-113 31931619-8 2020 In vivo, mice with beta-cell NOX5 expression developed aggravated impairment of glucose-induced insulin secretion compared to control mice when challenged with 14 weeks of high-fat diet. Glucose 80-87 insulin Homo sapiens 96-103 32176701-2 2020 Strategies aimed at enhancing beta-cell regeneration have long been pursued, but methods for reliably inducing human beta-cell proliferation with full retention of key functions such as glucose-stimulated insulin secretion (GSIS) are still very limited. Glucose 186-193 insulin Homo sapiens 205-212 32265649-4 2020 It contributes to the maintenance of glucose physiological levels namely by inhibiting insulin and glucagon secretion as well as controlling adiposity and satiation. Glucose 37-44 insulin Homo sapiens 87-94 32179729-1 2020 BACKGROUND Insulin lowers not only blood glucose levels but also serum potassium levels by driving potassium into the cells. Glucose 41-48 insulin Homo sapiens 11-18 32308680-1 2020 Background: Insulin promotes glucose consumption as the main cardiac energy source, while increasing myocardial efficiency. Glucose 29-36 insulin Homo sapiens 12-19 32163203-1 2020 Glucose-induced (physiological) insulin secretion from the islet beta-cell involves interplay between cationic (i.e., changes in intracellular calcium) and metabolic (i.e., generation of hydrophobic and hydrophilic second messengers) events. Glucose 0-7 insulin Homo sapiens 32-39 32164657-8 2020 CONCLUSIONS: This case story presents a patient with a gain-of-function mutation KCNQ1 R670K with low glucose-stimulated C-peptide secretion, additionally suggesting involvement of the voltage-gated potassium channel KCNQ1 in glucose-stimulated insulin regulation. Glucose 102-109 insulin Homo sapiens 245-252 32164657-8 2020 CONCLUSIONS: This case story presents a patient with a gain-of-function mutation KCNQ1 R670K with low glucose-stimulated C-peptide secretion, additionally suggesting involvement of the voltage-gated potassium channel KCNQ1 in glucose-stimulated insulin regulation. Glucose 226-233 insulin Homo sapiens 245-252 32178449-4 2020 The resulting downregulation of the insulin signaling cascade prevents the translocation of glucose transporter to the plasma membrane and glucose uptake into skeletal muscle, leading to metabolic disorders such as type 2 diabetes. Glucose 92-99 insulin Homo sapiens 36-43 32178449-4 2020 The resulting downregulation of the insulin signaling cascade prevents the translocation of glucose transporter to the plasma membrane and glucose uptake into skeletal muscle, leading to metabolic disorders such as type 2 diabetes. Glucose 139-146 insulin Homo sapiens 36-43 32168890-1 2020 Insulin secretion from the beta-cells of the islets of Langerhans is triggered mainly by nutrients such as glucose, and incretin hormones such as glucagon-like peptide-1 (GLP-1). Glucose 107-114 insulin Homo sapiens 0-7 32200183-3 2020 Epidemiological studies have shown that BPA concentrations are higher in human specimens of T2D when compared to healthy subjects, while experimental studies suggested that bisphenol A (BPA) impairs the pathway by which insulin stimulates glucose uptake. Glucose 239-246 insulin Homo sapiens 220-227 32069419-5 2020 More importantly, the excellent glucose-sensitivity of the hydrophobic domains enables the nanochaperones to release and refold insulin in native form in response to hyperglycemia. Glucose 32-39 insulin Homo sapiens 128-135 32200183-5 2020 Recent results demonstrated that BPA impairs several components of insulin-induced glucose uptake pathway and affect the expression of GLUT4. Glucose 83-90 insulin Homo sapiens 67-74 32200183-6 2020 Regular physical exercise delays or inhibits the development of T2D due to the physiologic processes taking place during muscle contraction, and the fact that skeletal muscle is the site for almost 80% of the glucose transported under insulin stimulation. Glucose 209-216 insulin Homo sapiens 235-242 32200183-8 2020 We hypothesize that during the development of insulin resistance, BPA contributes to the impairment of the molecular pathway by which insulin induces glucose uptake while contraction-induced glucose uptake is not impaired. Glucose 150-157 insulin Homo sapiens 46-53 32200183-8 2020 We hypothesize that during the development of insulin resistance, BPA contributes to the impairment of the molecular pathway by which insulin induces glucose uptake while contraction-induced glucose uptake is not impaired. Glucose 150-157 insulin Homo sapiens 134-141 32200183-8 2020 We hypothesize that during the development of insulin resistance, BPA contributes to the impairment of the molecular pathway by which insulin induces glucose uptake while contraction-induced glucose uptake is not impaired. Glucose 191-198 insulin Homo sapiens 46-53 32226901-1 2020 The monitoring of insulin, which is the only hormone that helps regulate blood glucose levels in the body, plays a key role in the diagnosis and treatment of diabetes. Glucose 79-86 insulin Homo sapiens 18-25 32210600-9 2020 Conclusion: Addition of insulin glargine to routine protocols more effectively reduces glucose levels and decreases incidence of hyperglycemic episodes and regular insulin usage. Glucose 87-94 insulin Homo sapiens 24-31 32156279-1 2020 BACKGROUND: The triglyceride glucose (TyG) index, a simple surrogate estimate of insulin resistance, has been demonstrated to predict cardiovascular (CV) disease morbidity and mortality in the general population and many patient cohorts. Glucose 29-36 insulin Homo sapiens 81-88 33455388-0 2020 Glucose-Sensitive Polyphosphoester Diblock Copolymer for an Insulin Delivery System. Glucose 0-7 insulin Homo sapiens 60-67 32256572-0 2020 Diagnostic Accuracy of the Triglyceride and Glucose Index for Insulin Resistance: A Systematic Review. Glucose 44-51 insulin Homo sapiens 62-69 32256572-2 2020 The triglyceride and glucose (TyG) index has been described as a biochemical marker of insulin resistance (IR); however, its diagnostic accuracy remains uncertain. Glucose 21-28 insulin Homo sapiens 87-94 32164195-4 2020 MetS is closely linked to altered glucose homeostasis, the plasma insulin/glucose ratio; i.e., the insulinogenic index helps to estimate the level of insulin secretion and also for assessing beta-cell function. Glucose 34-41 insulin Homo sapiens 99-106 33455388-6 2020 Fluorescein isothiocyanate (FITC)-insulin was loaded into the NPs and triggered to release in the presence of glucose. Glucose 110-117 insulin Homo sapiens 34-41 33455388-7 2020 The more the glucose in the release media, the more the FITC-insulin released and the faster the release rate. Glucose 13-20 insulin Homo sapiens 61-68 33455388-9 2020 All of these results verify that the glucose-sensitive polyphosphoester diblock copolymer is highly promising for an insulin delivery system. Glucose 37-44 insulin Homo sapiens 117-124 31753785-7 2020 Co-twins with higher Glucose iAUC also had higher waist circumference, body fat percentage, liver fat content, worse insulin-sensitivity and beta-cell function and higher cholesterol and triglyceride in plasma VLDL, IDL, and LDL. Glucose 21-28 insulin Homo sapiens 117-124 31954131-4 2020 Counterintuitively, glucagon seems also required for an optimal insulin secretion in response to glucose by acting on its cognate receptor and, even more importantly, on GLP-1 receptors. Glucose 97-104 insulin Homo sapiens 64-71 31628943-2 2020 The main function of these cells is to produce and secrete insulin in response to a rise in circulating levels of glucose and other nutrients. Glucose 114-121 insulin Homo sapiens 59-66 32150819-1 2020 Insulin, a hormone produced by pancreatic beta-cells, has a primary function of maintaining glucose homeostasis. Glucose 92-99 insulin Homo sapiens 0-7 32185116-1 2020 Insulin-stimulated glucose transport is a characteristic property of adipocytes and muscle cells and involves the regulated delivery of glucose transporter (GLUT4)-containing vesicles from intracellular stores to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 32031792-14 2020 The pH-stimulated release of insulin is controlled by the concentration of glucose. Glucose 75-82 insulin Homo sapiens 29-36 32219132-6 2020 WBC positively correlated with serum insulin at 0, 60, and 120 min during the oral glucose tolerance test (INS0: r = 0,221, p = 0,001; INS1: r = 0,194, p = 0,003; INS2: r = 0,022, p = 0,001), testosterone (r = 0,130, p = 0,046), androstenedione (r = 0,212, p = 0,001), and DHEAS (r = 0,178, p = 0,006) and negatively correlated with progesterone (r = -0,204, p = 0,002), estradiol (r = -0,140, p = 0,032), and SHBG (r = -0,308, p < 0,001). Glucose 83-90 insulin Homo sapiens 37-44 32219132-7 2020 CRP positively correlated with insulin concentration in 0, 60, and 120 min during the oral glucose tolerance test (INS0: r = 0,343, p < 0,001; INS1: r = 0,276, p = 0,001; INS2: r = 0,320, p < 001) and negatively correlated with progesterone (r = -0,194, p = 0,030) and SHBG (-0,244, p = 0,005). Glucose 91-98 insulin Homo sapiens 31-38 32031792-15 2020 While at normal glucose levels, the release of insulin is practically prohibited, the dose-controlled release of insulin in the entire concentration range of diabetic concern is demonstrated. Glucose 16-23 insulin Homo sapiens 113-120 32031792-16 2020 Also, switchable ON/OFF release of insulin is achieved highlighting an autonomous glucose-responsive microdevice operating as an "artificial pancreas" for the release of insulin. Glucose 82-89 insulin Homo sapiens 35-42 32031792-16 2020 Also, switchable ON/OFF release of insulin is achieved highlighting an autonomous glucose-responsive microdevice operating as an "artificial pancreas" for the release of insulin. Glucose 82-89 insulin Homo sapiens 170-177 32126857-6 2022 Women in the insulin-resistant group had higher fasting glucose levels in the first trimester (91, 98 and 102 mg/dL for women in the insulin sensitive-, comparison- and insulin-resistant groups, respectively; p = .01). Glucose 56-63 insulin Homo sapiens 13-20 32126857-7 2022 Women in the insulin-sensitive group had significantly better glycemic control (fasting glucose levels <=90 mg/dL and 1-hour and 2-hour postprandial glucose levels <=140 mg/dL and <=120 mg/dL for more than 80% of measurements) than those in the insulin-resistant group (70.3 versus 29.9%; p < .001). Glucose 88-95 insulin Homo sapiens 13-20 32126857-7 2022 Women in the insulin-sensitive group had significantly better glycemic control (fasting glucose levels <=90 mg/dL and 1-hour and 2-hour postprandial glucose levels <=140 mg/dL and <=120 mg/dL for more than 80% of measurements) than those in the insulin-resistant group (70.3 versus 29.9%; p < .001). Glucose 149-156 insulin Homo sapiens 13-20 32194426-1 2020 De novo hepatic glucose production or hepatic gluconeogenesis is the main contributor to hyperglycemia in the fasting state in patients with type 2 diabetes (T2D) owing to insulin resistance, which leads to at least twice as much glucose synthesis compared to healthy subjects. Glucose 16-23 insulin Homo sapiens 172-179 32126857-10 2022 However, those with higher insulin requirements have poorer glucose control and higher rates of CS than those with lower insulin requirements. Glucose 60-67 insulin Homo sapiens 27-34 32194426-1 2020 De novo hepatic glucose production or hepatic gluconeogenesis is the main contributor to hyperglycemia in the fasting state in patients with type 2 diabetes (T2D) owing to insulin resistance, which leads to at least twice as much glucose synthesis compared to healthy subjects. Glucose 230-237 insulin Homo sapiens 172-179 32293140-3 2020 Herein, a novel platform to perform glucose-stimulated insulin secretion (GSIS) assays with single islets is presented for studying the dynamics of insulin release at high temporal resolution. Glucose 36-43 insulin Homo sapiens 55-62 32293140-1 2020 Insulin is released from pancreatic islets in a biphasic and pulsatile manner in response to elevated glucose levels. Glucose 102-109 insulin Homo sapiens 0-7 33402916-11 2020 The multivariate logistic regression analysis showed that gender, serum glucose level, serum levels of triglycerides and high-density lipoprotein cholesterol, bodymass index and income status were associated with insulin resistance. Glucose 72-79 insulin Homo sapiens 213-220 31825657-7 2020 Consistently, insulin-stimulated glucose uptake and oxidative capacity were greatest in L6 myotubes. Glucose 33-40 insulin Homo sapiens 14-21 31825657-8 2020 Insulin-induced glycogen synthesis was highest in HSMCs, but C2C12 myotubes had higher baseline glucose oxidation. Glucose 96-103 insulin Homo sapiens 0-7 32108266-1 2020 Chronic mTORc1 hyperactivation via obesity-induced hyperleucinaemia has been implicated in the development of insulin resistance, yet the direct impact of leucine on insulin-stimulated glucose uptake in muscle cells remains unclear. Glucose 185-192 insulin Homo sapiens 166-173 31702069-5 2020 In the longer-term, a microvascular-metabolic mismatch in skeletal muscle reduces insulin-mediated muscle glucose uptake, leading to disturbances in whole body metabolic homeostasis. Glucose 106-113 insulin Homo sapiens 82-89 31814151-1 2020 Almost 100 years since the discovery of insulin, hypoglycaemia remains a barrier for people with type 1 diabetes to achieve and maintain blood glucose at levels which prevent long-term diabetes-related complications. Glucose 143-150 insulin Homo sapiens 40-47 31974099-12 2020 CONCLUSIONS: A novel rapid insulin-and-pramlintide artificial pancreas improves glucose control compared with a rapid insulin-alone artificial pancreas (ClinicalTrials.gov number NCT02814123). Glucose 80-87 insulin Homo sapiens 27-34 31974102-1 2020 OBJECTIVE: Impaired insulin-stimulated myocardial glucose uptake has occurred in patients with type 2 diabetes with or without coronary artery disease. Glucose 50-57 insulin Homo sapiens 20-27 31974102-7 2020 Univariate correlations showed that MRGlu was positively correlated with insulin-stimulated whole-body glucose disposal (r = 0.441; P = 0.019) and negatively correlated with 1-h (r = -0.422; P = 0.025) and 2-h (r = -0.374; P = 0.05) postload glucose levels, but not with fasting glucose. Glucose 103-110 insulin Homo sapiens 73-80 31608548-12 2020 A low FCP identifies a markedly insulin-deficient, insulin-sensitive subgroup/phenotype with an enhanced risk of hypoglycaemia, which requires a low initial basal insulin dose, cautious titration and earlier addition of prandial glucose-lowering therapy. Glucose 229-236 insulin Homo sapiens 32-39 31608548-12 2020 A low FCP identifies a markedly insulin-deficient, insulin-sensitive subgroup/phenotype with an enhanced risk of hypoglycaemia, which requires a low initial basal insulin dose, cautious titration and earlier addition of prandial glucose-lowering therapy. Glucose 229-236 insulin Homo sapiens 51-58 31873857-1 2020 INTRODUCTION: The aim of this meta-analysis was to investigate the impact of rapid-acting insulin analogues (RAIAs) and regular human insulin (RHI) on glycemic control, including long- and short-term glycemic variability as measured by glycated haemoglobin (HbA1c) and pre- and postprandial glucose (PPG). Glucose 291-298 insulin Homo sapiens 90-97 31980111-3 2020 Glucose-responsive automated insulin delivery enables the highest targets for time in range, lowest rate and duration of hypoglycemia, and favorable quality of life. Glucose 0-7 insulin Homo sapiens 29-36 31980117-1 2020 Treatment of type 1 diabetes with exogenous insulin often results in unpredictable daily glucose variability and hypoglycemia, which can be dangerous. Glucose 89-96 insulin Homo sapiens 44-51 31980117-2 2020 Automated insulin delivery systems can improve glucose control while reducing burden for people with diabetes. Glucose 47-54 insulin Homo sapiens 10-17 32163918-8 2020 We found higher fasting insulin levels on Mondays compared to the other days of the week, potentially indicating worsened glucose regulation after the weekend. Glucose 122-129 insulin Homo sapiens 24-31 31912958-8 2020 We hypothesized that low dose CO inhalation would improve glucose and insulin responses to an oral glucose bolus in overweight humans. Glucose 99-106 insulin Homo sapiens 70-77 31147381-7 2020 RESULTS: We observed a significant decrease in insulin sensitivity 2 weeks after allogenic METS-D FMT (median rate of glucose disappearance: from 40.6 to 34.0 micromol/kg/min; p<0.01). Glucose 118-125 insulin Homo sapiens 47-54 31195880-3 2020 The main limiting factor to achieve strict control of glucose levels in patients on intensive insulin therapy is the risk of severe hypoglycaemia. Glucose 54-61 insulin Homo sapiens 94-101 31324880-4 2020 The primary endpoint was insulin sensitivity (Matsuda Index) calculated from a 75-g oral glucose tolerance test. Glucose 89-96 insulin Homo sapiens 25-32 31624314-0 2020 Roux-en-Y gastric bypass surgery restores insulin-mediated glucose partitioning and mitochondrial dynamics in primary myotubes from severely obese humans. Glucose 59-66 insulin Homo sapiens 42-49 31624314-1 2020 BACKGROUND/OBJECTIVES: Impaired insulin-mediated glucose partitioning is an intrinsic metabolic defect in skeletal muscle from severely obese humans (BMI >= 40 kg/m2). Glucose 49-56 insulin Homo sapiens 32-39 31624314-8 2020 Finally, Drp1(Ser616) phosphorylation was negatively correlated with insulin-stimulated glucose oxidation (r = -0.49, P = 0.037). Glucose 88-95 insulin Homo sapiens 69-76 31608926-12 2020 CONCLUSION: These results suggest that the glucose-lowering effects of cotadutide are mediated by enhanced insulin secretion and delayed gastric emptying. Glucose 43-50 insulin Homo sapiens 107-114 31665349-10 2020 In exposed subjects, insulin secretion during graded IV glucose infusion and after arginine administration decreased by 17% (P = 0.02) and 22% (P = 0.002), respectively, while glucagon secretion after arginine increased. Glucose 56-63 insulin Homo sapiens 21-28 31126898-8 2020 A significant inverse correlation was also identified between fasting insulin level and elevated glucose on CGM, defined as AUC >7.8 mmol/L (rs = - 0.69, p = .027) or as % time > 7.8 (rs = - 0.76, p = .011). Glucose 97-104 insulin Homo sapiens 70-77 30678495-1 2020 INTRODUCTION:: Continuous glucose monitoring (CGM) is a better tool to detect hyper and hypoglycemia than capillary point of care in insulin-treated patients during hospitalization. Glucose 26-33 insulin Homo sapiens 133-140 31216874-3 2020 Currently, there are no FDA-approved insulin therapeutics whose bioactivity is regulated by blood glucose levels. Glucose 98-105 insulin Homo sapiens 37-44 31410924-14 2020 DATA CONCLUSION: ASL can be used to measure pancreatic flow in response to a glucose challenge, which could be linked to insulin release and secretion. Glucose 77-84 insulin Homo sapiens 121-128 31960210-0 2020 A diterpene derivative enhanced insulin signaling induced by high glucose level in HepG2 cells. Glucose 66-73 insulin Homo sapiens 32-39 31960210-7 2020 High glucose also inhibited the phosphorylation of insulin-dependent GSK3beta. Glucose 5-12 insulin Homo sapiens 51-58 32195965-2 2020 The deterioration of glucose metabolism are generally considered to be results of the impairment of the 4 factors: first, second insulin secretion (FPIS, SPIS, respectively), glucose effectiveness (GE), and insulin resistance. Glucose 21-28 insulin Homo sapiens 129-136 32195965-2 2020 The deterioration of glucose metabolism are generally considered to be results of the impairment of the 4 factors: first, second insulin secretion (FPIS, SPIS, respectively), glucose effectiveness (GE), and insulin resistance. Glucose 21-28 insulin Homo sapiens 207-214 31891768-4 2020 Glucagon only at a supra-physiological concentration (10-100 nM) significantly increased basal and insulin-stimulated glucose uptake by up to 1.5-fold. Glucose 118-125 insulin Homo sapiens 99-106 31982479-6 2020 RESULTS AND DISCUSSION: With most normalization methods, the obese subjects demonstrated reduced insulin-stimulated glucose disposal as compared to the lean subjects. Glucose 116-123 insulin Homo sapiens 97-104 31780780-1 2020 The ability of growth hormone (GH) to induce adipose tissue lipolysis has been known for over five decades; however, the molecular mechanisms that mediate this effect and the ability of GH to inhibit insulin-stimulated glucose uptake have scarcely been documented. Glucose 219-226 insulin Homo sapiens 200-207 32208561-9 2020 The emerging mobile toolbox for insulin dosing adjustments that will be reviewed in this paper includes insulin management Apps; diverse range of Apps to guide insulin adjustments such as in times of physical activity and eating; data management systems which enable visualization and analysis of insulin and glucose data of various devices; real-time alarms and glucose prediction Apps that help to prevent hypoglycemia and hyperglycemia events; various bolus calculators for meal time dosing; sophisticated decision support algorithms for people using insulin pump, multiple insulin injections and closed loop systems for real-time and retrospective insulin dosing adjustments. Glucose 309-316 insulin Homo sapiens 32-39 32208561-9 2020 The emerging mobile toolbox for insulin dosing adjustments that will be reviewed in this paper includes insulin management Apps; diverse range of Apps to guide insulin adjustments such as in times of physical activity and eating; data management systems which enable visualization and analysis of insulin and glucose data of various devices; real-time alarms and glucose prediction Apps that help to prevent hypoglycemia and hyperglycemia events; various bolus calculators for meal time dosing; sophisticated decision support algorithms for people using insulin pump, multiple insulin injections and closed loop systems for real-time and retrospective insulin dosing adjustments. Glucose 363-370 insulin Homo sapiens 32-39 31715213-2 2020 Glucose-dependent insulinotropic polypeptide (GIP) is secreted from the gut and potentiates insulin secretion in a glucose-dependent manner. Glucose 115-122 insulin Homo sapiens 18-25 31812593-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted primarily from enteroendocrine K cells in the duodenum and proximal jejunum following nutrient ingestion, primarily acting on islet beta-cells to potentiate insulin secretion in a glucose-dependent manner. Glucose 257-264 insulin Homo sapiens 18-25 31838219-3 2020 Conventionally, GIP is thought of as an important incretin hormone regulating postprandial insulin secretion in glucose tolerant individuals, but such effects are weak or absent in patients with type 2 diabetes, and GIP has been proposed to an obesity-promoting hormone, rather than the opposite. Glucose 112-119 insulin Homo sapiens 91-98 31935429-1 2020 Gastric inhibitory polypeptide (GIP) is best known as an incretin hormone released by enteroendocrine K-cells in response to feeding and stimulates insulin release to regulate blood glucose and nutrient homeostasis. Glucose 182-189 insulin Homo sapiens 148-155 32081451-2 2020 Augmentation of glucose mediated insulin release, the incretin effect, was discovered soon after GIP was first isolated and only much later was its important role in the pathogenesis of obesity, through mechanism other than its insulin secretion, appreciated. Glucose 16-23 insulin Homo sapiens 33-40 32126492-0 2020 Acacetin enhances glucose uptake through insulin-independent GLUT4 translocation in L6 myotubes. Glucose 18-25 insulin Homo sapiens 41-48 32126492-1 2020 BACKGROUND: Lowering blood glucose levels by increasing glucose uptake in insulin target tissues, such as skeletal muscle and adipose tissue, is one strategy to discover and develop antidiabetic drugs from natural products used as traditional medicines. Glucose 27-34 insulin Homo sapiens 74-81 32126492-1 2020 BACKGROUND: Lowering blood glucose levels by increasing glucose uptake in insulin target tissues, such as skeletal muscle and adipose tissue, is one strategy to discover and develop antidiabetic drugs from natural products used as traditional medicines. Glucose 56-63 insulin Homo sapiens 74-81 31724413-4 2020 We found that poor glucose regulation (higher insulin resistance) was consistently associated with lower levels of well-being among older men but not women. Glucose 19-26 insulin Homo sapiens 46-53 32190015-2 2020 Although the amount of insulin to be given per blood glucose range has been well described in guidelines, the amount of glucose to be given is not detailed well. Glucose 53-60 insulin Homo sapiens 23-30 32098413-2 2020 They are also referred to incretin for their ability to stimulate insulin secretion from pancreatic beta cells in a glucose-dependent manner. Glucose 116-123 insulin Homo sapiens 66-73 32058966-4 2020 As proof of concept, we investigated how 3T3-L1 cultured adipocytes acutely metabolize glucose in response to insulin. Glucose 87-94 insulin Homo sapiens 110-117 32058966-5 2020 Insulin rapidly stimulates glucose uptake, but intracellular pathways responded with differing speeds and magnitudes. Glucose 27-34 insulin Homo sapiens 0-7 32092909-7 2020 Insulin resistance was detected in 83% of subjects and associated with increased leptin, fasting plasma glucose and body mass index, and lower triglyceride levels. Glucose 104-111 insulin Homo sapiens 0-7 32079162-8 2020 The need for insulin therapy was associated with higher BM doses and the presence of marginal values in the 75-g oral glucose tolerance test (OGTT) at 60 min. Glucose 118-125 insulin Homo sapiens 13-20 31821855-3 2020 In pancreatic beta-cells, KATP channels composed of Kir6.2 and SUR1, encoded by KCNJ11 and ABCC8, respectively, play a key role in coupling blood glucose concentration to insulin secretion. Glucose 146-153 insulin Homo sapiens 171-178 32051343-3 2020 We show that SNAP23, when depleted in mouse beta cells in vivo and human beta cells (normal and type 2 diabetes [T2D] patients) in vitro, paradoxically increased biphasic glucose-stimulated insulin secretion corresponding to increased exocytosis of predocked and newcomer insulin granules. Glucose 171-178 insulin Homo sapiens 190-197 33464872-6 2020 Both xenogenic and allogenic versions of these coclusters were found to be viable and were able to respond to dynamic glucose stimulation with insulin release. Glucose 118-125 insulin Homo sapiens 143-150 32523723-0 2020 Correlation of plasma metabolites with glucose and lipid fluxes in human insulin resistance. Glucose 39-46 insulin Homo sapiens 73-80 32523723-9 2020 These metabolites may be used to predict the rate of glucose disposal in humans with obesity to a similar extend as HOMA, thus providing potential novel biomarkers for insulin resistance. Glucose 53-60 insulin Homo sapiens 168-175 31759099-3 2020 We found that treatment of the normal human liver cell LO2 with 1000 nM insulin for 48 h reduced glucose uptake and increased serine phosphorylation of insulin receptor substrate-1, indicating a reduction in insulin receptor signaling. Glucose 97-104 insulin Homo sapiens 72-79 31759099-6 2020 Cell treatment with S1P at 0.1-5.0 muM reversed the effects of high insulin concentrations on ROS generation, glucose uptake, and insulin signaling. Glucose 110-117 insulin Homo sapiens 68-75 31812226-8 2020 In patients on insulin before discharge, blood glucose values were significantly higher compared with those who were not (136 mg/dl vs 114 mg/dl at 1 to 3 months, 112 vs 100 at 4 to 6 months, 109 vs 98 at 8 to 12 months, all p <0.01). Glucose 47-54 insulin Homo sapiens 15-22 31794259-4 2020 Knockdown of Grb10 enhanced insulin-induced PI3K/Akt signaling and glucose uptake in myotubes, reinforcing the notion underlying its function as a negative regulator of insulin action in human muscle. Glucose 67-74 insulin Homo sapiens 28-35 31796987-12 2020 Interestingly, SCD knockdown by itself disrupted beta cell identity with a decrease in mature beta cell markers INS, MAFA and SLC30A8 and decreased insulin content and glucose-stimulated insulin secretion. Glucose 168-175 insulin Homo sapiens 187-194 31910030-6 2020 Using the glucose MM, MetSyn subjects had lower [-73% (-82, -57)] sensitivity to insulin (Si) and higher [138% (44, 293)] acute insulin response to glucose (AIRg). Glucose 148-155 insulin Homo sapiens 128-135 31866049-6 2020 Most importantly, ColV-containing microenvironment resulted in enhanced glucose responsive secretions of both insulin and glucagon hormone from organoids. Glucose 72-79 insulin Homo sapiens 110-117 32152146-7 2020 Insulin resistance was determined by means of the HOMA for insulin resistance (HOMA-IR) index and by an oral glucose tolerance test. Glucose 109-116 insulin Homo sapiens 0-7 31888883-8 2020 Superimposition of insulin to GLP-1 infusion did not further increase MBV or flow in either skeletal or cardiac muscle but raised the steady-state glucose infusion rate by ~20%. Glucose 147-154 insulin Homo sapiens 19-26 31915205-2 2020 We proposed that the insulin-deficient phenotype is genetically determined and tested this hypothesis by longitudinal modeling of insulin and glucose traits with diabetes risk genotypes in the EarlyBird cohort. Glucose 142-149 insulin Homo sapiens 21-28 31754750-6 2020 Insulin sensitivity is higher in women, who are also characterised by higher capacities for insulin secretion and incretin responses than men; although, these sex advantages all disappear when glucose tolerance deteriorates towards diabetes. Glucose 193-200 insulin Homo sapiens 0-7 32099025-1 2020 The Insulin/IGF-1 signalling (IIS) pathway plays an essential role in the regulation of glucose and lipid homeostasis. Glucose 88-95 insulin Homo sapiens 4-17 31889346-0 2020 Insulin-Delivery from Glucose-Responsive Self-Assembled Polyamine Nanoparticles: Smart "Sense-and-Treat" Nanocarriers Made Easy. Glucose 22-29 insulin Homo sapiens 0-7 31889346-2 2020 Here, a simple and fast multicomponent self-assembly process was used to construct crosslinked poly(allylamine hydrochloride)/phosphate PSAs (hydrodynamic diameter of 360 nm) containing glucose oxidase enzyme, as a glucose-responsive element, and human recombinant insulin, as a therapeutic agent for the treatment of diabetes mellitus (GI-PSA). Glucose 187-194 insulin Homo sapiens 266-273 31889346-2 2020 Here, a simple and fast multicomponent self-assembly process was used to construct crosslinked poly(allylamine hydrochloride)/phosphate PSAs (hydrodynamic diameter of 360 nm) containing glucose oxidase enzyme, as a glucose-responsive element, and human recombinant insulin, as a therapeutic agent for the treatment of diabetes mellitus (GI-PSA). Glucose 216-223 insulin Homo sapiens 266-273 31889346-3 2020 The addition of increasing glucose concentrations promotes the release of insulin due to the disassembly of the GI-PSAs triggered by the catalytic in-situ formation of gluconic acid. Glucose 27-34 insulin Homo sapiens 74-81 31866555-1 2020 Insulin and glucagon are important hormones for regulating blood glucose levels. Glucose 65-72 insulin Homo sapiens 0-7 32093050-1 2020 Pancreatic beta-cells secrete insulin to lower blood glucose, following a meal. Glucose 53-60 insulin Homo sapiens 30-37 32093050-8 2020 Enhanced mitochondrial calcium rises potentiated glucose-induced insulin secretion. Glucose 49-56 insulin Homo sapiens 65-72 32093050-9 2020 Conversely, the MCU inhibitor mitoxantrone inhibited mitochondrial Ca2+ uptake and prevented both glucose-induced insulin secretion and kaempferol-potentiated effects. Glucose 98-105 insulin Homo sapiens 114-121 31805307-5 2020 This impaired the capacity for glucose-induced insulin secretion in Cacna2d1-silenced cells. Glucose 31-38 insulin Homo sapiens 47-54 31805307-6 2020 Overexpression of alpha2delta-1 increased high-glucose/K+-stimulated insulin secretion. Glucose 47-54 insulin Homo sapiens 69-76 32041106-5 2020 The homeostasis model assessment of insulin resistance (HOMA-IR) was computed from third trimester fasting plasma glucose and insulin values. Glucose 114-121 insulin Homo sapiens 36-43 31494110-1 2020 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a novel class of medications that reduce plasma glucose concentrations through an insulin-independent mechanism of increased urinary glucose excretion, with concomitant natriuresis and diuresis. Glucose 7-14 insulin Homo sapiens 136-143 31850803-7 2020 Further, mutant cells demonstrate an increase in MFGE8 protein, milk fat globule-EGF factor-8, that influences insulin-signaling pathway by phosphorylating AktSer473 via phosphatidylinositide-3-kinase (PI3K) and mTOR (mammalian target of rapamycin).Conclusions: BMPR2 mutant cardiomyocytes have reduced metabolic plasticity and fail to respond to glucose. Glucose 347-354 insulin Homo sapiens 111-118 30937918-4 2020 FA acutely increase glucose-stimulated insulin secretion through cell-surface receptor and intracellular pathways. Glucose 20-27 insulin Homo sapiens 39-46 31392745-1 2020 Incretins are hormones secreted from enteroendocrine cells after nutrient intake that stimulate insulin secretion from beta cells in a glucose-dependent manner. Glucose 135-142 insulin Homo sapiens 96-103 32166667-1 2020 Thyroid hormones have a specific effect on glucose-induced insulin secretion from the pancreas. Glucose 43-50 insulin Homo sapiens 59-66 31740479-8 2020 Insulin (3.4 +- 0.8 mU/L; P < 0.01) and HOMA-IR (1.7 +- 0.1 vs. 2.4 +- 0.2; P < 0.01) rose, fasting GIP (-1.4 +- 0.8 pmol/L; P < 0.01) and AUC GIP dropped (2,524 +- 178 vs. 1,911 +- 162 [pmol/L] x min; P < 0.01), but fasting glucose (-0.3 +- 1.4 mg/dL), GLP-1 (1.3 +- 0.8 pmol/L), and AUC GLP-1 (2,956 +- 180 vs. 2,864 +- 93 [pmol/L] x min) remained unchanged. Glucose 225-232 insulin Homo sapiens 0-7 31902063-9 2020 Faster-acting insulin aspart is a relatively new option with the advantage of better postprandial glucose coverage. Glucose 98-105 insulin Homo sapiens 14-21 32097996-3 2020 However, most of the glucose-lowering therapies such as insulin, sulfonylureas, glinides, and thiazolidinediones induce weight gain, which makes the management of overweight/obese T2DM patients challenging. Glucose 21-28 insulin Homo sapiens 56-63 32293140-3 2020 Herein, a novel platform to perform glucose-stimulated insulin secretion (GSIS) assays with single islets is presented for studying the dynamics of insulin release at high temporal resolution. Glucose 36-43 insulin Homo sapiens 148-155 32077342-2 2020 This hurdle could be addressed by glucose-responsive insulin delivery based on real-time continuous glucose measurements.Areas covered: This review summaries recent advances of closed-loop systems in children and adolescents with type 1 diabetes, using both single- and dual-hormone closed-loop systems. Glucose 34-41 insulin Homo sapiens 53-60 31910150-10 2020 The patients with distinct insulin resistance and insulin release should be followed up, especially for those with reduced or even absent insulin response to glucose stimulation. Glucose 158-165 insulin Homo sapiens 27-34 31910150-10 2020 The patients with distinct insulin resistance and insulin release should be followed up, especially for those with reduced or even absent insulin response to glucose stimulation. Glucose 158-165 insulin Homo sapiens 50-57 31910150-10 2020 The patients with distinct insulin resistance and insulin release should be followed up, especially for those with reduced or even absent insulin response to glucose stimulation. Glucose 158-165 insulin Homo sapiens 50-57 32077342-2 2020 This hurdle could be addressed by glucose-responsive insulin delivery based on real-time continuous glucose measurements.Areas covered: This review summaries recent advances of closed-loop systems in children and adolescents with type 1 diabetes, using both single- and dual-hormone closed-loop systems. Glucose 100-107 insulin Homo sapiens 53-60 30951481-2 2020 State-of-the-art glucose control systems automatically regulate the basal insulin infusion. Glucose 17-24 insulin Homo sapiens 74-81 31534089-11 2020 Conclusion The present study showed that high plasma glucose levels and severe liver fibrosis stage influence insulin secretion levels in Japanese patients with NAFLD. Glucose 53-60 insulin Homo sapiens 110-117 31013208-2 2020 Blood glucose levels tend to decline during diving, probably because of changes in insulin requirements and resistance, due to increased physical activity and effects of hyperbaric environment on glucose tolerance. Glucose 6-13 insulin Homo sapiens 83-90 31806561-1 2020 BACKGROUND: The insulin-responsive glucose transporter 4 (GLUT4) plays prominent role in insulin-mediated facilitated glucose uptake into most of the cell types, majorly muscle, liver and adipose tissue. Glucose 35-42 insulin Homo sapiens 16-23 30945727-0 2020 The triglyceride-glucose index as a measure of insulin resistance and risk of obesity-related cancers. Glucose 17-24 insulin Homo sapiens 47-54 31449359-3 2020 On top of its glucose-lowering action, insulin may exert anti-inflammatory effects, rendering it an attractive therapeutic choice for a type of diabetes in which autoinflammation and beta cell insufficiency play major pathogenetic roles. Glucose 14-21 insulin Homo sapiens 39-46 31806561-1 2020 BACKGROUND: The insulin-responsive glucose transporter 4 (GLUT4) plays prominent role in insulin-mediated facilitated glucose uptake into most of the cell types, majorly muscle, liver and adipose tissue. Glucose 35-42 insulin Homo sapiens 89-96 31806561-1 2020 BACKGROUND: The insulin-responsive glucose transporter 4 (GLUT4) plays prominent role in insulin-mediated facilitated glucose uptake into most of the cell types, majorly muscle, liver and adipose tissue. Glucose 118-125 insulin Homo sapiens 16-23 31806561-1 2020 BACKGROUND: The insulin-responsive glucose transporter 4 (GLUT4) plays prominent role in insulin-mediated facilitated glucose uptake into most of the cell types, majorly muscle, liver and adipose tissue. Glucose 118-125 insulin Homo sapiens 89-96 32005719-7 2020 Conversely, insulin use increases the risk for hypoglycemia and requires close blood glucose monitoring and frequent adjustments to glucose infusion and insulin dosage. Glucose 85-92 insulin Homo sapiens 12-19 31735358-7 2020 Moreover, insulin reduced glucose production in rat proximal tubules and the expression of gluconeogenic genes in human and rat proximal tubules. Glucose 26-33 insulin Homo sapiens 10-17 31785256-8 2020 Insulin sensitivity was assessed via intravenous glucose tolerance test. Glucose 49-56 insulin Homo sapiens 0-7 32029226-9 2020 Functional characterization included glucose-stimulated insulin secretion and apoptosis assays. Glucose 37-44 insulin Homo sapiens 56-63 32005719-7 2020 Conversely, insulin use increases the risk for hypoglycemia and requires close blood glucose monitoring and frequent adjustments to glucose infusion and insulin dosage. Glucose 132-139 insulin Homo sapiens 12-19 31984772-6 2020 The continuous overdose of a single insulin for decades has resulted in hypoglycemic episodes almost daily, with consequent high fluctuations in blood glucose levels. Glucose 151-158 insulin Homo sapiens 36-43 31667906-4 2020 MIN6 cells were treated by TNF-alpha; then, viability, apoptosis, and insulin secretion were assessed by performing Cell Counting Kit-8 assay, flow cytometry, glucose-stimulated insulin secretion assay, and western blot. Glucose 159-166 insulin Homo sapiens 178-185 31677208-0 2020 beta-cell function, incretin response, and insulin sensitivity of glucose and fat metabolism in obese youth: Relationship to OGTT-time-to-glucose-peak. Glucose 66-73 insulin Homo sapiens 43-50 31677208-1 2020 BACKGROUND: In adults, the time-to-glucose-peak at or after 30 minutes during an oral glucose tolerance test (OGTT) identifies physiologically distinct groups with differences in insulin sensitivity, beta-cell function and risk for type 2 diabetes. Glucose 35-42 insulin Homo sapiens 179-186 31677208-1 2020 BACKGROUND: In adults, the time-to-glucose-peak at or after 30 minutes during an oral glucose tolerance test (OGTT) identifies physiologically distinct groups with differences in insulin sensitivity, beta-cell function and risk for type 2 diabetes. Glucose 86-93 insulin Homo sapiens 179-186 31677208-8 2020 CONCLUSIONS: In obese non-diabetic youth, those with a Late-peak vs an Early-peak glucose during an OGTT showed diminished beta-cell function, blunted incretin secretion, and lower insulin sensitivity of glucose and FFA metabolism. Glucose 82-89 insulin Homo sapiens 181-188 31677208-8 2020 CONCLUSIONS: In obese non-diabetic youth, those with a Late-peak vs an Early-peak glucose during an OGTT showed diminished beta-cell function, blunted incretin secretion, and lower insulin sensitivity of glucose and FFA metabolism. Glucose 204-211 insulin Homo sapiens 181-188 31911245-3 2020 Traditionally, T2D is considered a metabolic disorder epitomized by prolonged elevated levels of glucose due to insulin resistance and/or decreased insulin secretion resulting from pancreatic beta-cells dysfunction. Glucose 97-104 insulin Homo sapiens 112-119 31956961-3 2020 Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower insulin levels and sulfonylureas increase insulin levels, while both lower glucose levels. Glucose 7-14 insulin Homo sapiens 56-63 31765558-0 2020 Glucose-Responsive Nanoparticles for Rapid and Extended Self-Regulated Insulin Delivery. Glucose 0-7 insulin Homo sapiens 71-78 32005949-4 2020 Glargine U300 ("treat") and morning blood glucose level ("target") was significantly correlated with increasing insulin dose and decreasing blood glucose level in day 1-7, indicating that insulin amount was determined by target blood glucose level and lowered next target blood glucose level. Glucose 42-49 insulin Homo sapiens 112-119 32005949-4 2020 Glargine U300 ("treat") and morning blood glucose level ("target") was significantly correlated with increasing insulin dose and decreasing blood glucose level in day 1-7, indicating that insulin amount was determined by target blood glucose level and lowered next target blood glucose level. Glucose 42-49 insulin Homo sapiens 188-195 32005949-4 2020 Glargine U300 ("treat") and morning blood glucose level ("target") was significantly correlated with increasing insulin dose and decreasing blood glucose level in day 1-7, indicating that insulin amount was determined by target blood glucose level and lowered next target blood glucose level. Glucose 146-153 insulin Homo sapiens 188-195 32005949-4 2020 Glargine U300 ("treat") and morning blood glucose level ("target") was significantly correlated with increasing insulin dose and decreasing blood glucose level in day 1-7, indicating that insulin amount was determined by target blood glucose level and lowered next target blood glucose level. Glucose 146-153 insulin Homo sapiens 188-195 32005949-4 2020 Glargine U300 ("treat") and morning blood glucose level ("target") was significantly correlated with increasing insulin dose and decreasing blood glucose level in day 1-7, indicating that insulin amount was determined by target blood glucose level and lowered next target blood glucose level. Glucose 146-153 insulin Homo sapiens 188-195 32005949-7 2020 This method is pretty simple, flexible and cheap, and provides information about the dynamic pathophysiological alteration of insulin resistance and glucotoxicity from the profile of blood glucose levels and insulin shot. Glucose 189-196 insulin Homo sapiens 126-133 31765558-7 2020 Importantly, the concentration of human insulin in mouse serum is enhanced more than 3-fold with elevated glucose levels, providing direct evidence of glucose-responsiveness in animals. Glucose 106-113 insulin Homo sapiens 40-47 31996693-3 2020 Furthermore, a single high-dose of TCDD (200 microg/kg) suppressed both fasting and glucose-induced plasma insulin levels and promoted beta-cell apoptosis after 7 days in male mice. Glucose 84-91 insulin Homo sapiens 107-114 31765558-7 2020 Importantly, the concentration of human insulin in mouse serum is enhanced more than 3-fold with elevated glucose levels, providing direct evidence of glucose-responsiveness in animals. Glucose 151-158 insulin Homo sapiens 40-47 32550159-8 2020 These relationships were mediated by the presence of complications and the use of insulin, with lower levels of physical activity being found among patients with macrovascular complications and higher frequencies of glucose monitoring among patients on insulin. Glucose 216-223 insulin Homo sapiens 82-89 32051828-10 2020 There was a stepwise increase in the release of insulin and c-peptide, as a function of increasing glucose concentrations, indicating that the differentiated cells were glucose sensitive and insulin responsive. Glucose 99-106 insulin Homo sapiens 48-69 31979403-4 2020 As an alternative approach, human pluripotent stem cells (hPSCs) can provide an unlimited source of pancreatic cells that have the ability to secrete insulin in response to a high blood glucose level. Glucose 186-193 insulin Homo sapiens 150-157 32051828-10 2020 There was a stepwise increase in the release of insulin and c-peptide, as a function of increasing glucose concentrations, indicating that the differentiated cells were glucose sensitive and insulin responsive. Glucose 99-106 insulin Homo sapiens 48-55 32051828-10 2020 There was a stepwise increase in the release of insulin and c-peptide, as a function of increasing glucose concentrations, indicating that the differentiated cells were glucose sensitive and insulin responsive. Glucose 169-176 insulin Homo sapiens 48-69 32051828-10 2020 There was a stepwise increase in the release of insulin and c-peptide, as a function of increasing glucose concentrations, indicating that the differentiated cells were glucose sensitive and insulin responsive. Glucose 169-176 insulin Homo sapiens 48-55 32233537-3 2020 Intravenous glucose tolerance test (IVGTT) is such a protocol to determine an individual insulin sensitivity and glucose effectiveness indices. Glucose 12-19 insulin Homo sapiens 89-96 31937691-3 2020 Insulin doses can be adjusted based on blood glucose monitoring, which may compensate for lack of viability. Glucose 45-52 insulin Homo sapiens 0-7 31839542-4 2020 Here, we demonstrated that human SC islets reaggregated from cryopreserved cells display glucose-stimulated insulin secretion in vitro. Glucose 89-96 insulin Homo sapiens 108-115 31566370-1 2020 Sulfonylureas and glinides are commonly used oral insulin secretagogues (ISs) that act on the pancreatic ATP-sensitive potassium (KATP) channel to promote insulin secretion in order to lower the blood glucose level. Glucose 201-208 insulin Homo sapiens 50-57 31566370-1 2020 Sulfonylureas and glinides are commonly used oral insulin secretagogues (ISs) that act on the pancreatic ATP-sensitive potassium (KATP) channel to promote insulin secretion in order to lower the blood glucose level. Glucose 201-208 insulin Homo sapiens 155-162 31926090-2 2020 As an effort to attain rapid, gradually and more definite blood glucose, insulin is given intravenously. Glucose 64-71 insulin Homo sapiens 73-80 31883920-2 2020 Recent advances have led to the production of glucose-responsive insulin-secreting cells in vitro, but resulting cells remain less mature than their adult primary beta cell counterparts. Glucose 46-53 insulin Homo sapiens 65-72 31883920-7 2020 Ablation of LIN28B during human embryonic stem cell (hESC) differentiation toward beta cells led to a more mature glucose-stimulated insulin secretion profile and the suppression of juvenile-specific genes. Glucose 114-121 insulin Homo sapiens 133-140 31926091-0 2020 The effect of premixed insulin to blood glucose concentration in patients with type 2 diabetes mellitus. Glucose 40-47 insulin Homo sapiens 23-30 31926091-2 2020 This study aimed to examine the profile of premixed insulin related to blood glucose concentration and to identify the drug interactions due to the combination of premixed insulin with other drugs taken by T2DM patients. Glucose 77-84 insulin Homo sapiens 52-59 31936857-8 2020 IEC (intestinal epithelial cells) incubation with a high glucose + insulin dose produced an increase of p85alpha and p110beta. Glucose 57-64 insulin Homo sapiens 67-74 32377524-0 2020 Effect of Insulin on Proximal Tubules Handling of Glucose: A Systematic Review. Glucose 50-57 insulin Homo sapiens 10-17 32377524-2 2020 Modulation of glomerular filtration and renal glucose disposal are some of the insulin actions, but little is known about a possible insulin effect on tubular glucose reabsorption. Glucose 46-53 insulin Homo sapiens 79-86 32377524-3 2020 This review is aimed at synthesizing the current knowledge about insulin action on glucose handling by proximal tubules. Glucose 83-90 insulin Homo sapiens 65-72 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 248-255 insulin Homo sapiens 0-7 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 248-255 insulin Homo sapiens 176-183 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 248-255 insulin Homo sapiens 176-183 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 290-297 insulin Homo sapiens 0-7 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 290-297 insulin Homo sapiens 176-183 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 290-297 insulin Homo sapiens 176-183 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 290-297 insulin Homo sapiens 0-7 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 290-297 insulin Homo sapiens 176-183 32377524-8 2020 Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Glucose 290-297 insulin Homo sapiens 176-183 32377524-9 2020 Besides, insulin regulates SGLT2 inhibitor bioavailability, inhibits renal gluconeogenesis, and interferes with Na+K+ATPase activity impacting on glucose transport. Glucose 146-153 insulin Homo sapiens 9-16 31936632-7 2020 Mitochondrial localization of Nor1 reduced glucose oxidation, lowered ATP production rates, and inhibited glucose-stimulated insulin secretion. Glucose 106-113 insulin Homo sapiens 125-132 31919068-5 2020 Throughout his admission, there were incidental findings of asymptomatic hypoglycaemia (serum blood glucose <40 mg/dL), which was later found to be caused by anti-insulin monoclonal antibodies produced by the neoplastic plasma cells. Glucose 100-107 insulin Homo sapiens 166-173 31839261-1 2020 Two key prerequisites for glucose-stimulated insulin secretion (GSIS) in beta cells are the proximity of insulin granules to the plasma membrane and their anchoring or docking to the plasma membrane (PM). Glucose 26-33 insulin Homo sapiens 45-52 31839261-1 2020 Two key prerequisites for glucose-stimulated insulin secretion (GSIS) in beta cells are the proximity of insulin granules to the plasma membrane and their anchoring or docking to the plasma membrane (PM). Glucose 26-33 insulin Homo sapiens 105-112 31863584-1 2020 Glucose transporter 4 (GLUT4) is sequestered inside muscle and fat and then released by vesicle traffic to the cell surface in response to postprandial insulin for blood glucose clearance. Glucose 170-177 insulin Homo sapiens 152-159 31690627-4 2020 Insulin treatment increased glucose uptake and conversion to lactate, with the latter responding more to insulin than did other metabolic fates of glucose. Glucose 28-35 insulin Homo sapiens 0-7 31690627-4 2020 Insulin treatment increased glucose uptake and conversion to lactate, with the latter responding more to insulin than did other metabolic fates of glucose. Glucose 147-154 insulin Homo sapiens 0-7 31677889-0 2020 Insulin resistance, but not insulin response, during oral glucose tolerance test (OGTT) is associated to worse histological outcome in obese NAFLD. Glucose 58-65 insulin Homo sapiens 0-7 31839570-6 2020 Following entrainment, hPSC-derived islets gain persistent chromatin changes and rhythmic insulin responses with a raised glucose threshold, a hallmark of functional maturity, and function within days of transplantation. Glucose 122-129 insulin Homo sapiens 90-97 31646540-1 2020 Insulin secretion in humans is usually induced by mixed meals, which upon ingestion, increase the plasma concentration of glucose, fatty acids, amino acids, and incretins like glucagon-like peptide 1. Glucose 122-129 insulin Homo sapiens 0-7 32002800-4 2020 Insulin is a crucial hormone for glucose balance of the body. Glucose 33-40 insulin Homo sapiens 0-7 31711109-13 2020 Insulin resistance and uric acid concentrations were beneficially affected by replacement of fructose with glucose. Glucose 107-114 insulin Homo sapiens 0-7 31688066-13 2020 CONCLUSION: Second-generation insulin analogues and newer insulin infusion systems that automatically self-adjust according to patients continuous glucose monitor readings are important tools improving the treatment and quality of life of these women. Glucose 147-154 insulin Homo sapiens 30-37 31688066-13 2020 CONCLUSION: Second-generation insulin analogues and newer insulin infusion systems that automatically self-adjust according to patients continuous glucose monitor readings are important tools improving the treatment and quality of life of these women. Glucose 147-154 insulin Homo sapiens 58-65 31833871-7 2020 It enables adjustment of basal insulin to daily requirements and circadian needs, offers more precise treatment for meals and physical activity, and, when integrated with continuous glucose monitoring, allows glucose responsive insulin delivery. Glucose 209-216 insulin Homo sapiens 228-235 31773226-1 2020 Insulin oligosaccharide conjugates hold promise as potential glucose-responsive insulins (GRIs), which can improve the therapeutic index of insulins and mitigate the risk of hypoglycemia. Glucose 61-68 insulin Homo sapiens 0-7 33465774-1 2020 During normal pregnancy, increased insulin resistance acts as an adaptation to enhance materno-foetal nutrient transfer and meet the nutritional needs of the developing foetus, particularly in relation to glucose requirements. Glucose 205-212 insulin Homo sapiens 35-42 32229444-5 2020 RESULTS: Both incremental area under the curve (IAUC) 2h for glucose and insulin were higher in dinner at 21:00 than those in dinner at 18:00 (IAUC glucose: 449+-83 vs 216+-43 mmol/Lxmin, p<0.01, IAUC insulin:772+-104 vs 527+-107 muU/mLxmin, p<0.01, mean+-SEM). Glucose 61-68 insulin Homo sapiens 201-208 32115511-5 2020 Activation of PPARgamma by WSF-7 promotes adipogenesis, adiponectin oligomerization and insulin-induced glucose uptake. Glucose 104-111 insulin Homo sapiens 88-95 31864905-3 2020 The present study reported the optimization of Fla-CN to obtain a new derivative, 10b, which has improved glucose consumption at the nanomolar level (EC50 = 0.3 nM) in insulin resistant (IR) HepG2 cells. Glucose 106-113 insulin Homo sapiens 168-175 31958302-1 2020 INTRODUCTION: Risk of insulin resistance, dyslipidemia, diabetes and cardiac death is increased in Asians and Europeans with normal glucose tolerance (NGT) and 1-hour glucose >=8.6 mmol/L. Glucose 132-139 insulin Homo sapiens 22-29 31958302-1 2020 INTRODUCTION: Risk of insulin resistance, dyslipidemia, diabetes and cardiac death is increased in Asians and Europeans with normal glucose tolerance (NGT) and 1-hour glucose >=8.6 mmol/L. Glucose 167-174 insulin Homo sapiens 22-29 31892750-5 2020 Adjustments of insulin dosage were performed based on blood glucose concentrations measured with a continuous blood monitoring system (CGMS). Glucose 60-67 insulin Homo sapiens 15-22 31376318-7 2020 Measurement of insulin and the cleaved connecting peptide (C-peptide) in response to different concentrations of glucose, were performed using ELISA kits. Glucose 113-120 insulin Homo sapiens 15-22 31376318-7 2020 Measurement of insulin and the cleaved connecting peptide (C-peptide) in response to different concentrations of glucose, were performed using ELISA kits. Glucose 113-120 insulin Homo sapiens 59-68 32223315-0 2020 The Effect of Recovery Warm-up Time Following Cold Storage on the Dynamic Glucose-stimulated Insulin Secretion of Isolated Human Islets. Glucose 74-81 insulin Homo sapiens 93-100 32223315-2 2020 A critical component of islet cell quality is beta-cell function, and perifusion-based assessments of dynamic glucose-stimulated insulin secretion (GSIS) are the most informative method to assess this, as they provide the most complex in vitro evaluation of GSIS. Glucose 110-117 insulin Homo sapiens 129-136 32364405-6 2020 The isolated islets of the CORM-2 pretreatment group showed reduced apoptotic rate, improved viability, and higher glucose-stimulated insulin secretion, and functional gene expression in comparison to control group. Glucose 115-122 insulin Homo sapiens 134-141 30328570-1 2020 Traditional glucose-lowering chemical agents, including various types of insulin and insulin secretagogues, insulin sensitizers, gliptins, etc., are based on diabetic pathogenesis of insulin resistance (IR) and islet insufficiency. Glucose 12-19 insulin Homo sapiens 73-80 30328570-1 2020 Traditional glucose-lowering chemical agents, including various types of insulin and insulin secretagogues, insulin sensitizers, gliptins, etc., are based on diabetic pathogenesis of insulin resistance (IR) and islet insufficiency. Glucose 12-19 insulin Homo sapiens 85-92 31392840-2 2020 In Cohort 1, insulin tregopil administered 10 to 20 minutes before a meal resulted in optimal postmeal exposure and demonstrated better postprandial glucose-lowering effect (glucose area under concentration-time curve [AUC]) compared to the 30-minute group. Glucose 149-156 insulin Homo sapiens 13-20 31392840-2 2020 In Cohort 1, insulin tregopil administered 10 to 20 minutes before a meal resulted in optimal postmeal exposure and demonstrated better postprandial glucose-lowering effect (glucose area under concentration-time curve [AUC]) compared to the 30-minute group. Glucose 174-181 insulin Homo sapiens 13-20 31392840-8 2020 Insulin tregopil has a rapid onset of action of approximately 10 minutes and, when administered 10 to 20 minutes before a meal, demonstrated up to 13% to 18% reduction in blood glucose levels compared to baseline. Glucose 177-184 insulin Homo sapiens 0-7 31526351-1 2020 BACKGROUND: Diabetes is a metabolic disorder associated with abnormally high levels of glucose in the blood due to inadequate production of insulin or inadequate sensitivity of cells to the action of insulin. Glucose 87-94 insulin Homo sapiens 140-147 31526351-1 2020 BACKGROUND: Diabetes is a metabolic disorder associated with abnormally high levels of glucose in the blood due to inadequate production of insulin or inadequate sensitivity of cells to the action of insulin. Glucose 87-94 insulin Homo sapiens 200-207 31544698-8 2020 Then, a high association of glucose in blood beside insulin was found out. Glucose 28-35 insulin Homo sapiens 52-59 31686640-2 2020 Phosphorus, an essential micronutrient, is closely linked to the cellular metabolism of glucose for energy production, and serum inorganic phosphate is often transported into cells along with glucose during insulin therapy. Glucose 192-199 insulin Homo sapiens 207-214 31713487-6 2020 Higher secretion of glucocorticoids influence glucose metabolism by promoting gluconeogenesis in liver, suppressing glucose uptake (adipocytes and skeletal muscles), promoting lipolysis in adipocytes, suppressing insulin secretion, inflicting insulin resistance and inflammation. Glucose 46-53 insulin Homo sapiens 213-220 31713487-6 2020 Higher secretion of glucocorticoids influence glucose metabolism by promoting gluconeogenesis in liver, suppressing glucose uptake (adipocytes and skeletal muscles), promoting lipolysis in adipocytes, suppressing insulin secretion, inflicting insulin resistance and inflammation. Glucose 46-53 insulin Homo sapiens 243-250 31670620-4 2020 Abnormally lower insulin secretion from beta-cells, insulin insensitivity, and insulin tolerance lead to higher plasma glucose levels, resulting in metabolic complications. Glucose 119-126 insulin Homo sapiens 17-24 31670620-4 2020 Abnormally lower insulin secretion from beta-cells, insulin insensitivity, and insulin tolerance lead to higher plasma glucose levels, resulting in metabolic complications. Glucose 119-126 insulin Homo sapiens 52-59 31670620-4 2020 Abnormally lower insulin secretion from beta-cells, insulin insensitivity, and insulin tolerance lead to higher plasma glucose levels, resulting in metabolic complications. Glucose 119-126 insulin Homo sapiens 52-59 31612824-1 2020 Insulin (INS) therapy played a great role in patients with type 1 and type 2 diabetes to regulate blood glucose levels. Glucose 104-111 insulin Homo sapiens 0-7 32693765-2 2020 Because endothelium is also the barrier for insulin movement into tissue, it acts as a gate keeper for transport and glucose uptake. Glucose 117-124 insulin Homo sapiens 44-51 32851952-4 2020 Moreover, the review focuses on nanoscale based approaches i.e. closed-loop insulin delivery systems which detects any fluctuation in blood glucose levels and allow controlled release of a drug, thus are also called as selfregulating insulin release system. Glucose 140-147 insulin Homo sapiens 76-83 32851952-4 2020 Moreover, the review focuses on nanoscale based approaches i.e. closed-loop insulin delivery systems which detects any fluctuation in blood glucose levels and allow controlled release of a drug, thus are also called as selfregulating insulin release system. Glucose 140-147 insulin Homo sapiens 234-241 31746292-2 2020 It is also the primary site of insulin-mediated glucose uptake, and skeletal muscle insulin resistance, that is, diminished response to insulin, is characteristic of Type 2 diabetes (T2DM). Glucose 48-55 insulin Homo sapiens 31-38 32209037-3 2020 DM is characterized by high blood glucose levels that are caused by either lack of insulin (Type I) or resistance to the actions of insulin (Type II). Glucose 34-41 insulin Homo sapiens 83-90 32209037-3 2020 DM is characterized by high blood glucose levels that are caused by either lack of insulin (Type I) or resistance to the actions of insulin (Type II). Glucose 34-41 insulin Homo sapiens 132-139 32286938-2 2020 In pancreatic beta-cells, it plays chief role by controlling glucose-stimulated secretion of insulin and in liver hepatocyte cells, it controls metabolism of carbohydrates. Glucose 61-68 insulin Homo sapiens 93-100 32674731-2 2020 Multicellular organisms need to adequately control individual glucose uptake by the cells, and the insulin-glucagon endocrine system serves as the key glucose regulation mechanism. Glucose 151-158 insulin Homo sapiens 99-106 32674731-3 2020 Insulin allows for effective glucose entry into the cells when blood glucose levels are high, and glucagon acts as its opponent, balancing low blood glucose levels. Glucose 29-36 insulin Homo sapiens 0-7 32674731-3 2020 Insulin allows for effective glucose entry into the cells when blood glucose levels are high, and glucagon acts as its opponent, balancing low blood glucose levels. Glucose 69-76 insulin Homo sapiens 0-7 32674731-3 2020 Insulin allows for effective glucose entry into the cells when blood glucose levels are high, and glucagon acts as its opponent, balancing low blood glucose levels. Glucose 69-76 insulin Homo sapiens 0-7 32674731-4 2020 A lack of insulin will prevent glucose entry to the cells, resulting in glucose accumulation in the bloodstream. Glucose 31-38 insulin Homo sapiens 10-17 32674731-4 2020 A lack of insulin will prevent glucose entry to the cells, resulting in glucose accumulation in the bloodstream. Glucose 72-79 insulin Homo sapiens 10-17 31423551-2 2020 The contribution of the triggering/ATP-sensitive potassium (KATP)-dependent Ca2+ signalling and KATP-independent amplification pathways, that include anaplerosis and lipid signalling of glucose-stimulated insulin secretion (GSIS), are well established. Glucose 186-193 insulin Homo sapiens 205-212 31455688-6 2020 RESULTS: With the same insulin dose, increasing the amount of fat resulted in a significant dose-dependent reduction in incremental area under the curve for glucose (iAUCglucose) in the early postprandial period (0-2 h; P = 0.008) and increase in iAUCglucose in the late postprandial period (2-5 h; P = 0.004). Glucose 157-164 insulin Homo sapiens 23-30 31483167-0 2020 Examining the Relationship Between Pre- and Postprandial Glucose Levels and Insulin Bolus Timing Using Bluetooth-Enabled Insulin Pen Cap Technology and Continuous Glucose Monitoring. Glucose 57-64 insulin Homo sapiens 76-83 31483167-2 2020 New technology enabling tracking and logging of insulin doses, combined with continuous glucose monitoring (CGM), may provide insight into the relationship between insulin administration and glucose levels. Glucose 88-95 insulin Homo sapiens 164-171 31483167-2 2020 New technology enabling tracking and logging of insulin doses, combined with continuous glucose monitoring (CGM), may provide insight into the relationship between insulin administration and glucose levels. Glucose 191-198 insulin Homo sapiens 48-55 31483167-2 2020 New technology enabling tracking and logging of insulin doses, combined with continuous glucose monitoring (CGM), may provide insight into the relationship between insulin administration and glucose levels. Glucose 191-198 insulin Homo sapiens 164-171 31483167-10 2020 Conclusions: The use of Bluetooth-enabled pen caps, with CGM, in persons with T1D on MDI can illustrate the relationship between insulin bolus timing and postprandial glucose. Glucose 167-174 insulin Homo sapiens 129-136 31483167-11 2020 These data may help clinicians and patients understand the impact of timing of insulin doses on glucose levels and glycemic control. Glucose 96-103 insulin Homo sapiens 79-86 31575640-11 2020 CONCLUSIONS: Fully closed-loop insulin delivery using either faster or standard insulin aspart was safe and efficient in achieving near-normal glucose concentrations outside postprandial periods. Glucose 143-150 insulin Homo sapiens 31-38 32342455-1 2020 In insulin resistance, alterations occur in the signalling pathways that modulate glucose uptake into cells, especially skeletal muscle cells, resulting in impaired glucose homeostasis. Glucose 82-89 insulin Homo sapiens 3-10 32342455-2 2020 Glucose uptake into cells is controlled by a number of pathways, some of which are insulin-dependent. Glucose 0-7 insulin Homo sapiens 83-90 31567147-8 2020 THERAPEUTIC ADVANCES: New insulin formulations (ultralong basal and ultrarapid analogues) were designed to obtain a prolonged, flatter profile, with less hypoglycemia and improvement of postprandial glucose control, respectively. Glucose 199-206 insulin Homo sapiens 26-33 31567147-9 2020 The next generation of insulin therapy is probably best represented by the "smart" (glucose-responsive) insulins, which deliver it according to an endogenous glucose-sensing feedback mechanism. Glucose 84-91 insulin Homo sapiens 23-30 31567147-9 2020 The next generation of insulin therapy is probably best represented by the "smart" (glucose-responsive) insulins, which deliver it according to an endogenous glucose-sensing feedback mechanism. Glucose 158-165 insulin Homo sapiens 23-30 31567175-2 2020 But even with the availability of oral glucose-lowering drugs, insulin supplementation was often needed to achieve good glucose control in type 2 diabetes. Glucose 39-46 insulin Homo sapiens 63-70 31567175-2 2020 But even with the availability of oral glucose-lowering drugs, insulin supplementation was often needed to achieve good glucose control in type 2 diabetes. Glucose 120-127 insulin Homo sapiens 63-70 31567175-7 2020 THERAPEUTIC ADVANCES: Adding new oral glucose-lowering drugs to insulin such as DPP-4 inhibitors lead to a modest HbA1c reduction without weight gain and no increase in hypoglycemia. Glucose 38-45 insulin Homo sapiens 64-71 31567175-13 2020 CONCLUSIONS: Aggressive weight loss strategies together with the new glucose-lowering drugs which do not cause hypoglycemia nor weight gain should limit the number of patients with type 2 diabetes needing insulin. Glucose 69-76 insulin Homo sapiens 205-212 31876563-6 2020 The longer acting insulins can provide stable, reproducible basal insulin with reduced rates of hypoglycemia, particularly nocturnal hypoglycemia, greater efficacy in reducing mean glucose and glucose variability while increasing time in glucose target range. Glucose 181-188 insulin Homo sapiens 18-25 31876563-6 2020 The longer acting insulins can provide stable, reproducible basal insulin with reduced rates of hypoglycemia, particularly nocturnal hypoglycemia, greater efficacy in reducing mean glucose and glucose variability while increasing time in glucose target range. Glucose 193-200 insulin Homo sapiens 18-25 31876563-6 2020 The longer acting insulins can provide stable, reproducible basal insulin with reduced rates of hypoglycemia, particularly nocturnal hypoglycemia, greater efficacy in reducing mean glucose and glucose variability while increasing time in glucose target range. Glucose 193-200 insulin Homo sapiens 18-25 31465760-11 2020 Nonsignificant (9%) lowering of the area under a glucose tolerance curve following bionic ambulation required 20% less insulin than at rest. Glucose 49-56 insulin Homo sapiens 119-126 32226004-1 2020 Background: Congenital hyperinsulinism is a disease of the glucose metabolism, relevant in pediatric endocrinology because of the elevated production of insulin according to blood glucose level, which leads to persistent severe hypoglycemia. Glucose 59-66 insulin Homo sapiens 28-35 31662305-4 2020 RESEARCH DESIGN AND METHODS: Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp (M value) (glucose infusion rate in mg/kglean/min) and renal hemodynamic function by urinary inulin (GFR) and para-aminohippuric acid (effective renal plasma flow [ERPF]) clearances in participants with T2D without overt kidney disease. Glucose 110-117 insulin Homo sapiens 29-36 31776611-2 2020 Given the critical role of regulated insulin secretion in maintaining glucose homeostasis, environmental chemicals that reach the endocrine pancreas and cause beta cell injury are of particular concern. Glucose 70-77 insulin Homo sapiens 37-44 31776611-12 2020 Direct TCDD exposure to human and mouse islets in vitro resulted in suppressed glucose-induced insulin secretion. Glucose 79-86 insulin Homo sapiens 95-102 31813092-1 2020 Sodium-glucose cotransporter 2 (SGLT2) inhibitor clinical studies in type 1 diabetes mellitus (T1DM) have demonstrated reduced HbA1c and lower glucose variability with increased time in optimal glucose range as well as additional benefits of reductions in weight and insulin dose without increasing the incidence of hypoglycaemia. Glucose 7-14 insulin Homo sapiens 267-274 31653693-1 2020 BACKGROUND: Dextrose is commonly administered with insulin during the management of hyperkalaemia to avoid hypoglycaemia. Glucose 12-20 insulin Homo sapiens 51-58 31653693-3 2020 The aim of this study was to better characterise the changes in blood glucose and to identify patients who may have an increased response to insulin. Glucose 70-77 insulin Homo sapiens 141-148 31679138-6 2020 Insulin-resistant hepatocytes were cultured with different concentrations of DEX for 24 h, and the glucose concentration in the supernatant was measured. Glucose 99-106 insulin Homo sapiens 0-7 31679138-9 2020 RESULTS: After 48-h of culturing with 10 mug/mL insulin, glucose consumption in hepatocytes was found to be reduced. Glucose 57-64 insulin Homo sapiens 48-55 32334506-2 2020 It is a metabolic disorder characterized by high blood glucose level either as a result of impaired insulin secretion and/or insulin action usually termed insulin resistance. Glucose 55-62 insulin Homo sapiens 100-107 32334506-2 2020 It is a metabolic disorder characterized by high blood glucose level either as a result of impaired insulin secretion and/or insulin action usually termed insulin resistance. Glucose 55-62 insulin Homo sapiens 125-132 32416711-5 2020 The drug indirectly participates in the regulation of carbohydrate metabolism, influencing the increase in insulin sensitivity, supporting cellular uptake of glucose. Glucose 158-165 insulin Homo sapiens 107-114 32901912-1 2020 INTRODUCTION: Sodium glucose cotransporter 2 (SGLT2) inhibitors are insulin-independent and glucose-dependent anti-hyperglycaemic drugs that have shown potential as an adjuvant therapy to insulin for the treatment of type 1 diabetes mellitus (T1DM). Glucose 21-28 insulin Homo sapiens 68-75 32901912-1 2020 INTRODUCTION: Sodium glucose cotransporter 2 (SGLT2) inhibitors are insulin-independent and glucose-dependent anti-hyperglycaemic drugs that have shown potential as an adjuvant therapy to insulin for the treatment of type 1 diabetes mellitus (T1DM). Glucose 21-28 insulin Homo sapiens 188-195 31808097-9 2020 Combined phthalates influence on glucose and lipid metabolism may increase the possibility for NAFLD and insulin resistance development among exposed individuals. Glucose 33-40 insulin Homo sapiens 105-112 31625959-1 2020 OBJECTIVE: Insulin resistance (IR) has been established as a major risk factor for nonalcoholic fatty liver disease (NAFLD) where it exerts effects on plasma glucose homeostasis, cellular anabolism, and organ glucose uptake. Glucose 158-165 insulin Homo sapiens 11-18 31625959-1 2020 OBJECTIVE: Insulin resistance (IR) has been established as a major risk factor for nonalcoholic fatty liver disease (NAFLD) where it exerts effects on plasma glucose homeostasis, cellular anabolism, and organ glucose uptake. Glucose 209-216 insulin Homo sapiens 11-18 30396212-9 2020 Peripherally it amplified insulin action as demonstrated by a significant inhibition of endogenous glucose production and increased glucose infusion rate. Glucose 99-106 insulin Homo sapiens 26-33 30396212-9 2020 Peripherally it amplified insulin action as demonstrated by a significant inhibition of endogenous glucose production and increased glucose infusion rate. Glucose 132-139 insulin Homo sapiens 26-33 31614121-3 2020 Several lines of research converge to suggest that the insulin-responsive glucose transporter GluT4 plays a central role in hippocampal memory processes, and that reduced activation of this transporter may underpin the cognitive impairments seen as a consequence of insulin resistance. Glucose 74-81 insulin Homo sapiens 55-62 31614121-3 2020 Several lines of research converge to suggest that the insulin-responsive glucose transporter GluT4 plays a central role in hippocampal memory processes, and that reduced activation of this transporter may underpin the cognitive impairments seen as a consequence of insulin resistance. Glucose 74-81 insulin Homo sapiens 266-273 31771391-1 2020 Introduction: The activation of free fatty acid receptor 1 (FFAR1) induces insulin secretion in a glucose-dependent manner, and thereby is considered as an attractive anti-diabetic target. Glucose 98-105 insulin Homo sapiens 75-82 31914605-7 2020 In addition, ex vivo perifusion of recovered human islet grafts demonstrated glucose-stimulated insulin secretion. Glucose 77-84 insulin Homo sapiens 96-103 31755075-3 2020 This study aimed at enhancing the regenerative solution for diabetes by improving the differentiation of mesenchymal stromal cells (MSC) into glucose-sensitive, insulin-secreting cells through an epigenetic modification approach. Glucose 142-149 insulin Homo sapiens 161-168 31755075-7 2020 The cells responded to the high glucose challenge by secreting insulin in the media, as shown by ELISA. Glucose 32-39 insulin Homo sapiens 63-70 33040071-7 2020 Oral glucose tolerance testing showed severely increased plasma insulin concentration (>300 mU/L) with hypoglycemia (glucose 1.6 mmol/L) at 2.5 h. She was initially managed on dietary modifications, cornstarch, and then trialed on acarbose for postprandial hyperinsulinemic hypoglycemia (PPHH) with some response. Glucose 5-12 insulin Homo sapiens 64-71 31251175-7 2020 CONCLUSION: Our data show the feasibility of open- and closed-loop glucose control in diabetes patients using a device that combines insulin delivery and glucose sensing at a single tissue site. Glucose 67-74 insulin Homo sapiens 133-140 32854859-4 2020 Insulin not only regulates blood glucose levels, but also acts as a growth factor that is important for neuronal activity and repair. Glucose 33-40 insulin Homo sapiens 0-7 31863132-2 2020 The closed-loop system directs subcutaneous insulin delivery corresponding to the glucose concentration using a control algorithm. Glucose 82-89 insulin Homo sapiens 44-51 31512724-7 2020 Similar effects on blood glucose were observed with scores of insulin-sensitivity-reducing, insulin-secretion-reducing and glucose-raising alleles, respectively. Glucose 25-32 insulin Homo sapiens 62-69 31180589-2 2020 Insulin and glucagon oppositely modulate blood glucose levels in health, but a combined decline in insulin secretion together with increased glucagon secretion contribute to hyperglycemia in diabetes. Glucose 47-54 insulin Homo sapiens 0-7 32654995-7 2020 Besides routine glucose- and lipid-related parameters, we determined insulin sensitivity as the rate of glucose disappearance in a 2-step hyperinsulinemic-euglycemic clamp and the abdominal visceral fat area (VFA) by magnetic resonance imaging. Glucose 104-111 insulin Homo sapiens 69-76 31117804-12 2020 CONCLUSION: A safety system for an insulin dose recommender has been proven to be a viable solution to reduce the number of adverse events associated to glucose control in type 1 diabetes. Glucose 153-160 insulin Homo sapiens 35-42 31179612-0 2020 Impaired early-phase suppression of glucagon secretion after glucose load is associated with insulin requirement during pregnancy in gestational diabetes. Glucose 61-68 insulin Homo sapiens 93-100 31179612-8 2020 The early-phase glucagon secretion after glucose load, as determined by the changes in glucagon from the baseline to 30 min, was paradoxically augmented during mid-gestation in the Insulin group, but not in the Diet group. Glucose 41-48 insulin Homo sapiens 181-188 31216873-4 2020 METHODS: Our aim was to improve maternal glucose control in a cohort of insulin-requiring pregnant women enrolled in a telemedicine diabetes program. Glucose 41-48 insulin Homo sapiens 72-79 31216873-12 2020 CONCLUSION: For pregnancies complicated by insulin-requiring diabetes, use of cellular-enabled glucometers as part of a perinatal diabetes program improves glucose control at delivery with timely transmission of accurate values throughout gestation. Glucose 156-163 insulin Homo sapiens 43-50 31222973-0 2020 Proinsulin is sensitive to reflect glucose intolerance. Glucose 35-42 insulin Homo sapiens 0-10 31245904-0 2020 Proinsulin associates with poor beta-cell function, glucose-dependent insulinotropic peptide, and insulin resistance in persistent type 2 diabetes after Roux-en-Y gastric bypass in humans. Glucose 52-59 insulin Homo sapiens 0-10 31245904-0 2020 Proinsulin associates with poor beta-cell function, glucose-dependent insulinotropic peptide, and insulin resistance in persistent type 2 diabetes after Roux-en-Y gastric bypass in humans. Glucose 52-59 insulin Homo sapiens 3-10 31738010-1 2020 on "Accuracy of flash glucose monitoring in insulin-treated patients with type 2 diabetes". Glucose 22-29 insulin Homo sapiens 44-51 31697642-0 2020 microRNA-375 regulates glucose metabolism-related signaling for insulin secretion. Glucose 23-30 insulin Homo sapiens 64-71 31697642-1 2020 Enhanced beta cell glycolytic and oxidative metabolism are necessary for glucose-induced insulin secretion. Glucose 73-80 insulin Homo sapiens 89-96 31697642-5 2020 Additionally, miR-375 expression and glucose-induced insulin secretion were compared in islets from rats at different developmental ages. Glucose 37-44 insulin Homo sapiens 53-60 31697642-6 2020 We found that overexpressing of miR-375 in rat and human islet cells blunted insulin secretion in response to glucose but not to alpha-ketoisocaproate or KCl. Glucose 110-117 insulin Homo sapiens 77-84 31697642-10 2020 Finally, reduced miR-375 expression was associated with maturation of fetal rat beta cells and acquisition of glucose-induced insulin secretion function. Glucose 110-117 insulin Homo sapiens 126-133 31575640-11 2020 CONCLUSIONS: Fully closed-loop insulin delivery using either faster or standard insulin aspart was safe and efficient in achieving near-normal glucose concentrations outside postprandial periods. Glucose 143-150 insulin Homo sapiens 80-87 31512724-7 2020 Similar effects on blood glucose were observed with scores of insulin-sensitivity-reducing, insulin-secretion-reducing and glucose-raising alleles, respectively. Glucose 25-32 insulin Homo sapiens 92-99 31954050-4 2020 The rubrics of gluco-phenotype, endo-phenotype, metabolic phenotype, glucagon: insulin ratio, and adenosine monophosphate activated protein kinase (AMPK) status in planning glucose lowering therapy are explained. Glucose 173-180 insulin Homo sapiens 79-86 31678069-2 2020 Insulin and insulin like growth factor 1 (IGF-1) share many intracellular processes with both known to play a key role in glucose and protein metabolism in skeletal muscle. Glucose 122-129 insulin Homo sapiens 0-7 31666181-8 2020 During infections, an increase in blood glucose occurs and usually an increase in insulin dose is required. Glucose 40-47 insulin Homo sapiens 82-89 31425383-6 2020 Intestinal insulin-stimulated glucose uptake (GU) and fatty acid uptake (FAU) from circulation were measured using PET. Glucose 30-37 insulin Homo sapiens 11-18 31696935-0 2020 Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise. Glucose 41-48 insulin Homo sapiens 0-7 31696935-2 2020 Previous studies of insulin-stimulated GLUT4 translocation to the skeletal muscle membrane found insufficient increases to explain the increases in glucose uptake. Glucose 148-155 insulin Homo sapiens 20-27 31696935-3 2020 By determination of leg glucose uptake and interstitial muscle glucose concentration we calculated insulin-induced muscle membrane permeability to glucose 4 h after one-legged knee-extensor exercise during a submaximal euglycaemic hyperinsulinaemic clamp. Glucose 24-31 insulin Homo sapiens 99-106 31696935-3 2020 By determination of leg glucose uptake and interstitial muscle glucose concentration we calculated insulin-induced muscle membrane permeability to glucose 4 h after one-legged knee-extensor exercise during a submaximal euglycaemic hyperinsulinaemic clamp. Glucose 63-70 insulin Homo sapiens 99-106 31696935-4 2020 We found during submaximal insulin stimulation that muscle membrane permeability to glucose in humans increases twice as much in previously exercised vs. rested muscle and it outstrips the supply of glucose which then becomes limiting for glucose uptake. Glucose 84-91 insulin Homo sapiens 27-34 31696935-5 2020 This methodology can now be employed to determine muscle membrane permeability to glucose in people with diabetes, who have reduced insulin action, and in principle can also be used to determine membrane permeability to other substrates or metabolites. Glucose 82-89 insulin Homo sapiens 132-139 31696935-8 2020 Here we used leg glucose uptake (LGU) and interstitial muscle glucose concentration to calculate insulin-induced muscle membrane permeability to glucose, a variable not previously possible to quantify in humans. Glucose 17-24 insulin Homo sapiens 97-104 31696935-8 2020 Here we used leg glucose uptake (LGU) and interstitial muscle glucose concentration to calculate insulin-induced muscle membrane permeability to glucose, a variable not previously possible to quantify in humans. Glucose 62-69 insulin Homo sapiens 97-104 31696935-13 2020 We conclude that it is possible to measure functional muscle membrane permeability to glucose in humans and it increases twice as much in exercised vs. rested muscle during submaximal insulin stimulation. Glucose 86-93 insulin Homo sapiens 184-191 31644972-5 2020 However, the reduction of glucose transport into the muscle cells due to insulin resistance / insufficiency, leads to reduction in the ATP producing capacity of the mitochondria. Glucose 26-33 insulin Homo sapiens 73-80 31701450-4 2020 Here, we detail an in vitro method to analyze glucose uptake in conditionally immortalized human podocytes (Saleem, J Am Soc Nephrol 13:630-638, 2002; Coward, Diabetes 54:3095-3102, 2005); this assay is useful for detecting changes in podocyte metabolism, nutrient sensing, and insulin sensitivity. Glucose 46-53 insulin Homo sapiens 278-285 32180200-1 2020 Insulin is a hormone produced and secreted by the beta-cells of the pancreatic islets of Langerhans in response to increased blood glucose levels after a meal. Glucose 131-138 insulin Homo sapiens 0-7 32180200-3 2020 This signaling pathway is responsible for the pleiotropic actions of insulin on different tissues, such as regulation of glucose and lipid metabolism, proliferation, and differentiation. Glucose 121-128 insulin Homo sapiens 69-76 31689708-13 2020 This reaction could, for example, contribute to late postprandial glucose regulation by suppressing hepatic glucose production by portal venous insulin. Glucose 66-73 insulin Homo sapiens 144-151 31536778-7 2020 At this concentration, insulin-stimulated glucose uptake was increased, which corresponded to an increased phosphorylation of the insulin signaling protein Akt, and increased glycolysis measured by extracellular acidification rate (ECAR). Glucose 42-49 insulin Homo sapiens 23-30 31536778-7 2020 At this concentration, insulin-stimulated glucose uptake was increased, which corresponded to an increased phosphorylation of the insulin signaling protein Akt, and increased glycolysis measured by extracellular acidification rate (ECAR). Glucose 42-49 insulin Homo sapiens 130-137 31613996-0 2020 Reducing glucose variability with continuous subcutaneous insulin infusion is associated with reversal of axonal dysfunction in type 1 diabetes mellitus. Glucose 9-16 insulin Homo sapiens 58-65 31689708-13 2020 This reaction could, for example, contribute to late postprandial glucose regulation by suppressing hepatic glucose production by portal venous insulin. Glucose 108-115 insulin Homo sapiens 144-151 32564586-4 2020 After 48 hours of treatment with fluids and insulin infusion the serum glucose level and acidosis normalised. Glucose 71-78 insulin Homo sapiens 44-51 31841747-9 2020 Fasting serum glucose concentrations, even with higher serum insulin concentrations, were higher in the VLCA than ACA, indicating increased insulin resistance in VLCA. Glucose 14-21 insulin Homo sapiens 140-147 32721871-6 2020 Positive linear correlations of rCBF, body fat, and the serum levels of glucose and insulin were found, but no associations were detected using linear regression. Glucose 72-79 insulin Homo sapiens 84-91 31746289-1 2020 BACKGROUND: Insulin is a peptide hormone used for regulating blood glucose levels. Glucose 67-74 insulin Homo sapiens 12-19 31755817-7 2020 Furthermore, glucose consumption was 2.68 times that of control samples when tested with insulin-resistant HepG2 cell, showing potential use in type 2 diabetes. Glucose 13-20 insulin Homo sapiens 89-96 31495985-4 2020 The effect of chelator exposure on islet viability and recovery was assessed using flow cytometry, while glucose-stimulated insulin release (GSIR) assay was used to measure effects on islet function. Glucose 105-112 insulin Homo sapiens 124-131 33905473-1 2020 BACKGROUND: Diabetes is a chronic, metabolic disease, which is commonly associated with increased blood glucose levels caused by impaired secretion or function of insulin. Glucose 104-111 insulin Homo sapiens 163-170 32248180-5 2020 Decreases in postprandial glucose are also observed in people with a pre-diabetes condition in which insulin secretion is disturbed. Glucose 26-33 insulin Homo sapiens 101-108 32238640-4 2020 They have been used for home parenteral nutrition, with insulin injected into the bags for patients whose blood glucose becomes elevated. Glucose 112-119 insulin Homo sapiens 56-63 32370702-6 2020 By balancing pro-inflammatory and anti-inflammatory effects, the adipokines control insulin sensitivity and related glucose metabolism changes, lipid accumulation in the liver and other organs, and finally gonadal function. Glucose 116-123 insulin Homo sapiens 84-91 32046372-1 2020 Lipid metabolism-associated molecule abhydrolase domain containing 5 (ABHD5) has been reported to have a role in insulin-mediated glucose uptake, the deregulation of it is associated with gestational diabetes mellitus (GDM). Glucose 130-137 insulin Homo sapiens 113-120 32731709-7 2020 A positive correlation was found between some anthropometric indices and the following glycemic parameters: fasting blood glucose, HOMA-IR suggested that insulin resistance contributed to the growth of glycated compounds leading not only to the progression of NASH and affect the dysfunction of chondrocytes, but also influencing destruction of subchondral bone in osteoarthritis. Glucose 122-129 insulin Homo sapiens 154-161 31956633-8 2019 Conclusion: According to this study, basal-bolus insulin protocol, which supervised by clinical pharmacy service, showed better blood glucose control and infection remission compared to the sliding-scale protocol. Glucose 134-141 insulin Homo sapiens 49-56 31740584-1 2019 Insulin promotes glucose uptake by triggering the translocation of glucose transporter type 4 (GLUT4) from intracellular vesicles to the plasma membrane through exocytosis. Glucose 17-24 insulin Homo sapiens 0-7 31869355-6 2019 Insulin-modified frequently sampled intravenous glucose tolerance tests were performed before and after MCT to measure changes in Si, acute insulin response (AIR), disposition index (DI), and glucose effectiveness (Sg). Glucose 48-55 insulin Homo sapiens 0-7 31877933-2 2019 gamma-conglutin induced up-regulated transcriptomic and protein levels of insulin signalling pathway IRS-1, Glut-4, and PI3K, improving glucose uptake, while decreasing pro-inflammatory mediators as iNOs, TNFalpha, IL-1beta, INFgamma, IL-6, IL-12, IL-17, and IL-27; (4) Conclusion: These results suggest a promising use of NLL gamma-conglutin protein in functional foods, which could also be implemented in alternative diagnosis and therapeutic molecular tools helping to prevent and treat inflammatory-related diseases. Glucose 136-143 insulin Homo sapiens 74-81 31885383-3 2019 In addition, the insulin-producing cells differentiated from human pluripotent stem cells have limited ability to secrete sufficient hormones that can regulate the blood glucose level; therefore, improving the maturation by culturing cells with proper microenvironmental cues is strongly required. Glucose 170-177 insulin Homo sapiens 17-24 31697318-1 2019 It is accepted that insulin-secreting beta-cells release insulin in response to glucose even in the absence of functional ATP-sensitive K+ (KATP)-channels, which play a central role in a "consensus model" of secretion broadly accepted and widely reproduced in textbooks. Glucose 80-87 insulin Homo sapiens 20-27 31697318-1 2019 It is accepted that insulin-secreting beta-cells release insulin in response to glucose even in the absence of functional ATP-sensitive K+ (KATP)-channels, which play a central role in a "consensus model" of secretion broadly accepted and widely reproduced in textbooks. Glucose 80-87 insulin Homo sapiens 57-64 31462593-1 2019 In type 2 diabetes mellitus, metformin suppresses excessive insulin secretion in relation to the intake of glucose. Glucose 107-114 insulin Homo sapiens 60-67 31908508-7 2019 Reduced level of carnitine in T2D patients is known to participate in the impaired insulin-stimulated glucose utilization, while reduced betaine level in T2D patients is known as a common feature of this metabolic syndrome and can result in the reduced glycine production and the occurrence of insulin resistance. Glucose 102-109 insulin Homo sapiens 83-90 32042407-6 2019 The primary outcome was postprandial response in glucose metabolism, measured by samples of serum glucose and insulin in 20 min intervals for 120 min. Glucose 49-56 insulin Homo sapiens 110-117 31942227-11 2019 Flash glucose monitoring was more effective than self-monitoring of blood glucose in reducing the average time spent in hypoglycemia (-0.47 h [95% CI -0.73 to -0.21]) and the average number of hypoglycemia events (-0.16 [95% CI -0.29 to -0.03]) among adults with type 2 diabetes requiring intensive insulin therapy (GRADE: Moderate). Glucose 6-13 insulin Homo sapiens 299-306 31942227-19 2019 Conclusions: Based on an assessment of several glycemic outcomes, moderate-quality evidence shows that flash glucose monitoring improves diabetes management among adults with well-controlled type 1 diabetes and adults with type 2 diabetes requiring intensive insulin therapy. Glucose 109-116 insulin Homo sapiens 259-266 31942227-20 2019 We estimate that publicly funding flash glucose monitoring in Ontario for people with type 1 diabetes and for people with type 2 diabetes requiring intensive insulin therapy who are eligible for coverage under the Ontario Drug Benefit program would result in additional costs of between $14.6 million and $38.6 million annually over the next 5 years. Glucose 40-47 insulin Homo sapiens 158-165 31886089-1 2019 Background Despite conventional insulin treatment being considered an effective approach for glycemic regulation during renal dysfunction, there is still a major clinical need for better insulin therapy to stabilize fluctuations in glucose levels. Glucose 232-239 insulin Homo sapiens 187-194 31827338-4 2019 Recent decades have also seen the development of technologies such as continuous glucose monitors, faster-acting insulins and commercially available insulin pumps to allow for the real-time observation of interstitial glucose levels, and more precise adjustments to insulin dosage before, during and after activity. Glucose 218-225 insulin Homo sapiens 149-156 31817678-0 2019 Continuous Glucose Monitors and Activity Trackers to Inform Insulin Dosing in Type 1 Diabetes: The University of Virginia Contribution. Glucose 11-18 insulin Homo sapiens 60-67 31829209-1 2019 BACKGROUND: Glucose tolerance testing is a tool used to estimate glucose effectiveness and insulin sensitivity in diabetic patients. Glucose 12-19 insulin Homo sapiens 91-98 31829209-2 2019 The importance of such tests has prompted the development and utilisation of mathematical models that describe glucose kinetics as a function of insulin activity. Glucose 111-118 insulin Homo sapiens 145-152 31829209-3 2019 The hormone glucagon, also plays a fundamental role in systemic plasma glucose regulation and is secreted reciprocally to insulin, stimulating catabolic glucose utilisation. Glucose 153-160 insulin Homo sapiens 122-129 31829209-6 2019 This study presents two mathematical models of a glucose tolerance test that incorporate glucose-insulin-glucagon dynamics. Glucose 49-56 insulin Homo sapiens 97-104 31829209-6 2019 This study presents two mathematical models of a glucose tolerance test that incorporate glucose-insulin-glucagon dynamics. Glucose 89-96 insulin Homo sapiens 97-104 32233598-0 2019 Former gestational diabetes: Mathematical modeling of intravenous glucose tolerance test for the assessment of insulin clearance and its determinants. Glucose 66-73 insulin Homo sapiens 111-118 32233598-2 2019 Insulin clearance represents one of the processes regulating glucose tolerance but has been scarcely investigated for its possible impairment in high-risk subjects. Glucose 61-68 insulin Homo sapiens 0-7 32233598-4 2019 A detailed model-based analysis of a regular 3-hour, insulin-modified intravenous glucose tolerance test (IM-IVGTT) has been performed in women with a previous history of GDM (pGDM, n = 115) and in women who had a healthy pregnancy (CNT, n = 41) to assess total, first-phase and second-phase insulin clearance (ClINS-TOT, ClINS-FP and ClINS-SP) and other metabolic parameters (insulin sensitivity SI, glucose effectiveness SG, beta-cell function and disposition index DI). Glucose 82-89 insulin Homo sapiens 53-60 32233598-6 2019 Disposition index, accounting for the combined contribution of insulin sensitivity and beta-cell function, and glucose effectiveness were identified as possible determinants of insulin clearance in women with a previous history of GDM. Glucose 111-118 insulin Homo sapiens 177-184 31908262-2 2019 The established CMD monitoring allowed subsequent titration of insulin respecting acceptable cerebral and systemic glucose levels. Glucose 115-122 insulin Homo sapiens 63-70 31905447-7 2019 However, their blood glucose was well-controlled even with small doses of insulin, and the treatment was able to be changed to metformin therapy. Glucose 21-28 insulin Homo sapiens 74-81 31593505-0 2019 The exocyst complex regulates insulin-stimulated glucose uptake of skeletal muscle cells. Glucose 49-56 insulin Homo sapiens 30-37 31593505-1 2019 Skeletal muscle handles ~80-90% of the insulin-induced glucose uptake. Glucose 55-62 insulin Homo sapiens 39-46 31593505-2 2019 In skeletal muscle, insulin binding to its cell surface receptor triggers redistribution of intracellular glucose transporter GLUT4 protein to the cell surface, enabling facilitated glucose uptake. Glucose 106-113 insulin Homo sapiens 20-27 31593505-2 2019 In skeletal muscle, insulin binding to its cell surface receptor triggers redistribution of intracellular glucose transporter GLUT4 protein to the cell surface, enabling facilitated glucose uptake. Glucose 182-189 insulin Homo sapiens 20-27 31593505-3 2019 In adipocytes, the eight-protein exocyst complex is an indispensable constituent in insulin-induced glucose uptake, as it is responsible for the targeted trafficking and plasma membrane-delivery of GLUT4. Glucose 100-107 insulin Homo sapiens 84-91 31593505-5 2019 Here we demonstrate that the exocyst is a necessary factor in insulin-induced glucose uptake in skeletal muscle cells as well. Glucose 78-85 insulin Homo sapiens 62-69 31642978-5 2019 During decidualization in early pregnancy, serum levels of insulin, E2, P4, LH, FSH and blood glucose were significantly altered in mice treated with high insulin levels. Glucose 94-101 insulin Homo sapiens 155-162 31644699-0 2019 Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation. Glucose 40-47 insulin Homo sapiens 90-97 31693217-3 2019 Here, to investigate the role of AMPK in the protective effect of adiponectin against insulin resistance, we established the model of high-glucose (HG)- and high-lipid (HL)-induced insulin resistance in INS-1 pancreatic beta cells. Glucose 139-146 insulin Homo sapiens 181-188 31802311-4 2019 Though the mechanism of the antihyperglycemic effect is still unknown, ranolazine may exert the effect through beta cell preservation, inhibition of glucose secretion, and enhancement of insulin secretion in a glucose-dependent manner. Glucose 210-217 insulin Homo sapiens 187-194 31470221-0 2019 Multi-input stochastic prediction of insulin sensitivity for tight glycaemic control using insulin sensitivity and blood glucose data. Glucose 121-128 insulin Homo sapiens 37-44 31002426-3 2019 CASE REPORT: We present a case of a hospitalized individual whose glucose was managed with closed-loop insulin delivery within a randomized controlled trial setting during a period of terminal illness. Glucose 66-73 insulin Homo sapiens 103-110 31002426-4 2019 During the time in which closed-loop insulin delivery was used, glucose control was safe, with no glucose-related harm. Glucose 64-71 insulin Homo sapiens 37-44 31257946-8 2019 Conclusion: To sum up, the aim was to develop a non-injection system for insulin, INS@FDKP-MPs powder inhalation with high dose, low toxicity, and good lung deposition inhalation could rapidly decrease the blood glucose level without immune stimulation, which shows remarkably potential on diabetes treatment by pulmonary delivery route. Glucose 212-219 insulin Homo sapiens 73-80 31464063-3 2019 Basal-bolus regimen was replaced by model predictive control algorithm-directed insulin delivery based on sensor glucose levels. Glucose 113-120 insulin Homo sapiens 80-87 31464063-9 2019 In conclusion, short-term fully closed-loop in type 2 diabetes may require higher dose of faster insulin aspart compared with standard insulin aspart to achieve comparable glucose control. Glucose 172-179 insulin Homo sapiens 97-104 31624901-13 2019 Ex vivo, islet Mt1 and Mt2 mRNA and MT1 and MT2 protein levels were downregulated after culture with glucose at 10-30 mmol/l vs 2-5 mmol/l, in association with increased insulin secretion. Glucose 101-108 insulin Homo sapiens 170-177 31707004-0 2019 The relationship between glucose variability and insulin sensitivity and oxidative stress in subjects with prediabetes. Glucose 25-32 insulin Homo sapiens 49-56 31707004-1 2019 AIM: The present study assessed the relationship between glucose variability (GV) and insulin levels, insulin resistance and oxidative stress at early stages of glucose intolerance. Glucose 57-64 insulin Homo sapiens 86-93 31707004-11 2019 Insulin levels and HOMA-IR are positively related to plasma glucose and reciprocally to CV and M-Value in prediabetes, since the latter association is with borderline significance after adjustment for hypertension and smoking. Glucose 60-67 insulin Homo sapiens 0-7 31580427-5 2019 The lack of impairment in HFD-fed fl/fl/Cre mice was partly due to an improved islet glucose-stimulated NADPH/NADP+ ratio and glucose-stimulated insulin secretion. Glucose 126-133 insulin Homo sapiens 145-152 31884738-8 2019 Patients with a measured fasting plasma glucose (m-FPG) lower than their predicted FPG (p-FPG) by regression from HbA1c showed a significant HbA1c reduction caused by the change to IDegAsp, even without a significantly increased insulin dose. Glucose 40-47 insulin Homo sapiens 229-236 31884738-11 2019 CONCLUSION: We observed a significant glucose-lowering effect by replacing basal insulin with IDegAsp, especially in patients with a lower m-FPG than p-FPG. Glucose 38-45 insulin Homo sapiens 81-88 31636016-0 2019 Strict Control of Blood Glucose With an Intravenous Insulin Infusion Decreases the Risk of Post-operative Lower Extremity Weakness After Complex Endovascular Aortic Aneurysm Repair. Glucose 24-31 insulin Homo sapiens 52-59 31636016-2 2019 The purpose of this study was to determine whether a post-operative insulin infusion protocol (IIP) to achieve tight blood glucose control decreases the rate of LEW. Glucose 123-130 insulin Homo sapiens 68-75 31402604-5 2019 We determined basal and insulin-stimulated 2-deoxy-glucose uptake using isotopic tracers in vivo. Glucose 51-58 insulin Homo sapiens 24-31 31402604-7 2019 RESULTS: Fst288 muscle overexpression markedly increased in vivo insulin-stimulated (but not basal) glucose uptake (+75%, P < 0.05) and increased protein expression and intracellular insulin signalling of AKT, TBC1D4, PAK1, pyruvate dehydrogenase-E1alpha, and p70S6K, while decreasing TBC1D1 signaling (P < 0.05). Glucose 100-107 insulin Homo sapiens 65-72 31402604-9 2019 Importantly, Fst288 completely normalized muscle glucose uptake in insulin-resistant diet-induced obese mice. Glucose 49-56 insulin Homo sapiens 67-74 31575461-6 2019 Insulin in the absence of EPS increased glucose uptake and AS160Thr642 phosphorylation, and both effects were significantly enhanced by prior EPS. Glucose 40-47 insulin Homo sapiens 0-7 31575461-8 2019 Despite a comparable degree of AMPK activation following EPS, the action of insulin on glucose uptake (p < 0.05) and AS160Thr642 phosphorylation (p < 0.001) was decreased in the diabetic vs control myotubes. Glucose 87-94 insulin Homo sapiens 76-83 31575461-9 2019 CONCLUSION: EPS mediated AMPK activation enhances the effect of insulin on glucose uptake and AS160Thr642 phosphorylation in control myotubes replicating key metabolic benefits of exercise on insulin action in man. Glucose 75-82 insulin Homo sapiens 64-71 31575461-10 2019 Conversely, insulin mediated glucose uptake and AS160Thr642 phosphorylation remain significantly decreased in diabetic vs control myotubes despite a comparable degree of AMPK activation following EPS. Glucose 29-36 insulin Homo sapiens 12-19 29883217-6 2019 Hyperinsulinism was assessed via a 75 g oral glucose tolerance test (OGTT) with insulin studies. Glucose 45-52 insulin Homo sapiens 5-12 31571122-1 2019 A model for the homeostasis of glucose through the regulating hormones glucagon and insulin is described. Glucose 31-38 insulin Homo sapiens 84-91 30348064-0 2019 Initial increase in glucose variability during Ramadan fasting in non-insulin-treated patients with diabetes type 2 using continuous glucose monitoring. Glucose 20-27 insulin Homo sapiens 70-77 31446532-1 2019 Insulin resistance (IR), a pathological condition of type 2 diabetes mellitus (T2DM) is characterized by an inability of body"s tissue to respond the secreted or administered insulin, a necessary step for cellular glucose transportation. Glucose 214-221 insulin Homo sapiens 0-7 31446532-1 2019 Insulin resistance (IR), a pathological condition of type 2 diabetes mellitus (T2DM) is characterized by an inability of body"s tissue to respond the secreted or administered insulin, a necessary step for cellular glucose transportation. Glucose 214-221 insulin Homo sapiens 175-182 31767182-2 2019 Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent beta-cell proliferation. Glucose 54-61 insulin Homo sapiens 87-94 31610222-4 2019 Insulin-dependent metabolic activity assays included inhibition of lipolysis in in vitro differentiated human adipocytes, glucose uptake in L6-myocytes, and repression of glucose-6-phosphatase gene expression in human hepatocytes. Glucose 122-129 insulin Homo sapiens 0-7 31473874-13 2019 Two piglets expressing insulin showed normal glucose levels similar to that in the wild-type control. Glucose 45-52 insulin Homo sapiens 23-30 31774631-1 2019 BAY55-9837, a potential therapeutic peptide in the treatment of type 2 diabetes mellitus (T2DM), is capable of inducing glucose (GLC)-dependent insulin secretion. Glucose 120-127 insulin Homo sapiens 144-151 31774631-1 2019 BAY55-9837, a potential therapeutic peptide in the treatment of type 2 diabetes mellitus (T2DM), is capable of inducing glucose (GLC)-dependent insulin secretion. Glucose 129-132 insulin Homo sapiens 144-151 31779625-0 2019 Insulin resistance and systemic metabolic changes in oral glucose tolerance test in 5340 individuals: an interventional study. Glucose 58-65 insulin Homo sapiens 0-7 31789119-1 2019 Aim: Inaccurate blood glucose monitoring system (BGMS) results may lead to insulin dosing errors and adverse clinical outcomes. Glucose 22-29 insulin Homo sapiens 75-82 31724717-9 2019 Moreover, sampling of media following modeled transplantation showed secretory profiles that were correlated with imaging analyses as well as with islet function using glucose-stimulated insulin secretion. Glucose 168-175 insulin Homo sapiens 187-194 31819571-3 2019 Genetic polymorphism of cytokines like tumor necrosis factor-alpha (TNF-alpha) is suggestive of interference with insulin-sensitive glucose uptake and induces insulin resistance that ultimately could lead to T2DM. Glucose 132-139 insulin Homo sapiens 114-121 31775749-3 2019 METHODS: We retrospectively identified non-critically ill hospitalized insulin requiring patients who were undergoing bedside glucose monitoring and received either carvedilol or a selective beta blocker (metoprolol or atenolol). Glucose 126-133 insulin Homo sapiens 71-78 31756973-3 2019 In cell models, insulin secretion rate and beta cell proliferation were assessed in normal and high glucose after treating uPA siRNA, uPA, or anti-uPA antibody. Glucose 100-107 insulin Homo sapiens 16-23 31788032-0 2019 Fasting triglycerides and glucose index: a useful screening test for assessing insulin resistance in patients diagnosed with rheumatoid arthritis and systemic lupus erythematosus. Glucose 26-33 insulin Homo sapiens 79-86 31807264-2 2019 The risk of hypoglycemia, side effects of weight gain, and high glucose variability associated with insulin use have prompted researchers to explore additional therapies to treat this condition. Glucose 64-71 insulin Homo sapiens 100-107 31749022-4 2019 RECENT FINDINGS: The ability of adipocytes to synthesize lipids from glucose is a marker of metabolic fitness, e.g., low de novo lipogenesis (DNL) in adipocytes correlates with insulin resistance in obesity. Glucose 69-76 insulin Homo sapiens 177-184 31766373-5 2019 Metabolic-interfering effects of Fet-A have thus been shown to highly exacerbate insulin resistance (IR) through blocking insulin-stimulated glucose transporter 4 (GLUT-4) translocation and protein kinase B (Akt) activation. Glucose 141-148 insulin Homo sapiens 122-129 31756973-6 2019 In cell models, insulin secretion rate and cell proliferation declined in high glucose after uPA silencing either by siRNA or by anti-uPA antibody. Glucose 79-86 insulin Homo sapiens 16-23 31839754-8 2019 Differentiated IPCs expressed insulin and glucagon mRNA and protein, and these IPCs also secreted insulin in response to glucose stimulation. Glucose 121-128 insulin Homo sapiens 98-105 25905362-7 2000 In contrast, obesity is strongly related to Diabetes Mellitus type 2 (DM2) mainly through inducing insulin resistance which is the impaired ability of insulin to effectively induce glucose uptake by cells. Glucose 181-188 insulin Homo sapiens 99-106 25905362-7 2000 In contrast, obesity is strongly related to Diabetes Mellitus type 2 (DM2) mainly through inducing insulin resistance which is the impaired ability of insulin to effectively induce glucose uptake by cells. Glucose 181-188 insulin Homo sapiens 151-158 31839754-9 2019 In conclusion, we found that hUDSCs can be directly differentiated into IPCs, which secrete insulin in response to glucose. Glucose 115-122 insulin Homo sapiens 92-99 31798905-7 2019 Results: All the four surrogate indexes showed a significant correlation with insulin-stimulated glucose disposal in the whole study population. Glucose 97-104 insulin Homo sapiens 78-85 31828146-7 2019 An insulin resistance model was established by exposing mature adipocytes to excessive glucose and insulin. Glucose 87-94 insulin Homo sapiens 3-10 31781045-1 2019 Vildagliptin blocks glucagon like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) inactivation of the meal induced increases in GLP-1 and GIP so that elevated GLP-1 and GIP levels are maintained over 24 h. The primary insulin secretion effect of vildagliptin is to improve the impaired sensitivity of the beta-cells to glucose in subjects with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) and in patients with type 2 diabetes mellitus (T2DM); this effect was seen acutely and maintained over at least 2 years in patients with T2DM. Glucose 56-63 insulin Homo sapiens 74-81 31696345-3 2019 We have further shown that this released insulin retains bioactivity and reduces blood glucose. Glucose 87-94 insulin Homo sapiens 41-48 31499040-3 2019 The liver is the first organ where insulin reaches after being secreted from pancreas and liver regulates glucose storage and disposal as per the body"s demand in response to insulin. Glucose 106-113 insulin Homo sapiens 35-42 31499040-3 2019 The liver is the first organ where insulin reaches after being secreted from pancreas and liver regulates glucose storage and disposal as per the body"s demand in response to insulin. Glucose 106-113 insulin Homo sapiens 175-182 31690291-1 2019 BACKGROUND: The shape of the glucose response curve during an oral glucose tolerance test (OGTT) can predict beta-cell function and insulin resistance. Glucose 29-36 insulin Homo sapiens 132-139 31690291-1 2019 BACKGROUND: The shape of the glucose response curve during an oral glucose tolerance test (OGTT) can predict beta-cell function and insulin resistance. Glucose 67-74 insulin Homo sapiens 132-139 32514450-8 2020 Hepatic glucose production increased, and there was impairment of glucose disposal during the low-dose insulin infusion. Glucose 66-73 insulin Homo sapiens 103-110 31686215-8 2019 Using mouse pancreatic islets, a dynamic glucose-stimulated insulin secretion test was performed to examine the performance of the fluidic system. Glucose 41-48 insulin Homo sapiens 60-67 31686215-9 2019 The system successfully analyzed levels and patterns of insulin secretion upon exposure of the islets to low- and high-glucose solutions in turns, thus demonstrating its capacity to assess islet functions more easily and cost-effectively. Glucose 119-126 insulin Homo sapiens 56-63 31686274-0 2019 Subcutaneous Insulin Dosing Calculators for Inpatient Glucose Control. Glucose 54-61 insulin Homo sapiens 13-20 31686274-1 2019 PURPOSE OF REVIEW: The goal of this review is to summarize information about insulin dosing software and calculators used as computerized decision support systems or electronic glucose management systems (eGMS). Glucose 177-184 insulin Homo sapiens 77-84 31707881-2 2019 Attaining the recommended glucose levels is challenging with standard insulin therapy. Glucose 26-33 insulin Homo sapiens 70-77 31707881-4 2019 Fully automated insulin delivery (closed-loop) has been shown to be safe, and achieves superior glucose control than standard insulin therapy in the hospital, including in those patients receiving haemodialysis and enteral or parenteral nutrition where glucose control can be particularly challenging. Glucose 96-103 insulin Homo sapiens 16-23 31707881-4 2019 Fully automated insulin delivery (closed-loop) has been shown to be safe, and achieves superior glucose control than standard insulin therapy in the hospital, including in those patients receiving haemodialysis and enteral or parenteral nutrition where glucose control can be particularly challenging. Glucose 253-260 insulin Homo sapiens 16-23 30709732-2 2019 T1DM treatment is shifting from exogenous insulin replacement therapy toward pancreatic beta-cell replacement, to restore physiologically responsive insulin secretion to variations in blood glucose levels. Glucose 190-197 insulin Homo sapiens 149-156 31430566-10 2019 As for diabetes-related biochemical indicators, fasting plasma glucose (FPG) was non-linearly related to cognitive disorders; the elevated levels of 2 -h postload glucose (2h-PG), glycosylated hemoglobin (HbA1c), low and high levels of fasting plasma insulin (FPI) were associated with an increased risk of dementia. Glucose 63-70 insulin Homo sapiens 251-258 31479304-5 2019 In addition, glucose-stimulated insulin secretion was quantified in isolated pancreatic islets and beta-cell differentiation markers and insulin secretion machinery were characterized by RT-PCR. Glucose 13-20 insulin Homo sapiens 32-39 31479304-9 2019 Unexpectedly, we found 60% increase in Glut1 (a high-affinity/low-Km glucose transporter), suggesting increased glucose transport into the beta-cell at low glucose levels, which may be related to constitutive insulin secretion. Glucose 69-76 insulin Homo sapiens 209-216 31479304-9 2019 Unexpectedly, we found 60% increase in Glut1 (a high-affinity/low-Km glucose transporter), suggesting increased glucose transport into the beta-cell at low glucose levels, which may be related to constitutive insulin secretion. Glucose 112-119 insulin Homo sapiens 209-216 31479304-9 2019 Unexpectedly, we found 60% increase in Glut1 (a high-affinity/low-Km glucose transporter), suggesting increased glucose transport into the beta-cell at low glucose levels, which may be related to constitutive insulin secretion. Glucose 112-119 insulin Homo sapiens 209-216 31479304-11 2019 We conclude that IDE is required for glucose-stimulated insulin secretion. Glucose 37-44 insulin Homo sapiens 56-63 31479304-12 2019 When IDE is inhibited, insulin secretion machinery is perturbed, causing either inhibition of insulin release at high glucose concentrations or constitutive secretion. Glucose 118-125 insulin Homo sapiens 23-30 31479304-12 2019 When IDE is inhibited, insulin secretion machinery is perturbed, causing either inhibition of insulin release at high glucose concentrations or constitutive secretion. Glucose 118-125 insulin Homo sapiens 94-101 31939483-1 2019 GH is one of the insulin counterregulatory hormones which acts in the opposite way to insulin, increasing the glucose production by the liver and kidneys and decreasing glucose uptake from peripheral tissues, thus being a hyperglycemic hormone. Glucose 110-117 insulin Homo sapiens 17-24 31939483-1 2019 GH is one of the insulin counterregulatory hormones which acts in the opposite way to insulin, increasing the glucose production by the liver and kidneys and decreasing glucose uptake from peripheral tissues, thus being a hyperglycemic hormone. Glucose 110-117 insulin Homo sapiens 86-93 31939483-1 2019 GH is one of the insulin counterregulatory hormones which acts in the opposite way to insulin, increasing the glucose production by the liver and kidneys and decreasing glucose uptake from peripheral tissues, thus being a hyperglycemic hormone. Glucose 169-176 insulin Homo sapiens 17-24 31939483-1 2019 GH is one of the insulin counterregulatory hormones which acts in the opposite way to insulin, increasing the glucose production by the liver and kidneys and decreasing glucose uptake from peripheral tissues, thus being a hyperglycemic hormone. Glucose 169-176 insulin Homo sapiens 86-93 31539748-4 2019 Further studies on cell viability and cellular activity revealed that compound 10m could enhance insulin-stimulated glucose uptake with no significant cytotoxicity. Glucose 116-123 insulin Homo sapiens 97-104 31206976-10 2019 CONCLUSIONS: Both longitudinal and cross-sectional analyses support the hypothesis that insulin resistance is associated with increased red blood cells count and haematocrit in young adults, even within normal ranges of insulin and glucose. Glucose 232-239 insulin Homo sapiens 88-95 31335204-1 2019 Background: Euglyca is a mobile application which we developed for children and adolescents suffering type 1 diabetes mellitus (T1DM) for calculation of the appropriate insulin bolus dose by importing in the equation carbohydrates, lipids, glucose levels, and personalized parameters. Glucose 241-248 insulin Homo sapiens 170-177 31399433-4 2019 Insulin sensitivity was defined based on the median of insulin stimulated glucose disposal (M) measured during the hyperinsulinemic-euglycemic clamp. Glucose 74-81 insulin Homo sapiens 0-7 31399433-4 2019 Insulin sensitivity was defined based on the median of insulin stimulated glucose disposal (M) measured during the hyperinsulinemic-euglycemic clamp. Glucose 74-81 insulin Homo sapiens 55-62 31602234-1 2019 Sustained virological response (SVR) in hepatitis C virus (HCV) patients treated with pegylated interferon alpha-2a and ribavirin is associated with reduced insulin resistance (IR), measured as a reduction of homeostasis model assessment (HOMA) scores after 24 weeks of therapy, and reduced fasting serum insulin and serum glucose levels. Glucose 323-330 insulin Homo sapiens 157-164 31216011-3 2019 Incretin hormones are secreted by enteroendocrine cells in response to enteral nutrients and potentiate insulin release from pancreatic beta cells in a glucose-dependent manner, thereby reducing the risk of insulin-induced hypoglycemia. Glucose 152-159 insulin Homo sapiens 104-111 31666083-1 2019 Gestational diabetes mellitus (GDM) is defined as the presence of high blood glucose levels with the onset, or detected for the first time during pregnancy, as a result of increased insulin resistance. Glucose 77-84 insulin Homo sapiens 182-189 31243192-0 2019 Continuous subcutaneous insulin infusion combined with liraglutide reduced glycemic variability and oxidative stress in type 2 diabetes mellitus: a study based on the flash glucose monitoring system. Glucose 173-180 insulin Homo sapiens 24-31 31922025-1 2020 Aims: This study aims to assess insulin secretion and resistance through oral glucose tolerance test (OGTT) among young Japanese individuals. Glucose 78-85 insulin Homo sapiens 32-39 31922025-6 2020 ROC curves of disposition index reflecting the composition of insulin secretion and sensitivity classified the prolonged glucose elevation group (group III + IV) from the rapid glucose lowering group (group II; AUC = 0.847). Glucose 121-128 insulin Homo sapiens 62-69 31922025-6 2020 ROC curves of disposition index reflecting the composition of insulin secretion and sensitivity classified the prolonged glucose elevation group (group III + IV) from the rapid glucose lowering group (group II; AUC = 0.847). Glucose 177-184 insulin Homo sapiens 62-69 31472061-0 2019 Triglyceride/glucose index is a reliable alternative marker for insulin resistance in South American overweight and obese children and adolescents. Glucose 13-20 insulin Homo sapiens 64-71 31472061-1 2019 Background The aim of the present study was to investigate the correlation between the triglyceride/glucose index (TyG index) and homeostasis model assessment of insulin resistance (HOMA-IR). Glucose 100-107 insulin Homo sapiens 162-169 31663302-1 2019 Diabetes mellitus is a chronic metabolic condition characterised by an elevation of blood glucose levels, resulting from defects in insulin secretion, insulin action, or both. Glucose 90-97 insulin Homo sapiens 132-139 31663302-1 2019 Diabetes mellitus is a chronic metabolic condition characterised by an elevation of blood glucose levels, resulting from defects in insulin secretion, insulin action, or both. Glucose 90-97 insulin Homo sapiens 151-158 31652867-6 2019 In addition, PFFA dose-dependently inhibited d-ribose and d-glucose induced non-enzymatic insulin glycation. Glucose 58-67 insulin Homo sapiens 90-97 31652867-8 2019 Interestingly, PFFA strongly interacted with the Phe1 in insulin chain-B, and this interaction could block d-glucose access to the glycation site of insulin. Glucose 107-116 insulin Homo sapiens 57-64 31652867-8 2019 Interestingly, PFFA strongly interacted with the Phe1 in insulin chain-B, and this interaction could block d-glucose access to the glycation site of insulin. Glucose 107-116 insulin Homo sapiens 149-156 31641146-8 2019 In T2D patients, relative change in weight from 1 y to late after RYGB correlated with relative change in fasting glucose and HbA1c, whereas relative changes in glucose-stimulated insulin release correlated inversely with relative changes in postprandial glucose excursions. Glucose 161-168 insulin Homo sapiens 180-187 31641146-8 2019 In T2D patients, relative change in weight from 1 y to late after RYGB correlated with relative change in fasting glucose and HbA1c, whereas relative changes in glucose-stimulated insulin release correlated inversely with relative changes in postprandial glucose excursions. Glucose 161-168 insulin Homo sapiens 180-187 31641146-11 2019 Weight loss and improved beta-cell function both contribute to maintenance of long-term glycemic control in patients with type 2 diabetes, and increased glucose stimulated insulin secretion may contribute to postprandial hypoglycemia in NGT subjects. Glucose 153-160 insulin Homo sapiens 172-179 31781667-10 2019 Conclusions: There is inconsistent evidence for upregulated beta cell function in BA adults, and they may in fact exhibit greater deficits in insulin secretory function as glucose intolerance develops. Glucose 172-179 insulin Homo sapiens 142-149 31619585-5 2019 This glucose intolerance was due to a reduced insulin response to glucose as opposed to any effect on insulin sensitivity. Glucose 5-12 insulin Homo sapiens 46-53 31619585-5 2019 This glucose intolerance was due to a reduced insulin response to glucose as opposed to any effect on insulin sensitivity. Glucose 66-73 insulin Homo sapiens 46-53 31619585-7 2019 Furthermore, in pregnant women circulating kisspeptin levels significantly correlated with insulin responses to oral glucose challenge and were significantly lower in women with gestational diabetes (GDM) compared with those without GDM. Glucose 117-124 insulin Homo sapiens 91-98 31798905-13 2019 Conclusion: Among the surrogate TG/HDL-C ratio, VAI, LAP and TyG indexes of insulin sensitivity, LAP index showed a significant association with insulin-stimulated glucose disposal across the different glucose tolerance categories and the highest ability to detect insulin resistance and subclinical vascular damage. Glucose 164-171 insulin Homo sapiens 76-83 31798905-13 2019 Conclusion: Among the surrogate TG/HDL-C ratio, VAI, LAP and TyG indexes of insulin sensitivity, LAP index showed a significant association with insulin-stimulated glucose disposal across the different glucose tolerance categories and the highest ability to detect insulin resistance and subclinical vascular damage. Glucose 164-171 insulin Homo sapiens 145-152 31798905-13 2019 Conclusion: Among the surrogate TG/HDL-C ratio, VAI, LAP and TyG indexes of insulin sensitivity, LAP index showed a significant association with insulin-stimulated glucose disposal across the different glucose tolerance categories and the highest ability to detect insulin resistance and subclinical vascular damage. Glucose 164-171 insulin Homo sapiens 145-152 31798905-13 2019 Conclusion: Among the surrogate TG/HDL-C ratio, VAI, LAP and TyG indexes of insulin sensitivity, LAP index showed a significant association with insulin-stimulated glucose disposal across the different glucose tolerance categories and the highest ability to detect insulin resistance and subclinical vascular damage. Glucose 202-209 insulin Homo sapiens 145-152 31798905-13 2019 Conclusion: Among the surrogate TG/HDL-C ratio, VAI, LAP and TyG indexes of insulin sensitivity, LAP index showed a significant association with insulin-stimulated glucose disposal across the different glucose tolerance categories and the highest ability to detect insulin resistance and subclinical vascular damage. Glucose 202-209 insulin Homo sapiens 145-152 31828166-5 2019 The adjusted-insulin group had higher plasma glucose levels at the 2nd hour of dialysis than those of the nonadjusted-insulin group. Glucose 45-52 insulin Homo sapiens 13-20 31711271-24 2019 Where data could not be combined, single studies showed lower mean fasting glucose (MD -0.40; 95% CI -0.72 to -0.08) and higher means for two-hour glucose response (MD 1.08; 95% CI 0.45 to 1.71) and insulin area under the curve (AUC) (MD 20.30; 95% CI 4.24 to 36.36). Glucose 147-154 insulin Homo sapiens 199-206 33405670-6 2019 The hybrid MN autonomously released insulin well-correspondent to the glucose change pattern via the regulation of the skin layer formed on the surface. Glucose 70-77 insulin Homo sapiens 36-43 31717308-1 2019 The pancreas has an essential role in the regulation of glucose homeostasis by secreting insulin, the only hormone with a blood glucose lowering effect in mammals. Glucose 56-63 insulin Homo sapiens 89-96 31717308-1 2019 The pancreas has an essential role in the regulation of glucose homeostasis by secreting insulin, the only hormone with a blood glucose lowering effect in mammals. Glucose 128-135 insulin Homo sapiens 89-96 31703434-2 2019 Both fatty acids and amino acids stimulate insulin secretion by distinct mechanisms; fatty acids enhance glucose-stimulated insulin secretion, while amino acids may have a direct effect on pancreatic beta cells. Glucose 105-112 insulin Homo sapiens 124-131 31781030-5 2019 Expression silencing of PLCXD3 in INS-1 (832/13) cells was found to reduce glucose-stimulated insulin secretion (GSIS) and insulin content. Glucose 75-82 insulin Homo sapiens 94-101 31588013-4 2019 Insulin sensitivity, assessed as glucose disposal rate during insulin infusion, was ~45% greater after BPD than RYGB, whereas beta cell function was not different between groups. Glucose 33-40 insulin Homo sapiens 0-7 31588013-4 2019 Insulin sensitivity, assessed as glucose disposal rate during insulin infusion, was ~45% greater after BPD than RYGB, whereas beta cell function was not different between groups. Glucose 33-40 insulin Homo sapiens 62-69 31694157-9 2019 In conclusion, the glucose-lowering effect of the preload may relate to delayed small intestinal glucose absorption and insulin stimulation, rather than slowing of gastric emptying. Glucose 19-26 insulin Homo sapiens 120-127 31684154-6 2019 In this review, we will first highlight age-related changes to skeletal muscle which can contribute to insulin resistance, followed by a comparison of endurance and resistance training adaptations to insulin-stimulated glucose metabolism in older adults. Glucose 219-226 insulin Homo sapiens 200-207 32863472-0 2019 Simulation Software for Assessment of Nonlinear and Adaptive Multivariable Control Algorithms: Glucose - Insulin Dynamics in Type 1 Diabetes. Glucose 95-102 insulin Homo sapiens 105-112 32863472-3 2019 Nonlinear models are developed to describe glucose concentration (GC) variations based on user-defined scenarios for meal consumption, insulin administration, and physical activity. Glucose 43-50 insulin Homo sapiens 135-142 31655714-2 2019 It functions by providing the patient with a continuous subcutaneous infusion of a rapid acting insulin and allows the patient to administer boluses throughout the day for food and correction of high glucose levels. Glucose 200-207 insulin Homo sapiens 96-103 31655714-4 2019 Insulin pump technology continues to rapidly evolve, and many options are now on the market, including those that are used in conjunction with continuous glucose monitoring. Glucose 154-161 insulin Homo sapiens 0-7 31635936-8 2019 Furthermore, insulin secretion at high glucose concentration was significantly higher in cells differentiated on PLLA scaffold than those cultured on Silk scaffold (P-value: 0.012). Glucose 39-46 insulin Homo sapiens 13-20 31442763-2 2019 The glucose metabolism of humans is regulated by a balanced ratio of insulin and hIAPP. Glucose 4-11 insulin Homo sapiens 69-76 31273408-12 2019 CONCLUSIONS/INTERPRETATION: This study identified a COS that will help bring consistency and uniformity to outcome selection and reporting in clinical trials and other studies involving the follow-up at 1 year and beyond of women diagnosed with GDM treated with insulin and/or oral glucose-lowering agents during pregnancy. Glucose 282-289 insulin Homo sapiens 262-269 31364266-2 2019 In contrast, the main mechanism of action of basal insulin is to reduce elevated FG by inhibiting hepatic glucose production. Glucose 106-113 insulin Homo sapiens 51-58 31648183-11 2019 In addition, there was a positive association between serum IL-34 and insulin resistance and glucose concentrations. Glucose 93-100 insulin Homo sapiens 70-77 31536965-7 2019 During OGTT contrary to the control group, subjects with insulin resistance presented suppression of cOC and total OC decrease after 1 and 2 hour of oral glucose load. Glucose 154-161 insulin Homo sapiens 57-64 31162534-9 2019 CONCLUSIONS: In the presence of diabetes with advanced CKD, the insulin regimen should be individualized based on knowledge of the daily glucose patterns. Glucose 137-144 insulin Homo sapiens 64-71 31298704-7 2019 Insulin sensitivity was derived from an oral glucose tolerance test (ISOGTT). Glucose 45-52 insulin Homo sapiens 0-7 30901505-8 2019 RESULTS: Japanese-American men showed higher area under the curve values for serum insulin concentrations during the oral glucose tolerance test and lower Matsuda Index than native Japanese men. Glucose 122-129 insulin Homo sapiens 83-90 31067999-1 2019 BACKGROUND: In type 1 diabetes (T1D), closed-loop systems provide excellent overnight fasting blood glucose control by adjusting the insulin infusion rate based on corresponding changes in sensor glucose levels. Glucose 100-107 insulin Homo sapiens 133-140 31067999-1 2019 BACKGROUND: In type 1 diabetes (T1D), closed-loop systems provide excellent overnight fasting blood glucose control by adjusting the insulin infusion rate based on corresponding changes in sensor glucose levels. Glucose 196-203 insulin Homo sapiens 133-140 31067999-2 2019 In patients on multiple daily insulin (MDI) injections, such control in overnight glucose levels has not been possible due to the inability to alter the absorption rate of long-acting insulin after injection. Glucose 82-89 insulin Homo sapiens 30-37 31195815-2 2019 For people with diabetes who cannot achieve acceptable glycemic control despite the use of intensive insulin therapy and continuous glucose measurement, there exists the possibility of continuous intraperitoneal insulin delivery via an implantable pump or a percutaneous port system that is connected to an external insulin pump. Glucose 132-139 insulin Homo sapiens 212-219 31195815-2 2019 For people with diabetes who cannot achieve acceptable glycemic control despite the use of intensive insulin therapy and continuous glucose measurement, there exists the possibility of continuous intraperitoneal insulin delivery via an implantable pump or a percutaneous port system that is connected to an external insulin pump. Glucose 132-139 insulin Homo sapiens 212-219 31595784-4 2019 METHODS: A new insulin sensitivity adaptation (ISA) algorithm is presented that updates each patient"s insulin sensitivity during nonmeal periods to reduce the error between the actual glucose levels and the process model. Glucose 185-192 insulin Homo sapiens 15-22 31595784-4 2019 METHODS: A new insulin sensitivity adaptation (ISA) algorithm is presented that updates each patient"s insulin sensitivity during nonmeal periods to reduce the error between the actual glucose levels and the process model. Glucose 185-192 insulin Homo sapiens 103-110 31291451-0 2019 The Rate of Glucose Appearance Is Related to Postprandial Glucose and Insulin Responses in Adults: A Systematic Review and Meta-analysis of Stable Isotope Studies. Glucose 12-19 insulin Homo sapiens 70-77 31291451-1 2019 BACKGROUND: It is often assumed that lower postprandial glucose (PPG) and insulin (PPI) responses are induced by slower glucose influx from the gut (e.g., by delayed carbohydrate digestion). Glucose 120-127 insulin Homo sapiens 74-81 31691163-5 2019 AMPK is also expressed in pancreatic beta cells and is largely regulated by glucose, which is the main physiological stimulator of insulin secretion. Glucose 76-83 insulin Homo sapiens 131-138 31691163-6 2019 Results of in vitro studies clearly show that glucose-induced insulin release is associated with a concomitant inhibition of AMPK in beta cells. Glucose 46-53 insulin Homo sapiens 62-69 31691163-7 2019 However, pharmacological activation of AMPK significantly potentiates the insulin-secretory response of beta cells to glucose and to some other stimuli. Glucose 118-125 insulin Homo sapiens 74-81 31672937-5 2019 Our approach involved the creation of a multichannel perifusion system to monitor dynamic insulin secretion and intracellular calcium flux simultaneously, enabling the systematic evaluation of glucose-stimulated insulin secretion under multiple conditions. Glucose 193-200 insulin Homo sapiens 212-219 31400387-1 2019 Glutamate dehydrogenase 1 (GDH1) contributes to glucose-stimulated insulin secretion in murine beta-cells, but not to basic insulin release. Glucose 48-55 insulin Homo sapiens 67-74 31725665-2 2019 The triglyceride glucose (TyG) index is a marker of insulin resistance which is also implicated in the risk of nephropathy among people with type 2 diabetes. Glucose 17-24 insulin Homo sapiens 52-59 31383505-3 2019 Recently, some scholars have proposed that triglycerides-glucose index (TyG) is an important indicator of insulin resistance. Glucose 57-64 insulin Homo sapiens 106-113 31271247-7 2019 During OGTT, children with obesity and high insulin had a worse suppression of glucagon during the first 10 minutes after glucose intake. Glucose 122-129 insulin Homo sapiens 44-51 31969308-0 2019 Ameliorating effect of sesamin on insulin resistance of hepatic L02 cells induced by high glucose/high insulin. Glucose 90-97 insulin Homo sapiens 34-41 31969308-1 2019 Sesamin (SES) has the ameliorating effect on L02 hepatocyte model of insulin resistance induced by high glucose and high insulin, based on insulin receptor signaling pathway IRS/PI3K/Akt. Glucose 104-111 insulin Homo sapiens 69-76 31798905-8 2019 However, only LAP index had a significant association with insulin sensitivity across the different glucose tolerance groups. Glucose 100-107 insulin Homo sapiens 59-66 31798905-9 2019 LAP index showed the highest area under the receiver operating characteristic curve (0.728) to detect individuals with insulin resistance defined as the bottom quartile of insulin-stimulated glucose disposal, followed by TG/HDL-C ratio (0.693), TyG index (0.688) and VAI (0.688). Glucose 191-198 insulin Homo sapiens 119-126 31798905-9 2019 LAP index showed the highest area under the receiver operating characteristic curve (0.728) to detect individuals with insulin resistance defined as the bottom quartile of insulin-stimulated glucose disposal, followed by TG/HDL-C ratio (0.693), TyG index (0.688) and VAI (0.688). Glucose 191-198 insulin Homo sapiens 172-179 31431258-1 2019 Insulin is a small protein with 51 residues that mediates glucose uptake, and an interesting model for studying protein misfolding and aggregation. Glucose 58-65 insulin Homo sapiens 0-7 31600232-6 2019 The model can thus represent both fasting and postprandial glycemic levels and describe the effect of interventions acting on insulin-enhanced tissue glucose disposal or on insulin-inhibited hepatic glucose output, as well as on insulin secretion and beta-cell replicating ability. Glucose 150-157 insulin Homo sapiens 126-133 31601983-9 2019 Blood glucose levels decreased in response to human insulin administration. Glucose 6-13 insulin Homo sapiens 52-59 31597288-2 2019 However, accurate long-term glucose predictions (e.g., >60 min), which are usually needed in applications such as precision insulin dosing (e.g., an artificial pancreas), still remain a challenge. Glucose 28-35 insulin Homo sapiens 124-131 31374326-9 2019 Diabetic human islets displayed a reduced cAMP generation and insulin secretory capacity in response to glucose. Glucose 104-111 insulin Homo sapiens 62-69 31581241-1 2019 Given the association of disturbances in non-esterified fatty acid (NEFA) metabolism with the development of Type 2 Diabetes and Non-Alcoholic Fatty Liver Disease, computational models of glucose-insulin dynamics have been extended to account for the interplay with NEFA. Glucose 188-195 insulin Homo sapiens 196-203 31632354-1 2019 The detailed characterization and quantification of the kinetics of glucose-stimulated insulin secretion (GSIS) by normal pancreatic islets is of considerable interest for characterizing beta-cell dysfunction, assessing the quality of isolated islets, and improving the design of artificial pancreas devices. Glucose 68-75 insulin Homo sapiens 87-94 31632354-3 2019 In both species, insulin responses were biphasic (a transient first-phase peak followed by a sustained second-phase), and the amount of insulin released showed a sigmoid-type dependence on glucose concentration. Glucose 189-196 insulin Homo sapiens 136-143 31446050-6 2019 The resulting islet organoids express beta cell and other endocrine markers and are functional, capable of undergoing glucose-stimulated insulin secretion. Glucose 118-125 insulin Homo sapiens 137-144 31446050-10 2019 Despite successes generating beta cells, the cell type responsible for glucose-stimulated insulin secretion within the islets of Langerhans found in the pancreas, successful assembly with other non-endocrine cell types, particularly endothelial cells, has been technically challenging. Glucose 71-78 insulin Homo sapiens 90-97 32377245-7 2019 The odds ratio for fasting blood glucose level in insulin-treated obese GDM group was 1.081 (95% CI =1.004 - 1.163) (p=0.039); and it was 0.982 (95% CI =0.924 - 1.002) (p=0.048) for the weight gained during pregnancy, in only-diet treated obese GDM patients. Glucose 33-40 insulin Homo sapiens 50-57 30450940-5 2019 The resulting altered redox signaling, diminished insulin secretion responses to various secretagogues including glucose, may lead to excretion of cytokines or chemokines by beta-cells or excretion of endosomes. Glucose 113-120 insulin Homo sapiens 50-57 31514971-10 2019 The results of multivariate logistic regression model indicate that when controlling other variables in the multivariate logistic regression model, a higher fasting plasma glucose level and a longer diagnosis duration are associated with higher odds of insulin therapy commencement, but higher body mass index and some comorbidities, such as obesity and hyperlipidemia, are associated with higher odds of being a GLP-1-RA user. Glucose 172-179 insulin Homo sapiens 253-260 31433306-2 2019 However, the field has been limited in the ability to generate beta-like cells with both phenotypic maturation and functional glucose-stimulated insulin secretion that is similar to primary human islets. Glucose 126-133 insulin Homo sapiens 145-152 31077529-12 2019 It correlates to the recovery of beta cell function, contributing to insulin-induced glucose control. Glucose 85-92 insulin Homo sapiens 69-76 31335199-0 2019 Acceptability of Continuous Glucose Monitoring in Elderly Diabetes Patients Using Multiple Daily Insulin Injections. Glucose 28-35 insulin Homo sapiens 97-104 31440989-1 2019 Advances in continuous glucose monitoring and insulin pumps have allowed people with type 1 diabetes (T1D) and caregivers to accurately and continuously measure their glucose levels and make adjustments to insulin infusion. Glucose 167-174 insulin Homo sapiens 46-53 31440989-2 2019 In recent years, algorithms for subcutaneous insulin dosing have been developed that can respond to changes in glucose in an automated fashion and "close the loop". Glucose 111-118 insulin Homo sapiens 45-52 31485918-2 2019 Prandial insulin analogues have been developed to replicate the physiology of normal endogenous insulin secretion and action, with the aim of limiting postprandial glucose excursions. Glucose 164-171 insulin Homo sapiens 9-16 31485918-2 2019 Prandial insulin analogues have been developed to replicate the physiology of normal endogenous insulin secretion and action, with the aim of limiting postprandial glucose excursions. Glucose 164-171 insulin Homo sapiens 96-103 31581129-2 2019 The liver is the first organ to receive insulin and through a cascade of complex series of steps, insulin not only plays a key role in the intrahepatic regulation of glucose and lipid metabolism but also in the regulation of systemic glucose and lipid concentrations. Glucose 166-173 insulin Homo sapiens 40-47 31581129-2 2019 The liver is the first organ to receive insulin and through a cascade of complex series of steps, insulin not only plays a key role in the intrahepatic regulation of glucose and lipid metabolism but also in the regulation of systemic glucose and lipid concentrations. Glucose 166-173 insulin Homo sapiens 98-105 31581129-2 2019 The liver is the first organ to receive insulin and through a cascade of complex series of steps, insulin not only plays a key role in the intrahepatic regulation of glucose and lipid metabolism but also in the regulation of systemic glucose and lipid concentrations. Glucose 234-241 insulin Homo sapiens 40-47 31581129-2 2019 The liver is the first organ to receive insulin and through a cascade of complex series of steps, insulin not only plays a key role in the intrahepatic regulation of glucose and lipid metabolism but also in the regulation of systemic glucose and lipid concentrations. Glucose 234-241 insulin Homo sapiens 98-105 31412375-6 2019 In both patient groups, basal insulin reduced fasting plasma glucose into the target range (6.6+-1.3 vs. 5.7+-0.8 mmol/l), however, in those needing treatment intensification, post-breakfast plasma glucose remained substantially higher after basal insulin titration (12.6+-2.0 vs.9.4+-1.6 mmol/l, p<0.0001). Glucose 61-68 insulin Homo sapiens 30-37 31412375-6 2019 In both patient groups, basal insulin reduced fasting plasma glucose into the target range (6.6+-1.3 vs. 5.7+-0.8 mmol/l), however, in those needing treatment intensification, post-breakfast plasma glucose remained substantially higher after basal insulin titration (12.6+-2.0 vs.9.4+-1.6 mmol/l, p<0.0001). Glucose 198-205 insulin Homo sapiens 30-37 31412375-8 2019 CONCLUSIONS: Basal insulin therapy can provide satisfactory glucose control in more than 70% of patients with type 2 diabetes. Glucose 60-67 insulin Homo sapiens 19-26 31572507-7 2019 Insulin secretion stimulated by glucose was determined using ELISA. Glucose 32-39 insulin Homo sapiens 0-7 31311314-5 2019 Moreover, treatment of chemerin attenuated insulin-stimulated glucose uptake by decreasing phosphorylation of insulin receptor substrate (IRS)1/2 Tyr612, phosphorylation of protein kinase B Ser473, and membrane translocation of glucose transporter type 4 through increasing Ser307 phosphorylation of IRS1 in cultured hGLs. Glucose 62-69 insulin Homo sapiens 43-50 30772836-8 2019 However, incretin-stimulated ISRs, adjusted for insulin sensitivity and glucose-stimulated insulin secretion, were even more attenuated in the GB subjects, by threefold to fourfold (AUCISR(90-240 min) during GLP-1 and GIP: 47+-8 and 44+-12 nmol in GB and 116+-16 and 161+-44 in CN; p<0.01). Glucose 72-79 insulin Homo sapiens 91-98 30772836-9 2019 CONCLUSION: After GB, the sensitivity of insulin secretion to both glucose and incretins is diminished. Glucose 67-74 insulin Homo sapiens 41-48 32184874-12 2019 Results have shown insulin expression in different glucose concentrates. Glucose 51-58 insulin Homo sapiens 19-26 31074785-0 2019 Impaired Glucose-Stimulated Proinsulin Secretion Is an Early Marker of beta-Cell Impairment Before Prediabetes Stage. Glucose 9-16 insulin Homo sapiens 28-38 31074785-3 2019 However, the dynamic changes of glucose stimulated proinsulin secretion (GSPS) among nondiabetic individuals remain obscure. Glucose 32-39 insulin Homo sapiens 51-61 31074785-4 2019 OBJECTIVE: To examine GSPS and glucose-stimulated insulin secretion (GSIS) among individuals with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) and to evaluate whether impaired GSPS is an early biomarker of beta-cell impairment in individuals with NGT who have subthreshold postprandial plasma glucose (PPG). Glucose 31-38 insulin Homo sapiens 50-57 30712903-6 2019 Further, women with PCOS and MetS exhibited exacerbated insulin and glucose responses to a 75-g oral glucose tolerance test and greater acanthosis nigricans, hirsutism, TC/HDL-C, TC, and sex hormone-binding globulin concentrations compared with their BMI-adjusted counterparts without MetS (P < 0.05). Glucose 101-108 insulin Homo sapiens 56-63 31127824-1 2019 CONTEXT: Use of continuous glucose monitoring (CGM) is increasing for insulin-requiring patients with diabetes. Glucose 27-34 insulin Homo sapiens 70-77 30450664-6 2019 Despite no change in body weight, fasting C-peptide insulin resistance index (p = 0.01) as well as insulin and C-peptide levels at 60 min during the oral glucose tolerance test (p < 0.02) were reduced. Glucose 154-161 insulin Homo sapiens 99-106 30450664-6 2019 Despite no change in body weight, fasting C-peptide insulin resistance index (p = 0.01) as well as insulin and C-peptide levels at 60 min during the oral glucose tolerance test (p < 0.02) were reduced. Glucose 154-161 insulin Homo sapiens 111-120 31443772-5 2019 This paper explores the evidence that increased insulin resistance that is commonly associated with increased adiposity possibly because of shared locations on the genome is a phenotypic plastic adaptation to the increased consumption of refined carbohydrates and their predisposition to cause increased fluctuations in plasma insulin and plasma glucose and post-prandial reactive hypoglycaemia both of which have negative impacts on the metabolism. Glucose 346-353 insulin Homo sapiens 48-55 31443772-5 2019 This paper explores the evidence that increased insulin resistance that is commonly associated with increased adiposity possibly because of shared locations on the genome is a phenotypic plastic adaptation to the increased consumption of refined carbohydrates and their predisposition to cause increased fluctuations in plasma insulin and plasma glucose and post-prandial reactive hypoglycaemia both of which have negative impacts on the metabolism. Glucose 346-353 insulin Homo sapiens 327-334 31443772-6 2019 Obesity, that is a relatively stable state of increased adiposity and insulin resistance has adaptive and defensive features to these fluctuations in plasma insulin and glucose in that metabolic disorders associated with refined carbohydrate consumption are often mitigated and modified as exemplified by the obesity paradox. Glucose 169-176 insulin Homo sapiens 70-77 31420304-5 2019 RESULTS: SNRK ablation is sufficient to inhibit insulin-stimulated AKT phosphorylation and glucose uptake in both WAT and BAT. Glucose 91-98 insulin Homo sapiens 48-55 31362031-2 2019 We hypothesize that prolonged exposure of beta-cells to low concentrations of IL-1beta induce beta-cell dedifferentiation characterized by impaired glucose-stimulated insulin secretion, reduced expression of key beta-cell genes and changes in histone modifications at gene loci known to affect beta-cell function. Glucose 148-155 insulin Homo sapiens 167-174 31420304-9 2019 Dephosphorylated PPP2R5D promotes constitutive assembly of PP2A-AKT complex, therefore inhibits insulin-induced AKT phosphorylation and subsequent glucose uptake in both BAT and WAT. Glucose 147-154 insulin Homo sapiens 96-103 31591827-3 2019 Since DAG activates protein kinase D1 (PKD1) to potentiate glucose-stimulated insulin release, we hypothesized that autocrine ATP signaling activates downstream PKD1 to regulate insulin secretion. Glucose 59-66 insulin Homo sapiens 78-85 31444134-10 2019 Despite the absence of Akt signaling, in vivo and ex vivo insulin-stimulated glucose uptake were normal in M-AktDKO mice. Glucose 77-84 insulin Homo sapiens 58-65 31444134-13 2019 Mechanistically, chronic ablation of Akt induced mitochondrial dysfunction and activation of AMPK, which was required for insulin-stimulated glucose uptake in the absence of Akt. Glucose 141-148 insulin Homo sapiens 122-129 31444134-15 2019 Therefore, since insulin-stimulated glucose disposal in skeletal muscle is markedly impaired in insulin-resistant states, we hypothesize that alterations in signaling molecules in addition to skeletal muscle Akt are necessary to perturb glucose tolerance and insulin sensitivity in vivo. Glucose 36-43 insulin Homo sapiens 17-24 31565976-8 2019 Insulin resistant and diabetic patients showed a decrease in fasting glucose from baseline to end of follow-up (5.47 +- 0.66 vs. 5.08 +- 0.60, p<0.001; 7.90 +- 2.67 vs. 7.04 +- 2.75, p = 0.006), as did both the sustained responder and non-responder groups. Glucose 69-76 insulin Homo sapiens 0-7 31591827-7 2019 Finally, qPCR analysis confirmed PKD1 transcript (PRKD1) expression in human islets, and insulin secretion assays showed that inhibition of either P2Y1 or PKD1 signaling impaired glucose-stimulated insulin secretion. Glucose 179-186 insulin Homo sapiens 89-96 31031134-7 2019 The case group showed higher levels of oral glucose tolerance test (OGTT) 2-h glucose (mean difference (MD) = 0.32 mmol/L, 95% confidence interval (CI) 0.13-0.52 mmol/L, P = 0.0009) and fasting and OGTT 2-h insulin than the control group (respectively, MD = 7.47 pmol/L, 95% CI 1.77-13.17 pmol/L, P = 0.01 and MD = 105.55 pmol/L, 95% CI 65.43-145.66 pmol/L, P < 0.00001). Glucose 44-51 insulin Homo sapiens 207-214 31591827-7 2019 Finally, qPCR analysis confirmed PKD1 transcript (PRKD1) expression in human islets, and insulin secretion assays showed that inhibition of either P2Y1 or PKD1 signaling impaired glucose-stimulated insulin secretion. Glucose 179-186 insulin Homo sapiens 198-205 31583121-2 2019 Pancreatic beta cells are especially relevant because of their involvement in the coordination of insulin secretion when glucose concentration arises in the local milieu. Glucose 121-128 insulin Homo sapiens 98-105 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 387-394 insulin Homo sapiens 0-7 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 387-394 insulin Homo sapiens 54-61 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 387-394 insulin Homo sapiens 125-132 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 387-394 insulin Homo sapiens 125-132 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 421-428 insulin Homo sapiens 0-7 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 421-428 insulin Homo sapiens 54-61 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 421-428 insulin Homo sapiens 125-132 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 421-428 insulin Homo sapiens 125-132 31569345-3 2019 Measures of insulin resistance were calculated using both fasting and postprandial glucose and insulin concentrations. Glucose 83-90 insulin Homo sapiens 12-19 33778342-9 2019 Inverse associations were observed for plasma fasting glucose, insulin, and HOMA of insulin resistance for both exposures, exposure windows, before and after adjustment. Glucose 54-61 insulin Homo sapiens 84-91 31557884-3 2019 IH, hallmark of SAS, plays an important role in the pathogenesis of SAS and experimental studies with animal and cellular models indicate that IH leads to attenuation of glucose-induced insulin secretion from pancreatic beta cells and to enhancement of insulin resistance in peripheral tissues and cells, such as liver (hepatocytes), adipose tissue (adipocytes), and skeletal muscles (myocytes). Glucose 170-177 insulin Homo sapiens 186-193 31557953-7 2019 Two studies reported improved peripheral insulin sensitivity (rate of glucose disappearance, RD) at 6 weeks in patients receiving donor FMT versus patients receiving the placebo control. Glucose 70-77 insulin Homo sapiens 41-48 31556504-0 2019 [Insulin pump regulated by a glucose sensor; one step closer to closing the loop for type 1 diabetes patients]. Glucose 29-36 insulin Homo sapiens 1-8 31598135-10 2019 Plasma glucose: probiotics reduced the plasma glucose level by 4.45 mg/dl and the insulin level by 0.63. Glucose 7-14 insulin Homo sapiens 82-89 31571966-8 2019 Moreover, serum CTRP3 concentrations significantly decreased, while glucose and insulin concentrations significantly increased after a 3 hrs oral glucose tolerance test in obese children. Glucose 146-153 insulin Homo sapiens 80-87 31543708-2 2019 Insulin stimulation mobilizes GSVs, so that these vesicles fuse at the cell surface and insert GLUT4 glucose transporters into the plasma membrane. Glucose 101-108 insulin Homo sapiens 0-7 31555430-2 2019 In diabetic use, the DPP-4 inhibitor can block the DDP-4 to attenuate GLP-1 degradation and prolong GLP-1 its action and sensitize insulin activity for the purpose of lowering blood glucose. Glucose 182-189 insulin Homo sapiens 131-138 31620090-10 2019 Conclusions: Disposition index suggests that although reduced insulin sensitivity is characteristic of active acromegaly it is the impaired insulin secretion that mainly drives glucose intolerance. Glucose 177-184 insulin Homo sapiens 140-147 31247380-7 2019 Furthermore, when compared to suspension cultures, the scaffold culture showed increased insulin secretion in response to glucose stimulus indicating the development of functional beta-cells. Glucose 122-129 insulin Homo sapiens 89-96 31247380-10 2019 These results suggest the microporous scaffold culture provides a conducive environment that drives in vitro differentiation of hPSC-derived insulin-producing glucose-responsive beta-cells and demonstrates the feasibility of these scaffolds as a biomanufacturing platform. Glucose 159-166 insulin Homo sapiens 141-148 31540317-7 2019 Mean glucose and insulin responses varied among foods (p < 0.001) with insulin (p = 0.0037), but not glucose (p = 0.054), varying significantly among labs. Glucose 5-12 insulin Homo sapiens 71-78 31519950-3 2019 The insulin secretion of the generated IPCs was investigated using surface markers by: fluorescence activated cell sorting (FACS) analysis; cytokine release; proliferation ability of ADSCs; in vitro (glucose-stimulated insulin secretion: (GSIS) test/in vivo (transplantation into streptozotocin-induced diabetic nude mice). Glucose 200-207 insulin Homo sapiens 4-11 31519950-3 2019 The insulin secretion of the generated IPCs was investigated using surface markers by: fluorescence activated cell sorting (FACS) analysis; cytokine release; proliferation ability of ADSCs; in vitro (glucose-stimulated insulin secretion: (GSIS) test/in vivo (transplantation into streptozotocin-induced diabetic nude mice). Glucose 200-207 insulin Homo sapiens 219-226 31474750-9 2019 CONCLUSIONS: In obese T2D subjects, exercise training improves whole-body glucose metabolism, in part, by improving insulin-mediated suppression of EGP and enhancing muscle glucose uptake, which occur despite reduced SGU during an oral glucose challenge. Glucose 74-81 insulin Homo sapiens 116-123 31474750-9 2019 CONCLUSIONS: In obese T2D subjects, exercise training improves whole-body glucose metabolism, in part, by improving insulin-mediated suppression of EGP and enhancing muscle glucose uptake, which occur despite reduced SGU during an oral glucose challenge. Glucose 173-180 insulin Homo sapiens 116-123 31474750-9 2019 CONCLUSIONS: In obese T2D subjects, exercise training improves whole-body glucose metabolism, in part, by improving insulin-mediated suppression of EGP and enhancing muscle glucose uptake, which occur despite reduced SGU during an oral glucose challenge. Glucose 173-180 insulin Homo sapiens 116-123 30348487-8 2019 Sixty-six (93%) reported that insulin was commenced at blood glucose concentrations >10 mmol/L and titrated to achieve a blood glucose concentration between 6.0 and 10.0 mmol/L. Glucose 61-68 insulin Homo sapiens 30-37 30348487-8 2019 Sixty-six (93%) reported that insulin was commenced at blood glucose concentrations >10 mmol/L and titrated to achieve a blood glucose concentration between 6.0 and 10.0 mmol/L. Glucose 127-134 insulin Homo sapiens 30-37 31029825-2 2019 A proper membrane structure is critical in pancreatic beta-cells for glucose-mediated insulin secretion, and alterations in cellular cholesterol content may negatively affect this process, leading to beta-cell dysfunction. Glucose 69-76 insulin Homo sapiens 86-93 31175100-1 2019 Muscle insulin sensitivity for stimulating glucose uptake is enhanced in the period after a single bout of exercise. Glucose 43-50 insulin Homo sapiens 7-14 31175100-7 2019 In contrast, 3 h after contraction or 6 h after AICAR stimulation, enhanced insulin-stimulated glucose uptake was evident in muscle from wild-type mice only. Glucose 95-102 insulin Homo sapiens 76-83 31262951-7 2019 RESULTS: Galectin-3 and S100A9 were overexpressed in tumors with PCDM and dose-dependently suppressed insulin-stimulated glucose uptake in C2C12 myotubes. Glucose 121-128 insulin Homo sapiens 102-109 31345519-3 2019 Recent advances including Continuous Glucose Monitoring Systems, Continuous Subcutaneous Insulin Infusion, Closed Loop Devices and very Fast Acting Insulin Aspart analogs offer new possibilities to increase glucose time in target in selected, motivated patients, however their relative roles and indication for use require further elucidation. Glucose 207-214 insulin Homo sapiens 89-96 31345519-3 2019 Recent advances including Continuous Glucose Monitoring Systems, Continuous Subcutaneous Insulin Infusion, Closed Loop Devices and very Fast Acting Insulin Aspart analogs offer new possibilities to increase glucose time in target in selected, motivated patients, however their relative roles and indication for use require further elucidation. Glucose 207-214 insulin Homo sapiens 148-155 31163256-12 2019 In addition, myricetin was observed to enhance PDX-1 and insulin mRNA expression and potentiate glucose stimulated insulin secretion (GSIS). Glucose 96-103 insulin Homo sapiens 115-122 31501648-10 2019 This suggests that visfatin and chemerin levels might affect insulin sensitivity in conjunction with thyroid hormones and thus may alter the metabolism of glucose and leads to insulin resistance. Glucose 155-162 insulin Homo sapiens 61-68 31524229-12 2019 The present findings suggest that in palmitate-induced insulin-resistant HSMM, GLP-1 activates SIRT1 through the PKA/cAMP pathway, which in turn enhances glucose uptake through GLUT4 and the insulin signaling pathway. Glucose 154-161 insulin Homo sapiens 55-62 31396651-2 2019 By the use of ultrarapid insulin analogues postprandial glucose increases can be significantly reduced. Glucose 56-63 insulin Homo sapiens 25-32 31385938-1 2019 To control both fasting and prandial plasma glucose levels in people with diabetes, insulin therapy must mimic "normal" physiological insulin secretion as much as possible. Glucose 44-51 insulin Homo sapiens 84-91 30920624-7 2019 MAIN OUTCOME MEASURES: The primary outcome measure was insulin sensitivity index - Matsuda, derived from a 75-g oral glucose tolerance test. Glucose 117-124 insulin Homo sapiens 55-62 31081169-2 2019 These cells are highly specialized for the secretion of insulin in response to low increasing of blood glucose levels. Glucose 103-110 insulin Homo sapiens 56-63 31081255-0 2019 The molecular mechanism study of insulin in promoting wound healing under high-glucose conditions. Glucose 79-86 insulin Homo sapiens 33-40 30768859-0 2019 Assessment of optimal insulin administration timing for standard carbohydrates-rich meals using continuous glucose monitoring in children with type 1 diabetes: A cross-over randomized study. Glucose 107-114 insulin Homo sapiens 22-29 30661364-6 2019 METHOD: We hypothesized that this goal could be achieved with a modeling tool that determined the optimal basal insulin supply based on the patient"s anamnestic data and monitored glucose values. Glucose 180-187 insulin Homo sapiens 112-119 30678470-3 2019 METHODS: The insulin balanced infusion system (IBIS) is a closed-loop system that uses a system controller, two syringe pumps, and capillary glucose sensor intravenously infusing regular insulin and/or dextrose. Glucose 202-210 insulin Homo sapiens 13-20 30852757-0 2019 Decrease of FGF19 contributes to the increase of fasting glucose in human in an insulin-independent manner. Glucose 57-64 insulin Homo sapiens 80-87 30854885-6 2019 RESULTS: Induced stresses in the study using unpredicted stimuli of intravenous or oral glucose and intravenous insulin boluses, was contained with glucose remaining in target 43.8% of the time. Glucose 148-155 insulin Homo sapiens 112-119 31274675-4 2019 Insulin resistance was calculated by the triglyceride glucose index (TyG). Glucose 54-61 insulin Homo sapiens 0-7 31097391-2 2019 Within the liver, excess fat worsens hepatic responsiveness to insulin, leading to increased glucose production. Glucose 93-100 insulin Homo sapiens 63-70 31133457-0 2019 Fully closed-loop insulin delivery improves glucose control of inpatients with type 2 diabetes receiving hemodialysis. Glucose 44-51 insulin Homo sapiens 18-25 31133457-3 2019 Compared to control patients receiving conventional subcutaneous insulin therapy, those patients receiving closed-loop insulin delivery significantly increased the proportion of time when a continuous glucose monitor was in the target range of 5.6-10.0 mmol/l by 37.6 percent without increasing the risk of hypoglycemia. Glucose 201-208 insulin Homo sapiens 65-72 31133457-3 2019 Compared to control patients receiving conventional subcutaneous insulin therapy, those patients receiving closed-loop insulin delivery significantly increased the proportion of time when a continuous glucose monitor was in the target range of 5.6-10.0 mmol/l by 37.6 percent without increasing the risk of hypoglycemia. Glucose 201-208 insulin Homo sapiens 119-126 31133457-4 2019 Thus, closed-loop insulin delivery offers a novel way to achieve effective and safe glucose control in this vulnerable patient population. Glucose 84-91 insulin Homo sapiens 18-25 31147046-5 2019 In vivo animal trials revealed fast insulin action with excellent hypoglycaemia control and lower glucose levels achieved within 60 min, combined with steady state plasma glucose over 4 h compared to subcutaneous injections. Glucose 98-105 insulin Homo sapiens 36-43 31310433-0 2019 Preventive Effects of Thermosensitive Biopolymer-Conjugated C-Peptide against High Glucose-Induced Endothelial Cell Dysfunction. Glucose 83-90 insulin Homo sapiens 60-69 31310433-7 2019 K9-C-peptide inhibits high glucose-induced intracellular reactive oxygen species generation, transglutaminase 2 activation, and apoptosis, similar to the inhibitory effects of human C-peptide. Glucose 27-34 insulin Homo sapiens 3-12 31500828-11 2019 During maturation, enhancers tend to become demethylated in association with increased activation of beta cell function genes and increased functionality, as indicated by glucose stimulated insulin secretion. Glucose 171-178 insulin Homo sapiens 190-197 31500831-7 2019 MAJOR CONCLUSIONS: Different beta-cell regeneration approaches result in a similar outcome: glucose-sensitive, insulin-positive cells that mimic the native beta-cell phenotype but which lack normal plasticity. Glucose 92-99 insulin Homo sapiens 111-118 31055182-5 2019 A homeostatic model assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Glucose 91-98 insulin Homo sapiens 34-41 31375395-1 2019 Skeletal muscle (SM) insulin resistance (IR) plays an important role in the burden of obesity, particularly because it leads to glucose intolerance and type 2 diabetes. Glucose 128-135 insulin Homo sapiens 21-28 31375395-4 2019 Given that SM accounts for the majority of insulin-stimulated glucose uptake, this review integrates recent observational and mechanistic works with the sole focus on questioning the role of DAGs in SM IR. Glucose 62-69 insulin Homo sapiens 43-50 31464196-5 2019 METHODS: This research presents a model-free data-driven RL algorithm, namely Q-learning, that recommends insulin doses to regulate the blood glucose level of a T1DM patient, considering his or her state defined by glycated hemoglobin (HbA1c) levels, body mass index, engagement in physical activity, and alcohol usage. Glucose 142-149 insulin Homo sapiens 106-113 31464196-8 2019 The reward is calculated as a function of the difference between the actual blood glucose level achieved in response to the insulin dose and the targeted HbA1c level. Glucose 82-89 insulin Homo sapiens 124-131 32377086-3 2019 When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal. Glucose 64-71 insulin Homo sapiens 21-28 31534973-1 2019 Background: Insulin resistance (IR) is a physiological condition related to type 2 diabetes mellitus (T2DM) and obesity, which is associated with high blood insulin and glucose. Glucose 169-176 insulin Homo sapiens 12-19 31455007-8 2019 The obtained data implies that glucose-induced insulin secretion (GIS) in pancreatic beta cells is significantly attenuated by IH, and that IH increases selenoprotein P, which is one of the hepatokines, as well as TNF-alpha, CCL-2, and resistin, members of adipokines, to induce insulin resistance via direct cellular mechanisms. Glucose 31-38 insulin Homo sapiens 47-54 31442224-5 2019 Inhibition of PDE1 or PDE4, but not PDE3, potentiated glucose-stimulated insulin secretion in INS-1 cells. Glucose 54-61 insulin Homo sapiens 73-80 31442224-11 2019 Our results suggest that inhibition of PDE1 may be a useful strategy to potentiate glucose-stimulated insulin secretion, and to protect beta-cells from the toxic effects of excess fatty acids. Glucose 83-90 insulin Homo sapiens 102-109 31969308-4 2019 In conclusion, SES has the ameliorating effect on L02 hepatocyte model of insulin resistance induced by high glucose/high insulin, which might be related to its effect on promoting expression of insulin receptor and its associated proteins of IRS-PI3K-Akt passway, and thus promoting insulin sensitivity. Glucose 109-116 insulin Homo sapiens 74-81 32309058-1 2019 In classical approaches for an artificial pancreas, continuous glucose monitoring (CGM) is the only measured variable used for insulin dosing and additional control functions. Glucose 63-70 insulin Homo sapiens 127-134 31464325-1 2019 Pancreatic beta cell function is compromised in diabetes and is typically assessed by measuring insulin secretion during glucose stimulation. Glucose 121-128 insulin Homo sapiens 96-103 31464325-2 2019 Traditionally, measurement of glucose-stimulated insulin secretion involves manual liquid handling, heterogeneous stimulus delivery, and enzyme-linked immunosorbent assays that require large numbers of islets and processing time. Glucose 30-37 insulin Homo sapiens 49-56 32025933-5 2019 Serum K+ continued to increase to a maximum level of 7.4 mEq/L, despite the infusion of glucose with insulin during surgery. Glucose 88-95 insulin Homo sapiens 101-108 31265840-6 2019 The functionality of the islets was investigated using glucose-induced insulin and c-peptide secretion assay. Glucose 55-62 insulin Homo sapiens 71-78 31487959-8 2019 However, the serum insulin concentration at 30 min after 75 g glucose loading was significantly higher in the PD group. Glucose 62-69 insulin Homo sapiens 19-26 31508240-6 2019 Taken together, these results suggest that the glucose minimization is achieved by suppressing the peak value of insulin concentration, rather than by enhancing insulin concentration. Glucose 47-54 insulin Homo sapiens 113-120 31282029-8 2019 In conclusion, these results suggest that it is possible to increase the blood insulin response by supplementing dextrose to a high nutrient diet, thus, improving WSI interval and litter growth during heat stress. Glucose 113-121 insulin Homo sapiens 79-86 31044622-5 2019 Whether glucose-targeted insulin and glucose infusion have advantages over glucose-insulin-potassium infusion remains controversial. Glucose 8-15 insulin Homo sapiens 25-32 31069935-0 2019 Fast-acting insulin aspart in people with type 2 diabetes: Earlier onset and greater initial exposure and glucose-lowering effect compared with insulin aspart. Glucose 106-113 insulin Homo sapiens 12-19 34007540-12 2019 Conclusion: Integration of the clinical pharmacy services for insulin titration positively affected patients" degree of glucose control. Glucose 120-127 insulin Homo sapiens 62-69 31105125-5 2019 PGE2, the catalytic product of COX-2, downregulated the functional gene expression of PDX1, NKX6.1, and MAFA and blunted the glucose induced insulin secretion of human islets. Glucose 125-132 insulin Homo sapiens 141-148 31461451-0 2019 Delineating the role of FANCA in glucose-stimulated insulin secretion in beta cells through its protein interactome. Glucose 33-40 insulin Homo sapiens 52-59 31461451-3 2019 Therefore, we sought to evaluate the functional role of FANCA, the most commonly mutated gene in FA, in glucose-stimulated insulin secretion (GSIS). Glucose 104-111 insulin Homo sapiens 123-130 31692532-9 2019 Moreover, addition of DPP4 inhibitors to insulin was associated with significantly reduced fasting blood glucose (WMD: -0.47mmol/L, p<0.001), postprandial glucose at 2 hrs (WMD: -2.03 mmol/L, p<0.001), and daily dose of insulin (WMD: -2.73U/d, p<0.001), while body weight (WMD: 0.02 g, p=0.81) or risk of symptomatic hypoglycemia (risk ratio: 0.92, p=0.37) were not affected. Glucose 105-112 insulin Homo sapiens 41-48 31692532-9 2019 Moreover, addition of DPP4 inhibitors to insulin was associated with significantly reduced fasting blood glucose (WMD: -0.47mmol/L, p<0.001), postprandial glucose at 2 hrs (WMD: -2.03 mmol/L, p<0.001), and daily dose of insulin (WMD: -2.73U/d, p<0.001), while body weight (WMD: 0.02 g, p=0.81) or risk of symptomatic hypoglycemia (risk ratio: 0.92, p=0.37) were not affected. Glucose 158-165 insulin Homo sapiens 41-48 31496996-1 2019 Resistance to insulin is a pathophysiological state related to the decreased response of peripheral tissues to the insulin action, hyperinsulinemia and raised blood glucose levels caused by increased hepatic glucose outflow. Glucose 165-172 insulin Homo sapiens 14-21 31496996-1 2019 Resistance to insulin is a pathophysiological state related to the decreased response of peripheral tissues to the insulin action, hyperinsulinemia and raised blood glucose levels caused by increased hepatic glucose outflow. Glucose 208-215 insulin Homo sapiens 14-21 31078658-1 2019 The integrated multiscale mathematical model we present in this paper is built on two of our previous ones: a model of electrical oscillation in beta-cells connected to neighboring cells within a three-dimensional (3D) network, and a model of glucose-induced beta-cell intracellular insulin granule trafficking and insulin secretion. Glucose 243-250 insulin Homo sapiens 283-290 31078658-1 2019 The integrated multiscale mathematical model we present in this paper is built on two of our previous ones: a model of electrical oscillation in beta-cells connected to neighboring cells within a three-dimensional (3D) network, and a model of glucose-induced beta-cell intracellular insulin granule trafficking and insulin secretion. Glucose 243-250 insulin Homo sapiens 315-322 31078658-0 2019 Integrated multiscale mathematical modeling of insulin secretion reveals the role of islet network integrity for proper oscillatory glucose-dose response. Glucose 132-139 insulin Homo sapiens 47-54 31078658-4 2019 Numerical analysis of our new model shows that a single step increase in glucose concentration yields the experimentally observed characteristic biphasic insulin release. Glucose 73-80 insulin Homo sapiens 154-161 31078658-6 2019 The plateau fraction (the time that the beta-cells spend in their active firing phase) increases with increasing glucose dose, as does the total insulin secretion. Glucose 113-120 insulin Homo sapiens 145-152 31078658-8 2019 Our results also demonstrate how insulin secretion characteristics in various glucose protocols depend on the degree of beta-cell loss, highlighting the potential impact from disease. Glucose 78-85 insulin Homo sapiens 33-40 31170414-8 2019 RESULTS: We found that a low-dose exposure (0.25 ppm iAs in drinking water) caused glucose intolerance in adult male C57BL/6 mice, likely by disrupting glucose-induced insulin secretion without affecting peripheral insulin sensitivity. Glucose 152-159 insulin Homo sapiens 168-175 32259078-1 2019 Glucagon-like peptide-1 (GLP-1) has been in focus since the early 1980s as a long looked for incretin hormone, released from the gastrointestinal tract and with an important effect on glucose-dependent insulin secretion, providing efficient glucose lowering, with little risk for hypoglycemia. Glucose 184-191 insulin Homo sapiens 202-209 31474046-2 2019 The patient repeatedly used the same needle to inject insulin subcutaneously in the unsterilized right thigh, and his blood glucose was badly controlled in the long term. Glucose 124-131 insulin Homo sapiens 54-61 31430994-3 2019 In this study, we prepared phenylboronic acid-modified insulin (PBA-Ins) to evaluate its glucose-lowering activity and cell adhesiveness. Glucose 89-96 insulin Homo sapiens 55-62 31095939-6 2019 In this study, we aimed to investigate whether PAQR3 regulates phosphorylation of FoxO1 via NF-kappaB pathway in palmitic acid (PA)-induced insulin-resistant HepG2 cells, thereby causing glucose and lipid metabolism disorders. Glucose 187-194 insulin Homo sapiens 140-147 31095939-9 2019 Taken together, in PA-induced insulin-resistant HepG2 cells, PAQR3 might regulate the phosphorylation of FoxO1 and the expressions of GCK and LDLR through NF-kappaB pathway, thereby regulating the glucose and lipid metabolism disorders induced by insulin resistance. Glucose 197-204 insulin Homo sapiens 30-37 31170414-10 2019 Insulin Clamp analysis showed that 2.5 ppm iAs actually enhanced systemic insulin sensitivity by simultaneously enhancing insulin-stimulated glucose uptake in skeletal muscles and improved insulin-mediated suppression of endogenous glucose production. Glucose 141-148 insulin Homo sapiens 122-129 31170414-10 2019 Insulin Clamp analysis showed that 2.5 ppm iAs actually enhanced systemic insulin sensitivity by simultaneously enhancing insulin-stimulated glucose uptake in skeletal muscles and improved insulin-mediated suppression of endogenous glucose production. Glucose 141-148 insulin Homo sapiens 122-129 31378674-2 2019 However, it has been challenging to generate competent beta cells with dynamic insulin-secretory capacity to glucose and incretin stimulations. Glucose 109-116 insulin Homo sapiens 79-86 31398847-1 2019 Diabetes belongs to a group of metabolic disorders characterized by long term high blood glucose levels due to either inadequate production of insulin (Type 1 diabetes, T1DM) or poor response of the recipient cell to insulin (Type 2 diabetes, T2DM). Glucose 89-96 insulin Homo sapiens 143-150 31053371-5 2019 After treatment with an injection of calcium gluconate, insulin with glucose, bicarbonate, and an enema with polystyrene sulfonate, the patient"s serum potassium level normalized and the bradyarrhythmia converted to a normal sinus rhythm. Glucose 69-76 insulin Homo sapiens 56-63 31440170-1 2019 Skeletal muscle is a main target of insulin action that plays a pivotal role in postprandial glucose disposal. Glucose 93-100 insulin Homo sapiens 36-43 31331425-0 2019 Continuous Glucose Monitoring for In-Flight Measurement of Glucose Levels of Insulin-Treated Pilots. Glucose 11-18 insulin Homo sapiens 77-84 31331425-0 2019 Continuous Glucose Monitoring for In-Flight Measurement of Glucose Levels of Insulin-Treated Pilots. Glucose 59-66 insulin Homo sapiens 77-84 31084489-6 2019 Hep3B Fet-A was phosphorylated (Ser312) and inhibited insulin-stimulated glucose uptake and glycogen synthesis in L6GLUT4 myoblasts. Glucose 73-80 insulin Homo sapiens 54-61 31117834-1 2019 The objective of this cross-sectional analysis was to investigate in 109 adults with type 1 diabetes the relationship between sleep, circadian parameters and insulin sensitivity, as assessed by estimated glucose disposal rate (eGDR). Glucose 204-211 insulin Homo sapiens 158-165 31170380-0 2019 An insulin-dose error assessment grid: A new tool to evaluate glucose meter performance. Glucose 62-69 insulin Homo sapiens 3-10 30767123-1 2019 Controlled release insulin delivery systems possess multiple advantages over conventional ones, including maintaining desired blood glucose levels for prolonged periods and minimizing complications due to insulin overdose. Glucose 132-139 insulin Homo sapiens 19-26 31050109-10 2019 iGlarLixi was safe and well tolerated, and would be expected to provide the 24-hour plasma glucose-lowering effects of insulin glargine and the postprandial antihyperglycaemic effects of lixisenatide. Glucose 91-98 insulin Homo sapiens 119-126 31187420-1 2019 The use of insulin in children and adolescents with type 1 diabetes (T1D) is a challenge because of the heterogeneity of these patients and their lifestyles, with consequent unpredictability in blood glucose levels. Glucose 200-207 insulin Homo sapiens 11-18 31187420-2 2019 A new ultra-long-acting basal insulin, insulin degludec (degludec), has the potential to mitigate some of these challenges, notably variability in the glucose-lowering action of the basal insulin component of an insulin regimen, and consequent risks of hypo- and hyperglycemia. Glucose 151-158 insulin Homo sapiens 30-37 31383551-0 2019 The imprinted gene Delta like non-canonical notch ligand 1 (Dlk1) associates with obesity and triggers insulin resistance through inhibition of skeletal muscle glucose uptake. Glucose 160-167 insulin Homo sapiens 103-110 31271255-10 2019 Although we cannot conclude a causal association, the safety of insulin and alternative glucose-lowering treatments in HF needs to be evaluated in clinical trials. Glucose 88-95 insulin Homo sapiens 64-71 31028829-1 2019 In the periphery insulin plays a critical role in the regulation of metabolic homeostasis by stimulating glucose uptake into peripheral organs. Glucose 105-112 insulin Homo sapiens 17-24 31375001-6 2019 Added insulin increased the epithelial cell layer tightness in normal glucose concentrations, and the effect was more evident in type 2 diabetics than in healthy control hiPSC-RPE cells. Glucose 70-77 insulin Homo sapiens 6-13 30908701-0 2019 Undercarboxylated Osteocalcin Improves Insulin-Stimulated Glucose Uptake in Muscles of Corticosterone-Treated Mice. Glucose 58-65 insulin Homo sapiens 39-46 30908701-3 2019 To test the hypothesis that ucOC directly ameliorates impaired insulin-stimulated glucose uptake (ISGU) induced by short-term GC administration in mice muscle and to identify the molecular mechanisms, mice were implanted with placebo or corticosterone (CS) slow-release pellets. Glucose 82-89 insulin Homo sapiens 63-70 30790280-5 2019 As a new choice for transplantation, we have proposed glucose-regulated insulin-producing hepatocyte-like cells, which produce insulin dependent on glucose levels. Glucose 54-61 insulin Homo sapiens 72-79 30790280-5 2019 As a new choice for transplantation, we have proposed glucose-regulated insulin-producing hepatocyte-like cells, which produce insulin dependent on glucose levels. Glucose 54-61 insulin Homo sapiens 127-134 30790280-5 2019 As a new choice for transplantation, we have proposed glucose-regulated insulin-producing hepatocyte-like cells, which produce insulin dependent on glucose levels. Glucose 148-155 insulin Homo sapiens 72-79 30790280-5 2019 As a new choice for transplantation, we have proposed glucose-regulated insulin-producing hepatocyte-like cells, which produce insulin dependent on glucose levels. Glucose 148-155 insulin Homo sapiens 127-134 30790280-13 2019 They were functionally active by releasing insulin in response to elevated glucose concentrations in vitro. Glucose 75-82 insulin Homo sapiens 43-50 30938760-3 2019 OBJECTIVE: We hypothesized that the ingestion of glucose and fructose may differentially stimulate GLP-1 and insulin response in lean adolescents and adolescents with obesity. Glucose 49-56 insulin Homo sapiens 109-116 30938764-10 2019 RESULTS: Between-group differences in change in insulin sensitivity favored metformin regarding whole-body IR [change in glucose infusion rate 1.3 (0.1, 2.4) mg/kg/min, P = 0.03] and peripheral IR [change in metabolic clearance rate 0.923 (-0.002, 1.867) dL/kg/min, P = 0.05]. Glucose 121-128 insulin Homo sapiens 48-55 30701438-1 2019 PURPOSE: To evaluate the relationship between surrogate estimates of insulin resistance and a direct measurement of insulin-mediated glucose uptake women with and without PCOS. Glucose 133-140 insulin Homo sapiens 69-76 30701438-1 2019 PURPOSE: To evaluate the relationship between surrogate estimates of insulin resistance and a direct measurement of insulin-mediated glucose uptake women with and without PCOS. Glucose 133-140 insulin Homo sapiens 116-123 31452966-1 2019 Repaglinide (RPG) regulates the amount of glucose by stimulating the pancreas to release insulin in the blood. Glucose 42-49 insulin Homo sapiens 89-96 30964769-2 2019 INTRODUCTION: Hyperglycemia is common during acute illness, and current recommendations for patients with altered glucose metabolism is the use of intravenous insulin therapy. Glucose 114-121 insulin Homo sapiens 159-166 31353352-3 2019 We adjusted the insulin amount according to the glucose level of the device before surgery and prevented prolonged hypoglycemia. Glucose 48-55 insulin Homo sapiens 16-23 30945019-6 2019 While, not all of the T2DM-associated genetic variants are related to pregnant glucose tolerance, such as genes involved in fasting insulin/C-peptide regulation. Glucose 79-86 insulin Homo sapiens 132-139 30945019-8 2019 And certain genes may be particularly involved in this process via specific mechanisms, such as HKDC1, MTNR1B, BACE2, genes encoding cell cycle regulators, adipocyte regulators, inflammatory factors and hepatic factors related to gestational glucose sensing and insulin signaling. Glucose 242-249 insulin Homo sapiens 262-269 31087499-3 2019 METHODS AND RESULTS: It is found that TBI affects glucose metabolism and signaling proteins for insulin and growth hormone in the liver; these effects are exacerbated by fructose ingestion. Glucose 50-57 insulin Homo sapiens 96-103 31534762-2 2019 They alter insulin absorption, causing higher insulin requirements (and costs), fluctuating blood glucose and episodes of unpredictable hypoglycemia. Glucose 98-105 insulin Homo sapiens 11-18 31353426-7 2019 Therapy with dipeptidyl peptidase-4 (DPP-4) inhibitors, alone or in combination with basal insulin, may effectively control glucose levels in patients with mild to moderate hyperglycemia. Glucose 124-131 insulin Homo sapiens 91-98 31344028-7 2019 The fundamental limitation identified in these cells was a critical lack of expression of the insulin sensitive glucose transporter GLUT4. Glucose 112-119 insulin Homo sapiens 94-101 31344867-6 2019 The insulin signaling pathway was activated by KMOS, with stimulation of GLUT2 membrane translocation and glucose uptake in HepG2 cells via the AMPK pathway. Glucose 106-113 insulin Homo sapiens 4-11 31303487-2 2019 We find that when glucose metabolism induces insulin secretion, it also increases formation of Golgi-derived microtubules (GDMTs), notably with the same biphasic kinetics as insulin exocytosis. Glucose 18-25 insulin Homo sapiens 45-52 31039435-1 2019 Insulin is a peptide hormone responsible for stable glycemia, is entirely secreting from pancreatic beta cells at the core of glucose homeostatic regulation. Glucose 126-133 insulin Homo sapiens 0-7 31323061-4 2019 Islets, DPS, and islets + DPS (100 islets + 75 DPS, or 100 islets + 200 DPS) were cultured and glucose-stimulated insulin secretion, beta-cell apoptosis, and gene expression was determined. Glucose 95-102 insulin Homo sapiens 114-121 31311971-0 2019 Glucose, adrenaline and palmitate antagonistically regulate insulin and glucagon secretion in human pseudoislets. Glucose 0-7 insulin Homo sapiens 60-67 31360518-3 2019 The proliferation and spread of breast cancer is intimately linked to cellular glucose metabolism, given that glucose is an essential cellular metabolic substrate and that insulin signalling has mitogenic effects. Glucose 79-86 insulin Homo sapiens 172-179 31468825-2 2019 It involves an elevated level of glucose in the blood, which develops as a result of the body"s inability to produce insulin or process insulin effectively. Glucose 33-40 insulin Homo sapiens 117-124 31092478-6 2019 Low-dose insulin infusion suppressed endogenous glucose production similarly in all groups and suppressed nonesterified fatty acids similarly between control subjects and GCK-MODY, but to a lesser extent for type 1 diabetes. Glucose 48-55 insulin Homo sapiens 9-16 31092478-7 2019 High-dose insulin infusion stimulated glucose disposal similarly in control subjects and GCK-MODY but was 29% and 22% less effective in type 1 diabetes, respectively. Glucose 38-45 insulin Homo sapiens 10-17 31409982-0 2019 Downregulated level of insulin in COPD patients during AE; role beyond glucose control? Glucose 71-78 insulin Homo sapiens 23-30 31363388-5 2019 In this report we described a Thai MODY 3 patient who had excellence plasma glucose control by treating with glicazide 20 mg per day and insulin therapy can be discontinued. Glucose 76-83 insulin Homo sapiens 137-144 31112719-3 2019 When it is injected into the human body, it automatically releases the corresponding amount of insulin according to the blood glucose level of the human body. Glucose 126-133 insulin Homo sapiens 95-102 31296514-1 2019 BACKGROUND: Intravenous insulin infusions are considered the treatment of choice for critically ill patients and non-critically ill patients with persistent raised blood glucose who are unable to eat, to achieve optimal blood glucose levels. Glucose 170-177 insulin Homo sapiens 24-31 31296514-1 2019 BACKGROUND: Intravenous insulin infusions are considered the treatment of choice for critically ill patients and non-critically ill patients with persistent raised blood glucose who are unable to eat, to achieve optimal blood glucose levels. Glucose 226-233 insulin Homo sapiens 24-31 31295897-3 2019 The macronutrient composition of the meal, the rate of gastric emptying and premeal insulin administration are key factors affecting the PP glucose response in T1DM. Glucose 140-147 insulin Homo sapiens 84-91 31295897-4 2019 Although the use of continuous insulin infusion systems has improved PP glucose control compared to conventional insulin therapy, there is still need for further ameliorations. Glucose 72-79 insulin Homo sapiens 31-38 30970232-0 2019 Baicalein improves glucose metabolism in insulin resistant HepG2 cells. Glucose 19-26 insulin Homo sapiens 41-48 31296225-1 2019 BACKGROUND: The triglyceride-glucose index (TyG index) is a tool for insulin resistance evaluation, however, little is known about its association with coronary artery disease (CAD), which is the major cardiovascular death cause, and what factors may be associated with TyG index. Glucose 29-36 insulin Homo sapiens 69-76 31468825-2 2019 It involves an elevated level of glucose in the blood, which develops as a result of the body"s inability to produce insulin or process insulin effectively. Glucose 33-40 insulin Homo sapiens 136-143 31592406-1 2019 A 74-year-old woman of insulin-dependent diabetes mellitus presented with gradually improvement of blood glucose control and finally discontinuation of insulin therapy, for some unknown reason. Glucose 105-112 insulin Homo sapiens 23-30 31165524-8 2019 This work is the first demonstration of a glucose-responsive glucagon-delivery MN patch for the prevention of hypoglycemia, which has a tremendous potential to reduce the dangers of intensive insulin therapy and improve the quality of life of patients with diabetes and their caregivers. Glucose 42-49 insulin Homo sapiens 192-199 30748094-6 2019 CXCL12 enhanced glucose-stimulated insulin secretion activity of SC-beta cells and induced expression of genes associated with beta-cell function in vitro. Glucose 16-23 insulin Homo sapiens 35-42 30912960-0 2019 Chronic fructose renders pancreatic beta-cells hyper-responsive to glucose-stimulated insulin secretion through extracellular ATP signaling. Glucose 67-74 insulin Homo sapiens 86-93 30912960-8 2019 Addition of an ectonucleotidase inhibitor or P2Y1 agonists to naive beta-cells potentiated insulin secretion stimulated by intermediate glucose, mimicking the fructose treatment. Glucose 136-143 insulin Homo sapiens 91-98 31042416-4 2019 As consideration of daily variation in insulin secretion is necessary to accurately describe glucose-stimulated insulin secretion, we describe a mathematical model that incorporates the circadian modulation via insulin granule trafficking. Glucose 93-100 insulin Homo sapiens 39-46 31042416-4 2019 As consideration of daily variation in insulin secretion is necessary to accurately describe glucose-stimulated insulin secretion, we describe a mathematical model that incorporates the circadian modulation via insulin granule trafficking. Glucose 93-100 insulin Homo sapiens 112-119 31042416-4 2019 As consideration of daily variation in insulin secretion is necessary to accurately describe glucose-stimulated insulin secretion, we describe a mathematical model that incorporates the circadian modulation via insulin granule trafficking. Glucose 93-100 insulin Homo sapiens 112-119 31274486-13 2019 Total 75 (58.1%) patients did not require insulin and 54 (41.9%) were treated with insulin intraoperatively to keep the blood glucose level less than 200 g/dl. Glucose 126-133 insulin Homo sapiens 83-90 31947429-8 2019 The methodology is also successful in reconstructing of "non-accessible" glucose-insulin fluxes, i.e. glucose rate of appearance and plasma insulin. Glucose 73-80 insulin Homo sapiens 81-88 31946507-7 2019 The results show the model captures glucose-insulin dynamics in pre-diabetic post-surgical patients, and insulin Detemir may be useful to support individuals with pre-diabetes in reducing blood glucose levels. Glucose 36-43 insulin Homo sapiens 44-51 31946507-7 2019 The results show the model captures glucose-insulin dynamics in pre-diabetic post-surgical patients, and insulin Detemir may be useful to support individuals with pre-diabetes in reducing blood glucose levels. Glucose 194-201 insulin Homo sapiens 44-51 31946507-7 2019 The results show the model captures glucose-insulin dynamics in pre-diabetic post-surgical patients, and insulin Detemir may be useful to support individuals with pre-diabetes in reducing blood glucose levels. Glucose 194-201 insulin Homo sapiens 105-112 31947092-2 2019 Without the crucial hormone insulin, which is necessary to equilibrate the blood glucose level, the patient must inject insulin subcutaneously. Glucose 81-88 insulin Homo sapiens 28-35 31947092-2 2019 Without the crucial hormone insulin, which is necessary to equilibrate the blood glucose level, the patient must inject insulin subcutaneously. Glucose 81-88 insulin Homo sapiens 120-127 30845346-0 2019 Acute interaction between oral glucose (75 g as Lucozade) and inorganic nitrate: Decreased insulin clearance, but lack of blood pressure-lowering. Glucose 31-38 insulin Homo sapiens 91-98 30845346-2 2019 Whilst this is commonly assumed to be a consequence of chronic hyperglycaemia/hyperinsulinaemia, we hypothesized that acute physiological elevations in plasma [glucose]/[insulin] blunt the haemodynamic responses to NO3 - , a pertinent question for carbohydrate-rich Western diets. Glucose 160-167 insulin Homo sapiens 83-90 30955189-2 2019 The triglyceride-glucose index (TyG index) has been suggested as a marker of moderate insulin resistance. Glucose 17-24 insulin Homo sapiens 86-93 31371853-2 2019 If insulin is delivered intramuscularly, its uptake and action become variably faster, leading to suboptimal, inconsistent glucose control. Glucose 123-130 insulin Homo sapiens 3-10 30869182-3 2019 The primary outcome was change in insulin sensitivity (SI ) as estimated by insulin-modified frequently sampled intravenous glucose tolerance tests. Glucose 124-131 insulin Homo sapiens 34-41 30869182-3 2019 The primary outcome was change in insulin sensitivity (SI ) as estimated by insulin-modified frequently sampled intravenous glucose tolerance tests. Glucose 124-131 insulin Homo sapiens 76-83 31010960-9 2019 Silencing of ECHDC3 in adipocytes significantly reduced insulin-stimulated glucose uptake and Akt Ser473 phosphorylation. Glucose 75-82 insulin Homo sapiens 56-63 31036546-1 2019 OBJECTIVE: To assess treatment satisfaction and the effectiveness of a flash glucose monitoring (FGM) system in patients with type 2 diabetes using insulin. Glucose 77-84 insulin Homo sapiens 148-155 31271312-0 2019 Reduction in HbA1c using professional flash glucose monitoring in insulin-treated type 2 diabetes patients managed in primary and secondary care settings: A pilot, multicentre, randomised controlled trial. Glucose 44-51 insulin Homo sapiens 66-73 31271312-1 2019 AIM: Analyse the effects of professional flash glucose monitoring system (FreeStyle Libre Pro ) on glycaemic control in insulin-treated type 2 diabetes. Glucose 47-54 insulin Homo sapiens 120-127 30959417-0 2019 The protective effect of silk fibroin on high glucose induced insulin resistance in HepG2 cells. Glucose 46-53 insulin Homo sapiens 62-69 31079201-2 2019 Thus, the purpose of this study was to examine the effect of exercise pattern on post-exercise insulin and glucose responses following a glucose challenge. Glucose 137-144 insulin Homo sapiens 95-102 31215021-5 2019 Moreover, accumulating evidence indicates that N-glycans have a major role in preventing the impairment of glucose-stimulated insulin secretion by maintaining the glucose transporter in proper orientation, indicating that interindividual variation in protein N-glycosylation might be a novel risk factor contributing to diabetes development. Glucose 107-114 insulin Homo sapiens 126-133 31215021-5 2019 Moreover, accumulating evidence indicates that N-glycans have a major role in preventing the impairment of glucose-stimulated insulin secretion by maintaining the glucose transporter in proper orientation, indicating that interindividual variation in protein N-glycosylation might be a novel risk factor contributing to diabetes development. Glucose 163-170 insulin Homo sapiens 126-133 30810506-1 2019 Background: Medical professionals attribute a crucial role in the development of several age-related, chronic health maladies to glucose-insulin perturbations - particularly, discernible insulin resistance (IR). Glucose 129-136 insulin Homo sapiens 137-144 30810506-1 2019 Background: Medical professionals attribute a crucial role in the development of several age-related, chronic health maladies to glucose-insulin perturbations - particularly, discernible insulin resistance (IR). Glucose 129-136 insulin Homo sapiens 187-194 30689903-9 2019 Mean adipocyte size significantly reduced, more at 4 than at 24 weeks; at 4 weeks, glucose uptake per adipocyte was lowered, and isoproterenol-stimulated lipolysis tended to increase, whereas the fold insulin effects on glucose uptake and lipolysis were unchanged. Glucose 220-227 insulin Homo sapiens 201-208 30789980-0 2019 Mild Physiologic Hyperglycemia Induces Hepatic Insulin Resistance in Healthy Normal Glucose-Tolerant Participants. Glucose 84-91 insulin Homo sapiens 47-54 30789980-9 2019 The hepatic insulin resistance index (basal EGP x fasting plasma insulin) markedly increased following glucose infusion (20.1 +- 1.8 to 51.7 +- 6.6; P < 0.005) in both FH+ and FH- subjects. Glucose 103-110 insulin Homo sapiens 12-19 30582774-2 2019 We examined whether the reduction of plasma glucose using a sodium-glucose cotransporter 2 inhibitor, in inpatient diabetes management, has any effect on: (i) treatment period and basal-bolus dosage of insulin that achieve euglycemia; (ii) fasting/postprandial energy expenditure (EE); and (iii) energy substrate oxidation. Glucose 44-51 insulin Homo sapiens 202-209 30711385-0 2019 The main mechanism associated with progression of glucose intolerance in older patients with cystic fibrosis is insulin resistance and not reduced insulin secretion capacity. Glucose 50-57 insulin Homo sapiens 112-119 31084947-8 2019 Several strategies can reduce the risk of hypoglycemia with insulin therapy, which include using insulin 5 units or 0.1 units/kg instead of 10 units, administering dextrose 50 g instead of 25 g, or administering dextrose as a prolonged infusion instead of a rapid intravenous bolus. Glucose 164-172 insulin Homo sapiens 60-67 31084947-8 2019 Several strategies can reduce the risk of hypoglycemia with insulin therapy, which include using insulin 5 units or 0.1 units/kg instead of 10 units, administering dextrose 50 g instead of 25 g, or administering dextrose as a prolonged infusion instead of a rapid intravenous bolus. Glucose 212-220 insulin Homo sapiens 60-67 31579190-1 2019 BACKGROUND: Various indices for estimating insulin sensitivity, based on glucose tolerance test and fasting insulin levels, have been devised. Glucose 73-80 insulin Homo sapiens 43-50 30895514-6 2019 The compound controller is designed in such a way that eIMC predicts insulin doses when the glucose rate increase detector of meal detection module is positive, otherwise conventional IMC takes the control action. Glucose 92-99 insulin Homo sapiens 69-76 30999003-8 2019 In FABP4-challenged HL-1 cells, extracellular FABP4 increased intracellular lipid accumulation, which led to impairment of the insulin-signalling pathway and reduced insulin-stimulated glucose uptake. Glucose 185-192 insulin Homo sapiens 166-173 30999003-9 2019 However, these effects were partially reversed by FABP4 inhibition with BMS309403, which attenuated the intracellular lipid content and improved insulin signalling and insulin-stimulated glucose uptake. Glucose 187-194 insulin Homo sapiens 168-175 31029770-1 2019 The incretin effect, the amplification of insulin secretion occurring when glucose is taken in orally as compared to infused intravenously, is one of the factors that help the body to tolerate carbohydrate/glucose ingestion. Glucose 75-82 insulin Homo sapiens 42-49 31029770-1 2019 The incretin effect, the amplification of insulin secretion occurring when glucose is taken in orally as compared to infused intravenously, is one of the factors that help the body to tolerate carbohydrate/glucose ingestion. Glucose 206-213 insulin Homo sapiens 42-49 31018989-1 2019 Insulin-stimulated glucose uptake is known to involve microtubules, although the function of microtubules and the microtubule-regulating proteins involved in insulin action are poorly understood. Glucose 19-26 insulin Homo sapiens 0-7 31018989-2 2019 CLASP2, a plus-end tracking microtubule-associated protein (+TIP) that controls microtubule dynamics, was recently implicated as the first +TIP associated with insulin-regulated glucose uptake. Glucose 178-185 insulin Homo sapiens 160-167 31036449-14 2019 Islets from WSD/CTR offspring secreted a greater amount of insulin in response to glucose ex vivo. Glucose 82-89 insulin Homo sapiens 59-66 31117739-2 2019 The aim of this method is to release insulin from a shallow dermal depot in response to blood glucose information, using transcutaneous irradiation. Glucose 94-101 insulin Homo sapiens 37-44 31054312-3 2019 Islet must survive from possible cellular damages during the isolation procedure, storage time, islet injection process and post-transplantation immune rejection, only then the survived islets could produce insulin, actively regulating the blood glucose level. Glucose 246-253 insulin Homo sapiens 207-214 31111222-0 2019 Correction to: Sweet taste receptors as a tool for an amplifying pathway of glucose-stimulated insulin secretion in pancreatic beta cells. Glucose 76-83 insulin Homo sapiens 95-102 31253200-6 2019 Using a stepwise multiple logistic regression analysis, we observed 4 CpGs (cg27655935, cg02000426, cg10184328, and cg23085143) whose methylation levels independently predicted the insulin-resistant state at a higher confidence than that of clinical risk factors typically associated with insulin resistance (i.e., fasting glucose, 120-min oral glucose tolerance test, Framingham Risk Score, and Total to HDL cholesterol ratio). Glucose 323-330 insulin Homo sapiens 181-188 31253200-6 2019 Using a stepwise multiple logistic regression analysis, we observed 4 CpGs (cg27655935, cg02000426, cg10184328, and cg23085143) whose methylation levels independently predicted the insulin-resistant state at a higher confidence than that of clinical risk factors typically associated with insulin resistance (i.e., fasting glucose, 120-min oral glucose tolerance test, Framingham Risk Score, and Total to HDL cholesterol ratio). Glucose 345-352 insulin Homo sapiens 181-188 31253846-1 2019 The Muscle Insulin Sensitivity Index (MISI) has been developed to estimate muscle-specific insulin sensitivity based on oral glucose tolerance test (OGTT) data. Glucose 125-132 insulin Homo sapiens 91-98 31218342-2 2019 Skeletal muscle is one of the major target organs of insulin-mediated glucose uptake, metabolism and utilization, and it is the earliest and most important site of insulin resistance. Glucose 70-77 insulin Homo sapiens 53-60 31499737-8 2019 Results show that key metabolic factors improve after surgery, such as the effect of insulin inhibition of FFA on insulin and glucose regulation, results that do match prior clinical studies. Glucose 126-133 insulin Homo sapiens 85-92 31499737-9 2019 These findings indicate that the reduction in weight or body mass due to surgery improve insulin action for the regulation of glucose, FFA, and insulin levels. Glucose 126-133 insulin Homo sapiens 89-96 31499737-10 2019 This reinforces what we know, namely, that insulin action is essential for regulating FFA and glucose levels and is a robust effect that can be observed not only in the long-term, but also in the short-term; thereby preventing the manifestation of T2DM. Glucose 94-101 insulin Homo sapiens 43-50 30968941-8 2019 Significant changes in tai chi-related effects were observed in lowering fasting plasma glucose (standardized mean difference; SMD -0.67; 95% confidence interval (95% CI) -0.87 to -0.47; p <0.001), HbA1c (mean difference; MD-0.88%; 95% CI -1.45% to -0.31%; p =0.002) and insulin resistance (MD -0.41; 95% CI -0.78 to -0.04; p = 0.029). Glucose 88-95 insulin Homo sapiens 274-281 30992164-1 2019 The free fatty acid receptor 1 (FFA1) is considered as a promising anti-diabetic target based on its function of glucose-stimulated insulin secretion. Glucose 113-120 insulin Homo sapiens 132-139 31214645-4 2019 Insulin sensitivity index was derived from oral glucose tolerance tests. Glucose 48-55 insulin Homo sapiens 0-7 30755013-3 2019 RESULTS: Insulin resistance was significantly greater in persons with normal glucose tolerance whose 60-min glucose concentration was >=8.6, associated with higher blood pressure, plasma concentrations of glucose, insulin, triglyceride and lower high-density lipoprotein cholesterol concentrations. Glucose 77-84 insulin Homo sapiens 9-16 30755013-3 2019 RESULTS: Insulin resistance was significantly greater in persons with normal glucose tolerance whose 60-min glucose concentration was >=8.6, associated with higher blood pressure, plasma concentrations of glucose, insulin, triglyceride and lower high-density lipoprotein cholesterol concentrations. Glucose 108-115 insulin Homo sapiens 9-16 30755013-3 2019 RESULTS: Insulin resistance was significantly greater in persons with normal glucose tolerance whose 60-min glucose concentration was >=8.6, associated with higher blood pressure, plasma concentrations of glucose, insulin, triglyceride and lower high-density lipoprotein cholesterol concentrations. Glucose 108-115 insulin Homo sapiens 9-16 31188872-0 2019 Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation. Glucose 103-110 insulin Homo sapiens 67-74 31188872-2 2019 We hypothesized that insulin, which is elevated in obesity-driven insulin resistance, would increase tumor glucose oxidation in obesity-associated tumors. Glucose 107-114 insulin Homo sapiens 21-28 31188872-2 2019 We hypothesized that insulin, which is elevated in obesity-driven insulin resistance, would increase tumor glucose oxidation in obesity-associated tumors. Glucose 107-114 insulin Homo sapiens 66-73 31188872-6 2019 The observed increase in glucose oxidation in response to insulin correlated with a dose-dependent increase in cell division in obesity-associated tumor cell lines when grown in insulin, whereas no alteration in cell division was seen in tumor types not associated with obesity. Glucose 25-32 insulin Homo sapiens 58-65 31188872-6 2019 The observed increase in glucose oxidation in response to insulin correlated with a dose-dependent increase in cell division in obesity-associated tumor cell lines when grown in insulin, whereas no alteration in cell division was seen in tumor types not associated with obesity. Glucose 25-32 insulin Homo sapiens 178-185 31164368-1 2019 INTRODUCTION: Closed-loop systems titrate insulin based on sensor glucose levels, providing novel means to reduce the risk of hypoglycaemia while improving glycaemic control. Glucose 66-73 insulin Homo sapiens 42-49 30585698-4 2019 RESULTS: Insulin-stimulated glucose clearance in T legs was ~30% higher compared with UT legs in both groups due to increased blood flow in T vs UT legs and maintained glucose extraction. Glucose 28-35 insulin Homo sapiens 9-16 30585698-4 2019 RESULTS: Insulin-stimulated glucose clearance in T legs was ~30% higher compared with UT legs in both groups due to increased blood flow in T vs UT legs and maintained glucose extraction. Glucose 168-175 insulin Homo sapiens 9-16 30860881-0 2019 A novel measure of glucose homeostasis (or loss thereof) comprising the joint dynamics of glucose, insulin, glucagon, and cortisol. Glucose 19-26 insulin Homo sapiens 99-106 30892916-7 2019 Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity P = 0.002; acute insulin response to glucose P = 0.23). Glucose 194-201 insulin Homo sapiens 14-21 31244307-8 2019 Results: Serum Adiponectin was significantly lower in patients with hepatocellular carcinoma(p=0.000 ) and it is inversely correlated to tumor size and the number (p= 0.0001).Meanwhile, Insulin Resistanceparameters (Fasting s. Insulin, Fasting s. Glucose, HOMA IR) were significantly higher in HCC patients than CLDpatients (p= 0.0001). Glucose 247-254 insulin Homo sapiens 186-193 30738170-8 2019 In response to insulin infusion during the euglycemic hyperinsulinemic clamp, patients developing PTDM had lower whole body glucose utilization (P = .047) and decreased peripheral/skeletal muscle uptake (P = .031) before and after transplant, respectively, when compared with non-PTDM patients. Glucose 124-131 insulin Homo sapiens 15-22 30958599-0 2019 The caveolin-3 P104L mutation in LGMD-1C patients inhibits non-insulin-stimulated glucose metabolism and growth but promotes myocyte proliferation. Glucose 82-89 insulin Homo sapiens 63-70 31129998-1 2019 Background Thiazolidinediones (rosiglitazone, pioglitazone) are oral insulin-sensitizing medications used in type 2 diabetes mellitus that reduce glucose with minimal risk of hypoglycemia and potential benefits on atherosclerosis. Glucose 146-153 insulin Homo sapiens 69-76 31232038-1 2019 BACKGROUND: GLP-1 as an incretin, has the ability to decrease blood sugar levels in a glucose-dependent manner by enhancing the secretion of insulin. Glucose 86-93 insulin Homo sapiens 141-148 30604595-5 2019 RESULTS: The insulinogenic index (IGI30) obtained from the OGTT was significantly correlated with the acute insulin response to glucose (AIRg) obtained from the FSIVGTT. Glucose 128-135 insulin Homo sapiens 13-20 30936148-0 2019 Identification of Insulin-Responsive Transcription Factors That Regulate Glucose Production by Hepatocytes. Glucose 73-80 insulin Homo sapiens 18-25 31059282-1 2019 Background: Real-time continuous glucose monitoring (CGM) devices help detect glycemic excursions associated with exercise, meals, and insulin dosing in patients with type 1 diabetes (T1D). Glucose 33-40 insulin Homo sapiens 135-142 31121275-2 2019 Many children with type 1 diabetes (T1D) treated with multiple daily injections as well as with continuous subcutaneous insulin infusion (CSII) switched from self-monitoring of blood glucose to isCGM to monitor their treatment. Glucose 183-190 insulin Homo sapiens 120-127 30900204-9 2019 CONCLUSIONS: PCOS subjects have increased magnitudes of insulin resistance when compared to ovulatory controls, when controlling for age, BMI, fasting glucose, and insulin levels. Glucose 151-158 insulin Homo sapiens 56-63 30927376-11 2019 Blood glucose and insulin increased 30 min after glucose ingestion (P < 0.001), with no difference between phases. Glucose 49-56 insulin Homo sapiens 18-25 30644120-14 2019 Our findings revealed albumin excretion was attenuated by glucose administration to fasting individuals implying a regulatory role for insulin in PT albumin reabsorption. Glucose 58-65 insulin Homo sapiens 135-142 30317615-4 2019 IR underpins many metabolic disorders such as type 2 diabetes and metabolic syndrome, impairments in insulin signaling disrupting entry of glucose into the adipocytes, and skeletal muscle cells. Glucose 139-146 insulin Homo sapiens 101-108 29301456-0 2019 Can we stratify the risk for insulin need in women diagnosed early with gestational diabetes by fasting blood glucose? Glucose 110-117 insulin Homo sapiens 29-36 29301456-7 2019 In the logistic regression model, maternal age, prepregnancy body mass index, fasting blood glucose (FBG) value, prior GDM, and family history of diabetes were significant independent variables for the prediction of insulin need. Glucose 92-99 insulin Homo sapiens 216-223 31018156-9 2019 By contrast, the ability of IGF-II to lower blood glucose was blunted in insulin-resistant triprolyl human-amylin transgenic mice, whereas vesiculin"s ability to lower blood glucose remained unaffected. Glucose 50-57 insulin Homo sapiens 73-80 31132018-4 2019 Recent studies have demonstrated the usefulness of triglyceride-glucose index (TyG) as a simple surrogate of insulin resistance. Glucose 64-71 insulin Homo sapiens 109-116 30921636-3 2019 Skeletal muscle is the main contributor to insulin-mediated glucose uptake, and a defect in this muscle-related mechanism triggers insulin resistance and glucose intolerance. Glucose 60-67 insulin Homo sapiens 43-50 30921636-3 2019 Skeletal muscle is the main contributor to insulin-mediated glucose uptake, and a defect in this muscle-related mechanism triggers insulin resistance and glucose intolerance. Glucose 154-161 insulin Homo sapiens 43-50 30921636-4 2019 We have studied the chain of events that connect the loss of SELENON with defects in insulin-mediated glucose uptake in muscle cells and the effects of this on muscle performance. Glucose 102-109 insulin Homo sapiens 85-92 30921636-5 2019 Here, we show that saturated fatty acids are more lipotoxic in SELENON-devoid cells, and blunt the insulin-mediated glucose uptake of SELENON-devoid myotubes by increasing ER stress and mounting a maladaptive ER stress response. Glucose 116-123 insulin Homo sapiens 99-106 30036160-3 2019 Its objective is to help patients to perform insulin titration to reach target fasting blood glucose levels. Glucose 93-100 insulin Homo sapiens 45-52 31164926-9 2019 Beta-cell function derived from the oral glucose tolerance setting was calculated as changes in insulin secretion per unit changes in glucose concentration (Btotal) and whole-body insulin resistance using ISIcomposite. Glucose 41-48 insulin Homo sapiens 96-103 31164926-13 2019 Conclusions: The insulinotropic drug liraglutide may without increasing the insulin concentration reduce postprandial glucose but not glucagon excursions and improve beta-cell function in newly diagnosed and well-controlled T2DM.Trial registration Clinicaltrials.gov ID: NCT01595789. Glucose 118-125 insulin Homo sapiens 17-24 30726950-10 2019 Significant changes were observed in glucose homeostasis (fasting glucose and serum insulin) and, in addition, a reduction in the parameters of oxidative stress and DNA damage. Glucose 37-44 insulin Homo sapiens 84-91 31191220-3 2019 It has been shown that insulin stimulates the production of leptin when adipocytes are exposed to glucose to encourage satiety; while leptin, via a negative feedback, decreases the insulin release and enhances tissue sensitivity to it, leading to glucose uptake for energy utilization or storage. Glucose 98-105 insulin Homo sapiens 23-30 31191220-3 2019 It has been shown that insulin stimulates the production of leptin when adipocytes are exposed to glucose to encourage satiety; while leptin, via a negative feedback, decreases the insulin release and enhances tissue sensitivity to it, leading to glucose uptake for energy utilization or storage. Glucose 247-254 insulin Homo sapiens 23-30 30779918-1 2019 Destructive glucose and lipid metabolism in the liver is a crucial characteristic of type 2 diabetes mellitus (T2DM), eventually leading to insulin resistance and subsequent hyperglycemia and hyperlipidemia. Glucose 12-19 insulin Homo sapiens 140-147 31178708-7 2019 Strikingly, differences in plasma insulin levels between hunger and satiety states after glucose administration at the time of the scan were negatively related to brain activity in the posterior insula and superior frontal gyrus (SFG), while plasma glucose levels were positively associated with activity changes in the fusiform gyrus. Glucose 89-96 insulin Homo sapiens 34-41 31178708-7 2019 Strikingly, differences in plasma insulin levels between hunger and satiety states after glucose administration at the time of the scan were negatively related to brain activity in the posterior insula and superior frontal gyrus (SFG), while plasma glucose levels were positively associated with activity changes in the fusiform gyrus. Glucose 249-256 insulin Homo sapiens 34-41 31038150-5 2019 The nanogels displayed glucose-responsive release of insulin and the release rate could be promoted by the incorporation of glucose oxidase (GOx), which generated H2O2 at high glucose levels and H2O2 further oxidizes and hydrolyzes the phenylboronic ester group. Glucose 23-30 insulin Homo sapiens 53-60 31038150-5 2019 The nanogels displayed glucose-responsive release of insulin and the release rate could be promoted by the incorporation of glucose oxidase (GOx), which generated H2O2 at high glucose levels and H2O2 further oxidizes and hydrolyzes the phenylboronic ester group. Glucose 124-131 insulin Homo sapiens 53-60 31191043-2 2019 The discovery of insulin as a key regulator of glucose metabolism has revolutionized our understanding of DM and provided several therapeutic avenues. Glucose 47-54 insulin Homo sapiens 17-24 31187077-7 2019 There, oral glucose tolerance test showed fasting glucose and insulin of 80 mg/dL and 63.1 mIU/mL, respectively. Glucose 12-19 insulin Homo sapiens 62-69 31058966-1 2019 CONTEXT: Little is known about the individual response of glucose-regulating factors to administration of exogenous insulin infusion in extremely preterm infants. Glucose 58-65 insulin Homo sapiens 116-123 31058966-2 2019 OBJECTIVE: To evaluate longitudinal serum concentrations of insulin, C-peptide, and plasma glucose levels in a high frequency sampling regimen in extremely preterm infants treated with insulin due to hyperglycemia. Glucose 91-98 insulin Homo sapiens 185-192 31058966-8 2019 Individual insulin sensitivity based on the non-fasting plasma glucose/insulin ratio at the start of insulin infusion correlated with the initial decrease in serum DeltaC-peptide[After 12h] (p = 0.007) and the degree of lasting decrease in serum DeltaC-peptide[After end of infusion] (p = 0.015). Glucose 63-70 insulin Homo sapiens 11-18 30198923-3 2019 Variations in insulin pharmacokinetics and responsiveness over time in addition to illness, stress, and a myriad of other factors make ideal glucose control a challenge. Glucose 141-148 insulin Homo sapiens 14-21 30198923-7 2019 In this system, insulin delivery is continually adjusted to a glucose concentration, and the patient inputs meal-time information to modify insulin delivery as needed. Glucose 62-69 insulin Homo sapiens 16-23 30724369-4 2019 The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) score was calculated from fasting glucose and insulin values. Glucose 99-106 insulin Homo sapiens 36-43 30370783-3 2019 METHODS: This review examines the complementary mechanisms of action of glucagon-like peptide 1 (GLP-1) receptor agonists and basal insulin; they both enhance glucose-stimulated insulin release and suppress glucagon secretion. Glucose 159-166 insulin Homo sapiens 132-139 30455375-9 2019 Serum C-peptide levels demonstrated significant glucose responsiveness (fasted vs. stimulated) (P < 0.01). Glucose 48-55 insulin Homo sapiens 6-15 30796112-0 2019 Improved Open-Loop Glucose Control With Basal Insulin Reduction 90 Minutes Before Aerobic Exercise in Patients With Type 1 Diabetes on Continuous Subcutaneous Insulin Infusion. Glucose 19-26 insulin Homo sapiens 159-166 30885955-8 2019 Tissue-specific insulin-stimulated glucose uptake did not change in skeletal muscle, liver, myocardium, or white and brown adipose tissue, and endogenous glucose production remained unaffected. Glucose 35-42 insulin Homo sapiens 16-23 31009254-8 2019 Conclusions: Storage conditions of insulin are known to have an impact on its blood glucose-lowering effect. Glucose 84-91 insulin Homo sapiens 35-42 30720336-0 2019 PERCEPTION OF GRADUATING ENDOCRINOLOGY, DIABETES, AND METABOLISM FELLOWS ON THE BENEFITS OF WEARING A CONTINUOUS GLUCOSE MONITOR AND/OR INSULIN PUMP FOR THEIR EDUCATION. Glucose 113-120 insulin Homo sapiens 136-143 30782532-8 2019 RESULTS: Basal (5.5 mM glucose) islet insulin secretion was not affected by BPA exposure. Glucose 23-30 insulin Homo sapiens 38-45 30782532-9 2019 However, stimulated (11 mM glucose) insulin secretion was enhanced by about 50% in islets isolated from BPA0.5-exposed 5- and 52-week-old female and male offspring and by 80% in islets from dams, compared with control. Glucose 27-34 insulin Homo sapiens 36-43 30914352-4 2019 Insulin-resistance HepG2 cell model was used to elucidate the effect of CE on glucose metabolism. Glucose 78-85 insulin Homo sapiens 0-7 31197173-3 2019 We identify CpGs in LETM1, RBM20, IRS2, MAN2A2 and the 1q25.3 region associated with fasting insulin, and in FCRL6, SLAMF1, APOBEC3H and the 15q26.1 region with fasting glucose. Glucose 169-176 insulin Homo sapiens 93-100 30879985-6 2019 Remarkably, the ability of beta cells to secrete insulin in response to glucose was rescued almost completely by pharmacological inhibition of GSK3. Glucose 72-79 insulin Homo sapiens 49-56 31159924-1 2019 CHC22 clathrin plays a key role in intracellular membrane traffic of the insulin-responsive glucose transporter GLUT4 in humans. Glucose 92-99 insulin Homo sapiens 73-80 30977236-6 2019 Glucose-stimulated maximum increase in plasma insulin immunoreactivity was 42 +- 6.6 and 81 +- 7.4 mU/ml (p < 0.05) after the test and the control meals, respectively. Glucose 0-7 insulin Homo sapiens 46-53 30852232-5 2019 Treated insulin-resistant HepG2 cells with 0.0115 mg/ml of P. lobata increased the glucose uptake by two times compared with the negative control. Glucose 83-90 insulin Homo sapiens 8-15 29980312-6 2019 Meta-analysis showed in the treatment arm a reduction in fasting plasma glucose (Mean difference (MD) -0.44 mmol/l, 95% CI -0.65, -0.23), 2 h PG after 75 g OGTT (MD -0.69 mmol/l, 95% CI -1.14, -0.23), abnormal glucose tolerance (Relative risk (RR) 0.28, 95% CI 0.12, 0.66), fasting insulin (MD -38.49 pmol/l, 95% CI -52.63, -24.36), and HOMA-IR (MD -1.96 mmol x mUI/l, 95% CI -2.62, -1.30). Glucose 72-79 insulin Homo sapiens 282-289 31060838-5 2019 A standardized glucose management protocol determined administration of insulin. Glucose 15-22 insulin Homo sapiens 72-79 31011777-5 2019 Insulin sensitivity was measured as the glucose infusion rate from a euglycaemic-hyperinsulinaemic clamp. Glucose 40-47 insulin Homo sapiens 0-7 31257745-1 2019 BACKGROUND: Recently, the triglyceride glucose (TyG) index has been considered a surrogate marker of insulin resistance which is a well-known pathogenic factor in nonalcoholic fatty liver disease (NAFLD). Glucose 39-46 insulin Homo sapiens 101-108 31205332-11 2019 Standard insulin doses may not be appropriate in some cases like patients with lower baseline blood glucose. Glucose 100-107 insulin Homo sapiens 9-16 30277539-7 2019 Associations with breast cancer risk were found for genetically predicted fasting insulin [odds ratio (OR) = 1.71 per standard deviation (SD) increase, 95% confidence interval (CI) = 1.26-2.31, p = 5.09 x 10-4], 2-h glucose (OR = 1.80 per SD increase, 95% CI = 1.3 0-2.49, p = 4.02 x 10-4), BMI (OR = 0.70 per 5-unit increase, 95% CI = 0.65-0.76, p = 5.05 x 10-19) and WHRadj BMI (OR = 0.85, 95% CI = 0.79-0.91, p = 9.22 x 10-6). Glucose 220-227 insulin Homo sapiens 82-89 30277539-9 2019 CONCLUSIONS: We confirmed the previously reported inverse association of genetically predicted BMI with breast cancer risk, and showed a positive association of genetically predicted fasting insulin and 2-h glucose and an inverse association of WHRadj BMI with breast cancer risk. Glucose 207-214 insulin Homo sapiens 191-198 30277539-10 2019 Our study suggests that genetically determined obesity and glucose/insulin-related traits have an important role in the aetiology of breast cancer. Glucose 59-66 insulin Homo sapiens 67-74 30859189-0 2019 Letter regarding article, "Associations of obesity and circulating insulin and glucose with breast cancer risk: a Mendelian randomization analysis". Glucose 79-86 insulin Homo sapiens 67-74 30991014-5 2019 The GCK sensing system is, however, used to control release of both insulin and glucagon, the preeminant hormonal regulators of blood glucose, as well as glucose sensitive neuronal activity. Glucose 134-141 insulin Homo sapiens 68-75 30548348-7 2019 In addition, insulin and C-peptide secreted in response to varying concentrations of glucose in the 3D scaffold group was significantly higher than that in 2D culture. Glucose 85-92 insulin Homo sapiens 13-20 30597042-6 2019 However, after endurance exercise training, fasting blood glucose was greater with SGLT2 inhibition, and increased insulin sensitivity (oral glucose tolerance test/Matsuda index) was abrogated with SGLT2 inhibition (exercise training x treatment interaction, P < 0.01). Glucose 141-148 insulin Homo sapiens 115-122 30629195-9 2019 CONCLUSIONS: Younger age at diabetes diagnosis, higher baseline insulin sensitivity, and lower glucose levels after insulin treatment significantly favored a 2-year glycemic remission. Glucose 95-102 insulin Homo sapiens 116-123 30649347-9 2019 Adipose-IR positively correlated with serum androgen and log of fasting triglyceride (TG) levels, percentage of small adipocytes (P < 0.01, all correlations), and acute insulin response to glucose (P < 0.05); and negatively correlated with insulin sensitivity (Si; P < 0.025) and serum adiponectin levels (P < 0.05). Glucose 189-196 insulin Homo sapiens 169-176 30689904-0 2019 Correlates of Insulin-Stimulated Glucose Disposal in Recent-Onset Type 1 and Type 2 Diabetes. Glucose 33-40 insulin Homo sapiens 14-21 30689904-1 2019 CONTEXT AND OBJECTIVE: Not only type 2 diabetes (T2D), but also type 1 diabetes (T1D), can be associated with insulin resistance, as assessed using insulin-stimulated whole-body glucose disposal (M-value). Glucose 178-185 insulin Homo sapiens 110-117 30689904-1 2019 CONTEXT AND OBJECTIVE: Not only type 2 diabetes (T2D), but also type 1 diabetes (T1D), can be associated with insulin resistance, as assessed using insulin-stimulated whole-body glucose disposal (M-value). Glucose 178-185 insulin Homo sapiens 148-155 30689904-11 2019 CONCLUSIONS: Fasting glycemia correlated with insulin-stimulated glucose disposal in both diabetes types. Glucose 65-72 insulin Homo sapiens 46-53 30689904-12 2019 However, altered liver and adipose tissue function were associated with insulin-stimulated glucose disposal only in T2D, underpinning the specific differences between these diabetes types. Glucose 91-98 insulin Homo sapiens 72-79 31143312-7 2019 In the insulin introduction group, the six-divided diet was less common and the 75-g glucose tolerance test result was positive a significantly greater number of times compared with the non-introduction group. Glucose 85-92 insulin Homo sapiens 7-14 31143312-8 2019 The factor associated with the insulin introduction status was the number of positive 75-g glucose tolerance test results (odds ratio (OR) 2.04, 95% confidence interval (CI): 1.09 - 3.81, P value = 0.025). Glucose 91-98 insulin Homo sapiens 31-38 30685858-3 2019 As a result, the dynamics of insulin release from the pancreas are currently described by mathematical models that reproduce the behavior of the beta cells using exclusively glucose levels and other hormones as inputs. Glucose 174-181 insulin Homo sapiens 29-36 31086331-2 2019 The metalloprotease insulin-degrading enzyme (IDE) modulates blood glucose levels by cleaving insulin, a hormone that promotes glucose clearance. Glucose 67-74 insulin Homo sapiens 20-27 31086331-2 2019 The metalloprotease insulin-degrading enzyme (IDE) modulates blood glucose levels by cleaving insulin, a hormone that promotes glucose clearance. Glucose 127-134 insulin Homo sapiens 20-27 30891858-0 2019 Associations of HbA1c with the timing of C-peptide responses during the oral glucose tolerance test at the diagnosis of type 1 diabetes. Glucose 77-84 insulin Homo sapiens 41-50 30891858-3 2019 OBJECTIVES: We assessed the contribution of the timing of C-peptide responsiveness during oral glucose tolerance tests (OGTTs) to hemoglobin A1c (HbA1c) variation at T1D diagnosis. Glucose 95-102 insulin Homo sapiens 58-67 30891858-11 2019 Similar associations were seen between the 2-hour glucose and the C-peptide measures. Glucose 50-57 insulin Homo sapiens 66-75 31074547-6 2019 Our results demonstrated that HES decreased the levels of TNF-alpha and IL-6, attenuated the glucose content in culture medium and increased glucose uptake in insulin-resistant HepG2 cells in vitro. Glucose 141-148 insulin Homo sapiens 159-166 30747254-4 2019 The homeostasis model of assessment of insulin resistance (HOMA-IR) was calculated based on fasting blood levels of insulin and glucose. Glucose 128-135 insulin Homo sapiens 39-46 30950163-5 2019 Delivery of blood glucose and insulin to the brain occurs through their respective carrier (Glucose transporter 1) and receptor (insulin receptor), enacting bona fide transcytosis. Glucose 92-99 insulin Homo sapiens 30-37 31213973-6 2019 In fact, its excess increases the activity of the renin-angiotensin system in the brain, thus reducing insulin-mediated glucose uptake, which has a major impact on brain functioning. Glucose 120-127 insulin Homo sapiens 103-110 30967259-5 2019 Following 48 h of treatment with 30 mM high glucose, Hv1 KO beta cells showed higher cell viability, lower cell apoptosis and a more stable insulin gene expression level compared to WT beta cells. Glucose 44-51 insulin Homo sapiens 140-147 31126031-2 2019 It is characterized by pancreas failure to produce insulin, which involves high blood glucose levels. Glucose 86-93 insulin Homo sapiens 51-58 30977635-6 2019 Inspired by the structure and response mechanism of pancreatic beta-cells, we synthesized a series of insulin granule-like vesicles that can respond to high blood or intestinal glucose levels for aiding in transdermal or oral insulin delivery, respectively. Glucose 177-184 insulin Homo sapiens 102-109 31112275-10 2019 CONCLUSION: We propose that maternal insulin stimulates placental glucose transport by promoting GLUT4 trafficking to the BM, which may enhance glucose transfer to the fetus in response to postprandial hyperinsulinemia in women with normal BMI. Glucose 66-73 insulin Homo sapiens 37-44 31112275-10 2019 CONCLUSION: We propose that maternal insulin stimulates placental glucose transport by promoting GLUT4 trafficking to the BM, which may enhance glucose transfer to the fetus in response to postprandial hyperinsulinemia in women with normal BMI. Glucose 144-151 insulin Homo sapiens 37-44 31113929-7 2019 Consistent with animal experimental data, the degree of obesity and insulin resistance demonstrated by the body mass index, fasting blood glucose and HbA1c correlated negatively with the expression of Sirt6 in human visceral fat tissues. Glucose 138-145 insulin Homo sapiens 68-75 31156561-14 2019 Despite stopping her insulin, she continued to have hypoglycemia necessitating the administration of high concentrations of intravenous dextrose. Glucose 136-144 insulin Homo sapiens 21-28 31088046-0 2019 Triglyceride Glucose Index as a Surrogate Measure of Insulin Sensitivity in a Caucasian Pediatric Population Objective: The triglyceride and glucose (TyG) index has been proposed as a simple surrogate of insulin resistance (IR) with high sensitivity as an IR index besides the well known homeostasis model assessment of IR (HOMA-IR). Glucose 141-148 insulin Homo sapiens 53-60 31085831-1 2019 Impaired insulin secretion in type 2 diabetes (T2D) is linked to reduced insulin granule docking, disorganization of the exocytotic site, and an impaired glucose-dependent facilitation of insulin exocytosis. Glucose 154-161 insulin Homo sapiens 9-16 31061431-3 2019 Glucose-dependent excitability is lost in islets from KATP-knockout (KATP-KO) mice, in which beta-cells are permanently hyperexcited, [Ca2+]i, is chronically elevated and insulin is constantly secreted. Glucose 0-7 insulin Homo sapiens 171-178 31061431-6 2019 Wild-type islets showed rapid loss of insulin content when chronically incubated in high-glucose, an effect that was reversed by subsequently switching to low glucose media. Glucose 89-96 insulin Homo sapiens 38-45 31107439-1 2019 Mitophagy is an essential mitochondrial quality control pathway, which is crucial for pancreatic islet beta cell bioenergetics to fuel glucose-stimulated insulin release. Glucose 135-142 insulin Homo sapiens 154-161 31110526-5 2019 Insulin resistance was assessed according to the HOMA-IR method and insulin resistance (Belfiore) index (IRI) derived from glucose and insulin during the oral glucose tolerance test. Glucose 159-166 insulin Homo sapiens 0-7 30610874-1 2019 Normal glucose homeostasis depends on the capacity of pancreatic beta-cells to adjust insulin secretion in response to a change of tissue insulin sensitivity. Glucose 7-14 insulin Homo sapiens 86-93 30610874-2 2019 In cold environments, for example, the dramatic increase of insulin sensitivity required to ensure a sufficient supply of glucose to thermogenic tissues is offset by a proportionate reduction of insulin secretion, such that overall glucose tolerance is preserved. Glucose 122-129 insulin Homo sapiens 60-67 30610874-5 2019 To test this hypothesis, we used a thermode to cool the POA area, and found that as predicted, short-term (8-h) intense POA cooling reduced glucose-stimulated insulin secretion (GSIS), yet glucose tolerance remained unchanged due to an increase of insulin sensitivity. Glucose 140-147 insulin Homo sapiens 159-166 30772337-5 2019 Insulin resistance and sensitivity were assessed by triglyceride glucose (TyG) index, homeostatic model assessment (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and beta-cell function by HOMA-B. Glucose 65-72 insulin Homo sapiens 0-7 30855284-8 2019 High-intensity insulin therapy was designed to rapidly normalize blood glucose levels with bolus doses of insulin and rapid insulin titration. Glucose 71-78 insulin Homo sapiens 15-22 30855284-9 2019 Moderate-intensity insulin therapy was designed to mitigate glycemic variability and hypoglycemia through avoidance of bolus dosing, a liberalized blood glucose target, and gradual insulin titration. Glucose 153-160 insulin Homo sapiens 19-26 30706538-3 2019 Insulin resistance was assessed according to estimated glucose disposal rate. Glucose 55-62 insulin Homo sapiens 0-7 30706538-6 2019 The higher the estimated glucose disposal rate, the lower the insulin resistance. Glucose 25-32 insulin Homo sapiens 62-69 30833465-0 2019 Postprandial Aminogenic Insulin and Glucagon Secretion Can Stimulate Glucose Flux in Humans. Glucose 69-76 insulin Homo sapiens 24-31 30833465-1 2019 Insulin and glucagon exert opposing actions on glucose metabolism, and their secretion is classically viewed as being inversely regulated. Glucose 47-54 insulin Homo sapiens 0-7 30833465-10 2019 Finally, we argue that glucagon is a bona fide postprandial hormone that evolved to concurrently and synergistically work with insulin to regulate glucose, amino acid, and nitrogen metabolism. Glucose 147-154 insulin Homo sapiens 127-134 30893645-5 2019 Insulin secretion was estimated as acute insulin response to glucose (AIRg) and disposition index (DI), modeled from an intravenous glucose tolerance test. Glucose 61-68 insulin Homo sapiens 0-7 30893645-5 2019 Insulin secretion was estimated as acute insulin response to glucose (AIRg) and disposition index (DI), modeled from an intravenous glucose tolerance test. Glucose 61-68 insulin Homo sapiens 41-48 30893645-5 2019 Insulin secretion was estimated as acute insulin response to glucose (AIRg) and disposition index (DI), modeled from an intravenous glucose tolerance test. Glucose 132-139 insulin Homo sapiens 0-7 30910328-7 2019 Increased glucose administration using higher percentages of dextrose (10 or 20%) are required to facilitate the concomitant administration of the relatively large amounts of insulin that are needed to correct the severe acidosis in these patients. Glucose 10-17 insulin Homo sapiens 175-182 30910328-7 2019 Increased glucose administration using higher percentages of dextrose (10 or 20%) are required to facilitate the concomitant administration of the relatively large amounts of insulin that are needed to correct the severe acidosis in these patients. Glucose 61-69 insulin Homo sapiens 175-182 30742833-8 2019 Larger, but more transient increases in levels of plasma glucose and amino acids were accompanied by higher secretion of insulin, glucagon-like peptide 1, peptide YY, and cholecystokinin after RYGB, whereas levels of ghrelin were lower after SG, compared with RYGB and controls. Glucose 57-64 insulin Homo sapiens 121-128 30566676-7 2019 HIE was positively correlated with insulin sensitivity [rate of glucose disposal (Rd; low r = +0.7, P < 0.001; high r = +0.6, P = 0.001), adiponectin (r = +0.55, P = 0.004), and insulin-mediated suppression of clamp nonesterified free fatty acid (NEFA; r = +0.67, P < 0.001)] but was not associated with fasting NEFA, insulin-mediated suppression of glucose production, or measures of adiposity. Glucose 64-71 insulin Homo sapiens 35-42 30566676-7 2019 HIE was positively correlated with insulin sensitivity [rate of glucose disposal (Rd; low r = +0.7, P < 0.001; high r = +0.6, P = 0.001), adiponectin (r = +0.55, P = 0.004), and insulin-mediated suppression of clamp nonesterified free fatty acid (NEFA; r = +0.67, P < 0.001)] but was not associated with fasting NEFA, insulin-mediated suppression of glucose production, or measures of adiposity. Glucose 350-357 insulin Homo sapiens 35-42 30307128-0 2019 Accuracy of flash glucose monitoring in insulin-treated patients with type 2 diabetes. Glucose 18-25 insulin Homo sapiens 40-47 30677460-12 2019 This is the first study evaluating the contribution of all 3 direct determinants of insulin-dependent glucose regulation using a sophisticated mathematical model. Glucose 102-109 insulin Homo sapiens 84-91 30913535-5 2019 We demonstrated that the glucose uptake in cultured GCs and lactate accumulation in the culture medium were stimulated by insulin, but the effects of insulin were attenuated by PA treatment. Glucose 25-32 insulin Homo sapiens 122-129 30876866-1 2019 OBJECTIVE: We hypothesized that DA and L-DOPA derived from nutritional tyrosine and the resultant observed postprandial plasma excursions of L-DOPA and DA might affect glucose tolerance via their ability to be taken-up by beta cells and inhibit glucose-stimulated beta-cell insulin secretion. Glucose 168-175 insulin Homo sapiens 274-281 30876866-8 2019 DA and L-DOPA derived from nutritional tyrosine may serve to defend against hypoglycemia via inhibition of glucose-stimulated beta-cell insulin secretion as proposed by the anti-incretin hypothesis. Glucose 107-114 insulin Homo sapiens 136-143 30948306-5 2019 We evaluated glucose-induced insulin and C-peptide secretions as AUC of plasma insulin and C-peptide during intravenous-glucose-tolerance tests (IVGTT) and IS via hyperinsulinemic-euglycemic clamps. Glucose 13-20 insulin Homo sapiens 29-36 30948306-5 2019 We evaluated glucose-induced insulin and C-peptide secretions as AUC of plasma insulin and C-peptide during intravenous-glucose-tolerance tests (IVGTT) and IS via hyperinsulinemic-euglycemic clamps. Glucose 13-20 insulin Homo sapiens 79-86 30420708-5 2019 Baroreflex sensitivity reactivity was reduced with sleep fragmentation, but only for subjects with low insulin sensitivity and/or low first-phase insulin response to glucose. Glucose 166-173 insulin Homo sapiens 146-153 30892125-1 2019 Objectives: Recent studies have identified triglyceride-glucose index (TyG) as a surrogate of insulin resistance. Glucose 56-63 insulin Homo sapiens 94-101 31061619-1 2019 The aim of this study is to discuss the non-catechin flavonoids (NCF) from Camellia sinensis (L.) O. Kuntze seed improving TNF-alpha impaired insulin stimulated glucose uptake and insulin signaling. Glucose 161-168 insulin Homo sapiens 142-149 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 14-21 insulin Homo sapiens 47-54 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 14-21 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 14-21 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 47-54 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 47-54 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 47-54 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 105-112 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 69-76 insulin Homo sapiens 105-112 30980160-7 2019 Insulin should be switched to subcutaneous injections only after correction of the acidosis and stable glucose concentrations within an acceptable range. Glucose 103-110 insulin Homo sapiens 0-7 30936244-1 2019 Amino acids are increasingly recognised as modulators of nutrient disposal, including their role in regulating blood glucose through interactions with insulin signalling. Glucose 117-124 insulin Homo sapiens 151-158 31119141-7 2019 The oral glucose tolerance test showed impaired glucose tolerance and obviously increased insulin and C-peptide levels. Glucose 9-16 insulin Homo sapiens 90-97 31019221-2 2019 One of the key pathological traits of this disease is insulin resistance at "glucose sink" tissues (mostly skeletal muscle), and this remains one of the features of this disease most intractable to therapeutic intervention. Glucose 77-84 insulin Homo sapiens 54-61 31127822-11 2019 CONCLUSIONS: Vitamin D may play a role in regulating fetal insulin secretion, potentially impacting glucose regulation and growth. Glucose 100-107 insulin Homo sapiens 59-66 31013265-9 2019 RESULTS These hub genes were significantly enriched in "response to insulin", "response to glucose", and "fat cell differentiation". Glucose 91-98 insulin Homo sapiens 68-75 31018587-0 2019 Menaquinone-4 Amplified Glucose-Stimulated Insulin Secretion in Isolated Mouse Pancreatic Islets and INS-1 Rat Insulinoma Cells. Glucose 24-31 insulin Homo sapiens 43-50 31018587-5 2019 Glucose-stimulated insulin secretion significantly increased in isolated islets and INS-1 cells treated with MK-4. Glucose 0-7 insulin Homo sapiens 19-26 31018587-7 2019 A novel function of MK-4 on glucose-stimulated insulin secretion was found, suggesting that MK-4 might act as a potent amplifier of the incretin effect. Glucose 28-35 insulin Homo sapiens 47-54 31334442-7 2019 Conditional analyses using the two largest European ancestry cohorts in the study showed that insulin levels accounted for most of the interaction of PNPLA3-rs738409 with BMI, glucose, and TG in nondiabetic individuals. Glucose 176-183 insulin Homo sapiens 94-101 31001701-3 2019 We showcase this method using the Integrated Glucose Insulin (IGI) model and the Integrated Minimal Model (IMM). Glucose 45-52 insulin Homo sapiens 53-60 31001701-9 2019 The strongest parameter correlations were found for: insulin-dependent glucose clearance (IGI) ~ insulin sensitivity (IMM); insulin-independent glucose clearance (IGI) ~ glucose effectiveness (IMM); and insulin effect parameter (IGI) ~ insulin action (IMM). Glucose 71-78 insulin Homo sapiens 53-60 30884946-3 2019 In this study, a modular microfluidic system was developed to quantitatively measure the effect of insulin dynamics on glucose consumption by a human hepatocarcinoma cell line, HepG2. Glucose 119-126 insulin Homo sapiens 99-106 30884946-7 2019 By optimizing the mixing time of the reagents, the dynamic range of the enzymatic assay was adjusted to 0-12 mM glucose and had a time resolution of 96 +- 12 s. The system was used to observe rapid changes in insulin-induced glucose consumption from HepG2 cells. Glucose 112-119 insulin Homo sapiens 209-216 30884946-7 2019 By optimizing the mixing time of the reagents, the dynamic range of the enzymatic assay was adjusted to 0-12 mM glucose and had a time resolution of 96 +- 12 s. The system was used to observe rapid changes in insulin-induced glucose consumption from HepG2 cells. Glucose 225-232 insulin Homo sapiens 209-216 30992480-2 2019 Professional continuous glucose monitoring (p-CGM) is blinded recording of glucose trends over 5-7 days and helps physicians to guide insulin titration to patient. Glucose 24-31 insulin Homo sapiens 134-141 31139762-4 2019 Results: All glucose and insulin values from the OGTT were positively correlated with the steady-state plasma glucose (SSPG) value of the PST. Glucose 110-117 insulin Homo sapiens 25-32 31508171-6 2019 Results: TM treatment reduced insulin-stimulated glucose consumption by 19.7% in 3T3-L1 adipocytes. Glucose 49-56 insulin Homo sapiens 30-37 31508171-8 2019 Ex-4 augmented insulin-stimulated glucose consumption in adipocytes by 14.9%. Glucose 34-41 insulin Homo sapiens 15-22 30784942-6 2019 Moreover, the islets function was evaluated through the glucose-induced insulin and C-peptide secretion assay. Glucose 56-63 insulin Homo sapiens 72-79 30551936-7 2019 Insulin-stimulated glucose uptake was measured. Glucose 19-26 insulin Homo sapiens 0-7 30551936-10 2019 HG- vs. NG-differentiated adipocytes displayed an inhibition of insulin-stimulated glucose uptake. Glucose 83-90 insulin Homo sapiens 64-71 30552787-7 2019 By contrast, pharmacological delivery of insulin to the brain might modulate insulin effectiveness in glucose-producing tissue when circulating insulin levels are elevated; therefore, the metabolic consequences of brain insulin action appear to be dependent on metabolic prandial status. Glucose 102-109 insulin Homo sapiens 41-48 30552787-7 2019 By contrast, pharmacological delivery of insulin to the brain might modulate insulin effectiveness in glucose-producing tissue when circulating insulin levels are elevated; therefore, the metabolic consequences of brain insulin action appear to be dependent on metabolic prandial status. Glucose 102-109 insulin Homo sapiens 77-84 30696708-3 2019 Here, using a mouse model of diabetes in the latter half of pregnancy to mimic human GDM, we find that the efficient insulin therapy for GDM confers significant protection against glucose intolerance and obesity in offspring fed a normal chow diet. Glucose 180-187 insulin Homo sapiens 117-124 30721451-0 2019 Effect of Remote Glucose Monitoring Utilizing Computerized Insulin Dose Adjustment Algorithms: A Pilot Project. Glucose 17-24 insulin Homo sapiens 59-66 30788807-0 2019 C-Peptide Area Under the Curve at Glucagon Stimulation Test Predicts Glucose Improvements by GLP-1 Receptor Analogue: A Retrospective Observational Study. Glucose 69-76 insulin Homo sapiens 0-9 30794834-3 2019 Measurement of glucose/C peptide ratios may be useful to guide dosing in those patients who receive powerful insulin secretogogues as glomerular function decreases with age and disease. Glucose 15-22 insulin Homo sapiens 109-116 30794834-8 2019 Glucose C-peptide ratios were lowest in the quartile of patients with the lowest eGFR (<50 ml/min). Glucose 0-7 insulin Homo sapiens 8-17 30794834-9 2019 CONCLUSION: Diminished renal function and advanced age are associated with the lowest glucose/C-peptide ratios, independent of achieved glycemic control. Glucose 86-93 insulin Homo sapiens 94-103 30794834-12 2019 In patients with reduced renal function (eGFR < 50 ml/min), use of insulin secretogogues may be associated with lower glucose/C-peptide ratios associated with higher risks for hypoglycemic reactions. Glucose 121-128 insulin Homo sapiens 70-77 30753523-5 2019 Progression of insulin resistance (IR) was lessened by ImE compared with placebo under both fasting and IV glucose-stimulated conditions, plateauing in all groups between 24 and 30 months. Glucose 107-114 insulin Homo sapiens 15-22 30818268-6 2019 In vitro glucose uptake assay defined six compounds as insulin-sensitive and the other two as insulin-independent glucose uptake enhancers. Glucose 9-16 insulin Homo sapiens 55-62 30589572-6 2019 E-Syt1 knockdown resulted in prolonged accumulation of DAG in the PM, resulting in increased glucose-stimulated insulin secretion. Glucose 93-100 insulin Homo sapiens 112-119 30707625-7 2019 Whole-body insulin sensitivity and insulin-stimulated leg glucose uptake were reduced ( P < 0.01; ~20%) to a similar extent compared to Con after both HFDs. Glucose 58-65 insulin Homo sapiens 35-42 30142748-8 2019 Advisory-mode analysis based on clinical data indicates that the method can reduce glucose levels through suggesting additional safe amounts of insulin on top of those suggested by the zone MPC used in the study. Glucose 83-90 insulin Homo sapiens 144-151 29892037-7 2019 CONCLUSIONS: These data suggest that with severe obesity the partitioning of glucose toward anaerobic glycolysis in response to insulin is a resilient characteristic of human skeletal muscle. Glucose 77-84 insulin Homo sapiens 128-135 29915365-7 2019 RESULTS: In human cohorts, we show that the 12 bp del associates with improved glucose metabolism (lower fasting plasma glucose, fasting plasma insulin, and HOMA IR). Glucose 79-86 insulin Homo sapiens 144-151 30544235-9 2019 In women with PCOS, the insulin-stimulated glucose oxidation was reduced and insulin-stimulated dephosphorylation of pyruvate dehydrogenase (PDH) Ser293 was absent. Glucose 43-50 insulin Homo sapiens 24-31 30623452-0 2019 Adipocyte expression of glucose transporter 1 and 4 in PCOS: Relationship to insulin-mediated and non-insulin-mediated whole-body glucose uptake. Glucose 24-31 insulin Homo sapiens 77-84 30623452-0 2019 Adipocyte expression of glucose transporter 1 and 4 in PCOS: Relationship to insulin-mediated and non-insulin-mediated whole-body glucose uptake. Glucose 24-31 insulin Homo sapiens 102-109 30623452-0 2019 Adipocyte expression of glucose transporter 1 and 4 in PCOS: Relationship to insulin-mediated and non-insulin-mediated whole-body glucose uptake. Glucose 130-137 insulin Homo sapiens 102-109 30623452-2 2019 In IR states, non-insulin-mediated glucose uptake (NIMGU) may increase to compensate for declining insulin-mediated glucose uptake (IMGU), although this does not appear to be the case in PCOS. Glucose 35-42 insulin Homo sapiens 18-25 30623452-2 2019 In IR states, non-insulin-mediated glucose uptake (NIMGU) may increase to compensate for declining insulin-mediated glucose uptake (IMGU), although this does not appear to be the case in PCOS. Glucose 116-123 insulin Homo sapiens 99-106 30643924-0 2019 Preserved glucose response to low-dose glucagon after exercise in insulin-pump-treated individuals with type 1 diabetes: a randomised crossover study. Glucose 10-17 insulin Homo sapiens 66-73 30645667-14 2019 Attenuating sphingolipid metabolism in islets impairs glucose-stimulated insulin secretion. Glucose 54-61 insulin Homo sapiens 73-80 30659420-1 2019 INTRODUCTION: Some type 2 diabetes (T2DM) patients treated with premixed insulin alone or in combination with oral glucose-lowering agents (without sulfonylureas) cannot reach the required glucose targets. Glucose 189-196 insulin Homo sapiens 73-80 30721451-3 2019 METHODS: Patients taking insulin for at least 6 months with HbA1c levels of at least 8.0% measured glucose levels with a meter attached to their smartphones. Glucose 99-106 insulin Homo sapiens 25-32 30721451-13 2019 CONCLUSION: Remote glucose monitoring utilizing computerized insulin dose adjustment algorithms saved time for both providers and patients while effectively improving glycemia. Glucose 19-26 insulin Homo sapiens 61-68 31081593-4 2019 Across randomized trials of up to 52 weeks, SGLT-2 inhibitors or SGLT-1/2 inhibitors as an adjunct to insulin demonstrated significant reductions in glycated haemoglobin, glucose exposure, and measures of glycaemic variability, as well as increased time in the target glycaemic range, compared with placebo. Glucose 171-178 insulin Homo sapiens 102-109 30995433-0 2019 EVALUATION OF INSULIN GLARGINE AND EXENATIDE ALONE AND IN COMBINATION: A RANDOMIZED CLINICAL TRIAL WITH CONTINUOUS GLUCOSE MONITORING AND AMBULATORY GLUCOSE PROFILE ANALYSIS. Glucose 115-122 insulin Homo sapiens 14-21 30995433-0 2019 EVALUATION OF INSULIN GLARGINE AND EXENATIDE ALONE AND IN COMBINATION: A RANDOMIZED CLINICAL TRIAL WITH CONTINUOUS GLUCOSE MONITORING AND AMBULATORY GLUCOSE PROFILE ANALYSIS. Glucose 149-156 insulin Homo sapiens 14-21 30843740-7 2019 In this review, we examine the literature concerning the effects of insulin and thyroid hormones on glucose metabolism and discuss alterations of glucose metabolism in hyperthyroid conditions and the cellular and molecular mechanisms that may underline them. Glucose 100-107 insulin Homo sapiens 68-75 30818268-6 2019 In vitro glucose uptake assay defined six compounds as insulin-sensitive and the other two as insulin-independent glucose uptake enhancers. Glucose 114-121 insulin Homo sapiens 94-101 30191995-4 2019 The aim of this study was to compare the efficacy of metformin and insulin in regulating blood glucose levels and fetal outcomes in GDM. Glucose 95-102 insulin Homo sapiens 67-74 30877363-0 2019 Sweet taste receptors as a tool for an amplifying pathway of glucose-stimulated insulin secretion in pancreatic beta cells. Glucose 61-68 insulin Homo sapiens 80-87 30849076-8 2019 RESULTS: Results of paired sample t-tests revealed that although plasma insulin levels were significantly lower during the closed-loop than in the open-loop (Mean difference 36.51 pmol/l; t(13) = 2.13, p = .03, effect size d = 0.57), blood glucose levels did not vary between conditions (mean difference 0.76 mmol/l; t(13) = 1.24, p = .12, d = 0.37). Glucose 240-247 insulin Homo sapiens 72-79 30845237-1 2019 The triglyceride glucose (TyG) index, a product of triglyceride and fasting glucose, is a reliable marker for insulin resistance (IR). Glucose 17-24 insulin Homo sapiens 110-117 30845237-1 2019 The triglyceride glucose (TyG) index, a product of triglyceride and fasting glucose, is a reliable marker for insulin resistance (IR). Glucose 76-83 insulin Homo sapiens 110-117 29989486-6 2019 However, the insulin response to an oral glucose challenge was preserved. Glucose 41-48 insulin Homo sapiens 13-20 30352123-7 2019 In Caco-2 cells, GLUT12 translocation to the apical membrane and alpha-methyl- d-glucose uptake by the transporter are stimulated by protons, glucose, insulin, tumor necrosis factor-alpha (TNF-alpha), protein kinase C, and AMP-activated protein kinase. Glucose 81-88 insulin Homo sapiens 151-158 30763457-0 2019 A Whole-Grain Diet Increases Glucose-Stimulated Insulin Secretion Independent of Gut Hormones in Adults at Risk for Type 2 Diabetes. Glucose 29-36 insulin Homo sapiens 48-55 30763457-1 2019 INTRODUCTION: The effect of whole-grain (WG) versus refined-grain (RG) diets on glucose-stimulated insulin secretion (GSIS) and beta-cell function is unclear. Glucose 80-87 insulin Homo sapiens 99-106 30997973-4 2019 For a similar glucose control (reduction in glycated haemoglobin), less hypoglycaemic episodes were recorded, including severe hypoglycaemia, during the nocturnal period, with insulin degludec than with insulin glargine U100. Glucose 14-21 insulin Homo sapiens 176-183 30932004-1 2019 The islet beta-cells integrate external signals to modulate insulin secretion to better regulate blood glucose levels during periods of changing metabolic demand. Glucose 103-110 insulin Homo sapiens 60-67 30932004-7 2019 In beta-cell cultures obtained from nondiabetic donors, incubation at non-stimulatory glucose concentrations promotes a shift in vesicle diameter towards the more mature insulin vesicles at the expense of the larger immature insulin secretory vesicle population. Glucose 86-93 insulin Homo sapiens 170-177 30773442-12 2019 Prospective studies are important to dissect the contributions of weight loss, dietary factors, and systemic metabolism, and to determine the relationship with increased insulin-independent glucose uptake and reductions in glycemia. Glucose 190-197 insulin Homo sapiens 170-177 31091943-4 2019 Even there are available insulin pumps which can serve as continuous glucose monitoring signal receiver themselves and are capable to stop automatically basal insulin infusion to prevent hypoglycemia. Glucose 69-76 insulin Homo sapiens 25-32 31091945-1 2019 Insulin resistance (IR) is defined as insufficient insulin metabolic effect in target tissues, including glucose utilisation in skeletal muscle, suppression of hepatic glucose production and suppression of lipolysis in fat tissue. Glucose 105-112 insulin Homo sapiens 0-7 31091945-1 2019 Insulin resistance (IR) is defined as insufficient insulin metabolic effect in target tissues, including glucose utilisation in skeletal muscle, suppression of hepatic glucose production and suppression of lipolysis in fat tissue. Glucose 168-175 insulin Homo sapiens 0-7 30922303-7 2019 Many investigators have proved that statin use contribute to the genesis of diabetes, reports vary between 1 and 46%, where marked elevation of blood glucose fasting levels and glycosylated hemoglobin have been observed, be it by increased tissue resistance to insulin or by reduced beta-cell insulin secretion. Glucose 150-157 insulin Homo sapiens 261-268 30922303-7 2019 Many investigators have proved that statin use contribute to the genesis of diabetes, reports vary between 1 and 46%, where marked elevation of blood glucose fasting levels and glycosylated hemoglobin have been observed, be it by increased tissue resistance to insulin or by reduced beta-cell insulin secretion. Glucose 150-157 insulin Homo sapiens 293-300 25905329-0 2000 Emergencies in Childhood Diabetes Insulin is the hormone of feeding and has its" main actions in moving glucose from the blood into muscles for energy and brain for brain functioning, and inhibiting fat breakdown. Glucose 104-111 insulin Homo sapiens 34-41 25905329-6 2000 In all persons, the brain cannot store glucose and since in health glucose is the only fuel to operate it, when blood glucose levels fall after an inappropriately large dose of insulin is given, symptoms of hypoglycemia are seen. Glucose 39-46 insulin Homo sapiens 177-184 25905329-6 2000 In all persons, the brain cannot store glucose and since in health glucose is the only fuel to operate it, when blood glucose levels fall after an inappropriately large dose of insulin is given, symptoms of hypoglycemia are seen. Glucose 67-74 insulin Homo sapiens 177-184 30817300-5 2019 Omentin-1 has been shown to increase insulin-mediated glucose uptake, especially in the adipose tissue. Glucose 54-61 insulin Homo sapiens 37-44 30908518-14 2019 However, in patients who did not receive exogenous epinephrine during resuscitation, changes in blood glucose correlated with changes in insulin (r = 0.59, p = 0.04) and glucagon (r = 0.65, p = 0.05) levels, demonstrating that lowering glucose values was associated with a simultaneous lowering of insulin and glucagon levels. Glucose 102-109 insulin Homo sapiens 137-144 30908518-14 2019 However, in patients who did not receive exogenous epinephrine during resuscitation, changes in blood glucose correlated with changes in insulin (r = 0.59, p = 0.04) and glucagon (r = 0.65, p = 0.05) levels, demonstrating that lowering glucose values was associated with a simultaneous lowering of insulin and glucagon levels. Glucose 102-109 insulin Homo sapiens 298-305 30908521-1 2019 BACKGROUND: Studies on adults have reported inverse association between the homeostatic model assessment (HOMA) of adiponectin (HOMA-Adiponectin) and the insulin resistance assessed by the glucose clamp technique. Glucose 189-196 insulin Homo sapiens 154-161 30908521-3 2019 OBJECTIVES: To evaluate the association between the HOMA-Adiponectin and the insulin resistance assessed by the glucose clamp technique in adolescents, and to compare the accuracy of HOMA-Adiponectin and HOMA-insulin resistance (HOMA-IR) for identifying insulin resistance. Glucose 112-119 insulin Homo sapiens 77-84 30777938-9 2019 Indeed, islets isolated from VSG mice had increased glucose-stimulated insulin secretion and a left-shifted glucose sensitivity curve compared with islets from PF-Sham mice. Glucose 52-59 insulin Homo sapiens 71-78 30893335-1 2019 The Glucose-Insulin-Glucagon nonlinear model accurately describes how the body responds to exogenously supplied insulin and glucagon in patients affected by Type I diabetes. Glucose 4-11 insulin Homo sapiens 12-19 30918810-7 2019 In a multivariate analysis adjusting for blood glucose level, insulin treatment was the only significant factor associated with an increased risk of PCE (OR 3.9, 95%CI 1.0-15.0, P=0.04) compared to patients without insulin treatment. Glucose 47-54 insulin Homo sapiens 62-69 30715843-6 2019 In this study, four physiologically relevant monosaccharides, methylglyoxal, glucose, fructose, and ribose were used to glycate human insulin and two C-terminus truncated insulin analogues. Glucose 77-84 insulin Homo sapiens 134-141 30715843-6 2019 In this study, four physiologically relevant monosaccharides, methylglyoxal, glucose, fructose, and ribose were used to glycate human insulin and two C-terminus truncated insulin analogues. Glucose 77-84 insulin Homo sapiens 171-178 30808512-2 2019 The d-Nav Insulin Guidance System (Hygieia, Livonia, MI, USA) is a handheld device that is used to measure glucose, determine glucose patterns, and automatically determine the appropriate next insulin dose. Glucose 107-114 insulin Homo sapiens 10-17 30808512-2 2019 The d-Nav Insulin Guidance System (Hygieia, Livonia, MI, USA) is a handheld device that is used to measure glucose, determine glucose patterns, and automatically determine the appropriate next insulin dose. Glucose 126-133 insulin Homo sapiens 10-17 30886164-1 2019 Key to whole body glucose homeostasis is the ability of fat and muscle cells to sequester the facilitative glucose transporter GLUT4 in an intracellular compartment from where it can be mobilized in response to insulin. Glucose 18-25 insulin Homo sapiens 211-218 30886164-1 2019 Key to whole body glucose homeostasis is the ability of fat and muscle cells to sequester the facilitative glucose transporter GLUT4 in an intracellular compartment from where it can be mobilized in response to insulin. Glucose 107-114 insulin Homo sapiens 211-218 30886164-5 2019 Furthermore depletion of USP25 from adipocytes reduces cellular levels of GLUT4 and concomitantly blunts the ability of insulin to stimulate glucose transport. Glucose 141-148 insulin Homo sapiens 120-127 30814273-6 2019 AZD treatment also restored glucose-stimulated insulin secretion from pancreatic islets exposed to hIAPP. Glucose 28-35 insulin Homo sapiens 47-54 30875909-1 2019 Insulin exists in the central nervous system, where it executes two important functions in the hypothalamus: the suppression of food intake and the improvement of glucose metabolism. Glucose 163-170 insulin Homo sapiens 0-7 30871530-7 2019 After oral glucose tolerance test (OGTT), PCOS patients showed higher levels of both glucose and insulin as compared to controls. Glucose 11-18 insulin Homo sapiens 97-104 30923733-19 2019 Mechanisms of action point to normalization of homeostatic negative feedback loops resetting/restoring lipid synthesis/utilization and glucose (insulin)/fatty acid (glucagon) utilization/production in both the body and brain, resulting in increased cerebral metabolism, improved cognition, and reversal of T2DM via renewed cellular insulin sensitivity. Glucose 135-142 insulin Homo sapiens 144-151 30862104-0 2019 Discovery of Galangin as a Potential DPP-4 Inhibitor That Improves Insulin-Stimulated Skeletal Muscle Glucose Uptake: A Combinational Therapy for Diabetes. Glucose 102-109 insulin Homo sapiens 67-74 30862104-7 2019 These findings suggest the beneficial effect of the use of galangin, both alone or in combination with insulin, to reduce glucose levels and improve skeletal muscle health in diabetes mellitus. Glucose 122-129 insulin Homo sapiens 103-110 30707901-5 2019 When evaluated in vivo using insulin-loaded mucoadhesive patches, iontophoresis produced profound hypoglycemia (63% blood glucose drop in 3 h) without damaging the intestinal tissue and the efficacy depended on insulin dose and current density. Glucose 122-129 insulin Homo sapiens 29-36 30861997-1 2019 Efforts to identify a preferable diet for weight management based on macronutrient composition have largely failed, but recent evidence suggests that satiety effects of carbohydrates may depend on the individual"s insulin-mediated cellular glucose uptake. Glucose 240-247 insulin Homo sapiens 214-221 30956666-9 2019 This was followed by the characterization of pancreatic transdifferentiation via reverse transcriptase polymerase chain reaction (RT-PCR) and static and glucose-stimulated insulin secretion (GSIS). Glucose 153-160 insulin Homo sapiens 172-179 30587573-1 2019 Neuroendocrine-type ATP-sensitive K+ (KATP) channels are metabolite sensors coupling membrane potential with metabolism, thereby linking insulin secretion to plasma glucose levels. Glucose 165-172 insulin Homo sapiens 137-144 30849076-2 2019 BACKGROUND: Studies have shown that overnight closed-loop insulin delivery can improve glucose control and reduce the risk of hypoglycemia and hence may improve metabolic outcomes and reduce burden for children with type 1 diabetes and their families. Glucose 87-94 insulin Homo sapiens 58-65 30846785-1 2019 Metabolic clearance rate of insulin (MCRI) is thought to help maintain glucose homeostasis even in healthy subjects. Glucose 71-78 insulin Homo sapiens 28-35 30838644-1 2019 BACKGROUND: Obesity is known to induce a deterioration of insulin sensitivity (SI ), one of the insulin-dependent components of glucose tolerance. Glucose 128-135 insulin Homo sapiens 58-65 30838644-2 2019 However, few studies investigated whether obesity affects also the insulin-independent component, that is glucose effectiveness (SG ). Glucose 106-113 insulin Homo sapiens 67-74 30873220-8 2019 With the advancing of unfavorable glucose metabolism, the insulin resistance (HOMA-IR and Adipo-IR) and beta-cell function (FCPRI, PCPRI) deteriorated (P trend < 0.05 for all indices). Glucose 34-41 insulin Homo sapiens 58-65 30832662-0 2019 Adiponectin and insulin resistance are related to restenosis and overall new PCI in subjects with normal glucose tolerance: the prospective AIRE Study. Glucose 105-112 insulin Homo sapiens 16-23 30832546-8 2019 Chronic exposure to insulin or DHT aberrantly increased IRS1/IRS2 phosphorylation and protein levels of GLUT1 and GLUT12 in hESCs, suggesting that not only hyperinsulinemic but also hyperandrogenic conditions affect insulin signaling and glucose metabolism. Glucose 238-245 insulin Homo sapiens 20-27 30620637-1 2019 Glucose-stimulated insulin secretion from pancreatic beta-cells is controlled by a triggering pathway that culminates in calcium influx and regulated exocytosis of secretory granules, and by a less understood amplifying pathway that augments calcium-induced exocytosis. Glucose 0-7 insulin Homo sapiens 19-26 30620637-2 2019 In response to an abrupt increase in glucose concentration, insulin secretion exhibits a first peak followed by a lower sustained second phase. Glucose 37-44 insulin Homo sapiens 60-67 30586628-1 2019 AIMS/HYPOTHESIS: Salt-inducible kinase 2 (SIK2) is downregulated in adipose tissue from obese or insulin-resistant individuals and inhibition of SIK isoforms results in reduced glucose uptake and insulin signalling in adipocytes. Glucose 177-184 insulin Homo sapiens 97-104 30586628-1 2019 AIMS/HYPOTHESIS: Salt-inducible kinase 2 (SIK2) is downregulated in adipose tissue from obese or insulin-resistant individuals and inhibition of SIK isoforms results in reduced glucose uptake and insulin signalling in adipocytes. Glucose 177-184 insulin Homo sapiens 196-203 30183096-2 2019 Closed-loop glucose-responsive insulin delivery guided by real-time sensor glucose readings can accommodate highly variable day-to-day insulin requirements and reduce the hypoglycaemia risk observed with tight glycaemic control in Type 1 diabetes. Glucose 12-19 insulin Homo sapiens 31-38 30242901-0 2019 Physical activity is associated with lower insulin and C-peptide during glucose challenge in children and adolescents with family background of diabetes. Glucose 72-79 insulin Homo sapiens 55-64 30242901-5 2019 RESULTS: MVPA was negatively associated with insulin and C-peptide during challenge with an oral glucose tolerance test. Glucose 97-104 insulin Homo sapiens 45-52 30242901-5 2019 RESULTS: MVPA was negatively associated with insulin and C-peptide during challenge with an oral glucose tolerance test. Glucose 97-104 insulin Homo sapiens 57-66 30506451-4 2019 RESULTS: Insulin withdrawal increased levels of glucose (6.1 +- 0.5 vs 18.6 +- 0.5 mmol/l), NEFA, 3-OHB (127 +- 18 vs 1837 +- 298 mumol/l), glucagon, cortisol and growth hormone and decreased HCO3- and pH, without affecting catecholamine or cytokine levels. Glucose 48-55 insulin Homo sapiens 9-16 30506451-8 2019 Insulin therapy decreased plasma glucose concentrations dramatically after insulin withdrawal, without any detectable effect on net forearm glucose uptake. Glucose 33-40 insulin Homo sapiens 0-7 30515958-2 2019 In order to achieve optimal glucose control, it is often necessary to rely on combination therapy of multiple drugs or insulin because uncontrolled glucose levels result in T2DM progression and enhanced risk of complications and mortality. Glucose 148-155 insulin Homo sapiens 119-126 30523024-4 2019 These observations suggest that FGF1 acts in the brain to stimulate insulin-independent glucose clearance. Glucose 88-95 insulin Homo sapiens 68-75 30523024-5 2019 On the basis of our finding that icv FGF1 treatment increases hepatic glucokinase gene expression, we considered the possibility that increased hepatic glucose uptake (HGU) contributes to the insulin-independent glucose-lowering effect of icv FGF1. Glucose 152-159 insulin Homo sapiens 192-199 30552111-9 2019 In conclusion, exosome-derived extracellular miR-20b-5p is a circulating biomarker associated with type 2 diabetes that plays an intracellular role in modulating insulin-stimulated glucose metabolism via AKT signaling. Glucose 181-188 insulin Homo sapiens 162-169 30716347-5 2019 In a subset of patients, insulin sensitivity was assessed based on the glucose infusion rate (GIR) during a hyperinsulinemic euglycemic clamp test. Glucose 71-78 insulin Homo sapiens 25-32 30785311-1 2019 BACKGROUND: Hybrid closed-loop (HCL) systems combine continuous glucose monitoring with continuous subcutaneous insulin infusion (CSII) to continuously self-adjust basal insulin delivery. Glucose 64-71 insulin Homo sapiens 170-177 31014093-4 2019 Insulin-mediated glucose disposal (a direct measure of peripheral insulin sensitivity) was measured using the modified insulin suppression test. Glucose 17-24 insulin Homo sapiens 0-7 31014093-4 2019 Insulin-mediated glucose disposal (a direct measure of peripheral insulin sensitivity) was measured using the modified insulin suppression test. Glucose 17-24 insulin Homo sapiens 66-73 31014093-10 2019 CONCLUSION: Insulin sensitivity, as assessed by a direct measure of insulin-mediated glucose disposal, and its relationship to triglyceride concentration vary across five race/ethnic groups. Glucose 85-92 insulin Homo sapiens 12-19 31014093-10 2019 CONCLUSION: Insulin sensitivity, as assessed by a direct measure of insulin-mediated glucose disposal, and its relationship to triglyceride concentration vary across five race/ethnic groups. Glucose 85-92 insulin Homo sapiens 68-75 31014100-4 2019 Among glucose-lowering agents, metformin and thiazolidinediones provide cellular actions that counter some effects of insulin resistance: reduced glucotoxicity and weight-lowering with antidiabetic therapies also improve insulin action, except that endogenously- or exogenously-created hyperinsulinaemia may partially compromise these benefits. Glucose 6-13 insulin Homo sapiens 221-228 30267353-6 2019 Finally, negative feedback loops between spexin and insulin were found, indicating the presence of multilateral relationships between glucose, insulin, and spexin inside pancreatic islets. Glucose 134-141 insulin Homo sapiens 52-59 30913015-6 2019 The insulin peak after glucose load occurred after 30 minutes in CON, after 90 minutes in CF-noDM, and was missing in CFRD. Glucose 23-30 insulin Homo sapiens 4-11 30166639-0 2019 Consuming glucose-sweetened, not fructose-sweetened, beverages increases fasting insulin in healthy humans. Glucose 10-17 insulin Homo sapiens 81-88 30166639-5 2019 In conclusion, in contrast to our hypothesis, insulin resistance was increased with higher glucose vs. fructose content of the beverages in this short-term trial. Glucose 91-98 insulin Homo sapiens 46-53 30576640-6 2019 Nevertheless, recent evidence supports the role of brain insulin as a mediator of glucose metabolism through several means, including altering glucose transporters. Glucose 82-89 insulin Homo sapiens 57-64 30362832-2 2019 Short-term exposure is followed by transient hyperglycemia, mainly triggered by the activation of the sympathetic system, whereas long-term exposure results in lower plasma glucose concentrations, mediated by improved insulin sensitivity and augmented peripheral glucose disposal. Glucose 173-180 insulin Homo sapiens 218-225 30458627-2 2019 Diabetes results from the limited absorption of glucose into insulin-sensitive tissues. Glucose 48-55 insulin Homo sapiens 61-68 30502436-5 2019 The other contribution of the study is the experimental validation that the insulin-loaded microgels with different hydrogel-network compositions (based on Con A-sugar affinity) respond to different glucose concentrations. Glucose 199-206 insulin Homo sapiens 76-83 30502436-6 2019 Particularly, the result of the in vitro insulin release suggests that the microgels be able to maintain bolus and basal insulin release in response to different glucose concentrations and the network composition be able to affect the burst release, release rate and overall release amount of insulin. Glucose 162-169 insulin Homo sapiens 41-48 30458627-9 2019 Diabetes decreased protein content of both GLUT4 (the predominate insulin-sensitive glucose transporter) and AS160 (Akt Substrate at 160 kDa, the downstream protein in the signaling cascade that regulates GLUT4 trafficking) in striated muscle of diabetic rats, with a more pronounced alteration after diltiazem treatment. Glucose 84-91 insulin Homo sapiens 66-73 30285125-11 2019 Conclusions: These observations indicate that beta2-agonist alters net leg glucose uptake and clearance, as well as FFA balance in humans, which is associated with myocellular beta2-adrenergic and insulin-dependent signaling. Glucose 75-82 insulin Homo sapiens 176-204 30043095-2 2019 Insulin degludec, an ultralong acting analogue with a "peakless" and stable pharmacokinetic profile, has the potential advantage of reducing hypoglycaemia and glucose variability compared to other basal insulins. Glucose 159-166 insulin Homo sapiens 0-7 30590569-8 2019 Insulin sensitivity was derived from an oral glucose tolerance test (ISOGTT). Glucose 45-52 insulin Homo sapiens 0-7 30870813-6 2019 Insulin secretion in 11mM glucose also correlated reasonably well for islet area (R2=0.69), protein (R2=0.49), and insulin content (R2=0.58). Glucose 26-33 insulin Homo sapiens 0-7 30527564-4 2019 CASE REPORT: We discuss the case of a 30-year-old male bodybuilder presenting with coma due to severe hypoglycemia from unknown cause, necessitating iterative glucose infusions, which was subsequently found to be related to cryptic insulin injections. Glucose 159-166 insulin Homo sapiens 232-239 30537870-0 2019 A New Algorithm Dedicated to Blood Glucose Monitoring in Insulin-Treated Elderly Dependent People With Diabetes. Glucose 35-42 insulin Homo sapiens 57-64 30578020-5 2019 One of the mechanisms contributing to aging associated hyperglycemia is resistance to insulin-mediated glucose disposal. Glucose 103-110 insulin Homo sapiens 86-93 30870813-6 2019 Insulin secretion in 11mM glucose also correlated reasonably well for islet area (R2=0.69), protein (R2=0.49), and insulin content (R2=0.58). Glucose 26-33 insulin Homo sapiens 115-122 30712315-7 2019 Furthermore, the regulation of blood glucose levels via the activation of pancreatic sweet taste receptors and subsequent insulin secretion, as well as the influence of bitter compounds on thyroid hormone release, is addressed. Glucose 37-44 insulin Homo sapiens 122-129 30554789-4 2019 The primary outcome was the change in insulin-stimulated glucose disposal by a 3-hour hyperinsulinemic-euglycemic clamp. Glucose 57-64 insulin Homo sapiens 38-45 29968251-6 2019 A heightened inflammatory state is associated with major and rapid changes in muscle protein turnover and mass, and dampened insulin-stimulated glucose disposal and oxidation in both rodents and humans. Glucose 144-151 insulin Homo sapiens 125-132 30688831-2 2019 In response to increased glucose levels, insulin is secreted, and several studies have shown that insulin-induced AKT signaling can regulate tumor cell proliferation and apoptosis. Glucose 25-32 insulin Homo sapiens 41-48 30688831-2 2019 In response to increased glucose levels, insulin is secreted, and several studies have shown that insulin-induced AKT signaling can regulate tumor cell proliferation and apoptosis. Glucose 25-32 insulin Homo sapiens 98-105 30679095-7 2019 Weekly insulin dose titration aimed to achieve a self-measured fasting plasma glucose (FPG) concentration of 4 4-7 0 mmol/L. Glucose 78-85 insulin Homo sapiens 7-14 30606545-1 2019 The closed-loop delivery of insulin in response to change of the blood glucose level and long-term supply of insulin are both important for diabetes patients. Glucose 71-78 insulin Homo sapiens 28-35 30606545-3 2019 The purpose of the present study is to design a synthetic artificial pancreas by integration of chitosan hydrogels with insulin-loaded glucose-responsive microspheres to deliver insulin in a close-looped and long-term way for diabetes care. Glucose 135-142 insulin Homo sapiens 120-127 30554789-8 2019 After adjusting for age and sex, insulin-stimulated glucose disposal increased (P < .05) in all groups, with the increase in the aerobic exercise group being greater than the resistance exercise group (1.7 +- 0.1 vs 0.7 +- 0.1 mg/kg/min, P < .05) but not different from the combined group (1.2 +- 0.1 mg/kg/min). Glucose 52-59 insulin Homo sapiens 33-40 30382764-1 2019 The hybrid closed-loop insulin delivery system, a form of "artificial pancreas," is composed of an insulin pump, a standardized algorithm, and a continuous glucose monitor. Glucose 156-163 insulin Homo sapiens 23-30 30382764-2 2019 The system streamlines insulin delivery by connecting continuous glucose monitor data with an insulin pump and an algorithm to drive basal insulin delivery. Glucose 65-72 insulin Homo sapiens 23-30 30760930-0 2019 Diabetes relief in mice by glucose-sensing insulin-secreting human alpha-cells. Glucose 27-34 insulin Homo sapiens 43-50 30294842-5 2019 At 10 to 12 years, IS was measured with the Matsuda-insulin sensitivity index; insulin secretion was measured with the ratio of the area under the curve (AUC) of insulin to the AUC of glucose over a 2-hour oral glucose tolerance test. Glucose 184-191 insulin Homo sapiens 79-86 30713129-3 2019 During pancreatic dysfunction, insulin mediated suppression of glucagon is impaired leading to uncontrolled glucose production by liver and state of hyperglycemia. Glucose 108-115 insulin Homo sapiens 31-38 30537059-7 2019 METHODS: We used an insulin-modified frequent sample intravenous glucose tolerance test to study acute insulin response (AIR), insulin sensitivity (SI), and disposition index (DI) in children and adolescents with obesity. Glucose 65-72 insulin Homo sapiens 20-27 30912283-8 2019 Clamp-derived glucose disposal rates correlated with Nur77 (r2 = 0.14) and NOR1 (r2 = 0.12) protein expression responses to insulin, whereas age (Nur77: r2 = 0.22; NOR1: r2 = 0.25) and BMI (Nur77: r2 = 0.22; NOR1: r2 = 0.42) showed inverse correlations, corroborating preclinical data. Glucose 14-21 insulin Homo sapiens 126-133 30542047-2 2019 However, it remains controversial issue that glucose intolerance on pheochromocytoma is caused by impaired insulin secretion and/or by increased insulin resistance. Glucose 45-52 insulin Homo sapiens 107-114 30816192-0 2019 Low density lipoprotein mimics insulin action on autophagy and glucose uptake in endothelial cells. Glucose 63-70 insulin Homo sapiens 31-38 30989864-8 2019 The results showed that the glucose consumption was significantly decreased in the insulin resistance cells after incubation with 25. Glucose 28-35 insulin Homo sapiens 83-90 30815757-5 2019 In vivo studies in diabetic animals demonstrated low levels of plasma glucose for almost 24 h. Pharmacological availability (PA) of insulin administered through Ch-PSS-PGA NPs (17.28 +- 0.9) was significantly higher as compared to that of insulin administered through control NPs, i.e., Ch-PGA NPs (10.9 +- 1.5) and Ch-PSS NPs (12.9 +- 1.8). Glucose 70-77 insulin Homo sapiens 132-139 30816192-4 2019 The present study firstly demonstrated that LDL can suppress endothelial autophagy through activation of the PI3K/Akt/mTOR signaling pathway and can promote glucose uptake by translocating glucose transporter 1 (GLUT1) from cytoplasm to cell membrane, actions similar to those of insulin. Glucose 157-164 insulin Homo sapiens 280-287 30767782-6 2019 Flow cytometry and ELISA were performed to detect differentiation efficiency and insulin content and secretion from iPSCs-derived IPCs in response to stimulation at different concentration of glucose. Glucose 192-199 insulin Homo sapiens 81-88 30814610-2 2019 A key pathological trait associated with this disease is the failure of normal glucose-stimulated insulin secretion (GSIS) from pancreatic beta cells. Glucose 79-86 insulin Homo sapiens 98-105 30866459-1 2019 Diabetic patients need long-term and frequent glucose monitoring to assist in insulin intake. Glucose 46-53 insulin Homo sapiens 78-85 30481552-10 2019 For glucose parameters associations were found between C allele of rs7258674 (CARD8) and higher glucose levels, and between C allele of rs212704 (NLRC4) and G allele of rs455060 (NLRC4) and insulin levels. Glucose 4-11 insulin Homo sapiens 190-197 30639280-2 2019 Natural insulin secretion limits the fluctuation of the narrow and high surge of blood glucose levels. Glucose 87-94 insulin Homo sapiens 8-15 30783538-6 2019 In addition, hyperglycaemia in most cases is characterised by a significantly blunted acute first phase of insulin secretion in response to an oral or intravenous glucose load and pancreatic beta cell secretory dysfunction, rather than peripheral insulin resistance predominates. Glucose 163-170 insulin Homo sapiens 107-114 30763000-0 2019 [Exposure of beta-cells to chronic fructose potentiates glucose-stimulated insulin secretion through ATP signaling]. Glucose 56-63 insulin Homo sapiens 75-82 30760321-10 2019 ECFC and MSC co-culture as well as conditioned media of co-cultures resulted in a significant increased expression of pancreatic-specific genes and an increase in glucose-regulated insulin secretion, compared with IPCs alone. Glucose 163-170 insulin Homo sapiens 181-188 30763000-3 2019 Our results reveal that chronic fructose induces extracellular ATP signaling in the beta-cell, resulting in the potentiation of glucose-stimulated insulin secretion. Glucose 128-135 insulin Homo sapiens 147-154 30755634-4 2019 In this work, we fabricated microwell spheroid culture devices made of oxygen-permeable polydimethylsiloxane (PDMS), with which hypoxia in the core of bioartificial islets was alleviated and glucose-stimulated insulin secretion was increased ~2.5-fold compared to a device with the same configuration but made of non-oxygen-permeable plastic. Glucose 191-198 insulin Homo sapiens 210-217 30608155-6 2019 Furthermore, the successful glucose-triggered release of FITC-insulin from the polymeric micelles was investigated. Glucose 28-35 insulin Homo sapiens 62-69 30661993-2 2019 While these stem cell-derived beta (SC-beta) cells are capable of undergoing glucose-stimulated insulin secretion (GSIS), insulin secretion per cell remains low compared with islets and cells lack dynamic insulin release. Glucose 77-84 insulin Homo sapiens 96-103 30899527-7 2019 In subgroup analyses, studies with higher PUFA dose (upper tertiles) reduced insulin (-6.7, -10.5 to -2.9 pmol/L) and HOMA-IR (-0.28, -0.45 to -0.12 units), but not glucose (-0.09, 95% CI -0.18 to 0.01 mmol/L), as compared with an isocaloric control. Glucose 165-172 insulin Homo sapiens 77-84 30899529-9 2019 Conclusions: Higher adiponectin and lower orosomucoid were associated with 70 or lower mg/dL of postload glucose, a possible inverse marker for dysglycemia, in young women independently of DXA-derived fat mass and distribution, insulin secretion and IR. Glucose 105-112 insulin Homo sapiens 228-235 30718702-0 2019 Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle. Glucose 70-77 insulin Homo sapiens 0-57 30718702-3 2019 Incubation of primary human skeletal muscle cells (HSKMCs) with apoA-I increased insulin-dependent and insulin-independent glucose uptake in a time- and concentration-dependent manner. Glucose 123-130 insulin Homo sapiens 64-110 29861377-8 2019 Lower glucose prior to insulin (adjusted odds ratio [aOR] 0.90; 95% confidence interval [95% CI] 0.85 to 0.96), higher doses of insulin (aOR 1.07; 95% CI 1.01 to 1.15) and lower doses of D50 (aOR 0.98; 95% CI 0.97 to 0.99) were independently associated with hypoglycemia in the multivariate analysis. Glucose 6-13 insulin Homo sapiens 23-30 30863457-3 2019 Indeed such low-level chronic inflammation affects the pancreatic production of insulin and triggers the development of insulin resistance, eventually leading to an impaired control of the blood glucose concentration. Glucose 195-202 insulin Homo sapiens 80-87 30863457-3 2019 Indeed such low-level chronic inflammation affects the pancreatic production of insulin and triggers the development of insulin resistance, eventually leading to an impaired control of the blood glucose concentration. Glucose 195-202 insulin Homo sapiens 120-127 30612202-1 2019 AIMS: Glucose effectiveness (GE) refers to the ability of glucose to influence its own metabolism through insulin-independent mechanisms. Glucose 58-65 insulin Homo sapiens 106-113 30562061-5 2019 Insulin action was measured with a four-phase hyperinsulinemic-euglycemic clamp (basal, 10, 16, and 80 mU m-2 min-1 for studying adipose, hepatic, and peripheral IR, respectively) with glucose and glycerol isotope tracers. Glucose 185-192 insulin Homo sapiens 0-7 30592226-16 2019 Importantly, this study shows that in those with the rs10830963 GG genotype, insulin sensitivity deteriorated the most significantly across the 6.8-year follow-up if the daylight length on the oral glucose tolerance testing date at the follow-up was shorter than at the baseline. Glucose 198-205 insulin Homo sapiens 77-84 30466006-0 2019 Ellagic acid ameliorates oxidative stress and insulin resistance in high glucose-treated HepG2 cells via miR-223/keap1-Nrf2 pathway. Glucose 73-80 insulin Homo sapiens 46-53 30419762-8 2019 An insulin response toward glucose challenge was present in all experimental groups, but the stimulation index was significantly decreased using collagenase plus NP (2.0 +- 0.12) compared with supplementation with CP (3.16 +- 0.4, P < 0.001). Glucose 27-34 insulin Homo sapiens 3-10 30465877-1 2019 At present, the main form of insulin administration is the invasive subcutaneous (s.c.) route and, for many patients, this means managing their glucose levels with multiple daily injections, which is both painful and difficult to administer chronically. Glucose 144-151 insulin Homo sapiens 29-36 30351989-12 2019 Glucose variation showed a decrease after surgery with acrophase in summer-fall and plasminogen activator inhibitor-1 (PAI-1) and homeostatic model assessment-insulin resistance (HOMA-IR) in spring-summer. Glucose 0-7 insulin Homo sapiens 159-166 30125349-1 2019 The goal of this investigation was to examine clinical translation of glucose responsiveness of MK-2640, which is a novel insulin saccharide conjugate that can bind the insulin receptor or mannose receptor C type 1 (MRC1), the latter dependent upon glucose concentration. Glucose 70-77 insulin Homo sapiens 122-129 30125349-1 2019 The goal of this investigation was to examine clinical translation of glucose responsiveness of MK-2640, which is a novel insulin saccharide conjugate that can bind the insulin receptor or mannose receptor C type 1 (MRC1), the latter dependent upon glucose concentration. Glucose 70-77 insulin Homo sapiens 169-176 30125349-6 2019 These pharmacokinetic (PK) and pharmacodynamic (PD) data provide crucial insights into next steps for developing an insulin saccharide conjugate as a clinically effective glucose-responsive insulin analog. Glucose 171-178 insulin Homo sapiens 116-123 30125349-6 2019 These pharmacokinetic (PK) and pharmacodynamic (PD) data provide crucial insights into next steps for developing an insulin saccharide conjugate as a clinically effective glucose-responsive insulin analog. Glucose 171-178 insulin Homo sapiens 190-197 30523032-0 2019 Insulin Clearance After Oral and Intravenous Glucose Following Gastric Bypass and Gastric Banding Weight Loss. Glucose 45-52 insulin Homo sapiens 0-7 30572005-9 2019 Knockdown of two of the deleted genes (Dnajc24 or Immp1l) with Pax6 impaired glucose-stimulated insulin secretion. Glucose 77-84 insulin Homo sapiens 96-103 30523032-2 2019 We hypothesized that the improvement in insulin clearance rates (ICRs) under fasting conditions and in response to oral and intravenous (IV) glucose would improve similarly after Roux-en-Y gastric bypass (RYGB) and adjustable gastric banding (AGB) as a function of weight loss; the difference in ICR after oral and IV glucose stimulation will be enhanced after RYGB compared with AGB, an effect mediated by glucagon-like peptide 1 (GLP-1). Glucose 141-148 insulin Homo sapiens 40-47 30523032-2 2019 We hypothesized that the improvement in insulin clearance rates (ICRs) under fasting conditions and in response to oral and intravenous (IV) glucose would improve similarly after Roux-en-Y gastric bypass (RYGB) and adjustable gastric banding (AGB) as a function of weight loss; the difference in ICR after oral and IV glucose stimulation will be enhanced after RYGB compared with AGB, an effect mediated by glucagon-like peptide 1 (GLP-1). Glucose 318-325 insulin Homo sapiens 40-47 30368796-9 2019 The areas under the concentration-time curve for glucose and insulin for the entire population were significantly lower following ingestion of honey than glucose solution (P < 0.001) both at the beginning and at the end of study. Glucose 154-161 insulin Homo sapiens 61-68 29236165-5 2019 Compared with D0C meal, we found significant linear dose-response reductions in the 3-h postprandial incremental AUC (iAUC) for CGM glucose of 19% and 32% during D1C and D2C meals respectively (p < 0.05) and non-significant linear dose response reductions in iAUC of insulin (p = 0.089). Glucose 132-139 insulin Homo sapiens 270-277 30779092-11 2019 Increased values of insulin resistance indicators in the BD group point to the necessity of monitoring glucose and triglycerides levels and measurement of waist circumference in bipolar patients in the routine clinical practice. Glucose 103-110 insulin Homo sapiens 20-27 30576500-2 2019 SUMMARY ANSWER: Women with PCOS, particularly obese subjects, have dysregulated plasma NEFA kinetics in response to changes in plasma insulin and glucose levels, which are associated with insulin resistance (IR) independently of the fasting plasma NEFA levels. Glucose 146-153 insulin Homo sapiens 188-195 30226812-1 2019 Insulin is a critical signaling molecule in reducing blood glucose levels, and pyruvate dehydrogenase (PDH) is an essential enzyme in regulating glucose metabolism. Glucose 59-66 insulin Homo sapiens 0-7 30226812-1 2019 Insulin is a critical signaling molecule in reducing blood glucose levels, and pyruvate dehydrogenase (PDH) is an essential enzyme in regulating glucose metabolism. Glucose 145-152 insulin Homo sapiens 0-7 30793568-2 2019 Effective monitoring of blood glucose can aid in maintaining the body"s insulin level, and thus reduce disease severities, secondary complications, and related mortalities. Glucose 30-37 insulin Homo sapiens 72-79 30467902-8 2019 The intraoperative immunoreactive insulin/glucose ratio was significantly higher in patients with hypoglycemia than in those without hypoglycemia. Glucose 42-49 insulin Homo sapiens 34-41 30717198-6 2019 These findings were further supported by marked stimulation of genes involved in glucose metabolism, such as insulin receptor (Insr) and insulin receptor substrate 1 and 2 (Irs1 and Irs2), as well as those involved in lipid metabolism, including Forkhead box protein O1 (FOXO1) and carnitine palmitoyl transferase 1 (CPT1) following GRE treatment. Glucose 81-88 insulin Homo sapiens 109-116 30717198-6 2019 These findings were further supported by marked stimulation of genes involved in glucose metabolism, such as insulin receptor (Insr) and insulin receptor substrate 1 and 2 (Irs1 and Irs2), as well as those involved in lipid metabolism, including Forkhead box protein O1 (FOXO1) and carnitine palmitoyl transferase 1 (CPT1) following GRE treatment. Glucose 81-88 insulin Homo sapiens 137-144 30339268-0 2019 Toward Better Understanding of Insulin Therapy by Translation of a PK-PD Model to Visualize Insulin and Glucose Action Profiles. Glucose 104-111 insulin Homo sapiens 31-38 30339268-7 2019 Visualizations of insulin and glucose profiles for commonly prescribed regimens could be rapidly generated by implementing the linked subcutaneous insulin PK-IGI model using the R statistical program (version 3.4.4) and a contemporary web-based interface, which could enhance clinical education on glycemic control with insulin therapy. Glucose 30-37 insulin Homo sapiens 147-154 30339268-7 2019 Visualizations of insulin and glucose profiles for commonly prescribed regimens could be rapidly generated by implementing the linked subcutaneous insulin PK-IGI model using the R statistical program (version 3.4.4) and a contemporary web-based interface, which could enhance clinical education on glycemic control with insulin therapy. Glucose 30-37 insulin Homo sapiens 147-154 30721136-5 2019 Since skeletal muscle is the major tissue for insulin-stimulated glucose uptake understanding the functional role of vaspin in human muscle insulin signalling is critical in determining its role in glucose homeostasis. Glucose 65-72 insulin Homo sapiens 46-53 30468944-2 2019 Amylin is complementary to insulin in regulating and maintaining blood glucose levels in the human body. Glucose 71-78 insulin Homo sapiens 27-34 30468781-3 2019 We estimated insulin sensitivity and secretion using oral glucose tolerance test-based validated indices. Glucose 58-65 insulin Homo sapiens 13-20 30032866-7 2019 Si, Sg acute insulin response to glucose (AIRg) and disposition index (DI) were calculated using minimal model method. Glucose 33-40 insulin Homo sapiens 13-20 30710150-6 2019 eBCs display glucose-stimulated insulin secretion as early as three days after transplantation in mice. Glucose 13-20 insulin Homo sapiens 32-39 30528280-8 2019 Importantly, glucose and insulin suppress mitochondrial activity (i.e. ATP-linked respiration) significantly only in preadipocytes of female donors, reflecting their trends towards higher insulin sensitivity. Glucose 13-20 insulin Homo sapiens 188-195 30699907-2 2019 Muscle is a major insulin target that is responsible for the majority of insulin-stimulated glucose use. Glucose 92-99 insulin Homo sapiens 18-25 30766490-5 2019 Insulin resistance/sensitivity was measured using HOMAIR and glucose infusion rate during euglycemic hyperinsulinemic clamp. Glucose 61-68 insulin Homo sapiens 0-7 30694176-5 2019 Conserved in mammalians, calcineurin/NFAT prompted high-glucose-stimulated insulin secretion of neonatal mouse islets cultured in vitro. Glucose 56-63 insulin Homo sapiens 75-82 30694176-6 2019 However, the reduction in low-glucose-stimulated insulin secretion was dependent on optimal glucose but independent of calcineurin/NFAT. Glucose 30-37 insulin Homo sapiens 49-56 30694176-6 2019 However, the reduction in low-glucose-stimulated insulin secretion was dependent on optimal glucose but independent of calcineurin/NFAT. Glucose 92-99 insulin Homo sapiens 49-56 30699907-2 2019 Muscle is a major insulin target that is responsible for the majority of insulin-stimulated glucose use. Glucose 92-99 insulin Homo sapiens 73-80 30699907-3 2019 Evidence confirms that muscle microvasculature is an important insulin action site and critically regulates insulin delivery to muscle and action on myocytes, thereby affecting insulin-mediated glucose disposal. Glucose 194-201 insulin Homo sapiens 108-115 30699907-3 2019 Evidence confirms that muscle microvasculature is an important insulin action site and critically regulates insulin delivery to muscle and action on myocytes, thereby affecting insulin-mediated glucose disposal. Glucose 194-201 insulin Homo sapiens 108-115 30699907-5 2019 Insulin"s microvascular actions closely couple with its metabolic actions in muscle and blockade of insulin-mediated microvascular perfusion reduces insulin-stimulated muscle glucose disposal. Glucose 175-182 insulin Homo sapiens 0-7 30699907-5 2019 Insulin"s microvascular actions closely couple with its metabolic actions in muscle and blockade of insulin-mediated microvascular perfusion reduces insulin-stimulated muscle glucose disposal. Glucose 175-182 insulin Homo sapiens 100-107 30699907-5 2019 Insulin"s microvascular actions closely couple with its metabolic actions in muscle and blockade of insulin-mediated microvascular perfusion reduces insulin-stimulated muscle glucose disposal. Glucose 175-182 insulin Homo sapiens 149-156 30557648-7 2019 These values represented a remarkable increase in bioavailability of intranasal insulin, causing a significant decrease in blood glucose levels within one hour. Glucose 129-136 insulin Homo sapiens 80-87 30809553-4 2019 The model was used to quantify PA-induced lipid accumulation in the two cell lines treated with various concentrations of mangiferin simultaneously for 24 h. We found that mangiferin significantly increased insulin-stimulated glucose uptake, via phosphorylation of protein kinase B (P-AKT), glucose transporter 2 (GLUT2), and glucose transporter 4 (GLUT4) protein expressions, and markedly decreased glucose content, respectively, in HepG2 and C2C12 cells induced by PA. Glucose 226-233 insulin Homo sapiens 207-214 30525462-1 2019 Good glucose management through an insulin dose regime based on the metabolism of glucose helps millions of people worldwide manage their diabetes. Glucose 5-12 insulin Homo sapiens 35-42 30525462-1 2019 Good glucose management through an insulin dose regime based on the metabolism of glucose helps millions of people worldwide manage their diabetes. Glucose 82-89 insulin Homo sapiens 35-42 30525462-2 2019 Since Banting and Best extracted insulin, glucose management has improved due to the introduction of insulin analogues that act from 30 minutes to 28 days, improved insulin dose regimes, and portable glucose meters, with a current focus on alternative sampling sites that are less invasive. Glucose 42-49 insulin Homo sapiens 101-108 30525462-2 2019 Since Banting and Best extracted insulin, glucose management has improved due to the introduction of insulin analogues that act from 30 minutes to 28 days, improved insulin dose regimes, and portable glucose meters, with a current focus on alternative sampling sites that are less invasive. Glucose 42-49 insulin Homo sapiens 101-108 30525462-4 2019 The ability to measure both glucose and insulin concurrently will enable better glucose control by providing an improved estimate for insulin sensitivity, minimizing variability in control, and maximizing safety from hypoglycaemia. Glucose 28-35 insulin Homo sapiens 134-141 30525462-4 2019 The ability to measure both glucose and insulin concurrently will enable better glucose control by providing an improved estimate for insulin sensitivity, minimizing variability in control, and maximizing safety from hypoglycaemia. Glucose 80-87 insulin Homo sapiens 40-47 30525462-4 2019 The ability to measure both glucose and insulin concurrently will enable better glucose control by providing an improved estimate for insulin sensitivity, minimizing variability in control, and maximizing safety from hypoglycaemia. Glucose 80-87 insulin Homo sapiens 134-141 30809553-4 2019 The model was used to quantify PA-induced lipid accumulation in the two cell lines treated with various concentrations of mangiferin simultaneously for 24 h. We found that mangiferin significantly increased insulin-stimulated glucose uptake, via phosphorylation of protein kinase B (P-AKT), glucose transporter 2 (GLUT2), and glucose transporter 4 (GLUT4) protein expressions, and markedly decreased glucose content, respectively, in HepG2 and C2C12 cells induced by PA. Glucose 291-298 insulin Homo sapiens 207-214 30682147-4 2019 We hypothesised that the amount of food a person consumes differs substantially after a fasting period even after the energy deficit was partially removed by glucose ingestion and endocrine signals like insulin and C-peptide indicated a high glucose metabolic status. Glucose 242-249 insulin Homo sapiens 203-210 30678043-2 2019 Skeletal muscles are quantitatively the biggest glucose users in response to insulin and are considered as main targets in development of insulin-resistance. Glucose 48-55 insulin Homo sapiens 77-84 30678043-2 2019 Skeletal muscles are quantitatively the biggest glucose users in response to insulin and are considered as main targets in development of insulin-resistance. Glucose 48-55 insulin Homo sapiens 138-145 30485790-8 2019 In conclusion, ginsenoside-Rg1 can alleviate the insulin resistance through increasing the uptake of glucose and decreasing the output of glucose. Glucose 101-108 insulin Homo sapiens 49-56 30485790-8 2019 In conclusion, ginsenoside-Rg1 can alleviate the insulin resistance through increasing the uptake of glucose and decreasing the output of glucose. Glucose 138-145 insulin Homo sapiens 49-56 30566152-9 2019 The immune-metabolic correlation has been studied by monitoring adiponectin and IL-6 expression, as well as glucose uptake upon treatment with insulin. Glucose 108-115 insulin Homo sapiens 143-150 30861665-4 2019 Since the parameters in the blood glucose regulation system differ in people, such a robust controller is useful in the insulin pump technology: an insulin pump equipped with such a robust controller could be used in a group of people. Glucose 34-41 insulin Homo sapiens 120-127 30861665-4 2019 Since the parameters in the blood glucose regulation system differ in people, such a robust controller is useful in the insulin pump technology: an insulin pump equipped with such a robust controller could be used in a group of people. Glucose 34-41 insulin Homo sapiens 148-155 30879083-10 2019 Insulin induced glucose uptake, inhibited lipolysis and influenced vasculature-related genes. Glucose 16-23 insulin Homo sapiens 0-7 30485790-0 2019 Investigations on the effects of ginsenoside-Rg1 on glucose uptake and metabolism in insulin resistant HepG2 cells. Glucose 52-59 insulin Homo sapiens 85-92 30273662-12 2019 Homozygous A of rs9939609 showed significantly higher fasting glucose compared to other genotypes (p = 0.04) with a trend of higher insulin level and HOMA-2IR. Glucose 62-69 insulin Homo sapiens 132-139 30626738-2 2019 Insulin regulates both glucose and lipid homeostasis. Glucose 23-30 insulin Homo sapiens 0-7 30774850-0 2019 Blood Glucose Level Prediction for Diabetics Based on Nutrition and Insulin Administration Logs Using Personalized Mathematical Models. Glucose 6-13 insulin Homo sapiens 68-75 30729133-0 2019 High Glucose with Insulin Induces Cell Cycle Progression and Activation of Oncogenic Signaling of Bladder Epithelial Cells Cotreated with Metformin and Pioglitazone. Glucose 5-12 insulin Homo sapiens 18-25 30621663-6 2019 Marked hyperinsulinemia (4500 muU/mL) and high titers of insulin antibodies (80.4%) with high binding capacity and low affinity indicated that IAS-like insulin antibodies were causing severe glucose fluctuations. Glucose 191-198 insulin Homo sapiens 57-64 30621663-10 2019 Therefore, compared to exogenously injected insulin, endogenously secreted insulin directly and rapidly acts on hepatocytes and suppresses postprandial glucose output. Glucose 152-159 insulin Homo sapiens 75-82 30621663-11 2019 CONCLUSIONS: Proper enhancement of postprandial endogenous insulin aimed at suppressing postprandial glucose output without stimulating excessive glucose uptake in the periphery is potentially useful for treating diabetes with insulin antibody-induced glycemic instability. Glucose 101-108 insulin Homo sapiens 59-66 30621663-11 2019 CONCLUSIONS: Proper enhancement of postprandial endogenous insulin aimed at suppressing postprandial glucose output without stimulating excessive glucose uptake in the periphery is potentially useful for treating diabetes with insulin antibody-induced glycemic instability. Glucose 101-108 insulin Homo sapiens 227-234 30621663-11 2019 CONCLUSIONS: Proper enhancement of postprandial endogenous insulin aimed at suppressing postprandial glucose output without stimulating excessive glucose uptake in the periphery is potentially useful for treating diabetes with insulin antibody-induced glycemic instability. Glucose 146-153 insulin Homo sapiens 59-66 30622653-0 2019 Short-acting insulin analogues versus regular human insulin on postprandial glucose and hypoglycemia in type 1 diabetes mellitus: a systematic review and meta-analysis. Glucose 76-83 insulin Homo sapiens 13-20 30622653-0 2019 Short-acting insulin analogues versus regular human insulin on postprandial glucose and hypoglycemia in type 1 diabetes mellitus: a systematic review and meta-analysis. Glucose 76-83 insulin Homo sapiens 52-59 30622653-1 2019 Introduction: Strict glucose control using multiple doses of insulin is the standard treatment for type 1 diabetes mellitus (T1DM), but increased risk of hypoglycemia is a frequent drawback. Glucose 21-28 insulin Homo sapiens 61-68 30622653-2 2019 Regular insulin in multiple doses is important for achieving strict glycemic control for T1DM, but short-acting insulin analogues may be better in reducing hypoglycemia and postprandial glucose levels. Glucose 186-193 insulin Homo sapiens 112-119 30622653-13 2019 Conclusions: Short-acting insulin analogues are superior to regular human insulin in T1DM patients for the following outcomes: total hypoglycemic episodes, nocturnal hypoglycemia, severe hypoglycemia, postprandial glucose, and HbA1c. Glucose 214-221 insulin Homo sapiens 26-33 30507613-1 2019 Using an integrated approach to characterize the pancreatic tissue and isolated islets from a 33-year-old with 17 years of type 1 diabetes (T1D), we found that donor islets contained beta cells without insulitis and lacked glucose-stimulated insulin secretion despite a normal insulin response to cAMP-evoked stimulation. Glucose 223-230 insulin Homo sapiens 242-249 30507613-3 2019 In one of the first studies of human pancreatic islets with a disease-causing HNF1A variant associated with the most common form of monogenic diabetes, we found that HNF1A dysfunction leads to insulin-insufficient diabetes reminiscent of T1D by impacting the regulatory processes critical for glucose-stimulated insulin secretion and suggest a rationale for a therapeutic alternative to current treatment. Glucose 293-300 insulin Homo sapiens 193-200 30604094-2 2019 The beta cells produce insulin with respect to blood glucose level. Glucose 53-60 insulin Homo sapiens 23-30 30604094-4 2019 The blood glucose increases in body when insulin secretion is low from pancreas, termed as Diabetes mellititus. Glucose 10-17 insulin Homo sapiens 41-48 30623004-10 2019 We confirmed the secretion of human insulin and glucagon dependent on the blood glucose level in vivo. Glucose 80-87 insulin Homo sapiens 36-43 31281219-0 2019 Metformin poisoning treated with high dose insulin dextrose therapy: a case series. Glucose 51-59 insulin Homo sapiens 43-50 31281219-2 2019 Methods: Patients presenting with refractory lactic acidosis believed to be secondary to metformin poisoning were included.High dose insulin dextrose at 0.5units/kg/hour was infused in 50% dextrose. Glucose 141-149 insulin Homo sapiens 133-140 29791774-6 2019 In fact, 5-HT may serve an essential role in regulating the release of insulin and glucagon, the two main hormones that control glucose and lipid homoeostasis. Glucose 128-135 insulin Homo sapiens 71-78 30293894-3 2019 In this review, we describe the physiological function of PLCbetas in the regulation of glucose-stimulated insulin secretion and discuss emerging data on GPCR/PLCbeta signaling that is being developed as a target for the treatment of diabetes mellitus. Glucose 88-95 insulin Homo sapiens 107-114 30608898-3 2019 A 32-year-old woman was treated with insulin for gestational diabetes at age 32 years; post-partum, her fasting blood glucose was 6.0 mmol/L and 2-h glucose was 11.8 mmol/L following an oral glucose tolerance test, and she was maintained on diet alone. Glucose 118-125 insulin Homo sapiens 37-44 30608898-3 2019 A 32-year-old woman was treated with insulin for gestational diabetes at age 32 years; post-partum, her fasting blood glucose was 6.0 mmol/L and 2-h glucose was 11.8 mmol/L following an oral glucose tolerance test, and she was maintained on diet alone. Glucose 149-156 insulin Homo sapiens 37-44 30608898-3 2019 A 32-year-old woman was treated with insulin for gestational diabetes at age 32 years; post-partum, her fasting blood glucose was 6.0 mmol/L and 2-h glucose was 11.8 mmol/L following an oral glucose tolerance test, and she was maintained on diet alone. Glucose 149-156 insulin Homo sapiens 37-44 30153063-2 2019 Metformin is commonly used to treat insulin resistance-glucose intolerance, and flutamide, an androgen receptor (AR) antagonist, is used to target hyperandrogenemia and dyslipidemia. Glucose 55-62 insulin Homo sapiens 36-43 31659910-8 2019 When in combination with hypoglycemic agents or insulin, GGFs enhanced the glucose-lowering effect as well as the lipid-lowering effects. Glucose 75-82 insulin Homo sapiens 48-55 30549138-4 2019 Diabetic myotubes express a primary coordinated impairment of lipid oxidation, oxidative phosphorylation (OXPHOS) and insulin-stimulated glucose metabolism. Glucose 137-144 insulin Homo sapiens 118-125 30404557-5 2019 Moreover, GLP-1/Glb increased glucose-stimulated insulin secretion in a dose-dependent manner. Glucose 30-37 insulin Homo sapiens 49-56 31037970-8 2019 Patients on linagliptin-basal insulin had fewer hypoglycaemic events (blood glucose < 70 mg/dL) (p < .001). Glucose 76-83 insulin Homo sapiens 30-37 30404071-1 2019 Local renin-angiotensin system (RAS) in the pancreas is linked to the modulation of glucose-stimulated insulin secretion (GSIS) in beta cells and insulin sensitivity in target tissues, emerging as a promising tool in the prevention and/or treatment of obesity, diabetes, and systemic arterial hypertension. Glucose 84-91 insulin Homo sapiens 103-110 31117067-8 2019 Fluorescence glucose uptake assays revealed that hair cells take up glucose and that addition of insulin (10 nM or 1 microM) approximately doubled the rate of uptake. Glucose 13-20 insulin Homo sapiens 97-104 31117067-9 2019 Pioglitazone conferred a small but nonsignificant potentiation of glucose uptake at the highest concentration of insulin. Glucose 66-73 insulin Homo sapiens 113-120 31117067-12 2019 Together, these data show that insulin-stimulated glucose uptake occurs in the OC and may be associated with upregulation of both the IR and GLUT1. Glucose 50-57 insulin Homo sapiens 31-38 30123993-7 2019 Insulin secretion under different concentrations of glucose was measured using radioimmunoassay method. Glucose 52-59 insulin Homo sapiens 0-7 31474712-1 2019 Glucose-stimulated insulin secretion is controlled by both exocytosis and endocytosis in pancreatic beta-cells. Glucose 0-7 insulin Homo sapiens 19-26 31474712-3 2019 We have previously shown that in response to high concentrations of glucose, guanosine 5"-diphosphate (GDP)-bound Rab27a is recruited to the plasma membrane where IQ motif-containing guanosine 5"-triphosphatase (GTPase)-activating protein 1 (IQGAP1) is expressed, and that complex formation promotes endocytosis of secretory membranes after insulin secretion. Glucose 68-75 insulin Homo sapiens 341-348 30124003-3 2019 Elevated fasting glucose level and higher concentrations of innate immunity soluble molecules are not only related with insulin resistance, but inflammation is also an important factor in beta cell dysfunction in T2DM. Glucose 17-24 insulin Homo sapiens 120-127 30739869-2 2019 Although insulin normally promotes anabolic metabolism in the liver by increasing glucose consumption and lipid synthesis, insulin-resistant individuals fail to inhibit hepatic glucose production and paradoxically have increased liver lipid synthesis, leading to hyperglycemia and hypertriglyceridemia. Glucose 82-89 insulin Homo sapiens 9-16 30343320-3 2019 While hepatic simple steatosis seems to be a rather benign manifestation of hepatic triglyceride accumulation, the buildup of highly toxic free fatty acids associated with insulin resistance-induced massive free fatty acid mobilization from adipose tissue and the increased de novo hepatic fatty acid synthesis from glucose acts as the "first hit" for NAFLD development. Glucose 316-323 insulin Homo sapiens 172-179 30739869-2 2019 Although insulin normally promotes anabolic metabolism in the liver by increasing glucose consumption and lipid synthesis, insulin-resistant individuals fail to inhibit hepatic glucose production and paradoxically have increased liver lipid synthesis, leading to hyperglycemia and hypertriglyceridemia. Glucose 177-184 insulin Homo sapiens 123-130 30739869-3 2019 Here, we detail the intrahepatic and extrahepatic pathways mediating insulin"s control of glucose and lipid metabolism. Glucose 90-97 insulin Homo sapiens 69-76 30339034-7 2019 Homeostasis model assessment-estimated insulin resistance (HOMA-IR) was calculated using glucose and insulin levels. Glucose 89-96 insulin Homo sapiens 39-46 32422019-7 2019 In the fed state, when insulin secretion is stimulated and glucagon secretion is inhibited, EGP decreases and glucose uptake in splanchnic (liver and gut) and peripheral (primarily muscle) tissues increases. Glucose 110-117 insulin Homo sapiens 23-30 30461450-4 2019 The article reviews potential mechanisms and literature evidence suggesting a role in improving glucose tolerance in patients with illness associated with insulin resistance, as well as the preliminary evidence for the increased incidence of postexercise hypoglycemia in T1D after oral glutamine. Glucose 96-103 insulin Homo sapiens 155-162 30101716-4 2019 Methods & Results: In response to glycosuria, a compensatory rise in endogenous glucose production, sustained by a decrease in plasma insulin with an increase in glucagon has been described. Glucose 80-87 insulin Homo sapiens 134-141 29032755-4 2019 Improving insulin sensitivity is anticipated to both lower the plasma glucose concentration and decrease CVD risk in T2DM patients, independent of glucose control. Glucose 70-77 insulin Homo sapiens 10-17 29032755-4 2019 Improving insulin sensitivity is anticipated to both lower the plasma glucose concentration and decrease CVD risk in T2DM patients, independent of glucose control. Glucose 147-154 insulin Homo sapiens 10-17 30426902-1 2019 Pregnancy hypertensive disorders such as Preeclampsia (PE) are strongly correlated with insulin resistance, a condition in which the metabolic handling of D-glucose is deficient. Glucose 155-164 insulin Homo sapiens 88-95 30205799-6 2019 A reduction in the removal of the extracellular D-glucose is seen in states of insulin resistance, such as in diabetes mellitus and obesity. Glucose 48-57 insulin Homo sapiens 79-86 31512997-3 2019 Insulin signaling regulates metabolic homeostasis by regulating glucose and lipid turnover in the liver, skeletal muscle and adipose tissue. Glucose 64-71 insulin Homo sapiens 0-7 30488797-5 2019 Insulin resistance is defined as a pathological condition characterized by reduced sensitivity of skeletal muscles, liver, and adipose tissue, to insulin and its downstream metabolic effects under normal serum glucose concentrations. Glucose 210-217 insulin Homo sapiens 0-7 30714526-3 2019 Diabetes type II, the Non Insulin Dependent Type (NIDDM) is the most common type, characterized by the impairment in activation of the intracellular mechanism leading to the insertion and usage of glucose after interaction of insulin with its receptor, known as insulin resistance. Glucose 197-204 insulin Homo sapiens 26-33 30714526-3 2019 Diabetes type II, the Non Insulin Dependent Type (NIDDM) is the most common type, characterized by the impairment in activation of the intracellular mechanism leading to the insertion and usage of glucose after interaction of insulin with its receptor, known as insulin resistance. Glucose 197-204 insulin Homo sapiens 226-233 31660832-4 2019 In late-stage T2DM, impaired insulin production requires the patients to receive insulin replacement therapy for maintaining their glucose homeostasis. Glucose 131-138 insulin Homo sapiens 29-36 30714526-3 2019 Diabetes type II, the Non Insulin Dependent Type (NIDDM) is the most common type, characterized by the impairment in activation of the intracellular mechanism leading to the insertion and usage of glucose after interaction of insulin with its receptor, known as insulin resistance. Glucose 197-204 insulin Homo sapiens 262-269 30573674-2 2019 My early studies focused on understanding how insulin promotes glucose transport into adipocytes, a classic model of highly insulin-responsive target cells. Glucose 63-70 insulin Homo sapiens 46-53 30573674-2 2019 My early studies focused on understanding how insulin promotes glucose transport into adipocytes, a classic model of highly insulin-responsive target cells. Glucose 63-70 insulin Homo sapiens 124-131 31336505-5 2019 Accordingly, insulin resistance estimated by glucose tolerance tests is better predictor of future cardiovascular events than fasting glucose level in nondiabetic individuals. Glucose 45-52 insulin Homo sapiens 13-20 31405694-6 2019 Moreover, the proposed index based on the oral glucose tolerance test (OGTT), which considers the glucose metabolism process and the hepatic and peripheral insulin sensitivity, showed stronger correlations with the Stumvoll method and lower intergroup variability than the fasting one. Glucose 47-54 insulin Homo sapiens 156-163 31425958-0 2019 Use of flash glucose monitoring system in assessing safety of the SGLT2 inhibitors during Ramadan fasting in high risk insulin treated patients with type 2 diabetes. Glucose 13-20 insulin Homo sapiens 119-126 30047223-0 2019 Closed-loop driven by control-to-range algorithm outperforms threshold-low-glucose-suspend insulin delivery on glucose control albeit not on nocturnal hypoglycaemia in prepubertal patients with type 1 diabetes in a supervised hotel setting. Glucose 111-118 insulin Homo sapiens 91-98 30315341-6 2019 Insulin sensitivity was assessed by oral glucose insulin sensitivity index and beta-cell function by mathematical modelling of the plasma glucose, insulin and C-peptide concentrations. Glucose 41-48 insulin Homo sapiens 0-7 30620643-7 2019 CONCLUSIONS: Results suggest that insulin bolus delivery with fast delivery speed may result in more rapid insulin absorption and, thus, may provide a better control of meal-related glucose excursions than that obtained with bolus delivery using slow delivery speeds. Glucose 182-189 insulin Homo sapiens 34-41 30641711-0 2019 Triglycerides and glucose index as an insulin resistance marker in a sample of healthy adults. Glucose 18-25 insulin Homo sapiens 38-45 30641711-1 2019 AIM: To assess the association between elevated triglycerides/glucose index (TGI) and insulin resistance (IR) or hyperinsulinemia after oral glucose tolerance test (OGTT) in a sample of healthy adults. Glucose 62-69 insulin Homo sapiens 86-93 30641711-1 2019 AIM: To assess the association between elevated triglycerides/glucose index (TGI) and insulin resistance (IR) or hyperinsulinemia after oral glucose tolerance test (OGTT) in a sample of healthy adults. Glucose 141-148 insulin Homo sapiens 86-93 30641715-2 2019 The elevated blood glucose level results due to impairment in the production and action of insulin. Glucose 19-26 insulin Homo sapiens 91-98 30641727-1 2019 Type 1 and type 2 diabetes mellitus is a serious and lifelong condition commonly characterised by abnormally elevated blood glucose levels due to a failure in insulin production or a decrease in insulin sensitivity and function. Glucose 124-131 insulin Homo sapiens 159-166 30641727-1 2019 Type 1 and type 2 diabetes mellitus is a serious and lifelong condition commonly characterised by abnormally elevated blood glucose levels due to a failure in insulin production or a decrease in insulin sensitivity and function. Glucose 124-131 insulin Homo sapiens 195-202 31332996-5 2019 Insulin Producing Cells was induced to differentiate from human Umbilical Cord-Mesenchymal Stem Cells and characterized by morphology under phase contrast inverted microscope and staining of secretory granules by DTZ (diphenylthiocarbonazone) stain, then therapeutic effect was evaluated both in vitro and in vivo through glucose challenge test and hyperglycemia correction in STZ (streptozotocin)- induced diabetic rats. Glucose 322-329 insulin Homo sapiens 0-7 30175925-0 2019 Optimising use of rate-of-change trend arrows for insulin dosing decisions using the FreeStyle Libre flash glucose monitoring system. Glucose 107-114 insulin Homo sapiens 50-57 30175925-1 2019 Continuous glucose monitoring and flash glucose monitoring systems are increasingly used by people with diabetes on multiple daily injections of insulin and continuous subcutaneous insulin infusion. Glucose 40-47 insulin Homo sapiens 145-152 30175925-1 2019 Continuous glucose monitoring and flash glucose monitoring systems are increasingly used by people with diabetes on multiple daily injections of insulin and continuous subcutaneous insulin infusion. Glucose 40-47 insulin Homo sapiens 181-188 31235164-1 2019 AIMS: Plasma glucose and insulin concentrations in fasting and postprandial reflect the metabolism of glucose by the human body and are useful in the diagnosis of metabolic diseases, such as diabetes and insulin resistance. Glucose 13-20 insulin Homo sapiens 204-211 31235164-1 2019 AIMS: Plasma glucose and insulin concentrations in fasting and postprandial reflect the metabolism of glucose by the human body and are useful in the diagnosis of metabolic diseases, such as diabetes and insulin resistance. Glucose 102-109 insulin Homo sapiens 25-32 31235164-1 2019 AIMS: Plasma glucose and insulin concentrations in fasting and postprandial reflect the metabolism of glucose by the human body and are useful in the diagnosis of metabolic diseases, such as diabetes and insulin resistance. Glucose 102-109 insulin Homo sapiens 204-211 31235164-5 2019 RESULTS AND CONCLUSION: The process of deterioration of glucose metabolism advances with the age of the subject, more than half of the prediabetics have impaired glucose levels in fasting but normal in postprandial and normal insulin levels in fasting and postprandial, and one third of diabetics have diabetic glucose levels in fasting and postprandial and normal insulin levels in fasting and postprandial. Glucose 56-63 insulin Homo sapiens 226-233 31235164-5 2019 RESULTS AND CONCLUSION: The process of deterioration of glucose metabolism advances with the age of the subject, more than half of the prediabetics have impaired glucose levels in fasting but normal in postprandial and normal insulin levels in fasting and postprandial, and one third of diabetics have diabetic glucose levels in fasting and postprandial and normal insulin levels in fasting and postprandial. Glucose 56-63 insulin Homo sapiens 365-372 30651864-0 2019 Correlation of insulin-resistance with blood fat and glucose in elder patients after surgery for hepatic carcinoma. Glucose 53-60 insulin Homo sapiens 15-22 30172767-1 2019 INTRODUCTION AND OBJECTIVE: Hypoglycemia associated to insulin or other glucose-lowering agents is one of the most common causes of visits to the emergency department for adverse drug reactions. Glucose 72-79 insulin Homo sapiens 55-62 30172767-9 2019 Insulin with or without other concomitant glucose-lowering agents was associated to 78.7% of episodes in type 2 DM patients. Glucose 42-49 insulin Homo sapiens 0-7 30827271-4 2019 Insulin sensitivity by the peripheral glucose uptake tissues is also changed by the altered epigenetic mechanisms. Glucose 38-45 insulin Homo sapiens 0-7 30020828-7 2019 After palmitate treatment, triacylglycerol accumulation, insulin-induced Akt (Ser-473) phosphorylation, and insulin-stimulated glucose uptake were significantly reduced in FIT2 knockdown adipocytes compared with control cells. Glucose 127-134 insulin Homo sapiens 108-115 30869153-10 2019 After the transplantation of the beta cell progenitors into immunocompromised diabetic mice, a few weeks have to pass before the increased insulin levels in response to glucose load appear. Glucose 169-176 insulin Homo sapiens 139-146 30326225-8 2019 The glucose consumption increased 46.4%, 50.5%, 82.1% and 53.6%; 86.8%, 81.6%, 86.8% and 84.2% at the concentration of 20 mug/mL, respectively, without or with insulin. Glucose 4-11 insulin Homo sapiens 160-167 30141098-4 2019 Insulin is capable to increase glucose uptake in human brown adipose tissue fivefold to fasting conditions. Glucose 31-38 insulin Homo sapiens 0-7 31177228-1 2019 BACKGROUND: In addition to glucose metabolism, adipocytokine Nicotinamide phosphoribosyltransferase (Nampt) has been proposed as a multifunctional protein involved in insulin resistance. Glucose 27-34 insulin Homo sapiens 167-174 30232738-1 2019 Hypertensive patients with normal glucose tolerance (NGT) but 1-h post-load plasma glucose >= 155 mg/dl (1-h high), during an oral glucose tolerance test (OGTT), show higher insulin resistance and multiple target organ damages. Glucose 83-90 insulin Homo sapiens 177-184 30232738-1 2019 Hypertensive patients with normal glucose tolerance (NGT) but 1-h post-load plasma glucose >= 155 mg/dl (1-h high), during an oral glucose tolerance test (OGTT), show higher insulin resistance and multiple target organ damages. Glucose 83-90 insulin Homo sapiens 177-184 30371795-5 2019 In contrast, insulin-mediated glucose disposal was comparable in both groups. Glucose 30-37 insulin Homo sapiens 13-20 30458503-2 2019 It intends to investigate PA"s immediate effect on insulin-independent glucose variation and PA"s prolonged effect on insulin sensitivity. Glucose 71-78 insulin Homo sapiens 51-58 30398029-1 2019 Previous study has shown that thiazolidinediones (TZDs) improved endothelium insulin resistance (IR) induced by high glucose concentration (HG)/hyperglycaemia through a PPARgamma-dependent-NFkappaB trans-repression mechanism. Glucose 117-124 insulin Homo sapiens 77-84 30252100-7 2019 Main Outcome Measures: Insulin sensitivity (insulin-mediated glucose uptake normalized for steady-state insulin; hyperinsulinemic-euglycemic clamp), postprandial glucose, insulin and fatty acid concentrations, insulin secretion (mixed meal tolerance test with mathematical modeling), insulin clearance, body composition and fat distribution (dual-energy X-ray absorptiometry, MRI, and spectroscopy), cardiorespiratory fitness (maximal oxygen uptake; graded exercise test), and handgrip strength (dynamometry). Glucose 61-68 insulin Homo sapiens 44-51 30252100-10 2019 The postprandial glucose concentrations were ~8% lower, the insulin-mediated glucose uptake was ~16% greater, and the meal-induced suppression of fatty acid concentrations was significantly greater in women than in men (P < 0.05 for all). Glucose 77-84 insulin Homo sapiens 60-67 30371795-8 2019 Conclusions: The results of the present study have demonstrated that (i) glucose-mediated glucose disposal is impaired in those with IFG; (ii) insulin-mediated glucose uptake in IFG is normal; and (iii) insulin action to suppress EGP is impaired. Glucose 73-80 insulin Homo sapiens 203-210 29848104-0 2019 In Silico Assessment of Literature Insulin Bolus Calculation Methods Accounting for Glucose Rate of Change. Glucose 84-91 insulin Homo sapiens 35-42 29848105-1 2019 Antidiabetic therapeutics, including insulin as well as glucagon-like peptide 1 (GLP-1) and its analogs, are essential for people with diabetes to regulate their blood glucose levels. Glucose 168-175 insulin Homo sapiens 37-44 29940703-1 2019 Diabetes mellitus type 1 and type 2 are diseases characterized by impaired regulation of blood glucose due to decreased insulin production and insulin resistance, respectively. Glucose 95-102 insulin Homo sapiens 120-127 29940703-1 2019 Diabetes mellitus type 1 and type 2 are diseases characterized by impaired regulation of blood glucose due to decreased insulin production and insulin resistance, respectively. Glucose 95-102 insulin Homo sapiens 143-150 29746812-7 2019 Moderate correlation of all indicators (waist-to-height ratio, triglycerides/glucose index, and triglycerides-to-HDL-C ratio) with homeostatic model assessment for insulin resistance was observed for both sexes. Glucose 77-84 insulin Homo sapiens 164-171 30958080-6 2019 The insulin-loaded PEC could decrease blood glucose levels effectively and prolong insulin release after oral administration to diabetic rats. Glucose 44-51 insulin Homo sapiens 4-11 29457996-1 2019 OBJECTIVE: To investigate the factors associated with insulin resistance in children aged 4-7 years, and to identify the cutoff point of the triglyceride-glucose index for the prediction of insulin resistance in this population. Glucose 154-161 insulin Homo sapiens 190-197 29457996-10 2019 CONCLUSION: The present study identified that total and central body adiposity and shorter time spent in lively activities was positively associated with insulin resistance, evaluated through the triglyceride-glucose index. Glucose 209-216 insulin Homo sapiens 154-161 30071248-0 2019 1,25-Dihydroxyvitamin D3 enhances glucose-stimulated insulin secretion in mouse and human islets: a role for transcriptional regulation of voltage-gated calcium channels by the vitamin D receptor. Glucose 34-41 insulin Homo sapiens 53-60 30414190-1 2019 KEY POINTS: Exercise/exercise training can enhance insulin sensitivity through adaptations in skeletal muscle, the primary site of insulin-mediated glucose disposal; however, in humans the range of improvement can vary substantially. Glucose 148-155 insulin Homo sapiens 51-58 30414190-1 2019 KEY POINTS: Exercise/exercise training can enhance insulin sensitivity through adaptations in skeletal muscle, the primary site of insulin-mediated glucose disposal; however, in humans the range of improvement can vary substantially. Glucose 148-155 insulin Homo sapiens 131-138 30414190-8 2019 Prior to muscle contraction, insulin action was compromised in myotubes from the severely obese as was evident from reduced insulin-stimulated glycogen synthesis, glucose oxidation, glucose uptake, insulin signal transduction (IRS1, Akt, TBC1D4), and insulin-stimulated GLUT4 translocation. Glucose 163-170 insulin Homo sapiens 29-36 30414190-8 2019 Prior to muscle contraction, insulin action was compromised in myotubes from the severely obese as was evident from reduced insulin-stimulated glycogen synthesis, glucose oxidation, glucose uptake, insulin signal transduction (IRS1, Akt, TBC1D4), and insulin-stimulated GLUT4 translocation. Glucose 182-189 insulin Homo sapiens 29-36 30325018-3 2019 Studies in mice suggest that the AMPK-TBC1D4 signalling axis is important for the increased insulin-stimulated glucose uptake after a single bout of exercise. Glucose 111-118 insulin Homo sapiens 92-99 30071248-1 2019 AIM: Vitamin D deficiency in rodents negatively affects glucose-stimulated insulin secretion (GSIS) and human epidemiological studies connect poor vitamin D status with type 2 diabetes. Glucose 56-63 insulin Homo sapiens 75-82 30471281-2 2019 Type 2 diabetes is characterized by enhanced blood glucose level that promotes insulin resistance and hampers cellular glucose metabolism. Glucose 51-58 insulin Homo sapiens 79-86 31200402-0 2019 [Insulin resistance is an alimentary deficiency of energy substrates (glucose) in the biological reaction of exotrophy and aphysiology compensation by fatty acids via the biological reaction of endothrophy.] Glucose 70-77 insulin Homo sapiens 1-8 31200402-15 2019 Insulin resistance is a pathology associated primarily with FA and secondarily with glucose. Glucose 84-91 insulin Homo sapiens 0-7 30694188-3 2019 To achieve this control, it is necessary to adjust insulin doses, in type 1 or insulinized type 2 DM persons, based on traditional capillary glucose self-monitoring, which has limitations to generate an adequate data record, is invasive and has low adherence. Glucose 141-148 insulin Homo sapiens 51-58 30444986-7 2019 IPCs released insulin in response to glucose challenge. Glucose 37-44 insulin Homo sapiens 14-21 30247432-7 2019 In the fasted state, plasma glucose levels transiently dropped below 4.0 mmol L in five subjects, who had substantially higher serum insulin levels at the start of exercise, compared with those who did not develop hypoglycemia. Glucose 28-35 insulin Homo sapiens 133-140 30325018-4 2019 The present study is the first longitudinal intervention study to show that, although exercise training increases insulin-stimulated glucose uptake in skeletal muscle at rest, it diminishes the ability of a single bout of exercise to enhance muscle insulin-stimulated glucose uptake. Glucose 133-140 insulin Homo sapiens 114-121 30325018-4 2019 The present study is the first longitudinal intervention study to show that, although exercise training increases insulin-stimulated glucose uptake in skeletal muscle at rest, it diminishes the ability of a single bout of exercise to enhance muscle insulin-stimulated glucose uptake. Glucose 268-275 insulin Homo sapiens 249-256 30325018-6 2019 ABSTRACT: Not only chronic exercise training, but also a single bout of exercise, increases insulin-stimulated glucose uptake in skeletal muscle. Glucose 111-118 insulin Homo sapiens 92-99 30325018-15 2019 Interestingly, insulin-stimulated glucose uptake in the acutely exercised leg was not enhanced further by training. Glucose 34-41 insulin Homo sapiens 15-22 30325018-16 2019 Thus, the increase in insulin-stimulated glucose uptake following a single bout of one-legged exercise was lower in the trained vs. untrained state. Glucose 41-48 insulin Homo sapiens 22-29 30003444-0 2019 Insulin-dependent, glucose transporter 1 mediated glucose uptake and tube formation in the human placental first trimester trophoblast cells. Glucose 19-26 insulin Homo sapiens 0-7 30328623-4 2019 ABSTRACT: The vasodilator actions of insulin contribute to glucose uptake by skeletal muscle, and previous studies have demonstrated that acute and chronic physical activity improves insulin-stimulated vasodilatation and glucose uptake. Glucose 59-66 insulin Homo sapiens 37-44 30328623-4 2019 ABSTRACT: The vasodilator actions of insulin contribute to glucose uptake by skeletal muscle, and previous studies have demonstrated that acute and chronic physical activity improves insulin-stimulated vasodilatation and glucose uptake. Glucose 59-66 insulin Homo sapiens 183-190 30328623-4 2019 ABSTRACT: The vasodilator actions of insulin contribute to glucose uptake by skeletal muscle, and previous studies have demonstrated that acute and chronic physical activity improves insulin-stimulated vasodilatation and glucose uptake. Glucose 221-228 insulin Homo sapiens 37-44 32694809-2 2019 Here we identify a pathway linking the lipolytic enzyme hormone-sensitive lipase (HSL) to insulin action via the glucose-responsive transcription factor ChREBP and its target, the fatty acid elongase ELOVL6. Glucose 113-120 insulin Homo sapiens 90-97 30497926-5 2019 METHODS AND RESULTS: Healthy volunteers with BMI 25-29.9 kg/m2 underwent detailed metabolic phenotyping including insulin-mediated-glucose disposal, fasting/daylong glucose, insulin, triglycerides, FFA, and cholesterol. Glucose 131-138 insulin Homo sapiens 114-121 31258562-9 2019 Conclusion: The combination of insulin Glargine and Acarbose can significantly control the blood glucose level of elderly patients with diabetes, improve the biochemical indicators, and enhance the quality of life. Glucose 97-104 insulin Homo sapiens 31-38 30191503-1 2019 BACKGROUND: Obesity-induced insulin resistance leads to abnormalities in glucose, lipid, and amino acid metabolism. Glucose 73-80 insulin Homo sapiens 28-35 30191503-2 2019 Our study examined the differences in insulin-mediated glucose, amino acid, and lipid metabolism between morbidly obese subjects with non-obese controls and the associated changes following sleeve gastrectomy (SG). Glucose 55-62 insulin Homo sapiens 38-45 30191503-8 2019 Body weight significantly reduced at 6 months after bariatric surgery (92.5 +- 6.3 vs. 115.2 +- 6.9 kg), together with improvements in insulin-mediated glucose uptake, and suppression of BCAAs, non-esterified fatty acids, and lipid-related metabolites. Glucose 152-159 insulin Homo sapiens 135-142 30095738-6 2019 Islets were subsequently isolated, and preparations in each group matched for SCS or total preservation time were compared using dynamic glucose-stimulated insulin secretion as a measure of beta-cell function and RNA sequencing to elucidate transcriptomic changes. Glucose 137-144 insulin Homo sapiens 156-163 29558846-2 2019 Prompt early diagnosis is important, as insulin reduces glucose supply to the brain, resulting in significant brain injury and risk of death. Glucose 56-63 insulin Homo sapiens 40-47 30095738-7 2019 RESULTS: Persufflated pancreata had reduced SCS time, which resulted in islets with higher glucose-stimulated insulin secretion compared to islets from SCS only pancreata. Glucose 91-98 insulin Homo sapiens 110-117 30693047-1 2018 Background: Type-1 diabetes is a condition caused by the lack of insulin hormone, which leads to an excessive increase in blood glucose level. Glucose 128-135 insulin Homo sapiens 65-72 30707879-15 2019 However, only 23.7% (14/59) of patients with hyperglycemia were treated with insulin, the initiation of insulin therapy was triggered when median blood glucose level was 19.8 (16.8, 24.5) mmol/L. Glucose 152-159 insulin Homo sapiens 77-84 30707879-15 2019 However, only 23.7% (14/59) of patients with hyperglycemia were treated with insulin, the initiation of insulin therapy was triggered when median blood glucose level was 19.8 (16.8, 24.5) mmol/L. Glucose 152-159 insulin Homo sapiens 104-111 30746502-0 2019 Association Between Serum Adipsin Levels and Insulin Resistance in Subjects With Various Degrees of Glucose Intolerance. Glucose 100-107 insulin Homo sapiens 45-52 30590050-1 2018 Glucose-stimulated insulin secretion from islet beta cells is mediated by KATP channels. Glucose 0-7 insulin Homo sapiens 19-26 30568042-2 2018 Our aim was to identify primary (independent of insulin resistance) insulin hypersecretion in subjects with normal glucose tolerance and its role in the progression of dysglycemia. Glucose 115-122 insulin Homo sapiens 68-75 30568042-12 2018 CONCLUSION: Primary insulin hypersecretion, independent of insulin resistance, is associated with a worse clinical and metabolic phenotype in adults and adolescents and predicts deterioration of glucose control over time. Glucose 195-202 insulin Homo sapiens 20-27 30570241-7 2018 Moreover, C-reactive protein (CRP) levels were associated with plasma glucose and insulin levels measured 120 min after the glucose load (beta=0.91, p=0.0003 and beta=0.77, p=0.0006, respectively); ISI and EISI were predicted by CRP (beta=-0.79, p=0.0006; beta=-0.80, p=0.0001, respectively). Glucose 124-131 insulin Homo sapiens 82-89 30433876-6 2018 Insulin resistance was evaluated (homeostatic model assessment of insulin resistance [HOMA-IR]) by performing the oral glucose tolerance test (OGTT). Glucose 119-126 insulin Homo sapiens 0-7 30619718-7 2019 A major metabolic effect of insulin is the accumulation of glucose as glycogen in the liver. Glucose 59-66 insulin Homo sapiens 28-35 30572687-4 2018 Theaflavins significantly increased glucose uptake of insulin-resistant cells at noncytotoxic doses. Glucose 36-43 insulin Homo sapiens 54-61 30572687-7 2018 Mdivi-1, a selective mitochondrial division inhibitor, could attenuate TFs-induced promotion of glucose uptake in insulin-resistant HepG2 cells. Glucose 96-103 insulin Homo sapiens 114-121 30619717-6 2019 CGM-measured 24 h mean glucose level decreased significantly from 157.7 +- 22.9 to 152.3 +- 17.8 mg/dL, especially in the early glucose surge after the midnight nadir (from 28.3 +- 15.0 to 18.2 +- 9.9 mg/dL), and until supper with a significant improvement in homeostasis model assessment of insulin resistance from 4.0 +- 2.8 to 2.9 +- 1.6, respectively. Glucose 23-30 insulin Homo sapiens 292-299 30088095-9 2018 The inhibitor also increased glucose-stimulated insulin secretion in islets from donors with T2D, while having no effect on islets from non-diabetic donors. Glucose 29-36 insulin Homo sapiens 48-55 31457032-6 2018 Also, insulin secretion from the encapsulated and PEGylated groups was stimulated by glucose (i.e., 5.6 and 16.7 mM of glucose, respectively); showed insulin secretion similar to the naked islets, without coating, after 30 and 60 min of incubation. Glucose 85-92 insulin Homo sapiens 6-13 31457032-6 2018 Also, insulin secretion from the encapsulated and PEGylated groups was stimulated by glucose (i.e., 5.6 and 16.7 mM of glucose, respectively); showed insulin secretion similar to the naked islets, without coating, after 30 and 60 min of incubation. Glucose 119-126 insulin Homo sapiens 6-13 30574122-9 2018 In this review, we summarize recent advances in the understanding of the functions of Sirtuins in various insulin resistance-associated physiological processes, including inflammation, mitochondrial dysfunction, the insulin signaling pathway, glucose, and lipid metabolism. Glucose 243-250 insulin Homo sapiens 106-113 30655940-1 2019 GPR40 is a G-protein-coupled receptor which mediates fatty acid-induced glucose-stimulated insulin secretion from pancreatic beta cells and incretion release from enteroendocrine cells of the small intestine. Glucose 72-79 insulin Homo sapiens 91-98 30088095-10 2018 CONCLUSIONS: HDAC7 inhibition protects beta-cells from mitochondrial dysfunction and apoptosis, and increases glucose-stimulated insulin secretion in islets from human T2D donors. Glucose 110-117 insulin Homo sapiens 129-136 30106594-11 2018 Metabolism (MTT) quantification, dithizone staining, and glucose-stimulated insulin secretion assessment allow to discriminate, using a minimal number of animals, between treatments and validate the system. Glucose 57-64 insulin Homo sapiens 76-83 30191503-9 2019 CONCLUSIONS: Morbid obesity in Asian individuals was associated with impairment in the regulatory actions of insulin on glucose, amino acid, and lipid metabolism, and these obesity-induced regulatory dysfunctions improved significantly 6 months after SG. Glucose 120-127 insulin Homo sapiens 109-116 29268636-6 2018 The main focus of this review is to describe what we know to date of herbal extracts, along with their glucose-lowering mechanisms, which are either through insulin-mimicking activity, enhanced beta-cells regeneration, or glucose uptake. Glucose 103-110 insulin Homo sapiens 157-164 29514765-0 2018 Plasma fetuin-B concentrations are associated with insulin resistance and first-phase glucose-stimulated insulin secretion in individuals with different degrees of glucose tolerance. Glucose 86-93 insulin Homo sapiens 105-112 30372824-1 2018 Insulin, as the most important drug for the treatment of diabetes, can effectively control the blood glucose concentration in humans. Glucose 101-108 insulin Homo sapiens 0-7 30372824-2 2018 Due to its instability, short half-life, easy denaturation and side effects, the administration way of insulin are limited to subcutaneous injection accompany with poor glucose control and low patient compliance. Glucose 169-176 insulin Homo sapiens 103-110 29050649-5 2018 Insulin sensitivity was evaluated through frequently sampled intravenous glucose tolerance tests with minimal model analysis. Glucose 73-80 insulin Homo sapiens 0-7 30003666-7 2018 Triglycerides and triglyceride-rich VLDL (large and medium size fractions) were associated with both basal and glucose-stimulated insulin secretion, after adjustment for age, sex, ethnicity, BMI z-score, plasma glucose, and insulin sensitivity. Glucose 111-118 insulin Homo sapiens 130-137 30293953-0 2018 FITC-labeled d-glucose analog is suitable as a probe for detecting insulin-dependent glucose uptake. Glucose 13-22 insulin Homo sapiens 67-74 30293953-0 2018 FITC-labeled d-glucose analog is suitable as a probe for detecting insulin-dependent glucose uptake. Glucose 15-22 insulin Homo sapiens 67-74 30293953-1 2018 The detection of the insulin-dependent glucose uptake is a vital part in the research of diabetes. Glucose 39-46 insulin Homo sapiens 21-28 29514765-7 2018 CONCLUSION: Patients with nT2DM have significantly higher concentrations of plasma fetuin-B compared with NGT subjects and plasma fetuin-B is strongly associated with glucose and lipid metabolism, chronic inflammation and first-phase glucose-stimulated insulin secretion and insulin resistance. Glucose 234-241 insulin Homo sapiens 253-260 29514765-7 2018 CONCLUSION: Patients with nT2DM have significantly higher concentrations of plasma fetuin-B compared with NGT subjects and plasma fetuin-B is strongly associated with glucose and lipid metabolism, chronic inflammation and first-phase glucose-stimulated insulin secretion and insulin resistance. Glucose 234-241 insulin Homo sapiens 275-282 29907546-0 2018 Clinical value of Flash glucose monitoring in patients with type 1 diabetes treated with continuous subcutaneous insulin infusion. Glucose 24-31 insulin Homo sapiens 113-120 30302721-17 2018 CONCLUSION: Upon switching basaI insulin to Gla-300, overall glucose control significantly improved and glycemic targets were achieved with a low rate of hypoglycemia in T2D patients under real-world conditions in Switzerland. Glucose 61-68 insulin Homo sapiens 33-40 30305364-4 2018 This study in immune-compromised mice demonstrates that subcutaneous implants of Alg-encapsulated porcine prenatal islet cells with 4 x 105 beta-cells form, over 10 weeks, a FBM that results in glucose-induced plasma C-peptide >2 ng/mL and metabolic control over the following 10 weeks, with higher efficiency than nonencapsulated, while failing in peritoneum. Glucose 194-201 insulin Homo sapiens 217-226 30232211-6 2018 Their glucose levels began to diverge at 30 min of the OGTT with increasing insulin levels, and by 120 min, their insulin levels were three times higher. Glucose 6-13 insulin Homo sapiens 76-83 29907546-1 2018 AIM: To analyze the clinical impact of the Flash glucose monitoring system in patients with type 1 diabetes mellitus (T1DM) treated with continuous subcutaneous insulin infusion (CSII). Glucose 49-56 insulin Homo sapiens 161-168 30692335-6 2018 Furthermore, her blood glucose level is well controlled with insulin therapy. Glucose 23-30 insulin Homo sapiens 61-68 30289728-6 2018 Strategies addressing weight excess and abdominal adiposity, from lifestyle modification to insulin sensitizers, may improve insulin resistance and glucose tolerance in women with PCOS. Glucose 148-155 insulin Homo sapiens 92-99 30307821-5 2018 beta-Cell function was defined from glucose-stimulated insulin secretion (GSIS, deconvolution modeling) and the disposition index (DI). Glucose 36-43 insulin Homo sapiens 55-62 31239850-11 2018 In addition, the patients who use insulin better control their blood glucose, thus reducing the need of newborns for intensive care. Glucose 69-76 insulin Homo sapiens 34-41 30311825-7 2018 Glucose and HbA1c levels were significantly reduced after supplementation (135.7 +- 19.5 mg/dL vs. 126.5 +- 16.8 mg/dL and 8.3% +- 0.3% vs. 6.03% +- 0.58%, respectively, P < .05); however, insulin was significantly increased (3.6 +- 0.7 muIU/mL vs. 6.8 +- 0.2 muIU/mL, P < .05). Glucose 0-7 insulin Homo sapiens 192-199 30311825-10 2018 Daily supplementation with an individualized ALA, carnosine, and thiamine supplement effectively reduced glucose concentration in type 2 diabetic patients, probably by increasing insulin production from the pancreas. Glucose 105-112 insulin Homo sapiens 179-186 30392154-6 2018 The insulin kinetics model suggests that the increase in surface area associated with exercise-induced capillary recruitment significantly increases [Formula: see text] and [Formula: see text], which explains why insulin concentrations in plasma and skeletal muscle increase during exercise, ultimately enhancing insulin-dependent glucose uptake. Glucose 331-338 insulin Homo sapiens 4-11 30326527-0 2018 Altering Physical Activity Influences Insulin Responses to Glucose Ingestion in Healthy Adults. Glucose 59-66 insulin Homo sapiens 38-45 30109666-12 2018 As VAT is associated with insulin resistance, this reduction may account for the profound impact of this surgery on glucose metabolism. Glucose 116-123 insulin Homo sapiens 26-33 30439604-8 2018 Simultaneously, the inhibitory effects of HG on insulin-triggered glucose uptake and nephrin expression were overturned after celastrol exposure. Glucose 66-73 insulin Homo sapiens 48-55 30392154-6 2018 The insulin kinetics model suggests that the increase in surface area associated with exercise-induced capillary recruitment significantly increases [Formula: see text] and [Formula: see text], which explains why insulin concentrations in plasma and skeletal muscle increase during exercise, ultimately enhancing insulin-dependent glucose uptake. Glucose 331-338 insulin Homo sapiens 213-220 30392154-6 2018 The insulin kinetics model suggests that the increase in surface area associated with exercise-induced capillary recruitment significantly increases [Formula: see text] and [Formula: see text], which explains why insulin concentrations in plasma and skeletal muscle increase during exercise, ultimately enhancing insulin-dependent glucose uptake. Glucose 331-338 insulin Homo sapiens 213-220 30160046-7 2018 Pathway analysis and miRNA target prediction suggested that these miRNAs were particularly involved in insulin signalling, glucose transport, insulin resistance, cholesterol and lipid metabolism. Glucose 123-130 insulin Homo sapiens 103-110 30207079-0 2018 Exercise and glucose control in children with insulin resistance: prevalence of non-responders. Glucose 13-20 insulin Homo sapiens 46-53 30592185-1 2018 Ras-related C3 botulinum toxin substrate 1 (Rac1) is required for normal insulin-stimulated glucose transport in skeletal muscle and evidence indicates Rac1 may be negatively regulated by lipids. Glucose 92-99 insulin Homo sapiens 73-80 30664340-2 2018 IR can be selective, involving only certain aspects of insulin action, i.e. only its impact on hepatic glucose disposal. Glucose 103-110 insulin Homo sapiens 55-62 30664340-10 2018 Physiologic situations that require organisms to reserve priority nutrient access for an emerging metabolic requirement, for example immune system activation or foetal development, promote the decrease of systemic insulin sensitivity, reducing nutrient uptake by non-priority tissues and reserving glucose for priority cells. Glucose 298-305 insulin Homo sapiens 214-221 30120825-0 2018 Adjusting Insulin Delivery to Activity (AIDA) clinical trial: Effects of activity-based insulin profiles on glucose control in children with type 1 diabetes. Glucose 108-115 insulin Homo sapiens 88-95 30132574-7 2018 These cells also produced and released insulin in a glucose-responsive manner. Glucose 52-59 insulin Homo sapiens 39-46 30185719-10 2018 In conclusion, the t1/2 for insulin was elongated 2 to 7 times after massive overdosing, explaining why glucose supplementation is needed for long periods in these cases. Glucose 104-111 insulin Homo sapiens 28-35 30254065-9 2018 Placental exosomes from GDM pregnancies decreased insulin-stimulated migration and glucose uptake in primary skeletal muscle cells obtained from patients with normal insulin sensitivity. Glucose 83-90 insulin Homo sapiens 50-57 30656194-4 2019 The oral glucose tolerance test (OGTT) provides 1.2- to 3.5-fold more diagnoses of impaired glucose homeostasis and diabetes, and adequately measures insulin sensitivity, insulin secretion, and beta-cell function. Glucose 9-16 insulin Homo sapiens 150-157 30656194-4 2019 The oral glucose tolerance test (OGTT) provides 1.2- to 3.5-fold more diagnoses of impaired glucose homeostasis and diabetes, and adequately measures insulin sensitivity, insulin secretion, and beta-cell function. Glucose 9-16 insulin Homo sapiens 171-178 30228187-2 2018 Here, we sought to investigate the mechanism by which the secreted protein complement 1q-like-3 (C1ql3) regulates insulin secretion from pancreatic beta-cells, a key process affecting whole-body glucose metabolism. Glucose 195-202 insulin Homo sapiens 114-121 30228187-4 2018 However, to a lesser extent, C1ql3 also reduced insulin secretion in response to KCl, the potassium channel blocker tolbutamide, and high glucose. Glucose 138-145 insulin Homo sapiens 48-55 30228187-9 2018 We found that siRNA-mediated Bai3 knockdown in INS1(832/13) cells increased glucose-stimulated insulin secretion. Glucose 76-83 insulin Homo sapiens 95-102 30519194-19 2018 The study suggests that insulin might affect UGE through other ways, in addition to the direct blood glucose-lowering effect, thereby resulting in reduced UGE. Glucose 101-108 insulin Homo sapiens 24-31 30584465-8 2018 The major effects of IL-4 on the liver were to promote energy storage by boosting insulin-stimulated glucose uptake and lipid synthesis. Glucose 101-108 insulin Homo sapiens 82-89 30459202-2 2018 This interest is related to the importance of the GLUTs as archetypical membrane transport facilitators, as key limiters of the supply of glucose to cell metabolism, as targets of cell insulin and exercise signalling and of regulated membrane traffic, and as potential drug targets to combat cancer and metabolic diseases such as type 2 diabetes and obesity. Glucose 138-145 insulin Homo sapiens 185-192 30415638-4 2018 CONCLUSIONS: Because he showed elevated levels for insulin and prolonged high insulin levels in an oral glucose tolerance test, our case supports the theory that portocaval shunts cause a reduced hepatic insulin reduction due to the high blood volume bypassing the liver. Glucose 104-111 insulin Homo sapiens 78-85 30410753-7 2018 These results indicated that under nutritional restriction, reduced insulin-mediated glucose uptake and metabolism and increased lipolysis in adipose tissues was related to extracellular high glutamate concentration. Glucose 85-92 insulin Homo sapiens 68-75 30183308-1 2018 In obese children with high circulating concentrations of free fatty acid palmitate, we have observed that insulin levels at fasting and in response to a glucose challenge were several times higher than in obese children with low concentrations of the fatty acid as well as in lean controls. Glucose 154-161 insulin Homo sapiens 107-114 30256894-8 2018 Insulin resistance and insulin secretion were assessed in an oral-glucose-tolerance test and a meal-glucose-tolerance test. Glucose 66-73 insulin Homo sapiens 0-7 30325644-8 2018 Insulin therapy should be initiated if there are signs of ketosis or ketoacidosis, or if the patient has significant hyperglycemia (A1C greater than 9% or a random plasma glucose level of 250 mg per dL or greater). Glucose 171-178 insulin Homo sapiens 0-7 29553285-1 2018 Intravenous insulin with glucose is used in urgent treatment for hyperkalemia but has a significant risk of hypoglycemia. Glucose 25-32 insulin Homo sapiens 12-19 29444588-5 2018 Insulin sensitivity was determined by oral glucose tolerance test and carotid intima-media thickness (cIMT) by high-resolution ultrasound. Glucose 43-50 insulin Homo sapiens 0-7 30206707-3 2018 Furthermore, Tau can also ameliorate glucose metabolism through the enhancement of insulin signaling. Glucose 37-44 insulin Homo sapiens 83-90 29210770-4 2018 This strategy yielded 85.61% glucose-responsive insulin-positive cells in vitro, which was seven times higher than the basal level, and electron microscopy images revealed the presence of mature beta-cell secretory granules. Glucose 29-36 insulin Homo sapiens 48-55 29210770-5 2018 The generation of glucose-responsive insulin-secreting beta-like cells from human-induced pluripotent stem cells (hiPSCs) in vitro would provide a promising approach to produce an unprecedented cell source for cell transplantation therapy in diabetes without the ethical obstacle of embryonic stem cells and would bypass immune rejection. Glucose 18-25 insulin Homo sapiens 37-44 29524196-2 2018 The importance of V is attributed due to its multifaceted biological roles, i.e., glucose and lipid metabolism as an insulin-mimetic, antilipemic and a potent stress alleviating agent in diabetes when vanadium is administered at lower doses. Glucose 82-89 insulin Homo sapiens 117-124 29524196-4 2018 The intracellular enzyme protein tyrosine phosphatase, causing the dephosphorylation at beta subunit of the insulin receptor, is inhibited by vanadium, thus facilitating the uptake of glucose inside the cell but only in the presence of insulin. Glucose 184-191 insulin Homo sapiens 108-115 29524196-4 2018 The intracellular enzyme protein tyrosine phosphatase, causing the dephosphorylation at beta subunit of the insulin receptor, is inhibited by vanadium, thus facilitating the uptake of glucose inside the cell but only in the presence of insulin. Glucose 184-191 insulin Homo sapiens 236-243 30632974-4 2018 On the one hand, HDL are involved in the regulation of insulin secretion by b-cells and insulin-independent absorption of glucose. Glucose 122-129 insulin Homo sapiens 88-95 29947924-6 2018 Although elevated insulin levels and adipogenesis remodel the Kv phenotype, which could lead to multiple heteromeric complexes, Kv1.3 markedly participates in the insulin-dependent regulation of glucose uptake in mature adipocytes. Glucose 195-202 insulin Homo sapiens 163-170 29885045-10 2018 Whether long-term improvements in insulin-induced muscle perfusion may prove beneficial for glucose disposal remains to be determined. Glucose 92-99 insulin Homo sapiens 34-41 30063816-10 2018 People with conversion to normal glucose tolerance showed a greater increase in the 60-min insulinogenic index and disposition index and a smaller decrease in the composite insulin sensitivity index compared with people without conversion during 10 years of follow-up (all p-values < 0.001). Glucose 33-40 insulin Homo sapiens 91-98 30063816-11 2018 CONCLUSION: A higher insulin secretory capacity at baseline and during follow-up and higher baseline muscle to fat ratio were independently associated with an improvement in glucose tolerance in Korean adults with prediabetes. Glucose 174-181 insulin Homo sapiens 21-28 30213882-2 2018 Both hormones are lacking in type 1 diabetes, and postprandial glucose control using insulin therapy alone is difficult. Glucose 63-70 insulin Homo sapiens 85-92 29226733-8 2018 The enteric-coated insulin microparticles delivered by iturin plus surfactin showed a classical profile for controlled release in the intestine with a relative bioavailability of 7.67% after oral administration, which could effectively control the postprandial blood glucose at a level about 50% of the initial one just like the subcutaneous injection. Glucose 267-274 insulin Homo sapiens 19-26 29226733-9 2018 Collectively, iturin plus surfactin is more efficient for oral delivering insulin than the sole one, and the resultant enteric-coated insulin microparticles are potential for the development of oral insulin to control postprandial blood glucose in diabetic patients. Glucose 237-244 insulin Homo sapiens 134-141 29688087-8 2018 Moreover, co-administration of insulin plus l-TCTP-PTD 13M2 reduced blood glucose levels compared to levels in diabetic rats treated with insulin plus l-TCTP-PTD 13. Glucose 74-81 insulin Homo sapiens 31-38 30430019-7 2018 Results: Indices of peripheral insulin sensitivity, including glucose-disposal rate (M value) and glucose infusion rate, were significantly increased after RYGB. Glucose 62-69 insulin Homo sapiens 31-38 30430019-7 2018 Results: Indices of peripheral insulin sensitivity, including glucose-disposal rate (M value) and glucose infusion rate, were significantly increased after RYGB. Glucose 98-105 insulin Homo sapiens 31-38 30559718-1 2018 Dysregulation of metabolic pathways leads to type 2 diabetes, characteristic of high glucose concentration caused by insulin resistance. Glucose 85-92 insulin Homo sapiens 117-124 30474549-0 2018 Relationship of insulin resistance estimated by triglyceride glucose index to arterial stiffness. Glucose 61-68 insulin Homo sapiens 16-23 30305465-1 2018 Insulin degludec (IDeg) is a new insulin formulation that facilitates long-term control of glucose level in humans. Glucose 91-98 insulin Homo sapiens 0-7 30305465-1 2018 Insulin degludec (IDeg) is a new insulin formulation that facilitates long-term control of glucose level in humans. Glucose 91-98 insulin Homo sapiens 33-40 30470728-0 2018 Withdrawal: Glucose regulates MafA transcription factor abundance and insulin gene expression by inhibiting AMP-activated protein kinase in pancreatic beta-cells. Glucose 12-19 insulin Homo sapiens 70-77 30524370-1 2018 Introduction: We have previously shown that fetuses of mothers with gestational diabetes mellitus (GDM) and insulin resistance exhibit a prolongation of fetal auditory event-related brain responses (fAER) compared to fetuses of normal glucose tolerant women during an oral glucose tolerance test (oGTT). Glucose 235-242 insulin Homo sapiens 108-115 30524370-1 2018 Introduction: We have previously shown that fetuses of mothers with gestational diabetes mellitus (GDM) and insulin resistance exhibit a prolongation of fetal auditory event-related brain responses (fAER) compared to fetuses of normal glucose tolerant women during an oral glucose tolerance test (oGTT). Glucose 273-280 insulin Homo sapiens 108-115 30451893-4 2018 Here, we monitored parameters that constitute the glucose-triggering pathway of insulin release. Glucose 50-57 insulin Homo sapiens 80-87 30451893-5 2018 Both cell lines respond to glucose (6 and 20 mM) with 2- to 3-fold stimulation of insulin secretion which correlated with an elevation of [Ca2+]i, membrane depolarisation and increased action potential firing. Glucose 27-34 insulin Homo sapiens 82-89 30581872-0 2018 Fasting Plasma Glucose Indicates Reversibility of the Acute Insulin Response after Short-Term Intensive Insulin Therapy in Patients with Various Duration of Type 2 Diabetes. Glucose 15-22 insulin Homo sapiens 60-67 30581872-0 2018 Fasting Plasma Glucose Indicates Reversibility of the Acute Insulin Response after Short-Term Intensive Insulin Therapy in Patients with Various Duration of Type 2 Diabetes. Glucose 15-22 insulin Homo sapiens 104-111 30428550-4 2018 Gluten peptides enter the pancreas where they affect the morphology and might induce beta-cell stress by enhancing glucose- and palmitate-stimulated insulin secretion. Glucose 115-122 insulin Homo sapiens 149-156 29295631-3 2018 Mitochondrial energy production is essential for the major task of beta cells (the secretion of insulin in response to glucose). Glucose 119-126 insulin Homo sapiens 96-103 30487972-14 2018 If repeatable in humans, the more rapid glucose response may be of importance in a dual-hormone artificial pancreas using the intraperitoneal route for administration of insulin and glucagon. Glucose 40-47 insulin Homo sapiens 170-177 30099506-11 2018 Knockdown of TF in differentiated Simpson-Golabi-Behmel syndrome adipocytes by short hairpin RNA decreased intracellular iron, reduced maximal insulin-stimulated glucose uptake, and reduced Akt phosphorylation. Glucose 162-169 insulin Homo sapiens 143-150 30344817-3 2018 Meal-induced insulin response (MIR) was calculated as the ratio between the incremental insulin and glucose concentrations during the first 30 min of meal tests. Glucose 100-107 insulin Homo sapiens 13-20 29537733-0 2018 Delay in glucose peak time during the oral glucose tolerance test as an indicator of insulin resistance and insulin secretion in type 2 diabetes patients. Glucose 9-16 insulin Homo sapiens 85-92 29537733-0 2018 Delay in glucose peak time during the oral glucose tolerance test as an indicator of insulin resistance and insulin secretion in type 2 diabetes patients. Glucose 43-50 insulin Homo sapiens 85-92 29537733-8 2018 CONCLUSIONS: Delay in glucose peak time indicated an increase in blood glucose and a decrease in insulin sensitivity and secretion. Glucose 22-29 insulin Homo sapiens 97-104 29582571-6 2018 RESULTS: The rates of endogenous glucose production during fasting were similar, and endogenous glucose production was completely suppressed during insulin clamp for both ethnic groups. Glucose 96-103 insulin Homo sapiens 148-155 29624902-0 2018 One-hour oral glucose tolerance test plasma glucose at gestational diabetes diagnosis is a common predictor of the need for insulin therapy in pregnancy and postpartum impaired glucose tolerance. Glucose 14-21 insulin Homo sapiens 124-131 29624902-0 2018 One-hour oral glucose tolerance test plasma glucose at gestational diabetes diagnosis is a common predictor of the need for insulin therapy in pregnancy and postpartum impaired glucose tolerance. Glucose 44-51 insulin Homo sapiens 124-131 29624902-7 2018 Logistic regression analysis showed that gestational weeks at GDM diagnosis, 1-h glucose levels in a 75-g OGTT and glycated hemoglobin were significant predictors of the need for insulin therapy, and 1-h glucose levels in a 75-g OGTT at diagnosis and ketone bodies in a urine test were significant predictors for postpartum IGT. Glucose 81-88 insulin Homo sapiens 179-186 29624902-8 2018 CONCLUSIONS: Antepartum 1-h glucose levels in a 75-g OGTT was a predictor of the need for insulin therapy in pregnancy and postpartum IGT. Glucose 28-35 insulin Homo sapiens 90-97 29885744-0 2018 Continuous glucose monitoring guided insulin therapy is associated with improved clinical outcomes in cystic fibrosis-related diabetes. Glucose 11-18 insulin Homo sapiens 37-44 30288999-1 2018 AIMS: Closed-loop insulin delivery has the potential to improve day-to-day glucose control in type 1 diabetes pregnancy. Glucose 75-82 insulin Homo sapiens 18-25 30407917-7 2018 At later chase times or at steady state, Kalirin/Trio manipulations decreased glucose stimulated insulin output. Glucose 78-85 insulin Homo sapiens 97-104 30239760-5 2018 Glucose recovery time (GRT) was defined as the interval from cessation of insulin infusion to discontinuation of dextrose infusion. Glucose 0-7 insulin Homo sapiens 74-81 30322801-1 2018 Insulin resistance is a condition in which there is a defect in insulin actions to induce glucose uptake into the cells. Glucose 90-97 insulin Homo sapiens 0-7 30322801-6 2018 In this study, we demonstrate that chronic treatment with salbutamol, salmeterol, and formoterol inhibited insulin-induced glucose uptake and GLUT4 synthesis in H9c2 myoblast cells. Glucose 123-130 insulin Homo sapiens 107-114 29560554-0 2018 Effects of exosomes from LPS-activated macrophages on adipocyte gene expression, differentiation, and insulin-dependent glucose uptake. Glucose 120-127 insulin Homo sapiens 102-109 30383280-6 2018 Insulin secretion was assessed by the ratio of the area under the curve of insulin to the area under the curve of glucose at 30 min and at 120 min of an oral-glucose-tolerance test. Glucose 114-121 insulin Homo sapiens 0-7 30383280-6 2018 Insulin secretion was assessed by the ratio of the area under the curve of insulin to the area under the curve of glucose at 30 min and at 120 min of an oral-glucose-tolerance test. Glucose 158-165 insulin Homo sapiens 0-7 30403576-0 2018 Cost-effectiveness of Initiating an Insulin Pump in T1D Adults Using Continuous Glucose Monitoring Compared with Multiple Daily Insulin Injections: The DIAMOND Randomized Trial. Glucose 80-87 insulin Homo sapiens 36-43 30009519-6 2018 Three of the four individuals with impaired fasting glucose also had insulin resistance, as measured by HOMA-IR; an additional four subjects with normal glucose tolerance were insulin resistant. Glucose 52-59 insulin Homo sapiens 69-76 29725915-3 2018 Changes in a patient"s lifestyle, stress, exercise, or other activities may modify their blood glucose system, making it necessary to retune or change the insulin dosing algorithm. Glucose 95-102 insulin Homo sapiens 155-162 29923910-5 2018 RESULTS: After training, hypoxia, but not normoxia, decreased the area under the curve of plasma insulin (-49%; P = 0.001) and glucose levels (-14%; P = 0.005) during oral glucose tolerance test. Glucose 172-179 insulin Homo sapiens 97-104 29923910-7 2018 CONCLUSIONS: Hypoxic exercise training was particularly efficient at improving glucose tolerance and insulin response to a glucose challenge in adolescents with obesity. Glucose 123-130 insulin Homo sapiens 101-108 29885044-8 2018 Proinsulin secretory ratios were higher under hyperglycemic clamp conditions in PI-IGT and CFRD (P < .05 vs PI-NGT), and correlated with 1-hour glucose in PI-CF (P < .01). Glucose 147-154 insulin Homo sapiens 0-10 30315968-3 2018 Indeed, prominent pathways involved in glucose metabolism such as phosphatidylinositol 3-kinase/ protein kinase B (PI3-K/AKT) and 5" AMP-activated protein kinase (AMPK) are impaired in an insulin resistant state. Glucose 39-46 insulin Homo sapiens 188-195 30260514-7 2018 TNF-alpha-treated adipocytes showed a significant 64% decrease in insulin-stimulated glucose uptake as compared with control cells, whereas infliximab reversed TNF-alpha actions by significantly improving glucose incorporation. Glucose 85-92 insulin Homo sapiens 66-73 30487974-0 2018 Mealtime dosing of a rapid-acting insulin analog reduces glucose variability and suppresses daytime cardiac sympathetic activity: a randomized controlled study in hospitalized patients with type 2 diabetes. Glucose 57-64 insulin Homo sapiens 34-41 30052287-6 2018 API also had the highest glucose-stimulated insulin secretion response during a dynamic insulin secretion assay and had 50-fold higher total insulin content compared to NPI and JPI. Glucose 25-32 insulin Homo sapiens 44-51 30487974-10 2018 Conclusions: Mealtime insulin aspart reduced glucose variability to a greater extent than bedtime insulin detemir in patients with type 2 diabetes. Glucose 45-52 insulin Homo sapiens 22-29 30377436-7 2018 When dividing women with PCOS above and below the mean cutoff for insulin resistance, the insulin resistant women with PCOS had lower rates of non-oxidative glucose metabolism (p = 0.0001), higher levels of percent free testosterone (p = 0.04), a higher free androgen index (p = 0.006), more visceral adipose tissue (p = 0.02), and were less metabolically flexible (p = 0.007). Glucose 157-164 insulin Homo sapiens 90-97 30416973-0 2018 A higher blood glucose level pre-breakfast in comparison to bedtime is a contraindication for intensification of prandial insulin therapy in patients with type 2 diabetes - The impact of a negative BeAM value. Glucose 15-22 insulin Homo sapiens 122-129 30347680-6 2018 In addition, sulforhodamine B (SRB) assay, the quantification of insulin and glucose levels in differentiated skeletal muscle cell supernatants, reveals that functional dispersion regulates glucose and insulin levels to promote skeletal muscle cell proliferation. Glucose 77-84 insulin Homo sapiens 202-209 30347680-6 2018 In addition, sulforhodamine B (SRB) assay, the quantification of insulin and glucose levels in differentiated skeletal muscle cell supernatants, reveals that functional dispersion regulates glucose and insulin levels to promote skeletal muscle cell proliferation. Glucose 190-197 insulin Homo sapiens 65-72 30961089-0 2018 Preparation of Microparticles Capable of Glucose-Induced Insulin Release under Physiological Conditions. Glucose 41-48 insulin Homo sapiens 57-64 30336536-9 2018 CONCLUSIONS: Plasma insulin and HbA1c levels were significantly decreased in young adult malnourished patients without disease who had normal fasting glucose levels. Glucose 150-157 insulin Homo sapiens 20-27 30076159-6 2018 At baseline, insulin secretion was assessed by an oral glucose tolerance test (OGTT). Glucose 55-62 insulin Homo sapiens 13-20 30292578-21 2018 INTERPRETATION: Hybrid closed-loop insulin delivery improves glucose control while reducing the risk of hypoglycaemia across a wide age range in patients with suboptimally controlled type 1 diabetes. Glucose 61-68 insulin Homo sapiens 35-42 30307959-9 2018 Currently, a set of indices called HOMA-IR and HOMA-beta are used to represent insulin resistance and glucose-stimulated insulin response by beta cells respectively. Glucose 102-109 insulin Homo sapiens 121-128 30207680-6 2018 In the subsequent study, the bioactivity of encapsulated insulin during the cellular transportation was innovatively monitored by a glucose consumption assay. Glucose 132-139 insulin Homo sapiens 57-64 30697608-4 2019 Excellent therapeutic effects of islet transplantation as a result of accurate blood glucose level-reactive insulin secretion, which cannot be reproduced by current drug therapy, have been confirmed. Glucose 85-92 insulin Homo sapiens 108-115 30016674-8 2018 Moreover, the development of glucose-responsive systems for achieving MSN-based self-regulated insulin delivery, decorated with various components serving as sensors - glucose oxidase (GODx) and phenylboronic acid (PBA) that can control the insulin dosage, avoiding overdose leading to serious hypoglycemia. Glucose 29-36 insulin Homo sapiens 95-102 30016674-8 2018 Moreover, the development of glucose-responsive systems for achieving MSN-based self-regulated insulin delivery, decorated with various components serving as sensors - glucose oxidase (GODx) and phenylboronic acid (PBA) that can control the insulin dosage, avoiding overdose leading to serious hypoglycemia. Glucose 29-36 insulin Homo sapiens 241-248 30344510-7 2018 Compared to saline, lipid infusion lowered the rate of insulin stimulated glucose disposal (M value; mg/kg/min) by 67 +- 5% (from 0.5 +- 0.03 to -0.25 +- 0.2, p = 0.01) in PCOS, and by 49 +- 7% (from 0.65 +- 0.06 to 0.3 +- 0.1, p = 0.01) in controls. Glucose 74-81 insulin Homo sapiens 55-62 30291295-5 2018 Our results indicated that insulin-free high glucose culture significantly increased the size of and NPPB, SGLT1 and SGLT2 expression of hiPSC-derived cardiomyocytes. Glucose 45-52 insulin Homo sapiens 27-34 30078554-5 2018 Recovery of first-phase insulin response (0.04[-0.05-0.32] to 0.11[0.0005-0.51] nmol/min/m2, p < 0.0001) defined those who returned to non-diabetic glucose control and this was durable at 12 months (0.11[0.005-0.81] nmol/min/m2, p = 0.0001). Glucose 148-155 insulin Homo sapiens 24-31 29931422-1 2018 AIMS: Minimal model analysis of intravenous glucose tolerance test (IVGTT) data represents the reference method to assess insulin sensitivity (SI) and glucose effectiveness (SG) that quantify the insulin-dependent and insulin-independent processes of glucose disappearance, respectively. Glucose 151-158 insulin Homo sapiens 196-203 29931422-1 2018 AIMS: Minimal model analysis of intravenous glucose tolerance test (IVGTT) data represents the reference method to assess insulin sensitivity (SI) and glucose effectiveness (SG) that quantify the insulin-dependent and insulin-independent processes of glucose disappearance, respectively. Glucose 151-158 insulin Homo sapiens 196-203 29931422-8 2018 CONCLUSIONS: The interest for insulin-independent glucose disappearance is increasing, due to the recent availability of SGLT2 pharmacological agents, lowering glycemic levels without requiring insulin action. Glucose 50-57 insulin Homo sapiens 30-37 29931422-8 2018 CONCLUSIONS: The interest for insulin-independent glucose disappearance is increasing, due to the recent availability of SGLT2 pharmacological agents, lowering glycemic levels without requiring insulin action. Glucose 50-57 insulin Homo sapiens 194-201 30631000-1 2018 Insulin resistance is the disturbance of glucose regulation characterized by higher insulin level. Glucose 41-48 insulin Homo sapiens 0-7 30631000-1 2018 Insulin resistance is the disturbance of glucose regulation characterized by higher insulin level. Glucose 41-48 insulin Homo sapiens 84-91 30239554-0 2018 Adipose tissue and skeletal muscle insulin-mediated glucose uptake in insulin resistance: role of blood flow and diabetes. Glucose 52-59 insulin Homo sapiens 35-42 30239554-0 2018 Adipose tissue and skeletal muscle insulin-mediated glucose uptake in insulin resistance: role of blood flow and diabetes. Glucose 52-59 insulin Homo sapiens 70-77 30239554-1 2018 Background: Adipose tissue glucose uptake is impaired in insulin-resistant states, but ex vivo studies of human adipose tissue have yielded heterogeneous results. Glucose 27-34 insulin Homo sapiens 57-64 30239554-3 2018 Objective: The aim of this study was to test the flow dependency of in vivo insulin-mediated glucose uptake in fat tissues, and to contrast it with that of skeletal muscle. Glucose 93-100 insulin Homo sapiens 76-83 30239554-4 2018 Design: We reanalyzed data from 159 individuals in which adipose tissue depots-subcutaneous abdominal and femoral, and intraperitoneal-and femoral skeletal muscle were identified by MRI, and insulin-stimulated glucose uptake ([18F]-fluoro-2-deoxyglucose) and blood flow ([15O]-H2O) were measured simultaneously by positron emission tomography scanning. Glucose 210-217 insulin Homo sapiens 191-198 30239554-10 2018 Rates of glucose uptake were directly related to the degree of insulin resistance in all fat depots as well as in skeletal muscle. Glucose 9-16 insulin Homo sapiens 63-70 30239554-14 2018 Conclusions: Reduced blood supply is an important factor for the impairment of in vivo insulin-mediated glucose uptake in both subcutaneous and visceral fat. Glucose 104-111 insulin Homo sapiens 87-94 30239554-15 2018 In contrast, the insulin resistance of glucose uptake in resting skeletal muscle is predominantly a cellular defect. Glucose 39-46 insulin Homo sapiens 17-24 29878846-5 2018 The central action of insulin relies on autonomic outflow through the vagal innervation of the liver, where insulin is able to modulate the production of glucose at this organ level. Glucose 154-161 insulin Homo sapiens 22-29 29878846-5 2018 The central action of insulin relies on autonomic outflow through the vagal innervation of the liver, where insulin is able to modulate the production of glucose at this organ level. Glucose 154-161 insulin Homo sapiens 108-115 29260593-5 2018 We also aimed to investigate glucose-stimulated insulin and glucagon-like peptide-1 secretions as early pathogenetic mechanisms responsible for the development of carbohydrate intolerance. Glucose 29-36 insulin Homo sapiens 48-55 29260593-8 2018 We studied glucose-stimulated insulin and glucagon-like peptide-1 secretion during a 75 g oral glucose tolerance test. Glucose 11-18 insulin Homo sapiens 30-37 30251567-7 2018 ibeta basally secreted C-peptide, glucagon and ghrelin and released insulin in response either to increasing concentration of glucose or a depolarizing stimulus. Glucose 126-133 insulin Homo sapiens 68-75 29885025-0 2018 Adjusting insulin doses in patients with type 1 diabetes who use insulin pump and continuous glucose monitoring: Variations among countries and physicians. Glucose 93-100 insulin Homo sapiens 10-17 29856114-4 2018 The mean (SD) AUC glucose concentration for insulin dosing for both protein and carbohydrate was 8.3 (2.1) mmol/L compared with 10.0 (2.2) mmol/L for carbohydrate alone. Glucose 18-25 insulin Homo sapiens 44-51 30961089-7 2018 A 1 mg quantity of these particles released up to 10 mug insulin in the presence 10 mM glucose under physiological conditions. Glucose 87-94 insulin Homo sapiens 57-64 29885025-1 2018 AIMS: To evaluate physicians" adjustments of insulin pump settings based on continuous glucose monitoring (CGM) for patients with type 1 diabetes and to compare these to automated insulin dose adjustments. Glucose 87-94 insulin Homo sapiens 45-52 29939421-8 2018 CONCLUSION: Irrespective of the levels at which glycaemia is maintained, there is a 20-min low exogenous glucose demand period during which the exogenous glucose requirements to maintain stable glycaemia do not increase during moderate exercise performed at basal insulin level. Glucose 105-112 insulin Homo sapiens 264-271 30054673-10 2018 Glucose-stimulated first-phase insulin secretion and potassium-stimulated insulin secretion decreased by 53% and 59%, respectively, in perfused pancreases of 10-week-old Wfs1-/- mice compared with wild-type (WT) mice. Glucose 0-7 insulin Homo sapiens 31-38 30065032-2 2018 This effect may be mediated by inhibition of glucose-stimulated insulin secretion as well as reduced insulin sensitivity. Glucose 45-52 insulin Homo sapiens 64-71 30117055-4 2018 The addition of a DPP4 inhibitor to basal insulin is an attractive option, because they lower both postprandial and fasting plasma glucose concentrations without increasing the risk of hypoglycemia or weight gain. Glucose 131-138 insulin Homo sapiens 42-49 30082324-3 2018 We hypothesized that interrupting sitting with short bouts of moderate-intensity walking would decrease insulin area under the curve (AUC) during an oral glucose tolerance test (OGTT) compared with uninterrupted sitting. Glucose 154-161 insulin Homo sapiens 104-111 30054673-13 2018 The physiological relevance of the effects of Ex-4 was shown by the fact that a single administration potentiated glucose-stimulated insulin secretion and improved glucose tolerance in Wfs1-/- mice. Glucose 114-121 insulin Homo sapiens 133-140 30194951-4 2018 To evaluate the glucose-dependent insulin/glucagon responses without/with liraglutide, a 75-g oral glucose tolerance test (OGTT) was performed twice, before (1st-OGTT) and 2-days after (2nd-OGTT) liraglutide administration. Glucose 16-23 insulin Homo sapiens 34-41 30251560-1 2018 INTRODUCTION: Skeletal muscle is the major site of insulin-stimulated glucose uptake and imparts the beneficial effects of exercise, and hence is an important site of insulin resistance in obesity and type 2 diabetes (T2D). Glucose 70-77 insulin Homo sapiens 51-58 30194951-9 2018 CONCLUSIONS: Enhancement of glucose-dependent insulin-response under liraglutide administration is a potential predictor of long-term glycaemic control after switching the therapies. Glucose 28-35 insulin Homo sapiens 46-53 30207748-0 2018 Improved Postprandial Glucose with Inhaled Technosphere Insulin Compared with Insulin Aspart in Patients with Type 1 Diabetes on Multiple Daily Injections: The STAT Study. Glucose 22-29 insulin Homo sapiens 56-63 30299889-4 2018 As a morning dose of isophane insulin has a pharmacokinetic pattern that matches this pattern of glucose elevation, treatment comprising a basal dose of morning isophane insulin in combination with short-acting insulin boluses is generally recommended. Glucose 97-104 insulin Homo sapiens 30-37 30145684-0 2018 Valproate inhibits glucose-stimulated insulin secretion in beta cells. Glucose 19-26 insulin Homo sapiens 38-45 29637572-1 2018 Insulin is critical for the regulation of de novo fatty acid synthesis, which converts glucose to lipid in the liver. Glucose 87-94 insulin Homo sapiens 0-7 30145684-6 2018 Consequently, a reduction of glucose-stimulated insulin secretion is observed following VPA exposure. Glucose 29-36 insulin Homo sapiens 48-55 28959911-1 2018 Brain insulin-stimulated glucose uptake (GU) is increased in obese and insulin resistant subjects but normalizes after weight loss along with improved whole-body insulin sensitivity. Glucose 25-32 insulin Homo sapiens 6-13 29363047-8 2018 (iv) Finally, the need for greater appropriateness in the evaluation of possible coexistence is highlighted, in patients with PCOS who have fasting or glucose-stimulated very high insulin levels, or severe insulin-resistant states. Glucose 151-158 insulin Homo sapiens 180-187 30307162-0 2018 Mechanisms of beneficial effects of metformin on fatty acid-treated human islets Elevated levels of palmitate accentuate glucose-stimulated insulin secretion (GSIS) after short-term and cause beta-cell dysfunction after prolonged exposure. Glucose 121-128 insulin Homo sapiens 140-147 28959911-1 2018 Brain insulin-stimulated glucose uptake (GU) is increased in obese and insulin resistant subjects but normalizes after weight loss along with improved whole-body insulin sensitivity. Glucose 25-32 insulin Homo sapiens 71-78 28959911-1 2018 Brain insulin-stimulated glucose uptake (GU) is increased in obese and insulin resistant subjects but normalizes after weight loss along with improved whole-body insulin sensitivity. Glucose 25-32 insulin Homo sapiens 71-78 29864080-7 2018 RESULTS: Pedal desk use required significantly less insulin to maintain glucose concentrations compared with STD condition (peak insulin concentration, 42.1 muU mL vs 66.9 muU mL; P = 0.03; and area under the curve, 302.6 vs 441.8 muU min mL; P < 0.001). Glucose 72-79 insulin Homo sapiens 52-59 29762253-1 2018 PURPOSE: The optimal short-term exercise dose to improve glucose tolerance in relation to metabolic flexibility and/or insulin resistance is unknown. Glucose 57-64 insulin Homo sapiens 119-126 30016718-3 2018 Nano-encapsulated islets maintained physiological glucose-stimulated insulin secretion by both static incubation and perifusion studies. Glucose 50-57 insulin Homo sapiens 69-76 30098928-2 2018 While mitochondrial respiration is essential for glucose-stimulated insulin secretion, little is known regarding heterogeneity in mitochondrial function at the individual islet level. Glucose 49-56 insulin Homo sapiens 68-75 30204939-1 2018 OBJECTIVE: This study aimed to elucidate the relationship between glucose levels and insulin resistance and sensitivity obtained from oral glucose tolerance tests and neurophysiological indices of attention among adults with overweight and obesity. Glucose 66-73 insulin Homo sapiens 85-92 30214565-7 2018 Level of postoperative blood glucose of the DM group was significantly higher than that of the non-DM group (P<0.05), while the level of blood glucose in the insulin treatment group was significantly lower than that in the control group (P<0.05). Glucose 146-153 insulin Homo sapiens 161-168 30370689-4 2018 Characterization of pseudoislets cultured for 1 week revealed better preservation of first-phase glucose-stimulated insulin secretion (GSIS) compared with cultured-intact islets and insulin secretion profiles similar to fresh islets when challenged by glibenclamide and KCl. Glucose 97-104 insulin Homo sapiens 116-123 30267202-5 2018 Higher islet yield and lower preoperative glucose levels are among the strongest predictors of short-term post-operative insulin independence. Glucose 42-49 insulin Homo sapiens 121-128 30199253-4 2018 This compound did not activate the PPARgamma-dependent program of adipocyte differentiation inducing a very less severe lipid accumulation compared to rosiglitazone but increased the insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Glucose 202-209 insulin Homo sapiens 183-190 30261059-10 2018 Furthermore, their plasma levels of insulin increased from 8.1 +- 1.4 to 19.8 +- 3.4 muU/ml, which indicated endogenous secretion stimulated by glucose in dialysate and meal intake. Glucose 144-151 insulin Homo sapiens 36-43 30261059-13 2018 The depletion of the insulin through extracorporeal circulation may inhibit the transportation of glucose from the blood into the muscles, with the consequence of cell starvation. Glucose 98-105 insulin Homo sapiens 21-28 30112543-6 2018 Quantitative assays of glucose-stimulated insulin secretion were demonstrated at 15 second temporal resolution while detecting as low as 10 amol per droplet, revealing fast insulin oscillations that mirror well-known intracellular calcium signals. Glucose 23-30 insulin Homo sapiens 42-49 30246878-6 2018 OBJECTIVES: To examine the efficacy and safety of insulin and other pharmacological interventions for lowering glucose levels in people with diabetes and CKD. Glucose 111-118 insulin Homo sapiens 50-57 30249058-3 2018 Beneficial effects of CGA in glucose metabolism were confirmed in insulin-treated human hepatocarcinoma HepG2 cells. Glucose 29-36 insulin Homo sapiens 66-73 30249008-2 2018 This is the core tissue of insulin-mediated glucose uptake via glucose transporter type 4 (GLUT4). Glucose 44-51 insulin Homo sapiens 27-34 30231981-2 2018 (2018) show that glucose-stimulated beta cells secrete insulin B chain peptides relevant to autoimmunity in type 1 diabetes. Glucose 17-24 insulin Homo sapiens 55-62 30223606-3 2018 Current therapies are able to adjust insulin levels according to blood glucose peak, but they only partly reach the goal to abrogate the consequent inflammatory milieu responsible for diabetes-related diseases. Glucose 71-78 insulin Homo sapiens 37-44 29409957-4 2018 Morphological (including confocal microscopy), ultrastructural (electron microscopy, EM), functional (glucose-stimulated insulin secretion), survival (EM and nuclear dyes) and molecular (RNAseq, qPCR and western blot) studies were performed under several different experimental conditions. Glucose 102-109 insulin Homo sapiens 121-128 29409957-9 2018 Finally, DPP-4 inhibition augmented glucose-stimulated insulin secretion, reduced apoptosis and improved ultrastructure in T2D beta cells. Glucose 36-43 insulin Homo sapiens 55-62 30006347-1 2018 In adipose tissue, resistance to insulin"s ability to increase glucose uptake can be induced by multiple factors, including obesity. Glucose 63-70 insulin Homo sapiens 33-40 30271382-4 2018 Data from our lab and others document that several nutrients and environmental toxins can stimulate insulin secretion at non-stimulatory glucose in the absence of insulin resistance. Glucose 137-144 insulin Homo sapiens 100-107 30302422-0 2018 Experimental BPA Exposure and Glucose-Stimulated Insulin Response in Adult Men and Women. Glucose 30-37 insulin Homo sapiens 49-56 30302422-3 2018 Insulin response was assessed in two cross-over experiments using an oral glucose tolerance test (OGTT; experiment 1) and a hyperglycemic (HG) clamp (experiment 2). Glucose 74-81 insulin Homo sapiens 0-7 30302422-7 2018 In the HG clamp study, focusing on the later-phase insulin response to a stable level of glucose, several measures of insulin and C-peptide appeared suppressed during the BPA session relative to the control session; the change in insulin maximum concentration (Cmax) was negatively correlated with HbA1c and the Cmax of bioactive serum BPA. Glucose 89-96 insulin Homo sapiens 51-58 30302422-7 2018 In the HG clamp study, focusing on the later-phase insulin response to a stable level of glucose, several measures of insulin and C-peptide appeared suppressed during the BPA session relative to the control session; the change in insulin maximum concentration (Cmax) was negatively correlated with HbA1c and the Cmax of bioactive serum BPA. Glucose 89-96 insulin Homo sapiens 118-125 30302422-7 2018 In the HG clamp study, focusing on the later-phase insulin response to a stable level of glucose, several measures of insulin and C-peptide appeared suppressed during the BPA session relative to the control session; the change in insulin maximum concentration (Cmax) was negatively correlated with HbA1c and the Cmax of bioactive serum BPA. Glucose 89-96 insulin Homo sapiens 118-125 30302422-8 2018 Conclusions: This exploratory study suggests that BPA exposure to a dose considered safe by US regulators may alter glucose-stimulated insulin response in humans. Glucose 116-123 insulin Homo sapiens 135-142 30206243-4 2018 In particular, the clock of the pancreatic beta cell rhythmically regulates the transcription of genes involved in glucose-stimulated insulin secretion. Glucose 115-122 insulin Homo sapiens 134-141 30815569-5 2018 The time during which intravenous glucose was required to maintain euglycaemia following a 200-unit dose of U-500 insulin was significantly greater than the time following a 100-unit dose. Glucose 34-41 insulin Homo sapiens 114-121 30233176-1 2018 Background: Despite years of experience and rigorous research, injectable insulin is the sole trusted treatment method to control the blood glucose level in diabetes type 1 patients, but injection of insulin is painful and poses a lot of stress to the patients, especially children, therefore, development of a non-injectable formulation of insulin is a major breakthrough in the history of medicine and pharmaceutical sciences. Glucose 140-147 insulin Homo sapiens 74-81 29981896-0 2018 A stimuli-responsive insulin delivery system based on reversible phenylboronate modified cyclodextrin with glucose triggered host-guest interaction. Glucose 107-114 insulin Homo sapiens 21-28 29981896-3 2018 In this study, a smart drug carrier that can release insulin depending on the changes in blood glucose levels was designed. Glucose 95-102 insulin Homo sapiens 53-60 30183740-5 2018 72h of fasting in lean participants reduced insulin-stimulated glucose uptake to levels similar to obese participants fasted for 12h. Glucose 63-70 insulin Homo sapiens 44-51 30183752-7 2018 This report further describes an improved differentiation protocol that, coupled with SR1423, generated populations of greater than 60% insulin-expressing cells that secrete insulin in response to glucose and are capable of reversing diabetes in rodents. Glucose 197-204 insulin Homo sapiens 136-143 30183752-7 2018 This report further describes an improved differentiation protocol that, coupled with SR1423, generated populations of greater than 60% insulin-expressing cells that secrete insulin in response to glucose and are capable of reversing diabetes in rodents. Glucose 197-204 insulin Homo sapiens 174-181 30535090-8 2018 An increased acute insulin response to glucose from 577 mU L-1 min (350-1040 mU L-1 min) to 671 mU L-1 min (376-1010 mU L-1 min) (P = 0.04) was observed in the sucralose group for participants with adequate adherence. Glucose 39-46 insulin Homo sapiens 19-26 29950394-8 2018 These data suggest that human beta-cells transition between states with high rates of biosynthesis to fulfill the body"s insulin requirements to maintain normal blood glucose levels and UPR-mediated recovery from ER stress due to high insulin production. Glucose 167-174 insulin Homo sapiens 121-128 30230181-10 2018 In this review, we focus on beta-cell function and describe miRNAs involved in insulin biosynthesis and processing, glucose uptake and metabolism, electrical activity and Ca2+ -influx and exocytosis of the insulin granules. Glucose 116-123 insulin Homo sapiens 206-213 30230185-2 2018 Prevailing glucose concentrations, which oscillate pre- and postprandially, exert major dynamic variation in preproinsulin biosynthesis. Glucose 11-18 insulin Homo sapiens 109-122 29673097-9 2018 The systemic effect of insulin was assessed by measuring the blood glucose levels and total body weight. Glucose 67-74 insulin Homo sapiens 23-30 30142362-2 2018 The Arg-325 risk variant shows accelerated zinc (Zn) transport kinetic and reduced glucose-stimulated insulin secretion in pancreatic cells. Glucose 83-90 insulin Homo sapiens 102-109 30109329-6 2018 Chronic incubation (48 h) with 5-PAHSA significantly increased glucose-stimulated insulin secretion (GSIS) in murine islets compared to chronic incubation without the lipid or in the presence of palmitic acid (PA). Glucose 63-70 insulin Homo sapiens 82-89 30206293-0 2018 Serum IgG2 levels are specifically associated with whole-body insulin-mediated glucose disposal in non-diabetic offspring of type 2 diabetic individuals: a cross-sectional study. Glucose 79-86 insulin Homo sapiens 62-69 30206293-8 2018 In a multivariable regression analysis including variables known to affect insulin sensitivity such as age, gender, BMI, smoking, lipids, inflammatory markers, fasting and 2-h post-load glucose levels, IgG2 levels were independently associated with insulin-stimulated glucose disposal (beta = -0.115, 95% CI: -0.541 to -0.024; P = 0.03). Glucose 186-193 insulin Homo sapiens 75-82 30206293-8 2018 In a multivariable regression analysis including variables known to affect insulin sensitivity such as age, gender, BMI, smoking, lipids, inflammatory markers, fasting and 2-h post-load glucose levels, IgG2 levels were independently associated with insulin-stimulated glucose disposal (beta = -0.115, 95% CI: -0.541 to -0.024; P = 0.03). Glucose 268-275 insulin Homo sapiens 249-256 29860065-5 2018 The functionality of differentiated IPCs was assessed by C-peptide and insulin release in response to glucose stimulation test. Glucose 102-109 insulin Homo sapiens 71-78 29860065-9 2018 These cells in both groups secreted insulin and C-peptide in a glucose challenge test by ELISA showing in vitro maturation. Glucose 63-70 insulin Homo sapiens 48-57 29981896-6 2018 Moreover, beta-CD-EPDME can successfully encapsulate insulin and almost completely release insulin in the presence of glucose. Glucose 118-125 insulin Homo sapiens 91-98 29981896-7 2018 The detached phenylboronic acid moiety triggered by glucose can attack the beta-CD cavity and form a host-guest complex, which can force out the encapsulated insulin within the cavity. Glucose 52-59 insulin Homo sapiens 158-165 29183809-4 2018 RESULTS: While islets kept at 5.6 mM glucose secreted significantly more insulin in response to short term glucose-stimulation (p = 0.0067), islets exposed to high glucose for 48 h were desensitised and unresponsive to short term glucose-stimulation with respect to insulin secretion (p = 0.32). Glucose 37-44 insulin Homo sapiens 73-80 29183809-4 2018 RESULTS: While islets kept at 5.6 mM glucose secreted significantly more insulin in response to short term glucose-stimulation (p = 0.0067), islets exposed to high glucose for 48 h were desensitised and unresponsive to short term glucose-stimulation with respect to insulin secretion (p = 0.32). Glucose 107-114 insulin Homo sapiens 73-80 29183809-4 2018 RESULTS: While islets kept at 5.6 mM glucose secreted significantly more insulin in response to short term glucose-stimulation (p = 0.0067), islets exposed to high glucose for 48 h were desensitised and unresponsive to short term glucose-stimulation with respect to insulin secretion (p = 0.32). Glucose 107-114 insulin Homo sapiens 73-80 29183809-4 2018 RESULTS: While islets kept at 5.6 mM glucose secreted significantly more insulin in response to short term glucose-stimulation (p = 0.0067), islets exposed to high glucose for 48 h were desensitised and unresponsive to short term glucose-stimulation with respect to insulin secretion (p = 0.32). Glucose 107-114 insulin Homo sapiens 73-80 29534258-4 2018 This protocol introduced standardized algorithms based on maternal insulin requirements to drive real-time maternal glucose control during labor as well as provided guidelines for postpartum glycemic control. Glucose 116-123 insulin Homo sapiens 67-74 29943626-1 2018 Background Insulin is involved in a glucose homeostatic regulation and a cellular metabolism via phosphorylation of phosphoinositide 3 kinase (PI3K) pathway and mitogen-activated protein kinase (MAPK) pathway. Glucose 36-43 insulin Homo sapiens 11-18 29890222-6 2018 Insulin therapy restores maternal glycaemia, but this beneficial effect is not reflected in the foetus and newborn metabolism, suggesting that other factors than d-glucose may be involved in the pathophysiology of GDM. Glucose 162-171 insulin Homo sapiens 0-7 29935230-2 2018 To achieve this, most closed-loop control strategies need to compute the optimal insulin action on the basis of precedent glucose and insulin levels. Glucose 122-129 insulin Homo sapiens 81-88 29761615-4 2018 Titration of insulin was guided by a fasting plasma glucose (FPG)-based dosing algorithm. Glucose 52-59 insulin Homo sapiens 13-20 30026335-3 2018 Insulin dose was adjusted by investigators according to self-monitored glucose readings, local guidance, and individual circumstances. Glucose 71-78 insulin Homo sapiens 0-7 30059978-1 2018 Insulin production by the pancreatic beta cell is critical for the glucose homeostasis of the whole organism. Glucose 67-74 insulin Homo sapiens 0-7 30060183-2 2018 Islets and taste bud cells express the hormones glucagon and ghrelin, the same ATP-sensitive potassium channel responsible for depolarizing the insulin-secreting beta cell during glucose-induced insulin secretion, as well as the propeptide-processing enzymes PC1/3 and PC2. Glucose 179-186 insulin Homo sapiens 144-151 30349598-1 2018 Flash glucose monitoring - an alternative to traditional self-monitoring of blood glucose (SMBG) - prevents hypoglycaemic events without impacting glycated haemoglobin (HbA1c).21 Given the potential benefits, this study assessed the cost-effectiveness of using flash monitoring versus SMBG alone in patients with type 1 diabetes (T1D) receiving intensive insulin treatment in Sweden. Glucose 6-13 insulin Homo sapiens 355-362 29691896-4 2018 We tested this hypothesis with an intronic MTNR1B SNP, rs10830963, which is associated with acute insulin response to glucose, a dynamic measure of insulin secretion. Glucose 118-125 insulin Homo sapiens 98-105 29916530-10 2018 The results of the present study suggested that targeting AdipoR1 with miR-6835-3p inhibitors may be a potential strategy for promoting glucose-stimulated insulin secretion, and thereby, may be an effective treatment for type 2-DM. Glucose 136-143 insulin Homo sapiens 155-162 29432659-6 2018 The acute insulin response and area under the curve showed a progressive decrease in the normal glucose tolerance and IGT groups, and decreased to the lowest levels in the type 2 diabetes mellitus group (P < 0.05). Glucose 96-103 insulin Homo sapiens 10-17 30060692-1 2018 BACKGROUND: In insulin therapy, the blood glucose level is constrained from below by the hypoglycemic threshold, that is, the blood glucose level must remain above this threshold. Glucose 42-49 insulin Homo sapiens 15-22 30060692-1 2018 BACKGROUND: In insulin therapy, the blood glucose level is constrained from below by the hypoglycemic threshold, that is, the blood glucose level must remain above this threshold. Glucose 132-139 insulin Homo sapiens 15-22 30060692-4 2018 Hence, a desirable insulin input is one that minimizes the maximum glucose concentration while causing it to remain above the hypoglycemic, or higher, threshold. Glucose 67-74 insulin Homo sapiens 19-26 30235745-7 2018 The first-phase glucose and insulin secretion of the intravenous glucose tolerance test improved in both groups, especially in the repaglinide group. Glucose 65-72 insulin Homo sapiens 28-35 29937364-1 2018 Insulin, a key hormone produced by pancreatic beta cells precisely regulates glucose metabolism in vertebrates. Glucose 77-84 insulin Homo sapiens 0-7 29778648-6 2018 Low dose (LD) glucose was administered to avoid insulin-induced hypoglycemia. Glucose 14-21 insulin Homo sapiens 48-55 29778648-13 2018 LD and HD glucose administration combined with insulin improved the FCD and decreased the adherence of leukocytes in endotoxemic animals as did HD glucose administration alone. Glucose 147-154 insulin Homo sapiens 47-54 29778648-15 2018 CONCLUSIONS: Insulin administration, as well as an endogenous insulin response triggered by HD glucose administration, improved the FCD and decreased leukocyte activation in endotoxemic rats. Glucose 95-102 insulin Homo sapiens 62-69 30227796-4 2018 More and more insulin pump systems are linked up to continuous glucose monitoring, which thereby become ever more self-regulating. Glucose 63-70 insulin Homo sapiens 14-21 29578310-4 2018 EXPERIMENTAL DESIGN: Label-free mass spectrometry based proteomic analysis is performed on samples from a longitudinal study of differentiation of human induced pluripotent stem cells toward glucose responsive insulin producing cells. Glucose 191-198 insulin Homo sapiens 210-217 29578310-6 2018 The analysis of proteomes of the implanted cells in a longitudinal study shows that the neovascularization process linked to the extracellular matrix environment is time-dependent and conditions the proper maturation of the cells in beta-like cells secreting insulin in response to glucose. Glucose 282-289 insulin Homo sapiens 259-266 29995705-0 2018 Glucose Intolerance After Pancreatectomy Was Associated With Preoperative Hemoglobin A1c, Insulin Resistance, and Histological Pancreatic Fatty Infiltration. Glucose 0-7 insulin Homo sapiens 90-97 30166558-2 2018 The progression of beta cell failure to type 2 diabetes is preceded by an early positive increase in the insulin secretory response to glucose, which is only later followed by a loss in the secretion capacity of pancreatic islets. Glucose 135-142 insulin Homo sapiens 105-112 30170598-4 2018 Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance is characterized by defects in uptake and oxidation of glucose, a decrease in glycogen synthesis, and, to a lesser extent, the ability to suppress lipid oxidation. Glucose 165-172 insulin Homo sapiens 0-7 30170598-4 2018 Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance is characterized by defects in uptake and oxidation of glucose, a decrease in glycogen synthesis, and, to a lesser extent, the ability to suppress lipid oxidation. Glucose 165-172 insulin Homo sapiens 66-73 30170598-4 2018 Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance is characterized by defects in uptake and oxidation of glucose, a decrease in glycogen synthesis, and, to a lesser extent, the ability to suppress lipid oxidation. Glucose 165-172 insulin Homo sapiens 91-98 30170598-7 2018 For instance, insulin resistance can induce an imbalance in glucose metabolism that generates chronic hyperglycemia, which in turn triggers oxidative stress and causes an inflammatory response that leads to cell damage. Glucose 60-67 insulin Homo sapiens 14-21 30052036-6 2018 HucMSC-ex partially reversed insulin resistance in T2DM indirectly to accelerate glucose metabolism. Glucose 81-88 insulin Homo sapiens 29-36 29969227-5 2018 In the presence of glucose, the nanoparticles are unlocked, resulting in the release of insulin. Glucose 19-26 insulin Homo sapiens 88-95 29969227-6 2018 The release of insulin is controlled by the concentration of glucose. Glucose 61-68 insulin Homo sapiens 15-22 30133442-7 2018 Mature adipocytes differentiated in the presence of BPA were insulin resistant, with an approximate 25% reduction in insulin-stimulated glucose uptake. Glucose 136-143 insulin Homo sapiens 117-124 30211231-5 2018 Results: Insulin and HOMA-IR levels were the highest in newly diagnosed diabetes and were lowest in normal fasting glucose (NFG) (P < 0.001). Glucose 115-122 insulin Homo sapiens 9-16 30147674-4 2018 In type 2 diabetes patients, metformin reduces hyperglycemia and increases insulin sensitivity by enhancing insulin-stimulated glucose uptake in muscles, liver, and adipose tissue and by reducing glucose output by the liver. Glucose 127-134 insulin Homo sapiens 75-82 30121746-3 2018 RECENT FINDINGS: Recent studies have found that the integration of CGM with continuous subcutaneous insulin infusion (CSII) therapy, a system known as sensor-augmented pump (SAP) therapy, very significantly reduces the occurrence of these conditions by providing real-time glucose readings/trends and automatically suspending insulin infusion when glucose is low (LGS) or, even, before glucose is low but is predicted to soon be low (PLGS). Glucose 273-280 insulin Homo sapiens 100-107 30121746-3 2018 RECENT FINDINGS: Recent studies have found that the integration of CGM with continuous subcutaneous insulin infusion (CSII) therapy, a system known as sensor-augmented pump (SAP) therapy, very significantly reduces the occurrence of these conditions by providing real-time glucose readings/trends and automatically suspending insulin infusion when glucose is low (LGS) or, even, before glucose is low but is predicted to soon be low (PLGS). Glucose 348-355 insulin Homo sapiens 100-107 30121746-3 2018 RECENT FINDINGS: Recent studies have found that the integration of CGM with continuous subcutaneous insulin infusion (CSII) therapy, a system known as sensor-augmented pump (SAP) therapy, very significantly reduces the occurrence of these conditions by providing real-time glucose readings/trends and automatically suspending insulin infusion when glucose is low (LGS) or, even, before glucose is low but is predicted to soon be low (PLGS). Glucose 348-355 insulin Homo sapiens 100-107 31193891-5 2019 Based on the findings of Otto Warburg and his physiological reasoning he started to experiment with insulin administration and KDs in his patients with head and neck cancers, aiming to maximally lower blood glucose concentrations. Glucose 207-214 insulin Homo sapiens 100-107 30127860-0 2018 Twice-daily insulin degludec/insulin aspart effectively improved morning and evening glucose levels and quality of life in patients previously treated with premixed insulin: an observational study. Glucose 85-92 insulin Homo sapiens 12-19 30111834-0 2018 The IRE1alpha-XBP1s pathway promotes insulin-stimulated glucose uptake in adipocytes by increasing PPARgamma activity. Glucose 56-63 insulin Homo sapiens 37-44 30104309-2 2018 Automated insulin delivery devices incorporate an insulin pump with continuous glucose monitoring(CGM) and an algorithm, and adjust insulin in real time. Glucose 79-86 insulin Homo sapiens 10-17 30147674-4 2018 In type 2 diabetes patients, metformin reduces hyperglycemia and increases insulin sensitivity by enhancing insulin-stimulated glucose uptake in muscles, liver, and adipose tissue and by reducing glucose output by the liver. Glucose 196-203 insulin Homo sapiens 75-82 30215903-12 2018 Advances in diabetes care, including the bionic pancreas and the closed-loop system of glucose monitoring with an automated insulin pump, may have a significant effect on type 1 diabetes care in the years ahead. Glucose 87-94 insulin Homo sapiens 124-131 30038024-8 2018 Our data suggest that the SLC30A8 R138X LOF mutation may exert beneficial effects on glucose metabolism by increasing the capacity of beta-cells to secrete insulin under hyperglycemic conditions. Glucose 85-92 insulin Homo sapiens 156-163 30140092-2 2018 Dysfunction of CDKAL1 impairs the translation of proinsulin, which leads to glucose intolerance. Glucose 76-83 insulin Homo sapiens 49-59 29351487-5 2018 We found that olanzapine led to an increase in the acute insulin response to glucose, which was not seen with placebo, and was attenuated in the olanzapine group by atropine. Glucose 77-84 insulin Homo sapiens 57-64 29750952-2 2018 When continuous intravenous insulin infusion is needed, standardized insulin dosing charts have been used for titration of insulin to maintain glucose in target range. Glucose 143-150 insulin Homo sapiens 69-76 29750952-2 2018 When continuous intravenous insulin infusion is needed, standardized insulin dosing charts have been used for titration of insulin to maintain glucose in target range. Glucose 143-150 insulin Homo sapiens 69-76 29750952-3 2018 The GlucoStabilizer software program (Indiana University Health Inc, Indianapolis, IN) is a software-guided insulin dosing system that calculates the dose of intravenous insulin that is needed based on metabolic parameters, target glucose concentration, and an individual"s response to insulin. Glucose 231-238 insulin Homo sapiens 170-177 29750952-3 2018 The GlucoStabilizer software program (Indiana University Health Inc, Indianapolis, IN) is a software-guided insulin dosing system that calculates the dose of intravenous insulin that is needed based on metabolic parameters, target glucose concentration, and an individual"s response to insulin. Glucose 231-238 insulin Homo sapiens 170-177 29750952-5 2018 OBJECTIVE: The purpose of this study was to determine whether the use of intravenous insulin dosing software in women with pregestational or gestational diabetes mellitus that requires intrapartum insulin infusion can improve the rate of glucose concentration in target range (70-100 mg/dL; 3.9-5.5 mmol/L) at the time delivery. Glucose 238-245 insulin Homo sapiens 85-92 29750952-5 2018 OBJECTIVE: The purpose of this study was to determine whether the use of intravenous insulin dosing software in women with pregestational or gestational diabetes mellitus that requires intrapartum insulin infusion can improve the rate of glucose concentration in target range (70-100 mg/dL; 3.9-5.5 mmol/L) at the time delivery. Glucose 238-245 insulin Homo sapiens 197-204 29763373-1 2018 Skeletal muscle microvascular (capillary) blood flow increases in the postprandial state or during insulin infusion due to dilation of precapillary arterioles to augment glucose disposal. Glucose 170-177 insulin Homo sapiens 99-106 28673690-11 2018 CONCLUSION: Our study suggests a discordant association of lipid parameters with blood glucose level and TG/HDL-C is a better marker for evaluating insulin resistance and diabetes in Chinese population when compared with other routine lipid measures. Glucose 87-94 insulin Homo sapiens 148-155 29380240-5 2018 Short- and long-term treatments with tacrolimus, cyclosporin A or another CNI deltamethrin (herbicide) decreased basal and insulin-dependent glucose uptake in adipocytes, without any additive effects observed when added together. Glucose 141-148 insulin Homo sapiens 123-130 30051890-3 2018 As p110alpha mediates virtually all cellular responses to insulin, targeted inhibition of this enzyme disrupts glucose metabolism in multiple tissues. Glucose 111-118 insulin Homo sapiens 58-65 30051890-4 2018 For example, blocking insulin signalling promotes glycogen breakdown in the liver and prevents glucose uptake in the skeletal muscle and adipose tissue, resulting in transient hyperglycaemia within a few hours of PI3K inhibition. Glucose 95-102 insulin Homo sapiens 22-29 30051890-5 2018 The effect is usually transient because compensatory insulin release from the pancreas (insulin feedback) restores normal glucose homeostasis3. Glucose 122-129 insulin Homo sapiens 53-60 30051890-5 2018 The effect is usually transient because compensatory insulin release from the pancreas (insulin feedback) restores normal glucose homeostasis3. Glucose 122-129 insulin Homo sapiens 88-95 30220280-0 2018 [Effects of insulin caliper for blood glucose control on glucose control in emergent and critical patients]. Glucose 38-45 insulin Homo sapiens 12-19 30220280-12 2018 CONCLUSIONS: For emergent and critical patients, insulin caliper for blood glucose control presents favorable application value for achieving glucose control target, reducing glycemic fluctuation, and lowering the incidence of hypoglycemia. Glucose 75-82 insulin Homo sapiens 49-56 30060632-2 2018 Frequent glucose monitoring allows the adjustment of insulin therapy to improve metabolic control with near-normal blood glucose concentrations. Glucose 9-16 insulin Homo sapiens 53-60 30060632-2 2018 Frequent glucose monitoring allows the adjustment of insulin therapy to improve metabolic control with near-normal blood glucose concentrations. Glucose 121-128 insulin Homo sapiens 53-60 30087656-5 2018 In podocytes cultured under NG conditions, AngII inhibited insulin-stimulated glucose uptake. Glucose 78-85 insulin Homo sapiens 59-66 30087656-10 2018 These findings demonstrate that AngII modulates podocyte basal, as well as insulin-dependent glucose uptake by regulating glucose transporters and insulin signaling. Glucose 93-100 insulin Homo sapiens 75-82 30087656-10 2018 These findings demonstrate that AngII modulates podocyte basal, as well as insulin-dependent glucose uptake by regulating glucose transporters and insulin signaling. Glucose 93-100 insulin Homo sapiens 147-154 32026957-4 2018 A potassium concentration after recovery from VT was 6.4 mEq/L, which was normalized by the administration of calcium gluconate, furosemide, and insulin with glucose. Glucose 158-165 insulin Homo sapiens 145-152 30123264-8 2018 Conclusions: Serotonin system may play a role in glucose-stimulated insulin secretion in patients with insulin resistance (IR) and decreased insulin sensitivity. Glucose 49-56 insulin Homo sapiens 68-75 30123264-8 2018 Conclusions: Serotonin system may play a role in glucose-stimulated insulin secretion in patients with insulin resistance (IR) and decreased insulin sensitivity. Glucose 49-56 insulin Homo sapiens 103-110 29723655-4 2018 The net whole-body anabolic (protein balance) response to hyperinsulinemia was lower in the elderly vs young (p = 0.007) and was highly correlated with the clamp glucose rate of disposal (r = 0.671, p < 0.001), indicating insulin resistance of protein metabolism concurrent with that of glucose. Glucose 162-169 insulin Homo sapiens 63-70 29723655-4 2018 The net whole-body anabolic (protein balance) response to hyperinsulinemia was lower in the elderly vs young (p = 0.007) and was highly correlated with the clamp glucose rate of disposal (r = 0.671, p < 0.001), indicating insulin resistance of protein metabolism concurrent with that of glucose. Glucose 290-297 insulin Homo sapiens 63-70 30013127-1 2018 Mammalian glucose homeostasis is controlled by the antagonistic hormones insulin and glucagon, secreted by pancreatic beta and alpha cells respectively. Glucose 10-17 insulin Homo sapiens 73-80 25905189-3 2000 The glucose clamp method is the reference standard for direct measurement of insulin sensitivity. Glucose 4-11 insulin Homo sapiens 77-84 29995924-5 2018 At 100 muM, the pure ANC enhanced glucose-stimulated insulin secretion (GSIS) in INS-1E cells ranging from 18% to 40% (p<0.05) compared to untreated cells. Glucose 34-41 insulin Homo sapiens 53-60 30042734-13 2018 Men with OSA secreted significantly more insulin than women with OSA in order to achieve similar glucose levels. Glucose 97-104 insulin Homo sapiens 41-48 29941553-6 2018 Low insulin doses (3-10 U/kg) brought about a significant decrease in blood glucose levels, which were sustained for longer periods (up to 12 hours), unlike s.c. injected insulin. Glucose 76-83 insulin Homo sapiens 4-11 29941553-7 2018 When 10 U/kg insulin-CAGE was orally delivered in enterically coated capsules using an oral gavage, a sustained decrease in blood glucose of up to 45% was observed. Glucose 130-137 insulin Homo sapiens 13-20 33435111-0 2018 Microneedles Integrated with ZnO Quantum-Dot-Capped Mesoporous Bioactive Glasses for Glucose-Mediated Insulin Delivery. Glucose 85-92 insulin Homo sapiens 102-109 33435111-1 2018 A self-responsive insulin delivery system is highly desirable because of its high sensitivity dependent on blood glucose levels. Glucose 113-120 insulin Homo sapiens 18-25 33435111-2 2018 Herein, a smart pH-triggered and glucose-mediated transdermal delivery system, insulin-loaded and ZnO quantum dots (ZnO QDs) capped mesoporous bioactive glasses (MBGs) integrated with microneedles (MNs), was developed to achieve control and painless administration. Glucose 33-40 insulin Homo sapiens 79-86 29773651-1 2018 Insulin stimulates the exocytic translocation of specialized vesicles in adipocytes, which inserts GLUT4 glucose transporters into the plasma membrane to enhance glucose uptake. Glucose 105-112 insulin Homo sapiens 0-7 32232085-2 2018 Traditionally, control has involved external insulin injection in response to elevated blood glucose to substitute the role of the beta cells in the pancreas which would otherwise perform this function in a healthy individual. Glucose 93-100 insulin Homo sapiens 45-52 32232085-3 2018 The central nervous system (CNS), however, also plays a vital role in glucose homoeostasis through the control of pancreatic secretion and insulin sensitivity which could potentially be used as a pathway for enhancing glucose control. Glucose 70-77 insulin Homo sapiens 139-146 30116732-1 2018 Variability in the effect of subcutaneously administered insulin represents a major challenge in insulin therapy where precise dosing is required in order to achieve targeted glucose levels. Glucose 175-182 insulin Homo sapiens 57-64 30116732-1 2018 Variability in the effect of subcutaneously administered insulin represents a major challenge in insulin therapy where precise dosing is required in order to achieve targeted glucose levels. Glucose 175-182 insulin Homo sapiens 97-104 29966534-5 2018 In fact, 2-3 days after starting each 7-day cycle of 5-azacitidine, he reported higher blood glucose levels, requiring an increased dose of self-administered insulin. Glucose 93-100 insulin Homo sapiens 158-165 29947782-7 2018 Main Outcome Measures: Correlation of MRI-measured pancreatic fat content with early insulin release in an oral glucose tolerance test (OGGT) [insulin increment within the first 30 minutes of the OGTT (IR30)] and first-phase insulin response (FPIR) in an intravenous glucose tolerance test (n = 65), both adjusted for insulin sensitivity index (ISI). Glucose 112-119 insulin Homo sapiens 143-150 29947782-7 2018 Main Outcome Measures: Correlation of MRI-measured pancreatic fat content with early insulin release in an oral glucose tolerance test (OGGT) [insulin increment within the first 30 minutes of the OGTT (IR30)] and first-phase insulin response (FPIR) in an intravenous glucose tolerance test (n = 65), both adjusted for insulin sensitivity index (ISI). Glucose 112-119 insulin Homo sapiens 143-150 29947782-7 2018 Main Outcome Measures: Correlation of MRI-measured pancreatic fat content with early insulin release in an oral glucose tolerance test (OGGT) [insulin increment within the first 30 minutes of the OGTT (IR30)] and first-phase insulin response (FPIR) in an intravenous glucose tolerance test (n = 65), both adjusted for insulin sensitivity index (ISI). Glucose 112-119 insulin Homo sapiens 143-150 29909972-7 2018 These findings suggest that substrates preferred by BAT in postprandial state are glucose or LPL-released NEFAs due to insulin stimulation. Glucose 82-89 insulin Homo sapiens 119-126 29789944-8 2018 CONCLUSIONS: These results suggest that the associations between age at menarche and risk of gestational diabetes and raised pregnancy glucose concentrations may be mediated by insulin resistance. Glucose 135-142 insulin Homo sapiens 177-184 29982277-13 2018 Conclusions: PP elicits greater postprandial increases in glucagon than does CP and consequently requires higher insulin to control glucose metabolism, which appears to be related to the rate of amino acid appearance. Glucose 132-139 insulin Homo sapiens 113-120 29698057-0 2018 Differential associations between plasma concentrations of insulin and glucose and intestinal expression of key genes involved in chylomicron metabolism. Glucose 71-78 insulin Homo sapiens 59-66 29698057-2 2018 The objective of this study was to evaluate the association between the plasma levels of insulin and glucose and the intestinal expression of key genes involved in chylomicron metabolism in a large sample of nondiabetic men displaying various degrees of IR. Glucose 101-108 insulin Homo sapiens 89-96 29698057-13 2018 Alterations in intestinal lipoprotein metabolism associated with insulin resistance may be regulated by plasma levels of both insulin and glucose concurrently and are therefore likely modified by the onset of insulin insufficiency. Glucose 138-145 insulin Homo sapiens 65-72 28527646-12 2018 Continuous IV insulin maintained normoglycaemia by inhibiting EGP and increasing glucose clearance. Glucose 81-88 insulin Homo sapiens 14-21 29706019-8 2018 Multivariable logistic regression analysis showed insulinogenic index/fasting immunoreactive insulin and summation of glucose levels, assessed during pregnancy oral glucose tolerance tests (total glucose), to be independent risk factors for postpartum glucose intolerance. Glucose 165-172 insulin Homo sapiens 50-57 29706019-8 2018 Multivariable logistic regression analysis showed insulinogenic index/fasting immunoreactive insulin and summation of glucose levels, assessed during pregnancy oral glucose tolerance tests (total glucose), to be independent risk factors for postpartum glucose intolerance. Glucose 165-172 insulin Homo sapiens 50-57 29706019-8 2018 Multivariable logistic regression analysis showed insulinogenic index/fasting immunoreactive insulin and summation of glucose levels, assessed during pregnancy oral glucose tolerance tests (total glucose), to be independent risk factors for postpartum glucose intolerance. Glucose 165-172 insulin Homo sapiens 50-57 29706019-10 2018 Decision-curve analysis showed that combining insulinogenic index/fasting immunoreactive insulin <1.1 with basic clinical information resulted in superior net benefits for prediction of postpartum glucose intolerance. Glucose 200-207 insulin Homo sapiens 46-53 29706019-11 2018 CONCLUSIONS: Insulinogenic index/fasting immunoreactive insulin calculated using oral glucose tolerance test results during pregnancy is potentially useful for predicting early postpartum glucose intolerance in Japanese women with gestational diabetes. Glucose 86-93 insulin Homo sapiens 56-63 29706019-11 2018 CONCLUSIONS: Insulinogenic index/fasting immunoreactive insulin calculated using oral glucose tolerance test results during pregnancy is potentially useful for predicting early postpartum glucose intolerance in Japanese women with gestational diabetes. Glucose 188-195 insulin Homo sapiens 56-63 29844095-6 2018 Also, carriers had a lower insulin response after the oral glucose challenge. Glucose 59-66 insulin Homo sapiens 27-34 29844095-7 2018 Following an oral glucose tolerance test in the presence of metformin, carriers of the p.E508K variant with diabetes had a lower maximum insulin peak and total and incremental insulin AUC value as compared with noncarriers with diabetes (P < 0.05). Glucose 18-25 insulin Homo sapiens 137-144 29853473-8 2018 RESULTS: We identified four different glucose response patterns, which differed with regard to insulin sensitivity and acute insulin response, obesity, and plasma levels of lipids and inflammatory markers. Glucose 38-45 insulin Homo sapiens 95-102 29853473-8 2018 RESULTS: We identified four different glucose response patterns, which differed with regard to insulin sensitivity and acute insulin response, obesity, and plasma levels of lipids and inflammatory markers. Glucose 38-45 insulin Homo sapiens 125-132 29853473-10 2018 Time to glucose peak was driven mainly by insulin sensitivity, whereas glucose peak size was related to both insulin sensitivity and secretion. Glucose 8-15 insulin Homo sapiens 42-49 29853473-10 2018 Time to glucose peak was driven mainly by insulin sensitivity, whereas glucose peak size was related to both insulin sensitivity and secretion. Glucose 71-78 insulin Homo sapiens 109-116 29577536-1 2018 Glucose excursion was assessed prior to and post hypoglycaemia to increase understanding of hypoglycaemia incidence and recovery during hybrid closed-loop insulin delivery. Glucose 0-7 insulin Homo sapiens 155-162 29603872-1 2018 Glucagon-like peptide-1 receptor agonists lower blood glucose in type 2 diabetes (T2D) partially through glucose-dependent stimulation of insulin secretion. Glucose 54-61 insulin Homo sapiens 138-145 29652108-0 2018 Skeletal muscle-specific overexpression of heat shock protein 72 improves skeletal muscle insulin-stimulated glucose uptake but does not alter whole body metabolism. Glucose 109-116 insulin Homo sapiens 90-97 29652108-5 2018 RESULTS: IM injection of the AAV:Hsp72 significantly improved skeletal muscle insulin-stimulated glucose clearance in treated hind-limb muscles, as compared with untreated muscles of the contralateral leg when mice were fed an HFD. Glucose 97-104 insulin Homo sapiens 78-85 29652108-8 2018 CONCLUSIONS: At the levels of Hsp72 over-expression reported herein, skeletal muscle-specific Hsp72 overexpression via IM injection has the capacity to increase insulin-stimulated glucose clearance in this muscle. Glucose 180-187 insulin Homo sapiens 161-168 29732475-1 2018 AIMS/HYPOTHESIS: Incretin effect-the potentiation of glucose-stimulated insulin release induced by the oral vs the i.v. Glucose 53-60 insulin Homo sapiens 72-79 29807104-4 2018 Also, the fasting plasma glucose or post-prandial 2 h glucose were comparably decreased in dapagliflozin or insulin glargine. Glucose 25-32 insulin Homo sapiens 108-115 29807104-4 2018 Also, the fasting plasma glucose or post-prandial 2 h glucose were comparably decreased in dapagliflozin or insulin glargine. Glucose 54-61 insulin Homo sapiens 108-115 29979618-3 2018 Expert systems, from automated insulin delivery to advisory systems, are a key missing element to richer, more personalized, glucose management in diabetes. Glucose 125-132 insulin Homo sapiens 31-38 30025475-2 2018 Inhibition of the sodium--glucosecotransporter-2 (SGLT2) can increase urinary glucose excretion and decrease plasma glucose levels in an insulin-independent manner. Glucose 26-33 insulin Homo sapiens 137-144 29543533-1 2018 Postprandial insulin desensitization plays a critical role in maintaining whole-body glucose homeostasis by avoiding the excessive absorption of blood glucose; however, the detailed mechanisms that underlie how the major player, skeletal muscle, desensitizes insulin action remain to be elucidated. Glucose 85-92 insulin Homo sapiens 13-20 29543533-1 2018 Postprandial insulin desensitization plays a critical role in maintaining whole-body glucose homeostasis by avoiding the excessive absorption of blood glucose; however, the detailed mechanisms that underlie how the major player, skeletal muscle, desensitizes insulin action remain to be elucidated. Glucose 151-158 insulin Homo sapiens 13-20 29543533-3 2018 The inhibition of the transcriptional activity of Egr-1 enhanced the phosphorylation of the insulin receptor (InsR) and Akt, thus increasing glucose uptake in L6 myotubes after insulin stimulation, whereas overexpression of Egr-1 decreased insulin sensitivity. Glucose 141-148 insulin Homo sapiens 92-99 30001566-0 2018 Altered Glucose Uptake in Muscle, Visceral Adipose Tissue, and Brain Predict Whole-Body Insulin Resistance and may Contribute to the Development of Type 2 Diabetes: A Combined PET/MR Study. Glucose 8-15 insulin Homo sapiens 88-95 30001566-1 2018 We assessed glucose uptake in different tissues in type 2 diabetes (T2D), prediabetes, and control subjects to elucidate its impact in the development of whole-body insulin resistance and T2D. Glucose 12-19 insulin Homo sapiens 165-172 30001566-10 2018 Impaired glucose uptake in skeletal muscle and VAT together with elevated glucose uptake in brain were independently associated with whole-body insulin resistance, and these tissue-specific alterations may contribute to T2D development. Glucose 9-16 insulin Homo sapiens 144-151 30001566-10 2018 Impaired glucose uptake in skeletal muscle and VAT together with elevated glucose uptake in brain were independently associated with whole-body insulin resistance, and these tissue-specific alterations may contribute to T2D development. Glucose 74-81 insulin Homo sapiens 144-151 29860335-10 2018 Insulin area under curve after oral glucose was reduced for betaine treatment compared with placebo (P = 0.038). Glucose 36-43 insulin Homo sapiens 0-7 29982723-6 2018 The primary outcome tested was the change in insulin sensitivity as assessed by the Matsuda Insulin Sensitivity Index (MISI) after an oral glucose load. Glucose 139-146 insulin Homo sapiens 45-52 29874115-8 2018 RESULTS: Circulating levels of 25(OH)D were related to glucose parameters (negatively with HOMA2-%B and insulin levels and positively with HOMA2-%S) in women with PMO, resulting in an indicator of insulin sensitivity independent of age, body mass index, percent body fat, and undercarboxylated osteocalcin. Glucose 55-62 insulin Homo sapiens 104-111 29874115-8 2018 RESULTS: Circulating levels of 25(OH)D were related to glucose parameters (negatively with HOMA2-%B and insulin levels and positively with HOMA2-%S) in women with PMO, resulting in an indicator of insulin sensitivity independent of age, body mass index, percent body fat, and undercarboxylated osteocalcin. Glucose 55-62 insulin Homo sapiens 197-204 29898210-12 2018 From baseline to week 12, insulin-stimulated change in glucose rate of disappearance increased by 2.30% for risperidone and decreased by 29.34% for olanzapine and 30.26% for aripiprazole, with no significant difference across medications (time by treatment interaction, P < .07). Glucose 55-62 insulin Homo sapiens 26-33 30047711-3 2018 Hypoglycaemia is a side effect of some treatments for diabetes, whereby injected insulin or oral medicines that stimulate insulin secretion cause an abnormally low blood glucose level. Glucose 170-177 insulin Homo sapiens 81-88 30047711-3 2018 Hypoglycaemia is a side effect of some treatments for diabetes, whereby injected insulin or oral medicines that stimulate insulin secretion cause an abnormally low blood glucose level. Glucose 170-177 insulin Homo sapiens 122-129 30055649-4 2018 The Quantitative insulin sensitivity check index (QUICKI) was computed from the fasting insulin and glucose levels. Glucose 100-107 insulin Homo sapiens 17-24 30050503-0 2018 Commentary: Glucose Self-monitoring in Non-Insulin-Treated Patients With Type 2 Diabetes in Primary Care Settings: A Randomized Trial. Glucose 12-19 insulin Homo sapiens 43-50 30002559-6 2018 The GG genotype of rs2281939 was associated with a higher risk of diabetes at baseline, an earlier onset of diabetes, and higher steady-state plasma glucose levels in the modified insulin suppression test. Glucose 149-156 insulin Homo sapiens 180-187 29989097-6 2018 Insulin resistance was determined by glucose disposal rate (eGDR). Glucose 37-44 insulin Homo sapiens 0-7 29288549-9 2018 Recovered devices displayed a blunted glucose-stimulated insulin response, and amyloid formation in the endocrine tissue. Glucose 38-45 insulin Homo sapiens 57-64 29590558-3 2018 Therefore, we tested the hypothesis that insulin increases ventilation in humans during a hyperinsulinemic-euglycemic clamp in which insulin was elevated to postprandial concentrations while glucose was maintained at fasting concentrations. Glucose 191-198 insulin Homo sapiens 41-48 30440244-3 2018 The recent approval by the U.S. Food and Drug Administration to use the measurements collected by wearable continuous glucose monitoring (CGM) sensors for insulin dosing of fers new perspectives. Glucose 118-125 insulin Homo sapiens 155-162 30440244-8 2018 Then, a fully-connected feedforward NN was trained, with the aim of estimating the insulin bolus needed to obtain the best glycemic outcomes according to the blood glucose risk index (BGRI). Glucose 164-171 insulin Homo sapiens 83-90 30448236-5 2018 Inhibition of SphK2 also prevented insulin repressed PEPCK and G6Pase expression as well as glucose production levels. Glucose 92-99 insulin Homo sapiens 35-42 29729427-9 2018 In addition, GC-induced changes in P1NP were negatively related to changes in insulin-mediated suppression of hepatic glucose production (r = -0.582; p = 0.001), and were positively related to insulin-stimulated glucose uptake (r = 0.638; p < 0.001). Glucose 118-125 insulin Homo sapiens 78-85 29202888-3 2018 However, in patients with a functional pancreas, exogenous dextrose administration may precipitate endogenous insulin release leading to rebound hypoglycemia. Glucose 59-67 insulin Homo sapiens 110-117 29493118-0 2018 Greater early postprandial suppression of endogenous glucose production and higher initial glucose disappearance is achieved with fast-acting insulin aspart compared with insulin aspart. Glucose 53-60 insulin Homo sapiens 142-149 29493118-0 2018 Greater early postprandial suppression of endogenous glucose production and higher initial glucose disappearance is achieved with fast-acting insulin aspart compared with insulin aspart. Glucose 91-98 insulin Homo sapiens 142-149 29493118-1 2018 AIM: To investigate the mechanisms behind the lower postprandial glucose (PPG) concentrations achieved with fast-acting insulin aspart (faster aspart) than with insulin aspart (IAsp). Glucose 65-72 insulin Homo sapiens 120-127 29536605-0 2018 Effects of intranasal insulin on endogenous glucose production in insulin-resistant men. Glucose 44-51 insulin Homo sapiens 22-29 29536605-0 2018 Effects of intranasal insulin on endogenous glucose production in insulin-resistant men. Glucose 44-51 insulin Homo sapiens 66-73 29536605-1 2018 The effects of intranasal insulin on the regulation of endogenous glucose production (EGP) in individuals with insulin resistance were assessed in a single-blind, crossover study. Glucose 66-73 insulin Homo sapiens 26-33 29536605-1 2018 The effects of intranasal insulin on the regulation of endogenous glucose production (EGP) in individuals with insulin resistance were assessed in a single-blind, crossover study. Glucose 66-73 insulin Homo sapiens 111-118 29602762-7 2018 A decrease in the expression of LPL was observed in SCs of high glucose condition and it was reversed upon insulin treatment. Glucose 64-71 insulin Homo sapiens 107-114 29932731-10 2018 Ambulatory glucose monitoring on a subset of patients confirmed that the mean glucose, MAGE, and CONGA were higher when subjects injected insulin at LH sites than at non-LH sites. Glucose 11-18 insulin Homo sapiens 138-145 29766601-10 2018 An oral glucose tolerance test was used to derive measures of insulin sensitivity. Glucose 8-15 insulin Homo sapiens 62-69 29524488-0 2018 Regulated basal and bolus insulin release from glucose-responsive core-shell microspheres based on concanavalin A-sugar affinity. Glucose 47-54 insulin Homo sapiens 26-33 29524488-3 2018 Our study shows the feasibility of using a photo-crosslinkable shell layer to regulate basal and bolus insulin release from glucose-responsive Con A-polysaccharides network. Glucose 124-131 insulin Homo sapiens 103-110 29618067-8 2018 In addition, cortisol attenuated insulin-stimulated glucose uptake in EECs, which was mediated by inhibition of Akt phosphorylation and glucose transporter type 4 translocation via induction of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Glucose 52-59 insulin Homo sapiens 33-40 29047219-5 2018 The postprandial plasma glucose-lowering efficacies was also significantly greater with DPP-4i/INS than with placebo/insulin (weighted mean difference -1.65 mmol/L, 95% CI: -2.34, -0.96, P < 0.05). Glucose 24-31 insulin Homo sapiens 117-124 29047219-8 2018 Sodium-glucose cotransporter 2 inhibitor/insulin treatment achieved better placebo-corrected efficacy in lowering postprandial plasma glucose, with less weight gain and no higher risk of hypoglycemia. Glucose 7-14 insulin Homo sapiens 41-48 29265719-5 2018 Insulin resistance was estimated by the oral glucose insulin sensitivity index, an oral glucose tolerance test-derived measure. Glucose 45-52 insulin Homo sapiens 0-7 29188534-5 2018 Treatment with 1,25(OH)2D3, coupled with insulin, enhanced GLUT4 translocation and glucose uptake compared to treatment with either insulin or 1,25(OH)2D3 alone in HG-treated myotubes, which suggests that insulin-independent signaling molecules can contribute to the higher glucose metabolism observed in 1,25(OH)2D3 and insulin-treated cells. Glucose 83-90 insulin Homo sapiens 41-48 29767231-5 2018 Inactivation of PTEN enhanced the activation of insulin-induced protein kinase B (AKT), leading to increased glucose transporter 4 (GLUT4) redistribution and glucose uptake in 3T3-L1 adipocytes. Glucose 109-116 insulin Homo sapiens 48-55 29767231-7 2018 It was also revealed that insulin-induced AKT activation, GLUT4 translocation to cell membrane and glucose uptake were significantly inhibited in chronic ROS-treated 3T3-L1 adipocytes. Glucose 99-106 insulin Homo sapiens 26-33 29773871-5 2018 Factors released by neighbouring alpha-cells or beta-cells amplify the glucose-induced effects on somatostatin secretion from delta-cells, which act locally within the islets as paracrine or autocrine inhibitors of insulin, glucagon and somatostatin secretion. Glucose 71-78 insulin Homo sapiens 215-222 28859884-0 2018 A network of insulin peptides regulate glucose uptake by astrocytes: Potential new druggable targets for brain hypometabolism. Glucose 39-46 insulin Homo sapiens 13-20 29615289-0 2018 Fasting and post-glucose load measures of insulin resistance and risk of incident atrial fibrillation: The Cardiovascular Health Study. Glucose 17-24 insulin Homo sapiens 42-49 29977497-1 2018 Background: Fast-acting insulin aspart is a new formulation of the rapid-acting insulin analogue insulin aspart and represents an advancement over current rapid-acting insulin analogues in terms of onset of action and postprandial glucose control. Glucose 231-238 insulin Homo sapiens 24-31 32219200-2 2018 GLP-1R agonists improve T2DM by enhancing glucose-stimulated insulin secretion, delaying gastric transit, decreasing glucagon levels, and reducing body weight due to anorexigenic actions. Glucose 42-49 insulin Homo sapiens 61-68 29954380-4 2018 MAIN BODY: The real advantage of a CLS compared to last-generation sensor-augmented pumps is the gradual modulation of basal insulin infusion in response to glycaemic variations (towards both hyperglycaemia and hypoglycaemia), which has the aim of improving the proportion of time spent in the target glucose range and reducing the mean glucose level without increasing the risk of hypoglycaemia. Glucose 301-308 insulin Homo sapiens 125-132 29954380-4 2018 MAIN BODY: The real advantage of a CLS compared to last-generation sensor-augmented pumps is the gradual modulation of basal insulin infusion in response to glycaemic variations (towards both hyperglycaemia and hypoglycaemia), which has the aim of improving the proportion of time spent in the target glucose range and reducing the mean glucose level without increasing the risk of hypoglycaemia. Glucose 337-344 insulin Homo sapiens 125-132 30019009-1 2018 Variable rate intravenous insulin infusions (VRIII) are used to maintain stable blood glucose in hospitalised patients with diabetes who are unable to eat or have a severe illness where good glycaemic control is paramount. Glucose 86-93 insulin Homo sapiens 26-33 29929988-8 2018 However, insulin-stimulated cardiac glucose uptake and glucose oxidation were significantly diminished at 10 and 20 weeks, which indicates cardiac insulin resistance starting before the onset of mitochondrial and contractile dysfunction. Glucose 36-43 insulin Homo sapiens 9-16 29914537-8 2018 He was treated with beta-blocker, orally administered potassium iodine, a relatively low dose of prednisolone, and insulin injection therapy to control his blood glucose, resulting in an improvement in thyroid function and his symptoms. Glucose 162-169 insulin Homo sapiens 115-122 25905325-0 2000 Hypoglycemia During Therapy of Diabetes Hypoglycemia, caused by treatment with a sulfonylurea, a glinide or insulin coupled with compromised defenses against the resulting falling plasma glucose concentrations, is the limiting factor in the glycemic management of diabetes. Glucose 187-194 insulin Homo sapiens 108-115 29730292-9 2018 Insulin content was positively correlated with newborn birth weight and placental weight while HbA1c and blood glucose were positively correlated with insulin concentration (r = 0.92, P < 0.01, r = 0.85, P < 0.01). Glucose 111-118 insulin Homo sapiens 151-158 29909496-4 2018 Some of these new approaches are in clinical trials, but more research is needed to determine how sufficient beta-cell mass can be transplanted in a clinically applicable device size, and that insulin is secreted with kinetics that will safely provide adequate controls of glucose levels. Glucose 273-280 insulin Homo sapiens 193-200 29909550-2 2018 In addition, the OGTT is utilized for surrogate measures of insulin sensitivity and the insulin response to enteral glucose and has been widely applied in the evaluation of beta-cell dysfunction in obesity, prediabetes, and type 2 diabetes. Glucose 116-123 insulin Homo sapiens 88-95 29909550-4 2018 RECENT FINDINGS: Advantages of using the OGTT for measures of diabetes risk include its accessibility and the incorporation of physiological contributions of the gut-pancreas axis in the measures of insulin response to glucose. Glucose 219-226 insulin Homo sapiens 199-206 29909550-6 2018 Disadvantages include individual differences in the rate of glucose absorption that modify insulin responses, imperfect control of the glycemic stimulus, and poor intraindividual reproducibility. Glucose 60-67 insulin Homo sapiens 91-98 29914129-5 2018 Insulin resistance was calculated using an oral glucose tolerance test. Glucose 48-55 insulin Homo sapiens 0-7 29191483-3 2018 A typical example is glucose-responsive insulin delivery system, which can mimic the pancreatic beta cells to release insulin with a proper dose at a proper time point by responding to plasma glucose levels. Glucose 21-28 insulin Homo sapiens 40-47 29599083-0 2018 Corrigendum to "The effect of perioperative glucose control on postoperative insulin resistance" [Clin Nutr 31 (5) (2012) 676-681]. Glucose 44-51 insulin Homo sapiens 77-84 29069937-21 2018 The duration of glucose administration after ceasing insulin increased with the rate and total insulin administered during HIE. Glucose 16-23 insulin Homo sapiens 53-60 29069937-21 2018 The duration of glucose administration after ceasing insulin increased with the rate and total insulin administered during HIE. Glucose 16-23 insulin Homo sapiens 95-102 29429377-2 2018 Due to the progressive nature of the disease, many people with T2D require insulin at some point, most commonly a long-acting (basal) insulin to assist with 24-h control of glucose levels. Glucose 173-180 insulin Homo sapiens 75-82 29429377-2 2018 Due to the progressive nature of the disease, many people with T2D require insulin at some point, most commonly a long-acting (basal) insulin to assist with 24-h control of glucose levels. Glucose 173-180 insulin Homo sapiens 134-141 29429377-8 2018 CONCLUSIONS: It is possible to implement an effective basal-bolus insulin regimen in people with T2D in a way that improves glucose control while minimizing negative effects on quality-of-life, treatment satisfaction, and psychological well-being. Glucose 124-131 insulin Homo sapiens 66-73 29431272-4 2018 Corrected for study effects, the magnitude of differences in postprandial glucose and insulin responses between the 2 conditions was significantly exacerbated with poorer baseline levels of fasting glucose, insulin and/or surrogate markers of beta-cell function and insulin resistance. Glucose 74-81 insulin Homo sapiens 207-214 29431272-4 2018 Corrected for study effects, the magnitude of differences in postprandial glucose and insulin responses between the 2 conditions was significantly exacerbated with poorer baseline levels of fasting glucose, insulin and/or surrogate markers of beta-cell function and insulin resistance. Glucose 74-81 insulin Homo sapiens 207-214 29431272-4 2018 Corrected for study effects, the magnitude of differences in postprandial glucose and insulin responses between the 2 conditions was significantly exacerbated with poorer baseline levels of fasting glucose, insulin and/or surrogate markers of beta-cell function and insulin resistance. Glucose 198-205 insulin Homo sapiens 86-93 29623593-6 2018 RESULTS: In people on CSII, rapid-acting insulin analogs lowered postprandial plasma glucose post-breakfast to a greater extent than did regular human insulin (RHI) (mean difference: - 1.63 mmol/L [95% confidence interval - 1.71; - 1.54]), with a comparable risk of hypoglycemia and a trend for lower glycated hemoglobin. Glucose 85-92 insulin Homo sapiens 41-48 29725969-2 2018 The aim of this study was to evaluate the quality of glucose control achieved with basal plus-correction insulin in surgical patients with and without a history of DM receiving PN. Glucose 53-60 insulin Homo sapiens 105-112 29744819-8 2018 Percentage of the time that the blood glucose value was > 7.8 mmol/L decreased after insulin glargine use (P < 0.05) but not with the exenatide intervention. Glucose 38-45 insulin Homo sapiens 88-95 29372538-5 2018 During the 21-day period, the islets co-encapsulated with the exenatide-loaded microspheres exhibited improved survival and glucose-stimulated insulin secretion, compared to those without. Glucose 124-131 insulin Homo sapiens 143-150 28866479-1 2018 OBJECTIVE: Type-1 diabetes (T1D) treatment requires exogenous insulin administrations finely tuned based on glucose monitoring to avoid hyper/hypoglycemia. Glucose 108-115 insulin Homo sapiens 62-69 29962739-6 2018 The SI levels were derived by fitting the blood glucose levels, insulin infusion and glucose input rates into the Intensive Control of Insulin-Nutrition-Glucose model. Glucose 153-160 insulin Homo sapiens 135-142 29735266-4 2018 The major objective of the current work was to reveal the molecular mechanism by which NEU1 desialylation activates the IR and to test if increase of NEU1 activity in insulin target tissues reverses insulin resistance and glucose intolerance. Glucose 222-229 insulin Homo sapiens 167-174 29747733-3 2018 Insulin is the preferred medication to optimize glucose control in women with pregestational diabetes. Glucose 48-55 insulin Homo sapiens 0-7 30869250-2 2018 Insulin therapy in type 1 diabetes aims at keeping blood glucose level in a near-normal range. Glucose 57-64 insulin Homo sapiens 0-7 30869250-6 2018 The combination of continuous glucose monitoring to insulin pumps has opened the way toward glucose-driven insulin therapy, which showed its efficacy in the reduction of hypoglycemia, and more recently on total glucose control through the first hybrid artificial pancreas. Glucose 92-99 insulin Homo sapiens 52-59 30869250-6 2018 The combination of continuous glucose monitoring to insulin pumps has opened the way toward glucose-driven insulin therapy, which showed its efficacy in the reduction of hypoglycemia, and more recently on total glucose control through the first hybrid artificial pancreas. Glucose 92-99 insulin Homo sapiens 52-59 29760049-7 2018 In women, a highly significant negative correlation between FGF23 plasma concentration and increase in plasma insulin level following an oral glucose load was found. Glucose 142-149 insulin Homo sapiens 110-117 28917079-3 2018 An oral glucose tolerance test (OGTT) showed high blood glucose levels diagnostic for diabetes mellitus at 120 min and hypoglycemia with inappropriately high insulin levels at 240 min. Glucose 8-15 insulin Homo sapiens 158-165 29693104-3 2018 Insulin resistance was induced by high glucose (HG) in human hepatocellular carcinoma (HepG2) cells. Glucose 39-46 insulin Homo sapiens 0-7 29745409-2 2018 The system relies on the MOF response to glucose stimulation and this can promote insulin delivery. Glucose 41-48 insulin Homo sapiens 82-89 29745409-3 2018 This nanosystem was successfully applied for glucose-responsive and self-regulated insulin release. Glucose 45-52 insulin Homo sapiens 83-90 29212576-7 2018 Improved peripheral insulin resistance reduces the excess delivery of free fatty acids and glucose for free fatty acid synthesis to the liver. Glucose 91-98 insulin Homo sapiens 20-27 29768196-4 2018 Accordingly, insulin signaling is impaired in Abhd15-KO adipocytes, as indicated by reduced AKT phosphorylation, glucose uptake, and de novo lipogenesis. Glucose 113-120 insulin Homo sapiens 13-20 29768196-8 2018 Notably, ABHD15 expression is decreased in humans with obesity and diabetes compared to humans with obesity and normal glucose tolerance, identifying ABHD15 as a potential therapeutic target to mitigate insulin resistance. Glucose 119-126 insulin Homo sapiens 203-210 29588341-4 2018 Insulin sensitivity, expressed by the homeostasis model assessment (HOMA) of insulin sensitivity (HOMA index = (fasting insulin x fasting glucose)/22.5). Glucose 138-145 insulin Homo sapiens 0-7 29588341-4 2018 Insulin sensitivity, expressed by the homeostasis model assessment (HOMA) of insulin sensitivity (HOMA index = (fasting insulin x fasting glucose)/22.5). Glucose 138-145 insulin Homo sapiens 77-84 29277329-2 2018 Evidence indicates that this increased risk is linked to an altered cardiac substrate preference of the insulin resistant heart, which shifts from a balanced utilization of glucose and long-chain fatty acids (FAs) towards an almost complete reliance on FAs as main fuel source. Glucose 173-180 insulin Homo sapiens 104-111 29277329-5 2018 Using functional metabolic assays we demonstrate that, similar to rodent studies, hESC-CMs subjected to 16h of high palmitate (HP) treatment develop the main features of IR, i.e., decreased insulin-stimulated glucose and FA uptake, as well as loss of endosomal acidification and insulin signaling. Glucose 209-216 insulin Homo sapiens 190-197 29314667-1 2018 BACKGROUND: We aimed to determine the clinical characteristics of type 2 diabetes patients on basal insulin therapy with inadequate glucose control due to discordance between glycated haemoglobin (HbA1c ) and fasting plasma glucose (FPG) in the real world. Glucose 132-139 insulin Homo sapiens 100-107 29314667-1 2018 BACKGROUND: We aimed to determine the clinical characteristics of type 2 diabetes patients on basal insulin therapy with inadequate glucose control due to discordance between glycated haemoglobin (HbA1c ) and fasting plasma glucose (FPG) in the real world. Glucose 224-231 insulin Homo sapiens 100-107 29436377-7 2018 Murine and human islets exposed to elevated levels of M-acylCs developed defects in glucose-stimulated insulin secretion and this was directly linked to reduced mitochondrial respiratory capacity and subsequent ability to couple glucose metabolism to insulin secretion. Glucose 84-91 insulin Homo sapiens 103-110 29576523-13 2018 CONCLUSION: As women with higher fasting glucose levels have higher chance of necessitating insulin in later pregnancies, appropriate addition of insulin at metformin initiation for these women could help better glycaemic control throughout pregnancy. Glucose 41-48 insulin Homo sapiens 92-99 29428999-5 2018 RESULTS: Postoperatively, weight loss and SI-FSIVGTT improvement was similar in both groups, whereas the acute insulin response to glucose (AIRglu) decreased in the non-diabetic participants and increased in the participants with type 2 diabetes. Glucose 131-138 insulin Homo sapiens 111-118 29470589-0 2018 Can insulin response patterns predict metabolic disease risk in individuals with normal glucose tolerance? Glucose 88-95 insulin Homo sapiens 4-11 29478099-10 2018 Humans with high levels of IFI16 exhibited larger adipocytes, an enhanced inflammatory state and impaired insulin-stimulated glucose uptake in white adipose tissue. Glucose 125-132 insulin Homo sapiens 106-113 29487953-5 2018 Adipocytes were isolated and insulin-stimulated incorporation of radiolabelled glucose into lipids was used to quantify adipocyte insulin sensitivity. Glucose 79-86 insulin Homo sapiens 29-36 29502267-0 2018 Can insulin response patterns predict metabolic disease risk in individuals with normal glucose tolerance? Glucose 88-95 insulin Homo sapiens 4-11 29526680-4 2018 Insulin sensitivity (Si) was evaluated by frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis and by HOMA-IR, insulin secretion by acute insulin response (AIR) (calculated from the first 8 min of FSIGTT) and by disposition index (DI) (Si x AIR). Glucose 73-80 insulin Homo sapiens 0-7 29083246-7 2018 Insulin sensitivity, determined by the insulin-stimulated glucose uptake (M-value), was lower in the patients group (4.2 +- 1.6 mg/min*kg versus 5.8 +- 1.7, age-adjusted p-value = 0.0205). Glucose 58-65 insulin Homo sapiens 0-7 29083246-7 2018 Insulin sensitivity, determined by the insulin-stimulated glucose uptake (M-value), was lower in the patients group (4.2 +- 1.6 mg/min*kg versus 5.8 +- 1.7, age-adjusted p-value = 0.0205). Glucose 58-65 insulin Homo sapiens 39-46 30440879-2 2018 Diabetes is characterized by elevated glucose levels, that may be treated with insulin. Glucose 38-45 insulin Homo sapiens 79-86 29664632-10 2018 Finally, the oral administration of insulin-loaded microgels to STZ-induced diabetic rats led to a continuous decline in the fasting blood glucose level within 2 to 4 h, and the hypoglycemic effect maintained over 6 h in vivo. Glucose 139-146 insulin Homo sapiens 36-43 33445271-3 2018 Herein, we described a new kind of bifunctional polymeric nanogels for efficient loading and glucose-triggered release of insulin. Glucose 93-100 insulin Homo sapiens 122-129 33445271-6 2018 The structure, morphology, and drug-loading properties of the nanogels were well-characterized, and glucose-triggered insulin release was achieved based on the glucose-responsiveness of PBA groups. Glucose 100-107 insulin Homo sapiens 118-125 33445271-6 2018 The structure, morphology, and drug-loading properties of the nanogels were well-characterized, and glucose-triggered insulin release was achieved based on the glucose-responsiveness of PBA groups. Glucose 160-167 insulin Homo sapiens 118-125 33445271-8 2018 This kind of bifunctional nanogels would be promising candidates for glucose-responsive delivery of insulin in the future. Glucose 69-76 insulin Homo sapiens 100-107 29886443-3 2018 The objective of the present study is to determine the effectiveness of 6 months" closed-loop compared with manually determined insulin dosing on time-in-target glucose range in adults with type 1 diabetes. Glucose 161-168 insulin Homo sapiens 128-135 29875472-0 2018 Glucose challenge metabolomics implicates medium-chain acylcarnitines in insulin resistance. Glucose 0-7 insulin Homo sapiens 73-80 29875472-10 2018 In mouse 3T3-L1 adipocytes exposed to different acylcarnitines, we observed blunted insulin-stimulated glucose uptake after treatment with C10- or C12-carnitine. Glucose 103-110 insulin Homo sapiens 84-91 29866735-4 2018 We hypothesise that preoperative liraglutide (a synthetic GLP-1 analogue) will reduce the number of patients requiring insulin to achieve glucose values<8 mmol l-1 in the intraoperative period. Glucose 138-145 insulin Homo sapiens 119-126 29865281-5 2018 Insulin secretion rates (ISR) were determined by deconvolution modeling to assess glucose-stimulated insulin secretion ([GSIS: ISR/glucose total area under the curve (tAUC)]) and ss-cell function (Disposition Index [DI: GSIS/IR]) relative to skeletal muscle (Matsuda Index), hepatic (HOMA-IR) and adipose (Adipose-IRfasting) insulin resistance (IR). Glucose 82-89 insulin Homo sapiens 101-108 29607651-9 2018 In HIV-positive persons, lower levels of plasma acylcarnitines, including the C2 product of complete fatty acid oxidation, are a more prominent feature of insulin resistance than changes in BCAA, suggesting impaired fatty acid uptake and/or mitochondrial oxidation is a central aspect of glucose intolerance in this population. Glucose 288-295 insulin Homo sapiens 155-162 28699407-9 2018 Future directions highlighting the H2S-mediated homeostatic control of glucose metabolism under physiological and insulin-resistant conditions are also discussed. Glucose 71-78 insulin Homo sapiens 114-121 29604334-5 2018 Blockage of Cav-2 ATI protects against insulin resistance by preventing Cav-2beta-PTP1B-directed IR desensitization, thereby normalizing insulin sensitivity and glucose uptake. Glucose 161-168 insulin Homo sapiens 39-46 29704509-6 2018 Thus it responds to endogenous medium and long chain unsaturated fatty acids, resulting in enhancement of insulin secretion during increased glucose levels. Glucose 141-148 insulin Homo sapiens 106-113 29069937-5 2018 Associations between insulin and glucose/electrolyte homeostasis were explored by comparing insulin administration and glucose or electrolyte concentrations and replacement. Glucose 33-40 insulin Homo sapiens 21-28 29069937-20 2018 Glucose was administered for a median of 18h after ceasing insulin. Glucose 0-7 insulin Homo sapiens 59-66 29509570-5 2018 INTERVENTIONS: Liberal control patients received insulin therapy if glucose was greater than 14 mmol/L (target: 10-14 mmol/L [180-252 mg/dL]). Glucose 68-75 insulin Homo sapiens 49-56 29509570-6 2018 Conventional control patients received insulin therapy if glucose was greater than 10 mmol/L (target: 6-10 mmol/L [108-180 mg/dL]). Glucose 58-65 insulin Homo sapiens 39-46 29619751-1 2018 INTRODUCTION: Although reduction in the incidence of nocturnal hypoglycemia, as estimated by symptom or self-monitored plasma glucose, was shown to be more pronounced with 300 units/mL insulin glargine (Gla-300) than with 100 units/mL insulin glargine (Gla-100) in type 2 diabetes patients, the exact frequency of nocturnal hypoglycemia estimated with continuous glucose monitoring (CGM) has not been reported. Glucose 126-133 insulin Homo sapiens 185-192 29619751-1 2018 INTRODUCTION: Although reduction in the incidence of nocturnal hypoglycemia, as estimated by symptom or self-monitored plasma glucose, was shown to be more pronounced with 300 units/mL insulin glargine (Gla-300) than with 100 units/mL insulin glargine (Gla-100) in type 2 diabetes patients, the exact frequency of nocturnal hypoglycemia estimated with continuous glucose monitoring (CGM) has not been reported. Glucose 363-370 insulin Homo sapiens 185-192 29621562-0 2018 Development and validation of a scoring system for prediction of insulin requirement for optimal control of blood glucose during glucocorticoid treatments. Glucose 114-121 insulin Homo sapiens 65-72 29621562-1 2018 AIMS: We have developed and validated a novel scoring system to predict insulin requirement for optimal control of blood glucose during glucocorticoid (GC) treatments, by retrospective analyses of clinical parameters before GC treatment. Glucose 121-128 insulin Homo sapiens 72-79 29873517-3 2018 Development and rapid improvement of continuous glucose sensor technology has recently allowed swift progress toward a fully closed-loop insulin delivery system. Glucose 48-55 insulin Homo sapiens 137-144 29873517-5 2018 When in auto mode, this is a hybrid closed-loop insulin delivery system that automatically adjusts basal insulin delivery every 5 min based on sensor glucose to maintain blood glucose levels as close to a specific target as possible. Glucose 150-157 insulin Homo sapiens 48-55 29873517-5 2018 When in auto mode, this is a hybrid closed-loop insulin delivery system that automatically adjusts basal insulin delivery every 5 min based on sensor glucose to maintain blood glucose levels as close to a specific target as possible. Glucose 150-157 insulin Homo sapiens 105-112 29916738-2 2018 These advances enable more meaningful monitoring of blood glucose values with the facilitation of more optimal insulin dosing and delivery. Glucose 58-65 insulin Homo sapiens 111-118 29488154-1 2018 BACKGROUND AND AIMS: Fasiglifam, a potent, selective novel agonist of G protein-coupled receptor 40, stimulates insulin secretion at elevated blood glucose levels in a glucose-dependent manner. Glucose 168-175 insulin Homo sapiens 112-119 29887987-0 2018 Insulin degludec overdose in an adolescent with type 1 diabetes: proactive management including monitoring using the Freestyle Libre flash glucose monitoring system. Glucose 139-146 insulin Homo sapiens 0-7 28577150-3 2018 RESULTS: Men yogurt consumers had a lower body weight, BMI, % body fat, waist circumference and lower plasma insulin, and C-peptide concentrations in response to oral glucose, while women yogurt consumers had lower waist circumference, BMI, % body fat, plasma glucose, insulin, and C-peptide compared with non-consumers (P < 0.05). Glucose 167-174 insulin Homo sapiens 109-116 28577150-3 2018 RESULTS: Men yogurt consumers had a lower body weight, BMI, % body fat, waist circumference and lower plasma insulin, and C-peptide concentrations in response to oral glucose, while women yogurt consumers had lower waist circumference, BMI, % body fat, plasma glucose, insulin, and C-peptide compared with non-consumers (P < 0.05). Glucose 167-174 insulin Homo sapiens 122-131 29911757-7 2018 RESULTS: Reduction in elevated blood triglyceride and glucose levels in hospitalized diabetic patients resulted in a rapid decline in glucose levels and in the need for insulin therapy. Glucose 54-61 insulin Homo sapiens 169-176 29669812-1 2018 Tankyrase 1 and 2, members of the poly(ADP-ribose) polymerase family, have previously been shown to play a role in insulin-mediated glucose uptake in adipocytes. Glucose 132-139 insulin Homo sapiens 115-122 29669812-3 2018 Treatment of differentiated L6 myotubes with the small molecule tankyrase inhibitor XAV939 resulted in insulin resistance as determined by impaired insulin-stimulated glucose uptake. Glucose 167-174 insulin Homo sapiens 148-155 29669812-6 2018 Inhibition of the proteasome using MG132 rescued GSV protein levels as well as insulin-stimulated glucose uptake in XAV939-treated L6 myotubes. Glucose 98-105 insulin Homo sapiens 79-86 29082896-0 2018 Optimal Cut-off Points of Fasting and Post-Glucose Stimulus Surrogates of Insulin Resistance as Predictors of Metabolic Syndrome in Adolescents According to Several Definitions OBJECTIVE: The aim of this study was to determine optimal cut-off points for fasting and post-glucose stimulus surrogates of insulin resistance to predict metabolic syndrome in adolescents according to several definitions. Glucose 43-50 insulin Homo sapiens 74-81 29082896-0 2018 Optimal Cut-off Points of Fasting and Post-Glucose Stimulus Surrogates of Insulin Resistance as Predictors of Metabolic Syndrome in Adolescents According to Several Definitions OBJECTIVE: The aim of this study was to determine optimal cut-off points for fasting and post-glucose stimulus surrogates of insulin resistance to predict metabolic syndrome in adolescents according to several definitions. Glucose 271-278 insulin Homo sapiens 74-81 29150756-5 2018 Insulin-treated patients had higher fasting OGTT glucose than patients on diet therapy (p = 0.003). Glucose 49-56 insulin Homo sapiens 0-7 29762376-5 2018 In the fed state, the effects on glucose metabolism are related to the effects of SCFA on insulin sensitivity, possibly the consequence of their influence on lipid metabolism. Glucose 33-40 insulin Homo sapiens 90-97 29572336-0 2018 GPR40-Mediated Galpha12 Activation by Allosteric Full Agonists Highly Efficacious at Potentiating Glucose-Stimulated Insulin Secretion in Human Islets. Glucose 98-105 insulin Homo sapiens 117-124 29572336-6 2018 In this study, we described the discovery and characterization of Compound A, a newly identified GPR40 allosteric full agonist highly efficacious in human islets at potentiating glucose-stimulated insulin secretion. Glucose 178-185 insulin Homo sapiens 197-204 29735266-13 2018 CONCLUSION: Together our results demonstrate that increase of NEU1 activity in insulin target tissues reverses insulin resistance and glucose intolerance suggesting that a pharmacological modulation of NEU1 activity may be potentially explored for restoring insulin sensitivity and resolving hyperglycemia associated with T2DM. Glucose 134-141 insulin Homo sapiens 79-86 29665988-1 2018 Insulin plays roles in lipid uptake, lipolysis, and lipogenesis, in addition to controlling blood glucose levels. Glucose 98-105 insulin Homo sapiens 0-7 29623975-2 2018 Herein, we developed an excellent glucose-responsive insulin delivery system using a pH-sensitive peptide hydrogel loaded with insulin and a glucose-specific enzyme. Glucose 34-41 insulin Homo sapiens 53-60 29623975-4 2018 When hyperglycemia is encountered, the enzymatic conversion of glucose into gluconic acid leads to a decrease in the local pH, and the hydrogel is disassembled because of the strong inter- and intramolecular electrostatic repulsions between ornithine (Orn) residues; this is followed by the release of insulin. Glucose 63-70 insulin Homo sapiens 302-309 29623975-5 2018 The glucose-responsive hydrogel system was characterized by studying its structure, conformation, rheology, morphology, acid sensitivity and the amounts of consistent release of insulin in vitro and in vivo. Glucose 4-11 insulin Homo sapiens 178-185 29851323-1 2018 Systems for continuous glucose monitoring (CGM) are changing the management of insulin treated patient providing dynamic glucose information. Glucose 23-30 insulin Homo sapiens 79-86 29851323-1 2018 Systems for continuous glucose monitoring (CGM) are changing the management of insulin treated patient providing dynamic glucose information. Glucose 121-128 insulin Homo sapiens 79-86 29813102-0 2018 Palmitate and insulin counteract glucose-induced thioredoxin interacting protein (TXNIP) expression in insulin secreting cells via distinct mechanisms. Glucose 33-40 insulin Homo sapiens 14-21 29813102-0 2018 Palmitate and insulin counteract glucose-induced thioredoxin interacting protein (TXNIP) expression in insulin secreting cells via distinct mechanisms. Glucose 33-40 insulin Homo sapiens 103-110 29813102-16 2018 In conclusion, glucose-induced TXNIP expression is efficiently antagonized by two independent mechanisms, namely via an autocrine activation of insulin/IGF-1 receptors involving HDAC and by palmitate attenuating oxidative stress of beta-cells. Glucose 15-22 insulin Homo sapiens 144-151 29892261-10 2018 First, elevated glucose induces glycolytic genes in pancreatic beta cells, which induces a semi-stable persistent increase in insulin secretion, which could drive obesity and insulin resistance, and also due to glucose toxicity could eventually lead to beta-cell decompensation and diabetes. Glucose 16-23 insulin Homo sapiens 126-133 29867778-3 2018 Genetic defects in the pancreatic beta-cells result in the decrease of insulin production required for glucose utilization thereby lead to early-onset diabetes (often <25 years). Glucose 103-110 insulin Homo sapiens 71-78 29540530-5 2018 Both transporters are also required for optimum glucose-stimulated insulin secretion, likely via complementary roles. Glucose 48-55 insulin Homo sapiens 67-74 29540530-8 2018 Its knockdown caused similar defective stability of young granules and glucose-stimulated insulin secretion, neither of which were rescued with exogenous cholesterol. Glucose 71-78 insulin Homo sapiens 90-97 29760587-4 2018 Main body: The adipokines leptin, resistin, visfatin and adiponectin have all been shown to affect skeletal muscle insulin sensitivity by impacting on the activity of components within insulin signalling pathways, affecting GLUT4 translocation and modulating insulin-mediated skeletal muscle glucose uptake. Glucose 292-299 insulin Homo sapiens 115-122 29760587-4 2018 Main body: The adipokines leptin, resistin, visfatin and adiponectin have all been shown to affect skeletal muscle insulin sensitivity by impacting on the activity of components within insulin signalling pathways, affecting GLUT4 translocation and modulating insulin-mediated skeletal muscle glucose uptake. Glucose 292-299 insulin Homo sapiens 185-192 29738707-1 2018 Immature beta cells secrete insulin at a lower glucose threshold compared to mature beta cells. Glucose 47-54 insulin Homo sapiens 28-35 29477658-2 2018 It not only promoted glucose metabolism, but also advanced glucose-stimulated insulin secretion. Glucose 59-66 insulin Homo sapiens 78-85 29477658-8 2018 In NIT cell line, it promoted glucose-stimulated insulin secretion at the 20 mmol/l of glucose. Glucose 30-37 insulin Homo sapiens 49-56 29477658-8 2018 In NIT cell line, it promoted glucose-stimulated insulin secretion at the 20 mmol/l of glucose. Glucose 87-94 insulin Homo sapiens 49-56 29501738-12 2018 Finally, the efficacy of insulin SDS-NPs was demonstrated in vivo (100 or 250 UI insulin/kg) with a reduction of blood glucose levels in diabetic rats. Glucose 119-126 insulin Homo sapiens 25-32 29501738-12 2018 Finally, the efficacy of insulin SDS-NPs was demonstrated in vivo (100 or 250 UI insulin/kg) with a reduction of blood glucose levels in diabetic rats. Glucose 119-126 insulin Homo sapiens 81-88 29351421-6 2018 After intravenous glucose administration, insulin clearance during first phase insulin secretion was markedly higher in DIRKO than in WT mice (0.68 +- 0.06 10-3 l/min in DIRKO mice vs. 0.54 +- 0.03 10-3 1/min in WT mice, P = 0.02). Glucose 18-25 insulin Homo sapiens 42-49 29351421-6 2018 After intravenous glucose administration, insulin clearance during first phase insulin secretion was markedly higher in DIRKO than in WT mice (0.68 +- 0.06 10-3 l/min in DIRKO mice vs. 0.54 +- 0.03 10-3 1/min in WT mice, P = 0.02). Glucose 18-25 insulin Homo sapiens 79-86 29316197-5 2018 Peripheral glucose uptake, which indicates insulin sensitivity, increased significantly (M value by 0.90 and M/I ratio by 0.49; both P < .05). Glucose 11-18 insulin Homo sapiens 43-50 29258910-4 2018 The advent and progress of ambulatory glucose sensor technology has enabled continuous glucose monitoring based on real-time glucose levels to be integrated with insulin therapy. Glucose 38-45 insulin Homo sapiens 162-169 29258910-4 2018 The advent and progress of ambulatory glucose sensor technology has enabled continuous glucose monitoring based on real-time glucose levels to be integrated with insulin therapy. Glucose 87-94 insulin Homo sapiens 162-169 29258910-4 2018 The advent and progress of ambulatory glucose sensor technology has enabled continuous glucose monitoring based on real-time glucose levels to be integrated with insulin therapy. Glucose 87-94 insulin Homo sapiens 162-169 29540328-3 2018 This process is responsible for the insulin stimulation of glucose uptake in muscle and fat. Glucose 59-66 insulin Homo sapiens 36-43 29318412-1 2018 Recently, great attention is paid to cardiovascular impact of non-insulin glucose-lowering drugs, particularly in terms of major cardiovascular events and risk of heart failure. Glucose 74-81 insulin Homo sapiens 66-73 29535167-0 2018 Insulin-stimulated glucose uptake in skeletal muscle, adipose tissue and liver: a positron emission tomography study. Glucose 19-26 insulin Homo sapiens 0-7 29535167-1 2018 OBJECTIVE: Insulin resistance is reflected by the rates of reduced glucose uptake (GU) into the key insulin-sensitive tissues, skeletal muscle, liver and adipose tissue. Glucose 67-74 insulin Homo sapiens 11-18 29535167-1 2018 OBJECTIVE: Insulin resistance is reflected by the rates of reduced glucose uptake (GU) into the key insulin-sensitive tissues, skeletal muscle, liver and adipose tissue. Glucose 67-74 insulin Homo sapiens 100-107 29215704-9 2018 The higher levels of glucose in the sPTD group might be due to increased insulin resistance, which is associated with a higher risk of sPTD. Glucose 21-28 insulin Homo sapiens 73-80 29150935-6 2018 Furthermore, the immunoassay tests showed that these differentiated cells in these two groups are functional and secreted C-peptide and insulin in a glucose stimulation challenge. Glucose 149-156 insulin Homo sapiens 136-143 29409041-10 2018 Compared with age-, sex-, and body mass index-matched control subjects, fasting glucose and insulin levels were significantly higher in subjects with BBS (glucose: BBS, 5.2 +- 1.2 mmol/L vs control, 4.9 +- 0.9 mmol/L, P = 0.04; insulin: BBS, 24.2 +- 17.0 pmol/L vs control, 14.2 +- 14.8 pmol/L, P < 0.001). Glucose 155-162 insulin Homo sapiens 92-99 29546329-6 2018 Main Outcome: Dynamic measures were obtained from the frequently sampled intravenous glucose tolerance test and included insulin sensitivity and acute insulin response to glucose. Glucose 171-178 insulin Homo sapiens 151-158 29546329-12 2018 Acute insulin response to glucose was associated with six metabolites; glucose had the strongest association (P = 5.68 x 10-16). Glucose 26-33 insulin Homo sapiens 6-13 29546329-12 2018 Acute insulin response to glucose was associated with six metabolites; glucose had the strongest association (P = 5.68 x 10-16). Glucose 71-78 insulin Homo sapiens 6-13 29284290-9 2018 CONCLUSIONS: Insulin pump users should not blindly rely on occlusion alarms but perform regular glucose monitoring and manufacturers should develop mechanisms that allow an earlier detection at low basal rates. Glucose 96-103 insulin Homo sapiens 13-20 29295634-0 2018 The Need to Calculate Target Glucose Levels When Measuring Changes in Insulin Sensitivity During Interventions for Individuals With Type 2 Diabetes. Glucose 29-36 insulin Homo sapiens 70-77 29295634-1 2018 BACKGROUND: Physiological models that are used with dynamic test data to assess insulin sensitivity (SI) assume that the metabolic target glucose concentration ( GTARGET) is equal to fasting glucose concentration ( G0). Glucose 138-145 insulin Homo sapiens 80-87 29295634-7 2018 Participants underwent three insulin-modified intravenous glucose tolerance tests (IM-IVGTT) at 0, 12, and 24 weeks. Glucose 58-65 insulin Homo sapiens 29-36 29390915-3 2018 One such scenario involves an insulin infusion site failure, where the insulin that is recorded as delivered fails to affect the patient"s glucose as expected. Glucose 139-146 insulin Homo sapiens 30-37 29390915-3 2018 One such scenario involves an insulin infusion site failure, where the insulin that is recorded as delivered fails to affect the patient"s glucose as expected. Glucose 139-146 insulin Homo sapiens 71-78 28541810-11 2018 CONCLUSION: Rectal cancer surgery induced profound insulin resistance, affecting glucose and fatty acid metabolism. Glucose 81-88 insulin Homo sapiens 51-58 29533157-1 2018 BACKGROUND: Previous evaluations in nondiabetic subjects revealed statistically significant correlations between fasting blood glucose (FBG) levels used as an estimate of insulin resistance and many components constituting the metabolic syndrome. Glucose 127-134 insulin Homo sapiens 171-178 29542348-4 2018 This is a summary of our experience attempting to use such devices to enhance continuous glucose monitoring-augmented insulin pump therapy. Glucose 89-96 insulin Homo sapiens 118-125 29566547-1 2018 BACKGROUND: The artificial pancreas (AP) system, a technology that automatically administers exogenous insulin in people with type 1 diabetes mellitus (T1DM) to regulate their blood glucose concentrations, necessitates the estimation of the amount of active insulin already present in the body to avoid overdosing. Glucose 182-189 insulin Homo sapiens 103-110 29794749-0 2018 The relationship of insulin resistance estimated by triglyceride glucose index and coronary plaque characteristics. Glucose 65-72 insulin Homo sapiens 20-27 28541810-7 2018 RESULTS: Hepatic insulin sensitivity (insulin-mediated suppression of glucose production) decreased significantly after surgery in both groups, with no differences between the groups. Glucose 70-77 insulin Homo sapiens 17-24 28541810-8 2018 Peripheral insulin sensitivity (glucose rate of disappearance, Rd) was significantly decreased after surgery in both groups (S: 37.2 [19.1-50.9] vs 20.6 [13.9-27.9]; P: 23.8 [15.7-35.5] vs 15.3 [12.6-19.1] micromol/kg min) but less pronounced in the supplemented group (P = .04). Glucose 32-39 insulin Homo sapiens 11-18 29665232-3 2018 Herein, a trehalose-based hydrogel is reported that stabilizes insulin to elevated temperatures prior to glucose-triggered release. Glucose 105-112 insulin Homo sapiens 63-70 29665232-6 2018 Dissolution of the hydrogel is triggered upon addition of glucose as a stronger binder to boronic acid (Kb = 2.57 vs 0.48 m-1 for trehalose), allowing the insulin that is entrapped during gelation to be released in a glucose-responsive manner. Glucose 58-65 insulin Homo sapiens 155-162 29794749-1 2018 The triglyceride glucose (TyG) index is a useful surrogate marker for insulin resistance, which is an important risk factor for coronary artery disease (CAD). Glucose 17-24 insulin Homo sapiens 70-77 29665232-6 2018 Dissolution of the hydrogel is triggered upon addition of glucose as a stronger binder to boronic acid (Kb = 2.57 vs 0.48 m-1 for trehalose), allowing the insulin that is entrapped during gelation to be released in a glucose-responsive manner. Glucose 217-224 insulin Homo sapiens 155-162 29305946-4 2018 Insulin resistance and glucose metabolism was assessed using an oral glucose tolerance test combined with isotopic tracers of [6,6-2H2]-glucose and [U-13C]-glucose, and indirect calorimetry. Glucose 69-76 insulin Homo sapiens 0-7 29305946-12 2018 Changes in peripheral insulin resistance and metabolic flexibility correlated with improved glucose tolerance (P < 0.05). Glucose 92-99 insulin Homo sapiens 22-29 29171129-10 2018 The association between fasting glucose and C-peptide decreased markedly when fasting C-peptide values were adjusted (r = 0.30, P < .01 to r = 0.07, n.s.). Glucose 32-39 insulin Homo sapiens 44-53 29649378-5 2018 Insulin resistance was calculated from fasting glucose and insulin with the homeostasis model assessment of insulin resistance (HOMA2-IR) method. Glucose 47-54 insulin Homo sapiens 0-7 29526746-5 2018 NaAsO2 significantly decreased insulin-mediated glucose uptake, as well as GLUT1 and 3 membrane translocation. Glucose 48-55 insulin Homo sapiens 31-38 29171129-10 2018 The association between fasting glucose and C-peptide decreased markedly when fasting C-peptide values were adjusted (r = 0.30, P < .01 to r = 0.07, n.s.). Glucose 32-39 insulin Homo sapiens 86-95 29769806-2 2018 Variability in glucose readings can present a significant challenge for care providers, patients and families alike and recent research demonstrates that insulin selection and site-related lipohypertrophy can significantly influence blood glucose levels. Glucose 15-22 insulin Homo sapiens 154-161 29769806-2 2018 Variability in glucose readings can present a significant challenge for care providers, patients and families alike and recent research demonstrates that insulin selection and site-related lipohypertrophy can significantly influence blood glucose levels. Glucose 239-246 insulin Homo sapiens 154-161 29769806-6 2018 As well, glucose sensors are now available that can be used for insulin dosing while reducing the number of capillary blood sugar checks. Glucose 9-16 insulin Homo sapiens 64-71 29262294-2 2018 Thus, insulin administration is an effective treatment for diabetes, which is characterized by chronic elevation of blood glucose. Glucose 122-129 insulin Homo sapiens 6-13 29724293-1 2018 The pancreatic hormone preptin amplifies glucose-mediated insulin secretion, and we investigated its circulating levels in patients with essential hypertension and possible association with carotid atherosclerosis. Glucose 41-48 insulin Homo sapiens 58-65 29734117-7 2018 Furthermore, functional characterization of the isolated cells demonstrated that glucose-stimulated insulin secretion is mainly confined to the NKX6.1-positive cells. Glucose 81-88 insulin Homo sapiens 100-107 29776493-3 2018 We find that the improved glucose tolerance is due the following events: a negative energy balance and resulting weight loss, which improve first hepatic and later peripheral insulin sensitivity, in combination with increased postprandial insulin secretion elicited particularly by exaggerated glucagon-like peptide-1 responses. Glucose 26-33 insulin Homo sapiens 175-182 29776493-3 2018 We find that the improved glucose tolerance is due the following events: a negative energy balance and resulting weight loss, which improve first hepatic and later peripheral insulin sensitivity, in combination with increased postprandial insulin secretion elicited particularly by exaggerated glucagon-like peptide-1 responses. Glucose 26-33 insulin Homo sapiens 239-246 29853879-12 2018 Conclusions: The deterioration of glucose metabolism induced by SSA treatment is caused by the less reduction of GH and the more inhibition of insulin secretion, which can be predicted by the baseline BG120 during OGTT. Glucose 34-41 insulin Homo sapiens 143-150 29451713-1 2018 BACKGROUND: Although the ability of glucose to mediate its own in vivo metabolism is long documented, the quantitative measurement of whole body glucose-mediated glucose disposal at basal insulin levels (glucose effectiveness [GE]), followed the introduction of the Minimal Model intravenous glucose tolerance test technique. Glucose 145-152 insulin Homo sapiens 188-195 29451713-1 2018 BACKGROUND: Although the ability of glucose to mediate its own in vivo metabolism is long documented, the quantitative measurement of whole body glucose-mediated glucose disposal at basal insulin levels (glucose effectiveness [GE]), followed the introduction of the Minimal Model intravenous glucose tolerance test technique. Glucose 145-152 insulin Homo sapiens 188-195 29451713-1 2018 BACKGROUND: Although the ability of glucose to mediate its own in vivo metabolism is long documented, the quantitative measurement of whole body glucose-mediated glucose disposal at basal insulin levels (glucose effectiveness [GE]), followed the introduction of the Minimal Model intravenous glucose tolerance test technique. Glucose 145-152 insulin Homo sapiens 188-195 29451713-1 2018 BACKGROUND: Although the ability of glucose to mediate its own in vivo metabolism is long documented, the quantitative measurement of whole body glucose-mediated glucose disposal at basal insulin levels (glucose effectiveness [GE]), followed the introduction of the Minimal Model intravenous glucose tolerance test technique. Glucose 145-152 insulin Homo sapiens 188-195 29339110-3 2018 KEY RESULTS: on 2-NBDG glucose uptake assay using HepG2 and L6 cells, extracts from A. cominia enhanced insulin activity by increasing glucose uptake. Glucose 23-30 insulin Homo sapiens 104-111 29687501-2 2018 Cystic fibrosis-related diabetes differs from Type 1 and Type 2 diabetes in several ways; there is a pattern of insulin deficiency with reduced and delayed insulin response to carbohydrates but a sparing of basal insulin that results in glucose abnormalities, which are frequently characterized by normal fasting glucose and postprandial hyperglycaemia. Glucose 237-244 insulin Homo sapiens 112-119 29584406-5 2018 As a proof of concept, we developed specific circuits for insulin or glucagon production in response to different glucose levels. Glucose 114-121 insulin Homo sapiens 58-65 29713388-10 2018 While glucose profiles are associated with long-term mortality in patients without diabetes, after adjusting for potential confounding variables such as age, cause of transplantation, MELD, nutrition, immunosuppressive drugs, and units of insulin administered, this does not occur among patients with diabetes. Glucose 6-13 insulin Homo sapiens 239-246 29675266-0 2018 Evaluation of insulin sensitivity by hyperinsulinemic-euglycemic clamps using stable isotope-labeled glucose. Glucose 101-108 insulin Homo sapiens 14-21 29686650-5 2018 At the cellular level, the mechanisms leading to the development of insulin resistance include mutations in the insulin receptor gene, impairments in the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway, or perturbations in the trafficking of glucose transporters (GLUTs), which mediate the uptake of glucose into cells. Glucose 249-256 insulin Homo sapiens 68-75 29518335-1 2018 Characterization of molecular mechanisms underlying pancreatic beta-cell function in relation to glucose-stimulated insulin secretion is incomplete, especially with respect to global response in the nuclear environment. Glucose 97-104 insulin Homo sapiens 116-123 29619630-3 2018 All the clinical studies that used the oral glucose tolerance test to examine insulin sensitivity found that, after glucose load, there is in migraine patients a significant increase of both plasmatic insulin and glucose concentrations in comparison with controls. Glucose 44-51 insulin Homo sapiens 78-85 29619630-3 2018 All the clinical studies that used the oral glucose tolerance test to examine insulin sensitivity found that, after glucose load, there is in migraine patients a significant increase of both plasmatic insulin and glucose concentrations in comparison with controls. Glucose 44-51 insulin Homo sapiens 201-208 29619630-3 2018 All the clinical studies that used the oral glucose tolerance test to examine insulin sensitivity found that, after glucose load, there is in migraine patients a significant increase of both plasmatic insulin and glucose concentrations in comparison with controls. Glucose 116-123 insulin Homo sapiens 78-85 29619630-3 2018 All the clinical studies that used the oral glucose tolerance test to examine insulin sensitivity found that, after glucose load, there is in migraine patients a significant increase of both plasmatic insulin and glucose concentrations in comparison with controls. Glucose 116-123 insulin Homo sapiens 201-208 29619630-3 2018 All the clinical studies that used the oral glucose tolerance test to examine insulin sensitivity found that, after glucose load, there is in migraine patients a significant increase of both plasmatic insulin and glucose concentrations in comparison with controls. Glucose 116-123 insulin Homo sapiens 78-85 29619630-3 2018 All the clinical studies that used the oral glucose tolerance test to examine insulin sensitivity found that, after glucose load, there is in migraine patients a significant increase of both plasmatic insulin and glucose concentrations in comparison with controls. Glucose 116-123 insulin Homo sapiens 201-208 29610904-0 2018 Continuous Glucose Monitoring Versus Usual Care in Patients With Type 2 Diabetes Receiving Multiple Daily Insulin Injections. Glucose 11-18 insulin Homo sapiens 106-113 29610905-0 2018 Continuous Glucose Monitoring Versus Usual Care in Patients With Type 2 Diabetes Receiving Multiple Daily Insulin Injections. Glucose 11-18 insulin Homo sapiens 106-113 29504946-2 2018 Here, we demonstrate that chronic administration of a long-acting form of FKN, FKN-Fc, can exert durable effects to improve glucose tolerance with increased glucose-stimulated insulin secretion and decreased beta cell apoptosis in obese rodent models. Glucose 157-164 insulin Homo sapiens 176-183 29504946-5 2018 This results in increased glucose-stimulated insulin secretion and decreased glucagon secretion. Glucose 26-33 insulin Homo sapiens 45-52 31149264-4 2018 Recent studies indicated that insulin rapidly and dose-dependently regulates gene expression of the same complex, but the relationship with systemic insulin resistance and glucose levels is complex. Glucose 172-179 insulin Homo sapiens 30-37 31149264-4 2018 Recent studies indicated that insulin rapidly and dose-dependently regulates gene expression of the same complex, but the relationship with systemic insulin resistance and glucose levels is complex. Glucose 172-179 insulin Homo sapiens 149-156 29091741-6 2018 Long-term health consequences of PAE-related skeletal abnormalities include impaired glucose metabolism in the skeletal muscle, resulting in glucose intolerance and insulin resistance, leading to an increased risk of type 2 diabetes. Glucose 85-92 insulin Homo sapiens 165-172 29477089-6 2018 Insulin-stimulated glucose uptake was tested by the radioactivity of tritium-labeled glucose in 3T3-L1 adipocytes. Glucose 19-26 insulin Homo sapiens 0-7 29477089-6 2018 Insulin-stimulated glucose uptake was tested by the radioactivity of tritium-labeled glucose in 3T3-L1 adipocytes. Glucose 85-92 insulin Homo sapiens 0-7 29477089-9 2018 Moreover, insulin-stimulated glucose uptake of 3T3-L1 was suppressed by treatment with LPS-induced macrophage conditioned media (CM), whereas the opposite effect was showed after treatment with the CM of macrophages transfected with miR-17. Glucose 29-36 insulin Homo sapiens 10-17 29658081-2 2018 At the decompensation stage, along with the increased content of glucose and glycated hemoglobin, a pronounced (3-fold) increase in proinsulin concentration was observed. Glucose 65-72 insulin Homo sapiens 132-142 29326365-2 2018 Whereas skeletal muscle is the primary site of insulin-mediated glucose uptake and the main target for alterations in insulin-resistant states, the relevance of MAM integrity in muscle insulin resistance is unknown. Glucose 64-71 insulin Homo sapiens 47-54 29619926-6 2018 The glucose cohort was given a continuous 5% glucose infusion with 2 IU rapid-acting insulin per 10 g of carbohydrate. Glucose 4-11 insulin Homo sapiens 85-92 29172109-1 2018 The aim of this study was to investigate the relationship between laminitis development in ponies and insulin/glucose concentrations in response to the oral glucose test (OGT) and a dietary challenge high in nonstructural carbohydrates (NSCs). Glucose 157-164 insulin Homo sapiens 102-109 29410149-0 2018 Cost calculation for a flash glucose monitoring system for UK adults with type 1 diabetes mellitus receiving intensive insulin treatment. Glucose 29-36 insulin Homo sapiens 119-126 29410149-8 2018 CONCLUSIONS: The flash monitoring system has a modest impact on glucose monitoring costs for the UK NHS for patients with T1DM using intensive insulin. Glucose 64-71 insulin Homo sapiens 143-150 29508275-12 2018 If the desired glucose targets are not met, rapid-acting or short-acting (bolus or prandial) insulin can be added at mealtime to control the expected postprandial raise in glucose. Glucose 172-179 insulin Homo sapiens 93-100 29508275-13 2018 An insulin regimen should be adopted and individualized but should, to the extent possible, closely resemble a natural physiologic state and avoid, to the extent possible, wide fluctuating glucose levels (C). Glucose 189-196 insulin Homo sapiens 3-10 29631902-6 2018 We found a T allele-dosage effect on insulin synthesis and on glucose tolerance status, therefore insulin synthesis was higher among T-allele carriers with type 2 diabetes than in wild-type individuals. Glucose 62-69 insulin Homo sapiens 98-105 29638161-2 2018 This might be partly explained by insulin or hypoglycemia-induced changes in the plasma interstitial subcutaneous (SC) fluid glucose gradient. Glucose 125-132 insulin Homo sapiens 34-41 29638161-3 2018 The aim of the present study was to assess the role of plasma insulin (PI) and hypoglycemia itself in the plasma and interstitial SC fluid glucose concentration in patients with type 1 diabetes mellitus. Glucose 139-146 insulin Homo sapiens 62-69 29404902-0 2018 Comment on "The pros and cons of continuous glucose monitoring for patients with type 1 diabetes on multiple daily injections of insulin". Glucose 44-51 insulin Homo sapiens 129-137 29196878-7 2018 However, simultaneously, SCFA participates in glucose-stimulated insulin secretion from the pancreatic beta-cells through interaction with the FFA2 and FFA3 receptors, and release of peptide hormones which control appetite. Glucose 46-53 insulin Homo sapiens 65-72 29350334-1 2018 The study aims to assess the utility of the triglyceride-glucose index (TyG) as a marker of insulin resistance (IR) in neonates. Glucose 57-64 insulin Homo sapiens 92-99 29745912-8 2018 Intensive treatment of both conditions with diet, physical activity, fenofibrates and insulin is important, as it aims to reduce TG values and normalize glucose profile. Glucose 153-160 insulin Homo sapiens 86-93 29745913-8 2018 Patient was hospitalized and based on the revealed glucose values insulin therapy was initiated with long-acting insulin analogue - Levemir and rapid-acting insulin analogue - NovoRapid. Glucose 51-58 insulin Homo sapiens 66-73 29745913-13 2018 At her 21st week of gestation patient"s glucose levels are compensated on insulin therapy and she is feeling well. Glucose 40-47 insulin Homo sapiens 74-81 29421190-2 2018 ABA stimulates insulin independent glucose uptake in myocytes and adipocytes via LANCL2 binding in vitro, improves glucose tolerance in vivo and induces brown fat activity in vitro and in vivo. Glucose 35-42 insulin Homo sapiens 15-22 29300979-2 2018 Inositol hexakisphosphate kinase-1 (IP6K1) may inhibit insulin-stimulated glucose transport in this tissue type. Glucose 74-81 insulin Homo sapiens 55-62 29373734-7 2018 Insulin sensitivity was estimated as the steady-state plasma glucose (SSPG) concentration at equilibrium during octreotide and insulin administration. Glucose 61-68 insulin Homo sapiens 0-7 29408994-0 2018 Impact of C-Peptide Status on the Response of Glucagon and Endogenous Glucose Production to Induced Hypoglycemia in T1DM. Glucose 70-77 insulin Homo sapiens 10-19 29330151-5 2018 The effect of HG + LIGHT impairing glucose-stimulated insulin secretion was reversed by IL-22. Glucose 35-42 insulin Homo sapiens 54-61 29683975-7 2018 Delta-Tp(P-V)24 hours showed a negative correlation with C-peptide increment in the glucagon stimulation test and the area under the curve of insulin level in oral glucose tolerance test. Glucose 164-171 insulin Homo sapiens 142-149 29602916-3 2018 The homeostasis model assessment of insulin resistance (HOMA-IR) score was calculated using fasting blood glucose and insulin levels measured 8.3 +- 7.8 days after onset. Glucose 106-113 insulin Homo sapiens 36-43 30008760-0 2018 Insulin Monotherapy Versus Insulin Combined with Other Glucose-Lowering Agents in Type 2 Diabetes: A Narrative Review. Glucose 55-62 insulin Homo sapiens 0-7 29679039-7 2018 In a multivariable log-binomial regression, the mean postprandial glucose was significantly associated with GDM recurrence (p = 0.017) after adjusting for maternal age, family history of diabetes, insulin use, and inter-pregnancy interval (PR = 1.04 [95% CI: 1.01, 1.07]). Glucose 66-73 insulin Homo sapiens 197-204 29257872-2 2018 Although insulin is transported across the blood-brain barrier, peripheral routes of administration are problematic due to systemic effects of insulin on blood glucose. Glucose 160-167 insulin Homo sapiens 9-16 29257872-2 2018 Although insulin is transported across the blood-brain barrier, peripheral routes of administration are problematic due to systemic effects of insulin on blood glucose. Glucose 160-167 insulin Homo sapiens 143-150 29862021-11 2018 Furthermore, reductions in pre- and post-prandial blood glucose were also observed between Basalin initiation, insulin switch and hospital discharge. Glucose 56-63 insulin Homo sapiens 111-118 29658882-6 2018 Moreover, basal and insulin-stimulated glucose uptake were significantly reduced upon CLOCK depletion. Glucose 39-46 insulin Homo sapiens 20-27 29599125-6 2018 Human insulin was detected in the blood circulation of transplanted mice for months after transplantation and increased upon glucose stimulation. Glucose 125-132 insulin Homo sapiens 6-13 29459019-0 2018 Real-time continuous glucose monitoring in adults with type 1 diabetes and impaired hypoglycaemia awareness or severe hypoglycaemia treated with multiple daily insulin injections (HypoDE): a multicentre, randomised controlled trial. Glucose 21-28 insulin Homo sapiens 160-167 28582271-7 2018 Insulin was administered when the blood glucose level was >180 mg/dL. Glucose 40-47 insulin Homo sapiens 0-7 29159483-8 2018 The pancreatic progenitor marker, nestin and beta-cell differentiation markers were assessed by qRT-PCR, while the functionality of the generated IPCs was assessed by glucose-stimulated insulin secretion (GSIS). Glucose 167-174 insulin Homo sapiens 186-193 29427946-7 2018 Most importantly, insulin analog-loaded NPs significantly increased glucose consumption in HepG2 cultures confirming protein stability and retention of protein function. Glucose 68-75 insulin Homo sapiens 18-25 29339110-3 2018 KEY RESULTS: on 2-NBDG glucose uptake assay using HepG2 and L6 cells, extracts from A. cominia enhanced insulin activity by increasing glucose uptake. Glucose 135-142 insulin Homo sapiens 104-111 29356072-7 2018 Glucose data can be visualized in multiple devices and platforms, and summarized in an ambulatory glucose profile to aid pattern recognition and insulin dose adjustment. Glucose 0-7 insulin Homo sapiens 145-152 29479811-5 2018 The resulting microneedle patch can release insulin with rapid responsiveness under hyperglycemic conditions owing to an oxidative and acidic environment because of glucose oxidation, and can therefore effectively regulate blood glucose levels within a normal range on a chemically induced type 1 diabetic mouse model with enhanced biocompatibility. Glucose 165-172 insulin Homo sapiens 44-51 28655281-7 2018 Our results showed that the insulin-loaded HEMA nanogel was able to efficiently control blood glucose as a delivery system, suggesting the HEMA nanogel using emulsion polymerization could be an alternative carrier for oral insulin delivery. Glucose 94-101 insulin Homo sapiens 28-35 29676875-3 2018 The pharmacokinetic characteristics of insulin faster aspart have the potential to better reproduce the fast endogenous prandial insulin secretion and thereby to improve postprandial glucose control compared with insulin aspart. Glucose 183-190 insulin Homo sapiens 39-46 29572460-7 2018 Further, the impaired insulin secretion in pancreatic beta-cells observed due to cytokine stress has been restored by activation of Nrf2 as assessed by glucose-stimulated insulin secretion (GSIS). Glucose 152-159 insulin Homo sapiens 22-29 29455516-3 2018 This gel-based device can partially dissociate and subsequently release insulin when triggered by hydrogen peroxide (H2O2) generated during the oxidation of glucose by a glucose-specific enzyme covalently attached inside the gel. Glucose 157-164 insulin Homo sapiens 72-79 29455516-3 2018 This gel-based device can partially dissociate and subsequently release insulin when triggered by hydrogen peroxide (H2O2) generated during the oxidation of glucose by a glucose-specific enzyme covalently attached inside the gel. Glucose 170-177 insulin Homo sapiens 72-79 29455516-5 2018 Utilizing a chemically induced type 1 diabetic mouse model, we demonstrated that this smart insulin patch with a bioresponsive core and protective shell could effectively regulate the blood glucose levels within a normal range with improved biocompatibility. Glucose 190-197 insulin Homo sapiens 92-99 29459424-1 2018 In healthy individuals, any rise in blood glucose levels is rapidly countered by the release of insulin from the beta-cells of the pancreas which in turn promotes the uptake and storage of the glucose in peripheral tissues. Glucose 42-49 insulin Homo sapiens 96-103 29459424-1 2018 In healthy individuals, any rise in blood glucose levels is rapidly countered by the release of insulin from the beta-cells of the pancreas which in turn promotes the uptake and storage of the glucose in peripheral tissues. Glucose 193-200 insulin Homo sapiens 96-103 29459424-4 2018 Elevated glucose levels trigger an influx of Ca2+ that allows fusion of the small number of insulin containing vesicles that are pre-docked at the plasma membrane but glucose also stimulates processes that allow other insulin containing vesicles located further in the cell to move to and fuse with the plasma membrane. Glucose 9-16 insulin Homo sapiens 92-99 29459424-4 2018 Elevated glucose levels trigger an influx of Ca2+ that allows fusion of the small number of insulin containing vesicles that are pre-docked at the plasma membrane but glucose also stimulates processes that allow other insulin containing vesicles located further in the cell to move to and fuse with the plasma membrane. Glucose 9-16 insulin Homo sapiens 218-225 29562908-1 2018 BACKGROUND: The triglyceride glucose (TyG) index has been suggested as a simple surrogate marker of insulin resistance. Glucose 29-36 insulin Homo sapiens 100-107 29459424-4 2018 Elevated glucose levels trigger an influx of Ca2+ that allows fusion of the small number of insulin containing vesicles that are pre-docked at the plasma membrane but glucose also stimulates processes that allow other insulin containing vesicles located further in the cell to move to and fuse with the plasma membrane. Glucose 167-174 insulin Homo sapiens 218-225 29446615-10 2018 Moreover, by taking advantage of the reversible interaction between glucose-derivative-modified insulin and the red blood cell membrane, we constructed a glucose-responsive smart insulin delivery system for long-term maintenance of blood glucose levels within a normal range. Glucose 68-75 insulin Homo sapiens 96-103 29446615-10 2018 Moreover, by taking advantage of the reversible interaction between glucose-derivative-modified insulin and the red blood cell membrane, we constructed a glucose-responsive smart insulin delivery system for long-term maintenance of blood glucose levels within a normal range. Glucose 68-75 insulin Homo sapiens 179-186 29446615-10 2018 Moreover, by taking advantage of the reversible interaction between glucose-derivative-modified insulin and the red blood cell membrane, we constructed a glucose-responsive smart insulin delivery system for long-term maintenance of blood glucose levels within a normal range. Glucose 154-161 insulin Homo sapiens 96-103 29446615-10 2018 Moreover, by taking advantage of the reversible interaction between glucose-derivative-modified insulin and the red blood cell membrane, we constructed a glucose-responsive smart insulin delivery system for long-term maintenance of blood glucose levels within a normal range. Glucose 154-161 insulin Homo sapiens 179-186 29446615-10 2018 Moreover, by taking advantage of the reversible interaction between glucose-derivative-modified insulin and the red blood cell membrane, we constructed a glucose-responsive smart insulin delivery system for long-term maintenance of blood glucose levels within a normal range. Glucose 154-161 insulin Homo sapiens 96-103 29446615-10 2018 Moreover, by taking advantage of the reversible interaction between glucose-derivative-modified insulin and the red blood cell membrane, we constructed a glucose-responsive smart insulin delivery system for long-term maintenance of blood glucose levels within a normal range. Glucose 154-161 insulin Homo sapiens 179-186 29560274-1 2018 Insulin plays a central role in glucose homeostasis, and impairment of insulin action causes glucose intolerance and leads to type 2 diabetes mellitus (T2DM). Glucose 32-39 insulin Homo sapiens 0-7 29560274-2 2018 A decrease in the transient peak and sustained increase of circulating insulin following an infusion of glucose accompany T2DM pathogenesis. Glucose 104-111 insulin Homo sapiens 71-78 29610610-7 2018 Homeostatic model assessment for insulin resistance (HOMA-IR) index was calculated as fasting insulin concentration (microunits per millilitre) x fasting glucose concentration (millimolar)/22.5. Glucose 154-161 insulin Homo sapiens 33-40 29539434-6 2018 Engrafted organoids differentiated toward insulin-positive (INS+) cells, and circulating human C-peptide was detected upon glucose challenge 1 month after transplantation. Glucose 123-130 insulin Homo sapiens 95-104 29280758-6 2018 Those with incident insulin resistance underwent 2-h oral glucose tolerance test and HbA1c. Glucose 58-65 insulin Homo sapiens 20-27 29530008-9 2018 After initiation of insulin therapy, capillary glucose normalized, and serum sodium rose from 133 on admission to 144 mmol/l during the hospital stay. Glucose 47-54 insulin Homo sapiens 20-27 29707577-7 2018 Furthermore, there was a direct association between FAI levels and frequency of glucose intolerance (OR = 2.480, 95% CI 1.387-4.434), even after adjusting for age, BMI, waist circumference, hypertension, fasting insulin, testosterone, SHBG, and family history of diabetes. Glucose 80-87 insulin Homo sapiens 212-219 29518094-9 2018 During the first post-operative week glucose control in CSII patients was overall superior compared to standard-of-care as well as once-daily insulin isophane for fasting and post-supper glucose. Glucose 187-194 insulin Homo sapiens 142-149 29549243-5 2018 Whole-body IR and insulin-mediated suppression of hepatic endogenous glucose production were measured using euglycaemic-hyperinsulinemic clamps with [6-62H2] glucose infusion. Glucose 69-76 insulin Homo sapiens 18-25 29224132-9 2018 Glycemia at the time of treatment (< 3.2 mmol/L; p < 0.001) and a higher proportion of total daily insulin from basal doses (p = 0.03) were associated with a slower post-treatment plasma glucose rise. Glucose 193-200 insulin Homo sapiens 105-112 29604374-2 2018 Insulin is one of the hormones for modulating blood glucose level and the products of which is indispensable for most diabetes patients. Glucose 52-59 insulin Homo sapiens 0-7 29220547-5 2018 Insulin secretion was measured using graded glucose infusion test. Glucose 44-51 insulin Homo sapiens 0-7 29316087-11 2018 High-levels of A-FABP might increase insulin resistance by causing glucose and lipid metabolism disorders and ultimately inducing the occurrence and development of pre-eclampsia. Glucose 67-74 insulin Homo sapiens 37-44 29604374-3 2018 Introducing microneedles (MNs) to insulin delivery is promising to pave the way for modulating glucose level noninvasively of diabetes patients, as which born to be painless, easy to handle and no need of any power supply. Glucose 95-102 insulin Homo sapiens 34-41 28922582-4 2018 In each simulation, one of ten different and individualized subcutaneous insulin boluses was administered to decrease plasma glucose (PG) from 7.0 to <=3.9 mmol/l. Glucose 125-132 insulin Homo sapiens 73-80 29230803-2 2018 Patients were randomly allocated using a web-based randomisation program to premedication with liraglutide (liraglutide group), glucose-insulin-potassium infusion (insulin infusion group) or insulin bolus regimen (insulin bolus group), targeting a glucose < 8.0 mmol.l-1 . Glucose 128-135 insulin Homo sapiens 136-143 29442075-9 2018 Testosterone improves metabolic CV risk factors including body composition, insulin resistance, and hypercholesterolemia by improving both glucose utilization and lipid metabolism by a combination of genomic and nongenomic actions of glucose uptake and utilization expression of the insulin receptor, glucose transporters, and expression on regulatory enzymes of key metabolic pathways. Glucose 234-241 insulin Homo sapiens 283-290 29307653-1 2018 Insulin secretion and sensitivity play an essential role in maintaining normal glucose level and their abnormalities result in diabetes mellitus. Glucose 79-86 insulin Homo sapiens 0-7 29307653-7 2018 Its effect on insulin-stimulated glucose uptake in the adipose tissue is controversial; both stimulation and inhibition have been reported. Glucose 33-40 insulin Homo sapiens 14-21 29153750-6 2018 Insulin-stimulated lipogenesis was assessed by measuring the incorporation of radiolabelled glucose into fat-cell lipids. Glucose 92-99 insulin Homo sapiens 0-7 29068547-2 2018 The high level of expression in pancreatic beta cells and the dependence of glucose on stimulating the secretion of insulin led to great excitement in this field. Glucose 76-83 insulin Homo sapiens 116-123 28892258-4 2018 Here we have addressed these gaps and their effects on glucose-stimulated insulin secretion (GSIS). Glucose 55-62 insulin Homo sapiens 74-81 28892258-15 2018 CONCLUSION: Local regulation of pancreatic PYY, rather than GLP-1, by DPP-IV inhibition or RYGB can directly modulate the insulin secretory response to glucose, indicating a novel role of pancreatic PYY in diabetes and weight-loss surgery. Glucose 152-159 insulin Homo sapiens 122-129 29044708-5 2018 Pharmacokinetic and pharmacodynamic studies of rapid-acting insulin analogues, together with postprandial glucose excursion data, suggest that administering these 15-20 min before food would provide optimal postprandial glucose control. Glucose 220-227 insulin Homo sapiens 60-67 29044708-6 2018 Data from clinical studies involving people with Type 1 diabetes receiving structured meals and rapid-acting insulin analogues support this, showing a reduction in post-meal glucose levels of ~30% and less hypoglycaemia when meal insulin was taken 15-20 min before a meal compared with immediately before the meal. Glucose 174-181 insulin Homo sapiens 109-116 29565719-0 2018 Effect of Insulin Analogs on Frequency of Non-Severe Hypoglycemia in Patients with Type 1 Diabetes Prone to Severe Hypoglycemia: Much Higher Rates Detected by Continuous Glucose Monitoring than by Self-Monitoring of Blood Glucose-The HypoAna Trial. Glucose 222-229 insulin Homo sapiens 10-17 29044708-6 2018 Data from clinical studies involving people with Type 1 diabetes receiving structured meals and rapid-acting insulin analogues support this, showing a reduction in post-meal glucose levels of ~30% and less hypoglycaemia when meal insulin was taken 15-20 min before a meal compared with immediately before the meal. Glucose 174-181 insulin Homo sapiens 230-237 29196782-7 2018 Following an oral glucose challenge, there was a progressive increase in the total integrated insulin response from the most insulin-sensitive to the most insulin-resistant tertiles (p < 0.001). Glucose 18-25 insulin Homo sapiens 94-101 29196782-7 2018 Following an oral glucose challenge, there was a progressive increase in the total integrated insulin response from the most insulin-sensitive to the most insulin-resistant tertiles (p < 0.001). Glucose 18-25 insulin Homo sapiens 125-132 29196782-7 2018 Following an oral glucose challenge, there was a progressive increase in the total integrated insulin response from the most insulin-sensitive to the most insulin-resistant tertiles (p < 0.001). Glucose 18-25 insulin Homo sapiens 125-132 28593616-9 2018 When compared to normo-glucose tolerant patients, the diabetic patients had a significantly lower insulin-to-glucose ratio at 30 and 60 min of the oral glucose tolerance test. Glucose 23-30 insulin Homo sapiens 98-105 28593616-9 2018 When compared to normo-glucose tolerant patients, the diabetic patients had a significantly lower insulin-to-glucose ratio at 30 and 60 min of the oral glucose tolerance test. Glucose 109-116 insulin Homo sapiens 98-105 28593616-9 2018 When compared to normo-glucose tolerant patients, the diabetic patients had a significantly lower insulin-to-glucose ratio at 30 and 60 min of the oral glucose tolerance test. Glucose 109-116 insulin Homo sapiens 98-105 28866834-7 2018 Concomitantly, insulin secretion was significantly impaired in rat INS-1 beta-cells treated with conditioned medium from insulin resistant MG-63 cells or cells exposed to high glucose concentrations. Glucose 176-183 insulin Homo sapiens 15-22 29235560-4 2018 Insulin sensitivity was evaluated by oral glucose tolerance test (OGTT) and plasma free fatty acids. Glucose 42-49 insulin Homo sapiens 0-7 31008333-5 2018 Results: We found low-quality evidence from clinical trials in ischemic or haemorrhagic stroke exploring the use of intravenous insulin aimed to achieve a tight glycaemic control with different glucose level targets and several other sources of heterogeneity. Glucose 194-201 insulin Homo sapiens 128-135 29380352-0 2018 Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1). Glucose 14-21 insulin Homo sapiens 33-40 29380352-5 2018 The left-shifted dose-response curve reveals excessive insulin secretion even under low glucose, corresponding to fasting conditions. Glucose 88-95 insulin Homo sapiens 55-62 29380352-7 2018 To conclude, our results indicate that IF1 is a negative regulator of insulin secretion involved in pancreatic beta-cell glucose sensing. Glucose 121-128 insulin Homo sapiens 70-77 29460641-6 2018 Non-insulin adjunctive therapies may improve not only glucose control, but also insulin sensitivity, in addition to preserving beta-cell function in T1D patients. Glucose 54-61 insulin Homo sapiens 4-11 29286159-7 2018 miRNA-gene networks, Kyoto Encyclopedia of Genes and Genomes pathway analysis of differentially expressed miRNAs, and miRNA overexpression in HepG2 cells revealed the critical role of insulin signaling, via miR-327, miR-466f-3p and miR-223-3p, in the effects of early life Cr restriction on glucose metabolism. Glucose 291-298 insulin Homo sapiens 184-191 28864828-5 2018 Treatment with intravenous fluid replacement, insulin, glucose, potassium and buffer solution led to a normalisation of pH and serum glucose levels. Glucose 133-140 insulin Homo sapiens 46-53 29151531-4 2018 Our case suggests that the adaption of insulin secretion to the rapid loss of weight and to the recovery of weight may require a long period of time, leading to the excessive secretion of insulin relative to the glucose level and repeated hypoglycemic episodes with postprandial hyperinsulinemia. Glucose 212-219 insulin Homo sapiens 39-46 29416587-7 2018 In PCOS patients, stepwise multiple regression including C-peptide as the criterion variable and other predictors of cardiovascular disease risk provided a significant model in which the fasting C-peptide/glucose ratio, glucose, body weight, and free estrogen index (FEI) were retained (adjusted R2 = 0.988, F = 7.161, P = 0.008). Glucose 205-212 insulin Homo sapiens 57-66 29416587-7 2018 In PCOS patients, stepwise multiple regression including C-peptide as the criterion variable and other predictors of cardiovascular disease risk provided a significant model in which the fasting C-peptide/glucose ratio, glucose, body weight, and free estrogen index (FEI) were retained (adjusted R2 = 0.988, F = 7.161, P = 0.008). Glucose 220-227 insulin Homo sapiens 57-66 29457786-1 2018 The compensatory proliferation of insulin-producing beta cells is critical to maintaining glucose homeostasis at the early stage of type 2 diabetes. Glucose 90-97 insulin Homo sapiens 34-41 29457786-5 2018 The diminished insulin signaling was partly contributed to by the hypersensitivity to glucose-induced, Ca2+-dependent activation of Erk and the mTORC1 effector p85 S6K1. Glucose 86-93 insulin Homo sapiens 15-22 28952380-1 2018 BACKGROUND: The objective of this study was to identify the minimum basal insulin infusion rates and bolus insulin doses that would result in clinically relevant changes in blood glucose levels in the most insulin sensitive subjects with type 1 diabetes. Glucose 179-186 insulin Homo sapiens 74-81 28952380-1 2018 BACKGROUND: The objective of this study was to identify the minimum basal insulin infusion rates and bolus insulin doses that would result in clinically relevant changes in blood glucose levels in the most insulin sensitive subjects with type 1 diabetes. Glucose 179-186 insulin Homo sapiens 107-114 28952380-1 2018 BACKGROUND: The objective of this study was to identify the minimum basal insulin infusion rates and bolus insulin doses that would result in clinically relevant changes in blood glucose levels in the most insulin sensitive subjects with type 1 diabetes. Glucose 179-186 insulin Homo sapiens 107-114 28952380-6 2018 The bolus insulin doses required to change blood glucose by the target amounts in the respective populations were 0.10, 0.28, and 0.30 U and 0.19, 0.55, and 0.60 U. Glucose 49-56 insulin Homo sapiens 10-17 28952380-7 2018 CONCLUSIONS: In silico modeling suggests that only a very small percentage of individuals with type 1 diabetes, corresponding to children with high insulin sensitivity and low body weight, will exhibit a clinically relevant change in blood glucose with very low basal insulin rate changes or bolus doses. Glucose 240-247 insulin Homo sapiens 148-155 28952380-7 2018 CONCLUSIONS: In silico modeling suggests that only a very small percentage of individuals with type 1 diabetes, corresponding to children with high insulin sensitivity and low body weight, will exhibit a clinically relevant change in blood glucose with very low basal insulin rate changes or bolus doses. Glucose 240-247 insulin Homo sapiens 268-275 29395839-0 2018 Lipid accumulation product and triglycerides/glucose index are useful predictors of insulin resistance. Glucose 45-52 insulin Homo sapiens 84-91 29493356-0 2018 A Neural-Network-Based Approach to Personalize Insulin Bolus Calculation Using Continuous Glucose Monitoring. Glucose 90-97 insulin Homo sapiens 47-54 29493356-1 2018 BACKGROUND: In type 1 diabetes (T1D) therapy, the calculation of the meal insulin bolus is performed according to a standard formula (SF) exploiting carbohydrate intake, carbohydrate-to-insulin ratio, correction factor, insulin on board, and target glucose. Glucose 249-256 insulin Homo sapiens 74-81 29431147-2 2018 Type 2 diabetes evolves when beta-cells fail to release appropriate amounts of insulin in response to glucose. Glucose 102-109 insulin Homo sapiens 79-86 28264604-11 2018 Continuous subcutaneous insulin infusion with continuous glucose monitoring is an alternative treatment option for pregnant women with type 1 diabetes before or during pregnancy. Glucose 57-64 insulin Homo sapiens 24-31 28879656-3 2018 Our 3D tissue engineering approach established lipolytic responses and changes in insulin-stimulated glucose uptake from small volumes of human lipoaspirate, making this methodology useful for patient specific sample source assessments of treatment strategies, drug responses, disease mechanisms, and other responses that vary between patients. Glucose 101-108 insulin Homo sapiens 82-89 29491345-3 2018 In the present study, we investigated the effect of Gln on the hypoglycemic action of insulin in skeletal muscle L6 cells at high glucose levels through the insulin signaling pathway and glycogen synthesis pathway. Glucose 130-137 insulin Homo sapiens 86-93 29292863-0 2018 Extracellular Vesicles from Hypoxic Adipocytes and Obese Subjects Reduce Insulin-Stimulated Glucose Uptake. Glucose 92-99 insulin Homo sapiens 73-80 29292863-4 2018 Cultured adipocytes are incubated with EVs and activation of insulin signalling cascades and insulin-stimulated glucose transport are measured. Glucose 112-119 insulin Homo sapiens 93-100 29449181-10 2018 Insulin secretion changed proportional to glucose levels and insulin clearance increased after reversal. Glucose 42-49 insulin Homo sapiens 0-7 29625946-12 2018 Average insulin to glucose ratio was 0.10+-0.044 in NDHF patients which was significantly (p<0.0001) lowered in controls i.e., 0.073+-0.039. Glucose 19-26 insulin Homo sapiens 8-15 29337272-2 2018 Gestational diabetes mellitus (GDM) is defined as a state of glucose intolerance characterized by beta-cell dysfunction and insulin resistance. Glucose 61-68 insulin Homo sapiens 124-131 29536672-2 2018 Preparations from normal donors were tested with a standardized protocol evaluating dynamic insulin secretion induced by glucose, tolbutamide, and cAMP (forskolin). Glucose 121-128 insulin Homo sapiens 92-99 29536672-4 2018 Low purity (25-45%) of the preparation (n = 8) blunted the first phase of insulin secretion induced by glucose or tolbutamide and increased basal secretion, resulting in threefold lower stimulation index than in more pure (55-95%) preparations (n = 43). Glucose 103-110 insulin Homo sapiens 74-81 29322561-4 2018 We evaluated the effects of the oxygen-generating PDMS + CaO2 scaffold on viability, caspase-3 and caspase-7 activity, oxygen consumption rate (OCR), glucose-stimulated insulin secretion (GSIS), hypoxic cell marker expression, and reactive oxygen species (ROS) levels in porcine neonatal pancreatic cell clusters (NPCCs). Glucose 150-157 insulin Homo sapiens 169-176 25905339-1 2000 It is well established that decreased peripheral glucose uptake (mainly muscle) combined with augmented endogenous glucose production are characteristic features of insulin resistance. Glucose 49-56 insulin Homo sapiens 165-172 25905339-1 2000 It is well established that decreased peripheral glucose uptake (mainly muscle) combined with augmented endogenous glucose production are characteristic features of insulin resistance. Glucose 115-122 insulin Homo sapiens 165-172 25905339-3 2000 Compensatory insulin secretion by the pancreatic beta-cells may at first maintain normal plasma glucose levels, but beta-cell function is already abnormal at this stage, and progressively worsens over time. Glucose 96-103 insulin Homo sapiens 13-20 25905339-6 2000 Moreover, hypothalamic insulin resistance (central nervous system) also impairs the ability of circulating insulin to suppress glucose production, and renal tubular glucose reabsorption capacity may be enhanced despite hyperglycemia in T2DM. Glucose 127-134 insulin Homo sapiens 23-30 29534385-13 2018 Multivariate linear regression analysis also found that there were significant relationships between handgrip, insulin, insulin resistance levels and glucose and lipid metabolic disorders. Glucose 150-157 insulin Homo sapiens 111-118 29534385-13 2018 Multivariate linear regression analysis also found that there were significant relationships between handgrip, insulin, insulin resistance levels and glucose and lipid metabolic disorders. Glucose 150-157 insulin Homo sapiens 120-127 29577107-7 2018 Main Outcome Measure: Insulin secretion rate (ISR) was estimated from peripheral plasma C-peptide levels after a 3-hour 75-g oral glucose tolerance test done at baseline and week 24. Glucose 130-137 insulin Homo sapiens 22-29 25905343-0 2000 Classification of Diabetes Mellitus Diabetes is a heterogeneous, complex metabolic disorder characterized by elevated blood glucose concentration secondary to either resistance to the action of insulin, insufficient insulin secretion, or both. Glucose 124-131 insulin Homo sapiens 194-201 25905343-3 2000 The absolute plasma insulin concentration (both fasting and meal-stimulated) usually is increased, although "relative" to the severity of insulin resistance, the plasma insulin concentration is insufficient to maintain normal glucose homeostasis. Glucose 226-233 insulin Homo sapiens 20-27 29471797-6 2018 Compared to baseline, oral glucose tolerance tests showed reduced glucose and insulin levels at all time points following the exercise training (all P < 0.001). Glucose 27-34 insulin Homo sapiens 78-85 30603362-3 2018 Together with the inhibitory effects of synthetic human IAPP (hIAPP) on insulin secretion, our studies, using hIAPP transgenic mice, in which glucose-stimulated insulin secretion was moderately reduced without amyloid deposit, and hIAPP gene-transfected beta-cell lines, in which insulin secretion was markedly impaired without amyloid, predicted that soluble hIAPP-related molecules would exert cytotoxicity on beta-cells. Glucose 142-149 insulin Homo sapiens 161-168 30603362-3 2018 Together with the inhibitory effects of synthetic human IAPP (hIAPP) on insulin secretion, our studies, using hIAPP transgenic mice, in which glucose-stimulated insulin secretion was moderately reduced without amyloid deposit, and hIAPP gene-transfected beta-cell lines, in which insulin secretion was markedly impaired without amyloid, predicted that soluble hIAPP-related molecules would exert cytotoxicity on beta-cells. Glucose 142-149 insulin Homo sapiens 161-168 29458348-8 2018 Having easy access to blood glucose data on a continuous basis also allowed participants to develop a better understanding of how insulin, activity and food impacted on blood glucose. Glucose 28-35 insulin Homo sapiens 130-137 29675042-7 2018 CC genotype carriers at rs9840992 showed higher insulin levels at 120 min after a 75 g glucose load than noncarriers. Glucose 87-94 insulin Homo sapiens 48-55 28895655-3 2018 MATERIALS AND METHODS: Self-titration of insulin doses targeting a fasting plasma glucose <=5.3 mmoL/L (95 mg/dL) was promoted at every visit and cardiovascular and other serious health outcomes were ascertained. Glucose 82-89 insulin Homo sapiens 41-48 29282201-1 2018 Although the mechanisms by which glucose regulates insulin secretion from pancreatic beta-cells are now well described, the way glucose modulates gene expression in such cells needs more understanding. Glucose 33-40 insulin Homo sapiens 51-58 29285796-10 2018 CONCLUSIONS: Weight-based treatment using 0.3 g/kg glucose was more effective for symptomatic hypoglycaemia in children and adults with Type 1 diabetes who were using continuous subcutaneous insulin infusion than treatment based on current international recommendations. Glucose 51-58 insulin Homo sapiens 191-198 29565719-0 2018 Effect of Insulin Analogs on Frequency of Non-Severe Hypoglycemia in Patients with Type 1 Diabetes Prone to Severe Hypoglycemia: Much Higher Rates Detected by Continuous Glucose Monitoring than by Self-Monitoring of Blood Glucose-The HypoAna Trial. Glucose 170-177 insulin Homo sapiens 10-17 29449893-10 2018 We also observe increased AUC of glucose (p < 0.001) and insulin during oGTT, featuring a frame of hyperglycemia and hyperinsulinemia, suggesting insulin resistance. Glucose 33-40 insulin Homo sapiens 125-132 29193093-5 2018 Insulin-stimulated adipose tissue glucose uptake rates are lower in obese versus lean individuals, but this difference is abolished when values are normalised to whole-body fat mass. Glucose 34-41 insulin Homo sapiens 0-7 29193093-14 2018 Lower insulin-stimulated glucose uptake rates in obese versus lean individuals were eradicated when normalised to whole-body fat mass (P = 0.416). Glucose 25-32 insulin Homo sapiens 6-13 29193093-17 2018 Finally, lower insulin-stimulated SCAT glucose uptake rates in obese individuals are proportional to whole-body fat mass, suggesting a compensatory down-regulation, presumably to prevent excessive de novo lipogenesis in adipose tissue. Glucose 39-46 insulin Homo sapiens 15-22 29619381-3 2018 Insulin is considered the most effective glucose-lowering therapy available and is required by people with type 1 diabetes mellitus to control their blood glucose levels; yet, many people with type 2 diabetes mellitus will also eventually require insulin therapy, due to the progressive nature of the disease. Glucose 41-48 insulin Homo sapiens 0-7 29456931-4 2018 Homeostatic model of insulin resistance (HOMA-IR) was calculated using the formula (Fasting Blood Glucose *Insulin/405). Glucose 98-105 insulin Homo sapiens 21-28 29419919-8 2018 During the first 2 full days of insulin therapy, mean plasma glucose was 8.2 mmol/L for IV, 9.5 for SC (P = .025). Glucose 61-68 insulin Homo sapiens 32-39 29421825-1 2018 Insulin and leptin have an overlapping anorexigenic action as well as opposite effects on glucose and lipid metabolism. Glucose 90-97 insulin Homo sapiens 0-7 29316397-1 2018 G protein-coupled receptor 40 (GPR40) has become an attractive target for the treatment of diabetes since it was shown clinically to promote glucose-stimulated insulin secretion. Glucose 141-148 insulin Homo sapiens 160-167 28943275-8 2018 CONCLUSIONS: Mifepristone enhanced insulin-stimulated glucose uptake through a mechanism that involves a decrease in mitochondrial function and AMPK activation in skeletal muscle cells. Glucose 54-61 insulin Homo sapiens 35-42 29414682-3 2018 (2018), who demonstrate that glucose-induced 20-hydroxyeicosatetraenoic acid (20-HETE) amplifies insulin secretion through autocrine activation of FFAR1. Glucose 29-36 insulin Homo sapiens 97-104 28943275-0 2018 Mifepristone enhances insulin-stimulated Akt phosphorylation and glucose uptake in skeletal muscle cells. Glucose 65-72 insulin Homo sapiens 22-29 28943275-4 2018 PURPOSE: To determine the effects of mifepristone on insulin-stimulated glucose uptake on a model of L6 rat-derived skeletal muscle cells. Glucose 72-79 insulin Homo sapiens 53-60 29414687-8 2018 Blocking GPR40 reverses improvements in glucose tolerance and insulin sensitivity in PAHSA-treated chow- and HFD-fed mice and directly inhibits PAHSA augmentation of glucose-stimulated insulin secretion in human islets. Glucose 166-173 insulin Homo sapiens 185-192 29396395-1 2018 Pancreatic beta cells are highly specialized to regulate systemic glucose levels by secreting insulin. Glucose 66-73 insulin Homo sapiens 94-101 28943275-5 2018 RESULTS: Mifepristone enhanced insulin-dependent glucose uptake, GLUT4 translocation to the plasma membrane and Akt Ser473 phosphorylation in L6 myotubes. Glucose 49-56 insulin Homo sapiens 31-38 29402319-0 2018 Makes FLASH the difference between the intervention group and the treatment-as-usual group in an evaluation study of a structured education and treatment programme for flash glucose monitoring devices in people with diabetes on intensive insulin therapy: study protocol for a randomised controlled trial. Glucose 174-181 insulin Homo sapiens 238-245 29393871-0 2018 Combination Treatment of Deep Sea Water and Fucoidan Attenuates High Glucose-Induced Insulin-Resistance in HepG2 Hepatocytes. Glucose 69-76 insulin Homo sapiens 85-92 29396395-3 2018 In contrast, proliferation is robust in neonatal beta cells that are functionally immature as defined by a lower set point for glucose-stimulated insulin secretion. Glucose 127-134 insulin Homo sapiens 146-153 28780983-11 2018 Adjusting the ratio of insulin and glucose could provide a novel train of thought for freely treating patients with severe traumatic injury with different dosages of insulin according to the degree of inflammation. Glucose 35-42 insulin Homo sapiens 166-173 29134285-0 2018 Impact of variations in duodenal glucose load on insulin clearance in health and type 2 diabetes. Glucose 33-40 insulin Homo sapiens 49-56 29118024-8 2018 Instead, early insulin release during glucose challenge was attenuated relative to the rise in glycemia. Glucose 38-45 insulin Homo sapiens 15-22 29506229-4 2018 Insulin resistance in cancer patients is characterized by increased hepatic glucose production and gluconeogenesis, and unlike type 2 diabetes, normal fasting glucose with high, normal or low levels of insulin. Glucose 76-83 insulin Homo sapiens 0-7 32169204-4 2018 Insulin resistance in cancer patients is characterized by increased hepatic glucose production and gluconeogenesis, and unlike type 2 diabetes, normal fasting glucose with high, normal or low levels of insulin. Glucose 76-83 insulin Homo sapiens 0-7 28921001-8 2018 Activation of C3aR and C5aR1 potentiated glucose-induced insulin secretion from human and mouse islets, increased [Ca2+]i and ATP generation, and protected islets against apoptosis induced by a pro-apoptotic cytokine cocktail or palmitate. Glucose 41-48 insulin Homo sapiens 57-64 29223807-1 2018 The free fatty acid receptor 1 (FFA1) is a potential target due to its function in enhancement of glucose-stimulated insulin secretion. Glucose 98-105 insulin Homo sapiens 117-124 29120677-7 2018 The serum 25-hydroxyvitamin D and fasting insulin levels were measured, and insulin resistance was calculated using the formula: fasting plasma glucose (mg/dl) x fasting insulin (mIU/l)/405. Glucose 144-151 insulin Homo sapiens 76-83 29479386-4 2018 Blockade of the L-type calcium channels that mediate the antihypertensive effect of CCBs also decreases the release of insulin from pancreatic beta-islet cells and reduces glucose uptake by tissues (insulin resistance). Glucose 172-179 insulin Homo sapiens 199-206 29120677-7 2018 The serum 25-hydroxyvitamin D and fasting insulin levels were measured, and insulin resistance was calculated using the formula: fasting plasma glucose (mg/dl) x fasting insulin (mIU/l)/405. Glucose 144-151 insulin Homo sapiens 76-83 29392186-6 2018 Since beta-cell death or dysfunction lies at the heart of both T2DM as well as type 1 diabetes mellitus (T1DM), environmental endocrine disrupting chemicals (EDCs) that disrupt the production or regulated release of the glucose-lowering hormone insulin are likely contributors to diabetes risk. Glucose 220-227 insulin Homo sapiens 245-252 29274892-9 2018 African-Americans had higher baseline acute insulin response to glucose (AIRg measured by frequently sampled intravenous glucose tolerance test) compared to Caucasians, despite having less visceral adipose tissue mass and intrahepatic lipid; all other glycemic variables were similar between races. Glucose 64-71 insulin Homo sapiens 44-51 29393039-2 2018 Individuals with type 1 diabetes are therefore recommended to frequently inject insulin subcutaneously to keep near-normal blood glucose levels, preventing the progression and onset of diabetes-related complications, i.e. kidney failure, blindness, amputation, stroke and heart attack. Glucose 129-136 insulin Homo sapiens 80-87 29393039-6 2018 We showed that the glucose response to low-dose glucagon was dose-dependent but was impaired during high blood levels of insulin, after one week of low carbohydrate diet and perhaps 8-9 hours after ethanol intake. Glucose 19-26 insulin Homo sapiens 121-128 29044702-11 2018 CONCLUSIONS: In studies randomizing pregnant women to glucose-lowering therapy, metformin was associated with lower gestational weight gain and a lower risk of pre-eclampsia compared with insulin. Glucose 54-61 insulin Homo sapiens 188-195 29141982-0 2018 A Partial Loss-of-Function Variant in AKT2 Is Associated With Reduced Insulin-Mediated Glucose Uptake in Multiple Insulin-Sensitive Tissues: A Genotype-Based Callback Positron Emission Tomography Study. Glucose 87-94 insulin Homo sapiens 70-77 28948712-0 2018 Decline in the acute insulin response in relationship to plasma glucose concentrations. Glucose 64-71 insulin Homo sapiens 21-28 28948712-6 2018 RESULTS: In certain groups, the relationship between acute insulin response and increasing plasma glucose levels was non-linear. Glucose 98-105 insulin Homo sapiens 59-66 28948712-10 2018 However, the relationship between acute insulin response and increasing plasma glucose varies and was not always non-linear. Glucose 79-86 insulin Homo sapiens 40-47 29141982-0 2018 A Partial Loss-of-Function Variant in AKT2 Is Associated With Reduced Insulin-Mediated Glucose Uptake in Multiple Insulin-Sensitive Tissues: A Genotype-Based Callback Positron Emission Tomography Study. Glucose 87-94 insulin Homo sapiens 114-121 29141982-3 2018 The effects of the p.Pro50Thr AKT2 variant (p.P50T/AKT2) on insulin-stimulated glucose uptake (GU) in the whole body and in different tissues have not previously been investigated. Glucose 79-86 insulin Homo sapiens 60-67 29293363-0 2018 Relation Between Hypoglycemia and Glycemic Variability in Type 2 Diabetes Patients with Insulin Therapy: A Study Based on Continuous Glucose Monitoring. Glucose 133-140 insulin Homo sapiens 88-95 29293363-9 2018 CONCLUSIONS: MBG and SD of glucose levels were identified as significant and independent determinants of hypoglycemia in T2DM on insulin therapy. Glucose 27-34 insulin Homo sapiens 129-136 29269206-4 2018 Insulin sensitivity was estimated for each subject from fasting plasma glucose and insulin using the Homeostasis Model Assessment II. Glucose 71-78 insulin Homo sapiens 0-7 28681964-5 2018 We later find that the beta-cells secrete insulin and glucagon, which synchronously stimulate or suppress glycogenolysis, and that insulin is essential for glucose intake into the cell. Glucose 156-163 insulin Homo sapiens 131-138 29199404-10 2018 CONCLUSION: The reimbursement for SMBG resulted in a significant improvement in HbA1c in T2DM subjects using insulin, which was more prominent in subjects with poor glucose control at baseline or covered under the Medical Aid system. Glucose 165-172 insulin Homo sapiens 109-116 29203256-3 2018 The correlations between 11 surrogate estimates of insulin resistance, using either fasting or post-oral glucose challenge values, and a direct measure of insulin-mediated glucose uptake (SSPG concentration during the Insulin Suppression Test) were determined as well as the ability of the surrogate estimates to identify insulin resistant individuals. Glucose 172-179 insulin Homo sapiens 155-162 29203256-3 2018 The correlations between 11 surrogate estimates of insulin resistance, using either fasting or post-oral glucose challenge values, and a direct measure of insulin-mediated glucose uptake (SSPG concentration during the Insulin Suppression Test) were determined as well as the ability of the surrogate estimates to identify insulin resistant individuals. Glucose 172-179 insulin Homo sapiens 155-162 29203256-8 2018 For identification of insulin resistant individuals, indices based on post-glucose challenge measurements performed better than those based on fasting measurements, with the exception of McAuley index. Glucose 75-82 insulin Homo sapiens 22-29 29288757-2 2018 When an abundance of glucose and saturated fat enter the cell, impaired blood flow, hypoxia, inflammation and macrophage infiltration in obese adipose tissue may induce oxidative stress and insulin resistance. Glucose 21-28 insulin Homo sapiens 190-197 29211893-5 2018 Insulin sensitivity was assessed by determining whole-body glucose disposal during a hyperinsulinemic clamp. Glucose 59-66 insulin Homo sapiens 0-7 29095990-4 2018 Main Outcome Measures: We evaluated changes in glucose tolerance, beta cell function, insulin clearance, and insulin sensitivity by modeling plasma glucose, insulin, and C-peptide levels during the OGTT. Glucose 148-155 insulin Homo sapiens 109-116 29095990-4 2018 Main Outcome Measures: We evaluated changes in glucose tolerance, beta cell function, insulin clearance, and insulin sensitivity by modeling plasma glucose, insulin, and C-peptide levels during the OGTT. Glucose 148-155 insulin Homo sapiens 109-116 28544644-6 2018 RESULTS: Early phase insulin responses to oral glucose were significantly decreased in women with IPH versus those with impaired glucose tolerance (IGT) and normal glucose tolerance (geometric mean [95% confidence interval] insulinogenic index 61 [54-79] vs 90 [83-97] and 105 [96-116], respectively; P < 0.0001). Glucose 47-54 insulin Homo sapiens 21-28 28544644-6 2018 RESULTS: Early phase insulin responses to oral glucose were significantly decreased in women with IPH versus those with impaired glucose tolerance (IGT) and normal glucose tolerance (geometric mean [95% confidence interval] insulinogenic index 61 [54-79] vs 90 [83-97] and 105 [96-116], respectively; P < 0.0001). Glucose 129-136 insulin Homo sapiens 21-28 28803366-4 2018 METHODS: Insulin-naive Dutch people with T2DM in suboptimal glycaemic control (HbA1c >53 mmol/mol; 7.0%) on maximum dose of oral glucose-lowering medications were included from 363 primary care practices (n = 911). Glucose 132-139 insulin Homo sapiens 9-16 28544644-7 2018 In addition, there were significant decreases in late-phase insulin release as metabolic status shifted from normal glucose tolerance to IGT to IPH. Glucose 116-123 insulin Homo sapiens 60-67 28544644-10 2018 There were significant decreases in early and late-phase insulin release as glucose intolerance escalated. Glucose 76-83 insulin Homo sapiens 57-64 29490093-4 2018 Methods: Kinetics of arginine and related metabolites were measured with stable isotope tracers, and insulin secretory responses to arginine and glucose were determined under euglycemic and hyperglycemic conditions in 6 KPD patients and 6 age-, gender-, and body mass index-matched control participants. Glucose 145-152 insulin Homo sapiens 101-108 29094433-4 2018 Insulin sensitivity was calculated with the Matsuda insulin sensitivity index (ISI) based on an oral glucose tolerance test. Glucose 101-108 insulin Homo sapiens 0-7 29490093-8 2018 In both euglycemia and hyperglycemia, the first-phase insulin responses to glucose stimulation were lower in KPD patients (euglycemic insulin AUC 282 +- 108 compared with 926 +- 257 min muU mL-1, P = 0.02; hyperglycemic insulin AUC 358 +- 79 compared with 866 +- 292 min muU mL-1, P = 0.05), but exogenous arginine restored first-phase insulin secretion in KPD patients to the level of control participants. Glucose 75-82 insulin Homo sapiens 54-61 29490093-8 2018 In both euglycemia and hyperglycemia, the first-phase insulin responses to glucose stimulation were lower in KPD patients (euglycemic insulin AUC 282 +- 108 compared with 926 +- 257 min muU mL-1, P = 0.02; hyperglycemic insulin AUC 358 +- 79 compared with 866 +- 292 min muU mL-1, P = 0.05), but exogenous arginine restored first-phase insulin secretion in KPD patients to the level of control participants. Glucose 75-82 insulin Homo sapiens 134-141 28370959-5 2018 Percent Free "Immunoreactive" Insulin (%FII) as assessed by polyethylene glycol precipitation studies and its relationship to plasma glucose and serum insulin concentration. Glucose 133-140 insulin Homo sapiens 30-37 29307553-2 2018 While glucagon and insulin work together to achieve optimal plasma glucose concentrations in healthy individuals, the usual regulatory balance between these 2 critical pancreatic hormones is awry in patients with diabetes. Glucose 67-74 insulin Homo sapiens 19-26 29307512-8 2018 Both in vitro and in vivo, we observed a clear insulin response to glucose, and, in vitro, we found a significant increase in insulin secretion from EndoC-betaH1 pseudoislets compared to monolayer cultures for both glucose and incretins. Glucose 67-74 insulin Homo sapiens 47-54 28838782-3 2018 Dupre demonstrated that secretin given intravenously with glucose increased its rate of disappearance from the blood, McIntyre and co-workers established that hyperglycaemia evoked by oral glucose stimulated more insulin secretion than comparable hyperglycaemia produced by intravenous glucose and Marks and Samols established the insulinotropic properties of glucagon. Glucose 58-65 insulin Homo sapiens 213-220 28370959-8 2018 TPE increased %FII (23.8 +- 2.0 before TPE vs 83.6 +- 2.5 after TPE, P < .0001) and reestablished plasma glucose responsiveness to exogenous insulin. Glucose 108-115 insulin Homo sapiens 144-151 28838782-3 2018 Dupre demonstrated that secretin given intravenously with glucose increased its rate of disappearance from the blood, McIntyre and co-workers established that hyperglycaemia evoked by oral glucose stimulated more insulin secretion than comparable hyperglycaemia produced by intravenous glucose and Marks and Samols established the insulinotropic properties of glucagon. Glucose 189-196 insulin Homo sapiens 213-220 28838782-3 2018 Dupre demonstrated that secretin given intravenously with glucose increased its rate of disappearance from the blood, McIntyre and co-workers established that hyperglycaemia evoked by oral glucose stimulated more insulin secretion than comparable hyperglycaemia produced by intravenous glucose and Marks and Samols established the insulinotropic properties of glucagon. Glucose 189-196 insulin Homo sapiens 213-220 28370959-11 2018 CONCLUSION: TPE is an effective method for removing IICs and normalizing insulin-mediated glucose responses. Glucose 90-97 insulin Homo sapiens 73-80 29115018-10 2018 There was a significant relationship between glucose and insulin values obtained by OGTT with EC in a sample of non-diabetic patients with preserved lung function. Glucose 45-52 insulin Homo sapiens 57-64 29412821-2 2018 Insulin is the primary regulator of glucose and its secretion from beta-cells is tightly regulated in response to physiological demands. Glucose 36-43 insulin Homo sapiens 0-7 29412837-4 2018 Proof of concept has been established for non-cellular glucose-responsive insulin delivery ("smart insulins") to release insulin from implants or circulating depots in proportion to circulating glucose. Glucose 55-62 insulin Homo sapiens 74-81 29389978-11 2018 Furthermore, analysis shows that cART alters several regulators of blood glucose levels, including C-peptide, chromogranin-A and leptin. Glucose 73-80 insulin Homo sapiens 99-108 29289437-2 2018 Central to the process of glucose homeostasis are pancreatic beta cells, which sense elevations in plasma glucose and additional dietary components and respond by releasing the appropriate quantity of insulin, ensuring the arrest of hepatic glucose output and glucose uptake in peripheral tissues. Glucose 26-33 insulin Homo sapiens 201-208 28904260-0 2018 Impaired beta-cell function and decreased insulin sensitivity in subjects with normal oral glucose tolerance but isolated high glycosylated hemoglobin. Glucose 91-98 insulin Homo sapiens 42-49 29383544-2 2018 RECENT FINDINGS: The latest evidence suggests that continuous glucose monitoring (CGM) should be offered to all women on intensive insulin therapy in early pregnancy. Glucose 62-69 insulin Homo sapiens 131-138 29383544-4 2018 Despite new studies comparing insulin pump therapy to multiple daily injections, its effectiveness in improving glucose and pregnancy outcomes remains unclear. Glucose 112-119 insulin Homo sapiens 30-37 29382104-3 2018 Insulin and glucagon help to maintain the homeostasis of glucose and lipids through signaling cascades. Glucose 57-64 insulin Homo sapiens 0-7 29382104-4 2018 Pancreatic hormones stimulate translocation of the glucose transporter isoform 4 (GLUT4) from an intracellular location to the cell surface and facilitate the rapid insulin-dependent storage of glucose in muscle and fat cells. Glucose 51-58 insulin Homo sapiens 165-172 29382104-5 2018 Malfunction in glucose uptake mechanisms, primarily contribute to insulin resistance in type 2 diabetes. Glucose 15-22 insulin Homo sapiens 66-73 29322773-2 2018 Using spatially uniform 3D gold-nanoparticle sensors, we have demonstrated surface-enhanced Raman sensing of insulin in the secretions from human pancreatic islets under low and high glucose environments without the use of labels such as antibodies or aptamers. Glucose 183-190 insulin Homo sapiens 109-116 29552281-7 2018 In cultured C2C12 myotubes, treatment with high dose testosterone activated mTORC1, reduced autophagy, impaired mitochondria, decreased insulin-stimulated glucose uptake, and induced IR. Glucose 155-162 insulin Homo sapiens 136-143 29373583-0 2018 Zinc stimulates glucose oxidation and glycemic control by modulating the insulin signaling pathway in human and mouse skeletal muscle cell lines. Glucose 16-23 insulin Homo sapiens 73-80 29373583-7 2018 Glucose oxidation assays were performed on skeletal muscle cells treated with insulin, zinc, or a combination of both and resulted in a significant induction of glucose consumption in mouse (p<0.01) and human (p<0.05) skeletal muscle cells when treated with zinc alone. Glucose 161-168 insulin Homo sapiens 78-85 29373583-8 2018 Insulin, as expected, increased glucose oxidation in mouse (p<0.001) and human (0.001) skeletal muscle cells, however the combination of zinc and insulin did not augment glucose consumption in these cells. Glucose 32-39 insulin Homo sapiens 0-7 29370267-10 2018 CONCLUSION: Obese children with insulin resistance show increased levels of oxidative stress biomarkers, and a stunted antioxidant response to an OGTT leading to increased oxidative stress after a single glucose load, as detected in erythrocytes, but not in plasma. Glucose 204-211 insulin Homo sapiens 32-39 30393315-7 2018 By performing blood analyses, infusion of more-concentrated insulin (200 IU/mL, international units (IU)) exhibited similar blood glucose level drop (5-7%) compared to insulin of standard concentration (100 IU/mL), however, significant increase of serum insulin (40-50%) with respect to the preinfusion values was determined. Glucose 130-137 insulin Homo sapiens 60-67 29198302-8 2018 Homeostasis Model Assessment of insulin resistance was derived from measurements of fasting glucose and C-peptide levels. Glucose 92-99 insulin Homo sapiens 32-39 29330456-0 2018 20-HETE promotes glucose-stimulated insulin secretion in an autocrine manner through FFAR1. Glucose 17-24 insulin Homo sapiens 36-43 29330456-2 2018 Synthetic FFAR1 agonists can be used as antidiabetic drugs to promote glucose-stimulated insulin secretion (GSIS). Glucose 70-77 insulin Homo sapiens 89-96 29552281-8 2018 Inhibition of mTORC1 or induction of autophagy restored mitochondrial function, up-regulated insulin-stimulated glucose uptake, and increased insulin sensitivity. Glucose 112-119 insulin Homo sapiens 93-100 29552281-10 2018 Our findings suggest that the mTORC1-autophagy pathway might contribute to androgen excess-induced skeletal muscle IR in prepubertal female mice by impairing mitochondrial function and reducing insulin-stimulated glucose uptake. Glucose 213-220 insulin Homo sapiens 194-201 29321379-6 2018 These studies demonstrate that a glucose-dependent locus of insulin clearance and, hence, insulin action can be achieved by targeting MR and IR concurrently. Glucose 33-40 insulin Homo sapiens 90-97 29321379-0 2018 A glucose-responsive insulin therapy protects animals against hypoglycemia. Glucose 2-9 insulin Homo sapiens 21-28 28867301-3 2018 Peripheral insulin resistance indirectly influences hepatic glucose and lipid metabolism by increasing flux of substrates that promote lipogenesis (glucose and fatty acids) and gluconeogenesis (glycerol and fatty acid-derived acetyl-CoA, an allosteric activator of pyruvate carboxylase). Glucose 60-67 insulin Homo sapiens 11-18 29321379-2 2018 The concept of modifying insulin to render its glucose-responsive release from an injection depot (of an insulin complexed exogenously with a recombinant lectin) was proposed approximately 4 decades ago but has been challenging to achieve. Glucose 47-54 insulin Homo sapiens 25-32 29321379-2 2018 The concept of modifying insulin to render its glucose-responsive release from an injection depot (of an insulin complexed exogenously with a recombinant lectin) was proposed approximately 4 decades ago but has been challenging to achieve. Glucose 47-54 insulin Homo sapiens 105-112 29321379-3 2018 Data presented here demonstrate that mannosylated insulin analogs can undergo an additional route of clearance as result of their interaction with endogenous mannose receptor (MR), and this can occur in a glucose-dependent fashion, with increased binding to MR at low glucose. Glucose 205-212 insulin Homo sapiens 50-57 29321379-3 2018 Data presented here demonstrate that mannosylated insulin analogs can undergo an additional route of clearance as result of their interaction with endogenous mannose receptor (MR), and this can occur in a glucose-dependent fashion, with increased binding to MR at low glucose. Glucose 268-275 insulin Homo sapiens 50-57 29321379-6 2018 These studies demonstrate that a glucose-dependent locus of insulin clearance and, hence, insulin action can be achieved by targeting MR and IR concurrently. Glucose 33-40 insulin Homo sapiens 60-67 30673191-4 2018 Phylogenetically, in vivo insulin is primarily involved in the metabolism of fatty acids (FA) and only in the second turn in glucose metabolism; regulation of FA metabolism in cells started millions of years earlier than that of glucose metabolism. Glucose 125-132 insulin Homo sapiens 26-33 29311680-4 2018 Insulin resistance was induced by palmitic acid (PA) in human HK-2 cells, shown as the decrease of insulin-stimulated AKT phosphorylation, glucose transporter-4 (GLUT4), glucose uptake and enhanced phosphorylation of insulin receptor substrate 1(IRS-1) at site serine 307 (pIRS-1ser307) and downregulated expression of IRS-1. Glucose 139-146 insulin Homo sapiens 0-7 29311680-4 2018 Insulin resistance was induced by palmitic acid (PA) in human HK-2 cells, shown as the decrease of insulin-stimulated AKT phosphorylation, glucose transporter-4 (GLUT4), glucose uptake and enhanced phosphorylation of insulin receptor substrate 1(IRS-1) at site serine 307 (pIRS-1ser307) and downregulated expression of IRS-1. Glucose 139-146 insulin Homo sapiens 99-106 29537934-3 2018 Insulin secretion is stimulated by glucose, amino acids, and glucagon- like peptide-1 in tissue containing high levels of n-3 Polyunsaturated Fatty acids than lower level of n-3 Polyunsaturated Fatty acids. Glucose 35-42 insulin Homo sapiens 0-7 29289263-1 2018 BACKGROUND: The changes in insulin resistance and insulin secretion and their association with changes in glucose regulation status in Asians with prediabetes remain uncertain. Glucose 106-113 insulin Homo sapiens 27-34 28868790-4 2018 Here, we review some of the molecular mechanisms through which insulin modulates hepatic gluconeogenesis, thus controlling glucose production by the liver to ultimately maintain normoglycemia. Glucose 123-130 insulin Homo sapiens 63-70 29433332-4 2018 The functionality of differentiated cells was determined by insulin and C-peptide release in response to glucose challenges. Glucose 105-112 insulin Homo sapiens 72-81 29433332-6 2018 Furthermore, the immunoassay showed that differentiated cells in both culture plates and PES scaffolds groups are functional and secrete C-peptide and insulin in response to glucose challenges. Glucose 174-181 insulin Homo sapiens 137-146 29433332-6 2018 Furthermore, the immunoassay showed that differentiated cells in both culture plates and PES scaffolds groups are functional and secrete C-peptide and insulin in response to glucose challenges. Glucose 174-181 insulin Homo sapiens 151-158 29486602-7 2018 Furthermore, we showed that concentration of insulin and C-peptide in PLLA/PVA scaffold and/or 2 D culture in response to various concentrations of glucose increased but the difference between them were not significant. Glucose 148-155 insulin Homo sapiens 45-52 30284475-6 2018 In addition, insulin and C-peptide secretion in various glucose concentrations was evaluated by ELISA. Glucose 56-63 insulin Homo sapiens 13-20 30284475-6 2018 In addition, insulin and C-peptide secretion in various glucose concentrations was evaluated by ELISA. Glucose 56-63 insulin Homo sapiens 25-34 30284483-7 2018 Although differentiated cells in both groups are functional and secrete C-peptide and insulin in response to glucose challenges according to the immunoassay result. Glucose 109-116 insulin Homo sapiens 86-93 29384340-1 2018 The objective is to present the case of a 21-yr-old athlete observed with non-physiological immediate postprandial insulin response (1162 pmol/l; normal glucose excursion: 6.6 mmol/l), in a warm environment. Glucose 153-160 insulin Homo sapiens 115-122 29799764-2 2018 Pancreatic islet beta-cells, which release insulin in response to circulating blood glucose levels, are particularly susceptible to mitochondrial dysfunction due to their high metabolic activity and energy requirements for insulin processing, maturation, and secretion. Glucose 84-91 insulin Homo sapiens 43-50 29863077-4 2018 Glucose take-up, utilization levels, and oil red O recoloring were distinguished to confirm their impact on improving insulin resistance. Glucose 0-7 insulin Homo sapiens 118-125 29863077-8 2018 The insulin-resistant HepG2 cells prompted by insulin mediated the impact of polydatin on glucose and lipid digestion. Glucose 90-97 insulin Homo sapiens 4-11 29863077-8 2018 The insulin-resistant HepG2 cells prompted by insulin mediated the impact of polydatin on glucose and lipid digestion. Glucose 90-97 insulin Homo sapiens 46-53 28865118-0 2018 Glucose-stimulated insulin release: Parallel perifusion studies of free and hydrogel encapsulated human pancreatic islets. Glucose 0-7 insulin Homo sapiens 19-26 29577067-1 2018 Insulin release by pancreatic beta cells plays a key role in regulating blood glucose levels in humans, and to understand the mechanism for insulin secretion may reveal therapeutic strategies for diabetes. Glucose 78-85 insulin Homo sapiens 0-7 29768267-12 2018 Results from further analyses showed that AKT-ROS-dependent upregulations of expression, binding and centrosome translocation of ROCK1 and 14-3-3sigma was the molecular pathway underlying the centrosome amplification in vitro triggered by high glucose, insulin and palmitic acid. Glucose 244-251 insulin Homo sapiens 253-260 29950545-4 2018 Furthermore, bone-derived osteocalcin stimulates insulin secretion, thereby regulates the whole body glucose metabolism. Glucose 101-108 insulin Homo sapiens 49-56 28081696-2 2018 Insulin resistance is currently recognized by the estimated glucose disposal rate. Glucose 60-67 insulin Homo sapiens 0-7 28081696-5 2018 METHODS: 40 T1DM male >= 18 years of age were screened for insulin resistance (defined using estimated glucose disposal rate). Glucose 106-113 insulin Homo sapiens 62-69 29210631-8 2018 Besides this deficiency in the withdrawal of estrogen and progesterone, the insulin/ glucose pathway, adhesion molecules, cytokines and the inflammatory cascade, together with the establishment of a pro-oxidative status, lead to an imbalance in the uterine function, which in turn leads to implantation failure or even endometrial cancer. Glucose 85-92 insulin Homo sapiens 76-83 29210631-12 2018 The present review describes the role of hormones, metabolites, cytokines, adhesion molecules and the insulin/glucose pathway related to the uterine endometrium in women with PCOS and their role in implantation failure and development of endometrial cancer. Glucose 110-117 insulin Homo sapiens 102-109 29283045-1 2018 BACKGROUND: Insulin increases glucose uptake in muscles and fat and inhibits hepatic glucose production, thus serving as the primary regulator of the blood glucose level. Glucose 30-37 insulin Homo sapiens 12-19 29283045-1 2018 BACKGROUND: Insulin increases glucose uptake in muscles and fat and inhibits hepatic glucose production, thus serving as the primary regulator of the blood glucose level. Glucose 85-92 insulin Homo sapiens 12-19 29283045-1 2018 BACKGROUND: Insulin increases glucose uptake in muscles and fat and inhibits hepatic glucose production, thus serving as the primary regulator of the blood glucose level. Glucose 85-92 insulin Homo sapiens 12-19 29283045-2 2018 In type 2 diabetes, insufficient insulin release and suppressed insulin action [named insulin resistance] lead to increased glucose production in liver and decreased glucose uptake by muscles and fat tissues, resulting in elevated blood glucose concentration which is dangerous to human health. Glucose 124-131 insulin Homo sapiens 33-40 29283045-2 2018 In type 2 diabetes, insufficient insulin release and suppressed insulin action [named insulin resistance] lead to increased glucose production in liver and decreased glucose uptake by muscles and fat tissues, resulting in elevated blood glucose concentration which is dangerous to human health. Glucose 124-131 insulin Homo sapiens 64-71 29283045-2 2018 In type 2 diabetes, insufficient insulin release and suppressed insulin action [named insulin resistance] lead to increased glucose production in liver and decreased glucose uptake by muscles and fat tissues, resulting in elevated blood glucose concentration which is dangerous to human health. Glucose 166-173 insulin Homo sapiens 33-40 29283045-2 2018 In type 2 diabetes, insufficient insulin release and suppressed insulin action [named insulin resistance] lead to increased glucose production in liver and decreased glucose uptake by muscles and fat tissues, resulting in elevated blood glucose concentration which is dangerous to human health. Glucose 166-173 insulin Homo sapiens 64-71 29283045-2 2018 In type 2 diabetes, insufficient insulin release and suppressed insulin action [named insulin resistance] lead to increased glucose production in liver and decreased glucose uptake by muscles and fat tissues, resulting in elevated blood glucose concentration which is dangerous to human health. Glucose 166-173 insulin Homo sapiens 33-40 29283045-2 2018 In type 2 diabetes, insufficient insulin release and suppressed insulin action [named insulin resistance] lead to increased glucose production in liver and decreased glucose uptake by muscles and fat tissues, resulting in elevated blood glucose concentration which is dangerous to human health. Glucose 166-173 insulin Homo sapiens 64-71 29283045-5 2018 RESULTS: The current brief opinion proposes an original feedback control of glucose-lowering regulation and its models which allow comparing two distinct strategies of glucose level correction, i.e., one of them allows reducing the increased threshold of insulin resistance, whereas the other allows overcoming this threshold/barrier using exogenous insulin treatment. Glucose 76-83 insulin Homo sapiens 255-262 29283045-5 2018 RESULTS: The current brief opinion proposes an original feedback control of glucose-lowering regulation and its models which allow comparing two distinct strategies of glucose level correction, i.e., one of them allows reducing the increased threshold of insulin resistance, whereas the other allows overcoming this threshold/barrier using exogenous insulin treatment. Glucose 76-83 insulin Homo sapiens 350-357 29283045-5 2018 RESULTS: The current brief opinion proposes an original feedback control of glucose-lowering regulation and its models which allow comparing two distinct strategies of glucose level correction, i.e., one of them allows reducing the increased threshold of insulin resistance, whereas the other allows overcoming this threshold/barrier using exogenous insulin treatment. Glucose 168-175 insulin Homo sapiens 255-262 29283045-5 2018 RESULTS: The current brief opinion proposes an original feedback control of glucose-lowering regulation and its models which allow comparing two distinct strategies of glucose level correction, i.e., one of them allows reducing the increased threshold of insulin resistance, whereas the other allows overcoming this threshold/barrier using exogenous insulin treatment. Glucose 168-175 insulin Homo sapiens 350-357 28936587-2 2018 In this study we examined the association of metabolite levels and pairwise metabolite ratios with insulin responses after glucose, glucagon-like peptide-1 (GLP-1) and arginine stimulation. Glucose 123-130 insulin Homo sapiens 99-106 29133343-5 2018 Insulin resistance was estimated during an oral glucose tolerance test using the Matsuda Index. Glucose 48-55 insulin Homo sapiens 0-7 28904022-12 2018 Of importance, our data challenge the concept that PI3Kgamma is required for insulin secretion in response to glucose in vivo, and indicate that PI3Kgamma ablation protects db/db mice from beta-cell apoptosis and improves fasting insulin levels. Glucose 110-117 insulin Homo sapiens 77-84 28678568-8 2018 CONCLUSIONS: Moderately elevated testosterone concentrations together with obesity-related inflammatory factors modify glucose homeostasis by increasing insulin resistance and early insulin secretion. Glucose 119-126 insulin Homo sapiens 153-160 29136166-16 2018 WIDER IMPLICATIONS: While the effects of regulating the hyperglycemia by the use of insulin and other modulators of glucose metabolism have been reported, more clinical trials providing high quality evidence and specifically addressing the beneficial effects on male reproduction are required. Glucose 116-123 insulin Homo sapiens 84-91 29938757-3 2018 However, insulin injections often fail to achieve full glucose control, which in the long-term leads to multiple complications and mortality. Glucose 55-62 insulin Homo sapiens 9-16 29938757-4 2018 Beta-cells, the natural producers and secretors of insulin, remain the gold-standard in regulating blood glucose levels. Glucose 105-112 insulin Homo sapiens 51-58 29083418-4 2018 Under hyperglycemic conditions, high glucose uptake and oxidation generate a low pH (<5.6), which then induces steric deshielding of peptides tethered to the insulin-loaded inner small liposomal vesicles. Glucose 37-44 insulin Homo sapiens 161-168 27554132-0 2018 Relationship between serum betatrophin levels and the first-phase of glucose-stimulated insulin secretion. Glucose 69-76 insulin Homo sapiens 88-95 30786677-7 2018 The insulin pumps integrated with CGM automatically suspending insulin infusion when glucose is predicted to soon be low (PLGS) should be preferred in patient with hypoglycaemia unawareness. Glucose 85-92 insulin Homo sapiens 4-11 29791427-3 2018 Psychiatry describes an abnormal mental examination and diagnosed double depression; however, the patient had the Whipple triad and insulin/glucose ratio higher than 0.3. Glucose 140-147 insulin Homo sapiens 132-139 29261667-3 2017 METHODS: In this uncontrolled, change from baseline study design, insulin sensitivity and glucose-stimulated insulin secretion were measured in 9 normal glucose tolerant subjects before and after 3 day lipid infusion to elevate plasma FFA concentration. Glucose 90-97 insulin Homo sapiens 109-116 29261667-5 2017 RESULTS: Increased plasma FFA (440+-93 mumol/Lto 997+-242 muM, p<0.001) decreased insulin-stimulated total glucose disposal (TGD) by 25% (p = 0.008), impaired suppression of endogenous glucose production (p = 0.01), and reduced mitochondrial ATP synthesis with complex 1 (34%, p<0.05) and complex 2 (30%, p<0.05) substrates. Glucose 110-117 insulin Homo sapiens 85-92 29261667-5 2017 RESULTS: Increased plasma FFA (440+-93 mumol/Lto 997+-242 muM, p<0.001) decreased insulin-stimulated total glucose disposal (TGD) by 25% (p = 0.008), impaired suppression of endogenous glucose production (p = 0.01), and reduced mitochondrial ATP synthesis with complex 1 (34%, p<0.05) and complex 2 (30%, p<0.05) substrates. Glucose 188-195 insulin Homo sapiens 85-92 29262332-1 2017 Insulin triggers an extensive signaling cascade to coordinate adipocyte glucose metabolism. Glucose 72-79 insulin Homo sapiens 0-7 29262332-2 2017 It is considered that the major role of insulin is to provide anabolic substrates by activating GLUT4-dependent glucose uptake. Glucose 112-119 insulin Homo sapiens 40-47 29262332-8 2017 We refer to this phenomenon as metabolic priming, whereby insulin signaling creates a demand-driven system to "pull" glucose into specific anabolic pathways. Glucose 117-124 insulin Homo sapiens 58-65 29262332-9 2017 This complements the supply-driven regulation of anabolism by substrate accumulation and highlights an additional role for insulin action in adipocyte glucose metabolism. Glucose 151-158 insulin Homo sapiens 123-130 29242563-3 2017 Here we report that in human and murine adipocytes CK2-inhibition decreases the insulin-induced glucose-uptake by counteracting Akt-signaling and GLUT4-translocation to the plasma membrane. Glucose 96-103 insulin Homo sapiens 80-87 28158621-3 2017 Methods: Insulin-stimulated rates of glucose disposal (Rd) were determined using the hyperinsulinemic euglycemic clamp before and after completing 16 weeks of either calorie restriction to induce weight loss (N = 7) or moderate exercise (N = 10). Glucose 37-44 insulin Homo sapiens 9-16 29050941-2 2017 Skeletal muscle tissue and adipocyte tissue are the major sites of postprandial glucose disposal, and enhancing glucose uptake into this tissue may decrease insulin resistance in type 2 diabetes patients. Glucose 112-119 insulin Homo sapiens 157-164 29222456-0 2017 BMPs as new insulin sensitizers: enhanced glucose uptake in mature 3T3-L1 adipocytes via PPARgamma and GLUT4 upregulation. Glucose 42-49 insulin Homo sapiens 12-19 29222456-3 2017 We show that BMP2 and BMP6 lead to enhanced insulin-mediated glucose uptake in both insulin-sensitive and -insensitive adipocytes. Glucose 61-68 insulin Homo sapiens 44-51 29222456-3 2017 We show that BMP2 and BMP6 lead to enhanced insulin-mediated glucose uptake in both insulin-sensitive and -insensitive adipocytes. Glucose 61-68 insulin Homo sapiens 84-91 28974477-4 2017 Herein, we report a novel implantable insulin hydrogel for glucose-regulated delivery of insulin based on a unique particle-hydrogel hybrid platform featuring fast glucose responsiveness at physiological pH, shear-thinning behavior for injection, tissue-adhesive function for long-lasting adherence, and full biodegradability for safe use. Glucose 59-66 insulin Homo sapiens 38-45 28974477-4 2017 Herein, we report a novel implantable insulin hydrogel for glucose-regulated delivery of insulin based on a unique particle-hydrogel hybrid platform featuring fast glucose responsiveness at physiological pH, shear-thinning behavior for injection, tissue-adhesive function for long-lasting adherence, and full biodegradability for safe use. Glucose 59-66 insulin Homo sapiens 89-96 28974477-4 2017 Herein, we report a novel implantable insulin hydrogel for glucose-regulated delivery of insulin based on a unique particle-hydrogel hybrid platform featuring fast glucose responsiveness at physiological pH, shear-thinning behavior for injection, tissue-adhesive function for long-lasting adherence, and full biodegradability for safe use. Glucose 164-171 insulin Homo sapiens 38-45 28974477-4 2017 Herein, we report a novel implantable insulin hydrogel for glucose-regulated delivery of insulin based on a unique particle-hydrogel hybrid platform featuring fast glucose responsiveness at physiological pH, shear-thinning behavior for injection, tissue-adhesive function for long-lasting adherence, and full biodegradability for safe use. Glucose 164-171 insulin Homo sapiens 89-96 28974477-11 2017 Building upon a unique particle-hydrogel hybrid platform, herein we report a novel implantable insulin storage and delivery system with multifunctionalities including fast glucose-sensitiveness at physiological pH, shear-thinning behavior for injection, tissue-adhesive function for long-lasting adherence, biodegradable materials for safe use and well-controlled insulin release. Glucose 172-179 insulin Homo sapiens 95-102 29399544-3 2017 MicroRNAs in islet beta-cells regulate beta-cell differentiation, proliferation, insulin transcription and glucose-stimulated insulin secretion. Glucose 107-114 insulin Homo sapiens 126-133 29399544-4 2017 Furthermore, miRNAs play key roles in the regulation of glucose and lipid metabolisms and modify insulin sensitivity by controlling metabolic functions in main target organs of insulin such as skeletal muscle, liver and adipose tissue. Glucose 56-63 insulin Homo sapiens 177-184 28497374-5 2017 RESULTS: Overall, 20 (44.4%) patients required insulin to achieve target blood glucose. Glucose 79-86 insulin Homo sapiens 47-54 28497374-8 2017 Increases in c-peptide were positively correlated with an increase in blood glucose both in patients who did (r = 0.54, P = 0.01) and did not (r = 0.56, P = 0.004) receive insulin. Glucose 76-83 insulin Homo sapiens 13-22 28699150-8 2017 A glucose control monitoring system indicated a trend towards differences in the duration of hypoglycaemia (blood glucose level below 70 mg dl-1 (3.9 mmol l-1) over 1000 h of insulin infusion (9.7 +- 25.0 h in the standard group versus 4.4 +- 14.8 h in the optimised group, p = 0.059) and in the number of patients experiencing at least one hypoglycaemia incident (25.7 vs. 12.9%, p = 0.052). Glucose 2-9 insulin Homo sapiens 175-182 29250326-5 2017 As multi-drug resistance proteins require energy to operate, the present report evaluated the potential clinical efficacy of lowering blood glucose with insulin during chemotherapy for a patient with advanced pulmonary adenocarcinoma with multiple metastases. Glucose 140-147 insulin Homo sapiens 153-160 29063963-13 2017 Additionally, insulin and antioxidative treatment proved to be efficient in reversing the deleterious effects of high glucose and associated OS. Glucose 118-125 insulin Homo sapiens 14-21 28416367-7 2017 CONCLUSIONS: The higher serum galanin levels as well as the negative correlation between galanin levels and 1-hour glucose content in patients with IGT may result from the interaction between insulin and galanin in differing conditions, suggesting that the galanin level may be used as a potential biomarker for the prediction of IGT in clinical settings. Glucose 115-122 insulin Homo sapiens 192-199 29044699-5 2017 He was treated with insulin, and his glucose levels were well maintained. Glucose 37-44 insulin Homo sapiens 20-27 29044799-4 2017 A combined intravenous glucose tolerance-euglycaemic clamp test showed severe insulin resistance, as expected, but also showed strongly diminished first-phase insulin secretion. Glucose 23-30 insulin Homo sapiens 78-85 28374151-4 2017 In animal models of diabetes and in patients with type 1 diabetes mellitus, C-peptide replacement improves renal function, skin and skeletal muscle blood flow, nerve conduction, glucose utilization, and other diabetes-related complications. Glucose 178-185 insulin Homo sapiens 76-85 29019715-5 2017 Subgroup analysis was performed to see if insulin dose was related to glucose control. Glucose 70-77 insulin Homo sapiens 42-49 29028535-7 2017 In this study, BG and its three metabolites (M1-M3) were examined their effects on glucose consumption in insulin resistant HepG-2 cells with a commercial glucose assay kit. Glucose 83-90 insulin Homo sapiens 106-113 29028203-0 2017 An Information Theoretical Analysis of Human Insulin-Glucose System Toward the Internet of Bio-Nano Things. Glucose 53-60 insulin Homo sapiens 45-52 29074437-7 2017 Such approaches demonstrate that insulin resistance and T2D have far reaching metabolic effects beyond raised blood glucose and how the disease impacts systemic metabolism. Glucose 116-123 insulin Homo sapiens 33-40 28935388-3 2017 METHODS: Thirty-nine adolescents with recently diagnosed T2DM and 32 obese adolescent controls with normal glucose tolerance had acute insulin response to glucose, homeostatic model assessment of insulin resistance, and disposition index measured serially over 2 years. Glucose 155-162 insulin Homo sapiens 135-142 28784695-4 2017 We have previously demonstrated that Galphaq/11-biased agonism of FFA2 can potentiate glucose stimulated insulin secretion (GSIS) as well as promote beta cell proliferation. Glucose 86-93 insulin Homo sapiens 105-112 28688190-2 2017 HCV plays a direct role in glucose metabolism leading to both insulin resistance and type 2 diabetes. Glucose 27-34 insulin Homo sapiens 62-69 29390469-6 2017 An oral glucose tolerance test showed elevated insulin concentrations with disproportionately elevated C-peptide levels. Glucose 8-15 insulin Homo sapiens 47-54 28992089-6 2017 The insulin pathway in the presence of p-cresol, p-CG and/or p-CS was further evaluated in vitro on C2C12 muscle cells by measuring insulin-stimulated glucose uptake and the insulin signalling pathway (protein kinase B, PKB/Akt) by western blot. Glucose 151-158 insulin Homo sapiens 4-11 28992089-6 2017 The insulin pathway in the presence of p-cresol, p-CG and/or p-CS was further evaluated in vitro on C2C12 muscle cells by measuring insulin-stimulated glucose uptake and the insulin signalling pathway (protein kinase B, PKB/Akt) by western blot. Glucose 151-158 insulin Homo sapiens 132-139 28992089-6 2017 The insulin pathway in the presence of p-cresol, p-CG and/or p-CS was further evaluated in vitro on C2C12 muscle cells by measuring insulin-stimulated glucose uptake and the insulin signalling pathway (protein kinase B, PKB/Akt) by western blot. Glucose 151-158 insulin Homo sapiens 132-139 29128793-8 2017 As Kv2.1 channels play a prominent role in glucose-stimulated insulin secretion, our findings contribute to our understanding of the putative mechanism by which these phytochemicals exert their reported hypoglycemic effects. Glucose 43-50 insulin Homo sapiens 62-69 29186653-11 2017 Proinsulin has only 10~20% of the glucose-lowering effect of insulin. Glucose 34-41 insulin Homo sapiens 0-10 29186653-11 2017 Proinsulin has only 10~20% of the glucose-lowering effect of insulin. Glucose 34-41 insulin Homo sapiens 3-10 29181745-7 2017 Ketonemia, acidic urine with glycosuria, ketonuria, and high blood glucose prompted an insulin infusion. Glucose 67-74 insulin Homo sapiens 87-94 28986255-4 2017 Prdx3 KD cells exhibit a two-fold increase in H2O2, reduced insulin-stimulated glucose transport and attenuated S473 phosphorylation of the mTORC2 substrate, Akt. Glucose 79-86 insulin Homo sapiens 60-67 28972173-5 2017 Despite the lack of recovery from metformin-induced impairment of mitochondrial energy metabolism (glucose oxidation, O2 consumption, and ATP production), insulin secretion was almost completely restored at elevated glucose concentrations. Glucose 216-223 insulin Homo sapiens 155-162 29164254-5 2017 The main study group (n = 389) had first-phase insulin release on an intravenous glucose tolerance test that was higher than the threshold. Glucose 81-88 insulin Homo sapiens 47-54 29158477-3 2017 Here we show that sirolimus impairs glucose-stimulated insulin secretion both in human and murine pancreatic islets and in clonal beta cells in a dose- and time-dependent manner. Glucose 36-43 insulin Homo sapiens 55-62 29180325-1 2017 OBJECTIVE: To investigate the correlation between liver and skeletal muscle fat contents and insulin resistance in obese individuals with different levels of glucose tolerance. Glucose 158-165 insulin Homo sapiens 93-100 28972183-3 2017 Insulin signaling in muscle requires p21-activated kinase-1 (PAK1), whose downstream signaling triggers actin remodeling, which promotes GLUT4 vesicle translocation and glucose uptake into skeletal muscle cells. Glucose 169-176 insulin Homo sapiens 0-7 28972183-10 2017 These results expand the model of insulin-stimulated glucose uptake in skeletal muscle cells by implicating p41ARC as a new component of the insulin-signaling cascade and connecting PAK1 signaling to N-WASP-cortactin-mediated actin polymerization and GLUT4 vesicle translocation. Glucose 53-60 insulin Homo sapiens 34-41 29151130-1 2017 Islets of Langerhans need to maintain their round morphology and to be fast revascularized after transplantation to preserve functional insulin secretion in response to glucose stimulation. Glucose 169-176 insulin Homo sapiens 136-143 28714403-4 2017 Inhibition of GSK3 by insulin boosts the dephosphorylation of glycogen synthase, hence its activation to convert UDP glucose into glycogen. Glucose 117-124 insulin Homo sapiens 22-29 29046394-8 2017 rhIAPP exposure also affected glucose-stimulated insulin secretion from isolated pancreatic islets. Glucose 30-37 insulin Homo sapiens 49-56 28986361-3 2018 The development of insulin resistance in cardiac tissue decreases cellular glucose import and enhances mitochondrial fatty acid uptake. Glucose 75-82 insulin Homo sapiens 19-26 29590649-1 2018 BACKGROUND/AIMS: The islet is an important endocrine organ to secrete insulin to regulate the metabolism of glucose and maintain the stability of blood glucose. Glucose 108-115 insulin Homo sapiens 70-77 29590649-1 2018 BACKGROUND/AIMS: The islet is an important endocrine organ to secrete insulin to regulate the metabolism of glucose and maintain the stability of blood glucose. Glucose 152-159 insulin Homo sapiens 70-77 29295838-4 2018 METHODS: Genetic instruments of variation of insulin secretion [assessed as insulin concentration 30 min after oral glucose (insulin-30)] were used to estimate the causal relationship between increased insulin secretion and body mass index (BMI), using bidirectional Mendelian randomization analysis of genome-wide association studies. Glucose 116-123 insulin Homo sapiens 45-52 29295838-10 2018 CONCLUSIONS: Mendelian randomization analyses provide evidence for a causal relationship of glucose-stimulated insulin secretion on body weight, consistent with the carbohydrate-insulin model of obesity. Glucose 92-99 insulin Homo sapiens 111-118 28714382-11 2018 However, regular screening for insulin resistance is recommended in CHC patients with age >= 40 years and fasting blood glucose >= 100 mg/dl. Glucose 123-130 insulin Homo sapiens 31-38 29792143-2 2018 Insulin is mainly required to regulate glucose metabolism in type 1 diabetes mellitus patients; however, many patients with type 2 diabetes mellitus also require insulin, especially when their condition cannot be controlled solely by oral hypoglycemic agents. Glucose 39-46 insulin Homo sapiens 0-7 30605054-9 2018 All the oral glucose-lowering drugs can be used, but insulin is the most studied drug and the medication recommended for severe hyperglycemia, for patients with pre-existing diabetes or for those patients who have to undergo prolonged therapy over time. Glucose 13-20 insulin Homo sapiens 53-60 28474496-2 2018 Recent scientific breakthroughs enabled derivation of large quantities of human pancreatic beta-like cells in vitro, although with varied glucose-stimulated insulin secretion kinetics. Glucose 138-145 insulin Homo sapiens 157-164 28983693-2 2018 METHODS: We compared continuous glucose monitoring-assessed SD of blood glucose and hypoglycaemia duration in 17 patients with insulin-treated type 2 diabetes and severe insulin deficiency (rCP < 200 pmol/l) and 17 matched insulin-treated control patients with type 2 diabetes but who had preserved endogenous insulin (rCP > 600 pmol/l). Glucose 32-39 insulin Homo sapiens 170-177 28983693-5 2018 In those with low vs high C-peptide, SD of glucose was 4.2 (95% CI 3.7, 4.6) vs 3.0 (2.6, 3.4) mmol/l (p < 0.001). Glucose 43-50 insulin Homo sapiens 26-35 29044772-1 2018 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) have attracted considerable scientific and clinical interest due largely to their insulin-releasing and glucose-lowering properties. Glucose 22-29 insulin Homo sapiens 40-47 28551774-0 2018 Continuous glucose monitoring for patients with type 1 diabetes on multiple daily injections of insulin: pros and cons. Glucose 11-18 insulin Homo sapiens 96-103 28551774-1 2018 Continuous glucose monitoring associated with intensive insulin regimens represents a useful tool to lower HbA1c in selected adults with type 1 diabetes. Glucose 11-18 insulin Homo sapiens 56-63 28551774-4 2018 Pros and Cons of using continuous glucose monitoring in type 1 diabetic patients with multiple daily injections of insulin are here discussed. Glucose 34-41 insulin Homo sapiens 115-122 28646379-0 2018 Comment on "The pros and cons of continuous glucose monitoring for patients with type 1 diabetes on multiple daily injections of insulin." Glucose 44-51 insulin Homo sapiens 129-136 29952407-7 2018 The multivariate logistic regression analysis revealed that the duration of diabetes, body mass index, microvascular complications, inpatient days, HbA1C level, and self-monitoring of blood glucose (SMBG) were positively correlated with insulin titration in group B, C, and D, compared with group A. Glucose 190-197 insulin Homo sapiens 237-244 29952411-4 2018 Insulin resistance was assessed by the homeostasis model (HOMA-IR), HOMA beta, insulinogenic index (IGI), Matsuda insulin sensitivity index (ISI), and AUC for glucose. Glucose 159-166 insulin Homo sapiens 0-7 29064852-9 2018 Given the high prevalence of diabetes, avoiding excess or unnecessary insulin use to control the blood glucose may offer a potential public health benefit in reducing liver cancer risk. Glucose 103-110 insulin Homo sapiens 70-77 29070511-10 2018 Regarding all the analysed outcomes, only cesarean delivery rates and postpartum glucose levels were higher in women requiring insulin supplementation. Glucose 81-88 insulin Homo sapiens 127-134 30142036-1 2018 Islet beta-cells are responsible for secreting all circulating insulin in response to rising plasma glucose concentrations. Glucose 100-107 insulin Homo sapiens 63-70 30142036-3 2018 In mice, certain beta-cells (termed "hubs") have been shown to be crucial for dictating the islet response to high glucose, with inhibition of these hub cells abolishing the coordinated Ca2+ oscillations necessary for driving insulin secretion. Glucose 115-122 insulin Homo sapiens 226-233 29314873-9 2018 The guidelines review identifying and monitoring patients at risk for developing DM, which are important for avoiding unnecessary insulin therapy in patients with transient hyperglycemia or mildly elevated blood glucose. Glucose 212-219 insulin Homo sapiens 130-137 29029082-12 2018 In the hypertensive subjects, insulin-mediated glucose disposal was ~45% lower (460 +- 44 vs 792 +- 67 mg/kg LBM per hour, P < 0.0005) than in normotensive controls and was positively correlated with the increase of trans-sulfuration (P < 0.0015). Glucose 47-54 insulin Homo sapiens 30-37 29523408-4 2018 Tissue sensitivity to insulin was assessed on the basis of glucose distribution rate (GDR) obtained in the course of hyperinsulinemic-euglycemic clamp. Glucose 59-66 insulin Homo sapiens 22-29 28371567-4 2018 Patients receiving insulin peglispro (n = 192) showed a greater reduction in glycated hemoglobin from baseline compared with glargine (n = 196); -1.6 vs -1.4%, P = 0.005) and in fasting serum glucose (-61.2 vs -54.8 mg/dL, P = 0.02). Glucose 192-199 insulin Homo sapiens 19-26 31404422-12 2018 While type 1 diabetes has a very complex daily glucose pattern, the approach to type 2 diabetics on insulin could become simplified. Glucose 47-54 insulin Homo sapiens 100-107 28730907-2 2018 Mutations in the PAX4 gene may be associated with impaired differentiation/development of pancreatic islet beta cells during fetal development and, consequently, a compromised insulin response to high blood glucose. Glucose 207-214 insulin Homo sapiens 176-183 29310812-4 2018 The glucose levels of the medium were decreased by insulin, demonstrating insulin promoted glucose uptake into cell. Glucose 4-11 insulin Homo sapiens 51-58 29310812-4 2018 The glucose levels of the medium were decreased by insulin, demonstrating insulin promoted glucose uptake into cell. Glucose 4-11 insulin Homo sapiens 74-81 29310812-4 2018 The glucose levels of the medium were decreased by insulin, demonstrating insulin promoted glucose uptake into cell. Glucose 91-98 insulin Homo sapiens 51-58 29310812-4 2018 The glucose levels of the medium were decreased by insulin, demonstrating insulin promoted glucose uptake into cell. Glucose 91-98 insulin Homo sapiens 74-81 29310812-5 2018 However, TNF-alpha inhibited glucose uptake into cells treated with insulin. Glucose 29-36 insulin Homo sapiens 68-75 29310812-10 2018 In conclusion, this study found that TNF-alpha inhibited insulin stimulated glucose uptake and aggravated related proteins expressions, suggesting that it might cause insulin resistance. Glucose 76-83 insulin Homo sapiens 57-64 29457119-4 2018 In the GI group, regular insulin was continuously applied with glucose-added acetate Ringer"s solution (5-10 g glucose per 500 mL). Glucose 63-70 insulin Homo sapiens 25-32 30550084-25 2018 Insulin activates absorption of glucose by cells with purpose to use it for synthesis of oleic fatty acids. Glucose 32-39 insulin Homo sapiens 0-7 30768879-10 2018 Regulatory action of insulin was the directed conversion of exogenous glucose into omega-6 C18: 1 cis-oleic FA. Glucose 70-77 insulin Homo sapiens 21-28 27629995-1 2018 Diabetes is a chronic metabolic disorder characterized by increased level of glucose in the blood due to defects in insulin action, insulin secretion or both. Glucose 77-84 insulin Homo sapiens 116-123 29193779-1 2018 OBJECTIVE: Diets high in saturated fat induce obesity and insulin resistance and impair insulin access to skeletal muscle, leading to reduced insulin levels at the muscle cell surface available to bind insulin receptors and induce glucose uptake. Glucose 231-238 insulin Homo sapiens 88-95 29193779-1 2018 OBJECTIVE: Diets high in saturated fat induce obesity and insulin resistance and impair insulin access to skeletal muscle, leading to reduced insulin levels at the muscle cell surface available to bind insulin receptors and induce glucose uptake. Glucose 231-238 insulin Homo sapiens 88-95 29383306-11 2018 As blood glucose has almost no fluctuation in this age group, even in the presence of IR, fasting plasma insulin detected the same cases of IR that would be detected by HOMA-IR. Glucose 9-16 insulin Homo sapiens 105-112 29212789-1 2018 The pancreatic beta-cell plays a key role in glucose homeostasis by secreting insulin, the only hormone capable of lowering the blood glucose concentration. Glucose 45-52 insulin Homo sapiens 78-85 29379255-8 2017 Whereas, (3beta)-stigmast-5-en-3-ol isolated from Adathoda vasica and Aloe emodin isolated from Cassia fistula showed significant insulin mimetic effects favoring glucose uptake in L6 myotubes (an in vitro model mimicking skeletal muscle cells). Glucose 163-170 insulin Homo sapiens 130-137 29379255-9 2017 These extracts and molecules showed glucose uptake through activation of PI3K, an important insulin signaling intermediate. Glucose 36-43 insulin Homo sapiens 92-99 29071734-1 2017 KEY POINTS: People with insulin resistance or type 2 diabetes can substantially increase their skeletal muscle glucose uptake during exercise and insulin sensitivity after exercise. Glucose 111-118 insulin Homo sapiens 24-31 29250938-2 2017 Those who administer insulin should understand how it works, in particular its link to blood glucose levels. Glucose 93-100 insulin Homo sapiens 21-28 29228058-1 2017 AIMS/HYPOTHESIS: Failure in glucose response to insulin is a common pathology associated with obesity. Glucose 28-35 insulin Homo sapiens 48-55 28819992-1 2017 INTRODUCTION: Nocturnal glucose control remains challenging in children and adolescents with type 1 diabetes due to highly variable overnight insulin requirements. Glucose 24-31 insulin Homo sapiens 142-149 28769120-3 2017 METHODS: Subcutaneous and omental adipose tissue from obese, insulin-resistant donors was cultured in the presence of macrophage and T-cell stimuli, and the conditioned medium tested for its ability to inhibit insulin-stimulated glucose uptake into human Simpson-Golabi-Behmel Syndrome (SGBS) adipocytes. Glucose 229-236 insulin Homo sapiens 210-217 28993036-1 2017 BACKGROUND: Hyperglycemia is frequently encountered in the emergency department (ED), and insulin and intravenous fluid are commonly administered to reduce glucose prior to discharge. Glucose 156-163 insulin Homo sapiens 90-97 29225740-7 2017 Since acutely ill patients who receive insulin infusion are at a higher risk of hypoglycemia, a reliable devices for measuring blood glucose concentrations, such as an arterial blood gas analyzer, should be used frequently. Glucose 133-140 insulin Homo sapiens 39-46 29416197-2 2017 Goal: To determine the optimal insulin delivery method for the prevention of hypoglycemia recorded by continuous monitoring of glucose in patients with insulin pump and PEN. Glucose 127-134 insulin Homo sapiens 31-38 29416197-2 2017 Goal: To determine the optimal insulin delivery method for the prevention of hypoglycemia recorded by continuous monitoring of glucose in patients with insulin pump and PEN. Glucose 127-134 insulin Homo sapiens 152-159 28251726-7 2017 CONCLUSION: In our pediatric cohort, algorithmic adaptations of insulin doses were associated with better outcomes in terms of postexercise glucose control in patients with CSII therapy but not with MDI treatment. Glucose 140-147 insulin Homo sapiens 64-71 29101297-6 2017 RESULTS: We show that co-culture with hASCs improves human islet secretory function in vitro, as measured by glucose-stimulated insulin secretion, confirming previous reports using rodent tissues. Glucose 109-116 insulin Homo sapiens 128-135 29202033-1 2017 Although previous studies have attempted to create "electronics-free" insulin delivery systems using glucose oxidase and sugar-binding lectins as a glucose-sensing mechanism, no successful clinical translation has hitherto been made. Glucose 101-108 insulin Homo sapiens 70-77 29202033-6 2017 As a result, glucose metabolism was controlled in response to interstitial glucose fluctuation under both insulin-deficient and insulin-resistant conditions with at least 3-week durability. Glucose 13-20 insulin Homo sapiens 106-113 29202033-6 2017 As a result, glucose metabolism was controlled in response to interstitial glucose fluctuation under both insulin-deficient and insulin-resistant conditions with at least 3-week durability. Glucose 75-82 insulin Homo sapiens 106-113 29200880-6 2017 Based on the rates of glucose-lowering drug use in Italian patients with diabetes, the annual risk of undergoing a serious hypoglycemic event was estimated at 1.27% for subjects treated with insulin alone, the highest (p<0.00001) as compared with insulin + OHA (0.41%) or OHA alone, either in monotherapy or in multiple therapy (0.1% and 0.17%, respectively). Glucose 22-29 insulin Homo sapiens 191-198 29209279-6 2017 These new insights provide an enriched understanding into the process of glucose transport and yield potential new targets for interventions aimed to improve insulin sensitivity and remediate insulin resistance, pre-diabetes, and the progression to type 2 diabetes. Glucose 73-80 insulin Homo sapiens 158-165 29209279-6 2017 These new insights provide an enriched understanding into the process of glucose transport and yield potential new targets for interventions aimed to improve insulin sensitivity and remediate insulin resistance, pre-diabetes, and the progression to type 2 diabetes. Glucose 73-80 insulin Homo sapiens 192-199 29176006-9 2017 The receptor is also involved in the maturation of adipocytes, the modulation of insulin signalling pathways, the regulation of glucose metabolism, and the secretion of intestinal hormones. Glucose 128-135 insulin Homo sapiens 81-88 30673191-4 2018 Phylogenetically, in vivo insulin is primarily involved in the metabolism of fatty acids (FA) and only in the second turn in glucose metabolism; regulation of FA metabolism in cells started millions of years earlier than that of glucose metabolism. Glucose 229-236 insulin Homo sapiens 26-33 30673191-7 2018 Biological role of insulin consists in the formation of the biological function of locomotion, i.e., movement arising from contraction of striated myocytes provided with substrates (FA and glucose) for energy production as macroergic ATP. Glucose 189-196 insulin Homo sapiens 19-26 29431385-1 2017 Glucose management in hospitalized patients poses challenges to physicians, including identifying blood glucose targets, judicious use of oral diabetes mellitus medications, and implementing appropriate insulin regimens. Glucose 0-7 insulin Homo sapiens 203-210 29431385-12 2017 Historically, sliding scale insulin regimens have been used, but they have no proven benefit, increase the risk of hypoglycemia and large fluctuations in blood glucose levels, and are not recommended. Glucose 160-167 insulin Homo sapiens 28-35 28844890-6 2017 Moreover, decreased brain activity in the arcuate nucleus predicted future elevation of blood insulin during the first 10 min after glucose ingestion. Glucose 132-139 insulin Homo sapiens 94-101 28960798-4 2017 Utilizing this nanodevice, we not only accurately quantified intracellular glucose but also developed its further application for facile insulin sensitizer screening. Glucose 75-82 insulin Homo sapiens 137-144 29118381-2 2017 We analyzed the impact of first-phase and pulsatile insulin release on glucose and lipid control with various hepatic insulin signaling networks. Glucose 71-78 insulin Homo sapiens 52-59 29118381-6 2017 Based on these findings, we propose a sequential model of postprandial hepatic control of glucose and lipid by insulin, according to which delayed aPKC switch-off contributes to selective hepatic insulin resistance, which is a long-standing paradox in the field. Glucose 90-97 insulin Homo sapiens 111-118 29117552-0 2017 Circulating Glucagon 1-61 Regulates Blood Glucose by Increasing Insulin Secretion and Hepatic Glucose Production. Glucose 42-49 insulin Homo sapiens 64-71 29264467-1 2017 Type B insulin resistance is a rare syndrome characterized by fluctuating glucose levels (ranging from hyperglycemia with extreme insulin resistance to intractable hypoglycemia without exogenous insulin administration), high serum insulin levels, and insulin receptor autoantibodies. Glucose 74-81 insulin Homo sapiens 7-14 29264467-4 2017 We report the case of a 60-year-old African American woman with history of systemic lupus erythematosus presenting with extreme fluctuations in glucose levels, ranging from severe hyperglycemia to refractory hypoglycemia, with high serum concentration of insulin in both phases. Glucose 144-151 insulin Homo sapiens 255-262 28662366-4 2017 In this review, we follow the most central triggering pathway to insulin secretion from its very beginning when glucose enters the beta cell to the calcium oscillations it produces to trigger fusion of insulin containing granules with the plasma membrane. Glucose 112-119 insulin Homo sapiens 65-72 29096722-6 2017 Likewise, MAFA binds to the enhancer/promoter region of the insulin gene and drives insulin expression in response to glucose. Glucose 118-125 insulin Homo sapiens 60-67 29096722-6 2017 Likewise, MAFA binds to the enhancer/promoter region of the insulin gene and drives insulin expression in response to glucose. Glucose 118-125 insulin Homo sapiens 84-91 29096724-6 2017 Insulin resistance was confirmed by glycogen assay kit and glucose assay kit. Glucose 59-66 insulin Homo sapiens 0-7 28475354-6 2017 MEASUREMENTS AND MAIN RESULTS: In critically ill patients, infusing glucose with insulin did not lower glucagon, whereas parenteral nutrition containing amino acids increased glucagon. Glucose 68-75 insulin Homo sapiens 81-88 29180325-0 2017 [Correlation between ectopic fat accumulation and insulin sensitivity in obese individuals with different glucose tolerance levels]. Glucose 106-113 insulin Homo sapiens 50-57 28841775-1 2017 A glucose responsive insulin (GRI) is a therapeutic that modulates its potency, concentration, or dosing of insulin in relation to a patient"s dynamic glucose concentration, thereby approximating aspects of a normally functioning pancreas. Glucose 2-9 insulin Homo sapiens 21-28 28698280-2 2017 In fact, NEFA infusion reduces glucose-stimulated insulin secretion, and high-fat diets predict diabetes development. Glucose 31-38 insulin Homo sapiens 50-57 28698280-5 2017 Insulin sensitivity and secretion were computed by the oral glucose minimal model. Glucose 60-67 insulin Homo sapiens 0-7 28835436-8 2017 Prolonged EPS increased non-insulin-stimulated glucose uptake (83%, P = 0.002), Akt (Thr308) phosphorylation (P = 0.005), and insulin receptor substrate-1 (IRS-1)-associated PI3Kalpha activity (P = 0.048). Glucose 47-54 insulin Homo sapiens 28-35 28835436-9 2017 Palmitate reduced insulin-specific action on glucose uptake (-49%, P < 0.001) and inhibited insulin-stimulated Akt phosphorylation (P = 0.049) and whole cell PI3Kalpha activity (P = 0.009). Glucose 45-52 insulin Homo sapiens 18-25 29040103-0 2017 Insulin for Perioperative Glucose Control: Settled Science? Glucose 26-33 insulin Homo sapiens 0-7 29027136-0 2017 Oligonol promotes glucose uptake by modulating the insulin signaling pathway in insulin-resistant HepG2 cells via inhibiting protein tyrosine phosphatase 1B. Glucose 18-25 insulin Homo sapiens 51-58 29027136-0 2017 Oligonol promotes glucose uptake by modulating the insulin signaling pathway in insulin-resistant HepG2 cells via inhibiting protein tyrosine phosphatase 1B. Glucose 18-25 insulin Homo sapiens 80-87 29027136-1 2017 Insulin resistance and protein tyrosine phosphatase 1B (PTP1B) overexpression are strongly associated with type 2 diabetes mellitus (T2DM), which is characterized by defects in insulin signaling and glucose intolerance. Glucose 199-206 insulin Homo sapiens 0-7 29027136-5 2017 Oligonol significantly increased insulin-provoked glucose uptake and decreased PTP1B expression, followed by modulation of ERK phosphorylation. Glucose 50-57 insulin Homo sapiens 33-40 28899227-6 2017 Furthermore, PEITC restored impaired insulin-stimulated glucose uptake, translocation of glucose transporter 4 and insulin signaling by H2O2. Glucose 56-63 insulin Homo sapiens 37-44 28903186-4 2017 We showed that MA decreased the ROS level, inhibited the inflammatory cytokines expression, facilitated insulin-mediated IRS-1/PI3K/Akt/eNOS signaling and suppressed the cellular apoptosis ratio induced by high glucose. Glucose 211-218 insulin Homo sapiens 104-111 29029784-1 2017 The control of insulin release from pancreatic beta cells helps ensure proper blood glucose level, which is critical for human health. Glucose 84-91 insulin Homo sapiens 15-22 29029784-3 2017 After glucose stimulation, calcium influx into beta cells triggers exocytosis of insulin-containing dense-core granules and activates protein kinase C via calcium-dependent phospholipase C-mediated generation of diacylglycerol. Glucose 6-13 insulin Homo sapiens 81-88 29195308-4 2017 The intravenous glucose tolerance test (IVGTT) is an effective protocol to determine the insulin sensitivity, glucose effectiveness, and pancreatic beta-cell functionality, through the analysis and parameter estimation of a proper differential equation model. Glucose 16-23 insulin Homo sapiens 89-96 28724742-2 2017 Recombinant irisin stimulated insulin biosynthesis and glucose-stimulated insulin secretion (GSIS) in a PKA-dependent manner and prevented saturated fatty acid-induced apoptosis in human and rat pancreatic beta-cells, as well as in human and murine pancreatic islets, via AKT/BCL2 signaling. Glucose 55-62 insulin Homo sapiens 74-81 28811274-7 2017 Loss of Rab20 impairs insulin-stimulated glucose uptake in human and mouse skeletal muscle by blocking the translocation of GLUT4 to the cell surface. Glucose 41-48 insulin Homo sapiens 22-29 28851712-0 2017 Downregulation of Insulin Sensitivity After Oral Glucose Administration: Evidence for the Anti-Incretin Effect. Glucose 49-56 insulin Homo sapiens 18-25 28851712-9 2017 Monte Carlo mathematical simulations were used to test whether insulin secretion induced by oral glucose could cause hypoglycemia when coupled with the levels of insulin sensitivity measured during IGIV. Glucose 97-104 insulin Homo sapiens 63-70 28851712-10 2017 Despite isoglycemic conditions, insulin sensitivity was lower during oral than during IV glucose administration. Glucose 89-96 insulin Homo sapiens 32-39 28851712-14 2017 This study demonstrates an anti-incretin effect of intestinal glucose stimulation, which downregulates insulin sensitivity. Glucose 62-69 insulin Homo sapiens 103-110 29061658-2 2017 Insulin secretion together with reciprocal inhibition of glucagon secretion contributes to glucose tolerance. Glucose 91-98 insulin Homo sapiens 0-7 29115211-2 2017 The discoveries of insulin- and appetite-modulating chemical signals, including glucagon-like peptide-1 (GLP-1), secreted from the gastrointestinal system, led to development of a new group of drugs which now are being used for glucose-lowering therapy and weight loss. Glucose 228-235 insulin Homo sapiens 19-26 29115211-12 2017 This glucagon variant may be of importance for glucose homeo-stasis, as we were able to show that it, unexpectedly, activates the glucagon receptor, leading to increased glycogenolysis in hepatocytes and insulin secretion from pancreatic beta-cells. Glucose 47-54 insulin Homo sapiens 204-211 27986406-0 2017 Addition of once daily prandial lixisenatide to basal insulin therapy in patients with type-2 diabetes results in a reduction of HbA1c as an effect of postprandial glucose lowering. Glucose 164-171 insulin Homo sapiens 54-61 27986406-1 2017 AIMS: Basal insulin has been shown to effectively reduce fasting blood glucose (FBG), but postprandial plasma glucose (PPG) excursions may remain higher than normal. Glucose 71-78 insulin Homo sapiens 12-19 28365222-2 2017 Insulin pathway is very important for the regulation of glucose, lipid, and energy homeostasis, growth and mitogenic. Glucose 56-63 insulin Homo sapiens 0-7 28407415-3 2017 First- and second-phase insulin secretion during an intravenous glucose challenge were calculated. Glucose 64-71 insulin Homo sapiens 24-31 28407415-9 2017 Thus, lixisenatide and, to a lesser extent, insulin glargine, increase glucose-stimulated insulin secretion in an additive manner. Glucose 71-78 insulin Homo sapiens 44-51 28407415-9 2017 Thus, lixisenatide and, to a lesser extent, insulin glargine, increase glucose-stimulated insulin secretion in an additive manner. Glucose 71-78 insulin Homo sapiens 90-97 28433617-3 2017 It has been suggested that signaling errors within this homeostatic system, characterized by impaired switching of substrate oxidation from glucose to fat in response to insulin, can contribute to the etiology of metabolic syndrome and occurs before the development of type II diabetes. Glucose 140-147 insulin Homo sapiens 170-177 28433617-4 2017 Glucose regulation with restored insulin sensitivity facilitated through clinically regulated, benign dietary ketosis (BDK), may significantly reduce, regulate and reverse the adverse pathologies common to MetS and obesity. Glucose 0-7 insulin Homo sapiens 33-40 28852804-5 2017 Podocyte insulin responses were investigated with western blotting, cellular glucose uptake assays and automated fluorescent imaging of the actin cytoskeleton. Glucose 77-84 insulin Homo sapiens 9-16 28852804-8 2017 RESULTS: Podocytes exposed to a diabetic environment (high glucose, high insulin and the proinflammatory cytokines TNF-alpha and IL-6) become insulin resistant with respect to glucose uptake and activation of phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signalling. Glucose 59-66 insulin Homo sapiens 142-149 28852804-11 2017 Stable expression of nephrin is also required for the insulin-stimulated glucose uptake response in podocytes and for efficient insulin-stimulated remodelling of the actin cytoskeleton. Glucose 73-80 insulin Homo sapiens 54-61 28888993-2 2017 The precise incidence of nocturnal hypoglycaemia is difficult to determine with no agreed definition, but continuous glucose monitoring has shown that it occurs frequently in people taking insulin. Glucose 117-124 insulin Homo sapiens 189-196 28918342-4 2017 The ultra-long-acting insulin analogue, insulin degludec (IDeg), presents a flat and stable glucose-lowering effect both in Type 1 and Type 2 diabetes patients. Glucose 92-99 insulin Homo sapiens 22-29 29201240-0 2017 Glucagon-like peptide-1 potentiates glucose-stimulated insulin secretion via the transient receptor potential melastatin 2 channel. Glucose 36-43 insulin Homo sapiens 55-62 29201240-2 2017 It is known that glucose-stimulated insulin secretion (GSIS) can be potentiated by glucagon like peptide-1 (GLP-1), and that the changes in the extracellular glucose concentration alter the levels of intracellular adenosine ATP and cAMP. Glucose 17-24 insulin Homo sapiens 36-43 29201240-2 2017 It is known that glucose-stimulated insulin secretion (GSIS) can be potentiated by glucagon like peptide-1 (GLP-1), and that the changes in the extracellular glucose concentration alter the levels of intracellular adenosine ATP and cAMP. Glucose 158-165 insulin Homo sapiens 36-43 29201240-5 2017 In addition, the results of current recordings of TRPM2 and measurement of the resulting insulin secretion in beta-cells in the presence of GLP-1 and various concentrations of glucose suggest that GLP-1 regulates GSIS via the TRPM2 channel. Glucose 176-183 insulin Homo sapiens 89-96 28951307-2 2017 Glucose transport into the neurons is achieved by regulatory induction of surface glucose transporter-3 (GLUT3) instead of the insulin. Glucose 0-7 insulin Homo sapiens 127-134 28951307-10 2017 Insulin supplementation to high glucose decreased NOx synthesis and GLUT3 levels, in contrast oxidative stress increased three-fold. Glucose 32-39 insulin Homo sapiens 0-7 28473214-4 2017 CONCLUSIONS: Insulin is required if glucose levels are very high. Glucose 36-43 insulin Homo sapiens 13-20 28675705-0 2017 Assessment of insulin resistance in Chinese PCOS patients with normal glucose tolerance. Glucose 70-77 insulin Homo sapiens 14-21 28675705-1 2017 The study aimed to investigate insulin resistance (IR) status in polycystic ovary syndrome (PCOS) women with normal glucose tolerance (NGT), and further to evaluate feasible diagnostic method for those patients. Glucose 116-123 insulin Homo sapiens 31-38 29285445-14 2017 Conclusion: When compared to the standard basal-bolus insulin protocol, the new protocol showed lower mean blood glucose and lower glycemic variability. Glucose 113-120 insulin Homo sapiens 54-61 29084322-2 2017 The homoeostasis model assessment (HOMA) is a measure of insulin resistance based on fasting blood glucose and insulin levels. Glucose 99-106 insulin Homo sapiens 57-64 28544529-2 2017 Glucose triggers insulin secretion by causing exocytosis of insulin granules from pancreatic beta-cells. Glucose 0-7 insulin Homo sapiens 17-24 29023304-6 2017 RESULTS: The change in serum insulin level at 120 minutes after an oral glucose tolerance test was positively associated with changes in peroneal nerve conduction velocities and F-wave mean, sural nerve conduction and medial plantar nerve conduction velocities. Glucose 72-79 insulin Homo sapiens 29-36 28449590-0 2017 Continuous Glucose Monitoring in Older Adults With Type 1 and Type 2 Diabetes Using Multiple Daily Injections of Insulin: Results From the DIAMOND Trial. Glucose 11-18 insulin Homo sapiens 113-120 28523459-0 2017 Plasma vascular endothelial growth factor B levels are increased in patients with newly diagnosed type 2 diabetes mellitus and associated with the first phase of glucose-stimulated insulin secretion function of beta-cell. Glucose 162-169 insulin Homo sapiens 181-188 28523459-1 2017 PURPOSE: To detect plasma vascular endothelial growth factor B (VEGF-B) in individuals with different glucose tolerance and investigate the relationship between plasma VEGF-B levels and the first phase of glucose-stimulated insulin secretion. Glucose 205-212 insulin Homo sapiens 224-231 28654314-0 2017 Cross-Validation of a Glucose-Insulin-Glucagon Pharmacodynamics Model for Simulation Using Data From Patients With Type 1 Diabetes. Glucose 22-29 insulin Homo sapiens 30-37 28654314-11 2017 CONCLUSIONS: The PD model accurately simulates glucose excursions based on plasma insulin and glucagon concentrations. Glucose 47-54 insulin Homo sapiens 82-89 28681638-1 2017 The accompanying article by Groat et al in this issue presents a methodology to compare glucose outcomes from insulin bolus dose recommendations observed retrospectively from a novel iDecide bolus calculator with glucose outcomes from the prospective bolus recommendations provided by a current insulin pump. Glucose 88-95 insulin Homo sapiens 110-117 28681638-1 2017 The accompanying article by Groat et al in this issue presents a methodology to compare glucose outcomes from insulin bolus dose recommendations observed retrospectively from a novel iDecide bolus calculator with glucose outcomes from the prospective bolus recommendations provided by a current insulin pump. Glucose 88-95 insulin Homo sapiens 295-302 28884599-0 2017 A Simplified Approach Using Rate of Change Arrows to Adjust Insulin With Real-Time Continuous Glucose Monitoring. Glucose 94-101 insulin Homo sapiens 60-67 28954814-4 2017 Here, we utilized the model of high insulin/glucose (HIHG)-induced insulin resistance, determined by measuring Akt phosphorylation (T308 and S473) and glucose uptake in L6 skeletal muscle cells. Glucose 44-51 insulin Homo sapiens 67-74 28954814-4 2017 Here, we utilized the model of high insulin/glucose (HIHG)-induced insulin resistance, determined by measuring Akt phosphorylation (T308 and S473) and glucose uptake in L6 skeletal muscle cells. Glucose 151-158 insulin Homo sapiens 36-43 28127888-6 2017 Three weeks after implantation, the islets displayed intact morphology, intensive hormone staining and glucose-sensitive insulin release. Glucose 103-110 insulin Homo sapiens 121-128 28317340-8 2017 Moreover, differentiated beta-cells secreted insulin in response to increased glucose in vitro. Glucose 78-85 insulin Homo sapiens 45-52 28901503-3 2017 High glucose and high insulin conditions resulted in increased viability, proliferation, and invasion in MCF-7 cells compared with normal glucose and low insulin conditions. Glucose 138-145 insulin Homo sapiens 22-29 28901503-4 2017 Reverse transcription-quantitative polymerase chain reaction and western blot analyses revealed that insulin receptor substrate 1 (IRS1) was significantly upregulated following high glucose and high insulin treatment compared with normal glucose and low insulin conditions. Glucose 182-189 insulin Homo sapiens 101-108 28901503-4 2017 Reverse transcription-quantitative polymerase chain reaction and western blot analyses revealed that insulin receptor substrate 1 (IRS1) was significantly upregulated following high glucose and high insulin treatment compared with normal glucose and low insulin conditions. Glucose 238-245 insulin Homo sapiens 101-108 29107295-5 2017 METHODS: We recruited 40 Roux-en-Y gastric bypass patients and assessed the serum FGF21 response to fructose (75-g fructose tolerance test) and basal and insulin-mediated glucose and lipid fluxes during a 2-step hyperinsulinemic-euglycemic clamp with infusion of [6,6-2H2] glucose and [1,1,2,3,3-2H5] glycerol. Glucose 171-178 insulin Homo sapiens 154-161 28527919-1 2017 Pancreatic islet beta cells secrete insulin in response to nutrient secretagogues, like glucose, dependent on calcium influx and nutrient metabolism. Glucose 88-95 insulin Homo sapiens 36-43 29122960-4 2017 Here, we aim to determine the specific role of miR-335 during development of T2D, and the influence of this miRNA on glucose-stimulated insulin secretion and Ca2+-dependent exocytosis. Glucose 117-124 insulin Homo sapiens 136-143 29122960-6 2017 Overexpression of miR-335 in human EndoC-betaH1 and in rat INS-1 832/13 cells (OE335) resulted in decreased glucose-stimulated insulin secretion, and OE335 cells showed concomitant reduction in three exocytotic proteins: SNAP25, Syntaxin-binding protein 1 (STXBP1), and synaptotagmin 11 (SYT11). Glucose 108-115 insulin Homo sapiens 127-134 28673470-3 2017 OBJECTIVES: To investigate the acute and chronic effects of RYGB surgery on insulin-stimulated glucose metabolism in cultured human primary myotubes derived from nondiabetic severely obese humans. Glucose 95-102 insulin Homo sapiens 76-83 28263224-8 2017 Insulin secretion was also diminished, with ischemic beta cells losing their insulin secretory response to stimulatory glucose levels (P < 0.01). Glucose 119-126 insulin Homo sapiens 77-84 29063103-5 2017 Glucose and lipid levels in circulation and dietary habits may influence the effect of insulin on GH secretion. Glucose 0-7 insulin Homo sapiens 87-94 29016121-6 2017 Evaluation of lead compounds 1 and 2 (CHIR-611 or CT-98014) in rodent models of type 2 diabetes revealed that single oral doses lowered hyperglycemia within 60 min, enhanced insulin-stimulated glucose transport, and improved glucose disposal without increasing insulin levels. Glucose 193-200 insulin Homo sapiens 174-181 28910454-0 2017 FDA Approval of Nonadjunctive Use of Continuous Glucose Monitors for Insulin Dosing: A Potentially Risky Decision. Glucose 48-55 insulin Homo sapiens 69-76 29069585-5 2017 Surprisingly, adipocytes lacking ChREBP display a cell-autonomous reduction in insulin-stimulated glucose transport that is mediated by impaired Glut4 translocation and exocytosis, not lower Glut4 levels. Glucose 98-105 insulin Homo sapiens 79-86 29069585-9 2017 Thus, loss of adipose-ChREBP is sufficient to cause insulin resistance, potentially by regulating AT glucose transport and flux through specific lipogenic pathways. Glucose 101-108 insulin Homo sapiens 52-59 29130725-3 2017 Also, severe hypoglycemia was detected as a consequence of intensive insulin treatment that provokes deleterious effects in their clinical evolution, so a correct monitoring of plasma glucose would contribute to reduce morbidity and mortality. Glucose 184-191 insulin Homo sapiens 69-76 29130725-4 2017 In critically ill patients, glucose metabolism is in allostasis stage as a consequence of metabolic stress, producing an increase in peripheral resistance to insulin that causes an imbalance with the pancreatic beta-cell function, increasing insulin secretion to maintain plasma glucose levels within normality ranges. Glucose 28-35 insulin Homo sapiens 158-165 29130725-4 2017 In critically ill patients, glucose metabolism is in allostasis stage as a consequence of metabolic stress, producing an increase in peripheral resistance to insulin that causes an imbalance with the pancreatic beta-cell function, increasing insulin secretion to maintain plasma glucose levels within normality ranges. Glucose 28-35 insulin Homo sapiens 242-249 29058131-4 2017 RECENT FINDINGS: Preclinical studies suggest that insulin has positive effects of facilitating glucose entry into cells and maintaining euglycemia and negative effects of favoring obesity and atherogenesis under certain conditions. Glucose 95-102 insulin Homo sapiens 50-57 28717057-6 2017 RESULTS: Target glucose levels (71-180 mg/dL) were achieved during 97.1 +- 5.5% and 86.4 +- 19.0% of the continuous insulin infusion and subcutaneous injection periods, respectively. Glucose 16-23 insulin Homo sapiens 116-123 29085222-3 2017 Several studies have demonstrated that insulin action is not only relevant for glucose control, but also for vascular homeostasis. Glucose 79-86 insulin Homo sapiens 39-46 29042645-0 2017 Effects of intranasal insulin application on the hypothalamic BOLD response to glucose ingestion. Glucose 79-86 insulin Homo sapiens 22-29 29042645-3 2017 In this study, we assessed whether intranasal insulin can be used to enhance neuronal hypothalamic responses to glucose ingestion. Glucose 112-119 insulin Homo sapiens 46-53 28970466-6 2017 The total insulin dose and achievement rate of the target blood glucose level were 113.9+-51.4 U and 23.7+-15.6%, per 24 h, respectively. Glucose 64-71 insulin Homo sapiens 10-17 28984038-1 2017 Diabetes is characterized by elevated levels of blood glucose as a result of insufficient production of insulin from loss or dysfunction of pancreatic islet beta-cells. Glucose 54-61 insulin Homo sapiens 104-111 28930338-0 2017 Biomedical nanomotors: efficient glucose-mediated insulin release. Glucose 33-40 insulin Homo sapiens 50-57 28930338-1 2017 We report herein the design of an autonomous glucose-responsive smart nanomachine for insulin (In) delivery based on ultrasound (US)-propelled nanomotors combined with an enzyme-based sensing-effector unit. Glucose 45-52 insulin Homo sapiens 86-93 28930338-3 2017 Glucose-induced protonation of the PBA groups triggers the opening of the pH-driven gate and uncapping of the insulin-loaded nanovalves. Glucose 0-7 insulin Homo sapiens 110-117 28930338-4 2017 The insulin-loaded MS-Au nanomotors displayed an efficient US-driven movement that dramatically accelerates the glucose-triggered insulin release when compared to their static counterparts. Glucose 112-119 insulin Homo sapiens 4-11 28930338-4 2017 The insulin-loaded MS-Au nanomotors displayed an efficient US-driven movement that dramatically accelerates the glucose-triggered insulin release when compared to their static counterparts. Glucose 112-119 insulin Homo sapiens 130-137 28970466-8 2017 The total insulin dose and achievement rate of the target blood glucose level were 156.5+-57.5 U and 20.2+-20.0% per 24 h, respectively. Glucose 64-71 insulin Homo sapiens 10-17 30291065-10 2017 CONCLUSIONS: Insulin- and noninsulin-using subjects were each more inclined to act when glucose results were shown with color, and associating glucose results with color was viewed as particularly beneficial by subjects with lower numeracy. Glucose 88-95 insulin Homo sapiens 13-20 28647826-0 2017 Numerical simulation of a glucose sensitive composite membrane closed-loop insulin delivery system. Glucose 26-33 insulin Homo sapiens 75-82 29078846-3 2017 Moderate downregulation of 11beta-HSD1 can attenuate insulin insensitivity and the impairment of glucose-stimulated insulin secretion. Glucose 97-104 insulin Homo sapiens 116-123 28720584-2 2017 Because skeletal muscle is responsible for the majority of whole body insulin-stimulated glucose uptake, regulation of glucose metabolism in this tissue is of particular importance. Glucose 89-96 insulin Homo sapiens 70-77 28720584-5 2017 PKN2 knockdown in vitro decreased insulin-stimulated glucose uptake, incorporation into glycogen, and oxidation. Glucose 53-60 insulin Homo sapiens 34-41 28647826-1 2017 Closed-loop insulin delivery system works on pH modulation by gluconic acid production from glucose, which in turn allows regulation of insulin release across membrane. Glucose 92-99 insulin Homo sapiens 12-19 28647826-1 2017 Closed-loop insulin delivery system works on pH modulation by gluconic acid production from glucose, which in turn allows regulation of insulin release across membrane. Glucose 92-99 insulin Homo sapiens 136-143 28370947-4 2017 At baseline, posttreatment, and 1 year, depressive symptoms were assessed, and whole body insulin sensitivity (WBISI) was estimated from oral glucose tolerance tests. Glucose 142-149 insulin Homo sapiens 90-97 28863979-1 2017 OBJECTIVE: A glucose clamp procedure is the most reliable way to quantify insulin pharmacokinetics and pharmacodynamics, but skilled and trained research personnel are required to frequently adjust the glucose infusion rate. Glucose 13-20 insulin Homo sapiens 74-81 28863979-4 2017 Each virtual subject simulates plasma glucose and insulin concentrations in response to intravenous insulin and glucose infusions. Glucose 38-45 insulin Homo sapiens 100-107 28863979-4 2017 Each virtual subject simulates plasma glucose and insulin concentrations in response to intravenous insulin and glucose infusions. Glucose 112-119 insulin Homo sapiens 50-57 28863979-7 2017 RESULTS: Plasma glucose and insulin concentrations were predicted by the virtual subjects in response to glucose infusions determined by a trained research staff performing a simulated hyperglycemic clamp experiment. Glucose 105-112 insulin Homo sapiens 28-35 28318098-0 2017 Decreased insulin-stimulated brown adipose tissue glucose uptake after short-term exercise training in healthy middle-aged men. Glucose 50-57 insulin Homo sapiens 10-17 28371223-6 2017 During closed-loop insulin delivery, t max,IA was positively correlated with glucose variability ( P < .05). Glucose 77-84 insulin Homo sapiens 19-26 28318098-3 2017 Insulin-stimulated glucose uptake was measured using 2-[18 F]flouro-2-deoxy-D-glucose positron-emission tomography in BAT, skeletal muscle, and abdominal and femoral subcutaneous and visceral white adipose tissue (WAT) depots before and after the training interventions. Glucose 19-26 insulin Homo sapiens 0-7 28318098-4 2017 RESULTS: Training improved VO2peak (P = .0005), insulin-stimulated glucose uptake into the quadriceps femoris muscle (P = .0009) and femoral subcutaneous WAT (P = .02) but not into BAT, with no difference between the training modes. Glucose 67-74 insulin Homo sapiens 48-55 28802779-3 2017 Closed loop insulin delivery systems operate as an artificial pancreas by making automated insulin dose adjustments based on real time continuous glucose monitoring. Glucose 146-153 insulin Homo sapiens 12-19 28802779-3 2017 Closed loop insulin delivery systems operate as an artificial pancreas by making automated insulin dose adjustments based on real time continuous glucose monitoring. Glucose 146-153 insulin Homo sapiens 91-98 28318098-6 2017 Interestingly, training decreased insulin-stimulated BAT glucose uptake in the high BAT group (4.0 [2.8, 5.5] vs 2.5 [1.7, 3.6]; training*BAT, P = .02), whereas there was no effect of training in the low BAT group (1.5 [1.2, 1.9] vs 1.6 [1.2, 2.0] micromol/100 g/min). Glucose 57-64 insulin Homo sapiens 34-41 28768703-10 2017 Thus, PDH-E1alpha expression and covalent regulation, and hence the tricarboxylic acid cycle influx of pyruvate-derived acetyl-CoA relative to beta-oxidation-derived acetyl-CoA, are suggested to impact on insulin-stimulated glucose uptake. Glucose 224-231 insulin Homo sapiens 205-212 28318098-9 2017 Short-term exercise training decreased insulin-stimulated BAT glucose uptake in participants with active BAT, suggesting that training does not work as a potent stimulus for BAT activation. Glucose 62-69 insulin Homo sapiens 39-46 28609547-0 2017 Intensive insulin therapy combined with metformin is associated with reduction in both glucose variability and nocturnal hypoglycaemia in patients with type 2 diabetes. Glucose 87-94 insulin Homo sapiens 10-17 28609547-1 2017 BACKGROUND: The effect on glucose variability in patients with intensive insulin therapy has not been fully understood. Glucose 26-33 insulin Homo sapiens 73-80 28710139-3 2017 By using a recently developed mathematical model that uses insulin and C-peptide measurements from the insulin-modified, frequently sampled intravenous glucose tolerance test (FSIGT), we estimated hepatic versus extrahepatic insulin clearance in 29 EA and 18 AA healthy women. Glucose 152-159 insulin Homo sapiens 103-110 28768703-11 2017 Taken together, the oxidative metabolic fluxes of glucose and FA are powerful and opposite regulators of insulin action in muscle. Glucose 50-57 insulin Homo sapiens 105-112 28720696-4 2017 Mathematical model-based insulin secretion indices were estimated by using a 2-h seven-sample oral glucose tolerance test. Glucose 99-106 insulin Homo sapiens 25-32 28790139-4 2017 These highly blood-perfused islets had better glucose-stimulated insulin secretion capacity than other islets and developed more amyloid deposits after 10 months of high-fat diet. Glucose 46-53 insulin Homo sapiens 65-72 28938465-7 2017 Insulin sensitivity of glucose production (Ra) was measured by the euglycemic hyperinsulinemic clamp technique in which a low insulin dose (0.4 mU/kg/min for 240 minutes) was combined with D-[3-3H] glucose infusion to measure rates of Ra and utilization and insulin action on antilipolysis from suppression of serum free fatty acids. Glucose 23-30 insulin Homo sapiens 0-7 28661564-24 2017 Recent animal studies suggest a potential mechanism for such clinical benefits: beta-cells dedifferentiate to endocrine progenitor-like cells during stress-induced hyperglycemia, and strictly normalizing blood glucose by insulin therapy could induce dedifferentiated cell redifferentiation to mature beta-cells, and hence restoration of drug responsivity. Glucose 210-217 insulin Homo sapiens 221-228 28508346-1 2017 PURPOSE: Testosterone by promoting different metabolic pathways contributes to short-term homeostasis of skeletal muscle, the largest insulin-sensitive tissue and the primary site for insulin-stimulated glucose utilization. Glucose 203-210 insulin Homo sapiens 184-191 27440134-3 2017 In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores. Glucose 184-191 insulin Homo sapiens 147-154 28661564-25 2017 In addition to its glucose-lowering activity, insulin may contribute to improved beta-cell function by its antilipolytic, anti-inflammatory, and antiapoptotic effects. Glucose 19-26 insulin Homo sapiens 46-53 28577886-7 2017 CONCLUSION: The time-point 4-6weeks after Ramadan was distinguished by greater glucose exposure and wider glucose variability that may reflect ongoing changes in insulin sensitivity in response to altering lifestyle patterns in non-diabetic young adults across the spectrum of body weight. Glucose 106-113 insulin Homo sapiens 162-169 29362600-13 2017 When the insulin resistant HepG2 cells were treated alone with EGCG and pioglitazone, the glucose production reduced by 50 and 55%, respectively. Glucose 90-97 insulin Homo sapiens 9-16 28653461-1 2017 OBJECTIVE: The minimal model is used to estimate insulin sensitivity in patients with diabetes, following an intravenous glucose tolerance test (IVGTT). Glucose 121-128 insulin Homo sapiens 49-56 28653461-6 2017 An integrated glucose-insulin model was used to simulate glucose and insulin concentrations following new glucose inputs. Glucose 57-64 insulin Homo sapiens 22-29 28850155-9 2017 In cohort 1, serum CCDC80 correlated negatively with the acute insulin response to glucose and IGF1 levels, and positively with blood neutrophil count, independently of BMI, but not with insulin sensitivity. Glucose 83-90 insulin Homo sapiens 63-70 29033899-5 2017 We have demonstrated that PTM occurs during endoplasmic reticulum (ER) stress, a process to which beta cells are uniquely susceptible due to the high rate of insulin production in response to dynamic glucose sensing. Glucose 200-207 insulin Homo sapiens 158-165 29158827-4 2017 Using insulin-resistant HepG2 cell and diabetic KKAy mice as models, in vitro and in vivo assessments have demonstrated that biomineralized insulin nanoparticles can trigger glucose metabolism, and this improvement extends after the treatment. Glucose 174-181 insulin Homo sapiens 140-147 28828487-0 2017 Continuous Glucose Monitoring Versus Usual Care in Patients With Type 2 Diabetes Receiving Multiple Daily Insulin Injections: A Randomized Trial. Glucose 11-18 insulin Homo sapiens 106-113 28921900-6 2017 The mean estimated treatment difference (IDegAsp group - basal insulin group) of the mean plasma glucose level was -28 mg/dL (95% confidence interval -47 to -8, P = 0.008) after 4 weeks and that of the area under the glucose concentration vs time curve for 2 h was -2,800 mg/min/dL (95% confidence interval -5,300 to -350, P = 0.028), confirming the superiority of IDegAsp to basal insulin. Glucose 97-104 insulin Homo sapiens 63-70 28921900-9 2017 CONCLUSIONS: After switching from basal insulin, the IDegAsp dose can be uptitrated by 60% based on fasting plasma glucose data. Glucose 115-122 insulin Homo sapiens 40-47 28755973-0 2017 l-Cysteine supplementation increases insulin sensitivity mediated by upregulation of GSH and adiponectin in high glucose treated 3T3-L1 adipocytes. Glucose 113-120 insulin Homo sapiens 37-44 28755973-2 2017 This study examined the hypothesis that LC supplementation positively up regulates the effects of insulin on GSH and glucose metabolism in 3T3-L1 adipocyte model. Glucose 117-124 insulin Homo sapiens 98-105 28755973-6 2017 Treatment with insulin alone significantly (p < 0.05) reduced ROS levels as well as increased DsbA-L, adiponectin, GCLC, GCLM, GSH, and GLUT-4 protein levels, glucose utilization, and improved total and HMW adiponectin secretion in HG treated adipocytes compared to HG alone. Glucose 162-169 insulin Homo sapiens 15-22 28755973-9 2017 Furthermore, LC and insulin increases GLUT-4 protein expression (65% Vs LC, 18% Vs Insulin), glucose utilization (57% Vs LC, 27% Vs insulin) compared with the either insulin or LC alone in HG-treated cells. Glucose 93-100 insulin Homo sapiens 20-27 28755973-10 2017 Similarly, LC supplementation increased insulin action significantly in cells maintained in medium contained control glucose. Glucose 117-124 insulin Homo sapiens 40-47 28915272-7 2017 The results indicate that insulin action appears to be lower in DM than in control myotubes in terms of protein activation and glucose uptake. Glucose 127-134 insulin Homo sapiens 26-33 28903774-1 2017 BACKGROUND: Hypertension and the triglyceride and glucose index both have been associated with insulin resistance; however, the longitudinal association remains unclear. Glucose 50-57 insulin Homo sapiens 95-102 28898241-13 2017 DISCUSSION/CONCLUSION: This study indicates that prenatal and lactational exposure influences glucose metabolism in adolescents, presumably through a negative effect on insulin secretion by pancreatic beta cells. Glucose 94-101 insulin Homo sapiens 169-176 28726640-6 2017 Overexpressing mouse or human CTRP6 impaired glucose disposal in peripheral tissues in response to glucose and insulin challenge in wild-type mice. Glucose 45-52 insulin Homo sapiens 111-118 28924481-6 2017 Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. Glucose 114-121 insulin Homo sapiens 67-74 28662368-6 2017 Spheroids were tested for yield, viability, diameter, cellular composition, and glucose-stimulated insulin secretion. Glucose 80-87 insulin Homo sapiens 99-106 28662368-11 2017 The glucose-stimulated insulin secretion was not statistically different for the 50, 75, or 90 groups when exposed to 2.4, 16.8, or 22.4 mM glucose. Glucose 4-11 insulin Homo sapiens 23-30 28678625-10 2017 The effects of the reviewed additives, ECM or scaffolds on islet viability, apoptosis and function (glucose-stimulated insulin secretion - GSIS) were heterogeneous, making any major conclusion hard to sustain. Glucose 100-107 insulin Homo sapiens 119-126 28869506-4 2017 Beyond a role in cellular lipid homeostasis, ABCG1 equally participates to glucose and lipid metabolism by controlling the secretion and activity of insulin and lipoprotein lipase. Glucose 75-82 insulin Homo sapiens 149-179 28837492-0 2017 Routine Glucose Self-Monitoring Unnecessary for Non-Insulin-Treated Patients with Type 2 Diabetes. Glucose 8-15 insulin Homo sapiens 52-59 28180948-8 2017 Unlike previous studies, TBT at noncytotoxic concentrations significantly increased glucose-stimulated insulin secretion and intracellular Ca2+ ([Ca2+]i) in beta-cells. Glucose 84-91 insulin Homo sapiens 103-110 28180948-11 2017 Similarly, islets treated with TBT significantly increased glucose-stimulated insulin secretion, which could be reversed by ICI182780, NAC, and PKC inhibitor. Glucose 59-66 insulin Homo sapiens 78-85 28751575-1 2017 OBJECTIVE: Insulin administered directly into the brain acutely suppresses hepatic glucose production and triglyceride-rich lipoprotein (TRL) secretion in rodents. Glucose 83-90 insulin Homo sapiens 11-18 28751575-2 2017 In addition, intranasally administered insulin, which selectively raises cerebrospinal fluid insulin concentration, suppresses hepatic glucose production in humans; however, its effect on TRL secretion in humans has not previously been examined. Glucose 135-142 insulin Homo sapiens 39-46 28751575-3 2017 In this study, we examined whether intranasal insulin, administered at a dose that has previously been shown to suppress hepatic glucose production, modulates TRL particle secretion by the liver and intestine in humans. Glucose 129-136 insulin Homo sapiens 46-53 29226203-10 2017 Similarly, insulin-dependent diabetic patients had an average increase in fasting glucose level of 99 mg/dL versus 50 mg/dL in non-insulin-dependent diabetic patients (P<0.001). Glucose 82-89 insulin Homo sapiens 11-18 28529179-5 2017 In this review, we discuss the effects of obesity and insulin resistance on skeletal muscle, an important organ for the control of postprandial glucose. Glucose 144-151 insulin Homo sapiens 54-61 28500659-5 2017 METHODS: We assessed insulin sensitivity by Matsuda index (oral glucose tolerance test). Glucose 64-71 insulin Homo sapiens 21-28 28574177-5 2017 The first critical step is to optimize basal insulin dosing to reach a fasting glucose concentration of ~6.7 mmol/l; this allows ~40% of patients with baseline HbA1c >75 mmol/mol (9%) to be controlled with only one basal insulin injection per day. Glucose 79-86 insulin Homo sapiens 45-52 28596236-0 2017 Acute Hypoglycemia in Healthy Humans Impairs Insulin-Stimulated Glucose Uptake and Glycogen Synthase in Skeletal Muscle: A Randomized Clinical Study. Glucose 64-71 insulin Homo sapiens 45-52 28596236-2 2017 Skeletal muscle is the predominant site of insulin-mediated glucose disposal. Glucose 60-67 insulin Homo sapiens 43-50 28596236-6 2017 Hypoglycemia impaired insulin-stimulated glucose disposal and glucose clearance in skeletal muscle, whereas insulin signaling in glucose transport was unaffected by hypoglycemia. Glucose 41-48 insulin Homo sapiens 22-29 28596236-6 2017 Hypoglycemia impaired insulin-stimulated glucose disposal and glucose clearance in skeletal muscle, whereas insulin signaling in glucose transport was unaffected by hypoglycemia. Glucose 62-69 insulin Homo sapiens 22-29 28596236-6 2017 Hypoglycemia impaired insulin-stimulated glucose disposal and glucose clearance in skeletal muscle, whereas insulin signaling in glucose transport was unaffected by hypoglycemia. Glucose 62-69 insulin Homo sapiens 22-29 28684634-1 2017 Insulin clamp studies have shown that the suppressive actions of insulin on endogenous glucose production (EGP) are markedly more sensitive than for stimulating glucose disposal (Rd). Glucose 87-94 insulin Homo sapiens 0-7 28684634-1 2017 Insulin clamp studies have shown that the suppressive actions of insulin on endogenous glucose production (EGP) are markedly more sensitive than for stimulating glucose disposal (Rd). Glucose 87-94 insulin Homo sapiens 65-72 28684634-1 2017 Insulin clamp studies have shown that the suppressive actions of insulin on endogenous glucose production (EGP) are markedly more sensitive than for stimulating glucose disposal (Rd). Glucose 161-168 insulin Homo sapiens 0-7 28684634-7 2017 This suggests that after glucose ingestion, the body preferentially permits a transient and optimal degree of postprandial hyperglycemia to efficiently enhance insulin-induced changes in glucose fluxes, thereby minimizing the demand for insulin secretion. Glucose 25-32 insulin Homo sapiens 160-167 28684634-7 2017 This suggests that after glucose ingestion, the body preferentially permits a transient and optimal degree of postprandial hyperglycemia to efficiently enhance insulin-induced changes in glucose fluxes, thereby minimizing the demand for insulin secretion. Glucose 187-194 insulin Homo sapiens 160-167 28687542-1 2017 OBJECTIVE: Insulin increases glucose disposal in part by enhancing microvascular blood flow (MBF) and substrate delivery to myocytes. Glucose 29-36 insulin Homo sapiens 11-18 28743063-1 2017 Pancreatic beta-cells secrete insulin in response to circulating glucose, thereby maintaining euglycemia. Glucose 65-72 insulin Homo sapiens 30-37 28880482-3 2017 The current article summarizes recent insights gained from application of metabolomics tools to the specific process of glucose-stimulated insulin secretion, revealing 2 new mechanisms that may provide targets for improving insulin secretion in diabetes. Glucose 120-127 insulin Homo sapiens 139-146 28579536-8 2017 Insulin kinetics were calculated from oral glucose tolerance tests. Glucose 43-50 insulin Homo sapiens 0-7 28666850-1 2017 Previously published studies strongly suggested that insulin- and exercise-induced skeletal muscle glucose uptake require nitric oxide (NO) production. Glucose 99-106 insulin Homo sapiens 53-60 28666850-2 2017 However, the signal transduction mechanisms by which insulin and contraction regulated NO production and subsequent glucose transport are not known. Glucose 116-123 insulin Homo sapiens 53-60 28666850-8 2017 We conclude that nNOS phosphorylation and subsequently increased NO production are required for both insulin- and H2O2-stimulated glucose transport. Glucose 130-137 insulin Homo sapiens 101-118 28666850-10 2017 Thus, insulin and H2O2-activated signaling pathways converge on nNOS, which is a common mediator of glucose uptake in both pathways. Glucose 100-107 insulin Homo sapiens 6-13 28666850-11 2017 However, the fact that different kinases are utilized provides a basis for the use of exercise to activate glucose transport in the face of insulin resistance. Glucose 107-114 insulin Homo sapiens 140-147 27794176-8 2017 CONCLUSIONS: High fasting insulin concentrations may be a pivotal glucose metabolic predictor for the severity of hepatic fibrosis beyond the glycemic status in NAFLD patients before development of T2DM. Glucose 66-73 insulin Homo sapiens 26-33 28989869-1 2017 INTRODUCTION: Endogenous hyperinsulinemic hypoglycemia (EHH) is a condition in which the insulin levels are inappropriately high in the presence of low plasma glucose. Glucose 159-166 insulin Homo sapiens 30-37 28762247-0 2017 Deterioration of insulin release rate response to glucose during oral glucose tolerance test is associated with an increased risk of incident diabetes in normal glucose tolerance subjects. Glucose 50-57 insulin Homo sapiens 17-24 28762247-0 2017 Deterioration of insulin release rate response to glucose during oral glucose tolerance test is associated with an increased risk of incident diabetes in normal glucose tolerance subjects. Glucose 70-77 insulin Homo sapiens 17-24 28762247-7 2017 Insulin release rate (IRRINS ) in the function of glucose (IRRINS response to glucose [IRRG]) during OGTT was compared with betaCGS. Glucose 50-57 insulin Homo sapiens 0-7 28762247-7 2017 Insulin release rate (IRRINS ) in the function of glucose (IRRINS response to glucose [IRRG]) during OGTT was compared with betaCGS. Glucose 78-85 insulin Homo sapiens 0-7 28895791-2 2017 Recent reports indicate that fasting glucose levels in non-diabetic patients correlate appropriately with the development of certain elements in metabolic syndrome, which suggest a cause-effect relationship with insulin resistance. Glucose 37-44 insulin Homo sapiens 212-219 28303725-0 2017 Long-Term Effects of Continuous Subcutaneous Insulin Infusion on Glucose Control and Microvascular Complications in Patients With Type 1 Diabetes. Glucose 65-72 insulin Homo sapiens 45-52 28303725-1 2017 BACKGROUND: We investigated the long-term effects of continuous subcutaneous insulin infusion (CSII) on glucose control and microvascular complications in patients with type 1 diabetes (T1D). Glucose 104-111 insulin Homo sapiens 77-84 28332406-1 2017 BACKGROUND: Reliability of continuous glucose monitors (CGM) is a prerequisite for therapeutic dosing of insulin without the need for confirmatory blood glucose meter measurements. Glucose 38-45 insulin Homo sapiens 105-112 28720321-7 2017 RESULTS: Multivariate analysis showed "Age", "BMI" and "use of steroids" to be significantly related, in different combinations, to the glucose metabolism parameters "insulin resistance", "fasting insulin level" and "stimulated insulin secretion". Glucose 136-143 insulin Homo sapiens 167-174 28778962-5 2017 However, antioxidant supplementation combined with endurance training increases glucose transport in insulin-resistant skeletal muscle in an additive fashion only when antioxidants that are able to increase the expression of antioxidant enzymes and/or the activity of components of the insulin signaling pathway are used. Glucose 80-87 insulin Homo sapiens 101-108 27358332-2 2017 This can be an adaptation to relative abundancy of fatty acid over glucose caused by insulin resistance. Glucose 67-74 insulin Homo sapiens 85-92 27915035-1 2017 Pancreatic beta cells are functionally programmed to release insulin in response to changes in plasma glucose concentration. Glucose 102-109 insulin Homo sapiens 61-68 27915035-2 2017 Insulin secretion is precisely regulated so that, under normal physiological conditions, fasting plasma glucose concentrations are kept within a narrow range of 3 5-5 5 mmol/L. Glucose 104-111 insulin Homo sapiens 0-7 27915035-3 2017 In hyperinsulinaemic hypoglycaemia, insulin secretion becomes dysregulated (ie, uncoupled from glucose metabolism) so that insulin secretion persists in the presence of low plasma glucose concentrations. Glucose 95-102 insulin Homo sapiens 8-15 28711468-0 2017 Effect of initiating use of an insulin pump in adults with type 1 diabetes using multiple daily insulin injections and continuous glucose monitoring (DIAMOND): a multicentre, randomised controlled trial. Glucose 130-137 insulin Homo sapiens 31-38 28711468-1 2017 BACKGROUND: The benefit of initiation of insulin pump therapy (continuous subcutaneous insulin infusion; CSII) in patients with type 1 diabetes using continuous glucose monitoring (CGM) has not been studied. Glucose 161-168 insulin Homo sapiens 41-48 28398950-3 2017 In animals and in the presence of glucose, D-beta-hydroxybutyrate promotes insulin secretion and increases glycogen synthesis. Glucose 34-41 insulin Homo sapiens 75-82 28398950-8 2017 During the 2-h glucose clamps, insulin levels were twofold higher (31 vs 16 mU L, P < 0.01) and glucose uptake 32% faster (1.66 vs 1.26 g kg, P < 0.001). Glucose 15-22 insulin Homo sapiens 31-38 28398950-10 2017 CONCLUSION: In the presence of constant high glucose concentrations, a ketone ester drink increased endogenous insulin levels, glucose uptake, and muscle glycogen synthesis. Glucose 45-52 insulin Homo sapiens 111-118 28885369-3 2017 A total of 366 cases of hospitalized patients with T2D using insulin therapy, whom received continuous glucose monitoring from January 2014 to December 2016, were enrolled for this study. Glucose 103-110 insulin Homo sapiens 61-68 28885369-7 2017 Otherwise, serum levels of C-peptide, premixed insulin injection, history of cardiovascular disease, and serum concentration of uric acid were inversely associated with GV parameters.Dysfunction of pancreatic beta-cell and better insulin sensitivity were independent contributors to the fluctuation of blood glucose. Glucose 308-315 insulin Homo sapiens 230-237 28885369-8 2017 Moreover, premixed insulin therapy may obtain better glucose control and lower within-day and day-to-day glucose variability for Chinese T2D patients with insulin therapy. Glucose 53-60 insulin Homo sapiens 19-26 28885369-8 2017 Moreover, premixed insulin therapy may obtain better glucose control and lower within-day and day-to-day glucose variability for Chinese T2D patients with insulin therapy. Glucose 105-112 insulin Homo sapiens 19-26 28885369-8 2017 Moreover, premixed insulin therapy may obtain better glucose control and lower within-day and day-to-day glucose variability for Chinese T2D patients with insulin therapy. Glucose 105-112 insulin Homo sapiens 155-162 28244187-5 2017 This literature review will focus on randomized controlled trials comparing intensive insulin therapy to conventional insulin therapy, with an objective to identify optimal blood glucose level targets for critically ill adult patients. Glucose 179-186 insulin Homo sapiens 86-93 28244187-10 2017 The need for uniformed glucometrics for unbiased reporting and further research for optimal blood glucose target is required, especially in light of new technological advancements in closed-loop insulin delivery and monitoring devices. Glucose 98-105 insulin Homo sapiens 195-202 27925205-7 2017 Our differentiated cells in two groups secreted insulin and C-peptide in a glucose stimulation test by ELISA showing in vitro functional. Glucose 75-82 insulin Homo sapiens 48-55 27925205-7 2017 Our differentiated cells in two groups secreted insulin and C-peptide in a glucose stimulation test by ELISA showing in vitro functional. Glucose 75-82 insulin Homo sapiens 60-69 28731188-1 2017 Skeletal muscle serves an important role in the utilization of glucose during insulin-stimulated conditions. Glucose 63-70 insulin Homo sapiens 78-85 29038359-7 2017 In human islets, hyperoxia significantly reduced glucose-stimulated insulin secretion by 42.2 +- 5.3% and viability assessed by MTT by 22.5 +- 5.4%. Glucose 49-56 insulin Homo sapiens 68-75 28689096-1 2017 The free fatty acid receptor 1 (FFA1) has emerged as an attractive anti-diabetic target that mediates glucose-stimulated insulin secretion. Glucose 102-109 insulin Homo sapiens 121-128 28962589-3 2017 METHODS: Human MSC and human islets (or pseudoislets, obtained after digestion and reaggregation of islet cells) were cocultured with or without cellular contact and glucose-stimulated insulin secretion assays were performed to assess cell function. Glucose 166-173 insulin Homo sapiens 185-192 28739256-1 2017 High blood glucose triggers the release of insulin from pancreatic beta cells, but if chronic, causes cellular stress, partly due to impaired Ca2+ homeostasis. Glucose 11-18 insulin Homo sapiens 43-50 28979168-4 2017 The development of algorithms that allow the suspension of the infusion of insulin during hypoglycemia gave rise to the integrated therapy or sensor-augmented insulin pump therapy with low glucose suspend, which has proven to be an effective and safe alternative in the treatment of diabetic patients with high risk of hypoglycemia. Glucose 189-196 insulin Homo sapiens 75-82 28979168-4 2017 The development of algorithms that allow the suspension of the infusion of insulin during hypoglycemia gave rise to the integrated therapy or sensor-augmented insulin pump therapy with low glucose suspend, which has proven to be an effective and safe alternative in the treatment of diabetic patients with high risk of hypoglycemia. Glucose 189-196 insulin Homo sapiens 159-166 31289747-9 2017 Further evaluation of islet functionality was assessed by a glucose-stimulated insulin secretion test. Glucose 60-67 insulin Homo sapiens 79-86 31289747-10 2017 The PA-encapsulated islets showed greater insulin secretion response to glucose stimulation than the bare islets with the differentiated U937 cells after 3 and 7 days. Glucose 72-79 insulin Homo sapiens 42-49 28726640-11 2017 CTRP6-overexpressing mice or CTRP6-treated adipocytes had reduced insulin-stimulated Akt phosphorylation and glucose uptake. Glucose 109-116 insulin Homo sapiens 66-73 28878826-9 2017 CONCLUSION: Impairment of insulin secretion is the most important factor to predict glucose intolerance in NAFLD; severity of histological findings is associated with insulin sensitivity independent of adiposity in NAFLD. Glucose 84-91 insulin Homo sapiens 26-33 28666974-1 2017 Diabetes mellitus is a metabolic disorder in which a person has high blood glucose levels due to inadequate insulin production by the pancreas. Glucose 75-82 insulin Homo sapiens 108-115 29424410-5 2017 The index case is a patient who presented severe neonatal hyperglycemia (831 mg/dl, without ketosis) requiring continuous infusion of insulin, which was suspended after 48 hours with normalization of blood glucose. Glucose 206-213 insulin Homo sapiens 134-141 28674284-7 2017 Glucose utilisation test revealed that the glucose utilisation rate of mature adipocytes was improved by CTRP1 in the presence of insulin. Glucose 0-7 insulin Homo sapiens 130-137 28674284-7 2017 Glucose utilisation test revealed that the glucose utilisation rate of mature adipocytes was improved by CTRP1 in the presence of insulin. Glucose 43-50 insulin Homo sapiens 130-137 28854965-7 2017 Treatment response was defined by the percentage of recipients reaching normoglycemia, and by the area under the curve for glucose and c-peptide in a glucose tolerance test. Glucose 150-157 insulin Homo sapiens 135-144 28846649-1 2017 Type 2 diabetes is characterized by insulin resistance, which leads to increased blood glucose levels. Glucose 87-94 insulin Homo sapiens 36-43 28360105-4 2017 Here, we used induced pluripotent stem (iPS) cells derived from patients with T1D to generate glucose-responsive, insulin-producing cells (IPCs) via 3D culture. Glucose 94-101 insulin Homo sapiens 114-121 28360105-6 2017 The cells responded to high-glucose stimulation by secreting insulin in vitro The shape, size, and number of their granules, as observed by transmission electron microscopy, were identical to those found in cadaveric beta cells. Glucose 28-35 insulin Homo sapiens 61-68 28763212-2 2017 Cafestol, a bioactive substance in coffee, increases glucose-stimulated insulin secretion in vitro and increases glucose uptake in human skeletal muscle cells. Glucose 53-60 insulin Homo sapiens 72-79 28830471-1 2017 BACKGROUND: The triglyceride glucose (TyG) index has been considered a simple surrogate marker of insulin resistance. Glucose 29-36 insulin Homo sapiens 98-105 31662726-1 2019 Insulin resistance is a condition characterized by decreased sensitivity of a skeletal or adipose cell to insulin, resulting in decreased glucose uptake by the cell. Glucose 138-145 insulin Homo sapiens 0-7 31662726-1 2019 Insulin resistance is a condition characterized by decreased sensitivity of a skeletal or adipose cell to insulin, resulting in decreased glucose uptake by the cell. Glucose 138-145 insulin Homo sapiens 106-113 31662726-3 2019 Insulin resistance is one of the primary factors contributing to metabolic syndrome (MetS), causing elevated glucose and fatty acid concentrations in the blood. Glucose 109-116 insulin Homo sapiens 0-7 28824164-5 2017 The insulin expressing cells obtained after H1152 treatment show increased expression of mature beta cell markers and improved glucose stimulated insulin secretion. Glucose 127-134 insulin Homo sapiens 4-11 28814745-5 2017 Interestingly, insulin-stimulated Akt/eNOS signaling was increased only by normalizing the glucose concentration in human umbilical vein endothelial cells (HUVECs) with GRK2 overexpression, suggesting of an important role of hepatic GRK2. Glucose 91-98 insulin Homo sapiens 15-22 28493326-8 2017 Hyperglycaemia induced HA synthesis while insulin diminished HA production by directing glucose metabolites to glycolysis. Glucose 88-95 insulin Homo sapiens 42-49 28493326-11 2017 Thus, the cellular shift in glucose usage from catabolism of glucose to anabolism of HA driven by hyperglycaemia and insulin resistance may represent an important link between diabetes and cancer progression. Glucose 28-35 insulin Homo sapiens 117-124 28801559-5 2017 Our data showed that linagliptin significantly improved glucose-stimulated insulin secretion for both non-diabetic and diabetic human islets, but its effectiveness on T2D islets was lower than on normal islets. Glucose 56-63 insulin Homo sapiens 75-82 28714308-0 2017 Supersensitive Oxidation-Responsive Biodegradable PEG Hydrogels for Glucose-Triggered Insulin Delivery. Glucose 68-75 insulin Homo sapiens 86-93 28793331-7 2017 This is explained in part by an increase in 83% in insulin levels than induced with glucose alone, which is mainly mediated by a low insulin degradation ratio (determined by c-peptide ratio), incretins and likely also by the modulation of the antioxidant environment. Glucose 84-91 insulin Homo sapiens 51-58 28793331-7 2017 This is explained in part by an increase in 83% in insulin levels than induced with glucose alone, which is mainly mediated by a low insulin degradation ratio (determined by c-peptide ratio), incretins and likely also by the modulation of the antioxidant environment. Glucose 84-91 insulin Homo sapiens 174-183 28559285-9 2017 Thus, the expression of HCV proteins in the liver is sufficient to induce insulin resistance by impairing insulin signaling and glucose uptake. Glucose 128-135 insulin Homo sapiens 74-81 28791547-1 2017 Predicting glucose values on the basis of insulin and food intakes is a difficult task that people with diabetes need to do daily. Glucose 11-18 insulin Homo sapiens 42-49 28791547-4 2017 In this work, several machine learning techniques are used for the modeling and prediction of glucose concentrations using as inputs the values measured by a continuous monitoring glucose system as well as also previous and estimated future carbohydrate intakes and insulin injections. Glucose 94-101 insulin Homo sapiens 266-273 28791547-6 2017 We propose two new enhanced modeling algorithms for glucose prediction, namely (i) a variant of grammatical evolution which uses an optimized grammar, and (ii) a variant of tree-based genetic programming which uses a three-compartment model for carbohydrate and insulin dynamics. Glucose 52-59 insulin Homo sapiens 262-269 29375810-0 2017 Optimal cutoff for the evaluation of insulin resistance through triglyceride-glucose index: A cross-sectional study in a Venezuelan population. Glucose 77-84 insulin Homo sapiens 37-44 28767692-6 2017 Our data indicate that in insulin secreting beta cells in which either ENPP1 was up-regulated or insulin receptor was down-regulated, GLP-1 positive effects on several pancreatic beta cell activities, including glucose-induced insulin secretion, cell proliferation and cell survival, were strongly reduced. Glucose 211-218 insulin Homo sapiens 26-33 28592611-0 2017 Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis. Glucose 24-31 insulin Homo sapiens 96-103 28646031-2 2017 Studies of muscle cells have suggested that leucine alters the insulin response for glucose transport by activating an insulin-negative feedback loop driven by the mammalian target of rapamycin/p70 ribosomal S6 kinase (mTOR/p70S6K) pathway. Glucose 84-91 insulin Homo sapiens 63-70 28592611-6 2017 Peak postprandial blood triglyceride concentrations did not significantly increase.Conclusions: Strong evidence exists that substituting fructose for glucose or sucrose in food or beverages lowers peak postprandial blood glucose and insulin concentrations. Glucose 150-157 insulin Homo sapiens 233-240 28646031-2 2017 Studies of muscle cells have suggested that leucine alters the insulin response for glucose transport by activating an insulin-negative feedback loop driven by the mammalian target of rapamycin/p70 ribosomal S6 kinase (mTOR/p70S6K) pathway. Glucose 84-91 insulin Homo sapiens 119-126 28646031-4 2017 Leucine was indeed able to curb glucose uptake after insulin stimulation in both cultured cardiomyocytes and perfused hearts. Glucose 32-39 insulin Homo sapiens 53-60 28646031-7 2017 Incubation of cardiomyocytes with [13C]leucine ascertained its metabolism to ketone bodies (KBs), which had a similar negative impact on insulin-stimulated glucose transport. Glucose 156-163 insulin Homo sapiens 137-144 28646031-12 2017 They offer new insights into the establishment of insulin resistance in the heart.NEW & NOTEWORTHY Catabolism of the branched-chain amino acid leucine into ketone bodies efficiently inhibits cardiac glucose uptake through decreased translocation of glucose transporter 4 to the plasma membrane. Glucose 203-210 insulin Homo sapiens 50-57 28608050-5 2017 Insulin resistance was assessed by 3-h oral glucose tolerance test (OGTT). Glucose 44-51 insulin Homo sapiens 0-7 28453944-4 2017 Homeostasis model assessment of insulin resistance index (HOMA-IR) was assessed on the basis of fasting glucose and insulin. Glucose 104-111 insulin Homo sapiens 32-39 28490609-5 2017 The fasting glucose-raising allele near PDX1, a known key insulin transcription factor, was strongly associated with lower first-phase insulin secretion but has no evidence for an effect on type 2 diabetes risk. Glucose 12-19 insulin Homo sapiens 58-65 28700249-2 2017 METHODS: Seven stepwise, glucose-driven insulin dose-titration algorithms were evaluated with a model-based simulation approach by using insulin lispro. Glucose 25-32 insulin Homo sapiens 40-47 28700249-5 2017 RESULTS: Of the seven dosing algorithms assessed, daily adjustment of insulin lispro dose, when glucose targets were met at pre-breakfast, pre-lunch, and pre-dinner, sequentially, demonstrated greater HbA1c reduction at 24 weeks, compared with the other dosing algorithms. Glucose 96-103 insulin Homo sapiens 70-77 28721686-3 2017 Exogenous basal insulin is titrated to address control of fasting plasma glucose and may preserve residual beta-cell function, thus promoting a greater endogenous prandial insulin response. Glucose 73-80 insulin Homo sapiens 16-23 28404742-1 2017 A single bout of low-frequency electroacupuncture (EA) causing muscle contractions increases whole-body glucose uptake in insulin-resistant rats. Glucose 104-111 insulin Homo sapiens 122-129 28669481-8 2017 This effect can be inhibited by opioid antagonists, resulting in a decrease of circulating insulin levels in response to glucose challenge. Glucose 121-128 insulin Homo sapiens 91-98 28666704-3 2017 We performed microdialysis evaluation of adipose tissue and skeletal muscle before and during an insulin-modified frequently sampled intravenous glucose tolerance test (IM-FSIGT). Glucose 145-152 insulin Homo sapiens 97-104 28969110-8 2017 Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) was evaluated from fasting plasma glucose and serum insulin levels. Glucose 95-102 insulin Homo sapiens 32-39 28266884-6 2017 When insulin-loaded micropatches were administered with a permeation enhancer and protease inhibitor, a peak efficacy of 34% drop in blood glucose levels was observed within 3 h. Efficacy further improved to 41% when micropatches were administered in multiple doses. Glucose 139-146 insulin Homo sapiens 5-12 28490443-9 2017 On the other hand, the glucose uptake capacity in response to exogenous insulin was impaired when ILK was blocked in vivo and in vitro, although IR/IRS/AKT phosphorylation states were increased but not different between groups. Glucose 23-30 insulin Homo sapiens 72-79 28490443-10 2017 We conclude that ILK depletion modifies the transcription of GLUT4, which results in reduced peripheral insulin sensitivity and glucose uptake, suggesting ILK as a molecular target and a prognostic biomarker of insulin resistance. Glucose 128-135 insulin Homo sapiens 211-218 28737991-0 2017 Lowering Cost Share May Improve Rates of Home Glucose Monitoring Among Patients with Diabetes Using Insulin. Glucose 46-53 insulin Homo sapiens 100-107 27112737-6 2017 Although numerous opportunities for medication errors exist with the use of U-500 insulin, this case outlines the safe use of concentrated intravenous insulin when clinically indicated for patients requiring extremely high doses of insulin to control blood glucose. Glucose 257-264 insulin Homo sapiens 151-158 27112737-6 2017 Although numerous opportunities for medication errors exist with the use of U-500 insulin, this case outlines the safe use of concentrated intravenous insulin when clinically indicated for patients requiring extremely high doses of insulin to control blood glucose. Glucose 257-264 insulin Homo sapiens 151-158 28625360-4 2017 Glucose stimulated insulin secretion was assayed by Insulin ELISA Kit. Glucose 0-7 insulin Homo sapiens 19-26 28625360-4 2017 Glucose stimulated insulin secretion was assayed by Insulin ELISA Kit. Glucose 0-7 insulin Homo sapiens 52-59 28532044-9 2017 A maximum insulin secretion by glucose stimulation was obtained with a higher concentration (2muM) of RA. Glucose 31-38 insulin Homo sapiens 10-17 28316059-4 2017 Therefore, insulin analogues that are used to normalize blood glucose are tested for their ability to preferentially activate Akt/PKB but not ERK1/2 and mitogenesis. Glucose 62-69 insulin Homo sapiens 11-18 28969360-5 2017 For example, they affect hepatic glucose production via adenosine monophosphate-activated protein kinase and/or insulin-signaling pathways. Glucose 33-40 insulin Homo sapiens 112-119 27380934-9 2017 Those who performed >= 5 glucose checks/day adjusted basal insulin during exercise more frequently than those with fewer daily glucose checks (33% vs. 13%, p = 0.05, chi-squared = 3.7), and were more likely to report decreasing insulin dose for the bedtime snack following exercise (50% vs. 17%, p = 0.004, chi-squared = 8.2). Glucose 28-35 insulin Homo sapiens 62-69 28980863-8 2017 In human islets both a high glucose concentration and palmitate promoted increased IAPP mRNA levels, resulting in an augmented IAPP/insulin mRNA ratio. Glucose 28-35 insulin Homo sapiens 132-139 28672086-2 2017 Recent studies have provided evidence of the modulation of insulin action by branched-chain amino acids (BCAAs) and suggested novel mechanistic relationships between glucose and amino acid metabolic pathways. Glucose 166-173 insulin Homo sapiens 59-66 28285191-5 2017 Moreover, PCB-153 concentration-dependently inhibited insulin-dependent glucose uptake and lipid accumulation in cultured hepatocytes and adipocytes. Glucose 72-79 insulin Homo sapiens 54-61 28751630-8 2017 Then the glucose uptake ratio after cells were stimulated by insulin was measured. Glucose 9-16 insulin Homo sapiens 61-68 28756769-2 2017 Compared to intermittent monitoring systems, continuous glucose monitoring (CGM) can offer benefit in the prevention of severe hyperglycemia and hypoglycemia by enabling insulin infusions to be adjusted more rapidly and potentially more accurately because trends in glucose concentrations can be more readily identified. Glucose 56-63 insulin Homo sapiens 170-177 30603331-11 2017 DPP-4 inhibitors or micronutrients may contribute to the immune regulation of glucose and lipid metabolism by regulating macrophage polarization, thereby reducing insulin resistance and preventing the progression of NAFLD. Glucose 78-85 insulin Homo sapiens 163-170 28798723-1 2017 A significant drawback of the exogenous administration of insulin to diabetics is the non-physiological profile of insulin action resulting in the insufficient suppression of hepatic glucose production, which is the main contributing factor to diabetic hyperglycemia under fasting conditions and the basis of the challenge to restore a more physiological glucose profile in diabetes. Glucose 183-190 insulin Homo sapiens 58-65 28742858-9 2017 Treatment of Min6-B1 cells with palmitate altered glucose-stimulated insulin secretion, increased ER stress and significantly reduced ER-mitochondrial interactions. Glucose 50-57 insulin Homo sapiens 69-76 28710148-7 2017 Another important factor for reducing morbidity is the maintenance of blood glucose concentrations at 120-150 mg/dL, which is accomplished with the use of insulin and lower doses of glucose of 1-2 g kg-1 d-1, because this prevents the risk of hypoglycemia and is associated with a better prognosis according to recent studies. Glucose 76-83 insulin Homo sapiens 155-162 28710353-3 2017 Mediation analyses consistently indicated that these associations were mediated mainly by insulin resistance (IR) as measured by the homeostasis model (HOMA-IR), followed by triglyceride (TG) and total cholesterol (TC), and fasting glucose (FG) in the three studies. Glucose 232-239 insulin Homo sapiens 90-97 27476611-1 2017 Cell-based therapies for the treatment of diabetes, generally aim to provide long-term glucose regulated-insulin delivery using insulin producing cells. Glucose 87-94 insulin Homo sapiens 105-112 27476611-1 2017 Cell-based therapies for the treatment of diabetes, generally aim to provide long-term glucose regulated-insulin delivery using insulin producing cells. Glucose 87-94 insulin Homo sapiens 128-135 27476611-4 2017 These unique capsules were used to entrap human liver cells and mesenchymal stem cells that were induced to differentiate into glucose-regulated insulin-producing cells. Glucose 127-134 insulin Homo sapiens 145-152 28683803-6 2017 RESULTS: Compared with the native Japanese, the Japanese-Americans had significantly lower Matsuda index and higher area under the curve values for serum insulin concentration during OGTT in the normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) groups, but not in the diabetes mellitus (DM) group. Glucose 202-209 insulin Homo sapiens 154-161 28680093-3 2017 We have demonstrated that palmitate enhances glucose-stimulated insulin secretion from isolated human islets via free fatty acid receptor 1 (FFAR1/GPR40). Glucose 45-52 insulin Homo sapiens 64-71 28366423-1 2017 BACKGROUND: Glucagon-like peptide 1 (GLP-1) is an incretin hormone, which stimulates glucose-dependent insulin secretion from the pancreas and holds immune-regulatory properties. Glucose 85-92 insulin Homo sapiens 103-110 28688482-1 2017 BACKGROUND AND OBJECTIVE: Current prototypes of closed-loop systems for glucose control in type 1 diabetes mellitus, also referred to as artificial pancreas systems, require a pre-meal insulin bolus to compensate for delays in subcutaneous insulin absorption in order to avoid initial post-prandial hyperglycemia. Glucose 72-79 insulin Homo sapiens 185-192 28174292-0 2017 Hypothalamic and Striatal Insulin Action Suppresses Endogenous Glucose Production and May Stimulate Glucose Uptake During Hyperinsulinemia in Lean but Not in Overweight Men. Glucose 63-70 insulin Homo sapiens 26-33 28174292-0 2017 Hypothalamic and Striatal Insulin Action Suppresses Endogenous Glucose Production and May Stimulate Glucose Uptake During Hyperinsulinemia in Lean but Not in Overweight Men. Glucose 100-107 insulin Homo sapiens 26-33 28174292-7 2017 Glucose infusion rates (GIRs) had to be increased more after nasal insulin than after placebo to maintain euglycemia in lean but not in overweight people. Glucose 0-7 insulin Homo sapiens 67-74 28174292-9 2017 Suppression of endogenous glucose production by circulating insulin was more pronounced after administration of nasal insulin than after placebo. Glucose 26-33 insulin Homo sapiens 60-67 28174292-9 2017 Suppression of endogenous glucose production by circulating insulin was more pronounced after administration of nasal insulin than after placebo. Glucose 26-33 insulin Homo sapiens 118-125 28174292-10 2017 Furthermore, glucose uptake into tissue tended to be higher after nasal insulin application. Glucose 13-20 insulin Homo sapiens 72-79 28174292-12 2017 By increasing insulin-mediated suppression of endogenous glucose production and stimulating peripheral glucose uptake, brain insulin may improve glucose metabolism during systemic hyperinsulinemia. Glucose 57-64 insulin Homo sapiens 14-21 28174292-12 2017 By increasing insulin-mediated suppression of endogenous glucose production and stimulating peripheral glucose uptake, brain insulin may improve glucose metabolism during systemic hyperinsulinemia. Glucose 103-110 insulin Homo sapiens 14-21 28174292-12 2017 By increasing insulin-mediated suppression of endogenous glucose production and stimulating peripheral glucose uptake, brain insulin may improve glucose metabolism during systemic hyperinsulinemia. Glucose 103-110 insulin Homo sapiens 14-21 28617838-6 2017 MAIN OUTCOME MEASURE: Relative insulin response following oral ingestion of glucose. Glucose 76-83 insulin Homo sapiens 31-38 28589878-0 2017 Distinct Akt phosphorylation states are required for insulin regulated Glut4 and Glut1-mediated glucose uptake. Glucose 96-103 insulin Homo sapiens 53-60 28589878-1 2017 Insulin, downstream of Akt activation, promotes glucose uptake into fat and muscle cells to lower postprandial blood glucose, an enforced change in cellular metabolism to maintain glucose homeostasis. Glucose 48-55 insulin Homo sapiens 0-7 28589878-1 2017 Insulin, downstream of Akt activation, promotes glucose uptake into fat and muscle cells to lower postprandial blood glucose, an enforced change in cellular metabolism to maintain glucose homeostasis. Glucose 117-124 insulin Homo sapiens 0-7 28589878-6 2017 We show that insulin-stimulated Glut4-mediated glucose uptake requires PDPK1 phosphorylation of the kinase domain but not mTORC2 phosphorylation of the HM domain. Glucose 47-54 insulin Homo sapiens 13-20 28585545-6 2017 SOX5 overexpression reverses the expression perturbations observed in a mouse model of T2D, increases the expression of key beta-cell genes and improves glucose-stimulated insulin secretion in human islets from donors with T2D. Glucose 153-160 insulin Homo sapiens 172-179 28591651-5 2017 This advancement mitigates chronic foreign-body response, utilizes a device- and growth factor-free approach, facilitates in vivo differentiation of PECs into glucose-responsive insulin-producing cells, and reliably restores glycemic control. Glucose 159-166 insulin Homo sapiens 178-185 28452488-3 2017 To investigate the effects of inflammation and hypoxia, the main obstacles hampering the survival and function of isolated, cultured, and transplanted islets, we conducted a comprehensive metabolomics evaluation of human islets in parallel with dynamic glucose-stimulated insulin release (GSIR) perifusion studies for functional evaluation. Glucose 253-260 insulin Homo sapiens 272-279 28337855-8 2017 For PCB-insulin, there is a 24% increase of in vivo pharmacological activity of lowering blood glucose compared with native insulin. Glucose 95-102 insulin Homo sapiens 8-15 28794822-11 2017 These agents exert their effects by improving glucose-dependent insulin release, suppressing glucagon release, suppressing hepatic glucose output, and decreasing the rate of gastric emptying, thereby reducing appetite. Glucose 46-53 insulin Homo sapiens 64-71 28364599-0 2017 Flavonoids from Enicostema littorale blume enhances glucose uptake of cells in insulin resistant human liver cancer (HepG2) cell line via IRS-1/PI3K/Akt pathway. Glucose 52-59 insulin Homo sapiens 79-86 28364599-2 2017 Insulin resistance is a main pathogenic event in Type 2 Diabetes Mellitus (T2DM) leading to a reduction in glucose uptake by peripheral tissue and increased hepatic glucose output. Glucose 107-114 insulin Homo sapiens 0-7 28364599-6 2017 Insulin resistant HepG2 (IR/HepG2) model was established by inducing insulin resistance in HepG2 cells to investigate the effect of these fractions on IR/HepG2 cell line for their glucose uptake. Glucose 180-187 insulin Homo sapiens 0-7 28454670-5 2017 In addition, prunin significantly enhanced glucose uptake in a dose-dependent manner in insulin-resistant HepG2 cells. Glucose 43-50 insulin Homo sapiens 88-95 28568813-1 2017 Technosphere insulin (TI), an inhaled insulin with a fast onset of action, provides a novel option for the control of prandial glucose. Glucose 127-134 insulin Homo sapiens 13-20 28568813-2 2017 A euglycemic glucose clamp study was performed to compare the effects of TI and regular human insulin (RHI) on the induced glucose infusion rate (GIR) in healthy volunteers. Glucose 123-130 insulin Homo sapiens 94-101 28619307-10 2017 Insulin resistance was determined from fasting insulin and glucose, and dual energy x-ray absorptiometry was used to assess body composition. Glucose 59-66 insulin Homo sapiens 0-7 28659725-1 2017 BACKGROUND: Type 2 diabetes (T2D) is a common multi-factorial disease that is primarily ac-counted to ineffective insulin action in lowering blood glucose level and later escalates to impaired insu-lin secretion by pancreatic beta cells. Glucose 147-154 insulin Homo sapiens 114-121 25752319-9 2017 Insulin secretion in response to glucose challenge was predicted by BMI, body fat mass and antipsychotic medication. Glucose 33-40 insulin Homo sapiens 0-7 28098426-7 2017 CONCLUSIONS: Over 14 days, decreasing the insulin dose diminished the glucose-lowering effect of dapagliflozin-insulin combination therapy and increased levels of beta-hydroxybutyrate. Glucose 70-77 insulin Homo sapiens 42-49 28098426-7 2017 CONCLUSIONS: Over 14 days, decreasing the insulin dose diminished the glucose-lowering effect of dapagliflozin-insulin combination therapy and increased levels of beta-hydroxybutyrate. Glucose 70-77 insulin Homo sapiens 111-118 28127851-0 2017 Impact of insulin sensitivity, beta-cell function and glycaemic control on initiation of second-line glucose-lowering treatment in newly diagnosed type 2 diabetes. Glucose 101-108 insulin Homo sapiens 10-17 28292969-3 2017 Importantly, infusion of the nitric oxide synthase inhibitor l-NG-monomethyl-l-arginine acetate (l-NMMA) into both femoral arteries reversed the insulin-stimulated increase in microvascular perfusion in both legs and abrogated the greater glucose uptake in the exercised compared with the rested leg. Glucose 239-246 insulin Homo sapiens 145-152 28385685-0 2017 Improvement of Glucose Control and Reduction of Hypoglycemia Following Intravenous Immune Globulins in a Child With Type 1 Diabetes and High Levels of Insulin Antibodies. Glucose 15-22 insulin Homo sapiens 151-158 28401454-1 2017 INTRODUCTION: Published evaluations of sensor glucose monitoring use in insulin treated type 2 diabetes are limited. Glucose 46-53 insulin Homo sapiens 72-79 28401454-13 2017 CONCLUSION: The use of flash glucose-sensing technology for glycemic management in individuals with type 2 diabetes treated by intensive insulin therapy over 12 months was associated with a sustained reduction in hypoglycemia and safely and effectively replaced SMBG. Glucose 29-36 insulin Homo sapiens 137-144 28401444-1 2017 PURPOSE: Basal insulin controls primarily fasting plasma glucose but causes hypoglycaemia and weight gain, whilst glucagon like peptide 1 receptor agonists induce weight loss without increasing risk for hypoglycaemia. Glucose 57-64 insulin Homo sapiens 15-22 28405880-2 2017 Genetic variants in STEAP4 have been associated with numerous metabolic disorders related to obesity, including putative defects in the acute insulin response to glucose in type 2 diabetes. Glucose 162-169 insulin Homo sapiens 142-149 31008309-8 2017 Within 6 months, adjusting for age and National Institute of Health Stroke Scale, every month 2-h glucose reduced by 4.5% (p < 0.001), Homeostasis Model Assessment of Insulin Sensitivity improved 3% (p = 0.04) and fat mass decreased 490 g (95% confidence interval 325, 655; p = 0.01). Glucose 98-105 insulin Homo sapiens 170-177 31008309-9 2017 For every extra kilogram of body fat, 2-h glucose increased by 1.02 mmol/L (95% confidence interval 1.01, 1.02; p = 0.001); Homeostasis Model Assessment of Insulin Sensitivity reduced by 0.98% (95% confidence interval 0.97, 0.99; p = 0.001). Glucose 42-49 insulin Homo sapiens 156-163 28238527-3 2017 To verify our hypothesis, human islets and human EndoC-betaH1 cells were exposed to IFNalpha and tested for ER stress markers, glucose stimulated insulin secretion (GSIS) and insulin content. Glucose 127-134 insulin Homo sapiens 146-153 28278045-0 2017 Multiboronic acid-conjugated chitosan scaffolds with glucose selectivity to insulin release. Glucose 53-60 insulin Homo sapiens 76-83 28278045-6 2017 Insulin release from FPBA nanoparticles (FPBAINP) and FTBA nanoparticles (FTBAINP) were both concentration-dependent within glyceamically relevant values (1-3 mg/ml glucose and 0.002 mg/ml fructose). Glucose 165-172 insulin Homo sapiens 0-7 28278045-8 2017 Both FPBAINP and FTBAINP have the potential for development as a glucose-selective insulin delivery system in physiological settings. Glucose 65-72 insulin Homo sapiens 83-90 28323969-7 2017 Conclusions: These results suggest that links between PAPP-A concentrations in early pregnancy and subsequent glucose concentrations and blood pressures may be mediated by changes in insulin sensitivity (and secretion). Glucose 110-117 insulin Homo sapiens 183-190 28400405-5 2017 In addition, inflammatory mediators, e.g., proinflammatory cytokines, and excessive nutrients, e.g., glucose and fatty acids, act together to aggravate local insulin resistance and form a vicious cycle to further disturb the local metabolic pathways and exacerbate systemic metabolic dysregulation. Glucose 101-108 insulin Homo sapiens 158-165 28700767-0 2017 Effect of non-insulin-based glucose-lowering therapies on cardiovascular outcomes in patients with type 2 diabetes. Glucose 28-35 insulin Homo sapiens 14-21 28700767-4 2017 In this review, we aim to present the basic mechanisms for each class of commonly used non-insulin-based glucose-lowering drugs and to discuss the effect of these medications on CV events. Glucose 105-112 insulin Homo sapiens 91-98 28509691-1 2017 PURPOSE OF REVIEW: The complexity of modern insulin-based therapy for type I and type II diabetes mellitus and the risks associated with excursions in blood-glucose concentration (hyperglycemia and hypoglycemia) have motivated the development of "smart insulin" technologies (glucose-responsive insulin, GRI). Glucose 157-164 insulin Homo sapiens 253-260 28598888-2 2017 RECENT FINDINGS: Effective blood glucose control by insulin delays progression of microvascular complications and probably improves survival in type 1 diabetes. Glucose 33-40 insulin Homo sapiens 52-59 28754022-4 2017 Over the last decade, a body of work has focussed on establishing the mechanisms by which polyphenolic compounds exert beneficial effects to limit carbohydrate digestion, enhance insulin-mediated glucose uptake, down-regulate hepatic gluconeogenesis and decrease oxidative stress; the latter anti-oxidative property being the most documented. Glucose 196-203 insulin Homo sapiens 179-186 28753929-5 2017 RESULTS: The meta-analysis of the 14 studies testing the acute effects of WG foods showed significant reductions of the post-prandial values of the glucose iAUC (0-120 min) by -29.71 mmol min/L (95% CI: -43.57, -15.85 mmol min/L), the insulin iAUC (0-120 min) by -2.01 nmol min/L (95% CI: -2.88, -1.14 nmol min/L), and the maximal glucose and insulin response. Glucose 148-155 insulin Homo sapiens 235-242 28753929-5 2017 RESULTS: The meta-analysis of the 14 studies testing the acute effects of WG foods showed significant reductions of the post-prandial values of the glucose iAUC (0-120 min) by -29.71 mmol min/L (95% CI: -43.57, -15.85 mmol min/L), the insulin iAUC (0-120 min) by -2.01 nmol min/L (95% CI: -2.88, -1.14 nmol min/L), and the maximal glucose and insulin response. Glucose 148-155 insulin Homo sapiens 343-350 28464351-2 2017 The mammalian target of rapamycin complex 2 (mTORC2) is an important regulator of muscle glucose uptake in response to insulin stimulation. Glucose 89-96 insulin Homo sapiens 119-126 28464351-6 2017 ABSTRACT: Exercise increases glucose uptake into insulin-resistant muscle. Glucose 29-36 insulin Homo sapiens 49-56 28464351-8 2017 The mammalian target of rapamycin complex 2 (mTORC2), a regulator of insulin-controlled glucose uptake, has been reported to interact with ras-related C3 botulinum toxin substrate 1 (Rac1), which plays a role in exercise-induced glucose uptake in muscle. Glucose 88-95 insulin Homo sapiens 69-76 28464351-8 2017 The mammalian target of rapamycin complex 2 (mTORC2), a regulator of insulin-controlled glucose uptake, has been reported to interact with ras-related C3 botulinum toxin substrate 1 (Rac1), which plays a role in exercise-induced glucose uptake in muscle. Glucose 229-236 insulin Homo sapiens 69-76 28700945-6 2017 Remarkably, decreased insulin led to lower fasting glucose and improved insulin sensitivity in aged mice. Glucose 51-58 insulin Homo sapiens 22-29 28683241-8 2017 With further impairment in glucose metabolism, the glucose and lipid level gradually increased (P<0.05), while the impaired glucose regulation (IGR) group showed greater insulin response than a type 2 diabetes mellitus (T2DM) group. Glucose 27-34 insulin Homo sapiens 173-180 28729841-0 2017 Prevalence of Non-responders for Glucose Control Markers after 10 Weeks of High-Intensity Interval Training in Adult Women with Higher and Lower Insulin Resistance. Glucose 33-40 insulin Homo sapiens 145-152 28678303-1 2017 BACKGROUND: Type 1 diabetes requires frequent testing and monitoring of blood glucose levels in order to determine appropriate type and dosage of insulin administration. Glucose 78-85 insulin Homo sapiens 146-153 28680477-2 2017 However, the consistent generation of glucose-responsive insulin-releasing cells remains challenging. Glucose 38-45 insulin Homo sapiens 57-64 28438760-3 2017 We therefore characterized the dose-response curve for whole body glucose uptake using recombinant human insulin in the adult guinea pig. Glucose 66-73 insulin Homo sapiens 105-112 28438760-6 2017 Although human insulin infusion increased rates of glucose utilization (up to 68%) and storage and, at high concentrations, increased rates of glycolysis in females, glucose production was only partially suppressed (~23%), even at high insulin doses. Glucose 51-58 insulin Homo sapiens 15-22 28685604-4 2017 Recent studies show that potential mediators of insulin resistance such as adipokines - adiponectin, leptin and resistin are important for glucose and lipid metabolism. Glucose 139-146 insulin Homo sapiens 48-55 28403644-2 2017 Their plasma levels are adversely affected in patients with dysglycaemia, and glucose normalization with insulin glargine might improve the levels of these factors. Glucose 78-85 insulin Homo sapiens 105-112 28473464-1 2017 Systemic hyperaminoacidemia, induced by either intravenous amino acid infusion or protein ingestion, reduces insulin-stimulated glucose disposal. Glucose 128-135 insulin Homo sapiens 109-116 28473464-5 2017 Ingestion of protein, but not leucine, decreased insulin-stimulated glucose disposal (P < 0.05) and prevented both the HECP-mediated decrease in 3-HIB and increase in FGF21 concentration in plasma. Glucose 68-75 insulin Homo sapiens 49-56 28637827-7 2017 This Perspective focuses on the physiological possibilities and limitations of an encapsulation strategy to establish near-normoglycemia in subjects with T1D, assuming that glucose-responsive insulin-producing cells are available for transplantation. Glucose 173-180 insulin Homo sapiens 192-199 28389705-9 2017 Circulating concentrations of glucose and 3-hydroxybutyrate increased during KET (mean +- SEM 17.7 +- 0.6 mmol/l and 1.6 +- 0.2 mmol/l, respectively), then decreased after insulin treatment (6.6 +- 0.7 mmol/l and 0.1 +- 0.07 mmol/l, respectively). Glucose 30-37 insulin Homo sapiens 172-179 28389705-14 2017 Insulin stimulation during early phases of DKA is associated with reduced glucose disposal in skeletal muscle, impaired glycogen synthase function and lower glucose oxidation. Glucose 74-81 insulin Homo sapiens 0-7 28389705-14 2017 Insulin stimulation during early phases of DKA is associated with reduced glucose disposal in skeletal muscle, impaired glycogen synthase function and lower glucose oxidation. Glucose 157-164 insulin Homo sapiens 0-7 28463010-0 2017 Behavioral Patterns and Associations with Glucose Control During 12-Week Randomized Free-Living Clinical Trial of Day and Night Hybrid Closed-Loop Insulin Delivery in Adults with Type 1 Diabetes. Glucose 42-49 insulin Homo sapiens 147-154 28584168-3 2017 Primary human myotubes were pretreated with palmitate, oleate or their combination for 12 h. Glucose uptake was determined by intracellular accumulation of [3H]-2-deoxy-d-glucose, insulin signalling and activation of endoplasmic reticulum (ER) stress by Western blotting, and mitochondrial reactive oxygen species (ROS) production by fluorescent dye MitoSOX. Glucose 93-100 insulin Homo sapiens 180-187 28584168-6 2017 However, an exposure to palmitate, oleate or their combination reduced insulin-stimulated glucose uptake. Glucose 90-97 insulin Homo sapiens 71-78 28294170-3 2017 Although the effects of insulin secretion on metabolic organs such as liver, skeletal muscle and adipose is directly relevant for improving glucose uptake and reduce hyperglycemia, the ability of pancreatic beta-cells to crosstalk with multiple non-metabolic tissues is providing novel insights into potential opportunities for improving beta-cell function and/or mass that could have beneficial effects in patients with diabetes. Glucose 140-147 insulin Homo sapiens 24-31 28437809-6 2017 Insulin-treated patients (with or without oral agents) had higher glucose levels (+1.7 mmol/l, 5-95% CI 0.5-3.0, and +1.2 mmol/l, -0.1 to -2.5) than patients using oral agents only. Glucose 66-73 insulin Homo sapiens 0-7 26930674-1 2017 OBJECTIVE: Faults in subcutaneous glucose concentration readings with a continuous glucose monitoring (CGM) may affect the computation of insulin infusion rates that can lead to hypoglycemia or hyperglycemia in artificial pancreas control systems for patients with type 1 diabetes (T1D). Glucose 34-41 insulin Homo sapiens 138-145 26930674-1 2017 OBJECTIVE: Faults in subcutaneous glucose concentration readings with a continuous glucose monitoring (CGM) may affect the computation of insulin infusion rates that can lead to hypoglycemia or hyperglycemia in artificial pancreas control systems for patients with type 1 diabetes (T1D). Glucose 83-90 insulin Homo sapiens 138-145 26930674-3 2017 A nonlinear first principle glucose/insulin/meal dynamic model is developed. Glucose 28-35 insulin Homo sapiens 36-43 27448377-5 2017 We consider here nine candidate models of glucagon action featuring a number of possible characteristics: insulin-independent glucagon action, insulin/glucagon ratio effect on hepatic glucose production, insulin-dependent suppression of glucagon action, and the effect of rate of change of glucagon. Glucose 184-191 insulin Homo sapiens 143-150 27448377-5 2017 We consider here nine candidate models of glucagon action featuring a number of possible characteristics: insulin-independent glucagon action, insulin/glucagon ratio effect on hepatic glucose production, insulin-dependent suppression of glucagon action, and the effect of rate of change of glucagon. Glucose 184-191 insulin Homo sapiens 143-150 28137482-5 2017 Insulin secretion was reduced by EGCG upon glucose stimulation and blocked in response to glutamine combined with the allosteric GDH activator BCH (2-aminobicyclo-[2,2,1] heptane-2-carboxylic acid). Glucose 43-50 insulin Homo sapiens 0-7 28255821-0 2017 One-hour post-load plasma glucose levels associated with decreased insulin sensitivity and secretion and early makers of cardiometabolic risk. Glucose 26-33 insulin Homo sapiens 67-74 28406034-1 2017 While only used initially in cases with resistance to subcutaneous insulin therapy, intraperitoneal insulin therapy provides an overall more stable glucose control than subcutaneous insulin therapy thanks to its pharmacokinetics as pointed by Garcia-Verdugo et al from the experience of implantable insulin pumps. Glucose 148-155 insulin Homo sapiens 100-107 28406034-1 2017 While only used initially in cases with resistance to subcutaneous insulin therapy, intraperitoneal insulin therapy provides an overall more stable glucose control than subcutaneous insulin therapy thanks to its pharmacokinetics as pointed by Garcia-Verdugo et al from the experience of implantable insulin pumps. Glucose 148-155 insulin Homo sapiens 100-107 28420260-0 2017 The Safety of Nonadjunctive Use of Continuous Glucose Monitors for Insulin Dosing: Still Not Resolved. Glucose 46-53 insulin Homo sapiens 67-74 28540756-0 2017 Nonadjunctive Use of Continuous Glucose Monitors for Insulin Dosing: Is It Safe? Glucose 32-39 insulin Homo sapiens 53-60 28654305-0 2017 Commentary Regarding Shapiro, "Nonadjunctive Use of Continuous Glucose Monitors for Insulin Dosing: Is It Safe?" Glucose 63-70 insulin Homo sapiens 84-91 28592518-5 2017 C-peptide and glucose values were used to calculate the computer model-derived homeostatic model assessment of insulin resistance (HOMA2-IR). Glucose 14-21 insulin Homo sapiens 111-118 28271502-8 2017 CONCLUSIONS: The beneficial effect of TRG on insulin sensitivity and glucose/ lipid homeostasis is mediated by the enhancement of the insulin signaling and antioxidant property. Glucose 69-76 insulin Homo sapiens 134-141 28600913-0 2017 Glucose Self-monitoring in Non-Insulin-Treated Patients With Type 2 Diabetes in Primary Care Settings: A Randomized Trial. Glucose 0-7 insulin Homo sapiens 31-38 28105546-1 2017 Objectives To study if there is any relationship about higher cutoff values for 100 g oral glucose tolerance test and the need for insulin in women diagnosed with gestational diabetes. Glucose 91-98 insulin Homo sapiens 131-138 28105546-7 2017 Fasting blood glucose levels were significantly higher in women with further need for insulin than those who only needed diet and exercise (p < 0.001). Glucose 14-21 insulin Homo sapiens 86-93 28105546-10 2017 Conclusions Fasting cutoff vales for 100 g oral glucose tolerance test are consistently higher in women diagnosed with Gestational Diabetes that further needed insulin to achieve adequate blood glucose control. Glucose 48-55 insulin Homo sapiens 160-167 28673573-8 2017 Our hypothesis is that this training protocol may minimize the exercise-associated rapid drop of glucose levels in T1DM, due to glucoregulatory hormones and transient reduction of insulin-mediated glucose uptake. Glucose 197-204 insulin Homo sapiens 180-187 28764828-2 2017 During pregnancy, women with GDM develop insulin resistance, which results in altered glucose tolerance. Glucose 86-93 insulin Homo sapiens 41-48 28704134-4 2017 We assessed insulin signaling and insulin-mediated glucose uptake in human endothelial cells with and without mutations in BMPR2. Glucose 51-58 insulin Homo sapiens 34-41 28704134-8 2017 BMPR2 mutation impaired insulin-mediated endothelial glucose uptake via reduced glucose transporter translocation despite intact insulin signaling. Glucose 53-60 insulin Homo sapiens 24-31 28362116-1 2017 Assessment of insulin sensitivity based on a single measurement of insulin and glucose, is both easy to understand and simple to perform. Glucose 79-86 insulin Homo sapiens 14-21 28362116-8 2017 We also computed point estimates (single value estimates) of the insulin sensitivity index based on the different number of insulin/glucose samples (1-45 consecutive samples). Glucose 132-139 insulin Homo sapiens 65-72 28416361-1 2017 During insulin-resistant states such as type 2 diabetes mellitus (T2DM), insulin fails to suppress hepatic glucose production but promotes lipid synthesis leading to hyperglycemia and hypertriglyceridemia. Glucose 107-114 insulin Homo sapiens 73-80 28900377-6 2017 The homeostasis model assessment estimate of insulin resistance (HOMA-IR) has been determined from serum insulin and glucose values. Glucose 117-124 insulin Homo sapiens 45-52 28652605-1 2017 The pancreatic beta-cells control glucose homeostasis by secreting insulin in response to nutrient intake. Glucose 34-41 insulin Homo sapiens 67-74 28671646-3 2017 In muscle cells, glucose transporter type 4 (GLUT4) proteins translocate to the plasma membrane in response to insulin, thus allowing massive entry of glucose into the cell. Glucose 17-24 insulin Homo sapiens 111-118 28671646-4 2017 The ability of muscle cells to respond to insulin by increasing the rate of glucose uptake is one of the standard readouts to quantify muscle cell sensitivity to insulin. Glucose 76-83 insulin Homo sapiens 42-49 28671646-4 2017 The ability of muscle cells to respond to insulin by increasing the rate of glucose uptake is one of the standard readouts to quantify muscle cell sensitivity to insulin. Glucose 76-83 insulin Homo sapiens 162-169 28671646-7 2017 Measurements of the glucose uptake rate in differentiated myotubes reflect insulin sensitivity. Glucose 20-27 insulin Homo sapiens 75-82 28672734-9 2017 Significant differences were observed in the 2-h oral glucose tolerance test (OGTT) (p = 0.003 for glucose and p = 0.046 for insulin). Glucose 54-61 insulin Homo sapiens 125-132 28636637-3 2017 Insulin secretion was assessed using indexes derived from oral glucose tolerance test (OGTT). Glucose 63-70 insulin Homo sapiens 0-7 28301717-0 2017 Glucose-Triggered Insulin Release from Fe3+ -Cross-linked Alginate Hydrogel: Experimental Study and Theoretical Modeling. Glucose 0-7 insulin Homo sapiens 18-25 28301717-1 2017 We study the mechanisms involved in the release, triggered by the application of glucose, of insulin entrapped in Fe3+ -cross-linked alginate hydrogel particles further stabilized with a polyelectrolyte. Glucose 81-88 insulin Homo sapiens 93-100 28479244-8 2017 In addition, islet-like cells displayed glucose-stimulated insulin secretion in vitro. Glucose 40-47 insulin Homo sapiens 59-66 28450454-6 2017 As a result, Glut4 cannot reach the insulin-responsive compartment, and insulin-stimulated glucose uptake in adipocytes is suppressed. Glucose 91-98 insulin Homo sapiens 72-79 28535046-4 2017 Piceatannol also partially improved the malfunction of insulin-stimulated glucose uptake, which was reduced by TNF-alpha in 3T3-L1 adipocytes. Glucose 74-81 insulin Homo sapiens 55-62 28535046-6 2017 In addition, the Akt-dependent forkhead box O1 (FoxO1) signaling pathway was involved in the restoration of insulin-stimulated glucose uptake through suppressing the down-regulation of phosphorylation of Akt and FoxO1 expressions. Glucose 127-134 insulin Homo sapiens 108-115 29931910-9 2017 Glucose consumption experiment indicated that medium and high concentration of LBP could increase the glucose consumption of insulin-resistant HepG2 cells significantly, but low concentration of LBP had no significant impacted on glucose consumption of insulin-resistant HepG2 cells. Glucose 102-109 insulin Homo sapiens 125-132 28508651-2 2017 It is a long-term pain for those who are affected and must regulate their blood glucose level by frequent subcutaneous injection of insulin every day. Glucose 80-87 insulin Homo sapiens 132-139 28591573-0 2017 Phosphorylation of TXNIP by AKT Mediates Acute Influx of Glucose in Response to Insulin. Glucose 57-64 insulin Homo sapiens 80-87 28591573-1 2017 Growth factors, such as insulin, can induce both acute and long-term glucose uptake into cells. Glucose 69-76 insulin Homo sapiens 24-31 28190265-1 2017 Insulin plays a crucial physiological role in glucose control by initiating a number of signaling events on binding and activating its cell surface receptor. Glucose 46-53 insulin Homo sapiens 0-7 28394194-3 2017 Tissue sensitivity to insulin was assessed on the basis of the glucose disposal rate (GDR) analyzed during hyperinsulinemic-euglycemic clamp. Glucose 63-70 insulin Homo sapiens 22-29 30603331-12 2017 A detailed understanding of the immune regulation of glucose and lipid homeostasis can lead to the development of a novel therapy for insulin resistance, type 2 diabetes, and NAFLD. Glucose 53-60 insulin Homo sapiens 134-141 28521878-5 2017 Insulin sensitivity was derived from the frequently sampled intravenous glucose tolerance test. Glucose 72-79 insulin Homo sapiens 0-7 28562560-2 2017 Triglyceride (TG) and glucose index combined with body mass index (TyG-BMI) has been proposed as a favorable marker of insulin resistance. Glucose 22-29 insulin Homo sapiens 119-126 28236091-4 2017 Moreover, long-term exposure to high glucose leads to inhibition of autophagy as well as to the development of insulin resistance in podocytes. Glucose 37-44 insulin Homo sapiens 111-118 28236091-5 2017 Furthermore, impairment of autophagy is involved in alteration of insulin-dependent glucose uptake in podocytes, suggesting a relationship between these two processes. Glucose 84-91 insulin Homo sapiens 66-73 28236091-6 2017 Taken together, our findings suggest that downregulation of podocyte autophagy, observed after long-term exposure to high glucose, results from their suppressed sensitivity to insulin, and may therefore lead to diminished podocyte cell viability as well as their reduced number in glomerulus. Glucose 122-129 insulin Homo sapiens 176-183 28393248-3 2017 The aim of the present study was to examine the effect of EGCG on insulin resistance in human HepG2 cells pretreated with high concentrations of glucose. Glucose 145-152 insulin Homo sapiens 66-73 28393248-12 2017 ROS is known to serve a major role in high glucose induced-insulin resistance by increasing JNK and IRS1 serine phosphorylation. Glucose 43-50 insulin Homo sapiens 59-66 28393248-14 2017 EGCG ameliorated high glucose-induced insulin resistance in the hepatocytes by potentially decreasing ROS-induced JNK/IRS1/AKT/GSK signaling. Glucose 22-29 insulin Homo sapiens 38-45 28655753-0 2017 The thermodynamic basis of glucose-stimulated insulin release: a model of the core mechanism. Glucose 27-34 insulin Homo sapiens 46-53 28521865-9 2017 At target glucose levels of ~52mg/dL, insulin mediated glucose disposal (IMGD) was decreased by ~40% (P=0.02) in PCOS, compared to control women, despite ~20% higher steady-state insulin levels (P=0.03). Glucose 10-17 insulin Homo sapiens 38-45 28521865-9 2017 At target glucose levels of ~52mg/dL, insulin mediated glucose disposal (IMGD) was decreased by ~40% (P=0.02) in PCOS, compared to control women, despite ~20% higher steady-state insulin levels (P=0.03). Glucose 55-62 insulin Homo sapiens 38-45 28429889-5 2017 Glucose uptake by EAT and SAT explants was determined after insulin, omentin, or combined treatment. Glucose 0-7 insulin Homo sapiens 60-67 28283687-7 2017 Since studies in animal models have suggested that Wnt signaling augments insulin secretion, we also examined the effect of Wnt signaling on glucose-stimulated insulin secretion on human pancreatic islets. Glucose 141-148 insulin Homo sapiens 160-167 28655753-9 2017 Applied to the reported glucose concentration-dependent release of insulin by perifused islet preparations (Doliba et al. Glucose 24-31 insulin Homo sapiens 67-74 28570579-7 2017 These genes are enriched in pathways related to glucose and amino acid metabolism, cellular respiration, and insulin signaling, and include genes such as SLC2A4, AKT2, as well as genes coding for enzymes in the mitochondria respiratory chain. Glucose 48-55 insulin Homo sapiens 109-116 28570579-13 2017 KFL15 and SLC25A10 are inhibitors of insulin-stimulated lipogenesis under conditions when glucose transport is the rate limiting step. Glucose 90-97 insulin Homo sapiens 37-44 30970879-6 2017 Among them, much effort has been devoted to the glucose-triggered insulin delivery systems, which are constructed by encapsulating insulin in PBA-modified LbL films and microcapsules. Glucose 48-55 insulin Homo sapiens 66-73 30970879-6 2017 Among them, much effort has been devoted to the glucose-triggered insulin delivery systems, which are constructed by encapsulating insulin in PBA-modified LbL films and microcapsules. Glucose 48-55 insulin Homo sapiens 131-138 30970879-7 2017 Insulin is released from the PBA-modified LbL assemblies upon the addition of glucose resulting from changes in the permeability of the films or decomposition of the film entity. Glucose 78-85 insulin Homo sapiens 0-7 30970879-8 2017 Research into insulin DDS is currently focused on the development of high-performance devices that release insulin in response to diabetic levels of glucose (>10 mM) but remain stable at normal levels (~5 mM) under physiological conditions. Glucose 149-156 insulin Homo sapiens 14-21 28536423-4 2017 FAM3B is co-secreted with insulin from the beta-cell upon glucose stimulation and regulates glucose homeostasis. Glucose 58-65 insulin Homo sapiens 26-33 28542421-0 2017 Insulin resistance according to beta-cell function in women with polycystic ovary syndrome and normal glucose tolerance. Glucose 102-109 insulin Homo sapiens 0-7 28604327-1 2017 BACKGROUND: To maintain fasting blood glucose levels within near to the normal range in type 1 diabetes mellitus (DM), frequent insulin dose adjustments may be required with short-, intermediate- and long-acting insulin formulations. Glucose 38-45 insulin Homo sapiens 128-135 28515362-5 2017 As tumor cells consume glucose in an insulin-independent manner, they shift glucose away from cardiomyocytes. Glucose 23-30 insulin Homo sapiens 37-44 28515362-5 2017 As tumor cells consume glucose in an insulin-independent manner, they shift glucose away from cardiomyocytes. Glucose 76-83 insulin Homo sapiens 37-44 28515362-6 2017 Since cardiomyocytes in both tumor models remained insulin responsive, low-dose insulin supplementation by subcutaneous implantation of insulin-releasing pellets improved cardiac glucose uptake, atrophy, and function, with no adverse side effects. Glucose 179-186 insulin Homo sapiens 80-87 28515362-6 2017 Since cardiomyocytes in both tumor models remained insulin responsive, low-dose insulin supplementation by subcutaneous implantation of insulin-releasing pellets improved cardiac glucose uptake, atrophy, and function, with no adverse side effects. Glucose 179-186 insulin Homo sapiens 80-87 31646121-3 2017 In contrast, glucose-lowering drugs that work as insulin sensitizing agents have been postulated to reduce CV complications. Glucose 13-20 insulin Homo sapiens 49-56 28082240-7 2017 This biosensor was exposed to buffer conditioned by glucose-stimulated human islets, with the result showing a positive response and a high degree of selectivity towards insulin capture. Glucose 52-59 insulin Homo sapiens 170-177 28427228-2 2017 miR-29a plays crucial roles in decreasing glucose-stimulated insulin secretion, as well as in regulating breast cancer cell proliferation and EMT. Glucose 42-49 insulin Homo sapiens 61-68 28082240-8 2017 The obtained results correlated well with the ELISA used in the clinic for assaying glucose-stimulated insulin release from donor islets. Glucose 84-91 insulin Homo sapiens 103-110 28259806-13 2017 This leads to two alternative interpretations regarding long-term insulin IND in mice: 1) It causes an initial stage of insulin resistance to dampen the behaviors that would normally be modulated under acute insulin IND, but ability to clear a glucose challenge is still retained, or 2) There is a lack of behavioral modulation at high concentration of insulin attributed to the twice daily intervals of hyperinsulinemia caused by insulin IND administration without any insulin resistance, per se. Glucose 244-251 insulin Homo sapiens 66-73 28328176-5 2017 Moreover, FITC-labeled insulin was used to evaluate the release behavior of insulin, and it was demonstrated that high glucose concentration could facilitate the quick release of insulin, suggesting a smart drug delivery system for potential application in controlled insulin release only under hyperglycemic conditions. Glucose 119-126 insulin Homo sapiens 23-30 28328176-5 2017 Moreover, FITC-labeled insulin was used to evaluate the release behavior of insulin, and it was demonstrated that high glucose concentration could facilitate the quick release of insulin, suggesting a smart drug delivery system for potential application in controlled insulin release only under hyperglycemic conditions. Glucose 119-126 insulin Homo sapiens 76-83 27729095-1 2017 The islets of Langerhans are endocrine tissue clusters that secrete hormones that regulate the body"s glucose, carbohydrate, and fat metabolism, the most important of which is insulin, a hormone secreted by beta-cells within the islets. Glucose 102-109 insulin Homo sapiens 176-183 28328176-5 2017 Moreover, FITC-labeled insulin was used to evaluate the release behavior of insulin, and it was demonstrated that high glucose concentration could facilitate the quick release of insulin, suggesting a smart drug delivery system for potential application in controlled insulin release only under hyperglycemic conditions. Glucose 119-126 insulin Homo sapiens 76-83 28328176-5 2017 Moreover, FITC-labeled insulin was used to evaluate the release behavior of insulin, and it was demonstrated that high glucose concentration could facilitate the quick release of insulin, suggesting a smart drug delivery system for potential application in controlled insulin release only under hyperglycemic conditions. Glucose 119-126 insulin Homo sapiens 76-83 28322789-9 2017 Impaired insulin signaling as well as reduced insulin stimulated glucose uptake was observed in high glucose treated L6 muscle cells. Glucose 101-108 insulin Homo sapiens 9-16 28487511-5 2017 By testing all possible motifs governing the interactions of these three cell types, we found that a unique set of positive/negative intra-islet interactions between different islet cell types functions not only to reduce the superficially wasteful zero-sum action of glucagon and insulin but also to enhance/suppress the synchronization of hormone secretions between islets under high/normal glucose conditions. Glucose 393-400 insulin Homo sapiens 281-288 28322789-9 2017 Impaired insulin signaling as well as reduced insulin stimulated glucose uptake was observed in high glucose treated L6 muscle cells. Glucose 101-108 insulin Homo sapiens 46-53 28322789-9 2017 Impaired insulin signaling as well as reduced insulin stimulated glucose uptake was observed in high glucose treated L6 muscle cells. Glucose 65-72 insulin Homo sapiens 46-53 27982680-8 2017 Our data suggest that decreased insulin sensitivity observed in lean women with GDM and PCOS is associated with distinct hormonal response of fat and gastrointestinal tissue to glucose load. Glucose 177-184 insulin Homo sapiens 32-39 28484241-5 2017 Herein, by mimicking those conditions in vitro, we have shown that GDNF significantly improved glucose stimulated insulin secretion, reduced apoptosis and proinsulin:insulin ratio in nutrient deprived human islets. Glucose 95-102 insulin Homo sapiens 114-121 28218949-0 2017 The triglyceride and glucose index is useful for recognising insulin resistance in children. Glucose 21-28 insulin Homo sapiens 61-68 28321016-4 2017 Pancreatic beta-cells synthesize a large amount of insulin in response to high glucose stimulation, and IRE1alpha plays an important role in insulin secretion from pancreatic beta-cells. Glucose 79-86 insulin Homo sapiens 51-58 28346946-8 2017 Based on review of the insulin/glucose chart in the electronic medical record, recommendations for insulin changes were entered in a vGMS note, which could be seen by all clinicians. Glucose 31-38 insulin Homo sapiens 99-106 28202439-2 2017 Surrogate indices of insulin sensitivity calculated from insulin and glucose concentrations at fasting or after an oral glucose tolerance test (OGTT) are frequently used, but have not been validated after RYGB. Glucose 120-127 insulin Homo sapiens 21-28 28267235-2 2017 Here the authors report the development of a new glucose-responsive insulin delivery system based on the potential interaction between the glucose derivative-modified insulin (Glc-Insulin) and glucose transporters on erythrocytes (or red blood cells, RBCs) membrane. Glucose 49-56 insulin Homo sapiens 68-75 28267235-2 2017 Here the authors report the development of a new glucose-responsive insulin delivery system based on the potential interaction between the glucose derivative-modified insulin (Glc-Insulin) and glucose transporters on erythrocytes (or red blood cells, RBCs) membrane. Glucose 49-56 insulin Homo sapiens 180-187 28213469-0 2017 Insulin signaling via the PI3-kinase/Akt pathway regulates airway glucose uptake and barrier function in a CFTR-dependent manner. Glucose 66-73 insulin Homo sapiens 0-7 28213469-3 2017 The response to insulin by human airway epithelial cells was characterized by quantitative PCR, immunoblot, immunofluorescence, and glucose uptake assays. Glucose 132-139 insulin Homo sapiens 16-23 28213469-5 2017 We found that normal human primary airway epithelial cells expressed glucose transporter 4 and that application of insulin stimulated cytochalasin B-inhibitable glucose uptake, consistent with a requirement for glucose transporter translocation. Glucose 161-168 insulin Homo sapiens 115-122 28213469-7 2017 This provides the first demonstration that airway cells express insulin-regulated glucose transporters that act in concert with tight junctions to form an airway glucose barrier. Glucose 82-89 insulin Homo sapiens 64-71 28213469-10 2017 These results indicate that the airway glucose barrier is regulated by insulin and is dysfunctional in CF. Glucose 39-46 insulin Homo sapiens 71-78 28202439-2 2017 Surrogate indices of insulin sensitivity calculated from insulin and glucose concentrations at fasting or after an oral glucose tolerance test (OGTT) are frequently used, but have not been validated after RYGB. Glucose 69-76 insulin Homo sapiens 21-28 27829479-16 2017 Results of the glucose tolerance test indicate that a lesser insulin response was necessary to properly clear the glucose in the EW heifers, suggesting enhanced insulin sensitivity. Glucose 15-22 insulin Homo sapiens 61-68 27829479-16 2017 Results of the glucose tolerance test indicate that a lesser insulin response was necessary to properly clear the glucose in the EW heifers, suggesting enhanced insulin sensitivity. Glucose 15-22 insulin Homo sapiens 161-168 28133970-5 2017 DATA SYNTHESIS: Lixisenatide lowers blood glucose through a glucose-dependent increase in insulin release from pancreatic beta-cells and a decreased release of glucagon from pancreatic alpha-cells. Glucose 60-67 insulin Homo sapiens 90-97 27829479-16 2017 Results of the glucose tolerance test indicate that a lesser insulin response was necessary to properly clear the glucose in the EW heifers, suggesting enhanced insulin sensitivity. Glucose 114-121 insulin Homo sapiens 61-68 27933750-10 2017 Participants diagnosed with diabetes by plasma glucose criteria had lower body mass index, smaller waist circumference, and lower insulinogenic and disposition indices, but higher homeostatic model assessment of insulin resistance, than those diagnosed by HbA1c . Glucose 47-54 insulin Homo sapiens 130-137 28284804-2 2017 Glucose phosphorylation by GK in the pancreatic beta-cell is the rate-limiting step that controls glucose-stimulated insulin secretion. Glucose 0-7 insulin Homo sapiens 117-124 28284804-2 2017 Glucose phosphorylation by GK in the pancreatic beta-cell is the rate-limiting step that controls glucose-stimulated insulin secretion. Glucose 98-105 insulin Homo sapiens 117-124 28198575-6 2017 Transduced Tat-BLVRA also recovered hIAPP-induced dysfunction in basal and glucose-stimulated insulin secretions. Glucose 75-82 insulin Homo sapiens 94-101 28235722-4 2017 Insulin Depots (ID) are parenteral formulations designed to release the insulin over a specified period of time, to control the plasma blood glucose level for intended duration. Glucose 141-148 insulin Homo sapiens 0-7 28235722-4 2017 Insulin Depots (ID) are parenteral formulations designed to release the insulin over a specified period of time, to control the plasma blood glucose level for intended duration. Glucose 141-148 insulin Homo sapiens 72-79 28235722-9 2017 In closed-loop systems insulin will be released in response to plasma glucose. Glucose 70-77 insulin Homo sapiens 23-30 28078385-2 2017 While several factors promoting beta cell proliferation have been identified, in the context of nutrient excess the roles of glucose or NEFA in relation to insulin resistance remain unclear. Glucose 125-132 insulin Homo sapiens 156-163 28078385-3 2017 Here we tested the hypothesis that glucose and NEFA synergistically and reversibly promote beta cell proliferation in the context of nutrient-induced insulin resistance. Glucose 35-42 insulin Homo sapiens 150-157 28221823-1 2017 BACKGROUND: Predictions based on continuous glucose monitoring (CGM) data are the basis for automatic suspension and resumption of insulin delivery by a predictive low-glucose management feature termed "suspend before low," which is part of the Medtronic MiniMed 640G combined insulin pump and CGM system. Glucose 44-51 insulin Homo sapiens 131-138 28078385-8 2017 Insulin sensitivity was equally decreased in GLU and GLU+CLI infusions. Glucose 45-48 insulin Homo sapiens 0-7 28078385-8 2017 Insulin sensitivity was equally decreased in GLU and GLU+CLI infusions. Glucose 53-56 insulin Homo sapiens 0-7 28099755-1 2017 AIMS: To assess the difference between analogue and human insulin with regard to nocturnal glucose profiles and risk of hypoglycaemia in people with recurrent severe hypoglycaemia. Glucose 91-98 insulin Homo sapiens 58-65 28099755-5 2017 RESULTS: During insulin analogue treatment, the mean nocturnal plasma glucose level was significantly higher than during treatment with human insulin (10.6 vs 8.1 mmol/l). Glucose 70-77 insulin Homo sapiens 16-23 28221823-1 2017 BACKGROUND: Predictions based on continuous glucose monitoring (CGM) data are the basis for automatic suspension and resumption of insulin delivery by a predictive low-glucose management feature termed "suspend before low," which is part of the Medtronic MiniMed 640G combined insulin pump and CGM system. Glucose 44-51 insulin Homo sapiens 278-285 28099755-8 2017 CONCLUSIONS: Treatment with insulin analogue reduces the occurrence of nocturnal hypoglycaemia assessed by nocturnal glucose profiles in people with Type 1 diabetes prone to severe hypoglycaemia. Glucose 117-124 insulin Homo sapiens 28-35 28099755-9 2017 Nocturnal glucose profiles provide a more comprehensive assessment of clinical benefit of insulin regimens as compared to conventional recording of hypoglycaemia. Glucose 10-17 insulin Homo sapiens 90-97 28221823-1 2017 BACKGROUND: Predictions based on continuous glucose monitoring (CGM) data are the basis for automatic suspension and resumption of insulin delivery by a predictive low-glucose management feature termed "suspend before low," which is part of the Medtronic MiniMed 640G combined insulin pump and CGM system. Glucose 168-175 insulin Homo sapiens 131-138 28221823-1 2017 BACKGROUND: Predictions based on continuous glucose monitoring (CGM) data are the basis for automatic suspension and resumption of insulin delivery by a predictive low-glucose management feature termed "suspend before low," which is part of the Medtronic MiniMed 640G combined insulin pump and CGM system. Glucose 168-175 insulin Homo sapiens 278-285 28221823-4 2017 The "suspend before low" feature was set at 65 mg/dL, and as a result, the predictive algorithm suspended insulin delivery when the forecasted glucose was predicted to be <=85 mg/dL in 30 min (a 20 mg/dL safety buffer). Glucose 143-150 insulin Homo sapiens 106-113 28432081-7 2017 After one hour of glucose administration, the serum potassium level significantly decreased from baseline, and the urinary potassium-to-creatinine ratio increased gradually and peaked at 2 h. CONCLUSIONS: Glucose metabolism and insulin secretion were impaired in GS patients, but insulin sensitivity was comparable between GS patients and patients with type 2 DM. Glucose 18-25 insulin Homo sapiens 228-235 28104918-0 2017 Triglycerides/glucose index is a useful surrogate marker of insulin resistance among adolescents. Glucose 14-21 insulin Homo sapiens 60-67 28470093-2 2017 This review summarizes four major mechanisms by which arsenic induces diabetes, namely inhibition of insulin-dependent glucose uptake, pancreatic beta-cell damage, pancreatic beta-cell dysfunction and stimulation of liver gluconeogenesis that are supported by both in vivo and in vitro studies. Glucose 119-126 insulin Homo sapiens 101-108 28300563-1 2017 Impaired insulin-stimulated glucose uptake in skeletal muscle serves a critical role in the development of insulin resistance (IR), whereas the precise mechanism of the process remains unknown. Glucose 28-35 insulin Homo sapiens 9-16 28300563-1 2017 Impaired insulin-stimulated glucose uptake in skeletal muscle serves a critical role in the development of insulin resistance (IR), whereas the precise mechanism of the process remains unknown. Glucose 28-35 insulin Homo sapiens 107-114 28300563-4 2017 In view of the potential protective effects of autophagy on the physiological and the pathological regulatory processes via the regulation of energy homeostasis and metabolism, we investigated the effects of Sesn2 on the components of the insulin signaling pathway and insulin-stimulated glucose uptake in palmitate-induced insulin-resistant C2C12 myotubes. Glucose 288-295 insulin Homo sapiens 269-276 28300563-4 2017 In view of the potential protective effects of autophagy on the physiological and the pathological regulatory processes via the regulation of energy homeostasis and metabolism, we investigated the effects of Sesn2 on the components of the insulin signaling pathway and insulin-stimulated glucose uptake in palmitate-induced insulin-resistant C2C12 myotubes. Glucose 288-295 insulin Homo sapiens 269-276 28104918-1 2017 OBJECTIVES: Our aim was to investigate the association between the triglycerides/glucose index (TyG index) and the homeostasis model assessment-estimated insulin resistance (HOMA-IR) in the prediction of insulin resistance (IR) among adolescents. Glucose 81-88 insulin Homo sapiens 154-161 28104918-1 2017 OBJECTIVES: Our aim was to investigate the association between the triglycerides/glucose index (TyG index) and the homeostasis model assessment-estimated insulin resistance (HOMA-IR) in the prediction of insulin resistance (IR) among adolescents. Glucose 81-88 insulin Homo sapiens 204-211 28658751-9 2017 RESULTS: Fasting insulin was correlating significantly with 30, 60 and 120 minute OGTT insulin showing that hyperinsulinemia in the fasting state was related to hyperinsulinemia in the post glucose load states. Glucose 190-197 insulin Homo sapiens 17-24 28658751-9 2017 RESULTS: Fasting insulin was correlating significantly with 30, 60 and 120 minute OGTT insulin showing that hyperinsulinemia in the fasting state was related to hyperinsulinemia in the post glucose load states. Glucose 190-197 insulin Homo sapiens 87-94 28213398-0 2017 FoxO integration of insulin signaling with glucose and lipid metabolism. Glucose 43-50 insulin Homo sapiens 20-27 27697848-1 2017 BACKGROUND: The accuracy of point-of-care blood glucose (BG) meters is important for the detection of dysglycemia, calculation of insulin doses, and the calibration of continuous glucose monitors. Glucose 48-55 insulin Homo sapiens 130-137 27762088-3 2017 Insulin doses were adjusted to maintain normal blood glucose levels. Glucose 53-60 insulin Homo sapiens 0-7 28318372-4 2017 Insulin resistance was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR) index [(insulin (IU/mL) x fasting glucose (mg/dL)/18)/22.5]. Glucose 138-145 insulin Homo sapiens 0-7 28745095-3 2017 METHOD: Optimal insulin dosage by Zone-MPC is calculated by solving an optimization problem in which a scalar index is minimized by penalizing relative input deviations and glucose predictions out of the reference zone. Glucose 173-180 insulin Homo sapiens 16-23 26947770-0 2017 Influence of initial insulin dosage on blood glucose dynamics of children and adolescents with newly diagnosed type 1 diabetes mellitus. Glucose 45-52 insulin Homo sapiens 21-28 28724042-7 2017 The median administered subcutaneous regular human insulin was 6 IU and among the factors evaluated only blood glucose levels were associated with the choice of insulin dose administered. Glucose 111-118 insulin Homo sapiens 161-168 28724042-8 2017 Conclusion:: Clinical characteristics such as diet, medications and diagnosis of diabetes mellitus are clearly ignored in the decision-making regarding insulin dose to be administered for glucose control in critically ill patients with hyperglycemia. Glucose 188-195 insulin Homo sapiens 152-159 29264537-2 2017 This study assessed the associations of postabsorptive AAs with IR directly measured by insulin-mediated glucose disposal and determined the quantitative value of AAs and conventional IR predictors. Glucose 105-112 insulin Homo sapiens 88-95 29090554-0 2017 [Puerariae Lobatae Radix elevated expression levels of OB-R, IRS2, GLUT1 and GLUT2 to regulate glucose metabolism in insulin-resistance HepG2 cells]. Glucose 95-102 insulin Homo sapiens 117-124 28970434-8 2017 However, on the seventh or last day of basal-bolus treatment, whichever came first, 36.36% of patients receiving insulin detemir (n = 88) achieved the blood glucose reading goal compared to 52.00% in patients receiving insulin glargine (n = 100) (p = 0.03). Glucose 157-164 insulin Homo sapiens 113-120 28430816-9 2017 CONCLUSIONS: Insulin resistance most likely increases during ACS; however, DeltaK was positively correlated with plasma glucose level, which overwhelmed insulin resistance condition. Glucose 120-127 insulin Homo sapiens 153-160 28422162-3 2017 The A3 receptor (ADORA3) was expressed only in mouse islets and the A3 agonist MRS 5698 inhibited glucose-induced insulin secretion from mouse islets, with no effect on human islets. Glucose 98-105 insulin Homo sapiens 114-121 28426788-6 2017 In a linear regression analysis model including several atherosclerotic risk factors such as gender, age, BMI, inflammatory factors, lipid profile, insulin-stimulated glucose disposal, fasting insulin, uric acid, and blood pressure, HGI was the major predictor of IMT (beta = 0.35; P = 0.001). Glucose 167-174 insulin Homo sapiens 148-155 28513455-7 2017 Nevertheless, a crucial role in the hyperglycemic activity seems to be played by a peripheral glucose uptake reduction, principally in the skeletal muscle, which is responsible for the decrease of insulin sensitivity, and can manifest itself in the increase of postprandial blood glucose levels. Glucose 94-101 insulin Homo sapiens 197-204 28513455-8 2017 If they are used in higher doses and for a prolonged period, they can also reduce the inhibitory effect of insulin on hepatic glucose production, which can lead to an increase of fasting plasma glucose. Glucose 126-133 insulin Homo sapiens 107-114 28513455-8 2017 If they are used in higher doses and for a prolonged period, they can also reduce the inhibitory effect of insulin on hepatic glucose production, which can lead to an increase of fasting plasma glucose. Glucose 194-201 insulin Homo sapiens 107-114 28560263-7 2017 By inhibiting glucose-stimulated insulin secretion, dopamine D2 and dopamine D3 receptors are important mediators of pancreatic insulin release. Glucose 14-21 insulin Homo sapiens 33-40 28219664-3 2017 Patients (n = 30) were administered pioglitazone (45 mg/day) for 8 weeks, and measurements were made before and after intervention of insulin action (insulin-mediated glucose uptake by the insulin suppression test), C-reactive protein, lipid/lipoprotein profile, and gene expression profile of periumbilical subcutaneous fat tissue. Glucose 167-174 insulin Homo sapiens 150-157 28219664-3 2017 Patients (n = 30) were administered pioglitazone (45 mg/day) for 8 weeks, and measurements were made before and after intervention of insulin action (insulin-mediated glucose uptake by the insulin suppression test), C-reactive protein, lipid/lipoprotein profile, and gene expression profile of periumbilical subcutaneous fat tissue. Glucose 167-174 insulin Homo sapiens 150-157 28955746-5 2017 The bio-printed liver tissue displayed glucose production via cAMP/protein kinase A signaling, which could be suppressed with insulin. Glucose 39-46 insulin Homo sapiens 126-133 33429624-1 2017 A glucose-responsive closed-loop insulin delivery system represents an ideal form of treatment for type 1 diabetes mellitus. Glucose 2-9 insulin Homo sapiens 33-40 33429624-6 2017 The pH-lowering induced by the enzymatic MCF in high glucose concentration resulted in swelling of the chitosan microgels and the subsequent release of the encapsulated model protein drug, such as bovine serum albumin and insulin. Glucose 53-60 insulin Homo sapiens 222-229 28406435-6 2017 Linear regression analysis revealed a positive association of glucose intake with insulin sensitivity in the fully adjusted model (standardized beta (95% CI) 0.07 (0.05, 0.14) SD for >=23 g vs. <10 g of glucose). Glucose 62-69 insulin Homo sapiens 82-89 28406435-6 2017 Linear regression analysis revealed a positive association of glucose intake with insulin sensitivity in the fully adjusted model (standardized beta (95% CI) 0.07 (0.05, 0.14) SD for >=23 g vs. <10 g of glucose). Glucose 209-216 insulin Homo sapiens 82-89 28406435-9 2017 In conclusion, higher intake of glucose, not fructose and sucrose, was associated with higher insulin sensitivity, independent of dietary fibre. Glucose 32-39 insulin Homo sapiens 94-101 28156154-6 2017 The insulin timing algorithm altered the time when the meal dose of insulin was injected or infused from 30 minutes before the meal to 15 minutes after the meal, depending upon the premeal blood glucose concentration. Glucose 195-202 insulin Homo sapiens 4-11 28428756-6 2017 Insulin sensitivity was assessed by homeostasis model (HOMA-IR) and Matsuda Insulin Sensitivity Index (ISI) derived from 75-g oral glucose tolerance test. Glucose 131-138 insulin Homo sapiens 0-7 28368334-1 2017 Dietary protein and fiber independently influence insulin-mediated glucose control. Glucose 67-74 insulin Homo sapiens 50-57 28130099-4 2017 Through the introduction of an instantaneous glucose-dependent insulin response, explicit conditions for the existence of periodic solutions in the linearised model are formulated, significantly reducing the complexity of identifying an oscillatory regime. Glucose 45-52 insulin Homo sapiens 63-70 28387485-7 2017 Secondary analysis found significant correlations between the numerical values of baseline total plasma insulin level and fasting plasma glucose level at baseline (r = 0.492, P < .001), 3 months (r = 0.247, P = .035), and 6 months (r = 0.723, P < .001). Glucose 137-144 insulin Homo sapiens 104-111 28387485-9 2017 Conclusions: Baseline total plasma insulin levels were strongly correlated with parameters affected directly by alterations in glucose up to 6 months after admission but were weakly correlated or not correlated with other metabolic parameters. Glucose 127-134 insulin Homo sapiens 35-42 28277977-9 2017 Focusing on the top-ranking 30 and another 37 CpG sites mapped to genes enriched in pathways of metabolism (q = 0.0036) and cancer (q = 0.0001) all together, 59 NASH-associated CpG sites correlated with fasting insulin levels independently of age, fasting glucose, or T2D. Glucose 256-263 insulin Homo sapiens 211-218 28156154-6 2017 The insulin timing algorithm altered the time when the meal dose of insulin was injected or infused from 30 minutes before the meal to 15 minutes after the meal, depending upon the premeal blood glucose concentration. Glucose 195-202 insulin Homo sapiens 68-75 27976833-13 2017 glucose bolus, increased the second-phase insulin response and enhanced beta-cell function. Glucose 0-7 insulin Homo sapiens 42-49 28251932-0 2017 Inhibition of sweet chemosensory receptors alters insulin responses during glucose ingestion in healthy adults: a randomized crossover interventional study. Glucose 75-82 insulin Homo sapiens 50-57 28213130-8 2017 Our data suggest that hepatic DPP-4 induces a selective pathway of insulin resistance with reduced glycogen storage, enhanced glucose output and increased lipid accumulation in the liver. Glucose 126-133 insulin Homo sapiens 67-74 27505857-12 2017 These results suggest that an increase in insulin secretion and whole insulin sensitivity was associated with improvement in glucose tolerance in these recipients. Glucose 125-132 insulin Homo sapiens 42-49 28293907-8 2017 For most of these, the association reflects their correlation with the maternal risk allele which raises maternal glucose, thus increasing fetal insulin-mediated growth. Glucose 114-121 insulin Homo sapiens 145-152 27981615-4 2017 Hepatic insulin sensitivity (suppression of endogenous glucose production by insulin) was affected early on after IHTG content was ~1.5% and remained uniformly impaired (~40%-45%), regardless of further IHTG accumulation. Glucose 55-62 insulin Homo sapiens 8-15 28130310-2 2017 Although insulin plays a key role in glucose regulation, the importance of glucagon is increasingly acknowledged. Glucose 37-44 insulin Homo sapiens 9-16 28130310-5 2017 Dispersed islet cells secrete aberrant levels of glucagon and insulin at basal and elevated glucose levels. Glucose 92-99 insulin Homo sapiens 62-69 28220460-10 2017 CONCLUSION: Switching to IDegLira, mostly from regimens using insulin in conjunction with oral antidiabetic medications in a real-world population of patients with type 2 diabetes, resulted in improved glucose control with a lower insulin dose and weight loss. Glucose 202-209 insulin Homo sapiens 62-69 28220460-10 2017 CONCLUSION: Switching to IDegLira, mostly from regimens using insulin in conjunction with oral antidiabetic medications in a real-world population of patients with type 2 diabetes, resulted in improved glucose control with a lower insulin dose and weight loss. Glucose 202-209 insulin Homo sapiens 231-238 28221814-1 2017 BACKGROUND: Labeling prohibits delivery of insulin at the site of subcutaneous continuous glucose monitoring (CGM). Glucose 90-97 insulin Homo sapiens 43-50 28429367-5 2017 At today after one year and a half from the onset of T1D, the subject shows a near-normal blood glucose with the administration of 1.5-2 UI of insulin once a day. Glucose 96-103 insulin Homo sapiens 143-150 28347174-1 2017 Patients with diabetes have a high level of blood glucose because their body cannot produce enough insulin or properly respond to this hormone. Glucose 50-57 insulin Homo sapiens 99-106 28276155-2 2017 It can occur due to impaired secretion or action of the hormone insulin, which is produced by pancreatic beta-cells to promote the entry of glucose into the cells. Glucose 140-147 insulin Homo sapiens 64-71 27779772-2 2017 BACKGROUND: Insulin therapy is recommended to facilitate the regulation of plasma glucose; however, patient"s acceptance of insulin therapy is generally low. Glucose 82-89 insulin Homo sapiens 12-19 28324055-8 2017 Fasting-induced insulin resistance was abrogated by GHA (P < 0.01) primarily due to reduced endogenous glucose production (P = 0.003). Glucose 106-113 insulin Homo sapiens 16-23 28571200-3 2017 Insulin is administered by injection or continuous infusion to control glucose levels mainly in Type I diabetes. Glucose 71-78 insulin Homo sapiens 0-7 28025059-1 2017 BACKGROUND & AIMS: The paradox of selective hepatic insulin resistance, wherein the insulin-resistant liver fails to suppress glucose production but continues to produce lipids, has been central to the pathophysiology of hepatosteatosis and hyperglycemia. Glucose 130-137 insulin Homo sapiens 56-63 28025059-1 2017 BACKGROUND & AIMS: The paradox of selective hepatic insulin resistance, wherein the insulin-resistant liver fails to suppress glucose production but continues to produce lipids, has been central to the pathophysiology of hepatosteatosis and hyperglycemia. Glucose 130-137 insulin Homo sapiens 88-95 28025059-9 2017 By simultaneously modulating lipogenesis and insulin signaling, microRNA-206 reduced lipid (p=0.006) and glucose (p=0.018) production in human hepatocytes and livers of dietary obese mice (p<0.001 and p<0.01 respectively). Glucose 105-112 insulin Homo sapiens 45-52 28025059-11 2017 CONCLUSIONS: MicroRNA-206 is a potent inhibitor of lipid and glucose production by simultaneously facilitating insulin signaling and impairing hepatic lipogenesis. Glucose 61-68 insulin Homo sapiens 111-118 28298537-7 2017 Furthermore, the association between MDS and fasting glucose was fully mediated by adiposity, especially by WC in men aged <45 y and in premenopausal women.Conclusion: Our results suggest that reducing abdominal obesity may play an important role in the pathway through which Med-diet consumption reduces insulin resistance and inflammation. Glucose 53-60 insulin Homo sapiens 308-315 32263598-8 2017 The in vivo study showed that insulin-loaded NPs-C16 (20%) generated an obvious hypoglycemic effect, with a maximal 46% reduction of the blood glucose level. Glucose 143-150 insulin Homo sapiens 30-37 28685559-4 2017 Insulin release and content (at 11.0 and 20 mmol/L glucose) were significantly (p less than 0.01) stimulated by 1-100 nmol/L T2 and 0.1 nmol/L-1.0 mumol/L T3, and inhibited with higher concentrations of both (110 mumol/L T2 and 10 mumol/L T3). Glucose 51-58 insulin Homo sapiens 0-7 28094136-2 2017 We aimed to investigate whether day-and-night hybrid closed-loop insulin delivery can improve glucose control while alleviating the risk of hypoglycaemia in adults with HbA1c below 7 5% (58 mmol/mol). Glucose 94-101 insulin Homo sapiens 65-72 28094136-15 2017 INTERPRETATION: Use of day-and-night hybrid closed-loop insulin delivery under unsupervised, free-living conditions for 4 weeks in adults with type 1 diabetes and HbA1c below 7 5% is safe and well tolerated, improves glucose control, and reduces hypoglycaemia burden. Glucose 217-224 insulin Homo sapiens 56-63 28401743-6 2017 Hypoglycemia can result from consistently high levels of insulin after reaching normal glucose level. Glucose 87-94 insulin Homo sapiens 57-64 28228611-8 2017 Down-regulation of Gprc5c led to both moderately reduced glucose-stimulated insulin release and also reduced cAMP content in mouse islets. Glucose 57-64 insulin Homo sapiens 76-83 28346464-6 2017 Following agonist stimulation and glucose infusion, endogenous insulin release inhibited lipolysis in the presence of norepinephrine, which was more rapid and pronounced in healthy obese controls than in T2D subjects (p = 0.024 obese vs T2D subjects). Glucose 34-41 insulin Homo sapiens 63-70 30755920-8 2017 Large solid tumours can occasionally produce loosely bound or free Big IGF-2 molecules which circulate throughout the plasma and bind to insulin as well as IGF receptors, thus increasing glucose intake by body tissues, decreasing the release of glucose to the bloodstream by the liver and causing feedback suppression of insulin, IGF-1 and growth hormone production. Glucose 187-194 insulin Homo sapiens 137-144 30755920-8 2017 Large solid tumours can occasionally produce loosely bound or free Big IGF-2 molecules which circulate throughout the plasma and bind to insulin as well as IGF receptors, thus increasing glucose intake by body tissues, decreasing the release of glucose to the bloodstream by the liver and causing feedback suppression of insulin, IGF-1 and growth hormone production. Glucose 245-252 insulin Homo sapiens 137-144 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 77-84 insulin Homo sapiens 168-175 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 77-84 insulin Homo sapiens 295-302 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 77-84 insulin Homo sapiens 295-302 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 186-193 insulin Homo sapiens 168-175 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 186-193 insulin Homo sapiens 295-302 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 186-193 insulin Homo sapiens 295-302 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 186-193 insulin Homo sapiens 168-175 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 186-193 insulin Homo sapiens 295-302 28333091-3 2017 We summarized here recent advances in our understanding of the regulation of glucose metabolism using bioactive peptides from natural proteins, including regulation of insulin-regulated glucose metabolism, such as protection and reparation of pancreatic beta-cells, enhancing glucose-stimulated insulin secretion and influencing the sensitivity of insulin and the signaling pathways, and inhibition of bioactive peptides to dipeptidyl peptidase IV, alpha-amylase and alpha-glucosidase activities. Glucose 186-193 insulin Homo sapiens 295-302 28540053-2 2017 The state of insulin resistance created by hormonal changes in pregnancy enables free flow of glucose to the foetus and allows its absorption through facilitated diffusion. Glucose 94-101 insulin Homo sapiens 13-20 28304381-5 2017 In the present study, we discovered that TNF-alpha might stimulate PA transcytosis across cardiac microvascular endothelial cells, which further impaired the insulin-stimulated glucose uptake by cardiomyocytes and promoted insulin resistance. Glucose 177-184 insulin Homo sapiens 158-165 29955699-9 2017 Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated by using fasting serum glucose and insulin. Glucose 99-106 insulin Homo sapiens 32-39 27758118-6 2017 GS inhibition also decreases insulin-mediated glucose uptake in microglia. Glucose 46-53 insulin Homo sapiens 29-36 28215845-5 2017 Physiological studies demonstrated that converted alpha cells acquire hallmark beta cell electrophysiology and show glucose-stimulated insulin secretion. Glucose 116-123 insulin Homo sapiens 135-142 28253305-0 2017 Chitosan-assisted differentiation of porcine adipose tissue-derived stem cells into glucose-responsive insulin-secreting clusters. Glucose 84-91 insulin Homo sapiens 103-110 28253305-3 2017 Here, we report on the isolation and conversion of pADSCs into glucose-responsive insulin-secreting cells. Glucose 63-70 insulin Homo sapiens 82-89 28253305-6 2017 Upon glucose challenge, these PILC secreted high amounts of insulin in a dose-dependent manner. Glucose 5-12 insulin Homo sapiens 60-67 28106608-1 2017 BACKGROUND: Diabetic patients receiving insulin should have periodic intraoperative glucose measurement. Glucose 84-91 insulin Homo sapiens 40-47 28443256-7 2017 Fasting insulin and HOMA-IR were increased in the patient group; fasting glucose-to-insulin ratio and QUICKI were increased in the control group (all P<0.001). Glucose 73-80 insulin Homo sapiens 84-91 28225861-3 2017 Insulin sensitivity was assessed by estimated glucose disposal rate (eGDR), and metabolic syndrome (MS) was defined by the World Health Organization criteria. Glucose 46-53 insulin Homo sapiens 0-7 28126826-5 2017 Insulin-stimulated skeletal muscle perfusion is impaired in several insulin-resistant states and is believed to contribute to impaired skeletal muscle glucose uptake and consequently impaired whole-body glucose disposal. Glucose 151-158 insulin Homo sapiens 0-7 28189039-6 2017 Hepatic insulin sensitivity was estimated from percentage suppression of endogenous glucose production and peripheral insulin sensitivity as glucose infusion rate (M/I) during a hyperinsulinaemic-euglycaemic clamp. Glucose 84-91 insulin Homo sapiens 8-15 28189039-6 2017 Hepatic insulin sensitivity was estimated from percentage suppression of endogenous glucose production and peripheral insulin sensitivity as glucose infusion rate (M/I) during a hyperinsulinaemic-euglycaemic clamp. Glucose 141-148 insulin Homo sapiens 8-15 29026411-8 2017 RESULTS: The results of linear regression determined a significant inverse association between HEI score and homeostasis model assessment of insulin resistance [HOMA-IR, beta = -0.238 (-0.426, -0.048)], fasting blood glucose [beta = -0.194 (-0.383, -0.004)], and high-sensitivity C-reactive protein [hs-CRP, beta = -0.196, (-0.386, -0.005)]. Glucose 217-224 insulin Homo sapiens 141-148 28197835-3 2017 This article concentrates on three trace metals (selenium, vanadium, and chromium) that may play crucial roles in controlling blood glucose concentrations possibly through their insulin-mimetic effects. Glucose 132-139 insulin Homo sapiens 178-185 28099035-9 2017 Manual resumption of insulin delivery followed by carbohydrate intake resulted in significantly higher glucose levels 1 h after suspension compared to SmartGuard suspensions with automatic resume (190.8 +- 26.5 vs. 138.7 +- 10.3 mg/dL; P < 0.001). Glucose 103-110 insulin Homo sapiens 21-28 28359089-6 2017 In parallel experiments with goldfish hepatocytes and brain cell culture, insulin signal induced by glucose was shown to exert a dual role in SPX regulation, namely (1) acting as an autocrine/paracrine signal to trigger SPX mRNA expression in the liver and (2) serving as an endocrine signal to induce SPX gene expression in the brain. Glucose 100-107 insulin Homo sapiens 74-81 28359089-8 2017 Our findings indicate that an insulin component inducible by glucose is present in the liver of the fish model and may serve as the postprandial signal linking food intake with SPX expression both in the central as well as at the hepatic level. Glucose 61-68 insulin Homo sapiens 30-37 27870552-11 2017 Conclusions: Normal preoperative glucose status and lower fasting and postchallenge OGTT glucose values are significant predictors of insulin independence after TPIAT. Glucose 33-40 insulin Homo sapiens 134-141 27870552-11 2017 Conclusions: Normal preoperative glucose status and lower fasting and postchallenge OGTT glucose values are significant predictors of insulin independence after TPIAT. Glucose 89-96 insulin Homo sapiens 134-141 28183449-5 2017 The insulin sensitivity index (ISI) was calculated from the last 30min of a continuous low-dose insulin (25mU/kg h) and glucose (4mg/kg min) infusion test (LDIGIT 120-150min) at the end of each diet. Glucose 120-127 insulin Homo sapiens 4-11 28183452-10 2017 Priming dose of insulin may not be required, and fixed rate insulin infusion represents the best option to suppress hepatic glucose production, ketogenesis, and lipolysis. Glucose 124-131 insulin Homo sapiens 60-67 26799689-2 2017 Previously we demonstrated that for the same degree of insulin sensitivity, Black youth have an upregulated beta-cell function and insulin hypersecretion, in response to intravenous (iv) glucose, compared with Whites. Glucose 187-194 insulin Homo sapiens 131-138 28292880-5 2017 117 subjects (women, n = 50, men, n = 67; age= 37.6 +- 10.8; BMI=31.1 +- 7.7 kg/m2) underwent an insulin-modified frequently sampled intravenous glucose tolerance test (FSIVGTT) at the NIH Clinical Research Center. Glucose 145-152 insulin Homo sapiens 97-104 28292880-7 2017 The Quantitative Insulin Sensitivity Check Index (QUICKI) was calculated from fasting insulin and glucose values. Glucose 98-105 insulin Homo sapiens 17-24 28129048-2 2017 Insulin acting on adipocyte receptors produces less glucose uptake than does comparable interaction with myocyte receptors. Glucose 52-59 insulin Homo sapiens 0-7 28292497-1 2017 BACKGROUND: Glucose monitoring is important for patients with diabetes treated with insulin. Glucose 12-19 insulin Homo sapiens 84-91 28238223-17 2017 One study showed that more intensive insulin therapy resulted in a lower mean HbA1c (10 +- 0.8% versus 13 +- 0.9%) and lower fasting blood glucose (7.22 +- 0.5 mmol/L versus 13.44 +- 1.22 mmol/L) at 13 months compared with standard insulin therapy. Glucose 139-146 insulin Homo sapiens 37-44 28077579-8 2017 Interestingly, Rbfox1 silencing modulates the splicing of the actin-remodeling protein gelsolin, increasing gelsolin expression and leading to faster glucose-induced actin depolymerization and increased insulin release. Glucose 150-157 insulin Homo sapiens 203-210 28067391-4 2017 The effects of HF diets on gene expression are mediated by insulin, leptin and nutrients such as fatty acids (FA) and glucose that alter insulin signalling. Glucose 118-125 insulin Homo sapiens 137-144 30229209-11 2017 The glucose levels of patients in all of these groups responded well to insulin. Glucose 4-11 insulin Homo sapiens 72-79 28263805-1 2017 AIMS: Several studies have indicated that insulin that is used in reducing blood glucose is also affective on wound healing by various mechanisms. Glucose 81-88 insulin Homo sapiens 42-49 28407130-8 2017 Additional matching for OGTT glucose concentrations revealed significantly lower insulin sensitivity in ESRD patients than in controls. Glucose 29-36 insulin Homo sapiens 81-88 27648697-12 2017 CONCLUSION: IL-18 may reduce blood glucose by modulating insulin signaling in the liver during sepsis-induced hyperglycemia. Glucose 35-42 insulin Homo sapiens 57-64 28095749-6 2017 PCOS girls were more insulin resistant than controls (glucose infusion rate 5.24+-1.86 mg/kg/min vs 9.10+-2.69; p<0.001). Glucose 54-61 insulin Homo sapiens 21-28 28070056-10 2017 By means of multiple daily insulin injection therapy, his glycemic control has been well maintained (HbA1c approximately 6.0%), with relatively small glycemic fluctuations evaluated by continuous glucose monitoring. Glucose 196-203 insulin Homo sapiens 27-34 28100871-4 2017 We found that hepatocytes could be directly reprogrammed into insulin-producing cells after PNM gene transfection by non-viral hydrodynamics injection, and fasting blood glucose was reduced to normal, and lasted until 100 days after transfection. Glucose 170-177 insulin Homo sapiens 62-69 28100871-5 2017 Intraperitoneal glucose tolerance test (IPGTT) showed that glucose regulation ability was improved gradually and the serum insulin level approached to the level of normal mice with time. Glucose 16-23 insulin Homo sapiens 123-130 28408838-4 2017 In each study, the insulin secretory rate relative to glucose (ISR/G 0-2h) during glucose load (standard meal or oral glucose tolerance test) was assessed at baseline and end of study. Glucose 82-89 insulin Homo sapiens 19-26 28408838-4 2017 In each study, the insulin secretory rate relative to glucose (ISR/G 0-2h) during glucose load (standard meal or oral glucose tolerance test) was assessed at baseline and end of study. Glucose 82-89 insulin Homo sapiens 19-26 28358037-7 2017 A cure is not available, and patients depend on lifelong insulin injections; novel approaches to insulin treatment, such as insulin pumps, continuous glucose monitoring and hybrid closed-loop systems, are in development. Glucose 150-157 insulin Homo sapiens 97-104 28424732-1 2017 The two main types of diabetes mellitus have distinct etiologies, yet a similar outcome: loss of islet beta-cell function that is solely responsible for the secretion of the insulin hormone to reduce elevated plasma glucose toward euglycemic levels. Glucose 216-223 insulin Homo sapiens 174-181 28352665-0 2017 Insulin"s direct hepatic effect explains the inhibition of glucose production caused by insulin secretion. Glucose 59-66 insulin Homo sapiens 0-7 28352665-1 2017 Insulin can inhibit hepatic glucose production (HGP) by acting directly on the liver as well as indirectly through effects on adipose tissue, pancreas, and brain. Glucose 28-35 insulin Homo sapiens 0-7 28462075-13 2017 In NW class 2-arachidonoylglycerol correlations were found with insulin (P = 0.003) and HOMA-IR (P = 0.001), both enhanced by aging (both P = 0.004), and with glucose (P = 0.015) and HDL (P = 0.004). Glucose 159-166 insulin Homo sapiens 64-71 28325894-4 2017 Glucose-dependent de-SUMOylation of tomosyn1 at K298 releases syntaxin1A and controls the amplification of exocytosis in concert with a recently-identified tomosyn1-interacting partner; the Ca2+-binding protein secretagogin, which dissociates from tomosyn1 in response to Ca2+-raising stimuli and is required for insulin granule trafficking and exocytosis downstream of Ca2+ influx. Glucose 0-7 insulin Homo sapiens 313-320 28161417-5 2017 The hepatocytes exposed to palmitate (0.75mM) for 48h exhibited reduced both basal and insulin-stimulated glucose uptake, mitochondrial dysfunction, leading to increased mitochondrial oxidative stress with diminished fatty acid oxidation. Glucose 106-113 insulin Homo sapiens 87-94 28344558-6 2017 More recently, a role has been attributed to the parasympathetic nervous system (PNS) in modulating both adipose tissue insulin-mediated glucose uptake and fatty free acid (FFA) metabolism in an anabolic way and its endocrine function. Glucose 137-144 insulin Homo sapiens 120-127 28272368-1 2017 An artificial pancreas (AP) computes the optimal insulin dose to be infused through an insulin pump in people with Type 1 Diabetes (T1D) based on information received from a continuous glucose monitoring (CGM) sensor. Glucose 185-192 insulin Homo sapiens 49-56 27965206-3 2017 In this context, we postulated that lactation could potentially induce postweaning beneficial effects on glucose tolerance by modifying the natural history of insulin sensitivity and/or pancreatic beta-cell function over time. Glucose 105-112 insulin Homo sapiens 159-166 27974316-5 2017 Glucose kinetics after OGTT was described by a one-compartment model with an effect compartment to describe delayed insulin effects on glucose clearance. Glucose 0-7 insulin Homo sapiens 116-123 27974316-5 2017 Glucose kinetics after OGTT was described by a one-compartment model with an effect compartment to describe delayed insulin effects on glucose clearance. Glucose 135-142 insulin Homo sapiens 116-123 27974316-7 2017 Baseline glucose concentration was estimated to be only marginally higher in nondiabetic obese subjects (4.9 vs. 5.2 mmol/l), whereas insulin-dependent glucose clearance in nondiabetic obese subjects was found to be cut in half compared with lean controls (0.052 vs. 0.029 l/min) and the insulin concentration associated with 50% of insulin-dependent glucose elimination rate was approximately twofold higher in nondiabetic obese subjects compared with lean controls (7.1 vs. 15.3 muU/ml). Glucose 152-159 insulin Homo sapiens 134-141 27974316-7 2017 Baseline glucose concentration was estimated to be only marginally higher in nondiabetic obese subjects (4.9 vs. 5.2 mmol/l), whereas insulin-dependent glucose clearance in nondiabetic obese subjects was found to be cut in half compared with lean controls (0.052 vs. 0.029 l/min) and the insulin concentration associated with 50% of insulin-dependent glucose elimination rate was approximately twofold higher in nondiabetic obese subjects compared with lean controls (7.1 vs. 15.3 muU/ml). Glucose 152-159 insulin Homo sapiens 288-295 27974316-7 2017 Baseline glucose concentration was estimated to be only marginally higher in nondiabetic obese subjects (4.9 vs. 5.2 mmol/l), whereas insulin-dependent glucose clearance in nondiabetic obese subjects was found to be cut in half compared with lean controls (0.052 vs. 0.029 l/min) and the insulin concentration associated with 50% of insulin-dependent glucose elimination rate was approximately twofold higher in nondiabetic obese subjects compared with lean controls (7.1 vs. 15.3 muU/ml). Glucose 152-159 insulin Homo sapiens 288-295 27974316-7 2017 Baseline glucose concentration was estimated to be only marginally higher in nondiabetic obese subjects (4.9 vs. 5.2 mmol/l), whereas insulin-dependent glucose clearance in nondiabetic obese subjects was found to be cut in half compared with lean controls (0.052 vs. 0.029 l/min) and the insulin concentration associated with 50% of insulin-dependent glucose elimination rate was approximately twofold higher in nondiabetic obese subjects compared with lean controls (7.1 vs. 15.3 muU/ml). Glucose 152-159 insulin Homo sapiens 134-141 27974316-7 2017 Baseline glucose concentration was estimated to be only marginally higher in nondiabetic obese subjects (4.9 vs. 5.2 mmol/l), whereas insulin-dependent glucose clearance in nondiabetic obese subjects was found to be cut in half compared with lean controls (0.052 vs. 0.029 l/min) and the insulin concentration associated with 50% of insulin-dependent glucose elimination rate was approximately twofold higher in nondiabetic obese subjects compared with lean controls (7.1 vs. 15.3 muU/ml). Glucose 152-159 insulin Homo sapiens 288-295 27974316-7 2017 Baseline glucose concentration was estimated to be only marginally higher in nondiabetic obese subjects (4.9 vs. 5.2 mmol/l), whereas insulin-dependent glucose clearance in nondiabetic obese subjects was found to be cut in half compared with lean controls (0.052 vs. 0.029 l/min) and the insulin concentration associated with 50% of insulin-dependent glucose elimination rate was approximately twofold higher in nondiabetic obese subjects compared with lean controls (7.1 vs. 15.3 muU/ml). Glucose 152-159 insulin Homo sapiens 288-295 28186649-1 2017 A direct link between development of insulin resistance and the presence of chronic inflammation, in case of obesity exists, with cytokines playing an important role in glucose metabolism. Glucose 169-176 insulin Homo sapiens 37-44 28186649-5 2017 In this study, BMP-7 and -4 have been demonstrated to have antagonistic effects on insulin signaling and thereby on glucose homeostasis. Glucose 116-123 insulin Homo sapiens 83-90 28186649-6 2017 BMP-7 augmented glucose uptake in the insulin sensitive tissues such as the adipose and muscle by increasing Glut4 translocation to the plasma membrane through phosphorylation and activation of PDK1 and Akt, and phosphorylation and translocation of FoxO1 to the cytoplasm in liver/HepG2 cells. Glucose 16-23 insulin Homo sapiens 38-45 28134564-0 2017 Glucose Outcomes with the In-Home Use of a Hybrid Closed-Loop Insulin Delivery System in Adolescents and Adults with Type 1 Diabetes. Glucose 0-7 insulin Homo sapiens 62-69 27967226-2 2017 The use of an electronic glucose management system (eGMS) to guide intravenous (IV) insulin infusion has been found to significantly improve blood glucose (BG) control. Glucose 25-32 insulin Homo sapiens 84-91 28073130-11 2017 Conclusions: In males with hypertension, the link between insulin sensitivity and hypothalamic-pituitary-gonadal axis is maintained along the entire spectrum of glucose tolerance. Glucose 161-168 insulin Homo sapiens 58-65 28149010-0 2017 Association of Interleukin-6 and Myeloperoxidase with Insulin Resistance in Impaired Fasting Glucose Subjects. Glucose 93-100 insulin Homo sapiens 54-61 27967291-12 2017 Unusual oscillating glucose and insulin responses to oral glucose were seen in both cases and carriers. Glucose 58-65 insulin Homo sapiens 32-39 28406767-6 2017 Insulin resistance was assessed by calculating HOMA-IR using the formula (fasting glucose x fasting insulin)/405, taking normal value <2 in adults and hyperinsulinemia based on fasting insulin levels >=12 microIU/ml. Glucose 82-89 insulin Homo sapiens 0-7 27705031-1 2017 BACKGROUND AND AIMS: Insulin degludec is an insulin analog with an ultra-long duration of action that exhibits less intra-patient variability in its glucose-lowering activity, and reduces nocturnal, overall, and severe hypoglycemia relative to insulin glargine. Glucose 149-156 insulin Homo sapiens 21-28 28041666-4 2017 Corrected insulin response (CIR) was calculated as measure of insulin secretion, corrected for glucose (CIR30, CIR60, CIR120). Glucose 95-102 insulin Homo sapiens 10-17 27739515-3 2017 Exercise-stimulated glucose uptake is preserved in insulin-resistant muscle, emphasizing exercise as a therapeutic cornerstone among patients with metabolic diseases such as diabetes mellitus. Glucose 20-27 insulin Homo sapiens 51-58 27390032-5 2017 RESULTS: Multiple daily injection (MDI) treatment with insulin lispro or other rapid-acting insulins, mainly using neutral protamine Hagedorn (NPH) insulin as the basal component, was associated with reduced postprandial glucose excursions, similar or improved HbA1c levels, and similar or reduced risks of severe hypoglycemia when compared with regular human insulin across all age-groups. Glucose 221-228 insulin Homo sapiens 55-62 27390032-5 2017 RESULTS: Multiple daily injection (MDI) treatment with insulin lispro or other rapid-acting insulins, mainly using neutral protamine Hagedorn (NPH) insulin as the basal component, was associated with reduced postprandial glucose excursions, similar or improved HbA1c levels, and similar or reduced risks of severe hypoglycemia when compared with regular human insulin across all age-groups. Glucose 221-228 insulin Homo sapiens 92-99 27390032-5 2017 RESULTS: Multiple daily injection (MDI) treatment with insulin lispro or other rapid-acting insulins, mainly using neutral protamine Hagedorn (NPH) insulin as the basal component, was associated with reduced postprandial glucose excursions, similar or improved HbA1c levels, and similar or reduced risks of severe hypoglycemia when compared with regular human insulin across all age-groups. Glucose 221-228 insulin Homo sapiens 92-99 27717184-9 2017 Furthermore, proteins acting as negative modulators involved in negative regulation of gene expression, insulin stimulated glucose uptake, and cytoskeletal organization showed a decrease in their nuclear abundance and/or phosphorylation levels during the first 4 h of adipogenesis. Glucose 123-130 insulin Homo sapiens 104-111 28000288-1 2017 To investigate the impact of kidney transplantation (KTx) on insulin sensitivity affecting glucose metabolism. Glucose 91-98 insulin Homo sapiens 61-68 28000288-11 2017 In conclusion, insulin sensitivity is reduced 6 months after KTx and characterized mainly by impaired suppression of the endogenous glucose production. Glucose 132-139 insulin Homo sapiens 15-22 28235104-0 2017 Phase modulation of insulin pulses enhances glucose regulation and enables inter-islet synchronization. Glucose 44-51 insulin Homo sapiens 20-27 28235104-2 2017 The amplitude and phase (shape) of insulin secretion are modulated by numerous factors including glucose. Glucose 97-104 insulin Homo sapiens 35-42 28235104-5 2017 Here we asked how the phase modulation of insulin pulses contributes to glucose regulation. Glucose 72-79 insulin Homo sapiens 42-49 28235104-6 2017 To directly answer this question, we developed a phenomenological oscillator model that drastically simplifies insulin secretion, but precisely incorporates the observed phase modulation of insulin pulses in response to glucose stimuli. Glucose 220-227 insulin Homo sapiens 190-197 28235104-7 2017 Then, we mathematically modeled how insulin pulses regulate the glucose concentration in the body. Glucose 64-71 insulin Homo sapiens 36-43 28235104-9 2017 The data-based model demonstrates that the existence of phase modulation narrows the range within which the glucose concentration is maintained through the suppression/enhancement of insulin secretion in conjunction with the amplitude modulation of this secretion. Glucose 108-115 insulin Homo sapiens 183-190 28235104-12 2017 Thus, we conclude that the phase modulation of insulin pulses is essential for glucose regulation and inter-islet synchronization. Glucose 79-86 insulin Homo sapiens 47-54 28195217-1 2017 A 5-day High-Fat High-Calorie diet (HFHC-diet) reduces insulin-stimulated glucose disposal (Rd) in South Asian, but not Caucasian healthy lean males. Glucose 74-81 insulin Homo sapiens 55-62 28228847-5 2017 The three C-peptide parameters were independently associated with DPN (all P < 0.05) after adjusting for age, sex, diabetes duration, smoking status, systolic pressure, body mass index, angiotensin-converting enzyme inhibitors/angiotensin receptor blocker use, fasting plasma glucose, HbA1c, triglyceride and estimated glomerular filtration rate. Glucose 279-286 insulin Homo sapiens 10-19 28881687-0 2017 OGTT 1h serum C-peptide to plasma glucose concentration ratio is more related to beta cell function and diabetes mellitus. Glucose 34-41 insulin Homo sapiens 14-23 28228657-4 2017 Insulin sensitivity was measured by the glucose infusion rate during a hyperinsulinemic euglycemic clamp (80 mU m-2 min-1) at baseline and 10 and 30 days after HBOT sessions. Glucose 40-47 insulin Homo sapiens 0-7 28881687-6 2017 C-peptide index was calculated as the ratio of C-peptide to plasma glucose. Glucose 67-74 insulin Homo sapiens 0-9 28881687-13 2017 CONCLUSION: C-peptide index after oral glucose ingestion may reflect the maximal beta-cell function and is more related to diabetes. Glucose 39-46 insulin Homo sapiens 12-21 28179267-4 2017 Metabolically, obese women have increased insulin resistance in early pregnancy, which becomes manifest clinically in late gestation as glucose intolerance and fetal overgrowth. Glucose 136-143 insulin Homo sapiens 42-49 28132686-2 2017 The risk alleles impair glucose-induced insulin secretion and, paradoxically but characteristically, are associated with decreased proinsulin:insulin ratios, indicating improved proinsulin conversion. Glucose 24-31 insulin Homo sapiens 40-47 28178560-3 2017 (2016) generate insulin-producing cells from a somatic embryonic kidney cell line through minimal genetic modification capable of regulating glucose levels in diabetic mice. Glucose 141-148 insulin Homo sapiens 16-23 28032772-8 2017 Additionally, SPRA-insulin provided a prolonged and peakless blood glucose profile when compared with insulin glargine. Glucose 67-74 insulin Homo sapiens 19-26 28165405-6 2017 We measured plasma metabolites using proton nuclear magnetic resonance (1H-NMR) and insulin-dependent tissue-specific glucose uptake in skeletal muscle was assessed. Glucose 118-125 insulin Homo sapiens 84-91 27931981-5 2017 Whole-body insulin sensitivity (IS) was determined as glucose disposal rate during a euglycemic-hyperinsulinemic clamp. Glucose 54-61 insulin Homo sapiens 11-18 28135624-12 2017 CONCLUSIONS: Ethnicity modifies the predictive relationship between insulin and glucose with sub-clinical indicators of carotid atherosclerosis but not consistently so. Glucose 80-87 insulin Homo sapiens 68-75 26996519-5 2017 Moreover, fasting plasma glucose, waist-to-height ratio, wrist circumference and lower hip circumference were significantly associated with incident insulin resistance only among women (all P < 0.05). Glucose 25-32 insulin Homo sapiens 149-156 28357064-1 2017 In vivo insulin secretion is predominantly affected by blood glucose concentration, blood concentration of amino acids, gastrointestinal hormones and free nerve functional status, in addition to other factors. Glucose 61-68 insulin Homo sapiens 8-15 28182362-6 2017 The high level of FoxO 1FoxO 1 phosphorylation enhanced the TLR-4 signaling in response to LPS, and the FoxO FoxO 1 knockdown inhibited the insulin-induced glucose uptake in PCOS macrophages. Glucose 156-163 insulin Homo sapiens 140-147 28569662-2 2017 The most commonly prescribed insulin therapy for patients in long-term care is sliding-scale insulin (SSI): the use of finger-stick blood glucose testing to assess the need for insulin administration based on current blood glucose levels. Glucose 138-145 insulin Homo sapiens 29-36 28569662-2 2017 The most commonly prescribed insulin therapy for patients in long-term care is sliding-scale insulin (SSI): the use of finger-stick blood glucose testing to assess the need for insulin administration based on current blood glucose levels. Glucose 138-145 insulin Homo sapiens 93-100 28569662-2 2017 The most commonly prescribed insulin therapy for patients in long-term care is sliding-scale insulin (SSI): the use of finger-stick blood glucose testing to assess the need for insulin administration based on current blood glucose levels. Glucose 138-145 insulin Homo sapiens 93-100 27554476-5 2017 Oxytocin attenuated the peak excursion of plasma glucose and augmented the early increases in insulin and C-peptide concentrations in response to the glucose challenge, while slightly blunting insulin and C-peptide peaks. Glucose 150-157 insulin Homo sapiens 94-101 27709794-6 2017 Glucose (AUCglucose 319 +- 30 [placebo] vs 315 +- 18 mmol.L-1 .min-1 [sitagliptin], Delta 7 [95% confidence interval -50 to 63] mmol.L-1 .min-1 ), insulin, C-peptide and glucagon concentrations were not affected significantly by sitagliptin treatment ( P = .60-1.00). Glucose 0-7 insulin Homo sapiens 147-154 27709794-6 2017 Glucose (AUCglucose 319 +- 30 [placebo] vs 315 +- 18 mmol.L-1 .min-1 [sitagliptin], Delta 7 [95% confidence interval -50 to 63] mmol.L-1 .min-1 ), insulin, C-peptide and glucagon concentrations were not affected significantly by sitagliptin treatment ( P = .60-1.00). Glucose 0-7 insulin Homo sapiens 156-165 27761989-8 2017 Human islet beta-cells expressed FFAR2 and propionate potentiated dynamic glucose-stimulated insulin secretion in vitro, an effect that was dependent on signalling via protein kinase C. Propionate also protected human islets from apoptosis induced by the NEFA sodium palmitate and inflammatory cytokines. Glucose 74-81 insulin Homo sapiens 93-100 27761989-9 2017 CONCLUSIONS: Our results indicate that propionate has beneficial effects on beta-cell function in vivo, and in vitro analyses demonstrated that it has direct effects to potentiate glucose-stimulated insulin release and maintain beta-cell mass through inhibition of apoptosis. Glucose 180-187 insulin Homo sapiens 199-206 27796420-6 2017 In all type 2 diabetic donors, potential correlations of insulitis with dynamic glucose-stimulated insulin secretion in vitro or age, BMI, HbA1c or autoantibody positivity were examined. Glucose 80-87 insulin Homo sapiens 99-106 27807598-0 2017 Salt-inducible kinase 2 and -3 are downregulated in adipose tissue from obese or insulin-resistant individuals: implications for insulin signalling and glucose uptake in human adipocytes. Glucose 152-159 insulin Homo sapiens 81-88 27807598-11 2017 Silencing or inhibiting SIK1-3 in adipocytes results in reduced phosphorylation of HDAC4 and PKB/Akt, less GLUT4 at the plasma membrane, and lower basal and insulin-stimulated glucose uptake in adipocytes. Glucose 176-183 insulin Homo sapiens 157-164 28000140-17 2017 CONCLUSION: Flash glucose-sensing technology use in type 2 diabetes with intensive insulin therapy results in no difference in HbA1c change and reduced hypoglycemia, thus offering a safe, effective replacement for SMBG. Glucose 18-25 insulin Homo sapiens 83-90 28092788-10 2017 CONCLUSIONS: Pooled results from treat-to-target trials in insulin-naive people with type 2 diabetes demonstrate a significantly lower overall and nocturnal hypoglycaemia risk across different plasma glucose definitions with Gla-100 versus NPH insulin at similar glycaemic control. Glucose 200-207 insulin Homo sapiens 59-66 28118045-3 2017 Recent ICU recommendations suggest using insulin infusion protocols that can minimize glucose variability and hypoglycemic risk. Glucose 86-93 insulin Homo sapiens 41-48 27045210-0 2017 Hyperuricemia is associated with the increase of insulin release in non-obese subjects with normal glucose tolerance. Glucose 99-106 insulin Homo sapiens 49-56 27819771-2 2017 We describe the results of a peri-operative glycemic control program that standardized intravenous insulin with a target glucose (BG) range of 120 to 180 mg/dL for patients with diabetes presenting with a BG level >180 mg/dL and included transition to subcutaneous insulin. Glucose 121-128 insulin Homo sapiens 99-106 28270559-9 2017 BL at night was associated with significant increases in plasma glucose and insulin suggestive of glucose intolerance and insulin insensitivity. Glucose 98-105 insulin Homo sapiens 76-83 28025127-2 2017 Clinical data suggests that both type 1 and type 2 diabetes are risk factors for AD-related dementia and several clinical studies have demonstrated that AD patients show alterations in peripheral glucose regulation characterized by insulin resistance (hyperinsulinemia) or hypoinsulinemia. Glucose 196-203 insulin Homo sapiens 232-239 29231010-1 2017 Insulin as a common clinical hypoglycemic agent can effectively control serves to lower the concentration of blood glucose. Glucose 115-122 insulin Homo sapiens 0-7 28270515-3 2017 The marked heterogeneity long after maturation raises the prospect that diverse populations harbor distinct roles aside from glucose-stimulated insulin secretion. Glucose 125-132 insulin Homo sapiens 144-151 27926952-5 2017 Insulin sensitivity (Matsuda index) was calculated before and after the glucose load. Glucose 72-79 insulin Homo sapiens 0-7 27879196-10 2017 CONCLUSIONS: This real-world study shows that both in Poland and Germany treatment persistence of newly-prescribed basal insulin is influenced by type of insulin (analog vs. NPH) and by glucose-lowering and other comedications. Glucose 186-193 insulin Homo sapiens 121-128 28457028-1 2017 INSTRUCTION: Insulin is the oldest of the currently available treatment options in Type 2 diabetes mellitus (T2DM) and is considered as the most effective glucose lowering agent. Glucose 155-162 insulin Homo sapiens 13-20 28457028-10 2017 CONCLUSIONS: The consensus based recommendations mentioned in this paper will be a useful reference tool for health care practitioners, to initiate, optimise and intensify insulin therapy and to successfully achieve optimal glucose control. Glucose 224-231 insulin Homo sapiens 172-179 27404023-2 2017 Insulin is a crucial mediator of the glucose and lipid metabolism that has been implicated in atherosclerotic and inflammatory processes. Glucose 37-44 insulin Homo sapiens 0-7 27845180-4 2017 One aim was to explore predictors for the initiation of a basal insulin supported therapy in patients with type 2 diabetes initially prescribed to glucose-lowering drugs alone. Glucose 147-154 insulin Homo sapiens 64-71 28183563-14 2017 CONCLUSIONS: Our study shows that the percent of normal insulin dose given the evening before surgery directly impacts perioperative glucose levels in ambulatory surgery patients. Glucose 133-140 insulin Homo sapiens 56-63 28182362-4 2017 Then we investigated the influence of phosphorylation level of FoxO 1FoxO 1 on the induction of proinflammatory cytokines in the macrophages and the influence by FoxO FoxO 1 knockdown on the insulin-induced glucose uptake in PCOS macrophages. Glucose 207-214 insulin Homo sapiens 191-198 27904934-0 2017 Part-2: Analytical Expressions of Concentrations of Glucose, Oxygen, and Gluconic Acid in a Composite Membrane for Closed-Loop Insulin Delivery for the Non-steady State Conditions. Glucose 52-59 insulin Homo sapiens 127-134 27904934-7 2017 This predicted model is very much useful for designing the glucose-responsive composite membranes for closed-loop insulin delivery. Glucose 59-66 insulin Homo sapiens 114-121 27155940-0 2017 Modelling the effect of insulin on the disposal of meal-attributable glucose in type 1 diabetes. Glucose 69-76 insulin Homo sapiens 24-31 30615382-7 2017 To synthesize endogenous oleic mono unsaturated fatty acid the late in phylogenesis insulin expresses two enzymes of coupled biochemical reactions: palmitoyl-KoA-elongase andstearyl-KoA-desaturase, activating synthesis of fatty acids following the path glucose-endogenous palmitic unsaturated fatty acid-stearic unsaturated fatty acid-oleic mono unsaturated fatty acid. Glucose 253-260 insulin Homo sapiens 84-91 27155940-5 2017 Six compartmental models (all a priori identifiable) were proposed to investigate the remote effect of circulating plasma insulin on the disposal of those glucose tracers from the non-accessible compartments, representing e.g. interstitium. Glucose 155-162 insulin Homo sapiens 122-129 27155940-9 2017 Consequently, our mechanistic model suggests non-homogeneous changes in the disposal rates for meal-attributable glucose in relation to plasma insulin. Glucose 113-120 insulin Homo sapiens 143-150 27506476-0 2017 Casein glycomacropeptide-derived peptide IPPKKNQDKTE ameliorates high glucose-induced insulin resistance in HepG2 cells via activation of AMPK signaling. Glucose 70-77 insulin Homo sapiens 86-93 27991711-4 2017 A 2D finite element model of glucose transport was applied to predict glucose and insulin uptake in PP and fasting conditions using the same range of CD. Glucose 29-36 insulin Homo sapiens 82-89 27506476-4 2017 Effects of IPPKKNQDKTE on glucose metabolism and expression levels of the hepatic insulin signaling proteins in high glucose-induced insulin-resistant HepG2 cells were evaluated. Glucose 117-124 insulin Homo sapiens 82-89 27506476-5 2017 Results showed that IPPKKNQDKTE dose-dependently increased glucose uptake and intracellular glycogen in insulin-resistant HepG2 cells without affecting cell viability. Glucose 59-66 insulin Homo sapiens 104-111 27506476-10 2017 CONCLUSION: IPPKKNQDKTE prevents high glucose-induced insulin resistance in HepG2 cells by modulating the IRS-1/PI3K/Akt signaling pathway through AMPK activation, indicating that IPPKKNQDKTE plays a potential role in the prevention and treatment of hepatic insulin resistance and type 2 diabetes. Glucose 38-45 insulin Homo sapiens 54-61 28107204-1 2017 The most common method used for minimizing the occurrence of diabetes complications is frequent glucose testing to adjust the insulin dose. Glucose 96-103 insulin Homo sapiens 126-133 28000428-5 2017 RESULTS: Compared with the insulin-sensitive/overweight group, the insulin-sensitive/obesity had significantly higher insulin area under the curve (AUC) and ISR AUC during the graded-glucose infusion test (P < 0.001). Glucose 183-190 insulin Homo sapiens 67-74 28000428-5 2017 RESULTS: Compared with the insulin-sensitive/overweight group, the insulin-sensitive/obesity had significantly higher insulin area under the curve (AUC) and ISR AUC during the graded-glucose infusion test (P < 0.001). Glucose 183-190 insulin Homo sapiens 67-74 28000428-7 2017 The insulin-resistant/obesity group had higher insulin AUC and ISR AUC compared with the insulin-sensitive/obesity but also had higher glucose AUC and decreased ICR (P < 0.01). Glucose 135-142 insulin Homo sapiens 4-11 27749021-4 2017 The article by Karampatakis and colleagues in this week"s edition of the journal is important because it addresses the hypothesis that altered glucose metabolism/insulin resistance associates with bronchial hyperresponsiveness (BHR), a central and objectively measured marker of asthma. Glucose 143-150 insulin Homo sapiens 162-169 28025104-0 2017 Adrenoceptors promote glucose uptake into adipocytes and muscle by an insulin-independent signaling pathway involving mechanistic target of rapamycin complex 2. Glucose 22-29 insulin Homo sapiens 70-77 28025104-2 2017 Insulin released from beta-islet cells of the pancreas promotes glucose uptake in these target tissues by stimulating translocation of GLUT4 transporters to the cell surface. Glucose 64-71 insulin Homo sapiens 0-7 28025104-9 2017 The identification of insulin-independent mechanisms that promote glucose uptake should facilitate novel treatment strategies for metabolic disease. Glucose 66-73 insulin Homo sapiens 22-29 28952262-5 2017 The results showed that piperine, rosiglitazone and AMPK agonist AICAR could significantly elevate the glucose consumption in insulin resistance cell models, enhance the level of APN, promote APN mRNA transcripts and increase the protein expression of Adipo receptor. Glucose 103-110 insulin Homo sapiens 126-133 28242817-1 2017 The oral disposition index, the product of the early insulin secretory response during an oral glucose tolerance test and insulin sensitivity, is used widely for both the prediction of, and evaluation of the response to interventions, in type 2 diabetes. Glucose 95-102 insulin Homo sapiens 53-60 28242817-7 2017 The early insulin secretory response was estimated by the ratio of the change in insulin ( I0-30) to that of glucose at 30 min ( G0-30) represented as I0-30/ G0-30 Insulin sensitivity was estimated as 1/fasting insulin and the DI was then calculated as I0-30/ G0-30 x 1/fasting insulin. Glucose 109-116 insulin Homo sapiens 10-17 27955719-0 2017 Promotion of glucose utilization by insulin enhances granulosa cell proliferation and developmental competence of porcine oocyte grown in vitro. Glucose 13-20 insulin Homo sapiens 36-43 27955719-3 2017 GC proliferation depends on glycolysis and insulin-mediated AKT/mTOR signaling pathway; therefore, addition of culture medium containing insulin and glucose may potentially promote GC proliferation and hence improve oocyte development. Glucose 149-156 insulin Homo sapiens 43-50 27955719-5 2017 In the presence of 5.5 mM of glucose (Low), a comparison of 10 versus 20 mug/ml insulin showed that high insulin enhanced GC proliferation but exhausted glucose from the medium, which resulted in low energy status including lipid and adenosine triphosphate of the oocyte. Glucose 29-36 insulin Homo sapiens 80-87 27955719-5 2017 In the presence of 5.5 mM of glucose (Low), a comparison of 10 versus 20 mug/ml insulin showed that high insulin enhanced GC proliferation but exhausted glucose from the medium, which resulted in low energy status including lipid and adenosine triphosphate of the oocyte. Glucose 29-36 insulin Homo sapiens 105-112 27955719-6 2017 Whereas, in the presence of 20 mug/ml insulin, medium with 11 mM glucose (High) enhanced GC proliferation and oocyte energy status as well as developmental ability up to the blastocyst stage. Glucose 65-72 insulin Homo sapiens 38-45 28017719-5 2017 Simultaneously, miR-217 repression restored HG-disrupted insulin resistance by elevating glucose uptake and nephrin expression, an essential component for insulin-induced glucose uptake. Glucose 89-96 insulin Homo sapiens 57-64 27725372-0 2017 Diagnosis of insulinoma using the ratios of serum concentrations of insulin and C-peptide to glucose during a 5-hour oral glucose tolerance test. Glucose 93-100 insulin Homo sapiens 13-20 27725372-0 2017 Diagnosis of insulinoma using the ratios of serum concentrations of insulin and C-peptide to glucose during a 5-hour oral glucose tolerance test. Glucose 122-129 insulin Homo sapiens 13-20 27725372-9 2017 Subjects with insulinoma had significantly different insulin-to-glucose and C-peptide-to-glucose ratios from reactive hypoglycemia at the times of fasting, 4-hour post glucose load and 5-hour post glucose load. Glucose 89-96 insulin Homo sapiens 76-85 27725372-9 2017 Subjects with insulinoma had significantly different insulin-to-glucose and C-peptide-to-glucose ratios from reactive hypoglycemia at the times of fasting, 4-hour post glucose load and 5-hour post glucose load. Glucose 89-96 insulin Homo sapiens 76-85 28017719-5 2017 Simultaneously, miR-217 repression restored HG-disrupted insulin resistance by elevating glucose uptake and nephrin expression, an essential component for insulin-induced glucose uptake. Glucose 171-178 insulin Homo sapiens 155-162 28007348-7 2017 Autonomously adaptive dosing algorithms used data from a continuous glucose monitor to control subcutaneous delivery of insulin and glucagon. Glucose 68-75 insulin Homo sapiens 120-127 27983846-2 2017 In cellular assays, 13 and 14 inhibited Wnt-signaling, enhanced insulin-stimulated glucose uptake, and inhibited the proliferation of DLD-1 colorectal adenocarcinoma cells to a greater extent than 1. Glucose 83-90 insulin Homo sapiens 64-71 28051306-4 2017 The polymeric vesicles function as both moieties of the glucose sensing element (GOx) and the insulin release actuator to provide basal insulin release as well as promote insulin release in response to hyperglycemic states. Glucose 56-63 insulin Homo sapiens 136-143 28051306-4 2017 The polymeric vesicles function as both moieties of the glucose sensing element (GOx) and the insulin release actuator to provide basal insulin release as well as promote insulin release in response to hyperglycemic states. Glucose 56-63 insulin Homo sapiens 136-143 28051306-5 2017 In the current study, insulin release responds quickly to elevated glucose and its kinetics can be modulated by adjusting the concentration of GOx loaded into the microneedles. Glucose 67-74 insulin Homo sapiens 22-29 28118454-2 2017 Objective: To evaluate the effects of continuous glucose monitoring in adults with type 1 diabetes treated with multiple daily insulin injections. Glucose 49-56 insulin Homo sapiens 127-134 28118454-13 2017 Conclusions and Relevance: Among patients with inadequately controlled type 1 diabetes treated with multiple daily insulin injections, the use of continuous glucose monitoring compared with conventional treatment for 26 weeks resulted in lower HbA1c. Glucose 157-164 insulin Homo sapiens 115-122 30603317-4 2017 Beta cells have been assigned the important task of secreting insulin when blood glucose is increased to lower the glucose level. Glucose 81-88 insulin Homo sapiens 62-69 30603317-4 2017 Beta cells have been assigned the important task of secreting insulin when blood glucose is increased to lower the glucose level. Glucose 115-122 insulin Homo sapiens 62-69 28108466-0 2017 Post-Glucose Load Measures of Insulin Resistance and Prognosis of Nondiabetic Patients With Ischemic Stroke. Glucose 5-12 insulin Homo sapiens 30-37 28108466-2 2017 This study aimed to estimate the association between post-glucose load measures of insulin resistance and prognosis of nondiabetic patients with ischemic stroke. Glucose 58-65 insulin Homo sapiens 83-90 28108466-12 2017 CONCLUSIONS: In this large-scale registry, post-glucose load measures of insulin resistance with the ISI(composite) and the ISI0,120 were associated with 12-month poor outcomes of nondiabetic patients with ischemic stroke. Glucose 48-55 insulin Homo sapiens 73-80 27871946-8 2017 Trivaric acid also enhanced the ability of insulin to stimulate the IR/IRS/Akt/GLUT2 pathway and increase the glucose consumption in HepG2 cells. Glucose 110-117 insulin Homo sapiens 43-50 28098809-7 2017 CGM with automated insulin infusion improved time in target and mean glucose in one trial and two trials showed a decrease in hypoglycemic episodes and time in hypoglycemia. Glucose 69-76 insulin Homo sapiens 19-26 28123396-1 2016 Pancreatic beta-cells regulate glucose metabolism by secreting insulin, which in turn stimulates the utilization or storage of the sugar by peripheral tissues. Glucose 31-38 insulin Homo sapiens 63-70 28458724-2 2017 The ability to measure dynamic changes in insulin levels upon glucose stimulation from single islets will allow testing of therapeutics and investigating mechanisms of defective secretion observed in metabolic diseases. Glucose 62-69 insulin Homo sapiens 42-49 28458724-9 2017 The capability of this system for measuring insulin secretion from single islets was shown by stimulating an islet with varying glucose levels. Glucose 128-135 insulin Homo sapiens 44-51 28060898-0 2017 Proportional Insulin Infusion in Closed-Loop Control of Blood Glucose. Glucose 62-69 insulin Homo sapiens 13-20 28060898-2 2017 The model accounts for the intake of food, expenditure of calories and the control of glucose levels by insulin and glucagon. Glucose 86-93 insulin Homo sapiens 104-111 28060898-6 2017 Feedback provided by insulin plays a key role in the control of the blood glucose level. Glucose 74-81 insulin Homo sapiens 21-28 27566229-4 2017 Insulin secretory response to 20 mM glucose was attenuated after 7 days in islets exposed to palmitate but inclusion of exendin-4 restored secretion. Glucose 36-43 insulin Homo sapiens 0-7 28045398-2 2017 Under normal conditions, skeletal muscle is responsible for the majority of insulin-stimulated whole-body glucose disposal; thus, dysregulation of skeletal muscle metabolism can strongly influence whole-body glucose homeostasis and insulin sensitivity. Glucose 106-113 insulin Homo sapiens 76-83 27624579-2 2017 Islet amyloid polypeptide (IAPP) is co-secreted with insulin, but its secretion profile and relationship to insulin and C-peptide in response to glucose and non-glucose stimuli has not been clearly defined. Glucose 145-152 insulin Homo sapiens 120-129 27759899-4 2017 The homoeostatic model assessment of insulin resistance (HOMA-IR) was calculated from 12-hour fasting plasma glucose and serum insulin at eight-and-a-half years of age. Glucose 109-116 insulin Homo sapiens 37-44 28551803-2 2017 Insulin resistance contributes to multiple tissue defects characteristic of T2D, including reduced insulin-stimulated glucose uptake in insulin-sensitive tissues, increased hepatic glucose production, increased lipolysis in adipose tissue, and altered insulin secretion. Glucose 118-125 insulin Homo sapiens 0-7 28551803-2 2017 Insulin resistance contributes to multiple tissue defects characteristic of T2D, including reduced insulin-stimulated glucose uptake in insulin-sensitive tissues, increased hepatic glucose production, increased lipolysis in adipose tissue, and altered insulin secretion. Glucose 118-125 insulin Homo sapiens 99-106 28551803-2 2017 Insulin resistance contributes to multiple tissue defects characteristic of T2D, including reduced insulin-stimulated glucose uptake in insulin-sensitive tissues, increased hepatic glucose production, increased lipolysis in adipose tissue, and altered insulin secretion. Glucose 118-125 insulin Homo sapiens 136-143 28551803-2 2017 Insulin resistance contributes to multiple tissue defects characteristic of T2D, including reduced insulin-stimulated glucose uptake in insulin-sensitive tissues, increased hepatic glucose production, increased lipolysis in adipose tissue, and altered insulin secretion. Glucose 181-188 insulin Homo sapiens 0-7 28933059-1 2017 Adipose tissue is an endocrine organ which is responsible for postprandial uptake of glucose and fatty acids, consequently producing a broad range of adipokines controlling several physiological functions like appetite, insulin sensitivity and secretion, immunity, coagulation, and vascular tone, among others. Glucose 85-92 insulin Homo sapiens 220-227 27458792-7 2017 The predicted target genes (e.g. Irs2, Pik3r1, Akt2, and Gsk3b) were involved in glucose import and the insulin signaling pathway. Glucose 81-88 insulin Homo sapiens 104-111 28035081-1 2017 Insulin resistance is characterized by the reduced ability of insulin to stimulate tissue uptake and disposal of glucose including cardiac muscle. Glucose 113-120 insulin Homo sapiens 0-7 28035081-1 2017 Insulin resistance is characterized by the reduced ability of insulin to stimulate tissue uptake and disposal of glucose including cardiac muscle. Glucose 113-120 insulin Homo sapiens 62-69 28584815-7 2017 The release of insulin and c-peptide in response to a glucose challenge was also quantitated. Glucose 54-61 insulin Homo sapiens 15-22 28584815-7 2017 The release of insulin and c-peptide in response to a glucose challenge was also quantitated. Glucose 54-61 insulin Homo sapiens 27-36 28392373-5 2017 Systemic glucose metabolism was examined by concentrations of circulating glucose and insulin. Glucose 9-16 insulin Homo sapiens 86-93 28392373-11 2017 CONCLUSIONS: Our data confirm that tDCS reduces blood glucose through an insulin-independent mechanism. Glucose 54-61 insulin Homo sapiens 73-80 29186709-0 2017 Dynamic Profiling of Insulin Secretion and ATP Generation in Isolated Human and Mouse Islets Reveals Differential Glucose Sensitivity. Glucose 114-121 insulin Homo sapiens 21-28 29186709-8 2017 CONCLUSION: The high affinity of GLUT1/3 for glucose reflects the left-shifted glucose-induced insulin secretory response of human islets and the impairment of insulin secretion from human islets after STF-31 treatment indicates an important role for GLUT1 in human islet stimulus-secretion coupling. Glucose 45-52 insulin Homo sapiens 95-102 29186709-8 2017 CONCLUSION: The high affinity of GLUT1/3 for glucose reflects the left-shifted glucose-induced insulin secretory response of human islets and the impairment of insulin secretion from human islets after STF-31 treatment indicates an important role for GLUT1 in human islet stimulus-secretion coupling. Glucose 79-86 insulin Homo sapiens 95-102 27797410-1 2017 Skeletal muscle is an important site for insulin to regulate blood glucose levels. Glucose 67-74 insulin Homo sapiens 41-48 27797410-2 2017 It is estimated that skeletal muscle is responsible for ~80% of insulin-mediated glucose disposal in the post-prandial period. Glucose 81-88 insulin Homo sapiens 64-71 27797410-3 2017 The classical action of insulin to increase muscle glucose uptake involves insulin binding to insulin receptors on myocytes to stimulate glucose transporter 4 (GLUT 4) translocation to the cell surface membrane, enhancing glucose uptake. Glucose 51-58 insulin Homo sapiens 24-31 27797410-4 2017 However, an additional role of insulin that is often under-appreciated is its action to increase muscle perfusion thereby improving insulin and glucose delivery to myocytes. Glucose 144-151 insulin Homo sapiens 31-38 27908300-5 2017 Insulin sensitivity index (ISI) was calculated with the equation proposed by Matsuda et al., from dynamic values of glucose and insulin obtained during OGTT. Glucose 116-123 insulin Homo sapiens 0-7 28077204-2 2017 Although oral agents (i.e., metformin) are the preferred first-line therapy, older adults often eventually require the addition of insulin to control their blood glucose. Glucose 162-169 insulin Homo sapiens 131-138 28077204-5 2017 When compared with the standard of care, long-acting insulin product insulin glargine U-100, insulin degludec, and insulin glargine U-300 had similar glucose-lowering effects, longer half-lives and durations of action, and a more even distribution over a 24-hour period. Glucose 150-157 insulin Homo sapiens 53-60 28436331-10 2017 Both leptin and insulin regulate appetite, body weight, and glucose levels in the body. Glucose 60-67 insulin Homo sapiens 16-23 26648072-3 2017 A hallmark of T2DM is failure of insulin secretion from pancreatic beta-cell to regulate blood glucose disposal into peripheral tissues, such as skeletal muscle, termed insulin resistance, as well as deregulation of pancreatic alpha-cell function. Glucose 95-102 insulin Homo sapiens 33-40 28462703-7 2017 The presence of IRS2 in skeletal muscle is negligible for insulin-induced glucose uptake and the general role of IRS2 in muscle is still not fully understood. Glucose 74-81 insulin Homo sapiens 58-65 27981906-6 2017 Six months of locomotor training in individuals with SCI resulted in significant decreases in glucose (15%) and insulin (33%) areas under the curve during oral glucose tolerance tests. Glucose 160-167 insulin Homo sapiens 112-119 28120721-4 2017 Progranulin impairs insulin signaling and reduces insulin-induced glucose uptake both in vitro and in vivo whereas progranulin deficiency protects from high fat diet-induced insulin resistance. Glucose 66-73 insulin Homo sapiens 50-57 28128062-1 2017 BACKGROUND: Type-2 Diabetes is a long lasting disease characterized by high glucose concentration in the blood due to insulin resistance. Glucose 76-83 insulin Homo sapiens 118-125 27887844-4 2017 Using the fluorescent tagged glucose analogues, 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxy-D-glucose (2-NBDG), insulin mimetics were screened with compounds 1-19 in 3T3-L1 adipocytes. Glucose 29-36 insulin Homo sapiens 123-130 27887844-6 2017 Taken together, these anthraquinones showed the potential action as insulin mimetic to improve glucose uptake via activation of AMPK. Glucose 95-102 insulin Homo sapiens 68-75 28641547-1 2017 BACKGROUND: Insulin resistance is a pathological condition characterized by the failure of target cells to uptake and metabolize glucose in response to insulin. Glucose 129-136 insulin Homo sapiens 12-19 28641547-1 2017 BACKGROUND: Insulin resistance is a pathological condition characterized by the failure of target cells to uptake and metabolize glucose in response to insulin. Glucose 129-136 insulin Homo sapiens 152-159 28677502-3 2017 Insulin controls energy storage and the whole body glucose homeostasis. Glucose 51-58 insulin Homo sapiens 0-7 28055230-1 2017 BACKGROUND: Faster aspart is insulin aspart (IAsp) in a new formulation, which in continuous subcutaneous insulin infusion (CSII) in subjects with type 1 diabetes has shown a faster onset and offset of glucose-lowering effect than IAsp. Glucose 202-209 insulin Homo sapiens 29-36 28055230-1 2017 BACKGROUND: Faster aspart is insulin aspart (IAsp) in a new formulation, which in continuous subcutaneous insulin infusion (CSII) in subjects with type 1 diabetes has shown a faster onset and offset of glucose-lowering effect than IAsp. Glucose 202-209 insulin Homo sapiens 106-113 33834090-4 2017 Many components of insulin signaling pathways associated with glucose metabolic regulation have been evaluated in IUGR tissues for adaptive changes. Glucose 62-69 insulin Homo sapiens 19-26 33834090-6 2017 However, recent findings demonstrate that beta2 adrenoceptors (beta2AR) appear to activate an insulin-independent pathway or pathways that modify glucose metabolism via mTORC1/2 complexes. Glucose 146-153 insulin Homo sapiens 94-101 27605038-6 2017 Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin. Glucose 48-55 insulin Homo sapiens 0-7 27605038-8 2017 These changes, combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test, explained 63 % of the variance (p < 0.0001) in insulin sensitivity improvements. Glucose 42-49 insulin Homo sapiens 60-67 28819951-8 2017 The blood glucose-lowering effect of the drug is a consequence of hepatic glucose production inhibition, and of peripheral tissue (muscle tissue, fatty tissue) sensitisation to the effect of insulin of both endogenous and exogenous origin. Glucose 10-17 insulin Homo sapiens 191-198 29168546-2 2017 They counteract insulin by decreasing peripheral glucose uptake and stimulating hepatic gluconeogenesis, although they are best known for inducing insulin resistance (IR). Glucose 49-56 insulin Homo sapiens 16-23 29168546-7 2017 Although their insulin levels are elevated, they present lower insulin output in response to glucose than obese individuals. Glucose 93-100 insulin Homo sapiens 63-70 27826704-11 2017 Insulin resistance reflecting a high glucose and insulin condition resulted in higher IP-10 mRNA expression in the monocyte cell line only with concomitant TLR-2 stimulation. Glucose 37-44 insulin Homo sapiens 0-7 28372488-2 2017 To address this issue, we evaluated insulin sensitivity and secretion in patients with sickle cell disease (SCD) and normal oral glucose tolerance test (OGTT). Glucose 129-136 insulin Homo sapiens 36-43 28391281-4 2017 METHODS: We performed a cohort study of 153 severely obese children and adolescents evaluated with a 5-point OGTT at baseline and at follow-up with measurements of glucose, insulin, and C-peptide to estimate several empirical parameters of insulin sensitivity (includ ing oral glucose insulin sensitivity [OGIS] and OGTT-derived glucose effectiveness) and secretion. Glucose 277-284 insulin Homo sapiens 240-247 28880188-2 2017 The AP encompasses an algorithm that determines the amount of insulin (and other hormones) to be administered to the patient via a continuous subcutaneous insulin infusion pump using information provided by a continuous glucose monitor and other sensors. Glucose 220-227 insulin Homo sapiens 62-69 28855921-2 2017 Insulin, the only glucose lowering hormone secreted from pancreatic beta-cells, plays the key role in glucose homeostasis. Glucose 18-25 insulin Homo sapiens 0-7 27719550-5 2017 The release of insulin from the nanoparticles slowed down because of the presence of disulfide bonds and increased with increasing glucose level in the medium. Glucose 131-138 insulin Homo sapiens 15-22 27719550-8 2017 The simplicity of this strategy along with a high loading capacity, glucose sensitivity, and cytocompatibility of the produced nanoparticles should significantly boost their application in self-regulated insulin delivery. Glucose 68-75 insulin Homo sapiens 204-211 27778639-11 2017 Hyperglycemic clamp revealed increased glucose-stimulated insulin secretion and insulin resistance. Glucose 39-46 insulin Homo sapiens 58-65 27778640-10 2017 Conclusions: Matched for pubertal stage, PCOS daughters have similar levels of urinary androgens and gonadotropins as well as glucose-challenged salivary insulin levels. Glucose 126-133 insulin Homo sapiens 154-161 27809652-0 2017 Liver Fat and Insulin Sensitivity Define Metabolite Profiles During a Glucose Tolerance Test in Young Adult Twins. Glucose 70-77 insulin Homo sapiens 14-21 27184687-8 2017 Importantly, rats that maintained mild hyperglycemia showed nearly normal glucose-stimulated insulin secretion, glucose disposal and random blood glucose levels, suggesting almost full restoration of the islet function. Glucose 74-81 insulin Homo sapiens 93-100 27240324-10 2017 Insulin was released in response to glucose stimulation in a manner similar to that of adult human islets. Glucose 36-43 insulin Homo sapiens 0-7 26862136-1 2017 BACKGROUND: Insulin bolus calculators assist people with Type 1 diabetes (T1D) to calculate the amount of insulin required for meals to achieve optimal glucose levels but lack adaptability and personalization. Glucose 152-159 insulin Homo sapiens 12-19 26862136-1 2017 BACKGROUND: Insulin bolus calculators assist people with Type 1 diabetes (T1D) to calculate the amount of insulin required for meals to achieve optimal glucose levels but lack adaptability and personalization. Glucose 152-159 insulin Homo sapiens 106-113 26862136-11 2017 CONCLUSIONS: Results from the 6-week study indicate the potential benefit of including parameters exercise, alcohol and glucose-rate of change for insulin dosing decision support. Glucose 120-127 insulin Homo sapiens 147-154 27170635-0 2017 Personal Insulin Pump With Predictive Low Glucose Management Technology at High Altitude. Glucose 42-49 insulin Homo sapiens 9-16 27189155-3 2017 Insulin-pump therapy was first introduced in the 1970s as an approach to mimic physiological insulin delivery and attain normal glucose in patients with type 1 diabetes. Glucose 128-135 insulin Homo sapiens 0-7 27495225-5 2017 Fasting proinsulin-to-C-peptide and proinsulin secretory ratios during glucose potentiation were higher in PI-CF, suggesting impaired proinsulin processing. Glucose 71-78 insulin Homo sapiens 8-18 27495225-5 2017 Fasting proinsulin-to-C-peptide and proinsulin secretory ratios during glucose potentiation were higher in PI-CF, suggesting impaired proinsulin processing. Glucose 71-78 insulin Homo sapiens 36-46 27495225-5 2017 Fasting proinsulin-to-C-peptide and proinsulin secretory ratios during glucose potentiation were higher in PI-CF, suggesting impaired proinsulin processing. Glucose 71-78 insulin Homo sapiens 36-46 27501510-7 2017 Dose-dependent increases in fasting plasma glucagon were observed, but glucagon levels decreased and insulin levels increased after an oral glucose load in T2DM subjects. Glucose 140-147 insulin Homo sapiens 101-108 27569727-0 2017 Glucose variability indices predict the episodes of nocturnal hypoglycemia in elderly type 2 diabetic patients treated with insulin. Glucose 0-7 insulin Homo sapiens 124-131 27593206-2 2017 Several mechanisms of protraction have been used in pursuit of a basal insulin, for which a low injection frequency would provide tolerable and reproducible glucose control; these mechanisms have met with varying degrees of success. Glucose 157-164 insulin Homo sapiens 71-78 27593206-7 2017 Newer basal insulin analogues have used up-concentration in addition to precipitation (insulin glargine U300), and multihexamer formation in addition to albumin binding (insulin degludec), to further increase duration of action and/or decrease the day-to-day variability of the glucose-lowering profile. Glucose 278-285 insulin Homo sapiens 12-19 28264177-2 2017 The aim of the study was to determine the impact of the expert system, supporting the patient"s decision on meal bolus programming, on the time in range of diurnal glucose excursion in patients treated with continuous subcutaneous insulin infusion (CSII). Glucose 164-171 insulin Homo sapiens 231-238 28264177-10 2017 CONCLUSION: The expert system in meal insulin dosing allows improvement in glucose control without increasing the rates of hypoglycemia or the insulin requirement. Glucose 75-82 insulin Homo sapiens 38-45 28286777-0 2017 Effect of Human Myotubes-Derived Media on Glucose-Stimulated Insulin Secretion. Glucose 42-49 insulin Homo sapiens 61-68 28286777-1 2017 Fasting to postprandial transition requires a tight adjustment of insulin secretion to its demand, so tissue (e.g., skeletal muscle) glucose supply is assured while hypo-/hyperglycemia are prevented. Glucose 133-140 insulin Homo sapiens 66-73 28286777-2 2017 High muscle glucose disposal after meals is pivotal for adapting to increased glycemia and might drive insulin secretion through muscle-released factors (e.g., myokines). Glucose 12-19 insulin Homo sapiens 103-110 28286777-3 2017 We hypothesized that insulin influences myokine secretion and then increases glucose-stimulated insulin secretion (GSIS). Glucose 77-84 insulin Homo sapiens 21-28 28286777-3 2017 We hypothesized that insulin influences myokine secretion and then increases glucose-stimulated insulin secretion (GSIS). Glucose 77-84 insulin Homo sapiens 96-103 28367451-5 2017 In addition, we will discuss how membrane cholesterol levels affect glucose transport by modulating the insertion into the membrane of the main insulin-sensitive glucose transporter GLUT4. Glucose 68-75 insulin Homo sapiens 144-151 28428964-1 2017 The solute carrier family 2 facilitated glucose transporter member 4 (GLUT4) plays a key role in the insulin-induced glucose uptake by muscle and adipose tissues. Glucose 40-47 insulin Homo sapiens 101-108 28491872-10 2017 Independent risk factors for glucose intolerance were FPG >= 100 at the time of OGTT (OR 3.86; 95% CI; 1.60-9.32), earlier diagnosis of GDM (OR 0.92; 95% CI; 0.88-0.97), systolic blood pressure (OR 1.02; 95% CI; 1.002-1.04), and insulin or metformin therapy (OR 3.14; 95% CI; 1.20-8.21). Glucose 29-36 insulin Homo sapiens 232-239 28529958-1 2017 Insulin increases glucose uptake and storage in muscle and adipose cells, which is accomplished through the mobilization of intracellular GLUT4 storage vesicles (GSVs) to the cell surface upon stimulation. Glucose 18-25 insulin Homo sapiens 0-7 28913363-1 2017 AIM: To find the association between biochemical hypoglycemia on a 2-hour screening oral glucose tolerance test (OGTT) and insulin resistance. Glucose 89-96 insulin Homo sapiens 123-130 29201919-0 2017 Dynamics of Insulin Secretion from EndoC-betaH1 beta-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues. Glucose 86-93 insulin Homo sapiens 12-19 29201919-5 2017 The dynamics of insulin secretion from EndoC-betaH1 pseudoislets were characterized by an insulin secretory response to glucose starting within 1-2 min and passing over without interruption into a sustained phase of insulin release for the whole stimulation period. Glucose 120-127 insulin Homo sapiens 16-23 29201919-5 2017 The dynamics of insulin secretion from EndoC-betaH1 pseudoislets were characterized by an insulin secretory response to glucose starting within 1-2 min and passing over without interruption into a sustained phase of insulin release for the whole stimulation period. Glucose 120-127 insulin Homo sapiens 90-97 32691008-2 2017 Objective: We assessed the relationship between self-reported disinhibition scores and insulin resistance assessed during an oral glucose tolerance test (OGTT). Glucose 130-137 insulin Homo sapiens 87-94 27306986-5 2017 However, C-peptide signalling in this cell type appears to depend at least in part on extracellular glucose concentration and its interaction with insulin. Glucose 100-107 insulin Homo sapiens 9-18 29332906-4 2017 By targeting this nuclear factor, pharmacological or nutraceutical induction of AREBP gene expression is expected to reduce blood glucose levels in patient with insulin resistance. Glucose 130-137 insulin Homo sapiens 161-168 24737702-4 2017 Newly formed pseudo-islets were analysed for dimensions, morphology, glucose-stimulated insulin secretion (GSIS) and total insulin content. Glucose 69-76 insulin Homo sapiens 88-95 30840368-4 2017 The biological role of insulin consists in regulation of metabolism of fatty acids mainly unesterified fatty acids and in absorption of glucose by all insulin-dependent cells. Glucose 136-143 insulin Homo sapiens 23-30 30840368-4 2017 The biological role of insulin consists in regulation of metabolism of fatty acids mainly unesterified fatty acids and in absorption of glucose by all insulin-dependent cells. Glucose 136-143 insulin Homo sapiens 151-158 30840368-10 2017 At the late stages of phylogenesis, under becoming of biological function of locomotion (motion at the expense of contraction of cross-striated skeletal myocytes) insulin began to activate absorption of glucose by cells with subsequent synthesis of endogenous omega-9 oleic mono-saturated fatty acid out of it. Glucose 203-210 insulin Homo sapiens 163-170 31509656-13 2017 The concentration of proinsulin at the stage of decompensation positively correlated with level of glucose and concentration of triglycerides. Glucose 99-106 insulin Homo sapiens 21-31 27770892-3 2017 The insulin release behaviors were evaluated triggered by pH and glucose in vitro. Glucose 65-72 insulin Homo sapiens 4-11 28072690-0 2017 Comparison of jet injector and insulin pen in controlling plasma glucose and insulin concentrations in type 2 diabetic patients. Glucose 65-72 insulin Homo sapiens 31-38 28072690-9 2017 Efficacy of the insulin jet injector in treatment of type 2 diabetic patients is obviously superior to the insulin pen in regulating plasma glucose and insulin levels. Glucose 140-147 insulin Homo sapiens 16-23 28072690-9 2017 Efficacy of the insulin jet injector in treatment of type 2 diabetic patients is obviously superior to the insulin pen in regulating plasma glucose and insulin levels. Glucose 140-147 insulin Homo sapiens 107-114 28072690-9 2017 Efficacy of the insulin jet injector in treatment of type 2 diabetic patients is obviously superior to the insulin pen in regulating plasma glucose and insulin levels. Glucose 140-147 insulin Homo sapiens 107-114 28122381-6 2017 In addition, this review highlights insulin transport into the brain, signaling pathways associated with hypothalamic insulin receptor expression in the regulation of hepatic glucose production, and finally the perturbation of systemic glucose homeostasis as a consequence of central insulin resistance. Glucose 175-182 insulin Homo sapiens 118-125 27925416-6 2017 Moreover, the variant had a remarkable correlation with abdominal visceral fat area (P = 0.004) and was associated with 2-h plasma insulin (P = 0.009) and the Matsuda index (P = 0.027) after an oral glucose tolerance test in young subjects with obesity. Glucose 199-206 insulin Homo sapiens 131-138 27896979-3 2017 To test this hypothesis, single nucleotide polymorphisms (SNPs) nominally associated with acute insulin response to glucose (AIRg), a dynamic measure of first-phase insulin secretion, and previously associated with T2D in genome-wide association studies (GWAS) were identified in African Americans from the Insulin Resistance Atherosclerosis Family Study (IRASFS; n=492 subjects). Glucose 116-123 insulin Homo sapiens 96-103 29422987-1 2017 Insulin-like growth factor binding protein-2 (IGFBP-2) is the predominant IGF binding protein produced during adipogenesis and is known to increase the insulin-stimulated glucose uptake (GU) in myotubes. Glucose 171-178 insulin Homo sapiens 152-159 29253032-2 2017 AIM OF STUDY: The aim of the present study was to evaluate the association between MetS and estimates of insulin sensitivity and beta-cell function obtained from oral glucose tolerance test (OGTT)-derived indices in lean and obese children. Glucose 167-174 insulin Homo sapiens 105-112 29253032-9 2017 CONCLUSIONS: Children burdened by the accumulation of components of MetS exhibited a disturbed glucose metabolism as expressed by lowered peripheral insulin sensitivity and beta-cell function. Glucose 95-102 insulin Homo sapiens 149-156 29574469-3 2017 The literature data indicate that not only disturbed glucose concentration, especially hyperglycemia, is a crucial factor of the development of dementia but those data also emphasize that hyperphysiological concentrations of insulin and insulin resistance of brain tissue is an increasingly significant factor. Glucose 53-60 insulin Homo sapiens 225-232 29574469-3 2017 The literature data indicate that not only disturbed glucose concentration, especially hyperglycemia, is a crucial factor of the development of dementia but those data also emphasize that hyperphysiological concentrations of insulin and insulin resistance of brain tissue is an increasingly significant factor. Glucose 53-60 insulin Homo sapiens 237-244 29574469-4 2017 The aim of this study was to evaluate the influence of glucose and insulin concentration reached in human carbohydrate metabolism disorders such as i.e. impaired fasting glucose, impaired glucose tolerance and diabetes state as well as averageand high degree hyperinsulinemia, on the survival of PC12 cell line. Glucose 170-177 insulin Homo sapiens 67-74 27630249-2 2017 If approved, this claim will allow users to make day-to-day treatment decisions, including insulin dosing directly from the glucose values and rate of changes arrows generated by the CGM device, without the requirement of a confirmatory measurement with a self-monitoring blood glucose (SMBG) meter. Glucose 124-131 insulin Homo sapiens 91-98 28042862-4 2016 Some studies suggest that H2S inhibits insulin-induced glucose uptake and that excess of H2S contributes to adipose tissue insulin resistance in metabolic syndrome. Glucose 55-62 insulin Homo sapiens 39-46 29799179-3 2017 We assessed clinical and biochemical characteristics and determined insulin resistance through estimated glucose dispose rate (eGDR). Glucose 105-112 insulin Homo sapiens 68-75 30035393-10 2017 Neonate`s serum glucose correlated positively with insulin levels (r= 0.3, p=0.006) and HOMA-IR (r= 0.6, p < 0.0001); and negatively with HOMA-S (r= -0.6, p < 0.0001) and QUICKI (r= -0.5, p < 0.0001). Glucose 16-23 insulin Homo sapiens 51-58 28334539-2 2017 Current national and international guidelines list insulin treatment as a possible second choice therapy in patient with unsatisfactory glucose control on monotherapy with metformin. Glucose 136-143 insulin Homo sapiens 51-58 27647480-7 2016 Insulin secretion relative to glucose elevation (ISG; defined as AUC insulin/AUC glucose) increased significantly in the ADD-ON, although the mean change in fasting insulin level was significantly decreased in the ADD-ON (p=0.015 and p=0.026). Glucose 81-88 insulin Homo sapiens 0-7 28168232-6 2016 The patient was treated with a fluid infusion, and serum glucose level was controlled with insulin. Glucose 57-64 insulin Homo sapiens 91-98 28035984-3 2016 Moreover, we examined the effects of alaternin and emodin on stimulation of glucose uptake by insulin-resistant human HepG2 cells. Glucose 76-83 insulin Homo sapiens 94-101 28035984-4 2016 The results showed that alaternin and emodin significantly increased the insulin-provoked glucose uptake. Glucose 90-97 insulin Homo sapiens 73-80 27749056-1 2016 The G protein-coupled receptor 40 (GPR40) also known as free fatty acid receptor 1 (FFAR1) is highly expressed in pancreatic, islet beta-cells and responds to endogenous fatty acids, resulting in amplification of insulin secretion only in the presence of elevated glucose levels. Glucose 264-271 insulin Homo sapiens 213-220 28082906-2 2016 Patients with T1D are typically dependent on the administration of externally provided insulin in order to manage blood glucose levels. Glucose 120-127 insulin Homo sapiens 87-94 27810898-4 2016 Thus, the MID sensitized insulin signaling and increased insulin-elicited glucose uptake with an elevated level of IRS-1 in C2C12 myotubes. Glucose 74-81 insulin Homo sapiens 57-64 27777306-1 2016 The processes regulating glucose-stimulated insulin secretion (GSIS) and its modulation by incretins in pancreatic beta-cells are only partly understood. Glucose 25-32 insulin Homo sapiens 44-51 27996048-2 2016 The aberrant glucose metabolism is one of the hallmarks of cancer cells, and as a branch of glucose metabolism, hexosamine biosynthesis pathway (HBP) has been reported to play a critical role in the insulin resistance and progression of cancer. Glucose 13-20 insulin Homo sapiens 199-206 27777306-8 2016 We show that beta-catenin depletion disrupts the intracellular actin cytoskeleton, and by using total internal reflectance fluorescence (TIRF) microscopy, we found that beta-catenin is required for the glucose- and incretin-induced depletion of insulin vesicles from near the plasma membrane. Glucose 202-209 insulin Homo sapiens 245-252 27777306-9 2016 In conclusion, we find that beta-catenin levels modulate Ca2+-dependent insulin exocytosis under conditions of glucose, GLP-1, or KCl stimulation through a role in modulating insulin secretory vesicle localization and/or fusion via actin remodeling. Glucose 111-118 insulin Homo sapiens 72-79 27942596-5 2016 Hepatocyte glucose output increased with decreased insulin sensitivity. Glucose 11-18 insulin Homo sapiens 51-58 27922115-8 2016 In addition, we demonstrate that down-regulation of PLIN5 in skeletal muscle inhibits insulin-mediated glucose uptake under normal chow feeding condition, while paradoxically improving insulin sensitivity upon high-fat feeding. Glucose 103-110 insulin Homo sapiens 86-93 27981043-0 2016 Adding to the spectrum of insulin sensitive populations for mixed meal tolerance test glucose reliability assessment. Glucose 86-93 insulin Homo sapiens 26-33 27981043-8 2016 Indeed, the interclass coefficient revealed high glucose response repeatability during the MMTT in insulin-sensitive men. Glucose 49-56 insulin Homo sapiens 99-106 27815072-2 2016 Increased blood glucose level triggers release of insulin from pancreatic beta-cells. Glucose 16-23 insulin Homo sapiens 50-57 27815072-3 2016 Insulin represses hepatic glucose production and increases glucose accumulation. Glucose 26-33 insulin Homo sapiens 0-7 27771766-3 2016 To assess insulin sensitivity, several methods based on glucose and insulin levels during a 75-g oral glucose tolerance test (OGTT) exist. Glucose 56-63 insulin Homo sapiens 10-17 27552831-1 2016 AIMS: In vitro, beta cells immediately secrete stored but readily releasable insulin in response to a rise of glucose. Glucose 110-117 insulin Homo sapiens 77-84 27552834-12 2016 The fasting glucose-to-insulin ratio was significantly lower in the HNF4A-IGT cohort when compared to the normal control group (0.13 vs. 0.24, p = 0.03). Glucose 12-19 insulin Homo sapiens 23-30 27605456-9 2016 Torres participants consistently scored low on "knowledge" items in the ITAS, especially those which would guide insulin initiation (insulin improves glucose control and prevents complications). Glucose 150-157 insulin Homo sapiens 113-120 27552834-14 2016 CONCLUSIONS: In a young adult HNF4A-IGT cohort, we demonstrate preserved glucose, insulin and C-peptide secretory responses to oral glucose. Glucose 132-139 insulin Homo sapiens 82-89 27552834-14 2016 CONCLUSIONS: In a young adult HNF4A-IGT cohort, we demonstrate preserved glucose, insulin and C-peptide secretory responses to oral glucose. Glucose 132-139 insulin Homo sapiens 94-103 26898181-3 2016 miRNAs have been shown to be dysregulated in a number of different tissues under conditions of obesity and insulin resistance, and have been demonstrated to be important regulators of a number of critical metabolic functions, including insulin secretion in the pancreas, lipid and glucose metabolism in the liver, and nutrient signaling in the hypothalamus. Glucose 281-288 insulin Homo sapiens 107-114 27686967-6 2016 Consequently, both insulin-induced glucose transporter 4 (GLUT4) translocation to the plasma membrane and glucose uptake were decreased. Glucose 35-42 insulin Homo sapiens 19-26 27450071-6 2016 The level of glycaemic control, represented by baseline glycosylated haemoglobin was identified as a significant covariate for steady-state glucose, insulin-dependent glucose clearance and the magnitude of the incretin effect, while baseline body mass index was a significant covariate for steady-state insulin levels. Glucose 167-174 insulin Homo sapiens 149-156 27450071-8 2016 The developed model was used to simulate glucose and insulin profiles in different groups of T2DM patients, across a range of glycaemic control, and it was found accurately to characterize their response to the standard oral glucose challenge. Glucose 225-232 insulin Homo sapiens 53-60 27796854-5 2016 Glucose uptake in the exercising muscle occurs through insulin-independent mechanisms whose downstream signaling events ultimately converge with insulin-signaling pathways, a fact that may explain why exercise and insulin have additive effect on skeletal muscle glucose uptake. Glucose 0-7 insulin Homo sapiens 55-62 27796854-5 2016 Glucose uptake in the exercising muscle occurs through insulin-independent mechanisms whose downstream signaling events ultimately converge with insulin-signaling pathways, a fact that may explain why exercise and insulin have additive effect on skeletal muscle glucose uptake. Glucose 0-7 insulin Homo sapiens 145-152 27796854-5 2016 Glucose uptake in the exercising muscle occurs through insulin-independent mechanisms whose downstream signaling events ultimately converge with insulin-signaling pathways, a fact that may explain why exercise and insulin have additive effect on skeletal muscle glucose uptake. Glucose 0-7 insulin Homo sapiens 145-152 27796854-5 2016 Glucose uptake in the exercising muscle occurs through insulin-independent mechanisms whose downstream signaling events ultimately converge with insulin-signaling pathways, a fact that may explain why exercise and insulin have additive effect on skeletal muscle glucose uptake. Glucose 262-269 insulin Homo sapiens 145-152 27796854-5 2016 Glucose uptake in the exercising muscle occurs through insulin-independent mechanisms whose downstream signaling events ultimately converge with insulin-signaling pathways, a fact that may explain why exercise and insulin have additive effect on skeletal muscle glucose uptake. Glucose 262-269 insulin Homo sapiens 145-152 26511673-5 2016 Insulin resistance and sensitivity were evaluated using oral glucose tolerance test-derived indices that were validated by hyperinsulinaemic-euglycaemic and hyperglycaemic clamps. Glucose 61-68 insulin Homo sapiens 0-7 27589584-3 2016 Insulin secretion in response to intravenous glucose and arginine stimulus was measured. Glucose 45-52 insulin Homo sapiens 0-7 27679559-1 2016 Impaired GLUT4-dependent glucose uptake is a contributing factor in the development of whole-body insulin resistance in obese patients and obese animal models. Glucose 25-32 insulin Homo sapiens 98-105 27679559-3 2016 A likely mechanism underlying increased insulin sensitivity is increased glucose uptake in skeletal muscle. Glucose 73-80 insulin Homo sapiens 40-47 27695899-8 2016 Furthermore, the glucose-lowering drug, metformin, prevented IR cleavage accompanied by inhibition of calpain 2 release in exosomes, and re-established insulin signalling. Glucose 17-24 insulin Homo sapiens 152-159 27996320-0 2016 Mitigating Reductions in Glucose During Exercise on Closed-Loop Insulin Delivery: The Ex-Snacks Study. Glucose 25-32 insulin Homo sapiens 64-71 26832341-6 2016 In Gly2-GLP-2-treated mice, we found significant increase in glucose tolerance and exogenous insulin sensitivity, reduction in glucose-stimulated plasma insulin and in the increase in beta-cell mass in comparison with pair-aged HFD untreated animals. Glucose 127-134 insulin Homo sapiens 153-160 27754787-0 2016 Combined Deletion of Slc30a7 and Slc30a8 Unmasks a Critical Role for ZnT8 in Glucose-Stimulated Insulin Secretion. Glucose 77-84 insulin Homo sapiens 96-103 27754787-2 2016 SLC30A8 is predominantly expressed in pancreatic islet beta-cells, but surprisingly, multiple knockout mouse studies have shown little effect of Slc30a8 deletion on glucose tolerance or glucose-stimulated insulin secretion (GSIS). Glucose 186-193 insulin Homo sapiens 205-212 27652800-7 2016 Among all patients, 34.1% thought that insulin lowered blood glucose levels to an extreme degree and 14.9% disagreed. Glucose 61-68 insulin Homo sapiens 39-46 27322922-3 2016 Beside their pro-inflammatory activity, they may also affect glucose and lipid metabolism, possibly promoting insulin resistance and obesity. Glucose 61-68 insulin Homo sapiens 110-117 28210522-2 2016 In this case report, we present the case of a 36-year-old woman suffering from Type 1 diabetes mellitus who developed recurrent episodes of psychosis following poor adherence to her insulin therapy, leading to significantly high levels of blood glucose. Glucose 245-252 insulin Homo sapiens 182-189 28210522-3 2016 Adequate control of blood glucose levels by improving the adherence with insulin led to lack of recurrence of psychosis. Glucose 26-33 insulin Homo sapiens 73-80 27603902-10 2016 Insulin-stimulated glucose disappearance was lower in NFG/IGT (24.6 +- 2.2 vs 35.0 +- 3.6 mumol/kg/min; P = .03). Glucose 19-26 insulin Homo sapiens 0-7 27603902-13 2016 However, insulin-stimulated glucose disposal is impaired, exacerbating defects in beta-cell function. Glucose 28-35 insulin Homo sapiens 9-16 27834301-10 2016 Conclusion The insulin-mediated glucose disposal rate was significantly improved with the normalization of blood glucose levels following transient IIT. Glucose 32-39 insulin Homo sapiens 15-22 27834301-10 2016 Conclusion The insulin-mediated glucose disposal rate was significantly improved with the normalization of blood glucose levels following transient IIT. Glucose 113-120 insulin Homo sapiens 15-22 27500951-3 2016 Insulin-stimulated myocardial glucose uptake was decreased by training without any significantly different response between the groups, whereas free fatty acid uptake remained unchanged. Glucose 30-37 insulin Homo sapiens 0-7 27500951-9 2016 Cardiac magnetic resonance imaging (CMRI) was performed to measure cardiac structure and function and positron emission tomography was used to measure myocardial perfusion at baseline and during adenosine stimulation, insulin-stimulated glucose uptake (MGU) and fasting free fatty acid uptake (MFFAU). Glucose 237-244 insulin Homo sapiens 218-225 27612686-0 2016 A composite hydrogel system containing glucose-responsive nanocarriers for oral delivery of insulin. Glucose 39-46 insulin Homo sapiens 92-99 27612686-2 2016 In this study, a glucose-responsive nanocarriers for loading of insulin has been prepared firstly. Glucose 17-24 insulin Homo sapiens 64-71 27612686-4 2016 The insulin release behaviors were evaluated triggered by pH and glucose in vitro. Glucose 65-72 insulin Homo sapiens 4-11 27612686-5 2016 In order to enhance the oral bioavailability of insulin, the insulin-loaded glucose-responsive nanocarriers were further encapsulated into a three-dimensional (3D) hyaluronic acid (HA) hydrogel environment for overcoming multiple barriers and providing multi-protection for insulin during the transport process. Glucose 76-83 insulin Homo sapiens 48-55 27612686-5 2016 In order to enhance the oral bioavailability of insulin, the insulin-loaded glucose-responsive nanocarriers were further encapsulated into a three-dimensional (3D) hyaluronic acid (HA) hydrogel environment for overcoming multiple barriers and providing multi-protection for insulin during the transport process. Glucose 76-83 insulin Homo sapiens 61-68 27612686-5 2016 In order to enhance the oral bioavailability of insulin, the insulin-loaded glucose-responsive nanocarriers were further encapsulated into a three-dimensional (3D) hyaluronic acid (HA) hydrogel environment for overcoming multiple barriers and providing multi-protection for insulin during the transport process. Glucose 76-83 insulin Homo sapiens 61-68 27612686-7 2016 After oral administration to the diabetic rats, the released insulin from hydrogel systems containing insulin-loaded glucose-responsive nanocarriers exhibited an effective hypoglycemic effect for longer time compared with insulin-loaded nanocarriers. Glucose 117-124 insulin Homo sapiens 61-68 27612686-7 2016 After oral administration to the diabetic rats, the released insulin from hydrogel systems containing insulin-loaded glucose-responsive nanocarriers exhibited an effective hypoglycemic effect for longer time compared with insulin-loaded nanocarriers. Glucose 117-124 insulin Homo sapiens 102-109 27612686-7 2016 After oral administration to the diabetic rats, the released insulin from hydrogel systems containing insulin-loaded glucose-responsive nanocarriers exhibited an effective hypoglycemic effect for longer time compared with insulin-loaded nanocarriers. Glucose 117-124 insulin Homo sapiens 102-109 27612799-0 2016 Synthesis and evaluation of temperature- and glucose-sensitive nanoparticles based on phenylboronic acid and N-vinylcaprolactam for insulin delivery. Glucose 45-52 insulin Homo sapiens 132-139 27956466-6 2016 Alanine and total amino acid levels tended to be negatively associated with the insulin-stimulated glucose uptake after overfeeding. Glucose 99-106 insulin Homo sapiens 80-87 27639595-2 2016 It is a basis for a number of chronic diseases like hypertension, dyslipidemia, glucose intolerance, coronary heart disease, cerebral vascular disease along with T2DM, thus the key is to cure and prevent insulin resistance. Glucose 80-87 insulin Homo sapiens 204-211 27896318-0 2016 Insulin elevates leptin secretion and mRNA levels via cyclic AMP in 3T3-L1 adipocytes deprived of glucose. Glucose 98-105 insulin Homo sapiens 0-7 27497876-0 2016 Comment on "Management of postprandial glucose: Recommended targets and treatment with biphasic insulin". Glucose 39-46 insulin Homo sapiens 96-104 27878229-6 2016 Furthermore, we observed that lipopolysaccharide (LPS)-induced macrophage conditioned media could impair insulin-stimulated glucose uptake. Glucose 124-131 insulin Homo sapiens 105-112 28116330-1 2017 BACKGROUND: HNF1A gene regulates liver-specific genes, and genes that have a role in glucose metabolism, transport, and secretion of insulin. Glucose 85-92 insulin Homo sapiens 133-140 27933189-0 2016 Insulin resistance of protein anabolism accompanies that of glucose metabolism in lean, glucose-tolerant offspring of persons with type 2 diabetes. Glucose 60-67 insulin Homo sapiens 0-7 27896318-5 2016 RESULTS: Insulin significantly increased the secretion and mRNA levels of leptin under the depletion of glucose. Glucose 104-111 insulin Homo sapiens 9-16 27892898-1 2016 Skeletal muscle is the main tissue responsible for insulin-stimulated glucose uptake. Glucose 70-77 insulin Homo sapiens 51-58 27911357-3 2016 Interpretation of an IVGTT is done through measurement of changes in glucose and insulin levels over time in relation to the dextrose challenge. Glucose 125-133 insulin Homo sapiens 81-88 27743890-10 2016 In conclusion, our data indicate that simvastatin decreased both basal and insulin-stimulated glucose uptake through inhibiting the critical steps in IR/IRS-1/AKT signaling cascade, and by hindering GLUT4 function and normal regulation of glycogen synthesis, contributing to insulin resistance. Glucose 94-101 insulin Homo sapiens 75-82 27743890-10 2016 In conclusion, our data indicate that simvastatin decreased both basal and insulin-stimulated glucose uptake through inhibiting the critical steps in IR/IRS-1/AKT signaling cascade, and by hindering GLUT4 function and normal regulation of glycogen synthesis, contributing to insulin resistance. Glucose 94-101 insulin Homo sapiens 275-282 27488665-2 2016 Insulin controls the translocation of several solutes that are involved in energetic cellular metabolism, including glucose. Glucose 116-123 insulin Homo sapiens 0-7 27827363-1 2016 Obesity-related insulin resistance represents the core component of the metabolic syndrome, promoting glucose intolerance, pancreatic beta cell failure and type 2 diabetes. Glucose 102-109 insulin Homo sapiens 16-23 27712062-1 2016 Glucose-stimulated insulin secretion from pancreatic beta-cells within islets of Langerhans plays a critical role in maintaining glucose homeostasis. Glucose 0-7 insulin Homo sapiens 19-26 27605560-8 2016 CBA/SIV macaques had significantly decreased circulating adiponectin and resistin levels relative to SUC/SIV macaques and reduced disposition index and acute insulin response to glucose, insulin, and C-peptide release during frequently sampled intravenous glucose tolerance test, irrespective of ART status. Glucose 178-185 insulin Homo sapiens 158-165 27712062-5 2016 Both [Ca2+]i and insulin were oscillatory during application of 10 mM glucose with temporal and quantitative profiles similar to what has been observed elsewhere. Glucose 70-77 insulin Homo sapiens 17-24 27712062-6 2016 In previous work, sinusoidal glucose levels have been used to test the entrainment of islets while monitoring either [Ca2+]i or insulin levels; using this newly developed system, we show unambiguously that oscillations of both [Ca2+]i and insulin release are entrained to oscillatory glucose levels and that the temporal correlation of these are maintained throughout the experiment. Glucose 29-36 insulin Homo sapiens 128-135 27712062-6 2016 In previous work, sinusoidal glucose levels have been used to test the entrainment of islets while monitoring either [Ca2+]i or insulin levels; using this newly developed system, we show unambiguously that oscillations of both [Ca2+]i and insulin release are entrained to oscillatory glucose levels and that the temporal correlation of these are maintained throughout the experiment. Glucose 29-36 insulin Homo sapiens 239-246 27234693-9 2016 CONCLUSIONS: In patients with T2D, BIL with insulin lispro provided greater improvement in glycaemic control with less nocturnal hypoglycaemia, lower glucose variability and less weight gain compared with glargine. Glucose 150-157 insulin Homo sapiens 44-51 27478065-1 2016 Expression of adaptor protein, phosphotyrosine interaction, pleckstrin homology domain, and leucine zipper containing 1 (APPL1) promoted glucose transporter 4 (GLUT4) translocation and glucose uptake in adipose and muscle tissues in response to stimulation with insulin, adiponectin, or exercise. Glucose 137-144 insulin Homo sapiens 262-269 27870481-1 2016 Glucokinase enhances glucose conversion to glucose-6-phosphate, causing glucose-stimulated insulin secretion from pancreatic beta cells and increased hepatic glucose uptake. Glucose 21-28 insulin Homo sapiens 91-98 27870481-1 2016 Glucokinase enhances glucose conversion to glucose-6-phosphate, causing glucose-stimulated insulin secretion from pancreatic beta cells and increased hepatic glucose uptake. Glucose 43-50 insulin Homo sapiens 91-98 27870481-1 2016 Glucokinase enhances glucose conversion to glucose-6-phosphate, causing glucose-stimulated insulin secretion from pancreatic beta cells and increased hepatic glucose uptake. Glucose 43-50 insulin Homo sapiens 91-98 27504013-0 2016 Insulin Resistance Is Accompanied by Increased Fasting Glucagon and Delayed Glucagon Suppression in Individuals With Normal and Impaired Glucose Regulation. Glucose 137-144 insulin Homo sapiens 0-7 27561922-6 2016 It was strongly associated with higher glucose (effect size +3.3 mmol/L; P = 2.5 x 10-6) and insulin (effect size +175 pmol/L; P = 0.04) 2 h after an oral glucose load in homozygote carriers. Glucose 155-162 insulin Homo sapiens 93-100 27561923-7 2016 RESULTS: Dapagliflozin reduced fasting plasma glucose (167 +- 13 to 128 +- 6 mg/dL) and increased insulin-stimulated glucose disposal by 36% (P < 0.01). Glucose 117-124 insulin Homo sapiens 98-105 27567623-5 2016 Insulin secretion in response to glucose was evaluated in vitro by static and dynamic (perifusion) assays, and in vivo by EB transplantation into immunodeficient mice. Glucose 33-40 insulin Homo sapiens 0-7 27612500-7 2016 Improved glucose control during closed-loop was associated with increased variability of basal insulin delivery (P < 0.001) and an increase in the total daily insulin dose (53.5 [39.5-72.1] vs. 51.5 [37.6-64.3] units/day; P = 0.006). Glucose 9-16 insulin Homo sapiens 95-102 27860496-1 2016 BACKGROUND: A simulation methodology based on the net effect, a signal estimated from continuous glucose monitoring (CGM) and insulin data accounting for sources of glucose variability, for example, meals and exercise, has been proposed. Glucose 165-172 insulin Homo sapiens 126-133 27662042-9 2016 RESULTS: Regular human insulin by jet injection had a faster onset of glucose-lowering effect compared to aspart by conventional pen (T-GIR50%, 30.8+-2.9 versus 43.1+-3.2min, P<0.01). Glucose 70-77 insulin Homo sapiens 23-30 27708432-7 2016 Moreover, insulinemia was increased and caused a decrease in glucose production despite an increased resistance to insulin. Glucose 61-68 insulin Homo sapiens 10-17 27758845-1 2016 Bromocriptine is a glucose-lowering drug, which was shown to be effective in obese subjects with insulin resistance. Glucose 19-26 insulin Homo sapiens 97-104 27882141-5 2016 The best wound healing rate found was that of the low-dose insulin injection group where all the parameters measured improved significantly: The healing time was shorter; the blood flow volume, the flap survival, the number of fibroblasts and new vessels increased; the re-epithelialization occurred faster; the infiltration of inflammatory cells was reduced; the expression levels of heat shock protein-90, vascular endothelial growth factor, transforming growth factor-beta and interleukin-1 were higher; and the plasma glucose levels only fluctuated slightly. Glucose 522-529 insulin Homo sapiens 59-66 27882141-6 2016 The results clearly demonstrate that a local low-dose insulin regime after flap transplantation can accelerate the healing time and improve the surgical outcome without exerting detrimental secondary effects on the glucose plasma level of deep burn patients. Glucose 215-222 insulin Homo sapiens 54-61 27994380-3 2016 The purpose of this study was to determine the difference between blood glucose concentrations obtained from POC glucometers and laboratory results in critically ill patients with intensive insulin therapy. Glucose 72-79 insulin Homo sapiens 190-197 27895387-6 2016 The effects of excess extracellular acetylcarnitine on insulin resistance were studied in cultured skeletal muscle cells (C2C12 and human myotubes), and insulin-dependent glucose uptake was significantly and dose-dependently inhibited by addition of acetylcarnitine. Glucose 171-178 insulin Homo sapiens 55-62 27895387-6 2016 The effects of excess extracellular acetylcarnitine on insulin resistance were studied in cultured skeletal muscle cells (C2C12 and human myotubes), and insulin-dependent glucose uptake was significantly and dose-dependently inhibited by addition of acetylcarnitine. Glucose 171-178 insulin Homo sapiens 153-160 27669460-8 2016 Moreover, fructose activated ChREBP and induced G6pc in the absence of Foxo1a, indicating that carbohydrate-induced activation of ChREBP and G6PC dominates over the suppressive effects of insulin to enhance glucose production. Glucose 207-214 insulin Homo sapiens 188-195 27738482-1 2016 BACKGROUND: Some patients with type 2 diabetes mellitus (T2DM) on insulin have poor glycemic control and require add-on therapy to reach target glucose values. Glucose 144-151 insulin Homo sapiens 66-73 27613867-6 2016 However, treated mice showed significantly improved glucose tolerance with enhanced serum insulin levels, reduced beta cell death, and increased beta cell mass. Glucose 52-59 insulin Homo sapiens 90-97 27573238-1 2016 ATP-sensitive potassium (KATP) channels play a key role in mediating glucose-stimulated insulin secretion by coupling metabolic signals to beta-cell membrane potential. Glucose 69-76 insulin Homo sapiens 88-95 27754361-9 2016 The divergent findings between muscle and adipose tissue with regard to the association between 25(OH)D and insulin signaling proteins may suggest a tissue-specific interaction with varying effects on glucose homeostasis. Glucose 201-208 insulin Homo sapiens 108-115 27504013-10 2016 Therefore, glucose maintenance during insulin resistance may depend not only on hyperinsulinemia but also on the ability to suppress glucagon early after glucose intake. Glucose 11-18 insulin Homo sapiens 38-45 27504013-10 2016 Therefore, glucose maintenance during insulin resistance may depend not only on hyperinsulinemia but also on the ability to suppress glucagon early after glucose intake. Glucose 154-161 insulin Homo sapiens 38-45 27137456-0 2016 Evaluation of the Effect of Carbohydrate Intake on Postprandial Glucose in Patients With Type 1 Diabetes Treated With Insulin Pumps. Glucose 64-71 insulin Homo sapiens 118-125 27181199-12 2016 CONCLUSIONS: Basal insulin therapy was associated with a decrease in HbA1c and fasting blood glucose, and an improved treatment satisfaction. Glucose 93-100 insulin Homo sapiens 19-26 27207890-1 2016 BACKGROUND: We developed a system to suspend insulin pump delivery overnight when the glucose trend predicts hypoglycemia. Glucose 86-93 insulin Homo sapiens 45-52 26689349-4 2016 Irisin is a newly discovered myokine that is able to regulate glucose and lipid levels, thus improving insulin sensitivity. Glucose 62-69 insulin Homo sapiens 103-110 26769102-6 2016 Additionally, 1-h and 2-h glucose levels on 100 g OGTT were found to be predictive for the insulin need in achieving good glycemic control in GDM (OR: 1.022, 95% CI: 1.005-1.038, p = 0.010 and OR: 1.019, 95% CI: 1.004-1.035, p = 0.015). Glucose 26-33 insulin Homo sapiens 91-98 26769102-8 2016 Also, increased 1-h and 2-h glucose levels on 100 g OGTT can predict the need for insulin treatment for GDM. Glucose 28-35 insulin Homo sapiens 82-89 27699898-8 2016 This leads to hypertrophic, dysfunctional and insulin-resistant adipose cells with a reduced content of GLUT4, the major insulin-regulated glucose transporter, which in turn reduces adipose tissue glucose uptake and de novo lipogenesis. Glucose 139-146 insulin Homo sapiens 46-53 27699898-8 2016 This leads to hypertrophic, dysfunctional and insulin-resistant adipose cells with a reduced content of GLUT4, the major insulin-regulated glucose transporter, which in turn reduces adipose tissue glucose uptake and de novo lipogenesis. Glucose 139-146 insulin Homo sapiens 121-128 27699898-10 2016 FAHFAs have beneficial metabolic effects, including enhancing insulin-stimulated glucose transport and glucose-stimulated GLP1 and insulin secretion, as well as powerful anti-inflammatory effects. Glucose 81-88 insulin Homo sapiens 62-69 27739225-6 2016 These proteins work in concert with cofactors such as PGC-1alpha and CRTC2, and chromatin-modifying enzymes including DNA methyltransferases and histone acetyltransferases, to regulate key genes that promote insulin-stimulated glucose uptake, gluconeogenesis or other pathways that affect systemic insulin action. Glucose 227-234 insulin Homo sapiens 208-215 27739225-6 2016 These proteins work in concert with cofactors such as PGC-1alpha and CRTC2, and chromatin-modifying enzymes including DNA methyltransferases and histone acetyltransferases, to regulate key genes that promote insulin-stimulated glucose uptake, gluconeogenesis or other pathways that affect systemic insulin action. Glucose 227-234 insulin Homo sapiens 298-305 27613819-0 2016 MicroRNA-593-3p regulates insulin-promoted glucose consumption by targeting Slc38a1 and CLIP3. Glucose 43-50 insulin Homo sapiens 26-33 27613819-1 2016 Insulin plays an important role in the regulation of glucose metabolism. Glucose 53-60 insulin Homo sapiens 0-7 27613819-5 2016 Further studies demonstrated that Slc38a1 and CLIP3 mediate insulin-regulated glucose metabolism. Glucose 78-85 insulin Homo sapiens 60-67 27613819-7 2016 Taken together, this study indicates that inhibition of miRNA-593-3p by insulin promotes glucose metabolism through the regulation of Slc38a1 and CLIP3 expression, and provides a new insight into the role and mechanism of insulin-induced glycolysis. Glucose 89-96 insulin Homo sapiens 72-79 27733521-10 2016 CONCLUSIONS: These data suggest that consumption of a high-HAM-RS2 bagel improves glycemic efficiency by reducing the amount of insulin required to manage postprandial glucose while improving fasting insulin sensitivity in adults at increased risk of T2D. Glucose 168-175 insulin Homo sapiens 128-135 27959282-4 2016 Offspring of diabetic mothers compensate excess glucose concentrations by producing higher levels of insulin causing transient hyperinsulinemia. Glucose 48-55 insulin Homo sapiens 101-108 28760224-2 2016 The increased glucose reabsorption from the urine to the proximal tubule and subsequently to the bloodstream, has three direct effects on the prognosis of patients with DM2: a) it increases the daily glucose load by raising the renal threshold for glucose, thus augmenting requirements for oral antidiabetics and insulin. Glucose 14-21 insulin Homo sapiens 313-320 27733250-6 2016 Whole body insulin resistance was estimated as steady state plasma glucose (SSPG) concentrations during the last 30min of a 3-h insulin suppression test. Glucose 67-74 insulin Homo sapiens 11-18 27746033-2 2016 Our expanded mathematical model of the insulin signal transduction pathway was previously shown to effectively predict glucose clearance rates using mRNA levels of key components of the pathway in a mouse model. Glucose 119-126 insulin Homo sapiens 39-46 27061687-4 2016 RESULTS: Patients showed high insulin responsiveness to glucose and low insulin sensitivity. Glucose 56-63 insulin Homo sapiens 30-37 27664094-0 2016 MicroRNA-463-3p/ABCG4: A new axis in glucose-stimulated insulin secretion. Glucose 37-44 insulin Homo sapiens 56-63 27664094-1 2016 OBJECTIVE: Glucose-stimulated insulin secretion (GSIS) is known to be essential in the control of metabolic fuel homeostasis, though the molecular mechanisms involved remain unclear. Glucose 11-18 insulin Homo sapiens 30-37 27900046-4 2016 Metformin at a low dose potently inhibited the insulin action, decreasing the ability of the endometrial cancer (EC) cell line to migrate and invade in a high and normal glucose environment, and decreasing the migration ability of the primary eEPs. Glucose 170-177 insulin Homo sapiens 47-54 27900046-5 2016 In the EC cell line, the insulin treatment increased the proliferation, without any subsequent reduction of proliferation by the addition of 0.1 mM metformin; however, relative cell proliferation sensitivity to metformin was observed in the range between 1 and 5 mM regardless of the glucose concentration present. Glucose 284-291 insulin Homo sapiens 25-32 27900046-7 2016 However, at this concentration, metformin can inhibit the insulin action in endometrial epithelial cancer cells, demonstrating an anti-metastatic effect in high and normal glucose environments. Glucose 172-179 insulin Homo sapiens 58-65 26701831-0 2016 Evaluation of a novel continuous glucose monitoring guided system for adjustment of insulin dosing - PumpTune: a randomized controlled trial. Glucose 33-40 insulin Homo sapiens 84-91 26701831-1 2016 OBJECTIVE: Retrospective continuous glucose monitoring (CGM) can guide insulin pump adjustments, however, interpretation of data and recommending new pump settings is complex and subjective. Glucose 36-43 insulin Homo sapiens 71-78 26334252-2 2016 Glucose pellets with delayed release in the time of the maximum effect of insulin can not only prevent hypoglycemia but also eliminate the preventive carbohydrate intake. Glucose 0-7 insulin Homo sapiens 74-81 27550085-1 2016 AIMS: We hypothesised that the expected increase in insulin resistance over three years" time in individuals with impaired glucose tolerance (IGT) and/or impaired fasting glucose could be attenuated by an intervention with focus on physical activity in ordinary primary care. Glucose 123-130 insulin Homo sapiens 52-59 27139723-12 2016 The response to an oral glucose tolerance test following exercise intervention was for a decrease in the area under the curve for insulin (mean 162 muU/mul, 95 % CI 93-231; ES large) and blood glucose (mean 39 mg/dl, 95 % CI 9.4-69; ES moderate). Glucose 24-31 insulin Homo sapiens 130-137 27405779-9 2016 Furthermore, in vitro HDDC-derived beta cells (called beta-HDDCs) secreted human insulin and C-peptide in response to glucose, KCl, 3-isobutyl-1-methylxanthine, and tolbutamide stimulation. Glucose 118-125 insulin Homo sapiens 81-88 27796348-0 2016 Metabolomics reveals the protective of Dihydromyricetin on glucose homeostasis by enhancing insulin sensitivity. Glucose 59-66 insulin Homo sapiens 92-99 27796348-8 2016 In addition, the exposure of HepG2 cells to high glucose concentrations impaired the insulin-stimulated phosphorylation of Akt2 Ser474 and insulin receptor substrate-1 (IRS-1) Ser612, increased GSK-3beta phosphorylation, and upregulated G6Pase and PEPCK expression. Glucose 49-56 insulin Homo sapiens 85-92 27321586-1 2016 In pancreatic beta-cells, glucose-induced closure of the ATP-sensitive K+ (KATP) channel is an initial process triggering glucose-stimulated insulin secretion (GSIS). Glucose 26-33 insulin Homo sapiens 141-148 27321586-1 2016 In pancreatic beta-cells, glucose-induced closure of the ATP-sensitive K+ (KATP) channel is an initial process triggering glucose-stimulated insulin secretion (GSIS). Glucose 122-129 insulin Homo sapiens 141-148 27693789-8 2016 These data suggest that a desensitization to insulin during aging, possibly at the level of skeletal muscle ACC phosphorylation, results in a diminished ability to transition to glucose oxidation indicative of metabolic inflexibility. Glucose 178-185 insulin Homo sapiens 45-52 27994949-6 2016 BSCFAs inhibited both cAMP-mediated lipolysis and insulin-stimulated de novo lipogenesis at 10 mM, whereas isobutyric acid potentiated insulin-stimulated glucose uptake by all concentrations (1, 3 and 10 mM) in rat adipocytes. Glucose 154-161 insulin Homo sapiens 135-142 27994949-11 2016 To conclude, BSCFAs have effects on adipocyte lipid and glucose metabolism that can contribute to improved insulin sensitivity in individuals with disturbed metabolism. Glucose 56-63 insulin Homo sapiens 107-114 27788129-1 2016 Pancreatic islets manage elevations in blood glucose level by secreting insulin into the bloodstream in a pulsatile manner. Glucose 45-52 insulin Homo sapiens 72-79 27599528-2 2016 Therefore, glucose and caloric balances become negative, reducing both the blood glucose level and insulin secretion. Glucose 11-18 insulin Homo sapiens 99-106 27704066-10 2016 In summary, bioactive compounds in AP may play an important role in regulating the glucose metabolism in insulin-resistant HepG2 cells and could be developed as a promising natural material for diabetes prevention and treatment. Glucose 83-90 insulin Homo sapiens 105-112 27681976-3 2016 As skeletal muscle is the largest insulin-sensitive tissue in the body, low muscle mass in sarcopenia likely results in reduced capacity for glucose disposal. Glucose 141-148 insulin Homo sapiens 34-41 27690486-3 2016 When used in tandem, the insulin pump and continuous glucose monitor have prompted the Artificial Pancreas initiative, aimed at developing control system for fully automating glucose monitoring and insulin delivery. Glucose 175-182 insulin Homo sapiens 25-32 27311688-5 2016 Early-phase insulin secretion was estimated using the insulinogenic index (IGI [DeltaInsulin(30-0 min)/DeltaGlucose(30-0 min)]) during a 75-g oral glucose tolerance test. Glucose 147-154 insulin Homo sapiens 12-19 27581470-9 2016 The inclusion of whey protein in cereal bar formulations to reduce glycemic response requires caution because this may be associated with a disproportionate increase in insulin as judged by an increased insulin-to-glucose iAUC ratio. Glucose 214-221 insulin Homo sapiens 169-176 27333897-4 2016 Primary outcomes were baseline to post-intervention changes in CES-D and whole body insulin sensitivity index (WBISI), derived from 2-h oral glucose tolerance tests. Glucose 141-148 insulin Homo sapiens 84-91 27614289-2 2016 Glucose-responsive carbohydrate responsive element binding protein (ChREBP) has yet to be studied in hibernating organisms, which prepare for the cold winter months by feeding until they exhibit an obesity-like state that is accompanied by naturally-induced and completely reversible insulin resistance. Glucose 0-7 insulin Homo sapiens 284-291 27356203-1 2016 Meal-dependent fluctuations of blood glucose and corresponding endocrine signals such as insulin are thought to provide important regulatory input for central nervous processing of hunger and satiety. Glucose 37-44 insulin Homo sapiens 89-96 27517612-3 2016 Initial theories proposed that glucose was beneficial in the context of myocardial ischemia and insulin was required to enable glucose cell uptake. Glucose 127-134 insulin Homo sapiens 96-103 27544192-5 2016 We found that fucosterol enhanced insulin-provoked glucose uptake and conjointly decreased PTP1B expression level in insulin-resistant HepG2 cells. Glucose 51-58 insulin Homo sapiens 34-41 27380442-5 2016 More importantly, insulin loaded, dual ligand functionalized NC could increase the plasma insulin level and efficiently regulate the glycemic response for a prolonged period of time (~1 day) upon oral administration to diabetic rats, whereas delivery of insulin by single ligand functionalized NCs, either by chitosan or peptide, as well as by unmodified NC and free insulin, could not induce the effective regulation of the blood glucose level. Glucose 431-438 insulin Homo sapiens 18-25 27103506-2 2016 We also aimed to investigate the effect of mtDNA content on basal and oral glucose-stimulated insulin secretion. Glucose 75-82 insulin Homo sapiens 94-101 27103506-15 2016 CONCLUSIONS: Decreased peripheral blood mtDNA content was more closely associated with glucose-stimulated insulin secretion than with basal secretion. Glucose 87-94 insulin Homo sapiens 106-113 27103506-16 2016 Reduction in glucose-stimulated insulin secretion causes postprandial hyperglycaemia. Glucose 13-20 insulin Homo sapiens 32-39 27265844-8 2016 Insulin-stimulated glucose disposal rates did not change in response to TRT compared with placebo (p = 0.18). Glucose 19-26 insulin Homo sapiens 0-7 27324560-1 2016 The hyperinsulinaemic-euglycaemic glucose clamp has always been regarded as the "gold standard" for the assessment of pharmacodynamic (PD) properties of insulin preparations; however, there has been controversy over a variety of methodogical details, such as study population, dosing time and the initial stabilization of blood glucose (BG) concentrations at the clamp target level, among clamp groups. Glucose 34-41 insulin Homo sapiens 9-16 27376543-5 2016 RESULTS: Both [Formula: see text] (r = 0.39, p < 0.0001) and DeltaRQ (r = 0.32, p < 0.0001) correlated positively with whole-body insulin sensitivity, even after adjusting for anthropometric variables, glycaemia and glucose-lowering medication, but not after adjusting for NEFA. Glucose 222-229 insulin Homo sapiens 136-143 27660130-1 2016 Glucose Variability in a 26-Week Randomized Comparison of Mealtime Treatment With Rapid-Acting Insulin Versus GLP-1 Agonist in Participants With Type 2 Diabetes at High Cardiovascular Risk. Glucose 0-7 insulin Homo sapiens 95-102 27105622-1 2016 The insulin-secreting beta cells in the endocrine pancreas regulate blood glucose levels, and loss of functional beta cells leads to insulin deficiency, hyperglycemia (high blood glucose) and diabetes mellitus. Glucose 74-81 insulin Homo sapiens 4-11 27660131-1 2016 Glucose Variability in a 26-Week Randomized Comparison of Mealtime Treatment With Rapid-Acting Insulin Versus GLP-1 Agonist in Participants With Type 2 Diabetes at High Cardiovascular Risk. Glucose 0-7 insulin Homo sapiens 95-102 27672710-1 2016 BACKGROUND: Automated insulin management features of the MiniMed 640G sensor-augmented pump system include suspension in response to predicted low sensor glucose (SG) values ("suspend before low"), suspension in response to existing low SG values ("suspend on low"), and automatic restarting of basal insulin delivery upon SG recovery. Glucose 155-162 insulin Homo sapiens 22-29 27466218-9 2016 Compared with GLAR, EXE increased insulin secretion at 8 mmol/L glucose throughout the study period (P < 0.01). Glucose 64-71 insulin Homo sapiens 34-41 27697134-3 2016 Specifically, the mechanisms by which low-grade inflammation may affect the normal stimulatory effect of insulin on glucose and fat storage are reviewed. Glucose 116-123 insulin Homo sapiens 105-112 26908204-6 2016 Oral administration in the alloxan-induced diabetic mice of the mixture loaded in elastic anionic niosomes with the insulin doses at 25, 50 and 100 IU/kg body weight indicated significant hypoglycemic activity with the percentage fasting blood glucose reduction of 1.95, 2.10 and 2.10 folds of the subcutaneous insulin injection at 12 h, respectively. Glucose 244-251 insulin Homo sapiens 116-123 27060004-11 2016 Slopes of increasing follow-up glucose with baseline BMI, measured as regression coefficients (beta), were significantly greater in insulin-resistant than in insulin-sensitive individuals (beta = 0.86 vs. 0.38, p = 0.009 for difference in slopes). Glucose 31-38 insulin Homo sapiens 132-139 27060004-11 2016 Slopes of increasing follow-up glucose with baseline BMI, measured as regression coefficients (beta), were significantly greater in insulin-resistant than in insulin-sensitive individuals (beta = 0.86 vs. 0.38, p = 0.009 for difference in slopes). Glucose 31-38 insulin Homo sapiens 158-165 27521895-4 2016 The petroleum (PE) extract of the plant showed a significant increase in insulin stimulated glucose uptake by L6 myotubes. Glucose 92-99 insulin Homo sapiens 73-80 27459025-4 2016 Sodium glucose co-transporter type 2 (SGLT2) inhibitors present a novel glucose-lowering therapy, inducing glycosuria in an insulin-independent fashion. Glucose 7-14 insulin Homo sapiens 124-131 27514733-8 2016 Further, these cells exhibited elevated expression of INS gene at 10 mM glucose upon inducing with different glucose concentrations. Glucose 72-79 insulin Homo sapiens 54-57 27514733-8 2016 Further, these cells exhibited elevated expression of INS gene at 10 mM glucose upon inducing with different glucose concentrations. Glucose 109-116 insulin Homo sapiens 54-57 27521895-6 2016 The compound induced a dose dependent increase in insulin stimulated glucose uptake in L6 myotubes with an EC50 of 22.96muM. Glucose 69-76 insulin Homo sapiens 50-57 27296445-0 2016 Enzyme coated beta-cyclodextrin for effective adsorption and glucose-responsive closed-loop insulin delivery. Glucose 61-68 insulin Homo sapiens 92-99 27444630-1 2016 The differentiation of glucose-responsive, insulin-producing cells from ESCs in vitro is promising as a cellular therapy for the treatment of diabetes, a devastating and common disease. Glucose 23-30 insulin Homo sapiens 43-50 27589991-1 2016 Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Glucose 14-21 insulin Homo sapiens 56-63 27405860-2 2016 The international IRIS trial assessed whether pioglitazone, a glucose-lowering insulin-sensitizing drug, would reduce recurrent vascular events in patients with ischaemic stroke or transient ischaemic attack. Glucose 62-69 insulin Homo sapiens 79-86 27554111-5 2016 C-peptide also inhibited persistent upregulation of p53 and activation of mitochondrial adaptor p66(shc) after glucose normalization. Glucose 111-118 insulin Homo sapiens 0-9 27554111-6 2016 Further, C-peptide replacement therapy prevented persistent generation of ROS and ONOO(-) in the aorta of diabetic mice whose glucose levels were normalized by the administration of insulin. Glucose 126-133 insulin Homo sapiens 9-18 27589991-2 2016 Therefore, it is not surprising that insulin release from pancreatic beta-cells of the islets of Langerhans is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose 166-173 insulin Homo sapiens 37-44 27589991-3 2016 Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (KATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca2+ channels (VDCC). Glucose 0-7 insulin Homo sapiens 17-24 27461066-1 2016 BACKGROUND: Glucose effectiveness (GE) is the capacity of glucose to increase its own uptake and to maintain endogenous hepatic glucose output under basal insulin levels. Glucose 58-65 insulin Homo sapiens 155-162 27580020-1 2016 This study evaluated the capacity of mulberry anthocyanin extract (MAE) on insulin resistance amelioration in HepG2 cells induced by high glucose and palmitic acid and diabetes-related metabolic changes in type 2 diabetic mice. Glucose 138-145 insulin Homo sapiens 75-82 30358288-0 2016 [Difficult Perioperative Glucose Management in a Type 2 Diabetic Patient with Anti-insulin Antibody Undergoing Laparoscopic Partial Liver Resection]. Glucose 25-32 insulin Homo sapiens 83-90 30358288-8 2016 It should be born in mind that preoperative poor glucose control might be caused by anti-insulin antibodies and lead to difficult perioperative glucose management. Glucose 49-56 insulin Homo sapiens 89-96 30358288-8 2016 It should be born in mind that preoperative poor glucose control might be caused by anti-insulin antibodies and lead to difficult perioperative glucose management. Glucose 144-151 insulin Homo sapiens 89-96 27681957-11 2016 CONCLUSION: Insulin has metabolic and vasodilatory effects in the skin both when given locally and after systemic delivery through an oral glucose load. Glucose 139-146 insulin Homo sapiens 12-19 27374266-4 2016 During the hospitalization in cardiac intensive care unit, a treatment with insulin will be started when plasma glucose is>=1.80g/L (10.0mmol/L). Glucose 112-119 insulin Homo sapiens 76-83 27533789-5 2016 Intriguingly, oxidation of cholesterol affected glucose-stimulated insulin secretion only modestly, whereas basal insulin release was elevated. Glucose 48-55 insulin Homo sapiens 67-74 27865354-8 2016 Homeostasis model assessment of insulin resistance index was calculated from insulin and glucose levels. Glucose 89-96 insulin Homo sapiens 32-39 27374266-5 2016 In a patient with previously known diabetes, a treatment with insulin will also be started when preprandial plasma glucose is 1.40g/L (7.8mmol/L). Glucose 115-122 insulin Homo sapiens 62-69 27374266-7 2016 Insulin dosage will be determined according to the capillary glucose monitoring. Glucose 61-68 insulin Homo sapiens 0-7 28074994-7 2016 A diagnosis of normoglycemic diabetic ketoacidosis was formulated and treatment with hydration and regular insulin according to capillary blood glucose levels was started. Glucose 144-151 insulin Homo sapiens 107-114 27582250-2 2016 This review applies an external bioenergetic critique to the central processes of glucose-stimulated insulin secretion, including glycolytic and mitochondrial metabolism, the cytosolic adenine nucleotide pool, and its interaction with plasma membrane ion channels. Glucose 82-89 insulin Homo sapiens 101-108 27921433-3 2016 As critical illness is connected with so-called insulin resistance, it is recommended to reduce the glucose dose and maintain normal blood glucose. Glucose 100-107 insulin Homo sapiens 48-55 27921433-3 2016 As critical illness is connected with so-called insulin resistance, it is recommended to reduce the glucose dose and maintain normal blood glucose. Glucose 139-146 insulin Homo sapiens 48-55 27669747-0 2016 Assessment of three fasting plasma glucose targets for insulin glargine-based therapy in people with type 2 diabetes mellitus in China: study protocol for a randomized controlled trial. Glucose 35-42 insulin Homo sapiens 55-62 27376416-7 2016 Insulin level inversely correlated with insulin sensitivity and positively with glucose (r = -0.893, r = 0.166, respectively). Glucose 80-87 insulin Homo sapiens 0-7 27680512-3 2016 Transcriptomic meta-analysis and network analysis of blood microarrays from untreated patients with PD and depression identified genes enriched in pathways related to the immune system, metabolism of lipids, glucose, fatty acids, nicotinamide, lysosome, insulin signaling and type 1 diabetes. Glucose 208-215 insulin Homo sapiens 254-261 27682598-1 2016 The Triglyceride Glucose Index (TyG index) is considered a surrogate marker of insulin resistance. Glucose 17-24 insulin Homo sapiens 79-86 27677243-2 2016 Overlaps in the regulation of glucose and energy homeostasis have been reported between leptin and insulin. Glucose 30-37 insulin Homo sapiens 99-106 27669747-2 2016 The aim of this study is to identify the fasting plasma glucose (FPG) target that will provide the highest control rate of HbA1c <7 % in Chinese patients with T2DM treated with an insulin glargine-based regimen as an adjunct to an established OAD regimen. Glucose 56-63 insulin Homo sapiens 183-190 27662374-0 2016 Tissue-Specific Stem Cells Obtained by Reprogramming of Non-Obese Diabetic (NOD) Mouse-Derived Pancreatic Cells Confer Insulin Production in Response to Glucose. Glucose 153-160 insulin Homo sapiens 119-126 27521895-7 2016 OEA also increased the phosphorylation of IRS-1, Akt and AS160 leading to increased GLUT4 translocation to the plasma membrane indicating that it promotes insulin stimulated glucose uptake in L6 myotubes by activating the PI3K pathway. Glucose 174-181 insulin Homo sapiens 155-162 27662374-6 2016 In this study, we showed that glucose-sensitive insulin-producing cells are successfully generated by transfecting primary pancreatic cells from NOD mice (aged 6 months old) with a plasmid harboring the cDNAs for Oct-3/4, Sox2, Klf4, and c-Myc. Glucose 30-37 insulin Homo sapiens 48-55 27662374-11 2016 Induction of these cells to the pancreatic beta-cell lineage demonstrated their capability to produce insulin in response to glucose. Glucose 125-132 insulin Homo sapiens 102-109 27699280-5 2016 High glucose exposure resulted in a modest increase in PTB and TIAR binding to an insulin mRNA sequence. Glucose 5-12 insulin Homo sapiens 82-89 27640062-28 2016 AUTHORS" CONCLUSIONS: The addition of all oral glucose-lowering agents in people with type 2 diabetes and inadequate glycaemic control who are on insulin therapy has positive effects on glycaemic control and insulin requirements. Glucose 47-54 insulin Homo sapiens 146-153 27501754-3 2016 Glucose uptake and consumption assay indicated that pretreatment with 80 muM H2O2 for 2 h inhibited insulin-stimulated glucose uptake in C2C12 myotubes, and the reason for it, is that chronic H2O2 treatment decreased insulin-induced glucose transporter 4 (GLUT4) translocation from cell plasma to cell membrane. Glucose 119-126 insulin Homo sapiens 100-107 27501754-3 2016 Glucose uptake and consumption assay indicated that pretreatment with 80 muM H2O2 for 2 h inhibited insulin-stimulated glucose uptake in C2C12 myotubes, and the reason for it, is that chronic H2O2 treatment decreased insulin-induced glucose transporter 4 (GLUT4) translocation from cell plasma to cell membrane. Glucose 119-126 insulin Homo sapiens 217-224 27640062-28 2016 AUTHORS" CONCLUSIONS: The addition of all oral glucose-lowering agents in people with type 2 diabetes and inadequate glycaemic control who are on insulin therapy has positive effects on glycaemic control and insulin requirements. Glucose 47-54 insulin Homo sapiens 208-215 27640062-31 2016 Other well-known adverse effects of oral glucose-lowering agents have to be taken into account when prescribing oral glucose-lowering agents in addition to insulin therapy. Glucose 41-48 insulin Homo sapiens 156-163 27621482-2 2016 Insulin, a peptide hormone, is produced in and secreted from pancreatic beta-cells following elevated blood glucose levels. Glucose 108-115 insulin Homo sapiens 0-7 27695421-8 2016 Conclusion:These findings support a role for redox homeostasis and SAPK signaling in insulin-stimulated glucose uptake which may contribute to the enhancement of insulin sensitivity in obese men 3 h after HIIE. Glucose 104-111 insulin Homo sapiens 85-92 27695421-8 2016 Conclusion:These findings support a role for redox homeostasis and SAPK signaling in insulin-stimulated glucose uptake which may contribute to the enhancement of insulin sensitivity in obese men 3 h after HIIE. Glucose 104-111 insulin Homo sapiens 162-169 27621482-3 2016 Upon its release, insulin induces the removal of excessive exogenous glucose from the bloodstream primarily by stimulating glucose uptake into insulin-dependent tissues as well as promoting hepatic glycogenesis. Glucose 69-76 insulin Homo sapiens 18-25 27621482-3 2016 Upon its release, insulin induces the removal of excessive exogenous glucose from the bloodstream primarily by stimulating glucose uptake into insulin-dependent tissues as well as promoting hepatic glycogenesis. Glucose 69-76 insulin Homo sapiens 143-150 27621482-3 2016 Upon its release, insulin induces the removal of excessive exogenous glucose from the bloodstream primarily by stimulating glucose uptake into insulin-dependent tissues as well as promoting hepatic glycogenesis. Glucose 123-130 insulin Homo sapiens 18-25 27621482-3 2016 Upon its release, insulin induces the removal of excessive exogenous glucose from the bloodstream primarily by stimulating glucose uptake into insulin-dependent tissues as well as promoting hepatic glycogenesis. Glucose 123-130 insulin Homo sapiens 143-150 27594926-6 2016 An index of whole-body insulin sensitivity was estimated from oral glucose tolerance tests. Glucose 67-74 insulin Homo sapiens 23-30 27818934-4 2016 RESULTS: We identified increased glucose-6-phosphate dehydrogenase (G6PDH) activity as a common intracellular adaptation that occurs in parallel with the induction of insulin resistance in skeletal muscle and is present across animal and human disease states with an underlying pathology of insulin resistance and glucose intolerance. Glucose 33-40 insulin Homo sapiens 167-174 27818934-4 2016 RESULTS: We identified increased glucose-6-phosphate dehydrogenase (G6PDH) activity as a common intracellular adaptation that occurs in parallel with the induction of insulin resistance in skeletal muscle and is present across animal and human disease states with an underlying pathology of insulin resistance and glucose intolerance. Glucose 33-40 insulin Homo sapiens 291-298 27818934-6 2016 Furthermore, attenuation of G6PDH activity in skeletal muscle cells via (a) increased nNOSmu/NOS activity, (b) pharmacological G6PDH inhibition, or (c) genetic G6PDH inhibition increases insulin-independent glucose uptake. Glucose 207-214 insulin Homo sapiens 187-194 27626415-3 2016 The effect of theophylline is dose- and cell line-dependent, resulting in a minimal stimulation index of five followed by a rapid return to baseline insulin secretion by reducing glucose concentrations after a first high glucose stimulation. Glucose 179-186 insulin Homo sapiens 149-156 27626415-3 2016 The effect of theophylline is dose- and cell line-dependent, resulting in a minimal stimulation index of five followed by a rapid return to baseline insulin secretion by reducing glucose concentrations after a first high glucose stimulation. Glucose 221-228 insulin Homo sapiens 149-156 27505441-7 2016 Importantly, 9c restores the ER stress-impaired glucose-stimulated insulin secretion response and survival in primary human islet beta-cells. Glucose 48-55 insulin Homo sapiens 67-74 27363333-4 2016 Due to stimulated gluconeogenesis, insulin-stimulated glucose uptake was decreased in HepG2 cells. Glucose 54-61 insulin Homo sapiens 35-42 27488662-0 2016 Ketoisocaproic acid, a metabolite of leucine, suppresses insulin-stimulated glucose transport in skeletal muscle cells in a BCAT2-dependent manner. Glucose 76-83 insulin Homo sapiens 57-64 27488662-3 2016 Here, we first showed that the inhibitory effect of leucine on insulin-stimulated glucose transport in L6 myotubes was dampened when other amino acids were present, due in part to a 140% stimulation of basal glucose transport (P < 0.05). Glucose 82-89 insulin Homo sapiens 63-70 27488662-3 2016 Here, we first showed that the inhibitory effect of leucine on insulin-stimulated glucose transport in L6 myotubes was dampened when other amino acids were present, due in part to a 140% stimulation of basal glucose transport (P < 0.05). Glucose 208-215 insulin Homo sapiens 63-70 27488662-4 2016 Importantly, we also showed that alpha-ketoisocaproic acid (KIC), an obligatory metabolite of leucine, stimulated mTORC1 signaling but suppressed insulin-stimulated glucose transport (-34%, P < 0.05) in an mTORC1-dependent manner. Glucose 165-172 insulin Homo sapiens 146-153 27488662-5 2016 The effect of KIC on insulin-stimulated glucose transport was abrogated in cells depleted of branched-chain aminotransferase 2 (BCAT2), the enzyme that catalyzes the reversible transamination of KIC to leucine. Glucose 40-47 insulin Homo sapiens 21-28 26443937-9 2016 RESULTS: We observed that insulin concentration was significantly reduced at 120 min after the administration of glucose in Pro251 allele carriers, whereas glucose levels were similar in Pro251 allele carriers and non-carriers throughout the OGTT. Glucose 113-120 insulin Homo sapiens 26-33 27531029-4 2016 Through specific binding of glucose with boronic acid moieties on the R6G-APB PNs and insulin-APB PNs, glucose induces expansion of the APB PNs, leading to release of R6G and insulin molecules, respectively. Glucose 28-35 insulin Homo sapiens 167-182 27531029-4 2016 Through specific binding of glucose with boronic acid moieties on the R6G-APB PNs and insulin-APB PNs, glucose induces expansion of the APB PNs, leading to release of R6G and insulin molecules, respectively. Glucose 103-110 insulin Homo sapiens 86-93 27531029-4 2016 Through specific binding of glucose with boronic acid moieties on the R6G-APB PNs and insulin-APB PNs, glucose induces expansion of the APB PNs, leading to release of R6G and insulin molecules, respectively. Glucose 103-110 insulin Homo sapiens 167-182 27531029-6 2016 Release of insulin from insulin-APB PNs is significant and rapid when the glucose concentration is higher than 7 mM. Glucose 74-81 insulin Homo sapiens 11-18 27531029-6 2016 Release of insulin from insulin-APB PNs is significant and rapid when the glucose concentration is higher than 7 mM. Glucose 74-81 insulin Homo sapiens 24-31 27531029-7 2016 Having advantages of low cost, simple preparation, biocompatibility, and continuous response to glucose, the insulin-APB PNs hold great potential as an alternative for treating diabetic patients. Glucose 96-103 insulin Homo sapiens 109-116 27531029-8 2016 Graphical Abstract Quantitation of glucose and release of insulin by glucose responsive 3-aminophenylboronic acid polymer nanoparticles. Glucose 69-76 insulin Homo sapiens 58-65 27046086-14 2016 CONCLUSIONS: In a safety cohort of critically ill diabetic patients, a blood glucose concentration target of 10-14 mmol/L resulted in fewer episodes of negative glycemic distance or relative hypoglycemia and reduced insulin administration compared with a target of 6-10 mmol/L. Glucose 77-84 insulin Homo sapiens 216-223 26954230-4 2016 Compared with the control, plasma glucose concentration was significantly decreased after insulin treatment of 3, 5, 10, and 20 IU for 4 h in chicks with ad libitum feeding (p<0.05). Glucose 34-41 insulin Homo sapiens 90-97 26954230-5 2016 In fasted chicks, 10 and 20 IU insulin treatments significantly decreased the plasma glucose level for 4 h (p<0.05). Glucose 85-92 insulin Homo sapiens 31-38 27020663-0 2016 Long-term efficacy of real-time continuous glucose monitoring in patients with brittle or high-hypoglycaemic-risk type 1 diabetes treated by insulin pump: A single-centre experience. Glucose 43-50 insulin Homo sapiens 141-148 26445403-6 2016 Obestatin is a 23-amino-acid peptide, which is not only thought to suppress food intake and decrease gastric emptying but also found to exert survival effects in pancreatic beta cells, increase glucose-stimulated insulin secretion, and reduce insulin resistance and inflammation. Glucose 194-201 insulin Homo sapiens 213-220 26789012-0 2016 Effectiveness of the low-glucose suspend feature of insulin pump during fasting during Ramadan in type 1 diabetes mellitus. Glucose 25-32 insulin Homo sapiens 52-59 27475999-10 2016 Before the DTTP, 42 of 72 patients (58.3%) adjusted their insulin dose to correct high blood glucose levels by adjustment rules (factor for correction or correction scheme) and 20 of 72 people (27.8%) by personal experience/feeling. Glucose 93-100 insulin Homo sapiens 58-65 27388474-4 2016 RESULTS: With the same insulin dose, the HFHP increased the glucose incremental area under the curve over twofold (13,320 +- 2,960 vs. 27,092 +- 1,709 mg/dL min; P = 0.0013). Glucose 60-67 insulin Homo sapiens 23-30 27388474-5 2016 To achieve target glucose control following the HFHP, 65% more insulin was required (range 17%-124%) with a 30%/70% split over 2.4 h. CONCLUSIONS: This study demonstrates that insulin dose calculations need to consider meal composition in addition to carbohydrate content and provides the foundation for new insulin-dosing algorithms to cover meals of varying macronutrient composition. Glucose 18-25 insulin Homo sapiens 63-70 27388474-5 2016 To achieve target glucose control following the HFHP, 65% more insulin was required (range 17%-124%) with a 30%/70% split over 2.4 h. CONCLUSIONS: This study demonstrates that insulin dose calculations need to consider meal composition in addition to carbohydrate content and provides the foundation for new insulin-dosing algorithms to cover meals of varying macronutrient composition. Glucose 18-25 insulin Homo sapiens 176-183 27388474-5 2016 To achieve target glucose control following the HFHP, 65% more insulin was required (range 17%-124%) with a 30%/70% split over 2.4 h. CONCLUSIONS: This study demonstrates that insulin dose calculations need to consider meal composition in addition to carbohydrate content and provides the foundation for new insulin-dosing algorithms to cover meals of varying macronutrient composition. Glucose 18-25 insulin Homo sapiens 176-183 27615131-1 2016 The highly sophisticated identity of pancreatic beta-cells is geared to accomplish its unique feat of providing insulin for organismal glucose and lipid homeostasis. Glucose 135-142 insulin Homo sapiens 112-119 27407117-6 2016 In the AST, insulin secretory response to arginine at basal glucose and during hyperglycemia was lower in T2DM compared with NGT and PDM (>58%; all P < 0.001). Glucose 60-67 insulin Homo sapiens 12-19 27615132-3 2016 The effects of ageing on beta-cell function, namely glucose-stimulated insulin secretion (GSIS), have not been studied as extensively. Glucose 52-59 insulin Homo sapiens 71-78 27411698-0 2016 Insulin Injection Into Lipohypertrophic Tissue: Blunted and More Variable Insulin Absorption and Action and Impaired Postprandial Glucose Control. Glucose 130-137 insulin Homo sapiens 0-7 27615132-4 2016 Recent work revealed that, surprisingly, beta-cells of mature mice and humans secrete more insulin than young beta-cells in response to high glucose concentrations, potentially serving to counteract age-related peripheral insulin resistance. Glucose 141-148 insulin Homo sapiens 91-98 27411698-8 2016 CONCLUSIONS: Insulin absorption and action are blunted and considerably more variable with LHT injection, leading to profound deterioration in postprandial glucose control. Glucose 156-163 insulin Homo sapiens 13-20 27615132-4 2016 Recent work revealed that, surprisingly, beta-cells of mature mice and humans secrete more insulin than young beta-cells in response to high glucose concentrations, potentially serving to counteract age-related peripheral insulin resistance. Glucose 141-148 insulin Homo sapiens 222-229 27615132-9 2016 This leads to an overall reduction in the amplitude of insulin secretion between low and high glucose at old age, which may contribute to a deterioration in metabolic control. Glucose 94-101 insulin Homo sapiens 55-62 27615135-4 2016 In this review, we discuss mechanisms of beta-cell metabolic and functional adaptation in the context of two physiological states that alter glucose-stimulated insulin secretion: fasting and insulin resistance. Glucose 141-148 insulin Homo sapiens 160-167 27333446-1 2016 BACKGROUND: Technosphere( ) insulin (TI), an inhaled human insulin with a fast onset of action, provides a novel option for the control of prandial glucose. Glucose 148-155 insulin Homo sapiens 28-35 27615135-4 2016 In this review, we discuss mechanisms of beta-cell metabolic and functional adaptation in the context of two physiological states that alter glucose-stimulated insulin secretion: fasting and insulin resistance. Glucose 141-148 insulin Homo sapiens 191-198 27333446-1 2016 BACKGROUND: Technosphere( ) insulin (TI), an inhaled human insulin with a fast onset of action, provides a novel option for the control of prandial glucose. Glucose 148-155 insulin Homo sapiens 59-66 27505305-2 2016 The predictive low glucose management (PLGM) system employs a predictive algorithm that suspends basal insulin when hypoglycemia is predicted. Glucose 19-26 insulin Homo sapiens 103-110 27364997-2 2016 Glucose-responsive insulin delivery above and below a preset insulin amount informed by sensor glucose readings differentiates closed-loop systems from conventional, threshold-suspend and predictive-suspend insulin pump therapy. Glucose 95-102 insulin Homo sapiens 19-26 27364997-2 2016 Glucose-responsive insulin delivery above and below a preset insulin amount informed by sensor glucose readings differentiates closed-loop systems from conventional, threshold-suspend and predictive-suspend insulin pump therapy. Glucose 95-102 insulin Homo sapiens 61-68 27207534-6 2016 Then, experimentally lowering glucose sensing, specifically in the ARC, resulted in glucose intolerance due to deficient insulin secretion and no significant effect in the VMN, but in the LHA it resulted in a lowering of the glucose threshold that improved glucose tolerance and/or improved insulin sensitivity, with an exaggerated counter-regulatory response for glucagon secretion. Glucose 30-37 insulin Homo sapiens 121-128 27505305-5 2016 The predictive algorithm suspended basal insulin when sensor glucose was predicted to be below the preset hypoglycemic threshold in 30 min. Glucose 61-68 insulin Homo sapiens 41-48 27491070-2 2016 His seminal discoveries have shed light on the regulation of ion pumps and other transport proteins, insulin-mediated regulation of glucose metabolism and the role of signal transduction networks in cell transformation. Glucose 132-139 insulin Homo sapiens 101-108 27580280-2 2016 Understanding the wide variety of insulin preparations available will assist the clinician in guiding people with diabetes and their caregivers through the complexities of self-care and promote safe and optimal glucose control. Glucose 211-218 insulin Homo sapiens 34-41 30085613-5 2016 The glucose might influenced the bioactivity of insulin in the SAA-insulin and SAB-insulin systems by changing the binding constants of SAA (or SAB) with insulin and exacerbating the changes of insulin conformation and relative contents of alpha-belices. Glucose 4-11 insulin Homo sapiens 48-55 30085613-5 2016 The glucose might influenced the bioactivity of insulin in the SAA-insulin and SAB-insulin systems by changing the binding constants of SAA (or SAB) with insulin and exacerbating the changes of insulin conformation and relative contents of alpha-belices. Glucose 4-11 insulin Homo sapiens 67-74 30085613-5 2016 The glucose might influenced the bioactivity of insulin in the SAA-insulin and SAB-insulin systems by changing the binding constants of SAA (or SAB) with insulin and exacerbating the changes of insulin conformation and relative contents of alpha-belices. Glucose 4-11 insulin Homo sapiens 67-74 27735027-6 2016 After withdrawing insulin completely, 13.2 months later, there is a reincrease in the level of blood glucose of the patient. Glucose 101-108 insulin Homo sapiens 18-25 27377425-6 2016 Variants in GCKR, GCK, DGKB/TMEM195 (P for interactions = 0.02, 0.02, and 0.01), especially, showed interactions with obesity: obese, inactive, and high fat-diet women had greater increases in fasting glucose, insulin, and HOMA-IR levels. Glucose 201-208 insulin Homo sapiens 210-217 26969516-4 2016 These drugs have pleiotropic effects on glucose metabolism and different actions complementary to those of insulin-this Review reports the effects of these drugs on glycaemic control, glucose variability, hypoglycaemia, insulin requirements, and bodyweight. Glucose 184-191 insulin Homo sapiens 107-114 26660513-6 2016 RESULTS: The three-compartment model of insulin kinetics, coupled with HE depending on glucose concentration, showed the best fit and a good ability to precisely estimate the parameters. Glucose 87-94 insulin Homo sapiens 40-47 26439243-6 2016 The AUCs of plasma insulin levels or insulin resistance index (IRI): (AUCs of insulin) x (AUCs of glucose) as the insulin resistance marker were greater in diabetic CAD group than non-diabetic CAD group (insulin, P = 0.0373; IRI, P = 0.0228). Glucose 98-105 insulin Homo sapiens 37-44 26439243-6 2016 The AUCs of plasma insulin levels or insulin resistance index (IRI): (AUCs of insulin) x (AUCs of glucose) as the insulin resistance marker were greater in diabetic CAD group than non-diabetic CAD group (insulin, P = 0.0373; IRI, P = 0.0228). Glucose 98-105 insulin Homo sapiens 37-44 26439243-6 2016 The AUCs of plasma insulin levels or insulin resistance index (IRI): (AUCs of insulin) x (AUCs of glucose) as the insulin resistance marker were greater in diabetic CAD group than non-diabetic CAD group (insulin, P = 0.0373; IRI, P = 0.0228). Glucose 98-105 insulin Homo sapiens 37-44 26439243-6 2016 The AUCs of plasma insulin levels or insulin resistance index (IRI): (AUCs of insulin) x (AUCs of glucose) as the insulin resistance marker were greater in diabetic CAD group than non-diabetic CAD group (insulin, P = 0.0373; IRI, P = 0.0228). Glucose 98-105 insulin Homo sapiens 37-44 27142278-6 2016 Of particular interest in this space are the recent inventions of a low-glucose suspend feature in the portable systems that automatically stops insulin delivery 2 h following a glucose sensor value <70 mg/dL and a bio-hormonal pump system consisting of insulin and glucagon pumps. Glucose 72-79 insulin Homo sapiens 145-152 27142278-6 2016 Of particular interest in this space are the recent inventions of a low-glucose suspend feature in the portable systems that automatically stops insulin delivery 2 h following a glucose sensor value <70 mg/dL and a bio-hormonal pump system consisting of insulin and glucagon pumps. Glucose 72-79 insulin Homo sapiens 257-264 27142278-6 2016 Of particular interest in this space are the recent inventions of a low-glucose suspend feature in the portable systems that automatically stops insulin delivery 2 h following a glucose sensor value <70 mg/dL and a bio-hormonal pump system consisting of insulin and glucagon pumps. Glucose 178-185 insulin Homo sapiens 145-152 27235672-3 2016 With developments in insulin therapy still happening, it is worth keeping up to date on trends in the use of this powerful glucose-lowering agent. Glucose 123-130 insulin Homo sapiens 21-28 27484094-0 2016 Atorvastatin ameliorates endothelium-specific insulin resistance induced by high glucose combined with high insulin. Glucose 81-88 insulin Homo sapiens 46-53 27054677-2 2016 PURPOSE: This study aimed to quantify how acute passive cycling affects glucose and insulin responses to an oral glucose tolerance test (OGTT) and basic cognition compared with sitting and moderate-intensity active cycling. Glucose 113-120 insulin Homo sapiens 84-91 27506738-0 2016 Autophagy protects human podocytes from high glucose-induced injury by preventing insulin resistance. Glucose 45-52 insulin Homo sapiens 82-89 27506738-2 2016 In the present study, we aimed to investigate the high glucose-induced insulin resistance and cell injury in human podocytes and the putative role of autophagy in this process. Glucose 55-62 insulin Homo sapiens 71-78 27506738-9 2016 CONCLUSIONS: The presence or activation of autophagy was found to play a protective role in human podocytes against high glucose-induced insulin resistance and cell injury, which indicates a novel cellular mechanism and provides a potential therapeutic target for diabetic nephropathy (DN). Glucose 121-128 insulin Homo sapiens 137-144 27436126-1 2016 Pancreatic beta cells, unique cells that secrete insulin in response to an increase in glucose levels, play a significant role in glucose homeostasis. Glucose 87-94 insulin Homo sapiens 49-56 30228507-5 2016 Furthermore the Asian Indian population is particularly susceptible to exaggerated rises in postprandial glucose and triglycerides because they are genetically predisposed to metabolic syndrome (MetSyn), insulin resistance, and T2D. Glucose 105-112 insulin Homo sapiens 204-211 26251318-4 2016 RESULTS: Insulin-stimulated glucose disposal (Rd) declined significantly across the glycemic groups from OB-NGT to OB-preDM to OB-T2DM with a corresponding increase in TyG index (8.3 +- 0.5, 8.6 +- 0.5, 8.9 +- 0.6, p < 0.0001). Glucose 28-35 insulin Homo sapiens 9-16 27157469-7 2016 Insulin secretion was significantly higher for SP20 and SP40 than that for SP0 before and at 15 min after oral glucose consumption. Glucose 111-118 insulin Homo sapiens 0-7 27411561-1 2016 Insulin resistance results from impaired insulin signaling in target tissues that leads to increased levels of insulin required to control plasma glucose levels. Glucose 146-153 insulin Homo sapiens 0-7 27411561-1 2016 Insulin resistance results from impaired insulin signaling in target tissues that leads to increased levels of insulin required to control plasma glucose levels. Glucose 146-153 insulin Homo sapiens 41-48 27597765-3 2016 Using human myotubes, we demonstrated that overexpression of miR-148b decreased NRAS and ROCK1 protein levels, and PKB phosphorylation and glucose uptake in response to insulin. Glucose 139-146 insulin Homo sapiens 169-176 27582778-0 2016 Fatty acids stimulate insulin secretion from human pancreatic islets at fasting glucose concentrations via mitochondria-dependent and -independent mechanisms. Glucose 80-87 insulin Homo sapiens 22-29 27506420-12 2016 RESULTS: Following pancreatectomy and splenectomy, the animals showed a quick recovery from surgery and initial analgetic medication and volume substitution could be terminated within 24 h. A rapid increase in blood glucose was observed immediately following pancreatectomy necessitating insulin therapy. Glucose 216-223 insulin Homo sapiens 288-295 30193421-3 2016 In the endocrine pancreas the regulation of the main function of ss-cells, such as glucose-stimulated insulin secretion is carried out via this system. Glucose 83-90 insulin Homo sapiens 102-109 27582778-6 2016 RESULTS: The average increase in insulin secretion, measured from statically incubated and dynamically perifused human islets, was about 2-fold for saturated free fatty acids (SFAs) (palmitate and stearate) and 3-fold for mono-unsaturated free fatty acids (MUFAs) (palmitoleate and oleate) compared with 5.5 mmol/l glucose alone. Glucose 315-322 insulin Homo sapiens 33-40 27582778-12 2016 CONCLUSIONS: The findings suggest that long-chain FFAs acutely induce insulin secretion from human islets at physiologically fasting glucose concentrations, with MUFAs being more potent than SFAs, and that this effect is associated with increased glycolytic flux and mitochondrial respiration. Glucose 133-140 insulin Homo sapiens 70-77 27554943-0 2016 Frequent interruptions of sedentary time modulates contraction- and insulin-stimulated glucose uptake pathways in muscle: Ancillary analysis from randomized clinical trials. Glucose 87-94 insulin Homo sapiens 68-75 27334121-12 2016 Multiple linear regression analysis confirmed that the ratio of the incremental insulin to glucose responses over the first 30 min during OGTT (DeltaIns30/DeltaG30), average insulin dose before achieving targets, initial insulin dose and LDL-c were independent predictors for TGG. Glucose 91-98 insulin Homo sapiens 80-87 27554943-4 2016 Contraction- and insulin-mediated glucose uptake signaling pathways as well as changes in oxidative phosphorylation proteins were examined. Glucose 34-41 insulin Homo sapiens 17-24 27184690-1 2016 BACKGROUND: The closed-loop (CL) system delivers insulin in a glucose-responsive manner and optimal postprandial glycemic control is difficult to achieve with the algorithm and insulin available. Glucose 62-69 insulin Homo sapiens 49-56 27596552-5 2016 Compared with insulin glargine, insulin degludec was more effective in reducing fasting blood glucose (MD=-0.40, 95%CI: -0.65--0.16, P=0.001), but less effective in improving levels of glycated hemoglobin (MD=0.13, 95%CI: 0.08-0.17, P<0.001). Glucose 94-101 insulin Homo sapiens 32-39 27381030-5 2016 The quantification of how much insulin and CHO information improves glucose prediction is missing in the literature and is investigated, in an open-loop setting, in this proof-of-concept study. Glucose 68-75 insulin Homo sapiens 31-38 27381030-14 2016 CONCLUSIONS: In an open-loop setting, with PH >= 30 minutes, information on CHO and insulin improves short-term glucose prediction in the 2-hour time window following a meal, but not during the night. Glucose 115-122 insulin Homo sapiens 87-94 27534260-7 2016 The median sensor glucose concentration was 5.0 (2.7-7.3) mmol/L, and correlated with fasting plasma glucose concentrations (rs = 0.190, p = 0.046), serum insulin concentrations (rs = 0.218, p = 0.021), and HOMA-IR (rs = 0.230, p = 0.015). Glucose 18-25 insulin Homo sapiens 155-162 27534260-10 2016 Children with insulin resistance had higher median sensor glucose concentrations and a larger hyperglycaemic sensor glucose AUC, which are both associated with specific parameters predicting cardiovascular disease risk. Glucose 58-65 insulin Homo sapiens 14-21 27387397-8 2016 Further study indicated that genistein (an insulin receptor tyrosine kinase inhibitor) altered the effect of marein on glucose uptake, and both LY294002 (a phosphatidylinositol 3-kinase inhibitor) and compound C (an AMP-activated protein kinase inhibitor) significantly decreased marein-stimulated 2-NBDG uptake. Glucose 119-126 insulin Homo sapiens 43-50 27387397-12 2016 CONCLUSIONS: Consequently, marein improved insulin resistance induced by high glucose in HepG2 cells through CaMKK/AMPK/GLUT1 to promote glucose uptake, through IRS/Akt/GSK-3beta to increase glycogen synthesis, and through Akt/FoxO1 to decrease gluconeogenesis. Glucose 78-85 insulin Homo sapiens 43-50 27387397-12 2016 CONCLUSIONS: Consequently, marein improved insulin resistance induced by high glucose in HepG2 cells through CaMKK/AMPK/GLUT1 to promote glucose uptake, through IRS/Akt/GSK-3beta to increase glycogen synthesis, and through Akt/FoxO1 to decrease gluconeogenesis. Glucose 137-144 insulin Homo sapiens 43-50 27516571-8 2016 In type 2 diabetes mellitus, both chemerin and omentin enhance the body sensitivity to insulin, which results in increased glucose uptake. Glucose 123-130 insulin Homo sapiens 87-94 27518102-11 2016 Insulin infusion raised glucose disposal slightly lower post-transplant compared to pre-transplant, but not significantly, thus concluding differences in insulin sensitivity were similar. Glucose 24-31 insulin Homo sapiens 0-7 27547409-3 2016 METHODS: Isolated human islets were infected with different strains of coxsackievirus B (CVB) virus and the glucose-stimulated insulin release (GSIS) was measured in a dynamic perifusion system. Glucose 108-115 insulin Homo sapiens 127-134 28003935-8 2016 Cell aggregation improved glucose-stimulated insulin secretion, demonstrating the benefit of cell-cell contacts. Glucose 26-33 insulin Homo sapiens 45-52 27515427-7 2016 Differentiated IPCs were assessed by the expression of various beta-cell-related markers using quantitative RT-PCR, and functionally by measuring glucose-stimulated insulin secretion. Glucose 146-153 insulin Homo sapiens 165-172 27689010-8 2016 RESULTS: In both instances glucose-stimulated insulin release was not inhibited. Glucose 27-34 insulin Homo sapiens 46-53 27527213-1 2016 Diabetes is a metabolic, endocrine disorder which is characterized by hyperglycemia and glucose intolerance due to insulin resistance. Glucose 88-95 insulin Homo sapiens 115-122 26831749-3 2016 The availability of continuous subcutaneous insulin infusion pumps (CSII) in combination with continuous glucose monitoring systems (CGM) provides an opportunity to monitor glucose levels more closely and deliver insulin more safely. Glucose 105-112 insulin Homo sapiens 213-220 26831749-3 2016 The availability of continuous subcutaneous insulin infusion pumps (CSII) in combination with continuous glucose monitoring systems (CGM) provides an opportunity to monitor glucose levels more closely and deliver insulin more safely. Glucose 173-180 insulin Homo sapiens 44-51 27606384-16 2016 Subjects taking metformin demonstrated increased insulin sensitivity [glucose disposal per unit plasma insulin difference between means during high-dose insulin 0.02 mg/kg, 95% CI 0.001 to 0.03 mg/kg (fat-free mass)/minute/microIU/l; p = 0.04] compared with those taking placebo and enhanced endogenous glucose production [difference between means 0.54 mg/kg, 95% CI 0.08 to 1.00 mg/kg (fat-free mass)/minute; p = 0.02]. Glucose 70-77 insulin Homo sapiens 49-56 27194722-9 2016 By their combined actions, glucagon and insulin, working in a combinatory mode, could ensure an independent regulation of both plasma glucose and plasma K concentrations. Glucose 134-141 insulin Homo sapiens 40-47 27245333-1 2016 It is known that for a given insulin level glucose clearance depends on glucose concentration. Glucose 43-50 insulin Homo sapiens 29-36 27245333-1 2016 It is known that for a given insulin level glucose clearance depends on glucose concentration. Glucose 72-79 insulin Homo sapiens 29-36 27245333-4 2016 A mathematical model was developed in which glucose utilization was represented as a Michaelis-Menten function of glucose with constant Km and insulin-controlled Vmax, consistently with the basic notions of glucose transport. Glucose 44-51 insulin Homo sapiens 143-150 27245333-4 2016 A mathematical model was developed in which glucose utilization was represented as a Michaelis-Menten function of glucose with constant Km and insulin-controlled Vmax, consistently with the basic notions of glucose transport. Glucose 114-121 insulin Homo sapiens 143-150 27245333-4 2016 A mathematical model was developed in which glucose utilization was represented as a Michaelis-Menten function of glucose with constant Km and insulin-controlled Vmax, consistently with the basic notions of glucose transport. Glucose 114-121 insulin Homo sapiens 143-150 27245333-8 2016 Median model-derived glucose clearance at 600 pmol/l insulin was reduced from 246 to 158 ml min(-1) m(-2) when glucose was raised from 5 to 10 mmol/l. Glucose 21-28 insulin Homo sapiens 53-60 27245333-8 2016 Median model-derived glucose clearance at 600 pmol/l insulin was reduced from 246 to 158 ml min(-1) m(-2) when glucose was raised from 5 to 10 mmol/l. Glucose 111-118 insulin Homo sapiens 53-60 27406738-0 2016 Imeglimin lowers glucose primarily by amplifying glucose-stimulated insulin secretion in high-fat-fed rodents. Glucose 49-56 insulin Homo sapiens 68-75 27492703-4 2016 A fasting serum insulin assay performed on a Modular platform (Modular analytic E170, Roche Diagnostic, Meylan, France) showed a highly elevated value of 194.7 mIU/L, whereas on the same sample glucose and C-peptide levels were normal. Glucose 194-201 insulin Homo sapiens 16-23 28268592-2 2016 The blood glucose regulation PBPK/PD model simulates the distribution and metabolization of glucose, insulin and glucagon on an organ and whole body level. Glucose 10-17 insulin Homo sapiens 101-108 28324962-2 2016 In a dual hormone AP, insulin and glucagon are delivered automatically to the body based on glucose sensor measurements using a control algorithm that calculates the amount of hormones to be infused. Glucose 92-99 insulin Homo sapiens 22-29 28325022-5 2016 The oral glucose tolerance test (OGTT) is a medical test used to screen for prediabetes, type 2 diabetes and insulin resistance. Glucose 9-16 insulin Homo sapiens 109-116 28325022-10 2016 Insulin secretion decreases in marathon runners due to a significant reduction in plasma glucose concentration, but insulin secretion does not decrease in metabolic syndrome subjects due to insulin resistance, consequently plasma glucose concentration does not achieve normal levels. Glucose 89-96 insulin Homo sapiens 0-7 27502601-2 2016 Its mechanism of action for lowering blood glucose is essentially via inhibition of the rapid degradation of incretin hormones, such as glucagon-like peptide (GLP)-1 and gastric inhibitory polypeptide (GIP), thus the plasma concentration of GLP-1 increases, which promotes insulin secretion from the pancreatic beta cells and suppresses glucagon secretion from the alpha cells. Glucose 43-50 insulin Homo sapiens 273-280 27487295-3 2016 Using pancreatic beta-cells, insulin secretion was impaired by fA-I in the lipid-free and reconstituted HDL (rHDL) states, by up to 35%, and 40%, respectively, under hyperglycemic conditions (25 mmol/L glucose). Glucose 202-209 insulin Homo sapiens 29-36 27312935-4 2016 Many variants associated with insulin resistance are directly involved in glucose metabolism; however, functional studies are required to assess the contribution of other variants to the development of insulin resistance. Glucose 74-81 insulin Homo sapiens 30-37 27312935-4 2016 Many variants associated with insulin resistance are directly involved in glucose metabolism; however, functional studies are required to assess the contribution of other variants to the development of insulin resistance. Glucose 74-81 insulin Homo sapiens 202-209 27337958-14 2016 Postpartum, insulin doses must be reduced and glucoses closely monitored in women with T1DM because of the enhanced insulin sensitivity after delivery. Glucose 46-54 insulin Homo sapiens 116-123 27246911-6 2016 During high-dose insulin infusion, whole-body glucose disposal was low and remained unchanged after RDN, indicating persistent peripheral insulin resistance (IR). Glucose 46-53 insulin Homo sapiens 17-24 27293201-8 2016 CONCLUSIONS: In obese youth without diabetes, the risk imparted by the monophasic glucose curve compared with biphasic glucose curve, independent of fasting and 2-h glucose and insulin concentrations, is reflected in lower insulin sensitivity and poorer beta-cell function, which are two major pathophysiological biomarkers of type 2 diabetes in youth. Glucose 82-89 insulin Homo sapiens 223-230 27293201-8 2016 CONCLUSIONS: In obese youth without diabetes, the risk imparted by the monophasic glucose curve compared with biphasic glucose curve, independent of fasting and 2-h glucose and insulin concentrations, is reflected in lower insulin sensitivity and poorer beta-cell function, which are two major pathophysiological biomarkers of type 2 diabetes in youth. Glucose 119-126 insulin Homo sapiens 223-230 27352152-1 2016 Obesity resulting from the delivery of an excess amount of energy to adipose tissue from glucose or free fatty acids is associated with insulin resistance and adipose tissue inflammation. Glucose 89-96 insulin Homo sapiens 136-143 27168348-2 2016 Caveolae are especially abundant in fat tissue, playing a consistent role in a number of processes, such as the insulin-dependent glucose uptake and transmembrane transport of lipids underlying differentiation, maintenance and adaptive hypertrophy of adipocytes. Glucose 130-137 insulin Homo sapiens 112-119 27290979-6 2016 MEASUREMENTS: Glucose management data was extracted from electronic medical records to determine compliance to institutional glucose management protocol that prescribes hourly glucose measurements and insulin doses to maintain glucose levels between 100 to 140mg/dL. Glucose 125-132 insulin Homo sapiens 201-208 27288245-12 2016 However, insulin and glucose-dependent insulinotropic peptide secretion preceded GLP-1 release suggesting circulating GLP-1 does not mediate exaggerated insulin release after RYGB. Glucose 21-28 insulin Homo sapiens 39-46 27464858-2 2016 Such therapies offer the potential to stimulate endogenous insulin activity in proportion to circulating glucose levels; thereby, lowering the risk of hypoglycemic episodes. Glucose 105-112 insulin Homo sapiens 59-66 27483311-2 2016 It plays a particularly pivotal role in glucose homeostasis, as it can account for up to 40% of the body and for up to 80%-90% of insulin-stimulated glucose disposal. Glucose 40-47 insulin Homo sapiens 130-137 29652465-7 2016 With the titrationof insulin glargine, target fasting glucose levels were not achieved. Glucose 54-61 insulin Homo sapiens 21-28 27273909-1 2016 BACKGROUND: The oral minimal model is a simple, useful tool for the assessment of beta-cell function and insulin sensitivity across the spectrum of glucose tolerance, including normal glucose tolerance (NGT), prediabetes, and type 2 diabetes mellitus (T2DM) in humans. Glucose 148-155 insulin Homo sapiens 105-112 27422345-1 2016 The peroxisome proliferator-activated receptor gamma (PPARgamma) regulates osteoblast and osteoclast differentiation, and is the molecular target of thiazolidinediones (TZDs), insulin sensitizers that enhance glucose utilization and adipocyte differentiation. Glucose 209-216 insulin Homo sapiens 176-183 27624108-8 2016 Antibiotic therapy was initiated with doripenem and she was restrictively treated with intravenous insulin to control her plasma glucose. Glucose 129-136 insulin Homo sapiens 99-106 27309039-7 2016 A concomitant decrease of 11.6% +- 4.6% in whole-body insulin sensitivity was also observed (delta = -1.6 +- 0.7 mg/kg min glucose; P < .05). Glucose 125-132 insulin Homo sapiens 54-61 27215753-5 2016 BDSW containing COS synergistically increased glucose uptake; this was dependent on the activation of insulin receptor substrate 1 and protein kinase C in insulin-dependent signaling pathways as well as liver kinase B1, AMP-activated protein kinase, and mammalian target of rapamycin in insulin-independent signaling pathways. Glucose 46-53 insulin Homo sapiens 102-109 27215753-5 2016 BDSW containing COS synergistically increased glucose uptake; this was dependent on the activation of insulin receptor substrate 1 and protein kinase C in insulin-dependent signaling pathways as well as liver kinase B1, AMP-activated protein kinase, and mammalian target of rapamycin in insulin-independent signaling pathways. Glucose 46-53 insulin Homo sapiens 155-162 27170092-0 2016 Association of morning fasting blood glucose variability with insulin antibodies and clinical factors in type 1 diabetes. Glucose 37-44 insulin Homo sapiens 62-69 27170092-2 2016 This study aimed to identify association of morning fasting blood glucose concentration variability with insulin antibodies and clinical factors. Glucose 66-73 insulin Homo sapiens 105-112 27170092-11 2016 In some patients with a high insulin antibody titer, the antibody may have an effect on the variability of the fasting glucose concentration in type 1 diabetes. Glucose 119-126 insulin Homo sapiens 29-36 27448167-3 2016 To test this hypothesis, single nucleotide polymorphisms (SNPs) associated with acute insulin response to glucose (AIRg), a dynamic measure of first-phase insulin secretion, were identified in African Americans from the Insulin Resistance Atherosclerosis Family Study (IRASFS; n = 492 subjects). Glucose 106-113 insulin Homo sapiens 86-93 27441367-3 2016 In this approach, an Actor-Critic (AC) learning algorithm is designed and developed for the optimisation of insulin infusion for personalised glucose regulation. Glucose 142-149 insulin Homo sapiens 108-115 27447049-1 2016 Insulin secretion from pancreatic beta cells is regulated by the blood glucose concentration and occurs through Ca(2+)-triggered exocytosis. Glucose 71-78 insulin Homo sapiens 0-7 27441998-2 2016 Interrupting or blocking the binding between host insulin and the schistosome insulin receptors (IRs) may result in reduced glucose uptake leading to starvation and stunting of worms with a reduction in egg output. Glucose 124-131 insulin Homo sapiens 50-57 27441998-2 2016 Interrupting or blocking the binding between host insulin and the schistosome insulin receptors (IRs) may result in reduced glucose uptake leading to starvation and stunting of worms with a reduction in egg output. Glucose 124-131 insulin Homo sapiens 78-85 27446819-0 2015 Dietary insulin load and insulin index are associated with the risk of insulin resistance: a prospective approach in tehran lipid and glucose study. Glucose 134-141 insulin Homo sapiens 8-15 27446819-0 2015 Dietary insulin load and insulin index are associated with the risk of insulin resistance: a prospective approach in tehran lipid and glucose study. Glucose 134-141 insulin Homo sapiens 25-32 27434075-0 2016 High Glucose Impairs Insulin Signaling in the Glomerulus: An In Vitro and Ex Vivo Approach. Glucose 5-12 insulin Homo sapiens 21-28 27434075-7 2016 Prolonged insulin treatment caused a significant decrease of IR levels, while alterations in glucose concentrations for various time intervals demonstrated changes of IR, p-IR and p-Akt levels, suggesting that the IR signaling pathway is regulated by glucose levels. Glucose 251-258 insulin Homo sapiens 10-17 27434443-2 2016 OBJECTIVE: To estimate the relative efficacy and safety associated with glucose-lowering drugs including insulin. Glucose 72-79 insulin Homo sapiens 105-112 27130501-9 2016 With adipocytes and myotubes, insulin-dependent increases in glucose uptake have been measured with 10- and 2-fold assay windows, respectively. Glucose 61-68 insulin Homo sapiens 30-37 27146011-4 2016 Next, we discuss three scenarios in which aberrant gene expression causes abnormal glucose-induced insulin release and the epigenetic regulation of the hidden face in beta cells. Glucose 83-90 insulin Homo sapiens 99-106 26387753-7 2016 Our results suggest that ANGPTL8/betatrophin might play an important role in glucose metabolism in the context of insulin resistance. Glucose 77-84 insulin Homo sapiens 114-121 27270669-1 2016 Pancreatic islet dysfunction leading to insufficient glucose-stimulated insulin secretion triggers the clinical onset of diabetes. Glucose 53-60 insulin Homo sapiens 72-79 27422524-1 2016 BACKGROUND: The effects of insulin on cardiomyocytes, such as positive inotropic action and glucose uptake are well described. Glucose 92-99 insulin Homo sapiens 27-34 27346353-1 2016 Dysregulated mitochondrial metabolism during hepatic insulin resistance may contribute to pathophysiologies ranging from elevated glucose production to hepatocellular oxidative stress and inflammation. Glucose 130-137 insulin Homo sapiens 53-60 27399229-5 2016 These subpopulations are always present in normal adult islets and have diverse gene expression profiles and distinct basal and glucose-stimulated insulin secretion. Glucose 128-135 insulin Homo sapiens 147-154 27040307-6 2016 Treatment with Akti-1/2 and wortmannin suggested that Akt and PI3K are mediators of insulin effect on PAK2 and glucose uptake. Glucose 111-118 insulin Homo sapiens 84-91 27354378-1 2016 RAB10 is a regulator of insulin-stimulated translocation of the GLUT4 glucose transporter to the plasma membrane (PM) of adipocytes, which is essential for whole-body glucose homeostasis. Glucose 70-77 insulin Homo sapiens 24-31 27101299-0 2016 Insulin/glucose induces natriuretic peptide clearance receptor in human adipocytes: a metabolic link with the cardiac natriuretic pathway. Glucose 8-15 insulin Homo sapiens 0-7 27101299-10 2016 Low-glucose medium, used to simulate in vivo starving conditions, hampered the insulin effect on NPRC through modulation of insulin/glucose-regulated pathways, allowing atrial natriuretic peptide to induce lipolysis and thermogenic genes. Glucose 4-11 insulin Homo sapiens 79-86 27101299-10 2016 Low-glucose medium, used to simulate in vivo starving conditions, hampered the insulin effect on NPRC through modulation of insulin/glucose-regulated pathways, allowing atrial natriuretic peptide to induce lipolysis and thermogenic genes. Glucose 4-11 insulin Homo sapiens 124-131 27101299-12 2016 Insulin/glucose-dependent NPRC induction in adipocytes might be a key factor linking hyperinsulinemia, metabolic syndrome, and higher blood pressure by reducing NP effects on adipocytes. Glucose 8-15 insulin Homo sapiens 0-7 27751372-0 2016 Fasting Triglycerides and Glucose Index as a Diagnostic Test for Insulin Resistance in Young Adults. Glucose 26-33 insulin Homo sapiens 65-72 27751372-1 2016 BACKGROUND AND AIMS: Although the Glucose and Triglyceride levels (TyG) index is useful for identification of insulin resistance (IR) in different ethnic groups, it has not been evaluated in young adults. Glucose 34-41 insulin Homo sapiens 110-117 27395465-6 2016 The dysfunction of insulin signaling could directly lead to disrupted glucose utilization in the AD brain. Glucose 70-77 insulin Homo sapiens 19-26 27492405-2 2016 In the control group, the mean concentrations of glucose and immunoreactive insulin were significantly higher in the evening at all test terms (0, 60 and 120 min), which is indicative of physiological insulin resistance in the evening. Glucose 49-56 insulin Homo sapiens 201-208 27492405-5 2016 In case of gynoid obesity, glucose load was followed by hyperinsulinemia and hypoglycemia; in android obesity, it was followed by hyperinsulinemia, hyperglycemia, and insulin resistance irrespective of the time of the day. Glucose 27-34 insulin Homo sapiens 61-68 26670479-8 2016 RESULTS: OGTT calculations of insulin sensitivity (Matsuda) and plasma insulin response [ratio of insulin/glucose area-under-the-curve (AUC) or insulin total AUC] provided the expected hyperbolic relationship [beta = -0.95, 95% CI (-1.09, -0.82); -1.06 (-1.14, -0.98)]. Glucose 106-113 insulin Homo sapiens 71-78 26670479-8 2016 RESULTS: OGTT calculations of insulin sensitivity (Matsuda) and plasma insulin response [ratio of insulin/glucose area-under-the-curve (AUC) or insulin total AUC] provided the expected hyperbolic relationship [beta = -0.95, 95% CI (-1.09, -0.82); -1.06 (-1.14, -0.98)]. Glucose 106-113 insulin Homo sapiens 71-78 26670479-8 2016 RESULTS: OGTT calculations of insulin sensitivity (Matsuda) and plasma insulin response [ratio of insulin/glucose area-under-the-curve (AUC) or insulin total AUC] provided the expected hyperbolic relationship [beta = -0.95, 95% CI (-1.09, -0.82); -1.06 (-1.14, -0.98)]. Glucose 106-113 insulin Homo sapiens 71-78 26740634-4 2016 RESULTS: The proportion of time when the sensor glucose level was in the target range (3.9-10 mmol/L) was increased during closed-loop insulin delivery compared with sensor-augmented pump therapy (72 vs. 53%, P < 0.001; primary end point), the mean glucose concentration was lowered (8.7 vs. 10.1 mmol/L, P = 0.028), and the time spent above the target level was reduced (P = 0.005) without changing the total daily insulin amount (P = 0.55). Glucose 48-55 insulin Homo sapiens 135-142 26740634-7 2016 Compared with sensor-augmented insulin pump therapy, closed-loop insulin delivery may improve glucose control without increasing the risk of hypoglycemia in adolescents with suboptimally controlled type 1 diabetes. Glucose 94-101 insulin Homo sapiens 65-72 27033560-9 2016 However CFRD is the largest extra-pulmonary co-morbidity and rapidly accelerates lung decline Recent experimental evidence shows that functional CFTR channels are required for normal patterns of first phase insulin secretion from the pancreatic beta cell Current clinical recommendations suggest that insulin is more effective than oral glucose-lowering drugs for the treatment of CFRD. Glucose 341-348 insulin Homo sapiens 305-312 27148807-2 2016 The aim of this study was to determine whether predictive low glucose management (PLGM) system is effective in preventing insulin-induced hypoglycemia in controlled experiments. Glucose 62-69 insulin Homo sapiens 122-129 27148807-7 2016 The predictive algorithm was programmed to suspend basal insulin infusion when sensor glucose was predicted to be <80 mg/dL in 30 min. Glucose 86-93 insulin Homo sapiens 57-64 27207520-1 2016 Synaptotagmin (Syt)-7, a major component of the exocytotic machinery in neurons, is also the major Syt in rodent pancreatic beta-cells shown to mediate glucose-stimulated insulin secretion (GSIS). Glucose 152-159 insulin Homo sapiens 171-178 27207544-6 2016 In addition, obese adolescents demonstrated attenuated suppression of serum acyl-ghrelin and increased circulating insulin level after glucose ingestion; furthermore, the change in acyl-ghrelin and insulin levels after both glucose and fructose ingestion was associated with increased hypothalamic, thalamic, and hippocampal blood flow in obese relative to lean adolescents. Glucose 135-142 insulin Homo sapiens 115-122 27207544-6 2016 In addition, obese adolescents demonstrated attenuated suppression of serum acyl-ghrelin and increased circulating insulin level after glucose ingestion; furthermore, the change in acyl-ghrelin and insulin levels after both glucose and fructose ingestion was associated with increased hypothalamic, thalamic, and hippocampal blood flow in obese relative to lean adolescents. Glucose 135-142 insulin Homo sapiens 198-205 27207544-6 2016 In addition, obese adolescents demonstrated attenuated suppression of serum acyl-ghrelin and increased circulating insulin level after glucose ingestion; furthermore, the change in acyl-ghrelin and insulin levels after both glucose and fructose ingestion was associated with increased hypothalamic, thalamic, and hippocampal blood flow in obese relative to lean adolescents. Glucose 224-231 insulin Homo sapiens 198-205 27145003-7 2016 Insulin resistance was present in PMHAF with higher plasma insulin, normal fasting blood glucose, abnormal oral glucose tolerance test, and higher nonfasting blood glucose. Glucose 89-96 insulin Homo sapiens 0-7 27145003-7 2016 Insulin resistance was present in PMHAF with higher plasma insulin, normal fasting blood glucose, abnormal oral glucose tolerance test, and higher nonfasting blood glucose. Glucose 112-119 insulin Homo sapiens 0-7 27006448-8 2016 Furthermore, preadipocytes differentiated on matrix derived from CPX-1 knockdown cells exhibited reduced Glut4 expression and insulin-stimulated glucose uptake. Glucose 145-152 insulin Homo sapiens 126-133 27417862-5 2016 Although providers explain the importance of the ICU insulin regimen for glucose control, she either refuses the insulin or requests a lower dose. Glucose 73-80 insulin Homo sapiens 53-60 27578133-7 2016 Insulin sensitivity was assessed using equation derived from euglycemic-hyperinsulinemic clamp studies-estimated glucose disposal rate. Glucose 113-120 insulin Homo sapiens 0-7 27630879-1 2016 INTRODUCTION: Mastication has potential to affect postprandial blood glucose levels by affecting cephalic phase of insulin release. Glucose 69-76 insulin Homo sapiens 115-122 27630879-8 2016 CONCLUSION: In normoglycaemic group, postprandial blood glucose concentration upon thorough mastication was significantly lower, due to early-phase insulin secretion. Glucose 56-63 insulin Homo sapiens 148-155 26333348-1 2016 BACKGROUND: Insulin regulates glucose homeostasis but can also promote vascular smooth muscle (VSMC) proliferation, important in atherogenesis. Glucose 30-37 insulin Homo sapiens 12-19 27182042-3 2016 The insulin dose was fixed for 16 weeks, and titrated based on self-measured plasma glucose thereafter. Glucose 84-91 insulin Homo sapiens 4-11 27220352-8 2016 Curcumin decreased adipose lipolysis by attenuating ER stress through the cAMP/PKA pathway, reduced FFA influx into the liver by blocking FFA trafficking, and thereby improved insulin sensitivity to inhibit hepatic glucose production. Glucose 215-222 insulin Homo sapiens 176-183 27273792-1 2016 IMPORTANCE: Intensive glucose-lowering treatment among patients with non-insulin-requiring type 2 diabetes may increase the risk of hypoglycemia. Glucose 22-29 insulin Homo sapiens 73-80 27399115-5 2016 In multiple regression analysis, age, lower BMI, stimulated glucose, GA, and urinary ACR predicted increased urinary NAG.In conclusion, increase in urinary NAG may be related to glycemic parameters reflecting glucose fluctuation and decreased insulin secretory capacity in patients with T2DM. Glucose 209-216 insulin Homo sapiens 243-250 27571724-7 2016 The factors predicting the need for insulin therapy were: previous GDM, family history of diabetes, a previous infant weighing >= 4500 gram, Middle-East/North-African descent, multiparity, pre-gestational BMI >= 30 kg/m2, and an increased fasting glucose level >= 5.5 mmol/l (OR 6.03;CI 3.56-10.22) and two-hour glucose level >= 9.4 mmol/l after a 75-gram oral glucose tolerance test at GDM diagnosis. Glucose 253-260 insulin Homo sapiens 36-43 27571724-7 2016 The factors predicting the need for insulin therapy were: previous GDM, family history of diabetes, a previous infant weighing >= 4500 gram, Middle-East/North-African descent, multiparity, pre-gestational BMI >= 30 kg/m2, and an increased fasting glucose level >= 5.5 mmol/l (OR 6.03;CI 3.56-10.22) and two-hour glucose level >= 9.4 mmol/l after a 75-gram oral glucose tolerance test at GDM diagnosis. Glucose 321-328 insulin Homo sapiens 36-43 27571724-7 2016 The factors predicting the need for insulin therapy were: previous GDM, family history of diabetes, a previous infant weighing >= 4500 gram, Middle-East/North-African descent, multiparity, pre-gestational BMI >= 30 kg/m2, and an increased fasting glucose level >= 5.5 mmol/l (OR 6.03;CI 3.56-10.22) and two-hour glucose level >= 9.4 mmol/l after a 75-gram oral glucose tolerance test at GDM diagnosis. Glucose 321-328 insulin Homo sapiens 36-43 27003812-1 2016 PURPOSE: We report transient ocular wavefront and blood glucose data for one patient with acute type 1 diabetes mellitus after the treatment with insulin has been initiated. Glucose 56-63 insulin Homo sapiens 146-153 27441367-5 2016 Automatic, personalised tuning of AC is based on the estimation of information transfer (IT) from insulin to glucose signals. Glucose 109-116 insulin Homo sapiens 98-105 27441367-6 2016 Insulin-to-glucose IT is linked to patient-specific characteristics related to total daily insulin needs and insulin sensitivity (SI). Glucose 11-18 insulin Homo sapiens 0-7 27441367-6 2016 Insulin-to-glucose IT is linked to patient-specific characteristics related to total daily insulin needs and insulin sensitivity (SI). Glucose 11-18 insulin Homo sapiens 91-98 26526047-5 2016 Insulin resistance was assessed by HEGC (glucose disposal rate [GDR]), homeostatic model assessment of IR (HOMA-IR), HOMA-IR corrected by adiponectin (HOMA-AD), leptin adiponectin ratio (LAR), quantitative insulin sensitivity check index (QUICKI), McAuley"s index, and oral glucose tolerance test (OGTT) at each time point for a total of 18 studies. Glucose 41-48 insulin Homo sapiens 0-7 27441367-6 2016 Insulin-to-glucose IT is linked to patient-specific characteristics related to total daily insulin needs and insulin sensitivity (SI). Glucose 11-18 insulin Homo sapiens 109-116 27353345-8 2016 Insulin signaling and glucose uptake levels were lower in MCF-7 cells treated with modified insulin than in cells treated with native insulin. Glucose 22-29 insulin Homo sapiens 92-99 27656397-2 2016 Recent work has highlighted the important role of insulin"s action in the nervous system on glucose and energy homeostasis, memory, and mood. Glucose 92-99 insulin Homo sapiens 50-57 27485848-2 2016 Incorrect insulin application technique can lead to complications both local (lipohypertrophy, scars) and systemic (high variability of insulin absorption and action, unexpected hypoglycemia or hyperglycemia, suboptimal overall glucose control). Glucose 228-235 insulin Homo sapiens 10-17 27485848-9 2016 KEY WORDS: glucose variability - insulin application - lipohypertrophy - needles. Glucose 11-18 insulin Homo sapiens 33-40 27638898-3 2016 In addition, insulin resistance affects 86 million Americans, or more than one-third of the adult population, as manifested by impaired fasting glucose tolerance with random glucose values ranging from >=100 to <126 mg/dL. Glucose 144-151 insulin Homo sapiens 13-20 27353345-8 2016 Insulin signaling and glucose uptake levels were lower in MCF-7 cells treated with modified insulin than in cells treated with native insulin. Glucose 22-29 insulin Homo sapiens 134-141 27282931-7 2016 We further report that (E)-4-Chloro-2-(1-(2-(2,4,6-trichlorophenyl) hydrazono) ethyl) phenol (small molecule M1) prevents the cholesterol mediated blunting of cellular respiration and potentiates Glucose stimulated insulin secretion which was abolished in pancreatic beta cells on cholesterol accumulation. Glucose 196-203 insulin Homo sapiens 215-222 27312339-0 2016 Long-term exposure to abnormal glucose levels alters drug metabolism pathways and insulin sensitivity in primary human hepatocytes. Glucose 31-38 insulin Homo sapiens 82-89 27312339-4 2016 In contrast to declining PHH monocultures, micropatterned co-cultures (MPCCs) of PHHs and 3T3-J2 murine embryonic fibroblasts maintain insulin-sensitive glucose metabolism for several weeks. Glucose 153-160 insulin Homo sapiens 135-142 27312339-7 2016 In contrast, hyperglycemic MPCCs displayed significant hepatic lipid accumulation in the presence of insulin, while also showing decreased sensitivity to insulin-mediated inhibition of glucose output relative to a normoglycemic control. Glucose 185-192 insulin Homo sapiens 154-161 26994512-0 2016 PDX1 and ISL1 differentially coordinate with epigenetic modifications to regulate insulin gene expression in varied glucose concentrations. Glucose 116-123 insulin Homo sapiens 82-89 26994512-1 2016 The mechanism of insulin gene transcription control in response to glucose concentration is poorly defined. Glucose 67-74 insulin Homo sapiens 17-24 26994512-3 2016 However, their contribution and hierarchical organization in insulin expression control based on glucose concentration remain unknown. Glucose 97-104 insulin Homo sapiens 61-68 26994512-6 2016 The ISL1-recruited cofactors SET9 and JMJD3 facilitated insulin gene histone modifications under normal glucose. Glucose 104-111 insulin Homo sapiens 56-63 26994512-7 2016 In high-glucose concentrations, PDX1 formed a complex with BETA2 to enhance insulin gene expression. Glucose 8-15 insulin Homo sapiens 76-83 26994512-9 2016 This is the first evidence transcription factors orchestrate epigenetic modifications to control insulin gene expression based on glucose concentration. Glucose 130-137 insulin Homo sapiens 97-104 27210795-0 2016 Fabrication of Biobased Polyelectrolyte Capsules and Their Application for Glucose-Triggered Insulin Delivery. Glucose 75-82 insulin Homo sapiens 93-100 27210795-1 2016 To enhance the glucose sensitivity and self-regulated release of insulin, biobased capsules with glucose-responsive and competitive properties were fabricated based on poly(gamma-glutamic acid) (gamma-PGA) and chitosan oligosaccharide (CS) polyelectrolytes. Glucose 97-104 insulin Homo sapiens 65-72 27210795-7 2016 The encapsulated insulin was able to undergo self-regulated release from the capsules depending on the glucose level and APBA composition. Glucose 103-110 insulin Homo sapiens 17-24 27210795-8 2016 The amount of insulin release increased with incubation in higher glucose concentration and decreased with higher APBA composition. Glucose 66-73 insulin Homo sapiens 14-21 27210795-9 2016 Moreover, the on-off regulation of insulin release from the (gamma-PGA-g-APBA/GC)5 capsules could be triggered with a synchronizing and variation of the external glucose concentration, whereas the capsules without the LA functional groups did not show the on-off regulated release. Glucose 162-169 insulin Homo sapiens 35-42 27210795-11 2016 These (gamma-PGA-g-APBA/GC)5 with good stability, glucose response, and controlled insulin delivery are expected to be used for future applications to glucose-triggered insulin delivery. Glucose 50-57 insulin Homo sapiens 169-176 27210795-11 2016 These (gamma-PGA-g-APBA/GC)5 with good stability, glucose response, and controlled insulin delivery are expected to be used for future applications to glucose-triggered insulin delivery. Glucose 151-158 insulin Homo sapiens 83-90 27210795-11 2016 These (gamma-PGA-g-APBA/GC)5 with good stability, glucose response, and controlled insulin delivery are expected to be used for future applications to glucose-triggered insulin delivery. Glucose 151-158 insulin Homo sapiens 169-176 27279214-2 2016 Here we show that increased production of acetate by an altered gut microbiota in rodents leads to activation of the parasympathetic nervous system, which, in turn, promotes increased glucose-stimulated insulin secretion, increased ghrelin secretion, hyperphagia, obesity and related sequelae. Glucose 184-191 insulin Homo sapiens 203-210 26992575-2 2016 In particular, Akt is a key mediator of glucose transport in response to insulin. Glucose 40-47 insulin Homo sapiens 73-80 26215312-4 2016 Our objective was to evaluate the relationship between the 60-min OGTT insulin and glucose values and markers of clinical degradation in adult patients with CF. Glucose 83-90 insulin Homo sapiens 71-78 31239889-2 2016 Insulin analogues are primarily used to mediate the regulation of blood glucose concentrations; however, their use has also been implicated or suspected as a cause of death in suicides, accidents, and homicides. Glucose 72-79 insulin Homo sapiens 0-7 27072496-1 2016 The graded glucose infusion (GGI) examines insulin secretory response patterns to continuously escalating glycemia. Glucose 11-18 insulin Homo sapiens 43-50 27072496-4 2016 Insulin secretory response was measured as changes in insulin, C-peptide, insulin secretion rates (ISR), and ratio of ISR to prevailing glucose (ISR/G). Glucose 136-143 insulin Homo sapiens 0-7 27072496-8 2016 Collectively, the findings of this investigational series bolster confidence that the GGI has solid attributes for assessing insulin secretory response to glucose across populations and pharmacology. Glucose 155-162 insulin Homo sapiens 125-132 27234585-6 2016 The roles of glucose and of insulin-mediated uptake of glucose in folliculogenesis are discussed. Glucose 55-62 insulin Homo sapiens 28-35 27234585-7 2016 It is suggested that glucose in addition to its well-established role of providing energy for cellular function may also have insulin-mediated signalling functions in ovarian cells, involving AMPK (AMP-dependent protein kinase) and/or hexosamine. Glucose 21-28 insulin Homo sapiens 126-133 27245161-1 2016 BACKGROUND: The insulin signalling pathway (ISP) is an important biochemical pathway, which regulates some fundamental biological functions such as glucose and lipid metabolism, protein synthesis, cell proliferation, cell differentiation and apoptosis. Glucose 148-155 insulin Homo sapiens 16-23 27208730-9 2016 Altogether, insulin stimulates glucose uptake in the nucleus accumbens. Glucose 31-38 insulin Homo sapiens 12-19 26597252-11 2016 The effects of liraglutide on insulin and glucagon secretion are glucose dependent, and hence the risk of hypoglycaemia is low. Glucose 65-72 insulin Homo sapiens 30-37 26955646-1 2016 In peripheral tissues insulin activates signaling cascades to facilitate glucose uptake from the blood into tissues like liver, muscle and fat. Glucose 73-80 insulin Homo sapiens 22-29 26955646-2 2016 While insulin appears to play a minor role in the regulation of glucose uptake in the central nervous system (CNS), insulin is known to play a major role in regulating synaptic plasticity in brain regions like the hippocampus. Glucose 64-71 insulin Homo sapiens 6-13 27023630-4 2016 To replenish these intracellular lipid stores, brown adipocytes take up both glucose and triglyceride-derived fatty acids, resulting in attenuation of dyslipidaemia, insulin resistance and atherosclerosis. Glucose 77-84 insulin Homo sapiens 166-173 27023630-6 2016 Notably, insulin resistance during ageing or weight gain reduces the capacity of BAT to internalize glucose, without reducing fatty acid uptake or oxidative metabolism. Glucose 100-107 insulin Homo sapiens 9-16 26773271-3 2016 Glucagon-like peptide 1 (GLP-1), a hormone with a spectrum of favourable metabolic actions, including glucose-dependent stimulation of insulin and inhibition of glucagon secretion, provided the endocrine basis from which the idea of using DPP-4 inhibitors as anti-diabetic agents was developed. Glucose 102-109 insulin Homo sapiens 135-142 26880114-2 2016 Insulin secretion by beta-cells of the pancreatic islets is tightly coupled to blood glucose concentration and modulated by a large number of blood-borne or locally released mediators, including endocannabinoids. Glucose 85-92 insulin Homo sapiens 0-7 27282931-0 2016 Restoring Mitochondrial Function: A Small Molecule-mediated Approach to Enhance Glucose Stimulated Insulin Secretion in Cholesterol Accumulated Pancreatic beta cells. Glucose 80-87 insulin Homo sapiens 99-106 26888164-6 2016 CDCA elicited a small increase in plasma insulin : glucose ratio compared with colesevelam, CDCA + colesevelam and placebo in both groups. Glucose 51-58 insulin Homo sapiens 41-48 26948394-4 2016 RESULTS: Insulin was required in eight women (25%) in the myoinositol group who, compared with the 24 who did not need insulin, were older (37+-5 vs. 32+-5 years, respectively; P=0.018) and had a larger percentage of high self-monitored glucose values (45+-8% vs. 32+-14%; P<0.0001) during the week prior to the introduction of myoinositol treatment. Glucose 237-244 insulin Homo sapiens 9-16 26888164-9 2016 We speculate that bile acid-induced activation of TGR5 on L cells increases GLP-1 secretion, which, in turn, may result in amplification of glucose-stimulated insulin secretion. Glucose 140-147 insulin Homo sapiens 159-166 27208320-0 2016 Glucose Variability in a 26-Week Randomized Comparison of Mealtime Treatment With Rapid-Acting Insulin Versus GLP-1 Agonist in Participants With Type 2 Diabetes at High Cardiovascular Risk. Glucose 0-7 insulin Homo sapiens 95-102 26993071-0 2016 Hepatic and Extrahepatic Insulin Clearance Are Differentially Regulated: Results From a Novel Model-Based Analysis of Intravenous Glucose Tolerance Data. Glucose 130-137 insulin Homo sapiens 25-32 26993071-2 2016 We developed a novel model-based method to estimate both hepatic and extrahepatic insulin clearance using plasma insulin and C-peptide profiles obtained from the insulin-modified frequently sampled intravenous glucose tolerance test. Glucose 210-217 insulin Homo sapiens 82-89 26993071-6 2016 Parameters of insulin clearance were correlated with measures of insulin sensitivity and acute insulin response to glucose. Glucose 115-122 insulin Homo sapiens 14-21 27222390-10 2016 Elevated levels of glucose, free fatty acids, and inflammatory cytokines due to diabetes and insulin resistance selectively inhibit insulin"s antiatherogenic actions via the IRS/PI3K/Akt pathway. Glucose 19-26 insulin Homo sapiens 132-139 27222546-3 2016 The subsequent digestion and absorption of nutrients are associated with the release of a set of hormones that feeds back to regulate subsequent gastric emptying and regulates the release of insulin, resulting in downregulation of hepatic glucose production and deposition of glucose in insulin-sensitive tissues. Glucose 239-246 insulin Homo sapiens 191-198 27208343-10 2016 CONCLUSIONS: Addition of 1.2 mg and 1.8 mg liraglutide to insulin over a 12-week period in overweight and obese patients with T1D results in modest reductions of weekly mean glucose levels with significant weight loss, small insulin dose reductions, and frequent gastrointestinal side effects. Glucose 174-181 insulin Homo sapiens 58-65 27222546-3 2016 The subsequent digestion and absorption of nutrients are associated with the release of a set of hormones that feeds back to regulate subsequent gastric emptying and regulates the release of insulin, resulting in downregulation of hepatic glucose production and deposition of glucose in insulin-sensitive tissues. Glucose 276-283 insulin Homo sapiens 191-198 27222546-3 2016 The subsequent digestion and absorption of nutrients are associated with the release of a set of hormones that feeds back to regulate subsequent gastric emptying and regulates the release of insulin, resulting in downregulation of hepatic glucose production and deposition of glucose in insulin-sensitive tissues. Glucose 276-283 insulin Homo sapiens 287-294 27222390-10 2016 Elevated levels of glucose, free fatty acids, and inflammatory cytokines due to diabetes and insulin resistance selectively inhibit insulin"s antiatherogenic actions via the IRS/PI3K/Akt pathway. Glucose 19-26 insulin Homo sapiens 93-100 27035557-6 2016 Two of the T2D-associated monogenic diabetes genes-potassium inward-rectifying channel, subfamily J, member 11 (KCNJ11), which controls glucose-stimulated insulin secretion in the beta-cell; and peroxisome proliferator-activated receptor gamma (PPARG), which impacts multiple tissue targets in relation to inflammation and insulin sensitivity-have been developed as major antidiabetic drug targets. Glucose 136-143 insulin Homo sapiens 155-162 26817478-1 2016 The purpose of this study was to fabricate insulin-loaded double-walled and single-polymer poly(lactide-co-glycolide) (PLGA) microspheres using a fast degrading glucose core, hydroxyl-terminated poly(lactide-co-glycolide) (Glu-PLGA), and a moderate degrading carboxyl-terminated PLGA polymers. Glucose 161-168 insulin Homo sapiens 43-50 27035557-6 2016 Two of the T2D-associated monogenic diabetes genes-potassium inward-rectifying channel, subfamily J, member 11 (KCNJ11), which controls glucose-stimulated insulin secretion in the beta-cell; and peroxisome proliferator-activated receptor gamma (PPARG), which impacts multiple tissue targets in relation to inflammation and insulin sensitivity-have been developed as major antidiabetic drug targets. Glucose 136-143 insulin Homo sapiens 323-330 27032901-3 2016 Insulin sensitivity was measured via intravenous glucose tolerance in sedentary obese adults (OB; n = 14), individuals with type 2 diabetes (T2D; n = 15), and endurance-trained athletes (ATH; n = 15). Glucose 49-56 insulin Homo sapiens 0-7 27218271-11 2016 Antidiabetic medications (other than insulin) attenuated the air pollution effect on serum glucose. Glucose 91-98 insulin Homo sapiens 37-44 27055279-1 2016 OBJECTIVES: Administration of ghrelin inhibits the acute insulin response to glucose and worsens IV glucose tolerance in healthy subjects. Glucose 77-84 insulin Homo sapiens 57-64 26629879-5 2016 The insulin release in response to high glucose stimulation was hampered in all infected cells (P < 0.05) when no evidence of cytolysis was present; however, the adverse effect of E16 and E30 on insulin secretion appeared to be higher than that of the E4 strain. Glucose 40-47 insulin Homo sapiens 4-11 27427584-6 2016 According to the characterizations of size, morphology, drug loading efficiency, controlled insulin release behavior, glucose sensitivity and cytotoxicity, we conclude that this delicately designed glucose-responsive nanomicelle would be an efficient self-regulated carrier for controlled insulin release for potential DM therapy. Glucose 198-205 insulin Homo sapiens 92-99 27427584-6 2016 According to the characterizations of size, morphology, drug loading efficiency, controlled insulin release behavior, glucose sensitivity and cytotoxicity, we conclude that this delicately designed glucose-responsive nanomicelle would be an efficient self-regulated carrier for controlled insulin release for potential DM therapy. Glucose 198-205 insulin Homo sapiens 289-296 26660757-1 2016 Insulin secretion and insulin sensitivity indexes are related by hyperbolic functions, allowing the calculation of the disposition index (DI) as the product of the acute insulin response (AIR) and the insulin sensitivity index (Si) from intravenous glucose tolerance test (IVGTT). Glucose 249-256 insulin Homo sapiens 0-7 26992090-5 2016 RESULTS: Women using metformin (23.4% needing supplemental insulin) gained less weight (P < 0.001), and had lower fasting glucose during the first and last 2 weeks of treatment (P = 0.014 and 0.008, respectively) when compared with insulin monotherapy. Glucose 125-132 insulin Homo sapiens 59-66 26992090-6 2016 Insulin supplementation in the metformin group was related to initial body mass index, HbA1c, oral glucose tolerance test (GTT), and first week mean glucose level. Glucose 99-106 insulin Homo sapiens 0-7 26992090-7 2016 The 1-h glucose level during initial GTT (Hr1-GTT) and the mean fasting glucose level during the first week of therapy (Wk1-mFG) were the two independent parameters associated with requiring supplemental insulin. Glucose 8-15 insulin Homo sapiens 204-211 26992090-7 2016 The 1-h glucose level during initial GTT (Hr1-GTT) and the mean fasting glucose level during the first week of therapy (Wk1-mFG) were the two independent parameters associated with requiring supplemental insulin. Glucose 72-79 insulin Homo sapiens 204-211 26660757-7 2016 An adequate statistical fit for a rectangular hyperbola was found between the area under the curve of insulin-to-glucose ratio (AUCI/G-R) and the Matsuda ISI-COMP index (study 1). Glucose 113-120 insulin Homo sapiens 102-109 26876794-1 2016 The incretin effect describes the phenomenon whereby oral glucose elicits higher insulin secretory responses than does intravenous glucose, despite inducing similar levels of glycaemia, in healthy individuals. Glucose 58-65 insulin Homo sapiens 81-88 23897763-9 2016 Finally, insulin release upon glucose stimulation was detected in our differentiated clusters. Glucose 30-37 insulin Homo sapiens 9-16 26988411-4 2016 The development of an insulin therapy that is responsive to glucose concentration remains an ultimate goal, with initial prototypes now reaching the proof-of-concept stage. Glucose 60-67 insulin Homo sapiens 22-29 26875731-6 2016 Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B. Glucose 67-74 insulin Homo sapiens 39-46 26875731-6 2016 Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B. Glucose 67-74 insulin Homo sapiens 318-325 26875731-6 2016 Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B. Glucose 145-152 insulin Homo sapiens 39-46 27390726-0 2016 Association between Dietary Acid Load and Insulin Resistance: Tehran Lipid and Glucose Study. Glucose 79-86 insulin Homo sapiens 42-49 27083135-11 2016 CONCLUSIONS: All three solutions, when infused at 10 ml kg(-1) h(-1) , are equally effective in maintaining glucose homeostasis, but 1% dextrose-containing fluid promotes catabolism, insulin resistance, rebound hyperglycemia, and acidosis. Glucose 137-145 insulin Homo sapiens 184-191 27426087-9 2016 They were functionally active as demonstrated by release of physiological insulin and C-peptide in response to elevated glucose concentrations. Glucose 120-127 insulin Homo sapiens 74-81 27917299-4 2016 Despite dramatic increase in insulin step by step up to 1110 IU of concomitant short and intermediate acting insulin per day by subcutaneous route, his blood glucose remained over 12 mmol/L persistently, in all the fasting, pre-prandial, postprandial and random samples. Glucose 158-165 insulin Homo sapiens 109-116 27917299-6 2016 However, intravenous infusion of insulin over 4 hours caused a plummet in the glucose level. Glucose 78-85 insulin Homo sapiens 33-40 27195491-10 2016 Mice overexpressing RCAN1 had reduced in vivo glucose-stimulated insulin secretion and their beta-cells displayed mitochondrial dysfunction including hyperpolarised membrane potential, reduced oxidative phosphorylation and low ATP production. Glucose 46-53 insulin Homo sapiens 65-72 27105912-1 2016 Insulin maintains glucose homeostasis by stimulating glucose uptake from extracellular environment to adipose and muscle tissue through glucose transporter (GLUT4). Glucose 18-25 insulin Homo sapiens 0-7 27105912-1 2016 Insulin maintains glucose homeostasis by stimulating glucose uptake from extracellular environment to adipose and muscle tissue through glucose transporter (GLUT4). Glucose 53-60 insulin Homo sapiens 0-7 27105912-8 2016 The results suggest that exposure of cells to insulin in low glucose conditions made these cells insulin resistant within 10 passages, while the same level of insulin in the presence of high glucose did not result in insulin resistance. Glucose 61-68 insulin Homo sapiens 46-53 27105912-8 2016 The results suggest that exposure of cells to insulin in low glucose conditions made these cells insulin resistant within 10 passages, while the same level of insulin in the presence of high glucose did not result in insulin resistance. Glucose 61-68 insulin Homo sapiens 97-104 27105912-8 2016 The results suggest that exposure of cells to insulin in low glucose conditions made these cells insulin resistant within 10 passages, while the same level of insulin in the presence of high glucose did not result in insulin resistance. Glucose 61-68 insulin Homo sapiens 97-104 27105912-8 2016 The results suggest that exposure of cells to insulin in low glucose conditions made these cells insulin resistant within 10 passages, while the same level of insulin in the presence of high glucose did not result in insulin resistance. Glucose 61-68 insulin Homo sapiens 97-104 26936971-1 2016 Insulin increases glucose uptake by increasing the rate of exocytosis of the facilitative glucose transporter isoform 4 (Glut4) relative to its endocytosis. Glucose 18-25 insulin Homo sapiens 0-7 26983645-1 2016 Lots of experimental and clinical evidences indicate that chronic exposure to saturated fatty acids and high level of glucose is implicated in insulin resistance, beta cell failure and ultimately type 2 diabetes. Glucose 118-125 insulin Homo sapiens 143-150 26970180-2 2016 This effect is explained by the role of the kcnq1 protein as a potassium channel that in the pancreatic beta-cells drives an electrical signal that facilitates glucose-stimulated insulin secretion. Glucose 160-167 insulin Homo sapiens 179-186 27187341-2 2016 METHODS: A model of insulin resistant cells was established in HepG2 by treatment with high glucose and insulin. Glucose 92-99 insulin Homo sapiens 20-27 27187341-8 2016 CONCLUSIONS: The mechanism by which treatment with AME improves insulin resistance in HepG2 cells may involve the PI3K-Akt signaling pathway, the processes of glucose oxygenolysis, glycogen synthesis, gluconeogenesis and inflammatory cytokine expression. Glucose 159-166 insulin Homo sapiens 64-71 27408772-3 2016 Thus, our objective was two-fold; to determine the signalling pathway by which acute PI3K inhibition enhances glucose-stimulated insulin secretion (GSIS) and to examine the role of this pathway in islets from type-2 diabetic (T2D) donors. Glucose 110-117 insulin Homo sapiens 129-136 27163678-5 2016 Knockdown of miR-194 in L6 skeletal muscle cells induced an increase in basal and insulin-stimulated glucose uptake and glycogen synthesis. Glucose 101-108 insulin Homo sapiens 82-89 30603297-6 2016 The insulin group had a higher pre-gestational BMI, higher fasting glucose level, higher area under the curve (AUC) for serum C-peptide level, higher HbA1c level, and a younger gestational age at diagnosis than the nutrition group (p < 0.05, all). Glucose 67-74 insulin Homo sapiens 4-11 27148740-14 2016 Because the risk of hypoglycemia is increased with using large insulin doses, sufficient glucose (60 grams with the administration of 20 units of insulin and 50 grams with the administration of 10 units) should be given to prevent hypoglycemia, and plasma glucose should be frequently monitored. Glucose 89-96 insulin Homo sapiens 63-70 26979523-9 2016 The lower incretin effect calculated for the obese subjects with NGT is driven by a disproportionately greater insulin response to iv glucose and does not affect postprandial glucose regulation. Glucose 134-141 insulin Homo sapiens 111-118 26581879-3 2016 Many people with diabetes measure their blood glucose levels regularly to determine the insulin dose. Glucose 46-53 insulin Homo sapiens 88-95 27138453-6 2016 The regulatory properties of adenylyl cyclase isoforms determine fluctuations in cytoplasmic cAMP concentration and reveal a synergistic action of glucose, GLP-1 and GIP on insulin secretion. Glucose 147-154 insulin Homo sapiens 173-180 27138453-7 2016 On the other hand, the regulatory properties of phospholipase C isoforms determine the interaction of glucose, acetylcholine and free fatty acids (FFA) (that act through the FFA receptors) on insulin secretion. Glucose 102-109 insulin Homo sapiens 192-199 27236392-7 2016 The acute insulin response after a glucose load (AIRg), Si, disposition index (DI), and glucose effectiveness (GE) were determined. Glucose 35-42 insulin Homo sapiens 10-17 27249943-3 2016 The islets are responsible for secretion of glucose-regulating hormones, mainly glucagon and insulin, which are released in distinct pulses. Glucose 44-51 insulin Homo sapiens 93-100 26831299-2 2016 Insulin has greater glucose-lowering properties when administered in pulses compared with a constant i.v. Glucose 20-27 insulin Homo sapiens 0-7 26818894-7 2016 Verapamil users had on average 10mg/dL lower serum glucose compared to CCB non-users with substantially greater differences among insulin users: 24mg/dL lower serum glucose among users of insulin in combination with oral agents and 37mg/dL lower among users of insulin alone. Glucose 165-172 insulin Homo sapiens 130-137 26818894-7 2016 Verapamil users had on average 10mg/dL lower serum glucose compared to CCB non-users with substantially greater differences among insulin users: 24mg/dL lower serum glucose among users of insulin in combination with oral agents and 37mg/dL lower among users of insulin alone. Glucose 165-172 insulin Homo sapiens 188-195 26818894-7 2016 Verapamil users had on average 10mg/dL lower serum glucose compared to CCB non-users with substantially greater differences among insulin users: 24mg/dL lower serum glucose among users of insulin in combination with oral agents and 37mg/dL lower among users of insulin alone. Glucose 165-172 insulin Homo sapiens 188-195 26884438-4 2016 With weight gain (3.1 +- 1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin suppression of lipolysis and only 8% worsening of insulin-mediated glucose uptake (IMGU). Glucose 186-193 insulin Homo sapiens 169-176 26886065-2 2016 This cross-sectional study analyzes different insulin response patterns during the oral glucose tolerance test (OGTT) and their implications on glycemia in normoglycemic individuals. Glucose 88-95 insulin Homo sapiens 46-53 26886065-13 2016 CONCLUSIONS: A delayed insulin pattern was associated with higher postprandial glucose levels. Glucose 79-86 insulin Homo sapiens 23-30 26886198-10 2016 Partial knockdown of ANT1 in C2C12 myotubes decreased sensitivity to the FA-induced uncoupling (p = 0.008) and insulin-stimulated glucose uptake (p = 0.025) compared with controls. Glucose 130-137 insulin Homo sapiens 111-118 26184417-0 2016 Reducing glucose variability with continuous subcutaneous insulin infusion increases endothelial progenitor cells in type 1 diabetes: an observational study. Glucose 9-16 insulin Homo sapiens 58-65 26526605-1 2016 The purpose of this study was to investigate how renal loss of both C-peptide and glucose during oral glucose tolerance test (OGTT) relate to and affect plasma-derived oral minimal model (OMM) indices. Glucose 102-109 insulin Homo sapiens 68-77 26526605-13 2016 Both C-peptide and glucose in urine collected during OGTT might be used as non-invasive measures for endogenous insulin secretion and glucose tolerance state. Glucose 134-141 insulin Homo sapiens 5-14 27322451-0 2016 sLRP1ng Up Glucose: LRP1 Regulates Hepatic Insulin Responses. Glucose 11-18 insulin Homo sapiens 43-50 27017290-11 2016 Among diabetes patients treated with insulin, there was increased survival with increasing serum glucose, most prominent for bladder cancer (HR 0.91, 95% CI 0.84-0.99, per 1 mmol/l increase). Glucose 97-104 insulin Homo sapiens 37-44 27017290-13 2016 Among insulin-treated patients, higher glucose levels may be associated with improved survival. Glucose 39-46 insulin Homo sapiens 6-13 26786351-6 2016 Insulin sensitivity was evaluated with oral glucose tolerance tests and calculated as homeostasis model assessment-insulin resistance (HOMA-IR)/liver insulin resistance (Liver IR) index for hepatic insulin sensitivity and oral glucose insulin sensitivity (OGIS)/Matsuda for peripheral insulin sensitivity. Glucose 44-51 insulin Homo sapiens 0-7 26967690-10 2016 Glucose infusion rate, during the low-dose insulin infusion, was lower after anastrozole administration (12.16 +- 1.33 vs 14.15 +- 1.55 mumol/kg min, P = .024). Glucose 0-7 insulin Homo sapiens 43-50 26606271-7 2016 RESULTS: Plasma glucose responses did not differ between treatments (ANOVA, P = 0.096), but plasma insulin and lactate concentrations were elevated during GLU + FRU and GLU + SUC when compared with GLU (P < 0.01). Glucose 155-158 insulin Homo sapiens 99-106 26606271-7 2016 RESULTS: Plasma glucose responses did not differ between treatments (ANOVA, P = 0.096), but plasma insulin and lactate concentrations were elevated during GLU + FRU and GLU + SUC when compared with GLU (P < 0.01). Glucose 169-172 insulin Homo sapiens 99-106 26606271-7 2016 RESULTS: Plasma glucose responses did not differ between treatments (ANOVA, P = 0.096), but plasma insulin and lactate concentrations were elevated during GLU + FRU and GLU + SUC when compared with GLU (P < 0.01). Glucose 169-172 insulin Homo sapiens 99-106 27175665-0 2016 Type 2 Diabetes Risk Allele UBE2E2 Is Associated With Decreased Glucose-Stimulated Insulin Release in Elderly Chinese Han Individuals. Glucose 64-71 insulin Homo sapiens 83-90 26976796-7 2016 Under the same conditions, aleglitazar also reversed the TNF-alpha-mediated suppression of insulin-stimulated ser473 Akt phosphorylation and decreased the TNF-alpha-induced ser312 IRS1 phosphorylation, two major switches in insulin-mediated metabolic activities, restoring glucose uptake in insulin-resistant adipocytes. Glucose 273-280 insulin Homo sapiens 91-98 26965153-8 2016 Insulin secretion normalized to plasma glucose was significantly lower in PEAK patients, and the disposition index was reduced (35% to 41% of the values in NOPEAK patients). Glucose 39-46 insulin Homo sapiens 0-7 27052261-4 2016 now report that activation of a specific set of AgRP neurons results in an impairment of insulin-stimulated glucose uptake in brown fat through a myogenic signature program. Glucose 108-115 insulin Homo sapiens 89-96 27124282-2 2016 Secreted FABP4 as a novel adipokine leads to insulin resistance via increased hepatic glucose production (HGP). Glucose 86-93 insulin Homo sapiens 45-52 27113465-10 2016 This mini-review focuses on CADD approach on currently approved drugs and new therapeutic agents-indevelopment that may achieve suitable glucose levels and decrease the risk of hypoglycemia, which is a major obstacle to glucose control and a special concern for therapies that increase insulin levels. Glucose 137-144 insulin Homo sapiens 286-293 27110224-13 2016 CONCLUSIONS: In a fasted and glycogen-reduced state ingestion of a CHO solution during high-intensity exercise enhanced performance through stimulation of insulin-mediated glucose uptake. Glucose 172-179 insulin Homo sapiens 155-162 27104960-5 2016 In addition, our results show that stimulation of insulin secretion by GPR142 in pancreatic islets is strictly glucose-dependent. Glucose 111-118 insulin Homo sapiens 50-57 27073847-6 2016 CRP concentrations during pregnancy were positively correlated with a measure of insulin resistance, namely, the estimated glucose disposal rate, assessed in the first trimester (I, P = 0.01; II, P = 0.0165; III, P = 0.0062). Glucose 123-130 insulin Homo sapiens 81-88 27063927-3 2016 beta cells form irregular locally connected clusters within islets that act in concert to secrete insulin upon glucose stimulation. Glucose 111-118 insulin Homo sapiens 98-105 27061400-1 2016 BACKGROUND: Islet cell transplantation is a method to stabilize type 1 diabetes patients with hypoglycemia unawareness and unstable blood glucose levels by reducing insulin dependency and protecting against severe hypoglycemia through restoring endogenous insulin secretion. Glucose 138-145 insulin Homo sapiens 165-172 26998551-9 2016 It has been demonstrated that the glucose-responsive release behaviors of insulin and RSM in buffer or in human serum can be quantified in real-time through evaluating the changes of fluorescence signal. Glucose 34-41 insulin Homo sapiens 74-81 27143349-1 2016 OBJECTIVES: Nine classes of glucose-lowering agents (GLAs) are available for patients with type 2 diabetes prior to starting insulin. Glucose 28-35 insulin Homo sapiens 125-132 26727993-9 2016 Differentiated cells secreted insulin in a glucose-responsive manner. Glucose 43-50 insulin Homo sapiens 30-37 27054119-9 2016 IHC analysis showed higher expression of insulin protein in the hanging drop group, and CLIA revealed a significant higher insulin production in hanging drops compared with the monolayer group following the glucose challenge test. Glucose 207-214 insulin Homo sapiens 123-130 27034277-5 2016 The changes range from activation of proximal insulin signaling pathways that may contribute to adverse left ventricular remodeling and mitochondrial dysfunction to repression of distal elements of insulin signaling pathways such as forkhead box O transcriptional signaling or glucose transport, which may also impair cardiac metabolism, structure, and function. Glucose 277-284 insulin Homo sapiens 198-205 26706229-4 2016 More specifically, FGF19 and FGF21 signaling pathways have been linked to different glucose metabolic processes, including hepatic glucose synthesis, glycogen synthesis, glucose uptake, and insulin sensitivity, among others, and these molecules have been further related to the pathophysiology of diabetes mellitus. Glucose 84-91 insulin Homo sapiens 190-197 27034187-7 2016 The overall aim of this PhD thesis was to investigate how the blood glucose level affects the glucagon and insulin responses to GIP in healthy subjects (Study 1) and patients with Type 2 diabetes (Study 2), and more specifically to investigate the effects of GIP and GLP-1 at low blood glucose in patients with Type 1 diabetes without endogenous insulin secretion (Study 3). Glucose 68-75 insulin Homo sapiens 107-114 27034187-13 2016 The results from the three studies indicate that GIP has effects on insulin and glucagon responses highly dependent upon the blood glucose levels. Glucose 131-138 insulin Homo sapiens 68-75 27034187-18 2016 In conclusion, the studies position GIP as a bifunctional blood glucose stabilising hormone that glucose-dependently regulates insulin and glucagon responses in humans. Glucose 97-104 insulin Homo sapiens 127-134 26662378-5 2016 RESULTS: Circadian clock disruption resulted in a significant decrease in both acute and chronic glucose-stimulated insulin secretion. Glucose 97-104 insulin Homo sapiens 116-123 26740601-4 2016 Having previously developed an in vivo mouse hyperglycemia model, we tested whether glucose induces beta-cell proliferation through insulin signaling. Glucose 84-91 insulin Homo sapiens 132-139 26791990-1 2016 The physiologically predominant signal for pancreatic beta cells to secrete insulin is glucose. Glucose 87-94 insulin Homo sapiens 76-83 26791990-2 2016 While circulating glucose levels and beta cell glucose metabolism regulate the amount of released insulin, additional signals emanating from other tissues and from neighbouring islet endocrine cells modulate beta cell function. Glucose 18-25 insulin Homo sapiens 98-105 26791990-2 2016 While circulating glucose levels and beta cell glucose metabolism regulate the amount of released insulin, additional signals emanating from other tissues and from neighbouring islet endocrine cells modulate beta cell function. Glucose 47-54 insulin Homo sapiens 98-105 26791990-3 2016 To this end, each individual beta cell can be viewed as a sensor of a multitude of stimuli that are integrated to determine the extent of glucose-dependent insulin release. Glucose 138-145 insulin Homo sapiens 156-163 26791990-4 2016 This review discusses recent advances in our understanding of inter-organ communications that regulate beta cell insulin release in response to elevated glucose levels. Glucose 153-160 insulin Homo sapiens 113-120 26868492-7 2016 Interestingly, the high expression of ALOX12 is associated with the alteration in first-phase glucose-stimulated insulin secretion in human type 2 diabetic islets. Glucose 94-101 insulin Homo sapiens 113-120 26908914-7 2016 In PTDM patients, glucose-induced glucagon suppression was significantly less pronounced (maximal suppression from baseline: 43 +- 12 vs. 65 +- 12%, P < 0.001), while first- and second-phase insulin secretion were significantly lower. Glucose 18-25 insulin Homo sapiens 194-201 27094871-6 2016 CONCLUSION: Correction of vitamin D deficiency leads to increased insulin sensitivity that was significantly able to maintain glucose in the normal range with lower levels of insulin. Glucose 126-133 insulin Homo sapiens 66-73 26419850-0 2016 Elevated 1-hour plasma glucose levels are associated with dysglycemia, impaired beta-cell function, and insulin sensitivity: a pilot study from a real world health care setting. Glucose 23-30 insulin Homo sapiens 104-111 26774673-8 2016 RESULTS: AA supplementation significantly increased insulin-mediated glucose disposal (delta rate of glucose disappearance; Rd) (p=0.009), peripheral insulin-sensitivity index (p=0.046), skeletal muscle AA concentration (p=0.017) and muscle SVCT2 protein expression (p=0.008); but significantly decreased skeletal muscle DCFH oxidation during hyperinsulinaemia (p=0.007) when compared with placebo. Glucose 69-76 insulin Homo sapiens 52-59 26485752-0 2016 Insulin-stimulated glucose uptake in healthy and insulin-resistant skeletal muscle. Glucose 19-26 insulin Homo sapiens 0-7 26485752-0 2016 Insulin-stimulated glucose uptake in healthy and insulin-resistant skeletal muscle. Glucose 19-26 insulin Homo sapiens 49-56 26485752-1 2016 Skeletal muscle is the largest tissues in the human body and is considered the primary target for insulin-stimulated glucose disposal. Glucose 117-124 insulin Homo sapiens 98-105 26485752-2 2016 In skeletal muscle, binding of the insulin to insulin receptor (IR) initiates a signaling cascade that results in the translocation of the insulin-sensitive glucose transporter protein 4 (GLUT4) to the plasma membrane which leads to facilitated diffusion of glucose into the cell. Glucose 157-164 insulin Homo sapiens 35-42 26485752-2 2016 In skeletal muscle, binding of the insulin to insulin receptor (IR) initiates a signaling cascade that results in the translocation of the insulin-sensitive glucose transporter protein 4 (GLUT4) to the plasma membrane which leads to facilitated diffusion of glucose into the cell. Glucose 157-164 insulin Homo sapiens 46-53 26485752-3 2016 Understanding the precise signaling events guiding insulin-stimulated glucose uptake is pivotal, because impairment in these signaling events leads to development of insulin resistance and type 2 diabetes. Glucose 70-77 insulin Homo sapiens 51-58 26485752-3 2016 Understanding the precise signaling events guiding insulin-stimulated glucose uptake is pivotal, because impairment in these signaling events leads to development of insulin resistance and type 2 diabetes. Glucose 70-77 insulin Homo sapiens 166-173 26485752-4 2016 This review summarizes current understanding of insulin signaling pathways mediating glucose uptake in healthy and insulin-resistant skeletal muscle. Glucose 85-92 insulin Homo sapiens 48-55 26485752-4 2016 This review summarizes current understanding of insulin signaling pathways mediating glucose uptake in healthy and insulin-resistant skeletal muscle. Glucose 85-92 insulin Homo sapiens 115-122 26910750-9 2016 Specifically, physiological and molecular functions of several adipokines are defined with particular focus on interactions within the insulin-signaling pathway and subsequent regulation of glucose uptake in both standard and obesity-induced dysregulated conditions. Glucose 190-197 insulin Homo sapiens 135-142 27235674-11 2016 Furthermore, exogenous ghrelin administration was shown to decrease glucose-induced insulin release and increase glucose level in both humans and rodents. Glucose 68-75 insulin Homo sapiens 84-91 27123196-12 2016 In addition, we observed a direct correlation between fasting insulin with fasting glucose and HOMA-IR. Glucose 83-90 insulin Homo sapiens 62-69 26617254-4 2016 The primary and secondary outcome measures were insulin sensitivity assessed using a frequently sampled intravenous glucose tolerance test and hepatic triglyceride content with magnetic resonance spectroscopy. Glucose 116-123 insulin Homo sapiens 48-55 26400568-0 2016 Nephrin Trafficking beyond the Kidney--Role in Glucose-Stimulated Insulin Secretion in beta Cells. Glucose 47-54 insulin Homo sapiens 66-73 26400569-4 2016 Nephrin deficiency, however, resulted in glucose intolerance in vivo and impaired glucose-stimulated insulin release ex vivo Glucose intolerance was also observed in eight patients with nephrin mutations compared with three patients with other genetic forms of nephrotic syndrome or nine healthy controls.In vitro experiments were conducted to investigate if nephrin affects autocrine signaling through insulin receptor A (IRA) and B (IRB), which are both expressed in human podocytes and pancreatic islets. Glucose 82-89 insulin Homo sapiens 101-108 27358133-8 2016 All the above findings suggest that insulin pump can improve ulcer healing of patients suffering from diabetic foot ulcers as it effectively controls blood glucose level, restrains inflammatory reaction and prevents spreading of infection. Glucose 156-163 insulin Homo sapiens 36-43 26829441-9 2016 Conversely, insulin suppression of endogenous glucose production was similar in the groups. Glucose 46-53 insulin Homo sapiens 12-19 26859105-1 2016 Glucose entropy was inversely correlated with insulin resistance in a series of non-diabetic individuals with low glucose variability. Glucose 114-121 insulin Homo sapiens 46-53 26909799-10 2016 Insulin secretion improved in the liraglutide group vs placebo, as measured by the area under the curve of C-peptide (P = .002) and the area under the curves ratio of C-peptide to glucose (P = .003). Glucose 180-187 insulin Homo sapiens 0-7 27186348-4 2016 Further studies showed that GIP strongly stimulated the secretion of insulin, in the presence of elevated glucose, and this "incretin" action is now considered to be its most important; an alternative for the GIP acronym, glucose-dependent insulinotropic polypeptide, was therefore introduced. Glucose 106-113 insulin Homo sapiens 69-76 27226181-6 2016 At fasting leptin and adiponectin, as well as every 30 minutes of OGTT and every 2 hours of OLTT blood concentration of GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, insulin, triglycerides, free fatty acids, glutathione peroxidase, interleukin-6, sE-selectin, monocyte chemoattractant protein-1 (MCP1) and visfatin were measured. Glucose 127-134 insulin Homo sapiens 145-152 25647655-4 2016 The homeostasis model assessment of insulin sensitivity (HOMA) was calculated using glucose and insulin levels. Glucose 84-91 insulin Homo sapiens 36-43 27050068-8 2016 RESULTS: Compared to controls, insulin treated donors had a significant lower blood glucose 4.8 (4-6.9) vs. 9 (5.6-11.7) mmol/L, p<0.01); the net decreases of pro-inflammatory cytokines, such as IL-6 and MCP-1, and the net increase of anti-inflammatory cytokine, such as IL-10, reached significant level in insulin treated donors compared with those in controls. Glucose 84-91 insulin Homo sapiens 31-38 27186563-2 2016 The flexibility of an insulin regime or preparation is defined as their ability to be injected at variable times, with variable injection-meal time gaps, in a dose frequency and quantum determined by shared decision making, with a minimal requirement of glucose monitoring and health professional consultation, with no compromise on safety, efficiency and tolerability. Glucose 254-261 insulin Homo sapiens 22-29 26910514-7 2016 The future will increasingly focus on the refinement of structure to meet medicinal purposes that have long been pursued, such as the development of a glucose-sensitive insulin. Glucose 151-158 insulin Homo sapiens 169-176 26919485-2 2016 The insulin independent glucose transporter 1 (GLUT1) plays a key role in brain metabolism while the insulin-dependent GLUT4 is the major glucose transporter for skeletal and cardiac muscle. Glucose 24-31 insulin Homo sapiens 4-11 27085782-1 2016 AIM: Elevated basal endogenous glucose production (EGP), impaired suppression of EGP by insulin and reduced insulin-stimulated glucose disposal are cornerstones of the pathogenesis of hyperglycemia in patients with type 2 diabetes. Glucose 127-134 insulin Homo sapiens 108-115 26842771-7 2016 Strawberry intake reduced the insulin demand to manage postmeal glucose in obese individuals with IR, which was related to plasma anthocyanin/pelargonidin concentrations. Glucose 64-71 insulin Homo sapiens 30-37 26678022-6 2016 Insulin resistance (HOMA2 IR) was calculated from fasting blood glucose and insulin concentrations. Glucose 64-71 insulin Homo sapiens 0-7 27143182-0 2016 [The correlation between serum uric acid level and early-phase insulin secretion in subjects with normal glucose regulation]. Glucose 105-112 insulin Homo sapiens 63-70 27111219-0 2016 Exercise Intensity Modulates Glucose-Stimulated Insulin Secretion when Adjusted for Adipose, Liver and Skeletal Muscle Insulin Resistance. Glucose 29-36 insulin Homo sapiens 48-55 27111219-1 2016 Little is known about the effects of exercise intensity on compensatory changes in glucose-stimulated insulin secretion (GSIS) when adjusted for adipose, liver and skeletal muscle insulin resistance (IR). Glucose 83-90 insulin Homo sapiens 102-109 25581640-5 2016 We have shown that insulin can enhance blood flow to the microvasculature in muscle thus improving the access of glucose and insulin to the myocytes to augment glucose disposal. Glucose 113-120 insulin Homo sapiens 19-26 25581640-5 2016 We have shown that insulin can enhance blood flow to the microvasculature in muscle thus improving the access of glucose and insulin to the myocytes to augment glucose disposal. Glucose 160-167 insulin Homo sapiens 19-26 25581640-5 2016 We have shown that insulin can enhance blood flow to the microvasculature in muscle thus improving the access of glucose and insulin to the myocytes to augment glucose disposal. Glucose 160-167 insulin Homo sapiens 125-132 26902174-5 2016 Furthermore, LPS-, poly(I:C)- or TNF-alpha-induced insulin resistance was improved following suppression of ER stress, by increasing insulin-stimulated phosphorylation of IR-beta, IRS-1, GLUT-4 expression and glucose uptake. Glucose 209-216 insulin Homo sapiens 51-58 26902174-5 2016 Furthermore, LPS-, poly(I:C)- or TNF-alpha-induced insulin resistance was improved following suppression of ER stress, by increasing insulin-stimulated phosphorylation of IR-beta, IRS-1, GLUT-4 expression and glucose uptake. Glucose 209-216 insulin Homo sapiens 133-140 27076077-5 2016 Notably, forced expression of ERRgamma in iPSC-derived beta-like cells enables glucose-responsive secretion of human insulin in vitro, obviating in vivo maturation to achieve functionality. Glucose 79-86 insulin Homo sapiens 117-124 27347379-2 2016 GLP-1 also synergises insulin-dependent net hepatic glucose uptake (NHGU). Glucose 52-59 insulin Homo sapiens 22-29 27070593-0 2016 Pancreatic Transdifferentiation and Glucose-Regulated Production of Human Insulin in the H4IIE Rat Liver Cell Line. Glucose 36-43 insulin Homo sapiens 74-81 27070593-7 2016 Regulated secretion of insulin to glucose (0-20 mmol/L) was seen in the H4IIEins/ND cell line. Glucose 34-41 insulin Homo sapiens 23-30 27699257-3 2016 In the present work, we find that the ability of IL-1beta to amplify glucose-stimulated insulin secretion from human islets correlates with donor BMI. Glucose 69-76 insulin Homo sapiens 88-95 26739488-1 2016 Glucagon-like peptide-1 (GLP-1) is a gut L-cell hormone that enhances glucose-stimulated insulin secretion. Glucose 70-77 insulin Homo sapiens 89-96 26814014-6 2016 Insulin-stimulated [(14)C]glucose uptake and isoproterenol-stimulated lipolysis were measured in isolated epicardial and subcutaneous adipocytes. Glucose 26-33 insulin Homo sapiens 0-7 26447463-4 2016 Insulin sensitivity index (SI) was defined as steady-state glucose disposal divided by the steady-state plasma insulin. Glucose 59-66 insulin Homo sapiens 0-7 26861783-8 2016 The associated hormonal milieu (lower insulin-to-glucagon ratio) favors glucose release and ketogenesis. Glucose 72-79 insulin Homo sapiens 38-45 26968899-2 2016 These effects are realized through the insulin controlled transport of blood glucose into the insulin-responsive cells such as muscle, fat and liver cells. Glucose 77-84 insulin Homo sapiens 39-46 26968899-2 2016 These effects are realized through the insulin controlled transport of blood glucose into the insulin-responsive cells such as muscle, fat and liver cells. Glucose 77-84 insulin Homo sapiens 94-101 26968899-3 2016 Reduction in the ability of these cells to take glucose from the blood in response to normal circulating levels of insulin is known as insulin resistance (IR). Glucose 48-55 insulin Homo sapiens 115-122 26968899-3 2016 Reduction in the ability of these cells to take glucose from the blood in response to normal circulating levels of insulin is known as insulin resistance (IR). Glucose 48-55 insulin Homo sapiens 135-142 26763130-8 2016 CONCLUSION: The combination of glucose, fructose, and CFA could successfully induce metabolic disorders in HepG2 cells, including dyslipidemia, insulin resistance, hyperuricemia, and oxidative stress. Glucose 31-38 insulin Homo sapiens 144-151 26950362-3 2016 We found that beta cell-specific activation of p16(Ink4a) in transgenic mice enhances glucose-stimulated insulin secretion (GSIS). Glucose 86-93 insulin Homo sapiens 105-112 26781599-4 2016 RESULTS: The glucose-stimulated acute insulin response was restored in the T2D patients after SG. Glucose 13-20 insulin Homo sapiens 38-45 26709911-6 2016 The insulin area under the curve during the oral glucose tolerance test was lower for genotype CA/AA. Glucose 49-56 insulin Homo sapiens 4-11 26709911-7 2016 Despite the lower insulin levels, the glucose area under the curve was unchanged, resulting in a higher insulin sensitivity index. Glucose 38-45 insulin Homo sapiens 104-111 27035570-7 2016 When beta cells were selectively removed to mimic diabetic conditions, the anti-synchronicity of insulin and glucagon pulses was deteriorated at high glucose, but it could be partially recovered when the re-aggregation of remaining cells was considered. Glucose 150-157 insulin Homo sapiens 97-104 27065949-1 2016 Under normal physiological conditions, pancreatic beta-cells secrete insulin to maintain fasting blood glucose levels in the range 3.5-5.5 mmol/L. Glucose 103-110 insulin Homo sapiens 69-76 26997281-7 2016 This was associated with diminished glucose-stimulated insulin secretion, increased ROS formation, and accumulation of proinsulin, all characteristics of human diabetes. Glucose 36-43 insulin Homo sapiens 55-62 26986485-12 2016 These preliminary results suggest that FGF-21 might play a protective role as against the development of insulin resistance over time in patients undergoing a continuous glucose load. Glucose 170-177 insulin Homo sapiens 105-112 26714849-6 2016 The relationship between muscle metabolic insulin resistance and the vascular action of insulin in muscle continues to indicate an important role for the microvasculature as a target for insulin action and that impairing insulin"s microvascular action significantly affects body glucose metabolism. Glucose 279-286 insulin Homo sapiens 88-95 26714849-6 2016 The relationship between muscle metabolic insulin resistance and the vascular action of insulin in muscle continues to indicate an important role for the microvasculature as a target for insulin action and that impairing insulin"s microvascular action significantly affects body glucose metabolism. Glucose 279-286 insulin Homo sapiens 88-95 26744506-0 2016 Resistance training enhances insulin suppression of endogenous glucose production in elderly women. Glucose 63-70 insulin Homo sapiens 29-36 27066358-0 2016 Heart rate variability is associated with interstitial glucose fluctuations in type 2 diabetic women treated with insulin. Glucose 55-62 insulin Homo sapiens 114-121 27066358-3 2016 In this study we investigated the associations of frequency-domain HRV parameters with current and antecedent interstitial glucose fluctuations in insulin-treated type 2 diabetic women at high cardiovascular risk. Glucose 123-130 insulin Homo sapiens 147-154 27066358-13 2016 Both postprandial and antecedent nocturnal glucose fluctuations affect daytime frequency-domain HRV parameters in insulin-treated type 2 diabetic women. Glucose 43-50 insulin Homo sapiens 114-121 26996422-2 2016 The incretin effect is defined as the difference in the insulin secretory response between the oral glucose tolerance test and an isoglycemic intravenous glucose infusion study. Glucose 100-107 insulin Homo sapiens 56-63 26220149-8 2016 The decline in blood glucose concentration between peak and 125 min after exercise was greater in the insulin exercise session than in the no-insulin session (3.3 +- 1.0 vs. 1.3 +- 0.4 mmol/l: P = 0.015). Glucose 21-28 insulin Homo sapiens 102-109 26435365-0 2016 Twice-daily insulin degludec/insulin aspart provides superior fasting plasma glucose control and a reduced rate of hypoglycaemia compared with biphasic insulin aspart 30 in insulin-naive adults with Type 2 diabetes. Glucose 77-84 insulin Homo sapiens 12-19 26435365-5 2016 Insulin degludec/insulin aspart was superior in lowering fasting plasma glucose (estimated treatment difference -1.00 mmol/l; 95% CI -1.4, -0.6; P < 0.001) and reducing overall and nocturnal confirmed hypoglycaemia at a similar overall insulin dose compared with biphasic insulin aspart 30. Glucose 72-79 insulin Homo sapiens 0-7 26435365-5 2016 Insulin degludec/insulin aspart was superior in lowering fasting plasma glucose (estimated treatment difference -1.00 mmol/l; 95% CI -1.4, -0.6; P < 0.001) and reducing overall and nocturnal confirmed hypoglycaemia at a similar overall insulin dose compared with biphasic insulin aspart 30. Glucose 72-79 insulin Homo sapiens 17-24 26484727-10 2016 For individuals with Type 1 diabetes mellitus, nocturnal hypoglycaemia risk was significantly lower with insulin degludec during the maintenance period for the original definition (plasma glucose < 3.1 mmol/l, timescale 00.01-05.59) and in the extension trial set population for all hypoglycaemia definitions except for the nocturnal timescale 00.01-07.59. Glucose 188-195 insulin Homo sapiens 105-112 26948978-3 2016 Benefiting from the response capability of phenylboronic acid moiety toward glucose, the encapsulated insulin could be specifically released and the corresponding targeted DNA could efficiently express insulin in HepG2 cell, accompanied by the high-level insulin release in vitro. Glucose 76-83 insulin Homo sapiens 102-109 26948978-3 2016 Benefiting from the response capability of phenylboronic acid moiety toward glucose, the encapsulated insulin could be specifically released and the corresponding targeted DNA could efficiently express insulin in HepG2 cell, accompanied by the high-level insulin release in vitro. Glucose 76-83 insulin Homo sapiens 202-209 26948978-3 2016 Benefiting from the response capability of phenylboronic acid moiety toward glucose, the encapsulated insulin could be specifically released and the corresponding targeted DNA could efficiently express insulin in HepG2 cell, accompanied by the high-level insulin release in vitro. Glucose 76-83 insulin Homo sapiens 202-209 26942445-0 2016 Mechanisms Regulating Insulin Response to Intragastric Glucose in Lean and Non-Diabetic Obese Subjects: A Randomized, Double-Blind, Parallel-Group Trial. Glucose 55-62 insulin Homo sapiens 22-29 26942445-1 2016 BACKGROUND/OBJECTIVES: The changes in blood glucose concentrations that result from an oral glucose challenge are dependent on the rate of gastric emptying, the rate of glucose absorption and the rate of insulin-driven metabolism that include the incretins, glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). Glucose 44-51 insulin Homo sapiens 204-211 26942445-1 2016 BACKGROUND/OBJECTIVES: The changes in blood glucose concentrations that result from an oral glucose challenge are dependent on the rate of gastric emptying, the rate of glucose absorption and the rate of insulin-driven metabolism that include the incretins, glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). Glucose 92-99 insulin Homo sapiens 204-211 26942445-1 2016 BACKGROUND/OBJECTIVES: The changes in blood glucose concentrations that result from an oral glucose challenge are dependent on the rate of gastric emptying, the rate of glucose absorption and the rate of insulin-driven metabolism that include the incretins, glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). Glucose 92-99 insulin Homo sapiens 204-211 26934053-8 2016 Indeed, we found reduced levels of insulin receptor, PI3K, AKT, all important molecules in insulin signaling and glucose uptake by cells. Glucose 113-120 insulin Homo sapiens 35-42 26934990-1 2016 BACKGROUND: Quantitative evaluation of insulin regulation on plasma glucose and free fatty acid (FFA) in response to external glucose challenge is clinically important to assess the development of insulin resistance (World J Diabetes 1:36-47, 2010). Glucose 68-75 insulin Homo sapiens 39-46 26934990-1 2016 BACKGROUND: Quantitative evaluation of insulin regulation on plasma glucose and free fatty acid (FFA) in response to external glucose challenge is clinically important to assess the development of insulin resistance (World J Diabetes 1:36-47, 2010). Glucose 68-75 insulin Homo sapiens 197-204 26934990-1 2016 BACKGROUND: Quantitative evaluation of insulin regulation on plasma glucose and free fatty acid (FFA) in response to external glucose challenge is clinically important to assess the development of insulin resistance (World J Diabetes 1:36-47, 2010). Glucose 126-133 insulin Homo sapiens 39-46 26934990-1 2016 BACKGROUND: Quantitative evaluation of insulin regulation on plasma glucose and free fatty acid (FFA) in response to external glucose challenge is clinically important to assess the development of insulin resistance (World J Diabetes 1:36-47, 2010). Glucose 126-133 insulin Homo sapiens 197-204 26934990-2 2016 Mathematical minimal models (MMs) based on insulin modified frequently-sampled intravenous glucose tolerance tests (IM-FSIGT) are widely applied to ascertain an insulin sensitivity index (IEEE Rev Biomed Eng 2:54-96, 2009). Glucose 91-98 insulin Homo sapiens 43-50 26934990-2 2016 Mathematical minimal models (MMs) based on insulin modified frequently-sampled intravenous glucose tolerance tests (IM-FSIGT) are widely applied to ascertain an insulin sensitivity index (IEEE Rev Biomed Eng 2:54-96, 2009). Glucose 91-98 insulin Homo sapiens 161-168 26934990-3 2016 Furthermore, it is important to investigate insulin regulation on glucose and FFA in postprandial state as a normal physiological condition. Glucose 66-73 insulin Homo sapiens 44-51 26934990-5 2016 METHODS: A new MM is developed to simulate the insulin modulation of plasma glucose and FFA, combining IM-FSIGT with a mixed meal tolerance test (MT). Glucose 76-83 insulin Homo sapiens 47-54 26714848-2 2016 Hyperinsulinemic clamps with stable isotope tracers can simultaneously measure insulin"s ability to suppress lipolysis and hepatic glucose release. Glucose 131-138 insulin Homo sapiens 5-12 26714848-12 2016 Both STS and MEM can model lipolysis and endogenous glucose release in insulin-dependent states when basal Ra cannot be accurately measured. Glucose 52-59 insulin Homo sapiens 71-78 26599793-14 2016 Adequate intraoperative glucose management by initiating insulin infusion when glucose level exceeds 140 mg/dL to prevent hyperglycemia is associated with lower postoperative glucose levels and fewer incidences of postoperative hyperglycemia. Glucose 24-31 insulin Homo sapiens 57-64 26599793-14 2016 Adequate intraoperative glucose management by initiating insulin infusion when glucose level exceeds 140 mg/dL to prevent hyperglycemia is associated with lower postoperative glucose levels and fewer incidences of postoperative hyperglycemia. Glucose 79-86 insulin Homo sapiens 57-64 26599793-14 2016 Adequate intraoperative glucose management by initiating insulin infusion when glucose level exceeds 140 mg/dL to prevent hyperglycemia is associated with lower postoperative glucose levels and fewer incidences of postoperative hyperglycemia. Glucose 79-86 insulin Homo sapiens 57-64 26551662-13 2016 Once insulin or sulfonylurea-induced hypoglycaemia has developed, it should be initially treated with an intravenous dextrose bolus. Glucose 117-125 insulin Homo sapiens 5-12 25994513-4 2016 An increasing interest is reported in sodium-glucose co-transporter-2 inhibitors, a relatively novel class of glucose-lowering drugs that act independently of insulin, provide benefits beyond glucose-lowering actions and show a better tolerability compared with traditional medications for type 2 diabetes. Glucose 45-52 insulin Homo sapiens 159-166 26786574-12 2016 CONCLUSIONS: Glucose levels <180 mg/dL are associated with better outcomes in most patients, but worse outcomes in patients with diabetes with a history of prior insulin use. Glucose 13-20 insulin Homo sapiens 165-172 26803354-1 2016 This study using simultaneous Holter and continuous glucose monitoring demonstrates that prolongation of QT interval can occur with hypoglycaemia in an ambulatory setting in people with type 1 and type 2 diabetes treated with insulin. Glucose 52-59 insulin Homo sapiens 226-233 26806457-3 2016 Increasing the full-length human Klotho levels has a positive effect on blood glucose through increasing insulin secretion. Glucose 78-85 insulin Homo sapiens 105-112 29632582-2 2016 Insulin users need to frequently monitor their blood glucose levels and take multiple injections per day and/or multiple boluses through an insulin infusion pump, with the consequences of failing to match the insulin dose to the body"s needs resulting in hypoglycaemia and hyperglycaemia. Glucose 53-60 insulin Homo sapiens 0-7 26996422-2 2016 The incretin effect is defined as the difference in the insulin secretory response between the oral glucose tolerance test and an isoglycemic intravenous glucose infusion study. Glucose 154-161 insulin Homo sapiens 56-63 26194122-4 2016 Insulin was infused when the blood glucose level reached 120 mg/dL or higher, and glucose was infused when the level fell to 100 mg/dL or lower. Glucose 35-42 insulin Homo sapiens 0-7 26824281-7 2016 MAIN OUTCOME MEASURE: Odds ratios and 95% confidence intervals for a clinical diagnosis of type 1 diabetes or for insulin treatment by deciles of (a) fasting C-peptide, (b) C-peptide/glucose ratios, and (c) HOMA-ssC-peptide-index. Glucose 183-190 insulin Homo sapiens 114-121 26899161-7 2016 This report firstly showed that TBF could recover the redox status of insulin-resistant HepG2 cells, suggesting that TBF significantly protected the cells against high glucose-induced oxidative stress, and these beneficial effects of TBF on redox balance and insulin resistance were mediated by targeting MAPKs. Glucose 168-175 insulin Homo sapiens 70-77 26395744-9 2016 Secretions of CD56(-)CD15(+) cells differentiated into functional white adipocytes reduced insulin-mediated non-oxidative glucose disposal (P=0.0002) and insulin signaling. Glucose 122-129 insulin Homo sapiens 91-98 26471343-8 2016 Both single and double lipase knockdown reduced insulin-stimulated glucose uptake, which was attributable to impaired insulin signaling. Glucose 67-74 insulin Homo sapiens 48-55 30586235-1 2016 The insulin regulation of metabolism of fatty acids, number of double binds and cell absorption of glucose]. Glucose 99-106 insulin Homo sapiens 4-11 30586235-7 2016 The insulin expresses synthesis of Palmitoyl-KoA-elongase, stearyl-KoA-desaturase and glucose transporters 4, activates glucose absorption by cells with the purpose of synthesis endogenous oleic saturated fatty acid. Glucose 86-93 insulin Homo sapiens 4-11 26194122-7 2016 After total parenteral nutrition was started in the intensive care unit (ICU), the blood glucose level increased, and the artificial pancreas controlled the blood glucose level through automatic insulin administration. Glucose 163-170 insulin Homo sapiens 195-202 26874564-2 2016 Therefore, glucose and caloric balances become negative, making the blood glucose level as well as insulin secretion both reduced. Glucose 11-18 insulin Homo sapiens 99-106 26228765-5 2016 Recommendations accepted by the bedside clinicians directly link the subsequent blood glucose values to eProtocol-insulin recommendations and provide a unique clinical database. Glucose 86-93 insulin Homo sapiens 114-121 26224050-1 2016 The integrated glucose-insulin (IGI) model is a previously published semimechanistic model that describes plasma glucose and insulin concentrations after glucose challenges. Glucose 15-22 insulin Homo sapiens 23-30 26224050-1 2016 The integrated glucose-insulin (IGI) model is a previously published semimechanistic model that describes plasma glucose and insulin concentrations after glucose challenges. Glucose 113-120 insulin Homo sapiens 23-30 25753338-5 2016 Insulin resistance was quantified using the estimated glucose disposal rate (eGDR). Glucose 54-61 insulin Homo sapiens 0-7 26765576-7 2016 Compared to baseline, insulin-mediated glucose disposal increased significantly at week 2 (from 4.48 +- 0.50 to 5.30 +- 0.50 mg/kg min; P < .05). Glucose 39-46 insulin Homo sapiens 22-29 26765576-8 2016 However, insulin-mediated glucose disposal at week 3 (after the addition of acipimox) did not differ significantly from that at week 2. Glucose 26-33 insulin Homo sapiens 9-16 26765576-10 2016 CONCLUSION: Lowering the plasma glucose concentration with dapagliflozin improves both insulin sensitivity and beta-cell function, whereas lowering plasma FFA concentration by addition of acipimox to dapagliflozin improves beta-cell function without significantly affecting insulin sensitivity. Glucose 32-39 insulin Homo sapiens 87-94 26765576-1 2016 AIM: To investigate the effect of lowering the plasma glucose and free fatty acid (FFA) concentrations with dapagliflozin and acipimox, respectively, on insulin sensitivity and insulin secretion in T2DM individuals. Glucose 54-61 insulin Homo sapiens 153-160 26857733-8 2016 MAIN OUTCOMES AND MEASURES: Insulin sensitivity was measured by the homeostatic model assessment of insulin resistance and an oral glucose tolerance test-based index (Matsuda insulin sensitivity index). Glucose 131-138 insulin Homo sapiens 28-35 26857733-9 2016 Insulin secretion was measured using the area under the curve of insulin to glucose during the first 30 minutes of the oral glucose tolerance test and using the area under the curve of insulin to glucose over 2 hours. Glucose 124-131 insulin Homo sapiens 0-7 26880451-3 2016 Currently recommended insulin regimens provide too little insulin to achieve blood levels with a maximal kalemic effect and too little glucose to avoid hypoglycemia. Glucose 135-142 insulin Homo sapiens 22-29 26923398-5 2016 Insulin-stimulated glucose disposal was assessed using the hyperinsulinemic-euglycemic clamp to calculate glucose disposal rate into lean mass, the primary site of insulin-stimulated glucose disposal. Glucose 19-26 insulin Homo sapiens 0-7 26923398-5 2016 Insulin-stimulated glucose disposal was assessed using the hyperinsulinemic-euglycemic clamp to calculate glucose disposal rate into lean mass, the primary site of insulin-stimulated glucose disposal. Glucose 106-113 insulin Homo sapiens 0-7 26923398-5 2016 Insulin-stimulated glucose disposal was assessed using the hyperinsulinemic-euglycemic clamp to calculate glucose disposal rate into lean mass, the primary site of insulin-stimulated glucose disposal. Glucose 106-113 insulin Homo sapiens 0-7 26474432-5 2016 Islets were assessed for glucose-stimulated insulin release (GSIR) and apoptosis (Annexin V/caspase-3). Glucose 25-32 insulin Homo sapiens 44-51 26930652-0 2016 Triglyceride Glucose-Body Mass Index Is a Simple and Clinically Useful Surrogate Marker for Insulin Resistance in Nondiabetic Individuals. Glucose 13-20 insulin Homo sapiens 92-99 26723525-8 2016 In vivo evaluation of the system in a diabetic mouse model revealed that the fasted blood glucose level could be maintained in the normal range for 10days with a single injection of insulin-loaded CHC-lysozyme gel. Glucose 90-97 insulin Homo sapiens 182-189 26882284-4 2016 Knock-down of Jagn1 caused an increase in glucose-stimulated insulin secretion resulting from an increase in proinsulin biosynthesis. Glucose 42-49 insulin Homo sapiens 61-68 26882284-4 2016 Knock-down of Jagn1 caused an increase in glucose-stimulated insulin secretion resulting from an increase in proinsulin biosynthesis. Glucose 42-49 insulin Homo sapiens 109-119 27120723-4 2016 RESULTS: The glucose submodel specifies the dynamics of glucose absorption following meals, hepatic glucose production and uptake, peripheral glucose uptake, kidney excretion, and insulin-independent uptake of glucose in the brain and red blood cells. Glucose 13-20 insulin Homo sapiens 180-187 27120723-7 2016 Algebraic equations are used to specify (i) how the hormones affect glucose production and utilisation in various compartments such as liver, muscle and fat tissues, and (ii) how glucose levels modify insulin and glucagon release from the pancreas. Glucose 179-186 insulin Homo sapiens 201-208 28248217-2 2016 It accounts for ~80% of insulin stimulated glucose disposal. Glucose 43-50 insulin Homo sapiens 24-31 27313851-9 2016 BCAA were also associated with parameters of insulin sensitivity (Matsuda index: R -0 50, P = 0 0004; glucose AUC: R 0 53, P < 0 001). Glucose 102-109 insulin Homo sapiens 45-52 26840737-1 2016 Pancreatic islets respond to elevated blood glucose by secreting pulses of insulin that parallel oscillations in beta-cell metabolism, intracellular Ca(2+) concentration, and bursting electrical activity. Glucose 44-51 insulin Homo sapiens 75-82 25620470-7 2016 Insulin resistance (IR) was estimated using the Homeostasis Model of Assessment equation: HOMA-IR=[fasting insulin (mU/L)xfasting glucose (mmol/L)]/22.5. Glucose 130-137 insulin Homo sapiens 0-7 26646072-2 2016 It can provide early warning of the onset of hyperglycemia and hypoglycemia and has the functionality to suspend insulin delivery if sensor glucose levels fall below a predefined threshold. Glucose 140-147 insulin Homo sapiens 113-120 26893621-12 2016 In conclusion, local injection of insulin into the base of a diabetic foot ulcer has a significant effect on systemic blood glucose and may promote wound healing by improving the growth of granulation tissue. Glucose 124-131 insulin Homo sapiens 34-41 26652932-5 2016 A subgroup of 201 subjects also underwent a frequently sampled IV glucose tolerance test and the acute insulin response to glucose, insulin sensitivity, and glucose effectiveness (SG) estimated (MINMOD model). Glucose 123-130 insulin Homo sapiens 103-110 26394161-8 2016 Liraglutide increased hepatic insulin sensitivity (-9.36 vs. -2.54% suppression of hepatic endogenous glucose production with low-dose insulin; p<0.05). Glucose 102-109 insulin Homo sapiens 30-37 26361380-2 2016 A rise in circulating insulin in response to food-related sensory stimulation may prepare tissues to break down ingested glucose, e.g. by stimulating rate-limiting glycolytic enzymes. Glucose 121-128 insulin Homo sapiens 22-29 27455563-7 2016 Increasing of content of unesterifed fatty acids in blood plasma, as it always occurs in vivo, stops absorption of glucose by cells initiating hyperglycemia, hyperinsulinemia, and syndrome of resistance to insulin. Glucose 115-122 insulin Homo sapiens 163-170 26547662-1 2016 BACKGROUND: The use of oral glucose-lowering therapies with insulin is common, but the cardiovascular effects are largely unknown. Glucose 28-35 insulin Homo sapiens 60-67 26472664-7 2016 Glucose controls also basal and compensatory beta-cell proliferation and, along with fatty acids, regulates insulin biosynthesis. Glucose 0-7 insulin Homo sapiens 108-115 26598517-0 2016 O-Linked beta-N-acetylglucosamine (O-GlcNAc) Acts as a Glucose Sensor to Epigenetically Regulate the Insulin Gene in Pancreatic Beta Cells. Glucose 55-62 insulin Homo sapiens 101-108 26819233-10 2016 RESULTS: Subcutaneous regular insulin lowered both mean glucose concentrations and glucose variability in a linear fashion. Glucose 56-63 insulin Homo sapiens 30-37 26819233-10 2016 RESULTS: Subcutaneous regular insulin lowered both mean glucose concentrations and glucose variability in a linear fashion. Glucose 83-90 insulin Homo sapiens 30-37 26819233-12 2016 Although subcutaneous Lispro insulin lowered mean glucose concentrations, glucose variability increased in a nonlinear fashion. Glucose 50-57 insulin Homo sapiens 29-36 26819233-16 2016 CONCLUSIONS: Subcutaneous regular insulin consistently lowered mean glucose concentrations and glucose variability; its linear dose-response curve rendered the preparation better suited for a sliding-scale protocol. Glucose 68-75 insulin Homo sapiens 34-41 26819233-16 2016 CONCLUSIONS: Subcutaneous regular insulin consistently lowered mean glucose concentrations and glucose variability; its linear dose-response curve rendered the preparation better suited for a sliding-scale protocol. Glucose 95-102 insulin Homo sapiens 34-41 27276742-8 2016 Insulin secretion rate was measured using area under the curve (AUC) of insulin and AUC of insulin/glucose ratio. Glucose 99-106 insulin Homo sapiens 0-7 27276742-10 2016 AUC of insulin was greater after high-dose MO (4 g) than after baseline or low-dose MO capsule (1 g) (24.0 +- 3.5 vs. 14.5 +- 1.8 or 16.1 +- 2.0, respectively; p = 0.03), while there was no difference in AUC of glucose. Glucose 211-218 insulin Homo sapiens 7-14 27276742-11 2016 Accordingly, insulin secretion rate represented by AUC of insulin/glucose ratio after high-dose MO was significantly increased by 74% (P = 0.041), as compared with that of baseline. Glucose 66-73 insulin Homo sapiens 13-20 26767523-0 2016 Erratum to: Short-term glucagon stimulation test of C-peptide effect on glucose utilization in patients with type 1 diabetes mellitus. Glucose 72-79 insulin Homo sapiens 52-61 26835874-12 2016 CONCLUSIONS: Collectively, these findings provide a mechanism by which FSE exerts antihyperglycemic effects similar to metformin and insulin that occurs via enhanced insulin signaling, gene expression, and increasing glucose uptake. Glucose 217-224 insulin Homo sapiens 133-140 26842973-2 2016 Insulin therapy is essential and lifesaving in individuals with type 1 diabetes and beneficial for those with type 2 diabetes who fail to achieve optimal glycaemic targets with other classes of glucose-lowering therapies. Glucose 194-201 insulin Homo sapiens 0-7 26740469-2 2016 In insulin-secreting beta cells, glutamate acts as an intracellular messenger, and its transport into secretory granules promotes glucose- and incretin-stimulated insulin secretion. Glucose 130-137 insulin Homo sapiens 3-10 26888756-5 2016 Efficient knockdown of either Insr or Irs1/2 was achieved by conditional shRNA expression, severely attenuating insulin-stimulated AKT phosphorylation and glucose uptake. Glucose 155-162 insulin Homo sapiens 112-119 26801563-6 2016 Compared to normoxia and hypoxia, hyperoxia alleviated the loss of islet volume, maintaining higher islet viability and metabolism as measured by oxygen consumption and glucose-stimulated insulin secretion responses. Glucose 169-176 insulin Homo sapiens 188-195 26767403-2 2016 In this study, we compared demographic and clinical data between six GDM subjects and six normal glucose tolerance (NGT; healthy controls) subjects and found that homeostasis model of assessment for insulin resistance index (HOMA-IR) increased in GDM. Glucose 97-104 insulin Homo sapiens 199-206 26608654-2 2016 In this work, we describe the development of a physiologically based model and its application to data from 154 patients who underwent an insulin-modified intravenous glucose tolerance test (IM-IVGTT). Glucose 167-174 insulin Homo sapiens 138-145 26583890-1 2016 BACKGROUND: The purpose of this study was to evaluate the performance of an insulin infusion protocol targeting a blood glucose (BG) level of 140-180 mg/dL and to characterize protocol adherence. Glucose 120-127 insulin Homo sapiens 76-83 26784129-1 2016 BACKGROUND: Recent advances in accuracy and reliability of continuous glucose monitoring (CGM) devices have focused renewed interest on the use of such technology for therapeutic dosing of insulin without the need for independent confirmatory blood glucose meter measurements. Glucose 70-77 insulin Homo sapiens 189-196 26784131-5 2016 The first commercial product for partial automation of insulin administration used insulin delivery shutoff at a predefined glucose level. Glucose 124-131 insulin Homo sapiens 55-62 26895276-1 2016 OBJECTIVE: Glucose dependent insulinotropic peptide (GIP) belongs to the incretins which are responsible for 70% of the insulin release after oral glucose intake. Glucose 147-154 insulin Homo sapiens 29-36 26467793-0 2016 Impact of keratin intermediate filaments on insulin-mediated glucose metabolism regulation in the liver and disease association. Glucose 61-68 insulin Homo sapiens 44-51 26467793-2 2016 In insulin-targeted cells, such as hepatocytes, proper glucose utilization requires an elaborate interplay between the insulin receptor, the glucose transporter, and mitochondria that involves the participation of actin microfilaments and microtubules. Glucose 55-62 insulin Homo sapiens 3-10 26467793-6 2016 There are accumulating examples of K8/K18 involvement in the glucose-insulin cross-talk, including the modulation of plasma glucose levels, insulin release from pancreatic beta-cells, and insulin-mediated glucose uptake and glycogen production in hepatocytes after a K8/K18 loss. Glucose 61-68 insulin Homo sapiens 69-76 26467793-6 2016 There are accumulating examples of K8/K18 involvement in the glucose-insulin cross-talk, including the modulation of plasma glucose levels, insulin release from pancreatic beta-cells, and insulin-mediated glucose uptake and glycogen production in hepatocytes after a K8/K18 loss. Glucose 61-68 insulin Homo sapiens 140-147 26467793-6 2016 There are accumulating examples of K8/K18 involvement in the glucose-insulin cross-talk, including the modulation of plasma glucose levels, insulin release from pancreatic beta-cells, and insulin-mediated glucose uptake and glycogen production in hepatocytes after a K8/K18 loss. Glucose 124-131 insulin Homo sapiens 69-76 26467793-7 2016 This review integrates the mechanistic features that support such an impact of K8/K18 IFs on insulin-dependent glucose metabolism regulation in liver and its implication in glucose- or insulin-associated diseases. Glucose 111-118 insulin Homo sapiens 93-100 26774399-0 2016 Estimation of glucose utilization in a type 2 diabetes mellitus patient on insulin analogs with tumor hypoglycemia induced by IGF-II. Glucose 14-21 insulin Homo sapiens 75-82 26597568-4 2016 At physiological conditions, the glucose-induced volume phase transition and release profile of the model drug Alizarin Red with 1,2-diol structure (comparative to insulin as a drug as well as a dye for bio separation) were studied at various glucose concentrations, pH and ionic strengths. Glucose 33-40 insulin Homo sapiens 164-171 26725077-0 2016 The impact of basal insulin analogues on glucose variability in patients with type 2 diabetes undergoing renal replacement therapy for end-stage renal disease. Glucose 41-48 insulin Homo sapiens 20-27 26725077-1 2016 PURPOSE: We aimed to analyze the impact of basal insulin analogues on glucose variability (GV) in patients with type 2 diabetes (DM) undergoing renal replacement therapy. Glucose 70-77 insulin Homo sapiens 49-56 26683831-4 2016 We found that the insulin secretagogue glucose promotes phosphatidylinositol (3,4,5)-trisphosphate (PIP3) generation through phosphoinositide 3-kinase (PI3K), thereby recruiting ARNO to the intracellular side of the plasma membrane. Glucose 39-46 insulin Homo sapiens 18-25 26709968-5 2016 Insulin-stimulated glucose disposal, the suppression of endogenous glucose production during hyperinsulinemia, and homeostatic model assessment of insulin resistance were tested for associations with 11 potential predictors. Glucose 19-26 insulin Homo sapiens 0-7 26774163-1 2016 Neonatal glucose levels correlate negatively with umbilical cord levels of C-peptide, a polypeptide secreted with insulin. Glucose 9-16 insulin Homo sapiens 75-84 26774163-1 2016 Neonatal glucose levels correlate negatively with umbilical cord levels of C-peptide, a polypeptide secreted with insulin. Glucose 9-16 insulin Homo sapiens 114-121 26776262-4 2016 In this study we present an explicit solution to the minimal model which allows for separating the glucose and insulin dynamics of the minimal model and for identifying patient-specific parameters of glucose trajectories from IVGTT. Glucose 200-207 insulin Homo sapiens 111-118 26259649-7 2016 METHODS: Glucose uptake was examined in C2C12 myotubes that express GPRC6A following treatment with insulin alone or with insulin and increasing ucOC concentrations (0.3, 3, 10 and 30 ng/ml). Glucose 9-16 insulin Homo sapiens 100-107 26259649-7 2016 METHODS: Glucose uptake was examined in C2C12 myotubes that express GPRC6A following treatment with insulin alone or with insulin and increasing ucOC concentrations (0.3, 3, 10 and 30 ng/ml). Glucose 9-16 insulin Homo sapiens 122-129 26259649-11 2016 ucOC significantly increased insulin-stimulated glucose uptake dose-dependently up to 10 ng/ml, in differentiated mouse C2C12 myotubes. Glucose 48-55 insulin Homo sapiens 29-36 26259649-12 2016 Insulin increased EDL glucose uptake (~30 %, p < 0.05) and p-AKT and p-AKT/AKT compared with rest (all p < 0.05). Glucose 22-29 insulin Homo sapiens 0-7 26259649-14 2016 ucOC after contraction increased insulin-stimulated muscle glucose uptake (~12 % p < 0.05) and p-AS160 (<0.05) more than contraction plus insulin alone but without effect on p-AKT. Glucose 59-66 insulin Homo sapiens 33-40 26259649-17 2016 ucOC treatment augments insulin-stimulated skeletal muscle glucose uptake in C2C12 myotubes and following ex vivo muscle contraction. Glucose 59-66 insulin Homo sapiens 24-31 26146025-2 2016 OSA could alter glucose metabolism, generating insulin resistance and favoring the development of T2DM. Glucose 16-23 insulin Homo sapiens 47-54 27799841-1 2016 PURPOSE: The purpose of this study was to evaluate the optimization of fasting blood glucose (FBG) levels in patients with type 2 diabetes mellitus newly initiated on insulin glargine who were enrolled in the Australian Diabetes CoStars Patient Support Program (PSP). Glucose 85-92 insulin Homo sapiens 167-174 28031946-5 2016 For patients without pretransplant DM, the need for insulin at discharge increased 23% for every 5-year age increase (odds ratio: 1.23; 95% CI: 1.06-1.44; p = 0.007) and 51% for every five units of glucose measurements >180 mg/dl (OR: 1.51; 95% CI: 1.23-1.95; p < 0.01). Glucose 198-205 insulin Homo sapiens 52-59 26857733-9 2016 Insulin secretion was measured using the area under the curve of insulin to glucose during the first 30 minutes of the oral glucose tolerance test and using the area under the curve of insulin to glucose over 2 hours. Glucose 76-83 insulin Homo sapiens 0-7 26857733-9 2016 Insulin secretion was measured using the area under the curve of insulin to glucose during the first 30 minutes of the oral glucose tolerance test and using the area under the curve of insulin to glucose over 2 hours. Glucose 76-83 insulin Homo sapiens 65-72 26857733-9 2016 Insulin secretion was measured using the area under the curve of insulin to glucose during the first 30 minutes of the oral glucose tolerance test and using the area under the curve of insulin to glucose over 2 hours. Glucose 124-131 insulin Homo sapiens 0-7 26788115-12 2016 A minor effect was also observed on insulin-stimulated glucose uptake albeit only with the combination of DHA and AC. Glucose 55-62 insulin Homo sapiens 36-43 26772807-0 2016 Effects of analogue insulin in multiple daily injection therapy of type 2 diabetes on postprandial glucose control and cardiac function compared to human insulin: a randomized controlled long-term study. Glucose 99-106 insulin Homo sapiens 20-27 26772807-2 2016 Both short and long-acting insulin analogues (AI) have been shown to reduce glucose variability and provide potential benefit for cardiovascular disease although the effects on cardiac function have not yet been evaluated. Glucose 76-83 insulin Homo sapiens 27-34 26607804-6 2016 Furthermore, intrinsically recovered PDI levels were able to restore the effect of high glucose- and palmitate-induced beta-cell dysfunction by increasing 3.9-fold the glucose-stimulated insulin secretion levels and restoring insulin content up to basal control values. Glucose 88-95 insulin Homo sapiens 187-194 26607804-6 2016 Furthermore, intrinsically recovered PDI levels were able to restore the effect of high glucose- and palmitate-induced beta-cell dysfunction by increasing 3.9-fold the glucose-stimulated insulin secretion levels and restoring insulin content up to basal control values. Glucose 168-175 insulin Homo sapiens 187-194 26758205-9 2016 Glucose uptake by insulin target tissues, measured in vivo using (3)H-2-deoxyglucose, showed that CETP expression had no effect on the glucose uptake in liver, muscle, perigonadal, perirenal, subcutaneous and brown adipose tissues. Glucose 0-7 insulin Homo sapiens 18-25 26735686-11 2016 CONCLUSIONS: HCV-positive renal transplant recipients show significantly improved glucose-stimulated insulin sensitivity and overall glucose tolerance after conversion from tacrolimus to cyclosporine A. Glucose 82-89 insulin Homo sapiens 101-108 26742071-4 2016 Polyphenols may also enhance insulin-dependent glucose uptake, activate 5" adenosine monophosphate-activated protein kinase (AMPK), modify the microbiome and have anti-inflammatory effects. Glucose 47-54 insulin Homo sapiens 29-36 27645817-5 2016 Inaccurate blood glucose information can result in unsafe insulin delivery which causes poor glucose control and can be fatal. Glucose 17-24 insulin Homo sapiens 58-65 26542602-1 2016 Diabetes is a common chronic disease due to an altered glucose metabolism, caused by the quantitative and/or qualitative dysfunction of the insulin hormone. Glucose 55-62 insulin Homo sapiens 140-147 28514553-2 2016 It was found that in the group of hypertensive patients with low mass and muscle strength significantly increased indices of insulin resistance and more expressed signs of the left ventricle myocardial dysfunction and functional class of heart failure, probably as a result of disorders of energy homeostasis, resulting from the deterioration of glucose into the muscle cells of the heart and skeletal muscles. Glucose 346-353 insulin Homo sapiens 125-132 26571012-9 2016 There was a significant reduction in insulin resistance measured by the homeostatic model assessment in the isolated-impaired fasting glucose (p < 0.05) but not in the isolated-impaired glucose tolerance groups (p = 0.59). Glucose 134-141 insulin Homo sapiens 37-44 26973184-2 2016 This condition is manifested in the reduction of peripheral tissues sensitivity to the biological action of insulin and is expressed in the inhibition of cellular glucose absorption and metabolism in response to hormonal stimulation. Glucose 163-170 insulin Homo sapiens 108-115 26628048-5 2016 After culture viability, glucose-stimulated insulin release, DNA content as well as Bax and Bcl-2 gene expression were measured. Glucose 25-32 insulin Homo sapiens 44-51 26628048-8 2016 Decreased viability corresponded with a significant increase in the Bax/Bcl-2 mRNA ratio at 300 and 600 IEQ/cm(2) and with a sigificantly reduced glucose-stimulated insulin secretion and insulin content compared to 75 or 150 IEQ/cm(2) (p < 0.01). Glucose 146-153 insulin Homo sapiens 165-172 26877090-9 2016 Insulin secretions in response to high-glucose stimulation were 5.1 +- 1.6, 9.4 +- 3.8, and 23.5 +- 12.4 microIU/islet, and interleukin-6 (IL-6) secretions were 3.0 +- 0.7, 5.1 +- 1.2, and 7.3 +- 1.0 ng/day, respectively. Glucose 39-46 insulin Homo sapiens 0-7 27669369-1 2016 In primary aldosteronism (PA), insulin response to glucose is not fully understood. Glucose 51-58 insulin Homo sapiens 31-38 26819233-9 2016 These end points were interpreted by how the ultradian oscillations of glucose concentration were affected by each insulin preparation. Glucose 71-78 insulin Homo sapiens 115-122 26343364-0 2016 Real-time estimation of plasma insulin concentration from continuous glucose monitor measurements. Glucose 69-76 insulin Homo sapiens 31-38 26343364-2 2016 These control systems use an insulin feedback to maintain plasma glucose concentration within a narrow and safe range, and thus to avoid health complications. Glucose 65-72 insulin Homo sapiens 29-36 26343364-5 2016 In order to reduce these limitations, our objective is to perform a real-time estimation of plasma insulin concentration from continuous glucose monitoring (CGM). Glucose 137-144 insulin Homo sapiens 99-106 26343364-10 2016 Hence, real-time estimations for plasma insulin concentration based on subcutaneous glucose monitoring can be beneficial for increasing the efficiency of control algorithms for the artificial pancreas. Glucose 84-91 insulin Homo sapiens 40-47 26643928-1 2016 BACKGROUND: Alternative insulin therapy with continuous subcutaneous insulin infusion (CSII) is offered with an objective of achieving better glycemic control, minimising glucose variability and thereby, preventing or reducing the risk of microvascular and macrovascular complications in people with type 1 or type 2 diabetes. Glucose 171-178 insulin Homo sapiens 24-31 26643928-1 2016 BACKGROUND: Alternative insulin therapy with continuous subcutaneous insulin infusion (CSII) is offered with an objective of achieving better glycemic control, minimising glucose variability and thereby, preventing or reducing the risk of microvascular and macrovascular complications in people with type 1 or type 2 diabetes. Glucose 171-178 insulin Homo sapiens 69-76 27229720-1 2016 DNA methylation, a major regulator of epigenetic modifications has been shown to alter the expression of genes that are involved in aspects of glucose metabolism such as glucose intolerance, insulin resistance, beta-cell dysfunction and other conditions, and it ultimately leads to the pathogenesis of type 2 diabetes mellitus (T2DM). Glucose 143-150 insulin Homo sapiens 191-198 25708430-3 2016 Insulin released from islets grafted in CNS was shown to cross the blood-brain barrier and to act as a regulator of peripheral glucose metabolism. Glucose 127-134 insulin Homo sapiens 0-7 25708430-4 2016 In diabetic animals, sufficient nutrition and oxygen supply to islets grafted in the CNS provide adequate insulin response to increase glucose level resulting in rapid normoglycemia. Glucose 135-142 insulin Homo sapiens 106-113 26607485-3 2016 As expected with this improved pharmacokinetic profile, insulin aspart demonstrates a greater glucose-lowering effect compared with regular human insulin. Glucose 94-101 insulin Homo sapiens 56-63 26447084-0 2016 Central insulin-mediated regulation of hepatic glucose production [Review]. Glucose 47-54 insulin Homo sapiens 8-15 26447084-1 2016 Insulin controls hepatic glucose production (HGP) and maintains glucose homeostasis through the direct action of hepatic insulin receptors, as well as the indirect action of insulin receptors in the central nervous system. Glucose 25-32 insulin Homo sapiens 0-7 26447084-1 2016 Insulin controls hepatic glucose production (HGP) and maintains glucose homeostasis through the direct action of hepatic insulin receptors, as well as the indirect action of insulin receptors in the central nervous system. Glucose 64-71 insulin Homo sapiens 0-7 26447084-5 2016 It has become evident that nutrients such as glucose, fatty acids, and amino acids act upon the hypothalamus together with insulin, affecting HGP. Glucose 45-52 insulin Homo sapiens 123-130 27364374-1 2016 Insulin therapy is the most effective method of lowering blood glucose. Glucose 63-70 insulin Homo sapiens 0-7 26618219-11 2016 Development of glucose-responsive automated closed-loop insulin delivery systems may reduce the burden of disease management and improve outcomes in type 1 diabetes. Glucose 15-22 insulin Homo sapiens 56-63 27812978-2 2016 As skeletal muscle is a major sink for glucose disposal, understanding the molecular mechanisms involved in maintaining insulin sensitivity of this tissue could potentially benefit millions of people that are diagnosed with insulin resistance. Glucose 39-46 insulin Homo sapiens 120-127 27812978-4 2016 A single bout of exercise has long been known to increase glucose disposal in skeletal muscle in response to physiological insulin concentrations. Glucose 58-65 insulin Homo sapiens 123-130 26344944-3 2016 Insulin, a central anabolic hormone, is one such hormone, as its roles and effectiveness in regulation of blood glucose levels remain to be examined in squamates. Glucose 112-119 insulin Homo sapiens 0-7 26652306-11 2016 Independent predictors of maximum glucose post-event were type 1 diabetes (p = 0.0003), history of any diabetes (p = 0.013), and total bolus dose of insulin (p < 0.0001). Glucose 34-41 insulin Homo sapiens 149-156 27595543-1 2016 BACKGROUND: Growth hormone (GH) influences glucose homeostasis by negatively affecting insulin sensitivity, leading to a compensatory increase in insulin secretion. Glucose 43-50 insulin Homo sapiens 87-94 27478440-8 2016 Multivariate analysis showed that higher FBG at time of OGTT, first 75 g OGTT 2 h plasma glucose, and HbA1c concentration at diagnosis lead to more likely need of insulin therapy. Glucose 89-96 insulin Homo sapiens 163-170 27478440-10 2016 The probability of insulin therapy can be estimated in pregnant women with GDM based on fasting and 2 h glucose values during OGTT and HbA1c value at diagnosis of GDM. Glucose 104-111 insulin Homo sapiens 19-26 26273793-1 2016 Autoimmune antibodies, induced by exogenous insulin preparations, may result in labile glucose control and frequent hypoglycemia in some rare cases. Glucose 87-94 insulin Homo sapiens 44-51 26472876-10 2016 Training-induced changes in the vasculature and in insulin signaling in the muscle fibers and vasculature augment glucose and insulin delivery as well as glucose uptake. Glucose 114-121 insulin Homo sapiens 51-58 26668677-1 2016 The new drug for type 2 diabetes, the sodium-glucose cotransporter 2 (SGLT-2) inhibitor, is reversible inhibitor of SGLT-2, leading to reduction of renal glucose reabsorption and decrease of plasma glucose, in an insulin-independent manner. Glucose 45-52 insulin Homo sapiens 213-220 26770991-0 2016 Assessment of Insulin Resistance in Subjects with Normal Glucose Tolerance, Hyperinsulinemia with Normal Blood Glucose Tolerance, Impaired Glucose Tolerance, and Newly Diagnosed Type 2 Diabetes (Prediabetes Insulin Resistance Research). Glucose 57-64 insulin Homo sapiens 14-21 26770991-0 2016 Assessment of Insulin Resistance in Subjects with Normal Glucose Tolerance, Hyperinsulinemia with Normal Blood Glucose Tolerance, Impaired Glucose Tolerance, and Newly Diagnosed Type 2 Diabetes (Prediabetes Insulin Resistance Research). Glucose 111-118 insulin Homo sapiens 14-21 26770991-0 2016 Assessment of Insulin Resistance in Subjects with Normal Glucose Tolerance, Hyperinsulinemia with Normal Blood Glucose Tolerance, Impaired Glucose Tolerance, and Newly Diagnosed Type 2 Diabetes (Prediabetes Insulin Resistance Research). Glucose 111-118 insulin Homo sapiens 14-21 27382574-1 2016 The "incretin effect" is used to describe the observation that more insulin is secreted after the oral administration of glucose compared to that after the intravenous administration of the same amount of glucose. Glucose 121-128 insulin Homo sapiens 68-75 27382574-1 2016 The "incretin effect" is used to describe the observation that more insulin is secreted after the oral administration of glucose compared to that after the intravenous administration of the same amount of glucose. Glucose 205-212 insulin Homo sapiens 68-75 27686029-0 2016 Efficacy and safety of dextrose-insulin in unmasking non-diagnostic Brugada ECG patterns. Glucose 23-31 insulin Homo sapiens 32-39 27686029-3 2016 We report our experience with unmasking J-ST changes in response to a dextrose-insulin test. Glucose 70-78 insulin Homo sapiens 79-86 27686029-11 2016 The maximum changes of the J-ST segment were observed 41.3+-31.4minutes (range 3-90minutes) after dextrose-insulin infusion. Glucose 98-106 insulin Homo sapiens 107-114 28050568-9 2016 High glucose media enhanced insulin expression by about 4-18 fold, suggesting a glucose-dependent effect in the proliferated islet-derived cells. Glucose 5-12 insulin Homo sapiens 28-35 28050568-9 2016 High glucose media enhanced insulin expression by about 4-18 fold, suggesting a glucose-dependent effect in the proliferated islet-derived cells. Glucose 80-87 insulin Homo sapiens 28-35 26466813-0 2016 Insulin resistance and lipid profile during an oral glucose tolerance test in women with and without gestational diabetes mellitus. Glucose 52-59 insulin Homo sapiens 0-7 26466813-1 2016 We aimed to compare changes in insulin levels during an oral glucose tolerance test (OGTT) between women with normal glucose tolerance (NGT) during pregnancy and those with gestational diabetes mellitus (GDM). Glucose 61-68 insulin Homo sapiens 31-38 26466813-1 2016 We aimed to compare changes in insulin levels during an oral glucose tolerance test (OGTT) between women with normal glucose tolerance (NGT) during pregnancy and those with gestational diabetes mellitus (GDM). Glucose 117-124 insulin Homo sapiens 31-38 31529902-6 2016 The late in phylogenesis humoral insulin regulates no stages of glucose metabolism; they are completed a billion years before hormone synthesis. Glucose 64-71 insulin Homo sapiens 33-40 31529902-17 2016 The insulin activates absorption by myocytes, cardiomyocytes of glucose as substrate of synthesis out of it in situ de novo omega-9 oleic mono unsaturated fatty acid. Glucose 64-71 insulin Homo sapiens 4-11 31529916-2 2016 Inconsistency of Randle cycle, regulation metabolism of fatty acids and glucose by insulin.] Glucose 72-79 insulin Homo sapiens 83-90 31529916-6 2016 The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. Glucose 47-54 insulin Homo sapiens 4-11 31529916-6 2016 The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. Glucose 47-54 insulin Homo sapiens 108-115 31529916-6 2016 The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. Glucose 201-208 insulin Homo sapiens 4-11 31529916-6 2016 The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. Glucose 201-208 insulin Homo sapiens 108-115 31529916-7 2016 The insulin activates absorption of glucose only by insulin-dependent cells by force of decreasing of "bioavailability" of fatty acids. Glucose 36-43 insulin Homo sapiens 4-11 31529916-7 2016 The insulin activates absorption of glucose only by insulin-dependent cells by force of decreasing of "bioavailability" of fatty acids. Glucose 36-43 insulin Homo sapiens 52-59 27150090-2 2016 Diagnostic criteria are elevated fasting or postprandial blood glucose levels, a consequence of insulin resistance. Glucose 63-70 insulin Homo sapiens 96-103 27150090-7 2016 We review here commonly used methods to measure endpoints relevant to glucose metabolism which show good translatability to the diagnostic of type 2 diabetes in humans: baseline fasting glucose and insulin, glucose tolerance test, insulin sensitivity index, and body type composition. Glucose 70-77 insulin Homo sapiens 198-205 27150090-7 2016 We review here commonly used methods to measure endpoints relevant to glucose metabolism which show good translatability to the diagnostic of type 2 diabetes in humans: baseline fasting glucose and insulin, glucose tolerance test, insulin sensitivity index, and body type composition. Glucose 70-77 insulin Homo sapiens 231-238 26808535-12 2016 RESULTS: BDDE increased the insulin-resisted glucose uptake in HepG2 cells. Glucose 45-52 insulin Homo sapiens 28-35 27189471-5 2016 Insulin is a multipotent hormone regulating, not only glucose levels, but also cell survival and synaptic plasticity mechanisms of neurons. Glucose 54-61 insulin Homo sapiens 0-7 26795016-3 2016 Further DNA codon optimization of the insulin gene construct resulted in approximately 3-10 times more human C-peptide secreted in the blood of codon optimized treated animals thereby reducing the number of vector particles required to achieve the same extent of reduction in blood glucose levels as the non-codon optimized vector. Glucose 282-289 insulin Homo sapiens 38-45 26795016-3 2016 Further DNA codon optimization of the insulin gene construct resulted in approximately 3-10 times more human C-peptide secreted in the blood of codon optimized treated animals thereby reducing the number of vector particles required to achieve the same extent of reduction in blood glucose levels as the non-codon optimized vector. Glucose 282-289 insulin Homo sapiens 109-118 27928958-6 2016 Fasting glucose, fasting and postprandial triglyceride and C-peptide levels were also reduced by NPH insulin whereas postprandial insulin was decreased by sitagliptin. Glucose 8-15 insulin Homo sapiens 101-108 26486356-6 2016 Muscle insulin sensitivity of glucose uptake was measured using 18F-fluoro-2-deoxyglucose and positron emission tomography with computed tomography during a hyperinsulinaemic-euglycaemic clamp. Glucose 30-37 insulin Homo sapiens 7-14 26622051-4 2016 Insulin sensitivity was calculated from the glucose infusion rate (GIR) during hyperinsulinemic-euglycemic clamp. Glucose 44-51 insulin Homo sapiens 0-7 26628414-7 2016 First-phase insulin response to a stepped intravenous glucose infusion did not change in NGT (0.24 [0.13-0.46] to 0.23 [0.19-0.37] nmol min(-1) m(-2)) but normalized in T2DM (0.08 [-0.01 to -0.10] to 0.22 [0.07-0.30]) nmol min(-1) m(-2) at week 8 (P = 0.005). Glucose 54-61 insulin Homo sapiens 12-19 26522272-9 2016 Degludec is an effective and promising long-acting insulin that reduced hypoglycemia and daily blood glucose variability in participants with type 1 diabetes. Glucose 101-108 insulin Homo sapiens 51-58 26606946-11 2016 Multivariate analysis showed that the 1-h OGTT plasma glucose level at diagnosis was an independent predictor of the need for insulin. Glucose 54-61 insulin Homo sapiens 126-133 27933175-5 2016 An oral glucose tolerance test revealed persistent high serum levels of total insulin and undetectable C-peptide. Glucose 8-15 insulin Homo sapiens 78-85 26541603-5 2016 Insulin resistance was estimated by the HOMA index (considering serum fasting glucose and insulin determinations). Glucose 78-85 insulin Homo sapiens 0-7 27818698-7 2016 Norepinephrine was higher, whereas the dynamic changes in glucose and insulin during an oral glucose tolerance test were lower in those with cold extremities, particularly hands. Glucose 93-100 insulin Homo sapiens 70-77 26560137-5 2016 Furthermore, the integration of continuous glucose monitoring with insulin pump therapy enables on-going adjustment of insulin delivery to optimize glycemic control throughout the day and night. Glucose 43-50 insulin Homo sapiens 119-126 25998484-6 2016 Moreover, the single nucleotide polymorphism (SNP) was significantly associated with increased glucose levels at 0, 60 and 120 min during the OGTT (all p < 0.0038) and with the increased homeostasis model assessment of insulin resistance (p < 0.001) in the GDM group. Glucose 95-102 insulin Homo sapiens 222-229 25903416-2 2016 Type 1 and type 2 diabetes arise from different etiologies but lead to similar metabolic derangements constituted by an absolute or relative lack of insulin that results in elevated plasma glucose. Glucose 189-196 insulin Homo sapiens 149-156 26542377-5 2016 The plausible linkages between these two pathophysiological conditions are altered levels of insulin signaling proteins such as IR-beta, IRS-1, PI3K, Akt, Glut4 and PGC-1alpha that hamper insulin-mediated glucose uptake as well as other functions of insulin in the cardiomyocytes and the endothelial cells of the heart. Glucose 205-212 insulin Homo sapiens 93-100 26542377-5 2016 The plausible linkages between these two pathophysiological conditions are altered levels of insulin signaling proteins such as IR-beta, IRS-1, PI3K, Akt, Glut4 and PGC-1alpha that hamper insulin-mediated glucose uptake as well as other functions of insulin in the cardiomyocytes and the endothelial cells of the heart. Glucose 205-212 insulin Homo sapiens 188-195 26542377-5 2016 The plausible linkages between these two pathophysiological conditions are altered levels of insulin signaling proteins such as IR-beta, IRS-1, PI3K, Akt, Glut4 and PGC-1alpha that hamper insulin-mediated glucose uptake as well as other functions of insulin in the cardiomyocytes and the endothelial cells of the heart. Glucose 205-212 insulin Homo sapiens 188-195 26721672-5 2016 The balance between the utilization and production of glucose is primarily maintained at equilibrium by two opposing hormones, insulin and glucagon. Glucose 54-61 insulin Homo sapiens 127-134 26721672-6 2016 In response to an elevation in plasma glucose and amino acids (after consumption of a meal), insulin is released from the beta cells of the islets of Langerhans in the pancreas. Glucose 38-45 insulin Homo sapiens 93-100 26721672-9 2016 At the same time, insulin serves as the major physiological anabolic agent, promoting the synthesis and storage of glucose, lipids, and proteins and inhibiting their degradation and release back into the circulation. Glucose 115-122 insulin Homo sapiens 18-25 26721672-10 2016 This chapter will focus mainly on signal transduction mechanisms by which insulin exerts its plethora of effects in liver, muscle, and fat cells, focusing on those pathways that are crucial in the control of glucose and lipid homeostasis. Glucose 208-215 insulin Homo sapiens 74-81 26904466-1 2016 The gradual decline in beta-cell function is inevitable in type 2 diabetes mellitus and therefore, substantial proportions of patients require insulin subsequently, in order to achieve optimal glucose control. Glucose 193-200 insulin Homo sapiens 143-150 27882052-5 2016 Our results confirm that myoinositol and D-chiro inositol acutely reduce insulin increase after glucose intake mainly in children with high basal insulin level. Glucose 96-103 insulin Homo sapiens 73-80 26883301-0 2016 Differentiation with elaidate tends to impair insulin-dependent glucose uptake and GLUT4 translocation in 3T3-L1 adipocytes. Glucose 64-71 insulin Homo sapiens 46-53 26883301-4 2016 We show here that elaidate impairs insulin-dependent glucose uptake in adipocytes. Glucose 53-60 insulin Homo sapiens 35-42 26883301-5 2016 Differentiation with 10 muM elaidate, which is close to physiological plasma concentration, reduces insulin-dependent glucose uptake. Glucose 118-125 insulin Homo sapiens 100-107 26883301-8 2016 Thus, our findings reveal that differentiation with elaidate tends to affect insulin-dependent glucose uptake through alternation of GLUT4 translocation from cytosol to the plasma membrane. Glucose 95-102 insulin Homo sapiens 77-84 26765145-0 2016 Phenylboronic acid as a glucose-responsive trigger to tune the insulin release of glycopolymer nanoparticles. Glucose 24-31 insulin Homo sapiens 63-70 26765145-4 2016 Insulin was efficiently encapsulated within the nanoparticles (up to 15%), and the release of insulin increased with an increase in the level of glucose in the medium. Glucose 145-152 insulin Homo sapiens 0-7 26765145-4 2016 Insulin was efficiently encapsulated within the nanoparticles (up to 15%), and the release of insulin increased with an increase in the level of glucose in the medium. Glucose 145-152 insulin Homo sapiens 94-101 26574958-6 2016 Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated from glucose and insulin. Glucose 81-88 insulin Homo sapiens 32-39 26727229-2 2016 Ectopic lipid accumulation in liver and skeletal muscle triggers pathways that impair insulin signaling, leading to reduced muscle glucose uptake and decreased hepatic glycogen synthesis. Glucose 131-138 insulin Homo sapiens 86-93 26727229-3 2016 Muscle insulin resistance, due to ectopic lipid, precedes liver insulin resistance and diverts ingested glucose to the liver, resulting in increased hepatic de novo lipogenesis and hyperlipidemia. Glucose 104-111 insulin Homo sapiens 7-14 26697503-6 2016 The reduction of blood glucose levels in response to per unit of insulin (RBG/RI) was recorded. Glucose 23-30 insulin Homo sapiens 65-72 26770984-3 2016 Genetic and pharmacological studies have demonstrated that the nitric oxide (NO) synthase (NOS) genes are critically involved in the regulation of insulin-mediated glucose disposal. Glucose 164-171 insulin Homo sapiens 147-154 27274997-3 2016 Yet hypoxia is also known to encourage glucose transport using insulin-dependent mechanisms, largely reliant on the metabolic master switch, 5" AMP-activated protein kinase (AMPK). Glucose 39-46 insulin Homo sapiens 63-70 27274997-6 2016 How is it that the same stress can seemingly cause insulin resistance while increasing glucose uptake? Glucose 87-94 insulin Homo sapiens 51-58 27568916-1 2016 AIMS: This study aimed to assess whether insulin secretion patterns during oral glucose tolerance tests (OGTTs) could predict future type 2 diabetes (T2D) in Chinese normal glucose tolerance (NGT) subjects. Glucose 80-87 insulin Homo sapiens 41-48 27568916-1 2016 AIMS: This study aimed to assess whether insulin secretion patterns during oral glucose tolerance tests (OGTTs) could predict future type 2 diabetes (T2D) in Chinese normal glucose tolerance (NGT) subjects. Glucose 173-180 insulin Homo sapiens 41-48 27819007-6 2016 These changes were associated with improvements in insulin resistance as determined with intravenous glucose tolerance testing. Glucose 101-108 insulin Homo sapiens 51-58 27117849-1 2016 Uncoupling protein 3 (UCP3) and pyruvate dehydrogenase kinase 4 (PDK4) in skeletal muscle are key regulators of the glucose and lipid metabolic processes that are involved in insulin resistance. Glucose 116-123 insulin Homo sapiens 175-182 27554916-5 2016 In response to increasing concentrations of glucose, all 3 groups increased insulin release, but the cultured beta-cells (2D and 3D) were more sensitive to glucose (EC50 5.85mM for 2D beta-cells, 16.24mM for 3D beta-cell spheroids) than the human islet spheroids (EC50 53.69mM). Glucose 44-51 insulin Homo sapiens 76-83 27183727-5 2016 The phylogenetically late insulin used after billions years the same dependencies at formation of regulation ofmetabolism offatty acids and cells" absorption of glucose. Glucose 161-168 insulin Homo sapiens 26-33 31529916-13 2016 The syndrome of resistance to insulin is, at the first place, pathology of metabolism of fatty acids and only in the second place metabolism of glucose. Glucose 144-151 insulin Homo sapiens 30-37 26154337-1 2016 PURPOSE: This study aims to establish whether changes in indices of insulin sensitivity (Si) derived from fasting glucose and an oral glucose tolerance test (OGTT) are comparable to Si determined by the oral minimal model (OMM) in response to acute moderate-intensity exercise (MIE) and high-intensity exercise (HIE). Glucose 114-121 insulin Homo sapiens 68-75 26154337-1 2016 PURPOSE: This study aims to establish whether changes in indices of insulin sensitivity (Si) derived from fasting glucose and an oral glucose tolerance test (OGTT) are comparable to Si determined by the oral minimal model (OMM) in response to acute moderate-intensity exercise (MIE) and high-intensity exercise (HIE). Glucose 134-141 insulin Homo sapiens 68-75 26538022-1 2016 Insulin promotes glucose uptake into skeletal muscle through recruitment of glucose transporter 4 (GLUT4) to the plasma membrane. Glucose 17-24 insulin Homo sapiens 0-7 27313601-3 2016 The treatment of DM2 has been directed toward the reduction of hyperglycemia using different drugs such as insulin sensitizers, as the case of TZDs, which are able to lower blood glucose levels and circulating triglycerides by binding to the nuclear peroxisome proliferator-activated receptor gamma (PPARgamma) as full agonists. Glucose 179-186 insulin Homo sapiens 107-114 27951535-4 2016 RESULTS: Glucose disposal per kilogram of fat free mass (a marker of peripheral insulin sensitivity) increased significantly in all groups, especially after 1 month. Glucose 9-16 insulin Homo sapiens 80-87 26652903-1 2016 Insulin resistance is a condition in which cells are defective in response to the actions of insulin in tissue glucose uptake. Glucose 111-118 insulin Homo sapiens 0-7 26652903-1 2016 Insulin resistance is a condition in which cells are defective in response to the actions of insulin in tissue glucose uptake. Glucose 111-118 insulin Homo sapiens 93-100 26652903-4 2016 In this study, we demonstrate that sustained betaAR stimulation resulted in the inhibition of insulin-induced glucose uptake, and a reduction of insulin induced glucose transporter (GLUT)4 expression that were mediated by the beta2AR subtype in cardiomyocytes and heart tissue. Glucose 110-117 insulin Homo sapiens 94-101 29677418-3 2016 The aim of thestudy was to analyse the test resultsof oral load of 75g of glucose as a predictorof need for insulin in the treatmentof gestational diabetes and toprovide 2nd trimester characteristicsof women eventually requiring insulinas compared with those in behaviouralapproach was sufficient. Glucose 74-81 insulin Homo sapiens 108-115 27397605-3 2016 Insulin exerts diverse effects on cells by targeting distinct functions such as gene expression, fatty acid synthesis, glucose transport and receptor translocation. Glucose 119-126 insulin Homo sapiens 0-7 26350474-10 2016 CONCLUSIONS: The improvement of glucose tolerance in morbidly obese patients with severe obstructive sleep apnea, without changes in homeostasis model assessment of insulin resistance, supports an improvement in peripheral insulin resistance after continuous positive airway pressure treatment. Glucose 32-39 insulin Homo sapiens 223-230 27425836-13 2016 CONCLUSION: BPD restores the glucose entrainment of high-frequency insulin oscillations in obese NGT and T2D patients after marked weight loss and normalizes glucose levels and insulin sensitivity, thus demonstrating recovery of beta-cell glucose sensing. Glucose 29-36 insulin Homo sapiens 67-74 27425836-13 2016 CONCLUSION: BPD restores the glucose entrainment of high-frequency insulin oscillations in obese NGT and T2D patients after marked weight loss and normalizes glucose levels and insulin sensitivity, thus demonstrating recovery of beta-cell glucose sensing. Glucose 158-165 insulin Homo sapiens 67-74 27425836-13 2016 CONCLUSION: BPD restores the glucose entrainment of high-frequency insulin oscillations in obese NGT and T2D patients after marked weight loss and normalizes glucose levels and insulin sensitivity, thus demonstrating recovery of beta-cell glucose sensing. Glucose 158-165 insulin Homo sapiens 67-74 29159123-6 2016 With premix 75/25 insulin, insulin AUC was lower and incremental glucose AUC was greater at lunch compared to the healthy and glargine/glulisine. Glucose 65-72 insulin Homo sapiens 18-25 26583784-0 2015 Insulin-coated gold nanoparticles as a new concept for personalized and adjustable glucose regulation. Glucose 83-90 insulin Homo sapiens 0-7 26583784-3 2015 In this study we present a novel strategy for controlled and prolonged glucose regulation, based on the administration of insulin-coated gold nanoparticles (INS-GNPs). Glucose 71-78 insulin Homo sapiens 122-129 26513554-9 2015 Thus, efficient differentiation of therapeutic insulin-producing cells was attained in vivo through the use of extracellular vesicle-mimetic NVs, which maintained physiological glucose levels. Glucose 177-184 insulin Homo sapiens 47-54 26487009-0 2015 Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise. Glucose 42-49 insulin Homo sapiens 23-30 26487009-0 2015 Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise. Glucose 42-49 insulin Homo sapiens 71-78 26487009-2 2015 This review focuses on potential mechanisms for greater postexercise and insulin-stimulated glucose uptake (ISGU) by muscle in individuals with normal or reduced insulin sensitivity. Glucose 92-99 insulin Homo sapiens 73-80 26487009-3 2015 A model is proposed for the processes underlying this improvement; i.e., triggers initiate events that activate subsequent memory elements, which store information that is relayed to mediators, which translate memory into action by controlling an end effector that directly executes increased insulin-stimulated glucose transport. Glucose 312-319 insulin Homo sapiens 293-300 26472870-3 2015 We hypothesized that a reduction in insulin sensitivity via reductions in physical activity would reduce cardiac BRS at rest and following an oral glucose tolerance test (OGTT). Glucose 147-154 insulin Homo sapiens 36-43 25724479-5 2015 GLP-1 analogs were long presumed to affect glucose control through their ability to increase insulin levels through peripheral action on beta cells. Glucose 43-50 insulin Homo sapiens 93-100 26507143-3 2015 The aim of this study was to test whether insulin resistance is associated with obesity parameters, peritoneal transport rate, and glucose absorption. Glucose 131-138 insulin Homo sapiens 42-49 26507143-14 2015 A total of 18 patients (35.3%) who had insulin resistance presented with higher LAR and rel.FM (7.3 [12.3, interquartile range] versus 0.7 [1.4, interquartile range], P<0.001, and 39.4 +- 10.1% versus 27.2 +- 11.5%, P=0.002, respectively), lower IGFBP-1 (8.2 +- 7.2 versus 21.0 +- 16.3 ng/ml, P=0.002), but similar glucose absorption and small-solute transport compared with patients without insulin resistance. Glucose 318-325 insulin Homo sapiens 39-46 26507143-16 2015 CONCLUSIONS: Insulin resistance in nondiabetic peritoneal dialysis patients is associated with obesity and LAR independent of glucose absorption and small-solute transport status. Glucose 126-133 insulin Homo sapiens 13-20 26677767-3 2015 Following the transplant, basal human C-peptide levels were consistently higher in mice compared with rats, but only rats showed robust meal- and glucose-responsive human C-peptide secretion by 19-21 weeks. Glucose 146-153 insulin Homo sapiens 171-180 26362689-2 2015 With the availability of glucose from nutrient metabolism, insulin action in muscle results in increased glucose disposal via uptake from the circulation and storage of excess, thereby maintaining euglycemia. Glucose 25-32 insulin Homo sapiens 59-66 26362689-2 2015 With the availability of glucose from nutrient metabolism, insulin action in muscle results in increased glucose disposal via uptake from the circulation and storage of excess, thereby maintaining euglycemia. Glucose 105-112 insulin Homo sapiens 59-66 26362689-3 2015 This major action of insulin is executed by redistribution of the glucose transporter protein, GLUT4 from intracellular storage sites to the plasma membrane and storage of glucose in the form of glycogen which also involves modulation of actin dynamics that govern trafficking of all the signal proteins of insulin signal transduction. Glucose 66-73 insulin Homo sapiens 21-28 26362689-3 2015 This major action of insulin is executed by redistribution of the glucose transporter protein, GLUT4 from intracellular storage sites to the plasma membrane and storage of glucose in the form of glycogen which also involves modulation of actin dynamics that govern trafficking of all the signal proteins of insulin signal transduction. Glucose 66-73 insulin Homo sapiens 307-314 26549228-3 2015 In this study, we identified the Groucho protein AES (Amino-terminal Enhancer of Split) as a HNF1alpha-specific physical binding partner and functional repressor of HNF1alpha-mediated transcription, which has a direct link to glucose-stimulated insulin secretion in beta-cells that is impaired in the HNF1alpha mutation-driven diabetes. Glucose 226-233 insulin Homo sapiens 245-252 26249206-11 2015 CONCLUSIONS: Twenty-four-week treatment with exenatide, insulin and pioglitazone improved glucose control in patients with newly diagnosed type 2 diabetes, but had no impact on bone turnover markers or BMD. Glucose 90-97 insulin Homo sapiens 56-63 26537944-5 2015 Gastric emptying (with the use of 3-dimensional ultrasound), plasma cholecystokinin, glucagon-like peptide 1, glucose-dependent insulinotropic peptide, insulin, glucagon, total amino acids, and blood glucose were measured for 180 min after consumption of the drinks, and energy intake at a buffet-style lunch was quantified. Glucose 110-117 insulin Homo sapiens 128-135 26445303-11 2015 CONCLUSIONS: A less intensive subcutaneous insulin correction protocol in hospitalized patients resulted in similar glucose values with less severe hypoglycemia. Glucose 116-123 insulin Homo sapiens 43-50 26607016-3 2015 After administration of glucocorticoids, changing insulin formulations or discontinuing the insulin and switching to oral antidiabetic agents, the level of insulin antibodies decreased and the plasma glucose restored. Glucose 200-207 insulin Homo sapiens 92-99 26607016-3 2015 After administration of glucocorticoids, changing insulin formulations or discontinuing the insulin and switching to oral antidiabetic agents, the level of insulin antibodies decreased and the plasma glucose restored. Glucose 200-207 insulin Homo sapiens 92-99 26607016-4 2015 Thus, we recommend to identify the presence of high insulin antibodies in patients with type 2 diabetes who experience unexplained high plasma glucose or frequent reoccurrence of hypoglycemia. Glucose 143-150 insulin Homo sapiens 52-59 26458376-2 2015 Insulin resistance is a general term meaning that insulin does not exert its normal effects in insulin-sensitive target tissues, such as skeletal muscle, adipose tissue, and liver, the major target tissues for insulin action in glucose metabolism. Glucose 228-235 insulin Homo sapiens 0-7 25996848-2 2015 Previously, individuals with high AMY1 CNVs exhibited low postprandial glucose levels and postprandial early insulin surge, suggesting that high AMY1 gene copy numbers may play a role in lowering the risk of insulin resistance. Glucose 71-78 insulin Homo sapiens 208-215 26305390-4 2015 Insulin was infused using a modified Yale protocol targeting a blood glucose level between 80 and 120 mg/dL. Glucose 69-76 insulin Homo sapiens 0-7 26305390-11 2015 CONCLUSIONS: RT-CGM did not ameliorate glucose control or variability; neither did it reduce the number of hypoglycemic events, but our insulin infusion protocol led to overall good glucose control without a significant hypoglycemia risk, making further improvement difficult. Glucose 182-189 insulin Homo sapiens 136-143 26341113-5 2015 Determined by the frequently sampled intravenous glucose tolerance test, insulin resistance was defined as the lowest sex-specific quartile of insulin sensitivity. Glucose 49-56 insulin Homo sapiens 73-80 26376795-5 2015 RESULTS: We found that individual beta cells respond to increases in glucose concentration by releasing insulin granules in very discrete bursts with periods consistent with in vivo pulsatile insulin secretion. Glucose 69-76 insulin Homo sapiens 104-111 26376795-6 2015 In successive secretory bursts during prolonged exposure to high glucose levels, secretory events progressively localised to preferential release sites, coinciding with the transition to second phase insulin secretion. Glucose 65-72 insulin Homo sapiens 200-207 26537705-1 2015 Pre-diabetes and diabetes occur secondary to a constellation of pathophysiological abnormalities that culminate in insulin resistance, which results in reduced cellular glucose uptake and increased glucose production. Glucose 169-176 insulin Homo sapiens 115-122 26537705-1 2015 Pre-diabetes and diabetes occur secondary to a constellation of pathophysiological abnormalities that culminate in insulin resistance, which results in reduced cellular glucose uptake and increased glucose production. Glucose 198-205 insulin Homo sapiens 115-122 26774018-0 2015 Physiological aspects of the combination of insulin and GLP-1 in the regulation of blood glucose control. Glucose 89-96 insulin Homo sapiens 44-51 26774018-3 2015 Insulin increases glucose utilization and retards hepatic glucose production through direct actions in muscle, adipose tissue and the liver. Glucose 18-25 insulin Homo sapiens 0-7 26531841-1 2015 OBJECTIVE: Insulin pump therapy associated with continuous glucose monitoring has shown a positive clinical impact on diabetes control and reduction of hypoglycemia episodes. Glucose 59-66 insulin Homo sapiens 11-18 26140358-11 2015 Sensing of D-glucose and of di- and tripeptides is particularly relevant for the secretion of the incretins glucose-dependent insulinotrophic polypeptide and glucagon-like peptide 1 that promote insulin output from beta-cells and mediate beta-cell protection. Glucose 11-20 insulin Homo sapiens 126-133 26546820-2 2015 Insulin secretion is controlled by metabolic stimuli (glucose, fatty acids), but also by monoamine neurotransmitters, like dopamine, serotonin, and norepinephrine. Glucose 54-61 insulin Homo sapiens 0-7 26425886-7 2015 MAIN OUTCOMES AND MEASURES: The study"s main outcome was insulin-mediated glucose disposal (glucose disposal rate [GDR]) via hyperinsulinemic-euglycemic clamp. Glucose 74-81 insulin Homo sapiens 57-64 26155920-6 2015 RESULTS: Cutoff points for insulin-mediated suppression of endogenous glucose production (EGP) and insulin-stimulated glucose disappearance rate (Rd) were 46.5% and 37.3 mumol kg(-)(1) min(-)(1), respectively. Glucose 70-77 insulin Homo sapiens 27-34 26155920-6 2015 RESULTS: Cutoff points for insulin-mediated suppression of endogenous glucose production (EGP) and insulin-stimulated glucose disappearance rate (Rd) were 46.5% and 37.3 mumol kg(-)(1) min(-)(1), respectively. Glucose 118-125 insulin Homo sapiens 99-106 26425886-7 2015 MAIN OUTCOMES AND MEASURES: The study"s main outcome was insulin-mediated glucose disposal (glucose disposal rate [GDR]) via hyperinsulinemic-euglycemic clamp. Glucose 92-99 insulin Homo sapiens 57-64 26457543-15 2015 The association between serum glucose and odds of TOF indicates the need for additional epidemiological and mechanistic investigations into the risk conferred by insulin signaling and glucose metabolism during early pregnancy. Glucose 30-37 insulin Homo sapiens 162-169 26580240-10 2015 MAIN OUTCOME MEASURES: The primary outcomes of the study were insulin sensitivity and glucose-stimulated insulin secretion. Glucose 86-93 insulin Homo sapiens 105-112 26571400-1 2015 Strategies aimed at mimicking or enhancing the action of the incretin hormone glucagon-like peptide 1 (GLP-1) therapeutically improve glucose-stimulated insulin secretion (GSIS); however, it is not clear whether GLP-1 directly drives insulin secretion in pancreatic islets. Glucose 134-141 insulin Homo sapiens 153-160 26294351-5 2015 Insulin sensitivity was assessed by the glucose infusion rate during clamp (M value); insulin secretion by Insulinogenic index, Oral Disposition Index (DIo) and AUC(2h-insulin) during OGTT; and insulin clearance by the metabolic clearance rate of insulin (MCRI) during clamp. Glucose 40-47 insulin Homo sapiens 0-7 26452501-6 2015 KPNbeta1 knockdown reversed PA-induced pro-inflammatory cytokines expression and insulin-stimulated glucose uptake in HepG2 cells. Glucose 100-107 insulin Homo sapiens 81-88 26308671-4 2015 In response to insulin, forearm glucose uptake was significantly increased to a lesser extent (-40%) in patients with CKD than controls. Glucose 32-39 insulin Homo sapiens 15-22 26308671-6 2015 Besides blunting muscle glucose uptake, CKD and acidosis interfere with the normal suppression of protein degradation in response to a moderate rise in plasma insulin. Glucose 24-31 insulin Homo sapiens 159-166 25673317-0 2015 A receptor state space model of the insulin signalling system in glucose transport. Glucose 65-72 insulin Homo sapiens 36-43 26607818-0 2015 Short-term glucagon stimulation test of C-peptide effect on glucose utilization in patients with type 1 diabetes mellitus. Glucose 60-67 insulin Homo sapiens 40-49 25673317-1 2015 Insulin is a potent peptide hormone that regulates glucose levels in the blood. Glucose 51-58 insulin Homo sapiens 0-7 26607818-1 2015 This work aimed to evaluate the use of a four-point glucagon stimulation test of C-peptide effect on glucose utilization in type 1 diabetic patients using a new mathematical model. Glucose 101-108 insulin Homo sapiens 81-90 25673317-2 2015 Insulin-sensitive cells respond to insulin stimulation with the translocation of glucose transporter 4 (GLUT4) to the plasma membrane (PM), enabling the clearance of glucose from the blood. Glucose 81-88 insulin Homo sapiens 0-7 26607818-3 2015 Pharmacokinetic and pharmacokinetic/pharmacodynamic models of C-peptide effect on glucose utilization versus area under curve (AUC) were used. Glucose 82-89 insulin Homo sapiens 62-71 26607818-6 2015 The high correlation (r = 0.97) between modeled coefficient of whole-body glucose utilization and numerically calculated AUC C-peptide/AUC glucose ratio related to entire cohort indicated the stability of used method. Glucose 74-81 insulin Homo sapiens 125-134 25673317-2 2015 Insulin-sensitive cells respond to insulin stimulation with the translocation of glucose transporter 4 (GLUT4) to the plasma membrane (PM), enabling the clearance of glucose from the blood. Glucose 81-88 insulin Homo sapiens 35-42 25673317-4 2015 One widely cited model of insulin signalling leading to glucose transport is that of Sedaghat et al. Glucose 56-63 insulin Homo sapiens 26-33 25731746-1 2015 Insulin resistance, clinically defined as the inability of insulin to increase glucose uptake and utilization, has been found to be associated with the progression of Alzheimer disease (AD). Glucose 79-86 insulin Homo sapiens 0-7 25994778-6 2015 The insulin response to glucose did not change in LAGB participants, whereas their fasting C-peptide/insulin ratio increased. Glucose 24-31 insulin Homo sapiens 4-11 26623647-0 2015 Glucose Homeostatic Law: Insulin Clearance Predicts the Progression of Glucose Intolerance in Humans. Glucose 0-7 insulin Homo sapiens 25-32 25778467-0 2015 Genetic modifiers of response to glucose-insulin-potassium (GIK) infusion in acute coronary syndromes and associations with clinical outcomes in the IMMEDIATE trial. Glucose 33-40 insulin Homo sapiens 41-48 26201694-1 2015 PURPOSE: Insulin resistance in patients undergoing invasive surgery impairs glucose and lipid metabolism and increases muscle protein catabolism, which may result in delayed recovery and prolonged hospital stay. Glucose 76-83 insulin Homo sapiens 9-16 26727116-8 2015 Serum ATX and BMI also independently predicted glucose infusion rate during a hyperinsulinemic euglycemic clamp and homeostatic model assessment of insulin resistance after controlling for sex and medication use. Glucose 47-54 insulin Homo sapiens 83-90 26623647-1 2015 Homeostatic control of blood glucose is regulated by a complex feedback loop between glucose and insulin, of which failure leads to diabetes mellitus. Glucose 29-36 insulin Homo sapiens 97-104 26623647-3 2015 We made a mathematical model of the feedback loop between glucose and insulin using time course of blood glucose and insulin during consecutive hyperglycemic and hyperinsulinemic-euglycemic clamps in 113 subjects with variety of glucose tolerance including normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). Glucose 58-65 insulin Homo sapiens 70-77 26623647-3 2015 We made a mathematical model of the feedback loop between glucose and insulin using time course of blood glucose and insulin during consecutive hyperglycemic and hyperinsulinemic-euglycemic clamps in 113 subjects with variety of glucose tolerance including normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). Glucose 105-112 insulin Homo sapiens 70-77 26623647-3 2015 We made a mathematical model of the feedback loop between glucose and insulin using time course of blood glucose and insulin during consecutive hyperglycemic and hyperinsulinemic-euglycemic clamps in 113 subjects with variety of glucose tolerance including normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). Glucose 105-112 insulin Homo sapiens 70-77 26623647-6 2015 Importantly, insulin clearance, an insulin degradation rate, significantly declined from NGT, IGT to T2DM along the progression of glucose intolerance in the mathematical model. Glucose 131-138 insulin Homo sapiens 13-20 26385108-9 2015 Stepwise multiple regression analysis identified insulin resistance, insulin and the PANSS positive symptom subscore as significant predictor factors for glucose level. Glucose 154-161 insulin Homo sapiens 49-56 26385108-9 2015 Stepwise multiple regression analysis identified insulin resistance, insulin and the PANSS positive symptom subscore as significant predictor factors for glucose level. Glucose 154-161 insulin Homo sapiens 69-76 26623647-8 2015 Insulin clearance was correlated negatively with postprandial glucose at 2h after oral glucose tolerance test. Glucose 62-69 insulin Homo sapiens 0-7 26623647-8 2015 Insulin clearance was correlated negatively with postprandial glucose at 2h after oral glucose tolerance test. Glucose 87-94 insulin Homo sapiens 0-7 26623647-10 2015 Insulin clearance shows a conserved relationship with the capacity of glucose disposal among the NGT, IGT and T2DM subjects. Glucose 70-77 insulin Homo sapiens 0-7 27141664-4 2015 They can decrease blood glucose via protecting pancreatic/p cells or/and improving insulin sensitivity. Glucose 24-31 insulin Homo sapiens 83-90 26549253-6 2015 Reduced insulin sensitivity was compensated by an increased insulin response to glucose, which may reflect an initial physiological adaptation to maintain normal blood sugar levels during sleep loss. Glucose 80-87 insulin Homo sapiens 60-67 26635731-4 2015 In this study, we aimed to determine the differences in glucose metabolism between severely obese men and women using tissue-specific measurements of insulin sensitivity. Glucose 56-63 insulin Homo sapiens 150-157 26648697-8 2015 Insulin secretion stimulated by a high concentration of glucose (28 mmol/L) was significantly higher than a physiologic concentration of glucose (5.6 mmol/L) in all treatment groups. Glucose 56-63 insulin Homo sapiens 0-7 26618110-4 2015 Insulin sensitivity and beta cell function were calculated from fasting glucose and insulin concentrations. Glucose 72-79 insulin Homo sapiens 0-7 26567860-6 2015 METHODS: The incretin effect (i.e., the relative difference between the insulin response to oral and intravenous glucose administration) was investigated in a cross-sectional case-control study. Glucose 113-120 insulin Homo sapiens 72-79 26378251-1 2015 Insulin resistance (IR) is a metabolic disorder characterized by impaired insulin signaling and cellular glucose uptake. Glucose 105-112 insulin Homo sapiens 0-7 26555895-5 2015 Furthermore, characteristic insulin secretory response to challenge maneuvers have been described, such as frequency entrainment upon sinusoidal glycemic stimulation; substantial insulin peaks following minimal glucose administration; progressively strengthened insulin secretion response after repeated administration of the same amount of glucose; insulin and glucose characteristic curves after Intra-Venous administration of glucose boli in healthy and pre-diabetic subjects as well as in Type 2 Diabetes Mellitus. Glucose 211-218 insulin Homo sapiens 28-35 26753001-4 2015 We also evaluate the association between 3 oral glucose tolerance test (OGTT) based insulin sensitivity indexes (Matsuda, STUMVOLL-ISI and OGIS) and CAD. Glucose 48-55 insulin Homo sapiens 84-91 26555895-5 2015 Furthermore, characteristic insulin secretory response to challenge maneuvers have been described, such as frequency entrainment upon sinusoidal glycemic stimulation; substantial insulin peaks following minimal glucose administration; progressively strengthened insulin secretion response after repeated administration of the same amount of glucose; insulin and glucose characteristic curves after Intra-Venous administration of glucose boli in healthy and pre-diabetic subjects as well as in Type 2 Diabetes Mellitus. Glucose 341-348 insulin Homo sapiens 28-35 26555895-5 2015 Furthermore, characteristic insulin secretory response to challenge maneuvers have been described, such as frequency entrainment upon sinusoidal glycemic stimulation; substantial insulin peaks following minimal glucose administration; progressively strengthened insulin secretion response after repeated administration of the same amount of glucose; insulin and glucose characteristic curves after Intra-Venous administration of glucose boli in healthy and pre-diabetic subjects as well as in Type 2 Diabetes Mellitus. Glucose 341-348 insulin Homo sapiens 28-35 26555895-5 2015 Furthermore, characteristic insulin secretory response to challenge maneuvers have been described, such as frequency entrainment upon sinusoidal glycemic stimulation; substantial insulin peaks following minimal glucose administration; progressively strengthened insulin secretion response after repeated administration of the same amount of glucose; insulin and glucose characteristic curves after Intra-Venous administration of glucose boli in healthy and pre-diabetic subjects as well as in Type 2 Diabetes Mellitus. Glucose 341-348 insulin Homo sapiens 28-35 26556598-3 2015 Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated from fasting serum glucose and insulin. Glucose 95-102 insulin Homo sapiens 32-39 25910875-1 2015 Insulin secretion from pancreatic beta cells plays a central role in the control of blood glucose levels. Glucose 90-97 insulin Homo sapiens 0-7 26556780-0 2015 Insulin pumps improve glucose control in children with type 1 diabetes, study finds. Glucose 22-29 insulin Homo sapiens 0-7 26556368-3 2015 If the liver is fatty due to causes of insulin resistance such as obesity and physical inactivity, it overproduces glucose and triglycerides leading to hyperinsulinemia and a low high-density lipoprotein (HDL) cholesterol concentration. Glucose 115-122 insulin Homo sapiens 39-46 26041603-2 2015 A fundamental aim of such therapy is to mimic the pattern of "normal" physiological insulin secretion, thereby controlling basal and meal-time plasma glucose and fatty acid turnover. Glucose 150-157 insulin Homo sapiens 84-91 26224101-4 2015 We measured plasma glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), pancreatic polypeptide (PP), NEFA and glucose tracers, and calculated glucose fluxes, beta cell function variables, insulin sensitivity and clearance. Glucose 81-88 insulin Homo sapiens 99-106 26224101-4 2015 We measured plasma glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), pancreatic polypeptide (PP), NEFA and glucose tracers, and calculated glucose fluxes, beta cell function variables, insulin sensitivity and clearance. Glucose 81-88 insulin Homo sapiens 99-106 26224101-6 2015 This reduction:more pronounced across classes of glucose tolerance (NGT -32%, IGT -37%, type 2 diabetes -49%; p < 0.002):was the result of different combinations of slower exogenous glucose rate of appearance, improved beta cell function and reduced insulin clearance, in this order of relevance, which were associated with an only mild stimulation of GIP and GLP-1. Glucose 49-56 insulin Homo sapiens 253-260 26224101-6 2015 This reduction:more pronounced across classes of glucose tolerance (NGT -32%, IGT -37%, type 2 diabetes -49%; p < 0.002):was the result of different combinations of slower exogenous glucose rate of appearance, improved beta cell function and reduced insulin clearance, in this order of relevance, which were associated with an only mild stimulation of GIP and GLP-1. Glucose 185-192 insulin Homo sapiens 253-260 26041603-6 2015 Physiologically, meal-time insulin release begins rapidly in response to reflex activity and incretins, continuing with the rise in glucose and amino acid concentrations. Glucose 132-139 insulin Homo sapiens 27-34 26248647-1 2015 Until recently, type 2 diabetes was seen as a disease caused by an impaired ability of insulin to promote the uptake and utilisation of glucose. Glucose 136-143 insulin Homo sapiens 87-94 26271343-0 2015 Tissue factor/factor VIIa signalling promotes cytokine-induced beta cell death and impairs glucose-stimulated insulin secretion from human pancreatic islets. Glucose 91-98 insulin Homo sapiens 110-117 26522487-17 2015 Paper II: Five-year weight changes were associated with blood pressure alterations and had a substantial impact on both fasting and two-hour post-glucose serum insulin levels. Glucose 146-153 insulin Homo sapiens 160-167 26613332-5 2015 RESULTS: BOLD responses to food pictures were reduced during a glucose challenge in numerous corticolimbic brain regions in insulin-sensitive but not insulin-resistant subjects. Glucose 63-70 insulin Homo sapiens 124-131 26541763-2 2015 DPP-4 inhibitors control glucose levels by preventing the breakdown of the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), which stimulate insulin secretion in response to the increased levels of glucose in the period following meals. Glucose 25-32 insulin Homo sapiens 111-118 26541763-2 2015 DPP-4 inhibitors control glucose levels by preventing the breakdown of the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), which stimulate insulin secretion in response to the increased levels of glucose in the period following meals. Glucose 93-100 insulin Homo sapiens 111-118 26031570-1 2015 BACKGROUND: Few data are so far available on the relation between increased glucose values and insulin resistance and mortality at short-term in patients with acute heart failure (AHF). Glucose 76-83 insulin Homo sapiens 95-102 26613332-6 2015 Furthermore, the degree of insulin resistance positively correlated with the corticolimbic BOLD response in the medial prefrontal cortex (mPFC), orbitofrontal cortex (OFC), anterior cingulate and ventral tegmental area (VTA) in response to HC pictures, and in the dorsolateral prefrontal cortex (DLPFC), mPFC, anterior cingulate, and insula in response to LC pictures following a glucose challenge. Glucose 380-387 insulin Homo sapiens 27-34 26613332-8 2015 CONCLUSION: We conclude that the normal inhibition of corticolimbic brain responses to food pictures during a glucose challenge is compromised in insulin-resistant subjects. Glucose 110-117 insulin Homo sapiens 146-153 25395350-7 2015 RESULTS: Compared with standard noodles, the plasma glucose and insulin after consumption of oral glucose were higher at 30 min (both P < 0.001) and 60 min (both P < 0.001), while lower at 180 min (both P < 0.001), but no differences were found at 120 min. Glucose 98-105 insulin Homo sapiens 64-71 26378474-5 2015 Secondarily, top tertile subjects for endogenous glucose production suppression during the low-dose insulin clamp were deemed Liversen and the remainder Liverres. Glucose 49-56 insulin Homo sapiens 100-107 26378474-10 2015 When subjects were grouped by both glucose infusion rate during the high-dose insulin clamp and endogenous glucose production suppression, insulin sensitivity at either muscle or liver conferred apparent protection from the adverse metabolic features that characterized subjects insulin resistant at both sites. Glucose 35-42 insulin Homo sapiens 139-146 26378474-10 2015 When subjects were grouped by both glucose infusion rate during the high-dose insulin clamp and endogenous glucose production suppression, insulin sensitivity at either muscle or liver conferred apparent protection from the adverse metabolic features that characterized subjects insulin resistant at both sites. Glucose 35-42 insulin Homo sapiens 139-146 26673888-14 2015 SAD in relation to glucose metabolism, had a better correlation with OGTT followed by HOMA-IR and fasting Insulin. Glucose 19-26 insulin Homo sapiens 106-113 26378474-10 2015 When subjects were grouped by both glucose infusion rate during the high-dose insulin clamp and endogenous glucose production suppression, insulin sensitivity at either muscle or liver conferred apparent protection from the adverse metabolic features that characterized subjects insulin resistant at both sites. Glucose 107-114 insulin Homo sapiens 139-146 26378474-10 2015 When subjects were grouped by both glucose infusion rate during the high-dose insulin clamp and endogenous glucose production suppression, insulin sensitivity at either muscle or liver conferred apparent protection from the adverse metabolic features that characterized subjects insulin resistant at both sites. Glucose 107-114 insulin Homo sapiens 139-146 25395350-10 2015 In normal glucose tolerance (NGT), oral glucose elicited a higher insulin response to the corresponding AGLP-1 (P < 0.001), which was represented by iAUC(0 -120 min) -INS /iAUC(0 -120 min)- AGLP-1, while in type 2 diabetes mellitus (T2DM), standard noodles did (P = 0.001). Glucose 40-47 insulin Homo sapiens 66-73 26543546-8 2015 RESULTS: The 12 weeks of SQF treatment in combination with insulin significantly decreased the fasting and postprandial blood glucose levels. Glucose 126-133 insulin Homo sapiens 59-66 26363548-7 2015 Insulin sensitivity index increased 300% (P < .01), acute insulin response to glucose decreased 56% (P < .01), leading to a nearly 2-fold increase in the disposition index (P < .01). Glucose 81-88 insulin Homo sapiens 61-68 26352439-4 2015 Insulin sensitivity was determined by measuring the glucose uptake rate. Glucose 52-59 insulin Homo sapiens 0-7 26501581-2 2015 This article describes a recently approved inhaled insulin that appears to control blood glucose as well as rapid-acting injectable insulin. Glucose 89-96 insulin Homo sapiens 51-58 26352439-7 2015 The results of the present study demonstrated that insulin-induced glucose uptake was reduced in IR HepG2 cells; however, this reduction was reversed by 4-HIL in a dose-dependent manner. Glucose 67-74 insulin Homo sapiens 51-58 26356502-3 2015 Of particular interest is the intertwined regulation of glucose and non-esterified fatty acids (NEFA), due to the association between disturbed NEFA metabolism and insulin resistance. Glucose 56-63 insulin Homo sapiens 164-171 26063787-2 2015 Glucose-based peritoneal dialysis (PD) solutions are thought to intensify insulin resistance due to the continuous glucose absorption from the peritoneal cavity. Glucose 0-7 insulin Homo sapiens 74-81 26063787-2 2015 Glucose-based peritoneal dialysis (PD) solutions are thought to intensify insulin resistance due to the continuous glucose absorption from the peritoneal cavity. Glucose 115-122 insulin Homo sapiens 74-81 26063787-3 2015 The aim of our study was to analyse the effect of the substitution of glucose for icodextrin on insulin resistance in non-diabetic PD patients in a multicentric randomized clinical trial. Glucose 70-77 insulin Homo sapiens 96-103 26063787-11 2015 CONCLUSIONS: The substitution of glucose for icodextrin for the long dwell improved insulin resistance measured by HOMA index in non-diabetic APD patients. Glucose 33-40 insulin Homo sapiens 84-91 26218256-7 2015 INTERVENTIONS: Insulin titration was performed based on blood glucose value and rate of change of blood glucose using an algorithm developed for the Control of Hyperglycemia in Pediatric Intensive Care trial. Glucose 62-69 insulin Homo sapiens 15-22 26270573-4 2015 Insulin sensitivity was measured by fasting plasma glucose and insulin. Glucose 51-58 insulin Homo sapiens 0-7 26416226-5 2015 We show that EMPs constructed by seeding whole islets, freshly enzymatically-dissociated islets or even dissociated islets grown first in standard monolayer cultures express high levels of key beta-cell specific genes and secrete quantities of insulin per cell similar to freshly isolated human islets in a glucose-regulated manner for more than 3 months in vitro. Glucose 307-314 insulin Homo sapiens 244-251 26568812-2 2015 Basal insulin is commonly prescribed initially, alone or with one or more rapid-acting prandial insulin doses, to limit mealtime glucose excursions (a basal-bolus regimen). Glucose 129-136 insulin Homo sapiens 6-13 26568812-6 2015 Insulin degludec is an ultra-long-acting insulin analogue with a flat and stable glucose-lowering profile, a duration of action exceeding 30 h and less inter-patient variation in glucose-lowering effect than insulin glargine. Glucose 81-88 insulin Homo sapiens 0-7 26568812-6 2015 Insulin degludec is an ultra-long-acting insulin analogue with a flat and stable glucose-lowering profile, a duration of action exceeding 30 h and less inter-patient variation in glucose-lowering effect than insulin glargine. Glucose 179-186 insulin Homo sapiens 0-7 26568812-8 2015 Pharmacokinetic and pharmacodynamic studies have shown that the distinct, long basal glucose-lowering action of insulin degludec and the prandial glucose-lowering effect of insulin aspart are maintained in the co-formulation. Glucose 85-92 insulin Homo sapiens 112-119 26582989-3 2015 HDL may mediate effects on glucose metabolism through actions in multiple organs (e.g., pancreas, skeletal muscle, heart, adipose, liver, brain) by three distinct mechanisms: (i) Insulin secretion from pancreatic beta cells, (ii) Insulin-independent glucose uptake, (iii) Insulin sensitivity. Glucose 27-34 insulin Homo sapiens 179-186 26514124-7 2015 Co-ingestion of P with glucose improved, at time 60 min, postprandial glucose (P < 0.05), insulin (P < 0.05), and insulin sensitivity index (p < 0.006), while P pre-ingestion failed to exert similar effect. Glucose 23-30 insulin Homo sapiens 93-100 26514124-7 2015 Co-ingestion of P with glucose improved, at time 60 min, postprandial glucose (P < 0.05), insulin (P < 0.05), and insulin sensitivity index (p < 0.006), while P pre-ingestion failed to exert similar effect. Glucose 23-30 insulin Homo sapiens 120-127 26505901-3 2015 Long chain fatty acids (LCFA) increase intracellular calcium concentration and amplify glucose-stimulated insulin secretion by activating GPR40. Glucose 87-94 insulin Homo sapiens 106-113 26342081-5 2015 Pharmacological inhibition of PFKFB3 suppressed insulin-stimulated glucose uptake, GLUT4 translocation, and Akt signaling in 3T3-L1 adipocytes. Glucose 67-74 insulin Homo sapiens 48-55 26527864-10 2015 The insulin-induced glucose uptake was reduced by 67% in 3T3-L1 adipocytes, which indicated the presence of an IR-like state. Glucose 20-27 insulin Homo sapiens 4-11 26909308-8 2015 Such massive increase was accompanied by enhanced insulin secretion upon glucose stimulation. Glucose 73-80 insulin Homo sapiens 50-57 26543756-5 2015 Direct intragastric delivery of glucose or clipping the nose induced a downward shift in both BGC and serum insulin response curves (IRC), resulting in a decrease of the area under the BGC, positively correlated with the area under the IRC and satisfaction scores, respectively. Glucose 32-39 insulin Homo sapiens 108-115 26269521-5 2015 Following insulin infusion, whole body glucose disposal rates (GDR; mg/kg/min) were lower (P < 0.05) in the T2D vs. the control group. Glucose 39-46 insulin Homo sapiens 10-17 26318486-2 2015 In this study we have analysed proliferation, apoptosis, beta cell size and glucose-stimulated insulin secretion in human islets overexpressing either PKBalpha or PKBbeta. Glucose 76-83 insulin Homo sapiens 95-102 26330080-4 2015 Three hydrazone derivatives of benzimidazole significantly increased the cellular ATP levels, reduced caspase-3 activity, reduced nitrite production and increased glucose-stimulated insulin secretion in the presence of proinflammatory cytokines. Glucose 163-170 insulin Homo sapiens 182-189 26469794-1 2015 A new study shows that components of the unfolded protein pathway are needed to help manage the production of vast amounts of insulin by pancreatic beta cells in response to glucose stimulation. Glucose 174-181 insulin Homo sapiens 126-133 26446863-1 2015 BACKGROUND: In patients with type-2 diabetes receiving oral antidiabetic drugs (OADs), the addition of insulin is frequently required to achieve sufficient control over blood glucose levels. Glucose 175-182 insulin Homo sapiens 103-110 26387957-3 2015 Here, we provide evidence that in pancreatic beta cells, knockdown of PI3K-C2alpha expression results in rerouting of the insulin signal from insulin receptor (IR)-B/PI3K-C2alpha/PKB-mediated metabolic signaling to IR-B/Shc/ERK-mediated mitogenic signaling, which allows the beta cell to switch from a highly glucose-responsive, differentiated state to a proliferative state. Glucose 309-316 insulin Homo sapiens 122-129 26387957-3 2015 Here, we provide evidence that in pancreatic beta cells, knockdown of PI3K-C2alpha expression results in rerouting of the insulin signal from insulin receptor (IR)-B/PI3K-C2alpha/PKB-mediated metabolic signaling to IR-B/Shc/ERK-mediated mitogenic signaling, which allows the beta cell to switch from a highly glucose-responsive, differentiated state to a proliferative state. Glucose 309-316 insulin Homo sapiens 142-149 26437649-6 2015 Fasting glucose and insulin were used to derive the HOMA-index of insulin resistance (HOMA-IR). Glucose 8-15 insulin Homo sapiens 66-73 25697600-10 2015 CONCLUSIONS: Calculating prandial insulin bolus based on glycaemic load counting is feasible in a real-life setting and may improve postprandial glucose control in people with T1D. Glucose 145-152 insulin Homo sapiens 34-41 25749806-9 2015 The large number of unrecognized HE and VT in vulnerable patients treated with insulin or sulfonylurea should encourage the practitioner to focus on stable glucose control and to search for silent HE. Glucose 156-163 insulin Homo sapiens 79-86 26264556-4 2015 When perifused normal human islets were stimulated with 15 mmol/l glucose (G15), the proinsulin/insulin ratio in secretory products rapidly and reversibly decreased (~50%) and did not reaugment with time. Glucose 66-73 insulin Homo sapiens 85-95 26264556-4 2015 When perifused normal human islets were stimulated with 15 mmol/l glucose (G15), the proinsulin/insulin ratio in secretory products rapidly and reversibly decreased (~50%) and did not reaugment with time. Glucose 66-73 insulin Homo sapiens 88-95 26143144-4 2015 Insulin-stimulated glucose uptake, phosphorylation of PKB, IRS-1-associated PI3K, and IRS-1 tyrosine phosphorylation were all inhibited by ET-1 and 8-bromo cAMP in a synergistic manner. Glucose 19-26 insulin Homo sapiens 0-7 26143144-8 2015 Furthermore, ET-1 and beta-adrenergic agonists had similar synergistic inhibition on insulin-stimulated glucose uptake. Glucose 104-111 insulin Homo sapiens 85-92 25683266-5 2015 MEASUREMENTS: Insulin sensitivity was measured in the morning following the 3rd intervention night by minimal modelling of 19 samples collected during a 2-h oral glucose tolerance test. Glucose 162-169 insulin Homo sapiens 14-21 26359268-6 2015 Insulin sensitivity and beta cell function were calculated using fasting glucose and insulin levels according to the homeostatic model assessment 2. Glucose 73-80 insulin Homo sapiens 0-7 26339797-7 2015 A Western blot analysis showed that the membranous expression of GLUT1 in KD cells was elevated by glucose and/or insulin treatments, indicating that the GI-induced glucose uptake is mediated by the increased translocation of GLUT1 on the cell membrane. Glucose 165-172 insulin Homo sapiens 114-121 26330140-4 2015 When mimicked in newborn islet cells, modifications in the level of specific microRNAs result in a switch in the expression of metabolic enzymes and cause the acquisition of glucose-induced insulin release. Glucose 174-181 insulin Homo sapiens 190-197 25388277-4 2015 Children"s insulin sensitivity was measured using intravenous glucose tolerance tests and Bergman"s minimal model. Glucose 62-69 insulin Homo sapiens 11-18 25918234-5 2015 Haploinsufficiency of SIK1 led to the improved glucose tolerance due to the increased glucose-stimulated insulin secretion. Glucose 86-93 insulin Homo sapiens 105-112 26153273-7 2015 Furthermore, in volunteers with type 1 diabetes 1 h after increasing basal insulin delivery twofold, glucose levels dropped to 58 +- 5 mg/dL, whereas hypoglycemia was prevented by inhaled formoterol (P < 0.001). Glucose 101-108 insulin Homo sapiens 75-82 25964024-1 2015 Development of type 2 diabetes mellitus (T2DM) is preceded by insulin resistance (IR), which may evolve to impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). Glucose 124-131 insulin Homo sapiens 62-69 26034075-5 2015 Insulin sensitivity was assessed by the OGIS index and insulin secretion and beta-cell glucose sensitivity at both baseline and 3 years. Glucose 87-94 insulin Homo sapiens 0-7 25982907-7 2015 The insulin-treated patient group had significantly higher maximum blood glucose levels and higher cumulative IV salbutamol dose than the non-treated group. Glucose 73-80 insulin Homo sapiens 4-11 25686566-9 2015 This was accompanied by increased isoproterenol-induced lipolysis and reduced insulin-stimulated glucose uptake. Glucose 97-104 insulin Homo sapiens 78-85 26190660-10 2015 Plasma glucose was associated with increased insulin and a lower glucose-to-insulin ratio. Glucose 7-14 insulin Homo sapiens 45-52 26190660-10 2015 Plasma glucose was associated with increased insulin and a lower glucose-to-insulin ratio. Glucose 7-14 insulin Homo sapiens 76-83 26190660-10 2015 Plasma glucose was associated with increased insulin and a lower glucose-to-insulin ratio. Glucose 65-72 insulin Homo sapiens 76-83 26190660-12 2015 Paradoxically, increased cytokines were associated with an increased glucose-to-insulin ratio (EST: 0.21 (+-0.03) mmol/mumol; P < .001). Glucose 69-76 insulin Homo sapiens 80-87 26028283-8 2015 Dynamic glucose-modulated GH release was determined by insulin negatively (P=0.0039) and power positively (P=0.0034) (R(2)=0.454). Glucose 8-15 insulin Homo sapiens 55-62 26028283-10 2015 CONCLUSION: In healthy men, dynamic GH perturbations induced by exercise and glucose are strongly related to physical power, insulin, estradiol, and body composition, thus suggesting a network of regulatory pathways. Glucose 77-84 insulin Homo sapiens 125-132 26031505-2 2015 MATERIALS AND METHODS: In a sample of 93 healthy adults, insulin resistance was defined as steady state plasma glucose (SSPG)>=180 mg/dL and insulin sensitive as <120 mg/dL. Glucose 111-118 insulin Homo sapiens 57-64 26125313-2 2015 Of concern is that insulin and insulin-sensitizing medications detrimentally "flood" the heart with energy-providing substrates, including fats and glucose. Glucose 148-155 insulin Homo sapiens 19-26 26125313-2 2015 Of concern is that insulin and insulin-sensitizing medications detrimentally "flood" the heart with energy-providing substrates, including fats and glucose. Glucose 148-155 insulin Homo sapiens 31-38 26638442-3 2015 The initiation of insulin therapy (glargine in > 50%) was justified by insufficient glycaemic control (96%) and its intensification (replacement of insulin NPH or premixed insulins by insulin glargine, eventually with the addition of a short-acting insulin analogue) aimed at improving glucose control (58%), avoiding hypoglycaemia (17%) or both (17%). Glucose 289-296 insulin Homo sapiens 18-25 26629404-0 2015 TUSC5 regulates insulin-mediated adipose tissue glucose uptake by modulation of GLUT4 recycling. Glucose 48-55 insulin Homo sapiens 16-23 26322160-4 2015 Intracellular Mg plays a key role in regulating insulin action, insulin-mediated-glucose-uptake and vascular tone. Glucose 81-88 insulin Homo sapiens 64-71 26623647-11 2015 The decrease of insulin clearance predicts the progression of glucose intolerance. Glucose 62-69 insulin Homo sapiens 16-23 26981161-4 2015 Moreover, the patients" insulin and C-peptide level are significantly higher than those before intervention (P < 0.05); before intervention, their blood glucose and glycated hemogiobin level are higher than normal, after intervention, they are weakened, but there"s no significant difference (P > 0.05). Glucose 156-163 insulin Homo sapiens 24-31 26981161-4 2015 Moreover, the patients" insulin and C-peptide level are significantly higher than those before intervention (P < 0.05); before intervention, their blood glucose and glycated hemogiobin level are higher than normal, after intervention, they are weakened, but there"s no significant difference (P > 0.05). Glucose 156-163 insulin Homo sapiens 36-45 26487791-0 2015 Therapeutic Options for the Management of Postprandial Glucose in Patients With Type 2 Diabetes on Basal Insulin. Glucose 55-62 insulin Homo sapiens 105-112 25644898-4 2015 CASE REPORT: A Niuean women, first evaluated at age 6 years for severe acanthosis nigricans, hirsutism, poor growth and cognitive impairment, had extremely elevated fasting insulin levels of 10740 IU/l (fasting reference range 4-24 IU/l) and a normal glucose concentration (4.9 mmol/l). Glucose 251-258 insulin Homo sapiens 173-180 25711172-0 2015 Presence of hypertension modifies the impact of insulin resistance on incident cardiovascular disease in a Middle Eastern population: the Tehran Lipid and Glucose Study. Glucose 155-162 insulin Homo sapiens 48-55 26068543-1 2015 Intramuscular signaling and glucose transport mechanisms contribute to improvements in insulin sensitivity after aerobic exercise training. Glucose 28-35 insulin Homo sapiens 87-94 26068543-2 2015 This study tested the hypothesis that increases in skeletal muscle capillary density (CD) also contribute to exercise-induced improvements in whole-body insulin sensitivity (insulin-stimulated glucose uptake per unit plasma insulin [M/I]) independent of other mechanisms. Glucose 193-200 insulin Homo sapiens 153-160 26068543-2 2015 This study tested the hypothesis that increases in skeletal muscle capillary density (CD) also contribute to exercise-induced improvements in whole-body insulin sensitivity (insulin-stimulated glucose uptake per unit plasma insulin [M/I]) independent of other mechanisms. Glucose 193-200 insulin Homo sapiens 174-181 26068543-2 2015 This study tested the hypothesis that increases in skeletal muscle capillary density (CD) also contribute to exercise-induced improvements in whole-body insulin sensitivity (insulin-stimulated glucose uptake per unit plasma insulin [M/I]) independent of other mechanisms. Glucose 193-200 insulin Homo sapiens 174-181 26116696-5 2015 Group B (three patients with fasting hypoglycemic episodes) was mainly characterized by large insulin responses to 1 mmol/L glucose, resulting in very high basal secretion rates that were inhibited by diazoxide and restored by tolbutamide but were not further augmented by other agents except for high levels of CaCl2. Glucose 124-131 insulin Homo sapiens 94-101 26155745-7 2015 RESULTS: In control Ins1(-/-):Ins2(+/+) mice, HFD resulted in elevated fasting and glucose-stimulated insulin secretion between 8 weeks and 27 weeks of age. Glucose 83-90 insulin Homo sapiens 102-109 26172028-9 2015 All levels of measurable C-peptide were responsive to acute fluctuations in blood glucose levels as assessed by 1,5-Anhydroglucitol (P < 0.0001). Glucose 82-89 insulin Homo sapiens 25-34 26220945-5 2015 RESULTS: Compared with YesB, lunch area under the curves for 0-180 min (AUC0-180) for plasma glucose, FFA, and glucagon were 36.8, 41.1, and 14.8% higher, respectively, whereas the AUC0-180 for insulin and iGLP-1 were 17% and 19% lower, respectively, on the NoB day (P < 0.0001). Glucose 93-100 insulin Homo sapiens 194-201 26188234-1 2015 OBJECTIVE: To monitor and control the blood glucose levels in inefficiently insulin-treated patients with type 1 and 2 diabetes mellitus (DM) using a telemonitoring system and determine whether the improvement of HbA1c has a lasting effect following its discontinuation. Glucose 44-51 insulin Homo sapiens 76-83 25999046-10 2015 MiR-26b promotes insulin-stimulated glucose uptake and increases insulin-stimulated glucose transporter type 4 translocation to the plasma membrane in human mature adipocytes. Glucose 36-43 insulin Homo sapiens 17-24 26233474-1 2015 Insulin is well known as a hormone regulating glucose homeostasis across phyla. Glucose 46-53 insulin Homo sapiens 0-7 26233474-2 2015 Although there are insulin-independent mechanisms for glucose uptake in the mammalian brain, which had contributed to a perception of the brain as an insulin-insensitive organ for decades, the finding of insulin and its receptors in the brain revolutionized the concept of insulin signaling in the brain. Glucose 54-61 insulin Homo sapiens 19-26 26276137-4 2015 Diabetes standards for inmates contain diagnostic and treatment management guidelines that incorporate personal glucose monitoring for insulin users. Glucose 112-119 insulin Homo sapiens 135-142 26276137-5 2015 In December 2009, the Federal Bureau of Prisons initiated a program to distribute glucose meters to insulin-dependent inmates to facilitate self-monitoring blood glucose. Glucose 82-89 insulin Homo sapiens 100-107 25499901-6 2015 Capillary glucose (CG) was monitored for adjusting insulin perfusion according to the ICU protocol. Glucose 10-17 insulin Homo sapiens 51-58 26496258-4 2015 Her glucose even reached 1.22 mmol/L while the serum glycosylated hemoglobin was normal and previous history of diabetes or use of oral hypoglycemic agents and insulin denied.The laboratory examination showed that the low level of insulin, C-peptide, and growth hormone levels in the course of hypoglycemic episodes suggesting to the diagnosis of hypoglycemia induced by nonislet cell tumor, and the decreased levels of insulin-like growth factor (IGF)-I and IGFBP3 and the high expression of big IGF-II in the serum further confirmed the diagnosis of NICTH. Glucose 4-11 insulin Homo sapiens 231-238 26232910-0 2015 Insulin degludec results in lower rates of nocturnal hypoglycaemia and fasting plasma glucose vs. insulin glargine: A meta-analysis of seven clinical trials. Glucose 86-93 insulin Homo sapiens 0-7 26232910-2 2015 Insulin degludec (IDeg) is a new basal insulin that forms soluble multihexamers after subcutaneous injection resulting in an ultra-long duration of action and stable glucose-lowering effect. Glucose 166-173 insulin Homo sapiens 0-7 26232910-2 2015 Insulin degludec (IDeg) is a new basal insulin that forms soluble multihexamers after subcutaneous injection resulting in an ultra-long duration of action and stable glucose-lowering effect. Glucose 166-173 insulin Homo sapiens 39-46 26316298-9 2015 CONCLUSIONS: Among subjects with GB, the response of insulin and glucagon secretion to decreasing blood glucose is blunted, but meal-induced insulin secretion is stimulated even at fixed systemic sub-basal glycemia. Glucose 104-111 insulin Homo sapiens 53-60 26565267-1 2015 The activity of pancreatic beta cells can be described by biological networks of coupled nonlinear oscillators that, via electrochemical synchronization, release insulin in response to augmented glucose levels. Glucose 195-202 insulin Homo sapiens 162-169 26685566-10 2015 CONCLUSIONS: The implementation of a specific insulin protocol in patients receiving TH contributes to improve the blood glucose levels. Glucose 121-128 insulin Homo sapiens 46-53 26727843-2 2015 After subcutaneous injection, insulin lispro has a more favourable pharmacokinetics/pharmacodynamics profile than human insulin, characterized by a faster resorption and a more rapid and less prolonged glucose-lowering activity. Glucose 202-209 insulin Homo sapiens 30-37 26749702-6 2015 Insulin initiation requires specific educational program for the acceptation of injection and to learn insulin injection, capillary blood glucose test and adjustment of insulin regimens. Glucose 138-145 insulin Homo sapiens 0-7 26304037-14 2015 The implant can engraft and respond to glucose by secreting insulin, thus potentially replacing the beta cells lost in patients with T1D. Glucose 39-46 insulin Homo sapiens 60-67 26426068-2 2015 This review focuses on the glucose metabolic effects of alcohol, primarily in the muscle, liver and adipose tissue, under basal postabsorptive conditions and in response to insulin stimulation. Glucose 27-34 insulin Homo sapiens 173-180 26240143-1 2015 Insulin signaling augments glucose transport by regulating glucose transporter 4 (GLUT4) trafficking from specialized intracellular compartments, termed GLUT4 storage vesicles (GSVs), to the plasma membrane. Glucose 27-34 insulin Homo sapiens 0-7 26240143-6 2015 siRNA-mediated knockdown of TUSC5 decreased insulin-stimulated glucose uptake, although overexpression of TUSC5 had the opposite effect, implicating TUSC5 as a positive regulator of insulin-stimulated glucose transport in adipocytes. Glucose 63-70 insulin Homo sapiens 44-51 26240143-6 2015 siRNA-mediated knockdown of TUSC5 decreased insulin-stimulated glucose uptake, although overexpression of TUSC5 had the opposite effect, implicating TUSC5 as a positive regulator of insulin-stimulated glucose transport in adipocytes. Glucose 63-70 insulin Homo sapiens 182-189 26240143-6 2015 siRNA-mediated knockdown of TUSC5 decreased insulin-stimulated glucose uptake, although overexpression of TUSC5 had the opposite effect, implicating TUSC5 as a positive regulator of insulin-stimulated glucose transport in adipocytes. Glucose 201-208 insulin Homo sapiens 44-51 26240143-6 2015 siRNA-mediated knockdown of TUSC5 decreased insulin-stimulated glucose uptake, although overexpression of TUSC5 had the opposite effect, implicating TUSC5 as a positive regulator of insulin-stimulated glucose transport in adipocytes. Glucose 201-208 insulin Homo sapiens 182-189 26299925-1 2015 Insulin increases glucose transport in fat and muscle cells by stimulating the exocytosis of specialized vesicles containing the glucose transporter GLUT4. Glucose 18-25 insulin Homo sapiens 0-7 26376914-8 2015 Using stringent criteria (Fold change > 1.5; FDR < 0.05), three genes were found to be significantly and differently expressed in the intestine of insulin-resistant compared to insulin-sensitive subjects: the transcripts of the insulinotropic glucose-dependant peptide (GIP) and of the beta-microseminoprotein (MSMB) were significantly reduced, but that of the humanin like-1 (MTRNR2L1) was significantly increased. Glucose 249-256 insulin Homo sapiens 153-160 26376914-8 2015 Using stringent criteria (Fold change > 1.5; FDR < 0.05), three genes were found to be significantly and differently expressed in the intestine of insulin-resistant compared to insulin-sensitive subjects: the transcripts of the insulinotropic glucose-dependant peptide (GIP) and of the beta-microseminoprotein (MSMB) were significantly reduced, but that of the humanin like-1 (MTRNR2L1) was significantly increased. Glucose 249-256 insulin Homo sapiens 183-190 26126685-7 2015 Culturing LIV0APOLY cells in high glucose increased a marker of endoplasmic reticulum stress and attenuated insulin-stimulated Akt phosphorylation whereas low glucose and exogenous fatty acids increased AMPK phosphorylation. Glucose 34-41 insulin Homo sapiens 108-115 27005142-0 2015 Glucose-sensitive nanogel for controlled release of insulin and its blood safety. Glucose 0-7 insulin Homo sapiens 52-59 26305973-4 2015 Insulin-stimulated rates of muscle glucose uptake were reduced by 25% (P<0.01) in the elderly subjects and were associated with ~70% (P<0.04) increase in IMCL, assessed by 1H magnetic resonance spectroscopy. Glucose 35-42 insulin Homo sapiens 0-7 25976662-5 2015 Here, using a rat model of BD, we demonstrate that exendin-4 administration to the brain-dead donors increases both islet viability and glucose-stimulated insulin secretion. Glucose 136-143 insulin Homo sapiens 155-162 26212549-6 2015 In addition, the ability of exogenous D-glucose to rescue cellular stress and impaired contractile function occurred through GLUT1-mediated but insulin/GLUT4-independent mechanisms. Glucose 38-47 insulin Homo sapiens 144-151 26176316-9 2015 However, most differentiated cells obtained using these techniques are functionally immature and show poor glucose-stimulated insulin secretion compared with native beta cells. Glucose 107-114 insulin Homo sapiens 126-133 25927357-0 2015 Taking a Closer Look--Continuous Glucose Monitoring in Non-Critically Ill Hospitalized Patients with Type 2 Diabetes Mellitus Under Basal-Bolus Insulin Therapy. Glucose 33-40 insulin Homo sapiens 144-151 25974209-3 2015 Next the clinical significance of hypomagnesaemic conditions with regard to the management of glucose in prediabetic stages, such as insulin resistance/impaired glucose tolerance and in type 2 diabetes mellitus are characterized. Glucose 94-101 insulin Homo sapiens 133-140 26117686-7 2015 The pooled estimates of metformin-insulin differences were very small and statistically non-significant in fasting plasma glucose, postprandial plasma glucose and HbA1c, measured at 36-37 weeks of gestation. Glucose 122-129 insulin Homo sapiens 34-41 25595190-7 2015 Glucose uptake was dose dependent on insulin stimulus and high levels of adipokines were secreted (i.e. displaying not only the morphology but also expressing mature adipocytes" specific genes and functional characteristics). Glucose 0-7 insulin Homo sapiens 37-44 26068615-1 2015 Obesity and type 2 diabetes have been shown to alter the insulin sensitivity of glucose and protein metabolism in middle-aged women. Glucose 80-87 insulin Homo sapiens 57-64 26068615-6 2015 In contrast, the insulin-mediated glucose disposal (healthy: 9.72+-0.67) was decreased with obesity (6.96+-0.86) and further with diabetes (5.23+-0.27mg kg fat free mass(-1) min(-1); ANOVA p<0.001). Glucose 34-41 insulin Homo sapiens 17-24 26625615-4 2015 The elevation of the content of cortisol leads to the increase of the glucose level in the blood and the stimulation of the production of insulin, which can, like excessive consumption of food, give rise to irreversible decline in the number of insulin receptors on the cell surface, and thus--to a steady reduction in the ability of cells to utilize glucose, i.e. to type 2 diabetes or its aggravation. Glucose 351-358 insulin Homo sapiens 138-145 26625615-4 2015 The elevation of the content of cortisol leads to the increase of the glucose level in the blood and the stimulation of the production of insulin, which can, like excessive consumption of food, give rise to irreversible decline in the number of insulin receptors on the cell surface, and thus--to a steady reduction in the ability of cells to utilize glucose, i.e. to type 2 diabetes or its aggravation. Glucose 351-358 insulin Homo sapiens 245-252 26350813-6 2015 RESULTS: Plasma apoB correlated positively with fasting and postprandial triglycerides and chylomicron clearance (R = 0.44-0.66) and glucose-stimulated insulin secretion (R = 0.24) and negatively with insulin sensitivity (R = -0.28) and gynoid WAT in situ lipoprotein lipase activity (ie, ex vivo WAT function, R(2) = 0.34). Glucose 133-140 insulin Homo sapiens 152-159 26330484-5 2015 Such systems are currently being tested under everyday conditions, although it is not possible to predict when they will actually reach the market.There are, however, such couplings where algorithms are responsible for shutting off insulin delivery when the glucose concentration reaches a defined level or if it will be reached in the foreseeable future. Glucose 258-265 insulin Homo sapiens 232-239 26417414-8 2015 Then, insulin secretion relative to glucose elevation (ISG) (DeltaISG0-180 min: DeltaAUC0-180 min insulin/AUC0-180 min glucose) was significantly enhanced by nateglinide compared with sitagliptin. Glucose 119-126 insulin Homo sapiens 6-13 26592060-8 2015 The 2-hour oral glucose tolerance test with glucose and insulin concentrations was the most common IR screening test used (45%). Glucose 16-23 insulin Homo sapiens 56-63 28465738-6 2015 Seven months after the identification of liver metastases and after initiation of oncological therapy with Interferon and Somatostatin, the patient presented severe hypoglycemia (serum glucose 13-70 mg/dl) proved to be due to insulin-like factors (serum insulin level 64.9 iU/ml) secreted by metastases. Glucose 185-192 insulin Homo sapiens 226-233 25907108-1 2015 AIM: The aim of this study was to clarify the relationship between insulin resistance (IR) and glucose and lipid metabolism in peritoneal dialysis (PD) patients. Glucose 95-102 insulin Homo sapiens 67-74 25907108-14 2015 CONCLUSION: Insulin resistance may play an important role in the pathophysiology of glucose and lipid metabolism. Glucose 84-91 insulin Homo sapiens 12-19 26319827-5 2015 The insulin secretion and insulin sensitivity was determined with the insulin-modified intravenous glucose tolerance test according to the Bergman"s minimal model. Glucose 99-106 insulin Homo sapiens 4-11 26181299-6 2015 Using provided supplies and dosing references, subjects prepared doses of calcium chloride, calcium gluconate, sodium bicarbonate, and regular insulin with dextrose. Glucose 156-164 insulin Homo sapiens 143-150 26181299-12 2015 Insulin with dextrose took significantly longer to prepare than the other medications, and there was no difference between the calcium salts: (sodium bicarbonate, 1.9 [0.8-2.6] vs calcium chloride, 2.1 [1.2-3.1] vs calcium gluconate, 2.4 [2.1-3.0] vs insulin with dextrose, 5.1 min [3.7-7.7 min], respectively; p < 0.001). Glucose 13-21 insulin Homo sapiens 0-7 26181299-14 2015 CONCLUSIONS: Medication preparation for hyperkalemia takes significantly longer for smaller children and preparation of insulin with dextrose takes the longest. Glucose 133-141 insulin Homo sapiens 120-127 26206285-8 2015 In islets isolated from T2D donors the amine significantly increased release of insulin in response to glucose. Glucose 103-110 insulin Homo sapiens 80-87 26343738-3 2015 Hypoglycemia-associated autonomic failure, characterized by ineffective glucose counterregulation during hypoglycemia, is well described in children and adults on insulin therapy for diabetes mellitus. Glucose 72-79 insulin Homo sapiens 163-170 26629404-1 2015 OBJECTIVE: Failure to properly dispose of glucose in response to insulin is a serious health problem, occurring during obesity and is associated with type 2 diabetes development. Glucose 42-49 insulin Homo sapiens 65-72 26629404-2 2015 Insulin-stimulated glucose uptake is facilitated by the translocation and plasma membrane fusion of vesicles containing glucose transporter 4 (GLUT4), the rate-limiting step of post-prandial glucose disposal. Glucose 19-26 insulin Homo sapiens 0-7 26629404-2 2015 Insulin-stimulated glucose uptake is facilitated by the translocation and plasma membrane fusion of vesicles containing glucose transporter 4 (GLUT4), the rate-limiting step of post-prandial glucose disposal. Glucose 120-127 insulin Homo sapiens 0-7 26629404-3 2015 METHODS: We analyzed the role of Tusc5 in the regulation of insulin-stimulated Glut4-mediated glucose uptake in vitro and in vivo. Glucose 94-101 insulin Homo sapiens 60-67 26629404-5 2015 RESULTS: Herein, we report that TUSC5 controls insulin-stimulated glucose uptake in adipocytes, in vitro and in vivo. Glucose 66-73 insulin Homo sapiens 47-54 26629404-6 2015 TUSC5 facilitates the proper recycling of GLUT4 and other key trafficking proteins during prolonged insulin stimulation, thereby enabling proper protein localization and complete vesicle formation, processes that ultimately enable insulin-stimulated glucose uptake. Glucose 250-257 insulin Homo sapiens 100-107 26629404-6 2015 TUSC5 facilitates the proper recycling of GLUT4 and other key trafficking proteins during prolonged insulin stimulation, thereby enabling proper protein localization and complete vesicle formation, processes that ultimately enable insulin-stimulated glucose uptake. Glucose 250-257 insulin Homo sapiens 231-238 26629404-9 2015 CONCLUSIONS: Collectively, these findings establish TUSC5 as an adipose tissue-specific protein that enables proper protein recycling, linking the ubiquitous vesicle traffic machinery with tissue-specific insulin-mediated glucose uptake into adipose tissue and the maintenance of a healthy metabolic phenotype in mice and humans. Glucose 222-229 insulin Homo sapiens 205-212 26297582-9 2015 RESULTS: In normal glucose, the active phosphorylated forms of AKT, eNOS, ERK1/2, p38 and JNK were increased in insulin treated cells, in a dose-dependent manner. Glucose 19-26 insulin Homo sapiens 112-119 26937415-7 2015 Oral glucose tolerance test showed normal baseline blood levels of glucose, insulin and lactate, and their increase following glucose intake. Glucose 5-12 insulin Homo sapiens 76-83 30603261-0 2016 Red wine enhances glucose-dependent insulinotropic peptide (GIP) and insulin responses in type 2 diabetes during an oral glucose tolerance test. Glucose 18-25 insulin Homo sapiens 36-43 30603261-3 2016 The purposes of this study were to evaluate the potential involvement of glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) in alcohol-induced augmentation of the insulin response and to determine if red wine acutely improves glucose tolerance during an oral glucose tolerance test (OGTT). Glucose 73-80 insulin Homo sapiens 91-98 26356502-8 2015 Finally, the model is used to show that NEFA may mediate up to 30-45% of the postprandial increase in insulin-dependent glucose uptake at two hours after a glucose meal. Glucose 120-127 insulin Homo sapiens 102-109 26356502-8 2015 Finally, the model is used to show that NEFA may mediate up to 30-45% of the postprandial increase in insulin-dependent glucose uptake at two hours after a glucose meal. Glucose 156-163 insulin Homo sapiens 102-109 26139601-0 2015 Loss of Liver Kinase B1 (LKB1) in Beta Cells Enhances Glucose-stimulated Insulin Secretion Despite Profound Mitochondrial Defects. Glucose 54-61 insulin Homo sapiens 73-80 26139601-2 2015 LKB1-dependent phosphorylation of distinct AMPK (adenosine monophosphate-activated protein kinase) family members determines proper beta cell polarity and restricts beta cell size, total beta cell mass, and glucose-stimulated insulin secretion (GSIS). Glucose 207-214 insulin Homo sapiens 226-233 26858907-5 2015 Plating efficiency at day 1, the confluency at day 3, and glucose-stimulated insulin secretion test at day 3 were performed. Glucose 58-65 insulin Homo sapiens 77-84 26858907-8 2015 Islet cells cultured on the HL-332-PIPAAm surfaces showed a positive response in the glucose-stimulated insulin secretion test. Glucose 85-92 insulin Homo sapiens 104-111 26121325-1 2015 The pancreatic islet beta cell plays an essential role in maintaining the normal blood glucose level by releasing insulin. Glucose 87-94 insulin Homo sapiens 114-121 26288660-11 2015 CONCLUSION: The low number of patients using insulin analogues in the target group, considered to be in good control, implies the need to reevaluate both level of patients self-care knowledge and glucose monitoring prior their inclusion in the insulin analogue dispense program. Glucose 196-203 insulin Homo sapiens 45-52 26288661-0 2015 Regulation of hepatic TRB3/Akt interaction induced by physical exercise and its effect on the hepatic glucose production in an insulin resistance state. Glucose 102-109 insulin Homo sapiens 127-134 26288661-3 2015 These responses are associated with the insulin signaling pathway and the reduction in the activity of key gluconeogenic enzymes, resulting in a decrease of hepatic glucose production. Glucose 165-172 insulin Homo sapiens 40-47 26184777-0 2015 Phenylboronic Acid Appended Pyrene-Based Low-Molecular-Weight Injectable Hydrogel: Glucose-Stimulated Insulin Release. Glucose 83-90 insulin Homo sapiens 102-109 26184777-1 2015 A pyrene-containing phenylboronic acid (PBA) functionalized low-molecular-weight hydrogelator was synthesized with the aim to develop glucose-sensitive insulin release. Glucose 134-141 insulin Homo sapiens 152-159 26184777-8 2015 Hence, the glucose-induced swelling of the hydrogel was exploited in the controlled release of insulin from the hydrogel. Glucose 11-18 insulin Homo sapiens 95-102 26266953-1 2015 Pancreatic islets of Langerhans consist of endocrine cells, primarily alpha, beta and delta cells, which secrete glucagon, insulin, and somatostatin, respectively, to regulate plasma glucose. Glucose 183-190 insulin Homo sapiens 123-130 26266953-2 2015 beta cells form irregular locally connected clusters within islets that act in concert to secrete insulin upon glucose stimulation. Glucose 111-118 insulin Homo sapiens 98-105 26258766-9 2015 CONCLUSIONS: In conclusion, we show for the first time that human oWAT fibrosis in severe obesity is consistent with a higher degree of insulin resistance measured by glucose clamp. Glucose 167-174 insulin Homo sapiens 136-143 26248027-10 2015 Improvement was linked to preoperatively elevated insulin resistance, which normalized after resection and was accompanied by a decrease in fasting- and glucose-stimulated insulin secretion. Glucose 153-160 insulin Homo sapiens 50-57 26248027-10 2015 Improvement was linked to preoperatively elevated insulin resistance, which normalized after resection and was accompanied by a decrease in fasting- and glucose-stimulated insulin secretion. Glucose 153-160 insulin Homo sapiens 172-179 26737276-1 2015 The diagnosis of low insulin sensitivity is commonly done through the HOMA-IR index, in which fasting insulin and glucose blood levels are evaluated. Glucose 114-121 insulin Homo sapiens 21-28 26388576-1 2015 Addition of Subetta to insulin (10 nM) increased insulin-stimulated glucose uptake 43% (p<0.001). Glucose 68-75 insulin Homo sapiens 23-30 25986006-0 2015 Blood glucose response to rescue dextrose in hypoglycemic, critically ill patients receiving an insulin infusion. Glucose 33-41 insulin Homo sapiens 96-103 26297582-13 2015 Insulin was able to increase phospho-IRbeta in normal glucose but not in high glucose, in which the total protein levels remained reduced. Glucose 54-61 insulin Homo sapiens 0-7 26297582-14 2015 CONCLUSIONS: Exposure to short-term high glucose negatively affects insulin signaling even when physiological insulin concentrations are added. Glucose 41-48 insulin Homo sapiens 68-75 26297582-14 2015 CONCLUSIONS: Exposure to short-term high glucose negatively affects insulin signaling even when physiological insulin concentrations are added. Glucose 41-48 insulin Homo sapiens 110-117 26297582-15 2015 The impairment of the PI3K/AKT/eNOS pathway after physiological insulin treatment could contribute to detrimental effects on cardiovascular homeostasis under high glucose conditions, and might shift toward the activation of certain mitogenic effectors, such as ERK1/2, p38 and JNK, the only ones that respond to physiological insulin treatment in high glucose. Glucose 163-170 insulin Homo sapiens 64-71 26297582-15 2015 The impairment of the PI3K/AKT/eNOS pathway after physiological insulin treatment could contribute to detrimental effects on cardiovascular homeostasis under high glucose conditions, and might shift toward the activation of certain mitogenic effectors, such as ERK1/2, p38 and JNK, the only ones that respond to physiological insulin treatment in high glucose. Glucose 352-359 insulin Homo sapiens 64-71 26388576-2 2015 Moreover, glucose uptake stimulated by insulin (10 nM) in the presence of Subetta was similar to that stimulated by 300 nM insulin. Glucose 10-17 insulin Homo sapiens 39-46 26388576-3 2015 These findings suggest that Subetta significantly enhanced insulin sensitivity of tissues through stimulation of glucose transport to myocytes mediated by glucose transporter 4. Glucose 113-120 insulin Homo sapiens 59-66 25930989-6 2015 The decrease in glucose levels was accompanied by reductions in serum insulin levels throughout the day. Glucose 16-23 insulin Homo sapiens 70-77 25476247-3 2015 Consequently, the exon 11-deleted IR isoform that is less sensitive to insulin is predominantly produced, leading to glucose intolerance in DM1. Glucose 117-124 insulin Homo sapiens 71-78 25659979-10 2015 Insulin infusion study: as compared with no infusion, glucose and glucose-insulin infusion prevented the postprandial decrease in FGF21 and resulted in higher FGF21 concentrations by up to 25% (P = 0 003). Glucose 54-61 insulin Homo sapiens 0-7 26084344-10 2015 In multiple linear regression analysis, the addition of sclerostin levels to the traditional risk factors for insulin resistance improved the r(2) associated with HOMA-IR (r(2) change: 0.055; F change: 28.893; P = 0.001) and insulin-mediated total body glucose disposal (r(2) change: 0.059; F change: 4.938; P = 0.033). Glucose 253-260 insulin Homo sapiens 110-117 26057180-13 2015 Compared with males, females display higher glucose, insulin, and c-peptide responses with greater insulin secretion, beta-cell sensitivity to glucose, insulin clearance, and equal insulin sensitivity. Glucose 143-150 insulin Homo sapiens 66-75 26057180-15 2015 In contrast, insulin clearance increases with age, especially in females, contributing to the deterioration in glucose tolerance. Glucose 111-118 insulin Homo sapiens 13-20 25839190-3 2015 These factors have previously been shown to affect insulin-mediated glucose uptake in differentiated adipocytes. Glucose 68-75 insulin Homo sapiens 51-58 25839190-5 2015 This study therefore aimed to examine the effect of obesity-associated inflammatory factors on the expression of insulin-independent glucose transporters (GLUT1 and GLUT3) and on the uptake of glucose within adipose stromal cells. Glucose 133-140 insulin Homo sapiens 113-120 25329006-8 2015 RESULTS: After controlling for age, sex and BMI, every 100 count increase in accelerometer derived total movement was associated with a 0.06 mmol L-1 9 hours decrease in glucose iAUC (95% CI 0.004-0.1; P = .035), but not associated with changes in insulin or triglyceride iAUC. Glucose 170-177 insulin Homo sapiens 248-255 26051044-5 2015 Availability of newer glucose-lowering drugs (such as glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors, and sodium-glucose co-transporter-2 inhibitors) also offers the opportunity for combination treatment; the results of the first trials in this area of research suggest that such treatment might lead to use of reduced insulin doses, less weight gain, and fewer hypoglycaemic episodes than insulin treatment alone. Glucose 22-29 insulin Homo sapiens 349-356 26051044-5 2015 Availability of newer glucose-lowering drugs (such as glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors, and sodium-glucose co-transporter-2 inhibitors) also offers the opportunity for combination treatment; the results of the first trials in this area of research suggest that such treatment might lead to use of reduced insulin doses, less weight gain, and fewer hypoglycaemic episodes than insulin treatment alone. Glucose 22-29 insulin Homo sapiens 420-427 25809135-2 2015 Present study investigates glucose and insulin response during oral glucose tolerance test (oGTT) in MS patients. Glucose 68-75 insulin Homo sapiens 39-46 25809135-8 2015 Insulin response to oral glucose load in MS was increased (p = 0.022). Glucose 25-32 insulin Homo sapiens 0-7 25944785-8 2015 CONCLUSION: This study showed that PCA stimulates the insulin signaling pathway in human adipocytes increasing GLUT4 translocation and glucose uptake. Glucose 135-142 insulin Homo sapiens 54-61 25962562-6 2015 Following insulin stimulation, the rate of glucose uptake was significantly reduced in the cells with glucosamine-induced insulin-resistance in comparison with those in the control group. Glucose 43-50 insulin Homo sapiens 10-17 25962562-6 2015 Following insulin stimulation, the rate of glucose uptake was significantly reduced in the cells with glucosamine-induced insulin-resistance in comparison with those in the control group. Glucose 43-50 insulin Homo sapiens 122-129 25962562-9 2015 Following treatment with bisperoxopicolinatooxovanadate (BPV) or metformin in the insulin-resistant skeletal muscle cells, there was an increase in the rate of glucose uptake, an increase in GLUT4 expression and its translocation, a reduction in the expression of PTEN and p-PTEN, and a decrease in cell apoptosis compared with untreated insulin-resistant cells. Glucose 160-167 insulin Homo sapiens 82-89 25670721-2 2015 The results showed the presence of receptors and their activation resulted in a dose-dependent increase in glucose-induced release of insulin. Glucose 107-114 insulin Homo sapiens 134-141 25809669-1 2015 Insulin secretion from pancreatic beta-cells in response to sudden glucose stimulation is biphasic. Glucose 67-74 insulin Homo sapiens 0-7 26170190-1 2015 The transcription factor forkhead box O1 (FoxO1) plays pleiotropic roles in insulin-mediated glucose and lipid metabolism. Glucose 93-100 insulin Homo sapiens 76-83 26170190-2 2015 In the liver, glucose production is finely controlled by insulin signaling that dampens FoxO1. Glucose 14-21 insulin Homo sapiens 57-64 26231186-8 2015 Similar to the approach providers use during clinical encounters, the device analyses stored glucose trends and constantly titrates insulin dosage without care providers" supervision. Glucose 93-100 insulin Homo sapiens 132-139 25980620-6 2015 Direct injection of PIP peptides 640 or 250 with human insulin into the lumen of rat jejunum caused a decrease in blood glucose levels that was PIP peptide and insulin dose-dependent and correlated with increased pMLC levels. Glucose 120-127 insulin Homo sapiens 55-62 25980620-6 2015 Direct injection of PIP peptides 640 or 250 with human insulin into the lumen of rat jejunum caused a decrease in blood glucose levels that was PIP peptide and insulin dose-dependent and correlated with increased pMLC levels. Glucose 120-127 insulin Homo sapiens 160-167 26206703-0 2015 Erratum: FoxO1 integrates direct and indirect effects of insulin on hepatic glucose production and glucose utilization. Glucose 76-83 insulin Homo sapiens 57-64 26204994-4 2015 The biological clock is also involved in regulation of glucose metabolism by modulating peripheral insulin sensitivity. Glucose 55-62 insulin Homo sapiens 99-106 26206703-0 2015 Erratum: FoxO1 integrates direct and indirect effects of insulin on hepatic glucose production and glucose utilization. Glucose 99-106 insulin Homo sapiens 57-64 26187303-1 2015 BACKGROUND: Diabetes patients are usually started on a low dose of insulin and their dose is adjusted or "titrated" according to their blood glucose levels. Glucose 141-148 insulin Homo sapiens 67-74 26196519-0 2015 Increased Insulin following an Oral Glucose Load, Genetic Variation near the Melatonin Receptor MTNR1B, but No Biochemical Evidence of Endothelial Dysfunction in Young Asian Men and Women. Glucose 36-43 insulin Homo sapiens 10-17 26196519-8 2015 CONCLUSIONS: Elevated non-fasting insulin exists in young South Asians of normal fasting glucose and insulin. Glucose 89-96 insulin Homo sapiens 34-41 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 20-27 insulin Homo sapiens 62-69 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 20-27 insulin Homo sapiens 109-116 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 20-27 insulin Homo sapiens 109-116 25991649-1 2015 Recently, a model was proposed to assess hepatic insulin sensitivity during a meal, i.e., the ability of insulin to suppress glucose production (EGP), SI (P). Glucose 125-132 insulin Homo sapiens 49-56 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 126-133 insulin Homo sapiens 109-116 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 126-133 insulin Homo sapiens 109-116 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 126-133 insulin Homo sapiens 109-116 25960379-5 2015 Steady-state plasma glucose concentrations derived during the insulin suppression test were used to quantify insulin-mediated glucose uptake; higher steady-state plasma glucose concentrations indicated greater insulin resistance. Glucose 126-133 insulin Homo sapiens 109-116 26244156-14 2015 In glucose challenge test a significant increase in insulin secretion from 0.91 +- 0.04 muIu/mL (2.8 mmol/L glucose) to to 8.34 +- 0.45 muIu/mL (16.7 mmol/L glucose) was recorded (P < 0.05). Glucose 3-10 insulin Homo sapiens 52-59 26244156-14 2015 In glucose challenge test a significant increase in insulin secretion from 0.91 +- 0.04 muIu/mL (2.8 mmol/L glucose) to to 8.34 +- 0.45 muIu/mL (16.7 mmol/L glucose) was recorded (P < 0.05). Glucose 108-115 insulin Homo sapiens 52-59 26244156-14 2015 In glucose challenge test a significant increase in insulin secretion from 0.91 +- 0.04 muIu/mL (2.8 mmol/L glucose) to to 8.34 +- 0.45 muIu/mL (16.7 mmol/L glucose) was recorded (P < 0.05). Glucose 108-115 insulin Homo sapiens 52-59 26071524-1 2015 Insulin-stimulated delivery of glucose transporters (GLUT4, also known as SLC2A4) from specialized intracellular GLUT4 storage vesicles (GSVs) to the surface of fat and muscle cells is central to whole-body glucose regulation. Glucose 31-38 insulin Homo sapiens 0-7 25953061-1 2015 Physical training decreases glucose- and arginine-stimulated insulin secretion. Glucose 28-35 insulin Homo sapiens 61-68 25953061-5 2015 The insulin response to glucose was measured during hyperglycaemic (20 mmol l(-1) ) clamps before and after the NA infusion period. Glucose 24-31 insulin Homo sapiens 4-11 26154605-5 2015 A graphical Markov model was used to describe the impact of the intervention, by dividing the effects into various pathways comprising changes in proportion of dietary saturated fat, physical activity and weight loss, and a genetic predisposition score (T2DM-GPS), on changes in insulin sensitivity (HOMA-IR), insulin secretion (HOMA-B) and short and long term glycaemia (glucose and HbA1c). Glucose 372-379 insulin Homo sapiens 279-286 30603256-5 2016 Delta glucagon showed a significant association with post-prandial glucose increase in the group with diminished insulin secretory capacity, C-peptide index (CPI) <0.8 (p = 0.016), while Delta C-peptide reached significant association in the group with relatively intact insulin secretory capacity, CPI >=0.8 (p = 0.017). Glucose 67-74 insulin Homo sapiens 113-120 30603256-5 2016 Delta glucagon showed a significant association with post-prandial glucose increase in the group with diminished insulin secretory capacity, C-peptide index (CPI) <0.8 (p = 0.016), while Delta C-peptide reached significant association in the group with relatively intact insulin secretory capacity, CPI >=0.8 (p = 0.017). Glucose 67-74 insulin Homo sapiens 141-150 30603256-8 2016 In conclusion, complementary glucagonostatic and insulinotropic effects of adding DPP-4 inhibitors are involved in the glucose-lowering action of Japanese patients with type 2 diabetes according to their insulin secretory capacity. Glucose 119-126 insulin Homo sapiens 49-56 26100900-1 2015 A glucose-responsive "closed-loop" insulin delivery system mimicking the function of pancreatic cells has tremendous potential to improve quality of life and health in diabetics. Glucose 2-9 insulin Homo sapiens 35-42 26041305-8 2015 As a proof of concept for detection of insulin resistance, we measured insulin-dependent glucose uptake by hAT from nondiabetic and T2DM subjects, mimicking the postprandial response. Glucose 89-96 insulin Homo sapiens 39-46 26041305-8 2015 As a proof of concept for detection of insulin resistance, we measured insulin-dependent glucose uptake by hAT from nondiabetic and T2DM subjects, mimicking the postprandial response. Glucose 89-96 insulin Homo sapiens 71-78 26413467-0 2015 Pannexin 1 is required for full activation of insulin-stimulated glucose uptake in adipocytes. Glucose 65-72 insulin Homo sapiens 46-53 26413467-1 2015 OBJECTIVE: Defective glucose uptake in adipocytes leads to impaired metabolic homeostasis and insulin resistance, hallmarks of type 2 diabetes. Glucose 21-28 insulin Homo sapiens 94-101 26413467-10 2015 Pharmacologic inhibition or selective genetic deletion of Panx1 from adipocytes decreased insulin-induced glucose uptake in vitro and in vivo and exacerbated diet-induced insulin resistance in mice. Glucose 106-113 insulin Homo sapiens 90-97 26413467-13 2015 CONCLUSIONS: We show that Panx1 channel activity regulates insulin-stimulated glucose uptake in adipocytes and thus contributes to control of metabolic homeostasis. Glucose 78-85 insulin Homo sapiens 59-66 26151207-1 2015 Diabetes is a chronic disease characterized by high blood glucose level that results either from a deficiency of insulin produced by the body, or the body"s resistance to the effects of insulin. Glucose 58-65 insulin Homo sapiens 113-120 26016867-6 2015 The primary outcome was insulin sensitivity assessed by using the Matsuda method from an oral-glucose-tolerance test. Glucose 94-101 insulin Homo sapiens 24-31 25897569-11 2015 MEASUREMENTS AND MAIN RESULTS: The overall glucose response was reduced (treatment difference: -1,276.9 [mg/dl] min [95% confidence interval, -2,392.4 to -161.5]; P = 0.03) and insulin sensitivity was improved (treatment difference: 0.77 [mU/L](-1) min(-1) [95% confidence interval, 0.03-1.52]; P = 0.04) with CPAP as compared with placebo. Glucose 43-50 insulin Homo sapiens 179-186 25267549-4 2015 The insulin response to intravenous glucose during the 60- to 120-min interval (Insiv) was calculated using a prediction method. Glucose 36-43 insulin Homo sapiens 4-11 25267549-5 2015 The insulin response to oral glucose (Ins(oral)) was calculated by subtracting the Insiv from the overall insulin response during the 60- to 120-min interval (Ins(overall)). Glucose 29-36 insulin Homo sapiens 4-11 25267549-5 2015 The insulin response to oral glucose (Ins(oral)) was calculated by subtracting the Insiv from the overall insulin response during the 60- to 120-min interval (Ins(overall)). Glucose 29-36 insulin Homo sapiens 106-113 25979318-8 2015 OUTCOMES: Insulin response to an oral glucose load is the primary outcome measure, and changes in physiological parameters, cardiorespiratory fitness, strength, body composition, and psychological well-being comprise the secondary outcomes. Glucose 38-45 insulin Homo sapiens 10-17 25677915-3 2015 Here we report the insulin secretion ability by in vitro glucose perifusion and explore the expression of insulin pathway genes in isolated islets of Langerhans from these patients. Glucose 57-64 insulin Homo sapiens 19-26 26047681-0 2015 Coefficient of variation of R-R interval closely correlates with glycemic variability assessed by continuous glucose monitoring in insulin-depleted patients with type 1 diabetes. Glucose 109-116 insulin Homo sapiens 131-138 25754957-9 2015 In nondiabetic individuals, enhanced glucose sensitivity and potentiation upregulate the insulin secretory response to carbohydrate overloading. Glucose 37-44 insulin Homo sapiens 89-96 25772444-0 2015 Insulin degludec/insulin aspart produces a dose-proportional glucose-lowering effect in subjects with type 1 diabetes mellitus. Glucose 61-68 insulin Homo sapiens 0-7 25772444-0 2015 Insulin degludec/insulin aspart produces a dose-proportional glucose-lowering effect in subjects with type 1 diabetes mellitus. Glucose 61-68 insulin Homo sapiens 17-24 25846340-6 2015 Faster-acting insulin aspart had a significantly greater glucose-lowering effect within 90 min after dosing [largest difference: area under the curve for the glucose infusion rate (AUC(GIR), 0-30 min) ratio 1.48, 95% CI 1.13; 2.02] and 17% earlier time to reach 50% maximum glucose infusion rate (38.3 vs 46.1 min; ratio 0.83, 95% CI 0.73; 0.94). Glucose 57-64 insulin Homo sapiens 14-21 25846340-6 2015 Faster-acting insulin aspart had a significantly greater glucose-lowering effect within 90 min after dosing [largest difference: area under the curve for the glucose infusion rate (AUC(GIR), 0-30 min) ratio 1.48, 95% CI 1.13; 2.02] and 17% earlier time to reach 50% maximum glucose infusion rate (38.3 vs 46.1 min; ratio 0.83, 95% CI 0.73; 0.94). Glucose 158-165 insulin Homo sapiens 14-21 25846340-6 2015 Faster-acting insulin aspart had a significantly greater glucose-lowering effect within 90 min after dosing [largest difference: area under the curve for the glucose infusion rate (AUC(GIR), 0-30 min) ratio 1.48, 95% CI 1.13; 2.02] and 17% earlier time to reach 50% maximum glucose infusion rate (38.3 vs 46.1 min; ratio 0.83, 95% CI 0.73; 0.94). Glucose 158-165 insulin Homo sapiens 14-21 25846340-9 2015 CONCLUSIONS: Faster-acting insulin aspart was found to have earlier onset and higher early exposure than insulin aspart, and a greater early glucose-lowering effect, with similar potency. Glucose 141-148 insulin Homo sapiens 27-34 25852206-10 2015 Hepatic insulin sensitivity, determined from the suppression of endogenous glucose production by insulin, exhibited a small but significant improvement with EPA+DHA compared with placebo. Glucose 75-82 insulin Homo sapiens 8-15 25870023-5 2015 RESULTS: Insulin-stimulated glucose uptake was lower in diabetic patients vs obese controls with or without prior exercise. Glucose 28-35 insulin Homo sapiens 9-16 25879401-3 2015 In healthy individuals, pancreatic islet beta-cells secrete insulin to regulate the increase in blood glucose levels. Glucose 102-109 insulin Homo sapiens 60-67 25940643-4 2015 RESULTS: Higher fasting glucose, insulin and HOMA-IR at 8 years predicted higher glucose, insulin, HOMA-IR, BP, lipids and IMT at 21 years. Glucose 24-31 insulin Homo sapiens 90-97 25940643-4 2015 RESULTS: Higher fasting glucose, insulin and HOMA-IR at 8 years predicted higher glucose, insulin, HOMA-IR, BP, lipids and IMT at 21 years. Glucose 81-88 insulin Homo sapiens 33-40 25963320-2 2015 Insulin degludec (IDeg) is a novel basal insulin with improved pharmacokinetic and pharmacodynamic properties compared to insulin glargine (IGlar) including a long half-life of ~25 h and a duration of action >42 h at steady state, providing a flat and stable blood glucose-lowering effect when injected once daily. Glucose 268-275 insulin Homo sapiens 0-7 26021979-9 2015 In the presence of high insulin, the effect of high glucose on target gene expression was altered. Glucose 52-59 insulin Homo sapiens 24-31 26391447-8 2015 T-MSCs had a differentiation capacity similar to that of A-MSCs and were capable of secreting insulin in response to glucose concentration. Glucose 117-124 insulin Homo sapiens 94-101 25899581-0 2015 Insulin resistance in patients with type 1 diabetes assessed by glucose clamp studies: systematic review and meta-analysis. Glucose 64-71 insulin Homo sapiens 0-7 25899581-4 2015 Primary outcome measures were pooled mean differences of insulin sensitivity of endogenous glucose production (EGP), of glucose uptake and of lipolysis. Glucose 91-98 insulin Homo sapiens 57-64 25899581-8 2015 Insulin sensitivity of glucose uptake was either reported as M value (M), glucose infusion rate (GIR), glucose disposal rate (GDR) or metabolic clearance rate (MCR). Glucose 23-30 insulin Homo sapiens 0-7 25899581-8 2015 Insulin sensitivity of glucose uptake was either reported as M value (M), glucose infusion rate (GIR), glucose disposal rate (GDR) or metabolic clearance rate (MCR). Glucose 74-81 insulin Homo sapiens 0-7 25899581-8 2015 Insulin sensitivity of glucose uptake was either reported as M value (M), glucose infusion rate (GIR), glucose disposal rate (GDR) or metabolic clearance rate (MCR). Glucose 74-81 insulin Homo sapiens 0-7 25935491-10 2015 The expressions of CB1 mRNA and endocannabinoids showed a significant positive correlation with 2-hour glucose and insulin levels 2 hours after glucose loading in the PBMCs and adipose tissue. Glucose 144-151 insulin Homo sapiens 115-122 26177098-3 2015 Indeed, in tissue such as the liver both molecules are involved in the insulin signaling, i.e. MI promotes glucose uptake and DCI glycogen synthesis. Glucose 107-114 insulin Homo sapiens 71-78 26036654-11 2015 For a rapid drop in potassium by shifting the potassium to the intracellular space, administration of glucose with insulin and high-dose inhalative administration of betamimetics can be used. Glucose 102-109 insulin Homo sapiens 115-122 26036655-4 2015 Owing to its insulin-dependent duality of action, glucose can represent an effective or an ineffective osmolyte. Glucose 50-57 insulin Homo sapiens 13-20 26721005-6 2015 Insulin resistance was assessed using the HOMA-IR formula derived from fasting insulin and glucose levels. Glucose 91-98 insulin Homo sapiens 0-7 26020765-0 2015 Is Insulin Action in the Brain Relevant in Regulating Blood Glucose in Humans? Glucose 60-67 insulin Homo sapiens 3-10 26020765-1 2015 PURPOSE: In addition to its direct action on the liver to lower hepatic glucose production, insulin action in the central nervous system (CNS) also lowers hepatic glucose production in rodents after 4 hours. Glucose 163-170 insulin Homo sapiens 92-99 26020765-5 2015 Hence, INI can address whether CNSIA regulates plasma glucose concentration in humans. Glucose 54-61 insulin Homo sapiens 7-10 26020765-8 2015 CONCLUSIONS: The early glucose-lowering effect of INI is likely due to spillover of insulin into the systemic circulation. Glucose 23-30 insulin Homo sapiens 50-53 26020765-8 2015 CONCLUSIONS: The early glucose-lowering effect of INI is likely due to spillover of insulin into the systemic circulation. Glucose 23-30 insulin Homo sapiens 84-91 26020765-10 2015 INI administration does lower plasma glucose independent of peripheral insulin concentration (between ~3 and 6 h after administration), suggesting that CNSIA may play a role in glucose homeostasis in the late postprandial period when its action is likely greatest and portal insulin concentration is at baseline. Glucose 37-44 insulin Homo sapiens 0-3 26098213-1 2015 Pancreatic beta cells secrete insulin in response to postprandial increases in glucose levels to prevent hyperglycemia and inhibit insulin secretion under fasting conditions to protect against hypoglycemia. Glucose 79-86 insulin Homo sapiens 30-37 26098213-2 2015 beta cells lack this functional capability at birth and acquire glucose-stimulated insulin secretion (GSIS) during neonatal life. Glucose 64-71 insulin Homo sapiens 83-90 26098213-3 2015 Here, we have shown that during postnatal life, the de novo DNA methyltransferase DNMT3A initiates a metabolic program by repressing key genes, thereby enabling the coupling of insulin secretion to glucose levels. Glucose 198-205 insulin Homo sapiens 177-184 26236094-3 2015 Aging and chronic diseases are strongly associated with markers for oxidative stress, especially advanced glycation end-products, and resistance to peripheral insulin-mediated glucose uptake. Glucose 176-183 insulin Homo sapiens 159-166 26221522-11 2015 CONCLUSION: The treatment of reducing the dose of insulin and using liraglutide in combination not only suppresses PBGs, but also stabilizes their blood glucose fluctuations. Glucose 153-160 insulin Homo sapiens 50-57 25691653-14 2015 Therefore, it is necessary to determine the correlation between blood glucose concentrations and under different conditions, for example, insulin levels, as well as correlate the results with clinical tests, for example, Hb1Ac. Glucose 70-77 insulin Homo sapiens 138-145 25655141-9 2015 There was a significant negative correlation between serum glucose and insulin levels and ocular blood flow velocity. Glucose 59-66 insulin Homo sapiens 71-78 26311994-2 2015 The main treatment of diabetes relies on subcutaneous insulin administration by injection or continuous infusion to control glucose levels, besides oral hypoglycemic agents for type 2 diabetes. Glucose 124-131 insulin Homo sapiens 54-61 26100900-2 2015 Here, we report a novel glucose-responsive insulin delivery device using a painless microneedle-array patch ("smart insulin patch") containing glucose-responsive vesicles (GRVs; with an average diameter of 118 nm), which are loaded with insulin and glucose oxidase (GOx) enzyme. Glucose 24-31 insulin Homo sapiens 43-50 26100900-2 2015 Here, we report a novel glucose-responsive insulin delivery device using a painless microneedle-array patch ("smart insulin patch") containing glucose-responsive vesicles (GRVs; with an average diameter of 118 nm), which are loaded with insulin and glucose oxidase (GOx) enzyme. Glucose 24-31 insulin Homo sapiens 116-123 26100900-4 2015 The local hypoxic microenvironment caused by the enzymatic oxidation of glucose in the hyperglycemic state promotes the reduction of HS-HA, which rapidly triggers the dissociation of vesicles and subsequent release of insulin. Glucose 72-79 insulin Homo sapiens 218-225 26100900-5 2015 The smart insulin patch effectively regulated the blood glucose in a mouse model of chemically induced type 1 diabetes. Glucose 56-63 insulin Homo sapiens 10-17 26100900-6 2015 The described work is the first demonstration, to our knowledge, of a synthetic glucose-responsive device using a hypoxia trigger for regulation of insulin release. Glucose 80-87 insulin Homo sapiens 148-155 25956568-8 2015 In insulin-sensitive adipocytes, adiponectin ablation reduced insulin-stimulated glucose uptake, expression of IRS-1 and GLUT4, and GLUT4 translocation to the membrane. Glucose 81-88 insulin Homo sapiens 62-69 25956568-5 2015 Insulin-stimulated glucose transport was measured and protein and mRNA levels were assessed by Western blot and RT-PCR. Glucose 19-26 insulin Homo sapiens 0-7 25815690-7 2015 PA attenuated insulin-mediated insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, leading to decreased glucose uptake, and phosphorylation of eNOS, leading to a reduction in the production of NO. Glucose 115-122 insulin Homo sapiens 14-21 25956568-6 2015 KEY FINDINGS: Prolonged incubation with insulin significantly reduced insulin-stimulated glucose uptake, suggesting the development of insulin resistance and adiponectin mRNA expression. Glucose 89-96 insulin Homo sapiens 40-47 25956568-6 2015 KEY FINDINGS: Prolonged incubation with insulin significantly reduced insulin-stimulated glucose uptake, suggesting the development of insulin resistance and adiponectin mRNA expression. Glucose 89-96 insulin Homo sapiens 70-77 25956568-6 2015 KEY FINDINGS: Prolonged incubation with insulin significantly reduced insulin-stimulated glucose uptake, suggesting the development of insulin resistance and adiponectin mRNA expression. Glucose 89-96 insulin Homo sapiens 70-77 25815690-7 2015 PA attenuated insulin-mediated insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, leading to decreased glucose uptake, and phosphorylation of eNOS, leading to a reduction in the production of NO. Glucose 115-122 insulin Homo sapiens 31-38 26054006-5 2015 The effect of MFAP5 knock-down by siRNA on gene expression and insulin action was examined with RT-qPCR, western blot, and insulin-stimulated glucose uptake. Glucose 142-149 insulin Homo sapiens 123-130 26061564-0 2015 Rp-cAMPS Prodrugs Reveal the cAMP Dependence of First-Phase Glucose-Stimulated Insulin Secretion. Glucose 60-67 insulin Homo sapiens 79-86 26277181-8 2015 It has been determined that omentin enhances insulin-stimulated glucose uptake in subcutaneous and visceral adipose tissue. Glucose 64-71 insulin Homo sapiens 45-52 25822155-8 2015 RESULTS: EndoC-BH1 cells secreted insulin in response to glucose in a dose-dependent manner, and the secretion was enhanced by GLP-1 (glucagon-like peptide 1). Glucose 57-64 insulin Homo sapiens 34-41 26132231-9 2015 The risks of type 2 diabetes, early IGT, and insulin resistance were perfectly predicted by comparing fasting glucose levels to the estimated Matsuda Index 3 (fasting levels of 10- and 12-(Z,E)-HODE/linoleic acids, insulin, and leptin/adiponectin). Glucose 110-117 insulin Homo sapiens 45-52 26710502-4 2015 Insulin resistance was assessed using eGDR (estimated glucose disposal rate) formula. Glucose 54-61 insulin Homo sapiens 0-7 26134834-1 2015 BACKGROUND: The Predictive Hypoglycemia Minimizer System ("Hypo Minimizer"), consisting of a zone model predictive controller (the "controller") and a safety supervision module (the "safety module"), aims to mitigate hypoglycemia by preemptively modulating insulin delivery based on continuous glucose monitor (CGM) measurements. Glucose 294-301 insulin Homo sapiens 257-264 26072915-4 2015 Plasma glucose and serum insulin concentrations increased significantly following glucose load in both conditions (P < 0.05). Glucose 82-89 insulin Homo sapiens 25-32 25641955-5 2015 Additionally, we survey nanoscale approaches to "closed-loop" insulin delivery strategies which automatically release insulin in response to fluctuating blood glucose levels (BGLs). Glucose 159-166 insulin Homo sapiens 62-69 25641955-5 2015 Additionally, we survey nanoscale approaches to "closed-loop" insulin delivery strategies which automatically release insulin in response to fluctuating blood glucose levels (BGLs). Glucose 159-166 insulin Homo sapiens 118-125 26134834-9 2015 The most aggressive setting was quickest to take action to reduce insulin delivery below basal and achieved the best glucose metrics. Glucose 117-124 insulin Homo sapiens 66-73 26107810-7 2015 Glucose ingestion induced significantly greater elevations in plasma glucose, insulin, GLP-1 and GIP, while feelings of fullness increased and prospective food consumption decreased relative to fructose. Glucose 0-7 insulin Homo sapiens 78-85 27252608-4 2015 There is increased blood glucose though insulin levels are above normal. Glucose 25-32 insulin Homo sapiens 40-47 25839799-4 2015 The results of glucose-stimulated insulin secretion (GSIS) showed that 7WA significantly augmented insulin secretion at high glucose level (25mM), however, such effect was not seen at low glucose level (5mM). Glucose 15-22 insulin Homo sapiens 34-41 25839799-4 2015 The results of glucose-stimulated insulin secretion (GSIS) showed that 7WA significantly augmented insulin secretion at high glucose level (25mM), however, such effect was not seen at low glucose level (5mM). Glucose 125-132 insulin Homo sapiens 99-106 25839799-4 2015 The results of glucose-stimulated insulin secretion (GSIS) showed that 7WA significantly augmented insulin secretion at high glucose level (25mM), however, such effect was not seen at low glucose level (5mM). Glucose 125-132 insulin Homo sapiens 99-106 26107810-9 2015 Moreover, compared to fructose, the increased rsFC after glucose positively correlated with the glucose-induced increase in insulin. Glucose 57-64 insulin Homo sapiens 124-131 25862960-3 2015 AIM OF THE STUDY: To investigate the ability of the selected plants to both increase insulin sensitivity through the enhancement of glucose uptake after insulin induction in adipocytes and suppress lipid production in the same target cells. Glucose 132-139 insulin Homo sapiens 85-92 26479872-2 2015 Depletion of the Sec1/Munc18 protein mVps45 significantly abrogates insulin-stimulated glucose transport and GLUT4 translocation. Glucose 87-94 insulin Homo sapiens 68-75 25862960-7 2015 The screening platform consists of insulin-induced glucose uptake, lipid accumulation, and cell viability. Glucose 51-58 insulin Homo sapiens 35-42 25862960-11 2015 RESULTS: Out of 59 plants, 13 plants demonstrated their ability to increase glucose uptake in 3T3-L1 adipocytes after insulin induction, and 4 of these plants" extracts suppressed lipid production of the cells. Glucose 76-83 insulin Homo sapiens 118-125 25862960-14 2015 CONCLUSIONS: Screening of selected Indonesian medicinal plants has uncovered the potentials of E. longifolia Jack (root) and P. nigrum L. (fruits) with dual active functions, increasing insulin sensitivity through the enhancement of glucose uptake and reducing lipid accumulation in adipose cells. Glucose 233-240 insulin Homo sapiens 186-193 25911095-2 2015 We previously showed that iEC-induced PIs display improved insulin expression and secretion in response to glucose stimulation. Glucose 107-114 insulin Homo sapiens 59-66 25931001-1 2015 In previous studies, we demonstrated that down-regulation of lipoprotein lipase in L6 muscle cells increased insulin-stimulated glucose uptake. Glucose 128-135 insulin Homo sapiens 109-116 26124635-4 2015 The reverse insulin distribution has short- and long-term effects on glucose metabolism. Glucose 69-76 insulin Homo sapiens 12-19 26068931-10 2015 Silencing of the PP2A catalytic subunit abrogated the negative effect of ZAG on insulin-stimulated AKT phosphorylation and glucose uptake but not on GLUT4 expression and basal glucose uptake. Glucose 123-130 insulin Homo sapiens 80-87 26455610-0 2015 The effect of insulin therapy algorithms on blood glucose levels in patients following cardiac surgery: A systematic review. Glucose 50-57 insulin Homo sapiens 14-21 26455610-2 2015 OBJECTIVES: The objective of this study was to investigate the effect of insulin therapy algorithms on blood glucose levels in patients in critical care environments following cardiac surgery. Glucose 109-116 insulin Homo sapiens 73-80 26455610-18 2015 Pooled data demonstrated significantly improved mean blood glucose levels (Weighted Means Differences -27.24, 95% Confidence Interval: -27.77 - -26.72), p < 0.00001 and achievement of target blood glucose levels range (Relative Risks 1.43, 95% Confidence Interval: 1.18 - 1.72), p = 0.0002, among participants who received the paper nomogram continuous intravenous insulin method of glucose control compared to the bolus regime group. Glucose 59-66 insulin Homo sapiens 368-375 26455610-19 2015 Studies that investigated paper nomogram directed continuous intravenous insulin compared to computer calculator directed continuous intravenous insulin demonstrated a statistically significant improved mean blood glucose levels (Weighted Means Differences -23.74, 95% Confidence Interval: -24.45 - -23.02), p <0.00001 and higher percentage of time in which glucose levels were within the target range in the computer calculator group. Glucose 214-221 insulin Homo sapiens 73-80 26455610-19 2015 Studies that investigated paper nomogram directed continuous intravenous insulin compared to computer calculator directed continuous intravenous insulin demonstrated a statistically significant improved mean blood glucose levels (Weighted Means Differences -23.74, 95% Confidence Interval: -24.45 - -23.02), p <0.00001 and higher percentage of time in which glucose levels were within the target range in the computer calculator group. Glucose 214-221 insulin Homo sapiens 145-152 26455610-19 2015 Studies that investigated paper nomogram directed continuous intravenous insulin compared to computer calculator directed continuous intravenous insulin demonstrated a statistically significant improved mean blood glucose levels (Weighted Means Differences -23.74, 95% Confidence Interval: -24.45 - -23.02), p <0.00001 and higher percentage of time in which glucose levels were within the target range in the computer calculator group. Glucose 361-368 insulin Homo sapiens 73-80 26068931-13 2015 CONCLUSIONS: ZAG inhibits insulin-induced glucose uptake in human adipocytes by impairing insulin signaling at the level of AKT in a beta2-AR- and PP2A-dependent manner. Glucose 42-49 insulin Homo sapiens 26-33 26052375-6 2015 Glucagon-like peptide-1 (GLP-1) is an intestinal mucosa-derived hormone which is secreted into the bloodstream in response to nutrient ingestion; it favors glucose-stimulated insulin secretion, inhibition of postprandial glucagon secretion and delayed gastric emptying. Glucose 156-163 insulin Homo sapiens 175-182 26110043-5 2015 The reduction of mtDNAn was strongly associated with insulin resistance (HOMA-IR: -0.703, p < 0.05; fasting insulin level: -0.015, p < 0.05); by contrast, the correlation between fasting glucose or lipid levels and mtDNAn was not significant. Glucose 193-200 insulin Homo sapiens 53-60 26061526-4 2015 Primary outcome was insulin sensitivity measured using intravenous glucose tolerance tests and Bergman"s minimal model. Glucose 67-74 insulin Homo sapiens 20-27 26047327-10 2015 Children who had both higher fasting insulin and weight at 5 years of age showed much higher levels of systolic blood pressures, fasting plasma glucose, the homeostasis model assessment for insulin resistance (HOMA-IR) and triglycerides at 10 years of age. Glucose 144-151 insulin Homo sapiens 37-44 26064180-4 2015 Subsequently, insulin-stimulated phosphorylation of Akt (pAkt) and glucose uptake were determined. Glucose 67-74 insulin Homo sapiens 14-21 26064180-7 2015 In contrast to M2 MVs, which enhanced the insulin-induced glucose uptake measured by 2-NBDG, M1 MVs decreased this effect in treated adipocytes. Glucose 58-65 insulin Homo sapiens 42-49 26110057-9 2015 Although plasma glucose levels remained unchanged, plasma insulin levels were significantly increased in the glucose tolerance test in 7-month-old SHRs. Glucose 109-116 insulin Homo sapiens 58-65 25118998-2 2015 IGF-1 can directly stimulate glucose transport into the muscle through either IGF-1 or insulin/IGF-1 hybrid receptors. Glucose 29-36 insulin Homo sapiens 87-94 26043030-5 2015 Longitudinal data in five patients with a decline in serum zinc over a two year follow up period (-19.0 +- 9.6 mug/dL), showed consistent increases in fasting glucose (3.6 +- 3.2 mg/dL) and insulin to glucose ratios at 120 min post glucose dose (p = 0.05). Glucose 159-166 insulin Homo sapiens 190-197 25381193-4 2015 RESULTS: Baseline first phase insulin response (sum of serum-insulin at 1 and 3 min during IvGTT; FPIR) <=3 muU/mL [HR 4.42 (CI 1.40-14.0) p = 0.011] and maximal plasma glucose >=11.1 mmol/L measured at 30, 60 and/or 90 min during OGTT [HR 6.13 (CI 1.79-21.0) p = 0.0039] were predictors for progression to diabetes. Glucose 172-179 insulin Homo sapiens 30-37 26191509-1 2015 Increasing evidence suggests an important role of the insulin-like growth factor (IGF)-IGF binding protein (IGFBP) axis in the maintenance of normal glucose and lipid metabolism. Glucose 149-156 insulin Homo sapiens 54-61 25864162-1 2015 AIMS: Intensive glucose control, often involving insulin treatment, failed to improve cardiovascular outcomes in several clinical trials. Glucose 16-23 insulin Homo sapiens 49-56 24993741-4 2015 In this study, we evaluated the effect of H. pylori eradication on insulin resistance in patients with normal blood glucose concentrations. Glucose 116-123 insulin Homo sapiens 67-74 24993741-12 2015 CONCLUSION: Eradication treatment has beneficial effects on insulin resistance in patients with normal glucose concentrations. Glucose 103-110 insulin Homo sapiens 60-67 24931756-3 2015 The aims of this study are to evaluate the incidence of hyperglycemic episodes and the need for exogenous insulin to maintain stable glucose levels in critically ill polytrauma patients supplemented with parenteral glutamine dipeptide (Dipeptiven( )) versus standard nutritional support. Glucose 133-140 insulin Homo sapiens 106-113 25576060-4 2015 Intranasal insulin transiently increased serum insulin levels followed by a gradual lowering of blood glucose in CON only. Glucose 102-109 insulin Homo sapiens 11-18 25605810-1 2015 A recent study identified a low-frequency variant at CCND2 associated with lower risk of type 2 diabetes, enhanced insulin response to a glucose challenge, higher height, and, paradoxically, higher BMI. Glucose 137-144 insulin Homo sapiens 115-122 26107810-9 2015 Moreover, compared to fructose, the increased rsFC after glucose positively correlated with the glucose-induced increase in insulin. Glucose 96-103 insulin Homo sapiens 124-131 25683256-5 2015 At molar increments of glucose, insulin concentrations were increased by 27% (p = 0.02), but ISR was unchanged. Glucose 23-30 insulin Homo sapiens 32-39 26107810-10 2015 Our findings suggest that glucose and fructose induce dissociable effects on rsFC within the basal ganglia/limbic network, which are probably mediated by different insulin levels. Glucose 26-33 insulin Homo sapiens 164-171 25694060-1 2015 AIMS: To assess the glucose-stimulated insulin secretion effect of imeglimin in patients with type 2 diabetes. Glucose 20-27 insulin Homo sapiens 39-46 25694060-6 2015 RESULTS: Imeglimin treatment for 7 days raised the insulin secretory response to glucose by +112% (iAUC0-45 , p = 0.035), first-phase ISR by +110% (p = 0.034) and second-phase ISR by +29% (p = 0.031). Glucose 81-88 insulin Homo sapiens 51-58 25694060-3 2015 Glucose-stimulated insulin secretion was assessed using a hyperglycaemic clamp. Glucose 0-7 insulin Homo sapiens 19-26 25818885-10 2015 This may provide some justification for earlier insulin introduction to improve glucose control to target. Glucose 80-87 insulin Homo sapiens 48-55 25716630-10 2015 Significant unadjusted results favoring treatment with insulin sensitizers were obtained for body mass index (BMI) (effect size [ES] of 0.58), waist to hip ratio (WHR) (ES of 0.02), low-density-lipoprotein cholesterol (LDL-C) (ES of 0.11), fasting insulin (ES of 2.82), fasting glucose (ES of 0.10), free testosterone (ES of 1.88), and androstenedione level (ES of 0.76). Glucose 278-285 insulin Homo sapiens 55-62 26124996-5 2015 WC was measured at the midpoint between the lower rib and the iliac crest, and insulin sensitivity was assessed by the rate constant of plasma glucose disappearance (Kitt %/min) using an insulin tolerance test. Glucose 143-150 insulin Homo sapiens 79-86 28834658-5 2015 Insulin sensitivity was assessed by intravenous glucose tolerance tests and minimal modelling analysis. Glucose 48-55 insulin Homo sapiens 0-7 25506681-2 2015 In this study, we aimed to examine the shape of plasma glucose response curves and study their relationship with insulin sensitivity, insulin secretion and components of the metabolic syndrome in end-pubertal obese girls. Glucose 55-62 insulin Homo sapiens 113-120 25716630-11 2015 CONCLUSION: Treatment with insulin sensitizers in women with PCOS results in improvement in CV factors such as BMI, WHR, LDL-C, fasting insulin, glucose, free testosterone, and androstenedione. Glucose 145-152 insulin Homo sapiens 27-34 25716635-12 2015 Additional studies are needed to determine appropriate insulin adjustments based on glucose trend data. Glucose 84-91 insulin Homo sapiens 55-62 26136963-6 2015 The drug and insulin doses in the treatment group were adjusted according to the patients" blood glucose, which allowed the fasting and postprandial blood glucose levels to attain the standards. Glucose 97-104 insulin Homo sapiens 13-20 26136963-6 2015 The drug and insulin doses in the treatment group were adjusted according to the patients" blood glucose, which allowed the fasting and postprandial blood glucose levels to attain the standards. Glucose 155-162 insulin Homo sapiens 13-20 25506681-7 2015 In conclusion, end-pubertal obese girls with a monophasic plasma glucose curve are at increased risk for insulin resistance, which can contribute to the development of type 2 diabetes mellitus and cardiovascular diseases. Glucose 65-72 insulin Homo sapiens 105-112 25630536-1 2015 Advances in cell-replacement strategies for diabetes have focused on renewable sources of glucose-responsive, insulin-producing cells (IPCs). Glucose 90-97 insulin Homo sapiens 110-117 25630536-7 2015 Cellular clusters were also able to secrete detectable amounts of insulin and C-peptide in a glucose dose-dependent manner. Glucose 93-100 insulin Homo sapiens 66-73 25630536-7 2015 Cellular clusters were also able to secrete detectable amounts of insulin and C-peptide in a glucose dose-dependent manner. Glucose 93-100 insulin Homo sapiens 78-87 25904635-13 2015 A variant rs705702-G near RAB5B and SUOX was associated with insulin (-0.16 +- 0.05, P = 0.0029) and glucose levels (-0.20 +- 0.05, P = 0.0002) 120 min after an oral glucose test. Glucose 166-173 insulin Homo sapiens 61-68 25904635-18 2015 The relationship between a variant near RAB5B and SUOX and glucose stimulated insulin and glucose levels suggests an influence of one of these genes on glucose tolerance, but the absence of a relationship with PCOS points to potential differences in the international PCOS patient populations. Glucose 59-66 insulin Homo sapiens 78-85 25966806-1 2015 PURPOSE: In patients with type 2 diabetes mellitus (DM), insulin-stimulated glucose uptake is impaired. Glucose 76-83 insulin Homo sapiens 57-64 25825943-9 2015 Fasting EGP and insulin-mediated glucose disposal did not differ significantly, but EGP during hyperinsulinemia was greater (0.60 +- 0.07 vs 0.46 +- 0.06 mg/kg/min; P = .013) with the high-fructose diet, suggesting blunted suppression of EGP. Glucose 33-40 insulin Homo sapiens 16-23 25875045-4 2015 Stimulation of CRFR2 by urocortin 2 (Ucn 2), a CRFR2-selective ligand, in C2C12 myotubes greatly attenuated insulin-induced glucose uptake. Glucose 124-131 insulin Homo sapiens 108-115 25602348-2 2015 More specifically it has been suggested that TLQP-21 has the ability to enhance glucose stimulated insulin secretion, making it a candidate for treatment of patients with type 2 diabetes.In this study, we investigated the impact of TLQP-21 on insulin, glucagon, and somatostatin secretion in the perfused rat pancreas. Glucose 80-87 insulin Homo sapiens 99-106 25602348-4 2015 Increasing TLQP-21 (200 nM) and glucose concentration (3.5 and 16 mM) led to a nonsignificant decrease in glucagon secretion, though insulin and somatostatin secretory patterns remained unaffected. Glucose 32-39 insulin Homo sapiens 133-140 25781493-1 2015 BACKGROUND: The objective of this study was to determine whether glucose tolerance status influences the associations between serum 25-hydroxyvitamin D [25(OH)D], insulin sensitivity, insulin secretion, and beta-cell function. Glucose 65-72 insulin Homo sapiens 163-170 25781493-8 2015 CONCLUSION: Vitamin D and glucose tolerance status are both independently associated with measures of insulin sensitivity, insulin secretion, and beta-cell function. Glucose 26-33 insulin Homo sapiens 102-109 25801485-12 2015 Hence insulin, as it promotes the absorption of glucose, is set in the center of interest regarding hypoxic conditions. Glucose 48-55 insulin Homo sapiens 6-13 25875045-1 2015 Type 2 corticotropin-releasing factor receptor (CRFR2) is expressed in skeletal muscle and stimulation of the receptor has been shown to inhibit the effect of insulin on glucose uptake in muscle cells. Glucose 170-177 insulin Homo sapiens 159-166 26627219-2 2015 This review examines the extent to which biological differences in glucose metabolism, specifically insulin resistance and beta cell function (BCF), contribute to this disparity. Glucose 67-74 insulin Homo sapiens 100-107 26627223-4 2015 In patients with T2DM, weight loss improves glycemia, while reducing the need for conventional glucose-lowering medicines, by affecting all three processes that produce and sustain the hyperglycemic state, namely via increments in peripheral insulin sensitivity with improvements in insulin signal transduction at the cellular level, more robust insulin secretory responses, and reduced rates of hepatic glucose production. Glucose 404-411 insulin Homo sapiens 283-290 26627223-4 2015 In patients with T2DM, weight loss improves glycemia, while reducing the need for conventional glucose-lowering medicines, by affecting all three processes that produce and sustain the hyperglycemic state, namely via increments in peripheral insulin sensitivity with improvements in insulin signal transduction at the cellular level, more robust insulin secretory responses, and reduced rates of hepatic glucose production. Glucose 404-411 insulin Homo sapiens 283-290 26093759-14 2015 The patient"s insulin requirement gradually decreased to one-half of the primary dose over the following several days, and he was discharged on day 10 with successful serum glucose regulation. Glucose 173-180 insulin Homo sapiens 14-21 25899916-2 2015 At altitude, his blood glucose levels began to rise, necessitating increased insulin delivery. Glucose 23-30 insulin Homo sapiens 77-84 26023321-0 2015 Insulin stimulates SGLT2-mediated tubular glucose absorption via oxidative stress generation. Glucose 42-49 insulin Homo sapiens 0-7 26023321-7 2015 An anti-oxidant, N-acetylcysteine completely blocked insulin-induced up-regulation of SGLT2 as well as increase in glucose absorption by tubular cells. Glucose 115-122 insulin Homo sapiens 53-60 26023321-9 2015 CONCLUSIONS: Our present study demonstrated that insulin could stimulate SGLT-2-mediated glucose entry into cultured proximal tubular cells via oxidative stress generation. Glucose 89-96 insulin Homo sapiens 49-56 25986700-5 2015 Additionally, we examined the role of inducible nitric oxide synthase (iNOS or NOS2), the source of the increase in NO availability, in modulating LPS-induced decrease in insulin-stimulated muscle glucose uptake (MGU). Glucose 197-204 insulin Homo sapiens 171-178 25986700-6 2015 METHODS: The impact of NO donor infusion on insulin-stimulated whole-body and muscle glucose uptake (hyperinsulinemic-euglycemic clamps), and the cardiovascular system was assessed in chronically catheterized, conscious mice wild-type (WT) mice. Glucose 85-92 insulin Homo sapiens 44-51 25993479-9 2015 C-peptide also reduced proteinuria (mean difference, -186.25 mg/day, p = 0.05), glomerular volume (p<0.00001), and mesangial matrix area (p<0.00001) in diabetic animals without affecting blood pressure or plasma glucose. Glucose 218-225 insulin Homo sapiens 0-9 25941364-8 2015 Ingestion of fructose relative to glucose resulted in smaller increases in plasma insulin levels and greater brain reactivity to food cues in the visual cortex (in whole-brain analysis) and left orbital frontal cortex (in region-of-interest analysis). Glucose 34-41 insulin Homo sapiens 82-89 25985092-2 2015 We compared responses of plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin and glucagon, and blood glucose to a standardised glucose infusion into the proximal jejunum and duodenum in healthy humans. Glucose 65-72 insulin Homo sapiens 83-90 25985092-9 2015 glucose elicits greater incretin hormone and insulin secretion than intraduodenal glucose in healthy humans, suggesting regional specificity of the gut-incretin axis. Glucose 0-7 insulin Homo sapiens 45-52 25986628-0 2015 Use of a Combined Blood-Glucose- and ss-Ketone-Measuring Device Improves Glycemic Control in Insulin-Treated Patients With Diabetes: The Gold Plus Study. Glucose 24-31 insulin Homo sapiens 93-100 25796170-6 2015 FU increased the insulin-provoked glucose uptake in insulin-resistant HepG2 cells, and also reduced blood glucose and lipid levels of type 2 diabetic KKAy mice. Glucose 34-41 insulin Homo sapiens 17-24 25796170-6 2015 FU increased the insulin-provoked glucose uptake in insulin-resistant HepG2 cells, and also reduced blood glucose and lipid levels of type 2 diabetic KKAy mice. Glucose 34-41 insulin Homo sapiens 52-59 25987960-2 2015 This helps the delivery of insulin itself but also that of substrates and of other signalling molecules to multiple tissues beds and facilitates glucose disposal and lipid kinetics. Glucose 145-152 insulin Homo sapiens 27-34 25972281-1 2015 Because of its ease and simplicity of its measurement, the morning fasting plasma glucose (FPG), has been as used a surrogate marker for the entire basal day when titrating once-nightly basal insulin. Glucose 82-89 insulin Homo sapiens 192-199 25969463-1 2015 Insulin- and contraction-stimulated increases in glucose uptake into skeletal muscle occur in part as a result of the translocation of glucose transporter 4 (GLUT4) from intracellular stores to the plasma membrane (PM). Glucose 49-56 insulin Homo sapiens 0-7 25961164-3 2015 We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. Glucose 62-69 insulin Homo sapiens 43-50 25943590-12 2015 CONCLUSIONS: The majority of insulin dose calculator apps provide no protection against, and may actively contribute to, incorrect or inappropriate dose recommendations that put current users at risk of both catastrophic overdose and more subtle harms resulting from suboptimal glucose control. Glucose 278-285 insulin Homo sapiens 29-36 26005328-12 2015 Both pharmacokinetic and pharmacodynamic actions of insulin were altered when different initial blood glucose levels of STZ diabetic rats were selected for testing. Glucose 102-109 insulin Homo sapiens 52-59 25725372-5 2015 Treatment of 3T3-L1 adipocytes with exogenous tmTNF-alpha promoted insulin-induced phosphorylation of IRS-1 and Akt, facilitated GLUT4 expression and membrane translocation, and increased glucose uptake while addition of sTNF-alpha resulted in the opposite effect. Glucose 188-195 insulin Homo sapiens 67-74 25941189-9 2015 The primary outcome will be the change in insulin sensitivity before and after 6 months of acupuncture treatment, as measured by an oral glucose tolerance test. Glucose 137-144 insulin Homo sapiens 42-49 25908470-4 2015 This resistance to insulin at the level of skeletal muscle tissue impairs glucose disposal/utilization through actions on the endothelium that include vascular rarefaction, reductions in vascular relaxation, and vascular remodeling. Glucose 74-81 insulin Homo sapiens 19-26 25394335-3 2015 Insulin sensitivity was assessed by the Matsuda method from an oral glucose tolerance test. Glucose 68-75 insulin Homo sapiens 0-7 25875045-5 2015 The inhibitory effect of CRFR2 signaling required cAMP production and is involved the mammalian target of rapamycine pathway, as rapamycin reversed the inhibitory effect of CRFR2 stimulation on insulin-induced glucose uptake. Glucose 210-217 insulin Homo sapiens 194-201 25875045-9 2015 In conclusion, the inhibitory effect of CRFR2 signaling on insulin action is mediated by cAMP in a mammalian target of rapamycine-dependent manner, and IRS-1 is a key nodal point where CRFR2 signaling modulates insulin-stimulated glucose uptake in muscle cells. Glucose 230-237 insulin Homo sapiens 59-66 25875045-9 2015 In conclusion, the inhibitory effect of CRFR2 signaling on insulin action is mediated by cAMP in a mammalian target of rapamycine-dependent manner, and IRS-1 is a key nodal point where CRFR2 signaling modulates insulin-stimulated glucose uptake in muscle cells. Glucose 230-237 insulin Homo sapiens 211-218 25424358-5 2015 Three patients had a glucose level <3.9 mmol/L, which was corrected after adjusting the dose of insulin infusion. Glucose 21-28 insulin Homo sapiens 99-106 25407468-8 2015 Overall, the ketosis-prone diabetes - insulin group had a higher BMI (P = 0.018), yet a lower fasting glucose concentration (P = 0.003) compared with the ketosis-prone diabetes + insulin group. Glucose 102-109 insulin Homo sapiens 38-45 25944628-5 2015 Insulin resistance was associated with CVD risk after adjusting for age and race/ethnicity with hazard ratios (95% confidence interval [CI]) per doubling in insulin of 1.21 (CI, 1.12-1.31), in HOMA-IR of 1.19 (CI, 1.11-1.28), in TG/HDL-C of 1.35 (CI, 1.26-1.45), and for impaired fasting glucose of 1.31 (CI, 1.05-1.64). Glucose 288-295 insulin Homo sapiens 0-7 25944628-5 2015 Insulin resistance was associated with CVD risk after adjusting for age and race/ethnicity with hazard ratios (95% confidence interval [CI]) per doubling in insulin of 1.21 (CI, 1.12-1.31), in HOMA-IR of 1.19 (CI, 1.11-1.28), in TG/HDL-C of 1.35 (CI, 1.26-1.45), and for impaired fasting glucose of 1.31 (CI, 1.05-1.64). Glucose 288-295 insulin Homo sapiens 157-164 25388434-3 2015 Intraduodenal glucose was infused at 2 kcal/min (60 g over 120 min), and blood pressure, heart rate, plasma glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide (total and intact), glucose, insulin and glucagon responses were evaluated. Glucose 136-143 insulin Homo sapiens 154-161 25388434-4 2015 RESULTS: In response to intraduodenal glucose infusion, heart rate (treatment effect: P = 0.001) and serum insulin concentration (treatment x time interaction: P = 0.041) were higher after sitagliptin treatment than placebo, without a significant difference in blood pressure, plasma glucagon or glucose. Glucose 38-45 insulin Homo sapiens 107-114 25475435-1 2015 Increased plasma branched-chain amino acid concentrations are associated with insulin resistance, and intravenous amino acid infusion blunts insulin-mediated glucose disposal. Glucose 158-165 insulin Homo sapiens 141-148 25475435-2 2015 We tested the hypothesis that protein ingestion impairs insulin-mediated glucose disposal by leucine-mediated mTOR signaling, which can inhibit AKT. Glucose 73-80 insulin Homo sapiens 56-63 25475435-5 2015 Whey protein ingestion decreased insulin-mediated glucose disposal (median 38.8 [quartiles 30.8, 61.8] vs. 51.9 [41.0, 77.3] micromol glucose/microU insulin mL(-1) min(-1); P < 0.01), whereas ingestion of leucine did not (52.3 [43.3, 65.4] vs. 52.3 [43.9, 73.2]). Glucose 50-57 insulin Homo sapiens 33-40 25484175-6 2015 After 16 weeks with muraglitazar, fasting plasma glucose declined by 31%, fasting plasma insulin decreased by 44%, insulin-stimulated glucose disposal increased by 81%, HbA1c decreased by 21% and plasma triglyceride decreased by 39% (all P < 0.05). Glucose 134-141 insulin Homo sapiens 115-122 25407468-10 2015 At 24 months, in spite of the higher BMI in the ketosis-prone diabetes - insulin group, mixed-meal tolerance test glucose and leptin concentrations were significantly lower (P < 0.0001 and P = 0.017, respectively), while adiponectin levels were higher (P = 0.023) compared with the ketosis-prone diabetes + insulin group. Glucose 114-121 insulin Homo sapiens 73-80 25407468-11 2015 CONCLUSIONS: In spite of the higher BMI in the ketosis-prone diabetes - insulin group, lower leptin and higher adiponectin levels may contribute to improved beta-cell function and insulin sensitivity, as evidenced by lower glucose and higher C-peptide levels. Glucose 223-230 insulin Homo sapiens 72-79 25492378-7 2015 RESULTS: The proportion of time when sensor glucose was in the target range (3.9-8.0 mmol/l) overnight (between 24:00 and 08:00 hours) was 18.5% greater during closed-loop insulin delivery than during sensor-augmented therapy (p < 0.001). Glucose 44-51 insulin Homo sapiens 172-179 25580665-4 2015 RESULTS: Glucose concentration decreased after insulin treatment as a result of suppression of endogenous glucose production, which occurred to a similar extent with both detemir and NPH insulin. Glucose 9-16 insulin Homo sapiens 47-54 25492378-10 2015 Lower mean overnight glucose levels during closed-loop therapy were brought about by increased overnight insulin delivery (p < 0.001) without changes to the total daily delivery (p = 0.84). Glucose 21-28 insulin Homo sapiens 105-112 25492378-11 2015 CONCLUSION: Overnight closed-loop insulin therapy at home in adults and adolescents with type 1 diabetes is feasible, showing improvements in glucose control and reducing the risk of nocturnal hypoglycaemia. Glucose 142-149 insulin Homo sapiens 34-41 25495067-7 2015 Ninety per cent of patients with duration <= 4 years and fasting glucose <= 8.0 mmol/l responded to intensive insulin therapy. Glucose 68-75 insulin Homo sapiens 116-123 25495067-9 2015 CONCLUSION: At baseline, shorter duration of diabetes and lower fasting glucose can identify patients most likely to benefit from short-term intensive insulin therapy. Glucose 72-79 insulin Homo sapiens 151-158 25580665-4 2015 RESULTS: Glucose concentration decreased after insulin treatment as a result of suppression of endogenous glucose production, which occurred to a similar extent with both detemir and NPH insulin. Glucose 106-113 insulin Homo sapiens 47-54 25611577-1 2015 BACKGROUND: The automatic Threshold Suspend (TS) feature of the MiniMed 530G system (Medtronic MiniMed, Inc., Northridge, CA), when enabled, suspends insulin delivery for up to 2 h when the sensor glucose (SG) value reaches a preset threshold. Glucose 197-204 insulin Homo sapiens 150-157 25785658-1 2015 BACKGROUND: Little is known about the influence of exogenous insulin and actual glucose levels on the release of endogenous insulin in insulin-treated type 2 diabetes mellitus (T2DM) patients. Glucose 80-87 insulin Homo sapiens 124-131 25622214-0 2015 A web-based study of the relationship of duration of insulin pump infusion set use and fasting blood glucose level in adults with type 1 diabetes. Glucose 101-108 insulin Homo sapiens 53-60 25626737-0 2015 Engineered commensal bacteria reprogram intestinal cells into glucose-responsive insulin-secreting cells for the treatment of diabetes. Glucose 62-69 insulin Homo sapiens 81-88 25892446-0 2015 Continuous glucose monitoring used with an insulin pump: should we recommend it to people with diabetes and can we afford it? Glucose 11-18 insulin Homo sapiens 43-50 25710929-0 2015 SIRT1 attenuates high glucose-induced insulin resistance via reducing mitochondrial dysfunction in skeletal muscle cells. Glucose 22-29 insulin Homo sapiens 38-45 25631620-1 2015 AIMS/HYPOTHESIS: The intestine is the main site for glucose absorption and it has been suggested that it exhibits insulin resistance. Glucose 52-59 insulin Homo sapiens 114-121 25631620-3 2015 Our aim was to evaluate the effects of insulin on intestinal glucose metabolism before and after bariatric surgery. Glucose 61-68 insulin Homo sapiens 39-46 25710929-2 2015 Sustained high glucose is an important extracellular environment that induces insulin resistance. Glucose 15-22 insulin Homo sapiens 78-85 25710929-6 2015 Here, we demonstrate that pcDNA3.1 vector-mediated overexpression of SIRT1 attenuates insulin resistance in the high glucose-induced insulin-resistant skeleton muscle cells. Glucose 117-124 insulin Homo sapiens 86-93 24956470-3 2015 This is achieved by means of applying a retrospective optimization of the insulin bolus therapy using a novel combination of run-to-run (R2R) that uses intermittent continuous glucose monitoring data, and case-based reasoning (CBR). Glucose 176-183 insulin Homo sapiens 74-81 25816888-4 2015 Insulin degludec effectively reduces fasting plasma glucose, but carries the risk of hypoglycemia and body weight gain. Glucose 52-59 insulin Homo sapiens 0-7 26120328-0 2015 Impacts of insulin infusion protocol on blood glucose level and outcomes in acute coronary syndrome patients with diabetes mellitus. Glucose 46-53 insulin Homo sapiens 11-18 26120328-3 2015 The aim of this study was to investigate the impact of insulin infusion protocol and conventional therapy on the blood glucose level and outcomes in acute coronary syndrome patients with diabetes mellitus. Glucose 119-126 insulin Homo sapiens 55-62 25603459-0 2015 A novel insulin resistance index to monitor changes in insulin sensitivity and glucose tolerance: the ACT NOW study. Glucose 79-86 insulin Homo sapiens 8-15 25959645-3 2015 Insulin degludec is a new-generation basal insulin analog with an ultra-long duration of action and low day-to-day and hour-to-hour intrapatient variability in blood glucose-lowering action. Glucose 166-173 insulin Homo sapiens 0-7 25675382-9 2015 Two months after initiation of rituximab therapy, fasting glucose levels ranged from 80 to 110 mg/dL and could be controlled with very low insulin doses. Glucose 58-65 insulin Homo sapiens 139-146 25883166-0 2015 Improved Postprandial Glucose Control Using the InsuPad Device in Insulin-Treated Type 2 Diabetes: Injection Site Warming to Improve Glycemic Control. Glucose 22-29 insulin Homo sapiens 66-73 25652563-3 2015 This study tested the hypothesis that improved glucose control, rather than insulin dose, is central to reduced oxidative stress in patients with type 2 diabetes following continuous subcutaneous insulin infusion (CSII). Glucose 47-54 insulin Homo sapiens 196-203 25883166-7 2015 DISCUSSION AND CONCLUSIONS: Use of the InsuPad to increase the rate of insulin absorption provides an effective means to achieve better control of postmeal glucose excursions in type 2 diabetic patients receiving premeal injections of rapid-acting insulin analogs. Glucose 156-163 insulin Homo sapiens 71-78 25883166-7 2015 DISCUSSION AND CONCLUSIONS: Use of the InsuPad to increase the rate of insulin absorption provides an effective means to achieve better control of postmeal glucose excursions in type 2 diabetic patients receiving premeal injections of rapid-acting insulin analogs. Glucose 156-163 insulin Homo sapiens 248-255 25687124-6 2015 Insulin sensitivity (SI) and the acute insulin response to glucose (AIRg) were measured using minimal model and beta-cell function was determined by disposition index (DI = S I*AIRg). Glucose 59-66 insulin Homo sapiens 39-46 25324439-1 2015 OBJECTIVE: Omentin, a newly identified adipokine, enhances insulin mediated glucose uptake in human adipocytes, thus, inducing systemic insulin-sensitizing effect. Glucose 76-83 insulin Homo sapiens 59-66 25324439-1 2015 OBJECTIVE: Omentin, a newly identified adipokine, enhances insulin mediated glucose uptake in human adipocytes, thus, inducing systemic insulin-sensitizing effect. Glucose 76-83 insulin Homo sapiens 136-143 25332294-0 2015 Insulin secretion response during oral glucose tolerance test is related to low cardiorespiratory fitness in obese adolescents. Glucose 39-46 insulin Homo sapiens 0-7 25747336-3 2015 Furthermore, PTEN lies upstream of Akt kinase, a key enzyme in insulin signalling regulating glucose uptake and cell growth. Glucose 93-100 insulin Homo sapiens 63-70 26020396-9 2015 Analysis of glucose and insulin values during OGTT revealed a reduction of both glucose (303.9 +- 73.4 mg/dL min versus 269.2 +- 69.5 mg/dL min, P = 0.009) and insulin (208.4 +- 119.7 mg/dL min versus 158.0 +- 95.3 mg/dL min, P = 0.01) area under the curves (AUCs). Glucose 12-19 insulin Homo sapiens 160-167 26020396-9 2015 Analysis of glucose and insulin values during OGTT revealed a reduction of both glucose (303.9 +- 73.4 mg/dL min versus 269.2 +- 69.5 mg/dL min, P = 0.009) and insulin (208.4 +- 119.7 mg/dL min versus 158.0 +- 95.3 mg/dL min, P = 0.01) area under the curves (AUCs). Glucose 80-87 insulin Homo sapiens 24-31 25695910-7 2015 Activation of MT signaling in human islets was shown to restore glucose-stimulated insulin secretion in islets exposed to chronic hyperglycemia as well as in T2DM islets. Glucose 64-71 insulin Homo sapiens 83-90 25712349-1 2015 SCOPE: Insulin-regulated glucose metabolism in cells is critical for proper metabolic functioning, and insulin resistance leads to type 2 diabetes. Glucose 25-32 insulin Homo sapiens 7-14 26137438-9 2015 Moreover, responsiveness of blood glucose levels to injected insulin was improved by streptozotocin and diazoxide treatments of obese mice without changes in body weight. Glucose 34-41 insulin Homo sapiens 61-68 25894829-1 2015 Type 2 diabetes (T2D) is characterized by chronic hyperglycemia resulting from a deficiency in insulin signaling, because of insulin resistance and/or defects in insulin secretion; it is also associated with increases in glucagon and endogenous glucose production (EGP). Glucose 245-252 insulin Homo sapiens 95-102 25770760-6 2015 Insulin resistance was estimated (estimated glucose disposal rate). Glucose 44-51 insulin Homo sapiens 0-7 25813686-3 2015 Insulin secretion was assessed using indexes derived from oral glucose tolerance test (OGTT) in the whole study group and from intravenous glucose tolerance test (IVGTT) in a subgroup (n = 110). Glucose 63-70 insulin Homo sapiens 0-7 25813686-3 2015 Insulin secretion was assessed using indexes derived from oral glucose tolerance test (OGTT) in the whole study group and from intravenous glucose tolerance test (IVGTT) in a subgroup (n = 110). Glucose 139-146 insulin Homo sapiens 0-7 24754380-9 2015 Adolescents with NAFLD had lower (p < 0.05) insulin-stimulated glucose disposal and lower peripheral IS compared with those without NAFLD. Glucose 66-73 insulin Homo sapiens 47-54 25952934-3 2015 This was a cross-sectional study of 182 nondiabetic individuals (118 women and 64 men) who had measurement of 24 AAs and steady-state plasma glucose (SSPG) concentration (insulin resistance) using the insulin suppression test. Glucose 141-148 insulin Homo sapiens 171-178 26034806-13 2015 A daily injection of long-acting insulin, added to on-going oral glucose-lowering therapy, lowers HbA1c by 0.7% to 2.5% on average but causes weight gain and increases the risk of hypoglycaemia. Glucose 65-72 insulin Homo sapiens 33-40 25627966-1 2015 The structure of insulin, a glucose homeostasis-controlling hormone, is highly conserved in all vertebrates and stabilized by three disulfide bonds. Glucose 28-35 insulin Homo sapiens 17-24 25348129-7 2015 Insulin resistance was quantified by determining steady-state plasma glucose (SSPG) concentrations during the insulin suppression test. Glucose 69-76 insulin Homo sapiens 0-7 25870289-7 2015 Third, these variations in glucose tolerance appeared to be explained, at least in part, by different mechanisms: during the biological evening by decreased pancreatic beta-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without change in early-phase insulin. Glucose 27-34 insulin Homo sapiens 210-217 25870289-7 2015 Third, these variations in glucose tolerance appeared to be explained, at least in part, by different mechanisms: during the biological evening by decreased pancreatic beta-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without change in early-phase insulin. Glucose 27-34 insulin Homo sapiens 277-284 25870289-7 2015 Third, these variations in glucose tolerance appeared to be explained, at least in part, by different mechanisms: during the biological evening by decreased pancreatic beta-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without change in early-phase insulin. Glucose 27-34 insulin Homo sapiens 277-284 25870289-7 2015 Third, these variations in glucose tolerance appeared to be explained, at least in part, by different mechanisms: during the biological evening by decreased pancreatic beta-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without change in early-phase insulin. Glucose 27-34 insulin Homo sapiens 277-284 25762724-9 2015 The results indicate that ISG phospholipids are in a dynamic state and are consistent with the idea that changes in ISG phospholipids facilitate fusion of ISG with the plasma membrane-enhancing glucose-stimulated insulin exocytosis. Glucose 194-201 insulin Homo sapiens 213-220 25792745-0 2015 Insulin and Insulin-like Growth Factor 1 (IGF-1) Modulate Cytoplasmic Glucose and Glycogen Levels but Not Glucose Transport across the Membrane in Astrocytes. Glucose 70-77 insulin Homo sapiens 0-7 25792745-8 2015 Stimulation of cells with insulin and IGF-1 decreased cytosolic glucose concentration, likely because of elevated glucose utilization for glycogen synthesis. Glucose 64-71 insulin Homo sapiens 26-33 25792745-8 2015 Stimulation of cells with insulin and IGF-1 decreased cytosolic glucose concentration, likely because of elevated glucose utilization for glycogen synthesis. Glucose 114-121 insulin Homo sapiens 26-33 29371512-8 2015 Results: Serum glucose was positively correlated with beta2M, insulin and HOMA-IR (r = 0.361, p = 0.002, r = 0.581, p = 0.001 and r = 0.753, p = 0.001 respectively). Glucose 15-22 insulin Homo sapiens 62-69 25922828-3 2015 We studied the relationship between glycemic control defined by glucose serum concentrations and insulin resistance, beta2M and markers of inflammation in patients on renal replacement therapies with or/and without diabetes mellitus. Glucose 64-71 insulin Homo sapiens 97-104 25922828-8 2015 Insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR).We examined the association of elevated serum glucose with inflammatory factors and we built a multivariable model to investigate if glucose could be a potential determinant of beta2M serum levels. Glucose 238-245 insulin Homo sapiens 0-7 25922828-8 2015 Insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR).We examined the association of elevated serum glucose with inflammatory factors and we built a multivariable model to investigate if glucose could be a potential determinant of beta2M serum levels. Glucose 238-245 insulin Homo sapiens 76-83 25898056-0 2015 MiniMed 530G: an insulin pump with low-glucose suspend automation. Glucose 39-46 insulin Homo sapiens 17-24 25873144-11 2015 Patients will be trained to adjust their insulin dose according to carbohydrate intake and blood glucose level. Glucose 97-104 insulin Homo sapiens 41-48 26131263-0 2015 Insulin secretion and tolerance of women with different gestational glucose regulation one year postpartum. Glucose 68-75 insulin Homo sapiens 0-7 25897360-8 2015 Glucose stimulation causes insulin exocytosis. Glucose 0-7 insulin Homo sapiens 27-34 25875935-2 2015 Insulin leads to high expression and activity of human cationic amino acid transporter 1 (hCAT-1), NO synthesis and vasodilation; thus, a protective role of insulin on high D-glucose-alterations in endothelial function is likely. Glucose 173-182 insulin Homo sapiens 157-164 25897356-4 2015 If beta-cell functioning is impaired, it results in an under production of insulin, impairs glucose stimulated insulin secretion, fasting hyperglycemia and eventually the development of T2DM. Glucose 92-99 insulin Homo sapiens 75-82 25875935-0 2015 Insulin reverses D-glucose-increased nitric oxide and reactive oxygen species generation in human umbilical vein endothelial cells. Glucose 17-26 insulin Homo sapiens 0-7 25875935-2 2015 Insulin leads to high expression and activity of human cationic amino acid transporter 1 (hCAT-1), NO synthesis and vasodilation; thus, a protective role of insulin on high D-glucose-alterations in endothelial function is likely. Glucose 173-182 insulin Homo sapiens 0-7 25875935-7 2015 High D-glucose-increased maximal transport velocity was blocked by insulin and correlated with lower hCAT-1 expression and SLC7A1 gene promoter activity. Glucose 5-14 insulin Homo sapiens 67-74 25875935-10 2015 Insulin, but not apocynin or tempol reversed high D-glucose-increased NO synthesis; however, tempol and Mn(III)TMPyP reversed the high D-glucose-reduced BH4 level. Glucose 50-59 insulin Homo sapiens 0-7 25875935-11 2015 Insulin and tempol blocked the high D-glucose-increased p42/44mapk phosphorylation. Glucose 36-45 insulin Homo sapiens 0-7 25875935-12 2015 Vascular dysfunction caused by high D-glucose is likely attenuated by insulin through the L-arginine/NO and O2 -/NADPH oxidase pathways. Glucose 36-45 insulin Homo sapiens 70-77 25735975-0 2015 Promotion of insulin-induced glucose uptake in C2C12 myotubes by osteocalcin. Glucose 29-36 insulin Homo sapiens 13-20 25701779-2 2015 Several studies reported mutations in mitochondrial genes as potentially pathogenic for diabetes, since mitochondrial oxidative phosphorylation plays an important role in glucose-stimulated insulin secretion from beta cells. Glucose 171-178 insulin Homo sapiens 190-197 25735975-7 2015 Furthermore, cell treatment with GluOC for a long period promoted insulin-induced Akt phosphorylation and glucose uptake in the myotubes, which was abolished by ERK signaling inhibition. Glucose 106-113 insulin Homo sapiens 66-73 26029722-2 2015 The initial liver cell line (Huh7ins) commenced secretion of insulin in response to a glucose concentration of 2.5 mmol/l. Glucose 86-93 insulin Homo sapiens 61-68 26029722-3 2015 After transfection of the Huh7ins cells with human islet glucokinase, the resultant Melligen cells secreted insulin in response to glucose within the physiological range; commencing at 4.25 mmol/l. Glucose 131-138 insulin Homo sapiens 108-115 25853252-0 2015 Both fasting and glucose-stimulated proinsulin levels predict hyperglycemia and incident type 2 diabetes: a population-based study of 9,396 Finnish men. Glucose 17-24 insulin Homo sapiens 36-46 25853252-9 2015 CONCLUSION: Our results suggest that proinsulin in the fasting state and after an oral glucose load similarly predict the worsening of hyperglycemia and conversion to type 2 diabetes. Glucose 87-94 insulin Homo sapiens 37-47 25460870-4 2015 RESULTS: Insulin infusion for 13.0 +- 0.8 (standard error of the mean) hours decreased blood glucose level from 16.6 +- 1.6 mmol/L to 8.7 +- 1.4 mmol/L (P = .002). Glucose 93-100 insulin Homo sapiens 9-16 25849815-10 2015 One standard deviation difference in BMI, visceral adipose tissue, waist circumference, waist/height ratio and body fat percentage corresponded approximately to 0.2mmol/l higher fasting glucose, 0.7mmol/l higher 2-hr glucose, 0.06-0.1% higher HbA1c, 30 % lower HOMA index of insulin sensitivity, 20% lower Gutt"s index of insulin sensitivity, and 100 unit higher Stumvoll"s index of beta-cell function. Glucose 186-193 insulin Homo sapiens 275-282 25849815-10 2015 One standard deviation difference in BMI, visceral adipose tissue, waist circumference, waist/height ratio and body fat percentage corresponded approximately to 0.2mmol/l higher fasting glucose, 0.7mmol/l higher 2-hr glucose, 0.06-0.1% higher HbA1c, 30 % lower HOMA index of insulin sensitivity, 20% lower Gutt"s index of insulin sensitivity, and 100 unit higher Stumvoll"s index of beta-cell function. Glucose 186-193 insulin Homo sapiens 322-329 25836621-1 2015 OBJECTIVE: To analyze the mechanism of neuroprotection of insulin and which blood glucose range was benefit for insulin exerting neuroprotective action. Glucose 82-89 insulin Homo sapiens 112-119 25727015-1 2015 Pancreatic beta-cells fire action potentials as do cardiac cells and neurons, and electrical activity plays a central role in glucose-stimulated insulin secretion, which is disturbed in diabetes. Glucose 126-133 insulin Homo sapiens 145-152 25430705-1 2015 AIMS: Insulin degludec is a new-generation ultra-long-acting basal insulin which offers a significantly more predictable glucose-lowering effect than other long-acting insulin analogues. Glucose 121-128 insulin Homo sapiens 6-13 25430705-1 2015 AIMS: Insulin degludec is a new-generation ultra-long-acting basal insulin which offers a significantly more predictable glucose-lowering effect than other long-acting insulin analogues. Glucose 121-128 insulin Homo sapiens 67-74 25788506-7 2015 When compared with regular sliding-scale insulin (SSI), fixed-dose insulin glargine with or without insulin glulisine was found to reduce the blood glucose concentration in patients with type 2 diabetes and reduce postoperative complications in surgical patients with diabetes. Glucose 148-155 insulin Homo sapiens 67-74 25788506-7 2015 When compared with regular sliding-scale insulin (SSI), fixed-dose insulin glargine with or without insulin glulisine was found to reduce the blood glucose concentration in patients with type 2 diabetes and reduce postoperative complications in surgical patients with diabetes. Glucose 148-155 insulin Homo sapiens 67-74 25831191-9 2015 Five (50%) patients are currently off insulin with excellent glucose control and HbA1c below 6. Glucose 61-68 insulin Homo sapiens 38-45 25552659-3 2015 We developed a constraint optimization algorithm to find the minimal glucose levels associated with the maximized combination of insulin sensitivity and beta-cell function, the two main mechanisms of glucose homeostasis. Glucose 69-76 insulin Homo sapiens 129-136 25552659-9 2015 The concept that optimization of glucose concentrations by direct measures of insulin sensitivity and beta-cell function identifies gender- and age-specific thresholds that bear on disease progression is proven in a physiologically sound, quantifiable manner. Glucose 33-40 insulin Homo sapiens 78-85 25831191-12 2015 The remaining five patients, who require insulin support, had present C-peptide in blood and experience good glucose control without incidence of severe hypoglycemic episodes. Glucose 109-116 insulin Homo sapiens 41-48 25762476-1 2015 This study assessed the association between glucose-lowering drug (GLD) use, including metformin, sulphonylurea derivatives and insulin, after breast cancer diagnosis and breast cancer-specific and all-cause mortality. Glucose 44-51 insulin Homo sapiens 128-135 25529872-2 2015 Insulin in turn acts on liver, muscle and fat tissue to store energy and normalize the blood glucose level. Glucose 93-100 insulin Homo sapiens 0-7 25399739-0 2015 Glucose-lowering with exogenous insulin monotherapy in type 2 diabetes: dose association with all-cause mortality, cardiovascular events and cancer. Glucose 0-7 insulin Homo sapiens 32-39 25617999-3 2015 Hence, a wealth of literature has focused on the crosstalk between NEFA and glucose in the pathogenesis of insulin resistance. Glucose 76-83 insulin Homo sapiens 107-114 25348655-5 2015 Therefore, developing a predictive model of the blood glucose of a person with type II diabetes mellitus is important when the glucose and insulin concentrations are only available at irregular intervals. Glucose 54-61 insulin Homo sapiens 139-146 25702040-7 2015 Insulin sensitivity was estimated by a frequently sampled intravenous glucose tolerance test. Glucose 70-77 insulin Homo sapiens 0-7 25872541-6 2015 Concomitant increases in insulin clearance at 1 week further highlights the liver as an important organ responsible for the early effects on glucose metabolism after surgery since insulin predominantly is cleared by the liver. Glucose 141-148 insulin Homo sapiens 180-187 25798622-7 2015 In a murine adipocyte cell line, silencing of NAT2 ortholog Nat1 decreased insulin-mediated glucose uptake, increased basal and isoproterenol-stimulated lipolysis, and decreased adipocyte differentiation, while Nat1 overexpression produced opposite effects. Glucose 92-99 insulin Homo sapiens 75-82 25872541-11 2015 In glucose tolerant subjects, the insulin response to iv glucose-glucagon declined after RYGB likely as an adaptation to increased insulin sensitivity. Glucose 3-10 insulin Homo sapiens 34-41 25872541-11 2015 In glucose tolerant subjects, the insulin response to iv glucose-glucagon declined after RYGB likely as an adaptation to increased insulin sensitivity. Glucose 3-10 insulin Homo sapiens 131-138 25872541-11 2015 In glucose tolerant subjects, the insulin response to iv glucose-glucagon declined after RYGB likely as an adaptation to increased insulin sensitivity. Glucose 57-64 insulin Homo sapiens 34-41 25872541-11 2015 In glucose tolerant subjects, the insulin response to iv glucose-glucagon declined after RYGB likely as an adaptation to increased insulin sensitivity. Glucose 57-64 insulin Homo sapiens 131-138 25922805-6 2015 A distinct relationship was confirmed between Matsuda index and total area under the curve (insulin/glucose) in each glucose tolerance group. Glucose 117-124 insulin Homo sapiens 92-99 25922805-8 2015 CONCLUSION: After rapid economic growth and changes in lifestyle patterns, insulin resistance has worsened across the glucose tolerance status; however, the insulin secretory function remained unchanged, which resulted in an increase in the susceptibility to the development of type 2 diabetes mellitus among Korean subjects without diabetes. Glucose 118-125 insulin Homo sapiens 75-82 25922806-1 2015 BACKGROUND: Endogenous hyperinsulinemic hypoglycemia (EHH) is characterized by an inappropriately high plasma insulin level, despite a low plasma glucose level. Glucose 146-153 insulin Homo sapiens 28-35 26217781-8 2015 FU caused significant enhancement in glucose consumption by insulin-resistant HepG2 cells compared with control cells. Glucose 37-44 insulin Homo sapiens 60-67 25328007-0 2015 High prevalence of insulin resistance assessed by the glucose clamp technique in hormonal and non-hormonal contraceptive users. Glucose 54-61 insulin Homo sapiens 19-26 25894177-4 2015 When the blood glucose level of a patient exceeded the target level, extra insulin was administered via a different intravenous route. Glucose 15-22 insulin Homo sapiens 75-82 25641023-5 2015 IR was esimated using the equation for insulin sensitivity derived from euglycemic-hyperinsulinemic clamp studies-estimated glucose disposal rate (eGDR). Glucose 124-131 insulin Homo sapiens 39-46 25613093-6 2015 Linear regression analyses revealed that glucose area under the curve (AUC)0-120 min was associated with glucagon-AUC0-30 min and insulin-AUC0-30 min in both OGTT and MTT. Glucose 41-48 insulin Homo sapiens 130-137 25791577-3 2015 In contrast, beta cells release insulin in response to elevated levels of glucose to stimulate peripheral glucose disposal. Glucose 74-81 insulin Homo sapiens 32-39 25973447-1 2015 These strategies can help you optimize glucose control in your patient with type 2 diabetes when basal insulin alone isn"t sufficient. Glucose 39-46 insulin Homo sapiens 103-110 25733449-1 2015 Congenital hyperinsulinism (CHI) is a complex heterogeneous condition in which insulin secretion from pancreatic beta-cells is unregulated and inappropriate for the level of blood glucose. Glucose 180-187 insulin Homo sapiens 16-23 25791577-3 2015 In contrast, beta cells release insulin in response to elevated levels of glucose to stimulate peripheral glucose disposal. Glucose 106-113 insulin Homo sapiens 32-39 25467852-2 2015 The change from a mainly vegetarian fare to meat consumption went along with brain growth and increased insulin resistance to improve brain"s glucose supply. Glucose 142-149 insulin Homo sapiens 104-111 26827442-4 2015 Results of this study provide evidence that obesity affects the expression of the subset of glucose metabolism-related genes in the blood cells and that insulin resistance in obesity is associated with changes in the expression level of PFKFB1, PFKFB3, HK2, and INSIG2 genes, which contribute to the development of insulin resistance as well as glucose intolerance. Glucose 92-99 insulin Homo sapiens 153-160 25645181-2 2015 In order to explain the rheological behavior of glucose-insulin we attempt to modify MINMOD Millennium with fractional-order differentiation of order alpha (0, 1]. Glucose 48-55 insulin Homo sapiens 56-63 25058329-6 2015 RESULTS: Change in overall PA was significantly associated with postprandial log-transformed plasma insulin (beta = -0.002; 95% confidence interval (CI), -0.003 to 0.000; P = 0.008), C-peptide (beta = -2.7; 95% CI, -4.9 to -0.5; P = 0.01), and glucose concentration (beta = -0.006; 95% CI, -0.01 to -0.002; P = 0.002). Glucose 244-251 insulin Homo sapiens 100-107 25637831-6 2015 We review the evidence that insulin pulsatility improves the efficacy of secreted insulin on its targets, particularly hepatic glucose production, but also examine evidence that pulsatility alters or is altered by changes in peripheral glucose uptake. Glucose 127-134 insulin Homo sapiens 28-35 25824547-3 2015 While recent large-scale "omics" studies have revealed the acetylome to be comparable in size to the phosphorylome, the acetylation of insulin signaling proteins and its functional relevance to insulin-stimulated glucose transport and glucose metabolism is not fully understood. Glucose 213-220 insulin Homo sapiens 135-142 25824547-3 2015 While recent large-scale "omics" studies have revealed the acetylome to be comparable in size to the phosphorylome, the acetylation of insulin signaling proteins and its functional relevance to insulin-stimulated glucose transport and glucose metabolism is not fully understood. Glucose 213-220 insulin Homo sapiens 194-201 25824547-3 2015 While recent large-scale "omics" studies have revealed the acetylome to be comparable in size to the phosphorylome, the acetylation of insulin signaling proteins and its functional relevance to insulin-stimulated glucose transport and glucose metabolism is not fully understood. Glucose 235-242 insulin Homo sapiens 135-142 25251562-2 2015 Activation of peroxisome proliferator-activated receptor gamma by agonists leads to a conformational change in the ligand-binding domain altering the transcription of several target genes involved in glucose and lipid metabolism, resulting in, for example, facilitation of glucose and lipid uptake and amelioration of insulin resistance, and other effects that are important in the treatment of type 2 diabetes. Glucose 200-207 insulin Homo sapiens 318-325 25755084-8 2015 CONCLUSIONS: Increased beta-cell response to oral stimuli and insulin-independent glucose disposal may both contribute to severe hypoglycemia after RYGB. Glucose 82-89 insulin Homo sapiens 62-69 25900868-2 2015 Insulin glargine and glyburide were reduced gradually with blood glucose monitoring and replaced by an increase in metformin, start of liraglutide, and eventually phentermine/topiramate and canagliflozin (Figure). Glucose 65-72 insulin Homo sapiens 0-7 25201287-2 2015 This phenomenon, which may impair insulin secretion, has been suggested to be a reason for the adverse effects on glucose metabolism associated with thiazide diuretic treatment of hypertension. Glucose 114-121 insulin Homo sapiens 34-41 25251562-2 2015 Activation of peroxisome proliferator-activated receptor gamma by agonists leads to a conformational change in the ligand-binding domain altering the transcription of several target genes involved in glucose and lipid metabolism, resulting in, for example, facilitation of glucose and lipid uptake and amelioration of insulin resistance, and other effects that are important in the treatment of type 2 diabetes. Glucose 273-280 insulin Homo sapiens 318-325 25889474-0 2015 Experimental evaluation and computational modeling of the effects of encapsulation on the time-profile of glucose-stimulated insulin release of pancreatic islets. Glucose 106-113 insulin Homo sapiens 125-132 25653143-13 2015 Insulin inhibited by ~30% LPS-induced increase in TF-PCA and high glucose reversed it. Glucose 66-73 insulin Homo sapiens 0-7 25894268-1 2015 Patients with type 1 diabetes are exposed to permanent burden consisting of careful glucose self-monitoring and precise insulin dosage based on measured glucose values, carbohydrates content in the food and both planned and non-planned physical activity. Glucose 153-160 insulin Homo sapiens 120-127 25894268-5 2015 Low glucose suspend (LGS) and Predictive Low Glucose Management (PLGM) use glucose sensor values to prevent hypoglycemia, shorten the time spent in hypoglycemic range and present further step forward to fully closed-loop system of insulin treatment. Glucose 75-82 insulin Homo sapiens 231-238 25889474-5 2015 METHODS: To improve our ability to quantitatively describe the glucose-stimulated insulin release (GSIR) of pancreatic islets in general and of micro-encapsulated islets in particular, we performed dynamic perifusion experiments with frequent sampling. Glucose 63-70 insulin Homo sapiens 82-89 25889474-9 2015 This model, which was further validated and calibrated here, can be used for arbitrary geometries and glucose stimulation sequences and is well suited for the quantitative characterization of the insulin response of cultured, perifused, transplanted, or encapsulated islets. Glucose 102-109 insulin Homo sapiens 196-203 25927630-0 2015 Impact of PTBP1 rs11085226 on glucose-stimulated insulin release in adult Danes. Glucose 30-37 insulin Homo sapiens 49-56 25927630-1 2015 BACKGROUND: The variant rs11085226 (G) within the gene encoding polypyrimidine tract binding protein 1 (PTBP1) was reported to associate with reduced insulin release determined by an oral glucose tolerance test (OGTT) as well as an intravenous glucose tolerance test (IVGTT). Glucose 188-195 insulin Homo sapiens 150-157 25927630-1 2015 BACKGROUND: The variant rs11085226 (G) within the gene encoding polypyrimidine tract binding protein 1 (PTBP1) was reported to associate with reduced insulin release determined by an oral glucose tolerance test (OGTT) as well as an intravenous glucose tolerance test (IVGTT). Glucose 244-251 insulin Homo sapiens 150-157 25927630-7 2015 Meta-analysis of IVGTT-derived quantitative traits showed a nominally significant association between the variant and reduced beta-cell responsiveness to glucose (beta = -0.1 mmol kg(-1) min(-1); 95% CI: -0.200.20 - -0.024; P = 0.01) assuming a dominant model of inheritance, but failed to replicate a previously reported association with area under the curve (AUC) for insulin. Glucose 154-161 insulin Homo sapiens 374-381 25564474-7 2015 Furthermore, we detected beta-cell death by TUNEL, beta-cell differentiation by RT-PCR, and beta-cell function by glucose-stimulated insulin secretion. Glucose 114-121 insulin Homo sapiens 133-140 29259409-0 2015 Insulin resistance in nonobese Japanese women with polycystic ovary syndrome is associated with poorer glucose tolerance, delayed insulin secretion, and enhanced insulin response. Glucose 103-110 insulin Homo sapiens 0-7 29259409-12 2015 As the presence of a continuous increase of insulin level reflects to some degree poorer glucose tolerance, delayed insulin secretion, and enhanced insulin response compared with non-continuous insulin increase, OGTT might not been excluded to determine IR and IGT for nonobese women with PCOS. Glucose 89-96 insulin Homo sapiens 44-51 25732404-8 2015 These data suggest that EGCG suppresses TLR4 signaling in LPS-stimulated adipocytes via 67LR and attenuates insulin-stimulated glucose uptake associated with decreased GLUT4 expression. Glucose 127-134 insulin Homo sapiens 108-115 25781654-0 2015 Effects of acute exposure to increased plasma branched-chain amino acid concentrations on insulin-mediated plasma glucose turnover in healthy young subjects. Glucose 114-121 insulin Homo sapiens 90-97 25781654-1 2015 BACKGROUND: Plasma branched-chain amino acids (BCAA) are inversely related to insulin sensitivity of glucose metabolism in humans. Glucose 101-108 insulin Homo sapiens 78-85 25781654-3 2015 OBJECTIVE: To determine the effects of acute exposure to increased plasma BCAA concentrations on insulin-mediated plasma glucose turnover in humans. Glucose 121-128 insulin Homo sapiens 97-104 25781654-7 2015 RESULTS: Insulin infusion completely suppressed the endogenous glucose production (EGP) across all groups. Glucose 63-70 insulin Homo sapiens 9-16 25781654-9 2015 Insulin infusion stimulated whole-body glucose disposal rate (GDR) across all groups. Glucose 39-46 insulin Homo sapiens 0-7 25781654-11 2015 Likewise, insulin stimulated the glucose metabolic clearance in all experiments (P < 0.05) with no differences between Control and BCAA in either of the experiments (P > 0.05). Glucose 33-40 insulin Homo sapiens 10-17 25628424-5 2015 In patients with type 2 diabetes, glucose levels normalized after RYGB, first-phase insulin secretion in response to iv glucose increased twofold, and HOMA-beta already improved 1 wk postoperatively, with further enhancements at 3 mo. Glucose 120-127 insulin Homo sapiens 84-91 26064343-0 2015 Effect of combined application insulin and insulin detemir on continous glucose monitor in children with type 1 diabetes mellitus. Glucose 72-79 insulin Homo sapiens 31-38 26064343-0 2015 Effect of combined application insulin and insulin detemir on continous glucose monitor in children with type 1 diabetes mellitus. Glucose 72-79 insulin Homo sapiens 43-50 26064343-2 2015 This study aims to explore the effects of insulin combined with insulin detemir on the continous glucose in children with type 1 diabetes mellitus. Glucose 97-104 insulin Homo sapiens 42-49 26064343-2 2015 This study aims to explore the effects of insulin combined with insulin detemir on the continous glucose in children with type 1 diabetes mellitus. Glucose 97-104 insulin Homo sapiens 64-71 25789109-6 2015 Continuous glucose monitoring systems and continuous subcutaneous insulin systems may play a role in those who require higher doses of insulin for sugar control. Glucose 11-18 insulin Homo sapiens 135-142 25766323-1 2015 Insulin release in response to glucose stimulation requires exocytosis of insulin-containing granules. Glucose 31-38 insulin Homo sapiens 0-7 25766323-1 2015 Insulin release in response to glucose stimulation requires exocytosis of insulin-containing granules. Glucose 31-38 insulin Homo sapiens 74-81 25766323-8 2015 Upon glucose stimulation BAG3 is phosphorylated by FAK and dissociates from SNAP-25 allowing the formation of the SNARE complex, destabilization of the F-actin network and insulin release. Glucose 5-12 insulin Homo sapiens 172-179 25817343-1 2015 Insulin is known to regulate blood&mdash;glucose level and promote its utilization as an energy source in cardiac tissues under normal physiological conditions as well as stimulates signaling pathways that involved cell growth and proliferation. Glucose 45-52 insulin Homo sapiens 0-7 25596527-0 2015 Zinc finger protein 407 (ZFP407) regulates insulin-stimulated glucose uptake and glucose transporter 4 (Glut4) mRNA. Glucose 62-69 insulin Homo sapiens 43-50 25596527-1 2015 The glucose transporter GLUT4 facilitates insulin-stimulated glucose uptake in peripheral tissues including adipose, muscle, and heart. Glucose 4-11 insulin Homo sapiens 42-49 25596527-3 2015 To better understand the regulation of GLUT4 function, a targeted siRNA screen was performed and led to the discovery that ZFP407 regulates insulin-stimulated glucose uptake in adipocytes. Glucose 159-166 insulin Homo sapiens 140-147 25596527-4 2015 The decrease in insulin-stimulated glucose uptake due to ZFP407 deficiency was attributed to a reduction in GLUT4 mRNA and protein levels. Glucose 35-42 insulin Homo sapiens 16-23 25707553-8 2015 Additionally, poly(I:C) decreased insulin stimulated GLUT-4 expression and glucose uptake in skeletal muscle from pregnant women. Glucose 75-82 insulin Homo sapiens 34-41 25741640-2 2015 METHODS: A total of 327 patients with inadequately controlled type 2 diabetes were enrolled by 72 physicians in this prospective observational study, which aimed to evaluate the efficacy of a 6-month course of insulin glargine therapy measured as development of glycaemic control (glycosylated haemoglobin [HbA1c] and fasting plasma glucose [FPG]) and weight change. Glucose 333-340 insulin Homo sapiens 210-217 25889091-4 2015 METHODS: We evaluated six competing models to describe the time course of endogenous insulin concentration as a function of the plasma glucose concentration and time. Glucose 135-142 insulin Homo sapiens 85-92 25889091-10 2015 The modelling results indicated that the excess amount of insulin can be attributed to the glucose-independent effect as the glucose-dependent effect was similar between visits (P > 0.05). Glucose 91-98 insulin Homo sapiens 58-65 25889091-10 2015 The modelling results indicated that the excess amount of insulin can be attributed to the glucose-independent effect as the glucose-dependent effect was similar between visits (P > 0.05). Glucose 125-132 insulin Homo sapiens 58-65 25889091-11 2015 CONCLUSIONS: A model to describe endogenous insulin concentration in T2D including components of posthepatic glucose-dependent and glucose-independent insulin secretion was identified and validated. Glucose 109-116 insulin Homo sapiens 44-51 25889091-11 2015 CONCLUSIONS: A model to describe endogenous insulin concentration in T2D including components of posthepatic glucose-dependent and glucose-independent insulin secretion was identified and validated. Glucose 131-138 insulin Homo sapiens 44-51 25889091-11 2015 CONCLUSIONS: A model to describe endogenous insulin concentration in T2D including components of posthepatic glucose-dependent and glucose-independent insulin secretion was identified and validated. Glucose 131-138 insulin Homo sapiens 151-158 25564476-1 2015 The objective of this study was to assess the insulin-independent effects of incretin hormones on glucose and glycerol metabolism and hemodynamics under euglycemic and hyperglycemic conditions. Glucose 98-105 insulin Homo sapiens 46-53 26148367-5 2015 One of such algorithms is eMPC, which predicts blood glucose levels and offers physician a choice of a rate of intravenous administration of insulin and the time of further control of the glucose level. Glucose 53-60 insulin Homo sapiens 141-148 26336020-6 2015 A frequently sampled intravenous glucose tolerance test was done to determine insulin sensitivity and acute insulin response after the glucose load, which is regarded as the 1st ISEC. Glucose 135-142 insulin Homo sapiens 108-115 25706655-1 2015 One exercise session can improve subsequent insulin-stimulated glucose uptake by skeletal muscle in healthy and insulin-resistant individuals. Glucose 63-70 insulin Homo sapiens 44-51 25706655-3 2015 Our second aim was to determine whether acute exercise that improved insulin-stimulated glucose uptake by muscles would attenuate activation of these pathways. Glucose 88-95 insulin Homo sapiens 69-76 25284330-6 2015 The subsequent low level of insulin leads to the high blood glucose level also known as hyperglycemia. Glucose 60-67 insulin Homo sapiens 28-35 25706655-5 2015 Some animals from each diet group were sedentary and others were studied 3 h postexercise, when insulin-stimulated glucose uptake was increased. Glucose 115-122 insulin Homo sapiens 96-103 25458549-8 2015 This improvement in glucose metabolism is influenced by factors such as sex, age, insulin treatment, duration of diabetes and degree of preoperative obesity. Glucose 20-27 insulin Homo sapiens 82-89 25041866-9 2015 Although blood levels of glucose were lower after administration of insulin (132 +- 7 mg/dL) than saline (211 +- 15 mg/dL; P = .0002), gastric emptying thalf was not lower after administration of insulin, compared with saline. Glucose 25-32 insulin Homo sapiens 68-75 24494790-8 2015 However, area under the curve for serum insulin concentrations after glucose ingestion significantly decreased in only 4-week group (6910 +- 763 versus 5812 +- 872 muIU ml(-1) 120 min, P <= 0.05). Glucose 69-76 insulin Homo sapiens 40-47 25644817-5 2015 Management of diabetes or glucocorticoid-induced hyperglycemia in the hospital generally requires insulin therapy, which is tailored based upon nutritional needs, baseline glucose control, and concomitant factors such as type and dose of glucocorticoid administration. Glucose 172-179 insulin Homo sapiens 98-105 25271207-1 2015 OBJECTIVE: Insulin adjustments to maintain glycemic control in individuals with type 1 diabetes often lead to wide glucose fluctuations, hypoglycemia, and increased body weight. Glucose 115-122 insulin Homo sapiens 11-18 25044768-6 2015 Peripheral insulin resistance (homeostasis model assessment) was calculated from fasting plasma glucose and fasting plasma insulin. Glucose 96-103 insulin Homo sapiens 11-18 25277390-4 2015 IN insulin dose-dependently decreased plasma glucose concentrations while reducing C-peptide and attenuating endogenous insulin levels. Glucose 45-52 insulin Homo sapiens 3-10 25288674-0 2015 Intranasal insulin suppresses endogenous glucose production in humans compared with placebo in the presence of similar venous insulin concentrations. Glucose 41-48 insulin Homo sapiens 11-18 25277393-5 2015 By reverse hemolytic plaque assay, we showed that glucose-stimulated insulin secretion of single beta-cells was increased by N-cad/Fc and E-cad/Fc adhesion compared with control. Glucose 50-57 insulin Homo sapiens 69-76 25277393-6 2015 In the presence of E-cad/Fc and after glucose stimulation, we showed that total insulin secretion was six times higher in spreading beta-cells compared with round beta-cells. Glucose 38-45 insulin Homo sapiens 80-87 25964036-5 2015 Insulin sensitivity was measured by the glucose infusion rate (GIR) during a hyperinsulinaemic euglycaemic clamp (80 mU m-2 min-1) at baseline and during the third HBOT session. Glucose 40-47 insulin Homo sapiens 0-7 25500952-0 2015 Glucose uptake in human brown adipose tissue is impaired upon fasting-induced insulin resistance. Glucose 0-7 insulin Homo sapiens 78-85 25500952-3 2015 Prolonged fasting is known to induce insulin resistance in peripheral tissues in order to spare glucose for the brain. Glucose 96-103 insulin Homo sapiens 37-44 25500952-4 2015 METHODS: We studied the effect of fasting-induced insulin resistance on the capacity of BAT to take up glucose during cold exposure as well as on cold-stimulated thermogenesis. Glucose 103-110 insulin Homo sapiens 50-57 25713189-5 2015 Overriding IR in an effort to lower plasma glucose levels, particularly with intensive insulin therapy, could therefore be harmful. Glucose 43-50 insulin Homo sapiens 87-94 25601634-7 2015 We hypothesize that lipid metabolism alterations in subjects with the PROX1 CC genotype may be a primary cause of higher glucose levels after glucose load, since the fatty acids can inhibit insulin-stimulated glucose uptake by decreasing carbohydrate oxidation. Glucose 121-128 insulin Homo sapiens 190-197 25715419-0 2015 Blinded continuous glucose monitoring during Yom Kippur fasting in patients with type 1 diabetes on continuous subcutaneous insulin infusion therapy. Glucose 19-26 insulin Homo sapiens 124-131 25876562-7 2015 The recent approval of insulin degludec/liraglutide administered in a fixed ratio combination is unique not simply for the additive benefits of the two agents, but because it now permits adjustable dosing of liraglutide together with insulin, providing better glucose control than with either agent alone at lower dose levels. Glucose 260-267 insulin Homo sapiens 23-30 25601634-7 2015 We hypothesize that lipid metabolism alterations in subjects with the PROX1 CC genotype may be a primary cause of higher glucose levels after glucose load, since the fatty acids can inhibit insulin-stimulated glucose uptake by decreasing carbohydrate oxidation. Glucose 142-149 insulin Homo sapiens 190-197 25601634-7 2015 We hypothesize that lipid metabolism alterations in subjects with the PROX1 CC genotype may be a primary cause of higher glucose levels after glucose load, since the fatty acids can inhibit insulin-stimulated glucose uptake by decreasing carbohydrate oxidation. Glucose 142-149 insulin Homo sapiens 190-197 25367013-0 2015 A strong correlation of glucose variability in non-insulin-treated patients with type 2 diabetes evaluated between continuous glucose monitoring and seven-point testing. Glucose 24-31 insulin Homo sapiens 51-58 25920313-2 2015 Insulin resistance (IR) is defined clinically as the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization. Glucose 130-137 insulin Homo sapiens 0-7 25920313-2 2015 Insulin resistance (IR) is defined clinically as the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization. Glucose 130-137 insulin Homo sapiens 110-117 25042861-11 2015 In addition, gammaT3 treatment in human adipocytes resulted in (1) activation of insulin-stimulated glucose uptake and (2) a significant suppression of MAP kinase and NFkappaB activation. Glucose 100-107 insulin Homo sapiens 81-88 25376729-3 2015 Insulin sensitivity was assessed using intravenous glucose tolerance test (IVGTT) 30 min, 24 h and 48 h post-exercise. Glucose 51-58 insulin Homo sapiens 0-7 25761221-5 2015 Individuals with type 2 diabetes mellitus have reduced insulin-stimulated glucose uptake in skeletal muscle due to the phenomenon of insulin resistance. Glucose 74-81 insulin Homo sapiens 55-62 25761221-5 2015 Individuals with type 2 diabetes mellitus have reduced insulin-stimulated glucose uptake in skeletal muscle due to the phenomenon of insulin resistance. Glucose 74-81 insulin Homo sapiens 133-140 25761221-7 2015 In this context, physical exercise is one of the most important interventions that stimulates glucose uptake by insulin-independent pathways, and the main molecules involved are adenosine monophosphate-activated protein kinase, nitric oxide, bradykinin, AKT, reactive oxygen species and calcium. Glucose 94-101 insulin Homo sapiens 112-119 25559400-1 2015 CONTEXT: Increased adiposity and insulin resistance are associated with hyperglycemia and previous studies have reported that higher glucoses are associated with lower rates of weight gain. Glucose 133-141 insulin Homo sapiens 33-40 24889731-14 2015 glucose infusion, amplifying the differences in the effects of DPP-4 inhibitors and glimepiride on insulin secretion. Glucose 0-7 insulin Homo sapiens 99-106 25511878-1 2015 OBJECTIVE: To evaluate whether the augmented insulin and glucose response to a glucose challenge is sufficient to compensate for defects in glucose utilization in obesity and type 2 diabetes, using a breath test measurement of integrated glucose metabolism. Glucose 79-86 insulin Homo sapiens 45-52 25511878-1 2015 OBJECTIVE: To evaluate whether the augmented insulin and glucose response to a glucose challenge is sufficient to compensate for defects in glucose utilization in obesity and type 2 diabetes, using a breath test measurement of integrated glucose metabolism. Glucose 79-86 insulin Homo sapiens 45-52 25591855-1 2015 The effects of transition by individuals with type 1 diabetes (T1D) to more recently available continuous glucose monitoring (CGM)-enabled insulin pumps from either multiple daily insulin injections (MDI) or older insulin pumps on treatment satisfaction have not been well studied. Glucose 106-113 insulin Homo sapiens 139-146 25591857-15 2015 Duo provided insulin infusion and glucose sensing capabilities in a single device, which provided accurate glucose readings during routine use, was safe to wear, and was acceptable to most patients. Glucose 107-114 insulin Homo sapiens 13-20 25802723-1 2015 AIMS/INTRODUCTION: To examine the association between liver histological features and organ-specific insulin resistance indices calculated from 75-g oral glucose tolerance test data in patients with non-alcoholic fatty liver disease. Glucose 154-161 insulin Homo sapiens 101-108 25802730-0 2015 Combined use of basal insulin analog and acarbose reduces postprandial glucose in patients with uncontrolled type 2 diabetes. Glucose 71-78 insulin Homo sapiens 22-29 25802730-12 2015 CONCLUSIONS: Combination therapy of basal insulin and acarbose in patients with type 2 diabetes improved glucose control, and had no drug-specific safety concerns, suggesting that the treatment might benefit individuals who cannot control blood glucose with basal insulin alone. Glucose 105-112 insulin Homo sapiens 42-49 25767368-1 2015 Drugs raise blood glucose concentrations via two broad mechanisms: By reducing insulin biosynthesis or secretion, or by reducing tissue sensitivity to insulin. Glucose 18-25 insulin Homo sapiens 79-86 25767368-1 2015 Drugs raise blood glucose concentrations via two broad mechanisms: By reducing insulin biosynthesis or secretion, or by reducing tissue sensitivity to insulin. Glucose 18-25 insulin Homo sapiens 151-158 25407031-2 2015 The aim of this study was to assess the cost-effectiveness of starting basal insulin treatment with insulin detemir in people with type 2 diabetes (T2D) inadequately controlled on oral glucose-lowering drugs (OGLDs) in Mexico, South Korea, India, Indonesia, and Algeria. Glucose 185-192 insulin Homo sapiens 100-107 25733459-12 2015 Insulin, C-peptide, and GIP concentrations demonstrate the second-meal phenomenon and most likely aid in keeping the glucose concentrations controlled in response to the subsequent meal. Glucose 117-124 insulin Homo sapiens 0-7 25733459-12 2015 Insulin, C-peptide, and GIP concentrations demonstrate the second-meal phenomenon and most likely aid in keeping the glucose concentrations controlled in response to the subsequent meal. Glucose 117-124 insulin Homo sapiens 9-18 25781537-4 2015 Outcome measures were assessed pre-and post-intervention/control condition and included SI, acute insulin response to glucose (AIR) and disposition index (DI), fasting glucose, 2-h glucose, body composition using waist-hip circumferences, body mass index (BMI), dual energy X-ray absorptiometry (DEXA) scan, blood pressure, and strength by 1-repetition maximum. Glucose 118-125 insulin Homo sapiens 98-105 25512220-4 2015 The authors will share education tips and practical applications for diabetes educators to facilitate education and sustained use of Enlite glucose sensors in children and adolescents using insulin pump therapy. Glucose 140-147 insulin Homo sapiens 190-197 25196736-4 2015 IR was assessed directly with an insulin suppression test by measuring steady-state plasma glucose (SSPG) levels during continuous infusions of octreotide, glucose and insulin. Glucose 91-98 insulin Homo sapiens 33-40 25354240-4 2015 Gene silencing in rats showed that while insulin receptor substrate (IRS)1 mediates the insulin effect on glucose uptake into adipocytes, IRS2 mediates the insulin effect on proximal tubule transport. Glucose 106-113 insulin Homo sapiens 41-48 25354240-4 2015 Gene silencing in rats showed that while insulin receptor substrate (IRS)1 mediates the insulin effect on glucose uptake into adipocytes, IRS2 mediates the insulin effect on proximal tubule transport. Glucose 106-113 insulin Homo sapiens 88-95 25354240-5 2015 The stimulatory effect of insulin on glucose uptake into adipocytes was severely reduced, but its stimulatory effect on NBCe1 activity was completely preserved in insulin-resistant Otsuka Long-Evans Tokushima Fatty (OLETF) rats and patients with insulin resistance. Glucose 37-44 insulin Homo sapiens 26-33 25723632-3 2015 demonstrate in rodents and humans with insulin resistance that while the stimulatory effect of insulin on glucose uptake in adipocytes, mediated via insulin receptor substrate 1 (IRS1), was severely diminished, its effect on salt reabsorption in the kidney proximal tubule, mediated via IRS2, was preserved. Glucose 106-113 insulin Homo sapiens 95-102 25516476-11 2015 GlcN inhibited the insulin response under low (5 mM) glucose conditions, whereas it restored the insulin response for Akt phosphorylation under high (25 mM) glucose conditions in HepG2 and 3T3-L1 cells. Glucose 157-164 insulin Homo sapiens 97-104 25516476-12 2015 Uptake of 2-DG increased upon GlcN treatment under 5 mM glucose compared to control, whereas insulin-stimulated 2-DG uptake decreased under 5 mM and increased under 25 mM glucose in differentiated 3T3-L1 cells. Glucose 171-178 insulin Homo sapiens 93-100 25516476-13 2015 CONCLUSION: Our results show that GlcN increased body weight gain and reduced the insulin response for glucose maintenance when fed to normal CD mice, whereas it alleviated body weight gain and insulin resistance in HFD mice. Glucose 103-110 insulin Homo sapiens 82-89 25594249-5 2015 Knockdown of ME3, but not ME1 or ME2 alone or together, inhibited insulin release stimulated by glucose, pyruvate or 2-aminobicyclo [2,2,1]heptane-2-carboxylic acid-plus-glutamine. Glucose 96-103 insulin Homo sapiens 66-73 25812371-2 2015 Generating of rapid-acting insulin analogs, mimicking physiologic insulin action enables us to provide better control of post-prandial glucose level and lower incidence of hypoglycemia compared with human regular insulin. Glucose 135-142 insulin Homo sapiens 27-34 25812371-2 2015 Generating of rapid-acting insulin analogs, mimicking physiologic insulin action enables us to provide better control of post-prandial glucose level and lower incidence of hypoglycemia compared with human regular insulin. Glucose 135-142 insulin Homo sapiens 66-73 25812371-2 2015 Generating of rapid-acting insulin analogs, mimicking physiologic insulin action enables us to provide better control of post-prandial glucose level and lower incidence of hypoglycemia compared with human regular insulin. Glucose 135-142 insulin Homo sapiens 66-73 25812373-4 2015 As for ideal basal insulin, to maintain desirable pre-prandial glucose levels, duration of action should be long enough, profiles such as flat time-action and less day-to-day variation would be mandatory. Glucose 63-70 insulin Homo sapiens 19-26 25812383-3 2015 GK activator potentiates glucose-stimulated insulin secretion from beta cells and stimulates glucose uptake into the liver. Glucose 25-32 insulin Homo sapiens 44-51 25812383-4 2015 GPR40 agonists and GPR119 agonist stimulate glucose-dependent insulin secretion from beta cells. Glucose 44-51 insulin Homo sapiens 62-69 23944770-1 2015 AIMS: Intravenous glucose tolerance testing (IVGTT) is a common test of beta-cell function in which a glucose load is administered and insulin and/or C-peptide responses are monitored. Glucose 18-25 insulin Homo sapiens 135-142 23944770-5 2015 Areas under the curve (AUC) calculations represent early insulin or C-peptide responses from 0 through 10 min post-glucose challenge. Glucose 115-122 insulin Homo sapiens 68-77 25754657-5 2015 The antihyperglycemic effects of gliptins are attributed to inhibition of the DPP-IV enzyme, thereby prolonging the half-life (t1/2 ) of incretin hormones (substrates) to promote glucose-stimulated insulin secretion. Glucose 179-186 insulin Homo sapiens 198-205 25804263-8 2015 A synergistic increase in serum insulin was unmasked by both father/son HFD consumption, concomitant with increased sera glucose. Glucose 121-128 insulin Homo sapiens 32-39 25758883-2 2015 It reduces glucose levels by increasing insulin sensitivity, reducing hepatic glucose release and increasing muscle uptake. Glucose 11-18 insulin Homo sapiens 40-47 25760748-4 2015 With these bases, several associations have recommended the treatment of hospital hyperglycemia through insulin administration, with the therapeutic goal of maintaining a fasting blood glucose level between 100-140 mg/dL and glucose at any time of day less than 180 mg/dL. Glucose 185-192 insulin Homo sapiens 104-111 25760748-4 2015 With these bases, several associations have recommended the treatment of hospital hyperglycemia through insulin administration, with the therapeutic goal of maintaining a fasting blood glucose level between 100-140 mg/dL and glucose at any time of day less than 180 mg/dL. Glucose 225-232 insulin Homo sapiens 104-111 25665923-8 2015 Moreover, human C-peptide secretion into mouse bloodstream was stimulated by glucose challenges after in vivo maturation. Glucose 77-84 insulin Homo sapiens 16-25 26360670-0 2015 Insulin Control of Blood Glucose and GLUT4 Expression in the Skeletal Muscle of Septic Rats. Glucose 25-32 insulin Homo sapiens 0-7 26360670-2 2015 The level at which the serum glucose should be maintained using insulin infusions for optimal utilization by skeletal muscles is not yet established. Glucose 29-36 insulin Homo sapiens 64-71 26360670-12 2015 Glucose infusion rate during hyperinsulinaemic-euglycaemic clamp experiment was slower in septic rats, suggesting that they were insulin resistant. Glucose 0-7 insulin Homo sapiens 34-41 26360670-17 2015 CONCLUSION: Blood glucose concentration of 8-10 mmol/L results in more glucose utilization than 6-8 mmol/L in the skeletal muscle of septic rats during insulin therapy. Glucose 18-25 insulin Homo sapiens 152-159 26360670-17 2015 CONCLUSION: Blood glucose concentration of 8-10 mmol/L results in more glucose utilization than 6-8 mmol/L in the skeletal muscle of septic rats during insulin therapy. Glucose 71-78 insulin Homo sapiens 152-159 25630516-7 2015 Glucose AUC values increased by 10 % (from 817 (SE 45) to 899 (SE 39) mmol/l per 120 min, P< 0 05) and whole-body insulin sensitivity decreased by 27 % (from 5 3 (SE 1 4) to 3 9 (SE 0 9), P< 0 05) in the control group, whereas normal insulin sensitivity was maintained in the probiotic group (4 4 (SE 0 8) and 4 5 (SE 0 9) before and after overeating, respectively (P>0 05). Glucose 0-7 insulin Homo sapiens 240-247 25848166-1 2015 Normal blood glucose level depends on the availability of insulin and its ability to bind insulin receptor (IR) that regulates the downstream signaling pathway. Glucose 13-20 insulin Homo sapiens 58-65 25848166-3 2015 The study of genetic variation of insulin, blood glucose level and diabetics symptoms development in Aves is interesting because of its optimal high blood glucose level than mammals. Glucose 155-162 insulin Homo sapiens 34-41 26312919-1 2015 BACKGROUND: The closed-loop system (artificial pancreas) delivers insulin in a glucose-responsive manner by the use of a control algorithm that automatically directs insulin delivery, based on real-time sensor glucose concentrations. Glucose 79-86 insulin Homo sapiens 66-73 26312919-1 2015 BACKGROUND: The closed-loop system (artificial pancreas) delivers insulin in a glucose-responsive manner by the use of a control algorithm that automatically directs insulin delivery, based on real-time sensor glucose concentrations. Glucose 79-86 insulin Homo sapiens 166-173 26312919-1 2015 BACKGROUND: The closed-loop system (artificial pancreas) delivers insulin in a glucose-responsive manner by the use of a control algorithm that automatically directs insulin delivery, based on real-time sensor glucose concentrations. Glucose 210-217 insulin Homo sapiens 66-73 26312919-1 2015 BACKGROUND: The closed-loop system (artificial pancreas) delivers insulin in a glucose-responsive manner by the use of a control algorithm that automatically directs insulin delivery, based on real-time sensor glucose concentrations. Glucose 210-217 insulin Homo sapiens 166-173 26312919-15 2015 Lower mean overnight glucose was associated with increased overnight insulin delivery (p<0 0001) without changing total daily insulin amount (p=0 84). Glucose 21-28 insulin Homo sapiens 69-76 25716779-6 2015 METHODS: Insulin sensitivity was estimated for each subject from fasting plasma glucose and insulin using the Homeostasis Model Assessment II. Glucose 80-87 insulin Homo sapiens 9-16 30603240-9 2016 Glucose-stimulated insulin secretion was similarly increased by the MIT and SIT treatments. Glucose 0-7 insulin Homo sapiens 19-26 25523372-8 2015 RESULTS: Compared with the dried POL extract, the fresh POL extract significantly increased the consumption of extracellular glucose in insulin-resistant HepG2 cells (P<0.05). Glucose 125-132 insulin Homo sapiens 136-143 25675515-4 2015 Here, we demonstrate a strategy for the chemical modification of insulin intended to promote both long-lasting and glucose-responsive activity through the incorporation of an aliphatic domain to facilitate hydrophobic interactions, as well as a phenylboronic acid for glucose sensing. Glucose 115-122 insulin Homo sapiens 65-72 25675515-4 2015 Here, we demonstrate a strategy for the chemical modification of insulin intended to promote both long-lasting and glucose-responsive activity through the incorporation of an aliphatic domain to facilitate hydrophobic interactions, as well as a phenylboronic acid for glucose sensing. Glucose 268-275 insulin Homo sapiens 65-72 25675515-5 2015 These synthetic insulin derivatives enable rapid reversal of blood glucose in a diabetic mouse model following glucose challenge, with some derivatives responding to repeated glucose challenges over a 13-h period. Glucose 67-74 insulin Homo sapiens 16-23 25675515-5 2015 These synthetic insulin derivatives enable rapid reversal of blood glucose in a diabetic mouse model following glucose challenge, with some derivatives responding to repeated glucose challenges over a 13-h period. Glucose 111-118 insulin Homo sapiens 16-23 25675515-5 2015 These synthetic insulin derivatives enable rapid reversal of blood glucose in a diabetic mouse model following glucose challenge, with some derivatives responding to repeated glucose challenges over a 13-h period. Glucose 111-118 insulin Homo sapiens 16-23 25675515-6 2015 The best-performing insulin derivative provides glucose control that is superior to native insulin, with responsiveness to glucose challenge improved over a clinically used long-acting insulin derivative. Glucose 48-55 insulin Homo sapiens 20-27 25675515-6 2015 The best-performing insulin derivative provides glucose control that is superior to native insulin, with responsiveness to glucose challenge improved over a clinically used long-acting insulin derivative. Glucose 123-130 insulin Homo sapiens 20-27 25675515-8 2015 This synthetic approach to insulin modification could afford both long-term and glucose-mediated insulin activity, thereby reducing the number of administrations and improving the fidelity of glycemic control for insulin therapy. Glucose 80-87 insulin Homo sapiens 27-34 25675515-8 2015 This synthetic approach to insulin modification could afford both long-term and glucose-mediated insulin activity, thereby reducing the number of administrations and improving the fidelity of glycemic control for insulin therapy. Glucose 80-87 insulin Homo sapiens 97-104 25675515-8 2015 This synthetic approach to insulin modification could afford both long-term and glucose-mediated insulin activity, thereby reducing the number of administrations and improving the fidelity of glycemic control for insulin therapy. Glucose 80-87 insulin Homo sapiens 97-104 25675515-9 2015 The described work is to our knowledge the first demonstration of a glucose-binding modified insulin molecule with glucose-responsive activity verified in vivo. Glucose 68-75 insulin Homo sapiens 93-100 25675515-9 2015 The described work is to our knowledge the first demonstration of a glucose-binding modified insulin molecule with glucose-responsive activity verified in vivo. Glucose 115-122 insulin Homo sapiens 93-100 25706805-2 2015 These patients require insulin and enzyme replacement therapy to survive, grow, and maintain normal blood glucose levels. Glucose 106-113 insulin Homo sapiens 23-30 25973389-0 2015 Munc18c mediates exocytosis of pre-docked and newcomer insulin granules underlying biphasic glucose stimulated insulin secretion in human pancreatic beta-cells. Glucose 92-99 insulin Homo sapiens 55-62 25973389-3 2015 Although shown to influence glucose-stimulated insulin secretion (GSIS) in rodents the precise role of Munc18c in insulin SG exocytosis has not been elucidated. Glucose 28-35 insulin Homo sapiens 47-54 25685285-8 2015 Also, experimental and clinical findings on the effects of C-peptide on whole-body glucose utilization, adipose tissue metabolism and tissues blood flow are summarized and discussed. Glucose 83-90 insulin Homo sapiens 59-68 25474044-1 2015 A microfluidic system was developed to investigate the entrainment of insulin secretion from islets of Langerhans to oscillatory glucose levels. Glucose 129-136 insulin Homo sapiens 70-77 25474044-5 2015 At 11 mM glucose, insulin secretion from single islets was oscillatory with a period ranging from 3-6 min. Glucose 9-16 insulin Homo sapiens 18-25 25474044-6 2015 Application of a small amplitude sinusoidal wave of glucose with a period of 5 or 10 min, shifted the period of the insulin oscillations to this forcing period. Glucose 52-59 insulin Homo sapiens 116-123 25474044-7 2015 Exposing groups of 6-10 islets to a sinusoidal glucose wave synchronized their behavior, producing a coherent pulsatile insulin response from the population. Glucose 47-54 insulin Homo sapiens 120-127 25529453-5 2015 When INS1 cells and primary rat islets were incubated with 10nM NERPs for 3 days, glucose-stimulated insulin secretion levels were blunted by NERP-1 and -2. Glucose 82-89 insulin Homo sapiens 101-108 25529453-6 2015 The number of insulin granules released from the readily releasable pool, which is associated with the first phase of glucose-stimulated insulin release, was decreased by NERP-1 and -2. Glucose 118-125 insulin Homo sapiens 14-21 25529453-6 2015 The number of insulin granules released from the readily releasable pool, which is associated with the first phase of glucose-stimulated insulin release, was decreased by NERP-1 and -2. Glucose 118-125 insulin Homo sapiens 137-144 25658116-0 2015 Long-term pancreatic beta cell exposure to high levels of glucose but not palmitate induces DNA methylation within the insulin gene promoter and represses transcriptional activity. Glucose 58-65 insulin Homo sapiens 119-126 25658116-7 2015 Experimental-high-glucose conditions significantly suppressed insulin mRNA and increased DNA methylation at all five CpG sites within the Ins1 promoter, including the cAMP response element, in a time-dependent and glucose concentration-dependent manner. Glucose 18-25 insulin Homo sapiens 62-69 25658116-9 2015 Artificial methylation of Ins1 promoter significantly suppressed promoter-driven luciferase activity, and a DNA methylation inhibitor significantly improved insulin mRNA suppression by experimental-high-glucose conditions. Glucose 203-210 insulin Homo sapiens 157-164 25640178-1 2015 Strategies that simultaneously enhance the survival and glucose responsiveness of insulin-producing beta cells will greatly augment beta cell replacement therapies in type 1 diabetes (T1D). Glucose 56-63 insulin Homo sapiens 82-89 25645672-7 2015 Insulin (n = 151) resulted in a stronger reduction in HbA1c (-0.9 +- 2.0% vs. -0.5 +- 1.0%; p = 0.003), and fasting plasma glucose (-24 +- 70 mg/dl vs. -19 +- 42 mg/dl; p = 0.001), but was associated with increased bodyweight (0.8 +- 9.0 kg vs. -1.5 +- 5.0 kg; p = 0.028). Glucose 123-130 insulin Homo sapiens 0-7 25830090-7 2015 RESULTS: Rodent beta-cells chronically exposed to high glucose had diminished responses to GLP-1R agonists including: diminished insulin secretory response; reduced phosphorylation of (CREB); impaired cAMP response, attributable to chronically increased cAMP levels. Glucose 55-62 insulin Homo sapiens 129-136 24791963-10 2015 As their early insulin response correlates strongly with both glucose disposal and late insulin response, alterations in beta-cell dynamics may give an explanation to their extreme early onset of T2D, although larger prospective studies are required. Glucose 62-69 insulin Homo sapiens 15-22 25132463-2 2015 Fetal glucose availability is critically dependent on placental transfer and is linked to fetal growth by regulating the release of fetal growth hormones such as insulin. Glucose 6-13 insulin Homo sapiens 162-169 25138785-8 2015 In the entire group, 25(OH)D concentration significantly correlated with magnitude of insulin resistance (steady-state plasma glucose concentration; r = -0.20; P = 0.02). Glucose 126-133 insulin Homo sapiens 86-93 25501695-4 2015 The consequence of a decrease in insulin sensitivity is a significant change in protein and glucose metabolism characterized by an increase in the production of endogenous hepatic glucose, a decrease in the uptake of peripheral glucose, and an increase in the breakdown of protein. Glucose 92-99 insulin Homo sapiens 33-40 25501695-4 2015 The consequence of a decrease in insulin sensitivity is a significant change in protein and glucose metabolism characterized by an increase in the production of endogenous hepatic glucose, a decrease in the uptake of peripheral glucose, and an increase in the breakdown of protein. Glucose 180-187 insulin Homo sapiens 33-40 25501695-5 2015 Muscle is the main tissue for uptake of insulin-mediated glucose, and consequent with the reduced activation of a specific glucose transporter protein (GLUT 4), glucose cannot be transported into the muscle cells. Glucose 57-64 insulin Homo sapiens 40-47 25501695-5 2015 Muscle is the main tissue for uptake of insulin-mediated glucose, and consequent with the reduced activation of a specific glucose transporter protein (GLUT 4), glucose cannot be transported into the muscle cells. Glucose 123-130 insulin Homo sapiens 40-47 25511640-2 2015 Continuous glucose monitoring was performed in four Japanese insulin-treated inpatients with type 2 diabetes. Glucose 11-18 insulin Homo sapiens 61-68 25457209-6 2015 The effect of insulin on glucose production and lipolysis were significantly higher in the TM6SF2EK/KK than in the TM6SF2EE group. Glucose 25-32 insulin Homo sapiens 14-21 25187364-2 2015 Studies suggest that insulin-mediated glucose metabolism is different between muscle fiber types. Glucose 38-45 insulin Homo sapiens 21-28 25255697-8 2015 CONCLUSIONS: Free triiodothyronine is associated with both basal and glucose-stimulated insulin secretion in people with prediabetes who are euthyroid; therefore, the regulation of insulin secretion by thyroid hormones is a potentially novel therapeutic target for the treatment of diabetes. Glucose 69-76 insulin Homo sapiens 88-95 25255697-8 2015 CONCLUSIONS: Free triiodothyronine is associated with both basal and glucose-stimulated insulin secretion in people with prediabetes who are euthyroid; therefore, the regulation of insulin secretion by thyroid hormones is a potentially novel therapeutic target for the treatment of diabetes. Glucose 69-76 insulin Homo sapiens 181-188 25323312-1 2015 AIMS: The recent type 2 diabetes American Diabetes Association/European Association for the Study of Diabetes (ADA/EASD) position statement suggested insulin is the most effective glucose-lowering therapy, especially when glycated haemoglobin (HbA1c) is very high. Glucose 180-187 insulin Homo sapiens 150-157 25322843-1 2015 AIMS/HYPOTHESIS: The aim of this study was to determine the protective effects of human insulin and its analogues, B28Asp human insulin (insulin aspart) and B29Lys(epsilon-tetradecanoyl),desB30 human insulin (insulin detemir), against glucose-induced lifespan reduction and neuronal damage in the model organism Caenorhabditis elegans and to elucidate the underlying mechanisms. Glucose 235-242 insulin Homo sapiens 88-95 25322843-5 2015 RESULTS: Insulin and its analogues reversed the life-shortening effect of HG conditions and prevented the glucose-induced neuronal impairment. Glucose 106-113 insulin Homo sapiens 9-16 25322843-6 2015 Insulin treatment under HG conditions was associated with reduced concentration of glucose, as well as a reduced formation of ROS and AGEs, and increased SOD activity. Glucose 83-90 insulin Homo sapiens 0-7 25348609-3 2015 METHODS: We evaluated the early insulin response to glucose (using frequently sampled intravenous glucose tolerance testing) by R325W genotype before and after 14 days of supplementation with oral zinc acetate (50 mg elemental zinc) twice daily in healthy non-diabetic Amish individuals (N = 55). Glucose 52-59 insulin Homo sapiens 32-39 25348609-4 2015 RESULTS: Individuals with RW/WW genotypes (n = 32) had the lowest insulin response to glucose at 5 and 10 min at baseline (vs RR homozygotes [n = 23]). Glucose 86-93 insulin Homo sapiens 66-73 25348609-5 2015 After zinc supplementation, the RW/WW group experienced 15% and 14% increases in the insulin response to glucose at 5 and 10 min, respectively (p <= 0.04), and, compared with RR homozygotes, experienced a 26% (p = 0.04) increase in insulin at 5 min. Glucose 105-112 insulin Homo sapiens 85-92 25348609-7 2015 CONCLUSIONS/INTERPRETATION: Zinc supplementation appears to affect the early insulin response to glucose differentially by rs13266634 genotype and could be beneficial for diabetes prevention and/or treatment for some individuals based on SLC30A8 variation. Glucose 97-104 insulin Homo sapiens 77-84 25421524-3 2015 In pancreatic beta cells, GLUT2 is required for glucose-stimulated insulin secretion. Glucose 48-55 insulin Homo sapiens 67-74 25297660-11 2015 CONCLUSION: Patient-led insulin glargine titration achieved near-target blood glucose levels in Asian patients with uncontrolled type 2 diabetes who were on 2 oral glucose-lowering drugs, demonstrating that Asian patients can self-uptitrate insulin dose effectively when guided. Glucose 78-85 insulin Homo sapiens 24-31 25297660-11 2015 CONCLUSION: Patient-led insulin glargine titration achieved near-target blood glucose levels in Asian patients with uncontrolled type 2 diabetes who were on 2 oral glucose-lowering drugs, demonstrating that Asian patients can self-uptitrate insulin dose effectively when guided. Glucose 164-171 insulin Homo sapiens 24-31 25342129-1 2015 Insulin resistance causes diminished glucose uptake in similar regions of the brain in Alzheimer"s disease (AD) and type 2 diabetes mellitus (DM2). Glucose 37-44 insulin Homo sapiens 0-7 25534140-6 2015 This knowledge has led to possible drug therapies in clinical trials, particularly insulin secretagogues that are glucose-dependent. Glucose 114-121 insulin Homo sapiens 83-90 25089371-6 2015 Serum WNT5 correlated inversely with weight both in PCOS and reference women, and correlated directly with insulin response during oral glucose tolerance test in PCOS women. Glucose 136-143 insulin Homo sapiens 107-114 25636955-5 2015 Current experimental evidence suggests that insulin resistance and a chronic, subclinical inflammation in the visceral fat are the major metabolic events causing alterations in the levels of insulin, glucose, free fatty acids, insulin-like growth factor 1 (IGF-1) and 2, adipose tissue-derived proinflammatory cytokines and other bioactive molecules, such as adipokines (e.g. leptin and adiponectin), vascular endothelial growth factor (VEGF), sex hormones, gut microbiota and secondary bile acids. Glucose 200-207 insulin Homo sapiens 44-51 25859477-2 2015 Hypothyroidism has been associated with disorders of glucose and insulin metabolism involving defective insulin secretion in response to glucose, hyperinsulinemia, altered peripheral glucose disposal and insulin resistance. Glucose 137-144 insulin Homo sapiens 65-72 24583757-12 2015 At the end of the treatment, insulin resistance (serum glucose and HOMA) worsened with PUFA but not placebo. Glucose 55-62 insulin Homo sapiens 29-36 25375983-12 2015 The adaptation at larger meals results in identical glucose excursions, whereas after a lower caloric lunch, the insulin response is high, resulting in a postpeak suppression of glucose below baseline. Glucose 178-185 insulin Homo sapiens 113-120 25387258-5 2015 MAIN OUTCOME MEASURES: Insulin resistance (the lowest whole-body glucose uptake quartile) was measured by the euglycemic-hyperinsulinemic clamp. Glucose 65-72 insulin Homo sapiens 23-30 25387263-6 2015 RESULTS: Individuals with prediabetes or T2D diagnosed by fasting glucose had lower absolute insulin release (P <= .01) and higher insulin sensitivity in response to glucose intake (P <= .01) but a similar disposition index (P >= .36), compared with individuals with elevated 2-hour glucose concentrations. Glucose 66-73 insulin Homo sapiens 93-100 25393642-4 2015 In particular, total fat mass and fat distribution were assessed by dual-energy x-ray absorptiometry, serum-free T by liquid chromatography mass spectrometry and equilibrium dialysis and insulin sensitivity by the glucose clamp technique. Glucose 214-221 insulin Homo sapiens 187-194 25328153-4 2015 METHODS: Insulin-stimulated glucose disposal was determined by using the hyperinsulinemic-euglycemic clamp procedure with stable isotope glucose tracer infusion in nine lean and nine obese subjects, and in a separate group of nine obese subjects before and 1 year after Roux-en-Y gastric bypass (RYGB) surgery (38% weight loss). Glucose 28-35 insulin Homo sapiens 9-16 25581519-1 2015 Type 2 diabetes is a major health problem worldwide, and one of its key features is the inability of elevated glucose to stimulate the release of sufficient amounts of insulin from pancreatic beta cells to maintain normal blood glucose levels. Glucose 110-117 insulin Homo sapiens 168-175 25452199-1 2015 OBJECTIVE: In insulin-resistant states, resistance of protein anabolism occurs concurrently with that of glucose, but can be compensated for by abundant amino acid (AA) provision. Glucose 105-112 insulin Homo sapiens 14-21 25328153-4 2015 METHODS: Insulin-stimulated glucose disposal was determined by using the hyperinsulinemic-euglycemic clamp procedure with stable isotope glucose tracer infusion in nine lean and nine obese subjects, and in a separate group of nine obese subjects before and 1 year after Roux-en-Y gastric bypass (RYGB) surgery (38% weight loss). Glucose 137-144 insulin Homo sapiens 9-16 25173880-4 2015 PE cells co-cultured with islet cells or islet cell-derived conditioned medium (CM) showed increased expression levels of beta-cell markers; significantly higher levels of proinsulin- and Newport Green (NG)-positive cells, which revealed the characteristics of insulin producing cells; and increased insulin secretion upon glucose stimulation. Glucose 323-330 insulin Homo sapiens 261-268 25678954-2 2015 Dapagliflozin significantly reduces glucose reabsorption and decreases serum glucose concentration in an insulin-independent manner. Glucose 77-84 insulin Homo sapiens 105-112 25604903-10 2015 RESULTS: Glucose increased the circulating concentration of glucose (P < 0.05) and insulin (P < 0.05). Glucose 9-16 insulin Homo sapiens 86-93 25629318-7 2015 Serum glucose levels gradually declined to either normal or near normal levels over 150 days, suggesting that the IPCs were secreting insulin. Glucose 6-13 insulin Homo sapiens 134-141 25650514-2 2015 By mimicking the effects of the native GLP-1, it enhances the glucose-dependent secretion of insulin, suppresses elevated glucagon secretion, increases satiety and slows down gastric emptying. Glucose 62-69 insulin Homo sapiens 93-100 25598507-7 2015 Moreover, we show that the observed non-linear functional relationship between different network metrics and glucose concentration represents a well-balanced setup that parallels physiological insulin release. Glucose 109-116 insulin Homo sapiens 193-200 25604903-15 2015 CONCLUSIONS: These data suggest that the effect of glucose in small follicles is a direct action of glucose that increases the number of small follicles while the effect of glucose in oestrogenic follicles is an indirect insulin-mediated action. Glucose 51-58 insulin Homo sapiens 221-228 25406263-0 2015 Somatostatin and insulin mediate glucose-inhibited glucagon secretion in the pancreatic alpha-cell by lowering cAMP. Glucose 33-40 insulin Homo sapiens 17-24 25406263-5 2015 Thus, we conclude that somatostatin and insulin together are critical paracrine mediators of glucose-inhibited glucagon secretion and function by lowering cAMP/PKA signaling with increasing glucose. Glucose 93-100 insulin Homo sapiens 40-47 25406263-5 2015 Thus, we conclude that somatostatin and insulin together are critical paracrine mediators of glucose-inhibited glucagon secretion and function by lowering cAMP/PKA signaling with increasing glucose. Glucose 190-197 insulin Homo sapiens 40-47 25400106-9 2015 Postprandial plasma glucose, insulin and C-peptide concentrations were measured regularly for 3 h. The results of the present study showed that the peak plasma concentration, time to reach peak plasma concentration or AUC values of glucose, insulin and C-peptide were not altered after consumption of the test meals. Glucose 232-239 insulin Homo sapiens 253-262 25611002-2 2015 Protocols that include insulin infusions are commonly followed to achieve target blood glucose levels. Glucose 87-94 insulin Homo sapiens 23-30 25614674-1 2015 Skeletal muscle insulin resistance manifests as a decreased ability of insulin to stimulate glucose uptake in consequence of an impairment in its intracellular signaling. Glucose 92-99 insulin Homo sapiens 16-23 25565210-1 2015 Defects in insulin secretion play a central role in the pathogenesis of type 2 diabetes, yet the mechanisms driving beta-cell dysfunction remain poorly understood, and therapies to preserve glucose-dependent insulin release are inadequate. Glucose 190-197 insulin Homo sapiens 208-215 25445050-4 2015 An incubation of L6 myotubes with palmitate inhibited insulin-stimulated glucose uptake and translocation of GLUT4 to cell surface. Glucose 73-80 insulin Homo sapiens 54-61 25569521-2 2015 injection of insulin in the fed state is dependent on the action of a second hormone, hepatic insulin sensitizing substance (HISS), which is released from the liver and stimulates glucose uptake in muscle, heart and kidneys. Glucose 180-187 insulin Homo sapiens 13-20 26662988-2 2015 Insulin is released from pancreatic beta-cells in response to increasing blood glucose levels and acts on insulin-sensitive tissues such as skeletal muscle and liver in order to maintain normal glucose homeostasis. Glucose 79-86 insulin Homo sapiens 0-7 25601841-1 2014 Insulin resistance, "a relative impairment in the ability of insulin to exert its effects on glucose, protein and lipid metabolism in target tissues," has many detrimental effects on metabolism and is strongly correlated to deposition of lipids in non-adipose tissues. Glucose 93-100 insulin Homo sapiens 0-7 25601841-1 2014 Insulin resistance, "a relative impairment in the ability of insulin to exert its effects on glucose, protein and lipid metabolism in target tissues," has many detrimental effects on metabolism and is strongly correlated to deposition of lipids in non-adipose tissues. Glucose 93-100 insulin Homo sapiens 61-68 25705395-1 2015 Our current understanding of glucose homeostasis is centered on glucose-induced secretion of insulin from pancreatic islets and insulin action on glucose metabolism in peripheral tissues. Glucose 29-36 insulin Homo sapiens 93-100 25705395-1 2015 Our current understanding of glucose homeostasis is centered on glucose-induced secretion of insulin from pancreatic islets and insulin action on glucose metabolism in peripheral tissues. Glucose 29-36 insulin Homo sapiens 128-135 25705395-1 2015 Our current understanding of glucose homeostasis is centered on glucose-induced secretion of insulin from pancreatic islets and insulin action on glucose metabolism in peripheral tissues. Glucose 64-71 insulin Homo sapiens 93-100 26215992-2 2015 Glucocorticoids promote gluconeogenesis in liver, whereas in skeletal muscle and white adipose tissue they decrease glucose uptake and utilization by antagonizing insulin response. Glucose 116-123 insulin Homo sapiens 163-170 26215992-6 2015 Moreover, glucocorticoids modulate the function of pancreatic alpha and beta cells to regulate the secretion of glucagon and insulin, two hormones that play a pivotal role in the regulation of blood glucose levels. Glucose 199-206 insulin Homo sapiens 125-132 26662988-2 2015 Insulin is released from pancreatic beta-cells in response to increasing blood glucose levels and acts on insulin-sensitive tissues such as skeletal muscle and liver in order to maintain normal glucose homeostasis. Glucose 194-201 insulin Homo sapiens 0-7 27032232-2 2015 Specific negative influences of high dietary glucose and lipid consumption, as well as undernutrition, are associated with development of metabolic syndrome, insulin resistance and diabetes in the offspring. Glucose 45-52 insulin Homo sapiens 158-165 25370850-2 2015 Insulin-stimulated glucose uptake is decreased in differentiated diabetic cultured myotubes, which is in keeping with a retained genetic/epigenetic defect of insulin action. Glucose 19-26 insulin Homo sapiens 0-7 25370850-2 2015 Insulin-stimulated glucose uptake is decreased in differentiated diabetic cultured myotubes, which is in keeping with a retained genetic/epigenetic defect of insulin action. Glucose 19-26 insulin Homo sapiens 158-165 26736985-3 2015 Inhaled insulin appears an important candidate to improve post-prandial glucose control given its rapid appearance in plasma. Glucose 72-79 insulin Homo sapiens 8-15 26736768-1 2015 In type 1 diabetes (T1D) therapy, continuous glucose monitoring (CGM) sensors, which provide glucose concentration in the subcutis every 1-5 min for 7 consecutive days, should allow in principle a more efficient insulin dosing than that based on the conventional 3-4 self-monitoring of blood glucose (SMBG) measurements per day. Glucose 45-52 insulin Homo sapiens 212-219 26736768-1 2015 In type 1 diabetes (T1D) therapy, continuous glucose monitoring (CGM) sensors, which provide glucose concentration in the subcutis every 1-5 min for 7 consecutive days, should allow in principle a more efficient insulin dosing than that based on the conventional 3-4 self-monitoring of blood glucose (SMBG) measurements per day. Glucose 93-100 insulin Homo sapiens 212-219 25757931-1 2015 The effects of green tea catechins on glucose-stimulated insulin secretion (GSIS) were investigated in the beta-cell line INS-1D. Glucose 38-45 insulin Homo sapiens 57-64 25947911-9 2015 We also demonstrated that the insulin secretagogue glucose converts Rab27a from its GTP- to GDP-bound forms. Glucose 51-58 insulin Homo sapiens 30-37 25947913-5 2015 Inhibition of this receptor by gurmarin or deletion of the T1R3 gene attenuates glucose-induced insulin secretion from beta-cells. Glucose 80-87 insulin Homo sapiens 96-103 26662988-2 2015 Insulin is released from pancreatic beta-cells in response to increasing blood glucose levels and acts on insulin-sensitive tissues such as skeletal muscle and liver in order to maintain normal glucose homeostasis. Glucose 194-201 insulin Homo sapiens 106-113 25701261-4 2015 We found that insulin priming is necessary and specific for estradiol-induced cancer cell growth, and induces anaplerotic shunting of glucose into macromolecule biosynthesis in the estradiol treated cells. Glucose 134-141 insulin Homo sapiens 14-21 26488284-1 2015 BACKGROUNDS/AIMS: The lipid induced insulin resistance is a major pathophysiologic mechanism underlying glucose intolerance of varying severity. Glucose 104-111 insulin Homo sapiens 36-43 25397866-8 2015 Purified dithizone(+) 3D aggregates generated by our refined protocol produced pancreatic hormones and released insulin in response to both glucose and pharmacological drugs in vitro. Glucose 140-147 insulin Homo sapiens 112-119 25612477-2 2015 Foxo1, a member of the FOXO transcription factor family, is an important player in insulin signaling due to its inhibitory role in glucose uptake and utilization in skeletal muscle. Glucose 131-138 insulin Homo sapiens 83-90 26303164-11 2015 In addition, we demonstrated that 100 nM insulin up-regulated the expression of the hERG channel and rescued the hERG channel repression caused by high glucose. Glucose 152-159 insulin Homo sapiens 41-48 26303164-13 2015 Furthermore, insulin promotes the expression of the hERG channel and ameliorates the high-glucose-induced inhibition of the hERG channel. Glucose 90-97 insulin Homo sapiens 13-20 25154650-7 2015 Diabetes status and insulin infusion were associated with differences in the metabolic clearance rate of glucose, (P < 0 001 for each) and insulin infusion increased LBF (P < 0 001). Glucose 105-112 insulin Homo sapiens 20-27 25429672-5 2015 The most important problems related to diabetes management, such as self-monitoring of blood glucose levels and insulin injections, can now be conquered due to progress in nanomedicine, which offers glucose nanosensors, the layer-by-layer technique, carbon nanotubes, quantum dots, oral insulins, microspheres, artificial pancreases and nanopumps. Glucose 199-206 insulin Homo sapiens 112-119 25776871-1 2015 A closed-loop system that provides both the sensing of glucose and the appropriate dosage of insulin could dramatically improve treatment options for insulin-dependent diabetics. Glucose 55-62 insulin Homo sapiens 93-100 25415617-2 2015 While it was initially thought that the consequences of altered insulin signaling to podocyte function was strictly related to altered glucose uptake, it has become clear that upstream signaling events involved in cell survival, lipid metabolism or nutrient sensing and modulated by insulin are strong independent contributors to podocyte function. Glucose 135-142 insulin Homo sapiens 64-71 25981637-12 2015 ELISA analysis validate the insulin secretion of islet-like cell clusters in response to glucose stimulation. Glucose 89-96 insulin Homo sapiens 28-35 26122098-5 2015 Here we describe a simple and easy-to-use lentiviral transduction protocol that allows the transduction of approximately 80 % of mouse and human islet cells while preserving islet architecture, metabolic function and glucose-dependent stimulation of insulin secretion. Glucose 217-224 insulin Homo sapiens 250-257 25345658-2 2015 Continuous subcutaneous insulin infusion and other diabetes technologies, such as continuous glucose monitoring, are now an established and evidence-based part of diabetes care, but there has been some confusion about effectiveness and best use, particularly because of conflicting results from meta-analyses. Glucose 93-100 insulin Homo sapiens 24-31 24916838-11 2015 CONCLUSIONS: There were modest, transient differences in glucose control between IV and SQ insulin in hospitalized CHF patients. Glucose 57-64 insulin Homo sapiens 91-98 24957785-4 2015 Weekly insulin titration aimed to achieve median prebreakfast and nocturnal plasma glucose levels <=5.5 mmol/l, while limiting values <=4.4 mmol/l. Glucose 83-90 insulin Homo sapiens 7-14 24957785-11 2015 This study confirms, in a globally heterogeneous population, the reduction achieved in nocturnal hypoglycaemia while attaining good glycaemic control with insulin glargine compared with NPH, even when titrating basal insulin to prevent nocturnal hypoglycaemia rather than treating according to normal fasting glucose levels. Glucose 309-316 insulin Homo sapiens 155-162 25053587-4 2015 The first hour, plasma glucose was lowered by insulin infusion, and the second hour constituted a "recovery phase." Glucose 23-30 insulin Homo sapiens 46-53 25131451-5 2015 In both men and women, fasting insulin and homeostasis model assessment of insulin resistance (>= 75th percentile) were significantly associated with incident diabetes and combined impaired fasting glucose/impaired glucose tolerance; however, reduced beta-cell function as measured by homeostasis model assessment of beta-cell function (< 25th percentile) was associated with incident isolated impaired fasting glucose solely in men [hazard ratio 1.35 (95% CI 1.02-1.78)] in multivariable analysis including waist-hip ratio). Glucose 201-208 insulin Homo sapiens 31-38 25205223-7 2015 Patients receiving metformin + insulin were younger and had less comorbidity and a longer history of glucose-lowering treatment. Glucose 101-108 insulin Homo sapiens 31-38 25263215-8 2015 When plasma glucose levels were >5.0 mmol/l (>90 mg/dl), albiglutide increased pancreatic beta-cell secretion of C-peptide in a glucose-dependent manner to a greater extent than did placebo, and it was suppressed in each group when levels were <4.0 mmol/l (<72 mg/dl). Glucose 12-19 insulin Homo sapiens 119-128 25263215-8 2015 When plasma glucose levels were >5.0 mmol/l (>90 mg/dl), albiglutide increased pancreatic beta-cell secretion of C-peptide in a glucose-dependent manner to a greater extent than did placebo, and it was suppressed in each group when levels were <4.0 mmol/l (<72 mg/dl). Glucose 134-141 insulin Homo sapiens 119-128 25280670-0 2015 Roles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscle. Glucose 63-70 insulin Homo sapiens 30-37 25280670-1 2015 This review focuses on two paralogue Rab GTPase activating proteins known as TBC1D1 Tre-2/BUB2/cdc 1 domain family (TBC1D) 1 and TBC1D4 (also called Akt Substrate of 160 kDa, AS160) and their roles in controlling skeletal muscle glucose transport in response to the independent and combined effects of insulin and exercise. Glucose 229-236 insulin Homo sapiens 302-309 25280670-2 2015 Convincing evidence implicates Akt2-dependent TBC1D4 phosphorylation on T642 as a key part of the mechanism for insulin-stimulated glucose uptake by skeletal muscle. Glucose 131-138 insulin Homo sapiens 112-119 25280670-5 2015 Several studies that evaluated both normal and insulin-resistant skeletal muscle stimulated with a physiological insulin concentration after a single exercise session found that greater post-exercise insulin-stimulated glucose uptake was accompanied by greater TBC1D4 phosphorylation on several sites. Glucose 219-226 insulin Homo sapiens 47-54 25280670-5 2015 Several studies that evaluated both normal and insulin-resistant skeletal muscle stimulated with a physiological insulin concentration after a single exercise session found that greater post-exercise insulin-stimulated glucose uptake was accompanied by greater TBC1D4 phosphorylation on several sites. Glucose 219-226 insulin Homo sapiens 113-120 25280670-5 2015 Several studies that evaluated both normal and insulin-resistant skeletal muscle stimulated with a physiological insulin concentration after a single exercise session found that greater post-exercise insulin-stimulated glucose uptake was accompanied by greater TBC1D4 phosphorylation on several sites. Glucose 219-226 insulin Homo sapiens 113-120 25280670-8 2015 In summary, TBC1D1 and TBC1D4 have important, but distinct roles in regulating muscle glucose transport in response to insulin and exercise. Glucose 86-93 insulin Homo sapiens 119-126 25422169-5 2015 Continuous glucose monitoring was undertaken in the week preceding each assessment and the relationship between C-peptide and glucose control evaluated by mixed Poisson regression. Glucose 126-133 insulin Homo sapiens 112-121 25422169-7 2015 Increasing beta-cell function across predefined C-peptide groups was associated with reduced insulin dose, HbA1c, mean glucose (low [<200 pmol/L] 10.7 vs. excellent [>1,000 pmol/L] 7.5 mmol/L), and glucose SD (low, 4.4 vs. excellent, 1.4 mmol/L). Glucose 119-126 insulin Homo sapiens 48-57 25422169-8 2015 Highly statistically significant continuous associations between stimulated C-peptide and mean interstitial glucose (lower by 2.5% [95% CI 1.5-3.5%] per 100 pmol/L higher C-peptide), glucose SD, time outside glucose target range, and measures of hyper-/hypoglycemia risk were confirmed. Glucose 108-115 insulin Homo sapiens 76-85 25422169-8 2015 Highly statistically significant continuous associations between stimulated C-peptide and mean interstitial glucose (lower by 2.5% [95% CI 1.5-3.5%] per 100 pmol/L higher C-peptide), glucose SD, time outside glucose target range, and measures of hyper-/hypoglycemia risk were confirmed. Glucose 108-115 insulin Homo sapiens 171-180 25450815-6 2015 More insulin-resistant patients were defined as those having an estimated glucose disposal rate (eGDR) value below the first quartile. Glucose 74-81 insulin Homo sapiens 5-12 25156483-9 2015 This data suggest that the oral insulin microparticles were able to reduce glucose levels in disease conditions and would be a favorable route of administration to patients as an alternative to daily subcutaneous injections. Glucose 75-82 insulin Homo sapiens 32-39 25355081-0 2015 An inverse U-shaped association of late and peak insulin levels during an oral glucose load with glucose intolerance in a Japanese population: a cross-sectional study. Glucose 79-86 insulin Homo sapiens 49-56 25355081-0 2015 An inverse U-shaped association of late and peak insulin levels during an oral glucose load with glucose intolerance in a Japanese population: a cross-sectional study. Glucose 97-104 insulin Homo sapiens 49-56 25355081-1 2015 The current study investigated the association of post-load insulin levels with glucose tolerance in a Japanese population. Glucose 80-87 insulin Homo sapiens 60-67 25355081-4 2015 A penalized cubic regression spline model analysis revealed that the 60- and 120-min insulin levels, but not 0- or 30-min insulin levels, had an inverse U-shaped relationship to the 120-min glucose level. Glucose 190-197 insulin Homo sapiens 85-92 25355081-5 2015 Furthermore, peak insulin level followed an inverse U shape in relation to the 120-min glucose level, whereas the peak of insulin appeared at a later point in time as the 120-min glucose level increased. Glucose 87-94 insulin Homo sapiens 18-25 25355081-5 2015 Furthermore, peak insulin level followed an inverse U shape in relation to the 120-min glucose level, whereas the peak of insulin appeared at a later point in time as the 120-min glucose level increased. Glucose 179-186 insulin Homo sapiens 122-129 25355081-7 2015 Peak insulin levels also demonstrated an inverse U shape in association with 0-min glucose levels and indices of beta cell function, assessed by the disposition index and the beta-cell function index. Glucose 83-90 insulin Homo sapiens 5-12 25355081-8 2015 In conclusion, peak insulin levels followed an inverse U shape in relation to glucose intolerance in a Japanese population, whereas the impairment of glucose tolerance was associated with a delay in the time to reach peak insulin levels. Glucose 78-85 insulin Homo sapiens 20-27 25392020-7 2015 Stepwise multiple regression analysis identified post-breakfast glucose levels before titrating insulin as an independent determinant of the insulin requirement profile [Std beta (standard regression coefficient) = 0.228, p<0.01 for TDD, Std beta = -0.189, p<0.01 for B/TD ratio]. Glucose 64-71 insulin Homo sapiens 141-148 25458401-6 2015 A weak, positive and significant correlation was seen between fasting blood glucose and insulin levels in women with PCOS (P < .05). Glucose 76-83 insulin Homo sapiens 88-95 25735969-3 2015 Their blood glucose levels were tightly regulated by modifying lifestyles and insulin treatment. Glucose 12-19 insulin Homo sapiens 78-85 26073866-3 2015 When 3T3-L1 adipocytes were exposed to ROS, insulin-mediated glucose uptake was suppressed, but such phenomena were not observed in the presence of azelnidipine. Glucose 61-68 insulin Homo sapiens 44-51 26191411-1 2015 UNLABELLED: Drugs that inhibit the sodium-glucose co-transporter-2 (SGLT2) are an exciting novel, insulin-independent treatment for diabetes that block glucose reabsorption from the proximal tubules of the kidney, leading to increased glucose excretion and lower blood glucose levels. Glucose 42-49 insulin Homo sapiens 98-105 26191411-1 2015 UNLABELLED: Drugs that inhibit the sodium-glucose co-transporter-2 (SGLT2) are an exciting novel, insulin-independent treatment for diabetes that block glucose reabsorption from the proximal tubules of the kidney, leading to increased glucose excretion and lower blood glucose levels. Glucose 152-159 insulin Homo sapiens 98-105 25323013-0 2015 The negative impact of insulin therapy for acute hyperglycemia secondary to glucose load on plasma amino acid profiles in a rat model of sepsis. Glucose 76-83 insulin Homo sapiens 23-30 25323013-1 2015 BACKGROUND: In critical illnesses, insulin therapy under overfed conditions with an excessive glucose infusion may cause metabolic disturbances in skeletal muscle mainly through muscle cell glucose uptake and the inhibition of physiological protein breakdown. Glucose 94-101 insulin Homo sapiens 35-42 25323013-1 2015 BACKGROUND: In critical illnesses, insulin therapy under overfed conditions with an excessive glucose infusion may cause metabolic disturbances in skeletal muscle mainly through muscle cell glucose uptake and the inhibition of physiological protein breakdown. Glucose 190-197 insulin Homo sapiens 35-42 26291462-2 2015 Pharmacological inhibition of the sodium-glucose cotransporter-2 (SGLT2; SLC5A2) increases urinary glucose excretion, decreasing plasma glucose levels in an insulin-independent manner. Glucose 41-48 insulin Homo sapiens 157-164 26118715-9 2015 Moreover, insulin-induced glucose uptake and Akt phosphorylation at the Ser473 residue were decreased concurrently in adipocytes differentiated from 3T3-L1 preadipocytes after knockdown of Mfrn1/2. Glucose 26-33 insulin Homo sapiens 10-17 25553366-1 2015 Type 2 diabetes is a common metabolic disorder characterized by resistance to the actions of insulin to stimulate skeletal muscle glucose disposal. Glucose 130-137 insulin Homo sapiens 93-100 25338918-2 2015 Patients with type 1 diabetes control their blood glucose levels using several daily injections of exogenous insulin; however, this does not eliminate the long-term complications of hyperglycaemia. Glucose 50-57 insulin Homo sapiens 109-116 25774588-7 2015 Many studies based on intensive insulin treatment protocols targeting normal blood glucose values have in fact documented both an increased incidence of hypoglycemia and an increased mortality risk. Glucose 83-90 insulin Homo sapiens 32-39 26288254-1 2015 AIMS/INTRODUCTION: The aim of this study in patients with gestational diabetes mellitus (GDM) was to evaluate the relationship of insulin resistance and secretion to area-under-the-sensor glucose concentration-time curve from before to 120 min postmeal (CGM-AUC(0-120 min)) as determined with continuous glucose monitoring (CGM). Glucose 188-195 insulin Homo sapiens 130-137 26288254-1 2015 AIMS/INTRODUCTION: The aim of this study in patients with gestational diabetes mellitus (GDM) was to evaluate the relationship of insulin resistance and secretion to area-under-the-sensor glucose concentration-time curve from before to 120 min postmeal (CGM-AUC(0-120 min)) as determined with continuous glucose monitoring (CGM). Glucose 304-311 insulin Homo sapiens 130-137 25263249-2 2015 Strict postoperative glucose control by insulin infusion has been shown to lower morbidity, but not specifically SSI rates. Glucose 21-28 insulin Homo sapiens 40-47 25767510-3 2015 In Phase I, baseline insulin infusion was optimized to minimize the differences in fasting glucose levels to less than 30 mg/dL between any two time points between 9 a.m. and 3 p.m. Glucose 91-98 insulin Homo sapiens 21-28 25815010-8 2015 All participants received a frequently sampled intravenous glucose tolerance test, and acute insulin response after the glucose load (AIRg) was obtained. Glucose 120-127 insulin Homo sapiens 93-100 26089893-2 2015 The role of phospholipase D (PLD) as a positive modulator of glucose uptake activation by insulin in muscle and adipose cells has been demonstrated. Glucose 61-68 insulin Homo sapiens 90-97 26089893-3 2015 The role of PLD in the regulation of glucose metabolism by insulin in the primary hepatocytes has been determined in this study. Glucose 37-44 insulin Homo sapiens 59-66 26640487-0 2015 Influence of Acarbose on Plasma Glucose Fluctuations in Insulin-Treated Patients with Type 2 Diabetes: A Pilot Study. Glucose 32-39 insulin Homo sapiens 56-63 26640487-10 2015 Patients in acarbose plus insulin group achieved a significant improvement of MAGE compared to that of insulin therapy only group (5.56 +- 2.16 versus 7.50 +- 3.28 mmol/L, P = 0.044), accompanied by a significant decrease in the incremental AUC of plasma glucose concentration above 10.0 mmol/L (0.5 [0.03, 0.9] versus 0.85 [0.23,1.4] mmol/L per day, P = 0.037). Glucose 255-262 insulin Homo sapiens 26-33 26640487-12 2015 Add-on acarbose to insulin therapy further improves glucose fluctuation in patients with T2DM. Glucose 52-59 insulin Homo sapiens 19-26 26082830-8 2015 In response to high glucose medium, insulin release was detected by chemiluminescence enzyme immunoassay. Glucose 20-27 insulin Homo sapiens 36-43 26082830-12 2015 In response to glucose challenge test, secretion of insulin hormone in the medium with high glucose concentration significantly increased in the PDX-1-transduced cells related to medium with low glucose concentration. Glucose 15-22 insulin Homo sapiens 52-59 26082830-12 2015 In response to glucose challenge test, secretion of insulin hormone in the medium with high glucose concentration significantly increased in the PDX-1-transduced cells related to medium with low glucose concentration. Glucose 92-99 insulin Homo sapiens 52-59 26082830-12 2015 In response to glucose challenge test, secretion of insulin hormone in the medium with high glucose concentration significantly increased in the PDX-1-transduced cells related to medium with low glucose concentration. Glucose 92-99 insulin Homo sapiens 52-59 25709695-0 2015 Prediction of glucose intolerance at 24-28 weeks of gestation by glucose and insulin level measurements in the first trimester. Glucose 14-21 insulin Homo sapiens 77-84 25709695-4 2015 This study aimed to define the predictive value of fasting plasma glucose (FPG) and fasting plasma insulin (FPI) test in first trimester concerning the positive result of oral glucose challenge test (OGCT). Glucose 176-183 insulin Homo sapiens 99-106 26452321-4 2015 Our aim was to validate a 96-well plate-based single islet insulin secretion assay that would be as robust as previously published methods to quantify glucose-stimulated insulin secretion from mouse and human islets. Glucose 151-158 insulin Homo sapiens 59-66 26452321-4 2015 Our aim was to validate a 96-well plate-based single islet insulin secretion assay that would be as robust as previously published methods to quantify glucose-stimulated insulin secretion from mouse and human islets. Glucose 151-158 insulin Homo sapiens 170-177 26752360-3 2015 The purpose of this study was to identify possible differences in the early phase of glucose-stimulated insulin biosynthesis between large and small islets. Glucose 85-92 insulin Homo sapiens 104-111 26752360-10 2015 At the translational level, high glucose increased the proinsulin levels, and large islets showed a higher proinsulin content per cell than small islets. Glucose 33-40 insulin Homo sapiens 55-65 25864761-1 2015 Metabolic syndrome (MS), a series of physiological and metabolic disorders caused by insulin resistance, combines clinical syndrome of abdominal obesity, diabetes or impaired glucose regulation, dyslipidemia, hypertension and other metabolic diseases. Glucose 175-182 insulin Homo sapiens 85-92 25250633-0 2015 Influence of liver triglycerides on suppression of glucose production by insulin in men. Glucose 51-58 insulin Homo sapiens 73-80 25250633-1 2015 CONTEXT: The ability of insulin to suppress hepatic glucose production is impaired among subjects with increased intrahepatic triglycerides (IHTG). Glucose 52-59 insulin Homo sapiens 24-31 25250633-2 2015 However, little is known about the roles of insulin on the supporting fluxes of glucose production among patients with fatty liver. Glucose 80-87 insulin Homo sapiens 44-51 25250633-3 2015 OBJECTIVE: To evaluate the effects of insulin on fluxes through the three potential sources of plasma glucose (glycerol, the citric acid cycle, and glycogen) among patients with fatty liver. Glucose 102-109 insulin Homo sapiens 38-45 25250633-10 2015 Overproduction of glucose during hyperinsulinemia in men with fatty liver results from inadequate suppression of all the supporting fluxes of glucose production in response to insulin. Glucose 18-25 insulin Homo sapiens 38-45 25500886-5 2015 In a high-fat diet-fed mouse model of impaired glucose tolerance and type 2 diabetes, dibenzazepine administration increased L cell numbers in the intestine, improved the early insulin response to glucose, and restored glucose tolerance. Glucose 197-204 insulin Homo sapiens 177-184 25160667-2 2015 Advances in insulin formulations and insulin delivery devices have markedly improved the ability to achieve normal glucose homeostasis. Glucose 115-122 insulin Homo sapiens 12-19 25160667-2 2015 Advances in insulin formulations and insulin delivery devices have markedly improved the ability to achieve normal glucose homeostasis. Glucose 115-122 insulin Homo sapiens 37-44 25305282-1 2015 The premise of effective closed-loop insulin therapy for type 1 diabetes (T1D) relies on the accuracy of continuous interstitial fluid glucose sensing that represents the crucial afferent arm of such a system. Glucose 135-142 insulin Homo sapiens 37-44 25305282-5 2015 Plasma glucose was maintained at 113.7 +- 6.3 mg/dl using a continuous intravenous insulin infusion. Glucose 7-14 insulin Homo sapiens 83-90 25621136-2 2015 However, theoretically adding rosiglitazone to insulin could help insulin to decrease the glucose level. Glucose 90-97 insulin Homo sapiens 47-54 25621136-2 2015 However, theoretically adding rosiglitazone to insulin could help insulin to decrease the glucose level. Glucose 90-97 insulin Homo sapiens 66-73 25621136-11 2015 CONCLUSIONS: Rosiglitazone could help type 2 diabetes patients with poorly controlled glucose with insulin therapy to decrease glucose levels and reduce their daily insulin dose, but at the cost of increased total cholesterol level, hypoglycemia and edema risk. Glucose 86-93 insulin Homo sapiens 99-106 25621136-11 2015 CONCLUSIONS: Rosiglitazone could help type 2 diabetes patients with poorly controlled glucose with insulin therapy to decrease glucose levels and reduce their daily insulin dose, but at the cost of increased total cholesterol level, hypoglycemia and edema risk. Glucose 86-93 insulin Homo sapiens 165-172 25621136-11 2015 CONCLUSIONS: Rosiglitazone could help type 2 diabetes patients with poorly controlled glucose with insulin therapy to decrease glucose levels and reduce their daily insulin dose, but at the cost of increased total cholesterol level, hypoglycemia and edema risk. Glucose 127-134 insulin Homo sapiens 99-106 26064976-0 2015 Vinegar Consumption Increases Insulin-Stimulated Glucose Uptake by the Forearm Muscle in Humans with Type 2 Diabetes. Glucose 49-56 insulin Homo sapiens 30-37 26064976-3 2015 The aim of this randomised, crossover study was to investigate the effect of vinegar on glucose metabolism in muscle which is the most important tissue for insulin-stimulated glucose disposal. Glucose 88-95 insulin Homo sapiens 156-163 26064976-3 2015 The aim of this randomised, crossover study was to investigate the effect of vinegar on glucose metabolism in muscle which is the most important tissue for insulin-stimulated glucose disposal. Glucose 175-182 insulin Homo sapiens 156-163 26064976-10 2015 Vinegar"s effect on carbohydrate metabolism may be partly accounted for by an increase in glucose uptake, demonstrating an improvement in insulin action in skeletal muscle. Glucose 90-97 insulin Homo sapiens 138-145 26075283-8 2015 This may have consequences on lipid and glucose metabolism in adipose tissue and lead to a vicious cycle between impaired myokines production and insulin resistance. Glucose 40-47 insulin Homo sapiens 146-153 26273676-2 2015 Understanding the temporal secretory pattern of insulin and zinc corelease after a glucose challenge is essential for proper timing of administration of zinc sensing probes. Glucose 83-90 insulin Homo sapiens 48-55 26273679-7 2015 Unlike what is reported in cardiomyocytes, overexpression of miR-223 in human differentiated adipocytes was associated with a reduction in GLUT4 protein content and insulin-stimulated glucose uptake. Glucose 184-191 insulin Homo sapiens 165-172 26453161-1 2015 A grand challenge in the field of "smart" drug delivery has been the quest to create formulations that can sense glucose and respond by delivering an appropriate dose of insulin. Glucose 113-120 insulin Homo sapiens 170-177 26568959-1 2015 Pancreatic beta cells not only use glucose as an energy source, but also sense blood glucose levels for insulin secretion. Glucose 85-92 insulin Homo sapiens 104-111 26568959-2 2015 While pyruvate and NADH metabolic pathways are known to be involved in regulating insulin secretion in response to glucose stimulation, the roles of many other components along the metabolic pathways remain poorly understood. Glucose 115-122 insulin Homo sapiens 82-89 25750607-6 2015 Insulin sensitivity (SI ) is defined as the body response to the effects of insulin by lowering blood glucose levels. Glucose 102-109 insulin Homo sapiens 0-7 25750607-6 2015 Insulin sensitivity (SI ) is defined as the body response to the effects of insulin by lowering blood glucose levels. Glucose 102-109 insulin Homo sapiens 76-83 28356822-5 2015 RESULTS: Depending on criteria we used, insulin resistance was confirmed in 62-100% of obese patients, predominantly in the group with BMI SDS > 3. oGTT revealed isolated impaired fasting glucose (IFG) in 13.9%, impaired glucose tolerance (IGT) in 20.8% and combined IFG and IGT only in 2.8% of the obese patients. Glucose 191-198 insulin Homo sapiens 40-47 25527674-1 2015 Both genetics and lifestyle contribute to type 2 diabetes (T2D), a condition of elevated circulating glucose induced by a collection of metabolic defects including peripheral insulin resistance, elevated hepatic glucose output, and impaired pancreatic insulin secretion. Glucose 101-108 insulin Homo sapiens 175-182 25439770-8 2015 Glucose control was achieved with intravenous insulin infusion with a strict glucose monitoring protocol. Glucose 0-7 insulin Homo sapiens 46-53 25874297-4 2015 Without insulin resistance secretion of insulin in 2 hours after glucose load increased up to 3 times and content of individual fatty acids decreases in greater extent. Glucose 65-72 insulin Homo sapiens 40-47 25434967-5 2015 During visits when the patient used the single-hormone artificial pancreas, insulin was delivered based on glucose sensor readings and a predictive dosing algorithm. Glucose 107-114 insulin Homo sapiens 76-83 25131451-5 2015 In both men and women, fasting insulin and homeostasis model assessment of insulin resistance (>= 75th percentile) were significantly associated with incident diabetes and combined impaired fasting glucose/impaired glucose tolerance; however, reduced beta-cell function as measured by homeostasis model assessment of beta-cell function (< 25th percentile) was associated with incident isolated impaired fasting glucose solely in men [hazard ratio 1.35 (95% CI 1.02-1.78)] in multivariable analysis including waist-hip ratio). Glucose 201-208 insulin Homo sapiens 75-82 25131451-7 2015 CONCLUSIONS: Fasting hyperinsulinaemia and insulin resistance were strong risk factors for progression to diabetes and combined impaired fasting glucose/impaired glucose tolerance in a population with normal fasting glucose/normal glucose tolerance. Glucose 145-152 insulin Homo sapiens 26-33 25131451-7 2015 CONCLUSIONS: Fasting hyperinsulinaemia and insulin resistance were strong risk factors for progression to diabetes and combined impaired fasting glucose/impaired glucose tolerance in a population with normal fasting glucose/normal glucose tolerance. Glucose 162-169 insulin Homo sapiens 26-33 25621692-0 2015 Professional continuous glucose monitoring for the identification of type 1 diabetes mellitus among subjects with insulin therapy. Glucose 24-31 insulin Homo sapiens 114-121 25621692-9 2015 The good performance was validated by the leave-one-out method (sensitivity 83.3%, specificity 73.1%).Professional continuous glucose monitoring is a useful tool that improves identification of type 1 diabetes among diabetic patients receiving insulin therapy. Glucose 126-133 insulin Homo sapiens 244-251 26693205-6 2015 Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Glucose 131-138 insulin Homo sapiens 0-7 26202190-10 2015 Nevertheless, findings concerning the effect on ACS-related mortality of the control of glucose levels by intravenous infusion of insulin have been conflicting and intervention trials are needed to optimize the definition of hyperglycemia and to establish appropriate modalities and goals of glucose lowering treatment. Glucose 88-95 insulin Homo sapiens 130-137 25215442-2 2015 Under normal circumstances, insulin facilitates glucose uptake in skeletal muscle and adipose tissue by stimulating glucose transporter 4 (GLUT4) translocation and activity. Glucose 48-55 insulin Homo sapiens 28-35 25468647-4 2015 Furthermore, we show that inputting gene expression data of key components of the insulin signal transduction pathway leads to sensible predictions of glucose clearance rates in agreement with reported clinical measurements. Glucose 151-158 insulin Homo sapiens 82-89 25430866-3 2015 Glucose nanosensors are being incorporated in implantable devices that enable more accurate and patient-friendly real-time tracking of blood glucose levels, and are also providing the basis for glucose-responsive nanoparticles that better mimic the body"s physiological needs for insulin. Glucose 194-201 insulin Homo sapiens 280-287 25610945-0 2015 A new flavonol triglycoside derived from Anoectochilus elwesii on stimulating glucose uptake in insulin-induced human HepG2 cells. Glucose 78-85 insulin Homo sapiens 96-103 25610945-5 2015 The effects of 1-7 were evaluated on insulin-treated human HepG2 cells under high glucose conditions for stimulating glucose uptake activities. Glucose 117-124 insulin Homo sapiens 37-44 25610945-6 2015 The novel compound (4) displayed highly potent dose-dependent effect on the stimulation of glucose uptake in insulin-resistant human HepG2 cells. Glucose 91-98 insulin Homo sapiens 109-116 25687107-3 2015 Glucose metabolism activity of four compounds was tested, compounds 3 and 4 showed effect on the glucose consumption of insulin-resistant HepG2 cells. Glucose 97-104 insulin Homo sapiens 120-127 26044515-5 2015 Hyperinsulinism was diagnosed as hypoglycemia concomitant with high serum insulin in babies requiring >6 mg/kg/min intravenous glucose and THI as hyperinsulinism without maternal diabetes or genetic disorders. Glucose 130-137 insulin Homo sapiens 5-12 26387380-5 2015 METHODS: Using continuous glucose monitor (CGM), we evaluated the differences in glucose variability of 3 type 2 diabetic HD patients with poor glycemic control when switching from insulin glargine to degludec. Glucose 81-88 insulin Homo sapiens 181-188 26171112-5 2015 As regards the altered glucose metabolism, hyperinsulinaemia, both endogenous due to insulin-resistance and drug-induced, appears to promote tumour cell growth through the involvement of innate immune activation, platelet activation, increased reactive oxygen species, exposure to protumorigenic and proangiogenic cytokines, and increased substrate availability to neoplastic cells. Glucose 23-30 insulin Homo sapiens 48-55 25560470-1 2015 Glinides, including repaglinide, nateglinide and mitiglinide, are a type of fasting insulin secretagogue that could help to mimic early-phase insulin release, thus providing improved control of the postprandial glucose levels. Glucose 211-218 insulin Homo sapiens 84-91 25709214-2 2015 In a previous study, we have reported that quercetin stimulated glucose uptake in cultured C2C12 skeletal muscle through an insulin-independent mechanism involving adenosine monophosphate-activated protein kinase (AMPK). Glucose 64-71 insulin Homo sapiens 124-131 26359949-7 2015 Clinicians should be familiar with the risk factors for hypoglycemia, especially the profiles of the different classes of glucose-lowering medications such as the sulfonylureas and insulin. Glucose 122-129 insulin Homo sapiens 181-188 26428031-4 2015 Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) mimic the action of the endogenous gastrointestinal hormone GLP-1 to activate the insulin response in pancreatic beta cells in a glucose-dependent manner. Glucose 183-190 insulin Homo sapiens 136-143 26477909-10 2015 It is now well established that there are different proximal signaling pathways that mediate the effects of exercise and insulin on glucose uptake, and these distinct mechanisms are consistent with the ability of exercise to increase glucose uptake in the face of insulin resistance in people with type 2 diabetes. Glucose 132-139 insulin Homo sapiens 121-128 26477909-10 2015 It is now well established that there are different proximal signaling pathways that mediate the effects of exercise and insulin on glucose uptake, and these distinct mechanisms are consistent with the ability of exercise to increase glucose uptake in the face of insulin resistance in people with type 2 diabetes. Glucose 234-241 insulin Homo sapiens 121-128 26544055-2 2015 BACKGROUND: Treatment of diabetic ketoacidosis (DKA) requires hourly controls of blood glucose, which define changes in the intravenous glucose and insulin administration. Glucose 87-94 insulin Homo sapiens 148-155 25565442-3 2015 These new routes of insulin administration may help to suppress hypoglycemia episodes and aid to control weight gain and post-meal glucose. Glucose 131-138 insulin Homo sapiens 20-27 26846080-2 2015 This is associated with a "closed loop" insulin pump development (it controls an insulin infusion depending on the blood glucose level). Glucose 121-128 insulin Homo sapiens 40-47 26846080-2 2015 This is associated with a "closed loop" insulin pump development (it controls an insulin infusion depending on the blood glucose level). Glucose 121-128 insulin Homo sapiens 81-88 25382150-9 2015 All animals exhibited insulin, C-peptide, and glucagon responses to both glucose and arginine challenge; however, significant interindividual variation was observed. Glucose 73-80 insulin Homo sapiens 22-29 25801056-4 2015 Consistently, high insulin could give rise to the same results in the high-glucose DMEM condition, which mimicked T2D, in primary mouse hepatocytes. Glucose 75-82 insulin Homo sapiens 19-26 25801056-8 2015 The responsiveness of human hepatoma (HepG2) cells to high insulin in high-glucose condition was similar to that of primary mouse hepatocytes in terms of the altered expression of carboxylesterases. Glucose 75-82 insulin Homo sapiens 59-66 25801056-10 2015 The knockdown of HIF-1alpha or DEC1 with shRNA construct abrogated the decrease of the CES1 and CES2 expression induced by the insulin in high glucose condition in HepG2 cells. Glucose 143-150 insulin Homo sapiens 127-134 27905781-1 2014 Combination therapy In combination with other glucose-lowering medicinal products including basal insulin, when these, together with diet and exercise, do not provide adequate glycaemic control. Glucose 46-53 insulin Homo sapiens 98-105 25220191-1 2014 BACKGROUND: Combination treatment with a glucagon-like peptide-1 (GLP-1) agonist and basal insulin has been proposed as a treatment strategy for type 2 diabetes that could provide robust glucose-lowering capability with low risk of hypoglycaemia or weight gain. Glucose 187-194 insulin Homo sapiens 91-98 25279668-6 2014 These compounds also restored ER stress-impaired glucose-stimulated insulin secretion responses. Glucose 49-56 insulin Homo sapiens 68-75 25598831-4 2014 Inhibitors of SGLT2 lower blood glucose independent of the secretion and action of insulin by inhibiting renal reabsorption of glucose, thereby promoting the increased urinary excretion of excess glucose. Glucose 127-134 insulin Homo sapiens 83-90 25566193-2 2014 After a meal, insulin stimulates glycogen and lipid synthesis in the liver; in the fasted state, glucagon induces gluconeogenesis and ketogenesis, which produce glucose and ketone bodies for other tissues to use as energy sources. Glucose 161-168 insulin Homo sapiens 14-21 25515398-7 2014 RESULTS: Glucose and sucrose supplementation initially resulted in a significant increase in glucose and insulin levels compared to fructose supplementation and returned to near baseline values within 2 hours. Glucose 9-16 insulin Homo sapiens 105-112 25497641-1 2014 Continuous glucose monitoring enables innovative insulin pumps to stop infusion of insulin at selected blood glucose thresholds. Glucose 11-18 insulin Homo sapiens 49-56 25497641-1 2014 Continuous glucose monitoring enables innovative insulin pumps to stop infusion of insulin at selected blood glucose thresholds. Glucose 11-18 insulin Homo sapiens 83-90 25497641-1 2014 Continuous glucose monitoring enables innovative insulin pumps to stop infusion of insulin at selected blood glucose thresholds. Glucose 109-116 insulin Homo sapiens 49-56 25497641-1 2014 Continuous glucose monitoring enables innovative insulin pumps to stop infusion of insulin at selected blood glucose thresholds. Glucose 109-116 insulin Homo sapiens 83-90 25495645-7 2014 These data suggest liver-specific mechanisms involved in the reported insulin-sensitive phenotype of ANGPTL3-deficient humans, featuring lower plasma insulin and glucose levels. Glucose 162-169 insulin Homo sapiens 70-77 25514561-5 2014 Homeostasis model assessment for insulin resistance (HOMA-IR) was calculated using fasting blood glucose and insulin levels. Glucose 97-104 insulin Homo sapiens 33-40 25422441-2 2014 Although it has long been established that stimulation of the beta-adrenergic receptor inhibits insulin-stimulated glucose uptake in adipocytes, the mechanism has remained unclear. Glucose 115-122 insulin Homo sapiens 96-103 25320065-6 2014 During pregnancy, for example, the thresholds increase consistently to strengthen the mother"s insulin resistance to meet the increasing glucose demand of the expanding fetal brain. Glucose 137-144 insulin Homo sapiens 95-102 25320065-8 2014 Contrary to the common belief that insulin promotes glucose disposal, the results imply that insulin is the body"s "ration stamp" to restricting glucose utilization by peripheral tissues and that insulin resistance is primarily a well-evolved mechanism. Glucose 52-59 insulin Homo sapiens 35-42 25320065-8 2014 Contrary to the common belief that insulin promotes glucose disposal, the results imply that insulin is the body"s "ration stamp" to restricting glucose utilization by peripheral tissues and that insulin resistance is primarily a well-evolved mechanism. Glucose 145-152 insulin Homo sapiens 93-100 25320065-8 2014 Contrary to the common belief that insulin promotes glucose disposal, the results imply that insulin is the body"s "ration stamp" to restricting glucose utilization by peripheral tissues and that insulin resistance is primarily a well-evolved mechanism. Glucose 145-152 insulin Homo sapiens 93-100 25474091-8 2014 Insulin-stimulated glucose uptake activity was restored with the enhancement of insulin signaling pathways. Glucose 19-26 insulin Homo sapiens 0-7 25472607-2 2014 Glucose control in obese patients can be challenging due to insulin resistance. Glucose 0-7 insulin Homo sapiens 60-67 25472724-11 2014 The primary outcome is the difference between groups in insulin resistance calculated by a glucose tolerance test administered pre-operatively and 24 hours postoperatively. Glucose 91-98 insulin Homo sapiens 56-63 25517766-5 2014 RESULTS: Glucose-stimulated insulin secretion is higher in female versus male islets. Glucose 9-16 insulin Homo sapiens 28-35 25358836-1 2014 AIMS: This study was based on the hypothesis that: (1) coronary heart disease (CHD) risk is accentuated in the insulin-resistant subset of persons with normal glucose tolerance (NGT) or prediabetes (PreDM); (2) the prevalence of insulin resistance, and associated abnormalities, is greater in subjects with PreDM; and (3) insulin resistance is the major contributor to increased CHD risk in these individuals. Glucose 159-166 insulin Homo sapiens 111-118 25249503-4 2014 Interestingly, C-peptide appears to reverse the deleterious effects of high glucose in some tissues, including the kidney, the peripheral nerves, and the vasculature. Glucose 76-83 insulin Homo sapiens 15-24 25150534-5 2014 Insulin treatment alleviated the stimulatory effects of high glucose on pro-inflammatory cytokines and RANKL expression by hPDL cells. Glucose 61-68 insulin Homo sapiens 0-7 25341798-4 2014 APPROACH AND RESULTS: Healthy overweight or obese human subjects underwent adipose-tissue biopsies and quantification of insulin-mediated glucose disposal by the modified insulin suppression test. Glucose 138-145 insulin Homo sapiens 121-128 24917169-2 2014 Specifically, the insulin hormone triggers a cascade of intracellular signals in target cells mediating the uptake of glucose. Glucose 118-125 insulin Homo sapiens 18-25 24917169-3 2014 Insulin signaling triggers cellular relocalization of the glucose transporter protein GLUT4 to the cell surface, which is primarily responsible for regulated glucose import. Glucose 58-65 insulin Homo sapiens 0-7 25039620-1 2014 BACKGROUND AND PURPOSE: Insulin stimulates the transport of glucose in target tissues by triggering the translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Glucose 60-67 insulin Homo sapiens 24-31 25262585-1 2014 BACKGROUND/OBJECTIVE: Cytokines released from the adipose tissue and fatty acids (FAs) derived from lipolysis or uptake of fats go in to competition with glucose to be uptaken from the liver leads to insulin resistance (IR). Glucose 154-161 insulin Homo sapiens 200-207 25737689-4 2014 Furthermore, insulin resistance (IR) in the skeletal muscle vasculature results in impaired skeletal muscle glucose uptake and altered whole-body glucose homeostasis. Glucose 108-115 insulin Homo sapiens 13-20 25737689-7 2014 Understanding the effects of insulin and other metabolically active hormones in the vasculature should facilitate the development of new therapeutic strategies targeted at the modulation of IR and improvement of whole-body glucose tolerance. Glucose 223-230 insulin Homo sapiens 29-36 25556062-4 2014 Differentiated 3T3-L1 adipocytes were stimulated with conditioned medium derived from activated macrophages to induce insulin resistance and observed the effects of Mac-CM on insulin-mediated glucose uptake along the insulin receptor substrate-1/PI3K/Akt signaling pathway. Glucose 192-199 insulin Homo sapiens 175-182 25556062-4 2014 Differentiated 3T3-L1 adipocytes were stimulated with conditioned medium derived from activated macrophages to induce insulin resistance and observed the effects of Mac-CM on insulin-mediated glucose uptake along the insulin receptor substrate-1/PI3K/Akt signaling pathway. Glucose 192-199 insulin Homo sapiens 175-182 25556062-6 2014 mSMS enhanced AMPK phosphorylation and promoted basal glucose uptake in adipocytes; mSMS inhibited NF-kappaB activation by reducing P65 phosphorylation and improved insulin-stimulated IRS-1 tyrosine and Akt phosphorylation, leading to the restoration of insulin-mediated glucose uptake when cells were exposed to inflammatory stimulation. Glucose 54-61 insulin Homo sapiens 165-172 25556062-6 2014 mSMS enhanced AMPK phosphorylation and promoted basal glucose uptake in adipocytes; mSMS inhibited NF-kappaB activation by reducing P65 phosphorylation and improved insulin-stimulated IRS-1 tyrosine and Akt phosphorylation, leading to the restoration of insulin-mediated glucose uptake when cells were exposed to inflammatory stimulation. Glucose 271-278 insulin Homo sapiens 165-172 24656589-1 2014 Insulin resistance is strongly linked to type 2 diabetes and associated with a reduced uptake of glucose by muscle and adipose tissue. Glucose 97-104 insulin Homo sapiens 0-7 24656589-5 2014 After a meal when blood glucose levels rise, insulin is secreted by the pancreas, which, upon binding to its receptor, triggers an intracellular signaling cascade, leading to the translocation of GLUT4 from intracellular compartments to the cell surface, resulting in glucose uptake and normalization of the blood glucose levels. Glucose 24-31 insulin Homo sapiens 45-52 24656589-5 2014 After a meal when blood glucose levels rise, insulin is secreted by the pancreas, which, upon binding to its receptor, triggers an intracellular signaling cascade, leading to the translocation of GLUT4 from intracellular compartments to the cell surface, resulting in glucose uptake and normalization of the blood glucose levels. Glucose 268-275 insulin Homo sapiens 45-52 24656589-5 2014 After a meal when blood glucose levels rise, insulin is secreted by the pancreas, which, upon binding to its receptor, triggers an intracellular signaling cascade, leading to the translocation of GLUT4 from intracellular compartments to the cell surface, resulting in glucose uptake and normalization of the blood glucose levels. Glucose 268-275 insulin Homo sapiens 45-52 24910196-7 2014 Multiple linear regression analyses showed that hypertriglyceridaemic waist phenotype was significantly associated with insulin resistance after adjusting for age, BMI, family history, percentage of total body fat, smoking, alcohol intake, 2-h plasma glucose and HDL cholesterol level. Glucose 251-258 insulin Homo sapiens 120-127 24961673-9 2014 Each additional 1 mmol/l glucose challenge test result was associated with an increased likelihood of being prescribed insulin (odds ratio 1.33, 95% CI 1.17-1.51). Glucose 25-32 insulin Homo sapiens 119-126 25144424-11 2014 CONCLUSIONS: Addition of teneligliptin to insulin therapy led to a significant improvement in diurnal glycemic control and significant reductions in glucose fluctuations in 24-h periods without increasing hypoglycemia in Japanese patients with type 2 diabetes on insulin therapy, with or without other antidiabetes agents. Glucose 149-156 insulin Homo sapiens 42-49 25474091-8 2014 Insulin-stimulated glucose uptake activity was restored with the enhancement of insulin signaling pathways. Glucose 19-26 insulin Homo sapiens 80-87 25622739-6 2014 Logistic regression analysis revealed an odds ratio of 4.48(95%CI 1.53-13.15, P = 0.00) for total daily basal insulin dose within 0.2-0.3 units per kilogram, an OR of 1.31 (95%CI 1.05-1.63, P = 0.01) for self-monitoring of blood glucose (SMBG) and an OR of 3.43 (95%CI 1.18-10.01, P = 0.02) for males. Glucose 229-236 insulin Homo sapiens 110-117 25231898-0 2014 Each degree of glucose intolerance in pregnancy predicts distinct trajectories of beta-cell function, insulin sensitivity, and glycemia in the first 3 years postpartum. Glucose 15-22 insulin Homo sapiens 102-109 25231898-6 2014 RESULTS: At each of 3 months, 1 year, and 3 years postpartum, the prevalence of glucose intolerance increased from normal GCT NGT to abnormal GCT NGT to GIGT to GDM (all P < 0.001), whereas beta-cell function, assessed by the Insulin Secretion-Sensitivity Index-2 (ISSI-2), and insulin sensitivity (Matsuda index), progressively decreased across the groups (all P < 0.002). Glucose 80-87 insulin Homo sapiens 229-236 25231898-6 2014 RESULTS: At each of 3 months, 1 year, and 3 years postpartum, the prevalence of glucose intolerance increased from normal GCT NGT to abnormal GCT NGT to GIGT to GDM (all P < 0.001), whereas beta-cell function, assessed by the Insulin Secretion-Sensitivity Index-2 (ISSI-2), and insulin sensitivity (Matsuda index), progressively decreased across the groups (all P < 0.002). Glucose 80-87 insulin Homo sapiens 281-288 25231898-9 2014 CONCLUSIONS: Each degree of gestational glucose intolerance predicts distinct trajectories of beta-cell function, insulin sensitivity, and glycemia in the first 3 years postpartum that drive their differential risk of future T2DM. Glucose 40-47 insulin Homo sapiens 114-121 25273345-6 2014 Higher fasting and postload glucose levels were associated with higher cord-blood levels of insulin and leptin in all participants, irrespective of ethnicity. Glucose 28-35 insulin Homo sapiens 92-99 25414013-2 2014 Insulin in the central nervous system (CNS) affects feeding behavior and body energy stores, the metabolism of glucose and fats in the liver and adipose, and various aspects of memory and cognition. Glucose 111-118 insulin Homo sapiens 0-7 25414121-11 2014 Basal insulin can be added to a GLP-1 receptor agonist with a slow titration to target goal fasting plasma glucose. Glucose 107-114 insulin Homo sapiens 6-13 25554070-1 2014 Sodium-glucose cotransporter type 2 (SGLT-2) inhibitors (canagliflozin, dapagliflozin, empagliflozin) are new glucose-lowering agents that exert their therapeutic activity independently of insulin by facilitating glucose excretion through the kidneys. Glucose 7-14 insulin Homo sapiens 189-196 25588086-4 2014 As a result, after inhalation, there is a rapid drop in glucose levels which subsequently return to normal in a shorter time than after subcutaneous insulin administration. Glucose 56-63 insulin Homo sapiens 149-156 25787205-7 2014 A high correlation between the ratio of molar ellipticity at 208/222 nm and serum glucose levels (r (2) > 0.958) and serum insulin levels (r (2) > 0.952) strongly suggests the role of dissociation of insulin on enhanced absorption. Glucose 82-89 insulin Homo sapiens 206-213 25937839-1 2014 OBJECTIVE: To assess the presence of insulin resistance (IR) in patients with type 1 diabetes (T1DM) according to the estimated glucose disposal rate formula (eGDR) and the insulin sensitivity score (ISS) and to estimate the correlation between these two measures and identify the clinical and laboratory markers related to IR. Glucose 128-135 insulin Homo sapiens 37-44 24619287-2 2014 Diabetes was induced in monkeys by streptozotocin, and the animals were administered exogenous insulin to control blood glucose (BG). Glucose 120-127 insulin Homo sapiens 95-102 25174769-0 2014 Triglycerides and glucose index: a useful indicator of insulin resistance. Glucose 18-25 insulin Homo sapiens 55-62 25174769-3 2014 The aim of this study was to evaluate the triglycerides and glucose (TyG) index as a marker of insulin resistance and to compare it to the triglycerides/HDL cholesterol ratio (TG/HDL-C), in subjects with and without metabolic syndrome (MS). Glucose 60-67 insulin Homo sapiens 95-102 25159168-1 2014 INTRODUCTION: When insulin treatment is started in patients with type 2 diabetes mellitus (T2DM), there are many regimens that control serum glucose levels to a normal range. Glucose 141-148 insulin Homo sapiens 19-26 24903160-4 2014 Metformin enhanced basal and insulin-stimulated glucose uptake and GLUT4 translocation, reduced IRS-1 and Akt phosphorylation and ROS levels, and affected the expression of regulators of mitochondrial biogenesis in LYRM1-over-expressing adipocytes. Glucose 48-55 insulin Homo sapiens 29-36 25316597-8 2014 The risk of hypoglycemia appears to depend on coadministered glucose-lowering agents: when used as monotherapy, the frequency is comparable to that of placebo, but an increased risk is associated with concomitant use of sulfonylureas or insulin. Glucose 61-68 insulin Homo sapiens 237-244 25623546-2 2014 However, several clinical studies have reported that an intensive glucose-lowering treatment, especially when insulin or sulfonylureas are used, is associated with an increased risk of hypoglycemia and may exert negative effects on the cardiovascular risk. Glucose 66-73 insulin Homo sapiens 110-117 25705164-2 2014 With regard to the genetic factors that are altered by adiposity, a large meta-analysis on the interactions between genetic variants and body mass index with regard to fasting glucose and insulin levels was reported by the Meta-Analyses of Glucose- and Insulin-related trait Consortium (MAGIC), based on European ancestry. Glucose 240-247 insulin Homo sapiens 188-195 25826962-11 2014 CONCLUSIONS: Our findings show that IR is highly prevalent in patients with PCOS, and that this prevalence is even higher when insulin sensitivity is assessed using the glucose clamp technique. Glucose 169-176 insulin Homo sapiens 127-134 25295417-5 2014 Insulin secretion was estimated by the disposition index (DI) [(Delta insulin/Delta glucose (0-30 min) x (1/HOMA-IR)], which is an adjusted measure of beta-cell function relative to variations in insulin sensitivity. Glucose 84-91 insulin Homo sapiens 0-7 25823221-1 2014 The primary function of insulin is viewed as a hormone that controls blood glucose level. Glucose 75-82 insulin Homo sapiens 24-31 24861730-5 2014 Insulin sensitivity was determined by glucose infusion rate relative to body mass (GIR, mL/kg/min) as well as GIR per unit of insulin (M-value). Glucose 38-45 insulin Homo sapiens 0-7 25257875-6 2014 A positive correlation between endogenous glucose production and protein breakdown was observed in the insulin group (r(2) = 0.385). Glucose 42-49 insulin Homo sapiens 103-110 25093617-7 2014 After adjustment for putative confounding factors, the second, third, fourth, and fifth quintiles of total PCB were significantly inversely associated with serum insulin (-14.6%, -21.7%, -18.9%, -23.1%, P trend < .01), compared with the first quintile, but not with serum glucose (P = .45). Glucose 275-282 insulin Homo sapiens 162-169 25222757-13 2014 EAA infusion decreased (P < .05) the glucose infusion rates needed to maintain euglycemia during low (~ 40%) and high insulin (~ 24%). Glucose 40-47 insulin Homo sapiens 121-128 25271217-3 2014 Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. Glucose 163-170 insulin Homo sapiens 81-88 25271217-3 2014 Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. Glucose 163-170 insulin Homo sapiens 118-125 25271217-3 2014 Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. Glucose 205-212 insulin Homo sapiens 81-88 25271217-3 2014 Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. Glucose 205-212 insulin Homo sapiens 118-125 25671206-1 2014 PURPOSE: Insulin inhibits glucose release in the liver but increases glucose absorption in muscles. Glucose 26-33 insulin Homo sapiens 9-16 25671206-1 2014 PURPOSE: Insulin inhibits glucose release in the liver but increases glucose absorption in muscles. Glucose 69-76 insulin Homo sapiens 9-16 25671206-2 2014 When insulin cannot properly control glucose, it negatively affects glucose metabolism and, furthermore, contributes to the onset of metabolic syndrome and chronic disease. Glucose 37-44 insulin Homo sapiens 5-12 25671206-2 2014 When insulin cannot properly control glucose, it negatively affects glucose metabolism and, furthermore, contributes to the onset of metabolic syndrome and chronic disease. Glucose 68-75 insulin Homo sapiens 5-12 25842584-11 2014 CONCLUSION: Elevated ferritin levels without evident iron overload may affect glucose homeostasis, leading to insulin resistance in conjunction with inflammatory changes as seen by elevated C-reactive protein levels. Glucose 78-85 insulin Homo sapiens 110-117 25842594-1 2014 Insulin is an effective glucose lowering agent and key component of effective diabetes management. Glucose 24-31 insulin Homo sapiens 0-7 26885476-1 2014 BACKGROUND: Chronic exposure to high glucose-containing peritoneal dialysis solution and consequent abdominal obesity are potential sources of insulin resistance in patients requiring prevalent peritoneal dialysis. Glucose 37-44 insulin Homo sapiens 143-150 25073516-3 2014 Recently, a large-scale meta-analysis of genome-wide association studies for beta cell function and insulin resistance in the European ancestry was reported by the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC). Glucose 181-188 insulin Homo sapiens 100-107 25237037-2 2014 Insulin binding to cell surface insulin receptors engages many signaling intermediates operating in parallel and in series to control glucose, energy, and lipids while also regulating mitogenesis and development. Glucose 134-141 insulin Homo sapiens 0-7 25237037-2 2014 Insulin binding to cell surface insulin receptors engages many signaling intermediates operating in parallel and in series to control glucose, energy, and lipids while also regulating mitogenesis and development. Glucose 134-141 insulin Homo sapiens 32-39 25845046-3 2014 Glucose also regulates insulin gene transcription through PDX-1. Glucose 0-7 insulin Homo sapiens 23-30 25280207-7 2014 Excess exogenous insulin may also play a role in overcoming the decreased utilization and transport of glucose in patients with Alzheimer"s disease. Glucose 103-110 insulin Homo sapiens 17-24 25437865-8 2014 Insulin resistance was evaluated by HOMA-IR index and glucose tolerance test. Glucose 54-61 insulin Homo sapiens 0-7 25472042-13 2014 Culturing TallyHO morulae with the AMPK activator metformin led to a reversal of all the abnormal findings, including increased AMPK phosphorylation, improved insulin-stimulated glucose uptake and normalisation of lipid accumulation. Glucose 178-185 insulin Homo sapiens 159-166 25194457-8 2014 These data suggest that primary and secondary hyperaldosteronism may contribute to worsening glucose tolerance by impairing insulin sensitivity or insulin secretion in humans. Glucose 93-100 insulin Homo sapiens 124-131 25208321-4 2014 The expression of immunogenic, pluripotent, and pancreatic markers was examined, and glucose-stimulated insulin release in vitro was also assessed. Glucose 85-92 insulin Homo sapiens 104-111 25208321-5 2014 Insulin-producing cells that differentiated from PDPCs were transplanted under the kidney capsule of streptozotocin-induced diabetic mice, and glucose levels and glucose tolerance were measured. Glucose 143-150 insulin Homo sapiens 0-7 25208321-5 2014 Insulin-producing cells that differentiated from PDPCs were transplanted under the kidney capsule of streptozotocin-induced diabetic mice, and glucose levels and glucose tolerance were measured. Glucose 162-169 insulin Homo sapiens 0-7 25419971-8 2014 In adipose derived stem cells differentiated on a polycaprolactone-fiber matrix; an increased sensitivity in insulin-stimulated glucose uptake was detected when cells were grown on either aligned or random matrices. Glucose 128-135 insulin Homo sapiens 109-116 25410473-8 2014 After treatment intensification, there was an increased use of DPP-4 inhibitors, insulin, and GLP-1 analogues, achieving reductions in HbA1c, fasting plasma glucose, and postprandial glucose. Glucose 183-190 insulin Homo sapiens 81-88 25285200-1 2014 Blood glucose levels are controlled by well-known physiological feedback loops: high glucose levels promote insulin release from the pancreas, which in turn stimulates cellular glucose uptake. Glucose 6-13 insulin Homo sapiens 108-115 25184989-2 2014 The aim of this study was to use such information to determine insulin sensitivity and insulin secretion so as to calculate an oral glucose disposition index (DI(OGTT)) that is a measure of pancreatic beta-cell insulin secretory compensation for changing insulin sensitivity. Glucose 132-139 insulin Homo sapiens 63-70 25184989-11 2014 We hereby derive and validate a novel OGTT-derived measurement of insulin sensitivity across the entire glucose tolerance continuum and demonstrate that beta-cell compensation for changing insulin sensitivity can be readily calculated from clinical variables collected during OGTT. Glucose 104-111 insulin Homo sapiens 66-73 25091498-0 2014 Insulin drives glucose-dependent insulinotropic peptide expression via glucose-dependent regulation of FoxO1 and LEF1/beta-catenin. Glucose 15-22 insulin Homo sapiens 0-7 25091498-1 2014 Minutes after ingestion of fat or carbohydrates, vesicles stored in enteroendocrine cells release their content of incretin peptide hormones that, together with absorbed glucose, enhance insulin secretion by beta-pancreatic cells. Glucose 170-177 insulin Homo sapiens 187-194 25091498-3 2014 Here we show that insulin stimulates the expression of the major human incretin, glucose-dependent insulinotropic peptide (GIP) in enteroendocrine cells but requires glucose to do it. Glucose 81-88 insulin Homo sapiens 18-25 25091498-5 2014 Our results reveal a glucose-regulated feedback loop at the entero-insular axis, where glucose levels determine basal and insulin-induced Gip expression; GIP stimulation of insulin release, physiologically ensures a fine control of glucose homeostasis. Glucose 21-28 insulin Homo sapiens 122-129 25091498-5 2014 Our results reveal a glucose-regulated feedback loop at the entero-insular axis, where glucose levels determine basal and insulin-induced Gip expression; GIP stimulation of insulin release, physiologically ensures a fine control of glucose homeostasis. Glucose 87-94 insulin Homo sapiens 122-129 25084624-4 2014 Insulin secretion from pancreatic beta-cells is the primary mechanism by which the concentration of blood glucose is reduced. Glucose 106-113 insulin Homo sapiens 0-7 25217232-4 2014 In the insulin resistance state and diabetes this communication has been impaired leading to different disorders, for instance, diminished insulin production by pancreatic beta cells, reduced heart and skeletal muscle contractility, reduced NO production by endothelial cells, increased glucose production by liver, increased lipolysis by adipose cells, reduced immune responses, reduced cognitive functions, among others. Glucose 287-294 insulin Homo sapiens 7-14 25224502-2 2014 Insulin increases glucose uptake into muscle cells by stimulating glucose transporter (GLUT4) translocation from intracellular compartments to the cell surface. Glucose 18-25 insulin Homo sapiens 0-7 24879834-0 2014 The adaptor protein APPL2 inhibits insulin-stimulated glucose uptake by interacting with TBC1D1 in skeletal muscle. Glucose 54-61 insulin Homo sapiens 35-42 24879834-1 2014 Insulin stimulates glucose uptake by promoting the trafficking of GLUT4 to the plasma membrane in muscle cells, and impairment of this insulin action contributes to hyperglycemia in type 2 diabetes. Glucose 19-26 insulin Homo sapiens 0-7 24879834-1 2014 Insulin stimulates glucose uptake by promoting the trafficking of GLUT4 to the plasma membrane in muscle cells, and impairment of this insulin action contributes to hyperglycemia in type 2 diabetes. Glucose 19-26 insulin Homo sapiens 135-142 24879834-4 2014 We show that insulin-evoked plasma membrane recruitment of GLUT4 and glucose uptake are impaired by APPL2 overexpression but enhanced by APPL2 knockdown. Glucose 69-76 insulin Homo sapiens 13-20 24879834-8 2014 Substitution of serine 235 with alanine diminishes APPL2-mediated inhibition on insulin-dependent TBC1D1 phosphorylation on threonine 596 and the suppressive effects of TBC1D1 on insulin-induced glucose uptake and GLUT4 translocation to the plasma membrane in cultured myotubes. Glucose 195-202 insulin Homo sapiens 80-87 24879834-8 2014 Substitution of serine 235 with alanine diminishes APPL2-mediated inhibition on insulin-dependent TBC1D1 phosphorylation on threonine 596 and the suppressive effects of TBC1D1 on insulin-induced glucose uptake and GLUT4 translocation to the plasma membrane in cultured myotubes. Glucose 195-202 insulin Homo sapiens 179-186 24879834-9 2014 Therefore, the APPL2-TBC1D1 interaction is a key step to fine tune insulin-stimulated glucose uptake by regulating the membrane recruitment of GLUT4 in skeletal muscle. Glucose 86-93 insulin Homo sapiens 67-74 24947349-0 2014 Changes in glucose and fat metabolism in response to the administration of a hepato-preferential insulin analog. Glucose 11-18 insulin Homo sapiens 97-104 25047698-4 2014 Bivariate correlations were made between insulin sensitivity index, acute insulin response to glucose and disposition index and both adiposity measures (BMI, waist circumference and body fat mass) and total plasma free fatty acid levels. Glucose 94-101 insulin Homo sapiens 74-81 25047698-7 2014 Adiposity explained 13, 4 and 5% of the variation in insulin sensitivity index, acute insulin response to glucose and disposition index, respectively. Glucose 106-113 insulin Homo sapiens 86-93 25047698-8 2014 After adjustment, no adiposity measure was associated with free fatty acid level, but total plasma free fatty acid level was inversely associated with insulin sensitivity index (beta = -0.133), acute insulin response to glucose (beta = -0.148) and disposition index [beta = -0.218 (P values <0.01)]. Glucose 220-227 insulin Homo sapiens 200-207 25047698-9 2014 Plasma free fatty acid concentration accounted for 1.5, 2 and 4% of the variation in insulin sensitivity index, acute insulin response to glucose and disposition index, respectively. Glucose 138-145 insulin Homo sapiens 118-125 25071077-3 2014 We hypothesized that measured insulin sensitivity (glucose infusion rate [GIR]) would be associated with early markers of DN reflected by estimated glomerular filtration rate (eGFR) and albumin-creatinine ratio (ACR) in adolescents with type 2 diabetes. Glucose 51-58 insulin Homo sapiens 30-37 25112609-4 2014 RESULTS: Adding a dipeptidyl peptidase-4 inhibitor to insulin treatment resulted in a glucose-lowering effect of ~ 6.6-8.7 mmol/mol (0.60-0.80%) from a baseline HbA1c of 67-78 mmol/mol (8.3-9.3%), without increasing the risk of hypoglycaemia. Glucose 86-93 insulin Homo sapiens 54-61 25139882-10 2014 However, high insulin infusion rates prevent these doses of glucagon from significantly increasing glucose output and may reduce glucagon effectiveness in preventing hypoglycemia when used in the artificial pancreas. Glucose 99-106 insulin Homo sapiens 14-21 25287601-8 2014 Enzyme-linked immunosorbent assay analysis validated the insulin secretion of islet-like cell clusters in response to the glucose stimulation. Glucose 122-129 insulin Homo sapiens 57-64 24452875-2 2014 We examined the correlation between glucagon/insulin ratio (G/I) after glucose challenge and hemoglobin A1C (A1C) in subjects with and without pancreatic cancer. Glucose 71-78 insulin Homo sapiens 45-52 24423054-8 2014 RESULTS: The maximum increment in plasma insulin concentration in response to glucose was significantly higher in female (395 +- 58 ng/l) than male (172 +- 37 ng/l, P<0.05) pony foals 2 weeks after birth and the area under the insulin curve was significantly greater in females at this age. Glucose 78-85 insulin Homo sapiens 41-48 24423054-8 2014 RESULTS: The maximum increment in plasma insulin concentration in response to glucose was significantly higher in female (395 +- 58 ng/l) than male (172 +- 37 ng/l, P<0.05) pony foals 2 weeks after birth and the area under the insulin curve was significantly greater in females at this age. Glucose 78-85 insulin Homo sapiens 230-237 24423054-9 2014 At 12 weeks, the insulin increment in response to glucose was significantly greater in fillies 45 min post infusion. Glucose 50-57 insulin Homo sapiens 17-24 24142067-4 2014 According to our data, a relationship between renal function and glucose values and acute insulin resistance in the early phase of STEMI was detectable, since a significant, indirect correlation between eGFR, insulin values, and glycemia was observed. Glucose 65-72 insulin Homo sapiens 90-97 25364684-6 2014 Biochemical diagnostic criteria used were plasma concentrations of glucose <55 mg/dl with corresponding insulin level >3.0 muU/ml (18 pmol/L) and C-peptide of >0.6 ng/ml (0.2 nmol/L). Glucose 67-74 insulin Homo sapiens 107-114 24648294-12 2014 The low adipogenic ability of EAT-MCs might be associated with an insulin-resistant state because chronic insulin treatment reduced the inflammatory cytokine expression levels, improved the glucose consumption, and increased the post-translational modifications (PTMs) of the glycolytic enzyme phosphoglycerate mutase 1 (PGAM1). Glucose 190-197 insulin Homo sapiens 106-113 25119313-11 2014 Furthermore, the overall insulin sensitivity and beta-cell responsiveness for all glucose tolerance states were similar in Japanese and Caucasians after accounting for differences in body mass index. Glucose 82-89 insulin Homo sapiens 25-32 24835190-9 2014 Importantly, the rhythms in cortisol primarily but also insulin sensitivity drove the declines in evening glucose tolerance (r=0.86; p=0.002). Glucose 106-113 insulin Homo sapiens 56-63 25205589-0 2014 Use of microdialysis-based continuous glucose monitoring to drive real-time semi-closed-loop insulin infusion. Glucose 38-45 insulin Homo sapiens 93-100 25422763-10 2014 Treatment with insulin and incubation under a low glucose level decreased the ApoM levels in HepG2 cells. Glucose 50-57 insulin Homo sapiens 15-22 25332473-9 2014 Changes in plasma BCAAs across all diets were negatively correlated with changes in the metabolic clearance rate of insulin (rho = -0.18, P = 0.03) and positively correlated with changes in the acute insulin response to glucose (rho = 0.15, P = 0.05). Glucose 220-227 insulin Homo sapiens 200-207 25239597-1 2014 It is is well known that insulin stimulates glucose transport and epithelial Na(+) channel (ENaC)-mediated Na(+) reabsorption; however, the action of insulin on Cl(-) secretion is not fully understood. Glucose 44-51 insulin Homo sapiens 25-32 25264948-3 2014 Lowering the insulin dose may be advantageous in the initial hours of therapy when a gradual decrease in glucose, electrolytes, and resultant osmolality is desired. Glucose 105-112 insulin Homo sapiens 13-20 24637346-5 2014 Insulin resistance was assessed using the euglycemic-hyperinsulinemic clamp (40 mU m(-2) min(-1)) with isotope dilution ([6,6-H2]-glucose). Glucose 134-141 insulin Homo sapiens 0-7 25176602-1 2014 BACKGROUND: Glucose-stimulated insulin secretion correlates inversely with the degree of whole-body insulin sensitivity suggesting a crosstalk between peripheral organs and pancreas. Glucose 12-19 insulin Homo sapiens 31-38 25211370-3 2014 Stage (S) 7 cells expressed key markers of mature pancreatic beta cells, including MAFA, and displayed glucose-stimulated insulin secretion similar to that of human islets during static incubations in vitro. Glucose 103-110 insulin Homo sapiens 122-129 25538363-6 2014 PATIENTS AND METHODS: The weight of hundred pregnant women was measured between 24 to 32 weeks of pregnancy and their insulin resistance was measured using Homeostatic Model Assessment (HOMA-IR) from fasting serum glucose and fasting serum insulin. Glucose 214-221 insulin Homo sapiens 118-125 25355031-11 2014 However, this review suggests that scheduled insulin (basal-bolus) is effective in attainment of glucose targets. Glucose 97-104 insulin Homo sapiens 45-52 25333402-7 2014 Despite improvement of exogenous insulin therapy, more than 50% of these patients experience severe glucose control problems, which cause up to 50% long-term mortality. Glucose 100-107 insulin Homo sapiens 33-40 25108160-13 2014 CONCLUSION: In this case-control study, individuals with PTSD had a hyperinsulinemic response to oral glucose challenge compared to controls, suggestive of insulin resistance. Glucose 102-109 insulin Homo sapiens 73-80 25796774-2 2014 These disorders could have some impact on other systems such as the glucose metabolism regulation with an increased risk of insulin resistance and type 2 diabetes. Glucose 68-75 insulin Homo sapiens 124-131 25473328-3 2014 A novel approach of treatment is to target the incretin mimetic hormones, which are secreted by intestinal cells in response to food intake, provoking glucose-dependent insulin secretion from the pancreas. Glucose 151-158 insulin Homo sapiens 169-176 25443077-12 2014 The insulin response to glucose alone fell progressively over 12 months but the glucose clearance/metabolism (M of H-clamp) did not change significantly until 12 months. Glucose 24-31 insulin Homo sapiens 4-11 25028245-1 2014 Insulin resistance, a hallmark of impaired glucose tolerance and type 2 diabetes (T2D), arises from dysfunction of insulin action and subsequent glucose uptake by peripheral tissues, predominantly skeletal muscle and fat. Glucose 43-50 insulin Homo sapiens 0-7 25582477-8 2014 The oral glucose tolerance test (OGTT) showed fasting glucose 8.17 mmol/L, insulin <2.0 mU/L, 2 h glucose 8.69 mmol/L, insulin 5.06 mU /L. Glucose 9-16 insulin Homo sapiens 75-82 25203779-5 2014 Taking all these factors together, sulfonylthiourea 7 acts as an insulin secretagogue and insulinomimetic agent on glucose homeostasis, and does not exhibit toxicity in acute treatment. Glucose 115-122 insulin Homo sapiens 65-72 25024374-5 2014 Paradoxically, both glucose- and glutamine-stimulated insulin secretion were severely impaired in H454Y mice. Glucose 20-27 insulin Homo sapiens 54-61 25028522-5 2014 After insulin spray application in lean subjects, a higher glucose infusion rate was necessary to maintain euglycemia compared with placebo. Glucose 59-66 insulin Homo sapiens 6-13 25441945-3 2014 Administration of FFAR1 agonists has been proved to potentiate glucose-stimulated insulin secretion from pancreatic beta-cells. Glucose 63-70 insulin Homo sapiens 82-89 25185805-2 2014 Strong evidence indicates that glucocorticoids impair insulin-mediated glucose uptake and food intake. Glucose 71-78 insulin Homo sapiens 54-61 26137510-5 2014 Fasting plasma glucose levels were decreased by 3.74 mg/dL (- 5.28%: 95% CI - 4.37 to - 3.09 mg/dL, p = 0.029) in MS and by 14.97 mg/dL (10.40%: 95% CI - 15.79 to 14.15 mg/dL, p < 0.001) in T2DM, and insulin levels were also reduced by 10.39% and 25.93%, respectively. Glucose 15-22 insulin Homo sapiens 203-210 25376904-2 2014 Insulin promotes glucose uptake by cardiomyocytes and its use as a substrate for glycolysis and mitochondrial oxidation in order to maintain the high cardiac energy demands. Glucose 17-24 insulin Homo sapiens 0-7 25377857-2 2014 Rab2A knockdown inhibited glucose-stimulated insulin secretion and concomitantly enlarged the ERGIC in insulin-secreting cells. Glucose 26-33 insulin Homo sapiens 45-52 25383562-2 2014 The cascade of molecular events encompassing the initial sensing and transport of glucose into the beta cell, culminating with the exocytosis of the insulin large dense core granules (LDCVs) is termed "stimulus-secretion coupling." Glucose 82-89 insulin Homo sapiens 149-156 25267863-1 2014 Prandial glucose regulation is a major challenge for the artificial pancreas using subcutaneous insulin (without a feedforward bolus) due to insulin"s slow absorption-peak (50-60 min). Glucose 9-16 insulin Homo sapiens 96-103 25267863-1 2014 Prandial glucose regulation is a major challenge for the artificial pancreas using subcutaneous insulin (without a feedforward bolus) due to insulin"s slow absorption-peak (50-60 min). Glucose 9-16 insulin Homo sapiens 141-148 25418087-1 2014 In pancreatic ?-cells, K,ATP channels respond to changes in glucose to regulate cell excitability and insulin release. Glucose 60-67 insulin Homo sapiens 102-109 25365322-4 2014 Insulin signaling under these conditions was assessed by measuring tyrosine phosphorylation of insulin receptor (InsR), insulin receptor substrate-1 (IRS-1), and serine 473 phosphorylation of Akt, followed by a functional assay using 14C-2-deoxyglucose [14C]-2DG to measure glucose uptake in these cells. Glucose 245-252 insulin Homo sapiens 0-7 25365322-5 2014 FGF21 alone caused a modest increase of glucose uptake, but treatment with FGF21 in combination with insulin had a synergistic effect on glucose uptake in these cells. Glucose 137-144 insulin Homo sapiens 101-108 25365322-6 2014 The presence of FGF21 also effectively lowered the insulin concentration required to achieve the same level of glucose uptake compared to the absence of FGF21 by 10-fold. Glucose 111-118 insulin Homo sapiens 51-58 25365322-9 2014 Taken together, our data demonstrate that acute co-treatment of hASC-adipocytes with FGF21 and insulin can result in a synergistic improvement in glucose uptake. Glucose 146-153 insulin Homo sapiens 95-102 26021685-9 2014 CONCLUSIONS: An intravenous bolus of 10 units regular insulin with 10 gram glucose was able to decrease the serum -potassium level effectively and additionally increase serum glucose in LDLT patients. Glucose 75-82 insulin Homo sapiens 54-61 26021685-9 2014 CONCLUSIONS: An intravenous bolus of 10 units regular insulin with 10 gram glucose was able to decrease the serum -potassium level effectively and additionally increase serum glucose in LDLT patients. Glucose 175-182 insulin Homo sapiens 54-61 25395942-6 2014 RESULTS: Insulin dosing was targeted to obtain a mean daily glucose level < 7.8 mmol/l. Glucose 60-67 insulin Homo sapiens 9-16 25373904-3 2014 We show here, using a metabolomics-based approach, that cytosolic glutamate derived from the malate-aspartate shuttle upon glucose stimulation underlies the stimulatory effect of incretins and that glutamate uptake into insulin granules mediated by cAMP/PKA signaling amplifies insulin release. Glucose 123-130 insulin Homo sapiens 220-227 25373904-3 2014 We show here, using a metabolomics-based approach, that cytosolic glutamate derived from the malate-aspartate shuttle upon glucose stimulation underlies the stimulatory effect of incretins and that glutamate uptake into insulin granules mediated by cAMP/PKA signaling amplifies insulin release. Glucose 123-130 insulin Homo sapiens 278-285 25383313-8 2014 These findings indicate that (1) WH activates AMPK and insulin independently enhances glucose uptake following translocation of Glut4 to the plasma membrane, (2) activation of AMPKalpha by WH is mediated by the LKB1 pathway, without altering the Ca(2+)-dependent pathway, and (3) L6 myotubes express only one type of peptide transporter (PHT1; SLC15a4), which incorporates WH into cells to activate AMPKalpha. Glucose 86-93 insulin Homo sapiens 55-62 24931673-3 2014 Building upon recent successes in mathematical modeling of the human glucose-insulin system, we show that both food intake and insulin therapy likely demand increasingly precise control over insulin sensitivity if oscillations at a healthy average glucose concentration are to be maintained. Glucose 69-76 insulin Homo sapiens 77-84 24931673-3 2014 Building upon recent successes in mathematical modeling of the human glucose-insulin system, we show that both food intake and insulin therapy likely demand increasingly precise control over insulin sensitivity if oscillations at a healthy average glucose concentration are to be maintained. Glucose 69-76 insulin Homo sapiens 127-134 25331725-3 2014 Insulin sensitivity was assessed by the Matsuda method from an oral glucose tolerance test. Glucose 68-75 insulin Homo sapiens 0-7 25325535-0 2014 Molecular mechanisms for the regulation of insulin-stimulated glucose uptake by small guanosine triphosphatases in skeletal muscle and adipocytes. Glucose 62-69 insulin Homo sapiens 43-50 25325535-1 2014 Insulin is a hormone that regulates the blood glucose level by stimulating various physiological responses in its target tissues. Glucose 46-53 insulin Homo sapiens 0-7 25325535-2 2014 In skeletal muscle and adipose tissue, insulin promotes membrane trafficking of the glucose transporter GLUT4 from GLUT4 storage vesicles to the plasma membrane, thereby facilitating the uptake of glucose from the circulation. Glucose 84-91 insulin Homo sapiens 39-46 25325535-3 2014 Detailed mechanisms underlying insulin-dependent intracellular signal transduction for glucose uptake remain largely unknown. Glucose 87-94 insulin Homo sapiens 31-38 25325535-4 2014 In this article, I give an overview on the recently identified signaling network involving Rab, Ras, and Rho family small guanosine triphosphatases (GTPases) that regulates glucose uptake in insulin-responsive tissues. Glucose 173-180 insulin Homo sapiens 191-198 25179575-1 2014 The increase in insulin response to oral glucose compared with glucose given by intravenous injection is termed the incretin effect and is mediated by two peptide hormones secreted from the gut in response to nutrient intake: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Glucose 41-48 insulin Homo sapiens 16-23 25330241-10 2014 Raptor knock-down enhanced the effect of insulin on glucose transport in insulin resistant adipocytes. Glucose 52-59 insulin Homo sapiens 41-48 25330241-10 2014 Raptor knock-down enhanced the effect of insulin on glucose transport in insulin resistant adipocytes. Glucose 52-59 insulin Homo sapiens 73-80 25313899-5 2014 Although brite differentiation of adipocytes as well as browning of white adipose tissue entailed substantially elevated glucose uptake by adipose tissue, the capacity of insulin to stimulate glucose uptake surprisingly was not higher in the brite state. Glucose 192-199 insulin Homo sapiens 171-178 25317246-7 2014 Artificial pancreas has enabled to a certain extent to close the loop between blood glucose level and insulin delivery with devices armed with meal and exercise announcements, dual hormone delivery and pramlintide infusion. Glucose 84-91 insulin Homo sapiens 102-109 25180545-2 2014 Insulin-loaded PLGA nanoparticles with a size around 450 nm were dehydrated using a standard freeze-drying cycle, using trehalose, glucose, sucrose, fructose, and sorbitol at 10% (w/v) as cryoprotectants. Glucose 131-138 insulin Homo sapiens 0-7 25307742-6 2014 We document a similar pattern in the early phases of diet-induced insulin resistance, and propose that FoxOs are required to enable the liver to direct nutritionally derived carbons to glucose versus lipid metabolism. Glucose 185-192 insulin Homo sapiens 66-73 25303528-9 2014 In adipocytes, PAHSAs signal through GPR120 to enhance insulin-stimulated glucose uptake. Glucose 74-81 insulin Homo sapiens 55-62 25303535-5 2014 Furthermore, these cells secrete human insulin into the serum of mice shortly after transplantation in a glucose-regulated manner, and transplantation of these cells ameliorates hyperglycemia in diabetic mice. Glucose 105-112 insulin Homo sapiens 39-46 25417447-1 2014 BACKGROUND: Insulin degludec (IDeg) is a basal insulin with a stable, flat action profile and an even distribution of the blood glucose lowering effect over 24 hou rs. Glucose 128-135 insulin Homo sapiens 12-19 25507175-1 2014 BACKGROUND: Insulin degludec (IDeg) is a basal insulin with a stable, flat action profile and an even distribution of the blood glucose lowering effect over 24 hou rs. Glucose 128-135 insulin Homo sapiens 12-19 25285200-1 2014 Blood glucose levels are controlled by well-known physiological feedback loops: high glucose levels promote insulin release from the pancreas, which in turn stimulates cellular glucose uptake. Glucose 85-92 insulin Homo sapiens 108-115 25285200-1 2014 Blood glucose levels are controlled by well-known physiological feedback loops: high glucose levels promote insulin release from the pancreas, which in turn stimulates cellular glucose uptake. Glucose 85-92 insulin Homo sapiens 108-115 24998009-1 2014 BACKGROUND: Many patients with advanced type 2 diabetes do not meet their glycated haemoglobin targets and randomised controlled studies comparing the efficacy of pump treatment and multiple daily injections for lowering glucose in insulin-treated patients have yielded inconclusive results. Glucose 221-228 insulin Homo sapiens 232-239 25241191-3 2014 This inhibitory effect further inhibits insulin stimulated glucose uptake due to decreased cell membrane translocation of glucose transporter 4 (GLUT4), resulting in impaired cancer cell proliferation. Glucose 59-66 insulin Homo sapiens 40-47 25242225-1 2014 Type 2 diabetes is caused by insulin resistance coupled with an inability to produce enough insulin to control blood glucose, and thiazolidinediones (TZDs) are the only current antidiabetic agents that function primarily by increasing insulin sensitivity. Glucose 117-124 insulin Homo sapiens 92-99 25242225-1 2014 Type 2 diabetes is caused by insulin resistance coupled with an inability to produce enough insulin to control blood glucose, and thiazolidinediones (TZDs) are the only current antidiabetic agents that function primarily by increasing insulin sensitivity. Glucose 117-124 insulin Homo sapiens 92-99 25561123-6 2014 Insulin resistance was calculated according to the oral glucose tolerance test with 1.75 g/kg glucose maximum 75 g glucose. Glucose 56-63 insulin Homo sapiens 0-7 25561123-6 2014 Insulin resistance was calculated according to the oral glucose tolerance test with 1.75 g/kg glucose maximum 75 g glucose. Glucose 94-101 insulin Homo sapiens 0-7 25561123-6 2014 Insulin resistance was calculated according to the oral glucose tolerance test with 1.75 g/kg glucose maximum 75 g glucose. Glucose 94-101 insulin Homo sapiens 0-7 24687695-2 2014 In a preclinical proof-of-concept trial, the performance of the glucose measurement at the site of insulin infusion was assessed. Glucose 64-71 insulin Homo sapiens 99-106 24687695-6 2014 These preclinical in vivo results demonstrate that single-port glucose monitoring is feasible at the site of insulin infusion. Glucose 63-70 insulin Homo sapiens 109-116 28324382-1 2014 Glucose-dependent insulinotropic polypeptide (GIP), a gut peptide released in response to food intake brings about secretion of insulin in a glucose-dependent manner upon binding to its receptor, GIPR. Glucose 141-148 insulin Homo sapiens 18-25 25104497-3 2014 Glucocorticoid blockade lowered fasting glucose and insulin levels and improved insulin sensitivity of FFA and glycerol turnover and hepatic glucose production. Glucose 141-148 insulin Homo sapiens 80-87 25282010-7 2014 Insulin lispro, insulin aspart, and insulin glulisine are rapidly absorbed after injection and thus provide better coverage of the post-prandial glucose surge compared with human insulin. Glucose 145-152 insulin Homo sapiens 0-7 25282010-7 2014 Insulin lispro, insulin aspart, and insulin glulisine are rapidly absorbed after injection and thus provide better coverage of the post-prandial glucose surge compared with human insulin. Glucose 145-152 insulin Homo sapiens 16-23 25282010-7 2014 Insulin lispro, insulin aspart, and insulin glulisine are rapidly absorbed after injection and thus provide better coverage of the post-prandial glucose surge compared with human insulin. Glucose 145-152 insulin Homo sapiens 36-43 25256761-2 2014 Although alterations in glucose metabolism (i.e. insulin resistance), in the presence of excessive fat tissue are often explained by the consequences of dysfunctional adipose tissue, evidence is emerging that also altered brain functions might be an important determinant of insulin resistance. Glucose 24-31 insulin Homo sapiens 49-56 25233421-1 2014 Insulin plays a fundamental role in whole-body glucose homeostasis. Glucose 47-54 insulin Homo sapiens 0-7 25187163-7 2014 Furthermore, we found that PDLSC-derived ICCs were capable of secreting insulin in response to high concentrations of glucose, validating their functional differentiation into islet cells. Glucose 118-125 insulin Homo sapiens 72-79 24169498-3 2014 We recently proposed a pato-physiology-based glucose control protocol which takes into account patient glucose/carbohydrate intake and insulin resistance. Glucose 45-52 insulin Homo sapiens 135-142 25161114-3 2014 This study evaluated the contribution of continuous glucose monitoring (CGM) to the management of insulin regimen. Glucose 52-59 insulin Homo sapiens 98-105 24702712-4 2014 RESULTS: Human skeletal muscle exhibited increased glucose uptake with insulin (1.85-fold; p < 0.05) and stimulated phosphorylation of PKB/Akt and AMPK (0.98 +- 0.23 and 1.49 +- 0.13, respectively, phosphorylated: total; p < 0.05). Glucose 51-58 insulin Homo sapiens 71-78 24702738-4 2014 RESULTS: Acute exposure of clonal beta cells to human C-peptide resulted in concentration-dependent inhibitory effects on insulin secretion at 5.6 mM (p < 0.05-p < 0.001) and 16.7 mM (p < 0.01-p < 0.001) glucose. Glucose 216-223 insulin Homo sapiens 54-63 24702738-9 2014 C-peptide also inhibited in vivo glucose-stimulated insulin release and impaired glucose tolerance in mice. Glucose 33-40 insulin Homo sapiens 0-9 24702738-9 2014 C-peptide also inhibited in vivo glucose-stimulated insulin release and impaired glucose tolerance in mice. Glucose 33-40 insulin Homo sapiens 52-59 25047649-0 2014 Estimates of insulin sensitivity from the intravenous-glucose-modified-clamp test depend on suppression of lipolysis in type 2 diabetes: a randomised controlled trial. Glucose 54-61 insulin Homo sapiens 13-20 25311817-3 2014 RESULTS: Patients taking clozapine had higher fasting levels of glucose (103.5+-31.6 vs. 87.8+-11.7mg/dL, z=-2.03, p=0.04), there was no difference for insulin concentrations and markers of insulin resistance. Glucose 64-71 insulin Homo sapiens 152-159 25311817-3 2014 RESULTS: Patients taking clozapine had higher fasting levels of glucose (103.5+-31.6 vs. 87.8+-11.7mg/dL, z=-2.03, p=0.04), there was no difference for insulin concentrations and markers of insulin resistance. Glucose 64-71 insulin Homo sapiens 190-197 25012984-5 2014 Moreover, cell migration triggered by insulin occurred through GPER1 and its main target gene CTGF, whereas the insulin-induced expression of GPER1 boosted cell-cycle progression and the glucose uptake stimulated by estrogens. Glucose 187-194 insulin Homo sapiens 112-119 24878388-1 2014 BACKGROUND: Insulin aspart (IAsp) is used by many diabetics as a meal-time insulin to control post-prandial glucose levels. Glucose 108-115 insulin Homo sapiens 12-19 24878388-1 2014 BACKGROUND: Insulin aspart (IAsp) is used by many diabetics as a meal-time insulin to control post-prandial glucose levels. Glucose 108-115 insulin Homo sapiens 75-82 25139488-4 2014 Interventions which improve insulin sensitivity and/or preserve beta-cell function are logical strategies to delay the conversion of IGT/IFG to T2DM or revert glucose tolerance to normal. Glucose 159-166 insulin Homo sapiens 28-35 24835122-2 2014 The aim of this study was to design and clinically evaluate a system that integrates a control algorithm with off-the-shelf subcutaneous sensors and pumps to automate the delivery of the hormones glucagon and insulin in response to continuous glucose sensor measurements. Glucose 243-250 insulin Homo sapiens 209-216 25001269-9 2014 Glucose use improved during autonomic blockade in insulin-resistant subjects (MBW 3.8+-0.3 blocked versus 3.1+-0.3 mg/kg per minute intact; P=0.025), with no effect in the insulin-sensitive group. Glucose 0-7 insulin Homo sapiens 50-57 24937535-1 2014 AIMS AND HYPOTHESIS: The insulin secretion/insulin resistance (IR) (disposition) index (DeltaI/DeltaG / IR, where Delta is change from baseline, I is insulin, and G is glucose) is commonly used as a measure of beta-cell function. Glucose 168-175 insulin Homo sapiens 25-32 24937535-10 2014 The net result was a decline in the plasma insulin response to hyperglycemia during the oral glucose tolerance test. Glucose 93-100 insulin Homo sapiens 43-50 24937535-11 2014 These findings demonstrate a physiologic control mechanism wherein the increase in ISR ensures adequate insulin delivery into the portal circulation to suppress hepatic glucose production while delivering a reduced but sufficient amount of insulin to peripheral tissues to maintain the pioglitazone-mediated improvement in insulin sensitivity without excessive hyperinsulinemia. Glucose 169-176 insulin Homo sapiens 104-111 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Glucose 97-104 insulin Homo sapiens 116-123 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Glucose 97-104 insulin Homo sapiens 154-163 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Glucose 97-104 insulin Homo sapiens 228-235 25050902-4 2014 glucose tolerance test (IVGTT)-induced acute (0-30 min) insulin release (insulinogenic index IGIOGTT and IGIIVGTT), and IHA were calculated in 19 REL and 18 CON subjects by cross-correlation linear regression slope analyses of the OGTT (0-30 min) matched insulin/glucose profiles vs the early (0-5 min) and delayed (10-30 min) IVGTT profiles. Glucose 0-7 insulin Homo sapiens 56-63 25057876-7 2014 MAIN OUTCOME MEASURES: Glucose infusion rate during 90-120 minutes of insulin infusion was measured. Glucose 23-30 insulin Homo sapiens 70-77 25180600-5 2014 The beta cell insulin secretory defect was distal to glucose-dependent Ca2+ influx and resulted from reduced proinsulin biosynthesis and insulin content. Glucose 53-60 insulin Homo sapiens 14-21 24060547-4 2014 Increasing doses of insulin is mandatory under close monitoring of blood glucose levels, in particular according to the protocol proposed by Kaushal et al. Glucose 73-80 insulin Homo sapiens 20-27 24060547-5 2014 : infusion of insulin adapted to the results of glucose levels, as a supplementation to the usual doses in each patient. Glucose 48-55 insulin Homo sapiens 14-21 25374987-1 2014 PURPOSE: Insulin improves glycemic control in several ways, for example, by stimulating glucose uptake in the muscle and inhibiting hepatic glucose production. Glucose 88-95 insulin Homo sapiens 9-16 25823168-1 2014 Sodium glucose transporter 2 (SGLT2) inhibitors including dapagliflozin, canagliflozin and empagliflozin act by a novel insulin-independent mechanism by blocking glucose reabsorption in the proximal convoluted tubules resulting in markedly increased glycosuria, a mechanism not limited by the degree of insulin resistance or beta-cell dysfunction, and which results in weight loss due to loss of 300 to 400kcal/day. Glucose 7-14 insulin Homo sapiens 120-127 25823168-1 2014 Sodium glucose transporter 2 (SGLT2) inhibitors including dapagliflozin, canagliflozin and empagliflozin act by a novel insulin-independent mechanism by blocking glucose reabsorption in the proximal convoluted tubules resulting in markedly increased glycosuria, a mechanism not limited by the degree of insulin resistance or beta-cell dysfunction, and which results in weight loss due to loss of 300 to 400kcal/day. Glucose 7-14 insulin Homo sapiens 303-310 25473629-6 2014 Anthropometric indices and laboratory tests (fasting and glucose-stimulated insulin levels, lipid profile and androgens) were measured. Glucose 57-64 insulin Homo sapiens 76-83 25884071-10 2014 According the phylogenetic theory of general pathology, the effect of insulin on metabolism of glucose is mediated by fatty acids. Glucose 95-102 insulin Homo sapiens 70-77 25884071-12 2014 The insulin is depriving all cells of possibility to absorb unesterified fatty acids and "forces" them to absorb glucose increasing hereby number of GLUT4 on cell membrane. Glucose 113-120 insulin Homo sapiens 4-11 25146550-2 2014 Insulin secretion is often enhanced during obesity or insulin resistance to maintain glucose and lipid homeostasis, whereas a loss of insulin secretion is associated with type 2 diabetes. Glucose 85-92 insulin Homo sapiens 0-7 25146550-2 2014 Insulin secretion is often enhanced during obesity or insulin resistance to maintain glucose and lipid homeostasis, whereas a loss of insulin secretion is associated with type 2 diabetes. Glucose 85-92 insulin Homo sapiens 54-61 25146550-5 2014 Insulin, in turn, regulates lipolysis and promotes glucose uptake and lipid storage in adipocytes. Glucose 51-58 insulin Homo sapiens 0-7 25103239-0 2014 A Rab10:RalA G protein cascade regulates insulin-stimulated glucose uptake in adipocytes. Glucose 60-67 insulin Homo sapiens 41-48 25103239-1 2014 Insulin-stimulated glucose uptake in fat and muscle is mediated by the major facilitative glucose transporter Glut4. Glucose 19-26 insulin Homo sapiens 0-7 25103239-7 2014 Together these studies identify a new G protein cascade in the regulation of insulin-stimulated Glut4 trafficking and glucose uptake. Glucose 118-125 insulin Homo sapiens 77-84 25293551-4 2014 Conversely, analyses of studies administering caffeine prior to either an oral glucose tolerance test or insulin clamp showed a decline in whole-body glucose disposal of ~30%. Glucose 150-157 insulin Homo sapiens 105-112 25356031-6 2014 This may be related to disturbances in postprandial glucose, insulin, and ghrelin levels, which, in turn, appear to be associated to insulin resistance, a common finding in cirrhosis. Glucose 52-59 insulin Homo sapiens 133-140 25181343-7 2014 The hDPSCs-derived IPCs expressed PRO-INSULIN and released C-PEPTIDE upon glucose stimulation in dose-dependent manner. Glucose 74-81 insulin Homo sapiens 59-68 25181343-9 2014 Notch inhibition during the last induction step or throughout the protocol disturbed the ability of C-PEPTIDE release upon glucose stimulation. Glucose 123-130 insulin Homo sapiens 100-109 25452875-10 2014 The AUC for predicting 1 h glucose >=155 mg/dL was 0.82 for a base model that included age, gender, BMI, fasting glucose, glycated hemoglobin (HbA1c), and insulin, and increased to 0.86 with alpha-HB added (p=0.015), with a net reclassification index of 52% (p<0.0001). Glucose 27-34 insulin Homo sapiens 158-165 25043058-3 2014 Here we show that parenteral delivery of a single dose of recombinant FGF1 (rFGF1) results in potent, insulin-dependent lowering of glucose levels in diabetic mice that is dose-dependent but does not lead to hypoglycaemia. Glucose 132-139 insulin Homo sapiens 102-109 25043058-4 2014 Chronic pharmacological treatment with rFGF1 increases insulin-dependent glucose uptake in skeletal muscle and suppresses the hepatic production of glucose to achieve whole-body insulin sensitization. Glucose 73-80 insulin Homo sapiens 55-62 25043058-4 2014 Chronic pharmacological treatment with rFGF1 increases insulin-dependent glucose uptake in skeletal muscle and suppresses the hepatic production of glucose to achieve whole-body insulin sensitization. Glucose 148-155 insulin Homo sapiens 178-185 25226365-8 2014 Glucose clamp studies indicated that both Ab positive and Ab negative patients exhibited peripheral insulin resistance in a similar fashion. Glucose 0-7 insulin Homo sapiens 100-107 24833725-7 2014 Insulin-stimulated glucose uptake and secretion of adiponectin by the Cisd2 KO adipocytes were decreased. Glucose 19-26 insulin Homo sapiens 0-7 25222615-5 2014 Importantly, studies of serum hormone levels showed that variants in CDKAL1 are associated with glucose-induced GIP and insulin responses (p<0.05). Glucose 96-103 insulin Homo sapiens 120-127 25217974-4 2014 In the presence of resistin, insulin only slightly increased glucose uptake and glycolysis, and did not alter the flux profile around pyruvate induced by resistin. Glucose 61-68 insulin Homo sapiens 29-36 24769252-1 2014 Increased glucose variability (GV) is an independent risk factor for mortality in the critically ill; unfortunately, the optimal insulin therapy that minimizes GV is not known. Glucose 10-17 insulin Homo sapiens 129-136 25002582-4 2014 We hypothesized that glucose-dependent stimulation of insulin secretion from beta-cells must involve reversing the inhibitory action of tomosyn. Glucose 21-28 insulin Homo sapiens 54-61 25002582-8 2014 Using (32)P labeling and mass spectrometry, we showed that tomosyn-2 is phosphorylated in response to high glucose, phorbol esters, and analogs of cAMP, all key insulin secretagogues. Glucose 107-114 insulin Homo sapiens 161-168 25130462-2 2014 Skeletal muscle is the major site of insulin mediated glucose disposal and the skeletal muscle tissue is capable to synthesize, convert and degrade androgens. Glucose 54-61 insulin Homo sapiens 37-44 25181406-6 2014 Patients treated with the basal-bolus insulin regimen attained lower fasting blood glucose (10.8 +- 2.3 versus 11.6 +- 3.5 mmol/L; p = 0.028) and mean glucose levels throughout severe/acute hyperglycemia (12.3 +- 1.9 versus 12.8 +- 2.2; p = 0.021) compared with sliding-scale insulin regimens. Glucose 83-90 insulin Homo sapiens 38-45 25181406-6 2014 Patients treated with the basal-bolus insulin regimen attained lower fasting blood glucose (10.8 +- 2.3 versus 11.6 +- 3.5 mmol/L; p = 0.028) and mean glucose levels throughout severe/acute hyperglycemia (12.3 +- 1.9 versus 12.8 +- 2.2; p = 0.021) compared with sliding-scale insulin regimens. Glucose 151-158 insulin Homo sapiens 38-45 24802182-8 2014 In addition, several adipocyte-secreted proteins related to insulin resistance showed a reversed expression after low-glucose CR. Glucose 118-125 insulin Homo sapiens 60-67 24949886-6 2014 T2DM is characterized by high blood glucose levels resulting from increased hepatic glucose production, impaired insulin production and peripheral insulin resistance, which close resemble to the brain insulin resistance observed in AD patients. Glucose 36-43 insulin Homo sapiens 113-120 24949886-6 2014 T2DM is characterized by high blood glucose levels resulting from increased hepatic glucose production, impaired insulin production and peripheral insulin resistance, which close resemble to the brain insulin resistance observed in AD patients. Glucose 36-43 insulin Homo sapiens 147-154 24771405-5 2014 Incubation of 3T3-L1 adipocytes with 1 microM FCCP for 12 h decreased insulin-stimulated glucose uptake, reduced intracellular ATP synthesis, increased intracellular reactive oxygen species (ROS) production, impaired insulin-stimulated Glucose transporter type 4 (GLUT4) translocation, and diminished insulin-stimulated tyrosine phosphorylation of Insulin receptor substrate-1 (IRS-1) and serine phosphorylation of Protein Kinase B (Akt). Glucose 89-96 insulin Homo sapiens 70-77 24771405-6 2014 Knockdown of LYRM1 restored insulin-stimulated glucose uptake, rescued intracellular ATP synthesis, reduced intracellular ROS production, restored insulin-stimulated GLUT4 translocation, and rescued insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt in FCCP-treated 3T3-L1 adipocytes. Glucose 47-54 insulin Homo sapiens 28-35 25169436-16 2014 The clusters were positive for insulin and NGN3 proteins, and C-peptide and insulin secretion increased in response to changes in the glucose concentration (2.8 mM and 16.7 mM). Glucose 134-141 insulin Homo sapiens 31-38 25169436-16 2014 The clusters were positive for insulin and NGN3 proteins, and C-peptide and insulin secretion increased in response to changes in the glucose concentration (2.8 mM and 16.7 mM). Glucose 134-141 insulin Homo sapiens 76-83 24956263-4 2014 Insulin resistance (IR) was assessed by estimated glucose disposal rate (eGDR) calculation with cut-off point 7.5 mg/kg/min. Glucose 50-57 insulin Homo sapiens 0-7 24611892-5 2014 The decline in insulin-stimulated whole-body glucose infusion rate, muscle PDCa (pyruvate dehydrogenase complex activation) and glycogen storage associated with n6PUFA compared with Control was prevented with n3PUFA. Glucose 45-52 insulin Homo sapiens 15-22 24611892-8 2014 These findings demonstrate that n3PUFA exert beneficial effects on insulin-stimulated skeletal muscle glucose storage and oxidation independently of total acylcarnitine accumulation, which does not always reflect mitochondrial lipid overload. Glucose 102-109 insulin Homo sapiens 67-74 24890901-1 2014 In patients with acute heart failure (AHF) syndromes, little data are so far available on the relation between glucose values and insulin resistance and mortality, both in the short and long term. Glucose 111-118 insulin Homo sapiens 130-137 24495158-1 2014 Insulin degludec (IDeg) is a new basal insulin with an ultra-long and stable glucose-lowering effect. Glucose 77-84 insulin Homo sapiens 0-7 24495158-1 2014 Insulin degludec (IDeg) is a new basal insulin with an ultra-long and stable glucose-lowering effect. Glucose 77-84 insulin Homo sapiens 39-46 24521245-0 2014 Lixisenatide resensitizes the insulin-secretory response to intravenous glucose challenge in people with type 2 diabetes--a study in both people with type 2 diabetes and healthy subjects. Glucose 72-79 insulin Homo sapiens 30-37 24521245-1 2014 AIMS: Glucagon-like peptide-1 (GLP-1) receptor agonists improve blood glucose control by enhancing glucose-sensitive insulin release, delaying gastric emptying and reducing postprandial glucagon secretion. Glucose 99-106 insulin Homo sapiens 117-124 24521245-2 2014 The studies reported here investigated the insulin response to an intravenous (iv) glucose challenge after injection of lixisenatide (LIXI) 20 microg or placebo. Glucose 83-90 insulin Homo sapiens 43-50 24521245-10 2014 CONCLUSIONS: LIXI resensitized the insulin response to an iv glucose challenge in people with T2DM, thereby accelerating glucose disposal to nearly physiological intensity, and did not impair counter-regulation to low glucose levels by glucagon. Glucose 61-68 insulin Homo sapiens 35-42 24589127-8 2014 RESULTS: At 6 months, subjects receiving liraglutide plus insulin experienced statistically significant reductions in HbA1c, weight, insulin dose and glycaemic variability (GV) by continuous glucose monitor (CGM) compared with the control group receiving insulin only. Glucose 191-198 insulin Homo sapiens 58-65 24735100-1 2014 BACKGROUND: Implanted insulin pumps using the peritoneal route provide long-term improvement of glucose control compared with subcutaneous insulin therapy in type 1 diabetes (T1D) patients. Glucose 96-103 insulin Homo sapiens 22-29 24914241-6 2014 Compared with women with normal glucose and weight, obese women with normal glucose had increased beta-cell secretory function (odds ratio [OR] 0.09 [95% CI 0.02-0.37]) and insulin resistance (OR 17.4 [95% CI 9.47-31.9]). Glucose 76-83 insulin Homo sapiens 173-180 24939431-9 2014 In human islets, there was a significant positive correlation between DPP-4 activity and insulin secretory response to 16.7 mmol/l glucose. Glucose 131-138 insulin Homo sapiens 89-96 24969577-1 2014 OBJECTIVE: Agents that augment GLP-1 effects enhance glucose-dependent beta-cell insulin production and secretion and thus are hoped to prevent progressive impairment in insulin secretion characteristic of type 2 diabetes (T2D). Glucose 53-60 insulin Homo sapiens 81-88 24969577-4 2014 Acute insulin responses to arginine (AIRarg) were measured at baseline and after 6 months of treatment with 5 days of drug washout under fasting, 230 mg/dL (glucose potentiation of arginine-induced insulin release [AIRpot]), and 340 mg/dL (maximum arginine-induced insulin release [AIRmax]) hyperglycemic clamp conditions, in which AIRmax provides the beta-cell secretory capacity. Glucose 157-164 insulin Homo sapiens 198-205 24969577-4 2014 Acute insulin responses to arginine (AIRarg) were measured at baseline and after 6 months of treatment with 5 days of drug washout under fasting, 230 mg/dL (glucose potentiation of arginine-induced insulin release [AIRpot]), and 340 mg/dL (maximum arginine-induced insulin release [AIRmax]) hyperglycemic clamp conditions, in which AIRmax provides the beta-cell secretory capacity. Glucose 157-164 insulin Homo sapiens 198-205 25200290-6 2014 A conflict arises because reduced insulin/IGF1 signalling in the CNS is associated with longevity, but can dysregulate glucose and energy homeostasis, and promote overweight. Glucose 119-126 insulin Homo sapiens 34-41 25200301-1 2014 Intracellular glucose signalling pathways control the secretion of glucagon and insulin by pancreatic islet alpha- and beta-cells, respectively. Glucose 14-21 insulin Homo sapiens 80-87 25200303-4 2014 Within islets, glucose-stimulated beta-cells couple via gap junctions to generate synchronized insulin pulses. Glucose 15-22 insulin Homo sapiens 95-102 25200303-7 2014 Further glucose elevation will stimulate pulsatile insulin release and co-secretion of neurotransmitters. Glucose 8-15 insulin Homo sapiens 51-58 25051539-11 2014 By inhibiting glucose-driven maternal insulin secretion, ghrelin might ensure adequate fasting glucose and nutrient supplies to the fetus while limiting overall fetal adipose tissue deposition. Glucose 14-21 insulin Homo sapiens 38-45 24932807-1 2014 Glucose transporter isoform 4 (GLUT4) is the insulin-responsive glucose transporter mediating glucose uptake in adipose and skeletal muscle. Glucose 64-71 insulin Homo sapiens 45-52 24932807-7 2014 This model suggests that an early event in the development of insulin-resistant glucose transport in adipose tissue is to alter the intracellular localization of GLUT4 to a compartment that does not efficiently equilibrate with the cell surface when insulin levels are elevated for prolonged periods of time. Glucose 80-87 insulin Homo sapiens 62-69 24932807-7 2014 This model suggests that an early event in the development of insulin-resistant glucose transport in adipose tissue is to alter the intracellular localization of GLUT4 to a compartment that does not efficiently equilibrate with the cell surface when insulin levels are elevated for prolonged periods of time. Glucose 80-87 insulin Homo sapiens 250-257 24972836-3 2014 This invited review argues that in addition to the hypothalamus, insulin signalling in the dorsal vagal complex regulates hepatic glucose production and food intake. Glucose 130-137 insulin Homo sapiens 65-72 24846393-0 2014 Interplay of adiponectin, TNFalpha and insulin on gene expression, glucose uptake and PPARgamma, AKT and TOR pathways in rainbow trout cultured adipocytes. Glucose 67-74 insulin Homo sapiens 39-46 24846393-8 2014 Both adipokines stimulated glucose uptake without modifying AKT or TOR phosphorylation; however, glucose uptake in insulin-treated adipocytes was enhanced by TNFalpha but not by adiponectin. Glucose 97-104 insulin Homo sapiens 115-122 25236446-8 2014 Studies in Tpcn2 knockout mice demonstrated a significant decrease in fasting glucose levels and insulin response to a glucose challenge relative to those in wild-type mice. Glucose 119-126 insulin Homo sapiens 97-104 24911977-6 2014 Permethrin significantly reduced insulin-stimulated glucose uptake in myotubes. Glucose 52-59 insulin Homo sapiens 33-40 24796924-0 2014 Strong association between insulin-mediated glucose uptake and the 2-hour, not the fasting plasma glucose concentration, in the normal glucose tolerance range. Glucose 44-51 insulin Homo sapiens 27-34 24796924-1 2014 AIM: The aim of this study was to examine the relationship between whole-body insulin-mediated glucose disposal and the fasting plasma glucose concentration in nondiabetic individuals. Glucose 95-102 insulin Homo sapiens 78-85 24796924-1 2014 AIM: The aim of this study was to examine the relationship between whole-body insulin-mediated glucose disposal and the fasting plasma glucose concentration in nondiabetic individuals. Glucose 135-142 insulin Homo sapiens 78-85 24971665-8 2014 After insulin administration blood glucose control deteriorated acutely without any apparent cause, whereas C-peptide levels rapidly decreased to insulin-deficient levels. Glucose 35-42 insulin Homo sapiens 6-13 25049364-1 2014 Maintaining euglycemia for people with type 1 diabetes is highly challenging, and variations in glucose absorption rates with meal composition require meal type specific insulin delivery profiles for optimal blood glucose control. Glucose 96-103 insulin Homo sapiens 170-177 25172875-1 2014 Computerized insulin infusion protocols have facilitated more effective blood glucose (BG) control in intensive care units (ICUs). Glucose 78-85 insulin Homo sapiens 13-20 25172878-0 2014 Treatment with novel galactomannan derivative reduces 2-hour postprandial glucose excursions in individuals with type 2 diabetes treated with oral medications and/or insulin. Glucose 74-81 insulin Homo sapiens 166-173 25411619-2 2014 Recently, it was suggested that the C-peptide-to-glucose ratio after oral glucose ingestion is a better predictor of beta-cell mass than that during fasting. Glucose 49-56 insulin Homo sapiens 36-45 25411619-2 2014 Recently, it was suggested that the C-peptide-to-glucose ratio after oral glucose ingestion is a better predictor of beta-cell mass than that during fasting. Glucose 74-81 insulin Homo sapiens 36-45 25411623-8 2014 Furthermore, interestingly, near normalization of glycemic control with insulin therapy for 1-2 weeks brought out the long-term effectiveness of sitagliptin on glucose tolerance for 24 weeks, which was not observed with other antidiabetic drugs. Glucose 160-167 insulin Homo sapiens 72-79 24819347-2 2014 Since zinc mimics the function of insulin, it may provide benefit to the heart via stimulating Akt-mediated glucose metabolism. Glucose 108-115 insulin Homo sapiens 34-41 25049364-10 2014 The novel insulin delivery profiles present new waveforms that provide better control of postprandial glucose excursions than existing schemes. Glucose 102-109 insulin Homo sapiens 10-17 24943065-0 2014 Home use of closed-loop insulin delivery for overnight glucose control in adults with type 1 diabetes: a 4-week, multicentre, randomised crossover study. Glucose 55-62 insulin Homo sapiens 24-31 24943065-2 2014 We aimed to assess whether overnight home use of automated closed-loop insulin delivery would improve glucose control. Glucose 102-109 insulin Homo sapiens 71-78 24943065-13 2014 INTERPRETATION: Unsupervised overnight closed-loop insulin delivery at home is feasible and could improve glucose control in adults with type 1 diabetes. Glucose 106-113 insulin Homo sapiens 51-58 25015014-9 2014 In this same sense, lower adiponectin levels significantly related to low HDL-C and high triglyceride levels; and higher insulin and HOMA-IR values related to high triglyceride and glucose levels, respectively. Glucose 181-188 insulin Homo sapiens 121-128 25437460-2 2014 Glucagon-like peptide 1 (GLP-1) is secreted from enteroendocrine L-cells in response to oral nutrient intake and elicits glucose-stimulated insulin secretion while suppressing glucagon secretion. Glucose 121-128 insulin Homo sapiens 140-147 24997500-6 2014 Higher FKBP5 gene expression in omental adipose tissue was associated with reduced insulin effects on glucose uptake in both depots. Glucose 102-109 insulin Homo sapiens 83-90 25034385-6 2014 Exposure of myotubes to 17beta-estradiol reduced glucose oxidation under basal and insulin-stimulated conditions. Glucose 49-56 insulin Homo sapiens 83-90 25034385-7 2014 However, testosterone treatment enhanced basal palmitate oxidation and prevented insulin action on glucose and palmitate oxidation. Glucose 99-106 insulin Homo sapiens 81-88 25074384-1 2014 SCOPE: There is a growing interest in food constituents that could reduce intestinal glucose absorption to prevent overshooting plasma glucose and insulin levels in patients with prediabetes and diabetes mellitus type 2. Glucose 85-92 insulin Homo sapiens 147-154 25074384-5 2014 An oral glucose tolerance test performed in volunteers with prior administration of the apple extract reduced venous blood glucose and plasma insulin levels, similar to findings obtained in C57BL/6N mice. Glucose 8-15 insulin Homo sapiens 142-149 24829088-5 2014 RESULTS: In RYGB subjects, the glucose drink emptied very rapidly (PE t50 = 3 +- 1 min) and intestinal glucose infusion was associated with higher blood glucose and plasma 3-OMG, but lower plasma GLP-1, GIP, insulin, and GI symptoms than oral glucose (all P < 0.001), and comparable to volunteers. Glucose 31-38 insulin Homo sapiens 208-215 24829088-5 2014 RESULTS: In RYGB subjects, the glucose drink emptied very rapidly (PE t50 = 3 +- 1 min) and intestinal glucose infusion was associated with higher blood glucose and plasma 3-OMG, but lower plasma GLP-1, GIP, insulin, and GI symptoms than oral glucose (all P < 0.001), and comparable to volunteers. Glucose 103-110 insulin Homo sapiens 208-215 24829088-5 2014 RESULTS: In RYGB subjects, the glucose drink emptied very rapidly (PE t50 = 3 +- 1 min) and intestinal glucose infusion was associated with higher blood glucose and plasma 3-OMG, but lower plasma GLP-1, GIP, insulin, and GI symptoms than oral glucose (all P < 0.001), and comparable to volunteers. Glucose 103-110 insulin Homo sapiens 208-215 24891156-3 2014 RESULTS: Insulin sensitivity (insulin-stimulated glucose disposal during a clamp procedure), oral glucose tolerance (postprandial plasma glucose area under the curve), and beta-cell function (insulin secretion in relationship to insulin sensitivity) improved after weight loss, and were not different between surgical groups. Glucose 49-56 insulin Homo sapiens 30-37 25157925-10 2014 The differences between normal and DM subjects in glucose and insulin dynamics in the pancreas, liver and peripheral tissues, such as insulin resistance, insulin secretion and the relative roles of glucose disposal in each organ, were demonstrated clearly and quantitatively in a time-dependent manner. Glucose 50-57 insulin Homo sapiens 134-141 25157925-10 2014 The differences between normal and DM subjects in glucose and insulin dynamics in the pancreas, liver and peripheral tissues, such as insulin resistance, insulin secretion and the relative roles of glucose disposal in each organ, were demonstrated clearly and quantitatively in a time-dependent manner. Glucose 198-205 insulin Homo sapiens 62-69 25157925-11 2014 CONCLUSION: This study revealed the quantitative dynamic interaction between glucose and insulin using OGTT data and revealed organ function during the OGTT. Glucose 77-84 insulin Homo sapiens 89-96 25517049-0 2014 [Evaluation of serum insulin levels after an oral glucose load for the diagnosis of insulin resistance]. Glucose 50-57 insulin Homo sapiens 21-28 25517049-0 2014 [Evaluation of serum insulin levels after an oral glucose load for the diagnosis of insulin resistance]. Glucose 50-57 insulin Homo sapiens 84-91 25517049-1 2014 BACKGROUND: In our country, the assessment of insulin resistance (IR) measuring serum insulin levels at 60 and 120 minutes after a 75 g oral glucose tolerance test (OGTT), is usual. Glucose 141-148 insulin Homo sapiens 46-53 25517049-1 2014 BACKGROUND: In our country, the assessment of insulin resistance (IR) measuring serum insulin levels at 60 and 120 minutes after a 75 g oral glucose tolerance test (OGTT), is usual. Glucose 141-148 insulin Homo sapiens 86-93 25294758-17 2014 CONCLUSION: In the common clinical practice setting, the initiation of treatment with insulin glargine using the basal-bolus regime in patients with previous insulin therapy resulted in a reduction in the incidence of hypoglycemic events, including severe hypoglycemia and severe nocturnal hypoglycemia, and improved metabolic control in patients with diabetes (reduced glycated hemoglobin, fasting glucose values and 6-point blood glucose profile). Glucose 399-406 insulin Homo sapiens 86-93 25125454-0 2014 Continuous glucose monitoring in insulin-treated patients in non-ICU settings. Glucose 11-18 insulin Homo sapiens 33-40 25294764-3 2014 In the clinical conditions we usually define it as the impairment of insulin action in glucose metabolism, although it is true that the impairment may concern different effects of insulin and different cell structures. Glucose 87-94 insulin Homo sapiens 69-76 25509784-5 2014 The expressions of specific markers [alpha-fetoprotein (AFP), Nestin, and smooth muscle actin (SMA)] were measured by immunohistochemical method; and the ability of glucose-stimulated insulin secretion was analyzed. Glucose 165-172 insulin Homo sapiens 184-191 25509784-9 2014 The islet-like cell clusters could release insulin significantly in response to elevated concentrations of glucose in vitro (t = 7.444, P = 0.002). Glucose 107-114 insulin Homo sapiens 43-50 25509784-10 2014 The insulin contents were (23.2 +- 5.3) mU/L and (7.0 +- 0.5) mU/L in high and low glucose media, respectively. Glucose 83-90 insulin Homo sapiens 4-11 25175981-4 2014 The hypothesis of our study was that adding a DPP4-inhibitor at the beginning of insulin treatment could lead to less exogenous insulin requirement, a reduction of hyperinsulinemia and side effects (hypoglycemia and weight gain), less glucose variability and improvement of insulin and glucagon dynamics during a mixed meal test. Glucose 235-242 insulin Homo sapiens 81-88 24896237-8 2014 Women who at 28 weeks of gestation developed glucose intolerance, despite the low-GI diet, had a higher BMI and higher glucose concentrations in early pregnancy with more insulin resistance. Glucose 45-52 insulin Homo sapiens 171-178 27896108-8 2014 Furthermore, the genetic variant of PCSK1 might influence glucose homeostasis by altered insulin resistance independently of BMI, incretin level or proinsulin conversion, and may be associated with the occurrence of type 2 diabetes in Japanese. Glucose 58-65 insulin Homo sapiens 89-96 24837539-1 2014 BACKGROUND: In patients with type 1 diabetes, insulin antibodies (IA), altering the pharmacokinetics of circulating insulin, might be associated with high glucose concentration, prolonged hypoglycemia, and higher insulin requirement. Glucose 155-162 insulin Homo sapiens 46-53 24837539-1 2014 BACKGROUND: In patients with type 1 diabetes, insulin antibodies (IA), altering the pharmacokinetics of circulating insulin, might be associated with high glucose concentration, prolonged hypoglycemia, and higher insulin requirement. Glucose 155-162 insulin Homo sapiens 116-123 25150967-10 2014 The protective effects of insulin tended to be weaker in subjects with elevated fasting glucose, implying that the relation between FPI and incident AF could be dependent on the status of individual"s glucose metabolism. Glucose 88-95 insulin Homo sapiens 26-33 25139609-0 2014 Insulin treatment guided by subcutaneous continuous glucose monitoring compared to frequent point-of-care measurement in critically ill patients: a randomized controlled trial. Glucose 52-59 insulin Homo sapiens 0-7 25141237-8 2014 A positive relationship was found between changes in GIP and those of glucose and immunoreactive insulin in diabetic patients (p<0.001 and p<0.001, respectively) and between changes in PYY and those of glucose (p<0.01). Glucose 70-77 insulin Homo sapiens 97-104 25141237-8 2014 A positive relationship was found between changes in GIP and those of glucose and immunoreactive insulin in diabetic patients (p<0.001 and p<0.001, respectively) and between changes in PYY and those of glucose (p<0.01). Glucose 208-215 insulin Homo sapiens 97-104 25138792-1 2014 UNLABELLED: Differential activation/deactivation of insulin signaling, PI-3K and MAP-K pathways by high glucose and palmitate, with/out the insulin sensitizer pioglitazone (PIO), have been previously shown in vascular smooth muscle cells (VSMCs). Glucose 104-111 insulin Homo sapiens 52-59 25138792-1 2014 UNLABELLED: Differential activation/deactivation of insulin signaling, PI-3K and MAP-K pathways by high glucose and palmitate, with/out the insulin sensitizer pioglitazone (PIO), have been previously shown in vascular smooth muscle cells (VSMCs). Glucose 104-111 insulin Homo sapiens 140-147 25138792-10 2014 CONCLUSION: These results confirm that high glucose and palmitate stimulate VSMCs migration and proliferation in vitro, which is attenuated by coincubation with the insulin sensitizer PIO. Glucose 44-51 insulin Homo sapiens 165-172 25400046-11 2014 Also waist circumference, fasting plasma glucose and hemoglobin A1c levels were independently associated with total daily insulin dose per kilogram. Glucose 41-48 insulin Homo sapiens 122-129 25126394-1 2014 Type 2 diabetes is characterized by a decreased ability of insulin to facilitate glucose uptake into insulin sensitive tissue, i.e., skeletal muscle. Glucose 81-88 insulin Homo sapiens 59-66 25126394-1 2014 Type 2 diabetes is characterized by a decreased ability of insulin to facilitate glucose uptake into insulin sensitive tissue, i.e., skeletal muscle. Glucose 81-88 insulin Homo sapiens 101-108 25152631-8 2014 Paradoxically, rational insulin therapy, dosed according to a patient"s clinical status and the results of home blood glucose monitoring, so as to achieve and maintain recommended glycemic goals, can be an effective method for the prevention of hypoglycemia and falls in the elderly. Glucose 118-125 insulin Homo sapiens 24-31 25043022-4 2014 Here we show that homozygous carriers of this variant have markedly higher concentrations of plasma glucose (beta = 3.8 mmol l(-1), P = 2.5 x 10(-35)) and serum insulin (beta = 165 pmol l(-1), P = 1.5 x 10(-20)) 2 hours after an oral glucose load compared with individuals with other genotypes (both non-carriers and heterozygous carriers). Glucose 234-241 insulin Homo sapiens 161-168 25043022-8 2014 These findings are concomitant with a severely decreased insulin-stimulated glucose uptake in muscle, leading to postprandial hyperglycaemia, impaired glucose tolerance and T2D. Glucose 76-83 insulin Homo sapiens 57-64 25105579-5 2014 The induced beta cells resemble islet beta cells in morphology and histology, express genes essential for beta cell function, and release insulin after glucose challenge. Glucose 152-159 insulin Homo sapiens 138-145 25100389-1 2014 OBJECTIVE: Continuous subcutaneous insulin infusion (CSII) programming for an early morning increase in insulin delivery is frequently recommended to counteract the rise in glucose prior to breakfast (dawn phenomenon). Glucose 173-180 insulin Homo sapiens 35-42 24370925-1 2014 Eating behavior, body weight regulation, peripheral glucose metabolism, and cognitive function depend on adequate insulin action in the brain, and recent studies in humans suggested that impaired insulin action in the brain emerges upon fat intake, obesity, and genetic variants. Glucose 52-59 insulin Homo sapiens 114-121 27419209-0 2014 Adding of Sitagliptin on Insulin Therapy Effectively and Safely Reduces a Hemoglobin A1c Level and Glucose Fluctuation in Japanese Patients with Type 2 Diabetes. Glucose 99-106 insulin Homo sapiens 25-32 24965303-9 2014 Insulin was lower with intravenous ex9-39 during intraduodenal glucose (P <= 0.05). Glucose 63-70 insulin Homo sapiens 0-7 24806638-0 2014 Leucine facilitates the insulin-stimulated glucose uptake and insulin signaling in skeletal muscle cells: involving mTORC1 and mTORC2. Glucose 43-50 insulin Homo sapiens 24-31 24806638-3 2014 Our results showed that leucine alone did not have an effect on glucose uptake or phosphorylation of protein kinase B (AKT), but facilitated the insulin-induced glucose uptake and AKT phosphorylation. Glucose 161-168 insulin Homo sapiens 145-152 24806638-4 2014 The insulin-stimulated glucose uptake and AKT phosphorylation were inhibited by the phosphatidylinositol 3-kinase inhibitor, wortmannin, but the inhibition was partially reversed by leucine. Glucose 23-30 insulin Homo sapiens 4-11 24806638-5 2014 The inhibitor of mammalian target of rapamycin complex 1 (mTORC1), rapamycin, had no effect on the insulin-stimulated glucose uptake, but eliminated the facilitating effect of leucine in the insulin-stimulated glucose uptake and AKT phosphorylation. Glucose 210-217 insulin Homo sapiens 191-198 24806638-7 2014 Together, these findings show that leucine can facilitate the insulin-induced insulin signaling and glucose uptake in skeletal muscle cells through both mTORC1 and mTORC2, implicating the potential importance of this amino acid in glucose homeostasis and providing new mechanistic insights. Glucose 100-107 insulin Homo sapiens 62-69 24933032-0 2014 Insulin-induced glucose control improves HDL cholesterol levels but not reverse cholesterol transport in type 2 diabetic patients. Glucose 16-23 insulin Homo sapiens 0-7 24768767-1 2014 Insulin and muscle contraction each stimulate translocation of the glucose transporter GLUT4 to the plasma membrane in skeletal muscle, an important process regulating whole-body glucose homeostasis. Glucose 67-74 insulin Homo sapiens 0-7 24903496-2 2014 HDLs may also exert anti-diabetogenic functions on the beta cells of the endocrine pancreas, notably by potently inhibiting stress-induced cell death and enhancing glucose-stimulated insulin secretion. Glucose 164-171 insulin Homo sapiens 183-190 24903496-3 2014 HDLs have also been found to stimulate insulin-dependent and insulin-independent glucose uptake into skeletal muscle, adipose tissue, and liver. Glucose 81-88 insulin Homo sapiens 39-46 24903496-3 2014 HDLs have also been found to stimulate insulin-dependent and insulin-independent glucose uptake into skeletal muscle, adipose tissue, and liver. Glucose 81-88 insulin Homo sapiens 61-68 24612121-3 2014 Insulin sensitivity was measured using frequently sampled intravenous glucose tests and Bergman"s minimal model. Glucose 70-77 insulin Homo sapiens 0-7 24824749-3 2014 During oral glucose tolerance test, the rise in plasma insulin (beta = 34.0) and the insulinogenic index (beta = 4.1) were independently associated with the day/night ratio of W-ExcR. Glucose 12-19 insulin Homo sapiens 55-62 25150579-2 2014 We tested whether acute beta2-adrenoceptor stimulation increased insulin-induced glucose uptake in human forearm skeletal muscle. Glucose 81-88 insulin Homo sapiens 65-72 24353180-6 2014 Acipimox 1) markedly reduced the fasting plasma FFA concentration and enhanced suppression of plasma FFA during oral glucose tolerance tests and insulin clamp in obese NGT and T2DM subjects and 2) enhanced insulin-mediated muscle glucose disposal and suppression of hepatic glucose production. Glucose 230-237 insulin Homo sapiens 206-213 24353180-6 2014 Acipimox 1) markedly reduced the fasting plasma FFA concentration and enhanced suppression of plasma FFA during oral glucose tolerance tests and insulin clamp in obese NGT and T2DM subjects and 2) enhanced insulin-mediated muscle glucose disposal and suppression of hepatic glucose production. Glucose 230-237 insulin Homo sapiens 206-213 24724616-7 2014 Although rs1800497 was not associated with insulin secretion, we did find another single nucleotide polymorphism in this locus, rs6275, to be associated with increased first-phase glucose-stimulated insulin secretion in women (P = 5.5*104) but again not in men (P = 0.34). Glucose 180-187 insulin Homo sapiens 199-206 25215276-10 2014 CONCLUSION: These results revealed that serum TG and HDL-C levels have different impacts on early-phase insulin secretion on the basis of their glucose tolerance status. Glucose 144-151 insulin Homo sapiens 104-111 24224943-7 2014 RESULTS: In general, the joint action of physical exercise and dietary glucose supplement could up-regulate glucose and insulin transport into the brain, as well as augmenting the release of insulin growth factor-1 and brain-derived neurotrophic factor. Glucose 71-78 insulin Homo sapiens 120-127 24224943-7 2014 RESULTS: In general, the joint action of physical exercise and dietary glucose supplement could up-regulate glucose and insulin transport into the brain, as well as augmenting the release of insulin growth factor-1 and brain-derived neurotrophic factor. Glucose 71-78 insulin Homo sapiens 191-198 24828607-4 2014 Those who needed insulin had a stronger family history of diabetes and higher first hour plasma glucose along with multiple (>1) abnormal values during oral glucose tolerance test (OGTT) in univariate analysis (p < 0.05). Glucose 96-103 insulin Homo sapiens 17-24 24828607-4 2014 Those who needed insulin had a stronger family history of diabetes and higher first hour plasma glucose along with multiple (>1) abnormal values during oral glucose tolerance test (OGTT) in univariate analysis (p < 0.05). Glucose 160-167 insulin Homo sapiens 17-24 24886904-5 2014 The inhibition of KCNIP1 led to increased insulin secretion in a glucose-dependent manner, but had no effect on insulin gene transcription as well as cell apoptosis. Glucose 65-72 insulin Homo sapiens 42-49 25150967-10 2014 The protective effects of insulin tended to be weaker in subjects with elevated fasting glucose, implying that the relation between FPI and incident AF could be dependent on the status of individual"s glucose metabolism. Glucose 201-208 insulin Homo sapiens 26-33 24224883-3 2014 However, maintaining optimal glucose levels is challenging because insulin requirements are not uniform throughout the course of the pregnancy. Glucose 29-36 insulin Homo sapiens 67-74 24476772-9 2014 Higher plasma glucose concentrations during exercise, and the attenuated serum insulin response at rest, may explain the significantly longer times to exhaustion produced by Gal compared with Glu. Glucose 192-195 insulin Homo sapiens 79-86 25079023-2 2014 Among older men with and without moderate CKD, Jia and colleagues compared insulin resistance estimated from glucose and insulin concentrations obtained while fasting or during an oral glucose tolerance test vs. insulin resistance measured by the gold-standard hyperinsulinemic euglycemic clamp and tested associations of each with mortality. Glucose 109-116 insulin Homo sapiens 75-82 24685436-8 2014 PRINCIPAL OBSERVATIONS: Intragastric glucose elevated plasma glucose, insulin, and GLP-1, and reduced gall bladder volume (an in vivo assay for CCK secretion). Glucose 37-44 insulin Homo sapiens 70-77 25089237-5 2014 The result shows that 11 of the 16 medicinal plants enhanced glucose uptake of DXMS-induced insulin resistant HepG2 cells, thereby demonstrating their ability to increase insulin sensitivity, other five medicinal plants including Astragalus membranaceus were found ineffective. Glucose 61-68 insulin Homo sapiens 92-99 24719315-4 2014 Insulin resistance and sensitivity were assessed by euglycemic-hyperinsulinemic clamp (glucose infusion rate <60 and >70 mumol kg(-1) min(-1) , respectively) (1), or by HOMA-IR and TG/HDL ratio (2). Glucose 87-94 insulin Homo sapiens 0-7 25110569-8 2014 CONCLUSIONS: Moderate weight loss due to caloric restriction with reduction in insulin resistance improves glucose tolerance and insulin sensitivity in middle-aged obese women and thereby may help prevent the development of type 2 diabetes mellitus. Glucose 107-114 insulin Homo sapiens 79-86 24746186-3 2014 However, the subsequent sustained phase of glucose-stimulated insulin secretion arises from newcomer granules that have a minimal residence time at the PM before fusion. Glucose 43-50 insulin Homo sapiens 62-69 25354857-4 2014 The correlation between these blood glucose levels and their glycosylated hemoglobin (HbA1c) levels were analyzed by comparing the average value, the maximum and the minimum value of blood glucose, and the appeared time of these extremum values in these two monitoring methods, and the amount of insulin usage was recorded as well. Glucose 36-43 insulin Homo sapiens 296-303 25354857-22 2014 For those patients who received insulin treatment, after CGMS, 64% (16/25) of them adjusted the insulin dosage according to their blood glucose levels. Glucose 136-143 insulin Homo sapiens 32-39 25354857-22 2014 For those patients who received insulin treatment, after CGMS, 64% (16/25) of them adjusted the insulin dosage according to their blood glucose levels. Glucose 136-143 insulin Homo sapiens 96-103 25429818-1 2014 Since its discovery in 1921, insulin has been considered to be the most important hormone in the regulation of glucose and fat metabolism. Glucose 111-118 insulin Homo sapiens 29-36 24931572-3 2014 The automatically adaptive algorithm of the bionic pancreas received data from a continuous glucose monitor to control subcutaneous delivery of insulin and glucagon. Glucose 92-99 insulin Homo sapiens 144-151 25058613-1 2014 Ceramides are known to promote insulin resistance in a number of metabolically important tissues including skeletal muscle, the predominant site of insulin-stimulated glucose disposal. Glucose 167-174 insulin Homo sapiens 148-155 29159095-0 2014 Optimizing insulin injection technique and its effect on blood glucose control. Glucose 63-70 insulin Homo sapiens 11-18 25052490-1 2014 Increases in insulin-mediated glucose uptake following endurance training (ET) and sprint interval training (SIT) have in part been attributed to concomitant increases in glucose transporter 4 (GLUT4) protein content in skeletal muscle. Glucose 30-37 insulin Homo sapiens 13-20 25025664-1 2014 AIMS/HYPOTHESIS: Recently, cardiotrophin-1, a member of the interleukin-6 family of cytokines was described to protect beta-cells from apoptosis, to improve glucose-stimulated insulin secretion and insulin resistance, and to prevent streptozotocin-induced diabetes in mice. Glucose 157-164 insulin Homo sapiens 176-183 25009980-11 2014 These cells secreted insulin/C-peptide following glucose stimulation, similarly to adult human islets. Glucose 49-56 insulin Homo sapiens 21-28 25009980-11 2014 These cells secreted insulin/C-peptide following glucose stimulation, similarly to adult human islets. Glucose 49-56 insulin Homo sapiens 29-38 25071716-8 2014 Insulin tolerance tests at week 7 showed that both insulin treatments significantly reduced glucose concentrations and increased insulin levels compared with the Sham group, CRI significantly reduced glucose at 4 and 6 h relative to Reg-In (P < 0.05), suggesting the effects of CRI on reducing glucose last longer than Reg-In. Glucose 92-99 insulin Homo sapiens 51-58 26237474-1 2014 This review focuses on how insulin signals to metabolic processes in health, why this signaling is frequently deranged in Western/Westernized societies, how these derangements lead to, or abet development of, insulin-resistant states of obesity, the metabolic syndrome and type 2 diabetes mellitus, and what our options are for restoring insulin signaling, and glucose/lipid homeostasis. Glucose 361-368 insulin Homo sapiens 27-34 26237474-1 2014 This review focuses on how insulin signals to metabolic processes in health, why this signaling is frequently deranged in Western/Westernized societies, how these derangements lead to, or abet development of, insulin-resistant states of obesity, the metabolic syndrome and type 2 diabetes mellitus, and what our options are for restoring insulin signaling, and glucose/lipid homeostasis. Glucose 361-368 insulin Homo sapiens 209-216 26237474-1 2014 This review focuses on how insulin signals to metabolic processes in health, why this signaling is frequently deranged in Western/Westernized societies, how these derangements lead to, or abet development of, insulin-resistant states of obesity, the metabolic syndrome and type 2 diabetes mellitus, and what our options are for restoring insulin signaling, and glucose/lipid homeostasis. Glucose 361-368 insulin Homo sapiens 209-216 24971679-0 2014 Comparison of glucose tolerance tests to detect the insulin sensitizing effects of a bout of continuous exercise. Glucose 14-21 insulin Homo sapiens 52-59 24971679-1 2014 The aim of the present study was to determine which of the available glucose tolerance tests (oral (OGTT) vs. intravenous (IVGTT)) could more readily detect the insulin sensitizing effects of a bout of continuous exercise. Glucose 69-76 insulin Homo sapiens 161-168 24210541-10 2014 Oral glucose-stimulated insulin levels increased and GLP-1 levels also increased significantly. Glucose 5-12 insulin Homo sapiens 24-31 24755066-3 2014 Estimating non-insulin-mediated brain glucose uptake by the central nervous system in these models is typically done using population-based body weight models, which may not be ideal. Glucose 38-45 insulin Homo sapiens 15-22 24819559-2 2014 The core metabolic abnormality in MetS is insulin resistance, or impaired insulin-mediated glucose regulation that results in elevated plasma insulin concentration. Glucose 91-98 insulin Homo sapiens 74-81 25123125-5 2014 In several studies, we have investigated insulin action on glucose and lipid metabolism, and at the molecular level, insulin signaling to glucose transport and glycogen synthesis in skeletal muscle from healthy individuals and in obesity, PCOS and type 2 diabetes. Glucose 59-66 insulin Homo sapiens 41-48 25123125-5 2014 In several studies, we have investigated insulin action on glucose and lipid metabolism, and at the molecular level, insulin signaling to glucose transport and glycogen synthesis in skeletal muscle from healthy individuals and in obesity, PCOS and type 2 diabetes. Glucose 138-145 insulin Homo sapiens 117-124 25123125-9 2014 Type 2 diabetes, obesity and PCOS are characterized by pronounced defects in the insulin-stimulated glucose uptake, in particular glycogen synthesis and to a lesser extent glucose oxidation, and the ability of insulin to suppress lipid oxidation. Glucose 100-107 insulin Homo sapiens 81-88 25123125-9 2014 Type 2 diabetes, obesity and PCOS are characterized by pronounced defects in the insulin-stimulated glucose uptake, in particular glycogen synthesis and to a lesser extent glucose oxidation, and the ability of insulin to suppress lipid oxidation. Glucose 172-179 insulin Homo sapiens 81-88 25123125-10 2014 In inherited insulin resistance, however, only insulin action on glucose uptake and glycogen synthesis is impaired. Glucose 65-72 insulin Homo sapiens 13-20 25123125-14 2014 Insulin in physiological concentrations stimulates glucose uptake in human skeletal muscle in vivo by activation of the insulin signaling cascade to glucose transport through the enzymes IRS1, PI3K, Akt2, AS160/TBC1D4 and RAC1, and to glycogen synthesis through Akt2, inhibition of GSK3 and activation of glycogen synthase (GS) via dephosphorylation of serine residues in both the NH2-terminal (site 2+2a) and the COOH-terminal end (site 3a+3b). Glucose 51-58 insulin Homo sapiens 0-7 25123125-14 2014 Insulin in physiological concentrations stimulates glucose uptake in human skeletal muscle in vivo by activation of the insulin signaling cascade to glucose transport through the enzymes IRS1, PI3K, Akt2, AS160/TBC1D4 and RAC1, and to glycogen synthesis through Akt2, inhibition of GSK3 and activation of glycogen synthase (GS) via dephosphorylation of serine residues in both the NH2-terminal (site 2+2a) and the COOH-terminal end (site 3a+3b). Glucose 51-58 insulin Homo sapiens 120-127 25123125-14 2014 Insulin in physiological concentrations stimulates glucose uptake in human skeletal muscle in vivo by activation of the insulin signaling cascade to glucose transport through the enzymes IRS1, PI3K, Akt2, AS160/TBC1D4 and RAC1, and to glycogen synthesis through Akt2, inhibition of GSK3 and activation of glycogen synthase (GS) via dephosphorylation of serine residues in both the NH2-terminal (site 2+2a) and the COOH-terminal end (site 3a+3b). Glucose 149-156 insulin Homo sapiens 0-7 25123125-14 2014 Insulin in physiological concentrations stimulates glucose uptake in human skeletal muscle in vivo by activation of the insulin signaling cascade to glucose transport through the enzymes IRS1, PI3K, Akt2, AS160/TBC1D4 and RAC1, and to glycogen synthesis through Akt2, inhibition of GSK3 and activation of glycogen synthase (GS) via dephosphorylation of serine residues in both the NH2-terminal (site 2+2a) and the COOH-terminal end (site 3a+3b). Glucose 149-156 insulin Homo sapiens 120-127 25123125-15 2014 In type 2 diabetes, obesity and PCOS, there is, although with some variation from study to study, defects in insulin signaling through IRS1, PI3K, Akt2 and AS160/TBC1D4, which can explain reduced insulin action on glucose transport. Glucose 214-221 insulin Homo sapiens 109-116 25123125-15 2014 In type 2 diabetes, obesity and PCOS, there is, although with some variation from study to study, defects in insulin signaling through IRS1, PI3K, Akt2 and AS160/TBC1D4, which can explain reduced insulin action on glucose transport. Glucose 214-221 insulin Homo sapiens 196-203 25123125-16 2014 In type 2 diabetes an altered intracellular distribution of SNAP23 and impaired activation of RAC1 also seem to play a role for reduced insulin action on glucose transport. Glucose 154-161 insulin Homo sapiens 136-143 25123125-19 2014 In these individuals, however, a markedly reduced insulin clearance seems to partially rescue insulin signaling to glucose transport and GS. Glucose 115-122 insulin Homo sapiens 50-57 25123125-19 2014 In these individuals, however, a markedly reduced insulin clearance seems to partially rescue insulin signaling to glucose transport and GS. Glucose 115-122 insulin Homo sapiens 94-101 25123125-21 2014 We demonstrated a strong correlation between plasma adiponectin and insulin action on glucose disposal and glycogen synthesis in obesity, type 2 diabetes and PCOS. Glucose 86-93 insulin Homo sapiens 68-75 25123125-27 2014 The results from these studies demonstrate that the well-established abnormalities in insulin action on glucose uptake and glycogen synthesis are reflected by defects in insulin signaling to these cellular processes in type 2 diabetes, obesity, and PCOS, and as expected also in inherited insulin resistance caused by a mutation in INSR. Glucose 104-111 insulin Homo sapiens 86-93 24320159-6 2014 Results indicated that a calibrated bedtime snack based on bedtime blood glucose (BG) level could be effective to reduce NH occurrence for patients treated with human or animal insulin (short-acting combined with lente, ultralente and/or intermediate-acting insulin), but there is no evidence for patients treated with insulin analogues as part of multiple daily injections or insulin pump regimen. Glucose 73-80 insulin Homo sapiens 177-184 24320159-6 2014 Results indicated that a calibrated bedtime snack based on bedtime blood glucose (BG) level could be effective to reduce NH occurrence for patients treated with human or animal insulin (short-acting combined with lente, ultralente and/or intermediate-acting insulin), but there is no evidence for patients treated with insulin analogues as part of multiple daily injections or insulin pump regimen. Glucose 73-80 insulin Homo sapiens 258-265 24320159-6 2014 Results indicated that a calibrated bedtime snack based on bedtime blood glucose (BG) level could be effective to reduce NH occurrence for patients treated with human or animal insulin (short-acting combined with lente, ultralente and/or intermediate-acting insulin), but there is no evidence for patients treated with insulin analogues as part of multiple daily injections or insulin pump regimen. Glucose 73-80 insulin Homo sapiens 258-265 24320159-6 2014 Results indicated that a calibrated bedtime snack based on bedtime blood glucose (BG) level could be effective to reduce NH occurrence for patients treated with human or animal insulin (short-acting combined with lente, ultralente and/or intermediate-acting insulin), but there is no evidence for patients treated with insulin analogues as part of multiple daily injections or insulin pump regimen. Glucose 73-80 insulin Homo sapiens 258-265 24705606-1 2014 AIMS/HYPOTHESIS: Insulin secretion from pancreatic beta cells and insulin-stimulated glucose uptake into skeletal muscle are processes regulated by similar isoforms of the soluble N-ethylmaleimide-sensitive factor-attachment protein receptor (SNARE) and mammalian homologue of unc-18 (Munc18) protein families. Glucose 85-92 insulin Homo sapiens 66-73 24728127-1 2014 AIMS/HYPOTHESIS: Glucokinase (GCK) plays a role in glucose metabolism and glucose-stimulated insulin secretion. Glucose 74-81 insulin Homo sapiens 93-100 24842248-0 2014 Emerging parameters of the insulin and glucose response on the oral glucose tolerance test: reproducibility and implications for glucose homeostasis in individuals with and without diabetes. Glucose 68-75 insulin Homo sapiens 27-34 24842248-1 2014 AIMS: Recent studies have suggested that novel parameters of the insulin and glucose response on the oral glucose tolerance test (OGTT) can provide metabolic insight beyond glucose tolerance, but have not evaluated their reproducibility. Glucose 106-113 insulin Homo sapiens 65-72 24842248-1 2014 AIMS: Recent studies have suggested that novel parameters of the insulin and glucose response on the oral glucose tolerance test (OGTT) can provide metabolic insight beyond glucose tolerance, but have not evaluated their reproducibility. Glucose 106-113 insulin Homo sapiens 65-72 24929430-3 2014 Insulin dose was to remain stable in weeks 1-18, adjusted to meet glucose targets in weeks 19-40, then stable in weeks 41-52. Glucose 66-73 insulin Homo sapiens 0-7 24962805-4 2014 RESULTS: Hepatic and muscle insulin sensitivity were decreased in patients with NASH compared with controls, as demonstrated by reduced suppression of hepatic glucose production and glucose disposal (Gd) rates following insulin infusion. Glucose 159-166 insulin Homo sapiens 220-227 24962805-4 2014 RESULTS: Hepatic and muscle insulin sensitivity were decreased in patients with NASH compared with controls, as demonstrated by reduced suppression of hepatic glucose production and glucose disposal (Gd) rates following insulin infusion. Glucose 182-189 insulin Homo sapiens 220-227 24962915-3 2014 However, hypoglycemia becomes an issue if glycemic control is accomplished with a sulfonylurea, a glinide, or insulin, particularly in the setting of absolute endogenous insulin deficiency with loss of the normal decrease in circulating insulin and increase in glucagon secretion and attenuation of the sympathoadrenal response as plasma glucose concentrations fall. Glucose 338-345 insulin Homo sapiens 110-117 24962915-3 2014 However, hypoglycemia becomes an issue if glycemic control is accomplished with a sulfonylurea, a glinide, or insulin, particularly in the setting of absolute endogenous insulin deficiency with loss of the normal decrease in circulating insulin and increase in glucagon secretion and attenuation of the sympathoadrenal response as plasma glucose concentrations fall. Glucose 338-345 insulin Homo sapiens 170-177 24963110-8 2014 CONCLUSIONS: Compared with SAP, 1 week of closed-loop insulin delivery at home reduces mean glucose and increases time in target without increasing the risk of hypoglycemia in adults with relatively well-controlled type 1 diabetes. Glucose 92-99 insulin Homo sapiens 54-61 24736486-5 2014 Insulin sensitivity was measured with estimated glucose disposal rate (eGDR) calculated with the equation: eGDR=24.31-(12.22xWHR)-(3.29xAHT)-(0.57xHbA1c). Glucose 48-55 insulin Homo sapiens 0-7 24825420-1 2014 OBJECTIVE: To develop and validate a specific simple measure of insulin sensitivity using oral glucose tolerance test (OGTT) values for lean polycystic ovary syndrome (PCOS) women. Glucose 95-102 insulin Homo sapiens 64-71 24944613-7 2014 The fasting plasma glucose level in the insulin-glargine group was significantly lower than that observed in the standard-care group. Glucose 19-26 insulin Homo sapiens 40-47 24813197-11 2014 A positive relationship was also found in both study groups between F/L and the FSIVGTT measures insulin sensitivity (Si) and acute insulin response to glucose (AIRg). Glucose 152-159 insulin Homo sapiens 132-139 25143904-7 2014 RESULTS: Analysis of glucose levels both fasting and post-prandial glucose levels revealed that after using insulin lispro, the number of episodes of post-prandial hyperglycemia (1 h plasma glucose >120 mg/dL) was minimal and so was the incidence of hypoglycemia. Glucose 21-28 insulin Homo sapiens 108-115 25143904-7 2014 RESULTS: Analysis of glucose levels both fasting and post-prandial glucose levels revealed that after using insulin lispro, the number of episodes of post-prandial hyperglycemia (1 h plasma glucose >120 mg/dL) was minimal and so was the incidence of hypoglycemia. Glucose 67-74 insulin Homo sapiens 108-115 25143904-7 2014 RESULTS: Analysis of glucose levels both fasting and post-prandial glucose levels revealed that after using insulin lispro, the number of episodes of post-prandial hyperglycemia (1 h plasma glucose >120 mg/dL) was minimal and so was the incidence of hypoglycemia. Glucose 67-74 insulin Homo sapiens 108-115 25668933-6 2014 Critically ill patients with hyperglycaemia should primarily be managed with intravenous insulin infusion to allow dynamic adjustment of treatment to suit the rapid changes in blood glucose values in these patients. Glucose 182-189 insulin Homo sapiens 89-96 24712570-13 2014 In addition, IL-34 augmented fat accumulation and inhibited the stimulatory effects of insulin on glucose transport. Glucose 98-105 insulin Homo sapiens 87-94 24446385-1 2014 Insulin therapy for diabetes patients is designed to mimic the endogenous insulin response of healthy subjects and thereby generate normal blood glucose levels. Glucose 145-152 insulin Homo sapiens 0-7 24446385-2 2014 In order to control the blood glucose in insulin-treated diabetes patients, it is important to be able to predict the effect of exogenous insulin on blood glucose. Glucose 30-37 insulin Homo sapiens 41-48 24446385-2 2014 In order to control the blood glucose in insulin-treated diabetes patients, it is important to be able to predict the effect of exogenous insulin on blood glucose. Glucose 155-162 insulin Homo sapiens 41-48 24446385-4 2014 Thus the aim of this work was to extend the previously developed integrated glucose-insulin (IGI) model to predict 24-hour glucose profiles for patients with Type 2 diabetes following exogenous insulin administration. Glucose 76-83 insulin Homo sapiens 84-91 24876430-2 2014 Difficulties with insulin dose calculations may lead to poor adherence to blood glucose monitoring and insulin treatment regimes, resulting in poor metabolic control. Glucose 80-87 insulin Homo sapiens 18-25 24876431-4 2014 The Dynamic Insulin Sensitivity and Secretion Test (DISST) model was used with the glucose and basal insulin measurements from an Oral Glucose Tolerance Test (OGTT) to predict patient insulin responses. Glucose 83-90 insulin Homo sapiens 12-19 24876431-4 2014 The Dynamic Insulin Sensitivity and Secretion Test (DISST) model was used with the glucose and basal insulin measurements from an Oral Glucose Tolerance Test (OGTT) to predict patient insulin responses. Glucose 83-90 insulin Homo sapiens 184-191 24876431-5 2014 The insulin response to the OGTT was determined via population based regression analysis that incorporated the 60-minute glucose and basal insulin values. Glucose 121-128 insulin Homo sapiens 4-11 24876440-2 2014 The initial data suggesting significant benefit of normalization of blood glucose levels in critically ill patients using intensive intravenous insulin therapy have been challenged or even neglected by some later studies. Glucose 74-81 insulin Homo sapiens 144-151 24880813-12 2014 Therefore, it may disturb glucose metabolism via the insulin resistance of beta cells, but confirmation in humans is needed. Glucose 26-33 insulin Homo sapiens 53-60 25411603-0 2014 Oral glucose-stimulated serum C-peptide predicts successful switching from insulin therapy to liraglutide monotherapy in Japanese patients with type 2 diabetes and renal impairment. Glucose 5-12 insulin Homo sapiens 30-39 25411603-0 2014 Oral glucose-stimulated serum C-peptide predicts successful switching from insulin therapy to liraglutide monotherapy in Japanese patients with type 2 diabetes and renal impairment. Glucose 5-12 insulin Homo sapiens 75-82 25411603-12 2014 CONCLUSIONS: Measurement of oral glucose-stimulated DeltaCPR120 min is recommended when considering switching Japanese type 2 diabetes patients with renal impairment from insulin to liraglutide monotherapy. Glucose 33-40 insulin Homo sapiens 171-178 24898834-2 2014 In this planned substudy of the Outcome Reduction with Initial Glargine Intervention (ORIGIN) trial, we assessed whether normalising glucose with insulin glargine or administering omega-3 fatty acids in this population may slow this process or affect the development of cognitive impairment. Glucose 133-140 insulin Homo sapiens 146-153 24719245-10 2014 Results imply that MetS is equal to poorly controlled T2DM concerning the disturbances of plasma lipid metabolism examined here, and suggest that there are different thresholds for the insulin action on glucose and lipids. Glucose 203-210 insulin Homo sapiens 185-192 24444138-1 2014 OBJECTIVE: Insulin-induced capillary recruitment is considered a significant regulator of overall insulin-stimulated glucose uptake. Glucose 117-124 insulin Homo sapiens 11-18 24444138-1 2014 OBJECTIVE: Insulin-induced capillary recruitment is considered a significant regulator of overall insulin-stimulated glucose uptake. Glucose 117-124 insulin Homo sapiens 98-105 24444138-5 2014 We further assessed the role of capillary recruitment in the association between vasomotion and insulin-mediated glucose uptake. Glucose 113-120 insulin Homo sapiens 96-103 24444138-7 2014 RESULTS: Insulin-induced increase in the neurogenic vasomotion domain was positively related to insulin-augmented capillary recruitment (r = 0.51, p = 0.04), and both parameters were related to insulin-mediated glucose uptake (r = 0.47, p = 0.06 and r = 0.73, p = 0.001, respectively). Glucose 211-218 insulin Homo sapiens 9-16 24444138-7 2014 RESULTS: Insulin-induced increase in the neurogenic vasomotion domain was positively related to insulin-augmented capillary recruitment (r = 0.51, p = 0.04), and both parameters were related to insulin-mediated glucose uptake (r = 0.47, p = 0.06 and r = 0.73, p = 0.001, respectively). Glucose 211-218 insulin Homo sapiens 96-103 24444138-8 2014 The change in insulin-augmented capillary recruitment could, at least statistically, largely explain the association between the neurogenic domain and insulin-mediated glucose uptake. Glucose 168-175 insulin Homo sapiens 14-21 24444138-10 2014 These data suggest that insulin"s action to recruit capillaries may in part involve action on the neurogenic vasomotion domain, thereby enhancing capillary perfusion and glucose uptake. Glucose 170-177 insulin Homo sapiens 24-31 24854384-11 2014 On the other hand, the glucose-independent secretion of insulin was preserved. Glucose 23-30 insulin Homo sapiens 56-63 24718781-8 2014 In derived insulin producing cells (IPCs), secreted insulin and C-peptide was in a glucose dependent manner. Glucose 83-90 insulin Homo sapiens 11-18 24718781-8 2014 In derived insulin producing cells (IPCs), secreted insulin and C-peptide was in a glucose dependent manner. Glucose 83-90 insulin Homo sapiens 64-73 24618283-0 2014 Potential role of skeletal muscle glucose metabolism on the regulation of insulin secretion. Glucose 34-41 insulin Homo sapiens 74-81 24618283-2 2014 Insulin secretion is regulated by many factors including glucose, incretins, and sympathetic and parasympathetic tones among other physiological factors. Glucose 57-64 insulin Homo sapiens 0-7 24618283-5 2014 Considering that skeletal muscle is the largest organ in non-obese subjects and a major site of insulin- and exercise-stimulated glucose disposal, it appears plausible that muscle might interact with the pancreas and modulate insulin secretion for appropriate peripheral intracellular glucose utilization. Glucose 129-136 insulin Homo sapiens 96-103 24618283-5 2014 Considering that skeletal muscle is the largest organ in non-obese subjects and a major site of insulin- and exercise-stimulated glucose disposal, it appears plausible that muscle might interact with the pancreas and modulate insulin secretion for appropriate peripheral intracellular glucose utilization. Glucose 285-292 insulin Homo sapiens 226-233 24985106-4 2014 METHODS: Insulin resistance is a condition in which a normal or elevated insulin level results in an abnormal biologic response, e.g., glucose uptake. Glucose 135-142 insulin Homo sapiens 9-16 24985106-4 2014 METHODS: Insulin resistance is a condition in which a normal or elevated insulin level results in an abnormal biologic response, e.g., glucose uptake. Glucose 135-142 insulin Homo sapiens 73-80 24582776-1 2014 Insulin and Insulin Growth Factor-1 (IGF-1) play a major role in body homeostasis and glucose regulation. Glucose 86-93 insulin Homo sapiens 0-7 25372910-1 2014 OBJECTIVE: This study aims to investigate whether pre-operative Homeostasis Model Assessment Insulin Resistance (HOMA-IR) value is a predictor in non-diabetic coronary artery bypass grafting patients in combination with hemoglobin A1c, fasting blood glucose and insulin levels. Glucose 250-257 insulin Homo sapiens 93-100 25372910-10 2014 The risk factors of fasting blood glucose and cardiopulmonary bypass time were more associated with high Homeostasis Model Assessment Insulin Resistance levels. Glucose 34-41 insulin Homo sapiens 134-141 25396404-8 2014 PPARgamma is the molecular target of thiazolidinediones, which are used clinically as insulin sensitizers to lower blood glucose levels in diabetes type 2 patients. Glucose 121-128 insulin Homo sapiens 86-93 25131089-2 2014 Current islet product release criteria include viability based on cell membrane integrity stains, glucose-stimulated insulin release, and islet equivalent (IE) dose based on counts. Glucose 98-105 insulin Homo sapiens 117-124 25131089-8 2014 IE dose was also highly predictive, while glucoses stimulated insulin release and membrane integrity stains were not. Glucose 42-50 insulin Homo sapiens 62-69 25131094-7 2014 RESULTS: p3MTChins-hepatocytes secreted insulin during glucose challenge, but glucose levels did not change with increasing glucose concentrations. Glucose 55-62 insulin Homo sapiens 40-47 25233627-0 2014 [The synergistic effect of FGF-21 and insulin on regulating glucose metabolism and its mechanism]. Glucose 60-67 insulin Homo sapiens 38-45 25233627-3 2014 This study was designed to elucidate the mechanism of synergistic effect of FGF-21 and insulin in the regulation of glucose metabolism. Glucose 116-123 insulin Homo sapiens 87-94 25233627-4 2014 The synergistic effect of FGF-21 and insulin on regulating glucose metabolism was demonstrated by investigating the glucose absorption rate by insulin resistance HepG2 cell model and the blood glucose chances in type 2 diabetic db/db mice after treatments with different concentrations of FGF-21 or/and insulin; The synergistic metabolism was revealed through detecting GLUT1 and GLUT4 transcription levels in the liver by real-time PCR method. Glucose 59-66 insulin Homo sapiens 37-44 25233627-4 2014 The synergistic effect of FGF-21 and insulin on regulating glucose metabolism was demonstrated by investigating the glucose absorption rate by insulin resistance HepG2 cell model and the blood glucose chances in type 2 diabetic db/db mice after treatments with different concentrations of FGF-21 or/and insulin; The synergistic metabolism was revealed through detecting GLUT1 and GLUT4 transcription levels in the liver by real-time PCR method. Glucose 116-123 insulin Homo sapiens 37-44 25233627-4 2014 The synergistic effect of FGF-21 and insulin on regulating glucose metabolism was demonstrated by investigating the glucose absorption rate by insulin resistance HepG2 cell model and the blood glucose chances in type 2 diabetic db/db mice after treatments with different concentrations of FGF-21 or/and insulin; The synergistic metabolism was revealed through detecting GLUT1 and GLUT4 transcription levels in the liver by real-time PCR method. Glucose 116-123 insulin Homo sapiens 143-150 25233627-4 2014 The synergistic effect of FGF-21 and insulin on regulating glucose metabolism was demonstrated by investigating the glucose absorption rate by insulin resistance HepG2 cell model and the blood glucose chances in type 2 diabetic db/db mice after treatments with different concentrations of FGF-21 or/and insulin; The synergistic metabolism was revealed through detecting GLUT1 and GLUT4 transcription levels in the liver by real-time PCR method. Glucose 116-123 insulin Homo sapiens 143-150 25233627-5 2014 The experimental results showed that FGF-21 and insulin have a synergistic effect on the regulation of glucose metabolism. Glucose 103-110 insulin Homo sapiens 48-55 25233627-12 2014 FGF-21 and insulin exert a synergistic effect on glucose metabolism through mutual sensitization. Glucose 49-56 insulin Homo sapiens 11-18 25024747-9 2014 A positive correlation between fasting glucose and insulin levels (r = 0.28; p < 0.015) was detected in the fhMetS participants. Glucose 39-46 insulin Homo sapiens 51-58 25083136-6 2014 Switching to insulin degludec resulted in clinically meaningful reductions in hypoglycemia, along with reduced fasting plasma glucose and glycosylated hemoglobin and improved satisfaction with treatment. Glucose 126-133 insulin Homo sapiens 13-20 24949970-5 2014 Indeed, pancreatic Clec16a is required for normal glucose-stimulated insulin release. Glucose 50-57 insulin Homo sapiens 69-76 24933368-3 2014 It was found that on a fine scale in parameter variation, the less insulin required to process glucose, a condition that correlates with good health, the more predictable glucose values were. Glucose 95-102 insulin Homo sapiens 67-74 24933368-3 2014 It was found that on a fine scale in parameter variation, the less insulin required to process glucose, a condition that correlates with good health, the more predictable glucose values were. Glucose 171-178 insulin Homo sapiens 67-74 24678915-1 2014 The glucose stimulation of insulin secretion by pancreatic beta-cells depends on increased production of metabolic coupling factors, among which changes in NADPH and ROS (reactive oxygen species) may alter the glutathione redox state (EGSH) and signal through changes in thiol oxidation. Glucose 4-11 insulin Homo sapiens 27-34 24735819-2 2014 Insulin resistance was estimated in apparently healthy elderly control (HC, n=21) and neurodegenerative disease (Alzheimer"s disease (AD), n=20; Parkinson"s disease (PD), n=22) groups using Homeostasis Model Assessment of Insulin Resistance 2 (HOMA2) and intravenous glucose tolerance test (IVGTT). Glucose 267-274 insulin Homo sapiens 0-7 28609059-1 2014 Combination therapy: as combination therapy with other blood-glucose lowering drugs including insulin, when these, together with diet and exercise, do not provide adequate glycaemic control. Glucose 61-68 insulin Homo sapiens 94-101 24917242-2 2014 The GK protein acts in pancreatic islets as a "glucose sensor" that couples fluctuations in the blood glucose concentration to changes in cellular function and insulin secretion. Glucose 47-54 insulin Homo sapiens 160-167 25392748-4 2014 Insulin sensitivity (Si) was determined by a 2-stage glucose clamp, liver and intramyocellular lipid by 1H-MR spectroscopy and body composition by DEXA. Glucose 53-60 insulin Homo sapiens 0-7 25392748-6 2014 Whole body (WB) Si improved by 21% (0.76 +- 1.57 dL/min per microU/mL, p=0.04) and insulin-stimulated glucose uptake (Rd) by 24% (0.91 +- 1.74 dL/min per microU/mL, p=0.03). Glucose 102-109 insulin Homo sapiens 83-90 24747137-8 2014 NOGP inhibitory studies identified PKCbetaII as a key downstream player in lowering insulin-mediated glucose uptake. Glucose 101-108 insulin Homo sapiens 84-91 25392592-1 2014 BACKGROUND: Diabetes is a disease characterized by high blood glucose levels that result from the body"s inability to produce and/or use insulin. Glucose 62-69 insulin Homo sapiens 137-144 24155214-4 2014 Insulin-glucose dynamics were determined by an intravenous glucose tolerance test, and vitamin D metabolites were measured. Glucose 8-15 insulin Homo sapiens 0-7 24656994-12 2014 CONCLUSION: In psoriasis patients plasma levels of lipid and glucose metabolism-related miRNA-33 are increased and correlated with insulin. Glucose 61-68 insulin Homo sapiens 131-138 24668897-7 2014 Array comparative genomic hybridization (array CGH) detected a 3.2 Mb duplication of 17p13.1-p13.2 encompassing TP53, FXR2, NLGN2, and SLC2A4, which encodes the insulin-responsive glucose transporter 4 (GLUT4) associated with insulin-stimulated glucose uptake in adipocytes and muscle. Glucose 180-187 insulin Homo sapiens 161-168 24668897-7 2014 Array comparative genomic hybridization (array CGH) detected a 3.2 Mb duplication of 17p13.1-p13.2 encompassing TP53, FXR2, NLGN2, and SLC2A4, which encodes the insulin-responsive glucose transporter 4 (GLUT4) associated with insulin-stimulated glucose uptake in adipocytes and muscle. Glucose 245-252 insulin Homo sapiens 161-168 24740208-10 2014 The associations between dairy fat intake and glucose tolerance were attenuated by adjusting for insulin sensitivity or liver fat, but strengthened by adjusting for beta-cell function. Glucose 46-53 insulin Homo sapiens 97-104 33833847-2 2014 Unlike for majority of existing mathematical models of glucose-insulin dynamics, parameters in our model are estimable from a relatively small number of noisy observations of plasma glucose and insulin concentrations. Glucose 55-62 insulin Homo sapiens 63-70 24823464-10 2014 Dutasteride, but not finasteride, reduced stimulation of glucose disposal by high-dose insulin (dutasteride by -5.7 [3.2] mumol/kg fat-free mass/min, versus finasteride +7.2 [3.0], and tamsulosin +7.0 [2.0]). Glucose 57-64 insulin Homo sapiens 87-94 24641508-5 2014 KEY RESULTS: Insulin secretion from rat islets, human islets and human re-aggregated cell clusters was concentration-dependently increased by glucose. Glucose 142-149 insulin Homo sapiens 13-20 24630174-2 2014 The balance between glucose storage and mobilization is primarily regulated by the counteracting effects of insulin and glucagon. Glucose 20-27 insulin Homo sapiens 108-115 24011971-9 2014 During the glucose tolerance test, c-peptide, but not insulin, remained elevated in patients compared with all non-malignant females. Glucose 11-18 insulin Homo sapiens 35-44 24715548-9 2014 Insulin sensitivity increased from baseline to week 8 as measured by the Insulin Sensitivity Index derived from an oral glucose tolerance test (0.98 +- 0.3; p < 0.001). Glucose 120-127 insulin Homo sapiens 0-7 24715548-9 2014 Insulin sensitivity increased from baseline to week 8 as measured by the Insulin Sensitivity Index derived from an oral glucose tolerance test (0.98 +- 0.3; p < 0.001). Glucose 120-127 insulin Homo sapiens 73-80 24296717-9 2014 A fourth cluster (TCF7L2, SLC30A8, HHEX/IDE, CDKAL1, CDKN2A/2B) was defined by loci influencing insulin processing and secretion without a detectable change in fasting glucose levels. Glucose 168-175 insulin Homo sapiens 96-103 24477669-9 2014 CONCLUSION: Insulin aspart therapy was well tolerated and was associated with improved glucose control over 24 weeks in people with T2DM. Glucose 87-94 insulin Homo sapiens 12-19 24604100-2 2014 In addition, single nucleotide polymorphisms (SNPs) having an exclusive effect on either glucose- or tolbutamide-stimulated insulin release were identified. Glucose 89-96 insulin Homo sapiens 124-131 24656963-4 2014 Postprandial glucose was regulated by sensor-responsive insulin and glucagon delivery. Glucose 13-20 insulin Homo sapiens 56-63 24658843-1 2014 AIMS/HYPOTHESIS: Oral glucose elicits a higher insulin secretory response than intravenous glucose at matched glucose concentrations. Glucose 22-29 insulin Homo sapiens 47-54 24658843-2 2014 This potentiation, known as the incretin effect, is typically expressed as the difference between the total insulin response to oral vs intravenous glucose. Glucose 148-155 insulin Homo sapiens 108-115 24671273-4 2014 Insulin sensitivity was determined by glucose and insulin measurements at 0, 60 and 120 min. Glucose 38-45 insulin Homo sapiens 0-7 24671273-8 2014 There was a negative correlation between maternal insulin sensitivity and fetal response latencies 60 min after glucose ingestion (r = 0.68, p = 0.02). Glucose 112-119 insulin Homo sapiens 50-57 24705613-10 2014 South Asians may have lower beta-cell function and an inability to compensate adequately for higher glucose levels from insulin resistance. Glucose 100-107 insulin Homo sapiens 120-127 24888256-1 2014 INTRODUCTION: Several studies have shown that dipeptidyl peptidase-4 (DPP-4) inhibitors improve insulin secretion during oral glucose tolerance tests. Glucose 126-133 insulin Homo sapiens 96-103 24114405-7 2014 The proportion of insulin use for glucose control was significantly higher in the group of CA 19-9 >= 37 U/mL (75.0 %) as compared with the group of CA 19-9 < 37 U/mL (34.0 %). Glucose 34-41 insulin Homo sapiens 18-25 24654786-9 2014 Silencing IGFBP-2 lowered leptin- and insulin-stimulated protein kinase B phosphorylation and glucose uptake. Glucose 94-101 insulin Homo sapiens 38-45 24712876-1 2014 beta-Cells rapidly secrete insulin in response to acute increases in plasma glucose but, upon further continuous exposure to glucose, insulin secretion progressively decreases. Glucose 76-83 insulin Homo sapiens 27-34 24162448-2 2014 Furthermore, insulin and markers of insulin resistance, such as abdominal obesity, high blood glucose, high serum testosterone and metabolic syndrome, may affect both BC incidence and prognosis. Glucose 94-101 insulin Homo sapiens 13-20 24162448-2 2014 Furthermore, insulin and markers of insulin resistance, such as abdominal obesity, high blood glucose, high serum testosterone and metabolic syndrome, may affect both BC incidence and prognosis. Glucose 94-101 insulin Homo sapiens 36-43 24568842-1 2014 Insulin binding changes conformation of the insulin receptor kinase (IRK) domain and initiates glucose uptake through the insulin, IGF-1, phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways; human biliverdin reductase (hBVR) is an IRK substrate and pathway effector. Glucose 95-102 insulin Homo sapiens 0-7 24568842-1 2014 Insulin binding changes conformation of the insulin receptor kinase (IRK) domain and initiates glucose uptake through the insulin, IGF-1, phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways; human biliverdin reductase (hBVR) is an IRK substrate and pathway effector. Glucose 95-102 insulin Homo sapiens 44-51 24568842-1 2014 Insulin binding changes conformation of the insulin receptor kinase (IRK) domain and initiates glucose uptake through the insulin, IGF-1, phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways; human biliverdin reductase (hBVR) is an IRK substrate and pathway effector. Glucose 95-102 insulin Homo sapiens 122-129 24845703-8 2014 Using the research-grade human pancreata, the effective method showed high efficacy in the differentiation of NEPEC into insulin-positive cells that secreted insulin in response to a glucose challenge and improved diabetes after being transplanted into diabetic athymic mice. Glucose 183-190 insulin Homo sapiens 121-128 24845703-8 2014 Using the research-grade human pancreata, the effective method showed high efficacy in the differentiation of NEPEC into insulin-positive cells that secreted insulin in response to a glucose challenge and improved diabetes after being transplanted into diabetic athymic mice. Glucose 183-190 insulin Homo sapiens 158-165 24227120-4 2014 Insulin sensitivity index (ISI) was derived from oral-glucose-tolerance test. Glucose 54-61 insulin Homo sapiens 0-7 24606105-11 2014 Glucose Ra increased during the day (21.4 [19.5, 23.5] vs 18.6 [17.0, 21.6) mumol/kg/min, P = .019) and decreased overnight (9.7 [8.5, 11.4] vs 11.6 [10.3, 12.9] mumol/kg/min, P = .004) when the usual therapy was discontinued and replaced with insulin. Glucose 0-7 insulin Homo sapiens 244-251 24617664-5 2014 RESULTS: The glucose and insulin responses to meal ingestion were shifted upward and to the left after GB, with the largest early insulin response and the lowest nadir glucose levels in patients with a history of hypoglycemia, particularly those with neuroglycopenic symptoms. Glucose 13-20 insulin Homo sapiens 130-137 24628556-10 2014 In study 3 (intensified insulin treatment), intensification of glucose control with insulin resulted in a concomitant and parallel reduction of average weekly glucose and GCD59 within 2 weeks. Glucose 63-70 insulin Homo sapiens 24-31 24628556-10 2014 In study 3 (intensified insulin treatment), intensification of glucose control with insulin resulted in a concomitant and parallel reduction of average weekly glucose and GCD59 within 2 weeks. Glucose 63-70 insulin Homo sapiens 84-91 24628556-10 2014 In study 3 (intensified insulin treatment), intensification of glucose control with insulin resulted in a concomitant and parallel reduction of average weekly glucose and GCD59 within 2 weeks. Glucose 159-166 insulin Homo sapiens 24-31 24628556-10 2014 In study 3 (intensified insulin treatment), intensification of glucose control with insulin resulted in a concomitant and parallel reduction of average weekly glucose and GCD59 within 2 weeks. Glucose 159-166 insulin Homo sapiens 84-91 24667247-5 2014 The altered metabolism of nutrients by insulin-sensitive target tissues (muscle, adipose tissue and liver) can result in high circulating levels of glucose and various lipids, which further impact on pancreatic beta-cell function, IR and progression of the metabolic syndrome. Glucose 148-155 insulin Homo sapiens 39-46 24681827-4 2014 For instance, significant changes in protein kinase activities and in protein phosphorylation patterns occur subsequent to the stimulation of insulin release by glucose. Glucose 161-168 insulin Homo sapiens 142-149 24833582-3 2014 Although it is well established that many metabolic pathways (ie, oxidative phosphorylation, insulin-stimulated glucose uptake) decline with age, it often remains uncertain if these are a cause or consequence of the aging process. Glucose 112-119 insulin Homo sapiens 93-100 24398779-1 2014 Insulin, a pancreatic hormone, is best known for its peripheral effects on the metabolism of glucose, fats and proteins. Glucose 93-100 insulin Homo sapiens 0-7 24814528-2 2014 Women with PCOS present elevated plasma insulin levels, both fasting and after a glucose load, as an indirect evidence of insulin resistance. Glucose 81-88 insulin Homo sapiens 40-47 24814528-2 2014 Women with PCOS present elevated plasma insulin levels, both fasting and after a glucose load, as an indirect evidence of insulin resistance. Glucose 81-88 insulin Homo sapiens 122-129 25632404-4 2014 Changes in plasma glucose levels (hyper- or hypoglycemia) have been associated with altered BBB transport functions (e.g., glucose, insulin, choline, amino acids, etc. Glucose 18-25 insulin Homo sapiens 132-139 24766140-1 2014 Incretins such as glucagon-like peptide 1 (GLP-1) are released from the gut and potentiate insulin release in a glucose-dependent manner. Glucose 112-119 insulin Homo sapiens 91-98 24955299-3 2014 It"s noteworthy that compound 2, the major constituent of this plant, can significantly stimulate glucose absorption in insulin resistant HepG2 cells without affecting cell viability. Glucose 98-105 insulin Homo sapiens 120-127 24955299-4 2014 Furthermore, this compound can also restore the glucose absorption in DXMS-induced insulin resistant 3T3-L1 cells. Glucose 48-55 insulin Homo sapiens 83-90 24814346-5 2014 We demonstrate the nature of PTEN as an IRS1 phosphatase by direct biochemical analysis and cellular reconstitution, showing that NEDD4 supports insulin-mediated glucose metabolism and is required for the proliferation of IGF1 receptor-dependent but not EGF receptor-dependent tumor cells. Glucose 162-169 insulin Homo sapiens 145-152 24420961-6 2014 RESULTS: Whole body insulin resistance in skeletal muscle (insulin-stimulated glucose disposal) and adipose tissue (insulin-suppressed lipolysis) were independently related to trunk FM (r = -0.336 and 0.484, respectively), but not leg FM (r = -0.142 and -0.148, respectively). Glucose 78-85 insulin Homo sapiens 20-27 24420961-6 2014 RESULTS: Whole body insulin resistance in skeletal muscle (insulin-stimulated glucose disposal) and adipose tissue (insulin-suppressed lipolysis) were independently related to trunk FM (r = -0.336 and 0.484, respectively), but not leg FM (r = -0.142 and -0.148, respectively). Glucose 78-85 insulin Homo sapiens 59-66 24420961-6 2014 RESULTS: Whole body insulin resistance in skeletal muscle (insulin-stimulated glucose disposal) and adipose tissue (insulin-suppressed lipolysis) were independently related to trunk FM (r = -0.336 and 0.484, respectively), but not leg FM (r = -0.142 and -0.148, respectively). Glucose 78-85 insulin Homo sapiens 59-66 24345292-6 2014 The release of C-peptide was regulated by glucose concentration in the SVF cells. Glucose 42-49 insulin Homo sapiens 15-24 24345292-8 2014 In glucose perfusion experiments, C-peptide was released in response to high glucose concentrations in the mesenteric perfusate, opposite to insulin release. Glucose 3-10 insulin Homo sapiens 34-43 24345292-8 2014 In glucose perfusion experiments, C-peptide was released in response to high glucose concentrations in the mesenteric perfusate, opposite to insulin release. Glucose 77-84 insulin Homo sapiens 34-43 24559166-2 2014 For example, insulin stimulates glucose uptake in adipose tissue and skeletal muscle but not in liver. Glucose 32-39 insulin Homo sapiens 13-20 24559166-3 2014 In liver glucose influx will increase as insulin stimulates the phosphorylation of glucose and eventual storage in the form of glycogen. Glucose 9-16 insulin Homo sapiens 41-48 24559166-4 2014 Insulin also increases glucose oxidation, decreases glucose production, decreases lipolysis, increases protein synthesis and inhibits protein degradation in addition to others. Glucose 23-30 insulin Homo sapiens 0-7 24856123-4 2014 METHODS: Insulin sensitivity (SI) and the acute response to glucose (AIRg) were calculated by MINMOD analysis from glucose and insulin obtained during a modified frequently sampled intravenous glucose tolerance test. Glucose 115-122 insulin Homo sapiens 9-16 24856123-4 2014 METHODS: Insulin sensitivity (SI) and the acute response to glucose (AIRg) were calculated by MINMOD analysis from glucose and insulin obtained during a modified frequently sampled intravenous glucose tolerance test. Glucose 115-122 insulin Homo sapiens 9-16 25169637-4 2014 Serum insulin level of 2 hours after 75 g glucose intake was significantly higher in GG+AG groups than that of AA group at rs2479106 of DENND1A gene[(71 +- 65), (64 +- 50) mU/L; P = 0.05 ], and the prevalence of type II diabetes in first-degree relatives of patients were also increased [9.9% (66/666), 6.9% (52/751); P < 0.05]. Glucose 42-49 insulin Homo sapiens 6-13 24885604-9 2014 The augmentation of insulin secretion at 16.7 mM glucose by activation of CFTR by cAMP (forskolin (FSK) or GLP-1) was significantly inhibited when CFTR antagonists (GlyH-101 and/or CFTRinh-172) were added. Glucose 49-56 insulin Homo sapiens 20-27 24885604-11 2014 Finally, our studies demonstrate that CFTR act upstream of the chloride channel Anoctamin 1 (ANO1; TMEM16A) in the regulation of cAMP- and glucose-stimulated insulin secretion. Glucose 139-146 insulin Homo sapiens 158-165 24679060-7 2014 The use of glucose-lowering medications, including insulin, was lower in the surgical groups than in the medical-therapy group. Glucose 11-18 insulin Homo sapiens 51-58 24853756-4 2014 One hypothesis is that coordination is achieved through an insulin-dependent negative feedback action of the liver onto the glucose level. Glucose 124-131 insulin Homo sapiens 59-66 24892003-5 2014 Whole body insulin sensitivity was estimated by ISIMatsuda, glucose-stimulated insulin secretion by [deltaIRI0-30/deltaPG0-30] and Stumvoll indices, hepatic insulin sensitivity by quantitative insulin sensitivity check index (QUICKI) and 1/fasting IRI, beta cell function by oral disposition index (DIO) ([deltaIRI0-30/deltaPG0-30] [ISIMatsuda]), and glucose effectiveness by an OGTT-derived index (SgIO). Glucose 60-67 insulin Homo sapiens 79-86 24895054-1 2014 For almost 30 years, scientists have demonstrated that human fetal ICCs transplanted under the kidney capsule of nude mice matured into functioning endocrine cells, as evidenced by a significant increase in circulating human C-peptide following glucose stimulation(1-9). Glucose 245-252 insulin Homo sapiens 225-234 24936385-8 2014 Quenching of lipotoxicity mediated oxidative stress by antioxidant reverted its deleterious impacts and restored insulin stimulated glucose uptake. Glucose 132-139 insulin Homo sapiens 113-120 24792735-1 2014 The Immediate Myocardial Metabolic Enhancement During Initial Assessment and Treatment in Emergency care Trial of very early intravenous glucose-insulin-potassium (GIK) for acute coronary syndromes (ACS) in out-of-hospital emergency medical service (EMS) settings showed 80% reduction in infarct size at 30 days, suggesting potential longer-term benefits. Glucose 137-144 insulin Homo sapiens 145-152 24835010-5 2014 In this study, we showed that Imatinib significantly induced insulin expression in both glucose-stimulated and resting beta cells. Glucose 88-95 insulin Homo sapiens 61-68 24835010-7 2014 Unexpectedly, high concentrations of glucose significantly induced c-Abl expression, suggesting c-Abl may play a role in balancing insulin production during glucose stimulation. Glucose 37-44 insulin Homo sapiens 131-138 24636949-1 2014 Myosin 1c (Myo1c) plays a key role in supporting motile events that underlie cell migration, vesicle trafficking, insulin-stimulated glucose uptake and hearing. Glucose 133-140 insulin Homo sapiens 114-121 24636949-8 2014 This complex has been implicated in the exocytosis of glucose transporter 4 storage vesicles during insulin-stimulated glucose uptake. Glucose 54-61 insulin Homo sapiens 100-107 24847313-6 2014 Insulin, amylin, and preptin are co-secreted from pancreatic beta cells in response to increased glucose levels after feeding, and are also found in high circulating levels in obesity. Glucose 97-104 insulin Homo sapiens 0-7 24810050-6 2014 Glucose-mediated IR was characterized by basal activation of mTORC1 and its poor inducibility by insulin. Glucose 0-7 insulin Homo sapiens 97-104 24887638-10 2014 The cell clusters expressed a broad gene profile related to pancreatic islet cells, released insulin and c-peptide in a glucose concentration-dependent manner, and normalized hyperglycemia of streptozocin-induced mice for at least 80 days following xenograft. Glucose 120-127 insulin Homo sapiens 93-100 24746806-4 2014 Lineage-tracing experiments show that dedifferentiated cells can subsequently redifferentiate to mature neurogenin3-negative, insulin-positive beta cells after lowering of blood glucose by insulin therapy. Glucose 178-185 insulin Homo sapiens 189-196 25364722-1 2014 Type II diabetes mellitus (T2DM) is a widespread metabolic disorder characterized by insulin resistance precipitating abnormally high blood glucose levels. Glucose 140-147 insulin Homo sapiens 85-92 24641631-2 2014 Insulin regulates glucose metabolism by phosphorylation-dependent signaling and has been shown to stimulate ATP synthesis in human skeletal muscle. Glucose 18-25 insulin Homo sapiens 0-7 24843779-1 2014 AIMS/INTRODUCTION: To establish the validity of the plasma glucose disappearance rate (KITT), derived from an insulin-tolerance test (ITT), for evaluating the insulin sensitivity of patients with type 2 diabetes after insulin therapy. Glucose 59-66 insulin Homo sapiens 110-117 24843779-1 2014 AIMS/INTRODUCTION: To establish the validity of the plasma glucose disappearance rate (KITT), derived from an insulin-tolerance test (ITT), for evaluating the insulin sensitivity of patients with type 2 diabetes after insulin therapy. Glucose 59-66 insulin Homo sapiens 159-166 24843779-1 2014 AIMS/INTRODUCTION: To establish the validity of the plasma glucose disappearance rate (KITT), derived from an insulin-tolerance test (ITT), for evaluating the insulin sensitivity of patients with type 2 diabetes after insulin therapy. Glucose 59-66 insulin Homo sapiens 159-166 24462809-2 2014 The purpose of this study was to show the effects of insulin-derived amyloidosis on blood glucose levels, insulin dose requirements, and insulin absorption. Glucose 90-97 insulin Homo sapiens 53-60 24241533-6 2014 Insulin-mediated glucose disposal and suppression of fatty acids did not improve immediately after surgery but increased at 3 months and 1 year; this increase likely was related to the reduction in body weight. Glucose 17-24 insulin Homo sapiens 0-7 24241533-7 2014 Insulin secretion increased after RYGB only in patients with T2D and only in response to oral glucose, underscoring the importance of the changed gut anatomy. Glucose 94-101 insulin Homo sapiens 0-7 24353179-0 2014 Proinsulin-transferrin fusion protein as a novel long-acting insulin analog for the inhibition of hepatic glucose production. Glucose 106-113 insulin Homo sapiens 3-10 24379354-6 2014 These findings indicated that IG20/MADD plays a critical role in glucose-induced insulin release from beta-cells and that its functional disruption can cause type 2 diabetes. Glucose 65-72 insulin Homo sapiens 81-88 24526524-0 2014 MicroRNA-492 reverses high glucose-induced insulin resistance in HUVEC cells through targeting resistin. Glucose 27-34 insulin Homo sapiens 43-50 24526524-9 2014 Together, our findings indicate that miR-492 contributes to insulin resistance and endothelial dysfunction induced by high glucose, via directly downregulating resistin expression, and involving STAT3 phosphorylation, SOCS, and P-selectin activation. Glucose 123-130 insulin Homo sapiens 60-67 24585202-7 2014 In Study 3, beta cell glucose sensitivity was minimally affected, but the insulin secretion rate at 9 mmol/l glucose increased to similar degrees from baseline with canagliflozin and sitagliptin [LSM (SEM) changes 38 (8) and 28 (9) pmol min(-1) m(-2), respectively; p < 0.05 for both]. Glucose 109-116 insulin Homo sapiens 74-81 24595633-1 2014 OBJECTIVE: Transcapillary transport of insulin is one determinant of glucose uptake by skeletal muscle; thus, a reduction in capillary density (CD) may worsen insulin sensitivity. Glucose 69-76 insulin Homo sapiens 39-46 24841710-0 2014 Complementary Approaches to Improving Glucose Control-Insulin and Incretins: Patient Case Studies in Action. Glucose 38-45 insulin Homo sapiens 54-61 24841710-6 2014 CONCLUSION: Insulin remains the most potent glucose-lowering agent available for the treatment of type 2 diabetes but has limitations, primarily of hypoglycemia and secondarily of weight gain. Glucose 44-51 insulin Homo sapiens 12-19 24841710-7 2014 The addition of incretin-based therapies complements the glucose-lowering potential of basal insulin, without increasing the risk of hypoglycemia, potentially allowing for lower doses of insulin and without increasing weight gain (DPP-4 inhibitors) or possibly with weight loss (GLP-1 receptor agonists). Glucose 57-64 insulin Homo sapiens 93-100 24601884-8 2014 The results showed that the expressions of ERalpha and GLUT4, the insulin-stimulated translocation of GLUT4 from the cytoplasm to the cell membrane and glucose uptake in mature adipocytes were dramatically increased (P < .01). Glucose 152-159 insulin Homo sapiens 66-73 24710644-6 2014 In polycystic ovary syndrome condition, due to insulin resistance, the actions like glucose uptake and glycogen synthesis gets declined along with exhibiting steroidogenic effect in ovaries. Glucose 84-91 insulin Homo sapiens 47-54 24710644-10 2014 The inhibition of phophatidylinositide-3 kinase in ovary leads to decreased androgen synthesis and the activation affects the positive actions of insulin like glucose uptake. Glucose 159-166 insulin Homo sapiens 146-153 24554534-4 2014 Similarly, in primary cultured adipocytes, both carboxylated and uncarboxylated osteocalcin increased basal and insulin-stimulated glucose transport as well as insulin sensitivity. Glucose 131-138 insulin Homo sapiens 112-119 24554534-5 2014 Osteocalcin also increased basal and insulin-stimulated glucose oxidation, though there was no effect on fatty acid synthesis or lipolysis. Glucose 56-63 insulin Homo sapiens 37-44 24759285-1 2014 The glucose story begins with Claude Bernard"s discovery of glycogen and milieu interieur, continued with Banting"s and Best"s discovery of insulin and with Rudolf Schoenheimer"s paradigm of dynamic body constituents. Glucose 4-11 insulin Homo sapiens 140-147 24569874-1 2014 Insulin signaling includes generation of low levels of H2O2; however, its origin and contribution to insulin-stimulated glucose transport are unknown. Glucose 120-127 insulin Homo sapiens 0-7 24569874-1 2014 Insulin signaling includes generation of low levels of H2O2; however, its origin and contribution to insulin-stimulated glucose transport are unknown. Glucose 120-127 insulin Homo sapiens 101-108 24569874-2 2014 We tested the impact of H2O2 on insulin-dependent glucose transport and GLUT4 translocation in skeletal muscle cells. Glucose 50-57 insulin Homo sapiens 32-39 24569874-9 2014 We propose that, in addition to the canonical alpha,beta phosphatidylinositol 3-kinase to Akt pathway, insulin engages both RyR-mediated Ca(2+) release and IP3-receptor-mediated mitochondrial Ca(2+) uptake, and that these signals jointly stimulate glucose uptake. Glucose 248-255 insulin Homo sapiens 103-110 24517151-0 2014 TNFalpha dynamics during the oral glucose tolerance test vary according to the level of insulin resistance in pregnant women. Glucose 34-41 insulin Homo sapiens 88-95 24606093-9 2014 Glucose effectiveness (P = .002) and the acute insulin response to glucose (P = .002) increased, and basal glucose levels (P = .001) decreased after metformin treatment. Glucose 67-74 insulin Homo sapiens 47-54 24667639-1 2014 Diabetic patients exhibit a reduction in beta cells, which secrete insulin to help regulate glucose homeostasis; however, little is known about the factors that regulate proliferation of these cells in human pancreas. Glucose 92-99 insulin Homo sapiens 67-74 24895484-8 2014 Moreover, Deltaplasma glucose was higher in individuals in the high Deltaserum insulin group than in the low Deltaserum insulin group. Glucose 22-29 insulin Homo sapiens 79-86 24895484-8 2014 Moreover, Deltaplasma glucose was higher in individuals in the high Deltaserum insulin group than in the low Deltaserum insulin group. Glucose 22-29 insulin Homo sapiens 120-127 24560135-7 2014 Insulin-stimulated whole-body glucose disposal (35.4+/-3.1 versus 33.2+/-3.0 mumol/kg/min) and nadir endogenous glucose production (6.2+/-1.4 versus 7.0+/-1.1 mumol/kg/min) revealed no significant differences in effects of the treatments. Glucose 30-37 insulin Homo sapiens 0-7 24560135-7 2014 Insulin-stimulated whole-body glucose disposal (35.4+/-3.1 versus 33.2+/-3.0 mumol/kg/min) and nadir endogenous glucose production (6.2+/-1.4 versus 7.0+/-1.1 mumol/kg/min) revealed no significant differences in effects of the treatments. Glucose 112-119 insulin Homo sapiens 0-7 24876619-1 2014 The dose response of postprandial plasma glucose (PPG) to add-on, premeal oral hepatic-directed vesicle-insulin (HDV-I), an investigational lipid bio-nanoparticle hepatocyte-targeted insulin delivery system, was evaluated in a 3-test-meal/day model in type 2 diabetes patients. Glucose 41-48 insulin Homo sapiens 104-111 24876621-0 2014 Can glucose be monitored accurately at the site of subcutaneous insulin delivery? Glucose 4-11 insulin Homo sapiens 64-71 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 25-32 insulin Homo sapiens 8-15 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 25-32 insulin Homo sapiens 127-134 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 104-111 insulin Homo sapiens 8-15 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 104-111 insulin Homo sapiens 127-134 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 104-111 insulin Homo sapiens 8-15 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 104-111 insulin Homo sapiens 127-134 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 104-111 insulin Homo sapiens 8-15 24876621-1 2014 Because insulin promotes glucose uptake into adipocytes, it has been assumed that during measurement of glucose at the site of insulin delivery, the local glucose level would be much lower than systemic glucose. Glucose 104-111 insulin Homo sapiens 127-134 24876621-5 2014 Another is that insulin monomers and dimers (from hexamer disassociation) might be absorbed into the circulation before they can increase glucose uptake locally. Glucose 138-145 insulin Homo sapiens 16-23 24876621-9 2014 In summary, when measured at the site of insulin delivery, the decline in subcutaneous glucose level appears to be minimal, though the literature base is not large. Glucose 87-94 insulin Homo sapiens 41-48 24283382-14 2014 CONCLUSIONS: These results suggest that the Zbed3 protein may be a cytokine associated with insulin resistance in humans that is influenced by glucose and insulin levels. Glucose 143-150 insulin Homo sapiens 92-99 24090427-15 2014 Increases in muscle mass might have induced improvements in whole body insulin-induced glucose uptake. Glucose 87-94 insulin Homo sapiens 71-78 24937972-3 2014 RESULTS: Insulin levels were positively correlated with glucose levels (p < 0.001). Glucose 56-63 insulin Homo sapiens 9-16 24716635-5 2014 Peripheral insulin sensitivity improved (glucose infusion rate during high-dose insulin increased from 10.1 +- 1.6 to 12 +- 2.1 mg/kg/min/, P = 0.025), with no change in hepatic insulin response following successful viral eradication, without any accompanying change in muscle, liver or abdominal fat depots. Glucose 41-48 insulin Homo sapiens 11-18 24716635-5 2014 Peripheral insulin sensitivity improved (glucose infusion rate during high-dose insulin increased from 10.1 +- 1.6 to 12 +- 2.1 mg/kg/min/, P = 0.025), with no change in hepatic insulin response following successful viral eradication, without any accompanying change in muscle, liver or abdominal fat depots. Glucose 41-48 insulin Homo sapiens 80-87 25675756-4 2014 As a consequence of this a level of insulin and a HOMA index was noted, what have had promoted a reduction of a revealing rate of glucose tolerance violation (GTV) and diabetes mellitus (DM) type II. Glucose 130-137 insulin Homo sapiens 36-43 24785155-1 2014 BACKGROUND: Osteocalcin has been reported to be relevant to glucose and lipid metabolism, indicating it may stimulate insulin secretion and improve insulin resistance. Glucose 60-67 insulin Homo sapiens 118-125 24755593-6 2014 Finally, we show proof-of-concept enzyme-powered devices that autonomously deliver small molecules and proteins in response to specific chemical stimuli, including the release of insulin in response to glucose. Glucose 202-209 insulin Homo sapiens 179-186 24535382-1 2014 OBJECTIVE: The aim of this study was to develop a protocol for normalizing blood glucose levels in diabetic patients by subcutaneously administering rapid-acting insulin before administering (18)F-fluorodeoxyglucose ((18)F-FDG) without hindering the quality of PET/computed tomography (CT) studies. Glucose 81-88 insulin Homo sapiens 162-169 24535382-12 2014 CONCLUSION: Subcutaneous administration of rapid-acting insulin normalizes blood glucose levels without compromising the quality of PET-CT studies when (18)F-FDG is administered not earlier than 4 h later. Glucose 81-88 insulin Homo sapiens 56-63 24470352-4 2014 Insulin sensitivity was estimated by an oral glucose tolerance test and the Matsuda Index. Glucose 45-52 insulin Homo sapiens 0-7 24754463-1 2014 Insulin resistance is defined as a state where insulin produces a diminished biological response, primarily in its capacity as a glucose-regulating hormone. Glucose 129-136 insulin Homo sapiens 0-7 24754463-1 2014 Insulin resistance is defined as a state where insulin produces a diminished biological response, primarily in its capacity as a glucose-regulating hormone. Glucose 129-136 insulin Homo sapiens 47-54 24827702-3 2014 It is mediated by autoreactive cytotoxic CD4+ and CD8+ T-cells that infiltrate the pancreatic islets of Langerhans and destroy insulin-secreting beta-cells, leading to abnormal levels of glucose in affected individuals. Glucose 187-194 insulin Homo sapiens 127-134 26327840-10 2014 From different insulin measurements HOMA index turned out to have the strongest correlations with the metabolic parameters triglycerides and glucose. Glucose 141-148 insulin Homo sapiens 15-22 24788670-23 2014 Where data could not be combined, single studies showed lower mean fasting glucose (MD -0.40; 95% CI -0.72 to -0.08) and higher means for two-hour glucose response (MD 1.08; 95% CI 0.45 to 1.71) and insulin area under the curve (AUC) (MD 20.30; 95% CI 4.24 to 36.36).Three trials examined the etonogestrel vaginal ring and one examined an etonogestrel implant. Glucose 147-154 insulin Homo sapiens 199-206 24886864-0 2014 Coefficient of glucose variation is independently associated with mortality in critically ill patients receiving intravenous insulin. Glucose 15-22 insulin Homo sapiens 125-132 25191617-1 2014 Produce rich in phytochemicals may alter postprandial glucose and insulin responses by interacting with the pathways that regulate glucose uptake and insulin secretion in humans. Glucose 54-61 insulin Homo sapiens 150-157 25191617-1 2014 Produce rich in phytochemicals may alter postprandial glucose and insulin responses by interacting with the pathways that regulate glucose uptake and insulin secretion in humans. Glucose 131-138 insulin Homo sapiens 66-73 24790417-6 2014 The insulin-independent mechanism results in decreased serum glucose, without hypoglycemia or weight gain. Glucose 61-68 insulin Homo sapiens 4-11 24610809-2 2014 Cdc42, the small Rho family GTPase recognized as the proximal glucose-specific trigger to elicit second-phase insulin secretion, signals downstream to activate the p21-activated kinase (PAK1), which then signals to Raf-1/MEK/ERK to induce filamentous actin (F-actin) remodeling, to ultimately mobilize insulin granules to the plasma membrane. Glucose 62-69 insulin Homo sapiens 110-117 24610809-2 2014 Cdc42, the small Rho family GTPase recognized as the proximal glucose-specific trigger to elicit second-phase insulin secretion, signals downstream to activate the p21-activated kinase (PAK1), which then signals to Raf-1/MEK/ERK to induce filamentous actin (F-actin) remodeling, to ultimately mobilize insulin granules to the plasma membrane. Glucose 62-69 insulin Homo sapiens 302-309 24610809-4 2014 Toward this, we identified the involvement of the Src family kinases (SFKs), based upon the ability of SFK inhibitors to block glucose-stimulated Cdc42 and PAK1 activation events as well as the amplifying pathway of glucose-stimulated insulin release, in MIN6 beta cells. Glucose 127-134 insulin Homo sapiens 235-242 24025723-6 2014 Applying multiple regressions, adjusting for age and weight status (normal weight vs. obese), serum MR-proANP concentrations were significantly inversely associated with serum insulin concentrations (beta = -0.39; P < 0.0001) and plasma glucose concentrations (beta = -0.21; P = 0.02) but not with total (beta = 0.00), android (beta = -0.01), or gynoid (beta = 0.03) fat mass percentage (P > 0.76). Glucose 240-247 insulin Homo sapiens 176-183 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 57-64 insulin Homo sapiens 38-45 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 196-203 insulin Homo sapiens 38-45 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 196-203 insulin Homo sapiens 179-186 24473436-12 2014 In summary, although IL-6 induced local and systemic responses, the insulin-stimulated glucose uptake was not affected. Glucose 87-94 insulin Homo sapiens 68-75 24502221-3 2014 The unintentional use of a glucose-containing solution has resulted in artefactually high glucose concentrations in blood samples drawn from the arterial line, leading to insulin administration causing hypoglycaemia and fatal neuroglycopenic brain injury. Glucose 27-34 insulin Homo sapiens 171-178 24502221-3 2014 The unintentional use of a glucose-containing solution has resulted in artefactually high glucose concentrations in blood samples drawn from the arterial line, leading to insulin administration causing hypoglycaemia and fatal neuroglycopenic brain injury. Glucose 90-97 insulin Homo sapiens 171-178 24535192-3 2014 The phosphoinositide 3"-kinase (PI3K)/Akt signaling pathway plays an important role in insulin signaling by controlling glucose metabolism, in part through regulating the activity of FoxO transcription factors. Glucose 120-127 insulin Homo sapiens 87-94 24122936-4 2014 This led to diminished uptake of insulin-induced glucose. Glucose 49-56 insulin Homo sapiens 33-40 24122936-6 2014 Therefore, development of specific inhibitors targeting 11beta-HSD1 might be a promising way to improve impaired insulin-stimulated glucose uptake. Glucose 132-139 insulin Homo sapiens 113-120 24430017-7 2014 The measured glucose concentrations were used to alter insulin infusion rates according to established treatment protocols. Glucose 13-20 insulin Homo sapiens 55-62 24530467-3 2014 DESIGN AND METHODS: Serum insulin levels were measured by electrochemiluminescence immunoassay in 5786 participants of the Tehran Lipid and Glucose Study. Glucose 140-147 insulin Homo sapiens 26-33 24530467-8 2014 Age, waist circumference, and systolic blood pressures were biological determinants of fasting insulin in both genders; in addition, insulin was modulated by triglycerides in men and fasting glucose in women. Glucose 191-198 insulin Homo sapiens 133-140 24577625-5 2014 Resting muscle sympathetic nerve activity (MSNA) was measured with microneurography and insulin sensitivity of glucose and free fatty acid metabolism was measured during a hyperinsulinemic-euglycemic clamp with two levels of insulin. Glucose 111-118 insulin Homo sapiens 88-95 24748202-1 2014 Since insulin resistance can lead to hyperglycemia, improving glucose uptake into target tissues is critical for regulating blood glucose levels. Glucose 62-69 insulin Homo sapiens 6-13 24748202-1 2014 Since insulin resistance can lead to hyperglycemia, improving glucose uptake into target tissues is critical for regulating blood glucose levels. Glucose 130-137 insulin Homo sapiens 6-13 24748202-3 2014 This study aimed to investigate the role of GPR41 in modulating basal and insulin-stimulated glucose uptake in insulin-sensitive cells including adipocytes and skeletal muscle cells. Glucose 93-100 insulin Homo sapiens 74-81 24748202-3 2014 This study aimed to investigate the role of GPR41 in modulating basal and insulin-stimulated glucose uptake in insulin-sensitive cells including adipocytes and skeletal muscle cells. Glucose 93-100 insulin Homo sapiens 111-118 24748202-7 2014 Both propionic acid and valeric acid increased insulin-stimulated glucose uptake in 3T3-L1 adipocyte, which did not occur in cells transfected with siRNA for GPR41 (siGPR41). Glucose 66-73 insulin Homo sapiens 47-54 24583185-4 2014 The insulin sensitive group showed reduced blood oxygen level dependent (BOLD) signal in response to food pictures following glucose ingestion in numerous corticolimbic brain regions, whereas the insulin resistant group did not. Glucose 125-132 insulin Homo sapiens 4-11 24583185-5 2014 There was a significant interaction between insulin sensitivity (sensitive vs resistant) and condition (water vs glucose). Glucose 113-120 insulin Homo sapiens 44-51 24583185-7 2014 Furthermore, BOLD signal in the anterior cingulate, medial frontal gyrus, posterior cingulate/precuneus, and parietal cortex during a glucose challenge correlated negatively with insulin sensitivity. Glucose 134-141 insulin Homo sapiens 179-186 24583185-8 2014 We conclude the PCOS women with insulin resistance have an impaired brain response to a glucose challenge. Glucose 88-95 insulin Homo sapiens 32-39 24727515-2 2014 Increased risk of infection following hyperglycemia has been reported in hospitalized patients and infections may also cause insulin resistance which complicates the control of blood glucose level. Glucose 183-190 insulin Homo sapiens 125-132 24944908-4 2014 Strikingly, ss-cells exposed to this high-glucose pulse paradigm exhibited significantly stronger insulin secretion. Glucose 42-49 insulin Homo sapiens 98-105 24748926-4 2014 It is believed that, among individuals destined to develop T2DM, hyperinsulinemia is the mechanism by which the pancreatic beta-cell initially compensates for deteriorating peripheral insulin sensitivity, thus ensuring normal glucose tolerance. Glucose 226-233 insulin Homo sapiens 70-77 24748929-1 2014 Chromium is considered to have positive effects on insulin sensitivity and is marketed as an adjunctive therapy for inducing glucose tolerance in cases of insulin resistance ("the glucose tolerance factor"). Glucose 125-132 insulin Homo sapiens 155-162 24748929-1 2014 Chromium is considered to have positive effects on insulin sensitivity and is marketed as an adjunctive therapy for inducing glucose tolerance in cases of insulin resistance ("the glucose tolerance factor"). Glucose 180-187 insulin Homo sapiens 155-162 24765237-2 2014 As the only glucose-lowering hormone in the body, insulin not only alleviates the detrimental effects of hyperglycemia through its metabolic regulation, but also directly modulates inflammatory mediators and acts upon immune cells to enhance immunocompetence. Glucose 12-19 insulin Homo sapiens 50-57 24725803-1 2014 BACKGROUND: Insulin aspart (IAsp) and its biphasic preparations BIAsp50 and BIAsp70 (containing 50% and 70% IAsp, respectively) have distinct glucose-lowering properties as compared to human insulin (HI). Glucose 142-149 insulin Homo sapiens 12-19 24722187-2 2014 We previously demonstrated that the DNA encoding the insulin gene is uniquely unmethylated in these cells and then developed a methylation-specific PCR (MSP) assay to identify circulating beta cell DNA in streptozotocin-treated mice prior to the rise in blood glucose. Glucose 260-267 insulin Homo sapiens 53-60 24713709-4 2014 However, we paradoxically observed increased insulin sensitivity evaluated by a hyperinsulinaemic-euglycaemic clamp (glucose infusion rate: 64.83 mumol/kg/min). Glucose 117-124 insulin Homo sapiens 45-52 24705280-0 2014 Insulin dynamics in young women with polycystic ovary syndrome and normal glucose tolerance across categories of body mass index. Glucose 74-81 insulin Homo sapiens 0-7 24705280-7 2014 CONCLUSION: Women with PCOS show higher insulin resistance but also larger insulin secretion to maintain normal glucose homeostasis than age-, BMI- and insulin resistance-matched controls. Glucose 112-119 insulin Homo sapiens 75-82 23420066-1 2014 Insulin-mediated glucose disposal varies severalfold in apparently healthy individuals, and approximately one-third of the most insulin resistant of these individuals is at increased risk to develop various adverse clinical syndromes. Glucose 17-24 insulin Homo sapiens 0-7 23420066-1 2014 Insulin-mediated glucose disposal varies severalfold in apparently healthy individuals, and approximately one-third of the most insulin resistant of these individuals is at increased risk to develop various adverse clinical syndromes. Glucose 17-24 insulin Homo sapiens 128-135 23420066-3 2014 The objective of this study was to compare FPI as an estimate of insulin-mediated glucose disposal with values generated by HOMA-IR in 758 apparently healthy nondiabetic individuals. Glucose 82-89 insulin Homo sapiens 65-72 23420066-4 2014 Measurements were made of FPG, FPI, triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C) concentrations, and insulin-mediated glucose uptake was quantified by determining steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 141-148 insulin Homo sapiens 124-131 23420066-8 2014 In conclusion, FPI and HOMA-IR are highly correlated in nondiabetic individuals, with each estimate accounting for ~40% of the variability (variance) in a direct measure of insulin-mediated glucose disposal. Glucose 190-197 insulin Homo sapiens 173-180 23848509-2 2014 We aimed to assess whether treatment with metformin, an oral insulin-sensitising agent, improved lung function or symptoms in individuals with COPD and glucose intolerance. Glucose 152-159 insulin Homo sapiens 61-68 24569548-3 2014 Information gained from these studies was used to develop human embryonic stem cell (hESC) differentiation protocols with the goal of generating functional glucose-responsive, insulin-producing human beta-cells. Glucose 156-163 insulin Homo sapiens 176-183 24379346-4 2014 Treatment with 1-deoxysphinganine induced dose-dependent cytotoxicity with senescent, necrotic, and apoptotic characteristics and compromised glucose-stimulated insulin secretion. Glucose 142-149 insulin Homo sapiens 161-168 24442447-0 2014 Single injections of apoA-I acutely improve in vivo glucose tolerance in insulin-resistant mice. Glucose 52-59 insulin Homo sapiens 73-80 24461623-3 2014 Since humans spend most of their time in the postprandial state, the present study aims to evaluate the relationship of insulin resistance (IR) in the basal state with dyslipidemia and systemic inflammation (hs-CRP, IL-6 and TNF-a), in the fasting state, 2h and 4h after a mixed meal, in Indian adults with normal glucose tolerance, and new onset type-2 diabetes. Glucose 314-321 insulin Homo sapiens 120-127 24462282-4 2014 RESULTS: Compared to control islets, human islets cultured with high glucose showed a reduced glucose-stimulated insulin secretion that was associated with lower ATP levels and a lower ATP/ADP ratio. Glucose 69-76 insulin Homo sapiens 113-120 24462282-4 2014 RESULTS: Compared to control islets, human islets cultured with high glucose showed a reduced glucose-stimulated insulin secretion that was associated with lower ATP levels and a lower ATP/ADP ratio. Glucose 94-101 insulin Homo sapiens 113-120 24496806-5 2014 Insulin secretory rate (ISR) was calculated by C-peptide deconvolution from plasma glucose and C-peptide levels measured during oral glucose tolerance tests (OGTTs) performed at baseline and after 16-20 weeks of leptin replacement. Glucose 83-90 insulin Homo sapiens 0-7 24496806-5 2014 Insulin secretory rate (ISR) was calculated by C-peptide deconvolution from plasma glucose and C-peptide levels measured during oral glucose tolerance tests (OGTTs) performed at baseline and after 16-20 weeks of leptin replacement. Glucose 133-140 insulin Homo sapiens 0-7 24507950-1 2014 Type 1 diabetes (T1D) is due to the loss of both beta-cell insulin secretion and glucose sensing, leading to glucose variability and a lack of predictability, a daily issue for patients. Glucose 109-116 insulin Homo sapiens 59-66 24651807-8 2014 Adding a glucose tracer to the oral dose significantly enhances the assessment of insulin action by segregating insulin sensitivity into its glucose disposal and hepatic components. Glucose 9-16 insulin Homo sapiens 82-89 24651807-8 2014 Adding a glucose tracer to the oral dose significantly enhances the assessment of insulin action by segregating insulin sensitivity into its glucose disposal and hepatic components. Glucose 9-16 insulin Homo sapiens 112-119 24651807-8 2014 Adding a glucose tracer to the oral dose significantly enhances the assessment of insulin action by segregating insulin sensitivity into its glucose disposal and hepatic components. Glucose 141-148 insulin Homo sapiens 82-89 24808450-25 2014 Frequently, diabetes is a comorbid condition that exists among heart failure patients and with the reduction of the systemic inflammatory and stress response produced by the support of a nonpulsatile LVAD, many patients may benefit from a reduction in their blood glucose levels, as well as insulin requirements. Glucose 264-271 insulin Homo sapiens 291-298 24757334-6 2014 Rapid-acting insulin analogs seem to be safe and efficient in reducing postprandial glucose levels more proficiently than regular human insulin, with less hypoglycemia. Glucose 84-91 insulin Homo sapiens 13-20 24424487-8 2014 We next examined the effect of each ARB on insulin-mediated glucose metabolism in 3T3-L1 preadipocytes. Glucose 60-67 insulin Homo sapiens 43-50 24783939-1 2014 Insulin is involved in regulation of glucose utilization in the body. Glucose 37-44 insulin Homo sapiens 0-7 25080793-11 2014 On surface of membrane, insulin increases number of glucose carriers GLUT4. Glucose 52-59 insulin Homo sapiens 24-31 25080798-2 2014 The insulin expressed synthesis of apoE glucose carrier 4 and stearyl-KoA-desaturase. Glucose 40-47 insulin Homo sapiens 4-11 25080798-3 2014 These occurrences confirm that syndrome of insulin resistance primarily is the pathology of metabolism of fatty acids and only secondary the pathology metabolism of glucose. Glucose 165-172 insulin Homo sapiens 43-50 24469400-1 2014 Insulin stimulates glucose transport into fat and muscle cells by increasing the exocytic trafficking rate of the GLUT4 facilitative glucose transporter from intracellular stores to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 24910876-3 2014 The in vitro release of insulin from the nanoparticles was evaluated in 3 mg/ml glucose medium. Glucose 80-87 insulin Homo sapiens 24-31 24910876-7 2014 The insulinloaded nanoparticles showed the rapid insulin release in 3 mg/ml glucose medium. Glucose 76-83 insulin Homo sapiens 4-11 24910876-9 2014 Furthermore, the insulin-loaded nanoparticles overcame mucosal barriers and significantly decreased plasma glucose levels. Glucose 107-114 insulin Homo sapiens 17-24 24458650-10 2014 The safety and success of a prescribed insulin regimen is, therefore, dependent on self-monitoring of blood glucose and/or a continuous glucose monitoring system to avoid critical hypoglycemia and glucose variability. Glucose 108-115 insulin Homo sapiens 39-46 24458650-12 2014 New therapy options such as sensor-augmented insulin pump therapy, which integrates CSII with a continuous glucose sensor, along with emerging therapies such as the artificial pancreas, will likely continue to improve safe insulin therapy in the near future. Glucose 107-114 insulin Homo sapiens 45-52 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 195-202 insulin Homo sapiens 71-78 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 195-202 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 195-202 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 195-202 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 195-202 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 404-411 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 404-411 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 404-411 insulin Homo sapiens 147-154 23447466-3 2014 The objectives of this study were to: (i) determine the association of insulin sensitivity assessed by liquid meal test with that determined by an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT); (ii) examine the association of insulin sensitivity derived from each test with measures of body composition, fat distribution and metabolic health (lipids, fasting insulin and glucose, and surrogate indices of insulin sensitivity); and (iii) examine the associations of indices of beta-cell function derived from each test with total and regional adiposity. Glucose 404-411 insulin Homo sapiens 147-154 24724584-3 2014 The endothelial cells of the blood brain barrier, neurons and glia express typical and different receptors of the glucose metabolism (glucose transporters, insulin receptors and glucagon-like peptide-1 receptors). Glucose 114-121 insulin Homo sapiens 156-163 24931352-1 2014 Persistent hyperinsulinaemic hypoglycaemia in infancy (PHHI) is a heterogeneous condition characterised by unregulated insulin secretion in response to a low blood glucose level. Glucose 164-171 insulin Homo sapiens 16-23 24652432-0 2014 Identification of insulin resistance in subjects with normal glucose tolerance. Glucose 61-68 insulin Homo sapiens 18-25 23989864-7 2014 The difference between the two obese subgroups remained significant after adjusting for gender, age, waist circumference, fat mass, and insulin-stimulated glucose disposal (P = 0.03). Glucose 155-162 insulin Homo sapiens 136-143 24684803-6 2014 Insulin glargine was titrated to achieve a target fasting glucose level of 70-130 mg/dL as a first step (STEP0). Glucose 58-65 insulin Homo sapiens 0-7 24684803-14 2014 CONCLUSIONS: The two-step addition of postprandial hypoglycemic agents to basal insulin therapy is potentially effective and safe for decreasing both the fasting and postprandial glucose levels. Glucose 179-186 insulin Homo sapiens 80-87 24671002-1 2014 AIMS/HYPOTHESIS: Islet amyloid polypeptide (IAPP) is a beta cell hormone secreted together with insulin upon glucose stimulation. Glucose 109-116 insulin Homo sapiens 96-103 24671046-4 2014 The cells that differentiated into INSULIN-positive and C-PEPTIDE-positive cells secreted insulin in response to glucose stimulation, indicating a functional IPC phenotype. Glucose 113-120 insulin Homo sapiens 90-97 24666736-6 2014 RESULTS: Treatment of n-STZ rats with GPR40 agonist CNX-011-67 enhanced insulin secretion in response to oral glucose load on day 0 and this response persisted during the treatment period. Glucose 110-117 insulin Homo sapiens 72-79 24666736-7 2014 The treatment also produced a "memory effect" during which insulin secretion in response to oral glucose load remained enhanced, for a week, even in absence of the agonist. Glucose 97-104 insulin Homo sapiens 59-66 24666736-8 2014 Activation of GPR40 enhanced responsiveness of islets to glucose and increased glucose induced insulin secretion and islet insulin content. Glucose 79-86 insulin Homo sapiens 95-102 24315620-2 2014 If insulin resistance is present, beta cells maintain normal glucose tolerance by increasing insulin output. Glucose 61-68 insulin Homo sapiens 3-10 24315620-2 2014 If insulin resistance is present, beta cells maintain normal glucose tolerance by increasing insulin output. Glucose 61-68 insulin Homo sapiens 93-100 24315620-3 2014 Only when beta cells cannot release sufficient insulin in the presence of insulin resistance do glucose concentrations rise. Glucose 96-103 insulin Homo sapiens 47-54 24315620-3 2014 Only when beta cells cannot release sufficient insulin in the presence of insulin resistance do glucose concentrations rise. Glucose 96-103 insulin Homo sapiens 74-81 24651439-3 2014 Skeletal muscle is responsible for 75% of total insulin-dependent glucose uptake; consequently, skeletal muscle IR is considered to be the primary defect of systemic IR development. Glucose 66-73 insulin Homo sapiens 48-55 25364717-4 2014 Although hyperglycemia can be improved by insulin administration, exogenous insulin injection cannot successfully mimic the insulin secretion from normal beta cells, which keeps blood glucose levels within the normal range all the time. Glucose 184-191 insulin Homo sapiens 76-83 25364717-4 2014 Although hyperglycemia can be improved by insulin administration, exogenous insulin injection cannot successfully mimic the insulin secretion from normal beta cells, which keeps blood glucose levels within the normal range all the time. Glucose 184-191 insulin Homo sapiens 76-83 24412390-7 2014 Thus, a right combination of basal insulin which has lowering effect on fasting plasma glucose and GLP-1 mimetic with its lowering effect on postprandial plasma glucose with minimal gastrointestinal adverse effects, seems the right therapy choice from a clinical point of view for some diabetic patients. Glucose 87-94 insulin Homo sapiens 35-42 24412390-7 2014 Thus, a right combination of basal insulin which has lowering effect on fasting plasma glucose and GLP-1 mimetic with its lowering effect on postprandial plasma glucose with minimal gastrointestinal adverse effects, seems the right therapy choice from a clinical point of view for some diabetic patients. Glucose 161-168 insulin Homo sapiens 35-42 24492615-11 2014 Our results indicate that increased utilization of glucose induced a ROS-driven proinflammatory phenotype in MPhis, which may play an integral role in the promotion of obesity-associated insulin resistance. Glucose 51-58 insulin Homo sapiens 187-194 24944906-4 2014 The insulinotropic action of FABP4 was identified using an in vitro system that recapitulates adipocyte to beta-cell endocrine signalling, with glucose-stimulated insulin secretion (GSIS) as a functional readout, coupled with quantitative proteomics. Glucose 144-151 insulin Homo sapiens 4-11 24374234-0 2014 Regulation of myosin IIA and filamentous actin during insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Glucose 73-80 insulin Homo sapiens 54-61 24374234-1 2014 Insulin stimulated glucose uptake requires the colocalization of myosin IIA (MyoIIA) and the insulin-responsive glucose transporter 4 (GLUT4) at the plasma membrane for proper GLUT4 fusion. Glucose 19-26 insulin Homo sapiens 0-7 24374234-1 2014 Insulin stimulated glucose uptake requires the colocalization of myosin IIA (MyoIIA) and the insulin-responsive glucose transporter 4 (GLUT4) at the plasma membrane for proper GLUT4 fusion. Glucose 19-26 insulin Homo sapiens 93-100 24374234-3 2014 In adipocytes F-actin reorganization is required for insulin-stimulated glucose uptake. Glucose 72-79 insulin Homo sapiens 53-60 24653645-3 2014 Muscle, in addition to its mechanical role, is critical in maintaining systemic energy homeostasis and accounts for about 80% of insulin-directed glucose disposal. Glucose 146-153 insulin Homo sapiens 129-136 24741361-5 2014 RESULTS: On day 21 of BR, AUC(120 min) of glucose concentration was increased by 28.8 (5.2)% and AUC(120 min) of insulin by 35.9 (10.2)% (glucose: P < 0.001; insulin: P = 0.02). Glucose 138-145 insulin Homo sapiens 113-120 24594290-1 2014 Diabetes is characterized by high blood glucose level due to either autoimmune destruction of islet beta-cells or insufficient insulin secretion or glucose non-responsive production of insulin by beta-cells. Glucose 40-47 insulin Homo sapiens 127-134 24354538-2 2014 However, rise of glucose can also lower [Ca(2+) ]i and inhibit insulin release. Glucose 17-24 insulin Homo sapiens 63-70 24354538-10 2014 Patients with type 2 diabetes often respond to intravenous bolus injection of glucose with 5-10 min of late suppression of circulating insulin. Glucose 78-85 insulin Homo sapiens 135-142 24354574-1 2014 AIM: After both oral and intravenous glucose administration, peripheral insulin concentrations are lower in trained compared with untrained humans. Glucose 37-44 insulin Homo sapiens 72-79 24354574-9 2014 CONCLUSION: With no difference in incretin effect and insulin clearance between the two groups, the lower plasma insulin concentrations found in trained compared with untrained, young, healthy men are most likely explained by lower beta-cell sensitivity to glucose and enhanced glucose uptake in skeletal muscle in the former group. Glucose 257-264 insulin Homo sapiens 113-120 24354574-9 2014 CONCLUSION: With no difference in incretin effect and insulin clearance between the two groups, the lower plasma insulin concentrations found in trained compared with untrained, young, healthy men are most likely explained by lower beta-cell sensitivity to glucose and enhanced glucose uptake in skeletal muscle in the former group. Glucose 278-285 insulin Homo sapiens 113-120 23709472-6 2014 Best Practice Advice 1: Clinicians should target a blood glucose level of 7.8 to 11.1 mmol/L (140 to 200 mg/dL) if insulin therapy is used in SICU/MICU patients. Glucose 57-64 insulin Homo sapiens 115-122 24457840-5 2014 Experimental manipulation of the insulin/glucose milieu and suppression of endogenous testicular function suggests the relationship between androgens and insulin sensitivity is bidirectional. Glucose 41-48 insulin Homo sapiens 154-161 23725211-9 2014 Insulin secretion of hUDSCs(PDX1+) in the high-glucose medium was 1.8 muU/mL. Glucose 47-54 insulin Homo sapiens 0-7 24529205-1 2014 Estimation of insulin sensitivity plays a crucial role in the diagnosis and clinical investigation of glucose related diseases. Glucose 102-109 insulin Homo sapiens 14-21 24529205-2 2014 The Bergman minimal model provides a non-invasive approach for estimating insulin sensitivity from the glucose insulin time series data of intravenous glucose tolerance test (IVGTT). Glucose 103-110 insulin Homo sapiens 74-81 23657630-6 2014 Generated 56 IS-MSC cell-lines were glucose responsive i.e. mean C-Peptide and insulin secretion levels were measured 0.41 ng/ml and 13.13 muU/ml, respectively, in absence of glucose which rose to 1.18 ng/ml and 83.42 muU/ml, respectively, following glucose challenge (p < 0.001). Glucose 36-43 insulin Homo sapiens 65-74 24247476-1 2014 OBJECTIVES: Intensive insulin therapy for tight glycemic control in critically ill surgical patients has been shown to reduce mortality; however, intensive insulin therapy is associated with iatrogenic hypoglycemia and increased variability of blood glucose levels. Glucose 250-257 insulin Homo sapiens 22-29 24247476-1 2014 OBJECTIVES: Intensive insulin therapy for tight glycemic control in critically ill surgical patients has been shown to reduce mortality; however, intensive insulin therapy is associated with iatrogenic hypoglycemia and increased variability of blood glucose levels. Glucose 250-257 insulin Homo sapiens 156-163 24247476-3 2014 We hypothesized that the addition of continuous infusion of glucagon-like peptide-1 to intensive insulin therapy would result in better glucose control, reduced requirement of exogenous insulin administration, and fewer hypoglycemic events. Glucose 136-143 insulin Homo sapiens 97-104 24247476-15 2014 Improved stability of blood glucose is a favorable outcome, which enhances the safety of intensive insulin therapy. Glucose 28-35 insulin Homo sapiens 99-106 24222345-6 2014 The increase in insulin-stimulated glucose transport was less (P < 0.01) in T2D (twofold) than in NW (sevenfold) or OB (sixfold) subjects. Glucose 35-42 insulin Homo sapiens 16-23 24237386-4 2014 Insulin sensitivity was assessed by measuring the glucose disappearance rate (GDR) during the last 40 min of a 5-h hyperinsulinemic, euglycemic clamp. Glucose 50-57 insulin Homo sapiens 0-7 24237386-5 2014 Insulin secretion was determined as the acute insulin response to glucose (AIRg) during the first 10 min of a frequently sampled intravenous glucose tolerance test. Glucose 66-73 insulin Homo sapiens 0-7 24237386-5 2014 Insulin secretion was determined as the acute insulin response to glucose (AIRg) during the first 10 min of a frequently sampled intravenous glucose tolerance test. Glucose 66-73 insulin Homo sapiens 46-53 24237386-5 2014 Insulin secretion was determined as the acute insulin response to glucose (AIRg) during the first 10 min of a frequently sampled intravenous glucose tolerance test. Glucose 141-148 insulin Homo sapiens 0-7 24326527-8 2014 Primary outcome was insulin secretory function, which was evaluated in response to graded infusions of glucose and day-long mixed meals. Glucose 103-110 insulin Homo sapiens 20-27 24508419-2 2014 Insulin degludec (IDeg) is a basal insulin with an ultralong duration of action and a flat and stable glucose-lowering effect profile. Glucose 102-109 insulin Homo sapiens 0-7 24341419-3 2014 The metabolic dysfunction includes impaired insulin response, decreased hepatic suppression of glucose production during insulin infusion and decreased insulin-stimulated glucose uptake in skeletal muscle, i.e. peripheral insulin resistance. Glucose 95-102 insulin Homo sapiens 121-128 24341419-3 2014 The metabolic dysfunction includes impaired insulin response, decreased hepatic suppression of glucose production during insulin infusion and decreased insulin-stimulated glucose uptake in skeletal muscle, i.e. peripheral insulin resistance. Glucose 95-102 insulin Homo sapiens 121-128 24341419-3 2014 The metabolic dysfunction includes impaired insulin response, decreased hepatic suppression of glucose production during insulin infusion and decreased insulin-stimulated glucose uptake in skeletal muscle, i.e. peripheral insulin resistance. Glucose 95-102 insulin Homo sapiens 121-128 24341419-4 2014 The insulin resistance in normal glucose tolerance pregnancy is related to a decrease in the post-receptor insulin signalling cascade, specifically decreased insulin receptor substrate 1 tyrosine phosphorylation. Glucose 33-40 insulin Homo sapiens 4-11 24341419-4 2014 The insulin resistance in normal glucose tolerance pregnancy is related to a decrease in the post-receptor insulin signalling cascade, specifically decreased insulin receptor substrate 1 tyrosine phosphorylation. Glucose 33-40 insulin Homo sapiens 107-114 24429578-6 2014 First and second phases of glucose-stimulated insulin secretion were determined by perifusion. Glucose 27-34 insulin Homo sapiens 46-53 24456994-2 2014 METHODS: A retrospective review was performed on 1276 medical admissions (801 patients) in which insulin was given, >=6 point of care glucose (POCG) measurements and length of stay (LOS) 2-30 days. Glucose 137-144 insulin Homo sapiens 97-104 24462281-2 2014 We compare 3 insulin regimens with the aim of improving glucose control and reducing hypoglycaemia. Glucose 56-63 insulin Homo sapiens 13-20 24246336-1 2014 OBJECTIVE: Determine the relationship between mean glucose (MG), as assessed by continuous glucose monitoring (CGM), and hemoglobin A1c (A1C) in insulin-requiring adults in a clinical practice setting and examine the persistence of this relationship over time. Glucose 51-58 insulin Homo sapiens 145-152 24316260-4 2014 Clinical and demographic information was collected from all participants, and insulin sensitivity was measured using the insulin-modified intravenous glucose tolerance test. Glucose 150-157 insulin Homo sapiens 78-85 24316260-4 2014 Clinical and demographic information was collected from all participants, and insulin sensitivity was measured using the insulin-modified intravenous glucose tolerance test. Glucose 150-157 insulin Homo sapiens 121-128 23681273-7 2014 The cosine curve was fitted to all measured values in each QT measurement and RR for 24 h. Insulin resistance (glucose infusion rate (GIR)) was measured using the euglycemic hyperinsulinemic glucose clamp method. Glucose 111-118 insulin Homo sapiens 91-98 24557504-1 2014 Insulin secretion from pancreatic beta-cells is tightly regulated to maintain fasting blood glucose level between 3.5-5.5 mmol/l. Glucose 92-99 insulin Homo sapiens 0-7 23736362-5 2014 RESULTS: The threshold for insulin resistance (90th percentile) was 2.21 (mg dl(-1) fasting glucose x mU l(-1) fasting insulin divided by 405) for HOMA-IR and 6.118 (mg glucose per kg body weight per minute) for clamp. Glucose 92-99 insulin Homo sapiens 27-34 23736362-5 2014 RESULTS: The threshold for insulin resistance (90th percentile) was 2.21 (mg dl(-1) fasting glucose x mU l(-1) fasting insulin divided by 405) for HOMA-IR and 6.118 (mg glucose per kg body weight per minute) for clamp. Glucose 92-99 insulin Homo sapiens 119-126 23736362-5 2014 RESULTS: The threshold for insulin resistance (90th percentile) was 2.21 (mg dl(-1) fasting glucose x mU l(-1) fasting insulin divided by 405) for HOMA-IR and 6.118 (mg glucose per kg body weight per minute) for clamp. Glucose 169-176 insulin Homo sapiens 27-34 24876585-0 2014 Personalized State-space Modeling of Glucose Dynamics for Type 1 Diabetes Using Continuously Monitored Glucose, Insulin Dose, and Meal Intake: An Extended Kalman Filter Approach. Glucose 37-44 insulin Homo sapiens 112-119 24876585-2 2014 In this article, we present a new data-driven state-space dynamic model with time-varying coefficients that are used to explicitly quantify the time-varying patient-specific effects of insulin dose and meal intake on blood glucose fluctuations. Glucose 223-230 insulin Homo sapiens 185-192 24876590-1 2014 The aim was to evaluate changes in insulin requirements from onset of continuous subcutaneous insulin infusion (CSII) until glucose optimization in type 1 diabetes and to determine patient characteristics to be considered when CSII is implemented. Glucose 124-131 insulin Homo sapiens 35-42 23902932-3 2014 METHODS: We utilized an octreotide, basal glucagon replacement, multistage insulin infusion, and the concomitant infusion of [6,6 (2)H2]glucose to derive insulin-mediated suppression of glucose production and insulin-stimulated glucose disposal in nine older, overweight individuals (body mass index 28.1 +- 1.7 kg m(-2); 39.9% +- 1.9% fat). Glucose 136-143 insulin Homo sapiens 154-161 23902932-3 2014 METHODS: We utilized an octreotide, basal glucagon replacement, multistage insulin infusion, and the concomitant infusion of [6,6 (2)H2]glucose to derive insulin-mediated suppression of glucose production and insulin-stimulated glucose disposal in nine older, overweight individuals (body mass index 28.1 +- 1.7 kg m(-2); 39.9% +- 1.9% fat). Glucose 136-143 insulin Homo sapiens 154-161 23902932-3 2014 METHODS: We utilized an octreotide, basal glucagon replacement, multistage insulin infusion, and the concomitant infusion of [6,6 (2)H2]glucose to derive insulin-mediated suppression of glucose production and insulin-stimulated glucose disposal in nine older, overweight individuals (body mass index 28.1 +- 1.7 kg m(-2); 39.9% +- 1.9% fat). Glucose 186-193 insulin Homo sapiens 154-161 23902932-3 2014 METHODS: We utilized an octreotide, basal glucagon replacement, multistage insulin infusion, and the concomitant infusion of [6,6 (2)H2]glucose to derive insulin-mediated suppression of glucose production and insulin-stimulated glucose disposal in nine older, overweight individuals (body mass index 28.1 +- 1.7 kg m(-2); 39.9% +- 1.9% fat). Glucose 186-193 insulin Homo sapiens 154-161 23902932-7 2014 Insulin-mediated suppression of glucose production was modest prior to bed rest and was further reduced (>15% +- 2%) by bed rest. Glucose 32-39 insulin Homo sapiens 0-7 23902932-9 2014 There was also a significant bed rest-induced decline (>2.0 +- 0.6 mg kg FFM(-1) min(-1)) in insulin-stimulated glucose disposal. Glucose 115-122 insulin Homo sapiens 96-103 24616587-1 2014 The incretin effect, which is a unique stimulus of insulin secretion in response to oral ingestion of nutrients, is calculated by the difference in insulin secretory responses from an oral glucose tolerance test (OGTT) and a corresponding isoglycemic intravenous glucose infusion (IIGI) study. Glucose 189-196 insulin Homo sapiens 51-58 24359593-8 2014 The glucose testing frequency was lowest among basal-only insulin patients and pre-mixed insulin patients (mean=576.2 [median=450] and mean=599.5 [median=500], respectively; non-significantly different) compared to other insulin types. Glucose 4-11 insulin Homo sapiens 58-65 24359593-8 2014 The glucose testing frequency was lowest among basal-only insulin patients and pre-mixed insulin patients (mean=576.2 [median=450] and mean=599.5 [median=500], respectively; non-significantly different) compared to other insulin types. Glucose 4-11 insulin Homo sapiens 89-96 24359593-8 2014 The glucose testing frequency was lowest among basal-only insulin patients and pre-mixed insulin patients (mean=576.2 [median=450] and mean=599.5 [median=500], respectively; non-significantly different) compared to other insulin types. Glucose 4-11 insulin Homo sapiens 89-96 24152890-5 2014 RESULTS: A total of 25 out of 76 (32.9%) patients had abnormal fasting and/or glucose-stimulated insulin levels. Glucose 78-85 insulin Homo sapiens 97-104 25080782-3 2014 The regulation of metabolism of glucose is billions years older than system of insulin and biological function of locomotion (function of motion). Glucose 32-39 insulin Homo sapiens 79-86 25080782-5 2014 The insulin in physiological way deprives mitochondrions a possibility to metabolize ketone bodies, short chain, medium chain and long chain fatty acids and "forces" them to oxidize glucose which phylogenetically is not an optimal substrate. Glucose 182-189 insulin Homo sapiens 4-11 25080782-9 2014 In these conditions, insulin enhances absorption of glucose by cells through glucose carriers--GLUT4. Glucose 52-59 insulin Homo sapiens 21-28 25080782-9 2014 In these conditions, insulin enhances absorption of glucose by cells through glucose carriers--GLUT4. Glucose 77-84 insulin Homo sapiens 21-28 24576898-2 2014 The AMPK-related kinase SIK2 (salt-inducible kinase 2) is now shown to be stabilized in pancreatic beta-cells following glucose stimulation, leading to improved systemic glucose homeostasis by regulating cellular calcium flux and insulin secretion. Glucose 120-127 insulin Homo sapiens 230-237 23666871-2 2014 We sought to clarify this by quantifying adipose cell size distribution, body fat, and insulin-mediated glucose uptake in overweight to moderately-obese individuals. Glucose 104-111 insulin Homo sapiens 87-94 23666871-3 2014 METHODS: A total of 148 healthy nondiabetic subjects with BMI 25-38 kg/m2 underwent subcutaneous adipose tissue biopsies and quantification of insulin-mediated glucose uptake with steady-state plasma glucose (SSPG) concentrations during the modified insulin suppression test. Glucose 160-167 insulin Homo sapiens 143-150 24568287-1 2014 BACKGROUND: Adiponectin is a major regulator of glucose and lipid homeostasis by its insulin sensitizer properties. Glucose 48-55 insulin Homo sapiens 85-92 24900864-2 2014 Examples from this series have promising in vivo pharmacokinetics and increase glucose-stimulated insulin secretion in human whole and dispersed islets. Glucose 79-86 insulin Homo sapiens 98-105 24555815-1 2014 BACKGROUND: Insulin sensitivity can be estimated using glucose disposal rate (M) measured during a hyperinsulinemic euglycemic clamp (HEC) or insulin sensitivity index (SI) derived from a frequently sampled intravenous glucose tolerance test (FSIVGTT). Glucose 55-62 insulin Homo sapiens 12-19 24555815-1 2014 BACKGROUND: Insulin sensitivity can be estimated using glucose disposal rate (M) measured during a hyperinsulinemic euglycemic clamp (HEC) or insulin sensitivity index (SI) derived from a frequently sampled intravenous glucose tolerance test (FSIVGTT). Glucose 219-226 insulin Homo sapiens 12-19 24555815-2 2014 The commonly used homeostatic model assessment of insulin resistance (HOMA-IR) which utilizes fasting glucose and insulin has been validated against M across several populations (r = 0.5-0.8). Glucose 102-109 insulin Homo sapiens 50-57 24535122-0 2014 Subcellular glucose exposure biases the spatial distribution of insulin granules in single pancreatic beta cells. Glucose 12-19 insulin Homo sapiens 64-71 24535122-6 2014 In addition, the imaging of a cell expressing GFP-tagged insulin showed that continuous subcellular exposure to glucose biased the spatial distribution of insulin granules toward the site where the glucose was delivered. Glucose 112-119 insulin Homo sapiens 57-64 24535122-6 2014 In addition, the imaging of a cell expressing GFP-tagged insulin showed that continuous subcellular exposure to glucose biased the spatial distribution of insulin granules toward the site where the glucose was delivered. Glucose 112-119 insulin Homo sapiens 155-162 24535122-6 2014 In addition, the imaging of a cell expressing GFP-tagged insulin showed that continuous subcellular exposure to glucose biased the spatial distribution of insulin granules toward the site where the glucose was delivered. Glucose 198-205 insulin Homo sapiens 57-64 24535122-6 2014 In addition, the imaging of a cell expressing GFP-tagged insulin showed that continuous subcellular exposure to glucose biased the spatial distribution of insulin granules toward the site where the glucose was delivered. Glucose 198-205 insulin Homo sapiens 155-162 24338022-5 2014 The rank order of efficacy to inhibit insulin-stimulated glucose uptake was: PST-297S > PST-287K > PST-WT. Glucose 57-64 insulin Homo sapiens 38-45 24567800-0 2014 Insulin plus incretin: A glucose-lowering strategy for type 2-diabetes. Glucose 25-32 insulin Homo sapiens 0-7 24567800-1 2014 There are many advantages of combining incretin therapy [glucagon-like peptide-1 (GLP-1) receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors] with insulin therapy as a glucose-lowering strategy in type 2 diabetes. Glucose 180-187 insulin Homo sapiens 159-166 24611020-3 2014 Two distinct pathways encourage glucose transport activity in skeletal muscle, ie, the contraction-stimulated pathway reliant on Ca(2+)/5"-monophosphate-activated protein kinase (AMPK)-dependent mechanisms and an insulin-dependent pathway activated via upregulation of serine/threonine protein kinase Akt/PKB. Glucose 32-39 insulin Homo sapiens 213-220 24835766-7 2014 Insulin could be loaded onto the glycopolymer NPs with high efficiency (up to 10%), and insulin release increased with enhancement of the glucose level in the medium. Glucose 138-145 insulin Homo sapiens 0-7 24835766-7 2014 Insulin could be loaded onto the glycopolymer NPs with high efficiency (up to 10%), and insulin release increased with enhancement of the glucose level in the medium. Glucose 138-145 insulin Homo sapiens 88-95 24504462-8 2014 By contrast, concerted or sequential administration of the ectopic 3pTFs in an indirect hierarchical mode resulted in the generation of insulin and somatostatin co-producing cells and diminished glucose regulated processed insulin secretion. Glucose 195-202 insulin Homo sapiens 223-230 24652432-3 2014 In this study, we built models using data from metabolic syndrome (Mets) components and the oral glucose tolerance test (OGTT) to detect insulin resistance in subjects with normal glucose tolerance (NGT). Glucose 97-104 insulin Homo sapiens 137-144 24652432-3 2014 In this study, we built models using data from metabolic syndrome (Mets) components and the oral glucose tolerance test (OGTT) to detect insulin resistance in subjects with normal glucose tolerance (NGT). Glucose 180-187 insulin Homo sapiens 137-144 24652432-6 2014 The steady-state plasma glucose (SSPG) level derived from the IST was the measurement of insulin action. Glucose 24-31 insulin Homo sapiens 89-96 24212054-1 2014 Insulin is essential for the regulation of fuel metabolism and triggers the uptake of glucose by skeletal muscle. Glucose 86-93 insulin Homo sapiens 0-7 24212054-2 2014 The imported glucose is either stored or broken down, as insulin stimulates glycogenesis and ATP synthesis. Glucose 13-20 insulin Homo sapiens 57-64 24212054-5 2014 We demonstrate that a 20-min insulin exposure significantly increases (i) the cell respiratory control ratio, (ii) the coupling efficiency of oxidative phosphorylation, and (iii) the glucose sensitivity of anaerobic glycolysis. Glucose 183-190 insulin Homo sapiens 29-36 23591152-6 2014 Protein to carbohydrate ratio correlated negatively with pre-meal glucose due to improved efficacy of insulin action rather than to increased insulin concentrations. Glucose 66-73 insulin Homo sapiens 102-109 24130361-10 2014 A dose of 50-60% of the prepregnancy insulin requirement resulted in the lowest rate of hypoglycemia and glucose excursions. Glucose 105-112 insulin Homo sapiens 37-44 24150606-6 2014 Here, we show that transient overexpression of human OATP1B3 in a murine beta-cell line (MIN6)-which exhibits glucose and glibenclamide-sensitive insulin secretion-significantly enhances the insulinotropic effect of glibenclamide without affecting glucose-stimulated insulin secretion. Glucose 248-255 insulin Homo sapiens 191-198 24390813-9 2014 Glucose concentrations between 120-160 mg/dL can serve as a reasonable target for insulin infusion protocols. Glucose 0-7 insulin Homo sapiens 82-89 24186866-9 2014 Insulin secretion with sitagliptin treatment was similarly stimulated with oral and "isoglycemic" intravenous glucose. Glucose 110-117 insulin Homo sapiens 0-7 24233056-4 2014 Glucose-stimulated insulin secretion was assessed using isolated islets and studies were performed using independent ND islet preparations after 24 h exposure to 22.2 mmol/l glucose. Glucose 0-7 insulin Homo sapiens 19-26 23910952-7 2014 In the algorithm group, significantly more glucose values <3.9 mmol/l were detected in the afternoon relative to other times (p < 0.05), a finding mainly related to pronounced morning glucose excursions and requirements for corrective bolus insulin at lunch. Glucose 43-50 insulin Homo sapiens 247-254 24190582-5 2014 Glucose metabolism was studied, and glucose-stimulated insulin secretion was measured in vivo and in vitro. Glucose 36-43 insulin Homo sapiens 55-62 24233056-7 2014 Glucose-stimulated insulin secretion was 40-50% lower from type 2 diabetic islets (p < 0.01), which again was mimicked by culturing non-diabetic islets in high glucose. Glucose 0-7 insulin Homo sapiens 19-26 24233056-7 2014 Glucose-stimulated insulin secretion was 40-50% lower from type 2 diabetic islets (p < 0.01), which again was mimicked by culturing non-diabetic islets in high glucose. Glucose 163-170 insulin Homo sapiens 19-26 24217936-7 2014 Conversely, after 1-year rhGH, a significant worsening of insulin sensitivity (i.e. increase in fasting glucose levels and homeostasis model assessment of insulin resistance) and a significant improvement in lipid profile (i.e. reduction in total cholesterol and LDL-cholesterol) were recorded only in homozygous subjects. Glucose 104-111 insulin Homo sapiens 58-65 24485398-9 2014 The ratio between C-peptide/glucose increased significantly (P < 0.001) with glimepiride, both fasting and postprandially and, in a stepwise multiple regression analysis of possible predictive factors for response, a more pronounced decrease in HbA1c was associated with the magnitude of the increment in C-peptide/glucose. Glucose 318-325 insulin Homo sapiens 18-27 24257458-7 2014 MAIN OUTCOME MEASURES: Insulin resistance shown by dynamic tests (the IVGTT and the glucose clamp) were compared to static tests [the quantitative insulin sensitivity check index (QUICKI) and the homeostatic model assessment-insulin resistance (HOMA-IR)], which use only the plasma glucose and insulin concentrations at baseline. Glucose 84-91 insulin Homo sapiens 23-30 24257458-7 2014 MAIN OUTCOME MEASURES: Insulin resistance shown by dynamic tests (the IVGTT and the glucose clamp) were compared to static tests [the quantitative insulin sensitivity check index (QUICKI) and the homeostatic model assessment-insulin resistance (HOMA-IR)], which use only the plasma glucose and insulin concentrations at baseline. Glucose 282-289 insulin Homo sapiens 23-30 24257458-8 2014 RESULTS: The linear correlation coefficients for the relationship between insulin resistance as obtained with the glucose clamp and the other methods before or after surgery were 0.76 (IVGTT), 0.58 (QUICKI) and -0.65 (HOMA). Glucose 114-121 insulin Homo sapiens 74-81 24257458-10 2014 Surgery-induced insulin resistance amounted to 45% (glucose clamp), 26% (IVGTT), 4% (QUICKI) and 3% (HOMA). Glucose 52-59 insulin Homo sapiens 16-23 24554506-8 2014 Furthermore, the insulin mRNA and protein expression in beta-cells also decreased after cultured with high-glucose-lipid medium compared with the control cells.We conclude that chronic glucolipotoxicity could induce aberrant DNA methylation of some genes and may affect these genes expression in beta-cells, which might contribute to beta-cell function failure in T2DM and be helpful to explain, at least partially, the mechanism of glucolipotoxicity on beta-cells deterioration. Glucose 107-114 insulin Homo sapiens 17-24 24262486-0 2014 Cocoa flavonoids attenuate high glucose-induced insulin signalling blockade and modulate glucose uptake and production in human HepG2 cells. Glucose 32-39 insulin Homo sapiens 48-55 24463448-2 2014 Here, we examined whether reduction of plasma glucose with a sodium-glucose cotransporter 2 (SGLT2) inhibitor could improve insulin-mediated tissue glucose disposal in patients with type 2 diabetes. Glucose 46-53 insulin Homo sapiens 124-131 24463448-4 2014 We measured insulin-mediated whole body glucose uptake and endogenous glucose production (EGP) at baseline and 2 weeks after treatment using the euglycemic hyperinsulinemic clamp technique. Glucose 40-47 insulin Homo sapiens 12-19 24463448-6 2014 Insulin-mediated tissue glucose disposal increased by approximately 18% after 2 weeks of dapagliflozin treatment, while placebo-treated subjects had no change in insulin sensitivity. Glucose 24-31 insulin Homo sapiens 0-7 24463448-8 2014 Together, our data indicate that reduction of plasma glucose with an agent that works specifically on the kidney to induce glucosuria improves muscle insulin sensitivity. Glucose 53-60 insulin Homo sapiens 150-157 24344872-5 2014 MAIN OUTCOME MEASURES: Main outcome measures are insulin sensitivity as percent change (%Delta) in glucose disposal rates (GDR) from a two-step euglycemic clamp (GDR1 and 2), and %FM and %FFM by dual X-ray absorptiometry scan. Glucose 99-106 insulin Homo sapiens 49-56 24332562-6 2014 Indeed, a strict regulation of blood serum glucose by the use of insulin promotes a better outcome for TBI patients. Glucose 43-50 insulin Homo sapiens 65-72 23836730-8 2014 The acute overfeeding-induced development of insulin resistant glucose metabolism therefore does not appear to be directly mediated by plasma FFA availability. Glucose 63-70 insulin Homo sapiens 45-52 24030901-3 2014 Insulin secretion was measured using HOMA2-%B, area under the curve (AUC) of insulin to glucose over the first 30 minutes (AUC I/G(t30min)) of the OGTT and AUC I/G(t120min) over 2 hours. Glucose 88-95 insulin Homo sapiens 0-7 24461317-4 2014 Blood glucose and insulin levels were elevated after glucose loading with and without CPP, with no significant differences between treatments. Glucose 53-60 insulin Homo sapiens 18-25 23674813-7 2014 There is evidence that hyperinsulinemia-euglycemia therapy is superior to other therapies for CCB poisoning, and the mechanism is thought to be the insulin-mediated active transport of glucose into the cells, which counters the CCB-induced intra-cellular carbohydrate-deficient state. Glucose 185-192 insulin Homo sapiens 28-35 24262486-7 2014 These findings suggest that EC and CPE improved insulin sensitivity of HepG2 treated with high glucose, preventing or delaying a potential hepatic dysfunction through the attenuation of the insulin signalling blockade and the modulation of glucose uptake and production. Glucose 95-102 insulin Homo sapiens 48-55 23871132-10 2014 The concentrations of gastrointestinal hormones (glucose-dependent insulinotropic polypeptide, glucagon-like peptide (GLP) 1 and GLP2), insulin and glucose were determined. Glucose 49-56 insulin Homo sapiens 67-74 24479866-8 2014 An oral glucose tolerance test demonstrated impaired glucose tolerance and diabetes mellitus with marked insulin resistance (the peak insulin level for each patient was 197 and 279 muU/mL, respectively, while the 120" insulin level of each patient was 167 and 234 muU/mL, respectively). Glucose 8-15 insulin Homo sapiens 105-112 24479866-8 2014 An oral glucose tolerance test demonstrated impaired glucose tolerance and diabetes mellitus with marked insulin resistance (the peak insulin level for each patient was 197 and 279 muU/mL, respectively, while the 120" insulin level of each patient was 167 and 234 muU/mL, respectively). Glucose 8-15 insulin Homo sapiens 134-141 24479866-8 2014 An oral glucose tolerance test demonstrated impaired glucose tolerance and diabetes mellitus with marked insulin resistance (the peak insulin level for each patient was 197 and 279 muU/mL, respectively, while the 120" insulin level of each patient was 167 and 234 muU/mL, respectively). Glucose 8-15 insulin Homo sapiens 134-141 24055273-5 2014 Treatment of adipose tissue with IL-1beta decreased insulin-stimulated phosphorylation of IRS-1, GLUT-4 expression and glucose uptake. Glucose 119-126 insulin Homo sapiens 52-59 24468049-5 2014 Addition of human insulin to parasite larvae led to increased glucose uptake and enhanced phosphorylation of Echinococcus insulin signalling components, including an insulin receptor-like kinase, EmIR1, for which we demonstrate predominant expression in the parasite"s glycogen storage cells. Glucose 62-69 insulin Homo sapiens 18-25 24453023-3 2014 OBJECTIVES: To determine whether intensively monitoring insulin therapy aimed at maintaining serum glucose within a specific normal range (4 to 7.5 mmol/L) in the first 24 hours of acute ischaemic stroke influences outcome. Glucose 99-106 insulin Homo sapiens 56-63 24453023-16 2014 AUTHORS" CONCLUSIONS: After updating the results of our previous review, we found that the administration of intravenous insulin with the objective of maintaining serum glucose within a specific range in the first hours of acute ischaemic stroke does not provide benefit in terms of functional outcome, death, or improvement in final neurological deficit and significantly increased the number of hypoglycaemic episodes. Glucose 169-176 insulin Homo sapiens 121-128 24453023-17 2014 Specifically, those people whose glucose levels were maintained within a tighter range with intravenous insulin experienced a greater risk of symptomatic and asymptomatic hypoglycaemia than those people in the control group. Glucose 33-40 insulin Homo sapiens 104-111 24401367-5 2014 Insulin is the key hormone required to maintain the blood glucose level in normal range. Glucose 58-65 insulin Homo sapiens 0-7 24465779-7 2014 In untreated adipocytes, Sfrp5 decreased the insulin-mediated phosphorylation of Akt-Ser473, Akt-Thr308, GSK3alpha-Ser21 and PRAS40-Thr246 by 34% (p<0.01), 31% (p<0.05), 37% (p<0.05) and 34% (p<0.01), respectively, and the stimulation of glucose uptake by 25% (p<0.05). Glucose 250-257 insulin Homo sapiens 45-52 24291354-7 2014 The combined results provide evidence that a temporal link exists between glucose-stimulation, first phase insulin secretion and the action of TG on histone H3 both in INS-1E and human pancreatic islets. Glucose 74-81 insulin Homo sapiens 107-114 24323910-4 2014 This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. Glucose 201-208 insulin Homo sapiens 105-112 24323910-4 2014 This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. Glucose 201-208 insulin Homo sapiens 164-171 23880340-7 2014 The replacement of available carbohydrates with PDX or SCF reduced the peak glucose response, which was accompanied by reduced postprandial insulin responses. Glucose 76-83 insulin Homo sapiens 140-147 24240093-1 2014 Although insulin acutely stimulates glucose uptake by promotion of GLUT4 translocation from intracellular compartments to the plasma membrane in adipocytes and muscles, long term insulin stimulation causes GLUT4 depletion that is particularly prominent in the insulin-responsive GLUT4 storage compartment. Glucose 36-43 insulin Homo sapiens 9-16 24262853-3 2014 IR is manifested as a reduced response of cells to insulin expressed by lowered Akt kinase phosphorylation and decreased insulin-dependent glucose uptake. Glucose 139-146 insulin Homo sapiens 51-58 25344989-3 2014 Upon insulin stimulation (and contraction in muscle), GLUT4 translocates from these compartments to the cell surface where it transports glucose from the extracellular milieu into the cell. Glucose 137-144 insulin Homo sapiens 5-12 25344989-4 2014 Its implication in insulin-regulated glucose uptake makes GLUT4 not only a key player in normal glucose homeostasis but also an important element in insulin resistance and type 2 diabetes. Glucose 37-44 insulin Homo sapiens 19-26 25344989-4 2014 Its implication in insulin-regulated glucose uptake makes GLUT4 not only a key player in normal glucose homeostasis but also an important element in insulin resistance and type 2 diabetes. Glucose 37-44 insulin Homo sapiens 149-156 25946840-3 2014 In old animals after the glucose administration (standard dose) in control period, a reduced glucose "disappearance" rate and a higher values of insulin and C-peptide peaks (5 and 15 min after the glucose injection) were observed in comparison with young animals in similar experiments. Glucose 25-32 insulin Homo sapiens 145-152 24153346-3 2014 DESIGN: Four variables of insulin resistance and sensitivity were defined from oral-glucose-tolerance tests in 86 overweight and obese subjects with metabolic syndrome. Glucose 84-91 insulin Homo sapiens 26-33 24262853-3 2014 IR is manifested as a reduced response of cells to insulin expressed by lowered Akt kinase phosphorylation and decreased insulin-dependent glucose uptake. Glucose 139-146 insulin Homo sapiens 121-128 25164450-0 2014 Intra-operative administration of low-dose IV glucose attenuates post-operative insulin resistance. Glucose 46-53 insulin Homo sapiens 80-87 24815457-7 2014 The results indicated that glucose consumption was reduced in insulin-resistant cells. Glucose 27-34 insulin Homo sapiens 62-69 23792151-10 2014 These observations suggest the co-existence of insulin resistant glucose metabolism and insulin sensitive lipid metabolism in the metabolic syndrome. Glucose 65-72 insulin Homo sapiens 47-54 25164450-4 2014 This study aimed to investigate the effect of intra-operative administration of low-dose glucose on the post-operative insulin resistance. Glucose 89-96 insulin Homo sapiens 119-126 25164450-6 2014 Insulin resistance quantified by the mean glucose infusion rate (the glucose infusion rate) was evaluated by glucose clamp using the STG-22TM instrument on the previous day and on the next day of surgery. Glucose 42-49 insulin Homo sapiens 0-7 25164450-6 2014 Insulin resistance quantified by the mean glucose infusion rate (the glucose infusion rate) was evaluated by glucose clamp using the STG-22TM instrument on the previous day and on the next day of surgery. Glucose 69-76 insulin Homo sapiens 0-7 25164450-6 2014 Insulin resistance quantified by the mean glucose infusion rate (the glucose infusion rate) was evaluated by glucose clamp using the STG-22TM instrument on the previous day and on the next day of surgery. Glucose 69-76 insulin Homo sapiens 0-7 25164450-13 2014 CONCLUSIONS: Intra-operative small-dose of glucose administration may suppress ketogenesis and attenuate the post-operative insulin resistance without causing hyperglycemia. Glucose 43-50 insulin Homo sapiens 124-131 25471531-6 2014 Moreover, the ILCs from the INGAP-PP group secreted higher levels of insulin and C-peptide than those from the Scrambled-P group in response to both a low (5.6 mM) and high (25 mM) glucose challenge and secreted 6 times more hormones under the high-glucose challenge. Glucose 181-188 insulin Homo sapiens 69-76 24818157-8 2014 There was a stepwise increase in insulin and c-peptide release in response to glucose challenge, but the released amounts were low when compared with those of pancreatic islets. Glucose 78-85 insulin Homo sapiens 33-40 24818157-8 2014 There was a stepwise increase in insulin and c-peptide release in response to glucose challenge, but the released amounts were low when compared with those of pancreatic islets. Glucose 78-85 insulin Homo sapiens 45-54 25486190-1 2014 In insulin-resistant states (obesity, pre-diabetes, and type 2 diabetes), hepatic production of glucose and lipid synthesis are heightened in concert, implying that insulin deficiency and insulin excess coexists in this setting. Glucose 96-103 insulin Homo sapiens 3-10 25486190-4 2014 In particular, we focus on the hypothesis that insulin resistance accentuates differences in periportal and perivenous hepatocytes, namely periportal glucose production and perivenous lipid synthesis. Glucose 150-157 insulin Homo sapiens 47-54 25486190-5 2014 Subsequently, excessive production of glucose and accumulation of lipids could be expected in the livers of patients with obesity and insulin resistance. Glucose 38-45 insulin Homo sapiens 134-141 25486190-6 2014 Overall, in this review, we provide our integrative perspective regarding how excessive production of glucose in periportal hepatocytes and accumulation of lipids in perivenous hepatocytes interact in insulin resistant states. Glucose 102-109 insulin Homo sapiens 201-208 24731998-9 2014 It was also documented that insulin stimulates the net uptake of D-glucose by ductal rings prepared from submandibulary salivary glands, the relative magnitude of such an enhancing action being comparable to that found in hemidiaphragms. Glucose 65-74 insulin Homo sapiens 28-35 25171750-6 2014 DPPE also inhibited insulin-stimulated GLUT4 translocation to the cell surface and reduced insulin-stimulated glucose uptake into adipocytes. Glucose 110-117 insulin Homo sapiens 91-98 24373998-11 2014 The pharmacodynamic effect of PT302 on the postprandial response of insulin and C-peptide was significant on days 21 to 28 at the 4-mg dose and was positively correlated with plasma exenatide concentrations, whereas the correlations with glucose and glucagon were not significant. Glucose 238-245 insulin Homo sapiens 68-75 24373998-15 2014 A single 4-mg dose of PT302 significantly increased the insulin and C-peptide response to oral glucose loading and was well tolerated in healthy individuals. Glucose 95-102 insulin Homo sapiens 56-63 24589955-4 2014 Each patient was given at least 1 U of insulin for every 10 grams of glucose infused. Glucose 69-76 insulin Homo sapiens 39-46 24384568-2 2014 Insulin signaling regulates glucose, lipid, and energy homeostasis, predominantly via action on liver, skeletal muscle, and adipose tissue. Glucose 28-35 insulin Homo sapiens 0-7 24998439-2 2014 Consumption of food or glucose stimulates synthesis and secretion of GLP-1 in the bloodstream, which in turn stimulates insulin secretion from pancreas and delays gastric emptying. Glucose 23-30 insulin Homo sapiens 120-127 23282162-1 2014 This paper proposes a scheme for the control of the blood glucose in subjects with type-1 diabetes mellitus based on the subcutaneous (s.c.) glucose measurement and s.c. insulin administration. Glucose 58-65 insulin Homo sapiens 170-177 23282162-3 2014 The control consists of a mixed feedback and feedforward contribution whose parameters are tuned through an iterative learning process that is based on the day-by-day automated analysis of the glucose response to the infusion of exogenous insulin. Glucose 193-200 insulin Homo sapiens 239-246 24934349-3 2014 It has been demonstrated that oxidative stress and alterations in glucose and lipid homeostasis (e.g. hyperinsulinemia, hyperglycemia, insulin resistance and dyslipidemia) are linked to mitochondrial impairment and that all of them contribute to endothelial dysfunction. Glucose 66-73 insulin Homo sapiens 107-114 25360712-3 2014 It achieves this through a number of mechanisms, including stimulating insulin release by pancreatic beta-cells in a glucose-dependent manner; inhibition of glucagon release by pancreatic alpha-cells (also in a glucose-dependent manner); induction of central appetite suppression and by delaying gastric empting thereby inducing satiety and also reducing the rate of absorption of nutrients. Glucose 117-124 insulin Homo sapiens 71-78 23627981-1 2014 Although the brain has long been considered an insulin-independent organ, recent research has shown that insulin has significant effects on the brain, where it plays a role in maintaining glucose and energy homeostasis. Glucose 188-195 insulin Homo sapiens 105-112 25245380-4 2014 IR has traditionally been defined as a decreased ability of insulin to mediate the metabolic actions on glucose uptake, glucose production, and/or lipolysis. Glucose 104-111 insulin Homo sapiens 60-67 25245380-4 2014 IR has traditionally been defined as a decreased ability of insulin to mediate the metabolic actions on glucose uptake, glucose production, and/or lipolysis. Glucose 120-127 insulin Homo sapiens 60-67 23939544-7 2014 RESULTS During the MMTT, glucose levels were suppressed with exenatide in patients with or without residual insulin production (P = 0.0003). Glucose 25-32 insulin Homo sapiens 108-115 23949560-0 2014 Differential associations of oral glucose tolerance test-derived measures of insulin sensitivity and pancreatic beta-cell function with coronary artery calcification and microalbuminuria in type 2 diabetes. Glucose 34-41 insulin Homo sapiens 77-84 23949560-1 2014 OBJECTIVE We evaluated relationships of oral glucose tolerance testing (OGTT)-derived measures of insulin sensitivity and pancreatic beta-cell function with indices of diabetes complications in a cross-sectional study of patients with type 2 diabetes who are free of overt cardiovascular or renal disease. Glucose 45-52 insulin Homo sapiens 98-105 23974920-4 2014 Insulin resistance was confirmed through an intravenous glucose tolerance test. Glucose 56-63 insulin Homo sapiens 0-7 24194506-9 2014 RESULTS: Primary outcomes are clamp-derived glucose-stimulated C-peptide secretion and maximal C-peptide response to arginine during hyperglycemia. Glucose 44-51 insulin Homo sapiens 63-72 24319120-1 2014 OBJECTIVE: The goal was to develop a new index of insulin sensitivity in patients with type 1 diabetes estimated from continuous glucose monitoring (CGM) and subcutaneous insulin delivery data under carefully controlled conditions. Glucose 129-136 insulin Homo sapiens 50-57 24357688-2 2014 Its central function is to accurately sense glucose levels in the blood and consequently release appropriate amounts of insulin. Glucose 44-51 insulin Homo sapiens 120-127 24357702-8 2014 Furthermore, a 5-day HFHC diet decreased the insulin-stimulated (nonoxidative) glucose disposal rate only in SA. Glucose 79-86 insulin Homo sapiens 45-52 24367934-3 2014 RESULTS: Time to peak insulin action and time to half-maximal action occurred earlier with a greater early glucodynamic effect (area under the curve [AUC] for glucose infusion rate from 0 to 30 min) with IP(40) than without the IP(40), whereas the AUC for the time-action profile and the peak action did not differ with and without infusion site warming. Glucose 159-166 insulin Homo sapiens 22-29 23772634-0 2014 Intraportal injection of insulin-producing cells generated from human bone marrow mesenchymal stem cells decreases blood glucose level in diabetic rats. Glucose 121-128 insulin Homo sapiens 25-32 24152998-12 2014 Area-under-curves of glucose 0-180 min was correlated with height (r =-0.282; p=0.029), fasting glucose (r =0.742; p<0.0001), log area-under-curves of insulin 0-180 min (r =-0.258; p=0.047) and log 1st-phase insulin secretion (r =-0.518; p<0.0001). Glucose 21-28 insulin Homo sapiens 154-161 24460047-1 2014 AIMS: The KCNJ11 gene has a strong effect on glucose-stimulated insulin secretion. Glucose 45-52 insulin Homo sapiens 64-71 24549605-6 2014 Multiple methods of assessing insulin resistance are based on the concurrent measurements of glucose and insulin levels in blood serum. Glucose 93-100 insulin Homo sapiens 30-37 24549605-9 2014 The current "gold standard" in the assessment of insulin sensitivity is the determination of tissue glucose utilisation using the metabolic clamp technique. Glucose 100-107 insulin Homo sapiens 49-56 25109752-8 2014 The degree of maternal insulin resistance in mid-pregnancy was associated with birthweight and the risk of giving birth to an LGA infant in normal pregnancies, independent of maternal obesity and glucose levels. Glucose 196-203 insulin Homo sapiens 23-30 23689561-0 2014 Calcium co-ingestion augments postprandial glucose-dependent insulinotropic peptide(1-42), glucagon-like peptide-1 and insulin concentrations in humans. Glucose 43-50 insulin Homo sapiens 61-68 25070829-7 2014 Besides glucose metabolism, amino acid metabolism and lipid metabolism derived metabolites mediate the optimal glucose response of beta-cells to secrete insulin. Glucose 8-15 insulin Homo sapiens 153-160 25070829-7 2014 Besides glucose metabolism, amino acid metabolism and lipid metabolism derived metabolites mediate the optimal glucose response of beta-cells to secrete insulin. Glucose 111-118 insulin Homo sapiens 153-160 24120394-3 2014 miR-375 is also important to glucose-regulated insulin secretion through the regulation of the expression of Mtpn and Pdk1 genes. Glucose 29-36 insulin Homo sapiens 47-54 25410224-9 2014 In a critically ill patient a glucose range of 140-180mg/dL (7.8-10.0mmol/L) should be maintained via continuous intravenous insulin infusion. Glucose 30-37 insulin Homo sapiens 125-132 24155250-2 2014 Insufficient insulin secretion in compensation for insulin resistance leads to glucose intolerance. Glucose 79-86 insulin Homo sapiens 13-20 24403427-7 2014 As a good candidate for the full closed-loop insulin delivery method, this new combination can control the glucose level by bringing it to a safe range promptly thereby reducing the risk of death. Glucose 107-114 insulin Homo sapiens 45-52 24711817-1 2014 The importance of thyroid hormone, catecholamines, and insulin in modification of the thermogenic effect of glucose (TEG) was examined in 34 healthy and 32 hypothyroid subjects. Glucose 108-115 insulin Homo sapiens 55-62 25309595-0 2014 Genetic Variations in the Kir6.2 Subunit (KCNJ11) of Pancreatic ATP-Sensitive Potassium Channel Gene Are Associated with Insulin Response to Glucose Loading and Early Onset of Type 2 Diabetes in Childhood and Adolescence in Taiwan. Glucose 141-148 insulin Homo sapiens 121-128 25309595-8 2014 Furthermore, in normal glucose-tolerant children/adolescents, K23 allele carriers had a higher insulin response to oral glucose loading. Glucose 23-30 insulin Homo sapiens 95-102 25309595-8 2014 Furthermore, in normal glucose-tolerant children/adolescents, K23 allele carriers had a higher insulin response to oral glucose loading. Glucose 120-127 insulin Homo sapiens 95-102 23649472-2 2014 Rodent experiments suggest that this system also affects glucose metabolism, in particular by modulating peripheral insulin sensitivity independently of its effect on adiposity. Glucose 57-64 insulin Homo sapiens 116-123 24492686-0 2014 Insulin resistance correlates with the arterial stiffness before glucose intolerance. Glucose 65-72 insulin Homo sapiens 0-7 24492686-4 2014 The homeostasis model assessment (HOMA) index was used as a quantitative assessment of the fasting insulin resistance (FIR), and the plasma insulin level after glucose loading was adopted as an index of the post-challenge insulin resistance (PIR). Glucose 160-167 insulin Homo sapiens 140-147 24492686-4 2014 The homeostasis model assessment (HOMA) index was used as a quantitative assessment of the fasting insulin resistance (FIR), and the plasma insulin level after glucose loading was adopted as an index of the post-challenge insulin resistance (PIR). Glucose 160-167 insulin Homo sapiens 140-147 24492686-9 2014 CONCLUSION: The insulin resistance correlated with the arterial stiffness before glucose intolerance. Glucose 81-88 insulin Homo sapiens 16-23 25322829-1 2014 Mathematical modeling of the electrical activity of the pancreatic beta-cell has been extremely important for understanding the cellular mechanisms involved in glucose-stimulated insulin secretion. Glucose 160-167 insulin Homo sapiens 179-186 25833251-11 2014 Further, this is also the first report that links direct effects of activin A with the ability to restore glucose-stimulated insulin secretion in human islets from type 2 diabetic donors thereby establishing the relevance of targeting activin for therapeutic drug development. Glucose 106-113 insulin Homo sapiens 125-132 25120925-12 2014 The insulin area response increased by 24% after ingestion of Leu + Gly + glucose compared to ingestion of glucose alone. Glucose 74-81 insulin Homo sapiens 4-11 25330626-7 2014 Hypoglycaemia is one of the important barrier which limits the use of insulin therapy and incidence of hypoglycaemia increases with increased variability in glucose lowering effects of Insulin when one tries to achieve stricter glycaemic targets. Glucose 157-164 insulin Homo sapiens 70-77 25330626-7 2014 Hypoglycaemia is one of the important barrier which limits the use of insulin therapy and incidence of hypoglycaemia increases with increased variability in glucose lowering effects of Insulin when one tries to achieve stricter glycaemic targets. Glucose 157-164 insulin Homo sapiens 185-192 25330626-10 2014 Insulin degludec is designed to have a flat and stable glucose-lowering effect for more than 42 hours with less risk of hypoglycaemia. Glucose 55-62 insulin Homo sapiens 0-7 25330627-6 2014 The glucose-lowering effect is evenly distributed across a 24-hour dosing interval with insulin degludec having 4 times lower variability than insulin glargine. Glucose 4-11 insulin Homo sapiens 88-95 24025703-9 2014 CONCLUSIONS: When predicting the presence of insulin resistance using general health checkup data in Japanese employees with metabolic risk factors, it is important to take into consideration the BMI and fasting plasma glucose and HDL cholesterol levels. Glucose 219-226 insulin Homo sapiens 45-52 24009260-1 2014 Insulin regulates heart metabolism through the regulation of insulin-stimulated glucose uptake. Glucose 80-87 insulin Homo sapiens 0-7 24009260-1 2014 Insulin regulates heart metabolism through the regulation of insulin-stimulated glucose uptake. Glucose 80-87 insulin Homo sapiens 61-68 24876534-3 2014 The model of glucose kinetics in hypoglycemia has been improved, implementing the notion that insulin-dependent utilization increases nonlinearly when glucose decreases below a certain threshold. Glucose 13-20 insulin Homo sapiens 94-101 24026542-4 2014 During closed-loop visits, the subjects" routine diabetes therapy was replaced with model predictive control algorithm-driven subcutaneous insulin pump delivery based on real-time continuous glucose monitoring. Glucose 191-198 insulin Homo sapiens 139-146 24026542-9 2014 RESULTS: Compared with conventional therapy, 24 h of closed-loop insulin delivery increased overall the median time in target plasma glucose (3.9-8.0 mmol/L) from 24 to 40% (P = 0.016), despite sensor under-reading by a median of 1.2 mmol/L. Glucose 133-140 insulin Homo sapiens 65-72 24028151-6 2014 Insulin resistance was assessed by using the homeostasis assessment model (HOMA-IR) using the following formula: fasting insulin (muIU/mL)xfasting glucose (mmol/L)/22.5. Glucose 147-154 insulin Homo sapiens 0-7 24672804-2 2014 Keeping insulin secretion at rest after a rise of glucose prevents exhaustion and ultimately failure of beta-cells. Glucose 50-57 insulin Homo sapiens 8-15 24876556-0 2014 Use of a Smart Glucose Monitoring System to Guide Insulin Dosing in Patients With Diabetes in Regular Clinical Practice. Glucose 15-22 insulin Homo sapiens 50-57 24876557-0 2014 Use of Real-Time Continuous Glucose Monitoring in Patients on Insulin Pump Therapy: Real-Life Experience in an Endocrinology Office. Glucose 28-35 insulin Homo sapiens 62-69 24691385-0 2014 A quadruply-asymmetric sigmoid to describe the insulin-glucose relationship during intravenous insulin infusion. Glucose 55-62 insulin Homo sapiens 47-54 24691385-0 2014 A quadruply-asymmetric sigmoid to describe the insulin-glucose relationship during intravenous insulin infusion. Glucose 55-62 insulin Homo sapiens 95-102 25264066-4 2014 Her blood glucose level was controlled using the artificial endocrine pancreas, which enabled continuous blood glucose monitoring and computer-operated glucose and insulin infusion to maintain the blood glucose level at a steady state. Glucose 10-17 insulin Homo sapiens 164-171 24782919-5 2014 Second, during hyperglycemic-hyperinsulinemic intervals, high amounts of glucose enter muscle and fat tissues, which are insulin sensitive. Glucose 73-80 insulin Homo sapiens 34-41 24782919-6 2014 Intracellular glucose is metabolized by phosphorylation, which leads to a reduction in plasma Pi, and subsequent deleterious effects on glucose metabolism in insulin insensitive tissues. Glucose 14-21 insulin Homo sapiens 158-165 24782919-6 2014 Intracellular glucose is metabolized by phosphorylation, which leads to a reduction in plasma Pi, and subsequent deleterious effects on glucose metabolism in insulin insensitive tissues. Glucose 136-143 insulin Homo sapiens 158-165 25165577-3 2014 Evidences have provided that after a period of poor glucose control insulin or diabetes drug treatment fails to prevent the development and progression of DR even when good glycemic control is reinstituted (glucose normalization), suggesting a metabolic memory phenomenon. Glucose 52-59 insulin Homo sapiens 68-75 26556194-2 2014 Insulin is used for the treatment of diabetes mellitus, which is characterized by the elevated glucose level (above the normal range) in the blood stream, that is, hyperglycemia. Glucose 95-102 insulin Homo sapiens 0-7 25110634-4 2014 Fat mass was measured by dual-energy X-ray absorptiometry, and insulin sensitivity index (SI) was calculated from an insulin-modified intravenous glucose tolerance test using the minimal model. Glucose 146-153 insulin Homo sapiens 63-70 25110634-4 2014 Fat mass was measured by dual-energy X-ray absorptiometry, and insulin sensitivity index (SI) was calculated from an insulin-modified intravenous glucose tolerance test using the minimal model. Glucose 146-153 insulin Homo sapiens 117-124 25782302-3 2014 Insulin blocks the ability of mitochondria to oxidize ketone bodies, short-, medium- and long-chain FA and makes them oxidize glucose, i.e. a physiologically unoptimal substrate. Glucose 126-133 insulin Homo sapiens 0-7 23202146-1 2014 Metabolism of glucose during pregnancy reflects the equilibrium between lactogenic hormones stimulating insulin production and counterregulatory hormones inducing insulin resistance. Glucose 14-21 insulin Homo sapiens 104-111 23202146-1 2014 Metabolism of glucose during pregnancy reflects the equilibrium between lactogenic hormones stimulating insulin production and counterregulatory hormones inducing insulin resistance. Glucose 14-21 insulin Homo sapiens 163-170 23202146-2 2014 In physiological pregnancies, insulin-mediated glucose uptake is substantially decreased and insulin secretion increased to maintain euglycemia. Glucose 47-54 insulin Homo sapiens 30-37 23546809-4 2014 Obese adolescents with insulin resistance had significantly higher HOMA-IR, glucose response curve (AUC), insulin AUC, PT 1.2, FPA and fibrinogen and aggregation (to collagen 1 mug/ml, ADP 10 mumol/L and AA 0.5 mmol/L) comparison with obese adolescents without insulin resistance (P < 0.05). Glucose 76-83 insulin Homo sapiens 23-30 25782302-5 2014 Most antidiabetic medicines exhibit hypoglycemic activity, like insulin; they reduce the level of lipid substrates of oxidation in cytosol and mitochondria have to oxidize glucose. Glucose 172-179 insulin Homo sapiens 64-71 25980295-9 2014 Omega-3 eicosanoids act as peroxisome proliferators and oxidize excess palmitic acid The hypolipidemic action of insulin is mediated through transformation of all palmitic FA synthesized from glucose into oleinic FA. Glucose 192-199 insulin Homo sapiens 113-120 25326838-2 2014 Glucagon-like peptide 1 (GLP-1) is secreted from enteroendocrine L-cells in response to oral nutrient intake and elicits glucose-stimulated insulin secretion while suppressing glucagon secretion. Glucose 121-128 insulin Homo sapiens 140-147 25226799-1 2014 Physical training is known to markedly increase insulin-mediated glucose uptake. Glucose 65-72 insulin Homo sapiens 48-55 24268273-6 2014 Closed-loop insulin delivery systems that can release insulin in response to changes in glucose concentration have also been constructed with LbL films and microcapsules. Glucose 88-95 insulin Homo sapiens 12-19 24268273-7 2014 Glucose-sensitive materials, such as glucose oxidase, concanavalin A, and phenylboronic acid, have been incorporated into insulin-containing LbL assemblies. Glucose 0-7 insulin Homo sapiens 122-129 25226800-1 2014 Skeletal muscle is the major site of insulin-stimulated glucose utilization in the body. Glucose 56-63 insulin Homo sapiens 37-44 25226800-3 2014 Therefore, defects in the biogenesis of this organelle can impact the ability of muscle to oxidize substrates and can have grave consequences on the action of insulin on glucose uptake. Glucose 170-177 insulin Homo sapiens 159-166 24317490-1 2014 Glucokinase (GK) is a glucose-phosphorylating enzyme that regulates insulin release and hepatic metabolism, and its loss of function is implicated in diabetes pathogenesis. Glucose 22-29 insulin Homo sapiens 68-75 24648662-3 2014 Here, we aimed at investigating whether diabetic toxic products (glycated serum (GS) or high levels of glucose (HG)) may affect viability, function, and insulin sensitivity of the GLP-1 secreting cell line GLUTag. Glucose 103-110 insulin Homo sapiens 153-160 24692847-4 2014 However, it is unclear whether TNF-alpha may also affect endogenous glucose production (EGP) during fasting and glucose-stimulated insulin secretion (GSIS) in vivo. Glucose 112-119 insulin Homo sapiens 131-138 24576893-5 2014 Administration of 10 units of insulin with 100 ml of 50% glucose (50 g) was compared with the administration of 100 ml of 50% glucose only. Glucose 57-64 insulin Homo sapiens 30-37 24980865-0 2014 Stimulating effect of a new triterpene derived from Anoectochilus elwesii on glucose uptake in insulin-resistant human HepG2 cells. Glucose 77-84 insulin Homo sapiens 95-102 24980865-3 2014 The isolated compounds were evaluated on insulin-resistant human HepG2 cells for stimulating glucose uptake activity and the new compound displayed highly potent effect on the stimulation of glucose uptake in human HepG2 cells. Glucose 191-198 insulin Homo sapiens 41-48 23601331-3 2014 Insulin secretion was assessed using both indexes derived from oral glucose tolerance test (OGTT), and intravenous glucose tolerance test (IVGTT). Glucose 68-75 insulin Homo sapiens 0-7 23601331-3 2014 Insulin secretion was assessed using both indexes derived from oral glucose tolerance test (OGTT), and intravenous glucose tolerance test (IVGTT). Glucose 115-122 insulin Homo sapiens 0-7 24897498-4 2014 Obesity and insulin resistance were induced through 5 weeks of high-fat (HF) diet feeding and insulin resistance was confirmed by intraperitoneal glucose tolerance testing. Glucose 146-153 insulin Homo sapiens 94-101 23919587-0 2013 Insulin sensitivity and secretion in Arab Americans with glucose intolerance. Glucose 57-64 insulin Homo sapiens 0-7 24032487-1 2013 BACKGROUND: We used simulation modeling to relate glucose meter performance criteria to insulin dosing errors for patients on a moderate glycemic control protocol (glucose target, 110-150 mg/dL) and empirically validated assumptions from simulation models using observed glucose meter and laboratory glucose values obtained nearly simultaneously. Glucose 50-57 insulin Homo sapiens 88-95 24032487-1 2013 BACKGROUND: We used simulation modeling to relate glucose meter performance criteria to insulin dosing errors for patients on a moderate glycemic control protocol (glucose target, 110-150 mg/dL) and empirically validated assumptions from simulation models using observed glucose meter and laboratory glucose values obtained nearly simultaneously. Glucose 164-171 insulin Homo sapiens 88-95 24032487-1 2013 BACKGROUND: We used simulation modeling to relate glucose meter performance criteria to insulin dosing errors for patients on a moderate glycemic control protocol (glucose target, 110-150 mg/dL) and empirically validated assumptions from simulation models using observed glucose meter and laboratory glucose values obtained nearly simultaneously. Glucose 164-171 insulin Homo sapiens 88-95 24032487-1 2013 BACKGROUND: We used simulation modeling to relate glucose meter performance criteria to insulin dosing errors for patients on a moderate glycemic control protocol (glucose target, 110-150 mg/dL) and empirically validated assumptions from simulation models using observed glucose meter and laboratory glucose values obtained nearly simultaneously. Glucose 164-171 insulin Homo sapiens 88-95 24032487-3 2013 Simulation models were used to relate glucose meter analytical performance to insulin dosing errors assuming 10%, 15%, or 20% total allowable error (TEa). Glucose 38-45 insulin Homo sapiens 78-85 24032487-7 2013 When insulin dosing error rates were measured empirically by comparing paired glucose meter and laboratory glucose values, insulin dosing error rates were very similar to those predicted for the 20% TEa condition. Glucose 78-85 insulin Homo sapiens 5-12 24032487-7 2013 When insulin dosing error rates were measured empirically by comparing paired glucose meter and laboratory glucose values, insulin dosing error rates were very similar to those predicted for the 20% TEa condition. Glucose 107-114 insulin Homo sapiens 5-12 24032487-8 2013 CONCLUSIONS: Both simulation models and empiric data demonstrate that glucose meters that perform at >=20% TEa allow large insulin dosing errors during a moderate glycemic control protocol. Glucose 70-77 insulin Homo sapiens 126-133 24156868-1 2013 Metabolic consequences of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are the result of enhanced glucose-stimulated insulin secretion, inhibition of glucagon release, delayed gastric emptying and increased satiety. Glucose 107-114 insulin Homo sapiens 126-133 24404517-2 2013 Skeletal muscle plays a central role in insulin-mediated glucose disposal; however, little is known about the association between muscle mass and metabolic syndrome (MS). Glucose 57-64 insulin Homo sapiens 40-47 24396690-1 2013 Glucagon-like peptide 1 (GLP-1) is secreted from enteroendocrine L-cells in response to oral nutrient intake and elicits glucose-stimulated insulin secretion while suppressing glucagon secretion. Glucose 121-128 insulin Homo sapiens 140-147 24072034-3 2013 The purpose of this study was to test the hypothesis that adiposity attenuates improvements in insulin sensitivity and glucose-stimulated insulin secretion (INS0-60/GLC0-60) after both acute resistance exercise (ARE) and progressive training (PRT). Glucose 119-126 insulin Homo sapiens 138-145 23412585-0 2013 Guidelines on glucose self-monitoring in non-insulin users are not evidence-based. Glucose 14-21 insulin Homo sapiens 45-52 24034940-6 2013 MAIN OUTCOME MEASURE(S): Liver fat, abdominal adiposity, in vivo insulin-stimulated glucose disposal, whole-body lipolysis, fat oxidation, lipoprotein particle size and concentration, and liver enzymes (alanine aminotransferase and aspartate aminotransferase). Glucose 84-91 insulin Homo sapiens 65-72 24034940-11 2013 In a multiple regression analysis, age, total T, race, and insulin-stimulated glucose disposal explained 43% of the variance (R(2) = 0.43) in fatty liver index, with age (R(2) = 0.28) and total T (R(2) = 0.11) being independent contributors. Glucose 78-85 insulin Homo sapiens 59-66 22780425-2 2013 In addition to its plasma glucose lowering effect, insulin may also have antioxidant activity and was shown to downregulate NADPH oxidase expression in vitro. Glucose 26-33 insulin Homo sapiens 51-58 24075894-2 2013 A single bout of exercise improves glucose uptake in skeletal muscle through insulin-dependent and insulin-independent signal transduction mechanisms. Glucose 35-42 insulin Homo sapiens 77-106 24075894-4 2013 The decrease in glucose utilization is caused by decreased insulin-stimulated glucose uptake in damaged muscles with inhibition of the membrane translocation of glucose transporter 4 through phosphatidyl 3-kinase/Akt signaling. Glucose 16-23 insulin Homo sapiens 59-66 24075894-4 2013 The decrease in glucose utilization is caused by decreased insulin-stimulated glucose uptake in damaged muscles with inhibition of the membrane translocation of glucose transporter 4 through phosphatidyl 3-kinase/Akt signaling. Glucose 78-85 insulin Homo sapiens 59-66 24090664-11 2013 Insulin analogues protect pericytes and blood-retinal barrier by decreasing blood glucose level. Glucose 82-89 insulin Homo sapiens 0-7 24094981-1 2013 The metabolic syndrome (MS) is a cluster of metabolic disorders arising from insulin resistance, characterized by the presence of central obesity, impaired fasting glucose level, dyslipidemia and hypertension. Glucose 164-171 insulin Homo sapiens 77-84 24081837-4 2013 Continuous insulin infusion was used to maintain target serum glucose levels of 80-120 mg/dL (4.4-6.7 mmol/L). Glucose 62-69 insulin Homo sapiens 11-18 23818490-1 2013 PURPOSE: Insulin responses to oral and intravenous glucose markedly differ by ethnicity. Glucose 51-58 insulin Homo sapiens 9-16 24119040-4 2013 As a result, hypoglycemia and hyperglycemia are rare occurrences in normal individuals, but they occur commonly inpatients with type 1 diabetes mellitus (T1DM) due to a dysfunction of peripheral glucose-insulin-glucagon responses and non-physiologic doses of exogenous insulin, which imperfectly mimic normal physiology. Glucose 195-202 insulin Homo sapiens 203-210 24119040-4 2013 As a result, hypoglycemia and hyperglycemia are rare occurrences in normal individuals, but they occur commonly inpatients with type 1 diabetes mellitus (T1DM) due to a dysfunction of peripheral glucose-insulin-glucagon responses and non-physiologic doses of exogenous insulin, which imperfectly mimic normal physiology. Glucose 195-202 insulin Homo sapiens 269-276 23959343-5 2013 Similar to its systemic effect, insulin signaling in the brain lowers glucose production. Glucose 70-77 insulin Homo sapiens 32-39 23959343-7 2013 Future studies that aim to dissect insulin and glucagon signaling in the CNS that regulate energy and glucose homeostasis could unveil novel signaling molecules to lower body weight and glucose levels in obesity and diabetes. Glucose 102-109 insulin Homo sapiens 35-42 24396871-1 2013 Nur77 is a stress sensor in pancreatic beta-cells, which negatively regulates glucose-stimulated insulin secretion. Glucose 78-85 insulin Homo sapiens 97-104 24169049-1 2014 Insulin stimulated translocation of the glucose transporter GLUT4 from the cytosol to the plasma membrane in a concentration (1 nM-1 muM)-dependent manner and increased glucose uptake in 3T3-L1 adipocytes. Glucose 40-47 insulin Homo sapiens 0-7 24843702-0 2013 Glucose-stimulated insulin secretion: A newer perspective. Glucose 0-7 insulin Homo sapiens 19-26 24843702-1 2013 Existing concepts and models for glucose-stimulated insulin secretion (GSIS) are overviewed and a newer perspective has been formulated toward the physiological understanding of GSIS. Glucose 33-40 insulin Homo sapiens 52-59 24843703-4 2013 Thiazolidinediones affect glucose and lipid metabolism in insulin-sensitive tissues, which in turn reduces the lipid content in the liver by modulating several mediators. Glucose 26-33 insulin Homo sapiens 58-65 24312178-9 2013 The insulin-response following the single Mediterranean-style lunch-meal was more pronounced than during the low-fat diet lunch (insulin increase-ratio of the low-fat diet: 4.35 +- 2.2, of Mediterranean-style diet: 8.12 +- 5.2, p = 0.001) while postprandial glucose levels were similar. Glucose 258-265 insulin Homo sapiens 4-11 24895527-0 2014 Insulin regulates glucose consumption and lactate production through reactive oxygen species and pyruvate kinase M2. Glucose 18-25 insulin Homo sapiens 0-7 24184593-2 2014 The hallmark of insulin resistance is a gradual break-down of insulin-regulative glucose uptake by muscle and adipose tissues in subjects. Glucose 81-88 insulin Homo sapiens 16-23 24184593-2 2014 The hallmark of insulin resistance is a gradual break-down of insulin-regulative glucose uptake by muscle and adipose tissues in subjects. Glucose 81-88 insulin Homo sapiens 62-69 24564667-3 2014 Now we review UCP2 physiological roles emphasizing its roles in pancreatic beta-cells, such as antioxidant role, possible tuning of redox homeostasis (consequently UCP2 participation in redox regulations), and fine regulation of glucose-stimulated insulin secretion (GSIS). Glucose 229-236 insulin Homo sapiens 248-255 23527528-1 2014 The relation between high on-treatment platelet reactivity (HPR), and the level of glucose intolerance and insulin resistance (IR) was studied in clopidogrel-treated patients with minor ischemic stroke or TIA. Glucose 83-90 insulin Homo sapiens 107-114 24391482-1 2014 Electrical activity plays a pivotal role in glucose-stimulated insulin secretion from pancreatic beta-cells. Glucose 44-51 insulin Homo sapiens 63-70 24373235-2 2014 Studies have shown that GPR40 not only directly mediates FFA amplification of glucose-stimulated insulin secretion but also indirectly enhances insulin secretion by stimulating incretin release. Glucose 78-85 insulin Homo sapiens 97-104 24275002-0 2014 Decrease of serum S100B during an oral glucose tolerance test correlates inversely with the insulin response. Glucose 39-46 insulin Homo sapiens 92-99 24275002-9 2014 However, the decrease of serum-S100B 1h after glucose ingestion correlated inversely with the respective changes of serum-insulin (r = -0.484, P=0.049) and serum-C-peptide (r = -0.570, P = 0.017). Glucose 46-53 insulin Homo sapiens 122-129 25185980-4 2014 Low levels of Insulin causes decreased utilization of glucose by body cells, increased mobilization of fats from fat storage cells and depletion of proteins in the tissues of the body, keeping the body in crisis. Glucose 54-61 insulin Homo sapiens 14-21 24975640-5 2014 These are systems with chemical sensors for glucose, linked to reactions that trigger glucose mediated insulin delivery. Glucose 44-51 insulin Homo sapiens 103-110 24975640-5 2014 These are systems with chemical sensors for glucose, linked to reactions that trigger glucose mediated insulin delivery. Glucose 86-93 insulin Homo sapiens 103-110 24774260-1 2014 INTRODUCTION AND OBJECTIVES: Intensive glucose control with insulin in patients with an acute coronary syndrome reduces platelet reactivity during hospitalization, compared to conventional control. Glucose 39-46 insulin Homo sapiens 60-67 24774260-3 2014 METHODS: This is a prospective, randomized trial evaluating the effects of optimized glucose control (target glucose, 80-120mg/dL) with insulin, compared with conventional control (target glucose, <180 mg/dL), on platelet reactivity after hospital discharge in patients with an acute coronary syndrome and hyperglycemia. Glucose 85-92 insulin Homo sapiens 136-143 24774260-3 2014 METHODS: This is a prospective, randomized trial evaluating the effects of optimized glucose control (target glucose, 80-120mg/dL) with insulin, compared with conventional control (target glucose, <180 mg/dL), on platelet reactivity after hospital discharge in patients with an acute coronary syndrome and hyperglycemia. Glucose 109-116 insulin Homo sapiens 136-143 24774260-3 2014 METHODS: This is a prospective, randomized trial evaluating the effects of optimized glucose control (target glucose, 80-120mg/dL) with insulin, compared with conventional control (target glucose, <180 mg/dL), on platelet reactivity after hospital discharge in patients with an acute coronary syndrome and hyperglycemia. Glucose 109-116 insulin Homo sapiens 136-143 24583585-6 2014 According as administration of acetic Ringer"s solution and insulin injection, the laboratory data 14 hours after admission showed glucose 235 mg/dl, serum osmolality 290 mOsm/l and serum sodium 131 mEq/l. Glucose 131-138 insulin Homo sapiens 60-67 24592619-4 2014 The diagnostic clue to his erroneous glucose monitoring results was the lack of intra-day variation in this patient on insulin therapy. Glucose 37-44 insulin Homo sapiens 119-126 24754068-10 2014 Adipokine-induced insulin resistance appeared as increases in the concentrations of glucose, insulin, and HOMA-IR, as compared to those in the control group. Glucose 84-91 insulin Homo sapiens 18-25 24656006-3 2014 Homeostasis model assessment of insulin resistance (HOMA-IR), which is calculated as [fasting plasma glucose (mmol/L) x fasting insulin (mU/L)]/22.5, is widely used as an index of insulin resistance. Glucose 101-108 insulin Homo sapiens 32-39 24246648-4 2014 Obese dogs, like obese humans, are known to develop resistance to the glucose-lowering effects of insulin, and develop increased circulating concentrations of triglycerides, cholesterol and blood pressure. Glucose 70-77 insulin Homo sapiens 98-105 24391442-3 2014 Dipeptidyl peptidase-4 (DPP-4) inhibitors modulate insulin and glucagon secretion in a glucose-dependent manner, and consequently a low propensity of hypoglycemia has consistently been reported across different patient populations with these agents. Glucose 87-94 insulin Homo sapiens 51-58 24559912-5 2014 Glucose is the most important insulin secretagogue as it is the primary fuel source in food. Glucose 0-7 insulin Homo sapiens 30-37 24559918-3 2014 Exogenous SST strongly inhibits the secretion of the blood glucose-regulating hormones insulin and glucagon from pancreatic beta-cells and alpha-cells, respectively. Glucose 59-66 insulin Homo sapiens 87-94 24559927-2 2014 The primary cause of MODY is an impairment of glucose-stimulated insulin secretion by pancreatic beta-cells, indicating the important roles of HNF1alpha and HNF4alpha in beta-cells. Glucose 46-53 insulin Homo sapiens 65-72 24559927-7 2014 Studies of MODY have led to a better understanding of the molecular mechanism of glucose-stimulated insulin secretion by pancreatic beta-cells. Glucose 81-88 insulin Homo sapiens 100-107 24386218-0 2013 A tripeptide Diapin effectively lowers blood glucose levels in male type 2 diabetes mice by increasing blood levels of insulin and GLP-1. Glucose 45-52 insulin Homo sapiens 119-126 24399968-2 2013 In pancreatic beta-cells, KATP channels play a key role in glucose-stimulated insulin secretion, and gain or loss of channel function results in neonatal diabetes or congenital hyperinsulinism, respectively. Glucose 59-66 insulin Homo sapiens 78-85 24376889-3 2013 Insulin stimulated glucose uptake was measured using radioactive isotope. Glucose 19-26 insulin Homo sapiens 0-7 24376889-6 2013 RESULTS: Our results revealed that both short and prolonged time of inhibition of SPT by myriocin was sufficient to prevent ceramide accumulation and simultaneously reverse palmitate induced inhibition of insulin-stimulated glucose transport. Glucose 224-231 insulin Homo sapiens 205-212 24376889-7 2013 In contrast, prolonged inhibition of SphK1 intensified the effect of PA on insulin-stimulated glucose uptake and attenuated further the activity of insulin signaling proteins (pGSK3beta/GSK3beta ratio) in L6 myotubes. Glucose 94-101 insulin Homo sapiens 75-82 24255133-2 2014 The aim of this study was to define the changes in insulin sensitivity and/or secretion in relation to glucose tolerance categories in newly diagnosed CS patients. Glucose 103-110 insulin Homo sapiens 51-58 24255133-8 2014 CONCLUSIONS: Impairment of glucose tolerance is characterized by the inability of beta-cells to adequately compensate for insulin resistance through increased insulin secretion. Glucose 27-34 insulin Homo sapiens 122-129 24255133-8 2014 CONCLUSIONS: Impairment of glucose tolerance is characterized by the inability of beta-cells to adequately compensate for insulin resistance through increased insulin secretion. Glucose 27-34 insulin Homo sapiens 159-166 24174531-4 2013 Accordingly, we observed significant reduction of multiple signaling events in EBF1 knockdown cells as well as a reduction in insulin-stimulated glucose uptake and lipogenesis. Glucose 145-152 insulin Homo sapiens 126-133 24187134-5 2013 Mammalian two-hybrid and fluorescence resonance energy transfer analyses confirmed the interaction between glucokinase and the ubiquitin-like domain in insulin-secreting MIN6 cells and revealed the highest binding affinity at low glucose. Glucose 230-237 insulin Homo sapiens 152-159 24322663-0 2013 MiniMed 530G: an insulin pump with low-glucose suspend automation. Glucose 39-46 insulin Homo sapiens 17-24 24349194-5 2013 Treatment with 1 nM BPA significantly inhibited insulin-stimulated glucose utilization, without grossly interfering with adipocyte differentiation. Glucose 67-74 insulin Homo sapiens 48-55 24319275-8 2013 PRIMARY OUTCOME MEASURES: The outcome, insulin resistance, was measured by the HOMA, calculated as fasting insulin (muU/mL)xfasting glucose (mmol/L)/22.5. Glucose 132-139 insulin Homo sapiens 39-46 22994366-12 2013 The study confirms previous findings that insulin use, longer diabetes duration and higher levels of blood glucose are associated with retinopathy in persons with diabetes. Glucose 107-114 insulin Homo sapiens 42-49 23212668-0 2013 Postprandial serum C-peptide to plasma glucose ratio predicts future insulin therapy in Japanese patients with type 2 diabetes. Glucose 39-46 insulin Homo sapiens 19-28 23212668-0 2013 Postprandial serum C-peptide to plasma glucose ratio predicts future insulin therapy in Japanese patients with type 2 diabetes. Glucose 39-46 insulin Homo sapiens 69-76 23407994-1 2013 Skeletal muscle is important in insulin-stimulated glucose uptake. Glucose 51-58 insulin Homo sapiens 32-39 23994506-8 2013 Plasma glucose and serum insulin were significantly greater throughout exercise and rest following the GLU trial compared with the GAL and PLA trials (P<0.05). Glucose 103-106 insulin Homo sapiens 25-32 24135019-7 2013 In murine islets, an increase in miR-145 expression decreased ABCA1 protein expression, increased total islet cholesterol levels, and decreased glucose-stimulated insulin secretion. Glucose 144-151 insulin Homo sapiens 163-170 24135019-8 2013 Inhibiting miR-145 produced the opposite effect of increasing ABCA1 protein levels and improving glucose-stimulated insulin secretion. Glucose 97-104 insulin Homo sapiens 116-123 24319752-3 2013 In addition to hypocalcemic effect, this substance produced significant hyperglycemic effects, decreased glycogen amount in the liver, inhibited insulin-induced glucose consumption by muscular and adipose tissues in vivo and in vitro, slowed down insulin secretion during glucose load, and impaired glucose tolerance. Glucose 161-168 insulin Homo sapiens 145-152 23917335-9 2013 Insulin action was evaluated in both groups using the glucose infusion rate. Glucose 54-61 insulin Homo sapiens 0-7 23794242-1 2013 Insulin is a secreted peptide hormone identified in human pancreas to promote glucose utilization. Glucose 78-85 insulin Homo sapiens 0-7 24092826-6 2013 RESULTS: Long-acting insulin, titrated to reduce fasting glucose to 7 mM, lowered hemoglobin A1c from 8.6% +- 0.2% to 7.1% +- 0.2% over 8 weeks. Glucose 57-64 insulin Homo sapiens 21-28 24092826-9 2013 CONCLUSION: Intensified insulin treatment to improve glycemic control led to a disproportionate improvement of insulin secretion in response to oral compared with iv glucose stimulation in patients with type 2 diabetes. Glucose 166-173 insulin Homo sapiens 24-31 24551652-10 2013 Early initiation of insulin treatment in confirmed cases of Type 2 diabetics not only helps in controlling blood glucose level but also helps in keeping MPV low and thereby preventing possibility of impending acute vascular events. Glucose 113-120 insulin Homo sapiens 20-27 24576893-10 2014 In the insulin group, there was a fall of 0.83 +- 0.53 mmol/l at 60 min (p < 0.001) and a lower serum [K(+)] at that time compared to the glucose-only group (5.18 +- 0.76 vs. 5.73 +- 1.12 mmol/l, respectively; p = 0.01). Glucose 141-148 insulin Homo sapiens 7-14 24576893-11 2014 In the glucose-only group, the glucose area under the curve (AUC) was greater and the insulin AUC was smaller. Glucose 7-14 insulin Homo sapiens 86-93 24045867-3 2013 Insulin and C-peptide responses to an OGTT were used to define the first- and second-phase disposition index (DI; beta-cell function = glucose-stimulated insulin secretion x clamp-derived insulin sensitivity). Glucose 135-142 insulin Homo sapiens 154-161 24260440-1 2013 The glucose transporter 4 (GLUT4) plays a key role in glucose uptake in insulin target tissues. Glucose 4-11 insulin Homo sapiens 72-79 23986202-9 2013 Insulin/exendin-4 also significantly stimulate acute and long-term GLP-1 secretion in the presence of glucose, suggesting novel beneficial effects of insulin signaling and GLP-1R activation on glycemia through enhanced mass of GLP-1-producing cells and enhanced GLP-1 secretion. Glucose 102-109 insulin Homo sapiens 0-7 23986202-9 2013 Insulin/exendin-4 also significantly stimulate acute and long-term GLP-1 secretion in the presence of glucose, suggesting novel beneficial effects of insulin signaling and GLP-1R activation on glycemia through enhanced mass of GLP-1-producing cells and enhanced GLP-1 secretion. Glucose 102-109 insulin Homo sapiens 150-157 24064339-10 2013 Increased clamp-derived peripheral insulin sensitivity was also correlated with enhanced metabolic flexibility, reduced fasting RQ, and higher nonoxidative glucose disposal (P < 0.05). Glucose 156-163 insulin Homo sapiens 35-42 23523565-5 2013 GCs suppress insulin-stimulated glucose uptake and utilization and glycogen synthesis, and play a permissive role for catecholamine-induced glycogenolysis, thus preserving the level of circulating glucose, the major energy source for the brain. Glucose 32-39 insulin Homo sapiens 13-20 24201279-2 2013 However, insulin-independent mechanisms, referred to as "glucose effectiveness", account for roughly 50% of overall glucose disposal, and reduced glucose effectiveness also contributes importantly to diabetes pathogenesis. Glucose 57-64 insulin Homo sapiens 9-16 24201279-2 2013 However, insulin-independent mechanisms, referred to as "glucose effectiveness", account for roughly 50% of overall glucose disposal, and reduced glucose effectiveness also contributes importantly to diabetes pathogenesis. Glucose 116-123 insulin Homo sapiens 9-16 24201279-4 2013 Here we present evidence of a brain-centred glucoregulatory system (BCGS) that can lower blood glucose levels via both insulin-dependent and -independent mechanisms, and propose a model in which complex and highly coordinated interactions between the BCGS and pancreatic islets promote normal glucose homeostasis. Glucose 95-102 insulin Homo sapiens 119-126 24172269-2 2013 Intracorporeal glucose disposal was assumed as insulin-independent (lambda) in the central high-flow compartment comprising blood, brain, and internal organs, including pancreatic insulin secretion (a, C1) and hepatic insulin clearance (alpha). Glucose 15-22 insulin Homo sapiens 47-54 24363940-0 2013 Insulin sensitivity assessed by stable isotopes with oral glucose administration: validation with euglycaemic clamp. Glucose 58-65 insulin Homo sapiens 0-7 24363940-1 2013 Methods of determining insulin sensitivity that use an oral challenge of glucose are preferred to those using intravenous administration since the measurement is made in conditions more akin to normal physiology. Glucose 73-80 insulin Homo sapiens 23-30 23725973-1 2013 BACKGROUND: In peritoneal dialysis, the high glucose load absorbed from dialysis fluid contributes to several metabolic abnormalities, including insulin resistance. Glucose 45-52 insulin Homo sapiens 145-152 23725973-6 2013 OUTCOMES & MEASUREMENTS: The primary outcome was insulin sensitivity, measured by the magnitude of change from baseline in glucose infusion rate (in milligrams per kilogram of body weight per minute) during a euglycemic hyperinsulinemic clamp. Glucose 127-134 insulin Homo sapiens 53-60 24022868-9 2013 Further consistent with glucocorticoid-opposing effects of DHEA, insulin-independent glucose uptake was significantly enhanced by DHEA treatment. Glucose 85-92 insulin Homo sapiens 65-72 24172269-3 2013 Insulin-dependent (gamma) glucose utilization was allocated to the low-flow system comprising muscle, skin, and bone. Glucose 26-33 insulin Homo sapiens 0-7 24229692-0 2013 Efficacy and safety of insulin treatment in type 2 diabetes using a new index called glucose safety control index. Glucose 85-92 insulin Homo sapiens 23-30 23921548-4 2013 However, sulfonylureas are ineffective for long-term treatments and ultimately result in the administration of insulin to control glucose levels. Glucose 130-137 insulin Homo sapiens 111-118 24229669-15 2013 Basal insulin therapy strategy, including a single injection of basal insulin and basal insulin plus preprandial insulin injection subcutaneously, is superior to premixed insulin therapy in the perioperative blood glucose management, and it could be viewed as the best choice in glucose control during perioperative period. Glucose 214-221 insulin Homo sapiens 6-13 23838194-7 2013 More importantly, for the oral administration of insulin-loaded PLA-P85-PLA vesicles at insulin doses of 200 IU/kg, the minimum blood glucose concentration was observed in the diabetic mice test after 2.5h, which was 15% of initial glucose level. Glucose 134-141 insulin Homo sapiens 49-56 23838194-7 2013 More importantly, for the oral administration of insulin-loaded PLA-P85-PLA vesicles at insulin doses of 200 IU/kg, the minimum blood glucose concentration was observed in the diabetic mice test after 2.5h, which was 15% of initial glucose level. Glucose 232-239 insulin Homo sapiens 49-56 23965946-8 2013 CONCLUSION: Insulin resistance on glucose load (log post-glucose-IR), plasma high-density lipoprotein cholesterol levels, and smoking were significantly associated with CSA (r=0.225, P=0.004; r=-0.313, P<0.001; and r=0.258, P=0.001, respectively). Glucose 34-41 insulin Homo sapiens 12-19 23965946-8 2013 CONCLUSION: Insulin resistance on glucose load (log post-glucose-IR), plasma high-density lipoprotein cholesterol levels, and smoking were significantly associated with CSA (r=0.225, P=0.004; r=-0.313, P<0.001; and r=0.258, P=0.001, respectively). Glucose 57-64 insulin Homo sapiens 12-19 23835342-3 2013 In both groups postsurgery, tracer-derived appearance of oral glucose was biphasic, a rapid increase followed by a sharp drop, a pattern that was mirrored by postprandial glucose levels and insulin secretion. Glucose 62-69 insulin Homo sapiens 190-197 23835342-5 2013 Endogenous glucose production, however, was less suppressed during the MMT as the combined result of a relative hyperglucagonemia and the rapid fall in plasma glucose and insulin levels. Glucose 11-18 insulin Homo sapiens 171-178 23846812-7 2013 Lower baseline SI predicted the decline in physical activity measured by accelerometry, whereas higher baseline acute insulin response to glucose predicted the decline in physical activity measured by self-report. Glucose 138-145 insulin Homo sapiens 118-125 23863810-5 2013 Higher final glucose tolerance status (NGT > IGT > T2DM) was associated with improvements in insulin sensitivity (OR 0.61 [95% CI 0.54-0.80]), IS (OR 0.61 [95% CI 0.50-0.75]), and beta-cell function (ln IS/IR index and ln ISR/IR index) (OR 0.26 [95% CI 0.19-0.37]; all P < 0.0001). Glucose 13-20 insulin Homo sapiens 99-106 23952326-4 2013 Basal insulin was titrated to target pre-breakfast plasma glucose 3.9-4.9 mmol/l. Glucose 58-65 insulin Homo sapiens 6-13 24089542-0 2013 Needle-free jet injection of rapid-acting insulin improves early postprandial glucose control in patients with diabetes. Glucose 78-85 insulin Homo sapiens 42-49 23933953-11 2013 In addition, prednisolone 7.5 mg and 30 mg reduced insulin sensitivity (M value) by -11.4 +- 4.5 mumol kg(-1) min(-1) and -25.1 +- 4.1 mumol kg(-1) min(-1) (p < 0.001) and increased postprandial glucose levels by 11 +- 5% and 27 +- 9% (p < 0.001), respectively. Glucose 198-205 insulin Homo sapiens 51-58 23933953-13 2013 Prednisolone-induced changes in insulin-stimulated capillary recruitment were associated with insulin sensitivity (r = +0.76; p < 0.001), postprandial glucose concentrations (r = -0.52; p < 0.03) and systolic blood pressure (r = -0.62; p < 0.001). Glucose 154-161 insulin Homo sapiens 32-39 23933953-17 2013 CONCLUSIONS/INTERPRETATION: Prednisolone-induced impairment of insulin-stimulated capillary recruitment was paralleled by insulin resistance, increased postprandial glucose levels, hypertension and increased circulating resistin concentrations in healthy men. Glucose 165-172 insulin Homo sapiens 63-70 23807520-1 2013 OBJECTIVE: Because approximately 40% of patients with type 1 diabetes have the metabolic syndrome, we tested the hypothesis that addition of liraglutide to insulin in obese patients with type 1 diabetes will result in an improvement in plasma glucose concentrations, a reduction in hemoglobin A1c (HbA1c), a fall in systolic blood pressure, and weight loss. Glucose 243-250 insulin Homo sapiens 156-163 24035997-2 2013 Although acute exposure to FFAs stimulates glucose-stimulated insulin secretion (GSIS), prolonged exposure impairs GSIS and causes apoptosis. Glucose 43-50 insulin Homo sapiens 62-69 23180239-6 2013 Insulin resistance (IR) was assessed by glucose infusion rate (GIR; mg/kg/min) at euglycemia. Glucose 40-47 insulin Homo sapiens 0-7 23071070-1 2013 Glucose metabolism of children with drug-resistant epilepsy, controlled by antiepileptic drugs epilepsy, and first-time nonfebrile seizures was studied through the performance of an oral glucose tolerance test and through insulin, C-peptide, and glycosylated hemoglobin measurements. Glucose 0-7 insulin Homo sapiens 222-229 23665535-1 2013 AIM: The aim of this study was to determine the correlation between the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis and glucose intolerance in acromegaly during the early postoperative period. Glucose 138-145 insulin Homo sapiens 92-99 23890682-9 2013 CONCLUSIONS: Our results suggest that taking into account the impact of age and BMI on insulin sensitivity, it would be expected that the relatives of patients with type 1 diabetes with "high-normal" glucose levels would become gradually unable to compensate for increasing insulin resistance. Glucose 200-207 insulin Homo sapiens 87-94 24351171-8 2013 Results indicate that the proposed method delivers insulin more conservatively during nighttime than during daytime while maintaining safe blood glucose levels at all times. Glucose 145-152 insulin Homo sapiens 51-58 24351192-0 2013 Assessment of impaired fasting glucose in obese and overweight insulin-resistant children by continuous glucose monitoring. Glucose 31-38 insulin Homo sapiens 63-70 24351192-0 2013 Assessment of impaired fasting glucose in obese and overweight insulin-resistant children by continuous glucose monitoring. Glucose 104-111 insulin Homo sapiens 63-70 23948373-4 2013 We compared the insulin activation of PI3K-Akt (glucose uptake) and ERK-MAPK (pro-inflammation) signaling pathways, intracellular and mitochondrial oxidative stress (DCF and MitoSOX Red), and their responses to the antioxidant N-acetylcysteine (NAC). Glucose 48-55 insulin Homo sapiens 16-23 23948373-8 2013 Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake. Glucose 266-273 insulin Homo sapiens 91-98 23352957-6 2013 A secondary goal was to assess the relationship between non-HDL-C and insulin resistance, defined as the upper tertile of steady-state plasma glucose concentrations measured during the insulin suppression test. Glucose 142-149 insulin Homo sapiens 70-77 24397179-4 2013 It is known that GPR40 agonist stimulates insulin secretion in glucose independent manner. Glucose 63-70 insulin Homo sapiens 42-49 24397179-5 2013 GKA potentiates glucose-stimulated insulin secretion from pancreatic beta cells and stimulates glucose uptake into the liver. Glucose 16-23 insulin Homo sapiens 35-42 23554353-4 2013 DESIGN AND METHODS: Using positron emission tomography (PET), cold- and insulin-stimulated glucose uptake and blood flow in the BAT of obese and lean humans were quantified. Glucose 91-98 insulin Homo sapiens 72-79 23659762-0 2013 Vascular function and glucose variability improve transiently following initiation of continuous subcutaneous insulin infusion in children with type 1 diabetes. Glucose 22-29 insulin Homo sapiens 110-117 24179609-8 2013 Insulin secretion of hADSCs(PDX1+) in the high-glucose medium was detected by electrochemiluminescence test. Glucose 47-54 insulin Homo sapiens 0-7 24179609-17 2013 The insulin secretion of hADSCs(PDX1+) in the high glucose medium was 2.32 muU/mL. Glucose 51-58 insulin Homo sapiens 4-11 24148878-5 2013 Insulin sensitivity, given as the Glucose Infusion Rate (GIR) and Insulin Sensitivity Index (ISI), was calculated from the two euglycemic clamp steps. Glucose 34-41 insulin Homo sapiens 0-7 24512852-1 2013 Nur77 is a stress sensor in pancreatic beta-cells, which negatively regulates glucose-stimulated insulin secretion. Glucose 78-85 insulin Homo sapiens 97-104 24148878-12 2013 CONCLUSIONS: Compared with Norwegian patients, Pakistani patients with T2DM had lower insulin sensitivity, affecting both glucose and lipid metabolism. Glucose 122-129 insulin Homo sapiens 86-93 24194886-0 2013 Decreased insulin clearance in individuals with elevated 1-h post-load plasma glucose levels. Glucose 78-85 insulin Homo sapiens 10-17 24194903-7 2013 P1736 caused dose dependent increase in glucose uptake (EC50-400 nM) in the insulin resistant 3T3 adipocytes. Glucose 40-47 insulin Homo sapiens 76-83 24194886-7 2013 The differences in insulin clearance remained significant after adjustment for fasting glucose (P = 0.02) in addition to gender, age, and BMI. Glucose 87-94 insulin Homo sapiens 19-26 24194886-8 2013 In univariate analyses adjusted for gender and age, insulin clearance was inversely correlated with body weight, body mass index, waist, fat mass, 1-h and 2-h post-load glucose levels, fasting, 1-h and 2-h post-load insulin levels, and insulin-stimulated glucose disposal. Glucose 169-176 insulin Homo sapiens 52-59 24194886-8 2013 In univariate analyses adjusted for gender and age, insulin clearance was inversely correlated with body weight, body mass index, waist, fat mass, 1-h and 2-h post-load glucose levels, fasting, 1-h and 2-h post-load insulin levels, and insulin-stimulated glucose disposal. Glucose 255-262 insulin Homo sapiens 52-59 23876463-7 2013 After the insulin infusion, mean plasma glucose during peri-procedural period was greater in CGC group than in IGC group (P < 0.001). Glucose 40-47 insulin Homo sapiens 10-17 23992862-4 2013 Identified lead thiazolyl-phthalazinone acetamide (7114863) increased glucose uptake (EC50 of 0.07+-0.02 muM) in differentiated skeletal muscle cells in presence of insulin. Glucose 70-77 insulin Homo sapiens 165-172 23798495-6 2013 Ranolazine at therapeutically effective dose significantly recruited muscle microvasculature by increasing muscle microvascular blood volume (~2-fold, P < 0.05) and increased insulin-mediated whole body glucose disposal (~30%, P = 0.02). Glucose 206-213 insulin Homo sapiens 178-185 23792187-1 2013 In the endocrine fraction of the pancreas, the beta-cell rapidly reacts to fluctuations in blood glucose concentrations by adjusting the rate of insulin secretion. Glucose 97-104 insulin Homo sapiens 145-152 23792187-3 2013 Mitochondria play a central role in this process by connecting glucose metabolism to insulin release. Glucose 63-70 insulin Homo sapiens 85-92 23792187-7 2013 The coupling factors are additive to the Ca(2+) signal and participate to the amplifying pathway of glucose-stimulated insulin secretion. Glucose 100-107 insulin Homo sapiens 119-126 23904152-6 2013 The HGC model incorporates insulin-dependent glucose clearance and glucose-induced insulin secretion. Glucose 45-52 insulin Homo sapiens 27-34 24130551-7 2013 Group A dolphins with high insulin (greater than 14 muIU/ml) had higher glucose, iron, GGT, and BMI compared to Group A dolphins with lower insulin. Glucose 72-79 insulin Homo sapiens 27-34 24063815-2 2013 Interleukin-6 (IL-6), a multifunctional cytokine, could influence conditions of altered glucose metabolism such as insulin resistance in diabetic patients. Glucose 88-95 insulin Homo sapiens 115-122 23904152-10 2013 Insulin-dependent glucose clearance for the HGC was about 3-fold greater than for the MTT (0.0111 vs. 0.00425 L/min/[mU/L]). Glucose 18-25 insulin Homo sapiens 0-7 23904152-12 2013 The lack of palosuran effect coupled with a population-based analysis provided quantitative insights into the variability of glucose and insulin regulation in patients with T2DM following multiple glucose tolerance tests. Glucose 197-204 insulin Homo sapiens 137-144 23924045-4 2013 The acute C-peptide response to glucose (ACRglu) and disposition index from FSIVGTT correlated modestly with the islet equivalents per kilogram body weight (IEQ/kg). Glucose 32-39 insulin Homo sapiens 10-19 24634515-1 2013 Novel glucose-sensitive systems for the release of insulin from poly(diethylaminoethyl methacrylate) (PDEAEM) micro-particles and nanoparticles decorated with glucose oxidase and catalase enzymes have been developed. Glucose 6-13 insulin Homo sapiens 51-58 24634515-4 2013 Microparticles exhibited a responsive (pH) or intelligent (glucose) release of insulin from a stimulus. Glucose 59-66 insulin Homo sapiens 79-86 23924045-6 2013 In multivariate logistic regression modeling, normal fasting glucose (<100 mg/dL) and stimulated C-peptide on MMTT >=4 ng/mL were associated with greater odds of receiving an islet mass >=2500 IEQ/kg (OR 0.93 for fasting glucose, CI 0.87-1.0; OR 7.9 for C-peptide, CI 1.75-35.6). Glucose 230-237 insulin Homo sapiens 100-109 23859800-2 2013 In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect (that is, higher insulin release in response to an oral glucose challenge compared to an equal intravenous glucose load). Glucose 77-84 insulin Homo sapiens 95-102 23859800-2 2013 In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect (that is, higher insulin release in response to an oral glucose challenge compared to an equal intravenous glucose load). Glucose 241-248 insulin Homo sapiens 95-102 23921483-12 2013 Chromium supplementation could be beneficial in patients with DM2 treated with insulin, most likely due to lowered insulin resistance leading to improved glucose tolerance. Glucose 154-161 insulin Homo sapiens 79-86 23510756-2 2013 Both insulin-dependent and insulin-independent processes contribute to fasting and postprandial plasma glucose regulation. Glucose 103-110 insulin Homo sapiens 5-34 23510756-4 2013 Muscle and adipose tissue are responsive to insulin and can use either glucose or ketones and free fatty acids as their primary metabolic fuel. Glucose 71-78 insulin Homo sapiens 44-51 23685312-5 2013 Insulin-stimulated glucose uptake and glycogen synthesis were normal in FH+ myotubes. Glucose 19-26 insulin Homo sapiens 0-7 24500556-0 2013 A comparison of internet monitoring with continuous glucose monitoring in insulin-requiring type 2 diabetes mellitus. Glucose 52-59 insulin Homo sapiens 74-81 24157161-4 2013 Insulin resistance was calculated by the homeostasis model of assessment for insulin resistance (HOMA-IR) approach, calculated as fasting insulin (microunits/ml)x fasting blood glucose (mmol/L)/22.5. Glucose 177-184 insulin Homo sapiens 0-7 23996678-4 2013 Thus, insulin resistance is increased and the sensitivity to insulin is reset, so increasing levels of insulin are required to maintain body glucose and metabolic homeostasis. Glucose 141-148 insulin Homo sapiens 6-13 23955813-2 2013 GLP-1 receptor agonists stimulate insulin production and secretion from the pancreatic beta cells in a glucose-dependent manner, improve gastric emptying, favor weight reduction, and reduce postabsorptive glucagon secretion from pancreatic alpha cells. Glucose 103-110 insulin Homo sapiens 34-41 23996678-4 2013 Thus, insulin resistance is increased and the sensitivity to insulin is reset, so increasing levels of insulin are required to maintain body glucose and metabolic homeostasis. Glucose 141-148 insulin Homo sapiens 61-68 23996678-4 2013 Thus, insulin resistance is increased and the sensitivity to insulin is reset, so increasing levels of insulin are required to maintain body glucose and metabolic homeostasis. Glucose 141-148 insulin Homo sapiens 61-68 23996678-7 2013 Insulin acts as a YIN factor to lower blood glucose level by increasing cellular glucose uptake, whereas glucagon acts as a YANG factor to counter the action of insulin by increasing glucose production. Glucose 44-51 insulin Homo sapiens 0-7 23996678-7 2013 Insulin acts as a YIN factor to lower blood glucose level by increasing cellular glucose uptake, whereas glucagon acts as a YANG factor to counter the action of insulin by increasing glucose production. Glucose 81-88 insulin Homo sapiens 0-7 23818527-1 2013 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones that control the secretion of insulin, glucagon, and somatostatin to facilitate glucose disposal. Glucose 36-43 insulin Homo sapiens 54-61 23835328-7 2013 While the population in general had improved glucose regulation during the 5-year follow-up period, each additional allele in the genetic risk score was associated with a relative increase in fasting, 30-min, and 120-min plasma glucose values and a relative decrease in measures of beta-cell function over the 5-year period, whereas indices of insulin sensitivity were unaffected. Glucose 228-235 insulin Homo sapiens 344-351 23835684-4 2013 Peripheral insulin resistance was quantified by measuring the steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 82-89 insulin Homo sapiens 11-18 23893303-2 2013 We hypothesised that the driving force for the changed postprandial glucose profiles after RYGB is rapid entry of glucose into the systemic circulation due to modified gastrointestinal anatomy, causing hypersecretion of insulin and other hormones influencing glucose disappearance and endogenous glucose production. Glucose 68-75 insulin Homo sapiens 220-227 23893303-2 2013 We hypothesised that the driving force for the changed postprandial glucose profiles after RYGB is rapid entry of glucose into the systemic circulation due to modified gastrointestinal anatomy, causing hypersecretion of insulin and other hormones influencing glucose disappearance and endogenous glucose production. Glucose 114-121 insulin Homo sapiens 220-227 23893303-2 2013 We hypothesised that the driving force for the changed postprandial glucose profiles after RYGB is rapid entry of glucose into the systemic circulation due to modified gastrointestinal anatomy, causing hypersecretion of insulin and other hormones influencing glucose disappearance and endogenous glucose production. Glucose 114-121 insulin Homo sapiens 220-227 23893303-2 2013 We hypothesised that the driving force for the changed postprandial glucose profiles after RYGB is rapid entry of glucose into the systemic circulation due to modified gastrointestinal anatomy, causing hypersecretion of insulin and other hormones influencing glucose disappearance and endogenous glucose production. Glucose 114-121 insulin Homo sapiens 220-227 23893303-5 2013 These changes were brought about by changes in glucose kinetics: (1) a more rapid appearance of ingested glucose in the systemic circulation, and a concomitant increase in insulin and glucagon-like peptide-1 secretion; (2) postprandial glucose disappearance was maintained at a high rate for a longer time after RYGB. Glucose 47-54 insulin Homo sapiens 172-179 23907381-0 2013 Insulin-mediated suppression of lipolysis in adipose tissue and skeletal muscle of obese type 2 diabetic men and men with normal glucose tolerance. Glucose 129-136 insulin Homo sapiens 0-7 24199158-6 2013 However, life style intervention such as exercise, which is the most potent physiological activator of muscle PDC, along with pharmacological intervention such as administration of dichloroacetate or L-carnitine can prove to be viable strategies for treating muscle insulin resistance in obesity and T2D as they can potentially restore whole body glucose disposal. Glucose 347-354 insulin Homo sapiens 266-273 24290089-3 2013 At first, treatment with insulin therapy consisted of bolus insulin before each meal and basal insulin at bed time commenced to improve every preprandial glucose levels below 130 mg/dL. Glucose 154-161 insulin Homo sapiens 25-32 23651392-5 2013 Vitamin D insufficiency (VDI) was defined as 25(OH)D < 75 nmol/L; insulin sensitivity was determined using a 2-h continuous infusion of glucose model assessment with homeostasis (CIGMA-HOMA), using the trapezoidal model to calculate the incremental insulin and glucose areas under the curve (AUCins and AUGglu, respectively). Glucose 139-146 insulin Homo sapiens 69-76 23651392-5 2013 Vitamin D insufficiency (VDI) was defined as 25(OH)D < 75 nmol/L; insulin sensitivity was determined using a 2-h continuous infusion of glucose model assessment with homeostasis (CIGMA-HOMA), using the trapezoidal model to calculate the incremental insulin and glucose areas under the curve (AUCins and AUGglu, respectively). Glucose 264-271 insulin Homo sapiens 69-76 23039765-0 2013 Post-glucose load changes of plasma key metabolite and insulin concentrations during pregnancy and lactation in ewes with different susceptibility to pregnancy toxaemia. Glucose 5-12 insulin Homo sapiens 55-62 23039765-4 2013 The glucose elimination rate and the glucose-stimulated first-phase insulin secretion were significantly (p < 0.05) lower in the HR, in relation to the LR group combining the data of all gestational stages. Glucose 37-44 insulin Homo sapiens 68-75 23039765-7 2013 Results indicate an insulin resistance in the HR ewes regarding the glucose utilization and the ketone body formation during late pregnancy. Glucose 68-75 insulin Homo sapiens 20-27 24051373-2 2013 Zn2+ binds insulin in pancreatic beta cells to form crystalline aggregates in dense core vesicles (DCVs), which are released in response to physiological signals such as increased blood glucose. Glucose 186-193 insulin Homo sapiens 11-18 23876704-0 2013 Evaluation of glucose variability when converting from insulin infusion to basal-bolus regimen in a surgical-trauma intensive care unit. Glucose 14-21 insulin Homo sapiens 55-62 23876704-1 2013 PURPOSE: This study aimed to identify predictive factors resulting in glucose values greater than 200 mg/dL in patients with trauma transitioned from an insulin infusion to a basal-bolus subcutaneous insulin regimen. Glucose 70-77 insulin Homo sapiens 153-160 23876704-1 2013 PURPOSE: This study aimed to identify predictive factors resulting in glucose values greater than 200 mg/dL in patients with trauma transitioned from an insulin infusion to a basal-bolus subcutaneous insulin regimen. Glucose 70-77 insulin Homo sapiens 200-207 24358443-5 2013 Fetal insulin was measured under basal, glucose-stimulated insulin secretion (GSIS) and glucose-potentiated arginine-stimulated insulin secretion (GPAIS) conditions in the absence and presence of an ADR-block. Glucose 40-47 insulin Homo sapiens 59-66 23924694-2 2013 We previously identified mitogen-activated protein kinase kinase kinase kinase 4 (Map4k4), a sterile 20 protein kinase reported to be upstream of c-Jun NH2-terminal kinase (JNK) signaling, as a novel negative regulator of insulin-stimulated glucose transport in adipocytes. Glucose 241-248 insulin Homo sapiens 222-229 23831440-0 2013 Postprandial serum C-peptide to plasma glucose concentration ratio correlates with oral glucose tolerance test- and glucose clamp-based disposition indexes. Glucose 39-46 insulin Homo sapiens 19-28 23831440-0 2013 Postprandial serum C-peptide to plasma glucose concentration ratio correlates with oral glucose tolerance test- and glucose clamp-based disposition indexes. Glucose 88-95 insulin Homo sapiens 19-28 23831440-0 2013 Postprandial serum C-peptide to plasma glucose concentration ratio correlates with oral glucose tolerance test- and glucose clamp-based disposition indexes. Glucose 88-95 insulin Homo sapiens 19-28 23831440-1 2013 OBJECTIVE: The C-peptide index (CPI), a ratio of serum C-peptide to plasma glucose levels, is a readily measured index of beta-cell function. Glucose 75-82 insulin Homo sapiens 15-24 23831440-3 2013 MATERIALS/METHODS: We investigated the relationship of the two CPIs to indexes of insulin secretion measured with an oral glucose tolerance test (OGTT) or with hyperglycemic and hyperinsulinemic-euglycemic clamp analyses as well as to disposition indexes (indexes of insulin secretion adjusted for insulin sensitivity) calculated from OGTT- or clamp-based analyses. Glucose 122-129 insulin Homo sapiens 82-89 24037093-0 2013 Cross-talk between hypoxia and insulin signaling through Phd3 regulates hepatic glucose and lipid metabolism and ameliorates diabetes. Glucose 80-87 insulin Homo sapiens 31-38 23574533-1 2013 AIMS: Thiazoledinediones decrease blood glucose by their insulin-sensitizing properties. Glucose 40-47 insulin Homo sapiens 57-64 23765184-6 2013 Basal and insulin-stimulated glucose uptake was measured and the effect on plasma membrane translocation of glucose transporter 4 (GLUT4) was assayed. Glucose 29-36 insulin Homo sapiens 10-17 23765184-9 2013 LXR activation also diminished insulin-stimulated glucose transport and lipogenesis in adipocytes obtained from overweight individuals. Glucose 50-57 insulin Homo sapiens 31-38 23765184-11 2013 CONCLUSIONS/INTERPRETATION: In contrast to murine models, LXR downregulates insulin-stimulated glucose uptake in human adipocytes from overweight individuals. Glucose 95-102 insulin Homo sapiens 76-83 23786228-2 2013 Insulin remains the only glucose-lowering therapy that is efficacious throughout this continuum. Glucose 25-32 insulin Homo sapiens 0-7 24003936-1 2013 Glucagon-like peptide-1 (GLP-1) is one of the hormones responsible for the incretin effect, a term that refers to the observation that orally administered glucose results in a larger increase in plasma insulin levels and insulin-dependent decrease in blood glucose concentration when compared to the same amount of glucose given intravenously. Glucose 155-162 insulin Homo sapiens 202-209 24003936-3 2013 Upon secretion, GLP-1 targets different cell types and exerts a wide variety of actions such as potentiation of glucose-stimulated insulin secretion, reduction of appetite, delay of gastric emptying and increase in beta-cell mass. Glucose 112-119 insulin Homo sapiens 131-138 24086950-4 2013 In clinical trials of up to 1 year duration in patients with type 2 diabetes, treatment with lixisenatide alone and in combination with insulin and various oral antidiabetics conferred significant reductions in HbA1c, fasting and postprandial plasma glucose. Glucose 250-257 insulin Homo sapiens 136-143 24191388-2 2013 The pancreas and insulin are both key to normal glucose metabolism and glucose control.Nearly any body stressor that alters a patient"s metabolism can impair normal insulin function and trigger hyperglycemia. Glucose 48-55 insulin Homo sapiens 17-24 24191388-2 2013 The pancreas and insulin are both key to normal glucose metabolism and glucose control.Nearly any body stressor that alters a patient"s metabolism can impair normal insulin function and trigger hyperglycemia. Glucose 48-55 insulin Homo sapiens 165-172 23765198-3 2013 Amylin is co-secreted with insulin and controls influx of glucose into the blood. Glucose 58-65 insulin Homo sapiens 27-34 23765198-9 2013 A significant (p < 0.05) time effect occurred for glucose, insulin, and glucagon with reduced insulin across the exercise trial and increases in glucose and glucagon later in the trial, but there were no differences between the EFX and MLX trials. Glucose 53-60 insulin Homo sapiens 97-104 23700321-2 2013 Insulin exerts its metabolic function by activating the PI3K/Akt pathway and favoring glucose uptake. Glucose 86-93 insulin Homo sapiens 0-7 22721642-5 2013 Plasma levels of insulin and glucose during an oral 75 g glucose loading were decreased only in miglitol group. Glucose 57-64 insulin Homo sapiens 17-24 23925524-3 2013 In this work, we demonstrate the importance of rational design of both the individual organ and its relationship with other organs, using a simple two-compartment system simulating insulin-dependent glucose uptake in adipose tissues. Glucose 199-206 insulin Homo sapiens 181-188 24213304-1 2013 Insulin secretion from pancreatic beta-cells is initiated by the closure of ATP-sensitive K+ channels (KATP) in response to high concentrations of glucose, and this action of glucose is counteracted by the hormone leptin, an adipokine that signals through the Ob-Rb receptor to increase KATP channel activity. Glucose 147-154 insulin Homo sapiens 0-7 24213304-1 2013 Insulin secretion from pancreatic beta-cells is initiated by the closure of ATP-sensitive K+ channels (KATP) in response to high concentrations of glucose, and this action of glucose is counteracted by the hormone leptin, an adipokine that signals through the Ob-Rb receptor to increase KATP channel activity. Glucose 175-182 insulin Homo sapiens 0-7 23796568-6 2013 MAIN OUTCOME MEASURES: Indices of insulin sensitivity and insulin release were calculated using insulin and glucose values from a standard oral glucose tolerance test (120 minutes, 75 g glucose). Glucose 108-115 insulin Homo sapiens 34-41 23824421-9 2013 Compared with healthy controls, NLSDM patients showed impaired insulin response to glucose possibly related to the severe pancreatic steatosis, preserved whole-body insulin sensitivity, and a shift toward glucose metabolism in the heart. Glucose 83-90 insulin Homo sapiens 63-70 24179883-8 2013 These decreased levels of trace elements cause disturbances in glucose transport across cell membrane lead to insufficient formation and secretion of insulin by pancreas which compromise in the antioxidant defense mechanisms. Glucose 63-70 insulin Homo sapiens 150-157 23551748-4 2013 However, mounting evidence indicates that short-term intensive insulin therapy used in the early stages of type 2 diabetes could improve beta-cell function, resulting in better glucose control and more extended glycemic remission than oral antidiabetic agents. Glucose 177-184 insulin Homo sapiens 63-70 24124956-3 2013 Safe insulin dosing requires timely and accurate glucose measurements, especially during dynamic changes in nutrition, insulin sensitivity, and physiological stress. Glucose 49-56 insulin Homo sapiens 5-12 24124956-3 2013 Safe insulin dosing requires timely and accurate glucose measurements, especially during dynamic changes in nutrition, insulin sensitivity, and physiological stress. Glucose 49-56 insulin Homo sapiens 119-126 24124961-0 2013 A novel insulin combination of insulin degludec and insulin aspart achieves a more stable overnight glucose profile than insulin glargine: results from continuous glucose monitoring in a proof-of-concept trial. Glucose 100-107 insulin Homo sapiens 8-15 24124961-0 2013 A novel insulin combination of insulin degludec and insulin aspart achieves a more stable overnight glucose profile than insulin glargine: results from continuous glucose monitoring in a proof-of-concept trial. Glucose 100-107 insulin Homo sapiens 31-38 24124961-0 2013 A novel insulin combination of insulin degludec and insulin aspart achieves a more stable overnight glucose profile than insulin glargine: results from continuous glucose monitoring in a proof-of-concept trial. Glucose 163-170 insulin Homo sapiens 8-15 24124961-0 2013 A novel insulin combination of insulin degludec and insulin aspart achieves a more stable overnight glucose profile than insulin glargine: results from continuous glucose monitoring in a proof-of-concept trial. Glucose 163-170 insulin Homo sapiens 31-38 24124965-1 2013 It has been more than 7 years since the first fully automated closed-loop insulin delivery system that linked subcutaneous insulin delivery and glucose sensing was published. Glucose 144-151 insulin Homo sapiens 74-81 24968533-1 2013 Optimal dosing of basal insulin is needed to achieve target fasting blood glucose and to avoid hypoglycaemia on the other hand in patients of type 2 diabetes on bedtime basal insulin and daytime sulfonylureas. Glucose 74-81 insulin Homo sapiens 24-31 23701262-10 2013 Glucose improvements were associated with decreased insulin concentrations and measures of enhanced insulin sensitivity. Glucose 0-7 insulin Homo sapiens 52-59 23701262-10 2013 Glucose improvements were associated with decreased insulin concentrations and measures of enhanced insulin sensitivity. Glucose 0-7 insulin Homo sapiens 100-107 27335827-3 2013 Insulin regulates metabolism, at least in part, via the control of the expression of the hepatic genes involved in glucose and fatty acid metabolism. Glucose 115-122 insulin Homo sapiens 0-7 27335827-4 2013 Insulin resistance is always associated with profound changes of the expression of hepatic genes for glucose and lipid metabolism. Glucose 101-108 insulin Homo sapiens 0-7 27335827-10 2013 This paper also summarizes the effects of VA status and RA treatments on the glucose and lipid metabolism in vivo and the effects of retinoid treatments on the expression of insulin-regulated genes involved in the glucose and fatty acid metabolism in the primary hepatocytes. Glucose 214-221 insulin Homo sapiens 174-181 23742882-6 2013 The DAB-based insulin loaded microneedle shows similar bioavailability (96.6+-2.4%) and down regulation of glucose level compared with subcutaneous injection. Glucose 107-114 insulin Homo sapiens 14-21 22465098-4 2013 Aldosterone exerts its biological roles via the mineralocorticoid receptor (MR), and inhibition of MR signaling in adipose tissue ameliorates inflammation, with upregulation of insulin-mediated glucose transport and adipocyte differentiation. Glucose 194-201 insulin Homo sapiens 177-184 22684034-1 2013 Metabolic actions of insulin to promote glucose disposal are augmented by nitric oxide (NO)-dependent increases in microvascular blood flow to skeletal muscle. Glucose 40-47 insulin Homo sapiens 21-28 22684034-3 2013 Angiotensin II acting on AT2 receptor increases capillary blood flow to increase insulin-mediated glucose disposal. Glucose 98-105 insulin Homo sapiens 81-88 24327951-2 2013 Elevation of extracellular glucose and/or GLP-1 levels triggers a rapid upregulation of insulin biosynthesis through the activation of post-transcriptional mechanisms. Glucose 27-34 insulin Homo sapiens 88-95 24056309-9 2013 Results showed that the peaks of insulin and C peptide appeared at 0.5-1 h after glucose administration in Group A, which was earlier than that before therapy, but the maximal levels were no more than 2 times those of baseline levels. Glucose 81-88 insulin Homo sapiens 33-40 24069257-4 2013 Insulin resistance was assessed using a homeostasis model assessment of insulin resistance (HOMA-IR), which is calculated from fasting blood glucose and insulin levels. Glucose 141-148 insulin Homo sapiens 0-7 24069257-4 2013 Insulin resistance was assessed using a homeostasis model assessment of insulin resistance (HOMA-IR), which is calculated from fasting blood glucose and insulin levels. Glucose 141-148 insulin Homo sapiens 72-79 23850833-8 2013 Two of the gallotannins (4 and 5) also increased PPARalpha and PPARgamma protein expression, while all three (3-5) enhanced insulin-stimulated glucose uptake into HepG2 cells. Glucose 143-150 insulin Homo sapiens 124-131 23850833-11 2013 CONCLUSION: Three gallotannins (3-5) from Terminalia fruits acting as enhancers of both PPARalpha and PPARgamma signaling increased insulin-stimulated glucose uptake without inducing the adipogenesis, with 1,2,3,6-tetra-O-galloyl-beta-D-glucose (4) being the most effective in stimulating glucose uptake and 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (5) being most effective in increasing PPAR protein expression. Glucose 151-158 insulin Homo sapiens 132-139 23857978-2 2013 It is usually defined as a state characterised by reduced glucose-lowering activity of insulin, but it is also sometimes used as a shorthand label for a clinical syndrome encompassing major pathologies such as type 2 diabetes, polycystic ovary syndrome, fatty liver disease and atherosclerosis. Glucose 58-65 insulin Homo sapiens 87-94 23984871-0 2013 Multifunctional cyclic D,L-alpha-peptide architectures stimulate non-insulin dependent glucose uptake in skeletal muscle cells and protect them against oxidative stress. Glucose 87-94 insulin Homo sapiens 69-76 24012759-2 2013 Proteins that interact with insulin to direct its sequential synthesis, folding, trafficking, and packaging into reserve granules in order to manage release in response to elevated glucose remain largely unknown. Glucose 181-188 insulin Homo sapiens 28-35 24012759-4 2013 The insulin BIN revealed an abundant C2 domain-containing transmembrane protein 24 (TMEM24) that manages glucose-stimulated insulin secretion from a reserve pool of granules, a critical event impaired in patients with T2D. Glucose 105-112 insulin Homo sapiens 4-11 23937086-4 2013 Co-incubation of cytokine-treated human islets with GLP-1 resulted in a marked protection of beta-cells against cytokine-induced apoptosis and significantly attenuated cytokine-mediated inhibition of glucose-stimulated insulin secretion. Glucose 200-207 insulin Homo sapiens 219-226 25905178-1 2000 First, resistance to insulin develops primarily in the skeletal muscle and adipose tissue leading to reduced insulin mediated glucose uptake, and in the liver to excessive glucose production. Glucose 126-133 insulin Homo sapiens 21-28 25905178-1 2000 First, resistance to insulin develops primarily in the skeletal muscle and adipose tissue leading to reduced insulin mediated glucose uptake, and in the liver to excessive glucose production. Glucose 126-133 insulin Homo sapiens 109-116 25905178-1 2000 First, resistance to insulin develops primarily in the skeletal muscle and adipose tissue leading to reduced insulin mediated glucose uptake, and in the liver to excessive glucose production. Glucose 172-179 insulin Homo sapiens 21-28 24250303-11 2013 This makes it necessary for persons with hypertensive to have regular screening for diabetes and other categories of glucose intolerance as the increased insulin increases their risk of developing type 2 diabetes mellitus. Glucose 117-124 insulin Homo sapiens 154-161 24285449-3 2013 Insulin resistance is typically defined as decreased sensitivity or responsiveness to metabolic actions of insulin, such as insulin-mediated glucose disposal in skeletal muscle and adipose tissue and inhibition of hepatic glucose production. Glucose 141-148 insulin Homo sapiens 0-7 24285449-3 2013 Insulin resistance is typically defined as decreased sensitivity or responsiveness to metabolic actions of insulin, such as insulin-mediated glucose disposal in skeletal muscle and adipose tissue and inhibition of hepatic glucose production. Glucose 141-148 insulin Homo sapiens 107-114 24285449-3 2013 Insulin resistance is typically defined as decreased sensitivity or responsiveness to metabolic actions of insulin, such as insulin-mediated glucose disposal in skeletal muscle and adipose tissue and inhibition of hepatic glucose production. Glucose 141-148 insulin Homo sapiens 124-131 24285449-3 2013 Insulin resistance is typically defined as decreased sensitivity or responsiveness to metabolic actions of insulin, such as insulin-mediated glucose disposal in skeletal muscle and adipose tissue and inhibition of hepatic glucose production. Glucose 222-229 insulin Homo sapiens 0-7 24285449-3 2013 Insulin resistance is typically defined as decreased sensitivity or responsiveness to metabolic actions of insulin, such as insulin-mediated glucose disposal in skeletal muscle and adipose tissue and inhibition of hepatic glucose production. Glucose 222-229 insulin Homo sapiens 107-114 23831329-3 2013 Although epidemiologic studies and randomized clinical trials suggest that glycemic control plays a major role in the development of vascular complications of diabetes, insulin therapies for control of glucose metabolism cannot prevent long-term retinal complications. Glucose 202-209 insulin Homo sapiens 169-176 24624855-7 2013 However in 64% of cases patients needed insulin therapy Used systems of continuous glucose monitoring in the ICU allow improving the safety for patients receiving artificial nutrition and intravenous insulin therapy. Glucose 83-90 insulin Homo sapiens 40-47 24624855-7 2013 However in 64% of cases patients needed insulin therapy Used systems of continuous glucose monitoring in the ICU allow improving the safety for patients receiving artificial nutrition and intravenous insulin therapy. Glucose 83-90 insulin Homo sapiens 200-207 23855508-4 2013 Incretins are gut-derived peptides that stimulate in a glucose-dependent mechanism insulin secretion and action. Glucose 55-62 insulin Homo sapiens 83-90 23633524-8 2013 CONCLUSIONS: These data demonstrate that sucralose affects the glycemic and insulin responses to an oral glucose load in obese people who do not normally consume NNS. Glucose 105-112 insulin Homo sapiens 76-83 24088800-3 2013 Nevertheless, the rapid-acting insulin analog pharmacokinetics and pharmacodynamics are still far from replicating physiologic insulin action resulting in poorly controlled after meal blood glucose levels. Glucose 190-197 insulin Homo sapiens 31-38 23670996-11 2013 We conclude that hepatic and peripheral insulin sensitivity should be targeted by glucose-lowering therapy for glucocorticoid-induced diabetes. Glucose 82-89 insulin Homo sapiens 40-47 23809477-4 2013 Insulin action was quantified by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 69-76 insulin Homo sapiens 0-7 23809477-6 2013 RESULTS: For purposes of analysis, the population was divided into tertiles, and the results demonstrated that the greater the 1) fasting plasma glucose (FPG) concentration, 2) incremental plasma insulin response to meals, and 3) SSPG concentration, the more adverse the CHD risk profile (p<0.05). Glucose 145-152 insulin Homo sapiens 196-203 23657252-5 2013 in this issue of the journal addresses the capacity of agonists acting at the beta2-adrenoceptor to engender signalling bias in relation to glucose uptake in isolated skeletal muscle, an area of considerable potential interest in targeting insulin-independent pathways for the treatment of type 2 diabetes. Glucose 140-147 insulin Homo sapiens 240-247 23810798-1 2013 Diabetes is characterized by high levels of blood glucose due to either the loss of insulin-producing beta-cells in the pancreas, leading to a deficiency of insulin in type 1 diabetes, or due to increased insulin resistance, leading to reduced insulin sensitivity and productivity in type 2 diabetes. Glucose 50-57 insulin Homo sapiens 84-91 23810798-1 2013 Diabetes is characterized by high levels of blood glucose due to either the loss of insulin-producing beta-cells in the pancreas, leading to a deficiency of insulin in type 1 diabetes, or due to increased insulin resistance, leading to reduced insulin sensitivity and productivity in type 2 diabetes. Glucose 50-57 insulin Homo sapiens 157-164 23872069-1 2013 Dipeptidyl peptidase-4 (DPP-4) is a circulating glycoprotein that impairs insulin-stimulated glucose uptake and is linked to obesity and metabolic syndrome. Glucose 93-100 insulin Homo sapiens 74-81 23810798-1 2013 Diabetes is characterized by high levels of blood glucose due to either the loss of insulin-producing beta-cells in the pancreas, leading to a deficiency of insulin in type 1 diabetes, or due to increased insulin resistance, leading to reduced insulin sensitivity and productivity in type 2 diabetes. Glucose 50-57 insulin Homo sapiens 157-164 23806034-2 2013 Short-term moderate altitude exposure plus endurance physical activity has been found to improve glucose tolerance (not fasting glucose) in humans, which is associated with the improvement in the whole-body insulin sensitivity. Glucose 97-104 insulin Homo sapiens 207-214 23952705-5 2013 After 1 month on ivacaftor, the insulin response to oral glucose improved by 66-178% in all subjects except one with long-standing diabetes. Glucose 57-64 insulin Homo sapiens 32-39 24125298-2 2013 It has been observed that alpha and beta cells generate out-of-phase synchronization in the release of glucagon and insulin, counter-regulatory hormones for increasing and decreasing glucose levels, while beta and delta cells produce in-phase synchronization in the release of the insulin and somatostatin. Glucose 183-190 insulin Homo sapiens 116-123 23576172-1 2013 The Bergman"s minimal model of glucose and insulin plasma levels is commonly used to analyse the results of glucose tolerance tests in humans. Glucose 108-115 insulin Homo sapiens 43-50 23576172-2 2013 In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Glucose 125-132 insulin Homo sapiens 65-72 23576172-2 2013 In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Glucose 125-132 insulin Homo sapiens 195-202 23576172-2 2013 In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Glucose 167-174 insulin Homo sapiens 65-72 23576172-2 2013 In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Glucose 167-174 insulin Homo sapiens 195-202 23576172-2 2013 In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Glucose 167-174 insulin Homo sapiens 65-72 23576172-2 2013 In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Glucose 167-174 insulin Homo sapiens 195-202 23829493-4 2013 These pathways contribute to cell functions as major and diverse as glutamatergic activity in the neurons, membrane homeostasis in Schwann cell myelination, insulin stimulation of glucose transport in adipocytes, or endothelial secretion of the hemostatic protein, von Willebrand factor (VWF). Glucose 180-187 insulin Homo sapiens 157-164 24062005-3 2013 These molecular are related to the metabolism of glucose, functions of islet cells and sensitivity of insulin. Glucose 49-56 insulin Homo sapiens 102-109 24023652-8 2013 RESULTS: During insulin infusion, blood glucose decreased from 5.1 (SD+-0.2) to 3.0 (+-0.5) mmol/L at 60 min (p<0.001). Glucose 40-47 insulin Homo sapiens 16-23 23834678-7 2013 Finally, we demonstrated that these microgels with enzyme nanocapsules facilitate insulin release and result in a reduction of blood glucose levels in a mouse model of type 1 diabetes. Glucose 133-140 insulin Homo sapiens 82-89 23834678-0 2013 Glucose-responsive microgels integrated with enzyme nanocapsules for closed-loop insulin delivery. Glucose 0-7 insulin Homo sapiens 81-88 23834678-1 2013 A glucose-responsive closed-loop insulin delivery system represents the ideal treatment of type 1 diabetes mellitus. Glucose 2-9 insulin Homo sapiens 33-40 23834678-2 2013 In this study, we develop uniform injectable microgels for controlled glucose-responsive release of insulin. Glucose 70-77 insulin Homo sapiens 100-107 23984780-4 2013 Glucagon-like peptide-1 (GLP-1) receptor agonists stimulate glucose-medicated insulin secretion, suppress glucagon secretion, delay gastric emptying and decrease appetite. Glucose 60-67 insulin Homo sapiens 78-85 23984780-6 2013 Prospective interventional trials demonstrate that GLP-1 receptor agonists added to basal insulin decrease postprandial glucose levels, lower HbA1c levels, decrease weight and lower basal insulin requirements without increasing the risk of major hypoglycaemic events. Glucose 120-127 insulin Homo sapiens 90-97 23800880-0 2013 Exercise training favors increased insulin-stimulated glucose uptake in skeletal muscle in contrast to adipose tissue: a randomized study using FDG PET imaging. Glucose 54-61 insulin Homo sapiens 35-42 23800880-2 2013 We investigated the effect of aerobic exercise training on insulin-stimulated glucose uptake in five individual femoral muscle groups and four different adipose tissue regions, using dynamic (femoral region) and static (abdominal region) 2-deoxy-2-[18F]fluoro-d-glucose (FDG) PET/CT methodology during steady-state insulin infusion (40 mU m-2 min-1). Glucose 78-85 insulin Homo sapiens 59-66 23800880-5 2013 At baseline, insulin-stimulated glucose uptake was highest in femoral skeletal muscle followed by intraperitoneal visceral adipose tissue (VAT), retroperitoneal VAT, abdominal (anterior + posterior) subcutaneous adipose tissue (SAT), and femoral SAT (P < 0.0001 between tissues). Glucose 32-39 insulin Homo sapiens 13-20 23800880-9 2013 In conclusion, aerobic exercise training increases insulin-stimulated glucose uptake in skeletal muscle but not in adipose tissue, which demonstrates some interregional differences. Glucose 70-77 insulin Homo sapiens 51-58 23831466-0 2013 Pinusolide improves high glucose-induced insulin resistance via activation of AMP-activated protein kinase. Glucose 25-32 insulin Homo sapiens 41-48 23791483-3 2013 Fuel stimuli, including glucose, free fatty acids, and amino acids, promote insulin granule exocytosis primarily via their metabolism in beta cells and the production of key signaling metabolites. Glucose 24-31 insulin Homo sapiens 76-83 23831466-3 2013 An insulin resistance state was induced by exposing cells to 30mM glucose, as indicated by reduced insulin-stimulated tyrosine phosphorylation of IRS-1 and glucose uptake. Glucose 66-73 insulin Homo sapiens 3-10 23831466-3 2013 An insulin resistance state was induced by exposing cells to 30mM glucose, as indicated by reduced insulin-stimulated tyrosine phosphorylation of IRS-1 and glucose uptake. Glucose 66-73 insulin Homo sapiens 99-106 23831466-3 2013 An insulin resistance state was induced by exposing cells to 30mM glucose, as indicated by reduced insulin-stimulated tyrosine phosphorylation of IRS-1 and glucose uptake. Glucose 156-163 insulin Homo sapiens 3-10 23831466-3 2013 An insulin resistance state was induced by exposing cells to 30mM glucose, as indicated by reduced insulin-stimulated tyrosine phosphorylation of IRS-1 and glucose uptake. Glucose 156-163 insulin Homo sapiens 99-106 23831466-6 2013 Moreover, this treatment increased insulin-stimulated glucose uptake via AMPK activation. Glucose 54-61 insulin Homo sapiens 35-42 23430192-1 2013 We investigated whether basal insulin as first-line treatment in recently diagnosed type 2 diabetes (T2D) can improve glucose control, microvascular function and preserve insulin secretion in comparison with metformin (MET). Glucose 118-125 insulin Homo sapiens 30-37 21997325-10 2013 Insulin at high dose (100 IU/ml) dramatically enhanced the upregulatory effects of glucose on MCP-1 and IL-6 and reduced per se TLR2 mRNA expression. Glucose 83-90 insulin Homo sapiens 0-7 23803895-13 2013 Protein also regulates blood glucose by stimulating insulin and glucagon. Glucose 29-36 insulin Homo sapiens 52-59 23579070-7 2013 miR-135a also attenuated insulin stimulated phosphorylation and activation of PI3Kp85alpha and Akt and glucose uptake. Glucose 103-110 insulin Homo sapiens 25-32 23880204-5 2013 Univariate correlations showed that age, BMI, waist, blood pressure, triglycerides, fasting and 2-h post-load glucose and insulin levels were positively correlated with carotid IMT whereas HDL, insulin clearance, and insulin-stimulated glucose disposal were negatively correlated with IMT. Glucose 236-243 insulin Homo sapiens 122-129 23423695-7 2013 Most PLL patients exhibited little or no insulin-mediated glucose uptake after subtraction of non-insulin-mediated glucose uptake. Glucose 115-122 insulin Homo sapiens 98-105 23080424-7 2013 Inhibited CSE by its potent inhibitors significantly attenuates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes, whereas H2 S treatment of 3T3-L1 adipocytes impairs insulin-stimulated glucose consumption and uptake. Glucose 194-201 insulin Homo sapiens 175-182 23721205-0 2013 Insulin secreted from genetically engineered intestinal cells reduces blood glucose levels in diabetic mice. Glucose 76-83 insulin Homo sapiens 0-7 23721205-10 2013 The decrease in blood glucose level in the first week of treatment was greater in mice with K-cell specific insulin expression compared with mice with L-cell-specific insulin expression. Glucose 22-29 insulin Homo sapiens 108-115 23721205-10 2013 The decrease in blood glucose level in the first week of treatment was greater in mice with K-cell specific insulin expression compared with mice with L-cell-specific insulin expression. Glucose 22-29 insulin Homo sapiens 167-174 23423695-10 2013 These T2DM patients exhibit symmetrical lipodystrophy of the distal limbs, acanthosis nigricans, marked insulin resistance with little insulin-mediated glucose uptake, hypertriglyceridemia, and hepatic transaminase elevations, which are greater in severity than observed in patients with common T2DM. Glucose 152-159 insulin Homo sapiens 135-142 23451796-0 2013 Variability of glucose-lowering effect as a limiting factor in optimizing basal insulin therapy: a review. Glucose 15-22 insulin Homo sapiens 80-87 23451796-3 2013 Furthermore, this glucose variability is, to some extent, a reflection of variability in the glucose-lowering action of the insulin therapy itself. Glucose 18-25 insulin Homo sapiens 124-131 23451796-3 2013 Furthermore, this glucose variability is, to some extent, a reflection of variability in the glucose-lowering action of the insulin therapy itself. Glucose 93-100 insulin Homo sapiens 124-131 23451796-5 2013 The scope for insulin-induced glucose variability is particularly great with basal insulins because of their prolonged absorption from high-dose depots. Glucose 30-37 insulin Homo sapiens 14-21 23493575-8 2013 We conclude that obesity is associated with increased insulin-stimulated glucose metabolism in the brain and that this abnormality can be reversed by bariatric surgery. Glucose 73-80 insulin Homo sapiens 54-61 23756090-1 2013 Closed-loop insulin delivery systems often implement glucose measurement and insulin administration in the subcutis. Glucose 53-60 insulin Homo sapiens 12-19 23557703-4 2013 Islet function was assessed, in vivo, by measuring insulin and glucagon concentrations during oral glucose tolerance test, and, in vitro, by measuring glucose-stimulated insulin and glucagon secretion from human pancreatic islets. Glucose 151-158 insulin Homo sapiens 170-177 23756090-2 2013 However some existing models for glucose-insulin system ignored the dynamics of subcutaneous glucose and subcutaneously-injected insulin. Glucose 33-40 insulin Homo sapiens 41-48 23756090-7 2013 The new glucose-insulin model can mimic dynamics of glucose and insulin under the disturbance of insulin injections and meals. Glucose 8-15 insulin Homo sapiens 16-23 23756090-7 2013 The new glucose-insulin model can mimic dynamics of glucose and insulin under the disturbance of insulin injections and meals. Glucose 8-15 insulin Homo sapiens 64-71 23596179-0 2013 Use of the estimated glucose disposal rate as a measure of insulin resistance in an urban multiethnic population with type 1 diabetes. Glucose 21-28 insulin Homo sapiens 59-66 23596179-2 2013 Estimated glucose disposal rate (eGDR) is a validated clinical tool for estimating insulin sensitivity in type 1 diabetes. Glucose 10-17 insulin Homo sapiens 83-90 23610058-7 2013 Resultant cells were able to secrete insulin in response to glucose and on transplantation were able to normalize blood glucose levels in streptozotocin diabetic NOD/SCID mice. Glucose 60-67 insulin Homo sapiens 37-44 23610058-7 2013 Resultant cells were able to secrete insulin in response to glucose and on transplantation were able to normalize blood glucose levels in streptozotocin diabetic NOD/SCID mice. Glucose 120-127 insulin Homo sapiens 37-44 23643565-9 2013 Either the cytosol to nucleus translocation of pancreatic and duodenal homebox-1, either the expression of insulin, are regulated by glucose concentration changes. Glucose 133-140 insulin Homo sapiens 107-114 23643565-10 2013 Day 21 islet-like structures derived from both human amniotic fluid stem cells and human dental pulp stem cell release insulin in a glucose-dependent manner. Glucose 132-139 insulin Homo sapiens 119-126 23557704-3 2013 We compared the short-term effects of FFA elevation on fasting and glucose-stimulated C-peptide-modeled insulin secretion in prepubertal normal-weight AA versus C peers during a 2-h hyperglycemic clamp (12.5 mmol/L) on two occasions: 1) infusion of normal saline and 2) infusion of 20% intralipid (IL). Glucose 67-74 insulin Homo sapiens 104-111 23557704-5 2013 Glucose sensitivity of first- and second-phase insulin secretion showed a significant condition x race interaction being higher in AA youth. Glucose 0-7 insulin Homo sapiens 47-54 23286324-4 2013 RESULTS: After intensive insulin therapy, fasting plasma glucose and HbA1c levels decreased. Glucose 57-64 insulin Homo sapiens 25-32 23648584-1 2013 Diabetes mellitus is a metabolic disorder that is characterized by high blood glucose because of the insulin-resistance and insulin-deficiency in Type 2, while the insulin deficiency due to destruction of islet cells in the pancreas in Type 1. Glucose 78-85 insulin Homo sapiens 101-108 23428611-1 2013 The artificial pancreas aims at the automatic delivery of insulin for glycemic control in patients with type 1 diabetes, i.e., closed-loop glucose control. Glucose 139-146 insulin Homo sapiens 58-65 23428611-5 2013 It acts on the glucose reference sent to the main controller shaping it so as to avoid violating given constraints on the insulin-on-board. Glucose 15-22 insulin Homo sapiens 122-129 24772944-8 2013 In patients with glucose levels >100 mg/dl, mean BMI, HOMA-IR, insulin, TG, TC and leptin levels were significantly higher than in patients with glucose levels <100 mg/dl. Glucose 17-24 insulin Homo sapiens 66-73 23750032-4 2013 Primary outcome was insulin sensitivity measured using iv glucose tolerance tests and Bergman"s minimal model. Glucose 58-65 insulin Homo sapiens 20-27 23292288-6 2013 Insulin sensitivity (homeostatic model assessment-insulin resistance) was derived from fasting glucose and insulin. Glucose 95-102 insulin Homo sapiens 0-7 24621937-1 2013 OBJECTIVES: This study sought to investigate plasma levels of glucose and free fatty acids (FFA) and their relationship with adrenergic activation and insulin resistance (IR) in patients with advanced congestive heart failure (CHF). Glucose 62-69 insulin Homo sapiens 151-158 24005625-2 2013 Insulin release is chiefly stimulated by glucose, but also modulated by other nutrients, including long-chain fatty acids which potentiate glucose-induced insulin secretion. Glucose 41-48 insulin Homo sapiens 0-7 24005625-2 2013 Insulin release is chiefly stimulated by glucose, but also modulated by other nutrients, including long-chain fatty acids which potentiate glucose-induced insulin secretion. Glucose 139-146 insulin Homo sapiens 0-7 23741049-1 2013 Insulin stimulates glucose transport in fat and muscle cells by regulating delivery of the facilitative glucose transporter, glucose transporter isoform 4 (GLUT4), to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 23741049-6 2013 Depletion of mVps45 in 3T3-L1 adipocytes results in decreased GLUT4 levels and impaired insulin-stimulated glucose transport. Glucose 107-114 insulin Homo sapiens 88-95 23744894-3 2013 We review the literature underlying our current understanding of dopaminergic signaling that can down-regulate glucose-stimulated insulin secretion from pancreatic islets. Glucose 111-118 insulin Homo sapiens 130-137 23744894-4 2013 In this negative feedback loop, dopamine is synthesized in the beta-cells from circulating L-dopa, serves as an autocrine signal that is cosecreted with insulin, and causes a tonic inhibition on glucose-stimulated insulin secretion. Glucose 195-202 insulin Homo sapiens 214-221 23804653-1 2013 Adipocyte glucose uptake in response to insulin is essential for physiological glucose homeostasis: stimulation of adipocytes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose uptake. Glucose 10-17 insulin Homo sapiens 40-47 23804653-1 2013 Adipocyte glucose uptake in response to insulin is essential for physiological glucose homeostasis: stimulation of adipocytes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose uptake. Glucose 10-17 insulin Homo sapiens 131-138 23804653-1 2013 Adipocyte glucose uptake in response to insulin is essential for physiological glucose homeostasis: stimulation of adipocytes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose uptake. Glucose 79-86 insulin Homo sapiens 40-47 23804653-1 2013 Adipocyte glucose uptake in response to insulin is essential for physiological glucose homeostasis: stimulation of adipocytes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose uptake. Glucose 79-86 insulin Homo sapiens 131-138 23804653-1 2013 Adipocyte glucose uptake in response to insulin is essential for physiological glucose homeostasis: stimulation of adipocytes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose uptake. Glucose 79-86 insulin Homo sapiens 40-47 23804653-1 2013 Adipocyte glucose uptake in response to insulin is essential for physiological glucose homeostasis: stimulation of adipocytes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose uptake. Glucose 79-86 insulin Homo sapiens 131-138 23663508-8 2013 Moreover, glucose tolerance during glucose load was abnormal in patients, combining hyperglycemic insulin resistance and hyperinsulinism patterns, while fasting values for glycemia, insulin sensitivity, and insulin concentrations were normal. Glucose 10-17 insulin Homo sapiens 98-105 23663508-8 2013 Moreover, glucose tolerance during glucose load was abnormal in patients, combining hyperglycemic insulin resistance and hyperinsulinism patterns, while fasting values for glycemia, insulin sensitivity, and insulin concentrations were normal. Glucose 10-17 insulin Homo sapiens 126-133 23663508-8 2013 Moreover, glucose tolerance during glucose load was abnormal in patients, combining hyperglycemic insulin resistance and hyperinsulinism patterns, while fasting values for glycemia, insulin sensitivity, and insulin concentrations were normal. Glucose 35-42 insulin Homo sapiens 98-105 23663508-8 2013 Moreover, glucose tolerance during glucose load was abnormal in patients, combining hyperglycemic insulin resistance and hyperinsulinism patterns, while fasting values for glycemia, insulin sensitivity, and insulin concentrations were normal. Glucose 35-42 insulin Homo sapiens 126-133 23549962-8 2013 The insulin response to glucose also tended to be increased after GGF repair, however no concomitant increase in GLP-1 was observed. Glucose 24-31 insulin Homo sapiens 4-11 23585246-7 2013 Insulin sensitivity was evaluated by insulin-mediated glucose utilization (M value), which was obtained using a euglycemic hyperinsulinemic clamp. Glucose 54-61 insulin Homo sapiens 0-7 23585246-7 2013 Insulin sensitivity was evaluated by insulin-mediated glucose utilization (M value), which was obtained using a euglycemic hyperinsulinemic clamp. Glucose 54-61 insulin Homo sapiens 37-44 23585246-9 2013 In a linear regression analysis, the VAI was an independent determinant of the insulin sensitivity after controlling for age, systolic blood pressure, fasting glucose, fasting insulin, and testosterone levels. Glucose 159-166 insulin Homo sapiens 79-86 23997935-2 2013 Because insulin resistance promotes the preservation of glucose and oxidation of fat, it has been suggested to be an adaptive response to food deprivation. Glucose 56-63 insulin Homo sapiens 8-15 23997935-5 2013 Because GLP-1 facilitates glucose-stimulated insulin secretion, these infusions provide a method to assess pancreatic insulin-secreting capacity. Glucose 26-33 insulin Homo sapiens 45-52 24303139-1 2013 Human immunodeficiency virus (HIV)-infected patients with lipodystrophy have decreased insulin-stimulated glucose uptake. Glucose 106-113 insulin Homo sapiens 87-94 24303139-2 2013 Both endurance and resistance training improve insulin-stimulated glucose uptake in skeletal muscle of HIV-infected patients, but the mechanisms are unknown. Glucose 66-73 insulin Homo sapiens 47-54 24303139-3 2013 This study aims to identify the molecular pathways involved in the beneficial effects of training on insulin-stimulated glucose uptake in skeletal muscle of HIV-infected patients. Glucose 120-127 insulin Homo sapiens 101-108 24303139-9 2013 Despite improving insulin-stimulated glucose uptake, neither endurance nor strength training changed the phosphorylation status of insulin signaling proteins or affected GS activity. Glucose 37-44 insulin Homo sapiens 18-25 24303139-11 2013 HIV-infected patients with lipodystrophy have decreased insulin-stimulated glucose uptake in skeletal muscle and defects in insulin-stimulated phosphorylation of Akt(thr308). Glucose 75-82 insulin Homo sapiens 56-63 24303139-12 2013 Endurance and strength training increase insulin-stimulated glucose uptake in these patients, and the muscular training adaptation is associated with improved capacity for phosphorylation of glucose by HKII, rather than changes in markers of insulin signaling to glucose uptake or glycogen synthesis. Glucose 60-67 insulin Homo sapiens 41-48 23936417-2 2013 The pancreatic islets of Langerhans are responsible for secreting the hormone insulin in response to glucose stimulation. Glucose 101-108 insulin Homo sapiens 78-85 23218116-2 2013 Insulin resistance was indexed using homeostasis model assessment of insulin resistance (HOMA-IR) (US formula: fasting insulin (muU/ml) x fasting glucose (mg/dl)/405 international formula: fasting glucose (mmol/l) x fasting insulin (muU/l)/22.5). Glucose 146-153 insulin Homo sapiens 0-7 23218116-2 2013 Insulin resistance was indexed using homeostasis model assessment of insulin resistance (HOMA-IR) (US formula: fasting insulin (muU/ml) x fasting glucose (mg/dl)/405 international formula: fasting glucose (mmol/l) x fasting insulin (muU/l)/22.5). Glucose 197-204 insulin Homo sapiens 0-7 23883613-1 2013 INTRODUCTION: Closed-loop (CL) systems modulate insulin delivery according to glucose levels without nurse input. Glucose 78-85 insulin Homo sapiens 48-55 23894584-1 2013 BACKGROUND: The glucokinase regulatory protein encoded by GCKR plays an important role in glucose metabolism and a single nucleotide polymorphism (SNP) rs1260326 (P446L) in the gene has been associated with several age-related biomarkers, including triglycerides, glucose, insulin and apolipoproteins. Glucose 90-97 insulin Homo sapiens 273-280 23752741-3 2013 This novel kind of microgel with a narrow size distribution (~250 nm) is suitable for diabetes because it can adapt to the surrounding medium of different glucose concentrations over a clinically relevant range (0-20 mM), control the release of preloaded insulin and is highly stable under physiological conditions (pH 7.4, 0.15 M NaCl, 37 C). Glucose 155-162 insulin Homo sapiens 255-262 23879510-1 2013 OBJECTIVE: To examine the relationships between birthweight, current size, and fasting glucose and fasting insulin levels in Aboriginal adolescents. Glucose 87-94 insulin Homo sapiens 107-114 23789889-1 2013 BACKGROUND: The threshold-suspend feature of sensor-augmented insulin pumps is designed to minimize the risk of hypoglycemia by interrupting insulin delivery at a preset sensor glucose value. Glucose 177-184 insulin Homo sapiens 62-69 23866690-5 2013 RESULTS: Palmitate-induced cellular insulin resistance was clarified by the reduced Akt phosphorylation, glucose uptake and Glut4 expression. Glucose 105-112 insulin Homo sapiens 36-43 23868462-4 2013 Insulin resistance is associated with a decrease in glucose uptake by neurons, an increase in Amyloid beta production and secretion, in the formation of senile plaques, and also in tau protein phosphorylation. Glucose 52-59 insulin Homo sapiens 0-7 23875003-4 2013 3xTg-AD mice fed 0.23% w/v lipoic acid in drinking water for 4 weeks showed an insulin mimetic effect that consisted of increased brain glucose uptake, activation of the insulin receptor substrate and of the PI3K/Akt signaling pathway. Glucose 136-143 insulin Homo sapiens 79-86 23874650-1 2013 Insulin increases cellular glucose uptake and metabolism in the postprandial state by acutely stimulating the translocation of the Glut4 glucose transporter from intracellular membrane compartments to the cell surface in muscle and fat cells. Glucose 27-34 insulin Homo sapiens 0-7 23849162-8 2013 Their oral glucose tolerance tests showed extremely high levels of insulinemia, revealing major insulin resistance. Glucose 11-18 insulin Homo sapiens 67-74 23819910-12 2013 Insulin treatment was associated with HOMA-IR (<1.29 vs. >2.89), OR: 3.37, fasting glucose (<=6.11 vs. >6.11 mmol/dl), OR: 2.61, age (<=30 vs. >30 y. Glucose 89-96 insulin Homo sapiens 0-7 23958569-8 2013 Insulin analogues statistically significantly improved glucose control (HbA1c, FPG and PPPG, p < 0.001) at Week 24. Glucose 55-62 insulin Homo sapiens 0-7 23969997-2 2013 Pancreatic islet beta cells secrete insulin in response to nutrient stimuli, and insulin then travels through the circulation promoting glucose uptake into insulin-responsive tissues such as liver, skeletal muscle and adipose. Glucose 136-143 insulin Homo sapiens 81-88 23819910-15 2013 Maximum insulin dose was associated with HOMA-IR, OR: 2.00, after adjustment for family history of diabetes, and 2-h OGTT glucose. Glucose 122-129 insulin Homo sapiens 8-15 23844030-6 2013 This reduction in insulin exocytosis was attributed mainly to reduction in recruitment and exocytosis of newcomer insulin granules that undergo minimal docking time at the plasma membrane, but which encompassed a larger portion of biphasic glucose stimulated insulin secretion. Glucose 240-247 insulin Homo sapiens 18-25 23823221-1 2013 Glucose-stimulated insulin secretion is pulsatile and driven by intrinsic oscillations in metabolism, electrical activity, and Ca(2+) in pancreatic islets. Glucose 0-7 insulin Homo sapiens 19-26 23823221-2 2013 Periodic variations in glucose can entrain islet Ca(2+) and insulin secretion, possibly promoting interislet synchronization. Glucose 23-30 insulin Homo sapiens 60-67 23274913-6 2013 In addition, co-overexpression of TFAM-enhanced insulin-stimulated glucose uptake by increasing Glucose transporter type 4 (GLUT4) translocation to the PM in NYGGF4-overexpressing adipocytes. Glucose 67-74 insulin Homo sapiens 48-55 23651848-6 2013 Our data reveal that sTWEAK ameliorates TNF-alpha-induced insulin resistance on glucose uptake, GLUT4 translocation and insulin signaling without affecting other metabolic effects of TNF-alpha such as lipolysis or apoptotis. Glucose 80-87 insulin Homo sapiens 58-65 23838633-1 2013 Plasma glucose level depends on the peripheral intra-islet crosstalk between A cells (glucagon) + B-cells (insulin) and D-cells (somatostatin). Glucose 7-14 insulin Homo sapiens 107-114 23838633-2 2013 Gastrointestinal hormones (secretin, CCK-PZ, gastrin, and serotonin) modulate the glucose- and amino acids-induced secretions of insulin and glucagon, respectively. Glucose 82-89 insulin Homo sapiens 129-136 23110868-3 2013 Euglycemic hyperinsulinemic clamp is a method of estimating insulin sensitivity, based on the assumption that during steady-state hyperinsulinemic euglycemia, glucose infusion rate equals tissue glucose uptake, that is, the higher the glucose infusion rate, the higher the insulin sensitivity. Glucose 159-166 insulin Homo sapiens 16-23 23110868-3 2013 Euglycemic hyperinsulinemic clamp is a method of estimating insulin sensitivity, based on the assumption that during steady-state hyperinsulinemic euglycemia, glucose infusion rate equals tissue glucose uptake, that is, the higher the glucose infusion rate, the higher the insulin sensitivity. Glucose 159-166 insulin Homo sapiens 60-67 23110868-3 2013 Euglycemic hyperinsulinemic clamp is a method of estimating insulin sensitivity, based on the assumption that during steady-state hyperinsulinemic euglycemia, glucose infusion rate equals tissue glucose uptake, that is, the higher the glucose infusion rate, the higher the insulin sensitivity. Glucose 195-202 insulin Homo sapiens 60-67 23110868-3 2013 Euglycemic hyperinsulinemic clamp is a method of estimating insulin sensitivity, based on the assumption that during steady-state hyperinsulinemic euglycemia, glucose infusion rate equals tissue glucose uptake, that is, the higher the glucose infusion rate, the higher the insulin sensitivity. Glucose 195-202 insulin Homo sapiens 60-67 23939605-11 2013 Insulin therapy may be required to maintain serum glucose levels less than 180 mg per dL. Glucose 50-57 insulin Homo sapiens 0-7 23459193-5 2013 Endogenous GLP-1 is an incretin hormone composed by a 30-amino acid peptide and is secreted from L-cells in distal small intestine in response to calorie intake, causing a glucose-dependent beta-cell response resulting in a restoration of the first-phase insulin response. Glucose 172-179 insulin Homo sapiens 255-262 23524173-11 2013 Logistic regression analysis showed that gestational age at diagnosis and mean pretreatment glucose level were predictors of the need for supplemental insulin therapy in women initially treated with metformin. Glucose 92-99 insulin Homo sapiens 151-158 24116330-3 2013 AIM: This study was intended to assess the effects of antioxidants; alpha lipoic acid (ALA), omega 3 fatty acid and vitamin E on parameters of insulin sensitivity (blood glucose and HbA1c) in patients of type 2 diabetes mellitus with documented insulin resistance. Glucose 170-177 insulin Homo sapiens 143-150 23042260-4 2013 Hesperetin was also found to inhibit insulin-induced glucose uptake through impaired cell membrane translocation of glucose transporter 4 (GLUT4). Glucose 53-60 insulin Homo sapiens 37-44 23325573-3 2013 Specifically, the effect of a 50-g glucose challenge test (GCT) on heat shock protein and insulin levels in the circulation 1 h later was evaluated. Glucose 35-42 insulin Homo sapiens 90-97 23325573-11 2013 The release of hsp72 may regulate the extent of insulin production in response to a glucose challenge and, thereby, protect the mother and/or fetus from development of hyperglycemia, hyperinsulinemia, and/or immune system alterations. Glucose 84-91 insulin Homo sapiens 48-55 23393209-10 2013 CONCLUSIONS: At 36 weeks, maternal triglycerides were related to glucose control in women treated with insulin and ethnicity in women treated with metformin. Glucose 65-72 insulin Homo sapiens 103-110 23370777-5 2013 Vaspin treatment of isolated pancreatic islets leads to increased insulin concentration in the media upon glucose stimulation without influencing insulin secretion. Glucose 106-113 insulin Homo sapiens 66-73 23423565-5 2013 Interestingly, the delivery of cytosol from control ASCs into obese-derived ASCs using a lipid-based, protein-capture methodology restored insulin sensitivity on glucose and lipid metabolism and reversed the proinflammatory cytokine profile, in part due to the restoration of Lin28 protein levels. Glucose 162-169 insulin Homo sapiens 139-146 23436340-2 2013 Interventions that help improve glucose tolerance by attenuating pregnancy-induced insulin resistance or achieve glycaemic control may therefore help in preventing and managing GDM. Glucose 32-39 insulin Homo sapiens 83-90 23454694-4 2013 After 6 h, whole-body insulin sensitivity was reduced by iv fat, po fat, and LPS to 60, 67, and 48%, respectively (all P < 0.01), which was due to decreased nonoxidative glucose utilization, while hepatic insulin sensitivity was unaffected. Glucose 173-180 insulin Homo sapiens 22-29 23454694-7 2013 Po fat ingestion rapidly induces insulin resistance by reducing nonoxidative glucose disposal, which associates with PKCtheta activation and a rise in distinct myocellular membrane DAG, while endotoxin-induced insulin resistance is exclusively associated with stimulation of inflammatory pathways. Glucose 77-84 insulin Homo sapiens 33-40 23463496-5 2013 Insulin resistance was assessed by measurement of fasting circulating insulin levels before and after an oral glucose tolerance test and by HOMA-IR. Glucose 110-117 insulin Homo sapiens 0-7 23463496-7 2013 Importantly, lower insulin levels were also observed 2 h after oral glucose tolerance test in C allele carriers (p = 0.009). Glucose 68-75 insulin Homo sapiens 19-26 23493574-8 2013 These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of the syndrome. Glucose 75-82 insulin Homo sapiens 56-63 23578166-0 2013 Hypoglycemia observed during continuous glucose monitoring in patients with type 2 diabetes mellitus treated by subcutaneous insulin injection. Glucose 40-47 insulin Homo sapiens 125-132 23578166-1 2013 BACKGROUND: The relationship between hypoglycemia and the dose of insulin used in patients with type 2 diabetes mellitus was investigated by continuous glucose monitoring (CGM). Glucose 152-159 insulin Homo sapiens 66-73 23578166-4 2013 The proportion of time in the hypoglycemic range (blood glucose<3.9 mmol/L) during CGM was positively correlated with the bolus insulin ratio (bolus/total insulin dose, r=0.22, P=0.04), although it was not associated with the total dose of insulin or the hemoglobin A1c (HbA1c) level. Glucose 56-63 insulin Homo sapiens 131-138 23604550-5 2013 RESULTS: Insulin secretory responses to glucose, pyruvate, KIC and glutamine were higher in pseudoislets than monolayers and comparable to those of human islets. Glucose 40-47 insulin Homo sapiens 9-16 23604550-8 2013 PI3K inhibition only slightly attenuated glucose-stimulated insulin secretion from monolayers, but substantially reduced that from pseudoislets and human and mouse islets without suppressing the glucose-induced [Ca(2+)]c response. Glucose 41-48 insulin Homo sapiens 60-67 23512401-1 2013 The correlation between once-daily basal insulin doses to the fasting plasma glucose in type 2 diabetes. Glucose 77-84 insulin Homo sapiens 41-48 23677932-2 2013 Here, we report that Crtc2 is essential both for glucose-stimulated insulin secretion and cell survival in the beta-cell. Glucose 49-56 insulin Homo sapiens 68-75 23411637-1 2013 Early alterations in glucose homeostasis increase the risk of developing insulin resistance and obesity later in life. Glucose 21-28 insulin Homo sapiens 73-80 23592224-6 2013 An oral glucose tolerance test measured areas under the curve (AUC) for insulin (AUC 2h insulin) and for glucose (AUC 2h glucose). Glucose 8-15 insulin Homo sapiens 72-79 23592224-6 2013 An oral glucose tolerance test measured areas under the curve (AUC) for insulin (AUC 2h insulin) and for glucose (AUC 2h glucose). Glucose 8-15 insulin Homo sapiens 88-95 23961474-8 2013 In addition, therapy must be linked to monitoring of blood glucose to enable effective use of insulin therapy. Glucose 59-66 insulin Homo sapiens 94-101 23069666-3 2013 As a result of the increases in circulating fatty acids and insulin resistance that accompanies excess fat storage, several of the proteins and genes that are responsible for fatty acid uptake and metabolism are upregulated, and the metabolic machinery responsible for glucose utilization and oxidation are inhibited. Glucose 269-276 insulin Homo sapiens 60-67 23748472-10 2013 Both polymorphisms influenced insulin related traits (2 h glucose, fasting insulin and HOMA-IR) and improved glucose metabolism in these women. Glucose 58-65 insulin Homo sapiens 30-37 23616151-5 2013 Insulin sensitivity was estimated from an oral glucose tolerance test (OGTT), and mononuclear cells were isolated to assess reactive oxygen species production during the OGTT. Glucose 47-54 insulin Homo sapiens 0-7 23666972-8 2013 Insulin resistance (19.8 +- 0.8 mumol min-1 kg(ffm)-1, P < .001 vs 40.9 +- 5.3 of controls) resolved already at 2 months (34.2 +- 2.8) and was sustained at 1 year (34.7 +- 1.6), although insulin-mediated suppression of endogenous glucose production remained impaired. Glucose 237-244 insulin Homo sapiens 0-7 23998049-2 2013 Insulin is a hormone that regulates the body"s use of glucose. Glucose 54-61 insulin Homo sapiens 0-7 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 118-125 insulin Homo sapiens 80-87 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 118-125 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 118-125 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 118-125 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 224-231 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 224-231 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 224-231 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 224-231 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 224-231 insulin Homo sapiens 169-176 23911169-5 2013 RESULTS: Among cases selected for analysis (n = 119), examination of changes in insulin use based on tertiles of mean glucose showed that use of basal plus short-acting insulin increased from 10% in the lowest tertile (mean glucose, 120 mg/dl) to 18% in the highest tertile (mean glucose, 198 mg/dl; p < .01); however, 70% of patients in the highest tertile continued to receive short-acting insulin only, with 12% receiving no insulin. Glucose 224-231 insulin Homo sapiens 169-176 23911174-9 2013 CONCLUSIONS: Improved glucose regulation was demonstrated using the dIOB where circadian insulin sensitivity is used to adjust IOB estimation. Glucose 22-29 insulin Homo sapiens 89-96 23911175-2 2013 The availability of a simulator that incorporates glucagon as a counterregulatory hormone to insulin would allow more efficient design of bihormonal glucose controllers. Glucose 149-156 insulin Homo sapiens 93-100 23911175-13 2013 CONCLUSIONS: A novel composite model, which can be easily identified with standard clinical data, is able to account for the effect of exogenous insulin and glucagon infusion on glucose dynamics. Glucose 178-185 insulin Homo sapiens 145-152 23911176-2 2013 This article presents results from the comparative analysis of the parametric MM and a nonparametric Laguerre based Volterra Model (LVM) applied to the analysis of insulin modified (IM) intravenous glucose tolerance test (IVGTT) data from a clinical study of gestational diabetes mellitus (GDM). Glucose 198-205 insulin Homo sapiens 164-171 23911176-5 2013 In the nonparametric LVM analysis, the glucose and insulin data were used to calculate the first-order kernel, from which a diagnostic scalar index representing the integrated effect of insulin on glucose was derived. Glucose 197-204 insulin Homo sapiens 186-193 23911176-8 2013 CONCLUSIONS: It was found that the data based nonparametric LVM revealed additional insights about the manner in which infused insulin affects blood glucose concentration. Glucose 149-156 insulin Homo sapiens 127-134 23911178-10 2013 CONCLUSIONS: The on-device Pattern tool identified meaningful blood glucose patterns, highlighting potential opportunities for improving glycemic control in patients who self-adjust their insulin. Glucose 68-75 insulin Homo sapiens 188-195 23911183-2 2013 The Paradigm Veo system may mitigate nocturnal hypoglycemia by automatically suspending insulin when a prespecified sensor glucose threshold is reached. Glucose 125-132 insulin Homo sapiens 90-97 23911183-5 2013 The treatment arm used sensor-augmented pump therapy with threshold suspend, which automatically suspends the insulin pump in response to a sensor glucose value at or below a prespecified threshold. Glucose 147-154 insulin Homo sapiens 110-117 26120590-2 2013 Since skeletal muscle is responsible for 70-80% of insulin-stimulated glucose uptake, skeletal muscle IR is a key pathological component of type 2 diabetes (T2D). Glucose 70-77 insulin Homo sapiens 51-58 23864804-8 2013 Insulin sensitivity was estimated using the metabolic clearance rate (MCR) of glucose calculated from the oral glucose tolerance test. Glucose 78-85 insulin Homo sapiens 0-7 23864804-8 2013 Insulin sensitivity was estimated using the metabolic clearance rate (MCR) of glucose calculated from the oral glucose tolerance test. Glucose 111-118 insulin Homo sapiens 0-7 24341187-5 2013 The syndrome of resistance to insulin consists in the derangement of humoral regulation of metabolism of fatty acids and glucose at the phylogenetically different levels in vivo both in paracrine cells cenosis and at the level of organism. Glucose 121-128 insulin Homo sapiens 30-37 24341187-10 2013 Primarily, insulin regulates metabolism of fatty acids and only secondly metabolic transformations of glucose. Glucose 102-109 insulin Homo sapiens 11-18 23357530-2 2013 Among these changes are decreased reliance on the counter-regulatory dynamics by insulin-glucagon due to reduced glucose utilization, and increased concentrations of lipid substrates in plasma to meet the energetic demands of peripheral tissues. Glucose 113-120 insulin Homo sapiens 81-88 23660596-1 2013 The reduction in the expression of glucose-responsive insulin gene transcription factor MafA accompanies the development of beta-cell dysfunction under oxidative stress/diabetic milieu. Glucose 35-42 insulin Homo sapiens 54-61 23178285-1 2013 UNLABELLED: Distinct biochemical, electrochemical and electromechanical coupling processes of pancreatic beta-cells may well underlie different response patterns of insulin release from glucose and capsaicin stimulation. Glucose 186-193 insulin Homo sapiens 165-172 23743464-7 2013 Within the 500 units/mL concentrated insulin cohort, after initiation of this medication, fasting and postprandial blood glucose concentrations improved. Glucose 121-128 insulin Homo sapiens 37-44 23827131-4 2013 Insulin sensitivity was calculated using the homeostatic model assessment of insulin resistance We hypothesized that IGF-I, insulin, and glucose concentrations would decrease and IGFBP-3 concentration would increase in response to the low-fat diets. Glucose 137-144 insulin Homo sapiens 0-7 23455976-5 2013 Insulin resistance was evaluated at baseline by the homeostasis model assessment method (HOMA-IR) using fasting glucose and insulin levels. Glucose 112-119 insulin Homo sapiens 0-7 23957200-5 2013 Measuring C-peptide routinely in Type 1 diabetes provides valuable information to the patient and clinician about glucose variability, risk of hypoglycemia and ketoacidosis. Glucose 114-121 insulin Homo sapiens 10-19 24303118-9 2013 These results indicate that insulin sensitivity following exercise is blunted by H1- and H2-receptor blockade and suggest that postexercise H1- and H2-receptor-mediated skeletal muscle vasodilatation benefits glucose regulation in healthy humans. Glucose 209-216 insulin Homo sapiens 28-35 23840881-4 2013 Primary outcome was insulin sensitivity measured using intravenous glucose tolerance tests and Bergman"s minimal model. Glucose 67-74 insulin Homo sapiens 20-27 23840881-7 2013 There was a compensatory increase in acute insulin response among post-term children (418 vs 304 mU/l; p=0.037), who also displayed lower glucose effectiveness than those born at term (2.25 vs 3.11 x10-2 min-1; p=0.047). Glucose 138-145 insulin Homo sapiens 43-50 23900470-6 2013 Clinical parameters of diagnostic importance were noted, and homeostatic model assessment of insulin resistance (HOMA-IR) was calculated using fasting insulin and fasting blood glucose ratio. Glucose 177-184 insulin Homo sapiens 93-100 23909258-2 2013 In the metabolism of saccharides GLP1 stimulates synthesis of glycogen and reduces glucose production - thus acting like insulin. Glucose 83-90 insulin Homo sapiens 122-129 23690508-6 2013 Furthermore, insulin treatment under a high-glucose condition resulted in increased histone H3 phosphorylation and de-acetylation only in MDA-MB-231 cells. Glucose 44-51 insulin Homo sapiens 13-20 23826284-1 2013 BACKGROUND: Neighboring genes PIK3CA and KCNMB3 are both important for insulin signaling and beta-cell function, but their associations with glucose-related traits are unclear. Glucose 141-148 insulin Homo sapiens 71-78 23826312-5 2013 We have developed gene constructs which cause glucose-concentration-dependent human insulin production in liver cells. Glucose 46-53 insulin Homo sapiens 84-91 23826312-7 2013 Hepatocytes transduced with the new constructs, ex vivo, produced large amounts of glucose-inducible human insulin. Glucose 83-90 insulin Homo sapiens 107-114 23826312-10 2013 Intraperitoneal glucose tolerance test (IPGT) demonstrated in vivo glucose-responsive changes in insulin levels to correct hyperglycemia within 45 minutes. Glucose 16-23 insulin Homo sapiens 97-104 23826312-10 2013 Intraperitoneal glucose tolerance test (IPGT) demonstrated in vivo glucose-responsive changes in insulin levels to correct hyperglycemia within 45 minutes. Glucose 67-74 insulin Homo sapiens 97-104 23826312-13 2013 Non-viral insulin minicircle DNA-based TA1m mediated glucose-dependent insulin production in liver may represent a safe and promising approach to treat T1DM. Glucose 53-60 insulin Homo sapiens 10-17 23825606-5 2013 Insulin effectively reduces glucose levels and thereby contributes to protection. Glucose 28-35 insulin Homo sapiens 0-7 23805253-6 2013 Middle-aged sedentary cells had intact insulin-stimulated Akt phosphorylation however, the same cell showed ablated insulin-stimulated glucose uptake and GLUT4 translocation to the plasma membrane. Glucose 135-142 insulin Homo sapiens 116-123 23805253-7 2013 On the other hand, middle-aged active cells retained both insulin-stimulated increases in glucose uptake and GLUT4 translocation to the plasma membrane. Glucose 90-97 insulin Homo sapiens 58-65 23099275-5 2013 Oral delivery of proinsulin or exendin-4 expressed in plant cells regulated blood glucose levels similar to injections. Glucose 82-89 insulin Homo sapiens 17-27 23592483-6 2013 Chronic insulin treatment of diabetic rats, which nearly normalized glucose levels, markedly reduced neuronal damage induced by severe hypoglycemia. Glucose 68-75 insulin Homo sapiens 8-15 23589285-10 2013 Furthermore, A347S disrupted KLF11-mediated increases in basal insulin levels and promoter activity and blunted glucose-stimulated insulin secretion. Glucose 112-119 insulin Homo sapiens 131-138 23702482-6 2013 In L6 muscle cells treated with insulin and chloroquine, the phosphorylation of Akt and glucose uptake were dramatically increased compared to cells treated with insulin alone, suggesting that chloroquine is a potent activator of Akt and glucose uptake in these cells. Glucose 88-95 insulin Homo sapiens 32-39 23702482-6 2013 In L6 muscle cells treated with insulin and chloroquine, the phosphorylation of Akt and glucose uptake were dramatically increased compared to cells treated with insulin alone, suggesting that chloroquine is a potent activator of Akt and glucose uptake in these cells. Glucose 238-245 insulin Homo sapiens 32-39 23798995-9 2013 We used this and other information to formulate a mathematical model to estimate the local insulin concentration within a single islet as a function of glucose. Glucose 152-159 insulin Homo sapiens 91-98 23798995-12 2013 Model analysis predicted that the majority of monomeric insulin in the islet is that which has been returned from the periphery, and the concentration of intra-islet monomeric insulin varies from ~50-300 pM when glucose is in the physiological range. Glucose 212-219 insulin Homo sapiens 176-183 23799144-2 2013 The 12Ala allele carriers display a significantly improved insulin sensitivity that may result in better glucose utilisation in working skeletal muscles. Glucose 105-112 insulin Homo sapiens 59-66 23776620-11 2013 Importantly, glucose-stimulated insulin secretion and content were not downregulated by L-WRN medium treatment. Glucose 13-20 insulin Homo sapiens 32-39 23776669-1 2013 BACKGROUND: Plasma interleukin-6 (IL-6) concentrations decrease acutely 1 h after ingestion of a glucose load or mixed meals and this may be mediated by an anti-inflammatory effect of insulin. Glucose 97-104 insulin Homo sapiens 184-191 23776669-8 2013 Circulating insulin concentrations were significantly (P<0.001) and 2.8 fold higher following oral compared with intravenous glucose administration. Glucose 128-135 insulin Homo sapiens 12-19 23776669-9 2013 CONCLUSIONS: These data show that plasma IL-6 concentrations did not decrease during isoglycemic, intravenous glucose administration suggesting that the markedly higher circulating insulin levels and/or gut-related factors may mediate the acute decrease in plasma IL-6 after oral glucose intake in overweight/obese subjects. Glucose 280-287 insulin Homo sapiens 181-188 23589428-9 2013 Higher C-peptide levels were associated with increased mortality among strata of glycated hemoglobin and fasting serum glucose. Glucose 119-126 insulin Homo sapiens 7-16 23752133-5 2013 Consistent with the clamp findings, T2D subjects had impaired insulin-stimulated phosphorylation of AS160 Thr(642), a site previously shown to be important in glucose uptake in rodents. Glucose 159-166 insulin Homo sapiens 62-69 23752133-8 2013 Impaired insulin-stimulated glucose uptake in T2D subjects is accompanied by dysregulation of AS160 and TBC1D1 phosphorylation in skeletal muscle, suggesting that these proteins may regulate glucose uptake in humans. Glucose 28-35 insulin Homo sapiens 9-16 23752133-8 2013 Impaired insulin-stimulated glucose uptake in T2D subjects is accompanied by dysregulation of AS160 and TBC1D1 phosphorylation in skeletal muscle, suggesting that these proteins may regulate glucose uptake in humans. Glucose 191-198 insulin Homo sapiens 9-16 23736775-7 2013 The differentiated cells appropriately processed C-peptide and insulin in response to increasing glucose stimulation as shown by enzyme-linked immunosorbent assay (ELISA), fluorescence-activated cell sorting analysis, western blotting, and immunofluorescence staining. Glucose 97-104 insulin Homo sapiens 63-70 23844380-5 2013 Muscle biopsies performed during euglycemic hyperinsulinemic clamp showed a significant reduction in glucose uptake, and insulin-mediated IRS-2 increased significantly in skeletal muscle. Glucose 101-108 insulin Homo sapiens 49-56 22215127-14 2013 Insulin sensitivity appears to be incompletely described by functions of fasting glucose and insulin values alone and the use of other indices, such as LAP could be suggested. Glucose 81-88 insulin Homo sapiens 0-7 22907764-1 2013 Primary objective was to evaluate whether an intensified insulin therapy (IIT) incorporating the target of normal fasting glucose and HbA1c levels could halve the incidence of restenosis/amputation/SCA/death at 6 months after peripheral angioplasty compared with standard care (SC) in patients with type 2 diabetes (DMT2) affected by critical limb ischemia (CLI). Glucose 122-129 insulin Homo sapiens 57-64 23633267-2 2013 We present our experience of glucose-sensitive insulin-secreting mesenchymal stem cells (IS-MSC) generated and differentiated from human adipose tissue (h-AD) with application of specific differentiation media, sans xenogenic material. Glucose 29-36 insulin Homo sapiens 47-54 23968657-9 2013 The blood glucose concentration was significantly increased and consequently, consumption of insulin was increased on the 2(nd) day of ICU admission. Glucose 10-17 insulin Homo sapiens 93-100 23584594-9 2013 Overall, the glucose-modified insulin molecules under reducing and nonreducing systems display different structural features having significant consequences on aggregation behaviors and surface tension properties. Glucose 13-20 insulin Homo sapiens 30-37 23633267-8 2013 IS-MSC showed presence of all three transcriptional factors and showed rise in insulin and c-peptide level in presence of glucose stimuli. Glucose 122-129 insulin Homo sapiens 91-100 23633267-9 2013 It can be concluded that the specific extrinsic factors used in the defined differentiation media effectively and safely promote differentiation of glucose-sensitive insulin-secreting cells from human adipose tissue, without any genetic modulation. Glucose 148-155 insulin Homo sapiens 166-173 23683103-1 2013 Carbohydrate metabolism in humans is regulated by insulin secretion from pancreatic beta-cells and glucose disposal by insulin-sensitive tissues. Glucose 99-106 insulin Homo sapiens 119-126 23499910-1 2013 The small GTPase Rac1 plays a pivotal role in insulin-stimulated glucose uptake in skeletal muscle, which is mediated by GLUT4 translocation to the plasma membrane. Glucose 65-72 insulin Homo sapiens 46-53 23423567-0 2013 Rac1 signaling is required for insulin-stimulated glucose uptake and is dysregulated in insulin-resistant murine and human skeletal muscle. Glucose 50-57 insulin Homo sapiens 31-38 23423567-2 2013 However, involvement of Rac1 and its downstream signaling in glucose transport in insulin-sensitive and insulin-resistant mature skeletal muscle has not previously been investigated. Glucose 61-68 insulin Homo sapiens 82-89 23423567-2 2013 However, involvement of Rac1 and its downstream signaling in glucose transport in insulin-sensitive and insulin-resistant mature skeletal muscle has not previously been investigated. Glucose 61-68 insulin Homo sapiens 104-111 23423567-3 2013 We hypothesized that Rac1 and its downstream target, p21-activated kinase (PAK), are regulators of insulin-stimulated glucose uptake in mouse and human skeletal muscle and are dysregulated in insulin-resistant states. Glucose 118-125 insulin Homo sapiens 99-106 23423567-4 2013 Muscle-specific inducible Rac1 knockout (KO) mice and pharmacological inhibition of Rac1 were used to determine whether Rac1 regulates insulin-stimulated glucose transport in mature skeletal muscle. Glucose 154-161 insulin Homo sapiens 135-142 23423567-6 2013 Inhibition and KO of Rac1 decreased insulin-stimulated glucose transport in mouse soleus and extensor digitorum longus muscles ex vivo. Glucose 55-62 insulin Homo sapiens 36-43 23423567-10 2013 These findings show that Rac1 is a regulator of insulin-stimulated glucose uptake and a novel candidate involved in skeletal muscle insulin resistance. Glucose 67-74 insulin Homo sapiens 48-55 23683103-2 2013 Insulin facilitates glucose utilization in peripheral tissues and suppresses hepatic glucose production. Glucose 20-27 insulin Homo sapiens 0-7 23683103-2 2013 Insulin facilitates glucose utilization in peripheral tissues and suppresses hepatic glucose production. Glucose 85-92 insulin Homo sapiens 0-7 23250633-2 2013 More than just a means of recording and storing data, some blood glucose meters (BGMs) are now designed with an embedded automated bolus calculator (ABC) with the goal to propose patients recommendations about insulin dosage. Glucose 65-72 insulin Homo sapiens 210-217 23061470-5 2013 Short-acting GLP-1 RAs such as exenatide twice daily are particularly effective at reducing postprandial glucose while basal insulin has a greater effect on fasting glucose, providing a physiological rationale for this complementary approach. Glucose 165-172 insulin Homo sapiens 125-132 23587481-4 2013 The results were interpreted as the slope of the changes of plasma insulin against the glucose levels. Glucose 87-94 insulin Homo sapiens 67-74 23757032-11 2013 CONCLUSION: Insulin aspart +- OGLDs is associated with significant improvements in glycemic control and HRQoL, without increased risk of hypoglycemia, in people with type 2 diabetes and sub-optimal glucose control. Glucose 198-205 insulin Homo sapiens 12-19 23704681-6 2013 RESEARCH DESIGN AND METHODS: We identified studies that measured the insulin sensitivity index (SI) and acute insulin response to glucose (AIRg) in three major ethnic groups: Africans, Caucasians, and East Asians. Glucose 130-137 insulin Homo sapiens 110-117 23315993-2 2013 Syntaxin-1a -(Stx-1a) is one of two t-SNAREs involved in insulin exocytosis and decreased expression of Stx-1a protein impairs glucose-stimulated insulin secretion (GSIS) in isolated rat pancreatic islets. Glucose 127-134 insulin Homo sapiens 57-64 23713695-3 2013 Furthermore, type 2 diabetes mellitus (T2DM), a condition in which an individual"s ability to respond to insulin is lowered, is treated by drugs called thiazolidinediones (TZDs) that are known to activated PPAR-gamma, thus augmenting insulin signaling and glucose uptake by adipose tissue. Glucose 256-263 insulin Homo sapiens 105-112 23493357-0 2013 A ~60-min brisk walk increases insulin-stimulated glucose disposal but has no effect on hepatic and adipose tissue insulin sensitivity in older women. Glucose 50-57 insulin Homo sapiens 31-38 23493357-4 2013 The insulin-mediated decrease in glucose Ra during stage 1 of the clamp was also not different after rest and exercise (82.2% +- 3.4% and 77.7% +- 2.1%, respectively), but glucose rate of disappearance (Rd) during stage 2 of the clamp was significantly greater (P < 0.05) after exercise than rest (88.0 +- 5.9 and 78.4 +- 6.5 mumol/kg fat-free mass per min, respectively). Glucose 33-40 insulin Homo sapiens 4-11 23539730-14 2013 CONCLUSION: Aldosterone excess has a direct negative effect on beta-cell function in patients with PA. After adrenalectomy, glucose-induced first-phase insulin secretion improves significantly in the patients. Glucose 124-131 insulin Homo sapiens 152-159 24640202-6 2013 These two metabolic parameters were used to derive (Homeostatic Model Assessment) HOMA index for insulin resistance and Glucose-to-Insulin Ratio (GIR). Glucose 120-127 insulin Homo sapiens 131-138 23589527-1 2013 BACKGROUND: Infusion of ghrelin to supraphysiologic levels inhibits glucose-stimulated insulin secretion, reduces insulin sensitivity, and worsens glucose tolerance in humans. Glucose 68-75 insulin Homo sapiens 87-94 23589527-6 2013 Insulin secretion was measured as the acute insulin response to glucose (AIRg) and the disposition index was computed as AIRg x SI. Glucose 64-71 insulin Homo sapiens 0-7 23589527-6 2013 Insulin secretion was measured as the acute insulin response to glucose (AIRg) and the disposition index was computed as AIRg x SI. Glucose 64-71 insulin Homo sapiens 44-51 23529132-5 2013 Insulin-stimulated total glucose disposal (TGD), plasma FFA species, muscle insulin signalling, IBalpha protein, c-Jun phosphorylation, inflammatory gene (toll-like receptor 4 and monocyte chemotactic protein 1) expression, and ceramide and diacylglycerol (DAG) content were measured in muscle from a group of obese and T2DM subjects before and after administration of the antilipolytic drug acipimox for 7 days, and the results were compared to lean individuals. Glucose 25-32 insulin Homo sapiens 0-7 23579487-1 2013 Central resistance to the actions of insulin and leptin is associated with the onset of obesity and type 2 diabetes mellitus, whereas leptin and insulin signaling is essential for both glucose and energy homeostasis. Glucose 185-192 insulin Homo sapiens 145-152 23511925-5 2013 Ultrashort-acting insulin was intravenously injected when patients showed high glucose levels (>190 mg/dl). Glucose 79-86 insulin Homo sapiens 18-25 23511925-9 2013 RESULTS: The group administered ultrashort-acting insulin (n=52, blood glucose level: 243.7 +- 46.2 mg/dl) showed a significantly higher glucose level compared with the group not administered ultrashort-acting insulin (n=53, 177.1 +- 5.2 mg/dl). Glucose 71-78 insulin Homo sapiens 50-57 23511925-9 2013 RESULTS: The group administered ultrashort-acting insulin (n=52, blood glucose level: 243.7 +- 46.2 mg/dl) showed a significantly higher glucose level compared with the group not administered ultrashort-acting insulin (n=53, 177.1 +- 5.2 mg/dl). Glucose 137-144 insulin Homo sapiens 50-57 23622737-8 2013 Early clinical use of insulin provided mixed results due to insufficiently controlled glucose levels and heterogeneity of patient population. Glucose 86-93 insulin Homo sapiens 22-29 23729940-8 2013 Short-sleep insomnia sufferers had lower fasting and postchallenge serum insulin concentrations associated with lower estimates of fasting and glucose-stimulated insulin secretion, and increased insulin sensitivity. Glucose 143-150 insulin Homo sapiens 73-80 23729940-8 2013 Short-sleep insomnia sufferers had lower fasting and postchallenge serum insulin concentrations associated with lower estimates of fasting and glucose-stimulated insulin secretion, and increased insulin sensitivity. Glucose 143-150 insulin Homo sapiens 162-169 23729940-8 2013 Short-sleep insomnia sufferers had lower fasting and postchallenge serum insulin concentrations associated with lower estimates of fasting and glucose-stimulated insulin secretion, and increased insulin sensitivity. Glucose 143-150 insulin Homo sapiens 162-169 23206662-7 2013 Insulin sensitivity was assessed by the reciprocal of the square root of insulin (RISQI) and the insulin:glucose ratio. Glucose 105-112 insulin Homo sapiens 0-7 23638642-0 2013 Injectable nano-network for glucose-mediated insulin delivery. Glucose 28-35 insulin Homo sapiens 45-52 23638642-2 2013 An artificial "closed-loop" system able to mimic pancreas activity and release insulin in response to glucose level changes has the potential to improve patient compliance and health. Glucose 102-109 insulin Homo sapiens 79-86 23638642-3 2013 Herein we develop a glucose-mediated release strategy for the self-regulated delivery of insulin using an injectable and acid-degradable polymeric network. Glucose 20-27 insulin Homo sapiens 89-96 23638642-4 2013 Formed by electrostatic interaction between oppositely charged dextran nanoparticles loaded with insulin and glucose-specific enzymes, the nanocomposite-based porous architecture can be dissociated and subsequently release insulin in a hyperglycemic state through the catalytic conversion of glucose into gluconic acid. Glucose 109-116 insulin Homo sapiens 223-230 23638642-4 2013 Formed by electrostatic interaction between oppositely charged dextran nanoparticles loaded with insulin and glucose-specific enzymes, the nanocomposite-based porous architecture can be dissociated and subsequently release insulin in a hyperglycemic state through the catalytic conversion of glucose into gluconic acid. Glucose 292-299 insulin Homo sapiens 97-104 23638642-4 2013 Formed by electrostatic interaction between oppositely charged dextran nanoparticles loaded with insulin and glucose-specific enzymes, the nanocomposite-based porous architecture can be dissociated and subsequently release insulin in a hyperglycemic state through the catalytic conversion of glucose into gluconic acid. Glucose 292-299 insulin Homo sapiens 223-230 23638642-5 2013 In vitro insulin release can be modulated in a pulsatile profile in response to glucose concentrations. Glucose 80-87 insulin Homo sapiens 9-16 23679951-2 2013 It improves peripheral and liver sensitivity to insulin, reduces basal hepatic glucose production, increases insulin-stimulated uptake and utilization of glucose by peripheral tissues, decreases hunger and causes weight reduction.Recently, much attention has been made toward the possible kidney protective efficacy of metformin. Glucose 154-161 insulin Homo sapiens 109-116 23670537-3 2013 To address this issue, we experimentally measured metabolites in glucose metabolism in response to insulin. Glucose 65-72 insulin Homo sapiens 99-106 23670537-4 2013 Step stimulation of insulin induced transient response of glycolysis and glycogenesis, and sustained response of gluconeogenesis and extracellular glucose concentration (GLC(ex)). Glucose 147-154 insulin Homo sapiens 20-27 23670537-5 2013 Based on the experimental results, we constructed a simple computational model that characterises response of insulin-signalling-dependent glucose metabolism. Glucose 139-146 insulin Homo sapiens 110-117 23670537-9 2013 These results demonstrate the selective control mechanism of glucose metabolism by temporal patterns of insulin. Glucose 61-68 insulin Homo sapiens 104-111 23620200-2 2013 Insulin degludec has a flat, stable glucose-lowering profile with a duration of action of >42 h, and less within-patient day-to-day variability in glucose-lowering effect than the long-acting insulin analogue insulin glargine. Glucose 36-43 insulin Homo sapiens 0-7 23553859-7 2013 Insulin sensitivity was measured by glucose disposal rate. Glucose 36-43 insulin Homo sapiens 0-7 23548572-1 2013 The glucose transporter isoform, GLUT2, -mediated glucose sensing is essential for maintaining normal glucose-stimulated insulin secretion in pancreatic beta cells. Glucose 4-11 insulin Homo sapiens 121-128 23548572-1 2013 The glucose transporter isoform, GLUT2, -mediated glucose sensing is essential for maintaining normal glucose-stimulated insulin secretion in pancreatic beta cells. Glucose 50-57 insulin Homo sapiens 121-128 23558840-5 2013 IV insulin was given when glucose concentration exceeded 215 mg/dL. Glucose 26-33 insulin Homo sapiens 3-10 23453199-4 2013 These "FH-B-TPN" cells were shown to release insulin in response to physiological glucose stimulation both, in vitro and in vivo. Glucose 82-89 insulin Homo sapiens 45-52 23274898-1 2013 Skeletal muscle glucose uptake in response to exercise is preserved in insulin-resistant conditions, but the signals involved are debated. Glucose 16-23 insulin Homo sapiens 71-78 23665900-5 2013 It is from GSVs that GLUT4 is mobilized to the cell surface in response to insulin, where it increases the rate of glucose uptake into the cell. Glucose 115-122 insulin Homo sapiens 75-82 23669476-7 2013 Octreotide and diazoxide were not successful in preventing the hypoglycemic attacks, whereas continuous insulin therapy with an insulin pump helped to stabilize the blood glucose level temporarily. Glucose 171-178 insulin Homo sapiens 104-111 23669476-7 2013 Octreotide and diazoxide were not successful in preventing the hypoglycemic attacks, whereas continuous insulin therapy with an insulin pump helped to stabilize the blood glucose level temporarily. Glucose 171-178 insulin Homo sapiens 128-135 23667771-11 2013 Erythromycin potentiated the effect of insulin on blood glucose level and serum insulin level whereas other prokinetic agents failed to do so after repeated dose administration in diabetic mice. Glucose 56-63 insulin Homo sapiens 39-46 25885830-16 2013 To achieve normoglycemia by intravenous bolus dose of human regular insulin, significantly higher doses are required in patients receiving dextrose containing saline as maintenance fluid. Glucose 139-147 insulin Homo sapiens 68-75 22978318-10 2013 The mean terminal elimination half-life ranged between 3.11 and 5.28 h. All CarboCarrier insulin dose groups showed decreases in the mean change from baseline of plasma glucose concentrations compared with the placebo group. Glucose 170-177 insulin Homo sapiens 90-97 23688537-6 2013 In the intensive care setting, insulin infusions are now widely endorsed to quickly achieve and maintain glucose control. Glucose 105-112 insulin Homo sapiens 31-38 23223345-8 2013 For our primary outcome, we calculated the quantitative insulin sensitivity check index (QUICKI) using the end-of-period fasting serum glucose and insulin. Glucose 135-142 insulin Homo sapiens 56-63 23237882-5 2013 The major asset of the insulin secretion of the beta-cell is that it is glucose-sensitive and thus, in periods without meals, no peaks of insulin release will occur, but more importantly, when metabolism needs to switch to catabolism, also the basal secretion will diminish and shut down, allowing gluconeogenesis and glycogenolysis in liver to occur. Glucose 72-79 insulin Homo sapiens 23-30 23274905-8 2013 We also showed that the knockdown of Prox1 expression by small interfering RNAs in INS-1E cells resulted in a 1.7-fold reduction in glucose-stimulated insulin secretion. Glucose 132-139 insulin Homo sapiens 151-158 23275353-1 2013 OBJECTIVE: To examine whether the patterns of insulin concentration during the oral glucose tolerance test (OGTT) predict type 2 diabetes. Glucose 84-91 insulin Homo sapiens 46-53 23275356-4 2013 Homeostasis model assessment of insulin resistance (HOMA-IR) and fasting insulin were positively correlated with glucose, triglycerides, systolic blood pressure, and diastolic blood pressure, and were negatively correlated with adiponectin (P < 0.05). Glucose 113-120 insulin Homo sapiens 32-39 23275356-4 2013 Homeostasis model assessment of insulin resistance (HOMA-IR) and fasting insulin were positively correlated with glucose, triglycerides, systolic blood pressure, and diastolic blood pressure, and were negatively correlated with adiponectin (P < 0.05). Glucose 113-120 insulin Homo sapiens 73-80 23275356-6 2013 HOMA-IR and fasting insulin remained significantly and positively related to glucose, triglycerides, and blood pressure after adjustment for body composition. Glucose 77-84 insulin Homo sapiens 20-27 23460019-6 2013 Furthermore, insulin-stimulated glucose uptake was reduced by 20% in PRAS40-KD myotubes (p < 0.05). Glucose 32-39 insulin Homo sapiens 13-20 23643349-4 2013 In non-diabetic subjects, the incretin effect is responsible for 50-70% of insulin release during oral glucose administration. Glucose 103-110 insulin Homo sapiens 75-82 23643349-5 2013 In type 2 diabetes patients, the incretin effect is impaired and contributes to only 20-35% of the insulin response to oral glucose. Glucose 124-131 insulin Homo sapiens 99-106 23620200-2 2013 Insulin degludec has a flat, stable glucose-lowering profile with a duration of action of >42 h, and less within-patient day-to-day variability in glucose-lowering effect than the long-acting insulin analogue insulin glargine. Glucose 150-157 insulin Homo sapiens 0-7 23329581-8 2013 Patients were satisfied with the treatment with bolus calculator, according to the treatment satisfaction scale.Insulin pump bolus calculators are effective and safe in prandial insulin calculation with a positive impact on glucose profile. Glucose 224-231 insulin Homo sapiens 112-119 23305648-3 2013 Although human embryonic stem cells and induced pluripotent stem cells are capable of generating insulin-producing cells in vitro when provided with the appropriate inductive cues, the insulin-expressing cells that develop behave more like immature beta-cells with minimal sensitivity to glucose stimulation. Glucose 288-295 insulin Homo sapiens 185-192 23235922-1 2013 Obesity and insulin resistance are associated with low-grade systemic inflammation, which is related to increased concentrations of plasma FFAs, glucose, or insulin. Glucose 145-152 insulin Homo sapiens 12-19 23230283-11 2013 These observations document that GTN therapy modifies glucose metabolism causing evidence of increased insulin resistance during sustained therapy in normal humans. Glucose 54-61 insulin Homo sapiens 103-110 24421496-5 2013 RESULTS: Appropriate glucose control via administration of insulin within hospitals has been acknowledged as an important goal and is consistent with achieving patient safety. Glucose 21-28 insulin Homo sapiens 59-66 23533232-10 2013 After 6 months the mean insulin (picomoles per liter) to glucose ratio (millimoles per liter) decreased by 7.2 [95%CI -12.0 to -2.3], body mass index, expressed as a percentage of the 95th centile, decreased by 9% (95% CI -3 to -15), but there was no significant change in the lipids. Glucose 57-64 insulin Homo sapiens 24-31 23526462-3 2013 RESEARCH DESIGN AND METHODS: Glucose-stimulated insulin secretion was modeled, from glucose and C-peptide concentrations during a 2-hour hyperglycemic (225 mg/dL) clamp in 22 AA and 24 AW OW/OB adolescents, on 2 occasions after a 12-hour overnight infusion of either normal saline or intralipid (IL) in a random sequence. Glucose 29-36 insulin Homo sapiens 48-55 23526462-3 2013 RESEARCH DESIGN AND METHODS: Glucose-stimulated insulin secretion was modeled, from glucose and C-peptide concentrations during a 2-hour hyperglycemic (225 mg/dL) clamp in 22 AA and 24 AW OW/OB adolescents, on 2 occasions after a 12-hour overnight infusion of either normal saline or intralipid (IL) in a random sequence. Glucose 29-36 insulin Homo sapiens 96-105 23526462-3 2013 RESEARCH DESIGN AND METHODS: Glucose-stimulated insulin secretion was modeled, from glucose and C-peptide concentrations during a 2-hour hyperglycemic (225 mg/dL) clamp in 22 AA and 24 AW OW/OB adolescents, on 2 occasions after a 12-hour overnight infusion of either normal saline or intralipid (IL) in a random sequence. Glucose 84-91 insulin Homo sapiens 48-55 23526462-8 2013 beta-Cell glucose sensitivity of first- and second-phase insulin secretion did not change significantly during IL infusion in either group, but DI in each phase decreased significantly and similarly in AAs and AWs. Glucose 10-17 insulin Homo sapiens 57-64 23539729-6 2013 The prevalence of cells positive for both insulin and glucagon or somatostatin also increased in these patients compared with those with normal glucose tolerance. Glucose 144-151 insulin Homo sapiens 42-49 23539736-0 2013 Elevated 1-hour postload plasma glucose levels identify subjects with normal glucose tolerance but impaired beta-cell function, insulin resistance, and worse cardiovascular risk profile: the GENFIEV study. Glucose 32-39 insulin Homo sapiens 128-135 23539736-10 2013 CONCLUSIONS: Among subjects with NGT, those with 1-hour OGTT glucose of >155 mg/dL showed lower insulin sensitivity, impaired beta-cell function, and worse cardiovascular risk profile and therefore are at greater risk of developing T2DM and cardiovascular disease. Glucose 61-68 insulin Homo sapiens 99-106 23543661-9 2013 LPS thus directly inhibits insulin-stimulated glucose uptake and increases palmitate release in the perfused human leg without detectable effects on amino acid metabolism. Glucose 46-53 insulin Homo sapiens 27-34 23759396-7 2013 The insulin-glucose time variant data form the boundaries of OVAL, defined as the ellipse enclosing the 95% confidence intervals of the insulin and glucose concentrations plotted on an x-y scatter graph and normalized to ensure equal weighting of insulin and glucose. Glucose 12-19 insulin Homo sapiens 4-11 23759396-7 2013 The insulin-glucose time variant data form the boundaries of OVAL, defined as the ellipse enclosing the 95% confidence intervals of the insulin and glucose concentrations plotted on an x-y scatter graph and normalized to ensure equal weighting of insulin and glucose. Glucose 148-155 insulin Homo sapiens 4-11 23759396-7 2013 The insulin-glucose time variant data form the boundaries of OVAL, defined as the ellipse enclosing the 95% confidence intervals of the insulin and glucose concentrations plotted on an x-y scatter graph and normalized to ensure equal weighting of insulin and glucose. Glucose 148-155 insulin Homo sapiens 4-11 23363580-13 2013 However, reductions in fasting glucose, one hour insulin and insulin area under the curve with the low sucrose diet on glucose tolerance testing may indicate a beneficial effect and further work is required to determine if this is the case. Glucose 119-126 insulin Homo sapiens 61-68 23682221-0 2013 beta-Cell dysfunction and insulin resistance in gestational glucose intolerance. Glucose 60-67 insulin Homo sapiens 26-33 23467766-4 2013 Furthermore, we investigated the effects of C10orf116 on glucose uptake and demonstrated that the ectopic expression of C10orf116 significantly increases insulin-stimulated glucose uptake in adipocytes by increasing glucose transporter type 4 (GLUT4) expression levels. Glucose 57-64 insulin Homo sapiens 154-161 23107353-1 2013 BACKGROUND AND OBJECTIVE: Subcutaneously injected rapid-acting insulin analogs do not replicate physiologic insulin action due to delays in their onset and peak action resulting in postprandial glucose excursions. Glucose 194-201 insulin Homo sapiens 63-70 23650507-8 2013 Furthermore, MSDC-0160 in combination with IGF-1 and 8 mM glucose increased beta-cell specific gene expression of insulin, pdx1, nkx6.1, and nkx2.2, and maintained insulin content without altering glucose-stimulated insulin secretion. Glucose 58-65 insulin Homo sapiens 114-121 23650507-8 2013 Furthermore, MSDC-0160 in combination with IGF-1 and 8 mM glucose increased beta-cell specific gene expression of insulin, pdx1, nkx6.1, and nkx2.2, and maintained insulin content without altering glucose-stimulated insulin secretion. Glucose 58-65 insulin Homo sapiens 164-171 23650507-8 2013 Furthermore, MSDC-0160 in combination with IGF-1 and 8 mM glucose increased beta-cell specific gene expression of insulin, pdx1, nkx6.1, and nkx2.2, and maintained insulin content without altering glucose-stimulated insulin secretion. Glucose 58-65 insulin Homo sapiens 164-171 23726614-11 2013 CONCLUSIONS: Renal transplant recipients with glucose intolerance had increased IMT and baPWV, suggesting that glucose intolerance in renal transplant recipients may induce atherosclerosis and that the rise in insulin resistance may contribute to the increased IMT in renal transplant recipients. Glucose 46-53 insulin Homo sapiens 210-217 23637927-7 2013 Via interrogation of publicly available data from the Meta-Analyses of Glucose and Insulin-related traits Consortium, rs726344"s effect on insulin sensitivity was replicated. Glucose 71-78 insulin Homo sapiens 139-146 23595176-3 2013 An oral glucose tolerance test revealed high serum insulin and C peptide, suggesting hyperinsulinaemia, and it was used to ascertain the relationship between insulin, glucose and C peptide levels. Glucose 8-15 insulin Homo sapiens 51-58 23595176-3 2013 An oral glucose tolerance test revealed high serum insulin and C peptide, suggesting hyperinsulinaemia, and it was used to ascertain the relationship between insulin, glucose and C peptide levels. Glucose 8-15 insulin Homo sapiens 90-97 23475748-0 2013 Glucose regulates secretion of exogenously expressed insulin from HepG2 cells in vitro and in a mouse model of diabetes mellitus in vivo. Glucose 0-7 insulin Homo sapiens 53-60 23475748-1 2013 Glucose-controlled insulin secretion is a key component of its regulation. Glucose 0-7 insulin Homo sapiens 19-26 23475748-2 2013 Here, we examined whether liver cell secretion of insulin derived from an engineered construct can be regulated by glucose. Glucose 115-122 insulin Homo sapiens 50-57 23475748-10 2013 In streptozotocin-induced diabetic mice, when infected with adenovirus expressing mature insulin, glucose levels declined. Glucose 98-105 insulin Homo sapiens 89-96 23475748-11 2013 Our data show that glucose regulates release of exogenously expressed insulin from the ER of liver cells. Glucose 19-26 insulin Homo sapiens 70-77 23517533-0 2013 A pH gated, glucose-sensitive nanoparticle based on worm-like mesoporous silica for controlled insulin release. Glucose 12-19 insulin Homo sapiens 95-102 23517533-6 2013 In vitro experiment shows that the cumulative release of insulin is dependent on glucose concentration, and the glucose sensitivity could be adjusted simply by different pH values. Glucose 81-88 insulin Homo sapiens 57-64 23517533-6 2013 In vitro experiment shows that the cumulative release of insulin is dependent on glucose concentration, and the glucose sensitivity could be adjusted simply by different pH values. Glucose 112-119 insulin Homo sapiens 57-64 23802208-5 2013 AIM: To document blood glucose exposure in response to increasing carbohydrate loads on fixed carbohydrate-to-insulin ratios. Glucose 23-30 insulin Homo sapiens 110-117 23802208-9 2013 RESULTS: Increasing carbohydrate loads using a fixed carbohydrate-to-insulin ratio resulted in increasing glucose AUC. Glucose 106-113 insulin Homo sapiens 69-76 23566334-1 2013 BACKGROUND: Glucagon-like Peptide-1 (GLP-1) is an incretin hormone secreted from the gastrointestinal tract that facilitates the glucose-dependent insulin response. Glucose 129-136 insulin Homo sapiens 147-154 23577002-8 2013 Insulin sensitivity of glucose and lipid metabolism was not affected by chronic FA1 exposure in myotubes established from lean, obese, and T2D subjects. Glucose 23-30 insulin Homo sapiens 0-7 21604201-1 2013 Cellular resistance to insulin caused by reduced glucose transport and metabolism is a primary defect leading to the development of metabolic disease. Glucose 49-56 insulin Homo sapiens 23-30 23496914-7 2013 Intramuscular islet graft function after transplantation was confirmed by documenting the acute insulin response to intravenous glucose in 5/11 pancreatectomized animals. Glucose 128-135 insulin Homo sapiens 96-103 22967513-3 2013 At the level of glucose metabolism reduced metabolic adaptation in most cases is characterized by impaired stimulation of transarcolemmal glucose transport in the cardiomyocytes in response to insulin, referred to as insulin resistance, or to other stimuli such as energy deficiency. Glucose 16-23 insulin Homo sapiens 193-200 22967513-3 2013 At the level of glucose metabolism reduced metabolic adaptation in most cases is characterized by impaired stimulation of transarcolemmal glucose transport in the cardiomyocytes in response to insulin, referred to as insulin resistance, or to other stimuli such as energy deficiency. Glucose 16-23 insulin Homo sapiens 217-224 22967513-3 2013 At the level of glucose metabolism reduced metabolic adaptation in most cases is characterized by impaired stimulation of transarcolemmal glucose transport in the cardiomyocytes in response to insulin, referred to as insulin resistance, or to other stimuli such as energy deficiency. Glucose 138-145 insulin Homo sapiens 193-200 22967513-3 2013 At the level of glucose metabolism reduced metabolic adaptation in most cases is characterized by impaired stimulation of transarcolemmal glucose transport in the cardiomyocytes in response to insulin, referred to as insulin resistance, or to other stimuli such as energy deficiency. Glucose 138-145 insulin Homo sapiens 217-224 23126339-4 2013 KEY RESULTS: Glucose (25 mM) had no effect on aldolase A gene expression, but insulin (100 nM) up-regulated aldolase A mRNA and protein levels in the absence or presence of 25 mM glucose in adipocytes. Glucose 179-186 insulin Homo sapiens 78-85 23126339-5 2013 Treatment with insulin increased levels of basal or glucose (25 mM)-induced MG and glucose 6-phosphate. Glucose 52-59 insulin Homo sapiens 15-22 23467766-4 2013 Furthermore, we investigated the effects of C10orf116 on glucose uptake and demonstrated that the ectopic expression of C10orf116 significantly increases insulin-stimulated glucose uptake in adipocytes by increasing glucose transporter type 4 (GLUT4) expression levels. Glucose 173-180 insulin Homo sapiens 154-161 23086116-4 2013 Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 17-24 insulin Homo sapiens 0-7 24070800-5 2013 This notion was further supported by studies, which noted decreases in the effectiveness of insulin-mediated glucose uptake the following morning. Glucose 109-116 insulin Homo sapiens 92-99 23481229-4 2013 Specifically, PPARdelta activation in the liver stimulates glucose utilization and inhibits gluconeogenesis, which improves insulin resistance and hyperglycemia. Glucose 59-66 insulin Homo sapiens 124-131 23137345-1 2013 AIMS: Insulin aspart has a higher ability to treat postprandial glucose than regular human insulin, which may have favourable cardiovascular effects. Glucose 64-71 insulin Homo sapiens 6-13 23225242-2 2013 Tyrosine phosphorylation of the insulin receptor (IR) by insulin promotes glucose uptake by activating the PI3K/Akt pathway. Glucose 74-81 insulin Homo sapiens 32-39 23223406-12 2013 CONCLUSIONS Insulin sensitivity indices based on glucose and insulin levels should be used cautiously as measures of peripheral insulin sensitivity when comparing mixed gender and mixed race populations. Glucose 49-56 insulin Homo sapiens 12-19 23344726-9 2013 CONCLUSIONS/INTERPRETATION: These results highlight non-linearity in Akt signalling and suggest that: (1) the pathway from Akt to glucose transport is complex; and (2) pathways, particularly FOXO, that are not insulin-resistant, are likely to be hyperactivated in response to hyperinsulinaemia. Glucose 130-137 insulin Homo sapiens 210-217 23507269-5 2013 By both lowering plasma glucose and improving the lipid profile, insulin exerts beneficial effects on CV outcomes. Glucose 24-31 insulin Homo sapiens 65-72 23641356-3 2013 We recruited 50 patients with type 2 diabetes over the age of 60 who had used insulin pens for glucose control. Glucose 95-102 insulin Homo sapiens 78-85 23442069-3 2013 Indeed, previous studies have shown that GPR119 promotes glucose-stimulated insulin secretion, pancreatic beta-cell function and glucagon-like peptide-1 release, all of which provide valid mechanisms through which GPR119 may improve systemic glucose homeostasis. Glucose 57-64 insulin Homo sapiens 76-83 23336594-10 2013 Insulin sensitivity, expressed as glucose-to-insulin ratio and HOMA index resulted significantly improved after 12 weeks of treatment. Glucose 34-41 insulin Homo sapiens 0-7 23086116-4 2013 Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 17-24 insulin Homo sapiens 108-115 23086116-4 2013 Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 68-75 insulin Homo sapiens 0-7 23933689-2 2013 Glucose regulation by insulin depends on the suppression of endogenous glucose production and stimulation of glucose disposal. Glucose 0-7 insulin Homo sapiens 22-29 23450052-0 2013 Effects of endogenous androgens and abdominal fat distribution on the interrelationship between insulin and non-insulin-mediated glucose uptake in females. Glucose 129-136 insulin Homo sapiens 96-103 23933689-2 2013 Glucose regulation by insulin depends on the suppression of endogenous glucose production and stimulation of glucose disposal. Glucose 71-78 insulin Homo sapiens 22-29 23933689-2 2013 Glucose regulation by insulin depends on the suppression of endogenous glucose production and stimulation of glucose disposal. Glucose 109-116 insulin Homo sapiens 22-29 23933689-4 2013 Moreover, the sensitivity of glucose metabolism to insulin is impaired both in muscle (due to defects in insulin-stimulated glucose utilization and decreased blood flow) and in adipose tissue (due to decreased blood flow). Glucose 29-36 insulin Homo sapiens 51-58 23933689-5 2013 However, recent studies suggest that expanded total fat mass becomes a major consumer of glucose providing a sink for glucose and compensating for insulin resistance. Glucose 89-96 insulin Homo sapiens 147-154 23545891-3 2013 Most patients with T2DM eventually require insulin replacement therapy to attain and preserve satisfactory glucose control. Glucose 107-114 insulin Homo sapiens 43-50 23418316-1 2013 CONTEXT: In vitro and animal studies suggest that bile acids have the capacity to reduce blood glucose by stimulating glucagon-like peptide-1 (GLP-1) and, thereby, insulin. Glucose 95-102 insulin Homo sapiens 164-171 23476073-4 2013 Insulin sensitivity was measured by the glucose clamp technique. Glucose 40-47 insulin Homo sapiens 0-7 23450052-0 2013 Effects of endogenous androgens and abdominal fat distribution on the interrelationship between insulin and non-insulin-mediated glucose uptake in females. Glucose 129-136 insulin Homo sapiens 112-119 23450052-2 2013 Glucose disposal occurs via noninsulin-mediated glucose uptake (NIMGU) and insulin-mediated glucose uptake (IMGU). Glucose 48-55 insulin Homo sapiens 31-38 23450055-6 2013 MAIN OUTCOME MEASURES: Glucose, insulin, and FFA were measured during insulin-modified frequently sampled iv glucose tolerance tests. Glucose 109-116 insulin Homo sapiens 70-77 23365108-11 2013 These results suggest than when WB is consumed with berries, less insulin is needed for maintenance of normal or slightly improved postprandial glucose metabolism. Glucose 144-151 insulin Homo sapiens 66-73 24475558-6 2013 The mordality of treatment is continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1g/kg body weight/hour, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance is required. Glucose 104-111 insulin Homo sapiens 73-80 23259588-8 2013 Both TG and fasting glucose levels were significantly and positively correlated with fasting insulin (p<0.001), homeostasis model assessment (HOMA) (p<0.001). Glucose 20-27 insulin Homo sapiens 93-100 23151437-0 2013 Measurement of insulin-mediated glucose uptake: direct comparison of the modified insulin suppression test and the euglycemic, hyperinsulinemic clamp. Glucose 32-39 insulin Homo sapiens 15-22 23151437-1 2013 BACKGROUND: Two direct measurements of peripheral insulin sensitivity are the M value derived from the euglycemic, hyperinsulinemic clamp (EC) and the steady-state plasma glucose (SSPG) concentration derived from the insulin suppression test (IST). Glucose 171-178 insulin Homo sapiens 50-57 23512499-0 2013 Cardamonin ameliorates insulin resistance induced by high insulin and high glucose through the mTOR and signal pathway. Glucose 75-82 insulin Homo sapiens 23-30 23164480-1 2013 AIM: Glucocorticoids impair glucose tolerance by inducing insulin resistance. Glucose 28-35 insulin Homo sapiens 58-65 23348026-2 2013 The pancreatic beta cells are the source of insulin that keeps blood glucose normal. Glucose 69-76 insulin Homo sapiens 44-51 23384946-1 2013 Plasma glucose and ketone concentrations are much higher in birds than in humans and birds exhibit resistance to insulin-mediated glucose uptake into muscle. Glucose 7-14 insulin Homo sapiens 113-120 23384946-1 2013 Plasma glucose and ketone concentrations are much higher in birds than in humans and birds exhibit resistance to insulin-mediated glucose uptake into muscle. Glucose 130-137 insulin Homo sapiens 113-120 23404499-5 2013 We further show that leucine facilitated the insulin-mediated suppression of glucose production and expression of key gluconeogenic genes in a Galphai1 protein-dependent manner in cultured primary hepatocytes. Glucose 77-84 insulin Homo sapiens 45-52 23542897-3 2013 Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated glucose concentrations prevail. Glucose 46-53 insulin Homo sapiens 75-82 23542897-5 2013 With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Glucose 59-66 insulin Homo sapiens 14-21 23542897-5 2013 With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Glucose 59-66 insulin Homo sapiens 34-41 23542897-8 2013 Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis. Glucose 95-102 insulin Homo sapiens 70-77 23376105-5 2013 Insulin resistance and its prevention by Sutherlandia frutescens were measured by glucose uptake, gluconeogenesis and lipid accumulation in the cell cultures. Glucose 82-89 insulin Homo sapiens 0-7 23376105-7 2013 RESULTS: The insulin resistant Chang liver cells took up significantly less 2-[(3)H]-deoxyglucose (p<0.05) than controls, released more glucose into the culture medium (p<0.05) and accumulated more intracellular lipid (p<0.05). Glucose 90-97 insulin Homo sapiens 13-20 24843647-7 2013 Insulin secretion was assessed by measuring circulating GFP and endogenous C-peptide levels after glucose injection. Glucose 98-105 insulin Homo sapiens 0-7 24843651-4 2013 All of the patients were treated with medical nutrition therapy plus insulin therapy to improve fasting plasma glucose (FPG) and postprandial glucose below 150 and 200 mg/dL, respectively. Glucose 111-118 insulin Homo sapiens 69-76 24843651-4 2013 All of the patients were treated with medical nutrition therapy plus insulin therapy to improve fasting plasma glucose (FPG) and postprandial glucose below 150 and 200 mg/dL, respectively. Glucose 142-149 insulin Homo sapiens 69-76 23246867-6 2013 IPA3 also ablated glucose-stimulated insulin granule accumulation at the plasma membrane, consistent with its role in sustained/second-phase insulin release. Glucose 18-25 insulin Homo sapiens 37-44 23246867-10 2013 Taken together, these data suggest that glucose-mediated activation of Cdc42 leads to activation of PAK1 and prompts activation of its downstream targets Raf-1, MEK1/2 and ERK1/2 to elicit F-actin remodeling and recruitment of insulin granules to the plasma membrane to support the sustained phase of insulin release. Glucose 40-47 insulin Homo sapiens 227-234 23246867-10 2013 Taken together, these data suggest that glucose-mediated activation of Cdc42 leads to activation of PAK1 and prompts activation of its downstream targets Raf-1, MEK1/2 and ERK1/2 to elicit F-actin remodeling and recruitment of insulin granules to the plasma membrane to support the sustained phase of insulin release. Glucose 40-47 insulin Homo sapiens 301-308 23341496-4 2013 Bolus intraperitoneal injection of GW-9508 in mice showed a slight decrease in blood glucose, with an increase in plasma insulin levels under glucose stimuli. Glucose 142-149 insulin Homo sapiens 121-128 23076551-2 2013 The required balance between insulin sensitivity/resistance and insulin secretion is necessary to maintain normal glucose metabolism. Glucose 114-121 insulin Homo sapiens 29-36 23076551-5 2013 Skeletal muscle is quantitatively the most important tissue in the body for insulin-stimulated glucose disposal and is composed of diverse myofibers that vary in their properties between healthy and insulin-resistant muscle. Glucose 95-102 insulin Homo sapiens 76-83 23246353-5 2013 Chemically induced reduction of proteasome activity was associated with lower glucose-stimulated insulin secretion, which was partly reproduced by palmitate exposure. Glucose 78-85 insulin Homo sapiens 97-104 23416070-1 2013 Circulating levels of insulin and glucagon reflect the nutritional state of animals and elicit regulatory responses in the liver that maintain glucose and lipid homeostasis. Glucose 143-150 insulin Homo sapiens 22-29 23471249-4 2013 The insulin receptor within the central nervous system is widely distributed, reflecting insulin"s diverse range of actions, including acting as an adiposity signal to reduce food intake and increase energy expenditure, regulation of systemic glucose responses, altering sympathetic activity, and involvement in cognitive function. Glucose 243-250 insulin Homo sapiens 4-11 23277185-6 2013 Finally, skeletal muscle is the major site of dietary glucose disposal; therefore, muscle insulin resistance is essential to the development of whole body insulin resistance. Glucose 54-61 insulin Homo sapiens 90-97 23299501-9 2013 Lipid infusion abolished insulin-mediated increases in muscle MBV and MBF and lowered insulin-stimulated whole body glucose disposal (P = 0.0001), which were reversed by losartan administration. Glucose 116-123 insulin Homo sapiens 86-93 23512499-11 2013 However, neither cardamonin nor rapamycin increased the expression of glucose transport 4 which decreased in insulin-resistant vascular smooth muscle cells. Glucose 70-77 insulin Homo sapiens 109-116 23533158-2 2013 However, it is now known that components of the insulin-mediated glucose uptake pathway, including neuronal insulin synthesis and the insulin-dependent glucose transporter GLUT4, are present in brain tissue, particularly in the hippocampus. Glucose 65-72 insulin Homo sapiens 48-55 23533158-2 2013 However, it is now known that components of the insulin-mediated glucose uptake pathway, including neuronal insulin synthesis and the insulin-dependent glucose transporter GLUT4, are present in brain tissue, particularly in the hippocampus. Glucose 65-72 insulin Homo sapiens 108-115 23533158-13 2013 This provides supporting evidence for a physiological role for insulin signaling in facilitating increased neuronal glucose uptake during sustained cognitive activity. Glucose 116-123 insulin Homo sapiens 63-70 23190266-2 2013 Initially insulin was considered only important for rapid control of blood glucose by its action on a restricted number of tissues; however, it has now become clear that this hormone controls an array of cellular processes in many different tissues. Glucose 75-82 insulin Homo sapiens 10-17 23209190-8 2013 In conclusion, early in the development of prediabetes/type 2 diabetes in youth, ChREBPbeta expression in adipose tissue predicts insulin resistance and, therefore, might play a role in the regulation of glucose tolerance. Glucose 204-211 insulin Homo sapiens 130-137 23448196-2 2013 Since its introduction as a therapeutic modality almost 100 years ago, insulin therapy has undergone remarkable changes in purity and ability to provide more physiologic control of blood glucose levels. Glucose 187-194 insulin Homo sapiens 71-78 24396652-5 2013 After glucose loading, serum glucose, and total insulin levels increased abnormally. Glucose 6-13 insulin Homo sapiens 48-55 30736179-7 2013 In the hospital, insulin therapy of hyperglycemia is preferred due to the ability to flexibly manage glucose levels without side effects associated with many alternative antidiabetic agents. Glucose 101-108 insulin Homo sapiens 17-24 23104421-1 2013 We have previously reported that members of the NR4A family of orphan nuclear receptors can augment insulin"s ability to stimulate glucose transport in adipocytes. Glucose 131-138 insulin Homo sapiens 100-107 23104421-4 2013 The NR4A3 hyper-expression construct led to a significant increase in glucose transport rates in the presence of maximal insulin while the NR4A3 knock-down exhibited a significant reduction in insulin-stimulated glucose transport rates. Glucose 70-77 insulin Homo sapiens 121-128 23104421-4 2013 The NR4A3 hyper-expression construct led to a significant increase in glucose transport rates in the presence of maximal insulin while the NR4A3 knock-down exhibited a significant reduction in insulin-stimulated glucose transport rates. Glucose 212-219 insulin Homo sapiens 193-200 23104421-7 2013 PGA2 augmented insulin-stimulated glucose uptake in C2C12 myocytes and AKT phosphorylation after 12-h treatment, without significant effects on basal transport or basal AKT phosphorylation. Glucose 34-41 insulin Homo sapiens 15-22 23104421-8 2013 More importantly, we demonstrated that PGA2 led to a greater improvement in insulin-stimulated glucose rates in NR4A3 overexpressing C2C12 myocytes, when compared with Lac-Z controls stimulated with insulin and PGA2. Glucose 95-102 insulin Homo sapiens 76-83 23315061-5 2013 MATERIALS, SETTING, METHODS: In an academic clinic setting, glucose infusion rate (GIR) on euglycaemic-hyperinsulinaemic clamp was investigated as a marker of insulin sensitivity. Glucose 60-67 insulin Homo sapiens 108-115 23584214-9 2013 Due to the metabolic variability among individuals, optimum blood glucose management is a formidable task to accomplish despite the presence of novel insulin analogs. Glucose 66-73 insulin Homo sapiens 150-157 23305978-4 2013 We show here that large differences exist between men and women with regard to apparent adiponectin regulation of insulin-stimulated glucose uptake in skeletal muscle. Glucose 133-140 insulin Homo sapiens 114-121 23345093-9 2013 On the other hand, insulin-induced suppression of glucose production, gluconeogenesis, glycogenolysis, and stimulation of glucose disappearance all were normal. Glucose 50-57 insulin Homo sapiens 19-26 23345093-9 2013 On the other hand, insulin-induced suppression of glucose production, gluconeogenesis, glycogenolysis, and stimulation of glucose disappearance all were normal. Glucose 122-129 insulin Homo sapiens 19-26 23345093-10 2013 Although fasting glucose production also was increased (P = .0002) in subjects with IFG/IGT, insulin-induced suppression of glucose production, gluconeogenesis, and glycogenolysis and stimulation of glucose disappearance were impaired (P = .005). Glucose 17-24 insulin Homo sapiens 93-100 23345093-10 2013 Although fasting glucose production also was increased (P = .0002) in subjects with IFG/IGT, insulin-induced suppression of glucose production, gluconeogenesis, and glycogenolysis and stimulation of glucose disappearance were impaired (P = .005). Glucose 124-131 insulin Homo sapiens 93-100 23345093-10 2013 Although fasting glucose production also was increased (P = .0002) in subjects with IFG/IGT, insulin-induced suppression of glucose production, gluconeogenesis, and glycogenolysis and stimulation of glucose disappearance were impaired (P = .005). Glucose 124-131 insulin Homo sapiens 93-100 23434589-1 2013 Insulin-secreting beta cells and glucagon-secreting alpha cells maintain physiological blood glucose levels, and their malfunction drives diabetes development. Glucose 93-100 insulin Homo sapiens 0-7 23454764-1 2013 Insulin resistance is typically defined as a reduced ability of insulin to induce glucose uptake by target tissues such as fat and skeletal muscle cells. Glucose 82-89 insulin Homo sapiens 0-7 23454764-1 2013 Insulin resistance is typically defined as a reduced ability of insulin to induce glucose uptake by target tissues such as fat and skeletal muscle cells. Glucose 82-89 insulin Homo sapiens 64-71 23454764-3 2013 Outside of its effects on blood glucose levels, insulin resistance is also associated with a 2- to 3-fold increased risk of cardiovascular mortality. Glucose 32-39 insulin Homo sapiens 48-55 23035699-0 2013 Effect of different blood glucose target levels on the incidence of hypoglycemia during insulin therapy in the intensive care unit. Glucose 26-33 insulin Homo sapiens 88-95 23140910-1 2013 OBJECTIVE: To determine the prevalence of a negative insulinogenic index (change in plasma insulin/change in plasma glucose from 0 to 30 min) from an oral glucose tolerance test according to glucose tolerance category. Glucose 116-123 insulin Homo sapiens 53-60 23140910-1 2013 OBJECTIVE: To determine the prevalence of a negative insulinogenic index (change in plasma insulin/change in plasma glucose from 0 to 30 min) from an oral glucose tolerance test according to glucose tolerance category. Glucose 155-162 insulin Homo sapiens 53-60 23140910-1 2013 OBJECTIVE: To determine the prevalence of a negative insulinogenic index (change in plasma insulin/change in plasma glucose from 0 to 30 min) from an oral glucose tolerance test according to glucose tolerance category. Glucose 155-162 insulin Homo sapiens 53-60 23566996-1 2013 BACKGROUND: Subcutaneously infused insulin may interfere with the function of nearby glucose-sensing electrodes and vice versa. Glucose 85-92 insulin Homo sapiens 35-42 22522662-5 2013 However, insulin was more effective than GLP-1 analogues in lowering the fasting plasma glucose concentration, while GLP-1 agonists were more effective in lowering the postprandial glucose concentration. Glucose 88-95 insulin Homo sapiens 9-16 23277190-7 2013 Reduction of stimulated glucose transport by 1nM CT-1 was associated with overexpression of SOCS-3, a protein known to hinder proximal insulin signaling, and increased phosphorylation of STAT5. Glucose 24-31 insulin Homo sapiens 135-142 23277190-9 2013 Insulin-stimulated glucose transport and signaling were restored by inhibition of STAT5 activity. Glucose 19-26 insulin Homo sapiens 0-7 26064836-1 2013 BACKGROUND: Insulin resistance is a major factor in the development of metabolic syndrome and is associated with central obesity and glucose intolerance. Glucose 133-140 insulin Homo sapiens 12-19 26064836-9 2013 CONCLUSION: High doses of resveratrol block the insulin signaling pathway, thereby reducing glucose uptake and lipid accumulation in vitro. Glucose 92-99 insulin Homo sapiens 48-55 23107359-4 2013 Insulin resistance and islet beta-cell function changes were observed with the oral glucose tolerance test and insulin release test. Glucose 84-91 insulin Homo sapiens 0-7 23107359-10 2013 Insulin resistance in women with GDM is higher than in pregnant women with normal metabolism of glucose. Glucose 96-103 insulin Homo sapiens 0-7 23140239-1 2013 It is now accepted that several pharmacological drug treatments trigger clinical manifestations of glucose dysregulation, such as hyperglycaemia, glucose intolerance and insulin resistance, in part through poorly understood mechanisms. Glucose 99-106 insulin Homo sapiens 170-177 23435445-1 2013 Insulin therapy is the most physiological and effective glucose-lowering treatment for diabetic patients, in which the risk of complications increases proportionally to HbA1c levels. Glucose 56-63 insulin Homo sapiens 0-7 23802496-0 2013 Relationship of glucose values to sliding scale insulin (correctional insulin) dose delivery and meal time in acute care patients with diabetes mellitus. Glucose 16-23 insulin Homo sapiens 48-55 23802496-0 2013 Relationship of glucose values to sliding scale insulin (correctional insulin) dose delivery and meal time in acute care patients with diabetes mellitus. Glucose 16-23 insulin Homo sapiens 70-77 23315940-9 2013 In these mithramycin-treated cells, both cortical filamentous actin structure and insulin-stimulated glucose transport were restored. Glucose 101-108 insulin Homo sapiens 82-89 23250295-1 2013 The objective of this study was to evaluate the usefulness and impact of insulin administration before an F-FDG PET/computed tomography (CT) examination in diabetic patients in order to propose an optimized protocol that can reduce blood glucose levels without increasing muscular F-FDG uptake. Glucose 238-245 insulin Homo sapiens 73-80 22817137-5 2013 This improvement in glucose control was supported by corresponding reductions in the net area under the curve for glucose, insulin, and c-peptide, although there was no change in postprandial suppression of fatty acids. Glucose 20-27 insulin Homo sapiens 123-130 22817137-5 2013 This improvement in glucose control was supported by corresponding reductions in the net area under the curve for glucose, insulin, and c-peptide, although there was no change in postprandial suppression of fatty acids. Glucose 20-27 insulin Homo sapiens 136-145 23299657-4 2013 This results in a net increase of the overall number of perfused nutritive capillary networks and thereby increases insulin-mediated glucose uptake by skeletal muscle. Glucose 133-140 insulin Homo sapiens 116-123 23306779-2 2013 It acts as a "first-responder" to environmental stimuli such as nutrients, cytokines, chemokines and physical activity and regulates insulin delivery to muscle and adipose tissue and thereby affecting insulin-mediated glucose disposal by these tissues. Glucose 218-225 insulin Homo sapiens 133-140 23306779-2 2013 It acts as a "first-responder" to environmental stimuli such as nutrients, cytokines, chemokines and physical activity and regulates insulin delivery to muscle and adipose tissue and thereby affecting insulin-mediated glucose disposal by these tissues. Glucose 218-225 insulin Homo sapiens 201-208 23306779-3 2013 In addition, it also regulates the delivery of insulin and other appetite regulating signals from peripheral tissues to the central nervous system thus influencing the activity of nuclei that regulate hepatic glucose production, adipose tissue lipolysis and lipogenesis, as well as food consumption. Glucose 209-216 insulin Homo sapiens 47-54 23397462-1 2013 Insulin resistance affects the vascular endothelium, and contributes to systemic insulin resistance by directly impairing the actions of insulin to redistribute blood flow as part of its normal actions driving muscle glucose uptake. Glucose 217-224 insulin Homo sapiens 0-7 23397462-1 2013 Insulin resistance affects the vascular endothelium, and contributes to systemic insulin resistance by directly impairing the actions of insulin to redistribute blood flow as part of its normal actions driving muscle glucose uptake. Glucose 217-224 insulin Homo sapiens 81-88 23397462-1 2013 Insulin resistance affects the vascular endothelium, and contributes to systemic insulin resistance by directly impairing the actions of insulin to redistribute blood flow as part of its normal actions driving muscle glucose uptake. Glucose 217-224 insulin Homo sapiens 137-144 23582559-4 2013 Animal models have shown positive changes in glucose (lower plasma glucose and insulin levels) and in lipid metabolism (reduced visceral fat tissue and increased plasma adiponectin level), and an increased resistance to stress. Glucose 45-52 insulin Homo sapiens 79-86 22481243-4 2013 METHODS: Nondiabetic, overweight to obese volunteers underwent direct quantification of insulin sensitivity by measuring steady-state plasma glucose concentrations during the insulin suppression test. Glucose 141-148 insulin Homo sapiens 88-95 22481243-7 2013 RESULTS: Insulin-mediated glucose disposal differed threefold (p < 0.001) between equally obese, insulin-resistant (n = 22) and insulin-sensitive (n = 14) individuals, associated with higher fasting insulin and triglyceride and lower high-density lipoprotein cholesterol (HDL-C) concentrations in insulin-resistant individuals. Glucose 26-33 insulin Homo sapiens 9-16 23348005-6 2013 OA induced insulin resistance which was evident by inhibition of glucose uptake and cell proliferation. Glucose 65-72 insulin Homo sapiens 11-18 23348005-7 2013 Quercetin (10 muM) increased cell proliferation by 3.05 folds with decreased TAG content (45%) and was effective in increasing insulin mediated glucose uptake by 2.65 folds. Glucose 144-151 insulin Homo sapiens 127-134 23406308-10 2013 During static incubation, small islets released 2.89-fold (1.39 +- 0.2 ng/IE) higher insulin level under low glucose induction (3.3 mm) and simultaneously 2.92-fold (2.95 +- 0.33 ng/IE) more insulin under high glucose condition (16.7 mm) in comparison to large islets at the same islet equivalents (P < 0.05). Glucose 109-116 insulin Homo sapiens 85-92 23545829-3 2013 For glucose metabolism, microRNAs are related to insulin secretion, insulin sensitivity, glucose uptake, glycolysis, oxidation and mitochondrial function. Glucose 4-11 insulin Homo sapiens 49-56 23445093-7 2013 RESULTS: On nights when the artificial pancreas was used, versus nights when the sensor-augmented insulin pump was used, there were significantly fewer episodes of nighttime glucose levels below 63 mg per deciliter (7 vs. 22) and significantly shorter periods when glucose levels were below 60 mg per deciliter (P=0.003 and P=0.02, respectively, after adjustment for multiplicity). Glucose 174-181 insulin Homo sapiens 98-105 23443033-2 2013 Different studies provide evidence that vitamin D may play a functional role in glucose tolerance through its effects on insulin secretion and insulin sensitivity. Glucose 80-87 insulin Homo sapiens 121-128 22766107-3 2013 In this review, we discuss our current understanding of the role of AMPK in central functions of the pancreatic beta cell, including glucose-stimulated insulin secretion (GSIS), proliferation, and survival. Glucose 133-140 insulin Homo sapiens 152-159 23297408-1 2013 Glucokinase is the predominant hexokinase expressed in hepatocytes and pancreatic beta-cells, with a pivotal role in regulating glucose-stimulated insulin secretion, illustrated by glucokinase gene mutations causing monogenic diabetes and congenital hyperinsulinemic hypoglycemia. Glucose 128-135 insulin Homo sapiens 147-154 23239154-9 2013 MEASUREMENTS AND MAIN RESULTS: We performed successive muscle biopsies and assessed systemic insulin sensitivity and signal transduction pathways of glucose utilization at the mRNA and protein level and glucose transporter-4 (GLUT4) localization in skeletal muscle tissue. Glucose 149-156 insulin Homo sapiens 93-100 23269410-5 2013 Glucose tolerance and insulin sensitivity, measured with an intravenous glucose tolerance test (IVGTT), were impaired after starvation, but in EX the response was attenuated or abolished. Glucose 72-79 insulin Homo sapiens 22-29 23164509-8 2013 Together, the results uncover a key K8/K18 regulation of glucose metabolism in normal and cancerous hepatic cells through differential modulations of mitochondrial HK status and insulin-mediated signaling. Glucose 57-64 insulin Homo sapiens 178-185 23399272-7 2013 The 17% HA-insulin conjugate showed a lowering effect on blood glucose level for up to 6h, while free insulin exhausted its action after 1h. Glucose 63-70 insulin Homo sapiens 11-18 23352416-2 2013 EA-dependent activation of PKCtheta induces an insulin-resistant phenotype, limiting the access of tumor cells to glucose. Glucose 114-121 insulin Homo sapiens 47-54 22349573-1 2013 CONTEXT: Uncoupling protein 2 (UCP2) is involved in regulating ATP synthesis, generation of reactive oxygen species and glucose-stimulated insulin secretion in beta-cells. Glucose 120-127 insulin Homo sapiens 139-146 22349573-12 2013 Insulin sensitivity measured during intravenous glucose tolerance test in young Caucasian subjects (n=377) was decreased in carriers of the GG genotype (P=0.05). Glucose 48-55 insulin Homo sapiens 0-7 23225242-6 2013 To explore the mechanism associated with this condition, cultured endometrial cells (T-HESC) were exposed to high glucose (25 mM, 24 h), an experimental condition that leads to insulin resistance in other cell types. Glucose 114-121 insulin Homo sapiens 177-184 23225242-13 2013 In conclusion, in PCOSE-IR the impaired phosphorylation of IR downstream molecules such as phospho-Y14caveolin-1 suggests a diminished insulin sensitivity in endometria, condition that could be supported in vitro by the ability of T-HESCs to become insulin resistant when they are exposed to high glucose. Glucose 297-304 insulin Homo sapiens 135-142 22758403-4 2013 Because they more closely mimic the physiologic action of endogenous insulin, insulin analogs are associated with more effective glucose control, a lower risk of hypoglycemia, greater convenience, and, in some instances, less weight gain. Glucose 129-136 insulin Homo sapiens 69-76 22758403-4 2013 Because they more closely mimic the physiologic action of endogenous insulin, insulin analogs are associated with more effective glucose control, a lower risk of hypoglycemia, greater convenience, and, in some instances, less weight gain. Glucose 129-136 insulin Homo sapiens 78-85 23228565-5 2013 We suggest that destabilization of FBPase-Z-line interaction is a universal cellular mechanism of glyconeogenesis down-regulation, allowing for preferential utilization of glucose for insulin-stimulated muscle glycogen synthesis. Glucose 172-179 insulin Homo sapiens 184-191 23410642-3 2013 Intravenous insulin infusions are frequently preferred in the critical care setting to control glucose, because they can be titrated for changing insulin requirements and can be cleared from the system rapidly. Glucose 95-102 insulin Homo sapiens 12-19 23020608-3 2013 Furthermore, we aimed to characterize metformin-treated patients needing additional insulin to achieve prespecified glucose targets. Glucose 116-123 insulin Homo sapiens 84-91 23020608-8 2013 Compared with the patients on metformin only, those needing additional insulin were older (p = 0.04), their oral glucose tolerance test had been performed earlier and diabetes therapy started earlier in gestation (p = 0.01 and p = 0.004, respectively). Glucose 113-120 insulin Homo sapiens 71-78 23180812-9 2013 Results of this study demonstrate that reduced glucose availability associated with insulin resistance and a reduction in GLUT4-mediated glucose transport impairs electrical activity during hypoxia, and may contribute to cardiac vulnerability to arrhythmias in diabetic patients. Glucose 47-54 insulin Homo sapiens 84-91 24278841-4 2013 Receiving standard intensified insulin therapy, she still had poor glucose control with frequent mild and severe hypoglycemic episodes. Glucose 67-74 insulin Homo sapiens 31-38 23104421-10 2013 These results show for the first time that: (i) PGA2 augments insulin action in myocytes as manifested by enhanced stimulation of glucose transport and AKT phosphorylation; and (ii) the insulin sensitizing effect is dependent upon the orphan nuclear receptor NR4A3. Glucose 130-137 insulin Homo sapiens 62-69 23398881-11 2013 Coexistence of high glycemia levels with normal intravascular lipid metabolism may be related to differences in exogenous insulin bioavailabity and different insulin mechanisms of action on glucose and lipids. Glucose 190-197 insulin Homo sapiens 158-165 23154190-4 2013 In response to a single step increase in glucose concentration, our model reproduces the characteristic biphasic insulin release observed in multiple experimental systems, including perfused pancreata and isolated islets of rodent or human origin. Glucose 41-48 insulin Homo sapiens 113-120 23154190-7 2013 When the glucose protocol consists of multiple changes in sequence (a so-called glucose staircase), our model predicts insulin spikes of increasing height, as has been seen experimentally. Glucose 9-16 insulin Homo sapiens 119-126 23154190-7 2013 When the glucose protocol consists of multiple changes in sequence (a so-called glucose staircase), our model predicts insulin spikes of increasing height, as has been seen experimentally. Glucose 80-87 insulin Homo sapiens 119-126 23154190-8 2013 This increase stems from the glucose-dependent increase in the fusion rate of insulin granules at the plasma membrane of single beta-cells. Glucose 29-36 insulin Homo sapiens 78-85 23154190-10 2013 In light of experimental data indicating limited heterogeneous activation for beta-cells within intact islets, our findings suggest that a graded, dose-dependent cell response to glucose may contribute to insulin secretion patterns observed in multiple experiments, and thus regulate in vivo insulin release. Glucose 179-186 insulin Homo sapiens 205-212 23395167-4 2013 LRP6 mutation carriers exhibited hyperinsulinemia and reduced insulin sensitivity compared to noncarrier relatives in response to oral glucose ingestion, which correlated with a significant decline in tissue expression of the insulin receptor and insulin signaling activity. Glucose 135-142 insulin Homo sapiens 38-45 23395167-4 2013 LRP6 mutation carriers exhibited hyperinsulinemia and reduced insulin sensitivity compared to noncarrier relatives in response to oral glucose ingestion, which correlated with a significant decline in tissue expression of the insulin receptor and insulin signaling activity. Glucose 135-142 insulin Homo sapiens 62-69 21080005-2 2013 During the normalization of blood glucose with insulin, the patient developed acute hemolysis. Glucose 34-41 insulin Homo sapiens 47-54 22382775-4 2013 To this end, we labeled INS-1E that are capable of secreting insulin upon glucose stimulation in the physiologic range, with an artificial acyl acceptor (biotinamido-pentylamine) or donor (biotinylated peptide), in basal condition and after stimulus with glucose for 2, 5, and 8 min. Glucose 74-81 insulin Homo sapiens 61-68 22382775-8 2013 Physical interaction between TG2 and cytoplasmic actin during glucose-stimulated first-phase insulin secretion was confirmed by co-immunoprecipitation. Glucose 62-69 insulin Homo sapiens 93-100 23274498-7 2013 Anesthesia with propofol induced a marked whole-body insulin resistance compared with conscious rats, as reflected by significantly decreased glucose infusion rate to maintain euglycemia. Glucose 142-149 insulin Homo sapiens 53-60 23274498-8 2013 Insulin-stimulated tissue glucose uptake was decreased in skeletal muscle and heart, and hepatic glucose output was increased in propofol anesthetized rats. Glucose 26-33 insulin Homo sapiens 0-7 23274498-9 2013 Anesthesia with propofol induces systemic insulin resistance along with decreases in insulin-stimulated glucose uptake in skeletal and heart muscle and attenuation of the insulin-mediated suppression of hepatic glucose output in rats. Glucose 104-111 insulin Homo sapiens 85-92 23274498-9 2013 Anesthesia with propofol induces systemic insulin resistance along with decreases in insulin-stimulated glucose uptake in skeletal and heart muscle and attenuation of the insulin-mediated suppression of hepatic glucose output in rats. Glucose 104-111 insulin Homo sapiens 85-92 23384742-2 2013 Oral contraceptives (OCs) modify surrogate markers such as lipoproteins, insulin response to glucose, and coagulation factors, that have been associated with cardiovascular and venous risk. Glucose 93-100 insulin Homo sapiens 73-80 23375129-7 2013 Importantly, the at-risk alleles of both MC4R rs17782313 and NPC1 rs1805081 showed significant effect on increased fasting glucose levels (beta = 0.36 mmol/L; P = 1.47 x 10(-3)) and decreased fasting serum insulin levels (beta = -0.10 muU/mL; P = 1.21 x 10(-3)), respectively. Glucose 123-130 insulin Homo sapiens 206-213 22324306-13 2013 Increased insulin secretion was related to insulin resistance-induced higher glucose concentrations but also to increased dynamic beta-cell responsivity. Glucose 77-84 insulin Homo sapiens 10-17 23135865-4 2013 The benefits of this therapy over conventional sulfonylureas or insulin injections, such as fewer hypoglycemic events and reduced body weight gain, derive from the glucose-dependent insulinotropic effect. Glucose 164-171 insulin Homo sapiens 64-71 21940063-4 2013 Model-based targeted glucose control can adapt insulin and dextrose interventions to match identified patient insulin sensitivity. Glucose 21-28 insulin Homo sapiens 47-54 21940063-4 2013 Model-based targeted glucose control can adapt insulin and dextrose interventions to match identified patient insulin sensitivity. Glucose 21-28 insulin Homo sapiens 110-117 21940063-4 2013 Model-based targeted glucose control can adapt insulin and dextrose interventions to match identified patient insulin sensitivity. Glucose 59-67 insulin Homo sapiens 110-117 22244505-0 2013 Estimating insulin sensitivity from glucose levels only: Use of a non-linear mixed effects approach and maximum a posteriori (MAP) estimation. Glucose 36-43 insulin Homo sapiens 11-18 22244505-2 2013 It can be derived for a particular patient using data derived from some glucose challenge tests using measured glucose and insulin levels at various times. Glucose 72-79 insulin Homo sapiens 123-130 22244505-4 2013 This paper investigates an approach to measure insulin sensitivity from glucose levels only. Glucose 72-79 insulin Homo sapiens 47-54 23337559-6 2013 In both patients and controls, the increase in the level of C-peptide after honey was significant when compared with either glucose or sucrose (P < 0.01). Glucose 124-131 insulin Homo sapiens 60-69 23022130-4 2013 The glucose-dependency of their glucagon-inhibiting and insulin-enhancing effects, together with their weight-sparing properties, make the incretin therapies a logical proposition for use in combination with exogenous basal insulin therapy. Glucose 4-11 insulin Homo sapiens 56-63 23126686-3 2013 Glucose therapy intensification was defined as new start of insulin or oral hypoglycaemic agents, or addition of prandial insulin or insulin mixtures. Glucose 0-7 insulin Homo sapiens 60-67 23130654-2 2013 Insulin degludec (IDeg) has an ultra-long and stable glucose-lowering effect, with low day-to-day variability. Glucose 53-60 insulin Homo sapiens 0-7 23139352-4 2013 Treating cultured myotubes with LDL containing ceramide promoted ceramide accrual in cells and was accompanied by reduced insulin-stimulated glucose uptake, Akt phosphorylation, and GLUT4 translocation compared with LDL deficient in ceramide. Glucose 141-148 insulin Homo sapiens 122-129 23139352-6 2013 Finally, infusing LDL-ceramide into lean mice reduced insulin-stimulated glucose uptake, and this was due to impaired insulin action specifically in skeletal muscle. Glucose 73-80 insulin Homo sapiens 54-61 23182035-6 2013 Insulin secretion was estimated using three model-based parameters of insulin secretion (beta-cell glucose sensitivity, the potentiation factor ratio, and beta-cell rate sensitivity). Glucose 99-106 insulin Homo sapiens 0-7 23199058-9 2013 In each trial comprising the meta-analysis, fasting plasma glucose and confirmed overall and nocturnal (00.01-05.59 h) hypoglycaemia were all numerically or significantly lower with insulin degludec vs. insulin glargine. Glucose 59-66 insulin Homo sapiens 182-189 23229155-8 2013 CACNA1D siRNA reduced glucose-stimulated insulin release in INS-1 832/13 cells and exocytosis in human beta cells. Glucose 22-29 insulin Homo sapiens 41-48 22926738-4 2013 Insulin dosing algorithms based on CGM glucose trends have proven useful in dissecting the large volume of data generated daily by these devices, although these are imperfect tools, particularly in children. Glucose 39-46 insulin Homo sapiens 0-7 23144046-1 2013 AIMS: Hyperglycaemia during hospitalization for acute myocardial infarction (AMI) is a risk predictor, but attempts to improve the prognosis by insulin-based glucose control have not been consistently successful. Glucose 158-165 insulin Homo sapiens 144-151 23144046-4 2013 METHOD AND RESULTS: We studied 578 T2DM patients who had glucose levels measured hourly while receiving an insulin-glucose infusion during the first 48 h of hospitalization for AMI. Glucose 115-122 insulin Homo sapiens 107-114 22923231-4 2013 In control small interfering RNA-treated cells, insulin increased (P < 0.05) glucose (by 31%) and palmitate uptake (by 20%) and decreased (P < 0.05) palmitate oxidation (by 35%). Glucose 80-87 insulin Homo sapiens 48-55 23118029-8 2013 In vitro C5a and C3a (100 nM) exhibited novel insulin-like effects on 3T3-L1 adipocytes, promoting energy conservation by increasing glucose and fatty acid uptake while inhibiting cAMP signaling and lipolysis, and induced PGE(2) release from macrophages, effects all blocked by each respective antagonist (10 muM). Glucose 133-140 insulin Homo sapiens 46-53 23253816-7 2013 We found an attenuation of the insulin response as indicated by lower glucose uptake and decreased phosphorylation of Akt upon insulin stimulation of adipocytes with mitochondrial dysfunction. Glucose 70-77 insulin Homo sapiens 31-38 23160185-4 2013 Over the past 10 years, numerous studies have demonstrated that genistein has anti-diabetic effects, in particular, direct effects on beta-cell proliferation, glucose-stimulated insulin secretion and protection against apoptosis, independent of its functions as an estrogen receptor agonist, antioxidant, or tyrosine kinase inhibitor. Glucose 159-166 insulin Homo sapiens 178-185 23127112-0 2013 Insulin resistance and cardiovascular risk factors in women with PCOS who have normal glucose tolerance test. Glucose 86-93 insulin Homo sapiens 0-7 23127112-1 2013 INTRODUCTION: We aimed to determine the insulin resistance in women with PCOS patients who have normal oral glucose tolerance test (OGTT) and to evaluate cardiovascular risk by measuring C-reactive protein (CRP) and carotid intimae-media thickness (CIMT). Glucose 108-115 insulin Homo sapiens 40-47 23208300-12 2013 Using a dominant model, the GG + AG group for rs2479106 in DENND1A was associated with elevated serum insulin levels 2 h after a glucose load in the patients with PCOS (P = 0.02). Glucose 129-136 insulin Homo sapiens 102-109 22852864-13 2013 Intravenous insulin therapy significantly lowers glucose levels when compared with controls but adherence to glucose monitoring and treatment protocols appeared to pose considerable challenge on nurses in routine stroke care. Glucose 49-56 insulin Homo sapiens 12-19 23351630-2 2013 Treatment of hyperglycemia with insulin to achieve optimal blood glucose control is challenging and potentially associated with increased risk of the development of hypoglycemia. Glucose 65-72 insulin Homo sapiens 32-39 23299502-6 2013 Multiple linear regression suggested that postload glucose levels at 60 min (60"-PLG) were a better predictor for insulin sensitivity [beta: -0.10, 95% confidence interval (CI) -0.14 to -0.05, P < 0.001] and disposition index (DI) (beta: -0.07, 95% CI -0.12 to -0.02, P = 0.004) estimated from the FSIGT compared with other time points during the OGTT. Glucose 51-58 insulin Homo sapiens 114-121 23627043-7 2013 The efficacy of insulin-loaded LSCS sub micro particles (LSCS-ins) was investigated in diabetic rats by measuring the blood glucose level and found to be an effective reduction of the blood glucose level after oral administration of LSCS-ins. Glucose 124-131 insulin Homo sapiens 16-23 23627043-7 2013 The efficacy of insulin-loaded LSCS sub micro particles (LSCS-ins) was investigated in diabetic rats by measuring the blood glucose level and found to be an effective reduction of the blood glucose level after oral administration of LSCS-ins. Glucose 190-197 insulin Homo sapiens 16-23 23341487-1 2013 CONTEXT: Obesity is characterized by decreased insulin-stimulated glucose uptake in muscle and shift from glucose to lipid oxidation, the so-called metabolic inflexibility. Glucose 66-73 insulin Homo sapiens 47-54 23088748-0 2013 Subcutaneous versus intravenous insulin therapy for glucose control in non-diabetic trauma patients. Glucose 52-59 insulin Homo sapiens 32-39 22704782-3 2013 We demonstrate that acute exposure of L6 myotubes to cis-9, trans-11 (c9,t11) and trans-10, cis-12 (t10,c12) CLA isomers mimics insulin action by stimulating glucose uptake and glucose transporter-4 (GLUT4) trafficking. Glucose 158-165 insulin Homo sapiens 128-135 23117226-0 2013 Analytical expressions for the steady-state concentrations of glucose, oxygen and gluconic acid in a composite membrane for closed-loop insulin delivery. Glucose 62-69 insulin Homo sapiens 136-143 23117226-1 2013 The mathematical model of Abdekhodaie and Wu (J Membr Sci 335:21-31, 2009) of glucose-responsive composite membranes for closed-loop insulin delivery is discussed. Glucose 78-85 insulin Homo sapiens 133-140 22704782-7 2013 Intriguingly, CLA isomers sensitized insulin-Akt-responsive glucose uptake and prevented high insulin-induced Akt desensitisation. Glucose 60-67 insulin Homo sapiens 37-44 23179858-2 2013 It has been shown to adequately describe insulin and glucose profiles in both type 2 diabetics and healthy volunteers following various glucose tolerance tests. Glucose 136-143 insulin Homo sapiens 41-48 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 42-49 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 107-114 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 107-114 22956272-2 2013 Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. Glucose 26-33 insulin Homo sapiens 0-7 22956272-2 2013 Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. Glucose 26-33 insulin Homo sapiens 98-105 22118957-6 2013 Glucose control in smokers was significantly worse than in non-smokers at baseline and during follow-up (mean HbA1c during 5047 patient-years of follow-up 7.9 +- 1.3% in smokers and 7.3 +- 1.1% in non-smokers, p < 0.001) despite a higher insulin dosage in smokers (0.71 +- 0.30 U/kg vs. 0.65 +- 0.31 U/kg in non-smokers, p = 0.046). Glucose 0-7 insulin Homo sapiens 241-248 23401297-6 2013 RESULTS AND CONCLUSION: IL-1beta inhibited insulin-induced activation of Akt phosphorylation, glucose transport, and fatty acid uptake. Glucose 94-101 insulin Homo sapiens 43-50 22805161-1 2013 OBJECTIVES: To describe the design of a clinical trial testing the hypothesis that children randomized to tight glycemic control with intensive insulin therapy after cardiac surgery will have improved clinical outcomes compared to children randomized to conventional blood glucose management. Glucose 273-280 insulin Homo sapiens 144-151 22805161-7 2013 Continuous glucose monitoring is performed during insulin infusion to minimize the risks of hypoglycemia. Glucose 11-18 insulin Homo sapiens 50-57 22566008-4 2013 The in vitro data of rice bran directly translate into in vivo data of rats by using a glucose tolerance test (increase in plasma insulin). Glucose 87-94 insulin Homo sapiens 130-137 22566008-5 2013 Tocotrienols are well known for their apoptotic effect on tumor cells; nevertheless, an attempt was made to study glucose uptake in HEP-G2 cells, which needs to induce an insulin-resistant state by TNF-alpha. Glucose 114-121 insulin Homo sapiens 171-178 23231880-6 2013 Insulin secretion was measured as the area under the curve (AUC(insulin)) generated by levels recorded at baseline, 30, 60 and 120 min after the intake of 75 g of glucose. Glucose 163-170 insulin Homo sapiens 0-7 23231880-6 2013 Insulin secretion was measured as the area under the curve (AUC(insulin)) generated by levels recorded at baseline, 30, 60 and 120 min after the intake of 75 g of glucose. Glucose 163-170 insulin Homo sapiens 64-71 23231880-8 2013 RESULTS: The post-challenge AUC(insulin) was independently predicted by AUC(glucose), waist circumference, triglyceride levels and younger age (p<0.0001); non-smoking status (p=0.0012); and treatment with clozapine (p=0.021). Glucose 76-83 insulin Homo sapiens 32-39 23328189-3 2013 Insulin sensitivity was determined from intravenous glucose tolerances tests before and after each 8-week intervention. Glucose 52-59 insulin Homo sapiens 0-7 23265947-0 2013 CNS insulin signaling in the control of energy homeostasis and glucose metabolism - from embryo to old age. Glucose 63-70 insulin Homo sapiens 4-11 24843632-4 2013 During the trial, basal insulin was titrated according to a prespecified algorithm in order to achieve a fasting plasma glucose target of 80-109 mg/dL. Glucose 120-127 insulin Homo sapiens 24-31 23348588-4 2013 TRAIL inhibited insulin-stimulated glucose uptake and de novo lipogenesis in human adipocytes. Glucose 35-42 insulin Homo sapiens 16-23 23339473-0 2013 20/(fasting C-peptide x fasting plasma glucose) is a simple and effective index of insulin resistance in patients with type 2 diabetes mellitus: a preliminary report. Glucose 39-46 insulin Homo sapiens 12-21 23339473-0 2013 20/(fasting C-peptide x fasting plasma glucose) is a simple and effective index of insulin resistance in patients with type 2 diabetes mellitus: a preliminary report. Glucose 39-46 insulin Homo sapiens 83-90 23339473-1 2013 BACKGROUND: We developed a simple and new insulin resistance index derived from a glucose clamp and a meal tolerance test (MTT) in Japanese patients with type 2 diabetes mellitus. Glucose 82-89 insulin Homo sapiens 42-49 25374688-2 2013 High plasma levels of insulin and glucose due to insulin resistance are a major component of the metabolic disorder. Glucose 34-41 insulin Homo sapiens 49-56 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 42-49 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 107-114 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 107-114 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 42-49 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 107-114 23263773-3 2013 The model captured endogenous glucose and insulin dynamics, including the amplifying effects of glucose on insulin production and of insulin on glucose elimination, as well as the inhibitory influence of glucose and insulin on hepatic glucose production. Glucose 96-103 insulin Homo sapiens 107-114 23334490-4 2013 She was treated with calcium chloride, glucagon, a dextrose-insulin infusion and three vasopressors, but remained hypotensive. Glucose 51-59 insulin Homo sapiens 60-67 23211512-1 2013 Pancreatic beta-cells regulate glucose homeostasis by secreting insulin in response to glucose elevation and G protein-coupled receptor (GPCR) activation. Glucose 31-38 insulin Homo sapiens 64-71 23211512-1 2013 Pancreatic beta-cells regulate glucose homeostasis by secreting insulin in response to glucose elevation and G protein-coupled receptor (GPCR) activation. Glucose 87-94 insulin Homo sapiens 64-71 23255780-0 2013 Meta-analysis investigating associations between healthy diet and fasting glucose and insulin levels and modification by loci associated with glucose homeostasis in data from 15 cohorts. Glucose 74-81 insulin Homo sapiens 86-93 23324111-5 2013 CONCLUSIONS: Women with GDM had more unfavorable lipid profile and higher blood glucose values at three months after delivery, the metabolic profile being worst in women requiring insulin. Glucose 80-87 insulin Homo sapiens 180-187 23256685-1 2013 Insulin degludec, an engineered acylated insulin, was recently reported to form a soluble depot after subcutaneous injection with a subsequent slow release of insulin and an ultralong glucose-lowering effect in excess of 40 h in humans. Glucose 184-191 insulin Homo sapiens 0-7 23256685-1 2013 Insulin degludec, an engineered acylated insulin, was recently reported to form a soluble depot after subcutaneous injection with a subsequent slow release of insulin and an ultralong glucose-lowering effect in excess of 40 h in humans. Glucose 184-191 insulin Homo sapiens 41-48 23291205-0 2013 [A case of glucose-sensitive insulinoma accompanied by slightly elevated serum insulin levels and persisting convulsions after the surgically removed neuroendocrine tumor]. Glucose 11-18 insulin Homo sapiens 29-36 23207292-3 2013 A growing body of evidence suggests that insulin and IGF1 receptors mediate their effects on regulating cell proliferation, differentiation, apoptosis, glucose transport, and energy metabolism by signaling downstream through insulin receptor substrate molecules and thus play a pivotal role in cell fate determination. Glucose 152-159 insulin Homo sapiens 41-48 23207292-3 2013 A growing body of evidence suggests that insulin and IGF1 receptors mediate their effects on regulating cell proliferation, differentiation, apoptosis, glucose transport, and energy metabolism by signaling downstream through insulin receptor substrate molecules and thus play a pivotal role in cell fate determination. Glucose 152-159 insulin Homo sapiens 225-232 23316165-2 2012 Under normal conditions, insulin and glucagon operate in concert to maintain the glucose level within a narrow physiological range. Glucose 81-88 insulin Homo sapiens 25-32 23316165-5 2012 Defects in the insulin-glucagon fine-tuning machinery may result in beta-cell glucose incompetence, leading to unsuppressed glucagon secretion and subsequent hyperglycemia, which often occur under extreme conditions of glucose influx or efflux. Glucose 78-85 insulin Homo sapiens 15-22 23280226-13 2013 Fructose vs glucose ingestion resulted in lower peak levels of serum glucose (mean difference, 41.0 mg/dL [95% CI, 27.7-54.5]; P < .001), insulin (mean difference, 49.6 muU/mL [95% CI, 38.2-61.1]; P < .001), and glucagon-like polypeptide 1 (mean difference, 2.1 pmol/L [95% CI, 0.9-3.2]; P = .01). Glucose 12-19 insulin Homo sapiens 141-148 23280226-14 2013 CONCLUSION AND RELEVANCE: In a series of exploratory analyses, consumption of fructose compared with glucose resulted in a distinct pattern of regional CBF and a smaller increase in systemic glucose, insulin, and glucagon-like polypeptide 1 levels. Glucose 101-108 insulin Homo sapiens 200-207 23121166-3 2013 METHODS: Insulin resistance was measured as [HOMA-IR = Insulin (IU/mL)*glucose (mmol/L)/22.5]. Glucose 71-78 insulin Homo sapiens 9-16 22543593-4 2013 Islet beta-cell function was assessed by disposition index (DI) for the acute insulin response to glucose (AIRg) using intravenous glucose tolerance test. Glucose 98-105 insulin Homo sapiens 78-85 22543593-4 2013 Islet beta-cell function was assessed by disposition index (DI) for the acute insulin response to glucose (AIRg) using intravenous glucose tolerance test. Glucose 131-138 insulin Homo sapiens 78-85 23092914-4 2013 Human subcutaneous preadipocyte-derived adipocytes, differentiated in vitro, were treated with human GIP to analyze mRNA expression and protein secretion of cytokines, glycerol, and free fatty acid release and insulin-induced glucose uptake. Glucose 226-233 insulin Homo sapiens 210-217 23540230-1 2013 INTRODUCTION AND OBJECTIVE: The ability to perceive the symptoms of hypoglycemia during the early decrease in plasma glucose concentration may be critical for the safety of T1DM patients treated with intensive insulin therapy, including those treated with continuous subcutaneous insulin infusion (CSII). Glucose 117-124 insulin Homo sapiens 210-217 23540230-1 2013 INTRODUCTION AND OBJECTIVE: The ability to perceive the symptoms of hypoglycemia during the early decrease in plasma glucose concentration may be critical for the safety of T1DM patients treated with intensive insulin therapy, including those treated with continuous subcutaneous insulin infusion (CSII). Glucose 117-124 insulin Homo sapiens 280-287 23235393-9 2013 A dose-effect relationship was found between the effectiveness of insulin-related glucose control (worst 180-250 mg/dL, best <130 mg/dL) and adverse outcomes. Glucose 82-89 insulin Homo sapiens 66-73 24110480-4 2013 The control algorithm provides daily updates of the basal rate and insulin-to-carbohydrate (IC) ratio in order to optimize glucose regulation. Glucose 123-130 insulin Homo sapiens 67-74 24110588-7 2013 First, significant reduction of hypoglycaemic risk by reducing the undershoot in glucose levels in response to added insulin. Glucose 81-88 insulin Homo sapiens 117-124 22974438-7 2013 Here we discuss the properties of human pancreatic beta cells: their glucose sensing, the ion channel complement underlying glucose-induced electrical activity that culminates in exocytotic release of insulin, the cellular control of exocytosis, and the modulation of insulin secretion by circulating hormones and locally released neurotransmitters. Glucose 124-131 insulin Homo sapiens 201-208 23107043-8 2013 OGTT-derived insulin sensitivity index (ISI) was assessed in 829 individuals with fasting glucose <126 mg/dl. Glucose 90-97 insulin Homo sapiens 13-20 24066304-9 2013 Our results showed that GTP is capable of enhancing insulin-mediated glucose and lipid metabolism by regulating enzymes involved in glycogen synthesis and lipogenesis. Glucose 69-76 insulin Homo sapiens 52-59 24565418-1 2013 BACKGROUND: Insulin secreted by pancreatic islet beta-cells is the principal regulating hormone of glucose metabolism and plays a key role in controlling glucose level in blood. Glucose 99-106 insulin Homo sapiens 12-19 23578341-5 2013 An estimate of insulin resistance by homeostasis model assessment (HOMA-IR index) was calculated from fasting insulin and glucose. Glucose 122-129 insulin Homo sapiens 15-22 23339089-6 2013 hPdx1-treated hES cells synthesise and release insulin in response to glucose challenge. Glucose 70-77 insulin Homo sapiens 47-54 22710060-11 2013 There was a stepwise increase in human insulin and c-peptide release by IPCs in response to increasing glucose concentrations. Glucose 103-110 insulin Homo sapiens 39-46 22710060-11 2013 There was a stepwise increase in human insulin and c-peptide release by IPCs in response to increasing glucose concentrations. Glucose 103-110 insulin Homo sapiens 51-60 23109550-4 2013 Insulin sensitivity was assessed by the oral 75 g glucose tolerance test. Glucose 50-57 insulin Homo sapiens 0-7 22974359-8 2013 Insulin is secreted primarily in response to glucose, while other nutrients such as free fatty acids and amino acids can augment glucose-induced insulin secretion. Glucose 45-52 insulin Homo sapiens 0-7 22834840-3 2013 Restoration of first phase insulin secretion has been shown to improve blood glucose in T2D by suppressing hepatic glucose production and priming insulin sensitive tissue to more readily take up glucose and has thus prompted numerous studies into its regulation. Glucose 77-84 insulin Homo sapiens 27-34 22834840-3 2013 Restoration of first phase insulin secretion has been shown to improve blood glucose in T2D by suppressing hepatic glucose production and priming insulin sensitive tissue to more readily take up glucose and has thus prompted numerous studies into its regulation. Glucose 115-122 insulin Homo sapiens 27-34 22834840-3 2013 Restoration of first phase insulin secretion has been shown to improve blood glucose in T2D by suppressing hepatic glucose production and priming insulin sensitive tissue to more readily take up glucose and has thus prompted numerous studies into its regulation. Glucose 115-122 insulin Homo sapiens 27-34 22776039-4 2013 Stimulation of insulin secretion from pancreatic beta-cells by glucagon-like peptide 1 receptor (GLP-1R) agonists is known to be glucose-dependent. Glucose 129-136 insulin Homo sapiens 15-22 22776039-5 2013 GLP-1R agonists potentiate glucose-stimulated insulin secretion and have little or no activity on insulin secretion in the absence of elevated blood glucose concentrations. Glucose 27-34 insulin Homo sapiens 46-53 22776039-9 2013 This review aims to discuss the current understanding of the mechanisms by which GLP-1R signalling promotes insulin secretion from pancreatic beta-cells via a glucose-dependent process. Glucose 159-166 insulin Homo sapiens 108-115 22830987-1 2013 We recently showed in a euglycaemic glucose clamp study among 18 healthy volunteers that using jet injectors rather than conventional pens significantly improved the time-action profiles of rapid-acting insulin analogs. Glucose 36-43 insulin Homo sapiens 203-210 22961574-1 2013 OBJECTIVE: To test whether early, insulin-mediated microvascular recruitment in skeletal muscle predicts steady-state glucose metabolism in the setting of physiological elevation of free fatty acid concentrations. Glucose 118-125 insulin Homo sapiens 34-41 22961574-11 2013 CONCLUSIONS: Early microvascular responses to insulin strongly associate with steady state skeletal muscle insulin-mediated glucose uptake. Glucose 124-131 insulin Homo sapiens 46-53 22961574-11 2013 CONCLUSIONS: Early microvascular responses to insulin strongly associate with steady state skeletal muscle insulin-mediated glucose uptake. Glucose 124-131 insulin Homo sapiens 107-114 22966097-5 2013 Intensive insulin therapy was defined as three or more injections (or pump) and four or more glucose tests daily. Glucose 93-100 insulin Homo sapiens 10-17 24157813-7 2013 Moreover, in the GDM group, these SNPs were associated with increased fasting plasma glucose concentrations (p < 0.001) and increased homeostasis model assessment of insulin resistance (p < 0.001). Glucose 85-92 insulin Homo sapiens 169-176 23379555-2 2013 Insulin resistance is associated with a decrease in glucose uptake by muscle and adipose cells and also with a decrease in glycogen synthesis on retention of glucose synthesis by liver cells. Glucose 52-59 insulin Homo sapiens 0-7 23379555-2 2013 Insulin resistance is associated with a decrease in glucose uptake by muscle and adipose cells and also with a decrease in glycogen synthesis on retention of glucose synthesis by liver cells. Glucose 158-165 insulin Homo sapiens 0-7 23555075-1 2013 AIM: In postcardiac surgery patients, we assessed the performance of a system for intensive intravenous insulin therapy using continuous glucose monitoring (CGM) and enhanced model predictive control (eMPC) algorithm. Glucose 137-144 insulin Homo sapiens 104-111 23314346-2 2013 This disorder involves multiple physiological defects that result from high blood glucose content and eventually lead to the onset of insulin resistance. Glucose 82-89 insulin Homo sapiens 134-141 24222881-2 2013 Liraglutide lowers blood glucose levels by stimulating insulin secretion and decreasing glucagon release in glucose-dependent manners, increases satiety, and delays gastric emptying. Glucose 25-32 insulin Homo sapiens 55-62 24296476-2 2013 The present study investigated the effects of the saturated FFA stearic acid on protein tyrosine phosphatase 1B (PTP1B) activity, Akt activity, and glucose uptake into cells relevant to insulin signal. Glucose 148-155 insulin Homo sapiens 186-193 24296476-6 2013 For 3T3-L1- GLUT4myc adipocytes insulin phosphorylated insulin receptor at Tyr1185 and Akt at Thr308 and Ser473 in a concentration (100 fM-100 nM)-dependent manner and stimulated glucose uptake into cells in a concentration (0.1-100 nM)-dependent manner. Glucose 179-186 insulin Homo sapiens 32-39 23420163-10 2013 CONCLUSION: The multiple regression model demonstrated that in addition to age and glycemia (two well-known factors that are directly involved in glucose metabolism), adrenomedullin and IL-6 levels were independent factors associated with lower insulin concentrations. Glucose 146-153 insulin Homo sapiens 245-252 24260042-1 2013 Automated closed-loop control of blood glucose concentration is a daily challenge for type 1 diabetes mellitus, where insulin and glucagon are two critical hormones for glucose regulation. Glucose 39-46 insulin Homo sapiens 118-125 24260042-1 2013 Automated closed-loop control of blood glucose concentration is a daily challenge for type 1 diabetes mellitus, where insulin and glucagon are two critical hormones for glucose regulation. Glucose 169-176 insulin Homo sapiens 118-125 23448488-1 2013 Insulin resistance is associated with the impairment of the response of insulin receptor to insulin, resulting in the reduction of glucose uptake, leading to the alteration of myocardial glucose metabolism, impairment of cardiac electrophysiology, and increased susceptibility to ischemia-induced myocardial injury. Glucose 131-138 insulin Homo sapiens 0-7 23448488-1 2013 Insulin resistance is associated with the impairment of the response of insulin receptor to insulin, resulting in the reduction of glucose uptake, leading to the alteration of myocardial glucose metabolism, impairment of cardiac electrophysiology, and increased susceptibility to ischemia-induced myocardial injury. Glucose 131-138 insulin Homo sapiens 72-79 23489203-2 2013 Physiologically, insulin is a potent hypoglycaemic agent, which is vital in order for plasma glucose levels to be maintained within the normal range of 4- 7mmol/L. Glucose 93-100 insulin Homo sapiens 17-24 23627940-3 2013 Obesity-associated insulin resistance, which is characterized by reduced uptake and utilization of glucose in muscle, adipose and liver tissues, is a key predictor of metabolic syndrome and T2DM. Glucose 99-106 insulin Homo sapiens 19-26 23021431-9 2013 Estimated energy needs were 3626+-710 kcal, of which 84+-21% were met by enteral feeding with intensive insulin treatment (glucose 80-110 mg/ml). Glucose 123-130 insulin Homo sapiens 104-111 22646532-6 2013 The combination of a GLP-1RA and insulin might thus be highly effective for optimal glucose control, ameliorating the adverse effects typically associated with insulin. Glucose 84-91 insulin Homo sapiens 33-40 22923476-4 2013 C-peptide (1 nmol/L) prevented endothelial cell death by inhibiting protein kinase C- and NADPH oxidase-dependent intracellular ROS generation and by abolishing high glucose-induced TG2 activation, without affecting intracellular Ca(2+) levels. Glucose 166-173 insulin Homo sapiens 0-9 22933433-8 2013 RESULTS: Hepatic suppression of glucose production during the clamp was significantly lower after HF (59.4 +- 11.0%) than HG (70.3 +- 10.5%, P < 0.05), whereas fasting glucose, insulin, and C-peptide did not differ between the interventions. Glucose 32-39 insulin Homo sapiens 180-187 22933436-10 2013 In response to combined arginine and glucose stimulation, maximal insulin response was reduced. Glucose 37-44 insulin Homo sapiens 66-73 22933441-1 2013 OBJECTIVE: We aimed to examine insulin clearance, a compensatory mechanism to changes in insulin sensitivity, across sex, race/ethnicity populations, and varying states of glucose tolerance. Glucose 172-179 insulin Homo sapiens 31-38 22933441-5 2013 CONCLUSIONS: Insulin sensitivity, insulin secretion, and adiposity are correlates of insulin clearance and appear to explain differences in insulin clearance by race/ethnicity and glucose tolerance status. Glucose 180-187 insulin Homo sapiens 13-20 22936679-10 2013 Insulin resistance in type 1 diabetes involves both lipolysis, hepatic and peripheral glucose metabolism. Glucose 86-93 insulin Homo sapiens 0-7 23046396-0 2013 Assessing performance of closed-loop insulin delivery systems by continuous glucose monitoring: drawbacks and way forward. Glucose 76-83 insulin Homo sapiens 37-44 23126579-0 2013 Periodic extraction of interstitial fluid from the site of subcutaneous insulin infusion for the measurement of glucose: a novel single-port technique for the treatment of type 1 diabetes patients. Glucose 112-119 insulin Homo sapiens 72-79 23126579-1 2013 BACKGROUND: Treatment of type 1 diabetes patients could be simplified if the site of subcutaneous insulin infusion could also be used for the measurement of glucose. Glucose 157-164 insulin Homo sapiens 98-105 23126579-4 2013 RESULTS: Although periodically interrupted for extracting glucose (every hour for approximately 10 min), insulin infusion with the cannula was adequate to achieve euglycemia during fasting and to restore euglycemia after glucose ingestion. Glucose 221-228 insulin Homo sapiens 105-112 23126579-8 2013 CONCLUSIONS: Results show that ISF glucose concentrations measured at the insulin infusion site during periodic short-term interruptions of CSII closely reflect blood glucose levels, thus suggesting that glucose monitoring and insulin delivery may be performed alternately at the same tissue site. Glucose 35-42 insulin Homo sapiens 74-81 23126579-8 2013 CONCLUSIONS: Results show that ISF glucose concentrations measured at the insulin infusion site during periodic short-term interruptions of CSII closely reflect blood glucose levels, thus suggesting that glucose monitoring and insulin delivery may be performed alternately at the same tissue site. Glucose 167-174 insulin Homo sapiens 74-81 23126579-8 2013 CONCLUSIONS: Results show that ISF glucose concentrations measured at the insulin infusion site during periodic short-term interruptions of CSII closely reflect blood glucose levels, thus suggesting that glucose monitoring and insulin delivery may be performed alternately at the same tissue site. Glucose 167-174 insulin Homo sapiens 74-81 22972222-6 2013 Also, parameters reflecting the glucose-stimulated insulin secretion, such as the insulinogenic index and oral disposition index, were significantly higher in the responder group than in the non-responder group, whereas insulin sensitivity was similar between the two groups. Glucose 32-39 insulin Homo sapiens 51-58 22972222-6 2013 Also, parameters reflecting the glucose-stimulated insulin secretion, such as the insulinogenic index and oral disposition index, were significantly higher in the responder group than in the non-responder group, whereas insulin sensitivity was similar between the two groups. Glucose 32-39 insulin Homo sapiens 82-89 22972222-7 2013 These results suggest that the difference in the degree of improvement of the glucose tolerance between the responder group and non-responder group in this study could be associated with the effect of vildagliptin on the glucose-stimulated insulin secretion, but not on the insulin sensitivity. Glucose 78-85 insulin Homo sapiens 240-247 22972222-7 2013 These results suggest that the difference in the degree of improvement of the glucose tolerance between the responder group and non-responder group in this study could be associated with the effect of vildagliptin on the glucose-stimulated insulin secretion, but not on the insulin sensitivity. Glucose 78-85 insulin Homo sapiens 274-281 22972222-7 2013 These results suggest that the difference in the degree of improvement of the glucose tolerance between the responder group and non-responder group in this study could be associated with the effect of vildagliptin on the glucose-stimulated insulin secretion, but not on the insulin sensitivity. Glucose 221-228 insulin Homo sapiens 240-247 24616775-11 2013 LEARNING POINTS: THERE IS A COMPLEX INTERPLAY BETWEEN GH AND INSULIN RESISTANCE: chronically, both GH excess and deficiency lead to insulin resistance, but there is also an acute mechanism that is less well appreciated by clinicians.GH activates hormone-sensitive lipase to release FFA into the circulation; these may inhibit the uptake of glucose leading to hyperglycaemia and ketosis in the type 1 diabetic patient.The Randle cycle, or glucose-fatty acid cycle, outlines the mechanism for this acute relationship.Monitoring the adequacy of GH replacement in patients with type 1 diabetes is difficult, with IGF1 an unreliable marker. Glucose 340-347 insulin Homo sapiens 61-68 23983791-8 2013 In mature 3T3-L1 adipocytes, naringenin reduced the ability of insulin to induce IRS-1 tyrosine phosphorylation and substantially inhibited insulin-stimulated glucose uptake in a dose-dependent manner and over a time frame of 1.5 to 24 hours. Glucose 159-166 insulin Homo sapiens 140-147 23662132-8 2013 In this review, we select and discuss blood glucose-lowering medicinal herbs that have the ability to modulate one or more of the pathways that regulate insulin resistance, beta-cell function, GLP-1 homeostasis, and glucose (re)absorption. Glucose 44-51 insulin Homo sapiens 153-160 23036788-1 2013 The mechanism(s) behind the decreased ability of insulin to facilitate glucose uptake in insulin sensitive tissues as seen in type 2 diabetes is not resolved. Glucose 71-78 insulin Homo sapiens 49-56 23036788-1 2013 The mechanism(s) behind the decreased ability of insulin to facilitate glucose uptake in insulin sensitive tissues as seen in type 2 diabetes is not resolved. Glucose 71-78 insulin Homo sapiens 89-96 22310476-3 2013 Conversely, when insulin signaling is impaired in obesity or diabetes, the insulin-independent Ras pathway may be valuable for enhancing glucose disposal. Glucose 137-144 insulin Homo sapiens 17-24 22310476-3 2013 Conversely, when insulin signaling is impaired in obesity or diabetes, the insulin-independent Ras pathway may be valuable for enhancing glucose disposal. Glucose 137-144 insulin Homo sapiens 75-82 22310476-17 2013 CONCLUSIONS: Overall, the study offers Ras/Glut4 pathway as an alternate to enhance glucose disposal when insulin signaling is impaired, and, importantly, provides Ad36 as a tool to understand the modulation of that pathway. Glucose 84-91 insulin Homo sapiens 106-113 24190150-2 2013 A 75 g oral glucose tolerance test (75 gOGTT) showed a marked increase in the plasma insulin level and impaired glucose tolerance. Glucose 12-19 insulin Homo sapiens 85-92 23370747-2 2013 Her fasting plasma glucose level was 54 mg/dL with an extremely high serum immunoreactive insulin level (1210 muU/mL). Glucose 19-26 insulin Homo sapiens 90-97 23431467-1 2013 Insulin resistance is a common finding in chronic kidney disease (CKD) and is manifested by mild fasting hyperglycemia and abnormal glucose tolerance testing. Glucose 132-139 insulin Homo sapiens 0-7 23984046-0 2013 Ingestion of leucine + phenylalanine with glucose produces an additive effect on serum insulin but less than additive effect on plasma glucose. Glucose 42-49 insulin Homo sapiens 87-94 23100584-8 2013 The maximum increment in plasma insulin achieved in response to exogenous glucose was less in ACTH-treated foals at both 2 and 12 wk of age (P<0.05). Glucose 74-81 insulin Homo sapiens 32-39 23100584-9 2013 By 12 wk of age, developmental changes also occurred in the magnitude and biphasic pattern of glucose-stimulated insulin release. Glucose 94-101 insulin Homo sapiens 113-120 24482983-10 2013 Fasting plasma glucose values decreased by 70 mg/dL and 50 mg/dL in insulin naive and insulin experienced, respectively and the difference from baseline was statistically significant (P < 0.001). Glucose 15-22 insulin Homo sapiens 68-75 24482983-10 2013 Fasting plasma glucose values decreased by 70 mg/dL and 50 mg/dL in insulin naive and insulin experienced, respectively and the difference from baseline was statistically significant (P < 0.001). Glucose 15-22 insulin Homo sapiens 86-93 24482983-11 2013 The post prandial glucose value was also significantly (p < 0.001) reduced by 105 mg/dL for insulin naive subjects and 55 mg/dL for insulin experienced subjects. Glucose 18-25 insulin Homo sapiens 95-102 24482983-11 2013 The post prandial glucose value was also significantly (p < 0.001) reduced by 105 mg/dL for insulin naive subjects and 55 mg/dL for insulin experienced subjects. Glucose 18-25 insulin Homo sapiens 135-142 23489701-0 2013 Insulin resistance in first-trimester pregnant women with pre-pregnant glucose tolerance and history of recurrent spontaneous abortion. Glucose 71-78 insulin Homo sapiens 0-7 23489701-11 2013 In conclusion, woman with recurrent spontaneous abortion and normal pre-pregnant glucose metabolism tends to be more insulin resistant during first trimester pregnancy than healthy controls, no matter whether she has PCOS or not. Glucose 81-88 insulin Homo sapiens 117-124 23150678-3 2013 OBJECTIVE: The aim of the study was to measure adipose tissue insulin sensitivity and plasma triglyceride composition in individuals with type 1 diabetes after overnight insulin infusion to lower fasting glucose. Glucose 204-211 insulin Homo sapiens 62-69 23150678-3 2013 OBJECTIVE: The aim of the study was to measure adipose tissue insulin sensitivity and plasma triglyceride composition in individuals with type 1 diabetes after overnight insulin infusion to lower fasting glucose. Glucose 204-211 insulin Homo sapiens 170-177 23367497-2 2013 She had elevated fasting (422.95 pmol/L) and post-glucose insulin levels(>2083 pmol/L). Glucose 50-57 insulin Homo sapiens 58-65 23423872-9 2013 A positive correlation between insulin levels (basal and after oral glucose load) and cIMT of common, internal and external carotid artery was found in obese subjects (p < 0.03). Glucose 68-75 insulin Homo sapiens 31-38 23439156-5 2013 Blood glucose changes were induced by oral carbohydrate intake and insulin injections, and capillary blood glucose samples were obtained from the finger tip. Glucose 6-13 insulin Homo sapiens 67-74 24190036-4 2013 Over-expression of wild-type CSP1 led to attenuated insulin-stimulated glucose uptake without any change in GLUT4 content in the plasma membrane, rather it inhibits docking by blocking the association of VAMP2 with syntaxin 4. Glucose 71-78 insulin Homo sapiens 52-59 24190036-5 2013 In contrast, knockdown of CSP1 enhanced insulin-stimulated glucose uptake. Glucose 59-66 insulin Homo sapiens 40-47 24190037-5 2013 RESULTS: The mean and SD of blood glucose concentration during surgery (Glu-Ave and Glu-SD, respectively) for the programmed insulin group were lower than for the manual insulin group. Glucose 34-41 insulin Homo sapiens 125-132 22819549-5 2013 In cell culture, glucose induced the secretion of hepcidin and insulin into the supernatant of INS-1E cultures, but did not change the amount of hepcidin detectable in the hepatocyte cell culture HepG2. Glucose 17-24 insulin Homo sapiens 63-70 23457308-6 2013 We also show that exposure of HUVECs to high-glucose conditions inhibits the insulin-mediated activation of Akt/eNOS signalling and the subsequent NO generation in a dose-dependent manner (p<0.05). Glucose 45-52 insulin Homo sapiens 77-84 24025781-6 2013 Insulin stimulated glucose uptake was reduced by imidacloprid in all three cell culture models. Glucose 19-26 insulin Homo sapiens 0-7 22982177-7 2013 Oral glucose challenge in human islet transplanted mice resulted in an immediate incremental increase of plasma human C-peptide, while the plasma mouse C-peptide was undetectable. Glucose 5-12 insulin Homo sapiens 118-127 23086867-7 2013 Insulin secretion is regulated by plasma glucose concentration which acts through intracellular metabolism to influence intracellular [Ca(2+)]. Glucose 41-48 insulin Homo sapiens 0-7 23705494-9 2013 Mutations of INSR induce insulin resistance, lipodystrophy, other pathology, and suggest an important role of insulin in glucose level regulation and in stimulation of fat accumulation as well. Glucose 121-128 insulin Homo sapiens 110-117 23148893-9 2013 In 3T3-L1 adipocytes, insulin resistance induced by TNFalpha increased Mt2a mRNA levels (p=3x10(-4)) and insulin-stimulated glucose uptake was significantly inhibited by 53% (p=8x10(-4)) compared to vehicle, when 3T3-L1 adipocytes were treated with Mt protein. Glucose 124-131 insulin Homo sapiens 22-29 23148893-9 2013 In 3T3-L1 adipocytes, insulin resistance induced by TNFalpha increased Mt2a mRNA levels (p=3x10(-4)) and insulin-stimulated glucose uptake was significantly inhibited by 53% (p=8x10(-4)) compared to vehicle, when 3T3-L1 adipocytes were treated with Mt protein. Glucose 124-131 insulin Homo sapiens 105-112 24364208-1 2013 Type 2 diabetes mellitus (T2DM) is a metabolic disease caused by insulin resistance that leads to changes in glucose metabolism. Glucose 109-116 insulin Homo sapiens 65-72 23920897-1 2013 Gestational diabetes is a condition occurring in up to 18% [1] of pregnant women that results in an increase in blood glucose levels due to the body"s inability to produce sufficient insulin given the additional needs of the baby, and/or hormonal changes that lower the body"s sensitivity to insulin. Glucose 118-125 insulin Homo sapiens 183-190 23920897-1 2013 Gestational diabetes is a condition occurring in up to 18% [1] of pregnant women that results in an increase in blood glucose levels due to the body"s inability to produce sufficient insulin given the additional needs of the baby, and/or hormonal changes that lower the body"s sensitivity to insulin. Glucose 118-125 insulin Homo sapiens 292-299 23431062-4 2013 These drawbacks may be overcome by combining insulin with incretin-based therapies as these increase glucose sensitivity of both the alpha- and beta-cells, resulting in improved postprandial glycemia without the hypoglycemia and weight gain associated with increasing the dose of insulin. Glucose 101-108 insulin Homo sapiens 45-52 23637538-2 2013 Glucose-lowering medications that increase circulating insulin in a glucose-independent manner, such as insulin and sulfonylurea therapy, are the most common cause of hypoglycemia. Glucose 0-7 insulin Homo sapiens 55-62 23637538-2 2013 Glucose-lowering medications that increase circulating insulin in a glucose-independent manner, such as insulin and sulfonylurea therapy, are the most common cause of hypoglycemia. Glucose 0-7 insulin Homo sapiens 104-111 23637538-2 2013 Glucose-lowering medications that increase circulating insulin in a glucose-independent manner, such as insulin and sulfonylurea therapy, are the most common cause of hypoglycemia. Glucose 68-75 insulin Homo sapiens 55-62 23256222-18 2004 GLUT4 and HKII are the major transporter and HK isoform in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. Glucose 128-135 insulin Homo sapiens 111-118 23213228-4 2012 Such a secretion-biosynthesis coupling has been demonstrated for insulin; however, because of insulin"s unique role as the sole blood glucose-decreasing peptide hormone, this coupling is considered an exception rather than a more generally used mechanism. Glucose 134-141 insulin Homo sapiens 94-101 23251132-5 2012 The beta cells of the pancreatic islets of Langerhans respond to changes in blood glucose concentration by varying the rate of insulin synthesis and secretion. Glucose 82-89 insulin Homo sapiens 127-134 22975396-5 2012 The presence of a mixture of insulin and glucose affected the molecular packing in the DPPC monolayer differently than the pure insulin or glucose solutions, and the glucose-insulin mixture was seen to be able to penetrate through the monolayer. Glucose 41-48 insulin Homo sapiens 128-135 23045302-9 2013 Fasting glucose level was normal associated with high insulin levels at baseline and during an oral glucose tolerance test. Glucose 8-15 insulin Homo sapiens 54-61 23208166-10 2012 Patients with insulinoma had lower glucose levels and higher insulin and C-peptide levels overall than did control patients at the end of prolonged fasts, but there was considerable overlap. Glucose 35-42 insulin Homo sapiens 14-21 23208166-11 2012 The amended insulin-glucose ratio correctly identified 48 of 49 patients with insulinoma and excluded the diagnosis in 64 of 65 control patients, resulting in positive and negative predictive values of 0.98 (95% CI, 0.89 to 1.00) and 0.99 (CI, 0.92 to 1.00), respectively, compared with 0.75 (CI, 0.63 to 0.85) and 0.98 (CI, 0.89 to 1.00), respectively, for glucose, insulin, and C-peptide concentration criteria. Glucose 20-27 insulin Homo sapiens 12-19 23208166-13 2012 CONCLUSION: The amended insulin-glucose ratio showed improved diagnostic accuracy over established criteria that use glucose, insulin, and C-peptide concentrations. Glucose 32-39 insulin Homo sapiens 24-31 24533206-6 2012 Insulin sensitivity and secretion were measured using intravenous glucose tolerance test and minimal model. Glucose 66-73 insulin Homo sapiens 0-7 22902301-5 2012 Our studies elucidate two size-dependent phenomena: (1) as the cluster size increases from 40mum to 60mum, glucose stimulation results in a greater amount of insulin produced per cell; and (2) as the cluster size increases beyond 60mum, sustained glucose stimulation results in a greater amount of insulin secreted per cell. Glucose 107-114 insulin Homo sapiens 158-165 22902301-5 2012 Our studies elucidate two size-dependent phenomena: (1) as the cluster size increases from 40mum to 60mum, glucose stimulation results in a greater amount of insulin produced per cell; and (2) as the cluster size increases beyond 60mum, sustained glucose stimulation results in a greater amount of insulin secreted per cell. Glucose 107-114 insulin Homo sapiens 298-305 22902301-5 2012 Our studies elucidate two size-dependent phenomena: (1) as the cluster size increases from 40mum to 60mum, glucose stimulation results in a greater amount of insulin produced per cell; and (2) as the cluster size increases beyond 60mum, sustained glucose stimulation results in a greater amount of insulin secreted per cell. Glucose 247-254 insulin Homo sapiens 158-165 22902301-5 2012 Our studies elucidate two size-dependent phenomena: (1) as the cluster size increases from 40mum to 60mum, glucose stimulation results in a greater amount of insulin produced per cell; and (2) as the cluster size increases beyond 60mum, sustained glucose stimulation results in a greater amount of insulin secreted per cell. Glucose 247-254 insulin Homo sapiens 298-305 22902821-0 2012 The influence of arrangement sequence on the glucose-responsive controlled release profiles of insulin-incorporated LbL films. Glucose 45-52 insulin Homo sapiens 95-102 22902821-3 2012 The insulin release in vitro could be tuned to linear release and obtain desired "on-off" sensitivity in response to stepwise glucose challenge, just by rearranging the assembly sequence of LbL building blocks. Glucose 126-133 insulin Homo sapiens 4-11 22902821-5 2012 In addition to provide a potential glucose-responsive delivery system for insulin, the strategy described in this paper could be valuable for various drug-incorporated LbL systems with three or more components. Glucose 35-42 insulin Homo sapiens 74-81 20473530-0 2012 Decreased beta cell function and insulin sensitivity contributed to increasing fasting glucose in Chinese. Glucose 87-94 insulin Homo sapiens 33-40 20473530-6 2012 Both the impairment of beta cell function and insulin sensitivity started at the low point of FPG within the normoglycemic range and contributed to the deterioration of fasting glucose. Glucose 177-184 insulin Homo sapiens 46-53 22249339-5 2012 Consequently, we evaluated the viability, the induction of apoptosis, the glucose-stimulated insulin secretion, and the expression of beta-cell function genes (Isl1, Pax6, Glut-2, glucokinase) and apoptosis-related genes (Bax and Bcl2). Glucose 74-81 insulin Homo sapiens 93-100 22249339-8 2012 A twofold increase in apoptotic cells was observed in human islets after MPA exposure associated with strong inhibition of glucose-stimulated insulin secretion. Glucose 123-130 insulin Homo sapiens 142-149 22836490-4 2012 Secondly, "PPG-without insulin/with Sg" was obtained from inverse correlation between log(10)DI(O) and 2-h post-glucose plasma glucose at OGTT (2hPG) in each glucose tolerance category: DI(O) denotes oral disposition index, a product of the Matsuda Index and deltaIRI(0-30)/deltaPG(0-30). Glucose 112-119 insulin Homo sapiens 23-30 22836490-4 2012 Secondly, "PPG-without insulin/with Sg" was obtained from inverse correlation between log(10)DI(O) and 2-h post-glucose plasma glucose at OGTT (2hPG) in each glucose tolerance category: DI(O) denotes oral disposition index, a product of the Matsuda Index and deltaIRI(0-30)/deltaPG(0-30). Glucose 127-134 insulin Homo sapiens 23-30 22836490-4 2012 Secondly, "PPG-without insulin/with Sg" was obtained from inverse correlation between log(10)DI(O) and 2-h post-glucose plasma glucose at OGTT (2hPG) in each glucose tolerance category: DI(O) denotes oral disposition index, a product of the Matsuda Index and deltaIRI(0-30)/deltaPG(0-30). Glucose 127-134 insulin Homo sapiens 23-30 23141431-2 2012 Metformin increases insulin-stimulated glucose uptake and has direct effects on ovarian steroidogenesis in humans. Glucose 39-46 insulin Homo sapiens 20-27 22916958-1 2012 The specific and direct contribution of the stress-activated serine kinase c-Jun N-terminal kinase (JNK) in the development of oxidative stress-induced insulin resistance of the glucose transport system in mammalian skeletal muscle is not fully understood. Glucose 178-185 insulin Homo sapiens 152-159 22916958-3 2012 Importantly, insulin-stimulated glucose transport activity in the presence of H(2)O(2) was moderately improved with the selective JNK inhibitor SP600125. Glucose 32-39 insulin Homo sapiens 13-20 23168276-4 2012 In response to a glucose rise, nucleotides and metabolites are generated by mitochondria and participate, together with cytosolic calcium, in the stimulation of insulin release. Glucose 17-24 insulin Homo sapiens 161-168 22827292-2 2012 Traditional medicines for type 2 diabetes, such as sulfonylureas, pioglitazone, and insulin have glucose lowering effects; however, they also increase the frequency of hypoglycemia and/or body weight and thus may cancel out the benefits of glucose lowering on the development of atherosclerosis. Glucose 97-104 insulin Homo sapiens 84-91 22827292-2 2012 Traditional medicines for type 2 diabetes, such as sulfonylureas, pioglitazone, and insulin have glucose lowering effects; however, they also increase the frequency of hypoglycemia and/or body weight and thus may cancel out the benefits of glucose lowering on the development of atherosclerosis. Glucose 240-247 insulin Homo sapiens 84-91 23381670-1 2012 Insulin (INS) metabolic signaling is important for normal cardiovascular and renal function as well as for exerting the classic actions of INS, such as glucose uptake in skeletal muscle tissue. Glucose 152-159 insulin Homo sapiens 0-7 22890005-3 2012 Working in concert with insulin, glucagon is involved in regulating circulating glucose concentrations. Glucose 80-87 insulin Homo sapiens 24-31 22682085-3 2012 Insulin resistance is important in various states such as starvation, immune activation, growth and cancer, to spare glucose for different biosynthetic purposes such as the production of NADPH, nucleotides in the pentose phosphate pathway and oxaloacetate for anaplerosis. Glucose 117-124 insulin Homo sapiens 0-7 23195963-7 2012 RESULTS: Glucose infusion rates increased after administration of either NPH or oral enteric insulin. Glucose 9-16 insulin Homo sapiens 93-100 23164767-7 2012 We suggest that the insulin regimen and monitoring system be designed to avoid and detect hypoglycemia (blood glucose <= 70 mg/dL) and to minimize glycemic variability.Important processes of care for insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monitoring, and avoidance of finger-stick glucose testing through the use of arterial or venous glucose samples. Glucose 110-117 insulin Homo sapiens 20-27 23164767-7 2012 We suggest that the insulin regimen and monitoring system be designed to avoid and detect hypoglycemia (blood glucose <= 70 mg/dL) and to minimize glycemic variability.Important processes of care for insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monitoring, and avoidance of finger-stick glucose testing through the use of arterial or venous glucose samples. Glucose 110-117 insulin Homo sapiens 203-210 23164767-7 2012 We suggest that the insulin regimen and monitoring system be designed to avoid and detect hypoglycemia (blood glucose <= 70 mg/dL) and to minimize glycemic variability.Important processes of care for insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monitoring, and avoidance of finger-stick glucose testing through the use of arterial or venous glucose samples. Glucose 110-117 insulin Homo sapiens 203-210 23164767-7 2012 We suggest that the insulin regimen and monitoring system be designed to avoid and detect hypoglycemia (blood glucose <= 70 mg/dL) and to minimize glycemic variability.Important processes of care for insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monitoring, and avoidance of finger-stick glucose testing through the use of arterial or venous glucose samples. Glucose 287-294 insulin Homo sapiens 20-27 23164767-7 2012 We suggest that the insulin regimen and monitoring system be designed to avoid and detect hypoglycemia (blood glucose <= 70 mg/dL) and to minimize glycemic variability.Important processes of care for insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monitoring, and avoidance of finger-stick glucose testing through the use of arterial or venous glucose samples. Glucose 287-294 insulin Homo sapiens 203-210 23164767-7 2012 We suggest that the insulin regimen and monitoring system be designed to avoid and detect hypoglycemia (blood glucose <= 70 mg/dL) and to minimize glycemic variability.Important processes of care for insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monitoring, and avoidance of finger-stick glucose testing through the use of arterial or venous glucose samples. Glucose 287-294 insulin Homo sapiens 203-210 23164767-8 2012 The essential components of an insulin infusion system include use of a validated insulin titration program, availability of appropriate staffing resources, accurate monitoring technology, and standardized approaches to infusion preparation, provision of consistent carbohydrate calories and nutritional support, and dextrose replacement for hypoglycemia prevention and treatment. Glucose 317-325 insulin Homo sapiens 31-38 22540883-7 2012 Exenatide + metformin gave a greater increase in M value (+34%), and disposition index (+55%) compared with placebo + metformin; first (+21%) and second phase (+34%) C-peptide response to glucose and C-peptide response to arginine (+25%) were also improved by exenatide + metformin treatment, but not by placebo + metformin. Glucose 188-195 insulin Homo sapiens 166-175 22726220-9 2012 CONCLUSIONS: The trend towards improving ISR relative to glucose 0-0.5 h in patients treated with insulin supports the hypothesis that insulin secretion can be improved by blocking IL-1beta. Glucose 57-64 insulin Homo sapiens 98-105 22891212-1 2012 Increased lipid availability reduces insulin-stimulated glucose disposal in skeletal muscle, which is generally explained by fatty acid-mediated inhibition of insulin signaling. Glucose 56-63 insulin Homo sapiens 37-44 22891212-2 2012 It remains unclear whether lipids also impair transcapillary transport of insulin and glucose, which could become rate controlling for glucose disposal. Glucose 135-142 insulin Homo sapiens 74-81 22891212-3 2012 We hypothesized that lipid-induced insulin resistance is induced by inhibiting myocellular glucose uptake and not by interfering with the delivery of insulin or glucose. Glucose 91-98 insulin Homo sapiens 35-42 22891212-5 2012 Lipid infusion reduced insulin-stimulated glucose disposal by ~70% (P < 0.05) during clamps and dynamic insulin sensitivity by ~12% (P < 0.05) during oral glucose loading. Glucose 42-49 insulin Homo sapiens 23-30 22891212-5 2012 Lipid infusion reduced insulin-stimulated glucose disposal by ~70% (P < 0.05) during clamps and dynamic insulin sensitivity by ~12% (P < 0.05) during oral glucose loading. Glucose 161-168 insulin Homo sapiens 23-30 22891212-5 2012 Lipid infusion reduced insulin-stimulated glucose disposal by ~70% (P < 0.05) during clamps and dynamic insulin sensitivity by ~12% (P < 0.05) during oral glucose loading. Glucose 161-168 insulin Homo sapiens 107-114 22965294-0 2012 The use and efficacy of continuous glucose monitoring in type 1 diabetes treated with insulin pump therapy: a randomised controlled trial. Glucose 35-42 insulin Homo sapiens 86-93 23043166-3 2012 Insulin was titrated to achieve prebreakfast plasma glucose (PG) of 3.9-4.9 mmol/L. Glucose 52-59 insulin Homo sapiens 0-7 23068961-1 2012 The amelioration of glucose tolerance by liraglutide was associated with a significant improvement of early insulin-response during OGTT. Glucose 20-27 insulin Homo sapiens 108-115 23182460-6 2012 Insulin-stimulated glucose uptake was determined by measuring 2-deoxy-D-[(3)H] glucose uptake. Glucose 19-26 insulin Homo sapiens 0-7 23182460-11 2012 Moreover, NOD1 activation reduced insulin-induced glucose uptake, leading to insulin resistance. Glucose 50-57 insulin Homo sapiens 34-41 23182460-11 2012 Moreover, NOD1 activation reduced insulin-induced glucose uptake, leading to insulin resistance. Glucose 50-57 insulin Homo sapiens 77-84 23098366-2 2012 Alternative delivery routes of insulin are expected to overcome some limitations, mainly concerned with the possibility of hypoglycemia episodes, weight gain and inadequate post-meal glucose control, in order to lead a better patient compliance. Glucose 183-190 insulin Homo sapiens 31-38 22985947-6 2012 MAIN OUTCOME MEASURE(S): Insulin sensitivity (IS(FSIVGTT)) determined by frequently sampled IV glucose tolerance testing (GTT) and insulin-induced nonesterified fatty acid (NEFA) suppression, estimated by the log-linear slope of NEFA levels during the first 20 minutes of GTT. Glucose 95-102 insulin Homo sapiens 25-32 22960655-9 2012 Adrenomedullin and conditioned media from pancreatic cell lines inhibited glucose-stimulated insulin secretion from beta cell lines and islets isolated from mice; the effects of conditioned media from pancreatic cancer cells were reduced by small hairpin RNA-mediated knockdown of adrenomedullin. Glucose 74-81 insulin Homo sapiens 93-100 23258124-7 2012 The combination of GLP-1 analogs and insulin might be highly effective to maintain glucose control, and to attenuate the adverse effects usually associated with insulin therapy. Glucose 83-90 insulin Homo sapiens 37-44 23223771-8 2012 Daily physical activity and a reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles. Glucose 71-78 insulin Homo sapiens 115-122 23565488-2 2012 Although little is known about the process of leptin secretion, insulin, which has an important role in the metabolism of glucose and lipids, is believed to regulate leptin secretion through a posttranscriptional mechanism in the short term, and via glucose metabolism in the long term. Glucose 122-129 insulin Homo sapiens 64-71 22645077-1 2012 BACKGROUND: Insulin, glucose, and other insulin-related proteins that mediate insulin signaling are associated with colorectal neoplasia risk, but associations with common genetic variation in insulin axis genes are less clear. Glucose 21-28 insulin Homo sapiens 78-85 26052434-8 2012 Mitochondrial H2O2 emission is a major regulator of protein redox state, as well as the overall cellular redox environment, raising the intriguing possibility that elevated H2O2 emission from nutrient overload may represent the underlying basis for the development of insulin resistance due to disruption of normal redox control mechanisms regulating protein function, including the insulin signaling and glucose transport processes. Glucose 405-412 insulin Homo sapiens 268-275 21544537-1 2012 No data is so far available on the relation between glucose values and insulin resistance and mortality, both at short- and long-term, in patients with acute heart failure syndromes (AHF). Glucose 52-59 insulin Homo sapiens 71-78 23316320-1 2012 BACKGROUND: Insulin resistance, characterized by hyperinsulinemia and normal or elevated serum glucose, is an established precursor to diabetes and cardiovascular disease. Glucose 95-102 insulin Homo sapiens 12-19 22968630-3 2012 Our data showed that the metformin pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in NYGGF4 overexpression adipocytes. Glucose 87-94 insulin Homo sapiens 68-75 23027922-7 2012 Insulin sensitivity index was derived from a 75-g oral glucose tolerance test. Glucose 55-62 insulin Homo sapiens 0-7 23043193-9 2012 RESULTS: Insulin secretion was correlated with glucagon suppression in subjects with normal glucose tolerance only. Glucose 92-99 insulin Homo sapiens 9-16 23043193-10 2012 Individuals with type 2 diabetes had lower insulin sensitivity (-33 +- 11%) and insulin secretory responses to glucose, GLP-1, and arginine (-40 +- 11, -58 +- 7, and -36 +- 13%, respectively) and higher plasma glucagon and endogenous glucose production compared with normal glucose-tolerant subjects (all P < 0.05). Glucose 111-118 insulin Homo sapiens 80-87 23131894-7 2012 Although insulin levels at 0 minute were similar in both groups of subjects, insulin levels were significantly higher in the patients treated with AP at all times after the glucose load than in the healthy subjects. Glucose 173-180 insulin Homo sapiens 77-84 23131894-8 2012 In analyses of NFG subjects, insulin levels were significantly higher in the patients treated with AP compared with the healthy subjects at all times after glucose loading. Glucose 156-163 insulin Homo sapiens 29-36 23131894-10 2012 These results suggest that APs affect the glucose-insulin response, which may lead to subclinical insulin resistance before the onset of overt glucose intolerance. Glucose 42-49 insulin Homo sapiens 50-57 23737780-0 2013 Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals. Glucose 121-128 insulin Homo sapiens 31-38 23737653-1 2013 The primary function of pancreatic beta-cells is to produce and release insulin in response to increment in extracellular glucose concentrations, thus maintaining glucose homeostasis. Glucose 122-129 insulin Homo sapiens 72-79 23849871-0 2013 Effects of H2O2 on insulin signaling the glucose transport system in mammalian skeletal muscle. Glucose 41-48 insulin Homo sapiens 19-26 23849871-2 2013 In the absence of insulin, H2O2 in the low micromolar range engages the canonical IRS-1/PI3K/Akt-dependent insulin signaling pathway, as well as other signaling elements (AMPK and p38 MAPK), to increase basal glucose transport activity. Glucose 209-216 insulin Homo sapiens 107-114 23024191-11 2013 The final effect on insulin secretion depends on many parameters, including the actual glucose and drug concentration, protein binding of the drug, and the drug by itself. Glucose 87-94 insulin Homo sapiens 20-27 23183535-7 2013 Successful generation of glucose-responsive INS-producing cells required silencing of stemness programs as well as the induction of stage-specific pancreatic transcription factors. Glucose 25-32 insulin Homo sapiens 44-47 23204326-0 2013 Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation. Glucose 44-51 insulin Homo sapiens 25-32 23204326-1 2013 Impaired insulin-mediated glucose uptake characterizes cardiac muscle in humans and animals with insulin resistance and diabetes, despite preserved or enhanced phosphatidylinositol 3-kinase (PI3K) and the serine-threonine kinase, Akt-signaling, via mechanisms that are incompletely understood. Glucose 26-33 insulin Homo sapiens 9-16 23204326-1 2013 Impaired insulin-mediated glucose uptake characterizes cardiac muscle in humans and animals with insulin resistance and diabetes, despite preserved or enhanced phosphatidylinositol 3-kinase (PI3K) and the serine-threonine kinase, Akt-signaling, via mechanisms that are incompletely understood. Glucose 26-33 insulin Homo sapiens 97-104 23204326-3 2013 To gain mechanistic insights by which constitutive activation of PI3K or Akt may desensitize insulin-mediated glucose uptake in cardiomyocytes, we examined mice with cardiomyocyte-restricted, constitutive or inducible overexpression of a constitutively activated PI3K or a myristoylated Akt1 (myrAkt1) transgene that also expressed a myc-epitope-tagged glucose transporter type 4 protein (GLUT4). Glucose 110-117 insulin Homo sapiens 93-100 23204326-5 2013 However, insulin-mediated glucose uptake was reduced by 50-80%. Glucose 26-33 insulin Homo sapiens 9-16 24326773-1 2013 Functional pancreatic neuroendocrine tumours (PNETs) are mainly represented by insulinoma, which secrete insulin independent of glucose and cause hypoglycaemia. Glucose 128-135 insulin Homo sapiens 79-86 24326136-13 2013 Insulin administration should be considered when serum glucose concentrations are no longer declining adequately with fluid administration alone. Glucose 55-62 insulin Homo sapiens 0-7 24382044-5 2013 The required insulin dose is calculated and administered on the basis of continuous glucose measurements, taking over a large part of the treatment from the patient. Glucose 84-91 insulin Homo sapiens 13-20 23043683-4 2013 The primary outcome was an improvement in insulin resistance (glucose disposal rate, GDR) at 6 months (quantified by hyperinsulinaemic euglycaemic clamp). Glucose 62-69 insulin Homo sapiens 42-49 22947694-5 2013 Insulin resistance was quantified by calculation of glucose disposal and metabolic clearance rate during a euglycemic hyperinsulinemic clamp on two insulin levels (1 and 10 mIU/kg/min). Glucose 52-59 insulin Homo sapiens 0-7 23502135-3 2013 Amino acids and glucose also stimulate the secretion of IGF-I and insulin. Glucose 16-23 insulin Homo sapiens 66-73 23505173-7 2013 This subgroup was then divided as insulin resistant and insulin sensitive according to the glucose uptake (<= or >5 mg kg(-1) min(-1), respectively). Glucose 91-98 insulin Homo sapiens 56-63 23577222-5 2013 Insulin analog plus metformin treatment significantly reduced glucose variability. Glucose 62-69 insulin Homo sapiens 0-7 23577222-9 2013 On the contrary, decreased levels of oxidative stress markers following treatment with insulin analogs were significantly correlated with mean blood glucose levels. Glucose 149-156 insulin Homo sapiens 87-94 24327825-7 2013 Furthermore, Stevia extracts were able to revert the effect of the reduction of glucose uptake caused by methylglyoxal, an inhibitor of the insulin receptor/PI3K/Akt pathway. Glucose 80-87 insulin Homo sapiens 140-147 22438091-5 2013 Moreover, sinensetin inhibited insulin-stimulated glucose uptake by decreasing the phosphorylation of insulin receptor substrate and Akt. Glucose 50-57 insulin Homo sapiens 31-38 22438091-5 2013 Moreover, sinensetin inhibited insulin-stimulated glucose uptake by decreasing the phosphorylation of insulin receptor substrate and Akt. Glucose 50-57 insulin Homo sapiens 102-109 23234418-6 2013 The greatest total C-peptide response was induced by OWGT (36 % higher than glucose). Glucose 76-83 insulin Homo sapiens 19-28 23489182-7 2013 Fasting transiently reduced insulin-mediated glucose disposal in the clamp (from 9.69+/-1.48 to 6.78+/-1.21 mg min(-1) kg(-1), P<0.001). Glucose 45-52 insulin Homo sapiens 28-35 23489182-9 2013 We conclude that one week of fasting transiently decreased insulin-mediated glucose disposal in T1DM patients. Glucose 76-83 insulin Homo sapiens 59-66 23431266-8 2013 In human adipocytes, HSL gene silencing led to improved insulin-stimulated glucose uptake, resulting in increased de novo lipogenesis and activation of cognate gene expression. Glucose 75-82 insulin Homo sapiens 56-63 23577182-6 2013 Insulin resistance at four weeks was assessed by insulin resistance indices, lnHOMA-IR and lnMatsuda, and AUC insulin during a 2-hour glucose tolerance test. Glucose 134-141 insulin Homo sapiens 0-7 23565276-5 2013 Using the insulin-secreting cell line INS-1E, we found that glucose stimulation induced rapid mitochondrial shortening and recovery. Glucose 60-67 insulin Homo sapiens 10-17 23441155-1 2013 BACKGROUND: Glucokinase (GCK) is the key glucose phosphorylation enzyme which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its enzyme function as the first rate-limiting step in the glycolysis pathway and regulates glucose-stimulated insulin secretion. Glucose 41-48 insulin Homo sapiens 281-288 23441155-1 2013 BACKGROUND: Glucokinase (GCK) is the key glucose phosphorylation enzyme which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its enzyme function as the first rate-limiting step in the glycolysis pathway and regulates glucose-stimulated insulin secretion. Glucose 262-269 insulin Homo sapiens 281-288 23418416-8 2013 Whole body glucose disposal (WGD) was higher at baseline and lower after insulin stimulation. Glucose 11-18 insulin Homo sapiens 73-80 23437184-1 2013 BACKGROUND: Emerging evidence suggests that high density lipoprotein (HDL) may modulate glucose metabolism through multiple mechanisms including pancreatic insulin secretion as well as insulin-independent glucose uptake into muscle. Glucose 88-95 insulin Homo sapiens 156-163 23437184-5 2013 This conditioned media was then applied to primary human skeletal myotubes derived from vastus lateralis biopsies taken from patients with type 2 diabetes to examine insulin-stimulated glucose uptake. Glucose 185-192 insulin Homo sapiens 166-173 23437184-6 2013 RESULTS: Conditioned media from acLDL-treated primary and THP-1 macrophages reduced insulin-stimulated glucose uptake in primary human skeletal myotubes compared with vehicle (primary macrophages, 168+-21% of basal uptake to 104+-19%; THP-1 macrophages, 142+-8% of basal uptake to 108+-6%; P<0.05). Glucose 103-110 insulin Homo sapiens 84-91 23437184-10 2013 CONCLUSION: Inhibition of insulin-stimulated glucose uptake in primary human skeletal myotubes by conditioned media from macrophages pre-incubated with acLDL was restored by co-treatment with HDL. Glucose 45-52 insulin Homo sapiens 26-33 23383084-1 2013 Pyruvate carboxylase (PC) is an enzyme that plays a crucial role in many biosynthetic pathways in various tissues including glucose-stimulated insulin secretion. Glucose 124-131 insulin Homo sapiens 143-150 23928867-12 2013 This can be possibly explained by better glucose control, which improved insulin sensitivity of the peripheral tissues and reduced body mass in this patient group. Glucose 41-48 insulin Homo sapiens 73-80 23111651-4 2012 The main outcome measure was insulin-stimulated glucose infusion rate during the last 20 minutes of a hyperinsulinemic-euglycemic glucose clamp study. Glucose 48-55 insulin Homo sapiens 29-36 23231797-8 2012 RESULTS: The insulin-glucose infusion was used in 47% of women with type 1, type 2, and gestational diabetes requiring >= 0.5 units/kg/day of insulin during pregnancy and in 8% of women with GDM treated by diet or < 0.5 units/kg/day of insulin. Glucose 21-28 insulin Homo sapiens 13-20 23231797-8 2012 RESULTS: The insulin-glucose infusion was used in 47% of women with type 1, type 2, and gestational diabetes requiring >= 0.5 units/kg/day of insulin during pregnancy and in 8% of women with GDM treated by diet or < 0.5 units/kg/day of insulin. Glucose 21-28 insulin Homo sapiens 146-153 23231797-8 2012 RESULTS: The insulin-glucose infusion was used in 47% of women with type 1, type 2, and gestational diabetes requiring >= 0.5 units/kg/day of insulin during pregnancy and in 8% of women with GDM treated by diet or < 0.5 units/kg/day of insulin. Glucose 21-28 insulin Homo sapiens 146-153 23231797-11 2012 In women with type 1 and type 2 diabetes and high-dose insulin-requiring GDM, the rate of blood glucose values outside the range of 3.6 to 6.9 mmol/L was lower in those using the intravenous protocol (16.7%) than in those not using it (34.8%), but this reduction was not statistically significant. Glucose 96-103 insulin Homo sapiens 55-62 23231797-12 2012 CONCLUSION: Standardized management for diabetic women in labour using an intravenous insulin-glucose protocol was effective in achieving stable maternal blood glucose levels with low rates of neonatal hypoglycemia. Glucose 94-101 insulin Homo sapiens 86-93 22748969-7 2012 The insulin sensitivity index (S(I)) was assessed by using a frequently sampled intravenous glucose tolerance test with minimal model analysis. Glucose 92-99 insulin Homo sapiens 4-11 22811028-1 2012 PURPOSE: Effects of resistance training and detraining on glucose and insulin responses to an oral glucose load, muscle fiber type, and muscular performance in the offspring of those with type 2 diabetes (familial insulin resistant (FIR)) were investigated. Glucose 99-106 insulin Homo sapiens 70-77 22811028-11 2012 CONCLUSION: FIR appears to have exaggerated responses to resistance training and detraining, with a greater reduction in insulin release with glucose ingestion after training and increase when training ceases. Glucose 142-149 insulin Homo sapiens 121-128 22627913-4 2012 These morphological changes were accompanied by increases in the adipogenic marker expression and improved adipocyte metabolic phenotypes: enhanced responses to beta-adrenergically stimulated lipolysis and to insulin-stimulated glucose metabolism into triglyceride (TG). Glucose 228-235 insulin Homo sapiens 209-216 22627913-8 2012 Rates of insulin-stimulated glucose uptake were higher in adipocytes differentiated with 3% FBS, whereas the sensitivity to insulin was almost identical between the two groups. Glucose 28-35 insulin Homo sapiens 9-16 23107259-5 2012 In addition, the insulin resistance related to obesity results not only in defective insulin-stimulated glucose disposal but has also detrimental consequences on protein metabolism at the skeletal muscle level and whole-body level. Glucose 104-111 insulin Homo sapiens 17-24 23107259-5 2012 In addition, the insulin resistance related to obesity results not only in defective insulin-stimulated glucose disposal but has also detrimental consequences on protein metabolism at the skeletal muscle level and whole-body level. Glucose 104-111 insulin Homo sapiens 85-92 21747410-0 2012 Association between the GIPR gene and the insulin level after glucose loading in schizophrenia patients treated with olanzapine. Glucose 62-69 insulin Homo sapiens 42-49 22759245-10 2012 Oral glucose tolerance test revealed elevated free insulin concentrations with disproportionately elevated total insulin levels. Glucose 5-12 insulin Homo sapiens 51-58 22759245-10 2012 Oral glucose tolerance test revealed elevated free insulin concentrations with disproportionately elevated total insulin levels. Glucose 5-12 insulin Homo sapiens 113-120 23324191-9 2012 Case number of study group on glucose/insulin ratio < 4.5 was more than that of the control group, statistical difference was found (OR = 3.37, 95%CI: 1.90 to 5.99, P < 0.01). Glucose 30-37 insulin Homo sapiens 38-45 21856022-6 2012 Primary endpoint was the change of whole body insulin sensitivity after 4 months of treatment assessed by intravenous glucose tolerance testing and minimal modeling. Glucose 118-125 insulin Homo sapiens 46-53 23230428-5 2012 The role of xenin, a neurotensin-related peptide, on the regulation of insulin release by glucose-dependent insulinotropic polypeptide is summarized. Glucose 90-97 insulin Homo sapiens 71-78 23025244-3 2012 7h exhibited potent glucose-lowering effects on insulin-resistant HepG2 cells and regulated adiponectin and leptin expression in 3T3-L1 adipocytes. Glucose 20-27 insulin Homo sapiens 48-55 23075099-1 2012 The stable isotopes of hydrogen (delta(2)H) and oxygen (delta(18)O) in human urine are measured during studies of total energy expenditure by the doubly labeled water method, measurement of total body water, and measurement of insulin resistance by glucose disposal among other applications. Glucose 249-256 insulin Homo sapiens 227-234 23166963-17 2004 GLUT4 and HKII are the major transporter and HK isoform in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. Glucose 128-135 insulin Homo sapiens 111-118 22936689-6 2012 In addition, for measures based on intravenous glucose tolerance test, ORs (95% CI) associated with type 2 diabetes risk were 0.24 (0.08-0.74) (P = 0.01) and 0.14 (0.04-0.48) (P = 0.002) for per 1 standard deviation increment in insulin sensitivity index and disposition index, respectively. Glucose 47-54 insulin Homo sapiens 229-236 22865588-0 2012 Glucose-regulated insulin release from acid-disintegrable microgels covalently immobilized with glucose oxidase and catalase. Glucose 0-7 insulin Homo sapiens 18-25 22865588-3 2012 The above two factors both synergistically contribute to the prominently enhanced insulin release at high glucose levels (~10-20 mM) compared to that in the absence of glucose. Glucose 106-113 insulin Homo sapiens 82-89 22865588-3 2012 The above two factors both synergistically contribute to the prominently enhanced insulin release at high glucose levels (~10-20 mM) compared to that in the absence of glucose. Glucose 168-175 insulin Homo sapiens 82-89 22992739-1 2012 Insulin stimulates the mobilization of glucose transporter 4 (GLUT4) storage vesicles to the plasma membrane, resulting in an influx of glucose into target tissues such as muscle and fat. Glucose 39-46 insulin Homo sapiens 0-7 22992739-8 2012 Furthermore, siRNA mediated knockdown of CLASP2 in 3T3-L1 adipocytes inhibited insulin-stimulated glucose transport. Glucose 98-105 insulin Homo sapiens 79-86 23062564-4 2012 The Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) trial, published in 1995, evaluated the role of adjustable-dose insulin infusion to lower blood glucose. Glucose 183-190 insulin Homo sapiens 151-158 22990033-10 2012 CONCLUSIONS: Slower intestinal uptake of glucose from a starchy food product can result in lower postprandial insulin and GIP concentrations, but not necessarily in a lower glycemic response, because of a slower GCR. Glucose 41-48 insulin Homo sapiens 110-117 22967498-5 2012 PET images of tissue [18F]FDG activity were coregistered with MRI to derive K values for insulin-stimulated rates of fractional glucose uptake within tissue. Glucose 128-135 insulin Homo sapiens 89-96 22967498-10 2012 We conclude that rates of fractional glucose uptake within GFAT and VAT are significantly and positively associated with systemic insulin sensitivity in nonobese subjects. Glucose 37-44 insulin Homo sapiens 130-137 22897387-6 2012 Insulin synthesis de novo was confirmed by C-peptide ELISA of culture supernatant in response to varying concentrations of glucose as well as agonist and antagonist of functional 3D beta islet cells in vitro. Glucose 123-130 insulin Homo sapiens 0-7 22934551-7 2012 In BBB and BTB the insulin signaling is also distinct from other tissues and organs thus evidencing their importance in protecting against or exacerbating the effects of diabetes on glucose metabolism. Glucose 182-189 insulin Homo sapiens 19-26 22672227-1 2012 AIMS: To quantify and compare associations between femoral-gluteal adiposity and insulin sensitivity in adults with Type 1 diabetes mellitus with adults with normal glucose tolerance. Glucose 165-172 insulin Homo sapiens 81-88 22672227-3 2012 Insulin sensitivity was defined as whole-body glucose disposal measured by hyperinsulinaemic-euglycaemic clamps. Glucose 46-53 insulin Homo sapiens 0-7 22672227-7 2012 Higher % leg fat mass was independently associated with higher insulin sensitivity in individuals with normal glucose tolerance (P < 0.01) after similar adjustment; significant associations were not observed in Type 1 diabetes. Glucose 110-117 insulin Homo sapiens 63-70 22687049-11 2012 Defective glucose-stimulated insulin release upon induction of iNOS was restored by iNOS inhibitor aminoguanidine. Glucose 10-17 insulin Homo sapiens 29-36 22733799-5 2012 The relative increase in insulin release after glucose ingestion at fixed hyperglycemia, a surrogate for the incretin effect, was similar among all three studies. Glucose 47-54 insulin Homo sapiens 25-32 22733799-7 2012 Between the two LOW studies, the reproducibility of insulin release in response to intravenous glucose alone and intravenous plus ingested glucose was similar. Glucose 95-102 insulin Homo sapiens 52-59 22733799-7 2012 Between the two LOW studies, the reproducibility of insulin release in response to intravenous glucose alone and intravenous plus ingested glucose was similar. Glucose 139-146 insulin Homo sapiens 52-59 22851577-8 2012 Insulin-stimulated glucose uptake was higher in the prior exercised leg in the saline and the lipid trials. Glucose 19-26 insulin Homo sapiens 0-7 22851577-9 2012 In the lipid trial, prior exercise normalized insulin-stimulated glucose uptake to the level observed in the resting control leg in the saline trial. Glucose 65-72 insulin Homo sapiens 46-53 22865650-0 2012 Overexpression of ZAC impairs glucose-stimulated insulin translation and secretion in clonal pancreatic beta-cells. Glucose 30-37 insulin Homo sapiens 49-56 22865650-8 2012 Furthermore, glucose-stimulated proinsulin biosynthesis was inhibited despite an increase in insulin transcript level. Glucose 13-20 insulin Homo sapiens 35-42 22912423-9 2012 After ingestion of a glucose load, men with OSA had 27% lower insulin sensitivity (estimated by Matsuda index) and 37% higher total insulin secretion (incAUC(ins)) than the control subjects, despite comparable glucose levels (incAUC(glu)). Glucose 21-28 insulin Homo sapiens 62-69 23003329-0 2012 Evaluation of a novel continuous glucose monitoring-based method for mealtime insulin dosing--the iBolus--in subjects with type 1 diabetes using continuous subcutaneous insulin infusion therapy: a randomized controlled trial. Glucose 33-40 insulin Homo sapiens 78-85 23003329-1 2012 OBJECTIVE: Prandial insulin dosing is an empirical practice associated frequently with poor reproducibility in postprandial glucose response. Glucose 124-131 insulin Homo sapiens 20-27 23003329-2 2012 Based on continuous glucose monitoring (CGM), a method for prandial insulin administration (iBolus) is presented and evaluated for people with type 1 diabetes using CSII therapy. Glucose 20-27 insulin Homo sapiens 68-75 23055336-4 2012 RESULTS: CGM showed that compared to insulin alone, the addition of either sitagliptin or miglitol, or both, to insulin achieved better glucose control. Glucose 136-143 insulin Homo sapiens 112-119 22948221-5 2012 ISO induction of glucose uptake in adipocytes was abolished by inhibitors of the insulin signaling pathway. Glucose 17-24 insulin Homo sapiens 81-88 22924552-2 2012 Autoimmune attack and functional inhibition of the insulin-producing beta cells in the pancreas lead to the inability of beta cells to metabolize glucose, and thus results the hallmark clinical symptom of diabetes: abnormally high blood glucose levels. Glucose 146-153 insulin Homo sapiens 51-58 22924552-2 2012 Autoimmune attack and functional inhibition of the insulin-producing beta cells in the pancreas lead to the inability of beta cells to metabolize glucose, and thus results the hallmark clinical symptom of diabetes: abnormally high blood glucose levels. Glucose 237-244 insulin Homo sapiens 51-58 22578200-1 2012 OBJECTIVE: Insulin glulisine has a higher efficacy in reducing postprandial glucose excursions and in restoring normal postprandial microcirculation than rapid human insulin. Glucose 76-83 insulin Homo sapiens 11-18 22842625-5 2012 The blood samples were collected to monitor blood glucose and serum insulin levels for 12 h. Blood glucose was lowered in proportion to the concentration of insulin loaded in lyophilized hydrogel patches (R(2)=0.99), with a longer duration of action compared to subcutaneous injection. Glucose 50-57 insulin Homo sapiens 157-164 22842625-5 2012 The blood samples were collected to monitor blood glucose and serum insulin levels for 12 h. Blood glucose was lowered in proportion to the concentration of insulin loaded in lyophilized hydrogel patches (R(2)=0.99), with a longer duration of action compared to subcutaneous injection. Glucose 99-106 insulin Homo sapiens 68-75 22842625-5 2012 The blood samples were collected to monitor blood glucose and serum insulin levels for 12 h. Blood glucose was lowered in proportion to the concentration of insulin loaded in lyophilized hydrogel patches (R(2)=0.99), with a longer duration of action compared to subcutaneous injection. Glucose 99-106 insulin Homo sapiens 157-164 23247575-9 2012 Insulin content and insulin biosynthesis, however, were significantly reduced under the combination of nutrients compared with glucose alone. Glucose 127-134 insulin Homo sapiens 0-7 22871300-0 2012 Relationship of angiographically defined coronary artery disease with insulin sensitivity and secretion in subjects with different glucose tolerance. Glucose 131-138 insulin Homo sapiens 70-77 22871300-3 2012 The aim of this study was to investigate the association between insulin sensitivity, insulin secretion, and CAD in patients with different glucose metabolic status. Glucose 140-147 insulin Homo sapiens 65-72 22871300-10 2012 CONCLUSIONS: Insulin resistance is closely related to the presence of CAD in newly diagnosed patients with different glucose metabolic status. Glucose 117-124 insulin Homo sapiens 13-20 22977275-8 2012 Glucose infusion rate during insulin infusion was 5.5 +- 1.0 mg kg fat-free mass(-1) min(-1). Glucose 0-7 insulin Homo sapiens 29-36 23143631-2 2012 This study investigated when during the oral glucose tolerance test (OGTT) the plasma glucose, urine glucose, and insulin levels correlate most strongly with urinary N-acetyl-beta-d-glucosaminidase (NAG) levels in prediabetic subjects. Glucose 45-52 insulin Homo sapiens 114-121 23294785-3 2012 Using an insulin pen with memory function might facilitate corrective dosing to avoid postprandial blood glucose peaks and therefore might improve overall glycemic control. Glucose 105-112 insulin Homo sapiens 9-16 23294788-1 2012 BACKGROUND: Diabetes patients in the intensive care unit (ICU) and either nil per os, on enteral feedings, or on total parenteral nutrition are often treated with sliding-scale insulin (despite lack of evidence showing benefit) or intravenous insulin (IVI) infusion, a nursing intensive procedure requiring hourly glucose measurements, and insulin rate adjustments. Glucose 314-321 insulin Homo sapiens 177-184 23294788-2 2012 We introduced a subcutaneous insulin algorithm (SQIA) that would equal the glucose goals for IVI but have the simplicity of q4 hour adjustable sliding-scale insulin. Glucose 75-82 insulin Homo sapiens 29-36 23294789-1 2012 OBJECTIVE: Set-inversion-based prandial insulin delivery is a new model-based bolus advisor for postprandial glucose control in type 1 diabetes mellitus (T1DM). Glucose 109-116 insulin Homo sapiens 40-47 23217597-6 2012 RESULTS: Although metformin remained the mainstay of anti-diabetic treatment, patients receiving combination therapy of oral glucose-lowering agents, either with or without insulin, significantly increased, from approximately 40% in 2000 to 60% in 2009, particularly in relation to the newer agents, including glinides, alpha-glucosidase inhibitors, and long-acting insulin analogues. Glucose 125-132 insulin Homo sapiens 366-373 22926010-7 2012 Increase in glucose did not alter osteoblasts" function significantly but further enhanced the effects of insulin. Glucose 12-19 insulin Homo sapiens 106-113 22941440-5 2012 To test this hypothesis, 10,12 CLA-treated human adipocytes were supplemented with oleic acid for 12 h to 7 days, and inflammatory gene expression, insulin-stimulated glucose uptake, and lipid content were measured. Glucose 167-174 insulin Homo sapiens 148-155 23305008-8 2012 Under insulin resistance, saturated palmitic fatty acid synthesized by hepatocytes from glucose, does not further transform into oleic monoenic fatty acid. Glucose 88-95 insulin Homo sapiens 6-13 22859723-1 2012 Activation of FFA1 (GPR40), a member of G protein-coupling receptor family A, is mediated by medium- and long-chain fatty acids and leads to amplification of glucose-stimulated insulin secretion, suggesting a potential role for free fatty acid 1 (FFA1) as a target for type 2 diabetes. Glucose 158-165 insulin Homo sapiens 177-184 22993210-6 2012 Glucose-stimulated insulin secretion is augmented by incretin hormones, which increase cAMP levels and leads to MyRIP phosphorylation, its interaction with BR-MyoVa, and phosphorylation of the BR-MyoVa receptor rabphilin-3A (Rph-3A). Glucose 0-7 insulin Homo sapiens 19-26 23085536-5 2012 We found that 3T3-L1 adipocytes, incubated with 5muM FCCP for 12h, had decreased levels of insulin-stimulated glucose uptake and had impaired insulin-stimulated GLUT4 translocation. Glucose 110-117 insulin Homo sapiens 91-98 23373312-9 2012 Furthermore, the serum insulin concentrations from 75 g glucose tolerance (75 g-OGTT) 30 minutes later, in one third of patients receiving olanzapine, registered more than 100 microU/ml. Glucose 56-63 insulin Homo sapiens 23-30 23373312-11 2012 Olanzapine may impair glucose tolerance due in part to increased insulin resistance. Glucose 22-29 insulin Homo sapiens 65-72 22577884-0 2012 The effect of bolus and food calculator Diabetics on glucose variability in children with type 1 diabetes treated with insulin pump: the results of RCT. Glucose 53-60 insulin Homo sapiens 119-126 22765260-10 2012 CONCLUSION: In patients with long-term T1D, meal-related insulin dosing based on carbohydrate plus fat/protein counting reduces the postprandial glucose levels (ClinicalTrials.gov NCT01400659). Glucose 145-152 insulin Homo sapiens 57-64 23090065-8 2012 The insulin released from the drug delivery system stimulated cell growth in previously inhibited cells, and ameliorated the impaired bone-forming ability of human MG-63 cells under high glucose conditions. Glucose 187-194 insulin Homo sapiens 4-11 22970724-1 2012 Insulin secretion from pancreatic beta-cells is tightly regulated by glucose and other nutrients, hormones, and neural factors. Glucose 69-76 insulin Homo sapiens 0-7 22970724-3 2012 Cyclic AMP is formed primarily in response to glucoincretin hormones and other G(s)-coupled receptor agonists, but generation of the nucleotide is critical also for an optimal insulin secretory response to glucose. Glucose 206-213 insulin Homo sapiens 176-183 23387076-0 2012 [Effect of mulberry leaves extracts on glucose uptake of insulin-resistant HepG2 cells and the mechanism]. Glucose 39-46 insulin Homo sapiens 57-64 23387076-1 2012 The effect and mechanism of mulberry leaves extracts (MLE) on glucose uptake of insulin-resistant HepG2 cells in vitro was explored. Glucose 62-69 insulin Homo sapiens 80-87 23387076-4 2012 Mulberry leaves polysaccharides, mulberry leaves flavonoids and mulberry leaves extracts advanced glucose uptake of insulin-resistant HepG2 cells; Mulberry leaves extracts enhance phosphorylation of AMPK. Glucose 98-105 insulin Homo sapiens 116-123 23088514-10 2012 CONCLUSIONS: The supplementation used decreased insulin resistance in type 2 diabetic patients, suggesting a positive action in blood glucose control as adjuvant therapy in conventional treatments. Glucose 134-141 insulin Homo sapiens 48-55 22914748-9 2012 Insulin regulation of synaptic input in the DMV may influence autonomic visceral regulation and thus systemic glucose metabolism. Glucose 110-117 insulin Homo sapiens 0-7 22795893-6 2012 Extraneuronal Cdk5 regulates critical biological processes including transcript-selective translation control for regulation of macrophage gene expression, glucose-inducible insulin secretion, hematopoietic cell differentiation, vascular angiogenesis, cell migration, senescence, and wound-healing, among others. Glucose 156-163 insulin Homo sapiens 174-181 23063129-7 2012 Intriguingly, activation of the Smo-Ampk axis in vivo drives robust insulin-independent glucose uptake in muscle and brown adipose tissue. Glucose 88-95 insulin Homo sapiens 68-75 23612026-9 2012 The Glucose Management System, already developed within the REACTION project, is able to monitor a range of parameters from various sources including glucose levels, nutritional intakes, administered drugs, and patient"s insulin sensitivity, offering decision support for insulin dosing to professional caregivers on a mobile tablet platform that fulfills the need of the users and supports medical workflow procedures in compliance with the Medical Device Directive requirements. Glucose 4-11 insulin Homo sapiens 221-228 23612026-9 2012 The Glucose Management System, already developed within the REACTION project, is able to monitor a range of parameters from various sources including glucose levels, nutritional intakes, administered drugs, and patient"s insulin sensitivity, offering decision support for insulin dosing to professional caregivers on a mobile tablet platform that fulfills the need of the users and supports medical workflow procedures in compliance with the Medical Device Directive requirements. Glucose 4-11 insulin Homo sapiens 272-279 22314192-2 2012 This is due to both reductions in hepatic glucose production, and likely improved insulin stimulated glucose disposal in skeletal muscle. Glucose 101-108 insulin Homo sapiens 82-89 23507897-8 2012 After freeze-drying with cryoprotectants, the amount of insulin released was higher for trehalose and lower for sucrose, glucose, fructose and sorbitol comparatively to freeze-dried PLGA-NP with no cryoprotectant added. Glucose 121-128 insulin Homo sapiens 56-63 22409999-0 2012 The effect of perioperative glucose control on postoperative insulin resistance. Glucose 28-35 insulin Homo sapiens 61-68 22409999-3 2012 This study aims to disclose the impact of perioperative glucose control on postoperative insulin resistance. Glucose 56-63 insulin Homo sapiens 89-96 22409999-5 2012 In the treatment group (n = 9) insulin was administered intravenously to keep blood glucose between 6 and 8 mmol/l during surgery. Glucose 84-91 insulin Homo sapiens 31-38 22688013-8 2012 Additionally, we evaluated if the culture medium glucose, enriched insulin, could influence the cytokine production. Glucose 49-56 insulin Homo sapiens 67-74 22804483-2 2012 Our aim was to re-evaluate the hypothesis of a pregnancy-induced increase by measuring plasma C-peptide concentration in women with stable blood glucose control under standardized fasting and meal-stimulated conditions. Glucose 145-152 insulin Homo sapiens 94-103 22804483-9 2012 Four women had detectable C-peptide; peak (range) early vs. late pregnancy 48.5 (10-115) vs. 40.0 pmol/l (80-105); P = 0.5, which was weakly associated with plasma glucose; R(2) = 0.15, P < 0.0001. Glucose 164-171 insulin Homo sapiens 26-35 22855730-8 2012 Insulin-to-glucose ratios were significantly lower during exendin-(9-39) infusion compared with vehicle. Glucose 11-18 insulin Homo sapiens 0-7 22911383-6 2012 RESULTS: TCF7L2 rs7903146 (T/T) was associated with reduced basal and glucose-stimulated insulin secretion in isolated human islets, and reduced islet density in whole pancreas. Glucose 70-77 insulin Homo sapiens 89-96 22928559-6 2012 The strength of the contact between INS and SYT8 is increased by glucose, and this results in stimulation of SYT8 expression. Glucose 65-72 insulin Homo sapiens 36-39 22928569-1 2012 Here, we outline how islet cells use autocrine and paracrine "circuits" of classical neurotransmitters and their corresponding receptors and transporters to communicate with vicinal beta-cells to regulate glucose-stimulated insulin secretion. Glucose 205-212 insulin Homo sapiens 224-231 22928576-4 2012 Rodents with tissue-specific knockout of the insulin receptor in the beta-cell (betaIRKO) show reduced first-phase glucose-stimulated insulin secretion (GSIS) and with aging develop glucose intolerance and diabetes, phenotypically similar to the process seen in human T2D. Glucose 115-122 insulin Homo sapiens 45-52 22727921-8 2012 Androgen levels and immunoreactive insulin during an oral glucose tolerance test had lower power for predicting increased cardiovascular risk than WC and WSR. Glucose 58-65 insulin Homo sapiens 35-42 22956257-4 2012 METHODS: Normal adipocytes and adipocytes transfected with pre-miR-21(pmiR-21) or negative control (pNeg) were treated with high glucose and high insulin for 24 h, insulin-stimulated glucose uptake was determined by 2-Deoxyglucose transport assay, miR-21 expression level was measured by using quantitative real-time RT-PCR (qRT-PCR). Glucose 183-190 insulin Homo sapiens 164-171 22956257-7 2012 Over-expression of miR-21 significantly increased insulin-induced glucose uptake and decreased PTEN protein expression, while it had no significant effect on PTEN mRNA expression in IR-adipocytes. Glucose 66-73 insulin Homo sapiens 50-57 22728514-4 2012 Six weeks after infusion of microbiota from lean donors, insulin sensitivity of recipients increased (median rate of glucose disappearance changed from 26.2 to 45.3 mumol/kg/min; P < .05) along with levels of butyrate-producing intestinal microbiota. Glucose 117-124 insulin Homo sapiens 57-64 23193740-11 2012 After plotting the graph from serum glucose and insulin used, the physician can estimate the 24-hour insulin requirement and switch insulin from intravenous to subcutaneous route immediately after the metabolic abnormality is resolved CONCLUSION: The very low dose insulin regimen plus pre-printed order of laboratory investigation, fluid and electrolyte treatment, and precipitating causes treatment following the Lerdsin DKA/HHS Hospital Protocol can improve the outcome of treatment in our hospital. Glucose 36-43 insulin Homo sapiens 101-108 23193740-11 2012 After plotting the graph from serum glucose and insulin used, the physician can estimate the 24-hour insulin requirement and switch insulin from intravenous to subcutaneous route immediately after the metabolic abnormality is resolved CONCLUSION: The very low dose insulin regimen plus pre-printed order of laboratory investigation, fluid and electrolyte treatment, and precipitating causes treatment following the Lerdsin DKA/HHS Hospital Protocol can improve the outcome of treatment in our hospital. Glucose 36-43 insulin Homo sapiens 101-108 23193740-11 2012 After plotting the graph from serum glucose and insulin used, the physician can estimate the 24-hour insulin requirement and switch insulin from intravenous to subcutaneous route immediately after the metabolic abnormality is resolved CONCLUSION: The very low dose insulin regimen plus pre-printed order of laboratory investigation, fluid and electrolyte treatment, and precipitating causes treatment following the Lerdsin DKA/HHS Hospital Protocol can improve the outcome of treatment in our hospital. Glucose 36-43 insulin Homo sapiens 101-108 22388654-7 2012 Other peptides such as pancreastatin were found to have significant effects on inhibition of glucose-stimulated insulin secretion and glucose up-take, induction of glycogenolysis in hepatocytes, and inhibition of lipogenesis. Glucose 93-100 insulin Homo sapiens 112-119 22528452-2 2012 Pancreatic islets of Langerhans secrete various endocrine hormones including insulin and glucagon to keep blood glucose level relatively constant. Glucose 112-119 insulin Homo sapiens 77-84 22806348-5 2012 Use of glucose-lowering drugs (non-insulin) may prevent progression from APN to SPN. Glucose 7-14 insulin Homo sapiens 35-42 22775461-0 2012 The effect of glucose concentrations in the medium on expression of insulin receptors in human lymphocytes B and T: an in vitro study. Glucose 14-21 insulin Homo sapiens 68-75 22775461-1 2012 CONTEXT: Insulin is one of the most-known factors that influence the intensity of cell-bound glucose transport. Glucose 93-100 insulin Homo sapiens 9-16 22775461-6 2012 RESULTS: Incubation for 24 h of lymphocytes in pathological glucose concentrations seems to only have a slight influence on the expression of insulin receptors. Glucose 60-67 insulin Homo sapiens 142-149 22775461-8 2012 Different concentrations of glucose in the incubation medium were found to only marginally influence expression of insulin receptors in lymphocytes B. Glucose 28-35 insulin Homo sapiens 115-122 22775461-9 2012 CONCLUSIONS: Pathological concentrations of glucose in medium cause a decrease in the percent of cells which show expression of insulin receptors in comparison with normal glucose concentration. Glucose 44-51 insulin Homo sapiens 128-135 22775461-9 2012 CONCLUSIONS: Pathological concentrations of glucose in medium cause a decrease in the percent of cells which show expression of insulin receptors in comparison with normal glucose concentration. Glucose 172-179 insulin Homo sapiens 128-135 22906130-8 2012 AZD6482 inhibited insulin-induced human adipocyte glucose uptake in vitro (IC(50) of 4.4 mum). Glucose 50-57 insulin Homo sapiens 18-25 22483976-6 2012 Plasma glucose and insulin concentrations significantly increased after dextrose and combined Intralipid and dextrose (all, p<0.05) and were not different from baseline during saline and lipid infusion. Glucose 72-80 insulin Homo sapiens 19-26 22483976-6 2012 Plasma glucose and insulin concentrations significantly increased after dextrose and combined Intralipid and dextrose (all, p<0.05) and were not different from baseline during saline and lipid infusion. Glucose 109-117 insulin Homo sapiens 19-26 23373019-0 2012 Analysis of the degree of insulin resistance in post menopausal women by using skin temperature measurements and fasting insulin and fasting glucose levels: a case control study. Glucose 141-148 insulin Homo sapiens 26-33 23373019-3 2012 AIM: To analyze the degree of insulin resistance in post menopausal women by using skin temperature measurements and to confirm the insulin resistance from the fasting insulin and the fasting glucose levels. Glucose 192-199 insulin Homo sapiens 132-139 23373019-3 2012 AIM: To analyze the degree of insulin resistance in post menopausal women by using skin temperature measurements and to confirm the insulin resistance from the fasting insulin and the fasting glucose levels. Glucose 192-199 insulin Homo sapiens 132-139 22977253-5 2012 The inability of hepatic glucose metabolism to effectively counterbalance a decline of the blood glucose level becomes even more pronounced in case of tightly controlled insulin treatment. Glucose 25-32 insulin Homo sapiens 170-177 23082798-7 2012 However, improved outcomes were only observed when glucose levels in the conventional glycemic control group were permitted to be relatively high [threshold for insulin administration > 200 mg/dl (> 11.1 mmol/L)], but not with more intermediate glycemic targets [threshold for insulin administration 140-180 mg/dl (7.8-10.0 mmol/L)]. Glucose 51-58 insulin Homo sapiens 161-168 23082798-7 2012 However, improved outcomes were only observed when glucose levels in the conventional glycemic control group were permitted to be relatively high [threshold for insulin administration > 200 mg/dl (> 11.1 mmol/L)], but not with more intermediate glycemic targets [threshold for insulin administration 140-180 mg/dl (7.8-10.0 mmol/L)]. Glucose 51-58 insulin Homo sapiens 283-290 22942287-2 2012 We recently described C1q/TNF-related protein-12 (CTRP12), a novel insulin-sensitizing adipokine that regulates glucose metabolism in liver and adipose tissue. Glucose 112-119 insulin Homo sapiens 67-74 22942287-12 2012 Further, only fCTRP12 improved insulin-stimulated glucose uptake in adipocytes. Glucose 50-57 insulin Homo sapiens 31-38 23070488-12 2012 Total body insulin sensitivity was assessed using a frequently sampled intravenous glucose tolerance test. Glucose 83-90 insulin Homo sapiens 11-18 22535698-5 2012 It is the only solution to a dilemma in glucose homeostasis: high insulin efficiency is required to confer rapidness in plasma glucose clearance, whereas an insulin sparing state is required to guarantee the brain"s safety during fasting. Glucose 40-47 insulin Homo sapiens 66-73 22902430-8 2012 Insulin content and insulin response to elevated glucose were also enhanced by both three-dimensional scaffolds. Glucose 49-56 insulin Homo sapiens 20-27 22871100-1 2012 The aim of this study was to assess red blood cell glutathione from insulin-sensitive and insulin-resistant individuals before and after an oral glucose dose. Glucose 145-152 insulin Homo sapiens 90-97 22871100-7 2012 Direct associations between postprandial glucose response and red blood cell total (r = 0.52; p < 0.05) and oxidized (r = 0.61; p = 0.02) glutathione concentrations were observed only in insulin-sensitive subjects. Glucose 41-48 insulin Homo sapiens 190-197 22871100-8 2012 In conclusion, healthy individuals differing in their degree of insulin resistance showed similar red blood cell glutathione concentrations under non-glucose- and glucose-stimulated conditions. Glucose 163-170 insulin Homo sapiens 64-71 22647419-8 2012 CONCLUSIONS: NSCLC patients with moderate cachexia showed considerable insulin resistance of glucose and of whole-body protein anabolism. Glucose 93-100 insulin Homo sapiens 71-78 22356444-13 2012 Her glucose level was subsequently very well controlled with multiple insulin injections and she successfully delivered a healthy baby. Glucose 4-11 insulin Homo sapiens 70-77 22933115-6 2012 Nox2-deficient islets stimulated with 22.8 mmol/L glucose exhibited potentiation of insulin release compared with controls, an effect confirmed with in vitro knockdown of Nox2. Glucose 50-57 insulin Homo sapiens 84-91 22803772-9 2012 Combined impairments in beta-cell function and insulin sensitivity were responsible for the increases in fasting and 2-h plasma glucose concentrations within the euglycemic range. Glucose 128-135 insulin Homo sapiens 47-54 22803772-11 2012 beta-Cell function and insulin sensitivity worsen in direct proportion with number of traits of metabolic syndrome and increases in glucose levels. Glucose 132-139 insulin Homo sapiens 23-30 22915827-1 2012 We describe a negative feedback autocrine regulatory circuit for glucose-stimulated insulin secretion in purified human islets in vitro. Glucose 65-72 insulin Homo sapiens 84-91 22915827-2 2012 Using chronoamperometry and in vitro glucose-stimulated insulin secretion measurements, evidence is provided that dopamine (DA), which is loaded into insulin-containing secretory granules by vesicular monoamine transporter type 2 in human beta-cells, is released in response to glucose stimulation. Glucose 37-44 insulin Homo sapiens 56-63 22915827-2 2012 Using chronoamperometry and in vitro glucose-stimulated insulin secretion measurements, evidence is provided that dopamine (DA), which is loaded into insulin-containing secretory granules by vesicular monoamine transporter type 2 in human beta-cells, is released in response to glucose stimulation. Glucose 278-285 insulin Homo sapiens 150-157 22915827-4 2012 We found that antagonism of receptors participating in islet DA signaling generally drive increased glucose-stimulated insulin secretion. Glucose 100-107 insulin Homo sapiens 119-126 22983116-3 2012 Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion. Glucose 52-59 insulin Homo sapiens 148-155 23018631-1 2012 Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, abnormally elevated hepatic glucose production, and reduced glucose-stimulated insulin secretion. Glucose 132-139 insulin Homo sapiens 151-158 23033046-1 2012 After food consumption, insulin-secreting pancreatic beta-cells detect increased glucose and incretin hormones, and respond by releasing insulin. Glucose 81-88 insulin Homo sapiens 24-31 23134918-17 2012 Serum fasting insulin and hip circumference were significantly higher among children and adolescents with IGT compared to that of normal glucose tolerance. Glucose 137-144 insulin Homo sapiens 14-21 22820012-2 2012 Produced nearly exclusively by the pancreas, insulin crosses the blood-brain barrier (BBB) using a saturable transporter, affecting feeding and cognition through CNS mechanisms largely independent of glucose utilization. Glucose 200-207 insulin Homo sapiens 45-52 22717091-11 2012 However, it failed to improve the large islet"s glucose-stimulated insulin secretion. Glucose 48-55 insulin Homo sapiens 67-74 22787138-7 2012 Lipid infusion reduced insulin-stimulated glucose uptake by 63% in untrained subjects (P < 0.05), whereas this effect was blunted in trained subjects (29%, P < 0.05). Glucose 42-49 insulin Homo sapiens 23-30 22668816-5 2012 Insulin resistance was assessed from fasting blood levels of glucose and insulin with the homeostasis model assessment. Glucose 61-68 insulin Homo sapiens 0-7 22814999-3 2012 Insulin activation of the phosphatidylinositol-3-kinase (PI3K) pathway promotes nitric oxide (NO) production in the endothelium and glucose uptake in insulin-sensitive tissues. Glucose 132-139 insulin Homo sapiens 0-7 22814999-3 2012 Insulin activation of the phosphatidylinositol-3-kinase (PI3K) pathway promotes nitric oxide (NO) production in the endothelium and glucose uptake in insulin-sensitive tissues. Glucose 132-139 insulin Homo sapiens 150-157 23163141-10 2012 CONCLUSION: SQNYPBF combined intensive insulin therapy could better improve the sepsis patients" immunity, decrease the plasma glucose level and duration, increase their survival rate, and improve their prognosis. Glucose 127-134 insulin Homo sapiens 39-46 22985663-5 2012 The intensive insulin treatment (basal-bolus regime with insulin-analogues) approaches the optimal insulin substitution and, with its use the adequate correction of each element of the glucose triad (fasting blood glucose, postprandial blood glucose, HbA1c) should be considered feasible even in patients with type 2 diabetes. Glucose 185-192 insulin Homo sapiens 14-21 22985663-5 2012 The intensive insulin treatment (basal-bolus regime with insulin-analogues) approaches the optimal insulin substitution and, with its use the adequate correction of each element of the glucose triad (fasting blood glucose, postprandial blood glucose, HbA1c) should be considered feasible even in patients with type 2 diabetes. Glucose 214-221 insulin Homo sapiens 14-21 22985663-5 2012 The intensive insulin treatment (basal-bolus regime with insulin-analogues) approaches the optimal insulin substitution and, with its use the adequate correction of each element of the glucose triad (fasting blood glucose, postprandial blood glucose, HbA1c) should be considered feasible even in patients with type 2 diabetes. Glucose 214-221 insulin Homo sapiens 14-21 22958920-7 2012 Despite increased obesity, glucose tolerance was increased with specific enhanced insulin sensitivity in the fat. Glucose 27-34 insulin Homo sapiens 82-89 22992414-2 2012 Obesity causes features of metabolic dysfunction in the adipose tissue that may contribute to later impairments of insulin action in skeletal muscle and liver; these include reduced insulin-stimulated glucose transport, reduced expression of GLUT4, altered expression of adipokines, and adipocyte hypertrophy. Glucose 201-208 insulin Homo sapiens 115-122 23101049-0 2007 Insulin Delivery and Glucose Monitoring Methods for Diabetes Mellitus: Comparative Effectiveness In response to a public request regarding the benefits and harms of current modes of intensive insulin therapy (continuous subcutaneous insulin infusion [CSII] vs. multiple daily injections [MDI]) and modes of blood glucose monitoring (real-time continuous glucose monitoring [rt-CGM] vs. self-monitoring of blood glucose [SMBG]), the Agency for Healthcare Research and Quality (AHRQ) contracted with the Evidence-based Practice Center at Johns Hopkins University to conduct a systematic review of these modalities. Glucose 313-320 insulin Homo sapiens 0-7 22969729-1 2012 Normal release of glucagon from pancreatic islet alpha-cells promotes glucose mobilization, which counteracts the hypoglycemic actions of insulin, thereby ensuring glucose homeostasis. Glucose 70-77 insulin Homo sapiens 138-145 22884032-3 2012 As insulin triggers glucose uptake, most tumors are or become insulin-dependent. Glucose 20-27 insulin Homo sapiens 3-10 22884032-3 2012 As insulin triggers glucose uptake, most tumors are or become insulin-dependent. Glucose 20-27 insulin Homo sapiens 62-69 22950924-1 2012 PURPOSE: Metabolic syndrome (MetS) is characterized by a constellation of metabolic risk factors that consist of the following: atherogenic dyslipidemia, elevated blood pressure, elevated glucose associated with insulin resistance, prothrombotic state, and proinflammatory state. Glucose 188-195 insulin Homo sapiens 212-219 22796579-7 2012 Insulin plays a complex role in regulating glucose metabolism, and it is not surprising that the role of insulin in VLDL and lipid metabolism will prove equally complex. Glucose 43-50 insulin Homo sapiens 0-7 22457223-3 2012 This study specifically investigated insulin-stimulated glucose metabolism in monocytes and examined the impact of HSP induction on insulin signalling. Glucose 56-63 insulin Homo sapiens 37-44 22895666-1 2012 Impaired insulin signaling is central to development of the metabolic syndrome and can promote cardiovascular disease indirectly through development of abnormal glucose and lipid metabolism, hypertension, and a proinflammatory state. Glucose 161-168 insulin Homo sapiens 9-16 22895668-2 2012 Impaired insulin-mediated glucose uptake is a uniformly observed characteristic of the heart in these states, although changes in upstream kinase signaling are variable and dependent on the severity and duration of the associated obesity or diabetes mellitus. Glucose 26-33 insulin Homo sapiens 9-16 22895668-6 2012 In addition to promoting glucose uptake, insulin regulates long-chain fatty acid uptake, protein synthesis, and vascular function in the normal cardiovascular system. Glucose 25-32 insulin Homo sapiens 41-48 23062636-4 2012 Nuclear factor-kappaB transcriptional activity and proinflammatory chemokine / cytokines production were determined by reporter plasmid assay and enzyme-linked immunosorbent assay, respectively.Insulin-stimulated glucose uptake was measured by 2-deoxy-D-[3H] glucose uptake assay. Glucose 213-220 insulin Homo sapiens 194-201 22698081-2 2012 Important outcomes of the reviewed studies appear to support the hypotheses that the flexibility of a membrane determined by the ratio of (poly)unsaturated to saturated fatty acyl chains of its phospholipids influences the effectiveness of glucose transport by insulin-independent glucose transporters (GLUTs) and the insulin-dependent GLUT4, and from the prediabetic stage on a shift from unsaturated towards saturated fatty acyl chains of membrane phospholipids directly induces a decrease in glucose effectiveness and insulin sensitivity. Glucose 240-247 insulin Homo sapiens 261-268 22698081-2 2012 Important outcomes of the reviewed studies appear to support the hypotheses that the flexibility of a membrane determined by the ratio of (poly)unsaturated to saturated fatty acyl chains of its phospholipids influences the effectiveness of glucose transport by insulin-independent glucose transporters (GLUTs) and the insulin-dependent GLUT4, and from the prediabetic stage on a shift from unsaturated towards saturated fatty acyl chains of membrane phospholipids directly induces a decrease in glucose effectiveness and insulin sensitivity. Glucose 240-247 insulin Homo sapiens 318-325 22665215-7 2012 ANCOVA after adjustment for age and fasting plasma glucose clearly shows the decreasing trend in fasting insulin levels and the increasing trend in BMI. Glucose 51-58 insulin Homo sapiens 105-112 22721966-0 2012 The role of endogenous incretin secretion as amplifier of glucose-stimulated insulin secretion in healthy subjects and patients with type 2 diabetes. Glucose 58-65 insulin Homo sapiens 77-84 22752026-5 2012 Insulin-mediated myocardial glucose disposal was determined with 2-deoxy-2-[(18)F]fluoroglucose PET. Glucose 28-35 insulin Homo sapiens 0-7 22827507-15 2012 CONCLUSIONS: This study confirms the advantages provided by insulin pump use in patients with diabetes were enhanced by the use of continuous glucose monitoring. Glucose 142-149 insulin Homo sapiens 60-67 22548946-5 2012 The product of acute insulin response to glucose and insulin sensitivity yielded the disposition index and estimated the degree of beta-cell compensation for insulin resistance. Glucose 41-48 insulin Homo sapiens 21-28 22548946-11 2012 CONCLUSIONS: Our findings suggest that acute insulin response to glucose does not proportionately change to match change in insulin sensitivity. Glucose 65-72 insulin Homo sapiens 45-52 22951902-2 2012 While origins of the pathogenesis of T2DM are poorly understood, an early defect in glucose-stimulated insulin secretion (GSIS) from pancreatic beta-cells is considered a hallmark of T2DM. Glucose 84-91 insulin Homo sapiens 103-110 22951902-3 2012 Upon a glucose stimulus, insulin is secreted in a biphasic manner with an early first-phase burst of insulin, which is followed by a second, more sustained phase of insulin output. Glucose 7-14 insulin Homo sapiens 25-32 22951902-3 2012 Upon a glucose stimulus, insulin is secreted in a biphasic manner with an early first-phase burst of insulin, which is followed by a second, more sustained phase of insulin output. Glucose 7-14 insulin Homo sapiens 101-108 23422597-2 2012 Insulin induces uptake of glucose in the peripheral tissues by upregulating the Glucose transporter 4 expression. Glucose 26-33 insulin Homo sapiens 0-7 22797309-4 2012 Insulin sensitivity was measured using an intravenous glucose tolerance test with the subsequent modeling of an insulin sensitivity index (S(I)). Glucose 54-61 insulin Homo sapiens 0-7 22723317-5 2012 EVIDENCE SYNTHESIS: Insulin has been shown to exert vasodilatory, antiinflammatory, and antiatherogenic effects in experimental models, independent of its glucose-lowering effects. Glucose 155-162 insulin Homo sapiens 20-27 22723317-7 2012 In this context, through its nonmetabolic and metabolic (glucose-lowering) effects, insulin is likely to be cardioprotective and to improve clinical outcomes in acute myocardial infarction. Glucose 57-64 insulin Homo sapiens 84-91 22745239-8 2012 Insulin sensitivity index was quantified using the minimal model of glucose kinetics. Glucose 68-75 insulin Homo sapiens 0-7 22745239-13 2012 During the frequently sampled iv glucose tolerance test, GH secretion was positively correlated with insulin sensitivity index with saline infusion. Glucose 33-40 insulin Homo sapiens 101-108 23063039-0 2012 Effect of insulin feedback on closed-loop glucose control: a crossover study. Glucose 42-49 insulin Homo sapiens 10-17 23063040-0 2012 Robust fault detection system for insulin pump therapy using continuous glucose monitoring. Glucose 72-79 insulin Homo sapiens 34-41 22851631-10 2012 The lower maximal standardized uptake value in the postprandial state may be explained by increased insulin-stimulated glucose uptake in muscle. Glucose 119-126 insulin Homo sapiens 100-107 23049592-7 2012 Homeostatic model assessment-insulin resistance (HOMA-IR) was calculated from the fasting insulin and glucose levels. Glucose 102-109 insulin Homo sapiens 29-36 22424820-6 2012 Insulin resistance and secretion were assessed using oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FS-IVGTT). Glucose 58-65 insulin Homo sapiens 0-7 22424822-1 2012 The objective was to determine the effect of metformin on the concentrations of resistin and other markers of insulin resistance or inflammation (C-reactive protein, cytokines, body weight, HbA1c, among others) in minors with glucose intolerance. Glucose 226-233 insulin Homo sapiens 110-117 22751929-2 2012 Here, we present the first report of the mechanisms by which SKIP specifically suppresses insulin signaling and the subsequent glucose uptake. Glucose 127-134 insulin Homo sapiens 90-97 22971680-5 2012 Additional CV risk factors in PD are related to the glucose load, leading to increasing insulin resistance and a more atherogenic lipid profile. Glucose 52-59 insulin Homo sapiens 88-95 22583576-5 2012 Insulin NPs maintained a continual blood glucose level for 24 h, which, however, was transient (<8 h) in the case of subcutaneous insulin and associated with severe hypoglycemic shock. Glucose 41-48 insulin Homo sapiens 0-7 22817340-6 2012 Basal insulin delivery was automatically adjusted by a model predictive control algorithm based on real-time continuous glucose monitor readings. Glucose 120-127 insulin Homo sapiens 6-13 22426845-0 2012 Insulin secretion and sensitivity after single-dose amisulpride, olanzapine or placebo in young male subjects: double blind, cross-over glucose clamp study. Glucose 136-143 insulin Homo sapiens 0-7 22694920-11 2012 CONCLUSIONS: These findings suggest that an increase in serum insulin and insulin/glucose levels may cause weight gain, possibly by stimulating appetite, and that weight changes seem to be reversible with intensive behavior therapy without discontinuation of VPA. Glucose 82-89 insulin Homo sapiens 74-81 22708619-4 2012 Insulin sensitivity was calculated as glucose disposal rate (GDR) and insulin sensitivity index (ISI), and also by HOMA-IR. Glucose 38-45 insulin Homo sapiens 0-7 22938893-8 2012 Nonsurvivors required greater doses of insulin to control glucose levels and had greater mean insulin to glucose ratios (t test; P = .025). Glucose 58-65 insulin Homo sapiens 39-46 22766318-1 2012 In pancreatic beta cells, mitochondria play a central role in coupling glucose metabolism to insulin exocytosis, thereby ensuring strict control of glucose-stimulated insulin secretion. Glucose 71-78 insulin Homo sapiens 93-100 22938664-6 2012 If blood glucose >=11.1 mmol/L was maintained twicely, the approach of insulin administration would convert from subcutaneous injection to venous pump-in using the computerized glucose control protocol. Glucose 9-16 insulin Homo sapiens 74-81 22938664-17 2012 CONCLUSIONS: Compared with the conventional subcutaneous insulin injection protocol, this protocol with insulin glargine combined regular insulin subcutaneous injection can control the glucose level effectively during EN in critical patients. Glucose 185-192 insulin Homo sapiens 104-111 22938664-17 2012 CONCLUSIONS: Compared with the conventional subcutaneous insulin injection protocol, this protocol with insulin glargine combined regular insulin subcutaneous injection can control the glucose level effectively during EN in critical patients. Glucose 185-192 insulin Homo sapiens 104-111 23290812-6 2012 RESULTS: There were differences noticed regarding the waist circumstances (WC), body mass index (BMI), lipids, 0 and 120 min insulin levels in different glucose tolerance status between the Hans and Uygurs. Glucose 153-160 insulin Homo sapiens 125-132 21392830-0 2012 Metabolic syndrome and insulin resistance are associated with abnormal left ventricular diastolic function and structure independent of blood pressure and fasting plasma glucose level. Glucose 170-177 insulin Homo sapiens 23-30 21392830-9 2012 CONCLUSIONS: MetS and insulin resistance are associated with abnormal LV diastolic function and structure independent of age, gender, blood pressure, and fasting plasma glucose level. Glucose 169-176 insulin Homo sapiens 22-29 21523426-1 2012 Diabetes is a chronic disease that is characterized by an increased blood glucose level due to insulin resistance. Glucose 74-81 insulin Homo sapiens 95-102 22586589-3 2012 Because insulin physiologically facilitates glucose uptake by most tissues of the body and thereby fosters intracellular energy supply, we hypothesized that intranasal insulin reduces food consumption via enhancement of the neuroenergetic level. Glucose 44-51 insulin Homo sapiens 8-15 22586589-3 2012 Because insulin physiologically facilitates glucose uptake by most tissues of the body and thereby fosters intracellular energy supply, we hypothesized that intranasal insulin reduces food consumption via enhancement of the neuroenergetic level. Glucose 44-51 insulin Homo sapiens 168-175 25099568-1 2012 An optimal state feedback controller is designed with the objective of minimizing the elevated glucose levels caused by meal intake in Type 1 diabetic subjects, by the minimal infusion of insulin. Glucose 95-102 insulin Homo sapiens 188-195 22722501-11 2012 Glucose sensitivity for insulin worsened significantly with olanzapine (P < 0.03), with no significant changes for paliperidone ER. Glucose 0-7 insulin Homo sapiens 24-31 22822059-10 2012 To further assess the importance of mPGES-1 to IL-1beta regulation of an islet physiologic response, glucose-stimulated insulin secretion was examined in isolated islets of WT and mPGES-1-deficient mice. Glucose 101-108 insulin Homo sapiens 120-127 22822059-11 2012 IL-1beta inhibited glucose-stimulated insulin secretion equally in both WT and mPGES-1(-/-) islets, indicating that COX-2, not mPGES-1, mediates IL-1beta-induced PGE(2) production and subsequent inhibition of insulin secretion. Glucose 19-26 insulin Homo sapiens 38-45 24843592-7 2012 Mean area under the curves of glucose (AUC-G) was significantly associated with II and insulin sensitivity index (ISI) composite in univariate analysis. Glucose 30-37 insulin Homo sapiens 87-94 24843593-0 2012 Insulin secretory capacity and insulin sensitivity in impaired fasting glucose in Japanese. Glucose 71-78 insulin Homo sapiens 0-7 24843593-0 2012 Insulin secretory capacity and insulin sensitivity in impaired fasting glucose in Japanese. Glucose 71-78 insulin Homo sapiens 31-38 24843593-9 2012 CONCLUSIONS: Although impaired early-phase insulin secretion plays the more important role in the elevation of postchallenge glucose in IFG100-109 patients, both impaired early-phase insulin secretion and decreased insulin sensitivity are involved in the deterioration of FPG in Japanese. Glucose 127-134 insulin Homo sapiens 45-52 22809065-3 2012 The results show that eriodictyol increased insulin-stimulated glucose uptake in both human hepatocellular liver carcinoma cells (HepG2) and differentiated 3T3-L1 adipocytes under high-glucose conditions. Glucose 63-70 insulin Homo sapiens 44-51 22809065-3 2012 The results show that eriodictyol increased insulin-stimulated glucose uptake in both human hepatocellular liver carcinoma cells (HepG2) and differentiated 3T3-L1 adipocytes under high-glucose conditions. Glucose 185-192 insulin Homo sapiens 44-51 22809065-5 2012 Furthermore, it reactivated Akt in HepG2 cells with high-glucose-induced insulin resistance. Glucose 57-64 insulin Homo sapiens 73-80 22270400-5 2012 In addition, the more rapid onset and shorter duration of action of rapid-acting insulin analogs are associated with greater control of postprandial glucose than regular human insulin. Glucose 149-156 insulin Homo sapiens 81-88 22669243-1 2012 The present analysis tests the hypothesis that quantifiable disruption of the glucose-stimulated insulin-secretion dose-response pathway mediates impaired fasting glycemia (IFG) and type 2 diabetes mellitus (DM). Glucose 78-85 insulin Homo sapiens 97-104 22669243-5 2012 Logistic dose-response functions were constructed analytically of the sensitivity, potency, and efficacy (in the pharmacological sense of slope, one-half maximal stimulation, and maximal effect) of glucose"s stimulation of prehepatic insulin (C-peptide) secretion. Glucose 198-205 insulin Homo sapiens 234-241 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Glucose 120-127 insulin Homo sapiens 13-20 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Glucose 120-127 insulin Homo sapiens 97-104 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Glucose 120-127 insulin Homo sapiens 97-104 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Glucose 148-155 insulin Homo sapiens 13-20 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Glucose 148-155 insulin Homo sapiens 97-104 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Glucose 148-155 insulin Homo sapiens 97-104 22969777-7 2012 However, Niaspan therapy caused a 22% reduction in insulin-mediated glucose disposal (p < 0.05). Glucose 68-75 insulin Homo sapiens 51-58 21973241-10 2012 In the T2DM group, insulin/glucose ratio decreased postbreakfast (P = 0 04) and increased postdinner (P = 0 03). Glucose 27-34 insulin Homo sapiens 19-26 21803437-0 2012 Identification of an integrated mathematical model of standard oral glucose tolerance test for characterization of insulin potentiation in health. Glucose 68-75 insulin Homo sapiens 115-122 21803437-4 2012 Model behaviour was tested vs. mean plasma glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucose and insulin measurements from two different laboratories, where glycemic profiles observed during a 75 g OGTT were matched in healthy subjects (HC1- and HC2-group, respectively) by means of an isoglycemic intravenous glucose (I-IVG) infusion. Glucose 76-83 insulin Homo sapiens 94-101 22233527-1 2012 Glucagon-like peptide-1 (GLP-1), a gut-derived hormone secreted in response to nutrients, has several glucose and weight regulating actions including enhancement of glucose-stimulated insulin secretion, suppression of glucagon secretion, slowing of gastric emptying and reduction in food intake. Glucose 165-172 insulin Homo sapiens 184-191 22435928-0 2012 Insulin secretion based on the late oral glucose tolerance test period and incident diabetes: the San Antonio Heart Study. Glucose 41-48 insulin Homo sapiens 0-7 22435928-1 2012 AIMS: The Insulinogenic Index from 0 to 30 min (DeltaI (0-30) /DeltaG(0-30) ), a measure of insulin secretion derived from the early period of the oral glucose tolerance test, predicts future diabetes. Glucose 152-159 insulin Homo sapiens 92-99 22435928-11 2012 CONCLUSIONS: An insulin secretory measure derived from the late oral glucose tolerance test period is useful for classifying individuals at risk of future diabetes independently of other risk factors, including insulin sensitivity and a secretory measure from the early oral glucose tolerance test period. Glucose 69-76 insulin Homo sapiens 16-23 22435928-11 2012 CONCLUSIONS: An insulin secretory measure derived from the late oral glucose tolerance test period is useful for classifying individuals at risk of future diabetes independently of other risk factors, including insulin sensitivity and a secretory measure from the early oral glucose tolerance test period. Glucose 275-282 insulin Homo sapiens 16-23 22486204-9 2012 For patients with diabetes or impaired glucose tolerance, meta-analysis showed a small effect on fasting glucose (-0.32 mmol/l, 95%CI -0.57 to -0.07) and a small improvement in insulin resistance (standard mean difference -0.25, 95%CI -0.48 to -0.03). Glucose 39-46 insulin Homo sapiens 177-184 22507373-0 2012 Glucocorticoid receptor gene polymorphisms are associated with reduced first-phase glucose-stimulated insulin secretion and disposition index in women, but not in men. Glucose 83-90 insulin Homo sapiens 102-109 22507373-1 2012 AIM: Glucocorticoids are efficacious anti-inflammatory agents, but, in susceptible individuals, these drugs may induce glucose intolerance and diabetes by affecting beta-cell function and insulin sensitivity. Glucose 119-126 insulin Homo sapiens 188-195 22507373-5 2012 From 2-h hyperglycaemic clamps, first- and second-phase glucose-stimulated insulin secretion, as well as insulin sensitivity index and disposition index, were calculated. Glucose 56-63 insulin Homo sapiens 75-82 22507373-9 2012 Also only in women, the ER22/23EK polymorphism was associated with reduced first-phase glucose-stimulated insulin secretion (P=0.011) and disposition index (P=0.003). Glucose 87-94 insulin Homo sapiens 106-113 22584726-10 2012 Many of the highly ranked genes are also involved in the regulation or metabolism of insulin, glucose or lipids. Glucose 94-101 insulin Homo sapiens 85-92 22740171-5 2012 As graft-derived insulin levels increased over time, diabetic mice were weaned from exogenous insulin and human C-peptide secretion was eventually regulated by meal and glucose challenges. Glucose 169-176 insulin Homo sapiens 17-24 22740171-5 2012 As graft-derived insulin levels increased over time, diabetic mice were weaned from exogenous insulin and human C-peptide secretion was eventually regulated by meal and glucose challenges. Glucose 169-176 insulin Homo sapiens 112-121 22853720-1 2012 UNLABELLED: Abstract Objective: Controlled inpatient studies on the effects of food, physical activity (PA), and insulin dosing on glucose excursions exist, but such outpatient data are limited. Glucose 133-140 insulin Homo sapiens 115-122 22246849-4 2012 Insulin sensitivity was measured with estimated glucose disposal rate calculated using the equation: eGDR = 24.31 - (12.22 x WHR) - (3.29 x HT) - (0.57 x HbA1c); WHR = waist-to-hip ratio, HT = hypertension. Glucose 48-55 insulin Homo sapiens 0-7 22653558-6 2012 In addition, prednisolone-treated high-fat diet-fed mice appeared less insulin sensitive by detailed analysis of basal glucose kinetics. Glucose 119-126 insulin Homo sapiens 71-78 22669333-12 2012 A decrease in first-phase insulin secretion may partially contribute to the short-term LC/HFD-induced increase in postprandial plasma glucose levels. Glucose 134-141 insulin Homo sapiens 26-33 22762724-2 2012 INTRODUCTION: Dysregulation of metabolic pathways, caused by imbalances in energy homeostasis, leads to type 2 diabetes characterized by high glucose concentration in the blood due to insulin resistance which is a major disorder in developed countries. Glucose 142-149 insulin Homo sapiens 184-191 22309514-0 2012 Insulin resistance but not impaired beta-cell function: a key feature in Chinese normal-weight PCOS women with normal glucose regulation. Glucose 118-125 insulin Homo sapiens 0-7 22064160-9 2012 Postprandial IS and glucose-stimulated insulin secretion remained unchanged, but glucose tolerance decreased. Glucose 20-27 insulin Homo sapiens 39-46 22064160-10 2012 RF decreased fasting and postprandial IS at increased glucose-stimulated insulin secretion. Glucose 54-61 insulin Homo sapiens 73-80 22064160-12 2012 Concomitantly, fasting and postprandial IS decreased at increased glucose-stimulated insulin secretion. Glucose 66-73 insulin Homo sapiens 85-92 22611253-5 2012 This antioxidant function preserves mitochondrial integrity and physiology, prerequisites for glucose-stimulated insulin secretion. Glucose 94-101 insulin Homo sapiens 113-120 21537854-2 2012 Such individuals must determine when insulin is needed to reduce glucose levels in their bodies, or when additional glucose must be administered to raise levels. Glucose 65-72 insulin Homo sapiens 37-44 22763825-6 2012 After the switching, the basal insulin was increased with reference to the self-monitoring of blood glucose results, with the aim of maintaining fasting blood sugar (FBS) level at 110 mg/dL, and simultaneously reducing the bolus insulin dosage to maintain the total daily insulin dosage. Glucose 100-107 insulin Homo sapiens 31-38 22560232-13 2012 CONCLUSIONS: Strict glucose control with a postoperative insulin infusion protocol significantly decreased the incidence of postoperative in-hospital wound infection in the diabetic population. Glucose 20-27 insulin Homo sapiens 57-64 22360160-0 2012 Insulin-induced microvascular recruitment in skin and muscle are related and both are associated with whole-body glucose uptake. Glucose 113-120 insulin Homo sapiens 0-7 22360160-1 2012 OBJECTIVE: Insulin-induced capillary recruitment is considered a determinant of insulin-mediated glucose uptake. Glucose 97-104 insulin Homo sapiens 11-18 22360160-1 2012 OBJECTIVE: Insulin-induced capillary recruitment is considered a determinant of insulin-mediated glucose uptake. Glucose 97-104 insulin Homo sapiens 80-87 22360160-9 2012 Insulin"s microvascular effects in skin and muscle showed comparable strong correlations with insulin-mediated glucose uptake (r = 0.73 and 0.68, respectively). Glucose 111-118 insulin Homo sapiens 0-7 22360160-9 2012 Insulin"s microvascular effects in skin and muscle showed comparable strong correlations with insulin-mediated glucose uptake (r = 0.73 and 0.68, respectively). Glucose 111-118 insulin Homo sapiens 94-101 22360160-10 2012 CONCLUSIONS: Insulin-augmented capillary recruitment in skin parallels insulin-mediated microvascular recruitment in muscle and both are related to insulin-mediated glucose uptake. Glucose 165-172 insulin Homo sapiens 13-20 22360160-10 2012 CONCLUSIONS: Insulin-augmented capillary recruitment in skin parallels insulin-mediated microvascular recruitment in muscle and both are related to insulin-mediated glucose uptake. Glucose 165-172 insulin Homo sapiens 71-78 22360160-10 2012 CONCLUSIONS: Insulin-augmented capillary recruitment in skin parallels insulin-mediated microvascular recruitment in muscle and both are related to insulin-mediated glucose uptake. Glucose 165-172 insulin Homo sapiens 148-155 22386942-0 2012 Increased action of pulsatile compared to non-pulsatile insulin delivery during a meal-like glucose exposure simulated by computerized infusion in healthy humans. Glucose 92-99 insulin Homo sapiens 56-63 22386942-8 2012 The hypoglycemic effect of insulin was measured as the integrated area under the curve of glucose during the four-hour infusion period. Glucose 90-97 insulin Homo sapiens 27-34 22894087-3 2012 Of course, dietary and exercise therapy are important, and oral hypoglycemic agents and insulin will be used appropriately further, to control not only the average of the blood glucose levels for but also the blood glucose change. Glucose 177-184 insulin Homo sapiens 88-95 22894087-3 2012 Of course, dietary and exercise therapy are important, and oral hypoglycemic agents and insulin will be used appropriately further, to control not only the average of the blood glucose levels for but also the blood glucose change. Glucose 215-222 insulin Homo sapiens 88-95 22850594-5 2012 Insulin sensitivity (oral glucose tolerance test, ISI) was measured when subjects were sedentary and at 16-24 h and 15 days after the final training bout. Glucose 26-33 insulin Homo sapiens 0-7 22967344-1 2012 OBJECTIVE: To investigate the effect of combined use of insulin and acarbose on glucose excursion in type 1 diabetic patients. Glucose 80-87 insulin Homo sapiens 56-63 24710481-4 2012 Here we will focus on the signalling pathways by which environmental glucose directly, i.e., independently of insulin and glucagon, regulates autophagy in mammalian cells, but we will also briefly mention some data in yeast. Glucose 69-76 insulin Homo sapiens 110-117 22582094-4 2012 Both zinc depletion and lipotoxicity (but not glucotoxicity) downregulated ZNT8 (SLC30A8) expression and altered the glucose-stimulated insulin secretion index (GSIS). Glucose 117-124 insulin Homo sapiens 136-143 22816025-9 2012 Continuous glucose monitoring devices that provide accurate measurement can contribute to minimizing the risk of hypoglycemia and improve insulin titration. Glucose 11-18 insulin Homo sapiens 138-145 22545627-1 2012 GLUT4 (glucose transporter 4) is responsible for the insulin-induced uptake of glucose by muscle and fat cells. Glucose 7-14 insulin Homo sapiens 53-60 22511259-1 2012 OBJECTIVE: This study was designed to determine a cutoff point for identifying insulin resistance from hyperinsulinemic-euglycemic clamp studies performed at 120 mU/m(2) min in a white population and to generate equations from routinely measured clinic and blood variables for predicting clamp-derived glucose disposal rate (GDR), i.e., insulin sensitivity. Glucose 302-309 insulin Homo sapiens 79-86 22610098-1 2012 To promote glucose uptake into fat and muscle cells, insulin causes the translocation of GLUT4 glucose transporters from intracellular vesicles to the cell surface. Glucose 11-18 insulin Homo sapiens 53-60 22610098-10 2012 Together with previous results, these data support a model whereby insulin stimulates TUG cleavage to liberate GLUT4 storage vesicles from the Golgi matrix, which promotes GLUT4 translocation to the cell surface and enhances glucose uptake. Glucose 225-232 insulin Homo sapiens 67-74 22613019-8 2012 Also, increased insulin levels were detected after administration of a glucose tolerance test (GTT), consistent with previous studies showing changes in insulin signaling in patients with schizophrenia. Glucose 71-78 insulin Homo sapiens 16-23 22613019-8 2012 Also, increased insulin levels were detected after administration of a glucose tolerance test (GTT), consistent with previous studies showing changes in insulin signaling in patients with schizophrenia. Glucose 71-78 insulin Homo sapiens 153-160 22608986-11 2012 CONCLUSIONS: In this cohort of acutely infected patients without established severe sepsis or shock, higher glucose concentrations within the first 72 hours in the nondiabetic population were associated with worse hospital outcomes and were less likely to be treated with insulin compared with diabetic patients. Glucose 108-115 insulin Homo sapiens 272-279 22322357-2 2012 Here, we address the question whether a heat-shock protein (HSP) co-inducer, insulin sensitizer drug candidate, BGP-15, can prevent AAPD-induced glucose, lipid, and weight changes. Glucose 145-152 insulin Homo sapiens 77-84 22579112-8 2012 However, none of the phenolic compounds tested in this study reversed the blunted glucose-stimulated insulin secretion after cytokines treatment. Glucose 82-89 insulin Homo sapiens 101-108 22413808-0 2012 Fasting plasma glucose 6-12 weeks after starting insulin glargine predicts likelihood of treatment success: a pooled analysis. Glucose 15-22 insulin Homo sapiens 49-56 22413808-1 2012 AIMS: To evaluate whether fasting plasma glucose values measured early during insulin therapy can identify patients with Type 2 diabetes who may not achieve adequate glycaemic control after 6 months and will require additional treatment. Glucose 41-48 insulin Homo sapiens 78-85 22555471-1 2012 The incretins are gut hormones secreted in response to nutrient/carbohydrate ingestion and act on the pancreatic beta cell to amplify glucose-stimulated insulin secretion. Glucose 134-141 insulin Homo sapiens 153-160 22584133-0 2012 Analysis of glucose responses to automated insulin suspension with sensor-augmented pump therapy. Glucose 12-19 insulin Homo sapiens 43-50 22584133-8 2012 The mean sensor glucose 2 h after insulin delivery resumed was 155 +- 10 mg/dL (8.6 +- 0.6 mmol/L). Glucose 16-23 insulin Homo sapiens 34-41 22584133-10 2012 CONCLUSIONS: Analyses of sensor glucose patterns following insulin suspension activated by LGS suggest that this technology is safe and unlikely to be associated with adverse outcomes. Glucose 32-39 insulin Homo sapiens 59-66 22522617-1 2012 Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). Glucose 63-70 insulin Homo sapiens 18-25 22619360-11 2012 Moreover, ER stress induced by high glucose and palmitate increased the expression of fetuin-A and further contributed to the development of insulin resistance. Glucose 36-43 insulin Homo sapiens 141-148 22548951-8 2012 Targeting insulin titration to this glucose level may result in excessive basal insulin dosing for the non-dawn phenomenon periods of the day. Glucose 36-43 insulin Homo sapiens 10-17 22548951-8 2012 Targeting insulin titration to this glucose level may result in excessive basal insulin dosing for the non-dawn phenomenon periods of the day. Glucose 36-43 insulin Homo sapiens 80-87 22492868-6 2012 The relative suppression of palmitate Ra correlated directly with the relative stimulation of glucose rate of disappearance during insulin infusion (r(s) = 0.530, P < 0.001). Glucose 94-101 insulin Homo sapiens 131-138 22529198-6 2012 INTERVENTIONS: Intravenous insulin was administered to achieve nadir plasma glucose (NPG) of 2.2 mmol/l (39.6 mg/dl). Glucose 76-83 insulin Homo sapiens 27-34 22212745-0 2012 Effect of vitamin D on insulin sensitivity in elderly patients with impaired fasting glucose. Glucose 85-92 insulin Homo sapiens 23-30 22212745-2 2012 The aim of the present study was to investigate the effect of vitamin D treatment on insulin sensitivity and metabolic parameters in elderly people with impaired fasting glucose. Glucose 170-177 insulin Homo sapiens 85-92 22212745-8 2012 CONCLUSION: We found that vitamin D treatment might modify insulin sensitivity in the elderly with impaired fasting glucose. Glucose 116-123 insulin Homo sapiens 59-66 22496506-2 2012 DESIGN: Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp [glucose disposal rate (GDR)]. Glucose 79-86 insulin Homo sapiens 8-15 22523335-2 2012 Insulin and bradykinin are meal-stimulated promoters of AT blood flow and glucose metabolism. Glucose 74-81 insulin Homo sapiens 0-7 22508711-12 2012 Insulin-mediated whole-body glucose disposal did not differ with or without candesartan pretreatment. Glucose 28-35 insulin Homo sapiens 0-7 22523335-9 2012 In the lean group, bradykinin increased insulin-mediated AT glucose uptake from 8.6 +- 1.6 to 12.3 +- 2.4 mumol/min kg (P = 0.038). Glucose 60-67 insulin Homo sapiens 40-47 22569236-18 2012 These changes are, however, not reflected in a higher insulin-stimulated glucose disposal rate. Glucose 73-80 insulin Homo sapiens 54-61 22539584-10 2012 CONCLUSIONS: The dynamic change of circulating FGF21 was associated with alterations in insulin levels in response to glucose challenge in humans. Glucose 118-125 insulin Homo sapiens 88-95 22920801-1 2012 Barriers to the use of prandial insulin regimens include inadequate synchronization of insulin action to postprandial plasma glucose excursions as well as a significant risk of hypoglycemia and weight gain. Glucose 125-132 insulin Homo sapiens 32-39 22920801-1 2012 Barriers to the use of prandial insulin regimens include inadequate synchronization of insulin action to postprandial plasma glucose excursions as well as a significant risk of hypoglycemia and weight gain. Glucose 125-132 insulin Homo sapiens 87-94 22920802-2 2012 Shorter time to peak and shorter duration of insulin action are important steps toward reducing high postprandial blood glucose concentrations in diabetes therapy and are critical for the development of a closed-loop insulin delivery system. Glucose 120-127 insulin Homo sapiens 45-52 22920802-2 2012 Shorter time to peak and shorter duration of insulin action are important steps toward reducing high postprandial blood glucose concentrations in diabetes therapy and are critical for the development of a closed-loop insulin delivery system. Glucose 120-127 insulin Homo sapiens 217-224 22437669-8 2012 After examining Meta-Analyses of Glucose and Insulin-Related Traits Consortium data, SNPs in 22 genes modulated by PPAR ligands were associated with fasting plasma glucose and the expression of 28 transcripts modulated by PPAR ligands was under control of local genetic regulators (cis-eQTLs) in adipose tissue of Multi Tissue Human Expression Resource study twins. Glucose 164-171 insulin Homo sapiens 45-52 22325254-5 2012 The insulin-based oDI estimates correlated with cDI overall (r >= 0.74, P < .001) and within each glucose tolerance group (r >= 0.40, P < .001). Glucose 104-111 insulin Homo sapiens 4-11 22577121-4 2012 Although hyperglycemia develops, muscle and fat uptake is reduced and other non-insulin-sensitive cells have an increase in glucose uptake as a result of the elevated glucose levels. Glucose 124-131 insulin Homo sapiens 80-87 22577121-4 2012 Although hyperglycemia develops, muscle and fat uptake is reduced and other non-insulin-sensitive cells have an increase in glucose uptake as a result of the elevated glucose levels. Glucose 167-174 insulin Homo sapiens 80-87 22577121-6 2012 The increased uptake of glucose in non-insulin-sensitive cells is involved in the development of several of the most common postoperative complications, including infections and cardiovascular problems. Glucose 24-31 insulin Homo sapiens 39-46 22676360-4 2012 Insulin sensitivity was measured directly by steady-state plasma glucose (SSPG) concentration during insulin suppression test. Glucose 65-72 insulin Homo sapiens 0-7 22552298-7 2012 Second, ICER Igamma overexpression controlled by this promoter region significantly blocked the glucose-mediated insulin transcription, such as that regulated by the viral promoter in the pancreatic beta cell line, MIN6. Glucose 108-115 insulin Homo sapiens 137-144 22914402-0 2012 Influence of breastfeeding during the postpartum oral glucose tolerance test on plasma glucose and insulin. Glucose 54-61 insulin Homo sapiens 99-106 22480751-7 2012 CONCLUSIONS: Exclusion of glucose passage through the proximal small bowel results in enhanced insulin and gut hormone responses in patients after gastric bypass. Glucose 26-33 insulin Homo sapiens 95-102 22721429-5 2012 RESULTS: Results showed that E2 influenced on protein levels of insulin receptor substrate-1 (IRS-1) and impaired insulin-induced Ser308 phosphorylation of Akt/PKB and Ser9 phosphorylation of GSK3beta in Huh7 cells, leading to an inhibition of glucose uptake and glycogen synthesis, respectively, and eventually insulin resistance. Glucose 244-251 insulin Homo sapiens 114-121 22833839-5 2012 These islet-like cells demonstrated time-dependent glucose-stimulated insulin release, and the ability to ameliorate hyperglycemia in chemically induced diabetic mice. Glucose 51-58 insulin Homo sapiens 70-77 22716962-1 2012 Hypoglycemia is a common complication of insulin treatment in type 1 diabetes mellitus and can occur in any patient with diabetes when glucose consumption exceeds supply. Glucose 135-142 insulin Homo sapiens 41-48 22480907-5 2012 These findings provide a molecular mechanism by which a botanical extract improves insulin stimulated glucose uptake, transport and metabolism at the cellular level resulting in enhanced whole body insulin sensitivity. Glucose 102-109 insulin Homo sapiens 83-90 22480907-5 2012 These findings provide a molecular mechanism by which a botanical extract improves insulin stimulated glucose uptake, transport and metabolism at the cellular level resulting in enhanced whole body insulin sensitivity. Glucose 102-109 insulin Homo sapiens 198-205 22681724-0 2012 Assessment of endogenous insulin secretion in insulin treated diabetes predicts postprandial glucose and treatment response to prandial insulin. Glucose 93-100 insulin Homo sapiens 25-32 22703645-2 2012 Insulin sensitivity defines the metabolic balance between insulin concentration and insulin-mediated glucose disposal. Glucose 101-108 insulin Homo sapiens 0-7 22703645-2 2012 Insulin sensitivity defines the metabolic balance between insulin concentration and insulin-mediated glucose disposal. Glucose 101-108 insulin Homo sapiens 84-91 22681724-2 2012 We aimed to assess the impact of endogenous insulin secretion on postprandial glucose increase and the effectiveness of prandial exogenous insulin. Glucose 78-85 insulin Homo sapiens 44-51 22681724-6 2012 RESULTS: Post meal glucose increment (90 minute - fasting) was inversely correlated with endogenous insulin secretion (90 minute C-peptide) (Spearman"s r = -0.70, p < 0.001). Glucose 19-26 insulin Homo sapiens 100-107 22685218-9 2012 Use of different types of glucose-lowering agents including human insulin, insulin analogues, as well as sulfonylureas were associated with a quantitatively similar and significantly increased RR of cancer of 1.2-1.3 compared with unexposed individuals after multivariable adjustment. Glucose 26-33 insulin Homo sapiens 66-73 22682537-4 2012 Insulin sensitivity was assessed according the rate constant for plasma glucose disappearance (Kitt) determined via the short insulin tolerance test. Glucose 72-79 insulin Homo sapiens 0-7 22685218-9 2012 Use of different types of glucose-lowering agents including human insulin, insulin analogues, as well as sulfonylureas were associated with a quantitatively similar and significantly increased RR of cancer of 1.2-1.3 compared with unexposed individuals after multivariable adjustment. Glucose 26-33 insulin Homo sapiens 75-82 22710978-9 2012 Therefore, through a systematical implementation plan, monitoring of patient blood glucose levels was switched from using a paper IV insulin protocol to a computerized glucose management system. Glucose 83-90 insulin Homo sapiens 133-140 22732222-1 2012 Uptake of circulating glucose into the cells happens via the insulin- mediated signalling pathway, which translocates the glucose transporter 4 (GLUT4) vesicles from the intracellular compartment to the plasma membrane. Glucose 22-29 insulin Homo sapiens 61-68 24843576-0 2012 Insulin-secretion capacity in normal glucose tolerance, impaired glucose tolerance, and diabetes in obese and non-obese Japanese patients. Glucose 37-44 insulin Homo sapiens 0-7 24843576-5 2012 ), calculated by dividing the increment in serum insulin by the increment in plasma glucose from 0 to 30 min during OGTT, decreased from NGT to IGT and to DM in patients with and without obesity. Glucose 84-91 insulin Homo sapiens 49-56 24843576-9 2012 CONCLUSIONS: These results show that early-phase insulin secretion in obese Japanese patients is higher than in non-obese patients in all stages of glucose tolerance, and delayed insulin-secretion capacity is also conserved in obese Japanese patients, even in IGT and DM, which is similar to Caucasian patients. Glucose 150-157 insulin Homo sapiens 51-58 24750613-0 2012 pH- and glucose-sensitive glycopolymer nanoparticles based on phenylboronic acid for triggered release of insulin. Glucose 8-15 insulin Homo sapiens 106-113 24750613-5 2012 Furthermore, the in vitro release profiles of insulin also revealed obvious pH- and glucose-sensitivity of the nanoparticles. Glucose 84-91 insulin Homo sapiens 46-53 22856231-2 2012 We investigated associations of renal parameters, including urinary albumin excretion rate (UAE), serum creatinine and creatinine clearance, with surrogate measure of insulin sensitivity calculated using a formula derived from euglycemic-hyperinsulinemic clamp studies (estimated glucose disposal rate, eGDR). Glucose 280-287 insulin Homo sapiens 167-174 22122457-4 2012 Thiazolidinediones are PPAR-gamma agonists regulating the expression of several genes involved in the regulation of glucose, lipid and protein metabolism, enhancing the action of insulin in insulin-sensitive tissue by increasing glucose uptake in skeletal muscle and adipose tissue, and decreasing hepatic glucose production. Glucose 229-236 insulin Homo sapiens 179-186 22122457-4 2012 Thiazolidinediones are PPAR-gamma agonists regulating the expression of several genes involved in the regulation of glucose, lipid and protein metabolism, enhancing the action of insulin in insulin-sensitive tissue by increasing glucose uptake in skeletal muscle and adipose tissue, and decreasing hepatic glucose production. Glucose 229-236 insulin Homo sapiens 190-197 22342294-7 2012 CONCLUSION: In critically ill patients, glucose measurements from capillary and arterial blood by glucose meter are inaccurate, and can potentially lead to inappropriate use of insulin-infusion protocols and failure to achieve glycaemic targets. Glucose 40-47 insulin Homo sapiens 177-184 22342294-7 2012 CONCLUSION: In critically ill patients, glucose measurements from capillary and arterial blood by glucose meter are inaccurate, and can potentially lead to inappropriate use of insulin-infusion protocols and failure to achieve glycaemic targets. Glucose 98-105 insulin Homo sapiens 177-184 22385830-1 2012 In 61 young adults with type 1 diabetes mellitus, the estimated glucose disposal rate (eGDR), a validated marker for insulin resistance, correlated positively with the prevalence of microvascular complications. Glucose 64-71 insulin Homo sapiens 117-124 22432118-4 2012 Insulin sensitivity index (ISI) was calculated from fasting and 2-h postload insulin and glucose concentrations. Glucose 89-96 insulin Homo sapiens 0-7 22449812-1 2012 PURPOSE OF REVIEW: To review the aberrations of insulin signaling to atypical protein kinase C (aPKC) in muscle and liver that generate cardiovascular risk factors, including obesity, hypertriglyceridemia, hypercholesterolemia, insulin resistance and glucose intolerance in type 2 diabetes mellitus (T2DM), and obesity-associated metabolic syndrome (MetSyn). Glucose 251-258 insulin Homo sapiens 48-55 22449812-2 2012 RECENT FINDINGS: aPKC and Akt mediate the insulin effects on glucose transport in muscle and synthesis of lipids, cytokines and glucose in liver. Glucose 61-68 insulin Homo sapiens 42-49 22449812-2 2012 RECENT FINDINGS: aPKC and Akt mediate the insulin effects on glucose transport in muscle and synthesis of lipids, cytokines and glucose in liver. Glucose 128-135 insulin Homo sapiens 42-49 22474039-1 2012 OBJECTIVE: To provide a comprehensive assessment of multiorgan insulin sensitivity in lean and obese subjects with normal glucose tolerance. Glucose 122-129 insulin Homo sapiens 63-70 22474039-4 2012 RESULTS: In obese subjects, palmitate and glucose R(a) in plasma decreased with increasing plasma insulin concentrations. Glucose 42-49 insulin Homo sapiens 98-105 22474039-5 2012 The decrease in endogenous glucose R(a) was greater during low-, medium-, and high-dose insulin infusions (69 +- 2, 74 +- 2, and 90 +- 2%) than the suppression of palmitate R(a) (52 +- 4, 68 +- 1, and 79 +- 1%). Glucose 27-34 insulin Homo sapiens 88-95 22474039-6 2012 Insulin-mediated increase in glucose disposal ranged from 24 +- 5% at low to 253 +- 19% at high physiological insulin concentrations. Glucose 29-36 insulin Homo sapiens 0-7 22474039-6 2012 Insulin-mediated increase in glucose disposal ranged from 24 +- 5% at low to 253 +- 19% at high physiological insulin concentrations. Glucose 29-36 insulin Homo sapiens 110-117 22474039-8 2012 CONCLUSIONS: Endogenous glucose production and adipose tissue lipolytic rate are both very sensitive to small increases in circulating insulin, whereas stimulation of muscle glucose uptake is minimal until high physiological plasma insulin concentrations are reached. Glucose 24-31 insulin Homo sapiens 135-142 22474039-9 2012 Hyperinsulinemia within the normal physiological range can compensate for both liver and adipose tissue insulin resistance, but not skeletal muscle insulin resistance, in obese people who have normal glucose tolerance. Glucose 200-207 insulin Homo sapiens 5-12 22650221-4 2012 Although there is a theoretical basis for the use of glucose-insulin-potassium infusion during AMI, lack of outcome efficacy (and inability to reach glycemic targets) in recent randomized trials has resulted in little enthusiasm for this strategy. Glucose 53-60 insulin Homo sapiens 61-68 22650221-5 2012 Based on the increasing understanding of the dangers of hypoglycemia, while at the same time appreciating the role of hyperglycemia in AMI patients, goal glucose levels of 140-180 mg/dL using an intravenous insulin infusion while not eating seem reasonable for most patients and hospital systems. Glucose 154-161 insulin Homo sapiens 207-214 22391949-10 2012 This kinase appears to be an interesting new mediator to be evaluated for therapeutic intervention in type 2 diabetes and related complications, as controlled increase in lipid oxidation and insulin-stimulated glucose uptake in skeletal muscle is favourable and can restore energy balance in metabolically compromised states. Glucose 210-217 insulin Homo sapiens 191-198 22236023-3 2012 In view of the impact of sexual hormones on glucose homeostasis, the molecular pathways involved in insulin resistance suggest a sex-gender specificity mechanism in the development of diabetic complications leading to the unmet need of sex-gender therapeutic approaches. Glucose 44-51 insulin Homo sapiens 100-107 22425588-3 2012 There was a negative correlation between insulin-mediated suppression of hepatic glucose production and intrahepatic diacylglycerol (r = -0.609; P = .012), but not with intrahepatic ceramide or acylcarnitine. Glucose 81-88 insulin Homo sapiens 41-48 22686416-1 2012 BACKGROUND: The provision of sufficient basal insulin to normalize fasting plasma glucose levels may reduce cardiovascular events, but such a possibility has not been formally tested. Glucose 82-89 insulin Homo sapiens 46-53 21635573-6 2012 It was concluded that dextrose and sucrose have the potential to stimulate fast and high insulin peaks, especially when combined with additional lactose. Glucose 22-30 insulin Homo sapiens 89-96 22425523-0 2012 Glucose-stimulated insulin secretion of various mesenchymal stem cells after insulin-producing cell differentiation. Glucose 0-7 insulin Homo sapiens 19-26 22425523-3 2012 Recently the generation of glucose-responsive insulin-producing cells (IPCs) from MSCs has shown immense potential for the treatment of type 1 diabetes mellitus (T1DM) due to a lack of pancreas donors. Glucose 27-34 insulin Homo sapiens 46-53 22528396-3 2012 Our data showed that the LA pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in NYGGF4 overexpression adipocytes. Glucose 80-87 insulin Homo sapiens 61-68 22438225-1 2012 CONTEXT: Fibroblast growth factor 21 (FGF-21), a potent activator of glucose uptake, has been proposed to be related to insulin resistance, metabolic syndrome (MetS), nonalcoholic fatty liver disease (NAFLD), and weight status. Glucose 69-76 insulin Homo sapiens 120-127 21740103-2 2012 Compounds 5, 11-15 (at lower concentration; 0.001 mg/ml) were able to increase insulin release in the presence of 5.6 mmol/l glucose. Glucose 125-132 insulin Homo sapiens 79-86 22798980-6 2012 Wepropose that a lifestyle that fosters increased weight gain, especially in the visceral adipose depot, promotes the development of insulin resistance which in turn exposes an underlying reduced beta-cell reserve in susceptible individuals, resulting in glucose intolerance and eventually in many the development of diabetes. Glucose 255-262 insulin Homo sapiens 133-140 22240107-4 2012 The primary outcome variable was the disposition index, computed from the acute insulin response to glucose corrected for insulin sensitivity (1/Homeostatic model assessment of insulin resistance). Glucose 100-107 insulin Homo sapiens 80-87 22495590-5 2012 The glucose infusion rate (adjusted for fat free mass and circulating insulin concentration) required to maintain blood glucose concentration at 5 mmol l-1 during administration of insulin was decreased in hypoxia compared with normoxia (225 +- 23 vs. 128 +- 30 nmol (kg fat free mass)-1 pmol l-1 min-1; P =0.03), and unchanged during normoxia and sympathetic inhibition (219 +- 19; P =0.86) and hypoxia and sympathetic inhibition (169 +- 23; P =0.23). Glucose 4-11 insulin Homo sapiens 70-77 22495590-5 2012 The glucose infusion rate (adjusted for fat free mass and circulating insulin concentration) required to maintain blood glucose concentration at 5 mmol l-1 during administration of insulin was decreased in hypoxia compared with normoxia (225 +- 23 vs. 128 +- 30 nmol (kg fat free mass)-1 pmol l-1 min-1; P =0.03), and unchanged during normoxia and sympathetic inhibition (219 +- 19; P =0.86) and hypoxia and sympathetic inhibition (169 +- 23; P =0.23). Glucose 4-11 insulin Homo sapiens 181-188 22437199-2 2012 Insulin, which regulates systemic glucose metabolism, has been recently shown both to regulate hippocampal metabolism and to be a mandatory component of hippocampally-mediated cognitive performance. Glucose 34-41 insulin Homo sapiens 0-7 22262157-7 2012 The area under the curve after glucose ingestion was ~20% lower for glucose but doubled for insulin and C-peptide at 12 months, compared with pre-surgery values (all P < 0.01). Glucose 31-38 insulin Homo sapiens 92-99 22554867-6 2012 The presence of metabolic syndrome was evaluated and quantified based on the sum of the standardized scores of the waist circumference, the triglyceride/c-HDL ratio, mean blood pressure and R-HOMA (Index of insulin resistance to glucose lowering effect). Glucose 229-236 insulin Homo sapiens 207-214 22122457-4 2012 Thiazolidinediones are PPAR-gamma agonists regulating the expression of several genes involved in the regulation of glucose, lipid and protein metabolism, enhancing the action of insulin in insulin-sensitive tissue by increasing glucose uptake in skeletal muscle and adipose tissue, and decreasing hepatic glucose production. Glucose 229-236 insulin Homo sapiens 190-197 22633150-8 2012 As no glycemic target is known, administration of insulin is required for glucose levels higher that 10 mmol/l. Glucose 74-81 insulin Homo sapiens 50-57 22122457-4 2012 Thiazolidinediones are PPAR-gamma agonists regulating the expression of several genes involved in the regulation of glucose, lipid and protein metabolism, enhancing the action of insulin in insulin-sensitive tissue by increasing glucose uptake in skeletal muscle and adipose tissue, and decreasing hepatic glucose production. Glucose 229-236 insulin Homo sapiens 179-186 22650646-1 2012 UNLABELLED: BACKGROUND: Reduction of dietary carbohydrates and corresponding insulin doses stabilizes and lowers mean blood glucose in individuals with type 1 diabetes within days. Glucose 125-132 insulin Homo sapiens 78-85 22736117-4 2012 The metabolic state of the surgical patients, anesthesia method, glucose infusion, stress-induced neuroendocrine responses and insulin resistance can affect the perioperative blood glucose levels, resulting in poor clinical outcomes. Glucose 181-188 insulin Homo sapiens 127-134 22333157-3 2012 At therapeutic concentration (0.01 muM) rapamycin reduced basal and insulin-stimulated glucose uptake by 20-30%, after short-term (15 min) or long-term (20 h) culture of subcutaneous (n=23 and n=10) and omental adipocytes (n=6 and n=7). Glucose 87-94 insulin Homo sapiens 68-75 22883195-6 2012 Fasting plasma glucose (FPG) was tested by glucose oxidase and home model insulin resistance index (HOMA-IR) calculated. Glucose 15-22 insulin Homo sapiens 74-81 22875295-2 2012 Self-monitoring of blood glucose levels can be helpful to people with diabetes in helping to maintain day-to-day control, adjusting insulin doses, detecting hypoglycaemia, assessing control during intercurrent illness and helping to provide information that can be used in the prevention of long-term complications. Glucose 25-32 insulin Homo sapiens 132-139 22617471-0 2012 Regulation of glucose transport by insulin: traffic control of GLUT4. Glucose 14-21 insulin Homo sapiens 35-42 22617471-1 2012 Despite daily fasting and feeding, plasma glucose levels are normally maintained within a narrow range owing to the hormones insulin and glucagon. Glucose 42-49 insulin Homo sapiens 125-132 22617471-2 2012 Insulin increases glucose uptake into fat and muscle cells through the regulated trafficking of vesicles that contain glucose transporter type 4 (GLUT4). Glucose 18-25 insulin Homo sapiens 0-7 22333157-7 2012 This is the first study to show that rapamycin reduces glucose uptake in human adipocytes through impaired insulin signalling and this may contribute to the development of insulin resistance associated with rapamycin therapy. Glucose 55-62 insulin Homo sapiens 107-114 22993929-11 2012 The conclusions of this theory substantiate the effectiveness of ketoacidosis treatment with offered method CONCLUSION: The offered technique for diabetic ketoacidosis treatment on the basis of the glucose solutions infusion throughout the treatment and "small" doses of insulin values pH and glucose in a safe range, even in patients with high risk of brain edema, which is confirmed by biological systems stability theory. Glucose 198-205 insulin Homo sapiens 271-278 22560217-1 2012 Lipid sensing and insulin signaling in the brain independently triggers a negative feedback system to lower glucose production and food intake. Glucose 108-115 insulin Homo sapiens 18-25 22993929-11 2012 The conclusions of this theory substantiate the effectiveness of ketoacidosis treatment with offered method CONCLUSION: The offered technique for diabetic ketoacidosis treatment on the basis of the glucose solutions infusion throughout the treatment and "small" doses of insulin values pH and glucose in a safe range, even in patients with high risk of brain edema, which is confirmed by biological systems stability theory. Glucose 293-300 insulin Homo sapiens 271-278 22488757-0 2012 Theoretical analysis of insulin-dependent glucose uptake heterogeneity in 3D bioreactor cell culture. Glucose 42-49 insulin Homo sapiens 24-31 22704848-1 2012 BACKGROUND AND AIMS: ATP-sensitive potassium (K(ATP)) channels of pancreatic beta-cells play a key role in glucose-stimulated insulin secretion mechanism. Glucose 107-114 insulin Homo sapiens 126-133 22341865-9 2012 There was a trend towards an increased microvessel density by 20% in atherosclerotic plaques derived from patients using insulin compared to plaques derived from patients using oral glucose lowering agents only (p=0.05). Glucose 182-189 insulin Homo sapiens 121-128 22488757-7 2012 The signaling model was integrated into this model, linking the local insulin concentration at cell membrane to the glucose uptake rate through glucose transporter type 4 (GLUT4) translocation from the cytosol to the cell membrane. Glucose 116-123 insulin Homo sapiens 70-77 22322917-1 2012 AIMS/HYPOTHESIS: In type 2 diabetes, reduced insulin-stimulated glucose disposal, primarily glycogen synthesis, is associated with defective insulin activation of glycogen synthase (GS) in skeletal muscle. Glucose 64-71 insulin Homo sapiens 45-52 21950636-2 2012 It potentiates the glucose-induced secretion of insulin from pancreatic beta cells, increases insulin expression, inhibits beta-cell apoptosis, promotes beta-cell neogenesis, reduces glucagon secretion, delays gastric emptying, promotes satiety and increases peripheral glucose disposal. Glucose 19-26 insulin Homo sapiens 48-55 21950636-2 2012 It potentiates the glucose-induced secretion of insulin from pancreatic beta cells, increases insulin expression, inhibits beta-cell apoptosis, promotes beta-cell neogenesis, reduces glucagon secretion, delays gastric emptying, promotes satiety and increases peripheral glucose disposal. Glucose 19-26 insulin Homo sapiens 94-101 21950636-2 2012 It potentiates the glucose-induced secretion of insulin from pancreatic beta cells, increases insulin expression, inhibits beta-cell apoptosis, promotes beta-cell neogenesis, reduces glucagon secretion, delays gastric emptying, promotes satiety and increases peripheral glucose disposal. Glucose 270-277 insulin Homo sapiens 48-55 22004512-0 2012 Effects of variations in duodenal glucose load on glycaemic, insulin, and incretin responses in type 2 diabetes. Glucose 34-41 insulin Homo sapiens 61-68 22004512-6 2012 In both groups, the stimulation of insulin and GLP-1 by increasing glucose loads was not linear; responses to G1 and G2 were minimal, whereas responses to G4 were much greater (P < 0.005 for each) (incremental area under the GLP-1 curve 224 +- 65, 756 +- 331 and 2807 +- 473 pmol/l.min, respectively, in Type 2 patients and 373 +- 231, 505 +- 161 and 1742 +- 456 pmol/l.min, respectively, in healthy controls). Glucose 67-74 insulin Homo sapiens 35-42 22391950-3 2012 Acute aerobic exercise first accelerates translocation of myocellular glucose transporters via AMP-activated protein kinase, calcium release and mitogen-activated protein kinase, but also improves insulin-dependent glucose transport/phosphorylation via distal components of insulin signalling (phosphoinositide-dependent kinase 1, TBC1 domain family, members 1 and 4, Rac1, protein kinase C). Glucose 70-77 insulin Homo sapiens 274-281 22396200-7 2012 Because adiponectin is suspected to have insulin-sensitizing proprieties, these epigenetic adaptations have the potential to induce sustained glucose metabolism changes in the mother and offspring later in life. Glucose 142-149 insulin Homo sapiens 41-48 22399695-4 2012 Insulin sensitivity was assessed directly with insulin suppression test by measuring steady-state plasma glucose (SSPG) concentration during a 240-min infusion of octreotide, glucose, and insulin. Glucose 105-112 insulin Homo sapiens 0-7 22399695-4 2012 Insulin sensitivity was assessed directly with insulin suppression test by measuring steady-state plasma glucose (SSPG) concentration during a 240-min infusion of octreotide, glucose, and insulin. Glucose 105-112 insulin Homo sapiens 47-54 22399695-4 2012 Insulin sensitivity was assessed directly with insulin suppression test by measuring steady-state plasma glucose (SSPG) concentration during a 240-min infusion of octreotide, glucose, and insulin. Glucose 175-182 insulin Homo sapiens 0-7 22403297-7 2012 Exercise enhanced insulin-stimulated leg glucose extraction both before and after bed rest, which was accompanied by higher GS activity in the prior-exercised leg than the rested leg. Glucose 41-48 insulin Homo sapiens 18-25 22403297-8 2012 The present findings demonstrate that physical inactivity-induced insulin resistance in muscle is associated with lower content/activity of key proteins in glucose transport/phosphorylation and storage. Glucose 156-163 insulin Homo sapiens 66-73 22322917-6 2012 RESULTS: During euglycaemia, insulin-stimulated glucose disposal, glucose oxidation and non-oxidative glucose metabolism were reduced in the diabetic group compared with both control groups (p < 0.05). Glucose 48-55 insulin Homo sapiens 29-36 22322917-8 2012 When studied under hyperglycaemia, all variables of insulin-stimulated glucose metabolism were normalised compared with the weight-matched controls. Glucose 71-78 insulin Homo sapiens 52-59 22068250-8 2012 CONCLUSIONS: Targeted pathophysiologic therapy based on oral glucose tolerance test-derived measures of insulin sensitivity and beta-cell function can be implemented in general internal medicine and endocrine practice and is associated with marked improvement in glucose tolerance and reversion of prediabetes to normal glucose tolerance in more than 50% of patients. Glucose 61-68 insulin Homo sapiens 104-111 22415876-3 2012 These pathways included those known to be affected by insulin such as glucose, amino acid and lipid metabolism, Krebs cycle, and immune responses and those hitherto unknown to be altered including prostaglandin, arachidonic acid, leukotrienes, neurotransmitters, nucleotides, and anti-inflammatory responses. Glucose 70-77 insulin Homo sapiens 54-61 22415876-5 2012 Although insulin treatment normalized plasma glucose and many other metabolites, there were 71 metabolites and 24 pathways that differed between nondiabetes and insulin-treated type 1 diabetes. Glucose 45-52 insulin Homo sapiens 9-16 22068250-8 2012 CONCLUSIONS: Targeted pathophysiologic therapy based on oral glucose tolerance test-derived measures of insulin sensitivity and beta-cell function can be implemented in general internal medicine and endocrine practice and is associated with marked improvement in glucose tolerance and reversion of prediabetes to normal glucose tolerance in more than 50% of patients. Glucose 263-270 insulin Homo sapiens 104-111 22068250-8 2012 CONCLUSIONS: Targeted pathophysiologic therapy based on oral glucose tolerance test-derived measures of insulin sensitivity and beta-cell function can be implemented in general internal medicine and endocrine practice and is associated with marked improvement in glucose tolerance and reversion of prediabetes to normal glucose tolerance in more than 50% of patients. Glucose 263-270 insulin Homo sapiens 104-111 22082043-1 2012 Potassium inwardly rectifying channel, subfamily-J, member 11 (KCNJ11) gene encodes Kir6.2 subunits of the adenosine triphosphate (ATP)-sensitive potassium channel involved in glucose-mediated metabolic signaling pathway and has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its function in glucose-stimulated insulin secretion. Glucose 176-183 insulin Homo sapiens 352-359 22396448-5 2012 Insulin signaling was measured by Western blotting and glucose uptake using 2-deoxy-d-[3H]glucose. Glucose 55-62 insulin Homo sapiens 0-7 22396448-8 2012 4-HNE induced a time- and dose-dependent decrease in insulin signaling and insulin-induced glucose uptake in muscle. Glucose 91-98 insulin Homo sapiens 75-82 22082043-1 2012 Potassium inwardly rectifying channel, subfamily-J, member 11 (KCNJ11) gene encodes Kir6.2 subunits of the adenosine triphosphate (ATP)-sensitive potassium channel involved in glucose-mediated metabolic signaling pathway and has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its function in glucose-stimulated insulin secretion. Glucose 333-340 insulin Homo sapiens 352-359 22440988-5 2012 On an isocaloric, 50% carbohydrate, fixed diet, the insulin to carbohydrate ratio was adjusted to achieve a 2- to 4-hour postbolus glucose value within +-20% of premeal glucose. Glucose 131-138 insulin Homo sapiens 52-59 22408172-0 2012 Insulin-stimulated glucose uptake occurs in specialized cells within the cumulus oocyte complex. Glucose 19-26 insulin Homo sapiens 0-7 22408172-4 2012 Insulin-stimulated glucose uptake is thought to be unique to adipocytes, skeletal and cardiac muscle, and the blastocyst. Glucose 19-26 insulin Homo sapiens 0-7 22408172-7 2012 We show that insulin-stimulated glucose uptake occurs in both compact and expanded cumulus cells of mice, as well as in human cumulus cells. Glucose 32-39 insulin Homo sapiens 13-20 22408172-9 2012 Insulin-stimulated glucose uptake in cumulus cells is mediated through phosphatidylinositol 3-kinase signaling as shown by inhibition of insulin-stimulated glucose uptake and Akt phosphorylation with the specific phosphatidylinositol 3-kinase inhibitor, LY294002. Glucose 19-26 insulin Homo sapiens 0-7 22408172-9 2012 Insulin-stimulated glucose uptake in cumulus cells is mediated through phosphatidylinositol 3-kinase signaling as shown by inhibition of insulin-stimulated glucose uptake and Akt phosphorylation with the specific phosphatidylinositol 3-kinase inhibitor, LY294002. Glucose 19-26 insulin Homo sapiens 137-144 22408172-9 2012 Insulin-stimulated glucose uptake in cumulus cells is mediated through phosphatidylinositol 3-kinase signaling as shown by inhibition of insulin-stimulated glucose uptake and Akt phosphorylation with the specific phosphatidylinositol 3-kinase inhibitor, LY294002. Glucose 156-163 insulin Homo sapiens 0-7 22408172-9 2012 Insulin-stimulated glucose uptake in cumulus cells is mediated through phosphatidylinositol 3-kinase signaling as shown by inhibition of insulin-stimulated glucose uptake and Akt phosphorylation with the specific phosphatidylinositol 3-kinase inhibitor, LY294002. Glucose 156-163 insulin Homo sapiens 137-144 22408172-11 2012 Both sets of cells displayed blunted insulin-stimulated glucose uptake. Glucose 56-63 insulin Homo sapiens 37-44 22408172-12 2012 Our studies identify another tissue that, through a classical insulin-signaling pathway, demonstrates insulin-stimulated glucose uptake. Glucose 121-128 insulin Homo sapiens 62-69 22408172-12 2012 Our studies identify another tissue that, through a classical insulin-signaling pathway, demonstrates insulin-stimulated glucose uptake. Glucose 121-128 insulin Homo sapiens 102-109 22440988-8 2012 Titrating insulin glargine to the morning glucose led to hypoglycemia during the rest of the day (2 PM to 4 AM). Glucose 42-49 insulin Homo sapiens 10-17 22440988-11 2012 CONCLUSIONS: Smaller insulin glargine doses to achieve control are in contrast to those much larger doses reported in clinical trials in multiple daily injection-treated type 1 diabetes in which the morning fasting glucose is the basal insulin target. Glucose 215-222 insulin Homo sapiens 236-243 22847496-0 2012 Metabolomic analysis of pancreatic beta-cell insulin release in response to glucose. Glucose 76-83 insulin Homo sapiens 45-52 22430284-5 2012 Furthermore GLP-1 was found to improve chronic heart failure by increasing insulin independent cellular glucose transport. Glucose 104-111 insulin Homo sapiens 75-82 22708029-2 2012 It acts synergistically with insulin in increasing glucose cellular uptake, stimulating glucose transfer to the muscle and adipose tissue, as well as in preventing hepatic glucose production. Glucose 51-58 insulin Homo sapiens 29-36 22708029-2 2012 It acts synergistically with insulin in increasing glucose cellular uptake, stimulating glucose transfer to the muscle and adipose tissue, as well as in preventing hepatic glucose production. Glucose 88-95 insulin Homo sapiens 29-36 22708029-2 2012 It acts synergistically with insulin in increasing glucose cellular uptake, stimulating glucose transfer to the muscle and adipose tissue, as well as in preventing hepatic glucose production. Glucose 88-95 insulin Homo sapiens 29-36 22847496-5 2012 These identified metabolites allowed us to perform a systematic analysis of key pathways involved in glucose-stimulated insulin secretion (GSIS). Glucose 101-108 insulin Homo sapiens 120-127 22442275-11 2012 Targeting near-normal glucose levels in insulin-treated patients should be reserved for those of younger age with a longer life expectancy, a shorter duration of diabetes, and little or no end-organ complications. Glucose 22-29 insulin Homo sapiens 40-47 22362823-3 2012 OBJECTIVE: We performed this study to determine muscle and liver insulin sensitivity individuals with type 1 diabetes after overnight insulin infusion to lower fasting glucose concentration. Glucose 168-175 insulin Homo sapiens 65-72 22362823-9 2012 The concentration of insulin required for 50% suppression of glucose Ra was 2-fold higher in subjects with type 1 diabetes. Glucose 61-68 insulin Homo sapiens 21-28 22521317-14 2012 CONCLUSIONS: Glucose readings are sufficient to adjust insulin therapy in a safe and effective manner, when adjustments are made on a weekly basis. Glucose 13-20 insulin Homo sapiens 55-62 22768892-3 2012 Developments in mathematical models of the beta-cell physiology of the pancreas have described the glucose-induced insulin release from pancreatic beta cells at a molecular level. Glucose 99-106 insulin Homo sapiens 115-122 22521317-0 2012 Frequent insulin dosage adjustments based on glucose readings alone are sufficient for a safe and effective therapy. Glucose 45-52 insulin Homo sapiens 9-16 22521317-3 2012 We hypothesize that glucose readings are sufficient to adjust insulin dosage provided that it is done on a weekly basis. Glucose 20-27 insulin Homo sapiens 62-69 20814956-3 2012 Insulin resistance is a major pathophysiological factor in the development of type 2 diabetes, occurring mainly in muscle, adipose tissues, and liver leading to reduced glucose uptake and utilization and increased glucose production. Glucose 169-176 insulin Homo sapiens 0-7 22834149-0 2012 [The insulin regulation of metabolism of fat acids and glucose next in the realization of biologic function of locomotion]. Glucose 55-62 insulin Homo sapiens 5-12 22834149-4 2012 To "force" the mitochondria starting to oxidize glucose first of all the insulin is to inhibit the biochemical reactions in all cells where releasing of polar non-etherified fatty acids and formation of their polar metabolites occurs. Glucose 48-55 insulin Homo sapiens 73-80 22834149-10 2012 Only second insulin effect is targeted to the glucose metabolic transformation. Glucose 46-53 insulin Homo sapiens 12-19 22160469-1 2012 Insulin resistance is a clinical condition that is characterized by reducing glucose uptake in response to insulin. Glucose 77-84 insulin Homo sapiens 0-7 22160469-1 2012 Insulin resistance is a clinical condition that is characterized by reducing glucose uptake in response to insulin. Glucose 77-84 insulin Homo sapiens 107-114 22173574-1 2012 Excessive metabolism of glucose and/or fatty acids may impair insulin signaling by increasing oxidative stress. Glucose 24-31 insulin Homo sapiens 62-69 22173574-4 2012 Insulin sensitivity was determined using an intravenous glucose tolerance test incorporating [6,6-(2)H(2)]-glucose, and a two-compartment mathematical model. Glucose 56-63 insulin Homo sapiens 0-7 21933317-5 2012 While insulin-stimulated glucose disposal was similar in AA and AW (7.5 +- 1.0 vs. 7.3 +- 0.9 mg/kg FFM/min), IS tended to be lower (2.5 +- 0.4 vs. 3.8 +- 0.6 mg/kg FFM/min per microU/mL, p = 0.081). Glucose 25-32 insulin Homo sapiens 6-13 22307937-2 2012 We show here that a dichloromethane extract of Ratanhiae radix ( RR_EX) dose-dependently inhibits human recombinant PTP1B in vitro and enhances insulin-stimulated glucose uptake in murine myocytes. Glucose 163-170 insulin Homo sapiens 144-151 22435393-8 2012 GLP-1 analogue and insulin as FDC or by co-administration, is a rational method of controlling fasting and postprandial glucose effectively. Glucose 120-127 insulin Homo sapiens 19-26 21784130-7 2012 The sustained, amplifying pathway of insulin release also depends on mitochondrial Ca(2+) signals, which likely influence the generation of glucose-derived metabolites serving as coupling factors. Glucose 140-147 insulin Homo sapiens 37-44 22108437-1 2012 Pancreatic beta-cells secrete insulin in response to fluctuations in blood fuel concentrations, in particular glucose and fatty acids. Glucose 110-117 insulin Homo sapiens 30-37 22314339-7 2012 Restoration of endogenous insulin secretion was accompanied by sustained normalization of fasting plasma glucose concentrations and HbA1c levels as well as significant improvement of total cholesterol, low-density lipoprotein-cholesterol, and blood pressure. Glucose 105-112 insulin Homo sapiens 26-33 22781771-5 2012 Insulin resistance was assessed with fasting plasma blood glucose (FPG), plasma insulin (FINS) and homeostatic model assessment of insulin resistance index (HOMA-IR). Glucose 58-65 insulin Homo sapiens 0-7 22298776-4 2012 In clinical trials, small molecule GK activators (GKAs) have been efficacious in lowering plasma glucose and enhancing glucose-stimulated insulin secretion, but they carry a risk of overly activating GK and causing hypoglycemia. Glucose 119-126 insulin Homo sapiens 138-145 22465118-7 2012 Furthermore, a fraction of the glucose-responsive nesfatin-1 neurons also responded to insulin, and vice versa. Glucose 31-38 insulin Homo sapiens 87-94 22513937-22 2012 Where data could not be combined, single studies showed lower mean fasting glucose (MD -0.40; 95% CI -0.72 to -0.08) and higher means for two-hour glucose response (MD 1.08; 95% CI 0.45 to 1.71) and insulin area under the curve (AUC) (MD 20.30; 95% CI 4.24 to 36.36).Three trials examined the etonogestrel vaginal ring and one examined an etonogestrel implant. Glucose 147-154 insulin Homo sapiens 199-206 22236133-4 2012 As a protein drug for treating diabetes, insulin is conventionally administered via subcutaneous (SC) injection, yet often fails to achieve the glucose homeostasis observed in nondiabetic subjects. Glucose 144-151 insulin Homo sapiens 41-48 22297305-7 2012 In agreement, sequoyitol increased the ability of insulin to suppress glucose production in primary hepatocytes and to stimulate glucose uptake into primary adipocytes. Glucose 70-77 insulin Homo sapiens 50-57 22374408-1 2012 BACKGROUND: Activation of free fatty acid receptor 1 (FFAR1; also known as G-protein-coupled receptor 40) by fatty acids stimulated glucose-dependent beta-cell insulin secretion in preclinical models. Glucose 132-139 insulin Homo sapiens 160-167 22395905-4 2012 The higher the concentration of glucose, the more production of insulin was noted. Glucose 32-39 insulin Homo sapiens 64-71 22808525-3 2012 During hospitalization in the ICU, continuous insulin treatment should be initiated in all patients when admission blood glucose levels are greater or equal to 180 mg/dL (10.0 mmol/L) and, in those with previously known diabetes, when preprandial glucose levels are greater or equal to 140 mg/dL (7.77 mmol/L) during follow-up. Glucose 121-128 insulin Homo sapiens 46-53 22094821-3 2012 The first phase is characterized by a transient stimulation of insulin to rapidly lower the blood glucose levels, which is followed by a second phase of insulin secretion to sustain the lowered blood glucose levels over a longer period of time. Glucose 98-105 insulin Homo sapiens 63-70 22094821-7 2012 Insulin secretion was stimulated by exposing the cells to glucose only (hepatic cells), meat hydrolysate only (GLUTag-INS), or to a cocktail of the two secretagogues. Glucose 58-65 insulin Homo sapiens 0-7 22068611-1 2012 Type-2 diabetes mellitus (T2DM) is a disorder that is characterized by high blood glucose concentration in the context of insulin resistance and/or relative insulin deficiency. Glucose 82-89 insulin Homo sapiens 122-129 22311610-4 2012 The induction of intestinal gluconeogenesis plays a major role in diminishing hunger, and in restoring insulin sensitivity of endogenous glucose production. Glucose 137-144 insulin Homo sapiens 103-110 22311610-5 2012 In parallel, the restoration of the secretion of glucagon-like peptide 1 and insulin plays a key additional role, in this context of recovered insulin sensitivity, to improve postprandial glucose tolerance. Glucose 188-195 insulin Homo sapiens 77-84 22311610-5 2012 In parallel, the restoration of the secretion of glucagon-like peptide 1 and insulin plays a key additional role, in this context of recovered insulin sensitivity, to improve postprandial glucose tolerance. Glucose 188-195 insulin Homo sapiens 143-150 22282162-9 2012 The abundance of multiple spots representing glycolytic and fast-muscle proteins correlated negatively with insulin action on glucose disposal, glucose oxidation and lipid oxidation, while several spots with proteins involved in oxidative metabolism and mitochondrial function correlated positively with these whole-body measures of insulin action. Glucose 144-151 insulin Homo sapiens 108-115 22198320-5 2012 We identified St. John"s Wort (SJW) extracts as inhibitors of adipogenesis of 3T3-L1 cells and demonstrated that these extracts also inhibited insulin-sensitive glucose uptake in mature fat cells. Glucose 161-168 insulin Homo sapiens 143-150 22198320-7 2012 We have shown that SJW also attenuates insulin-sensitive glucose uptake in human adipocytes. Glucose 57-64 insulin Homo sapiens 39-46 22198320-12 2012 Our novel studies indicate that the profound effects of SJW on adipogenesis, IRS-1 activation, and insulin-stimulated glucose uptake are not mediated by HI and/or HF. Glucose 118-125 insulin Homo sapiens 99-106 22449098-4 2012 RESULTS: Switching to insulin glargine was associated with significant reductions in levels of glycosylated haemoglobin (HbA(1c); 8.4 +- 0.6 to 7.9 +- 1.0%; p < 0.001) and fasting plasma glucose (FPG; 9.50 +- 2.10 to 6.58 +- 2.07 mmol/L; p < 0.001). Glucose 190-197 insulin Homo sapiens 22-29 22209680-3 2012 During hospitalization in the ICU, continuous insulin treatment should be initiated in all patients when admission blood glucose levels are greater or equal to 180mg/dL (10.0mmol/L) and, in those with previously known diabetes, when preprandial glucose levels are greater or equal to 140mg/dL (7.77mmol/L) during follow-up. Glucose 121-128 insulin Homo sapiens 46-53 22282161-7 2012 Insulin-stimulated glucose uptake was substantially elevated in contracting cells compared with control. Glucose 19-26 insulin Homo sapiens 0-7 22282162-9 2012 The abundance of multiple spots representing glycolytic and fast-muscle proteins correlated negatively with insulin action on glucose disposal, glucose oxidation and lipid oxidation, while several spots with proteins involved in oxidative metabolism and mitochondrial function correlated positively with these whole-body measures of insulin action. Glucose 126-133 insulin Homo sapiens 108-115 22374642-5 2012 RESULTS: Mixing the two insulins diminished the peak and overall early aspart insulin action with significantly lower maximum glucose infusion rate (GIR(max) separate 6.1 +- 0.7 mg/kg/min vs. mix 4.5 +- 0.5 mg/kg/min; P = 0.03) values and the area under curve for GIR during the first 3 h of the insulin action study (separate 757 +- 105 mg/kg vs. mix 491 +- 66 mg/kg; P = 0.04). Glucose 126-133 insulin Homo sapiens 24-31 22540046-3 2012 Diabetes, especially T2DM, causes dysregulation of various metabolic processes, which includes a defect in the insulin-mediated glucose function of adipocytes, and an impaired insulin action in the liver. Glucose 128-135 insulin Homo sapiens 111-118 23153982-4 2012 There is strong evidence that PDX-1 plays a role in activating the insulin promoter and increasing insulin levels in response to glucose. Glucose 129-136 insulin Homo sapiens 99-106 22180093-2 2012 This gene has been demonstrated to encode a functional receptor of acylation-stimulating protein (ASP), a G-protein-coupled receptor (GPCR), that has been shown to influence insulin secretion in cultured pancreatic islet cells in vitro and is a stimulator of triglyceride synthesis and glucose transport in vivo. Glucose 286-293 insulin Homo sapiens 174-181 22323472-1 2012 Glucagon-like peptide-1 (GLP-1) is an incretin hormone that enhances glucose-stimulated insulin secretion and exerts direct and indirect actions on the cardiovascular system. Glucose 69-76 insulin Homo sapiens 88-95 22355071-2 2012 However, cell-autonomous effects of ROCK1 on insulin-dependent glucose transport in adipocytes and muscle cells have not been elucidated. Glucose 63-70 insulin Homo sapiens 45-52 22355071-4 2012 Here, we show that small interfering RNA-mediated ROCK1 depletion decreased insulin-induced glucose transport in adipocytes and myoblasts, whereas adenovirus-mediated ROCK1 expression increased this in a dose-dependent manner, indicating that ROCK1 is permissive for glucose transport. Glucose 92-99 insulin Homo sapiens 76-83 22355071-6 2012 Importantly, the ED50 of insulin for adipocyte glucose transport was reduced when ROCK1 was expressed, leading to hypersensitivity to insulin. Glucose 47-54 insulin Homo sapiens 25-32 22355071-7 2012 These effects are dependent on actin cytoskeleton remodeling, because inhibitors of actin polymerization significantly decreased ROCK1"s effect to promote insulin-stimulated glucose transport. Glucose 174-181 insulin Homo sapiens 155-162 22355071-10 2012 Replacing IRS-1 serine 632/635 with alanine reduced insulin-stimulated phosphatidylinositol 3-kinase activation and glucose transport in 3T3-L1 adipocytes, indicating that phosphorylation of these serine residues of IRS-1, which are substrates of the ROCK2 isoform in vitro, are crucial for maximal stimulation of glucose transport by insulin. Glucose 116-123 insulin Homo sapiens 52-59 22355071-10 2012 Replacing IRS-1 serine 632/635 with alanine reduced insulin-stimulated phosphatidylinositol 3-kinase activation and glucose transport in 3T3-L1 adipocytes, indicating that phosphorylation of these serine residues of IRS-1, which are substrates of the ROCK2 isoform in vitro, are crucial for maximal stimulation of glucose transport by insulin. Glucose 314-321 insulin Homo sapiens 52-59 22355071-11 2012 Our studies identify ROCK1 as an important positive regulator of insulin action on glucose transport in adipocytes and muscle cells. Glucose 83-90 insulin Homo sapiens 65-72 22386248-3 2012 The rapid improvement of glucose levels within days after the surgery, in relation to change of meal pattern, rapid nutrient transit, enhanced incretin release and improved incretin effect on insulin secretion, suggest mechanisms independent of weight loss. Glucose 25-32 insulin Homo sapiens 192-199 22440045-1 2012 BACKGROUND: Hypoglycemia limits the efficacy of intensive insulin therapy, especially in patients with great glucose variability. Glucose 109-116 insulin Homo sapiens 58-65 22342592-8 2012 Other correlates were ethnicity, a low insulin-to-glucose response at 60 min, and gestational age. Glucose 50-57 insulin Homo sapiens 39-46 22615077-6 2012 The use of intravenous insulin via computerized or manual standardized protocols in critically ill patients has been shown to be effective in achieving glucose control; we focus on the barriers to the appropriate use of subcutaneous insulin in hospitalized patients with noncritical illness. Glucose 152-159 insulin Homo sapiens 23-30 22234281-9 2012 Insulin sensitivity indices were calculated from the measured glucose and insulin levels. Glucose 62-69 insulin Homo sapiens 0-7 22156222-6 2012 Importantly, this environment preserved beta-cell physiological function, as measured by glucose-stimulated insulin secretion. Glucose 89-96 insulin Homo sapiens 108-115 21543663-5 2012 The SGLT2 inhibitors increase urinary excretion of glucose and lower plasma glucose levels in an insulin-independent manner. Glucose 76-83 insulin Homo sapiens 97-104 22225552-8 2012 A statistically significant intergroup gradient from normal glucose tolerance to prediabetes and from prediabetes to diabetes mellitus was observed for waist circumference, triglycerides, fasting insulin levels, and frequency of metabolic syndrome (P = .02 to P < .0001). Glucose 60-67 insulin Homo sapiens 196-203 22319034-6 2012 CONCLUSIONS: These data show that impairment of the insulinotropic effect of both GIP and GLP-1 can be induced in healthy male subjects without risk factors for type 2 diabetes, indicating that the reduced insulinotropic effect of the incretin hormones observed in type 2 diabetes most likely is a consequence of insulin resistance and glucose intolerance rather than a primary event causing the disease. Glucose 336-343 insulin Homo sapiens 52-59 22000585-1 2012 Insulin is often infused based upon total body weight (TBW) or fat-free mass (FFM) for glucose clamp protocols. Glucose 87-94 insulin Homo sapiens 0-7 22536561-5 2012 TNF-alpha and IL-6 levels were also correlated with fasting plasma glucose of obese and nonobese diabetic patients after insulin therapy. Glucose 67-74 insulin Homo sapiens 121-128 22161170-8 2012 RESULTS: Five patients developed asymptomatic hypoglycaemia during the test (glucose level <50 mg/dl) with inappropriately high insulin levels and exaggerated GLP-1 response. Glucose 77-84 insulin Homo sapiens 131-138 21984197-1 2012 Both insulin resistance and estrogen deficiency result in complex metabolic disorder based mainly on defective cellular glucose uptake and on an atherogenic serum lipid profile. Glucose 120-127 insulin Homo sapiens 5-12 22203325-3 2012 RESULTS: PGC-formulations of native human insulin are able to control blood glucose to the same extent and for the same amount of time after s.c. injection as the insulin analogue insulin glargine. Glucose 76-83 insulin Homo sapiens 42-49 23077965-7 2012 The incretins (GLP-1--glucagon-like-peptide-1 and GIP--glucose-dependent insulin tropic peptide), are natural hormones that contribute to glucose homeostasis by acting on the pancreas, gastrointestinal tract, muscle and brain tissue. Glucose 55-62 insulin Homo sapiens 73-80 22649855-1 2012 Continuous glucose monitoring is a major element of the metabolic assessment of the diabetic patient, treated or not by insulin. Glucose 11-18 insulin Homo sapiens 120-127 20814956-3 2012 Insulin resistance is a major pathophysiological factor in the development of type 2 diabetes, occurring mainly in muscle, adipose tissues, and liver leading to reduced glucose uptake and utilization and increased glucose production. Glucose 214-221 insulin Homo sapiens 0-7 22071009-1 2012 Intravenous glucose tolerance tests have demonstrated lower whole-body insulin sensitivity (S(I)) among African Americans (AA) compared with European Americans (EA). Glucose 12-19 insulin Homo sapiens 71-78 22071009-2 2012 Whole-body S(I) represents both insulin-stimulated glucose disposal, primarily by skeletal muscle, and insulin"s suppression of endogenous glucose production (EGP) by liver. Glucose 51-58 insulin Homo sapiens 32-39 22781951-5 2012 Hyperinsulinemia was diagnosed with fasting serum insulin >= 15 mU/L and/or 2-hour serum insulin >= 80 mU/L after glucose loading. Glucose 120-127 insulin Homo sapiens 5-12 22364841-2 2012 METHODS: Injury leads to cellular reaction characterized by insulin resistance during which glucose cannot enter muscle and fat cells. Glucose 92-99 insulin Homo sapiens 60-67 22300409-11 2012 Therefore a rapid decrease in glucose level seems to enhance ROS toxicity, perhaps contributing to neural damage when insulin levels given to diabetic patients are not properly calibrated and plasma glucose levels are not adequately maintained. Glucose 30-37 insulin Homo sapiens 118-125 22355097-2 2012 Metformin, effective in treating type 2 diabetes and the insulin resistance syndromes, improves insulin resistance by reducing hepatic gluconeogenesis and by enhancing glucose uptake by skeletal muscle. Glucose 168-175 insulin Homo sapiens 96-103 22436702-9 2012 RESULTS: Our data show that insulin, metformin, BLX-1002, and rosuvastatin improved HCAEC viability and they could also significantly increase cell proliferation in low glucose. Glucose 169-176 insulin Homo sapiens 28-35 22436702-10 2012 The proliferative effect of insulin and BLX-1002 was also evident at 11 mM of glucose. Glucose 78-85 insulin Homo sapiens 28-35 22252939-10 2012 In addition, the glucose-induced fall in pulsatile LH secretion was exacerbated by higher fasting insulin concentrations (P = 0.054) and attenuated by higher adiponectin levels (P = 0.0037). Glucose 17-24 insulin Homo sapiens 98-105 22178787-5 2012 Glucose-stimulated TNFalpha release from MNC along with molecular markers of inflammation are associated with insulin resistance in PCOS. Glucose 0-7 insulin Homo sapiens 110-117 25745436-5 2012 These cells had glucose-stimulated secretion of human insulin and C-peptide. Glucose 16-23 insulin Homo sapiens 54-61 25745436-5 2012 These cells had glucose-stimulated secretion of human insulin and C-peptide. Glucose 16-23 insulin Homo sapiens 66-75 22370612-6 2012 After insulin tolerance testing (ITT), a significant decline was noted in glucose in both groups. Glucose 74-81 insulin Homo sapiens 6-13 22584561-1 2012 Hypoglycemia due to endogenous hyperinsulinism (EH) is diagnosed in a symptomatic patient with low levels of plasma glucose concomitant with elevated plasma insulin and C-peptide. Glucose 116-123 insulin Homo sapiens 36-43 22100871-8 2012 Applying the identifiability analysis to the trajectories of the insulin glucose system during an intravenous glucose tolerance test (IVGTT) shows the following result: (1) if only plasma glucose G(t) is measured, plasma insulin I(t) and S(G) can be estimated, but not S(I). Glucose 73-80 insulin Homo sapiens 65-72 22311976-1 2012 ATP-sensitive potassium (K(ATP)) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2 regulate insulin secretion by linking glucose metabolism with membrane potential. Glucose 134-141 insulin Homo sapiens 105-112 22311976-11 2012 The results suggest that physiological or pathological changes in Derlin-1 expression levels may affect glucose-stimulated insulin secretion by altering surface expression of K(ATP) channels. Glucose 104-111 insulin Homo sapiens 123-130 22344561-7 2012 In both experiments, intranasal insulin induced a slight decrease in plasma glucose but did not affect serum insulin concentrations. Glucose 76-83 insulin Homo sapiens 32-39 22357182-0 2012 Insulin sensitivity, beta-cell function, and incretin effect in individuals with elevated 1-hour postload plasma glucose levels. Glucose 113-120 insulin Homo sapiens 0-7 22357182-4 2012 Insulin secretion was assessed using both indexes derived from oral glucose tolerance test (OGTT) and intravenous glucose tolerance test (IVGTT). Glucose 68-75 insulin Homo sapiens 0-7 22357182-4 2012 Insulin secretion was assessed using both indexes derived from oral glucose tolerance test (OGTT) and intravenous glucose tolerance test (IVGTT). Glucose 114-121 insulin Homo sapiens 0-7 22357182-10 2012 CONCLUSIONS: NGT 1h-high individuals may represent an intermediate state of glucose intolerance between NGT and type 2 diabetes characterized by insulin resistance and reduced beta-cell function, the two main pathophysiological defects responsible for the development of type 2 diabetes. Glucose 76-83 insulin Homo sapiens 145-152 22100871-8 2012 Applying the identifiability analysis to the trajectories of the insulin glucose system during an intravenous glucose tolerance test (IVGTT) shows the following result: (1) if only plasma glucose G(t) is measured, plasma insulin I(t) and S(G) can be estimated, but not S(I). Glucose 110-117 insulin Homo sapiens 65-72 22442825-6 2012 Increased plasma glucose stimulated secretion of insulin which stimulated utilization of glucose. Glucose 17-24 insulin Homo sapiens 49-56 22442825-6 2012 Increased plasma glucose stimulated secretion of insulin which stimulated utilization of glucose. Glucose 89-96 insulin Homo sapiens 49-56 22100871-11 2012 Then, parameters of the insulin subsystem can be identified approximately from measurement of plasma glucose G(t) only. Glucose 101-108 insulin Homo sapiens 24-31 22803146-4 2012 Intensive glucose-induced generation of reactive oxygen species in these patients was associated with a decrease of cholesterolemia, of the C-peptide/insulin proportion, and a trend to higher urinary excretion of 4-hydroxyestrone, one of the most genotoxic catecholestrogens. Glucose 10-17 insulin Homo sapiens 150-157 22296781-5 2012 The objective of this study was to determine whether insulin-mediated glucose lowering reduces in-stent restenosis in patients with diabetes undergoing PCIs. Glucose 70-77 insulin Homo sapiens 53-60 22339447-26 2012 Vildagliptin increases the insulin levels following an OGTT and an intravenous glucose tolerance test (IVGTT), and the stimulation of insulin secretion is glucose dependent. Glucose 79-86 insulin Homo sapiens 27-34 21711376-5 2012 MEASUREMENTS: Insulin resistance was measured by glucose infusion rate on euglycaemic hyperinsulinaemic clamp, and fitness was assessed by VO(2max) . Glucose 51-58 insulin Homo sapiens 16-23 21767287-6 2012 The risk-conferring rs2237897 C alleles in the KCNQ1 gene were associated with higher fasting glucose (P = 0 009), lower HOMA-beta (P = 0 03), and lower first-phase insulin response in OGTT (P = 0 03). Glucose 94-101 insulin Homo sapiens 165-172 22051059-3 2012 We hypothesized that the angiotensin receptor antagonist losartan would improve insulin-mediated vasodilation, and thereby improve insulin-stimulated glucose uptake in skeletal muscle of insulin-resistant subjects. Glucose 150-157 insulin Homo sapiens 131-138 22229253-10 2012 Insulin resistance in the beta cell arises from defects in phosphorylation/activation of insulin receptor substrates (IRS) proteins, which result in impairment in glucose sensing, glucose stimulated insulin secretion, and also in increased loss of beta cells. Glucose 163-170 insulin Homo sapiens 0-7 22229253-10 2012 Insulin resistance in the beta cell arises from defects in phosphorylation/activation of insulin receptor substrates (IRS) proteins, which result in impairment in glucose sensing, glucose stimulated insulin secretion, and also in increased loss of beta cells. Glucose 163-170 insulin Homo sapiens 89-96 22229253-10 2012 Insulin resistance in the beta cell arises from defects in phosphorylation/activation of insulin receptor substrates (IRS) proteins, which result in impairment in glucose sensing, glucose stimulated insulin secretion, and also in increased loss of beta cells. Glucose 180-187 insulin Homo sapiens 0-7 22229253-10 2012 Insulin resistance in the beta cell arises from defects in phosphorylation/activation of insulin receptor substrates (IRS) proteins, which result in impairment in glucose sensing, glucose stimulated insulin secretion, and also in increased loss of beta cells. Glucose 180-187 insulin Homo sapiens 89-96 22301128-4 2012 RESEARCH DESIGN AND METHODS: Insulin sensitivity was calculated from fasting serum insulin and plasma glucose determinations using the homeostasis model assessment of insulin resistance (HOMA-IR) method. Glucose 102-109 insulin Homo sapiens 29-36 22167125-2 2012 METHODS: To characterise the abundance and regulation of key proteins involved in glucose-regulated insulin secretion in human islets, we examined the expression of MAFA, MAFB, GLUT2 (also known as SLC2A2), betaGK (also known as GCK) and PDX1 in isolated, highly purified human islets with an intact insulin secretory pattern. Glucose 82-89 insulin Homo sapiens 100-107 22167125-4 2012 RESULTS: Compared with mouse islets, human islets secreted more insulin at baseline glucose (5.6 mmol/l), but less upon stimulation with high glucose (16.7 mmol/l) or high glucose plus 3-isobutyl-1-methyl-xanthine. Glucose 84-91 insulin Homo sapiens 64-71 22167125-9 2012 CONCLUSIONS/INTERPRETATION: Our results suggest that human islets have a distinctive distribution and function of key regulators of the glucose-stimulated insulin secretion pathway, emphasising the urgent need to understand the processes that regulate human islet beta cell function. Glucose 136-143 insulin Homo sapiens 155-162 22051059-3 2012 We hypothesized that the angiotensin receptor antagonist losartan would improve insulin-mediated vasodilation, and thereby improve insulin-stimulated glucose uptake in skeletal muscle of insulin-resistant subjects. Glucose 150-157 insulin Homo sapiens 131-138 22173627-1 2012 AIMS/HYPOTHESIS: Insulin resistance is characterised by impaired glucose utilisation when measured by a euglycaemic-hyperinsulinaemic clamp. Glucose 65-72 insulin Homo sapiens 17-24 22315307-7 2012 In SkMCs, Hsp60 activated ERK1/2, JNK, and NF-kappaB and inhibits insulin signaling and insulin-stimulated glucose uptake. Glucose 107-114 insulin Homo sapiens 88-95 22051059-6 2012 Before and after treatment, under hyperinsulinaemic euglycaemic clamp conditions we measured whole-body insulin-stimulated glucose disposal, insulin-mediated vasodilation, and insulin-stimulated leg glucose uptake by the limb balance technique. Glucose 123-130 insulin Homo sapiens 104-111 22173627-8 2012 Resting metabolic rate was similar in the two groups before (p = 0.29) and after (p = 0.33-0.99 over time) glucose ingestion, whereas a trend for blunted glucose-induced thermogenesis was observed in insulin-resistant vs insulin-sensitive individuals (p = 0.06). Glucose 154-161 insulin Homo sapiens 200-207 22315319-5 2012 Adenoviral miR-33a overexpression in human or mouse islets reduced ABCA1 expression, decreased glucose-stimulated insulin secretion, and increased cholesterol levels. Glucose 95-102 insulin Homo sapiens 114-121 22051059-6 2012 Before and after treatment, under hyperinsulinaemic euglycaemic clamp conditions we measured whole-body insulin-stimulated glucose disposal, insulin-mediated vasodilation, and insulin-stimulated leg glucose uptake by the limb balance technique. Glucose 123-130 insulin Homo sapiens 104-111 22315322-4 2012 Insulin sensitivity decreased significantly across 2-h glucose NGT categories, while the highest NGT category and IGT group were similar. Glucose 55-62 insulin Homo sapiens 0-7 22173627-8 2012 Resting metabolic rate was similar in the two groups before (p = 0.29) and after (p = 0.33-0.99 over time) glucose ingestion, whereas a trend for blunted glucose-induced thermogenesis was observed in insulin-resistant vs insulin-sensitive individuals (p = 0.06). Glucose 154-161 insulin Homo sapiens 221-228 22051059-7 2012 RESULTS: Whole-body insulin-stimulated glucose disposal was not significantly increased by losartan. Glucose 39-46 insulin Homo sapiens 20-27 22173627-9 2012 However, over the 4 h after the 75 g glucose ingestion, glycolytic glucose disposal was the same in insulin-sensitive and insulin-resistant individuals (36.5 +- 3.7 and 36.2 +- 6.4 mmol, respectively; p = 0.99). Glucose 37-44 insulin Homo sapiens 100-107 22575405-1 2012 An input-output schematization of plasma glucose homeostasis provides quantitative information on glucose fluxes and their control by insulin. Glucose 41-48 insulin Homo sapiens 134-141 22166985-2 2012 Normally, a decrease in the plasma glucose concentration causes a decrease in beta-cell insulin secretion that signals an increase in alpha-cell glucagon secretion during hypoglycemia. Glucose 35-42 insulin Homo sapiens 88-95 22166985-3 2012 In contrast, an increase in the plasma glucose concentration, among other stimuli, causes an increase in beta-cell insulin secretion that signals a decrease, or at least no change, in alpha-cell glucagon secretion after a meal. Glucose 39-46 insulin Homo sapiens 115-122 22316089-2 2012 SUBJECTS AND METHODS: In this randomized crossover study, subjects used a sensor-augmented insulin pump system with a low glucose suspend (LGS) feature that automatically stops insulin delivery for 2 h following a sensor glucose (SG) value <=70 mg/dL. Glucose 221-228 insulin Homo sapiens 91-98 22354931-0 2012 Hypothalamic regulation of glucose-stimulated insulin secretion. Glucose 27-34 insulin Homo sapiens 46-53 22575405-2 2012 Insulin action is dependent on the target tissue, the route of delivery, and the kinetics of insulin activation and deactivation, which are different for glucose production and disposal and are a function of insulin resistance. Glucose 154-161 insulin Homo sapiens 0-7 22226490-6 2012 The insulin resistance index was calculated from the glucose and insulin concentrations obtained by oral glucose tolerance tests. Glucose 53-60 insulin Homo sapiens 4-11 22226490-6 2012 The insulin resistance index was calculated from the glucose and insulin concentrations obtained by oral glucose tolerance tests. Glucose 105-112 insulin Homo sapiens 4-11 22575405-2 2012 Insulin action is dependent on the target tissue, the route of delivery, and the kinetics of insulin activation and deactivation, which are different for glucose production and disposal and are a function of insulin resistance. Glucose 154-161 insulin Homo sapiens 93-100 22008406-2 2012 We designed an intravenous insulin protocol aiming at rapid and strict glucose control in hyperglycemic ischaemic stroke patients. Glucose 71-78 insulin Homo sapiens 27-34 22575405-3 2012 Under normal conditions, the closed-loop control of minute-by-minute insulin release by arterial glucose levels protects against both hyperglycemia and hypoglycemia. Glucose 97-104 insulin Homo sapiens 69-76 22575410-3 2012 Many studies show that glucose control is achievable with insulin safely in most patients with type 2 diabetes. Glucose 23-30 insulin Homo sapiens 58-65 22292451-4 2012 In vitro studies indicate that GPR119 agonists increase intracellular cAMP levels leading to enhanced glucose-induced insulin release and enhanced incretin hormone glucagon-like peptide 1 (GLP-1) secretion. Glucose 102-109 insulin Homo sapiens 118-125 22170727-2 2012 OBJECTIVE: Our objective was to test whether rimonabant improves insulin regulation of free fatty acid and glucose metabolism after controlling for fat loss. Glucose 107-114 insulin Homo sapiens 65-72 22627736-1 2012 Glucose is a metabolic regulator of insulin secretion from pancreatic beta-cells, which is regulated by intracellular Ca(2+) signaling. Glucose 0-7 insulin Homo sapiens 36-43 22627736-3 2012 Although F-actin remodeling is known to be an important step in glucose stimulated insulin secretion, the role of actin cytoskeleton in regulating Ca(2+) signaling in pancreatic beta-cells remain to be solved. Glucose 64-71 insulin Homo sapiens 83-90 22701849-0 2012 Ex vivo generation of glucose sensitive insulin secreting mesenchymal stem cells derived from human adipose tissue. Glucose 22-29 insulin Homo sapiens 40-47 22701849-2 2012 We present a prospective study of glucose-sensitive insulin-secreting mesenchymal stem cells (IS-MSC) generated from human adipose tissue (h-AD) sans xenogenic material. Glucose 34-41 insulin Homo sapiens 52-59 22701849-8 2012 In vitro glucose sensitivity assay was carried out by measuring levels of insulin and C-peptide secretion in absence of glucose followed by 2 hours incubation after glucose addition. Glucose 9-16 insulin Homo sapiens 74-81 22701849-13 2012 CONCLUSION: Insulin-secreting h-AD-MSC can be generated safely and effectively showing in vitro glucose responsive alteration in insulin and C-peptide secretion levels. Glucose 96-103 insulin Homo sapiens 12-19 22701849-13 2012 CONCLUSION: Insulin-secreting h-AD-MSC can be generated safely and effectively showing in vitro glucose responsive alteration in insulin and C-peptide secretion levels. Glucose 96-103 insulin Homo sapiens 129-136 22170727-7 2012 Insulin sensitivity was assessed as insulin concentration needed to suppress by 50% palmitate concentration [IC50(palmitate)], flux [IC50(palmitate)f], and hepatic glucose output [IC50(HGO)] and as insulin-stimulated glucose disposal (Delta glucose disappearance per Delta insulin concentration--glucose slope). Glucose 164-171 insulin Homo sapiens 0-7 22170727-7 2012 Insulin sensitivity was assessed as insulin concentration needed to suppress by 50% palmitate concentration [IC50(palmitate)], flux [IC50(palmitate)f], and hepatic glucose output [IC50(HGO)] and as insulin-stimulated glucose disposal (Delta glucose disappearance per Delta insulin concentration--glucose slope). Glucose 217-224 insulin Homo sapiens 0-7 22170727-7 2012 Insulin sensitivity was assessed as insulin concentration needed to suppress by 50% palmitate concentration [IC50(palmitate)], flux [IC50(palmitate)f], and hepatic glucose output [IC50(HGO)] and as insulin-stimulated glucose disposal (Delta glucose disappearance per Delta insulin concentration--glucose slope). Glucose 217-224 insulin Homo sapiens 0-7 22170727-11 2012 CONCLUSIONS: Improvements observed in insulin regulation of free fatty acid and glucose metabolism with rimonabant treatment in humans was not greater than that predicted by weight loss alone. Glucose 80-87 insulin Homo sapiens 38-45 22074132-1 2012 BACKGROUND: Glucose homeostasis relies on insulin to suppress hepatic glucose production and to stimulate glucose uptake by peripheral tissues (primarily skeletal muscle) during and after a meal or glucose load. Glucose 70-77 insulin Homo sapiens 42-49 22074132-1 2012 BACKGROUND: Glucose homeostasis relies on insulin to suppress hepatic glucose production and to stimulate glucose uptake by peripheral tissues (primarily skeletal muscle) during and after a meal or glucose load. Glucose 106-113 insulin Homo sapiens 42-49 22074132-1 2012 BACKGROUND: Glucose homeostasis relies on insulin to suppress hepatic glucose production and to stimulate glucose uptake by peripheral tissues (primarily skeletal muscle) during and after a meal or glucose load. Glucose 106-113 insulin Homo sapiens 42-49 21872284-7 2012 The insulin response to an oral glucose tolerance test was a significant predictor of fasting plasma IGFBP-1 concentrations at baseline and after exercise training (P = .02). Glucose 32-39 insulin Homo sapiens 4-11 22538145-0 2012 Commentary on "Performance of a glucose meter with a built-in automated bolus calculator versus manual bolus calculation in insulin-using subjects". Glucose 32-39 insulin Homo sapiens 124-131 22730862-0 2012 Timely bolus insulin for glucose control during cardiopulmonary bypass. Glucose 25-32 insulin Homo sapiens 13-20 22730862-9 2012 The timely bolus insulin method is more efficacious, but equally safe, in preventing hyperglycemia during CPB with glucose containing cardioplegia, compared with conventional (not standardized) insulin treatment in historical case-matched controls. Glucose 115-122 insulin Homo sapiens 17-24 21674205-1 2012 Insulin is a hormone that regulates the physiological glucose level in human blood. Glucose 54-61 insulin Homo sapiens 0-7 21674205-16 2012 The information obtained by identifying the parts of insulin molecules that are crucial to aggregate formation and stability can be used to design new analogs that can better control the blood glucose level. Glucose 193-200 insulin Homo sapiens 53-60 22199166-3 2012 Finally, this review deals with the signalling relaying the well-described increased sensitivity of glucose transport to insulin in the post-exercise period which can result in an overshoot of intramuscular glycogen resynthesis post exercise (glycogen supercompensation). Glucose 100-107 insulin Homo sapiens 121-128 22262463-1 2012 Glucose transporter isoform 4 (GLUT4), is the sole glucose transporter responsible for the effect of insulin on postprandial blood glucose clearance. Glucose 51-58 insulin Homo sapiens 101-108 22371083-1 2012 Insulin-expressing cells that have been differentiated from human pluripotent stem cells in vitro lack the glucose responsiveness characteristic of mature beta cells. Glucose 107-114 insulin Homo sapiens 0-7 22392952-0 2012 Adipocyte maturation arrest: a determinant of systemic insulin resistance to glucose disposal. Glucose 77-84 insulin Homo sapiens 55-62 22060105-0 2012 Slow-release insulin in cystic fibrosis patients with glucose intolerance: a randomized clinical trial. Glucose 54-61 insulin Homo sapiens 13-20 22315413-0 2012 Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion. Glucose 87-94 insulin Homo sapiens 106-113 21345499-6 2012 In the early phase of ST elevation myocardial infarction (STEMI), the acute glucose response to stress comprises not only hyperglycemia but also insulin-resistance (assessed by the Homeostatic Model Assessment). Glucose 76-83 insulin Homo sapiens 145-152 21345499-7 2012 Recently it has been documented in 346 STEMI patients submitted to mechanical revascularization that the acute glucose response to myocardial injury differs in respect to age, since older patients showed the highest glucose levels and the poorest glycemic control during ICCU stay in the lack of differences in insulin resistance incidence. Glucose 111-118 insulin Homo sapiens 311-318 22315413-1 2012 Postprandial insulin release is regulated by glucose, but other circulating nutrients may target beta cells and potentiate glucose-stimulated insulin secretion via distinct signaling pathways. Glucose 45-52 insulin Homo sapiens 13-20 22315413-1 2012 Postprandial insulin release is regulated by glucose, but other circulating nutrients may target beta cells and potentiate glucose-stimulated insulin secretion via distinct signaling pathways. Glucose 123-130 insulin Homo sapiens 13-20 22315413-1 2012 Postprandial insulin release is regulated by glucose, but other circulating nutrients may target beta cells and potentiate glucose-stimulated insulin secretion via distinct signaling pathways. Glucose 123-130 insulin Homo sapiens 142-149 22315413-2 2012 We demonstrate that fructose activates sweet taste receptors (TRs) on beta cells and synergizes with glucose to amplify insulin release in human and mouse islets. Glucose 101-108 insulin Homo sapiens 120-127 22315413-3 2012 Genetic ablation of the sweet TR protein T1R2 obliterates fructose-induced insulin release and its potentiating effects on glucose-stimulated insulin secretion in vitro and in vivo. Glucose 123-130 insulin Homo sapiens 142-149 22330739-5 2012 Whereas activation of ERalpha enhances glucose-stimulated insulin biosynthesis, reduces islet toxic lipid accumulation and promotes beta-cell survival from proapoptotic stimuli, activation of ERbeta increases glucose-stimulated insulin secretion. Glucose 39-46 insulin Homo sapiens 58-65 22330739-6 2012 However, activation of GPER protects beta cells from apoptosis, raises glucose-stimulated insulin secretion and lipid homeostasis without affecting insulin biosynthesis. Glucose 71-78 insulin Homo sapiens 90-97 22261942-12 2012 On hospital day 5, the patient"s triglyceride concentration decreased to 717 mg/dL; the insulin-dextrose infusion was discontinued. Glucose 96-104 insulin Homo sapiens 88-95 22281494-2 2012 Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes. Glucose 135-142 insulin Homo sapiens 80-87 22281494-7 2012 Moreover, S6K1 RNAi-mediated knockdown preserved insulin-stimulated Akt phosphorylation and glucose uptake in ER-stressed L6 myotubes, which was blocked by the phosphatidylinositol 3-kinase inhibitor wortmannin. Glucose 92-99 insulin Homo sapiens 49-56 21347608-4 2012 Insulin-stimulated glucose disposal (Rd) and substrate oxidation were assessed by euglycemic hyperinsulinemic clamps combined with indirect calorimetry. Glucose 19-26 insulin Homo sapiens 0-7 22296999-2 2012 Used in combination with glucose it can increase the insulin response and the post exercise re-synthesis of glycogen in man. Glucose 25-32 insulin Homo sapiens 53-60 22237064-0 2012 Weight-loss diets modify glucose-dependent insulinotropic polypeptide receptor rs2287019 genotype effects on changes in body weight, fasting glucose, and insulin resistance: the Preventing Overweight Using Novel Dietary Strategies trial. Glucose 25-32 insulin Homo sapiens 43-50 21816244-11 2012 Insulin suppresses activity of osteoblastic FoxO1 thus promoting beneficial effects of osteoblasts on glucose metabolism. Glucose 102-109 insulin Homo sapiens 0-7 22146232-2 2012 As insulin regulates glucose uptake and its disturbance/insensitivity is associated with diabetes mellitus, we aimed to determine the effect of insulin deprivation in human Sertoli cell (hSC) metabolism and metabolism-associated gene expression. Glucose 21-28 insulin Homo sapiens 3-10 22146232-9 2012 Insulin-deprived hSCs presented: 1) altered glucose consumption and lactate secretion; 2) altered expression of metabolism-associated genes involved in lactate production and export; 3) an adaptation of glucose uptake by modulating the expression of GLUT1 and GLUT3. Glucose 44-51 insulin Homo sapiens 0-7 22260657-7 2012 Increased blood glucose levels after food intake result in the secretion of insulin from pancreatic beta-cells. Glucose 16-23 insulin Homo sapiens 76-83 22157398-5 2012 The novel synthesis of selective, high-affinity BRS-3 agonists and antagonists has recently been accomplished and showed that BRS-3 regulates energy balance independent of other established pathways and glucose-stimulated insulin secretion in the pancreatic islet cells. Glucose 203-210 insulin Homo sapiens 222-229 21816244-5 2012 Hepatic glucose production is promoted and lipid metabolism is regulated by FoxO1 such that under insulin resistance they lead to hyperglycemia and dyslipidemia, two features of type 2 diabetes. Glucose 8-15 insulin Homo sapiens 98-105 21771385-2 2012 Tight glucose control with insulin therapy has been shown to improve outcomes, but is not common practice for children following cardiopulmonary bypass. Glucose 6-13 insulin Homo sapiens 27-34 21974813-2 2012 Aim of this study was to analyse the association of circulating insulin with nutritional status and lung function in CF patients with normal glucose tolerance (NGT). Glucose 141-148 insulin Homo sapiens 64-71 21781150-3 2012 METHODS: On day 4, a depot of insulin was excised from the patient"s abdominal wall; this was followed by a reduction in his glucose requirements and improvement in liver function. Glucose 125-132 insulin Homo sapiens 30-37 22275085-0 2012 Insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans. Glucose 24-31 insulin Homo sapiens 0-7 22210318-1 2012 As patients decline from health to type 2 diabetes, glucose-stimulated insulin secretion (GSIS) typically becomes impaired. Glucose 52-59 insulin Homo sapiens 71-78 22275085-0 2012 Insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans. Glucose 24-31 insulin Homo sapiens 43-50 22275085-0 2012 Insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans. Glucose 24-31 insulin Homo sapiens 76-83 22275085-2 2012 We hypothesized that insulin"s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. Glucose 52-59 insulin Homo sapiens 21-28 22275085-2 2012 We hypothesized that insulin"s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. Glucose 52-59 insulin Homo sapiens 71-78 21951345-0 2012 Association of beta-cell function and insulin sensitivity with fasting and 2-h plasma glucose in a large Chinese population. Glucose 86-93 insulin Homo sapiens 38-45 21951345-1 2012 AIM: Our aim was to provide a quantitative analysis of the changes in the principal determinants of insulin sensitivity and secretion in relation to fasting plasma glucose (FPG) or 2-h plasma glucose (2h PG) in a Chinese population with a wide range of glucose tolerance. Glucose 164-171 insulin Homo sapiens 100-107 22275085-2 2012 We hypothesized that insulin"s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. Glucose 52-59 insulin Homo sapiens 71-78 22275085-4 2012 The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or an isoglycemic-hyperinsulinemic clamp using B28-Asp-insulin (which can be distinguished immunologically from endogenous insulin) that raised insulin concentrations to high physiologic concentrations. Glucose 69-77 insulin Homo sapiens 4-11 22275085-7 2012 Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. Glucose 20-27 insulin Homo sapiens 0-7 21992270-11 2012 CONCLUSIONS: The ANN appears to be more appropriate for the prediction of glucose profile based on glucose and insulin data. Glucose 74-81 insulin Homo sapiens 111-118 22275085-7 2012 Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. Glucose 20-27 insulin Homo sapiens 39-46 22075915-8 2012 This translated into defective glucose-stimulated insulin secretion but, intriguingly, appropriate glucagon responses. Glucose 31-38 insulin Homo sapiens 50-57 22275085-7 2012 Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. Glucose 20-27 insulin Homo sapiens 60-67 22095234-5 2012 RESULTS: Insulin treatment normalised blood glucose concentrations, improved oral glucose tolerance, preserved insulin sensitivity and inhibited oxidative stress of Munich Ins2(C95S) mutant mice. Glucose 44-51 insulin Homo sapiens 9-16 22080230-11 2012 Early prandial insulin dosing may help to accelerate glucose disposal and potentially ameliorate postprandial hyperglycaemia in late pregnancy. Glucose 53-60 insulin Homo sapiens 15-22 22181063-0 2012 Glucose control in acute myocardial infarction: a pilot randomized study controlled by continuous glucose monitoring system comparing the use of insulin glargine with standard of care. Glucose 0-7 insulin Homo sapiens 145-152 22149546-5 2012 Insulin resistance was analyzed by homeostasis assessment model using the following expression: fasting insulin (muIU/mL)xfasting glucose (mmol/L)/22.5. Glucose 130-137 insulin Homo sapiens 0-7 22214489-8 2012 Extending the duration of insulin effect would also allow for greater flexibility and potentially reduce the frequency of blood glucose monitoring. Glucose 128-135 insulin Homo sapiens 26-33 22369975-5 2012 The artificial pancreas or closed-loop insulin delivery may improve outcomes, building on recent technological progress and combining continuous glucose monitoring with insulin pump therapy. Glucose 145-152 insulin Homo sapiens 39-46 22221106-5 2012 Insulin resistance (IR) of HepG2 cells was induced by 0.5 mm palmitate for 48 h. NO-1886 stimulated glucose consumption, glycogen synthesis and FFA absorption in insulin-resistant HepG2 cells. Glucose 100-107 insulin Homo sapiens 0-7 22187292-10 2012 Because of higher glucose levels (300-400 mg/dl) we started an intense insulin therapy. Glucose 18-25 insulin Homo sapiens 71-78 22174391-4 2012 The whole body insulin sensitivity index (S(I)) was determined using a frequently sampled intravenous glucose tolerance test. Glucose 102-109 insulin Homo sapiens 15-22 22221106-5 2012 Insulin resistance (IR) of HepG2 cells was induced by 0.5 mm palmitate for 48 h. NO-1886 stimulated glucose consumption, glycogen synthesis and FFA absorption in insulin-resistant HepG2 cells. Glucose 100-107 insulin Homo sapiens 162-169 22624461-4 2012 In the biologic reaction of exotrophy, the cells activatedly absorb glucose under effect of insulin through glucose carriers-4 and actively absorb fat acids in the form of nonpolar triglycerides in olein lipoproteins of very low density by force of receptor endocytosis. Glucose 108-115 insulin Homo sapiens 92-99 22624461-9 2012 In the biologic reaction of exotrophy insulin "decides": a) glucose can be deposited only in a limited way and can be consumed (oxidized in mitochondrion) in the first instance: b) fat acids can be stored and kept to be used in biologic function of locomotion. Glucose 60-67 insulin Homo sapiens 38-45 22624461-4 2012 In the biologic reaction of exotrophy, the cells activatedly absorb glucose under effect of insulin through glucose carriers-4 and actively absorb fat acids in the form of nonpolar triglycerides in olein lipoproteins of very low density by force of receptor endocytosis. Glucose 68-75 insulin Homo sapiens 92-99 22624461-10 2012 In the biologic reaction of exotrophy insulin "endeavors" as fast and full as possible use glucose and preserve in vivo as much as possible of fat acids as a substratum for further realization of biologic function of locomotion. Glucose 91-98 insulin Homo sapiens 38-45 22624461-11 2012 Insulin minimizes in cytosol the content of a) ketone bodies - metabolites of C4 butyric fat acid and b) short chained C6-C10 fat acids and C16 palmitic acid for which in mitochondrion exists specific carrier - carnitin-palmitoilacyltransferase and "forces" mitochondrion to oxidize glucose. Glucose 283-290 insulin Homo sapiens 0-7 21820684-3 2012 Body composition was measured by dual-energy x-ray absorptiometry; insulin sensitivity by insulin-modified, frequently sampled intravenous glucose tolerance test; substrate oxidation by indirect calorimetry; blood metabolite and hormone concentrations biochemically; and fatty acid flux by using stable isotope tracers. Glucose 139-146 insulin Homo sapiens 90-97 22123436-3 2012 The intravenous glucose tolerance test (IVGTT) has been considered as the most accurate method to determine the insulin sensitivity and glucose effectiveness. Glucose 16-23 insulin Homo sapiens 112-119 21869763-5 2012 Insulin sensitivity was assessed by both a frequently sampled intravenous glucose tolerance test (S(i)) and the homeostatic model assessment of insulin resistance (HOMA(IR)). Glucose 74-81 insulin Homo sapiens 0-7 22667123-9 2012 The result of insulin secretion stimulated by high glucose indicated that insulin increasingly secreted and then kept stable with prolongation of high glucose stimulation. Glucose 51-58 insulin Homo sapiens 14-21 22437766-3 2012 Insulin resistance diagnosis was performed using fasting insulin, HOMA-IR, QUICKI, insulin sensibility index and glucose/fasting insulin ratio. Glucose 113-120 insulin Homo sapiens 0-7 22667123-9 2012 The result of insulin secretion stimulated by high glucose indicated that insulin increasingly secreted and then kept stable with prolongation of high glucose stimulation. Glucose 151-158 insulin Homo sapiens 14-21 22277085-4 2012 Intensive insulin therapy was used to maintain serum glucose levels between 5.5 and 7.8 mmol/l. Glucose 53-60 insulin Homo sapiens 10-17 22227186-0 2012 Isolated mouse islets respond to glucose with an initial peak of glucagon release followed by pulses of insulin and somatostatin in antisynchrony with glucagon. Glucose 33-40 insulin Homo sapiens 104-111 22227186-1 2012 Recent studies of isolated human islets have shown that glucose induces hormone release with repetitive pulses of insulin and somatostatin in antisynchrony with those of glucagon. Glucose 56-63 insulin Homo sapiens 114-121 22227186-5 2012 Increase of glucose to 20mM resulted in an early secretory phase with a glucagon peak followed by peaks of insulin and somatostatin. Glucose 12-19 insulin Homo sapiens 107-114 22279598-2 2012 As a result, higher levels of insulin are needed to maintain normal glucose tolerance. Glucose 68-75 insulin Homo sapiens 30-37 21944265-2 2012 One-hundred thirty-four subjects with varying degrees of glucose tolerance received an insulin-modified intravenous glucose tolerance test and a standard oral glucose tolerance test with measurement of plasma insulin and C-peptide. Glucose 116-123 insulin Homo sapiens 87-94 21944265-2 2012 One-hundred thirty-four subjects with varying degrees of glucose tolerance received an insulin-modified intravenous glucose tolerance test and a standard oral glucose tolerance test with measurement of plasma insulin and C-peptide. Glucose 116-123 insulin Homo sapiens 87-94 21944267-4 2012 Insulin sensitivity and beta-cell response to glucose (basal, dynamic [PhiD], and static) were calculated by mathematical modeling using glucose, insulin, and C-peptide data obtained during a liquid meal tolerance test. Glucose 137-144 insulin Homo sapiens 0-7 21944267-8 2012 Eight weeks of a higher-carbohydrate/lower-fat diet resulted in higher insulin sensitivity in healthy, NGT, overweight/obese individuals, and lower fasting glucose and greater glucose-stimulated insulin secretion in individuals with IFG. Glucose 176-183 insulin Homo sapiens 195-202 22277085-1 2012 INTRODUCTION: We sought to determine the effect of nutritional support and insulin infusion therapy on serum and brain glucose levels and cerebral metabolic crisis after aneurysmal subarachnoid hemorrhage (SAH). Glucose 119-126 insulin Homo sapiens 75-82 22277085-12 2012 In the presence of metabolic distress, increased insulin administration was associated with a relative reduction of interstitial brain glucose concentrations (Wald=8.26, P=0.017), independent of serum glucose levels. Glucose 135-142 insulin Homo sapiens 49-56 22277085-13 2012 CONCLUSIONS: In the presence of metabolic distress, insulin administration is associated with reductions in brain glucose concentration that are independent of serum glucose levels. Glucose 114-121 insulin Homo sapiens 52-59 22277085-13 2012 CONCLUSIONS: In the presence of metabolic distress, insulin administration is associated with reductions in brain glucose concentration that are independent of serum glucose levels. Glucose 166-173 insulin Homo sapiens 52-59 23700508-4 2012 Adipose tissue dysfunction, characterized by an imbalanced secretion of pro- and anti-inflammatory adipokines and cytokines, decreased insulin-stimulated glucose uptake, dysregulation of lipid storage and release and mitochondrial dysfunction, has been linked to obesity and its associated metabolic disorders. Glucose 154-161 insulin Homo sapiens 135-142 22028408-2 2012 This is associated with the development of insulin resistance and a subsequent reduction of insulin-stimulated glucose uptake. Glucose 111-118 insulin Homo sapiens 92-99 22028408-5 2012 Insulin action on skeletal muscle was assessed by a hyperinsulinemic euglycemic clamp and by determining insulin signaling to glucose transport. Glucose 126-133 insulin Homo sapiens 0-7 22028408-9 2012 Intracellular insulin signaling to glucose transport was impaired by regulation of phosphorylation at specific sites on AS160 but not TBC1D1, both key regulators of glucose uptake. Glucose 35-42 insulin Homo sapiens 14-21 22028408-9 2012 Intracellular insulin signaling to glucose transport was impaired by regulation of phosphorylation at specific sites on AS160 but not TBC1D1, both key regulators of glucose uptake. Glucose 165-172 insulin Homo sapiens 14-21 22245737-2 2012 Here we examined how CD8(+) T cells kill human islet beta cells in type 1 diabetes via recognition of a human leukocyte antigen HLA-A*0201-restricted glucose-sensitive preproinsulin peptide by the autoreactive TCR 1E6. Glucose 150-157 insulin Homo sapiens 168-181 22230186-0 2012 High-dose clevudine impairs mitochondrial function and glucose-stimulated insulin secretion in INS-1E cells. Glucose 55-62 insulin Homo sapiens 74-81 22230186-9 2012 Insulin release in response to glucose application was markedly decreased in clevudine-treated INS-1E cells, which might be a consequence of mitochondrial dysfunction. Glucose 31-38 insulin Homo sapiens 0-7 22230186-10 2012 CONCLUSIONS: Our data suggest that high-dose treatment with clevudine induces mitochondrial defects associated with mtDNA depletion and impairs glucose-stimulated insulin secretion in insulin-releasing cells. Glucose 144-151 insulin Homo sapiens 163-170 22230186-10 2012 CONCLUSIONS: Our data suggest that high-dose treatment with clevudine induces mitochondrial defects associated with mtDNA depletion and impairs glucose-stimulated insulin secretion in insulin-releasing cells. Glucose 144-151 insulin Homo sapiens 184-191 21801810-6 2012 Our data suggest that in 3T3-L1 adipocytes NPY inhibits insulin-stimulated glucose uptake in a GLUT4-dependent manner. Glucose 75-82 insulin Homo sapiens 56-63 22559855-5 2012 Normal glucose regulation is maintained by an intricate interaction between pancreatic beta-cells (insulin/amylin), pancreatic alpha-cells (glucagon), and associated organs (eg, intestines, liver, skeletal muscle, adipose tissue). Glucose 7-14 insulin Homo sapiens 99-106 23393688-2 2012 This chapter concentrates on aspects of potential new strategies in the treatment of the disease going from nutritional preventive approaches towards currently utilized drugs for treatment that target the pancreatic beta cells with potentiation of glucose-stimulated insulin secretion. Glucose 248-255 insulin Homo sapiens 267-274 22399424-2 2012 How excessive caloric intake and weight gain cause insulin resistance has not completely been elucidated.Skeletal muscle is responsible for a major part of insulin stimulated whole-body glucose disposal and, hence, plays an important role in the pathogenesis of insulin resistance.It has been hypothesized that skeletal muscle mitochondrial dysfunction is involved in the accumulation of intramyocellular lipid metabolites leading to lipotoxicity and insulin resistance. Glucose 186-193 insulin Homo sapiens 156-163 22399424-2 2012 How excessive caloric intake and weight gain cause insulin resistance has not completely been elucidated.Skeletal muscle is responsible for a major part of insulin stimulated whole-body glucose disposal and, hence, plays an important role in the pathogenesis of insulin resistance.It has been hypothesized that skeletal muscle mitochondrial dysfunction is involved in the accumulation of intramyocellular lipid metabolites leading to lipotoxicity and insulin resistance. Glucose 186-193 insulin Homo sapiens 156-163 22399424-2 2012 How excessive caloric intake and weight gain cause insulin resistance has not completely been elucidated.Skeletal muscle is responsible for a major part of insulin stimulated whole-body glucose disposal and, hence, plays an important role in the pathogenesis of insulin resistance.It has been hypothesized that skeletal muscle mitochondrial dysfunction is involved in the accumulation of intramyocellular lipid metabolites leading to lipotoxicity and insulin resistance. Glucose 186-193 insulin Homo sapiens 156-163 21952036-1 2012 It was reported previously that isolated human islets from individuals with type 2 diabetes mellitus (T2DM) show reduced glucose-stimulated insulin release. Glucose 121-128 insulin Homo sapiens 140-147 23367159-1 2012 We know much about the glucose regulatory system, yet the application of this knowledge is limited because simultaneous measurements of insulin and glucose are difficult to obtain. Glucose 23-30 insulin Homo sapiens 136-143 22482906-1 2012 To enhance glucose uptake into muscle and fat cells, insulin stimulates the translocation of GLUT4 glucose transporters from intracellular membranes to the cell surface. Glucose 11-18 insulin Homo sapiens 53-60 22374243-8 2012 The differentiated cells significantly produced human insulin as compared to the undifferentiated ADSCs, and its production was increased with an increase of glucose concentration in the culture medium. Glucose 158-165 insulin Homo sapiens 54-61 22785470-3 2012 In it, palmitate decreased insulin-stimulated glucose uptake and consumption in a dose-dependent manner, and it reduced the insulin-stimulated phosphorylation of Akt at Thr308 and Ser473, but had no effect on the protein expression of PI3K-p85 or the activity of PI3K. Glucose 46-53 insulin Homo sapiens 27-34 22018645-2 2012 Recent findings in cellular models indicate that HDL may act on glucose homeostasis by improving insulin sensitivity and secretion. Glucose 64-71 insulin Homo sapiens 97-104 23275719-2 2012 Insulin, the principal hormone regulates uptake of glucose from the blood into most of the cells except central nervous system. Glucose 51-58 insulin Homo sapiens 0-7 22558802-2 2012 It is known to have an immune-mediated pathogenesis, which results in the loss of insulin-secreting beta-cells responsible for maintaining normal blood glucose levels. Glucose 152-159 insulin Homo sapiens 82-89 22606402-7 2012 25 mg of prednisolone was infused preoperatively, and intervention with insulin treatment was initiated when blood glucose level rose to 18 mmol/L at 2 hours. Glucose 115-122 insulin Homo sapiens 72-79 22080915-4 2012 Engrafted beta-cell mass was assessed by acute insulin and C-peptide responses to glucose (AIR(glu) and ACR(glu)) and arginine (AIR(arg) and ACR(arg)). Glucose 82-89 insulin Homo sapiens 59-68 22080915-5 2012 Insulin sensitivity (S(I)) was determined in naive and transplanted primates from an intravenous glucose tolerance test using the minimal model. Glucose 98-105 insulin Homo sapiens 0-7 22415069-2 2012 Insulin commands the glucose uptake by the cells and might control the processes in which there is need for energy such as mitogenesis and gene transcription. Glucose 21-28 insulin Homo sapiens 0-7 22415075-1 2012 BACKGROUND/AIMS: Stimulation of insulin release by D-glucose is accompanied by Cl(-) and HCO(3)(-) efflux from pancreatic islet cells. Glucose 51-60 insulin Homo sapiens 32-39 22490341-3 2012 After culture in vitro, the differentiated cells (hAM-ISCs) were intensively stained with dithizone and secreted insulin and c-peptide in a high-glucose-dependent manner. Glucose 146-153 insulin Homo sapiens 126-135 22830071-4 2012 The CREATE-ECLA study, which hypothesized that a fixed high dose of glucose, insulin, and potassium (GIK) would change myocardial substrate utilization from free fatty acids to glucose and therefore protect ischemic myocardium, failed to demonstrate improved clinical outcomes in AMI patients. Glucose 177-184 insulin Homo sapiens 77-84 22937295-3 2012 Glucose, insulin, and C-peptide response to a 2-hour glucose tolerance test were consistently improved across this time period, and calculated beta-cell mass increased by 67%. Glucose 53-60 insulin Homo sapiens 22-31 22195604-0 2012 Generation of glucose-responsive, insulin-producing cells from human umbilical cord blood-derived mesenchymal stem cells. Glucose 14-21 insulin Homo sapiens 34-41 22195604-1 2012 We sought to assess the potential of human cord blood-derived mesenchymal stem cells (CB-MSCs) to derive insulin-producing, glucose-responsive cells. Glucose 124-131 insulin Homo sapiens 105-112 22195604-3 2012 Transplantation of these cells in immune-deficient animals shows human C-peptide production in response to a glucose challenge. Glucose 110-117 insulin Homo sapiens 71-80 22785470-5 2012 Inhibition of Src by PP2 resulted in decreases in insulin-stimulated glucose uptake and phosphorylation of Src at Tyr416 and Akt at Thr308 and Ser473. Glucose 69-76 insulin Homo sapiens 50-57 22240352-1 2012 In studies using the intravenous glucose tolerance test with minimal model analysis we reported that low insulin sensitivity (SI) is associated with increased erythrocyte aggregability and plasma viscosity, that appeared to be markers of insulin resistance. Glucose 33-40 insulin Homo sapiens 105-112 22240352-1 2012 In studies using the intravenous glucose tolerance test with minimal model analysis we reported that low insulin sensitivity (SI) is associated with increased erythrocyte aggregability and plasma viscosity, that appeared to be markers of insulin resistance. Glucose 33-40 insulin Homo sapiens 238-245 22240352-2 2012 Recently, development of modelling has made available a new approach of insulin sensitivity from oral glucose tolerance test data (oral minimal model). Glucose 102-109 insulin Homo sapiens 72-79 22240354-2 2012 In studies using the intravenous glucose tolerance test with minimal model analysis we reported that low insulin sensitivity (SI) is associated with increased erythrocyte aggregability (EA). Glucose 33-40 insulin Homo sapiens 105-112 20870309-0 2012 Insulin dosage optimization based on prediction of postprandial glucose excursions under uncertain parameters and food intake. Glucose 64-71 insulin Homo sapiens 0-7 22372347-0 2012 Hemolysis is a major cause of variability in insulin measurement during oral glucose tolerance test in children. Glucose 77-84 insulin Homo sapiens 45-52 22372347-1 2012 BACKGROUND: The oral glucose tolerance test (OGTT) is widely employed to evaluate insulin resistance in children with growth hormone deficiency. Glucose 21-28 insulin Homo sapiens 82-89 27820154-3 2012 Diabetes is a group of diseases marked by high levels of blood glucose resulting from defects in insulin production, insulin action, or both.Type 2 diabetes was previously called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. Glucose 63-70 insulin Homo sapiens 117-124 27820154-27 2012 The fasting plasma glucose test measures fasting blood sugar levels and the postprandial plasma glucose test is often used to test the effectiveness of the body"s carbohydrate metabolism and the ability to produce insulin. Glucose 96-103 insulin Homo sapiens 214-221 22975062-5 2012 Pharmacological and genetic blockades of islet-derived ghrelin markedly augment glucose-induced insulin release. Glucose 80-87 insulin Homo sapiens 96-103 22975062-7 2012 Ghrelin attenuates the glucose-induced cAMP production and PKA activation, which drives activation of Kv channels and suppression of the glucose-induced [Ca(2+)](i) increase and insulin release in beta-cells. Glucose 23-30 insulin Homo sapiens 178-185 22975062-7 2012 Ghrelin attenuates the glucose-induced cAMP production and PKA activation, which drives activation of Kv channels and suppression of the glucose-induced [Ca(2+)](i) increase and insulin release in beta-cells. Glucose 137-144 insulin Homo sapiens 178-185 22893412-1 2012 Glucose disposal in skeletal muscle is a major target for insulin action and assessment of insulin-regulated glucose uptake under in vitro conditions allows the direct determination of insulin sensitivity in this organ. Glucose 109-116 insulin Homo sapiens 91-98 22893412-1 2012 Glucose disposal in skeletal muscle is a major target for insulin action and assessment of insulin-regulated glucose uptake under in vitro conditions allows the direct determination of insulin sensitivity in this organ. Glucose 109-116 insulin Homo sapiens 91-98 22057446-4 2012 Thus, glucose-responsive, insulin-producing cells from human origin are urgently needed. Glucose 6-13 insulin Homo sapiens 26-33 22095824-7 2012 Although the results have not always been consistent, gene variants that affect primary insulin action, and particularly their interaction with the environment, are important modulators of glucose metabolism. Glucose 189-196 insulin Homo sapiens 88-95 22067800-5 2012 RESULTS: At baseline, median gravidity, BMI, abdominal circumference, and acute insulin response to intravenous glucose were higher and high-density lipoprotein (HDL) cholesterol and insulin sensitivity (S(I) from FSIGTs) were lower in the 10 obese participants than the five normal-weight women (p<=.05 for each). Glucose 112-119 insulin Homo sapiens 80-87 22414059-5 2012 In addition, ROS activate UCP2 via peroxidation of the mitochondrial membrane phospholipids, which results in proton leak leading to reduced ATP synthesis and content in beta-cells - critical parameters in the regulation of glucose-stimulated insulin secretion. Glucose 224-231 insulin Homo sapiens 243-250 22519397-2 2012 Its main clinical effect is to reduce blood glucose levels by improving insulin resistance. Glucose 44-51 insulin Homo sapiens 72-79 23167795-0 2012 Estrogen receptor 1 agonist PPT stimulates Slc2a4 gene expression and improves insulin-induced glucose uptake in adipocytes. Glucose 95-102 insulin Homo sapiens 79-86 21790774-7 2012 Glucose monitoring took place in all residents who received insulin, but was monitored unnecessarily in those with diet-controlled diabetes (63%). Glucose 0-7 insulin Homo sapiens 60-67 21831167-4 2012 Hepatic/peripheral insulin sensitivity was evaluated at baseline and at week 12 by infusion of (3) H-labelled glucose followed by a 2-step hyperinsulinemic-euglycemic clamp. Glucose 110-117 insulin Homo sapiens 19-26 21877913-5 2012 Insulin dosage was titrated according to fasting capillary blood glucose levels, and treatment was stopped after 2 weeks. Glucose 65-72 insulin Homo sapiens 0-7 21922321-8 2012 Arginine-stimulated (p = 0.02) insulin secretion was reduced in vivo, which was further reflected by a reduction of glucose- and potassium-stimulated insulin secretion (p = 0.002 and p = 0.04, respectively) in human islets in vitro. Glucose 116-123 insulin Homo sapiens 150-157 22011715-6 2012 Baseline insulin and insulin levels at 30 min after taking glucose during the GTT were significantly higher following carrageenan treatment. Glucose 59-66 insulin Homo sapiens 9-16 22011715-6 2012 Baseline insulin and insulin levels at 30 min after taking glucose during the GTT were significantly higher following carrageenan treatment. Glucose 59-66 insulin Homo sapiens 21-28 22040838-5 2012 Before and after the intervention, insulin sensitivity was measured by euglycemic hyperinsulinemic (80 mU/m(2)/min) clamp enriched with [6,6-(2)H]glucose. Glucose 146-153 insulin Homo sapiens 35-42 22050786-8 2012 The static component (Phi(s)) estimates the rate of insulin secretion related to above-basal glucose concentration. Glucose 93-100 insulin Homo sapiens 52-59 22074724-6 2012 RESULTS: At 24 h, the mean glucose level was 1.41 mmol/L (95% CI 0.69-2.13) lower in the insulin (6.53 vs. 7.94 mmol/L). Glucose 27-34 insulin Homo sapiens 89-96 22074724-10 2012 CONCLUSIONS: A paper-based insulin algorithm targeting glucose levels of 5.0-6.5 mmol/L (90-117 mg/dL) can be feasibly implemented in the CCU. Glucose 55-62 insulin Homo sapiens 27-34 22124715-7 2012 The association between GLP-1 and insulin concentrations supports the idea that the incretins are involved in glucose control after GBP. Glucose 110-117 insulin Homo sapiens 34-41 22419881-6 2012 The level of the short chain fatty acids acetate, but not propionate or butyrate, was also negatively associated with fasting serum insulin and 2 hour insulin levels in the oral glucose tolerance test. Glucose 178-185 insulin Homo sapiens 132-145 21774670-1 2012 Glucose-stimulated insulin gene transcription is mainly regulated by a 340-bp promoter region upstream of the transcription start site by beta-cell-enriched transcription factors Pdx-1, MafA, and NeuroD1. Glucose 0-7 insulin Homo sapiens 19-26 21774670-4 2012 In this report we investigated the role of the additional HAT proteins CREB binding protein (CBP), p300/CBP-associated factor (PCAF), and general control of amino-acid synthesis 5 (GCN5) in regulation of glucose-stimulated insulin gene transcription. Glucose 204-211 insulin Homo sapiens 223-230 21774670-5 2012 Utilizing quantitative chromatin immunoprecipitation analysis, we demonstrate that glucose regulates the binding of p300, CBP, PCAF, and GCN5 to the proximal insulin promoter. Glucose 83-90 insulin Homo sapiens 158-165 21774670-7 2012 These data suggest that high glucose mediates the recruitment of p300, CBP, PCAF, and GCN5 to the insulin promoter and that all four HATs are important for insulin gene expression. Glucose 29-36 insulin Homo sapiens 98-105 22028447-5 2012 Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. Glucose 201-208 insulin Homo sapiens 74-81 22068110-0 2012 Insulin secretion and insulin sensitivity on the oral glucose tolerance test (OGTT) in middle-aged Japanese. Glucose 54-61 insulin Homo sapiens 0-7 22068110-0 2012 Insulin secretion and insulin sensitivity on the oral glucose tolerance test (OGTT) in middle-aged Japanese. Glucose 54-61 insulin Homo sapiens 22-29 22094999-0 2012 Hyperbolic correlation between insulin sensitivity and insulin secretion fades away in lean subjects with superb glucose regulation. Glucose 113-120 insulin Homo sapiens 31-38 22230809-1 2012 Recent studies have shown colestimide, a bile acid-binding resin, to also exert a glucose-lowering effect via amelioration of insulin resistance. Glucose 82-89 insulin Homo sapiens 126-133 22301938-2 2012 The alpha-glucosidase inhibitor (alpha-GI) miglitol is useful for controlling the early postprandial increase of glucose, but the combined effect of miglitol and multiple daily insulin injections (MDI) on glucose excursion has not been evaluated. Glucose 205-212 insulin Homo sapiens 177-184 22374239-5 2012 Insulin secretion and glucose tolerance were evaluated by a 75-g oral glucose tolerance test and an intravenous glucagon loading test. Glucose 70-77 insulin Homo sapiens 0-7 22744624-1 2012 INTRODUCTION: Insulin resistance is defined as reduction of insulin-stimulated glucose uptake in skeletal muscles and inadequate suppression of the production of endogenous glucose. Glucose 79-86 insulin Homo sapiens 14-21 22744624-1 2012 INTRODUCTION: Insulin resistance is defined as reduction of insulin-stimulated glucose uptake in skeletal muscles and inadequate suppression of the production of endogenous glucose. Glucose 79-86 insulin Homo sapiens 60-67 22744624-1 2012 INTRODUCTION: Insulin resistance is defined as reduction of insulin-stimulated glucose uptake in skeletal muscles and inadequate suppression of the production of endogenous glucose. Glucose 173-180 insulin Homo sapiens 14-21 22744627-8 2012 The mean initial glucose levels for the insulin group decreased significantly after the intravenous infusion of insulin (p < 0.001). Glucose 17-24 insulin Homo sapiens 40-47 22744627-8 2012 The mean initial glucose levels for the insulin group decreased significantly after the intravenous infusion of insulin (p < 0.001). Glucose 17-24 insulin Homo sapiens 112-119 22744627-10 2012 Moreover, the blood glucose concentration decrease during these two weeks was significantly higher in the insulin group (p = 0.01). Glucose 20-27 insulin Homo sapiens 106-113 22744627-14 2012 Insulin caused a greater reduction in blood glucose concentration but required more attention and trained personnel. Glucose 44-51 insulin Homo sapiens 0-7 22744628-2 2012 The impairment of cellular glucose transport observed in insulin resistance leads to glucose metabolism disturbances. Glucose 27-34 insulin Homo sapiens 57-64 22893453-4 2012 Insulin resistance and type 2 diabetes affects liver pathology, typically leading to nonalcoholic fatty liver disease (NAFLD) by dynamically altering the hepatic genes involved in glucose and lipid metabolism. Glucose 180-187 insulin Homo sapiens 0-7 22009494-11 2012 CONCLUSIONS: Morphologies of the glucose curve seem reflecting different metabolic phenotypes of insulin action and secretion, particularly when combined with morphologies of insulin curve or time of glucose peak. Glucose 33-40 insulin Homo sapiens 97-104 21915820-10 2012 Insulin was released in response to glucose stimulation in a manner comparable to that of adult human islets. Glucose 36-43 insulin Homo sapiens 0-7 23197975-6 2012 Functionally, isolated human islets released more glucose-stimulated insulin when preincubated in KU-32. Glucose 50-57 insulin Homo sapiens 69-76 22110477-5 2012 ROS activate UCP2, which results in proton leak across the mitochondrial inner membrane, and this leads to reduced beta-cell ATP synthesis and content, which is a critical parameter in regulating glucose-stimulated insulin secretion. Glucose 196-203 insulin Homo sapiens 215-222 22262970-9 2012 Our results suggest that insulin may play a significant role in the regulation of microvascular perfusion in patients with Type 1 diabetes through its vasodilation effect and can counteract the effect of acute glucose fluctuations. Glucose 210-217 insulin Homo sapiens 25-32 30736105-4 2012 Insulin degludec, appropriately labeled as an ultra-long-acting basal insulin, promises to achieve similar blood glucose control to currently available preparations (glargine and detemir insulin), with a reduced risk of hypoglycemia and greater flexibility in the day-to-day timing of insulin administration. Glucose 113-120 insulin Homo sapiens 0-7 21947415-1 2012 OBJECTIVE: We investigated C-peptide effects on inflammatory cytokine release and adhesion of monocytes exposed to high glucose and lipopolysaccharide (LPS) in vitro. Glucose 120-127 insulin Homo sapiens 27-36 22345880-8 2012 CONCLUSION: The novel excipient used could protect insulin from gastric and pancreatic enzymes and reduce blood glucose concentration in both healthy and diabetic rats suggesting that oral delivery of insulin is feasible in a near future. Glucose 112-119 insulin Homo sapiens 51-58 22345880-8 2012 CONCLUSION: The novel excipient used could protect insulin from gastric and pancreatic enzymes and reduce blood glucose concentration in both healthy and diabetic rats suggesting that oral delivery of insulin is feasible in a near future. Glucose 112-119 insulin Homo sapiens 201-208 22567007-0 2012 1-Hour OGTT Plasma Glucose as a Marker of Progressive Deterioration of Insulin Secretion and Action in Pregnant Women. Glucose 19-26 insulin Homo sapiens 71-78 22567007-2 2012 Our aim is to assess if changes in insulin action and secretion during pregnancy are related to 1-hour plasma glucose concentration during OGTT. Glucose 110-117 insulin Homo sapiens 35-42 22689376-1 2012 The beta cells of the pancreatic islets, which maintain glucose homeostasis by secreting insulin, are important cells for sustaining life. Glucose 56-63 insulin Homo sapiens 89-96 23037470-2 2012 We herein report the case of a 57-year-old diabetic CML patient who was resistant to imatinib and initially required 20 units of insulin daily to control his blood glucose levels. Glucose 164-171 insulin Homo sapiens 129-136 22504236-6 2012 RESULTS: Women with previous GDM treated with insulin in pregnancy had significantly higher fasting glucose, plasma PAI-1 levels and carotid IMT compared to women treated with MNT alone. Glucose 100-107 insulin Homo sapiens 46-53 22504236-7 2012 In multiple regression analysis, insulin need in pregnancy was associated with increased carotid IMT and plasma PAI-1 levels (corrected for age, BMI, postpartum duration, fasting glucose and lipids; model r(2)=0.132; beta=0.297, p=0.014 for carotid IMT; model r(2)=0.198; beta=0.345, p=0.003 for PAI-1). Glucose 179-186 insulin Homo sapiens 33-40 22143007-1 2012 The ability of the pancreatic beta-cells to adapt the rate of insulin release in accordance to changes in circulating glucose levels is essential for glucose homeostasis. Glucose 118-125 insulin Homo sapiens 62-69 22143007-3 2012 The first spatial barrier is overcome by the presence of a glucose transporter (GLUT) in the plasma membrane, whereas a low affinity hexokinase IV (glucokinase, GK) in the cytosol conveys glucose availability into a metabolic flux that triggers and accelerates insulin release. Glucose 59-66 insulin Homo sapiens 261-268 22192948-2 2012 Insulin secretion was measured by radioimmunoassay following perifusion of human, pig, rat and mouse isolated islets with kisspeptin-10 or kisspeptin-13 in the presence of 20 mM glucose. Glucose 178-185 insulin Homo sapiens 0-7 22192948-3 2012 Both peptides stimulated rapid, reversible potentiation of glucose-stimulated insulin secretion from islets of all species tested. Glucose 59-66 insulin Homo sapiens 78-85 23229989-7 2012 Pharmacist recommendations for insulin dose adjustments were made based on patient reported self-monitored glucose values. Glucose 107-114 insulin Homo sapiens 31-38 22016371-5 2012 Insulin sensitivity index (ISI) was determined from oral glucose tolerance test glucose and insulin levels. Glucose 57-64 insulin Homo sapiens 0-7 22016371-5 2012 Insulin sensitivity index (ISI) was determined from oral glucose tolerance test glucose and insulin levels. Glucose 80-87 insulin Homo sapiens 0-7 22785026-0 2012 Decreased beta cell function and insulin sensitivity contributed to coronary artery disease in patients with normal glucose tolerance. Glucose 116-123 insulin Homo sapiens 33-40 22785026-11 2012 CONCLUSION: Insulin resistance and beta cell function were closely related to the incidence of CAD in patients with normal glucose tolerance. Glucose 123-130 insulin Homo sapiens 12-19 22401319-1 2012 Studies on tight glycemic control by intensive insulin therapy abruptly changed the climate of limited interest in the problem of hyperglycemia in critically ill patients and reopened the discussion on accuracy and reliability of glucose sensor devices. Glucose 230-237 insulin Homo sapiens 47-54 22401333-3 2012 The bolus advisor improved overall glucose control and increased adherence by overcoming the patients" fear of hypoglycemia, giving them more confidence to give adequate doses of insulin to control hyperglycemia. Glucose 35-42 insulin Homo sapiens 179-186 22401339-0 2012 Continuous glucose monitoring-guided insulin dosing in pump-treated patients with type 1 diabetes: a clinical guide. Glucose 11-18 insulin Homo sapiens 37-44 22401339-1 2012 This article describes our methods for structured continuous glucose monitoring (CGM)-guided insulin dosing in pump-treated type 1 diabetes. Glucose 61-68 insulin Homo sapiens 93-100 21350243-3 2012 We sought to determine the relationship of insulin and glucose measurements from the oral glucose tolerance test (OGTT) with muscle mass in persons without diabetes. Glucose 90-97 insulin Homo sapiens 43-50 22613419-0 2012 Adipocytokines and insulin resistance across various degrees of glucose tolerance in pregnancy. Glucose 64-71 insulin Homo sapiens 19-26 22971482-11 2012 Liver AdipoR2-mediated glucose uptake is important in the prophylactic effect of pioglitazone on insulin resistance. Glucose 23-30 insulin Homo sapiens 97-104 22046973-7 2012 In each study the targeted glucose values for patients treated with insulin based on sonographic measurements were lower than for those treated exclusively with diet. Glucose 27-34 insulin Homo sapiens 68-75 22046973-9 2012 To support these findings, studies are needed in which glycemic targets comparing groups whose insulin treatment is based on maternal glucose results with those based on ultrasound measurements are identical. Glucose 134-141 insulin Homo sapiens 95-102 22235952-18 2012 CONCLUSION: For insulin users with at least 1 pharmacy claim for glucose test strips, SMBG-related costs accounted for about one-fourth of total insulin and SMBG-related pharmacy costs. Glucose 65-72 insulin Homo sapiens 16-23 22235952-18 2012 CONCLUSION: For insulin users with at least 1 pharmacy claim for glucose test strips, SMBG-related costs accounted for about one-fourth of total insulin and SMBG-related pharmacy costs. Glucose 65-72 insulin Homo sapiens 145-152 22474575-3 2012 Glucose uptake assays revealed that insulin stimulation caused a significant 2.54-fold decrease in 2-deoxyglucose uptake in transfected cells coupled with a significant upregulation of native mitogen-activated protein kinases (MAPKs), p38, and p44/42. Glucose 0-7 insulin Homo sapiens 36-43 22768668-2 2012 Glucose variability in infants with NDM treated with insulin can be extreme. Glucose 0-7 insulin Homo sapiens 53-60 27820140-16 2012 It is an average of blood glucose levels for the last 120 days, which is consistent with the average life span of a red blood cell (RBC).Compensation for the lack of insulin-secreting betaeta-cells is accomplished through administration of insulin. Glucose 26-33 insulin Homo sapiens 240-247 27820140-36 2012 The user must enter insulin dosing information into the pump, taking into account the present glucose level and duration of action of the insulin. Glucose 94-101 insulin Homo sapiens 20-27 27820154-3 2012 Diabetes is a group of diseases marked by high levels of blood glucose resulting from defects in insulin production, insulin action, or both.Type 2 diabetes was previously called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. Glucose 63-70 insulin Homo sapiens 97-104 24331168-7 2012 CONCLUSIONS: Insulin resistance was observed in overweight Japanese children, though their hemoglobin A1c and fasting glucose were within the normal range. Glucose 118-125 insulin Homo sapiens 13-20 21820870-0 2012 Baseline insulin/glucose ratio as a marker for the clinical course of hyperglycemic critically ill children treated with insulin. Glucose 17-24 insulin Homo sapiens 121-128 21820870-3 2012 METHODS: Sixty-four consecutively admitted critically ill children with hyperglycemia, defined as a blood glucose level higher than 8 mmol/L (>145 mg/dL) and treated with insulin according to a glucose-control protocol, were included. Glucose 197-204 insulin Homo sapiens 174-181 21820870-8 2012 A hyperinsulinemic response, indicated by an increased insulin/glucose ratio (>18 pmol/mmol), was seen in 55% of children. Glucose 63-70 insulin Homo sapiens 7-14 21820870-12 2012 It would be worthwhile to further investigate if the insulinemic response to hyperglycemia, determined by the insulin/glucose ratio in combination with the type of organ dysfunction, could be used in clinical practice to determine the need for insulin therapy. Glucose 118-125 insulin Homo sapiens 53-60 21872431-7 2012 The increase in plasma insulin concentrations, but not in glucose, after glucose administration (area under the curve) was significantly smaller in the MLCT group than in the LCT group (P < 0.01) and was significantly associated with mesenteric fat weight (P < 0.05). Glucose 73-80 insulin Homo sapiens 23-30 24155816-12 2012 Patients transitioned "per protocol" had better glucose control demonstrated by: less hyperglycemic events, lower mean blood glucose levels at 48 and 72 hours, and lower need for correctional insulin. Glucose 48-55 insulin Homo sapiens 192-199 23227203-10 2012 Glucose uptake by human skeletal muscle cells decreases 61.7% when the cells are incubated with pre UV-illuminated insulin during 1.5 h. The observations presented in this work highlight the importance of protecting insulin and other drugs from UV-light exposure, which is of outmost relevance to the pharmaceutical industry. Glucose 0-7 insulin Homo sapiens 115-122 23251403-6 2012 RESULTS: Incremental tertiles of the triglyceride-to-HDL cholesterol ratio demonstrated a significant positive association with levels of fasting insulin, HOMA1-IR, glucose: insulin ratio and a negative association with QUICKI in White European men (n = 255) and women (n = 250) and South Asian men (n = 124) (all p<0.05), but not South Asian women (n = 100). Glucose 165-172 insulin Homo sapiens 174-181 23300589-11 2012 In a random-effect meta-analysis the pooled relative risk of CHD (95% CI; I(2)) comparing high to low concentrations was 1.52 (1.31, 1.76; 62.4%) for glucose, 1.12 (0.92, 1.37; 41.0%) for insulin and 1.64 (1.35, 2.00; 0%) for HOMA-IR. Glucose 150-157 insulin Homo sapiens 188-195 23227203-10 2012 Glucose uptake by human skeletal muscle cells decreases 61.7% when the cells are incubated with pre UV-illuminated insulin during 1.5 h. The observations presented in this work highlight the importance of protecting insulin and other drugs from UV-light exposure, which is of outmost relevance to the pharmaceutical industry. Glucose 0-7 insulin Homo sapiens 216-223 23077502-0 2012 Polymorphism rs11085226 in the gene encoding polypyrimidine tract-binding protein 1 negatively affects glucose-stimulated insulin secretion. Glucose 103-110 insulin Homo sapiens 122-129 23133528-1 2012 Insulin is critical for controlling energy functions including glucose and lipid metabolism. Glucose 63-70 insulin Homo sapiens 0-7 23077502-8 2012 In the IVGTT subgroup, SNP rs11085226 was accordingly associated with lower insulin levels within the first ten minutes following glucose injection (p = 0.0103). Glucose 130-137 insulin Homo sapiens 76-83 23077502-11 2012 CONCLUSIONS: We conclude that common genetic variation in PTBP1 influences glucose-stimulated insulin secretion. Glucose 75-82 insulin Homo sapiens 94-101 23056264-10 2012 Basal and insulin stimulated glucose uptake, glycogen synthesis and glucose oxidation were not significantly modulated by Angptl4 overexpression. Glucose 29-36 insulin Homo sapiens 10-17 23077605-1 2012 In glucose-induced insulin secretion from pancreatic beta-cells, a population of insulin granules fuses with the plasma membrane without the typical docking process (newcomer granule fusions), however, its mechanism is unclear. Glucose 3-10 insulin Homo sapiens 19-26 22937169-8 2012 Importantly, we provide evidence that differentiation of human satellite cells in hyperglycemic (22.5 mM glucose) conditions increases GLUT1 expression, and renders the cells insulin resistant and interestingly GLP-1 resistant in terms of glucose uptake and glycogen synthesis. Glucose 105-112 insulin Homo sapiens 175-182 23056434-10 2012 The geometric mean insulin (log standard deviation) concentrations amongst 12,812 children were 3.0 mU/L (1.1) in boys and 4.0 mU/L (1.0) in girls and were positively associated with pubertal stage, measures of central and peripheral adiposity, height and fasting glucose. Glucose 264-271 insulin Homo sapiens 19-26 23056614-5 2012 Forkhead box O1 (FoxO1), a downstream effector of insulin signaling, plays a central role in hepatic glucose metabolism through the regulation of hepatic glucose production. Glucose 101-108 insulin Homo sapiens 50-57 23024780-0 2012 High glucose predisposes gene expression and ERK phosphorylation to apoptosis and impaired glucose-stimulated insulin secretion via the cytoskeleton. Glucose 91-98 insulin Homo sapiens 110-117 23024780-1 2012 Chronic high glucose (HG) inflicts glucotoxicity on vulnerable cell types such as pancreatic beta cells and contributes to insulin resistance and impaired insulin secretion in diabetic patients. Glucose 13-20 insulin Homo sapiens 123-130 23024780-3 2012 Chronic HG exposure which reduced glucose-stimulated insulin secretion (GSIS) increased transcript levels of 185 genes that clustered primarily in 5 processes namely cellular growth and proliferation; cell death; cellular assembly and organization; cell morphology; and cell-to-cell signaling and interaction. Glucose 34-41 insulin Homo sapiens 53-60 22606236-8 2012 Subjects of the French DESIR population, who carried the rs3743462 T-to-C polymorphism, located in the distal glucose-responsive promoter, displayed lower basal insulin levels and lower HOMA-IR index. Glucose 110-117 insulin Homo sapiens 161-168 22815837-5 2012 Assessment of the effect on insulin secretion was made at the end of each intervention using an insulin-modified frequently sampled intravenous glucose tolerance test (FSIVGTT). Glucose 144-151 insulin Homo sapiens 96-103 22720085-4 2012 Insulin sensitivity was measured as the glucose infusion rate during a euglycemic hyperinsulinemic clamp, body fat percentage was measured by dual X-ray absorptiometry, and CVD risk was estimated using the Framingham risk score. Glucose 40-47 insulin Homo sapiens 0-7 22720085-6 2012 RESULTS: Both fasting and 2-hour plasma glucose levels were associated with higher Framingham risk score (fasting glucose: r(2) = 0.21; 2-hour glucose: r(2) = 0.24; P<0.001 for both), and insulin sensitivity with lower Framingham risk score (r(2) = 0.36; P<0.001). Glucose 40-47 insulin Homo sapiens 191-198 22720085-8 2012 Likewise, when adjusting for insulin sensitivity and fasting glucose, the association between 2-hour glucose and Framingham risk score disappeared (P = 0.143). Glucose 101-108 insulin Homo sapiens 29-36 22720085-9 2012 In contrast, insulin sensitivity was still associated with Framingham risk score after adjusting for glucose levels (P<0.001). Glucose 101-108 insulin Homo sapiens 13-20 22720085-11 2012 CONCLUSION: The association between plasma glucose levels and CVD risk is mainly explained by insulin resistance, which raises the question of whether glucose lowering per se without changes in the processes that underlie hyperglycemia should be the sole clinical paradigm in the treatment of type 2 diabetes or its prevention. Glucose 43-50 insulin Homo sapiens 94-101 22720003-6 2012 Diabetic duration, BMI, HbA1c, fasting and postprandial blood glucose level were positively associated with daily insulin dose, while age was negatively associated with daily insulin dose. Glucose 62-69 insulin Homo sapiens 114-121 22606236-10 2012 CONCLUSIONS/SIGNIFICANCE: The rs3743462 polymorphism affects glucose-responsive NR2F2 promoter regulation and thereby may influence whole-body insulin sensitivity, suggesting a role of NR2F2 in the control of glucose homeostasis in humans. Glucose 61-68 insulin Homo sapiens 143-150 22348058-1 2012 Insulin/IGF-1 signaling plays a pivotal role in the regulation of cellular homeostasis through its control of glucose metabolism as well as due to its effects on cell proliferation. Glucose 110-117 insulin Homo sapiens 0-7 22412906-9 2012 N-glycosylation is also required for expression of the GIP receptor at the plasma membrane and efficient GIP potentiation of glucose-induced insulin secretion from the INS-1 pancreatic beta cell line. Glucose 125-132 insulin Homo sapiens 141-148 22509346-7 2012 The results show that the system"s metabolic profile changes dramatically in the presence of high concentrations of glucose, and that these changes are modulated by the presence of insulin. Glucose 116-123 insulin Homo sapiens 181-188 22272238-5 2012 In vitro, the particles demonstrated triggered release of insulin upon exposure to physiologically relevant concentrations of glucose (10 mmoles/L-40 mmoles/L). Glucose 126-133 insulin Homo sapiens 58-65 22403629-7 2012 The risk C-allele of rs151290 was nominally associated with reduced first-phase glucose-stimulated insulin secretion, while the non-risk T-allele of rs2237892 was significantly correlated with increased second-phase glucose-stimulated insulin secretion (p = 0.025 and 0.0016, respectively). Glucose 80-87 insulin Homo sapiens 99-106 22272238-6 2012 The agglomerates were also shown to be responsive to multiple spikes in glucose levels over several hours, releasing insulin at a rate defined by the concentration of the glucose trigger. Glucose 72-79 insulin Homo sapiens 117-124 22272238-6 2012 The agglomerates were also shown to be responsive to multiple spikes in glucose levels over several hours, releasing insulin at a rate defined by the concentration of the glucose trigger. Glucose 171-178 insulin Homo sapiens 117-124 23196582-4 2012 Low level of fasting plasma glucose is a characteristic feature in the early stage of glucose intolerance in DM1, Early intervention against insulin resistance in DM1 is suggested because glucose intolerance could deteriorate in a certain degree of cases. Glucose 28-35 insulin Homo sapiens 141-148 22347395-11 2012 Plasma IL-6 concentrations increase in response to glucose and insulin, consistent with both an early glucose-dependent response (detectable at 1-2 hours) and a late insulin-dependent response (detectable after 2 hours). Glucose 51-58 insulin Homo sapiens 166-173 22347395-11 2012 Plasma IL-6 concentrations increase in response to glucose and insulin, consistent with both an early glucose-dependent response (detectable at 1-2 hours) and a late insulin-dependent response (detectable after 2 hours). Glucose 102-109 insulin Homo sapiens 63-70 22994093-13 2012 CONCLUSION: The combination therapy with SUD and insulin sensitizers was stated to be effective in maintaining the reached blood glucose level, reducing the risk of hypoglycemic reactions, and positively affecting lipid metabolism. Glucose 129-136 insulin Homo sapiens 49-56 22990548-1 2012 The values of the glucose influence the status of the periodontium, but also the periodontitis influences the glucose balance by increasing the resistance to insulin. Glucose 18-25 insulin Homo sapiens 158-165 22990548-1 2012 The values of the glucose influence the status of the periodontium, but also the periodontitis influences the glucose balance by increasing the resistance to insulin. Glucose 110-117 insulin Homo sapiens 158-165 22247191-1 2011 GLUT4 is an insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat and muscle cells. Glucose 30-37 insulin Homo sapiens 12-19 22232606-12 2011 Indeed insulin-stimulated glucose uptake and glycogen synthesis is elevated after exercise, which, from an evolutional point of view, will favor glycogen repletion and preparation for new "fight or flight" events. Glucose 26-33 insulin Homo sapiens 7-14 22065581-10 2011 PASK p.G1117E-infected islets displayed a 4-fold decrease in glucose-stimulated (16.7 versus 3 mM) insulin secretion, chiefly reflecting a 4.5-fold increase in insulin release at low glucose. Glucose 61-68 insulin Homo sapiens 99-106 22002247-1 2011 Phosphoinositide 3-kinase (PI3K) signaling promotes the translocation of the glucose transporter, GLUT4, to the plasma membrane in insulin-sensitive tissues to facilitate glucose uptake. Glucose 77-84 insulin Homo sapiens 131-138 22002247-2 2011 In adipocytes, insulin-stimulated reorganization of the actin cytoskeleton has been proposed to play a role in promoting GLUT4 translocation and glucose uptake, in a PI3K-dependent manner. Glucose 145-152 insulin Homo sapiens 15-22 22834331-4 2012 This involves a) beta-oxidation of fatty acids in the mitochondria, b) synthesis of C 16:0 palmitic saturated fatty acid, c) glucose metabolism in pro- and eukaryotes, d) regulation of biochemical reactions in insulin-independent cells, e) humoral effects of mediators at the level of paracrine cell communities which are structural and functional units of all internal organs, and f) hormonal regulation at the entire organism level. Glucose 125-132 insulin Homo sapiens 210-217 22834331-9 2012 If insulin resistance results from changes in the primary structure of transport proteins, in glucose storage and cellular insulin reception, it can be referred to as type II diabetes mellitus. Glucose 94-101 insulin Homo sapiens 3-10 22247191-1 2011 GLUT4 is an insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat and muscle cells. Glucose 30-37 insulin Homo sapiens 74-81 21907249-5 2011 In contrast, the NPY increase during ITT was completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. Glucose 99-106 insulin Homo sapiens 117-124 27004135-9 2012 Maintenance of secretory granules and glucose-stimulated insulin secretion was confirmed following transport. Glucose 38-45 insulin Homo sapiens 57-64 22215075-28 2011 While the low oxygen stress does not cause a pronounced drop in viability, it is clearly impacting MIN6 aggregation and function as measured by glucose-stimulated insulin secretion. Glucose 144-151 insulin Homo sapiens 163-170 21828338-9 2011 Taken together, these data support a new model, wherein glucose stimulates Cav-1 and induces its dissociation from Cdc42, possibly via Src kinase activation to phosphorylate Cav-1(Tyr14), to promote Cdc42-betaPix binding and Cdc42 activation, and to trigger downstream signaling and ultimately sustain insulin release. Glucose 56-63 insulin Homo sapiens 302-309 21968139-11 2011 The Pro12Ala polymorphism was associated with significant changes in insulin-to-glucose ratio after treatment (P=0.015 and P=0.005). Glucose 80-87 insulin Homo sapiens 69-76 21968131-4 2011 Atazanavir sulfate + ritonavir treatment for 48 h completely prevented insulin stimulation of glucose uptake (P>0.05). Glucose 94-101 insulin Homo sapiens 71-78 21900125-4 2011 In this cohort, plasma PTX3 was negatively correlated with fasting triglyceride levels and insulin secretion after intravenous and oral glucose administration. Glucose 136-143 insulin Homo sapiens 91-98 21900125-10 2011 In conclusion, the negative correlation between PTX3 and glucose-stimulated insulin secretion suggests a role for PTX3 in metabolic control. Glucose 57-64 insulin Homo sapiens 76-83 21975647-2 2011 GLP-1 receptor (GLP-1R) agonists applied peripherally or centrally decrease food intake and increase glucose-stimulated insulin secretion. Glucose 101-108 insulin Homo sapiens 120-127 22158537-4 2011 GLIS3, which is involved in pancreatic beta cell development and insulin gene expression, is known for its association with fasting glucose levels. Glucose 132-139 insulin Homo sapiens 65-72 21735081-4 2011 Insulin sensitivity was measured with estimated glucose disposal rate calculated using the equation: eGDR = 24.31 - (12.22 x WHR) - (3.29 x HT) - (0.57 x HbA1c); WHR = waist to hip ratio, HT = hypertension. Glucose 48-55 insulin Homo sapiens 0-7 21924490-9 2011 The recovered cell spheroids released insulin in response to glucose treatment, demonstrating the cytocompatibility of thiol-ene hydrogels and the enzymatic mechanism of cell spheroids recovery. Glucose 61-68 insulin Homo sapiens 38-45 22247912-5 2011 Our studies found that visfatin is not only a surrogate marker of systemic inflammation in type 2 diabetic patients but is also up-regulated in diabetic kidney through the uptake of glucose into renal cells, which leads to the activation of the intracellular insulin signaling pathway and pro-inflammatory mechanisms. Glucose 182-189 insulin Homo sapiens 259-266 22078152-11 2011 beta-cell response to postprandial glucose increments was assessed by the ratio between incremental AUC of insulin and glucose during MTT. Glucose 35-42 insulin Homo sapiens 107-114 21736687-3 2011 Consequently, it is currently under debate whether the high doses of exogenous insulin that were administered in these trials to achieve strict target glucose levels could be responsible for these unexpected outcomes. Glucose 151-158 insulin Homo sapiens 79-86 21945562-1 2011 We assessed the oral glucose tolerance test"s (OGTT) ability to produce consistent results for estimating insulin sensitivity over four consecutive days. Glucose 21-28 insulin Homo sapiens 106-113 22028180-7 2011 Insulin sensitivity and beta-GS were the major determinants of mean OGTT glucose in both NGT and IGR, with a minor role for IISR. Glucose 73-80 insulin Homo sapiens 0-7 22348917-2 2011 However, when treating diabetes, clinical inertia seems to be the rule, despite the availability of effective therapies and recommendations for early insulin replacement to improve glucose control and prevent diabetes complications. Glucose 181-188 insulin Homo sapiens 150-157 21615395-4 2011 Donors" insulin sensitivity was calculated from plasma insulin and glucose levels during oral glucose tolerance test (OGTT) and hyperinsulinemic-euglycemic clamp. Glucose 67-74 insulin Homo sapiens 8-15 21615395-4 2011 Donors" insulin sensitivity was calculated from plasma insulin and glucose levels during oral glucose tolerance test (OGTT) and hyperinsulinemic-euglycemic clamp. Glucose 94-101 insulin Homo sapiens 8-15 21558143-7 2011 DISCUSSION: It has been demonstrated that AAS use, specifically growth hormone, can affect glucose homeostasis through increasing cellular insulin resistance and reducing glucose uptake. Glucose 91-98 insulin Homo sapiens 139-146 23204821-4 2011 Insulin resistance is a common feature of hypertension in both humans and animal models affecting glucose and lipid metabolism producing excess aldehydes including methylglyoxal. Glucose 98-105 insulin Homo sapiens 0-7 21946079-4 2011 The in vitro insulin release study revealed that the microhydrogels could quickly respond to the changes of glucose concentrations in the medium and small change in pH value of the environment. Glucose 108-115 insulin Homo sapiens 13-20 21792063-4 2011 Insulin resistance (IR) was estimated using the homeostatic model assessment (HOMA) (HOMA >= 3.8), which was calculated as fasting plasma glucose (mmol/L) times fasting serum insulin (mU/L) divided by 22.5. Glucose 141-148 insulin Homo sapiens 0-7 22208713-4 2011 In contrast, the latest real-time devices, whether linked or not to an insulin pump, give the patient access to glucose measurements and incorporate alarms that can be set. Glucose 112-119 insulin Homo sapiens 71-78 22208718-5 2011 The key obstacles to achieving permanent normal glucose control are related to the delay of insulin action when infused subcutaneously or, at a lesser extent, into the peritoneal cavity, and blood glucose estimation made by subcutaneous interstitial measurement. Glucose 48-55 insulin Homo sapiens 92-99 22408591-5 2011 Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated using fasting glucose and insulin level as a marker of IR. Glucose 90-97 insulin Homo sapiens 32-39 21631893-5 2011 Metformin achieves glycemic control by reducing hepatic glucose production and increasing the muscle intake of glucose, thus lowering levels of circulating glucose and, consequently, insulin. Glucose 111-118 insulin Homo sapiens 183-190 22207907-3 2011 Insulin, growth hormone (GH), and insulin-like growth factor 1 (IGF-1) are involved in glucose, protein, and fat metabolism, which regulates body composition. Glucose 87-94 insulin Homo sapiens 0-7 21956413-0 2011 Exogenous insulin enhances glucose-stimulated insulin response in healthy humans independent of changes in free fatty acids. Glucose 27-34 insulin Homo sapiens 10-17 21956413-0 2011 Exogenous insulin enhances glucose-stimulated insulin response in healthy humans independent of changes in free fatty acids. Glucose 27-34 insulin Homo sapiens 46-53 21956413-2 2011 Recent studies suggest insulin signaling is physiologically important for glucose sensing. Glucose 74-81 insulin Homo sapiens 23-30 21956413-3 2011 OBJECTIVE: Preexposure to insulin enhances glucose-stimulated insulin secretion (GSIS) in healthy humans. Glucose 43-50 insulin Homo sapiens 26-33 21956413-7 2011 INTERVENTIONS: Glucose-induced insulin response was assessed on three occasions after 4 h saline (low insulin/sham) or isoglycemic-hyperinsulinemic (high insulin) clamps with or without intralipid and heparin infusion, using B28 Asp-insulin that could be distinguished from endogenous insulin immunologically. Glucose 15-22 insulin Homo sapiens 31-38 21956413-7 2011 INTERVENTIONS: Glucose-induced insulin response was assessed on three occasions after 4 h saline (low insulin/sham) or isoglycemic-hyperinsulinemic (high insulin) clamps with or without intralipid and heparin infusion, using B28 Asp-insulin that could be distinguished from endogenous insulin immunologically. Glucose 15-22 insulin Homo sapiens 102-109 21956413-7 2011 INTERVENTIONS: Glucose-induced insulin response was assessed on three occasions after 4 h saline (low insulin/sham) or isoglycemic-hyperinsulinemic (high insulin) clamps with or without intralipid and heparin infusion, using B28 Asp-insulin that could be distinguished from endogenous insulin immunologically. Glucose 15-22 insulin Homo sapiens 102-109 21956413-7 2011 INTERVENTIONS: Glucose-induced insulin response was assessed on three occasions after 4 h saline (low insulin/sham) or isoglycemic-hyperinsulinemic (high insulin) clamps with or without intralipid and heparin infusion, using B28 Asp-insulin that could be distinguished from endogenous insulin immunologically. Glucose 15-22 insulin Homo sapiens 102-109 21956413-10 2011 RESULTS: Preexposure to exogenous insulin increased the endogenous insulin-secretory response to glucose by 32% compared with sham clamp (P = 0.001). Glucose 97-104 insulin Homo sapiens 34-41 21956413-10 2011 RESULTS: Preexposure to exogenous insulin increased the endogenous insulin-secretory response to glucose by 32% compared with sham clamp (P = 0.001). Glucose 97-104 insulin Homo sapiens 67-74 21956413-13 2011 CONCLUSIONS: Insulin potentiates glucose-stimulated insulin response independent of FFA concentrations in healthy humans. Glucose 33-40 insulin Homo sapiens 13-20 21956413-13 2011 CONCLUSIONS: Insulin potentiates glucose-stimulated insulin response independent of FFA concentrations in healthy humans. Glucose 33-40 insulin Homo sapiens 52-59 21631893-5 2011 Metformin achieves glycemic control by reducing hepatic glucose production and increasing the muscle intake of glucose, thus lowering levels of circulating glucose and, consequently, insulin. Glucose 111-118 insulin Homo sapiens 183-190 21556834-6 2011 Insulin-stimulated glucose uptake was measured with positron emission tomography using 2- [(18)F]-fluoro-2-deoxyglucose during euglycemic hyperinsulinemia. Glucose 19-26 insulin Homo sapiens 0-7 21556834-8 2011 Compared with controls, insulin-stimulated glucose uptake in adipose tissue was decreased by ~50% in all groups with the m.3243A > G mutation. Glucose 43-50 insulin Homo sapiens 24-31 22068124-7 2011 A slight, transient rise in plasma glucose (p<0.05) concomitant with the decline in serum insulin was also observed. Glucose 35-42 insulin Homo sapiens 93-100 21343902-2 2011 DESIGN: Cross sectional and longitudinal clinical study: we investigated the association of peripheral insulin concentrations in response to an oral glucose tolerance test (OGTT) with subsequent measures of ad libitum food intake and body weight change. Glucose 149-156 insulin Homo sapiens 103-110 21922329-1 2011 GLP-1 is an insulinotropic hormone that synergistically with glucose gives rise to an increased insulin response. Glucose 61-68 insulin Homo sapiens 12-19 22068124-8 2011 INTERPRETATION: It is possible that the effect of Mg(2+) on insulin may have been due to antagonism of Ca(2+) entry in pancreatic beta-cells, the insulin decline causing a subsequent rise in circulating glucose levels. Glucose 203-210 insulin Homo sapiens 60-67 21606871-4 2011 We hypothesized that (i) prediabetic subjects would have greater endurance training-induced changes in plasma glucose and insulin responses to an oral glucose challenge compared with age- and body mass index-matched normoglycemic subjects and (ii) training would completely reverse the abnormal glucose metabolism of prediabetic subjects. Glucose 151-158 insulin Homo sapiens 122-129 21820141-0 2011 Use of a two-stage insulin infusion study to assess the relationship between insulin suppression of lipolysis and insulin-mediated glucose uptake in overweight/obese, nondiabetic women. Glucose 131-138 insulin Homo sapiens 77-84 21632069-5 2011 Adiponectin stimulates insulin secretion by enhancing exocytosis of insulin granules and upregulating the expression of the insulin gene; however, this effect depends on the prevailing glucose concentration and status of insulin resistance. Glucose 185-192 insulin Homo sapiens 23-30 21632070-1 2011 The objective was to compare relationships between insulin-mediated glucose uptake and surrogate estimates of insulin action, particularly those using fasting triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) concentrations. Glucose 68-75 insulin Homo sapiens 51-58 21632070-2 2011 Insulin-mediated glucose uptake was quantified by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test in 455 nondiabetic subjects. Glucose 17-24 insulin Homo sapiens 0-7 21632070-2 2011 Insulin-mediated glucose uptake was quantified by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test in 455 nondiabetic subjects. Glucose 17-24 insulin Homo sapiens 126-133 21632070-2 2011 Insulin-mediated glucose uptake was quantified by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test in 455 nondiabetic subjects. Glucose 86-93 insulin Homo sapiens 0-7 21820141-0 2011 Use of a two-stage insulin infusion study to assess the relationship between insulin suppression of lipolysis and insulin-mediated glucose uptake in overweight/obese, nondiabetic women. Glucose 131-138 insulin Homo sapiens 77-84 21820141-2 2011 Resistance to insulin-mediated glucose disposal and higher daylong FFA concentrations occur more commonly in obese individuals. Glucose 31-38 insulin Homo sapiens 14-21 21820141-3 2011 However, the relationship between the ability of insulin to suppress FFA release from adipose tissue and stimulate glucose disposal in muscle has not been clearly defined in this population. Glucose 115-122 insulin Homo sapiens 49-56 21820141-4 2011 The current study was initiated to test the hypothesis that these 2 facets of insulin action are related, with greater defects in insulin-mediated glucose disposal associated with less effective insulin inhibition of FFA release from adipose tissue. Glucose 147-154 insulin Homo sapiens 78-85 21820141-4 2011 The current study was initiated to test the hypothesis that these 2 facets of insulin action are related, with greater defects in insulin-mediated glucose disposal associated with less effective insulin inhibition of FFA release from adipose tissue. Glucose 147-154 insulin Homo sapiens 130-137 21820141-4 2011 The current study was initiated to test the hypothesis that these 2 facets of insulin action are related, with greater defects in insulin-mediated glucose disposal associated with less effective insulin inhibition of FFA release from adipose tissue. Glucose 147-154 insulin Homo sapiens 130-137 21820141-5 2011 Subjects included 56 healthy nondiabetic overweight/moderately obese women classified as insulin resistant or insulin sensitive based on whole-body glucose disposal. Glucose 148-155 insulin Homo sapiens 110-117 21820141-10 2011 Overweight/moderately obese women exhibit dramatic differences in the ability of insulin to suppress plasma FFA, which correlate highly with differences in insulin-mediated glucose disposal. Glucose 173-180 insulin Homo sapiens 81-88 21820141-10 2011 Overweight/moderately obese women exhibit dramatic differences in the ability of insulin to suppress plasma FFA, which correlate highly with differences in insulin-mediated glucose disposal. Glucose 173-180 insulin Homo sapiens 156-163 21998054-0 2011 Fasting and post-glucose load measures of insulin resistance and risk of ischemic stroke in older adults. Glucose 17-24 insulin Homo sapiens 42-49 22002509-1 2011 The explanation for the rapid improvement in insulin resistance after Roux-en Y gastric bypass (RYGB) may involve mechanisms additional to caloric restriction and improvements in peripheral glucose disposal. Glucose 190-197 insulin Homo sapiens 45-52 22002509-8 2011 However, 6 days after RYGB, IVITT showed worsened insulin induced glucose uptake (p < 0.05). Glucose 66-73 insulin Homo sapiens 50-57 22590838-9 2011 Mean blood glucose level was not significantly different in the two groups at the beginning of the ICU admission; however, mean glucose level in insulin-metformin group, twelve hours after the initiation of the study, was significantly lower than insulin group (p < 0.05). Glucose 128-135 insulin Homo sapiens 145-152 22295709-10 2011 The levels of insulin and C peptide secretion increased with glucose stimulation. Glucose 61-68 insulin Homo sapiens 14-21 21998054-1 2011 BACKGROUND AND PURPOSE: Few studies have assessed post-glucose load measures of insulin resistance and ischemic stroke risk, and data are sparse for older adults. Glucose 55-62 insulin Homo sapiens 80-87 21998054-4 2011 The Gutt insulin sensitivity index was calculated from baseline body weight and from fasting and 2-hour postload insulin and glucose; a lower Gutt index indicates higher insulin resistance. Glucose 125-132 insulin Homo sapiens 9-16 21998054-10 2011 CONCLUSIONS: In nondiabetic, older adults, insulin resistance measured by Gutt index or 2-hour glucose, but not by fasting insulin, was associated with risk of incident ischemic stroke. Glucose 95-102 insulin Homo sapiens 43-50 22509554-10 2011 C-peptide content of the induced cells measured up to (195.10 +/- 8.88) pmol/L/h (P < 0.01), when exposed to 5.5 mmol/L glucose (P < 0.01). Glucose 123-130 insulin Homo sapiens 0-9 21880378-3 2011 At a cellular level, angiotensin II (Ang II) and aldosterone induce insulin resistance by increasing oxidative stress and altering insulin signaling, leading to decreased glucose transport. Glucose 171-178 insulin Homo sapiens 68-75 21880378-3 2011 At a cellular level, angiotensin II (Ang II) and aldosterone induce insulin resistance by increasing oxidative stress and altering insulin signaling, leading to decreased glucose transport. Glucose 171-178 insulin Homo sapiens 131-138 21880378-5 2011 Aldosterone diminishes glucose-stimulated insulin secretion in vivo and in vitro from isolated pancreatic islets and cultured beta cells through a mineralocorticoid receptor (MR)-independent mechanism. Glucose 23-30 insulin Homo sapiens 42-49 22340792-0 2011 [Effect of insulin by local injection on the level of systemic blood glucose and granulation tissue formation of wound in patients with diabetic foot ulcer]. Glucose 69-76 insulin Homo sapiens 11-18 22340792-1 2011 OBJECTIVE: To investigate the effects of local injection of insulin on the level of systemic blood glucose and granulation tissue formation of wound in patients with diabetic foot ulcer. Glucose 99-106 insulin Homo sapiens 60-67 22340792-13 2011 CONCLUSIONS: Local injection of insulin has a significant effect on systemic blood glucose in patients with diabetic foot ulcer, and it can promote the growth of granulation tissue and wound healing. Glucose 83-90 insulin Homo sapiens 32-39 22509554-11 2011 When stimulated with 22 mmol/L glucose, the c-peptide content of the induced cells increased to (340.99 +/- 7.91) pmol/L/h (P < 0.01 ). Glucose 31-38 insulin Homo sapiens 44-53 21948391-4 2011 For example, many intensive care units currently implement insulin infusion protocols to better control patients" blood glucose levels. Glucose 120-127 insulin Homo sapiens 59-66 21948391-10 2011 To illustrate these points, we present a detailed analysis of the relationship between blood glucose levels and insulin doses on the basis of data from an intensive care unit. Glucose 93-100 insulin Homo sapiens 112-119 22195816-0 2011 Modulated insulin release from glucose-sensitive multilayer films. Glucose 31-38 insulin Homo sapiens 10-17 21843518-1 2011 BACKGROUND: Detection of below-threshold first-phase insulin release or FPIR (1+3 minute insulin concentrations during an intravenous glucose tolerance test [IVGTT]) is important in type 1 diabetes prediction and prevention studies including the TrialNet Oral Insulin Prevention Trial. Glucose 134-141 insulin Homo sapiens 53-60 24843526-8 2011 These results show that chronic elevation of the glucose level might impair endogenous insulin secretion after meal load, but might have little effect on endogenous insulin secretion after glucagon load. Glucose 49-56 insulin Homo sapiens 87-94 21984830-2 2011 It is known that IAPP can inhibit glucose-stimulated insulin secretion; however, the mechanisms of action have not yet been established. Glucose 34-41 insulin Homo sapiens 53-60 21984830-4 2011 These cells showed intracellular oligomers and a strong alteration of glucose-stimulated insulin and IAPP secretion. Glucose 70-77 insulin Homo sapiens 89-96 21984830-10 2011 We concluded that the hIAPP overexpression inhibits insulin and IAPP secretion in response to glucose affecting the activity of K(ATP) channels and that the increased mitochondrial metabolism is a compensatory response to counteract the secretory defect of beta-cells. Glucose 94-101 insulin Homo sapiens 52-59 22654826-1 2011 Ever since the discovery of insulin and its role in the regulation of glucose uptake and utilization, there has been great interest in insulin, its structure and the way in which it interacts with its receptor and effects signal transduction. Glucose 70-77 insulin Homo sapiens 28-35 22654826-1 2011 Ever since the discovery of insulin and its role in the regulation of glucose uptake and utilization, there has been great interest in insulin, its structure and the way in which it interacts with its receptor and effects signal transduction. Glucose 70-77 insulin Homo sapiens 135-142 21843518-1 2011 BACKGROUND: Detection of below-threshold first-phase insulin release or FPIR (1+3 minute insulin concentrations during an intravenous glucose tolerance test [IVGTT]) is important in type 1 diabetes prediction and prevention studies including the TrialNet Oral Insulin Prevention Trial. Glucose 134-141 insulin Homo sapiens 89-96 22074365-9 2011 RESULTS: A meal x time effect (p = 0.0003) was noted for insulin, with values highest for the dextrose meals at the 0.5 hr and 1 hr times, and relatively unaffected by the lipid meals. Glucose 94-102 insulin Homo sapiens 57-64 21930600-2 2011 Gap-junctions coordinate oscillations in intracellular free-calcium ([Ca(2+)](i)) and insulin secretion in the islet following elevated glucose. Glucose 136-143 insulin Homo sapiens 86-93 22074365-12 2011 An AUC effect was noted for insulin (p = 0.001), with values higher for the dextrose meals compared to the lipid meals (p < 0.05). Glucose 76-84 insulin Homo sapiens 28-35 21075579-11 2011 Once an urgent situation has been handled with intravenous push of a 10% calcium salt, short-term measures should be started with agents that cause a transcellular shift of potassium, namely, insulin with glucose, beta2-agonist, and NaHCO(3). Glucose 205-212 insulin Homo sapiens 192-199 22071283-3 2011 Closed-loop insulin delivery (artificial pancreas) is a recent medical innovation, aiming to reduce the risk of hypoglycemia while achieving tight control of glucose. Glucose 158-165 insulin Homo sapiens 12-19 22071283-4 2011 Characterized by real-time glucose-responsive insulin administration, closed-loop systems combine glucose-sensing and insulin-delivery components. Glucose 27-34 insulin Homo sapiens 46-53 22071283-4 2011 Characterized by real-time glucose-responsive insulin administration, closed-loop systems combine glucose-sensing and insulin-delivery components. Glucose 27-34 insulin Homo sapiens 118-125 22071283-4 2011 Characterized by real-time glucose-responsive insulin administration, closed-loop systems combine glucose-sensing and insulin-delivery components. Glucose 98-105 insulin Homo sapiens 46-53 22071283-5 2011 In the most viable and researched configuration, a disposable sensor measures interstitial glucose levels, which are fed into a control algorithm controlling delivery of a rapid-acting insulin analog into the subcutaneous tissue by an insulin pump. Glucose 91-98 insulin Homo sapiens 185-192 22071283-5 2011 In the most viable and researched configuration, a disposable sensor measures interstitial glucose levels, which are fed into a control algorithm controlling delivery of a rapid-acting insulin analog into the subcutaneous tissue by an insulin pump. Glucose 91-98 insulin Homo sapiens 235-242 21757774-7 2011 The correlation between insulin and fasting glucose levels in AN-negative or AN-positive patients was low (R (2) = 13% to 17%). Glucose 44-51 insulin Homo sapiens 24-31 22009997-15 2011 CONCLUSIONS: An intravenous infusion including a dextrose:insulin ratio of 3.3:1, compared with a higher ratio, results in less hyperglycemia and appears to be as effective in decreasing potassium concentrations in newborns. Glucose 49-57 insulin Homo sapiens 58-65 21794908-4 2011 Modified islets retained the ability to control insulin release in response to glucose concentration changes. Glucose 79-86 insulin Homo sapiens 48-55 21488836-3 2011 Among these factors, the cAMP-responsive element-binding protein (CREB) has emerged as a key transcriptional element for the maintenance of an efficient glucose sensing, insulin exocytosis, insulin gene transcription and beta-cell survival. Glucose 153-160 insulin Homo sapiens 170-177 21635675-3 2011 The amount of glucose infused at steady-state to maintain stable blood glucose [90 mg/dl (4.95 mmol/l)] was used to calculate several indices of insulin sensitivity. Glucose 14-21 insulin Homo sapiens 145-152 21635675-9 2011 These observed changes in insulin sensitivity are likely to be clinically relevant, especially in individuals predisposed to develop glucose intolerance. Glucose 133-140 insulin Homo sapiens 26-33 21911750-6 2011 In addition, insulin-stimulated glucose uptake was completely suppressed in myocytes from obese impaired glucose tolerant and T2D subjects. Glucose 32-39 insulin Homo sapiens 13-20 22069287-4 2011 Conversion of PP to glucose-responsive insulin-secreting cells can be achieved by transplanting the progenitors in vivo where cell maturation occurs. Glucose 20-27 insulin Homo sapiens 39-46 21827318-5 2011 The primary objective was to assess the frequency of hypoglycemic episodes when using the LGS feature with an insulin delivery shutoff of a maximum of 2 h at a sensor glucose level below 70 mg/dL (3.9 mmol/L). Glucose 167-174 insulin Homo sapiens 110-117 21835486-1 2011 AIM: To examine the effects of glibenclamide and repaglinide on glucose stimulated insulin release, incretins, oxidative stress and cell adhesion molecules in patients with type 2 diabetes suboptimally treated with metformin. Glucose 64-71 insulin Homo sapiens 83-90 21919776-6 2011 We preferentially adjusted the basal insulin dose to control fasting and preprandial blood glucose. Glucose 91-98 insulin Homo sapiens 37-44 21988213-5 2011 RESULTS: Insulin detemir significantly improved glycemic control, with a decrease in mean HbA1c, fasting glucose and within-patient fasting glucose variability. Glucose 105-112 insulin Homo sapiens 9-16 21988213-5 2011 RESULTS: Insulin detemir significantly improved glycemic control, with a decrease in mean HbA1c, fasting glucose and within-patient fasting glucose variability. Glucose 140-147 insulin Homo sapiens 9-16 21871559-2 2011 Here, using IHECs stably transfected with promoter-luciferase reporter vectors, we found that insulin increased GCLc promoter activity, which required a prerequisite increase or decrease in medium glucose. Glucose 197-204 insulin Homo sapiens 94-101 21871559-6 2011 Insulin-tBH coadministration abrogated the low or high glucose requirement for promoter activation, suggesting possible ROS involvement. Glucose 55-62 insulin Homo sapiens 0-7 23525024-5 2011 RESULTS: Baseline plasma glucose levels in the group treated with insulin were higher. Glucose 25-32 insulin Homo sapiens 66-73 21841493-1 2011 Glucose management in patients with burn injury is often difficult because of their hypermetabolic state with associated hyperglycemia, hyperinsulinemia, and insulin resistance. Glucose 0-7 insulin Homo sapiens 141-148 21865364-5 2011 RESULTS: Insulin sensitivity (M-value, i.e. glucose infusion rate divided by lean body mass) during the last 60 min of the clamp was higher during infusion with atropine than saline (9.2 +- 1.0 vs. 7.6 +- 1.0 mg/kg lean body mass min, mean +- sem; P = 0.015) in all subjects. Glucose 44-51 insulin Homo sapiens 9-16 21623155-1 2011 OBJECTIVE: To establish if glucose management with continuous intravenous insulin infusion (CII) in the early post-operative period after coronary artery bypass graft (CABG) surgery is associated with complication rate and length of hospital stay (LOS) in patients with diabetes mellitus (DM). Glucose 27-34 insulin Homo sapiens 74-81 22226267-1 2011 BACKGROUND: The Paradigm Veo System includes a low glucose suspend (LGS) feature which suspends insulin delivery when a prespecified glucose threshold setting is reached by the associated continuous glucose monitoring (CGM) sensor. Glucose 52-59 insulin Homo sapiens 97-104 22226267-1 2011 BACKGROUND: The Paradigm Veo System includes a low glucose suspend (LGS) feature which suspends insulin delivery when a prespecified glucose threshold setting is reached by the associated continuous glucose monitoring (CGM) sensor. Glucose 134-141 insulin Homo sapiens 97-104 22226267-1 2011 BACKGROUND: The Paradigm Veo System includes a low glucose suspend (LGS) feature which suspends insulin delivery when a prespecified glucose threshold setting is reached by the associated continuous glucose monitoring (CGM) sensor. Glucose 134-141 insulin Homo sapiens 97-104 21750207-2 2011 Typically, insulin protocols require a dextrose solution to prevent hypoglycemia. Glucose 39-47 insulin Homo sapiens 11-18 21967317-8 2011 Insulin resistance resulted from a defect in glycogen synthesis, whereas insulin-mediated suppression of glucose production was unaltered. Glucose 105-112 insulin Homo sapiens 73-80 21550078-8 2011 Insulin therapy reduced blood glucose, inhibited pancreatic lipid accumulation and islet beta-cell apoptosis, and increased beta-cell proliferation and beta-cell area in glucose-intolerant rats. Glucose 30-37 insulin Homo sapiens 0-7 21875604-5 2011 If insulin"s effects on microcirculatory function indeed play a physiological role in regulating insulin-mediated glucose uptake, such effects should be demonstrable not only during steady-state hyperinsulinemia, but also after meal ingestion. Glucose 114-121 insulin Homo sapiens 3-10 21875604-5 2011 If insulin"s effects on microcirculatory function indeed play a physiological role in regulating insulin-mediated glucose uptake, such effects should be demonstrable not only during steady-state hyperinsulinemia, but also after meal ingestion. Glucose 114-121 insulin Homo sapiens 97-104 21878900-6 2011 Differentiated cells secreted insulin in a glucose responsive manner. Glucose 43-50 insulin Homo sapiens 30-37 22411395-7 2011 RESULTS: As quartile for cord blood insulin levels increased, glucose, the insulin/cortisol ratio and HOMA-IR (all p < 0.001) and IGF-I (p < 0.01) increased while QUICKI and the glucose/insulin ratio (both p < 0.001) and GH (p < 0.05) decreased. Glucose 62-69 insulin Homo sapiens 36-43 21593800-5 2011 Insulin-supplemented frequently-sampled intravenous glucose tolerance test (fsIVGTT) was performed before and after equivalent weight reduction. Glucose 52-59 insulin Homo sapiens 0-7 21593800-6 2011 MINMOD analysis of insulin sensitivity (Si), acute insulin response to glucose (AIRg) and C-peptide (ACPRg) response to glucose, and insulin secretion normalized to the degree of insulin resistance (disposition index (DI)) were analyzed. Glucose 71-78 insulin Homo sapiens 51-58 21593800-6 2011 MINMOD analysis of insulin sensitivity (Si), acute insulin response to glucose (AIRg) and C-peptide (ACPRg) response to glucose, and insulin secretion normalized to the degree of insulin resistance (disposition index (DI)) were analyzed. Glucose 71-78 insulin Homo sapiens 51-58 21593800-6 2011 MINMOD analysis of insulin sensitivity (Si), acute insulin response to glucose (AIRg) and C-peptide (ACPRg) response to glucose, and insulin secretion normalized to the degree of insulin resistance (disposition index (DI)) were analyzed. Glucose 71-78 insulin Homo sapiens 51-58 21847559-0 2011 Involvement of phosphatidylinositol 5-phosphate in insulin-stimulated glucose uptake in the L6 myotube model of skeletal muscle. Glucose 70-77 insulin Homo sapiens 51-58 21847559-1 2011 The phosphoinositide phospholipid PtdIns5P has previously been implicated in insulin-stimulated translocation of the glucose transporter GLUT4 into the plasma membrane of adipocytes, but its potential role in glucose transport in muscle has not been explored. Glucose 117-124 insulin Homo sapiens 77-84 21847559-2 2011 The involvement of PtdIns5P in insulin-stimulated glucose uptake was therefore investigated in myotubes of the skeletal muscle cell line L6. Glucose 50-57 insulin Homo sapiens 31-38 21847559-6 2011 Our results are consistent with a role for insulin-stimulated PtdIns5P production in regulating glucose transport by promoting PI 3-kinase signalling. Glucose 96-103 insulin Homo sapiens 43-50 21782840-1 2011 Insulin secretion from pancreatic beta cells is stimulated by glucagon-like peptide-1 (GLP-1), a blood glucose-lowering hormone that is released from enteroendocrine L cells of the distal intestine after the ingestion of a meal. Glucose 103-110 insulin Homo sapiens 0-7 21920379-8 2011 The explicit incorporation of Ca2+ channels, Ca2+ and cAMP dynamics allows the model to be further connected to current models for calcium and metabolic dynamics and provides an interpretation of the roles of the triggering and amplifying pathways of glucose-stimulated insulin secretion. Glucose 251-258 insulin Homo sapiens 270-277 22102801-1 2011 Insulin, the primary hormone regulating the level of glucose in the bloodstream, modulates a variety of cellular and enzymatic processes in normal and diseased cells. Glucose 53-60 insulin Homo sapiens 0-7 21638183-2 2011 METHODS: Insulin secretion and peripheral insulin sensitivity using the intravenous glucose tolerance test (IVGTT) were assessed in 18 obese type 2 diabetic patients and in 10 nondiabetic obese patients before and 3 days after SG, before any food intake and any weight change occurrence. Glucose 84-91 insulin Homo sapiens 42-49 21638183-5 2011 The early insulin area under the curve (AUC) significantly increased at the postoperative IVGTT, indicating an increased glucose-induced insulin secretion. Glucose 121-128 insulin Homo sapiens 10-17 21871813-4 2011 They interact with the Rab GTPase-activating proteins AS160 and TBC1D1 to regulate glucose uptake into target tissues in response to insulin and energy stress. Glucose 83-90 insulin Homo sapiens 133-140 22099772-8 2011 The viability of the sheets was measured using fluorescein diacetate (FDA)/propidium iodide (PI), and function was measured through glucose-stimulated insulin release, in which the sheets were incubated for an hour in low-glucose concentration (2.8 mmol/L) and then high (28 mmol/L), then high (28 mmol/L) plus 3-isobutyl-1-methylxanthine (50 mum). Glucose 132-139 insulin Homo sapiens 151-158 22099772-9 2011 Human islet sheets remained both viable, above 70%, and functional, with a stimulation index (insulin secretion in high glucose divided by insulin secretion in low glucose) above 1.5, over 8 weeks of culture or subcutaneous transplantation. Glucose 120-127 insulin Homo sapiens 94-101 22168140-12 2011 CONCLUSIONS: The substantially lower glucose-induced insulin response in adult porcine islet preparations as opposed to islets manufactured from humans or macaques combined with the much higher need for insulin in macaques than in humans creates an imbalance between the metabolic demand and the engrafted islet mass in the pig-to-NHP xenograft recipient. Glucose 37-44 insulin Homo sapiens 53-60 21803140-5 2011 Furthermore, we revealed that subcutaneous administration of an insulin glargine solution with SBE4-beta-CyD to rats enhanced the bioavailability of insulin glargine and sustained the glucose lowering effect, possibly due to the inhibitory effects of SBE4-beta-CyD on the enzymatic degradation at the injection site. Glucose 184-191 insulin Homo sapiens 64-71 21817852-0 2011 Insulin-dependent suppression of cholesterol 7alpha-hydroxylase is a possible link between glucose and cholesterol metabolisms. Glucose 91-98 insulin Homo sapiens 0-7 22675089-2 2011 Although the mechanism has not been clarified yet, increased insulin sensitivity as well as decreased insulin degradation is suggested to contribute to the reduction in serum glucose levels. Glucose 175-182 insulin Homo sapiens 61-68 22049574-9 2004 GLUT4 and HKII are the major transporter and HK isoform in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. Glucose 128-135 insulin Homo sapiens 111-118 22029671-6 2011 In addition, many cancer patients exhibit an altered glucose metabolism characterized by insulin resistance and may profit from an increased protein and fat intake.In this review, we address the possible beneficial effects of low CHO diets on cancer prevention and treatment. Glucose 53-60 insulin Homo sapiens 89-96 21801736-4 2011 Body fatness was evaluated using anthropometric techniques, and insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Glucose 121-128 insulin Homo sapiens 64-71 21813109-12 2011 Insulin-mediated suppression of nonesterified fatty acids during extended glucose tolerance test was significantly less effective during treatment than during placebo. Glucose 74-81 insulin Homo sapiens 0-7 21869742-3 2011 METHODS: Human islets were cultured in medium supplemented with or without GDNF (100 ng/mL) and in vitro islet survival and function assessed by analyzing beta-cell apoptosis and glucose stimulated insulin release. Glucose 179-186 insulin Homo sapiens 198-205 21854074-1 2011 The free fatty acid receptor 1 (FFA1, also known as GPR40) enhances glucose-stimulated insulin secretion from pancreatic beta-cells and is recognized as an interesting new target for treatment of type 2 diabetes. Glucose 68-75 insulin Homo sapiens 87-94 21635925-7 2011 The link high PYY(3-36)-high insulin level was evident in subjects with normal glucose tolerance (p<0.05). Glucose 79-86 insulin Homo sapiens 29-36 21975769-15 2011 Insulin infusion resulted in significant increases in non-protein energy intake, glucose intake, and short-term weight gain.Meetze 1998 compared insulin infusion with reduction of glucose infusion. Glucose 81-88 insulin Homo sapiens 0-7 21975769-15 2011 Insulin infusion resulted in significant increases in non-protein energy intake, glucose intake, and short-term weight gain.Meetze 1998 compared insulin infusion with reduction of glucose infusion. Glucose 180-187 insulin Homo sapiens 0-7 21975769-17 2011 Insulin infusion resulted in significant increases in glucose intake and total energy intake. Glucose 54-61 insulin Homo sapiens 0-7 21975772-20 2011 Refinement of algorithms to guide insulin infusion is needed to enable tight control of glucose concentrations within the target range. Glucose 88-95 insulin Homo sapiens 34-41 21982703-3 2011 (2011) show that high lipid levels induce nuclear exclusion of Foxa2 and HNF1alpha in beta cells, leading to impaired expression and glycosylation of proteins controlling glucose-stimulated insulin secretion. Glucose 171-178 insulin Homo sapiens 190-197 21969324-0 2011 Letter by Taegtmeyer and Khalaf regarding article, "Glucose-insulin-potassium reduces the incidence of low cardiac output episodes after aortic valve replacement for aortic stenosis in patients with left ventricular hypertrophy: results from the hypertrophy, insulin, glucose, and electrolytes (HINGE) trial". Glucose 268-275 insulin Homo sapiens 60-67 23346606-3 2011 Intensive insulin therapy is defined as an intravenous infusion of insulin and glucose with or without potassium. Glucose 79-86 insulin Homo sapiens 10-17 21693690-8 2011 Furthermore, NOD1 activation suppresses insulin signaling, as revealed by attenuated tyrosine phosphorylation and increased inhibitory serine phosphorylation, of IRS-1 and attenuated phosphorylation of Akt and downstream target GSK3alpha/3beta, resulting in decreased insulin-induced glucose uptake in 3T3-L1 adipocytes. Glucose 284-291 insulin Homo sapiens 40-47 21518259-6 2011 The postprandial glucose response differed significantly between insulin regimens with a postprandial increase on NPH insulin and a decrease on insulin aspart. Glucose 17-24 insulin Homo sapiens 65-72 21518259-9 2011 The rapid-acting insulin analogue aspart and the intermediate-acting insulin NPH had different effects on postprandial glucose response but similar postprandial effects on markers of inflammation and endothelial dysfunction. Glucose 119-126 insulin Homo sapiens 17-24 21518259-9 2011 The rapid-acting insulin analogue aspart and the intermediate-acting insulin NPH had different effects on postprandial glucose response but similar postprandial effects on markers of inflammation and endothelial dysfunction. Glucose 119-126 insulin Homo sapiens 69-76 21806589-6 2011 Women with GDM who required insulin therapy had greater body mass index (BMI), were more likely to have previous GDM, had higher fasting glucose level on 75-g oral glucose tolerance test (OGTT) and were diagnosed with GDM at an earlier stage of their pregnancy. Glucose 137-144 insulin Homo sapiens 28-35 21806589-6 2011 Women with GDM who required insulin therapy had greater body mass index (BMI), were more likely to have previous GDM, had higher fasting glucose level on 75-g oral glucose tolerance test (OGTT) and were diagnosed with GDM at an earlier stage of their pregnancy. Glucose 164-171 insulin Homo sapiens 28-35 21806589-7 2011 On multivariate logistic regression analysis, BMI, fasting glucose level and 2-h glucose level on OGTT and gestational week when GDM was diagnosed were all independent predictors for requirement of insulin therapy. Glucose 59-66 insulin Homo sapiens 198-205 21806589-7 2011 On multivariate logistic regression analysis, BMI, fasting glucose level and 2-h glucose level on OGTT and gestational week when GDM was diagnosed were all independent predictors for requirement of insulin therapy. Glucose 81-88 insulin Homo sapiens 198-205 21885970-7 2011 A variety of dynamic tests are available to directly measure insulin-mediated glucose uptake. Glucose 78-85 insulin Homo sapiens 61-68 21488836-3 2011 Among these factors, the cAMP-responsive element-binding protein (CREB) has emerged as a key transcriptional element for the maintenance of an efficient glucose sensing, insulin exocytosis, insulin gene transcription and beta-cell survival. Glucose 153-160 insulin Homo sapiens 190-197 21773684-0 2011 C-peptide reduces high-glucose-induced apoptosis of endothelial cells and decreases NAD(P)H-oxidase reactive oxygen species generation in human aortic endothelial cells. Glucose 23-30 insulin Homo sapiens 0-9 21569186-4 2011 However, the most probable explanation is that because of the lowering of insulin resistance there are decreases in hepatic glucose production and an increased uptake of glucose leading to decreased levels of postprandial glucose, free fatty acids and triglycerides, which cause decreases in inflammation, oxidative stress and accumulation of atheroma. Glucose 124-131 insulin Homo sapiens 74-81 21569186-4 2011 However, the most probable explanation is that because of the lowering of insulin resistance there are decreases in hepatic glucose production and an increased uptake of glucose leading to decreased levels of postprandial glucose, free fatty acids and triglycerides, which cause decreases in inflammation, oxidative stress and accumulation of atheroma. Glucose 170-177 insulin Homo sapiens 74-81 21773684-6 2011 We hypothesised that C-peptide reduces glucose-induced ROS generation by decreasing NAD(P)H oxidase activation and prevents apoptosis METHODS: Human aortic endothelial cells (HAEC) were exposed to 25 mmol/l glucose in the presence or absence of C-peptide and tested for protein quantity and activity of caspase-3 and other apoptosis markers by ELISA, TUNEL and immunoblotting. Glucose 39-46 insulin Homo sapiens 21-30 21779873-1 2011 AIMS/HYPOTHESIS: Individuals with impaired glucose tolerance have increased proinsulin levels, despite normal glucose or C-peptide levels. Glucose 43-50 insulin Homo sapiens 76-86 21782317-8 2011 Glucose stimulation test results showed that significantly greater amounts of C-peptide and insulin were released from differentiated cells than from undifferentiated cells. Glucose 0-7 insulin Homo sapiens 78-87 21782317-8 2011 Glucose stimulation test results showed that significantly greater amounts of C-peptide and insulin were released from differentiated cells than from undifferentiated cells. Glucose 0-7 insulin Homo sapiens 92-99 21773684-6 2011 We hypothesised that C-peptide reduces glucose-induced ROS generation by decreasing NAD(P)H oxidase activation and prevents apoptosis METHODS: Human aortic endothelial cells (HAEC) were exposed to 25 mmol/l glucose in the presence or absence of C-peptide and tested for protein quantity and activity of caspase-3 and other apoptosis markers by ELISA, TUNEL and immunoblotting. Glucose 207-214 insulin Homo sapiens 21-30 21796486-3 2011 METHODS: An unbiased metabolite profiling analysis (GC-time-of-flight-MS) was used to identify the time course of core metabolite patterns in rat beta cell line INS-1E during exposure to high glucose concentrations and its relation to insulin expression. Glucose 192-199 insulin Homo sapiens 235-242 21773684-12 2011 Glucose-induced ROS production was quenched by C-peptide and this was associated with a decreased NAD(P)H oxidase activity and reduced RAC-1 membrane production and GTPase activity. Glucose 0-7 insulin Homo sapiens 47-56 21773684-13 2011 CONCLUSIONS/INTERPRETATION: In glucose-exposed endothelial cells, C-peptide acts as an endogenous antioxidant molecule by reducing RAC-1 translocation to membrane and NAD(P)H oxidase activation. Glucose 31-38 insulin Homo sapiens 66-75 21773684-14 2011 By preventing oxidative stress, C-peptide protects endothelial cells from glucose-induced apoptosis. Glucose 74-81 insulin Homo sapiens 32-41 21774690-9 2011 In varying insulin sensitivity conditions, the percentage of time glucose levels were below 70 mg/dL was significantly reduced by approximately sevenfold (P<0.001). Glucose 66-73 insulin Homo sapiens 11-18 21873549-2 2011 Higher circulating proinsulin levels are associated with impaired beta-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Glucose 93-100 insulin Homo sapiens 19-29 21873549-2 2011 Higher circulating proinsulin levels are associated with impaired beta-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Glucose 93-100 insulin Homo sapiens 22-29 21873549-7 2011 The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 x 10(-4)), improved beta-cell function (P = 1.1 x 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 x 10(-6)). Glucose 75-82 insulin Homo sapiens 4-14 21873552-5 2011 Insulin sensitivity was assessed by glucose clamps. Glucose 36-43 insulin Homo sapiens 0-7 21923697-8 2011 We found a progressive significant increase (P < 0.001) of insulin resistance from subjects with normal glucose tolerance without the hypertriglyceridaemic waist phenotype with respect to patients with impaired glucose tolerance with the hypertriglyceridaemic waist phenotype. Glucose 107-114 insulin Homo sapiens 62-69 21933842-4 2011 METHODS: Insulin action was quantified by determining steady-state plasma glucose (SSPG) concentrations during the insulin suppression test. Glucose 74-81 insulin Homo sapiens 9-16 22010364-0 2011 The key to glucose: a guide to the hormone (and protein) insulin. Glucose 11-18 insulin Homo sapiens 57-64 22111033-4 2011 The glucose-regulatory actions of these agents function by increasing insulin secretion and suppressing glucagon. Glucose 4-11 insulin Homo sapiens 70-77 21846802-5 2011 Effects of NIK overexpression on insulin-stimulated glucose uptake were estimated using tritiated 2-deoxyglucose uptake. Glucose 52-59 insulin Homo sapiens 33-40 21846802-8 2011 Enhanced NIK expression in cultured L6 myotubes induced a dose-dependent decrease in insulin-stimulated glucose uptake. Glucose 104-111 insulin Homo sapiens 85-92 21846802-9 2011 The decrease in insulin-stimulated glucose uptake was associated with a significant decrease in PI3 kinase activity and protein kinase B/Akt phosphorylation. Glucose 35-42 insulin Homo sapiens 16-23 21775499-9 2011 Gene expression of NDUFA5, NDUFA10, COX11, and ATP6V1H correlated positively with glucose-stimulated insulin secretion (P<0.03). Glucose 82-89 insulin Homo sapiens 101-108 21707884-1 2011 AIM: Hepatitis C virus infection often complicates glucose intolerance, which can be caused by insulin resistance. Glucose 53-60 insulin Homo sapiens 97-104 22056828-2 2011 Intensive glucose lowering with insulin is generally favored for seriously ill hospitalized patients, but after discharge, patients often resume their prior regimens, which may include an array of oral or injected glucose-lowering agents. Glucose 10-17 insulin Homo sapiens 32-39 22281887-2 2011 The objective of this study was to investigate if hyperinsulinemia during the oral glucose tolerance test (GTT) stimulates Ct secretion in normal subjects as well as to examine the relationship between serum cortisol and Ct. DESIGN: In 26 normal subjects (9 men and 17 women) with detectable basal serum Ct, aged 22-70 yr [51.5+-14.6 (mean+-SD), median 55.5], we measured serum or plasma Ct, cortisol, ACTH, insulin, and blood glucose before (0 min) and at 30, 60, 90, and 120 min after ingestion of 75 g glucose. Glucose 83-90 insulin Homo sapiens 55-62 21792921-0 2011 Thyroid hormone promotes insulin-induced glucose uptake by enhancing Akt phosphorylation and VAMP2 translocation in 3T3-L1 adipocytes. Glucose 41-48 insulin Homo sapiens 25-32 21792921-1 2011 The purpose of this study was to test a hypothesis that T3 promotes glucose uptake via enhancing insulin-induced Akt phosphorylation and VAMP2 translocation in 3T3-L1 adipocytes. Glucose 68-75 insulin Homo sapiens 97-104 21792921-2 2011 T3 significantly enhanced insulin-induced phosphorylation of Akt, cytoplasma to cell membrane translocations of vesicle-associated membrane protein 2 (VAMP2) and glucose transporter 4 (GLUT4), and glucose uptake in adipocytes. Glucose 162-169 insulin Homo sapiens 26-33 21792921-4 2011 Knockdown of VAMP2 using siRNA abrogated the effects of T3 on insulin-induced GLUT4 translocation and glucose uptake, suggesting that VAMP2 is an important mediator of these processes. Glucose 102-109 insulin Homo sapiens 62-69 21792921-5 2011 These data suggest that T3 may promote glucose uptake via enhancing insulin-induced phosphorylation of Akt and subsequent translocations of VAMP2 and GLUT4 in 3T3-L1 adipocytes. Glucose 39-46 insulin Homo sapiens 68-75 21792921-7 2011 Further, VAMP2 is essential for T3 to increase insulin-stimulated translocation of GLUT4 and subsequent uptake of glucose in adipocytes. Glucose 114-121 insulin Homo sapiens 47-54 21241371-8 2011 Oral glucose tolerance tests yielded a correlation between the PASI and plasma levels for C-peptide (r = 0.73, P = 0.02) at t = 120 min in patients with a pathological Homeostasis Model Assessment (>2.5), indicating that the state of peripheral insulin resistance is driven at least in part by the severity of the psoriatic inflammation. Glucose 5-12 insulin Homo sapiens 248-255 21666414-2 2011 Recent observations suggest that a defective glucose stimulated insulin secretion by glucagon-like peptide-1 (GLP- 1) plays a role in the pathogenesis of DM2. Glucose 45-52 insulin Homo sapiens 64-71 21746792-0 2011 Intensive insulin treatment induces insulin resistance in diabetic rats by impairing glucose metabolism-related mechanisms in muscle and liver. Glucose 85-92 insulin Homo sapiens 10-17 21746792-0 2011 Intensive insulin treatment induces insulin resistance in diabetic rats by impairing glucose metabolism-related mechanisms in muscle and liver. Glucose 85-92 insulin Homo sapiens 36-43 21881525-3 2011 Here, we evaluated the associations between insulin sensitivity/resistance and central BP using the oral glucose tolerance test. Glucose 105-112 insulin Homo sapiens 44-51 21661079-1 2011 GLP-1 is an incretin peptide involved in the regulation of glucose metabolism and the glucose-dependent stimulation of insulin secretion. Glucose 86-93 insulin Homo sapiens 119-126 21914084-3 2011 To date, all human studies except for four where IR was evaluated in the HCV setting, an estimation of IR has been used rather than direct measurements of insulin-mediated glucose uptake. Glucose 172-179 insulin Homo sapiens 155-162 21914084-4 2011 The most commonly used estimation in the HCV population is the homeostasis model assessment of insulin resistance (HOMA-IR) which is calculated from a single measurement of fasting insulin and glucose. Glucose 193-200 insulin Homo sapiens 95-102 21616512-10 2011 At the end of surgery, plasma glucose concentration was significantly lower in the insulin group (4.2 +- 0.6 vs 7.3 +- 1.0 mmol/L, P = .0001), whereas plasma cortisol levels did not show any difference between groups. Glucose 30-37 insulin Homo sapiens 83-90 21861804-2 2011 What is incomprehensible is that the detrimental ROS also plays a substantial role in the normal insulin signal transduction and glucose-stimulated insulin secretion (GSIS) in beta-cell, which forces us to re-recognize the role of ROS under physiological and pathological conditions in a more broad way. Glucose 129-136 insulin Homo sapiens 148-155 21904878-1 2011 Glucagon-like peptide-1 (GLP-1) stimulates insulin secretion from pancreatic beta-cells in a glucose-dependent manner. Glucose 93-100 insulin Homo sapiens 43-50 21904878-5 2011 When beta-cells were exposed to a high concentration of glucose (25 mM), which stimulates insulin secretion, exe-4-induced cAMP formation declined gradually as exposure time was increased. Glucose 56-63 insulin Homo sapiens 90-97 21904878-7 2011 HNMPA was able to further increase the exe-4-induced insulin secretion when beta-cells were exposed to high glucose for 18 h. Treatment of beta-cells with insulin significantly decreased exe-4-induced cAMP formation in a dose-dependent manner. Glucose 108-115 insulin Homo sapiens 53-60 21904878-7 2011 HNMPA was able to further increase the exe-4-induced insulin secretion when beta-cells were exposed to high glucose for 18 h. Treatment of beta-cells with insulin significantly decreased exe-4-induced cAMP formation in a dose-dependent manner. Glucose 108-115 insulin Homo sapiens 155-162 21626002-7 2011 siRNA-mediated knock down of nm23-H1 and PHP in insulin-secreting INS 832/13 cells significantly attenuated glucose-induced insulin secretion. Glucose 108-115 insulin Homo sapiens 48-55 21829172-8 2011 The cells often lack the crucial function of regulated insulin secretion upon glucose stimulation. Glucose 78-85 insulin Homo sapiens 55-62 22046124-6 2011 These metabolic changes are accompanied by enhanced glucose-stimulated insulin secretion, normoglycemia, upregulation of insulinotropic amino acids in islets, elevated plasma leptin and adiponectin, and diminished gut microbial diversity of the Clostridium leptum group. Glucose 52-59 insulin Homo sapiens 71-78 22015080-9 2011 Impaired glucose metabolism ranges from insulin resistance to overt diabetes mellitus, which is a frequent finding and is associated with worse outcome. Glucose 9-16 insulin Homo sapiens 40-47 22262069-9 2011 Current studies are evaluating the potential benefits of combining incretin therapies with basal insulin to provide continuous glucose control before and after meals. Glucose 127-134 insulin Homo sapiens 97-104 22262075-1 2011 GLP-1-modulating therapies are a class of anti-diabetic drugs that improve glycemic control by stimulating glucose-dependent insulin secretion from pancreatic beta-cells. Glucose 107-114 insulin Homo sapiens 125-132 21922355-2 2011 However, conventional intensive insulin therapy (IIT), which consists of intermittent blood glucose measurement and manually controlled infusions of insulin, tends to induce hypoglycemia and glucose variability. Glucose 92-99 insulin Homo sapiens 32-39 21922355-2 2011 However, conventional intensive insulin therapy (IIT), which consists of intermittent blood glucose measurement and manually controlled infusions of insulin, tends to induce hypoglycemia and glucose variability. Glucose 191-198 insulin Homo sapiens 32-39 21922355-2 2011 However, conventional intensive insulin therapy (IIT), which consists of intermittent blood glucose measurement and manually controlled infusions of insulin, tends to induce hypoglycemia and glucose variability. Glucose 191-198 insulin Homo sapiens 149-156 22004441-13 2011 Intensive insulin therapy (80-110 mg/dL), which appears beneficial in critically ill surgical patients but requires frequent measurement of glucose to avoid hypoglycemia. Glucose 140-147 insulin Homo sapiens 10-17 21813649-10 2011 Together, these data demonstrate that TNF-alpha-mediated insulin resistance of glucose uptake can occur through a MEK/Erk-dependent activation of CDK5. Glucose 79-86 insulin Homo sapiens 57-64 21816162-0 2011 Human cholesteryl ester transfer protein enhances insulin-mediated glucose uptake in adipocytes. Glucose 67-74 insulin Homo sapiens 50-57 21816162-10 2011 SIGNIFICANCE: Human CETP expression increased cellular cholesterol levels and enhanced insulin-stimulated Akt phosphorylation and glucose uptake in adipocytes. Glucose 130-137 insulin Homo sapiens 87-94 21867683-1 2011 The aim of this study was to investigate whether cap-independent insulin mRNA translation occurs in human pancreatic islets at basal conditions, during stimulation at a high glucose concentration and at conditions of nitrosative stress. Glucose 174-181 insulin Homo sapiens 65-72 21867683-7 2011 We observed that in the presence of 1.67 mM glucose, approximately 70% of the insulin mRNA translation was inhibited by hippuristanol. Glucose 44-51 insulin Homo sapiens 78-85 21867683-9 2011 DETA/NO treatment significantly decreased the translation of insulin by 85% in high glucose incubated islets, and by 50% at a low glucose concentration. Glucose 84-91 insulin Homo sapiens 61-68 21867683-9 2011 DETA/NO treatment significantly decreased the translation of insulin by 85% in high glucose incubated islets, and by 50% at a low glucose concentration. Glucose 130-137 insulin Homo sapiens 61-68 21867683-10 2011 The lowered insulin biosynthesis rates of DETA/NO-exposed islets were further suppressed by hippuristanol with 55% at 16.7 mM glucose but not at 1.67 mM glucose. Glucose 126-133 insulin Homo sapiens 12-19 21867683-13 2011 In conclusion, our studies show that insulin biosynthesis is mainly cap-dependent at a high glucose concentration, but that the cap-independent biosynthesis of insulin can constitute as much as 40-100% of all insulin biosynthesis during conditions of nitrosative stress. Glucose 92-99 insulin Homo sapiens 37-44 21871446-2 2011 We have previously demonstrated that insulin-stimulated NO synthesis is inhibited under high culture glucose conditions, without altering Ca(2+)-stimulated NO synthesis or insulin-stimulated phosphorylation of eNOS. Glucose 101-108 insulin Homo sapiens 37-44 21779606-0 2011 A glucose-responsive controlled release of insulin system based on enzyme multilayers-coated mesoporous silica particles. Glucose 2-9 insulin Homo sapiens 43-50 21779606-1 2011 A novel glucose-responsive controlled release of insulin system is constructed through coating enzyme multilayers on mesoporous silica particles (MSPs). Glucose 8-15 insulin Homo sapiens 49-56 21779606-2 2011 The MSPs serve as the drug reservoir, and the enzyme multilayers cross-linked with glutaraldehyde act as a valve to control the release of insulin in response to the external glucose level. Glucose 175-182 insulin Homo sapiens 139-146 21901697-11 2011 AUTHORS" CONCLUSIONS: With the current evidence, we found that the administration of intravenous insulin with the objective of maintaining serum glucose within a specific range in the first hours of acute ischaemic stroke does not provide benefit in terms of functional outcome, death, or improvement in final neurological deficit and significantly increased the number of hypoglycaemic episodes. Glucose 145-152 insulin Homo sapiens 97-104 21553243-8 2011 The insulin secretion/insulin resistance (disposition) index was calculated as the ratio between incremental area under the ISR curve ( ISR[AUC]) to incremental area under the glucose curve ( G[AUC]) factored by the severity of insulin resistance (measured by Matsuda index during OGTT or glucose disposal during insulin clamp). Glucose 176-183 insulin Homo sapiens 4-11 21813803-9 2011 These cured mice maintain normal insulin content and were more sensitive to insulin than control mice, a compensatory mechanism that together with basal insulin secretion may be sufficient to maintain near-normal glucose levels. Glucose 213-220 insulin Homo sapiens 76-83 21813803-12 2011 Although untreated NDM mice rapidly lose insulin content and progress to permanently extremely elevated blood glucose levels, early tight control of blood glucose may permit this insulin-hypersensitivity, in combination with maintained basal insulin secretion, to provide long-term remission. Glucose 155-162 insulin Homo sapiens 179-186 21824260-0 2011 Brain glucose sensing and neural regulation of insulin and glucagon secretion. Glucose 6-13 insulin Homo sapiens 47-54 21824263-3 2011 As a corollary, during hypoglycaemia beta-cells would stop secreting insulin, which would permit alpha-cells to release glucagon into the hepatic portal circulation so it could travel to the liver to increase glucose production and thereby correct hypoglycaemia. Glucose 209-216 insulin Homo sapiens 69-76 21553243-8 2011 The insulin secretion/insulin resistance (disposition) index was calculated as the ratio between incremental area under the ISR curve ( ISR[AUC]) to incremental area under the glucose curve ( G[AUC]) factored by the severity of insulin resistance (measured by Matsuda index during OGTT or glucose disposal during insulin clamp). Glucose 289-296 insulin Homo sapiens 4-11 21126160-6 2011 Seventy-five grams oral glucose tolerance tests performed via feeding tubes in two patients after the successful treatment of HHS revealed increased insulin resistance and diminished early-phase insulin secretion with preserved total insulin secretion. Glucose 24-31 insulin Homo sapiens 149-156 21126160-6 2011 Seventy-five grams oral glucose tolerance tests performed via feeding tubes in two patients after the successful treatment of HHS revealed increased insulin resistance and diminished early-phase insulin secretion with preserved total insulin secretion. Glucose 24-31 insulin Homo sapiens 195-202 21126160-6 2011 Seventy-five grams oral glucose tolerance tests performed via feeding tubes in two patients after the successful treatment of HHS revealed increased insulin resistance and diminished early-phase insulin secretion with preserved total insulin secretion. Glucose 24-31 insulin Homo sapiens 195-202 22040435-11 2011 However, insulin levels increased significantly when INS-1 cells were exposed to a high glucose environment (P < 0.05). Glucose 88-95 insulin Homo sapiens 9-16 21865944-2 2011 SUMMARY OF BACKGROUND DATA: Maintaining serum glucose levels between 120 and 180 mg/dL with continuous insulin infusions decreases morbidity in diabetic patients undergoing CABG surgery. Glucose 46-53 insulin Homo sapiens 103-110 21865944-7 2011 Patients with aggressive control had a lower mean glucose at the end of 18 hours of insulin infusion (135 +- 12 mg/dL moderate vs 103 +- 17 mg/dL aggressive; P < 0.0001). Glucose 50-57 insulin Homo sapiens 84-91 21943503-1 2011 Short-term nutritional supplementation stimulates folliculogenesis in ewes probably by insulin-mediated actions of glucose in the follicle. Glucose 115-122 insulin Homo sapiens 87-94 21869620-2 2011 The aim of this study was to analyze and to compare the acute insulin response using a common but high glucose concentration in the dialysate representing a parenteral mode of glucose administration to oral glucose administration in stable and fasting nondiabetic hemodialysis patients during their routine hemodialysis session. Glucose 103-110 insulin Homo sapiens 62-69 21869620-2 2011 The aim of this study was to analyze and to compare the acute insulin response using a common but high glucose concentration in the dialysate representing a parenteral mode of glucose administration to oral glucose administration in stable and fasting nondiabetic hemodialysis patients during their routine hemodialysis session. Glucose 176-183 insulin Homo sapiens 62-69 21869620-2 2011 The aim of this study was to analyze and to compare the acute insulin response using a common but high glucose concentration in the dialysate representing a parenteral mode of glucose administration to oral glucose administration in stable and fasting nondiabetic hemodialysis patients during their routine hemodialysis session. Glucose 176-183 insulin Homo sapiens 62-69 21869620-4 2011 The insulin response per unit glucose stimulus was determined from the slope of paired insulin and glucose concentrations measured in 15-minute intervals using standard techniques. Glucose 30-37 insulin Homo sapiens 4-11 21869620-4 2011 The insulin response per unit glucose stimulus was determined from the slope of paired insulin and glucose concentrations measured in 15-minute intervals using standard techniques. Glucose 30-37 insulin Homo sapiens 87-94 21869620-4 2011 The insulin response per unit glucose stimulus was determined from the slope of paired insulin and glucose concentrations measured in 15-minute intervals using standard techniques. Glucose 99-106 insulin Homo sapiens 4-11 21869620-7 2011 Administration of glucose using dialysate thus leads to a blunted insulin response per unit glucose stimulus. Glucose 18-25 insulin Homo sapiens 66-73 21869620-7 2011 Administration of glucose using dialysate thus leads to a blunted insulin response per unit glucose stimulus. Glucose 92-99 insulin Homo sapiens 66-73 22479085-2 2011 Web-based, patient-specific insulin nomograms may facilitate improved glucose control. Glucose 70-77 insulin Homo sapiens 28-35 22479085-9 2011 CONCLUSIONS: A web-based insulin nomogram was an easy-to-use instrument for achieving tighter glucose control for patients in the cardiovascular surgery ICU. Glucose 94-101 insulin Homo sapiens 25-32 21076998-6 2011 Endogenous glucose production was similar in the two groups of patients in the postabsorptive state and was completely suppressed by insulin infusion. Glucose 11-18 insulin Homo sapiens 133-140 21076998-8 2011 In pooled patients, individual values of hemoglobin concentrations inversely correlated with the rates of insulin-mediated glucose infusion, both as absolute values (r = -0.58; P < 0.05) and as values normalized by steady-state plasma insulin concentration (r = -0.74; P < 0.001). Glucose 123-130 insulin Homo sapiens 106-113 21916833-3 2011 They have various effects, including augmentation of glucose-stimulated insulin secretion (GSIS), actions that promote the cellular assimilation and storage of dietary glucose and lipid as liver and skeletal muscle glycogen and adipocyte triacylglycerol (TAG) respectively. Glucose 53-60 insulin Homo sapiens 72-79 21778879-6 2011 This finding adds a new layer of complexity in the regulation of insulin secretion with implications for glucose and energy homeostasis. Glucose 105-112 insulin Homo sapiens 65-72 21354844-11 2011 CONCLUSION: Insulin analogues have differential effects on the expression of insulin-signaling molecules in human pancreatic islets that are also dependent on the degree of glucose exposure. Glucose 173-180 insulin Homo sapiens 12-19 21354844-5 2011 Functional (glucose-stimulated insulin secretion) and molecular (quantitative RT-PCR and immunoblot) studies were performed at the end of the different incubation conditions. Glucose 12-19 insulin Homo sapiens 31-38 21354844-11 2011 CONCLUSION: Insulin analogues have differential effects on the expression of insulin-signaling molecules in human pancreatic islets that are also dependent on the degree of glucose exposure. Glucose 173-180 insulin Homo sapiens 77-84 21354844-6 2011 RESULTS: Glucose-stimulated insulin secretion was blunted in islets cultured in 22.2 mmol/L of glucose, with no significant effects from the exogenous added insulins. Glucose 9-16 insulin Homo sapiens 28-35 21517955-5 2011 RESULTS: Post-meal, the prandial + basal insulin group had significantly higher insulin, lower glucose and triglycerides, as well as lower high-sensitivity C-reactive protein, tumour necrosis factor alpha and interleukin-6, than the basal insulin group. Glucose 95-102 insulin Homo sapiens 41-48 21354844-6 2011 RESULTS: Glucose-stimulated insulin secretion was blunted in islets cultured in 22.2 mmol/L of glucose, with no significant effects from the exogenous added insulins. Glucose 95-102 insulin Homo sapiens 28-35 21538777-7 2011 RESULTS: The glucose infusion rate required to maintain euglycaemia during the clamps, a marker of whole-body insulin sensitivity, decreased from 11.2 +- 3.7 mg kg(-1) min(-1) at baseline to 9.0 +- 2.6 mg kg(-1) min(-1) (p = 0.015) during the norepinephrine infusion. Glucose 13-20 insulin Homo sapiens 110-117 21488144-1 2011 BACKGROUND: Magnesium modulates insulin-mediated glucose uptake but data regarding its role in insulin secretion are scarce; therefore, in this study we determined whether decreased serum magnesium levels are associated with the impairment of insulin secretion in non-diabetic individuals. Glucose 49-56 insulin Homo sapiens 32-39 21679232-5 2011 Women treated with metformin and/or insulin had significantly higher BMIs compared with those in the diet group (P < 0.001) and had a higher fasting glucose at diagnosis (p < 0.001). Glucose 152-159 insulin Homo sapiens 36-43 21612404-5 2011 Following induction, siRNA-MOCK-transfected cells differentiated into beta-cell-like cells that expressed multiple islet cell markers and produced insulin and C-peptide in a glucose-regulated manner. Glucose 174-181 insulin Homo sapiens 159-168 21688198-13 2011 Secreted MEDA-7 attenuates insulin-stimulated glucose uptake in 3T3-L1 adipocytes, while downregulating glucose transporter-4 and upregulating both monocyte chemotactic protein-1 and suppressor of cytokine signalling-3. Glucose 46-53 insulin Homo sapiens 27-34 21711120-3 2011 Intensification in these circumstances has traditionally been achieved by the addition of short-acting insulin to cover postprandial glucose excursions that are not targeted by basal insulin. Glucose 133-140 insulin Homo sapiens 103-110 21750275-0 2011 Declining beta-cell function relative to insulin sensitivity with escalating OGTT 2-h glucose concentrations in the nondiabetic through the diabetic range in overweight youth. Glucose 86-93 insulin Homo sapiens 41-48 21750275-2 2011 We hypothesized that beta-cell function relative to insulin sensitivity decreases with increasing 2-h glucose levels based on an oral glucose tolerance test (OGTT) in overweight youth. Glucose 102-109 insulin Homo sapiens 52-59 21750275-6 2011 RESULTS: Insulin sensitivity, first-phase insulin, and DI declined significantly as 2-h glucose concentrations increased. Glucose 88-95 insulin Homo sapiens 9-16 21750275-9 2011 CONCLUSIONS: These data in overweight youth demonstrate that impairment in insulin secretion relative to insulin sensitivity is apparent even with normal glucose tolerance. Glucose 154-161 insulin Homo sapiens 75-82 21755313-11 2011 When transplanted into mouse models for diabetes, these insulin-producing cells could decrease blood glucose levels in approximately 50% of the mice. Glucose 101-108 insulin Homo sapiens 56-63 21775756-2 2011 We examined whether chronic basal insulin treatment with insulin glargine improves glucose-induced insulin secretion. Glucose 83-90 insulin Homo sapiens 34-41 21775756-2 2011 We examined whether chronic basal insulin treatment with insulin glargine improves glucose-induced insulin secretion. Glucose 83-90 insulin Homo sapiens 57-64 21775756-8 2011 In contrast, insulin and C-peptide responses to intravenous glucose administration were significantly greater after the glargine treatment period (P < 0.0001, respectively). Glucose 60-67 insulin Homo sapiens 13-20 21775756-8 2011 In contrast, insulin and C-peptide responses to intravenous glucose administration were significantly greater after the glargine treatment period (P < 0.0001, respectively). Glucose 60-67 insulin Homo sapiens 25-34 21775756-11 2011 CONCLUSIONS: Chronic supplementation of long-acting basal insulin improves glucose-induced insulin secretion in hyperglycemic patients with type 2 diabetes, whereas acute exogenous insulin administration reduces the beta-cell response to glucose administration. Glucose 75-82 insulin Homo sapiens 58-65 21775756-11 2011 CONCLUSIONS: Chronic supplementation of long-acting basal insulin improves glucose-induced insulin secretion in hyperglycemic patients with type 2 diabetes, whereas acute exogenous insulin administration reduces the beta-cell response to glucose administration. Glucose 75-82 insulin Homo sapiens 91-98 21788626-0 2011 Cross-sectional and longitudinal changes of glucose effectiveness in relation to glucose tolerance: the insulin resistance atherosclerosis study. Glucose 44-51 insulin Homo sapiens 104-111 21810597-11 2011 Insulin-mediated glucose disposal was significantly reduced in obese men. Glucose 17-24 insulin Homo sapiens 0-7 21810601-2 2011 Recently, a combined analysis of several genome-wide association studies (Meta-analysis of Glucose and Insulin-Related Traits Consortium [MAGIC]) showed association to postprandial insulin at the GIP receptor (GIPR) locus. Glucose 91-98 insulin Homo sapiens 181-188 21843305-3 2011 METHODS: Insulin-naive Dutch patients with Type 2 diabetes in suboptimal glycaemic control (HbA(1c) > 53 mmol/mol; 7%) on maximum dose of oral glucose-lowering medications were included from 363 primary care practices (n = 911). Glucose 146-153 insulin Homo sapiens 9-16 21868778-1 2011 OBJECTIVE: To evaluate a sensor-augmented insulin pump with a low glucose suspend (LGS) feature that automatically suspends basal insulin delivery for up to 2 h in response to sensor-detected hypoglycemia. Glucose 66-73 insulin Homo sapiens 42-49 21454236-1 2011 OBJECTIVE: To investigate whether changing the prandial regular insulin to rapid-acting insulin analogue in hospital medicine wards improves the timing of insulin delivery in relation to meals and improves patient safety and glucose control. Glucose 225-232 insulin Homo sapiens 64-71 21454236-1 2011 OBJECTIVE: To investigate whether changing the prandial regular insulin to rapid-acting insulin analogue in hospital medicine wards improves the timing of insulin delivery in relation to meals and improves patient safety and glucose control. Glucose 225-232 insulin Homo sapiens 88-95 21454236-1 2011 OBJECTIVE: To investigate whether changing the prandial regular insulin to rapid-acting insulin analogue in hospital medicine wards improves the timing of insulin delivery in relation to meals and improves patient safety and glucose control. Glucose 225-232 insulin Homo sapiens 88-95 21712361-2 2011 Evidence reveals a hidden cost of hyperinsulinemia on plasma membrane (PM) phosphatidylinositol 4,5-bisphosphate (PIP(2))-regulated filamentous actin (F-actin) structure, components critical to the normal operation of the insulin-regulated glucose transport system. Glucose 240-247 insulin Homo sapiens 39-46 21712361-3 2011 Here we delineated whether increased glucose flux through the hexosamine biosynthesis pathway (HBP) causes PIP(2)/F-actin dysregulation and subsequent insulin resistance. Glucose 37-44 insulin Homo sapiens 151-158 21286922-4 2011 Hyperglycemia (10 mM) with insulin infused at 300 mU/m(2)/min over a 2-h period resulted in a total glucose uptake of 275 g (assessed by the area under the curve) of which glucose storage accounted for about 73% (i.e. 198 g). Glucose 100-107 insulin Homo sapiens 27-34 21286922-4 2011 Hyperglycemia (10 mM) with insulin infused at 300 mU/m(2)/min over a 2-h period resulted in a total glucose uptake of 275 g (assessed by the area under the curve) of which glucose storage accounted for about 73% (i.e. 198 g). Glucose 172-179 insulin Homo sapiens 27-34 21494874-10 2011 Low-dose insulin (1 nM) decreased Psim, ROS production, and UCP-2, VEGF expression in BRECs at high glucose (30 mM); and high-dose insulin (10 nM, 100nM) recovered Psim, ROS production, and UCP-2, VEGF expression. Glucose 101-108 insulin Homo sapiens 9-16 21622071-1 2011 This paper aims at the development and evaluation of a personalized insulin infusion advisory system (IIAS), able to provide real-time estimations of the appropriate insulin infusion rate for type 1 diabetes mellitus (T1DM) patients using continuous glucose monitors and insulin pumps. Glucose 250-257 insulin Homo sapiens 68-75 21622071-1 2011 This paper aims at the development and evaluation of a personalized insulin infusion advisory system (IIAS), able to provide real-time estimations of the appropriate insulin infusion rate for type 1 diabetes mellitus (T1DM) patients using continuous glucose monitors and insulin pumps. Glucose 250-257 insulin Homo sapiens 166-173 21179000-5 2011 RESULTS: The intra-individual variability (coefficient of variation) ranged from 6% for basal glucose production to 21% for insulin-stimulated glucose disposal (percentage increase from basal). Glucose 143-150 insulin Homo sapiens 124-131 21750413-3 2011 Production of ROS for short periods is associated with an increase in GSIS (glucose-stimulated insulin secretion), but excessive or sustained production of ROS is negatively correlated with the insulin secretory process. Glucose 76-83 insulin Homo sapiens 95-102 21811103-1 2011 The definitive measure of beta-cell quality in an islet is the measurement of beta-cell function, i.e., the ability of the islets to release insulin in a controlled manner in response to minute changes in ambient glucose levels. Glucose 213-220 insulin Homo sapiens 141-148 21811103-2 2011 Continuous flow or dynamic perifusion of the solution containing glucose and secretagogues through the islets is the most accurate assessment of regulated insulin release in vitro. Glucose 65-72 insulin Homo sapiens 155-162 21811103-3 2011 Here, we describe in detail a low cost, mini-perifusion system that can be adapted to any laboratory to assess islet function by examining dynamic insulin release in response to elevated glucose concentrations and addition of secretagogues. Glucose 187-194 insulin Homo sapiens 147-154 21811103-5 2011 A prototypical biphasic response to elevated glucose concentrations was observed with an average 8-fold (above basal) increase in insulin concentration at peak values. Glucose 45-52 insulin Homo sapiens 130-137 21856529-3 2011 Children were classified as having IR if they had a homeostasis model assessment of insulin resistance (insulin [U/mL] x glucose [mmol/L]/22.5) of greater than 4.39.We created receiver operating characteristic curves predicting IR across various thresholds of WC and BMI, and area under the curve was compared. Glucose 121-128 insulin Homo sapiens 84-91 21991713-2 2011 OBJECTIVE: To study the effect of the recommendation to start insulin glargine or insulin determir (long-acting insulin treatment, LAI) at discharge from hospital, on glucose control in the community setting. Glucose 167-174 insulin Homo sapiens 62-69 21737826-1 2011 The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal; however, insulin-stimulated vasodilation is impaired in individuals with type 2 diabetes, limiting perfusion and delivery of glucose and insulin to target tissues. Glucose 78-85 insulin Homo sapiens 28-35 21737826-1 2011 The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal; however, insulin-stimulated vasodilation is impaired in individuals with type 2 diabetes, limiting perfusion and delivery of glucose and insulin to target tissues. Glucose 78-85 insulin Homo sapiens 61-68 21737826-1 2011 The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal; however, insulin-stimulated vasodilation is impaired in individuals with type 2 diabetes, limiting perfusion and delivery of glucose and insulin to target tissues. Glucose 78-85 insulin Homo sapiens 61-68 21737826-1 2011 The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal; however, insulin-stimulated vasodilation is impaired in individuals with type 2 diabetes, limiting perfusion and delivery of glucose and insulin to target tissues. Glucose 78-85 insulin Homo sapiens 61-68 21660954-7 2011 High glucose treatment also abolished the stimulatory effects of insulin on BK(Ca) current density, although insulin continued to increase phosphorylation of Erk and Akt under those conditions. Glucose 5-12 insulin Homo sapiens 65-72 21660954-8 2011 Therefore, in contrast to most other cell types, high glucose abrogates the effects of insulin in podocytes at relatively distal steps in its signaling pathway. Glucose 54-61 insulin Homo sapiens 87-94 21841312-8 2011 These findings suggest that glucose-stimulated translation of proinsulin may require fully modified tRNA(Lys)(UUU), which could potentially explain the molecular pathogenesis of T2D in patients carrying cdkal1 risk alleles. Glucose 28-35 insulin Homo sapiens 62-72 21865645-0 2011 A genetically engineered human pancreatic beta cell line exhibiting glucose-inducible insulin secretion. Glucose 68-75 insulin Homo sapiens 86-93 21865645-8 2011 The cells secreted insulin when stimulated by glucose or other insulin secretagogues, and cell transplantation reversed chemically induced diabetes in mice. Glucose 46-53 insulin Homo sapiens 19-26 22027306-0 2011 Usage and effectiveness of the low glucose suspend feature of the Medtronic Paradigm Veo insulin pump. Glucose 35-42 insulin Homo sapiens 89-96 22027318-1 2011 More than five million Americans use insulin every day for glucose control. Glucose 59-66 insulin Homo sapiens 37-44 22027329-1 2011 From an engineering perspective, controlling blood glucose appears to be a fairly straightforward single input (glucose), single output (insulin) control problem. Glucose 51-58 insulin Homo sapiens 137-144 22346090-0 2011 Post-glucose insulin level in polycystic ovarian syndrome. Glucose 5-12 insulin Homo sapiens 13-20 21618241-5 2011 FFAR1 facilitates glucose-stimulated insulin secretion from pancreatic beta-cells, whereas GPR120 regulates the secretion of glucagon-like peptide-1 in the intestine, as well as insulin sensitivity in macrophages. Glucose 18-25 insulin Homo sapiens 37-44 21914528-10 2011 Moreover, although the precise mechanisms for the arsenic-induced diabetogenic effect are still largely undefined, recent in vitro experimental studies indicated that inorganic arsenic or its metabolites impair insulin-dependent glucose uptake or glucose-stimulated insulin secretion. Glucose 229-236 insulin Homo sapiens 211-218 21855697-5 2011 In this context, it must be emphasized that CVD, 2DM, and hypertension are characterized by resistance to insulin-mediated glucose disposal and that insulin resistance and the compensatory hyperinsulinemia associated with insulin resistance have been shown to be independent predictors of all three clinical syndromes. Glucose 123-130 insulin Homo sapiens 106-113 21311355-9 2011 CONCLUSIONS: The increase in glucose disposal after l-Arg infusion during exercise is likely due to the significantly higher plasma insulin concentration. Glucose 29-36 insulin Homo sapiens 132-139 21489574-6 2011 Multiple regression analyses showed that the significant and positive correlations between serum Ca vs fasting plasma glucose and homeostasis model assessment insulin resistance in men still remained after adjustment for intact PTH as well as age, body weight, height, creatinine, albumin, phosphate, bone metabolic markers, and estradiol (P < .05). Glucose 118-125 insulin Homo sapiens 159-166 21489577-8 2011 After stratification for sex, rs2301699 was significantly associated with the ratio of AUC insulin 0 to 30 minutes to AUC glucose 0 to 30 minutes in women (P = .0097), but not in men (P = .3), in the dominant model. Glucose 122-129 insulin Homo sapiens 91-98 22165780-0 2011 Glucose control in the medical patient: bolus insulin dosing compared to basal-bolus insulin dosing. Glucose 0-7 insulin Homo sapiens 46-53 21850563-7 2011 While insulin therapy in subarachnoid hemorrhage patients was shown to effectively control plasma glucose levels, plasma glucose control was not necessarily reflective of cerebral glucose such that very tight glucose control may lead to neuroglycopenia. Glucose 98-105 insulin Homo sapiens 6-13 21945749-10 2011 Insulin secretion increased in the differentiated islet-like cells in response to high glucose exposure. Glucose 87-94 insulin Homo sapiens 0-7 21330118-10 2011 CONCLUSIONS: In type 1 diabetes, insulin adjustment to avoid hypoglycemia may be useful for meals in which the proportion of carbohydrate absorbed as glucose is <0.75, however the precise level which increases hypoglycaemic risk requires further research. Glucose 150-157 insulin Homo sapiens 33-40 21593812-5 2011 Insulin resistance in mice is linked to ROS production and increased level of protein carbonylation, mitochondrial dysfunction, decreased insulin-stimulated glucose transport, and altered adipokine secretion. Glucose 157-164 insulin Homo sapiens 0-7 21593812-5 2011 Insulin resistance in mice is linked to ROS production and increased level of protein carbonylation, mitochondrial dysfunction, decreased insulin-stimulated glucose transport, and altered adipokine secretion. Glucose 157-164 insulin Homo sapiens 138-145 22783644-6 2011 However, glucose counterregulatory responses are altered in patients with diabetes treated with insulin especially after repeated hypoglycemia or antecedent exercise. Glucose 9-16 insulin Homo sapiens 96-103 21312306-5 2011 Then, the insulin action on glucose disposal rate was measured using the glucose-insulin index, values of the areas under the curves of glucose and insulin during the intraperitoneal glucose tolerance test (IPGTT). Glucose 28-35 insulin Homo sapiens 10-17 21312306-5 2011 Then, the insulin action on glucose disposal rate was measured using the glucose-insulin index, values of the areas under the curves of glucose and insulin during the intraperitoneal glucose tolerance test (IPGTT). Glucose 28-35 insulin Homo sapiens 81-88 21312306-5 2011 Then, the insulin action on glucose disposal rate was measured using the glucose-insulin index, values of the areas under the curves of glucose and insulin during the intraperitoneal glucose tolerance test (IPGTT). Glucose 73-80 insulin Homo sapiens 10-17 21312306-5 2011 Then, the insulin action on glucose disposal rate was measured using the glucose-insulin index, values of the areas under the curves of glucose and insulin during the intraperitoneal glucose tolerance test (IPGTT). Glucose 73-80 insulin Homo sapiens 81-88 21312306-5 2011 Then, the insulin action on glucose disposal rate was measured using the glucose-insulin index, values of the areas under the curves of glucose and insulin during the intraperitoneal glucose tolerance test (IPGTT). Glucose 73-80 insulin Homo sapiens 10-17 21312306-5 2011 Then, the insulin action on glucose disposal rate was measured using the glucose-insulin index, values of the areas under the curves of glucose and insulin during the intraperitoneal glucose tolerance test (IPGTT). Glucose 73-80 insulin Homo sapiens 81-88 21312306-7 2011 An increase of insulin sensitivity by Chlorella was further evaluated using the plasma glucose lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Glucose 87-94 insulin Homo sapiens 15-22 21312306-7 2011 An increase of insulin sensitivity by Chlorella was further evaluated using the plasma glucose lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Glucose 87-94 insulin Homo sapiens 124-131 21336840-1 2011 Incretin hormones are intestinally derived peptides that are known to augment glucose-stimulated insulin secretion and suppress glucagon levels. Glucose 78-85 insulin Homo sapiens 97-104 21916595-1 2011 Pancreatic beta-cells sense and adjust the blood glucose level by secretion of insulin. Glucose 49-56 insulin Homo sapiens 79-86 21915367-2 2011 However, significant gaps in knowledge exist in the understanding of consequences of glucose load during pregnancy, a state of insulin resistance. Glucose 85-92 insulin Homo sapiens 127-134 21510988-4 2011 Sugar-sensitive LbL films and microcapsules have been studied mainly for the development of an artificial pancreas that can release insulin in response to the presence of glucose. Glucose 171-178 insulin Homo sapiens 132-139 21511450-0 2011 Magnolia dealbata Zucc and its active principles honokiol and magnolol stimulate glucose uptake in murine and human adipocytes using the insulin-signaling pathway. Glucose 81-88 insulin Homo sapiens 137-144 21511450-6 2011 Inhibitors of the insulin-signaling pathway abolished the glucose uptake induced by Magnolia dealbata preparations, suggesting that their antidiabetic effects are mediated by this signaling pathway. Glucose 58-65 insulin Homo sapiens 18-25 21511450-8 2011 In summary, Magnolia dealbata and its active principles HK and MG stimulate glucose uptake in insulin-sensitive and insulin-resistant murine and human adipocytes using the insulin signaling pathway. Glucose 76-83 insulin Homo sapiens 94-101 21590789-0 2011 Fitting dynamic models with forcing functions: application to continuous glucose monitoring in insulin therapy. Glucose 73-80 insulin Homo sapiens 95-102 21693703-8 2011 Endogenous knockdown of CREBH led to ablation of 2-AG-induced gluconeogenic gene expression and glucose production, and the CB1R antagonist AM251 or insulin exhibited repression of CREBH gene induction and subsequently inhibited gluconeogenesis in both rat and human primary hepatocytes. Glucose 96-103 insulin Homo sapiens 149-156 21512720-4 2011 Upon insulin stimulation, glucose uptake and glycogen synthesis increased but as the cellular proliferative capacity became gradually exhausted, the response dropped concomitantly. Glucose 26-33 insulin Homo sapiens 5-12 21750406-1 2011 Pancreatic beta-cells regulate glucose homeostasis by secreting insulin in response to metabolic demands. Glucose 31-38 insulin Homo sapiens 64-71 21271939-7 2011 Insulin responses to the glucose tolerance test also increased significantly (p<0.005). Glucose 25-32 insulin Homo sapiens 0-7 21388348-1 2011 Suppression of lipolysis by acipimox is known to improve insulin-stimulated glucose disposal, and this is an important phenomenon. Glucose 76-83 insulin Homo sapiens 57-64 21819291-13 2011 The mean duration of glucose infusion post-insulin was 25.2 h (SD 17.7). Glucose 21-28 insulin Homo sapiens 43-50 21547498-10 2011 Insulin-mediated suppression of EGP during lower dose insulin infusion and insulin-mediated peripheral glucose uptake during higher dose insulin infusion were comparable between FHBL participants and controls. Glucose 103-110 insulin Homo sapiens 75-82 21547498-10 2011 Insulin-mediated suppression of EGP during lower dose insulin infusion and insulin-mediated peripheral glucose uptake during higher dose insulin infusion were comparable between FHBL participants and controls. Glucose 103-110 insulin Homo sapiens 75-82 21562755-4 2011 Prednisolone 7.5 mg and prednisolone 30 mg decreased the ability of insulin to suppress endogenous glucose production (by 17 +- 6% and 46 +- 7%, respectively, vs placebo). Glucose 99-106 insulin Homo sapiens 68-75 21567299-9 2011 TNF-alpha alone did not induce beta cell death, but did abrogate preproinsulin precursor mRNA synthesis in response to high glucose stimulation, which was inversely associated with upregulation of BBC3 mRNA expression by TNF-alpha. Glucose 124-131 insulin Homo sapiens 65-78 21614570-5 2011 We measured insulin-stimulated glucose disposal (M) and substrate utilisation (euglycaemic clamp/indirect calorimetry), endogenous glucose production (EGP) by 6,6-[(2)H(2)]glucose, lipolysis (rate of appearance of [(2)H(5)]glycerol) and beta cell function (acute insulin response to i.v. Glucose 31-38 insulin Homo sapiens 12-19 21715522-7 2011 Jet injector insulin administration reduced the time to 50% glucose disposal by ~40 min (P < 0.0001). Glucose 60-67 insulin Homo sapiens 13-20 21715522-9 2011 CONCLUSIONS: Administration of insulin aspart by jet injection enhances insulin absorption and reduces the duration of glucose-lowering action. Glucose 119-126 insulin Homo sapiens 31-38 21715522-10 2011 This profile resembles more closely the pattern of endogenous insulin secretion and may help to achieve better meal insulin coverage and correction of postprandial glucose excursions. Glucose 164-171 insulin Homo sapiens 62-69 21864738-1 2011 Insulin therapy is considered to be the most effective therapy for the reduction of high glucose levels. Glucose 89-96 insulin Homo sapiens 0-7 21864741-4 2011 Continuous subcutaneous insulin infusion (CSII) using an external pump, offers both a better blood glucose stability as compared to multiple daily injections and a broader flexibility in life mode, and reduces the frequency of severe hypoglycemia. Glucose 99-106 insulin Homo sapiens 24-31 21864741-6 2011 However, experience with CSII indicates that candidates for insulin pump therapy must be carefully selected and strongly motivated to improve their glucose control. Glucose 148-155 insulin Homo sapiens 60-67 21864745-2 2011 RESEARCH DESIGN AND METHODS: During closed-loop glucose control, insulin infusion rates on a subcutaneous insulin pump are adjusted by a control algorithm according to subcutaneous glucose sensor readings. Glucose 48-55 insulin Homo sapiens 65-72 21864745-2 2011 RESEARCH DESIGN AND METHODS: During closed-loop glucose control, insulin infusion rates on a subcutaneous insulin pump are adjusted by a control algorithm according to subcutaneous glucose sensor readings. Glucose 181-188 insulin Homo sapiens 65-72 21864745-2 2011 RESEARCH DESIGN AND METHODS: During closed-loop glucose control, insulin infusion rates on a subcutaneous insulin pump are adjusted by a control algorithm according to subcutaneous glucose sensor readings. Glucose 181-188 insulin Homo sapiens 106-113 21864752-1 2011 The major effects of insulin on muscle and adipose tissue are: (1) Carbohydrate metabolism: (a) it increases the rate of glucose transport across the cell membrane, (b) it increases the rate of glycolysis by increasing hexokinase and 6-phosphofructokinase activity, (c) it stimulates the rate of glycogen synthesis and decreases the rate of glycogen breakdown. Glucose 121-128 insulin Homo sapiens 21-28 21864753-2 2011 It is widely recognised that both insulin resistance and beta-cell dysfunction are important in the pathogenesis of glucose intolerance. Glucose 116-123 insulin Homo sapiens 34-41 21864753-4 2011 However, as long as the beta cell is able to secrete sufficient amounts of insulin to offset the severity of insulin resistance, glucose tolerance remains normal. Glucose 129-136 insulin Homo sapiens 75-82 21864757-2 2011 Indeed, insulin promotes glucose uptake and its utilization via glycolysis. Glucose 25-32 insulin Homo sapiens 8-15 21864757-3 2011 Insulin, promoting glucose as the main cardiac energy substrate, reduces myocardial O(2) consumption and increases cardiac efficiency. Glucose 19-26 insulin Homo sapiens 0-7 21864758-6 2011 Nevertheless, we and others could show that a group of genes affect glucose-stimulated insulin secretion, a group incretin-stimulated insulin secretion (incretin sensitivity or secretion) and a group proinsulin-to-insulin conversion. Glucose 68-75 insulin Homo sapiens 87-94 21732177-8 2011 However, insulin-stimulated glucose transport was unaltered. Glucose 28-35 insulin Homo sapiens 9-16 21887902-0 2011 Insulin resistance is associated with increased cardiovascular risk in Asian Indians with normal glucose tolerance--the Chennai Urban Rural Epidemiology Study (CURES-66). Glucose 97-104 insulin Homo sapiens 0-7 21887902-1 2011 OBJECTIVE: The aim of the study was to assess the association of Insulin Resistance [IR] assessed by Homeostasis Assessment model (HOMA-IR) with cardiovascular risk factors in subjects with Normal Glucose Tolerance [NGT] in Asian Indians. Glucose 197-204 insulin Homo sapiens 65-72 21887902-4 2011 IR was calculated using the homeostasis assessment model (HOMA-IR) using the formula: fasting insulin (1IU/mL) fasting glucose (mmol/L)/22.5. Glucose 119-126 insulin Homo sapiens 94-101 21593106-0 2011 Higher acute insulin response to glucose may determine greater free fatty acid clearance in African-American women. Glucose 33-40 insulin Homo sapiens 13-20 21593106-2 2011 Because free fatty acids (FFA) participate in the development of these conditions, studying race differences in the regulation of FFA and glucose by insulin is essential. Glucose 138-145 insulin Homo sapiens 149-156 21593106-7 2011 INTERVENTIONS: Insulin-modified frequently sampled iv glucose tolerance tests were performed with data analyzed by separate minimal models for glucose and FFA. Glucose 54-61 insulin Homo sapiens 15-22 21593106-8 2011 MAIN OUTCOME MEASURES: Glucose measures were insulin sensitivity index (S(I)) and acute insulin response to glucose (AIRg). Glucose 108-115 insulin Homo sapiens 88-95 21593115-1 2011 CONTEXT: The incretin effect is responsible for the higher insulin response to oral glucose than to iv glucose at matching glucose levels. Glucose 84-91 insulin Homo sapiens 59-66 21593117-10 2011 CONCLUSIONS: After RYGB, fasting insulin decreases to levels like those of lean control subjects and diabetes is reversed (fasting blood glucose < 125 mg/dl). Glucose 137-144 insulin Homo sapiens 33-40 21613350-8 2011 RESULTS: Insulin sensitivity differed significantly between the GH-deficiency studies (P = 0.005) with distinct insulin resistance in study 2 and increased insulin sensitivity in study 0 [area under the glucose infusion rate curve (mg/kg min): 1663 +- 151 (study 0) vs. 1482 +- 166 (study 1) vs. 1123 +- 136 (study 2) vs. 1492 +- 229 (control group)]. Glucose 203-210 insulin Homo sapiens 9-16 21613350-11 2011 CONCLUSIONS: Very-low-dose GH exposure evokes acute insulin resistance that subsides after 5 h. This time-dependent reversibility should be considered when assessing the impact of GH on glucose homeostasis. Glucose 186-193 insulin Homo sapiens 52-59 21677042-8 2011 RESULTS: After oral glucose ingestion, mean arterial insulin levels were higher in obese women than in the lean group. Glucose 20-27 insulin Homo sapiens 53-60 21677044-12 2011 CONCLUSIONS: Insulin and GLP-1 are responsible for the rapid suppression of visfatin levels upon an oral glucose uptake in healthy probands. Glucose 105-112 insulin Homo sapiens 13-20 21803297-1 2011 We investigated the metabolism of human brown adipose tissue (BAT) in healthy subjects by determining its cold-induced and insulin-stimulated glucose uptake and blood flow (perfusion) using positron emission tomography (PET) combined with computed tomography (CT). Glucose 142-149 insulin Homo sapiens 123-130 21803297-5 2011 Insulin enhanced glucose uptake 5-fold in BAT independently of its perfusion, while the effect on WAT was weaker. Glucose 17-24 insulin Homo sapiens 0-7 21803297-7 2011 In conclusion, BAT appears to be differently activated by insulin and cold; in response to insulin, BAT displays high glucose uptake without increased perfusion, but when activated by cold, it dissipates energy in a perfusion-dependent manner. Glucose 118-125 insulin Homo sapiens 91-98 21624100-12 2011 CONCLUSION: Adrenaline directly increases lactate release and lipolysis and inhibits insulin-stimulated glucose uptake in the perfused human leg. Glucose 106-113 insulin Homo sapiens 87-94 21744143-0 2011 Influence of telmisartan on insulin response after glucose loading in obese patients with hypertension: ARB trial of hypertension in obese patients with hyperinsulinemia assessed by oral glucose tolerance test (ATHLETE). Glucose 51-58 insulin Homo sapiens 28-35 21744143-7 2011 A 75 g oral glucose tolerance test (OGTT) was performed before and after switching, and the effect of telmisartan on the insulin response to glucose loading was investigated. Glucose 141-148 insulin Homo sapiens 121-128 21744143-9 2011 The hyperinsulin response to glucose loading also significantly improved in those taking telmisartan, as well as homeostasis model assessment of insulin resistance (HOMA-IR). Glucose 29-36 insulin Homo sapiens 9-16 21602475-6 2011 The stimulation of glucose uptake by AMPK activators and insulin correlated with AMPK and protein kinase B (PKB/Akt) activation, respectively. Glucose 19-26 insulin Homo sapiens 57-64 21602475-8 2011 Together, insulin and AMPK activators acted synergistically to induce PKB/Akt overactivation, AS160 overphosphorylation, and glucose uptake overstimulation. Glucose 125-132 insulin Homo sapiens 10-17 21632466-1 2011 Several processes contribute to variation in fasting insulin concentration, including fasting glucose, insulin resistance, insulin secretion, and insulin clearance. Glucose 94-101 insulin Homo sapiens 53-60 21632466-7 2011 In multivariate analysis, MCRI, M, BMI, waist circumference, and fasting glucose were independently associated with fasting insulin. Glucose 73-80 insulin Homo sapiens 124-131 21632466-8 2011 Decreasing M and MCRI were associated with increasing fasting insulin, whereas increasing BMI, waist circumference, and fasting glucose were associated with increasing fasting insulin. Glucose 128-135 insulin Homo sapiens 176-183 21571600-4 2011 Obese young people with glucose intolerance are characterized by marked peripheral insulin resistance and relative beta-cell failure. Glucose 24-31 insulin Homo sapiens 83-90 21594601-9 2011 The baseline fasting insulin was statistically significantly lower and fasting glucose:insulin ratio was statistically significantly higher (P = 0.003, 0.002) in ovulatory compared with anovulatory patients. Glucose 79-86 insulin Homo sapiens 87-94 21353260-1 2011 Exercise has the potential to alleviate the resistance to insulin-mediated glucose uptake precipitated by elevated circulating free fatty acids (FFAs) in conditions such as obesity, lipid infusion, and starvation. Glucose 75-82 insulin Homo sapiens 58-65 21353260-3 2011 Insulin sensitivity was determined by intravenous glucose tolerance test, and intramyocellular lipid (IMCL) concentration was measured by (1)H magnetic resonance spectroscopy. Glucose 50-57 insulin Homo sapiens 0-7 20304617-4 2011 METHODS AND RESULTS: Healthy, non-diabetic volunteers underwent measurements of BMI, WC, blood pressure, fasting plasma glucose (FPG), lipoprotein concentrations, and direct quantification of insulin-mediated glucose uptake. Glucose 209-216 insulin Homo sapiens 192-199 20304617-5 2011 Insulin resistance was defined as the top tertile of steady-state plasma glucose (SSPG) concentrations. Glucose 73-80 insulin Homo sapiens 0-7 21249361-14 2011 Overexpression of SSTR5 P335 enhanced the inhibitory effect of SSTR5 agonist RPL-1980 on cell proliferation of Mia PaCa-2 cells and glucose-stimulated insulin secretion from mouse insulinoma cells, while overexpression of SSTR5 L335 blocked the inhibitory effect of RPL-1980. Glucose 132-139 insulin Homo sapiens 151-158 21443584-1 2011 OBJECTIVE: Insulin glargine offers sustained insulin delivery for 24 h. Change to glargine treatment consistently results in lower fasting glucose and fewer hypoglycemic episodes in children with type 1 diabetes compared to continuation of NPH, although glargine has not been shown to improve HbA1c in randomized trials. Glucose 139-146 insulin Homo sapiens 11-18 21249361-20 2011 Its overexpression blocked the inhibitory effect of an SSTR5-specific analog on human pancreatic cancer cell proliferation and on glucose-stimulated insulin secretion from mouse insulinoma cells. Glucose 130-137 insulin Homo sapiens 149-156 21812507-1 2011 The dipeptidyl peptidase (DPP)-4 inhibitors, which enhance glucose-dependent insulin secretion from pancreatic beta cells by preventing DPP-4-mediated degradation of endogenously released incretin hormones, represent a new therapeutic approach to the management of type 2 diabetes mellitus. Glucose 59-66 insulin Homo sapiens 77-84 22093562-4 2011 Insulin resistance index (IRI) was expressed by homeostasis model assessment for insulin resistance (HOMA-IR) calculated by the formula of [fasting serum glucose (mmol/L) x fasting plasma insulin (mU/L)]/22.5. Glucose 154-161 insulin Homo sapiens 0-7 22093562-4 2011 Insulin resistance index (IRI) was expressed by homeostasis model assessment for insulin resistance (HOMA-IR) calculated by the formula of [fasting serum glucose (mmol/L) x fasting plasma insulin (mU/L)]/22.5. Glucose 154-161 insulin Homo sapiens 81-88 22021788-6 2011 Participants received intravenous, then subcutaneous, insulin to control blood glucose to 4.4-6.5 mmol/l. Glucose 79-86 insulin Homo sapiens 54-61 21572040-0 2011 A hierarchical whole-body modeling approach elucidates the link between in Vitro insulin signaling and in Vivo glucose homeostasis. Glucose 111-118 insulin Homo sapiens 81-88 21572040-5 2011 Herein, we develop a hierarchical model of the adipose tissue, which links intracellular insulin control of glucose transport in human primary adipocytes with whole-body glucose homeostasis. Glucose 108-115 insulin Homo sapiens 89-96 21555120-2 2011 This inhibitor exhibited strong anti-alpha-glucosidase activity with an IC50 value of 170.62nM and stimulated a dose-dependent increase in the uptake of a fluorescent d-glucose analog, 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG), in HepG2 cells at a rate higher than that of insulin controls. Glucose 167-176 insulin Homo sapiens 305-312 21571245-6 2011 We observed a stable or increased association between waist circumference and insulin resistance (Homeostasis Model of Assessment-Insulin Resistance index) and fasting plasma glucose. Glucose 175-182 insulin Homo sapiens 78-85 21571245-6 2011 We observed a stable or increased association between waist circumference and insulin resistance (Homeostasis Model of Assessment-Insulin Resistance index) and fasting plasma glucose. Glucose 175-182 insulin Homo sapiens 130-137 21467301-6 2011 Insulin sensitivity was evaluated with fasting (QUICKI) and dynamic index (OGIS) and beta-cell function with a modified insulinogenic index as DeltaAUC(insulin)/DeltaAUC(glucose) and disposition index. Glucose 170-177 insulin Homo sapiens 0-7 21616080-1 2011 Human islet amyloid polypeptide (hIAPP) is a highly amyloidogenic protein co-secreted with insulin in response to glucose levels. Glucose 114-121 insulin Homo sapiens 91-98 21676673-13 2011 In children with increased cardiometabolic risk, the insulin/glucose ratio was similar in T1, T2-4 and T5 stages, however, it was significantly higher in T1 stage as compared to subjects without increased cardiometabolic risk (p = 0.04). Glucose 61-68 insulin Homo sapiens 53-60 21352505-11 2011 With regard to the interstitial glucose concentration microvascular perfusion is particular relevant as correlative evidence supports a connection between insulin sensitivity and microvascular perfusion. Glucose 32-39 insulin Homo sapiens 155-162 21613559-3 2011 OBJECTIVE: We determined whether the greater adverse effects of fructose than of glucose consumption were associated with glucose and insulin exposures. Glucose 81-88 insulin Homo sapiens 134-141 21474138-9 2011 CONCLUSION: The observed increase of triglycerides after glucose load in subjects with signs of insulin resistance and obesity suggests that post-glucose triglyceride change is a potential novel biomarker for early detection of metabolic risk. Glucose 57-64 insulin Homo sapiens 96-103 21505151-4 2011 Because the degree of metabolic function of beta-cells (reflected by the level of insulin output) increases in a glucose-dependent manner between 4 and 10 mM glucose, PMET was evaluated under these conditions. Glucose 113-120 insulin Homo sapiens 82-89 20963457-0 2011 Effects of oral L-carnitine supplementation on insulin sensitivity indices in response to glucose feeding in lean and overweight/obese males. Glucose 90-97 insulin Homo sapiens 47-54 21474138-9 2011 CONCLUSION: The observed increase of triglycerides after glucose load in subjects with signs of insulin resistance and obesity suggests that post-glucose triglyceride change is a potential novel biomarker for early detection of metabolic risk. Glucose 146-153 insulin Homo sapiens 96-103 21570480-0 2011 Insulin-stimulated glucose uptake and pathways regulating energy metabolism in skeletal muscle cells: the effects of subcutaneous and visceral fat, and long-chain saturated, n-3 and n-6 polyunsaturated fatty acids. Glucose 19-26 insulin Homo sapiens 0-7 21474138-10 2011 The specific association of post-glucose triglyceride change with abdominal obesity and fasting glucose suggests a link to hepatic steatosis and insulin resistance. Glucose 33-40 insulin Homo sapiens 145-152 21474138-10 2011 The specific association of post-glucose triglyceride change with abdominal obesity and fasting glucose suggests a link to hepatic steatosis and insulin resistance. Glucose 96-103 insulin Homo sapiens 145-152 21570480-3 2011 Insulin-stimulated glucose uptake, lipid content, mRNA expression of key genes involved in nutrient utilization and protein expression of inhibitor protein inhibitor kappa B (IkappaB)-alpha and mammalian target of rapamycin (mTOR) were measured. Glucose 19-26 insulin Homo sapiens 0-7 21570480-4 2011 RESULTS: PA and IAB fat reduced insulin-stimulated glucose uptake and their combined effect was similar to that of PA alone. Glucose 51-58 insulin Homo sapiens 32-39 21396140-0 2011 Effects of 4-week very-high-fructose/glucose diets on insulin sensitivity, visceral fat and intrahepatic lipids: an exploratory trial. Glucose 37-44 insulin Homo sapiens 54-61 21396140-5 2011 Insulin sensitivity was estimated from oral glucose tolerance tests. Glucose 44-51 insulin Homo sapiens 0-7 21429276-9 2011 This combination also resulted in a lower first-phase insulin release during glucose tolerance testing (P < 0.001). Glucose 77-84 insulin Homo sapiens 54-61 21396140-10 2011 Insulin sensitivity appeared to decrease both in the fructose and glucose groups. Glucose 66-73 insulin Homo sapiens 0-7 21435140-5 2011 D11 insulin secretion was induced by static incubation with low glucose (1.67 mmol/l), high glucose (16.7 mmol/l) and high glucose with 10 mmol/l theophylline (G+T) and assessed by enzyme-linked immunosorbent assay (ELISA). Glucose 64-71 insulin Homo sapiens 4-11 21598057-0 2011 Validation of the DeLiT Trial intravenous insulin infusion algorithm for intraoperative glucose control in noncardiac surgery: a randomized controlled trial. Glucose 88-95 insulin Homo sapiens 42-49 21598057-4 2011 Glucose was managed with a dynamic intravenous insulin infusion algorithm. Glucose 0-7 insulin Homo sapiens 47-54 21734082-0 2011 Comparison of insulin action on glucose versus potassium uptake in humans. Glucose 32-39 insulin Homo sapiens 14-21 21734082-1 2011 BACKGROUND AND OBJECTIVES: Insulin has several physiologic actions that include stimulation of cellular glucose and potassium uptake. Glucose 104-111 insulin Homo sapiens 27-34 21734082-2 2011 The ability of insulin to induce glucose uptake by cells is impaired in type 2 diabetes mellitus, but whether potassium uptake is similarly impaired is not known. Glucose 33-40 insulin Homo sapiens 15-22 21734082-12 2011 Conclusions Insulin-stimulated intracellular uptake of glucose and potassium are independent of each other. Glucose 55-62 insulin Homo sapiens 12-19 21966580-1 2011 Recently, M(3)-muscarinic receptor (M3R) has been identified as the bona fide receptor responsible for the cholinergic regulation of glucose-induced insulin release. Glucose 133-140 insulin Homo sapiens 149-156 22011855-5 2011 Predictive factors for insulin use were: screening fasting glucose (FG) >= 85, Oral Glucose Tolerance Test (OGTT) FG >= 95, 2h glucose after 75 g >= 200 mg/dL, previous GDM, obesity, HbA1c > 6%, and the association of risk factors including family history of diabetes mellitus and obesity or previous GDM, the last one the most relevant (p < 0,05). Glucose 59-66 insulin Homo sapiens 23-30 21484216-4 2011 Among persons with normal glucose tolerance (n = 266) this allele was associated with a higher mean acute insulin response during an intravenous glucose tolerance test (p = 0.005), higher mean 30 min insulin concentration during an oral glucose tolerance test (p = 0.017) and higher body fat percentage (p = 0.010). Glucose 26-33 insulin Homo sapiens 106-113 21484216-4 2011 Among persons with normal glucose tolerance (n = 266) this allele was associated with a higher mean acute insulin response during an intravenous glucose tolerance test (p = 0.005), higher mean 30 min insulin concentration during an oral glucose tolerance test (p = 0.017) and higher body fat percentage (p = 0.010). Glucose 26-33 insulin Homo sapiens 200-207 21484216-4 2011 Among persons with normal glucose tolerance (n = 266) this allele was associated with a higher mean acute insulin response during an intravenous glucose tolerance test (p = 0.005), higher mean 30 min insulin concentration during an oral glucose tolerance test (p = 0.017) and higher body fat percentage (p = 0.010). Glucose 145-152 insulin Homo sapiens 106-113 21484216-4 2011 Among persons with normal glucose tolerance (n = 266) this allele was associated with a higher mean acute insulin response during an intravenous glucose tolerance test (p = 0.005), higher mean 30 min insulin concentration during an oral glucose tolerance test (p = 0.017) and higher body fat percentage (p = 0.010). Glucose 145-152 insulin Homo sapiens 106-113 21602425-6 2011 We computed and mathematically modeled gut glucose absorption from insulin-mediated glucose disappearance and endogenous glucose production (EGP). Glucose 43-50 insulin Homo sapiens 67-74 21602425-6 2011 We computed and mathematically modeled gut glucose absorption from insulin-mediated glucose disappearance and endogenous glucose production (EGP). Glucose 84-91 insulin Homo sapiens 67-74 21602425-6 2011 We computed and mathematically modeled gut glucose absorption from insulin-mediated glucose disappearance and endogenous glucose production (EGP). Glucose 84-91 insulin Homo sapiens 67-74 21617098-12 2011 Lipid infusion abolished insulin-mediated microvascular recruitment in both skeletal and cardiac muscle and lowered insulin-stimulated whole body glucose disposal (P<0.001). Glucose 146-153 insulin Homo sapiens 116-123 21617098-13 2011 Salsalate treatment rescued insulin"s actions to recruit muscle microvasculature and improved insulin-stimulated whole body glucose disposal in the presence of high plasma FFAs. Glucose 124-131 insulin Homo sapiens 94-101 21521748-9 2011 Concentration-response studies on female islets from healthy controls and type 2 diabetic subjects showed that both E2 and G-1 displayed important antidiabetic actions by improving glucose-stimulated insulin release while suppressing glucagon and somatostatin secretion. Glucose 181-188 insulin Homo sapiens 200-207 21502328-0 2011 Identification of insulin secretory defects and insulin resistance during oral glucose tolerance test in a cohort of cystic fibrosis patients. Glucose 79-86 insulin Homo sapiens 18-25 21502328-9 2011 CF patients who attained glucose tolerance comparable to CON had lower beta-cell function and higher insulin sensitivity. Glucose 25-32 insulin Homo sapiens 101-108 21502328-10 2011 CONCLUSION: The major alteration in insulin secretion and insulin sensitivity of CF patients is slowly declining beta-cell function, consisting of delayed and reduced responsiveness to hyperglycemia, that in CF patients with normal glucose tolerance may be compensated by an increased insulin sensitivity. Glucose 232-239 insulin Homo sapiens 36-43 21569204-1 2011 Glucokinase (GK) is the central player in glucose-stimulated insulin release from pancreatic beta-cells, and catalytic activation by alpha-D-glucose binding has a key regulatory function. Glucose 42-49 insulin Homo sapiens 61-68 26396568-6 2011 Insulin resistance was determined with the fasting glucose (mmol/L) to insulin (mIU/L) ratio and HOMA-IR (Homeostasis model assessment-Insulin resistance). Glucose 51-58 insulin Homo sapiens 0-7 21508130-0 2011 Surrogate estimates of insulin sensitivity in obese youth along the spectrum of glucose tolerance from normal to prediabetes to diabetes. Glucose 80-87 insulin Homo sapiens 23-30 21062674-0 2011 The impact of continuous subcutaneous insulin infusion and multiple daily injections of insulin on glucose variability in older adults with type 2 diabetes. Glucose 99-106 insulin Homo sapiens 88-95 21601483-7 2011 Insulin sensitivity quantified by estimated glucose disposal rate (eGDR) was lower in patients with hypertension compared with normotensives (5.2+-1.4 vs. 9.1+-1.2 mg kg(-1) min(-1), P<.001) and showed a negative correlation with systolic blood pressure level (r=-0.612, P<.01). Glucose 44-51 insulin Homo sapiens 0-7 21880230-10 2011 CONCLUSIONS: Insulin pump therapy using a relatively simple dosing regimen safely improved glucose control and PROs in patients with T2DM who were unable to achieve glycemic targets with MDI therapy. Glucose 91-98 insulin Homo sapiens 13-20 21880241-5 2011 Insulin resistance was calculated using the homeostasis model assessment (HOMA-IR) using the following formula: fasting insulin (microIU/ml) x fasting glucose (mmol/liter)/22.5. Glucose 151-158 insulin Homo sapiens 0-7 21478228-4 2011 Results showed that insulin treatment, which effectively reduced plasma glucose level in diabetic mice, attenuated diabetes-increased intimal lesion size and significantly inhibited diabetes-increased MMP9 expression, but had no effect on tissue inhibitor of metalloproteinase 1 in atherosclerotic plaques. Glucose 72-79 insulin Homo sapiens 20-27 21476811-12 2011 The administration of insulin was related to a lowering of MD glucose and MD pyruvate, often to low levels even though plasma glucose values remained above 6 mmol/L. Glucose 62-69 insulin Homo sapiens 22-29 21476811-13 2011 After SAH, the administration of insulin could impede the glucose supply of the brain. Glucose 58-65 insulin Homo sapiens 33-40 21594678-0 2011 Computational assessment of insulin secretion and insulin sensitivity from 2-h oral glucose tolerance tests for clinical use for type 2 diabetes. Glucose 84-91 insulin Homo sapiens 28-35 21448693-0 2011 Dynamics of insulin action in hypertension: assessment from minimal model interpretation of intravenous glucose tolerance test data. Glucose 104-111 insulin Homo sapiens 12-19 21448693-1 2011 Based on glucose kinetics minimal model (GKMM) interpretation of frequently sampled intravenous glucose tolerance test (FSIGTT), the aim was to broaden the characterization of insulin-mediated glucose disposal in hypertension by aid of a dynamic insulin sensitivity index, S(D)(I), and the related efficiency, eta = S(D)(I) / S(I), of the metabolic system to convert the maximal individual response capacity, measured by S (I), into an effective insulin control on glucose. Glucose 9-16 insulin Homo sapiens 176-183 21448693-1 2011 Based on glucose kinetics minimal model (GKMM) interpretation of frequently sampled intravenous glucose tolerance test (FSIGTT), the aim was to broaden the characterization of insulin-mediated glucose disposal in hypertension by aid of a dynamic insulin sensitivity index, S(D)(I), and the related efficiency, eta = S(D)(I) / S(I), of the metabolic system to convert the maximal individual response capacity, measured by S (I), into an effective insulin control on glucose. Glucose 96-103 insulin Homo sapiens 176-183 21448693-1 2011 Based on glucose kinetics minimal model (GKMM) interpretation of frequently sampled intravenous glucose tolerance test (FSIGTT), the aim was to broaden the characterization of insulin-mediated glucose disposal in hypertension by aid of a dynamic insulin sensitivity index, S(D)(I), and the related efficiency, eta = S(D)(I) / S(I), of the metabolic system to convert the maximal individual response capacity, measured by S (I), into an effective insulin control on glucose. Glucose 96-103 insulin Homo sapiens 176-183 21448693-1 2011 Based on glucose kinetics minimal model (GKMM) interpretation of frequently sampled intravenous glucose tolerance test (FSIGTT), the aim was to broaden the characterization of insulin-mediated glucose disposal in hypertension by aid of a dynamic insulin sensitivity index, S(D)(I), and the related efficiency, eta = S(D)(I) / S(I), of the metabolic system to convert the maximal individual response capacity, measured by S (I), into an effective insulin control on glucose. Glucose 96-103 insulin Homo sapiens 176-183 21448693-5 2011 These findings suggest that, in spite of no change of efficiency, insulin resistance in normoglycemic hypertensive patients is primarily compensated by an increase in first-phase insulin secretion to preserve glucose tolerance to intravenous glucose load. Glucose 209-216 insulin Homo sapiens 66-73 21448693-5 2011 These findings suggest that, in spite of no change of efficiency, insulin resistance in normoglycemic hypertensive patients is primarily compensated by an increase in first-phase insulin secretion to preserve glucose tolerance to intravenous glucose load. Glucose 209-216 insulin Homo sapiens 179-186 21448693-5 2011 These findings suggest that, in spite of no change of efficiency, insulin resistance in normoglycemic hypertensive patients is primarily compensated by an increase in first-phase insulin secretion to preserve glucose tolerance to intravenous glucose load. Glucose 242-249 insulin Homo sapiens 179-186 21067784-8 2011 Compared with NO-SIT, insulin action, defined as whole-body rate of glucose disappearance normalized to mean plasma insulin, was reduced by 39% in SIT (P < .001) and by 18% in SIT-BAL (P = .07). Glucose 68-75 insulin Homo sapiens 22-29 21087777-5 2011 Insulin sensitivity was estimated using a 2-hour oral glucose tolerance test with oral glucose insulin sensitivity analysis. Glucose 54-61 insulin Homo sapiens 0-7 21461612-4 2011 After 10 ng/ml TNF-alpha treatment for 24 h, insulin-stimulated glucose uptake was reduced by 47% in 3T3-L1 adipocytes. Glucose 64-71 insulin Homo sapiens 45-52 21461612-6 2011 Treatment of 1,000 nM apelin for 60 min maximally augmented glucose uptake in insulin-resistant 3T3-L1 adipocytes. Glucose 60-67 insulin Homo sapiens 78-85 21461612-7 2011 Furthermore, apelin pre-incubation also increased adipocytes" insulin-stimulated glucose uptake, and PI3K/Akt pathway were involved in these effects. Glucose 81-88 insulin Homo sapiens 62-69 21514308-1 2011 OBJECTIVE: An effect of insulin that is crucial for stimulating glucose uptake is its ability to increase the number of perfused capillaries, and thereby enhance its own delivery, and that of glucose, to muscle cells. Glucose 64-71 insulin Homo sapiens 24-31 21514308-1 2011 OBJECTIVE: An effect of insulin that is crucial for stimulating glucose uptake is its ability to increase the number of perfused capillaries, and thereby enhance its own delivery, and that of glucose, to muscle cells. Glucose 192-199 insulin Homo sapiens 24-31 21470888-10 2011 While MHCIIa expression related positively with insulin-stimulated glucose uptake (P<0.01), MHCIIx/d expression related negatively with insulin-stimulated glucose uptake (P<0.05). Glucose 158-165 insulin Homo sapiens 139-146 21050717-7 2011 Basal and insulin-stimulated glucose transport and incorporation into glycogen were also assessed. Glucose 29-36 insulin Homo sapiens 10-17 21050717-9 2011 RESULTS: Insulin-stimulated glucose transport, muscle glycogen, and adenosine triphosphate content were decreased in patients with PDAC compared with controls, and insulin stimulation did not significantly increase glucose incorporation into glycogen in vitro in patients with PDAC. Glucose 28-35 insulin Homo sapiens 9-16 21494227-7 2011 After RYGB increase of C-peptide concentration following glucose ingestion was significantly higher compared to all other groups (dynamic-area under the curve (Dyn-AUC): 0-90 min: POST: 984 +- 115 ng min/ml, PRE: 590 +- 67 ng min/ml, CONob: 440 +- 44 ng min/ml, CON: 279 +- 22 ng min/ml, P < 0.01 respectively). Glucose 57-64 insulin Homo sapiens 23-32 21494227-10 2011 Insulin-stimulated glucose uptake tended to increase postoperatively (M-value: PRE: 1.8 +- 0.5, POST: 3.0 +- 0.3, not significant (n.s.)). Glucose 19-26 insulin Homo sapiens 0-7 21499957-5 2011 Insulin secretion was measured by insulinogenic index and area under the curve (AUC) during a standard oral glucose tolerance test (OGTT). Glucose 108-115 insulin Homo sapiens 0-7 21923457-12 2011 CONCLUSION: In patients with insulin-resistant diabetes who have requirements of more than 200 units/day or 100 units/injection, use of U-500 regular insulin provided the same or better glucose control compared with U-100 insulin, with fewer daily injections and reduced injection volume. Glucose 186-193 insulin Homo sapiens 150-157 21680986-2 2011 Clinicians are familiar with physiological effects of insulin on carbohydrate metabolism, including stimulation of glucose uptake in skeletal muscle and the suppression of glucose production from the liver. Glucose 115-122 insulin Homo sapiens 54-61 21680986-2 2011 Clinicians are familiar with physiological effects of insulin on carbohydrate metabolism, including stimulation of glucose uptake in skeletal muscle and the suppression of glucose production from the liver. Glucose 172-179 insulin Homo sapiens 54-61 21680986-5 2011 Insulin resistance, typically defined with respect to glucose metabolism, is a condition in which normal levels of insulin do not trigger the signal for glucose disposition. Glucose 54-61 insulin Homo sapiens 0-7 21680991-2 2011 Optimal glycemic control for patients with type 1 diabetes (T1DM) includes methods that provide glucose-regulated physiologic insulin replacement or secretion in association with glucose monitoring methods designed to predict and prevent acute extreme changes in glycemic variability. Glucose 96-103 insulin Homo sapiens 126-133 21680998-0 2011 Control of postprandial glucose levels with insulin in type 2 diabetes. Glucose 24-31 insulin Homo sapiens 44-51 20942606-7 2011 These cells also produced and released C-peptide in a glucose-responsive manner. Glucose 54-61 insulin Homo sapiens 39-48 21787464-1 2011 OBJECTIVE: To observe the trend of change in perioperative blood glucose level in patients undergoing deep hypothermic circulatory arrest (DHCA), in order to evaluate the influencing factors of inciting hyperglycemia and the clinical effects of insulin control. Glucose 65-72 insulin Homo sapiens 245-252 21787464-8 2011 One hundred and thirty-four patients (76.1%) insulin was given with intravenous micropump due to poor effect of intermittent subcutaneous injection of insulin in controlling blood glucose. Glucose 180-187 insulin Homo sapiens 45-52 21787464-8 2011 One hundred and thirty-four patients (76.1%) insulin was given with intravenous micropump due to poor effect of intermittent subcutaneous injection of insulin in controlling blood glucose. Glucose 180-187 insulin Homo sapiens 151-158 21508897-8 2011 The insulin response to glucose was significantly higher in rats treated with SIR compared with TAC (P<0.05). Glucose 24-31 insulin Homo sapiens 4-11 21646544-5 2011 Here we show in a model of chronic hyperinsulinemia that adipocytes develop selective insulin resistance in which translocation of the GLUT4 glucose transporter to the cell surface is blunted yet nuclear exclusion of the FoxO1 transcription factor is preserved, rendering uncoupled insulin-controlled carbohydrate and lipid metabolisms. Glucose 141-148 insulin Homo sapiens 40-47 21646544-5 2011 Here we show in a model of chronic hyperinsulinemia that adipocytes develop selective insulin resistance in which translocation of the GLUT4 glucose transporter to the cell surface is blunted yet nuclear exclusion of the FoxO1 transcription factor is preserved, rendering uncoupled insulin-controlled carbohydrate and lipid metabolisms. Glucose 141-148 insulin Homo sapiens 86-93 21693022-0 2011 A local glucose-and oxygen concentration-based insulin secretion model for pancreatic islets. Glucose 8-15 insulin Homo sapiens 47-54 21693022-4 2011 Insulin secretion rates depend on both the glucose concentration and its time-gradient, resulting in second-and first-phase responses, respectively. Glucose 43-50 insulin Homo sapiens 0-7 21693022-7 2011 RESULTS: The model was calibrated using experimental results from dynamic glucose-stimulated insulin release (GSIR) perifusion studies with isolated islets. Glucose 74-81 insulin Homo sapiens 93-100 21693022-8 2011 Further optimization is still needed, but calculated insulin responses to stepwise increments in the incoming glucose concentration are in good agreement with existing experimental insulin release data characterizing glucose and oxygen dependence. Glucose 110-117 insulin Homo sapiens 53-60 21693022-8 2011 Further optimization is still needed, but calculated insulin responses to stepwise increments in the incoming glucose concentration are in good agreement with existing experimental insulin release data characterizing glucose and oxygen dependence. Glucose 110-117 insulin Homo sapiens 181-188 21693022-8 2011 Further optimization is still needed, but calculated insulin responses to stepwise increments in the incoming glucose concentration are in good agreement with existing experimental insulin release data characterizing glucose and oxygen dependence. Glucose 217-224 insulin Homo sapiens 53-60 21693022-8 2011 Further optimization is still needed, but calculated insulin responses to stepwise increments in the incoming glucose concentration are in good agreement with existing experimental insulin release data characterizing glucose and oxygen dependence. Glucose 217-224 insulin Homo sapiens 181-188 21536389-1 2011 Pancreatic beta cells produce and release insulin, which decreases the blood glucose level. Glucose 77-84 insulin Homo sapiens 42-49 21606541-3 2011 These functions are required for glucose uptake by insulin-stimulated adipocytes. Glucose 33-40 insulin Homo sapiens 51-58 21211525-3 2011 This review attempts to highlight contributions to our current understanding of how numerous neuromodulators (leptin, insulin, and serotonin) integrate with the central melanocortin system to coordinate alterations in energy and glucose balance. Glucose 229-236 insulin Homo sapiens 118-125 21454638-7 2011 In good agreement with these in vitro data, Pin1 knock-out mice exhibited impaired insulin signaling with glucose intolerance, whereas adenoviral gene transfer of Pin1 into the ob/ob mouse liver mostly normalized insulin signaling and restored glucose tolerance. Glucose 106-113 insulin Homo sapiens 83-90 21647189-1 2011 Glucagon-like peptide 1 (GLP-1), a peptide secreted from the intestine in response to nutrient ingestion, is perhaps best known for its effect on glucose-stimulated insulin secretion. Glucose 146-153 insulin Homo sapiens 165-172 21524684-6 2011 In adipocytes glucose transport was 100-fold more sensitive to insulin than to IGFs and the maximal effect was higher with insulin. Glucose 14-21 insulin Homo sapiens 63-70 21524684-6 2011 In adipocytes glucose transport was 100-fold more sensitive to insulin than to IGFs and the maximal effect was higher with insulin. Glucose 14-21 insulin Homo sapiens 123-130 21524684-7 2011 In preadipocytes glucose accumulation and DNA synthesis was equally sensitive to insulin and IGFs but the maximal effect was higher with IGF-I. Glucose 17-24 insulin Homo sapiens 81-88 21602835-2 2011 In pancreatic beta cells, K(ATP) channels modulate insulin secretion in response to fluctuations in plasma glucose level, and play an important role in glucose homeostasis. Glucose 107-114 insulin Homo sapiens 51-58 21288502-3 2011 He suggested that fetal overgrowth was related to increased transplacental transfer of glucose, stimulating the release of insulin by the fetal beta cell and subsequent macrosomia. Glucose 87-94 insulin Homo sapiens 123-130 21420057-3 2011 Insulin sensitivity was estimated with an oral glucose tolerance test-derived insulin sensitivity index. Glucose 47-54 insulin Homo sapiens 0-7 21420057-3 2011 Insulin sensitivity was estimated with an oral glucose tolerance test-derived insulin sensitivity index. Glucose 47-54 insulin Homo sapiens 78-85 21386060-2 2011 We examined the effects of type I and type II IFN (IFN-beta and IFN-gamma) on insulin-induced metabolic signaling leading to glucose uptake in 3T3-L1 adipocytes. Glucose 125-132 insulin Homo sapiens 78-85 21386060-8 2011 In contrast, adenovirus-mediated expression of a dominant-negative STAT3 (F-STAT3) attenuated IFN-gamma-induced SOCS3 expression, reduction of IRS-1 protein, and suppression of insulin-induced glucose uptake but did not have any effect on the IFN-beta-mediated SOCS1 expression and inhibition of insulin-induced glucose uptake. Glucose 193-200 insulin Homo sapiens 177-184 21663839-2 2011 The use of in vitro model systems together with the investigation of drug-mediated effects on glucose homeostasis in animals and healthy human volunteers has provided important insight into the contribution of individual drugs to insulin resistance and affected cellular pathways. Glucose 94-101 insulin Homo sapiens 230-237 21083860-12 2011 Women with considerable obesity, high fasting blood glucose and an early need for pharmacological treatment may be more suitable for insulin therapy. Glucose 52-59 insulin Homo sapiens 133-140 23646067-7 2011 Simulations indicate that (1) regulation of lipoprotein lipase (LPL) reaction is important when the intracellular lipolysis is suppressed by insulin; (2) intracellular diglyceride levels can affect the regulatory mechanisms; and (3) glyceroneogenesis is the dominant pathway for glycerol-3-phosphate synthesis even in the presence of increased glucose uptake by the adipose tissue. Glucose 344-351 insulin Homo sapiens 141-148 23646067-9 2011 A parameter sensitivity analysis predicts that insulin-stimulated glucose uptake would be more severely affected by impairment of GLUT4 translocation and glycolysis than by impairment of glycogen synthesis and pyruvate oxidation. Glucose 66-73 insulin Homo sapiens 47-54 21435140-5 2011 D11 insulin secretion was induced by static incubation with low glucose (1.67 mmol/l), high glucose (16.7 mmol/l) and high glucose with 10 mmol/l theophylline (G+T) and assessed by enzyme-linked immunosorbent assay (ELISA). Glucose 92-99 insulin Homo sapiens 4-11 21435140-5 2011 D11 insulin secretion was induced by static incubation with low glucose (1.67 mmol/l), high glucose (16.7 mmol/l) and high glucose with 10 mmol/l theophylline (G+T) and assessed by enzyme-linked immunosorbent assay (ELISA). Glucose 92-99 insulin Homo sapiens 4-11 21492974-1 2011 Although insulin resistance in T2DM (type 2 diabetes mellitus) is usually referred to glucose and lipid metabolism, the question whether such a resistance affects also amino acid and protein metabolism is both relevant and not easy to be answered. Glucose 86-93 insulin Homo sapiens 9-16 21378565-1 2011 PURPOSE OF REVIEW: The metabolic syndrome incorporating obesity, hypertension, dyslipidaemia and elevated plasma glucose has reached epidemic proportions in many Western countries leading to a dramatic increase in insulin resistance, steatosis and type 2 diabetes. Glucose 113-120 insulin Homo sapiens 214-221 20541829-6 2011 Integral-based fitting methods were used to identify time-varying insulin sensitivity and non-insulin mediated glucose uptake profiles. Glucose 111-118 insulin Homo sapiens 94-101 21599535-4 2011 Though the pathways by which insulin controls hepatic glucose output have been of intense study in recent years, considerably less attention has been devoted to how lipid metabolism is regulated. Glucose 54-61 insulin Homo sapiens 29-36 21424899-3 2011 METHODS: We analysed the data from a population-based cohort of 1,048 non-diabetic, normotensive men and women (aged 30-60 years) in whom insulin sensitivity was measured by the glucose clamp technique (M/I index; average glucose infusion rate/steady-state insulin concentration) and beta cell function was estimated by mathematical modelling of the oral glucose tolerance test at baseline and 3 years later. Glucose 178-185 insulin Homo sapiens 138-145 21376417-4 2011 After fasting glucose was optimized by insulin glargine, nateglinide or acarbose was initiated and then crossed over after second wash out period. Glucose 14-21 insulin Homo sapiens 39-46 21424899-10 2011 Insulin sensitivity and beta cell glucose sensitivity predict and track changes in glucose tolerance independently of sex, age and obesity. Glucose 83-90 insulin Homo sapiens 0-7 21668337-3 2011 This stimulated a concerted effort to modify the properties of insulin in order to extend the duration of its blood glucose-lowering effect, minimize dosing frequency, and decrease the burden of treatment. Glucose 116-123 insulin Homo sapiens 63-70 21488799-10 2011 We identified a statistically significant difference in glucose profiles during the morning between insulin pump-treated and MDI-treated type 1 diabetes patients. Glucose 56-63 insulin Homo sapiens 100-107 21668333-6 2011 The findings of glucose clamp studies demonstrate that the two long-acting insulin analogs are different, to some extent, in both their PK and PD profiles. Glucose 16-23 insulin Homo sapiens 75-82 21668340-7 2011 This approach considers the addition of increasing injections of prandial insulin, beginning with the meal that has the major impact on postprandial glucose values. Glucose 149-156 insulin Homo sapiens 74-81 21386858-8 2011 Plasma triglycerides, leptin and glucose combined predicted about 60% of variation in insulin level whereas insulin was the only component that predicted the membrane fatty acids. Glucose 33-40 insulin Homo sapiens 86-93 21570642-3 2011 The aim of this study was to assess the effect of lower doses of a casein hydrolysate on the glucose and insulin responses to an oral glucose tolerance test in patients with type 2 diabetes. Glucose 134-141 insulin Homo sapiens 105-112 21463618-9 2011 Furthermore, SKLB102 could promote glucose consumption in HepG2 cells in the presence of 0.1 muM insulin. Glucose 35-42 insulin Homo sapiens 97-104 21447694-6 2011 An oral glucose tolerance test (75 g glucose) measured areas under the curve (AUC) for insulin (AUC(2h-insulin)) and for glucose (AUC(2h-glucose)). Glucose 8-15 insulin Homo sapiens 87-94 21501347-4 2011 Insulin enhanced glucose uptake in an additive fashion with increased phosphorylation of Akt and AS160 in FABP3-induced myotubes compared to control cells. Glucose 17-24 insulin Homo sapiens 0-7 21501347-5 2011 This increased glucose uptake in FABP3-induced myotubes with insulin stimulation was found even in the presence of palmitate, in which a significantly higher Akt phosphorylation was detected compared to controls. Glucose 15-22 insulin Homo sapiens 61-68 21321933-0 2011 Insulin regulates GLUT1-mediated glucose transport in MG-63 human osteosarcoma cells. Glucose 33-40 insulin Homo sapiens 0-7 21070095-4 2011 Insulin sensitivity was determined by the frequently sampled intravenous glucose tolerance test (FSIVGTT) in boys and by a 3-hour oral glucose tolerance test with multiple sampling calculations for the whole-body insulin sensitivity index (WBISI) in girls. Glucose 73-80 insulin Homo sapiens 0-7 20668935-7 2011 Insulin resistance was evaluated by the homeostasis model assessment method (HOMA-IR) using fasting glucose and insulin levels. Glucose 100-107 insulin Homo sapiens 0-7 20878500-7 2011 The significant correlation between GGT and acute glucose dysmetabolism (as indicated by admission glycemia and insulin-resistance) can account, at least in part, for the prognostic role of GGT. Glucose 50-57 insulin Homo sapiens 112-119 21647634-5 2011 After the application of anti-STEAP4 antibodies at 0.002 mg/mL, adipocytes exhibited reduced insulin-stimulated glucose transport by attenuating the phosphorylation of IRS-1, PI3K (p85), and Akt. Glucose 112-119 insulin Homo sapiens 93-100 21647634-7 2011 In conclusion, (i) STEAP4 regulates the function of IRS-1, PI3K, and Akt and decreases insulin-induced GLUT4 translocation and glucose uptake; (ii) ROS-related mitochondrial dysfunction may be related to a reduced IRS-1 correlation with the PI3K signaling pathway, leading to insulin resistance. Glucose 127-134 insulin Homo sapiens 87-94 21321933-11 2011 One possible mechanism through which insulin is involved in cancer progression is by increasing the amount of glucose available to the cancer cell. Glucose 110-117 insulin Homo sapiens 37-44 21411544-2 2011 RESEARCH DESIGN AND METHODS: Ten obese type 2 diabetic patients were infused with insulin (2 U/h with 100 ml 5% dextrose/h) for 4 h. Patients were also infused with 5% dextrose/h or normal physiological saline for 4 h, respectively, on two other days as controls. Glucose 112-120 insulin Homo sapiens 82-89 21508135-8 2011 Insulin sensitivity increased in controls (steady-state glucose infusion rate = 7.0 +- 2.0 mg/kg min pretraining training vs. 8.7 +- 3.1 mg/kg min posttraining; P < 0.01) but did not improve in MS subjects (3.3 +- 1.3 pre vs. 3.1 +- 1.0 post). Glucose 56-63 insulin Homo sapiens 0-7 21555852-2 2011 It has thus been suggested that primary and/or genetic abnormalities in mitochondrial function may lead to accumulation of toxic lipid species in muscle and elsewhere, impairing insulin action on glucose metabolism. Glucose 196-203 insulin Homo sapiens 178-185 21411549-8 2011 During the first 60 min of the oral glucose tolerance test, the rise in plasma insulin and the insulinogenic index were positively correlated with the D/N of V, even after adjustment for age, waist circumference, 24-h urine volume, and BP (P < 0.001 for both), suggesting inadequate insulin secretion in poor daytime excretors. Glucose 36-43 insulin Homo sapiens 79-86 21576825-6 2011 This resulted in increased insulin-induced suppression of hepatic gluconeogenesis, improved glucose tolerance, and reduced hepatosteatosis with aging. Glucose 92-99 insulin Homo sapiens 27-34 20631738-7 2011 Despite comparable anthropometric parameters and body fat distribution assessed by magnetic resonance imaging in both groups, newly diagnosed untreated young hypertensive male subjects showed decreased insulin sensitivity, augmented insulin response to both oral and intravenous glucose load (P<0.01; P<0.05 respectively) and "higher still normal" 2-h plasma glucose levels during OGTT. Glucose 279-286 insulin Homo sapiens 233-240 21505353-4 2011 Insulin sensitivity was estimated during a 75-g oral glucose tolerance test. Glucose 53-60 insulin Homo sapiens 0-7 21357660-0 2011 Dose-dependent modulatory effects of insulin on glucose-induced endothelial senescence in vitro and in vivo: a relationship between telomeres and nitric oxide. Glucose 48-55 insulin Homo sapiens 37-44 21268025-0 2011 Phenylboronic acid grafted chitosan as a glucose-sensitive vehicle for controlled insulin release. Glucose 41-48 insulin Homo sapiens 82-89 21268025-1 2011 To develop self-regulated insulin delivery system, the glucose-sensitive copolymers with a fraction of phenylboronic acid group were prepared by the coupling reaction of -COOH of N-(carboxyacyl) chitosan and -NH(2) of 3-aminophenylboronic acid. Glucose 55-62 insulin Homo sapiens 26-33 21357660-5 2011 Physiological concentrations of insulin preserved telomere length and delayed endothelial senescence under high-glucose conditions. Glucose 112-119 insulin Homo sapiens 32-39 21268025-2 2011 A sufficient glucose sensitivity of the copolymer was accomplished by the glucose-induced volume changes of the nanoparticles and release profiles of insulin in phosphate buffered saline (PBS, pH 7.4) with different glucose concentrations, which occurred in a remarkable glucose concentration-dependent manner. Glucose 13-20 insulin Homo sapiens 150-157 21268025-2 2011 A sufficient glucose sensitivity of the copolymer was accomplished by the glucose-induced volume changes of the nanoparticles and release profiles of insulin in phosphate buffered saline (PBS, pH 7.4) with different glucose concentrations, which occurred in a remarkable glucose concentration-dependent manner. Glucose 74-81 insulin Homo sapiens 150-157 21268025-2 2011 A sufficient glucose sensitivity of the copolymer was accomplished by the glucose-induced volume changes of the nanoparticles and release profiles of insulin in phosphate buffered saline (PBS, pH 7.4) with different glucose concentrations, which occurred in a remarkable glucose concentration-dependent manner. Glucose 74-81 insulin Homo sapiens 150-157 21357660-6 2011 The effect of insulin under high-glucose conditions was associated with reduced reactive oxygen species and increased nitric oxide (NO). Glucose 33-40 insulin Homo sapiens 14-21 21268025-2 2011 A sufficient glucose sensitivity of the copolymer was accomplished by the glucose-induced volume changes of the nanoparticles and release profiles of insulin in phosphate buffered saline (PBS, pH 7.4) with different glucose concentrations, which occurred in a remarkable glucose concentration-dependent manner. Glucose 74-81 insulin Homo sapiens 150-157 21357660-8 2011 Physiological concentrations of insulin also reversed high glucose-induced increases in p53 and vascular cell adhesion molecule-1 and decreases in senescence marker protein-30. Glucose 59-66 insulin Homo sapiens 32-39 21357660-9 2011 On the other hand, when insulin was given at any concentrations under normal glucose or at high concentrations under high glucose, its ability to promote cellular senescence was unrelated to endothelial NO. Glucose 77-84 insulin Homo sapiens 24-31 21357660-11 2011 Conclusively, the regulatory effects of insulin on endothelial senescence were modulated by the glucose environment. Glucose 96-103 insulin Homo sapiens 40-47 21357660-9 2011 On the other hand, when insulin was given at any concentrations under normal glucose or at high concentrations under high glucose, its ability to promote cellular senescence was unrelated to endothelial NO. Glucose 122-129 insulin Homo sapiens 24-31 20817212-2 2011 Glucokinase regulates insulin secretion via phosphorylation of glucose. Glucose 63-70 insulin Homo sapiens 22-29 21324373-0 2011 Expression and function of the insulin receptor in normal and osteoarthritic human chondrocytes: modulation of anabolic gene expression, glucose transport and GLUT-1 content by insulin. Glucose 137-144 insulin Homo sapiens 31-38 21401839-1 2011 One of the most important metabolic actions of insulin is catalysing glucose uptake into skeletal muscle and adipose tissue. Glucose 69-76 insulin Homo sapiens 47-54 21779726-7 2011 CONCLUSIONS: High glucose could inhibit biological function of hPDLF and such effect could be blocked by insulin. Glucose 18-25 insulin Homo sapiens 105-112 21454697-1 2011 Insulin-stimulated translocation of the glucose transporter GLUT4 to the cell surface in fat and muscle cells is the basis for insulin-stimulated glucose transport. Glucose 40-47 insulin Homo sapiens 0-7 21454710-8 2011 Glucose-stimulated human islets released insulin similarly to rat islets but formed much more acetoacetate. Glucose 0-7 insulin Homo sapiens 41-48 21666815-2 2011 Rosiglitazone exerts its glucose-lowering effects by improving insulin sensitivity. Glucose 25-32 insulin Homo sapiens 63-70 21462967-7 2011 Glucose uptake in 3T3-L1 and L6C5 cells as well as the hypoglycemic effect in mice was significantly reduced after treatment with adducted insulin compared to native insulin. Glucose 0-7 insulin Homo sapiens 139-146 21462967-7 2011 Glucose uptake in 3T3-L1 and L6C5 cells as well as the hypoglycemic effect in mice was significantly reduced after treatment with adducted insulin compared to native insulin. Glucose 0-7 insulin Homo sapiens 166-173 21454697-1 2011 Insulin-stimulated translocation of the glucose transporter GLUT4 to the cell surface in fat and muscle cells is the basis for insulin-stimulated glucose transport. Glucose 40-47 insulin Homo sapiens 127-134 21393240-1 2011 Glucose-stimulated insulin release from pancreatic islet beta-cells involves increased levels of reactive oxygen and nitrogen species. Glucose 0-7 insulin Homo sapiens 19-26 21569503-2 2011 Abnormalities of B-cell function and glucose regulation by insulin and glucagon have been postulated as causes but associated gastrointestinal dysfunction has not been reported. Glucose 37-44 insulin Homo sapiens 59-66 21573217-8 2011 Insulin-induced glucose uptake in untransfected L6 (60% increase over basal), was totally abolished in L6-K and L6-Q cells. Glucose 16-23 insulin Homo sapiens 0-7 21535887-0 2011 A simple intravenous glucose tolerance test for assessment of insulin sensitivity. Glucose 21-28 insulin Homo sapiens 62-69 21535887-1 2011 BACKGROUND: The aim of the study was to find a simple intravenous glucose tolerance test (IVGTT) that can be used to estimate insulin sensitivity. Glucose 66-73 insulin Homo sapiens 126-133 21251239-3 2011 In this present work, we sought to investigate whether visfatin/eNAMPT is able to reproduce insulin effects on glucose transport and lipid metabolism. Glucose 111-118 insulin Homo sapiens 92-99 21389182-6 2011 RESULTS: The rs2953171 SNP interacted with plasma total saturated fatty acid (SFA) concentrations, which were significantly associated with insulin sensitivity (P < 0.031 for fasting insulin, P < 0.028 for HOMA-IR, and P < 0.012 for glucose effectiveness). Glucose 242-249 insulin Homo sapiens 140-147 21270293-1 2011 Glucose transporter 1 (GLUT1) is widely distributed throughout various tissues and contributes to insulin-independent basal glucose uptake. Glucose 124-131 insulin Homo sapiens 98-105 21307364-3 2011 Parameters of the insulin kinetic model were estimated from the complete set of glucose and insulin data collected in 219 anesthetized nonfasted NMR-imaged mice after intravenous injection of glucose (1 g/kg) alone or with GLP-1 (0.03-100 nmol/kg). Glucose 80-87 insulin Homo sapiens 18-25 21307364-3 2011 Parameters of the insulin kinetic model were estimated from the complete set of glucose and insulin data collected in 219 anesthetized nonfasted NMR-imaged mice after intravenous injection of glucose (1 g/kg) alone or with GLP-1 (0.03-100 nmol/kg). Glucose 192-199 insulin Homo sapiens 18-25 21325105-2 2011 To assess the effect of antioxidant supplementation during endurance training on insulin-stimulated glucose uptake, 21 young healthy (age 29 +- 1 y, BMI 25 +- 3 kg/m(2)) men were randomly assigned to either an antioxidant [AO; 500 mg vitamin C and 400 IU vitamin E (alpha-tocopherol) daily] or a placebo (PL) group that both underwent a supervised intense endurance-training program 5 times/wk for 12 wk. Glucose 100-107 insulin Homo sapiens 81-88 21325105-5 2011 Although plasma levels of vitamin C (P < 0.05) and alpha-tocopherol (P < 0.05) increased markedly in the AO group, insulin-stimulated glucose uptake increased similarly in both the AO (17.2%, P < 0.05) and the PL (18.9%, P < 0.05) group in response to training. Glucose 140-147 insulin Homo sapiens 121-128 21350183-2 2011 Diabetes is characterized by a defect in insulin secretion or a decrease in sensitivity to insulin, which results in elevated fasting blood glucose. Glucose 140-147 insulin Homo sapiens 41-48 21529219-6 2011 The minimal model of glucose and insulin dynamics was used to estimate SI, glucose effectiveness, and acute insulin response to glucose from tolerance testing data. Glucose 21-28 insulin Homo sapiens 108-115 21529219-6 2011 The minimal model of glucose and insulin dynamics was used to estimate SI, glucose effectiveness, and acute insulin response to glucose from tolerance testing data. Glucose 75-82 insulin Homo sapiens 33-40 21529219-6 2011 The minimal model of glucose and insulin dynamics was used to estimate SI, glucose effectiveness, and acute insulin response to glucose from tolerance testing data. Glucose 75-82 insulin Homo sapiens 33-40 21456517-8 2011 The utility of this rapid preparation method (~5 min) was demonstrated through precise metabolite measurements (11% average relative standard deviation without internal standards) associated with step changes in glucose concentration that evoke insulin secretion in the clonal beta-cell line INS-1. Glucose 212-219 insulin Homo sapiens 245-252 21115555-2 2011 The availability of continuous glucose monitoring systems in combination with continuous subcutaneous insulin infusion pumps provides an opportunity to monitor glucose levels more closely and deliver insulin more safely. Glucose 31-38 insulin Homo sapiens 200-207 21115555-2 2011 The availability of continuous glucose monitoring systems in combination with continuous subcutaneous insulin infusion pumps provides an opportunity to monitor glucose levels more closely and deliver insulin more safely. Glucose 160-167 insulin Homo sapiens 102-109 21115555-3 2011 We report on a preterm infant with neonatal diabetes who had profound hypoglycaemia in response to bolus subcutaneous insulin therapy, but in whom we used the combination of continuous glucose monitoring and insulin pump therapy to manage glucose control in the neonatal period, and who was discharged home on pump therapy. Glucose 239-246 insulin Homo sapiens 208-215 21354306-3 2011 Insulin and insulin-like growth factor-1 (IGF-1) receptor signaling inhibits glucose-induced caspase-3 activation and apoptotic cell death. Glucose 77-84 insulin Homo sapiens 0-7 21382444-2 2011 Recently, 9-cis-RA has been identified in vivo in the pancreas, where it contributes to regulating glucose-stimulated insulin secretion. Glucose 99-106 insulin Homo sapiens 118-125 21532121-1 2011 It has been demonstrated that osteocalcin, osteoblast-derived molecule, regulates glucose/lipid metabolism through increasing insulin secretion from pancreas and insulin sensitivity in peripheral tissues. Glucose 82-89 insulin Homo sapiens 126-133 21532121-1 2011 It has been demonstrated that osteocalcin, osteoblast-derived molecule, regulates glucose/lipid metabolism through increasing insulin secretion from pancreas and insulin sensitivity in peripheral tissues. Glucose 82-89 insulin Homo sapiens 162-169 21532121-5 2011 This finding indicated that the osteoblasts is an important target cells used by insulin which playing a central role in glucose/lipid metabolism. Glucose 121-128 insulin Homo sapiens 81-88 21539509-3 2011 We describe the effects of ghrelin on all aspects of glucose homeostasis including glucose-stimulated insulin secretion, hepatic glucose production and insulin stimulated glucose disposal in the peripheral tissues. Glucose 83-90 insulin Homo sapiens 102-109 21539509-3 2011 We describe the effects of ghrelin on all aspects of glucose homeostasis including glucose-stimulated insulin secretion, hepatic glucose production and insulin stimulated glucose disposal in the peripheral tissues. Glucose 83-90 insulin Homo sapiens 102-109 21396732-0 2011 Contribution of first trimester fasting plasma insulin levels to the incidence of glucose intolerance in later pregnancy: Tanaka women"s clinic study. Glucose 82-89 insulin Homo sapiens 47-54 21411512-5 2011 Multiorgan insulin sensitivity before and after treatment was evaluated by using the hyperinsulinemic-euglycemic clamp procedure in conjunction with stable isotopically labeled tracer infusions to measure glucose, glycerol, and fatty acid kinetics. Glucose 205-212 insulin Homo sapiens 11-18 21467247-7 2011 CONCLUSIONS: Coordinating insulin administration, glucose monitoring, and meal delivery within the tight time frames required for rapid-acting insulin is a significant challenge not being met. Glucose 50-57 insulin Homo sapiens 143-150 21267535-0 2011 Type 2 diabetes risk allele near CENTD2 is associated with decreased glucose-stimulated insulin release. Glucose 69-76 insulin Homo sapiens 88-95 21267535-2 2011 Here we evaluate the effect of lead variants of these loci on estimates of insulin release and insulin resistance derived from an oral glucose tolerance test. Glucose 135-142 insulin Homo sapiens 75-102 21267535-11 2011 CONCLUSIONS/INTERPRETATION: Of the lead variants from 12 novel type 2 diabetes associated loci, CENTD2 significantly associated with increased plasma glucose values and decreased glucose-stimulated insulin release, suggesting that the diabetogenic effect of this locus is mediated through an impaired pancreatic beta cell function. Glucose 179-186 insulin Homo sapiens 198-205 21298414-7 2011 We therefore assessed the NAMPT dynamic following an oral glucose load and found a significant decline of NAMPT levels to 77.0 +- 0.1% as a function of time, and insulin-to-glucose ratio during an OGTT in obese insulin-resistant adolescents. Glucose 58-65 insulin Homo sapiens 162-169 22127804-4 2011 The pancreatic effects of GLP-1 receptor agonists include glucose-lowering effects by stimulating insulin secretion and inhibiting glucagon release in a strictly glucose-dependent manner, increased beta-cell proliferation, and decreased beta-cell apoptosis. Glucose 58-65 insulin Homo sapiens 98-105 21325017-1 2011 CONTEXT: Mitochondrial ATP production is important in the regulation of glucose-stimulated insulin secretion. Glucose 72-79 insulin Homo sapiens 91-98 21325017-4 2011 DESIGN AND METHODS: To find polymorphisms associated with glucose-stimulated insulin secretion, data from a genome-wide association study (GWAS) of 1467 non-diabetic individuals, including the Diabetes Genetic Initiative (DGI), was examined. Glucose 58-65 insulin Homo sapiens 77-84 21325017-7 2011 Insulinogenic index during an oral glucose tolerance test was used as a surrogate marker of glucose-stimulated insulin secretion. Glucose 92-99 insulin Homo sapiens 111-118 21325017-11 2011 CONCLUSION: Our study shows that genetic variation near genes involved in OXPHOS may influence glucose-stimulated insulin secretion in vivo. Glucose 95-102 insulin Homo sapiens 114-121 21104586-5 2011 The counter directional change in insulin and IGFBP-1 concentrations, expressed as a factor that takes into consideration the rate of insulin increase and IGFBP-1 decrease after glucose intake was approximately twice more pronounced in patients with diabetes than in healthy and hypoglycemic persons. Glucose 178-185 insulin Homo sapiens 34-41 21378389-11 2011 CONCLUSIONS: In this randomised trial, early intensive glucose control with insulin in patients with ACS presenting with hyperglycaemia was found to decrease platelet reactivity. Glucose 55-62 insulin Homo sapiens 76-83 21448848-6 2011 In CF patients, there was a decrease in first phase insulin secretion (FPIR) with progressive delay of insulin peak, which was correlated with worsening glucose tolerance (Stumvoll index: normal glucose tolerance: 450+-291; impaired fasting glucose: 252+-203; impaired glucose tolerance: 309+-254; CF related diabetes: 18+-41; controls: 950+-388) and high early post-challenge glucose peak (p<0.01 vs. controls). Glucose 195-202 insulin Homo sapiens 52-59 21448848-6 2011 In CF patients, there was a decrease in first phase insulin secretion (FPIR) with progressive delay of insulin peak, which was correlated with worsening glucose tolerance (Stumvoll index: normal glucose tolerance: 450+-291; impaired fasting glucose: 252+-203; impaired glucose tolerance: 309+-254; CF related diabetes: 18+-41; controls: 950+-388) and high early post-challenge glucose peak (p<0.01 vs. controls). Glucose 153-160 insulin Homo sapiens 52-59 21448848-6 2011 In CF patients, there was a decrease in first phase insulin secretion (FPIR) with progressive delay of insulin peak, which was correlated with worsening glucose tolerance (Stumvoll index: normal glucose tolerance: 450+-291; impaired fasting glucose: 252+-203; impaired glucose tolerance: 309+-254; CF related diabetes: 18+-41; controls: 950+-388) and high early post-challenge glucose peak (p<0.01 vs. controls). Glucose 195-202 insulin Homo sapiens 52-59 21448848-6 2011 In CF patients, there was a decrease in first phase insulin secretion (FPIR) with progressive delay of insulin peak, which was correlated with worsening glucose tolerance (Stumvoll index: normal glucose tolerance: 450+-291; impaired fasting glucose: 252+-203; impaired glucose tolerance: 309+-254; CF related diabetes: 18+-41; controls: 950+-388) and high early post-challenge glucose peak (p<0.01 vs. controls). Glucose 195-202 insulin Homo sapiens 52-59 21541992-8 2011 Through its endocrine actions on target tissues of insulin, FoxO1 acts by way of osteocalcin to suppress glucose production by pancreatic beta cells and hepatocytes and to decrease insulin production and sensitivity. Glucose 105-112 insulin Homo sapiens 51-58 21289240-6 2011 RESULTS: Lipid infusion reduced insulin-stimulated glucose disposal by approximately 40%, glucose oxidation (CHOox) by approximately 50%, and NOGD by approximately 35%. Glucose 51-58 insulin Homo sapiens 32-39 21289242-8 2011 RESULTS: Although subjects were identical with respect to age, body composition, energy expenditure, and lipid status, insulin-stimulated glucose disposal and maximum oxygen consumption showed progressive decline with increasing glucose intolerance. Glucose 138-145 insulin Homo sapiens 119-126 21289242-8 2011 RESULTS: Although subjects were identical with respect to age, body composition, energy expenditure, and lipid status, insulin-stimulated glucose disposal and maximum oxygen consumption showed progressive decline with increasing glucose intolerance. Glucose 229-236 insulin Homo sapiens 119-126 21289242-12 2011 CONCLUSIONS: Impaired muscle capillarization and reduced nutrient exposure to the metabolizing tissue may play a major role in the progression of insulin resistance across the glucose tolerance continuum, independent of age, adiposity, lipid status, and resting energy metabolism. Glucose 176-183 insulin Homo sapiens 146-153 21307134-12 2011 Data were further analyzed after dividing patients on the basis of pretreatment insulinemic response to the oral glucose tolerance test; metformin was effective in reducing insulin secretion, AMH levels, and, interestingly, ovarian volume exclusively in PCOS patients with hyperinsulinism; none of these changes occurred in the normoinsulinemic group. Glucose 113-120 insulin Homo sapiens 80-87 21325461-10 2011 However, measures of insulin sensitivity (glucose infusion and disappearance rates) correlated positively with C-terminal telopeptide of type I collagen levels. Glucose 42-49 insulin Homo sapiens 21-28 21335539-7 2011 Day 10 ICAs released insulin and C-peptide in a glucose-dependent manner, exhibiting in vitro functionality. Glucose 48-55 insulin Homo sapiens 21-28 21335539-7 2011 Day 10 ICAs released insulin and C-peptide in a glucose-dependent manner, exhibiting in vitro functionality. Glucose 48-55 insulin Homo sapiens 33-42 21346075-0 2011 Higher maternal gestational glucose concentration is associated with lower offspring insulin sensitivity and altered beta-cell function. Glucose 28-35 insulin Homo sapiens 85-92 21346075-2 2011 However, studies examining the effects of maternal glucose concentration on measures of insulin sensitivity and beta-cell response in prepubertal children are limited. Glucose 51-58 insulin Homo sapiens 88-95 21346075-3 2011 OBJECTIVE: We tested the hypothesis that maternal gestational glucose concentration would be inversely associated with children"s insulin sensitivity independent of adiposity and positively associated with children"s beta-cell response independent of adiposity and insulin sensitivity. Glucose 62-69 insulin Homo sapiens 130-137 21346075-3 2011 OBJECTIVE: We tested the hypothesis that maternal gestational glucose concentration would be inversely associated with children"s insulin sensitivity independent of adiposity and positively associated with children"s beta-cell response independent of adiposity and insulin sensitivity. Glucose 62-69 insulin Homo sapiens 265-272 21346075-8 2011 RESULTS: Maternal glucose concentration was significantly, inversely associated with children"s insulin sensitivity, independent of percent fat and ethnicity (P <0.05). Glucose 18-25 insulin Homo sapiens 96-103 21346075-10 2011 CONCLUSIONS: Maternal gestational glucose concentration was significantly associated with offspring insulin sensitivity and beta-cell response independent of adiposity. Glucose 34-41 insulin Homo sapiens 100-107 21346075-11 2011 These results suggest that maternal glucose may program the fetus both at the pancreas and at the level of insulin target tissues such as skeletal muscle and liver. Glucose 36-43 insulin Homo sapiens 107-114 21367930-0 2011 The effect of insulin feedback on closed loop glucose control. Glucose 46-53 insulin Homo sapiens 14-21 21722581-1 2011 BACKGROUND: Real-time continuous glucose monitoring (RT-CGM) improves hemoglobin A1c (A1C) and hypoglycemia in people with type 1 diabetes mellitus and those with type 2 diabetes mellitus (T2DM) on prandial insulin; however, it has not been tested in people with T2DM not taking prandial insulin. Glucose 33-40 insulin Homo sapiens 207-214 21722581-1 2011 BACKGROUND: Real-time continuous glucose monitoring (RT-CGM) improves hemoglobin A1c (A1C) and hypoglycemia in people with type 1 diabetes mellitus and those with type 2 diabetes mellitus (T2DM) on prandial insulin; however, it has not been tested in people with T2DM not taking prandial insulin. Glucose 33-40 insulin Homo sapiens 288-295 21722591-12 2011 Greater doses of insulin, but with dosing based on more accurate glucose levels, might result in less hypoglycemia, less hyperglycemia, and less glycemic variability. Glucose 65-72 insulin Homo sapiens 17-24 21118863-2 2011 An era of tight glucose control began when intensive insulin therapy was shown to improve outcomes in a single-center randomized trial. Glucose 16-23 insulin Homo sapiens 53-60 21531028-7 2011 Activation of key phosphatases play a major role in the regulation of glucose disposal by oxidative metabolism via PDH, and the non-oxidative storage by glycogen synthesis, both pathways classically known to be regulated by insulin. Glucose 70-77 insulin Homo sapiens 224-231 21393239-1 2011 The transcription factor PDX1 plays a critical role during beta-cell development and in glucose-induced insulin gene transcription in adult beta-cells. Glucose 88-95 insulin Homo sapiens 104-111 21527604-7 2011 RESULTS: After D-Glc infusion, plasma insulin concentrations increased significantly (period I, 6.6 +- 1.8 microU/mL; period II, 21.4 +- 2.1 microU/mL; P < .01). Glucose 15-20 insulin Homo sapiens 38-45 21280205-2 2011 Insulin increases the extraction of glucose from circulation into adipose tissue by recruiting the glucose transporter GLUT4 to the plasma membrane. Glucose 36-43 insulin Homo sapiens 0-7 20850158-10 2011 The ISI-Mat values were better correlated than HOMA(IR) (r = 0.875, P = .0001 and r = -0.631, P = .0001, respectively) with insulin sensitivity index obtained with intravenous glucose tolerance test. Glucose 176-183 insulin Homo sapiens 124-131 21280205-6 2011 A screening of representative flavonoids of different structural classes revealed the flavanone naringenin and the isoflavone daidzein to affect glucose transport significantly with half-maximal inhibition at concentrations of around 60-80 muM for basal and 70-110 muM for insulin-stimulated glucose uptake in both 3T3-L1 adipocytes and mature human adipocytes. Glucose 145-152 insulin Homo sapiens 273-280 21468601-0 2011 Knockdown of STEAP4 inhibits insulin-stimulated glucose transport and GLUT4 translocation via attenuated phosphorylation of Akt, independent of the effects of EEA1. Glucose 48-55 insulin Homo sapiens 29-36 21468601-2 2011 Our data demonstrated that siRNA-mediated STEAP4 deficiency significantly decreased insulin-stimulated glucose transport in mature human adipocytes by decreasing GLUT4 translocation to the plasma membrane through attenuated Akt phosphorylation. Glucose 103-110 insulin Homo sapiens 84-91 21468601-4 2011 In conclusion, this study revealed that the knockdown of STEAP4 inhibits insulin-stimulated glucose transport and GLUT4 translocation via the attenuated phosphorylation of Akt, independent of the effects of EEA1. Glucose 92-99 insulin Homo sapiens 73-80 21595275-3 2011 Pioglitazone, a thiazolidinedione class agent, is an insulin sensitizer and alogliptin belongs to DPP-4 (dipeptidyl peptidase-4) inhibitor class agents, which promote postprandial insulin secretion and suppress glucagon secretion in a blood glucose dependent fashion. Glucose 241-248 insulin Homo sapiens 180-187 21595276-4 2011 Liraglutide increases insulin secretion in a glucose-dependent manner, and improves first- and second-phase insulin responses. Glucose 45-52 insulin Homo sapiens 22-29 21595284-3 2011 Although the mechanisms by which TCF7L2 affects susceptibility to type 2 diabetes remain to be elucidated, several studies have shown that decreased TCF7L2 protein inhibits the insulin secretory response to oral glucose through impaired incretin action(GLP-1, GIP). Glucose 212-219 insulin Homo sapiens 177-184 21595265-2 2011 Not only enhancing glucose-stimulated insulin secretion, but incretins exert beta-cell mass maintaining effects by upregulation of proliferation and prevention of cell death (apoptosis). Glucose 19-26 insulin Homo sapiens 38-45 21214701-0 2011 Independent relationships of obesity and insulin resistance with serum proinsulin level in prepubertal children with normal glucose tolerance. Glucose 124-131 insulin Homo sapiens 41-48 20935589-5 2011 INTERVENTIONS: Glucose was monitored and insulin used for persistent hyperglycemia (glucose >140 mg/dL [7.8 mmol/L] for at least two observations separated by at least a 1-hr interval), with a target glucose during insulin use of 60-140 mg/dL (3.3-7.8 mmol/L). Glucose 84-91 insulin Homo sapiens 41-48 20935589-8 2011 Insulin infusion was most frequently started on day 1 (61%), with a glucose level at the time of 229 +- 79 mg/dL (12.7 +- 4.4 mmol/L). Glucose 68-75 insulin Homo sapiens 0-7 20935589-9 2011 The mean glucose level after 6 hrs of insulin was 172 +- 87 mg/dL (9.6 +- 4.8 mmol/L), and the time to achieve the target glucose range was 9.5 (2-20) hrs (median [interquartile range]). Glucose 9-16 insulin Homo sapiens 38-45 21214701-0 2011 Independent relationships of obesity and insulin resistance with serum proinsulin level in prepubertal children with normal glucose tolerance. Glucose 124-131 insulin Homo sapiens 71-81 21042331-0 2011 Insulin resistance in tetraplegia but not in mid-thoracic paraplegia: is the mid-thoracic spinal cord involved in glucose regulation? Glucose 114-121 insulin Homo sapiens 0-7 21518412-2 2011 OBJECTIVE: Here we assessed the relationship among fasting PI, clinical parameters, and carbohydrate metabolism, a potential difference of the PI/I ratio between overweight and obese youth with or without IGR in an oral glucose tolerance test (OGTT) and the predictive power of PI levels for IGR. Glucose 220-227 insulin Homo sapiens 59-61 21518412-2 2011 OBJECTIVE: Here we assessed the relationship among fasting PI, clinical parameters, and carbohydrate metabolism, a potential difference of the PI/I ratio between overweight and obese youth with or without IGR in an oral glucose tolerance test (OGTT) and the predictive power of PI levels for IGR. Glucose 220-227 insulin Homo sapiens 143-145 21518412-10 2011 CONCLUSIONS: Children and adolescents with IGR have disproportionately elevated PI levels, both during fasting and after acute glucose stimulation indicating beta-cell dysfunction. Glucose 127-134 insulin Homo sapiens 80-82 21673486-5 2011 Both insulin pump therapy and multiple daily injections are beneficial treatment options to lower average glucose levels; however, without continuous glucose monitoring, these treatment options typically increase the risk of hypoglycemia. Glucose 106-113 insulin Homo sapiens 5-12 21357685-0 2011 Glucose-stimulated translation regulation of insulin by the 5" UTR-binding proteins. Glucose 0-7 insulin Homo sapiens 45-52 21357685-1 2011 Insulin is the key regulator of glucose homeostasis in mammals, and glucose-stimulated insulin biosynthesis is essential for maintaining glucose levels in a narrow range in mammals. Glucose 32-39 insulin Homo sapiens 0-7 21357685-1 2011 Insulin is the key regulator of glucose homeostasis in mammals, and glucose-stimulated insulin biosynthesis is essential for maintaining glucose levels in a narrow range in mammals. Glucose 68-75 insulin Homo sapiens 87-94 21357685-2 2011 Glucose specifically promotes the translation of insulin in pancreatic beta-islet, and the untranslated regions of insulin mRNA play a role in such regulation. Glucose 0-7 insulin Homo sapiens 49-56 21357685-4 2011 In the present study we identify protein-disulfide isomerase (PDI) as a key regulator of glucose-stimulated insulin biosynthesis. Glucose 89-96 insulin Homo sapiens 108-115 21357685-6 2011 Immunodepletion of PDI from the islet extract results in loss of glucose-stimulated translation indicating a critical role for PDI in insulin biosynthesis. Glucose 65-72 insulin Homo sapiens 134-141 21195125-1 2011 Insulin increases muscle and fat cell glucose uptake by inducing the translocation of glucose transporter GLUT4 from intracellular compartments to the plasma membrane. Glucose 38-45 insulin Homo sapiens 0-7 21144097-10 2011 In conclusion, SI and insulin response to the glucose load differed between the COMT genotype groups, and this may be suggestive of a green tea extract and genotype interaction. Glucose 46-53 insulin Homo sapiens 22-29 21563902-25 2011 Glucose concentrations must be monitored regularly and supplementation of glucose will likely be required throughout therapy and for up to 24 h after discontinuation of high-dose insulin. Glucose 74-81 insulin Homo sapiens 179-186 21240641-3 2011 Studies of patients with diabetes have shown that the heart is resistant to insulin-mediated glucose uptake and that metabolism of nonesterified FA is upregulated. Glucose 93-100 insulin Homo sapiens 76-83 21279740-4 2011 Besides its classic actions, aldosterone and mineralocorticoid receptor (MR) activation affect glucose metabolism, inducing insulin resistance through various mechanisms that involve oxidative stress, inflammation, and downregulation of proteins involved in insulin signaling pathways. Glucose 95-102 insulin Homo sapiens 258-265 21249489-0 2011 The diabetogenic VPS13C/C2CD4A/C2CD4B rs7172432 variant impairs glucose-stimulated insulin response in 5,722 non-diabetic Danish individuals. Glucose 64-71 insulin Homo sapiens 83-90 21249489-5 2011 In analyses adjusted for concomitant insulin sensitivity levels the diabetogenic allele was associated with a lower acute glucose-stimulated insulin response (GSIR) as estimated by 30 min serum insulin (beta = -0.039, p = 2 x 10(-7)), insulinogenic index (beta = -0.057, p = 1 x 10(-8)) and BIGTT-acute insulin release (beta = -0.041, p = 9 x 10(-9)). Glucose 122-129 insulin Homo sapiens 37-44 21249489-5 2011 In analyses adjusted for concomitant insulin sensitivity levels the diabetogenic allele was associated with a lower acute glucose-stimulated insulin response (GSIR) as estimated by 30 min serum insulin (beta = -0.039, p = 2 x 10(-7)), insulinogenic index (beta = -0.057, p = 1 x 10(-8)) and BIGTT-acute insulin release (beta = -0.041, p = 9 x 10(-9)). Glucose 122-129 insulin Homo sapiens 141-148 21249489-5 2011 In analyses adjusted for concomitant insulin sensitivity levels the diabetogenic allele was associated with a lower acute glucose-stimulated insulin response (GSIR) as estimated by 30 min serum insulin (beta = -0.039, p = 2 x 10(-7)), insulinogenic index (beta = -0.057, p = 1 x 10(-8)) and BIGTT-acute insulin release (beta = -0.041, p = 9 x 10(-9)). Glucose 122-129 insulin Homo sapiens 141-148 21249489-5 2011 In analyses adjusted for concomitant insulin sensitivity levels the diabetogenic allele was associated with a lower acute glucose-stimulated insulin response (GSIR) as estimated by 30 min serum insulin (beta = -0.039, p = 2 x 10(-7)), insulinogenic index (beta = -0.057, p = 1 x 10(-8)) and BIGTT-acute insulin release (beta = -0.041, p = 9 x 10(-9)). Glucose 122-129 insulin Homo sapiens 141-148 21292340-4 2011 Thus, the aim of this analysis was to assess which features and parameters of insulin pump use are associated with better glucose control. Glucose 122-129 insulin Homo sapiens 78-85 21330640-5 2011 RESULTS: Valsartan increased first-phase (P = 0.028) and second-phase (P = 0.002) glucose-stimulated insulin secretion compared with placebo, whereas the enhanced arginine-stimulated insulin secretion was comparable between groups (P = 0.25). Glucose 82-89 insulin Homo sapiens 101-108 21330640-6 2011 In addition, valsartan increased the OGTT-derived insulinogenic index (representing first-phase insulin secretion after an oral glucose load; P = 0.027). Glucose 128-135 insulin Homo sapiens 50-57 21330640-10 2011 CONCLUSIONS: Twenty-six weeks of valsartan treatment increased glucose-stimulated insulin release and insulin sensitivity in normotensive subjects with IGM. Glucose 63-70 insulin Homo sapiens 82-89 21355717-4 2011 RESULTS: Intradermal insulin infusion using microneedles reached peak insulin concentrations in approximately half the time and led to greater reduction in plasma glucose levels than subcutaneous catheters. Glucose 163-170 insulin Homo sapiens 21-28 21355724-8 2011 CONCLUSIONS: Because there is some evidence that insulin injection can cause a minor perturbation (about <=10%) in the local glycemia, caution is warranted when co-locating glucose sensing and insulin injection sites. Glucose 176-183 insulin Homo sapiens 49-56 21355725-0 2011 Associations between improved glucose control and patient-reported outcomes after initiation of insulin pump therapy in patients with type 2 diabetes mellitus. Glucose 30-37 insulin Homo sapiens 96-103 21355725-1 2011 BACKGROUND: This study assessed the relationship between changes in glucose control and changes in patient-reported outcomes (PRO)--health-related quality of life (HR-QoL) and treatment satisfaction (TxSat)--in patients with type 2 diabetes initiating insulin pump therapy. Glucose 68-75 insulin Homo sapiens 252-259 21378173-7 2011 Conditioned medium from control myotubes increased proliferation and glucose-stimulated insulin secretion (GSIS) from primary beta-cells, whereas conditioned medium from TNF-alpha-treated insulin-resistant myotubes (TMs) exerted detrimental effects that were either independent (increased apoptosis and decreased proliferation) or dependent on the presence of TNF-alpha in TM (blunted GSIS). Glucose 69-76 insulin Homo sapiens 88-95 21378174-0 2011 Partial inhibition of insulin secretion results in glucose intolerance but not hyperglucagonemia. Glucose 51-58 insulin Homo sapiens 22-29 21378174-1 2011 OBJECTIVE: We tested the hypotheses that in nondiabetic individuals, partial inhibition of insulin secretion with the ATP-sensitive K(+) channel agonist (opener) diazoxide, compared with placebo, results in higher plasma glucose and higher plasma glucagon concentrations after a mixed meal and after administration of the sulfonylurea glimepiride. Glucose 221-228 insulin Homo sapiens 91-98 21457557-1 2011 Insulin is one of the major metabolic hormones regulating glucose homeostasis in the organism and a key growth factor for normal and neoplastic cells. Glucose 58-65 insulin Homo sapiens 0-7 21321112-7 2011 Phosphorylation at this site impaired insulin signaling in adipocytes and reduced glucose uptake. Glucose 82-89 insulin Homo sapiens 38-45 21300027-1 2011 Glucose-stimulated insulin secretion [GSIS] involves a sequence of metabolic events leading to small G-protein [e.g., Rac1]-mediated cytoskeletal remodeling to promote granule mobilization toward the plasma membrane for fusion and release of insulin. Glucose 0-7 insulin Homo sapiens 19-26 21349852-10 2011 Insulin significantly increased cytosolic glucose concentration in adipocytes by a factor of 3.6; however, we recorded no effect on delta ratio (DeltaR) in fibroblasts. Glucose 42-49 insulin Homo sapiens 0-7 21349852-12 2011 However, in adipocytes in insulin-stimulated conditions, glucose clearance was significantly faster following adrenaline addition in comparison with controls (p < 0.001). Glucose 57-64 insulin Homo sapiens 26-33 21493665-5 2011 INTERVENTION: During overnight closed loop delivery, sensor measurements of glucose were fed into a computer algorithm, which advised on insulin pump infusion rates at 15 minute intervals. Glucose 76-83 insulin Homo sapiens 137-144 21493665-11 2011 RESULTS: For the eating in scenario, overnight closed loop delivery of insulin increased the time plasma glucose levels were in target by a median 15% (interquartile range 3-35%), P = 0.002. Glucose 105-112 insulin Homo sapiens 71-78 21493665-15 2011 CONCLUSION: These two small crossover trials suggest that closed loop delivery of insulin may improve overnight control of glucose levels and reduce the risk of nocturnal hypoglycaemia in adults with type 1 diabetes. Glucose 123-130 insulin Homo sapiens 82-89 21559208-1 2011 Rosiglitazone, an agonist of peroxisome proliferator activated receptor (PPARgamma), improves insulin sensitivity by increasing insulin-stimulated glucose uptake into muscle tissue. Glucose 147-154 insulin Homo sapiens 128-135 21396911-0 2011 Prolonged inorganic arsenite exposure suppresses insulin-stimulated AKT S473 phosphorylation and glucose uptake in 3T3-L1 adipocytes: involvement of the adaptive antioxidant response. Glucose 97-104 insulin Homo sapiens 49-56 21396911-2 2011 One critical feature of T2D is insulin resistance in peripheral tissues, especially in mature adipocytes, the hallmark of which is decreased insulin-stimulated glucose uptake (ISGU). Glucose 160-167 insulin Homo sapiens 141-148 24843466-4 2011 First-phase insulin response to glucose is lost very early in the development of type 2 diabetes. Glucose 32-39 insulin Homo sapiens 12-19 24843467-9 2011 These insulin gene mutations with hyper(pro)insulinemia were very rare, showed only mild diabetes or glucose intolerance, and hyper(pro)insulinemia was the key for their diagnosis. Glucose 101-108 insulin Homo sapiens 6-13 24843473-1 2011 INTRODUCTION: The aim of the present study is to propose a novel index of insulin sensitivity instead of homeostasis model assessment of insulin resistance (HOMA-IR), which has a fundamental limitation of validity when applied to subjects with lower insulin secretions or high fasting plasma glucose (FPG) levels. Glucose 294-301 insulin Homo sapiens 76-83 21470398-4 2011 Insulin secretion in the presence of non-glycated human albumin (HA) and GA was measured under three different glucose concentrations, 3 mM (G3), 7 mM (G7), and 15 mM (G15), with various stimulators. Glucose 111-118 insulin Homo sapiens 0-7 21470398-10 2011 CONCLUSION: GA suppresses glucose-induced insulin secretion from rat pancreatic beta-cells through impairment of intracellular glucose metabolism. Glucose 26-33 insulin Homo sapiens 42-49 21496149-7 2011 CONCLUSIONS: This small sample suggests that adjusted insulin infusion efficiently lowers blood glucose in the ultra-acute phase of stroke and is feasible in the prehospital setting. Glucose 96-103 insulin Homo sapiens 54-61 21785179-5 2011 Its formulations have both basal and short or rapid-acting insulin capabilities, enabling them to cover both fasting and postprandial blood glucose levels. Glucose 140-147 insulin Homo sapiens 59-66 21304064-4 2011 Glucose infusion rates during low-dose insulin were not significantly different in GB compared with either L or O. Glucose 0-7 insulin Homo sapiens 39-46 21304064-5 2011 During high-dose insulin, glucose infusion rates were significantly greater in GB than in O but less than in L. Endogenous glucose production in GB was significantly lower than O only during low dose of insulin. Glucose 123-130 insulin Homo sapiens 203-210 21248305-10 2011 We also found that the type of glucose shape is often associated to similar insulin and C-peptide shape. Glucose 31-38 insulin Homo sapiens 76-83 21248305-10 2011 We also found that the type of glucose shape is often associated to similar insulin and C-peptide shape. Glucose 31-38 insulin Homo sapiens 88-97 21484623-7 2011 Using this framework, therapy with insulin may be used to achieve a targeted range of glucose avoiding an increased risk of hypoglycaemia. Glucose 86-93 insulin Homo sapiens 35-42 22468051-8 2011 While insulin level and HOMA-IR both were significantly positively correlated with BMI, waist-to-hip ratio, total cholesterol, VLDL-cholesterol, triglyceride and TGF-beta1; glucose, IL-6 and TNF-alpha levels were significantly positively correlated with HOMA-IR only. Glucose 173-180 insulin Homo sapiens 6-13 21249616-3 2011 However, skeletal muscle is the predominant site of insulin-mediated glucose disposal, which is known to be reduced in obesity. Glucose 69-76 insulin Homo sapiens 52-59 21282352-2 2011 Vaspin (SERPINA12) is a novel insulin-sensitizing adipokine that might be implicated in endogenous glucose regulation. Glucose 99-106 insulin Homo sapiens 30-37 22468049-4 2011 Some of these adipokines have been shown to directly or indirectly affect insulin sensitivity through modulation of insulin signaling and the molecules involved in glucose and lipid metabolism. Glucose 164-171 insulin Homo sapiens 74-81 21789431-7 2011 Insulin resistance were assessed by the insulin sensitivity check index (QUICKI) determined as follow: 1/[log(Io) + log(Go)], where Io is the fasting insulin, and Go is the fasting glucose. Glucose 181-188 insulin Homo sapiens 0-7 20856257-11 2011 Although vaspin"s association with obesity remains controversial, vaspin was increased with worsening insulin resistance already in children and was acutely down-regulated following glucose provocation in insulin-resistant adolescents independent of obesity. Glucose 182-189 insulin Homo sapiens 205-212 21239518-8 2011 CONCLUSIONS: DPP-4 inhibition augmented insulin secretory responses both after oral glucose and during isoglycemic iv glucose infusions, with no net change in the incretin effect. Glucose 84-91 insulin Homo sapiens 40-47 21239518-10 2011 Or, DPP-4 inhibitor-induced change in the incretin-related environment of islets may persist overnight, augmenting insulin secretory responses to iv glucose as well. Glucose 149-156 insulin Homo sapiens 115-122 21252243-8 2011 In individuals in the highest insulin quartile, the odds ratio for developing T2DM remained significant even after multivariate adjustment including baseline glucose concentration [2.42 (1.23-4.75)]. Glucose 158-165 insulin Homo sapiens 30-37 21476781-8 2011 The AHRQ systematic review indicated that premixed insulin analogues are more effective than long-acting insulin analogues in lowering postprandial glucose and hemoglobin A1c; however, in this comparison the premixed analogues were associated with higher rates of hypoglycemia and more weight gain. Glucose 148-155 insulin Homo sapiens 51-58 21505982-5 2011 The results showed that after the treatment with palmitic acid for 24 h, the insulin-stimulated glucose transport in HepG2 cells was inhibited, and the glucose consumption was substantially reduced. Glucose 96-103 insulin Homo sapiens 77-84 21476781-8 2011 The AHRQ systematic review indicated that premixed insulin analogues are more effective than long-acting insulin analogues in lowering postprandial glucose and hemoglobin A1c; however, in this comparison the premixed analogues were associated with higher rates of hypoglycemia and more weight gain. Glucose 148-155 insulin Homo sapiens 105-112 21356519-0 2011 Impaired insulin signaling in endothelial cells reduces insulin-induced glucose uptake by skeletal muscle. Glucose 72-79 insulin Homo sapiens 9-16 21348785-0 2011 The relationship between glycosylated haemoglobin (HbA1c) and measures of insulin resistance across a range of glucose tolerance. Glucose 111-118 insulin Homo sapiens 74-81 21348785-3 2011 All had specimens taken in the context of a standard oral glucose tolerance test at their first visit and had the insulin sensitivity parameter (Si) determined by frequently-sampled intravenous glucose tolerance test at a second visit. Glucose 194-201 insulin Homo sapiens 114-121 21614978-5 2011 Patients with triglyceride levels in excess of 10 mmol/l were treated with either standard supportive therapy or an insulin dextrose infusion. Glucose 124-132 insulin Homo sapiens 116-123 21484688-5 2011 Diagnosis was considered whenever hyperinsulinemia >= 10mu UI/ml was concomitant to hypoglycemia < 3mmol/l and/or high insulin to glucose ratio > 0.3 and/or positif glucagon test. Glucose 136-143 insulin Homo sapiens 39-46 21262219-9 2011 Furthermore, TS-021 exhibited a significant improvement in glucose tolerance by increasing the plasma insulin level during oral glucose tolerance tests at doses of 0.02-0.5mg/kg. Glucose 128-135 insulin Homo sapiens 102-109 21443773-10 2011 CONCLUSION: This report demonstrates that sitagliptin is effective and safe as an add-on therapy to insulin in reducing blood glucose levels in patients who absolutely lack the capacity for endogenous insulin secretion. Glucose 126-133 insulin Homo sapiens 100-107 24212773-4 2011 Of these, GLUT-4 is essential for insulin-stimulated glucose uptake. Glucose 53-60 insulin Homo sapiens 34-41 21252237-1 2011 Insulin regulates glucose uptake through effects on the trafficking of the glucose transporter Glut4. Glucose 18-25 insulin Homo sapiens 0-7 21437235-7 2011 HER2 over expression in MCF10A cells resulted in glucose uptake in the absence of insulin at a rate equal to insulin-induced glucose uptake in non-transduced cells. Glucose 125-132 insulin Homo sapiens 109-116 21437235-9 2011 To gain insight into how HER2 oncogene signaling affected increased insulin-independent glucose uptake we compared HER2-regulated gene expression signatures in MCF10A and HER2 over expressing MCF10A cells by differential analysis of time series gene expression data from cells treated with a HER2 inhibitor. Glucose 88-95 insulin Homo sapiens 68-75 21356519-6 2011 Taken together, our results show that insulin signaling in endothelial cells plays a pivotal role in the regulation of glucose uptake by skeletal muscle. Glucose 119-126 insulin Homo sapiens 38-45 21356520-5 2011 Here we show that these incretin-stimulated pathways converge at the level of snapin, and that PKA-dependent phosphorylation of snapin increases interaction among insulin secretory vesicle-associated proteins, thereby potentiating glucose-stimulated insulin secretion (GSIS). Glucose 231-238 insulin Homo sapiens 163-170 21356519-0 2011 Impaired insulin signaling in endothelial cells reduces insulin-induced glucose uptake by skeletal muscle. Glucose 72-79 insulin Homo sapiens 56-63 21356519-3 2011 We demonstrate that impaired insulin signaling in endothelial cells, due to reduced Irs2 expression and insulin-induced eNOS phosphorylation, causes attenuation of insulin-induced capillary recruitment and insulin delivery, which in turn reduces glucose uptake by skeletal muscle. Glucose 246-253 insulin Homo sapiens 29-36 21356519-3 2011 We demonstrate that impaired insulin signaling in endothelial cells, due to reduced Irs2 expression and insulin-induced eNOS phosphorylation, causes attenuation of insulin-induced capillary recruitment and insulin delivery, which in turn reduces glucose uptake by skeletal muscle. Glucose 246-253 insulin Homo sapiens 104-111 21356519-3 2011 We demonstrate that impaired insulin signaling in endothelial cells, due to reduced Irs2 expression and insulin-induced eNOS phosphorylation, causes attenuation of insulin-induced capillary recruitment and insulin delivery, which in turn reduces glucose uptake by skeletal muscle. Glucose 246-253 insulin Homo sapiens 104-111 21333978-3 2011 The complemented strategy allowed to assess parameters of NEFA kinetics and to get insight into their relationship with insulin during oral glucose tolerance tests in women with former gestational diabetes: (i) providing a reliable estimation of the model parameters, (ii) assuring the usability of the model, and (iii) promoting and facilitating its application in a clinical context. Glucose 140-147 insulin Homo sapiens 120-127 20617348-6 2011 Adverse events included abdominal distension and flatulence, which were significantly more frequent in Group M. The frequency of nocturnal hypoglycemia events tended to be reduced in Group M. Combined use of insulin and miglitol is useful for postprandial glucose regulation and improves glycemic control. Glucose 256-263 insulin Homo sapiens 208-215 21189360-10 2011 Thus, these data suggest that ROCK1 may play an important role in the pathogenesis of resistance to insulin action on glucose disposal in muscle of obese type 2 diabetic subjects. Glucose 118-125 insulin Homo sapiens 100-107 21244237-1 2011 AIM: Dextran methacrylate (dex-MA) and concanavalin A (con A)-methacrylamide were photopolymerized to produce covalently cross-linked glucose-sensitive gels for the basis of an implantable closed-loop insulin delivery device. Glucose 134-141 insulin Homo sapiens 201-208 20955160-4 2011 The main therapeutic option to type 1 diabetes mellitus is daily insulin injections which is shown to promote tighter glucose control and to reduce much of diabetic chronic complications. Glucose 118-125 insulin Homo sapiens 65-72 21178768-2 2011 A closed-loop glycemic control device (STG-22; NIKKISO, Tokyo, Japan) has been developed to maintain blood glucose levels within the target range through automatic infusion of insulin and glucose. Glucose 107-114 insulin Homo sapiens 176-183 21205113-7 2011 BOLD signal in the cortical control areas increased during glucose infusion (p = 0.002), corresponding with increased plasma glucose and insulin levels. Glucose 59-66 insulin Homo sapiens 137-144 21205115-5 2011 RESULTS: The area under the absolute glucose concentration-time curve between 0 and 1 h after insulin injection and maximal glucose concentration was significantly lower with glulisine than with aspart (p = 0.0455 and 0.0337, respectively). Glucose 37-44 insulin Homo sapiens 94-101 21291336-2 2011 The aim of the current study was to evaluate the effect of implementing an automated version of an existing insulin protocol for glucose regulation in the Intensive Cardiac Care Unit (ICCU) on compliance with the protocol and achievement of glycemic targets. Glucose 129-136 insulin Homo sapiens 108-115 21291336-7 2011 CONCLUSIONS: The CDSS implementation of an insulin protocol in an ICCU improved compliance, identified targets for further improvement of the protocol, and resulted in improved glucose regulation after implementation. Glucose 177-184 insulin Homo sapiens 43-50 21818994-5 2011 Basal insulin will help to control fasting plasma glucose (FPG) level, but postprandial glucose excursions make a significant contribution to the overall daily hyperglycemia of type 2 diabetic patients. Glucose 50-57 insulin Homo sapiens 6-13 21845205-3 2011 During pregnancy, the increase in maternal insulin resistance is compensated by maternal beta-cell hyperplasia and hyperfunctionality to maintain normal blood glucose. Glucose 159-166 insulin Homo sapiens 43-50 21309049-1 2011 AIMS: Since glucose levels during oral glucose tolerance test (OGTT) are determined both by insulin sensitivity and insulin secretion, we investigated whether the percentage increment (PG%) of 2-h plasma glucose (2hPG) over fasting plasma glucose (FPG) is related to validated indexes of insulin sensitivity and insulin secretion. Glucose 12-19 insulin Homo sapiens 92-99 21309049-6 2011 RESULTS: In each glucose tolerance group, beta-cell function was better preserved in lower PG% tertiles, demonstrating a correlation between PG% and insulin resistance. Glucose 17-24 insulin Homo sapiens 149-156 21309058-9 2011 FGF21 exposure increased basal and insulin-stimulated glucose uptake in human myotubes, coincident with increased glucose transporter 1 mRNA, and enhanced glucose transporter 1 abundance at the plasma membrane. Glucose 54-61 insulin Homo sapiens 35-42 21309058-10 2011 In isolated extensor digitorum longus muscle, FGF21 potentiated insulin-stimulated glucose transport, without altering phosphorylation of Akt or AMP-activated protein kinase. Glucose 83-90 insulin Homo sapiens 64-71 22127766-6 2011 CONCLUSION: These results suggest that GIP possibly facilitates insulin secretion in response to oral glucose load directly and active GLP-1 may exert the glucoregulatory action via the suppression of glucagon secretion in NGT subjects. Glucose 102-109 insulin Homo sapiens 64-71 21324828-4 2011 RESULTS: The biochemical diagnosis of insulinoma was established with concomitant low fasting blood glucose concentrations and inappropriately high insulin levels. Glucose 100-107 insulin Homo sapiens 38-45 21247848-3 2011 Endogenous hyperinsulinism was confirmed by a fasting test, which revealed a glucose level of 35 mg/dL and an insulin value of 23.7 muIU/mL. Glucose 77-84 insulin Homo sapiens 16-23 21372634-5 2011 In vitro, human islets with alpha-cell deficiency exhibited low glucose-induced insulin release compared with intact islets. Glucose 64-71 insulin Homo sapiens 80-87 21291346-1 2011 INTRODUCTION: The historical background of the discovery of incretins became of particular interest when insulin response was found to be much more pronounced when glucose was given orally, rather than intravenously. Glucose 164-171 insulin Homo sapiens 105-112 21291346-2 2011 The robust insulin secretion seen in response to oral glucose, as opposed to intravenous glucose, is due to incretin hormones. Glucose 54-61 insulin Homo sapiens 11-18 21426465-0 2011 Outside of the intensive care unit: the safety and effectiveness of an insulin-dextrose infusion protocol. Glucose 79-87 insulin Homo sapiens 71-78 21426465-1 2011 A review of patients who were on an insulin-dextrose (I-D) infusion protocol in general hospital wards over a 6-month period was conducted to compare glycaemic control before, during and following I-D infusion. Glucose 44-52 insulin Homo sapiens 36-43 21270239-10 2011 Knockdown of pericentrin in adipocytes had no effect on proximal insulin signaling but produced a twofold impairment in insulin-stimulated glucose uptake, approximately commensurate with an associated defect in cell proliferation and adipogenesis. Glucose 139-146 insulin Homo sapiens 120-127 21372634-6 2011 In islets deficient in alpha-cells, exogenous glucagon did not alone stimulate insulin release in the absence of glucose, but increased the glucose-induced insulin release in a dose-dependent manner. Glucose 140-147 insulin Homo sapiens 156-163 21372634-11 2011 These results indicated that glucagon-secreting alpha-cells have an important role in maintaining glucose-stimulated insulin release from beta-cells, and that alpha-cell loss from islets during isolation has a deleterious effect on insulin secretion. Glucose 98-105 insulin Homo sapiens 117-124 21372635-2 2011 Thus, segregation of islets into single cells is associated with a dramatic decline in stimulus secretion-coupling and glucose-induced insulin release. Glucose 119-126 insulin Homo sapiens 135-142 21372635-5 2011 Pseudoislets comprising insulin-secreting cell lines have been shown to closely mimic primary islets in both size and morphology, displaying a significantly enhanced response to glucose, nutrients and drugs over equivalent monolayer cultures. Glucose 178-185 insulin Homo sapiens 24-31 21209036-13 2011 CONCLUSION: This net increase in Glut-4 transporters in the plasma membrane has the potential to increase glucose uptake and metabolism by granulosa cells of the insulin-resistant polycystic ovary, thereby facilitating follicle growth. Glucose 106-113 insulin Homo sapiens 162-169 21054523-9 2011 Factors associated with advanced fibrosis were higher insulin levels at 120 min after oral glucose loading (P = 0.0001; odds ratio [OR], 3.56; 95% confidence interval [CI], 1.61-7.86), aspartate aminotransferase (P = 0.003; OR, 2.70; 95% CI: 1.19-6.12), and age (P = 0.02; OR, 2.49; 95% CI: 1.15-5.37) as determined by multivariate analysis. Glucose 91-98 insulin Homo sapiens 54-61 21209036-2 2011 OBJECTIVE: Our aim was to investigate the interaction of metformin with the other insulin-stimulated ovarian pathway, namely that leading to glucose uptake. Glucose 141-148 insulin Homo sapiens 82-89 21040499-4 2011 In the present study, the effect of combining rosiglitazone with metformin and/or insulin on beta-cell mass and glucose levels was examined in a rat model of Type 2 diabetes. Glucose 112-119 insulin Homo sapiens 82-89 21149438-10 2011 In addition, glucose-stimulated C-peptide release was significantly increased in the insulin-producing cells. Glucose 13-20 insulin Homo sapiens 85-92 20573523-1 2011 AIM: To examine which timing of blood glucose level is more important to achieve adequate blood glucose control with insulin lispro mixture-50 (Mix 50) three times daily (TID) monotherapy. Glucose 38-45 insulin Homo sapiens 117-124 20573523-6 2011 For the insulin-naive patients, only bedtime plasma glucose level also had a significant correlation with improvement in HbA1c at 6 months. Glucose 52-59 insulin Homo sapiens 8-15 20959387-5 2011 The SNP, rs10830963, was significantly associated with higher fasting plasma glucose concentrations (P < 0.001) and increased the area under the curve of plasma glucose levels during the OGTT (P < 0.001), as well as increased homeostasis model assessment of insulin resistance (HOMA-IR; P = 0.027). Glucose 77-84 insulin Homo sapiens 264-271 21103669-5 2011 Insulin resistance was measured at baseline and after 70 d by homeostatic model assessment (HOMA) index as well as by minimal model analysis of an intravenous glucose tolerance test. Glucose 159-166 insulin Homo sapiens 0-7 21465949-5 2011 Although diabetic ketoacidosis resolved in 24 hours, large doses of subcutaneous insulin (upto 130 units per day) were needed to keep serum glucose within the normal range. Glucose 140-147 insulin Homo sapiens 81-88 20959387-5 2011 The SNP, rs10830963, was significantly associated with higher fasting plasma glucose concentrations (P < 0.001) and increased the area under the curve of plasma glucose levels during the OGTT (P < 0.001), as well as increased homeostasis model assessment of insulin resistance (HOMA-IR; P = 0.027). Glucose 164-171 insulin Homo sapiens 264-271 21430606-7 2011 Plasma insulin levels decreased significantly by 30% to 50% in each time point of the oral glucose tolerance test. Glucose 91-98 insulin Homo sapiens 7-14 20096546-0 2011 Early phase insulin secretion is increased in subjects with normal fasting glucose and metabolic syndrome: a premature feature of beta-cell dysfunction. Glucose 75-82 insulin Homo sapiens 12-19 20096546-11 2011 The hyperinsulinemia might not only be an adaptive response to insulin resistance, but a primary defect of beta-cell function contributing to glucose intolerance. Glucose 142-149 insulin Homo sapiens 9-16 20473242-7 2011 Compared to the 34 children who received 0.1 units/kg/hr of insulin, the 33 children who received 0.05 units/kg/hr of insulin were younger (median age, 25 mos vs. 62 mos, p = .024) and had a more gradual reduction in the effective plasma osmolality over the first 12 hrs (p < .0005); this was because plasma glucose decreased more slowly (p = .004) and plasma sodium increased faster (p < .0005). Glucose 311-318 insulin Homo sapiens 118-125 21163946-0 2011 Resveratrol potentiates glucose-stimulated insulin secretion in INS-1E beta-cells and human islets through a SIRT1-dependent mechanism. Glucose 24-31 insulin Homo sapiens 43-50 21216617-1 2011 Solving how insulin regulates glucose transport into skeletal muscle and adipose tissue remains a fundamental challenge in biology and a significant issue in medicine. Glucose 30-37 insulin Homo sapiens 12-19 21163946-6 2011 Treatment of INS-1E cells for 24 h with 25 muM resveratrol resulted in marked potentiation of glucose-stimulated insulin secretion. Glucose 94-101 insulin Homo sapiens 113-120 21452510-6 2011 In the meantime adherence to insulin therapy is mandatory to achieve near physiological glucose levels. Glucose 88-95 insulin Homo sapiens 29-36 21235242-9 2011 Furthermore, the in vitro and in vivo effects of the active constituents of NNE, quercetin, and catechin, on glucose-induced insulin secretion and blood glucose regulation were evaluated. Glucose 109-116 insulin Homo sapiens 125-132 21870631-2 2011 The subsequent lack of insulin leads to increased blood and urine glucose. Glucose 66-73 insulin Homo sapiens 23-30 21475629-7 2011 RESULTS: The duration of disease was negatively correlated with both (125)I-insulin binding capacity (r = -0.70, P < 0.05) and basal and maximum insulin-stimulated glucose transport (r = -0.87, P < 0.01, and r = -0.88, P < 0.01, respectively). Glucose 167-174 insulin Homo sapiens 148-155 21475629-9 2011 Basal and maximum insulin-stimulated glucose transport was significantly higher in the group with less than 5 years of disease (P < 0.01). Glucose 37-44 insulin Homo sapiens 18-25 21241662-5 2011 In the presence of insulin, H2O2 decreased total protein expression of IRS-1 at 6 h and IRS-2 at 4 and 6 h. Phosphorylation of p38 MAPK Thr180/Tyr182 was transiently increased by H2O2 in the presence and absence of insulin at 2 and 4 h, but not at 6 h. Selective inhibition of p38 MAPK with A304000 partially rescued the H2O2-induced reduction in insulin-stimulated glucose transport activity. Glucose 366-373 insulin Homo sapiens 19-26 21241662-6 2011 These results indicate that direct in vitro exposure of isolated mammalian skeletal muscle to a low-level oxidant stress impairs distal insulin signaling and insulin-stimulated glucose transport activity, at least in part, due to a p38 MAPK-dependent mechanism. Glucose 177-184 insulin Homo sapiens 158-165 21364956-7 2011 Utilizing an in vitro system, we show that insulin stimulates heparanase secretion by kidney 293 cells, and even higher secretion is observed when insulin is added to cells maintained under high glucose conditions. Glucose 195-202 insulin Homo sapiens 43-50 21364956-7 2011 Utilizing an in vitro system, we show that insulin stimulates heparanase secretion by kidney 293 cells, and even higher secretion is observed when insulin is added to cells maintained under high glucose conditions. Glucose 195-202 insulin Homo sapiens 147-154 21241662-2 2011 Skeletal muscle is the primary site of insulin-dependent glucose disposal in the body; however, the effects of oxidative stress on insulin signaling and glucose transport activity in mammalian skeletal muscle are not well understood. Glucose 57-64 insulin Homo sapiens 39-46 21241662-3 2011 We therefore studied the effects of a low-level in vitro oxidant stress (30-40 muM H2O2) on basal and insulin-stimulated (5 mU/ml) glucose transport activity and insulin signaling at 2, 4, and 6 h in isolated rat soleus muscle. Glucose 131-138 insulin Homo sapiens 102-109 21241662-4 2011 H2O2 increased basal glucose transport activity at 2 and 4 h, but not at 6 h. This low-level oxidant stress significantly impaired insulin-stimulated glucose transport activity at all time points, and was associated with inhibition of insulin-stimulated phosphorylation of Akt Ser473 and GSK-3beta Ser9. Glucose 21-28 insulin Homo sapiens 131-138 21241662-4 2011 H2O2 increased basal glucose transport activity at 2 and 4 h, but not at 6 h. This low-level oxidant stress significantly impaired insulin-stimulated glucose transport activity at all time points, and was associated with inhibition of insulin-stimulated phosphorylation of Akt Ser473 and GSK-3beta Ser9. Glucose 21-28 insulin Homo sapiens 235-242 21241662-4 2011 H2O2 increased basal glucose transport activity at 2 and 4 h, but not at 6 h. This low-level oxidant stress significantly impaired insulin-stimulated glucose transport activity at all time points, and was associated with inhibition of insulin-stimulated phosphorylation of Akt Ser473 and GSK-3beta Ser9. Glucose 150-157 insulin Homo sapiens 131-138 21320941-10 2011 RECOMMENDATION 3: ACP recommends a target blood glucose level of 7.8 to 11.1 mmol/L (140 to 200 mg/dL) if insulin therapy is used in SICU/MICU patients (Grade: weak recommendation, moderate-quality evidence). Glucose 48-55 insulin Homo sapiens 106-113 21186142-4 2011 The daily glucose profile measured by the patients themselves through measurements performed in capillary blood obtained by finger stick provides valuable information needed to adjust insulin therapy. Glucose 10-17 insulin Homo sapiens 184-191 21163329-6 2011 In addition, primary hepatocytes treated with different doses of insulin in high glucose induced alteration of H6PDH and 11beta-HSD1 while in low glucose there was no significant effect. Glucose 81-88 insulin Homo sapiens 65-72 21163329-6 2011 In addition, primary hepatocytes treated with different doses of insulin in high glucose induced alteration of H6PDH and 11beta-HSD1 while in low glucose there was no significant effect. Glucose 146-153 insulin Homo sapiens 65-72 21070591-4 2011 Here, we compared groups of offspring from long-lived siblings and controls for the relation between insulin and glucose in nonfasted serum (n = 1848 subjects) and for quantitation of insulin action using a two-step hyperinsulinemic-euglycemic clamp (n = 24 subjects). Glucose 113-120 insulin Homo sapiens 101-108 21070591-6 2011 We observed a positive bi-phasic linear relationship between ln (insulin) levels and nonfasted glucose with a steeper slope from 10.7mU L(-1) insulin onwards in controls compared to offspring (P = 0.02). Glucose 95-102 insulin Homo sapiens 65-72 21070591-7 2011 During the clamp study, higher glucose infusion rate was required to maintain euglycemia during high-dose insulin infusion (P = 0.036) in offspring, reflecting higher whole-body insulin sensitivity. Glucose 31-38 insulin Homo sapiens 106-113 21070591-7 2011 During the clamp study, higher glucose infusion rate was required to maintain euglycemia during high-dose insulin infusion (P = 0.036) in offspring, reflecting higher whole-body insulin sensitivity. Glucose 31-38 insulin Homo sapiens 178-185 21070591-8 2011 After adjustment for sex, age, and fat mass, the insulin-mediated glucose disposal rate (GDR) was higher in offspring than controls (42.5 +- 2.7 vs. 33.2 +- 2.7 micromol kg(-1) min(-1) , mean +- SE, P = 0.025). Glucose 66-73 insulin Homo sapiens 49-56 21070591-9 2011 The insulin-mediated suppression of endogenous glucose production and lipolysis did not differ between groups (all P > 0.05). Glucose 47-54 insulin Homo sapiens 4-11 20195917-0 2011 Dietary intake and serum and hair concentrations of minerals and their relationship with serum lipids and glucose levels in hypertensive and obese patients with insulin resistance. Glucose 106-113 insulin Homo sapiens 161-168 21186142-9 2011 A basal amount of insulin is needed to regulate the endogenous glucose production, short-acting insulin shots are needed to handle exogenous glucose loads. Glucose 63-70 insulin Homo sapiens 18-25 21186142-9 2011 A basal amount of insulin is needed to regulate the endogenous glucose production, short-acting insulin shots are needed to handle exogenous glucose loads. Glucose 141-148 insulin Homo sapiens 96-103 21186142-20 2011 Insulin therapy during labour means short-acting insulin adjusted to achieve glucose levels between 4 and 8 mmol l(-1) to prevent neonatal hypoglycaemia as much as possible. Glucose 77-84 insulin Homo sapiens 0-7 21150617-2 2011 RECENT FINDINGS: Initial experience with simultaneous pancreas-kidney transplantation (SPKT) in patients with T2DM and end-stage renal disease (ESRD) suggested that augmentation of endogenous insulin production by PTX in patients with C-peptide-positive, insulin-requiring diabetes resulted in insulin independence, improved glucose counter-regulation, and enhanced quality of life. Glucose 325-332 insulin Homo sapiens 192-199 20594757-13 2011 Taken together, these results indicate that the mTOR pathway is an important modulator of the signals involved in the acute regulation of insulin-stimulated glucose metabolism, and at least, partly contributes to burn-induced insulin resistance. Glucose 157-164 insulin Homo sapiens 138-145 20594757-13 2011 Taken together, these results indicate that the mTOR pathway is an important modulator of the signals involved in the acute regulation of insulin-stimulated glucose metabolism, and at least, partly contributes to burn-induced insulin resistance. Glucose 157-164 insulin Homo sapiens 226-233 20941645-2 2011 Visceral adipose tissue is now known to secrete into the circulation a number of protein and nonprotein factors that regulate glucose metabolism in traditional insulin-sensitive tissue as well as nontraditional insulin-sensitive tissue including cardiovascular tissue. Glucose 126-133 insulin Homo sapiens 160-167 21057314-15 2011 Use of insulin therapy for glucose control in this patient population may need to be carefully targeted toward high-risk subsets of patients. Glucose 27-34 insulin Homo sapiens 7-14 21219433-8 2011 After the 25% insulin dose immediately pre-exercise glucose concentration was higher than after the full or 50% dose (P<0.05). Glucose 52-59 insulin Homo sapiens 14-21 21104225-4 2011 RESULTS: Insulin mRNA expression (p = 0.002), insulin content (p = 0.004) and glucose-stimulated insulin secretion (p = 0.04) were reduced in pancreatic islets from patients with type 2 diabetes compared with non-diabetic donors. Glucose 78-85 insulin Homo sapiens 97-104 21219435-0 2011 Effects of meals with different glycaemic index on postprandial blood glucose response in patients with Type 1 diabetes treated with continuous subcutaneous insulin infusion. Glucose 70-77 insulin Homo sapiens 157-164 21219436-9 2011 Statistically significant differences were seen in mean plasma glucose and mean glucose infusion rate, with the highest mean plasma glucose and the lowest mean glucose infusion rate with continuous intravenous insulin infusion, suggesting a slightly lower bioefficacy of continuous intravenous insulin infusion compared with subcutaneous bolus insulin injection and continuous subcutaneous insulin infusion. Glucose 63-70 insulin Homo sapiens 210-217 21219436-9 2011 Statistically significant differences were seen in mean plasma glucose and mean glucose infusion rate, with the highest mean plasma glucose and the lowest mean glucose infusion rate with continuous intravenous insulin infusion, suggesting a slightly lower bioefficacy of continuous intravenous insulin infusion compared with subcutaneous bolus insulin injection and continuous subcutaneous insulin infusion. Glucose 80-87 insulin Homo sapiens 210-217 21219436-9 2011 Statistically significant differences were seen in mean plasma glucose and mean glucose infusion rate, with the highest mean plasma glucose and the lowest mean glucose infusion rate with continuous intravenous insulin infusion, suggesting a slightly lower bioefficacy of continuous intravenous insulin infusion compared with subcutaneous bolus insulin injection and continuous subcutaneous insulin infusion. Glucose 80-87 insulin Homo sapiens 210-217 21219436-9 2011 Statistically significant differences were seen in mean plasma glucose and mean glucose infusion rate, with the highest mean plasma glucose and the lowest mean glucose infusion rate with continuous intravenous insulin infusion, suggesting a slightly lower bioefficacy of continuous intravenous insulin infusion compared with subcutaneous bolus insulin injection and continuous subcutaneous insulin infusion. Glucose 80-87 insulin Homo sapiens 210-217 21063673-8 2011 Glucose-stimulated insulin secretion was carried out in Tctp knockdown cells. Glucose 0-7 insulin Homo sapiens 19-26 21537406-4 2011 Independent risk factors for the development of diabetes in Korean women with previous GDM are pre-pregnancy body weight, gestational age at diagnosis, antepartum hyperglycemia on oral glucose tolerance test, low insulin response to oral glucose load, and family history of diabetes. Glucose 238-245 insulin Homo sapiens 213-220 21216852-1 2011 OBJECTIVE: Glucose is the major stimulus for insulin release. Glucose 11-18 insulin Homo sapiens 45-52 21216859-6 2011 RESULTS: During closed-loop insulin delivery, median (interquartile range) plasma glucose levels were 117 (100.8-154.8) mg/dL in early and 126 (109.8-140.4) mg/dL in late gestation (P = 0.72). Glucose 82-89 insulin Homo sapiens 28-35 21209021-1 2011 The euglycemic glucose clamp is the reference method for assessing insulin sensitivity in humans and animals. Glucose 15-22 insulin Homo sapiens 67-74 21205021-7 2011 During stimulation by insulin, type 1 diabetic patients exhibited approximately 50% (P < 0.001) lower whole-body glucose disposal along with approximately 42% (P = 0.003) lower intramyocellular g6p and approximately25% (P = 0.024) lower fATP. Glucose 116-123 insulin Homo sapiens 22-29 20865425-1 2011 In obesity, insulin-stimulated glucose uptake in skeletal muscle is decreased. Glucose 31-38 insulin Homo sapiens 12-19 20865425-11 2011 These results suggest a shared pathway between insulin- and exercise-induced glucose uptake and subsequent glycogen synthesis. Glucose 77-84 insulin Homo sapiens 47-54 21378423-3 2011 Critical blood sample revealed increased insulin: glucose ratio. Glucose 50-57 insulin Homo sapiens 41-48 21047922-9 2011 Lipid infusion lowered insulin-stimulated whole-body glucose disposal and abolished insulin-mediated increases in MBV and MBF in both cardiac and skeletal muscle. Glucose 53-60 insulin Homo sapiens 23-30 21219421-3 2011 Our objective was to explore the associations between insulin resistance (assessed by glucose infusion rate) and lipids in people with Type 1 diabetes and determine whether adiposity and/or average glycaemia influence these associations. Glucose 86-93 insulin Homo sapiens 54-61 21219422-11 2011 This indicates that, in remission, the residual islets maintain a secretion of insulin and glucagon of benefit for control of hepatic glucose production. Glucose 134-141 insulin Homo sapiens 79-86 21228246-4 2011 RESULTS: The mean daily glucose concentration after the 1st day of basal-bolus insulin and SSI was 145 +- 32 mg/dL and 172 +- 47 mg/dL, respectively (P < 0.01). Glucose 24-31 insulin Homo sapiens 79-86 21070775-4 2011 Insulin resistance (IR) was estimated by the homeostasis model assessment index (HOMA2-IR) based on fasting glucose and insulin levels. Glucose 108-115 insulin Homo sapiens 0-7 20639170-0 2011 Calculation of the best basal-bolus combination for postprandial glucose control in insulin pump therapy. Glucose 65-72 insulin Homo sapiens 84-91 21697536-3 2011 Parameters of insulin sensitivity and secretion were derived from 120-minute oral glucose tolerance tests. Glucose 82-89 insulin Homo sapiens 14-21 21106709-9 2011 RESULTS: Intermyofibrillar mitochondrial content was lower in the insulin-resistant nondiabetic subjects and type 2 diabetes mellitus groups, significantly correlating with glucose disposal in both men (R = 0.72, P < 0.01) and women (R = 0.53, P < 0.01). Glucose 173-180 insulin Homo sapiens 66-73 20153492-1 2011 In the present study, we investigated the effect of adrenaline on insulin-mediated regulation of glucose and fat metabolism with focus on regulation of skeletal muscle PKB, GSK-3, and glycogen synthase (GS) phosphorylation. Glucose 97-104 insulin Homo sapiens 66-73 20927436-0 2011 Novel use of fluorescent glucose analogues to identify a new class of triazine-based insulin mimetics possessing useful secondary effects. Glucose 25-32 insulin Homo sapiens 85-92 20927436-10 2011 Two inducers of glucose uptake were shown to be non-cytotoxic and confirmed as insulin mimetic compounds by their inhibition of epinephrine-stimulated free fatty acid release from adipocytes. Glucose 16-23 insulin Homo sapiens 79-86 20927436-12 2011 The discovery of new insulin mimetics using 6-NBDG validates the use of this probe in the development of large-scale, cell-based screening systems based on the uptake of fluorescent-tagged glucose analogues. Glucose 189-196 insulin Homo sapiens 21-28 21266695-4 2011 However, recent large multicenter trials have reported that intensive insulin therapy designed to normalize blood glucose resulted in an unacceptable increase in the incidence of hypoglycemia. Glucose 114-121 insulin Homo sapiens 70-77 21461038-2 2011 Therefore intensive glucose-lowering therapy with insulin (IGL) has been proposed in diabetic or hyperglycaemic patients and has been shown to improve survival and reduce incidence of adverse events. Glucose 20-27 insulin Homo sapiens 50-57 21461038-4 2011 Furthermore, systematic glucose-insulin-potassium infusion (GIK) has been studied to improve outcome after AMI. Glucose 24-31 insulin Homo sapiens 32-39 21127472-5 2011 We assessed insulin sensitivity with an intravenous glucose tolerance test (IVGTT) and the 24-h insulin area under the curve (AUC). Glucose 52-59 insulin Homo sapiens 12-19 21176778-1 2011 The role of protein kinase C (PKCs) isoforms in the regulation of glucose metabolism by insulin is complex, partly due to the large PKC family consisting of three sub-groups: conventional, novel and atypical. Glucose 66-73 insulin Homo sapiens 88-95 21146545-0 2011 Glucose-mediated spatial interactions of voltage dependent calcium channels and calcium sensing receptor in insulin producing beta-cells. Glucose 0-7 insulin Homo sapiens 108-115 21146545-3 2011 MAIN METHODS: The insulin producing beta-cells were exposed to 2.5, 5, 7.5, 10, and 15 mM glucose for 24 h at 37 C. The confocal fluorescence imaging data was obtained by using antibodies against CaR and L-type VDCC. Glucose 90-97 insulin Homo sapiens 18-25 21146545-8 2011 The insulin ELISA data showed a significant increase in the 1st phase of glucose-induced insulin secretion in beta-cells exposed to increasing concentrations of glucose. Glucose 73-80 insulin Homo sapiens 4-11 21244702-1 2011 BACKGROUND: Adiponectin is the most abundant plasma protein synthesized for the most part in adipose tissue, and it is an insulin-sensitive hormone, playing a central role in glucose and lipid metabolism. Glucose 175-182 insulin Homo sapiens 122-129 20851146-1 2011 Chicks genetically selected for low juvenile body weight had a lower threshold of central insulin-induced decreased food and water intake and whole blood glucose concentration than those selected for juvenile high body weight. Glucose 154-161 insulin Homo sapiens 90-97 21200004-0 2011 Glucose-insulin-potassium reduces the incidence of low cardiac output episodes after aortic valve replacement for aortic stenosis in patients with left ventricular hypertrophy: results from the Hypertrophy, Insulin, Glucose, and Electrolytes (HINGE) trial. Glucose 0-7 insulin Homo sapiens 207-214 21059654-5 2011 In this study, we confirm that siRNA-mediated knockdown of ARNT/HIF-1beta inhibits glucose-stimulated insulin secretion. Glucose 83-90 insulin Homo sapiens 102-109 21283811-9 2011 Positive associations were observed for fasting plasma glucose (OR = 1.42 [1.07; 1.87]), serum triglycerides (OR = 1.41 [1.05; 1.91]) and with fasting plasma insulin (OR = 1.48 [1.05; 2.08]) in stressed men at S-49. Glucose 55-62 insulin Homo sapiens 158-165 21059654-8 2011 Metabolic profiling of beta-cells treated with siRNAs against the ARNT/HIF-1beta gene revealed that glycolysis, anaplerosis, and glucose-induced fatty acid production were down-regulated, and all are key events involved in glucose-stimulated insulin secretion. Glucose 129-136 insulin Homo sapiens 242-249 21211036-0 2011 The minor C-allele of rs2014355 in ACADS is associated with reduced insulin release following an oral glucose load. Glucose 102-109 insulin Homo sapiens 68-75 21251326-10 2011 High doses of intravenous insulin with intravenous dextrose as required (hyperinsulinaemic euglycaemia or HIET), has also been successfully reported. Glucose 51-59 insulin Homo sapiens 26-33 21211036-2 2011 Chronic exposure to fatty acids due to an impaired beta-oxidation may down-regulate the glucose-stimulated insulin release and result in an increased risk of type 2 diabetes (T2D). Glucose 88-95 insulin Homo sapiens 107-114 21211036-3 2011 We aimed to investigate whether the two variants associate with altered insulin release following an oral glucose load or with T2D. Glucose 106-113 insulin Homo sapiens 72-79 21211036-10 2011 CONCLUSIONS: In glucose-tolerant individuals the minor C-allele of rs2014355 of ACADS was associated with reduced measures of glucose-stimulated insulin release during an OGTT, a finding which in part may be mediated through an impaired beta-oxidation of fatty acids. Glucose 16-23 insulin Homo sapiens 145-152 21169804-7 2011 Fluctuations in blood glucose were created using intravenous glucose and insulin. Glucose 22-29 insulin Homo sapiens 73-80 21195351-2 2011 Insulin release from the pancreatic beta cell is controlled by mitochondrial metabolism, which translates fluctuations in blood glucose into metabolic coupling signals. Glucose 128-135 insulin Homo sapiens 0-7 21195351-5 2011 These mice displayed lower expression of TFB1M in islets and impaired mitochondrial function and released less insulin in response to glucose in vivo and in vitro. Glucose 134-141 insulin Homo sapiens 111-118 22254332-7 2011 The system described in this paper is comprised of two sensors for measuring glucose, two pumps for independent delivery of insulin and glucagon, and a laptop computer running a custom software application that controls the sensor acquisition and insulin and glucagon delivery based on the glucose values recorded. Glucose 290-297 insulin Homo sapiens 247-254 20887712-9 2011 High glucose induced changes in O-GlcNAcylation and phosphorylation of mitochondrial proteins may be associated with mitochondrial dysfunction and insulin resistance. Glucose 5-12 insulin Homo sapiens 147-154 21960076-0 2011 Association of the serum glucose level with fetal-maternal complications of gestational diabetes with insulin therapy. Glucose 25-32 insulin Homo sapiens 102-109 21960076-2 2011 This study conducted to determine association the level of serum glucose with fetal-maternal complications of gestational diabetes with insulin therapy. Glucose 65-72 insulin Homo sapiens 136-143 22688918-0 2011 Insulin is secreted upon glucose stimulation by both gastrointestinal enteroendocrine K-cells and L-cells engineered with the preproinsulin gene. Glucose 25-32 insulin Homo sapiens 0-7 21057307-1 2011 The purpose of this study was to analyze the effect of peritoneal dialysis with glucose-based solution on plasma glucose and insulin responses in patients on continuous ambulatory peritoneal dialysis (CAPD), describe the glucose-insulin system using a mathematical model, and identify abnormalities in this system. Glucose 80-87 insulin Homo sapiens 125-132 21057307-3 2011 We used a mathematical model based on the previous works of Stolwijk and Hardy (1974) and Tolic et al (2000) to estimate the parameters of glucose-insulin system, insulin sensitivity index (Sl), and glucose effectiveness at basal (SG) and zero (GEZI) insulin. Glucose 139-146 insulin Homo sapiens 147-154 21057307-7 2011 We demonstrated a successful control of increasing plasma glucose by insulin, despite an increased insulin resistance, during CAPD. Glucose 58-65 insulin Homo sapiens 69-76 22688918-1 2011 Transgenic mice carrying the human insulin gene driven by the K-cell glucose-dependent insulinotropic peptide (GIP) promoter secrete insulin and display normal glucose tolerance tests after their pancreatic p-cells have been destroyed. Glucose 69-76 insulin Homo sapiens 35-42 22688918-3 2011 It is noted that in addition to GIP secreting K-cells, the glucagon-like peptide 1 (GLP-1) generating L-cells share/ many similarities to pancreatic p-cells, including the peptidases required for proinsulin processing, hormone storage and a glucose-stimulated hormone secretion mechanism. Glucose 241-248 insulin Homo sapiens 196-206 22688918-4 2011 In the present study, we demonstrate that not only K-cells, but also L-cells engineered with the human preproinsulin gene are able to synthesize, store and, upon glucose stimulation, release mature insulin. Glucose 162-169 insulin Homo sapiens 103-116 22688918-4 2011 In the present study, we demonstrate that not only K-cells, but also L-cells engineered with the human preproinsulin gene are able to synthesize, store and, upon glucose stimulation, release mature insulin. Glucose 162-169 insulin Homo sapiens 109-116 22688918-6 2011 Exposure to glucose of engineered STC-1 cells led to a marked insulin secretion, which was 7-fold greater when the insulin gene was driven by the CMV promoter (expressed both in K-cells and L-cells) than when it was driven by the GIP promoter (expressed only in K-cells). Glucose 12-19 insulin Homo sapiens 62-69 21240346-1 2011 We studied the correlation between the effect of alpha-lipoic acid, emoxipin, reamberin, and mexidol on LPO in vitro and the action of these drugs on insulin sensitivity and tolerance to glucose load in vivo. Glucose 187-194 insulin Homo sapiens 150-157 20934485-0 2011 The Unscented Kalman Filter estimates the plasma insulin from glucose measurement. Glucose 62-69 insulin Homo sapiens 49-56 20934485-4 2011 A novel approach using an Unscented Kalman Filter that provides an estimate of the current plasma insulin concentration is presented, which operates on the measurement of the plasma glucose and Bergman"s Minimal Model of the glucose insulin homeostasis. Glucose 182-189 insulin Homo sapiens 98-105 22255216-7 2011 To minimize the insulin infusion rate, and avoid the hypoglycemia risk, the glucose target is a dynamical profile. Glucose 76-83 insulin Homo sapiens 16-23 20887662-5 2011 Insulin secretory capacity was validated by glucose challenge and immunomodulatory potential characterized using a peripheral blood lymphocyte (PBL) proliferation assay. Glucose 44-51 insulin Homo sapiens 0-7 21404483-2 2011 Stress-induced hyperglycemia is the consequence of increased levels of cortisol, cytokines, growth hormones, catecholamines, and glucagon resulting in the stimulation of endogenous glucose production through glycogenolysis and gluconeogenesis as well as other mechanisms including central and peripheral insulin resistance. Glucose 181-188 insulin Homo sapiens 304-311 20719086-5 2011 C-peptide release, both spontaneous and after glucose challenge, was measured by ELISA. Glucose 46-53 insulin Homo sapiens 0-9 20719086-10 2011 Differentiated cells" C-peptide release in vitro increased after glucose challenge. Glucose 65-72 insulin Homo sapiens 22-31 21439131-7 2011 We also show that CLECs transduced with a modified human proinsulin gene were transplanted intraperitoneally into streptozotocin (STZ)-induced diabetic mice, resulting in significantly lower levels of serum glucose compared to control mice. Glucose 208-215 insulin Homo sapiens 57-67 21276273-9 2011 Blood glucose level on admission correlated positively with plasma insulin, C-peptide, cortisol, age and glucose intake. Glucose 6-13 insulin Homo sapiens 67-74 21721974-1 2011 Biliverdin reductase A (BLVRA) is a powerful intracellular antioxidant enzyme and an antagonist to insulin-mediated glucose uptake by the cells. Glucose 116-123 insulin Homo sapiens 99-106 22029179-3 2011 The glucose transporter 1 (GLUT1) plays an important role for fetal glucose uptake as well as for maternal-fetal glucose transfer, and it has been associated with insulin resistance in adults. Glucose 4-11 insulin Homo sapiens 163-170 22029179-3 2011 The glucose transporter 1 (GLUT1) plays an important role for fetal glucose uptake as well as for maternal-fetal glucose transfer, and it has been associated with insulin resistance in adults. Glucose 68-75 insulin Homo sapiens 163-170 22029179-4 2011 The present study hypothesized that the common fetal GLUT1 XbaI polymorphism might reduce fetal insulin sensitivity and/or glucose supply in utero, thus affecting fetal blood glucose and fetal growth. Glucose 175-182 insulin Homo sapiens 96-103 21276273-10 2011 Multiple regression analysis revealed that both age and plasma insulin on admission were significantly related to blood glucose. Glucose 120-127 insulin Homo sapiens 63-70 20870970-1 2011 OBJECTIVE: Suppression of Kinesin-1 by antisense oligonucleotides, or overexpression of dominant-negative acting kinesin heavy chain, has been reported to affect the sustained phase of glucose-stimulated insulin secretion in beta-cells in vitro. Glucose 185-192 insulin Homo sapiens 204-211 20921215-4 2011 Insulin is started if the preprandial glucose concentration is >=90 mg/dl and/or a 1-h postprandial glucose concentration is >=120 mg/dl. Glucose 38-45 insulin Homo sapiens 0-7 20921215-4 2011 Insulin is started if the preprandial glucose concentration is >=90 mg/dl and/or a 1-h postprandial glucose concentration is >=120 mg/dl. Glucose 103-110 insulin Homo sapiens 0-7 20876713-5 2011 RESULTS: Intranasal insulin, compared with placebo, increased postprandial energy expenditure, i.e., diet-induced thermogenesis, and decreased postprandial concentrations of circulating insulin and C-peptide, whereas postprandial plasma glucose concentrations did not differ from placebo values. Glucose 237-244 insulin Homo sapiens 20-27 20929990-11 2011 However, insulin therapy has to be combined with treatment of both peripheral and liver insulin resistance to normalize blood glucose, and in this case, the insulin regimen is less important. Glucose 126-133 insulin Homo sapiens 9-16 23008685-8 2011 Animals treated with oral niosome-encapsulated insulin (100 IU/kg) showed decreased levels of blood glucose and elevated serum insulin, which in the case of Brij 92 niosomes, hypoglycemic effect was significant (P<0.05). Glucose 100-107 insulin Homo sapiens 47-54 20978091-1 2011 OBJECTIVE: To assess insulin action on peripheral glucose utilization and nonesterified fatty acid (NEFA) suppression as a predictor of coronary artery calcification (CAC) in patients with type 1 diabetes and nondiabetic controls. Glucose 50-57 insulin Homo sapiens 21-28 20956497-1 2011 OBJECTIVE: We have previously shown that overnight fasted women have higher insulin-stimulated whole body and leg glucose uptake despite a higher intramyocellular triacylglycerol concentration than men. Glucose 114-121 insulin Homo sapiens 76-83 20956497-5 2011 RESULTS: Intralipid infusion reduced whole-body glucose infusion rate by 26% in women and 38% in men (P < 0.05), and insulin-stimulated leg glucose uptake was reduced significantly less in women (45%) than men (60%) after intralipid infusion. Glucose 143-150 insulin Homo sapiens 120-127 20956497-10 2011 CONCLUSIONS: Intralipid infusion causes less insulin resistance of muscle glucose uptake in women than in men. Glucose 74-81 insulin Homo sapiens 45-52 20929990-11 2011 However, insulin therapy has to be combined with treatment of both peripheral and liver insulin resistance to normalize blood glucose, and in this case, the insulin regimen is less important. Glucose 126-133 insulin Homo sapiens 88-95 20938636-1 2011 AIMS/HYPOTHESIS: Insulin-mediated glucose disposal rates (R(d)) are reduced in type 2 diabetic patients, a process in which intrinsic signalling defects are thought to be involved. Glucose 34-41 insulin Homo sapiens 17-24 21051097-0 2011 Impairment of insulin action in non-obese, normal-glucose tolerant, first-degree relatives of Chinese type 2 diabetic patients. Glucose 50-57 insulin Homo sapiens 14-21 21051097-10 2011 Insulin resistance is independent of obesity and blood glucose level. Glucose 55-62 insulin Homo sapiens 0-7 21114602-2 2011 The aim of this proof-of-concept study was to investigate the safety and efficacy of treatment with buccal spray insulin (Oral-lyn , Generex Biotechnology Corporation, Toronto, Ontario, Canada) on postprandial plasma glucose and insulin levels in subjects with impaired glucose tolerance (IGT). Glucose 217-224 insulin Homo sapiens 113-120 20978091-4 2011 Insulin-induced NEFA suppression was also lower in type 1 diabetic compared with nondiabetic subjects: NEFA levels (muM) during 8 mU/m2/min insulin infusion = 370 +- 27 vs. 185 +- 25, P < 0.0001, after adjustment for age, sex, BMI, fasting glucose, and time point insulin. Glucose 243-250 insulin Homo sapiens 0-7 21114606-10 2011 CONCLUSION: Co-administration of liraglutide 1.8 mg at steady state and insulin detemir produces an additive glucose-lowering effect without affecting the PK profile of either therapeutic agent suggesting that the addition of insulin detemir to patients treated with liraglutide will not require titration algorithms different from when insulin is added to OADs. Glucose 109-116 insulin Homo sapiens 72-79 21114601-1 2011 AIM: AS1535907, a small molecule agonist of GPR119, was assessed for its glucose-stimulated insulin secretory activity and pancreatic beta-cell function in type 2 diabetes. Glucose 73-80 insulin Homo sapiens 92-99 21218513-9 2011 Acute insulin response to glucose was reduced following hypoxic rest versus normoxic rest (p = 0.014). Glucose 26-33 insulin Homo sapiens 6-13 21218513-10 2011 CONCLUSIONS: this study demonstrated that (1) hypoxic-induced improvements in glucose tolerance in the 4 h following exposure can be attributed to improvements in peripheral insulin sensitivity (S( I)(2*) and (2) exercise and hypoxia have an additive effect on insulin sensitivity (S(I)(2*) in type 2 diabetic patients. Glucose 78-85 insulin Homo sapiens 174-181 21175273-1 2011 BACKGROUND: studies in younger patients with diabetes have shown that insulin profiles are more physiologic and postprandial glucose levels are lower with repaglinide than with glyburide. Glucose 125-132 insulin Homo sapiens 70-77 21218513-10 2011 CONCLUSIONS: this study demonstrated that (1) hypoxic-induced improvements in glucose tolerance in the 4 h following exposure can be attributed to improvements in peripheral insulin sensitivity (S( I)(2*) and (2) exercise and hypoxia have an additive effect on insulin sensitivity (S(I)(2*) in type 2 diabetic patients. Glucose 78-85 insulin Homo sapiens 261-268 21175274-7 2011 The subjects will be randomized to either the patient-led or the physician-led titration arm, where the insulin dose will be adjusted to achieve a target fasting plasma glucose (FPG) value of 110 mg/dL (6.1 mmol/L). Glucose 169-176 insulin Homo sapiens 104-111 21166853-7 2011 A quarter overall and 70% of those taking insulin tested their blood glucose. Glucose 69-76 insulin Homo sapiens 42-49 21175276-1 2011 BACKGROUND: applying the principles of the hyperinsulinemic-normoglycemic clamp technique we have introduced glucose and insulin administration while maintaining normoglycemia (GIN therapy) to surgical patients. Glucose 109-116 insulin Homo sapiens 48-55 21175277-0 2011 Are glucose readings sufficient to adjust insulin dosage? Glucose 4-11 insulin Homo sapiens 42-49 21175277-3 2011 We hypothesize that glucose readings are sufficient to adjust insulin dosage provided that dosage is adjusted every 1-4 weeks. Glucose 20-27 insulin Homo sapiens 62-69 21175266-0 2011 Hypoglycemia risk and glucose variability indices derived from routine self-monitoring of blood glucose are related to laboratory measures of insulin sensitivity and epinephrine counterregulation. Glucose 22-29 insulin Homo sapiens 142-149 21175266-0 2011 Hypoglycemia risk and glucose variability indices derived from routine self-monitoring of blood glucose are related to laboratory measures of insulin sensitivity and epinephrine counterregulation. Glucose 96-103 insulin Homo sapiens 142-149 21175266-6 2011 RESULTS: two glucose variability measures correlated positively (P < 0.01) with insulin sensitivity: the Average Daily Risk Range (ADRR) (rho = 0.5) and the Glycemic Lability Index (rho = 0.48). Glucose 13-20 insulin Homo sapiens 83-90 21175266-8 2011 CONCLUSIONS: higher insulin sensitivity and lower epinephrine response during hypoglycemia are related to increased glucose variability (as quantified by the ADRR), irrespective of HbA1c and other patient characteristics. Glucose 116-123 insulin Homo sapiens 20-27 21792327-7 2011 Mean blood glucose calculated from CGM values was significantly lower with insulin glargine compared with insulin detemir (9.6 +- 2.4 mmol/L versus 10.4 +- 2.8 mmol/L, P = 0.038). Glucose 11-18 insulin Homo sapiens 75-82 21262869-6 2011 Insulin was directly and significantly related to glycaemia (p = 0.0006), body mass index (BMI) (p = 0.00028) and lactate (p = 0.0096) In the early phase of STEMI without previously known diabetes the acute glucose dysmetabolism is quite complex, comprising increased glucose values and the development of acute insulin resistance. Glucose 207-214 insulin Homo sapiens 0-7 21262870-2 2011 The goal of this study was to quantify insulin action by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test in apparently healthy individuals with prehypertension (n=126) and to elucidate the relationship between insulin action and CVD risk.We found a marked heterogeneity in insulin sensitivity in the prehypertension group, and when we divided the population into insulin-sensitive, insulin-resistant and intermediate groups, there were significant (p<0.01) increases in plasma glucose and triglyceride concentrations and decreases in high-density lipoprotein cholesterol concentrations with progressive degrees of insulin resistance. Glucose 93-100 insulin Homo sapiens 39-46 21262870-2 2011 The goal of this study was to quantify insulin action by determining the steady-state plasma glucose (SSPG) concentration during the insulin suppression test in apparently healthy individuals with prehypertension (n=126) and to elucidate the relationship between insulin action and CVD risk.We found a marked heterogeneity in insulin sensitivity in the prehypertension group, and when we divided the population into insulin-sensitive, insulin-resistant and intermediate groups, there were significant (p<0.01) increases in plasma glucose and triglyceride concentrations and decreases in high-density lipoprotein cholesterol concentrations with progressive degrees of insulin resistance. Glucose 533-540 insulin Homo sapiens 39-46 21175277-12 2011 CONCLUSIONS/INTERPRETATION: glucose readings are sufficient to effectively adjust insulin dosage provided that adjustments are made every 1-4 weeks. Glucose 28-35 insulin Homo sapiens 82-89 21217102-3 2011 The Sensor-Augmented Pump Therapy for A1C Reduction (STAR) 3 trial demonstrated that initiating both CGM and CSII in selected adult and pediatric patients with type 1 diabetes unable to meet glycemic goals with intensive insulin injection therapy significantly improved glucose control. Glucose 270-277 insulin Homo sapiens 221-228 21894016-2 2011 The aim of this study was to evaluate insulin sensitivity (IS) and beta-cell function using the euglycemic hyperinsulinemic clamp (EHC) with the intravenous glucose tolerance test (IVGTT). Glucose 157-164 insulin Homo sapiens 38-45 20554486-5 2011 Insulin resistance/sensitivity was estimated in nonalcoholic fatty liver disease by the homeostasis model assessment and the oral glucose insulin sensitivity during oral glucose tolerance test. Glucose 130-137 insulin Homo sapiens 0-7 21415555-0 2011 Postprandial serum C-peptide to plasma glucose ratio as a predictor of subsequent insulin treatment in patients with type 2 diabetes. Glucose 39-46 insulin Homo sapiens 19-28 21187662-7 2011 Since glucose converts Rab27a from the GTP- to GDP-bound form, we suggested that Rab27a plays a crucial role in stimulus-endocytosis coupling in pancreatic beta-cells, and that this is the key molecule for membrane recycling of insulin granules. Glucose 6-13 insulin Homo sapiens 228-235 21490407-7 2011 The estimate of insulin resistance by HOMA score was calculated with the formula: fasting serum insulin (microIU/mL) x fasting plasma glucose (microM/L) / 22.5. Glucose 134-141 insulin Homo sapiens 16-23 21415555-0 2011 Postprandial serum C-peptide to plasma glucose ratio as a predictor of subsequent insulin treatment in patients with type 2 diabetes. Glucose 39-46 insulin Homo sapiens 82-89 21415555-9 2011 Among CPR values, postprandial serum CPR to plasma glucose ratio (CPR index) showed the greatest area under the receiver operating characteristic (ROC) curve for insulin therapy. Glucose 51-58 insulin Homo sapiens 162-169 21519152-5 2011 As a result, there was a significant correlation between recovery time from hypoglycemia and insulin dose (r=0.88, p<0.0001) and this correlation was expressed as y=0.045x; where y is time (h) and x is insulin dose (U), corresponding to that if 1000 U insulin is injected, hypoglycemia will persist for ~45 h. This equation may be useful to predict the duration of glucose supplementation for treatment of insulin overdose. Glucose 368-375 insulin Homo sapiens 93-100 21701075-8 2011 In the pancreatic beta cell, incretin hormones increase cAMP level, which enhances glucose-stimulated insulin release by protein kinase A-dependent and -independent mechanisms. Glucose 83-90 insulin Homo sapiens 102-109 21528473-5 2011 Insulin resistance was assessed by HOMA and Insulin Resistance Index derived from glucose and insulin concentrations during 75 gram oral glucose tolerance test. Glucose 82-89 insulin Homo sapiens 0-7 21528473-5 2011 Insulin resistance was assessed by HOMA and Insulin Resistance Index derived from glucose and insulin concentrations during 75 gram oral glucose tolerance test. Glucose 137-144 insulin Homo sapiens 0-7 21701075-6 2011 Glucose also stimulates insulin release independent of its action on K(ATP) channels. Glucose 0-7 insulin Homo sapiens 24-31 21701075-10 2011 The stimulatory level of ambient glucose is an absolute requirement for incretin to enhance insulin release. Glucose 33-40 insulin Homo sapiens 92-99 21785227-1 2011 Insulin secretion from pancreatic beta-cells is the only efficient means to decrease blood glucose concentrations. Glucose 91-98 insulin Homo sapiens 0-7 21986033-4 2011 The results showed that insulin aspart three times a day produced a greater improvement in plasma glucose, and particularly in mean postprandial plasma glucose, compared with insulin detemir once a day (p = 0.0006 for comparison of changes between the two insulin treatments). Glucose 98-105 insulin Homo sapiens 24-31 21986033-4 2011 The results showed that insulin aspart three times a day produced a greater improvement in plasma glucose, and particularly in mean postprandial plasma glucose, compared with insulin detemir once a day (p = 0.0006 for comparison of changes between the two insulin treatments). Glucose 152-159 insulin Homo sapiens 24-31 21986033-5 2011 The amount of insulin needed to approach the target levels of plasma glucose was larger in the insulin aspart group (26.0 +- 10.7 U/day vs. 13.7 +- 4.9 U/day; p < 0.0001). Glucose 69-76 insulin Homo sapiens 14-21 21986033-5 2011 The amount of insulin needed to approach the target levels of plasma glucose was larger in the insulin aspart group (26.0 +- 10.7 U/day vs. 13.7 +- 4.9 U/day; p < 0.0001). Glucose 69-76 insulin Homo sapiens 95-102 20956435-9 2011 Duration of the follow-up and extent of weight loss were similar among the three groups, as were fasting and glucose-stimulated insulin and indices of insulin resistance. Glucose 109-116 insulin Homo sapiens 128-135 20823899-7 2011 C-peptide levels were significantly higher after administration of both honeys after 1 and 2 h. CONCLUSIONS: For the first time it has been found out that honey ingestion leads to a rise of blood fructose concentration: in one case, this rise was lower than that achieved after fructose/glucose controls, in the other cases it was same as after the controls. Glucose 287-294 insulin Homo sapiens 0-9 21155690-3 2011 It couples insulin secretion in the pancreas with plasma glucose concentration and improves glucose utilization in the liver, thus, affecting two key aspects of glucose homeostasis. Glucose 57-64 insulin Homo sapiens 11-18 20840879-1 2011 Theca cells with dexamethasone-induced insulin resistance showed defective glucose uptake and excessive testosterone production, both of which were effectively antagonized by berberine. Glucose 75-82 insulin Homo sapiens 39-46 20951701-6 2011 Both protein and dextrose meals caused significant increases in plasma glucose during the 0-5 h post-prandial period; dolphins fed dextrose demonstrated a sustained hyperglycemia lasting 5-10 h. Fasting plasma insulin levels among healthy dolphins mimicked those found in humans with some insulin resistance. Glucose 17-25 insulin Homo sapiens 210-217 21196169-5 2011 In this respect, ERalpha is directly implicated in the E2-regulation of insulin content and secretion, while ERbeta is in the E2-potentiation of glucose-induced insulin release. Glucose 145-152 insulin Homo sapiens 161-168 21966779-9 2011 The triglycerides level correlated with insulin resistance (r = 0.325, p = 0.011), insulin resistance with glucose (r = 0.535, p = 0.000) and insulin resistance with BMI (r = 0.282, p = 0.28). Glucose 107-114 insulin Homo sapiens 83-90 21966779-9 2011 The triglycerides level correlated with insulin resistance (r = 0.325, p = 0.011), insulin resistance with glucose (r = 0.535, p = 0.000) and insulin resistance with BMI (r = 0.282, p = 0.28). Glucose 107-114 insulin Homo sapiens 83-90 21484579-3 2011 Most importantly, it serves as glucose sensor glucose sensor in pancreatic beta-cells mediating glucose-stimulated insulin biosynthesis and release and it governs the capacity of the liver to convert glucose to glycogen. Glucose 31-38 insulin Homo sapiens 115-122 21484579-3 2011 Most importantly, it serves as glucose sensor glucose sensor in pancreatic beta-cells mediating glucose-stimulated insulin biosynthesis and release and it governs the capacity of the liver to convert glucose to glycogen. Glucose 46-53 insulin Homo sapiens 115-122 20967757-5 2011 hCRP was associated with impaired insulin suppression of endogenous glucose production with no reduction in peripheral tissue glucose uptake, suggesting that hCRP mediated insulin resistance in the liver but not extrahepatic tissues. Glucose 68-75 insulin Homo sapiens 34-41 21135541-4 2011 RESULTS: Insulin sensitivity expressed as M value (glucose disposal mg/kg/min) was lower in AGA-non-PGR (8.9) than in SGA (11.0) or AGA-PGR subjects (10.4). Glucose 51-58 insulin Homo sapiens 9-16 21296741-6 2011 We found that European genetic admixture is positively associated with insulin sensitivity (S I ), and negatively associated with the acute insulin response to glucose, fasting insulin levels and the homeostasis model assessment of insulin resistance. Glucose 160-167 insulin Homo sapiens 140-147 21296741-6 2011 We found that European genetic admixture is positively associated with insulin sensitivity (S I ), and negatively associated with the acute insulin response to glucose, fasting insulin levels and the homeostasis model assessment of insulin resistance. Glucose 160-167 insulin Homo sapiens 140-147 21296741-6 2011 We found that European genetic admixture is positively associated with insulin sensitivity (S I ), and negatively associated with the acute insulin response to glucose, fasting insulin levels and the homeostasis model assessment of insulin resistance. Glucose 160-167 insulin Homo sapiens 140-147 23439402-3 2011 The author of this "expert opinion" presents her insights into the use of insulin in this setting and suggest that based on available evidence based medicine, insulin infusion, titrated to "normoglycemia" is a complex intervention, that not only requires the simple administration of a "drug", the hormone insulin, but also needs tools and skills to accurately measure and control blood glucose to achieve normoglycemia while avoiding hypoglycemia and large glucose fluctuations. Glucose 387-394 insulin Homo sapiens 159-166 23439402-3 2011 The author of this "expert opinion" presents her insights into the use of insulin in this setting and suggest that based on available evidence based medicine, insulin infusion, titrated to "normoglycemia" is a complex intervention, that not only requires the simple administration of a "drug", the hormone insulin, but also needs tools and skills to accurately measure and control blood glucose to achieve normoglycemia while avoiding hypoglycemia and large glucose fluctuations. Glucose 387-394 insulin Homo sapiens 159-166 23439402-3 2011 The author of this "expert opinion" presents her insights into the use of insulin in this setting and suggest that based on available evidence based medicine, insulin infusion, titrated to "normoglycemia" is a complex intervention, that not only requires the simple administration of a "drug", the hormone insulin, but also needs tools and skills to accurately measure and control blood glucose to achieve normoglycemia while avoiding hypoglycemia and large glucose fluctuations. Glucose 458-465 insulin Homo sapiens 159-166 23439402-3 2011 The author of this "expert opinion" presents her insights into the use of insulin in this setting and suggest that based on available evidence based medicine, insulin infusion, titrated to "normoglycemia" is a complex intervention, that not only requires the simple administration of a "drug", the hormone insulin, but also needs tools and skills to accurately measure and control blood glucose to achieve normoglycemia while avoiding hypoglycemia and large glucose fluctuations. Glucose 458-465 insulin Homo sapiens 159-166 22211009-6 2011 Fasting glucose levels were found to be negatively correlated with serum insulin levels. Glucose 8-15 insulin Homo sapiens 73-80 21056684-4 2011 Insulin maintains glucose homeostasis by stimulating glucose uptake into muscle and adipose tissue. Glucose 18-25 insulin Homo sapiens 0-7 21056684-4 2011 Insulin maintains glucose homeostasis by stimulating glucose uptake into muscle and adipose tissue. Glucose 53-60 insulin Homo sapiens 0-7 21686140-2 2011 We investigated the association between cytokine-mediated inflammation (high sensitivity C reactive protein [hsCRP] and interleukin [IL] 6) and insulin sensitivity (insulin-mediated glucose disposal rate, assessed by the euglycemic insulin clamp) in a community-based cohort, with subgroup analyses of normal weight individuals without diabetes mellitus and metabolic syndrome (NCEP). Glucose 182-189 insulin Homo sapiens 165-172 21686140-2 2011 We investigated the association between cytokine-mediated inflammation (high sensitivity C reactive protein [hsCRP] and interleukin [IL] 6) and insulin sensitivity (insulin-mediated glucose disposal rate, assessed by the euglycemic insulin clamp) in a community-based cohort, with subgroup analyses of normal weight individuals without diabetes mellitus and metabolic syndrome (NCEP). Glucose 182-189 insulin Homo sapiens 165-172 22028710-4 2011 Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells. Glucose 128-135 insulin Homo sapiens 147-154 22028710-6 2011 The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus. Glucose 106-113 insulin Homo sapiens 125-132 22267935-1 2011 INTRODUCTION: The goal of insulin therapy in patients with either type 1 diabetes mellitus (T1DM) or type 2 diabetes mellitus (T2DM) is to match as closely as possible normal physiologic insulin secretion to control fasting and postprandial plasma glucose. Glucose 248-255 insulin Homo sapiens 26-33 22007244-3 2011 At baseline, all fatness indices (i.e., percent body fat, visceral adipose tissue, BMI, and waist circumference) were significantly (P < 0.05) associated with unfavorable levels of insulin, glucose, systolic BP, diastolic BP, triglycerides, C-reactive protein (CRP), and fibrinogen. Glucose 193-200 insulin Homo sapiens 184-191 21266855-3 2011 In this study, we assessed insulin secretion per IEQ by our newly developed single islet glucose-stimulated insulin release test (SI-GSIRT). Glucose 89-96 insulin Homo sapiens 27-34 21266855-3 2011 In this study, we assessed insulin secretion per IEQ by our newly developed single islet glucose-stimulated insulin release test (SI-GSIRT). Glucose 89-96 insulin Homo sapiens 108-115 21266855-7 2011 There was a significantly strong correlation between insulin secretion stimulated by high glucose solution and low glucose solution (R(2) =0.90, p< 0.001) confirming our technical applicability for SI-GSIRT. Glucose 90-97 insulin Homo sapiens 53-60 21266855-8 2011 Insulin secretion stimulated by high glucose per IEQ was significantly lower in larger islets compared to smaller islets. Glucose 37-44 insulin Homo sapiens 0-7 20843946-9 2011 CONCLUSIONS: Islet up-regulation manifesting as basal elevated glucagon and c-peptide secretion that determines the suppressive effects of hyperinsulinemia appears early in the course of deteriorating glucose tolerance. Glucose 201-208 insulin Homo sapiens 76-85 20881262-6 2011 RESULTS: In the twin sample, carriers of the minor G-allele of rs2802292 showed reduced fasting plasma insulin [per allele effect (beta) = -13% (-24; -1) (95% confidence interval), P = 0.03] and lower incremental area under the curve 0-120 min for insulin after an oral glucose load [beta = -14% (-23; -5), P = 0.005]. Glucose 270-277 insulin Homo sapiens 103-110 20881262-7 2011 The G-allele was associated with increased peripheral insulin action [glucose disposal rate clamp, beta = 0.85 mg kg(fat-free mass)(-1) min(-1)() (0.049; 1.64), P = 0.04] and lower hepatic insulin resistance index [beta = -13% (-25; -1), P = 0.03]. Glucose 70-77 insulin Homo sapiens 54-61 20881262-9 2011 In the Inter99 sample, we found an association with reduced incremental area under the curve 0-120 min for insulin after an oral glucose load [beta = -3% (-5; -0.07), P = 0.04], but this association was not significant after adjustment for body mass index. Glucose 129-136 insulin Homo sapiens 107-114 20943777-5 2011 Secondary end points included insulin-stimulated glucose uptake as measured by euglycemic hyperinsulinemic clamp; IGF-I; and GH secretion parameters, including pulse area, pulse frequency, and basal secretion. Glucose 49-56 insulin Homo sapiens 30-37 20943777-10 2011 Moreover, although tesamorelin significantly increases IGF-I, peripheral insulin-stimulated glucose uptake appears to be preserved. Glucose 92-99 insulin Homo sapiens 73-80 21303619-12 2011 CONCLUSIONS: The use of a continuous glucose monitor changes the way patients manage their diabetes, as observed in the increased number of daily insulin bolus, the increased number of daily BG measurements, and the differences in the distribution of BG measurements throughout the day. Glucose 37-44 insulin Homo sapiens 146-153 22187651-0 2011 Effects of Selected Anionic beta-Cyclodextrins on Persistence of Blood Glucose Lowering by Insulin Glargine after Subcutaneous Injection to Rats. Glucose 71-78 insulin Homo sapiens 91-98 20237501-3 2011 Insulin sensitivity indices were obtained by using the homeostasis model assessment, after 75 g Dextrose oral glucose tolerance tests (Matsuda index) and the euglycemic hyperinsulinemic clamp (M-value) in 49 patients with arterial hypertension. Glucose 96-104 insulin Homo sapiens 0-7 20237501-3 2011 Insulin sensitivity indices were obtained by using the homeostasis model assessment, after 75 g Dextrose oral glucose tolerance tests (Matsuda index) and the euglycemic hyperinsulinemic clamp (M-value) in 49 patients with arterial hypertension. Glucose 110-117 insulin Homo sapiens 0-7 20972250-7 2011 Of these, rs693, which lies in the APOB gene, was also significantly associated with the homoeostasis model assessment for insulin resistance (p=6.68x10-6) and gamma-glutamyl transpeptidase (p=2.34x10-6), and rs174547, which lies in the FADS1 gene and was significantly associated with fasting plasma glucose (p=1.48x10-6). Glucose 301-308 insulin Homo sapiens 123-130 21281021-2 2011 Insulin resistance is defined as a diminution in the glucose response to a given amount of insulin. Glucose 53-60 insulin Homo sapiens 0-7 21281021-2 2011 Insulin resistance is defined as a diminution in the glucose response to a given amount of insulin. Glucose 53-60 insulin Homo sapiens 91-98 21281021-7 2011 Lifestyle modification to reduce weight in obese women and treatment with insulin-sensitising drugs such as metformin in women with glucose intolerance result in the improvement of some metabolic abnormalities and hyperandrogenic disorders with the consequent restoration of normal menstrual and ovulatory function in a significant number of women with polycystic ovaries. Glucose 132-139 insulin Homo sapiens 74-81 21932577-10 2011 CONCLUSION: Even with well-controlled glucose levels, the development of children with diabetes who had been receiving insulin pigment were still adversely affected. Glucose 38-45 insulin Homo sapiens 119-126 22308842-5 2011 Insulin secretory capacity was measured as acute insulin response and glucose disposal index. Glucose 70-77 insulin Homo sapiens 0-7 20809104-5 2011 Insulin synthesis was determined by in vitro translation of glucose induced insulin mRNA synthesis in the pancreatic beta cells. Glucose 60-67 insulin Homo sapiens 0-7 20809104-5 2011 Insulin synthesis was determined by in vitro translation of glucose induced insulin mRNA synthesis in the pancreatic beta cells. Glucose 60-67 insulin Homo sapiens 76-83 20809104-10 2011 These results indicated that dermcidin was a novel platelet aggregating agent, and potentiated the ADP induced thrombosis in the animal model as well as acutely inhibited glucose induced insulin synthesis. Glucose 171-178 insulin Homo sapiens 187-194 21148297-1 2011 Insulin stimulates glucose transport in muscle and adipose tissue by translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 21269980-0 2011 [Efficacy and safety evaluation of two insulin treatment protocols using a continuous glucose monitoring system]. Glucose 86-93 insulin Homo sapiens 39-46 21986470-7 2011 Indices of insulin sensitivity and resistance were determined following an oral glucose tolerance test (OGTT). Glucose 80-87 insulin Homo sapiens 11-18 21772735-0 2011 Efficacy of 2-hour post glucose insulin levels in predicting insulin resistance in polycystic ovarian syndrome with infertility. Glucose 24-31 insulin Homo sapiens 61-68 21772735-2 2011 AIMS: To evaluate if "2-hour post-glucose insulin level" is an effective indicator of IR and can aid in diagnosing IR in infertile PCOS women. Glucose 34-41 insulin Homo sapiens 42-49 21772735-8 2011 "2-hour post-glucose insulin levels" were elevated in 88% of PCOS individuals but were normal in all females not suffering from PCOS. Glucose 13-20 insulin Homo sapiens 21-28 21772735-10 2011 CONCLUSIONS: "2-hour post-glucose insulin levels" appears to be a good indicator of IR. Glucose 26-33 insulin Homo sapiens 34-41 22145455-1 2011 BACKGROUND: Magnesium, the second most abundant intracellular cation, plays a major role in regulating insulin effect and insulin mediated glucose uptake. Glucose 139-146 insulin Homo sapiens 122-129 22420194-5 2011 The Pearson correlation analysis revealed moderate negative correlation between 6-SOMT level in urine and insulin and glucose levels in plasma (r = 0.95). Glucose 118-125 insulin Homo sapiens 106-113 20356610-4 2011 Insulin resistance was quantified by determining the steady-state plasma glucose concentration during the insulin suppression test and insulin secretory function by homeostasis model assessment of beta-cell function (HOMA-beta) and the total integrated daylong plasma insulin responses to mixed meals (insulin area under the curve). Glucose 73-80 insulin Homo sapiens 0-7 20356610-7 2011 Insulin sensitivity improved (P < .001) after RSG administration, with decreases of 31% +- 23% and 21% +- 14% in steady-state plasma glucose concentration in nondiabetic and diabetic subjects, respectively. Glucose 136-143 insulin Homo sapiens 0-7 21766644-0 2011 [Approaches of assessing insulin resistance--euglycemic glucose clamp, steady state plasma glucose, and minimal model]. Glucose 56-63 insulin Homo sapiens 25-32 21154114-2 2011 This prospective study examined the association between insulin sensitivity measured directly using the frequently sampled intravenous glucose tolerance test (FSIGT) and later risk of colorectal adenomas. Glucose 135-142 insulin Homo sapiens 56-63 21159496-3 2011 Insulin and nitric oxide have an important role in the regulation of glucose transport and metabolism. Glucose 69-76 insulin Homo sapiens 0-7 22027284-8 2011 RESULTS: At discharge from hospital, only 3 of the 13 patients who used insulin preoperatively required small amounts of insulin (mean 21 IU per day, range 15-30) to keep fasting and postprandial plasma glucose levels below 200 mg/dl. Glucose 203-210 insulin Homo sapiens 72-79 22027284-8 2011 RESULTS: At discharge from hospital, only 3 of the 13 patients who used insulin preoperatively required small amounts of insulin (mean 21 IU per day, range 15-30) to keep fasting and postprandial plasma glucose levels below 200 mg/dl. Glucose 203-210 insulin Homo sapiens 121-128 24331010-0 2011 The use of adipose tissue-conditioned media to demonstrate the differential effects of fat depots on insulin-stimulated glucose uptake in a skeletal muscle cell line. Glucose 120-127 insulin Homo sapiens 101-108 24331010-4 2011 CM from visceral fat (1:128 dilution) reduced insulin-stimulated glucose uptake in L6 myotubes by 19% (P < 0.05), an effect mediated by a nuclear factor kappa B (NFkappaB)/mammalian target of rapamycin complex 1 (mTORC1)-dependent pathway and partially reversed by neutralizing IL-6. Glucose 65-72 insulin Homo sapiens 46-53 24331010-5 2011 IL-6 at a concentration comparable to that in CM from visceral fat reduced insulin-stimulated glucose uptake by 53% (P < 0.05), an effect abolished by inhibiting NFkappaB or mTORC1. Glucose 94-101 insulin Homo sapiens 75-82 21482586-14 2011 CONCLUSIONS: Everolimus normalizes plasma glucose levels in metastatic insulinoma within 14 days, coinciding with a lower glucose uptake in tumor and muscles and declining (pro)insulin levels. Glucose 42-49 insulin Homo sapiens 71-78 21673843-3 2011 Maternal glucose regulation is however affected by numerous factors including physiological changes of pregnancy (e.g. insulin resistance [IR]), pathological conditions (e.g. gestational diabetes mellitus) and maternal nutrition. Glucose 9-16 insulin Homo sapiens 119-126 21760856-8 2011 RESULTS: In both genders, insulin therapy (Group A) was associated with significant (p = 0.003 to <0.001) increases in weight, body mass index and leptin levels and significant decreases in glucose, HbA(1c) and NPY levels. Glucose 193-200 insulin Homo sapiens 26-33 21966327-5 2011 Insulin is a major metabolic hormone which has numerous functions in the body and one main role is to stimulate glucose uptake into body"s cells where it is utilized to provide energy. Glucose 112-119 insulin Homo sapiens 0-7 22248781-2 2011 The hallmark of insulin resistance is decreased tissue glucose uptake despite normal or elevated insulin concentration. Glucose 55-62 insulin Homo sapiens 16-23 22248782-3 2011 Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscles and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Glucose 61-68 insulin Homo sapiens 0-7 22248782-3 2011 Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscles and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Glucose 110-117 insulin Homo sapiens 0-7 22248782-3 2011 Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscles and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Glucose 110-117 insulin Homo sapiens 0-7 22056597-3 2011 Insulin-stimulated glucose uptake was measured in HepG2 cells and in differentiated 3T3-L1 adipocytes using 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG), a fluorescent D-glucose analog. Glucose 19-26 insulin Homo sapiens 0-7 22056597-3 2011 Insulin-stimulated glucose uptake was measured in HepG2 cells and in differentiated 3T3-L1 adipocytes using 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG), a fluorescent D-glucose analog. Glucose 163-172 insulin Homo sapiens 0-7 22056597-5 2011 Insulin-stimulated protein kinase B (Akt/PKB) phosphorylation was measured in high glucose-induced, insulin-resistant HepG2 cells. Glucose 83-90 insulin Homo sapiens 0-7 22056597-5 2011 Insulin-stimulated protein kinase B (Akt/PKB) phosphorylation was measured in high glucose-induced, insulin-resistant HepG2 cells. Glucose 83-90 insulin Homo sapiens 100-107 22056597-6 2011 Similar to 30 mumol/l rosiglitazone, treatment with 30 mumol/l aromadendrin significantly stimulated insulin-sensitive glucose uptake in both HepG2 cells and 3T3-L1 adipocytes. Glucose 119-126 insulin Homo sapiens 101-108 22056597-8 2011 In high glucose-induced, insulin-resistant HepG2 cells, aromadendrin reversed the inhibition of Akt/PKB phosphorylation in response to insulin, which could be abrogated by pretreatment with LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. Glucose 8-15 insulin Homo sapiens 25-32 22056597-8 2011 In high glucose-induced, insulin-resistant HepG2 cells, aromadendrin reversed the inhibition of Akt/PKB phosphorylation in response to insulin, which could be abrogated by pretreatment with LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. Glucose 8-15 insulin Homo sapiens 135-142 22194812-7 2011 Insulin was also detected in the culture medium following glucose stimulation, confirming an initial differentiation that resulted in glucose-sensitive endocrine secretion. Glucose 58-65 insulin Homo sapiens 0-7 22194812-7 2011 Insulin was also detected in the culture medium following glucose stimulation, confirming an initial differentiation that resulted in glucose-sensitive endocrine secretion. Glucose 134-141 insulin Homo sapiens 0-7 22073261-8 2011 Furthermore the C-allele was associated with increased insulin response following oral glucose stimulation in a meta-analysis based on Danish and Finnish non-diabetic individuals. Glucose 87-94 insulin Homo sapiens 55-62 22087313-1 2011 In type 2 Diabetes (T2D) free fatty acids (FFAs) in plasma are increased and hepatic insulin resistance is "selective", in the sense that the insulin-mediated decrease of glucose production is blunted while insulin"s effect on stimulating lipogenesis is maintained. Glucose 171-178 insulin Homo sapiens 85-92 22087313-1 2011 In type 2 Diabetes (T2D) free fatty acids (FFAs) in plasma are increased and hepatic insulin resistance is "selective", in the sense that the insulin-mediated decrease of glucose production is blunted while insulin"s effect on stimulating lipogenesis is maintained. Glucose 171-178 insulin Homo sapiens 142-149 22087313-6 2011 Accordingly, dose-response curves for insulin-mediated suppression of the FoxO1-induced gluconeogenic genes and for de novo glucose production were right shifted, and insulin-stimulated glucose oxidation and glycogen synthesis were impaired. Glucose 124-131 insulin Homo sapiens 38-45 22087313-6 2011 Accordingly, dose-response curves for insulin-mediated suppression of the FoxO1-induced gluconeogenic genes and for de novo glucose production were right shifted, and insulin-stimulated glucose oxidation and glycogen synthesis were impaired. Glucose 186-193 insulin Homo sapiens 167-174 22087313-12 2011 In conclusion, our findings indicate that FFAs may cause a selective impairment of insulin action upon hepatic glucose metabolism by increasing PP2A activity. Glucose 111-118 insulin Homo sapiens 83-90 22073153-1 2011 BACKGROUND: We have shown that 1,2,3,4,6-penta-O-galloyl-alpha-D-glucopyranose (alpha-PGG), an orally effective hypoglycemic small molecule, binds to insulin receptors and activates insulin-mediated glucose transport. Glucose 199-206 insulin Homo sapiens 150-157 22073153-1 2011 BACKGROUND: We have shown that 1,2,3,4,6-penta-O-galloyl-alpha-D-glucopyranose (alpha-PGG), an orally effective hypoglycemic small molecule, binds to insulin receptors and activates insulin-mediated glucose transport. Glucose 199-206 insulin Homo sapiens 182-189 21966466-2 2011 Indinavir has been shown to act as a potent reversible noncompetitive inhibitor of zero-trans glucose influx via direct interaction with the insulin responsive facilitative glucose transporter GLUT4. Glucose 94-101 insulin Homo sapiens 141-148 21949744-1 2011 BACKGROUND: The Meta-Analysis of Glucose and Insulin related traits Consortium (MAGIC) recently identified 16 loci robustly associated with fasting glucose, some of which were also associated with type 2 diabetes. Glucose 148-155 insulin Homo sapiens 45-52 21887289-0 2011 Glucose-raising genetic variants in MADD and ADCY5 impair conversion of proinsulin to insulin. Glucose 0-7 insulin Homo sapiens 72-82 21887289-0 2011 Glucose-raising genetic variants in MADD and ADCY5 impair conversion of proinsulin to insulin. Glucose 0-7 insulin Homo sapiens 75-82 21887289-11 2011 DISCUSSION: By examining parameters of glucose-stimulated proinsulin-to-insulin conversion during an OGTT, we show that the SNP in ADCY5 is implicated in defective proinsulin-to-insulin conversion. Glucose 39-46 insulin Homo sapiens 58-68 21887289-11 2011 DISCUSSION: By examining parameters of glucose-stimulated proinsulin-to-insulin conversion during an OGTT, we show that the SNP in ADCY5 is implicated in defective proinsulin-to-insulin conversion. Glucose 39-46 insulin Homo sapiens 61-68 21887289-11 2011 DISCUSSION: By examining parameters of glucose-stimulated proinsulin-to-insulin conversion during an OGTT, we show that the SNP in ADCY5 is implicated in defective proinsulin-to-insulin conversion. Glucose 39-46 insulin Homo sapiens 164-174 21887289-11 2011 DISCUSSION: By examining parameters of glucose-stimulated proinsulin-to-insulin conversion during an OGTT, we show that the SNP in ADCY5 is implicated in defective proinsulin-to-insulin conversion. Glucose 39-46 insulin Homo sapiens 72-79 21738722-15 2011 However, we found increased insulin-dependent glucose incorporation into glycogen. Glucose 46-53 insulin Homo sapiens 28-35 21687731-8 2011 These ICAs are shown to produce human C-peptide in a glucose dependent manner exhibiting in-vitro functionality. Glucose 53-60 insulin Homo sapiens 38-47 21913422-3 2011 These are key transcription factors determining, proper cellular metabolism of glucose and lipids, tissue sensitivity to insulin, appropriate immune responses including inflammatory processes and finally cell division and differentiation. Glucose 79-86 insulin Homo sapiens 121-128 20971778-4 2011 In vitro viability and the glucose-stimulation index for insulin were determined over the course of 2 weeks and analyzed by using a cross-sectional time series regression model. Glucose 27-34 insulin Homo sapiens 57-64 22074575-2 2011 One of the key metabolic actions of insulin is to control blood sugar levels by promoting glucose uptake into adipocyte and muscle cells. Glucose 90-97 insulin Homo sapiens 36-43 20678967-1 2011 BACKGROUND: Obesity is a strong risk factor for resistance to insulin-mediated glucose disposal, a precursor of type 2 diabetes and other disorders. Glucose 79-86 insulin Homo sapiens 62-69 21893886-3 2011 In order to support in-patient care, we designed a prototypical mobile in-patient glucose management system with decision support for insulin dosing. Glucose 82-89 insulin Homo sapiens 134-141 21353873-3 2011 Activins signaling, which is mediated by ALK4 and 7 together with ActRIIA and IIB, plays a critical role in glucose-stimulated insulin secretion, development/neogenesis, and glucose homeostatic control of pancreatic endocrine cells; the insulin gene is regulated by these signaling pathways via ALK7, which is a receptor for Activins AB and B and Nodal. Glucose 108-115 insulin Homo sapiens 127-134 21353873-3 2011 Activins signaling, which is mediated by ALK4 and 7 together with ActRIIA and IIB, plays a critical role in glucose-stimulated insulin secretion, development/neogenesis, and glucose homeostatic control of pancreatic endocrine cells; the insulin gene is regulated by these signaling pathways via ALK7, which is a receptor for Activins AB and B and Nodal. Glucose 108-115 insulin Homo sapiens 237-244 22241951-11 2011 CONCLUSION: Systolic heart failure and type 2 diabetes result in similar vascular insulin resistance and reduced muscular insulin-stimulated glucose uptake. Glucose 141-148 insulin Homo sapiens 122-129 21187969-1 2010 In response to insulin, glucose transporter GLUT4 translocates from intracellular compartments towards the plasma membrane where it enhances cellular glucose uptake. Glucose 24-31 insulin Homo sapiens 15-22 21353883-2 2011 Activins regulate glucose/energy metabolism by promoting the differentiation of insulin-producing and -responsive cells, and regulating function of the differentiated cells. Glucose 18-25 insulin Homo sapiens 80-87 21353883-3 2011 In the pancreas, activins stimulate the differentiation of beta cells and secretion of insulin, which enables the cells to respond to glucose uptake efficiently. Glucose 134-141 insulin Homo sapiens 87-94 21434307-7 2011 There is a positive correlation between serum iron and insulin resistance index and blood glucose. Glucose 90-97 insulin Homo sapiens 55-62 21628978-3 2011 This is because PPARgamma/RXR is known to be a target of thiazolidinediones (TZDs), which are used for the treatment of insulin resistance, LXR/RXR is reported to be involved in glucose/lipid metabolism, and these heterodimers can be activated by RXR agonists alone (permissive mechanism). Glucose 178-185 insulin Homo sapiens 120-127 21418880-5 2011 The dose response were insulin secretion rates at each time point during OGTT being plotted over the corresponding glucose levels, and the slopes of which quantified the insulin secretion responding to glucose. Glucose 202-209 insulin Homo sapiens 170-177 21418880-10 2011 CONCLUSIONS: It supports that with the alleviation of physiological insulin resistance after puberty, the gross hyperinsulinemia tends to ameliorate, and beta-cell secretion does not deteriorate over time as glucose homeostasis maintains. Glucose 208-215 insulin Homo sapiens 68-75 21418882-1 2011 OBJECTIVE: To investigate insulin sensitivity and beta cell function in female systemic lupus erythematosus (SLE) patients with different glucose tolerances. Glucose 138-145 insulin Homo sapiens 26-33 21223811-6 2010 Fasting plasma glucose (FPG) was tested by glucose oxidase and the home model insulin resistance index (HOMA-IR) calculated. Glucose 15-22 insulin Homo sapiens 78-85 21191479-3 2010 One prime candidate is insulin, which until recently was mainly related to its metabolic function for the transport and regulation of glucose in the periphery. Glucose 134-141 insulin Homo sapiens 23-30 21301591-8 2010 Overall, patients" ideal insulin treatment would provide better glucose control, result in fewer adverse reactions, have the lowest cost, and be administered orally. Glucose 64-71 insulin Homo sapiens 25-32 20934436-9 2010 Exposure to high glucose and/or tumor necrosis factor-alpha which is known to be a factor that induces insulin resistance, enhanced the mRNA levels of DUSP1, ANXA1, IL1B, S100A8, IL22RA2, S100A9 and IRF1 in human monocyte-like U937 cells. Glucose 17-24 insulin Homo sapiens 103-110 21167072-2 2010 This is particularly true for the vast set of processes involved in regulation of glucose homeostasis, being it in glucose metabolism itself or in hormonal control, especially insulin. Glucose 82-89 insulin Homo sapiens 176-183 21167072-2 2010 This is particularly true for the vast set of processes involved in regulation of glucose homeostasis, being it in glucose metabolism itself or in hormonal control, especially insulin. Glucose 115-122 insulin Homo sapiens 176-183 20826135-4 2010 In C2C12 myotubes, 24-h treatment with irbesartan significantly promoted both basal and insulin-stimulated glucose transport. Glucose 107-114 insulin Homo sapiens 88-95 20826135-9 2010 We conclude that irbesartan has a direct action, which can be additive to insulin, of promoting glucose transport in skeletal muscle. Glucose 96-103 insulin Homo sapiens 74-81 20472004-4 2010 Acutely, both GLP-1 and, more markedly so, GIP, significantly potentiated glucose-stimulated insulin release, with no apparent synergic action. Glucose 74-81 insulin Homo sapiens 93-100 21151894-0 2010 Protein markers for insulin-producing beta cells with higher glucose sensitivity. Glucose 61-68 insulin Homo sapiens 20-27 21036144-3 2010 This study was performed to determine the contribution of GPR40 to short- and/or long-term effects of FFAs on glucose-stimulated insulin secretion (GSIS) and the expression of PDX-1 and GLUT2 in pancreatic beta-cells, as well as the intervenient effects of pioglitazone on lipotoxicity of beta-cells. Glucose 110-117 insulin Homo sapiens 129-136 24843445-0 2010 Endogenous insulin secretion even at a very low level contributes to the stability of blood glucose control in fulminant type 1 diabetes. Glucose 92-99 insulin Homo sapiens 11-18 21151924-8 2010 Glucose-stimulated insulin secretion, beta-cell mass, islet size, body composition, serum metabolic profiles, lipogenesis, lipolysis, adipose hypertrophy and lipid deposition in the liver and muscle were also measured after 12 weeks of dosing. Glucose 0-7 insulin Homo sapiens 19-26 21151924-12 2010 Administration of Boc5 (3 mg) reduced basal but enhanced insulin-mediated glucose incorporation and noradrenaline-stimulated lipolysis in isolated adipocytes from obese mice. Glucose 74-81 insulin Homo sapiens 57-64 24843445-6 2010 In conclusion, our present results suggest that even very low levels of endogenous insulin secreting capacity can improve daily dosages of insulin and stabilize blood glucose levels. Glucose 167-174 insulin Homo sapiens 83-90 21152029-9 2010 AUC(C-Peptide(0-120))/AUC(Glucose(0-120)) was best-ranked for the detection of SNPs involved in incretin-stimulated insulin secretion. Glucose 26-33 insulin Homo sapiens 116-123 21152029-0 2010 Evaluation of fasting state-/oral glucose tolerance test-derived measures of insulin release for the detection of genetically impaired beta-cell function. Glucose 34-41 insulin Homo sapiens 77-84 20861177-5 2010 We determined the whole-body insulin sensitivity index (S(I)) with an intravenous glucose tolerance test and minimal modeling. Glucose 82-89 insulin Homo sapiens 29-36 21152029-1 2010 BACKGROUND: To date, fasting state- and different oral glucose tolerance test (OGTT)-derived measures are used to estimate insulin release with reasonable effort in large human cohorts required, e.g., for genetic studies. Glucose 55-62 insulin Homo sapiens 123-130 21152029-7 2010 This approach revealed area under the curve (AUC)(Insulin(0-30))/AUC(Glucose(0-30)) as the best-ranked index to detect SNP-dependent differences in insulin release. Glucose 69-76 insulin Homo sapiens 148-155 20823450-11 2010 5) We and others established that the indirect effect of insulin plays an important role in the regulation of glucose production in dogs. Glucose 110-117 insulin Homo sapiens 57-64 21274487-5 2010 Homeostatic model assessement of insulin resistance (HOMA-IR) was evaluated from fasting plasma glucose and serum insulin levels. Glucose 96-103 insulin Homo sapiens 33-40 20923961-10 2010 Given the importance of vasodilator reactivity in affecting glucose disposal and vascular homeostasis, this defect may then contribute to the development of metabolic and vascular complications in insulin-resistant states. Glucose 60-67 insulin Homo sapiens 197-204 21095317-3 2010 To improve postoperative glucose control at our institution, a patient-specific insulin-resistance-guided (IRG) protocol was developed. Glucose 25-32 insulin Homo sapiens 80-87 21095317-10 2010 The ability to adjust a patient"s insulin dosing based upon factors related to their insulin resistance results in improved blood glucose control and safety in cardiovascular surgery patients. Glucose 130-137 insulin Homo sapiens 34-41 21095317-10 2010 The ability to adjust a patient"s insulin dosing based upon factors related to their insulin resistance results in improved blood glucose control and safety in cardiovascular surgery patients. Glucose 130-137 insulin Homo sapiens 85-92 20868233-4 2010 However, higher concentrations of metformin (100-1000 mum) increased (1.3-1.5-fold; p<0.001) insulin release at basal glucose concentrations, but had no effect on glucose-stimulated insulin secretion. Glucose 121-128 insulin Homo sapiens 96-103 20868233-7 2010 Prolonged glucotoxic and lipotoxic conditions impaired beta-cell viability and insulin release in response to glucose and to a broad range of insulin secretagogues. Glucose 110-117 insulin Homo sapiens 79-86 20802253-3 2010 RESEARCH DESIGN AND METHODS: Insulin secretion was assessed by insulinogenic index and areas under the curve of C-peptide/glucose in 1,576 subjects using an oral glucose tolerance test (OGTT). Glucose 122-129 insulin Homo sapiens 29-36 22166651-8 2010 The time was shortest in Group C. The insulin doses needed to achieve glucose reduction of 20% in three treatment groups were (0.40 +- 0.04) Uxkg(-1)xd(-1) for Group A, (0.37 +- 0.04) Uxkg(-1)xd(-1) for Group B, and (0.35 +- 0.03) Uxkg(-1)xd(-1) for Group C, respectively. Glucose 70-77 insulin Homo sapiens 38-45 20584565-8 2010 But insulin sensitivity (glucose infusion rate) during the EH clamp was not different at the end of fiber and control treatments, 3.7 +- 1.8 and 3.8 +- 1.5 mg kg(-1) min(-1), respectively, nor fasting plasma glucose and insulin. Glucose 25-32 insulin Homo sapiens 4-11 20886378-4 2010 Investigations of more detailed physiologic phenotypes, such as the insulin response to intravenous glucose or the incretion hormones, are now emerging and give indications of more specific pathologic mechanisms for diabetes-related risk variants. Glucose 100-107 insulin Homo sapiens 68-75 20802253-3 2010 RESEARCH DESIGN AND METHODS: Insulin secretion was assessed by insulinogenic index and areas under the curve of C-peptide/glucose in 1,576 subjects using an oral glucose tolerance test (OGTT). Glucose 162-169 insulin Homo sapiens 29-36 20841609-4 2010 Insulin sensitivity was estimated from a 75-g oral glucose tolerance test (IS(OGTT)) and measured by a euglycemic hyperinsulinemic clamp (IS(clamp), n = 172). Glucose 51-58 insulin Homo sapiens 0-7 21074472-9 2010 This negative feedback may be exacerbated when cells are chronically exposed to elevated glucose concentrations and could thereby contribute to alterations in insulin signaling observed in diabetic patients. Glucose 89-96 insulin Homo sapiens 159-166 22127749-3 2010 In 163 of these hospitalized patients, insulin resistance was evaluated by the ITT after their blood glucose level was ameliorated. Glucose 101-108 insulin Homo sapiens 39-46 20926588-6 2010 Within 3 h, insulin resistance arose, characterized by reductions in each insulin-stimulated glucose uptake, GLUT4 translocation, Akt Ser(473) phosphorylation, and insulin receptor substrate 1 tyrosine phosphorylation. Glucose 93-100 insulin Homo sapiens 12-19 20926588-6 2010 Within 3 h, insulin resistance arose, characterized by reductions in each insulin-stimulated glucose uptake, GLUT4 translocation, Akt Ser(473) phosphorylation, and insulin receptor substrate 1 tyrosine phosphorylation. Glucose 93-100 insulin Homo sapiens 74-81 20926588-10 2010 This study provides supporting evidence for the integration of innate immune and metabolic responses through the involvement of NOD proteins and suggests the possible participation of cell autonomous immune responses in the development of insulin resistance in skeletal muscle, the major depot for postprandial glucose utilization. Glucose 311-318 insulin Homo sapiens 239-246 20972724-6 2010 Moreover, after glucose administration, the concentration of insulin at 60, 120, and 180 min were significantly higher in patients with TPP than those in pure hyperthyroidism patients. Glucose 16-23 insulin Homo sapiens 61-68 20648057-10 2010 Along with glucose ingestion TT subjects had lower INS(AUC) (insulin area under curve), as well as higher LF/HF(AUC) (LF/HF area under curve) values. Glucose 11-18 insulin Homo sapiens 61-68 21428797-1 2010 BACKGROUND: Benzylamine exerts insulin-like effects in adipocytes (e.g., glucose uptake and antilipolysis) and improves glucose handling in rodents. Glucose 73-80 insulin Homo sapiens 31-38 21428797-6 2010 CONCLUSION: Owing to the parallelism between the in vitro insulin mimicry and the in vivo improvement of glucose handling elicited by benzylamine in rodents, the SSAO/VAP-1 substrates, with stronger effects on human adipocytes than benzylamine, show promising applications for the treatment of insulin resistance. Glucose 105-112 insulin Homo sapiens 294-301 20886413-0 2010 Amelioration of insulin resistance by scopoletin in high-glucose-induced, insulin-resistant HepG2 cells. Glucose 57-64 insulin Homo sapiens 74-81 20886413-3 2010 To examine its effect on insulin resistance, we treated high-glucose-induced, insulin-resistant HepG2 cells with scopoletin and measured phosphatidylinositol 3-kinase (PI3 K)-linked protein kinase B (Akt/PKB) phosphorylation. Glucose 61-68 insulin Homo sapiens 78-85 20498658-0 2010 Fat mass largely contributes to insulin mediated glucose uptake in morbidly obese subjects. Glucose 49-56 insulin Homo sapiens 32-39 20498658-1 2010 OBJECTIVE: The aim of this study is to investigate the effect of body size on insulin-mediated, whole-body glucose uptake (M-value) in morbidly obese (MO) subjects, who have large amounts of fat mass. Glucose 107-114 insulin Homo sapiens 78-85 21070530-9 2010 CONCLUSION: In general medicine wards, modified prehospital hypoglycaemic regimens and a basal/bolus insulin regimen achieve similar glucose control. Glucose 133-140 insulin Homo sapiens 101-108 20853142-4 2010 Calculations of transcellular potassium shifts based on the combined effects of insulin-the increase in the electrical potential differences (hyperpolarization) of the cell membranes and the correction of the hyperglycemic intracellular dehydration through decrease in serum glucose concentration-produced quantitative predictions of the decrease in serum K(+) similar to the reported changes in serum K(+) during treatment of DH with insulin. Glucose 275-282 insulin Homo sapiens 80-87 20810569-1 2010 CONTEXT: ATP-sensitive potassium (KATP) channels regulate insulin secretion by coupling glucose metabolism to beta-cell membrane potential. Glucose 88-95 insulin Homo sapiens 58-65 20826583-3 2010 OBJECTIVE: Our objective was to investigate whether the impact of the SNP on variables of glucose-stimulated insulin secretion is influenced by glucose tolerance status. Glucose 90-97 insulin Homo sapiens 109-116 20826583-3 2010 OBJECTIVE: Our objective was to investigate whether the impact of the SNP on variables of glucose-stimulated insulin secretion is influenced by glucose tolerance status. Glucose 144-151 insulin Homo sapiens 109-116 20826583-11 2010 During the iv glucose tolerance test, an association of A-allele carriers with decreased first-phase insulin secretion was also observed only in NGT subjects (P=0.0053). Glucose 14-21 insulin Homo sapiens 101-108 20843942-8 2010 Associations with 1- and 2-h plasma glucose remained significant for adiponectin (P<0.001), PAI-1 (P<0.05), and CRP (P<0.01) after adjustment for BMI and C-peptide. Glucose 36-43 insulin Homo sapiens 163-172 20855446-9 2010 Insulin and C-peptide production in response to glucose was significantly higher in SB-EMSCs than in undifferentiated EMSC controls. Glucose 48-55 insulin Homo sapiens 0-7 20855446-9 2010 Insulin and C-peptide production in response to glucose was significantly higher in SB-EMSCs than in undifferentiated EMSC controls. Glucose 48-55 insulin Homo sapiens 12-21 20855446-13 2010 These data suggest that EMSCs not only play a novel role in the differentiation of pancreatic progenitors, but also can functionally enhance insulin production to restore the regulation of blood glucose levels in an in vivo transplantation model. Glucose 195-202 insulin Homo sapiens 141-148 20585307-2 2010 Blood glucose control with insulin mandates an adequate and precise assessment of blood glucose levels. Glucose 6-13 insulin Homo sapiens 27-34 20673928-9 2010 The area under the insulin and the C-peptide curve during the oral glucose tolerance test and the hepatic insulin extraction increased (P = .05), whereas no statistically significant changes occurred in insulin sensitivity. Glucose 67-74 insulin Homo sapiens 19-26 20673928-12 2010 Most patients with AGM had an improvement in glucose tolerance status, probably due to the augmented action of insulin in peripheral tissues. Glucose 45-52 insulin Homo sapiens 111-118 20826099-3 2010 In this study, we demonstrated that the overexpression of LYRM1 in 3T3-L1 adipocytes resulted in reduced insulin-stimulated glucose uptake, an abnormal mitochondrial morphology, and a decrease in intracellular ATP synthesis and mitochondrial membrane potential. Glucose 124-131 insulin Homo sapiens 105-112 21086066-1 2010 BACKGROUND: Studies devoted to intensive glucose control suggested that the intensive insulin therapy (IIT) approach could effectively reduce complications associated with critical illness. Glucose 41-48 insulin Homo sapiens 86-93 20306023-2 2010 In this large cohort of middle-aged and older Australian men and women without diabetes, elevated 2-h plasma glucose and pre-diabetes were associated with a reduced 5-year risk of low trauma and all fractures in women, independently of BMI, fasting insulin and other lifestyle factors. Glucose 109-116 insulin Homo sapiens 249-256 21078733-1 2010 OBJECTIVE: The goal was to describe the temporal pattern of neonatal plasma glucose levels and associations with maternal glucose levels, cord serum C-peptide levels, and neonatal size and adiposity. Glucose 76-83 insulin Homo sapiens 149-158 20688758-2 2010 The authors hypothesised that rates of hypoglycaemia in patients receiving an insulin infusion would be associated with the intensity of work of the bedside nurse in the preceding 72 h. METHODS: The authors identified ICU patients who had hypoglycaemia (glucose <=3.5 mmol/l, 63 mg/dl) between October 2006 and June 2007. Glucose 254-261 insulin Homo sapiens 78-85 21268471-7 2010 The area under the curves for insulin and glucose during the oral glucose tolerance test were also reduced in Days 3 and 25. Glucose 66-73 insulin Homo sapiens 30-37 25302511-7 2010 Therefore, ideal blood glucose sampling is relevant to prevent insulin solution management errors. Glucose 23-30 insulin Homo sapiens 63-70 20961181-4 2010 RESULTS: The insulin/glucose ratio at the 30th and 120th minute of the OGTT and the insulinogenic index [(insulin at 30 min - insulin at 0 min)/glucose at 30 min] were significantly lower (p = 0.018, p = 0.031 and p = 0.013, respectively) in the ADPKD group. Glucose 21-28 insulin Homo sapiens 13-20 20961181-4 2010 RESULTS: The insulin/glucose ratio at the 30th and 120th minute of the OGTT and the insulinogenic index [(insulin at 30 min - insulin at 0 min)/glucose at 30 min] were significantly lower (p = 0.018, p = 0.031 and p = 0.013, respectively) in the ADPKD group. Glucose 144-151 insulin Homo sapiens 84-91 20961181-4 2010 RESULTS: The insulin/glucose ratio at the 30th and 120th minute of the OGTT and the insulinogenic index [(insulin at 30 min - insulin at 0 min)/glucose at 30 min] were significantly lower (p = 0.018, p = 0.031 and p = 0.013, respectively) in the ADPKD group. Glucose 144-151 insulin Homo sapiens 84-91 20380516-8 2010 Data also evidenced that high glucose concentrations cause prominent disparities in nASCs and dASCs in expression of genes involved in insulin resistance such as adiponectin and resistin. Glucose 30-37 insulin Homo sapiens 135-142 20850340-5 2010 Under normal physiological conditions, changes in ER calcium levels, mediated by glucose and other insulin secretagogues, regulate PERK activity for the purpose of controlling insulin biogenesis. Glucose 81-88 insulin Homo sapiens 176-183 20849938-8 2010 The protective effect of BGP-15 on insulin stimulated glucose utilization had the highest magnitude in the values calculated for the muscle tissue (p=0.002). Glucose 54-61 insulin Homo sapiens 35-42 20807869-4 2010 RESULTS: Two-hour glucose from an OGTT most accurately predicted progression to disease compared with all other metabolic indicators with an area under the ROC curve of 0.67 (95% CI 0.59-0.76), closely followed by the ratio of first-phase insulin response (FPIR) to homeostasis model assessment of insulin resistance (HOMA-IR) with an area under the curve value of 0.66. Glucose 18-25 insulin Homo sapiens 239-246 20807869-4 2010 RESULTS: Two-hour glucose from an OGTT most accurately predicted progression to disease compared with all other metabolic indicators with an area under the ROC curve of 0.67 (95% CI 0.59-0.76), closely followed by the ratio of first-phase insulin response (FPIR) to homeostasis model assessment of insulin resistance (HOMA-IR) with an area under the curve value of 0.66. Glucose 18-25 insulin Homo sapiens 298-305 21036152-8 2010 In CHO cells constitutively expressing human insulin receptor (CHO-IR), there was a concentration dependent increase of promoter activity by insulin in the presence of glucose. Glucose 168-175 insulin Homo sapiens 45-52 21226273-5 2011 On the other hand, our NICE Study yielded better cardiovascular outcomes for those patients with intensive glucose-lowering therapy using rapid-acting insulin analogue reducing postprandial glucose levels with less hypoglycemia. Glucose 107-114 insulin Homo sapiens 151-158 21226273-5 2011 On the other hand, our NICE Study yielded better cardiovascular outcomes for those patients with intensive glucose-lowering therapy using rapid-acting insulin analogue reducing postprandial glucose levels with less hypoglycemia. Glucose 190-197 insulin Homo sapiens 151-158 21152264-1 2010 Insulin stimulates glucose transport in muscle and adipose cells by stimulating translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 20456283-6 2010 Islets from DEX rats secreted more insulin in response to increasing concentrations of glucose and other metabolic and non-metabolic stimuli, compared with that in the CTL group. Glucose 87-94 insulin Homo sapiens 35-42 20819080-3 2010 However, Akt also plays an essential role in other physiological processes, such as the insulin-regulated transport of glucose into muscle and fat cells. Glucose 119-126 insulin Homo sapiens 88-95 20937249-6 2010 In contrast, the sulfonylurea glibenclamide predominantly induced insulin release in the second phase at 16.8 mM glucose and also markedly stimulated insulin secretion at 2.8 mM glucose. Glucose 113-120 insulin Homo sapiens 66-73 21035759-1 2010 The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secretory proteins, termed hepatokines. Glucose 23-30 insulin Homo sapiens 109-116 21211306-0 2010 [Prediction of nocturnal hypoglycaemia with bedtime glucose level during continuous subcutaneous insulin infusion in type 2 diabetics]. Glucose 52-59 insulin Homo sapiens 97-104 21211306-1 2010 OBJECTIVE: To find out the features of glycemic excursion via continuous glucose monitoring system (CGMS) during continuous subcutaneous insulin infusion (CSII) treatment in type 2 diabetics and discuss the possibility of predicting nocturnal hypoglycaemia with bedtime glucose level. Glucose 73-80 insulin Homo sapiens 137-144 21085106-2 2010 Insulin release by the pancreas induces glucose uptake by insulin-sensitive tissues, most notably the brain, skeletal muscle, and adipocytes. Glucose 40-47 insulin Homo sapiens 0-7 21085106-2 2010 Insulin release by the pancreas induces glucose uptake by insulin-sensitive tissues, most notably the brain, skeletal muscle, and adipocytes. Glucose 40-47 insulin Homo sapiens 58-65 21085106-6 2010 Glucose transporter type 4 (GLUT4) is the major transporter that mediates glucose uptake by insulin sensitive tissues, such as the skeletal muscle. Glucose 74-81 insulin Homo sapiens 92-99 21085106-7 2010 Upon binding of insulin to its receptor, vesicles containing GLUT4 translocate from the cytoplasm to the plasma membrane, inducing glucose uptake. Glucose 131-138 insulin Homo sapiens 16-23 20810907-2 2010 We hypothesized that factors known to potentiate insulin action [e.g., AMP-activated protein kinase (AMPK) and p38] or to be involved in insulin signaling leading to glucose transport [e.g., Akt, PKCzeta, AS160, and ataxia telangiectasia mutated (ATM)] would be phosphorylated during serum starvation and would be responsible for increased insulin action after serum starvation. Glucose 166-173 insulin Homo sapiens 137-144 20810907-2 2010 We hypothesized that factors known to potentiate insulin action [e.g., AMP-activated protein kinase (AMPK) and p38] or to be involved in insulin signaling leading to glucose transport [e.g., Akt, PKCzeta, AS160, and ataxia telangiectasia mutated (ATM)] would be phosphorylated during serum starvation and would be responsible for increased insulin action after serum starvation. Glucose 166-173 insulin Homo sapiens 137-144 20810907-5 2010 Insulin had no effect on glucose transport in control cells but caused an increase in glucose uptake for serum-starved cells that was preventable by compound C (an AMPK inhibitor), by expression of dominant negative AMPK (AMPK-DN), and by KU55933 (an ATM inhibitor). Glucose 86-93 insulin Homo sapiens 0-7 20810907-7 2010 Thus, it appears that AMPK is required for the serum starvation-related increase in insulin-stimulated glucose transport, with ATM as a possible downstream effector. Glucose 103-110 insulin Homo sapiens 84-91 20724647-3 2010 Furthermore, the effect of C10 on insulin-mediated glucose uptake and on GLUT4 expression was assessed in L6 muscle cells in vitro. Glucose 51-58 insulin Homo sapiens 34-41 20949602-9 2010 The attachment of PEG to insulin resulted in a conjugated insulin derivative that was biologically active, orally bioavailable and that showed a dose-dependent glucose lowering effect in Type 2 diabetes patients. Glucose 160-167 insulin Homo sapiens 25-32 20949602-9 2010 The attachment of PEG to insulin resulted in a conjugated insulin derivative that was biologically active, orally bioavailable and that showed a dose-dependent glucose lowering effect in Type 2 diabetes patients. Glucose 160-167 insulin Homo sapiens 58-65 21046453-2 2010 Uncoupling of the insulin response to glucose variations may lead to type-2 diabetes mellitus. Glucose 38-45 insulin Homo sapiens 18-25 20699417-0 2010 Glucagon supports postabsorptive plasma glucose concentrations in humans with biologically optimal insulin levels. Glucose 40-47 insulin Homo sapiens 99-106 20699417-3 2010 Insulin was infused intravenously to hold plasma glucose concentrations at ~100 mg/dl (5.6 mmol/l) overnight and fixed from -60 to 240 min the following morning. Glucose 49-56 insulin Homo sapiens 0-7 21088805-5 2010 The insulin resistance index was measured using the estimated glucose disposal rate (eGDR). Glucose 62-69 insulin Homo sapiens 4-11 20879969-2 2010 It is characterized by high circulating levels of glucose resulting from insulin resistance and impaired insulin secretion. Glucose 50-57 insulin Homo sapiens 73-80 20705776-3 2010 This is due in part to impaired insulin-induced suppression of endogenous glucose production, which is observed early in the evolution of type 2 diabetes. Glucose 74-81 insulin Homo sapiens 32-39 20705776-5 2010 Insulin-induced stimulation of hepatic glucose uptake and hepatic glycogen synthesis are reduced in people with type 2 diabetes primarily due to decreased uptake of extracellular glucose presumably because of inadequate activation of hepatic glucokinase. Glucose 39-46 insulin Homo sapiens 0-7 20705776-6 2010 Delayed insulin secretion results in higher peak glucose concentrations particularly when suppression of glucagon is impaired, whereas insulin resistance prolongs the duration of hyperglycemia, which can be marked when both hepatic and extra-hepatic insulin resistance are present. Glucose 49-56 insulin Homo sapiens 8-15 20724647-8 2010 The insulin-dependent glucose uptake by L6 cells was increased in the presence of C10 (38.7+-10.3 vs. 11.4+-5.4%; P=0.026). Glucose 22-29 insulin Homo sapiens 4-11 20848328-13 2010 A temporary continuous intravenous insulin infusion may then be used in most patients to maintain the glucose closer to normal levels (eg, below 180 or 140 mg/dL). Glucose 102-109 insulin Homo sapiens 35-42 20714888-3 2010 Though the molecular mechanisms by which common genetic variation within these loci affects beta cell function are not completely understood, risk variants may alter glucose-stimulated insulin secretion, proinsulin conversion, and incretin signals. Glucose 166-173 insulin Homo sapiens 185-192 20724579-3 2010 We hypothesized that murine Pparg-P465L mutation leads to covert insulin resistance, which is masked by hyperinsulinemia and increased pancreatic islet mass, to retain normal plasma glucose. Glucose 182-189 insulin Homo sapiens 65-72 20724579-8 2010 In an insulin tolerance test, they showed smaller reduction in plasma glucose, indicating impaired insulin sensitivity. Glucose 70-77 insulin Homo sapiens 6-13 20811038-8 2010 Thus, they document that insulin is a beta-cell secretory product that, in concert with glucose and among other signals, reciprocally regulates alpha-cell glucagon secretion in humans. Glucose 88-95 insulin Homo sapiens 25-32 20439245-6 2010 Moreover, in comparison with human insulin, insulin lispro was reported to result in improved glycemic control, as demonstrated by lower postprandial glucose concentrations and hemoglobin A1c levels. Glucose 150-157 insulin Homo sapiens 44-51 20879966-3 2010 METHODS: The basal insulin profile is adjusted by the proposed algorithm every 30 min based on interstitial glucose level and its rate of change. Glucose 109-116 insulin Homo sapiens 19-26 20879966-5 2010 A conservative insulin bolus is administered, the size of which is determined based on glucose prediction and the subject-specific correction factor. Glucose 87-94 insulin Homo sapiens 15-22 21059029-1 2010 REASONS FOR PERFORMING STUDY: Providing protein or amino acid mixtures in combination with glucose to post exercise in man has resulted in increases in the post feeding insulin response and in muscle glycogen and protein synthesis rates. Glucose 91-98 insulin Homo sapiens 169-176 20628884-2 2010 Hyperglycemia and high intramuscular glucose levels mediate insulin resistance, a precursor state of type 2 diabetes. Glucose 37-44 insulin Homo sapiens 60-67 21129337-2 2010 This article presents pilot study results of the dynamic insulin sensitivity and secretion test (DISST), a high-resolution, low-intensity test to diagnose insulin sensitivity (IS) and characterize pancreatic insulin secretion in response to a (small) glucose challenge. Glucose 251-258 insulin Homo sapiens 57-64 20945272-5 2010 Accordingly, the insulin sensitivity index determined after a mixed meal and standardized glucose load was lower in A-allele carriers. Glucose 90-97 insulin Homo sapiens 17-24 20668044-0 2010 Differences in insulin resistance in Mexican and U.S. Pima Indians with normal glucose tolerance. Glucose 79-86 insulin Homo sapiens 15-22 20850803-8 2010 However, insulin-stimulated glucose uptake was normal in the infarcted hearts, consistent with normal insulin-induced phosphorylation of Akt and unchanged mRNA expression of glucose transporter type 4. Glucose 28-35 insulin Homo sapiens 9-16 20655673-6 2010 This in turn has direct effects on the endocrine pancreas to enhance insulin release in a glucose-dependent manner and suppress glucagon release, the net effects of which are to reduce post-prandial excursions of plasma glucose. Glucose 90-97 insulin Homo sapiens 69-76 20634790-0 2010 Insulin differentially influences brain glucose and lactate in traumatic brain injured patients. Glucose 40-47 insulin Homo sapiens 0-7 20811656-1 2010 Classical actions of insulin involve increased glucose uptake from the bloodstream and its metabolism in peripheral tissues, the most important and relevant effects for human health. Glucose 47-54 insulin Homo sapiens 21-28 20811656-2 2010 However, nonoxidative and oxidative glucose disposal by activation of glycogen synthase (GS) and mitochondrial pyruvate dehydrogenase (PDH) remain incompletely explained by current models for insulin action. Glucose 36-43 insulin Homo sapiens 192-199 20584260-7 2010 Glucose-dependent insulinotropic polypeptide 5 pmol kg(-1) min(-1) decreased postprandial glucose (P < 0.001) and insulin (P < 0.05) with increased insulinogenic index. Glucose 90-97 insulin Homo sapiens 18-25 20660478-2 2010 Here, we report the synthesis of a 130-nt mRNA sequence encoding a 33-amino-acid peptide that includes the sequence of glucagon-like peptide-1, a peptide that stimulates glucose-dependent insulin secretion from the pancreas. Glucose 170-177 insulin Homo sapiens 188-195 20421430-4 2010 RESULTS: Instillation of the 1.5% dextrose solution resulted in a modest change in plasma glucose, paralleled by a small increase in plasma insulin levels and plasma insulin-like growth factor (IGF-1). Glucose 34-42 insulin Homo sapiens 140-147 20421430-4 2010 RESULTS: Instillation of the 1.5% dextrose solution resulted in a modest change in plasma glucose, paralleled by a small increase in plasma insulin levels and plasma insulin-like growth factor (IGF-1). Glucose 34-42 insulin Homo sapiens 166-173 21063041-1 2010 AIM: to obtain prevalence of insulin resistance among siblings of subjects with type 2 DM and their metabolic abnormality profiles as measured by their BMI, waist circumference (WC), blood pressure, glucose intolerance, concentration of triglyceride, HDL cholesterol, and uric acid. Glucose 199-206 insulin Homo sapiens 29-36 20816753-1 2010 G-protein-coupled receptor (GPR) 119 is involved in glucose-stimulated insulin secretion (GSIS) and represents a promising target for the treatment of type 2 diabetes as it is highly expressed in pancreatic beta-cells. Glucose 52-59 insulin Homo sapiens 71-78 20570724-1 2010 Insulin and AMP-activated protein kinase (AMPK) signal pathways are involved in the regulation of glucose uptake. Glucose 98-105 insulin Homo sapiens 0-7 20570724-3 2010 In this work, stimulation of insulin and berberine conferred a glucose uptake or surface glucose transporter 4 (GLUT4) translocation that was less than simple summation of their effects in insulin-sensitive muscle cells. Glucose 63-70 insulin Homo sapiens 29-36 21520550-22 2010 The hyperinsulinism values after the intervention studied by means of the glucose/insulin ratio were abnormal in 70.5% (defined as ratio under 3). Glucose 74-81 insulin Homo sapiens 9-16 20717021-2 2010 RECENT FINDINGS: HIV protease inhibitor treatment may affect the normal stimulatory effect of insulin on glucose and fat storage. Glucose 105-112 insulin Homo sapiens 94-101 20592052-7 2010 Compared with adolescents with NGT, first-phase insulin was lower in those with IFG, IGT, and IFG/IGT with further deterioration in those with type 2 diabetes (P < 0.001), and beta-cell function relative to insulin sensitivity (glucose disposition index [GDI]) was also lower in those with IFG, IGT, and IFG/IGT (40, 47, and 47%, respectively), with a further decrease (80%) in those with type 2 diabetes (P < 0.001). Glucose 231-238 insulin Homo sapiens 48-55 20592052-9 2010 CONCLUSIONS: Obese adolescents who show signs of glucose dysregulation, including abnormal fasting glucose, glucose intolerance or both, are more likely to have impaired insulin secretion rather than reduced insulin sensitivity. Glucose 49-56 insulin Homo sapiens 170-177 20593160-10 2010 Assuming that the insulin secretion deficit is of pathogenetic importance in a network with insulin resistance as an aggravating factor, an insulinotropic glucose-lowering drug may do more good than harm if it relieves the beta cell from the stress of glucose overstimulation and does so without inducing hypoglycaemia. Glucose 155-162 insulin Homo sapiens 18-25 20593160-10 2010 Assuming that the insulin secretion deficit is of pathogenetic importance in a network with insulin resistance as an aggravating factor, an insulinotropic glucose-lowering drug may do more good than harm if it relieves the beta cell from the stress of glucose overstimulation and does so without inducing hypoglycaemia. Glucose 252-259 insulin Homo sapiens 18-25 20622164-1 2010 OBJECTIVE: Glucose-stimulated islet insulin or C-peptide secretion experiments are a fundamental tool for studying and assessing islet function. Glucose 11-18 insulin Homo sapiens 36-43 20693354-1 2010 OBJECTIVE: To assess the effect of three premeal timings of rapid-acting insulin on postprandial glucose excursions in type 1 diabetes. Glucose 97-104 insulin Homo sapiens 73-80 20693354-10 2010 CONCLUSIONS: Administration of rapid-acting insulin analogs 15 min before mealtime results in lower postprandial glucose excursions and more time spent in the 3.5-10.0 mmol/l range, without increased risk of hypoglycemia. Glucose 113-120 insulin Homo sapiens 44-51 20809678-7 2010 CONCLUSIONS: Insulin-treated diabetes patients on hemodialysis showed different glucose profiles between the HD and the FD. Glucose 80-87 insulin Homo sapiens 13-20 20920038-1 2010 BACKGROUND: The effectiveness of insulin therapy to lower blood glucose levels in patients with type 2 diabetes (T2D) may depend on a variety of factors. Glucose 64-71 insulin Homo sapiens 33-40 21029304-3 2010 Lipogenesis is an insulin- and glucose-dependent process that is under the control of specific transcription factors, sterol regulatory element binding protein 1c (SREBP-1c), activated by insulin and carbohydrate response element binding protein (ChREBP) activated by glucose. Glucose 31-38 insulin Homo sapiens 188-195 21211736-0 2010 Brain, liver, intestine: a triumvirate to coordinate insulin sensitivity of endogenous glucose production. Glucose 87-94 insulin Homo sapiens 53-60 20519325-5 2010 In the postprandial period, insulin-stimulated glucose uptake by the skeletal muscle has been found to be normal or increased, mainly due to increased blood flow. Glucose 47-54 insulin Homo sapiens 28-35 20519325-6 2010 Under hyperthyroid conditions, insulin-stimulated rates of glycogen synthesis in skeletal muscle are decreased, whereas there is a preferential increase in the rates of lactate formation vs. glucose oxidation leading to increased Cori cycle activity. Glucose 191-198 insulin Homo sapiens 31-38 20519325-8 2010 Moreover, lipolysis is rapidly suppressed to normal after the meal to facilitate the disposal of glucose by the insulin-resistant muscle. Glucose 97-104 insulin Homo sapiens 112-119 20643758-2 2010 DESIGN AND METHODS: To investigate this, we assessed the sensitivity of glucose metabolism to insulin in vivo (by an oral glucose tolerance test) and in vitro (by measuring insulin-stimulated rates of glucose transport in isolated monocytes) in 12 euthyroid subjects (EU), 16 patients with HR, and 10 patients with SHR. Glucose 72-79 insulin Homo sapiens 94-101 20643758-2 2010 DESIGN AND METHODS: To investigate this, we assessed the sensitivity of glucose metabolism to insulin in vivo (by an oral glucose tolerance test) and in vitro (by measuring insulin-stimulated rates of glucose transport in isolated monocytes) in 12 euthyroid subjects (EU), 16 patients with HR, and 10 patients with SHR. Glucose 122-129 insulin Homo sapiens 94-101 20643758-7 2010 CONCLUSIONS: Insulin-stimulated glucose transport in isolated monocytes of patients with HR was decreased compared with EU subjects. Glucose 32-39 insulin Homo sapiens 13-20 20939648-7 2010 The present study suggests that olanzapine might impair glucose tolerance to some extent because of an increase in insulin resistance compared with risperidone. Glucose 56-63 insulin Homo sapiens 115-122 19931080-11 2010 Treatment with DRP/EE20 significantly increased the glucose to insulin ratio index. Glucose 52-59 insulin Homo sapiens 63-70 20186475-3 2010 Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. Glucose 170-177 insulin Homo sapiens 104-111 20186475-6 2010 Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. Glucose 80-87 insulin Homo sapiens 28-35 20887299-4 2010 In preclinical studies, liraglutide demonstrated good glycaemic control, mediated by the glucose-dependent stimulation of insulin and suppression of glucagon secretion and by delayed gastric emptying. Glucose 89-96 insulin Homo sapiens 122-129 20949699-11 2010 As liraglutide increases insulin production in a glucose-dependent manner, the incidence of hypoglycaemia largely depends on the hypoglycaemic risk profile of the selected oral antidiabetic with which it is used. Glucose 49-56 insulin Homo sapiens 25-32 20514046-6 2010 This was accompanied by a commensurate defect in insulin-stimulated glucose uptake. Glucose 68-75 insulin Homo sapiens 49-56 20514046-8 2010 These results suggest that partial impairment of adipogenesis in Alstrom syndrome may contribute to the severity of the associated metabolic phenotype, whereas the ability of insulin to stimulate glucose uptake into adipocytes is grossly unimpaired. Glucose 196-203 insulin Homo sapiens 175-182 20531354-9 2010 The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated from glucose and insulin. Glucose 85-92 insulin Homo sapiens 36-43 20640452-8 2010 Recent work confirmed that a combination of intravenous and subcutaneous insulin as a glucose management strategy had beneficial effects identical with intravenous insulin therapy alone on the reduction of infection rates during the postoperative period. Glucose 86-93 insulin Homo sapiens 73-80 21080215-4 2010 The results revealed that NYGGF4 knockdown enhanced the glucose uptake of adipocytes, which reconfirmed the regulatory function of NYGGF4 in adipocyte insulin sensitivity. Glucose 56-63 insulin Homo sapiens 151-158 20660036-7 2010 Specifically, cortisol is negatively associated with potential compensatory mechanisms for insulin resistance, such as increased beta-cell function and increased insulin release to a glucose challenge, by exacerbating the progression toward insulin resistance in this population. Glucose 183-190 insulin Homo sapiens 91-98 20660036-7 2010 Specifically, cortisol is negatively associated with potential compensatory mechanisms for insulin resistance, such as increased beta-cell function and increased insulin release to a glucose challenge, by exacerbating the progression toward insulin resistance in this population. Glucose 183-190 insulin Homo sapiens 162-169 20660036-7 2010 Specifically, cortisol is negatively associated with potential compensatory mechanisms for insulin resistance, such as increased beta-cell function and increased insulin release to a glucose challenge, by exacerbating the progression toward insulin resistance in this population. Glucose 183-190 insulin Homo sapiens 162-169 20660049-8 2010 Insulin sensitivity was estimated from an oral glucose tolerance test. Glucose 47-54 insulin Homo sapiens 0-7 20142635-9 2010 In healthy subjects, basal glucose correlated with growth hormone Delta- AUC (r=0.820; p=0.004) and inversely with insulin Delta-AUC (r=-0.822; p=0.003). Glucose 27-34 insulin Homo sapiens 115-122 21063833-4 2010 We are led to conclude that insulin serves as a regulator in maintaining the balance between glucose and lipid metabolism in vivo, possibly through its effect on the differential expression of VLDLR subtypes. Glucose 93-100 insulin Homo sapiens 28-35 20601896-6 2010 Multiple regression analysis showed that waist circumference, diastolic blood pressure, 2-hour plasma insulin after glucose overload, and HbA1c were independently related factors influencing plasma chemerin levels. Glucose 116-123 insulin Homo sapiens 102-109 20153490-0 2010 Assessment of non-insulin-mediated glucose uptake: association with body fat and glycemic status. Glucose 35-42 insulin Homo sapiens 18-25 20153490-1 2010 In the fasting state, approximately 83% of glucose uptake occurs via non-insulin-mediated mechanisms. Glucose 43-50 insulin Homo sapiens 73-80 20153490-14 2010 NIMGU increases with declining glucose tolerance perhaps to preserve glucose uptake during increased insulin resistance. Glucose 31-38 insulin Homo sapiens 101-108 20204528-4 2010 Serum levels of hGH (human growth hormone), insulin, glucose and leptin increased significantly, which might induce insulin resistance. Glucose 53-60 insulin Homo sapiens 116-123 20861198-1 2010 BACKGROUND: The aim of this study was to analyse whether the insulin to glucose relationship following an intravenous glucose load in non-diabetic patients delivered during haemodialysis was affected by extracorporeal clearance and whether this relationship could be determined by an abridged sampling protocol. Glucose 72-79 insulin Homo sapiens 61-68 20861198-1 2010 BACKGROUND: The aim of this study was to analyse whether the insulin to glucose relationship following an intravenous glucose load in non-diabetic patients delivered during haemodialysis was affected by extracorporeal clearance and whether this relationship could be determined by an abridged sampling protocol. Glucose 118-125 insulin Homo sapiens 61-68 20861198-4 2010 The insulin to glucose relationship was examined for a period of 1 h following the infusion of glucose. Glucose 95-102 insulin Homo sapiens 4-11 20861198-8 2010 A linear relationship providing characteristic slopes k(IG) was observed between arterial insulin and glucose levels. Glucose 102-109 insulin Homo sapiens 90-97 20861198-12 2010 CONCLUSIONS: The insulin to glucose relationship is measurable within 10 min of glucose administration and unaffected by extracorporeal clearance. Glucose 28-35 insulin Homo sapiens 17-24 20861198-12 2010 CONCLUSIONS: The insulin to glucose relationship is measurable within 10 min of glucose administration and unaffected by extracorporeal clearance. Glucose 80-87 insulin Homo sapiens 17-24 20861198-13 2010 This could be helpful to characterize the insulin response to a glucose stimulus during haemodialysis. Glucose 64-71 insulin Homo sapiens 42-49 22453619-8 2010 CONCLUSIONS: : Operative vaginal delivery, episiotomy, increased infant birth weight and gestational diabetes requiring insulin for glucose control all appear to increase the risk of severe perineal laceration at the time of vaginal delivery in a teenage population. Glucose 132-139 insulin Homo sapiens 120-127 20727924-11 2010 Both insulin and MCD complexed insulin encapsulated PCP microparticles were effective in reducing blood glucose level in diabetic animal models. Glucose 104-111 insulin Homo sapiens 5-12 20727924-11 2010 Both insulin and MCD complexed insulin encapsulated PCP microparticles were effective in reducing blood glucose level in diabetic animal models. Glucose 104-111 insulin Homo sapiens 31-38 21129353-3 2010 It is anticipated that CGM devices will utilize constant feedback of analytical information from a glucose sensor to activate an insulin delivery pump, thereby ultimately realizing the concept of an artificial pancreas. Glucose 99-106 insulin Homo sapiens 129-136 20423743-4 2010 Intramyocellular lipid (IMCL) concentration was measured by 1H magnetic resonance spectroscopy, and insulin sensitivity was determined by intravenous glucose tolerance test. Glucose 150-157 insulin Homo sapiens 100-107 20634790-7 2010 Insulin administration was associated with significantly reduced cerebral glucose concentrations and significantly increased lactate-to-glucose ratios with arterial blood glucose levels <5 mM. Glucose 74-81 insulin Homo sapiens 0-7 20634790-7 2010 Insulin administration was associated with significantly reduced cerebral glucose concentrations and significantly increased lactate-to-glucose ratios with arterial blood glucose levels <5 mM. Glucose 136-143 insulin Homo sapiens 0-7 20634790-7 2010 Insulin administration was associated with significantly reduced cerebral glucose concentrations and significantly increased lactate-to-glucose ratios with arterial blood glucose levels <5 mM. Glucose 136-143 insulin Homo sapiens 0-7 20634790-8 2010 At arterial blood glucose levels >7 mM, insulin administration was associated with significantly increased interstitial glucose values, significantly decreased lactate concentrations, and markedly diminished lactate-to-glucose ratios. Glucose 18-25 insulin Homo sapiens 43-50 20634790-8 2010 At arterial blood glucose levels >7 mM, insulin administration was associated with significantly increased interstitial glucose values, significantly decreased lactate concentrations, and markedly diminished lactate-to-glucose ratios. Glucose 123-130 insulin Homo sapiens 43-50 20634790-8 2010 At arterial blood glucose levels >7 mM, insulin administration was associated with significantly increased interstitial glucose values, significantly decreased lactate concentrations, and markedly diminished lactate-to-glucose ratios. Glucose 123-130 insulin Homo sapiens 43-50 20634790-9 2010 CONCLUSION: Insulin exerts differential effects that depend strongly on the underlying arterial blood glucose concentrations. Glucose 102-109 insulin Homo sapiens 12-19 20634790-11 2010 However, at arterial blood glucose levels >7-8 mM, insulin administration appears to be encouraged to increase extracellular glucose concentrations and decrease energetic impairment reflected by reduced interstitial brain lactate and decreased lactate-to-glucose ratios. Glucose 27-34 insulin Homo sapiens 54-61 20634790-11 2010 However, at arterial blood glucose levels >7-8 mM, insulin administration appears to be encouraged to increase extracellular glucose concentrations and decrease energetic impairment reflected by reduced interstitial brain lactate and decreased lactate-to-glucose ratios. Glucose 128-135 insulin Homo sapiens 54-61 20634790-11 2010 However, at arterial blood glucose levels >7-8 mM, insulin administration appears to be encouraged to increase extracellular glucose concentrations and decrease energetic impairment reflected by reduced interstitial brain lactate and decreased lactate-to-glucose ratios. Glucose 128-135 insulin Homo sapiens 54-61 21174711-8 2010 Recently, there have been reports that intensive insulin therapy to maintain normal glucose levels in useful in the management of critically ill patients. Glucose 84-91 insulin Homo sapiens 49-56 21174711-9 2010 Maintenance of normal glucose levels is difficult in the clinical setting because hypoglycemia is extremely dangerous for patients, and the NICE-SUGAR study showed that intensive insulin therapy significantly increased the risk of hypoglycemia. Glucose 22-29 insulin Homo sapiens 179-186 21130299-1 2010 The levels of circulating nonesterified fatty acids increase during obesity and contribute to insulin resistance by inhibiting insulin-stimulated glucose transport and phosphorylation in human muscles. Glucose 146-153 insulin Homo sapiens 94-101 21130299-1 2010 The levels of circulating nonesterified fatty acids increase during obesity and contribute to insulin resistance by inhibiting insulin-stimulated glucose transport and phosphorylation in human muscles. Glucose 146-153 insulin Homo sapiens 127-134 21102380-14 2010 CONCLUSIONS: In clinical practice, treatment with insulin aspart in basal-bolus regimen is associated with low risk of hypoglycemia and leads to a significant improvement in glucose control, irrespective of diabetes type. Glucose 174-181 insulin Homo sapiens 50-57 20854370-1 2010 A major consequence of insulin binding its receptor on fat and muscle cells is translocation of the facilitative glucose transporter GLUT4 from an intracellular store to the cell surface where it serves to clear glucose from the bloodstream. Glucose 113-120 insulin Homo sapiens 23-30 21108056-0 2010 [Effects of preoperative oral glucose on perioperative insulin resistance and plasma proteins of intestinal surgery]. Glucose 30-37 insulin Homo sapiens 55-62 21108056-14 2010 CONCLUSION: Oral liquid intake 2 hours before surgery is not associated with increased risk of regurgitation or aspiration during intubation and extubation, and may glucose solution intake reduce insulin resistance and protein degradation after colorectal surgery. Glucose 165-172 insulin Homo sapiens 196-203 20595780-7 2010 Unadjusted analysis demonstrated that the fasting insulin quartiles (p=0.0256) and InsAUC quartiles (p<0.0001) were significantly associated with log (CAC+1), and the lowest fasting insulin quartiles (p<0.0001) and the lowest InsAUC quartile (p=0.0006) had lower glucose AUC. Glucose 269-276 insulin Homo sapiens 50-57 20813965-2 2010 Insulin blocks the generation of biochemical intermediates for glucose production by inhibiting autophagy. Glucose 63-70 insulin Homo sapiens 0-7 20937946-6 2010 MAIN OUTCOME MEASURES: Insulin sensitivity, expressed by the homeostasis model assessment (HOMA) of insulin sensitivity (HOMA index = [fasting insulin x fasting glucose] / 22.5). Glucose 161-168 insulin Homo sapiens 23-30 20937946-6 2010 MAIN OUTCOME MEASURES: Insulin sensitivity, expressed by the homeostasis model assessment (HOMA) of insulin sensitivity (HOMA index = [fasting insulin x fasting glucose] / 22.5). Glucose 161-168 insulin Homo sapiens 100-107 20506178-14 2010 The presence of insulin lowered glycerol uptake and corresponding fluxes involved in lipid metabolism for all glucose levels but otherwise exerted negligible effect on metabolism. Glucose 110-117 insulin Homo sapiens 16-23 20424221-7 2010 CONCLUSIONS: In individuals with both FPG and 2-h plasma glucose within the normoglycemic range, high 2-h plasma glucose was associated with insulin resistance and increased CVD mortality. Glucose 57-64 insulin Homo sapiens 141-148 20424221-7 2010 CONCLUSIONS: In individuals with both FPG and 2-h plasma glucose within the normoglycemic range, high 2-h plasma glucose was associated with insulin resistance and increased CVD mortality. Glucose 113-120 insulin Homo sapiens 141-148 20664017-1 2010 OBJECTIVE: To determine whether an electronic order template for basal-bolus insulin ordering improves mean blood glucose in hospitalized general medical patients with hyperglycemia and type 2 diabetes. Glucose 114-121 insulin Homo sapiens 77-84 20664017-7 2010 CONCLUSIONS: Access to a computer insulin order template was associated with improved mean glucose levels without increasing hypoglycemia in patients with type 2 diabetes. Glucose 91-98 insulin Homo sapiens 34-41 20667613-5 2010 Candesartan recovered decreased insulin content in MIN6 exposed to 25mM glucose with 0.5mM palmitate (P<0.01). Glucose 72-79 insulin Homo sapiens 32-39 20830736-1 2010 BACKGROUND: We investigated the concordance between glucose effectiveness (SG) and insulin sensitivity (SI), derived from the unmodified dynamic non-insulin-assisted intravenous glucose tolerance test (IVGTT) implemented by SG(MM) and SI(MM); simulation analysis and modelling/conversational interaction (SAAM/CONSAM) versus the eu/hyperglycaemic basal insulinaemic and the euglycaemic hyperinsulinaemic clamp (SG(CLAMP) and SI(CLAMP)). Glucose 178-185 insulin Homo sapiens 149-156 21029304-3 2010 Lipogenesis is an insulin- and glucose-dependent process that is under the control of specific transcription factors, sterol regulatory element binding protein 1c (SREBP-1c), activated by insulin and carbohydrate response element binding protein (ChREBP) activated by glucose. Glucose 268-275 insulin Homo sapiens 18-25 21029304-3 2010 Lipogenesis is an insulin- and glucose-dependent process that is under the control of specific transcription factors, sterol regulatory element binding protein 1c (SREBP-1c), activated by insulin and carbohydrate response element binding protein (ChREBP) activated by glucose. Glucose 268-275 insulin Homo sapiens 188-195 19962298-2 2010 In the present study, we first checked the efficacy of grapeseed procyanidin extract (GSPE) for stimulating glucose uptake in insulin-resistant 3T3-L1 adipocytes. Glucose 108-115 insulin Homo sapiens 126-133 19962298-9 2010 Similarly, a chronic GSPE treatment of insulin-resistant 3T3-L1 adipocytes down-regulated the mRNA levels of those adipocyte markers, although cells were still able to respond to the acute stimulation of glucose uptake. Glucose 204-211 insulin Homo sapiens 39-46 20854065-4 2010 RESULTS: Insulin-stimulated glucose disposal (Rd) (5.2 +/-0.4 vs. 9.0 +/-0.9 mg/kg-min, P < 0.01) and basal NOS activity (107 +/-45 vs. 459 +/- 100 pmol/min-mg protein, P < 0.05) were reduced in T2DM versus controls. Glucose 28-35 insulin Homo sapiens 9-16 20134415-3 2010 Insulin sensitivity was assessed by intravenous glucose tolerance test and body composition by total-body dual-energy X-ray absorptiometry. Glucose 48-55 insulin Homo sapiens 0-7 22043356-7 2010 CONCLUSION: Overall, the glucose/leptin ratio can be used in addition to glucose/insulin ratio, Quantitative Insulin-Sensitivity Check Index, and Homeostasis Model Assessment to accurately assess insulin resistance in subjects with hyperglycemia. Glucose 25-32 insulin Homo sapiens 196-203 20798069-7 2010 In the opinion of the experts, patients receiving continuous-infusion insulin and those receiving dextrose only via parenteral nutrition were at increased risk for insulin-related hypoglycaemia. Glucose 98-106 insulin Homo sapiens 164-171 20798069-8 2010 Lack of standardisation in insulin-dosing decisions and variation regarding when and how much to adjust insulin doses in response to changing glucose levels were identified as common causes of the adverse events. Glucose 142-149 insulin Homo sapiens 104-111 20800254-9 2010 Transfected islets demonstrated normal mitochondrial function, calcium influx, and insulin release when stimulated by glucose. Glucose 118-125 insulin Homo sapiens 83-90 20723550-7 2010 The level of insulin mRNA, by semi-quantitative RT-PCR, was significantly reduced at 33mM glucose concentration after 48h of incubation. Glucose 90-97 insulin Homo sapiens 13-20 20570597-8 2010 The improvement of glucose-stimulated insulin secretion provided by Lixisenatide occurred in a strictly glucose-dependent manner. Glucose 19-26 insulin Homo sapiens 38-45 20570597-8 2010 The improvement of glucose-stimulated insulin secretion provided by Lixisenatide occurred in a strictly glucose-dependent manner. Glucose 104-111 insulin Homo sapiens 38-45 20804735-0 2010 Identification of a novel GPR119 agonist, AS1269574, with in vitro and in vivo glucose-stimulated insulin secretion. Glucose 79-86 insulin Homo sapiens 98-105 20804735-2 2010 On activation, this receptor enhances the effect of glucose-stimulated insulin secretion (GSIS) via the elevation of intracellular cAMP concentrations. Glucose 52-59 insulin Homo sapiens 71-78 20804735-8 2010 In in vivo studies, a single administration of AS1269574 to normal mice reduced blood glucose levels after oral glucose loading based on the observed insulin secretion profiles. Glucose 112-119 insulin Homo sapiens 150-157 20811030-2 2010 SUMMARY: U-500 regular insulin has been available in the United States since 1952, but only recently has it become more commonly prescribed for patients requiring large amounts of insulin to improve their blood glucose control. Glucose 211-218 insulin Homo sapiens 23-30 20811030-2 2010 SUMMARY: U-500 regular insulin has been available in the United States since 1952, but only recently has it become more commonly prescribed for patients requiring large amounts of insulin to improve their blood glucose control. Glucose 211-218 insulin Homo sapiens 180-187 20816091-1 2010 While the glucose transporter-4 (GLUT4) is fundamental to insulin-regulated glucose metabolism, its dynamic spatial organization in the plasma membrane (PM) is unclear. Glucose 10-17 insulin Homo sapiens 58-65 20711225-2 2010 There are at least three types of K(+) channels (K(ATP), K(Ca), and Kv2.1 channels) that are involved in glucose-stimulated insulin secretion in pancreatic beta-cells, and one type (Kv1.3) that is associated with the regulation of insulin sensitivity in peripheral target tissues. Glucose 105-112 insulin Homo sapiens 124-131 20573988-6 2010 Thujone (6-12 h) fully rescued palmitate oxidation and insulin-stimulated glucose transport, but only partially restored GLUT4 translocation and AS160 phosphorylation, raising the possibility that an increased GLUT4 intrinsic activity may also have contributed to the restoration of glucose transport. Glucose 74-81 insulin Homo sapiens 55-62 20804351-0 2010 Continuous glucose monitoring-enabled insulin-pump therapy in diabetic pregnancy. Glucose 11-18 insulin Homo sapiens 38-45 20804351-1 2010 We describe the feasibility of continuous glucose monitoring (CGM)-enabled insulin-pump therapy during pregnancy in a woman with type 1 diabetes, who was treated with CGM-enabled insulin-pump therapy in her third pregnancy. Glucose 42-49 insulin Homo sapiens 75-82 20804351-1 2010 We describe the feasibility of continuous glucose monitoring (CGM)-enabled insulin-pump therapy during pregnancy in a woman with type 1 diabetes, who was treated with CGM-enabled insulin-pump therapy in her third pregnancy. Glucose 42-49 insulin Homo sapiens 179-186 20977082-2 2010 The effect of insulin administration in the condition of elevated glucose concentration on the E-selectin, intracellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) expression on human aortic endothelial cells (HAEC) was investigated. Glucose 66-73 insulin Homo sapiens 14-21 20977082-10 2010 In conditions of elevated glucose concentration (12 mM), addition of insulin significantly dropped E-selectin (27%) and increased VCAM-1 (23%) expression. Glucose 26-33 insulin Homo sapiens 69-76 20594161-1 2010 Insulin resistance of glucose transport and metabolism in insulin-sensitive tissues is a primary defect leading to the development of type 2 diabetes. Glucose 22-29 insulin Homo sapiens 0-7 20594161-1 2010 Insulin resistance of glucose transport and metabolism in insulin-sensitive tissues is a primary defect leading to the development of type 2 diabetes. Glucose 22-29 insulin Homo sapiens 58-65 20594161-4 2010 Evidence from muscle and fat cell lines and in skeletal muscle from a variety of obese rodent models and from type 2 diabetic humans supports a role of GSK-3 overactivity in the development of insulin resistance of glucose transport and glycogenesis. Glucose 215-222 insulin Homo sapiens 193-200 20547974-2 2010 This study tests the hypothesis that insulin acts directly in the brain to regulate critical glucose-sensing neurons in the hypothalamus to mediate the counterregulatory response to hypoglycemia. Glucose 93-100 insulin Homo sapiens 37-44 20547974-9 2010 CONCLUSIONS: Chronically, insulin acts in the brain to regulate the counterregulatory response to hypoglycemia by directly altering glucose sensing in hypothalamic neurons and shifting the glycemic levels necessary to elicit a normal sympathoadrenal response. Glucose 132-139 insulin Homo sapiens 26-33 20573749-3 2010 Prolonged fasting is a physiologic condition in which muscular insulin resistance develops in the presence of increased free fatty acid (FFA) levels, increased fat oxidation and low glucose and insulin levels. Glucose 182-189 insulin Homo sapiens 63-70 20573751-2 2010 We tested the hypothesis that maternal glucose tolerance in pregnancy affects fetal insulin sensitivity or beta-cell function. Glucose 39-46 insulin Homo sapiens 84-91 20573751-5 2010 RESULTS: Higher OGTT blood glucose levels were associated with significantly lower cord plasma glucose-to-insulin ratios (r = -0.31, P < 0.001) and higher proinsulin concentrations (r = 0.31, P < 0.001) but not with proinsulin-to-insulin ratios. Glucose 27-34 insulin Homo sapiens 106-113 20573751-5 2010 RESULTS: Higher OGTT blood glucose levels were associated with significantly lower cord plasma glucose-to-insulin ratios (r = -0.31, P < 0.001) and higher proinsulin concentrations (r = 0.31, P < 0.001) but not with proinsulin-to-insulin ratios. Glucose 27-34 insulin Homo sapiens 158-168 20573751-5 2010 RESULTS: Higher OGTT blood glucose levels were associated with significantly lower cord plasma glucose-to-insulin ratios (r = -0.31, P < 0.001) and higher proinsulin concentrations (r = 0.31, P < 0.001) but not with proinsulin-to-insulin ratios. Glucose 27-34 insulin Homo sapiens 222-232 20573751-5 2010 RESULTS: Higher OGTT blood glucose levels were associated with significantly lower cord plasma glucose-to-insulin ratios (r = -0.31, P < 0.001) and higher proinsulin concentrations (r = 0.31, P < 0.001) but not with proinsulin-to-insulin ratios. Glucose 27-34 insulin Homo sapiens 161-168 20570007-6 2010 CONCLUSIONS: The proposed kinetic model is able to describe the glucose-stimulated insulin response, account for the first-phase insulin release and identify a racially-based pharmacokinetic difference in insulin"s biphasic secretion behavior. Glucose 64-71 insulin Homo sapiens 83-90 20573751-8 2010 Significant changes in the glucose-to-insulin ratio and proinsulin concentration were also observed in obese (n = 31) mothers, but the differences became not statistically significant after adjustment for maternal glucose tolerance and fetal adiposity. Glucose 27-34 insulin Homo sapiens 38-45 20573751-9 2010 CONCLUSIONS: Maternal glucose intolerance may impair fetal insulin sensitivity (but not beta-cell function) and consequently "program" the susceptibility to type 2 diabetes. Glucose 22-29 insulin Homo sapiens 59-66 20584998-0 2010 Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans. Glucose 19-26 insulin Homo sapiens 38-45 20573754-10 2010 Single determinations of FPG and 2-h plasma glucose seem to be more precise correlates of insulin resistance and secretion than A1C and, in general, better for other metabolic disorders. Glucose 44-51 insulin Homo sapiens 90-97 20687863-1 2010 BACKGROUND: It is generally held that basal insulin substitution with continuous subcutaneous insulin infusion (CSII) provides less variable glucose levels than with long-acting insulin analogs, e.g., glargine, in patients with type 1 diabetes, although this has not been convincingly demonstrated by continuous glucose monitoring. Glucose 141-148 insulin Homo sapiens 44-51 20584998-3 2010 The goal of this study was to test the hypothesis that circulating ghrelin suppresses glucose-stimulated insulin secretion in healthy subjects. Glucose 86-93 insulin Homo sapiens 105-112 20584998-6 2010 The acute insulin response to intravenous glucose (AIRg) was calculated from plasma insulin concentrations between 2 and 10 min after the glucose bolus. Glucose 42-49 insulin Homo sapiens 10-17 20584998-6 2010 The acute insulin response to intravenous glucose (AIRg) was calculated from plasma insulin concentrations between 2 and 10 min after the glucose bolus. Glucose 42-49 insulin Homo sapiens 84-91 20584998-6 2010 The acute insulin response to intravenous glucose (AIRg) was calculated from plasma insulin concentrations between 2 and 10 min after the glucose bolus. Glucose 138-145 insulin Homo sapiens 10-17 20584998-11 2010 CONCLUSIONS: This is a robust proof-of-concept study showing that exogenous ghrelin reduces glucose-stimulated insulin secretion and glucose disappearance in healthy humans. Glucose 92-99 insulin Homo sapiens 111-118 20687863-1 2010 BACKGROUND: It is generally held that basal insulin substitution with continuous subcutaneous insulin infusion (CSII) provides less variable glucose levels than with long-acting insulin analogs, e.g., glargine, in patients with type 1 diabetes, although this has not been convincingly demonstrated by continuous glucose monitoring. Glucose 141-148 insulin Homo sapiens 94-101 20687863-1 2010 BACKGROUND: It is generally held that basal insulin substitution with continuous subcutaneous insulin infusion (CSII) provides less variable glucose levels than with long-acting insulin analogs, e.g., glargine, in patients with type 1 diabetes, although this has not been convincingly demonstrated by continuous glucose monitoring. Glucose 141-148 insulin Homo sapiens 94-101 20687863-1 2010 BACKGROUND: It is generally held that basal insulin substitution with continuous subcutaneous insulin infusion (CSII) provides less variable glucose levels than with long-acting insulin analogs, e.g., glargine, in patients with type 1 diabetes, although this has not been convincingly demonstrated by continuous glucose monitoring. Glucose 312-319 insulin Homo sapiens 44-51 20687863-1 2010 BACKGROUND: It is generally held that basal insulin substitution with continuous subcutaneous insulin infusion (CSII) provides less variable glucose levels than with long-acting insulin analogs, e.g., glargine, in patients with type 1 diabetes, although this has not been convincingly demonstrated by continuous glucose monitoring. Glucose 312-319 insulin Homo sapiens 94-101 20687863-1 2010 BACKGROUND: It is generally held that basal insulin substitution with continuous subcutaneous insulin infusion (CSII) provides less variable glucose levels than with long-acting insulin analogs, e.g., glargine, in patients with type 1 diabetes, although this has not been convincingly demonstrated by continuous glucose monitoring. Glucose 312-319 insulin Homo sapiens 94-101 20805276-0 2010 Declining beta-cell function relative to insulin sensitivity with increasing fasting glucose levels in the nondiabetic range in children. Glucose 85-92 insulin Homo sapiens 41-48 20862393-7 2010 Thus, GPR119 may represent an important new therapeutic target for the design of insulin secretagogues able to promote improvements in blood glucose control in patients with type 2 diabetes. Glucose 141-148 insulin Homo sapiens 81-88 20805281-0 2010 One-hour plasma glucose identifies insulin resistance and beta-cell dysfunction in individuals with normal glucose tolerance: cross-sectional data from the Relationship between Insulin Sensitivity and Cardiovascular Risk (RISC) study. Glucose 16-23 insulin Homo sapiens 35-42 20805281-0 2010 One-hour plasma glucose identifies insulin resistance and beta-cell dysfunction in individuals with normal glucose tolerance: cross-sectional data from the Relationship between Insulin Sensitivity and Cardiovascular Risk (RISC) study. Glucose 16-23 insulin Homo sapiens 177-184 20805281-6 2010 Participants with NGT with 1-h plasma glucose >8.95 mmol/l had larger waist circumference, higher BMI, lower insulin sensitivity, higher fasting glucose, and higher insulin secretion than their counterparts with 1-h plasma glucose <or=8.95 mmol/l (P < 0.001 for all comparisons). Glucose 38-45 insulin Homo sapiens 112-119 20439247-13 2010 CONCLUSION: Administration of oral glucose load via a meal is an effective alternative to the OGTT in diagnosing impaired glucose tolerance and insulin resistance and may be more sensitive, without the adverse effects of the oral glucose load in the OGTT. Glucose 35-42 insulin Homo sapiens 144-151 20805281-6 2010 Participants with NGT with 1-h plasma glucose >8.95 mmol/l had larger waist circumference, higher BMI, lower insulin sensitivity, higher fasting glucose, and higher insulin secretion than their counterparts with 1-h plasma glucose <or=8.95 mmol/l (P < 0.001 for all comparisons). Glucose 38-45 insulin Homo sapiens 168-175 20805281-9 2010 CONCLUSIONS: Higher values of 1-h plasma glucose may identify an intermediate condition between NGT and IGT characterized by greater insulin resistance, reduced beta-cell glucose sensitivity, and reduced beta-cell rate sensitivity. Glucose 41-48 insulin Homo sapiens 133-140 20439249-9 2010 Fasting blood glucose and glycemic excursions varied among racial/ethnic groups for the 3 insulin regimens. Glucose 14-21 insulin Homo sapiens 90-97 20723821-4 2010 Over the past 15 years, there has been widespread use of multiple-dose insulin regimens using a variety of insulin analogs, administered either by injection or insulin pump therapy, together with medical nutrition therapy, frequent self-monitoring of blood glucose and, more recently, continuous logo glucose monitoring. Glucose 257-264 insulin Homo sapiens 71-78 21099334-1 2010 Insulin secretion in beta-pancreatic cells after glucose stimulation requires the concerted action of a number of different ion channels. Glucose 49-56 insulin Homo sapiens 0-7 21191840-9 2010 It is concluded that resistin inhibits insulin induced glucose uptake in myocytes by downregulating the expression of GLUT4 and it has no effects on glucose oxidation and glycogen synthesis. Glucose 55-62 insulin Homo sapiens 39-46 20603780-9 2010 Insulin-induced glucose uptake was decreased and lipolysis increased. Glucose 16-23 insulin Homo sapiens 0-7 20603780-12 2010 Since stimulation is followed by decreased insulin-induced glucose uptake and increased lipolysis we conclude that TLRs may be important linking molecules in the generation of insulin resistance in fat tissue. Glucose 59-66 insulin Homo sapiens 43-50 20618882-4 2010 Key glucose-clamp studies that compare two basal insulin analogues - insulin glargine and insulin detemir - to Neutral Protamine Hagedorn insulin and to each other are then presented. Glucose 4-11 insulin Homo sapiens 49-56 21099334-3 2010 Recently two calcium activated nonselective (CAN) cation channels (TRPM4 and TRPM5) have been shown to influence efficient insulin response upon glucose stimulation. Glucose 145-152 insulin Homo sapiens 123-130 20177722-7 2010 These findings suggest that postmenopausal women treated with insulin or thiazolidinedione have a high risk of vertebral fractures independent of age, body stature, blood glucose level, insulin secretion, or BMD whereas treatment with sulfonylurea is associated with a decreased risk. Glucose 171-178 insulin Homo sapiens 62-69 20495126-13 2010 Recombinant human insulin was used at doses of 8, 20, 50, and 125 mU/kg of BW, as needed, to estimate (by linear regression) the dose of insulin causing a 50% decline in glucose concentrations (ED50). Glucose 170-177 insulin Homo sapiens 18-25 20623795-2 2010 However, the relative time course of insulin action in stimulating ATP turnover rate and glucose uptake in skeletal muscle has not been examined. Glucose 89-96 insulin Homo sapiens 37-44 20623795-4 2010 Glucose infusion rate rose rapidly from 0 to 2.90 +- 0.11 mg/kg(ffm)/min during the first 10 min of insulin infusion and further to 6.17 +- 0.57 mg/kg(ffm)/min between 15 and 45 min. Glucose 0-7 insulin Homo sapiens 100-107 20883237-6 2010 The primary efficacy measure was changed from baseline in the insulin sensitivity index (SI), calculated from oral glucose tolerance testing. Glucose 115-122 insulin Homo sapiens 62-69 20610601-9 2010 RESULTS: Glucose tolerance improved and insulin-mediated glucose uptake increased significantly during treatment. Glucose 57-64 insulin Homo sapiens 40-47 23554650-2 2010 The proposed method for the estimation of parameters for a system of ordinary differential equations (ODEs) that represent the time course of plasma glucose and insulin concentrations during glucose tolerance test (GTT) in physiological studies is presented. Glucose 191-198 insulin Homo sapiens 161-168 20920449-5 2010 Indeed, when selecting an insulin dose, the inaccuracy of the glucose reading has little effect compared with the inaccuracy in counting carbohydrates and the variability in insulin absorption. Glucose 62-69 insulin Homo sapiens 26-33 20920434-2 2010 This observation, in conjunction with the introduction of continuous glucose monitoring (CGM) devices, has set the stage for achieving tight glycemic control with systems that adjust the insulin pump settings based on measured glucose concentrations. Glucose 69-76 insulin Homo sapiens 187-194 20519313-2 2010 They are essential for glucose-stimulated insulin secretion from pancreatic beta-cells, contribute to the mechanisms by which hypoglycaemia stimulates glucagon release from pancreatic alpha-cells, and are involved in glucose uptake into skeletal muscle, glucose production and release from the liver, and feeding behaviour. Glucose 23-30 insulin Homo sapiens 42-49 20920434-2 2010 This observation, in conjunction with the introduction of continuous glucose monitoring (CGM) devices, has set the stage for achieving tight glycemic control with systems that adjust the insulin pump settings based on measured glucose concentrations. Glucose 227-234 insulin Homo sapiens 187-194 20920437-0 2010 Guidelines for insulin dosing in continuous subcutaneous insulin infusion using new formulas from a retrospective study of individuals with optimal glucose levels. Glucose 148-155 insulin Homo sapiens 15-22 20920437-3 2010 METHODS: Anonymous data downloads from 1020 insulin pumps used throughout the United States and overseen by a variety of clinicians were analyzed retrospectively to find insulin doses that provided the best glucose control. Glucose 207-214 insulin Homo sapiens 170-177 20920437-12 2010 Poor glucose outcomes among insulin pump users appear to be related to pump setting errors and being relatively underinsulinized, even though those in poor control use more total insulin per day. Glucose 5-12 insulin Homo sapiens 28-35 20920437-12 2010 Poor glucose outcomes among insulin pump users appear to be related to pump setting errors and being relatively underinsulinized, even though those in poor control use more total insulin per day. Glucose 5-12 insulin Homo sapiens 117-124 20920443-0 2010 Modeling the effects of subcutaneous insulin administration and carbohydrate consumption on blood glucose. Glucose 98-105 insulin Homo sapiens 37-44 20519313-2 2010 They are essential for glucose-stimulated insulin secretion from pancreatic beta-cells, contribute to the mechanisms by which hypoglycaemia stimulates glucagon release from pancreatic alpha-cells, and are involved in glucose uptake into skeletal muscle, glucose production and release from the liver, and feeding behaviour. Glucose 217-224 insulin Homo sapiens 42-49 20519313-2 2010 They are essential for glucose-stimulated insulin secretion from pancreatic beta-cells, contribute to the mechanisms by which hypoglycaemia stimulates glucagon release from pancreatic alpha-cells, and are involved in glucose uptake into skeletal muscle, glucose production and release from the liver, and feeding behaviour. Glucose 217-224 insulin Homo sapiens 42-49 20960553-5 2010 In normal circumstances, insulin stimulates glucose uptake into skeletal muscle, inhibits hepatic gluconeogenesis, and decreases adipose-tissue lipolysis and hepatic production of very-low-density lipoproteins. Glucose 44-51 insulin Homo sapiens 25-32 20379601-3 2010 The experimental support for this model of the binding interaction is provided by the consequences of the successful delivery of the CN-Cbl-insulin conjugate in the production of significantly decreased blood glucose levels in diabetic STZ-rat models. Glucose 209-216 insulin Homo sapiens 140-147 20960553-6 2010 Insulin signaling in the brain decreases appetite and prevents glucose production by the liver through neuronal signals from the hypothalamus. Glucose 63-70 insulin Homo sapiens 0-7 20922570-2 2010 The channel is key for glucose stimulated insulin release from the pancreatic beta cell. Glucose 23-30 insulin Homo sapiens 42-49 20934606-12 2010 In conclusion, in this study of 2 hexoses revealed an increase in adiponectin gene expression, suggesting that the effect of a glucose-rich diet on the development of insulin resistance is not related to the effect of these hexoses on adipocyte adiponectin gene expression. Glucose 127-134 insulin Homo sapiens 167-174 21205499-1 2010 In the gastrointestinal tract we produce hormones, called incretins, in response to food ingestion with a direct effect on pancreatic beta and alpha cell improving the insulin and glucagon response to glucose. Glucose 201-208 insulin Homo sapiens 168-175 20853714-0 2010 [Therapeutic education and continuous glucose monitoring in insulin-treated diabetic patients]. Glucose 38-45 insulin Homo sapiens 60-67 21205499-2 2010 The effect consisting in a greater secretion of insulin with a glucose stimulus from the gut or IV injection is called "the incretin effect." Glucose 63-70 insulin Homo sapiens 48-55 20202743-4 2010 Our results from the glucose tolerance test and the homeostasis model assessment show that alcohol consumption improved insulin sensitivity. Glucose 21-28 insulin Homo sapiens 120-127 20144748-6 2010 Finally, the efficacy of insulin-loaded particles in reducing the blood glucose level in streptozotocin-induced diabetic rats was investigated. Glucose 72-79 insulin Homo sapiens 25-32 20501875-2 2010 Facilitated glucose uptake into muscle fibers is mediated by increases in surface membrane levels of the glucose transporter GLUT4 via insulin- and/or muscle contraction-mediated GLUT4 translocation. Glucose 12-19 insulin Homo sapiens 135-142 20530733-9 2010 The capacities of insulin to stimulate glucose disposal and inhibit glucose production were reinforced by GLP-1. Glucose 39-46 insulin Homo sapiens 18-25 20489042-8 2010 Insulin sensitivity based on glucose infusion rate (4.69 +/- 1.82 vs. 4.85 +/- 2.37 mg.kg(-1).min(-1)) and glucose tracer-based rate of disappearance were unchanged (5.01 +/- 1.61 vs. 4.97 +/- 2.13 mg.kg(-1).min(-1)). Glucose 29-36 insulin Homo sapiens 0-7 20530733-9 2010 The capacities of insulin to stimulate glucose disposal and inhibit glucose production were reinforced by GLP-1. Glucose 68-75 insulin Homo sapiens 18-25 20530733-13 2010 In conclusion, peripheral administration of GLP-1 reinforces the ability of insulin to suppress endogenous glucose and VLDL-TG production (but not lipolysis) and boosts its capacity to stimulate glucose disposal in high-fat-fed C57Bl/6 mice. Glucose 107-114 insulin Homo sapiens 76-83 20832741-1 2010 Metformin lowers blood glucose by reducing hepatic glucose output, increasing insulin sensitivity and enhancing peripheral glucose uptake. Glucose 23-30 insulin Homo sapiens 78-85 20877750-1 2010 BACKGROUND: Many patients with type 2 diabetes need to progress to insulin use when oral glucose lowering therapies fail to maintain adequate glycaemic control. Glucose 89-96 insulin Homo sapiens 67-74 20419449-5 2010 RESULTS: Assuming an additive genetic model, carriers of the alleles increasing fasting glucose in DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B showed decreased glucose-stimulated insulin release as assessed by the BIGTT-acute insulin response index (2.7-3.5%; p < 0.005 for all) and by corrected insulin response (2.8-5.9%; p < 0.03 for all). Glucose 88-95 insulin Homo sapiens 174-181 20605096-3 2010 An isoflavone C-glucoside, puerarin (1), is known to enhance glucose uptake into the insulin sensitive cell and is thought to be a candidate for treatment of diabetes mellitus. Glucose 61-68 insulin Homo sapiens 85-92 20417083-3 2010 Insulin stimulates the translocation of these vesicles to the cell surface, inserting the transporters into the plasma membrane to enhance glucose uptake. Glucose 139-146 insulin Homo sapiens 0-7 20454776-4 2010 Insulin secretion and action were assessed based upon OGTT measurements of insulin and glucose. Glucose 87-94 insulin Homo sapiens 0-7 20419449-5 2010 RESULTS: Assuming an additive genetic model, carriers of the alleles increasing fasting glucose in DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B showed decreased glucose-stimulated insulin release as assessed by the BIGTT-acute insulin response index (2.7-3.5%; p < 0.005 for all) and by corrected insulin response (2.8-5.9%; p < 0.03 for all). Glucose 88-95 insulin Homo sapiens 221-228 20419449-5 2010 RESULTS: Assuming an additive genetic model, carriers of the alleles increasing fasting glucose in DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B showed decreased glucose-stimulated insulin release as assessed by the BIGTT-acute insulin response index (2.7-3.5%; p < 0.005 for all) and by corrected insulin response (2.8-5.9%; p < 0.03 for all). Glucose 88-95 insulin Homo sapiens 221-228 20419449-5 2010 RESULTS: Assuming an additive genetic model, carriers of the alleles increasing fasting glucose in DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B showed decreased glucose-stimulated insulin release as assessed by the BIGTT-acute insulin response index (2.7-3.5%; p < 0.005 for all) and by corrected insulin response (2.8-5.9%; p < 0.03 for all). Glucose 155-162 insulin Homo sapiens 174-181 20419449-5 2010 RESULTS: Assuming an additive genetic model, carriers of the alleles increasing fasting glucose in DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B showed decreased glucose-stimulated insulin release as assessed by the BIGTT-acute insulin response index (2.7-3.5%; p < 0.005 for all) and by corrected insulin response (2.8-5.9%; p < 0.03 for all). Glucose 155-162 insulin Homo sapiens 221-228 20419449-5 2010 RESULTS: Assuming an additive genetic model, carriers of the alleles increasing fasting glucose in DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B showed decreased glucose-stimulated insulin release as assessed by the BIGTT-acute insulin response index (2.7-3.5%; p < 0.005 for all) and by corrected insulin response (2.8-5.9%; p < 0.03 for all). Glucose 155-162 insulin Homo sapiens 221-228 20419449-8 2010 CONCLUSIONS/INTERPRETATION: We found that the lead variants at the DGKB/TMEM195, ADRA2A, GLIS3 and C2CD4B loci were associated with decreased glucose-stimulated insulin response. Glucose 142-149 insulin Homo sapiens 161-168 20422397-5 2010 Before and after training, insulin-stimulated glucose disposal was examined during a hyperinsulinaemic-euglycaemic clamp. Glucose 46-53 insulin Homo sapiens 27-34 20522590-6 2010 Among Pima Indians with normal glucose tolerance, the diabetes risk allele glycine of Gly54Asp was associated with a decreased acute insulin response to an intravenous glucose bolus infusion (P = 0.004, adjusted for age, sex, percent body fat, glucose disposal under physiological insulin stimulation, and family membership). Glucose 168-175 insulin Homo sapiens 133-140 20522590-6 2010 Among Pima Indians with normal glucose tolerance, the diabetes risk allele glycine of Gly54Asp was associated with a decreased acute insulin response to an intravenous glucose bolus infusion (P = 0.004, adjusted for age, sex, percent body fat, glucose disposal under physiological insulin stimulation, and family membership). Glucose 168-175 insulin Homo sapiens 133-140 20422397-10 2010 Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals. Glucose 96-103 insulin Homo sapiens 77-84 20615108-1 2010 BACKGROUND: We designed a system for diabetes patients treated with glargine, a long-acting insulin, to make an automatic adjustment of insulin dose based on glucose level data and to provide the patients with the needed insulin dose by using a short message service (SMS). Glucose 158-165 insulin Homo sapiens 92-99 20590745-1 2010 AIMS: To explore glucose lowering response to insulin initiation or switch to insulin glargine in obese and non-obese individuals with type 2 diabetes mellitus (T2DM) and to examine weight gain and hypoglycaemic episodes in this group. Glucose 17-24 insulin Homo sapiens 46-53 20590750-0 2010 Effects of in vitro antagonism of endocannabinoid-1 receptors on the glucose transport system in normal and insulin-resistant rat skeletal muscle. Glucose 69-76 insulin Homo sapiens 108-115 20590750-6 2010 The maximal increase in insulin-stimulated glucose transport for lean muscle ( approximately 30%) was achieved at 50 nM SR141716 and for obese muscle ( approximately 30%) at 100 nM SR141716. Glucose 43-50 insulin Homo sapiens 24-31 20590750-8 2010 CB1 receptor agonism (1 mM ACEA) significantly decreased both basal (15%) and insulin-stimulated (22%) glucose transport activity in isolated lean soleus. Glucose 103-110 insulin Homo sapiens 78-85 20615108-1 2010 BACKGROUND: We designed a system for diabetes patients treated with glargine, a long-acting insulin, to make an automatic adjustment of insulin dose based on glucose level data and to provide the patients with the needed insulin dose by using a short message service (SMS). Glucose 158-165 insulin Homo sapiens 136-143 20590750-11 2010 CONCLUSION: These results indicate that the engagement of CB1 receptor can negatively modulate both basal and insulin-dependent glucose transport activity in lean and obese skeletal muscles, and that these effects are not mediated by the engagement of elements of the canonical pathways regulating this process in mammalian skeletal muscle. Glucose 128-135 insulin Homo sapiens 110-117 20615108-1 2010 BACKGROUND: We designed a system for diabetes patients treated with glargine, a long-acting insulin, to make an automatic adjustment of insulin dose based on glucose level data and to provide the patients with the needed insulin dose by using a short message service (SMS). Glucose 158-165 insulin Homo sapiens 136-143 20501667-6 2010 We speculated that hyperinsulinemia minimized glucose-mediated VLDL changes and performed hyperglycemic-hypoinsulinemic clamp studies in which insulin was clamped near fasting levels with somatostatin (17 mm blood glucose, 0.25 mU/kg . Glucose 46-53 insulin Homo sapiens 24-31 20668152-1 2010 OBJECTIVE: To assess the effect of an Internet-based glucose monitoring system (IBGMS) on A1C levels in patients with type 2 diabetes treated with insulin. Glucose 53-60 insulin Homo sapiens 147-154 20501667-9 2010 We tested the extent that impaired inactivation of FoxO1 by insulin was sufficient for glucose to promote increased serum VLDL. Glucose 87-94 insulin Homo sapiens 60-67 20501667-10 2010 We found that, when the ability of insulin to inactivate FoxO1 is blocked after adenoviral delivery of constitutively active FoxO1, glucose increased serum VLDL triglyceride when given both by ip glucose tolerance testing (3.5-fold increase) and by a hyperglycemic clamp (4.6-fold). Glucose 132-139 insulin Homo sapiens 35-42 20501667-10 2010 We found that, when the ability of insulin to inactivate FoxO1 is blocked after adenoviral delivery of constitutively active FoxO1, glucose increased serum VLDL triglyceride when given both by ip glucose tolerance testing (3.5-fold increase) and by a hyperglycemic clamp (4.6-fold). Glucose 196-203 insulin Homo sapiens 35-42 20501667-12 2010 These data suggest that glucose more potently promotes increased serum VLDL when insulin action is impaired, with either low insulin levels or disrupted downstream signaling to the transcription factor FoxO1. Glucose 24-31 insulin Homo sapiens 81-88 19580964-5 2010 INTERVENTION(S): Peripheral insulin sensitivity was evaluated by the hyperinsulinemic euglycemic clamp, glucose tolerance by an oral glucose tolerance test (OGTT), and ovarian morphology by transvaginal ultrasonography (TVS). Glucose 104-111 insulin Homo sapiens 28-35 20670183-3 2010 By improving insulin sensitivity, hepatic glucose production decreases and glucose uptake increases in the peripheral tissues. Glucose 42-49 insulin Homo sapiens 13-20 19580964-5 2010 INTERVENTION(S): Peripheral insulin sensitivity was evaluated by the hyperinsulinemic euglycemic clamp, glucose tolerance by an oral glucose tolerance test (OGTT), and ovarian morphology by transvaginal ultrasonography (TVS). Glucose 133-140 insulin Homo sapiens 28-35 20444915-1 2010 INTRODUCTION: African-American children have a greater acute insulin response to iv glucose (AIR) compared with Latino children despite a similar degree of insulin resistance and body composition. Glucose 84-91 insulin Homo sapiens 61-68 20739722-10 2010 Mechanisms for the decreased magnitude of EPOC in the ABS trial include decreases in BLA, T(re), and perhaps epinephrine-mediated hepatic glucose production and insulin-mediated glucose uptake. Glucose 178-185 insulin Homo sapiens 161-168 20484615-0 2010 A model for glucose, insulin, and beta-cell dynamics in subjects with insulin resistance and patients with type 2 diabetes. Glucose 12-19 insulin Homo sapiens 70-77 20484481-8 2010 In cultured adipocytes, basal and insulin-stimulated glucose uptake were unaffected by 1-100 nM (normal/hyperaldosteronism) and impaired only by much higher, up to 10 microM, aldosterone concentrations. Glucose 53-60 insulin Homo sapiens 34-41 20498618-9 2010 The glucose responses were inversely related to insulin responses at the study conclusion. Glucose 4-11 insulin Homo sapiens 48-55 20498618-10 2010 CONCLUSION: The novel observation of this investigation was that the combination of valsartan and hydrochlorothiazide was associated with greater glucose-stimulated insulin secretory and lesser glycemic excursion responses than the amlodipine combination group. Glucose 146-153 insulin Homo sapiens 165-172 19756607-2 2010 Without detailing the chain of biochemical events giving rise to the delivery of insulin packets, the effect of the islets" bursting response to varying glucose concentration is described by a simple second order nonlinear model, of the same functional form for all islets, but with a random distribution of parameter values over the one million islets considered. Glucose 153-160 insulin Homo sapiens 81-88 20504157-2 2010 In contrast, it has been demonstrated that intensive insulin therapy to lower blood glucose can lead to an increased frequency of hypoglycemic episodes and poor outcome. Glucose 84-91 insulin Homo sapiens 53-60 20504157-8 2010 Insulin therapy to reduce blood glucose reverses this beneficial effect of hyperglycemia. Glucose 32-39 insulin Homo sapiens 0-7 20504157-9 2010 Taken together, our results indicate that an acute increase in blood glucose levels may not be harmful, and that intervention with insulin therapy to lower blood glucose levels in TBI patients may increase secondary brain damage. Glucose 162-169 insulin Homo sapiens 131-138 20519436-1 2010 Insulin stimulation of glucose uptake is achieved by redistribution of insulin-responsive glucose transporters, GLUT4, from intracellular storage compartment(s) to the plasma membrane in adipocytes and muscle cells. Glucose 23-30 insulin Homo sapiens 71-78 20501681-0 2010 Angiotensin II enhances insulin-stimulated whole-body glucose disposal but impairs insulin-induced capillary recruitment in healthy volunteers. Glucose 54-61 insulin Homo sapiens 24-31 20501681-1 2010 CONTEXT: Angiotensin II (AngII) increases insulin-mediated glucose uptake in healthy individuals. Glucose 59-66 insulin Homo sapiens 42-49 20501681-3 2010 AngII may increase glucose uptake through a direct effect on muscle cell insulin signaling or through increasing insulin delivery to muscle cells through effects on the microvasculature. Glucose 19-26 insulin Homo sapiens 73-80 20501681-4 2010 OBJECTIVE: Our objective was to determine whether AngII increases insulin-mediated glucose uptake through effects on insulin-induced capillary recruitment. Glucose 83-90 insulin Homo sapiens 66-73 20501681-10 2010 CONCLUSION: AngII increases insulin-mediated glucose uptake in healthy individuals. Glucose 45-52 insulin Homo sapiens 28-35 20519436-1 2010 Insulin stimulation of glucose uptake is achieved by redistribution of insulin-responsive glucose transporters, GLUT4, from intracellular storage compartment(s) to the plasma membrane in adipocytes and muscle cells. Glucose 23-30 insulin Homo sapiens 0-7 20819714-7 2010 This negative feedback may be exacerbated when cells are exposed to elevated glucose concentrations as observed in diabetic patients, and could thereby contribute to insulin resistance and worsening of hyperglycaemia. Glucose 77-84 insulin Homo sapiens 166-173 21189647-2 2010 New targets are addressed, as SGLT2 in the kidney or enzymes of glucose metabolism in the liver which might help to lower glucose levels and to overcome insulin resistance. Glucose 64-71 insulin Homo sapiens 153-160 20534694-3 2010 The defects in both glucose-stimulated insulin secretion and intracellular calcium oscillation are more pronounced than those in beta-cells lacking only Foxa2. Glucose 20-27 insulin Homo sapiens 39-46 20567248-4 2010 The high glucose load associated with peritoneal dialysis may lead to insulin resistance and to the development of an atherogenic lipid profile. Glucose 9-16 insulin Homo sapiens 70-77 20025694-7 2010 In addition, plasma membrane cholesterol normalization by chromium picolinate can fully restore insulin-stimulated glucose transport, further supporting the role of the adipocyte cholesterol imbalance in obesity and insulin resistance. Glucose 115-122 insulin Homo sapiens 96-103 20665189-0 2010 Glucose-stimulated insulin secretion in gastric bypass patients with hypoglycemic syndrome: no evidence for inappropriate pancreatic beta-cell function. Glucose 0-7 insulin Homo sapiens 19-26 19961550-1 2010 BACKGROUND: Adults with type 2 diabetes mellitus (T2DM) have broad impairments in beta-cell function, including severe attenuation of the first-phase insulin response to glucose, and reduced beta-cell mass. Glucose 170-177 insulin Homo sapiens 150-157 19961550-7 2010 RESULTS: The insulin response to increasing plasma glucose concentrations was blunted in the diabetic compared with control subjects (34.8 +/- 11.9 vs. 280.5 +/- 57.8 pmol/mmol; p < 0.0001), and AIR(max) was also significantly reduced in the diabetic group (1868 +/- 330 vs. 4445 +/- 606; p = 0.0005). Glucose 51-58 insulin Homo sapiens 13-20 20467340-2 2010 METHODS: Islets isolated from the pancreata of 40 surgical patients categorized as control group, patients with mild CP, and patients with advanced CP were assessed for their yield, size, and glucose-stimulated insulin secretion. Glucose 192-199 insulin Homo sapiens 211-218 20467340-7 2010 Islets obtained from the patients with advanced CP retained 53% glucose-stimulated insulin secretion function in comparison with those of the control group. Glucose 64-71 insulin Homo sapiens 83-90 20877251-4 2010 Advances in the integration of continuous glucose monitoring and insulin pumps already allow automated suspension of insulin delivery during hypoglycemia to limit its severity and duration. Glucose 42-49 insulin Homo sapiens 117-124 20877259-5 2010 The low glucose suspend (LGS) feature of the Medtronic Paradigm Veo (Medtronic MiniMed, Northridge, CA) pump allows CGM to suspend insulin delivery if preset hypoglycemic thresholds are achieved. Glucose 8-15 insulin Homo sapiens 131-138 20842820-13 2010 Negative correlation between C-peptide and glucose serum levels was found in control group (R = -0.71; p < 0.05). Glucose 43-50 insulin Homo sapiens 29-38 20600153-0 2010 High-glucose condition reduces cardioprotective effects of insulin against mechanical stress-induced cell injury. Glucose 5-12 insulin Homo sapiens 59-66 20600153-6 2010 However, high-glucose condition attenuated the insulin-induced Akt phosphorylation and cardioprotection. Glucose 14-21 insulin Homo sapiens 47-54 20600153-7 2010 To investigate the mechanisms that attenuated the effects of insulin in high-glucose condition, we examined the expression of tensin homologue deleted on chromosome 10 (PTEN), which is a negative regulator of the PI3 kinase/Akt pathway. Glucose 77-84 insulin Homo sapiens 61-68 20600153-8 2010 The expressions of PTEN and phosphorylated PTEN were significantly decreased by insulin, and those effects were attenuated in high-glucose condition. Glucose 131-138 insulin Homo sapiens 80-87 20600153-10 2010 Furthermore, we found that high-glucose condition prevented the decrease in PTEN expression and the cardioprotective effects induced by insulin. Glucose 32-39 insulin Homo sapiens 136-143 20628017-3 2010 Administration of a single dose of the insulin oligomer, defined here as the supramolecular insulin assembly II (SIA-II), to experimental animals rendered diabetic by streptozotocin or alloxan, released the hormone capable of maintaining physiologic glucose levels for >120 days for bovine and >140 days for recombinant human insulin without fasting hypoglycemia. Glucose 250-257 insulin Homo sapiens 92-99 20655470-3 2010 We show here that insulin signaling in osteoblasts is necessary for whole-body glucose homeostasis because it increases osteocalcin activity. Glucose 79-86 insulin Homo sapiens 18-25 20655470-6 2010 Accordingly, increasing or decreasing insulin signaling in osteoblasts promotes or hampers glucose metabolism in a bone resorption-dependent manner in mice and humans. Glucose 91-98 insulin Homo sapiens 38-45 20655470-7 2010 Hence, in a feed-forward loop, insulin signals in osteoblasts activate a hormone, osteocalcin, that promotes glucose metabolism. Glucose 109-116 insulin Homo sapiens 31-38 20668700-8 2010 Combined effect analyses showed individuals carrying more risk allele for high fasting glucose tended to have a higher glucose levels at both fasting and 2 h during OGTTs (p = 1.7x10(-13) and 0.0009, respectively), as well as lower HOMA-beta, insulinogenic index and both first- and second-phases insulin secretion (p = 0.0321-1.1x10(-7)). Glucose 87-94 insulin Homo sapiens 243-250 20668700-8 2010 Combined effect analyses showed individuals carrying more risk allele for high fasting glucose tended to have a higher glucose levels at both fasting and 2 h during OGTTs (p = 1.7x10(-13) and 0.0009, respectively), as well as lower HOMA-beta, insulinogenic index and both first- and second-phases insulin secretion (p = 0.0321-1.1x10(-7)). Glucose 119-126 insulin Homo sapiens 243-250 20642855-7 2010 CONCLUSIONS: When tested in-Silico, a commercially available subcutaneous glucose sensor allowed the stable functioning of a proportional-derivative Automatic Insulin Infusion System, which was able to maintain glucose within acceptable limits when using a well-established glucose response model simulating a patient. Glucose 74-81 insulin Homo sapiens 159-166 20642855-7 2010 CONCLUSIONS: When tested in-Silico, a commercially available subcutaneous glucose sensor allowed the stable functioning of a proportional-derivative Automatic Insulin Infusion System, which was able to maintain glucose within acceptable limits when using a well-established glucose response model simulating a patient. Glucose 211-218 insulin Homo sapiens 159-166 20642855-7 2010 CONCLUSIONS: When tested in-Silico, a commercially available subcutaneous glucose sensor allowed the stable functioning of a proportional-derivative Automatic Insulin Infusion System, which was able to maintain glucose within acceptable limits when using a well-established glucose response model simulating a patient. Glucose 211-218 insulin Homo sapiens 159-166 21437090-6 2010 The glucose-dependent mechanism of insulin release with incretin analog therapy holds potential clinical significance in the management of postprandial hyperglycemic excursions, with minimal risk of hypoglycemia when used with non-secretagogue medications. Glucose 4-11 insulin Homo sapiens 35-42 20513353-1 2010 PIKfyve is a protein and lipid kinase that plays an important role in membrane trafficking, including TGN to endosome retrograde sorting and in insulin-stimulated translocation of the GLUT4 glucose transporter from intracellular storage vesicles to the plasma membrane. Glucose 190-197 insulin Homo sapiens 144-151 20430894-6 2010 Acute oxidative stress restored normal insulin sensitivity and glucose uptake in insulin-resistant muscle cells, and this effect was dependent on MKP7. Glucose 63-70 insulin Homo sapiens 81-88 20615254-5 2010 During a clinic visit, the patient became confused and had a low plasma glucose, high plasma insulin, and high plasma C-peptide; symptoms were relieved with glucose. Glucose 157-164 insulin Homo sapiens 93-100 20515652-5 2010 Here we report that BBR mimics insulin action by increasing glucose uptake ability by 3T3-L1 adipocytes and L6 myocytes in an insulin-independent manner, inhibiting phosphatase activity of protein tyrosine phosphatase 1B (PTP1B), and increasing phosphorylation of IR, IRS1 and Akt in 3T3-L1 adipocytes. Glucose 60-67 insulin Homo sapiens 31-38 24900217-1 2010 The free fatty acid 1 receptor (FFA1 or GPR40), which is highly expressed on pancreatic beta-cells and amplifies glucose-stimulated insulin secretion, has emerged as an attractive target for the treatment of type 2 diabetes. Glucose 113-120 insulin Homo sapiens 132-139 20430890-2 2010 This study was undertaken to elucidate the molecular mechanism by which oxidative stress induced by paraquat impairs insulin-dependent glucose uptake in 3T3-L1 adipocytes. Glucose 135-142 insulin Homo sapiens 117-124 20430890-6 2010 Overexpression of active form Akt (myr-Akt) restored inhibition of insulin-dependent glucose uptake by paraquat, indicating that paraquat-induced oxidative stress inhibits insulin signals upstream of Akt. Glucose 85-92 insulin Homo sapiens 67-74 20407006-4 2010 Insulin-mediated glucose uptake (GU) increased (whole body and leg; P < 0.05) after training in CON but not in FDR, whereas glucose-mediated GU increased (P < 0.05) in both groups. Glucose 17-24 insulin Homo sapiens 0-7 20407006-7 2010 Glucose-stimulated insulin secretion was lower in FDR compared with CON, but no effect of training was seen. Glucose 0-7 insulin Homo sapiens 19-26 20463039-8 2010 In human adipocytes, resveratrol stimulated basal and insulin-stimulated glucose uptake. Glucose 73-80 insulin Homo sapiens 54-61 20715734-9 2010 Similar levels of glucose fluctuation were observed in intensive insulin therapy and conventional insulin therapy patients. Glucose 18-25 insulin Homo sapiens 65-72 20715734-9 2010 Similar levels of glucose fluctuation were observed in intensive insulin therapy and conventional insulin therapy patients. Glucose 18-25 insulin Homo sapiens 98-105 20516365-4 2010 STUDY SELECTION AND DATA EXTRACTION: All relevant English-language information on the pharmacology, efficacy, and safety of salicylates for glucose control related to insulin resistance or diabetes prevention were reviewed. Glucose 140-147 insulin Homo sapiens 167-174 20571106-14 2010 Insulin treatment regimens and protocols for non-critically ill patients in the acute care setting are evolving with recognition of ideal glucose targets to prevent adverse outcomes. Glucose 138-145 insulin Homo sapiens 0-7 20150286-10 2010 CONCLUSIONS: We concluded that insulin stimulation (day 4) and glucagon inhibition (day 3) contribute equally to the effect of GLP-1 on glucose turnover in patients with type 2 diabetes, and these changes explain the glucose-lowering effect of GLP-1 (day 5 vs. day 1). Glucose 136-143 insulin Homo sapiens 31-38 20495126-13 2010 Recombinant human insulin was used at doses of 8, 20, 50, and 125 mU/kg of BW, as needed, to estimate (by linear regression) the dose of insulin causing a 50% decline in glucose concentrations (ED50). Glucose 170-177 insulin Homo sapiens 137-144 20357360-9 2010 Tissue culture medium conditioned by CD11c(+) ATMs, but not CD11c(-) ATMs or other stromovascular cells, impaired insulin-stimulated glucose uptake by human adipocytes. Glucose 133-140 insulin Homo sapiens 114-121 20357364-7 2010 Insulin sensitivity was determined during an oral glucose tolerance test. Glucose 50-57 insulin Homo sapiens 0-7 20393152-3 2010 However, the link between elevated fasting glucose levels and insulin resistance in nondiabetic individuals, and the risk of cognitive impairment is unclear. Glucose 43-50 insulin Homo sapiens 62-69 20413510-11 2010 beta-Cells secreted GABA both by glucose-dependent exocytosis of insulin-containing granules and by a glucose-independent mechanism. Glucose 33-40 insulin Homo sapiens 65-72 20495453-1 2010 PURPOSE OF REVIEW: The present review outlines possible mechanisms by which high fatty acids, associated with high-fat diet and obesity, impose insulin resistance on glucose uptake into skeletal muscle. Glucose 166-173 insulin Homo sapiens 144-151 20200305-2 2010 Exercise and diet can alter glucose-induced insulin responses, but whether this is due to changes in beta-cell function per se is not clear. Glucose 28-35 insulin Homo sapiens 44-51 20200305-5 2010 beta-Cell function (oral glucose-induced insulin secretion corrected for insulin resistance assessed by hyperinsulinemic-euglycemic clamps) and the role of glucose-dependent insulinotropic polypeptide (GIP) were examined. Glucose 25-32 insulin Homo sapiens 41-48 20361178-2 2010 Insulin resistance is a hallmark of type 2 diabetes mellitus and is associated with a metabolic and cardiovascular cluster of disorders (dyslipidaemia, hypertension, obesity [especially visceral], glucose intolerance, endothelial dysfunction), each of which is an independent risk factor for cardiovascular disease (CVD). Glucose 197-204 insulin Homo sapiens 0-7 20372873-2 2010 High-dose growth hormone treatment often induces further impairment of insulin sensitivity, leading to an increase in insulin and glucose levels or even, in cases of preexisting beta cell defect, to overt diabetes. Glucose 130-137 insulin Homo sapiens 71-78 20372873-11 2010 Although the insulin response to glucose and arginine decreased slightly, the disposition index, integrating insulin sensitivity and secretion, significantly increased (p < 0.01), indicating an improvement in whole-body glucose metabolism. Glucose 33-40 insulin Homo sapiens 13-20 20736387-3 2010 The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are now known to play major roles in endogenous glucose control, including regulation of insulin, glucagon, and hepatic glucose metabolism. Glucose 59-66 insulin Homo sapiens 77-84 20350924-6 2010 Insulin glargine also yielded significantly greater reductions in fasting plasma glucose at all time points (end point difference, -34.9 mg/dL; 95% confidence interval, -47.6 to -22.2; P<.0001). Glucose 81-88 insulin Homo sapiens 0-7 20439243-4 2010 During the entire fasting test, highly specific insulin remained at <3 mIU/L, with a median value (and interquartile range) of 0.9 (0.8 to 2.3) mIU/L, when the glucose concentration was <50 mg/dL. Glucose 163-170 insulin Homo sapiens 48-55 20806184-0 2010 Insulin as the main regulator of cellular glucose utilization--aetiological aspects of insulin resistance. Glucose 42-49 insulin Homo sapiens 0-7 20806184-0 2010 Insulin as the main regulator of cellular glucose utilization--aetiological aspects of insulin resistance. Glucose 42-49 insulin Homo sapiens 87-94 20806184-1 2010 This review presents the advances in the molecular biology and the pathophysiology of insulin resistance with emphasis on disturbances in cellular glucose transport. Glucose 147-154 insulin Homo sapiens 86-93 20497462-5 2010 The level of blood glucose was assessed by fasting plasma glucose, fasting immunoreactive insulin, homeostasis model assessment (HOMA) index and haemoglobin A1c (HbA1c). Glucose 19-26 insulin Homo sapiens 90-97 20519242-6 2010 However, the difficult implementation of nurse-driven protocols for insulin infusion able to lead to rapid and effective blood glucose control without significant episodes of hypoglycaemia has led to poor implementations of insulin infusion protocols in coronary care units, and cardiologists now to consider alternative drugs for this purpose. Glucose 127-134 insulin Homo sapiens 68-75 20303351-6 2010 Muscle insulin sensitivity (percent increase in glucose uptake during insulin infusion) was greatest in the Lean group (576% +/- 70%). Glucose 48-55 insulin Homo sapiens 7-14 20578127-4 2010 Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during a 240-minute insulin suppression test. Glucose 17-24 insulin Homo sapiens 0-7 20578127-4 2010 Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during a 240-minute insulin suppression test. Glucose 17-24 insulin Homo sapiens 117-124 20578127-4 2010 Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during a 240-minute insulin suppression test. Glucose 68-75 insulin Homo sapiens 0-7 20236369-4 2010 A common cause of hypoglycaemia in people with type 2 diabetes is glucose-lowering medication, in particular, those which raise insulin independently of ambient glucose concentration such as sulphonylureas and exogenous insulin. Glucose 66-73 insulin Homo sapiens 128-135 20236369-4 2010 A common cause of hypoglycaemia in people with type 2 diabetes is glucose-lowering medication, in particular, those which raise insulin independently of ambient glucose concentration such as sulphonylureas and exogenous insulin. Glucose 66-73 insulin Homo sapiens 220-227 21099317-1 2010 Pancreatic beta-cells secrete insulin in response to changes in extracellular glucose concentration. Glucose 78-85 insulin Homo sapiens 30-37 20484475-0 2010 The product of triglycerides and glucose, a simple measure of insulin sensitivity. Glucose 33-40 insulin Homo sapiens 62-69 20045353-4 2010 In fact, mitochondrial genes may be plausible causative agents for diabetes, since mitochondrial oxidative phosphorylation plays an important role in glucose-stimulated insulin secretion from beta cells. Glucose 150-157 insulin Homo sapiens 169-176 20663451-3 2010 The net metabolic effect of insulin, defined as the total effect resulting from both reduced endogenous glucose production and increased glucose uptake, was used to define the insulin effectiveness (IE), a measure that indicates the amplitude of glucose lowering that a unit of active insulin can achieve at a given BG level. Glucose 104-111 insulin Homo sapiens 176-183 20663451-3 2010 The net metabolic effect of insulin, defined as the total effect resulting from both reduced endogenous glucose production and increased glucose uptake, was used to define the insulin effectiveness (IE), a measure that indicates the amplitude of glucose lowering that a unit of active insulin can achieve at a given BG level. Glucose 137-144 insulin Homo sapiens 176-183 20663451-3 2010 The net metabolic effect of insulin, defined as the total effect resulting from both reduced endogenous glucose production and increased glucose uptake, was used to define the insulin effectiveness (IE), a measure that indicates the amplitude of glucose lowering that a unit of active insulin can achieve at a given BG level. Glucose 137-144 insulin Homo sapiens 176-183 20154361-6 2010 Additionally, KN-62 attenuated 10,12 CLA induction of inflammatory and integrated stress response genes, increase in prostaglandin F2alpha, and suppression of peroxisome proliferator activated receptor gamma protein levels and insulin-stimulated glucose uptake. Glucose 246-253 insulin Homo sapiens 227-234 20044113-6 2010 The lower and upper 2.5%ile data of plasma glucose were prepared, which were used for mathematical basis of strong correlation between HOMA-R and serum insulin. Glucose 43-50 insulin Homo sapiens 152-159 20044113-7 2010 Subjects with higher insulin had higher plasma glucose, which was resulted in higher HOMA-R. Glucose 47-54 insulin Homo sapiens 21-28 20044113-9 2010 As two lines of the lower and upper 2.5%ile data of plasma glucose exists near, the correlation between HOMA-R and serum insulin became very strong. Glucose 59-66 insulin Homo sapiens 121-128 21060967-3 2010 beta-cells in the islets transcribe gene-encoding insulin, and subsequently process and secrete insulin, in response to circulating glucose. Glucose 132-139 insulin Homo sapiens 50-57 20392600-1 2010 Insulin is an important regulator of glucose, lipid, and protein metabolism. Glucose 37-44 insulin Homo sapiens 0-7 20853621-2 2010 TLRs activation leads to insulin resistance of adipose, hepatic and muscle cells, which increases glucose and lipids level in blood. Glucose 98-105 insulin Homo sapiens 25-32 20456670-2 2010 Adipokines affect insulin-stimulated glucose uptake in vitro but, to date there is little evidence for such a role in vivo. Glucose 37-44 insulin Homo sapiens 18-25 21060972-1 2010 Allogeneic islet transplantation serves as a source of insulin-secreting beta-cells for the maintenance of normal glucose levels and treatment of diabetes. Glucose 114-121 insulin Homo sapiens 55-62 21060975-12 2010 Both undifferentiated hPDMSCs and ILCs exihibited insulin secretion in response to glucose. Glucose 83-90 insulin Homo sapiens 50-57 20429700-2 2010 glucose bolus on insulin, leptin, ghrelin, peptide YY (PYY), free fatty acids (FFA), glucagon and glucagon-like peptide-1 (GLP-1) concentrations together with self-reported satiety ratings in lean and obese human subjects. Glucose 0-7 insulin Homo sapiens 17-24 20842888-2 2010 OBJECTIVE: The aim of this study was to establish relationship between basal glucose and insulin levels, insulin sensitivity and lipid panel and the degree of coronary atherosclerosis in nondiabetic patients. Glucose 77-84 insulin Homo sapiens 89-96 20096645-0 2010 Early insulin sensitivity after restrictive bariatric surgery, inconsistency between HOMA-IR and steady-state plasma glucose levels. Glucose 117-124 insulin Homo sapiens 6-13 20096645-6 2010 In the present study, we evaluated the use of steady-state plasma glucose (SSPG) levels to assess insulin sensitivity 2 months after bariatric surgery. Glucose 66-73 insulin Homo sapiens 98-105 20163204-10 2010 The results show that islets coated with the functional PEG conjugate are capable of secreting more insulin in response to high glucose levels compared to control islets. Glucose 128-135 insulin Homo sapiens 100-107 20303779-4 2010 Here, we show how the biological clock plays an important role in determining early morning (fasting) plasma glucose concentrations by affecting hepatic glucose production and glucose uptake, as well as glucose tolerance, by determining feeding-induced insulin responses. Glucose 109-116 insulin Homo sapiens 253-260 20303779-4 2010 Here, we show how the biological clock plays an important role in determining early morning (fasting) plasma glucose concentrations by affecting hepatic glucose production and glucose uptake, as well as glucose tolerance, by determining feeding-induced insulin responses. Glucose 153-160 insulin Homo sapiens 253-260 20303779-4 2010 Here, we show how the biological clock plays an important role in determining early morning (fasting) plasma glucose concentrations by affecting hepatic glucose production and glucose uptake, as well as glucose tolerance, by determining feeding-induced insulin responses. Glucose 153-160 insulin Homo sapiens 253-260 20597621-4 2010 Metformin induces higher glucose uptake, thus inducing a lower synthesis/secretion of insulin. Glucose 25-32 insulin Homo sapiens 86-93 20597621-6 2010 These are the basis of the many positive effects of this drug, such as the restoration of menstrual cyclicity, ovulatory cycles and fertility, because abnormal insulin levels affect the hypothalamus-pituitary-ovarian function, as well as the use of glucose in peripheral tissues. Glucose 249-256 insulin Homo sapiens 160-167 20939284-5 2010 Each treatment group, especially jatrorrhizine hydrochloride (in the concentration of 10.5 micromol x L(-1)) significantly decreased the concentration of glucose in 3T3-L1 adipocytes culture, at the same time improved insulin resistance. Glucose 154-161 insulin Homo sapiens 218-225 20842888-3 2010 METHODS: The coronary angiograms were evaluated for the presence of significant stenosis, insulin sensitivity was assessed using the intravenous glucose tolerance test with a minimal model according to Bergman, while baseline glucose (GO), insulin (10) and lipid panel measurements (TC, HDL, LDL, TG) were taken after a 12-hour fasting. Glucose 145-152 insulin Homo sapiens 90-97 20579360-7 2010 Moreover, the islet-like clusters could release insulin in response to glucose in vitro. Glucose 71-78 insulin Homo sapiens 48-55 20427569-2 2010 K(ATP) channels play a key role in glucose-stimulated insulin secretion by linking glucose metabolism to membrane excitability. Glucose 35-42 insulin Homo sapiens 54-61 20609972-2 2010 More than 40 years ago, Randle and colleagues postulated that lipids impaired insulin-stimulated glucose use by muscles through inhibition of glycolysis at key points. Glucose 97-104 insulin Homo sapiens 78-85 20609972-3 2010 However, work over the past two decades has shown that lipid-induced insulin resistance in skeletal muscle stems from defects in insulin-stimulated glucose transport activity. Glucose 148-155 insulin Homo sapiens 69-76 20609972-3 2010 However, work over the past two decades has shown that lipid-induced insulin resistance in skeletal muscle stems from defects in insulin-stimulated glucose transport activity. Glucose 148-155 insulin Homo sapiens 129-136 20609972-4 2010 The steatotic liver is also resistant to insulin in terms of inhibition of hepatic glucose production and stimulation of glycogen synthesis. Glucose 83-90 insulin Homo sapiens 41-48 20576133-8 2010 Insulin sensitivity decreased from diet initiation to mid-gestation (P = 0.04), and acute insulin response to glucose tended to be greater in OB150 ewes than C ewes (P = 0.09) and was greater than in OW125 ewes (P = 0.02). Glucose 110-117 insulin Homo sapiens 90-97 21437089-4 2010 In consequence, insulin detemir has shown a less variable pharmacodynamic profile than alternative basal insulins; this manifests as more consistent temporal glucose reduction profiles in repeat-clamp studies. Glucose 158-165 insulin Homo sapiens 16-23 21437089-6 2010 Given some recent associations that have been made in prospective and epidemiologic studies between glucose variability and/or hypoglycemia and increased cardiovascular risk, and the long-known association between excess weight and cardiovascular risk, it is possible that the clinical profile of insulin detemir may carry prognostic value with regard to cardiovascular safety, although this is yet to be substantiated. Glucose 100-107 insulin Homo sapiens 297-304 20303253-5 2010 The measured glucose concentration in human adipocytes or frog oocytes using our ZnO-nanorod sensor was consistent with values of glucose concentration reported in the literature; furthermore, the sensor was able to show that insulin increased the intracellular glucose concentration. Glucose 13-20 insulin Homo sapiens 226-233 20303253-5 2010 The measured glucose concentration in human adipocytes or frog oocytes using our ZnO-nanorod sensor was consistent with values of glucose concentration reported in the literature; furthermore, the sensor was able to show that insulin increased the intracellular glucose concentration. Glucose 130-137 insulin Homo sapiens 226-233 20303253-5 2010 The measured glucose concentration in human adipocytes or frog oocytes using our ZnO-nanorod sensor was consistent with values of glucose concentration reported in the literature; furthermore, the sensor was able to show that insulin increased the intracellular glucose concentration. Glucose 130-137 insulin Homo sapiens 226-233 20410133-1 2010 Insulin stimulates glucose uptake by regulating translocation of the GLUT4 glucose transporter from intracellular compartments to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 20427569-2 2010 K(ATP) channels play a key role in glucose-stimulated insulin secretion by linking glucose metabolism to membrane excitability. Glucose 83-90 insulin Homo sapiens 54-61 20179243-8 2010 All models share the common assumption that insulin secretion is made up of two components, one proportional to glucose rate of change through dynamic responsivity, Phi(d), and one proportional to glucose through static responsivity, Phi(s), but differing by modality of GLP-1 control. Glucose 112-119 insulin Homo sapiens 44-51 20534142-12 2010 The minor allele of SNP rs6232 was additionally associated with 15% higher OGTT-derived and 19% higher clamp-derived insulin sensitivity (pdom <or= 0.0047), 4.5% lower HOMAIR (pdom = 0.02) and 3.5% lower 120-min glucose (pdom = 0.0003) independently of BMI and proinsulin conversion. Glucose 215-222 insulin Homo sapiens 117-124 20534142-14 2010 CONCLUSIONS: Like rare mutations in PCSK1, the more common variants tested determine glucose-stimulated proinsulin conversion, but not insulin secretion. Glucose 85-92 insulin Homo sapiens 104-114 20534142-14 2010 CONCLUSIONS: Like rare mutations in PCSK1, the more common variants tested determine glucose-stimulated proinsulin conversion, but not insulin secretion. Glucose 85-92 insulin Homo sapiens 107-114 19936603-11 2010 The stimulus to maintain NGT elicits more insulin secretion, predisposing to worsening glucose tolerance when a faltering insulin secretion ensues. Glucose 87-94 insulin Homo sapiens 42-49 19936603-11 2010 The stimulus to maintain NGT elicits more insulin secretion, predisposing to worsening glucose tolerance when a faltering insulin secretion ensues. Glucose 87-94 insulin Homo sapiens 122-129 20179243-8 2010 All models share the common assumption that insulin secretion is made up of two components, one proportional to glucose rate of change through dynamic responsivity, Phi(d), and one proportional to glucose through static responsivity, Phi(s), but differing by modality of GLP-1 control. Glucose 197-204 insulin Homo sapiens 44-51 20332360-0 2010 Computational model of cellular metabolic dynamics: effect of insulin on glucose disposal in human skeletal muscle. Glucose 73-80 insulin Homo sapiens 62-69 20332360-1 2010 Identifying the mechanisms by which insulin regulates glucose metabolism in skeletal muscle is critical to understanding the etiology of insulin resistance and type 2 diabetes. Glucose 54-61 insulin Homo sapiens 36-43 20332360-1 2010 Identifying the mechanisms by which insulin regulates glucose metabolism in skeletal muscle is critical to understanding the etiology of insulin resistance and type 2 diabetes. Glucose 54-61 insulin Homo sapiens 137-144 20332360-6 2010 Insulin-mediated rate of glucose disposal was the primary model input. Glucose 25-32 insulin Homo sapiens 0-7 20510967-2 2010 Increases in each of the 3 values on the 75-g, 2-hour oral glucose tolerance test are associated with graded increases in the likelihood of pregnancy outcomes such as large for gestational age, cesarean section, fetal insulin levels, and neonatal fat content. Glucose 59-66 insulin Homo sapiens 218-225 20371732-7 2010 Basal and maximal insulin-stimulated glucose utilization was twice as high as in humans at approximately 5.5 and 21 mg kg(-1) min(-1). Glucose 37-44 insulin Homo sapiens 18-25 20587399-9 2010 On ECG, we noticed typical signs of hyperkalaemia.The patient was treated with a slow intravenous bolus of calcium gluconate and intravenous infusion of sodium chloride with insulin, glucose with insulin and sodium bicarbonte. Glucose 183-190 insulin Homo sapiens 196-203 20012307-5 2010 Insulin resistance was assessed by determining fasting insulin levels, fasting glucose levels, the fasting glucose/insulin ratio, as well as the HOMA and QUICKI indexes. Glucose 79-86 insulin Homo sapiens 0-7 20012307-5 2010 Insulin resistance was assessed by determining fasting insulin levels, fasting glucose levels, the fasting glucose/insulin ratio, as well as the HOMA and QUICKI indexes. Glucose 107-114 insulin Homo sapiens 0-7 20400899-12 2010 Intensive insulin therapy displayed a significantly higher glucose clamp infusion rate posttreatment (9.1 +/- 1.3 intensive insulin therapy versus 4.8 +/- 0.6 mg/kg x min conventional insulin therapy, p = .005). Glucose 59-66 insulin Homo sapiens 10-17 20031127-4 2010 Insulin sensitivity was determined by the hyperinsulinemic euglycemic clamp and insulin secretion with the intravenous glucose tolerance test. Glucose 119-126 insulin Homo sapiens 0-7 20400899-13 2010 Suppression of hepatic glucose release was significantly greater in the intensive insulin therapy after treatment compared with conventional insulin therapy (5.0 +/- 0.9 vs. 2.5 +/- 0.6 mg/kg x min; intensive insulin therapy vs. conventional insulin therapy; p = .03). Glucose 23-30 insulin Homo sapiens 82-89 20332342-0 2010 Fat cell-specific ablation of rictor in mice impairs insulin-regulated fat cell and whole-body glucose and lipid metabolism. Glucose 95-102 insulin Homo sapiens 53-60 20204321-0 2010 High normal fasting glucose level in obese youth: a marker for insulin resistance and beta cell dysregulation. Glucose 20-27 insulin Homo sapiens 63-70 20204321-10 2010 CONCLUSIONS/INTERPRETATION: These data suggest that in obese youth, independent of age, BMI z score, sex, family history and ethnicity, insulin sensitivity and secretion decline when moving from low to high normal fasting plasma glucose. Glucose 229-236 insulin Homo sapiens 136-143 20215429-8 2010 However, Ex-9 also reduced the insulin response to intravenous glucose (25 +/- 5% vs. 26 +/- 7%; diabetic vs. nondiabetic subjects), when plasma GLP-1 levels were undetectable. Glucose 63-70 insulin Homo sapiens 31-38 20332342-1 2010 OBJECTIVE: Rictor is an essential component of mammalian target of rapamycin (mTOR) complex (mTORC) 2, a kinase that phosphorylates and activates Akt, an insulin signaling intermediary that regulates glucose and lipid metabolism in adipose tissue, skeletal muscle, and liver. Glucose 200-207 insulin Homo sapiens 154-161 20215429-11 2010 Surprisingly, GLP-1 receptor signaling promotes glucose-stimulated insulin secretion independent of the mode of glucose entry. Glucose 48-55 insulin Homo sapiens 67-74 20215457-0 2010 Evaluation of an algorithm to guide patients with type 1 diabetes treated with continuous subcutaneous insulin infusion on how to respond to real-time continuous glucose levels: a randomized controlled trial. Glucose 162-169 insulin Homo sapiens 103-110 20332358-8 2010 RESULTS: Treatment with both doses of exenatide versus insulin monotherapy significantly reduced glucose excursions over 300 min (P < 0.0001). Glucose 97-104 insulin Homo sapiens 55-62 20215457-1 2010 OBJECTIVE: To evaluate an algorithm guiding responses of continuous subcutaneous insulin infusion (CSII)-treated type 1 diabetic patients using real-time continuous glucose monitoring (RT-CGM). Glucose 165-172 insulin Homo sapiens 81-88 20508226-0 2010 Continuous subcutaneous insulin infusion is better than multiple daily insulin injections in reducing glucose variability only in type 1 diabetes with good metabolic control. Glucose 102-109 insulin Homo sapiens 24-31 20349036-13 2010 CONCLUSIONS/INTERPRETATION: Pharmacological treatment of skeletal muscle with spermine NONOate increases glucose transport via insulin-independent signalling pathways involving increased intracellular cGMP levels and AMPK-alpha1-associated activity. Glucose 105-112 insulin Homo sapiens 127-134 20508226-0 2010 Continuous subcutaneous insulin infusion is better than multiple daily insulin injections in reducing glucose variability only in type 1 diabetes with good metabolic control. Glucose 102-109 insulin Homo sapiens 71-78 20515304-2 2010 With this increase has come a concomitant increase in the number of pregnant women using insulin to control their blood glucose in pregnancy. Glucose 120-127 insulin Homo sapiens 89-96 20515315-1 2010 Recent guidelines from the American Diabetes Association and the European Association for the Study of Diabetes promote the use of insulin sooner rather than later in patients with type 2 diabetes to achieve goal range glucose control (< 7%) but remain silent on a recommendation for delivery system. Glucose 219-226 insulin Homo sapiens 131-138 20061534-0 2010 Insulin-feedback via PI3K-C2alpha activated PKBalpha/Akt1 is required for glucose-stimulated insulin secretion. Glucose 74-81 insulin Homo sapiens 0-7 19338997-13 2010 CONCLUSION(S): In women with PCOS, [1] there is increased secretion of amylin, [2] insulin and amylin secretion is coregulated in the fasting state, [3] after glucose ingestion, glucose levels regulate amylin release, and [4] the insulin-sensitizing agent metformin, but not rosiglitazone, reduces amylin secretion. Glucose 159-166 insulin Homo sapiens 230-237 20061534-0 2010 Insulin-feedback via PI3K-C2alpha activated PKBalpha/Akt1 is required for glucose-stimulated insulin secretion. Glucose 74-81 insulin Homo sapiens 93-100 20061534-4 2010 Knockdown of PI3K-C2alpha expression and subsequent reduction of PKBalpha/Akt1 activity in the pancreatic beta-cell impaired glucose-stimulated insulin release, at least in part, due to reduced glucokinase expression and increased AS160 activity. Glucose 125-132 insulin Homo sapiens 144-151 20303969-0 2010 Insulin down-regulates the Na+/K+ ATPase in enterocytes but increases intestinal glucose absorption. Glucose 81-88 insulin Homo sapiens 0-7 20185348-0 2010 IGF-I stimulates reactive oxygen species (ROS) production and inhibits insulin-dependent glucose uptake via ROS in 3T3-L1 adipocytes. Glucose 89-96 insulin Homo sapiens 71-78 20185348-6 2010 DESIGN: To clarify the role of IGF-I on insulin sensitivity in adipocytes, we determined insulin-induced glucose uptake and IRS-1 status in 3T3-L1 adipocytes treated with IGF-I. Glucose 105-112 insulin Homo sapiens 89-96 20185348-8 2010 RESULTS: Preincubation of the adipocytes with IGF-I attenuated insulin-dependent glucose uptake. Glucose 81-88 insulin Homo sapiens 63-70 20303969-2 2010 Insulin increased apical glucose entry into the cells and decreased intestinal retention suggesting that serosal glucose transport was enhanced by the hormone. Glucose 25-32 insulin Homo sapiens 0-7 20185348-10 2010 Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS. Glucose 146-153 insulin Homo sapiens 128-135 20303969-2 2010 Insulin increased apical glucose entry into the cells and decreased intestinal retention suggesting that serosal glucose transport was enhanced by the hormone. Glucose 113-120 insulin Homo sapiens 0-7 20303969-5 2010 The cells also showed an increase in [(14)C] 3OMG uptake and intracellular glucose levels when treated with insulin and a lower Na(+)/K(+) ATPase activity. Glucose 75-82 insulin Homo sapiens 108-115 20303969-7 2010 The results showed that the effect of insulin on glucose uptake and intracellular glucose was still enhanced in presence of phloretin. Glucose 49-56 insulin Homo sapiens 38-45 20303969-7 2010 The results showed that the effect of insulin on glucose uptake and intracellular glucose was still enhanced in presence of phloretin. Glucose 82-89 insulin Homo sapiens 38-45 20601735-1 2010 This study determined whether disrupted glucose and insulin responses to an oral glucose-tolerance test (OGTT) induced by eccentric exercise were attenuated after a repeated bout. Glucose 81-88 insulin Homo sapiens 52-59 19531084-1 2010 Recent studies have revealed that insulin, the main regulator of the glucose homeostasis in somatic cells, is expressed in human spermatozoa which are also able to secrete it. Glucose 69-76 insulin Homo sapiens 34-41 20382691-6 2010 INTERVENTION: Plasma metabolic check-up was performed, and insulin sensitivity index was calculated from glucose and insulin responses to a 3-h oral glucose tolerance test. Glucose 105-112 insulin Homo sapiens 59-66 20371664-5 2010 Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies (from 1130 to 1430 h) with infusion of [6,6-(2)H(2)]glucose. Glucose 130-137 insulin Homo sapiens 0-7 20382691-6 2010 INTERVENTION: Plasma metabolic check-up was performed, and insulin sensitivity index was calculated from glucose and insulin responses to a 3-h oral glucose tolerance test. Glucose 149-156 insulin Homo sapiens 59-66 19963413-1 2010 STUDY OBJECTIVES: To estimate (1) the prevalence of insulin resistance (IR), by fasting glucose: insulin ratio (G:I<7.0) in adolescent girls with polycystic ovary syndrome (PCOS), (2) to compare the clinical and biochemical parameters between insulin-resistant and non-insulin resistant groups. Glucose 88-95 insulin Homo sapiens 52-59 20662332-7 2010 A higher frequency of hyperinsulinism was found in the case group: Fasting insulin > 15 mU/ml, 75% vs. 21% (case group vs. control group, respectively); fasting glucose to insulin ratio < 6, 72% vs. 24%; HOMA IR > 2.7, 83% vs. 14%; and decrease in QUICKI (< 0.3), 80% vs. 19% (p = 0.000). Glucose 164-171 insulin Homo sapiens 27-34 19962157-4 2010 Insulin resistance was directly quantified by measuring the steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 80-87 insulin Homo sapiens 0-7 20357092-2 2010 Insulin regulates gene expression of key enzymes in glucose and lipid metabolism by modulating the activity of specific Forkhead box transcriptional regulators (FoxO1 and FoxA2) via the phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway in the liver. Glucose 52-59 insulin Homo sapiens 0-7 20617073-5 2010 In obesity, inflammation develops when macrophages infiltrate adipose tissue and stimulate adipocyte secretion of inflammatory cytokines, that in turn affect energy balance, glucose and lipid metabolism, leading to insulin resistance. Glucose 174-181 insulin Homo sapiens 215-222 20617076-4 2010 Additionally, we analyzed the changes in early phase insulin secretion according to changes in fasting (Glc(0)), post-prandial (Glc(120)) glucose and HbA1c (A1c) levels. Glucose 104-107 insulin Homo sapiens 53-60 20617076-4 2010 Additionally, we analyzed the changes in early phase insulin secretion according to changes in fasting (Glc(0)), post-prandial (Glc(120)) glucose and HbA1c (A1c) levels. Glucose 128-131 insulin Homo sapiens 53-60 20617076-6 2010 Early phase insulin secretion decreased rapidly according to the increments of Glc(0), Glc(120) and A1c, and these changes were most prominent in the NGT stage. Glucose 79-82 insulin Homo sapiens 12-19 20617076-6 2010 Early phase insulin secretion decreased rapidly according to the increments of Glc(0), Glc(120) and A1c, and these changes were most prominent in the NGT stage. Glucose 87-90 insulin Homo sapiens 12-19 20005535-8 2010 The results were interpreted as the slope of the changes of plasma insulin against the glucose levels. Glucose 87-94 insulin Homo sapiens 67-74 20423560-2 2010 Chromium (Cr) supplementation improves glucose disposal in patients with insulin resistance and diabetes. Glucose 39-46 insulin Homo sapiens 73-80 20738033-2 2010 When patients with type 2 diabetes fail to achieve strict HbA1c control with oral glucose-lowering drugs, insulin is the standard recourse. Glucose 82-89 insulin Homo sapiens 106-113 21204007-1 2010 Insulin is a hormone that is essential for regulating energy storage and glucose metabolism in the body. Glucose 73-80 insulin Homo sapiens 0-7 21204007-2 2010 Insulin in liver, muscle, and fat tissues stimulates the cell to take up glucose from blood and store it as glycogen in liver and muscle. Glucose 73-80 insulin Homo sapiens 0-7 20208423-5 2010 SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. Glucose 56-63 insulin Homo sapiens 37-44 20520763-0 2010 High glucose suppresses human islet insulin biosynthesis by inducing miR-133a leading to decreased polypyrimidine tract binding protein-expression. Glucose 5-12 insulin Homo sapiens 36-43 20520763-4 2010 The aim of this study was therefore to investigate whether high glucose increased the levels of these three miRNAs in association with lower PTB levels and lower insulin biosynthesis rates. Glucose 64-71 insulin Homo sapiens 162-169 20520763-13 2010 However, both PTB protein levels and insulin biosynthesis rates were decreased in response to high glucose. Glucose 99-106 insulin Homo sapiens 37-44 20520763-14 2010 The miR-133a inhibitor prevented the high glucose-induced decrease in PTB and insulin biosynthesis, and the miR-133a precursor decreased PTB levels and insulin biosynthesis similarly to high glucose. Glucose 42-49 insulin Homo sapiens 78-85 20520763-15 2010 CONCLUSION: Prolonged high-glucose exposure down-regulates PTB levels and insulin biosynthesis rates in human islets by increasing miR-133a levels. Glucose 27-34 insulin Homo sapiens 74-81 20339002-7 2010 Activated Rap1A promotes glucose-stimulated insulin secretion, islet cell hypertrophy, and islet cell proliferation, the latter exclusively through mammalian target of rapamycin complex 1, suggesting that Rap1 is an important regulator of beta-cell function. Glucose 25-32 insulin Homo sapiens 44-51 20494121-1 2010 Pancreatic beta-cells release insulin in appropriate amounts in order to keep blood glucose levels within physiological limits. Glucose 84-91 insulin Homo sapiens 30-37 20494121-3 2010 The glucose-stimulus/insulin-secretion coupling represents a sophisticated interplay between glucose and a variety of modulatory factors. Glucose 4-11 insulin Homo sapiens 21-28 20494121-3 2010 The glucose-stimulus/insulin-secretion coupling represents a sophisticated interplay between glucose and a variety of modulatory factors. Glucose 93-100 insulin Homo sapiens 21-28 20383171-9 2010 RESULTS: The production of glucose stimulated with insulin was reduced. Glucose 27-34 insulin Homo sapiens 51-58 20031131-12 2010 The greater postprandial increases in plasma insulin and glucose in MS relatively to control subjects indicate decreased insulin sensitivity, not revealed in the fasted state. Glucose 57-64 insulin Homo sapiens 121-128 20433129-6 2010 A correctional insulin dose provides a final insulin adjustment based on the preprandial glucose value. Glucose 89-96 insulin Homo sapiens 15-22 20433129-6 2010 A correctional insulin dose provides a final insulin adjustment based on the preprandial glucose value. Glucose 89-96 insulin Homo sapiens 45-52 20394912-5 2010 The use of insulin sensitizers i.e. metformin in PCOS should be restricted to women with glucose intolerance and/or insulin resistance. Glucose 89-96 insulin Homo sapiens 11-18 20368410-6 2010 The insulin response to a mixed meal was blunted in both the RYGB and caloric restriction groups (113 +/- 67 to 65 +/- 33 and 85 +/- 59 to 65 +/- 56 nmol x l(-1) x min(-1), respectively; P < 0.05) without a change in the glucose response. Glucose 224-231 insulin Homo sapiens 4-11 20305674-3 2010 Insulin resistance was calculated by homeostasis model assessment (HOMA [fasting glucose x fasting insulin]/22.5) and quantitative insulin sensitivity check index (QUICKI; 1/[log (fasting insulin) + log (fasting glucose)]). Glucose 81-88 insulin Homo sapiens 0-7 20384568-0 2010 Direct inhibition by angiotensin II of insulin-dependent glucose transport activity in mammalian skeletal muscle involves a ROS-dependent mechanism. Glucose 57-64 insulin Homo sapiens 39-46 20384568-4 2010 Ang II caused significant (p < 0.05) inhibition of insulin-stimulated glucose transport (39%) and decreased phosphorylation of Akt Ser(473) (37%) and glycogen synthase kinase-3beta Ser(9) (42%) without affecting phosphorylation of IRS-1 Ser(307) or p38 MAPK. Glucose 73-80 insulin Homo sapiens 54-61 20384568-6 2010 Tempol partially reversed (42%) Ang II-induced inhibition of insulin-stimulated glucose transport. Glucose 80-87 insulin Homo sapiens 61-68 20384568-7 2010 These results indicate that Ang II inhibits distal insulin signalling and insulin-stimulated glucose transport in isolated mammalian skeletal muscle, and that this effect is partially mediated by ROS. Glucose 93-100 insulin Homo sapiens 74-81 20637370-5 2010 The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated by measuring fasting plasma glucose and insulin levels. Glucose 108-115 insulin Homo sapiens 36-43 20507288-9 2010 This work presents the way of automatic regulation of the basal dose of insulin through the synthesis of the functions of the insulin pump and the continuing glucose sensor. Glucose 158-165 insulin Homo sapiens 72-79 20026082-1 2010 Insulin induces a translocation of the glucose transporter GLUT4 from intracellular storage compartments towards the cell surface in adipocytes and skeletal muscle cells, allowing the cells to take up glucose. Glucose 39-46 insulin Homo sapiens 0-7 20507288-9 2010 This work presents the way of automatic regulation of the basal dose of insulin through the synthesis of the functions of the insulin pump and the continuing glucose sensor. Glucose 158-165 insulin Homo sapiens 126-133 20507288-10 2010 The aim is to give a contribution to the development of the controlling algorithm on the insulin pump for the automatic regulation of the glucose concentration in the blood. Glucose 138-145 insulin Homo sapiens 89-96 20685497-10 2010 Insulin doses were adjusted based on preprandial plasma glucose levels. Glucose 56-63 insulin Homo sapiens 0-7 20447065-13 2010 The presence of d3GHR allele, and not BMI or age, was a significant negative predictor of insulin levels 120 min after oral glucose load (beta = -80.8, P < 0.05). Glucose 124-131 insulin Homo sapiens 90-97 20404621-2 2010 A clinical nurse specialist-led interdisciplinary team developed standardized insulin orders with the goal of improving glucose control. Glucose 120-127 insulin Homo sapiens 78-85 20404621-3 2010 Of the 570 patients admitted from July to September 2006, 124 met glucose criteria to use standardized insulin orders. Glucose 66-73 insulin Homo sapiens 103-110 20404621-5 2010 A mean glucose of 175 mg/dL and median glucose of 149 mg/dL were the outcomes when standardized insulin orders were used versus a mean glucose of 206 mg/dL and median glucose of 190 mg/dL when standardized orders were not used. Glucose 7-14 insulin Homo sapiens 96-103 20714409-1 2010 Insulin triggers glucose uptake into muscle and adipose tissue by stimulating the translocation of the glucose transporter glut4 from intracellular vesicles to the plasma membrane (pm). Glucose 17-24 insulin Homo sapiens 0-7 20185745-3 2010 Insulin resistance was derived from blood chemistry measures of fasting insulin and glucose using the homeostasis model assessment method. Glucose 84-91 insulin Homo sapiens 0-7 20165829-10 2010 CONCLUSIONS/INTERPRETATION: In this work we show that glucosamine-induced ER stress causes insulin resistance in both human and rat myotubes and impairs GLUT4 production and insulin-induced glucose uptake via an ATF6-dependent decrease of the GLUT4 regulators MEF2A and PGC1alpha. Glucose 190-197 insulin Homo sapiens 174-181 20185807-2 2010 We aimed to characterize 19 such loci using detailed measures of insulin processing, secretion, and sensitivity to help elucidate their role in regulation of glucose control, insulin secretion and/or action. Glucose 158-165 insulin Homo sapiens 65-72 20185807-4 2010 RESULTS The glucose-raising allele in MADD was associated with abnormal insulin processing (a dramatic effect on higher proinsulin levels, but no association with insulinogenic index) at extremely persuasive levels of statistical significance (P = 2.1 x 10(-71)). Glucose 12-19 insulin Homo sapiens 120-130 20185807-6 2010 Abnormalities in early insulin secretion were suggested in glucose-raising allele carriers at MTNR1B, GCK, FADS1, DGKB, and PROX1 (lower insulinogenic index; no association with proinsulin or insulin sensitivity). Glucose 59-66 insulin Homo sapiens 23-30 20200310-4 2010 Blood samples were obtained at 0, 2, 4, and 6 h. RESULTS: Insulin infusion significantly suppressed the plasma concentrations of MCP-1, eotaxin, and RANTES and the expression of RANTES, macrophage inflammatory protein (MIP)-1beta, CCR-2, and CCR-5 in MNCs at 2 and 4 h. Dextrose and saline infusions did not alter these indexes. Glucose 270-278 insulin Homo sapiens 58-65 20388047-13 2010 An insulin kinetics study using glucose induction with different concentrations showed increased insulin secretion in response to glucose concentrations up to 20 mM. Glucose 32-39 insulin Homo sapiens 3-10 20388047-13 2010 An insulin kinetics study using glucose induction with different concentrations showed increased insulin secretion in response to glucose concentrations up to 20 mM. Glucose 32-39 insulin Homo sapiens 97-104 20388047-13 2010 An insulin kinetics study using glucose induction with different concentrations showed increased insulin secretion in response to glucose concentrations up to 20 mM. Glucose 130-137 insulin Homo sapiens 3-10 20388047-13 2010 An insulin kinetics study using glucose induction with different concentrations showed increased insulin secretion in response to glucose concentrations up to 20 mM. Glucose 130-137 insulin Homo sapiens 97-104 20466163-3 2010 Modern insulin analogs were designed to achieve improved blood glucose control with similar hypoglycemic risk compared with non-analog insulins (or similar blood glucose control with reduced hypoglycemic risk). Glucose 63-70 insulin Homo sapiens 7-14 20503260-3 2010 RESULTS: NGT and IFG subjects who returned their plasma glucose concentration following an ingested glucose load below FPG within 60 min had increased insulin sensitivity, greater insulin secretion and lower risk for future T2DM compared to NGT and IFG subjects whose post-load plasma glucose concentration required 120 min or longer to return their plasma glucose level to FPG level. Glucose 56-63 insulin Homo sapiens 151-158 20503260-3 2010 RESULTS: NGT and IFG subjects who returned their plasma glucose concentration following an ingested glucose load below FPG within 60 min had increased insulin sensitivity, greater insulin secretion and lower risk for future T2DM compared to NGT and IFG subjects whose post-load plasma glucose concentration required 120 min or longer to return their plasma glucose level to FPG level. Glucose 100-107 insulin Homo sapiens 151-158 20503260-3 2010 RESULTS: NGT and IFG subjects who returned their plasma glucose concentration following an ingested glucose load below FPG within 60 min had increased insulin sensitivity, greater insulin secretion and lower risk for future T2DM compared to NGT and IFG subjects whose post-load plasma glucose concentration required 120 min or longer to return their plasma glucose level to FPG level. Glucose 100-107 insulin Homo sapiens 151-158 20503260-3 2010 RESULTS: NGT and IFG subjects who returned their plasma glucose concentration following an ingested glucose load below FPG within 60 min had increased insulin sensitivity, greater insulin secretion and lower risk for future T2DM compared to NGT and IFG subjects whose post-load plasma glucose concentration required 120 min or longer to return their plasma glucose level to FPG level. Glucose 100-107 insulin Homo sapiens 151-158 20503260-4 2010 IGT subjects who had a lower plasma glucose concentration at 1-h compared to 2-h during OGTT had greater insulin sensitivity, better beta cell function and lower risk for future T2DM. Glucose 36-43 insulin Homo sapiens 105-112 20061290-1 2010 Reevaluation of insulin dosing estimation formulas using continuous glucose monitoring. Glucose 68-75 insulin Homo sapiens 16-23 20061290-6 2010 Bolus insulin was adjusted to achieve a 2- to 4-hour postbolus glucose value within 20% of the premeal glucose (ICR) or 80 to 120 mg/dL from premeal hyperglycemia (CF). Glucose 63-70 insulin Homo sapiens 6-13 20233798-1 2010 Hyperglycemia, a prevalent condition in premature infants, is thought to be a consequence of incomplete suppression of endogenous glucose production and reduced insulin-stimulated glucose disposal in peripheral tissues. Glucose 180-187 insulin Homo sapiens 161-168 20233798-9 2010 Reduced muscle content of key glucose transport-regulating proteins (GLUT1, GLUT4, AS160) could play a role in the pathogenesis of neonatal hyperglycemia and reduced insulin-stimulated glucose disposal. Glucose 30-37 insulin Homo sapiens 166-173 20233798-9 2010 Reduced muscle content of key glucose transport-regulating proteins (GLUT1, GLUT4, AS160) could play a role in the pathogenesis of neonatal hyperglycemia and reduced insulin-stimulated glucose disposal. Glucose 185-192 insulin Homo sapiens 166-173 20408756-6 2010 Insulin resistance was calculated from fasting insulin and glucose values using Homeostasis Model Assessment (HOMA). Glucose 59-66 insulin Homo sapiens 0-7 20602305-9 2010 These pathophysiological and clinical circumstances were the motivation for presenting a review of cellular glucose transport pathophysiology, which contributes to the aetiology of insulin resistance, cellular underutilization of glucose, and type 2 diabetes mellitus. Glucose 108-115 insulin Homo sapiens 181-188 20602305-10 2010 They underline the significance of cellular glucose transport as a target for prevention and therapy of type 2 diabetes mellitus and other insulin resistant conditions. Glucose 44-51 insulin Homo sapiens 139-146 20072961-1 2010 INTRODUCTION: Basal insulin dose requirements in patients with type 1 diabetes may be derived from the course of glucose concentrations in the fasting state; i. e. by skipping meals. Glucose 113-120 insulin Homo sapiens 20-27 20198556-6 2010 Functional laboratory tests ruled out heterozygous C21-hydroxylase deficiency and showed a moderate insulin resistance on the oral glucose tolerance test. Glucose 131-138 insulin Homo sapiens 100-107 20182520-0 2010 Insulin expressed from endogenously active glucose-responsive EGR1 promoter in bone marrow mesenchymal stromal cells as diabetes therapy. Glucose 43-50 insulin Homo sapiens 0-7 20182520-2 2010 We have recently demonstrated durable correction of murine and porcine diabetes by syngeneic and autologous implantation, respectively, of primary hepatocytes non-virally modified with a glucose-responsive promoter-regulated insulin transgene. Glucose 187-194 insulin Homo sapiens 225-232 19903118-1 2010 AIM: To estimate (1) the prevalence of insulin resistance (IR) by fasting glucose: insulin ratio (G:I) (G:I <or= 4.5) in overweight-obese polycystic ovary syndrome (PCOS) women, (2) to compare the clinical and biochemical parameters between insulin-resistant and insulin-sensitive groups. Glucose 74-81 insulin Homo sapiens 39-46 20123578-9 2010 The IIAS is used to close the loop between the insulin pump and the continuous glucose monitoring system, by providing the pump with the appropriate insulin infusion rate in order to keep the patient"s glucose levels within predefined limits. Glucose 79-86 insulin Homo sapiens 149-156 20123578-9 2010 The IIAS is used to close the loop between the insulin pump and the continuous glucose monitoring system, by providing the pump with the appropriate insulin infusion rate in order to keep the patient"s glucose levels within predefined limits. Glucose 202-209 insulin Homo sapiens 47-54 20123578-9 2010 The IIAS is used to close the loop between the insulin pump and the continuous glucose monitoring system, by providing the pump with the appropriate insulin infusion rate in order to keep the patient"s glucose levels within predefined limits. Glucose 202-209 insulin Homo sapiens 149-156 20212264-4 2010 Insulin sensitivity was estimated on the basis of glucose and insulin levels in the fasting state and after an oral glucose load. Glucose 50-57 insulin Homo sapiens 0-7 20212264-4 2010 Insulin sensitivity was estimated on the basis of glucose and insulin levels in the fasting state and after an oral glucose load. Glucose 116-123 insulin Homo sapiens 0-7 20225248-2 2010 GLP-1 functions as an incretin and stimulates glucose-mediated insulin production by pancreatic beta cells. Glucose 46-53 insulin Homo sapiens 63-70 19931409-10 2010 Accordingly, insulin stimulates mitochondrial NO synthase simultaneously with cellular glucose intake. Glucose 87-94 insulin Homo sapiens 13-20 20101247-8 2010 Using LPS-challenged MPhi-CM, GPE pretreatment attenuated MPhi-mediated inflammatory gene expression, activation of an NF-kappaB reporter and suppression of insulin-stimulated glucose uptake in human adipocytes. Glucose 176-183 insulin Homo sapiens 157-164 20207830-11 2010 ET-1 impaired basal and insulin-stimulated glucose uptake in cultured muscle cells (P < 0.01) via an effect that was prevented by ET(A)/ET(B) receptor blockade. Glucose 43-50 insulin Homo sapiens 24-31 20207830-12 2010 CONCLUSION: ET(A)/ET(B) receptor blockade enhances basal and insulin-stimulated glucose uptake in IR subjects. Glucose 80-87 insulin Homo sapiens 61-68 20513314-4 2010 Features of certain advanced pump models include the ability to connect wirelessly to a blood glucose meter or to a subcutaneous interstitial glucose sensor for semicontinuous glucose-driven insulin rate adjustment. Glucose 142-149 insulin Homo sapiens 191-198 20513322-1 2010 Bolus calculators are effective tools in controlling blood glucose levels in patients treated with insulin. Glucose 59-66 insulin Homo sapiens 99-106 20513337-6 2010 At exercise onset, blood [glucose] transiently rises before beginning to decline after approximately 30 min, causing a subsequent decline in blood [insulin] and rise in blood glucagon. Glucose 26-33 insulin Homo sapiens 148-155 20662347-17 2010 A correlation was found between serum glucose and insulin on the first day but not on day 3 or month 3. Glucose 38-45 insulin Homo sapiens 50-57 20496226-14 2010 A 75% reduction to pre-exercise insulin results in the greatest preservation of blood glucose, and a reduced dietary intake, for 24 h after running in individuals with type 1 diabetes. Glucose 86-93 insulin Homo sapiens 32-39 19919871-8 2010 After bed rest, there was a decrease in insulin sensitivity, as assessed by glucose uptake during hyperinsulinemia (from 9.1 +/- 1.3 [mean +/- SEM] to 5.2 +/- 0.7 mg/kg of leg per minute [P = .015]). Glucose 76-83 insulin Homo sapiens 40-47 20022616-7 2010 At preintervention, responders, defined as insulin sensitivity change from baseline of at least 10% or greater, had significantly lower insulin sensitivity and higher fasting glucose and A(1c) when compared with placebo and nonresponders, that is, insulin sensitivity change from baseline of less than 10%. Glucose 175-182 insulin Homo sapiens 43-50 20022616-10 2010 Clinical response to Cr is more likely in insulin-resistant subjects who have more elevated fasting glucose and A(1c) levels. Glucose 100-107 insulin Homo sapiens 42-49 19910937-7 2010 Insulin resistance (steady-state plasma insulin and glucose (SSPG)) decreased following pioglitazone (P < 0.001). Glucose 52-59 insulin Homo sapiens 0-7 20186136-1 2010 In subjects with obesity and type 2 diabetes mellitus (T2DM), biliopancreatic diversion (BPD) improves glucose stimulated insulin secretion, whereas the effects on other secretion mechanisms are still unknown. Glucose 103-110 insulin Homo sapiens 122-129 20186136-3 2010 In 16 morbid obese subjects (9 with T2DM and 7 with normal fasting glucose (NFG)), we measured insulin secretion after glucose-dependent arginine stimulation test and after intravenous glucose tolerance test (IVGTT) before and 1 month after BPD. Glucose 119-126 insulin Homo sapiens 95-102 20186136-3 2010 In 16 morbid obese subjects (9 with T2DM and 7 with normal fasting glucose (NFG)), we measured insulin secretion after glucose-dependent arginine stimulation test and after intravenous glucose tolerance test (IVGTT) before and 1 month after BPD. Glucose 119-126 insulin Homo sapiens 95-102 20186136-7 2010 In particular, acute insulin response to arginine at basal glucose concentrations (AIR(basal)) was reduced but insulin response at 14 mmol/l of plasma glucose (AIR(14)) was increased. Glucose 59-66 insulin Homo sapiens 21-28 20186136-7 2010 In particular, acute insulin response to arginine at basal glucose concentrations (AIR(basal)) was reduced but insulin response at 14 mmol/l of plasma glucose (AIR(14)) was increased. Glucose 151-158 insulin Homo sapiens 111-118 20186136-10 2010 In conclusion, in obese T2DM subjects 1 month after BPD we observed a great improvement of both glucose- and nonglucose-stimulated insulin secretions. Glucose 96-103 insulin Homo sapiens 131-138 19958460-0 2010 Use of a real-time continuous glucose monitoring system in children and young adults on insulin pump therapy: patients" and caregivers" perception of benefit. Glucose 30-37 insulin Homo sapiens 88-95 20463409-8 2010 A basal insulin should be initiated if glycemic control is not achieved with >or= 1 agents or if presenting glucose control is poor. Glucose 111-118 insulin Homo sapiens 8-15 20179324-4 2010 The cells also became insulin-resistant with impaired upstream insulin signaling and reduced glucose uptake. Glucose 93-100 insulin Homo sapiens 22-29 19799964-2 2010 Adipose tissue-specific elevation in hexosamine flux in animal models recapitulates whole-body insulin-resistant phenotypes, and increased hexosamine flux in adipocyte cell culture models impairs insulin-stimulated glucose uptake. Glucose 215-222 insulin Homo sapiens 196-203 20210336-7 2010 The encapsulated islets retained the ability to control insulin release in response to glucose concentration changes. Glucose 87-94 insulin Homo sapiens 56-63 19963442-9 2010 CONCLUSION: We have observed that the QTc interval is prolonged in insulin-resistant subjects with associated impaired glucose metabolism, while no difference was reported between insulin-resistant and non insulin-resistant subjects with normal glucose regulation. Glucose 119-126 insulin Homo sapiens 67-74 20106981-1 2010 Hepatic nuclear factor 1alpha (HNF1alpha) is a key regulator of development and function in pancreatic beta cells and is specifically involved in regulation of glycolysis and glucose-stimulated insulin secretion. Glucose 175-182 insulin Homo sapiens 194-201 20181829-1 2010 Insulin stimulates glucose transport by recruiting the GLUT4 glucose transporter to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 20407626-6 2010 The glycemic-lowering effects of pioglitazone alone occur slowly, whereas the addition of insulin to pioglitazone often shows a dramatic glucose-lowering effect. Glucose 137-144 insulin Homo sapiens 90-97 20128772-2 2010 hIPCs (human islet-derived precursor cells) are capable of proliferating and differentiating into cells that secrete insulin in response to glucose in vivo and in vitro. Glucose 140-147 insulin Homo sapiens 117-124 20226174-5 2010 Although archaeosomes have little effect on the transport of insulin across the Caco-2 cell monolayers, the in vivo experiments indicated that archaeosomes containing insulin induced lower levels of blood glucose than a conventional liposome formulation. Glucose 205-212 insulin Homo sapiens 167-174 20513939-4 2010 If administrated correctly, insulin is one of means that effectively control blood glucose level. Glucose 83-90 insulin Homo sapiens 28-35 20071560-6 2010 Insulin sensitivity was assessed 4 h postexercise with a euglycemic hyperinsulinemic (40 mU.m(2).min(-1)) clamp enriched with [6,6-(2)H]glucose. Glucose 136-143 insulin Homo sapiens 0-7 20071559-0 2010 Progesterone inhibits glucose uptake by affecting diverse steps of insulin signaling in 3T3-L1 adipocytes. Glucose 22-29 insulin Homo sapiens 67-74 20237381-4 2010 SUMMARY: Chromium supplementation has been hypothesized to potentiate the actions of insulin in facilitating cellular uptake of glucose. Glucose 128-135 insulin Homo sapiens 85-92 19861158-1 2010 GH/insulin/IGF-1 signaling is a vital pathway e.g. in the regulation of protein synthesis and glucose metabolism. Glucose 94-101 insulin Homo sapiens 3-10 20074919-0 2010 Glucose-responsive composite microparticles based on chitosan, concanavalin A and dextran for insulin delivery. Glucose 0-7 insulin Homo sapiens 94-101 19656159-8 2010 Young people with normal fasting glucose and fasting insulin < or =180 pmol/l had lower insulin resistance (homeostasis model assessment median 1.9 vs. 4.2, P < 0.001), higher insulin sensitivity index (2.4 vs. 1.0, P < 0.001) and a lower early insulin response (insulinogenic index 2.5 vs. 4.1, P < 0.001) compared to those with normal fasting glucose and higher fasting insulin levels. Glucose 33-40 insulin Homo sapiens 91-98 19656159-8 2010 Young people with normal fasting glucose and fasting insulin < or =180 pmol/l had lower insulin resistance (homeostasis model assessment median 1.9 vs. 4.2, P < 0.001), higher insulin sensitivity index (2.4 vs. 1.0, P < 0.001) and a lower early insulin response (insulinogenic index 2.5 vs. 4.1, P < 0.001) compared to those with normal fasting glucose and higher fasting insulin levels. Glucose 33-40 insulin Homo sapiens 91-98 19656159-8 2010 Young people with normal fasting glucose and fasting insulin < or =180 pmol/l had lower insulin resistance (homeostasis model assessment median 1.9 vs. 4.2, P < 0.001), higher insulin sensitivity index (2.4 vs. 1.0, P < 0.001) and a lower early insulin response (insulinogenic index 2.5 vs. 4.1, P < 0.001) compared to those with normal fasting glucose and higher fasting insulin levels. Glucose 33-40 insulin Homo sapiens 91-98 19656159-8 2010 Young people with normal fasting glucose and fasting insulin < or =180 pmol/l had lower insulin resistance (homeostasis model assessment median 1.9 vs. 4.2, P < 0.001), higher insulin sensitivity index (2.4 vs. 1.0, P < 0.001) and a lower early insulin response (insulinogenic index 2.5 vs. 4.1, P < 0.001) compared to those with normal fasting glucose and higher fasting insulin levels. Glucose 33-40 insulin Homo sapiens 91-98 19656159-8 2010 Young people with normal fasting glucose and fasting insulin < or =180 pmol/l had lower insulin resistance (homeostasis model assessment median 1.9 vs. 4.2, P < 0.001), higher insulin sensitivity index (2.4 vs. 1.0, P < 0.001) and a lower early insulin response (insulinogenic index 2.5 vs. 4.1, P < 0.001) compared to those with normal fasting glucose and higher fasting insulin levels. Glucose 357-364 insulin Homo sapiens 53-60 19656159-11 2010 CONCLUSION: Fasting glucose and insulin levels should be measured in young people with insulin resistance before undertaking a time- and resource-intensive OGTT. Glucose 20-27 insulin Homo sapiens 87-94 20124887-1 2010 OBJECTIVES: To assess the effect of intensive insulin therapy on blood glucose amplitude variation and pattern irregularity in critically ill patients. Glucose 71-78 insulin Homo sapiens 46-53 20074919-1 2010 Glucose-responsive systems are very useful for self-regulated insulin delivery. Glucose 0-7 insulin Homo sapiens 62-69 20074919-8 2010 The release profiles of insulin revealed that the insulin release was in response to the glucose concentration in the medium and the glucose sensitivity was reversible. Glucose 89-96 insulin Homo sapiens 24-31 20074919-8 2010 The release profiles of insulin revealed that the insulin release was in response to the glucose concentration in the medium and the glucose sensitivity was reversible. Glucose 89-96 insulin Homo sapiens 50-57 20074919-8 2010 The release profiles of insulin revealed that the insulin release was in response to the glucose concentration in the medium and the glucose sensitivity was reversible. Glucose 133-140 insulin Homo sapiens 24-31 20336586-2 2010 GPR43 is a GPCR that has been implicated in the regulation of fatty-acid and glucose homeostasis in adipose tissue and the intestines, thus having potential therapeutic relevance in the treatment of type 2 diabetes, insulin resistance and obesity. Glucose 77-84 insulin Homo sapiens 216-223 20074919-8 2010 The release profiles of insulin revealed that the insulin release was in response to the glucose concentration in the medium and the glucose sensitivity was reversible. Glucose 133-140 insulin Homo sapiens 50-57 20033802-3 2010 The expression of ex13-13b strongly correlated with proinsulin in glucose-stimulated pancreatic islets, suggesting a potential role for this form in the development of type 2 diabetes. Glucose 66-73 insulin Homo sapiens 52-62 20067967-0 2010 Effects of intravenous glucose load on insulin secretion in patients with ketosis-prone diabetes during near-normoglycemia remission. Glucose 23-30 insulin Homo sapiens 39-46 20060192-0 2010 Effects of short-term therapy with different insulin secretagogues on glucose metabolism, lipid parameters and oxidative stress in newly diagnosed Type 2 Diabetes Mellitus. Glucose 70-77 insulin Homo sapiens 45-52 20067969-1 2010 OBJECTIVE: To determine insulin resistance and response in patients with polycystic ovary syndrome (PCOS) and normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance, and combined glucose intolerance (CGI). Glucose 117-124 insulin Homo sapiens 24-31 20097778-0 2010 Glucose levels at the site of subcutaneous insulin administration and their relationship to plasma levels. Glucose 0-7 insulin Homo sapiens 43-50 20074827-5 2010 Insulin infusion was terminated when plasma glucose reached 1.8mmol/l or when the subjects showed obvious signs of cognitive dysfunction. Glucose 44-51 insulin Homo sapiens 0-7 20097778-1 2010 OBJECTIVE: To examine insulin"s effect on the tissue glucose concentration at the site of subcutaneous insulin administration. Glucose 53-60 insulin Homo sapiens 22-29 20103707-1 2010 OBJECTIVE: Insulin-mediated glucose uptake is highly sensitive to the levels of the facilitative GLUT protein GLUT4. Glucose 28-35 insulin Homo sapiens 11-18 20097778-1 2010 OBJECTIVE: To examine insulin"s effect on the tissue glucose concentration at the site of subcutaneous insulin administration. Glucose 53-60 insulin Homo sapiens 103-110 20097778-6 2010 RESULTS: Start of insulin delivery with MD and MP catheters resulted in a decline of the tissue glucose concentration and the tissue-to-plasma glucose ratio (TPR) for approximately 60 min (P < 0.05). Glucose 96-103 insulin Homo sapiens 18-25 20107109-9 2010 CONCLUSIONS: Healthy carriers of the T-allele of TCF7L2 rs7903146 exhibit a diminished increase of insulin secretion in response to intravenous glucose to compensate for insulin resistance as induced by bed rest. Glucose 144-151 insulin Homo sapiens 99-106 20097778-8 2010 After subsequent switch to insulin-free perfusate, tissue glucose concentration and TPR increased slowly and reattained preinsulin delivery levels by the end of the experiments. Glucose 58-65 insulin Homo sapiens 27-34 20097778-9 2010 CONCLUSIONS: The results show the attainment of a stable TPR value at the site of insulin administration, thus indicating that insulin delivery and glucose sensing may be performed simultaneously at the same adipose tissue site. Glucose 148-155 insulin Homo sapiens 82-89 20226708-0 2010 Peak-time determination of post-meal glucose excursions in insulin-treated diabetic patients. Glucose 37-44 insulin Homo sapiens 59-66 20210571-14 2010 As intravenous glucose tolerance tests (IVGTTs) were performed before and after DPP-IV implementation, we were able to assess their impact on insulin secretion under fasting conditions. Glucose 15-22 insulin Homo sapiens 142-149 20380657-5 2010 Insulin stimulated glucose uptake in subcutaneous preadipocyte-derived adipocytes from both non-obese and obese patients (p < 0.001 vs. basal). Glucose 19-26 insulin Homo sapiens 0-7 20380657-1 2010 To evaluate the effect of metformin on basal and insulin-induced glucose uptake in subcutaneous and visceral preadipocyte-derived adipocytes from obese and non-obese patients, preadipocytes were obtained from subcutaneous and visceral fat depots during abdominal surgery. Glucose 65-72 insulin Homo sapiens 49-56 20380657-9 2010 Combined treatment with metformin and insulin increased glucose uptake in subcutaneous preadipocyte-derived adipocytes from both non-obese and obese patients (p < 0.001 vs. insulin alone). Glucose 56-63 insulin Homo sapiens 38-45 20382779-10 2010 As glucose tolerance declined, insulin resistance worsened. Glucose 3-10 insulin Homo sapiens 31-38 20032049-2 2010 Acute alterations in glucose levels trigger rapid changes in insulin concentration and insulin signaling. Glucose 21-28 insulin Homo sapiens 61-68 20536523-0 2010 Suspended insulin infusion during overnight closed-loop glucose control in children and adolescents with Type 1 diabetes. Glucose 56-63 insulin Homo sapiens 10-17 20536523-1 2010 AIMS: We assessed an extended interruption of subcutaneous insulin delivery during overnight closed-loop glucose control in children and adolescents with Type 1 diabetes (T1D). Glucose 105-112 insulin Homo sapiens 59-66 20536523-6 2010 When insulin delivery restarted, plasma glucose was 6.4+/-2.2 mmol/l and peaked at 7.9+/-2.1 mmol/l in 60 min (P=0.01). Glucose 40-47 insulin Homo sapiens 5-12 20536523-8 2010 CONCLUSIONS: A prolonged interruption of insulin delivery during overnight closed-loop glucose control to prevent hypoglycaemia was not associated with an increased risk of hyperglycaemia in young people with T1D. Glucose 87-94 insulin Homo sapiens 41-48 20032049-2 2010 Acute alterations in glucose levels trigger rapid changes in insulin concentration and insulin signaling. Glucose 21-28 insulin Homo sapiens 87-94 20033205-0 2010 Use of continuous glucose monitoring in normoglycemic, insulin-resistant women. Glucose 18-25 insulin Homo sapiens 55-62 20960276-1 2010 To investigate the effects of resveratrol on the secretion of NO induced by insulin in high glucose cultured primary human umbilical vein endothelial cells (HUVEC). Glucose 92-99 insulin Homo sapiens 76-83 20960276-6 2010 Compared with control cells, high glucose decreased the secretion of NO induced by insulin. Glucose 34-41 insulin Homo sapiens 83-90 20204442-11 2010 Insulin secretion in response to glucose was not impaired after isolation and purification. Glucose 33-40 insulin Homo sapiens 0-7 20960276-10 2010 Resveratrol can improve the NO stimulating function of insulin in high glucose cultured HUVEC in SIRT1-dependent manner. Glucose 71-78 insulin Homo sapiens 55-62 20885773-4 2010 Insulin, released with increases in blood glucose promotes glucose uptake into the cells. Glucose 42-49 insulin Homo sapiens 0-7 20885773-4 2010 Insulin, released with increases in blood glucose promotes glucose uptake into the cells. Glucose 59-66 insulin Homo sapiens 0-7 20885773-5 2010 In response to glucose changes, pancreatic alpha-, beta-, and delta-cells regulate their electrical activity and Ca(2+) signals to release glucagon, insulin, and somatostatin, respectively. Glucose 15-22 insulin Homo sapiens 149-156 20885774-1 2010 Pancreatic beta-cells release insulin in response to increased glucose levels. Glucose 63-70 insulin Homo sapiens 30-37 20885774-2 2010 Compared to isolated beta-cells, beta-cells embedded within the islets of Langerhans network exhibit a coordinated and greater insulin secretion response to glucose. Glucose 157-164 insulin Homo sapiens 127-134 20110544-5 2010 As expected, the insulin response to meal ingestion was lower in HF than AF participants (insulin area under the curve(0-120): 2,314 +/- 171 vs. 4,028 +/- 460 microIU x ml(-1) x 120(-1), HF vs. AF, P < 0.05), with similar plasma glucose responses between groups. Glucose 232-239 insulin Homo sapiens 17-24 20110547-7 2010 Forearm insulin-stimulated glucose clearance decreased significantly in the CON and LBW groups in response to bedrest; in the FDR group, clearance was very low before bedrest and no change was observed. Glucose 27-34 insulin Homo sapiens 8-15 20456732-6 2010 The future direction of insulin pump development is targeted toward closing the loop, to allow feedback control between an insulin pump and a glucose sensor, and hence finer adjustment of insulin delivery rates as required. Glucose 142-149 insulin Homo sapiens 24-31 20130077-7 2010 Insulin sensitivity index (ISI) was calculated after a 75-g oral glucose load with glucose and insulin measurements at 0, 30, 60, and 120 min. Glucose 65-72 insulin Homo sapiens 0-7 20130077-7 2010 Insulin sensitivity index (ISI) was calculated after a 75-g oral glucose load with glucose and insulin measurements at 0, 30, 60, and 120 min. Glucose 83-90 insulin Homo sapiens 0-7 19955252-2 2010 It is postulated that alterations in the insulin-signalling pathway and subsequent glucose disposal are the underlying cause of insulin resistance in patients with GDM. Glucose 83-90 insulin Homo sapiens 41-48 19955252-2 2010 It is postulated that alterations in the insulin-signalling pathway and subsequent glucose disposal are the underlying cause of insulin resistance in patients with GDM. Glucose 83-90 insulin Homo sapiens 128-135 20156067-1 2010 BACKGROUND: Obese women with polycystic ovary syndrome (PCOS) manifest impaired insulin-stimulated release of a d-chiro-inositol-containing inositolphosphoglycan (DCI-IPG) insulin mediator during oral glucose tolerance testing (OGTT), which appears to be restored by the administration of metformin. Glucose 201-208 insulin Homo sapiens 80-87 21264119-4 2010 Decreased plasma glucose level and increased plasma insulin in normal and STZ-induced diabetic rat suggested the probable absorption of insulin through GI tract when insulin was administered by mixing with DG extract. Glucose 17-24 insulin Homo sapiens 136-143 21264119-4 2010 Decreased plasma glucose level and increased plasma insulin in normal and STZ-induced diabetic rat suggested the probable absorption of insulin through GI tract when insulin was administered by mixing with DG extract. Glucose 17-24 insulin Homo sapiens 136-143 19846393-2 2010 METHODS: Pre-diabetes and an insulin sensitivity index were estimated by an oral glucose tolerance test in 66 consecutive uraemic patients, without diabetes, being on the waiting list for the first renal transplantation. Glucose 81-88 insulin Homo sapiens 29-36 20428418-2 2010 Systemic insulin administration results in a reduction in circulating free fatty acids and an improvement in myocardial glucose uptake, which causes an efficiency improvement in the myocardial cell. Glucose 120-127 insulin Homo sapiens 9-16 19902270-4 2010 In addition, GH regulates substrate metabolism in muscle and in particular antagonizes insulin-stimulated glucose disposal. Glucose 106-113 insulin Homo sapiens 87-94 19902270-8 2010 Understanding the mechanisms whereby GH antagonizes insulin-stimulated glucose disposal in muscle is an important future research field with implications for a variety of clinical conditions ranging from malnutrition to obesity and type 2 diabetes. Glucose 71-78 insulin Homo sapiens 52-59 20102299-1 2010 BACKGROUND: The standard frequently-sampled intravenous glucose tolerance test (FSIVGTT) is an alternative procedure to the clamp technique for estimating the insulin sensitivity (Si) parameter. Glucose 56-63 insulin Homo sapiens 159-166 20102299-11 2010 The short protocol may give less acceptable results for insulin sensitivity in individuals who have normal glucose tolerance but high BMI. Glucose 107-114 insulin Homo sapiens 56-63 19501608-1 2010 This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H(2)O(2), act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Glucose 93-100 insulin Homo sapiens 191-198 20513276-4 2010 Insulin resistance was defined as HOMA index (fasting glucose in mmol/L x fasting insulin in mU/L/22.5) in the top quartile of the studied population. Glucose 54-61 insulin Homo sapiens 0-7 19501608-1 2010 This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H(2)O(2), act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Glucose 172-179 insulin Homo sapiens 191-198 20176932-0 2010 Insulin enhances glucose-stimulated insulin secretion in healthy humans. Glucose 17-24 insulin Homo sapiens 0-7 21811521-3 2010 Also, insulin resistance is generally considered to be of major importance in the pathophysiology of type 2 diabetes mellitus given that glucose intolerance and insulin resistance precede the development of overt diabetes, these factors would be associated with arterial stiffness. Glucose 137-144 insulin Homo sapiens 6-13 20085539-1 2010 Insulin stimulates glucose transport in fat and skeletal muscle cells primarily by inducing the translocation of GLUT4 (glucose transporter isoform 4) to the PM (plasma membrane) from specialized GSVs (GLUT4 storage vesicles). Glucose 19-26 insulin Homo sapiens 0-7 20085539-2 2010 Glycosphingolipids are components of membrane microdomains and are involved in insulin-regulated glucose transport. Glucose 97-104 insulin Homo sapiens 79-86 20176932-0 2010 Insulin enhances glucose-stimulated insulin secretion in healthy humans. Glucose 17-24 insulin Homo sapiens 36-43 20176932-2 2010 Recent evidence from rodents in vivo and from islets isolated from rodents or humans suggests that the insulin signaling pathway is physiologically important for glucose sensing. Glucose 162-169 insulin Homo sapiens 103-110 19962391-2 2010 The main goal of AEP is to replace the pancreatic insulin secretion in the blood glucose regulation loop by means of an automatic exogenous insulin infusion. Glucose 81-88 insulin Homo sapiens 50-57 20176932-6 2010 Preexposure to exogenous insulin increased the endogenous insulin secretory response to glucose by approximately 40%. Glucose 88-95 insulin Homo sapiens 25-32 19962391-6 2010 The inclusion of mathematical models of relations between glucose and chosen biosignals in the control loop generates an adequate insulin infusion pattern to compensate blood glucose variations during each metabolic scenario. Glucose 58-65 insulin Homo sapiens 130-137 20176932-6 2010 Preexposure to exogenous insulin increased the endogenous insulin secretory response to glucose by approximately 40%. Glucose 88-95 insulin Homo sapiens 58-65 19962391-6 2010 The inclusion of mathematical models of relations between glucose and chosen biosignals in the control loop generates an adequate insulin infusion pattern to compensate blood glucose variations during each metabolic scenario. Glucose 175-182 insulin Homo sapiens 130-137 20176932-9 2010 These studies demonstrate that insulin potentiates glucose-stimulated insulin secretion in vivo in healthy humans. Glucose 51-58 insulin Homo sapiens 31-38 20176932-9 2010 These studies demonstrate that insulin potentiates glucose-stimulated insulin secretion in vivo in healthy humans. Glucose 51-58 insulin Homo sapiens 70-77 20234779-3 2010 Many individuals with diabetes rely on subcutaneous insulin administration by injection or continuous infusion to control glucose levels. Glucose 122-129 insulin Homo sapiens 52-59 19996389-1 2010 Atypical protein kinase C (aPKC) isoforms mediate insulin effects on glucose transport in muscle and adipose tissues and lipid synthesis in liver and support other metabolic processes, expression of enzymes needed for islet insulin secretion and hepatic glucose production/release, CNS appetite suppression, and inflammatory responses. Glucose 69-76 insulin Homo sapiens 50-57 19904628-4 2010 In this study we evaluated body composition, glucose, and insulin responses to an oral glucose tolerance test and serum adipokines levels in 28 volunteers, who had been eating a CR diet for an average of 6.9 +/- 5.5 years, (mean age 53.0 +/- 11 years), in 28 age-, sex-, and body fat-matched endurance runners (EX), and 28 age- and sex-matched sedentary controls eating Western diets (WD). Glucose 87-94 insulin Homo sapiens 58-65 19996389-1 2010 Atypical protein kinase C (aPKC) isoforms mediate insulin effects on glucose transport in muscle and adipose tissues and lipid synthesis in liver and support other metabolic processes, expression of enzymes needed for islet insulin secretion and hepatic glucose production/release, CNS appetite suppression, and inflammatory responses. Glucose 254-261 insulin Homo sapiens 50-57 19996382-0 2010 Mammalian Tribbles homolog 3 impairs insulin action in skeletal muscle: role in glucose-induced insulin resistance. Glucose 80-87 insulin Homo sapiens 37-44 20028969-11 2010 In conclusion, low-dose intravenous insulin administered to maintain BG between 7-9 mmol/l is sufficient to limit lipolysis and endogenous glucose R(a) and increase glucose R(d). Glucose 139-146 insulin Homo sapiens 36-43 20028969-11 2010 In conclusion, low-dose intravenous insulin administered to maintain BG between 7-9 mmol/l is sufficient to limit lipolysis and endogenous glucose R(a) and increase glucose R(d). Glucose 165-172 insulin Homo sapiens 36-43 20032494-3 2010 OBJECTIVE: To address this issue, we quantified insulin-mediated glucose uptake (IMGU) by using the insulin suppression test in 96 apparently healthy, nondiabetic individuals and defined its relation to fasting urine pH. Glucose 65-72 insulin Homo sapiens 48-55 20207245-8 2010 Maternal glucose levels (below diabetes mellitus) had weaker associations with preeclampsia, particularly after adjustment for fasting C-peptide and BMI. Glucose 9-16 insulin Homo sapiens 135-144 19920215-4 2010 We have previously shown that in normal glucose tolerant subjects S(I)(D) provides a more comprehensive picture of insulin action on glucose metabolism than S(I). Glucose 133-140 insulin Homo sapiens 115-122 19920215-6 2010 We analyzed insulin-modified intravenous glucose tolerance test studies performed in 10 diabetic subjects and mixed meal glucose tolerance test studies exploiting the triple tracer technique in 14 diabetic subjects. Glucose 41-48 insulin Homo sapiens 12-19 19996382-0 2010 Mammalian Tribbles homolog 3 impairs insulin action in skeletal muscle: role in glucose-induced insulin resistance. Glucose 80-87 insulin Homo sapiens 96-103 20060466-3 2010 We found that FXR activation induces positive regulatory effects on glucose-induced insulin transcription and secretion by genomic and non-genomic activities. Glucose 68-75 insulin Homo sapiens 84-91 20053958-1 2010 Type 2 diabetes has been coined "a two-hit disease," as it involves specific defects of glucose-stimulated insulin secretion from the pancreatic beta cells in addition to defects in peripheral tissue insulin action required for glucose uptake. Glucose 88-95 insulin Homo sapiens 107-114 20369755-9 2010 Some authors still recommend glucose-potassium-insulin infusions for all patients with type 1 diabetes. Glucose 29-36 insulin Homo sapiens 47-54 20060466-5 2010 Indeed, results from silencing experiments of KLF11 demonstrate that this transcription factor is essential for FXR activity on glucose-induced insulin gene transcription. Glucose 128-135 insulin Homo sapiens 144-151 20060466-9 2010 These data established that an FXR-KLF11 regulated pathway has an essential role in the regulation of insulin transcription and secretion induced by glucose. Glucose 149-156 insulin Homo sapiens 102-109 19632735-3 2010 This paper presents a composite metabolic model, "Glucosafe", that integrates models and parameters from normal physiology and accounts for the reduced rate of glucose gut absorption and saturation of insulin action in patients with reduced insulin sensitivity. Glucose 160-167 insulin Homo sapiens 241-248 20132129-12 2010 Furthermore, the results suggest that a certain level of circulating insulin is necessary to obtain sufficient stimulation of glucose uptake in the exercising muscles. Glucose 126-133 insulin Homo sapiens 69-76 20168143-1 2010 BACKGROUND: Since Van den Berghe et al published their study on tight glucose control in 2001, intensive insulin therapy (IIT) has been increasingly used for critically ill patients worldwide. Glucose 70-77 insulin Homo sapiens 105-112 19890623-9 2010 CONCLUSIONS/INTERPRETATION: In type 1 and type 2 diabetes, insulin exerts an inhibitory effect on oxidative stress, a metabolic disorder that is significantly activated by sustained hyperglycaemia and glucose variability in non-insulin-treated type 2 diabetes. Glucose 201-208 insulin Homo sapiens 59-66 20007942-4 2010 Estimated glucose disposal rate (eGDR) (milligrams per kilogram per minute; a lower eGDR indicates greater insulin resistance) was calculated using A1C, waist circumference, and hypertension status. Glucose 10-17 insulin Homo sapiens 107-114 20007940-1 2010 OBJECTIVE The American Diabetes Association advocates insulin regimens for youth with type 1 diabetes that involve adjusting insulin dose based on carbohydrate intake and blood glucose level. Glucose 177-184 insulin Homo sapiens 54-61 20007940-1 2010 OBJECTIVE The American Diabetes Association advocates insulin regimens for youth with type 1 diabetes that involve adjusting insulin dose based on carbohydrate intake and blood glucose level. Glucose 177-184 insulin Homo sapiens 125-132 20009096-4 2010 In a multivariate model, the best predictors of adulthood glucose homeostasis variables were the change in BMI Z score from childhood to adulthood and childhood BMI Z score, followed by the corresponding childhood levels of glucose, insulin, and HOMA-IR. Glucose 58-65 insulin Homo sapiens 233-240 20028948-7 2010 Suppression of insulin-stimulated endogenous glucose production improved in both groups (-64%; P < 0.01 in control subjects and -52% in diabetic subjects; P < 0.01). Glucose 45-52 insulin Homo sapiens 15-22 20028948-11 2010 Insulin-mediated glucose disposal and metabolic flexibility improved in type 2 diabetic subjects in the face of near-significantly increased IMCL content. Glucose 17-24 insulin Homo sapiens 0-7 20032279-3 2010 Glucose excursions between 1330 and 1700 h were defined as relating to snacks with insulin or snacks with no insulin administered. Glucose 0-7 insulin Homo sapiens 83-90 20032280-0 2010 Estimates of insulin sensitivity using glucose and C-Peptide from the hyperglycemia and adverse pregnancy outcome glucose tolerance test. Glucose 39-46 insulin Homo sapiens 13-20 20032280-0 2010 Estimates of insulin sensitivity using glucose and C-Peptide from the hyperglycemia and adverse pregnancy outcome glucose tolerance test. Glucose 114-121 insulin Homo sapiens 13-20 20012012-3 2010 Insulin secretion and insulin sensitivity indices were derived from plasma glucose and insulin during an OGTT. Glucose 75-82 insulin Homo sapiens 0-7 20032280-1 2010 OBJECTIVE To determine if glucose and C-peptide values obtained as part of the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study could be used to estimate insulin sensitivity during late pregnancy. Glucose 26-33 insulin Homo sapiens 162-169 20012595-7 2010 Obese individuals with and without type 2 diabetes were characterised by impaired insulin-stimulated glucose disposal rates, and showed a approximately 30% higher phosphorylation of ATPsyn-beta at Tyr361 and Thr213 (within the nucleotide-binding region of ATP synthase) as well as a coordinated downregulation of ATPsyn-beta protein and other OxPhos components. Glucose 101-108 insulin Homo sapiens 82-89 20032280-7 2010 A new insulin sensitivity index was calculated using the glucose and C-peptide concentrations at 0 and 60 min to derive IS(HOMA C-pep), IS(QUICKI C-pep), and IS(OGTT C-pep). Glucose 57-64 insulin Homo sapiens 6-13 20032282-0 2010 Trends of earlier and later responses of C-peptide to oral glucose challenges with progression to type 1 diabetes in diabetes prevention trial-type 1 participants. Glucose 59-66 insulin Homo sapiens 41-50 20032282-1 2010 OBJECTIVE We studied the C-peptide response to oral glucose with progression to type 1 diabetes in Diabetes Prevention Trial-Type 1 (DPT-1) participants. Glucose 52-59 insulin Homo sapiens 25-34 20032282-10 2010 CONCLUSIONS A decreased early C-peptide response to oral glucose and an increased later response occur at least 2 years before the diagnosis of type 1 diabetes. Glucose 57-64 insulin Homo sapiens 30-39 20151766-8 2010 CONCLUSIONS: A bolus of rapid-acting insulin 20 min prior to a meal results in significantly better postprandial glucose control than when the meal insulin bolus is given just prior to the meal or 20 min after meal initiation. Glucose 113-120 insulin Homo sapiens 37-44 20040654-0 2010 Use of the site of subcutaneous insulin administration for the measurement of glucose in patients with type 1 diabetes. Glucose 78-85 insulin Homo sapiens 32-39 20040654-1 2010 OBJECTIVE To simplify and improve the treatment of patients with type 1 diabetes, we ascertained whether the site of subcutaneous insulin infusion can be used for the measurement of glucose. Glucose 182-189 insulin Homo sapiens 130-137 20040654-7 2010 Tissue glucose concentrations derived with the insulin-perfused catheter agreed well with plasma glucose levels. Glucose 7-14 insulin Homo sapiens 47-54 20040654-11 2010 CONCLUSIONS Our data suggest that estimation of plasma glucose concentrations from the glucose levels directly observed at the site of subcutaneous insulin infusion is feasible and its quality is comparable to that of estimating plasma glucose concentrations from glucose levels measured in insulin-unexposed subcutaneous tissue. Glucose 55-62 insulin Homo sapiens 148-155 20040654-11 2010 CONCLUSIONS Our data suggest that estimation of plasma glucose concentrations from the glucose levels directly observed at the site of subcutaneous insulin infusion is feasible and its quality is comparable to that of estimating plasma glucose concentrations from glucose levels measured in insulin-unexposed subcutaneous tissue. Glucose 87-94 insulin Homo sapiens 148-155 20040654-11 2010 CONCLUSIONS Our data suggest that estimation of plasma glucose concentrations from the glucose levels directly observed at the site of subcutaneous insulin infusion is feasible and its quality is comparable to that of estimating plasma glucose concentrations from glucose levels measured in insulin-unexposed subcutaneous tissue. Glucose 87-94 insulin Homo sapiens 148-155 20151998-12 2010 CONCLUSIONS: All five oral insulin formulations resulted in glucose and c-peptide reductions, where formulation 5 demonstrated the most pronounced effect on c-peptide concentration reduction. Glucose 60-67 insulin Homo sapiens 27-34 20040654-11 2010 CONCLUSIONS Our data suggest that estimation of plasma glucose concentrations from the glucose levels directly observed at the site of subcutaneous insulin infusion is feasible and its quality is comparable to that of estimating plasma glucose concentrations from glucose levels measured in insulin-unexposed subcutaneous tissue. Glucose 87-94 insulin Homo sapiens 148-155 20235101-1 2010 The elevated blood glucose following a meal is cleared by insulin-stimulated glucose entry into muscle and fat cells. Glucose 19-26 insulin Homo sapiens 58-65 20186999-0 2010 Serum gamma-glutamyltransferase levels are related to insulin sensitivity and secretion in subjects with abnormal glucose regulation. Glucose 114-121 insulin Homo sapiens 54-61 20464705-0 2010 Investigations of cellular glucose transport and its regulation under the influence of insulin in human peripheral blood lymphocytes. Glucose 27-34 insulin Homo sapiens 87-94 20122448-4 2010 The actions of insulin and IGF-I that may enhance performance include increased protein anabolism and glucose uptake and storage. Glucose 102-109 insulin Homo sapiens 15-22 20464705-1 2010 INTRODUCTION: We investigated the effects of insulin on glucose transport in human peripheral lymphocytes using flow cytometry. Glucose 56-63 insulin Homo sapiens 45-52 20464705-14 2010 CONCLUSIONS: Peripheral blood lymphocytes may become an interesting model system to study the effects of insulin on cellular glucose transport. Glucose 125-132 insulin Homo sapiens 105-112 19834875-4 2010 In all study patients, insulin infusion with the Portland Protocol was used to maintain stable blood glucose levels. Glucose 101-108 insulin Homo sapiens 23-30 20156251-0 2010 Measurement of C-peptide concentrations and responses to somatostatin, glucose infusion, and insulin resistance in horses. Glucose 71-78 insulin Homo sapiens 15-24 20156251-12 2010 C-peptide-to-insulin ratio significantly (P = 0.004) decreased during the glucose tolerance test from 3.60 + or - 1.95 prior to infusion to 1.03 + or - 0.18 during the first 20 min following dextrose administration. Glucose 74-81 insulin Homo sapiens 0-9 20156251-12 2010 C-peptide-to-insulin ratio significantly (P = 0.004) decreased during the glucose tolerance test from 3.60 + or - 1.95 prior to infusion to 1.03 + or - 0.18 during the first 20 min following dextrose administration. Glucose 191-199 insulin Homo sapiens 0-9 20156251-14 2010 CONCLUSIONS: Endogenous C-peptide secretion decreases in response to somatostatin and increases after dextrose infusion. Glucose 102-110 insulin Homo sapiens 24-33 20199368-2 2010 In that model, fasting plasma glucose and C-peptide levels are used to evaluate insulin sensitivity and beta-cell function. Glucose 30-37 insulin Homo sapiens 80-87 20127040-4 2010 2-Deoxy-D-[3H]-glucose uptake tests showed that STEAP4 promoted insulin-stimulated glucose uptake in mature human adipocytes. Glucose 15-22 insulin Homo sapiens 64-71 19342030-10 2010 CONCLUSION(S): Obesity and insulin resistance are associated with lower morning cortisol and DHEAS but increased cortisol and DHEA responses after glucose ingestion. Glucose 147-154 insulin Homo sapiens 27-34 19962985-4 2010 Insulin secretion was assessed after intravenous glucose. Glucose 49-56 insulin Homo sapiens 0-7 20127040-4 2010 2-Deoxy-D-[3H]-glucose uptake tests showed that STEAP4 promoted insulin-stimulated glucose uptake in mature human adipocytes. Glucose 83-90 insulin Homo sapiens 64-71 21099297-8 2010 This article provides a brief summary of the evidence suggesting that, in addition to metabolically-regulated K(ATP) channels, beta-cells are equipped with a volume-regulated anion channel that is activated by glucose concentrations within the range effective in modulating electrical activity and insulin release. Glucose 210-217 insulin Homo sapiens 298-305 21099302-8 2010 Islets isolated from Trif-(/)- mice have impaired glucose-stimulated insulin secretion, with a diminished first-phase insulin response to glucose. Glucose 50-57 insulin Homo sapiens 69-76 20187822-9 2010 This form of insulin administration may allow more control of glucose kinetics in these patients. Glucose 62-69 insulin Homo sapiens 13-20 19940230-8 2010 An additional control mechanism of insulin on glucose production improved the description of the data. Glucose 46-53 insulin Homo sapiens 35-42 20307399-8 2010 RESULTS: Alpha-glucosidase inhibitors (1.25), metformin (2.20), and thiazolidinediones (TZDs; 1.25-1.32) demonstrate a greater effect on glucose supply (SD ratio >1), while secretagogues (0.69-0.81), basal insulins (0.77-0.79), and bolus insulins (0.62-0.67) demonstrate a greater effect on insulin demand (SD ratio <1). Glucose 137-144 insulin Homo sapiens 209-216 20307400-2 2010 In the article entitled "Glucose Supply and Insulin Demand Dynamics of Antidiabetic Agents" in this issue of Journal of Diabetes Science and Technology, we presented data for a pharmacokinetic/pharmacodynamic model that characterizes the effect of conventional antidiabetic therapies on the glucose supply and insulin demand dynamic. Glucose 25-32 insulin Homo sapiens 310-317 20307400-2 2010 In the article entitled "Glucose Supply and Insulin Demand Dynamics of Antidiabetic Agents" in this issue of Journal of Diabetes Science and Technology, we presented data for a pharmacokinetic/pharmacodynamic model that characterizes the effect of conventional antidiabetic therapies on the glucose supply and insulin demand dynamic. Glucose 291-298 insulin Homo sapiens 44-51 20676394-3 2010 The incretin effect was measured as the difference in insulin levels in response to oral glucose and to an isoglycemic intravenous challenge. Glucose 89-96 insulin Homo sapiens 54-61 20515582-0 2010 Pre-mixed rapid-acting insulin 50/50 analogue twice daily is useful not only for controlling post-prandial blood glucose, but also for stabilizing the diurnal variation of blood glucose levels: switching from pre-mixed insulin 70/30 or 75/25 to pre-mixed insulin 50/50. Glucose 113-120 insulin Homo sapiens 23-30 20515582-0 2010 Pre-mixed rapid-acting insulin 50/50 analogue twice daily is useful not only for controlling post-prandial blood glucose, but also for stabilizing the diurnal variation of blood glucose levels: switching from pre-mixed insulin 70/30 or 75/25 to pre-mixed insulin 50/50. Glucose 178-185 insulin Homo sapiens 23-30 20515582-6 2010 In conclusion, switching to twice-daily Mix 50/50 insulin injections controlled post-prandial blood glucose levels and stabilized diurnal blood glucose variations in patients with type 2 diabetes mellitus who had poor glucose control on insulin 70/30 or 75/25. Glucose 100-107 insulin Homo sapiens 50-57 19952103-7 2010 Thus, in response to insulin increases in tyrosine phosphorylation of IR and insulin receptor substrate-1, downstream signaling to protein kinase B and glycogen synthase kinase 3 (GSK3) and glucose uptake were greater in cells overexpressing PKCdelta/alpha and the PKCdelta/delta domains than in cells expressing the PKCalpha/delta domains. Glucose 190-197 insulin Homo sapiens 21-28 20540435-3 2010 Under physiological circumstances K(ATP) channel closure plays a central role in glucose-stimulated insulin secretion from pancreatic beta cells. Glucose 81-88 insulin Homo sapiens 100-107 19745772-8 2010 Although insulin levels were higher in 21 hyperinsulinemic women at all times that oral glucose tolerance tests were performed, levels of glucose were also above those of 21 matched normoinsulinemic women at 1 and 2 hours and remained greater than 6.0 mmol/L at 2 hours. Glucose 88-95 insulin Homo sapiens 9-16 20004426-4 2010 The level of blood glucose was assessed by fasting plasma glucose, fasting immunoreactive insulin, homeostasis model assessment index, and hemoglobin A(1c). Glucose 19-26 insulin Homo sapiens 90-97 20011249-9 2010 In conclusion, human endometrium has the machinery for glucose uptake mediated by insulin. Glucose 55-62 insulin Homo sapiens 82-89 19500959-6 2010 Insulin sensitivity was calculated using the oral-glucose insulin-sensitivity index, and insulin secretion by C-peptide deconvolution. Glucose 50-57 insulin Homo sapiens 0-7 19841991-4 2010 All subjects underwent an oral glucose tolerance test, and insulin resistance was calculated by the homeostasis model assessment (HOMA) at baseline and by the oral glucose insulin sensitivity (OGIS) during the glucose and insulin curve. Glucose 164-171 insulin Homo sapiens 59-66 20031381-3 2010 The heart is an omnivore organ, relying on metabolic flexibility, which is compromised by the occurrence of defects in coronary flow reserve, insulin-mediated glucose disposal, and metabolic-mechanical coupling. Glucose 159-166 insulin Homo sapiens 142-149 19947956-10 2010 Those on twice daily insulin continued to have hyperglycaemia during the day whilst those on basal-bolus insulin showed a steady fall in blood glucose towards normal by the time of breaking their fast. Glucose 143-150 insulin Homo sapiens 105-112 20383938-6 2010 The in vitro release of insulin from gel network was observed spectrophotometrically which was good enough to maintain blood glucose level for six hour. Glucose 125-132 insulin Homo sapiens 24-31 22011639-8 2010 Insulin resistance indicated by increased glucose and insulin levels occurred starting 24 h postburn. Glucose 42-49 insulin Homo sapiens 0-7 20459024-6 2010 With insulin stimulation, the glucose remained in culture medium in insulin group was much lower than that in TNF-alpha group (P < 0.05). Glucose 30-37 insulin Homo sapiens 5-12 20459024-6 2010 With insulin stimulation, the glucose remained in culture medium in insulin group was much lower than that in TNF-alpha group (P < 0.05). Glucose 30-37 insulin Homo sapiens 68-75 20028975-9 2010 Finally, expression of a triple Y156F/S101A/S174A-RhoGDI mutant specifically inhibited only the second/granule mobilization phase of glucose-stimulated insulin secretion, overall supporting the integration of RhoGDI into the activation cycling mechanism of glucose-responsive small GTPases. Glucose 133-140 insulin Homo sapiens 152-159 20028975-9 2010 Finally, expression of a triple Y156F/S101A/S174A-RhoGDI mutant specifically inhibited only the second/granule mobilization phase of glucose-stimulated insulin secretion, overall supporting the integration of RhoGDI into the activation cycling mechanism of glucose-responsive small GTPases. Glucose 257-264 insulin Homo sapiens 152-159 20138357-1 2010 BACKGROUND: Closed-loop systems link continuous glucose measurements to insulin delivery. Glucose 48-55 insulin Homo sapiens 72-79 20005261-8 2010 In conclusion, amylin, C-peptide and proinsulin responses to glucose were unaffected by four weeks of near-normoglycaemia, whereas GLP-1 increased amylin and C-peptide secretion and amylin/C-peptide ratio. Glucose 61-68 insulin Homo sapiens 37-47 20371491-4 2010 Increased free fatty acid (FFA) concentrations in blood for 5 hours in nondiabetic, overweight subjects markedly suppressed insulin-stimulated glucose uptake and raised circulating PAI-1 concentrations, with a concomitant increase in the expression of the PAI-1 gene in adipose tissue. Glucose 143-150 insulin Homo sapiens 124-131 20641546-14 2004 GLUT4 and HKII are the major transporters and HK isoforms in skeletal, muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. Glucose 131-138 insulin Homo sapiens 114-121 20203102-7 2010 Unexpectedly, insulin-induced activation of Akt2 and glucose transporter 4 expression were reduced after chronic disruption of the mTORC1/S6K1 pathway, impairing insulin-mediated glucose uptake despite increased PI3K activation. Glucose 53-60 insulin Homo sapiens 14-21 20203102-9 2010 However, this study also shows that chronic inhibition of the mTORC1/S6K1 pathway uncouples IRS-1/PI3K signaling from insulin-induced glucose transport due to impaired activation of Akt2 and blunted glucose transporter 4 expression. Glucose 134-141 insulin Homo sapiens 118-125 20133841-1 2010 Insulin is a key protein hormone that regulates blood glucose levels and, thus, has widespread impact on lipid and protein metabolism. Glucose 54-61 insulin Homo sapiens 0-7 19897715-6 2010 Systemic insulin resistance was manifest by elevated fasting glucose and insulin, abnormal response to intravenous glucose tolerance testing, and blunted skeletal muscle phosphatidylinositol-3-kinase (PI 3-kinase) activation and protein kinase B (Akt) phosphorylation in response to insulin. Glucose 61-68 insulin Homo sapiens 9-16 19920219-1 2010 After a constant insulin infusion is initiated, determination of steady-state conditions for glucose infusion rates (GIR) typically requires >or=3 h. The glucose infusion follows a simple time-dependent rise, reaching a plateau at steady state. Glucose 157-164 insulin Homo sapiens 17-24 19897715-6 2010 Systemic insulin resistance was manifest by elevated fasting glucose and insulin, abnormal response to intravenous glucose tolerance testing, and blunted skeletal muscle phosphatidylinositol-3-kinase (PI 3-kinase) activation and protein kinase B (Akt) phosphorylation in response to insulin. Glucose 115-122 insulin Homo sapiens 9-16 19897715-7 2010 In myocardium, insulin-stimulated glucose uptake, PI 3-kinase activation, and Akt phosphorylation were also blunted in the intervention diet group. Glucose 34-41 insulin Homo sapiens 15-22 20166804-2 2010 They lower blood glucose predominantly via the stimulation of insulin release from pancreatic beta-cells. Glucose 17-24 insulin Homo sapiens 62-69 20075431-3 2010 In fish, GLUT4 also mediates insulin-regulated glucose entry into cells but differs from mammalian GLUT4 in its affinity for glucose and in protein motifs known to be important for the traffic of GLUT4. Glucose 47-54 insulin Homo sapiens 29-36 20166804-8 2010 Together these findings may provide a basis for the design of novel sulphonylureas with blood glucose-lowering activity relying on less pronounced stimulation of insulin release from pancreatic beta-cells and more pronounced insulin-independent stimulation of esterification as well as inhibition of release of fatty acids by adipocytes than provoked by the sulphonylureas currently used in therapy. Glucose 94-101 insulin Homo sapiens 162-169 20166804-8 2010 Together these findings may provide a basis for the design of novel sulphonylureas with blood glucose-lowering activity relying on less pronounced stimulation of insulin release from pancreatic beta-cells and more pronounced insulin-independent stimulation of esterification as well as inhibition of release of fatty acids by adipocytes than provoked by the sulphonylureas currently used in therapy. Glucose 94-101 insulin Homo sapiens 225-232 19767120-4 2010 Minimal modelling of C-peptide and insulin data provided beta-cell responsiveness to glucose perturbation (first, Phi(1), second, Phi(2), and basal, Phi(b), phase), insulin secretion rate, ISR(t) and total pre-hepatic insulin secretion, TIS, as well as insulin delivery rate, IDR(t), and total insulin delivery, TID, into plasma, over 5-h test. Glucose 85-92 insulin Homo sapiens 35-42 19767120-6 2010 In our H-group, insulin sensitivity, S(I), assessed by minimal model of glucose kinetics, showed a 56% reduction, which confirmed deterioration of insulin action in hypertension. Glucose 72-79 insulin Homo sapiens 16-23 19789438-13 2010 INTERVENTIONS: Insulin doses were calculated based on predicted serum glucose values from corrected point-of-care glucometer measurements. Glucose 70-77 insulin Homo sapiens 15-22 19789438-19 2010 CONCLUSIONS: A mathematical formula that corrects erroneous point-of-care glucose values due to anemia in intensive care unit patients reduces the prevalence of hypoglycemia during intensive insulin therapy. Glucose 74-81 insulin Homo sapiens 191-198 19809312-6 2010 Recent findings underscore the relevance of insulin resistance in mediating blunted sympathetic responsiveness to endogenous hyperinsulinemia induced by glucose ingestion. Glucose 153-160 insulin Homo sapiens 44-51 19934000-4 2010 Mathematical modeling was used to quantify insulin-secretory profiles during OGTT and glucose infusion protocols. Glucose 86-93 insulin Homo sapiens 43-50 19934000-6 2010 Dose-response curves relating insulin secretion to glucose concentrations were derived from the GGI. Glucose 51-58 insulin Homo sapiens 30-37 20103714-10 2010 RESULTS: In subjects with normal fasting glucose and impaired fasting glucose, IGF-I bioactivity progressively increased with increasing insulin resistance, peaked at fasting glucose levels just below 7.0 mmol/l, and dropped at higher glucose levels. Glucose 70-77 insulin Homo sapiens 137-144 20103714-10 2010 RESULTS: In subjects with normal fasting glucose and impaired fasting glucose, IGF-I bioactivity progressively increased with increasing insulin resistance, peaked at fasting glucose levels just below 7.0 mmol/l, and dropped at higher glucose levels. Glucose 70-77 insulin Homo sapiens 137-144 20103714-10 2010 RESULTS: In subjects with normal fasting glucose and impaired fasting glucose, IGF-I bioactivity progressively increased with increasing insulin resistance, peaked at fasting glucose levels just below 7.0 mmol/l, and dropped at higher glucose levels. Glucose 70-77 insulin Homo sapiens 137-144 20546261-12 2010 Strict control of FPG with insulin glargine was effective to control postprandial glucose excursion, but had no significant effect on sd and MAGE. Glucose 82-89 insulin Homo sapiens 27-34 19880583-5 2010 Correlation and multiple regression analyses were used to determine factors associated with maternal insulin sensitivity (IS) estimated using both OGTT-derived (IS(OGTT)) and fasting (using the homeostasis model assessment [HOMA]; IS(HOMA)) insulin and glucose concentrations. Glucose 253-260 insulin Homo sapiens 101-108 19889804-3 2010 Insulin sensitivity was estimated during an oral glucose tolerance test (OGTT) at baseline and after 9 months of lifestyle intervention and measured during the euglycemic-hyperinsulinemic clamp (n = 79). Glucose 49-56 insulin Homo sapiens 0-7 19890090-1 2010 Glucose-stimulated insulin secretion from the islet beta-cell involves a sequence of metabolic events and an interplay between a wide range of signaling pathways leading to the generation of second messengers (e.g., cyclic nucleotides, adenine and guanine nucleotides, soluble lipid messengers) and mobilization of calcium ions. Glucose 0-7 insulin Homo sapiens 19-26 19895637-5 2010 Glucose clamp studies have shown that premix analogues give serum insulin levels proportional to their percentage of rapid-acting uncomplexed insulin: the higher the proportion, the greater the maximum level reached. Glucose 0-7 insulin Homo sapiens 66-73 19895637-5 2010 Glucose clamp studies have shown that premix analogues give serum insulin levels proportional to their percentage of rapid-acting uncomplexed insulin: the higher the proportion, the greater the maximum level reached. Glucose 0-7 insulin Homo sapiens 142-149 19908022-6 2010 Conversely, PPARalpha upregulation preserved glucose-stimulated insulin secretion, essentially by increasing the response at a stimulatory concentration of glucose (15 mmol/l), a protection we also observed in human islets. Glucose 45-52 insulin Homo sapiens 64-71 19908022-6 2010 Conversely, PPARalpha upregulation preserved glucose-stimulated insulin secretion, essentially by increasing the response at a stimulatory concentration of glucose (15 mmol/l), a protection we also observed in human islets. Glucose 156-163 insulin Homo sapiens 64-71 19931932-5 2010 The level of blood glucose was assessed by fasting plasma glucose (FPG), fasting immunoreactive insulin (F-IRI), homeostasis model assessment (HOMA) index, and Hemoglobin A1c (HbA1c). Glucose 19-26 insulin Homo sapiens 96-110 19966179-7 2010 Insulin sensitivity was assessed using iv glucose tolerance tests. Glucose 42-49 insulin Homo sapiens 0-7 20022932-9 2010 Similarly, COX-2 inhibition impaired insulin-stimulated Akt phosphorylation and 2-deoxy-D-[(14)C]glucose uptake in palmitate-exposed skeletal muscle cells, and this effect was abolished in the presence of PGE(2). Glucose 97-104 insulin Homo sapiens 37-44 20056832-9 2010 Autocrine insulin signaling partly accounted for the effects of glucose on ERK phosphorylation. Glucose 64-71 insulin Homo sapiens 10-17 20105039-0 2010 Comparison of the post-meal glucose response to different insulin bolus waveforms in insulin pump- and pre-meal pramlintide-treated type 1 diabetes patients. Glucose 28-35 insulin Homo sapiens 58-65 20105039-0 2010 Comparison of the post-meal glucose response to different insulin bolus waveforms in insulin pump- and pre-meal pramlintide-treated type 1 diabetes patients. Glucose 28-35 insulin Homo sapiens 85-92 20105039-1 2010 BACKGROUND: Both pramlintide and insulin pump waveforms separately provide improved post-meal glucose control. Glucose 94-101 insulin Homo sapiens 33-40 20105041-1 2010 BACKGROUND: Lack of first-phase insulin (INS) secretion is regarded as causative for high postprandial glucose excursions in subjects with type 2 diabetes. Glucose 103-110 insulin Homo sapiens 32-39 19897566-8 2010 In contrast, there was a significant interaction of training and hypoxia (P < 0.05) on glucose metabolism, as follows: plasma insulin and glucose concentrations were significantly increased; glucose metabolic clearance rate was decreased; and the insulin to glucagon ratio was increased after training in the HYP group. Glucose 90-97 insulin Homo sapiens 129-136 19897566-8 2010 In contrast, there was a significant interaction of training and hypoxia (P < 0.05) on glucose metabolism, as follows: plasma insulin and glucose concentrations were significantly increased; glucose metabolic clearance rate was decreased; and the insulin to glucagon ratio was increased after training in the HYP group. Glucose 90-97 insulin Homo sapiens 250-257 19862665-9 2010 Short-term (60-240 min) stimulation of HUVECs with high glucose increased COUP-TFII expression independent of insulin. Glucose 56-63 insulin Homo sapiens 110-117 20377657-7 2010 This paradox has created a need for new technology that will facilitate optimal glucose control by recommending appropriate insulin doses while decreasing the risk of hypoglycaemia. Glucose 80-87 insulin Homo sapiens 124-131 19940100-0 2010 Leucine modulates contraction- and insulin-stimulated glucose transport and upstream signaling events in rat skeletal muscle. Glucose 54-61 insulin Homo sapiens 35-42 19940100-2 2010 We investigated the effects of leucine on contraction- and insulin-stimulated glucose transport in isolated rat epitrochlearis muscle in vitro. Glucose 78-85 insulin Homo sapiens 59-66 19362017-10 2010 CONCLUSIONS: The divided insulin dose regimen that specifically targets the risk factors for prereperfusion hyperkalemia is associated with significantly lower prereperfusion potassium and pre- and postreperfusion glucose levels and provides a useful alternative to the conventional large-bolus method in management of intraoperative hyperkalemia during liver transplantation. Glucose 214-221 insulin Homo sapiens 25-32 19765783-7 2010 5-Aminoimidazole-4-carboxamide 1-beta-d-ribonucleoside and insulin increased glucose transport rate 1.5-fold (P < .05) and 1.7-fold (P < .01) in isolated muscle strips, respectively. Glucose 77-84 insulin Homo sapiens 59-66 20081857-0 2010 Genetic variation in GIPR influences the glucose and insulin responses to an oral glucose challenge. Glucose 82-89 insulin Homo sapiens 53-60 19661962-2 2010 The objectives of this study were to assess the relationships between (i) maternal insulin sensitivity and glucose tolerance status in pregnancy and (ii) early infant weight gain and adiposity in the first year of life. Glucose 107-114 insulin Homo sapiens 83-90 19661962-9 2010 Independent of maternal glucose tolerance status, maternal insulin resistance during pregnancy is associated with increased infant weight gain and adiposity over the first year of life. Glucose 24-31 insulin Homo sapiens 59-66 19460122-10 2010 HOMA-IR and glucose-stimulated insulin levels were higher in patients with IGT than individuals with normal glucose tolerance (HOMA-IR = 4.4 +/- 2.5 vs. 3.4 +/- 2.3, p = 0.001). Glucose 12-19 insulin Homo sapiens 31-38 19460122-10 2010 HOMA-IR and glucose-stimulated insulin levels were higher in patients with IGT than individuals with normal glucose tolerance (HOMA-IR = 4.4 +/- 2.5 vs. 3.4 +/- 2.3, p = 0.001). Glucose 108-115 insulin Homo sapiens 31-38 19460122-12 2010 In multivariate analysis, age, fasting glucose, and insulin resistance influenced independently plasma glucose at 120 min of OGTT. Glucose 103-110 insulin Homo sapiens 52-59 19833727-1 2010 The pancreatic beta cell is sensitive to even small changes in PDX1 protein levels; consequently, Pdx1 haploinsufficiency can inhibit beta cell growth and decrease insulin biosynthesis and gene expression, leading to compromised glucose-stimulated insulin secretion. Glucose 229-236 insulin Homo sapiens 248-255 20098276-0 2010 Microassay for glucose-induced preproinsulin mRNA expression to assess islet functional potency for islet transplantation. Glucose 15-22 insulin Homo sapiens 31-44 20098276-2 2010 We developed a microassay that evaluates the potency of human islets by measuring changes in glucose-induced human insulin gene (INS) expression using a single islet in octuplicate samples. Glucose 93-100 insulin Homo sapiens 115-122 20098276-4 2010 Glucose-induced mature (postspliced) and premature (prespliced) insulin mRNA were quantified by reverse-transcriptase polymerase chain reaction using several insulin mRNA primers designed at different locations including, intron, exon, and an exon-intron junction. Glucose 0-7 insulin Homo sapiens 64-71 20040363-5 2010 Type 2 diabetes is associated with high blood glucose in the context of insulin resistance and relative insulin deficiency. Glucose 46-53 insulin Homo sapiens 72-79 20338842-1 2010 Pancreatic beta-cells sense the ambient blood-glucose concentration and secrete insulin to signal other tissues to take up glucose. Glucose 123-130 insulin Homo sapiens 80-87 18778861-5 2010 Skeletal muscle insulin sensitivity was assessed by intravenous glucose tolerance testing using a minimal modeling technique. Glucose 64-71 insulin Homo sapiens 16-23 20865534-7 2010 Nateglinide and Glimepiride are a class of insulin secretagog agents that lowers blood glucose levels by stimulating insulin secretion from the pancreas. Glucose 87-94 insulin Homo sapiens 43-50 20865534-7 2010 Nateglinide and Glimepiride are a class of insulin secretagog agents that lowers blood glucose levels by stimulating insulin secretion from the pancreas. Glucose 87-94 insulin Homo sapiens 117-124 21137206-2 2010 The analyses of retrospective and current sources of information about contra-insulin effect of calcitonin on the glucose metabolism has been revealed. Glucose 114-121 insulin Homo sapiens 78-85 21137206-4 2010 The impairment of glucose metabolism under calcitonin is established--hyperglycemia, insulin resistance and glucose intolerance. Glucose 18-25 insulin Homo sapiens 85-92 19923374-1 2010 BACKGROUND: The glucose-lowering effect of fat and protein is attenuated or absent in diabetic patients, which suggests that the same may occur in insulin-resistant subjects without diabetes. Glucose 16-23 insulin Homo sapiens 147-154 20714007-1 2010 Insulin resistance (IR) is a common pathophysiological condition where higher-than-normal concentrations of insulin are needed to maintain a normal glycemia and adequate glucose utilization in insulin target tissues. Glucose 170-177 insulin Homo sapiens 0-7 20714007-1 2010 Insulin resistance (IR) is a common pathophysiological condition where higher-than-normal concentrations of insulin are needed to maintain a normal glycemia and adequate glucose utilization in insulin target tissues. Glucose 170-177 insulin Homo sapiens 108-115 20714007-1 2010 Insulin resistance (IR) is a common pathophysiological condition where higher-than-normal concentrations of insulin are needed to maintain a normal glycemia and adequate glucose utilization in insulin target tissues. Glucose 170-177 insulin Homo sapiens 193-200 20134158-8 2010 This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Glucose 100-107 insulin Homo sapiens 73-80 20134158-8 2010 This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Glucose 134-141 insulin Homo sapiens 160-167 19782765-4 2010 The action of insulin is initiated by binding to its receptor and activation of the intrinsic protein tyrosine kinase activity of the receptor, resulting in the initiation of an intracellular signaling cascade that eventually leads to insulin-mediated alterations in a number of cellular processes, including an increase in glucose transport. Glucose 324-331 insulin Homo sapiens 14-21 19782765-4 2010 The action of insulin is initiated by binding to its receptor and activation of the intrinsic protein tyrosine kinase activity of the receptor, resulting in the initiation of an intracellular signaling cascade that eventually leads to insulin-mediated alterations in a number of cellular processes, including an increase in glucose transport. Glucose 324-331 insulin Homo sapiens 235-242 20606308-0 2010 Ghrelin modulates insulin sensitivity and tau phosphorylation in high glucose-induced hippocampal neurons. Glucose 70-77 insulin Homo sapiens 18-25 20606308-3 2010 The aim of this study was to investigate whether ghrelin increased high glucose-induced hippocampal neuron insulin sensitivity, and further modulated tau phosphorylation. Glucose 72-79 insulin Homo sapiens 107-114 20823563-3 2010 7-O-MA at 10 microM significantly stimulated insulin-induced glucose uptake measured by 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG) in both human hepatocellular liver carcinoma (HepG2) cells and differentiated 3T3-L1 adipocytes. Glucose 61-68 insulin Homo sapiens 45-52 20823563-5 2010 Moreover, 7-O-MA stimulated the reactivation of insulin-mediated phosphorylation of phosphatidylinositol 3-kinase (PI3K)-linked protein kinase B (Akt/PKB) and adenosine 5"-monophosphate-activated protein kinase (AMPK) in high glucose-induced, insulin-resistant HepG2 cells, and this effect was blocked by either LY294002, a PI3K inhibitor, or compound C, an AMPK inhibitor. Glucose 226-233 insulin Homo sapiens 48-55 20925278-9 2010 The average insulin sensitivity described as corrected glucose disposal (Mk) was 34.9 +/- 12.70 micromol/kg/min. Glucose 55-62 insulin Homo sapiens 12-19 20719072-4 2010 Transplantation of 5-20 million insulin-expressing porcine Sertoli cells into diabetic SCID mice significantly decreased blood glucose levels in a dose-dependent manner, with 20 million Sertoli cells decreasing blood glucose levels to 9.8 +- 2.7 mM. Glucose 127-134 insulin Homo sapiens 32-39 20719072-5 2010 Similar results were obtained when 20 million insulin-positive, BALB/c mouse Sertoli cells were transplanted; blood glucose levels dropped to 6.3 +- 2.4 mM and remained significantly lower for 5 days. Glucose 116-123 insulin Homo sapiens 46-53 20701787-13 2010 CONCLUSIONS: Patients receiving exenatide received significantly lower amounts of exogenous insulin to control plasma glucose levels. Glucose 118-125 insulin Homo sapiens 92-99 20727232-1 2010 The physiological response to blood glucose elevation is the pancreatic release of insulin, which blocks hepatic glucose production and release, and stimulates glucose uptake and storage in insulin-dependent tissues. Glucose 36-43 insulin Homo sapiens 83-90 20727232-1 2010 The physiological response to blood glucose elevation is the pancreatic release of insulin, which blocks hepatic glucose production and release, and stimulates glucose uptake and storage in insulin-dependent tissues. Glucose 36-43 insulin Homo sapiens 190-197 20727232-1 2010 The physiological response to blood glucose elevation is the pancreatic release of insulin, which blocks hepatic glucose production and release, and stimulates glucose uptake and storage in insulin-dependent tissues. Glucose 113-120 insulin Homo sapiens 83-90 20727232-1 2010 The physiological response to blood glucose elevation is the pancreatic release of insulin, which blocks hepatic glucose production and release, and stimulates glucose uptake and storage in insulin-dependent tissues. Glucose 113-120 insulin Homo sapiens 83-90 19833885-5 2010 RESULTS: Obese participants, independent of age, had reduced insulin sensitivity based on lower rates of glucose infusion during a hyperinsulinemic-euglycemic clamp. Glucose 105-112 insulin Homo sapiens 61-68 19833888-7 2010 RESULTS: Gene variants in CDC123/CAMK1D, ADAMTS9, BCL11A, and MTNR1B affected various aspects of the insulin response to glucose (all P < 6.9 x 10(-3)). Glucose 121-128 insulin Homo sapiens 101-108 19837793-8 2010 Markers of insulin resistance, particularly fasting glucose, were also positively associated with colorectal cancer risk. Glucose 52-59 insulin Homo sapiens 11-18 19846793-1 2010 OBJECTIVE: To determine how glucose control in women with GDM treated with metformin and/or insulin influenced pregnancy outcomes. Glucose 28-35 insulin Homo sapiens 92-99 19846793-9 2010 CONCLUSIONS: Glucose control in women with gestational diabetes mellitus treated with metformin and/or insulin is strongly related to outcomes. Glucose 13-20 insulin Homo sapiens 103-110 19846796-0 2010 Closed-loop insulin delivery using a subcutaneous glucose sensor and intraperitoneal insulin delivery: feasibility study testing a new model for the artificial pancreas. Glucose 50-57 insulin Homo sapiens 12-19 19846796-2 2010 We tested closed-loop intraperitoneal insulin infusion from an implanted pump driven by an subcutaneous glucose sensor via a proportional-integral-derivative (PID) algorithm. Glucose 104-111 insulin Homo sapiens 38-45 19943326-8 2010 In the obese, the insulin-mediated glucose disposal was approximately 50% lower (p < 0.03) than in controls, and it was inversely correlated with fibrinogen ASR during the clamp in both groups (r = - 0.58). Glucose 35-42 insulin Homo sapiens 18-25 19876614-0 2010 An empirical index of insulin sensitivity from short IVGTT: validation against the minimal model and glucose clamp indices in patients with different clinical characteristics. Glucose 101-108 insulin Homo sapiens 22-29 19876614-6 2010 A calculated S(I) (CS(I)) predictor, CS(I) = Alpha X K(G)/(DeltaAUC(INS)/T), was suggested, based on the calculation of the rate of glucose disappearance K(G) and the suprabasal AUC of insulin concentration DeltaAUC(INS) over T = 40 min. Glucose 132-139 insulin Homo sapiens 185-192 20924141-0 2010 Pharmacokinetic/pharmacodynamic modeling of glucose clamp effects of inhaled and subcutaneous insulin in healthy volunteers and diabetic patients. Glucose 44-51 insulin Homo sapiens 94-101 20924141-2 2010 We rationalized a model for the effects of inhaled insulin on glucose infusion rate during a euglycemic clamp study based on the mechanism of insulin action and compared parameter estimates between subcutaneous and inhaled insulin in healthy and diabetic subjects. Glucose 62-69 insulin Homo sapiens 51-58 20924141-7 2010 Insulin effects on glucose were described by an indirect response model. Glucose 19-26 insulin Homo sapiens 0-7 19756025-5 2010 Insulin resistance was defined as a homeostasis model assessment value of >3.99, based on fasting blood glucose and insulin concentrations. Glucose 107-114 insulin Homo sapiens 0-7 19834876-3 2010 In an open-label two period design, the effect of a single oral dose of 40 g of alcohol (168 ml 40% vodka) on an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT) and on endothelium-dependent (flow mediated, FMD) or endothelium-independent (glyceroltrinitrate (GTN)-induced) vasodilation of the brachial artery measured by ultrasound was studied. Glucose 161-168 insulin Homo sapiens 113-120 19815622-13 2010 The pancreatic beta cells were able to produce insulin in response to glucose and osteogenic-differentiated cells showed deposition of phosphate and calcium, demonstrating their functional capacity. Glucose 70-77 insulin Homo sapiens 47-54 19915938-3 2010 The aim of this work was to develop a method to characterize Na,K-ATPase activity in intact pancreatic beta-cells that will allow the investigation of putative Na,K-ATPase activity regulation by glucose and its possible role in insulin secretion signalling. Glucose 195-202 insulin Homo sapiens 228-235 20621207-9 2010 An insulin-dextrose infusion was indicated in 30 patients, of which 14 (46.7%) were treated according to protocol. Glucose 11-19 insulin Homo sapiens 3-10 20621207-11 2010 While an insulin-dextrose infusion was not indicated in 39 patients, 14 (35.9%) of these patients were inappropriately given insulin either as an infusion (8 patients) or according to a sliding scale (6 patients). Glucose 17-25 insulin Homo sapiens 9-16 20421697-5 2010 In AD, an age-related desynchronization of biological systems results, involving stress components, cortisol and noradrenaline, reactive oxygen species, and membrane damage as major candidates that precipitates an insulin resistant brain state (IRBS) with decreased glucose/energy metabolism and the increased formation of hyperphosphorylated tau protein and Abeta. Glucose 266-273 insulin Homo sapiens 214-221 21197403-6 2010 Furthermore, within this reconstructed network, interacting proteins which mediate the signal from insulin hormone to glucose transportation were identified using linear paths. Glucose 118-125 insulin Homo sapiens 99-106 21197403-7 2010 The identification of key components functioning in insulin action on glucose metabolism is crucial for the efforts of preventing and treating type 2 diabetes mellitus. Glucose 70-77 insulin Homo sapiens 52-59 19829142-3 2010 RESULTS: Highest glucose levels were associated with higher Killip class, lower ejection fraction and increased values of CPK, CPK-MB, troponin I, proBNP, lactic acid, leukocytes and insulin. Glucose 17-24 insulin Homo sapiens 183-190 19906788-4 2010 RESULTS: Olanzapine hampered insulin-mediated glucose disposal (by 1.3 mg x kg(-1) x min(-1)), whereas haloperidol did not have a significant effect. Glucose 46-53 insulin Homo sapiens 29-36 19906788-9 2010 CONCLUSIONS: Short-term treatment with olanzapine reduces fasting plasma free fatty acid concentrations and hampers insulin action on glucose disposal in healthy men, whereas haloperidol has less clear effects. Glucose 134-141 insulin Homo sapiens 116-123 21274335-5 2010 Two hours after glucose loading, the glucose tolerance test revealed a glucose level of 258 mg/dL, a HbA1c value of 6.8%, and an insulin level of 642.9 mIU/mL, documenting a state of insulin resistance and type 2 diabetes mellitus. Glucose 37-44 insulin Homo sapiens 183-190 21274335-5 2010 Two hours after glucose loading, the glucose tolerance test revealed a glucose level of 258 mg/dL, a HbA1c value of 6.8%, and an insulin level of 642.9 mIU/mL, documenting a state of insulin resistance and type 2 diabetes mellitus. Glucose 37-44 insulin Homo sapiens 183-190 20167176-0 2010 Continuous glucose monitoring during exercise in patients with type 1 diabetes on continuous subcutaneous insulin infusion. Glucose 11-18 insulin Homo sapiens 106-113 20167176-2 2010 The aim of this study was to assess glucose changes during and after physical exercise in patients with type 1 diabetes managed by continuous subcutaneous insulin infusion before and after a 14-day moderate or intense exercise program. Glucose 36-43 insulin Homo sapiens 155-162 20167186-9 2010 If the glucose level is high, then there will be a positive value multiplied to the weight, resulting in a positive amount of insulin to be injected. Glucose 7-14 insulin Homo sapiens 126-133 20167186-10 2010 If the user"s glucose level is low, then the weights will be multiplied by a negative value, resulting in a decrease in the overall insulin dose. Glucose 14-21 insulin Homo sapiens 132-139 20167187-1 2010 Amperometric glucose sensors have advanced the care of patients with diabetes and are being studied to control insulin delivery in the research setting. Glucose 13-20 insulin Homo sapiens 111-118 20839582-8 2010 In the ICU, it is best to use an insulin infusion protocol for glucose control. Glucose 63-70 insulin Homo sapiens 33-40 20121503-10 2010 A state of hyperinsulinaemia indicated by a low fasting glucose to insulin ratio was present, even in non-obese women with PCOS. Glucose 56-63 insulin Homo sapiens 16-23 21099306-0 2010 Targeting triglyceride/fatty acid cycling in beta-cells as a therapy for augmenting glucose-stimulated insulin secretion. Glucose 84-91 insulin Homo sapiens 103-110 21099306-1 2010 Insulin secretion from pancreatic beta-cells is triggered by signals arising from the metabolism of glucose and acting through separate initiation and amplification pathways. Glucose 100-107 insulin Homo sapiens 0-7 20377657-15 2010 Tools to help patients adjust their insulin dose at home should help in improving their glucose control. Glucose 88-95 insulin Homo sapiens 36-43 20377662-14 2010 This in turn requires that more insulin has to be applied to induce the same metabolic (blood glucose lowering) effect in patients with diabetes. Glucose 94-101 insulin Homo sapiens 32-39 19898246-5 2010 RESULTS: Insulin-stimulated peripheral glucose disposal decreased by 25% after 3 months in patients on zidovudine/lamivudine/lopinavir/ritonavir (ZDV/3TC/LPV/r) (P < 0.001) and this decreased rate persisted thereafter, followed by a transient decrease in insulin-mediated inhibition of lipolysis. Glucose 39-46 insulin Homo sapiens 9-16 19898246-5 2010 RESULTS: Insulin-stimulated peripheral glucose disposal decreased by 25% after 3 months in patients on zidovudine/lamivudine/lopinavir/ritonavir (ZDV/3TC/LPV/r) (P < 0.001) and this decreased rate persisted thereafter, followed by a transient decrease in insulin-mediated inhibition of lipolysis. Glucose 39-46 insulin Homo sapiens 258-265 20102853-9 2010 A positive association was observed between glucose and diastolic blood pressure with the intake of soft drinks/sweetened beverages, insulin concentrations and the intake of white bread, and triglyceride concentrations with the intake of added fats. Glucose 44-51 insulin Homo sapiens 133-140 19940100-9 2010 These results indicate that leucine activates contraction-stimulated glucose transport and inhibits insulin-stimulated glucose transport in skeletal muscle by activating mammalian target of rapamycin (mTOR)/p70S6K signaling. Glucose 119-126 insulin Homo sapiens 100-107 19755487-1 2010 Recent studies have discovered changes in the insulin-/IGF1 signaling affecting glucose metabolism and the molecular pathogenesis of human hepatocellular cancer. Glucose 80-87 insulin Homo sapiens 46-53 19929599-1 2010 BACKGROUND: Insulin resistance in pregnancy is consequent to the physiological adaptation necessary to provide glucose to the growing fetus. Glucose 111-118 insulin Homo sapiens 12-19 19506980-1 2010 BACKGROUND: Recently, vaspin was identified as a novel adipokine with insulin-sensitizing effects that might be implicated in endogenous glucose regulation. Glucose 137-144 insulin Homo sapiens 70-77 20158100-1 2010 The metabolic syndrome means the state of glucose intolerance caused by insulin resistance, and develops lipid abnormality and high blood pressure. Glucose 42-49 insulin Homo sapiens 72-79 19610024-5 2010 Insulin sensitivity was calculated using the composite whole body insulin sensitivity index (ISIcomp) during the oral glucose tolerance test. Glucose 118-125 insulin Homo sapiens 0-7 20337094-8 2010 Glucose-stimulated insulin secretion was expressed as stimulation index (SI). Glucose 0-7 insulin Homo sapiens 19-26 20236579-2 2010 The altered glucose homeostasis is caused by faulty insulin signal transduction, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. Glucose 12-19 insulin Homo sapiens 52-59 20236579-2 2010 The altered glucose homeostasis is caused by faulty insulin signal transduction, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. Glucose 108-115 insulin Homo sapiens 52-59 19925457-5 2010 Insulin-stimulated Ser-615 phosphorylation was abrogated by incubation with the PI3K (phosphoinositide 3-kinase) inhibitor wortmannin, infection with adenoviruses expressing a dominant-negative mutant PKB/Akt or pre-incubation with TNFalpha (tumour necrosis factor alpha), but was unaffected by high culture glucose concentrations. Glucose 308-315 insulin Homo sapiens 0-7 19965390-7 2010 Human pancreatic islets from risk allele carriers exhibited reduced granule docking and secreted less insulin in response to glucose; both effects were counteracted by pharmacological alpha(2A)AR antagonists. Glucose 125-132 insulin Homo sapiens 102-109 20217499-4 2010 In response to a glucose rise, nucleotides and metabolites are generated by mitochondria and participate, together with cytosolic calcium, to the stimulation of insulin release. Glucose 17-24 insulin Homo sapiens 161-168 20217507-8 2010 Experimental loss of TCF7L2 function in islets and polymorphisms in TCF7L2 alleles in humans impair glucose-stimulated insulin secretion, suggesting that perturbations in the Wnt signaling pathway may contribute substantially to the susceptibility for, and pathogenesis of, type 2 diabetes. Glucose 100-107 insulin Homo sapiens 119-126 19889821-8 2010 The insulin response was the same, whereas mean (+/-SEM) tissue glucose uptake was 30% higher (20.2 +/- 1.9 compared with 15.5 +/- 1.8 mL/2 h; P = 0.016) after the BA evening meal, which indicated higher peripheral insulin sensitivity (P = 0.001). Glucose 64-71 insulin Homo sapiens 215-222 20126806-2 2010 We validate the accuracy of oral glucose insulin sensitivity (OGIS) in the Chinese by comparing the OGIS120 and OGIS180, homeostasis model assessment of insulin resistance (HOMA-IR), and quantitative insulin sensitivity check index (OUICKI) with steady-state plasma glucose (SSPG) in different glucose tolerance subjects. Glucose 33-40 insulin Homo sapiens 41-48 20386078-2 2010 The aim of this study was to assess the effect on insulin sensitivity (determined by peripheral glucose uptake using a hyperinsulinaemic euglycaemic clamp) of tenofovir disoproxil fumarate (TDF) administration compared with placebo for 2 weeks in HIV-1-seronegative healthy male volunteers. Glucose 96-103 insulin Homo sapiens 50-57 20606308-10 2010 This study demonstrated that ghrelin increased insulin-stimulated neuronal glucose uptake in 25 mM or 75 mM glucose, raised insulin sensitivity, improved insulin resistance and decreased tau abnormal phosphorylation via the PI3-K/Akt-GSK pathway. Glucose 75-82 insulin Homo sapiens 47-54 20606308-10 2010 This study demonstrated that ghrelin increased insulin-stimulated neuronal glucose uptake in 25 mM or 75 mM glucose, raised insulin sensitivity, improved insulin resistance and decreased tau abnormal phosphorylation via the PI3-K/Akt-GSK pathway. Glucose 108-115 insulin Homo sapiens 47-54 19782393-8 2010 At the same time, these peptide-modified hydrogels were able to efficiently protect encapsulated cells against beta-cell specific T-lymphocytes and maintain glucose-stimulated insulin release by islet cells. Glucose 157-164 insulin Homo sapiens 176-183 20460728-2 2010 ATP-binding cassette (ABC) proteins are involved in the homeostasis of glucose and lipid in that they regulate insulin secretion and remove excess cholesterol from the body. Glucose 71-78 insulin Homo sapiens 111-118 21391351-1 2010 BACKGROUND: The disposition index represents insulin secretion related to the degree of insulin sensitivity, being constant for given degree of glucose tolerance. Glucose 144-151 insulin Homo sapiens 45-52 21391351-1 2010 BACKGROUND: The disposition index represents insulin secretion related to the degree of insulin sensitivity, being constant for given degree of glucose tolerance. Glucose 144-151 insulin Homo sapiens 88-95 19473183-7 2010 OUTCOME MEASURES: Insulin sensitivity and insulin secretion were measured by the frequently sampled intravenous glucose tolerance test (FSIGT) (n = 68) and homeostasis model assessment (HOMA) calculations (all). Glucose 112-119 insulin Homo sapiens 18-25 20236504-1 2010 A small study in patients with severe sepsis suggested that insulin infused to normalize blood glucose levels increased forearm flow. Glucose 95-102 insulin Homo sapiens 60-67 19808892-0 2010 Combined risk allele score of eight type 2 diabetes genes is associated with reduced first-phase glucose-stimulated insulin secretion during hyperglycemic clamps. Glucose 97-104 insulin Homo sapiens 116-123 19808892-6 2010 RESULTS: The risk allele score was associated with lower first-phase glucose-stimulated insulin secretion (GSIS) (P = 7.1 x 10(-6)). Glucose 69-76 insulin Homo sapiens 88-95 19808919-8 2010 CONCLUSIONS: Both insulin sensitivity and beta-cell function predict conversion to diabetes in different ethnic groups and various states of glucose tolerance, family history of diabetes, and obesity. Glucose 141-148 insulin Homo sapiens 18-25 19808930-5 2010 Insulin suppression of hepatic glucose production was determined using in vivo clamp techniques. Glucose 31-38 insulin Homo sapiens 0-7 19808930-7 2010 There was a strong correlation between hepatic glucose production suppression under low-dose insulin infusion and early-phase glucose excursions from the oral glucose tolerance test (r = -0.83; P < 0.001) in women with abdominal obesity, but not in women without (r = 0.44; P < 0.11). Glucose 47-54 insulin Homo sapiens 93-100 19808930-7 2010 There was a strong correlation between hepatic glucose production suppression under low-dose insulin infusion and early-phase glucose excursions from the oral glucose tolerance test (r = -0.83; P < 0.001) in women with abdominal obesity, but not in women without (r = 0.44; P < 0.11). Glucose 126-133 insulin Homo sapiens 93-100 19808930-7 2010 There was a strong correlation between hepatic glucose production suppression under low-dose insulin infusion and early-phase glucose excursions from the oral glucose tolerance test (r = -0.83; P < 0.001) in women with abdominal obesity, but not in women without (r = 0.44; P < 0.11). Glucose 126-133 insulin Homo sapiens 93-100 20460912-7 2010 Once fatty, the liver is resistant to the actions of insulin to inhibit both production of glucose and very-low-density lipoprotein, which results in mild hyperglycemia, compensatory hyperinsulinemia and hypertriglyceridemia. Glucose 91-98 insulin Homo sapiens 53-60 20460913-2 2010 Insulin resistance, the pathogenic driver of the metabolic syndrome, refers to a constellation of features such as overweight/obesity, glucose intolerance, dyslipidemia and hypertension, all of which are important risk factors for cardiovascular disease (CVD). Glucose 135-142 insulin Homo sapiens 0-7 20151762-11 2010 We founded a significant decrease in glycated hemoglobin HbA1c and insulin resistance measured using rate constant for plasma glucose disappearance (kITT) showed only a borderline decrease. Glucose 126-133 insulin Homo sapiens 67-74 20001427-8 2010 WHAT THE READER WILL GAIN: The reader is presented with evidence discussing the importance of postprandial hyperglycaemia and studies comparing different insulin regimes and in particular insulin analogue mix 50 and its potential to reduce postprandial glucose surges and reduce cardiovascular disease. Glucose 253-260 insulin Homo sapiens 154-161 20422863-7 2010 The postoperative course was uneventful and his blood glucose level had been controlled carefully with insulin formulation. Glucose 54-61 insulin Homo sapiens 103-110 20431277-6 2010 Multiple linear regression analysis showed that maternal fat mass explained 36% of the variation in insulin resistance, accounting for 62% of the variation in glucose production. Glucose 159-166 insulin Homo sapiens 100-107 20431277-9 2010 CONCLUSION: Fetal weight is dependent on maternal glucose production, which is in turn determined by the degree of insulin resistance, induced in part by the maternal fat mass. Glucose 50-57 insulin Homo sapiens 115-122 20414467-9 2010 The observed increase of serum IGF-1 and insulin-to-glucose ratio indicates that sleep restriction may result in an increased risk to develop type 2 diabetes. Glucose 52-59 insulin Homo sapiens 41-48 21099291-5 2010 In parallel, we also investigated the subcellular localization of polypyrimidine tract-binding protein 1 (PTBP1), whose nucleocytoplasmic translocation is involved in the rapid posttranscriptional up-regulation of insulin biosynthesis following islet stimulation with glucose and GLP-1. Glucose 268-275 insulin Homo sapiens 214-221 21099295-2 2010 Under hyperglycemic conditions, glucose enters the cell, generates ATP, leading to a subsequent closure of voltage-dependent ATP channels, membrane depolarization, Ca2(+) entry and exocytosis of insulin vesicles. Glucose 32-39 insulin Homo sapiens 195-202 19861722-2 2010 Activation of the GLP-1 receptor potentiates the synthesis and release of insulin from pancreatic beta-cells in a glucose-dependent manner. Glucose 114-121 insulin Homo sapiens 74-81 20445742-1 2010 Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Glucose 84-91 insulin Homo sapiens 0-7 20445742-1 2010 Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Glucose 84-91 insulin Homo sapiens 65-72 20445742-1 2010 Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Glucose 211-218 insulin Homo sapiens 0-7 20141689-8 2010 Insulin resistance was calculated from fasting plasma glucose and serum insulin levels, using homeostatic model assessment of insulin resistance (HOMA-IR). Glucose 54-61 insulin Homo sapiens 0-7 19770178-4 2010 Current theories of T2DM include a defect in insulin-mediated glucose uptake in muscle, a dysfunction of the pancreatic beta-cells, a disruption of secretory function of adipocytes, and an impaired insulin action in liver. Glucose 62-69 insulin Homo sapiens 45-52 20700410-7 2010 Insulin resistance was estimated from fasting insulin and glucose using the homeostatic model assessment method (i.e., HOMA) and was log-transformed. Glucose 58-65 insulin Homo sapiens 0-7 20010968-6 2010 The pathophysiology of diabetes mellitus in HH is thought to be due primarily to defects in the early insulin response to glucose. Glucose 122-129 insulin Homo sapiens 102-109 19766271-12 2010 Serum RBP4 appears to identify age-induced insulin resistance by physiologic changes due to aging or menopause and by increasing hepatic glucose production. Glucose 137-144 insulin Homo sapiens 43-50 20005465-1 2010 BACKGROUND: After discovery of insulin as a hypoglycemic agent in 1921 various routes of administration to control blood glucose were attempted. Glucose 121-128 insulin Homo sapiens 31-38 20336517-8 2010 The secretion of insulin and C-peptide by these cells corresponded to the variations in glucose levels. Glucose 88-95 insulin Homo sapiens 17-24 21603183-1 2010 BACKGROUND: Many insulin sensitivity (SI) tests identify a sensitivity metric that is proportional to the total available insulin and measured glucose disposal despite general acceptance that insulin action is saturable. Glucose 143-150 insulin Homo sapiens 17-24 24345621-2 2010 METHODS: Insulin resistance was assessed using the homeostasis model assessment for insulin resistance (HOMA-R) and was calculated as "Fasting plasma glucose x Fasting serum insulin)/405". Glucose 150-157 insulin Homo sapiens 9-16 21686295-2 2010 Rosiglitazone is an insulin-sensitizing agent used to control blood glucose levels in patients with type 2 diabetes. Glucose 68-75 insulin Homo sapiens 20-27 22039395-5 2010 Insulin sensitivity was assessed via intravenous glucose tolerance test. Glucose 49-56 insulin Homo sapiens 0-7 19666117-2 2010 While insulin alone produces a substantial reduction in blood-glucose levels and is thus the mainstay of treating type-1 diabetes, today"s peroral agents used in treating type-2 diabetes struggle to achieve satisfactory clinical results in the absence of endogenous or exogeneous insulin. Glucose 62-69 insulin Homo sapiens 6-13 21447273-2 2010 Calculation of prandial insulin dose is a complex process employing many variant factors such as pre-prandial glucose and carbohydrate (CHO) levels, glucose index, insulin to CHO ratio (ICR) and active insulin. Glucose 110-117 insulin Homo sapiens 24-31 21447273-2 2010 Calculation of prandial insulin dose is a complex process employing many variant factors such as pre-prandial glucose and carbohydrate (CHO) levels, glucose index, insulin to CHO ratio (ICR) and active insulin. Glucose 149-156 insulin Homo sapiens 24-31 21447273-3 2010 Bolus calculators are very effective in controlling blood glucose level in patients treated with continuous subcutaneous insulin infusion (CSII). Glucose 58-65 insulin Homo sapiens 121-128 19505210-0 2010 Glucose-sensitive gel rheology of dextran-concanavalin A mixtures suitable for self-regulating insulin delivery. Glucose 0-7 insulin Homo sapiens 95-102 19666117-4 2010 In fact, short-term insulin therapy appears to result in long-term improvement in blood-glucose control, especially when administered in early stages of type-2 diabetes. Glucose 88-95 insulin Homo sapiens 20-27 21812215-12 2010 If the insulin dosage is too high, the increase in muscular assimilation, combined with the shutdown of liver glucose production, may result in a severe hypoglycemia. Glucose 110-117 insulin Homo sapiens 7-14 20107299-3 2010 Insulin offers flexibility to address varying glucose levels and therefore is the preferred therapy to achieve recommended targets and manage hyperglycemia. Glucose 46-53 insulin Homo sapiens 0-7 20107299-4 2010 Traditional sliding-scale insulin regimens often ineffectively control blood glucose levels as they are unable to mimic physiologic insulin secretion. Glucose 77-84 insulin Homo sapiens 26-33 20107299-6 2010 Critical components of these programs include addressing barriers to glycemic control, understanding varying needs of different types of patients, and developing standardized subcutaneous insulin orders to achieve target glucose levels. Glucose 221-228 insulin Homo sapiens 188-195 20086080-6 2010 Thus, following an acute stimulus, particularly insulin or muscle contraction, specific fatty acid transporters translocate from intracellular stores to the plasma membrane to facilitate fatty acid uptake, just as these same stimuli recruit glucose transporters to increase glucose uptake. Glucose 241-248 insulin Homo sapiens 48-55 21067067-7 2010 Intensive insulin therapy appeared to lower blood glucose levels by ameliorating insulin sensitivity and stimulation of glucose uptake in skeletal muscle, whereas hepatic insulin resistance was not affected. Glucose 50-57 insulin Homo sapiens 10-17 21067067-7 2010 Intensive insulin therapy appeared to lower blood glucose levels by ameliorating insulin sensitivity and stimulation of glucose uptake in skeletal muscle, whereas hepatic insulin resistance was not affected. Glucose 120-127 insulin Homo sapiens 10-17 21067067-7 2010 Intensive insulin therapy appeared to lower blood glucose levels by ameliorating insulin sensitivity and stimulation of glucose uptake in skeletal muscle, whereas hepatic insulin resistance was not affected. Glucose 50-57 insulin Homo sapiens 81-88 21094896-1 2010 The insulin secretory response to a meal results largely from glucose stimulation of the pancreatic islets and both direct and indirect (autonomic) glucose-dependent stimulation by incretin hormones released from the gastrointestinal tract. Glucose 62-69 insulin Homo sapiens 4-11 21094908-2 2010 This is achieved either directly through Wnt receptors, or indirectly through the action of incretins, hormones that enhance glucose-stimulated insulin secretion and target extrapancreatic organs that cooperatively control whole body energy balance. Glucose 125-132 insulin Homo sapiens 144-151 21094896-1 2010 The insulin secretory response to a meal results largely from glucose stimulation of the pancreatic islets and both direct and indirect (autonomic) glucose-dependent stimulation by incretin hormones released from the gastrointestinal tract. Glucose 148-155 insulin Homo sapiens 4-11 20356474-11 2010 (2) Fasting insulin as well as 30 min and 120 min insulin levels after oral glucose tolerance test and insulin area under the curve in the metformin group were significantly reduced after 4 and 8 weeks of treatment as compared with those of baseline (P < 0.05 and P < 0.01). Glucose 76-83 insulin Homo sapiens 50-57 20356474-11 2010 (2) Fasting insulin as well as 30 min and 120 min insulin levels after oral glucose tolerance test and insulin area under the curve in the metformin group were significantly reduced after 4 and 8 weeks of treatment as compared with those of baseline (P < 0.05 and P < 0.01). Glucose 76-83 insulin Homo sapiens 50-57 20356475-7 2010 The multiples of the peak level and the base level of insulin secretion in the groups of newly diagnosed diabetes were significantly lower than those in the groups of normal glucose tolerance with and without family history (P < 0.05). Glucose 174-181 insulin Homo sapiens 54-61 20356475-9 2010 (3) The multiples of the peak level and the base level of insulin secretion in normal glucose tolerance group with family history of diabetes were 20.8% lower than those in the group without family history, being 7.27 and 9.18 respectively (P < 0.05). Glucose 86-93 insulin Homo sapiens 58-65 20551594-1 2010 Pancreatic beta-cells play a central role in the maintenance glucose homeostasis by secreting insulin, a key hormone that regulates blood glucose levels. Glucose 61-68 insulin Homo sapiens 94-101 20356475-12 2010 (5) When the normal glucose tolerance subjects with family history of diabetes progressed to suffer from diabetes, the multiples of the peak level and the base level of insulin secretion declined 43.6% (P < 0.05) more than those in the subjects still with normal glucose tolerance without family history. Glucose 20-27 insulin Homo sapiens 169-176 20356475-12 2010 (5) When the normal glucose tolerance subjects with family history of diabetes progressed to suffer from diabetes, the multiples of the peak level and the base level of insulin secretion declined 43.6% (P < 0.05) more than those in the subjects still with normal glucose tolerance without family history. Glucose 266-273 insulin Homo sapiens 169-176 20148062-0 2009 DISTq: An Iterative Analysis of Glucose Data for Low-Cost, Real-Time and Accurate Estimation of Insulin Sensitivity. Glucose 32-39 insulin Homo sapiens 96-103 20018749-4 2009 Exposure to IL-1beta in fasting glucose activated multiple protein kinases that associate with the insulin gene promoter and transiently increased insulin gene transcription in beta cells. Glucose 32-39 insulin Homo sapiens 99-106 20018749-4 2009 Exposure to IL-1beta in fasting glucose activated multiple protein kinases that associate with the insulin gene promoter and transiently increased insulin gene transcription in beta cells. Glucose 32-39 insulin Homo sapiens 147-154 20041157-1 2009 BACKGROUND: Intramyocellular lipid accumulation is strongly related to insulin resistance in humans, and we have shown that high glucose concentration induced de novo lipogenesis and insulin resistance in murin muscle cells. Glucose 129-136 insulin Homo sapiens 71-78 20041157-1 2009 BACKGROUND: Intramyocellular lipid accumulation is strongly related to insulin resistance in humans, and we have shown that high glucose concentration induced de novo lipogenesis and insulin resistance in murin muscle cells. Glucose 129-136 insulin Homo sapiens 183-190 20041157-8 2009 Stimulation of the Wnt/beta-catenin pathway i) drastically decreased SREBP-1c protein and intramyocellular lipid deposition in myotubes; ii) increased basal glucose transport in both insulin-sensitive and insulin-resistant myotubes through a differential activation of Akt and AMPK pathways; iii) restored insulin sensitivity in insulin-resistant myotubes. Glucose 157-164 insulin Homo sapiens 183-190 27713238-1 2009 Insulin, besides its glucose lowering effects, is involved in the modulation of lifespan, aging and memory and learning processes. Glucose 21-28 insulin Homo sapiens 0-7 21437134-7 2009 RESULTS: Maximal reductions of plasma glucose and glucagon plus exacerbated insulin rises were significantly greater throughout the oral glucose plus amantadine test than those registered throughout the oral glucose plus placebo challenge. Glucose 137-144 insulin Homo sapiens 76-83 21437134-7 2009 RESULTS: Maximal reductions of plasma glucose and glucagon plus exacerbated insulin rises were significantly greater throughout the oral glucose plus amantadine test than those registered throughout the oral glucose plus placebo challenge. Glucose 137-144 insulin Homo sapiens 76-83 19738036-0 2009 Short-term prednisone use antagonizes insulin"s anabolic effect on muscle protein and glucose metabolism in young healthy people. Glucose 86-93 insulin Homo sapiens 38-45 19738036-7 2009 Insulin infusion increased leg glucose uptake in both trials but was 65% lower with Pred than with placebo. Glucose 31-38 insulin Homo sapiens 0-7 19826103-9 2009 FEN improved insulin action on glucose uptake and glycogen levels in muscle, insulin-stimulated suppression of hepatic glucose production, and suppression of serum FFA levels in HFD mice. Glucose 31-38 insulin Homo sapiens 13-20 19826103-9 2009 FEN improved insulin action on glucose uptake and glycogen levels in muscle, insulin-stimulated suppression of hepatic glucose production, and suppression of serum FFA levels in HFD mice. Glucose 119-126 insulin Homo sapiens 77-84 19489690-4 2009 AGEs represent a heterogeneous group of chemical products resulting from a nonenzymatic reaction between reducing sugars and proteins, lipids, nucleic acids, or a combination of these.The glycation process (glucose fixation) affects circulating proteins (serum albumin, lipoprotein, insulin, hemoglobin),whereas the formation of AGEs implicates reactive intermediates such as methylglyoxal. Glucose 207-214 insulin Homo sapiens 283-290 19535078-2 2009 Skeletal muscles are responsible for approximately 75% of insulin stimulated whole body glucose disposal and therefore insulin resistance could underlie the relation between muscle mass and CVD. Glucose 88-95 insulin Homo sapiens 58-65 20108577-3 2009 Central insulin resistance, defined as increased hepatic gluconeogenesis and glucose output despite abundant endogenous insulin levels, appears pivotal to the occurrence of stress hyperglycaemia. Glucose 77-84 insulin Homo sapiens 8-15 20108577-6 2009 Significantly increased noninsulin-mediated glucose transport into the skeletal muscle overrules defective insulin-mediated glucose transport. Glucose 44-51 insulin Homo sapiens 27-34 20108577-6 2009 Significantly increased noninsulin-mediated glucose transport into the skeletal muscle overrules defective insulin-mediated glucose transport. Glucose 124-131 insulin Homo sapiens 27-34 20108577-8 2009 Still, exogenous insulin administration normalises blood glucose levels in this setting. Glucose 57-64 insulin Homo sapiens 17-24 20108577-10 2009 During prolonged critical illness, therapeutic insulin effects seem mediated by increased skeletal muscle glucose uptake and use. Glucose 106-113 insulin Homo sapiens 47-54 18848759-2 2009 Initial glucose levels ranging between 270 and 600 mg/dL decreased to 60-160 mg/dL following insulin, pharmacologic or dietary treatment. Glucose 8-15 insulin Homo sapiens 93-100 19966492-6 2009 The percent minimum reductions of the blood glucose concentration (%MRBG) produced by the insulin microcrystal powder and by an insulin solution reached 40.4% and 33.4% of the initial glucose levels respectively, and their bioavailability relative to subcutaneous injection (F) was 15% and 10% respectively. Glucose 44-51 insulin Homo sapiens 90-97 19966492-6 2009 The percent minimum reductions of the blood glucose concentration (%MRBG) produced by the insulin microcrystal powder and by an insulin solution reached 40.4% and 33.4% of the initial glucose levels respectively, and their bioavailability relative to subcutaneous injection (F) was 15% and 10% respectively. Glucose 184-191 insulin Homo sapiens 90-97 19622194-2 2009 The present study investigates mechanisms involved in the interaction between oleate and palmitate on insulin-stimulated glucose uptake by L6 skeletal muscle cells. Glucose 121-128 insulin Homo sapiens 102-109 19622194-4 2009 Insulin-stimulated glucose uptake, measured by uptake of 2-deoxy-d-[3H]glucose, was almost completely prevented by 300 microm-palmitate. Glucose 19-26 insulin Homo sapiens 0-7 19622194-5 2009 Cells incubated with oleate up to 750 micromol/l maintained a significant increase in insulin-stimulated glucose uptake. Glucose 105-112 insulin Homo sapiens 86-93 19622194-6 2009 Co-incubation of 50-300 microm-oleate with 300 microm-palmitate partially prevented the decrease in insulin-stimulated glucose uptake associated with palmitate. Glucose 119-126 insulin Homo sapiens 100-107 19765648-1 2009 Insulin stimulates trafficking of GLUT4 to the cell surface for glucose uptake into target cells, and phosphorylation of Ser703 of the Na+/H+ exchanger NHE1, which activates proton efflux. Glucose 64-71 insulin Homo sapiens 0-7 19765648-5 2009 In contrast, both NHE1 phosphorylation and insulin-stimulated uptake of glucose into 3T3-L1 adipocytes were blocked by inhibitors of the N-terminal kinase domain of p90RSK, namely BI-D1870 and SL0101, but not the FMK inhibitor of the C-terminal kinase domain of p90RSK, though in our hands FMK did not inhibit p90RSK in 3T3-L1 adipocytes. Glucose 72-79 insulin Homo sapiens 43-50 19952300-4 2009 The glucose-lowering properties of insulin and sulfonylureas are well known but they are also associated with weight gain. Glucose 4-11 insulin Homo sapiens 35-42 19821654-7 2009 Significantly lower plasma glucose levels were observed with BIAsp 30 post-dinner (BIAsp 30 - insulin glargine = -0.52 mmol/L, 95% CI [-1.02; -0.03], p = 0.04) and at bedtime (BIAsp 30 - insulin glargine = -0.78 mmol/L, 95% CI [-1.25; -0.31], p < 0.01). Glucose 27-34 insulin Homo sapiens 94-101 19821654-7 2009 Significantly lower plasma glucose levels were observed with BIAsp 30 post-dinner (BIAsp 30 - insulin glargine = -0.52 mmol/L, 95% CI [-1.02; -0.03], p = 0.04) and at bedtime (BIAsp 30 - insulin glargine = -0.78 mmol/L, 95% CI [-1.25; -0.31], p < 0.01). Glucose 27-34 insulin Homo sapiens 187-194 19720789-8 2009 Insulin resistance induced by bed rest was fully accounted for by the impairment of nonoxidative glucose metabolism in both groups (overall P < 0.001). Glucose 97-104 insulin Homo sapiens 0-7 19802603-1 2009 AIMS/HYPOTHESIS: The aim of the present study was to estimate the heritability of the beta cell insulin response to glucose and to glucose combined with glucagon-like peptide-1 (GLP-1) or with GLP-1 plus arginine. Glucose 116-123 insulin Homo sapiens 96-103 19802603-7 2009 RESULTS: The heritability of insulin levels in response to glucose was 52% and 77% for the first and second phase, respectively, 53% in response to glucose + GLP-1 and 80% in response to an additional arginine bolus. Glucose 59-66 insulin Homo sapiens 29-36 19802603-7 2009 RESULTS: The heritability of insulin levels in response to glucose was 52% and 77% for the first and second phase, respectively, 53% in response to glucose + GLP-1 and 80% in response to an additional arginine bolus. Glucose 148-155 insulin Homo sapiens 29-36 19802603-8 2009 Insulin responses to the administration of glucose, glucose + GLP-1 and glucose + GLP-1 + arginine were highly correlated (0.62< r <0.79). Glucose 43-50 insulin Homo sapiens 0-7 19802603-8 2009 Insulin responses to the administration of glucose, glucose + GLP-1 and glucose + GLP-1 + arginine were highly correlated (0.62< r <0.79). Glucose 52-59 insulin Homo sapiens 0-7 19802603-8 2009 Insulin responses to the administration of glucose, glucose + GLP-1 and glucose + GLP-1 + arginine were highly correlated (0.62< r <0.79). Glucose 52-59 insulin Homo sapiens 0-7 19878258-3 2009 The incretin hormones, such as glucagon-like peptide-1 (GLP-1), induce the glucose-dependent secretion of insulin, improve beta-cell function and induce slowing of gastric emptying and feelings of satiety - which result in reduced food intake and weight loss. Glucose 75-82 insulin Homo sapiens 106-113 20001676-0 2009 Responses to continuous glucose monitoring in subjects with type 1 diabetes using continuous subcutaneous insulin infusion or multiple daily injections. Glucose 24-31 insulin Homo sapiens 106-113 20001683-12 2009 CONCLUSIONS: The newly derived equation provides a better approximation than the CHO counting method of insulin secretion due to metabolized blood glucose energy from ingested carbohydrates for those without diabetes. Glucose 147-154 insulin Homo sapiens 104-111 20002470-2 2009 Recently, the demonstration of a hyperbolic relationship between indices of insulin secretion and insulin sensitivity derived from the oral glucose tolerance test (OGTT) has led to the introduction of two novel OGTT-based measures of B-cell function analogous to the disposition index: (i) the insulin secretion-sensitivity index-2 (ISSI-2) (defined as the ratio of the area-under-the-insulin-curve to the area-under-the-glucose curve, multiplied by the Matsuda index) and (ii) insulinogenic index (IGI)/fasting insulin. Glucose 140-147 insulin Homo sapiens 76-83 20002470-2 2009 Recently, the demonstration of a hyperbolic relationship between indices of insulin secretion and insulin sensitivity derived from the oral glucose tolerance test (OGTT) has led to the introduction of two novel OGTT-based measures of B-cell function analogous to the disposition index: (i) the insulin secretion-sensitivity index-2 (ISSI-2) (defined as the ratio of the area-under-the-insulin-curve to the area-under-the-glucose curve, multiplied by the Matsuda index) and (ii) insulinogenic index (IGI)/fasting insulin. Glucose 140-147 insulin Homo sapiens 98-105 20002470-2 2009 Recently, the demonstration of a hyperbolic relationship between indices of insulin secretion and insulin sensitivity derived from the oral glucose tolerance test (OGTT) has led to the introduction of two novel OGTT-based measures of B-cell function analogous to the disposition index: (i) the insulin secretion-sensitivity index-2 (ISSI-2) (defined as the ratio of the area-under-the-insulin-curve to the area-under-the-glucose curve, multiplied by the Matsuda index) and (ii) insulinogenic index (IGI)/fasting insulin. Glucose 140-147 insulin Homo sapiens 98-105 20152736-6 2009 In addition, the pattern of insulin secretion in response to oral glucose changes after GBP, with recovery of the early phase, and post-prandial glucose levels decrease significantly. Glucose 66-73 insulin Homo sapiens 28-35 19601918-2 2009 Increased adiposity, leading to increased free fatty acids (FFAs), contributes to insulin resistance by disrupting the signal transduction pathway of insulin mediated glucose disposal, and causes impaired insulin secretion. Glucose 167-174 insulin Homo sapiens 82-89 19601918-2 2009 Increased adiposity, leading to increased free fatty acids (FFAs), contributes to insulin resistance by disrupting the signal transduction pathway of insulin mediated glucose disposal, and causes impaired insulin secretion. Glucose 167-174 insulin Homo sapiens 150-157 19620249-10 2009 In addition to the well-known diabetogenic effect of glucocorticoids and anti-androgens, an increasing number of targeted anti-cancer molecules may interfere with glucose metabolism acting at different levels on the signaling substrates shared by IGF-I and insulin receptors. Glucose 163-170 insulin Homo sapiens 257-264 19819962-0 2009 Glucose generates coincident insulin and somatostatin pulses and antisynchronous glucagon pulses from human pancreatic islets. Glucose 0-7 insulin Homo sapiens 29-36 19819962-6 2009 Glucose caused pronounced stimulation of average insulin and somatostatin release. Glucose 0-7 insulin Homo sapiens 49-56 19819962-9 2009 The resulting greater than 20-fold variations of the insulin to glucagon ratio might be essential for minute-to-minute regulation of the hepatic glucose production. Glucose 145-152 insulin Homo sapiens 53-60 19887572-9 2009 In contrast to TNFalpha, basal and insulin-stimulated glucose uptake and lipolysis of terminally differentiated mature adipocytes and secretion of proinflammatory cytokines were not altered in the presence of TWEAK, and nuclear factor kappa B activity was only weakly induced. Glucose 54-61 insulin Homo sapiens 35-42 19755409-8 2009 MAIN OUTCOME MEASURE: Insulin sensitivity measured by euglycemic clamp and oral glucose tolerance test. Glucose 80-87 insulin Homo sapiens 22-29 19755409-11 2009 Treatment with pioglitazone significantly improved insulin sensitivity in CAH patients (glucose infusion rate (GIR) from 28.5+/-11.6 to 38.9+/-11.0 micromol/kg per min, P=0.000, GIR in controls 46.2+/-23.4 micromol/kg per min, P<0.05 versus CAH). Glucose 88-95 insulin Homo sapiens 51-58 19708000-5 2009 Insulin sensitivity was expressed as the amount of glucose infused during the last 30 min (glucose infusion rate, GIR) in micromol/min/kg. Glucose 51-58 insulin Homo sapiens 0-7 19708000-5 2009 Insulin sensitivity was expressed as the amount of glucose infused during the last 30 min (glucose infusion rate, GIR) in micromol/min/kg. Glucose 91-98 insulin Homo sapiens 0-7 19850481-4 2009 A pre-defined dose of intravenous insulin is infused for each glucose level. Glucose 62-69 insulin Homo sapiens 34-41 19686786-6 2009 The functionality of the encapsulated and differentiated cells was confirmed by their insulin production capability, whereby on glucose challenge the insulin production by the cells differentiated within alginate beads was found to be statistically significantly higher than for the cells from conventional two-dimensional differentiation system. Glucose 128-135 insulin Homo sapiens 150-157 20021538-5 2009 Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Glucose 113-120 insulin Homo sapiens 85-92 20021538-5 2009 Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Glucose 149-156 insulin Homo sapiens 85-92 20076797-3 2009 We designed an insulin infusion protocol for aggressive glucose control and investigated its efficacy and safety. Glucose 56-63 insulin Homo sapiens 15-22 20076797-9 2009 Glucose was significantly lowered from 160+/-57 mg/dL (8.9+/-3.2 mmol/L) at admission to 93+/-28 mg/dL (5.2+/-1.6 mmol/L) during insulin infusion (p<0.05). Glucose 0-7 insulin Homo sapiens 129-136 21386197-3 2009 We used selected ion flow tube mass spectrometry to monitor the breath of eight patients with type 1 diabetes mellitus during "insulin clamp" studies in which insulin and glucose were infused into patients to lower blood glucose levels in steps from normal values into the low glucose (hypoglycaemic) range. Glucose 221-228 insulin Homo sapiens 159-166 21386197-3 2009 We used selected ion flow tube mass spectrometry to monitor the breath of eight patients with type 1 diabetes mellitus during "insulin clamp" studies in which insulin and glucose were infused into patients to lower blood glucose levels in steps from normal values into the low glucose (hypoglycaemic) range. Glucose 221-228 insulin Homo sapiens 159-166 20700478-5 2009 insulin based on glucose measurements every 15 min. Glucose 17-24 insulin Homo sapiens 0-7 20182775-3 2009 Since O-GlcNAc serves as a glucose sensor by the way of hexosamine biosynthesis pathway, this glycosylation is often associated with glucose toxicity and development of insulin resistance. Glucose 27-34 insulin Homo sapiens 169-176 19952506-4 2009 By 30 min after intake of samples containing high glucose and high MG, the levels of plasma MG, glucose, insulin and uric acid had increased significantly, and then returned to basal levels by 120 min. Glucose 50-57 insulin Homo sapiens 105-112 19927140-1 2009 After a single bout of exercise, the ability of insulin to stimulate glucose uptake is markedly improved locally in the previously active muscles. Glucose 69-76 insulin Homo sapiens 48-55 19346115-8 2009 In H, the insulin-mediated glucose disposal (M) was approximately 25% lower, (although insignificantly) than in controls, showing no overall insulin resistance. Glucose 27-34 insulin Homo sapiens 10-17 20033363-2 2009 The current treatment of exogenous insulin supply is not fully capable of achieving tight control of glucose regulation, leading to long-term complications. Glucose 101-108 insulin Homo sapiens 35-42 19772694-3 2009 Inflammation seems to be rather central in causing damage to endothelial cells as well as exerting negative effects on glucose metabolism, ultimately leading to insulin resistance. Glucose 119-126 insulin Homo sapiens 161-168 19955549-4 2009 RESULTS: Mean blood glucose was found to be lower in patients receiving NPH every 4 hours and NPH every 6 hours than in patients receiving insulin aspart (P < .001). Glucose 20-27 insulin Homo sapiens 139-146 19963157-3 2009 We hypothesized that by suppressing endogenous insulin secretion, we could estimate the glucose absorption rate from an oral carbohydrate load and determine the effects of vinegar ingestion on this rate. Glucose 88-95 insulin Homo sapiens 47-54 19834016-14 2009 CONCLUSIONS: Insulin infusion for patients with acute ischemic stroke is feasible and safe using the insulin infusion protocol in the Glucose Regulation in Acute Stroke Patients (GRASP) trial. Glucose 134-141 insulin Homo sapiens 13-20 19628039-10 2009 Similarly, tacrolimus is also capable of blocking the glucose-stimulated secretion of insulin by MIN6 cells. Glucose 54-61 insulin Homo sapiens 86-93 20001333-4 2009 METHODS: Prospective study of 220 consecutive patients (February, 2003-March, 2006) who received an infusion of insulin for glucose control for >24 h by protocol. Glucose 124-131 insulin Homo sapiens 112-119 19566440-3 2009 However, upon exposure to several streptozotocin (STZ) concentrations, CM showed glucose-stimulated insulin release recovery and an increased synthesis of insulin mRNA. Glucose 81-88 insulin Homo sapiens 100-107 19245309-5 2009 ELISA analyses showed that the transduced cells secreted increasing amount of insulin in response to increasing concentration of glucose. Glucose 129-136 insulin Homo sapiens 78-85 20081678-3 2009 Congenital hyperinsulinism is characterized by the presence of insulin that is inappropriately high for the concentration of blood glucose. Glucose 131-138 insulin Homo sapiens 16-23 19797055-0 2009 Tight coupling between glucose and mitochondrial metabolism in clonal beta-cells is required for robust insulin secretion. Glucose 23-30 insulin Homo sapiens 104-111 19922417-4 2009 NO* synthesis is essential for vasodilation, the maintenance of blood pressure and glucose uptake and, thus, if levels of NO* are decreased, insulin resistance and hypertension will result. Glucose 83-90 insulin Homo sapiens 141-148 19797055-1 2009 The biochemical mechanisms underlying glucose-stimulated insulin secretion from pancreatic beta-cells are not completely understood. Glucose 38-45 insulin Homo sapiens 57-64 19797055-2 2009 To identify metabolic disturbances in beta-cells that impair glucose-stimulated insulin secretion, we compared two INS-1-derived clonal beta-cell lines, which are glucose-responsive (832/13 cells) or glucose-unresponsive (832/2 cells). Glucose 61-68 insulin Homo sapiens 80-87 19797055-4 2009 We found that despite a marked impairment of glucose-stimulated insulin secretion, 832/2 cells exhibited a higher rate of glycolysis. Glucose 45-52 insulin Homo sapiens 64-71 19797055-11 2009 We conclude that tight metabolic regulation enhancing mitochondrial metabolism and restricting glycolysis in 832/13 cells is required for clonal beta-cells to secrete insulin robustly in response to glucose. Glucose 199-206 insulin Homo sapiens 167-174 19716806-1 2009 Diabetes is characterized by high blood glucose which eventually impairs the secretion of insulin. Glucose 40-47 insulin Homo sapiens 90-97 19720047-3 2009 Forced expression of miR-133 decreased GLUT4 expression and reduced insulin-mediated glucose uptake in cardiomyocytes. Glucose 85-92 insulin Homo sapiens 68-75 19716806-7 2009 In conclusion, glucose-mediated inhibition of cholesterol biosynthesis perturbs lipid raft stability, resulting in a loss of syntaxin 1A from granule docking sites and inhibition of insulin secretion. Glucose 15-22 insulin Homo sapiens 182-189 19724017-6 2009 The AICAR and leptin treatments did not consistently reduce intramuscular lipids, but they did rescue palmitate oxidation and insulin-stimulated glucose transport, GLUT4 translocation, and AS160 phosphorylation. Glucose 145-152 insulin Homo sapiens 126-133 19776010-5 2009 IFNgamma induced sustained loss of insulin-stimulated glucose uptake in human adipocytes, coincident with reduced Akt phosphorylation and down-regulation of the insulin receptor, insulin receptor substrate-1, and GLUT4. Glucose 54-61 insulin Homo sapiens 35-42 19900993-6 2009 Insulin dose was adjusted aiming for a fasting plasma glucose concentration of 4.0-6.0 mmol/l. Glucose 54-61 insulin Homo sapiens 0-7 19679110-5 2009 Insulin also stimulates the translocation of GLUT4 to hippocampal plasma membranes in a time course that mirrors the increases in glucose uptake observed during the performance of hippocampal-dependent tasks. Glucose 130-137 insulin Homo sapiens 0-7 19679110-8 2009 These results demonstrate that insulin-stimulated translocation of GLUT4 to the plasma membrane in the rat hippocampus occurs via similar mechanisms as described in peripheral tissues and suggests that insulin-mediated translocation of GLUT4 may provide a mechanism through which hippocampal neurons rapidly increase glucose utilization during increases in neuronal activity associated with hippocampal-dependent learning. Glucose 317-324 insulin Homo sapiens 31-38 19679110-8 2009 These results demonstrate that insulin-stimulated translocation of GLUT4 to the plasma membrane in the rat hippocampus occurs via similar mechanisms as described in peripheral tissues and suggests that insulin-mediated translocation of GLUT4 may provide a mechanism through which hippocampal neurons rapidly increase glucose utilization during increases in neuronal activity associated with hippocampal-dependent learning. Glucose 317-324 insulin Homo sapiens 202-209 19508405-5 2009 Basal and insulin-stimulated glucose uptake, as well as glucose incorporation into glycogen, was similar in myotube cultures derived from male vs. female donors. Glucose 29-36 insulin Homo sapiens 10-17 19706785-6 2009 In a recent validation study in mice, we demonstrated that surrogates have a weaker correlation with glucose clamp estimates of insulin sensitivity/resistance than in humans. Glucose 101-108 insulin Homo sapiens 128-135 19810675-4 2009 Characterization of insulin-loaded micelles and their drug release in solutions with various glucose concentrations were further studied. Glucose 93-100 insulin Homo sapiens 20-27 19793849-10 2009 Insulin-stimulated glucose disposal (P < 0.001), insulin suppression of hepatic glucose production (P = 0.004), and postabsorptive fat oxidation (P = 0.03) improved equally in both groups after the intervention. Glucose 19-26 insulin Homo sapiens 0-7 19741193-9 2009 Under high glucose concentration conditions in the presence of insulin, migration of diabetic SV-SMC was greater than nondiabetic cells. Glucose 11-18 insulin Homo sapiens 63-70 19675138-5 2009 RESULTS: Dexamethasone decreased insulin-stimulated glucose uptake, decreased IRS1 mRNA and protein expression, and increased inactivating pSer(307) insulin receptor substrate (IRS)-1. Glucose 52-59 insulin Homo sapiens 33-40 19283340-2 2009 In cultured skeletal muscle cells, chromium augmented insulin-stimulated glucose uptake and metabolism as assessed by a reduced glucose concentration of culture medium. Glucose 73-80 insulin Homo sapiens 54-61 19283340-2 2009 In cultured skeletal muscle cells, chromium augmented insulin-stimulated glucose uptake and metabolism as assessed by a reduced glucose concentration of culture medium. Glucose 128-135 insulin Homo sapiens 54-61 19724224-3 2009 RECENT FINDINGS: Whereas normal podocytes take up glucose in response to insulin, diabetic podocytes become insulin resistant in experimental diabetic nephropathy prior to the development of significant albuminuria. Glucose 50-57 insulin Homo sapiens 73-80 19651814-4 2009 Insulin sensitivity was estimated during an oral glucose tolerance test and the euglycemic-hyperinsulinemic clamp (n = 222). Glucose 49-56 insulin Homo sapiens 0-7 19707744-7 2009 At and below plasma glucose concentrations of 3.5 mmol/l suppression of endogenous glucose production was greater with insulin detemir than with NPH insulin, whereas stimulation of peripheral glucose uptake was greater with NPH insulin than with insulin detemir. Glucose 83-90 insulin Homo sapiens 119-126 19651814-8 2009 Interestingly, insulin sensitivity (oral glucose tolerance test: P = 0.99; clamp: P = 0.32), serum C-reactive protein levels, lipids, or liver enzymes (all P > 0.14) were not different among the genotypes. Glucose 41-48 insulin Homo sapiens 15-22 19707744-7 2009 At and below plasma glucose concentrations of 3.5 mmol/l suppression of endogenous glucose production was greater with insulin detemir than with NPH insulin, whereas stimulation of peripheral glucose uptake was greater with NPH insulin than with insulin detemir. Glucose 83-90 insulin Homo sapiens 149-156 19675205-3 2009 RESEARCH DESIGN AND METHODS: We developed a standardized inpatient continuous subcutaneous insulin infusion protocol to produce a progressive fall in plasma glucose concentrations in insulin pump-treated patients. Glucose 157-164 insulin Homo sapiens 91-98 19707744-7 2009 At and below plasma glucose concentrations of 3.5 mmol/l suppression of endogenous glucose production was greater with insulin detemir than with NPH insulin, whereas stimulation of peripheral glucose uptake was greater with NPH insulin than with insulin detemir. Glucose 83-90 insulin Homo sapiens 119-126 19707744-7 2009 At and below plasma glucose concentrations of 3.5 mmol/l suppression of endogenous glucose production was greater with insulin detemir than with NPH insulin, whereas stimulation of peripheral glucose uptake was greater with NPH insulin than with insulin detemir. Glucose 83-90 insulin Homo sapiens 149-156 19675205-3 2009 RESEARCH DESIGN AND METHODS: We developed a standardized inpatient continuous subcutaneous insulin infusion protocol to produce a progressive fall in plasma glucose concentrations in insulin pump-treated patients. Glucose 157-164 insulin Homo sapiens 183-190 19817801-5 2009 It allowed studies of the regulation of insulin biosynthesis that highlighted the key role of glucose. Glucose 94-101 insulin Homo sapiens 40-47 19730809-6 2009 These alterations were reversed by aspirin treatment, in parallel with an improvement in insulin signalling and sensitivity, as measured by insulin tolerance test and glucose clamp. Glucose 167-174 insulin Homo sapiens 89-96 19546055-9 2009 CONCLUSION: Use of a simple intravenous insulin protocol can safely and effectively control the blood glucose level in patients in a non-ICU setting. Glucose 102-109 insulin Homo sapiens 40-47 19625243-9 2009 CONCLUSION: Sulfonylurea with and without use of a small dose of insulin glargine rapidly improved blood glucose levels and beta-cell function in patients with DM2. Glucose 105-112 insulin Homo sapiens 65-72 19817791-3 2009 The normal phenotype should differ from the state of overwork when beta-cells compensate for insulin resistance to keep glucose levels normal. Glucose 120-127 insulin Homo sapiens 93-100 19817800-2 2009 Glucose-stimulated insulin secretion is the principal mode of insulin secretion, and the mechanism potentiating the secretion is critical for physiological responses. Glucose 0-7 insulin Homo sapiens 19-26 19817800-2 2009 Glucose-stimulated insulin secretion is the principal mode of insulin secretion, and the mechanism potentiating the secretion is critical for physiological responses. Glucose 0-7 insulin Homo sapiens 62-69 19713424-7 2009 In all hyperandrogenic subjects and 14 controls, insulin sensitivity was measured by the glucose clamp technique. Glucose 89-96 insulin Homo sapiens 49-56 19745037-7 2009 RESULTS: Oral glucose load decreased anandamide plasma levels to an extent inversely correlated with BMI, waist circumference, subcutaneous fat, fasting insulin and total glucose, and insulin areas under the curve during the OGTT, and nonsignificantly in obese volunteers. Glucose 14-21 insulin Homo sapiens 153-160 19745037-7 2009 RESULTS: Oral glucose load decreased anandamide plasma levels to an extent inversely correlated with BMI, waist circumference, subcutaneous fat, fasting insulin and total glucose, and insulin areas under the curve during the OGTT, and nonsignificantly in obese volunteers. Glucose 14-21 insulin Homo sapiens 184-191 30780794-1 2009 Insulin sensitivity and insulin secretion are reciprocally related such that insulin resistance is adapted by increased insulin secretion to maintain normal glucose and lipid homeostasis. Glucose 157-164 insulin Homo sapiens 0-7 19723576-0 2009 Frailty in the elderly is associated with insulin resistance of glucose metabolism in the postabsorptive state only in the presence of increased abdominal fat. Glucose 64-71 insulin Homo sapiens 42-49 30780794-1 2009 Insulin sensitivity and insulin secretion are reciprocally related such that insulin resistance is adapted by increased insulin secretion to maintain normal glucose and lipid homeostasis. Glucose 157-164 insulin Homo sapiens 24-31 30780794-1 2009 Insulin sensitivity and insulin secretion are reciprocally related such that insulin resistance is adapted by increased insulin secretion to maintain normal glucose and lipid homeostasis. Glucose 157-164 insulin Homo sapiens 77-84 30780794-1 2009 Insulin sensitivity and insulin secretion are reciprocally related such that insulin resistance is adapted by increased insulin secretion to maintain normal glucose and lipid homeostasis. Glucose 157-164 insulin Homo sapiens 77-84 20090113-7 2009 It is not only maternal undernutrition that causes problems; gestational diabetes, a form of foetal overnutrition (glucose excess), is associated with increased adiposity and insulin resistance in the children, highlighting the adverse effects of the "double burden" of malnutrition in developing countries, where undernutrition and overnutrition co-exist. Glucose 115-122 insulin Homo sapiens 175-182 20090116-2 2009 During the third trimester increased maternal glucose production and insulin resistance improves fetal glucose availability. Glucose 103-110 insulin Homo sapiens 69-76 20108549-1 2009 BACKGROUND: Tight glucose control has been shown to improve the outcome of patients with severe acute illnesses who are hospitalized in intensive care units and on intravenous insulin-based regimens. Glucose 18-25 insulin Homo sapiens 176-183 19704410-5 2009 Peripheral insulin sensitivity was assessed by the euglycemic hyperinsulinemic clamp and determined as glucose disposal rate and insulin sensitivity index. Glucose 103-110 insulin Homo sapiens 11-18 19721448-1 2009 OBJECTIVE: To compare the ability of biochemical indices of insulin resistance (IR) with metabolic syndrome (MetS) classifications to predict changes in blood glucose control over a 3-year period in overweight and obese subjects. Glucose 159-166 insulin Homo sapiens 60-67 19820020-1 2009 OBJECTIVE: Proinflammatory cytokine IL-1beta is capable of decreasing insulin-induced glucose transport. Glucose 86-93 insulin Homo sapiens 70-77 19729590-3 2009 We assessed in vivo insulin action by measuring glucose tolerance (GT), insulin tolerance (IT), and insulin-assisted GT (IAGT). Glucose 48-55 insulin Homo sapiens 20-27 19814947-16 2009 CONCLUSIONS: The increase in insulin levels during olanzapine treatment may compensate for the increase in insulin resistance and serve to reduce fasting and postprandial glucose levels. Glucose 171-178 insulin Homo sapiens 29-36 19837931-1 2009 CONTEXT: Insulin-stimulated glucose disposal is impaired in obesity and type 2 diabetes mellitus (T2DM) and is tightly linked to impaired skeletal muscle glucose uptake and storage. Glucose 28-35 insulin Homo sapiens 9-16 20144377-1 2009 It is also perceived as the most important obstacle to tight glucose control using intensive insulin therapy in critically ill patients. Glucose 61-68 insulin Homo sapiens 93-100 20144377-4 2009 In the context of critical illness that limits endogenous glucose production and increases glucose utilization, inadequate nutrition, or insufficient provision of glucose, intensive insulin therapy is the most frequent cause of hypoglycemia. Glucose 58-65 insulin Homo sapiens 182-189 20144377-4 2009 In the context of critical illness that limits endogenous glucose production and increases glucose utilization, inadequate nutrition, or insufficient provision of glucose, intensive insulin therapy is the most frequent cause of hypoglycemia. Glucose 91-98 insulin Homo sapiens 182-189 20144377-4 2009 In the context of critical illness that limits endogenous glucose production and increases glucose utilization, inadequate nutrition, or insufficient provision of glucose, intensive insulin therapy is the most frequent cause of hypoglycemia. Glucose 91-98 insulin Homo sapiens 182-189 20144377-7 2009 In prospective randomized controlled studies comparing the effects of two glucose regimens, intensive insulin therapy aimed to reach strict glucose control (<110 mg/dl) but increased the incidence of severe hypoglycemia (<40 mg/dl) by four- to sixfold. Glucose 74-81 insulin Homo sapiens 102-109 20144377-7 2009 In prospective randomized controlled studies comparing the effects of two glucose regimens, intensive insulin therapy aimed to reach strict glucose control (<110 mg/dl) but increased the incidence of severe hypoglycemia (<40 mg/dl) by four- to sixfold. Glucose 140-147 insulin Homo sapiens 102-109 20144391-3 2009 Although several early studies in a mixed intensive care unit population indicated that insulin protocols aimed at strict glucose control improved outcome, later studies did not support this and, in fact, encountered increased complications due to hypoglycemia. Glucose 122-129 insulin Homo sapiens 88-95 20144400-9 2009 Fasting glucose values dropped after insulin infusion (-17.7%; p < .001). Glucose 8-15 insulin Homo sapiens 37-44 20144405-3 2009 Depending on the composition of the given meal and its glycemic index, this is an attempt to match the circulating insulin levels to the rate of glucose absorption from the gut in order to minimize postprandial glycemic excursions. Glucose 145-152 insulin Homo sapiens 115-122 19820026-1 2009 CONTEXT: Insulin action in the brain contributes to adequate regulation of body weight, neuronal survival, and suppression of endogenous glucose production. Glucose 137-144 insulin Homo sapiens 9-16 19697961-5 2009 The insulin resistance statuses were closely associated with the serum metabonomic changes in terms of glucose, fatty acid and protein/amino acid metabolisms. Glucose 103-110 insulin Homo sapiens 4-11 19556298-4 2009 In the kidney, glomerular podocytes are novel insulin-sensitive cells that have the ability to rapidly transport glucose. Glucose 113-120 insulin Homo sapiens 46-53 19443128-2 2009 Inositol phosphoglycans P-type belongs to a family of putative insulin mediators and was described to exert many insulin-like effects on lipid and glucose metabolism. Glucose 147-154 insulin Homo sapiens 63-70 19443128-2 2009 Inositol phosphoglycans P-type belongs to a family of putative insulin mediators and was described to exert many insulin-like effects on lipid and glucose metabolism. Glucose 147-154 insulin Homo sapiens 113-120 19556298-9 2009 RESULTS: We found that palmitate blocked insulin-stimulated glucose uptake in human podocytes. Glucose 60-67 insulin Homo sapiens 41-48 19849800-5 2009 Habitually short sleep durations could lead to insulin resistance by increasing sympathetic nervous system activity, raising evening cortisol levels and decreasing cerebral glucose utilization that over time could compromise beta-cell function and lead to diabetes. Glucose 173-180 insulin Homo sapiens 47-54 19557485-7 2009 CONCLUSIONS: Plasma glucose and insulin responses to oral glucose in patients with symptomatic hypoglycemia post-RYGB are minimally different when compared to individuals who remain asymptomatic, and both groups demonstrate hyperinsulinemia out of proportion to their degree of insulin sensitivity. Glucose 58-65 insulin Homo sapiens 32-39 19557485-7 2009 CONCLUSIONS: Plasma glucose and insulin responses to oral glucose in patients with symptomatic hypoglycemia post-RYGB are minimally different when compared to individuals who remain asymptomatic, and both groups demonstrate hyperinsulinemia out of proportion to their degree of insulin sensitivity. Glucose 58-65 insulin Homo sapiens 229-236 19602994-10 2009 Insulin treatment was initiated 4 hrs after the first episode of hyperglycemia was documented (median blood glucose, 11.4 mmol/L, [207 mg/dL] [9.7-14.5 mmol/L, 176-264 mg/dL]). Glucose 108-115 insulin Homo sapiens 0-7 20098797-1 2009 BACKGROUND: The homeostasis assessment model for insulin resistance (HOMA-IR) estimates insulin resistance using basal insulin and glucose values and has a good concordance with values obtained with the euglycemic clamp. Glucose 131-138 insulin Homo sapiens 49-56 20098797-1 2009 BACKGROUND: The homeostasis assessment model for insulin resistance (HOMA-IR) estimates insulin resistance using basal insulin and glucose values and has a good concordance with values obtained with the euglycemic clamp. Glucose 131-138 insulin Homo sapiens 88-95 20042050-12 2009 Human insulin was less effective at reducing blood glucose levels in rats than porcine insulin (P < 0.001). Glucose 51-58 insulin Homo sapiens 6-13 20042050-17 2009 Insulin diluent alone marginally increased blood glucose levels in all animals tested. Glucose 49-56 insulin Homo sapiens 0-7 20079327-7 2009 CONCLUSIONS: Normal glucose tolerance NAFLD patients may present with insulin resistance, mainly hepatic insulin resistance. Glucose 20-27 insulin Homo sapiens 70-77 19664593-3 2009 Therefore we investigated whether basal and insulin-stimulated (10(-6)M for 12h) glucose (2-deoxy-D-[(3)H]-glucose) uptake was affected by palmitate pre-treatment human THP-1 monocytes. Glucose 81-88 insulin Homo sapiens 44-51 19664593-4 2009 Palmitate-induced a time-dependent and concentration-dependent inhibition of insulin-stimulated glucose uptake, showing almost complete abolition of the insulin-stimulatory effect with 300 microM palmitate. Glucose 96-103 insulin Homo sapiens 77-84 19664593-6 2009 When palmitate was washed out, the inhibitory effect on insulin-stimulated glucose uptake persisted for at least 60 h. Glucose 75-82 insulin Homo sapiens 56-63 19602480-6 2009 Expression of this form in glucose-stimulated pancreatic islets correlated with expression of proinsulin (r(2) = 0.84-0.90, P < 0.00063). Glucose 27-34 insulin Homo sapiens 94-104 19807695-1 2009 With the already heightened demand placed on organ donation, stem cell therapy has become a tantalizing idea to provide glucose-responsive insulin-producing cells to Type 1 diabetic patients as an alternative to islet transplantation. Glucose 120-127 insulin Homo sapiens 139-146 19501121-4 2009 INGAP-PP treated animals had significantly higher HOMA-IR and HOMA-beta and their islets released more insulin in response to glucose; they had lower islet DNA content, significantly increased number of islets/unit area, beta-cell replication rate and mass, cells co-expressing Pdx-1/INGAP and islets in contact with ducts, and decreased beta-cell apoptosis rate. Glucose 126-133 insulin Homo sapiens 103-110 19878539-11 2009 Insulin treatment of glucose-stressed EPCs increased NO production, but did not change O2- generation and their ability to form colonies. Glucose 21-28 insulin Homo sapiens 0-7 19862325-10 2009 Analyses on the quantitative traits in the control subjects showed that THADA SNP rs7578597 was association with 2-h insulin during oral glucose tolerance tests (P = 0.0005, empirical P = 0.0090). Glucose 137-144 insulin Homo sapiens 117-124 19729450-0 2009 Cholesterol regulates glucose-stimulated insulin secretion through phosphatidylinositol 4,5-bisphosphate. Glucose 22-29 insulin Homo sapiens 41-48 19729450-1 2009 Membrane cholesterol modulates the ability of glucose to stimulate insulin secretion from pancreatic beta-cells. Glucose 46-53 insulin Homo sapiens 67-74 19729450-3 2009 Here, we show that in cultured beta-cells, cholesterol acts through phosphatidylinositol 4,5-bisphosphate (PIP(2)) to regulate actin dynamics, plasma membrane potential, and glucose-stimulated insulin secretion. Glucose 174-181 insulin Homo sapiens 193-200 19729450-4 2009 Cholesterol-overloaded beta-cells exhibited decreased PIP(2) hydrolysis, with diminished glucose-induced actin reorganization, membrane depolarization, and insulin secretion. Glucose 89-96 insulin Homo sapiens 156-163 20137268-5 2009 Insulin resistance was assessed with fasting plasma blood glucose (FBG), plasma insulin (FINS) and homeostatic model assessment of insulin resistance index (HOMA-IR). Glucose 58-65 insulin Homo sapiens 0-7 19628478-4 2009 We demonstrate that mutant huntingtin impairs glucose-stimulated insulin secretion in insulin-producing beta-cells, without altering stored levels of insulin. Glucose 46-53 insulin Homo sapiens 65-72 19628478-4 2009 We demonstrate that mutant huntingtin impairs glucose-stimulated insulin secretion in insulin-producing beta-cells, without altering stored levels of insulin. Glucose 46-53 insulin Homo sapiens 86-93 19628478-4 2009 We demonstrate that mutant huntingtin impairs glucose-stimulated insulin secretion in insulin-producing beta-cells, without altering stored levels of insulin. Glucose 46-53 insulin Homo sapiens 86-93 19647719-5 2009 Acute stimulation of cells in high glucose with insulin down-regulated PTP1B expression, slightly decreased ERK1/2 activity, and activated Akt, whereas oxidative stress up-regulated Akt and ERK1/2 phosphorylation. Glucose 35-42 insulin Homo sapiens 48-55 19647719-6 2009 In conclusion, long-term high glucose and acute oxidative stress and insulin stimulation imbalance the expression of activated kinases Akt and ERK1/2 and of dephosphorylating PTP1B in the insulin signaling pathway. Glucose 30-37 insulin Homo sapiens 188-195 19690174-0 2009 Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. Glucose 153-160 insulin Homo sapiens 172-179 19690174-5 2009 Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. Glucose 46-53 insulin Homo sapiens 65-72 19690174-6 2009 This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. Glucose 38-45 insulin Homo sapiens 96-103 20098797-1 2009 BACKGROUND: The homeostasis assessment model for insulin resistance (HOMA-IR) estimates insulin resistance using basal insulin and glucose values and has a good concordance with values obtained with the euglycemic clamp. Glucose 131-138 insulin Homo sapiens 88-95 19654285-5 2009 Insulin treatment normalized glucose levels, but plasma insulin levels were higher during insulin treatment than during insulin deprivation in T1DM and ND. Glucose 29-36 insulin Homo sapiens 0-7 19671019-3 2009 Elevated levels of fatty acids in the plasma and interstitial fluids lead to whole-body insulin resistance by disrupting normal insulin-regulated glucose uptake and glycogen storage in skeletal muscle. Glucose 146-153 insulin Homo sapiens 88-95 19671019-3 2009 Elevated levels of fatty acids in the plasma and interstitial fluids lead to whole-body insulin resistance by disrupting normal insulin-regulated glucose uptake and glycogen storage in skeletal muscle. Glucose 146-153 insulin Homo sapiens 128-135 20043611-2 2009 The insulin assay with the oral glucose tolerance provides the earliest diagnosis. Glucose 32-39 insulin Homo sapiens 4-11 19793504-3 2009 Under normal conditions, the pancreatic islet beta cells increase production of insulin sufficiently to maintain normal blood glucose concentrations despite insulin resistance. Glucose 126-133 insulin Homo sapiens 80-87 19707125-8 2009 In fact, glucose clearance in response to insulin was markedly impaired in septic mice. Glucose 9-16 insulin Homo sapiens 42-49 19669124-0 2009 A variant in the G6PC2/ABCB11 locus is associated with increased fasting plasma glucose, increased basal hepatic glucose production and increased insulin release after oral and intravenous glucose loads. Glucose 80-87 insulin Homo sapiens 146-153 19584308-5 2009 KCNQ1 expression (n = 18) and glucose-stimulated insulin secretion (n = 19) were measured in human islets from nondiabetic cadaver donors. Glucose 30-37 insulin Homo sapiens 49-56 19584308-8 2009 C-allele carriers showed reduced glucose-stimulated insulin secretion in human islets (P = 2.5 x 10(-6)). Glucose 33-40 insulin Homo sapiens 52-59 19485892-7 2009 It has been shown that insulin blocks D-glucose-increased L-arginine transport and cGMP accumulation in HUVEC, whereas in this cell type insulin also modulates high D-glucose effects by activating the transcriptional factors Sp1 and NFkappaB. Glucose 38-47 insulin Homo sapiens 23-30 19485892-7 2009 It has been shown that insulin blocks D-glucose-increased L-arginine transport and cGMP accumulation in HUVEC, whereas in this cell type insulin also modulates high D-glucose effects by activating the transcriptional factors Sp1 and NFkappaB. Glucose 165-174 insulin Homo sapiens 137-144 19485892-9 2009 Recent evidences suggest that insulin blocks the stimulatory effect of D-glucose on L-arginine transport by reducing the transcriptional activity of SLC7A1 via Sp1-, NFkappaB- and ROS-dependent mechanisms. Glucose 71-80 insulin Homo sapiens 30-37 19713099-3 2009 The major task of the fully differentiated beta-cell is the tight regulation of blood glucose levels by secreting insulin into the blood stream. Glucose 86-93 insulin Homo sapiens 114-121 19633828-8 2009 A 6 h lipid infusion into NGT individuals decreased insulin-stimulated glucose metabolism by 25% with increased TACE, decreased expression of the gene encoding TIMP3 and increased IL-6R release. Glucose 71-78 insulin Homo sapiens 52-59 19713099-4 2009 This requires molecular features to measure glucose and produce, process, and release insulin by exocytosis. Glucose 44-51 insulin Homo sapiens 86-93 19688613-5 2009 Anthropometric measures, 75 g oral glucose tolerance test (OGTT), and measurement of insulin sensitivity (insulin mediated glucose uptake; IMGU) using euglycemic hyperinsulinemic clamp technique were performed. Glucose 123-130 insulin Homo sapiens 85-92 19688613-5 2009 Anthropometric measures, 75 g oral glucose tolerance test (OGTT), and measurement of insulin sensitivity (insulin mediated glucose uptake; IMGU) using euglycemic hyperinsulinemic clamp technique were performed. Glucose 123-130 insulin Homo sapiens 106-113 19688613-8 2009 Women with glucose intolerance had higher BMI, waist circumference, free testosterone, fasting insulin, 2-h post-load insulin, total cholesterol, LDL cholesterol, triglyceride and lower sex hormone binding globulin and IMGU than women with normal glucose tolerance (NGT) (P < 0.05). Glucose 11-18 insulin Homo sapiens 95-102 19688613-8 2009 Women with glucose intolerance had higher BMI, waist circumference, free testosterone, fasting insulin, 2-h post-load insulin, total cholesterol, LDL cholesterol, triglyceride and lower sex hormone binding globulin and IMGU than women with normal glucose tolerance (NGT) (P < 0.05). Glucose 11-18 insulin Homo sapiens 118-125 19764108-1 2009 This pilot study was aimed to investigate whether there are humoral factors in serum from type 2 diabetic subjects that, in addition to glucose, insulin and free fatty acids are able to induce or contribute to peripheral insulin resistance with respect to glucose transport. Glucose 136-143 insulin Homo sapiens 221-228 19764108-1 2009 This pilot study was aimed to investigate whether there are humoral factors in serum from type 2 diabetic subjects that, in addition to glucose, insulin and free fatty acids are able to induce or contribute to peripheral insulin resistance with respect to glucose transport. Glucose 256-263 insulin Homo sapiens 145-152 19764108-1 2009 This pilot study was aimed to investigate whether there are humoral factors in serum from type 2 diabetic subjects that, in addition to glucose, insulin and free fatty acids are able to induce or contribute to peripheral insulin resistance with respect to glucose transport. Glucose 256-263 insulin Homo sapiens 221-228 19764108-4 2009 Serum from type 2 diabetic donors, compared to serum from controls, significantly reduced the maximal insulin eff ect to stimulate glucose uptake (approximately 40 %, p < 0.05) in adipocytes from control subjects, independent of surrounding glucose concentrations. Glucose 131-138 insulin Homo sapiens 102-109 19764108-7 2009 The present findings indicate the presence of biomolecules in the circulation of type 2 diabetic subjects, apart from glucose, insulin, and free fatty acids with the ability to induce peripheral insulin resistance. Glucose 118-125 insulin Homo sapiens 195-202 19647101-2 2009 Many studies have shown that intensive insulin therapy can combat insulin resistance, decrease blood glucose levels, and induce anabolic processes, thus, decreasing morbidity and mortality. Glucose 101-108 insulin Homo sapiens 39-46 20023776-9 2009 Furthermore, stimulation of insulin secretion by high glucose or acetylcholine administration to a levitated drop containing insulin-producing beta-cells resulted in inhibition of isoprenaline-induced lipolysis in adipocytes present in the same drop. Glucose 54-61 insulin Homo sapiens 28-35 20023776-9 2009 Furthermore, stimulation of insulin secretion by high glucose or acetylcholine administration to a levitated drop containing insulin-producing beta-cells resulted in inhibition of isoprenaline-induced lipolysis in adipocytes present in the same drop. Glucose 54-61 insulin Homo sapiens 125-132 19389739-0 2009 The molecular basis of insulin-stimulated glucose uptake: signalling, trafficking and potential drug targets. Glucose 42-49 insulin Homo sapiens 23-30 19389739-1 2009 The search for the underlying mechanism through which insulin regulates glucose uptake into peripheral tissues has unveiled a highly intricate network of molecules that function in concert to elicit the redistribution or "translocation" of the glucose transporter isoform GLUT4 from intracellular membranes to the cell surface. Glucose 72-79 insulin Homo sapiens 54-61 19389739-1 2009 The search for the underlying mechanism through which insulin regulates glucose uptake into peripheral tissues has unveiled a highly intricate network of molecules that function in concert to elicit the redistribution or "translocation" of the glucose transporter isoform GLUT4 from intracellular membranes to the cell surface. Glucose 244-251 insulin Homo sapiens 54-61 19901502-9 2009 CONCLUSION: The results indicate that tailored education for patients with diabetes on insulin therapy improve self-glucose test, management of insulin injection, and life style. Glucose 116-123 insulin Homo sapiens 87-94 19555970-7 2009 CONCLUSIONS: Patients with persistent MetS had accelerated fat gain, increased insulin response to oral glucose, and decreased sensitivity and beta cell function, indicators of progressively greater risk for type 2 diabetes. Glucose 104-111 insulin Homo sapiens 79-86 19602132-9 2009 During the insulin infusion, whole-body lipid oxidation was inversely correlated with insulin-stimulated glucose disposal (r=-0.48, P<0.0001), which was lower in subjects with NAFLD [3.7+/-0.2 mg/(kg fat-free mass min)] than in the control subjects [5.0+/-0.3 mg/(kg fat-free mass min), P=0.0008]. Glucose 105-112 insulin Homo sapiens 11-18 19602132-9 2009 During the insulin infusion, whole-body lipid oxidation was inversely correlated with insulin-stimulated glucose disposal (r=-0.48, P<0.0001), which was lower in subjects with NAFLD [3.7+/-0.2 mg/(kg fat-free mass min)] than in the control subjects [5.0+/-0.3 mg/(kg fat-free mass min), P=0.0008]. Glucose 105-112 insulin Homo sapiens 86-93 19654563-10 2009 RESULTS: For serum insulin levels measured after glucose application, a significant increase was determined, according to the period before glucose application (P<0.001). Glucose 49-56 insulin Homo sapiens 19-26 19654563-10 2009 RESULTS: For serum insulin levels measured after glucose application, a significant increase was determined, according to the period before glucose application (P<0.001). Glucose 140-147 insulin Homo sapiens 19-26 19686772-5 2009 When an insulin molecule docks on an adipocyte receptor, substantially fewer glucose molecules are cleared from the blood than when an insulin molecule docks on a myocyte insulin receptor. Glucose 77-84 insulin Homo sapiens 8-15 19686772-5 2009 When an insulin molecule docks on an adipocyte receptor, substantially fewer glucose molecules are cleared from the blood than when an insulin molecule docks on a myocyte insulin receptor. Glucose 77-84 insulin Homo sapiens 135-142 19686772-5 2009 When an insulin molecule docks on an adipocyte receptor, substantially fewer glucose molecules are cleared from the blood than when an insulin molecule docks on a myocyte insulin receptor. Glucose 77-84 insulin Homo sapiens 135-142 19789630-4 2009 METHODOLOGY/RESULTS: Oral and intravenous glucose stimulated insulin release (n = 849) and insulin sensitivity (n = 596) estimated from a hyperinsulinemic euglycemic clamp were measured in non-diabetic offspring of type 2 diabetic patients from five European populations. Glucose 42-49 insulin Homo sapiens 61-68 19789630-5 2009 Assuming an additive genetic model the diabetes-associated major C-allele of rs4607103 near ADAMTS9 associated with reduced insulin-stimulated glucose uptake (p = 0.002) during a hyperinsulinemic euglycemic clamp. Glucose 143-150 insulin Homo sapiens 124-131 19789630-6 2009 However, following intravenous and oral administration of glucose serum insulin release was increased in individuals with the C-allele (p = 0.003 and p = 0.01, respectively). Glucose 58-65 insulin Homo sapiens 72-79 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Glucose 232-239 insulin Homo sapiens 63-70 19738432-6 2009 There are both direct and indirect pathways by which insulin suppresses hepatic glucose production, and the indirect pathway via the hypothalamus is particularly impaired under relatively short-term overfeeding conditions, which in turn leads to compensatory enhancement of insulin signaling in the liver. Glucose 80-87 insulin Homo sapiens 53-60 19545616-4 2009 In vivo, the insulin and glucose profiles in plasma obtained by subcutaneous administration of a dose of particles containing 2 microg insulin to diabetic mice overlapped that obtained with 2 microg of insulin in solution. Glucose 25-32 insulin Homo sapiens 135-142 19725141-4 2009 In the insulin infusion algorithm, insulin is infused on the basis of its proportional and derivative actions, to blood glucose concentrations with a constant time delay. Glucose 120-127 insulin Homo sapiens 7-14 19725141-4 2009 In the insulin infusion algorithm, insulin is infused on the basis of its proportional and derivative actions, to blood glucose concentrations with a constant time delay. Glucose 120-127 insulin Homo sapiens 35-42 19023513-8 2009 Based on homeostasis model assessment (HOMA) calculations, diabetic patients had impaired beta-cell function and patients with elevated fasting glucose levels were insulin resistant. Glucose 144-151 insulin Homo sapiens 164-171 19082521-6 2009 We confirmed the significant associations of variants in CDKAL1, CDKN2B, HHEX/IDE, KCNJ11 and TCF7L2 with insulin secretion and also found associations of some of these variants with insulin sensitivity and glucose tolerance. Glucose 207-214 insulin Homo sapiens 106-113 19622787-4 2009 In this setting, increasing concentrations of amino acids dose-dependently reduced the insulin-stimulated rates of CO(2) production from glucose and palmitate (decrease in glucose oxidation induced by addition of 5.5, 11, 22, and 44 mmol/l amino acids:--16 +/- 3, -25 +/- 7, -44 +/- 4, -62 +/- 4%; P < 0.02 each). Glucose 137-144 insulin Homo sapiens 87-94 19532121-1 2009 In fat and muscle cells, insulin-stimulated glucose uptake is mainly mediated by glucose transporter 4 (GLUT4), which translocates from intracellular compartments to the cell surface in response to insulin stimulation. Glucose 44-51 insulin Homo sapiens 25-32 19532121-1 2009 In fat and muscle cells, insulin-stimulated glucose uptake is mainly mediated by glucose transporter 4 (GLUT4), which translocates from intracellular compartments to the cell surface in response to insulin stimulation. Glucose 44-51 insulin Homo sapiens 198-205 19473196-11 2009 In experiments with anti-miR-320 oligo, insulin sensitivity was increased in IR adipocytes, as evidenced by increases in p85 expression, phosphorylation of Akt and the protein expression of the glucose transporter GLUT-4, as well as insulin-stimulated glucose uptake. Glucose 194-201 insulin Homo sapiens 40-47 19721200-7 2009 Recently, many researches demonstrated that periodontitis affected diabetic condition, in which periodontal pathogen like P-LPS and TNF-alpha possibly elevated insulin resistance by inhibiting glucose incorporation into smooth muscle cells. Glucose 193-200 insulin Homo sapiens 160-167 19502541-2 2009 RESEARCH DESIGN AND METHODS: In 73 sedentary, overweight to obese, dyslipidemic individuals, insulin action was derived from a frequently sampled intravenous glucose tolerance test. Glucose 158-165 insulin Homo sapiens 93-100 19502541-7 2009 A factor containing fatty acids was inversely related to the acute insulin response to glucose (R(2) = 0.12). Glucose 87-94 insulin Homo sapiens 67-74 19565212-1 2009 AIMS/HYPOTHESIS: The aim of this prospective trial was to compare the effect of different long-acting insulin preparations injected at bedtime on glucose concentrations in patients with type 2 diabetes omitting breakfast and lunch the next day. Glucose 146-153 insulin Homo sapiens 102-109 19565212-8 2009 Symptomatic hypoglycaemia did not occur from 08:00 to 16:00 hours; glucose concentrations during this time were slightly lower with NPH insulin than with insulin detemir (p = 0.012) and insulin glargine (p = 0.049). Glucose 67-74 insulin Homo sapiens 136-143 19565212-8 2009 Symptomatic hypoglycaemia did not occur from 08:00 to 16:00 hours; glucose concentrations during this time were slightly lower with NPH insulin than with insulin detemir (p = 0.012) and insulin glargine (p = 0.049). Glucose 67-74 insulin Homo sapiens 154-161 19719704-5 2009 The IHF content was measured by proton magnetic resonance spectroscopy ((1)H-MRS), while insulin sensitivity was estimated based on fasting plasma glucose and insulin with the homestasis model assessment (HOMA) 2 method. Glucose 147-154 insulin Homo sapiens 89-96 19546347-2 2009 MC dysfunction arises from excessive glucose uptake through insulin-independent glucose transporter (GLUT1). Glucose 37-44 insulin Homo sapiens 60-67 19917185-7 2009 Insulin resistance was estimated using the HOMA-IR index based on fasting-glucose and fasting-insulin. Glucose 74-81 insulin Homo sapiens 0-7 19509102-5 2009 RESULTS: Among the 18 SNPs, rs290487 C allele was significantly associated with higher 60-, 90-, and 120-min glucose concentrations (P = 0.001, 0.01, and 0.02, respectively); higher 60- and 90-min insulin concentrations (P = 0.01 and 0.01, respectively); and a lower insulin sensitivity index (P = 0.04). Glucose 109-116 insulin Homo sapiens 197-204 19509102-5 2009 RESULTS: Among the 18 SNPs, rs290487 C allele was significantly associated with higher 60-, 90-, and 120-min glucose concentrations (P = 0.001, 0.01, and 0.02, respectively); higher 60- and 90-min insulin concentrations (P = 0.01 and 0.01, respectively); and a lower insulin sensitivity index (P = 0.04). Glucose 109-116 insulin Homo sapiens 267-274 19567513-7 2009 Nevertheless, this cytokine induced an insulin-resistant state in visceral adipocytes by impairing insulin-stimulated glucose uptake and insulin signaling at the insulin receptor substrate (IRS)-1/AKT level. Glucose 118-125 insulin Homo sapiens 39-46 19567513-7 2009 Nevertheless, this cytokine induced an insulin-resistant state in visceral adipocytes by impairing insulin-stimulated glucose uptake and insulin signaling at the insulin receptor substrate (IRS)-1/AKT level. Glucose 118-125 insulin Homo sapiens 99-106 19567513-7 2009 Nevertheless, this cytokine induced an insulin-resistant state in visceral adipocytes by impairing insulin-stimulated glucose uptake and insulin signaling at the insulin receptor substrate (IRS)-1/AKT level. Glucose 118-125 insulin Homo sapiens 99-106 19567513-9 2009 Accordingly, silencing JNK1/2 with either small interfering RNA or chemical inhibitors impaired serine phosphorylation of IRS1, restored downstream insulin signaling, and normalized insulin-induced glucose uptake in the presence of TNF-alpha. Glucose 198-205 insulin Homo sapiens 182-189 19567513-12 2009 CONCLUSIONS: TNF-alpha induces insulin resistance on glucose uptake in human visceral but not sc adipocytes, suggesting depot-specific effects of TNF-alpha on glucose uptake. Glucose 53-60 insulin Homo sapiens 31-38 19567513-12 2009 CONCLUSIONS: TNF-alpha induces insulin resistance on glucose uptake in human visceral but not sc adipocytes, suggesting depot-specific effects of TNF-alpha on glucose uptake. Glucose 159-166 insulin Homo sapiens 31-38 19567513-13 2009 Activation of JNK1/2 appears to be involved in serine phosphorylation of IRS1 and subsequently insulin resistance on glucose uptake, a state that can be reversed by liver X receptor agonists. Glucose 117-124 insulin Homo sapiens 95-102 19821760-0 2009 Capillary and venous blood glucose concentrations measured during intravenous insulin and glucose infusion: a comparison of steady and dynamic states. Glucose 27-34 insulin Homo sapiens 78-85 19821760-12 2009 As hospital insulin infusion protocols are widely implemented, healthcare providers need to be aware that glucose values may differ when blood is sampled from capillary and venous sites. Glucose 106-113 insulin Homo sapiens 12-19 19628574-4 2009 In murine and human beta-cells, LDL decreased both proliferation and maximal glucose-stimulated insulin secretion. Glucose 77-84 insulin Homo sapiens 96-103 19908933-8 2009 It is assumed that the above mentioned conditions, if persisting for a long time, might lead to decreased ability of insulin to maintain normal serum glucose level and consequently to insulin resistance which is highly prevalent in symptomatic DISH patients. Glucose 150-157 insulin Homo sapiens 117-124 19628651-13 2009 Since glucose concentration did not change in the first hour after Comb administration, our data suggest a strong improvement in insulin sensitivity. Glucose 6-13 insulin Homo sapiens 129-136 19955868-1 2009 Akt substrate of 160 kDa (called AS160 or TBC1D4) and TBC1D1, Rab GTPase-activating proteins that regulate glucose transport, become phosphorylated with exercise or insulin stimulation. Glucose 107-114 insulin Homo sapiens 165-172 19955868-2 2009 Evidence suggests that this convergence may prove to be imperfect, and each stimulus will produce a unique phosphosignature, providing a plausible mechanism for their apparently unique and overlapping roles in exercise- and insulin-stimulated glucose transport. Glucose 243-250 insulin Homo sapiens 224-231 19637187-5 2009 Insulin-mediated whole-body glucose disposal (M) and endogenous glucose production (iEGP) were assessed during euglycemic-hyperinsulinemic clamps. Glucose 28-35 insulin Homo sapiens 0-7 19497805-0 2009 Nonlinear modeling of the dynamic effects of infused insulin on glucose: comparison of compartmental with Volterra models. Glucose 64-71 insulin Homo sapiens 53-60 19497805-1 2009 This paper presents the results of a computational study that compares simulated compartmental (differential equation) and Volterra models of the dynamic effects of insulin on blood glucose concentration in humans. Glucose 182-189 insulin Homo sapiens 165-172 19291781-10 2009 Infliximab maintenance therapy has no deleterious effects on lipid profile and is accompanied by a decrease in glycemia and HbA1c concentrations, probably by reversing the impairment of tumor necrosis factor-induced insulin-mediated glucose uptake. Glucose 233-240 insulin Homo sapiens 216-223 19636533-0 2009 A prospective randomised multi-centre controlled trial on tight glucose control by intensive insulin therapy in adult intensive care units: the Glucontrol study. Glucose 64-71 insulin Homo sapiens 93-100 19680131-0 2009 The acute effects of HIV protease inhibitors on insulin suppression of glucose production in healthy HIV-negative men. Glucose 71-78 insulin Homo sapiens 48-55 19680131-1 2009 BACKGROUND: The effects of different HIV protease inhibitors (PIs) on peripheral insulin resistance have been described, but less is known about their effects on insulin suppression of endogenous glucose production (EGP). Glucose 196-203 insulin Homo sapiens 162-169 19602560-9 2009 ADRP content was negatively associated with insulin-stimulated glucose uptake (r = -0.50; P = 0.017). Glucose 63-70 insulin Homo sapiens 44-51 19857065-4 2009 Moreover, we found that inulin was able to increase the uptake of glucose in C2C12 myotubes in which insulin resistance was induced by exposing cells to high glucose concentrations. Glucose 66-73 insulin Homo sapiens 101-108 19857065-4 2009 Moreover, we found that inulin was able to increase the uptake of glucose in C2C12 myotubes in which insulin resistance was induced by exposing cells to high glucose concentrations. Glucose 158-165 insulin Homo sapiens 101-108 19785566-8 2009 CONCLUSIONS: Moderate intensity, water-based circuit-type exercises appear to be an effective exercise modality to improve glucose and insulin response to a glucose challenge in overweight women with IGT. Glucose 157-164 insulin Homo sapiens 135-142 19592051-11 2009 The area under the curve for insulin at 30 minutes after a glucose load during the OGTT was significantly larger in subjects with NGT or IFG than in those with DM (P < .05). Glucose 59-66 insulin Homo sapiens 29-36 19651146-1 2009 A new molecular mathematical model is developed by considering the kinetics of GLUT2, GLUT3, and GLUT4, the process of glucose mobilization by glycogen phosphorylase and glycogen synthase in liver, and the dynamics of the insulin signaling pathway. Glucose 119-126 insulin Homo sapiens 222-229 19545590-3 2009 Incretins are defined as being responsible for the higher insulin release after an oral glucose load compared to an intravenous glucose load. Glucose 88-95 insulin Homo sapiens 58-65 19345076-11 2009 Insulin-induced glucose uptake increased, while the rate of adipogenesis decreased with increasing THC concentration. Glucose 16-23 insulin Homo sapiens 0-7 19345076-12 2009 Insulin-resistance was induced using TNF-alpha, exposed to the extract and insulin-induced glucose uptake measured. Glucose 91-98 insulin Homo sapiens 0-7 19345076-12 2009 Insulin-resistance was induced using TNF-alpha, exposed to the extract and insulin-induced glucose uptake measured. Glucose 91-98 insulin Homo sapiens 75-82 19345076-13 2009 Insulin-induced glucose was increased in these cells after exposure to the extract. Glucose 16-23 insulin Homo sapiens 0-7 20039004-3 2009 To date, the key metrics that have been measured involving C-peptide and RBCs include an increase in glucose uptake by these cells and a subsequent increase in adenosine triphosphate (ATP) release. Glucose 101-108 insulin Homo sapiens 59-68 19578118-1 2009 Insulin-regulated stimulation of glucose entry and mobilization of fat/muscle-specific glucose transporter GLUT4 onto the cell surface require the phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P(2)) pathway for optimal performance. Glucose 33-40 insulin Homo sapiens 0-7 19531639-12 2009 Evidence generated over the past 10 years indicated that this defect contributes to altering glucose tolerance by impairing insulin action and insulin secretion and might play a role in the development of diabetes-associated neurological disorders. Glucose 93-100 insulin Homo sapiens 124-131 19602578-0 2009 Role of iduronate-2-sulfatase in glucose-stimulated insulin secretion by activation of exocytosis. Glucose 33-40 insulin Homo sapiens 52-59 19602578-6 2009 hIDS potentiated the glucose-stimulated insulin secretory response compared with controls (61%) with no changes in insulin mRNA levels or insulin peptide content. Glucose 21-28 insulin Homo sapiens 40-47 19602578-10 2009 We conclude that IDS has a role in glucose-stimulated insulin secretion via a mechanism that involves the activation of exocytosis through phosphorylation of PKCalpha and MARCKS. Glucose 35-42 insulin Homo sapiens 54-61 19638470-12 2009 The glucose-dependent mechanism of insulin release with GLP-1 agonist therapy holds potential clinical significance in the management of postprandial hyperglycemic excursions, with minimal risk of hypoglycemia. Glucose 4-11 insulin Homo sapiens 35-42 19496776-1 2009 Metformin as adjunct to intensive insulin therapy may improve glucose metabolism and thereby prevent the development of cardiovascular risk factors in patients with type 1 diabetes. Glucose 62-69 insulin Homo sapiens 34-41 19587026-9 2009 At 24-28 weeks gestation, and in women with GDM only, fasting insulin was correlated with liking of the glucose solutions (R(2) = 0.63, P = 0.004) and fasting leptin was correlated with sweetness liking of the 10% sucrose milk (R(2) = 0.42, P = 0.017). Glucose 104-111 insulin Homo sapiens 62-69 19344310-2 2009 Aralar1 overexpression increased long-term (24 h) and acute (20 min) glucose- and amino-acid-stimulated insulin secretion, cellular glucose metabolism, L-alanine and L-glutamine consumption, cellular ATP and glutamate concentrations, and stimulated glutamate release. Glucose 69-76 insulin Homo sapiens 104-111 19623043-12 2009 However, in glucose-infused mice, lipopolysaccharide induced a large and unexpected increase in circulating insulin without significant alteration in blood glucose. Glucose 12-19 insulin Homo sapiens 108-115 19496088-0 2009 Circulating insulin antibodies: influence of continuous subcutaneous or intraperitoneal insulin infusion, and impact on glucose control. Glucose 120-127 insulin Homo sapiens 12-19 19502091-4 2009 At the end of incubation, functional (glucose-stimulated insulin secretion), morphological (electron microscopy) and molecular (gene and protein expression) studies were performed. Glucose 38-45 insulin Homo sapiens 57-64 19531056-8 2009 Insulin-stimulated glucose disappearance rate (Rd) was lower in T2D vs. control subjects both before and after training. Glucose 19-26 insulin Homo sapiens 0-7 19533082-11 2009 Furthermore, rosiglitazone significantly increased basal and insulin-stimulated glucose uptake when podocytes were treated with the NEFA palmitate. Glucose 80-87 insulin Homo sapiens 61-68 19588121-1 2009 AIMS/HYPOTHESIS: The physiological increase in muscle protein anabolism induced by insulin is blunted in healthy, glucose-tolerant older adults. Glucose 114-121 insulin Homo sapiens 83-90 19640601-9 2009 Insulin mediated glucose extraction is reduced during concomitant maximal stimulation of forearm blood flow with endothelial-dependent vasodilators, despite maintaining flow. Glucose 17-24 insulin Homo sapiens 0-7 19662615-4 2009 Hyperinsulemic/euglycemic clamp studies in humans and carnitine supplementation studies in rodents provide "proof-of-concept" that carnitine is effective at improving insulin-stimulated glucose utilization and in reversing abnormalities of fuel metabolism associated with T2D. Glucose 186-193 insulin Homo sapiens 167-174 19662621-3 2009 Insulin is the most powerful agent that can be used to control blood glucose levels. Glucose 69-76 insulin Homo sapiens 0-7 19546347-11 2009 In contrast, after 72 hrs, glucose uptake was increased by 50%, only under insulin stimulus. Glucose 27-34 insulin Homo sapiens 75-82 19546347-13 2009 Results suggest that MCs can be highly susceptible to the HG environment since they uptake glucose in both an insulin-independent and insulin-dependent manner. Glucose 91-98 insulin Homo sapiens 110-117 19546347-13 2009 Results suggest that MCs can be highly susceptible to the HG environment since they uptake glucose in both an insulin-independent and insulin-dependent manner. Glucose 91-98 insulin Homo sapiens 134-141 19500665-1 2009 We have recently shown that direct exposure to an oxidant stress induces resistance to insulin in glucose transport activity in intact rat skeletal muscle. Glucose 98-105 insulin Homo sapiens 87-94 19500665-5 2009 Interestingly, the inhibitory effects of H(2)O(2) on insulin-stimulated glucose transport and Akt (Ser(473)) phosphorylation were attenuated by 43 and 75% in exercise-trained muscles. Glucose 72-79 insulin Homo sapiens 53-60 19500665-7 2009 We have demonstrated for the first time in mammalian skeletal muscle that endurance exercise training can partially protect against glucose transport resistance to insulin induced by oxidative stress, and this benefit of exercise training is at least in part mediated through the insulin signaling pathway and stress-activated signaling elements. Glucose 132-139 insulin Homo sapiens 164-171 19500665-7 2009 We have demonstrated for the first time in mammalian skeletal muscle that endurance exercise training can partially protect against glucose transport resistance to insulin induced by oxidative stress, and this benefit of exercise training is at least in part mediated through the insulin signaling pathway and stress-activated signaling elements. Glucose 132-139 insulin Homo sapiens 280-287 19572227-3 2009 Insulin resistance was evaluated as oral glucose index (OGIS); insulin and C-peptide secretion as the insulinogenic index in 30th min of OGTT. Glucose 41-48 insulin Homo sapiens 0-7 19639221-5 2009 Since PKB is instrumental in mediating the effects of insulin on glucose transport, glycogen synthesis and gluconeogenesis, it is reasonable to suggest that activation of this pathway by BMOV serves as a mechanism for its insulin-like effects. Glucose 65-72 insulin Homo sapiens 54-61 19549742-5 2009 Indices of insulin sensitivity and resistance were determined from an oral glucose tolerance test. Glucose 75-82 insulin Homo sapiens 11-18 19549745-2 2009 In GLUT4 null mice, insulin-stimulated glucose uptake into muscle was diminished but not eliminated, suggesting that another insulin-sensitive system was present. Glucose 39-46 insulin Homo sapiens 20-27 19567519-7 2009 He required diazoxide, a thiazide diuretic, phenytoin, and a constant infusion of glucose to control the hypoglycemia and elevated insulin levels. Glucose 82-89 insulin Homo sapiens 131-138 19584183-1 2009 OBJECTIVE: The objective of the study was to quantify insulin resistance in type 1 diabetes patients by estimated glucose disposal rate (eGDR), according to the presence or absence of the metabolic syndrome, and its relationship with chronic complications. Glucose 114-121 insulin Homo sapiens 54-61 20144418-3 2009 Insulin"s effects to increase glucose uptake and decrease endogenous glucose production were described by the Bergman minimal model, and compartmental models were used to describe the pharmacokinetics of subcutaneous insulin absorption and glucose appearance following meals. Glucose 69-76 insulin Homo sapiens 0-7 20144418-3 2009 Insulin"s effects to increase glucose uptake and decrease endogenous glucose production were described by the Bergman minimal model, and compartmental models were used to describe the pharmacokinetics of subcutaneous insulin absorption and glucose appearance following meals. Glucose 69-76 insulin Homo sapiens 0-7 20144418-4 2009 The composite model, comprised of only five equations and eight parameters, was identified with and without intraday variance in insulin sensitivity (S(I)), glucose effectiveness at zero insulin (GEZI), and endogenous glucose production (EGP) at zero insulin. Glucose 157-164 insulin Homo sapiens 187-194 20144418-4 2009 The composite model, comprised of only five equations and eight parameters, was identified with and without intraday variance in insulin sensitivity (S(I)), glucose effectiveness at zero insulin (GEZI), and endogenous glucose production (EGP) at zero insulin. Glucose 157-164 insulin Homo sapiens 187-194 20144418-6 2009 With intraday variation in these three parameters, plasma glucose and insulin were well fit by the model (R(2) = 0.933 +/- 0.00971 [mean +/- standard error of the mean] ranging from 0.879-0.974 for glucose; R(2) = 0.879 +/- 0.0151, range 0.819-0.972 for insulin). Glucose 198-205 insulin Homo sapiens 70-77 20144419-2 2009 Here the function and structure of a class of control algorithms designed to exert control to range, defined as insulin treatment optimizing glycemia within a predefined target range by preventing extreme glucose fluctuations, are studied. Glucose 205-212 insulin Homo sapiens 112-119 20144424-1 2009 BACKGROUND: Hypoglycemia and hyperglycemia during closed-loop insulin delivery based on subcutaneous (SC) glucose sensing may arise due to (1) overdosing and underdosing of insulin by control algorithm and (2) difference between plasma glucose (PG) and sensor glucose, which may be transient (kinetics origin and sensor artifacts) or persistent (calibration error [CE]). Glucose 106-113 insulin Homo sapiens 62-69 20144424-1 2009 BACKGROUND: Hypoglycemia and hyperglycemia during closed-loop insulin delivery based on subcutaneous (SC) glucose sensing may arise due to (1) overdosing and underdosing of insulin by control algorithm and (2) difference between plasma glucose (PG) and sensor glucose, which may be transient (kinetics origin and sensor artifacts) or persistent (calibration error [CE]). Glucose 236-243 insulin Homo sapiens 62-69 20144424-1 2009 BACKGROUND: Hypoglycemia and hyperglycemia during closed-loop insulin delivery based on subcutaneous (SC) glucose sensing may arise due to (1) overdosing and underdosing of insulin by control algorithm and (2) difference between plasma glucose (PG) and sensor glucose, which may be transient (kinetics origin and sensor artifacts) or persistent (calibration error [CE]). Glucose 236-243 insulin Homo sapiens 62-69 20923533-3 2009 In the present review, theoretical questions are raised as to the physiological validity of these estimates of insulin secretory function and experimental data are presented demonstrating that hourly measurements of plasma insulin and glucose concentrations in response to mixed meals throughout an 8-h day lead to a very different point of view. Glucose 235-242 insulin Homo sapiens 111-118 19602103-7 2009 However, the glucose-stimulated induction of insulin release was significantly reduced in the insulinoma-cell line expressing highly expanded huntingtin compared to cells expressing huntingtin with modestly elongated polyglutamine stretches. Glucose 13-20 insulin Homo sapiens 45-52 19625702-1 2009 Type 2 diabetes affects approximately 7% of the population in the United States and is characterized by decreased disposal of glucose in peripheral tissues due to insulin resistance and overproduction of glucose by the liver, defects in pancreatic beta-cell function, and decreased beta-cell mass. Glucose 126-133 insulin Homo sapiens 163-170 19684236-9 2009 In the first 12 hours, glucose profiles were lower in the groups treated with strict glucose control; median AUC was 90 mmol/l x 12 h (range 77-189) for the hyperglycaemic control group versus 81 mmol/l x 12 h (range 60-118) for the meal related insulin group (p = 0.03) and 74 mmol/l x 12 h (range 52-97) for the basal insulin group (p = 0.008). Glucose 85-92 insulin Homo sapiens 246-253 19684236-9 2009 In the first 12 hours, glucose profiles were lower in the groups treated with strict glucose control; median AUC was 90 mmol/l x 12 h (range 77-189) for the hyperglycaemic control group versus 81 mmol/l x 12 h (range 60-118) for the meal related insulin group (p = 0.03) and 74 mmol/l x 12 h (range 52-97) for the basal insulin group (p = 0.008). Glucose 85-92 insulin Homo sapiens 320-327 19325541-5 2009 Our results show that both insulin sensitivity, as measured from levels of fasting glucose and insulin, and central adiposity, estimated by subscapular skinfold thickness, were significantly associated to genetic variability in TFAP2B. Glucose 83-90 insulin Homo sapiens 27-34 19766074-6 2009 Mimicking normal pancreagenesis offers the best strategy for producing glucose-responsive insulin-producing cells in vitro for people with diabetes. Glucose 71-78 insulin Homo sapiens 90-97 19220776-5 2009 RESULTS: Twelve weeks of treatment with insulin detemir significantly reduced mean hemoglobin A1c (9.7-8.9%, p < 0.001) and mean fasting glucose [185-162 mg/dL (10.3-9 mmol/L), p < 0.01]. Glucose 140-147 insulin Homo sapiens 40-47 19220776-6 2009 Fasting glucose variability was also lower after treatment with insulin detemir than previously (on either NPH or glargine, p < 0.05). Glucose 8-15 insulin Homo sapiens 64-71 19172665-0 2009 Identification of plant extracts with potential antidiabetic properties: effect on human peroxisome proliferator-activated receptor (PPAR), adipocyte differentiation and insulin-stimulated glucose uptake. Glucose 189-196 insulin Homo sapiens 170-177 19172665-5 2009 Extracts from common medicinal/food plants were tested in a screening platform comprising a series of bioassays, including tests for PPARgamma, alpha and delta transactivation, adipocyte differentiation and insulin-stimulated glucose uptake, allowing identification of plants containing potentially interesting PPAR agonists. Glucose 226-233 insulin Homo sapiens 207-214 19172665-6 2009 Twenty-two plant extracts out of 133 were found to increase insulin-stimulated glucose uptake and 18 extracts were found to activate PPARgamma, 3 to activate PPARalpha and gamma, 6 to activate PPARdelta and gamma, and 9 to activate PPARgamma, alpha and delta. Glucose 79-86 insulin Homo sapiens 60-67 19172665-7 2009 Among the 24 different plant species tested in the platform, 50% were shown to contain compounds capable of activating PPARgamma and stimulating insulin-dependent glucose uptake with no or little effect on adipocyte differentiation warranting further studies and characterization. Glucose 163-170 insulin Homo sapiens 145-152 19688040-7 2009 CAPN10 SNP-43 and SNP-44 were genotyped and related to gene expression and insulin release in response to glucose, arginine and glibenclamide. Glucose 106-113 insulin Homo sapiens 75-82 19779253-7 2009 miR-375 persuades beta cells for glucose-induced insulin gene expression. Glucose 33-40 insulin Homo sapiens 49-56 19688040-11 2009 The G/G variant of SNP-43 was associated with reduced insulin release in response to glucose (P</=0.04) in non-diabetic donors. Glucose 85-92 insulin Homo sapiens 54-61 19501568-4 2009 Insulin resistance was subsequent to IRS1 phosphorylation defects and resulted in a concentration-dependent decrease of glucose uptake. Glucose 120-127 insulin Homo sapiens 0-7 19682370-1 2009 BACKGROUND: Neuron-derived orphan receptor (Nor) 1, nuclear receptor (Nur) 77, and nuclear receptor-related protein (Nurr) 1 constitute the NR4A family of orphan nuclear receptors which were recently found to modulate hepatic glucose production, insulin signalling in adipocytes, and oxidative metabolism in skeletal muscle. Glucose 226-233 insulin Homo sapiens 246-253 19486888-5 2009 In subjects with genotype Ser/Ser, the insulin secretion index, HOMA-beta, increased in the subjects with glucose intolerance and decreased in the subjects with diabetes, while, in subjects with genotypes Ser/Cys + Cys/Cys, HOMA-beta decreased as the glucose tolerance progressed (p for trend = 0.010). Glucose 106-113 insulin Homo sapiens 39-46 19486888-5 2009 In subjects with genotype Ser/Ser, the insulin secretion index, HOMA-beta, increased in the subjects with glucose intolerance and decreased in the subjects with diabetes, while, in subjects with genotypes Ser/Cys + Cys/Cys, HOMA-beta decreased as the glucose tolerance progressed (p for trend = 0.010). Glucose 251-258 insulin Homo sapiens 39-46 19524129-5 2009 In addition, treatment of cells with adenyl cyclase inhibitor SQ52236 ameliorated the effects of PTH on insulin-stimulated glucose uptake, whereas inhibition of phospholipase C alpha (U73122) did not significantly alter the effects of PTH. Glucose 123-130 insulin Homo sapiens 104-111 19524127-2 2009 The bursting electrical activity in beta-cells is crucial for the release of insulin, which acts to regulate the blood glucose level. Glucose 119-126 insulin Homo sapiens 77-84 19524129-3 2009 PTH (10 nM, 24 h) treatment induced a reduction in insulin-stimulated glucose uptake, AKT activity (phosphorylated AKT/total AKT protein expression) and a decrease in GLUT4 and IRS-1 protein expression compared to vehicle treated controls in differentiated adipocytes. Glucose 70-77 insulin Homo sapiens 51-58 20641809-1 2004 As a consequence of the beta cell destruction, the net mass of these cells in the islet cells is reduced and, due to reduced insulin production, maintenance of blood glucose to a proper physiological level is impaired. Glucose 166-173 insulin Homo sapiens 125-132 19748061-1 2009 The incretin effect, that is, the postprandial augmentation of insulin secretion by gastrointestinal hormones, mediates approximately 50-70% of the overall insulin responses after a mixed meal or glucose ingestion in healthy subjects. Glucose 196-203 insulin Homo sapiens 63-70 19454546-1 2009 BACKGROUND: Surgical trauma causes stress and inflammatory reactions with elevated serum free fatty acids (FFA) and glucose levels characteristic of intraoperative insulin resistance. Glucose 116-123 insulin Homo sapiens 164-171 19618407-1 2009 In a previous study, we showed that a synthetic human insulin 1-chain analog, named analog (3) was capable of mimicking in vitro effects of native insulin, including stimulation of cell proliferation, glucose uptake and glycogen synthesis. Glucose 201-208 insulin Homo sapiens 54-61 19396426-0 2009 Glucose inhibits the insulin-induced activation of the insulin-degrading enzyme in HepG2 cells. Glucose 0-7 insulin Homo sapiens 21-28 19396426-7 2009 RESULTS: In HepG2 cells, insulin increased IDE activity under normal glucose conditions with no change in IDE mRNA or protein levels. Glucose 69-76 insulin Homo sapiens 25-32 20144412-2 2009 Algorithms presented in this issue are affected by numerous quantifiable factors, including insulin pharmaco-kinetics, timing of meal carbohydrate appearance, meal size, amount of exercise, presence of stress, day-to-day variations in insulin sensitivity, insulin time-activity profiles, accuracy of glucose monitor calibration, metabolic profiles of both adults and neonates, and risks of hypoglycemia/hyperglycemia. Glucose 300-307 insulin Homo sapiens 92-99 20144412-2 2009 Algorithms presented in this issue are affected by numerous quantifiable factors, including insulin pharmaco-kinetics, timing of meal carbohydrate appearance, meal size, amount of exercise, presence of stress, day-to-day variations in insulin sensitivity, insulin time-activity profiles, accuracy of glucose monitor calibration, metabolic profiles of both adults and neonates, and risks of hypoglycemia/hyperglycemia. Glucose 300-307 insulin Homo sapiens 235-242 20144412-2 2009 Algorithms presented in this issue are affected by numerous quantifiable factors, including insulin pharmaco-kinetics, timing of meal carbohydrate appearance, meal size, amount of exercise, presence of stress, day-to-day variations in insulin sensitivity, insulin time-activity profiles, accuracy of glucose monitor calibration, metabolic profiles of both adults and neonates, and risks of hypoglycemia/hyperglycemia. Glucose 300-307 insulin Homo sapiens 235-242 20144413-5 2009 The glucose infusion rates are used to obtain insulin time-activity profiles, which are then used to generate IOB curves. Glucose 4-11 insulin Homo sapiens 46-53 20144418-3 2009 Insulin"s effects to increase glucose uptake and decrease endogenous glucose production were described by the Bergman minimal model, and compartmental models were used to describe the pharmacokinetics of subcutaneous insulin absorption and glucose appearance following meals. Glucose 30-37 insulin Homo sapiens 0-7 19630751-2 2009 Endothelial dysfunction is intricately related to insulin resistance through the parallel stimulatory effects of insulin on glucose disposal in metabolic tissues and NO production in the endothelium. Glucose 124-131 insulin Homo sapiens 50-57 19630751-2 2009 Endothelial dysfunction is intricately related to insulin resistance through the parallel stimulatory effects of insulin on glucose disposal in metabolic tissues and NO production in the endothelium. Glucose 124-131 insulin Homo sapiens 113-120 19522877-5 2009 It was only 2 years after the islet transplantation that this search became positive against class II antigens, reaching a peak of reactivity concomitantly with the appearance of a deterioration of glucose control requiring low-dose insulin therapy. Glucose 198-205 insulin Homo sapiens 233-240 19522877-10 2009 As the result of an improvement in glucose control, the patient was again insulin-free. Glucose 35-42 insulin Homo sapiens 74-81 20027320-5 2009 Isoptin did not affect the stimulating effect of insulin against the background of parathyrin administration and completely blocked the inhibitory effect of calcitonin on insulin-stimulated glucose consumption by the muscle and adipose tissues in vivo and in vitro, while Bay-K-8644 potentiated this effect of calcitonin in vitro. Glucose 190-197 insulin Homo sapiens 171-178 19628278-1 2009 Calcium serves as a second messenger in glucose-triggered insulin secretion of pancreatic cells. Glucose 40-47 insulin Homo sapiens 58-65 19524129-6 2009 Thus, PTH treatment of differentiated 3T3-L1 adipocytes suppresses insulin-stimulated glucose uptake and insulin signaling via cAMP pathway, potentially through the phosphorylation of IRS-1 at serine 307. Glucose 86-93 insulin Homo sapiens 67-74 19520181-3 2009 Phosphorylation of glucose by glucokinase in the liver promotes glycogen synthesis, while in the beta-cell it results in insulin release. Glucose 19-26 insulin Homo sapiens 121-128 19455303-6 2009 RESULTS: Low early insulin response to oral glucose challenge, but not low insulin sensitivity, was associated with a higher risk of Alzheimer"s disease (HR for 1 SD decrease 1.32; 95% CI 1.02, 1.69) after adjustment for diabetes, blood pressure, body mass index, cholesterol, smoking and educational level. Glucose 44-51 insulin Homo sapiens 19-26 19491206-7 2009 RESULTS: Insulin secretory responses to oral and intravenous glucose were reduced by approximately 40% in glucose-tolerant subjects homozygous for E23K. Glucose 61-68 insulin Homo sapiens 9-16 19491206-7 2009 RESULTS: Insulin secretory responses to oral and intravenous glucose were reduced by approximately 40% in glucose-tolerant subjects homozygous for E23K. Glucose 106-113 insulin Homo sapiens 9-16 19367171-0 2009 Efficacy of insulin glargine in perioperative glucose control in type 2 diabetic patients. Glucose 46-53 insulin Homo sapiens 12-19 19491206-12 2009 Initially, insulin sensitivity is enhanced, thereby maintaining normal glucose tolerance. Glucose 71-78 insulin Homo sapiens 11-18 19491206-13 2009 Presumably, over time, as insulin secretion falls further or insulin resistance develops, glucose levels rise resulting in type 2 diabetes. Glucose 90-97 insulin Homo sapiens 26-33 19698061-3 2009 The present study extended the theoretical potential of the model by defining hepatic glucose effectiveness (hS(G)(2)) as the ability of glucose per se to inhibit EGP and hepatic insulin sensitivity (hS(1)(2)) as the ability of insulin to enhance glucose suppression of EGP. Glucose 86-93 insulin Homo sapiens 179-186 19698061-3 2009 The present study extended the theoretical potential of the model by defining hepatic glucose effectiveness (hS(G)(2)) as the ability of glucose per se to inhibit EGP and hepatic insulin sensitivity (hS(1)(2)) as the ability of insulin to enhance glucose suppression of EGP. Glucose 137-144 insulin Homo sapiens 179-186 19698061-5 2009 Model parameters of the two-compartment minimal model and of liver glucose metabolism were simultaneously identified to assess insulin sensitivity specific to stimulate glucose uptake (S(1)(2*)) and that specific to inhibit EGP (hS(1)(2)). Glucose 67-74 insulin Homo sapiens 127-134 19698061-10 2009 CONCLUSIONS: Because insulin resistance in liver and peripheral tissue may play a differential role in the pathogenesis of diabetes, this analysis can serve as a simple one-step approach to obtain metabolic indexes specific to EGP suppression and stimulating glucose uptake. Glucose 259-266 insulin Homo sapiens 21-28 19506561-9 2009 CONCLUSIONS: Increased expression of MIF gene in adipose cells may be an important link between obesity characterized by enlarged adipocytes and insulin resistance in normal glucose tolerant people. Glucose 174-181 insulin Homo sapiens 145-152 19435828-2 2009 This study was undertaken in morbid obesity to investigate insulin action on glucose disposal in AD and muscle (M). Glucose 77-84 insulin Homo sapiens 59-66 19624785-5 2009 Their effects include potentiation of glucose-stimulated insulin secretion, glucose-dependent inhibition of glucagon secretion and reduction in gastric emptying, appetite, food intake and body weight. Glucose 38-45 insulin Homo sapiens 57-64 19396426-8 2009 Under conditions of high glucose, insulin increased mRNA levels of IDE without changes in IDE activity. Glucose 25-32 insulin Homo sapiens 34-41 19396426-9 2009 Both in normal and high glucose medium, insulin increased levels of the catalytically more active 15a IDE isoform compared with the 15b isoform. Glucose 24-31 insulin Homo sapiens 40-47 19435828-7 2009 CONCLUSION: In morbid obesity, the sensitivity of glucose metabolism to insulin is impaired in M, due to defects in insulin-stimulated glucose use and decreased BF, and in AD, at least in part, due to decreased BF. Glucose 50-57 insulin Homo sapiens 72-79 19370316-4 2009 Cells silenced for O-glycosyl transferase (OGT) showed improved insulin-stimulated glucose uptake (P < 0.05) but without any effect on ER chaperone upregulation. Glucose 83-90 insulin Homo sapiens 64-71 19491219-9 2009 The glucose-induced changes in glucagon levels were closely correlated to the respective increments in insulin and C-peptide concentrations (P < 0.01). Glucose 4-11 insulin Homo sapiens 103-110 19674222-8 2009 In comparison with baseline, fasting glucose significantly decreased in the insulin pen group (-57 +/- 14 mg dL(-1), P < 0.001), and the reduction was significantly greater than that in the syringe group (P = 0.003). Glucose 37-44 insulin Homo sapiens 76-83 19470633-1 2009 CONTEXT: Obesity-related insulin resistance of glucose and lipid metabolism may also affect protein kinetics, notably at the muscle level. Glucose 47-54 insulin Homo sapiens 25-32 19353625-4 2009 First phase insulin release (FPIR) was determined by intravenous glucose tolerance test (IVGTT). Glucose 65-72 insulin Homo sapiens 12-19 19470633-4 2009 RESULTS: Responses of WB glucose disposal rate and protein breakdown to insulin and amino acid infusion were significantly lower in obese than in nonobese subjects (P < 0.05). Glucose 25-32 insulin Homo sapiens 72-79 19481772-10 2009 After the coingestion of fructose and glucose with the resultant insulin response from the glucose, fructose is a significant contributor to glycogen synthesis. Glucose 38-45 insulin Homo sapiens 65-72 19481772-10 2009 After the coingestion of fructose and glucose with the resultant insulin response from the glucose, fructose is a significant contributor to glycogen synthesis. Glucose 91-98 insulin Homo sapiens 65-72 19481791-8 2009 Heifers calving at <775 d had a mean BW gain of 0.82+/-0.01kg from 30 to 180 d. Increased glucose concentration at 180 d was associated with a reduced AFB (P<0.01), but no associations were found between insulin and urea concentrations and any of the fertility traits recorded (P>0.1). Glucose 93-100 insulin Homo sapiens 210-217 19642985-2 2009 BACKGROUND: Diabetes Mellitus is a chronic disease and many patients of which require frequent subcutaneous insulin injection to maintain proper blood glucose levels. Glucose 151-158 insulin Homo sapiens 108-115 19544420-6 2009 Following differentiation in vitro, HEACs released insulin and c-peptide in a glucose-dependent manner. Glucose 78-85 insulin Homo sapiens 51-58 19544420-6 2009 Following differentiation in vitro, HEACs released insulin and c-peptide in a glucose-dependent manner. Glucose 78-85 insulin Homo sapiens 63-72 19588439-19 2009 Refinement of algorithms to guide insulin infusion is needed to enable tight control of glucose concentrations within the target range. Glucose 88-95 insulin Homo sapiens 34-41 20641617-14 2004 GLUT4 and HKII are the major transporters and HK isoforms in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. Glucose 130-137 insulin Homo sapiens 113-120 19587243-9 2009 Matching plasma insulin and glucagon with portal infusions led to higher plasma glucoses in the HFF rats (147 +/- 4 vs. 161 +/- 4 mg/dL, P = 0.05) with higher rates of EGP and gluconeogenesis. Glucose 80-88 insulin Homo sapiens 16-23 19093914-2 2009 The aim of the present study was to explore how IMCL levels relate to the insulin-mediated suppression of endogenous glucose production [hepatic SI (insulin sensitivity)] and increase in glucose disposal (peripheral SI). Glucose 117-124 insulin Homo sapiens 74-81 19161346-8 2009 The rise in plasma glucose after lunch was significantly less if breakfast had been taken (0.9+/-0.3 compared with 3.2+/-0.3 mmol/l, with and without breakfast respectively; P<0.001), despite comparable insulin responses. Glucose 19-26 insulin Homo sapiens 206-213 19435854-4 2009 We found that resistin at a concentration of 30 ng/ml decreased insulin-stimulated glucose uptake by 30-40% in soleus muscle and myotubes, whereas in EDL muscle insulin-stimulated glucose uptake was impaired at a resistin concentration of 100 ng/ml. Glucose 180-187 insulin Homo sapiens 161-168 19435854-3 2009 This was investigated by incubating mouse extensor digitorum longus (EDL) and soleus muscles and L6 myotubes with physiological concentrations of resistin and assessing insulin-stimulated glucose uptake, cellular signaling, suppressor of cytokine signaling 3 (SOCS-3) mRNA, and GLUT4 translocation. Glucose 188-195 insulin Homo sapiens 169-176 19435854-4 2009 We found that resistin at a concentration of 30 ng/ml decreased insulin-stimulated glucose uptake by 30-40% in soleus muscle and myotubes, whereas in EDL muscle insulin-stimulated glucose uptake was impaired at a resistin concentration of 100 ng/ml. Glucose 83-90 insulin Homo sapiens 64-71 19147142-5 2009 Insulin sensitivity was directly assessed by a rate constant for plasma glucose disappearance (Kitt) using short insulin tolerance test. Glucose 72-79 insulin Homo sapiens 0-7 19147142-5 2009 Insulin sensitivity was directly assessed by a rate constant for plasma glucose disappearance (Kitt) using short insulin tolerance test. Glucose 72-79 insulin Homo sapiens 113-120 19338578-10 2009 Also in normal primary pancreatic islets of transgenic mice, known to express high levels of PPARgamma, rosiglitazone inhibited glucose-stimulated insulin gene transcription. Glucose 128-135 insulin Homo sapiens 147-154 19573114-2 2009 Previous data suggest patients with Type 2 diabetes develop greater symptomatic and hormonal responses to hypoglycaemia at higher glucose concentrations than non-diabetic controls and these responses are lowered by insulin treatment. Glucose 130-137 insulin Homo sapiens 215-222 19320663-0 2009 A randomized clinical trial comparing the effect of basal insulin and inhaled mealtime insulin on glucose variability and oxidative stress. Glucose 98-105 insulin Homo sapiens 87-94 19320663-5 2009 RESULTS: Inhaled insulin improved overall and postprandial glucose control significantly better than insulin glargine (p < 0.0001). Glucose 59-66 insulin Homo sapiens 17-24 19320663-10 2009 These findings indicate also that lowering glucose using insulin treatment lowers oxidative stress over time, at least for the study period of 9 days, in type 2 diabetes patients. Glucose 43-50 insulin Homo sapiens 57-64 19333572-1 2009 Insulin action on metabolically active tissues is a complex process involving positive and negative feedback regulation to control whole body glucose homeostasis. Glucose 142-149 insulin Homo sapiens 0-7 19333572-2 2009 At the cellular level, glucose and lipid metabolism, as well as protein synthesis, are controlled through canonical insulin signalling cascades. Glucose 23-30 insulin Homo sapiens 116-123 19333572-6 2009 This review will focus on the use of siRNA to validate critical regulators controlling insulin action in human skeletal muscle, a key organ important for the control of whole body insulin-mediated glucose uptake and metabolism. Glucose 197-204 insulin Homo sapiens 87-94 19333572-6 2009 This review will focus on the use of siRNA to validate critical regulators controlling insulin action in human skeletal muscle, a key organ important for the control of whole body insulin-mediated glucose uptake and metabolism. Glucose 197-204 insulin Homo sapiens 180-187 19430760-0 2009 A genome-wide association scan for acute insulin response to glucose in Hispanic-Americans: the Insulin Resistance Atherosclerosis Family Study (IRAS FS). Glucose 61-68 insulin Homo sapiens 41-48 19430760-1 2009 AIMS/HYPOTHESIS: This study sought to identify genes and regions in the human genome that are associated with the acute insulin response to glucose (AIRg), an important predictor of type 2 diabetes, in Hispanic-American participants from the Insulin Resistance Atherosclerosis Family Study (IRAS FS). Glucose 140-147 insulin Homo sapiens 120-127 19430760-1 2009 AIMS/HYPOTHESIS: This study sought to identify genes and regions in the human genome that are associated with the acute insulin response to glucose (AIRg), an important predictor of type 2 diabetes, in Hispanic-American participants from the Insulin Resistance Atherosclerosis Family Study (IRAS FS). Glucose 140-147 insulin Homo sapiens 242-249 19572795-1 2009 Intensive insulin therapy aimed at achieving normal glucose levels significantly reduces the complications that are associated with diabetes but is also associated with an increased risk of low glucose levels (hypoglycemia). Glucose 52-59 insulin Homo sapiens 10-17 19572795-1 2009 Intensive insulin therapy aimed at achieving normal glucose levels significantly reduces the complications that are associated with diabetes but is also associated with an increased risk of low glucose levels (hypoglycemia). Glucose 194-201 insulin Homo sapiens 10-17 19572795-2 2009 The growing use of continuous glucose monitors has stimulated the development of the artificial pancreas, a closed-loop insulin-delivery system aimed at restoring near-normal glucose levels while reducing the risk of hypoglycemia. Glucose 30-37 insulin Homo sapiens 120-127 19572795-2 2009 The growing use of continuous glucose monitors has stimulated the development of the artificial pancreas, a closed-loop insulin-delivery system aimed at restoring near-normal glucose levels while reducing the risk of hypoglycemia. Glucose 175-182 insulin Homo sapiens 120-127 19572795-3 2009 The artificial pancreas comprises three components: a continuous glucose monitor, an insulin infusion pump and a control algorithm delivering insulin according to real-time glucose readings. Glucose 173-180 insulin Homo sapiens 142-149 19533481-5 2009 Pituitary function and insulin secretion were assessed before and after intervention by GnRH-TRH tests and oral glucose tolerance test induced insulin response. Glucose 112-119 insulin Homo sapiens 143-150 19552740-12 2009 We found a statistically significant negative correlation between duration of erythropoietin treatment, fasting blood glucose, insulin levels, and insulin resistance (r=-0.62, -0.71, and -0.57, P<0.001). Glucose 118-125 insulin Homo sapiens 147-154 21084851-1 2009 Previously, the insulin producing liver cell line HUH7-ins has been shown to synthesize, store and secrete insulin in response to glucose via secretory granules. Glucose 130-137 insulin Homo sapiens 16-23 19366854-9 2009 The insulin sensitivity of endogenous glucose production was significantly increased after pegvisomant [mean glucose Ra *insulin, 118.5 +/- 28 vs. 69.2 +/- 22 micromol/kg x min *(mU/liter); P = 0.04]. Glucose 38-45 insulin Homo sapiens 4-11 19366854-9 2009 The insulin sensitivity of endogenous glucose production was significantly increased after pegvisomant [mean glucose Ra *insulin, 118.5 +/- 28 vs. 69.2 +/- 22 micromol/kg x min *(mU/liter); P = 0.04]. Glucose 38-45 insulin Homo sapiens 121-128 20144337-1 2009 AIMS AND BACKGROUND: Model-based insulin sensitivity testing via the intravenous glucose tolerance test (IVGTT) or similar is clinically very intensive due to the need for frequent sampling to accurately capture the dynamics of insulin secretion and clearance. Glucose 81-88 insulin Homo sapiens 33-40 20144337-1 2009 AIMS AND BACKGROUND: Model-based insulin sensitivity testing via the intravenous glucose tolerance test (IVGTT) or similar is clinically very intensive due to the need for frequent sampling to accurately capture the dynamics of insulin secretion and clearance. Glucose 81-88 insulin Homo sapiens 228-235 20144337-2 2009 The goal of this study was to significantly reduce the number of samples required in intravenous glucose tolerance test protocols to accurately identify C-peptide and insulin secretion characteristics. Glucose 97-104 insulin Homo sapiens 167-174 20144345-0 2009 Numerical and clinical accuracy of a continuous glucose monitoring system during intravenous insulin therapy in the surgical and burn intensive care units. Glucose 48-55 insulin Homo sapiens 93-100 20144346-0 2009 Analysis: Continuous glucose monitoring during intensive insulin therapy. Glucose 21-28 insulin Homo sapiens 57-64 20144350-1 2009 People on insulin therapy are challenged with evaluation of numerous factors affecting the blood glucose in order to select the optimal dose for reaching their glucose target. Glucose 97-104 insulin Homo sapiens 10-17 20144350-1 2009 People on insulin therapy are challenged with evaluation of numerous factors affecting the blood glucose in order to select the optimal dose for reaching their glucose target. Glucose 160-167 insulin Homo sapiens 10-17 19617231-0 2009 Insulin resistance despite tight glucose control is associated with mortality in critically ill surgical patients. Glucose 33-40 insulin Homo sapiens 0-7 19670354-2 2009 OBJECTIVE: This study was conducted to determine if the application of hospital-wide insulin order sets improved inpatient safety by reducing the number of actual hypoglycemic and hyperglycemic events and increasing at-target blood glucose. Glucose 232-239 insulin Homo sapiens 85-92 19625881-4 2009 The disposition index (SI x the acute insulin response to glucose), which measures how the body compensates for insulin resistance to maintain a normal glucose level, was significantly lower in the group treated with clozapine than in the group treated with olanzapine (1067+/-1390 vs. 2521+/-2805; P=0.013), suggesting that the subjects treated with clozapine had a reduced compensatory response to IR compared with the subjects treated with olanzapine. Glucose 58-65 insulin Homo sapiens 38-45 19560684-11 2009 Insulin-resistant patients with recurrence had significantly lower levels of plasma insulin at 120 minutes in the oral glucose tolerance test compared with those without recurrence. Glucose 119-126 insulin Homo sapiens 0-7 19560684-11 2009 Insulin-resistant patients with recurrence had significantly lower levels of plasma insulin at 120 minutes in the oral glucose tolerance test compared with those without recurrence. Glucose 119-126 insulin Homo sapiens 84-91 19394979-0 2009 A numerical deconvolution method to estimate C-peptide secretion in humans after an intravenous glucose tolerance test. Glucose 96-103 insulin Homo sapiens 45-54 19428033-2 2009 However, in glucose-intolerance/insulin-resistant conditions, such as that induced by starvation, the flexibility of tissues to rapidly respond to change in substrate availability is diminished. Glucose 12-19 insulin Homo sapiens 32-39 19428033-8 2009 In contrast, large reductions in resting blood glucose (-21%, +/-14%) and moderate reductions in plasma insulin concentrations (-47%, +/-26%) were observed in the fast condition; but this effect was reversed for glucose (30%, +/- 24%) and negated for insulin by the end of exercise. Glucose 212-219 insulin Homo sapiens 104-111 19428033-8 2009 In contrast, large reductions in resting blood glucose (-21%, +/-14%) and moderate reductions in plasma insulin concentrations (-47%, +/-26%) were observed in the fast condition; but this effect was reversed for glucose (30%, +/- 24%) and negated for insulin by the end of exercise. Glucose 212-219 insulin Homo sapiens 251-258 19572292-1 2009 Insulin is a polypeptide hormone which is produced by the beta-cell of pancreas and controls the blood glucose level in the human body. Glucose 103-110 insulin Homo sapiens 0-7 19405039-1 2009 BACKGROUND: Although insulin has been reported to have an anti-inflammatory effect, whether this effect is independent of its property to reduce blood glucose with insulin treatment in type 2 diabetes has not been investigated in detail. Glucose 151-158 insulin Homo sapiens 21-28 19405039-9 2009 CONCLUSIONS: Our data suggest that insulin has an anti-inflammatory effect that is independent of the reduction it causes in blood glucose. Glucose 131-138 insulin Homo sapiens 35-42 19527481-9 2009 CONCLUSIONS: An insulin regimen using high-mix BIAsp (BIAsp 70) before breakfast and lunch and BIAsp 30 before dinner can achieve lower blood glucose levels during the day through reduced mealtime glucose excursions in particular at lunchtime than a twice-daily premix regimen. Glucose 142-149 insulin Homo sapiens 16-23 19524190-2 2009 Whether glucose control with multiple daily subcutaneous insulin injections (MDI) is beneficial in patients hospitalized in general medical wards is unknown. Glucose 8-15 insulin Homo sapiens 57-64 19769745-7 2009 TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. Glucose 135-142 insulin Homo sapiens 53-60 19769745-10 2009 Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. Glucose 175-182 insulin Homo sapiens 136-143 30781275-1 2009 Insulin exerts a fundamental role in glucose metabolism. Glucose 37-44 insulin Homo sapiens 0-7 19322745-5 2009 Insulin sensitivity was assessed by the Oral Glucose Sensitivity Index (OGIS). Glucose 45-52 insulin Homo sapiens 0-7 20409967-3 2009 The GLP-1 receptor agonists reduce blood glucose levels by stimulating insulin and inhibiting glucagon secretion and gastric emptying. Glucose 41-48 insulin Homo sapiens 71-78 19401372-2 2009 Estimates of insulin resistance in first-degree relatives of those with type 1 diabetes may be obtained using the minimal model of glucose kinetics incorporating a population approach. Glucose 131-138 insulin Homo sapiens 13-20 19401372-4 2009 DESIGN: Insulin sensitivity (SI) was assessed using the minimal model of glucose kinetics after an oral glucose tolerance test combined with nonlinear mixed-effects modeling. Glucose 73-80 insulin Homo sapiens 8-15 19401372-4 2009 DESIGN: Insulin sensitivity (SI) was assessed using the minimal model of glucose kinetics after an oral glucose tolerance test combined with nonlinear mixed-effects modeling. Glucose 104-111 insulin Homo sapiens 8-15 20144331-0 2009 Improved glycemic control through continuous glucose sensor-augmented insulin pump therapy: prospective results from a community and academic practice patient registry. Glucose 45-52 insulin Homo sapiens 70-77 20144334-16 2009 In addition to user-definable parameters, three special algorithm parameters discoverable in nature are described: the maximum rate of the spontaneous ascent of blood glucose during nonhypoglycemia, the glucose per daily dose of insulin exogenously mediated, and the MR at given patient time points. Glucose 203-210 insulin Homo sapiens 229-236 19369940-8 2009 These data show that obese subjects who display insulin resistance on insulin-mediated peripheral glucose uptake have the same sensitivity for the insulin-mediated suppression of ketogenesis. Glucose 98-105 insulin Homo sapiens 48-55 19369940-8 2009 These data show that obese subjects who display insulin resistance on insulin-mediated peripheral glucose uptake have the same sensitivity for the insulin-mediated suppression of ketogenesis. Glucose 98-105 insulin Homo sapiens 70-77 19369940-8 2009 These data show that obese subjects who display insulin resistance on insulin-mediated peripheral glucose uptake have the same sensitivity for the insulin-mediated suppression of ketogenesis. Glucose 98-105 insulin Homo sapiens 70-77 19435854-5 2009 Impaired insulin-stimulated glucose uptake was not associated with reduced Akt phosphorylation or IRS-1 protein or increased SOCS-3 mRNA expression. Glucose 28-35 insulin Homo sapiens 9-16 19435854-9 2009 We conclude that resistin impairs insulin-stimulated glucose uptake by mechanisms involving reduced plasma membrane GLUT4 translocation but independent of the proximal insulin-signaling cascade, AMPK, and SOCS-3. Glucose 53-60 insulin Homo sapiens 34-41 19435855-3 2009 As evidence that insulin resistance in high-fat diet-fed rats is due to high FFA, it has been reported that the insulin resistance is rapidly reversed by an overnight fast, a high-glucose meal, and an exercise bout. Glucose 180-187 insulin Homo sapiens 17-24 19435855-3 2009 As evidence that insulin resistance in high-fat diet-fed rats is due to high FFA, it has been reported that the insulin resistance is rapidly reversed by an overnight fast, a high-glucose meal, and an exercise bout. Glucose 180-187 insulin Homo sapiens 112-119 19435855-7 2009 An overnight fast and a high-glucose meal were followed by a large increase in insulin-stimulated muscle glucose transport. Glucose 29-36 insulin Homo sapiens 79-86 19435855-7 2009 An overnight fast and a high-glucose meal were followed by a large increase in insulin-stimulated muscle glucose transport. Glucose 105-112 insulin Homo sapiens 79-86 19397257-4 2009 The swelling behavior of the NPs and the in vitro release profiles of insulin at different glucose concentrations revealed definite glucose sensitivity of the glycopolymers. Glucose 91-98 insulin Homo sapiens 70-77 19715873-5 2009 Cell viability was determined by acridine orange/propidium iodide staining, and islet cell function by measuring glucose-stimulated insulin secretion expressed as the insulin stimulation index. Glucose 113-120 insulin Homo sapiens 132-139 19852296-3 2009 Insulin resistance of thecal cells was induced by Dex treatment for 48 h. Then the glucose utilization ratio of thecal cells was detected. Glucose 83-90 insulin Homo sapiens 0-7 19539082-10 2009 Whole-body insulin sensitivity increased by 33% (p <0.01), but insulin-stimulated myocardial glucose uptake remained unchanged (p = 0.90). Glucose 96-103 insulin Homo sapiens 66-73 19516902-0 2009 The type 2 diabetes associated minor allele of rs2237895 KCNQ1 associates with reduced insulin release following an oral glucose load. Glucose 121-128 insulin Homo sapiens 87-94 19516902-3 2009 METHODOLOGY/PRINCIPAL FINDINGS: Genotypes were examined for associations with serum insulin levels following an oral glucose tolerance test (OGTT) in a population-based sample of 6,039 middle-aged and treatment-naive individuals. Glucose 117-124 insulin Homo sapiens 84-91 19516902-5 2009 Applying an additive genetic model the minor C-allele of rs2237895 was associated with reduced serum insulin levels 30 min (mean+/-SD: (CC) 277+/-160 vs. (AC) 280+/-164 vs. (AA) 299+/-200 pmol/l, p = 0.008) after an oral glucose load, insulinogenic index (29.6+/-17.4 vs. 30.2+/-18.7vs. Glucose 221-228 insulin Homo sapiens 101-108 19516902-10 2009 CONCLUSION: The minor C-allele of rs2237895 of KCNQ1, which has a prevalence of about 42% among Caucasians was associated with reduced measures of insulin release following an oral glucose load suggesting that the increased risk of type 2 diabetes, previously reported for this variant, likely is mediated through an impaired beta cell function. Glucose 181-188 insulin Homo sapiens 147-154 19470471-7 2009 Two overweight family members with the mutation also manifested normal fasting glucose and insulin levels but disproportionately elevated insulin levels following an oral glucose challenge. Glucose 171-178 insulin Homo sapiens 138-145 19197265-4 2009 Insulin sensitivity was determined by intravenous glucose tolerance test (IVGTT) and minimal modeling; insulin secretion and clearance by C-peptide modeling; genetic ancestry by admixture analysis. Glucose 50-57 insulin Homo sapiens 0-7 19497719-4 2009 Insulin sensitivity was measured by intravenous glucose tolerance test. Glucose 48-55 insulin Homo sapiens 0-7 19497719-9 2009 We concluded that preeclamptic women have higher circulating FFA concentrations, which despite insulin resistance are suppressed by oral glucose loading. Glucose 137-144 insulin Homo sapiens 95-102 19397257-4 2009 The swelling behavior of the NPs and the in vitro release profiles of insulin at different glucose concentrations revealed definite glucose sensitivity of the glycopolymers. Glucose 132-139 insulin Homo sapiens 70-77 19397257-7 2009 The glycopolymers that responded to changes in the glucose concentration of the surrounding environment are being aimed for use in self-regulated insulin delivery. Glucose 51-58 insulin Homo sapiens 146-153 19322513-4 2009 Acromegalic patients are insulin resistant, both in the liver and in the periphery, displaying hyperinsulinemia and increased glucose turnover in the basal post-absorptive states. Glucose 126-133 insulin Homo sapiens 25-32 19231303-8 2009 The insulin-loaded microcapsules significantly improved glucose tolerance from 2 h (free insulin) to even 12 h (insulin-loaded microcapsules with 10 bilayers). Glucose 56-63 insulin Homo sapiens 4-11 19203789-0 2009 Triggered release of insulin from glucose-sensitive enzyme multilayer shells. Glucose 34-41 insulin Homo sapiens 21-28 19258492-1 2009 Obesity is associated with resistance of skeletal muscle to insulin-mediated glucose uptake, as well as resistance of different organs and tissues to other metabolic and vascular actions of insulin. Glucose 77-84 insulin Homo sapiens 60-67 19351807-0 2009 The glucose-dependent insulinotropic polypeptide and glucose-stimulated insulin response to exercise training and diet in obesity. Glucose 4-11 insulin Homo sapiens 22-29 19649376-1 2009 Insulin resistance of skeletal muscle glucose transport is a key-defect for the development of impaired glucose tolerance and type 2 diabetes. Glucose 38-45 insulin Homo sapiens 0-7 19662793-1 2009 The objective of this study was to analyze how preoperative glucose treatment influences the blood glucose level as a measured exponent of surgical stress and to establish the best postoperative replacement considering glucose solutions and insulin. Glucose 60-67 insulin Homo sapiens 241-248 19490822-5 2009 Conversely, in the fed state, insulin levels rise and stimulate uptake of glucose primarily into skeletal muscle and other organs, including adipose tissue. Glucose 74-81 insulin Homo sapiens 30-37 19491573-7 2009 Patients were treated intensively with IV insulin for 35 hours and had 23 glucose measurements in this time span on average. Glucose 74-81 insulin Homo sapiens 42-49 19183933-8 2009 Addition of rCD40L to adipocytes induced mitogen activated protein kinase (MAPK) activation, stimulated inflammatory adipocytokine production, and decreased insulin-induced glucose transport in parallel with a downregulation of IRS1 and GLUT4 (also known as SCL2A4). Glucose 173-180 insulin Homo sapiens 157-164 19244092-4 2009 C-peptide (detection limit: 6 pmol/l) was considered stimulated at a corresponding serum glucose concentration >or=5.0 mmol/l. Glucose 89-96 insulin Homo sapiens 0-9 19252135-4 2009 Insulin resistance was calculated from fasting insulin and glucose using the homeostasis model assessment method, whereas pancreatic beta-cell function was assessed using the corrected insulin response at 120 min (CIR(120)). Glucose 59-66 insulin Homo sapiens 0-7 19288074-5 2009 Bivariate model fitting was used to investigate the glucose and insulin responses to a glucose load, i.e. an OGTT. Glucose 87-94 insulin Homo sapiens 64-71 19288074-9 2009 CONCLUSIONS/INTERPRETATION: Exposure to a glucose challenge uncovers new genetic variance for glucose and amplifies the effects of genes that already influence the fasting insulin level. Glucose 42-49 insulin Homo sapiens 172-179 19296078-1 2009 AIMS/HYPOTHESIS: Glucose-stimulated insulin secretion is defective in patients with type 2 diabetes. Glucose 17-24 insulin Homo sapiens 36-43 19324940-0 2009 G-allele of intronic rs10830963 in MTNR1B confers increased risk of impaired fasting glycemia and type 2 diabetes through an impaired glucose-stimulated insulin release: studies involving 19,605 Europeans. Glucose 134-141 insulin Homo sapiens 153-160 19324940-6 2009 The G-allele was associated with a decreased insulin release after oral and intravenous glucose challenges (P < 0.01) but not after injection of tolbutamide. Glucose 88-95 insulin Homo sapiens 45-52 19349201-3 2009 Such accumulation is known to cause insulin resistance, particularly in skeletal muscle, by reducing insulin-stimulated glucose uptake. Glucose 120-127 insulin Homo sapiens 36-43 19349201-3 2009 Such accumulation is known to cause insulin resistance, particularly in skeletal muscle, by reducing insulin-stimulated glucose uptake. Glucose 120-127 insulin Homo sapiens 101-108 19406499-7 2009 When subjects were stratified by PA level (according to the median value), we found that high level of PA (>2h/week) was associated with smaller glucose area under the curve (AUC) and 2-h glucose levels in rs1885088 A/A homozygotes and with lower fasting C-peptide and insulin AUC in rs745975 T/T homozygotes. Glucose 148-155 insulin Homo sapiens 272-279 19433015-6 2009 Experimental data suggest that elevated blood glucose may contribute to infarct expansion directly through a number of maladaptive metabolic pathways and that treatment with insulin may attenuate these adverse effects. Glucose 46-53 insulin Homo sapiens 174-181 19459760-2 2009 This study tested the hypothesis that hollow microneedles can deliver insulin to modulate blood glucose levels in subjects with type 1 diabetes in a minimally invasive manner. Glucose 96-103 insulin Homo sapiens 70-77 19459760-6 2009 Bolus insulin delivery followed by consumption of a standardized meal in the second phase revealed that microneedles were effective in reducing postprandial glucose levels. Glucose 157-164 insulin Homo sapiens 6-13 19469676-2 2009 The perceived advantages of such a system include the ability for patients to view and be alerted of glucose information in real-time and affords them a method to adjust insulin delivery in response to these data. Glucose 101-108 insulin Homo sapiens 170-177 19469676-4 2009 The Paradigm REAL-Time system offers two distinct capabilities over conventional multiple daily injection therapy with self-monitoring of blood glucose, mainly the abilities to observe and react to glucose changes in a timely and appropriate manner using the Bolus Wizard calculator feature of the pump and to retrospectively review integrated glucose sensing and insulin delivery data. Glucose 198-205 insulin Homo sapiens 364-371 19469676-4 2009 The Paradigm REAL-Time system offers two distinct capabilities over conventional multiple daily injection therapy with self-monitoring of blood glucose, mainly the abilities to observe and react to glucose changes in a timely and appropriate manner using the Bolus Wizard calculator feature of the pump and to retrospectively review integrated glucose sensing and insulin delivery data. Glucose 198-205 insulin Homo sapiens 364-371 19469676-5 2009 Retrospective review of uploaded data allows patients and HCPs the opportunity to modify insulin therapy and to potentially improve glycemic control without the use of a traditional glucose diary. Glucose 182-189 insulin Homo sapiens 89-96 19505629-9 2009 Moreover, they were able to release insulin in a glucose-dependent manner and ameliorate the diabetic conditions of streptozotocin (STZ)-treated nude mice. Glucose 49-56 insulin Homo sapiens 36-43 19538232-8 2009 First-phase insulin secretion was inversely correlated with 1-h (r = -0.74; P < 0.0001) and 2-h glucose levels (r = -0.34; P < 0.05). Glucose 99-106 insulin Homo sapiens 12-19 19482713-5 2009 Recent studies have cast a new light on the role of the CNS in regulating peripheral glucose via a hypothalamic lipid-sensing device that detects nutrient availability and relays, through the autonomic nervous system, a negative feedback signal on food intake, insulin sensitivity and insulin secretion. Glucose 85-92 insulin Homo sapiens 261-268 20431732-10 2009 CONCLUSIONS: The clearance of HCV by the combination therapy of pegylated interferon alpha-2a and ribavirin improves insulin resistance by reducing fasting serum insulin and glucose levels. Glucose 174-181 insulin Homo sapiens 117-124 19232615-3 2009 Patients in intensive glucose control group (n=121) received continuous insulin infusion to maintain glucose levels between 4.4 m mol/l (80 mg/dl) and 6.1 m mol/l (110 mg/dl). Glucose 22-29 insulin Homo sapiens 72-79 19220548-4 2009 RESULTS: Although 32% patients had diabetes diagnosed before lung transplantation, 92% had random blood glucose levels > or =11.1 mmol/L requiring insulin during admission. Glucose 104-111 insulin Homo sapiens 150-157 19164770-7 2009 However, postexercise-increased amino acid availability is less important for inhibiting MPB than insulin, the secretion of which is stimulated most by glucose availability, without itself stimulating MPS. Glucose 152-159 insulin Homo sapiens 98-105 19556721-7 2009 CONCLUSIONS: Although the number of TD patients was very small in the current study, these observations indicated a possible mechanism that glucose-stimulated insulin secretion might be impaired in human TD patients with ABCA1 mutations. Glucose 140-147 insulin Homo sapiens 159-166 20929509-4 2009 Insulin secretion was assessed by DeltaI/DeltaG (increment in plasma insulin concentration/plasma glucose concentration 30 min after the oral administration of 75 g glucose) and the total area under the curve for insulin over 180 min (AUC-I). Glucose 98-105 insulin Homo sapiens 0-7 20929509-4 2009 Insulin secretion was assessed by DeltaI/DeltaG (increment in plasma insulin concentration/plasma glucose concentration 30 min after the oral administration of 75 g glucose) and the total area under the curve for insulin over 180 min (AUC-I). Glucose 165-172 insulin Homo sapiens 0-7 19627193-3 2009 Experimentally, cassia cinnamon (Cinnamomum cassia) supplementation facilitates glucose disposal in healthy humans, which may be achieved by enhancing (1) insulin sensitivity via increased phosphorylation of signaling proteins and (2) insulin-sensitive glucose transporter 4-mediated glucose uptake into muscle cells. Glucose 80-87 insulin Homo sapiens 155-162 19627193-3 2009 Experimentally, cassia cinnamon (Cinnamomum cassia) supplementation facilitates glucose disposal in healthy humans, which may be achieved by enhancing (1) insulin sensitivity via increased phosphorylation of signaling proteins and (2) insulin-sensitive glucose transporter 4-mediated glucose uptake into muscle cells. Glucose 80-87 insulin Homo sapiens 235-242 19627193-3 2009 Experimentally, cassia cinnamon (Cinnamomum cassia) supplementation facilitates glucose disposal in healthy humans, which may be achieved by enhancing (1) insulin sensitivity via increased phosphorylation of signaling proteins and (2) insulin-sensitive glucose transporter 4-mediated glucose uptake into muscle cells. Glucose 253-260 insulin Homo sapiens 235-242 19403722-8 2009 In addition, gamma-MG prevented the suppression by LPS of insulin-stimulated glucose uptake and PPAR-gamma and adiponectin gene expression. Glucose 77-84 insulin Homo sapiens 58-65 19522271-8 2009 Then, insulin infusion was continued to maintain blood glucose level around 150 mg x dl(-1). Glucose 55-62 insulin Homo sapiens 6-13 19368944-0 2009 Uncoupling protein 2 Ala55Val polymorphism is associated with a higher acute insulin response to glucose. Glucose 97-104 insulin Homo sapiens 77-84 19368944-2 2009 We hypothesized that 2 UCP2 polymorphisms, a -55C/T (Ala55Val) substitution in exon 4 and an exon 8 insertion, would alter the acute insulin response to glucose (AIRg). Glucose 153-160 insulin Homo sapiens 133-140 19375766-5 2009 Moreover, insulin-stimulated glucose uptake in isolated adipocytes was analyzed to address adipose tissue insulin sensitivity. Glucose 29-36 insulin Homo sapiens 10-17 19375766-10 2009 Insulin-induced rise in IL-6 correlated negatively to BMI (P = .001), waist to hip ratio (P = .05), and baseline (fasting) insulin (P = .03) and IL-6 (P = .02) levels and positively to insulin-stimulated glucose uptake in isolated adipocytes (P = .07). Glucose 204-211 insulin Homo sapiens 0-7 19273608-0 2009 Glucose effects on beta-cell growth and survival require activation of insulin receptors and insulin receptor substrate 2. Glucose 0-7 insulin Homo sapiens 71-78 19273608-0 2009 Glucose effects on beta-cell growth and survival require activation of insulin receptors and insulin receptor substrate 2. Glucose 0-7 insulin Homo sapiens 93-100 19273608-5 2009 Exogenous addition of either insulin or glucose activated proteins in the insulin signaling pathway in control beta-cell lines with the effects of insulin peaking earlier than glucose. Glucose 40-47 insulin Homo sapiens 74-81 19273608-5 2009 Exogenous addition of either insulin or glucose activated proteins in the insulin signaling pathway in control beta-cell lines with the effects of insulin peaking earlier than glucose. Glucose 40-47 insulin Homo sapiens 74-81 19273608-5 2009 Exogenous addition of either insulin or glucose activated proteins in the insulin signaling pathway in control beta-cell lines with the effects of insulin peaking earlier than glucose. Glucose 176-183 insulin Homo sapiens 29-36 19273608-5 2009 Exogenous addition of either insulin or glucose activated proteins in the insulin signaling pathway in control beta-cell lines with the effects of insulin peaking earlier than glucose. Glucose 176-183 insulin Homo sapiens 74-81 19273608-5 2009 Exogenous addition of either insulin or glucose activated proteins in the insulin signaling pathway in control beta-cell lines with the effects of insulin peaking earlier than glucose. Glucose 176-183 insulin Homo sapiens 74-81 19273608-9 2009 Together, these studies provide compelling evidence that the growth and survival effects of glucose on beta-cells require activation of proteins in the insulin signaling pathway. Glucose 92-99 insulin Homo sapiens 152-159 19164322-5 2009 Insulin resistance was calculated using fasting glucose and insulin, expressed as HOMA-IR. Glucose 48-55 insulin Homo sapiens 0-7 19463742-7 2009 NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. Glucose 37-44 insulin Homo sapiens 18-25 19842560-3 2009 At the time of admission, a continuous infusion of insulin (2-4 U/h) was pumped into the patients of IT group to maintain blood glucose level at 6-8 mmol/L. Glucose 128-135 insulin Homo sapiens 51-58 19496630-3 2009 Insulin glulisine and insulin lispro have similar effects on glucose levels. Glucose 61-68 insulin Homo sapiens 0-7 19496630-3 2009 Insulin glulisine and insulin lispro have similar effects on glucose levels. Glucose 61-68 insulin Homo sapiens 22-29 19364109-6 2009 These results suggested that c9,t11-CLA induced an insulin-independent enhancement of glucose and fatty acid metabolism. Glucose 86-93 insulin Homo sapiens 51-58 19433249-2 2009 The main functions of pancreatic beta-cells are the biosynthesis and release of insulin, the only hormone that can directly decrease blood glucose levels. Glucose 139-146 insulin Homo sapiens 80-87 26561693-1 2000 First suggested in beta-cells by the observations of Haist in 1940 (3), the notion that high glucose exerts multiple pathological effects on many cells and tissues has been established by abundant evidence for its causative role in the chronic microvascular complications of diabetes (4-6), its effects on insulin action in metabolic target tissues (7,8), and in several other adverse outcomes noted in people with diabetes, such as frequent fungal infections (9) and an increased frequency of congenital birth defects (10). Glucose 93-100 insulin Homo sapiens 306-313 19265681-1 2009 Post-menopausal women exhibit decreases in circulating estrogen levels and whole body insulin sensitivity, suggesting that estrogen regulates skeletal muscle glucose disposal. Glucose 158-165 insulin Homo sapiens 86-93 21437117-3 2009 RESULTS: Insulin detemir improves glycemic control, based on HbA(1C) reduction and fasting glucose levels, without increasing the risk of hypoglycemia and weight gain. Glucose 91-98 insulin Homo sapiens 9-16 21437117-4 2009 Insulin detemir has lower glycemic variability, with less intra-subject variability in blood glucose levels in patients with type 1 and type 2 diabetes, without increasing the risk of hypoglycemia. Glucose 93-100 insulin Homo sapiens 0-7 19429412-3 2009 ATP also triggers a positive feedback signal amplifying glucose-induced insulin release, which argues for a potential pharmacological application. Glucose 56-63 insulin Homo sapiens 72-79 19429412-6 2009 Activation of G-protein-coupled P2Y receptors triggers different signalling pathways and amplifies insulin release in a glucose-dependent way. Glucose 120-127 insulin Homo sapiens 99-106 19289105-0 2009 YM201636, an inhibitor of retroviral budding and PIKfyve-catalyzed PtdIns(3,5)P2 synthesis, halts glucose entry by insulin in adipocytes. Glucose 98-105 insulin Homo sapiens 115-122 19289105-7 2009 We suggest that apart from PIKfyve, there are at least two additional targets for YM201636 in the context of insulin signaling to GLUT4 and glucose uptake: the insulin-activated class IA PI 3-kinase and a here-unidentified high-affinity target responsible for the greater inhibition of glucose entry vs. GLUT4 translocation. Glucose 140-147 insulin Homo sapiens 109-116 19289105-7 2009 We suggest that apart from PIKfyve, there are at least two additional targets for YM201636 in the context of insulin signaling to GLUT4 and glucose uptake: the insulin-activated class IA PI 3-kinase and a here-unidentified high-affinity target responsible for the greater inhibition of glucose entry vs. GLUT4 translocation. Glucose 140-147 insulin Homo sapiens 160-167 19289105-7 2009 We suggest that apart from PIKfyve, there are at least two additional targets for YM201636 in the context of insulin signaling to GLUT4 and glucose uptake: the insulin-activated class IA PI 3-kinase and a here-unidentified high-affinity target responsible for the greater inhibition of glucose entry vs. GLUT4 translocation. Glucose 286-293 insulin Homo sapiens 109-116 19289105-8 2009 The profound inhibition of the net insulin effect on glucose influx at YM201636 doses markedly lower than those required for efficient retroviral budding disruption warns of severe perturbations in glucose homeostasis associated with potential YM201636 use in antiretroviral therapy. Glucose 53-60 insulin Homo sapiens 35-42 19827447-0 2009 [Insulin secretion is increased depending on glucose.. Metabolism regulation in type 2 diabetes mellitus over five paths]. Glucose 45-52 insulin Homo sapiens 1-8 19223652-0 2009 Insulin blunts the response of glucose-excited neurons in the ventrolateral-ventromedial hypothalamic nucleus to decreased glucose. Glucose 31-38 insulin Homo sapiens 0-7 19351807-7 2009 The glucose-stimulated insulin response was reduced after EX-HYPO (P = 0.02), as was the glucose-stimulated GIP response (P < 0.05). Glucose 4-11 insulin Homo sapiens 23-30 19351807-10 2009 We conclude that 1) a combination of caloric restriction and exercise reduces the GIP response to ingested glucose, 2) GIP may mediate the attenuated glucose-stimulated insulin response after exercise/diet interventions, and 3) the increased PYY(3-36) response represents an improved capacity to regulate satiety and potentially body weight in older, obese, insulin-resistant adults. Glucose 150-157 insulin Homo sapiens 169-176 19448209-5 2009 A review of the basal insulin dose revealed that it had been inappropriately increased to control elevated postprandial glucose. Glucose 120-127 insulin Homo sapiens 22-29 19459810-6 2009 Mathematical model analysis of an intravenous glucose tolerance test determined first-phase insulin secretion, insulin sensitivity and disposition index. Glucose 46-53 insulin Homo sapiens 92-99 19448691-7 2009 In contrast, when PGC-1alpha was overexpressed modestly, within physiological limits, mitochondrial fatty acid oxidation was increased, GLUT4 expression was upregulated, and insulin-stimulated glucose transport was increased. Glucose 193-200 insulin Homo sapiens 174-181 19448705-1 2009 Skeletal muscle is the largest tissue responsible for the insulin-stimulated disposal of glucose. Glucose 89-96 insulin Homo sapiens 58-65 19272350-0 2009 Inhibition of uncoupling protein 2 by genipin reduces insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Glucose 73-80 insulin Homo sapiens 54-61 19272350-2 2009 However, the role of UCP2 on insulin-stimulated glucose uptake in adipose tissue, which is an indispensable process in insulin-glucose homeostasis, remains unknown. Glucose 48-55 insulin Homo sapiens 29-36 19272350-4 2009 Importantly, insulin-stimulated glucose uptake in 3T3-L1 adipocytes was largely impaired in the presence of genipin, and recovered by CCCP, a mitochondrial uncoupler. Glucose 32-39 insulin Homo sapiens 13-20 19272350-6 2009 These results suggest that mitochondrial uncoupling in adipocytes positively regulates insulin-stimulated glucose uptake in adipocytes, and UCP2 may play an important role in insulin resistance. Glucose 106-113 insulin Homo sapiens 87-94 19476649-0 2009 Indices of insulin sensitivity and secretion from a standard liquid meal test in subjects with type 2 diabetes, impaired or normal fasting glucose. Glucose 139-146 insulin Homo sapiens 11-18 19671340-0 2009 [Expression of iPLA2 in human pancreatic islets and its important role in glucose-stimulated insulin secretion]. Glucose 74-81 insulin Homo sapiens 93-100 19671340-3 2009 Bromoenol lactone (BEL), a selective inhibitor of iPLA2, was used in a randomized controlled trial to compare its influence to glucose-stimulated insulin secretion. Glucose 127-134 insulin Homo sapiens 146-153 19671340-6 2009 Glucose-stimulated insulin secretory response was dramatically reduced in islets pretreated with BEL (0.8285 +/- 0.0803 ng x islet(-1) x h(-1)) as compared with the control (1.2264 +/- 0.0568 ng x islet(-1) x h(-1)) (P < 0.01). Glucose 0-7 insulin Homo sapiens 19-26 19671340-7 2009 BEL inhibited glucose stimulated insulin secretion from isolated human islets. Glucose 14-21 insulin Homo sapiens 33-40 19671340-8 2009 CONCLUSION: iPLA2 signaling plays an important role in glucose-stimulated insulin secretion under the physiological conditions. Glucose 55-62 insulin Homo sapiens 74-81 19428987-2 2009 A feedback loop was added to link the transportation of glucose into cells (by GLUT4 in the insulin-signaling pathways) and the insulin-dependent glucose uptake in the glucose regulation model using the Michaelis-Menten kinetic model. Glucose 56-63 insulin Homo sapiens 92-99 19428987-2 2009 A feedback loop was added to link the transportation of glucose into cells (by GLUT4 in the insulin-signaling pathways) and the insulin-dependent glucose uptake in the glucose regulation model using the Michaelis-Menten kinetic model. Glucose 56-63 insulin Homo sapiens 128-135 19428987-2 2009 A feedback loop was added to link the transportation of glucose into cells (by GLUT4 in the insulin-signaling pathways) and the insulin-dependent glucose uptake in the glucose regulation model using the Michaelis-Menten kinetic model. Glucose 146-153 insulin Homo sapiens 128-135 19428987-2 2009 A feedback loop was added to link the transportation of glucose into cells (by GLUT4 in the insulin-signaling pathways) and the insulin-dependent glucose uptake in the glucose regulation model using the Michaelis-Menten kinetic model. Glucose 146-153 insulin Homo sapiens 128-135 19428987-5 2009 Based on the results of this study, the combined model enables us to understand the overall dynamics of glucose at the systemic level, monitor the time profile of components in the insulin-signaling pathways at the cellular level and gives a good estimate of the K(m) value of glucose transportation by GLUT4. Glucose 277-284 insulin Homo sapiens 181-188 19372374-1 2009 Insulin secretion is biphasic in response to a step in glucose stimulation. Glucose 55-62 insulin Homo sapiens 0-7 19245657-5 2009 Understanding how these secreted signalling proteins regulate AMPK activity to control fatty acid oxidation, glucose uptake, gluconeogenesis and appetite may yield therapeutic treatments for metabolic disorders such as diabetes, insulin resistance and obesity. Glucose 109-116 insulin Homo sapiens 229-236 19279229-5 2009 Moreover, IGFBP-3 inhibits insulin-stimulated glucose uptake into adipocytes independent of IGF. Glucose 46-53 insulin Homo sapiens 27-34 19411582-10 2009 The magnitude of these differences calls into question the widespread practice of using point-of-care glucose testing to guide insulin titration for tight glucose control. Glucose 155-162 insulin Homo sapiens 127-134 19203789-1 2009 A glucose-sensitive multilayer shell, which was fabricated by the layer-by-layer (LbL) assembly method, can be used as a carrier for the encapsulation and controlled release of insulin. Glucose 2-9 insulin Homo sapiens 177-184 19203789-4 2009 When the external glucose was introduced, the release ratio of insulin from the protein multilayer can be increased observably. Glucose 18-25 insulin Homo sapiens 63-70 19203789-9 2009 Therefore, such CAT/GOD multilayer may have a great potential as a glucose-sensitive release carrier for insulin, and may open the way for the further application of LbL capsules in the drug delivery and controlled release, etc. Glucose 67-74 insulin Homo sapiens 105-112 19175375-13 2009 Some studies showed that rapid-acting insulin analogues frequently result in a better HbA1c or postprandial glucose without increase of hypoglycaemia than regular human insulin. Glucose 108-115 insulin Homo sapiens 38-45 19539098-7 2009 The effect of the device on insulin absorption and postprandial glucose excursions was tested by measuring blood glucose and insulin concentration profiles with and without the operation of the device. Glucose 113-120 insulin Homo sapiens 28-35 19196884-1 2009 OBJECTIVE: The purpose of this study was to characterize differences in the acute insulin response to glucose (AIR(g)) relative to insulin sensitivity (S(I)) in black and white premenopausal normoglycemic South African women matched for body fatness. Glucose 102-109 insulin Homo sapiens 82-89 19539098-17 2009 CONCLUSION: In this pilot study, use of the InsuPatch was associated with significant decreases in T(max) and T(50%max) and increases in insulin AUC and C(max) of subcutaneous infused rapid-acting insulin analogues, resulting in a lower postprandial glucose excursion in these patients with type 1 diabetes mellitus treated with CSII. Glucose 250-257 insulin Homo sapiens 137-144 19196884-8 2009 CONCLUSIONS: Black South African women are more insulin resistant than their white counterparts but compensate by increasing their insulin response to maintain normal glucose levels, suggesting an appropriate beta-cell response for the level of insulin sensitivity. Glucose 167-174 insulin Homo sapiens 131-138 19196887-7 2009 RESULTS: Treatment-induced change in combined glucose- and arginine-stimulated C-peptide secretion was 2.46-fold (95% CI 2.09-2.90, P < 0.0001) greater after a 52-week exenatide treatment compared with insulin glargine treatment. Glucose 46-53 insulin Homo sapiens 205-212 19196884-8 2009 CONCLUSIONS: Black South African women are more insulin resistant than their white counterparts but compensate by increasing their insulin response to maintain normal glucose levels, suggesting an appropriate beta-cell response for the level of insulin sensitivity. Glucose 167-174 insulin Homo sapiens 131-138 19196896-11 2009 In contrast, rates of postprandial glucose disappearance were substantially decreased due to defects in insulin secretion, insulin action, and glucose effectiveness. Glucose 35-42 insulin Homo sapiens 104-111 19208914-1 2009 OBJECTIVE: To test the hypotheses that decreased insulin-mediated glucose disposal in muscle is associated with a reduced muscle microvascular exchange capacity (Kf) and that 6 months of high-dose statin therapy would improve microvascular function in people with central obesity. Glucose 66-73 insulin Homo sapiens 49-56 19208914-4 2009 RESULTS: Kf was negatively associated with a measure of glycemia (A1C; r = -0.44, P = 0.006) and positively associated with insulin sensitivity (the ratio of insulin-stimulated glucose effectiveness, or M value, to the mean insulin concentration, or I value; r = 0.39, P = 0.02). Glucose 177-184 insulin Homo sapiens 158-165 19208914-4 2009 RESULTS: Kf was negatively associated with a measure of glycemia (A1C; r = -0.44, P = 0.006) and positively associated with insulin sensitivity (the ratio of insulin-stimulated glucose effectiveness, or M value, to the mean insulin concentration, or I value; r = 0.39, P = 0.02). Glucose 177-184 insulin Homo sapiens 158-165 19208914-8 2009 CONCLUSIONS: Decreased insulin-mediated glucose uptake in skeletal muscle is associated with impaired muscle microvascular exchange capacity (Kf), independently of visceral fat mass. Glucose 40-47 insulin Homo sapiens 23-30 19228868-5 2009 CONCLUSIONS: Childhood insulin response during an oral glucose challenge predicts adult AIR, indicating that beta-cell capacity may be set early in life. Glucose 55-62 insulin Homo sapiens 23-30 19236441-2 2009 AIMS: To use continuous glucose monitoring (CGMS) to compare glucose profiles in people with type 1 diabetes following injection of insulin into an area affected by lipohypertrophy vs. an area not affected by lipohypertrophy. Glucose 61-68 insulin Homo sapiens 132-139 19252892-3 2009 METHODS: In a cross-sectional study, subcutaneous abdominal adipose tissue biopsies from 59 people were examined in relation to fasting and post-glucose insulin sensitivity. Glucose 145-152 insulin Homo sapiens 153-160 19252894-1 2009 AIMS/HYPOTHESIS: TBC1 domain family, member 4 (TBC1D4; also known as AS160) is a cellular signalling intermediate to glucose transport regulated by insulin-dependent and -independent mechanisms. Glucose 117-124 insulin Homo sapiens 148-155 19252894-4 2009 METHODS: Insulin-regulated glucose metabolism was evaluated in 12 healthy moderately trained young men 4 h after one-legged exercise at basal and during a euglycaemic-hyperinsulinaemic clamp. Glucose 27-34 insulin Homo sapiens 9-16 19252894-6 2009 RESULTS: Insulin stimulation increased glucose uptake in both legs, with greater effects (approximately 80%, p < 0.01) in the previously exercised leg. Glucose 39-46 insulin Homo sapiens 9-16 19283361-1 2009 Evidence suggests that insulin delivery to skeletal muscle interstitium is the rate-limiting step in insulin-stimulated muscle glucose uptake and that this process is impaired by insulin resistance. Glucose 127-134 insulin Homo sapiens 23-30 19283361-1 2009 Evidence suggests that insulin delivery to skeletal muscle interstitium is the rate-limiting step in insulin-stimulated muscle glucose uptake and that this process is impaired by insulin resistance. Glucose 127-134 insulin Homo sapiens 101-108 19425877-0 2009 Use of short-term real-time continuous glucose monitoring in type 1 diabetes patients on continuous intraperitoneal insulin infusion: a feasibility study. Glucose 39-46 insulin Homo sapiens 116-123 19537357-8 2009 CONCLUSIONS: Prandial insulin therapy with EXU, using a higher daily insulin dose, reduces total daily glucose exposure--in particular postmeal glycemia--more effectively than a basal insulin analog. Glucose 103-110 insulin Homo sapiens 22-29 19106222-5 2009 Inhibition of Rho and of ROCK increased spreading and improved both short-term and prolonged glucose-stimulated insulin secretion but had no impact on basal secretion. Glucose 93-100 insulin Homo sapiens 112-119 19106222-9 2009 Overall these results show for the first time that the Rho-ROCK signaling pathway contributes to the stabilization of the actin cytoskeleton and inhibits glucose-stimulated insulin secretion in primary pancreatic beta-cells. Glucose 154-161 insulin Homo sapiens 173-180 19141606-2 2009 DESIGN AND METHODS: To investigate this, we assessed the sensitivity of glucose metabolism to insulin both in vivo (by an oral glucose tolerance test) and in vitro (by measuring insulin-stimulated rates of glucose transport in isolated monocytes with flow cytometry) in 21 euthyroid subjects (EU), 12 patients with HO, and 13 patients with SHO. Glucose 72-79 insulin Homo sapiens 94-101 19141606-2 2009 DESIGN AND METHODS: To investigate this, we assessed the sensitivity of glucose metabolism to insulin both in vivo (by an oral glucose tolerance test) and in vitro (by measuring insulin-stimulated rates of glucose transport in isolated monocytes with flow cytometry) in 21 euthyroid subjects (EU), 12 patients with HO, and 13 patients with SHO. Glucose 127-134 insulin Homo sapiens 94-101 19141606-6 2009 CONCLUSIONS: In patients with HO and SHO: i) insulin resistance was comparable; ii) insulin-stimulated rates of glucose transport in isolated monocytes were decreased due to impaired translocation of GLUT4 glucose transporters on the plasma membrane; iii) these findings could justify the increased risk for insulin resistance-associated disorders, such as cardiovascular disease, observed in patients with HO or SHO. Glucose 112-119 insulin Homo sapiens 84-91 19141606-6 2009 CONCLUSIONS: In patients with HO and SHO: i) insulin resistance was comparable; ii) insulin-stimulated rates of glucose transport in isolated monocytes were decreased due to impaired translocation of GLUT4 glucose transporters on the plasma membrane; iii) these findings could justify the increased risk for insulin resistance-associated disorders, such as cardiovascular disease, observed in patients with HO or SHO. Glucose 112-119 insulin Homo sapiens 84-91 19219452-1 2009 Recent evidence suggests that insulin sensitivity is relatively better preserved in arm muscle than in leg muscle in both healthy controls and type 2 DM, based on measurements of basal and insulin-mediated glucose clearance performed simultaneously in the two sets of muscles. Glucose 206-213 insulin Homo sapiens 30-37 19219452-1 2009 Recent evidence suggests that insulin sensitivity is relatively better preserved in arm muscle than in leg muscle in both healthy controls and type 2 DM, based on measurements of basal and insulin-mediated glucose clearance performed simultaneously in the two sets of muscles. Glucose 206-213 insulin Homo sapiens 189-196 19320939-5 2009 The level of blood glucose was assessed by fasting plasma glucose (FPG), fasting immunoreactive insulin, homeostasis model assessment (HOMA) index, and haemoglobin A1c. Glucose 19-26 insulin Homo sapiens 96-103 19389241-5 2009 Alternatively, we tested in a separate baboon population (n = 159), a simpler model based on body weight and fasting plasma glucose to predict the whole-body insulin sensitivity (Rd/SSPI) derived from the clamp. Glucose 124-131 insulin Homo sapiens 158-165 19223652-0 2009 Insulin blunts the response of glucose-excited neurons in the ventrolateral-ventromedial hypothalamic nucleus to decreased glucose. Glucose 123-130 insulin Homo sapiens 0-7 19223652-6 2009 Furthermore, insulin reduced the sensitivity of VMH GE neurons to a decrease in extracellular glucose level from 2.5 to 0.1 mM. Glucose 94-101 insulin Homo sapiens 13-20 19223652-7 2009 This change in the glucose sensitivity in the presence of insulin was reversed by the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin (10 nM) but not by the mitogen-activated kinase (MAPK) inhibitor PD-98059 (PD; 50 microM). Glucose 19-26 insulin Homo sapiens 58-65 19223652-9 2009 These data suggest that insulin attenuates the ability of VMH GE neurons to sense decreased glucose via the PI3K signaling pathway. Glucose 92-99 insulin Homo sapiens 24-31 19223652-11 2009 That is, in the presence of insulin, glucose levels must decline further before GE neurons respond. Glucose 37-44 insulin Homo sapiens 28-35 18565519-10 2009 Only fasting glucose and insulin, 2-hour insulin, HOMA-IR, age, androstenedione, and status (PCOS vs. control) had a significant impact on 2-hour glucose level. Glucose 146-153 insulin Homo sapiens 25-32 19208352-6 2009 Insulin-mediated glucose uptake did not change at 48 hours but increased similarly in both groups after 7% weight loss (48.4% +/- 14.3%; P < .05). Glucose 17-24 insulin Homo sapiens 0-7 19218574-2 2009 Phosphatidylinositol (PI) 3-kinase is an important enzyme in the early insulin signaling cascade and plays a key role in insulin-mediated glucose transport. Glucose 138-145 insulin Homo sapiens 121-128 19473593-5 2009 MATERIAL AND METHODS: Insulin sensitivity indices (SI indices) were obtained by analyzing fasting glucose and insulin concentration with homeostasis model assessment (HOMA), the glucose and insulin profiles after 75 g dextrose oral glucose tolerance tests (OGTT, Matsuda-Index) and euglycemic hyperinsulinemic clamp (m-value) in a double-blind placebo-controlled study in 60 patients with arterial hypertension before and after 4 months treatment with Pioglitazone 45 mg (PIO45). Glucose 98-105 insulin Homo sapiens 22-29 19473593-5 2009 MATERIAL AND METHODS: Insulin sensitivity indices (SI indices) were obtained by analyzing fasting glucose and insulin concentration with homeostasis model assessment (HOMA), the glucose and insulin profiles after 75 g dextrose oral glucose tolerance tests (OGTT, Matsuda-Index) and euglycemic hyperinsulinemic clamp (m-value) in a double-blind placebo-controlled study in 60 patients with arterial hypertension before and after 4 months treatment with Pioglitazone 45 mg (PIO45). Glucose 178-185 insulin Homo sapiens 22-29 19473593-5 2009 MATERIAL AND METHODS: Insulin sensitivity indices (SI indices) were obtained by analyzing fasting glucose and insulin concentration with homeostasis model assessment (HOMA), the glucose and insulin profiles after 75 g dextrose oral glucose tolerance tests (OGTT, Matsuda-Index) and euglycemic hyperinsulinemic clamp (m-value) in a double-blind placebo-controlled study in 60 patients with arterial hypertension before and after 4 months treatment with Pioglitazone 45 mg (PIO45). Glucose 178-185 insulin Homo sapiens 22-29 19391163-1 2009 Like insulin, muscle contraction (in vitro or in situ) and exercise increase glucose uptake into skeletal muscle. Glucose 77-84 insulin Homo sapiens 5-12 19391163-2 2009 However, the contraction/exercise pathway of glucose uptake in skeletal muscle is an independent pathway to that of insulin. Glucose 45-52 insulin Homo sapiens 116-123 19391163-3 2009 Indeed, skeletal muscle glucose uptake is normal during exercise in those who suffer from insulin resistance and diabetes. Glucose 24-31 insulin Homo sapiens 90-97 19265062-6 2009 The intravenous glucose tolerance test (IVGTT) was used to assess insulin-dependent and insulin-independent measures of glucose disposal. Glucose 16-23 insulin Homo sapiens 66-73 19265200-9 2009 Moreover, Smad3 deficiency results in improved glucose tolerance and enhanced glucose-stimulated insulin secretion in vivo. Glucose 78-85 insulin Homo sapiens 97-104 19265200-10 2009 In ex vivo perifusion assays, Smad3-deficient islets exhibit improved glucose-stimulated insulin release. Glucose 70-77 insulin Homo sapiens 89-96 19349879-5 2009 Insulin significantly reduced blood glucose in injured animals to levels no different from those seen in animals that were neither ethanol exposed nor burned. Glucose 36-43 insulin Homo sapiens 0-7 19190104-1 2009 CONTEXT: The purpose of this study was to examine the effect of continuous sc replacement of amylin and insulin for a 24-h period on glucose homeostasis in adolescents with type 1diabetes. Glucose 133-140 insulin Homo sapiens 104-111 19190104-10 2009 CONCLUSIONS: Simultaneous continuous sc pramlintide and insulin infusion has the potential of improving glucose concentrations by way of physiological replacement. Glucose 104-111 insulin Homo sapiens 56-63 19240154-8 2009 Glucose values were significantly augmented for 6 months post-burn (P < 0.05), associated with significant increases in serum C-peptide and insulin that remained significantly increased for 36 months compared to nonburned children (P < 0.05). Glucose 0-7 insulin Homo sapiens 143-150 19273501-1 2009 Insulin stimulates cardiac long-chain fatty acid (LCFA) and glucose uptake via translocation of human homolog of rat fatty acid translocase (CD36) and GLUT4 respectively, from intracellular membrane compartments to the sarcolemma, a process dependent on the activation of phosphatidylinositol-3 kinase. Glucose 60-67 insulin Homo sapiens 0-7 19273501-3 2009 Insulin-stimulated LCFA and glucose uptake were completely blunted by inhibition of PKC-zeta, but not by inhibition of conventional or novel PKCs. Glucose 28-35 insulin Homo sapiens 0-7 19273501-9 2009 However, PKC-zeta is already fully active under basal conditions and not further activated by insulin, indicating that its role in insulin-stimulated uptake of both glucose and LCFA is permissive rather than regulatory. Glucose 165-172 insulin Homo sapiens 131-138 20144285-1 2009 BACKGROUND: The importance of near-normal blood glucose in the immediate postoperative period is generally accepted and is best achieved in the perioperative period with a constant intravenous (IV) infusion of insulin. Glucose 48-55 insulin Homo sapiens 210-217 20144286-1 2009 BACKGROUND: This article provides a clinical update using a novel run-to-run algorithm to optimize prandial insulin dosing based on sparse glucose measurements from the previous day"s meals. Glucose 139-146 insulin Homo sapiens 108-115 20144293-2 2009 As a result, people with T1DM depend on exogenous insulin that is given either by multiple daily injections or by an insulin pump to control their blood glucose. Glucose 153-160 insulin Homo sapiens 50-57 20144293-2 2009 As a result, people with T1DM depend on exogenous insulin that is given either by multiple daily injections or by an insulin pump to control their blood glucose. Glucose 153-160 insulin Homo sapiens 117-124 20144293-4 2009 The core of such a system is a control algorithm that calculates the insulin dose based on automated glucose measurements. Glucose 101-108 insulin Homo sapiens 69-76 20144293-7 2009 RESULTS: The results emphasized the ability of the IOB constraint to significantly improve the glucose/insulin control trajectories in the presence of aggressive control actions. Glucose 95-102 insulin Homo sapiens 103-110 19321584-10 2009 There was a beverage x week interaction (P = 0.044) on insulin area under the curve showing a trend toward reduced insulin output with a glucose challenge after high-milk consumption (P = 0.062). Glucose 137-144 insulin Homo sapiens 55-62 19221053-5 2009 We also found that MOR-1 KO mice exhibit enhanced glucose tolerance that results from insulin hypersecretion that reflects increased beta-cell mass and increased secretory dynamics in the MOR-1 mutant mice compared with wild type. Glucose 50-57 insulin Homo sapiens 86-93 19221053-6 2009 Analysis of the isolated islets indicated that islet insulin hypersecretion is mediated directly by MOR expressed on islet cells via a mechanism downstream of ATP-sensitive K(+) channel activation by glucose. Glucose 200-207 insulin Homo sapiens 53-60 19375586-7 2009 The IR index from fasting plasma insulin and plasma glucose levels was estimated using the homeostasis model assessment (HOMA), as follows: fasting plasma insulin (in microliter units per milliliter) x fasting plasma glucose (in millimoles per liter)/22.5. Glucose 52-59 insulin Homo sapiens 155-162 19375593-0 2009 Insulin resistance predicts future deterioration of glucose tolerance in nondiabetic young African Americans. Glucose 52-59 insulin Homo sapiens 0-7 24345564-7 2009 Suppression of blood glucose by enhanced insulin secretion triggered by the increase of insulin resistance may begin to lose its effect as waist circumference becomes larger. Glucose 21-28 insulin Homo sapiens 41-48 24345564-7 2009 Suppression of blood glucose by enhanced insulin secretion triggered by the increase of insulin resistance may begin to lose its effect as waist circumference becomes larger. Glucose 21-28 insulin Homo sapiens 88-95 19307807-9 2009 The blood glucose threshold for starting insulin varied widely from 6.1 to>15 mmol x L(-1) (110-270 mg x dL(-1)) for each of the six scenarios,with poor agreement between intensivists within each center(intraclass correlation coefficient of 0.29). Glucose 10-17 insulin Homo sapiens 41-48 19201177-9 2009 APS could alleviate insulin resistance and ER stress induced by high glucose in vivo and in vitro, respectively. Glucose 69-76 insulin Homo sapiens 20-27 19460560-9 2009 Up to 20.1% of the cells in pancreatic 3-dimensional structures induced by 17.8 mmol/L glucose were positive for insulin, and <3.2%, for glucagon. Glucose 87-94 insulin Homo sapiens 113-120 19460560-10 2009 The positive ratio of immunoreactive staining was dependent on the glucose concentration; 17.8 mmol/L glucose effectively stimulated insulin- and glucagon-secreting cells. Glucose 67-74 insulin Homo sapiens 133-140 19460560-10 2009 The positive ratio of immunoreactive staining was dependent on the glucose concentration; 17.8 mmol/L glucose effectively stimulated insulin- and glucagon-secreting cells. Glucose 102-109 insulin Homo sapiens 133-140 19418413-1 2009 BACKGROUND: Patients with liver cirrhosis develop frequently disturbances of glucose metabolism e. g. glucose intolerance or hepatogenous diabetes which are caused by the hepatocellular functional loss and insulin resistance due to chronic liver disease. Glucose 77-84 insulin Homo sapiens 206-213 19237543-8 2009 Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is a key node in the convergence of FGF and insulin signaling pathways and functions as a key integrator for the regulation of glucose and bile acid metabolism. Glucose 221-228 insulin Homo sapiens 8-15 19237543-8 2009 Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is a key node in the convergence of FGF and insulin signaling pathways and functions as a key integrator for the regulation of glucose and bile acid metabolism. Glucose 221-228 insulin Homo sapiens 138-145 19389241-6 2009 RESULTS: In the first model, abdominal circumference explained 59% of total insulin mediated glucose uptake (Rd). Glucose 93-100 insulin Homo sapiens 76-83 19349317-2 2009 We hypothesized that HDL modulates glucose metabolism via elevation of plasma insulin and through activation of the key metabolic regulatory enzyme, AMP-activated protein kinase, in skeletal muscle. Glucose 35-42 insulin Homo sapiens 78-85 19349317-9 2009 CONCLUSIONS: rHDL reduced plasma glucose in patients with type 2 diabetes mellitus by increasing plasma insulin and activating AMP-activated protein kinase in skeletal muscle. Glucose 33-40 insulin Homo sapiens 104-111 19386915-1 2009 The insulin-sensitive isoform of the glucose transporting protein, Glut4, is expressed in fat as well as in skeletal and cardiac muscle and is responsible for the effect of insulin on blood glucose clearance. Glucose 37-44 insulin Homo sapiens 4-11 19386915-1 2009 The insulin-sensitive isoform of the glucose transporting protein, Glut4, is expressed in fat as well as in skeletal and cardiac muscle and is responsible for the effect of insulin on blood glucose clearance. Glucose 37-44 insulin Homo sapiens 173-180 19386915-4 2009 In cultured cerebellar neurons, insulin stimulates glucose uptake and causes translocation of Glut4 to the cell surface. Glucose 51-58 insulin Homo sapiens 32-39 19590752-1 2009 BACKGROUND: Endosomal small GTPases of the Rab family, among them Rab4a, play an essential role in the control of the glucose transporter GLUT4 trafficking, which is essential for insulin-mediated glucose uptake. Glucose 118-125 insulin Homo sapiens 180-187 31569894-1 2009 Insulin therapy is a pharmaceutical treatment used for patients with diabetes to normalize blood glucose level. Glucose 97-104 insulin Homo sapiens 0-7 31569894-2 2009 In patients receiving insulin therapy, optimization of blood glucose levels can be achieved using various types of insulin and various methods, such as MDI (multiple daily injections) and CSII (continuous subcutaneous insulin infusion). Glucose 61-68 insulin Homo sapiens 22-29 31569894-2 2009 In patients receiving insulin therapy, optimization of blood glucose levels can be achieved using various types of insulin and various methods, such as MDI (multiple daily injections) and CSII (continuous subcutaneous insulin infusion). Glucose 61-68 insulin Homo sapiens 115-122 31569894-2 2009 In patients receiving insulin therapy, optimization of blood glucose levels can be achieved using various types of insulin and various methods, such as MDI (multiple daily injections) and CSII (continuous subcutaneous insulin infusion). Glucose 61-68 insulin Homo sapiens 115-122 18728222-1 2009 Insulin signaling at target tissues is essential for growth and development and for normal homeostasis of glucose, fat, and protein metabolism. Glucose 106-113 insulin Homo sapiens 0-7 19190265-0 2009 Reduced malonyl-CoA content in recovery from exercise correlates with improved insulin-stimulated glucose uptake in human skeletal muscle. Glucose 98-105 insulin Homo sapiens 79-86 19190265-1 2009 This study evaluated whether improved insulin-stimulated glucose uptake in recovery from acute exercise coincides with reduced malonyl-CoA (MCoA) content in human muscle. Glucose 57-64 insulin Homo sapiens 38-45 19190265-4 2009 Four hours after exercise, insulin-stimulated glucose uptake was determined in both legs during a euglycemic-hyperinsulinemic clamp. Glucose 46-53 insulin Homo sapiens 27-34 19190265-6 2009 Four hours after exercise, insulin-stimulated glucose uptake was improved (approximately 70%, P<0.001) independent of diet composition and despite normal insulin-stimulated regulation of insulin receptor substrate-1-associated phosphatidylinositol 3-kinase, Akt, GSK-3, and glycogen synthase. Glucose 46-53 insulin Homo sapiens 27-34 19190265-7 2009 Interestingly, exercise resulted in a sustained reduction (approximately 20%, P<0.05) in MCoA content 4 h after exercise that correlated (r=0.65, P<0.001) with improved insulin-stimulated glucose uptake. Glucose 194-201 insulin Homo sapiens 175-182 19190265-9 2009 However, at the muscular level proximal insulin signaling and insulin-stimulated glucose uptake appeared to be compromised, although to a minor extent, by the Fat diet. Glucose 81-88 insulin Homo sapiens 62-69 19190265-10 2009 Collectively, this study indicates that reduced muscle MCoA content in recovery from exercise may be part of the adaptive response leading to improved insulin action on glucose uptake after exercise in human muscle. Glucose 169-176 insulin Homo sapiens 151-158 19336649-7 2009 Data analysis demonstrated significantly lower median blood glucose values with the use of subcutaneous insulin doses that were 60-70% of insulin infusion requirements when compared with all other groups. Glucose 60-67 insulin Homo sapiens 104-111 19336649-7 2009 Data analysis demonstrated significantly lower median blood glucose values with the use of subcutaneous insulin doses that were 60-70% of insulin infusion requirements when compared with all other groups. Glucose 60-67 insulin Homo sapiens 138-145 19076072-1 2009 Postprandial blood glucose clearance is mediated by GLUT4 (glucose transporter 4) which is translocated from an intracellular storage pool to the plasma membrane in response to insulin. Glucose 19-26 insulin Homo sapiens 177-184 19201021-8 2009 Insulin secretion ability by glucose stimulation was well maintained on these cell-encapsulated islets. Glucose 29-36 insulin Homo sapiens 0-7 19288584-0 2009 Noncompartmental pharmacokinetics analysis of glucose-stimulated insulin response in African-American and Caucasian youths. Glucose 46-53 insulin Homo sapiens 65-72 19288584-5 2009 African-American youths were found to have higher insulin responses after glucose stimulation and the insulin concentrations were more related to BMI in Caucasians compared with African-Americans. Glucose 74-81 insulin Homo sapiens 50-57 19288584-7 2009 The acute insulin response to glucose (AIR(g)) extended to 20 min resulted in a more significant racial difference (p<0.0006) compared with the calculation done over 10 min suggested in the past (p<0.001). Glucose 30-37 insulin Homo sapiens 10-17 19167374-1 2009 The self-monitoring of blood glucose (SMBG), traditionally performed by "point-of-care" (POC) devices called portable glucose monitors (PGM) is now considered an integral part of managed care of diabetic patients, especially type 1 diabetics and those on insulin therapy. Glucose 29-36 insulin Homo sapiens 255-262 19255591-3 2009 The differentiated human ES cells obtained by this approach comprised nearly 25% insulin-positive cells as assayed by flow cytometry analysis, which released insulin/C-peptide in response to glucose stimuli in a manner comparable to that of adult human islets. Glucose 191-198 insulin Homo sapiens 81-88 19255591-3 2009 The differentiated human ES cells obtained by this approach comprised nearly 25% insulin-positive cells as assayed by flow cytometry analysis, which released insulin/C-peptide in response to glucose stimuli in a manner comparable to that of adult human islets. Glucose 191-198 insulin Homo sapiens 158-165 19255591-3 2009 The differentiated human ES cells obtained by this approach comprised nearly 25% insulin-positive cells as assayed by flow cytometry analysis, which released insulin/C-peptide in response to glucose stimuli in a manner comparable to that of adult human islets. Glucose 191-198 insulin Homo sapiens 166-175 19266162-1 2009 Excessive nutrients, especially amino acids, impair insulin action on glucose metabolism in skeletal muscle. Glucose 70-77 insulin Homo sapiens 52-59 19266162-5 2009 Leucine also reduced insulin-stimulated Akt phosphorylation, glucose uptake and glucose incorporation to glycogen (39%, 39% and 37%, respectively), and this reduction was restored after S6K1 silencing. Glucose 61-68 insulin Homo sapiens 21-28 19266162-5 2009 Leucine also reduced insulin-stimulated Akt phosphorylation, glucose uptake and glucose incorporation to glycogen (39%, 39% and 37%, respectively), and this reduction was restored after S6K1 silencing. Glucose 80-87 insulin Homo sapiens 21-28 19266162-7 2009 In conclusion, S6K1 plays an important role in the regulation of insulin action on glucose metabolism in skeletal muscle. Glucose 83-90 insulin Homo sapiens 65-72 18793347-9 2009 CONCLUSIONS: Pre-gravid vigorous/sports activity is associated with a reduced risk of glucose intolerance in pregnancy, an effect likely mediated by enhanced insulin sensitivity. Glucose 86-93 insulin Homo sapiens 158-165 19243312-5 2009 In diabetic animals and Type 1 diabetic patients, short-term studies indicate that C-peptide also enhances glucose disposal and metabolic control. Glucose 107-114 insulin Homo sapiens 83-92 19372382-2 2009 Here, we investigated potential mechanisms underlying Akt isoform functional specificity by using Akt2-specific regulation of glucose transport in insulin-stimulated adipocytes as a model system. Glucose 126-133 insulin Homo sapiens 147-154 19337955-1 2009 Insulin suppresses the release of non-esterified fatty acids from adipocytes and suppresses glucose production from hepatocytes, but stimulates glucose uptake by skeletal muscle, liver and adipose tissue. Glucose 92-99 insulin Homo sapiens 0-7 19337955-1 2009 Insulin suppresses the release of non-esterified fatty acids from adipocytes and suppresses glucose production from hepatocytes, but stimulates glucose uptake by skeletal muscle, liver and adipose tissue. Glucose 144-151 insulin Homo sapiens 0-7 19089403-10 2009 The reduction of insulin-stimulated glucose uptake by CM was completely prevented by Rim. Glucose 36-43 insulin Homo sapiens 17-24 19169664-8 2009 Following pioglitazone, insulin-stimulated glucose disposal increased by 30% (p < 0.01), and muscle AMPK and acetyl-CoA carboxylase (ACC) phosphorylation increased by 38% and 53%, respectively (p < 0.05). Glucose 43-50 insulin Homo sapiens 24-31 19250850-10 2009 The scores were also lower in those who had shorter disease duration and fewer complications, were taking insulin, had less frequent insulin injections, performed less glucose monitoring and had lower HbA(1c) levels. Glucose 168-175 insulin Homo sapiens 106-113 19250850-10 2009 The scores were also lower in those who had shorter disease duration and fewer complications, were taking insulin, had less frequent insulin injections, performed less glucose monitoring and had lower HbA(1c) levels. Glucose 168-175 insulin Homo sapiens 133-140 19251449-3 2009 This defect is clearly the consequence of a decline of insulin response to glucose due to functional beta-cell deficiency. Glucose 75-82 insulin Homo sapiens 55-62 19344199-2 2009 Predicted glucose values can be used for early hypoglycemic/hyperglycemic alarms or for adjustment of insulin injections or insulin infusion rates of manual or automated pumps. Glucose 10-17 insulin Homo sapiens 102-109 19344199-2 2009 Predicted glucose values can be used for early hypoglycemic/hyperglycemic alarms or for adjustment of insulin injections or insulin infusion rates of manual or automated pumps. Glucose 10-17 insulin Homo sapiens 124-131 19344199-14 2009 The proposed modeling algorithm with small number of parameters is a good candidate for installation in portable devices for early hypoglycemic/hyperglycemic alarms and for closing the glucose regulation loop with an insulin pump. Glucose 185-192 insulin Homo sapiens 217-224 19036880-2 2009 Here we delineated whether increased glucose flux through the hexosamine biosynthesis pathway (HBP) causes the PIP(2)/F-actin dysregulation and insulin resistance induced by hyperinsulinemia. Glucose 37-44 insulin Homo sapiens 144-151 19240267-9 2009 GH is a counterregulatory hormone that antagonizes the hepatic and peripheral effects of insulin on glucose metabolism via mechanisms involving the concomitant increase in FFA flux and uptake. Glucose 100-107 insulin Homo sapiens 89-96 18693051-13 2009 Accumulation of glucose in PA was increased by insulin at 10nM and by IGF-I at 1 nM and 10nM. Glucose 16-23 insulin Homo sapiens 47-54 19303967-8 2009 Retinol-binding protein was also associated with insulin at 2 hours during an oral glucose tolerance test (r = 0.24, P = .03) and the area under the curve for insulin during the oral glucose tolerance test (r = 0.26, P = .02). Glucose 83-90 insulin Homo sapiens 49-56 19422140-6 2009 The primary end point was a change in the insulin sensitivity index derived from a frequently sampled intravenous glucose tolerance test. Glucose 114-121 insulin Homo sapiens 42-49 19422140-9 2009 However, CrPic increased acute insulin response to glucose (P 0.02). Glucose 51-58 insulin Homo sapiens 31-38 19165163-8 2009 The ghrelin variant, g.A-604G (rs27647), showed an association with insulin levels at 2-h post-oral glucose tolerance test (OGTT) (P = 0.009) in obese families. Glucose 100-107 insulin Homo sapiens 68-75 19323622-5 2009 Throughout approximately 3 years of treatment with these erythropoietin analogs, the patient"s total daily dose of insulin was reduced in response to his decreasing A1C values, despite elevated blood glucose levels and the absence of patient-reported hypoglycemic events. Glucose 200-207 insulin Homo sapiens 115-122 19164796-7 2009 The highest values of homeostasis model assessment for insulin resistance and immunoreactive insulin at 120 minutes after glucose loading were found in atherothrombotic infarction patients with abnormal glucose tolerance. Glucose 122-129 insulin Homo sapiens 93-100 19135066-4 2009 In particular, such features as paracrine signals of neighboring cells and cell-to-cell variations in response to external glucose concentrations as well as glucose dynamics, depending on insulin and glucagon hormone, are considered explicitly. Glucose 157-164 insulin Homo sapiens 188-195 19135066-6 2009 Second, the inhibitory interactions of delta-cells for glucagon and insulin secretion prevent the wasteful co-secretion of them at the normal glucose level. Glucose 142-149 insulin Homo sapiens 68-75 19135066-7 2009 Finally, the glucose dose-responses of insulin secretion is modified to become more pronounced at high glucose levels due to the inhibition by delta-cells. Glucose 13-20 insulin Homo sapiens 39-46 19135066-7 2009 Finally, the glucose dose-responses of insulin secretion is modified to become more pronounced at high glucose levels due to the inhibition by delta-cells. Glucose 103-110 insulin Homo sapiens 39-46 20161147-1 2009 The effectiveness of closed-loop insulin infusion algorithms is assessed for three different mathematical models describing insulin and glucose dynamics within a Type I diabetes patient. Glucose 136-143 insulin Homo sapiens 33-40 19255425-1 2009 Here, we report that Cdk5 activation is stimulated by insulin and plays a key role in the regulation of GLUT4-mediated glucose uptake in 3T3-L1 adipocytes. Glucose 119-126 insulin Homo sapiens 54-61 19255425-6 2009 These studies elucidate a previously unknown activity of Cdk5 and demonstrate the involvement of this kinase in the regulation of insulin-dependent glucose uptake in adipocytes. Glucose 148-155 insulin Homo sapiens 130-137 19171650-4 2009 In particular, far less is known about the mechanisms underlying Ca(2+)-triggered glucagon release from alpha-cells than insulin secretion from beta-cells, even though insulin and glucagon together regulate blood glucose levels. Glucose 213-220 insulin Homo sapiens 168-175 19295313-7 2009 At 12 months, acute insulin release to glucose in group 2 was markedly reduced as compared with baseline (5.62+/-1.21 microIU/mL, n=4 vs. 16.14+/-3.69 microIU/mL, n=8), whereas it remained stable in group 1 (22.36+/-4.98 microIU/mL, n=5 vs. 27.70+/-2.83 microIU/mL, n=5). Glucose 39-46 insulin Homo sapiens 20-27 19295313-8 2009 Acute insulin release to glucose, acute C-peptide release to glucose (ACpRg), and mixed meal stimulation index were significantly decreased and time-to-peak C-peptide, 90-min glucose, and area under the curve for glucose were significantly increased when measured at time points preceding intervals where IGD occurred compared with intervals where there was no IGD. Glucose 25-32 insulin Homo sapiens 6-13 19273773-11 2009 CONCLUSIONS: Glucose normalization after admission is associated with better survival in hyperglycemic patients hospitalized with acute myocardial infarction whether or not they receive insulin therapy. Glucose 13-20 insulin Homo sapiens 186-193 18777156-5 2009 Similar 24-h blood glucose profiles were obtained with repaglinide and insulin aspart treatment. Glucose 19-26 insulin Homo sapiens 71-78 18925358-2 2009 Established risk cardiovascular factors like hypertension, atherogenic dyslipidaemia, and glucose intolerance occur in the setting of insulin resistance and central adiposity, with genetic and environmental influences modulating the ultimate risk. Glucose 90-97 insulin Homo sapiens 134-141 19106250-8 2009 In conclusion, the 24-h fast was accompanied by substantial increases in fasting FFA levels and induced reductions in the acute glucose-simulated insulin response and insulin sensitivity. Glucose 128-135 insulin Homo sapiens 146-153 19135250-6 2009 Insulin secretion could be detected and increased significantly by adding KCL in high glucose concentration in vitro. Glucose 86-93 insulin Homo sapiens 0-7 19287907-5 2009 In the normal glucose tolerant phase, progressors presented: 1) a higher OGTT blood glucose response with hyperglycemia in the second hour and a similar insulin response vs non-progressors; 2) a reduced first-phase insulin secretion (2.0 +/- 0.3 vs 2.3 +/- 0.3 pmol/L; P < 0.02) with a similar insulin sensitivity index and a lower disposition index (3.9 +/- 0.2 vs 4.1 +/- 0.2 micromol.kg-1.min-1 ; P < 0.05) vs non-progressors. Glucose 14-21 insulin Homo sapiens 215-222 18564177-6 2009 Likewise, insulin and C-peptide levels rose to higher levels after oral glucose compared with mixed meal ingestion. Glucose 72-79 insulin Homo sapiens 10-17 19034419-0 2009 Paired box 6 (PAX6) regulates glucose metabolism via proinsulin processing mediated by prohormone convertase 1/3 (PC1/3). Glucose 30-37 insulin Homo sapiens 53-63 19073775-8 2009 CONCLUSIONS: Our findings show that subjects with m.3243A>G are insulin resistant in skeletal muscle even when beta-cell function is not markedly impaired or glucose control compromised. Glucose 161-168 insulin Homo sapiens 67-74 19104769-7 2009 Main outcomes were changes in insulin action assessed as rate of glucose disposal (R (d)) by euglycaemic-hyperinsulinaemic clamp (insulin infusion rate 40 mU m(-2) min(-1)) and glucose tolerance by 75 g OGTT. Glucose 65-72 insulin Homo sapiens 30-37 19124171-3 2009 Whole-body insulin-mediated glucose uptake was determined using a euglycemic hyperinsulinemic clamp test. Glucose 28-35 insulin Homo sapiens 11-18 19156705-9 2009 Lispro insulin mixtures provided lower HbA(1c) and post-prandial blood glucose values than glargine, but caused more daytime hypoglycaemia. Glucose 71-78 insulin Homo sapiens 7-14 19275680-4 2009 Patients with insulin resistance and/or type 2 diabetes have high levels of plasma free fatty acids, inflammatory cytokines, and/or glucose, and over-activation of the cardiovascular renin-angiotensin system, all are capable of activating p38 MAPK. Glucose 132-139 insulin Homo sapiens 14-21 19275680-6 2009 The roles of p38 MAPK in insulin-mediated glucose uptake in skeletal muscle and adipose tissue remain controversial. Glucose 42-49 insulin Homo sapiens 25-32 19499845-7 2009 The area under the plasma insulin curve after oral administration of glucose decreased from 8.54 +/- 1.149 to 5.535 +/- 1.792 microU/ml/min (placebo group: from 8.903 +/- 1.276 to 9.1 +/- 1.162 microU/ml/min; P = 0.03). Glucose 69-76 insulin Homo sapiens 26-33 19330922-9 2009 Insulin sensitivity was estimated by using the homeostasis model assessment index calculated from the fasting glucose and insulin concentrations. Glucose 110-117 insulin Homo sapiens 0-7 19098161-1 2009 Diabetic patients treated with inhaled insulin exhibit reduced fasting plasma glucose levels. Glucose 78-85 insulin Homo sapiens 39-46 19098161-8 2009 Notwithstanding, glucose utilization was greater when insulin was administered by inhalation. Glucose 17-24 insulin Homo sapiens 54-61 19098161-9 2009 At its peak, the peripheral glucose infusion rate was 4 mg/kg/min greater in the inhalation group, and a 50% difference between groups persisted over 8 h. Inhalation of insulin caused a greater increase in nonhepatic glucose uptake in the first 3 h after inhalation; thereafter, net hepatic glucose uptake was greater. Glucose 28-35 insulin Homo sapiens 169-176 19098161-9 2009 At its peak, the peripheral glucose infusion rate was 4 mg/kg/min greater in the inhalation group, and a 50% difference between groups persisted over 8 h. Inhalation of insulin caused a greater increase in nonhepatic glucose uptake in the first 3 h after inhalation; thereafter, net hepatic glucose uptake was greater. Glucose 217-224 insulin Homo sapiens 169-176 19098161-9 2009 At its peak, the peripheral glucose infusion rate was 4 mg/kg/min greater in the inhalation group, and a 50% difference between groups persisted over 8 h. Inhalation of insulin caused a greater increase in nonhepatic glucose uptake in the first 3 h after inhalation; thereafter, net hepatic glucose uptake was greater. Glucose 217-224 insulin Homo sapiens 169-176 19098161-10 2009 Inhalation of insulin was associated with greater than expected (based on insulin levels) glucose disposal. Glucose 90-97 insulin Homo sapiens 14-21 19098161-10 2009 Inhalation of insulin was associated with greater than expected (based on insulin levels) glucose disposal. Glucose 90-97 insulin Homo sapiens 74-81 19098161-11 2009 This may explain the reduced fasting glucose concentrations observed in humans after administration of certain inhaled insulin formulations compared with subcutaneous insulin. Glucose 37-44 insulin Homo sapiens 119-126 19223597-11 2009 The insulin secretion in response to glucose and the insulin content were preserved in human islets exposed to high glucose and loaded with the peptide. Glucose 37-44 insulin Homo sapiens 4-11 19223597-11 2009 The insulin secretion in response to glucose and the insulin content were preserved in human islets exposed to high glucose and loaded with the peptide. Glucose 116-123 insulin Homo sapiens 4-11 19794883-2 2009 Normal glucose homeostasis is a complex process involving several interacting mechanisms, such as insulin secretion, insulin sensitivity, glucose production, and glucose uptake. Glucose 7-14 insulin Homo sapiens 98-105 19081303-1 2009 The adipocytokine, visfatin, exerts a diverse variety of effects that include the ability to mimic the glucose-lowering effects of insulin. Glucose 103-110 insulin Homo sapiens 131-138 19168596-8 2009 Overexpression of TCF7L2 exerted minor inhibitory effects on glucose-regulated changes in [Ca2+]i and insulin release. Glucose 61-68 insulin Homo sapiens 102-109 19188436-1 2009 OBJECTIVE: In skeletal muscle, insulin stimulates glucose transport activity three- to fourfold, and a large part of this stimulation is associated with a net translocation of GLUT4 from an intracellular compartment to the cell surface. Glucose 50-57 insulin Homo sapiens 31-38 19188436-2 2009 We examined the extent to which insulin or the AMP-activated protein kinase activator AICAR can lead to a stimulation of the exocytosis limb of the GLUT4 translocation pathway and thereby account for the net increase in glucose transport activity. Glucose 220-227 insulin Homo sapiens 32-39 19188436-9 2009 CONCLUSIONS: Insulin stimulation of the GLUT4 exocytosis rate constant is sufficient to account for most of the observed increase in glucose transport activity in rat and human muscle. Glucose 133-140 insulin Homo sapiens 13-20 19095745-0 2009 Aldosterone inhibits insulin-induced glucose uptake by degradation of insulin receptor substrate (IRS) 1 and IRS2 via a reactive oxygen species-mediated pathway in 3T3-L1 adipocytes. Glucose 37-44 insulin Homo sapiens 21-28 19095745-2 2009 Because the underlying molecular mechanism is largely unknown, we examined the effect of aldosterone on insulin-induced metabolic signaling leading to glucose uptake in 3T3-L1 adipocytes. Glucose 151-158 insulin Homo sapiens 104-111 19364685-12 2009 CONCLUSIONS: Decreased need in total daily basal insulin is caused by increased glucose use during lactation. Glucose 80-87 insulin Homo sapiens 49-56 19364691-2 2009 METHODS: In this prospective study, insulin pump-treated patients with type 1 diabetes had insulin dosages optimally titrated on the basis of daily continuous glucose monitoring (CGM). Glucose 159-166 insulin Homo sapiens 36-43 19234050-0 2009 HIV-1 protease inhibitor induced oxidative stress suppresses glucose stimulated insulin release: protection with thymoquinone. Glucose 61-68 insulin Homo sapiens 80-87 19196913-3 2009 Insulin sensitivity (intravenous glucose tolerance test, S(I)) was measured when subjects were sedentary and at 16-24 h and 15 days after the final training bout. Glucose 33-40 insulin Homo sapiens 0-7 19295123-1 2009 The release of insulin from pancreatic islets requires negative regulation to ensure low levels of insulin release under resting conditions, as well as positive regulation to facilitate robust responsiveness to conditions of elevated fuel or glucose. Glucose 242-249 insulin Homo sapiens 15-22 19396979-4 2009 Under stress conditions, the release of stress hormones produces insulin resistance and, owing to ROS preventing beta-cells from secreting insulin at the level required to maintain homeostasis, diverts glucose to insulin-independent tissues such as the brain and the foetus. Glucose 202-209 insulin Homo sapiens 139-146 19396979-4 2009 Under stress conditions, the release of stress hormones produces insulin resistance and, owing to ROS preventing beta-cells from secreting insulin at the level required to maintain homeostasis, diverts glucose to insulin-independent tissues such as the brain and the foetus. Glucose 202-209 insulin Homo sapiens 139-146 19175899-0 2009 Prolonged use of continuous glucose monitors in children with type 1 diabetes on continuous subcutaneous insulin infusion or intensive multiple-daily injection therapy. Glucose 28-35 insulin Homo sapiens 105-112 19246065-11 2009 Capillary glucose (most often elevated) must be corrected using a pre-established insulin infusion algorithm. Glucose 10-17 insulin Homo sapiens 82-89 19151370-8 2009 In insulin-secreting cells, rescue of both mutant channels to the cell surface led to hyperpolarized membrane potentials and reduced insulin secretion upon glucose stimulation. Glucose 156-163 insulin Homo sapiens 3-10 19595057-9 2009 The fasting insulin level and insulin levels 30, 60, 120, and 180 min after the glucose uptake during OGTT of the PCOS group were all significantly higher than those of the control group (all P < 0.01). Glucose 80-87 insulin Homo sapiens 30-37 19595057-14 2009 CONCLUSION: With normal glucose tolerance, the PCOS women show (1) a backwardly-shifted peak of glucose -stimulated insulin secretion, (2) an abnormal mode of daily glucose change characterized by a delayed peak of post-breakfast plasma glucose level, and (3) significant decrease of peripheral insulin sensitivity with compensated increase of insulin secretion. Glucose 96-103 insulin Homo sapiens 116-123 19595057-14 2009 CONCLUSION: With normal glucose tolerance, the PCOS women show (1) a backwardly-shifted peak of glucose -stimulated insulin secretion, (2) an abnormal mode of daily glucose change characterized by a delayed peak of post-breakfast plasma glucose level, and (3) significant decrease of peripheral insulin sensitivity with compensated increase of insulin secretion. Glucose 96-103 insulin Homo sapiens 116-123 19595057-14 2009 CONCLUSION: With normal glucose tolerance, the PCOS women show (1) a backwardly-shifted peak of glucose -stimulated insulin secretion, (2) an abnormal mode of daily glucose change characterized by a delayed peak of post-breakfast plasma glucose level, and (3) significant decrease of peripheral insulin sensitivity with compensated increase of insulin secretion. Glucose 96-103 insulin Homo sapiens 116-123 19122000-1 2009 Growth hormone (GH) pretreatment of 3T3-L1 adipocytes resulted in a concentration- and time-dependent inhibition of insulin-stimulated glucose uptake. Glucose 135-142 insulin Homo sapiens 116-123 19122000-5 2009 In contrast, overexpression of IRS-2 or expression of a constitutively active Akt mutant prevented the GH-induced insulin resistance of glucose uptake. Glucose 136-143 insulin Homo sapiens 114-121 19122000-6 2009 Moreover, small interfering RNA-mediated IRS-2 knockdown also inhibited insulin-stimulated Akt activation and glucose uptake without affecting GLUT4 translocation and plasma membrane fusion. Glucose 110-117 insulin Homo sapiens 72-79 19091788-5 2009 Cells were incubated with TGF-beta1 either alone or with C-peptide in low or high glucose. Glucose 82-89 insulin Homo sapiens 57-66 19514447-2 2009 Due to its effects in decreasing the hepatic production of glucose and in increasing insulin sensitivity in peripheral tissues, such as adipose tissue and skeletal muscle, the agent is used in metabolic syndrome and type 2 diabetes mellitus and, in which insulin resistance is especially pronounced. Glucose 59-66 insulin Homo sapiens 255-262 19035854-6 2009 Insulin treatment stimulated both glucose uptake and GLUT4 translocation in these cells. Glucose 34-41 insulin Homo sapiens 0-7 19507343-0 2009 [Oral insulin preparations for the regulation of the glucose level in the blood]. Glucose 53-60 insulin Homo sapiens 6-13 19254570-5 2009 Furthermore, PGC-1beta ASO increased insulin-stimulated whole-body glucose disposal due to a threefold increase in glucose uptake in white adipose tissue. Glucose 67-74 insulin Homo sapiens 37-44 19254570-5 2009 Furthermore, PGC-1beta ASO increased insulin-stimulated whole-body glucose disposal due to a threefold increase in glucose uptake in white adipose tissue. Glucose 115-122 insulin Homo sapiens 37-44 19202389-5 2009 The landmark phenomenon is insulin resistance and changes in the metabolic fates of glucose and fat. Glucose 84-91 insulin Homo sapiens 27-34 19033407-3 2009 Insulin-dependent whole-body glucose disposal was measured by the euglycemic clamp, and glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were also measured. Glucose 29-36 insulin Homo sapiens 0-7 19048227-7 2009 Basal and insulin-stimulated D-[U-(14)C]glucose incorporation and lipolysis were measured. Glucose 40-47 insulin Homo sapiens 10-17 19048227-9 2009 RESULTS: Insulin-stimulated D-[U-(14)C]glucose incorporation into adipocytes isolated from HFD-fed mice was reduced by 50% compared with adipocytes from chow-fed mice. Glucose 39-46 insulin Homo sapiens 9-16 19073767-4 2009 RESULTS: Insulin-stimulated total, oxidative, and nonoxidative glucose disposal, and suppression of fat oxidation during hyperinsulinemia were significantly lower in Ab- compared with Ab+ clinically diagnosed type 2 diabetic and control subjects with no difference between the latter two. Glucose 63-70 insulin Homo sapiens 9-16 19074983-5 2009 Additionally, we looked at effects of LASY knockdown on cellular antioxidant status, inflammation, mitochondrial function, and insulin-stimulated glucose uptake. Glucose 146-153 insulin Homo sapiens 127-134 19074983-10 2009 RNAi-mediated downregulation of LASY induced a significant loss of mitochondrial membrane potential and decreased insulin-stimulated glucose uptake in skeletal muscle cells. Glucose 133-140 insulin Homo sapiens 114-121 19106380-1 2009 OBJECTIVE: To compare the glucose variability associated with insulin glargine and NPH/Lente insulin used as the basal insulin component of a multiple daily injection (MDI) regimen in pediatric patients with type 1 diabetes. Glucose 26-33 insulin Homo sapiens 62-69 19106380-5 2009 CONCLUSIONS: Insulin glargine is associated with greater reductions in glucose variability than NPH/Lente insulin in pediatric patients with type 1 diabetes. Glucose 71-78 insulin Homo sapiens 13-20 19216684-1 2009 BACKGROUND: Continuous glucose monitoring (CGM) has the potential to provide useful data for behavioral interventions targeting non-insulin-using, sedentary individuals with type 2 diabetes mellitus (T2DM). Glucose 23-30 insulin Homo sapiens 132-139 19318690-4 2009 Comprehensive patient education, carbohydrate counting, and frequent self-monitoring of blood glucose or continuous glucose monitoring are necessary components of successful insulin pump therapy. Glucose 94-101 insulin Homo sapiens 174-181 18726867-13 2009 Insulin sensitivity and insulin secretion were estimated from oral glucose tolerance testing. Glucose 67-74 insulin Homo sapiens 0-7 19284367-10 2009 It is necessary to supplement with short-acting insulin at mealtimes to control glucose surges after meals. Glucose 80-87 insulin Homo sapiens 48-55 19083274-2 2009 Altered insulin secretion combined with recommended high-fat intake could be associated with dysregulation of glucose and lipid metabolism. Glucose 110-117 insulin Homo sapiens 8-15 19262221-6 2009 Skeletal muscle and the liver, not adipose tissue, are the two key insulin-response tissues involved in maintaining glucose balance, although abnormal insulin action in the adipocytes also plays a role in development of the syndrome. Glucose 116-123 insulin Homo sapiens 67-74 19001411-1 2009 The insulin signaling pathway is critical in regulating glucose levels and is associated with diabetes, obesity, and longevity. Glucose 56-63 insulin Homo sapiens 4-11 19103747-5 2009 SIRT1 depletion inhibited insulin-stimulated glucose uptake and GLUT4 translocation. Glucose 45-52 insulin Homo sapiens 26-33 19217454-4 2009 Insulin sensitivity (steady-state plasma glucose concentration) significantly improved in both treatment groups, associated with significant decreases in daylong plasma concentrations of glucose, insulin, and FFA. Glucose 41-48 insulin Homo sapiens 0-7 19217454-4 2009 Insulin sensitivity (steady-state plasma glucose concentration) significantly improved in both treatment groups, associated with significant decreases in daylong plasma concentrations of glucose, insulin, and FFA. Glucose 187-194 insulin Homo sapiens 0-7 19002565-6 2009 Transduced islets were viable after incubation with the cocktail of TNF-alpha, IL-1beta and IFN-gamma, as evidenced by insulin release in response to glucose concentration. Glucose 150-157 insulin Homo sapiens 119-126 19418936-2 2009 It potentiates the insulin secretory response (incretin effect) by enhancing the endogenous post-prandial response of GLP-1 (incretin enhancer) in a glucose-dependent manner. Glucose 149-156 insulin Homo sapiens 19-26 19157785-5 2009 Clozapine and olanzapine had a rapid and potent effect on insulin sensitivity by lowering the glucose infusion rate and increasing hepatic glucose production. Glucose 94-101 insulin Homo sapiens 58-65 19157785-5 2009 Clozapine and olanzapine had a rapid and potent effect on insulin sensitivity by lowering the glucose infusion rate and increasing hepatic glucose production. Glucose 139-146 insulin Homo sapiens 58-65 19146827-1 2009 Insulin stimulated GLUT4 (glucose transporter 4) translocation and glucose uptake in muscles and adipocytes is important for the maintenance of blood glucose homeostasis in our body. Glucose 26-33 insulin Homo sapiens 0-7 19146827-2 2009 In this paper, we report the identification of kaempferitrin (kaempferol 3,7-dirhamnoside), a glycosylated flavonoid, as a compound that inhibits insulin stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes. Glucose 189-196 insulin Homo sapiens 146-153 19146827-4 2009 On the other hand, kaempferitrin acted as an inhibitor of insulin-stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes by inhibiting Akt activation. Glucose 101-108 insulin Homo sapiens 58-65 19141293-2 2009 Recently, it was reported that ARNT is essential for adequate insulin secretion in response to glucose input and that its expression is downregulated in the pancreatic islets of diabetic patients. Glucose 95-102 insulin Homo sapiens 62-69 19179212-3 2009 Regimens that infuse fixed doses of insulin with high rates of glucose are usually associated with hyperglycemia, which may neutralize the beneficial effects of insulin. Glucose 63-70 insulin Homo sapiens 36-43 19179212-3 2009 Regimens that infuse fixed doses of insulin with high rates of glucose are usually associated with hyperglycemia, which may neutralize the beneficial effects of insulin. Glucose 63-70 insulin Homo sapiens 161-168 19179212-4 2009 Therefore, we propose that such regimens should be avoided and instead replaced by insulin infusions that normalize and maintain blood glucose at a reasonably low level and ensure that plasma insulin is maintained at levels high enough to provide clinically relevant anti-inflammatory and cardioprotective effects. Glucose 135-142 insulin Homo sapiens 83-90 18800198-6 2009 In addition, the burn-induced insulin resistance, leading to protein catabolism, was emphasized, with higher plasma insulin, glucose, and leptin levels in zinc-deficient animals versus normal-fed rats. Glucose 125-132 insulin Homo sapiens 30-37 19146801-2 2009 Insulin activation of the phosphatidylinositol-3-kinase (PI3K) pathway promotes glucose uptake in insulin-responsive tissues and nitric oxide (NO) production in the endothelium. Glucose 80-87 insulin Homo sapiens 0-7 19143591-3 2009 Defects in GLUT4 membrane traffic contribute to loss of insulin-stimulated glucose uptake in insulin resistance and Type 2 diabetes. Glucose 75-82 insulin Homo sapiens 56-63 19143591-3 2009 Defects in GLUT4 membrane traffic contribute to loss of insulin-stimulated glucose uptake in insulin resistance and Type 2 diabetes. Glucose 75-82 insulin Homo sapiens 93-100 18996102-1 2009 BACKGROUND: The thiazolidinediones (TZDs) improve tissue sensitivity to insulin in patients with type II diabetes, resulting in reduced levels of fasting blood glucose and glycated hemoglobin. Glucose 160-167 insulin Homo sapiens 72-79 19146801-2 2009 Insulin activation of the phosphatidylinositol-3-kinase (PI3K) pathway promotes glucose uptake in insulin-responsive tissues and nitric oxide (NO) production in the endothelium. Glucose 80-87 insulin Homo sapiens 98-105 18518893-1 2009 AIMS/HYPOTHESIS: Insulin resistance and glucose effectiveness (S(G)) are major determinants of glucose tolerance and independently predict the development of type 2 diabetes in individuals with a family history of disease. Glucose 95-102 insulin Homo sapiens 17-24 19337148-3 2009 RECENT FINDINGS: Multiple groups have developed successful in-vitro protocols to differentiate human embryonic stem cells and selected tissue specific stem cells into progenitors capable of insulin production and glucose-stimulated insulin secretion. Glucose 213-220 insulin Homo sapiens 232-239 18518893-4 2009 Each subject underwent a 100-g oral glucose tolerance test (OGTT) and insulin modified frequently sampled intravenous glucose tolerance, analysed using the Bergman"s minimal model (MINMOD). Glucose 118-125 insulin Homo sapiens 70-77 18518893-9 2009 CONCLUSIONS: These results demonstrate that familial factors impart important physiological differences in the inter-relationship between insulin-dependent and insulin-independent glucose disposal, which may be important in modulating risk for development of disease. Glucose 180-187 insulin Homo sapiens 138-145 18518893-9 2009 CONCLUSIONS: These results demonstrate that familial factors impart important physiological differences in the inter-relationship between insulin-dependent and insulin-independent glucose disposal, which may be important in modulating risk for development of disease. Glucose 180-187 insulin Homo sapiens 160-167 18984742-2 2009 We tested the cis-regulatory effects of rs573225 on promoter activity and its association with insulin response to oral glucose. Glucose 120-127 insulin Homo sapiens 95-102 18957530-5 2009 Insulin response was estimated as the change in insulin divided by change in glucose from 0 to 30 min (DeltaI(0-30)/DeltaG(0-30)). Glucose 77-84 insulin Homo sapiens 0-7 19033398-1 2009 OBJECTIVE: Insulin stimulates glucose uptake in skeletal muscle and adipose tissues primarily by stimulating the translocation of vesicles containing a facilitative glucose transporter, GLUT4, from intracellular compartments to the plasma membrane. Glucose 30-37 insulin Homo sapiens 11-18 19017772-7 2009 CONCLUSIONS: African American and Caucasian adolescents respond to FFA elevation similarly through increased fasting insulin secretion to maintain fasting glucose homeostasis and reduced peripheral glucose uptake and insulin resistance. Glucose 155-162 insulin Homo sapiens 117-124 19037628-2 2009 The aim of the present study was to investigate whether 4 weeks of near-normalisation of the blood glucose level could improve insulin responses to GIP and GLP-1 in patients with type 2 diabetes. Glucose 99-106 insulin Homo sapiens 127-134 19033398-1 2009 OBJECTIVE: Insulin stimulates glucose uptake in skeletal muscle and adipose tissues primarily by stimulating the translocation of vesicles containing a facilitative glucose transporter, GLUT4, from intracellular compartments to the plasma membrane. Glucose 165-172 insulin Homo sapiens 11-18 19033398-10 2009 Expression of DOC2b in cultured adipocytes enhanced, while expression of the Ca(2+)-interacting domain mutant DCO2b or knockdown of DOC2b inhibited, insulin-stimulated glucose uptake. Glucose 168-175 insulin Homo sapiens 149-156 19033398-11 2009 CONCLUSIONS: These findings indicate that DOC2b is a positive SNARE regulator for GLUT4 vesicle fusion and mediates insulin-stimulated glucose transport in adipocytes. Glucose 135-142 insulin Homo sapiens 116-123 19449669-2 2009 Using a physician-selected glucose target range and a weight-based multiplier, it recommends an insulin infusion rate and interval to next glucose measurement. Glucose 27-34 insulin Homo sapiens 96-103 19848575-6 2009 On the first admission their basal insulin was increased until their blood glucose level was <60 mg/dL. Glucose 75-82 insulin Homo sapiens 35-42 18726828-7 2009 Insulin sensitivity for each of the four meals was calculated by using the minimal glucose model approach. Glucose 83-90 insulin Homo sapiens 0-7 19214922-5 2009 In patients with normal beta-cell function, insulin resistance is compensated by increased insulin release from the beta cells to keep blood glucose levels compensated. Glucose 141-148 insulin Homo sapiens 44-51 19214922-5 2009 In patients with normal beta-cell function, insulin resistance is compensated by increased insulin release from the beta cells to keep blood glucose levels compensated. Glucose 141-148 insulin Homo sapiens 91-98 19214922-7 2009 The coexistence of insulin resistance with functional beta cell failure results in loss of blood glucose control especially after a meal and increases the cardiovascular risk of these patients far beyond the increased glucose levels. Glucose 97-104 insulin Homo sapiens 19-26 18813913-0 2009 Time dependent decrease in blood glucose levels after sampling potentially affects intensive insulin therapy in the intensive care unit. Glucose 33-40 insulin Homo sapiens 93-100 19108584-1 2009 GLUT4 is a 12 transmembrane (TM) protein belonging to the Class I facilitated glucose transporter family that transports glucose into the cells in an insulin regulated manner. Glucose 78-85 insulin Homo sapiens 150-157 18984669-9 2009 Insulin-stimulated peripheral glucose uptake was higher in both clamps after LPS compared to the control setting (P = 0.006 and 0.010), despite a significant increase in the plasma concentrations of norepinephrine and cytokines in the LPS group during both clamps. Glucose 30-37 insulin Homo sapiens 0-7 19449669-2 2009 Using a physician-selected glucose target range and a weight-based multiplier, it recommends an insulin infusion rate and interval to next glucose measurement. Glucose 139-146 insulin Homo sapiens 96-103 19022264-2 2009 Daily compensation of the deficiency requires 4-6 insulin injections to be taken daily, the aim of this insulin therapy being to maintain normoglycemia - i.e., a blood glucose level between 4 and 7mmol/l. Glucose 168-175 insulin Homo sapiens 104-111 19022264-7 2009 The insulin subsystem aims to describe the absorption of injected insulin from the subcutaneous depots and the glucose subsystem the absorption of glucose from the gut following a meal. Glucose 111-118 insulin Homo sapiens 4-11 19022264-7 2009 The insulin subsystem aims to describe the absorption of injected insulin from the subcutaneous depots and the glucose subsystem the absorption of glucose from the gut following a meal. Glucose 147-154 insulin Homo sapiens 4-11 19022264-9 2009 Several black-box models and grey-box models describing the insulin/glucose interaction were developed and analyzed. Glucose 68-75 insulin Homo sapiens 60-67 19154955-0 2009 Validity of the reduced-sample insulin modified frequently-sampled intravenous glucose tolerance test using the nonlinear regression approach. Glucose 79-86 insulin Homo sapiens 31-38 19154955-1 2009 The disposition index, the product of the insulin sensitivity index (S(I)) and the acute insulin response to glucose, is linked in African Americans to chromosome 11q. Glucose 109-116 insulin Homo sapiens 89-96 19154955-2 2009 This link was determined with S(I) calculated with the nonlinear regression approach to the minimal model and data from the reduced-sample insulin-modified frequently-sampled intravenous glucose tolerance test (Reduced-Sample-IM-FSIGT). Glucose 187-194 insulin Homo sapiens 139-146 19039315-4 2009 Insulin sensitivity was assessed with intravenous glucose tolerance test and minimal modeling; fat distribution with computed tomography; body composition with dual-energy X-ray absorptiometry; markers of inflammation (tumor necrosis factor (TNF)-alpha, soluble tumor necrosis factor receptor (sTNFR)-1, sTNFR-2, C-reactive protein (CRP), and interleukin (IL)-6) with enzyme-linked immunosorbent assay (ELISA). Glucose 50-57 insulin Homo sapiens 0-7 19057529-5 2009 The glucose minimal model was identified on glucose and insulin data to estimate insulin sensitivity, S(I), which was compared to a reference measure, S(I)(ref), provided by a tracer method. Glucose 4-11 insulin Homo sapiens 56-63 19057529-5 2009 The glucose minimal model was identified on glucose and insulin data to estimate insulin sensitivity, S(I), which was compared to a reference measure, S(I)(ref), provided by a tracer method. Glucose 4-11 insulin Homo sapiens 81-88 19411712-2 2009 An intravenous glucose tolerance test and minimal modeling were used to derive the insulin sensitivity index (SI) and acute insulin response to glucose (AIRg). Glucose 144-151 insulin Homo sapiens 124-131 19028573-1 2009 Many diabetic patients depend on regular and well-controlled administration of insulin to avoid unacceptable excursions in plasma glucose. Glucose 130-137 insulin Homo sapiens 79-86 19049859-8 2009 The oxidative stress biomarkers significantly affected the indicators of insulin resistance, particularly glucose level. Glucose 106-113 insulin Homo sapiens 73-80 19160334-15 2009 Insulin infusion resulted in significant increases in non-protein energy intake, glucose intake, and short-term weight gain.Meetze 1998 compared insulin infusion with reduction of glucose infusion. Glucose 81-88 insulin Homo sapiens 0-7 19160334-15 2009 Insulin infusion resulted in significant increases in non-protein energy intake, glucose intake, and short-term weight gain.Meetze 1998 compared insulin infusion with reduction of glucose infusion. Glucose 180-187 insulin Homo sapiens 0-7 19160334-17 2009 Insulin infusion resulted in significant increases in glucose intake and total energy intake. Glucose 54-61 insulin Homo sapiens 0-7 18599191-2 2009 Insulin-antagonistic effects of hormones, cytokines and excess metabolic substrates such as glucose and fatty acids may be exerted via common mechanisms involving for example reactive oxygen species (ROS) accumulation and associated inflammatory responses. Glucose 92-99 insulin Homo sapiens 0-7 18621093-7 2009 The preproinsulin mRNA has a long half-life and changes in preproinsulin mRNA stability, induced by glucose, are likely to be regulated through specific mechanisms. Glucose 100-107 insulin Homo sapiens 4-17 18621093-7 2009 The preproinsulin mRNA has a long half-life and changes in preproinsulin mRNA stability, induced by glucose, are likely to be regulated through specific mechanisms. Glucose 100-107 insulin Homo sapiens 59-72 18621093-8 2009 Recent findings indicate that the polypyrimidine tract-binding protein (PTB), also named hnRNP I, by binding to the 3"-UTR (untranslated region) of the preproinsulin mRNA molecule, stabilizes the messenger, thereby participating in the glucose-induced increase in preproinsulin mRNA. Glucose 236-243 insulin Homo sapiens 152-165 18621093-8 2009 Recent findings indicate that the polypyrimidine tract-binding protein (PTB), also named hnRNP I, by binding to the 3"-UTR (untranslated region) of the preproinsulin mRNA molecule, stabilizes the messenger, thereby participating in the glucose-induced increase in preproinsulin mRNA. Glucose 236-243 insulin Homo sapiens 264-277 18621094-3 2009 Dyslipidemia in diabetes aggravates the glucose effects both by inducing insulin resistance and by direct effects on beta cells. Glucose 40-47 insulin Homo sapiens 73-80 18786605-2 2009 They potentiate glucose-induced insulin secretion and may be responsible for up to 70% of postprandial insulin secretion. Glucose 16-23 insulin Homo sapiens 32-39 18786605-2 2009 They potentiate glucose-induced insulin secretion and may be responsible for up to 70% of postprandial insulin secretion. Glucose 16-23 insulin Homo sapiens 103-110 18945247-5 2009 A nurse-driven intensive insulin therapy with a target blood glucose level of 4-6 mmol/l had been introduced earlier. Glucose 61-68 insulin Homo sapiens 25-32 19258676-7 2009 For metabolic syndrome, hypoadiponectinemia showed the OR value of 6.0 (95% CI 2.13 to 16.98); insulin resistance showed the OR value of 5.7 (95% CI 1.3 to 25.02), after adjustment for waist circumference, TG, HLD, blood pressure, fasting blood glucose. Glucose 245-252 insulin Homo sapiens 95-102 19738938-3 2009 The activity of adenosine deaminase in the cytosolic fraction was very low and was not affected by different glucose concentration, but in the membrane fraction of cells cultured with 25 mM glucose it was decreased by about 35% comparing to the activity in cells maintained in 5 mM glucose, irrespective of insulin concentration. Glucose 190-197 insulin Homo sapiens 307-314 19738938-3 2009 The activity of adenosine deaminase in the cytosolic fraction was very low and was not affected by different glucose concentration, but in the membrane fraction of cells cultured with 25 mM glucose it was decreased by about 35% comparing to the activity in cells maintained in 5 mM glucose, irrespective of insulin concentration. Glucose 190-197 insulin Homo sapiens 307-314 19536490-3 2009 Insulin and glucose infusions were used to clamp the plasma glucose in a step-wise decrease to 2.5,mmol/l over 4 hours while counter-regulatory hormones were measured.The hypoglycemic trajectories were similar under all three interventions (dopa-mine, hyperoxia and control), but the total glucose infused was significantly larger for hyperoxia than for dopamine. Glucose 60-67 insulin Homo sapiens 0-7 19536490-3 2009 Insulin and glucose infusions were used to clamp the plasma glucose in a step-wise decrease to 2.5,mmol/l over 4 hours while counter-regulatory hormones were measured.The hypoglycemic trajectories were similar under all three interventions (dopa-mine, hyperoxia and control), but the total glucose infused was significantly larger for hyperoxia than for dopamine. Glucose 60-67 insulin Homo sapiens 0-7 19145963-5 2009 Insulin can be used acutely in patients newly diagnosed with type 2 diabetes to normalize blood glucose, or it can be added to a regimen of oral medication to improve glycemic control. Glucose 96-103 insulin Homo sapiens 0-7 18703873-8 2009 Half of the insulin-resistant patients developed an impaired fasting glucose by 1 year and 14% were being treated for type 2 diabetes mellitus by 5 years. Glucose 69-76 insulin Homo sapiens 12-19 19025445-6 2009 Insulin resistance was evaluated by hyperinsulinemic euglycemic clamp (insulin-mediated glucose disposal, M-value). Glucose 88-95 insulin Homo sapiens 0-7 18837470-9 2009 The addition of BG slowed the appearance of glucose in plasma, resulting in longer-lasting insulin secretion which exerted a prolonged inhibition of EGP and lipolysis. Glucose 44-51 insulin Homo sapiens 91-98 18855190-0 2009 Effects of weight loss on visceral and abdominal subcutaneous adipose tissue blood-flow and insulin-mediated glucose uptake in healthy obese subjects. Glucose 109-116 insulin Homo sapiens 92-99 18812463-5 2009 Pancreatic beta-cells respond to glucose levels by both producing and secreting insulin. Glucose 33-40 insulin Homo sapiens 80-87 19025445-15 2009 As glucose tolerance declined, glycemic control deteriorated and insulin resistance worsened. Glucose 3-10 insulin Homo sapiens 65-72 18840759-5 2009 Conditioned medium from palmitate-treated RAW 264.7 macrophages inhibited myoblast insulin-stimulated glucose uptake, GLUT4 translocation, and Akt phosphorylation while activating JNK p38 MAPK, decreasing IkappaBalpha, and elevating inflammation markers. Glucose 102-109 insulin Homo sapiens 83-90 18840759-6 2009 Surprisingly, and opposite to its effects on adipose cells, conditioned medium from LPS-treated macrophages stimulated myoblast insulin-stimulated glucose uptake, GLUT4 translocation, and Akt phosphorylation without affecting stress kinases or inflammation indexes. Glucose 147-154 insulin Homo sapiens 128-135 18840763-6 2009 The essential role of glucagon and insulin and the importance of distributed control of glucose fluxes are highlighted in this review. Glucose 88-95 insulin Homo sapiens 35-42 19161389-1 2009 Pancreatic beta-cells secrete insulin in response to elevated blood glucose via Ca(2+)-dependent fusion of secretory granules with the plasma membrane (regulated exocytosis). Glucose 68-75 insulin Homo sapiens 30-37 19161386-1 2009 Neuroendocrine pancreatic islet beta-cells secrete the hormone insulin in response to glucose stimulation and adapt efficiently to increased demand by peripheral tissues to maintain glucose homeostasis. Glucose 86-93 insulin Homo sapiens 63-70 20066963-10 2009 I4 (1-100 micromol x L(-1)) also produced an insulin-independent increase in glucose consumption by Hep G2 cells, increased glycogen synthesis and glucokinase activity of these cells. Glucose 77-84 insulin Homo sapiens 45-52 19964000-1 2009 A device which integrates existing intravenous continuous glucose monitors and infusion pumps into a central hub for automated intravenous intensive insulin therapy, targeting non-diabetic critically-ill patients is presented. Glucose 58-65 insulin Homo sapiens 149-156 19092238-11 2009 CONCLUSIONS: The intensive intravenous insulin infusion protocol effectively lowers blood glucose levels with an increased risk of manageable hypoglycaemic events. Glucose 90-97 insulin Homo sapiens 39-46 18952196-7 2009 Endogenous lipids reduced insulin-mediated glucose oxidation. Glucose 43-50 insulin Homo sapiens 26-33 19106615-1 2009 Type 2 diabetes occurs when the endocrine pancreas can no longer secrete enough insulin to maintain glucose and lipid homeostasis. Glucose 100-107 insulin Homo sapiens 80-87 19471091-5 2009 In beta-cells proinsulin represents up to 50% of the total protein synthesis, and the rate of glucose-stimulated proinsulin translation is approximately 1 million molecules per minute per cell. Glucose 94-101 insulin Homo sapiens 113-123 20003200-1 2009 INTRODUCTION: Intensive insulin treatment of critically ill patients was seen as a promising method of treatment, though recent studies showed that reducing the blood glucose level below 6 mmol/l had a detrimental outcome. Glucose 167-174 insulin Homo sapiens 24-31 18570630-3 2009 In the present study, we hypothesized that in vivo in humans ischaemia- and insulin-induced glucose uptake are additive, and that the combined impact of ischaemia and contraction on glucose uptake is of a similar magnitude when each is applied separately. Glucose 92-99 insulin Homo sapiens 76-83 19435472-4 2009 Thus, it is logically possible that the benefit of intensive insulin therapy in the first Leuven trial was due to a decrease in mean glucose levels, a decrease in their variability, or both. Glucose 133-140 insulin Homo sapiens 61-68 19435472-6 2009 Decreasing the variability of blood glucose levels might be an important dimension of glucose management, a possible mechanism by which an intensive insulin protocol exerts its putative beneficial effects, and an important goal of glucose management in the intensive care unit. Glucose 36-43 insulin Homo sapiens 149-156 19435472-6 2009 Decreasing the variability of blood glucose levels might be an important dimension of glucose management, a possible mechanism by which an intensive insulin protocol exerts its putative beneficial effects, and an important goal of glucose management in the intensive care unit. Glucose 86-93 insulin Homo sapiens 149-156 19435472-6 2009 Decreasing the variability of blood glucose levels might be an important dimension of glucose management, a possible mechanism by which an intensive insulin protocol exerts its putative beneficial effects, and an important goal of glucose management in the intensive care unit. Glucose 86-93 insulin Homo sapiens 149-156 18852332-12 2009 CONCLUSIONS: In contrast to animals, in humans, prevention of portal hypoglycemia with oral glucose from the beginning of insulin-induced slow-fall hypoglycemia has no effect on sympathoadrenal and symptomatic responses to hypoglycemia. Glucose 92-99 insulin Homo sapiens 122-129 19156623-4 2009 Insulin sensitivity was measured by the frequent sample intravenous glucose tolerance test, and sCD36 by an in-house ELISA assay. Glucose 68-75 insulin Homo sapiens 0-7 18972094-1 2009 AIMS/HYPOTHESES: Insulin-stimulated glucose transport in muscle is impaired in type 2 diabetes, presumably reflecting reduced activation of atypical protein kinase C (aPKC) and protein kinase B (PKB/Akt). Glucose 36-43 insulin Homo sapiens 17-24 19132851-14 2009 Adjustment of insulin doses according to CHO intake allowed the reduction of glucose variability, increasingly recognized as an important, independent risk factor for cardiovascular events. Glucose 77-84 insulin Homo sapiens 14-21 19367016-5 2009 Her NME improved markedly after intravenous infusion of amino acids, and her plasma glucose was controlled reasonably well by intensive insulin therapy. Glucose 84-91 insulin Homo sapiens 136-143 19236187-4 2009 RESULTS/CONCLUSION: Exenatide improves fasting plasma glucose and HbA1c in type 2 diabetic patients not controlled on other antidiabetic drugs, due to its effects on glucose-dependent stimulation on insulin secretion, suppression elevated glucagon secretion, slowing the accelerated rate of gastric emptying, reduction of food intake and possible beta-cell preservation. Glucose 166-173 insulin Homo sapiens 199-206 19273250-2 2009 For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells. Glucose 288-295 insulin Homo sapiens 362-369 19273380-2 2009 A key factor is insulin resistance, defined as a reduced ability of insulin to stimulate glucose utilization and storage. Glucose 89-96 insulin Homo sapiens 16-23 19273380-2 2009 A key factor is insulin resistance, defined as a reduced ability of insulin to stimulate glucose utilization and storage. Glucose 89-96 insulin Homo sapiens 68-75 18855306-4 2009 When encapsulated in the minicell, insulin release from the pseudoislets in response to glucose stimulation was reduced. Glucose 88-95 insulin Homo sapiens 35-42 18855306-8 2009 The reduced release of insulin from the encapsulated pseudoislets could be compensated by overexpression of glucokinase in MIN6 cells, which resulted in an increased glucose responsiveness of the pseudoislets for stimulation with glucose. Glucose 166-173 insulin Homo sapiens 23-30 18855306-8 2009 The reduced release of insulin from the encapsulated pseudoislets could be compensated by overexpression of glucokinase in MIN6 cells, which resulted in an increased glucose responsiveness of the pseudoislets for stimulation with glucose. Glucose 230-237 insulin Homo sapiens 23-30 19690431-3 2009 At the age of 11 years, she was admitted to a local hospital and an oral glucose tolerance test showed high total insulin levels. Glucose 73-80 insulin Homo sapiens 114-121 19922039-6 2009 An intravenous glucose tolerance test was used to derive the insulin sensitivity index and acute insulin response to glucose (AIRg) diet by two 24 h recalls, and body composition by dual-energy x-ray absorptiometry (DXA). Glucose 117-124 insulin Homo sapiens 97-104 18661120-7 2009 Time-weighted average glucose concentrations in patients receiving eMPC advised insulin infusions were similar [104 mg/dL (5.8 mmol/L)] in both ICUs. Glucose 22-29 insulin Homo sapiens 80-87 18682916-0 2009 Plasma insulin concentration is useful to guide glucose supplement in insulin overdose. Glucose 48-55 insulin Homo sapiens 7-14 19542630-1 2009 Insulin, long known as an important regulator of blood glucose levels, plays important and multifaceted roles in the brain. Glucose 55-62 insulin Homo sapiens 0-7 18957498-12 2009 The proinsulin secretory ratio (PISR) during glucose-potentiated arginine was significantly greater with GLP-1 vs. placebo infusion in both groups (P < 0.05). Glucose 45-52 insulin Homo sapiens 4-14 18957505-2 2009 Consistent with this mechanism of action, DPP-4 inhibitors improve glucose tolerance after meals by increasing insulin and reducing glucagon levels in the plasma. Glucose 67-74 insulin Homo sapiens 111-118 18957505-9 2009 Major Outcome Measure: We measured insulin secretion in response to iv glucose and arginine before and after treatment and after drug washout. Glucose 71-78 insulin Homo sapiens 35-42 18957505-12 2009 DPP-4 inhibitor treatment improved the acute insulin and C-peptide responses to glucose (50 and 100% respectively; P < 0.05) and increased the slope of the C-peptide response to glucose (33%; P = 0.023). Glucose 80-87 insulin Homo sapiens 45-52 18957505-12 2009 DPP-4 inhibitor treatment improved the acute insulin and C-peptide responses to glucose (50 and 100% respectively; P < 0.05) and increased the slope of the C-peptide response to glucose (33%; P = 0.023). Glucose 80-87 insulin Homo sapiens 57-66 19500470-0 2009 Different effects of FK506, rapamycin, and mycophenolate mofetil on glucose-stimulated insulin release and apoptosis in human islets. Glucose 68-75 insulin Homo sapiens 87-94 19500470-5 2009 In the present study, we show that 24-h exposure to FK506 or MMF impairs glucose-stimulated insulin secretion in human islets. Glucose 73-80 insulin Homo sapiens 92-99 19500470-9 2009 Treating human islets with the GLP-1 agonist exenatide ameliorated the immunosuppressant-induced defects in glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 127-134 19133705-2 2009 The aim of the present study was to describe a 4-year course of glucose homeostasis in a cohort of HAART-treated children and adolescents, using glucose and insulin levels during an oral glucose tolerance test (OGTT) as outcome measures. Glucose 64-71 insulin Homo sapiens 157-164 19822000-0 2009 Computerized intensive insulin dosing can mitigate hypoglycemia and achieve tight glycemic control when glucose measurement is performed frequently and on time. Glucose 104-111 insulin Homo sapiens 23-30 19822000-13 2009 CONCLUSIONS: Glycemic control to a lower glucose target range can be achieved using a computerized insulin dosing protocol. Glucose 41-48 insulin Homo sapiens 99-106 19849827-5 2009 Such computerized clinical decision support systems (Cuss) use more complex logic to provide an insulin infusion rate based on previous blood glucose levels and other parameters. Glucose 142-149 insulin Homo sapiens 96-103 19747136-4 2009 It promotes glycogen synthesis in the liver and glucose-sensitive insulin release in the beta-cell. Glucose 48-55 insulin Homo sapiens 66-73 18835946-3 2009 The aim of this study was to investigate the differences in insulin sensitivity (IS) and secretion in obese adolescents with IGT compared with those with normal glucose tolerance (NGT) and type 2 diabetes. Glucose 161-168 insulin Homo sapiens 60-67 18835946-6 2009 RESULTS: Insulin-stimulated glucose disposal was significantly lower in subjects with type 2 diabetes compared with subjects with NGT and IGT, with no difference between the latter two. Glucose 28-35 insulin Homo sapiens 9-16 18984735-4 2009 Insulin signaling was monitored through the phosphorylation state of several key partners of the pathway and glucose transport. Glucose 109-116 insulin Homo sapiens 0-7 18984735-6 2009 In 3T3-L1 adipocytes, this inhibition of insulin receptor phosphorylation is followed by a decrease in the phosphorylation state of protein kinase B and AS160, as well as an inhibition of glucose transport in response to insulin. Glucose 188-195 insulin Homo sapiens 41-48 18671795-1 2009 AIM: Short-acting insulin analogues, in comparison with regular human insulin (HRI), provide a greater control of postprandial glucose, while their superiority on haemoglobin A1c (HbA1c) is controversial. Glucose 127-134 insulin Homo sapiens 18-25 18671795-7 2009 CONCLUSION: In type 2 diabetic patients, short-acting insulin analogues provide a better control of HbA1c and postprandial glucose than regular human insulin, without any significant reduction of the risk of severe hypoglycaemia. Glucose 123-130 insulin Homo sapiens 54-61 19145587-2 2009 IGF-I, a peptide hormone, shares amino acid sequence homology with insulin and has insulin-like activity; most notably, the promotion of glucose uptake by peripheral tissues. Glucose 137-144 insulin Homo sapiens 67-74 19145587-2 2009 IGF-I, a peptide hormone, shares amino acid sequence homology with insulin and has insulin-like activity; most notably, the promotion of glucose uptake by peripheral tissues. Glucose 137-144 insulin Homo sapiens 83-90 19224501-3 2009 Insulin resistance, leading to glucose intolerance is one of the most important contributory factors to the cardiovascular mortality in acromegaly. Glucose 31-38 insulin Homo sapiens 0-7 18835976-1 2009 OBJECTIVE: Based on fasting insulin and glucose, several indices of insulin sensitivity have been developed in adults. Glucose 40-47 insulin Homo sapiens 68-75 19727413-7 2009 Interestingly, PTHrP showed a positive correlation with insulin levels only among healthy individuals presumably due to defective glucose stimulated insulin secretion known to occur in type 2 diabetics. Glucose 130-137 insulin Homo sapiens 56-63 19727413-7 2009 Interestingly, PTHrP showed a positive correlation with insulin levels only among healthy individuals presumably due to defective glucose stimulated insulin secretion known to occur in type 2 diabetics. Glucose 130-137 insulin Homo sapiens 149-156 19273123-6 2009 Insulin analogs and secretagogues suppress glucose production and increase liver glucose utilization by both direct and indirect hepatic actions. Glucose 43-50 insulin Homo sapiens 0-7 19188736-8 2009 VPA can directly stimulate pancreatic beta-cells and indirectly enhance insulin resistance by suppressing insulin-mediated peripheral glucose uptake. Glucose 134-141 insulin Homo sapiens 106-113 21694920-4 2009 Adiponectin potentiates insulin in its post-receptor signaling resulting in glucose oxidation in mitochondria. Glucose 76-83 insulin Homo sapiens 24-31 18599564-11 2009 Insulin temporarily reduced vitreal glucose levels. Glucose 36-43 insulin Homo sapiens 0-7 19661616-6 2009 In sAD, this desynchronization may involve stress components, cortisol and noradrenaline, reactive oxygen species, and membrane damage as major candidates causing an insulin resistant brain state with decreased glucose/energy metabolism. Glucose 211-218 insulin Homo sapiens 166-173 19536630-6 2009 The glucose challenge tests revealed the production of insulin, and such production was regulated via physiological signaling pathways. Glucose 4-11 insulin Homo sapiens 55-62 18854391-7 2009 However, rates of maximal insulin-stimulated glucose transport (insulin responsiveness) into isolated adipocytes were comparable between all three groups, whereas PCOS subjects displayed impaired insulin sensitivity. Glucose 45-52 insulin Homo sapiens 26-33 18854391-7 2009 However, rates of maximal insulin-stimulated glucose transport (insulin responsiveness) into isolated adipocytes were comparable between all three groups, whereas PCOS subjects displayed impaired insulin sensitivity. Glucose 45-52 insulin Homo sapiens 64-71 18854391-8 2009 In contrast, myotubes from PCOS subjects displayed reduced insulin responsiveness for glucose uptake and normal sensitivity. Glucose 86-93 insulin Homo sapiens 59-66 18957505-12 2009 DPP-4 inhibitor treatment improved the acute insulin and C-peptide responses to glucose (50 and 100% respectively; P < 0.05) and increased the slope of the C-peptide response to glucose (33%; P = 0.023). Glucose 181-188 insulin Homo sapiens 159-168 18984671-11 2009 R84 islets were more likely to display relatively low glucose-stimulated insulin release (P = 0.04). Glucose 54-61 insulin Homo sapiens 73-80 19026267-10 2009 CONCLUSION: Olanzapine and risperidone may impair glucose tolerance due in part to increased insulin resistance. Glucose 50-57 insulin Homo sapiens 93-100 19337007-10 2009 In FH-, the cohort is an acquired trait restricted to pregnancy signaling transiently reduced insulin-stimulated glucose utilization; in FH+, instead, it unveils the existence of an inherited DM2-related background these women all have, that is awakened by pregnancy and as such lastingly impairs insulin-stimulated glucose utilization. Glucose 113-120 insulin Homo sapiens 94-101 19337007-10 2009 In FH-, the cohort is an acquired trait restricted to pregnancy signaling transiently reduced insulin-stimulated glucose utilization; in FH+, instead, it unveils the existence of an inherited DM2-related background these women all have, that is awakened by pregnancy and as such lastingly impairs insulin-stimulated glucose utilization. Glucose 316-323 insulin Homo sapiens 94-101 19337008-5 2009 Insulin and glucose responses to the oral glucose tolerance test (OGTT) were analyzed by calculating the areas under the curve for insulin (AUCI) and glucose by the trapezoidal methods.We used PCR and restriction fragment length polymorphism technique to examine Calpain 10 SNP 19, 43, 44, and 63 polymorphisms. Glucose 12-19 insulin Homo sapiens 131-138 19337008-5 2009 Insulin and glucose responses to the oral glucose tolerance test (OGTT) were analyzed by calculating the areas under the curve for insulin (AUCI) and glucose by the trapezoidal methods.We used PCR and restriction fragment length polymorphism technique to examine Calpain 10 SNP 19, 43, 44, and 63 polymorphisms. Glucose 42-49 insulin Homo sapiens 0-7 19337008-5 2009 Insulin and glucose responses to the oral glucose tolerance test (OGTT) were analyzed by calculating the areas under the curve for insulin (AUCI) and glucose by the trapezoidal methods.We used PCR and restriction fragment length polymorphism technique to examine Calpain 10 SNP 19, 43, 44, and 63 polymorphisms. Glucose 42-49 insulin Homo sapiens 131-138 19865614-7 2009 CONCLUSIONS: The increase in insulin delivery in response to persistent hyperglycemia observed with all the algorithms can be expected to bring subjects who respond to insulin to targeted glucose ranges. Glucose 188-195 insulin Homo sapiens 29-36 19865614-7 2009 CONCLUSIONS: The increase in insulin delivery in response to persistent hyperglycemia observed with all the algorithms can be expected to bring subjects who respond to insulin to targeted glucose ranges. Glucose 188-195 insulin Homo sapiens 168-175 19865614-8 2009 However, because the PID and P protocols did not alter the insulin delivery response curves, these algorithms can be expected to take longer to achieve target glucose levels in individuals who are insulin resistant and/or are exposed to increased carbohydrate loads (e.g., glucose infusions). Glucose 159-166 insulin Homo sapiens 197-204 20046650-5 2009 Recently, a new parsimonious model of exercise effect on glucose homeostasis has been proposed that links the change in insulin action and glucose effectiveness to heart rate (HR). Glucose 57-64 insulin Homo sapiens 120-127 20046650-7 2009 METHODS: The exercise model describes changes in glucose-insulin dynamics in two phases: a rapid on-and-off change in insulin-independent glucose clearance and a rapid-on/slow-off change in insulin sensitivity. Glucose 49-56 insulin Homo sapiens 57-64 20046650-7 2009 METHODS: The exercise model describes changes in glucose-insulin dynamics in two phases: a rapid on-and-off change in insulin-independent glucose clearance and a rapid-on/slow-off change in insulin sensitivity. Glucose 49-56 insulin Homo sapiens 118-125 20046653-0 2009 Coordinated basal-bolus infusion for tighter postprandial glucose control in insulin pump therapy. Glucose 58-65 insulin Homo sapiens 77-84 20046655-1 2009 BACKGROUND: Intensive insulin therapy reduces mortality and morbidity in critically ill patients but places great demands on medical staff who must take frequent blood samples for the determination of glucose levels. Glucose 201-208 insulin Homo sapiens 22-29 19140174-7 2009 ICU patients treated with intravenous insulin had significantly lower median glucose when compared to subcutaneous insulin. Glucose 77-84 insulin Homo sapiens 38-45 19848860-3 2009 Insulin pumps are used to deliver insulin in small quantities, allowing the glucose level to remain as close as possible to that of non-diabetics (near 100 mg dl(-1)). Glucose 76-83 insulin Homo sapiens 0-7 19131817-6 2009 The protocol calculates the insulin rate using a linear equation (rate = blood glucose - 60[M]). Glucose 79-86 insulin Homo sapiens 28-35 18809262-2 2009 It is characterized by pathway-specific inhibition of the PI3K/Akt signaling, which concerns the positive actions of insulin including glucose and lipid metabolism, while other pathways including the Ras/MAPK pathway, which accounts for the negative actions of insulin such as stimulation of smooth muscle proliferation and secretion of endothelin-1, stay unaffected. Glucose 135-142 insulin Homo sapiens 117-124 18809262-6 2009 The mechanisms may include the recently revealed anti-inflammatory effects of insulin as well as its conventional glucose and free fatty acids lowering effects, and possibly may also include changes in body fat distribution and plasma adiponectin level. Glucose 114-121 insulin Homo sapiens 78-85 19059535-0 2009 Insulin action and secretion in hypertension in the absence of metabolic syndrome: model-based assessment from oral glucose tolerance test. Glucose 116-123 insulin Homo sapiens 0-7 19059536-9 2009 Moreover, FDR demonstrated whole-body insulin resistance as well as decreased basal and insulin-stimulated forearm glucose uptake. Glucose 115-122 insulin Homo sapiens 88-95 19897102-5 2009 For each of 45 sets of glucose meter bias and imprecision conditions, 100 patients were simulated, and each patient was followed for 100 h. RESULTS: For both insulin regimens: Mean glucose was inversely related to assay bias; glucose variability increased with negative assay bias and assay imprecision; frequencies of glucose concentrations >160 mg/dL increased with negative assay bias and assay imprecision; and frequencies of hypoglycemia increased with positive assay bias and assay imprecision. Glucose 181-188 insulin Homo sapiens 158-165 19897102-5 2009 For each of 45 sets of glucose meter bias and imprecision conditions, 100 patients were simulated, and each patient was followed for 100 h. RESULTS: For both insulin regimens: Mean glucose was inversely related to assay bias; glucose variability increased with negative assay bias and assay imprecision; frequencies of glucose concentrations >160 mg/dL increased with negative assay bias and assay imprecision; and frequencies of hypoglycemia increased with positive assay bias and assay imprecision. Glucose 181-188 insulin Homo sapiens 158-165 19897102-7 2009 CONCLUSIONS: Errors in glucose measurement exert important regimen-dependent effects on glucose control in intensive IV insulin administration. Glucose 23-30 insulin Homo sapiens 120-127 19897102-7 2009 CONCLUSIONS: Errors in glucose measurement exert important regimen-dependent effects on glucose control in intensive IV insulin administration. Glucose 88-95 insulin Homo sapiens 120-127 19504248-5 2009 The primary mechanism for insulin stimulation of glucose uptake into muscle and fat is the translocation of glucose transporter 4 (GLUT4) to the cell surface from intracellular storage vesicles within the cell. Glucose 49-56 insulin Homo sapiens 26-33 19504248-6 2009 A major advantage in focussing on insulin regulation of glucose transport is that this represents the endpoint of multiple upstream signalling pathways. Glucose 56-63 insulin Homo sapiens 34-41 19504253-1 2009 Insulin resistance, the impaired ability of insulin to stimulate glucose utilization, is a major characteristic of type 2 diabetes. Glucose 65-72 insulin Homo sapiens 0-7 19504253-1 2009 Insulin resistance, the impaired ability of insulin to stimulate glucose utilization, is a major characteristic of type 2 diabetes. Glucose 65-72 insulin Homo sapiens 44-51 19504253-4 2009 The euglycemic clamp is widely used in clinics and laboratories to measure insulin action on glucose utilization in humans and animals for clinical and basic science research. Glucose 93-100 insulin Homo sapiens 75-82 19160674-3 2009 A role for PLD in regulating glucose homeostasis is emerging as the enzyme has recently been identified in events regulating exocytosis of insulin from pancreatic beta-cells and also in insulin-stimulated glucose uptake through controlling GLUT4 vesicle exocytosis in muscle and adipose tissue. Glucose 29-36 insulin Homo sapiens 139-146 19160674-3 2009 A role for PLD in regulating glucose homeostasis is emerging as the enzyme has recently been identified in events regulating exocytosis of insulin from pancreatic beta-cells and also in insulin-stimulated glucose uptake through controlling GLUT4 vesicle exocytosis in muscle and adipose tissue. Glucose 29-36 insulin Homo sapiens 186-193 18936159-3 2009 Here, we show that TZD prevents oxidative stress-induced insulin resistance in human skeletal muscle cells, as indicated by the increase in insulin-stimulated glucose uptake and insulin signaling. Glucose 159-166 insulin Homo sapiens 140-147 18936159-3 2009 Here, we show that TZD prevents oxidative stress-induced insulin resistance in human skeletal muscle cells, as indicated by the increase in insulin-stimulated glucose uptake and insulin signaling. Glucose 159-166 insulin Homo sapiens 140-147 19067524-6 2009 Transduced islets were viable as evidenced by insulin release upon glucose challenge. Glucose 67-74 insulin Homo sapiens 46-53 19139117-1 2009 The phosphatidylinositol 3-kinase (PI3K)/Akt signaling cascade is an important component of the insulin signaling in normal tissues leading to glucose uptake and homeostasis and for cell survival signaling in cancer cells. Glucose 143-150 insulin Homo sapiens 96-103 19060908-3 2009 Specifically, the risk genotype was associated with impairment of early insulin response to both oral and intravenous glucose and with faster deterioration of insulin secretion over time. Glucose 118-125 insulin Homo sapiens 72-79 19060908-6 2009 Insulin release from clonal beta cells in response to glucose was inhibited in the presence of melatonin. Glucose 54-61 insulin Homo sapiens 0-7 19212611-3 2009 (i) Intravenous bolus injection of short-acting insulin, one I.E. for each 0.6 mmol/l blood glucose above 7.0. Glucose 92-99 insulin Homo sapiens 48-55 19212611-4 2009 (ii) If 20 min after insulin administration plasma glucose is <or=7.0 mmol/l, proceed to (iii). Glucose 51-58 insulin Homo sapiens 21-28 19212611-6 2009 Compute insulin dose with the updated blood glucose level. Glucose 44-51 insulin Homo sapiens 8-15 23074525-23 2009 The insulin dose is adjusted in response to measured capillary glucose values in a fashion similar to MDI and is thus often seen as a preferred method to multiple injection therapy. Glucose 63-70 insulin Homo sapiens 4-11 19299910-1 2009 The insulin pathway is crucial for the regulation of intracellular and blood glucose levels and the prevention of diabetes. Glucose 77-84 insulin Homo sapiens 4-11 19299910-2 2009 Regulating blood glucose levels demands coordinated interaction between several tissues, which is facilitated by the release of and response to the hormone, insulin. Glucose 17-24 insulin Homo sapiens 157-164 19299910-3 2009 In response to an increase in circulating glucose levels, insulin is secreted by pancreatic beta cells to cause an increase in the uptake of glucose, fatty acids and amino acids into adipose tissue, muscle and the liver to subsequently promote the storage of these nutrients in the form of glycogen, lipids and protein, respectively, as well as suppress hepatic glucose release. Glucose 42-49 insulin Homo sapiens 58-65 19299910-3 2009 In response to an increase in circulating glucose levels, insulin is secreted by pancreatic beta cells to cause an increase in the uptake of glucose, fatty acids and amino acids into adipose tissue, muscle and the liver to subsequently promote the storage of these nutrients in the form of glycogen, lipids and protein, respectively, as well as suppress hepatic glucose release. Glucose 141-148 insulin Homo sapiens 58-65 19299910-3 2009 In response to an increase in circulating glucose levels, insulin is secreted by pancreatic beta cells to cause an increase in the uptake of glucose, fatty acids and amino acids into adipose tissue, muscle and the liver to subsequently promote the storage of these nutrients in the form of glycogen, lipids and protein, respectively, as well as suppress hepatic glucose release. Glucose 141-148 insulin Homo sapiens 58-65 19299910-4 2009 Insulin sensitivity is measured by the relative capacity of insulin to promote a decrease in blood glucose. Glucose 99-106 insulin Homo sapiens 0-7 19299910-4 2009 Insulin sensitivity is measured by the relative capacity of insulin to promote a decrease in blood glucose. Glucose 99-106 insulin Homo sapiens 60-67 19772820-1 2009 Insulin determines glucose transport to the most of cells. Glucose 19-26 insulin Homo sapiens 0-7 20384178-0 2009 [The relationship between plasma insulin and glucose, maximal oxygen uptake and body composition in young, lean men and women]. Glucose 45-52 insulin Homo sapiens 33-40 20384178-3 2009 AIM OF THE STUDY: The present study aimed at the evaluation of the association between plasma insulin and glucose, maximal oxygen uptake, and body composition in young, lean women and men. Glucose 106-113 insulin Homo sapiens 94-101 20455417-9 2009 Estimated glucose disposal rate (eGDR) as indicator of insulin resistance was calculated according to own formula. Glucose 10-17 insulin Homo sapiens 55-62 23226034-1 2009 Type 2 diabetes mellitus (T2DM) is characterized by three major metabolic abnormalities: impaired insulin-stimulated glucose uptake in muscle and adipose tissues, alterations in glucose-stimulated insulin secretion, and increased hepatic glucose production. Glucose 117-124 insulin Homo sapiens 98-105 23226034-1 2009 Type 2 diabetes mellitus (T2DM) is characterized by three major metabolic abnormalities: impaired insulin-stimulated glucose uptake in muscle and adipose tissues, alterations in glucose-stimulated insulin secretion, and increased hepatic glucose production. Glucose 178-185 insulin Homo sapiens 197-204 23226034-1 2009 Type 2 diabetes mellitus (T2DM) is characterized by three major metabolic abnormalities: impaired insulin-stimulated glucose uptake in muscle and adipose tissues, alterations in glucose-stimulated insulin secretion, and increased hepatic glucose production. Glucose 178-185 insulin Homo sapiens 197-204 19274082-9 2009 The mRNA level of ATP5O in skeletal muscle was positively related to insulin-stimulated glucose uptake (regression coefficient = 6.6; p = 0.02). Glucose 88-95 insulin Homo sapiens 69-76 19357775-6 2009 Instead, cell-to-cell variability in lipid droplet formation is dependent on the cascade responses of an insulin signaling pathway which includes insulin sensitivity, kinase activity, glucose import, expression of an insulin degradation enzyme, and insulin degradation rate. Glucose 184-191 insulin Homo sapiens 105-112 19424489-1 2009 BACKGROUND: Apolipoprotein C3 (APOC3) modulates triglyceride metabolism through inhibition of lipoprotein lipase, but is itself regulated by insulin, so that APOC3 represents a potential mechanism by which glucose metabolism may affect lipid metabolism. Glucose 206-213 insulin Homo sapiens 141-148 19179812-6 2009 Since these drugs improve insulin secretion in response to an increase in blood glucose, it seems appropriate to pair them with drugs that have a different mechanism of action, such as insulin sensitizers or metformin. Glucose 80-87 insulin Homo sapiens 26-33 21179921-2 2009 Both insulin resistance and lower insulin secretion in liver cirrhosis are important determinants of the degree of oral glucose tolerance. Glucose 120-127 insulin Homo sapiens 5-12 19731182-12 2009 Skinfold thickness, higher triglyceride and glucose levels, and being female were associated with increased serum insulin. Glucose 44-51 insulin Homo sapiens 114-121 19947447-1 2009 Insulin resistance (IR) is a leading factor of type 2 diabetes (T2D), the central and governing component of the metabolic syndrome (MS), that also appears as obesity, glucose intolerance, dyslipidemia, and essential hypertension. Glucose 168-175 insulin Homo sapiens 0-7 19171928-3 2009 We review molecular mechanisms by which the HIV protease inhibitor (PI) class of drugs may affect the normal stimulatory effect of insulin on glucose and fat storage. Glucose 142-149 insulin Homo sapiens 131-138 19249552-3 2009 Moreover, PACAP increases glucose-stimulated insulin release in vitro and in vivo. Glucose 26-33 insulin Homo sapiens 45-52 19249552-6 2009 We assessed beta-cell viability using FACS, cellular composition analysis by iCys/LSC, and glucose-stimulated insulin secretion. Glucose 91-98 insulin Homo sapiens 110-117 19249552-10 2009 Moreover, glucose-stimulated insulin secretion significantly improved in islets cultured with PACAP compared with controls, respectively (P < .05). Glucose 10-17 insulin Homo sapiens 29-36 19242868-10 2009 Plasma glucose levels were increased concomitantly with an unchanged serum insulin concentration which might reflect an insulin resistance state in addition to proteolytic glyconeogenesis. Glucose 7-14 insulin Homo sapiens 120-127 19242868-14 2009 A kindred nature of a presumed insulin-resistant state with less intracellular availability of glucose for erythrocytes was also indicated by the findings of decreased MCV together with increased MCHC (haemoconcentration) after the race. Glucose 95-102 insulin Homo sapiens 31-38 19590589-3 2009 Their unique pharmacokinetic and pharmacodynamic properties have offered tangible advantage over the conventional intermediate and long-acting insulin preparations in terms of improving glucose control as well as reducing risk of hypoglycemia and weight gain. Glucose 186-193 insulin Homo sapiens 143-150 19961265-5 2009 Studies of hormone secretion from the perfused pancreas of rats and mice revealed that glucose induces pulses of glucagon anti-synchronous with pulses of insulin and somatostatin. Glucose 87-94 insulin Homo sapiens 154-161 19961265-11 2009 The observation of reversed cycles of insulin and glucagon adds to the understanding how the islets regulate hepatic glucose production. Glucose 117-124 insulin Homo sapiens 38-45 19251038-3 2009 Insulin acts within minutes to mobilize these vesicles, translocating GLUT4 to the plasma membrane to enhance glucose uptake. Glucose 110-117 insulin Homo sapiens 0-7 19251039-5 2009 We see from this body of work that both the actin network and the microtubule cytoskeleton play roles as targets of insulin action and effectors of insulin signaling leading to changes in GLUT4 redistribution to the cell surface and insulin-mediated glucose uptake. Glucose 250-257 insulin Homo sapiens 116-123 19251039-5 2009 We see from this body of work that both the actin network and the microtubule cytoskeleton play roles as targets of insulin action and effectors of insulin signaling leading to changes in GLUT4 redistribution to the cell surface and insulin-mediated glucose uptake. Glucose 250-257 insulin Homo sapiens 148-155 19251039-5 2009 We see from this body of work that both the actin network and the microtubule cytoskeleton play roles as targets of insulin action and effectors of insulin signaling leading to changes in GLUT4 redistribution to the cell surface and insulin-mediated glucose uptake. Glucose 250-257 insulin Homo sapiens 148-155 19251040-1 2009 The presence of different nutrients regulates the beta-cell response to secrete insulin to maintain glucose in the physiological range and appropriate levels of fuels in different organs and tissues. Glucose 100-107 insulin Homo sapiens 80-87 19251040-2 2009 Glucose is the only nutrient secretagogue capable of promoting alone the release of insulin release. Glucose 0-7 insulin Homo sapiens 84-91 19251040-8 2009 However, FAs in the presence of glucose produce high concentration of malonyl-CoA that repress FA oxidation and increase the formation of LC-CoA amplifying the insulin release. Glucose 32-39 insulin Homo sapiens 160-167 19251041-0 2009 How insulin regulates glucose transport in adipocytes. Glucose 22-29 insulin Homo sapiens 4-11 19251041-1 2009 Insulin stimulates glucose storage and metabolism by the tissues of the body, predominantly liver, muscle and fat. Glucose 19-26 insulin Homo sapiens 0-7 19251041-5 2009 Work presented in this review focuses on the pathways responsible for the regulation of glucose transport by insulin. Glucose 88-95 insulin Homo sapiens 109-116 19251041-6 2009 We present some historical work to show how the prevailing model for regulation of glucose transport by insulin was originally developed, then some more recent data challenging this model. Glucose 83-90 insulin Homo sapiens 104-111 19251043-1 2009 Signaling of insulin and insulin-like growth factor-I (IGF-1) at target tissues is essential for growth, development and for normal homeostasis of glucose, fat, and protein metabolism. Glucose 147-154 insulin Homo sapiens 13-20 19251043-1 2009 Signaling of insulin and insulin-like growth factor-I (IGF-1) at target tissues is essential for growth, development and for normal homeostasis of glucose, fat, and protein metabolism. Glucose 147-154 insulin Homo sapiens 25-32 19251047-10 2009 The initial trigger for insulin granule fusion with the plasma membrane is a rise in intracellular calcium and in the case of glucose stimulation results from increased production of ATP, closure of the ATP-sensitive potassium channel and cellular depolarization. Glucose 126-133 insulin Homo sapiens 24-31 19251052-5 2009 In contrast to its role in liver, IL-6 is believed to be beneficial for insulin-regulated glucose metabolism in muscle. Glucose 90-97 insulin Homo sapiens 72-79 19251052-7 2009 Herein we review the in vivo and in vitro studies that have examined the role of IL-6 in insulin signaling and glucose metabolism in the insulin target tissues: liver, adipose, and skeletal muscle. Glucose 111-118 insulin Homo sapiens 137-144 20047115-1 2009 BACKGROUND: Thiazolidinediones represent a novel class of drugs that exert pleiotropic effects at various levels and lower blood glucose through reduction of insulin resistance in patients with type 2 diabetes mellitus. Glucose 129-136 insulin Homo sapiens 158-165 19108012-9 2008 CONCLUSION: The glucose lowering effects of TZDs by improving insulin resistance could be determined by using Kitt. Glucose 16-23 insulin Homo sapiens 62-69 19280885-1 2008 UNLABELLED: Insulin sensitivity is deteriorating with age leading to many metabolic complications, yet fasting glucose is the common metabolic predictor in preventive medicine. Glucose 111-118 insulin Homo sapiens 12-19 19280885-7 2008 However, all politicians were substantially insulin resistant, compared with their young descendents, evidenced by exaggerated glucose and insulin responses (>100% greater area under curves above baseline) under oral glucose challenged condition. Glucose 220-227 insulin Homo sapiens 139-146 19104401-10 2008 Acute effects of EXN during mixed meal tolerance test and intravenous glucose tolerance test results in improved first and second phase insulin release in response to intravenous glucose tolerance test and suppressed postprandial hyperglucagonemia after mixed meal tolerance test. Glucose 70-77 insulin Homo sapiens 136-143 19104401-10 2008 Acute effects of EXN during mixed meal tolerance test and intravenous glucose tolerance test results in improved first and second phase insulin release in response to intravenous glucose tolerance test and suppressed postprandial hyperglucagonemia after mixed meal tolerance test. Glucose 179-186 insulin Homo sapiens 136-143 18952604-9 2008 RNAi knockdown demonstrated an important role for S6K1 in mediating TNF-alpha-induced IRS-1 inhibition that led to impaired insulin-stimulated glucose uptake in adipocytes. Glucose 143-150 insulin Homo sapiens 124-131 20428328-1 2008 A mathematical model describing glucose-dependent pH swelling and insulin release is developed for pH-sensitive cationic hydrogels in which glucose oxidase and catalase have been immobilized and insulin imbibed. Glucose 32-39 insulin Homo sapiens 66-73 20428328-1 2008 A mathematical model describing glucose-dependent pH swelling and insulin release is developed for pH-sensitive cationic hydrogels in which glucose oxidase and catalase have been immobilized and insulin imbibed. Glucose 32-39 insulin Homo sapiens 195-202 20428328-6 2008 Glucose sensitivity, as measured by gluconic acid production and by the system pH, are functions of glucose oxidase loading and the concentration and pK(a) of the monomer used in the hydrogel.The necessarily submicron particle size results in very rapid device insulin depletion. Glucose 0-7 insulin Homo sapiens 261-268 18973876-7 2008 Insulin and IGF-1 increased the expression of genes decreased in schizophrenia, including those involved in mitochondrial functions, glucose and energy metabolism, hydrogen ion transport, and synaptic function. Glucose 133-140 insulin Homo sapiens 0-7 19090988-4 2008 It is speculated that angiotensin IV may interact with insulin-regulated amino peptidase to enhance neuronal glucose uptake, prevent metabolism of other neuroactive peptides, induce changes in extracellular matrix molecules, or induce release of acetylcholine and/or dopamine. Glucose 109-116 insulin Homo sapiens 55-62 18728221-2 2008 Glucose exerts its effects on insulin secretion via its metabolism in beta-cells to generate stimulus/secretion coupling factors, including a rise in the ATP/ADP ratio, which serves to suppress ATP-sensitive K(+) (K(ATP)) channels and activate voltage-gated Ca(2+) channels, leading to stimulation of insulin granule exocytosis. Glucose 0-7 insulin Homo sapiens 30-37 18940941-1 2008 Mammalian beta-cells are acutely and chronically regulated by sensing surrounding glucose levels that determine the rate at which insulin is secreted, to maintain euglycemia. Glucose 82-89 insulin Homo sapiens 130-137 18940941-4 2008 In this review, we have taken on the task of looking at the role that ion channels play in the regulation of this process, delineating the different families, and describing the signaling that parallels the glucose sensing process that results in insulin release. Glucose 207-214 insulin Homo sapiens 247-254 19084097-3 2008 Hyperinsulinemia, as demonstrated by elevated insulin levels on a 2-hour 75-g load glucose tolerance test, is an important parameter in deciding whether or not to initiate metformin therapy to women with PCOS with the hope of preventing or delaying the onset of type 2 diabetes mellitus (DM). Glucose 83-90 insulin Homo sapiens 5-12 18294642-0 2008 Human proinsulin C-peptide reduces high glucose-induced proliferation and NF-kappaB activation in vascular smooth muscle cells. Glucose 40-47 insulin Homo sapiens 17-26 18836005-1 2008 Here, we show that commensal bacteria can stimulate intestinal epithelial cells to secrete insulin in response to glucose. Glucose 114-121 insulin Homo sapiens 91-98 18836005-3 2008 Epithelia stimulated by engineered strains and glucose secreted up to 1 ng ml(-1) of insulin with no significant background secretion. Glucose 47-54 insulin Homo sapiens 85-92 18294642-8 2008 C-peptide at the physiological concentrations of 0.5 and 1 nmol/L decreased high glucose-induced proliferation of VSMCs that was accompanied by decreased phosphorylation of IkappaB and reduced NF-kappaB nuclear translocation. Glucose 81-88 insulin Homo sapiens 0-9 18294642-10 2008 In patients with T1D, physiological C-peptide levels may exert beneficial effects on the vasculature that, under high glucose conditions, is subject to progressive dysfunction. Glucose 118-125 insulin Homo sapiens 36-45 18945510-1 2008 AIMS: To investigate ethnic difference by focusing on fasting serum insulin (FSI) in inter-East Asian subjects with normal glucose tolerance (NGT) and impaired glucose regulation (IGR). Glucose 123-130 insulin Homo sapiens 68-75 18471092-8 2008 For the strongest glucose/insulin solution, this linear relationship had a correlation coefficient of 0.77 (n=386, P<0.0001). Glucose 18-25 insulin Homo sapiens 26-33 18936695-5 2008 INTERVENTIONS: Intensive insulin therapy (systemic glucose target: 4.4-6.7 mmol/L [80-120 mg/dL]). Glucose 51-58 insulin Homo sapiens 25-32 18936695-10 2008 Using multivariable analysis, and adjusting for intracranial pressure and cerebral perfusion pressure, systemic glucose concentration (adjusted odds ratio 1.23, 95% confidence interval [CI] 1.10-1.37, for each 1 mmol/L decrease, p < 0.001) and insulin dose (adjusted odds ratio 1.10, 95% CI 1.04-1.17, for each 1 U/hr increase, p = 0.02) independently predicted brain energy crisis. Glucose 112-119 insulin Homo sapiens 247-254 19005294-2 2008 Insulin resistance is defined as impairment of insulin-stimulated glucose and/or lipid metabolism, while endothelial dysfunction is defined as paradoxical or inadequate endothelial-mediated vasodilation. Glucose 66-73 insulin Homo sapiens 0-7 19046246-5 2008 Insulin resistance [homeostasis model assessment (HOMA) score] increased by 1.90% (95% CI 0.01, 3.82, n = 2526) per quintile of area deprivation after adjustment for individual SEP, while fasting blood glucose increased by 0.69% (95% CI 0.16, 1.22, n = 2875) after adjustment for individual SEP. Glucose 202-209 insulin Homo sapiens 0-7 19088809-1 2008 In animal studies, the whole-body glucose disposal effect of insulin is low in the fasted state or after atropine infusion, but doubles after a meal, consistent with the hepatic insulin-sensitizing substance (HISS) hypothesis. Glucose 34-41 insulin Homo sapiens 61-68 19040565-7 2008 Graft function was confirmed by secretion of human C-peptide in response to an oral bolus of glucose. Glucose 93-100 insulin Homo sapiens 51-60 18954705-2 2008 Randomized controlled trials and large observational trials of insulin therapy titrated to achieve glucose values approximating the normal range (80 to 110 mg/dL) demonstrate improved morbidity and mortality in heterogeneous populations and have led to recommendations for improved glucose control. Glucose 99-106 insulin Homo sapiens 63-70 18954705-2 2008 Randomized controlled trials and large observational trials of insulin therapy titrated to achieve glucose values approximating the normal range (80 to 110 mg/dL) demonstrate improved morbidity and mortality in heterogeneous populations and have led to recommendations for improved glucose control. Glucose 282-289 insulin Homo sapiens 63-70 18954705-4 2008 The recent Surviving Sepsis consensus statement recommends insulin therapy using validated protocols to lower glucose (less than 150 mg/dL) pending the results of adequately powered trials to determine if normalization (less than 110 mg/dL) of glucose is needed to optimize outcomes in patients who have severe sepsis. Glucose 110-117 insulin Homo sapiens 59-66 18809633-3 2008 Insulin stimulation of glucose disposal, and insulin suppression of endogenous glucose production (EGP) and nonesterified fatty acids (NEFAs), was studied using a 200-min two-step (10 mU x m(-2) body surface x min(-1) and 80 mU x m(-2) x min (-1) insulin infusion rates) euglycemic clamp with [6,6-(2)H(2)]glucose as the tracer. Glucose 23-30 insulin Homo sapiens 0-7 18809633-3 2008 Insulin stimulation of glucose disposal, and insulin suppression of endogenous glucose production (EGP) and nonesterified fatty acids (NEFAs), was studied using a 200-min two-step (10 mU x m(-2) body surface x min(-1) and 80 mU x m(-2) x min (-1) insulin infusion rates) euglycemic clamp with [6,6-(2)H(2)]glucose as the tracer. Glucose 79-86 insulin Homo sapiens 45-52 18809633-3 2008 Insulin stimulation of glucose disposal, and insulin suppression of endogenous glucose production (EGP) and nonesterified fatty acids (NEFAs), was studied using a 200-min two-step (10 mU x m(-2) body surface x min(-1) and 80 mU x m(-2) x min (-1) insulin infusion rates) euglycemic clamp with [6,6-(2)H(2)]glucose as the tracer. Glucose 79-86 insulin Homo sapiens 45-52 18476986-3 2008 METHODS: Fifty-seven insulin-resistant obese subjects had insulin-mediated glucose disposal quantified through the steady-state plasma glucose (SSPG) test, and associated metabolic risk markers quantified at baseline, after a 16-week dietary weight loss intervention, and in 25 subjects, at follow-up of 28.8 +/- 13 months. Glucose 75-82 insulin Homo sapiens 58-65 18476986-8 2008 Insulin-mediated glucose disposal remained significantly improved vs. baseline, as did plasma triglyceride and HDL cholesterol (HDL-C) concentrations, and improvement correlated with total amount of weight lost. Glucose 17-24 insulin Homo sapiens 0-7 18476986-14 2008 Fasting glucose and weight regain predict less long-term response in insulin sensitivity. Glucose 8-15 insulin Homo sapiens 69-76 19049379-0 2008 Better postprandial glucose stability during continuous subcutaneous infusion with insulin aspart compared with insulin lispro in patients with type 1 diabetes. Glucose 20-27 insulin Homo sapiens 83-90 19195626-4 2008 Insulin signals in the liver through its tyrosine-kinase receptors to negatively control hepatic glucose production (HGP), replenish glycogen stores and synthesize fatty acids (FA), leading to TG exported as VLDL. Glucose 97-104 insulin Homo sapiens 0-7 19195628-2 2008 Under the control of hormones, especially insulin, the liver stores or releases glucose as needed by the body"s systems. Glucose 80-87 insulin Homo sapiens 42-49 19049372-4 2008 Recent pump manufacturers have engineered a new feature called a bolus calculator, which calculates bolus insulin doses based on input from the pump wearer, which functions to help patients obtain optimum control over blood glucose levels. Glucose 224-231 insulin Homo sapiens 106-113 19079282-4 2008 The hormones insulin and glucagon not only regulate glycemic levels through their action on these organs and the sympathetic and parasympathetic branches of the autonomic nervous system, which are activated by glucose or lipid sensors, but also modulate pancreatic hormone secretion and liver, muscle and fat glucose and lipid metabolism. Glucose 210-217 insulin Homo sapiens 13-20 18805916-9 2008 Simpler methods to assess insulin resistance based on surrogate markers derived from an oral glucose tolerance test or from fasting insulin and glucose levels have been validated in children and adolescents and widely used. Glucose 93-100 insulin Homo sapiens 26-33 18805916-9 2008 Simpler methods to assess insulin resistance based on surrogate markers derived from an oral glucose tolerance test or from fasting insulin and glucose levels have been validated in children and adolescents and widely used. Glucose 144-151 insulin Homo sapiens 26-33 18926903-0 2008 Insulin stimulation of gamma-glutamylcysteine ligase catalytic subunit expression increases endothelial GSH during oxidative stress: influence of low glucose. Glucose 150-157 insulin Homo sapiens 0-7 18926903-5 2008 Notably, the effects of insulin were observed under low, but not normal, glucose conditions. Glucose 73-80 insulin Homo sapiens 24-31 19079282-4 2008 The hormones insulin and glucagon not only regulate glycemic levels through their action on these organs and the sympathetic and parasympathetic branches of the autonomic nervous system, which are activated by glucose or lipid sensors, but also modulate pancreatic hormone secretion and liver, muscle and fat glucose and lipid metabolism. Glucose 309-316 insulin Homo sapiens 13-20 19079282-7 2008 Work from several laboratories, including ours, has explored the physiological role of glucose as a signal that regulates these homeostatic processes and has tested the hypothesis that the mechanism of glucose sensing that controls insulin secretion by the pancreatic beta-cells is also used by other cell types. Glucose 202-209 insulin Homo sapiens 232-239 18765510-12 2008 CONCLUSIONS: Insulin sensitivity and glucose transport are greater in the postsurgery patients than predicted from the weight-matched group, suggesting that improved insulin sensitivity after bypass is due to something other than, or in addition to, weight loss. Glucose 37-44 insulin Homo sapiens 166-173 19155426-5 2008 In genetically prone individuals, malnutrition (i.e., excessive consumption of saturated fats and refined sugars) leads to the derangement of the adipose tissue architecture and homeostasis, the peripheral and hepatic resistance to insulin-stimulated glucose uptake, thus favoring a condition of chronic low-grade inflammation. Glucose 251-258 insulin Homo sapiens 232-239 19013300-15 2008 However, it increased the insulin area response to glucose by an additional 66%; that is, it almost doubled the response. Glucose 51-58 insulin Homo sapiens 26-33 18796522-10 2008 CONCLUSIONS: We conclude that variation marked by the Kir6.2 E23K and SUR1 A1369S mutations is associated with alterations in glucose-stimulated insulin secretion but not with other measures of glucose homeostasis in an African-American population. Glucose 126-133 insulin Homo sapiens 145-152 18827000-7 2008 RESULTS: Plasma insulin levels during hyperglycemia alone were similar in the two studies (control, 282.5 +/- 42 vs. Ex-9, 263.8 +/- 59 pmol/liter) but were reduced by approximately 30% by Ex-9 after glucose ingestion (control, 1154 +/- 203 vs. Ex-9, 835 +/- 120 pmol/liter; P < 0.05). Glucose 200-207 insulin Homo sapiens 16-23 19067533-0 2008 The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects. Glucose 23-30 insulin Homo sapiens 78-85 18923366-9 2008 Age, weight, body mass index, high fasting, 30, 60-, 90-, 120-min serum glucose, insulin and HgA1c levels were risk factors for glucose intolerance. Glucose 128-135 insulin Homo sapiens 81-88 19047536-5 2008 Activation of FFA1 has been proposed to mediate fatty acid augmentation of glucose-stimulated insulin secretion although it is unclear whether the known long-term detrimental effects of beta-cell exposure to high levels of fatty acids are also mediated through this receptor. Glucose 75-82 insulin Homo sapiens 94-101 18606622-8 2008 The increase of both glucose and insulin levels was more pronounced in patients with insulin resistance (11/22 patients). Glucose 21-28 insulin Homo sapiens 85-92 19078869-3 2008 This review has two aims: 1) to review the mechanisms of insulin resistance, specifically impaired insulin-stimulated glucose transport, in skeletal muscle and adipose tissue in PCOS, and 2) to assess whether mechanisms of insulin resistance in PCOS are distinct from those in type 2 diabetes. Glucose 118-125 insulin Homo sapiens 57-64 19078869-3 2008 This review has two aims: 1) to review the mechanisms of insulin resistance, specifically impaired insulin-stimulated glucose transport, in skeletal muscle and adipose tissue in PCOS, and 2) to assess whether mechanisms of insulin resistance in PCOS are distinct from those in type 2 diabetes. Glucose 118-125 insulin Homo sapiens 99-106 19202764-3 2008 In this work, we demonstrated that insulin could regulate glucose uptake in schistosomes and we investigated the implication of SmIR-1 and SmIR-2 in this process. Glucose 58-65 insulin Homo sapiens 35-42 18947221-2 2008 The preferred compound 20 (TUG-424, EC(50) = 32 nM) significantly increased glucose-stimulated insulin secretion at 100 nM and may serve to explore the role of FFA(1) in metabolic diseases such as diabetes or obesity. Glucose 76-83 insulin Homo sapiens 95-102 19060447-9 2008 A large amount of insulin (34 units/day) was required to control the blood glucose level. Glucose 75-82 insulin Homo sapiens 18-25 18824546-1 2008 Insulin maintains homeostasis of glucose by promoting its uptake into cells from the blood. Glucose 33-40 insulin Homo sapiens 0-7 18950630-5 2008 We observed that a prolonged effect of high levels of insulin on the presence of serum (15-24h) in glucose-deprived beta cells induced apoptosis. Glucose 99-106 insulin Homo sapiens 54-61 18782593-5 2008 The first one consists in delivering insulin with a glucose-responsive matrix. Glucose 52-59 insulin Homo sapiens 37-44 18782593-6 2008 Polymeric hydrogels that swell or shrink according to the glucose concentration allow delivering insulin doses adapted to the glucose concentration. Glucose 58-65 insulin Homo sapiens 97-104 18782593-6 2008 Polymeric hydrogels that swell or shrink according to the glucose concentration allow delivering insulin doses adapted to the glucose concentration. Glucose 126-133 insulin Homo sapiens 97-104 18782593-7 2008 The second strategy consists in modifying insulin itself with glucose-sensitive functional groups that trigger its activity. Glucose 62-69 insulin Homo sapiens 42-49 18784081-3 2008 Nanomolar ABA increases glucose-stimulated insulin secretion from RIN-m and INS-1 cells and from murine and human pancreatic islets. Glucose 24-31 insulin Homo sapiens 43-50 18804779-8 2008 Core-shell microgels with a response to glucose at physiological pH were obtained and used to encapsulate insulin. Glucose 40-47 insulin Homo sapiens 106-113 19030757-1 2008 The article by Ramkumar and Basti: "Reversal of Bilateral Rosette Cataracts with Glycemic Control", published in TheScientificWorldJournal, Vol 8 1150-1151, describes the acute onset of a bilateral cataract related to the onset of diabetes, and the eventual reversal of the lens opacities after accomplishing a fall in blood glucose levels with insulin therapy. Glucose 325-332 insulin Homo sapiens 345-352 18804779-9 2008 Insulin release was shown to be regulated by the presence of glucose. Glucose 61-68 insulin Homo sapiens 0-7 18782754-7 2008 The iPS-derived ILCs not only contain C-peptide-positive and glucagon-positive cells but also release C-peptide upon glucose stimulation. Glucose 117-124 insulin Homo sapiens 102-111 19205422-1 2008 Studies of replacement therapy of diabetes mellitus resulted in introduction of series of forms of insulin and new insulin analogs which exhibit better control of blood glucose level. Glucose 169-176 insulin Homo sapiens 99-106 18779333-6 2008 However, insulin-stimulated GLUT4 translocation to the cell surface and subsequent glucose transport are impaired in Tfam knockdown cells. Glucose 83-90 insulin Homo sapiens 9-16 18779333-8 2008 These studies reveal independent links between mitochondrial function, insulin signaling, and glucose transport, in which impaired respiratory chain activity enhances insulin signaling to Akt phosphorylation, but impairs GLUT4 translocation. Glucose 94-101 insulin Homo sapiens 167-174 18996863-1 2008 BACKGROUND: African Americans have a greater insulin response after glucose challenge than do European Americans. Glucose 68-75 insulin Homo sapiens 45-52 18765680-4 2008 Indeed, after controlling for insulin-stimulated glucose disposal rate (amount of glucose available for oxidation), metabolic flexibility is not altered in obesity regardless of the presence of type 2 diabetes. Glucose 49-56 insulin Homo sapiens 30-37 18765680-4 2008 Indeed, after controlling for insulin-stimulated glucose disposal rate (amount of glucose available for oxidation), metabolic flexibility is not altered in obesity regardless of the presence of type 2 diabetes. Glucose 82-89 insulin Homo sapiens 30-37 18765681-1 2008 The ability to accurately quantify indexes of the individual role of glucose (GE(L)) and insulin (S(I)(L)) in the suppression of endogenous glucose production (EGP) would improve the understanding of liver metabolism. Glucose 140-147 insulin Homo sapiens 89-96 18796548-2 2008 The glucose clamp is considered the gold standard for determining in vivo insulin sensitivity, both in human and in animal models. Glucose 4-11 insulin Homo sapiens 74-81 18796548-8 2008 We have performed a calibration analysis to evaluate the ability of these indexes to accurately predict insulin sensitivity as determined by the reference glucose clamp. Glucose 155-162 insulin Homo sapiens 104-111 18482007-1 2008 BACKGROUND INFORMATION: Insulin-stimulated glucose uptake into skeletal muscle is crucial for glucose homoeostasis, and depends on the recruitment of GLUT4 (glucose transporter 4) to the plasma membrane. Glucose 43-50 insulin Homo sapiens 24-31 18482007-9 2008 CONCLUSION: Collectively, Rac1 activation specifically in membrane ruffles by the GEF FLJ00068 is sufficient for insulin induction of glucose uptake into skeletal-muscle cells. Glucose 134-141 insulin Homo sapiens 113-120 19205422-1 2008 Studies of replacement therapy of diabetes mellitus resulted in introduction of series of forms of insulin and new insulin analogs which exhibit better control of blood glucose level. Glucose 169-176 insulin Homo sapiens 115-122 18612626-3 2008 It also modulates glucose uptake, glycolysis and insulin resistance in insulin target cells such as the adipocyte, myocyte and cardiomyocyte. Glucose 18-25 insulin Homo sapiens 71-78 18284435-0 2008 Adiponectin and its response to thiazolidinediones are associated with insulin-mediated glucose metabolism in type 2 diabetic patients and their first-degree relatives. Glucose 88-95 insulin Homo sapiens 71-78 18284435-7 2008 The troglitazone-mediated upregulation of plasma adiponectin was associated with increased insulin-stimulated Rd, NOGD and glucose storage in both groups. Glucose 123-130 insulin Homo sapiens 91-98 18284435-10 2008 In conclusion, plasma adiponectin in weight-matched FDR and T2D patients is comparably low and correlates with insulin-mediated glucose uptake and storage. Glucose 128-135 insulin Homo sapiens 111-118 18647954-7 2008 RESULTS: Four variants were modestly associated with early-onset type 2 diabetes in both general and within-family analyses (P = 0.004-0.04, recessive model), where the diabetes risk allele was also nominally associated with a lower insulin-mediated glucose disposal rate (P = 0.009-0.14, recessive model) in nondiabetic Pima Indians. Glucose 250-257 insulin Homo sapiens 233-240 18284435-11 2008 Moreover, these data provide evidence for an adiponectin-dependent insulin-sensitizing effect of TZDs at an early stage before development of T2D and that this effect is exerted mainly on insulin-mediated glucose metabolism. Glucose 205-212 insulin Homo sapiens 188-195 18694978-9 2008 Five patients in the no load group required supplemental insulin doses to decrease initial glucose levels by 10%; patients in the twice no load and load groups did not. Glucose 91-98 insulin Homo sapiens 57-64 18650373-1 2008 OBJECTIVE: To assess whether prandial insulin, in addition to basal insulin, has an effect on the rate of glucose appearance from a meal in people with type 1 diabetes. Glucose 106-113 insulin Homo sapiens 38-45 18768235-0 2008 Is fasting glucose level during oral glucose tolerance test an indicator of the insulin need in gestational diabetes? Glucose 11-18 insulin Homo sapiens 80-87 18678610-8 2008 CONCLUSIONS: Technosphere insulin was well tolerated and demonstrated significant improvement in glycemic control with clinically meaningful reductions in A1C levels and postprandial glucose concentrations after 12 weeks of treatment. Glucose 183-190 insulin Homo sapiens 26-33 18716044-6 2008 RESULTS: Insulin-induced glucose disposal and suppression of endogenous glucose production were higher in the trained young and older subjects, but no age effect was noted. Glucose 25-32 insulin Homo sapiens 9-16 18834446-7 2008 Most recently, the production in vivo of glucose-responsive insulin-producing cells with the capacity to correct Steptozotocin-induced hyperglycaemia in mice has been achieved. Glucose 41-48 insulin Homo sapiens 60-67 19046215-9 2008 The B-cell responsiveness to changes in plasma glucose, expressed as the slope of the linear relationship between the insulin secretion rate and the concomitant plasma glucose increased from 0.59 +/- 0.16 to 0.94 +/- 0.13 pmol kg(-1) min(-1)/ mmol l(-1) (P < 0.07). Glucose 47-54 insulin Homo sapiens 118-125 19046218-3 2008 Insulin sensitivity in skeletal muscle was measured as the insulin-stimulated rate of total glucose disposal during the insulin clamp divided by steady-state plasma insulin concentration (TGD/SSPI). Glucose 92-99 insulin Homo sapiens 0-7 19046218-3 2008 Insulin sensitivity in skeletal muscle was measured as the insulin-stimulated rate of total glucose disposal during the insulin clamp divided by steady-state plasma insulin concentration (TGD/SSPI). Glucose 92-99 insulin Homo sapiens 59-66 18768235-2 2008 The aim of this study is to investigate the utility of diagnostic oral glucose tolerance test (OGTT) in prediction of the need of insulin in patients with GDM. Glucose 71-78 insulin Homo sapiens 130-137 19046218-8 2008 Subjects with increased skeletal muscle insulin resistance had a higher 2-h plasma glucose concentration, greater incremental area under the plasma glucose concentration curve, lower fasting plasma insulin concentration and lower rate of basal hepatic glucose production compared with subjects with increased insulin resistance in liver. Glucose 83-90 insulin Homo sapiens 40-47 19046218-8 2008 Subjects with increased skeletal muscle insulin resistance had a higher 2-h plasma glucose concentration, greater incremental area under the plasma glucose concentration curve, lower fasting plasma insulin concentration and lower rate of basal hepatic glucose production compared with subjects with increased insulin resistance in liver. Glucose 148-155 insulin Homo sapiens 40-47 18768235-6 2008 Glucose levels obtained from the diagnostic OGTT were evaluated regarding the need of insulin during the rest of pregnancy. Glucose 0-7 insulin Homo sapiens 86-93 19046218-9 2008 CONCLUSION: In non-diabetic subjects, insulin resistance in skeletal muscle is an important determinant of the fasting and 2-h plasma glucose concentrations and strongly correlates with hepatic insulin resistance. Glucose 134-141 insulin Homo sapiens 38-45 18768235-7 2008 Fasting, 1h and 3h post-load glucose levels were significantly elevated in patients who required insulin. Glucose 29-36 insulin Homo sapiens 97-104 18768235-8 2008 Multivariate analysis showed that fasting glucose level on OGTT was an independent predictor for the insulin need. Glucose 42-49 insulin Homo sapiens 101-108 18768235-10 2008 Our results suggest that fasting glucose level on OGTT is a predictor of the need for insulin treatment in GDM. Glucose 33-40 insulin Homo sapiens 86-93 19031221-0 2008 Insulin response to oral glucose in healthy, lean young women and patients with polycystic ovary syndrome. Glucose 25-32 insulin Homo sapiens 0-7 19347813-8 2008 Oral glucose tolerance test was performed with estimation of glucose and insulin concentrations. Glucose 5-12 insulin Homo sapiens 73-80 19031221-4 2008 Thus the present study aimed to determine the insulin response to oral glucose in women with PCOS and healthy women. Glucose 71-78 insulin Homo sapiens 46-53 19031221-16 2008 Peak insulin was observed at 1 h. The difference between 1-h and 2-h post-glucose insulin decreased with worsening glucose tolerance. Glucose 74-81 insulin Homo sapiens 5-12 19031221-21 2008 CONCLUSION: Women with PCOS had an exaggerated insulin response to glucose. Glucose 67-74 insulin Homo sapiens 47-54 18713820-3 2008 Insulin sensitivity was assessed by the surrogate measures of fasting glucose to insulin ratio, whole-body insulin sensitivity index, and homeostasis model assessment of insulin resistance, and insulin secretion by the insulinogenic index with calculation of the glucose disposition index (GDI). Glucose 70-77 insulin Homo sapiens 0-7 19330070-3 2008 The work of numerous different researchers indicates a role of PKB in regulating insulin-stimulated glucose uptake. Glucose 100-107 insulin Homo sapiens 81-88 18713820-3 2008 Insulin sensitivity was assessed by the surrogate measures of fasting glucose to insulin ratio, whole-body insulin sensitivity index, and homeostasis model assessment of insulin resistance, and insulin secretion by the insulinogenic index with calculation of the glucose disposition index (GDI). Glucose 263-270 insulin Homo sapiens 0-7 19885293-7 2008 For IN doses, peak insulin levels were generally attained in 10-20 min and remained elevated for approximately 40-50 min; the resultant effect on glucose peaked at 40 min and waned approximately 2 h postdosing. Glucose 146-153 insulin Homo sapiens 19-26 18694627-10 2008 However, during this time, as insulin concentrations declined, blood glucose levels would increase, eventually overcoming the renal threshold, causing the renal diuresis and subsequent dehydration. Glucose 69-76 insulin Homo sapiens 30-37 19009015-7 2008 Since skeletal muscle is an important insulin target tissue and accounts for much of insulin-induced glucose disposal, it is important to determine its role in injury/infection-induced hyperglycemia. Glucose 101-108 insulin Homo sapiens 85-92 18940402-8 2008 However, significantly higher acute insulin response after glucose load and disposal index were noted in MetS+ and MetS (4,5) than in Met-, MetS (1,2), and MetS (3), respectively. Glucose 59-66 insulin Homo sapiens 36-43 18797431-4 2008 The study indicated that patients requiring glucose-lowering therapy (oral treatment, insulin, or combined insulin and oral therapy) exhibited a cardiovascular risk comparable to that of nondiabetic individuals with a prior myocardial infarction, irrespective of sex and type of diabetes. Glucose 44-51 insulin Homo sapiens 86-93 18797431-4 2008 The study indicated that patients requiring glucose-lowering therapy (oral treatment, insulin, or combined insulin and oral therapy) exhibited a cardiovascular risk comparable to that of nondiabetic individuals with a prior myocardial infarction, irrespective of sex and type of diabetes. Glucose 44-51 insulin Homo sapiens 107-114 19055134-4 2008 The favourable pathophysiological mechanisms in the insulin group may be related to the biological effects of insulin, such as reducing the toxic influence of glucose on beta-cells and so-called beta-cell rest. Glucose 159-166 insulin Homo sapiens 52-59 19055134-4 2008 The favourable pathophysiological mechanisms in the insulin group may be related to the biological effects of insulin, such as reducing the toxic influence of glucose on beta-cells and so-called beta-cell rest. Glucose 159-166 insulin Homo sapiens 110-117 18801852-8 2008 Exogenous forms of insulin and agents that stimulate insulin secretion in a glucose-independent manner (such as sulfonylureas and glinides) increase the propensity for hypoglycemia during low- to moderate-intensity aerobic exercise. Glucose 76-83 insulin Homo sapiens 19-26 18799296-0 2008 Insulin resistance to both glucose and aminoacid metabolism in a patient with Fatal Familial Insomnia. Glucose 27-34 insulin Homo sapiens 0-7 18801860-1 2008 The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Glucose 189-196 insulin Homo sapiens 117-124 18801860-5 2008 Additionally, a single session of aerobic exercise increases glucose uptake by muscle during exercise, increases the ability of insulin to promote glucose uptake, and increases glycogen accumulation after exercise, all of which are important to blood glucose control. Glucose 147-154 insulin Homo sapiens 128-135 18971490-8 2008 RESULTS: As compared with infants in the control group, infants in the early-insulin group had lower mean (+/-SD) glucose levels (6.2+/-1.4 vs. 6.7+/-2.2 mmol per liter [112+/-25 vs. 121+/-40 mg per deciliter], P=0.007). Glucose 114-121 insulin Homo sapiens 77-84 19020364-5 2008 However, intensive insulin therapy can increase the risk of hypoglycemia, which often results in the early abandonment of tight glycemic control strategies, or in some cases, no emphasis on glucose control at all. Glucose 190-197 insulin Homo sapiens 19-26 17851095-8 2008 Underfeeding was associated with a higher AUC for plasma glucose (P=0.02) and plasma insulin (P=0.05) resulting in a decreased glucose tolerance (AUC glucose/AUC insulin; P=0.008), probably due to a plasma cortisol increase caused by the reduced feed intake. Glucose 127-134 insulin Homo sapiens 85-92 17851095-8 2008 Underfeeding was associated with a higher AUC for plasma glucose (P=0.02) and plasma insulin (P=0.05) resulting in a decreased glucose tolerance (AUC glucose/AUC insulin; P=0.008), probably due to a plasma cortisol increase caused by the reduced feed intake. Glucose 127-134 insulin Homo sapiens 162-169 18727921-1 2008 SREBP1c (sterol regulatory element-binding protein 1c) is a metabolic-syndrome-associated transcription factor that controls fatty acid biosynthesis under glucose/insulin stimulation. Glucose 155-162 insulin Homo sapiens 163-170 19175181-2 2008 The goal of the study was to determine the insulin levels under a glucose-challenged condition for the sedentary and physical active females in early middle age. Glucose 66-73 insulin Homo sapiens 43-50 18794553-8 2008 Premixed insulin analogues were similar to premixed human insulin in decreasing fasting glucose levels, hemoglobin A(1c) levels, and the incidence of hypoglycemia but were more effective in decreasing postprandial glucose levels (mean difference, -1.1 mmol/L; 95% CI, -1.4 to -0.7 mmol/L [-19.2 mg/dL; 95% CI, -25.9 to -12.5 mg/dL]). Glucose 88-95 insulin Homo sapiens 9-16 18794553-8 2008 Premixed insulin analogues were similar to premixed human insulin in decreasing fasting glucose levels, hemoglobin A(1c) levels, and the incidence of hypoglycemia but were more effective in decreasing postprandial glucose levels (mean difference, -1.1 mmol/L; 95% CI, -1.4 to -0.7 mmol/L [-19.2 mg/dL; 95% CI, -25.9 to -12.5 mg/dL]). Glucose 214-221 insulin Homo sapiens 9-16 18697738-10 2008 The results confirm the central importance of PC and anaplerosis to generate metabolites from glucose that support insulin secretion and even suggest PC is important for insulin secretion stimulated by noncarbohydrate insulin secretagogues. Glucose 94-101 insulin Homo sapiens 115-122 18669636-0 2008 Use of Akt inhibitor and a drug-resistant mutant validates a critical role for protein kinase B/Akt in the insulin-dependent regulation of glucose and system A amino acid uptake. Glucose 139-146 insulin Homo sapiens 107-114 18669636-1 2008 Protein kinase B (PKB)/Akt has been strongly implicated in the insulin-dependent stimulation of GLUT4 translocation and glucose transport in skeletal muscle and fat cells. Glucose 120-127 insulin Homo sapiens 63-70 18650435-1 2008 Insulin increases glucose uptake into muscle by enhancing the surface recycling of GLUT4 transporters. Glucose 18-25 insulin Homo sapiens 0-7 18647881-2 2008 Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscle and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Glucose 61-68 insulin Homo sapiens 0-7 18647881-2 2008 Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscle and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Glucose 110-117 insulin Homo sapiens 0-7 18647881-2 2008 Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscle and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Glucose 110-117 insulin Homo sapiens 0-7 18685069-5 2008 In one category of models, a single insulin compartment acted on both glucose and FFA simultaneously. Glucose 70-77 insulin Homo sapiens 36-43 18685069-6 2008 In a second category, there were two insulin compartments, each acting on FFA and glucose independently. Glucose 82-89 insulin Homo sapiens 37-44 18685069-11 2008 In the best model, insulin suppressed lipolysis via a Hill function through a remote compartment that acted on both glucose and FFA simultaneously, and glucose dynamics obeyed the classic MMG. Glucose 116-123 insulin Homo sapiens 19-26 18923570-1 2008 One bout of exercise enhances insulin-stimulated glucose uptake (insulin action), but the effect is blunted by consumption of carbohydrate-containing food after exercise. Glucose 49-56 insulin Homo sapiens 30-37 18923570-1 2008 One bout of exercise enhances insulin-stimulated glucose uptake (insulin action), but the effect is blunted by consumption of carbohydrate-containing food after exercise. Glucose 49-56 insulin Homo sapiens 65-72 18923570-7 2008 Twelve hours later, insulin action was measured by continuous infusion of glucose with stable isotope tracer (CIG-SIT). Glucose 74-81 insulin Homo sapiens 20-27 18923570-13 2008 Following exercise, re-feeding expended energy, but not carbohydrate, increased fasting fat oxidation, and shifted insulin-mediated glucose disposal toward increased storage and away from oxidation. Glucose 132-139 insulin Homo sapiens 115-122 18793157-7 2008 PPARs exert important lipid-lowering effects in vivo, thereby opposing the development of lipid-induced insulin resistance by relieving the inhibition of insulin-stimulated glucose disposal by muscle and lowering the necessity for augmented GSIS to counter lipid-induced insulin resistance. Glucose 173-180 insulin Homo sapiens 154-161 18612041-7 2008 In addition, vascular dysfunction appears to be an early development in the onset of insulin resistance, with the consequence that impaired glucose delivery, more so than insulin delivery, accounts for the diminished glucose uptake by insulin-resistant muscle. Glucose 140-147 insulin Homo sapiens 85-92 18793157-7 2008 PPARs exert important lipid-lowering effects in vivo, thereby opposing the development of lipid-induced insulin resistance by relieving the inhibition of insulin-stimulated glucose disposal by muscle and lowering the necessity for augmented GSIS to counter lipid-induced insulin resistance. Glucose 173-180 insulin Homo sapiens 154-161 18793158-5 2008 Recent studies in our laboratory have shown that cyclical and alternate infusions of glucose and Intralipid in rats impair insulin gene expression, providing evidence that inhibition of the insulin gene under glucolipotoxic conditions is an early defect that might indeed contribute to beta-cell failure in Type 2 diabetes, although this hypothesis remains to be tested in humans. Glucose 85-92 insulin Homo sapiens 123-130 18793158-5 2008 Recent studies in our laboratory have shown that cyclical and alternate infusions of glucose and Intralipid in rats impair insulin gene expression, providing evidence that inhibition of the insulin gene under glucolipotoxic conditions is an early defect that might indeed contribute to beta-cell failure in Type 2 diabetes, although this hypothesis remains to be tested in humans. Glucose 85-92 insulin Homo sapiens 190-197 18793168-2 2008 Acute exposure of the pancreatic beta-cell to high glucose concentrations and/or saturated NEFAs results in a substantial increase in insulin release, whereas chronic exposure results in desensitization and suppression of secretion followed by induction of apoptosis. Glucose 51-58 insulin Homo sapiens 134-141 18855266-3 2008 In insulin-resistant states, like obesity and type 2 diabetes, altered glucose metabolism may lead to increased formation of methylglyoxal and other ketoaldehydes. Glucose 71-78 insulin Homo sapiens 3-10 18855585-4 2008 The human brain uses glucose as a primary fuel; insulin secreted by the pancreas cross the blood-brain barrier (BBB), reaching neurons and glial cells, and exerts a region-specific effect on glucose metabolism. Glucose 21-28 insulin Homo sapiens 48-55 18615850-7 2008 Insulin-stimulated glucose transport rate was unaltered by exposure to globular adiponectin in either group. Glucose 19-26 insulin Homo sapiens 0-7 18615850-8 2008 AICAR increased glucose transport and enhanced insulin-stimulated glucose transport in type 2 diabetic and non-diabetic muscles. Glucose 66-73 insulin Homo sapiens 47-54 18633101-11 2008 Increased TLR4 content and gene expression observed in muscle from insulin-resistant subjects were reproduced by treating myotubes from lean, normal-glucose-tolerant subjects with palmitate. Glucose 149-156 insulin Homo sapiens 67-74 18665347-5 2008 A small fraction of the beta cell population (20%) secreted more than 90% and 70% of total insulin at 2.2 and 22.2 mmol/l glucose, respectively. Glucose 122-129 insulin Homo sapiens 91-98 18665347-8 2008 Insulin secretion of beta cell pairs was increased compared with that of single beta cells and was higher at 22.2 than at 12.2 mmol/l glucose. Glucose 134-141 insulin Homo sapiens 0-7 18670752-0 2008 The interpretation of glucose clamp studies of long-acting insulin analogues: from physiology to marketing and back. Glucose 22-29 insulin Homo sapiens 59-66 18670752-1 2008 Glucose clamp studies assessing the time-action profile of long-acting insulin analogues have reported conflicting results. Glucose 0-7 insulin Homo sapiens 71-78 18670752-4 2008 (Un)conscious investigator-related bias, especially during manual studies, cannot be ruled out, despite attempts at blinding the study insulin during the clamp.The duration of action of study insulins is influenced by many factors, such as glucose and insulin levels prior to injection, endogenous insulin secretion, insulin dose, definitions used for onset and end of action, and insulin sensitivity (which is influenced by the necessity of fasting during the clamp). Glucose 240-247 insulin Homo sapiens 192-199 18670752-4 2008 (Un)conscious investigator-related bias, especially during manual studies, cannot be ruled out, despite attempts at blinding the study insulin during the clamp.The duration of action of study insulins is influenced by many factors, such as glucose and insulin levels prior to injection, endogenous insulin secretion, insulin dose, definitions used for onset and end of action, and insulin sensitivity (which is influenced by the necessity of fasting during the clamp). Glucose 240-247 insulin Homo sapiens 192-199 18670752-4 2008 (Un)conscious investigator-related bias, especially during manual studies, cannot be ruled out, despite attempts at blinding the study insulin during the clamp.The duration of action of study insulins is influenced by many factors, such as glucose and insulin levels prior to injection, endogenous insulin secretion, insulin dose, definitions used for onset and end of action, and insulin sensitivity (which is influenced by the necessity of fasting during the clamp). Glucose 240-247 insulin Homo sapiens 192-199 18726585-9 2008 Once established, the increased insulin secretion required to maintain plasma glucose levels will further increase liver fat deposition. Glucose 78-85 insulin Homo sapiens 32-39 18789871-8 2008 In summary, these data indicate that oral glucose uptake in insulin-sensitive adults is associated with elevated monocytic and reduced systemic CXCL8. Glucose 42-49 insulin Homo sapiens 60-67 18462969-5 2008 Body adiposity was determined by DEXA, and insulin resistance was estimated by HOMA-IR using the fasting serum glucose and insulin values. Glucose 111-118 insulin Homo sapiens 43-50 18401805-2 2008 Since glucose uptake during muscle contraction has been observed in the absence of insulin, the existence of an insulin-independent pathway has been suggested to explain this phenomenon. Glucose 6-13 insulin Homo sapiens 112-119 18926586-3 2008 Insulin was up-titrated to achieve fasting plasma glucose <6 mmol/l. Glucose 50-57 insulin Homo sapiens 0-7 18401805-6 2008 Therefore, the earliest concept that two different routes exist in skeletal muscle has been progressively modified to the notion that glucose uptake is induced by muscle contraction via components of the insulin pathway. Glucose 134-141 insulin Homo sapiens 204-211 18401805-7 2008 With further consideration, increased glucose uptake and enhanced insulin sensitivity observed during/after exercise might be explained by a metabolic- and calcium-dependent activation of several intermediate molecules of the insulin cascade. Glucose 38-45 insulin Homo sapiens 226-233 18628523-8 2008 We further studied the genotype-phenotype correlation in 70 Han Chinese using iv glucose tolerance test and found an association between SNP rs13266634 and acute insulin response to glucose and disposition index (adjusted P = 0.012 and 0.004, respectively). Glucose 81-88 insulin Homo sapiens 162-169 18208559-4 2008 Glucose utilization and insulin signalling were impaired in all key insulin target tissues in Tg972 mice. Glucose 0-7 insulin Homo sapiens 68-75 18611975-11 2008 CONCLUSION/INTERPRETATION: Nocturnal variations of EGP and Rd explain the reduced incidence of hypoglycemia and lower fasting glucose levels reported for insulin glargine compared with human NPH insulin. Glucose 126-133 insulin Homo sapiens 154-161 18628523-8 2008 We further studied the genotype-phenotype correlation in 70 Han Chinese using iv glucose tolerance test and found an association between SNP rs13266634 and acute insulin response to glucose and disposition index (adjusted P = 0.012 and 0.004, respectively). Glucose 182-189 insulin Homo sapiens 162-169 18628529-7 2008 RESULTS: Insulin-mediated glucose uptake increased with both endurance training (55.7 +/- 11 to 63.0 +/- 11 micromol glucose/kg lean mass.min, P = 0.02) and strength training (49.0 +/- 12 to 57.8 +/- 18 micromol glucose/kg lean mass.min, P = 0.005), irrespective of training modality (P = 0.24). Glucose 26-33 insulin Homo sapiens 9-16 18802479-0 2008 CTLs are targeted to kill beta cells in patients with type 1 diabetes through recognition of a glucose-regulated preproinsulin epitope. Glucose 95-102 insulin Homo sapiens 113-126 18802479-7 2008 Critically, at high glucose concentration, beta cell presentation of preproinsulin signal epitope increased, as did CTL killing. Glucose 20-27 insulin Homo sapiens 69-82 18802485-5 2008 They also report that beta cells upregulate PPI expression in the presence of high glucose levels, rendering these cells more susceptible to lysis and potentially accelerating disease. Glucose 83-90 insulin Homo sapiens 44-47 18669612-2 2008 This hormone counteracts hypoglycaemia and opposes insulin actions by stimulating hepatic glucose synthesis and mobilization, thereby increasing blood glucose concentrations. Glucose 90-97 insulin Homo sapiens 51-58 18797414-9 2008 Our data suggest a mechanism by which correct insulin action may exert a beneficial protective role against inflammation, independent of its immediate glucose-lowering effect. Glucose 151-158 insulin Homo sapiens 46-53 18806119-4 2008 Moreover, glutamine administration seems to have a positive effect on glucose metabolism in the state of insulin resistance. Glucose 70-77 insulin Homo sapiens 105-112 18589448-6 2008 The rate of confirmed glucose values <70 mg/dL was higher in the patients receiving insulin glargine (P = .0298). Glucose 22-29 insulin Homo sapiens 87-94 18812026-2 2008 The present study has been carried out to evaluate the effects of BFOV on insulin-resistant glucose metabolism using dexamethasone-treated 3T3-L1 adipocytes as an in-vitro model of insulin resistance. Glucose 92-99 insulin Homo sapiens 74-81 18812026-3 2008 The results showed that BFOV, similar to vanadyl sulfate and rosiglitazone, caused a concentration-dependent increase in glucose consumption by insulin-resistant adipocytes. Glucose 121-128 insulin Homo sapiens 144-151 18812026-4 2008 Moreover, BFOV enhanced the action of insulin and completely prevented the development of insulin resistance induced by dexamethasone, leading to glucose consumption equal to that by normal cells. Glucose 146-153 insulin Homo sapiens 90-97 18803944-9 2008 This suggests that, in women with PCOS, increased glucose-stimulated DCI-IPG release is significantly correlated with improved insulin sensitivity. Glucose 50-57 insulin Homo sapiens 127-134 18321693-7 2008 OD and O subjects had similar degrees of adiposity (BMI, waist circumference, fat mass) and insulin resistance (insulin stimulated glucose disposal and M/I). Glucose 131-138 insulin Homo sapiens 112-119 18080299-6 2008 Switching of cells to high-glucose culture further increased immunostaining for proinsulin and insulin. Glucose 27-34 insulin Homo sapiens 80-90 18080299-6 2008 Switching of cells to high-glucose culture further increased immunostaining for proinsulin and insulin. Glucose 27-34 insulin Homo sapiens 83-90 18755896-2 2008 In pancreatic beta-cells, ERK1/2 are required for transcription of the insulin gene and several other genes in response to glucose. Glucose 123-130 insulin Homo sapiens 71-78 18755896-3 2008 We show that binding of glucose-sensitive transcription activators and repressors to the insulin gene promoter depends on ERK1/2 activity. Glucose 24-31 insulin Homo sapiens 89-96 18755896-4 2008 We also find that glucose and NGF stimulate the binding of ERK1/2 to the insulin gene and other promoters. Glucose 18-25 insulin Homo sapiens 73-80 18776996-2 2008 However, limited availability of islet tissue means that new sources of insulin-producing cells that are responsive to glucose are required. Glucose 119-126 insulin Homo sapiens 72-79 18821289-1 2008 INTRODUCTION: It was found that vitamin D may have a direct effect on adipocyte differentiation and metabolism and might be involved in the glucose regulation of insulin secretion, as suggested from the discovery of a nuclear localization of 1,25-(OH)(2)D(3) in pancreatic islets. Glucose 140-147 insulin Homo sapiens 162-169 18653476-1 2008 The pathways implicated in the control of epithelial Na(+) channel (ENaC)-dependent Na(+) transport in renal collecting duct cells share substantial parallels with those implicated in insulin-regulated glucose metabolism. Glucose 202-209 insulin Homo sapiens 184-191 18653476-8 2008 In contrast to insulin-stimulated glucose uptake in muscle cells, p110-beta inhibition did not enhance sensitivity to p110-alpha inhibition. Glucose 34-41 insulin Homo sapiens 15-22 19045501-4 2008 Global coupling and synchronization result from the inhibition exerted by insulin on the production of glucose, which serves as the substrate for metabolic oscillations. Glucose 103-110 insulin Homo sapiens 74-81 18331610-9 2008 The change in insulin-stimulated adiponectin level after pioglitazone treatment was positively correlated to the change in insulin-stimulated total glucose disposal (R = 0.69, P = 0.04). Glucose 148-155 insulin Homo sapiens 14-21 18331610-9 2008 The change in insulin-stimulated adiponectin level after pioglitazone treatment was positively correlated to the change in insulin-stimulated total glucose disposal (R = 0.69, P = 0.04). Glucose 148-155 insulin Homo sapiens 123-130 18208402-1 2008 IGFs (insulin-like growth factors), which in an unbound form induce glucose and amino acid uptake, circulate bound to IGFBPs (IGF-binding proteins), which modulate their bioavailability and activity. Glucose 68-75 insulin Homo sapiens 6-13 18801953-4 2008 The rapid-acting analogs can be administered at mealtimes and produce a rapid and short-lived insulin spike to address postprandial glucose elevations, while the long-acting analogs come close to the ideal of a smooth, relatively flat, 24-hour basal insulin supply, with less variability in action compared to NPH insulin. Glucose 132-139 insulin Homo sapiens 94-101 18801953-7 2008 Beyond HbA1c comparisons, however, insulin analogs have been shown in many instances to be associated with lower risks of hypoglycemia, lower levels of postprandial glucose excursions, better patient adherence, greater quality of life, and higher satisfaction with treatment. Glucose 165-172 insulin Homo sapiens 35-42 18687201-5 2008 Therefore, recommendations regarding practical aspects of tight glucose control by intensive insulin therapy cannot be supported by currently available data. Glucose 64-71 insulin Homo sapiens 93-100 18798718-11 2008 CONCLUSIONS: The intensive insulin protocol was effective in lowering blood glucose in neurosurgical ICU patients. Glucose 76-83 insulin Homo sapiens 27-34 18034844-1 2008 Insulin resistance (IR) is defined as a reduced responsiveness of peripheral tissues to the effects of the hormone, referring to abated ability of insulin in stimulating glucose uptake in peripheral tissues and in inhibiting hepatic glucose output. Glucose 170-177 insulin Homo sapiens 0-7 18034844-1 2008 Insulin resistance (IR) is defined as a reduced responsiveness of peripheral tissues to the effects of the hormone, referring to abated ability of insulin in stimulating glucose uptake in peripheral tissues and in inhibiting hepatic glucose output. Glucose 170-177 insulin Homo sapiens 147-154 18535193-12 2008 A multivariate analysis of variance showed that maternal obesity and offspring sex concurred together with BMI and beta-cell glucose sensitivity to determine the differences in insulin sensitivity and secretion observed in offspring. Glucose 125-132 insulin Homo sapiens 177-184 18568334-5 2008 In individuals with abnormal glucose regulation, the diabetogenic risk A allele of rs734312 was associated in an allele-dependent manner with a decrease in insulinogenic index (p = 0.025) and decreased 30-min serum insulin levels (p = 0.047) after an oral glucose load. Glucose 29-36 insulin Homo sapiens 156-163 18568334-5 2008 In individuals with abnormal glucose regulation, the diabetogenic risk A allele of rs734312 was associated in an allele-dependent manner with a decrease in insulinogenic index (p = 0.025) and decreased 30-min serum insulin levels (p = 0.047) after an oral glucose load. Glucose 256-263 insulin Homo sapiens 156-163 18568334-6 2008 In glucose-tolerant individuals the same allele was associated with increased fasting serum insulin concentration (p = 0.019) and homeostasis model assessment of insulin resistance (HOMA-IR; p = 0.026). Glucose 3-10 insulin Homo sapiens 92-99 18568334-6 2008 In glucose-tolerant individuals the same allele was associated with increased fasting serum insulin concentration (p = 0.019) and homeostasis model assessment of insulin resistance (HOMA-IR; p = 0.026). Glucose 3-10 insulin Homo sapiens 162-169 18606978-10 2008 TGs were significantly higher in small for gestational age (SGA) newborns compared with AGA or LGA newborns, while insulin-to-glucose ratio and FFAs were the highest in LGA newborns. Glucose 126-133 insulin Homo sapiens 115-122 18615853-4 2008 Insulin-related indexes were calculated from levels of fasting plasma insulin (FPI) and fasting plasma glucose (FPG). Glucose 103-110 insulin Homo sapiens 0-7 18618095-9 2008 CONCLUSIONS: Variants of CDKAL1 and IGF2BP2 attenuate the first phase of glucose-stimulated insulin secretion but show no effect on the second phase of insulin secretion. Glucose 73-80 insulin Homo sapiens 92-99 18672308-1 2008 Insulin therapy in type 2 diabetes (T2DM) can produce greater improvements in fasting plasma glucose (FPG) and glycated haemoglobin (HbA1c) than oral antidiabetic drugs (OADs). Glucose 93-100 insulin Homo sapiens 0-7 18832292-6 2008 RESULTS: Subjects receiving insulin via pump had better glucose control and were on lower insulin doses. Glucose 56-63 insulin Homo sapiens 28-35 18832292-7 2008 Subjects with adequate glucose control used a lower insulin dose, checked blood glucose levels more frequently, and had fathers with a higher education level. Glucose 23-30 insulin Homo sapiens 52-59 18951116-9 2008 However, past experience with CSII indicates that candidates for insulin pump therapy must be carefully selected and strongly motivated to improve their glucose control. Glucose 153-160 insulin Homo sapiens 65-72 18775353-1 2008 Insulin-mediated glucose disposal varies at least sixfold in apparently healthy individuals. Glucose 17-24 insulin Homo sapiens 0-7 17554246-7 2008 Insulin sensitivity by an oral glucose tolerance test (OGTT) was not affected by moderate alcohol consumption, but 2 h glucose concentrations were lower (P=0.01) after beer (4.5+/-0.1 mmol/l) than alcohol-free beer (4.9+/-0.1 mmol/l). Glucose 31-38 insulin Homo sapiens 0-7 18710354-2 2008 Thiazolidindiones are able to lower the levels of fasting glucose and glycated hemoglobin significantly by improving insulin sensitivity, as well as improving some aspects of diabetic dyslipidemia: total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol tend to increase while triglycerides are generally decreased. Glucose 58-65 insulin Homo sapiens 117-124 18783081-6 2008 However, the difficult implementation of nurse-driven protocols for insulin infusion, able to achieve more rapid and effective blood glucose control without significant episodes of hypoglycemia, has led physicians to consider alternative drugs for this purpose. Glucose 133-140 insulin Homo sapiens 68-75 18958772-1 2008 AIM: Vitamin D could have a direct effect on adipocyte differentiation and metabolism and might be involved in glucose regulation of insulin secretion. Glucose 111-118 insulin Homo sapiens 133-140 18778246-0 2008 Glucose regulation of insulin gene expression in pancreatic beta-cells. Glucose 0-7 insulin Homo sapiens 22-29 18778246-2 2008 This is achieved by tight regulation of insulin synthesis and exocytosis from the beta-cells in response to changes in blood glucose levels. Glucose 125-132 insulin Homo sapiens 40-47 18778246-3 2008 The synthesis of insulin is regulated by blood glucose levels at the transcriptional and post-transcriptional levels. Glucose 47-54 insulin Homo sapiens 17-24 18778246-5 2008 These three transcription factors activate insulin gene expression in a co-ordinated and synergistic manner in response to increasing glucose levels. Glucose 134-141 insulin Homo sapiens 43-50 18778246-9 2008 The present review summarizes the recent findings on how glucose modulates the function of the beta-cell transcription factors Pdx-1, NeuroD1 and MafA, and thereby tightly regulates insulin synthesis in accordance with blood glucose levels. Glucose 57-64 insulin Homo sapiens 182-189 18778246-9 2008 The present review summarizes the recent findings on how glucose modulates the function of the beta-cell transcription factors Pdx-1, NeuroD1 and MafA, and thereby tightly regulates insulin synthesis in accordance with blood glucose levels. Glucose 225-232 insulin Homo sapiens 182-189 18792871-11 2008 Chronically increased insulin secretion could counteract the initial beneficial effect of reduced glucose excursions. Glucose 98-105 insulin Homo sapiens 22-29 18725817-2 2008 The risk of insulin resistance and diabetes in HIV-infected patients receiving antiretroviral treatment stems from 2 sources: exposure to the same environmental factors that have led to an increased incidence of these conditions in the general population and the negative effects on glucose metabolism inherent to components of antiretroviral treatment regimens. Glucose 283-290 insulin Homo sapiens 12-19 18544618-5 2008 RESULTS: Reduced insulin-mediated glucose disposal (P < 0.05) was associated with a lower insulin-stimulated GS activity in PCOS patients (P < 0.05), compared with controls. Glucose 34-41 insulin Homo sapiens 17-24 18544618-5 2008 RESULTS: Reduced insulin-mediated glucose disposal (P < 0.05) was associated with a lower insulin-stimulated GS activity in PCOS patients (P < 0.05), compared with controls. Glucose 34-41 insulin Homo sapiens 93-100 18544618-9 2008 Pioglitazone treatment improved insulin-stimulated glucose metabolism and GS activity in PCOS (all P < 0.05) and restored the ability of insulin to dephosphorylate GS at sites 2 and 2a. Glucose 51-58 insulin Homo sapiens 32-39 18583466-1 2008 BACKGROUND: Free fatty acids (FFAs) acutely stimulate but chronically impair glucose-stimulated insulin secretion from beta-cells. Glucose 77-84 insulin Homo sapiens 96-103 18583466-7 2008 In these subjects, insulin secretion (insulinogenic index derived from oral glucose tolerance test) was significantly lower than in 692 Gly/Gly carriers (86.0 +/- 48.2 vs. 183.7 +/- 134.4, P < 0.005). Glucose 76-83 insulin Homo sapiens 19-26 19020393-3 2008 Multiple studies have shown that in tissues previously deprived of GH, short-term stimulation with GH is able to mimic the actions of insulin, including stimulation of amino-acid and glucose transport, and lipogenesis. Glucose 183-190 insulin Homo sapiens 134-141 18951382-1 2008 Influential trials and guidelines supporting the value of glucose control in hospital settings, particularly in the intensive care and postoperative settings, has led to the widespread adoption of intravenous infusions of human regular insulin. Glucose 58-65 insulin Homo sapiens 236-243 18753395-6 2008 In the absence of vagal activation, which occurs when glucose is administered intragastrically, postprandial glucose levels are higher and insulin levels blunted compared with when there is activation of oropharyngeal receptors by food. Glucose 54-61 insulin Homo sapiens 139-146 18282177-8 2008 This is influenced by the body"s inability to soak up excess glucose as a result of insulin resistance. Glucose 61-68 insulin Homo sapiens 84-91 18551127-2 2008 The aim of this study was to analyze the association of peripheral (insulin-mediated glucose disposal--M) and hepatic (suppression of endogenous glucose production--EGP) insulin action with abdominal (subcutaneous abdominal AT-SAAT intraabdominal AT-IAAT) and thigh AT depots in obese individuals. Glucose 85-92 insulin Homo sapiens 68-75 18551127-2 2008 The aim of this study was to analyze the association of peripheral (insulin-mediated glucose disposal--M) and hepatic (suppression of endogenous glucose production--EGP) insulin action with abdominal (subcutaneous abdominal AT-SAAT intraabdominal AT-IAAT) and thigh AT depots in obese individuals. Glucose 145-152 insulin Homo sapiens 170-177 18850475-11 2008 The study group showed a high rate of impairement in insulin secretion by first-phase insulin response to glucose overload, despite the low rate of insulin resistance. Glucose 106-113 insulin Homo sapiens 53-60 18850475-11 2008 The study group showed a high rate of impairement in insulin secretion by first-phase insulin response to glucose overload, despite the low rate of insulin resistance. Glucose 106-113 insulin Homo sapiens 86-93 18692137-4 2008 Insulin decreased fasting glucose and free fatty acid levels and insulin resistance, while increasing HDL-cholesterol, but had no effect in inflammatory markers. Glucose 26-33 insulin Homo sapiens 0-7 19099161-11 2008 The serum glucose values were also higher in MS patients (p = 0.006), thus demonstrating that insulin resistance has a role in MS physiopathology. Glucose 10-17 insulin Homo sapiens 94-101 18628529-7 2008 RESULTS: Insulin-mediated glucose uptake increased with both endurance training (55.7 +/- 11 to 63.0 +/- 11 micromol glucose/kg lean mass.min, P = 0.02) and strength training (49.0 +/- 12 to 57.8 +/- 18 micromol glucose/kg lean mass.min, P = 0.005), irrespective of training modality (P = 0.24). Glucose 117-124 insulin Homo sapiens 9-16 18628529-7 2008 RESULTS: Insulin-mediated glucose uptake increased with both endurance training (55.7 +/- 11 to 63.0 +/- 11 micromol glucose/kg lean mass.min, P = 0.02) and strength training (49.0 +/- 12 to 57.8 +/- 18 micromol glucose/kg lean mass.min, P = 0.005), irrespective of training modality (P = 0.24). Glucose 117-124 insulin Homo sapiens 9-16 18698425-6 2008 We have found that CAPN10 gene in our population is mainly associated with two indicators of the presence of insulin resistance: glucose levels two hours after a 75-g oral glucose tolerance test (OGTT) and HOMA values, although cholesterol levels and blood pressure values are also influenced by CAPN10 variants. Glucose 172-179 insulin Homo sapiens 109-116 18714373-6 2008 Insulin sensitivity was derived from fasting glucose and insulin concentrations, oral glucose tolerance test (OGTT), and hyperinsulinemic-euglycemic clamp. Glucose 45-52 insulin Homo sapiens 0-7 18714373-6 2008 Insulin sensitivity was derived from fasting glucose and insulin concentrations, oral glucose tolerance test (OGTT), and hyperinsulinemic-euglycemic clamp. Glucose 86-93 insulin Homo sapiens 0-7 18636958-3 2008 METHODS: Endothelium-dependent vasodilation, insulin-mediated vasodilation, and whole-body and leg glucose uptake during use of a 1-h euglycemic hyperinsulinemic clamp (insulin infusion, 40 mU/m(2)/min) were measured in healthy men before and after 4 weeks of treatment with placebo (12 men), with 400 mg atazanavir per day (9 men), or with 400 mg lopinavir and 100 mg ritonavir twice per day (9 men). Glucose 99-106 insulin Homo sapiens 150-157 18636958-6 2008 The response to the endothelium-independent vasodilator nitroprusside was not different at week 4 for any group, nor was insulin-mediated vasodilation or leg or whole-body insulin-mediated glucose uptake (all within-group P values were 1.1). Glucose 189-196 insulin Homo sapiens 172-179 18591189-5 2008 Moreover, FeTPPS restored insulin-stimulated Akt phosphorylation and insulin-stimulated glucose uptake in isolated skeletal muscle in vitro. Glucose 88-95 insulin Homo sapiens 69-76 18591189-6 2008 Stimulation of peroxynitrite catalysis attenuates HFD-induced insulin resistance in mice by restoring insulin signalling and insulin-stimulated glucose uptake in skeletal muscle tissue. Glucose 144-151 insulin Homo sapiens 62-69 18698425-6 2008 We have found that CAPN10 gene in our population is mainly associated with two indicators of the presence of insulin resistance: glucose levels two hours after a 75-g oral glucose tolerance test (OGTT) and HOMA values, although cholesterol levels and blood pressure values are also influenced by CAPN10 variants. Glucose 129-136 insulin Homo sapiens 109-116 18695074-5 2008 Insulin sensitivity was estimated from oral glucose tolerance test results. Glucose 44-51 insulin Homo sapiens 0-7 18673579-1 2008 BACKGROUND: Insulin, the principal regulating hormone of blood glucose, is released through the bursting of the pancreatic islets. Glucose 63-70 insulin Homo sapiens 12-19 18641723-5 2008 For measurements of insulin-stimulated glucose disposal (M), insulin was infused at a constant rate of 240 pmol.m(-2).min(-1), and M was calculated between the 90th and 120th min of the hyperinsulinemic-euglycemic clamp. Glucose 39-46 insulin Homo sapiens 20-27 18492770-1 2008 To assess the relationship between the fasting plasma glucose (FPG) concentration and insulin secretion in normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) subjects, 531 nondiabetic subjects with NGT (n = 293) and IGT (n = 238; 310 Japanese and 232 Mexican Americans) received an oral glucose tolerance test (OGTT) with measurement of plasma glucose, insulin, and C-peptide every 30 min. Glucose 54-61 insulin Homo sapiens 86-93 18492770-3 2008 Insulin sensitivity (Matsuda index) was measured from plasma insulin and glucose concentrations. Glucose 73-80 insulin Homo sapiens 0-7 18690898-3 2008 It is important to realize that there are discrepancies between blood and interstitial glucose concentration, which (1) may impact the quality of the system calibration and thereby the accuracy of the data, (2) may jeopardize the specificity and the sensitivity of hypoglycaemic alarms based on these systems and (3) must be considered in the design of closed-loop insulin delivery systems. Glucose 87-94 insulin Homo sapiens 365-372 18678809-6 2008 MAIN OUTCOME MEASURES: Insulin resistance at baseline was calculated from fasting insulin and glucose levels (ie, homeostatic model assessment [HOMA]) and change in BMI z score from baseline to 12-week follow-up. Glucose 94-101 insulin Homo sapiens 23-30 18585970-5 2008 Likewise, eradication of hepatitis C virus in patients with insulin resistance or diabetes mellitus appears to improve glucose metabolism. Glucose 119-126 insulin Homo sapiens 60-67 18690906-4 2008 Current insulin titration is based upon discrete glucose measurements, which may miss fast changes in glycemia and which does not give a full picture of overall glycemic control. Glucose 49-56 insulin Homo sapiens 8-15 18690906-5 2008 Recent evidence suggests that continuous monitoring of glucose levels may help to signal glycemic excursions and eventually to optimize insulin titration in the ICU. Glucose 55-62 insulin Homo sapiens 136-143 18443205-7 2008 RESULTS: Insulin increased glucose uptake 1.7-fold (P < 0.05) and glucose incorporation into glycogen 3.8-fold (P < 0.05) in myotubes from nondiabetic subjects. Glucose 27-34 insulin Homo sapiens 9-16 18443205-8 2008 TNF-alpha exposure fully impaired insulin-mediated glucose uptake and metabolism. Glucose 51-58 insulin Homo sapiens 34-41 18443205-9 2008 IKKbeta siRNA protected against TNF-alpha-induced impairments in glucose metabolism, since insulin-induced increases in glucose uptake (1.5-fold; P < 0.05) and glycogen synthesis (3.5-fold; P < 0.05) were restored. Glucose 65-72 insulin Homo sapiens 91-98 18690909-1 2008 Improvements in accuracy of real-time continuous glucose monitoring facilitate the development of closed-loop systems consisting of a continuous glucose monitor, a control algorithm, and an insulin pump. Glucose 49-56 insulin Homo sapiens 190-197 18509205-4 2008 RESULTS: Insulin sensitivity was directly related to GFR (multivariable-adjusted regression coefficient for 1-unit higher M/I 1.19 [95% CI 0.69-1.68]; P < 0.001) after adjusting for age, glucometabolic variables (fasting plasma glucose, fasting plasma insulin, and 2-h glucose after an oral glucose tolerance test), cardiovascular risk factors (hypertension, dyslipidemia, and smoking), and lifestyle factors (BMI, physical activity, and consumption of tea, coffee, and alcohol). Glucose 231-238 insulin Homo sapiens 9-16 18493738-0 2008 Human C-peptide antagonises high glucose-induced endothelial dysfunction through the nuclear factor-kappaB pathway. Glucose 33-40 insulin Homo sapiens 6-15 18493738-9 2008 RESULTS: Physiological concentrations of C-peptide affect high glucose-induced endothelial dysfunction by: (1) decreasing VCAM-1 expression and U-937 cell adherence to HAEC; (2) reducing secretion of IL-8 and MCP-1; and (3) suppressing NF-kappaB activation. Glucose 63-70 insulin Homo sapiens 41-50 18509205-4 2008 RESULTS: Insulin sensitivity was directly related to GFR (multivariable-adjusted regression coefficient for 1-unit higher M/I 1.19 [95% CI 0.69-1.68]; P < 0.001) after adjusting for age, glucometabolic variables (fasting plasma glucose, fasting plasma insulin, and 2-h glucose after an oral glucose tolerance test), cardiovascular risk factors (hypertension, dyslipidemia, and smoking), and lifestyle factors (BMI, physical activity, and consumption of tea, coffee, and alcohol). Glucose 272-279 insulin Homo sapiens 9-16 18509205-4 2008 RESULTS: Insulin sensitivity was directly related to GFR (multivariable-adjusted regression coefficient for 1-unit higher M/I 1.19 [95% CI 0.69-1.68]; P < 0.001) after adjusting for age, glucometabolic variables (fasting plasma glucose, fasting plasma insulin, and 2-h glucose after an oral glucose tolerance test), cardiovascular risk factors (hypertension, dyslipidemia, and smoking), and lifestyle factors (BMI, physical activity, and consumption of tea, coffee, and alcohol). Glucose 272-279 insulin Homo sapiens 9-16 18509205-5 2008 The positive multivariable-adjusted association between insulin sensitivity and GFR also remained statistically significant in participants with normal fasting plasma glucose, normal glucose tolerance, and normal GFR (n = 443; P < 0.02). Glucose 167-174 insulin Homo sapiens 56-63 18509205-5 2008 The positive multivariable-adjusted association between insulin sensitivity and GFR also remained statistically significant in participants with normal fasting plasma glucose, normal glucose tolerance, and normal GFR (n = 443; P < 0.02). Glucose 183-190 insulin Homo sapiens 56-63 18551117-4 2008 To this end, 110 nonobese subjects and 87 obese subjects were stratified into quartile based on their insulin-stimulated glucose disposal (M(FFM)). Glucose 121-128 insulin Homo sapiens 102-109 24692813-2 2008 Accordingly, insulin resistance is a possible target for lowering plasma glucose concentration and preventing diabetic macroangiopathy. Glucose 73-80 insulin Homo sapiens 13-20 18979203-0 2008 Insulin sensitivity and first-phase insulin secretion in obese Chinese with hyperglycemia in 30 and/or 60 min during glucose tolerance tests. Glucose 117-124 insulin Homo sapiens 0-7 18979203-1 2008 The purpose of this study was to investigate insulin sensitivity and first-phase insulin secretion in obesity with hyperglycemia in 30 and/or 60 min during oral glucose tolerance (OGTT, glucose > or = 11.1 mmol/l, post-loading hyperglycemia, PLH) in Chinese population. Glucose 161-168 insulin Homo sapiens 45-52 18979203-1 2008 The purpose of this study was to investigate insulin sensitivity and first-phase insulin secretion in obesity with hyperglycemia in 30 and/or 60 min during oral glucose tolerance (OGTT, glucose > or = 11.1 mmol/l, post-loading hyperglycemia, PLH) in Chinese population. Glucose 186-193 insulin Homo sapiens 45-52 18493882-4 2008 Insulin was titrated to target fasting blood glucose levels 80-130 mg/dl at 06:00-07:00. Glucose 45-52 insulin Homo sapiens 0-7 18574072-4 2008 Vasodilation was measured by venous occlusion plethysmography after intra-arterial infusions of sodium nitroprusside and acetylcholine and insulin sensitivity by the intravenous glucose tolerance test using the minimal model technique. Glucose 178-185 insulin Homo sapiens 139-146 18705822-3 2008 Given the inevitable progression of beta-cell dysfunction, along with the relatively limited glucose-lowering capacity of other agents, many patients will eventually require insulin for optimal glycaemic management. Glucose 93-100 insulin Homo sapiens 174-181 18695473-1 2008 BACKGROUND: Strict glucose control with insulin is associated with decreased mortality in a mixed patient population in the intensive care unit. Glucose 19-26 insulin Homo sapiens 40-47 18640382-10 2008 Maximal insulin-stimulated glucose disposal was not different between the groups on either day, nor was endogenous glucose production. Glucose 27-34 insulin Homo sapiens 8-15 18496818-0 2008 Epigallocatechin gallate (EGCG) attenuates high glucose-induced insulin signaling blockade in human hepG2 hepatoma cells. Glucose 48-55 insulin Homo sapiens 64-71 18496818-3 2008 In the present study, the investigations of EGCG on insulin signaling are performed in insulin-responsive human HepG2 cells cotreated with high glucose. Glucose 144-151 insulin Homo sapiens 52-59 18496818-4 2008 We found that the high glucose condition causes significant increasing Ser307 phosphorylation of insulin receptor substrate-1 (IRS-1), leading to reduce insulin-stimulated phosphorylation of Akt. Glucose 23-30 insulin Homo sapiens 97-104 18496818-5 2008 As the results, the insulin metabolic effects of glycogen synthesis and glucose uptake are inhibited by high glucose. Glucose 72-79 insulin Homo sapiens 20-27 18496818-5 2008 As the results, the insulin metabolic effects of glycogen synthesis and glucose uptake are inhibited by high glucose. Glucose 109-116 insulin Homo sapiens 20-27 18670420-4 2008 Therefore, insulin sensitivity indices based on the oral glucose-tolerance test (OGTT) have been introduced. Glucose 57-64 insulin Homo sapiens 11-18 18670420-11 2008 More important, imposed alterations in beta-cell sensitivity and glucose absorption without simulated changes in insulin sensitivity did change insulin sensitivity indices. Glucose 65-72 insulin Homo sapiens 144-151 18551117-5 2008 Insulin secretion was estimated by acute insulin response (AIR) during an intravenous glucose-tolerance test (IVGTT), and the disposition index was calculated as AIR x M(FFM). Glucose 86-93 insulin Homo sapiens 0-7 18676549-5 2008 RESULTS: Insulin sensitivity expressed as Mi value (glucose disposal mg/kg/min (insulin levels pmol/l) x 100) was lower in infants in the POPS-AGA (18.2) and POPS-SGA (15.2) groups than in the CON group (24.7). Glucose 52-59 insulin Homo sapiens 9-16 18524416-1 2008 Visfatin is a novel-secreted 52kDa adipokine that appears to mimic the action of insulin, inducing glucose transport into mammalian cells. Glucose 99-106 insulin Homo sapiens 81-88 18524416-14 2008 At a concentration of 2nM, visfatin and insulin produced nearly identical increases in glucose transport. Glucose 87-94 insulin Homo sapiens 40-47 18676549-5 2008 RESULTS: Insulin sensitivity expressed as Mi value (glucose disposal mg/kg/min (insulin levels pmol/l) x 100) was lower in infants in the POPS-AGA (18.2) and POPS-SGA (15.2) groups than in the CON group (24.7). Glucose 52-59 insulin Homo sapiens 80-87 18677693-7 2008 The situation of frail elderly with diabetes sometimes can be improved by starting an insulin therapy because of its anabolic effects beyond the action of normalizing blood glucose. Glucose 173-180 insulin Homo sapiens 86-93 18646147-18 2008 AUTHORS" CONCLUSIONS: Long acting insulin preparations seem to exert a beneficial effect on nocturnal glucose levels. Glucose 102-109 insulin Homo sapiens 34-41 18795630-12 2008 As assessed by the IVGTT, acute insulin response of glucose (AIRg) tended to increase after the HFD administration (P = 0.06). Glucose 52-59 insulin Homo sapiens 32-39 18652694-1 2008 BACKGROUND: Animal and cell culture data suggest a critical role for Munc18c and Syntaxin 4 proteins in insulin mediated glucose transport in skeletal muscle, but no studies have been published in humans. Glucose 121-128 insulin Homo sapiens 104-111 18468514-3 2008 In the present study, we performed a detailed analysis of the molecular events of the insulin-independent glucose response of the liver-type pyruvate kinase (L-PK) gene. Glucose 106-113 insulin Homo sapiens 86-93 18570632-1 2008 Glucose entry into muscle cells is precisely regulated by insulin, through recruitment of GLUT4 (glucose transporter-4) to the membrane of muscle and fat cells. Glucose 0-7 insulin Homo sapiens 58-65 18772618-2 2008 Insulin is indispensable for serum glucose control and diabetes patients are on the relative or absolute deficient state of insulin. Glucose 35-42 insulin Homo sapiens 0-7 18772618-7 2008 In the presence of 1 nM concentration of insulin, the neuronal cell death curve showed the U-shape, and the minimum death point was 3-5mM glucose concentrations at the CA1. Glucose 138-145 insulin Homo sapiens 41-48 18772618-10 2008 We concluded that insulin has a double-edged effect on the neuronal cell death dependent on glucose concentration, and that the CA1 and the DG have a different sensitivity to insulin in terms of cell survival. Glucose 92-99 insulin Homo sapiens 18-25 18390897-2 2008 Indeed, insulin promotes glucose uptake and its utilization via glycolysis. Glucose 25-32 insulin Homo sapiens 8-15 20641767-0 2004 (67)Ga labeled cyclic diethylenetriamine pentaacetic acid Insulin Although the main role of insulin is considered to be the regulation of glucose transport and metabolism, insulin is known to influence directly or indirectly a variety of other metabolic processes in the cell such as protein synthesis, DNA transcription, and RNA translation in that insulin receptors are found in almost all cell types (1). Glucose 138-145 insulin Homo sapiens 92-99 18572033-2 2008 Consequently, measurements were made of the WC, BMI, blood pressure, glucose, and lipid components of metabolic syndrome (MS) and insulin-mediated glucose uptake. Glucose 147-154 insulin Homo sapiens 130-137 18492767-1 2008 The insulin-responsive glucose transporter 4 (GLUT4) plays a key role in glucose uptake and metabolism in insulin target tissues. Glucose 23-30 insulin Homo sapiens 4-11 18492767-1 2008 The insulin-responsive glucose transporter 4 (GLUT4) plays a key role in glucose uptake and metabolism in insulin target tissues. Glucose 23-30 insulin Homo sapiens 106-113 18492771-5 2008 Importantly, NCX 4016 further increased glucose transport induced by a physiological concentration of insulin. Glucose 40-47 insulin Homo sapiens 102-109 18714620-7 2008 However mean blood glucose level was found to be lower (6.56+/-0.82 mmol/l vs. 7.85+/-1.6 mmol/l, P=0.00055) in the subcutaneous insulin group. Glucose 19-26 insulin Homo sapiens 129-136 18495085-2 2008 However, the effects of TSA on insulin stimulated glucose utilization and insulin signaling transduction are still poorly understood. Glucose 50-57 insulin Homo sapiens 31-38 18495085-3 2008 Here we showed that TSA significantly enhanced insulin stimulated glucose uptake, glycogen synthesis and glycogen synthase activities in C2C12 myotubes. Glucose 66-73 insulin Homo sapiens 47-54 18191448-2 2008 Dysfunction of the organelle leads to impaired glucose-stimulated insulin secretion, as exemplified by the rare disease mitochondrial diabetes, which is caused by mutations in the mitochondrial DNA. Glucose 47-54 insulin Homo sapiens 66-73 18191448-8 2008 We hypothesize that the improvement of glucose-stimulated insulin secretion by sulfonylurea compounds in type 2 diabetic patients is in part due to their capacity to raise mitochondrial calcium, which is beneficial for the generation of metabolic coupling factors. Glucose 39-46 insulin Homo sapiens 58-65 18411240-4 2008 Deterioration of glucose tolerance between tests was associated with decreased insulin sensitivity, while insulin secretion remained stable. Glucose 17-24 insulin Homo sapiens 79-86 18411240-6 2008 However, the development of insulin resistance may have an important role in the deterioration of the glucose tolerance and in the long-term evolution of the disorder. Glucose 102-109 insulin Homo sapiens 28-35 18417751-3 2008 The aim of the present investigation was to assess whether glucose-stimulated insulin response is higher in AA versus AW adolescents who have comparable in vivo insulin sensitivity. Glucose 59-66 insulin Homo sapiens 78-85 18417751-5 2008 Insulin secretion relative to insulin sensitivity was calculated as the glucose disposition index. Glucose 72-79 insulin Homo sapiens 0-7 18417751-5 2008 Insulin secretion relative to insulin sensitivity was calculated as the glucose disposition index. Glucose 72-79 insulin Homo sapiens 30-37 18483800-5 2008 The effects on glucose uptake were additive to those of insulin. Glucose 15-22 insulin Homo sapiens 56-63 18577153-1 2008 Type 2 diabetes mellitus (T2DM) is a progressive disease characterized by both insulin resistance and beta-cell failure, resulting in a decline in insulin secretion and increased blood glucose levels. Glucose 185-192 insulin Homo sapiens 79-86 18577159-1 2008 In the early treatment of type 2 diabetes mellitus (T2DM), the addition of a basal insulin, such as insulin glargine, to existing oral therapy can help patients attain recommended glycaemic control targets, including haemoglobin A(1c) (HbA(1c)) <7% and fasting blood glucose <5.5 mmol/l (<100 mg/dl). Glucose 270-277 insulin Homo sapiens 83-90 18577159-2 2008 For patients close to but not at target, the management of postprandial glucose excursions with a rapid-acting insulin, such as insulin glulisine, can provide further improvements in glycaemic control. Glucose 72-79 insulin Homo sapiens 111-118 18490836-2 2008 However, it has been reported that insulinomas with normal levels of plasma insulin and a normal insulin to glucose ratio occur in patients with hypoglycemia. Glucose 108-115 insulin Homo sapiens 35-42 18603639-1 2008 For many patients with type 2 diabetes mellitus, metformin plus appropriate treatment for cardiovascular risk factors form the cornerstone of drug therapy.1 However, the progressive impairment of both the secretion and action of insulin in the condition mean that high blood glucose concentrations usually worsen over time, so necessitating escalation of hypoglycaemic therapy. Glucose 275-282 insulin Homo sapiens 229-236 18463890-0 2008 Interstitial glucose concentration in insulin-resistant human skeletal muscle: influence of one bout of exercise and of local perfusion with insulin or vanadate. Glucose 13-20 insulin Homo sapiens 38-45 18463890-8 2008 Microdialysis perfusion with insulin (14 mU/ml) or sodium metavanadate (100 mM) decreased the interstitial glucose concentration (P = 0.001) in both the exercised and rested leg. Glucose 107-114 insulin Homo sapiens 29-36 18463890-10 2008 This study shows that the interstitial glucose concentration in insulin-resistant skeletal muscle is markedly decreased for several hours following a single exercise session. Glucose 39-46 insulin Homo sapiens 64-71 18463890-12 2008 This change is accompanied by an increased insulin effect on the interstitial glucose concentration. Glucose 78-85 insulin Homo sapiens 43-50 19343122-0 2008 Effects of intermittent and long-term glucose-insulin-potassium infusion in patients with systolic heart failure. Glucose 38-45 insulin Homo sapiens 46-53 18437687-2 2008 Beta cell death and/or dysfunction result in an insufficient amount of insulin that leads to high glucose levels in the blood, a metabolic disorder known as Diabetes mellitus. Glucose 98-105 insulin Homo sapiens 71-78 18397976-6 2008 RESULTS: Insulin-mediated peripheral glucose uptake was significantly lower after 62-h fasting compared with 14-h fasting. Glucose 37-44 insulin Homo sapiens 9-16 18397976-10 2008 CONCLUSIONS: Fasting for 62 h decreases insulin-mediated peripheral glucose uptake with lower phosphorylation of AKT at serine(473). Glucose 68-75 insulin Homo sapiens 40-47 18397982-5 2008 MAIN OUTCOME MEASURES: Insulin response and insulin sensitivity were assessed by oral glucose tolerance test and euglycemic hyperinsulinemic clamp. Glucose 86-93 insulin Homo sapiens 23-30 18460559-1 2008 CONTEXT: Impairment of insulin-mediated capillary recruitment in skeletal muscle contributes to a hampered glucose uptake in obesity. Glucose 107-114 insulin Homo sapiens 23-30 18460571-5 2008 RESULTS: Insulin sensitivity improved after rosiglitazone (glucose infusion rate: 19.9 +/- 2.8 to 24.8 +/- 2.1 micromol/kg.min; P < 0.05). Glucose 59-66 insulin Homo sapiens 9-16 19885229-0 2008 Predicted blood glucose from insulin administration based on values from miscoded glucose meters. Glucose 16-23 insulin Homo sapiens 29-36 19885229-5 2008 It attempts to relate potential insulin dose errors to possible adverse blood glucose outcomes when glucose meters are miscoded. Glucose 78-85 insulin Homo sapiens 32-39 19885229-11 2008 RESULTS: Using insulin sensitivity data, it was determined that, given an actual blood glucose of 150-400 mg/dl, an error greater than +40 mg/dl would be required to calculate an insulin dose sufficient to produce a blood glucose of less than 70 mg/dl. Glucose 87-94 insulin Homo sapiens 15-22 19885229-11 2008 RESULTS: Using insulin sensitivity data, it was determined that, given an actual blood glucose of 150-400 mg/dl, an error greater than +40 mg/dl would be required to calculate an insulin dose sufficient to produce a blood glucose of less than 70 mg/dl. Glucose 87-94 insulin Homo sapiens 179-186 18545202-7 2008 Insulin sensitivity was calculated by dividing the glucose infusion rate by the average insulin infusion. Glucose 51-58 insulin Homo sapiens 0-7 18434594-1 2008 Phosphatidylinositol 3-phosphate (PI(3)P) plays an important role in insulin-stimulated glucose uptake. Glucose 88-95 insulin Homo sapiens 69-76 18434594-7 2008 Concomitant with its effect on PI(3)P levels, the knockdown of GAPEX-5 blocks insulin-stimulated Glut4 translocation and glucose uptake. Glucose 121-128 insulin Homo sapiens 78-85 18555828-5 2008 In 206 subjects, an insulin sensitivity index (S(I)) was obtained with a frequently sampled intravenous glucose tolerance test pre- and post-ET. Glucose 104-111 insulin Homo sapiens 20-27 18555850-12 2008 The major findings were that consumption of isoflavone-containing soy protein dose-dependently increased insulin responses to the glucose challenge and decreased plasma adiponectin, whereas isoflavone-depleted soy protein decreased body weight and had no effect on plasma adiponectin concentrations. Glucose 130-137 insulin Homo sapiens 105-112 18555852-6 2008 Finally, we demonstrate that resveratrol inhibits insulin-dependent changes in glucose uptake and glycogen levels and decreases insulin receptor substrate 1 and glucose transporter 4 protein levels, indicating that resveratrol represses insulin sensitivity in adipocytes. Glucose 79-86 insulin Homo sapiens 50-57 18636668-4 2008 RESULTS: Compared with the control group, the fasting blood glucose levels in the lavage and coloclysis groups were decreased significantly in 4 d (5.63 +/- 0.48 mmol/L and 5.07 +/- 0.37 mmol/L vs 22.12 +/- 1.31 mmol/L, respectively, P < 0.01), while the plasma insulin levels were much higher (32.26 +/- 1.81 microIU/mL and 32.79 +/- 1.84 microIU/mL vs 14.23 +/- 1.38 microIU/mL, respectively, P < 0.01). Glucose 60-67 insulin Homo sapiens 265-272 18636232-14 2008 CONCLUSION: Metformin plus insulin appears to lower the incidence of insulin resistance, lower insulin requirement while maintaining blood glucose level control, and consequently lower the incidence of adverse effects related to high-dose insulin therapy, particularly hypoglycaemia, and also declined nursing workload. Glucose 139-146 insulin Homo sapiens 27-34 18614723-8 2008 The insulin sensitivity index was calculated from the glucose and insulin data. Glucose 54-61 insulin Homo sapiens 4-11 18614743-6 2008 Insulin sensitivity was measured by fasting and 2-h post-oral-glucose-tolerance test (OGTT) insulin, the homeostasis model assessment of insulin resistance (HOMA-IR), and the insulin sensitivity index (ISI(0,120)). Glucose 62-69 insulin Homo sapiens 0-7 18580184-2 2008 The altered glucose homeostasis is caused by faulty signal transduction via the insulin signaling proteins, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. Glucose 12-19 insulin Homo sapiens 80-87 18580184-2 2008 The altered glucose homeostasis is caused by faulty signal transduction via the insulin signaling proteins, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. Glucose 135-142 insulin Homo sapiens 80-87 18635467-2 2008 In this study, we evaluated the safety and efficacy of a nurse-driven insulin protocol (the Aalst Glycemia Insulin Protocol) for achieving a target glucose level of 80-110 mg/dL during cardiac surgery and in the intensive care unit (ICU). Glucose 148-155 insulin Homo sapiens 70-77 18635467-5 2008 The algorithm adjusts insulin dosage based on blood glucose level and the projected insulin sensitivity (e.g., reduced sensitivity during cardiopulmonary bypass and normalizing sensitivity after surgery). Glucose 52-59 insulin Homo sapiens 22-29 18645345-7 2008 Baseline glycosylated hemoglobin was measured and homeostasis model assessment for insulin resistance was calculated from insulin and glucose levels. Glucose 134-141 insulin Homo sapiens 83-90 18629684-3 2008 The activation of proinflammatory pathways after exposure to TNF-alpha induces a state of insulin resistance in terms of glucose uptake in myocytes and adipocytes that impair insulin signalling at the level of the insulin receptor substrate (IRS) proteins. Glucose 121-128 insulin Homo sapiens 90-97 18433713-3 2008 Mitochondria play a central role in GSIS by coupling glucose oxidation to production of ATP, a signal that triggers a series of events that ultimately leads to insulin release. Glucose 53-60 insulin Homo sapiens 160-167 18495085-0 2008 Trichostatin A improves insulin stimulated glucose utilization and insulin signaling transduction through the repression of HDAC2. Glucose 43-50 insulin Homo sapiens 24-31 18542013-4 2008 An increased, similar or reduced insulin sensitivity has been reported in women than in men, which makes it unclear to what extent a disturbed insulin-mediated glucose disposal may contribute to increased postprandial glucose concentrations in women. Glucose 160-167 insulin Homo sapiens 143-150 18364392-12 2008 CONCLUSIONS: Weekly basal-bolus insulin adjustments based on premeal and bedtime glucose patterns resulted in significant reductions in A1C. Glucose 81-88 insulin Homo sapiens 32-39 18426862-6 2008 RESULTS: The Q allele of K121Q (rs1044498) was associated with increased fasting plasma glucose (FPG), A1C, fasting insulin, and insulin resistance by homeostasis model assessment (HOMA-IR; all P = 0.01-0.006). Glucose 88-95 insulin Homo sapiens 129-136 18458871-6 2008 RESULTS: Glucose infusion rates increased in response to insulin infusion, and significant differences were present between groups (T2D<IGT<CON<TR). Glucose 9-16 insulin Homo sapiens 57-64 18577159-2 2008 For patients close to but not at target, the management of postprandial glucose excursions with a rapid-acting insulin, such as insulin glulisine, can provide further improvements in glycaemic control. Glucose 72-79 insulin Homo sapiens 128-135 18577159-6 2008 A second and third dose of prandial insulin can then be added if HbA(1c) remains above target and to manage postprandial glucose excursions at other meals. Glucose 121-128 insulin Homo sapiens 36-43 18594063-3 2008 RESEARCH DESIGN AND METHODS: Insulin sensitivity was quantified by determining the steady-state plasma glucose (SSPG) concentration during an insulin suppression test in 446 individuals. Glucose 103-110 insulin Homo sapiens 29-36 18594063-4 2008 The integrated insulin response was calculated after a 75-g oral glucose challenge. Glucose 65-72 insulin Homo sapiens 15-22 18753097-9 2008 CONCLUSION: We are the first to report improvements in glucose control over an extended period with use of both hospital-wide intravenous and subcutaneous insulin protocols in an academic hospital setting. Glucose 55-62 insulin Homo sapiens 155-162 18753109-10 2008 In clinical trials, they have been shown to improve glycemic control by increasing glucose-stimulated insulin secretion and suppressing glucagon secretion. Glucose 83-90 insulin Homo sapiens 102-109 18777500-12 2008 IR was assessed by HOMA in all non-diabetic subjects and in subjects participating in study 1 also by Insulin Resistance Index (IRI), which takes into account glucose and insulin levels during OGTT. Glucose 159-166 insulin Homo sapiens 102-109 18777500-13 2008 RESULTS: Glucose administration resulted in significant increases in insulin and glucose (p < 0.0001). Glucose 9-16 insulin Homo sapiens 69-76 18474251-5 2008 Liver fat was determined by (1)H-MRS, body composition by magnetic resonance imaging, and insulin clearance and action on hepatic glucose production (HGP), glucose uptake, and serum FFA by the euglycemic insulin clamp technique (insulin 0.3 mU/kg x min) combined with infusion of [3-(3)H]glucose. Glucose 130-137 insulin Homo sapiens 90-97 18645711-0 2008 Abnormal response of insulin to glucose loading and assessment of insulin resistance in non-obese patients with polycystic ovary syndrome. Glucose 32-39 insulin Homo sapiens 21-28 18645711-1 2008 OBJECTIVES: To investigate the insulin response to glucose loading and to determine which method is best in order to evaluate insulin resistance in women with polycystic ovary syndrome (PCOS). Glucose 51-58 insulin Homo sapiens 31-38 18645711-9 2008 CONCLUSION: In the PCOS group, the abnormal response of insulin to glucose loading was suggested. Glucose 67-74 insulin Homo sapiens 56-63 18537181-8 2008 Secondary end points were changes in body weight, liver enzymes, and insulin sensitivity indices on 2-hour oral glucose tolerance test. Glucose 112-119 insulin Homo sapiens 69-76 18430770-7 2008 Nonoxidative glucose metabolism was calculated in insulin-stimulated conditions by subtracting glucose oxidation from total glucose metabolism. Glucose 13-20 insulin Homo sapiens 50-57 18430770-7 2008 Nonoxidative glucose metabolism was calculated in insulin-stimulated conditions by subtracting glucose oxidation from total glucose metabolism. Glucose 95-102 insulin Homo sapiens 50-57 18430770-7 2008 Nonoxidative glucose metabolism was calculated in insulin-stimulated conditions by subtracting glucose oxidation from total glucose metabolism. Glucose 95-102 insulin Homo sapiens 50-57 18430774-0 2008 Hyperinsulinemia induces insulin resistance on glucose and lipid metabolism in a human adipocytic cell line: paracrine interaction with myocytes. Glucose 47-54 insulin Homo sapiens 5-12 18430774-5 2008 RESULTS: Adipocytes differentiated for 14 d gain insulin sensitivity on glucose uptake and inhibition of lipolysis, but prolonged cultures develop an insulin-resistant state characterized by an increase in phosphatase and tensin homolog-deleted on chromosome 10 expression and defects in insulin signaling at the insulin receptor substrate-1/AKT level. Glucose 72-79 insulin Homo sapiens 49-56 18430774-9 2008 Pharmacological treatment of adipocytes with a liver X receptor agonist reestablishes insulin-stimulated glucose uptake, whereas treatment with a peroxisome proliferator-activated receptor-gamma agonist restored the antilipolytic action of insulin. Glucose 105-112 insulin Homo sapiens 86-93 18430778-8 2008 The incretin effect was measured as the difference in insulin levels in response to oral and to an isoglycemic iv glucose load. Glucose 114-121 insulin Homo sapiens 54-61 18413197-6 2008 Insulin resistance (insulin drip rate/glucose ratio) was higher in DM during Hours 1-12 (0.029 vs. 0.022 U h(-1) mg(-1) dl(-1); P<.001), but not during Hours 12-24 (P=.57). Glucose 38-45 insulin Homo sapiens 0-7 19885233-0 2008 Use of continuous glucose monitoring to estimate insulin requirements in patients with type 1 diabetes mellitus during a short course of prednisone. Glucose 18-25 insulin Homo sapiens 49-56 19885233-9 2008 CONCLUSIONS: For adults with T1DM, insulin requirements during prednisone induced insulin resistance may need to be increased by 70% or more to normalize blood glucose levels. Glucose 160-167 insulin Homo sapiens 35-42 19885236-1 2008 BACKGROUND: This study was conducted to develop case-based decision support software to improve glucose control in patients with type 1 diabetes mellitus (T1DM) on insulin pump therapy. Glucose 96-103 insulin Homo sapiens 164-171 18580507-4 2008 Insulin therapy was instituted for ICU patients admitted after July 1, 2005 with glucose >140 mg/dL. Glucose 81-88 insulin Homo sapiens 0-7 18589336-7 2008 Insulin resistance was defined by the homeostasis model assessment and the level of insulin at 120 minutes after consuming oral glucose. Glucose 128-135 insulin Homo sapiens 0-7 18589336-7 2008 Insulin resistance was defined by the homeostasis model assessment and the level of insulin at 120 minutes after consuming oral glucose. Glucose 128-135 insulin Homo sapiens 84-91 18572033-4 2008 The results indicated that WC and BMI significantly correlated (p <0.001) and were associated with differences in insulin-mediated glucose uptake to a similar degree in men (r = 0.57 and r = 0.59) and women (r = 0.53 and r = 0.52). Glucose 134-141 insulin Homo sapiens 117-124 18406351-1 2008 Cell-based treatments for insulin-dependent diabetes (IDD) may provide more physiologic regulation of blood glucose levels than daily insulin injections, thereby reducing the occurrence of secondary complications associated with diabetes. Glucose 108-115 insulin Homo sapiens 26-33 18635989-8 2008 In contrast, the traditional approach to glucose management, sliding-scale insulin administration, does not provide adequate control. Glucose 41-48 insulin Homo sapiens 75-82 19356462-11 2008 Lower myocardial glucose utilization was independently predicted by female gender (p < 0.05), and it independently predicted lower myocardial glucose utilization/plasma insulin (p < 0.05). Glucose 17-24 insulin Homo sapiens 172-179 18551039-2 2008 As sulfonylurea stimulate insulin secretion by an increased influx of Ca, we hypothesized that this polymorphism is associated with the glucose-lowering effect and mortality risk in sulfonylurea users. Glucose 136-143 insulin Homo sapiens 26-33 18795211-6 2008 In the diagnostic 2-hour oral glucose tolerance test, glucose values were slightly, but significantly, higher in the insulin group than in the metformin group (p < 0.003). Glucose 30-37 insulin Homo sapiens 117-124 18795211-6 2008 In the diagnostic 2-hour oral glucose tolerance test, glucose values were slightly, but significantly, higher in the insulin group than in the metformin group (p < 0.003). Glucose 54-61 insulin Homo sapiens 117-124 19024537-0 2008 [Evaluating the feature of hypoglycemia detected by continuous glucose monitoring system during temporary continuous subcutaneous insulin infusion in type 2 diabetes patients]. Glucose 63-70 insulin Homo sapiens 130-137 19058615-5 2008 This study showed that alteration in the proportion of fibroblast mtDNA A3243G mutation content directly affected basal and insulin-stimulated glucose uptake. Glucose 143-150 insulin Homo sapiens 124-131 18461096-4 2008 Serum glucose and plasma insulin reached their peak concentrations (p < 0.01) 15 min after glucose ingestion and declined at the onset of exercise. Glucose 94-101 insulin Homo sapiens 25-32 18374950-1 2008 In this paper, we propose a new mathematical control system for a simplified regulatory system of blood glucose by taking into account the dynamics of glucose and glycogen in liver and the dynamics of insulin and glucagon receptors at the molecular level. Glucose 104-111 insulin Homo sapiens 201-208 18374950-5 2008 The formula shows that the insulin sensitivity depends on various parameters that determine the insulin influence on insulin-dependent glucose utilization and reflect the efficiency of binding of insulin to its receptors. Glucose 135-142 insulin Homo sapiens 27-34 18374950-5 2008 The formula shows that the insulin sensitivity depends on various parameters that determine the insulin influence on insulin-dependent glucose utilization and reflect the efficiency of binding of insulin to its receptors. Glucose 135-142 insulin Homo sapiens 96-103 18374950-5 2008 The formula shows that the insulin sensitivity depends on various parameters that determine the insulin influence on insulin-dependent glucose utilization and reflect the efficiency of binding of insulin to its receptors. Glucose 135-142 insulin Homo sapiens 96-103 18374950-5 2008 The formula shows that the insulin sensitivity depends on various parameters that determine the insulin influence on insulin-dependent glucose utilization and reflect the efficiency of binding of insulin to its receptors. Glucose 135-142 insulin Homo sapiens 96-103 18560589-6 2008 Treatment with pioglitazone improved insulin-stimulated glucose metabolism and plasma adiponectin, and reduced fasting serum insulin (all P<0.05). Glucose 56-63 insulin Homo sapiens 37-44 18440169-8 2008 RESULTS: BHT potentiated insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Glucose 44-51 insulin Homo sapiens 25-32 18514090-5 2008 Trials of long-acting insulin analogues have consistently shown efficacy in controlling fasting plasma glucose and glycosylated hemoglobin (HbA1c), as well as a markedly reduced risk of hypoglycemia compared with neutral protamine Hagedorn insulin. Glucose 103-110 insulin Homo sapiens 22-29 18496372-9 2008 Insulin-mediated glucose disposal, during euglycemic clamp, as a measure of insulin sensitivity, significantly worsened between days 4 and 17 in group 1 but improved in groups 2 and 3. Glucose 17-24 insulin Homo sapiens 0-7 18536739-2 2008 These vesicles move slowly to the cell surface, but their translocation is markedly enhanced by insulin, resulting in higher glucose uptake. Glucose 125-132 insulin Homo sapiens 96-103 18481943-1 2008 The control of glucose metabolism by pancreatic endocrine cells throughout life relies on a tight regulation of the mass of insulin-producing beta-cells. Glucose 15-22 insulin Homo sapiens 124-131 18481944-4 2008 Knockdown of IR mRNA by siRNAs (small interfering RNAs) decreased IR protein expression without affecting IGF-1 receptor levels, and blocked glucose stimulation of preproinsulin gene expression. Glucose 141-148 insulin Homo sapiens 164-177 18481944-6 2008 Studies using the mouse MIN6 beta-cell line indicated that glucose protected beta-cells from undergoing apoptosis and that this was a consequence, at least in part, of insulin release in response to elevated glucose. Glucose 208-215 insulin Homo sapiens 168-175 18321782-0 2008 Ca(2+) and insulin-mediated glucose uptake. Glucose 28-35 insulin Homo sapiens 11-18 18321782-1 2008 Insulin stimulates glucose uptake in striated muscle and fat via a complex cascade of signaling events. Glucose 19-26 insulin Homo sapiens 0-7 18496372-9 2008 Insulin-mediated glucose disposal, during euglycemic clamp, as a measure of insulin sensitivity, significantly worsened between days 4 and 17 in group 1 but improved in groups 2 and 3. Glucose 17-24 insulin Homo sapiens 76-83 18496372-10 2008 Group 1 required significantly more insulin to control blood glucose, resulting in higher insulinemia (approximately 70 mIU in group 1 vs. approximately 25 mIU in groups 2 and 3). Glucose 61-68 insulin Homo sapiens 36-43 18520641-13 2008 Compared with the simple guideline, eProtocol-insulin glucose measurements within target increased from 21% to 39%, and mean blood glucose decreased from 142 to 115 mg/dL (generalized linear model p < .001). Glucose 54-61 insulin Homo sapiens 46-53 18332157-1 2008 OBJECTIVE: Data investigating the possible disturbing influence of insulin in the vicinity of continuous glucose monitoring (CGM) is lacking. Glucose 105-112 insulin Homo sapiens 67-74 18339441-3 2008 This study examined observational data taken from a previously reported randomised controlled trial of insulin therapy for myocardial infarction (The Hyperglycaemia: Intensive Insulin Infusion In Infarction Study), to determine optimal glucose levels for this period. Glucose 236-243 insulin Homo sapiens 103-110 18390794-1 2008 OBJECTIVE: To characterize the voltage-gated ion channels in human beta-cells from nondiabetic donors and their role in glucose-stimulated insulin release. Glucose 120-127 insulin Homo sapiens 139-146 18321782-3 2008 Recent research implicates an important role of Ca(2+) in insulin-mediated glucose uptake. Glucose 75-82 insulin Homo sapiens 58-65 18321782-4 2008 Maneuvers that increase or decrease Ca(2+) influx also increase or decrease insulin-mediated glucose uptake both in normal and insulin-resistant cells. Glucose 93-100 insulin Homo sapiens 76-83 18321782-4 2008 Maneuvers that increase or decrease Ca(2+) influx also increase or decrease insulin-mediated glucose uptake both in normal and insulin-resistant cells. Glucose 93-100 insulin Homo sapiens 127-134 18423105-5 2008 The level of blood glucose was assessed by fasting plasma glucose (FPG), fasting immunoreactive insulin (F-IRI), homeostasis model assessment (HOMA) index, and hemoglobin A(1c) (HbA1c). Glucose 19-26 insulin Homo sapiens 96-110 18435781-1 2008 AIM: To examine the impact of inhaled human insulin (Exubera, EXU) on patient or physician willingness to adopt insulin after oral glucose-lowering agent failure. Glucose 131-138 insulin Homo sapiens 44-51 18437349-4 2008 Insulin secretion was evaluated as the insulin response to intravenous arginine (5 g) injected at fasting glucose and after raising glucose to 13 to 15 mmol/l or to >28 mmol/l. Glucose 106-113 insulin Homo sapiens 0-7 18437349-4 2008 Insulin secretion was evaluated as the insulin response to intravenous arginine (5 g) injected at fasting glucose and after raising glucose to 13 to 15 mmol/l or to >28 mmol/l. Glucose 106-113 insulin Homo sapiens 39-46 18390794-10 2008 Blockade of L-type channels abolished glucose-stimulated insulin release, while inhibition of T- and P/Q-type Ca(2+) channels reduced glucose-induced (6 mmol/l) secretion by 60-70%. Glucose 38-45 insulin Homo sapiens 57-64 18437349-4 2008 Insulin secretion was evaluated as the insulin response to intravenous arginine (5 g) injected at fasting glucose and after raising glucose to 13 to 15 mmol/l or to >28 mmol/l. Glucose 132-139 insulin Homo sapiens 0-7 18405999-3 2008 All subjects underwent an insulin-modified frequently sampled intravenous glucose tolerance test to measure insulin sensitivity and insulin secretory function with minimal model analysis. Glucose 74-81 insulin Homo sapiens 26-33 18437349-9 2008 The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48+/-6% at fasting glucose, 61+/-8% at 13-15 mmol/l glucose and 62+/-8% at >28 mmol/l glucose (p<0.001 for all). Glucose 153-160 insulin Homo sapiens 41-48 18437349-9 2008 The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48+/-6% at fasting glucose, 61+/-8% at 13-15 mmol/l glucose and 62+/-8% at >28 mmol/l glucose (p<0.001 for all). Glucose 153-160 insulin Homo sapiens 84-91 18437349-9 2008 The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48+/-6% at fasting glucose, 61+/-8% at 13-15 mmol/l glucose and 62+/-8% at >28 mmol/l glucose (p<0.001 for all). Glucose 186-193 insulin Homo sapiens 41-48 18437349-9 2008 The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48+/-6% at fasting glucose, 61+/-8% at 13-15 mmol/l glucose and 62+/-8% at >28 mmol/l glucose (p<0.001 for all). Glucose 186-193 insulin Homo sapiens 84-91 18437349-9 2008 The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48+/-6% at fasting glucose, 61+/-8% at 13-15 mmol/l glucose and 62+/-8% at >28 mmol/l glucose (p<0.001 for all). Glucose 186-193 insulin Homo sapiens 41-48 18544104-0 2008 Relationships between insulin secretion after intravenous and oral glucose administration in subjects with glucose tolerance ranging from normal to overt diabetes. Glucose 67-74 insulin Homo sapiens 22-29 18437349-9 2008 The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48+/-6% at fasting glucose, 61+/-8% at 13-15 mmol/l glucose and 62+/-8% at >28 mmol/l glucose (p<0.001 for all). Glucose 186-193 insulin Homo sapiens 84-91 18544104-0 2008 Relationships between insulin secretion after intravenous and oral glucose administration in subjects with glucose tolerance ranging from normal to overt diabetes. Glucose 107-114 insulin Homo sapiens 22-29 18544104-1 2008 AIMS: Acute insulin release (AIR) in response to intravenous glucose injection (IVGTT) can be abolished in diabetic subjects when their response to oral glucose is maintained. Glucose 61-68 insulin Homo sapiens 12-19 18544104-1 2008 AIMS: Acute insulin release (AIR) in response to intravenous glucose injection (IVGTT) can be abolished in diabetic subjects when their response to oral glucose is maintained. Glucose 153-160 insulin Homo sapiens 12-19 22964124-0 2008 Continuous glucose monitoring in insulin pump treated children. Glucose 11-18 insulin Homo sapiens 33-40 22964124-10 2008 CONCLUSIONS: Insulin pump-treated children and adolescents showed an irregular interstitial glucose level and did not achieve normoglycemia. Glucose 92-99 insulin Homo sapiens 13-20 18263705-0 2008 Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases. Glucose 0-7 insulin Homo sapiens 86-93 18263705-0 2008 Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases. Glucose 67-74 insulin Homo sapiens 86-93 18693476-13 2008 On the basis of the Fasting Glucose-to-Insulin Resistance Ratio (FGIR), 46.7% of the children showed insulin resistance. Glucose 28-35 insulin Homo sapiens 39-46 18518780-3 2008 These two hormones then simulate the secretion of insulin in a glucose-dependent manner and inhibit glucagon secretion, thus reducing circulating glucose levels. Glucose 63-70 insulin Homo sapiens 50-57 18569013-4 2008 It demonstrated that Cr(VI) treatment significantly inhibited insulin-stimulated glucose uptake and attenuated insulin signalling. Glucose 81-88 insulin Homo sapiens 62-69 18569016-5 2008 ROS induced by chronic insulin treatment inhibited insulin signalling and glucose uptake, induced endoplasmic reticulum (ER) stress and JNK activation. Glucose 74-81 insulin Homo sapiens 23-30 18693476-13 2008 On the basis of the Fasting Glucose-to-Insulin Resistance Ratio (FGIR), 46.7% of the children showed insulin resistance. Glucose 28-35 insulin Homo sapiens 101-108 18375940-1 2008 UNLABELLED: BACKGROUND We have shown that American women with polycystic ovary syndrome (PCOS) have decreased glucose-stimulated release of a putative mediator of insulin action, D-chiro-inositol (DCI)-containing inositolphosphoglycan (DCI-IPG), and increased urinary clearance of DCI (uCl(DCI)), which was associated with hyperinsulinemia. Glucose 110-117 insulin Homo sapiens 163-170 18588656-5 2008 As diabetes progresses, insulin is the only hypoglycemic agent with unlimited potential to lower blood glucose; earlier initiation of insulin therapy can help many patients achieve glucose targets more rapidly and provide symptomatic relief. Glucose 103-110 insulin Homo sapiens 24-31 18509785-4 2008 In animal studies and phase I clinical trials, dosing with Eligen insulin led to a rapid elevation of plasma insulin and subsequent decrease in plasma glucose levels; the onset of activity was more rapid and insulin concentrations were higher with Eligen insulin than with injected insulin. Glucose 151-158 insulin Homo sapiens 66-73 18537708-5 2008 Strategies to induce production of new beta cells, ameliorate or evade the auto-immune response that leads to beta cell destruction, or simply delivering a modified insulin cDNA under the control of glucose-responsive promoters have all resulted in restoration of euglycaemia in a physiologically normal time frame in rodent models of diabetes. Glucose 199-206 insulin Homo sapiens 165-172 18588656-5 2008 As diabetes progresses, insulin is the only hypoglycemic agent with unlimited potential to lower blood glucose; earlier initiation of insulin therapy can help many patients achieve glucose targets more rapidly and provide symptomatic relief. Glucose 103-110 insulin Homo sapiens 134-141 18588656-5 2008 As diabetes progresses, insulin is the only hypoglycemic agent with unlimited potential to lower blood glucose; earlier initiation of insulin therapy can help many patients achieve glucose targets more rapidly and provide symptomatic relief. Glucose 181-188 insulin Homo sapiens 24-31 18588656-5 2008 As diabetes progresses, insulin is the only hypoglycemic agent with unlimited potential to lower blood glucose; earlier initiation of insulin therapy can help many patients achieve glucose targets more rapidly and provide symptomatic relief. Glucose 181-188 insulin Homo sapiens 134-141 18397986-5 2008 The primary endpoint was an insulin-dependent state defined by the sum of serum C-peptide values during the oral glucose tolerance test (SigmaC-peptide) less than 4 ng/ml (1.32 nmol/liter). Glucose 113-120 insulin Homo sapiens 28-35 18334585-6 2008 INTERVENTIONS: Subjects had oral glucose tolerance tests, insulin-modified frequently sampled iv glucose tolerance tests, and fasting lipid profiles. Glucose 97-104 insulin Homo sapiens 58-65 18349060-0 2008 Insulin-stimulated rates of glucose uptake in muscle in hyperthyroidism: the importance of blood flow. Glucose 28-35 insulin Homo sapiens 0-7 18397988-4 2008 Insulin sensitivity was assessed by iv glucose tolerance test. Glucose 39-46 insulin Homo sapiens 0-7 18349060-8 2008 CONCLUSIONS: These results suggest that, in hyperthyroidism, insulin-stimulated glucose uptake in muscle is impaired; this defect is corrected, at least in part, by the increases in BF. Glucose 80-87 insulin Homo sapiens 61-68 18384905-6 2008 Endogenous glucose production (EGP) and insulin-mediated whole body glucose uptake (wbGU) were determined by standard methods. Glucose 68-75 insulin Homo sapiens 40-47 18293064-1 2008 PURPOSE: The purpose of this study was to examine glucose- and metabolically modulation of insulin secretion by rAAV-mediated gene delivery in vitro and in vivo. Glucose 50-57 insulin Homo sapiens 91-98 18717244-3 2008 AIM: To evaluate glucose and insulin responses to oral glucose load in patients with FBS. Glucose 55-62 insulin Homo sapiens 29-36 18502253-2 2008 We explored the effects of non-insulin-dependent increase in glucose utilization and recombinant human growth hormone (rhGH) on glucose production, glycogenolysis, and GNG in both the fed and overnight-fasted condition. Glucose 61-68 insulin Homo sapiens 31-38 18520641-14 2008 Compared with the paper-based protocol, eProtocol-insulin glucose measurements within target increased from 28% to 42%, and mean blood glucose decreased from 134 to 116 mg/dL (generalized linear model p = .001). Glucose 58-65 insulin Homo sapiens 50-57 18686355-4 2008 RESULTS: The mean serum fasting glucose and insulin levels, thus insulin resistance index of women with polycystic ovary syndrome, were significantly higher than those of the control subjects. Glucose 32-39 insulin Homo sapiens 65-72 19083434-5 2008 Insulin sensitivity was measured by intravenous glucose tolerance testing, hyperinsulinemic-euglycemic clamps, and insulin-stimulated insulin receptor and protein kinase B phosphorylation levels in muscle. Glucose 48-55 insulin Homo sapiens 0-7 19083434-7 2008 We show that high isoflavones do not adversely affect insulin sensitivity but do significantly alter insulin secretion to glucose stimulation. Glucose 122-129 insulin Homo sapiens 101-108 18293064-4 2008 Glucose- and metabolically modulated secretion of human insulin in the streptozotocin (STZ)-induced diabetic mice was assessed by intrahepatic administration of rAAV-polyethylenimine (PEI) complexes, followed by intraperitoneal glucose tolerance test (IPGTT), with or without theophylline. Glucose 228-235 insulin Homo sapiens 56-63 18293064-5 2008 RESULTS: Glucose- and metabolically controlled human insulin secretion was obtained in the rAAV-transduced Huh7 cells. Glucose 9-16 insulin Homo sapiens 53-60 18293064-4 2008 Glucose- and metabolically modulated secretion of human insulin in the streptozotocin (STZ)-induced diabetic mice was assessed by intrahepatic administration of rAAV-polyethylenimine (PEI) complexes, followed by intraperitoneal glucose tolerance test (IPGTT), with or without theophylline. Glucose 0-7 insulin Homo sapiens 56-63 18293064-7 2008 Co-administration of glucose and theophylline in these animals augmented the secretion of human insulin, demonstrating metabolic modulation of insulin secretion in vivo. Glucose 21-28 insulin Homo sapiens 96-103 18293064-7 2008 Co-administration of glucose and theophylline in these animals augmented the secretion of human insulin, demonstrating metabolic modulation of insulin secretion in vivo. Glucose 21-28 insulin Homo sapiens 143-150 18503703-14 2008 Icodextrin solution could ameliorate insulin resistance by decreasing insulin levels due to a reduction in the glucose load and an increase in plasma adiponectin levels. Glucose 111-118 insulin Homo sapiens 70-77 18361919-1 2008 Pdx-1 is a key regulator of glucose-stimulated insulin gene transcription in beta-cells. Glucose 28-35 insulin Homo sapiens 47-54 18589153-9 2008 The metabolic picture in lung transplanted patients on low-dose steroid therapy was characterized by normal insulin-stimulated glucose, leucine, and free fatty acid metabolism. Glucose 127-134 insulin Homo sapiens 108-115 18381287-0 2008 Chronic suppression of acetyl-CoA carboxylase 1 in beta-cells impairs insulin secretion via inhibition of glucose rather than lipid metabolism. Glucose 106-113 insulin Homo sapiens 70-77 18381287-4 2008 Delivery of siACC1 decreased glucose-stimulated insulin secretion (GSIS) by 70% in 832/13 cells and by 33% in islets. Glucose 29-36 insulin Homo sapiens 48-55 18221434-0 2008 Indices of insulin action calculated from fasting glucose and insulin reflect hepatic, not peripheral, insulin sensitivity in African-American and Caucasian adolescents. Glucose 50-57 insulin Homo sapiens 11-18 18207474-1 2008 Failure of insulin to elicit an increase in glucose uptake and metabolism in target tissues such as skeletal muscle is a major characteristic of non-insulin dependent type 2 diabetes mellitus. Glucose 44-51 insulin Homo sapiens 11-18 18221434-1 2008 Insulin stimulates muscle glucose uptake and inhibits hepatic glucose production. Glucose 26-33 insulin Homo sapiens 0-7 18221434-1 2008 Insulin stimulates muscle glucose uptake and inhibits hepatic glucose production. Glucose 62-69 insulin Homo sapiens 0-7 18342897-2 2008 The latter is known to cause insulin resistance, in particularly in skeletal muscle, by reducing insulin stimulated glucose uptake, most likely via accumulation of lipid inside the muscle cell. Glucose 116-123 insulin Homo sapiens 29-36 18772605-7 2008 These results suggest that conventional kinesin is dispensable for insulin-induced GLUT4 translocation in cultured myoblasts and may thus reveal a cell-type specific role of the microtubules-based cytoskeleton in glucose transport in response to insulin. Glucose 213-220 insulin Homo sapiens 67-74 18342897-2 2008 The latter is known to cause insulin resistance, in particularly in skeletal muscle, by reducing insulin stimulated glucose uptake, most likely via accumulation of lipid inside the muscle cell. Glucose 116-123 insulin Homo sapiens 97-104 18342897-4 2008 Furthermore, type 2 diabetes is associated with impaired metabolic flexibility, i.e. an impaired switching from fatty acid to glucose oxidation in response to insulin. Glucose 126-133 insulin Homo sapiens 159-166 18451265-5 2008 We speculate that G6PC2 regulates FPG by modulating the set point for glucose-stimulated insulin secretion in pancreatic beta cells. Glucose 70-77 insulin Homo sapiens 89-96 18343214-1 2008 Insulin stimulates glucose uptake in fat and muscle primarily by stimulating the translocation of vesicles containing facilitative glucose transporters, GLUT4, from intracellular compartments to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 18492238-1 2008 BACKGROUND: Insulin stimulates glucose uptake by adipocytes through increasing translocation of the glucose transporter GLUT4 from an intracellular compartment to the plasma membrane. Glucose 31-38 insulin Homo sapiens 12-19 18402935-7 2008 However, investigating the possible roles of insulin in memory storage can be challenging, due to the powerful peripheral effects of insulin on glucose and the low concentration of insulin in the brain. Glucose 144-151 insulin Homo sapiens 133-140 18585125-1 2008 Glucose biosensors are key components of closed-loop glycaemic control (insulin delivery) systems for effective management of diabetes. Glucose 0-7 insulin Homo sapiens 72-79 18402935-7 2008 However, investigating the possible roles of insulin in memory storage can be challenging, due to the powerful peripheral effects of insulin on glucose and the low concentration of insulin in the brain. Glucose 144-151 insulin Homo sapiens 133-140 18402935-8 2008 Although peripheral for insulin, synthesized in the beta-cells of the pancreas, is primarily involved in regulating glucose, small amounts of insulin are also present in the brain. Glucose 116-123 insulin Homo sapiens 24-31 18469247-1 2008 BACKGROUND: The ingestion of caffeine (5 mg/kg body weight) and a 75-g oral glucose load has been shown to elicit an acute insulin-insensitive environment in healthy and obese individuals and in those with type 2 diabetes. Glucose 76-83 insulin Homo sapiens 123-130 18215134-1 2008 Multiple studies have suggested that the protein kinase Akt/PKB (protein kinase B) is required for insulin-stimulated glucose transport in skeletal muscle and adipose cells. Glucose 118-125 insulin Homo sapiens 99-106 18303120-1 2008 High-glucose/low-dose insulin-mediated insulin resistance of glucose transport was studied in 3T3-L1 adipocytes. Glucose 5-12 insulin Homo sapiens 39-46 18303120-1 2008 High-glucose/low-dose insulin-mediated insulin resistance of glucose transport was studied in 3T3-L1 adipocytes. Glucose 61-68 insulin Homo sapiens 22-29 18303120-1 2008 High-glucose/low-dose insulin-mediated insulin resistance of glucose transport was studied in 3T3-L1 adipocytes. Glucose 61-68 insulin Homo sapiens 39-46 18303120-6 2008 Treatment with rapamycin [a specific inhibitor of mammalian target of rapamycin complex 1 (mTORC1)] inhibited the increased PTEN expression and partially restored insulin-stimulated glucose transport and Akt activation to insulin-resistant cells. Glucose 182-189 insulin Homo sapiens 163-170 18322051-5 2008 A direct marker of insulin resistance, the insulin sensitivity index, was measured by the frequently sampled intravenous glucose tolerance test. Glucose 121-128 insulin Homo sapiens 19-26 18460534-0 2008 Glucose variance in ICU patients receiving insulin infusions. Glucose 0-7 insulin Homo sapiens 43-50 18322051-5 2008 A direct marker of insulin resistance, the insulin sensitivity index, was measured by the frequently sampled intravenous glucose tolerance test. Glucose 121-128 insulin Homo sapiens 43-50 19337387-6 2008 Salsalate increased glucose utilization during euglycemic hyperinsulinemic clamps, by approximately 50% and 15% at the high and standard doses, respectively, and insulin clearance was decreased. Glucose 20-27 insulin Homo sapiens 63-70 18473759-4 2008 RESULTS: The subjects with higher 2 hrs glucose levels 5.2 for NGT vs. 9.1 for IGT and 13.4 mmol/l for NIDDM, p<0.001, apo C-III level (12.8 (DM) vs. 8.9 mg/dl (normal), p<0.001), waist to hip ratio (0.91 (IGT) vs. 0.89 (Normal), p<0.01) and abdominal fat and were found to be highly insulin resistant. Glucose 40-47 insulin Homo sapiens 293-300 18394265-0 2008 Quantifying the effect of exenatide and insulin glargine on postprandial glucose excursions in patients with type 2 diabetes. Glucose 73-80 insulin Homo sapiens 40-47 18394265-2 2008 After 26 weeks of treatment, insulin glargine reduced fasting glucose to a greater extent than exenatide without significant effect on PPG excursion. Glucose 62-69 insulin Homo sapiens 29-36 18473760-1 2008 In healthy individuals, the ability of the pancreatic islets to sense and respond appropriately to changes in plasma glucose levels maintains plasma glucose levels within a narrow range despite broad fluctuations in nutrient intake and variable "demand" for insulin imposed by changes in insulin sensitivity. Glucose 117-124 insulin Homo sapiens 258-265 19017497-0 2008 Contribution of defects in glucose production and uptake to carbohydrate intolerance in insulin-resistant subjects. Glucose 27-34 insulin Homo sapiens 88-95 18473760-1 2008 In healthy individuals, the ability of the pancreatic islets to sense and respond appropriately to changes in plasma glucose levels maintains plasma glucose levels within a narrow range despite broad fluctuations in nutrient intake and variable "demand" for insulin imposed by changes in insulin sensitivity. Glucose 117-124 insulin Homo sapiens 288-295 18285554-6 2008 RESULTS: The glucose infusion rates required to maintain identical glucose levels during the similar insulin infusion rates were substantially lower in diabetic Indians than in the nondiabetic participants (P < 0.001), and they were lower in nondiabetic Indians than in nondiabetic Northern European Americans (P < 0.002). Glucose 13-20 insulin Homo sapiens 101-108 18268067-4 2008 RESULTS: Insulin glulisine injections resulted in higher postprandial insulin levels (means +/- SEM area under the curve [AUC](0-120) 51.0 +/- 6.8 vs. 38.2 +/- 5.4 mU/l; P = 0.004), while plasma glucose (AUC(0-240) 158 +/- 9 vs. 180 +/- 9 mg/dl; P < 0.05) and intact proinsulin (AUC(0-240) 26.2 +/- 3.5 vs. 31.2 +/- 4.3 pmol/l; P = 0.002) were lower. Glucose 195-202 insulin Homo sapiens 9-16 18268073-4 2008 Insulin dose was adjusted with algorithm-controlled titration to achieve premeal blood glucose of 4.4-6.1 mmol/l. Glucose 87-94 insulin Homo sapiens 0-7 18304675-3 2008 RESULTS: All three insulin regimes significantly reduced postprandial glucose increment (area under the curve AUC(-30 to 240 min)) and peak plasma glucose increment (DeltaC(max)) compared with placebo. Glucose 70-77 insulin Homo sapiens 19-26 18304675-3 2008 RESULTS: All three insulin regimes significantly reduced postprandial glucose increment (area under the curve AUC(-30 to 240 min)) and peak plasma glucose increment (DeltaC(max)) compared with placebo. Glucose 147-154 insulin Homo sapiens 19-26 18252903-9 2008 CONCLUSIONS: Closed-loop glucose control using an external sensor and insulin pump provides a means to achieve near-normal glucose concentrations in youth with type 1 diabetes during the overnight period. Glucose 25-32 insulin Homo sapiens 70-77 18252903-9 2008 CONCLUSIONS: Closed-loop glucose control using an external sensor and insulin pump provides a means to achieve near-normal glucose concentrations in youth with type 1 diabetes during the overnight period. Glucose 123-130 insulin Homo sapiens 70-77 18299316-7 2008 Insulin resistance was evaluated by homeostasis model assessment for insulin resistance (HOMA-IR), fasting plasma insulin level, Matsuda index, and area under the oral glucose tolerance test curve (AUC) of insulin. Glucose 168-175 insulin Homo sapiens 0-7 18410564-12 2008 In addition, exercise improves insulin resistance mainly by increasing non-oxidative glucose disposal in type 2 diabetes. Glucose 85-92 insulin Homo sapiens 31-38 18324385-8 2008 These diabetes-prone offspring are characterised by a 19% decrease in first-phase insulin release following an intravenous glucose load, suggesting a role for this variant in the pathogenesis of pancreatic beta cell dysfunction. Glucose 123-130 insulin Homo sapiens 82-89 17938503-3 2008 In mature beta-cells, PDX-1 transactivates the insulin and other genes involved in glucose sensing and metabolism such as GLUT2 and glucokinase. Glucose 83-90 insulin Homo sapiens 47-54 18048763-3 2008 In addition to their contribution to the deterioration of beta-cell function after the onset of the disease, elevations of plasma fatty acid levels that often accompany insulin resistance may, as glucose levels begin to rise outside of the normal range, also play a pathogenic role in the early stages of the disease. Glucose 196-203 insulin Homo sapiens 169-176 18184681-4 2008 From the results of the oral glucose tolerance test, an insulin sensitivity index (ISI) was calculated. Glucose 29-36 insulin Homo sapiens 56-63 18445172-4 2008 RESULTS: On the last day of each treatment period, the area under the curve (AUC) for glucose was 10% lower on the continuous subcutaneous infusion regimen compared with the insulin injection regimen (P = 0.002). Glucose 86-93 insulin Homo sapiens 174-181 18319317-2 2008 OBJECTIVE: We hypothesized that normalization of portal insulin in patients with portal pancreas graft drainage stimulates the GH/IGF-I axis and thereby contributes to glucose control. Glucose 168-175 insulin Homo sapiens 56-63 18355813-2 2008 The purpose of this study was to determine the relationship between intrahepatic triglyceride (IHTG) content and insulin action in liver (suppression of glucose production), skeletal muscle (stimulation of glucose uptake), and adipose tissue (suppression of lipolysis) in nondiabetic obese subjects. Glucose 153-160 insulin Homo sapiens 113-120 18355813-2 2008 The purpose of this study was to determine the relationship between intrahepatic triglyceride (IHTG) content and insulin action in liver (suppression of glucose production), skeletal muscle (stimulation of glucose uptake), and adipose tissue (suppression of lipolysis) in nondiabetic obese subjects. Glucose 206-213 insulin Homo sapiens 113-120 18355813-4 2008 RESULTS: Hepatic insulin sensitivity, assessed as a function of glucose production rate and plasma insulin concentration, was inversely correlated with IHTG content (r = -0.599; P < .001). Glucose 64-71 insulin Homo sapiens 17-24 18355813-5 2008 The ability of insulin to suppress fatty acid release from adipose tissue and to stimulate glucose uptake by skeletal muscle were also inversely correlated with IHTG content (adipose tissue: r = -0.590, P < .001; skeletal muscle: r = -0.656, P < .001). Glucose 91-98 insulin Homo sapiens 15-22 18303080-6 2008 Basal hepatic insulin resistance index (basal hepatic glucose production x fasting plasma insulin) was significantly increased in IFG, IGT, and IFG/IGT (P < 0.009) compared with NGT. Glucose 54-61 insulin Homo sapiens 14-21 18303080-7 2008 Glucose sensitivity of first-phase insulin secretion was progressively lower in IFG, IGT, and IFG/IGT compared with NGT. Glucose 0-7 insulin Homo sapiens 35-42 18319319-5 2008 Finally, when subjects were stratified on the basis of their respective concentrations of IL-6 and TNF-alpha (using the 50th percentile of their overall distribution), an ANOVA revealed an independent contribution of IL-6 to the variation of fasting insulin (P < 0.01) and each of these two cytokines to the variation of insulin levels measured after a 75-g oral glucose challenge (P <0.01 for IL-6 and P < 0.05 for TNF-alpha). Glucose 366-373 insulin Homo sapiens 250-257 19885199-5 2008 METHODS: We required attending physicians of eligible patients to independently intend to use intravenous insulin to normalize blood glucose. Glucose 133-140 insulin Homo sapiens 106-113 18434356-6 2008 After culture with prolactin and palmitate, acute stimulation with 10 mM glucose for 1 h showed a suppression of insulin release. Glucose 73-80 insulin Homo sapiens 113-120 19885199-6 2008 We used eProtocol-insulin for glucose control for a duration determined by the clinical caregivers. Glucose 30-37 insulin Homo sapiens 18-25 19885199-18 2008 CONCLUSIONS: A multicenter validation demonstrated that eProtocol-insulin is a valid, exportable tool that can assist clinicians in achieving control of glucose in critically ill adults and children. Glucose 153-160 insulin Homo sapiens 66-73 19885206-1 2008 BACKGROUND: In silico testing was used extensively in the European Commission-funded Closed Loop Insulin Infusion for Critically Ill Patients (Clinicip) project, which aimed to develop prototype systems for closed loop glucose control in the critically ill. Glucose 219-226 insulin Homo sapiens 97-104 18469500-2 2008 The effects of atorvastatin and pravastatin on insulin-induced glucose uptake and the related signal transduction in 3T3L1 adipocytes were studied. Glucose 63-70 insulin Homo sapiens 47-54 18633302-1 2008 Human insulin is a hormone well-known to regulate the blood glucose level. Glucose 60-67 insulin Homo sapiens 6-13 21479410-2 2008 Skeletal muscle represents the largest insulin-regulated glucose sink in the body, making insulin resistance and abnormal glucose disposal in muscle fibres a critical aspect of diabetes mellitus. Glucose 57-64 insulin Homo sapiens 39-46 18469500-11 2008 In conclusion, hydrophobic atorvastatin decreases the glucose uptake by 3T3L1 adipocytes since it can enter the cell and prevents lipid modification of some proteins that are involved in the insulin signal transduction process. Glucose 54-61 insulin Homo sapiens 191-198 17646121-0 2008 Glucose control in critical illness using a web-based insulin dose calculator. Glucose 0-7 insulin Homo sapiens 54-61 18442629-1 2008 There is a tight connection between insulin-like growth factor binding protein 1 (IGFBP-1) and nutrient/energy supply, suggesting modulation of the short-term insulin-like activity and glucose homeostasis by IGFBP-1. Glucose 185-192 insulin Homo sapiens 36-43 21479410-2 2008 Skeletal muscle represents the largest insulin-regulated glucose sink in the body, making insulin resistance and abnormal glucose disposal in muscle fibres a critical aspect of diabetes mellitus. Glucose 57-64 insulin Homo sapiens 90-97 21479410-2 2008 Skeletal muscle represents the largest insulin-regulated glucose sink in the body, making insulin resistance and abnormal glucose disposal in muscle fibres a critical aspect of diabetes mellitus. Glucose 122-129 insulin Homo sapiens 39-46 18401346-1 2008 Acquired resistance to the action of insulin to stimulate glucose transport in skeletal muscle is associated with obesity and promotes the development of type 2 diabetes. Glucose 58-65 insulin Homo sapiens 37-44 17931748-7 2008 Finally, in the absence of exogenous UII, both palosuran and urantide potentiated glucose-induced insulin release, thus supporting the concept that endogenous UII is an insulinostatic peptide. Glucose 82-89 insulin Homo sapiens 98-105 18427204-3 2008 METHODS: Insulin resistance was defined according to the homeostasis model of assessment-insulin resistance calculated as fasting insulin (mIU/l) x fasting glucose (mmol/l)/22.5. Glucose 156-163 insulin Homo sapiens 89-96 18427204-3 2008 METHODS: Insulin resistance was defined according to the homeostasis model of assessment-insulin resistance calculated as fasting insulin (mIU/l) x fasting glucose (mmol/l)/22.5. Glucose 156-163 insulin Homo sapiens 9-16 18468820-11 2008 Leptin secretion is acutely regulated by glucose levels in insulin presence. Glucose 41-48 insulin Homo sapiens 59-66 18331742-2 2008 We used an approach of two metabolic pathways (glucose oxidation and utilization) based on the measurement of 14CO2 and 3H2O production from D-[U-14C]-glucose and D-[5-(3)H]-glucose, respectively, in isolated islets incubated with 3.3 and 16.7 mM glucose alone, or with 5 or 15 mU/ml insulin, anti-insulin guinea-pig serum (1:500), 25 microM nifedipine, or 150 nM wortmannin. Glucose 47-54 insulin Homo sapiens 284-291 18331742-2 2008 We used an approach of two metabolic pathways (glucose oxidation and utilization) based on the measurement of 14CO2 and 3H2O production from D-[U-14C]-glucose and D-[5-(3)H]-glucose, respectively, in isolated islets incubated with 3.3 and 16.7 mM glucose alone, or with 5 or 15 mU/ml insulin, anti-insulin guinea-pig serum (1:500), 25 microM nifedipine, or 150 nM wortmannin. Glucose 47-54 insulin Homo sapiens 298-305 18331742-3 2008 Insulin release was measured by radioimmunoassay in islets incubated with 3.3 or 16.7 mM glucose, with or without 75, 150, and 300 nM wortmannin. Glucose 89-96 insulin Homo sapiens 0-7 18331742-5 2008 Addition of anti-insulin serum, nifedipine or wortmannin to the medium with 16.7 mM glucose decreased 14CO2 and 3H2O production in control but not in SRD islets. Glucose 84-91 insulin Homo sapiens 17-24 18331742-7 2008 We can conclude that the autocrine stimulatory effect of insulin upon glucose metabolism observed in normal islets is attenuated or even absent in islets from IR animals. Glucose 70-77 insulin Homo sapiens 57-64 18391974-2 2008 Glucose homeostasis is achieved by adjusting endogenous glucose production as well as glucose uptake by peripheral tissues in response to insulin. Glucose 86-93 insulin Homo sapiens 138-145 18258599-1 2008 Insulin increases glucose transport by stimulating the trafficking of intracellular GLUT4 to the cell surface, a process known as GLUT4 translocation. Glucose 18-25 insulin Homo sapiens 0-7 18405504-4 2008 For insulin sensitivity quantification in patients with type 1 diabetes the estimated glucose disposal rate (eGDR): it consists of calculating a score based on clinical factors of the patient, which shows an inverse relationship with the development of micro- and macrovascular complications. Glucose 86-93 insulin Homo sapiens 4-11 18378631-2 2008 Commonly used oral glucose-lowering agents include sulfonylureas, which are insulin secretagogues, and thiazolidinediones, which are insulin sensitizers. Glucose 19-26 insulin Homo sapiens 76-83 18400721-2 2008 Because insulin is secreted in response to elevated blood glucose concentrations, dietary factors that increase these concentrations may be important in pancreatic carcinogenesis. Glucose 58-65 insulin Homo sapiens 8-15 18230695-3 2008 Intriguingly, insulin appears to exert opposite actions, depending on glucose availability, with regard to the regulation of SIRT1 and FoxO3a abundance, which apparently contributes to modulating the potency of insulin"s myogenic action. Glucose 70-77 insulin Homo sapiens 14-21 18230695-4 2008 Namely, insulin exerts a potent myogenic effect in the presence of sufficient glucose, whereas insulin is unable to exert its myogenic action under LG conditions, since insulin evokes massive upregulation of both SIRT1 and FoxO3a in the absence of sufficient ambient glucose. Glucose 78-85 insulin Homo sapiens 8-15 18230695-4 2008 Namely, insulin exerts a potent myogenic effect in the presence of sufficient glucose, whereas insulin is unable to exert its myogenic action under LG conditions, since insulin evokes massive upregulation of both SIRT1 and FoxO3a in the absence of sufficient ambient glucose. Glucose 267-274 insulin Homo sapiens 8-15 18230695-5 2008 In addition, the hampered differentiation state under LG is significantly restored by sirtinol, a SIRT1 inhibitor, whereas insulin abolished this sirtinol-dependent restoration, indicating that insulin can function as a negative as well as a positive myogenic factor depending on glucose availability. Glucose 280-287 insulin Homo sapiens 123-130 18230695-5 2008 In addition, the hampered differentiation state under LG is significantly restored by sirtinol, a SIRT1 inhibitor, whereas insulin abolished this sirtinol-dependent restoration, indicating that insulin can function as a negative as well as a positive myogenic factor depending on glucose availability. Glucose 280-287 insulin Homo sapiens 194-201 18305020-4 2008 Insulin-stimulated (10 mU/ml) glucose transport was not different, relative to control, following exposure to palmitate (-10%) or P+gAd (-3%) in lean muscle. Glucose 30-37 insulin Homo sapiens 0-7 18305020-5 2008 In obese muscle, the absolute increase in glucose transport from basal to insulin-stimulated conditions was significantly decreased following palmitate (-55%) and P+gAd (-36%) exposure (control vs. palmitate; control vs. P+gAd, P < 0.05). Glucose 42-49 insulin Homo sapiens 74-81 18305020-7 2008 The palmitate-induced reduction in insulin-stimulated glucose transport in muscle from obese individuals may have been due to reduced Ser Akt (control vs. palmitate; P+gAd, P < 0.05) and Akt substrate 160 (AS160) phosphorylation (control vs. palmitate; P+gAd, P < 0.05). Glucose 54-61 insulin Homo sapiens 35-42 18347614-7 2008 Additionally, ERK1/2 are important for insulin gene transcription in pancreatic beta cells, which produce insulin in response to increases in circulating glucose to permit efficient glucose utilization and storage in the organism. Glucose 154-161 insulin Homo sapiens 39-46 18347614-7 2008 Additionally, ERK1/2 are important for insulin gene transcription in pancreatic beta cells, which produce insulin in response to increases in circulating glucose to permit efficient glucose utilization and storage in the organism. Glucose 154-161 insulin Homo sapiens 106-113 18347614-7 2008 Additionally, ERK1/2 are important for insulin gene transcription in pancreatic beta cells, which produce insulin in response to increases in circulating glucose to permit efficient glucose utilization and storage in the organism. Glucose 182-189 insulin Homo sapiens 39-46 18347614-7 2008 Additionally, ERK1/2 are important for insulin gene transcription in pancreatic beta cells, which produce insulin in response to increases in circulating glucose to permit efficient glucose utilization and storage in the organism. Glucose 182-189 insulin Homo sapiens 106-113 18418425-3 2008 To provide information on the underlying basis of these divergent actions of high glucose, the present study examined the hypothesis that the adverse effects of high glucose are linked to impaired insulin signaling, leading to a reduction in the levels of cytoprotective factors, and that the beneficial effects of high glucose occur in the absence of insulin and result in an improvement in Akt signaling. Glucose 166-173 insulin Homo sapiens 197-204 18418425-3 2008 To provide information on the underlying basis of these divergent actions of high glucose, the present study examined the hypothesis that the adverse effects of high glucose are linked to impaired insulin signaling, leading to a reduction in the levels of cytoprotective factors, and that the beneficial effects of high glucose occur in the absence of insulin and result in an improvement in Akt signaling. Glucose 166-173 insulin Homo sapiens 197-204 18418425-9 2008 Because high glucose diminishes insulin signaling, it reduces phospho-Akt levels and renders the cell susceptible to damaging insults. Glucose 13-20 insulin Homo sapiens 32-39 18201563-7 2008 Although the fasting HOMA insulin resistance did not change significantly in either group, glucose and insulin areas under the curve of 2 h-OGTT were significantly decreased, suggesting improvement in insulin sensitivity post glucose challenge. Glucose 226-233 insulin Homo sapiens 103-110 18201563-7 2008 Although the fasting HOMA insulin resistance did not change significantly in either group, glucose and insulin areas under the curve of 2 h-OGTT were significantly decreased, suggesting improvement in insulin sensitivity post glucose challenge. Glucose 226-233 insulin Homo sapiens 103-110 18187548-3 2008 A single bout of insulin-induced AH or RH for 3 consecutive days was used to deplete brain glucose and glycogen stores in rats. Glucose 91-98 insulin Homo sapiens 17-24 18324957-8 2008 Treatment with insulin detemir (+/- OADs) significantly reduced mean haemoglobin A(1c) (HbA(1c)) (-1.3%; p < 0.0001), fasting glucose (-3.7 mmol/l; p < 0.0001), and within-patient fasting glucose variability (-0.5 mmol/l; p < 0.0001). Glucose 129-136 insulin Homo sapiens 15-22 18324957-8 2008 Treatment with insulin detemir (+/- OADs) significantly reduced mean haemoglobin A(1c) (HbA(1c)) (-1.3%; p < 0.0001), fasting glucose (-3.7 mmol/l; p < 0.0001), and within-patient fasting glucose variability (-0.5 mmol/l; p < 0.0001). Glucose 194-201 insulin Homo sapiens 15-22 18499046-3 2008 With increasing ratio of d-glucose displayed on the surfaces, the cells showed a stretched shape in the culture with 10 mug/cm(3) insulin, reaching the highest extent of cell stretching at 100%d-glucose display, whereas round cells were predominant at 0%d-glucose display. Glucose 25-34 insulin Homo sapiens 130-137 18499046-3 2008 With increasing ratio of d-glucose displayed on the surfaces, the cells showed a stretched shape in the culture with 10 mug/cm(3) insulin, reaching the highest extent of cell stretching at 100%d-glucose display, whereas round cells were predominant at 0%d-glucose display. Glucose 193-202 insulin Homo sapiens 130-137 18499046-3 2008 With increasing ratio of d-glucose displayed on the surfaces, the cells showed a stretched shape in the culture with 10 mug/cm(3) insulin, reaching the highest extent of cell stretching at 100%d-glucose display, whereas round cells were predominant at 0%d-glucose display. Glucose 193-202 insulin Homo sapiens 130-137 18499046-8 2008 However, in the presence of insulin, the broad distribution of GLUT4 appeared on the basal and apical sides of cells at 100%d-glucose display, in contrast with its localization only on the apical side of cells at 0%d-glucose display. Glucose 124-133 insulin Homo sapiens 28-35 18499046-8 2008 However, in the presence of insulin, the broad distribution of GLUT4 appeared on the basal and apical sides of cells at 100%d-glucose display, in contrast with its localization only on the apical side of cells at 0%d-glucose display. Glucose 215-224 insulin Homo sapiens 28-35 18198225-8 2008 RESULTS: In the simple analysis, glucose utilization at the 40 mU insulin dose (6.3 +/- 2.8 vs. 9.1 +/- 3.4; P < 0.05), the index of the insulin resistance of basal hepatic glucose production (23.6 +/- 13.0 vs. 15.1 +/- 6.0; P < 0.05), and insulin-stimulated suppression of lipolysis (35 vs. 54%; P < 0.05) were significantly different between women with and without abdominal obesity, respectively. Glucose 33-40 insulin Homo sapiens 66-73 18445172-9 2008 CONCLUSIONS: Basal continuous subcutaneous infusion of a rapid-acting insulin analogue improved plasma insulin (more flat insulin profile with a lower variability) and glucose (lower AUC) profiles compared with once-daily subcutaneous injection of a long-acting insulin analogue in Type 2 diabetes. Glucose 168-175 insulin Homo sapiens 70-77 18396141-1 2008 The serine/threonine kinase Akt2 has been implicated in insulin-regulated glucose uptake into muscle and fat cells by promoting the translocation of glucose transporter 4 (GLUT4) to the cell surface. Glucose 74-81 insulin Homo sapiens 56-63 18414771-8 2008 Insulin resistance, assessed by the homeostasis model of assessment of insulin resistance (HOMA-IR), correlated with mean RR interval (beta coefficient = -0.189, P = 0.04) and BRS (beta coefficient = -0.246, P = 0.006) and similar correlations were seen with fasting serum glucose. Glucose 273-280 insulin Homo sapiens 0-7 18540789-7 2008 Insulin analogs, though slightly more expensive than human and isophane insulin, provide much more physiologic insulin action, resulting in better glucose control and lower rates of hypoglycemia. Glucose 147-154 insulin Homo sapiens 0-7 18540789-7 2008 Insulin analogs, though slightly more expensive than human and isophane insulin, provide much more physiologic insulin action, resulting in better glucose control and lower rates of hypoglycemia. Glucose 147-154 insulin Homo sapiens 111-118 17949938-9 2008 The proinsulin and insulin secretion pattern in response to glucose was significantly different between lean and obese cats but the pattern was similar within a group. Glucose 60-67 insulin Homo sapiens 4-14 18174496-4 2008 Insulin sensitivity was determined by glucose uptake (milligrams per kilogram per minute) adjusted for lean body mass (M(LBM)) and steady-state insulin (M(LBM)/ln SSI). Glucose 38-45 insulin Homo sapiens 0-7 18174523-12 2008 Moreover, glucose-stimulated insulin secretion and biosynthesis were impaired in islets treated with rapamycin. Glucose 10-17 insulin Homo sapiens 29-36 18184925-7 2008 Third, and finally, ICV lactate administration lowered glucose production in normal rodents with diet-induced insulin resistance. Glucose 55-62 insulin Homo sapiens 110-117 18192539-6 2008 The diabetes-associated alleles also associated strongly with a higher plasma glucose at 30 and 120 min and serum insulin at 120 min during an oral glucose tolerance test (all P < 0.006) and the minor allele of rs1889018 with a surrogate measure of insulin sensitivity (P = 0.03). Glucose 78-85 insulin Homo sapiens 252-259 18192539-6 2008 The diabetes-associated alleles also associated strongly with a higher plasma glucose at 30 and 120 min and serum insulin at 120 min during an oral glucose tolerance test (all P < 0.006) and the minor allele of rs1889018 with a surrogate measure of insulin sensitivity (P = 0.03). Glucose 148-155 insulin Homo sapiens 114-121 18192539-6 2008 The diabetes-associated alleles also associated strongly with a higher plasma glucose at 30 and 120 min and serum insulin at 120 min during an oral glucose tolerance test (all P < 0.006) and the minor allele of rs1889018 with a surrogate measure of insulin sensitivity (P = 0.03). Glucose 148-155 insulin Homo sapiens 252-259 18192544-8 2008 AIR insulin adverse events (cough, headache, and dizziness) were mild to moderate in intensity and have been previously reported or are typical of studies involving glucose clamp procedures. Glucose 165-172 insulin Homo sapiens 4-11 18202246-2 2008 RESEARCH DESIGN AND METHODS: Insulin-mediated glucose uptake and plasma total and high molecular weight (HMW) adiponectin concentrations were quantified in 52 women of South Asian (SA) and Caucasian (CAU) ancestry and compared. Glucose 46-53 insulin Homo sapiens 29-36 18260774-1 2008 BACKGROUND: Most glucose meter comparisons to date have focused on performance specifications likely to impact subcutaneous dosing of insulin. Glucose 17-24 insulin Homo sapiens 134-141 18260774-2 2008 We evaluated four hospital-based glucose meter technologies for accuracy, precision, and analytical interferences likely to be encountered in critically ill patients, with the goal of identifying and discriminating glucose meter performance specifications likely to impact intensive intravenous insulin dosing. Glucose 215-222 insulin Homo sapiens 295-302 18260776-1 2008 BACKGROUND: The use of patient models describing the dynamics of glucose, insulin, and possibly other metabolic species associated with glucose regulation allows diabetes researchers to gain insights regarding novel therapies via simulation. Glucose 136-143 insulin Homo sapiens 74-81 18285553-2 2008 We hypothesized that impaired insulin-stimulated glucose oxidation is a consequence of the lower cellular glucose uptake rate in type 2 diabetes. Glucose 49-56 insulin Homo sapiens 30-37 18285553-2 2008 We hypothesized that impaired insulin-stimulated glucose oxidation is a consequence of the lower cellular glucose uptake rate in type 2 diabetes. Glucose 106-113 insulin Homo sapiens 30-37 18285553-6 2008 RESULTS: Metabolic flexibility to glucose (change in respiratory quotient [RQ]) was mainly related to insulin-stimulated glucose disposal rate (R(2) = 0.46, P < 0.0001) with an additional 3% of variance accounted for by plasma free fatty acid concentration at the end of the clamp (P = 0.03). Glucose 34-41 insulin Homo sapiens 102-109 18285553-6 2008 RESULTS: Metabolic flexibility to glucose (change in respiratory quotient [RQ]) was mainly related to insulin-stimulated glucose disposal rate (R(2) = 0.46, P < 0.0001) with an additional 3% of variance accounted for by plasma free fatty acid concentration at the end of the clamp (P = 0.03). Glucose 121-128 insulin Homo sapiens 102-109 18285553-8 2008 Additionally, the increase in metabolic flexibility to glucose after weight loss was accounted for by the concomitant increase in insulin-stimulated glucose disposal rate. Glucose 55-62 insulin Homo sapiens 130-137 18285553-8 2008 Additionally, the increase in metabolic flexibility to glucose after weight loss was accounted for by the concomitant increase in insulin-stimulated glucose disposal rate. Glucose 149-156 insulin Homo sapiens 130-137 18292985-0 2008 Near normalisation of blood glucose improves the potentiating effect of GLP-1 on glucose-induced insulin secretion in patients with type 2 diabetes. Glucose 28-35 insulin Homo sapiens 97-104 18292985-0 2008 Near normalisation of blood glucose improves the potentiating effect of GLP-1 on glucose-induced insulin secretion in patients with type 2 diabetes. Glucose 81-88 insulin Homo sapiens 97-104 18292985-3 2008 We investigated whether 4 weeks of near normalisation of blood glucose (BG) improves the potentiation of glucose-stimulated insulin secretion by GLP-1. Glucose 105-112 insulin Homo sapiens 124-131 18292985-7 2008 The responsiveness to glucose or glucose+GLP-1 was expressed as the slope of the linear regression line relating insulin secretion rate (ISR) and plasma glucose concentration (pmol kg(-1) min(-1) [mmol/l](-1)). Glucose 22-29 insulin Homo sapiens 113-120 18292985-7 2008 The responsiveness to glucose or glucose+GLP-1 was expressed as the slope of the linear regression line relating insulin secretion rate (ISR) and plasma glucose concentration (pmol kg(-1) min(-1) [mmol/l](-1)). Glucose 33-40 insulin Homo sapiens 113-120 18292985-7 2008 The responsiveness to glucose or glucose+GLP-1 was expressed as the slope of the linear regression line relating insulin secretion rate (ISR) and plasma glucose concentration (pmol kg(-1) min(-1) [mmol/l](-1)). Glucose 33-40 insulin Homo sapiens 113-120 18333889-0 2008 Combination of the insulin sensitizer, pioglitazone, and the long-acting GLP-1 human analog, liraglutide, exerts potent synergistic glucose-lowering efficacy in severely diabetic ZDF rats. Glucose 132-139 insulin Homo sapiens 19-26 18387079-8 2008 AUC 0-120 min before delivery, mean glucose concentration 0-120 min before delivery and cord plasma insulin level were all significantly associated with the need for IV glucose in the newborn children. Glucose 169-176 insulin Homo sapiens 100-107 18446452-6 2008 Overexpression of human resistin impaired significantly insulin-stimulated glucose uptake and glycogen synthesis in HepG2 cells. Glucose 75-82 insulin Homo sapiens 56-63 18463047-3 2008 RESULTS: Insulin signaling in the periphery is known to affect hepatic glucose production and glucose uptake in muscle and adipose tissue. Glucose 71-78 insulin Homo sapiens 9-16 18463047-3 2008 RESULTS: Insulin signaling in the periphery is known to affect hepatic glucose production and glucose uptake in muscle and adipose tissue. Glucose 94-101 insulin Homo sapiens 9-16 18339003-13 2008 CONCLUSION: The data obtained show middle-aged T2DM-OFF with normal glucose tolerance displaying reduced total insulin sensitivity and impaired beta cell function, which relates to impaired insulin-dependent suppression of plasma FFA and increased ICA-IMT. Glucose 68-75 insulin Homo sapiens 111-118 18339003-13 2008 CONCLUSION: The data obtained show middle-aged T2DM-OFF with normal glucose tolerance displaying reduced total insulin sensitivity and impaired beta cell function, which relates to impaired insulin-dependent suppression of plasma FFA and increased ICA-IMT. Glucose 68-75 insulin Homo sapiens 190-197 18358253-3 2008 Although the relationship between blood glucose and insulin is linear, not all types of carbohydrate are fully metabolized to blood glucose. Glucose 40-47 insulin Homo sapiens 52-59 17940160-3 2008 Direct exposure to TNF-alpha induces a state of insulin resistance in terms of glucose uptake in myocytes and brown adipocytes because of the activation of proinflammatory pathways that impair insulin signaling at the level of the insulin receptor substrate (IRS) proteins. Glucose 79-86 insulin Homo sapiens 48-55 18375745-1 2008 Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are intestinal postprandial hormones that stimulate insulin release from the pancreas as long as circulating glucose concentrations are raised. Glucose 18-25 insulin Homo sapiens 36-43 18379571-6 2008 In this case, the combination of an initial episode of hypoglycemia and subsequent blood glucose levels below 95 mg per 100 ml led to a prolonged delay in the initiation of a planned insulin infusion for insulin coverage during the induction of labor. Glucose 89-96 insulin Homo sapiens 183-190 18379571-6 2008 In this case, the combination of an initial episode of hypoglycemia and subsequent blood glucose levels below 95 mg per 100 ml led to a prolonged delay in the initiation of a planned insulin infusion for insulin coverage during the induction of labor. Glucose 89-96 insulin Homo sapiens 204-211 18328348-11 2008 However, it is important to determine whether the glucose-lowering effect of RSG occurs mainly through direct enhancement of insulin sensitivity. Glucose 50-57 insulin Homo sapiens 125-132 18288110-0 2008 Pancreatic endoderm derived from human embryonic stem cells generates glucose-responsive insulin-secreting cells in vivo. Glucose 70-77 insulin Homo sapiens 89-96 18288110-3 2008 Upon glucose stimulation of the implanted mice, human insulin and C-peptide are detected in sera at levels similar to those of mice transplanted with approximately 3,000 human islets. Glucose 5-12 insulin Homo sapiens 54-61 18288110-6 2008 Together, these data provide definitive evidence that hES cells are competent to generate glucose-responsive, insulin-secreting cells. Glucose 90-97 insulin Homo sapiens 110-117 18634374-6 2008 In patients treated with peritoneal dialysis, a potential risk factor of insulin resistance is persistent glucose overload, used as an osmotic agent in dialysis fluids. Glucose 106-113 insulin Homo sapiens 73-80 18548166-2 2008 The most important stage in the development of insulin resistance is impairment of insulin-stimulated skeletal muscle glucose uptake. Glucose 118-125 insulin Homo sapiens 47-54 18660731-5 2008 Insulin resistance (IR) is a significant predictor of cardiovascular mortality and morbidity across a spectrum of glucose tolerance. Glucose 114-121 insulin Homo sapiens 0-7 18664175-3 2008 Insulin is an important hormone involving in lots of physiological functions such as transport of glucose, gene expression and DNA synthesis. Glucose 98-105 insulin Homo sapiens 0-7 18359095-2 2008 Pancreatic islets are a target for adverse effectors such as high concentrations of glucose, pro-inflammatory cytokines and increased free fatty acid concentrations - which are associated with adiposity, insulin resistance and the induction of beta-cell apoptosis. Glucose 84-91 insulin Homo sapiens 204-211 18630617-1 2008 "Incretin effect" refers to increased insulin response to oral glucose as compared to i.v. Glucose 63-70 insulin Homo sapiens 38-45 18350633-0 2008 Changes of ghrelin following oral glucose tolerance test in obese children with insulin resistance. Glucose 34-41 insulin Homo sapiens 80-87 18366646-2 2008 We hypothesized that common polymorphisms in the ARNT gene might increase the susceptibility to type 2 diabetes through impaired glucose-stimulated insulin secretion. Glucose 129-136 insulin Homo sapiens 148-155 18335029-3 2008 We wondered whether insulin-operated signaling pathways modulate mitochondrial respiration via NO, to alternatively release complete glucose oxidation to CO(2) and H(2)O or to drive glucose storage to glycogen. Glucose 133-140 insulin Homo sapiens 20-27 18178160-5 2008 Increasing concentrations of glucose enhanced hBD-1 expression and these levels were further elevated after insulin treatment. Glucose 29-36 insulin Homo sapiens 108-115 18178160-6 2008 Insulin treatment also led to the up-regulation of human sodium/glucose transporter 1 (hSGLT1), which further increases intracellular glucose levels. Glucose 64-71 insulin Homo sapiens 0-7 18178160-7 2008 Thus, our findings suggest for the first time that insulin signaling is important for hBD-1 optimal expression by elevating intracellular glucose levels and by mediating gene expression. Glucose 138-145 insulin Homo sapiens 51-58 18320053-5 2008 Ambient glucose concentrations appropriately altered human insulin mRNA expression and C-peptide secretion within minutes in vitro and in vivo. Glucose 8-15 insulin Homo sapiens 59-66 18089761-6 2008 In contrast, this oxidant stress significantly inhibited the expected insulin-mediated enhancements in glucose transport, glycogen synthesis, and these signaling factors and allowed GSK-3beta to retain a more active form. Glucose 103-110 insulin Homo sapiens 70-77 18089761-7 2008 In the presence of CT-98014, a selective GSK-3 inhibitor, the ability of insulin to stimulate glucose transport and glycogen synthesis during exposure to this oxidant stress was enhanced by 20% and 39% (P < 0.05), respectively, and insulin stimulation of the phosphorylation of insulin receptor, Akt, and GSK-3 was significantly increased by 36-58% (P < 0.05). Glucose 94-101 insulin Homo sapiens 73-80 18089761-8 2008 These results indicate that an oxidant stress can directly and rapidly induce substantial insulin resistance of skeletal muscle insulin signaling, glucose transport, and glycogen synthesis. Glucose 147-154 insulin Homo sapiens 90-97 18094066-3 2008 Insulin resistance in skeletal muscle is particularly important since it is normally responsible for more than 75% of all insulin-mediated glucose disposal. Glucose 139-146 insulin Homo sapiens 0-7 18094066-3 2008 Insulin resistance in skeletal muscle is particularly important since it is normally responsible for more than 75% of all insulin-mediated glucose disposal. Glucose 139-146 insulin Homo sapiens 122-129 18245813-6 2008 Deferoxamine consistently increased the phosphorylation status of Akt/PKB and its targets FoxO1 and Gsk3beta, which mediate the effect of insulin on gluconeogenesis and glycogen synthesis, and up-regulated genes involved in glucose uptake and utilization. Glucose 224-231 insulin Homo sapiens 138-145 18292688-2 2008 Insulin resistance, a state of decreased biologic response to physiologic concentrations of insulin, is a key component of this syndrome and seems to be the result of a primary defect at the skeletal muscle glucose transporter. Glucose 207-214 insulin Homo sapiens 0-7 18292688-2 2008 Insulin resistance, a state of decreased biologic response to physiologic concentrations of insulin, is a key component of this syndrome and seems to be the result of a primary defect at the skeletal muscle glucose transporter. Glucose 207-214 insulin Homo sapiens 92-99 18438538-3 2008 The objective of associating other drugs to insulin therapy is to achieve better metabolic control lowering postprandial blood glucose levels. Glucose 127-134 insulin Homo sapiens 44-51 17466309-3 2008 RESULTS: Patients were insulin resistant as shown by higher glucose and insulin concentrations and lower muscle glucose extraction than controls. Glucose 60-67 insulin Homo sapiens 23-30 17466309-3 2008 RESULTS: Patients were insulin resistant as shown by higher glucose and insulin concentrations and lower muscle glucose extraction than controls. Glucose 112-119 insulin Homo sapiens 23-30 17560580-4 2008 Insulin sensitivity was determined with the hyperinsulinemic-euglycemic clamp, insulin secretion with the intravenous glucose tolerance test, and abdominal fat distribution with computed tomography. Glucose 118-125 insulin Homo sapiens 0-7 17956227-1 2008 One of the most important actions of insulin is the stimulation of the uptake of glucose into fat and muscle cells. Glucose 81-88 insulin Homo sapiens 37-44 18086496-8 2008 When KYO-1 was used, islets still maintained the ability to release insulin in response to glucose stimulation, and agarose capsule showed morphological integrity, and mechanical properties. Glucose 91-98 insulin Homo sapiens 68-75 17708582-1 2008 Fatty acid (FA) and glucose transport into insulin-dependent cells are impaired in insulin resistance (IR; type 2 diabetes mellitus). Glucose 20-27 insulin Homo sapiens 43-50 17708582-1 2008 Fatty acid (FA) and glucose transport into insulin-dependent cells are impaired in insulin resistance (IR; type 2 diabetes mellitus). Glucose 20-27 insulin Homo sapiens 83-90 17708582-8 2008 These results suggest that: (1) AA inhibits glucose uptake by adipocytes exposed over a short period, probably by a membrane-associated mechanism, (2) insulin-dependent AA uptake is dependent on the body mass index (BMI) of the donor and the insulin sensitivity of their adipocytes. Glucose 44-51 insulin Homo sapiens 151-158 18172783-7 2008 Despite marked impairment of endothelial function and IMV with indinavir, only modest, inconsistent reductions in measures of insulin-stimulated glucose uptake occurred. Glucose 145-152 insulin Homo sapiens 126-133 18380275-9 2008 A physiological model of the effect of intramyocellular lipid accumulation on oxidative metabolism and insulin mediated glucose uptake is proposed. Glucose 120-127 insulin Homo sapiens 103-110 18071026-7 2008 Subsequently, glucose-stimulated insulin secretion (GSIS), beta-cell apoptosis [by transferase-mediated dUTP nick-end labeling assay and Western blotting for poly(ADP-ribose) polymerase and Caspase-3 cleavage], and beta-cell proliferation (by Ki67 immunostaining) were analyzed. Glucose 14-21 insulin Homo sapiens 33-40 18279410-3 2008 Insulin sensitivity was estimated by glucose uptake during an euglycaemic-hyperinsulinaemic clamp and was calculated as the average amount of glucose (M(lbm) = mg/kg(lbm)/min) required to maintain euglycaemia. Glucose 37-44 insulin Homo sapiens 0-7 17854943-2 2008 However, because of limited availability of islet tissue, new sources of insulin producing cells that are responsive to glucose are required. Glucose 120-127 insulin Homo sapiens 73-80 18279410-3 2008 Insulin sensitivity was estimated by glucose uptake during an euglycaemic-hyperinsulinaemic clamp and was calculated as the average amount of glucose (M(lbm) = mg/kg(lbm)/min) required to maintain euglycaemia. Glucose 142-149 insulin Homo sapiens 0-7 18301088-5 2008 In this setting, a reduction of systemic glucose below 6 mmol/l with exogenous insulin has been found to exacerbate brain metabolic distress. Glucose 41-48 insulin Homo sapiens 79-86 18307456-1 2008 AIMS: To investigate whether changes in glucose concentrations during an OGTT in obese children reflect the presence of peripheral insulin resistance and/or cardiovascular risk factors more closely than single measurements of fasting plasma glucose (FPG). Glucose 40-47 insulin Homo sapiens 131-138 18307456-6 2008 During the OGTT, FPG, glucose at 60 min and area under the glucose curve correlated highly with fasting insulin. Glucose 22-29 insulin Homo sapiens 104-111 18307456-6 2008 During the OGTT, FPG, glucose at 60 min and area under the glucose curve correlated highly with fasting insulin. Glucose 59-66 insulin Homo sapiens 104-111 18290850-5 2008 The blood glucose level was assessed by fasting plasma glucose (FPG), fasting immunoreactive insulin, Homeostasis Model Assessment (HOMA) Index and hemoglobin A1c. Glucose 10-17 insulin Homo sapiens 93-100 17586504-11 2008 Insulin sensitivity was assessed by insulin tolerance test and glucose infusion rate (GIR) during euglycemic clamp studies. Glucose 63-70 insulin Homo sapiens 0-7 18269435-2 2008 Elevated glucose levels following a meal stimulate pancreatic islet beta cells to secrete insulin and islet alpha cells to downregulate production of glucagon. Glucose 9-16 insulin Homo sapiens 90-97 18335328-10 2008 Insulin sensitivity, expressed as glucose-to-insulin ratio and HOMA index resulted significantly improved after 12 weeks of treatment. Glucose 34-41 insulin Homo sapiens 0-7 18334398-7 2008 Consistent with insulin concentrations, actively administered insulin resulted in a significant decrease of blood glucose levels. Glucose 114-121 insulin Homo sapiens 16-23 18334398-7 2008 Consistent with insulin concentrations, actively administered insulin resulted in a significant decrease of blood glucose levels. Glucose 114-121 insulin Homo sapiens 62-69 18269435-3 2008 With declining glucose and insulin levels, alpha-cell production of glucagon is increased to stimulate hepatic glucose production, preventing fasting hypoglycaemia. Glucose 111-118 insulin Homo sapiens 27-34 18269435-4 2008 In type 2 diabetes mellitus (T2DM), beta-cell insulin response to glucose is blunted, including absence of early acute response, and alpha-cell response to glucose is impaired, resulting in absolute or relative hyperglucagonaemia and inappropriate hepatic glucose output that contributes to fasting hyperglycaemia. Glucose 66-73 insulin Homo sapiens 46-53 18269435-6 2008 The role of the incretin hormone glucagon-like peptide-1 (GLP-1) in regulating glucose-dependent beta-cell insulin production and glucose-dependent alpha-cell glucagon production has been used to develop GLP-1-based therapies. Glucose 79-86 insulin Homo sapiens 107-114 18089699-5 2008 OBJECTIVE: We studied the influence of glycosphingolipid storage on whole body glucose and fat metabolism by measuring insulin-mediated (IMGU) and noninsulin-mediated glucose uptake (NIMGU) and suppression of free fatty acids by insulin. Glucose 167-174 insulin Homo sapiens 150-157 19885352-1 2008 Insulin pump development started in 1978, with the first commercially available glucose sensor marketed in 1999. Glucose 80-87 insulin Homo sapiens 0-7 18310441-2 2008 Chronic exposure of islets to oleate (OA) resulted in a significant reduction in glucose-stimulated insulin secretion (GSIS) compared with control (466+/-82 vs 234+/-57 ng/microg DNA, P<0.05). Glucose 81-88 insulin Homo sapiens 100-107 18575277-1 2008 OBJECTIVE: To demonstrate a role of early insulin secretion on plasma glucose levels after different amounts of oral glucose loads in pregnant women. Glucose 70-77 insulin Homo sapiens 42-49 18575277-1 2008 OBJECTIVE: To demonstrate a role of early insulin secretion on plasma glucose levels after different amounts of oral glucose loads in pregnant women. Glucose 117-124 insulin Homo sapiens 42-49 18575277-9 2008 CONCLUSION: The limited ability of early insulin secretion to increase when glucose load increased in the pregnant women could explain the high plasma glucose levels at 2 and 3 hours of 100-g OGTT compared to those of 75-g OGTT. Glucose 151-158 insulin Homo sapiens 41-48 18540249-4 2008 Insulin sensitivity and secretion were analyzed by the stable labeled intravenous glucose tolerance test and glucose and lipid kinetics using GCMS. Glucose 82-89 insulin Homo sapiens 0-7 18540249-4 2008 Insulin sensitivity and secretion were analyzed by the stable labeled intravenous glucose tolerance test and glucose and lipid kinetics using GCMS. Glucose 109-116 insulin Homo sapiens 0-7 18045815-0 2008 Insulin action on glucose and protein metabolism during L-carnitine supplementation in maintenance haemodialysis patients. Glucose 18-25 insulin Homo sapiens 0-7 18073298-13 2008 A high 2-h glucose level is characterized by peripheral insulin resistance with a high insulin level. Glucose 11-18 insulin Homo sapiens 56-63 18073298-13 2008 A high 2-h glucose level is characterized by peripheral insulin resistance with a high insulin level. Glucose 11-18 insulin Homo sapiens 87-94 18328342-0 2008 Use of oral glucose minimal model-derived index of insulin sensitivity in subjects with early type 1 diabetes mellitus. Glucose 12-19 insulin Homo sapiens 51-58 18328342-3 2008 Therefore, in this study, we obtain estimates of insulin sensitivity from a simpler experiment, the oral glucose tolerance test (OGTT), and compare them with those from a frequently sampled intravenous glucose tolerance test (FSIGT) in a population of subjects defined as having early type 1 diabetes mellitus (abnormal 2-hour glucose on OGTT) and a group of healthy controls. Glucose 105-112 insulin Homo sapiens 49-56 18328342-6 2008 Indices of insulin sensitivity (SI) were estimated from the recently derived oral glucose minimal model and the original minimal model of glucose kinetics for the OGTT and FSIGT, respectively. Glucose 82-89 insulin Homo sapiens 11-18 18328342-6 2008 Indices of insulin sensitivity (SI) were estimated from the recently derived oral glucose minimal model and the original minimal model of glucose kinetics for the OGTT and FSIGT, respectively. Glucose 138-145 insulin Homo sapiens 11-18 18045815-7 2008 Insulin-mediated glucose disappearance was improved by L-carnitine only in those patients (n = 5) (+18 +/- 3%, P < 0.05 vs placebo group, n = 5) with greater baseline insulin resistance, selected according to the median value of insulin sensitivity before treatment. Glucose 17-24 insulin Homo sapiens 0-7 18197457-5 2008 During normal diet and after overfeeding, insulin sensitivity was measured using steady state plasma glucose (SSPG) levels. Glucose 101-108 insulin Homo sapiens 42-49 17929061-2 2008 When insulin secretion cannot be increased adequately (type I diabetes defect) to overcome insulin resistance in maintaining glucose homeostasis, hyperglycemia and glucose intolerance ensues. Glucose 125-132 insulin Homo sapiens 5-12 18286202-5 2008 PRINCIPAL FINDINGS: Here we report that hyperactivation of IRE1alpha caused by chronic high glucose treatment or IRE1alpha overexpression leads to insulin mRNA degradation in pancreatic beta-cells. Glucose 92-99 insulin Homo sapiens 147-154 17502877-5 2008 Insulin sensitivity index (ISI) was determined via 2-h oral glucose challenge; standard lipid profile was determined from fasting blood samples. Glucose 60-67 insulin Homo sapiens 0-7 18374086-4 2008 These cells were able to differentiate into insulin-producing cells in vitro and secreted C-peptide in a glucose-dependent manner. Glucose 105-112 insulin Homo sapiens 44-51 18374086-4 2008 These cells were able to differentiate into insulin-producing cells in vitro and secreted C-peptide in a glucose-dependent manner. Glucose 105-112 insulin Homo sapiens 90-99 18286202-8 2008 CONCLUSIONS/SIGNIFICANCE: These results reveal a role of IRE1alpha in insulin mRNA expression under ER stress conditions caused by chronic high glucose. Glucose 144-151 insulin Homo sapiens 70-77 18240344-7 2008 RESULTS: After the intervention of palmic acid for 24 h, the insulin-stimulated glucose transport in 3T3-L1 adipocytes was inhibited by 67%. Glucose 80-87 insulin Homo sapiens 61-68 17889380-5 2008 Furthermore, studies with isolated Type 2 diabetic islets have consistently shown both quantitative and qualitative defects of glucose-stimulated insulin secretion. Glucose 127-134 insulin Homo sapiens 146-153 17964673-1 2008 CONTEXT: The "incretin" hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), account for some 60% of the stimulation of insulin by oral glucose, but the determinants of their secretion from the small intestine are poorly understood. Glucose 70-77 insulin Homo sapiens 88-95 18274620-1 2008 The gene encoding PDX1 (pancreatic duodenum homeobox 1), the main transcription factor regulating the glucose-dependent transactivation of the insulin promoter in pancreatic beta-cells, clusters with two closely related homeobox genes (Gsh1 and Cdx2/3), all of them belonging to the ParaHox gene family. Glucose 102-109 insulin Homo sapiens 143-150 18274620-7 2008 Noticeably, several ParaHox transcription factors are able to transactivate or inhibit the insulin promoter, depending on the cell type and glucose concentration, thus suggesting their possible participation in the regulation of similar target genes, such as insulin, either by silencing or activating them, in the absence of PDX1. Glucose 140-147 insulin Homo sapiens 91-98 18274620-7 2008 Noticeably, several ParaHox transcription factors are able to transactivate or inhibit the insulin promoter, depending on the cell type and glucose concentration, thus suggesting their possible participation in the regulation of similar target genes, such as insulin, either by silencing or activating them, in the absence of PDX1. Glucose 140-147 insulin Homo sapiens 259-266 18235977-1 2008 A gene therapy-based treatment of type 1 diabetes mellitus requires the development of a surrogate beta cell that can synthesize and secrete functionally active insulin in response to physiologically relevant changes in ambient glucose levels. Glucose 228-235 insulin Homo sapiens 161-168 18235977-4 2008 After glucose concentration in the culture medium was increased from 1 mM to 10 mM, secreted insulin rose from 40.3+/-0.8 to 56.3+/-3.2 microIU/ml (STC-1-2), and from 10.8+/-0.8 to 23.6+/-2.3 microIU/ml (STC-1-14). Glucose 6-13 insulin Homo sapiens 93-100 18235977-7 2008 Our data suggested that genetically engineered K cells secrete active insulin in a glucose-regulated manner, and in vivo study showed that hyperglycemia could be reversed by implantation of the cells, suggesting that the use of genetically engineered K cells to express human insulin might provide a glucose-regulated approach to treat diabetic hyperglycemia. Glucose 83-90 insulin Homo sapiens 70-77 18235977-7 2008 Our data suggested that genetically engineered K cells secrete active insulin in a glucose-regulated manner, and in vivo study showed that hyperglycemia could be reversed by implantation of the cells, suggesting that the use of genetically engineered K cells to express human insulin might provide a glucose-regulated approach to treat diabetic hyperglycemia. Glucose 300-307 insulin Homo sapiens 276-283 18258617-8 2008 Low insulin-mediated glucose disposal was associated with low plasma adiponectin (P = 0.02) and high IHL (P = 0.0003), SAT (P = 0.02), and VAT (P = 0.04). Glucose 21-28 insulin Homo sapiens 4-11 18258617-9 2008 High IHL was the only predictor of reduced insulin-mediated suppression of hepatic glucose production (P = 0.02) and the only independent predictor of insulin-mediated glucose disposal in a multivariate analysis. Glucose 83-90 insulin Homo sapiens 43-50 18003716-3 2008 The reference standard for measuring insulin sensitivity in both humans and animals is the euglycemic glucose clamp. Glucose 102-109 insulin Homo sapiens 37-44 18056794-8 2008 We conclude that subjects at risk for Type 2 diabetes have intrinsic differences in palmitate regulation of at least two enzymes (PP2A and glycogen synthase), contributing to abnormal insulin regulation of glucose metabolism. Glucose 206-213 insulin Homo sapiens 184-191 18293245-3 2008 Intensive Insulin Therapy (IIT) describes intravenous application of insulin to sustain a defined level of blood glucose to reduce negative effects of hyperglycemia. Glucose 113-120 insulin Homo sapiens 10-17 18293245-3 2008 Intensive Insulin Therapy (IIT) describes intravenous application of insulin to sustain a defined level of blood glucose to reduce negative effects of hyperglycemia. Glucose 113-120 insulin Homo sapiens 69-76 18347650-8 2008 Specifically, we will briefly describe the mechanisms of insulin-stimulated skeletal muscle glucose uptake and the potential mediators of oxidative stress induced insulin resistance, highlight data suggesting that antioxidant compounds can have beneficial effects on skeletal muscle insulin action, and discuss potential mechanisms mediating this effect. Glucose 92-99 insulin Homo sapiens 57-64 18198833-5 2008 Preliminary experiments suggest that such amphoteric PBA-microgels have a high capacity for insulin uptake and can selectively release more insulin at higher glucose concentrations under physiological conditions via glucose-induced, "on-off" switching of electrostatic attractions between insulin and the microgel. Glucose 158-165 insulin Homo sapiens 140-147 18198833-5 2008 Preliminary experiments suggest that such amphoteric PBA-microgels have a high capacity for insulin uptake and can selectively release more insulin at higher glucose concentrations under physiological conditions via glucose-induced, "on-off" switching of electrostatic attractions between insulin and the microgel. Glucose 158-165 insulin Homo sapiens 140-147 18198833-5 2008 Preliminary experiments suggest that such amphoteric PBA-microgels have a high capacity for insulin uptake and can selectively release more insulin at higher glucose concentrations under physiological conditions via glucose-induced, "on-off" switching of electrostatic attractions between insulin and the microgel. Glucose 216-223 insulin Homo sapiens 140-147 18198833-5 2008 Preliminary experiments suggest that such amphoteric PBA-microgels have a high capacity for insulin uptake and can selectively release more insulin at higher glucose concentrations under physiological conditions via glucose-induced, "on-off" switching of electrostatic attractions between insulin and the microgel. Glucose 216-223 insulin Homo sapiens 140-147 17803698-1 2008 OBJECTIVE: Recent studies suggested that the effect of adiponectin on insulin-stimulated glucose metabolism is mediated primarily by the high molecular weight (HMW) form of adiponectin. Glucose 89-96 insulin Homo sapiens 70-77 17803698-8 2008 Delta-total adiponectin levels correlated positively with the rate of Delta-insulin-stimulated glucose disposal (R(d)) (r = 0.89) and Delta-oxidative glucose metabolism (r = 0.71) and inversely with Delta-fasting free fatty acid (FFA) levels (r = -0.69) and Delta-lipid oxidation (r = -0.73) during insulin stimulation (all P < 0.01). Glucose 95-102 insulin Homo sapiens 76-83 17803698-9 2008 Weaker correlations were found between Delta-HMW adiponectin levels and Delta-measures of glucose and lipid metabolism during insulin stimulation than with Delta-total adiponectin. Glucose 90-97 insulin Homo sapiens 126-133 17803698-10 2008 CONCLUSION: A close correlation between increased total adiponectin levels and increased insulin-stimulated glucose metabolism during pioglitzone treatment supports the hypothesis that the insulin-sensitizing effect of pioglitazone in PCOS is, at least in part, mediated by adiponectin. Glucose 108-115 insulin Homo sapiens 89-96 17803698-10 2008 CONCLUSION: A close correlation between increased total adiponectin levels and increased insulin-stimulated glucose metabolism during pioglitzone treatment supports the hypothesis that the insulin-sensitizing effect of pioglitazone in PCOS is, at least in part, mediated by adiponectin. Glucose 108-115 insulin Homo sapiens 189-196 17706318-0 2008 Model-based assessment of insulin sensitivity of glucose disposal and endogenous glucose production from double-tracer oral glucose tolerance test. Glucose 49-56 insulin Homo sapiens 26-33 17706318-0 2008 Model-based assessment of insulin sensitivity of glucose disposal and endogenous glucose production from double-tracer oral glucose tolerance test. Glucose 81-88 insulin Homo sapiens 26-33 17706318-0 2008 Model-based assessment of insulin sensitivity of glucose disposal and endogenous glucose production from double-tracer oral glucose tolerance test. Glucose 81-88 insulin Homo sapiens 26-33 17706318-1 2008 A new mathematical model of short-term glucose regulation by insulin is proposed to exploit the oral glucose tolerance test (OGTT), which is commonly used for clinical diagnosis of glucose intolerance and diabetes. Glucose 39-46 insulin Homo sapiens 61-68 17706318-1 2008 A new mathematical model of short-term glucose regulation by insulin is proposed to exploit the oral glucose tolerance test (OGTT), which is commonly used for clinical diagnosis of glucose intolerance and diabetes. Glucose 101-108 insulin Homo sapiens 61-68 17706318-6 2008 Results indicate that insulin-independent glucose clearance does not vary significantly with gender or diabetic state and that the latter strongly affects, as expected, insulin-dependent clearance (insulin sensitivity). Glucose 42-49 insulin Homo sapiens 22-29 17854954-0 2008 Higher total ghrelin levels are associated with higher insulin-mediated glucose disposal in non-diabetic maintenance hemodialysis patients. Glucose 72-79 insulin Homo sapiens 55-62 17854954-5 2008 METHODS: Total (T-Ghr) and acylated (A-Ghr) ghrelin as well as insulin-mediated glucose disposal [(M): hyperinsulinemic-euglycemic clamp] were measured in non-diabetic non-obese ambulatory MHD patients (n=19, 16 Males). Glucose 80-87 insulin Homo sapiens 63-70 17694505-9 2008 CONCLUSIONS: The reduction in postprandial glucose excursions achieved with addition of pramlintide to rapid-acting insulin in type 2 diabetes was associated with a reduction in postprandial markers of oxidative stress. Glucose 43-50 insulin Homo sapiens 116-123 17977950-3 2008 RESEARCH DESIGN AND METHODS: We determined molecular mediators of insulin signaling to glucose transport in skeletal muscle biopsies of 24 PCOS patients and 14 matched control subjects metabolically characterized by euglycemic-hyperinsulinemic clamps and indirect calorimetry, and we examined the effect of 16 weeks of treatment with pioglitazone in PCOS patients. Glucose 87-94 insulin Homo sapiens 66-73 17977950-4 2008 RESULTS: Impaired insulin-mediated total (R(d)) oxidative and nonoxidative glucose disposal (NOGD) was paralleled by reduced insulin-stimulated Akt phosphorylation at Ser473 and Thr308 and AS160 phosphorylation in muscle of PCOS patients. Glucose 75-82 insulin Homo sapiens 18-25 17977950-4 2008 RESULTS: Impaired insulin-mediated total (R(d)) oxidative and nonoxidative glucose disposal (NOGD) was paralleled by reduced insulin-stimulated Akt phosphorylation at Ser473 and Thr308 and AS160 phosphorylation in muscle of PCOS patients. Glucose 75-82 insulin Homo sapiens 125-132 17977950-7 2008 Importantly, the pioglitazone-mediated improvement in insulin-stimulated glucose metabolism, which did not fully reach normal levels, was accompanied by normalization of insulin-mediated Akt phosphorylation at Ser473 and Thr308 and AS160 phosphorylation. Glucose 73-80 insulin Homo sapiens 54-61 18000176-7 2008 After adjusting for fat mass, sCD36 and oxLDL correlated inversely with measures of insulin-stimulated glucose metabolism and positively with lipid oxidation during insulin stimulation in PCOS patients and control subjects (n = 44). Glucose 103-110 insulin Homo sapiens 84-91 18000176-12 2008 Pioglitazone treatment reduced sCD36 while improving insulin-stimulated glucose metabolism, further supporting the association between sCD36 and insulin resistance in PCOS. Glucose 72-79 insulin Homo sapiens 53-60 18000182-0 2008 Decreased non-insulin-dependent glucose clearance contributes to the rise in fasting plasma glucose in the nondiabetic range. Glucose 32-39 insulin Homo sapiens 14-21 18000182-0 2008 Decreased non-insulin-dependent glucose clearance contributes to the rise in fasting plasma glucose in the nondiabetic range. Glucose 92-99 insulin Homo sapiens 14-21 18000182-3 2008 The basal and insulin-stimulated rates of glucose appearance, glucose disappearance, and glucose clearance and the basal hepatic insulin resistance index were calculated. Glucose 42-49 insulin Homo sapiens 14-21 18000182-10 2008 During the insulin clamp, glucose disposal declined with increasing BMI (r = -0.64, P < 0.0001) and correlated with the basal glucose clearance (r = 0.39, P < 0.0001). Glucose 26-33 insulin Homo sapiens 11-18 18000182-10 2008 During the insulin clamp, glucose disposal declined with increasing BMI (r = -0.64, P < 0.0001) and correlated with the basal glucose clearance (r = 0.39, P < 0.0001). Glucose 129-136 insulin Homo sapiens 11-18 18000184-2 2008 To subject this conclusion to further validation, we evaluated the relationship between glucose tolerance categories and peripheral insulin sensitivity in a large nondiabetic population. Glucose 88-95 insulin Homo sapiens 132-139 18000184-3 2008 RESEARCH DESIGN AND METHODS: Insulin sensitivity was directly quantified by determining the steady-state plasma glucose (SSPG) concentration during an insulin suppression test in 446 nondiabetic individuals divided into four groups: normal glucose tolerance (NGT, n = 318), isolated IFG (n = 63), isolated impaired glucose tolerance (IGT, n = 33), and combined IFG and IGT (IFG/IGT, n = 32). Glucose 112-119 insulin Homo sapiens 29-36 18039816-0 2008 A candidate type 2 diabetes polymorphism near the HHEX locus affects acute glucose-stimulated insulin release in European populations: results from the EUGENE2 study. Glucose 75-82 insulin Homo sapiens 94-101 18039816-4 2008 To assess glucose-stimulated insulin release, a subgroup of 758 subjects underwent an intravenous glucose tolerance test (IVGTT). Glucose 10-17 insulin Homo sapiens 29-36 18056889-9 2008 However, the 30-min interruption of basal insulin infusion resulted in significant glucose elevation; approximately 1 mg/dl for each minute basal insulin infusion was interrupted. Glucose 83-90 insulin Homo sapiens 42-49 18080107-0 2008 Loss of 50% of excess weight using a very low energy diet improves insulin-stimulated glucose disposal and skeletal muscle insulin signalling in obese insulin-treated type 2 diabetic patients. Glucose 86-93 insulin Homo sapiens 67-74 18080107-7 2008 RESULTS: Loss of 50% EWR (20.3+/-2.2 kg from day 2 to day of 50% EWR) normalised basal EGP and improved insulin sensitivity, especially insulin-stimulated glucose disposal (18.8+/-2.0 to 39.1+/-2.8 micromol kg fat-free mass(-1) min(-1), p=0.001). Glucose 155-162 insulin Homo sapiens 136-143 18201212-3 2008 First- and second-phase insulin release were measured by means of the insulin-modified frequently sampled intravenous glucose tolerance test. Glucose 118-125 insulin Homo sapiens 70-77 18206413-1 2008 BACKGROUND: Day-to-day glucose variability may cause difficulty for patients trying to adjust their insulin dosages and for healthcare providers when they have to make recommendations. Glucose 23-30 insulin Homo sapiens 100-107 18227473-5 2008 On the contrary, treatment with most insulin secretagogues has been associated with increased beta-cell apoptosis, reduced responsiveness to high glucose, and impairment of myocardial function during ischemic conditions. Glucose 146-153 insulin Homo sapiens 37-44 18227473-7 2008 Insulin treatment, especially with rapid-acting analogs, has been demonstrated to successfully control postprandial glucose excursions. Glucose 116-123 insulin Homo sapiens 0-7 18275363-0 2008 Glucose or carbohydrate supply during continuous intravenous insulin administration in the intensive care unit. Glucose 0-7 insulin Homo sapiens 61-68 18290857-5 2008 Those cases due to recent diagnosis of diabetes, inadequate treatment with diet, oral glucose-lowering agents or insulin, exacerbation of co-existent medical problems, recent stressful life-events and missed clinic appointments were all associated with significant improvement in HbA(1c) at 12 months. Glucose 86-93 insulin Homo sapiens 113-120 18290864-5 2008 A linear fall in plasma glucose to a nadir of 2.2 mmol/l within 60 min was induced by insulin infusion immediately after sleep onset ("early hypo") or after about 3.5 h of sleep ("late hypo"). Glucose 24-31 insulin Homo sapiens 86-93 18640585-2 2008 Multiple insulin secretory defects are present, including absence of pulsatility, loss of early phase of insulin secretion after glucose, decreased basal and stimulated plasma insulin concentrations, excess in prohormone secretion, and progressive decrease in insulin secretory capacity with time. Glucose 129-136 insulin Homo sapiens 9-16 18640588-1 2008 Incretin hormones are defined as intestinal hormones released in response to nutrient ingestion, which potentiate the glucose-induced insulin response. Glucose 118-125 insulin Homo sapiens 134-141 18640589-4 2008 GLP-1 improves glucose-stimulated insulin secretion, restores glucose competence in glucose-resistant beta-cells, and stimulates insulin gene expression and biosynthesis. Glucose 15-22 insulin Homo sapiens 34-41 18389389-9 2008 We have demonstrated in the present study the predominant role of beta cell dysfunction as compared to that of insulin resistance in the deterioration of glucose tolerance in non-obese women. Glucose 154-161 insulin Homo sapiens 111-118 17972239-12 2008 Obese normal glucose tolerant subjects were more insulin resistant than lean IFG patients. Glucose 13-20 insulin Homo sapiens 49-56 17972239-15 2008 Considering that both obesity and insulin resistance are independently associated to an increased cardiovascular risk, all overweight subjects, even with normal FPG, should be referred for OGTT evaluation to define glucose tolerance status in order to enforce adequate preventive actions. Glucose 215-222 insulin Homo sapiens 34-41 18190526-1 2008 Insulin stimulates glucose uptake by inducing translocation of glucose transporter 4 (GLUT4) from intracellular resides to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 18270458-0 2008 Insulin response to oral glucose load is associated with coronary artery disease in subjects with normal glucose tolerance. Glucose 25-32 insulin Homo sapiens 0-7 18270458-0 2008 Insulin response to oral glucose load is associated with coronary artery disease in subjects with normal glucose tolerance. Glucose 105-112 insulin Homo sapiens 0-7 18270458-2 2008 We investigated the association between secretion patterns of insulin after oral glucose load and the severity of coronary artery disease (CAD) in patients with normal glucose tolerance (NGT). Glucose 81-88 insulin Homo sapiens 62-69 18460477-8 2008 There was a strong negative correlation between fasting glucose and insulin levels at baseline and in the magnitude of change after the study (r = -0.93 and r = -0.85 respectively; p < 0.01). Glucose 56-63 insulin Homo sapiens 68-75 18029467-6 2008 Insulin-mediated peripheral glucose uptake was not different between patients and controls. Glucose 28-35 insulin Homo sapiens 0-7 18042649-3 2008 METHODS: In a group of 136 young adults, aged 18-24 yr, insulin sensitivity and disposition index were determined by frequent sampling iv glucose tolerance test. Glucose 138-145 insulin Homo sapiens 56-63 18056775-9 2008 RESULTS: Fasting decreased insulin-mediated peripheral glucose uptake by 46% after 60 h (P = 0.03). Glucose 55-62 insulin Homo sapiens 27-34 18066630-8 2008 Intensifications of scheduled and sliding scale insulin, but not oral medications, were associated with a 11.1 mg/dL (p < 0.0001) and 12.2 mg/dL (p < 0.0001) reduction in the average daily glucose, respectively. Glucose 195-202 insulin Homo sapiens 48-55 17497735-12 2008 The TCP microsphere based delayed release formulation of insulin has effected a decrease in elevated glucose level in induced diabetic rats, establishing its feasibility towards the development of a noninvasive delivery device. Glucose 101-108 insulin Homo sapiens 57-64 18206684-6 2008 (3) Insulin sensitivity was determined with the insulin-modified frequently sampled intravenous glucose tolerance test. Glucose 96-103 insulin Homo sapiens 4-11 18206684-6 2008 (3) Insulin sensitivity was determined with the insulin-modified frequently sampled intravenous glucose tolerance test. Glucose 96-103 insulin Homo sapiens 48-55 19190726-1 2008 As the "artificial pancreas" becomes closer to reality, automated insulin delivery based on real-time glucose measurements becomes feasible for people with diabetes. Glucose 102-109 insulin Homo sapiens 66-73 17717074-1 2008 Despite being one of the first recognized targets of insulin action, the acceleration of glucose transport into muscle and fat tissue remains one of the most enigmatic processes in the insulin action cascade. Glucose 89-96 insulin Homo sapiens 53-60 17717074-1 2008 Despite being one of the first recognized targets of insulin action, the acceleration of glucose transport into muscle and fat tissue remains one of the most enigmatic processes in the insulin action cascade. Glucose 89-96 insulin Homo sapiens 185-192 17717074-3 2008 The complexity in deciphering the molecular blueprint of insulin regulation of glucose transport arises because it represents a convergence of two convoluted biological systems-vesicular transport and signal transduction. Glucose 79-86 insulin Homo sapiens 57-64 18261396-5 2008 Current data indicate that this insulin is at least as effective as the sc in regards to glucose control. Glucose 89-96 insulin Homo sapiens 32-39 17579617-14 2008 CONCLUSIONS: Spasticity may counteract the risk of diabetes by inducing an insulin-independent glucose uptake. Glucose 95-102 insulin Homo sapiens 75-82 17693932-0 2008 Insulin regulates macrophage activation through activin A. UNLABELLED: Strict control of serum glucose with insulin has been associated with a reduction in the development of multiple organ dysfunction syndrome potentially through alterations in macrophage activation. Glucose 95-102 insulin Homo sapiens 0-7 17693932-0 2008 Insulin regulates macrophage activation through activin A. UNLABELLED: Strict control of serum glucose with insulin has been associated with a reduction in the development of multiple organ dysfunction syndrome potentially through alterations in macrophage activation. Glucose 95-102 insulin Homo sapiens 108-115 18035054-1 2008 It is well known that the activation of AMP-activated protein kinase (AMPK) represses insulin gene expression and glucose-stimulated insulin secretion. Glucose 114-121 insulin Homo sapiens 133-140 18035054-5 2008 These results demonstrate that the expressions of BETA2 and insulin gene are positively regulated by glucose and negatively by AMPK. Glucose 101-108 insulin Homo sapiens 60-67 18205930-7 2008 We then introduced an algorithm for intensive insulin therapy; aiming for arterial blood-glucose at 4.4 - 6.1 mmol/L. Glucose 89-96 insulin Homo sapiens 46-53 18197261-7 2008 These islet-like cell clusters were shown to contain human C-peptide and release human insulin in response to physiological glucose levels. Glucose 124-131 insulin Homo sapiens 87-94 18361065-6 2008 CONCLUSION: With satisfied fasting blood glucose level and fewer episode of hypoglycemia, perioperative glycemic control by insulin glargine in type 2 diabetic patients is safe, effective, and convenient. Glucose 41-48 insulin Homo sapiens 124-131 18271455-11 2008 Insulin therapy should be initiated before conception in women with preconceptional type 2 diabetes mellitus that requires glucose-lowering therapy. Glucose 123-130 insulin Homo sapiens 0-7 17618629-5 2008 Similar to the regulation of mammalian insulin, we found that increases of glucose (1-70 mM) and arginine (0.4-25 mM) induced insulin secretion. Glucose 75-82 insulin Homo sapiens 39-46 17662254-0 2008 Bridging the gap between protein carboxyl methylation and phospholipid methylation to understand glucose-stimulated insulin secretion from the pancreatic beta cell. Glucose 97-104 insulin Homo sapiens 116-123 17662254-1 2008 Recent findings have implicated post-translational modifications at C-terminal cysteines [e.g., methylation] of specific proteins [e.g., G-proteins] in glucose-stimulated insulin secretion [GSIS]. Glucose 152-159 insulin Homo sapiens 171-178 18286202-7 2008 Islets from mice heterozygous for IRE1alpha retain expression of more insulin mRNA after chronic high glucose treatment than do their wild-type littermates. Glucose 102-109 insulin Homo sapiens 70-77 18171435-1 2008 Individuals with insulin resistance are characterized by impaired insulin action on whole-body glucose uptake, in part due to impaired insulin-stimulated glucose uptake into skeletal muscle. Glucose 95-102 insulin Homo sapiens 17-24 17947242-5 2008 The insulin-regulated trafficking of GLUT4 to the plasma membrane serves to facilitate glucose uptake in adipocytes, and both SNAP23 and the exocyst have been implicated in this process. Glucose 87-94 insulin Homo sapiens 4-11 17947242-6 2008 In this study, depletion of Snapin in adipocytes using RNA interference inhibits insulin-stimulated glucose uptake. Glucose 100-107 insulin Homo sapiens 81-88 18167556-11 2008 UCP-3 overexpression improved glucose-stimulated insulin secretion. Glucose 30-37 insulin Homo sapiens 49-56 18167556-13 2008 Increased expression of UCP-2 and decreased expression of UCP-3 in humans with chronic hyperglycemia may contribute to impaired glucose-stimulated insulin secretion. Glucose 128-135 insulin Homo sapiens 147-154 18728914-13 2008 CONCLUSION: The 24-hour glucose profile performed after the diagnosis of GDM clearly distinguishes between low-risk (diet-treated) and high-risk (insulin-treated) for fetal macrosomia in GDM pregnancies. Glucose 24-31 insulin Homo sapiens 146-153 18171435-1 2008 Individuals with insulin resistance are characterized by impaired insulin action on whole-body glucose uptake, in part due to impaired insulin-stimulated glucose uptake into skeletal muscle. Glucose 154-161 insulin Homo sapiens 17-24 19163412-6 2008 Results show that the two most recent blood glucose measurements and the slope of recent changes in blood glucose concentration with respect to the change in insulin infusion are the most informative features. Glucose 106-113 insulin Homo sapiens 158-165 21607228-4 2008 Hypotension persisted with the development of progressive metabolic acidosis despite increasing inotropic support, haemofiltration and high dose insulin-dextrose infusions. Glucose 153-161 insulin Homo sapiens 145-152 18082485-2 2008 Thus, targeting normal fasting glucose levels with insulin may reduce CV events. Glucose 31-38 insulin Homo sapiens 51-58 17957034-8 2008 The hyperinsulinemic euglycemic glucose clamp and the insulin suppression test directly assess insulin-mediated glucose utilization under steady-state conditions that are both labor and time intensive. Glucose 32-39 insulin Homo sapiens 9-16 17957034-10 2008 Finally, simple surrogate indexes for insulin sensitivity/resistance are available (e.g., QUICKI, HOMA, 1/insulin, Matusda index) that are derived from blood insulin and glucose concentrations under fasting conditions (steady state) or after an oral glucose load (dynamic). Glucose 170-177 insulin Homo sapiens 38-45 17957034-11 2008 In particular, the quantitative insulin sensitivity check index (QUICKI) has been validated extensively against the reference standard glucose clamp method. Glucose 135-142 insulin Homo sapiens 32-39 17957036-5 2008 Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Glucose 86-93 insulin Homo sapiens 58-65 18167097-5 2008 Insulin sensitivity was calculated with proxies derived from basal serum insulin and plasma glucose concentrations. Glucose 92-99 insulin Homo sapiens 0-7 18481923-2 2008 In addition to glucose, the major nutrient factor, inputs from the nervous system, humoral components, and cell-cell communication within the islet of Langerhans act together to guarantee the release of appropriate amounts of insulin in response to changes in blood glucose levels. Glucose 15-22 insulin Homo sapiens 226-233 18171425-8 2008 The insulin promoter is both positively and negatively regulated by glucose and other nutrients. Glucose 68-75 insulin Homo sapiens 4-11 18481923-2 2008 In addition to glucose, the major nutrient factor, inputs from the nervous system, humoral components, and cell-cell communication within the islet of Langerhans act together to guarantee the release of appropriate amounts of insulin in response to changes in blood glucose levels. Glucose 266-273 insulin Homo sapiens 226-233 18572755-6 2008 The homeostasis model for assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Glucose 97-104 insulin Homo sapiens 40-47 18171425-9 2008 Exposure to glucose for minutes to hours causes an increase in the rate of insulin gene transcription. Glucose 12-19 insulin Homo sapiens 75-82 18171425-10 2008 In contrast, exposure to elevated glucose for 48 h or more results in inhibition of the insulin gene promoter. Glucose 34-41 insulin Homo sapiens 88-95 18171430-1 2008 Insulin stimulates glucose uptake into muscle and adipose tissues through glucose transporter 4 (GLUT4). Glucose 19-26 insulin Homo sapiens 0-7 18998755-3 2008 These actions complement those of insulin to regulate blood glucose concentrations. Glucose 60-67 insulin Homo sapiens 34-41 18171432-1 2008 Insulin stimulates glucose uptake into the target tissues of fat and muscle by recruiting or translocating Glut4 glucose transport proteins to their functional location at the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 18171432-1 2008 Insulin stimulates glucose uptake into the target tissues of fat and muscle by recruiting or translocating Glut4 glucose transport proteins to their functional location at the cell surface. Glucose 113-120 insulin Homo sapiens 0-7 18260137-2 2008 Together with insulin, it is an important regulator of glucose metabolism. Glucose 55-62 insulin Homo sapiens 14-21 19141955-12 2008 Evaluation of insulin production by enzyme linked immuno sorbent assay (ELISA) showed trends of dose and time dependency in all groups, with the highest levels in cells grown at 5% glucose and treated with 5% glucose. Glucose 181-188 insulin Homo sapiens 14-21 19141955-12 2008 Evaluation of insulin production by enzyme linked immuno sorbent assay (ELISA) showed trends of dose and time dependency in all groups, with the highest levels in cells grown at 5% glucose and treated with 5% glucose. Glucose 209-216 insulin Homo sapiens 14-21 17905511-0 2008 First phase release coefficient of insulin in subjects with normal glucose tolerance on glucose infusion analyzed by computer simulation. Glucose 67-74 insulin Homo sapiens 35-42 17905511-0 2008 First phase release coefficient of insulin in subjects with normal glucose tolerance on glucose infusion analyzed by computer simulation. Glucose 88-95 insulin Homo sapiens 35-42 17905511-1 2008 We report here a mathematical model using computer simulation to solve the phase fractionation coefficient (f) of instantaneous insulin release on glucose infusion. Glucose 147-154 insulin Homo sapiens 128-135 17905511-4 2008 In addition, the value of the factor f was shown to be independent of both the glucose infusion method and the non-insulin-dependent uptake of glucose. Glucose 143-150 insulin Homo sapiens 115-122 17761018-0 2008 Decreased levels of uric acid after oral glucose challenge is associated with triacylglycerol levels and degree of insulin resistance. Glucose 41-48 insulin Homo sapiens 115-122 17971659-8 2008 CONCLUSIONS: Proinsulin is a strong and statistically highly significant pre- dictor of coronary atherosclerosis independent of the other major risk factors including age, body mass index, blood pressure, fasting blood glucose, and blood lipid. Glucose 219-226 insulin Homo sapiens 13-23 17900551-8 2008 SdLDLC also decreased and was a minimum at 2 h after glucose ingestion and increased to the baseline by 3 h. The sdLDLC decrease was seen while serum insulin level was high. Glucose 53-60 insulin Homo sapiens 150-157 18345710-4 2008 This finding, coupled with epidemiological evidence that elevated postprandial glucose concentration is an independent risk factor for cardiovascular disease (CVD), and is associated with a greater CVD risk than elevated fasting glucose, points to the need to monitor and target postprandial glucose, as well as fasting glucose and HbA(1c) levels, when optimizing insulin therapy for patients with type 2 diabetes. Glucose 79-86 insulin Homo sapiens 364-371 18076356-0 2008 Assay-dependent variability of serum insulin levels during oral glucose tolerance test: influence on reference intervals for insulin and on cut-off values for insulin sensitivity indices. Glucose 64-71 insulin Homo sapiens 37-44 18076356-1 2008 BACKGROUND: The oral glucose tolerance test (oGTT) is the most common method to estimate indices of insulin sensitivity in clinical as well as in epidemiological studies. Glucose 21-28 insulin Homo sapiens 100-107 18076356-10 2008 At 120 min post glucose, gender was the relevant influencing factor on insulin levels of the LIA (r=0.40, p<0.001), AD (r=0.37, p<0.01) and EL (r=0.40 p<0.001) method. Glucose 16-23 insulin Homo sapiens 71-78 18345710-6 2008 Among the available rapid-acting insulin analogues, insulin lispro has been shown to reduce postprandial glucose concentrations to a significantly greater degree than regular human insulin in patients with type 2 diabetes. Glucose 105-112 insulin Homo sapiens 33-40 18345710-6 2008 Among the available rapid-acting insulin analogues, insulin lispro has been shown to reduce postprandial glucose concentrations to a significantly greater degree than regular human insulin in patients with type 2 diabetes. Glucose 105-112 insulin Homo sapiens 52-59 18345710-6 2008 Among the available rapid-acting insulin analogues, insulin lispro has been shown to reduce postprandial glucose concentrations to a significantly greater degree than regular human insulin in patients with type 2 diabetes. Glucose 105-112 insulin Homo sapiens 52-59 18345710-7 2008 Moreover, premixed combinations of insulin lispro with the longer acting analogue neutral insulin lispro protamine suspension in 25% : 75% or 50% : 50% combinations are significantly more effective in lowering postprandial blood glucose concentrations than premixed regular human insulin plus neutral protamine Hagedorn (NPH) 30% : 70%. Glucose 229-236 insulin Homo sapiens 35-42 18345710-7 2008 Moreover, premixed combinations of insulin lispro with the longer acting analogue neutral insulin lispro protamine suspension in 25% : 75% or 50% : 50% combinations are significantly more effective in lowering postprandial blood glucose concentrations than premixed regular human insulin plus neutral protamine Hagedorn (NPH) 30% : 70%. Glucose 229-236 insulin Homo sapiens 90-97 18698880-3 2008 Insulin aspart and insulin lispro have nearly identical pharmacokinetic and pharmacodynamic profiles and provide better postprandial glucose control and less hypoglycaemia (primarily nocturnal and severe hypoglycaemia in type 1 diabetes mellitus) than regular insulin. Glucose 133-140 insulin Homo sapiens 0-7 19410162-2 2008 Both IFG and IGT exhibit elevated glucose levels that are not sufficient to be classified as diabetes but that represent the development of insulin resistance. Glucose 34-41 insulin Homo sapiens 140-147 19410163-3 2008 Addition of insulin to sulfonylurea therapy, when maximal sulfonylurea does not adequately maintain fasting plasma glucose levels at < 108 mg/dL, has been found to be more effective than initiating insulin therapy after oral agents have failed to maintain glycemic control. Glucose 115-122 insulin Homo sapiens 12-19 18076215-7 2008 The pharmacodynamic profile of insulin glulisine reflects the absorption kinetics by demonstrating a greater rate of glucose utilization, which is completed earlier and at equipotency on a molar base compared with regular human insulin. Glucose 117-124 insulin Homo sapiens 31-38 18076215-8 2008 Dose-proportionality in glucose utilization has been established for insulin glulisine in patients with type 1 diabetes mellitus in the dose range of 0.075-0.15 U/kg, and a less than dose-proportional increase above 0.15 U/kg, indicating saturation of insulin action in general. Glucose 24-31 insulin Homo sapiens 69-76 18076215-8 2008 Dose-proportionality in glucose utilization has been established for insulin glulisine in patients with type 1 diabetes mellitus in the dose range of 0.075-0.15 U/kg, and a less than dose-proportional increase above 0.15 U/kg, indicating saturation of insulin action in general. Glucose 24-31 insulin Homo sapiens 252-259 18076215-10 2008 Furthermore, the early insulin exposure and action of insulin glulisine were slightly -- but consistently -- greater than those of insulin lispro in healthy volunteers across a wide range of BMIs.Meal studies in patients with type 1 diabetes show that insulin glulisine provides better postprandial blood glucose control than regular human insulin when administered immediately pre-meal, and equivalent control when given after the meal. Glucose 305-312 insulin Homo sapiens 54-61 18076215-10 2008 Furthermore, the early insulin exposure and action of insulin glulisine were slightly -- but consistently -- greater than those of insulin lispro in healthy volunteers across a wide range of BMIs.Meal studies in patients with type 1 diabetes show that insulin glulisine provides better postprandial blood glucose control than regular human insulin when administered immediately pre-meal, and equivalent control when given after the meal. Glucose 305-312 insulin Homo sapiens 54-61 18076215-10 2008 Furthermore, the early insulin exposure and action of insulin glulisine were slightly -- but consistently -- greater than those of insulin lispro in healthy volunteers across a wide range of BMIs.Meal studies in patients with type 1 diabetes show that insulin glulisine provides better postprandial blood glucose control than regular human insulin when administered immediately pre-meal, and equivalent control when given after the meal. Glucose 305-312 insulin Homo sapiens 54-61 18076215-10 2008 Furthermore, the early insulin exposure and action of insulin glulisine were slightly -- but consistently -- greater than those of insulin lispro in healthy volunteers across a wide range of BMIs.Meal studies in patients with type 1 diabetes show that insulin glulisine provides better postprandial blood glucose control than regular human insulin when administered immediately pre-meal, and equivalent control when given after the meal. Glucose 305-312 insulin Homo sapiens 54-61 18698880-3 2008 Insulin aspart and insulin lispro have nearly identical pharmacokinetic and pharmacodynamic profiles and provide better postprandial glucose control and less hypoglycaemia (primarily nocturnal and severe hypoglycaemia in type 1 diabetes mellitus) than regular insulin. Glucose 133-140 insulin Homo sapiens 19-26 18698880-5 2008 Insulin glargine was the first basal analogue approved for clinical use and has shown better fasting glucose control and less risk of hypoglycaemia than conventional human neutral protamine Hagedorn (NPH) insulin. Glucose 101-108 insulin Homo sapiens 0-7 18466639-0 2008 Pro/con debate: Is intensive insulin therapy targeting tight blood glucose control of benefit in critically ill patients? Glucose 67-74 insulin Homo sapiens 29-36 17942356-3 2008 The present study was undertaken to investigate whether a NO donor or a nitric oxide synthase (NOS) inhibitor influences basal or insulin-mediated glucose uptake in vivo in skeletal muscles of chickens. Glucose 147-154 insulin Homo sapiens 130-137 19055829-9 2008 RESULTS: Mean blood glucose levels in the Insulin group were lower compared to the Control group from rewarming on cardiopulmonary bypass onwards until ICU discharge (p < 0.0001). Glucose 20-27 insulin Homo sapiens 42-49 18218076-14 2008 Future studies might detect relevant metabolic derangements when insulin treatment starts at low cerebral glucose levels, and may allow us to design a strategy for avoidance of insulin-induced metabolic crisis in SAH patients. Glucose 106-113 insulin Homo sapiens 65-72 18218076-2 2008 The aim of this study was to determine the effect of insulin treatment for glucose control on cerebral metabolism in SAH patients. Glucose 75-82 insulin Homo sapiens 53-60 18423062-2 2008 Targeted insulin therapy for glycemic control might, on the contrary, have harmful effects by causing too low cerebral glucose levels. Glucose 119-126 insulin Homo sapiens 9-16 18218076-7 2008 Twenty-four patients were treated with insulin for glucose control. Glucose 51-58 insulin Homo sapiens 39-46 18218076-9 2008 Although blood glucose remained stable after initiation of insulin infusion, insulin induced a significant decrease in cerebral glucose at 3 hours after onset of the infusion until the end of the observation period (P < 0.05), reflecting high glucose utilization. Glucose 128-135 insulin Homo sapiens 77-84 18423062-3 2008 The study published by Schlenk and colleagues in the previous issue of Critical Care shows that insulin caused a significant decrease in the interstitial cerebral glucose concentration although the blood glucose level remained unaffected. Glucose 163-170 insulin Homo sapiens 96-103 18691043-2 2008 Visfatin binds to the insulin receptor at a site distinct from that of insulin and causes hypoglycaemia by reducing glucose release from liver cells and stimulating glucose utilization in adipocytes and myocytes. Glucose 116-123 insulin Homo sapiens 22-29 18423062-3 2008 The study published by Schlenk and colleagues in the previous issue of Critical Care shows that insulin caused a significant decrease in the interstitial cerebral glucose concentration although the blood glucose level remained unaffected. Glucose 204-211 insulin Homo sapiens 96-103 17510915-5 2008 Fasting glucose and insulin were used to estimate insulin sensitivity using the QUICKI index. Glucose 8-15 insulin Homo sapiens 50-57 18691043-2 2008 Visfatin binds to the insulin receptor at a site distinct from that of insulin and causes hypoglycaemia by reducing glucose release from liver cells and stimulating glucose utilization in adipocytes and myocytes. Glucose 165-172 insulin Homo sapiens 22-29 19128226-2 2008 All these metabolic disorders are characterized by insulin resistance, defined as decreased sensitivity and/or responsiveness to metabolic actions of insulin promoting glucose disposal. Glucose 168-175 insulin Homo sapiens 51-58 19128226-2 2008 All these metabolic disorders are characterized by insulin resistance, defined as decreased sensitivity and/or responsiveness to metabolic actions of insulin promoting glucose disposal. Glucose 168-175 insulin Homo sapiens 150-157 17914030-5 2008 In type 1 diabetes, glucose utilization increased with increasing plasma insulin and decreasing FFA levels. Glucose 20-27 insulin Homo sapiens 73-80 17909087-5 2008 From the FSIGT, the acute insulin response to glucose (AIR(g)) and insulin sensitivity index (S(I)) were determined and used to compute the disposition index (AIR(g) x S(I)) as a measure of beta-cell function. Glucose 46-53 insulin Homo sapiens 26-33 17914030-9 2008 However, its myocardial glucose and fatty acid metabolism still responds to changes in plasma insulin and plasma FFA levels. Glucose 24-31 insulin Homo sapiens 94-101 17914032-4 2008 Insulin-induced stimulation of glucose disappearance did not differ before and after treatment with either pioglitazone (23 +/- 3 vs. 24 +/- 2 micromol x kg(-1) x min(-1)) or metformin (22 +/- 2 vs. 24 +/- 3 micromol x kg(-1) x min(-1)). Glucose 31-38 insulin Homo sapiens 0-7 17914032-5 2008 In contrast, pioglitazone enhanced (P < 0.01) insulin-induced suppression of both glucose production (6.0 +/- 1.0 vs. 0.2 +/- 1.6 micromol x kg(-1) x min(-1)) and gluconeogenesis (n = 11; 4.5 +/- 0.9 vs. 0.8 +/- 1.2 micromol x kg(-1) x min(-1)). Glucose 85-92 insulin Homo sapiens 49-56 17914032-9 2008 On the other hand, both drugs have comparable effects on insulin-induced stimulation of glucose uptake. Glucose 88-95 insulin Homo sapiens 57-64 17936398-10 2008 Treatments with insulin and TNFalpha as well as stearic acid, a saturated free fatty acid, upregulated RELMbeta expression, while d-glucose downregulated RELMbeta. Glucose 130-139 insulin Homo sapiens 16-23 17921356-11 2008 Elevated flux is associated with greater visceral adiposity, REE, and insulin resistance of glucose. Glucose 92-99 insulin Homo sapiens 70-77 17942180-0 2008 New insulin sensitivity index from the oral glucose tolerance test. Glucose 44-51 insulin Homo sapiens 4-11 17942180-3 2008 The new insulin sensitivity index: oral glucose insulin sensitivity index (GSI) was calculated from five sets of plasma glucose and insulin levels obtained at 0, 30, 60, 90 and 120 min during OGTT using a formula based on an autoregressive model. Glucose 40-47 insulin Homo sapiens 8-15 17942180-3 2008 The new insulin sensitivity index: oral glucose insulin sensitivity index (GSI) was calculated from five sets of plasma glucose and insulin levels obtained at 0, 30, 60, 90 and 120 min during OGTT using a formula based on an autoregressive model. Glucose 40-47 insulin Homo sapiens 48-55 18199128-10 2008 In the normal control subjects, the SNP +5388 C>T was associated with serum C-peptide levels both fasting and 2 h after an oral glucose tolerance test (P = 0.0162 and P = 0.0075, respectively). Glucose 131-138 insulin Homo sapiens 79-88 18008059-8 2008 Insulin suppression of glucose rate of appearance and serum NEFA was significantly impaired in the high liver fat group. Glucose 23-30 insulin Homo sapiens 0-7 18199133-3 2008 The insulin sensitivity index (S(I)) was assessed by Bergman"s minimal model method with FSIGTT; insulin secretion was determined by acute insulin response to glucose (AIRg). Glucose 159-166 insulin Homo sapiens 97-104 18267999-2 2008 Unfortunately, the intensive insulin therapy required to achieve tight glucose control is also associated with a significantly increased risk of developing hypoglycemia. Glucose 71-78 insulin Homo sapiens 29-36 18268000-2 2008 The more recent view of diabetes as a disease that affects multiple hormones, including insulin, has led to the development of therapies more broadly aimed at restoring glucose homeostasis by correcting abnormalities in other glucoregulatory hormones, including amylin. Glucose 169-176 insulin Homo sapiens 88-95 17973096-8 2008 CONCLUSIONS/INTERPRETATION: The endogenous insulin production achieved by islet transplantation, combined with optimal insulin therapy, was sufficient for maintaining near-normal glucose levels. Glucose 179-186 insulin Homo sapiens 43-50 17973096-8 2008 CONCLUSIONS/INTERPRETATION: The endogenous insulin production achieved by islet transplantation, combined with optimal insulin therapy, was sufficient for maintaining near-normal glucose levels. Glucose 179-186 insulin Homo sapiens 119-126 17960360-10 2008 By contrast, adiponectin was secreted at threefold higher rates by visceral than by subcutaneous adipocytes while visceral adipocytes also showed two- to threefold higher insulin-stimulated glucose uptake. Glucose 190-197 insulin Homo sapiens 171-178 18273540-4 2008 Insulin resistance was comparatively evaluated by an euglycemic hyperinsulinemic glucose clamp (M value, mg/m(2) per minute) or by a 75g-oral glucose tolerance test (120-min immunoreactive insulin; 120" IRI, pmol/l). Glucose 81-88 insulin Homo sapiens 0-7 17965850-0 2008 Metal-activated C-peptide facilitates glucose clearance and the release of a nitric oxide stimulus via the GLUT1 transporter. Glucose 38-45 insulin Homo sapiens 16-25 17965850-8 2008 The increase in ATP release from the erythrocytes is due to metal-activated C-peptide stimulation of glucose transfer into the erythrocytes via the GLUT1 transporter. Glucose 101-108 insulin Homo sapiens 76-85 17965850-9 2008 In the presence of C-peptide complexed to Cr3+, the amount of glucose transferred into the erythrocyte increased by 31%. Glucose 62-69 insulin Homo sapiens 19-28 18238741-6 2008 The mean glucose concentration that triggered initiation of insulin treatment was 262 mg/dL, which is significantly higher (P<.001) than levels recommended by the American Diabetes Association (ADA) and the American College of Endocrinology (ACE). Glucose 9-16 insulin Homo sapiens 60-67 18389076-0 2008 Influence of C-peptide on glucose utilisation. Glucose 26-33 insulin Homo sapiens 13-22 18389076-3 2008 Moreover, there is evidence that C-peptide decreases glomerular hyperfiltration and increases glucose utilisation. Glucose 94-101 insulin Homo sapiens 33-42 18196905-4 2008 The insulin resistance was calculated by the measurement of fasting serum glucose and insulin levels, serum insulin response to an oral glucose tolerance test and homeostasis model assessment. Glucose 74-81 insulin Homo sapiens 4-11 18196905-4 2008 The insulin resistance was calculated by the measurement of fasting serum glucose and insulin levels, serum insulin response to an oral glucose tolerance test and homeostasis model assessment. Glucose 136-143 insulin Homo sapiens 4-11 18196937-16 2008 A linear relationship between oligomenorrhea, family history of diabetes, tonic LH, high fasting serum insulin levels, insulin resistance and an abnormal glucose tolerance test was revealed, keeping intrafamily marriage and BMI as dependent variables. Glucose 154-161 insulin Homo sapiens 103-110 18196937-16 2008 A linear relationship between oligomenorrhea, family history of diabetes, tonic LH, high fasting serum insulin levels, insulin resistance and an abnormal glucose tolerance test was revealed, keeping intrafamily marriage and BMI as dependent variables. Glucose 154-161 insulin Homo sapiens 119-126 18085503-4 2008 Insulin sensitivity was assessed at the end of experimental period by measuring glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during oral glucose tolerance test. Glucose 80-87 insulin Homo sapiens 0-7 18085503-4 2008 Insulin sensitivity was assessed at the end of experimental period by measuring glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during oral glucose tolerance test. Glucose 80-87 insulin Homo sapiens 88-95 18085503-4 2008 Insulin sensitivity was assessed at the end of experimental period by measuring glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during oral glucose tolerance test. Glucose 80-87 insulin Homo sapiens 168-175 18085503-4 2008 Insulin sensitivity was assessed at the end of experimental period by measuring glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during oral glucose tolerance test. Glucose 156-163 insulin Homo sapiens 0-7 18085503-4 2008 Insulin sensitivity was assessed at the end of experimental period by measuring glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during oral glucose tolerance test. Glucose 156-163 insulin Homo sapiens 88-95 18310964-4 2008 Insulin sensitivity was expressed as the amount of glucose infused during the last 30 minutes (glucose infusion rate, GIR) in mg/Kg/min. Glucose 51-58 insulin Homo sapiens 0-7 18547952-5 2008 RESULTS: Children were classified into quartiles of insulin sensitivity based on their glucose AUC/insulin AUC index. Glucose 87-94 insulin Homo sapiens 52-59 18437199-6 2008 Insulin pumps are designed to create artificial insulin perfusion while they largely rely on the blood glucose profile measurements and these measurements are achieved by one or more blood glucose sensors. Glucose 103-110 insulin Homo sapiens 0-7 18437199-9 2008 Controlling the amount of exogenous insulin to suppress the blood glucose levels requires complicated computations. Glucose 66-73 insulin Homo sapiens 36-43 18310964-4 2008 Insulin sensitivity was expressed as the amount of glucose infused during the last 30 minutes (glucose infusion rate, GIR) in mg/Kg/min. Glucose 95-102 insulin Homo sapiens 0-7 18306020-3 2008 Continuous intravenous infusion of insulin and volume loading with normal saline gradually achieved normalization of the serum glucose level and hemodynamic stability. Glucose 127-134 insulin Homo sapiens 35-42 18318957-4 2008 The dissociated islet cells formed tight cell clusters containing the normal insulin secretion against glucose concentration and the aggregation yield was significantly improved by treatment with atRA and ECM. Glucose 103-110 insulin Homo sapiens 77-84 18206156-3 2008 A physiologic model of glucose metabolism in man and its use to design and assess improved insulin therapies for diabetes. Glucose 23-30 insulin Homo sapiens 91-98 17900254-8 2008 Morphologic changes and elevation levels of ST segment were associated with changes in glucose-induced insulin levels after meals, being highest after dinner (47 +/- 33 microU/mL) and decreasing significantly at midnight (7 +/- 4 microU/mL) and at 3:00 a.m. (5 +/- 2 microU/mL). Glucose 87-94 insulin Homo sapiens 103-110 18053094-1 2008 Insulin secretion from the pancreatic beta-cell is regulated principally by the ambient concentration of glucose. Glucose 105-112 insulin Homo sapiens 0-7 18053094-0 2008 Protein prenylation in glucose-induced insulin secretion from the pancreatic islet beta cell: a perspective. Glucose 23-30 insulin Homo sapiens 39-46 18053094-2 2008 However, the molecular and cellular mechanisms underlying the stimulus-secretion coupling of glucose-stimulated insulin secretion (GSIS) remain only partially understood. Glucose 93-100 insulin Homo sapiens 112-119 17956948-8 2008 Hepatic insulin sensitivity, measured from the percent suppression of endogenous glucose production by insulin, increased from -40 +/- 7% to -89 +/- 12% (P = 0.001). Glucose 81-88 insulin Homo sapiens 8-15 18182920-2 2008 An intensive insulin protocol with target glucose values of less than 120 mg/dl was implemented in October 2005 in our regional Burn-Trauma intensive care unit. Glucose 42-49 insulin Homo sapiens 13-20 17726571-7 2008 The correlation"s insulin/glucose and insulin/glycohemoglobin change to positive within demented groups, indicating a different performance of insulin in demented and non-demented subjects. Glucose 26-33 insulin Homo sapiens 18-25 19885177-0 2008 Randomized forced titration to different doses of technosphere insulin demonstrates reduction in postprandial glucose excursions and hemoglobin A1c in patients with type 2 diabetes. Glucose 110-117 insulin Homo sapiens 63-70 19885177-1 2008 BACKGROUND: Individuals with type 2 diabetes mellitus have impairments in early insulin release, resulting in increased postprandial glucose excursions and suboptimal glycemic control. Glucose 133-140 insulin Homo sapiens 80-87 19885177-2 2008 Studies with Technosphere Insulin (TI) indicate that it has rapid systemic absorption and a short duration of glucose-lowering activity, making it well suited for controlling postprandial glucose levels. Glucose 110-117 insulin Homo sapiens 26-33 19885177-2 2008 Studies with Technosphere Insulin (TI) indicate that it has rapid systemic absorption and a short duration of glucose-lowering activity, making it well suited for controlling postprandial glucose levels. Glucose 188-195 insulin Homo sapiens 26-33 19885178-9 2008 The DETM offers the opportunity to evaluate the clinical relevance of these errors and their contribution to the increased risk of meal-related excessive glucose excursions during intensified insulin therapy. Glucose 154-161 insulin Homo sapiens 192-199 17726571-7 2008 The correlation"s insulin/glucose and insulin/glycohemoglobin change to positive within demented groups, indicating a different performance of insulin in demented and non-demented subjects. Glucose 26-33 insulin Homo sapiens 38-45 17726571-7 2008 The correlation"s insulin/glucose and insulin/glycohemoglobin change to positive within demented groups, indicating a different performance of insulin in demented and non-demented subjects. Glucose 26-33 insulin Homo sapiens 38-45 18062666-4 2008 After culture at 16.7 mM glucose for 48 h, 832/13 beta-cells exhibited a phenotype reminiscent of glucotoxicity with decreased content and secretion of insulin. Glucose 25-32 insulin Homo sapiens 152-159 18081560-11 2008 Insulin suppressed hepatic glucose production (HGP) to a greater extent in lean ob/ob than in obese ob/ob mice, but its impact remained considerably less than in wild-type mice (% suppression: 11.8 +/- 8.9 versus 1.3 +/- 1.1 versus 56.6 +/- 13.0%/nmol, for lean, obese ob/ob and wild-type mice, respectively; P < 0.05). Glucose 27-34 insulin Homo sapiens 0-7 18081560-12 2008 The insulin-mediated glucose disposal (GD) of lean ob/ob mice was also in between that of obese ob/ob and wild-type mice (37.5 +/- 21.4 versus 25.1 +/- 14.6 versus 59.6 +/- 17.3 mumol/min/kg/nmol of insulin, respectively; P < 0.05 wild-type versus obese ob/ob mice). Glucose 21-28 insulin Homo sapiens 4-11 18165443-0 2008 A computerized insulin infusion titration protocol improves glucose control with less hypoglycemia compared to a manual titration protocol in a trauma intensive care unit. Glucose 60-67 insulin Homo sapiens 15-22 18165443-11 2008 CONCLUSIONS: A computerized insulin titration protocol improves glucose control by (1) increasing the percentage of glucose values in range, (2) reducing hyperglycemia, and (3) reducing severe hypoglycemia. Glucose 64-71 insulin Homo sapiens 28-35 18165443-11 2008 CONCLUSIONS: A computerized insulin titration protocol improves glucose control by (1) increasing the percentage of glucose values in range, (2) reducing hyperglycemia, and (3) reducing severe hypoglycemia. Glucose 116-123 insulin Homo sapiens 28-35 18266182-14 2008 This analysis showed that in the group treated with insulin the glucose level at discharge was not an independent prognostic factor of one-year mortality (HR 1.07, 95% CI 0.95-1.22; p=0.27), whereas in patients treated with hypoglycaemic agents or diet it was significantly associated with a one-year mortality (HR 1.30, 95% CI 1.01-1.68; p=0.049). Glucose 64-71 insulin Homo sapiens 52-59 17766054-3 2008 As skeletal muscle is the main site for insulin-mediated glucose utilization, the research on this topic has been active since. Glucose 57-64 insulin Homo sapiens 40-47 18078859-4 2008 Our data show that treatment with lovastatin results in a marked improvement in insulin sensitivity characterized by an increase in glucose disappearance rate during the insulin tolerance test. Glucose 132-139 insulin Homo sapiens 80-87 18296974-7 2008 Insulin sensitivity was also estimated by fasting glucose and insulin. Glucose 50-57 insulin Homo sapiens 0-7 18078859-4 2008 Our data show that treatment with lovastatin results in a marked improvement in insulin sensitivity characterized by an increase in glucose disappearance rate during the insulin tolerance test. Glucose 132-139 insulin Homo sapiens 170-177 19008977-1 2008 CONTEXT: Intensive insulin therapy is recommended to control glucose elevations in the critically ill and has been shown to significantly improve outcomes among hospital inpatients with acute hyperglycemia or newly diagnosed diabetes. Glucose 61-68 insulin Homo sapiens 19-26 19118673-2 2008 Extracellular glucose stimulates insulin secretion from islet beta-cells through an increase in metabolic state, which can be measured using two-photon NAD(P)H imaging. Glucose 14-21 insulin Homo sapiens 33-40 20467584-3 2008 We have recently shown that arsenite and its methylated metabolites inhibit insulin-stimulated glucose uptake in cultured adipocytes by disrupting insulin-activated signal transduction pathway and preventing insulin-dependent translocation of GLUT4 transporters to the plasma membrane. Glucose 95-102 insulin Homo sapiens 76-83 19088850-6 2008 SNPs rs10830962, rs4753426, and rs10830963 were significantly associated with higher fasting plasma glucose concentrations (p < 0.0001) and reduced OGTT- and IVGTT-induced insulin release (p < or = 0.0007 and p < or = 0.01, respectively). Glucose 100-107 insulin Homo sapiens 175-182 19066040-1 2008 Insulin regulates the glucose uptake in muscle and adipose cells by acutely modulating the amount of the GLUT4 glucose transporter in the plasma membrane. Glucose 22-29 insulin Homo sapiens 0-7 19066041-1 2008 Postprandial blood glucose homeostasis is regulated by an insulin-stimulated increase in glucose transport into muscle and fat tissues via glucose transporter isoform 4 (GLUT4). Glucose 19-26 insulin Homo sapiens 58-65 19066041-3 2008 In order to achieve the insulin-stimulated increase in glucose flux, GLUT4 increases its cell surface abundance at the expense of preformed intracellular depots. Glucose 55-62 insulin Homo sapiens 24-31 18682704-0 2008 Metabolic profiling of the human response to a glucose challenge reveals distinct axes of insulin sensitivity. Glucose 47-54 insulin Homo sapiens 90-97 19088850-10 2008 CONCLUSIONS/SIGNIFICANCE: In conclusion, common genetic variation within MTNR1B determines glucose-stimulated insulin secretion and plasma glucose concentrations. Glucose 91-98 insulin Homo sapiens 110-117 19441676-12 2008 The insulin resistance ratio (HOMA-IR) was calculated for each patient according to the formula: [insulin (mU/ml) x glucose (mmol/l)]/22.5. Glucose 116-123 insulin Homo sapiens 4-11 19114996-5 2008 Here we show that 10-min treatment with MES at 5 V (0.1 ms pulse duration) together with HS at 42 degrees C increased the phosphorylation of insulin signaling molecules such as insulin receptor substrate (IRS) and Akt in HepG2 cells maintained in high-glucose medium. Glucose 252-259 insulin Homo sapiens 141-148 19114996-5 2008 Here we show that 10-min treatment with MES at 5 V (0.1 ms pulse duration) together with HS at 42 degrees C increased the phosphorylation of insulin signaling molecules such as insulin receptor substrate (IRS) and Akt in HepG2 cells maintained in high-glucose medium. Glucose 252-259 insulin Homo sapiens 177-184 19378424-0 2008 C-reactive protein and tumor necrosis factor-alpha in relation to insulin-mediated glucose uptake, smoking and atherosclerosis. Glucose 83-90 insulin Homo sapiens 66-73 18483661-5 2008 Defective glucose-stimulated insulin secretion by pancreatic B-cells could be alleviated with recombinant glucagon-like peptide (GLP-1) or agonists to the GLP-1 receptor. Glucose 10-17 insulin Homo sapiens 29-36 18827908-1 2008 Diabetes mellitus is characterized by a lack of insulin causing elevated blood glucose, often with associated insulin resistance. Glucose 79-86 insulin Homo sapiens 48-55 18314766-1 2008 Insulin is the important regulator of adipose cell metabolism and activates the branched out network of the signaling pathways supervising glucose transport, glycogen synthesis, lipogenesis stimulation, lipolysis inhibition and adipokine secretion. Glucose 139-146 insulin Homo sapiens 0-7 19337540-2 2008 It is caused by defects in insulin-mediated signal pathways, resulting in decreased glucose transportation from blood into muscle and fat cells. Glucose 84-91 insulin Homo sapiens 27-34 19066006-1 2008 OBJECTIVES: To investigate the long-term effect of continuous insulin infusion for glucose control on cerebral metabolism in aneurysmal subarachnoid hemorrhage (SAH) patients. Glucose 83-90 insulin Homo sapiens 62-69 19066006-7 2008 Though no insulin-induced hypoglycemia occurred, cerebral glucose decreased on days 1-4 after insulin onset without reaching critical levels. Glucose 58-65 insulin Homo sapiens 94-101 19066006-9 2008 CONCLUSIONS: Concerning cerebral metabolism, long-term continuous insulin infusion appears to be safe as long as cerebral glucose levels do not fall below the physiological range. Glucose 122-129 insulin Homo sapiens 66-73 19337542-1 2008 The proinsulin connecting peptide, C-peptide, is a cleavage product of insulin synthesis that is co-secreted with insulin by pancreatic beta-cells following glucose stimulation. Glucose 157-164 insulin Homo sapiens 4-14 19337542-1 2008 The proinsulin connecting peptide, C-peptide, is a cleavage product of insulin synthesis that is co-secreted with insulin by pancreatic beta-cells following glucose stimulation. Glucose 157-164 insulin Homo sapiens 35-44 18034458-7 2007 Insulin secretion stimulating activity of a single oral CK administration was also confirmed with an oral glucose tolerance test (OGTT) using ICR mice. Glucose 106-113 insulin Homo sapiens 0-7 17971304-0 2007 CXCL14 enhances insulin-dependent glucose uptake in adipocytes and is related to high-fat diet-induced obesity. Glucose 34-41 insulin Homo sapiens 16-23 17971304-8 2007 Intriguingly, incubation of 3T3-L1 adipocytes with CXCL14 stimulated insulin-dependent glucose uptake. Glucose 87-94 insulin Homo sapiens 69-76 18077353-11 2007 Importantly, FoxO-mediated increases in Akt activity diminish insulin signaling, as manifested by reduced Akt phosphorylation, reduced membrane translocation of Glut4, and decreased insulin-triggered glucose uptake. Glucose 200-207 insulin Homo sapiens 62-69 18077353-11 2007 Importantly, FoxO-mediated increases in Akt activity diminish insulin signaling, as manifested by reduced Akt phosphorylation, reduced membrane translocation of Glut4, and decreased insulin-triggered glucose uptake. Glucose 200-207 insulin Homo sapiens 182-189 17911348-4 2007 Nonobese Ins2(Akita) mice developed insulin resistance, as indicated by an approximately 80% reduction in glucose infusion rate during clamps. Glucose 106-113 insulin Homo sapiens 36-43 31627559-5 2007 Their use could cause a significant decrease in the fasting plasma level of glucose, by completely refusing 6.00 extra insulin doses. Glucose 76-83 insulin Homo sapiens 119-126 18033628-6 2007 RESULTS: Glycaemic control worsened substantially with increases of serum glucose requiring increases in insulin dosages. Glucose 74-81 insulin Homo sapiens 105-112 17911348-5 2007 Insulin resistance was due to approximately 50% decreases in glucose uptake in skeletal muscle and brown adipose tissue as well as hepatic insulin action. Glucose 61-68 insulin Homo sapiens 0-7 17894546-1 2007 Pancreatic beta-cells are specialized for the production and regulated secretion of insulin to control blood-glucose levels. Glucose 109-116 insulin Homo sapiens 84-91 18005774-2 2007 METHODS: Records for burn intensive care unit patients with 7 days of glucose control with insulin were reviewed. Glucose 70-77 insulin Homo sapiens 91-98 18005774-5 2007 RESULTS: Diurnal patterns of blood glucose and insulin requirement were noted (insulin troughs = noon; insulin peaks = midnight; glucose troughs = 5 am; glucose peaks = 5 pm). Glucose 35-42 insulin Homo sapiens 79-86 18005774-5 2007 RESULTS: Diurnal patterns of blood glucose and insulin requirement were noted (insulin troughs = noon; insulin peaks = midnight; glucose troughs = 5 am; glucose peaks = 5 pm). Glucose 129-136 insulin Homo sapiens 47-54 18005774-9 2007 The insulin requirement to blood glucose ratio increased, evidence that insulin resistance progresses over time. Glucose 33-40 insulin Homo sapiens 4-11 18005774-9 2007 The insulin requirement to blood glucose ratio increased, evidence that insulin resistance progresses over time. Glucose 33-40 insulin Homo sapiens 72-79 17932315-3 2007 METHODS AND RESULTS: We measured insulin sensitivity by glucose tolerance test and vascular function by ultrasound and venous occlusion plethysmography in 20 healthy subjects (14 men, 6 women) at baseline and during 5 days of bed rest. Glucose 56-63 insulin Homo sapiens 33-40 17932315-4 2007 Bed rest led to a 67% increase in the insulin response to glucose loading (P<0.001) suggesting increased insulin resistance and produced increases in total cholesterol and triglycerides. Glucose 58-65 insulin Homo sapiens 38-45 17932315-4 2007 Bed rest led to a 67% increase in the insulin response to glucose loading (P<0.001) suggesting increased insulin resistance and produced increases in total cholesterol and triglycerides. Glucose 58-65 insulin Homo sapiens 108-115 18042786-4 2007 We review the specifics of glucose management in patients undergoing cardiac surgery and hypothermic cardiopulmonary bypass, including the role that insulin may play in regulating blood glucose levels intraoperatively and the relationship between insulin and outcome. Glucose 186-193 insulin Homo sapiens 149-156 18059588-4 2007 Then, insulin action (glucose uptake per unit plasma insulin) was assessed by stable isotope dilution during a continuous glucose infusion 12 h after a standardized meal under 4 conditions. Glucose 22-29 insulin Homo sapiens 6-13 18059588-4 2007 Then, insulin action (glucose uptake per unit plasma insulin) was assessed by stable isotope dilution during a continuous glucose infusion 12 h after a standardized meal under 4 conditions. Glucose 122-129 insulin Homo sapiens 6-13 18209893-7 2007 When we evaluated insulin resistance alone, by using HOMA and QUICKI indices and the fasting glucose to insulin index, we have found statistical significance (p = 0.005; p = 0.005; p = 0.053). Glucose 93-100 insulin Homo sapiens 104-111 17125771-8 2007 The difference in the integrated responses for serum RLP-cholesterol concentration during OFTT between DAG and TAG in all subjects can be easily explained by the integrated response of insulin rather than glucose during oral glucose tolerance test (r=0.7, p<0.01). Glucose 225-232 insulin Homo sapiens 185-192 18054735-1 2007 Inhaled insulin has attractive pharmacodynamic properties with a fast onset of action which should lead to improved postprandial blood glucose concentrations. Glucose 135-142 insulin Homo sapiens 8-15 18054735-2 2007 Comparisons with regular subcutaneous (sc) insulin in clinical studies, however, showed lower fasting blood glucose concentrations. Glucose 108-115 insulin Homo sapiens 43-50 17920690-5 2007 Disturbances in insulin signalling appears to be the main common impairment that affects cell growth and differentiation, cellular repair mechanisms, energy metabolism, and glucose utilization. Glucose 173-180 insulin Homo sapiens 16-23 18220724-8 2007 The vascular effects of insulin are generally ignored in the clinical practice, despite the evidences that insulin infusion with algorithms aiming to provide an optimal blood glucose control improves the clinical outcomes of patients with severe acute illness and myocardial infarction. Glucose 175-182 insulin Homo sapiens 107-114 17950500-8 2007 Evidence concerning the mechanism and the effect of insulin on glucose and lipid metabolism in pediatric critical illness is scarce. Glucose 63-70 insulin Homo sapiens 52-59 17982337-5 2007 An increase in insulin resistance results in increases in maternal glucose and free fatty acid concentrations, allowing for greater substrate availability for fetal growth. Glucose 67-74 insulin Homo sapiens 15-22 17982345-2 2007 Self-blood glucose monitoring in combination with flexible or intensive insulin treatment including the use of newer insulin analogs and insulin pump therapy has dramatically improved glucose control in most pregnancies complicated by diabetes. Glucose 11-18 insulin Homo sapiens 117-124 17982345-2 2007 Self-blood glucose monitoring in combination with flexible or intensive insulin treatment including the use of newer insulin analogs and insulin pump therapy has dramatically improved glucose control in most pregnancies complicated by diabetes. Glucose 11-18 insulin Homo sapiens 117-124 18217467-8 2007 Insulin resistance is the result of the multiple effects of the antipsychotics, among which most common are: increased body mass and direct involvement of the antipsychotics in the glucose metabolism. Glucose 181-188 insulin Homo sapiens 0-7 17720897-1 2007 OBJECTIVE: Transport of insulin from the central circulation into muscle is rate limiting for the stimulation of glucose metabolism. Glucose 113-120 insulin Homo sapiens 24-31 17919068-5 2007 The second pathway amplifies the insulin/growth-factor signal for protein/DNA synthesis and glucose transport downstream of PI3K. Glucose 92-99 insulin Homo sapiens 33-40 17584514-11 2007 Upon stimulation by glucose alone, human islets secreted approximately 10x more insulin than pig islets, and the kinetics was characterized by a large first phase, a flat second phase, and rapid reversibility. Glucose 20-27 insulin Homo sapiens 80-87 17827400-6 2007 Interestingly, in middle-aged people, the rs1111875 C-allele of HHEX/KIF11/IDE strongly associated with lower acute insulin response during an oral glucose tolerance test (P = 6 x 10(-7)). Glucose 148-155 insulin Homo sapiens 116-123 17804762-10 2007 CONCLUSIONS: CDKAL1 and HHEX/IDE diabetes-associated alleles are associated with decreased pancreatic beta-cell function, including decreased beta-cell glucose sensitivity that relates insulin secretion to plasma glucose concentration. Glucose 152-159 insulin Homo sapiens 185-192 17804762-10 2007 CONCLUSIONS: CDKAL1 and HHEX/IDE diabetes-associated alleles are associated with decreased pancreatic beta-cell function, including decreased beta-cell glucose sensitivity that relates insulin secretion to plasma glucose concentration. Glucose 213-220 insulin Homo sapiens 185-192 17827400-10 2007 Importantly, variations within the HHEX/KIF11/IDE and CDKN2A/B loci confer impaired glucose- and tolbutamide-induced insulin release in middle-aged and young healthy subjects, suggesting a role for these variants in the pathogenesis of pancreatic beta-cell dysfunction. Glucose 84-91 insulin Homo sapiens 117-124 17827400-8 2007 Also, a reduced insulin release was observed for the CDKN2A/B rs10811661 T-allele after both oral and intravenous glucose challenges (P = 0.001 and P = 0.009, respectively). Glucose 114-121 insulin Homo sapiens 16-23 17934712-1 2007 AIMS/HYPOTHESIS: Glucose-stimulated insulin secretion is dependent on the electrical activity of beta cells; hence, genes encoding beta cell ion channels are potential candidate genes for type 2 diabetes. Glucose 17-24 insulin Homo sapiens 36-43 17848612-0 2007 Targeting glucose in acute myocardial infarction: has glucose, insulin, and potassium infusion missed the target? Glucose 10-17 insulin Homo sapiens 63-70 17928988-1 2007 AIMS/HYPOTHESIS: Clear evidence exists that TNF-alpha inhibits insulin signalling and thereby glucose uptake in myocytes and adipocytes. Glucose 94-101 insulin Homo sapiens 63-70 18034605-1 2007 BACKGROUND: Our objective was to use continuous glucose monitoring to derive the optimal basal insulin infusion rates in adults with type 1 diabetes and using continuous subcutaneous insulin infusion (CSII) pumps. Glucose 48-55 insulin Homo sapiens 95-102 18034605-4 2007 Subjects were asked to skip meals periodically in order to optimize basal insulin infusion rates, defined as the basal infusion rates that maintained glucose levels in the range of 65-120 mg/dL during the fasting state or between meals. Glucose 150-157 insulin Homo sapiens 74-81 17988918-6 2007 The continuous availability of glucose measurements permitted the patients to adjust their own insulin doses, food intake and physical activity and, thus, improve their glycaemic control. Glucose 31-38 insulin Homo sapiens 95-102 17629673-1 2007 Insulin regulates circulating glucose levels by suppressing hepatic glucose production and increasing glucose transport into muscle and adipose tissues. Glucose 30-37 insulin Homo sapiens 0-7 18042082-10 2007 CONCLUSION: Insulin glargine pre-bed can be used in three-injections-daily regimens in prepubertal children to lower and stabilize pre-breakfast glucose levels. Glucose 145-152 insulin Homo sapiens 12-19 17983933-5 2007 Recent data indicate that insulin independence after islet cell transplantation is associated with an improvement in glucose metabolism and quality of life and with a reduction in hypoglycemic episodes. Glucose 117-124 insulin Homo sapiens 26-33 18025761-11 2007 In conclusion, our study showed that both insulin sensitivity and impaired beta-cell function are associated with impaired glucose metabolism, and that beta-cell function may be more important in determining glucose disposal. Glucose 123-130 insulin Homo sapiens 42-49 18256939-7 2007 However, she still needed the insulin injection therapy to control her blood glucose level. Glucose 77-84 insulin Homo sapiens 30-37 18407031-2 2007 Insulin suppresses these effects, either indirectly by decreasing glucose levels or directly by stimulating nitric oxide production and inhibiting important pathways in the inflammatory cascade. Glucose 66-73 insulin Homo sapiens 0-7 18075971-5 2007 Spironolactone, but not its active metabolite canrenoic acid, significantly increased basal and insulin-stimulated glucose uptake in cultured IN VITRO-differentiated adipocytes of women, without affecting insulin sensitivity. Glucose 115-122 insulin Homo sapiens 96-103 18174660-6 2007 In subjects with fasting plasma glucose < or = 140mg/dL, FMD showed significant negative correlations with fasting insulin levels and homeostasis model assessment (HOMA)-R. Multivariate analysis revealed that insulin resistance as represented by HOMA-R and systolic blood pressure showed a significant association with impaired FMD. Glucose 32-39 insulin Homo sapiens 118-125 18174660-6 2007 In subjects with fasting plasma glucose < or = 140mg/dL, FMD showed significant negative correlations with fasting insulin levels and homeostasis model assessment (HOMA)-R. Multivariate analysis revealed that insulin resistance as represented by HOMA-R and systolic blood pressure showed a significant association with impaired FMD. Glucose 32-39 insulin Homo sapiens 212-219 17878257-5 2007 DESIGN: SI, acute insulin response to iv glucose (AIRg), maximally potentiated insulin response to arginine (AIRmax), and disposition indexes (DIs) (DI = SI * AIRg; DImax = SI * AIRmax) were compared among nondiabetic Caucasian and African-American individuals with and without a family history of diabetes. Glucose 41-48 insulin Homo sapiens 18-25 18035140-1 2007 OBJECTIVE: To investigate the use of insulin throughout the first week of life in very low birth weight (VLBW) infants (birth weight <1.5 kg) to improve glucose control and increase insulin-like growth factor-I (IGF-I) levels. Glucose 156-163 insulin Homo sapiens 37-44 18309686-0 2007 Differences in insulin sensitivity and secretory capacity based on OGTT in subjects with impaired glucose regulation. Glucose 98-105 insulin Homo sapiens 15-22 17375138-0 2007 Adiposity and insulin sensitivity derived from intravenous glucose tolerance tests in antipsychotic-treated patients. Glucose 59-66 insulin Homo sapiens 14-21 17375138-7 2007 In addition, BMI and waist circumference significantly predicted the acute plasma insulin response to the glucose challenge (AIR(G)), consistent with a beta cell compensatory response to insulin resistance (MinMod AIR(G) F(1,65)=22.42, p<0.0001 and F(1,49)=11.72, p=0.0013, respectively). Glucose 106-113 insulin Homo sapiens 82-89 18061818-3 2007 The vast majority of patients who have type 1 diabetes require a basal insulin to suppress hepatic glucose production in the fasting state, as well as prandial (mealtime) insulin to cover glycemic excursions that occur as carbohydrate absorption occurs in response to meals. Glucose 99-106 insulin Homo sapiens 71-78 18357861-2 2007 It is has been demonstrated that normalization of blood glucose level using intensive insulin therapy significantly improves prognosis of these patients. Glucose 56-63 insulin Homo sapiens 86-93 18198644-4 2007 RESULTS: Treatment with 0.5 mmol/L of palmic acid for 24 h made glucose consumption of 3T3-L1 adipocytes decrease by 41%; the insulin-stimulated glucose transportation inhibited by 67%; nuclear NF-kappaB p65 protein expression and nuclear translocation of NF-kappaB p65 significantly increased. Glucose 64-71 insulin Homo sapiens 126-133 18198644-4 2007 RESULTS: Treatment with 0.5 mmol/L of palmic acid for 24 h made glucose consumption of 3T3-L1 adipocytes decrease by 41%; the insulin-stimulated glucose transportation inhibited by 67%; nuclear NF-kappaB p65 protein expression and nuclear translocation of NF-kappaB p65 significantly increased. Glucose 145-152 insulin Homo sapiens 126-133 18049122-0 2007 Acute insulin responses to glucose and arginine as predictors of beta-cell secretory capacity in human islet transplantation. Glucose 27-34 insulin Homo sapiens 6-13 18049122-4 2007 We sought to determine whether acute insulin responses to intravenous glucose (AIR(glu)) or arginine (AIR(arg)) could predict beta-cell secretory capacity in islet recipients. Glucose 70-77 insulin Homo sapiens 37-44 17715127-7 2007 Depletion of SIRT4 from insulin-producing INS-1E cells results in increased insulin secretion in response to glucose. Glucose 109-116 insulin Homo sapiens 24-31 17848561-7 2007 Expression of either of these two minimal interaction domains resulted in inhibition of glucose-stimulated insulin secretion, consistent with a functional importance for the endogenous WNK1-Munc18c complex in exocytosis. Glucose 88-95 insulin Homo sapiens 107-114 17711984-3 2007 That dose of insulin raised plasma insulin concentrations approximately threefold, suppressed glucose production, and drove plasma glucose concentrations down to subphysiological levels (65 +/- 3 mg/dl, P < 0.0001 vs. saline), resulting in nearly complete suppression of insulin secretion (P < 0.0001) and stimulation of glucagon (P = 0.0059) and epinephrine (P = 0.0009) secretion. Glucose 94-101 insulin Homo sapiens 13-20 17711984-3 2007 That dose of insulin raised plasma insulin concentrations approximately threefold, suppressed glucose production, and drove plasma glucose concentrations down to subphysiological levels (65 +/- 3 mg/dl, P < 0.0001 vs. saline), resulting in nearly complete suppression of insulin secretion (P < 0.0001) and stimulation of glucagon (P = 0.0059) and epinephrine (P = 0.0009) secretion. Glucose 131-138 insulin Homo sapiens 13-20 17956305-1 2007 Insulin has a potent inhibitory effect on hepatic glucose production by direct action at hepatic receptors. Glucose 50-57 insulin Homo sapiens 0-7 17956314-3 2007 Recent work has led to the discovery of synthetic small-molecule activators of GK that stimulate beta-cell physiology and subsequently enhance the glucose-dependent release of insulin. Glucose 147-154 insulin Homo sapiens 176-183 17697007-5 2007 Insulin sensitivity and beta-cell function were calculated by minimal model method from the frequently sampled intravenous glucose tolerance test. Glucose 123-130 insulin Homo sapiens 0-7 17697007-8 2007 Acute insulin response (AIR) to intravenous glucose was elevated in BD as compared to control and RD groups (6079.9 +/- 841.8 pmol vs. 3339.8 +/- 356.4 pmol and 3494.8 +/- 337.7 pmol, P < 0.05, respectively). Glucose 44-51 insulin Homo sapiens 6-13 19162650-2 2008 Daily compensation of the deficiency requires 4-6 insulin injections to be taken daily, the aim of this insulin therapy being to maintain normoglycemia--i.e., a blood glucose level between 4-7 mmol/L. Glucose 167-174 insulin Homo sapiens 104-111 19162650-7 2008 The insulin subsystem aims to describe the absorbtion of injected insulin from the subcutaneous depots and the glucose subsystem the absorbtion of glucose from the gut following a meal. Glucose 111-118 insulin Homo sapiens 4-11 19162650-7 2008 The insulin subsystem aims to describe the absorbtion of injected insulin from the subcutaneous depots and the glucose subsystem the absorbtion of glucose from the gut following a meal. Glucose 147-154 insulin Homo sapiens 4-11 18003705-0 2007 Rip11 is a Rab11- and AS160-RabGAP-binding protein required for insulin-stimulated glucose uptake in adipocytes. Glucose 83-90 insulin Homo sapiens 64-71 18003705-1 2007 The translocation of GLUT4 to the plasma membrane underlies the ability of insulin to stimulate glucose uptake, an event that involves the activation of protein kinase B, several members of the Rab family of GTP-binding proteins and the phosphorylation of the Rab GTPase-activating protein AS160. Glucose 96-103 insulin Homo sapiens 75-82 18003705-8 2007 We propose that Rip11 is an AS160- and Rab-binding protein that coordinates the protein kinase signalling and trafficking machinery required to stimulate glucose uptake in response to insulin. Glucose 154-161 insulin Homo sapiens 184-191 18004125-1 2007 We investigated ghrelin, leptin, glucose, and insulin response to an oral glucose tolerance test among children receiving antipsychotics. Glucose 74-81 insulin Homo sapiens 46-53 18166691-6 2007 In men, there was an inverse relationship between SAF and insulin-stimulated glucose disposal (ISGD) (r= -.60, p=.01). Glucose 77-84 insulin Homo sapiens 58-65 17537518-3 2007 A family of putative insulin mediators, namely inositol phosphoglycans, were described to exert many insulin-like effects on lipid and glucose metabolism. Glucose 135-142 insulin Homo sapiens 21-28 17537518-3 2007 A family of putative insulin mediators, namely inositol phosphoglycans, were described to exert many insulin-like effects on lipid and glucose metabolism. Glucose 135-142 insulin Homo sapiens 101-108 18198296-5 2007 Insulin secretion was evaluated by an intravenous glucose tolerance test and insulin sensitivity and energy metabolism by the hyperinsulinemic euglycemic clamp and indirect calorimetry. Glucose 50-57 insulin Homo sapiens 0-7 17991135-3 2007 The major factor driving the development of compromised glucose metabolism in obese youth is severe insulin resistance. Glucose 56-63 insulin Homo sapiens 100-107 17848579-3 2007 By contrast, co-expression of Dyn/K44A with human growth hormone as an insulin secretory marker resulted in a marked inhibition of human growth hormone release by glucose, KCl, and a combination of multiple secretagogues. Glucose 163-170 insulin Homo sapiens 71-78 17848579-5 2007 Similarly, small interference RNA-mediated knockdown of dynamin resulted in marked inhibition of glucose-stimulated insulin secretion. Glucose 97-104 insulin Homo sapiens 116-123 17956278-1 2007 K(ATP) channels (ATP-sensitive potassium channels), comprising four subunits each of Kir6.2 (inwardly rectifying potassium channel 6.2) and the SUR1 (sulfonylurea receptor 1), play a central role in glucose-stimulated insulin secretion by the pancreatic beta-cell. Glucose 199-206 insulin Homo sapiens 218-225 17956334-7 2007 IL-6 treatment of myotubes increases fatty acid oxidation, basal and insulin-stimulated glucose uptake and translocation of GLUT4 to the plasma membrane. Glucose 88-95 insulin Homo sapiens 69-76 17956338-1 2007 SREBP-1c (sterol-regulatory-element-binding protein 1c) is a transcription factor that regulates genes associated with glucose and fatty acid metabolism and exhibits responsiveness to insulin and exercise. Glucose 119-126 insulin Homo sapiens 184-191 17902094-7 2007 Insulin-stimulated endogenous glucose release was similar before and after surgery in the high oral CHO group, but was higher after surgery in the low oral CHO group (P = 0.013) and compared with the high oral CHO group (P = 0.044). Glucose 30-37 insulin Homo sapiens 0-7 17902094-8 2007 CONCLUSION: Whole-body protein balance and the suppressive effect of insulin on endogenous glucose release are better maintained when patients receive a CHO-rich beverage before surgery. Glucose 91-98 insulin Homo sapiens 69-76 17900299-6 2007 Insulin sensitivity (HOMA-S) was determined from paired fasting plasma intact insulin and glucose values. Glucose 90-97 insulin Homo sapiens 0-7 17629673-1 2007 Insulin regulates circulating glucose levels by suppressing hepatic glucose production and increasing glucose transport into muscle and adipose tissues. Glucose 68-75 insulin Homo sapiens 0-7 17629673-1 2007 Insulin regulates circulating glucose levels by suppressing hepatic glucose production and increasing glucose transport into muscle and adipose tissues. Glucose 68-75 insulin Homo sapiens 0-7 17629673-3 2007 At the cellular level, insulin stimulates glucose uptake by inducing the translocation of the glucose transporter 4 (GLUT4) from intracellular storage sites to the plasma membrane, where the transporter facilitates the diffusion of glucose into striated muscle and adipocytes. Glucose 42-49 insulin Homo sapiens 23-30 17629673-3 2007 At the cellular level, insulin stimulates glucose uptake by inducing the translocation of the glucose transporter 4 (GLUT4) from intracellular storage sites to the plasma membrane, where the transporter facilitates the diffusion of glucose into striated muscle and adipocytes. Glucose 94-101 insulin Homo sapiens 23-30 17595353-10 2007 Although it is not possible to characterize clear predictors of outcome given the size and exploratory nature of the study, the data suggest that patients with longer disease duration, who are taking higher doses of insulin and have less endogenous beta-cell function, may experience deterioration in glucose control if exenatide is substituted for insulin therapy. Glucose 301-308 insulin Homo sapiens 216-223 17616474-4 2007 This was accompanied by reduced glucose-stimulated insulin secretion, as compared to non-diabetic islets (Stimulation Index, SI: 0.9 +/- 0.2 vs. 2.0 +/- 0.4, P<0.01), and by altered expression of insulin (approximately -60%), catalase (approximately +90%) and glutathione peroxidase (approximately +140%). Glucose 32-39 insulin Homo sapiens 51-58 17644447-2 2007 We report the case of a patient suffering from type 1 diabetes who was found comatose with a plasma glucose close to zero after having injected herself massive doses of both aspart and glargine insulin analogues. Glucose 100-107 insulin Homo sapiens 194-201 17644447-4 2007 This observation emphasizes again that clinicians should be aware of the extremely prolonged action of long acting insulin analogue glargine after intentional massive injection in order to avoid a too early interruption of glucose infusion and a subsequent risk of relapse of severe hypoglycaemic episodes. Glucose 223-230 insulin Homo sapiens 115-122 17660267-5 2007 RESULTS: Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Glucose 60-67 insulin Homo sapiens 23-30 17919177-1 2007 Maturity-onset diabetes of the young (MODY) is a monogenic form of type 2 diabetes mellitus that is characterized by impairment of glucose-stimulated insulin secretion from pancreatic beta-cells. Glucose 131-138 insulin Homo sapiens 150-157 17919181-3 2007 Pancreatic beta-cells may be extremely sensitive to the accumulation of mtDNA mutations, as insulin secretion requires the mitochondrial oxidation of glucose to CO(2). Glucose 150-157 insulin Homo sapiens 92-99 17924864-4 2007 Insulin-associated weight gain may result from a reduction of blood glucose to levels below the renal threshold without a compensatory reduction in calorie intake, a defensive or unconscious increase in calorie intake caused by the fear or experience of hypoglycaemia, or the "unphysiological" pharmacokinetic and metabolic profiles that follow subcutaneous administration. Glucose 68-75 insulin Homo sapiens 0-7 17924873-2 2007 Insulin detemir was to be started once-daily as add-on therapy to any other glucose-lowering regimens or as a replacement of prestudy basal insulin in patients with type 2 diabetes. Glucose 76-83 insulin Homo sapiens 0-7 18158076-0 2007 Mealtime 50/50 basal + prandial insulin analogue mixture with a basal insulin analogue, both plus metformin, in the achievement of target HbA1c and pre- and postprandial blood glucose levels in patients with type 2 diabetes: a multinational, 24-week, randomized, open-label, parallel-group comparison. Glucose 176-183 insulin Homo sapiens 32-39 18158076-0 2007 Mealtime 50/50 basal + prandial insulin analogue mixture with a basal insulin analogue, both plus metformin, in the achievement of target HbA1c and pre- and postprandial blood glucose levels in patients with type 2 diabetes: a multinational, 24-week, randomized, open-label, parallel-group comparison. Glucose 176-183 insulin Homo sapiens 70-77 18194936-3 2007 Homeostasis model assessment of insulin resistance was calculated from the fasting plasma glucose and insulin concentrations. Glucose 90-97 insulin Homo sapiens 32-39 18058599-9 2007 However, either three months or five years after SPK abnormal glucose tolerance was mainly due to a reduced glucose- and arginine-induced secretory response of insulin. Glucose 62-69 insulin Homo sapiens 160-167 18058599-9 2007 However, either three months or five years after SPK abnormal glucose tolerance was mainly due to a reduced glucose- and arginine-induced secretory response of insulin. Glucose 108-115 insulin Homo sapiens 160-167 17575262-10 2007 However, the sensitivity to insulin for downstream signaling to control of protein kinase B and glucose uptake was not affected by RBP4. Glucose 96-103 insulin Homo sapiens 28-35 17904132-4 2007 RESULTS: For both insulin and glucose, we found higher risk for subjects in the high quartile compared with the low quartile (OR, 1.56; 95% CI, 1.00-2.43 for insulin; OR, 1.49; 95% CI, 0.95-2.31 for glucose). Glucose 30-37 insulin Homo sapiens 158-165 17904132-4 2007 RESULTS: For both insulin and glucose, we found higher risk for subjects in the high quartile compared with the low quartile (OR, 1.56; 95% CI, 1.00-2.43 for insulin; OR, 1.49; 95% CI, 0.95-2.31 for glucose). Glucose 199-206 insulin Homo sapiens 18-25 17904132-4 2007 RESULTS: For both insulin and glucose, we found higher risk for subjects in the high quartile compared with the low quartile (OR, 1.56; 95% CI, 1.00-2.43 for insulin; OR, 1.49; 95% CI, 0.95-2.31 for glucose). Glucose 199-206 insulin Homo sapiens 158-165 17698912-8 2007 The weight-for-height adjusted serum insulin concentrations during the oral glucose tolerance test were elevated in the whole PA group, whereas the fasting insulin concentrations were increased and SHBG was decreased only in the PP-PA subgroup. Glucose 76-83 insulin Homo sapiens 37-44 17711920-7 2007 MAIN OUTCOME MEASURES: Insulin signaling cascade gene and protein expression and insulin-stimulated glucose uptake were determined. Glucose 100-107 insulin Homo sapiens 81-88 17711920-10 2007 Furthermore, GC induced IRS-2 mRNA expression (2.8-fold; P < 0.05) and increased insulin-stimulated glucose uptake [1.0 (control) 1.8 +/- 0.1 (insulin) vs. 2.8 +/- 0.2 (insulin + GC); P < 0.05]. Glucose 103-110 insulin Homo sapiens 84-91 17711920-11 2007 In contrast, in primary cultures of human muscle, GC decreased insulin-stimulated glucose uptake [1.0 (control) 1.9 +/- 0.2 (insulin) vs. GC 1.3 +/- 0.1 (insulin + GC); P < 0.05]. Glucose 82-89 insulin Homo sapiens 63-70 17785358-8 2007 Acutely normalizing hyperglycemia over 2-4 h resulted in a small ( approximately 7%) but significant decline in TF-PCA with no further decline over 24 h. Raising insulin levels alone raised TF-PCA by 30%, whereas raising insulin and glucose levels together increased TF-PCA (by 80%), thrombin-anti-thrombin complexes, and prothrombin fragment 1.2. Glucose 233-240 insulin Homo sapiens 162-169 17785360-13 2007 We have shown that women with an exaggerated 17-hydroxyprogesterone response to a GnRH agonist, buserelin, are characterized by more severe hyperandrogenemia, glucose-stimulated beta-cell insulin secretion, and worse insulin resistance than those without evidence of FOH. Glucose 159-166 insulin Homo sapiens 188-195 17651516-2 2007 Recently, Thomaseth & Pavan (2003) presented a compartmental model (Thomaseth model), which employs the pattern of plasma insulin concentrations in humans to predict the dynamic changes that occur in the plasma concentrations of glucose and NEFA during an intravenous glucose tolerance test (IVGTT). Glucose 233-240 insulin Homo sapiens 126-133 17651516-2 2007 Recently, Thomaseth & Pavan (2003) presented a compartmental model (Thomaseth model), which employs the pattern of plasma insulin concentrations in humans to predict the dynamic changes that occur in the plasma concentrations of glucose and NEFA during an intravenous glucose tolerance test (IVGTT). Glucose 272-279 insulin Homo sapiens 126-133 19756210-4 2007 Insulin infusion is computed from linear quadratic regulator feedback gains applied to these estimates, generally seeking to minimize squared deviations from a target glucose concentration and basal insulin rate. Glucose 167-174 insulin Homo sapiens 0-7 19885152-3 2007 Closed-loop control of blood glucose levels still poses technological challenges to the automatic control expert, most notable of which are the inevitable time delays between glucose sensing and insulin actuation. Glucose 29-36 insulin Homo sapiens 195-202 17763913-8 2007 Intensity of glucose self-monitoring remained lower among blacks than whites throughout follow-up [IRR for insulin = 0.41 (0.27-0.62); IRR for oral hypoglycemic = 0.75 (0.63, 0.90)], with both groups monitoring well below recommended standards. Glucose 13-20 insulin Homo sapiens 107-114 17951498-3 2007 The main reasons are that this hormone 1) is secreted by epithelial intestinal L-cells in response to glucose and lipids, 2) enhances glucose-stimulated insulin secretion, 3) improves blood glucose profiles of type 2 diabetic patients by means of several actions on pancreatic hormone secretions, 4) reduces body weight and food intake, and 5) slows gastric emptying. Glucose 134-141 insulin Homo sapiens 153-160 17940534-0 2007 Atypical antipsychotic drugs directly impair insulin action in adipocytes: effects on glucose transport, lipogenesis, and antilipolysis. Glucose 86-93 insulin Homo sapiens 45-52 18090240-11 2007 CONCLUSIONS: Study results indicate that, first, there was a significant decrease of insulin sensitivity and insulin secretion in subjects with fasting glucose from 100 to 109 mg/dL compared with subjects with normal fasting glucose. Glucose 152-159 insulin Homo sapiens 85-92 18090240-11 2007 CONCLUSIONS: Study results indicate that, first, there was a significant decrease of insulin sensitivity and insulin secretion in subjects with fasting glucose from 100 to 109 mg/dL compared with subjects with normal fasting glucose. Glucose 225-232 insulin Homo sapiens 85-92 17805200-0 2007 Lower insulin secretory response to glucose induced by artificial nutrition in children: prolonged and total parenteral nutrition. Glucose 36-43 insulin Homo sapiens 6-13 17805200-6 2007 The same demonstrated a lower insulin release under graded glucose infusion, although plasma glucose reached values as high as 15 mM. Glucose 59-66 insulin Homo sapiens 30-37 17805200-7 2007 These data emphasize that metabolic conditions induced by TPN can lead to lower insulin secretory response to glucose. Glucose 110-117 insulin Homo sapiens 80-87 17615265-8 2007 A significant insulin content, as well as glucose-stimulated insulin release, were demonstrated in vitro. Glucose 42-49 insulin Homo sapiens 61-68 18095618-5 2007 The concentration of blood glucose was stabilized gradually to normal level and therefore the injected insulin was stopped using to the patient at day 16 of post-operative days. Glucose 27-34 insulin Homo sapiens 103-110 17936091-1 2007 BACKGROUND: The aim of this study was to measure the circulating levels of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), and glucagon in patients who had undergone adjustable gastric banding (BND) or Roux-en-Y gastric bypass (RYGB) to understand the differences in glucose and insulin regulation after these procedures. Glucose 108-115 insulin Homo sapiens 126-133 17223212-7 2007 Short-acting insulin was started according to admission glucose and adjusted based on hourly measured glucose. Glucose 56-63 insulin Homo sapiens 13-20 17223212-7 2007 Short-acting insulin was started according to admission glucose and adjusted based on hourly measured glucose. Glucose 102-109 insulin Homo sapiens 13-20 17675296-2 2007 In low glucose medium without insulin, amounts of both FVII mRNA and secreted FVII protein were coordinately increased; in the presence of glucose with insulin, both were decreased. Glucose 139-146 insulin Homo sapiens 152-159 17675296-4 2007 Mutation of this element largely abrogated the glucose/insulin-responsive change in expression of the reporter gene. Glucose 47-54 insulin Homo sapiens 55-62 17785466-0 2007 NR4A orphan nuclear receptors modulate insulin action and the glucose transport system: potential role in insulin resistance. Glucose 62-69 insulin Homo sapiens 106-113 17785466-5 2007 Compared with LacZ expressing cells, hyperexpression of NR4A3 increased the ability of insulin to augment glucose transport activity, and the mechanism involved increased recruitment of GLUT4 glucose transporters to the plasma membrane. Glucose 106-113 insulin Homo sapiens 87-94 17785466-7 2007 Suppression of NR4A3 using lentiviral short hairpin RNA constructs reduced the ability of insulin to stimulate glucose transport and phosphorylate Insulin receptor substrate-1 and Akt. Glucose 111-118 insulin Homo sapiens 90-97 17887659-3 2007 More recently, ghrelin has been recognized to also play a role in controlling glucose-induced insulin secretion, which suggests another possible benefit for a GHS-R1a antagonist, namely, the role as an insulin secretagogue with potential value for diabetes treatment. Glucose 78-85 insulin Homo sapiens 94-101 17941991-6 2007 However in many cases, insulin secretion from non-beta cells engineered to produce insulin occurs in a glucose-independent manner. Glucose 103-110 insulin Homo sapiens 23-30 17941991-6 2007 However in many cases, insulin secretion from non-beta cells engineered to produce insulin occurs in a glucose-independent manner. Glucose 103-110 insulin Homo sapiens 83-90 17706338-2 2007 The unique function of the cell is to integrate all these ambient signals into an appropriate insulin secretory rate in order to maintain normal glucose homeostasis. Glucose 145-152 insulin Homo sapiens 94-101 17920636-0 2007 Glucose-regulated insulin production from genetically engineered human non-beta cells. Glucose 0-7 insulin Homo sapiens 18-25 17931417-6 2007 The method, "Revised Quantitative Insulin Sensitivity Check Index" (RQUICKI) is based on plasma concentrations of glucose, insulin and free fatty acids (FFA) and it generates good and linear correlations with different estimates of insulin sensitivity in human populations. Glucose 114-121 insulin Homo sapiens 232-239 17935674-9 2007 CONCLUSION: Insulin Aspart results in better control of blood glucose levels than regular human insulin (Novolin R) in diabetic patients during delivery by CSII. Glucose 62-69 insulin Homo sapiens 12-19 17851816-2 2007 The long-acting insulin analogue glargine has 24-h persistence and a peakless action profile, and could contribute to more stable daily plasma glucose levels and improved glycemic control. Glucose 143-150 insulin Homo sapiens 16-23 17875968-2 2007 METHODS AND RESULTS: Exposure of cultured human umbilical vein endothelial cells to either peroxynitrite (ONOO-) or high glucose significantly inhibited both basal and insulin-stimulated Akt phosphorylation at Ser473 and Akt activity in parallel with increased apoptosis, phosphorylation, and activity of phosphatase and tensin homologue deleted on chromosome 10 (PTEN). Glucose 121-128 insulin Homo sapiens 168-175 17680843-4 2007 Insulin resistance and insulin secretion were determined in response to oral loading of 75 g glucose. Glucose 93-100 insulin Homo sapiens 0-7 17680843-8 2007 Of the 212 CHC patients, 148 (61%) showed NGT, and the serum insulin response to oral glucose loading in these NGT patients with steatosis was significantly different from that in patients with NGT but no steatosis. Glucose 86-93 insulin Homo sapiens 61-68 18059606-3 2007 IL-6 increases insulin-stimulated glucose disposal and fatty acid oxidation in humans in vivo. Glucose 34-41 insulin Homo sapiens 15-22 18059607-1 2007 Regularly performed aerobic exercise leads to increases in skeletal muscle mitochondria and glucose transporter 4 (GLUT4) protein content, resulting in an enhanced capacity to oxidize substrates and improvements in insulin- and contraction-mediated glucose uptake. Glucose 92-99 insulin Homo sapiens 215-222 17553476-0 2007 Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart. Glucose 0-7 insulin Homo sapiens 40-47 17553476-1 2007 OBJECTIVE: Insulin regulates both glucose uptake and postnatal cardiac growth. Glucose 34-41 insulin Homo sapiens 11-18 17553476-5 2007 RESULTS: Although insulin enhanced Akt activity, phosphorylation of mTOR and its downstream targets (p70S6K and 4EBP1) required the addition of glucose. Glucose 144-151 insulin Homo sapiens 18-25 17553476-10 2007 CONCLUSION: Phosphorylation of glucose is necessary for insulin-dependent mTOR activity in the heart, suggesting a link between intermediary metabolism and cardiac growth. Glucose 31-38 insulin Homo sapiens 56-63 17979649-3 2007 Current published protocols use insulin alone to reduce blood glucose levels, require significant added clinical effort, and provide highly variable results. Glucose 62-69 insulin Homo sapiens 32-39 17606872-0 2007 Glucagon, in concert with insulin, supports the postabsorptive plasma glucose concentration in humans. Glucose 70-77 insulin Homo sapiens 26-33 17606872-1 2007 OBJECTIVE: Given the interest in glucagon antagonism as a potential treatment of diabetes, we tested the hypothesis that glucagon, in concert with insulin, supports the postabsorptive plasma glucose concentration in humans. Glucose 191-198 insulin Homo sapiens 147-154 17606872-3 2007 RESULTS: During combined insulin and glucagon deficiency, glucose production decreased and then increased, and mean (+/-SE) plasma glucose decreased from 83 +/- 1 to 63 +/- 2 mg/dl at 60 min and then increased to 89 +/- 3 mg/dl at 240 min. Glucose 58-65 insulin Homo sapiens 25-32 17606872-5 2007 Partial glucagon replacement raised plasma glucose to higher levels (P = 0.0469) during insulin deficiency and to higher levels (P = 0.0090) during insulin replacement. Glucose 43-50 insulin Homo sapiens 88-95 17606872-6 2007 CONCLUSIONS: These three findings provide direct evidence that glucagon, in concert with insulin, supports the postabsorptive plasma glucose concentration in humans. Glucose 133-140 insulin Homo sapiens 89-96 17626894-5 2007 Acute insulin response to glucose and fasting and 2-h glucose increased (beta = 0.019, beta = 0.002, and beta = 0.003, P < 0.01). Glucose 26-33 insulin Homo sapiens 6-13 17626894-5 2007 Acute insulin response to glucose and fasting and 2-h glucose increased (beta = 0.019, beta = 0.002, and beta = 0.003, P < 0.01). Glucose 54-61 insulin Homo sapiens 6-13 17686943-1 2007 OBJECTIVE: beta-Cell response to glucose is characterized by mitochondrial membrane potential (Delta Psi) hyperpolarization and the production of metabolites that serve as insulin secretory signals. Glucose 33-40 insulin Homo sapiens 172-179 17931052-1 2007 BACKGROUND: A model-based controller for an artificial beta-cell automatically regulates blood glucose levels based on available glucose measurements, insulin infusion and meal information, and model predictions of future glucose trends. Glucose 95-102 insulin Homo sapiens 151-158 17785428-6 2007 Little proof exists, however, that the development of insulin antibodies (IAs) to exogenous insulin therapy affects integrated glucose control, insulin dose requirements, and incidence of hypoglycemia, or contributes to beta-cell failure or to long-term complications of diabetes. Glucose 127-134 insulin Homo sapiens 54-61 17785428-6 2007 Little proof exists, however, that the development of insulin antibodies (IAs) to exogenous insulin therapy affects integrated glucose control, insulin dose requirements, and incidence of hypoglycemia, or contributes to beta-cell failure or to long-term complications of diabetes. Glucose 127-134 insulin Homo sapiens 92-99 17785428-6 2007 Little proof exists, however, that the development of insulin antibodies (IAs) to exogenous insulin therapy affects integrated glucose control, insulin dose requirements, and incidence of hypoglycemia, or contributes to beta-cell failure or to long-term complications of diabetes. Glucose 127-134 insulin Homo sapiens 92-99 18080040-2 2007 The stimulatory effect of insulin on glucose uptake in muscle and adipose tissue is a consequence of the rapid translocation of GLUT4 glucose transporters from an intracellular site to the cell surface. Glucose 37-44 insulin Homo sapiens 26-33 17922630-3 2007 All patients with Type 1 diabetes and many patients with Type 2 diabetes require intensive insulin therapy to achieve optimal glucose control. Glucose 126-133 insulin Homo sapiens 91-98 17931093-2 2007 It mirrors many of the effects of GLP-1, improving glycaemic control through a combination of mechanisms, which include glucose-dependent stimulation of insulin secretion, suppression of glucagon secretion, slowing of gastric emptying and reduced appetite. Glucose 120-127 insulin Homo sapiens 153-160 17559844-6 2007 MAIN OUTCOME MEASURE(S): Androgen levels and insulin-stimulated glucose disposal (metabolic insulin sensitivity), determined by euglycemic-hyperinsulinemic clamp (M-value). Glucose 64-71 insulin Homo sapiens 45-52 18018604-2 2007 METHODS: DM patients were aggressively treated with intensive insulin therapy to achieve a preoperative fasting blood glucose level of 140 mg/dl and a postoperative level of 200 mg/dl. Glucose 118-125 insulin Homo sapiens 62-69 17646573-11 2007 Furthermore, aldosterone pretreatment decreased insulin-stimulated (100 nmol/L; 60 minutes; n=4) glucose uptake by 50%, which was reversed by eplerenone (10 micromol/L; n=4). Glucose 97-104 insulin Homo sapiens 48-55 17952832-2 2007 Insulin regulates blood glucose levels primarily by promoting glucose uptake from the blood into multiple tissues and by suppressing glucose production from the liver. Glucose 24-31 insulin Homo sapiens 0-7 17952832-2 2007 Insulin regulates blood glucose levels primarily by promoting glucose uptake from the blood into multiple tissues and by suppressing glucose production from the liver. Glucose 62-69 insulin Homo sapiens 0-7 17952832-2 2007 Insulin regulates blood glucose levels primarily by promoting glucose uptake from the blood into multiple tissues and by suppressing glucose production from the liver. Glucose 62-69 insulin Homo sapiens 0-7 17952832-3 2007 The glucose transporter, GLUT4, mediates insulin-stimulated glucose uptake in muscle and adipose tissue. Glucose 4-11 insulin Homo sapiens 41-48 17952832-6 2007 However, functional defects in the intracellular trafficking and plasma membrane translocation of GLUT4 result in impaired insulin-stimulated glucose uptake in muscle. Glucose 142-149 insulin Homo sapiens 123-130 17897114-3 2007 CONCLUSIONS: Insulin therapy, if titrated appropriately, is the most physiological and effective intervention for lowering blood glucose and may help preserve beta-cell function in patients with type 2 diabetes. Glucose 129-136 insulin Homo sapiens 13-20 17931573-10 2007 In patients whose insulin requirements have increased as a result of increases in post-prandial glucose excursions, prandial insulin should be added following a stepwise approach to therapy. Glucose 96-103 insulin Homo sapiens 18-25 17931573-10 2007 In patients whose insulin requirements have increased as a result of increases in post-prandial glucose excursions, prandial insulin should be added following a stepwise approach to therapy. Glucose 96-103 insulin Homo sapiens 125-132 17953047-1 2007 (1) An open-loop insulin delivery system combines an external insulin pump with continuous monitoring of glucose levels via a subcutaneous sensor. Glucose 105-112 insulin Homo sapiens 17-24 17635945-5 2007 Insulin sensitivity and secretion were measured by shortened fasting iv glucose tolerance test. Glucose 72-79 insulin Homo sapiens 0-7 17906159-3 2007 The ability of the model to predict the incretin effect was assessed by simulating the observed difference in insulin response following an oral glucose tolerance test compared with an isoglycemic glucose infusion mimicking an oral glucose tolerance test profile. Glucose 145-152 insulin Homo sapiens 110-117 18051927-0 2007 Ghrelin serum levels during oral glucose tolerance test in prepubertal obese children with insulin resistance. Glucose 33-40 insulin Homo sapiens 91-98 17884452-2 2007 As often observed in patients with GSD1a, this patient has multiple risk factors for atherosclerosis including hyperlipidemia, hypertension, glucose intolerance with insulin resistance, and chronic kidney disease. Glucose 141-148 insulin Homo sapiens 166-173 17884454-4 2007 Insulin secretion was assessed by measuring insulin and glucose levels 30 minutes after an oral glucose load. Glucose 56-63 insulin Homo sapiens 0-7 17884454-4 2007 Insulin secretion was assessed by measuring insulin and glucose levels 30 minutes after an oral glucose load. Glucose 96-103 insulin Homo sapiens 0-7 17904198-3 2007 Insulin sensitivity was assessed with a 2-h oral glucose tolerance test, magnetic resonance spectroscopy was used to asses IMCL, LFAT and plasma lipids were measured before and after 6, 11 and 61 days of PPAR-alpha agonist (fenofibrate) administration in 19 elderly (age 70+/-1 years) volunteers. Glucose 49-56 insulin Homo sapiens 0-7 17979810-6 2007 Moreover, recent studies suggest that Cdk5 plays crucial roles in physiological functions in non-neuronal cells such as glucose-stimulated insulin secretion in pancreatic -cells. Glucose 120-127 insulin Homo sapiens 139-146 17925465-10 2007 DISCUSSION: To our knowledge, this is the first protein array data on a very early dysregulation of ScAT protein levels in insulin-resistant obese, but apparently healthy, subjects with normal glucose tolerance. Glucose 193-200 insulin Homo sapiens 123-130 17727385-7 2007 In addition, continuous glucose monitoring may teach us better ways to use insulin in children who do not have the technology available to them. Glucose 24-31 insulin Homo sapiens 75-82 18084670-4 2007 Oral inhibitors of DPP-4 increase GLP-1 levels and this leads to lower glucose levels caused by increased insulin secretion and decreased glucagon levels. Glucose 71-78 insulin Homo sapiens 106-113 17999597-7 2007 Insulin secretion from these ISILCs is regulated by glucose concentration in vitro, and transplantation of purified ISILCs normalizes hyperglycemia in streptozocin (STZ)- induced nonobese diabetic (NOD)/SCID mice. Glucose 52-59 insulin Homo sapiens 0-7 18218239-4 2007 Acute insulin secretion response (AIR(3 - 5)) during intravenous glucose tolerance test (IVGTT) was adopted to indicate the first phase insulin secretion with the ratio of insulin change from 0 min to 30 min to that of blood glucose from 0 min to 30 min (DeltaI(30)/DeltaG(30)) as the indicator of early insulin secretion and insulin sensitivity (ISI) was analyzed by the formula suggested by Cederholm during oral glucose tolerance (OGTT). Glucose 65-72 insulin Homo sapiens 6-13 18173967-4 2007 In particular, an understanding of the role of basal insulin in the regulation of glucose and the development of strategies to implement basal insulin therapy can provide a transition that is rational and highly effective in most patients. Glucose 82-89 insulin Homo sapiens 53-60 17644513-6 2007 We also demonstrate that PI3K-C2alpha contributes to maximal insulin-induced translocation of the glucose transporter GLUT4 to the plasma membrane and subsequent glucose uptake, definitely assessing the role of this enzyme in insulin signaling. Glucose 98-105 insulin Homo sapiens 61-68 17644513-6 2007 We also demonstrate that PI3K-C2alpha contributes to maximal insulin-induced translocation of the glucose transporter GLUT4 to the plasma membrane and subsequent glucose uptake, definitely assessing the role of this enzyme in insulin signaling. Glucose 98-105 insulin Homo sapiens 226-233 17895943-7 2007 Insulin therapy should be considered when plasma glucose levels exceed 8 mmol/L; the treatment target is 4-6 mmol/L. Glucose 49-56 insulin Homo sapiens 0-7 17724330-5 2007 Ingestion of glucose by alpha-gustducin null mice revealed deficiencies in secretion of GLP-1 and the regulation of plasma insulin and glucose. Glucose 13-20 insulin Homo sapiens 123-130 17490777-8 2007 Elevation in post-challenge glucose (120 min) and insulin levels (30 and 120 min) suggests that reduced insulin sensitivity during glucose loading occurs in subjects with A/A polymorphism. Glucose 28-35 insulin Homo sapiens 104-111 17490777-8 2007 Elevation in post-challenge glucose (120 min) and insulin levels (30 and 120 min) suggests that reduced insulin sensitivity during glucose loading occurs in subjects with A/A polymorphism. Glucose 131-138 insulin Homo sapiens 50-57 17490777-8 2007 Elevation in post-challenge glucose (120 min) and insulin levels (30 and 120 min) suggests that reduced insulin sensitivity during glucose loading occurs in subjects with A/A polymorphism. Glucose 131-138 insulin Homo sapiens 104-111 17490777-9 2007 The present study demonstrates that the A/A polymorphism of the MCP-1 gene at position -2518 is associated with insulin resistance during glucose loading in non-diabetic Japanese subjects. Glucose 138-145 insulin Homo sapiens 112-119 17490781-10 2007 Improving glucose control by adding insulin glargine to OAD therapy had a positive impact on TS and general QoL without complaints related to hypoglycemia. Glucose 10-17 insulin Homo sapiens 36-43 17593244-1 2007 AIMS: In muscle, resistance to insulin-mediated glucose uptake is thought to underlie the pre-Type 2 diabetic condition. Glucose 48-55 insulin Homo sapiens 31-38 18218239-4 2007 Acute insulin secretion response (AIR(3 - 5)) during intravenous glucose tolerance test (IVGTT) was adopted to indicate the first phase insulin secretion with the ratio of insulin change from 0 min to 30 min to that of blood glucose from 0 min to 30 min (DeltaI(30)/DeltaG(30)) as the indicator of early insulin secretion and insulin sensitivity (ISI) was analyzed by the formula suggested by Cederholm during oral glucose tolerance (OGTT). Glucose 225-232 insulin Homo sapiens 6-13 17846409-5 2007 RESULTS: In early AD, insulin and glucose AUCs were related to whole brain (insulin beta = 0.66, p < 0.001; glucose beta = 0.45, p < 0.01) and hippocampal volume (insulin beta = 0.42, p < 0.05; glucose beta = 0.46, p < 0.05). Glucose 34-41 insulin Homo sapiens 76-83 17846409-5 2007 RESULTS: In early AD, insulin and glucose AUCs were related to whole brain (insulin beta = 0.66, p < 0.001; glucose beta = 0.45, p < 0.01) and hippocampal volume (insulin beta = 0.42, p < 0.05; glucose beta = 0.46, p < 0.05). Glucose 108-115 insulin Homo sapiens 22-29 17718790-6 2007 High glucose-stimulated insulin response is associated with high plasma C20:3n-6 and C20:4n-6 values only in obese children with the G allele of the -866 G/A polymorphism. Glucose 5-12 insulin Homo sapiens 24-31 17828323-7 2007 Glucose from sucrose and starch increase blood glucose levels and stimulate insulin secretion. Glucose 0-7 insulin Homo sapiens 76-83 17550999-8 2007 Our study indicates that palmitate-induced insulin resistance is provoked by two distinct mechanisms: 1) an early phase (< or =6 h), during which lipid-mediated impairments in insulin signaling and GLUT4 translocation reduce insulin-stimulated glucose transport, followed by 2) a later phase (12 and 18 h), during which the intrinsic activity of GLUT4 is markedly reduced independently of any further alterations in intramuscular lipid accumulation, insulin signaling and GLUT4 translocation. Glucose 247-254 insulin Homo sapiens 179-186 17550999-1 2007 We examined, in soleus muscle, the effects of prolonged palmitate exposure (0, 6, 12, 18 h) on insulin-stimulated glucose transport, intramuscular lipid accumulation and oxidation, activation of selected insulin-signaling proteins, and the insulin-stimulated translocation of GLUT4. Glucose 114-121 insulin Homo sapiens 95-102 17550999-2 2007 Insulin-stimulated glucose transport was progressively reduced after 6 h (-33%), 12 h (-66%), and 18 h (-89%) of palmitate exposure. Glucose 19-26 insulin Homo sapiens 0-7 17550999-8 2007 Our study indicates that palmitate-induced insulin resistance is provoked by two distinct mechanisms: 1) an early phase (< or =6 h), during which lipid-mediated impairments in insulin signaling and GLUT4 translocation reduce insulin-stimulated glucose transport, followed by 2) a later phase (12 and 18 h), during which the intrinsic activity of GLUT4 is markedly reduced independently of any further alterations in intramuscular lipid accumulation, insulin signaling and GLUT4 translocation. Glucose 247-254 insulin Homo sapiens 179-186 17550999-8 2007 Our study indicates that palmitate-induced insulin resistance is provoked by two distinct mechanisms: 1) an early phase (< or =6 h), during which lipid-mediated impairments in insulin signaling and GLUT4 translocation reduce insulin-stimulated glucose transport, followed by 2) a later phase (12 and 18 h), during which the intrinsic activity of GLUT4 is markedly reduced independently of any further alterations in intramuscular lipid accumulation, insulin signaling and GLUT4 translocation. Glucose 247-254 insulin Homo sapiens 179-186 17827708-4 2007 Activation of PI 3-kinase and its downstream AKT has been demonstrated to be essential for almost all of the insulin-induced glucose and lipid metabolism such as glucose uptake, glycogen synthesis, suppression of glucose output and triglyceride synthesis as well as insulin-induced mitogenesis. Glucose 125-132 insulin Homo sapiens 109-116 17609256-5 2007 Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. Glucose 157-164 insulin Homo sapiens 0-7 17827708-4 2007 Activation of PI 3-kinase and its downstream AKT has been demonstrated to be essential for almost all of the insulin-induced glucose and lipid metabolism such as glucose uptake, glycogen synthesis, suppression of glucose output and triglyceride synthesis as well as insulin-induced mitogenesis. Glucose 162-169 insulin Homo sapiens 109-116 17583514-1 2007 beta-Carbolines stimulate insulin secretion in a glucose-dependent manner, probably by acting on I(3)-binding site. Glucose 49-56 insulin Homo sapiens 26-33 17583514-4 2007 Interestingly, with respect to the control, test compounds showed concentration-dependent insulin release, only in presence of glucose load (16.7 mmol). Glucose 127-134 insulin Homo sapiens 90-97 17767908-0 2007 Glucose recruits K(ATP) channels via non-insulin-containing dense-core granules. Glucose 0-7 insulin Homo sapiens 41-48 17767908-1 2007 beta cells rely on adenosine triphosphate-sensitive potassium (K(ATP)) channels to initiate and end glucose-stimulated insulin secretion through changes in membrane potential. Glucose 100-107 insulin Homo sapiens 119-126 17767908-7 2007 Our data suggest that glucose can recruit K(ATP) channels to the beta cell plasma membrane via non-insulin-containing dense-core granules in a Ca(2+)- and PKA-dependent manner. Glucose 22-29 insulin Homo sapiens 99-106 17846641-9 2007 These results suggest that insulin-stimulated Glut-4 translocation and glucose uptake are caveolae-independent events. Glucose 71-78 insulin Homo sapiens 27-34 17846641-1 2007 Caveolae and non-caveolar lipid rafts are two types of membrane lipid microdomains that play important roles in insulin-stimulated glucose uptake in adipocytes. Glucose 131-138 insulin Homo sapiens 112-119 17713396-7 2007 Insulin-stimulated glucose uptake is impaired following burn trauma, as is intracellular insulin signaling, palmitate oxidation, and mitochondrial oxidative capacity. Glucose 19-26 insulin Homo sapiens 0-7 17713399-10 2007 In conclusion, demonstration of the clinical benefits of intensive insulin therapy depends on the quality of blood glucose control and the statistical power of the studies. Glucose 115-122 insulin Homo sapiens 67-74 17713400-0 2007 Clinical experience with tight glucose control by intensive insulin therapy. Glucose 31-38 insulin Homo sapiens 60-67 17713400-1 2007 OBJECTIVE: To describe the current status and the clinical data related to the effects of tight glucose control by intensive insulin therapy in critically ill patients. Glucose 96-103 insulin Homo sapiens 125-132 17713400-5 2007 INTERVENTIONS: Tight glucose control by intensive insulin therapy. Glucose 21-28 insulin Homo sapiens 50-57 17713400-9 2007 CONCLUSIONS: Recommendations regarding the practical aspects of tight glucose control by intensive insulin therapy cannot be presently issued. Glucose 70-77 insulin Homo sapiens 99-106 17449130-2 2007 In pancreatic beta-cells, intracellular glucose metabolism regulates exocytosis of insulin granules, according to metabolism-secretion coupling in which glucose-induced mitochondrial ATP production plays an essential role. Glucose 40-47 insulin Homo sapiens 83-90 17449130-2 2007 In pancreatic beta-cells, intracellular glucose metabolism regulates exocytosis of insulin granules, according to metabolism-secretion coupling in which glucose-induced mitochondrial ATP production plays an essential role. Glucose 153-160 insulin Homo sapiens 83-90 17499540-7 2007 Analogically to QUICKI, we calculated a new formula derived from the OGTT measurements of glucose and insulin named simple index assessing insulin sensitivity (SI(is)OGTT)=1/[log(sum glucose t(0-30-90-120)) (mmol/l)+log(sum insulin t(0-30-90-120)) (microUI/ml)]. Glucose 90-97 insulin Homo sapiens 139-146 17499540-7 2007 Analogically to QUICKI, we calculated a new formula derived from the OGTT measurements of glucose and insulin named simple index assessing insulin sensitivity (SI(is)OGTT)=1/[log(sum glucose t(0-30-90-120)) (mmol/l)+log(sum insulin t(0-30-90-120)) (microUI/ml)]. Glucose 90-97 insulin Homo sapiens 139-146 17512083-12 2007 Insulin expression, both insulin mRNA and peptide levels, was increased and showed glucose dependent manner by ectopic expression of clusterin upon the culture of neogenic ductules when compared to the mock-transfected control, implying that the duct cells transformed functional beta cells. Glucose 83-90 insulin Homo sapiens 0-7 17512083-15 2007 In particular, by modulation of Pdx-1 and Ngn-3, clusterin induces remarkable differentiation of the functional beta cells secreting insulin in response to glucose stimulation. Glucose 156-163 insulin Homo sapiens 133-140 17575082-5 2007 Resulting blastocysts were compared with embryos cocultured with excess IGF-I plus metformin and embryos cultured in control medium for the following: AMPK phosphorylation, insulin-stimulated glucose uptake, and apoptosis. Glucose 192-199 insulin Homo sapiens 173-180 17575082-8 2007 Compared with control blastocysts, blastocysts exposed to high concentrations of IGF-I showed a decrease in AMPK activation and insulin-stimulated glucose uptake and an increase in the number of apoptotic nuclei. Glucose 147-154 insulin Homo sapiens 128-135 17595351-0 2007 The Clamp-Like Index: a novel and highly sensitive insulin sensitivity index to calculate hyperinsulinemic clamp glucose infusion rates from oral glucose tolerance tests in nondiabetic subjects. Glucose 113-120 insulin Homo sapiens 51-58 17595351-0 2007 The Clamp-Like Index: a novel and highly sensitive insulin sensitivity index to calculate hyperinsulinemic clamp glucose infusion rates from oral glucose tolerance tests in nondiabetic subjects. Glucose 146-153 insulin Homo sapiens 51-58 17606307-6 2007 The fasting plasma glucose (p<0.01) and post-glucose load plasma insulin (p<0.01) of women with PCOS were higher than those of controls. Glucose 48-55 insulin Homo sapiens 68-75 17606307-9 2007 Between IR and IS groups, DHEAS (p<0.01), post-glucose load plasma insulin (p<0.05) showed differences after the adjustment for BMI. Glucose 50-57 insulin Homo sapiens 70-77 17765682-1 2007 Insulin stimulates glucose transport in muscle and adipose tissue by producing translocation of the glucose transporter Glut4. Glucose 19-26 insulin Homo sapiens 0-7 17765682-5 2007 Disruption of RalA function by dominant-negative mutants or siRNA-mediated knockdown attenuates insulin-stimulated glucose transport. Glucose 115-122 insulin Homo sapiens 96-103 17609256-6 2007 Oral glucose administration led to an approximately 60% reduction in the C-peptide-to-insulin ratio (P < 0.0001), whereas intravenous glucose administration had no effect (P = 0.09). Glucose 5-12 insulin Homo sapiens 86-93 17609256-10 2007 An inverse nonlinear relationship was found between the C-peptide-to-insulin ratio and the integrated insulin levels after oral and during intravenous glucose administration. Glucose 151-158 insulin Homo sapiens 69-76 17609256-10 2007 An inverse nonlinear relationship was found between the C-peptide-to-insulin ratio and the integrated insulin levels after oral and during intravenous glucose administration. Glucose 151-158 insulin Homo sapiens 102-109 17609258-6 2007 The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r > 0.82, P < 0.05). Glucose 62-69 insulin Homo sapiens 13-20 17609258-8 2007 In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. Glucose 38-45 insulin Homo sapiens 103-110 17583689-4 2007 The HOMA-IR index (homeostasis model of insulin resistance) was calculated as [fasting serum glucose*fasting serum insulin/22.5], with lower values indicating a higher degree of insulin sensitivity. Glucose 93-100 insulin Homo sapiens 40-47 17270310-4 2007 RESULTS: In all subjects the model was able to simulate influences of the insulin plasma concentration and gastric emptying rate on glucose concentration and to determine time profiles of glucose fractions retained in stomach. Glucose 132-139 insulin Homo sapiens 74-81 17467844-0 2007 Negative and positive feedback regulation of insulin in glucose-stimulated Ca2+ response in pancreatic beta cells. Glucose 56-63 insulin Homo sapiens 45-52 17467844-2 2007 The present study has evaluated how exogenous insulin participates in cytosolic Ca(2+) response to high glucose, according to glucose concentration at which insulin is applied. Glucose 104-111 insulin Homo sapiens 46-53 17467844-2 2007 The present study has evaluated how exogenous insulin participates in cytosolic Ca(2+) response to high glucose, according to glucose concentration at which insulin is applied. Glucose 126-133 insulin Homo sapiens 46-53 17467844-2 2007 The present study has evaluated how exogenous insulin participates in cytosolic Ca(2+) response to high glucose, according to glucose concentration at which insulin is applied. Glucose 126-133 insulin Homo sapiens 157-164 17467844-3 2007 When 100 nM insulin was pretreated to the bath solution containing islet cells in the presence of basal level of glucose, the elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)) by subsequently applied 10mM glucose was remarkably attenuated. Glucose 113-120 insulin Homo sapiens 12-19 17467844-3 2007 When 100 nM insulin was pretreated to the bath solution containing islet cells in the presence of basal level of glucose, the elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)) by subsequently applied 10mM glucose was remarkably attenuated. Glucose 213-220 insulin Homo sapiens 12-19 17467844-4 2007 In contrast, the glucose-stimulated [Ca(2+)](c) elevation was more potentiated when insulin was superimposed on the high glucose stimulation. Glucose 17-24 insulin Homo sapiens 84-91 17467844-6 2007 By 100 nM insulin, phosphorylated form of AMP-activated protein kinases (p-AMPK) was dramatically decreased in basal glucose but increased in high glucose, when compared with their reciprocal controls. Glucose 117-124 insulin Homo sapiens 10-17 17467844-6 2007 By 100 nM insulin, phosphorylated form of AMP-activated protein kinases (p-AMPK) was dramatically decreased in basal glucose but increased in high glucose, when compared with their reciprocal controls. Glucose 147-154 insulin Homo sapiens 10-17 17467844-7 2007 These results may suggest that the extent of AMPK activation may be a tool for insulin receptors to monitor blood glucose level, with which insulin-induced insulin receptor activation determines the way to go negatively or positively toward [Ca(2+)](c). Glucose 114-121 insulin Homo sapiens 79-86 17467844-7 2007 These results may suggest that the extent of AMPK activation may be a tool for insulin receptors to monitor blood glucose level, with which insulin-induced insulin receptor activation determines the way to go negatively or positively toward [Ca(2+)](c). Glucose 114-121 insulin Homo sapiens 140-147 17467844-7 2007 These results may suggest that the extent of AMPK activation may be a tool for insulin receptors to monitor blood glucose level, with which insulin-induced insulin receptor activation determines the way to go negatively or positively toward [Ca(2+)](c). Glucose 114-121 insulin Homo sapiens 140-147 17563058-5 2007 We demonstrate that impaired insulin-stimulated total, oxidative and nonoxidative glucose disposal in PCOS patients are associated with a consistent downregulation of OXPHOS gene expression using GSEA and GenMAPP analysis. Glucose 82-89 insulin Homo sapiens 29-36 17575088-7 2007 Assessment of insulin sensitivity by clamp showed a significant decrease of the metabolic clearance rate of glucose with increasing aldosterone levels. Glucose 108-115 insulin Homo sapiens 14-21 17586744-0 2007 Coverage of postprandial blood glucose excursions with inhaled technosphere insulin in comparison to subcutaneously injected regular human insulin in subjects with type 2 diabetes. Glucose 31-38 insulin Homo sapiens 76-83 30736121-0 2007 Insulin aspart: rapid control for postmeal glucose excursions. Glucose 43-50 insulin Homo sapiens 0-7 17853331-14 2007 For patients it provides a better understanding of the effects of insulin or oral agents, nutrition and exercises to their glucose level. Glucose 123-130 insulin Homo sapiens 66-73 30736121-1 2007 Insulin aspart is a rapid-acting insulin analog that can be used to control prandial glucose levels as part of basal-bolus therapy, in continuous subcutaneous insulin infusion or in combination with oral antidiabetic drugs. Glucose 85-92 insulin Homo sapiens 0-7 30736121-1 2007 Insulin aspart is a rapid-acting insulin analog that can be used to control prandial glucose levels as part of basal-bolus therapy, in continuous subcutaneous insulin infusion or in combination with oral antidiabetic drugs. Glucose 85-92 insulin Homo sapiens 33-40 30736121-3 2007 Randomized clinical trials have shown efficacy and safety advantages with insulin aspart over human soluble insulin, in particular, improved postprandial glucose control and lower rates of hypoglycemia. Glucose 154-161 insulin Homo sapiens 74-81 30736121-3 2007 Randomized clinical trials have shown efficacy and safety advantages with insulin aspart over human soluble insulin, in particular, improved postprandial glucose control and lower rates of hypoglycemia. Glucose 154-161 insulin Homo sapiens 108-115 17767897-7 2007 Inhaled insulin is clinically effective, and is as good as short-acting soluble insulin in controlling blood glucose, plus it works slightly more quickly. Glucose 109-116 insulin Homo sapiens 8-15 17659530-1 2007 Hypoglycemia is a common and serious problem among diabetic patients receiving treatment with insulin or other glucose-lowering drugs. Glucose 111-118 insulin Homo sapiens 94-101 18051738-5 2007 Insulin regulates constitutive NOS gene expression in endothelial cells in vivo; vasodilation is an important component of Insulin-stimulated whole body glucose uptake. Glucose 153-160 insulin Homo sapiens 0-7 18051738-5 2007 Insulin regulates constitutive NOS gene expression in endothelial cells in vivo; vasodilation is an important component of Insulin-stimulated whole body glucose uptake. Glucose 153-160 insulin Homo sapiens 123-130 17609300-8 2007 CONCLUSIONS: Cortisol withdrawal increased insulin sensitivity in terms of increased glucose oxidation and decreased endogenous glucose production; this may induce hypoglycemia in adrenocortical failure. Glucose 85-92 insulin Homo sapiens 43-50 17609300-8 2007 CONCLUSIONS: Cortisol withdrawal increased insulin sensitivity in terms of increased glucose oxidation and decreased endogenous glucose production; this may induce hypoglycemia in adrenocortical failure. Glucose 128-135 insulin Homo sapiens 43-50 17766701-0 2007 An integrated model for glucose and insulin regulation in healthy volunteers and type 2 diabetic patients following intravenous glucose provocations. Glucose 128-135 insulin Homo sapiens 36-43 17689303-1 2007 Type-2 diabetes is a disorder characterized by disrupted insulin production leading to high blood glucose levels. Glucose 98-105 insulin Homo sapiens 57-64 17766701-1 2007 An integrated model for the regulation of glucose and insulin concentrations following intravenous glucose provocations in healthy volunteers and type 2 diabetic patients was developed. Glucose 99-106 insulin Homo sapiens 54-61 17786232-1 2007 Since the first diabetic was treated with insulin in 1922, millions of patients have relied on frequent insulin injections and glucose monitoring to combat the disease and its complications. Glucose 127-134 insulin Homo sapiens 42-49 19885138-6 2007 RESULTS: Compared to the control day, an 8-hour overnight insulin infusion during a 3-day period improved fasting plasma glucose (FPG) (mean differences +/- SEM; Delta59.0 +/- 10.1 mg/dl; p < 0.01) and 2-hour postprandial plasma glucose (PPPG) (Delta57.8 +/- 10.6 mg/dl; p < 0.01) after breakfast. Glucose 121-128 insulin Homo sapiens 58-65 17878754-4 2007 However, insulin increased actin reorganization and glucose uptake. Glucose 52-59 insulin Homo sapiens 9-16 17878754-7 2007 Either P38 or ERK1/2 inhibitors partially reversed the Ang II-inhibited actin reorganization and glucose uptake, suggesting that MAPK signaling pathways could be involved as downstream events in Ang II signaling, and this signaling may interfere with insulin-induced actin reorganization and glucose uptake. Glucose 292-299 insulin Homo sapiens 251-258 17878754-8 2007 These data imply that Ang II induces insulin resistance by decreasing glucose uptake via disarrangement of actin filaments, which provides a novel insight into understanding of insulin resistance by Ang II at the molecular level. Glucose 70-77 insulin Homo sapiens 37-44 17878754-8 2007 These data imply that Ang II induces insulin resistance by decreasing glucose uptake via disarrangement of actin filaments, which provides a novel insight into understanding of insulin resistance by Ang II at the molecular level. Glucose 70-77 insulin Homo sapiens 177-184 17540511-4 2007 Resistance to insulin seems to be accompanied by a greater risk of glucose intolerance, type 2 diabetes, lipidic anomalies and can involve the development of cardiovascular diseases. Glucose 67-74 insulin Homo sapiens 14-21 19885138-6 2007 RESULTS: Compared to the control day, an 8-hour overnight insulin infusion during a 3-day period improved fasting plasma glucose (FPG) (mean differences +/- SEM; Delta59.0 +/- 10.1 mg/dl; p < 0.01) and 2-hour postprandial plasma glucose (PPPG) (Delta57.8 +/- 10.6 mg/dl; p < 0.01) after breakfast. Glucose 232-239 insulin Homo sapiens 58-65 19885144-5 2007 Insulin sensitivity was estimated from the oral glucose tolerance test (OGTT) and measured by a euglycemic hyperinsulinemic clamp in a subgroup (n = 157). Glucose 48-55 insulin Homo sapiens 0-7 18038714-14 2007 However, metformin at a higher dose and in combination with rosiglitazone resulted in improvement of pancreatic beta-cell function, shown by markedly improved first-phase insulin response to glucose measured by AIR. Glucose 191-198 insulin Homo sapiens 171-178 17697856-1 2007 This study compares indices of insulin sensitivity derived from fasting and oral glucose tolerance test (OGTT) glucose and insulin measurements, with respect to the reference measure (M/I), obtained from the euglycemic-hyperinsulinemic clamp, in postmenopausal women with varying glucose tolerance status. Glucose 81-88 insulin Homo sapiens 31-38 17885284-13 2007 CONCLUSIONS: We suggest that hyperinsulinemia and insulin resistance could be associated with gallstone formation in individuals without clinical diagnosis of diabetes mellitus and with normal serum glucose level. Glucose 199-206 insulin Homo sapiens 34-41 17697856-1 2007 This study compares indices of insulin sensitivity derived from fasting and oral glucose tolerance test (OGTT) glucose and insulin measurements, with respect to the reference measure (M/I), obtained from the euglycemic-hyperinsulinemic clamp, in postmenopausal women with varying glucose tolerance status. Glucose 111-118 insulin Homo sapiens 31-38 17697856-6 2007 Finally, correlation coefficients between M/I and insulin sensitivity indices were generally lower in women with normal glucose tolerance compared with women with impaired glucose tolerance or type 2 diabetes mellitus. Glucose 120-127 insulin Homo sapiens 50-57 17958029-2 2007 Both of them potentiate glucose-induced insulin response, enhance insulin biosynthesis and, at least in rodents, preserve beta-cell mass through reduction of apoptosis and stimulation of beta-cell proliferation. Glucose 24-31 insulin Homo sapiens 40-47 18632035-0 2007 International survey of insulin pump users: Impact of continuous subcutaneous insulin infusion therapy on glucose control and quality of life. Glucose 106-113 insulin Homo sapiens 78-85 18064366-6 2007 The maximum levels of insulin and glucose were observed 60 minutes after the oral glucose load and they were expressed as rG/1. Glucose 82-89 insulin Homo sapiens 22-29 17715056-1 2007 Incretins, endogenous polypeptide hormones released in response to food intake, potentiate insulin secretion from pancreatic beta cells after oral glucose ingestion (the incretin effect). Glucose 147-154 insulin Homo sapiens 91-98 17953366-0 2007 [Mechanism of rosiglitasone to improve glucose-uptake of 3T3-L1 adipocyte with insulin resistance induced by dexamethasone and insulin]. Glucose 39-46 insulin Homo sapiens 79-86 17953366-0 2007 [Mechanism of rosiglitasone to improve glucose-uptake of 3T3-L1 adipocyte with insulin resistance induced by dexamethasone and insulin]. Glucose 39-46 insulin Homo sapiens 127-134 17953366-1 2007 OBJECTIVE: To study the mechanism of rosiglitasone to improve glucose-uptake of 3T3-L1 adipocyte with insulin resistance induced by dexamethasone and insulin. Glucose 62-69 insulin Homo sapiens 102-109 17623014-2 2007 Insulin is synthesized primarily by pancreatic beta-cells and is released in response to an increase in blood glucose levels (hyperglycaemia). Glucose 110-117 insulin Homo sapiens 0-7 17683181-2 2007 It also is indicated for a subset of nonuremic, insulin-dependent diabetics who experience extreme difficulties in maintaining proper glucose homeostasis by insulin therapy that compromises their productivity and safety. Glucose 134-141 insulin Homo sapiens 48-55 17425514-4 2007 Our results show an increase in insulin-mediated glucose disposal during euglycaemic clamp conditions that was significantly higher following the high-salt diet compared with the low-salt diet (7.41+/-0.41 compared with 6.11+/-0.40 mg x kg(-1) of body weight x min(-1) respectively; P=0.03). Glucose 49-56 insulin Homo sapiens 32-39 17468346-5 2007 On one condition, a linear fall of plasma glucose to 2.2 mmol/l was induced within 60 min by infusing insulin during early sleep. Glucose 42-49 insulin Homo sapiens 102-109 18220669-1 2007 Control of blood glucose levels in individuals with diabetes mellitus (DM) is directly affected by the balance between insulin and glucose-raising endocrine hormones, along with other metabolic factors, including fuel use and availability, exercise intensity and duration, training status, and visceral fat levels, all of which can impact the effect of physical activity on insulin action in diabetic or prediabetic individuals. Glucose 17-24 insulin Homo sapiens 119-126 18220669-1 2007 Control of blood glucose levels in individuals with diabetes mellitus (DM) is directly affected by the balance between insulin and glucose-raising endocrine hormones, along with other metabolic factors, including fuel use and availability, exercise intensity and duration, training status, and visceral fat levels, all of which can impact the effect of physical activity on insulin action in diabetic or prediabetic individuals. Glucose 17-24 insulin Homo sapiens 374-381 17473058-0 2007 Diagnosis of hyperglycemia in a cohort of Brazilian subjects: fasting plasma glucose- and oral glucose tolerance test-based glycemic status are associated with different profiles of insulin sensitivity and insulin secretion. Glucose 77-84 insulin Homo sapiens 182-189 18220669-2 2007 Current research suggests that type 2 DM can be prevented and controlled with increased physical activity, largely through improvements in the muscles" sensitivity to insulin that are affected by changes in both glucose and fat metabolism. Glucose 212-219 insulin Homo sapiens 167-174 17473058-0 2007 Diagnosis of hyperglycemia in a cohort of Brazilian subjects: fasting plasma glucose- and oral glucose tolerance test-based glycemic status are associated with different profiles of insulin sensitivity and insulin secretion. Glucose 95-102 insulin Homo sapiens 182-189 17513702-1 2007 The purpose of this study was to investigate the mechanisms explaining improved insulin-stimulated glucose uptake after exercise training in human skeletal muscle. Glucose 99-106 insulin Homo sapiens 80-87 17599013-3 2007 This review discusses recent literature on tight glucose control with insulin therapy and its effects in prevention and management of infection. Glucose 49-56 insulin Homo sapiens 70-77 17513702-3 2007 Fifteen hours after the last exercise bout, insulin-stimulated glucose uptake was approximately 60% higher (P < 0.01) in the trained compared with the untrained leg during a hyperinsulinemic-euglycemic clamp. Glucose 63-70 insulin Homo sapiens 44-51 17513702-9 2007 Our findings do not support generally improved insulin signaling after endurance training; rather it seems that improved insulin-stimulated glucose uptake may result from hemodynamic adaptations as well as increased cellular protein content of individual insulin signaling components and molecules involved in glucose transport and metabolism. Glucose 140-147 insulin Homo sapiens 121-128 17513702-9 2007 Our findings do not support generally improved insulin signaling after endurance training; rather it seems that improved insulin-stimulated glucose uptake may result from hemodynamic adaptations as well as increased cellular protein content of individual insulin signaling components and molecules involved in glucose transport and metabolism. Glucose 140-147 insulin Homo sapiens 121-128 17513702-9 2007 Our findings do not support generally improved insulin signaling after endurance training; rather it seems that improved insulin-stimulated glucose uptake may result from hemodynamic adaptations as well as increased cellular protein content of individual insulin signaling components and molecules involved in glucose transport and metabolism. Glucose 310-317 insulin Homo sapiens 121-128 17513702-9 2007 Our findings do not support generally improved insulin signaling after endurance training; rather it seems that improved insulin-stimulated glucose uptake may result from hemodynamic adaptations as well as increased cellular protein content of individual insulin signaling components and molecules involved in glucose transport and metabolism. Glucose 310-317 insulin Homo sapiens 121-128 17696868-2 2007 Various efforts have produced many potent small molecule inhibitors of GSK-3, which are being tested for modulation of glycogen metabolism, gene transcription, apoptosis and enhancement of insulin-stimulated glucose transport. Glucose 208-215 insulin Homo sapiens 189-196 17883998-3 2007 Specifically, the molecular mechanisms by which the HIV protease inhibitor class of drugs may affect the normal stimulatory effect of insulin on glucose and fat storage are reviewed. Glucose 145-152 insulin Homo sapiens 134-141 17940451-3 2007 They exhibit several properties, including glucose-dependent stimulation of insulin secretion, suppression of glucagon secretion, slowing of gastric emptying and induction of satiety, which result in improvements in glycemic control with weight loss in patients with type 2 diabetes. Glucose 43-50 insulin Homo sapiens 76-83 17940454-5 2007 The ability to recognize trends in blood glucose levels provides a new paradigm for making insulin dose decisions and treating hypo- and hyperglycemia. Glucose 41-48 insulin Homo sapiens 91-98 17525361-2 2007 This leads to capillary recruitment, vasodilation, increased blood flow, and subsequent augmentation of glucose disposal in classical insulin target tissues (e.g., skeletal muscle). Glucose 104-111 insulin Homo sapiens 134-141 17992607-5 2007 However, GLP-1 and exendin-4 increased insulin mediated glucose uptake in intact and TNF-alpha treated 3T3-L1 adipocytes by up-regulation of phophorylated IRbeta, IRS-1, Akt and GSK-3beta. Glucose 56-63 insulin Homo sapiens 39-46 17624545-2 2007 The objective of this study is to investigate the insulin and glucose responses to an oral glucose tolerance test (OGTT) following a high intensity bout of either EE or RE followed by post-exercise carbohydrate-protein hydrolysate ingestion. Glucose 91-98 insulin Homo sapiens 50-57 17666135-1 2007 ATP-sensitive potassium (KATP) channels play a key role in the regulation of insulin secretion by coupling glucose metabolism to the electrical activity of pancreatic beta-cells. Glucose 107-114 insulin Homo sapiens 77-84 17671651-8 2007 Overexpression of TCF7L2 in human islets reduced glucose-stimulated insulin secretion. Glucose 49-56 insulin Homo sapiens 68-75 17286287-3 2007 Long-acting insulin formulations are designed to meet the body"s basal needs, whereas rapid-acting insulin formulations are designed to cover mealtime glucose spikes. Glucose 151-158 insulin Homo sapiens 99-106 17540697-2 2007 Four hours after acute one-legged exercise, insulin-induced glucose uptake was approximately 80% higher (N = 12, P < 0.05) in previously exercised muscle, measured during a euglycaemic-hyperinsulinaemic clamp (100 microU ml(-1)). Glucose 60-67 insulin Homo sapiens 44-51 17765682-7 2007 This interaction is modulated by Calmodulin, which functions as the light chain for Myo1c during insulin-stimulated glucose uptake. Glucose 116-123 insulin Homo sapiens 97-104 17705692-6 2007 It was used to examine the change in blood glucose following the intake of carbohydrate and insulin. Glucose 43-50 insulin Homo sapiens 92-99 17294189-2 2007 Chronic beta-adrenergic stimulation has been implicated in insulin resistance in cultured cardiomyocytes in vitro, where sustained noradrenaline stimulation inhibited insulin-modulated glucose uptake. Glucose 185-192 insulin Homo sapiens 167-174 17785698-6 2007 Pilot studies confirmed that rhIGF-I could reduce glucose and insulin levels in subjects with type A insulin resistance and those with Rabson-Mendenhall syndrome with sustained beneficial effects on HbA1c. Glucose 50-57 insulin Homo sapiens 101-108 17574553-0 2007 Effect of insulin/IGF-I like peptides on glucose metabolism in the white shrimp Penaeus vannamei. Glucose 41-48 insulin Homo sapiens 10-17 17681171-10 2007 LF, but not VAT, was correlated with fasting insulin, insulin-stimulated glucose disposal, and impaired FFA suppression by insulin (all P < .05). Glucose 73-80 insulin Homo sapiens 54-61 17712721-6 2007 This leads to a maximum glucose phosphorylation capacity in-phase with food intake, enhanced glucose-stimulated insulin secretion, and prevents postprandial hyperglycemia. Glucose 24-31 insulin Homo sapiens 112-119 17712721-6 2007 This leads to a maximum glucose phosphorylation capacity in-phase with food intake, enhanced glucose-stimulated insulin secretion, and prevents postprandial hyperglycemia. Glucose 93-100 insulin Homo sapiens 112-119 17712721-7 2007 Perfusion experiments showed a reduction in glucose-stimulated insulin secretion in Goto-Kakizaki rat islets with an impaired first phase. Glucose 44-51 insulin Homo sapiens 63-70 17712721-8 2007 Hyperglycemia and hypoinsulinemia in newborn and up to 3-week-old Goto-Kakizaki rats are thus probably due to reduced pancreatic beta-cell content, reduced beta-cell insulin content and impaired glucose sensing. Glucose 195-202 insulin Homo sapiens 22-29 17593272-6 2007 The current review discusses the clinical implications of these newer therapeutic alternatives, which enhance insulin secretion through glucose-dependent and physiologic mechanisms. Glucose 136-143 insulin Homo sapiens 110-117 18667139-5 2007 Subsequently, a progressive loss of first-phase insulin response occurs, which is manifested by progressively increasing postprandial glucose (PPG) levels. Glucose 134-141 insulin Homo sapiens 48-55 17601993-11 2007 The present study provides direct evidence that suppression of lipolysis in patients with HIV lipodystrophy improves insulin-stimulated peripheral glucose uptake. Glucose 147-154 insulin Homo sapiens 117-124 17572128-0 2007 Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells. Glucose 73-80 insulin Homo sapiens 54-61 17685725-7 2007 Insulin sensitivity was also estimated by fasting glucose and insulin. Glucose 50-57 insulin Homo sapiens 0-7 17693836-3 2007 Varying amounts of insulin by infusion are required to maintain blood glucose levels within normal limits. Glucose 70-77 insulin Homo sapiens 19-26 17572128-5 2007 Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase). Glucose 162-169 insulin Homo sapiens 143-150 17661834-0 2007 Plasma insulin is removed by hemodialysis: evaluation of the relation between plasma insulin and glucose by using a dialysate with or without glucose. Glucose 97-104 insulin Homo sapiens 85-92 17629492-1 2007 The physiological incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), lower blood glucose levels through multiple mechanisms, including enhancement of glucose-stimulated insulin secretion. Glucose 29-36 insulin Homo sapiens 47-54 17629492-1 2007 The physiological incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), lower blood glucose levels through multiple mechanisms, including enhancement of glucose-stimulated insulin secretion. Glucose 129-136 insulin Homo sapiens 47-54 17615236-9 2007 The MARE-CEB is repressed by MafA, whereas the CEB-MARE site, which is homologous to the A2C1 component of the glucose-sensitive RIPE3b region of the insulin gene promoter, is activated by MafA. Glucose 111-118 insulin Homo sapiens 150-157 17616768-4 2007 Insulin sensitivity (S(I)) was measured with an intravenous glucose tolerance test in obese HIV+ women recruited because of their desire to lose weight (n=17) and in obese healthy controls (n=32). Glucose 60-67 insulin Homo sapiens 0-7 17540697-10 2007 Furthermore, endurance exercise increased the responsiveness of aPKC to PIP3 providing a possible link to improved insulin-stimulated glucose uptake after exercise. Glucose 134-141 insulin Homo sapiens 115-122 17699877-2 2007 Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at different anatomical sites and converge to the hypothalamus to cooperate with leptin and insulin in controlling the melanocortin pathway. Glucose 0-7 insulin Homo sapiens 202-209 17699877-2 2007 Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at different anatomical sites and converge to the hypothalamus to cooperate with leptin and insulin in controlling the melanocortin pathway. Glucose 71-78 insulin Homo sapiens 202-209 17637088-8 2007 Insulin is administered according to a relatively simple scale that is adjustable by nursing staff according to patients" glucose results. Glucose 122-129 insulin Homo sapiens 0-7 17510217-2 2007 Generation of glucose-responsive, insulin-producing beta cells from self-renewing, pluripotent human ESCs (hESCs) has immense potential for diabetes treatment. Glucose 14-21 insulin Homo sapiens 34-41 17510217-11 2007 In addition, the hESC-derived ILCs contained numerous secretory granules, as determined by electron microscopy, and secreted human C-peptide in a glucose-dependent manner. Glucose 146-153 insulin Homo sapiens 131-140 17660700-7 2007 The risk factors include waist-to-hip ratio (WHR), triglycerides, high-density lipoprotein (HDL)-cholesterol, blood pressure, and fasting plasma glucose, which are associated with metabolic syndrome and insulin resistance. Glucose 145-152 insulin Homo sapiens 203-210 17628546-5 2007 There is much evidence supporting that detrimental effects of glucose, fatty acids, hormones and cytokines leading to insulin resistance can be exerted via such a common pathway. Glucose 62-69 insulin Homo sapiens 118-125 17988556-0 2007 [Effects of insulin-like growth factor-1 and insulin on modulating glucose metabolism and functions of lung fibroblasts]. Glucose 67-74 insulin Homo sapiens 12-19 17548353-8 2007 Disruption of endogenous Munc18c-Doc2beta complexes by addition of the Doc2beta binding domain of Munc18c (residues 173-255) was found to selectively inhibit glucose-stimulated insulin release. Glucose 158-165 insulin Homo sapiens 177-184 17548353-9 2007 Moreover, increased expression of Doc2beta enhanced glucose-stimulated insulin secretion by approximately 40%, whereas siRNA-mediated depletion of Doc2beta attenuated insulin release. Glucose 52-59 insulin Homo sapiens 71-78 17616757-6 2007 Human trials to date have reported greater insulin-mediated glucose uptake but no effect on fasting glucose or insulin concentrations. Glucose 60-67 insulin Homo sapiens 43-50 17356008-5 2007 The purpose of this study was to determine whether Ad"s effects on FA oxidation and AMPK/ACC would be reduced following different HF diets, and if this coincided with the development of impaired maximal insulin-stimulated glucose transport. Glucose 222-229 insulin Homo sapiens 203-210 17356008-8 2007 LARD rats showed reduced rates of maximal insulin-stimulated glucose transport compared with CON and SAFF (+68 vs. +172 and +184%, P < or = 0.001). Glucose 61-68 insulin Homo sapiens 42-49 17356008-10 2007 Thus 4 wk of HF feeding results in the loss of gAd stimulatory effect on ACC phosphorylation and muscle FA oxidation, and this can occur independently of impaired maximal insulin-stimulated glucose transport. Glucose 190-197 insulin Homo sapiens 171-178 17440034-4 2007 A glucose clamp was performed at an insulin infusion of 80 mU x min(-1) x m(-2). Glucose 2-9 insulin Homo sapiens 36-43 17456637-3 2007 The model provides an interpretation of the roles of the triggering and amplifying pathways of glucose-stimulated insulin secretion. Glucose 95-102 insulin Homo sapiens 114-121 17619673-9 2007 Glitazones are an alternative to insulin, but for HbA1c, >or=9.5% insulin results in greater improvement in fasting glucose and HbA1c. Glucose 119-126 insulin Homo sapiens 69-76 17482433-5 2007 Antimycin A and oligomycin treatment induced insulin resistance at the level of glucose and palmitate uptake in all three study groups while, at the level of glycogen synthesis, insulin resistance was only seen in lean myotubes. Glucose 80-87 insulin Homo sapiens 45-52 17482433-6 2007 Primary insulin resistance in diabetic myotubes was significantly worsened at the level of glucose and lipid uptake. Glucose 91-98 insulin Homo sapiens 8-15 17391917-5 2007 However, DPI increases basal and insulin-stimulated glucose uptake in L6 cells, C(2)C(12) cells and primary muscle cells. Glucose 52-59 insulin Homo sapiens 33-40 17563470-5 2007 Intervention trials of insulin therapy are limited but overall demonstrate that glucose lowering significantly improves outcomes. Glucose 80-87 insulin Homo sapiens 23-30 17563474-2 2007 Insulin-stimulated nitric oxide mediates capillary recruitment, vasodilation, increased blood flow, and subsequent augmentation of glucose disposal in skeletal muscle. Glucose 131-138 insulin Homo sapiens 0-7 17563475-11 2007 Insulin therapy in hyperglycaemic subjects may be of benefit through effects of both insulin itself and lowered glucose concentration. Glucose 112-119 insulin Homo sapiens 0-7 17384344-8 2007 Changes in fat deposition were associated with decreased postprandial mRNA adiponectin levels in peripheral adipose tissue and lower insulin sensitivity index values from a frequently sampled insulin-assisted intravenous glucose tolerance test in patients fed a CHO-rich diet compared with a MUFA-rich diet (ANOVA P < 0.05). Glucose 221-228 insulin Homo sapiens 192-199 17393133-6 2007 Insulin secretion was assessed from an OGTT and a modified intravenous glucose tolerance test. Glucose 71-78 insulin Homo sapiens 0-7 17400929-5 2007 On two nights, a linear fall in plasma glucose to a nadir of 2.2 mmol/l within 60 min was induced by insulin infusion. Glucose 39-46 insulin Homo sapiens 101-108 17456839-4 2007 RESULTS: In subjects with chronic bronchitis and emphysema, AIR inhaled insulin administration resulted in reduced insulin exposure (area under the serum insulin concentration curve from time zero until time of return to baseline [AUC(0-t")]) (55.7%, P = 0.13 and 78.5%, P < 0.001, respectively) and reduced total insulin effect (total glucose infusion rate) (60.4%, P < 0.01 and 67.1%, P < 0.01, respectively) relative to healthy subjects. Glucose 339-346 insulin Homo sapiens 72-79 17468352-1 2007 OBJECTIVE: The homeostasis model assessment (HOMA), based on plasma levels of fasting glucose and insulin, has been widely validated and applied for quantifying insulin resistance and beta-cell function. Glucose 86-93 insulin Homo sapiens 161-168 17479246-5 2007 Cotransfections of INS-1E and beta-TC3 beta cells with a human (h)KLF11 expression plasmid and an hInsP-driven reporter plasmid resulted in a substantial dose-dependent and glucose-independent inhibition of proinsulin promoter activity. Glucose 173-180 insulin Homo sapiens 207-217 17596480-6 2007 The association of gestational glucose intolerance with gestational hypertension appears to be independent of obesity and ambient glycemia but explained in part by insulin resistance. Glucose 31-38 insulin Homo sapiens 164-171 17576204-5 2007 Insulin sensitivity was estimated from an oral glucose tolerance test (OGTT). Glucose 47-54 insulin Homo sapiens 0-7 17576204-13 2007 CONCLUSIONS: Moderate weight loss under a lifestyle intervention with reduction in total, visceral and ectopic fat and increase in insulin sensitivity improves glucose tolerance in individuals with IGT but not with NGT. Glucose 160-167 insulin Homo sapiens 131-138 17576204-14 2007 In individuals with NGT, the beneficial effects of a lifestyle intervention on fat distribution and insulin sensitivity possibly prevent future deterioration in glucose tolerance. Glucose 161-168 insulin Homo sapiens 100-107 17609404-10 2007 Finally, high-density lipoproteins and the area under curve for glucose/area under curve for insulin ratio also significantly increased (P<0.001), whereas low-density lipoproteins and area under curve for insulin were significantly reduced (P<0.001). Glucose 64-71 insulin Homo sapiens 93-100 17609405-2 2007 RESULTS: When blood glucose levels were below 2.5 mmol/l, insulin was <21 pmol/l in 8-35% of the patients and in all controls; C-peptide was >0.2 nmol/l in all insulinomas but not in the nesidioblastosis or in the controls; proinsulin was >5 pmol/l in all patients but not in the controls. Glucose 20-27 insulin Homo sapiens 58-65 17609405-3 2007 When fasting blood glucose levels reached 2.5-3.3 mmol/l, proinsulin was <22 pmol/l in all the controls and >22 pmol/l in 74% of the patients. Glucose 19-26 insulin Homo sapiens 58-68 17475247-1 2007 Insulin activates glucose transport by promoting translocation of the insulin-sensitive fat/muscle-specific glucose transporter GLUT4 from an intracellular storage compartment to the cell surface. Glucose 18-25 insulin Homo sapiens 0-7 17475247-1 2007 Insulin activates glucose transport by promoting translocation of the insulin-sensitive fat/muscle-specific glucose transporter GLUT4 from an intracellular storage compartment to the cell surface. Glucose 18-25 insulin Homo sapiens 70-77 17475247-2 2007 Here we report that an optimal insulin effect on glucose uptake in 3T3-L1 adipocytes is dependent upon expression of both PIKfyve, the sole enzyme for PtdIns 3,5-P(2) biosynthesis, and the PIKfyve activator, ArPIKfyve. Glucose 49-56 insulin Homo sapiens 31-38 17475247-3 2007 Small-interfering RNAs that selectively ablated PIKfyve or ArPIKfyve in this cell type depleted the PtdIns 3,5-P(2) pool and reduced insulin-activated glucose uptake to a comparable degree. Glucose 151-158 insulin Homo sapiens 133-140 17475247-8 2007 Together, the data demonstrate for the first time a physical association between functionally related PIKfyve and ArPIKfyve in 3T3-L1 adipocytes and indicate that the novel ArPIKfyve-PIKfyve-PtdIns 3,5-P(2) pathway is physiologically linked to insulin-activated GLUT4 translocation and glucose transport. Glucose 286-293 insulin Homo sapiens 244-251 30290427-6 2007 Exercise increases glucose uptake and lipid oxidation by an insulin-independent mechanism. Glucose 19-26 insulin Homo sapiens 60-67 30290427-10 2007 Activation of AMPK enhances GLUT4 translocation of glucose uptake in skeletal muscle from Type 2 diabetic patients and animal models of the disease by an insulin-independent mechanism. Glucose 51-58 insulin Homo sapiens 154-161 17276431-10 2007 RESULT(S): Both groups showed an insulin response to the glucose load above the normal range. Glucose 57-64 insulin Homo sapiens 33-40 17611903-8 2007 One patient with insulinoma had no neuroglycopenic symptoms, but was diagnosed by glucose and insulin levels during the 48-hour fast. Glucose 82-89 insulin Homo sapiens 17-24 17986744-4 2007 Rate constant for insulin tolerance test (KITT) was calculated using the formula KITT (%/min) = 0.693/t(1/2), where t(1/2) was calculated from the slope of plasma glucose concentration during 3-15 minutes after administration of intravenous insulin. Glucose 163-170 insulin Homo sapiens 18-25 17339414-14 2007 Insulin did not increase conversion of glucose to CO(2), lactate, or total lipid in steers fed hay but caused an increase (per cell) of 97 to 110% in glucose conversion to CO(2), 46 to 54% in glucose conversion to lactate, and 65 to 160% in glucose conversion to total lipid content in adipose tissue from steers fed corn. Glucose 150-157 insulin Homo sapiens 0-7 17339414-14 2007 Insulin did not increase conversion of glucose to CO(2), lactate, or total lipid in steers fed hay but caused an increase (per cell) of 97 to 110% in glucose conversion to CO(2), 46 to 54% in glucose conversion to lactate, and 65 to 160% in glucose conversion to total lipid content in adipose tissue from steers fed corn. Glucose 150-157 insulin Homo sapiens 0-7 17339414-14 2007 Insulin did not increase conversion of glucose to CO(2), lactate, or total lipid in steers fed hay but caused an increase (per cell) of 97 to 110% in glucose conversion to CO(2), 46 to 54% in glucose conversion to lactate, and 65 to 160% in glucose conversion to total lipid content in adipose tissue from steers fed corn. Glucose 150-157 insulin Homo sapiens 0-7 17339414-19 2007 adipose tissue from corn-fed steers to insulin resulted in a 165% increase in glucose incorporation into fatty acids. Glucose 78-85 insulin Homo sapiens 39-46 17339414-20 2007 These results suggest that feeding hay limited both glucose supply and tissue capacity to increase glucose utilization in response to insulin without altering acetate conversion to fatty acids. Glucose 99-106 insulin Homo sapiens 134-141 17488791-8 2007 Beta-cell function and secretory capacity were assessed by the insulin secretory responses to iv glucose, arginine (AIR(arg)), and glucose-potentiated arginine (AIR(pot)) before and at alloantibody detection. Glucose 97-104 insulin Homo sapiens 63-70 17488791-9 2007 The acute insulin response to glucose was almost entirely lost, whereas the AIR(arg) and AIR(pot) both decreased by approximately 50%. Glucose 30-37 insulin Homo sapiens 10-17 17592027-7 2007 Insulin-stimulated glucose utilization in adipose tissues decreases in 8 months, while in oxidative muscles it reaches significance only in older rats. Glucose 19-26 insulin Homo sapiens 0-7 19885105-1 2007 A study that glucose control can be achieved in 31 type 1 patients who follow a controlled diet and use an insulin pump that is programmed. Glucose 13-20 insulin Homo sapiens 107-114 19885117-7 2007 CONCLUSION: The recent introduction of rigorously implemented insulin titration algorithms when adding on basal insulin to oral drugs in inadequately treated type 2 diabetes patients has led to better average glycemic control with little risk of severe hypoglycemia, as long as the morning fasting plasma glucose target is not lower than 100 mg/dl. Glucose 305-312 insulin Homo sapiens 62-69 17512085-4 2007 Insulin resistance in hepatocytes distorts directly glucose metabolism, especially the control over glucose output into the circulation and interferes with cell survival and proliferation, while hepatic fatty acid synthesis remains stimulated by compensatory hyperinsulinaemia, resulting in steatosis. Glucose 52-59 insulin Homo sapiens 0-7 17512085-4 2007 Insulin resistance in hepatocytes distorts directly glucose metabolism, especially the control over glucose output into the circulation and interferes with cell survival and proliferation, while hepatic fatty acid synthesis remains stimulated by compensatory hyperinsulinaemia, resulting in steatosis. Glucose 100-107 insulin Homo sapiens 0-7 17598817-5 2007 We demonstrated significant nongenetic associations between birth weight and measures of glucose homeostasis in MZ twins, with a reduction in fasting plasma glucose, 120 min post-OGTT plasma glucose, fasting plasma insulin and HOMA-IR index of 15.7%, 25.5%, 26.4% and 37.2%, respectively, for every 1 kg increase in birth weight. Glucose 89-96 insulin Homo sapiens 215-222 17679067-8 2007 Insulin sensitivity was an independent predictor of increased myocardial glucose extraction fraction and utilization (P < .01 and P = .01, respectively). Glucose 73-80 insulin Homo sapiens 0-7 17849744-7 2007 Insulin sensitivity as calculated by quantitative insulin-sensitivity check index (QUICKI = 1/[log(I0) + log(G0)], where I0 is fasting insulin and G0 is fasting glucose) was computed following the visit. Glucose 161-168 insulin Homo sapiens 0-7 17515613-1 2007 Phosphatidylinositol 3-kinase activation of Akt signaling is critical to insulin-stimulated glucose transport and GLUT4 translocation. Glucose 92-99 insulin Homo sapiens 73-80 17515613-5 2007 Small interfering RNA-induced inhibition of myosin 5a and expression of dominant-negative myosin 5a attenuate insulin-stimulated glucose transport and GLUT4 translocation. Glucose 129-136 insulin Homo sapiens 110-117 17515613-6 2007 Furthermore, knockdown of Akt2 or expression of dominant-negative Akt (DN-Akt) abolished insulin-stimulated phosphorylation of myosin 5a, inhibited myosin 5a binding to actin, and blocked insulin-stimulated glucose transport. Glucose 207-214 insulin Homo sapiens 89-96 17570249-3 2007 Consequently, we defined the relationship between differences in insulin-mediated glucose uptake (IMGU), abdominal obesity, and various measures of lipoprotein metabolism known to increase CHD risk in 52 apparently healthy women of South Asian Indian ancestry. Glucose 82-89 insulin Homo sapiens 65-72 21603515-2 2007 Traditional hyperglycemic management has been done either by subcutaneous sliding scale or intravenous insulin infusions based on absolute glucose numbers. Glucose 139-146 insulin Homo sapiens 103-110 17575539-10 2007 The process appears vigorous and sensitive enough to account for a significant reduction in hepatic glucose output and may represent a major mechanism for insulin regulation of hepatic glucose production. Glucose 100-107 insulin Homo sapiens 155-162 17387600-7 2007 Administration of insulin resulted in a reduced plasma glucose independently of administration route (subcutaneous 7.5 +/- 4.2, n = 9, and intradermal 11 +/- 1.8, n = 9 after 240 min), but with less errors of the mean in the intradermal group. Glucose 55-62 insulin Homo sapiens 18-25 17594734-7 2007 Insulin is transported across the alveolar-epithelial barrier into the blood and has onset of glucose-lowering activity within 10-20 min of inhalation. Glucose 94-101 insulin Homo sapiens 0-7 17662202-8 2007 The incretin mimetics bind to GLP-1 receptors, increasing glucose-dependent secretion of insulin and decreasing glucose-dependent posprandial secretion of glucagon, slowing gastric emptying, and reducing food intake. Glucose 58-65 insulin Homo sapiens 89-96 17823693-3 2007 Insulin detemir improved glycemic control in type 1 patients, with decreases in mean HbA1c (-0.2%, p = 0.0026), fasting glucose (-1.7 mmol/l, p = 0.0033) and within-patient fasting glucose variability (-0.6 mmol/l, p = 0.0472). Glucose 120-127 insulin Homo sapiens 0-7 17823693-3 2007 Insulin detemir improved glycemic control in type 1 patients, with decreases in mean HbA1c (-0.2%, p = 0.0026), fasting glucose (-1.7 mmol/l, p = 0.0033) and within-patient fasting glucose variability (-0.6 mmol/l, p = 0.0472). Glucose 181-188 insulin Homo sapiens 0-7 17929538-1 2007 INTRODUCTION: The main causes of reduced glucose levels during metformin therapy appear to be an increase in insulin action in peripheral tissues and reduced hepatic glucose output due to inhibition gluconeogenesis. Glucose 41-48 insulin Homo sapiens 109-116 17983556-5 2007 The intimate relationship between insulin secretion and insulin sensitivity requires either appropriate tests that open the homeostatic feedback loop ("glucose clamp"), or sophisticated modeling approaches ("HOMA", "minimal model"). Glucose 152-159 insulin Homo sapiens 34-41 17646701-4 2007 Increase in glucose uptake by working skeletal muscle during prolonged exercise is due to an increase in the translocation of insulin and contraction sensitive glucose transporter-4 (GLUT4) proteins to the plasma membrane. Glucose 12-19 insulin Homo sapiens 126-133 17879738-4 2007 Insulin resistant HepG2 cells model was induced by high concentration of insulin, then the effects of ROS on glucose consumption in insulin resistant HepG2 cells were investigated. Glucose 109-116 insulin Homo sapiens 132-139 17879738-7 2007 ROS promoted the glucose consumption in insulin resistance of HepG2 cells, improved the sensitivity of insulin resistance of HepG2 cells to insulin. Glucose 17-24 insulin Homo sapiens 40-47 17619527-4 2007 Although insulin effectively helps patients attain glucose goals, the search for new agents continues. Glucose 51-58 insulin Homo sapiens 9-16 17543346-1 2007 Chronically administered insulin returns enhanced maximal glucose transport capacity induced by diabetes to its normal state. Glucose 58-65 insulin Homo sapiens 25-32 17543346-2 2007 In this study, the direct and acute effects of insulin on glucose transport in different parts of isolated small intestine were investigated. Glucose 58-65 insulin Homo sapiens 47-54 17543346-9 2007 The results of this study show that insulin can directly affect glucose transport in the small intestine; its physiological role must be examined. Glucose 64-71 insulin Homo sapiens 36-43 17624157-1 2007 Patients who are admitted to an intensive care unit for 3 days or longer have an increased survival rate if their blood-glucose levels are strictly controlled by means of intensive insulin therapy. Glucose 120-127 insulin Homo sapiens 181-188 17548418-0 2007 Effect of inhaled insulin on fasting and postprandial plasma glucose. Glucose 61-68 insulin Homo sapiens 18-25 17509989-7 2007 Capillary whole blood glucose levels correlate most closely with laboratory plasma glucose levels in patients receiving intensive intravenous insulin therapy after cardiac surgery. Glucose 22-29 insulin Homo sapiens 142-149 17509989-7 2007 Capillary whole blood glucose levels correlate most closely with laboratory plasma glucose levels in patients receiving intensive intravenous insulin therapy after cardiac surgery. Glucose 83-90 insulin Homo sapiens 142-149 17284580-4 2007 In subjects with normal glucose tolerance (NGT), the ln [insulinogenic index (IGI)] was described by a linear function of ln (x) (x, insulin sensitivity index) in regression analysis when the reciprocal of the insulin resistance index in homeostasis model assessment, Matsuda"s index, and oral glucose insulin sensitivity index were used as x. Glucose 24-31 insulin Homo sapiens 57-64 17299078-8 2007 There was an inverse correlation between fasting FFA and first-phase ISR (r2 = 0.31, P < 0.02) and acute (2-4 min) glucose-induced insulin release after acipimox (r2 =0.52, P < 0.04). Glucose 118-125 insulin Homo sapiens 134-141 17299078-9 2007 In this proof-of-concept study in FH+ individuals predisposed to T2DM, a 48-h reduction of plasma FFA improves day-long meal and glucose-stimulated insulin secretion. Glucose 129-136 insulin Homo sapiens 148-155 17299081-0 2007 Basal and insulin-regulated free fatty acid and glucose metabolism in humans. Glucose 48-55 insulin Homo sapiens 10-17 17299081-1 2007 These studies were done to examine the effects of body composition, resting energy expenditure (REE), sex, and fitness on basal and insulin-regulated FFA and glucose metabolism. Glucose 158-165 insulin Homo sapiens 132-139 17961657-1 2007 The development of an artificial pancreas allowing a continuous insulin infusion according to glucose measurement is closed to be an ideal device for type 1 diabetic patients and for the diabetologits. Glucose 94-101 insulin Homo sapiens 64-71 17510695-2 2007 However, in healthy first-degree relatives of type 2 diabetics, insulin resistance is often present years before glucose intolerance or diabetes becomes clinically manifest. Glucose 113-120 insulin Homo sapiens 64-71 17510697-0 2007 Role of Akt substrate of 160 kDa in insulin-stimulated and contraction-stimulated glucose transport. Glucose 82-89 insulin Homo sapiens 36-43 17510697-1 2007 Insulin and exercise, the most important physiological stimuli to increase glucose transport in skeletal muscle, trigger a redistribution of GLUT4 glucose transporter proteins from the cell interior to the cell surface, thereby increasing glucose transport capacity. Glucose 75-82 insulin Homo sapiens 0-7 17510697-1 2007 Insulin and exercise, the most important physiological stimuli to increase glucose transport in skeletal muscle, trigger a redistribution of GLUT4 glucose transporter proteins from the cell interior to the cell surface, thereby increasing glucose transport capacity. Glucose 147-154 insulin Homo sapiens 0-7 17510697-2 2007 The most distal insulin signaling protein that has been linked to GLUT4 translocation, Akt substrate of 160 kDa (AS160), becomes phosphorylated in insulin-stimulated 3T3-L1 adipocytes; this is important for insulin-stimulated GLUT4 translocation and glucose transport. Glucose 250-257 insulin Homo sapiens 16-23 17510697-2 2007 The most distal insulin signaling protein that has been linked to GLUT4 translocation, Akt substrate of 160 kDa (AS160), becomes phosphorylated in insulin-stimulated 3T3-L1 adipocytes; this is important for insulin-stimulated GLUT4 translocation and glucose transport. Glucose 250-257 insulin Homo sapiens 147-154 17510697-2 2007 The most distal insulin signaling protein that has been linked to GLUT4 translocation, Akt substrate of 160 kDa (AS160), becomes phosphorylated in insulin-stimulated 3T3-L1 adipocytes; this is important for insulin-stimulated GLUT4 translocation and glucose transport. Glucose 250-257 insulin Homo sapiens 147-154 17510697-4 2007 Available data from skeletal muscle support the concepts developed in adipocytes with regard to the role AS160 plays in the regulation of insulin-stimulated glucose transport. Glucose 157-164 insulin Homo sapiens 138-145 17922309-5 2007 Moreover, accumulating evidence that mitochondria failure, reduced glucose utilization and deficient energy metabolism occur already very early in the course of the disease suggests a role of impaired insulin signalling in the pathogenesis of AD. Glucose 67-74 insulin Homo sapiens 201-208 17433254-8 2007 The potential of these insulin producing cells derived from PDMSCs was also demonstrated functionally by the demonstration of secreted insulin in vitro and effective control of blood glucose levels in vivo. Glucose 183-190 insulin Homo sapiens 23-30 17496462-1 2007 OBJECTIVE: Insulin resistance is involved in glucose intolerance, type 2 diabetes mellitus and hypertension. Glucose 45-52 insulin Homo sapiens 11-18 17692716-3 2007 Insulin may be initiated as an add-on therapy to oral treatment using a single evening basal insulin dose and titrating according to fasting blood glucose (FBG) levels (with an ideal target of <5.5 mmol/L [<100 mg/dL] to achieve glycosylated hemoglobin [HbA1c] <7%). Glucose 147-154 insulin Homo sapiens 0-7 17092597-2 2007 We aimed to examine whether the restoration of a more physiological insulin profile using rapid-acting insulin analogues might, through effects on glucose toxicity, improve endogenous insulin secretion rate (ISR) and secondly improve markers of vascular risk. Glucose 147-154 insulin Homo sapiens 68-75 17092597-2 2007 We aimed to examine whether the restoration of a more physiological insulin profile using rapid-acting insulin analogues might, through effects on glucose toxicity, improve endogenous insulin secretion rate (ISR) and secondly improve markers of vascular risk. Glucose 147-154 insulin Homo sapiens 103-110 17092597-2 2007 We aimed to examine whether the restoration of a more physiological insulin profile using rapid-acting insulin analogues might, through effects on glucose toxicity, improve endogenous insulin secretion rate (ISR) and secondly improve markers of vascular risk. Glucose 147-154 insulin Homo sapiens 103-110 17329620-12 2007 In conclusion, rapamycin stimulates insulin-mediated glucose uptake in man under conditions known to activate the mTOR/S6K pathway. Glucose 53-60 insulin Homo sapiens 36-43 17363741-4 2007 Thus, IL-6 has also been suggested to promote insulin-mediated glucose utilization. Glucose 63-70 insulin Homo sapiens 46-53 17363741-14 2007 Insulin-stimulated glucose transport and insulin signaling were unchanged after IL-6 exposure. Glucose 19-26 insulin Homo sapiens 0-7 17369524-4 2007 Whole-body insulin action measured by glucose infusion rate decreased (P < 0.05) after a single exercise bout, whereas in response to repeated bouts of resistance exercise, the glucose infusion rate was similar to the rest trial. Glucose 38-45 insulin Homo sapiens 11-18 17381500-5 2007 Home-measured fasting plasma glucose (PG) was lower with insulin glargine than with insulin detemir (7.0 vs. 7.7 mmol/l, P < 0.001). Glucose 29-36 insulin Homo sapiens 57-64 17384334-4 2007 This was confirmed during preprandial insulin infusion when glucose disposal was lower (P < 0.05) and EGP higher (P < 0.05) in IFG than in NFG subjects. Glucose 60-67 insulin Homo sapiens 38-45 17384341-6 2007 Patients self-adjusted the insulin dose to achieve a fasting plasma glucose 4.0-5.5 mmol/l. Glucose 68-75 insulin Homo sapiens 27-34 17384342-4 2007 RESULTS: Insulin secretion/insulin resistance index (0- to 30- and 0- to 120-min time periods) had the greatest areas under the ROC curve (0.85 and 0.86, respectively), which were significantly greater than the 2-h plasma glucose concentration during the OGTT or the San Antonio Diabetes Prediction Model (SADPM) (P < 0.001 and P < 0.0001, respectively). Glucose 222-229 insulin Homo sapiens 9-16 17384342-4 2007 RESULTS: Insulin secretion/insulin resistance index (0- to 30- and 0- to 120-min time periods) had the greatest areas under the ROC curve (0.85 and 0.86, respectively), which were significantly greater than the 2-h plasma glucose concentration during the OGTT or the San Antonio Diabetes Prediction Model (SADPM) (P < 0.001 and P < 0.0001, respectively). Glucose 222-229 insulin Homo sapiens 27-34 17561792-8 2007 RESULTS: Following the switch from human regular insulin to aspart, hemoglobin A1c (HbA1c) decreased from 8.4 +/- 0.23% at baseline to 7.9 +/- 0.17% (P = 0.031), and thereafter to 7.5 +/- 0.20% (P < 0.001), while plasma glucose concentrations in 10-point profiles, daily insulin dose (37.1 +/- 1.39 IU/day), body mass index (BMI) (30.5 +/- 0.82 kg/m(2)), and frequency of hypo- and hyperglycemic episodes did not change (P > 0.05). Glucose 223-230 insulin Homo sapiens 49-56 17317782-1 2007 Glucokinase (GK) plays a key role in the regulation of glucose use and glucose-stimulated insulin secretion in pancreatic islet cells. Glucose 71-78 insulin Homo sapiens 90-97 17563269-9 2007 Their glucose-lowering effect results from improving insulin sensitivity in a complementary fashion: metformin reduces hepatic glucose production and TZDs increase skeletal muscle glucose use. Glucose 6-13 insulin Homo sapiens 53-60 17572128-7 2007 This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells. Glucose 71-78 insulin Homo sapiens 52-59 17550551-3 2007 At a physiologic level, glitazones stimulate adipocyte differentiation, enhance insulin-sensitive glucose uptake by muscle and fat cells, suppress angiogenesis, inhibit tumor cell growth, and normalize keratinocyte differentiation. Glucose 98-105 insulin Homo sapiens 80-87 17535961-1 2007 The Goto Kakizaki (GK) rat is a widely used animal model to study defective glucose-stimulated insulin release in type-2 diabetes (T2D). Glucose 76-83 insulin Homo sapiens 95-102 17693685-3 2007 Plasma glucose and insulin were elevated after DEX (P < 0.05) compared with UAMS, MAMS, and PLA. Glucose 47-50 insulin Homo sapiens 19-26 17541844-5 2007 Transfection of K-cells by a specific plasmid to produce insulin correlated to glucose level is being considered. Glucose 79-86 insulin Homo sapiens 57-64 17548021-2 2007 The objectives of this pilot trial were to evaluate the feasibility of a randomized trial of intensive insulin therapy with respect to (a) achieving target glucose values in the 2 ranges of 5 to 7 and 8 to 10 mmol/L and (b) uncovering problems with the protocol in anticipation of a larger trial. Glucose 156-163 insulin Homo sapiens 103-110 17548021-10 2007 Although the intensive insulin therapy group had more glucose measurements performed than the control group, a similar proportion of values were within the target range (682 [42.4%] of 1607 values in the 5- to 7-mmol/L range; 250 [38.7%] of 660 values in the 8- to 10-mmol/L range, P = .35). Glucose 54-61 insulin Homo sapiens 23-30 17548021-11 2007 Glucose values of less than 2.5 mmol/L developed 7 times in 5 patients, 4 of whom were in the intensive insulin therapy group; however, no adverse consequences were documented. Glucose 0-7 insulin Homo sapiens 104-111 17623580-0 2007 Insulin resistance in human subjects having impaired glucose regulation. Glucose 53-60 insulin Homo sapiens 0-7 17623580-1 2007 OBJECTIVE: To determine insulin resistance in human subjects having impaired glucose regulation (IGR) by Homeostasis Model Assessment for Insulin Resistance (HOMA-IR). Glucose 77-84 insulin Homo sapiens 24-31 17623580-1 2007 OBJECTIVE: To determine insulin resistance in human subjects having impaired glucose regulation (IGR) by Homeostasis Model Assessment for Insulin Resistance (HOMA-IR). Glucose 77-84 insulin Homo sapiens 138-145 17535961-11 2007 We conclude that a decrease in the sensitivity of the GK rat beta-cell to depolarization-evoked Ca(2+) influx is involved in defective glucose-stimulated insulin secretion. Glucose 135-142 insulin Homo sapiens 154-161 17623580-10 2007 CONCLUSION: Patients with impaired glucose regulation may have significant insulin resistance. Glucose 35-42 insulin Homo sapiens 75-82 17623580-11 2007 It is, thus, recommended that a vigorous search be made to measure insulin resistance in all cases diagnosed to have impaired glucose regulation. Glucose 126-133 insulin Homo sapiens 67-74 17567461-9 2007 By contrast, VDAC opening is proposed to stimulate oxidative phosphorylation and promote insulin release by glucose-stimulated pancreatic beta cells. Glucose 108-115 insulin Homo sapiens 89-96 17567459-6 2007 High plasma insulin levels compensate for insulin resistance in muscle and maintain normal blood glucose levels. Glucose 97-104 insulin Homo sapiens 12-19 17561793-4 2007 This program calculates an insulin drip rate based on the low and high blood glucose (BG) levels of the desired target range, the patient"s current and previous BG levels, and an insulin sensitivity factor, with a goal of safely and expeditiously achieving and maintaining the patient"s BG in the target range. Glucose 77-84 insulin Homo sapiens 27-34 17512306-5 2007 The formula for the homeostasis model assessment of insulin resistance (HOMA-IR) is as follows: fasting serum insulin (microU/mL) x fasting plasma glucose (mmol/L)/22.5. Glucose 147-154 insulin Homo sapiens 52-59 17613803-1 2007 OBJECTIVE: Insulin has vascular actions within the skeletal muscle microcirculation (capillary recruitment) that enhance its own access and that of glucose to the muscle cells. Glucose 148-155 insulin Homo sapiens 11-18 17613803-3 2007 Furthermore, agents that impair insulin"s vascular actions to recruit capillaries lead to acute insulin resistance in terms of muscle glucose uptake. Glucose 134-141 insulin Homo sapiens 32-39 17160355-3 2007 The critical factor for insulin gene therapy in surrogate cells is to select an appropriate site for insulin expression and a tissue-specific promoter that is responsive to both physiological glucose and insulin concentrations. Glucose 192-199 insulin Homo sapiens 24-31 17160355-6 2007 The chimeric promoter was inhibited by insulin in a dosage-dependent manner and activated by glucose, two features essential for glucose metabolism. Glucose 93-100 insulin Homo sapiens 39-46 17160355-8 2007 The construction of a chimeric promoter with stronger and more sensitive responsive activity to glucose and insulin in liver cells could further advance studies in insulin gene therapy. Glucose 96-103 insulin Homo sapiens 164-171 17448241-1 2007 Basal-prandial insulin therapy is a physiologic approach to insulin delivery that utilizes multiple daily injections to cover both basal (ie, overnight fasting and between-meal) and prandial (ie, glucose excursions above basal at mealtime) insulin needs. Glucose 196-203 insulin Homo sapiens 15-22 17561795-7 2007 The insulin dose was titrated to achieve a target fasting plasma glucose of <120 mg/dL and/or HbA(1c) of <7%. Glucose 65-72 insulin Homo sapiens 4-11 17563308-1 2007 The effect of inhaled insulin in subjects with diabetes and chronic lung disease, such as asthma or chronic obstructive pulmonary disease (COPD), is of particular interest because these diseases are quite common, and it is likely that patients with asthma or COPD who are poorly controlled on oral agents and are reluctant to start subcutaneous insulin would benefit from inhaled insulin to improve their glucose control. Glucose 405-412 insulin Homo sapiens 22-29 17512320-0 2007 Early-phase insulin secretion is disturbed in obese subjects with glucose intolerance. Glucose 66-73 insulin Homo sapiens 12-19 17512320-3 2007 We developed an analytical method to qualify the early-phase insulin secretion; that is, we measured C-peptide immunoreactivity (CPR) response to a selective increase in blood glucose level in portal vein during oral glucose load under a euglycemic hyperinsulinemic clamp (clamp-OGL). Glucose 176-183 insulin Homo sapiens 61-68 17512320-3 2007 We developed an analytical method to qualify the early-phase insulin secretion; that is, we measured C-peptide immunoreactivity (CPR) response to a selective increase in blood glucose level in portal vein during oral glucose load under a euglycemic hyperinsulinemic clamp (clamp-OGL). Glucose 176-183 insulin Homo sapiens 101-110 17512320-3 2007 We developed an analytical method to qualify the early-phase insulin secretion; that is, we measured C-peptide immunoreactivity (CPR) response to a selective increase in blood glucose level in portal vein during oral glucose load under a euglycemic hyperinsulinemic clamp (clamp-OGL). Glucose 217-224 insulin Homo sapiens 101-110 17512320-7 2007 The early-phase insulin secretion is well maintained in O-NGT; however, early-phase insulin secretion has already been disturbed in obese subjects with glucose intolerance. Glucose 152-159 insulin Homo sapiens 84-91 17259649-2 2007 Since peritoneal dialysis (PD) solution contains glucose, the insulin requirement of these patients often increases after commenced on PD. Glucose 49-56 insulin Homo sapiens 62-69 17550426-0 2007 Treatment with insulin glargine reduces asymptomatic hypoglycemia detected by continuous subcutaneous glucose monitoring in children and adolescents with type 1 diabetes. Glucose 102-109 insulin Homo sapiens 15-22 17503968-4 2007 Glucose-dependent suppression of glucagon release persisted when paracrine GABA or Zn(2+) signalling was blocked, but was reversed by low concentrations (1-20 muM) of the ATP-sensitive K(+) (KATP) channel opener diazoxide, which had no effect on insulin release or beta cell responses. Glucose 0-7 insulin Homo sapiens 246-253 17507345-4 2007 Serum insulin concentration at 30 minutes after a 75-g dose of oral glucose was determined at baseline as a measure of insulin secretion. Glucose 68-75 insulin Homo sapiens 6-13 17507345-10 2007 However, insulin concentration at 30 minutes after a dose of oral glucose was an effect modifier (group x time x insulin concentration at 30 minutes: P = .02 for body weight and P = .01 for body fat percentage). Glucose 66-73 insulin Homo sapiens 9-16 17507345-10 2007 However, insulin concentration at 30 minutes after a dose of oral glucose was an effect modifier (group x time x insulin concentration at 30 minutes: P = .02 for body weight and P = .01 for body fat percentage). Glucose 66-73 insulin Homo sapiens 113-120 17507345-13 2007 Insulin concentration at 30 minutes after a dose of oral glucose was not a significant effect modifier for cardiovascular disease risk factors. Glucose 57-64 insulin Homo sapiens 0-7 17379187-3 2007 Here we report that high glucose resulted in 96.6+/-0.2% inhibition of secretagogue-stimulated insulin secretion and 44.9+/-6.2% reduction in beta-cell insulin content. Glucose 25-32 insulin Homo sapiens 95-102 17379187-6 2007 In summary, high glucose results in almost total attenuation of stimulated insulin secretion, partial depletion of beta-cell insulin stores and dysregulation of SNARE protein expression. Glucose 17-24 insulin Homo sapiens 75-82 17383613-2 2007 Cell transplantation therapies providing a glucose-regulated supply of insulin have been implemented clinically, but are limited by safety, efficacy and supply considerations. Glucose 43-50 insulin Homo sapiens 71-78 17383613-5 2007 These cells integrate functions necessary for glucose responsive regulation of preproinsulin mRNA and expression of insulin C-peptide in vitro. Glucose 46-53 insulin Homo sapiens 79-92 17383613-5 2007 These cells integrate functions necessary for glucose responsive regulation of preproinsulin mRNA and expression of insulin C-peptide in vitro. Glucose 46-53 insulin Homo sapiens 85-92 17531117-13 2007 Insulin was secreted by these cells in response to different concentrations of glucose stimulation in a regulated manner (P<0.05). Glucose 79-86 insulin Homo sapiens 0-7 17213476-6 2007 This duration of pioglitazone improved insulin"s suppression of glucose production by 41% and enhanced stimulation of glucose uptake by 27% in concert with increased gene expression and plasma levels of adiponectin. Glucose 64-71 insulin Homo sapiens 39-46 17515702-6 2007 In patients who received 0.05 to 0.1 units/kg of insulin as a bolus dose, the decrease in serum glucose was greater than 100 mg/dL in 5 of 11 patients. Glucose 96-103 insulin Homo sapiens 49-56 17515702-8 2007 During the 243 hours of insulin infusion therapy, the decline in serum glucose was 0 to 100 mg/dL during 162 hours, 101 to 200 mg/dL during 49 hours, 201 to 300 mg/dL during 8 hours, and more than 300 mg/dL during 3 hours. Glucose 71-78 insulin Homo sapiens 24-31 17515702-9 2007 Of the 193 hours of 0.05 to 0.1 units/kg/h insulin administration, there were 47 hours (24%) during which the serum-glucose decrease was greater than 100 mg/dL. Glucose 116-123 insulin Homo sapiens 43-50 17515702-10 2007 Of the 21 hours of insulin administration at less than 0.05 units/kg/h, there was 1 hour (4.8%) where the serum-glucose decrease was greater than 100 mg/dL (P = 0.05 vs. insulin infusion at 0.05 to 0.1 units/kg/h). Glucose 112-119 insulin Homo sapiens 19-26 17515702-11 2007 Commonly used insulin dosing regimens of a bolus of 0.1 units/kg followed by an infusion of 0.05 to 0.1 units/kg/h frequently resulted in a decrease in serum glucose of greater than 100 mg/dL/h. Glucose 158-165 insulin Homo sapiens 14-21 17520998-3 2007 In our intensive care unit (ICU), we use a subcutaneous sliding scale insulin protocol to achieve glucose levels <140 mg/dL. Glucose 98-105 insulin Homo sapiens 70-77 17392722-6 2007 The decline in beta-cell function and mass is evidenced metabolically by loss of first-phase insulin response to an intravenous glucose challenge, and later by the appearance of impairment in glycemic regulation, manifested as dysglycemia--usually as impaired glucose tolerance, but occasionally as impaired fasting glucose. Glucose 128-135 insulin Homo sapiens 93-100 17488384-8 2007 Porcine insulin could be detected in the serum after a glucose challenge and insulin positive cells inside a removed device after two yr. No complications have arisen and no porcine endogenous retrovirus infection has been detected through PCR and RT-PCR. Glucose 55-62 insulin Homo sapiens 8-15 17697900-6 2007 RESULTS: IDPI is an inhaled dry powder form of regular human insulin (RHI) that is used as a premeal insulin to improve glycemic control by reducing postprandial glucose excursions. Glucose 162-169 insulin Homo sapiens 61-68 17697900-6 2007 RESULTS: IDPI is an inhaled dry powder form of regular human insulin (RHI) that is used as a premeal insulin to improve glycemic control by reducing postprandial glucose excursions. Glucose 162-169 insulin Homo sapiens 101-108 17414493-4 2007 Acute interleukin-6 administration to humans increases lipolysis, fat oxidation and insulin-mediated glucose disposal. Glucose 101-108 insulin Homo sapiens 84-91 18220662-1 2007 The dissection of mechanisms that regulate glucose transport by insulin has revealed an intricate network of signaling molecules scattered from the insulin receptor to the intracellular glucose transporter GLUT4. Glucose 43-50 insulin Homo sapiens 64-71 17001619-0 2007 Acute insulin response is an independent predictor of type 2 diabetes mellitus in individuals with both normal fasting and 2-h plasma glucose concentrations. Glucose 134-141 insulin Homo sapiens 6-13 17001619-1 2007 BACKGROUND: Earlier prospective studies have identified insulin action and secretion as predictors of T2DM in populations with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) (2-h OGTT < 7.8 and 7.8-11 mmol/L, respectively). Glucose 134-141 insulin Homo sapiens 56-63 17287471-8 2007 In a subgroup of 262 nondiabetic, full-heritage Pima Indians who had undergone detailed metabolic testing, the risk allele H also was associated with a lower mean insulin-mediated glucose disposal rate and a lower mean nonoxidative glucose storage rate after adjusting for age, sex, nuclear family membership, and percentage of body fat (P < or = 0.01). Glucose 180-187 insulin Homo sapiens 163-170 17303792-1 2007 OBJECTIVE: We propose a novel algorithm to adjust prandial insulin dose using sparse blood glucose measurements. Glucose 91-98 insulin Homo sapiens 59-66 17303792-9 2007 Subsequently, physicians made insulin bolus recommendations to normalize postprandial glucose concentrations. Glucose 86-93 insulin Homo sapiens 30-37 17317765-3 2007 Using expressed fluorescent vesicle cargo proteins and total internal reflection fluorescence (TIRF) microscopy, we demonstrate that glucose stimulates human pancreatic beta-cells to secrete insulin vesicles in short, coordinated bursts of approximately 70 vesicles each. Glucose 133-140 insulin Homo sapiens 191-198 17337488-5 2007 Periods of high rates of change of glucose were induced by insulin and glucose challenges. Glucose 35-42 insulin Homo sapiens 59-66 17391171-8 2007 The frequency of hypoglycaemia in insulin-treated patients showed a significant, positive association with duration of diabetes, number of insulin injections and fasting glucose variability but was inversely related to HbA(1c), fasting glucose and body mass index. Glucose 170-177 insulin Homo sapiens 34-41 17391171-8 2007 The frequency of hypoglycaemia in insulin-treated patients showed a significant, positive association with duration of diabetes, number of insulin injections and fasting glucose variability but was inversely related to HbA(1c), fasting glucose and body mass index. Glucose 236-243 insulin Homo sapiens 34-41 17570879-7 2007 There was a statistically significant difference (P=.033) between mean prelunch glucose levels for subjects who received insulin>45 minutes before breakfast and mean glucose levels for those who received insulin<45 minutes before breakfast. Glucose 80-87 insulin Homo sapiens 121-128 17570879-7 2007 There was a statistically significant difference (P=.033) between mean prelunch glucose levels for subjects who received insulin>45 minutes before breakfast and mean glucose levels for those who received insulin<45 minutes before breakfast. Glucose 169-176 insulin Homo sapiens 207-214 17570879-10 2007 A logistical regression model revealed that patients had a 5.3 times higher risk of having a prelunch blood glucose level>180 mg/dL when their breakfast time was >45 minutes after receiving insulin as compared to those whose insulin was given<45 minutes before breakfast (relative risk, 5.3; 95% confidence interval, 1.2-25; P=.031). Glucose 108-115 insulin Homo sapiens 196-203 17520061-3 2007 We have previously shown that trivalent metabolites of iAs, arsenite (iAs(III)) and methylarsonous acid (MAs(III)) inhibit insulin-stimulated glucose uptake (ISGU) in 3T3-L1 adipocytes by suppressing the insulin-dependent phosphorylation of protein kinase B (PKB/Akt). Glucose 142-149 insulin Homo sapiens 123-130 17520061-3 2007 We have previously shown that trivalent metabolites of iAs, arsenite (iAs(III)) and methylarsonous acid (MAs(III)) inhibit insulin-stimulated glucose uptake (ISGU) in 3T3-L1 adipocytes by suppressing the insulin-dependent phosphorylation of protein kinase B (PKB/Akt). Glucose 142-149 insulin Homo sapiens 204-211 17599852-6 2007 The mean blood glucose level for patients first treated with intravenous insulin infusion in the ICU was 125 mg/dL, in comparison with 145 mg/dL in the non-ICU patients whose treatment began directly with 0.3 U/kg of insulin glargine. Glucose 15-22 insulin Homo sapiens 73-80 17940983-12 2007 Glucose administration resulted in a highly significant increase in insulin (from 11.4 +/- 7.2 microU/mL at 0 min to 98.9 +/- 68.6 microU/mL at 60 min and 72.6 +/- 45.1 microU/mL at 120 minute of OGTT, p < 0.001 for 60 and 120 minutes in comparison to baseline). Glucose 0-7 insulin Homo sapiens 68-75 17478172-4 2007 Thus, the goal of this study was to evaluate the effect of suppression of endogenous ovarian hormone production on insulin-stimulated glucose disposal. Glucose 134-141 insulin Homo sapiens 115-122 17478172-8 2007 INTERVENTION(S): Insulin-stimulated glucose disposal was determined by hyperinsulinemic (40 mU/m(2)/min) clamp during the early to midfollicular and midluteal phase of the menstrual cycle. Glucose 36-43 insulin Homo sapiens 17-24 17478172-10 2007 MAIN OUTCOME MEASURE(S): Total, oxidative, and nonoxidative insulin-stimulated glucose disposal. Glucose 79-86 insulin Homo sapiens 60-67 17498512-7 2007 Hepatic insulin resistance is clearly exacerbated by systemic insulin resistance and impaired handling by skeletal muscle and adipose tissue of both glucose and free fatty acids. Glucose 149-156 insulin Homo sapiens 8-15 17498512-9 2007 Cytokines secreted by white adipose tissue, adipokines, have emerged as key players in glucose and fat metabolism previously thought controlled largely by insulin. Glucose 87-94 insulin Homo sapiens 155-162 24557677-3 2007 In the presence of 200 mumol of palmitate, insulin (10(-7) mol/L) stimulation of glycogenesis was inhibited, as evidenced by increased glucose in the medium and decreased intracellular glycogen. Glucose 135-142 insulin Homo sapiens 43-50 17533576-3 2007 Repeated intravenous injection of ginsenoside Rh2 (1 mg/kg per injection, 3 times daily) into rats which received fructose-rich chow for 3 consecutive days decreased the value of glucose-insulin index, the product of the areas under the curve of glucose and insulin during the intraperitoneal (i.p.) Glucose 179-186 insulin Homo sapiens 187-194 17533576-5 2007 This means that ginsenoside Rh2 has an ability to improve insulin action on glucose disposal. Glucose 76-83 insulin Homo sapiens 58-65 17533576-6 2007 The plasma glucose lowering action of tolbutamide, induced by the secretion of endogenous insulin, is widely used to characterize the formation of insulin resistance. Glucose 11-18 insulin Homo sapiens 90-97 17533576-6 2007 The plasma glucose lowering action of tolbutamide, induced by the secretion of endogenous insulin, is widely used to characterize the formation of insulin resistance. Glucose 11-18 insulin Homo sapiens 147-154 17533576-10 2007 Increase of insulin sensitivity by ginsenoside Rh2 was further identified using the plasma glucose lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Glucose 91-98 insulin Homo sapiens 12-19 17533576-10 2007 Increase of insulin sensitivity by ginsenoside Rh2 was further identified using the plasma glucose lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Glucose 91-98 insulin Homo sapiens 128-135 17368460-4 2007 The prevalence of overweight women was 30.4%, and the prevalence of insulin resistance was 12.8% using the glucose to insulin ratio (GIR) and 21.6% using the homesostasis model assessment (HOMA). Glucose 107-114 insulin Homo sapiens 68-75 17329722-6 2007 RESULTS: The computer-based protocol reduced time from first glucose measurement to initiation of insulin protocol, improved the percentage of all SICU glucose readings in the ideal range, and improved control in patients on IV insulin for > or =24 hours. Glucose 61-68 insulin Homo sapiens 98-105 17481538-0 2007 Intensive insulin protocol improves glucose control and is associated with a reduction in intensive care unit mortality. Glucose 36-43 insulin Homo sapiens 10-17 17481538-1 2007 BACKGROUND: Intensive insulin therapy to maintain serum glucose levels between 80 and 110 mg/dL has previously been shown to reduce mortality in the critically ill; recent data, however, have called this benefit into question. Glucose 56-63 insulin Homo sapiens 22-29 17481538-12 2007 CONCLUSIONS: Improvements in glucose control in the ICU can be achieved by using a protocol for intensive insulin therapy. Glucose 29-36 insulin Homo sapiens 106-113 17167773-5 2007 Both glucose limitation and 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) treatment during insulin pre-treatment curtailed glycogen accumulation, and concomitantly restored insulin-sensitive glycogen synthesis and GS activation, although GS de-phosphorylation and PKB phosphorylation remained impaired. Glucose 5-12 insulin Homo sapiens 108-115 17167773-5 2007 Both glucose limitation and 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) treatment during insulin pre-treatment curtailed glycogen accumulation, and concomitantly restored insulin-sensitive glycogen synthesis and GS activation, although GS de-phosphorylation and PKB phosphorylation remained impaired. Glucose 5-12 insulin Homo sapiens 190-197 17341555-7 2007 Both in the basal state and during insulin stimulation, we saw progressively decreased glucose disposal, nonoxidative glucose disposal, and forearm muscle glucose uptake at FFA levels above 500 micromol/liter. Glucose 87-94 insulin Homo sapiens 35-42 17341555-7 2007 Both in the basal state and during insulin stimulation, we saw progressively decreased glucose disposal, nonoxidative glucose disposal, and forearm muscle glucose uptake at FFA levels above 500 micromol/liter. Glucose 118-125 insulin Homo sapiens 35-42 17341555-7 2007 Both in the basal state and during insulin stimulation, we saw progressively decreased glucose disposal, nonoxidative glucose disposal, and forearm muscle glucose uptake at FFA levels above 500 micromol/liter. Glucose 118-125 insulin Homo sapiens 35-42 17442688-7 2007 Unlike findings during mixed-meal challenges, vildagliptin increases plasma insulin levels during oral glucose tolerance tests in patients with type 2 diabetes mellitus. Glucose 103-110 insulin Homo sapiens 76-83 17493545-7 2007 Insulin was administered twice daily and titrated to achieve normal capillary blood glucose levels. Glucose 84-91 insulin Homo sapiens 0-7 19885087-2 2007 A new meal simulation model has been proposed that incorporates state-of-the-art quantitative knowledge on glucose metabolism and its control by insulin at both organ/tissue and whole-body levels. Glucose 107-114 insulin Homo sapiens 145-152 19885088-4 2007 With the long-term goal of developing a closed-loop insulin delivery system operating under various physiological conditions, it is necessary to develop a model that is capable of predicting blood glucose concentration at rest and during physical activity. Glucose 197-204 insulin Homo sapiens 52-59 19885090-1 2007 BACKGROUND: We investigated the influence of parenteral glucose infusion on insulin-driven tight glucose control (4.4-6.1 mmol/liter) in the critically ill by appraising kinetic characteristics of the glucoregulatory system. Glucose 56-63 insulin Homo sapiens 76-83 19885090-1 2007 BACKGROUND: We investigated the influence of parenteral glucose infusion on insulin-driven tight glucose control (4.4-6.1 mmol/liter) in the critically ill by appraising kinetic characteristics of the glucoregulatory system. Glucose 97-104 insulin Homo sapiens 76-83 19885090-5 2007 This follows on from the accelerated glucose turnover brought about by the insulin-modulated glucose uptake, which increases in response to increasing exogenous insulin required to achieve tight glucose control. Glucose 37-44 insulin Homo sapiens 75-82 19885090-5 2007 This follows on from the accelerated glucose turnover brought about by the insulin-modulated glucose uptake, which increases in response to increasing exogenous insulin required to achieve tight glucose control. Glucose 37-44 insulin Homo sapiens 161-168 19885090-5 2007 This follows on from the accelerated glucose turnover brought about by the insulin-modulated glucose uptake, which increases in response to increasing exogenous insulin required to achieve tight glucose control. Glucose 93-100 insulin Homo sapiens 75-82 19885090-5 2007 This follows on from the accelerated glucose turnover brought about by the insulin-modulated glucose uptake, which increases in response to increasing exogenous insulin required to achieve tight glucose control. Glucose 93-100 insulin Homo sapiens 161-168 19885090-5 2007 This follows on from the accelerated glucose turnover brought about by the insulin-modulated glucose uptake, which increases in response to increasing exogenous insulin required to achieve tight glucose control. Glucose 93-100 insulin Homo sapiens 75-82 19885090-5 2007 This follows on from the accelerated glucose turnover brought about by the insulin-modulated glucose uptake, which increases in response to increasing exogenous insulin required to achieve tight glucose control. Glucose 93-100 insulin Homo sapiens 161-168 19885090-7 2007 CONCLUSIONS: The constant parenteral glucose infusion greater or equal to 2.4 mg/kg/min is expected to simplify the achievement of tight glucose control by reducing system delays and may facilitate the development of more intuitive, efficacious, and safer insulin-titration guidelines. Glucose 37-44 insulin Homo sapiens 256-263 19885090-7 2007 CONCLUSIONS: The constant parenteral glucose infusion greater or equal to 2.4 mg/kg/min is expected to simplify the achievement of tight glucose control by reducing system delays and may facilitate the development of more intuitive, efficacious, and safer insulin-titration guidelines. Glucose 137-144 insulin Homo sapiens 256-263 19885098-1 2007 Insulin-based regimens decrease morbidity and mortality among critically ill patients by way of keeping glucose at tight control. Glucose 104-111 insulin Homo sapiens 0-7 19885098-2 2007 Utilizing these regimens involves multiple measurements of glucose by way of finger pricking or through indwelling vascular catheters in order to adjust insulin doses. Glucose 59-66 insulin Homo sapiens 153-160 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 19-26 insulin Homo sapiens 78-85 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 19-26 insulin Homo sapiens 111-118 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 19-26 insulin Homo sapiens 111-118 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 153-160 insulin Homo sapiens 78-85 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 153-160 insulin Homo sapiens 111-118 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 153-160 insulin Homo sapiens 111-118 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 153-160 insulin Homo sapiens 78-85 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 153-160 insulin Homo sapiens 111-118 19885102-3 2007 In the presence of glucose above a threshold level the robot moves, releasing insulin from a lawn covered with insulin, but stops in its tracks whenever glucose decreases to a level below threshold; thus, the robot could provide an insulin release response to spikes in glucose concentration in real time. Glucose 153-160 insulin Homo sapiens 111-118 17434094-0 2007 Glucose-potassium-insulin infusions in the management of post-stroke hyperglycaemia: the UK Glucose Insulin in Stroke Trial (GIST-UK). Glucose 0-7 insulin Homo sapiens 18-25 16670819-13 2007 Glucose clamp technique revealed mean whole body glucose uptake was reduced in CD36-deficient patients, indicating the presence of insulin resistance. Glucose 0-7 insulin Homo sapiens 131-138 16670819-13 2007 Glucose clamp technique revealed mean whole body glucose uptake was reduced in CD36-deficient patients, indicating the presence of insulin resistance. Glucose 49-56 insulin Homo sapiens 131-138 17445546-3 2007 To examine which variables influence insulin sensitivity, we compared metabolic parameters, serum resistin, leptin, and adiponectin concentrations to the insulin sensitivity, obtained by frequently sampled intravenous glucose tolerance test using the minimal model analysis, in 113 Japanese patients with type 2 diabetes mellitus. Glucose 218-225 insulin Homo sapiens 154-161 17445549-1 2007 Selective resistance to the effects of insulin on glucose metabolism in skeletal muscle and adipose tissue is a key feature of polycystic ovary syndrome (PCOS). Glucose 50-57 insulin Homo sapiens 39-46 17476196-4 2007 RESULTS: Although the fasting serum insulin concentrations were quite similar between the patient and the control groups, serum insulin levels were significantly lower in the thalassemia patients one hour and two hours after oral glucose load ingestion compared with the healthy controls. Glucose 230-237 insulin Homo sapiens 128-135 17476196-7 2007 CONCLUSIONS: These data support the assumption that zinc deficiency might lead to an exacerbation of the inability of the pancreas to secrete sufficient amounts of insulin in response to glucose stimulation in beta-thalassemia patients. Glucose 187-194 insulin Homo sapiens 164-171 27741883-1 2007 In type 1 diabetes, the body is unable to produce insulin for glucose control so regular administration of insulin is the main treatment. Glucose 62-69 insulin Homo sapiens 107-114 27741883-3 2007 Insulin therapy is not required initially but may be required later as glucose metabolism deteriorates. Glucose 71-78 insulin Homo sapiens 0-7 27741883-4 2007 Insulin is indicated when there is inadequate control of blood glucose on oral hypoglycaemic drugs or in acute episodes such as myocardial infarction where survival rates are improved when patients are treated with insulin. Glucose 63-70 insulin Homo sapiens 0-7 17472435-3 2007 METHODS AND FINDINGS: We combined human insulin/glucose clamp physiological studies with genome-wide expression profiling to identify thioredoxin interacting protein (TXNIP) as a gene whose expression is powerfully suppressed by insulin yet stimulated by glucose. Glucose 48-55 insulin Homo sapiens 229-236 17472435-3 2007 METHODS AND FINDINGS: We combined human insulin/glucose clamp physiological studies with genome-wide expression profiling to identify thioredoxin interacting protein (TXNIP) as a gene whose expression is powerfully suppressed by insulin yet stimulated by glucose. Glucose 255-262 insulin Homo sapiens 229-236 17472435-7 2007 CONCLUSIONS: TXNIP regulates both insulin-dependent and insulin-independent pathways of glucose uptake in human skeletal muscle. Glucose 88-95 insulin Homo sapiens 34-63 25905389-0 2000 Insulin signaling and action: glucose, lipids, protein Diabetes is a chronic metabolic disorder affecting ~ 5% of the population in industrialized nations. Glucose 30-37 insulin Homo sapiens 0-7 17448241-7 2007 Based on home glucose monitoring data, patients may be converted from split-mixed or premixed insulin regimens to basal-prandial regimens with similar ease. Glucose 14-21 insulin Homo sapiens 94-101 17448994-2 2007 Within these islets, communication between beta cells inhibits basal insulin secretion and enhances glucose-stimulated insulin secretion, thus contributing to glucose homeostasis during fasting and feeding. Glucose 100-107 insulin Homo sapiens 119-126 17448994-4 2007 We provide evidence that ephrin-A5 is required for glucose-stimulated insulin secretion. Glucose 51-58 insulin Homo sapiens 70-77 17448994-6 2007 EphA forward signaling is downregulated in response to glucose, which indicates that, under basal conditions, beta cells use EphA forward signaling to suppress insulin secretion and that, under stimulatory conditions, they shift to ephrin-A reverse signaling to enhance insulin secretion. Glucose 55-62 insulin Homo sapiens 160-167 17448994-6 2007 EphA forward signaling is downregulated in response to glucose, which indicates that, under basal conditions, beta cells use EphA forward signaling to suppress insulin secretion and that, under stimulatory conditions, they shift to ephrin-A reverse signaling to enhance insulin secretion. Glucose 55-62 insulin Homo sapiens 270-277 17448994-7 2007 Thus, we explain how beta cell communication in pancreatic islets conversely affects basal and glucose-stimulated insulin secretion to improve glucose homeostasis. Glucose 95-102 insulin Homo sapiens 114-121 17955068-9 2007 These approaches include: (1) addition of a basal insulin analog to oral therapy to reduce and stabilize fasting plasma glucose, (2) supplementation of oral therapy with a rapid-acting mealtime insulin analog to control postprandial glucose excursions, and (3) addition of or switching to a premixed insulin analog, which can be used to control both fasting and postprandial glucose in 1 injection. Glucose 120-127 insulin Homo sapiens 50-57 17955068-9 2007 These approaches include: (1) addition of a basal insulin analog to oral therapy to reduce and stabilize fasting plasma glucose, (2) supplementation of oral therapy with a rapid-acting mealtime insulin analog to control postprandial glucose excursions, and (3) addition of or switching to a premixed insulin analog, which can be used to control both fasting and postprandial glucose in 1 injection. Glucose 233-240 insulin Homo sapiens 194-201 17955068-9 2007 These approaches include: (1) addition of a basal insulin analog to oral therapy to reduce and stabilize fasting plasma glucose, (2) supplementation of oral therapy with a rapid-acting mealtime insulin analog to control postprandial glucose excursions, and (3) addition of or switching to a premixed insulin analog, which can be used to control both fasting and postprandial glucose in 1 injection. Glucose 233-240 insulin Homo sapiens 194-201 17955068-9 2007 These approaches include: (1) addition of a basal insulin analog to oral therapy to reduce and stabilize fasting plasma glucose, (2) supplementation of oral therapy with a rapid-acting mealtime insulin analog to control postprandial glucose excursions, and (3) addition of or switching to a premixed insulin analog, which can be used to control both fasting and postprandial glucose in 1 injection. Glucose 233-240 insulin Homo sapiens 194-201 17955068-9 2007 These approaches include: (1) addition of a basal insulin analog to oral therapy to reduce and stabilize fasting plasma glucose, (2) supplementation of oral therapy with a rapid-acting mealtime insulin analog to control postprandial glucose excursions, and (3) addition of or switching to a premixed insulin analog, which can be used to control both fasting and postprandial glucose in 1 injection. Glucose 233-240 insulin Homo sapiens 194-201 17286248-0 2007 A statistical model for inter-temporal causal dynamics of glucose production and disposal with insulin level in diabetic patients. Glucose 58-65 insulin Homo sapiens 95-102 17286248-2 2007 The primary thrust of this paper is to model inter-temporal causal dynamics of endogenous and ingested glucose production and disposal with insulin in diabetic patients. Glucose 103-110 insulin Homo sapiens 140-147 17287212-2 2007 Because glucose and amino acids stimulate insulin release from pancreatic beta-cells by the regulation of metabolic intermediates, AMPK represents an attractive candidate for control of beta-cell function. Glucose 8-15 insulin Homo sapiens 42-49 17420421-4 2007 Main outcome measures included insulin-mediated glucose uptake as quantified by the insulin suppression test and metabolic variables known to increase the risk for type 2 diabetes and cardiovascular disease. Glucose 48-55 insulin Homo sapiens 31-38 17420421-6 2007 When compared with the most insulin-sensitive third, the most insulin-resistant third of the population had significantly higher (P<.001) systolic and diastolic blood pressure (139 +/- 20 vs 123 +/- 18 mm Hg, and 83 +/- 3 vs 75 +/- 10 mm Hg, respectively), higher fasting and 2-hour oral glucose load concentrations (103 +/- 11 vs 95 +/- 11 mg/dL [5.7 +/- 0.6 vs 5.3 +/- 0.6 mmol/L], and 139 +/- 30 vs 104 +/- 19 mg/dL [7.7 +/- 1.7 vs 5.8 +/- 1.1 mmol/L], respectively), higher plasma triglyceride concentrations (198 +/- 105 vs 114 +/- 51 mg/dL [2.2 +/- 1.2 vs 1.3 +/- 0.6 mmol/L]), lower plasma high-density lipoprotein cholesterol concentrations (41 +/- 9 vs 50 +/- 13 mg/dL [1.1 +/- 0.2 vs 1.3 +/- 0.3 mmol/L]), and more prevalent impaired glucose tolerance (47% vs 2%). Glucose 291-298 insulin Homo sapiens 62-69 17270303-2 2007 It has been found that skin pretreatment with iodine followed by a dermal application of insulin results in reduced glucose and elevated hormone levels in the plasma. Glucose 116-123 insulin Homo sapiens 89-96 17170237-2 2007 Glucose-sensing neurons alter their action potential frequency in response to physiological changes in extracellular glucose, insulin, and leptin. Glucose 0-7 insulin Homo sapiens 126-133 17170237-13 2007 Thus NO may mediate, in part, glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. Glucose 76-83 insulin Homo sapiens 51-58 17200159-10 2007 CaM-specific inhibitors blocked glucose transport stimulated by transforming growth factor-beta and insulin in mesangial cells. Glucose 32-39 insulin Homo sapiens 100-107 17239967-11 2007 Pleconaril treatment reduced the beta-cells" insulin secretion in response to glucose stimulation in some experiments and induced slight morphological changes to the islets compared to untreated controls. Glucose 78-85 insulin Homo sapiens 45-52 17962866-5 2007 Tumor necrosis factor affects insulin receptor substrate phosphorylation, resulting in decreased glucose uptake and compensatory hyperinsulinemia. Glucose 97-104 insulin Homo sapiens 30-37 17371253-6 2007 However, Akt is also the key enzyme in insulin signalling regulating glucose uptake and cell growth. Glucose 69-76 insulin Homo sapiens 39-46 18225446-6 2007 Glucose sensing can be modulated by other nutrients (particularly fatty acids) and also by hormones (insulin, leptin and ghrelin) and peptides (NPY). Glucose 0-7 insulin Homo sapiens 101-108 18225448-5 2007 This deficiency is characterised by an early loss of first-phase insulin response to glucose, followed by gradual collapse of the later insulin response as well as of the maximal secretory capacity of the beta-cell. Glucose 85-92 insulin Homo sapiens 65-72 17158030-2 2007 In earlier work we identified Rab11a to be present in GLUT4-containing vesicles after insulin stimulation and showed its involvement in insulin-dependent glucose uptake. Glucose 154-161 insulin Homo sapiens 136-143 17403369-2 2007 The major cellular mechanism that diminishes blood glucose when carbohydrates are ingested is insulin-stimulated glucose transport into skeletal muscle. Glucose 51-58 insulin Homo sapiens 94-101 17403369-2 2007 The major cellular mechanism that diminishes blood glucose when carbohydrates are ingested is insulin-stimulated glucose transport into skeletal muscle. Glucose 113-120 insulin Homo sapiens 94-101 17426693-7 2007 The secretion of insulin and C-peptide by these cells corresponded to the variations in glucose levels. Glucose 88-95 insulin Homo sapiens 17-24 17371479-4 2007 RESULTS: Forearm glucose uptake incremental area was significantly lower in Cushing"s disease and in the metabolic syndrome than in controls, suggesting a state of severe insulin resistance. Glucose 17-24 insulin Homo sapiens 171-178 17407632-8 2007 During the intervention period, the difference between mean admission and discharge day glucose levels was 43 mg/dL in patients treated with four times daily insulin injections, in contrast to no change noted in the other treatment groups. Glucose 88-95 insulin Homo sapiens 158-165 17407650-8 2007 Intestinal absorption of glucose stimulates secretion of these hormones, which act to increase insulin and decrease glucagon secretion. Glucose 25-32 insulin Homo sapiens 95-102 17007957-7 2007 Insulin sensitivity was measured by the steady-state plasma glucose (SSPG) method. Glucose 60-67 insulin Homo sapiens 0-7 17229943-1 2007 OBJECTIVE: To determine if glucose management in postcardiothoracic surgery patients with a combined intravenous (IV) and subcutaneous (SC) insulin regimen reduces mortality and morbidity in patients with diabetes and stress-induced hyperglycemia. Glucose 27-34 insulin Homo sapiens 140-147 17392539-4 2007 Insulin doses were titrated toward predefined glucose targets and A1C <6.5%. Glucose 46-53 insulin Homo sapiens 0-7 17395750-2 2007 Despite comparable glucose areas above basal, glucose-induced insulin secretion was higher (P < 0.05) and insulin action lower (P < 0.05) during the meal than the oral glucose tolerance test (OGTT) in all subgroups regardless of whether they had abnormal or normal glucose tolerance (NGT). Glucose 46-53 insulin Homo sapiens 62-69 17395750-2 2007 Despite comparable glucose areas above basal, glucose-induced insulin secretion was higher (P < 0.05) and insulin action lower (P < 0.05) during the meal than the oral glucose tolerance test (OGTT) in all subgroups regardless of whether they had abnormal or normal glucose tolerance (NGT). Glucose 46-53 insulin Homo sapiens 62-69 17395750-6 2007 We conclude that, whereas glucose-induced insulin secretion is impaired in people with abnormal glucose tolerance, nonglucose nutrient-induced secretion is intact, suggesting that a glucose-specific defect in the insulin secretory pathway is an early event in the evolution of type 2 diabetes. Glucose 26-33 insulin Homo sapiens 42-49 17395751-3 2007 We have recently shown this cell to be insulin sensitive with respect to glucose uptake, with kinetics similar to muscle cells. Glucose 73-80 insulin Homo sapiens 39-46 17425444-5 2007 RESULTS: Non-insulin-mediated glucose disposal increased during the luteal phase (0.009 +/- 0.004 min(1)) versus the follicular phase (0.005 +/- 0.003 min(1)) (P < 0.05). Glucose 30-37 insulin Homo sapiens 13-20 17425444-7 2007 CONCLUSIONS: Elevated blood glucose during the luteal phase may increase insulin-independent glucose disposal. Glucose 28-35 insulin Homo sapiens 73-80 17204559-1 2007 Prolonged exposure of beta-cells to high glucose (glucotoxicity) diminishes insulin secretion in response to glucose and has been linked to altered generation of metabolism-secretion coupling factors. Glucose 41-48 insulin Homo sapiens 76-83 17204559-1 2007 Prolonged exposure of beta-cells to high glucose (glucotoxicity) diminishes insulin secretion in response to glucose and has been linked to altered generation of metabolism-secretion coupling factors. Glucose 109-116 insulin Homo sapiens 76-83 17204559-6 2007 Insulin secretion was reduced not only by acute stimulation with either glucose or KCl but more importantly by direct calcium stimulation of permeabilized cells. Glucose 72-79 insulin Homo sapiens 0-7 17873317-3 2007 A total of 220 subjects underwent standard 75 g oral glucose tolerance test (OGTT) and insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 135-142 insulin Homo sapiens 87-94 17873317-5 2007 Insulin secretion capacities were determined by the insulinogenic index (I 30 min - I 0 min)/(G 30 min - G 0 min) in OGTT and the acute insulin response to glucose (AIR) in FSIGT. Glucose 156-163 insulin Homo sapiens 0-7 17849796-4 2007 The diagnosis of insulin resistance was achieved by model homeostasis assessment and the relationship glucose/insulin. Glucose 102-109 insulin Homo sapiens 17-24 17849796-4 2007 The diagnosis of insulin resistance was achieved by model homeostasis assessment and the relationship glucose/insulin. Glucose 102-109 insulin Homo sapiens 110-117 17704045-5 2007 South Asian post-GDM women had decreased -cell function [lower HOMA (%B) (73 (37-147) vs 124 (59-262) %, p=0.048 and acute insulin response to glucose (463 (131-1639) vs 1039 (393-2748) pmol/l h, p=0.052] than controls. Glucose 143-150 insulin Homo sapiens 123-130 17177048-5 2007 INTERVENTIONS: Five steps were taken to improve glucose regulation: (1) Nurses were authorised to adjust insulin dosage using a protocol. Glucose 48-55 insulin Homo sapiens 105-112 17177048-15 2007 CONCLUSIONS: The combined strategy of successively more ambitious nurse-driven (computerised) insulin protocols and bedside glucose measurement resulted in acceptably low glucose levels with very few episodes of hypoglycaemia. Glucose 171-178 insulin Homo sapiens 94-101 17082366-3 2007 The three major physiological stimuli of glucose transport in muscle are insulin, exercise/contraction, and hypoxia. Glucose 41-48 insulin Homo sapiens 73-80 17226789-6 2007 The differentiated PDX-1+ hMSCs expressed multiple islet-cell genes including neurogenin3 (Ngn3), insulin, GK, Glut2, and glucagon, produced and released insulin/C-peptide in a weak glucose-regulated manner. Glucose 182-189 insulin Homo sapiens 162-171 17244784-8 2007 Elevated intrafollicular insulin levels in overweight women (P=0.004) were accompanied by normal glucose and lactate levels. Glucose 97-104 insulin Homo sapiens 25-32 17449920-6 2007 The insulin sensitivity measured as the glucose infusion rate at steady state was similar in the two groups (p=0.088). Glucose 40-47 insulin Homo sapiens 4-11 17382119-1 2007 OBJECTIVE: To determine whether African-American adolescents have endothelial dysfunction compared with Caucasians and whether differences are a result of differences in insulin sensitivity calculated from total glucose (S(I)) or secretion. Glucose 212-219 insulin Homo sapiens 170-177 17382119-4 2007 S(I) and acute insulin response to glucose (AIRG) were measured using intravenous glucose tolerance tests and minimal modeling. Glucose 35-42 insulin Homo sapiens 15-22 18370816-5 2007 In multiple regression modeling, fasting insulin was independently related to more elements of the metabolic syndrome (fasting glucose, waist circumference, triglycerides, systolic and diastolic blood pressure) than were Si or AIRg (both related only to fasting glucose), after adjusting for ethnicity, age, and total fat or IAAT. Glucose 127-134 insulin Homo sapiens 41-48 18370816-5 2007 In multiple regression modeling, fasting insulin was independently related to more elements of the metabolic syndrome (fasting glucose, waist circumference, triglycerides, systolic and diastolic blood pressure) than were Si or AIRg (both related only to fasting glucose), after adjusting for ethnicity, age, and total fat or IAAT. Glucose 262-269 insulin Homo sapiens 41-48 17420302-1 2007 Exocytosis of insulin-containing secretory vesicles in pancreatic beta-cells is crucial to maintenance of plasma glucose levels. Glucose 113-120 insulin Homo sapiens 14-21 17454835-10 2007 Glucose concentration was lower before anaesthesia induction in the carbohydrate group, possibly due to increased insulin release. Glucose 0-7 insulin Homo sapiens 114-121 17397545-0 2007 The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study. Glucose 121-128 insulin Homo sapiens 101-108 17340661-2 2007 These polymer coatings permit the islets to respond to changes in glucose concentration by producing insulin with a dose-response profile that is substantially similar to that of unencapsulated islets. Glucose 66-73 insulin Homo sapiens 101-108 17451048-8 2007 In addition to its critical role as a peripheral signal integrating the complex network of hypothalamic neuropeptides and neurotransmitters that influence parameters of energy balance, central nervous insulin signalling is also implicated in the regulation of peripheral glucose metabolism. Glucose 271-278 insulin Homo sapiens 201-208 17316975-0 2007 IRS-3 mediates insulin-induced glucose uptake in differentiated IRS-2(-/-) brown adipocytes. Glucose 31-38 insulin Homo sapiens 15-22 17316975-1 2007 IRS-2 mediates insulin-induced glucose uptake in brown preadipocytes. Glucose 31-38 insulin Homo sapiens 15-22 17275862-6 2007 The 48-h glucose infusion elicited a metabolic profile of a glucose intolerant obese subjects, with increased plasma glucose, insulin and leptin (all P<0.01) and increased HOMA-IR (P<0.001). Glucose 9-16 insulin Homo sapiens 126-133 17275862-6 2007 The 48-h glucose infusion elicited a metabolic profile of a glucose intolerant obese subjects, with increased plasma glucose, insulin and leptin (all P<0.01) and increased HOMA-IR (P<0.001). Glucose 60-67 insulin Homo sapiens 126-133 17316975-4 2007 More importantly, insulin induced glucose uptake in differentiated IRS-2-deficient brown adipocytes in a wortmannin-dependent manner. Glucose 34-41 insulin Homo sapiens 18-25 17316975-6 2007 The reduction of IRS-3 expression by siRNA inhibited insulin-induced glucose uptake and also PKC zeta activation in differentiated IRS-2(-/-) brown adipocytes. Glucose 69-76 insulin Homo sapiens 53-60 17202135-0 2007 The glucose transporter 4-regulating protein TUG is essential for highly insulin-responsive glucose uptake in 3T3-L1 adipocytes. Glucose 4-11 insulin Homo sapiens 73-80 17414699-6 2007 RESULTS: The cultured monolayer cells secreted insulin in response to glucose stimulation and maintained endocrine gene expression. Glucose 70-77 insulin Homo sapiens 47-54 17227768-3 2007 Using small interfering RNA (siRNA) to suppress the expression of MAP4K4 protein 85% in primary human skeletal muscle cells, we provide evidence that TNF-alpha-induced insulin resistance on glucose uptake was completely prevented. Glucose 190-197 insulin Homo sapiens 168-175 17227768-5 2007 These results highlight the MAPK4K4/JNK/ERK/IRS module in the negative regulation of insulin signaling to glucose transport in response to TNF-alpha. Glucose 106-113 insulin Homo sapiens 85-92 17227768-6 2007 Depletion of MAP4K4 also prevented TNF-alpha-induced insulin resistance on Akt and the Akt substrate 160 (AS160), providing evidence that appropriate insulin signaling inputs for glucose metabolism were rescued. Glucose 179-186 insulin Homo sapiens 150-157 17227768-9 2007 Moreover, in myotubes from insulin-resistant type II diabetic patients, siRNA against MAP4K4, MAP2K4, or MAP2K1 restored insulin action on glucose uptake to levels observed in healthy subjects. Glucose 139-146 insulin Homo sapiens 27-34 17227768-9 2007 Moreover, in myotubes from insulin-resistant type II diabetic patients, siRNA against MAP4K4, MAP2K4, or MAP2K1 restored insulin action on glucose uptake to levels observed in healthy subjects. Glucose 139-146 insulin Homo sapiens 121-128 17202135-9 2007 Together, these findings demonstrate that TUG is required to retain GLUT4 intracellularly in 3T3-L1 adipocytes in the absence of insulin and further implicate the insulin-stimulated dissociation of TUG and GLUT4 as an important action by which insulin stimulates glucose uptake. Glucose 263-270 insulin Homo sapiens 163-170 17202135-9 2007 Together, these findings demonstrate that TUG is required to retain GLUT4 intracellularly in 3T3-L1 adipocytes in the absence of insulin and further implicate the insulin-stimulated dissociation of TUG and GLUT4 as an important action by which insulin stimulates glucose uptake. Glucose 263-270 insulin Homo sapiens 163-170 17202135-1 2007 Insulin stimulates glucose uptake in fat and muscle by redistributing GLUT4 glucose transporters from intracellular membranes to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 17303006-4 2007 The effects of YY20 on insulin-mediated glucose consumption were determined in the HepG2 human hepatocellular carcinoma line. Glucose 40-47 insulin Homo sapiens 23-30 17424761-3 2007 The blood glucose level as controlled by subcutaneous injection of insulin was maintained at the level of 110-140 mg/dL. Glucose 10-17 insulin Homo sapiens 67-74 17344488-3 2007 OBJECTIVE: We compared the effects of acute protein administration with those of glucose challenges on hormones related to obesity and insulin resistance (ie, cortisol and insulin), hirsutism [ie, dehydroepiandosterone (DHEA) and androstenedione], and hunger (ie, ghrelin). Glucose 81-88 insulin Homo sapiens 135-142 17344486-3 2007 The excess fatty acids are esterified and either stored or metabolized to various molecules that may participate or interfere with normal cellular signaling, particularly insulin-mediated signal transduction, thus altering cellular and, subsequently, whole-body glucose metabolism. Glucose 262-269 insulin Homo sapiens 171-178 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 44-51 insulin Homo sapiens 26-33 17106061-8 2007 Pioglitazone and rosiglitazone similarly improved FPG, mean plasma glucose during OGTT, Hb A1c, and insulin-mediated total body glucose disposal (Rd) and decreased mean plasma FFA during OGTT (all P<0.01, ANOVA). Glucose 128-135 insulin Homo sapiens 100-107 17106061-10 2007 Improved insulin secretion correlated positively with increased body weight, fat mass, and Rd and inversely with decreased plasma glucose and FFA during the OGTT. Glucose 130-137 insulin Homo sapiens 9-16 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 44-51 insulin Homo sapiens 122-129 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 44-51 insulin Homo sapiens 122-129 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 99-106 insulin Homo sapiens 26-33 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 99-106 insulin Homo sapiens 122-129 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 99-106 insulin Homo sapiens 122-129 17151925-8 2007 Changes in maximal activities, whether caused by exercise-induced changes in insulin, glucagon, or other hormones are shown to be needed to achieve the expected glucose output. Glucose 161-168 insulin Homo sapiens 77-84 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 99-106 insulin Homo sapiens 26-33 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 99-106 insulin Homo sapiens 122-129 17122093-1 2007 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high (25 mM) glucose, provided that insulin (0.6 nM) is included, Akt activation is impaired, and high glucose and insulin act synergistically. Glucose 99-106 insulin Homo sapiens 122-129 17122093-2 2007 Considerable evidence suggests that increased glucose flux via the hexosamine biosynthesis pathway enhances the O-GlcNAc modification (O-GlcNAcylation) of some critical protein(s) that may contribute to insulin resistance. Glucose 46-53 insulin Homo sapiens 203-210 17417692-1 2007 INTRODUCTION: The objective of this study was to evaluate glucose transport into lymphocytes in healthy subjects and patients with type 2 diabetes mellitus (DM) treated either with diet only or with insulin and to propose peripheral blood lymphocytes as a convenient model for cellular glucose transport studies. Glucose 58-65 insulin Homo sapiens 199-206 17339029-0 2007 A cis-element in the 5" untranslated region of the preproinsulin mRNA (ppIGE) is required for glucose regulation of proinsulin translation. Glucose 94-101 insulin Homo sapiens 51-64 17339021-3 2007 (2007) show that BMP signaling specifically regulates genes involved in insulin production and secretion and demonstrate that exogenous BMP4 administration augments glucose-stimulated insulin secretion in vivo. Glucose 165-172 insulin Homo sapiens 184-191 17339029-0 2007 A cis-element in the 5" untranslated region of the preproinsulin mRNA (ppIGE) is required for glucose regulation of proinsulin translation. Glucose 94-101 insulin Homo sapiens 54-64 17339029-1 2007 Insulin production in pancreatic beta cells is predominantly regulated through glucose control of proinsulin translation. Glucose 79-86 insulin Homo sapiens 98-108 17339029-5 2007 Glucose-responsive factor binding to this cis-element exhibited temporal and glucose-concentration-dependent patterns that paralleled proinsulin biosynthesis. Glucose 0-7 insulin Homo sapiens 134-144 17339029-5 2007 Glucose-responsive factor binding to this cis-element exhibited temporal and glucose-concentration-dependent patterns that paralleled proinsulin biosynthesis. Glucose 77-84 insulin Homo sapiens 134-144 17339029-6 2007 Mutating this cis-element abolished the ability of ppI mRNA UTRs to confer glucose regulation upon translation. Glucose 75-82 insulin Homo sapiens 51-54 17327503-7 2007 The fasting C-peptide concentration displayed an inverted-U pattern, with a maximum at a mean plasma glucose concentration during the OGTT of 9.6 mmol/L in the transition from GDM1 to GDM2. Glucose 101-108 insulin Homo sapiens 12-21 17425753-2 2007 Reduced early insulin response (EIR) after a meal leads to impaired suppression of endogenous glucose production and subsequently PPHG, which is a risk factor for cardiovascular disease. Glucose 94-101 insulin Homo sapiens 14-21 16952202-4 2007 RESULTS: Intermittent high glucose caused a significant decrease of glucose-stimulated insulin secretion, which was not further affected by either sulphonylurea. Glucose 27-34 insulin Homo sapiens 87-94 16874846-5 2007 RESULTS: Glucose-stimulated insulin secretion was not affected by C-peptide and, accordingly, mRNA expression of glucose transporter 2 and glucokinase did not differ between islets pre-cultured or not with the hormone. Glucose 9-16 insulin Homo sapiens 28-35 16952202-4 2007 RESULTS: Intermittent high glucose caused a significant decrease of glucose-stimulated insulin secretion, which was not further affected by either sulphonylurea. Glucose 68-75 insulin Homo sapiens 87-94 17069922-0 2007 Factors associated with improvement of fasting plasma glucose level by mealtime dosing of a rapid-acting insulin analog in type 2 diabetes. Glucose 54-61 insulin Homo sapiens 105-112 17216279-3 2007 Cell size and insulin action on glucose uptake capacity in vitro were assessed in isolated fat cells. Glucose 32-39 insulin Homo sapiens 14-21 17216279-6 2007 RESULTS: Negative correlations were found between subcutaneous fat cell size and insulin sensitivity assessed as M-value during clamp and as insulin action on glucose uptake in fat cells in vitro. Glucose 159-166 insulin Homo sapiens 141-148 17069922-1 2007 This study investigated whether strict control of plasma glucose levels with mealtime dosing of a rapid-acting insulin analog improves early morning fasting plasma glucose (FPG) levels in patients with type 2 diabetes. Glucose 57-64 insulin Homo sapiens 111-118 17069922-1 2007 This study investigated whether strict control of plasma glucose levels with mealtime dosing of a rapid-acting insulin analog improves early morning fasting plasma glucose (FPG) levels in patients with type 2 diabetes. Glucose 164-171 insulin Homo sapiens 111-118 17089369-1 2007 OBJECTIVES: To determine whether treatment with glucose-insulin-potassium (GIK), insulin and glucose, or insulin by itself is beneficial in limiting organ damage after acute myocardial infarction (AMI) and reducing mortality and morbidity among critically ill hyperglycaemic patients. Glucose 48-55 insulin Homo sapiens 56-63 17285007-5 2007 Furthermore, animal and in-vitro work further supports the finding that glucose control, rather than glycemia-independent effects of insulin, is the primary mechanism of action of intensive insulin therapy. Glucose 72-79 insulin Homo sapiens 190-197 17285001-2 2007 According to the glucose-fatty acid cycle of Randle, preferential oxidation of free fatty acids over glucose plays a major role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Glucose 17-24 insulin Homo sapiens 131-138 17285001-2 2007 According to the glucose-fatty acid cycle of Randle, preferential oxidation of free fatty acids over glucose plays a major role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Glucose 101-108 insulin Homo sapiens 131-138 17285009-8 2007 The threat of hypoglycemia is a barrier to intensive insulin therapy in critical care, supporting the need for frequent glucose monitoring, readily available concentrated intravenous dextrose infusions, better training of nurses and technological advances in glucose-sensing and insulin-dosing algorithms. Glucose 120-127 insulin Homo sapiens 53-60 17285001-4 2007 RECENT FINDINGS: Recent studies have suggested that local accumulation of fat metabolites such as ceramides, diacylglycerol or acyl-CoA, inside skeletal muscle and liver, may activate a serine kinase cascade leading to defects in insulin signalling and glucose transport. Glucose 253-260 insulin Homo sapiens 230-237 17285009-8 2007 The threat of hypoglycemia is a barrier to intensive insulin therapy in critical care, supporting the need for frequent glucose monitoring, readily available concentrated intravenous dextrose infusions, better training of nurses and technological advances in glucose-sensing and insulin-dosing algorithms. Glucose 183-191 insulin Homo sapiens 53-60 17327330-7 2007 Obesity status and glucose tolerance status influenced the relationships among visfatin, insulin sensitivity, and parameters of iron metabolism. Glucose 19-26 insulin Homo sapiens 89-96 17327334-0 2007 Insulin secretion and insulin sensitivity in relation to fasting glucose in healthy subjects. Glucose 65-72 insulin Homo sapiens 0-7 17327334-0 2007 Insulin secretion and insulin sensitivity in relation to fasting glucose in healthy subjects. Glucose 65-72 insulin Homo sapiens 22-29 17327334-1 2007 OBJECTIVE: This study evaluated insulin secretion and insulin sensitivity in healthy subjects with normal fasting glucose. Glucose 114-121 insulin Homo sapiens 32-39 17327334-4 2007 From this test, the acute insulin response (AIR) to arginine during the three glucose levels (AIR1, AIR2, and AIR3) were estimated. Glucose 78-85 insulin Homo sapiens 26-33 17327334-8 2007 CONCLUSIONS: It is concluded that 1) raised fasting glucose (albeit still within normal values) augments baseline and maximal arginine-induced insulin secretion in healthy subjects, and 2) this is associated with reduced insulin sensitivity. Glucose 52-59 insulin Homo sapiens 143-150 17327334-9 2007 This suggests that high, but still normal, fasting glucose may contribute to the augmented insulin secretion in subjects with low insulin sensitivity. Glucose 51-58 insulin Homo sapiens 91-98 17285009-8 2007 The threat of hypoglycemia is a barrier to intensive insulin therapy in critical care, supporting the need for frequent glucose monitoring, readily available concentrated intravenous dextrose infusions, better training of nurses and technological advances in glucose-sensing and insulin-dosing algorithms. Glucose 259-266 insulin Homo sapiens 53-60 17327345-4 2007 Insulin resistance was calculated using their estimated glucose disposal rate (eGDR). Glucose 56-63 insulin Homo sapiens 0-7 17327454-0 2007 Glucose regulation of insulin gene transcription and pre-mRNA processing in human islets. Glucose 0-7 insulin Homo sapiens 22-29 17327442-1 2007 Insulin resistance is associated with metabolic inflexibility, impaired switching of substrate oxidation from fatty acids to glucose in response to insulin. Glucose 125-132 insulin Homo sapiens 0-7 17327442-1 2007 Insulin resistance is associated with metabolic inflexibility, impaired switching of substrate oxidation from fatty acids to glucose in response to insulin. Glucose 125-132 insulin Homo sapiens 148-155 17327443-7 2007 Endothelin antagonism augmented skeletal muscle responses to insulin in obese subjects through changes in both leg blood flow (LBF) and glucose extraction. Glucose 136-143 insulin Homo sapiens 61-68 17327443-9 2007 These changes, combined with differential effects on glucose extraction, resulted in augmented insulin-stimulated leg glucose uptake in obese subjects (54.7 +/- 5.7 vs. 107.4 +/- 18.9 mg/min with BQ123), with no change in lean subjects (103.7 +/- 11.4 vs. 88.9 +/- 16.3, P = 0.04 comparing BQ123 across groups). Glucose 53-60 insulin Homo sapiens 95-102 17327443-9 2007 These changes, combined with differential effects on glucose extraction, resulted in augmented insulin-stimulated leg glucose uptake in obese subjects (54.7 +/- 5.7 vs. 107.4 +/- 18.9 mg/min with BQ123), with no change in lean subjects (103.7 +/- 11.4 vs. 88.9 +/- 16.3, P = 0.04 comparing BQ123 across groups). Glucose 118-125 insulin Homo sapiens 95-102 17327444-1 2007 Obesity-related glucose intolerance is a function of hepatic (homeostatic model assessment-insulin resistance [HOMA-IR]) and peripheral insulin resistance (S(i)) and beta-cell dysfunction. Glucose 16-23 insulin Homo sapiens 91-98 17327454-1 2007 Glucose is the primary regulator of insulin granule release from pancreatic islets. Glucose 0-7 insulin Homo sapiens 36-43 17327446-4 2007 In contrast, postmeal and intravenous glucose tolerance test change over time in insulin and C-peptide concentrations were greater (P < 0.05) in women after DHEA than after placebo. Glucose 38-45 insulin Homo sapiens 81-88 17327454-2 2007 In rodent islets, the role of glucose in the acute regulation of insulin gene transcription has remained unclear, primarily because the abundance and long half-life of insulin mRNA confounds analysis of transcription by traditional methods that measure steady-state mRNA levels. Glucose 30-37 insulin Homo sapiens 65-72 17327446-4 2007 In contrast, postmeal and intravenous glucose tolerance test change over time in insulin and C-peptide concentrations were greater (P < 0.05) in women after DHEA than after placebo. Glucose 38-45 insulin Homo sapiens 93-102 17327454-3 2007 To investigate the nature of glucose-regulated insulin gene transcription in human islets, we first quantitated the abundance and half-lives of insulin mRNA and pre-mRNAs after addition of actinomycin D (to stop transcription). Glucose 29-36 insulin Homo sapiens 47-54 17316975-7 2007 In addition, inhibition of PKC zeta totally blunted insulin-induced glucose uptake in those cells. Glucose 68-75 insulin Homo sapiens 52-59 17327454-6 2007 In response to elevated glucose, pre-mRNA species increased within 60 min, whereas increases in mature mRNA did not occur until 48 h, suggesting that measurement of mature mRNA species does not accurately reflect the acute transcriptional response of the insulin gene to glucose. Glucose 24-31 insulin Homo sapiens 255-262 17327454-6 2007 In response to elevated glucose, pre-mRNA species increased within 60 min, whereas increases in mature mRNA did not occur until 48 h, suggesting that measurement of mature mRNA species does not accurately reflect the acute transcriptional response of the insulin gene to glucose. Glucose 271-278 insulin Homo sapiens 255-262 17316975-8 2007 Our results provide evidences suggesting that IRS-3/PI 3-kinase/PKC zeta signaling is the main responsible for the insulin-induced glucose uptake observed upon differentiation of brown adipocytes lacking IRS-2. Glucose 131-138 insulin Homo sapiens 115-122 17454170-6 2007 After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. Glucose 228-235 insulin Homo sapiens 116-123 17321040-7 2007 Insulin treatment partially prevented the inhibitory effects of CLA on glucose uptake and induced a significant increase (P<0.05-0.01) in the percentage of glucose metabolized to lactate. Glucose 71-78 insulin Homo sapiens 0-7 17321040-7 2007 Insulin treatment partially prevented the inhibitory effects of CLA on glucose uptake and induced a significant increase (P<0.05-0.01) in the percentage of glucose metabolized to lactate. Glucose 159-166 insulin Homo sapiens 0-7 17158207-2 2007 We previously demonstrated a role for Akt in insulin regulation of protein kinase CbetaII alternative splicing through phosphorylation of serine/arginine-rich protein 40, a required mechanism for insulin-stimulated glucose uptake. Glucose 215-222 insulin Homo sapiens 45-52 17158207-2 2007 We previously demonstrated a role for Akt in insulin regulation of protein kinase CbetaII alternative splicing through phosphorylation of serine/arginine-rich protein 40, a required mechanism for insulin-stimulated glucose uptake. Glucose 215-222 insulin Homo sapiens 196-203 17454170-6 2007 After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. Glucose 228-235 insulin Homo sapiens 116-123 17496362-2 2007 A clear goal through the years has been to unravel the insulin signal transduction network regulating glucose transport. Glucose 102-109 insulin Homo sapiens 55-62 17313628-7 2007 Insulin detemir improved glycaemic control in type 1 and type 2 patients, with reductions in mean HbA(1c) (0.5% and 0.9%, respectively, p < 0.0001 for both), fasting glucose (1.7 and 2.6 mmol/l, p < 0.0001 for both) and within-patient fasting glucose variability (0.7 and 0.5 mmol/l, p < 0.0001 for both). Glucose 169-176 insulin Homo sapiens 0-7 17313628-7 2007 Insulin detemir improved glycaemic control in type 1 and type 2 patients, with reductions in mean HbA(1c) (0.5% and 0.9%, respectively, p < 0.0001 for both), fasting glucose (1.7 and 2.6 mmol/l, p < 0.0001 for both) and within-patient fasting glucose variability (0.7 and 0.5 mmol/l, p < 0.0001 for both). Glucose 249-256 insulin Homo sapiens 0-7 17496362-5 2007 In this review, we detail our current state of knowledge on the intricate insulin signaling network responsible for glucose transport in peripheral adipose and skeletal muscle tissues. Glucose 116-123 insulin Homo sapiens 74-81 17496364-5 2007 Moreover, insulin infusion while maintaining glucose and amino acid levels results in increase in muscle mitochondrial gene transcript levels and ATP production indicating that insulin is a key regulator of muscle mitochondrial biogenesis. Glucose 45-52 insulin Homo sapiens 10-17 17496364-5 2007 Moreover, insulin infusion while maintaining glucose and amino acid levels results in increase in muscle mitochondrial gene transcript levels and ATP production indicating that insulin is a key regulator of muscle mitochondrial biogenesis. Glucose 45-52 insulin Homo sapiens 177-184 16801926-0 2007 The glucose clamp reveals an association between adiponectin gene polymorphisms and insulin sensitivity in obese subjects. Glucose 4-11 insulin Homo sapiens 84-91 17402320-4 2007 METHODS: Following admission to the ICU, hyperglycemic patients were randomly assigned to a group treated intensively with insulin targeting glucose at 110-140 mg/dl, or to a conventional insulin therapy group, where glucose, upon exceeding 200 mg/dl, was controlled at 140-200 mg/dl. Glucose 141-148 insulin Homo sapiens 123-130 17402320-6 2007 RESULTS: In the 41 patients treated intensively with insulin the glucose level was 142 +/- 14 mg/dl, as compared to 174+/-20 mg/dl in the 48 patients on conventional insulin treatment. Glucose 65-72 insulin Homo sapiens 53-60 17192297-5 2007 MAIN OUTCOME MEASURES: Insulin secretion was evaluated by an iv glucose tolerance test, and insulin sensitivity and energy metabolism by the hyperinsulinemic euglycemic clamp and indirect calorimetry. Glucose 64-71 insulin Homo sapiens 23-30 17122377-1 2007 The purpose of this study was to compare insulin"s ability to stimulate glucose uptake in the arm and leg in a group of older hypertensive individuals (n = 13, 66 +/- 2 yr old). Glucose 72-79 insulin Homo sapiens 41-48 19888403-0 2007 Whole blood glucose standard is key to accurate insulin dosages. Glucose 12-19 insulin Homo sapiens 48-55 17332526-3 2007 Given that high androgen levels and insulin resistance are linked in women, we proposed that androgens may influence insulin-mediated glucose metabolism in adipose cells. Glucose 134-141 insulin Homo sapiens 117-124 17332526-7 2007 In the glucose metabolic pathway of insulin signaling, treatment of cells with T 10 nmol/l did not alter insulin-stimulated phosphorylation of insulin receptor substrate-1 or Akt, but insulin-stimulated phosphorylation of protein kinase C (PKC) zeta was impaired. Glucose 7-14 insulin Homo sapiens 36-43 17332528-0 2007 Glucose regulates AMP-activated protein kinase activity and gene expression in clonal, hypothalamic neurons expressing proopiomelanocortin: additive effects of leptin or insulin. Glucose 0-7 insulin Homo sapiens 170-177 17427537-8 2007 Euglycemia was achieved within 8 hours after fluid rehydration and only low dose insulin was required He maintained normal glucose levels without any antidiabetic drugs afterward. Glucose 123-130 insulin Homo sapiens 81-88 17367703-5 2007 METHODS AND RESULTS: In 158 never-treated hypertensive patients, we evaluated insulin resistance by HOMA index [insulin (microU/mL) x glucose (mmol/L)]/22.5 and LVM by echocardiograms. Glucose 134-141 insulin Homo sapiens 78-85 17372313-6 2007 RESULTS: Total and incremental glucose AUCs during the OGTT (but not the MT) were negatively associated with BW change (total, percent, and annual), both before and after adjusting for sex, age, initial BW, follow-up time, insulin action, RMR, fasting plasma glucose and insulin concentrations, and insulin response. Glucose 31-38 insulin Homo sapiens 223-230 17372313-6 2007 RESULTS: Total and incremental glucose AUCs during the OGTT (but not the MT) were negatively associated with BW change (total, percent, and annual), both before and after adjusting for sex, age, initial BW, follow-up time, insulin action, RMR, fasting plasma glucose and insulin concentrations, and insulin response. Glucose 31-38 insulin Homo sapiens 271-278 17372313-6 2007 RESULTS: Total and incremental glucose AUCs during the OGTT (but not the MT) were negatively associated with BW change (total, percent, and annual), both before and after adjusting for sex, age, initial BW, follow-up time, insulin action, RMR, fasting plasma glucose and insulin concentrations, and insulin response. Glucose 31-38 insulin Homo sapiens 271-278 17476613-4 2007 RESULTS: Patients with RA had marked insulin resistance (glucose infusion rate (GIR) area under the curve (AUC) was 499+/-55 mg/kg in the RA group compared to 710+/-77 mg/kg in the control group; p<0.05). Glucose 57-64 insulin Homo sapiens 37-44 17306374-7 2007 As well as short-term effects of enhancing glucose-induced insulin secretion, continuous GLP-1R activation also increases insulin synthesis, beta cell proliferation, and neogenesis. Glucose 43-50 insulin Homo sapiens 59-66 17314695-6 2007 There were significant relations between carotid artery IMT and insulin sensitivity indexes derived from fasting samples (fasting glucose to insulin ratio (FGIR; p = 0.004, r = -0.404), quantitative insulin-sensitivity check index (QUICK-I; p = 0.002, r = -0.401) and homeostasis model assessment of insulin resistance (HOMA-IR; p = 0.034, r = 0.300) in the obese group. Glucose 130-137 insulin Homo sapiens 64-71 17381690-11 2007 The retrieved capsules produced a small amount of insulin when placed in high glucose concentrations in vitro. Glucose 78-85 insulin Homo sapiens 50-57 17169456-6 2007 Isolated human pancreatic islets were infected and viral replication, viability and degree of cytolysis as well as insulin release in response to high glucose were measured. Glucose 151-158 insulin Homo sapiens 115-122 17327454-8 2007 Taken together, our data suggest that pre-mRNA species may be a more reliable reflection of acute changes to human insulin gene transcriptional rates and that glucose acutely enhances insulin transcription by a mechanism that enhances chromatin accessibility and leads to recruitment of basal transcriptional machinery. Glucose 159-166 insulin Homo sapiens 184-191 17311679-8 2007 CONCLUSION: Taken together our data indicate that only leptin is reduced by glucose uptake in insulin-sensitive probands whereas adiponectin and resistin are not altered. Glucose 76-83 insulin Homo sapiens 94-101 17547798-11 2007 The change at baseline in the study group was more than that in the control group [the change of AUC for plasma glucose (-6.42 +/- 8.62) h x mmol x L(-1) vs (-1.87 +/- 5.30) h x mmol x L(-1), P < 0.01; that of AUC for serum insulin (-36.94 +/- 49.77) h x mIU x L(-1) vs (-18.20 +/- 32.62) h x mIU x L(-1), P < 0.05]. Glucose 112-119 insulin Homo sapiens 227-234 17316471-4 2007 Serotonergic effects on energy balance lead to secondary effects on glucose homeostasis, based on a well-established link between obesity and insulin resistance. Glucose 68-75 insulin Homo sapiens 142-149 17311679-10 2007 Omentin was shown to enhance insulin-stimulated glucose uptake but systemic levels are not correlated to postprandial blood glucose. Glucose 48-55 insulin Homo sapiens 29-36 17302653-4 2007 Insulin dosage in each group was titrated to target fasting blood glucose (FBG) of 100 mg/dL or less (<or=5.6 mmol/L) using a weekly titration algorithm. Glucose 66-73 insulin Homo sapiens 0-7 17307055-3 2007 In this report, the investigators discuss data demonstrating an anti-inflammatory effect of insulin and a proinflammatory effect of glucose and free fatty acids and provide a mechanistic justification for the benefits of maintaining euglycemia with insulin infusions in hospitalized patients. Glucose 132-139 insulin Homo sapiens 249-256 17307055-4 2007 The regimens that infuse fixed doses of insulin with high rates of glucose are usually associated with hyperglycemia. Glucose 67-74 insulin Homo sapiens 40-47 17187250-7 2007 DNA chip analysis revealed that expression of genes involved in OXPHOS, which correlated with several nuclear factors, including estrogen-related receptor-alpha or peroxisome proliferator-activated receptor-gamma, was a predictor of fasting plasma glucose levels, independently of age, BMI, insulin resistance and fasting insulin levels (p = 0.04). Glucose 248-255 insulin Homo sapiens 291-298 17187250-7 2007 DNA chip analysis revealed that expression of genes involved in OXPHOS, which correlated with several nuclear factors, including estrogen-related receptor-alpha or peroxisome proliferator-activated receptor-gamma, was a predictor of fasting plasma glucose levels, independently of age, BMI, insulin resistance and fasting insulin levels (p = 0.04). Glucose 248-255 insulin Homo sapiens 322-329 17258929-5 2007 Insulin resistance was assessed using a validated estimation of the glucose disposal rate (eGDR). Glucose 68-75 insulin Homo sapiens 0-7 17259506-7 2007 Insulin sensitivity was determined by the minimal model technique using the frequently sampled intravenous glucose tolerance test. Glucose 107-114 insulin Homo sapiens 0-7 17259506-10 2007 beta-Cell function, as measured by the acute insulin response to glucose, was also lower in GDM-IGT. Glucose 65-72 insulin Homo sapiens 45-52 17259506-11 2007 CONCLUSIONS: High body fat content, especially visceral fat content, and a low insulin response to glucose seem to contribute simultaneously to the development of impaired glucose metabolism in Korean women with previous GDM. Glucose 99-106 insulin Homo sapiens 79-86 17316104-2 2007 TPG modeling allows determination of the separate effects of insulin on the disposal of glucose and on the hepatic production of glucose. Glucose 88-95 insulin Homo sapiens 61-68 27792092-4 2007 RECENT FINDINGS: Insulin gene therapy using non-beta cells has been improved by utilizing modified insulin constructs controlled by regulatory elements to confer nutrient responsiveness, and by inducing insulin production in endocrine cells that are equipped for rapid and in some cases glucose-responsive secretion. Glucose 287-294 insulin Homo sapiens 17-24 27792092-7 2007 SUMMARY: The major challenge associated with insulin gene therapy in non-beta cells is to achieve rapid, glucose-responsive secretion, while transdifferentiation approaches require additional characterization of the function and stability of insulin-producing cells. Glucose 105-112 insulin Homo sapiens 45-52 17082262-1 2007 Both the rate of overall translation and the specific acceleration of proinsulin synthesis are known to be glucose-regulated processes in the beta-cell. Glucose 107-114 insulin Homo sapiens 70-80 17381690-12 2007 An oral glucose tolerance test induced a small rise in serum of immuno-reactive insulin, identified as porcine by reversed phase high pressure liquid chromatography. Glucose 8-15 insulin Homo sapiens 80-87 17173660-2 2007 Calculations were made to account for the dependence of C-peptide secretion on glucose concentration (C-peptide/glucose ratio [CP/G]) and adjusted for renal function by calculating the C-peptide/glucose-creatinine ratio (CP/GCr). Glucose 79-86 insulin Homo sapiens 56-65 17173660-2 2007 Calculations were made to account for the dependence of C-peptide secretion on glucose concentration (C-peptide/glucose ratio [CP/G]) and adjusted for renal function by calculating the C-peptide/glucose-creatinine ratio (CP/GCr). Glucose 79-86 insulin Homo sapiens 102-111 17173660-2 2007 Calculations were made to account for the dependence of C-peptide secretion on glucose concentration (C-peptide/glucose ratio [CP/G]) and adjusted for renal function by calculating the C-peptide/glucose-creatinine ratio (CP/GCr). Glucose 79-86 insulin Homo sapiens 102-111 17173660-2 2007 Calculations were made to account for the dependence of C-peptide secretion on glucose concentration (C-peptide/glucose ratio [CP/G]) and adjusted for renal function by calculating the C-peptide/glucose-creatinine ratio (CP/GCr). Glucose 112-119 insulin Homo sapiens 56-65 17173660-2 2007 Calculations were made to account for the dependence of C-peptide secretion on glucose concentration (C-peptide/glucose ratio [CP/G]) and adjusted for renal function by calculating the C-peptide/glucose-creatinine ratio (CP/GCr). Glucose 112-119 insulin Homo sapiens 56-65 17306648-2 2007 STUDY DESIGN: Forty-five postmenopausal women, aged 55 +/- 7 years, were examined from a randomized, double-blind placebo-controlled trial evaluating the effect of HRT on insulin-stimulated glucose disposal and body composition. Glucose 190-197 insulin Homo sapiens 171-178 16818461-5 2007 Insulin was measured by radioimmunoassay every 30 min for 2 h. RESULTS: Three participants who were found to have previously undiagnosed abnormalities of glucose tolerance demonstrated significant (p = 0.04) incremental elevations in glucose levels after ingestion of glucosamine sulphate. Glucose 154-161 insulin Homo sapiens 0-7 17245174-7 2007 Insulin-stimulated glucose uptake increased significantly in FEN (4.3 +/- 0.6 vs. 4.5 +/- 0.7 PLA and 5.2 +/- 0.5 vs. 7.6 +/- 0.6 mg/kg per minute FEN; pretreatment vs. posttreatment; P = 0.003). Glucose 19-26 insulin Homo sapiens 0-7 17245174-8 2007 Insulin trended to suppress hepatic glucose release following fenofibrate treatment (P = 0.06). Glucose 36-43 insulin Homo sapiens 0-7 16808892-4 2007 Intracellular Mg plays a key role in regulating insulin action, insulin-mediated-glucose uptake and vascular tone. Glucose 81-88 insulin Homo sapiens 64-71 17522981-0 2007 Malonyl coenzyme A affects insulin-stimulated glucose transport in myotubes. Glucose 46-53 insulin Homo sapiens 27-34 17522981-2 2007 The purpose of the current study was to test the hypothesis that treatments designed to manipulate malonyl CoA concentrations would affect insulin-stimulated glucose transport in cultured C2C12 myotubes. Glucose 158-165 insulin Homo sapiens 139-146 17522981-4 2007 All three of these treatments prevented stimulation of glucose transport by insulin. Glucose 55-62 insulin Homo sapiens 76-83 17522981-6 2007 Three unrelated ACC inhibitors (diclofop, clethodim, and Pfizer CP-640186) all enhanced insulin-stimulated glucose transport. Glucose 107-114 insulin Homo sapiens 88-95 16950602-1 2007 The green tea flavonoid epigallocatechin gallate (EGCG) is one of several compounds that have been reported to have insulin-like glucose-lowering properties in mammals. Glucose 129-136 insulin Homo sapiens 116-123 16961464-1 2007 Minimal model analysis of glucose and insulin data from an IVGTT (intravenous glucose tolerance test) is widely used to estimate insulin sensitivity; however, the use of the model often requires intervention by a trained operator and some problems can occur in the estimation of model parameters. Glucose 26-33 insulin Homo sapiens 129-136 16961464-1 2007 Minimal model analysis of glucose and insulin data from an IVGTT (intravenous glucose tolerance test) is widely used to estimate insulin sensitivity; however, the use of the model often requires intervention by a trained operator and some problems can occur in the estimation of model parameters. Glucose 78-85 insulin Homo sapiens 38-45 16961464-1 2007 Minimal model analysis of glucose and insulin data from an IVGTT (intravenous glucose tolerance test) is widely used to estimate insulin sensitivity; however, the use of the model often requires intervention by a trained operator and some problems can occur in the estimation of model parameters. Glucose 78-85 insulin Homo sapiens 129-136 16961464-7 2007 Insulin sensitivity by GAMMOD was (3.86+/-0.19) compared with (4.33+/-0.20) x 10(-4) micro-units.ml(-1) x min(-1) by MINMOD; glucose effectiveness was 0.0236+/-0.0005 compared with 0.0229+/-0.0005 min(-1) respectively. Glucose 125-132 insulin Homo sapiens 0-7 17311546-7 2007 These pathways are ultimately linked to protein kinase B (Akt) and the insulin signaling pathways that determine the initial onset of glucose intolerance and the subsequent course to apoptotic cell injury. Glucose 134-141 insulin Homo sapiens 71-78 17940419-3 2007 Release of this peptide is stimulated by the ingestion of glucose and fat from the upper portion of the small intestine, which in turn enhances the release of insulin from the pancreas. Glucose 58-65 insulin Homo sapiens 159-166 16815586-2 2007 Aim of the present study is to compare the effects of glimepiride, repaglinide, and insulin glargine in type 2 diabetics during Ramadan fasting on the glucose metabolism. Glucose 151-158 insulin Homo sapiens 84-91 16887232-6 2007 We demonstrated a significant association between subtle disturbances of the glucose metabolism, assessed by subnormal levels of fasting glucose and insulin resistance parameters, and angiographically documented coronary artery disease. Glucose 77-84 insulin Homo sapiens 149-156 17119916-9 2007 CONCLUSIONS/INTERPRETATION: In patients with type 1 diabetes, exercise under peak therapeutic insulin concentrations increases exogenous glucose utilisation but does not spare muscle glycogen utilisation. Glucose 137-144 insulin Homo sapiens 94-101 17149589-8 2007 The effects of low-dose insulin on EGP and of high-dose insulin on glucose uptake and metabolic clearance rate were enhanced in the exercise group but not in the control group (p = 0.026; p = 0.007 and p = 0.04). Glucose 67-74 insulin Homo sapiens 56-63 17149589-10 2007 CONCLUSIONS/INTERPRETATION: Decreased availability of circulating NEFA may contribute to the observed improvement in the insulin sensitivity of EGP and glucose uptake following 6 weeks of moderate exercise. Glucose 152-159 insulin Homo sapiens 121-128 17151862-10 2007 In contrast, when plasma insulin was increased while maintaining normal blood glucose, the cerebral output of BDNF was not inhibited, indicating that high levels of glucose, but not insulin, inhibit the output of BDNF from the human brain. Glucose 165-172 insulin Homo sapiens 25-32 17318770-8 2007 TPTD seems to have an acute, subclinical adverse impact on stimulated glucose levels, possibly due to insulin resistance. Glucose 70-77 insulin Homo sapiens 102-109 17392602-4 2007 However, when dividing the 30 subjects in the upper and lower halves according to serum 25-hydroxyvitamin D levels (<59 and >58 nmol/l), those in the lower half had significantly higher 2-h serum insulin value at the OGTT, significantly higher insulin secretion during the last hour of the clamp, and significantly lower insulin sensitivity index (ISI; glucose infusion rate/insulin secretion during the last hour of the clamp). Glucose 359-366 insulin Homo sapiens 202-209 17090642-5 2007 Homeostasis model assessment for insulin resistance (HOMA-IR) (mU*mmol/liter2) was calculated as fasting insulin (mU/liter) times fasting glucose (mmol/liter) divided by 22.5. Glucose 138-145 insulin Homo sapiens 33-40 17321925-1 2007 STUDY OBJECTIVE: To investigate whether preinduction glucose is an important predictor for perioperative insulin management in patients undergoing cardiac surgery. Glucose 53-60 insulin Homo sapiens 105-112 17321925-12 2007 CONCLUSIONS: In cardiac surgical patients with a preinduction glucose above 110 mg/dL, even if diabetes was not previously suspected, perioperative insulin requirements were higher, and intraoperative insulin management is more difficult than in those with a preinduction glucose 110 mg/dL or lower. Glucose 62-69 insulin Homo sapiens 148-155 17380010-0 2007 Angiotensin II inhibits insulin-induced actin stress fiber formation and glucose uptake via ERK1/2. Glucose 73-80 insulin Homo sapiens 24-31 17380010-3 2007 In the presence of 100 nM of Ang II, insulin-induced glucose uptake was decreased and insulin-induced actin filament organization was inhibited. Glucose 53-60 insulin Homo sapiens 37-44 17234497-6 2007 A regression model, including gender, age, race, body mass index, serum glucose, high-density lipoprotein cholesterol, triglycerides, and blood pressure, explained 48% of insulin variance. Glucose 72-79 insulin Homo sapiens 171-178 17224332-6 2007 In addition, insulin-stimulated glucose uptake capacity was reduced by approximately 40% already after 2 hours (P < .05) and reached a maximal decline (by approximately 50%, P < .05) after a 6-hour culture in high glucose and high insulin. Glucose 32-39 insulin Homo sapiens 237-244 17396435-0 2007 Assessment of insulin sensitivity from measurements in fasting state and during an oral glucose tolerance test in obese children. Glucose 88-95 insulin Homo sapiens 14-21 17396435-2 2007 OBJECTIVE: To compare simple indices of insulin resistance calculated from fasting glucose and insulin levels with insulin sensitivity indices (area under the response curve [AUCinsulin], insulin sensitivity index [ISI-compositeL) determined by oral glucose tolerance testing (OGTT) in obese children. Glucose 83-90 insulin Homo sapiens 40-47 17224332-6 2007 In addition, insulin-stimulated glucose uptake capacity was reduced by approximately 40% already after 2 hours (P < .05) and reached a maximal decline (by approximately 50%, P < .05) after a 6-hour culture in high glucose and high insulin. Glucose 220-227 insulin Homo sapiens 13-20 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 41-48 insulin Homo sapiens 80-87 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 41-48 insulin Homo sapiens 80-87 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 99-106 insulin Homo sapiens 18-25 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 99-106 insulin Homo sapiens 80-87 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 99-106 insulin Homo sapiens 80-87 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 99-106 insulin Homo sapiens 18-25 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 99-106 insulin Homo sapiens 80-87 17224332-10 2007 Culture with high insulin alone (and low glucose, 6 mmol/L) decreased basal and insulin-stimulated glucose uptake in conformity with the high-glucose/high-insulin setting. Glucose 99-106 insulin Homo sapiens 80-87 16960657-0 2007 Chronic exposure to ketone bodies impairs glucose uptake in adult cardiomyocytes in response to insulin but not vanadate: the role of PI3-K. Glucose 42-49 insulin Homo sapiens 96-103 17224332-12 2007 We conclude that, in adipocytes from healthy humans, high insulin alone for 2 hours or more decrease glucose uptake capacity. Glucose 101-108 insulin Homo sapiens 58-65 16960657-2 2007 We have already shown that chronic exposure to the ketone body beta-hydroxybutyrate (OHB) decreases insulin-mediated activation of protein kinase B (PKB) and glucose uptake in cardiomyocytes. Glucose 158-165 insulin Homo sapiens 100-107 17224332-13 2007 Likewise, high glucose and high insulin in combination for 2 hours or more decrease glucose uptake to the same extent as when cells were cultured with high insulin alone but, in addition, with a diminishment in IRS-1 protein lagging behind. Glucose 15-22 insulin Homo sapiens 156-163 17224332-13 2007 Likewise, high glucose and high insulin in combination for 2 hours or more decrease glucose uptake to the same extent as when cells were cultured with high insulin alone but, in addition, with a diminishment in IRS-1 protein lagging behind. Glucose 84-91 insulin Homo sapiens 32-39 17224332-15 2007 High glucose alone induces only a minor insulin resistance in human fat cells. Glucose 5-12 insulin Homo sapiens 40-47 17258675-5 2007 Metformin (an insulin sensitizer) reduces hepatic glucose production. Glucose 50-57 insulin Homo sapiens 14-21 17379930-7 2007 Adding these drugs to standard oral glucose-lowering medication shows improvement in glucose and insulin concentrations and HbA1c compared with adding placebo. Glucose 36-43 insulin Homo sapiens 97-104 17326710-5 2007 In one night, a linear fall in plasma glucose to nadir levels of 2.2 mmol/l was induced by infusing insulin over a 1-h period starting as soon as polysomnographic recordings indicated that stage 2 sleep had been reached. Glucose 38-45 insulin Homo sapiens 100-107 17224784-4 2007 The beneficial anti-inflammatory effects of insulin in preclinical and clinical studies could possibly be due, at least in part, to the inhibition of GSK-3 and not directly correlated to the regulation of blood glucose. Glucose 211-218 insulin Homo sapiens 44-51 17343775-10 2007 Impaired fasting glucose often relates to defects in insulin secretion in addition to insulin resistance, and probably more than any other component of the syndrome predicts the increased incidence of type 2 diabetes. Glucose 17-24 insulin Homo sapiens 53-60 17233921-4 2007 The aim of this study was to examine whether the malignant potential of endometrial cancer enhanced by P-LAP/IRAP is due to increased glucose uptake via the P-LAP/IRAP-mediated activation of insulin signaling. Glucose 134-141 insulin Homo sapiens 191-198 17201925-7 2007 We will review islet transplantation, as well as the mechanisms underlying insulin transcription, translation and glucose stimulated insulin release. Glucose 114-121 insulin Homo sapiens 133-140 17224332-0 2007 Insulin resistance induced by high glucose and high insulin precedes insulin receptor substrate 1 protein depletion in human adipocytes. Glucose 35-42 insulin Homo sapiens 0-7 17224332-0 2007 Insulin resistance induced by high glucose and high insulin precedes insulin receptor substrate 1 protein depletion in human adipocytes. Glucose 35-42 insulin Homo sapiens 69-76 17224332-1 2007 The aim of this study was to investigate whether high glucose and/or high insulin produces cellular insulin resistance in human adipocytes and, if so, to evaluate the time course and content of key proteins in the insulin signaling pathway. Glucose 54-61 insulin Homo sapiens 100-107 17224332-1 2007 The aim of this study was to investigate whether high glucose and/or high insulin produces cellular insulin resistance in human adipocytes and, if so, to evaluate the time course and content of key proteins in the insulin signaling pathway. Glucose 54-61 insulin Homo sapiens 100-107 17224332-3 2007 Insulin action in vitro was studied by measurement of glucose uptake after incubation at a physiologic glucose level (6 mmol/L) for 24 hours or with the last 2, 6, or 24 hours at a high glucose level (20 mmol/L) with or without high insulin (10(4)microU/mL). Glucose 54-61 insulin Homo sapiens 0-7 17224332-3 2007 Insulin action in vitro was studied by measurement of glucose uptake after incubation at a physiologic glucose level (6 mmol/L) for 24 hours or with the last 2, 6, or 24 hours at a high glucose level (20 mmol/L) with or without high insulin (10(4)microU/mL). Glucose 103-110 insulin Homo sapiens 0-7 17224332-3 2007 Insulin action in vitro was studied by measurement of glucose uptake after incubation at a physiologic glucose level (6 mmol/L) for 24 hours or with the last 2, 6, or 24 hours at a high glucose level (20 mmol/L) with or without high insulin (10(4)microU/mL). Glucose 103-110 insulin Homo sapiens 0-7 17224332-5 2007 In contrast, the combination of high glucose and high insulin for 6 hours or more reduced basal glucose uptake by approximately 40% (P < .05). Glucose 96-103 insulin Homo sapiens 54-61 17224332-6 2007 In addition, insulin-stimulated glucose uptake capacity was reduced by approximately 40% already after 2 hours (P < .05) and reached a maximal decline (by approximately 50%, P < .05) after a 6-hour culture in high glucose and high insulin. Glucose 32-39 insulin Homo sapiens 13-20 17474309-4 2007 These molecular toxicities can affect non-adipose tissues, and together with secondary effects on lipid and glucose metabolism of changes in body fat mass, help to contribute to the dyslipidemia and insulin resistance characteristic of this syndrome. Glucose 108-115 insulin Homo sapiens 199-206 17049721-4 2007 The rate of glucose-6-phosphate formation, however, was decreased by resistin both in the absence and presence of insulin; in the absence of insulin, resistin decreased glucose-6-phosphate formation by reducing hexokinase type I activity without affecting glucose uptake; by contrast, in the presence of insulin, resistin decreased glucose-6-phosphate formation by reducing the Vmax of glucose uptake without changing hexokinase type I activity. Glucose 12-19 insulin Homo sapiens 114-121 17187615-5 2007 Insulin sensitivity was evaluated by oral glucose tolerance test, oral glucose insulin sensitivity (OGIS) and homeostasis is model assessment (HOMA) index. Glucose 42-49 insulin Homo sapiens 0-7 17187615-8 2007 Statistically significant differences between both groups were found for mean serum ALT levels, mean glucose levels after 30, 60 and 90 minutes and mean insulin levels after 60 minutes of the glucose tolerance test. Glucose 192-199 insulin Homo sapiens 153-160 17953471-3 2007 Repaglinide is an insulin secretagogue that lowers blood glucose levels in patients with T2DM. Glucose 57-64 insulin Homo sapiens 18-25 16968812-0 2007 Carotid artery intima-media thickness is associated with insulin-mediated glucose disposal in nondiabetic normotensive offspring of type 2 diabetic patients. Glucose 74-81 insulin Homo sapiens 57-64 16954337-5 2007 beta-Cell responsiveness was estimated as changes in insulin secretion rates in response to changes in postprandial plasma glucose (PG). Glucose 123-130 insulin Homo sapiens 53-60 16968813-6 2007 In contrast to metformin, pioglitazone improved S(I), glucose tolerance, and insulin-independent glucose disposal [glucose effectiveness (S(G))]. Glucose 97-104 insulin Homo sapiens 77-84 16968813-6 2007 In contrast to metformin, pioglitazone improved S(I), glucose tolerance, and insulin-independent glucose disposal [glucose effectiveness (S(G))]. Glucose 97-104 insulin Homo sapiens 77-84 16968813-8 2007 Insulin secretion in response to arginine at maximally potentiating glucose levels (AIR(max)) tended to increase after metformin and to decrease after pioglitazone; however, when adjusted for S(I), the changes were not significant. Glucose 68-75 insulin Homo sapiens 0-7 18025824-0 2007 Plasma arachidonic acid influences insulin-stimulated glucose uptake in healthy adult women. Glucose 54-61 insulin Homo sapiens 35-42 18003373-1 2007 This paper presents the results of computational studies that compare simulated parametric and nonparametric models in terms of their ability to obtain reliable quantitative descriptions of the dynamic effects of variable infusions of insulin on blood glucose concentration in human subjects. Glucose 252-259 insulin Homo sapiens 235-242 17582913-0 2007 Insulin sensitivity obtained from the oral glucose tolerance test and its relationship with birthweight. Glucose 43-50 insulin Homo sapiens 0-7 18003374-6 2007 The output of the model consists of short term glucose predictions and provides input to the NMPC, in order for the latter to estimate the optimum insulin infusion rates. Glucose 47-54 insulin Homo sapiens 147-154 18002320-0 2007 Prediction of glucose excursions under uncertain parameters and food intake in intensive insulin therapy for type 1 diabetes mellitus. Glucose 14-21 insulin Homo sapiens 89-96 18002680-1 2007 In this study we develop a system that uses some variables such as, level of exercise, stress, food intake, injected insulin and blood glucose level in previous intervals, as input and accurately predicts the blood glucose level in the next interval. Glucose 215-222 insulin Homo sapiens 117-124 17465853-3 2007 Postprandial glucose uptake by the liver is determined by the size of the glucose load reaching the liver, the rise in insulin concentration, and the route of glucose delivery. Glucose 13-20 insulin Homo sapiens 119-126 17210722-10 2007 Accordingly, insulin-stimulated glucose uptake was enhanced on IGF1R down-regulation. Glucose 32-39 insulin Homo sapiens 13-20 17666010-4 2007 In vitro and in vivo data also support an important role of amino acids in glucose homeostasis through modulation of insulin action on muscle glucose transport and hepatic glucose production, secretion of insulin and glucagon, as well as gene and protein expression in various tissues. Glucose 75-82 insulin Homo sapiens 117-124 17666010-4 2007 In vitro and in vivo data also support an important role of amino acids in glucose homeostasis through modulation of insulin action on muscle glucose transport and hepatic glucose production, secretion of insulin and glucagon, as well as gene and protein expression in various tissues. Glucose 142-149 insulin Homo sapiens 117-124 17206800-6 2007 The in vivo results clearly indicated that the insulin-loaded NPs could effectively reduce the blood glucose level in a diabetic rat model. Glucose 101-108 insulin Homo sapiens 47-54 17873339-5 2007 In insulin resistance, alterations in glucose and lipid metabolism lead to the production of excess aldehydes including glyoxal and methylglyoxal. Glucose 38-45 insulin Homo sapiens 3-10 17189207-1 2007 Insulin stimulates glucose uptake by promoting translocation of the Glut4 glucose transporter from intracellular storage compartments to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 17189207-7 2007 Insulin recruits the CIP4/Gapex-5 complex to the plasma membrane, thus reducing Rab31 activity and permitting Glut4 vesicles to translocate to the cell surface, where Glut4 docks and fuses to transport glucose into the cell. Glucose 202-209 insulin Homo sapiens 0-7 17709880-0 2007 Insulin signaling and glucose transport in insulin resistant human skeletal muscle. Glucose 22-29 insulin Homo sapiens 43-50 17709880-5 2007 The identification and characterization of pathways governing insulin action on glucose metabolism will facilitate the development of strategies to improve insulin sensitivity in an effort to prevent and treat Type 2 diabetes mellitus. Glucose 80-87 insulin Homo sapiens 62-69 17709880-5 2007 The identification and characterization of pathways governing insulin action on glucose metabolism will facilitate the development of strategies to improve insulin sensitivity in an effort to prevent and treat Type 2 diabetes mellitus. Glucose 80-87 insulin Homo sapiens 156-163 17709883-7 2007 The molecular mechanisms responsible for the glucose toxic effect on beta cell function involves disappearance of two important regulators of insulin promoter activity, PDX-1 and MafA. Glucose 45-52 insulin Homo sapiens 142-149 17635072-3 2007 METHODS: Insulin output in terms of area under the curve after an oral glucose tolerance test (AUC Ins OGTT) and lipid tolerance tests (AUC Ins OLTT) were measured in 167 overweight/obese patients. Glucose 71-78 insulin Homo sapiens 9-16 17635072-10 2007 Thus, the new insulin index NIOR may distinguish gene variant carriers into groups of glucose- or lipid-sensitive phenotypes. Glucose 86-93 insulin Homo sapiens 14-21 18357952-2 2007 Both IFG and IGT exhibit elevated glucose levels that are not sufficient to be classified as diabetes but that represent the development of insulin resistance. Glucose 34-41 insulin Homo sapiens 140-147 18154189-2 2007 The main metabolic actions of insulin are to stimulate glucose uptake in skeletal muscle and the heart and to suppress the production of glucose and very-low-density lipoprotein in the liver. Glucose 55-62 insulin Homo sapiens 30-37 18154189-2 2007 The main metabolic actions of insulin are to stimulate glucose uptake in skeletal muscle and the heart and to suppress the production of glucose and very-low-density lipoprotein in the liver. Glucose 137-144 insulin Homo sapiens 30-37 18154189-3 2007 Other metabolic effects of insulin include inhibition of glucose release from the liver, inhibition of the release of free fatty acids (FFAs) from adipose tissue, and stimulation of the process by which amino acids are incorporated into protein. Glucose 57-64 insulin Homo sapiens 27-34 18159645-1 2007 Insulin resistance (IR) is characterized by decreasing sensitivity of target tissues to the action of insulin, elevated blood glucose concentration, and increased hepatic production of atherogenic lipids. Glucose 126-133 insulin Homo sapiens 0-7 18357954-3 2007 Addition of insulin to sulfonylurea therapy, when maximal sulfonylurea does not adequately maintain fasting plasma glucose levels at <108 mg/dL, has been found to be more effective than initiating insulin therapy after oral agents have failed to maintain glycemic control. Glucose 115-122 insulin Homo sapiens 12-19 17132138-2 2007 Acute exposure of the pancreatic beta-cell to high glucose concentrations and/or saturated NEFAs results in a substantial increase in insulin release, whereas chronic exposure results in desensitization and suppression of secretion, followed by induction of apoptosis. Glucose 51-58 insulin Homo sapiens 134-141 18191067-12 2007 In addition, insulin aspart was associated with lowered postprandial blood glucose levels, as well as reduced risk of hypoglycemia, suggesting that it may offer clinical advantages in this population. Glucose 75-82 insulin Homo sapiens 13-20 17963523-8 2007 Toxicokinetic/toxicodynamic relationships between glucose infusion rates and insulin concentrations fit the maximum measured glucose infusion rate (Emax) model (Emax 29.5 [17.5 to 41.1] g/hour, concentration associated with the half-maximum glucose infusion rate [EC50] 46 [35 to 161] mIU/l, and R2 range 0.70 to 0.98; n = 6). Glucose 50-57 insulin Homo sapiens 77-84 17623086-3 2007 METHODS: At a general adult 22-bed intensive care unit, we implemented an intensive insulin therapy protocol in mechanically ventilated patients, aiming for a target glucose range of 4.4 to 6.1 mmol/l. Glucose 166-173 insulin Homo sapiens 84-91 17963523-8 2007 Toxicokinetic/toxicodynamic relationships between glucose infusion rates and insulin concentrations fit the maximum measured glucose infusion rate (Emax) model (Emax 29.5 [17.5 to 41.1] g/hour, concentration associated with the half-maximum glucose infusion rate [EC50] 46 [35 to 161] mIU/l, and R2 range 0.70 to 0.98; n = 6). Glucose 125-132 insulin Homo sapiens 77-84 17963523-8 2007 Toxicokinetic/toxicodynamic relationships between glucose infusion rates and insulin concentrations fit the maximum measured glucose infusion rate (Emax) model (Emax 29.5 [17.5 to 41.1] g/hour, concentration associated with the half-maximum glucose infusion rate [EC50] 46 [35 to 161] mIU/l, and R2 range 0.70 to 0.98; n = 6). Glucose 125-132 insulin Homo sapiens 77-84 17691941-6 2007 The insulin-resistant state is characterized by a failure to suppress hepatic glucose production and glycogenolysis, with enhanced fat accumulation in hepatocytes because of increased lipolysis, increased free fatty acid uptake by hepatocytes, and increased hepatic synthesis of triglycerides. Glucose 78-85 insulin Homo sapiens 4-11 17257475-2 2007 The Diabetes Control and Complications Clinical Trial demonstrated that intensive insulin therapy and the control of plasma glucose can significantly reduce the incidence of late diabetic complications and delay the progression of existing conditions in type 1 diabetes. Glucose 124-131 insulin Homo sapiens 82-89 16874843-2 2007 Near normalization of elevated blood glucose levels with IV insulin may improve outcome. Glucose 37-44 insulin Homo sapiens 60-67 17852199-0 2007 Co-transfection of GK and mhPINS genes into HepG2 cells confers glucose-stimulated insulin secretion. Glucose 64-71 insulin Homo sapiens 83-90 17852199-1 2007 BACKGROUND: The purpose of this study was to construct an "artificial beta cell" that can exhibit physiologic glucose-stimulated insulin secretion for the treatment of type 1 diabetes. Glucose 110-117 insulin Homo sapiens 129-136 17852199-5 2007 Finally, the dose-response effect of glucose on insulin secretion from those HepG2 cells that expressed both GK and mhPINS genes was tested with HepG2 cells that only expressed the mhPINS gene as a control. Glucose 37-44 insulin Homo sapiens 48-55 17852199-10 2007 The artificial beta cell, clone Beta, obtained a glucose-stimulated insulin secretion with maximal insulin secretion at 1.75-2.00 mmol/L glucose concentrations. Glucose 49-56 insulin Homo sapiens 68-75 17852199-10 2007 The artificial beta cell, clone Beta, obtained a glucose-stimulated insulin secretion with maximal insulin secretion at 1.75-2.00 mmol/L glucose concentrations. Glucose 49-56 insulin Homo sapiens 99-106 17852199-10 2007 The artificial beta cell, clone Beta, obtained a glucose-stimulated insulin secretion with maximal insulin secretion at 1.75-2.00 mmol/L glucose concentrations. Glucose 137-144 insulin Homo sapiens 68-75 16874843-6 2007 The intersection of the current and the previous blood glucose values on the matrix locates the appropriate cell containing the required change in insulin flow rate. Glucose 55-62 insulin Homo sapiens 147-154 17852199-10 2007 The artificial beta cell, clone Beta, obtained a glucose-stimulated insulin secretion with maximal insulin secretion at 1.75-2.00 mmol/L glucose concentrations. Glucose 137-144 insulin Homo sapiens 99-106 17852199-11 2007 DISCUSSION: An artificial beta cell that exhibits glucose-stimulated insulin secretion can be constructed successfully. Glucose 50-57 insulin Homo sapiens 69-76 17192339-1 2007 OBJECTIVE: To derive indexes for muscle and hepatic insulin sensitivity from the measurement of plasma glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 103-110 insulin Homo sapiens 52-59 17192339-1 2007 OBJECTIVE: To derive indexes for muscle and hepatic insulin sensitivity from the measurement of plasma glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Glucose 153-160 insulin Homo sapiens 52-59 17192339-5 2007 RESULTS: The product of total area under curve (AUC) for glucose and insulin during the first 30 min of the OGTT (glucose(0-30)[AUC] x insulin(0-30)[AUC]) strongly correlated with the hepatic insulin resistance index (fasting plasma insulin x basal endogenous glucose production) (r = 0.64, P < 0.0001). Glucose 57-64 insulin Homo sapiens 135-142 17192482-4 2007 Perifusion experiments with human islets indicated that PLA(2) inhibition inhibited glucose-stimulated insulin secretion, whereas inhibitors of COX-2 and 12-LOX enzymes enhanced basal insulin secretion and also secretory responses induced by 20 mmol/l glucose or by 50 mumol/l arachidonic acid. Glucose 84-91 insulin Homo sapiens 103-110 17192339-5 2007 RESULTS: The product of total area under curve (AUC) for glucose and insulin during the first 30 min of the OGTT (glucose(0-30)[AUC] x insulin(0-30)[AUC]) strongly correlated with the hepatic insulin resistance index (fasting plasma insulin x basal endogenous glucose production) (r = 0.64, P < 0.0001). Glucose 57-64 insulin Homo sapiens 135-142 17192488-6 2007 Hyperglycemia, insulin resistance, and insulin response to glucose, as well as dyslipidemia, were markedly and significantly ameliorated by the treatment. Glucose 59-66 insulin Homo sapiens 39-46 17199720-5 2007 The two groups were similar in age and body mass index, differing only in their insulin-mediated glucose uptake as quantified by the steady-state plasma glucose concentration determined during the insulin suppression test. Glucose 97-104 insulin Homo sapiens 80-87 17192339-5 2007 RESULTS: The product of total area under curve (AUC) for glucose and insulin during the first 30 min of the OGTT (glucose(0-30)[AUC] x insulin(0-30)[AUC]) strongly correlated with the hepatic insulin resistance index (fasting plasma insulin x basal endogenous glucose production) (r = 0.64, P < 0.0001). Glucose 114-121 insulin Homo sapiens 69-76 17199720-5 2007 The two groups were similar in age and body mass index, differing only in their insulin-mediated glucose uptake as quantified by the steady-state plasma glucose concentration determined during the insulin suppression test. Glucose 97-104 insulin Homo sapiens 197-204 17192339-5 2007 RESULTS: The product of total area under curve (AUC) for glucose and insulin during the first 30 min of the OGTT (glucose(0-30)[AUC] x insulin(0-30)[AUC]) strongly correlated with the hepatic insulin resistance index (fasting plasma insulin x basal endogenous glucose production) (r = 0.64, P < 0.0001). Glucose 114-121 insulin Homo sapiens 69-76 17192339-6 2007 The rate of decay of plasma glucose concentration from its peak value to its nadir during the OGTT divided by the mean plasma insulin concentration (dG/dt / I) strongly correlated with muscle insulin sensitivity measured with the insulin clamp (P = 0.78, P < 0.0001). Glucose 28-35 insulin Homo sapiens 192-199 17199734-5 2007 Insulin sensitivity, assessed by a frequently sampled intravenous glucose tolerance test [n=5], body composition, HbA(1c) and quality of life (QOL) were measured before and after treatment. Glucose 66-73 insulin Homo sapiens 0-7 17192339-6 2007 The rate of decay of plasma glucose concentration from its peak value to its nadir during the OGTT divided by the mean plasma insulin concentration (dG/dt / I) strongly correlated with muscle insulin sensitivity measured with the insulin clamp (P = 0.78, P < 0.0001). Glucose 28-35 insulin Homo sapiens 192-199 17008397-0 2007 A purine analog kinase inhibitor, calcium/calmodulin-dependent protein kinase II inhibitor 59, reveals a role for calcium/calmodulin-dependent protein kinase II in insulin-stimulated glucose transport. Glucose 183-190 insulin Homo sapiens 164-171 17008397-2 2007 We found that olomoucine blocked insulin"s ability to stimulate glucose transport. Glucose 64-71 insulin Homo sapiens 33-40 17008397-5 2007 One of the generated analogs inhibited insulin-stimulated glucose uptake with increased sensitivity compared with olomoucine. Glucose 58-65 insulin Homo sapiens 39-46 17220786-2 2007 Exenatide is a long acting analogue of Glucagon-like peptide-1 (GLP-1) that augments glucose induced insulin secretion, and may increase beta cell mass. Glucose 85-92 insulin Homo sapiens 101-108 17008397-6 2007 The IC(50) for inhibition of insulin-stimulated glucose uptake occurred at analog concentrations as low as 0.1 microM. Glucose 48-55 insulin Homo sapiens 29-36 17008397-9 2007 To investigate CaMKII involvement in insulin-stimulated glucose uptake, 3T3-L1 adipocytes were infected with retrovirus encoding green fluorescent protein (GFP)-hemagluttinin tag (HA)-tagged CaMKII wild-type or the ATP binding mutant, K42M. Glucose 56-63 insulin Homo sapiens 37-44 17008397-11 2007 Insulin-stimulated glucose transport was significantly decreased (approximately 80%) in GFP-HA-CaMKII K42M cells, compared with nontransfected cells, and cells expressing either GFP-HA-CaMKII or GFP-HA. Glucose 19-26 insulin Homo sapiens 0-7 17008399-0 2007 TC10alpha is required for insulin-stimulated glucose uptake in adipocytes. Glucose 45-52 insulin Homo sapiens 26-33 17008399-3 2007 Knockdown of TC10alpha but not TC10beta by RNA interference inhibited insulin-stimulated glucose uptake as well as the translocation of the insulin-sensitive glucose transporter GLUT4 from intracellular sites to the plasma membrane. Glucose 89-96 insulin Homo sapiens 70-77 17923765-4 2007 Transient neonatal diabetes can be caused by defects in the normal methylation pattern of an imprinted gene on chromosome 6 and by mutations in the 2 genes encoding the beta-cell ATP-sensitive potassium channel which is vital to normal glucose-stimulated insulin secretion. Glucose 236-243 insulin Homo sapiens 255-262 17038556-6 2007 Importantly, we found that prolonged IL-1beta treatment reduced the insulin-induced glucose uptake, whereas an acute treatment had no effect. Glucose 84-91 insulin Homo sapiens 68-75 17923775-7 2007 Pilot studies of insulin replacement in VLBW infants demonstrate improved glucose control, and increased circulating IGF-1 bioactivity. Glucose 74-81 insulin Homo sapiens 17-24 16962100-6 2007 Short-term exposure (12 h) of acetaldehyde (150 muM) facilitated glucose uptake in a rapamycin-dependent manner without affecting apoptosis, IRS-2 expression and insulin-stimulated glucose uptake in SH-SY5Y cells. Glucose 181-188 insulin Homo sapiens 162-169 17344645-1 2007 Insulin has long-term effects on glucose and lipid metabolism through its control on the expression of specific genes. Glucose 33-40 insulin Homo sapiens 0-7 30743746-3 2007 Efficient insulin gene therapy should have an effective insulin gene delivery mechanism, a system of regulation of the insulin biosynthesis that responds to glucose within extremely narrow physiological limits, a system of insulin processing into its active form and a choice of appropriate target cells, which possess biochemical characteristics similar to beta cells, but are not targets for beta-cell-specific self-reactivity. Glucose 157-164 insulin Homo sapiens 10-17 17057397-13 2007 Insulin mediated glucose disposal was lower in the normal weight women with IH than in those without hirsutism. Glucose 17-24 insulin Homo sapiens 0-7 17028439-3 2007 OBJECTIVE: To ascertain whether recovery from insulin-induced hypoglycaemia with an oral glucose solution produces a different response of growth hormone (GH) and cortisol at different times of the study compared with spontaneous recovery from hypoglycaemia. Glucose 89-96 insulin Homo sapiens 46-53 17028439-10 2007 CONCLUSIONS: Oral glucose solution administration when glycaemia was under 30 mg/dl in HIT produced a lower GH and cortisol response to insulin stimulus and a greater frequency of GH deficit diagnosis. Glucose 18-25 insulin Homo sapiens 136-143 17143549-0 2007 Significant change in insulin production, glucose tolerance and ER stress signaling in transgenic mice coexpressing insulin-siRNA and human IDE. Glucose 42-49 insulin Homo sapiens 116-123 17587854-11 2007 Exogenous insulin infusion partially reduces endogenous glucose production in preterm newborn infants. Glucose 56-63 insulin Homo sapiens 10-17 17763019-1 2007 The study aimed to assess the frequency of hypoglycaemia during the insulin-modified, frequently sampled intravenous glucose tolerance test (FSIVGTT) in overweight Hispanic children. Glucose 117-124 insulin Homo sapiens 68-75 18019848-0 2007 Glucose-sensing pulmonary delivery of human insulin to the systemic circulation of rats. Glucose 0-7 insulin Homo sapiens 44-51 18019848-4 2007 This work is a demonstration of an inhalable particle with long residence times in the lungs capable of modulating insulin release based on systemic glucose levels. Glucose 149-156 insulin Homo sapiens 115-122 17063460-1 2007 Fibroblast growth factor (FGF)-21 is a novel regulator of insulin-independent glucose transport in 3T3-L1 adipocytes and has glucose and triglyceride lowering effects in rodent models of diabetes. Glucose 78-85 insulin Homo sapiens 58-65 17179547-18 2007 Active follicular development was associated with prolonged secretion of insulin in response to glucose challenge. Glucose 96-103 insulin Homo sapiens 73-80 17062764-7 2007 HF diet reduced CHO oxidation under basal (by approximately 40%, P < 0.05) and clamp conditions (by approximately 20%, P < 0.05), increased insulin-mediated whole-body nonoxidative glucose disposal (by 30%, P < 0.05) and muscle glycogen storage (by approximately 25%, P < 0.05). Glucose 187-194 insulin Homo sapiens 146-153 17032721-10 2007 Insulin sensitivity, derived from iv glucose tolerance testing, tended (P > 0.1) to be higher with haplotype 1 (S(I) = 1.72) and lower with haplotype 4 (S(I)=1.38). Glucose 37-44 insulin Homo sapiens 0-7 17385686-11 2007 The insulin resistance index progressively increased when the glucose tolerance stage changed from NGT through diabetic subjects. Glucose 62-69 insulin Homo sapiens 4-11 17077128-7 2007 We observed nominal significant associations of genotype with increased area under the serum insulin curve during an oral glucose tolerance test (P = 0.03) and elevated fasting plasma glucose (P = 0.02) in homozygous Ala92 allele carriers, the latter strengthened by epistasis with the ADRB2 Gly16Arg variant in a double recessive model (P = 0.004). Glucose 122-129 insulin Homo sapiens 93-100 19888378-1 2007 BACKGROUND: Current bolus insulin dosing recommendations are based on retrospective studies of patients with Type 1 diabetes in whom the glucose control was not intensely established. Glucose 137-144 insulin Homo sapiens 26-33 17189870-5 2007 RESULTS: Insulin lispro was associated with significantly lower postprandial glucose (area under the curve0-5 h=43.54 vs. 57.65 mM/h; P<.001), elevated insulin concentrations, and acutely altered lipid fractions that included an early decrease followed by an increase in free fatty acids, lower triglycerides, elevated total cholesterol, elevated low-density lipoprotein cholesterol (LDL), and elevated high-density lipoprotein cholesterol. Glucose 77-84 insulin Homo sapiens 9-16 19888383-6 2007 Models are necessary for understanding the relationship between blood glucose levels and insulin dosing; developing algorithms to control insulin dosing; and customizing each user"s system based on individual responses to factors that influence glycemia. Glucose 70-77 insulin Homo sapiens 89-96 17143190-6 2007 APA patients showed a significant reduction of both plasma glucose (P=0.017) and insulin levels (P=0.001) after 75 g oral glucose tolerance test. Glucose 122-129 insulin Homo sapiens 81-88 17035674-6 2007 With respect to adipocyte function, adipose LPIN1 gene expression was strongly associated with both basal and insulin-mediated subcutaneous adipocyte glucose transport as well as mRNA levels of glucose transporter 4 (GLUT4). Glucose 150-157 insulin Homo sapiens 110-117 17441407-0 2007 Effects of multiple daily insulin injections on peripheral glucose disposal in Latin Americans with type 2 diabetes mellitus. Glucose 59-66 insulin Homo sapiens 26-33 17441407-1 2007 OBJECTIVE: To evaluate the effects of insulin in multiple daily injections (MDI) on peripheral glucose disposal in Latin American patients with type 2 diabetes. Glucose 95-102 insulin Homo sapiens 38-45 17978746-6 2007 Continuous insulin therapy using pumps offers both a better blood glucose stability than multiple daily injections and a broader flexibility in life mode. Glucose 66-73 insulin Homo sapiens 11-18 17978746-8 2007 The development of glucose sensors provides reinforced information on blood glucose, versus self-monitoring by capillary blood measurements, that contributes to a better adaptation of insulin therapy. Glucose 19-26 insulin Homo sapiens 184-191 17978746-8 2007 The development of glucose sensors provides reinforced information on blood glucose, versus self-monitoring by capillary blood measurements, that contributes to a better adaptation of insulin therapy. Glucose 76-83 insulin Homo sapiens 184-191 17978746-9 2007 First trials of connections between blood glucose data and insulin delivery open a perspective toward glucose-modulated insulin therapy, at least in periods outside meals, leading to first models of semi-automated artificial endocrine pancreas. Glucose 42-49 insulin Homo sapiens 59-66 17978746-9 2007 First trials of connections between blood glucose data and insulin delivery open a perspective toward glucose-modulated insulin therapy, at least in periods outside meals, leading to first models of semi-automated artificial endocrine pancreas. Glucose 42-49 insulin Homo sapiens 120-127 18613325-4 2007 By reducing hepatic glucose output it lowers blood glucose and insulin levels with minimal risk of hypoglycaemia, and when used as monotherapy can lower HbAlc by around 1.5%. Glucose 20-27 insulin Homo sapiens 63-70 17495816-0 2007 [Insulin-glucose parameters in healthy women and patients with arterial hypertension and ischemic heart disease in dependence on age and follicle-stimulating hormone levels]. Glucose 9-16 insulin Homo sapiens 1-8 17495816-1 2007 Insulin-glucose parameters in healthy women do not significantly change with changes of functional state of ovaries. Glucose 8-15 insulin Homo sapiens 0-7 17459601-2 2007 Although the first described action of insulin was on glucose transport, it is a hormone with many functions some of which may operate in a metabolic hierarchy depending on the relative importance of the action required. Glucose 54-61 insulin Homo sapiens 39-46 17459601-3 2007 Insulin also promotes the transport of potassium ions from the extracellular space to the intracellular space and it is suggested that there are occasions where this action may take place at the expense of glucose regulation. Glucose 206-213 insulin Homo sapiens 0-7 17145138-4 2007 The rationale for combination therapy is based on the assumption that, if evening insulin lowers the fasting glucose concentration to normal, then daytime oral agents will be more effective in controlling postprandial hyperglycemia. Glucose 109-116 insulin Homo sapiens 82-89 17145138-6 2007 In postprandial period, beta cell-originated insulin inhibits glucagon synthesis by paracrine effect and also inhibits hepatic glucose production by using half of its concentration that administered to portal system. Glucose 127-134 insulin Homo sapiens 45-52 17145138-7 2007 Since half of insulin that found in portal system is exposed to hepatic clearance to inhibit hepatic glucose production, portal insulin concentration is 2-4-folds higher than peripheral insulin concentration. Glucose 101-108 insulin Homo sapiens 14-21 17145138-7 2007 Since half of insulin that found in portal system is exposed to hepatic clearance to inhibit hepatic glucose production, portal insulin concentration is 2-4-folds higher than peripheral insulin concentration. Glucose 101-108 insulin Homo sapiens 128-135 17145138-7 2007 Since half of insulin that found in portal system is exposed to hepatic clearance to inhibit hepatic glucose production, portal insulin concentration is 2-4-folds higher than peripheral insulin concentration. Glucose 101-108 insulin Homo sapiens 128-135 17145138-10 2007 Thus, exogenous insulin that is used to inhibit hepatic glucose production requires higher concentrations than physiologic values. Glucose 56-63 insulin Homo sapiens 16-23 17145138-13 2007 For that reason, using OAD instead of bedtime insulin may be a more convenient way to inhibit hepatic glucose production. Glucose 102-109 insulin Homo sapiens 46-53 17179917-3 2007 Beta-cell failure is characterized by the inability of the beta-cell to secrete sufficient insulin in response to glucose, which ultimately results in hyperglycemia- the clinical hallmark of Type 2 diabetes. Glucose 114-121 insulin Homo sapiens 91-98 17179917-5 2007 The facilitative glucose transporter, GLUT-2, and glucose phosphorylating enzyme, glucokinase, are key for glucose sensing of the pancreatic beta-cell, the initial event in the pathway for glucose-stimulated insulin secretion. Glucose 17-24 insulin Homo sapiens 208-215 17179917-5 2007 The facilitative glucose transporter, GLUT-2, and glucose phosphorylating enzyme, glucokinase, are key for glucose sensing of the pancreatic beta-cell, the initial event in the pathway for glucose-stimulated insulin secretion. Glucose 50-57 insulin Homo sapiens 208-215 17179917-5 2007 The facilitative glucose transporter, GLUT-2, and glucose phosphorylating enzyme, glucokinase, are key for glucose sensing of the pancreatic beta-cell, the initial event in the pathway for glucose-stimulated insulin secretion. Glucose 50-57 insulin Homo sapiens 208-215 17179917-7 2007 A high fat diet is known to reduce both GLUT-2 and glucokinase expression thereby impairing glucose-stimulated insulin secretion. Glucose 92-99 insulin Homo sapiens 111-118 17179917-9 2007 Glucose sensing is the initial event of glucose-stimulated insulin secretion therefore it is imperative to maintain adequate expression levels of GLUT-2 and GK for ensuring normal beta-cell function. Glucose 0-7 insulin Homo sapiens 59-66 17179917-9 2007 Glucose sensing is the initial event of glucose-stimulated insulin secretion therefore it is imperative to maintain adequate expression levels of GLUT-2 and GK for ensuring normal beta-cell function. Glucose 40-47 insulin Homo sapiens 59-66 17179917-10 2007 The development of pharmaceutical agents that improve glucose-stimulated insulin secretion may replenish expression of these glucose sensing genes after their attenuation by high fat feeding. Glucose 54-61 insulin Homo sapiens 73-80 17179917-10 2007 The development of pharmaceutical agents that improve glucose-stimulated insulin secretion may replenish expression of these glucose sensing genes after their attenuation by high fat feeding. Glucose 125-132 insulin Homo sapiens 73-80 17408014-0 2007 [Critical evaluation of the oral glucose tolerance test for the diagnosis of insulin resistance in patients with polycystic ovary syndrome]. Glucose 33-40 insulin Homo sapiens 77-84 17408014-1 2007 Oral glucose tolerance test (OGTT) is the most commonly used method to evaluate insulin resistance (IR) in the clinical practice. Glucose 5-12 insulin Homo sapiens 80-87 17161222-23 2007 The significance of the increased insulin clearance by TZD therapy remains uncertain and deserves further investigation in patients with insulin resistance and glucose intolerance. Glucose 160-167 insulin Homo sapiens 34-41 17161224-8 2007 The best predictive equation for the whole postmeal glucose area under the curve (AUC) was found at 120 minutes and involved glucose, insulin, and nonesterified fatty acids (r(2) = 0.89; P < 10(-7)). Glucose 52-59 insulin Homo sapiens 134-141 17161228-6 2007 Glucose disposal increased in a linear fashion with plasma insulin concentrations. Glucose 0-7 insulin Homo sapiens 59-66 17161228-10 2007 The EC(50) for insulin suppression of lipolysis correlated linearly with plasma triglycerides (r = 0.52, P < .001) and exponentially with insulin sensitivity(glucose) (r = 0.70, P < .001). Glucose 161-168 insulin Homo sapiens 15-22 17161228-10 2007 The EC(50) for insulin suppression of lipolysis correlated linearly with plasma triglycerides (r = 0.52, P < .001) and exponentially with insulin sensitivity(glucose) (r = 0.70, P < .001). Glucose 161-168 insulin Homo sapiens 141-148 17161231-12 2007 A strong positive association was observed in the control population between H-Cr(pr) and fasting plasma insulin (n = 22; R = 0.6157; P < .01), and H-Cr(pr) and fasting plasma glucose (n = 24; R = 0.4118; P < .05), which is indicative of the interrelation of these parameters. Glucose 179-186 insulin Homo sapiens 105-112 17161234-3 2007 This study therefore examined the time course of changes in the insulin response to intravenous glucose (1 g/kg) in relation to glucose tolerance in female mice after 1, 3, 8, or 16 weeks of feeding with diets containing 11% fat (normal diet [ND]), 30% fat (medium-fat diet [MFD]), or 58% fat (high-fat diet [HFD]; by energy). Glucose 96-103 insulin Homo sapiens 64-71 17161234-9 2007 Insulin clearance, as judged by elimination of intravenous human insulin, was not altered in HFD, suggesting that the observed changes in insulin responses to glucose are due to changes in insulin secretion rather than to changes in insulin clearance. Glucose 159-166 insulin Homo sapiens 138-145 17161234-9 2007 Insulin clearance, as judged by elimination of intravenous human insulin, was not altered in HFD, suggesting that the observed changes in insulin responses to glucose are due to changes in insulin secretion rather than to changes in insulin clearance. Glucose 159-166 insulin Homo sapiens 138-145 17115034-1 2007 Insulin and insulin-like growth factor have an essential role in growth, development and the maintenance of metabolic homeostasis, including glucose uptake from the bloodstream. Glucose 141-148 insulin Homo sapiens 0-7 17115034-1 2007 Insulin and insulin-like growth factor have an essential role in growth, development and the maintenance of metabolic homeostasis, including glucose uptake from the bloodstream. Glucose 141-148 insulin Homo sapiens 12-19 17115034-4 2007 Like insulin, GAPDS increased both glucose uptake and the concentration of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) in mammalian preadipocytes. Glucose 35-42 insulin Homo sapiens 5-12 17493406-5 2007 Continuous insulin infusion can rapidly and safely improve intravenous glucose tolerance. Glucose 71-78 insulin Homo sapiens 11-18 18042313-0 2007 [Insulin glargine improves fasting blood glucose levels in prepubertal children with unsatisfactorily controlled type 1 diabetes]. Glucose 41-48 insulin Homo sapiens 1-8 16497094-1 2007 Insulin resistance (IR) is the result of long-lasting positive energy balance and the imbalance between the uptake of energy rich substrates (glucose, lipids) and energy output. Glucose 142-149 insulin Homo sapiens 0-7 16497094-4 2007 The decreased fat oxidation results into the accumulation of intermediates of fatty acid metabolism that are supposed to interfere with the insulin signaling cascade and in consequence negatively influence the glucose utilization. Glucose 210-217 insulin Homo sapiens 140-147 18605244-5 2007 The RIST uses as the index of insulin sensitivity, the total amount of glucose required to be infused to maintain euglycemia during insulin action following an i.v. Glucose 71-78 insulin Homo sapiens 132-139 18605244-12 2007 The RIST is a powerful research tool to assess the glucose utilization action of an insulin bolus in fasted and fed states both evaluated in the same day. Glucose 51-58 insulin Homo sapiens 84-91 17724873-7 2007 Insulin-resistance was defined as the highest quartile of the distribution of the HOMA-IR index assessed for population with normal glucose tolerance (NGT). Glucose 132-139 insulin Homo sapiens 0-7 17497442-3 2007 The purpose of this study was to examine the insulin resistance in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) with standard glucose and icodextrin containing solutions. Glucose 150-157 insulin Homo sapiens 45-52 17497442-7 2007 Morning fasting serum insulin levels were 20.59 +/- 17.86 in the glucose group and 10.15 +/- 6.87 in the icodextrin group (p = 0.0001). Glucose 65-72 insulin Homo sapiens 22-29 17454847-1 2007 OBJECTIVE: The aim of the study was to evaluate the relationship between postprandial blood glucose and first-phase insulin response and, furthermore, to assess whether the intravenous glucagon stimulation test can be used as a predictor for increased postprandial glucose in patients with recently diagnosed type 2 diabetes. Glucose 92-99 insulin Homo sapiens 116-123 17454847-5 2007 RESULTS: The first-phase insulin response at an intravenous glucose stimulation test was significantly correlated to the postprandial blood glucose increment (R(2)=0.21, p<0.05) and the maximal increment in plasma glucose concentration (R(2)=0.40, p<0.01) during the meal tolerance test. Glucose 60-67 insulin Homo sapiens 25-32 17454847-5 2007 RESULTS: The first-phase insulin response at an intravenous glucose stimulation test was significantly correlated to the postprandial blood glucose increment (R(2)=0.21, p<0.05) and the maximal increment in plasma glucose concentration (R(2)=0.40, p<0.01) during the meal tolerance test. Glucose 140-147 insulin Homo sapiens 25-32 17454847-5 2007 RESULTS: The first-phase insulin response at an intravenous glucose stimulation test was significantly correlated to the postprandial blood glucose increment (R(2)=0.21, p<0.05) and the maximal increment in plasma glucose concentration (R(2)=0.40, p<0.01) during the meal tolerance test. Glucose 140-147 insulin Homo sapiens 25-32 17454847-7 2007 CONCLUSION: Impaired first-phase insulin response is a significant predictor of the increase in postprandial blood glucose in patients with type 2 diabetes in near normal metabolic control, whereas beta-cell function, assessed by glucagon stimulation test, is not. Glucose 115-122 insulin Homo sapiens 33-40 17966438-6 2007 Because the increase in plasma glucose levels is a late indicator of the diabetogenic process (a decrease with more than 50% of beta cell mass/function), we propose as marker of the prehyperglycaemia the high levels of plasma proinsulin or of the proinsulin/insulin ratio. Glucose 31-38 insulin Homo sapiens 226-236 17966438-6 2007 Because the increase in plasma glucose levels is a late indicator of the diabetogenic process (a decrease with more than 50% of beta cell mass/function), we propose as marker of the prehyperglycaemia the high levels of plasma proinsulin or of the proinsulin/insulin ratio. Glucose 31-38 insulin Homo sapiens 247-257 17966438-6 2007 Because the increase in plasma glucose levels is a late indicator of the diabetogenic process (a decrease with more than 50% of beta cell mass/function), we propose as marker of the prehyperglycaemia the high levels of plasma proinsulin or of the proinsulin/insulin ratio. Glucose 31-38 insulin Homo sapiens 229-236 18214359-3 2007 Drugs facilitating weight loss also improve glucose control by reducing insulin resistance. Glucose 44-51 insulin Homo sapiens 72-79 19606275-10 2007 The most promising application is the selective interaction of covalently fixed boronic acid residues with glucose, which renders itself not only for sensing, but eventually also for delivery of drugs such as insulin. Glucose 107-114 insulin Homo sapiens 209-216 17703632-5 2007 With time action profiles that more closely mimic physiologic insulin secretion, rapid acting insulin analogues (RAAs) reduce post-prandial glucose excursions and hypoglycemia when compared to regular human insulin (RHI). Glucose 140-147 insulin Homo sapiens 94-101 17703632-12 2007 In summary, insulin glulisine is a safe, effective, and well tolerated rapid-acting insulin analogue across all BMIs and a worthy option for prandial glucose control in type 1 or 2 DM. Glucose 150-157 insulin Homo sapiens 12-19 18175561-7 2007 Other mechanisms which could be associated with insulin resistance in aging are related to leptin and adiponectin serum level or changes in mitochondrial energy metabolism and level of advanced glucose end products in diet. Glucose 194-201 insulin Homo sapiens 48-55 17236121-4 2007 In type 2 diabetes, as well as in liver disease, alterations in hepatic glucose metabolism like an increased post-absorptive glucose production together with diminished glucose uptake following carbohydrate ingestion occur, implying insulin resistance as a central pathological principle. Glucose 72-79 insulin Homo sapiens 233-240 17236121-4 2007 In type 2 diabetes, as well as in liver disease, alterations in hepatic glucose metabolism like an increased post-absorptive glucose production together with diminished glucose uptake following carbohydrate ingestion occur, implying insulin resistance as a central pathological principle. Glucose 125-132 insulin Homo sapiens 233-240 17347858-8 2007 In these patients, post-glucose, but not baseline plasma ghrelin levels correlated negatively with plasma insulin, C-peptide and blood glucose levels, whereas baseline plasma ghrelin correlated inversely with baseline plasma leptin. Glucose 24-31 insulin Homo sapiens 106-113 17347858-8 2007 In these patients, post-glucose, but not baseline plasma ghrelin levels correlated negatively with plasma insulin, C-peptide and blood glucose levels, whereas baseline plasma ghrelin correlated inversely with baseline plasma leptin. Glucose 24-31 insulin Homo sapiens 115-124 17458219-0 2006 [Insulin resistance in pancreatic beta-cells: possible implication in beta-cell glucose toxicity]. Glucose 80-87 insulin Homo sapiens 1-8 17458270-0 2006 [Assessment for insulin sensitivity (glucose clamp, SSPG, and minimal model)]. Glucose 37-44 insulin Homo sapiens 16-23 17084385-5 2006 When islets were continuously perifused with 5 mM glucose, short-term pretreatment with pioglitazone caused approximately 2-fold increase in insulin secretion after drug withdrawal. Glucose 50-57 insulin Homo sapiens 141-148 17158694-2 2006 SUMMARY: Insulin detemir is a long-acting, neutral, and soluble insulin analogue with a lower within-subject variability of fasting plasma glucose levels than isophane insulin human (NPH insulin) and insulin glargine. Glucose 139-146 insulin Homo sapiens 9-16 16478775-4 2006 In NGT, incretin-mediated insulin release [oral glucose tolerance test (OGTT)/IV ratio = 1.59 +/- 0.18, P = 0.004] amounted to 18 +/- 2 nmol/m(2) (32 +/- 4% of oral response), and its time course matched that of total insulin secretion. Glucose 48-55 insulin Homo sapiens 26-33 19888377-1 2007 BACKGROUND: Current basal insulin dosing recommendations are based on retrospective studies of Type 1 patients with diabetes in whom the glucose control was not intensely established. Glucose 137-144 insulin Homo sapiens 26-33 16849630-8 2006 Insulin-stimulated glucose uptake was inhibited by palmitate treatment, whereas the addition of effector caspase inhibitors [Ac-DEVD-aldehyde (DEVD-CHO), Z-DQMD-FMK] independently restored >80% of the insulin-stimulated glucose uptake. Glucose 19-26 insulin Homo sapiens 0-7 16835403-4 2006 In 3T3-L1 adipocytes, incubation in high glucose with insulin did not increase TRB3 mRNA expression. Glucose 41-48 insulin Homo sapiens 54-61 17213881-2 2006 The major part of insulin-mediated glucose disposal takes place in the skeletal muscle, and increased amounts of intramyocellular lipid has been associated with insulin resistance and linked to decreased activity of mitochondrial oxidative phosphorylation. Glucose 35-42 insulin Homo sapiens 18-25 17161338-1 2006 Insulin resistance is a feature of a number of clinical disorders, including type 2 diabetes/glucose intolerance, obesity, dyslipidaemia and hypertension clustering in the so-called metabolic syndrome. Glucose 93-100 insulin Homo sapiens 0-7 17161338-2 2006 Insulin resistance in skeletal muscle manifests itself primarily as a reduction in insulin-stimulated glycogen synthesis due to reduced glucose transport. Glucose 136-143 insulin Homo sapiens 0-7 17161338-2 2006 Insulin resistance in skeletal muscle manifests itself primarily as a reduction in insulin-stimulated glycogen synthesis due to reduced glucose transport. Glucose 136-143 insulin Homo sapiens 83-90 17075371-1 2006 OBJECTIVE: Intensive insulin therapy to normalize blood glucose may improve outcome in intensive care unit patients. Glucose 56-63 insulin Homo sapiens 21-28 17116183-1 2006 AIMS: To assess insulin sensitivity and secretion in the fasting state in regularly transfused patients with beta-thalassaemia major with normal glucose response during an oral glucose tolerance test and to estimate its possible relation to iron overload. Glucose 145-152 insulin Homo sapiens 16-23 17116183-1 2006 AIMS: To assess insulin sensitivity and secretion in the fasting state in regularly transfused patients with beta-thalassaemia major with normal glucose response during an oral glucose tolerance test and to estimate its possible relation to iron overload. Glucose 177-184 insulin Homo sapiens 16-23 17116188-2 2006 AIMS: Research into early life and childhood determinants of insulin resistance and Type 2 diabetes are complicated by requirements for fasting blood samples and glucose tolerance tests. Glucose 162-169 insulin Homo sapiens 61-68 17130228-0 2006 Intensive insulin therapy in the intensive care unit: assessment by continuous glucose monitoring: response to De Block et al. Glucose 79-86 insulin Homo sapiens 10-17 17130463-4 2006 As a first example, we were able to quantify the regulation of proinsulin mRNA abundance in beta-cells by food intake or by the glucose concentration in tissue culture. Glucose 128-135 insulin Homo sapiens 63-73 17130478-3 2006 Closed-loop insulin delivery was calculated using a model of the beta-cell"s multiphasic insulin response to glucose. Glucose 109-116 insulin Homo sapiens 12-19 17130502-5 2006 Net insulin action (S(i)) and insulin-stimulated glucose disposal (S(i)*) were reduced (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT or IFG/NGT. Glucose 49-56 insulin Homo sapiens 30-37 17130510-0 2006 Inhalation of human insulin (exubera) augments the efficiency of muscle glucose uptake in vivo. Glucose 72-79 insulin Homo sapiens 20-27 17130514-3 2006 Outcomes included BMI, percent body fat, insulin sensitivity (S(i)), acute insulin response to glucose (AIR(g)), and the disposition index (DI). Glucose 95-102 insulin Homo sapiens 75-82 17130640-2 2006 For the pancreatic beta-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of beta-cell compensation for insulin resistance. Glucose 78-85 insulin Homo sapiens 97-104 17130640-2 2006 For the pancreatic beta-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of beta-cell compensation for insulin resistance. Glucose 154-161 insulin Homo sapiens 173-180 17130640-2 2006 For the pancreatic beta-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of beta-cell compensation for insulin resistance. Glucose 154-161 insulin Homo sapiens 173-180 17130640-8 2006 The third arm involves FFA stimulation of the G-protein-coupled receptor GPR40/FFAR1, which results in enhancement of glucose-stimulated accumulation of cytosolic Ca2+ and consequently insulin secretion. Glucose 118-125 insulin Homo sapiens 185-192 17166343-5 2006 This review indicates that both insulin analogs demonstrate better glycemic control than NPH insulin, based on measurements of HbA1c, fasting glucose and intra-subject variability in blood glucose. Glucose 142-149 insulin Homo sapiens 32-39 17166343-5 2006 This review indicates that both insulin analogs demonstrate better glycemic control than NPH insulin, based on measurements of HbA1c, fasting glucose and intra-subject variability in blood glucose. Glucose 189-196 insulin Homo sapiens 32-39 17019595-0 2006 Exercise training increases insulin-stimulated glucose disposal and GLUT4 (SLC2A4) protein content in patients with type 2 diabetes. Glucose 47-54 insulin Homo sapiens 28-35 17019595-1 2006 AIMS/HYPOTHESIS: Exercise enhances insulin-stimulated glucose transport in skeletal muscle through changes in signal transduction and gene expression. Glucose 54-61 insulin Homo sapiens 35-42 17019595-2 2006 The aim of this study was to assess the impact of acute and short-term exercise training on whole-body insulin-mediated glucose disposal and signal transduction along the canonical insulin signalling cascade. Glucose 120-127 insulin Homo sapiens 103-110 17019595-2 2006 The aim of this study was to assess the impact of acute and short-term exercise training on whole-body insulin-mediated glucose disposal and signal transduction along the canonical insulin signalling cascade. Glucose 120-127 insulin Homo sapiens 181-188 17019595-4 2006 RESULTS: Insulin-mediated glucose disposal was unchanged following acute exercise in both groups. Glucose 26-33 insulin Homo sapiens 9-16 17019595-5 2006 Short-term exercise training increased insulin-mediated glucose disposal in obese type 2 diabetic (p<0.05), but not in obese non-diabetic subjects. Glucose 56-63 insulin Homo sapiens 39-46 17019595-8 2006 CONCLUSIONS/INTERPRETATION: Exercise training increased whole-body insulin-mediated glucose disposal in obese type 2 diabetic patients. Glucose 84-91 insulin Homo sapiens 67-74 17028898-1 2006 AIMS/HYPOTHESIS: Insulin-stimulated glucose transport in muscle is impaired in obesity and type 2 diabetes, but alterations in levels of relevant signalling factors, i.e. atypical protein kinase C (aPKC) and protein kinase B (PKB/Akt), are still uncertain. Glucose 36-43 insulin Homo sapiens 17-24 17028898-6 2006 RESULTS: In lean control subjects, the submaximal insulin concentration increased aPKC activity and glucose disposal to approximately 50% of the maximal level and PKBbeta activity to 25% of the maximal level, but PKBalpha activity was not increased. Glucose 100-107 insulin Homo sapiens 50-57 17008399-6 2007 These data indicate that TC10alpha is specifically required for insulin-stimulated glucose uptake in adipocytes. Glucose 83-90 insulin Homo sapiens 64-71 17296465-3 2006 Insulin glargine is a long-acting (up to 24-hour duration of effect), parenteral blood glucose-lowering agent. Glucose 87-94 insulin Homo sapiens 0-7 17130190-7 2006 RESULTS: Changes at study end were noted in 2-h OGTT glucose (T/V -0.21 +/- 0.36 vs. L/H +1.44 +/- 0.36 mmol/l; P < 0.001) and insulin level (-30.13 +/- 38.38 vs. +84.86 +/- 38.33 pmol/l, respectively; P = 0.025). Glucose 53-60 insulin Homo sapiens 130-137 17130209-3 2006 RESULTS: Fasting glucose and insulin concentrations were poor predictors of postprandial glucose area above basal (R2 = approximately 0.07, P < 0.001). Glucose 89-96 insulin Homo sapiens 29-36 17130209-4 2006 The correlation was stronger for 2-h glucose concentration (R2 = 0.55, P < 0.001) and improved slightly but significantly (P < 0.001) with the addition of fasting glucose, insulin, age, sex, and body weight to the model (r2 = 0.58). Glucose 37-44 insulin Homo sapiens 178-185 17130209-5 2006 The 2-h glucose concentration also predicted the peak glucose concentration (R2 = 0.37, P < 0.001) with strength of the prediction increasing (P < 0.001) modestly with the addition of fasting glucose, insulin, age, sex, and body weight to the model (R2 = 0.48, P < 0.001). Glucose 8-15 insulin Homo sapiens 207-214 17130209-5 2006 The 2-h glucose concentration also predicted the peak glucose concentration (R2 = 0.37, P < 0.001) with strength of the prediction increasing (P < 0.001) modestly with the addition of fasting glucose, insulin, age, sex, and body weight to the model (R2 = 0.48, P < 0.001). Glucose 54-61 insulin Homo sapiens 207-214 17130209-5 2006 The 2-h glucose concentration also predicted the peak glucose concentration (R2 = 0.37, P < 0.001) with strength of the prediction increasing (P < 0.001) modestly with the addition of fasting glucose, insulin, age, sex, and body weight to the model (R2 = 0.48, P < 0.001). Glucose 54-61 insulin Homo sapiens 207-214 17130210-3 2006 Insulin sensitivity was determined with the hyperinsulinemic-euglycemic clamp, insulin secretion with the intravenous glucose tolerance test, and abdominal fat distribution with computed tomography. Glucose 118-125 insulin Homo sapiens 0-7 17130495-5 2006 Long-term exposure to M16, but not to Cl-DICA, resulted in suppression of glucose-, arginine-, and K(+)-stimulated insulin secretion; inhibition of glucose-induced proinsulin biosynthesis; and depletion of islets insulin. Glucose 74-81 insulin Homo sapiens 115-122 17130495-5 2006 Long-term exposure to M16, but not to Cl-DICA, resulted in suppression of glucose-, arginine-, and K(+)-stimulated insulin secretion; inhibition of glucose-induced proinsulin biosynthesis; and depletion of islets insulin. Glucose 148-155 insulin Homo sapiens 167-174 17130651-1 2006 Recent studies using magnetic resonance spectroscopy have shown that decreased insulin-stimulated muscle glycogen synthesis due to a defect in insulin-stimulated glucose transport activity is a major factor in the pathogenesis of type 2 diabetes. Glucose 162-169 insulin Homo sapiens 79-86 17130651-1 2006 Recent studies using magnetic resonance spectroscopy have shown that decreased insulin-stimulated muscle glycogen synthesis due to a defect in insulin-stimulated glucose transport activity is a major factor in the pathogenesis of type 2 diabetes. Glucose 162-169 insulin Homo sapiens 143-150 17130651-2 2006 The molecular mechanism underlying defective insulin-stimulated glucose transport activity can be attributed to increases in intramyocellular lipid metabolites such as fatty acyl CoAs and diacylglycerol, which in turn activate a serine/threonine kinase cascade, thus leading to defects in insulin signaling through Ser/Thr phosphorylation of insulin receptor substrate (IRS)-1. Glucose 64-71 insulin Homo sapiens 45-52 17130651-2 2006 The molecular mechanism underlying defective insulin-stimulated glucose transport activity can be attributed to increases in intramyocellular lipid metabolites such as fatty acyl CoAs and diacylglycerol, which in turn activate a serine/threonine kinase cascade, thus leading to defects in insulin signaling through Ser/Thr phosphorylation of insulin receptor substrate (IRS)-1. Glucose 64-71 insulin Homo sapiens 289-296 17296510-4 2006 The K(ATP) channels play multiple physiological roles in the glucose metabolism regulation, especially in beta-cells where it regulates insulin secretion, in response to an increase in ATP concentration. Glucose 61-68 insulin Homo sapiens 136-143 16730846-8 2006 Lower glucose tolerance occurred in IGT after dinner, as in the NGT, and after breakfast associated with increased insulin response after breakfast, and similar proinsulin response after all three meals. Glucose 6-13 insulin Homo sapiens 115-122 17109593-1 2006 BACKGROUND: The mathematical models for patients with diabetes proposed in the literature since the late 1970s are mainly glucocentric (glucose-based); hence, the contribution of free fatty acid (FFA) metabolism in the body and its glucose-insulin interactions have been largely ignored. Glucose 232-239 insulin Homo sapiens 240-247 17130808-8 2006 Uploading of pump electronics by algorithms designed for closed-loop insulin delivery allowed in-patient 48 hour-trials aiming at automated glucose control. Glucose 140-147 insulin Homo sapiens 69-76 16849630-8 2006 Insulin-stimulated glucose uptake was inhibited by palmitate treatment, whereas the addition of effector caspase inhibitors [Ac-DEVD-aldehyde (DEVD-CHO), Z-DQMD-FMK] independently restored >80% of the insulin-stimulated glucose uptake. Glucose 223-230 insulin Homo sapiens 0-7 17182318-1 2006 The approach used by Medtronic MiniMed to close the insulin delivery loop using the subcutaneous site for both glucose sensing and insulin delivery relies on modeling insulin action and beta-cell insulin secretion. Glucose 111-118 insulin Homo sapiens 52-59 17087783-7 2006 In patients and in controls, there was an inverse correlation between the serum concentrations of insulin and of TNF-alpha during oGTT (for patients, a mean of both days, P = 0.009; for controls, P = 0.047), but not between the serum concentrations of glucose and TNF-alpha. Glucose 252-259 insulin Homo sapiens 98-105 16963622-7 2006 Thus, at the glucose dose and insulin levels chosen, peripheral insulin delivery was associated with greater whole-body glucose disposal than endogenous (portal) insulin secretion. Glucose 13-20 insulin Homo sapiens 64-71 17110071-4 2006 Second is the discovery that sirtuins, proteins that regulate lifespan in model organisms, enhance pancreatic insulin secretion in mice following a glucose challenge, suggesting the potential to regulate mammalian lifespan through regulation of the insulin signaling pathway. Glucose 148-155 insulin Homo sapiens 110-117 17194656-6 2006 Plasma insulin and C-peptide levels were appropriately suppressed, but a low concentration of beta-hydroxy-butyrate and normal increase of plasma glucose concentration after a glucagon injection suggested the presence of an insulin-like substance. Glucose 146-153 insulin Homo sapiens 224-231 16607383-4 2006 Insulin resistance was estimated by homeostasis model assessment insulin resistance (HOMA-IR) derived from fasting glucose and insulin concentrations. Glucose 115-122 insulin Homo sapiens 0-7 16607383-4 2006 Insulin resistance was estimated by homeostasis model assessment insulin resistance (HOMA-IR) derived from fasting glucose and insulin concentrations. Glucose 115-122 insulin Homo sapiens 65-72 16924660-0 2006 Insulin restores glucose inhibition of adenosine transport by increasing the expression and activity of the equilibrative nucleoside transporter 2 in human umbilical vein endothelium. Glucose 17-24 insulin Homo sapiens 0-7 16924660-4 2006 We have characterized insulin effect on adenosine transport in HUVEC cultured in normal (5 mM) or high (25 mM) D-glucose. Glucose 111-120 insulin Homo sapiens 22-29 16924660-5 2006 Insulin (1 nM) increased overall adenosine transport associated with higher hENT2-, but lower hENT1-mediated transport in normal D-glucose. Glucose 129-138 insulin Homo sapiens 0-7 16924660-6 2006 Insulin increased hENT2 protein abundance in normal or high D-glucose, but reduced hENT1 protein abundance in normal D-glucose. Glucose 60-69 insulin Homo sapiens 0-7 16924660-6 2006 Insulin increased hENT2 protein abundance in normal or high D-glucose, but reduced hENT1 protein abundance in normal D-glucose. Glucose 117-126 insulin Homo sapiens 0-7 16924660-7 2006 Insulin did not alter the reduced hENT1 protein abundance, but blocked the reduced hENT1 and hENT2 mRNA expression induced by high D-glucose. Glucose 131-140 insulin Homo sapiens 0-7 16924660-8 2006 Insulin effect on hENT1 mRNA expression in normal D-glucose was blocked by N(G)-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) and mimicked by S-nitroso-N-acetyl-L,D-penicillamine (SNAP, NO donor). Glucose 50-59 insulin Homo sapiens 0-7 17046094-5 2006 METHODS/RESULTS: : Cirrhotic animals were insulin resistant and this was associated with reduced glucose transport into muscles. Glucose 97-104 insulin Homo sapiens 42-49 17046094-6 2006 Interestingly, activity in the proximal part of the insulin signaling cascade was not decreased, as evinced by increased activity of key enzymes in the signal to glucose transport. Glucose 162-169 insulin Homo sapiens 52-59 17076764-8 2006 These gut hormones affect glucose metabolism at different levels: by altering food intake and body weight, and thereby insulin sensitivity; by affecting gastric delay and gut motility, and thereby meal-related fluctuations in glucose levels; by affecting insulin secretion, and thereby plasma glucose levels, and by affecting tissue specific insulin sensitivity of glucose metabolism. Glucose 26-33 insulin Homo sapiens 119-126 16963622-7 2006 Thus, at the glucose dose and insulin levels chosen, peripheral insulin delivery was associated with greater whole-body glucose disposal than endogenous (portal) insulin secretion. Glucose 13-20 insulin Homo sapiens 64-71 16963622-7 2006 Thus, at the glucose dose and insulin levels chosen, peripheral insulin delivery was associated with greater whole-body glucose disposal than endogenous (portal) insulin secretion. Glucose 120-127 insulin Homo sapiens 64-71 16963622-7 2006 Thus, at the glucose dose and insulin levels chosen, peripheral insulin delivery was associated with greater whole-body glucose disposal than endogenous (portal) insulin secretion. Glucose 120-127 insulin Homo sapiens 64-71 17237630-1 2006 BACKGROUND/AIM: The liver plays important roles in the homeostasis of glucose metabolism since it acts as a major target organ for insulin and a site for gluconeogenesis and glycogen storage. Glucose 70-77 insulin Homo sapiens 131-138 17142140-1 2006 We evaluated insulin action in skeletal muscle (glucose disposal), liver (glucose production), and adipose tissue (lipolysis) in 5 extremely obese women with acanthosis nigricans (AN), who had normal oral glucose tolerance, and 5 healthy lean subjects, by using a 5-stage pancreatic clamp and stable isotopically labeled tracer infusion. Glucose 48-55 insulin Homo sapiens 13-20 17165640-1 2006 The metabolic syndrome is an insulin-resistant state characterized by a cluster of cardiovascular risk factors, including various combinations of abdominal obesity, glucose intolerance, hypertension, and atherogenic dyslipidemia (elevated triglyceride values, low high-density lipoprotein cholesterol levels, and small dense low-density lipoprotein cholesterol particles). Glucose 165-172 insulin Homo sapiens 29-36 17146316-1 2006 PURPOSE: Chromium enhances insulin signaling and insulin-mediated glucose uptake in cultured cells. Glucose 66-73 insulin Homo sapiens 49-56 17142140-3 2006 During stage 1 of the clamp, glucose rate of appearance (R(a)) (2.6 +/- 0.3 vs 3.7 +/- 0.3 micromol x kg FFM(-1) x min(-1), P = .02) and palmitate R(a) (2.4 +/- 0.6 vs 7.0 +/- 1.5 micromol x kg FFM(-1) x min(-1), P < .05) were greater in obese subjects with AN than lean subjects despite slightly greater plasma insulin concentration in subjects with AN (3.0 +/- 0.7 vs 1.1 +/- 0.4 microU/mL, P < .05). Glucose 29-36 insulin Homo sapiens 315-322 17142140-8 2006 However, marked insulin hypersecretion can compensate for impaired insulin action, resulting in normal glucose and fatty acid metabolism during basal conditions. Glucose 103-110 insulin Homo sapiens 16-23 16842857-8 2006 Overexpression of PTEN and SKIP also inhibited insulin-induced phosphorylation of Akt and the uptake of glucose in cultured cells. Glucose 104-111 insulin Homo sapiens 47-54 17189547-5 2006 The mean percentage change in insulin sensitivity by a frequently sampled intravenous glucose tolerance test was +26% in the HG group and +24% in the LG group (p = 0.83); first-phase acute insulin release was -20% in the HG group and -21% in the LG group (p = 0.77). Glucose 86-93 insulin Homo sapiens 30-37 17165235-7 2006 (4) Inhalation of 1 mg of insulin powder has similar glucose-lowering effects as 3 units of subcutaneous insulin, but inhalation of 3 mg is comparable to 8 units rather than 9 units of injected insulin. Glucose 53-60 insulin Homo sapiens 26-33 16990588-10 2006 Enzyme-linked immunosorbent assay analysis demonstrated that insulin secretion was regulated by glucose. Glucose 96-103 insulin Homo sapiens 61-68 17260461-18 2006 The percentage of total body fat, levels of plasma glucose, serum insulin, total cholesterol and systolic blood pressure are independent risk factors of insulin resistance. Glucose 51-58 insulin Homo sapiens 153-160 17166358-7 2006 Intensive insulin therapy reduced the days of stay in ICU, TISS-28 score per day, time of the ventilatory support needed, time for retention of tracheal intubation, mean morning blood glucose levels (6 am) compared with those in CT group (P<0.05 or P<0.01), and patients receiving intensive insulin therapy were less likely to require intensive care. Glucose 184-191 insulin Homo sapiens 10-17 17166358-10 2006 CONCLUSION: Intensive insulin therapy maintaining blood glucose at a level 4.4-6.1 mmol/L reduces mortality rate among critically ill patients. Glucose 56-63 insulin Homo sapiens 22-29 17076994-1 2006 The amylin analogue pramlintide acts in concert with insulin to regulate glucose metabolism. Glucose 73-80 insulin Homo sapiens 53-60 17057046-7 2006 Although the mechanism of gatifloxacin-induced hyperglycemia is not known, in vitro studies have found that certain quinolone antimicrobials can lower serum glucose levels by blocking adenosine 5"-triphosphate-dependent potassium channels in the pancreatic beta-cell, stimulating insulin release. Glucose 157-164 insulin Homo sapiens 280-287 16757548-4 2006 OC subjects underwent a 6-mo caloric restriction resulting in a 7% decrease in body mass index (BMI) and a 21% improvement in insulin-stimulated whole body glucose disposal rate (GDR). Glucose 156-163 insulin Homo sapiens 126-133 16803855-2 2006 Akt2 is a key signaling intermediate for insulin-stimulated glucose uptake and glycogen synthesis in skeletal muscle. Glucose 60-67 insulin Homo sapiens 41-48 16803855-8 2006 Our data establish a key role for Akt2 in the regulation of GSK-3alpha Ser(21) phosphorylation with contraction and add genetic evidence to support the separation of the intracellular pathways regulated by insulin and exercise that converge on glucose uptake and glycogen synthesis in skeletal muscle. Glucose 244-251 insulin Homo sapiens 206-213 17052201-5 2006 Adiponectin has insulin-mimetic and -sensitizing actions including stimulation of glucose uptake in skeletal muscle and suppression of glucose production in liver. Glucose 82-89 insulin Homo sapiens 16-23 17100583-1 2006 A reduced ability of insulin to activate glucose transport in skeletal muscle, termed insulin resistance, is a primary defect leading to the development of impaired glucose tolerance and type 2 diabetes. Glucose 41-48 insulin Homo sapiens 21-28 17100583-1 2006 A reduced ability of insulin to activate glucose transport in skeletal muscle, termed insulin resistance, is a primary defect leading to the development of impaired glucose tolerance and type 2 diabetes. Glucose 41-48 insulin Homo sapiens 86-93 17100583-4 2006 Overexpression and overactivity of GSK-3 in skeletal muscle of rodent models of obesity and obese type 2 diabetic humans are associated with an impaired ability of insulin to activate glucose disposal and glycogen synthase. Glucose 184-191 insulin Homo sapiens 164-171 17100583-5 2006 New insights into the importance of GSK-3 as a regulator of insulin action on glucose transport activity in muscle have come from studies utilizing selective and sensitive inhibitors of GSK-3. Glucose 78-85 insulin Homo sapiens 60-67 17100583-6 2006 These studies have demonstrated that selective inhibition of GSK-3 in insulin-resistant skeletal muscle causes improvements in insulin-stimulated glucose transport activity that are likely caused by enhanced post-insulin receptor insulin signaling and GLUT-4 glucose transporter translocation. Glucose 146-153 insulin Homo sapiens 70-77 17100583-6 2006 These studies have demonstrated that selective inhibition of GSK-3 in insulin-resistant skeletal muscle causes improvements in insulin-stimulated glucose transport activity that are likely caused by enhanced post-insulin receptor insulin signaling and GLUT-4 glucose transporter translocation. Glucose 146-153 insulin Homo sapiens 127-134 17100583-6 2006 These studies have demonstrated that selective inhibition of GSK-3 in insulin-resistant skeletal muscle causes improvements in insulin-stimulated glucose transport activity that are likely caused by enhanced post-insulin receptor insulin signaling and GLUT-4 glucose transporter translocation. Glucose 146-153 insulin Homo sapiens 127-134 17066302-2 2006 The aim of this study was to determine whether the association between symptoms of depression and insulin resistance varies across glucose tolerance status and between men and women. Glucose 131-138 insulin Homo sapiens 98-105 17070421-9 2006 CONCLUSIONS: Directly measured insulin sensitivity index SSPG clustered with 2-h glucose and Log 2-h insulin in factor analysis in a cohort consisting entirely of hypertensive subjects. Glucose 81-88 insulin Homo sapiens 31-38 16822958-4 2006 Although similar to the effects of insulin to increase glucose transport in muscle, it is clear that the underlying mechanisms for AMPK-mediated glucose transport involve proximal signals that are distinct from that of insulin. Glucose 55-62 insulin Homo sapiens 35-42 16822958-6 2006 We also discuss evidence that AMPK may play a role in enhancing muscle and whole body insulin sensitivity for glucose transport under conditions such as exercise, as well as the use of the AMPK activator AICAR to reverse insulin-resistant conditions. Glucose 110-117 insulin Homo sapiens 86-93 17056939-5 2006 Exogenous insulin requirements to control blood glucose levels <or=10.0 mmol/L were used as a marker for PIR. Glucose 48-55 insulin Homo sapiens 10-17 17052207-12 2006 In animal models, transgenic mice lacking expression of the mitochondrial genome specifically in beta-cells are diabetic and their islets are incable of releasing insulin in response to glucose. Glucose 186-193 insulin Homo sapiens 163-170 17019598-6 2006 After phlebotomy, there was a 2.2-fold increase in insulin secretory capacity as determined by FSIVGTT (acute insulin response to glucose [AIRg], p<0.02) but a concomitant 70% fall in insulin sensitivity (Si, p<0.05). Glucose 130-137 insulin Homo sapiens 51-58 16506274-9 2006 Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. Glucose 177-184 insulin Homo sapiens 158-165 16506274-10 2006 This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Glucose 122-129 insulin Homo sapiens 176-183 16506274-13 2006 There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Glucose 102-109 insulin Homo sapiens 85-92 16624438-6 2006 RESULTS: The change in insulin sensitivity using the formula proposed by McAuley (exp(2.63-0.28 x ln(fasting insulin)-0.31 x ln(fasting triglyceride in mmol/l)) showed the greatest correlation with weight loss (r=-0.59, p<0.0001) and was statistically superior to change in fasting glucose, fasting insulin and homeostasis model assessment (HOMA). Glucose 285-292 insulin Homo sapiens 23-30 16703330-5 2006 RESULTS: As expected, cord insulin concentrations correlated with all measures of birth size (weight, length, head and arm circumferences, sum of skinfold thicknesses, ponderal index: r=0.16-0.4, p<0.01 for all) and maternal BMI (r=0.11, p=0.005), maternal glucose (r=0.25, p<0.001) and maternal insulin resistance (r=0.23, p<0.001). Glucose 260-267 insulin Homo sapiens 27-34 16703330-9 2006 This is consistent with heritability of insulin resistance from father to offspring and a compensatory increase in fetal insulin secretion, the latter occurring pre-natally before the homeostatic feedback loop between glucose and insulin is established. Glucose 218-225 insulin Homo sapiens 121-128 17019598-6 2006 After phlebotomy, there was a 2.2-fold increase in insulin secretory capacity as determined by FSIVGTT (acute insulin response to glucose [AIRg], p<0.02) but a concomitant 70% fall in insulin sensitivity (Si, p<0.05). Glucose 130-137 insulin Homo sapiens 110-117 17019598-6 2006 After phlebotomy, there was a 2.2-fold increase in insulin secretory capacity as determined by FSIVGTT (acute insulin response to glucose [AIRg], p<0.02) but a concomitant 70% fall in insulin sensitivity (Si, p<0.05). Glucose 130-137 insulin Homo sapiens 110-117 17065339-1 2006 Skeletal muscle accounts for a large proportion of insulin-stimulated glucose utilization. Glucose 70-77 insulin Homo sapiens 51-58 17065334-3 2006 We measured brain glucose metabolism, using [(18)F]fluorodeoxyglucose positron emission tomography, in seven insulin-sensitive (homeostasis model assessment of insulin resistance [HOMA-IR] = 1.3) and seven insulin-resistant (HOMA-IR = 6.3) men, during suppression of endogenous insulin by somatostatin, with and without an insulin infusion that elevated insulin to 24.6 +/- 5.2 and 23.2 +/- 5.8 mU/l (P = 0.76), concentrations similar to fasting levels of the resistant subjects and approximately threefold above those of the insulin-sensitive subjects. Glucose 18-25 insulin Homo sapiens 109-116 17065334-4 2006 Insulin-evoked change in global cerebral metabolic rate for glucose was reduced in insulin resistance (+7 vs. +17.4%, P = 0.033). Glucose 60-67 insulin Homo sapiens 0-7 17065334-4 2006 Insulin-evoked change in global cerebral metabolic rate for glucose was reduced in insulin resistance (+7 vs. +17.4%, P = 0.033). Glucose 60-67 insulin Homo sapiens 83-90 17065355-1 2006 Intensive insulin therapy (IIT) improves the outcome of prolonged critically ill patients, but concerns remain regarding potential harm and the optimal blood glucose level. Glucose 158-165 insulin Homo sapiens 10-17 17065339-9 2006 Insulin increased uptake of [(11)C]3-OMG substantially and strongly stimulated the kinetics of bidirectional glucose transport. Glucose 109-116 insulin Homo sapiens 0-7 17065339-13 2006 Thus, insulin evokes a broader distribution of control than during fasting conditions in governing glucose uptake into skeletal muscle. Glucose 99-106 insulin Homo sapiens 6-13 17069600-3 2006 RESULTS: In all subjects, the levels of plasma glucose and serum insulin significantly increased after glucose loading compared with baseline (5.1 +/- 0.6 vs 7.6 +/- 1.2 mM/l, 6 +/- 3 vs 49 +/- 13 microU/ml, respectively; P < 0.0001). Glucose 103-110 insulin Homo sapiens 65-72 17065362-3 2006 The presumed function of the SCHAD enzyme in glucose-stimulated insulin secretion led us to the hypothesis that common variants in HADHSC on chromosome 4q22-26 might be associated with development of type 2 diabetes. Glucose 45-52 insulin Homo sapiens 64-71 17090865-7 2006 Insulin resistance was defined by fasting glucose-to-insulin ratio <or=4.5. Glucose 42-49 insulin Homo sapiens 0-7 17090865-7 2006 Insulin resistance was defined by fasting glucose-to-insulin ratio <or=4.5. Glucose 42-49 insulin Homo sapiens 53-60 17190391-6 2006 The management of insulin perioperatively depends on the preparation normally taken by the patient, and the glucose level on the morning of surgery. Glucose 108-115 insulin Homo sapiens 18-25 17102160-5 2006 Illness-related factors of a longer duration of diabetes were strongly associated with glucose and blood pressure control, insulin use with glucose control and waist circumference, and antihypertensive use with blood pressure, triglycerides, and body mass index. Glucose 140-147 insulin Homo sapiens 123-130 17171192-2 2006 Peripheral insulin administration, which increases CNS insulin levels, is associated with increased insulin-stimulated glucose disposal and the release of counter-regulatory hormones--events that can confound CNS results. Glucose 119-126 insulin Homo sapiens 11-18 16916956-4 2006 Insulin-dependent glucose uptake into adipocytes and muscle was impaired, suggesting that these rats developed insulin resistance. Glucose 18-25 insulin Homo sapiens 0-7 16916956-4 2006 Insulin-dependent glucose uptake into adipocytes and muscle was impaired, suggesting that these rats developed insulin resistance. Glucose 18-25 insulin Homo sapiens 111-118 16916956-5 2006 In contrast, insulin-independent glucose uptake into hepatocytes from TG rats was significantly increased, and glycogen and lipid levels in livers of TG rats were remarkably high. Glucose 33-40 insulin Homo sapiens 13-20 16916956-8 2006 These results suggest that impairment of insulin-dependent glucose uptake by GH excess in adipose tissue and muscle is compensated by up-regulation of glucose uptake in liver and that potentiation of insulin signaling through insulin receptor substrate-2 in liver experiencing GH excess causes an increase in glycogen and lipid synthesis from incorporated glucose, resulting in accumulation of glycogen and lipids in liver. Glucose 59-66 insulin Homo sapiens 41-48 16916956-8 2006 These results suggest that impairment of insulin-dependent glucose uptake by GH excess in adipose tissue and muscle is compensated by up-regulation of glucose uptake in liver and that potentiation of insulin signaling through insulin receptor substrate-2 in liver experiencing GH excess causes an increase in glycogen and lipid synthesis from incorporated glucose, resulting in accumulation of glycogen and lipids in liver. Glucose 151-158 insulin Homo sapiens 41-48 17032347-2 2006 In this study the authors examine whether the product of insulin sensitivity and insulin secretion, assessed from the fasting state, predicts progression from normal glucose tolerance (NGT) to impaired fasting glucose (IFG) and from impaired glucose tolerance (IGT) to type 2 diabetes mellitus (T2DM). Glucose 166-173 insulin Homo sapiens 57-64 17177134-4 2006 At the start of the fasting tests, blood glucose concentrations were lowered to below 7 mmol/L using an insulin infusion. Glucose 41-48 insulin Homo sapiens 104-111 17177134-10 2006 CONCLUSIONS: Fasting blood glucose concentrations in the majority of insulin-treated patients with type 2 diabetes increase markedly after midnight. Glucose 27-34 insulin Homo sapiens 69-76 17213521-0 2006 Insulin resistance & secretion in subjects with normal fasting plasma glucose. Glucose 74-81 insulin Homo sapiens 0-7 17213521-5 2006 Steady state plasma glucose (SSPG) derived from insulin suppression test was used to quantify insulin resistance and 30 min insulinogenic index during an oral glucose tolerance test to measure acute insulin secretion. Glucose 20-27 insulin Homo sapiens 48-55 17213521-5 2006 Steady state plasma glucose (SSPG) derived from insulin suppression test was used to quantify insulin resistance and 30 min insulinogenic index during an oral glucose tolerance test to measure acute insulin secretion. Glucose 20-27 insulin Homo sapiens 94-101 17053832-5 2006 Moreover, mice lacking TLR4 are substantially protected from the ability of systemic lipid infusion to (a) suppress insulin signaling in muscle and (b) reduce insulin-mediated changes in systemic glucose metabolism. Glucose 196-203 insulin Homo sapiens 159-166 17185891-6 2006 Postprandial plasma glucose and serum insulin increased (p<0.001) with lower glucose responses in females (p=0.001) and lower insulin responses in males (p=0.012). Glucose 20-27 insulin Homo sapiens 129-136 17185891-6 2006 Postprandial plasma glucose and serum insulin increased (p<0.001) with lower glucose responses in females (p=0.001) and lower insulin responses in males (p=0.012). Glucose 80-87 insulin Homo sapiens 38-45 16988754-1 2006 We aimed to compare the effects of two different vasodilating principles, angiotensin II-receptor blockade and calcium channel blockade, on peripheral insulin-mediated glucose uptake in patients with hypertension and other cardiovascular risk factors. Glucose 168-175 insulin Homo sapiens 151-158 17718254-0 2006 Hyperthyroidism induces glucose intolerance by lowering both insulin secretion and peripheral insulin sensitivity. Glucose 24-31 insulin Homo sapiens 61-68 16803868-1 2006 APS (adaptor protein with PH and SH2 domains) initiates a phosphatidylinositol 3-kinase-independent pathway involved in insulin-stimulated glucose transport. Glucose 139-146 insulin Homo sapiens 120-127 16803868-3 2006 Because actin rearrangement is important for insulin-induced glucose transporter 4 (Glut 4) translocation, we studied the potential involvement of Enigma in insulin-induced glucose transport in 3T3-L1 adipocytes. Glucose 61-68 insulin Homo sapiens 45-52 16803868-9 2006 A physiological link between increased expression of Enigma and an alteration in insulin-induced glucose uptake was suggested by the increase in Enigma mRNA expression in adipose tissue of diabetic obese patients. Glucose 97-104 insulin Homo sapiens 81-88 16803868-10 2006 Taken together, these data strongly suggest that the interaction between APS and Enigma is involved in insulin-induced Glut 4 translocation by regulating cortical actin remodeling and raise the possibility that modification of APS/Enigma ratio could participate in the alteration of insulin-induced glucose uptake in adipose tissue. Glucose 299-306 insulin Homo sapiens 103-110 17053859-4 2006 insulin followed by FDG injection 60 minutes later could decrease the blood glucose level of hyperglycemic patients without altering muscular, liver, or lung FDG uptake. Glucose 76-83 insulin Homo sapiens 0-7 17053859-9 2006 RESULTS: After one or two boluses of insulin (mean 3.4 units), 39 diabetic patients decreased their blood glucose level from 9.4 +/- 1.8 to 6.1 +/- 1.3 mmol/l. Glucose 106-113 insulin Homo sapiens 37-44 17053859-10 2006 In 14 patients, two doses of insulin (mean 4.5 +/- 2.3 units) were not sufficient, but managed to decrease the blood glucose level from 10.6 +/- 2.1 to 9.1 +/- 2.1 mmol/l. Glucose 117-124 insulin Homo sapiens 29-36 17079565-6 2006 Insulin sensitivity (10(-4) min(-1) microU/mL) was calculated from a 90-minute frequently sampled intravenous glucose tolerance test. Glucose 110-117 insulin Homo sapiens 0-7 16941611-3 2006 Insulin action on the glucose disposal rate was measured using the glucose-insulin index, the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 22-29 insulin Homo sapiens 0-7 16941611-3 2006 Insulin action on the glucose disposal rate was measured using the glucose-insulin index, the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 22-29 insulin Homo sapiens 75-82 16941611-3 2006 Insulin action on the glucose disposal rate was measured using the glucose-insulin index, the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 67-74 insulin Homo sapiens 0-7 16941611-3 2006 Insulin action on the glucose disposal rate was measured using the glucose-insulin index, the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 67-74 insulin Homo sapiens 75-82 16941611-3 2006 Insulin action on the glucose disposal rate was measured using the glucose-insulin index, the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 67-74 insulin Homo sapiens 0-7 16941611-3 2006 Insulin action on the glucose disposal rate was measured using the glucose-insulin index, the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 67-74 insulin Homo sapiens 75-82 16941611-5 2006 The plasma glucose lowering action of tolbutamide, induced by secretion of endogenous insulin, is widely used to characterize the formation of insulin resistance. Glucose 11-18 insulin Homo sapiens 86-93 16941611-5 2006 The plasma glucose lowering action of tolbutamide, induced by secretion of endogenous insulin, is widely used to characterize the formation of insulin resistance. Glucose 11-18 insulin Homo sapiens 143-150 17112889-2 2006 Considering the clinical controversies in the study of infection in diabetes and the recognized effect of insulin on the oxidative metabolism of glucose in phagocytes, the present study sought to evaluate the formation of intraphagocytic oxygen-free radicals in diabetic patients undergoing simultaneous pancreas kidney transplantation (SPK). Glucose 145-152 insulin Homo sapiens 106-113 17097017-8 2006 RESULTS: Insulin increased specific membrane glucose transport in 3T3-L1 preadipocytes. Glucose 45-52 insulin Homo sapiens 9-16 17097017-12 2006 Oleate and palmitate treatment did not influence basal glucose transport (without insulin stimulation), whereas insulin-stimulated glucose transport was inhibited after overnight oleate and palmitate treatment in preadipocytes and adipocytes. Glucose 131-138 insulin Homo sapiens 112-119 17027570-1 2006 This study compared the abilities of body mass index (BMI) and waist circumference (WC) to identify resistance to insulin-mediated glucose uptake and related metabolic abnormalities in 261 apparently healthy patients. Glucose 131-138 insulin Homo sapiens 114-121 17027570-4 2006 Therefore, insulin-mediated glucose uptake was quantified in 261 apparently healthy adults by determining the steady-state plasma glucose concentrations during the insulin suppression test; the higher the concentration, the greater the defect in insulin action. Glucose 28-35 insulin Homo sapiens 11-18 17027570-4 2006 Therefore, insulin-mediated glucose uptake was quantified in 261 apparently healthy adults by determining the steady-state plasma glucose concentrations during the insulin suppression test; the higher the concentration, the greater the defect in insulin action. Glucose 28-35 insulin Homo sapiens 164-171 17027570-4 2006 Therefore, insulin-mediated glucose uptake was quantified in 261 apparently healthy adults by determining the steady-state plasma glucose concentrations during the insulin suppression test; the higher the concentration, the greater the defect in insulin action. Glucose 28-35 insulin Homo sapiens 164-171 17027570-4 2006 Therefore, insulin-mediated glucose uptake was quantified in 261 apparently healthy adults by determining the steady-state plasma glucose concentrations during the insulin suppression test; the higher the concentration, the greater the defect in insulin action. Glucose 130-137 insulin Homo sapiens 11-18 16934249-8 2006 In order to improve the efficiency of producing and selecting insulin-producing cells from undifferentiated cells, we have designed a novel beta-cell specific and glucose responsive promoter system designated pGL3.hINS-363 3x. Glucose 163-170 insulin Homo sapiens 62-69 16934249-12 2006 Here, we describe a novel beta-cell specific and glucose responsive artificial promoter system designed for analyzing and sorting beta-like insulin-producing cells that have differentiated from stem cells or other progenitor cells. Glucose 49-56 insulin Homo sapiens 140-147 17322583-6 2006 Insulin secretion was significantly increased in the presence of adiponectin for 6 h at high glucose concentration. Glucose 93-100 insulin Homo sapiens 0-7 17087289-6 2006 Improving insulin sensitivity of liver, delaying glucose flux to portal vein and reviving fast insulin secretion. Glucose 49-56 insulin Homo sapiens 10-17 17087306-4 2006 The agents that improve insulin resistance, such as metformin and pioglitazone, have multiple effects to improve glucose and lipid metabolism by increasing sensitivity for insulin without increasing insulin secretion and exert anti-atherogenic properties resulting in preventing development of atherosclerosis. Glucose 113-120 insulin Homo sapiens 24-31 17087306-4 2006 The agents that improve insulin resistance, such as metformin and pioglitazone, have multiple effects to improve glucose and lipid metabolism by increasing sensitivity for insulin without increasing insulin secretion and exert anti-atherogenic properties resulting in preventing development of atherosclerosis. Glucose 113-120 insulin Homo sapiens 172-179 16712872-4 2006 Applying the mass conservation law, we introduce two explicit time delays and propose a more robust alternative model for better understanding the glucose-insulin endocrine metabolic regulatory system and the ultradian insulin secretory oscillations for the cases of continuous enteral nutrition and constant glucose infusion. Glucose 147-154 insulin Homo sapiens 155-162 16705064-2 2006 However, it is unclear whether endothelial dysfunction per se is sufficient to impair insulin-mediated glucose uptake. Glucose 103-110 insulin Homo sapiens 86-93 16705064-5 2006 We measured insulin-mediated glucose disposal at the level of the whole body, skeletal muscle, and vasculature by performing hyperinsulinemic euglycemic clamp, and vascular function studies, in a separate group of HIV-negative healthy nonobese subjects (n = 13) before and after 4 wk of daily oral indinavir. Glucose 29-36 insulin Homo sapiens 12-19 16705064-10 2006 Thus our findings indicate that 1) endothelial dysfunction alone is insufficient to impair insulin-mediated glucose disposal, and 2) indinavir-induced endothelial dysfunction is likely due to a direct effect of the drug on the endothelium and is not coupled to the induction of insulin resistance. Glucose 108-115 insulin Homo sapiens 91-98 16735448-0 2006 Regulation of glucose transporters by insulin and extracellular glucose in C2C12 myotubes. Glucose 14-21 insulin Homo sapiens 38-45 16735448-1 2006 It is well established that insulin stimulation of glucose uptake in skeletal muscle cells is mediated through translocation of GLUT4 from intracellular storage sites to the cell surface. Glucose 51-58 insulin Homo sapiens 28-35 16735448-2 2006 However, the established skeletal muscle cell lines, with the exception of L6 myocytes, reportedly show minimal insulin-dependent glucose uptake and GLUT4 translocation. Glucose 130-137 insulin Homo sapiens 112-119 16735448-4 2006 However, this insulin stimulation of GLUT4 translocation was difficult to demonstrate with a conventional 2-deoxyglucose uptake assay because of markedly elevated basal glucose uptake via other glucose transporter(s). Glucose 113-120 insulin Homo sapiens 14-21 16735448-7 2006 Taken together, these findings indicate that regulation of the facilitative glucose transport system in differentiated C(2)C(12) myotubes can be achieved through surprisingly acute glucose-dependent modulation of the activity of glucose transporter(s), which apparently contributes to obscuring the insulin augmentation of glucose uptake elicited by GLUT4 translocation. Glucose 76-83 insulin Homo sapiens 299-306 16735448-7 2006 Taken together, these findings indicate that regulation of the facilitative glucose transport system in differentiated C(2)C(12) myotubes can be achieved through surprisingly acute glucose-dependent modulation of the activity of glucose transporter(s), which apparently contributes to obscuring the insulin augmentation of glucose uptake elicited by GLUT4 translocation. Glucose 181-188 insulin Homo sapiens 299-306 16735448-7 2006 Taken together, these findings indicate that regulation of the facilitative glucose transport system in differentiated C(2)C(12) myotubes can be achieved through surprisingly acute glucose-dependent modulation of the activity of glucose transporter(s), which apparently contributes to obscuring the insulin augmentation of glucose uptake elicited by GLUT4 translocation. Glucose 181-188 insulin Homo sapiens 299-306 16954338-1 2006 The intravenous glucose tolerance test (IVGTT) interpreted with the minimal model provides individual indexes of insulin sensitivity (S(I)) and glucose effectiveness (S(G)). Glucose 16-23 insulin Homo sapiens 113-120 17469342-8 2006 The glucose-insulin-potassium solution provides the glucose needed by the myocardium in reperfusion conditions and protects the cellular membrane"s integrity as well as pumps and ionic channels, it allows maintaining the action potential probably because ATP-depended channels block and prevent potassium loss, it reduces the cytosol calcium overload and prevent cardiac arrhythmias, preserves the sodium ATPasa pump avoiding the rise in cytosolic sodium; glucose prevents the production of free oxygen radicals. Glucose 4-11 insulin Homo sapiens 12-19 17469342-8 2006 The glucose-insulin-potassium solution provides the glucose needed by the myocardium in reperfusion conditions and protects the cellular membrane"s integrity as well as pumps and ionic channels, it allows maintaining the action potential probably because ATP-depended channels block and prevent potassium loss, it reduces the cytosol calcium overload and prevent cardiac arrhythmias, preserves the sodium ATPasa pump avoiding the rise in cytosolic sodium; glucose prevents the production of free oxygen radicals. Glucose 52-59 insulin Homo sapiens 12-19 16690177-11 2006 CONCLUSIONS: TPN-especially glucose-induces a neurohumoral response as shown here for leptin and insulin that is mainly depending on the fat mass. Glucose 28-35 insulin Homo sapiens 97-104 17063993-0 2006 The effect of icodextrin and glucose-containing solutions on insulin resistance in CAPD patients. Glucose 29-36 insulin Homo sapiens 61-68 17063993-6 2006 Insulin resistance (IR) was calculated according to the homeostasis model assesment (HOMA) formula: HOMA-IR = fasting glucose (mmol/l) x fasting insulin (microU/1/22.5. Glucose 118-125 insulin Homo sapiens 0-7 17063993-14 2006 CONCLUSION: These results suggest that insulin resistance is reduced in peritoneal dialysis patients using icodextrin-based dialysis fluid instead of glucose-based dialysis fluid. Glucose 150-157 insulin Homo sapiens 39-46 17157120-0 2006 A single-center, randomized, double-blind, three-way crossover study examining postchallenge glucose responses to human insulin 70/30 and insulin lispro fixed mixtures 75/25 and 50/50 in patients with type 2 diabetes mellitus. Glucose 93-100 insulin Homo sapiens 120-127 17157120-10 2006 Compared with those in healthy subjects, incremental glucose AUC values for the 4 hours after the meal (AUCglucose 0-4) for patients with type 2 DM were 6.4-fold higher with human insulin 70/30, 4.6-fold higher with insulin lispro 75/25, and 3.0-fold higher with insulin lispro 50/50. Glucose 53-60 insulin Homo sapiens 180-187 17157120-10 2006 Compared with those in healthy subjects, incremental glucose AUC values for the 4 hours after the meal (AUCglucose 0-4) for patients with type 2 DM were 6.4-fold higher with human insulin 70/30, 4.6-fold higher with insulin lispro 75/25, and 3.0-fold higher with insulin lispro 50/50. Glucose 53-60 insulin Homo sapiens 216-223 17157120-10 2006 Compared with those in healthy subjects, incremental glucose AUC values for the 4 hours after the meal (AUCglucose 0-4) for patients with type 2 DM were 6.4-fold higher with human insulin 70/30, 4.6-fold higher with insulin lispro 75/25, and 3.0-fold higher with insulin lispro 50/50. Glucose 53-60 insulin Homo sapiens 216-223 17157120-11 2006 Each insulin regimen produced AUC(glucose) 0-4 and 2-hour PPG values significantly different from all other regimens (all, P < 0.05). Glucose 34-41 insulin Homo sapiens 5-12 16943722-2 2006 Several further trials and meta-analyses investigating the role of insulin treatment, either aimed at tight control of blood glucose concentration or as part of a regimen including glucose and potassium, have been reported recently and are the subject of this review. Glucose 125-132 insulin Homo sapiens 67-74 16943722-2 2006 Several further trials and meta-analyses investigating the role of insulin treatment, either aimed at tight control of blood glucose concentration or as part of a regimen including glucose and potassium, have been reported recently and are the subject of this review. Glucose 181-188 insulin Homo sapiens 67-74 16943722-5 2006 The use of glucose-insulin-potassium regimens does not improve outcomes in patients with acute myocardial infarction who have undergone reperfusion therapy, but may be beneficial during cardiac surgery. Glucose 11-18 insulin Homo sapiens 19-26 16978369-2 2006 METHODS: Intramyocellular lipid (IMCL) was measured by proton magnetic resonance spectroscopy and insulin sensitivity via frequently sampled intravenous glucose tolerance test (IVGTT) after 67 h of two identical low carbohydrate/high fat (LC) diets which were used to elevate IMCL and plasma FFAs. Glucose 153-160 insulin Homo sapiens 98-105 16978378-0 2006 Performance of the continuous glucose monitoring system (CGMS) during development of ketosis in patients on insulin pump therapy. Glucose 30-37 insulin Homo sapiens 108-115 17076642-3 2006 MATERIALS AND METHODS: The decrease in blood glucose levels in five fasting rats following nasal administration of regular insulin solutions in the presence or absence of enhancers was determined by glucometric strips and used as an indication of insulin absorption. Glucose 45-52 insulin Homo sapiens 123-130 17076642-5 2006 Following the instillation of solutions containing insulin and different absorption enhancers into the right nostril of rats, the percentage decrease in initial blood glucose was as follows: 72.46% (+/- 2.39%) for ATS, 63.22 % (+/-11.06%) for QTS and 60.06% (+/-14.93%) for SC. Glucose 167-174 insulin Homo sapiens 51-58 17086934-6 2006 This review will discuss the possibility of targeting cAMP mechanisms in the treatment of type 2 diabetes mellitus, in which insulin release in response to glucose is impaired. Glucose 156-163 insulin Homo sapiens 125-132 16857754-5 2006 However, insulin-stimulated glucose uptake was reduced by approximately 52%. Glucose 28-35 insulin Homo sapiens 9-16 16896936-13 2006 CONCLUSIONS/INTERPRETATION: Our results indicate that sirolimus decreases ductal cell numbers in culture and alters glucose-stimulated insulin secretion in vivo. Glucose 116-123 insulin Homo sapiens 135-142 16944093-6 2006 Islet cell viability was assessed by fluorescence microscopy and beta cell function was determined via glucose-stimulated insulin secretion. Glucose 103-110 insulin Homo sapiens 122-129 17003332-0 2006 Interleukin-6 increases insulin-stimulated glucose disposal in humans and glucose uptake and fatty acid oxidation in vitro via AMP-activated protein kinase. Glucose 43-50 insulin Homo sapiens 24-31 17003332-3 2006 Because skeletal muscle accounts for most of the insulin-stimulated glucose disposal in vivo, we examined the mechanism(s) by which IL-6 may affect muscle metabolism using L6 myotubes. Glucose 68-75 insulin Homo sapiens 49-56 17003332-4 2006 IL-6 treatment increased fatty acid oxidation, basal and insulin-stimulated glucose uptake, and translocation of GLUT4 to the plasma membrane. Glucose 76-83 insulin Homo sapiens 57-64 17003332-8 2006 Our results demonstrate that acute IL-6 treatment enhances insulin-stimulated glucose disposal in humans in vivo, while the effects of IL-6 on glucose and fatty acid metabolism in vitro appear to be mediated by AMPK. Glucose 78-85 insulin Homo sapiens 59-66 17003335-7 2006 A similarly bimodal induction of FLIP, pancreatic duodenal homeobox (PDX)-1, and Pax4 mRNA expression, as well as glucose-stimulated insulin secretion, was observed. Glucose 114-121 insulin Homo sapiens 133-140 17003338-2 2006 A number of studies have led to the controversial proposal that CD38 mediates an alternate pathway for glucose-stimulated insulin release and contributes to the pathogenesis of diabetes. Glucose 103-110 insulin Homo sapiens 122-129 17003350-4 2006 Small interfering RNA-induced reductions in IR expression in human islets completely suppressed glucose-stimulated insulin gene expression, suggesting that insulin regulates its own gene expression in human beta-cells. Glucose 96-103 insulin Homo sapiens 115-122 17003350-4 2006 Small interfering RNA-induced reductions in IR expression in human islets completely suppressed glucose-stimulated insulin gene expression, suggesting that insulin regulates its own gene expression in human beta-cells. Glucose 96-103 insulin Homo sapiens 156-163 17322583-8 2006 It is concluded that adiponectin augments insulin secretion from pancreatic islet beta cells at high glucose concentration through AMPK activation. Glucose 101-108 insulin Homo sapiens 42-49 16962947-0 2006 PTHrP and insulin levels following oral glucose and calcium administration. Glucose 40-47 insulin Homo sapiens 10-17 16962947-4 2006 METHODS: In the present study, we examined the effect of an oral calcium (1 g elemental calcium) and glucose (75 g) load on insulin and PTHrP release in 16 healthy volunteers and of an oral calcium load in 16 non-insulin-dependent diabetes mellitus (NIDDM) patients. Glucose 101-108 insulin Homo sapiens 124-131 16990663-8 2006 When we looked for factors differentially associated with these glucose intolerant states, female sex, greater hip circumference, high triglyceride levels, low fasting insulin levels, and not being born in China were independently associated with isolated IGT compared with isolated IFG. Glucose 64-71 insulin Homo sapiens 168-175 17115351-11 2006 CONCLUSIONS: Starting insulin in Type 2 diabetes patients with twice-daily BIAsp 30 plus met can reduce HbA (1c) and mean prandial plasma glucose increment to a greater extent than once-daily glarg plus glim. Glucose 138-145 insulin Homo sapiens 22-29 18651033-3 2006 The authors suggest that insulin resistance is the key element in the pathogenesis of these diseases, and leads to abnormal glucose and lipid metabolism with an increase in reactive aldehydes. Glucose 124-131 insulin Homo sapiens 25-32 17027360-10 2006 [2] Participants with PCOS and lean controls exhibited different glucose and insulin responses to 75 g of glucose at 1 and 2 hours postchallenge, resulting in paradoxically similar GI ratios. Glucose 106-113 insulin Homo sapiens 77-84 16978135-7 2006 We found that glucose and insulin concentrations on an oral glucose tolerance test were significantly lowered by the mountaineering activity only in the high DHEA-S group. Glucose 60-67 insulin Homo sapiens 26-33 17075773-4 2006 Therefore, we embarked on a study to investigate an individual effect of peroral glucose challenge on serum insulin level and ROS generation by mononuclears (luminol-dependent/latex-induced chemiluminescence) in 20 healthy people aged between 28-75. Glucose 81-88 insulin Homo sapiens 108-115 19669468-1 2006 The relation between plasma glucose and insulin release from pancreatic beta-cells is not stationary in the sense that a given glucose concentration leads to a specific rate of insulin secretion. Glucose 28-35 insulin Homo sapiens 40-47 19669468-1 2006 The relation between plasma glucose and insulin release from pancreatic beta-cells is not stationary in the sense that a given glucose concentration leads to a specific rate of insulin secretion. Glucose 28-35 insulin Homo sapiens 177-184 19669468-1 2006 The relation between plasma glucose and insulin release from pancreatic beta-cells is not stationary in the sense that a given glucose concentration leads to a specific rate of insulin secretion. Glucose 127-134 insulin Homo sapiens 40-47 17070438-1 2006 OBJECTIVE: Insulin need for a given degree of glucose control varies markedly among individuals. Glucose 46-53 insulin Homo sapiens 11-18 19669468-1 2006 The relation between plasma glucose and insulin release from pancreatic beta-cells is not stationary in the sense that a given glucose concentration leads to a specific rate of insulin secretion. Glucose 127-134 insulin Homo sapiens 177-184 19669468-4 2006 The first phase, lasting up to 10 min, is a pulse of insulin release in response to fast changes in glucose concentration. Glucose 100-107 insulin Homo sapiens 53-60 19669468-5 2006 The second phase is a more steady increase of insulin release over minutes to hours, if the elevated glucose concentration is sustained. Glucose 101-108 insulin Homo sapiens 46-53 19669468-12 2006 Finally, the release of the insulin granules is assumed to be enhanced by previous glucose exposure, giving a so-called glucose memory to the beta-cells. Glucose 83-90 insulin Homo sapiens 28-35 16979403-7 2006 Insulin sensitivity by intravenous glucose tolerance test and circulating cardiovascular risk factors (including lipids, tissue plasminogen activator, and plasminogen activator inhibitor 1) were measured in a subset (n = 9). Glucose 35-42 insulin Homo sapiens 0-7 16883325-4 2006 Thiazolidinediones (TZDs) are a class of agents that lower blood glucose through reduction of insulin resistance in patients with type 2 diabetes. Glucose 65-72 insulin Homo sapiens 94-101 16979411-4 2006 Insulin action was estimated as glucose disposal (M), glucose metabolic clearance rate (MCR), and insulin sensitivity index (M/I) during a 10-hour hyperinsulinemic euglycemic clamp. Glucose 32-39 insulin Homo sapiens 0-7 16979411-4 2006 Insulin action was estimated as glucose disposal (M), glucose metabolic clearance rate (MCR), and insulin sensitivity index (M/I) during a 10-hour hyperinsulinemic euglycemic clamp. Glucose 54-61 insulin Homo sapiens 0-7 16979411-5 2006 The sum of immunoreactive insulin values from the oral glucose tolerance test was calculated. Glucose 55-62 insulin Homo sapiens 26-33 16914513-1 2006 Insulin modulates glucose disposal in muscle and adipose tissue by regulating the cellular redistribution of the GLUT4 glucose transporter. Glucose 18-25 insulin Homo sapiens 0-7 17716170-1 2006 One of the predominant aims of insulin therapy for diabetes is to appropriately mimic physiological insulin secretion levels and their correlation with glucose concentration in healthy individuals. Glucose 152-159 insulin Homo sapiens 31-38 17063804-1 2006 Insulin secretion is greater after peroral challenge than after intravenous glucose administration due to so-called incretin effect. Glucose 76-83 insulin Homo sapiens 0-7 17045646-7 2006 Islets of Langerhans from PYY knockout mice were found to hypersecrete insulin in response to 25 mM glucose (p<0.05). Glucose 100-107 insulin Homo sapiens 71-78 17038784-0 2006 [SOX6 attenuates glucose-stimulated insulin secretion by repressing PDX1 transcriptional activity]. Glucose 17-24 insulin Homo sapiens 36-43 16999652-8 2006 Appropriately timed, successive glucose measurements documented a decrement in elevated blood glucose values to within the target range of 90-130 mg/dl after 76 (12%) of 621 sliding-scale insulin injections. Glucose 94-101 insulin Homo sapiens 188-195 16978721-8 2006 Finally, we found that the hypoglycaemia induced by insulin can be corrected by simultaneous glucose infusion without modification of efficacy. Glucose 93-100 insulin Homo sapiens 52-59 17006329-10 2006 Finally, RDP58-treated islets displayed increased insulin secretion in response to both elevated glucose (1915.0+/-396.6 vs. 825.3+/-261.1 mU/L, P<0.01) and secretagogues (2294.3+/-529.5 vs. 939.8+/-333.7 mU/L, P<0.02). Glucose 97-104 insulin Homo sapiens 50-57 16887799-4 2006 Further, glucose enhances p35 gene expression, promoting the formation of active p35/CDK5 complexes that regulate the expression of the insulin gene. Glucose 9-16 insulin Homo sapiens 136-143 16887799-8 2006 Chronic exposure of INS-1 cells to high glucose (20-30 mm) reduced both insulin mRNA levels and the activity of an insulin promoter reporter gene. Glucose 40-47 insulin Homo sapiens 72-79 16887799-8 2006 Chronic exposure of INS-1 cells to high glucose (20-30 mm) reduced both insulin mRNA levels and the activity of an insulin promoter reporter gene. Glucose 40-47 insulin Homo sapiens 115-122 16831872-4 2006 We found that overexpression of mir-9 in insulin-secreting cells causes a reduction in exocytosis elicited by glucose or potassium. Glucose 110-117 insulin Homo sapiens 41-48 16815907-1 2006 Pancreatic islets of Langerhans display complex intracellular calcium changes in response to glucose that include fast (seconds), slow ( approximately 5 min), and mixed fast/slow oscillations; the slow and mixed oscillations are likely responsible for the pulses of plasma insulin observed in vivo. Glucose 93-100 insulin Homo sapiens 273-280 16952981-8 2006 There was a strong, inverse correlation between sCD36 and insulin-stimulated glucose disposal and a direct correlation with fasting plasma glucose, fasting insulin, and body mass index. Glucose 77-84 insulin Homo sapiens 58-65 16954722-10 2006 CONCLUSIONS: Both glucose uptake in vitro and clinical insulin sensitivity in healthy volunteers demonstrate differential effects on glucose metabolism by the combination PI atazanavir/ritonavir and lopinavir/ritonavir. Glucose 133-140 insulin Homo sapiens 55-62 16954722-3 2006 METHODS: Glucose uptake was measured following insulin stimulation in differentiated human adipocytes in the presence of ritonavir (2 micromol/l) combined with either atazanavir or lopinavir (3-30 micromol/l). Glucose 9-16 insulin Homo sapiens 47-54 16861328-3 2006 Insulin sensitivity was directly measured with a validated, 12-sample, insulin-enhanced, intravenous glucose tolerance test with minimal model analysis. Glucose 101-108 insulin Homo sapiens 0-7 16861328-3 2006 Insulin sensitivity was directly measured with a validated, 12-sample, insulin-enhanced, intravenous glucose tolerance test with minimal model analysis. Glucose 101-108 insulin Homo sapiens 71-78 17142216-6 2006 Both rosiglitazone (n=56) and insulin (n=56) significantly improved fasting glucose (2.4 and 3.7 mmol/L, respectively) and hemoglobin A1c concentrations (1.1% and 1.3%, respectively). Glucose 76-83 insulin Homo sapiens 30-37 16980199-1 2006 Insulin resistance is not simply a problem of decreased glucose uptake in response to insulin, but a multifaceted syndrome that significantly increases the risk for cardiovascular disease. Glucose 56-63 insulin Homo sapiens 86-93 17003352-7 2006 These findings implicate several factors in the insulin signaling pathway, which may be further dysregulated in HIV+IGT, and support the notion that insulin signaling pathways for glucose and leucine metabolism may be disrupted by increased proinflammatory adipocytokines (IL-8) and increased lipid oxidation. Glucose 180-187 insulin Homo sapiens 48-55 17003352-7 2006 These findings implicate several factors in the insulin signaling pathway, which may be further dysregulated in HIV+IGT, and support the notion that insulin signaling pathways for glucose and leucine metabolism may be disrupted by increased proinflammatory adipocytokines (IL-8) and increased lipid oxidation. Glucose 180-187 insulin Homo sapiens 149-156 17003358-0 2006 Common single nucleotide polymorphisms in TCF7L2 are reproducibly associated with type 2 diabetes and reduce the insulin response to glucose in nondiabetic individuals. Glucose 133-140 insulin Homo sapiens 113-120 17003358-2 2006 In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. Glucose 140-147 insulin Homo sapiens 99-106 17003358-2 2006 In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. Glucose 140-147 insulin Homo sapiens 202-209 17003358-2 2006 In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. Glucose 222-229 insulin Homo sapiens 99-106 17003358-2 2006 In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. Glucose 222-229 insulin Homo sapiens 202-209 17003361-7 2006 However, we found suggestive evidence for reduced insulin response to glucose (P = 0.05). Glucose 70-77 insulin Homo sapiens 50-57 16959033-3 2006 Impaired fasting plasma glucose has been previously associated with endothelial dysfunction, higher levels of inflammatory markers and increased risk of developing insulin resistance and cardiovascular events. Glucose 24-31 insulin Homo sapiens 164-171 16912247-7 2006 DISCUSSION: Thiazolidinediones, insulin sensitizers widely used in the treatment of type 2 diabetes, have been reported to have beneficial effects on lipids, such as triglyceride lowering and HDL-C elevation, in addition to their glucose-lowering effects. Glucose 230-237 insulin Homo sapiens 32-39 16678254-7 2006 The in vitro diffusion experiments also showed that differential delivery of insulin in response to glucose was possible with candidate polymerised glucose-responsive formulations, thus highlighting the potential of such a novel glucose-sensitive material to be used as part of implantable closed-loop insulin delivery device. Glucose 148-155 insulin Homo sapiens 302-309 16678254-7 2006 The in vitro diffusion experiments also showed that differential delivery of insulin in response to glucose was possible with candidate polymerised glucose-responsive formulations, thus highlighting the potential of such a novel glucose-sensitive material to be used as part of implantable closed-loop insulin delivery device. Glucose 100-107 insulin Homo sapiens 77-84 16678254-7 2006 The in vitro diffusion experiments also showed that differential delivery of insulin in response to glucose was possible with candidate polymerised glucose-responsive formulations, thus highlighting the potential of such a novel glucose-sensitive material to be used as part of implantable closed-loop insulin delivery device. Glucose 148-155 insulin Homo sapiens 77-84 16678254-7 2006 The in vitro diffusion experiments also showed that differential delivery of insulin in response to glucose was possible with candidate polymerised glucose-responsive formulations, thus highlighting the potential of such a novel glucose-sensitive material to be used as part of implantable closed-loop insulin delivery device. Glucose 148-155 insulin Homo sapiens 77-84 16678254-7 2006 The in vitro diffusion experiments also showed that differential delivery of insulin in response to glucose was possible with candidate polymerised glucose-responsive formulations, thus highlighting the potential of such a novel glucose-sensitive material to be used as part of implantable closed-loop insulin delivery device. Glucose 148-155 insulin Homo sapiens 302-309 16950132-2 2006 Work in this issue of Cell Metabolism (Lipson et al., 2006) identifies a novel role for UPR activation in beta cell function by demonstrating that the UPR effector IRE1 is a positive regulator of glucose-stimulated proinsulin biosynthesis. Glucose 196-203 insulin Homo sapiens 215-225 16733835-1 2006 The objective of this study was to analyse the PK/PD of the insulin-glucose physiology for glucose stimulated insulin secretion from beta-cells between lean and obese pre-pubertal children in an 18 month study. Glucose 68-75 insulin Homo sapiens 60-67 16950141-6 2006 In contrast, chronic exposure of beta cells to high glucose causes ER stress and hyperactivation of IRE1, leading to the suppression of insulin gene expression. Glucose 52-59 insulin Homo sapiens 136-143 16950141-3 2006 IRE1alpha phosphorylation is coupled to insulin biosynthesis in response to transient exposure to high glucose; inactivation of IRE1alpha signaling by siRNA or inhibition of IRE1alpha phosphorylation hinders insulin biosynthesis. Glucose 103-110 insulin Homo sapiens 40-47 16922822-5 2006 These thrifty traits, namely a decreased capacity for dietary thermogenesis and an increased resistance to insulin-mediated glucose uptake in skeletal muscle, would prolong survival during famine but predispose to obesity and diabetes in the face of abundance. Glucose 124-131 insulin Homo sapiens 107-114 16938587-5 2006 New, innovative isotopic approaches now being developed offer the potential to characterize whole-body glucose metabolism in a fashion that may eventually allow routine clinical testing of insulin sensitivity. Glucose 103-110 insulin Homo sapiens 189-196 16886163-0 2006 Single-dose lopinavir-ritonavir acutely inhibits insulin-mediated glucose disposal in healthy volunteers. Glucose 66-73 insulin Homo sapiens 49-56 17002258-3 2006 Thiazolidinediones are a relatively new class of compounds for the treatment of type 2 diabetes mellitus that lower glucose levels by decreasing insulin resistance and glucose production by the liver. Glucose 116-123 insulin Homo sapiens 145-152 16930111-1 2006 The use of intensive insulin therapy (IIT) to maintain blood glucose level below 8.3 mmol/L is recommended for management of severe sepsis by the Surviving Sepsis guidelines. Glucose 61-68 insulin Homo sapiens 21-28 16819611-10 2006 In the whole patient group, mean OGTT glucose levels were inversely related to both insulin sensitivity and beta cell glucose sensitivity (r (2)=0.67, partial r=-0.76 and -0.41, respectively). Glucose 38-45 insulin Homo sapiens 84-91 16819611-12 2006 CONCLUSIONS/INTERPRETATION: Following BPD, glucose tolerance was restored mainly as a result of a rapid and large improvement in insulin sensitivity. Glucose 43-50 insulin Homo sapiens 129-136 16918581-0 2006 Glucose control with insulin results in reduction of NF-kappaB-binding activity in mononuclear blood cells of patients with recently manifested type 1 diabetes. Glucose 0-7 insulin Homo sapiens 21-28 16826407-3 2006 The effects of KISS1 on basal and glucose-induced insulin secretion from mouse and human islets were measured in a perifusion system. Glucose 34-41 insulin Homo sapiens 50-57 16918591-0 2006 Insulin sensitivity during oral glucose tolerance test and its relations to parameters of glucose metabolism and endothelial function in type 2 diabetic subjects under metformin and thiazolidinedione. Glucose 32-39 insulin Homo sapiens 0-7 16826407-6 2006 Exposure of mouse and human islets to KISS1 caused a stimulation of glucose-induced (20 mmol/l) insulin secretion, but had no effect on the basal rate of secretion at a sub-stimulatory concentration of glucose (2 mmol/l). Glucose 68-75 insulin Homo sapiens 96-103 16918591-1 2006 AIM: This study was designed to assess the usefulness of a model-based index of insulin sensitivity during an oral glucose tolerance test (OGTT) in the identification of possible changes in this metabolic parameter produced by pharmacological agents known to be potent insulin sensitizers, that is metformin (M) and thiazolidinedione (T). Glucose 115-122 insulin Homo sapiens 80-87 16918591-1 2006 AIM: This study was designed to assess the usefulness of a model-based index of insulin sensitivity during an oral glucose tolerance test (OGTT) in the identification of possible changes in this metabolic parameter produced by pharmacological agents known to be potent insulin sensitizers, that is metformin (M) and thiazolidinedione (T). Glucose 115-122 insulin Homo sapiens 269-276 16918591-5 2006 Insulin sensitivity was calculated with homeostasis model assessment and with oral glucose insulin sensitivity (OGIS), which quantifies dynamic glucose clearance per unit change of insulin. Glucose 83-90 insulin Homo sapiens 0-7 16918591-5 2006 Insulin sensitivity was calculated with homeostasis model assessment and with oral glucose insulin sensitivity (OGIS), which quantifies dynamic glucose clearance per unit change of insulin. Glucose 83-90 insulin Homo sapiens 91-98 16918591-14 2006 CONCLUSIONS: Model-based indices of insulin sensitivity and secretion during an OGTT can be able to detect changes observed in patients under treatment with pharmacological agents such as M or T. Both the drugs improved glucose control similarly. Glucose 220-227 insulin Homo sapiens 36-43 17194639-4 2006 The data indicated resistin impaired, insulin-stimulated glucose utilization, which implied liver was a target tissue of resistin. Glucose 57-64 insulin Homo sapiens 38-45 16936218-7 2006 We also genotyped these SNPs in nondiabetic, non-Amish subjects (n = 48), in whom intravenous glucose tolerance tests were performed, and found an association between rs7901695 and rs7903146 and insulin sensitivity (P = 0.003 and P = 0.005, respectively) and disposition index (P = 0.04 and P = 0.007, respectively). Glucose 94-101 insulin Homo sapiens 195-202 16977256-2 2006 The subsequent first phase insulin response (also termed acute insulin response or AIR) to intravenous glucose or arginine has been quantified in a variety of ways, from the mean serum insulin measured at multiple times after glucose injection to the mean value above baseline of serum insulin at 2 to 10 min. Glucose 103-110 insulin Homo sapiens 27-34 16977256-2 2006 The subsequent first phase insulin response (also termed acute insulin response or AIR) to intravenous glucose or arginine has been quantified in a variety of ways, from the mean serum insulin measured at multiple times after glucose injection to the mean value above baseline of serum insulin at 2 to 10 min. Glucose 103-110 insulin Homo sapiens 63-70 16977256-2 2006 The subsequent first phase insulin response (also termed acute insulin response or AIR) to intravenous glucose or arginine has been quantified in a variety of ways, from the mean serum insulin measured at multiple times after glucose injection to the mean value above baseline of serum insulin at 2 to 10 min. Glucose 103-110 insulin Homo sapiens 63-70 16977256-2 2006 The subsequent first phase insulin response (also termed acute insulin response or AIR) to intravenous glucose or arginine has been quantified in a variety of ways, from the mean serum insulin measured at multiple times after glucose injection to the mean value above baseline of serum insulin at 2 to 10 min. Glucose 103-110 insulin Homo sapiens 63-70 16977256-2 2006 The subsequent first phase insulin response (also termed acute insulin response or AIR) to intravenous glucose or arginine has been quantified in a variety of ways, from the mean serum insulin measured at multiple times after glucose injection to the mean value above baseline of serum insulin at 2 to 10 min. Glucose 226-233 insulin Homo sapiens 27-34 17194639-8 2006 Moreover, resistin lowered mRNA levels of IRS-2 while stimulating SOCS-3 expression, which suggests it impairs glucose tolerance by blocking the insulin signal transduction pathway. Glucose 111-118 insulin Homo sapiens 145-152 16895803-6 2006 After selective accumulation in pancreatic beta cells, which are weakly protected against oxidative stress, the cytotoxic glucose analogue alloxan destroys these insulin-producing cells and causes a state of insulin-dependent diabetes mellitus through ROS-mediated toxicity in rodents and in other animal species, which express this glucose transporter isoform in their beta cells. Glucose 122-129 insulin Homo sapiens 162-169 16772346-1 2006 CONTEXT/OBJECTIVE: Insulin resistance in obese subjects results in the impaired disposal of glucose by skeletal muscle. Glucose 92-99 insulin Homo sapiens 19-26 16763943-15 2006 Insulin and/or heparin protect against high glucose-induced injury. Glucose 44-51 insulin Homo sapiens 0-7 17003289-2 2006 In depolarised cells, GLP-1 significantly augmented glucose-induced K(ATP) channel-independent insulin secretion in a glucose concentration-dependent manner. Glucose 52-59 insulin Homo sapiens 95-102 16822818-8 2006 RESULTS: After adjustment for age, gender, and body mass index, patients with primary aldosteronism had greater homeostasis model assessment index (P < 0.05) and plasma insulin response to an oral glucose load (P < 0.05) and lower quantitative insulin sensitivity check index (P < 0.01) than normotensive controls. Glucose 200-207 insulin Homo sapiens 172-179 17003271-3 2006 CaR activation initiated a marked but transient insulin secretory response from both human islets and MIN6 cells at a sub-stimulatory concentration of glucose, and further enhanced glucose-induced insulin secretion. Glucose 151-158 insulin Homo sapiens 48-55 17003272-1 2006 Insulin is capable of increasing intracellular magnesium, although very little is known about the effect of insulin on the biologically active fraction of magnesium, i.e. the ionized quota (Mg(i)(2+)), its interactions with glucose, and the cellular mechanisms involved in these processes. Glucose 224-231 insulin Homo sapiens 0-7 17003272-4 2006 We found that insulin significantly increases the Mg(i)(2+)(without insulin 227 +/- 14 microM, with 10 microU/ml, insulin 301 +/- 30 microM, P<0.0001, n = 12) in a dose-dependent manner in all three glucose concentrations tested (5, 7 and 15 mmol/l). Glucose 202-209 insulin Homo sapiens 14-21 17003289-2 2006 In depolarised cells, GLP-1 significantly augmented glucose-induced K(ATP) channel-independent insulin secretion in a glucose concentration-dependent manner. Glucose 118-125 insulin Homo sapiens 95-102 17003272-8 2006 Taking into account the relationship between insulin and glucose plasma levels and their opposing effects on Mg(i)(2+), this mechanism may represent the two limbs of a biphasic regulatory system of Mg(i)(2+) in both physiological and pathological conditions. Glucose 57-64 insulin Homo sapiens 45-52 16919540-8 2006 Basal and insulin-stimulated glucose disposal remained unchanged with overfeeding in all groups. Glucose 29-36 insulin Homo sapiens 10-17 16909480-2 2006 METHODS: 5-point capillary blood glucose was monitored in pre- and post-CSII and the insulin dose which could stabilize blood glucose was defined as the total daily dose of insulin, including basal and bolus total dose. Glucose 126-133 insulin Homo sapiens 85-92 16919548-2 2006 After a meal, the rise in postprandial glucose (PPG) is controlled by the rapid pancreatic release of insulin, stimulated by both glucose and the intestinal production of the incretins glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1. Glucose 39-46 insulin Homo sapiens 102-109 16919540-9 2006 Low-dose insulin suppression of endogenous glucose production was impaired after overfeeding in lean women (euenergetic, 1.92 +/- 0.36 to 0.36 +/- 0.16 mg x kg(-1) x min(-1); overfeeding: 2.13 +/- 0.17 to 0.86 +/- 0.12 mg x kg(-1) x min(-1); P = .04) but remained unchanged in the other groups. Glucose 43-50 insulin Homo sapiens 9-16 16919548-2 2006 After a meal, the rise in postprandial glucose (PPG) is controlled by the rapid pancreatic release of insulin, stimulated by both glucose and the intestinal production of the incretins glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1. Glucose 130-137 insulin Homo sapiens 102-109 16919548-2 2006 After a meal, the rise in postprandial glucose (PPG) is controlled by the rapid pancreatic release of insulin, stimulated by both glucose and the intestinal production of the incretins glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1. Glucose 130-137 insulin Homo sapiens 102-109 16919548-12 2006 New semisynthetic insulin analogues permit a more aggressive response to postprandial glucose elevation, with lower risk of hypoglycemia, than with regular insulin. Glucose 86-93 insulin Homo sapiens 18-25 16919540-10 2006 These findings demonstrate that insulin action is reduced in lean, obese-resistant women after short-term overfeeding primarily because of an inhibition of insulin-mediated suppression of endogenous glucose production, whereas short-term overfeeding does not appear to effect insulin action in lean men and RO individuals. Glucose 199-206 insulin Homo sapiens 32-39 16919540-10 2006 These findings demonstrate that insulin action is reduced in lean, obese-resistant women after short-term overfeeding primarily because of an inhibition of insulin-mediated suppression of endogenous glucose production, whereas short-term overfeeding does not appear to effect insulin action in lean men and RO individuals. Glucose 199-206 insulin Homo sapiens 156-163 16919540-10 2006 These findings demonstrate that insulin action is reduced in lean, obese-resistant women after short-term overfeeding primarily because of an inhibition of insulin-mediated suppression of endogenous glucose production, whereas short-term overfeeding does not appear to effect insulin action in lean men and RO individuals. Glucose 199-206 insulin Homo sapiens 156-163 16941278-2 2006 The objective of the present study was to determine whether ingested phenylalanine stimulates insulin and/or glucagon secretion, and if phenylalanine ingested with glucose modifies the insulin, glucagon or glucose response to the ingested glucose. Glucose 164-171 insulin Homo sapiens 185-192 16989702-6 2006 RESULT: In morbidly obese subjects, the SI (P<0.01), DI (P<0.01) and first-phase insulin release (P<0.02) started changing with serum glucose levels considered to be normal (5.00-5.28 mmol/L). Glucose 143-150 insulin Homo sapiens 87-94 16989702-10 2006 CONCLUSIONS: Morbidly obese subjects show slopes of insulin sensitivity and insulin secretion in accordance with their baseline serum glucose levels. Glucose 134-141 insulin Homo sapiens 52-59 16989702-11 2006 The fall in first-phase insulin release begins when serum glucose values are considered normal. Glucose 58-65 insulin Homo sapiens 24-31 16967593-3 2006 A systematic review of 6 randomised controlled trials comparing self-monitoring of blood glucose with standard care, self-monitoring of urine glucose, or both showed that self-monitoring of blood glucose may be effective in improving glycaemic control in patients with type 2 diabetes who are not using insulin. Glucose 89-96 insulin Homo sapiens 303-310 16893717-4 2006 The increased risk for mortality due to hyperglycemia provides a strong rationale for an intensive approach using insulin to control blood glucose levels in cardiac patients being treated in acute care and surgical settings. Glucose 139-146 insulin Homo sapiens 114-121 16877540-7 2006 Moreover, the insulin effect on spontaneous cortical activity correlated negatively with body mass index and percent body fat (all r < -0.4; all P < 0.05) and positively with insulin sensitivity of glucose disposal (theta band, r = 0.48, P = 0.017). Glucose 204-211 insulin Homo sapiens 14-21 16877540-7 2006 Moreover, the insulin effect on spontaneous cortical activity correlated negatively with body mass index and percent body fat (all r < -0.4; all P < 0.05) and positively with insulin sensitivity of glucose disposal (theta band, r = 0.48, P = 0.017). Glucose 204-211 insulin Homo sapiens 181-188 16740635-2 2006 In a manner analogous to insulin and exercise, neuregulins stimulate glucose transport through recruitment of glucose transporters to surface membranes in skeletal muscle. Glucose 69-76 insulin Homo sapiens 25-32 16740635-3 2006 Like muscle contraction, neuregulins have additive effects with insulin on glucose uptake. Glucose 75-82 insulin Homo sapiens 64-71 16214148-7 2006 Univariate analysis showed age, male gender, smoking, coronary artery disease, HDL-cholesterol, insulin levels in glucose tolerance test and homeostasis model assessment insulin resistance index (HOMA index) were found to be significant predictors of complex atherosclerotic lesions. Glucose 114-121 insulin Homo sapiens 96-103 16828894-1 2006 Insulin-stimulated glucose uptake through GLUT4 plays a pivotal role in maintaining normal blood glucose levels. Glucose 19-26 insulin Homo sapiens 0-7 16828894-1 2006 Insulin-stimulated glucose uptake through GLUT4 plays a pivotal role in maintaining normal blood glucose levels. Glucose 97-104 insulin Homo sapiens 0-7 16883035-2 2006 The absolute, and/or relative insulin lack state deteriorate the function and reduce the number of osteoblast, in addition, the osteoblast dysfunction is also caused by the sorbitol accumulation brought in the osteoblast as the result of the continuation of high blood glucose state. Glucose 269-276 insulin Homo sapiens 30-37 16980199-1 2006 Insulin resistance is not simply a problem of decreased glucose uptake in response to insulin, but a multifaceted syndrome that significantly increases the risk for cardiovascular disease. Glucose 56-63 insulin Homo sapiens 0-7 16890492-3 2006 New findings on gene modulation by ERalpha and ERbeta of insulin-sensitive tissues indicate that estradiol participates in glucose homeostasis by modulating the expression of genes that are involved in insulin sensitivity and glucose uptake. Glucose 123-130 insulin Homo sapiens 57-64 16890492-3 2006 New findings on gene modulation by ERalpha and ERbeta of insulin-sensitive tissues indicate that estradiol participates in glucose homeostasis by modulating the expression of genes that are involved in insulin sensitivity and glucose uptake. Glucose 123-130 insulin Homo sapiens 202-209 16765099-4 2006 Improvement of insulin sensitivity was measured as changes in levels of glucose, insulin, and adiponectin in ob/ob mice. Glucose 72-79 insulin Homo sapiens 15-22 17091602-6 2006 Insulin resistance may be improved in several ways, e.g. by changes in microcirculation or direct effects on insulin response and glucose transport in target organ cells. Glucose 130-137 insulin Homo sapiens 0-7 16828707-9 2006 Over-expression of a mutant form of Stx16 devoid of a transmembrane anchor was found to significantly slow the reversal of insulin-stimulated glucose transport. Glucose 142-149 insulin Homo sapiens 123-130 16828707-10 2006 Depletion of Stx16 using antisense approaches profoundly reduced insulin-stimulated glucose transport but was without effect on cell surface transferrin receptor levels, and also reduced the extent of Glut4 translocation to the plasma membrane in response to insulin. Glucose 84-91 insulin Homo sapiens 65-72 16885550-11 2006 Sulfonylurea treatment increased insulin secretion, which was more highly stimulated by oral glucose or a mixed meal than by intravenous glucose. Glucose 93-100 insulin Homo sapiens 33-40 16885550-11 2006 Sulfonylurea treatment increased insulin secretion, which was more highly stimulated by oral glucose or a mixed meal than by intravenous glucose. Glucose 137-144 insulin Homo sapiens 33-40 16478772-8 2006 In addition to insulin resistance at the whole body level (P = 0.012) and muscle (P = 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake (P = 0.040) and glucose extraction rate (P = 0.0006) compared with the low liver fat group. Glucose 159-166 insulin Homo sapiens 129-136 16569758-1 2006 We measured in vivo and in vitro nutrient-stimulated insulin secretion in late gestation fetal sheep to determine whether an intrinsic islet defect is responsible for decreased glucose-stimulated insulin secretion (GSIS) in response to chronic hypoglycemia. Glucose 177-184 insulin Homo sapiens 196-203 16569758-5 2006 Isolated pancreatic islets from chronically hypoglycemic fetuses had normal insulin and DNA content but decreased fractional insulin release when stimulated with glucose, leucine, arginine, or lysine. Glucose 162-169 insulin Homo sapiens 125-132 16845606-7 2006 Compatible with these findings, type 1 diabetic patients receiving insulin and C-peptide developed 66% more stimulation of glucose metabolism than when given insulin alone. Glucose 123-130 insulin Homo sapiens 67-74 16845606-7 2006 Compatible with these findings, type 1 diabetic patients receiving insulin and C-peptide developed 66% more stimulation of glucose metabolism than when given insulin alone. Glucose 123-130 insulin Homo sapiens 79-88 16621106-13 2006 Further studies are required to determine the impact of insulin pulses on glucose metabolism. Glucose 74-81 insulin Homo sapiens 56-63 16718465-8 2006 Insulin deprivation doubled endogenous glucose production, renal glucose production was unaltered by insulin deprivation and diabetes (ranging between 100 and 140 micromol/min). Glucose 39-46 insulin Homo sapiens 0-7 16736128-9 2006 Glucose-induced elevation of visfatin was prevented by co-infusion of insulin or somatostatin (p<0.05). Glucose 0-7 insulin Homo sapiens 70-77 16873679-1 2006 The insulin-signaling network regulates blood glucose levels, controls metabolism, and when dysregulated, may lead to the development of type 2 diabetes. Glucose 46-53 insulin Homo sapiens 4-11 16873700-7 2006 After partial pancreatectomy both basal and glucose-stimulated insulin secretion were decreased through the mechanism of a selective approximately 50 and approximately 80% deficit in insulin pulse mass, respectively (P < 0.05). Glucose 44-51 insulin Homo sapiens 63-70 16873700-9 2006 Partial pancreatectomy also caused a approximately 40% decrease in insulin-stimulated glucose disposal (P < 0.05), insulin sensitivity after partial pancreatectomy being related to insulin pulse amplitude (r = 0.9, P < 0.01). Glucose 86-93 insulin Homo sapiens 67-74 16873706-2 2006 Subsequent studies in insulin-resistant animal models and humans have consistently demonstrated a reduced strength of insulin signaling via the insulin receptor substrate (IRS)-1/phosphatidylinositol (PI) 3-kinase pathway, resulting in diminished glucose uptake and utilization in insulin target tissues. Glucose 247-254 insulin Homo sapiens 22-29 16873706-2 2006 Subsequent studies in insulin-resistant animal models and humans have consistently demonstrated a reduced strength of insulin signaling via the insulin receptor substrate (IRS)-1/phosphatidylinositol (PI) 3-kinase pathway, resulting in diminished glucose uptake and utilization in insulin target tissues. Glucose 247-254 insulin Homo sapiens 118-125 16873706-2 2006 Subsequent studies in insulin-resistant animal models and humans have consistently demonstrated a reduced strength of insulin signaling via the insulin receptor substrate (IRS)-1/phosphatidylinositol (PI) 3-kinase pathway, resulting in diminished glucose uptake and utilization in insulin target tissues. Glucose 247-254 insulin Homo sapiens 118-125 16873706-2 2006 Subsequent studies in insulin-resistant animal models and humans have consistently demonstrated a reduced strength of insulin signaling via the insulin receptor substrate (IRS)-1/phosphatidylinositol (PI) 3-kinase pathway, resulting in diminished glucose uptake and utilization in insulin target tissues. Glucose 247-254 insulin Homo sapiens 118-125 16873775-0 2006 Intensive insulin therapy in the intensive care unit: assessment by continuous glucose monitoring. Glucose 79-86 insulin Homo sapiens 10-17 16873775-2 2006 Using continuous glucose monitoring (CGM), we investigated whether intensive insulin therapy based on discontinuous glucose monitoring can achieve normoglycemia (80-110 mg/dl) in a medical intensive care unit (MICU). Glucose 116-123 insulin Homo sapiens 77-84 16873785-10 2006 CONCLUSIONS: Insulin glulisine renders postprandial glucose disposal closer to physiologic requirements compared with RHI and enables appropriate timing of prandial insulin administration. Glucose 52-59 insulin Homo sapiens 13-20 16873799-4 2006 We used the disposition index, derived as the product of insulin sensitivity and the first-phase insulin response to glucose as a measure of the activity of the beta-cells adjusted for insulin resistance. Glucose 117-124 insulin Homo sapiens 97-104 16873799-4 2006 We used the disposition index, derived as the product of insulin sensitivity and the first-phase insulin response to glucose as a measure of the activity of the beta-cells adjusted for insulin resistance. Glucose 117-124 insulin Homo sapiens 97-104 16941278-7 2006 When glucose was ingested with phenylalanine, the circulating phenylalanine, glucagon, AAN, and insulin area responses were approximately the sum of the responses to phenylalanine alone and glucose alone. Glucose 5-12 insulin Homo sapiens 96-103 16916082-2 2006 The optimal insulin delivery rate is obtained off-line as an explicit function of the current blood glucose concentration of the patient by using novel parametric programming algorithms, developed at Imperial College London. Glucose 100-107 insulin Homo sapiens 12-19 16957985-1 2006 Recent studies from multiple laboratories, including our own, provided fresh insights into the contributory roles for GTP-binding proteins (G-proteins) in glucose-stimulated insulin secretion (GSIS) from the islet beta cell. Glucose 155-162 insulin Homo sapiens 174-181 16684820-6 2006 Chronic treatment of adipocytes with insulin is accompanied by permanently elevated endocannabinoid signaling, whereas culturing of RIN-m5F beta-cells in high glucose transforms insulin down-regulation of endocannabinoid levels into up-regulation. Glucose 159-166 insulin Homo sapiens 178-185 16911007-11 2006 CONCLUSIONS: Screening with fasting glucose alone would have missed 70% of subjects with IGT in this population of insulin-resistant adolescents. Glucose 36-43 insulin Homo sapiens 115-122 18220639-4 2006 Current therapy of GDM focuses on tightly controlling maternal glucose levels, resulting in insulin therapy in up to 50% of women to reach the fasting glucose target of< 90 mg/dl and 2h-postprandial glucose < 120 mg/dl. Glucose 63-70 insulin Homo sapiens 92-99 18220639-4 2006 Current therapy of GDM focuses on tightly controlling maternal glucose levels, resulting in insulin therapy in up to 50% of women to reach the fasting glucose target of< 90 mg/dl and 2h-postprandial glucose < 120 mg/dl. Glucose 151-158 insulin Homo sapiens 92-99 18220639-4 2006 Current therapy of GDM focuses on tightly controlling maternal glucose levels, resulting in insulin therapy in up to 50% of women to reach the fasting glucose target of< 90 mg/dl and 2h-postprandial glucose < 120 mg/dl. Glucose 151-158 insulin Homo sapiens 92-99 18220641-3 2006 The insulin mRNA has a long half-life and changes in insulin mRNA stability, induced by glucose, are likely to be regulated through specific mechanisms. Glucose 88-95 insulin Homo sapiens 4-11 18220641-3 2006 The insulin mRNA has a long half-life and changes in insulin mRNA stability, induced by glucose, are likely to be regulated through specific mechanisms. Glucose 88-95 insulin Homo sapiens 53-60 18220641-4 2006 Recent findings indicate that the polypyrimidine tract binding protein (PTB), also named hnRNP I, by binding to the 3"-UTR (untranslated region) of the insulin mRNA molecule, stabilizes the messenger thereby participating in the glucose-induced increase in insulin mRNA. Glucose 229-236 insulin Homo sapiens 152-159 18220641-4 2006 Recent findings indicate that the polypyrimidine tract binding protein (PTB), also named hnRNP I, by binding to the 3"-UTR (untranslated region) of the insulin mRNA molecule, stabilizes the messenger thereby participating in the glucose-induced increase in insulin mRNA. Glucose 229-236 insulin Homo sapiens 257-264 16601071-1 2006 The stimulation of cells with physiological concentrations of insulin induces a variety of responses, e.g. an increase in glucose uptake, induction of glycogen and protein synthesis, and gene expression. Glucose 122-129 insulin Homo sapiens 62-69 16774611-4 2006 Moreover, the recent introduction of continuous glucose monitoring systems (CGMSs) offers the prospect of finally realizing the full potential of insulin pump therapy to normalize hemoglobin A1c (HbAlc) levels with minimal risk of hypoglycemia. Glucose 48-55 insulin Homo sapiens 146-153 16774615-2 2006 Continuous subcutaneous insulin infusion (CSII) is associated with lower blood glucose variability in children. Glucose 79-86 insulin Homo sapiens 24-31 16774618-2 2006 The goal of "closing the loop" is to develop an autonomous insulin delivery system attached to a device capable of continuous glucose sensing, thus mimicking the islet beta cells activity and its capability of maintaining normal blood glucose levels and freeing the patient from the need of constant calculations of daily insulin and carbohydrates. Glucose 126-133 insulin Homo sapiens 59-66 16774618-2 2006 The goal of "closing the loop" is to develop an autonomous insulin delivery system attached to a device capable of continuous glucose sensing, thus mimicking the islet beta cells activity and its capability of maintaining normal blood glucose levels and freeing the patient from the need of constant calculations of daily insulin and carbohydrates. Glucose 235-242 insulin Homo sapiens 59-66 17144094-9 2006 Fasting glucose and insulin concentration did not differ between CKD patients and control group but insulin/glucose ratio was higher in CKD group. Glucose 108-115 insulin Homo sapiens 100-107 17048997-2 2006 The Homeostasis Model for Assessment [HOMA= fasting insulin (mUI/ml) * fasting glucose (mmol/L) / 22.5] has proved useful in the measurement of insulin sensitivity in euglycemic patients. Glucose 79-86 insulin Homo sapiens 144-151 16889692-2 2006 We tested the hypothesis that impairment in insulin stimulated glucose-disposal in insulin resistant patients would be reflected in the gene expression profile of skeletal muscle. Glucose 63-70 insulin Homo sapiens 44-51 16815800-3 2006 Insulin and amylin are co-secreted by B-cells and provide a signal that reflects both circulating energy in the form of glucose and stored energy in the form of visceral adipose tissue. Glucose 120-127 insulin Homo sapiens 0-7 16815800-4 2006 Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight. Glucose 78-85 insulin Homo sapiens 0-7 16889692-2 2006 We tested the hypothesis that impairment in insulin stimulated glucose-disposal in insulin resistant patients would be reflected in the gene expression profile of skeletal muscle. Glucose 63-70 insulin Homo sapiens 83-90 16750510-2 2006 Insulin resistance in transgenic animals genetically rendered insulin resistant was confirmed with the use of intraperitoneal glucose tolerance tests. Glucose 126-133 insulin Homo sapiens 0-7 16750510-2 2006 Insulin resistance in transgenic animals genetically rendered insulin resistant was confirmed with the use of intraperitoneal glucose tolerance tests. Glucose 126-133 insulin Homo sapiens 62-69 16869959-5 2006 We tested for altered insulin secretion in 107 subjects who had undergone intravenous glucose tolerance tests to assess insulin sensitivity and insulin secretion. Glucose 86-93 insulin Homo sapiens 22-29 16464906-5 2006 Training significantly improved glucose tolerance, with a reduction in the area under the curve for glucose (P < 0.05) and insulin (P = 0.01) during an oral glucose tolerance test. Glucose 32-39 insulin Homo sapiens 126-133 16847295-3 2006 PURPOSE: To briefly review the pharmacologic characteristics of currently available insulin products and to suggest an initial insulin regimen based on common blood glucose profiles among patients with diabetes. Glucose 165-172 insulin Homo sapiens 127-134 16776662-0 2006 Gender differences in the insulin-like growth factor axis response to a glucose load. Glucose 72-79 insulin Homo sapiens 26-33 16776662-3 2006 METHODS: The intravenous glucose tolerance test (IVGTT) was used to quantify insulin sensitivity and insulin secretion in 160 adults aged 20-21 years in Adelaide, Australia. Glucose 25-32 insulin Homo sapiens 77-84 16478778-1 2006 Minimal model analysis of intravenous glucose tolerance test (IVGTT) glucose and insulin concentrations offers a validated approach to measuring insulin sensitivity, but model identification is not always successful. Glucose 38-45 insulin Homo sapiens 145-152 16478778-1 2006 Minimal model analysis of intravenous glucose tolerance test (IVGTT) glucose and insulin concentrations offers a validated approach to measuring insulin sensitivity, but model identification is not always successful. Glucose 69-76 insulin Homo sapiens 145-152 16464907-6 2006 Insulin sensitivity was assessed by measurement of whole body glucose uptake with the stable isotope tracer method during a euglycemic hyperinsulinemic clamp (20 mU.min(-1).kg(-1)), which was initiated 1 h after the IL-6-TNF-saline infusion. Glucose 62-69 insulin Homo sapiens 0-7 16464907-9 2006 Whole body insulin-mediated glucose uptake was significantly reduced during TNF infusion but remained unchanged during IL-6 infusion. Glucose 28-35 insulin Homo sapiens 11-18 16478780-7 2006 In both fiber types, basal and insulin-stimulated glucose oxidation were not significantly altered by metformin. Glucose 50-57 insulin Homo sapiens 31-38 16464907-11 2006 We conclude that TNF-induced insulin resistance of whole body glucose uptake is associated with increased IL-18 gene expression in muscle tissue, indicating that TNF and IL-18 interact, and both may have important regulatory roles in the pathogenesis of insulin resistance. Glucose 62-69 insulin Homo sapiens 29-36 16489105-0 2006 AMPK activation restores the stimulation of glucose uptake in an in vitro model of insulin-resistant cardiomyocytes via the activation of protein kinase B. Glucose 44-51 insulin Homo sapiens 83-90 16489105-4 2006 In this work, we studied the relationship between AMPK activation and glucose uptake stimulation by biguanides and oligomycin, another AMPK activator, in both insulin-sensitive and insulin-resistant cardiomyocytes. Glucose 70-77 insulin Homo sapiens 159-166 16464907-11 2006 We conclude that TNF-induced insulin resistance of whole body glucose uptake is associated with increased IL-18 gene expression in muscle tissue, indicating that TNF and IL-18 interact, and both may have important regulatory roles in the pathogenesis of insulin resistance. Glucose 62-69 insulin Homo sapiens 254-261 16489105-5 2006 In insulin-sensitive cardiomyocytes, insulin, biguanides and oligomycin were able to stimulate glucose uptake with the same efficiency. Glucose 95-102 insulin Homo sapiens 3-10 16489105-5 2006 In insulin-sensitive cardiomyocytes, insulin, biguanides and oligomycin were able to stimulate glucose uptake with the same efficiency. Glucose 95-102 insulin Homo sapiens 37-44 16489105-9 2006 Finally, an adenoviral-mediated expression of a constitutively active form of AMPK increased both PKB phosphorylation and glucose uptake in insulin-resistant cardiomyocytes. Glucose 122-129 insulin Homo sapiens 140-147 16489105-6 2006 Stimulation of glucose uptake by insulin or biguanides was correlated to protein kinase B (PKB) or AMPK activation, respectively, and were additive. Glucose 15-22 insulin Homo sapiens 33-40 16489105-7 2006 In insulin-resistant cardiomyocytes, where insulin stimulation of glucose uptake was greatly reduced, biguanides or oligomycin, in the absence of insulin, induced a higher stimulation of glucose uptake than that obtained in insulin-sensitive cells. Glucose 66-73 insulin Homo sapiens 43-50 16489105-7 2006 In insulin-resistant cardiomyocytes, where insulin stimulation of glucose uptake was greatly reduced, biguanides or oligomycin, in the absence of insulin, induced a higher stimulation of glucose uptake than that obtained in insulin-sensitive cells. Glucose 66-73 insulin Homo sapiens 43-50 16489105-10 2006 We concluded that AMPK activators, like biguanides and oligomycin, are able to restore glucose uptake stimulation, in the absence of insulin, in insulin-resistant cardiomyocytes via the additive activation of AMPK and PKB. Glucose 87-94 insulin Homo sapiens 145-152 16489105-7 2006 In insulin-resistant cardiomyocytes, where insulin stimulation of glucose uptake was greatly reduced, biguanides or oligomycin, in the absence of insulin, induced a higher stimulation of glucose uptake than that obtained in insulin-sensitive cells. Glucose 66-73 insulin Homo sapiens 43-50 17061445-14 2006 In oral glucose tolerance test, areas under the curve of insulin and glucose are significantly higher in PCOS patients with hypertension (respectively p = 0.06 and 0.02). Glucose 8-15 insulin Homo sapiens 57-64 16760337-2 2006 Adrenomedullin (1-100 pM) inhibited insulin secretion at both basal (3 mM) and high (15 mM) glucose concentrations, although this inhibitory effect was not observed at higher concentrations of adrenomedullin. Glucose 92-99 insulin Homo sapiens 36-43 16760337-3 2006 The inhibition of glucose-induced insulin secretion by adrenomedullin was restored with 12-h pretreatment with 1 microg/ml pertussis toxin (PTX), suggesting that this effect could be mediated by PTX-sensitive G proteins. Glucose 18-25 insulin Homo sapiens 34-41 16903823-6 2006 Exploring the molecular mechanisms and pathways by which PKCzeta mediates glucose transport will highlight the insulin-signaling pathway. Glucose 74-81 insulin Homo sapiens 111-118 16814735-1 2006 Type 2 diabetes is associated with defects in insulin signaling and the resulting abnormal glucose and lipid metabolism. Glucose 91-98 insulin Homo sapiens 46-53 16616054-9 2006 CONCLUSIONS: Glucose uptake, in response to insulin or ischemia, was lower in the chronically infarcted rat heart and associated with increased circulating FFA concentrations and decreased GLUT4 levels. Glucose 13-20 insulin Homo sapiens 44-51 16705481-9 2006 Diet-induced changes in SNS activity are regulated by insulin-mediated glucose uptake and metabolism in central neurons sensitive to insulin and located anatomically in the ventro-medial hypothalamus. Glucose 71-78 insulin Homo sapiens 54-61 16705481-9 2006 Diet-induced changes in SNS activity are regulated by insulin-mediated glucose uptake and metabolism in central neurons sensitive to insulin and located anatomically in the ventro-medial hypothalamus. Glucose 71-78 insulin Homo sapiens 133-140 16778577-6 2006 Finally, numerous data have demonstrated the modulation of glucose sensing by other nutrients, in particular fatty acids, hormones (insulin, leptin and ghrelin) and peptides (neuropeptide Y). Glucose 59-66 insulin Homo sapiens 132-139 16814735-7 2006 Unraveling the isoform-specific regulation of glucose and lipid metabolism by key elements along insulin signaling cascades through siRNA-mediated gene silencing in human tissues will facilitate the discovery of novel targets for the treatment of diabetes and related metabolic disorders. Glucose 46-53 insulin Homo sapiens 97-104 16817815-0 2006 Growth hormone and insulin-like growth factor binding protein-1 responses to oral glucose in patients with primary hyperparathyroidism. Glucose 82-89 insulin Homo sapiens 19-26 16776752-9 2006 Two-hour postprandial glucose values (for all three meals) and predinner glucose values were significantly less with IMT than with insulin glargine (p = 0.0034, 0.0001, 0.0066 and 0.0205). Glucose 22-29 insulin Homo sapiens 131-138 16538487-8 2006 Overall, patients with haemochromatosis and control subjects had similar values for acute insulin response to glucose and insulin sensitivity. Glucose 110-117 insulin Homo sapiens 90-97 16538487-9 2006 However, patients with haemochromatosis and IGT had a 68% decrease in acute insulin response to glucose (p<0.02) compared with those with NGT. Glucose 96-103 insulin Homo sapiens 76-83 16538487-11 2006 Haemochromatosis subjects with diabetes exhibited further declines in acute insulin response to glucose, insulin resistance, or both. Glucose 96-103 insulin Homo sapiens 76-83 16752186-5 2006 Insulin sensitivity was measured using the glucose clamp technique. Glucose 43-50 insulin Homo sapiens 0-7 16752186-12 2006 The relationship between adiponectin and insulin sensitivity was related to the decreased insulin regulation of glucose utilisation (r=0.55, p<0.001) but not of endogenous hepatic glucose production. Glucose 112-119 insulin Homo sapiens 41-48 16752186-12 2006 The relationship between adiponectin and insulin sensitivity was related to the decreased insulin regulation of glucose utilisation (r=0.55, p<0.001) but not of endogenous hepatic glucose production. Glucose 112-119 insulin Homo sapiens 90-97 16776753-12 2006 CONCLUSIONS: Moxonidine improved insulin sensitivity in response to glucose challenge in patients with evidence of metabolic syndrome. Glucose 68-75 insulin Homo sapiens 33-40 16752186-15 2006 The adiponectin changes relate to decreased insulin sensitivity of glucose disposal rather than alterations of lipid metabolism. Glucose 67-74 insulin Homo sapiens 44-51 16801571-0 2006 Continuous glucose monitoring-guided insulin adjustment in children and adolescents on near-physiological insulin regimens: a randomized controlled trial. Glucose 11-18 insulin Homo sapiens 37-44 16801587-5 2006 Early-phase insulin secretion was calculated as the ratio between the incremental plasma insulin and glucose concentrations during the first 30 min of the OGTT (DeltaI(0-30)/DeltaG(0-30)). Glucose 101-108 insulin Homo sapiens 12-19 16801587-6 2006 Total insulin secretion was calculated as the ratio between the incremental areas under the insulin and glucose curves during the OGTT [DeltaG(AUC)/DeltaI(AUC)]. Glucose 104-111 insulin Homo sapiens 6-13 16801587-11 2006 CONCLUSIONS: Subjects whose postload plasma glucose concentration returned to baseline (i.e., FPG level) more quickly had greater insulin sensitivity, a higher insulinogenic index, and a lower risk of developing type 2 diabetes after 8 years of follow-up compared with subjects whose postload glucose concentration returned to baseline more slowly. Glucose 44-51 insulin Homo sapiens 130-137 16801571-0 2006 Continuous glucose monitoring-guided insulin adjustment in children and adolescents on near-physiological insulin regimens: a randomized controlled trial. Glucose 11-18 insulin Homo sapiens 106-113 16801571-1 2006 OBJECTIVE: This randomized controlled trial assesses the effect on glycemic control of continuous glucose monitoring system (CGMS)-guided insulin therapy adjustment in young people with type 1 diabetes on intensive diabetes treatment regimens with continuous subcutaneous insulin infusion (CSII) or glargine. Glucose 98-105 insulin Homo sapiens 138-145 16804071-3 2006 Fasting plasma IL-6 concentration was negatively correlated with the rate of insulin-stimulated glucose disposal (M) (P = 0.001). Glucose 96-103 insulin Homo sapiens 77-84 16873591-2 2006 METHODS: The algorithm recommended specific doses of oral agents and insulin based on a patient"s medications and glucose or A1C levels at the time of the visit. Glucose 114-121 insulin Homo sapiens 69-76 16804071-7 2006 To estimate the independent contribution of plasma IL-6 levels to AIR, we carried out forward stepwise linear regression analysis in a model that included sex, age, BMI, waist-to-hip ratio, FFAs, and insulin-stimulated glucose disposal. Glucose 219-226 insulin Homo sapiens 200-207 16842476-0 2006 Insulin detemir lowers the risk of hypoglycaemia and provides more consistent plasma glucose levels compared with NPH insulin in Type 1 diabetes. Glucose 85-92 insulin Homo sapiens 0-7 16574795-10 2006 Thus, in skeletal myotubes, FAK regulates the insulin-mediated cytoskeletal rearrangement essential for normal glucose transport and glycogen synthesis. Glucose 111-118 insulin Homo sapiens 46-53 16905514-7 2006 Although the reasons for this are not clear, one study showed that patients with diabetes were more likely to receive insulin for any given blood glucose level. Glucose 146-153 insulin Homo sapiens 118-125 16905516-5 2006 Results from implementing this program have included a reduction in the average glucose level in the medical intensive care unit through use of protocols driven to initiate intravenous insulin once the glucose level exceeds 140 mg/dL. Glucose 80-87 insulin Homo sapiens 185-192 16905516-5 2006 Results from implementing this program have included a reduction in the average glucose level in the medical intensive care unit through use of protocols driven to initiate intravenous insulin once the glucose level exceeds 140 mg/dL. Glucose 202-209 insulin Homo sapiens 185-192 16899796-5 2006 RESULTS: Cholesterol synthesis markers correlated positively with IAF (r = 0.213 to 0.309, p < or = 0.027) and negatively with the rates of insulin-stimulated whole-body glucose uptake (r = -0.372 to -0.248, p < or = 0.010). Glucose 173-180 insulin Homo sapiens 143-150 16805937-5 2006 For the next 6 months blood glucose level was reduced with intensive insulin therapy (aim 4.4 < BG < 6.1 mmol L-1); 271 patients were included. Glucose 28-35 insulin Homo sapiens 69-76 16723378-2 2006 The present study investigated whether MG, a highly reactive metabolite of glucose, induced structural and functional changes of insulin. Glucose 75-82 insulin Homo sapiens 129-136 16750207-8 2006 RESULT(S): Insulin-induced glucose disposal was reduced by approximately 20% after treatment with testosterone alone, and after the combined treatment, but not by estrogen alone. Glucose 27-34 insulin Homo sapiens 11-18 30290456-2 2006 In pancreatic beta cells, free fatty acids potentiate glucose-stimulated insulin secretion precisely to the extent needed to compensate for the free fatty acid-induced insulin resistance. Glucose 54-61 insulin Homo sapiens 73-80 30290463-0 2006 Rapid-acting insulin glulisine: a new tool for postprandial glucose control. Glucose 60-67 insulin Homo sapiens 13-20 30290463-5 2006 Insulin glulisine is safe when used for pump therapy and its rapid-acting properties are maintained consistently across patient types and body mass indices, making it an effective and versatile tool for postprandial glucose control. Glucose 216-223 insulin Homo sapiens 0-7 16873964-1 2006 Glucose uptake and energy metabolism in the brain are regulated by insulin and insulin-like growth factors (IGF). Glucose 0-7 insulin Homo sapiens 67-74 16873964-1 2006 Glucose uptake and energy metabolism in the brain are regulated by insulin and insulin-like growth factors (IGF). Glucose 0-7 insulin Homo sapiens 79-86 16877762-1 2006 Insulin is stored in pancreatic beta cell granules, and released biphasically by the exocytotic mechanism induced by nutrient glucose. Glucose 126-133 insulin Homo sapiens 0-7 16877762-2 2006 Insulin exocytosis must be critically regulated to finely control body glucose homeostasis because insulin is the only hormone that can promptly reduce the blood glucose level. Glucose 71-78 insulin Homo sapiens 0-7 16877762-2 2006 Insulin exocytosis must be critically regulated to finely control body glucose homeostasis because insulin is the only hormone that can promptly reduce the blood glucose level. Glucose 71-78 insulin Homo sapiens 99-106 16877762-2 2006 Insulin exocytosis must be critically regulated to finely control body glucose homeostasis because insulin is the only hormone that can promptly reduce the blood glucose level. Glucose 162-169 insulin Homo sapiens 0-7 16877762-2 2006 Insulin exocytosis must be critically regulated to finely control body glucose homeostasis because insulin is the only hormone that can promptly reduce the blood glucose level. Glucose 162-169 insulin Homo sapiens 99-106 16877762-3 2006 Recent advanced techniques in molecular biology and electrophysiology revealed the molecular mechanism of insulin release in the process from glucose entry to increased [Ca(2+)](i). Glucose 142-149 insulin Homo sapiens 106-113 16621911-4 2006 OBJECTIVE: Our objective was to reveal the effect of ghrelin on insulin-mediated glucose disposal in gastrectomized patients. Glucose 81-88 insulin Homo sapiens 64-71 17679813-5 2006 Insulin and glucose were used in equations to estimate insulin sensitivity. Glucose 12-19 insulin Homo sapiens 55-62 17679820-3 2006 Obese and insulin-resistant individuals display elevated intramuscular lipids, impaired vasculature function, decreased fatty add oxidation during fasting, and reduced postprandial glucose metabolism. Glucose 181-188 insulin Homo sapiens 10-17 16772509-1 2006 Insulin is a major regulatory hormone in glucose and fat metabolism, vascular function, inflammation, tissue remodeling, and the somatotropic axis of growth. Glucose 41-48 insulin Homo sapiens 0-7 16772509-3 2006 In humans, altered insulin signaling is implicated in reduced glucose availability to insulin-sensitive cells, vasoconstriction and endothelial damage, and inflammatory response. Glucose 62-69 insulin Homo sapiens 19-26 16772509-3 2006 In humans, altered insulin signaling is implicated in reduced glucose availability to insulin-sensitive cells, vasoconstriction and endothelial damage, and inflammatory response. Glucose 62-69 insulin Homo sapiens 86-93 16819705-2 2006 In this situation close glucose monitoring is essential for adequate insulin treatment. Glucose 24-31 insulin Homo sapiens 69-76 16784958-9 2006 Serum glucose and glycoalbumin levels were substantially decreased by insulin treatment. Glucose 6-13 insulin Homo sapiens 70-77 16838661-3 2006 Recent evidence suggests that insulin action in the brain also plays an important role in the regulation of glucose metabolism in the liver. Glucose 108-115 insulin Homo sapiens 30-37 16838661-4 2006 Insulin signaling in pancreatic beta cells appears to regulate glucose-induced insulin secretion. Glucose 63-70 insulin Homo sapiens 0-7 16061274-4 2006 In recent years, development of a range of insulin analogs has led to better control of glucose levels, thus preventing secondary complications and improving the quality of life in diabetic patients. Glucose 88-95 insulin Homo sapiens 43-50 16916571-1 2006 Insulin is best known for its role in peripheral glucose homeostasis. Glucose 49-56 insulin Homo sapiens 0-7 16829342-7 2006 CONCLUSION: The onset of MS during the menopause is associated with a physiological shift in insulin resistance occurring even in normal glucose tolerant subjects, suggesting that it may depend upon critical metabolic changes occurring specifically in that age period. Glucose 137-144 insulin Homo sapiens 93-100 16985482-14 2006 CONCLUSION: A fasting glucose to insulin ratio is a simple and useful test for identifying insulin-resistant obese women with PCOS. Glucose 22-29 insulin Homo sapiens 33-40 16985482-14 2006 CONCLUSION: A fasting glucose to insulin ratio is a simple and useful test for identifying insulin-resistant obese women with PCOS. Glucose 22-29 insulin Homo sapiens 91-98 16904045-4 2006 Therefore, a modification in anyone of the proteins involved in the insulin signaling, can take place a dysfunction in the glucose metabolism. Glucose 123-130 insulin Homo sapiens 68-75 16904045-5 2006 The impaired glucose can be due because there are many proteins, ions and enzymes that participate in the downstream pathways of the insulin signaling, it has become difficult to find a single phatophysiologic level as cause of diabetes. Glucose 13-20 insulin Homo sapiens 133-140 16777491-4 2006 The effect of PPAR gamma activation is to enhance the action of insulin in insulin-sensitive tissue by increasing peripheral glucose disposal and decreasing hepatic glucose production. Glucose 125-132 insulin Homo sapiens 64-71 16777491-4 2006 The effect of PPAR gamma activation is to enhance the action of insulin in insulin-sensitive tissue by increasing peripheral glucose disposal and decreasing hepatic glucose production. Glucose 125-132 insulin Homo sapiens 75-82 16777491-4 2006 The effect of PPAR gamma activation is to enhance the action of insulin in insulin-sensitive tissue by increasing peripheral glucose disposal and decreasing hepatic glucose production. Glucose 165-172 insulin Homo sapiens 64-71 16777491-4 2006 The effect of PPAR gamma activation is to enhance the action of insulin in insulin-sensitive tissue by increasing peripheral glucose disposal and decreasing hepatic glucose production. Glucose 165-172 insulin Homo sapiens 75-82 16768722-4 2006 RESULTS: High glucose concentration and glucagon-like peptide 1 (GLP-1) were associated with maintenance either of insulin secretory patterns from the incubated cell monolayers, or expression of transcriptional markers associated with beta-cell like phenotypes. Glucose 14-21 insulin Homo sapiens 115-122 16644736-0 2006 Repletion of atypical protein kinase C following RNA interference-mediated depletion restores insulin-stimulated glucose transport. Glucose 113-120 insulin Homo sapiens 94-101 16644736-1 2006 The role of atypical protein kinase C (aPKC) in insulin-stimulated glucose transport in myocytes and adipocytes is controversial. Glucose 67-74 insulin Homo sapiens 48-55 16644736-3 2006 Moreover, there are no reports of aPKC knockdown in myocytes, wherein insulin effects on glucose transport are particularly relevant for understanding whole body glucose disposal. Glucose 89-96 insulin Homo sapiens 70-77 16644736-3 2006 Moreover, there are no reports of aPKC knockdown in myocytes, wherein insulin effects on glucose transport are particularly relevant for understanding whole body glucose disposal. Glucose 162-169 insulin Homo sapiens 70-77 16644736-6 2006 Accordingly, in L6 myotubes, RNAi-targeting PKC-zeta, but not PKC-lambda, markedly depleted aPKC and concomitantly inhibited insulin-stimulated glucose transport; more importantly, these depleting/inhibitory effects were rescued by adenovirally mediated expression of PKC-lambda. Glucose 144-151 insulin Homo sapiens 125-132 16644736-7 2006 Conversely, in 3T3/L1 adipocytes, RNAi constructs targeting PKC-lambda, but not PKC-zeta, markedly depleted aPKC and concomitantly inhibited insulin-stimulated glucose transport; here again, these depleting/inhibitory effects were rescued by adenovirally mediated expression of PKC-zeta. Glucose 160-167 insulin Homo sapiens 141-148 16644736-8 2006 These findings in knockdown and, more convincingly, rescue studies, strongly support the hypothesis that aPKCs are required for insulin-stimulated glucose transport in myocytes and adipocytes. Glucose 147-154 insulin Homo sapiens 128-135 16813735-2 2006 This question is highly relevant, since earlier targeted glycemic control trials utilizing conventional glucose-lowering strategies that increase insulin levels have generally failed to reduce CAD risk despite markedly reducing microvascular risk. Glucose 104-111 insulin Homo sapiens 146-153 16631207-1 2006 Insulin resistance (reduced ability of insulin to stimulate glucose utilization) is common in North American and Europe, where as many as one third of all older adults suffer from prodromal or clinical type 2 diabetes mellitus. Glucose 60-67 insulin Homo sapiens 0-7 16631207-1 2006 Insulin resistance (reduced ability of insulin to stimulate glucose utilization) is common in North American and Europe, where as many as one third of all older adults suffer from prodromal or clinical type 2 diabetes mellitus. Glucose 60-67 insulin Homo sapiens 39-46 16730838-10 2006 Animal studies showed that plasma glucose level was effectively reduced when liposomal insulin was delivered by inhalation route of using aerosolized insulin-encapsulated liposomes. Glucose 34-41 insulin Homo sapiens 87-94 16730838-10 2006 Animal studies showed that plasma glucose level was effectively reduced when liposomal insulin was delivered by inhalation route of using aerosolized insulin-encapsulated liposomes. Glucose 34-41 insulin Homo sapiens 150-157 16403776-6 2006 When glucose was ingested after exercise (ExGLU), glucose, insulin, VIP, gastrin, GLP-1, and GIP were all increased (P < 0.01). Glucose 5-12 insulin Homo sapiens 59-66 16403776-11 2006 In summary, when glucose is ingested after prolonged exercise, there is mild insulin resistance and a corresponding rapid transitory increase in plasma VIP. Glucose 17-24 insulin Homo sapiens 77-84 16449302-8 2006 Despite this, glucose Rd was reduced during afternoon hypoglycemia following morning hypoglycemia, indicating posthypoglycemic insulin resistance. Glucose 14-21 insulin Homo sapiens 127-134 16531507-9 2006 Addition of recombinant omentin in vitro did not affect basal but enhanced insulin-stimulated glucose uptake in both sc (47%, n = 9, P = 0.003) and omental (approximately 30%, n = 3, P < 0.05) human adipocytes. Glucose 94-101 insulin Homo sapiens 75-82 16638603-5 2006 CONCLUSION: Homeostasis model assessment, quick insulin sensitivity check index, and fasting glucose are sensitive screening tests for gestational diabetes mellitus and can avoid oral administration of glucose-containing solutions. Glucose 202-209 insulin Homo sapiens 48-55 16762930-1 2006 Values of insulin-mediated glucose disposal vary continuously throughout a population of apparently healthy persons, and a difference of > or = 600% exists between the most insulin-sensitive and the most insulin-resistant persons. Glucose 27-34 insulin Homo sapiens 10-17 16762930-1 2006 Values of insulin-mediated glucose disposal vary continuously throughout a population of apparently healthy persons, and a difference of > or = 600% exists between the most insulin-sensitive and the most insulin-resistant persons. Glucose 27-34 insulin Homo sapiens 176-183 16762930-1 2006 Values of insulin-mediated glucose disposal vary continuously throughout a population of apparently healthy persons, and a difference of > or = 600% exists between the most insulin-sensitive and the most insulin-resistant persons. Glucose 27-34 insulin Homo sapiens 176-183 16762930-3 2006 The more insulin-resistant a person, the more likely that he or she will develop some degree of glucose intolerance, high triacylglycerol and low HDL concentrations, essential hypertension, and procoagulant and proinflammatory states, all of which increase the risk of cardiovascular disease (CVD). Glucose 96-103 insulin Homo sapiens 9-16 16762941-9 2006 The insulin response was significantly related to the glucose response (r = 0.94, P = 0.005). Glucose 54-61 insulin Homo sapiens 4-11 16390860-0 2006 Dose-responsive insulin regulation of glucose transport in human skeletal muscle. Glucose 38-45 insulin Homo sapiens 16-23 16390860-1 2006 Glucose transport is regarded as the principal rate control step governing insulin-stimulated glucose utilization by skeletal muscle. Glucose 94-101 insulin Homo sapiens 75-82 16390860-10 2006 In summary, in healthy volunteers there is robust dose-responsive insulin stimulation of glucose transport in skeletal muscle. Glucose 89-96 insulin Homo sapiens 66-73 16772152-9 2006 Ovulatory PCOS patients with altered glucose tolerance and/or with dyslipidaemia may need treatment with insulin-sensitizing agents. Glucose 37-44 insulin Homo sapiens 105-112 16480697-3 2006 The most fundamental defect in these patients is resistance to cellular actions of insulin, particularly resistance to insulin-stimulated glucose uptake. Glucose 138-145 insulin Homo sapiens 83-90 16480697-3 2006 The most fundamental defect in these patients is resistance to cellular actions of insulin, particularly resistance to insulin-stimulated glucose uptake. Glucose 138-145 insulin Homo sapiens 119-126 16480697-4 2006 Insulin insensitivity appears to cause hyperinsulinemia, enhanced hepatic gluconeogenesis and glucose output, reduced suppression of lipolysis in adipose tissue leading to a high free fatty acid flux, and increased hepatic very low density lipoprotein (VLDL) secretion causing hypertriglyceridemia and reduced plasma levels of high density lipoprotein (HDL) cholesterol. Glucose 94-101 insulin Homo sapiens 0-7 16712665-6 2006 RESULTS: Correlations between the rate of glucose disappearance (G(Rd)) (the gold standard) and the HOMA-derived metabolic parameters of insulin sensitivity were significant, with a multiple R(2) of 43.5% (P = 0.003). Glucose 42-49 insulin Homo sapiens 137-144 16712665-10 2006 CONCLUSIONS: HOMA estimation of insulin resistance is appropriate for use during both the second and third trimesters of pregnancy and postpartum in obese women with normal glucose tolerance. Glucose 173-180 insulin Homo sapiens 32-39 16337067-11 2006 Hyperglycemia was seen in 61% (55/90) of the patients and insulin was administered to 53% (29/55) at an average glucose level of 19+/-3 mmol/l. Glucose 112-119 insulin Homo sapiens 58-65 18340223-2 2006 Normalization of blood glucose levels using intensive insulin infusion protocols improves clinical outcomes. Glucose 23-30 insulin Homo sapiens 54-61 16898570-2 2006 Hypothalamic centers involved in the regulation of energy balance and endogenous glucose production constantly sense fuel availability by receiving and integrating inputs from circulating nutrients and hormones such as insulin and leptin. Glucose 81-88 insulin Homo sapiens 219-226 16898571-1 2006 The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion from pancreatic beta cells. Glucose 157-164 insulin Homo sapiens 176-183 16439034-4 2006 The glucose infusion rate during hyperinsulinemic euglycemic clamp was 2.84 mg/kg/min, suggesting a high level of insulin resistance. Glucose 4-11 insulin Homo sapiens 38-45 16596361-0 2006 Differential effects of monounsaturated, polyunsaturated and saturated fat ingestion on glucose-stimulated insulin secretion, sensitivity and clearance in overweight and obese, non-diabetic humans. Glucose 88-95 insulin Homo sapiens 107-114 16596361-1 2006 AIMS/HYPOTHESIS: Prolonged elevation of plasma specific fatty acids may exert differential effects on glucose-stimulated insulin secretion (GSIS), insulin sensitivity and clearance. Glucose 102-109 insulin Homo sapiens 121-128 16609880-6 2006 Plasma adiponectin was positively associated with insulin-stimulated glucose disposal (r = 0.48), glucose oxidation (r = 0.54), respiratory quotient (r = 0.58) and non-oxidative glucose metabolism (r = 0.38), and negatively associated with lipid oxidation during insulin stimulation (r = -0.60) after adjustment for body fat (all p < 0.01). Glucose 69-76 insulin Homo sapiens 50-57 16609880-8 2006 CONCLUSIONS/INTERPRETATION: Our results indicate that plasma adiponectin may enhance insulin sensitivity by improving the capacity to switch from lipid to glucose oxidation and to store glucose as glycogen in response to insulin, and that low adiponectin may contribute to impaired insulin activation of GS in skeletal muscle of patients with type 2 diabetes. Glucose 155-162 insulin Homo sapiens 85-92 16731816-10 2006 Therefore, the joint action of basal insulin production and glucokinase activity may generate a "glucose sensor" in skeletal muscle that allows proper regulation of glycemia in diabetic animals and thus prevents secondary complications. Glucose 97-104 insulin Homo sapiens 37-44 16731846-7 2006 The differential effects of hyperglycemia and hyperinsulinemia suggest that patients with hyperglycemia due to insulin resistance are especially susceptible to thrombotic events by a concurrent insulin-driven impairment of fibrinolysis and a glucose-driven activation of coagulation. Glucose 242-249 insulin Homo sapiens 51-58 16759282-5 2006 Also, the addition of glucose to the culture medium triggered insulin release from differentiated cells, but transmission electron microscopy of the differentiated cells did not show typical beta-cell granules, even though secretary granules were detected. Glucose 22-29 insulin Homo sapiens 62-69 16799402-8 2006 CONCLUSION: Surrogate measures of insulin resistance, in particular fasting insulin, are simple tools appropriate for epidemiological studies that can be used as substitutes for the EH clamp to estimate glucose disposal and cardiovascular risk factors in overweight and obese postmenopausal women. Glucose 203-210 insulin Homo sapiens 34-41 16799402-8 2006 CONCLUSION: Surrogate measures of insulin resistance, in particular fasting insulin, are simple tools appropriate for epidemiological studies that can be used as substitutes for the EH clamp to estimate glucose disposal and cardiovascular risk factors in overweight and obese postmenopausal women. Glucose 203-210 insulin Homo sapiens 76-83 16800754-0 2006 Evaluation of the accuracy of a microdialysis-based glucose sensor during insulin-induced hypoglycemia, its recovery, and post-hypoglycemic hyperglycemia in humans. Glucose 52-59 insulin Homo sapiens 74-81 16800755-7 2006 RESULTS: Correlation between model-based insulin sensitivity, SI, and ISIG (ISI normalized by steady-state glucose) is r = 0.99 (n = 60) at steady state and r = 0.97 at transient state, respectively. Glucose 107-114 insulin Homo sapiens 41-48 16513829-8 2006 Chronic treatment with insulin for 18 h led to down-regulation of insulin-stimulated glucose transport. Glucose 85-92 insulin Homo sapiens 23-30 16513829-8 2006 Chronic treatment with insulin for 18 h led to down-regulation of insulin-stimulated glucose transport. Glucose 85-92 insulin Homo sapiens 66-73 16527842-0 2006 Diphenylhydantoin suppresses glucose-induced insulin release by decreasing cytoplasmic H+ concentration in pancreatic islets. Glucose 29-36 insulin Homo sapiens 45-52 16527842-1 2006 Diphenylhydantoin (DPH), which is clinically used in the treatment of epilepsy, inhibits glucose-induced insulin release from pancreatic islets by a mechanism that remains unknown. Glucose 89-96 insulin Homo sapiens 105-112 16527842-2 2006 In the present study, DPH is shown to suppress glucose-induced insulin release concentration-dependently. Glucose 47-54 insulin Homo sapiens 63-70 16527842-4 2006 DPH also suppressed insulin release in the presence of 16.7 mm glucose, 200 microm diazoxide, and 30 mm K+ without affecting the intracellular Ca2+ concentration. Glucose 63-70 insulin Homo sapiens 20-27 16556766-3 2006 In the pancreatic beta-cell, glucose carbons are quantitatively funneled to the mitochondria, where signals for the initiation and potentiation of insulin secretion are generated. Glucose 29-36 insulin Homo sapiens 147-154 16556766-6 2006 Patients with mitochondrial diabetes and a corresponding mouse model display defective glucose-stimulated insulin secretion and reduced beta-cell mass, leading to overt diabetes. Glucose 87-94 insulin Homo sapiens 106-113 16702775-1 2006 In skeletal muscle and adipose tissue, insulin-stimulated glucose uptake is dependent upon translocation of the insulin-responsive glucose transporter GLUT4 from intracellular storage compartments to the plasma membrane. Glucose 58-65 insulin Homo sapiens 39-46 16702775-1 2006 In skeletal muscle and adipose tissue, insulin-stimulated glucose uptake is dependent upon translocation of the insulin-responsive glucose transporter GLUT4 from intracellular storage compartments to the plasma membrane. Glucose 58-65 insulin Homo sapiens 112-119 16985482-0 2006 The frequency of insulin resistance calculated upon the basis of a fasting glucose to insulin ratio and characteristics of insulin resistant women with polycystic ovary syndrome. Glucose 75-82 insulin Homo sapiens 17-24 16985482-3 2006 A fasting glucose to insulin (G/I) ratio is a simple, reliable, sensitive and specific measurement of insulin sensitivity and is a useful test for the identification of IR in women with PCOS, who have to be treated with insulin sensitizers. Glucose 10-17 insulin Homo sapiens 21-34 16985482-3 2006 A fasting glucose to insulin (G/I) ratio is a simple, reliable, sensitive and specific measurement of insulin sensitivity and is a useful test for the identification of IR in women with PCOS, who have to be treated with insulin sensitizers. Glucose 10-17 insulin Homo sapiens 21-28 16985482-3 2006 A fasting glucose to insulin (G/I) ratio is a simple, reliable, sensitive and specific measurement of insulin sensitivity and is a useful test for the identification of IR in women with PCOS, who have to be treated with insulin sensitizers. Glucose 10-17 insulin Homo sapiens 102-109 16684128-5 2006 Disposition index (DI) was calculated as insulin sensitivity (Si(RD)) multiplied by the first-phase insulin response to intravenous glucose. Glucose 132-139 insulin Homo sapiens 100-107 16684128-9 2006 Incremental IP + SP/insulin ratio after an intravenous glucose bolus correlated inversely with DI (P < 0.01), but did not differ between study groups. Glucose 55-62 insulin Homo sapiens 20-27 16722815-2 2006 Exenatide is an incretin mimetic that improves glycaemic control in patients with diabetes through acute mechanisms, such as glucose-dependent stimulation of insulin secretion, suppression of inappropriate glucagon secretion and slowing of gastric emptying, as well as chronic mechanisms that include enhancement of beta-cell mass in rodent studies and weight loss and inhibition of food intake in humans. Glucose 125-132 insulin Homo sapiens 158-165 16905822-3 2006 Introduced as Syndrome X by Reaven in 1988 and also termed insulin resistance syndrome, metabolic syndrome is recognized clinically by the findings of abdominal obesity, elevated triglycerides, atherogenic dyslipidemia - i.e. low levels of high-density lipoprotein cholesterol (HDL-C), elevated blood pressure, high blood glucose and/or insulin resistance. Glucose 322-329 insulin Homo sapiens 59-66 16766777-1 2006 BACKGROUND: Acute exercise is associated with increased insulin sensitivity characterized by increased insulin-induced glucose transport for periods of up to 48 h after the bout of exercise. Glucose 119-126 insulin Homo sapiens 56-63 16766777-1 2006 BACKGROUND: Acute exercise is associated with increased insulin sensitivity characterized by increased insulin-induced glucose transport for periods of up to 48 h after the bout of exercise. Glucose 119-126 insulin Homo sapiens 103-110 16886777-0 2006 [Insulin sensitivity and beta cell function in different glucose tolerance status]. Glucose 57-64 insulin Homo sapiens 1-8 16886777-13 2006 In conclusion, the decrease of glucose tolerance was associated with the lowering of Insulin Sensitivity (IS). Glucose 31-38 insulin Homo sapiens 85-92 16569741-5 2006 INTERVENTION: We performed an insulin-modified frequently sampled iv glucose tolerance test to measure insulin sensitivity (S(I)), glucose effectiveness, and free fatty acid (FFA) dynamics. Glucose 69-76 insulin Homo sapiens 30-37 16569741-9 2006 The acute insulin response to glucose and the disposition index (D(I) = acute insulin response to glucose x S(I)) were significantly lower in the islet transplant group, compared with the control group (P < 0.05 for all comparisons). Glucose 30-37 insulin Homo sapiens 10-17 16569741-9 2006 The acute insulin response to glucose and the disposition index (D(I) = acute insulin response to glucose x S(I)) were significantly lower in the islet transplant group, compared with the control group (P < 0.05 for all comparisons). Glucose 98-105 insulin Homo sapiens 78-85 16595595-1 2006 CONTEXT: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease. Glucose 55-62 insulin Homo sapiens 16-23 16595595-1 2006 CONTEXT: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease. Glucose 55-62 insulin Homo sapiens 117-124 16595595-1 2006 CONTEXT: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease. Glucose 140-147 insulin Homo sapiens 16-23 16595595-1 2006 CONTEXT: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease. Glucose 140-147 insulin Homo sapiens 117-124 16595595-2 2006 OBJECTIVE: This study aimed to assess the counterregulatory impact of the insulin-induced fall of glucose on minimal model-derived indices of insulin sensitivity (S(I)) and glucose effectiveness. Glucose 98-105 insulin Homo sapiens 74-81 16595595-2 2006 OBJECTIVE: This study aimed to assess the counterregulatory impact of the insulin-induced fall of glucose on minimal model-derived indices of insulin sensitivity (S(I)) and glucose effectiveness. Glucose 98-105 insulin Homo sapiens 142-149 16595595-2 2006 OBJECTIVE: This study aimed to assess the counterregulatory impact of the insulin-induced fall of glucose on minimal model-derived indices of insulin sensitivity (S(I)) and glucose effectiveness. Glucose 173-180 insulin Homo sapiens 74-81 16595597-12 2006 After 24-h exposure to high (16.7 mmol/liter) glucose concentration, impairment of glibenclamide-induced insulin release was significantly (P = 0.01) worse with the E23K variant. Glucose 46-53 insulin Homo sapiens 105-112 16840831-8 2006 In males, age (beta=0.19, p<0.001) and insulin (beta=0.18, p<0.001) were independently associated with fasting glucose levels; and waist circumference (beta=0.17, p<0.001), triglycerides (beta=0.16, p<0.001) and insulin (beta=0.12, p=0.001) were independently associated with post-load glucose levels. Glucose 117-124 insulin Homo sapiens 42-49 16249033-5 2006 A slight and temporary reduction in insulin sensitivity was caused by a reduction in non-oxidative glucose metabolism (n=5). Glucose 99-106 insulin Homo sapiens 36-43 16713429-5 2006 We found that hydrogen peroxide treatment alone suppressed glucose uptake by insulin stimulation to 65.9%+/-7.8% of the corresponding controls (P<.01). Glucose 59-66 insulin Homo sapiens 77-84 16713429-7 2006 Treatment with the known anti-oxidant NAC also dose-dependently (0.1-10 mmol/L) restored insulin-induced glucose uptake in the presence of hydrogen peroxide. Glucose 105-112 insulin Homo sapiens 89-96 16682937-1 2006 Orally ingested glucose leads to a much higher insulin response than intravenous glucose leading to identical postprandial plasma glucose excursions. Glucose 16-23 insulin Homo sapiens 47-54 16855520-2 2006 Peripheral insulin resistance, tightly coupled with obesity in this age group, seems to be the major driving force of deteriorating glucose metabolism. Glucose 132-139 insulin Homo sapiens 11-18 16677709-5 2006 These results suggest that the NTS is a part of the ghrelin pathway that regulates the orexigenic signalling cascade, which may be triggered by a drop in blood glucose levels mediated by insulin. Glucose 160-167 insulin Homo sapiens 187-194 16861612-1 2006 OBJECTIVE: To determine the effects of weight loss (WL) alone and combined with aerobic exercise on visceral adipose tissue (VAT), intramuscular fat, insulin-stimulated glucose uptake, and the rate of decline in free fatty acid (FFA) concentrations during hyperinsulinemia. Glucose 169-176 insulin Homo sapiens 150-157 16859113-3 2006 Metabolic actions of insulin to promote glucose disposal are augmented by vascular actions of insulin in endothelium to stimulate production of the vasodilator nitric oxide (NO). Glucose 40-47 insulin Homo sapiens 21-28 16859113-4 2006 Indeed, NO-dependent increases in blood flow to skeletal muscle account for 25% to 40% of the increase in glucose uptake in response to insulin stimulation. Glucose 106-113 insulin Homo sapiens 136-143 16859113-5 2006 PI 3-kinase-dependent insulin signaling pathways in endothelium related to production of NO share striking similarities with metabolic pathways in skeletal muscle that promote glucose uptake. Glucose 176-183 insulin Homo sapiens 22-29 16783990-1 2006 This practical guide describes the most currently used insulins--classified according to their duration of action, the insulin pens and the glucose monitoring devices. Glucose 140-147 insulin Homo sapiens 55-62 16901800-12 2006 They also increase insulin secretion in the basal state and the first-phase insulin release after a glucose load. Glucose 100-107 insulin Homo sapiens 19-26 16905514-4 2006 In 2 prospective studies using glucose-insulin-potassium infusion, glucose levels did not reach target, and the results of both trials were negative with regard to the primary endpoint, mortality. Glucose 31-38 insulin Homo sapiens 39-46 16796924-1 2006 OBJECTIVE: To study the characteristics of insulin ultradian pulses of individuals with normal glucose tolerance, overweight, and impaired glucose tolerance (IGT). Glucose 95-102 insulin Homo sapiens 43-50 16570048-2 2006 Adiponectin, an adipocyte secreted endogenous insulin sensitizer, appears to play an important role not only in glucose and lipid metabolism but also in the development and progression of several obesity-related malignancies. Glucose 112-119 insulin Homo sapiens 46-53 16677372-1 2006 BACKGROUND: The protein tyrosine phosphatase-1B, a negative regulator for insulin and leptin signalling, potentially modulates glucose and energy homeostasis. Glucose 127-134 insulin Homo sapiens 74-81 16545776-6 2006 PKCtheta was found to be expressed in liver and treatment of human hepatoma cells (HepG2) with high insulin and glucose resulted in an increase in PKCtheta expression that correlated with a decrease in IRS-1 protein levels and the development of insulin resistance. Glucose 112-119 insulin Homo sapiens 246-253 16677372-12 2006 SNP rs2426159 exhibited evidence of association under a dominant model with glucose homeostasis related traits (p = 0.04 for fasting insulin and HOMA-B) and with lipid markers (0.02 = p = 0.04). Glucose 76-83 insulin Homo sapiens 133-151 16702795-2 2006 This review provides practical recommendations for adding insulin therapy for patients with type 2 diabetes whose glucose levels are inadequately controlled with oral medications. Glucose 114-121 insulin Homo sapiens 58-65 16734759-5 2006 Hyperosmotic dehydration in different cell types produces inactivation of signalling components around mTOR, thereby attenuating insulin-induced glucose uptake, glycogen synthesis, and lipogenesis in adipocytes, and MAP-kinase phosphatase MKP-1 expression in hepatoma cells. Glucose 145-152 insulin Homo sapiens 129-136 16327015-4 2006 Insulin-induced changes in glucose oxidation (GLUox) and fatty acid (FA) oxidation (FAox) were measured in isolated hearts from control and diabetic mice, perfused with both low as well as high concentration of glucose and FA: 10 mM glucose/0.5 mM palmitate and 28 mM glucose/1.1 mM palmitate. Glucose 27-34 insulin Homo sapiens 0-7 16327015-4 2006 Insulin-induced changes in glucose oxidation (GLUox) and fatty acid (FA) oxidation (FAox) were measured in isolated hearts from control and diabetic mice, perfused with both low as well as high concentration of glucose and FA: 10 mM glucose/0.5 mM palmitate and 28 mM glucose/1.1 mM palmitate. Glucose 211-218 insulin Homo sapiens 0-7 16327015-4 2006 Insulin-induced changes in glucose oxidation (GLUox) and fatty acid (FA) oxidation (FAox) were measured in isolated hearts from control and diabetic mice, perfused with both low as well as high concentration of glucose and FA: 10 mM glucose/0.5 mM palmitate and 28 mM glucose/1.1 mM palmitate. Glucose 211-218 insulin Homo sapiens 0-7 16327015-7 2006 During elevated FA and glucose supply, however, the effect of insulin was blunted in db/db hearts with respect to both FAox and GLUox. Glucose 23-30 insulin Homo sapiens 62-69 16327015-8 2006 Finally, insulin-stimulated deoxyglucose uptake was markedly reduced in isolated cardiomyocytes from db/db mice, whereas glucose uptake in isolated perfused db/db hearts was clearly responsive to insulin. Glucose 33-40 insulin Homo sapiens 9-16 16563942-3 2006 Novel investigational techniques based on magnetic resonance spectroscopy (MRS) have allowed real-time insight into the molecular defects in patients with type 2 diabetes, revealing that insulin resistance is a product of decreased insulin-stimulated skeletal muscle glycogen synthesis, which can mostly be attributed to decreased insulin-stimulated glucose transport (Glut 4) activity. Glucose 350-357 insulin Homo sapiens 187-194 16563942-3 2006 Novel investigational techniques based on magnetic resonance spectroscopy (MRS) have allowed real-time insight into the molecular defects in patients with type 2 diabetes, revealing that insulin resistance is a product of decreased insulin-stimulated skeletal muscle glycogen synthesis, which can mostly be attributed to decreased insulin-stimulated glucose transport (Glut 4) activity. Glucose 350-357 insulin Homo sapiens 232-239 16563942-3 2006 Novel investigational techniques based on magnetic resonance spectroscopy (MRS) have allowed real-time insight into the molecular defects in patients with type 2 diabetes, revealing that insulin resistance is a product of decreased insulin-stimulated skeletal muscle glycogen synthesis, which can mostly be attributed to decreased insulin-stimulated glucose transport (Glut 4) activity. Glucose 350-357 insulin Homo sapiens 232-239 16611332-5 2006 Glucose and arginine administered through the hepatic artery, but not through the portal vein, induced insulin release from the intraportally implanted islets. Glucose 0-7 insulin Homo sapiens 103-110 16611332-7 2006 The first phase of glucose-stimulated insulin release from both islets transplanted to the liver and kidney was delayed, and less prominent when compared to the pancreas. Glucose 19-26 insulin Homo sapiens 38-45 16679286-3 2006 Deletion of ghrelin increased basal insulin level, enhanced glucose-stimulated insulin secretion, and improved peripheral insulin sensitivity. Glucose 60-67 insulin Homo sapiens 79-86 16679286-3 2006 Deletion of ghrelin increased basal insulin level, enhanced glucose-stimulated insulin secretion, and improved peripheral insulin sensitivity. Glucose 60-67 insulin Homo sapiens 79-86 17699261-4 2006 Insulin secretion and insulin sensitivity were estimated by previously validated oral glucose tolerance test-derived indexes. Glucose 86-93 insulin Homo sapiens 0-7 17699261-4 2006 Insulin secretion and insulin sensitivity were estimated by previously validated oral glucose tolerance test-derived indexes. Glucose 86-93 insulin Homo sapiens 22-29 16557150-0 2006 Insulin reduces the multiple organ injury and dysfunction caused by coadministration of lipopolysaccharide and peptidoglycan independently of blood glucose: role of glycogen synthase kinase-3beta inhibition. Glucose 148-155 insulin Homo sapiens 0-7 18220630-7 2006 Metabolic secretagogues that stimulate insulin secretion by the activation of initial steps in the glucose-stimulated insulin secretion pathway can also lead to increased reactive species production and cellular destruction contributing to beta-cell damage and apoptosis. Glucose 99-106 insulin Homo sapiens 39-46 16557150-16 2006 We propose that the inhibitory effect of insulin on the activity of glycogen synthase kinase-3beta contributes to the protective effect of insulin against the organ injury/dysfunction caused by excessive systemic inflammation independently of any effects on blood glucose. Glucose 264-271 insulin Homo sapiens 41-48 16557150-16 2006 We propose that the inhibitory effect of insulin on the activity of glycogen synthase kinase-3beta contributes to the protective effect of insulin against the organ injury/dysfunction caused by excessive systemic inflammation independently of any effects on blood glucose. Glucose 264-271 insulin Homo sapiens 139-146 16607114-4 2006 RECENT FINDINGS: We examine recent attempts to define the anatomical nature of non-nutritive flow route in muscle, the quick onset of insulin action to recruit nutritive blood flow at doses lower than that which activates glucose uptake and bulk blood flow, actions of the inflammatory cytokine tumour necrosis factor alpha TNFalpha to oppose physiologic insulin action, interfibrillar fat depots that grow on the non-nutritive vasculature of muscle and underpin a "vascrine hypothesis", and drugs that reduce insulin resistance by ameliorating vascular dysfunction. Glucose 222-229 insulin Homo sapiens 134-141 18220630-7 2006 Metabolic secretagogues that stimulate insulin secretion by the activation of initial steps in the glucose-stimulated insulin secretion pathway can also lead to increased reactive species production and cellular destruction contributing to beta-cell damage and apoptosis. Glucose 99-106 insulin Homo sapiens 118-125 16634983-2 2006 Insulin resistance is central both to the progression from normal glucose tolerance to type 2 diabetes and to a constellation of cardiovascular risk factors known as the metabolic syndrome. Glucose 66-73 insulin Homo sapiens 0-7 16644635-4 2006 Insulin responsiveness to an oral glucose tolerance test (OGTT) was measured in nondiabetic subjects. Glucose 34-41 insulin Homo sapiens 0-7 16634992-0 2006 Energy expenditure, body composition and insulin response to glucose in male twins discordant for the Trp64Arg polymorphism of the beta3-adrenergic receptor gene. Glucose 61-68 insulin Homo sapiens 41-48 16634992-3 2006 METHODS: In 10 male twin pairs discordant for the Trp64Arg polymorphism, we examined insulin response to glucose by an oral glucose tolerance test (OGTT), a frequently sampled intravenous glucose tolerance test (FSIGT), body composition by the bioimpedance method, dual-energy X-ray absorptiometry scanning and energy expenditure by indirect and direct calorimetry. Glucose 105-112 insulin Homo sapiens 85-92 16634992-3 2006 METHODS: In 10 male twin pairs discordant for the Trp64Arg polymorphism, we examined insulin response to glucose by an oral glucose tolerance test (OGTT), a frequently sampled intravenous glucose tolerance test (FSIGT), body composition by the bioimpedance method, dual-energy X-ray absorptiometry scanning and energy expenditure by indirect and direct calorimetry. Glucose 124-131 insulin Homo sapiens 85-92 16634992-3 2006 METHODS: In 10 male twin pairs discordant for the Trp64Arg polymorphism, we examined insulin response to glucose by an oral glucose tolerance test (OGTT), a frequently sampled intravenous glucose tolerance test (FSIGT), body composition by the bioimpedance method, dual-energy X-ray absorptiometry scanning and energy expenditure by indirect and direct calorimetry. Glucose 124-131 insulin Homo sapiens 85-92 16634992-8 2006 CONCLUSIONS: In male twins with a high similarity in genetic and environmental background, the Trp64Arg polymorphism of the beta3AR gene is associated with lower fat mass, fasting insulin levels and an appropriate insulin response to glucose. Glucose 234-241 insulin Homo sapiens 214-221 16634996-2 2006 It is thought that the concomitant hyperinsulinaemia exacerbates vascular disease because resistance to insulin-induced glucose disposal is associated with resistance to certain effects of insulin which inhibit, but with no resistance to other effects which promote, neointimal hyperplasia. Glucose 120-127 insulin Homo sapiens 40-47 16634996-2 2006 It is thought that the concomitant hyperinsulinaemia exacerbates vascular disease because resistance to insulin-induced glucose disposal is associated with resistance to certain effects of insulin which inhibit, but with no resistance to other effects which promote, neointimal hyperplasia. Glucose 120-127 insulin Homo sapiens 104-111 16644693-2 2006 Analysis of human islets from cadaveric donors (age 16-70 years) was performed using glucose-stimulated insulin release (GSIR) (n = 93), islet ATP content (n = 27), diabetic nude mouse bioassay (n = 72), and the insulin secretory function after single-donor clinical islet allotransplantation (n = 7). Glucose 85-92 insulin Homo sapiens 104-111 16644676-9 2006 An important role for the ubiquitin-proteasome pathways in beta-cells is suggested by the findings that changes in glucose concentration influence expression of genes in the pathway and that blockade of the proteasome degradation machinery enhances glucose-stimulated insulin secretion. Glucose 249-256 insulin Homo sapiens 268-275 16644684-3 2006 Basal and submaximal insulin-stimulated (0.6 and 1.2 nmol/l) glucose transport was comparable between groups, whereas the maximal response (120 nmol/l) was 38% lower (P < 0.05) in the relatives. Glucose 61-68 insulin Homo sapiens 21-28 16644684-8 2006 In conclusion, the uncoupling of insulin action on Akt/AS160 signaling and glucose transport implicates defective GLUT4 trafficking as an early event in the pathogenesis of type 2 diabetes. Glucose 75-82 insulin Homo sapiens 33-40 16644696-4 2006 L-cysteine and the H(2)S donor NaHS inhibited glucose-induced insulin release from islets and MIN6 cells. Glucose 46-53 insulin Homo sapiens 62-69 16644701-5 2006 Insulin sensitivity was calculated as the total glucose disposal (TGD) during the last 30 min of the clamp. Glucose 48-55 insulin Homo sapiens 0-7 16644701-6 2006 Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated from fasting plasma glucose and insulin concentrations. Glucose 96-103 insulin Homo sapiens 32-39 16644701-9 2006 Insulin secretion, measured by the insulinogenic index (DeltaI(0-30)/DeltaG(0-30)) and by the ratio of the incremental area under the curve (AUC) of insulin to the incremental AUC of glucose (0-120 min), was reduced to the same extent in all three glucose-intolerant groups. Glucose 183-190 insulin Homo sapiens 0-7 16644702-2 2006 This facilitates glucose and insulin delivery to muscle, thus augmenting glucose uptake. Glucose 73-80 insulin Homo sapiens 29-36 16644702-9 2006 After 2 h of insulin infusion, whole-body glucose infusion rate was significantly lower in the obese versus lean group (19.3 +/- 3.2 and 37.4 +/- 2.6 mumol . Glucose 42-49 insulin Homo sapiens 13-20 16751350-0 2006 The physiology of amylin and insulin: maintaining the balance between glucose secretion and glucose uptake. Glucose 70-77 insulin Homo sapiens 29-36 16751350-0 2006 The physiology of amylin and insulin: maintaining the balance between glucose secretion and glucose uptake. Glucose 92-99 insulin Homo sapiens 29-36 16751350-2 2006 Historically, glucose homeostasis has been viewed somewhat narrowly--insulin from pancreatic beta cells regulated glucose disposal, while glucagon from pancreatic alpha [corrected] cells regulated glucose appearance during fasting states. Glucose 14-21 insulin Homo sapiens 69-76 16772655-12 2006 The novel chart-based insulin infusion algorithm chosen as the standard for this pilot was an effective tool for reducing the blood glucose to target range with no clinically significant hypoglycemia. Glucose 132-139 insulin Homo sapiens 22-29 16772658-0 2006 Physiologic insulin replacement in type 2 diabetes: optimizing postprandial glucose control. Glucose 76-83 insulin Homo sapiens 12-19 16772658-3 2006 METHODS: This article reviews the benefits of treating with a basal-prandial insulin approach and focuses on post-prandial glucose-targeted therapies, including rapid-acting insulin analogs. Glucose 123-130 insulin Homo sapiens 174-181 16784178-6 2006 TNF only suppressed glucose uptake in insulin-stimulated subcutaneous tissue and this suppression was only observed in tissue from lean subjects. Glucose 20-27 insulin Homo sapiens 38-45 16497805-8 2006 Chronic exposure of neuronal cells to insulin or leptin down-regulates Glut4 proteins and mRNA levels and abolishes the acute stimulation of glucose uptake in response to acute insulin or leptin. Glucose 141-148 insulin Homo sapiens 38-45 16497805-8 2006 Chronic exposure of neuronal cells to insulin or leptin down-regulates Glut4 proteins and mRNA levels and abolishes the acute stimulation of glucose uptake in response to acute insulin or leptin. Glucose 141-148 insulin Homo sapiens 177-184 16530875-4 2006 An intravenous injection of cationic emulsion containing proinsulin gene decreased blood glucose levels for 7 days within normal range. Glucose 89-96 insulin Homo sapiens 57-67 16530875-8 2006 Therefore, the cationic emulsion showed a promising result as a novel insulin gene therapy vehicle by decreasing blood glucose level for a month. Glucose 119-126 insulin Homo sapiens 70-77 17219488-11 2006 When adjusted for clinical factors, the use of sliding-scale insulin by itself was associated with a 20 mg/dL higher mean glucose level per patient-day. Glucose 122-129 insulin Homo sapiens 61-68 16614419-6 2006 We conclude that co-ingestion of a protein hydrolysate with or without additional free leucine strongly augments the insulin response after ingestion of a single bolus of carbohydrate, thereby significantly reducing postprandial blood glucose excursions in patients with long-standing Type 2 diabetes. Glucose 235-242 insulin Homo sapiens 117-124 16641887-3 2006 Insulin influences the production of pyruvate by its action on glucose metabolism and pyruvate is an insulin secretagogue. Glucose 63-70 insulin Homo sapiens 0-7 16641887-5 2006 This may have relevance to the use of glucose-insulin-potassium regimen in these clinical conditions, sepsis, and cancer. Glucose 38-45 insulin Homo sapiens 46-53 16622421-4 2006 This signalling pathway involves a catalytically inactive receptor tyrosine phosphatase, ICA512, whose cytoplasmic tail is cleaved on glucose-stimulated exocytosis of insulin secretory granules and then moves into the nucleus, where it upregulates insulin transcription. Glucose 134-141 insulin Homo sapiens 167-174 16622421-4 2006 This signalling pathway involves a catalytically inactive receptor tyrosine phosphatase, ICA512, whose cytoplasmic tail is cleaved on glucose-stimulated exocytosis of insulin secretory granules and then moves into the nucleus, where it upregulates insulin transcription. Glucose 134-141 insulin Homo sapiens 248-255 16771083-4 2006 Authors present their own research of the impact of plasmatic insulin levels on glucose metabolism. Glucose 80-87 insulin Homo sapiens 62-69 16771083-5 2006 It seems that the ability of critical patients to utilise and store glucose is significantly decreased due to their insulin resistance. Glucose 68-75 insulin Homo sapiens 116-123 16771083-7 2006 Glucose utilisation and oxidation in sepsis can be enhanced by administration of insulin. Glucose 0-7 insulin Homo sapiens 81-88 16676512-0 2006 [Inhaled insulin: a new route in the optimisation of glucose regulation]. Glucose 53-60 insulin Homo sapiens 9-16 16585665-3 2006 When a laboratory result that documented the diabetic patient"s severe hyperglycemia was entered into the other patient"s electronic medical record, the latter patient seemed to have a very high glucose level and was almost given what could have been a fatal dose of insulin. Glucose 195-202 insulin Homo sapiens 267-274 16611137-2 2006 Insulin is a peptide hormone secreted by the beta-cells of the pancreatic islets of Langerhans in response to increased circulating levels of glucose and amino acids and it is essential for appropriate tissue development, growth, and maintenance of whole-body glucose homeostasis by regulating carbohydrate, lipid and protein metabolism. Glucose 142-149 insulin Homo sapiens 0-7 16611137-2 2006 Insulin is a peptide hormone secreted by the beta-cells of the pancreatic islets of Langerhans in response to increased circulating levels of glucose and amino acids and it is essential for appropriate tissue development, growth, and maintenance of whole-body glucose homeostasis by regulating carbohydrate, lipid and protein metabolism. Glucose 260-267 insulin Homo sapiens 0-7 16256241-6 2006 Thus, LPL-deficient subjects with hypertriglyceridemia displayed an enhanced glucose-stimulated insulin response as well as lower blood glucose levels, the latter of which is not generally seen in those with hypertriglyceridemia and normolipidemia. Glucose 77-84 insulin Homo sapiens 96-103 16567515-8 2006 Conversely, insulin-stimulated Akt phosphorylation, glucose uptake, and GLUT4 translocation were not affected by siJAK2. Glucose 52-59 insulin Homo sapiens 12-19 16567531-1 2006 The purpose of this study was to examine longitudinally the relationship among glucose levels, pancreatic beta-cell function, and insulin resistance in women at high risk for type 2 diabetes. Glucose 79-86 insulin Homo sapiens 130-137 16567536-8 2006 These data shed light on the natural course of beta-cell function; over 5.2 years, mean insulin sensitivity declined in each glucose tolerance category. Glucose 125-132 insulin Homo sapiens 88-95 16567539-3 2006 When patients were stratified by insulin resistance, more severe insulin resistance was associated (P < 0.05) with overweight, central fat distribution, hypertension, and dyslipidemia (with similar sex distribution, age, fasting plasma glucose, and HbA1c). Glucose 239-246 insulin Homo sapiens 65-72 16396984-4 2006 Acute Intralipid infusion increased plasma free fatty acid levels from 1.0 +/- 0.1 to 2.5 +/- 0.3 mM, which subsequently caused reductions in skeletal muscle (insulin-stimulated glucose disposal rate) and liver (hepatic glucose production) insulin sensitivity by 30 and 45%, respectively. Glucose 178-185 insulin Homo sapiens 159-166 16396984-5 2006 CNTF pretreatment completely prevented the lipid-mediated reduction in insulin-stimulated glucose disposal rate and the blunted suppression of hepatic glucose production by insulin. Glucose 90-97 insulin Homo sapiens 71-78 16439461-6 2006 In addition, MCP-1 significantly reduced insulin-stimulated glucose uptake in the myocytes. Glucose 60-67 insulin Homo sapiens 41-48 16492903-3 2006 In metabolic tissues, insulin signaling via the phosphatidylinositol-3-kinase pathway leads to glucose uptake so that in insulin resistance a state of hyperglycemia occurs; other factors such as dyslipidemia and hypertension also arise. Glucose 95-102 insulin Homo sapiens 22-29 16492903-3 2006 In metabolic tissues, insulin signaling via the phosphatidylinositol-3-kinase pathway leads to glucose uptake so that in insulin resistance a state of hyperglycemia occurs; other factors such as dyslipidemia and hypertension also arise. Glucose 95-102 insulin Homo sapiens 121-128 16497797-8 2006 Interestingly, insulin-stimulated glucose uptake was only reduced by 50-60%, suggesting that another glucose transporter mediates part of this effect. Glucose 34-41 insulin Homo sapiens 15-22 16497797-9 2006 When siGLUT1 was introduced into GLUT4-deficient adipocytes, insulin-stimulated glucose uptake was essentially abolished, indicating that both GLUT4 and GLUT1 contribute to insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 80-87 insulin Homo sapiens 61-68 16497797-9 2006 When siGLUT1 was introduced into GLUT4-deficient adipocytes, insulin-stimulated glucose uptake was essentially abolished, indicating that both GLUT4 and GLUT1 contribute to insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 80-87 insulin Homo sapiens 173-180 16497797-9 2006 When siGLUT1 was introduced into GLUT4-deficient adipocytes, insulin-stimulated glucose uptake was essentially abolished, indicating that both GLUT4 and GLUT1 contribute to insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 192-199 insulin Homo sapiens 61-68 16497797-9 2006 When siGLUT1 was introduced into GLUT4-deficient adipocytes, insulin-stimulated glucose uptake was essentially abolished, indicating that both GLUT4 and GLUT1 contribute to insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 192-199 insulin Homo sapiens 173-180 16497805-0 2006 Insulin and leptin induce Glut4 plasma membrane translocation and glucose uptake in a human neuronal cell line by a phosphatidylinositol 3-kinase- dependent mechanism. Glucose 66-73 insulin Homo sapiens 0-7 16497805-4 2006 We show that insulin and leptin both induce Glut4 translocation to the PM of neuronal cells and activate glucose uptake. Glucose 105-112 insulin Homo sapiens 13-20 16497805-5 2006 Wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase, totally abolished insulin- and leptin-dependent Glut4 translocation and stimulation of glucose uptake. Glucose 154-161 insulin Homo sapiens 85-92 16337726-5 2006 Insulin resistance was estimated by fasting insulin level, fasting glucose/insulin ratio and 75 g 2 h glucose tolerance test. Glucose 67-74 insulin Homo sapiens 0-7 16337726-5 2006 Insulin resistance was estimated by fasting insulin level, fasting glucose/insulin ratio and 75 g 2 h glucose tolerance test. Glucose 102-109 insulin Homo sapiens 0-7 16804799-2 2006 Other approaches such as fasting- or oral glucose tolerance test-derived insulin sensitivity indices were proposed and validated with the euglycemic clamp. Glucose 42-49 insulin Homo sapiens 73-80 20476912-1 2006 Diabetes mellitus is characterized by a lack of insulin, causing elevated blood glucose, often with associated insulin resistance. Glucose 80-87 insulin Homo sapiens 48-55 16700870-9 2006 The plasma levels of leptin and insulin 120 min after a glucose load decreased after moxonidine administration from 27.2 +/- 3.5 to 22.6 +/- 2.9 pg/ml (p < 0.05) and from 139.7 +/- 31.2 to 76.0 +/- 15.2 U/ml (p < 0.05), respectively. Glucose 56-63 insulin Homo sapiens 32-39 16632233-1 2006 PURPOSE: To compare the effects of prandial insulin therapy focusing on postprandial glucose control vs. basal insulin therapy focusing on fasting glucose control in patients with type 2 diabetes. Glucose 85-92 insulin Homo sapiens 44-51 16631446-1 2006 There is a need for reliable measurements of insulin sensitivity (SI) simpler than the euglycemic hyperinsulinemic clamp or the intravenous glucose tolerance test (IVGTT), which could be used when the simpler surrogates based on fasting insulin (Ib) and glucose (Gb) lose their validity. Glucose 254-261 insulin Homo sapiens 45-52 16473497-7 2006 RESULTS: Three days after surgery insulin-stimulated whole-body glucose disposal decreased by 24 +/- 11% versus 28 +/- 23% in patients receiving TPN and hypocaloric glucose, respectively (P < 0.05 for both, not significant between groups). Glucose 64-71 insulin Homo sapiens 34-41 16473497-8 2006 Endogenous glucose production during insulin stimulation was increased only in the glucose group after surgery (P < 0.05 versus before). Glucose 11-18 insulin Homo sapiens 37-44 16473497-8 2006 Endogenous glucose production during insulin stimulation was increased only in the glucose group after surgery (P < 0.05 versus before). Glucose 83-90 insulin Homo sapiens 37-44 16473497-9 2006 After surgery, insulin-stimulated glucose oxidation was higher after treatment with TPN, whereas fat oxidation was lower (P < 0.05 for both versus glucose treatment). Glucose 34-41 insulin Homo sapiens 15-22 16473497-9 2006 After surgery, insulin-stimulated glucose oxidation was higher after treatment with TPN, whereas fat oxidation was lower (P < 0.05 for both versus glucose treatment). Glucose 150-157 insulin Homo sapiens 15-22 16672772-1 2006 In adipocytes, insulin stimulates glucose transport primarily by promoting the translocation of GLUT4 to the plasma membrane. Glucose 34-41 insulin Homo sapiens 15-22 16672772-5 2006 In addition, ML-7, a selective inhibitor of MLCK, as well as inhibitors of myosin II, such as blebbistatin and 2,3-butanedione monoxime, block insulin-stimulated GLUT4 translocation and subsequent glucose transport. Glucose 197-204 insulin Homo sapiens 143-150 16672772-6 2006 Our studies suggest that MLCK may be a regulatory target of Ca(2+)/calmodulin and may play an important role in insulin-stimulated glucose transport in adipocytes. Glucose 131-138 insulin Homo sapiens 112-119 16440350-0 2006 Use of glucose-responsive material to regulate insulin release from constitutively secreting cells. Glucose 7-14 insulin Homo sapiens 47-54 16440350-4 2006 Our objective consists of using such cells as an insulin source and of regulating insulin release by incorporating a glucose-responsive material, which acts as a control barrier for insulin in a cell-material hybrid device. Glucose 117-124 insulin Homo sapiens 82-89 16440350-4 2006 Our objective consists of using such cells as an insulin source and of regulating insulin release by incorporating a glucose-responsive material, which acts as a control barrier for insulin in a cell-material hybrid device. Glucose 117-124 insulin Homo sapiens 82-89 16440350-7 2006 Results demonstrated that the device released insulin at a higher rate in response to glucose challenges. Glucose 86-93 insulin Homo sapiens 46-53 16440350-8 2006 In contrast, a device containing an inert hydrogel instead of glucose-responsive material released insulin at an essentially constant rate, irrespective of the surrounding glucose concentration. Glucose 62-69 insulin Homo sapiens 99-106 16618833-3 2006 Metabolic actions of insulin to promote glucose disposal are augmented by vascular actions of insulin in endothelium to stimulate production of the vasodilator nitric oxide (NO). Glucose 40-47 insulin Homo sapiens 21-28 16618833-4 2006 Indeed, NO-dependent increases in blood flow to skeletal muscle account for 25% to 40% of the increase in glucose uptake in response to insulin stimulation. Glucose 106-113 insulin Homo sapiens 136-143 16618833-5 2006 Phosphatidylinositol 3-kinase-dependent insulin-signaling pathways in endothelium related to production of NO share striking similarities with metabolic pathways in skeletal muscle that promote glucose uptake. Glucose 194-201 insulin Homo sapiens 40-47 16476731-1 2006 Insulin secretion by pancreatic beta-cells is stimulated by glucose, amino acids, and other metabolic fuels. Glucose 60-67 insulin Homo sapiens 0-7 16603055-6 2006 Insulin resistance was evaluated with fasting insulin, fasting glucose/insulin ratio, and homeostasis model assessment index for insulin resistance (HOMAIR). Glucose 63-70 insulin Homo sapiens 0-7 16759519-9 2006 RESULTS: After stimulation of glucose the insulin concentration in the supernatant of the Ad-HO-1 group was 270 mIU/L +/- 89 mIU/L, significantly higher than those of the Ad-EGFP group (189 mIU/L +/- 88 mIU/L) and control group (182 mIU/L +/- 59 mIU/L, both P < 0.05). Glucose 30-37 insulin Homo sapiens 42-49 16278244-3 2006 It has been reported that in vivo insulin pulses can be entrained to a pulse interval of approximately 10 min by infused glucose oscillations. Glucose 121-128 insulin Homo sapiens 34-41 16278244-6 2006 We report that oscillatory glucose exposure does not entrain insulin pulse frequency, but it amplifies the mass of insulin secretory bursts that coincide with glucose oscillations (P < 0.001). Glucose 27-34 insulin Homo sapiens 115-122 16278244-6 2006 We report that oscillatory glucose exposure does not entrain insulin pulse frequency, but it amplifies the mass of insulin secretory bursts that coincide with glucose oscillations (P < 0.001). Glucose 159-166 insulin Homo sapiens 115-122 16278244-8 2006 The apparent entrainment of pulsatile insulin to infused glucose oscillations in nondiabetic humans in vivo might reflect the amplification of underlying insulin secretory bursts that are detected as entrained pulses at the peripheral sampling site, but without changes in the underlying pacemaker activity. Glucose 57-64 insulin Homo sapiens 38-45 16564941-10 2006 CONCLUSION: Systolic and diastolic blood pressures decreased with glucose in the dialysis fluid in patients with chronic renal failure, presumably because of insulin-induced vasodilatation in patients without diabetes. Glucose 66-73 insulin Homo sapiens 158-165 16545078-1 2006 Several members of the extensive family of small GTP-binding proteins are regulated by insulin, and have been implicated in insulin action on glucose uptake. Glucose 142-149 insulin Homo sapiens 87-94 16545078-1 2006 Several members of the extensive family of small GTP-binding proteins are regulated by insulin, and have been implicated in insulin action on glucose uptake. Glucose 142-149 insulin Homo sapiens 124-131 16545078-4 2006 We review recent evidence that this may be the case, and place specific emphasis on the role of these pathways in insulin-stimulated glucose uptake. Glucose 133-140 insulin Homo sapiens 114-121 16399832-3 2006 Currently, considerable information can be found about the signal transduction mechanisms that lead to glucose-mediated insulin release in the pancreatic beta-cell, mitochondrial activation being an essential step. Glucose 103-110 insulin Homo sapiens 120-127 16505973-6 2006 Hyperglycemia and hyperlipidemia impair this cycle and affect glucose-stimulated insulin release. Glucose 62-69 insulin Homo sapiens 81-88 28863744-5 2006 Morphology, viability, and glucose-responding insulin secretion were analyzed in the coculture system. Glucose 27-34 insulin Homo sapiens 46-53 16529680-2 2006 The patient and physician must work together to optimize glucose control involving both insulin administration and caloric intake. Glucose 57-64 insulin Homo sapiens 88-95 16256241-0 2006 Glucose-stimulated insulin response in non-diabetic patients with lipoprotein lipase deficiency and hypertriglyceridemia. Glucose 0-7 insulin Homo sapiens 19-26 16256241-2 2006 The objective of this study was to investigate the relationship between hypertriglyceridemia and glucose-stimulated insulin responsiveness in non-diabetic patients. Glucose 97-104 insulin Homo sapiens 116-123 16256241-4 2006 In response to a 75 g oral glucose tolerance test, plasma insulin levels in the LPL-deficient subjects were higher (106+/-11 microU/ml) than those in the hypertriglyceridemic (69+/-16 microU/ml) and normolipidemic (29+/-3 microU/ml) subjects, at 30 min. Glucose 27-34 insulin Homo sapiens 58-65 16703118-7 2006 Similarly to rapid-acting subcutaneous analogs, inhaled human insulin has a more rapid onset of glucose-lowering activity compared to subcutaneous regular insulin, allowing it to be administered shortly before meals. Glucose 96-103 insulin Homo sapiens 62-69 16703118-9 2006 Inhaled human insulin effectively controls postprandial glucose concentrations in patients with type 1 or type 2 diabetes without increasing the risk of hypoglycemia, and even improves fasting glucose levels compared to subcutaneous insulin. Glucose 56-63 insulin Homo sapiens 14-21 16703118-9 2006 Inhaled human insulin effectively controls postprandial glucose concentrations in patients with type 1 or type 2 diabetes without increasing the risk of hypoglycemia, and even improves fasting glucose levels compared to subcutaneous insulin. Glucose 193-200 insulin Homo sapiens 14-21 16734545-5 2006 Insulin was applied intravenously (rapid glucose decline) or subcutaneously (moderate glucose decline) in a dosage between 3 to 18 units 2 h later in a randomized sequence on two different days. Glucose 41-48 insulin Homo sapiens 0-7 16734545-5 2006 Insulin was applied intravenously (rapid glucose decline) or subcutaneously (moderate glucose decline) in a dosage between 3 to 18 units 2 h later in a randomized sequence on two different days. Glucose 86-93 insulin Homo sapiens 0-7 16396989-6 2006 beta-Cells expressed insulin and Pdx-1 mRNA in response to glucose. Glucose 59-66 insulin Homo sapiens 21-28 16644693-8 2006 These results show that insulin secretory response to glucose deteriorates with increasing age and that it may be related to changes in ATP generation in beta-cells. Glucose 54-61 insulin Homo sapiens 24-31 16494630-9 2006 CONCLUSION: Plasma triglyceride, alanine, glucagon, lactate and TNF-alpha may be associated with alterations in the first-phase prehepatic insulin secretion response to intravenous glucose in normoglycaemic lipodystrophic HIV-infected patients. Glucose 181-188 insulin Homo sapiens 139-146 16455755-1 2006 Skeletal muscle tissue is one of the main sites where glucose uptake occurs in response to insulin. Glucose 54-61 insulin Homo sapiens 91-98 16455755-2 2006 The glucose transporter type-4 (GLUT4) is primarily responsible for the insulin-stimulated increase in glucose uptake. Glucose 4-11 insulin Homo sapiens 72-79 16455755-8 2006 In fact, we demonstrate that lack of caveolin-3 significantly reduces insulin-stimulated glucose uptake in caveolin-3 null myotubes by inhibiting both PI3K and Akt, as well as the movement of GLUT4 to the plasma membrane. Glucose 89-96 insulin Homo sapiens 70-77 16455755-11 2006 Disruption of flotillin-1-based domains prevents the activation of C3G, movement of GLUT4 to the sarcolemma, and glucose uptake in response to insulin. Glucose 113-120 insulin Homo sapiens 143-150 16494630-0 2006 Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride, glucagon, lactate and TNF-alpha in patients with HIV-lipodystrophy. Glucose 0-7 insulin Homo sapiens 30-37 16807226-6 2006 2) Body mass index (BMI) was an important predictor of post-glucose load insulin levels both before (coefficient=1.051, p=0.004) and after chemotherapy (coefficient=0.711, p=0.003). Glucose 60-67 insulin Homo sapiens 73-80 16807226-9 2006 CONCLUSIONS: Post-glucose load insulin values significantly decrease after chemotherapy. Glucose 18-25 insulin Homo sapiens 31-38 16807226-10 2006 There is a positive relationship between BMI and post-glucose load insulin before and after chemotherapy. Glucose 54-61 insulin Homo sapiens 67-74 16449334-8 2006 This correlation is still significant, although attenuated, after inclusion of insulin-stimulated glucose disposal among the regressors and further attenuated when adjusted also for waist to thigh ratio. Glucose 98-105 insulin Homo sapiens 79-86 16464947-5 2006 MAIN OUTCOME MEASURES: Insulin sensitivity (IS) was derived from a 2-h 75-g oral glucose tolerance test (IS(OGTT)). Glucose 81-88 insulin Homo sapiens 23-30 16643134-5 2006 The insulin sensitivity (M), measured as the glucose utilization rate under steady-state conditions of euglycaemia, was significantly decreased (P = 0.001) in BD patients compared to the controls (4.09 +/- 0.16 vs. 5.60 +/- 0.27 mg/kg/min). Glucose 45-52 insulin Homo sapiens 4-11 16339278-3 2006 Concomitant with an increase in GLUT4 at the plasma membrane, insulin-stimulated glucose transport was enhanced by chromium treatment. Glucose 81-88 insulin Homo sapiens 62-69 16339278-9 2006 Interestingly, cholesterol add-back to the plasma membrane prevented the beneficial effect of chromium on both GLUT4 mobilization and insulin-stimulated glucose transport. Glucose 153-160 insulin Homo sapiens 134-141 16339278-11 2006 Together, these data reveal a novel mechanism by which chromium may enhance GLUT4 trafficking and insulin-stimulated glucose transport. Glucose 117-124 insulin Homo sapiens 98-105 16567515-9 2006 Interestingly, in two insulin-resistant states, siJAK2 led to partial restoration of Akt phosphorylation and glucose uptake stimulation but not of the MAPK pathway. Glucose 109-116 insulin Homo sapiens 22-29 16567515-10 2006 These results suggest that JAK2 may depress the Akt to glucose uptake signaling axis selectively in insulin-resistant states. Glucose 55-62 insulin Homo sapiens 100-107 16567530-1 2006 Glucose sensing is essential for the ability of pancreatic beta-cells to produce insulin in sufficient quantities to maintain blood glucose within the normal range. Glucose 0-7 insulin Homo sapiens 81-88 16567530-1 2006 Glucose sensing is essential for the ability of pancreatic beta-cells to produce insulin in sufficient quantities to maintain blood glucose within the normal range. Glucose 132-139 insulin Homo sapiens 81-88 16567530-2 2006 Stress causes the release of adrenergic hormones that increase circulating glucose by promoting glucose production and inhibiting insulin release. Glucose 75-82 insulin Homo sapiens 130-137 16528409-1 2006 Insulin resistance markedly increases cardiovascular disease risk in people with normal glucose tolerance, even after adjustment for known risk factors such as LDL, triglycerides, HDL, and systolic blood pressure. Glucose 88-95 insulin Homo sapiens 0-7 16549443-0 2006 Regulation of the insulin gene by glucose and fatty acids. Glucose 34-41 insulin Homo sapiens 18-25 16549443-3 2006 Glucose is the major physiologic regulator of insulin gene expression; it coordinately controls the recruitment of transcription factors [e.g., pancreatic/duodenal homeobox-1 (PDX-1), mammalian homologue of avian MafA/L-Maf (MafA), Beta2/Neuro D (B2), the rate of transcription, and the stability of insulin mRNA. Glucose 0-7 insulin Homo sapiens 46-53 16549443-3 2006 Glucose is the major physiologic regulator of insulin gene expression; it coordinately controls the recruitment of transcription factors [e.g., pancreatic/duodenal homeobox-1 (PDX-1), mammalian homologue of avian MafA/L-Maf (MafA), Beta2/Neuro D (B2), the rate of transcription, and the stability of insulin mRNA. Glucose 0-7 insulin Homo sapiens 300-307 16549443-4 2006 However, chronically elevated levels of glucose (glucotoxicity) and lipids (lipotoxicity) also contribute to the worsening of beta-cell function in type 2 diabetes, in part via inhibition of insulin gene expression. Glucose 40-47 insulin Homo sapiens 191-198 16612310-7 2006 Insulin treatment (2 IU/kg/hr) resulted in significantly lower blood glucose (p < 0.01) and improved 4 day survival (p < 0.03). Glucose 69-76 insulin Homo sapiens 0-7 16546484-1 2006 Multiple indices to assess insulin sensitivity calculated from mathematical equations based on fasting blood parameters or oral glucose tolerance data have been developed. Glucose 128-135 insulin Homo sapiens 27-34 16565728-3 2006 Coadministration of the peptide and insulin to the abdominal skin of diabetic rats resulted in elevated systemic levels of insulin and suppressed serum glucose levels for at least 11 h. Significant systemic bioavailability of human growth hormone was also achieved when topically coadministered with the peptide. Glucose 152-159 insulin Homo sapiens 36-43 16504534-2 2006 A gene therapy strategy using constructs designed to allow glucose-regulated insulin transcription when delivered to non-pancreatic tissues has not fully recreated the stringent control of blood glucose provided by the beta cell. Glucose 59-66 insulin Homo sapiens 77-84 16009423-1 2006 Insulin-dependent diabetes mellitus (Type I) is associated with disregulation of the glucose and oxygen metabolic pathways during pregnancy, both of which affect placental villous development. Glucose 85-92 insulin Homo sapiens 0-7 16722457-2 2006 Since insulin plays pivotal roles in energy homeostasis by transferring glucose into cells, type 1 diabetic patients can not survive without insulin replacement. Glucose 72-79 insulin Homo sapiens 6-13 16722457-3 2006 Insulin secretion is precisely controlled by ingested glucose as well as hormones and neural factors, therefore it is impossible to reproduce the physiological secretory pattern of insulin via exogenous insulin, even by multiple or continuous delivery by injection. Glucose 54-61 insulin Homo sapiens 0-7 16768096-19 2006 In addition, good control of serum glucose with an appropriate insulin treatment has abolished the involuntary movement episodes described above. Glucose 35-42 insulin Homo sapiens 63-70 16540333-3 2006 At the cellular level, glucose uptake results from the insulin-stimulated translocation of the glucose transporter 4 (GLUT4) from intracellular storage sites to the plasma membrane. Glucose 23-30 insulin Homo sapiens 55-62 16427608-6 2006 In addition, RAW-CM treatment decreased insulin-stimulated glucose uptake in adipocytes. Glucose 59-66 insulin Homo sapiens 40-47 16612838-2 2006 The glucose loading test (administration of 75 g orally given glucose) was evaluated in 14 human healthy subjects by the simultaneous measurement of plasma level of glucose, C-peptide and glucagon every 15 min for 4 h without and with (ED50) oral application of capsaicin. Glucose 4-11 insulin Homo sapiens 174-183 16612838-2 2006 The glucose loading test (administration of 75 g orally given glucose) was evaluated in 14 human healthy subjects by the simultaneous measurement of plasma level of glucose, C-peptide and glucagon every 15 min for 4 h without and with (ED50) oral application of capsaicin. Glucose 62-69 insulin Homo sapiens 174-183 16612838-2 2006 The glucose loading test (administration of 75 g orally given glucose) was evaluated in 14 human healthy subjects by the simultaneous measurement of plasma level of glucose, C-peptide and glucagon every 15 min for 4 h without and with (ED50) oral application of capsaicin. Glucose 62-69 insulin Homo sapiens 174-183 16612838-4 2006 The plasma levels of insulin and C-peptide increased from 90 to 165 min after glucose loading but there were no significant difference between the results obtained without and with capsaicin administration. Glucose 78-85 insulin Homo sapiens 21-28 16612838-4 2006 The plasma levels of insulin and C-peptide increased from 90 to 165 min after glucose loading but there were no significant difference between the results obtained without and with capsaicin administration. Glucose 78-85 insulin Homo sapiens 33-42 16249253-3 2006 Compared with 5 mM glucose, incubation of HAEC with 30 mM glucose for up to 48 h increased in a time-dependent manner expression of insulin receptor, insulin receptor substrate (IRS)-1, IRS-2, and GLUT1 proteins. Glucose 58-65 insulin Homo sapiens 132-139 16249253-3 2006 Compared with 5 mM glucose, incubation of HAEC with 30 mM glucose for up to 48 h increased in a time-dependent manner expression of insulin receptor, insulin receptor substrate (IRS)-1, IRS-2, and GLUT1 proteins. Glucose 58-65 insulin Homo sapiens 150-157 16249253-4 2006 High glucose also increased the specific binding of (125)I-labeled insulin in HAEC accompanied by accelerated production of interleukin (IL)-6 and IL-8. Glucose 5-12 insulin Homo sapiens 67-74 16249253-6 2006 However, an addition of insulin to high glucose-exposed endothelial cells led to a significant increase in [(14)C]glucose uptake in a glucose concentration- and time-dependent fashion, reaching a plateau at 48 h of incubation. Glucose 40-47 insulin Homo sapiens 24-31 16249253-6 2006 However, an addition of insulin to high glucose-exposed endothelial cells led to a significant increase in [(14)C]glucose uptake in a glucose concentration- and time-dependent fashion, reaching a plateau at 48 h of incubation. Glucose 114-121 insulin Homo sapiens 24-31 16249253-6 2006 However, an addition of insulin to high glucose-exposed endothelial cells led to a significant increase in [(14)C]glucose uptake in a glucose concentration- and time-dependent fashion, reaching a plateau at 48 h of incubation. Glucose 114-121 insulin Homo sapiens 24-31 16249253-7 2006 Furthermore, incubation of HAEC with 30 mM glucose resulted in a new insulin-stimulated extracellular signal-regulated kinase-1/2 mitogen-activated protein kinase phosphorylation and increased lipid peroxidation and production of reactive oxygen species. Glucose 43-50 insulin Homo sapiens 69-76 16249253-8 2006 These studies show for the first time that high glucose increases expression of insulin receptors and downstream elements of the insulin-signaling pathway and transforms "insulin-resistant" aortic endothelial cells into "insulin-sensitive" tissue regarding glucose uptake. Glucose 48-55 insulin Homo sapiens 80-87 16249253-8 2006 These studies show for the first time that high glucose increases expression of insulin receptors and downstream elements of the insulin-signaling pathway and transforms "insulin-resistant" aortic endothelial cells into "insulin-sensitive" tissue regarding glucose uptake. Glucose 48-55 insulin Homo sapiens 129-136 16249253-8 2006 These studies show for the first time that high glucose increases expression of insulin receptors and downstream elements of the insulin-signaling pathway and transforms "insulin-resistant" aortic endothelial cells into "insulin-sensitive" tissue regarding glucose uptake. Glucose 48-55 insulin Homo sapiens 129-136 16249253-8 2006 These studies show for the first time that high glucose increases expression of insulin receptors and downstream elements of the insulin-signaling pathway and transforms "insulin-resistant" aortic endothelial cells into "insulin-sensitive" tissue regarding glucose uptake. Glucose 48-55 insulin Homo sapiens 129-136 16758949-2 2006 Due to its effects in suppressing the hepatic production of endogenous glucose and in increasing insulin sensitivity in adipose tissue and skeletal muscle, the agent is used particularly in type 2 diabetes mellitus and metabolic syndrome, in which insulin resistance is especially pronounced. Glucose 71-78 insulin Homo sapiens 248-255 16412274-7 2006 RESULTS: Astragaloside IV can significantly potentiate insulin-induced preadipocyte differentiation at concentrations of 3, 10, and 30 microg/mL, improve high glucose-induced insulin resistance in adipocytes at a concentration of 30 microg/mL, and prevent tumor necrosis factor (TNF)-alpha-induced apoptosis and viability loss at concentrations of 10 and 30 microg/mL, and 30 microg/mL, respectively, in endothelial cells. Glucose 159-166 insulin Homo sapiens 175-182 16249253-0 2006 De novo emergence of insulin-stimulated glucose uptake in human aortic endothelial cells incubated with high glucose. Glucose 40-47 insulin Homo sapiens 21-28 16249253-0 2006 De novo emergence of insulin-stimulated glucose uptake in human aortic endothelial cells incubated with high glucose. Glucose 109-116 insulin Homo sapiens 21-28 16249253-2 2006 We hypothesized that incubation of human aortic endothelial cells (HAEC) with high glucose increases insulin signaling and develops the appearance of insulin-stimulated glucose uptake by the cells. Glucose 83-90 insulin Homo sapiens 101-108 16570557-5 2006 Insulin is the mainstay of perioperative glucose management, and intensive insulin therapy (to a target blood glucose of 110 mg/dL or lower) improves a range of clinical outcomes in critically ill patients relative to less aggressive insulin strategies. Glucose 41-48 insulin Homo sapiens 0-7 16752684-6 2006 The diagnosis of insulinoma was based on Whipple triad, high plasma insulin levels associated with low plasma glucose levels, as well as the symptomatic relief after intravenous glucose injection. Glucose 110-117 insulin Homo sapiens 17-24 16752684-6 2006 The diagnosis of insulinoma was based on Whipple triad, high plasma insulin levels associated with low plasma glucose levels, as well as the symptomatic relief after intravenous glucose injection. Glucose 178-185 insulin Homo sapiens 17-24 16505665-0 2006 Intensive insulin therapy reduces microdialysis glucose values without altering glucose utilization or improving the lactate/pyruvate ratio after traumatic brain injury. Glucose 48-55 insulin Homo sapiens 10-17 16505665-6 2006 MEASUREMENTS AND MAIN RESULTS: In 14 patients treated with intensive insulin therapy, there was a reduction in microdialysis glucose by 70% of baseline concentration compared with a 15% reduction in 33 patients treated with a loose insulin protocol. Glucose 125-132 insulin Homo sapiens 69-76 16505665-8 2006 However, intensive insulin therapy was associated with increased incidence of microdialysis markers of cellular distress, namely elevated glutamate (38+/-37% vs. 10+/-17%, p<.01), elevated lactate/pyruvate ratio (38+/-37% vs. 19+/-26%, p<.03) and low glucose (26+/-17% vs. 11+/-15%, p<.05, and increased global oxygen extraction fraction. Glucose 257-264 insulin Homo sapiens 19-26 16505665-10 2006 CONCLUSIONS: Intensive insulin therapy results in a net reduction in microdialysis glucose and an increase in microdialysis glutamate and lactate/pyruvate without conveying a functional outcome advantage. Glucose 83-90 insulin Homo sapiens 23-30 16214255-6 2006 Moreover, in the euglycemic hyperinsulinemic clamp test, glucose infusion rate was significantly increased by nateglinide treatment, indicating that nateglinide functions to decrease insulin resistance. Glucose 57-64 insulin Homo sapiens 33-40 16456682-3 2006 The aim of this study was to evaluate the early insulin response and insulin clearance in response to an oral glucose load in obese children and adolescents. Glucose 110-117 insulin Homo sapiens 48-55 16456682-3 2006 The aim of this study was to evaluate the early insulin response and insulin clearance in response to an oral glucose load in obese children and adolescents. Glucose 110-117 insulin Homo sapiens 69-76 16456682-11 2006 The greater early insulin response needed to maintain glucose tolerance in young people of ethnic minorities may partially explain their greater tendency to develop type 2 diabetes. Glucose 54-61 insulin Homo sapiens 18-25 16477177-4 2006 By these actions, insulin preserves mitochondrial function, enhances adiponectin secretion and probably modulates AMP-activated protein kinase activity, which in turn depletes lipid depots in tissues and restores glucose uptake and oxidation. Glucose 213-220 insulin Homo sapiens 18-25 16477177-8 2006 A tight control of glucose levels by intense insulin therapy reduced morbidity in critically ill patients. Glucose 19-26 insulin Homo sapiens 45-52 16477178-2 2006 Insulin is used to achieve a tight glucose control or as part of glucose-insulin-potassium therapy. Glucose 35-42 insulin Homo sapiens 0-7 16477178-8 2006 Some recent evidence confirms a substantial benefit of insulin administered either alone to achieve a tight glucose control or as a component of glucose-insulin-potassium therapy. Glucose 108-115 insulin Homo sapiens 55-62 16477438-1 2006 AIMS/HYPOTHESIS: Insulin resistance, which manifests itself as endogenous glucose overproduction and reduced insulin-mediated glucose uptake, is a core defect in type 2 diabetes. Glucose 74-81 insulin Homo sapiens 17-24 16477438-1 2006 AIMS/HYPOTHESIS: Insulin resistance, which manifests itself as endogenous glucose overproduction and reduced insulin-mediated glucose uptake, is a core defect in type 2 diabetes. Glucose 126-133 insulin Homo sapiens 17-24 16477438-1 2006 AIMS/HYPOTHESIS: Insulin resistance, which manifests itself as endogenous glucose overproduction and reduced insulin-mediated glucose uptake, is a core defect in type 2 diabetes. Glucose 126-133 insulin Homo sapiens 109-116 16477438-7 2006 RESULTS: Both TZDs and metformin enhance insulin suppression of endogenous glucose production and fasting plasma glucose clearance. Glucose 75-82 insulin Homo sapiens 41-48 16477438-7 2006 RESULTS: Both TZDs and metformin enhance insulin suppression of endogenous glucose production and fasting plasma glucose clearance. Glucose 113-120 insulin Homo sapiens 41-48 16477438-8 2006 TZDs, but not metformin, also improve insulin-mediated glucose uptake at all insulin levels. Glucose 55-62 insulin Homo sapiens 38-45 16505238-2 2006 Exposure of INS-1 beta-cells to elevated glucose leads to reduced insulin gene transcription, and this is associated with diminished binding of pancreatic duodenal homeobox factor 1 (PDX-1) and mammalian homologue of avian MafA/l-Maf (MafA). Glucose 41-48 insulin Homo sapiens 66-73 16505238-4 2006 The low-potency PARP inhibitors nicotinamide, 3-aminobenzamide, or PD128763 increased expression of a human insulin reporter gene suppressed by elevated glucose. Glucose 153-160 insulin Homo sapiens 108-115 16505250-5 2006 Experiments in human adipocytes confirmed that the gene is upregulated in response to insulin in a glucose-dependent fashion. Glucose 99-106 insulin Homo sapiens 86-93 16505505-3 2006 Insulin glargine was forced-titrated to target fasting plasma glucose (FPG) < or =5.5-6.7 mmol/l (< or =100-120 mg/dl), and rosiglitazone was increased to 8 mg/day any time after 6 weeks if FPG was >5.5 mmol/l. Glucose 62-69 insulin Homo sapiens 0-7 16505516-7 2006 The significant association between proinsulin and HRT status persisted after adjustment for age, waist-to-hip ratio, pulse pressure, LDL-to-HDL cholesterol ratio, triglycerides, fasting and postchallenge glucose, and intact insulin. Glucose 205-212 insulin Homo sapiens 36-46 16505516-7 2006 The significant association between proinsulin and HRT status persisted after adjustment for age, waist-to-hip ratio, pulse pressure, LDL-to-HDL cholesterol ratio, triglycerides, fasting and postchallenge glucose, and intact insulin. Glucose 205-212 insulin Homo sapiens 39-46 16505516-11 2006 Increased postchallenge glucose in HRT, however, suggests insulin resistance and would be expected to increase the risk of heart disease. Glucose 24-31 insulin Homo sapiens 58-65 16505525-4 2006 Insulin resistance was estimated using the insulin sensitivity index (ISI) of Matsuda and DeFronzo [ISI = 10,000/square root of (fasting glucose x fasting insulin) x (mean glucose x mean insulin during an oral glucose tolerance test); lower ISI = greater insulin resistance]. Glucose 137-144 insulin Homo sapiens 0-7 16505544-0 2006 Decreased insulin secretion but not insulin sensitivity in normal glucose tolerant Thai subjects. Glucose 66-73 insulin Homo sapiens 10-17 16554425-4 2006 The discovery in the 1950s of the pancreatic hormone glucagon, which opposes insulin by increasing glucose appearance in the circulation, resulted in a bihormonal model of glucose homeostasis. Glucose 99-106 insulin Homo sapiens 77-84 16554425-6 2006 Therapies for diabetes have focused on compensation for deficient insulin action through stimulation of insulin secretion, administration of insulin itself, reduction of peripheral insulin resistance, or decreased glucose absorption from the intestine. Glucose 214-221 insulin Homo sapiens 66-73 16423804-2 2006 Every 2 weeks subcutaneous administration made their blood glucose level depend on the insulin release and food intake. Glucose 59-66 insulin Homo sapiens 87-94 16690465-4 2006 While he continued treatment with propoxyphene, 58 hours into a 72-hour fast the plasma glucose concentration was 38 mg/dL, in conjunction with a beta-hydroxybutyric acid level of 0.9 mmol/L and inappropriately elevated plasma insulin, serum C-peptide, and proinsulin levels. Glucose 88-95 insulin Homo sapiens 227-234 16690465-4 2006 While he continued treatment with propoxyphene, 58 hours into a 72-hour fast the plasma glucose concentration was 38 mg/dL, in conjunction with a beta-hydroxybutyric acid level of 0.9 mmol/L and inappropriately elevated plasma insulin, serum C-peptide, and proinsulin levels. Glucose 88-95 insulin Homo sapiens 257-267 16234828-7 2006 RESULTS: The study shows that a modest dietary modification, confined to a lowering of the GI character and increasing cereal DF of the bread products, improved insulin economy as judged from the fact that all women lowered their insulin responses to the intravenous glucose challenge on average by 35% (0-60 min), in the absence of effect on glycaemia. Glucose 267-274 insulin Homo sapiens 161-168 16234828-7 2006 RESULTS: The study shows that a modest dietary modification, confined to a lowering of the GI character and increasing cereal DF of the bread products, improved insulin economy as judged from the fact that all women lowered their insulin responses to the intravenous glucose challenge on average by 35% (0-60 min), in the absence of effect on glycaemia. Glucose 267-274 insulin Homo sapiens 230-237 16337941-0 2006 Insulin regulates neuronal glucose uptake by promoting translocation of glucose transporter GLUT3. Glucose 27-34 insulin Homo sapiens 0-7 16337941-2 2006 In this in vitro study, the effect of insulin on neuronal glucose uptake was studied by assaying glucose uptake, translocation of glucose transporter isoform GLUT3, and fusion of GLUT3 vesicles with the plasma membrane. Glucose 58-65 insulin Homo sapiens 38-45 16337941-2 2006 In this in vitro study, the effect of insulin on neuronal glucose uptake was studied by assaying glucose uptake, translocation of glucose transporter isoform GLUT3, and fusion of GLUT3 vesicles with the plasma membrane. Glucose 97-104 insulin Homo sapiens 38-45 16337941-2 2006 In this in vitro study, the effect of insulin on neuronal glucose uptake was studied by assaying glucose uptake, translocation of glucose transporter isoform GLUT3, and fusion of GLUT3 vesicles with the plasma membrane. Glucose 97-104 insulin Homo sapiens 38-45 16337941-5 2006 In cells pre-exposed to insulin, depolarization with 40 mM KCl markedly increased fusion of GLUT3 with plasma membrane and neuronal uptake of glucose. Glucose 142-149 insulin Homo sapiens 24-31 16337941-6 2006 Based on these data, we propose that insulin regulates neuronal glucose uptake by promoting translocation of GLUT3 to the plasma membrane, and that insulin enables neurons to respond to demand for energy induced by increased neuronal activity. Glucose 64-71 insulin Homo sapiens 37-44 16503818-2 2006 In clinical trials, pioglitazone as monotherapy or in combination with other oral antidiabetic drugs or insulin has demonstrated to effectively improve blood glucose levels, long-term glucose control and the lipid profile. Glucose 158-165 insulin Homo sapiens 104-111 16532763-5 2006 Then, by resorting to real and synthetic data, we show both in IVGTT MM and clamp studies why this new index SD(I) offers, in comparison with SI, a more comprehensive picture of the control of insulin on glucose. Glucose 204-211 insulin Homo sapiens 193-200 23105586-4 2006 The correlation between glucose and insulin sensitivity is consistent with the idea that the degree of chronic hyperglycemia is a cause of excessive insulin resistance in type 2 diabetes, i.e. the insulin resistance which characterizes type 2 diabetes but not nondiabetic subjects matched for age, gender, family history and duration of diabetes. Glucose 24-31 insulin Homo sapiens 36-43 23105586-4 2006 The correlation between glucose and insulin sensitivity is consistent with the idea that the degree of chronic hyperglycemia is a cause of excessive insulin resistance in type 2 diabetes, i.e. the insulin resistance which characterizes type 2 diabetes but not nondiabetic subjects matched for age, gender, family history and duration of diabetes. Glucose 24-31 insulin Homo sapiens 149-156 16352680-12 2006 Insulin sensitivity improved within 4 wk after beginning of metformin as shown by an increased area under the curve glucose to insulin ratio, compared with baseline (P < 0.005). Glucose 116-123 insulin Homo sapiens 0-7 16352680-12 2006 Insulin sensitivity improved within 4 wk after beginning of metformin as shown by an increased area under the curve glucose to insulin ratio, compared with baseline (P < 0.005). Glucose 116-123 insulin Homo sapiens 127-134 16352688-5 2006 Endothelial function, insulin-stimulated endothelial function, and insulin-stimulated glucose uptake were measured before and after quinapril treatment. Glucose 86-93 insulin Homo sapiens 67-74 16352689-9 2006 During both clamp steps, RSG enhanced insulin-mediated glucose clearance (by 26% and 31%; P = 0.01 and P < 0.02, respectively). Glucose 55-62 insulin Homo sapiens 38-45 16384854-10 2006 This may relieve tissues from the burden of NEFAs after the meal, thus facilitating muscle glucose disposal by insulin. Glucose 91-98 insulin Homo sapiens 111-118 16394086-9 2006 RESULTS: After glucose infusion, mean plasma glucose was increased by 16.8% (P < 0.0001), and plasma insulin was increased by 99.4% (P < 0.0001) compared with after saline infusion. Glucose 15-22 insulin Homo sapiens 104-111 16394086-10 2006 Significant decreases in homeostasis model assessment indicated a decrease in insulin sensitivity (saline, 0.52 + 0.13; glucose, 0.34 + 0.12; P < 0.0001). Glucose 120-127 insulin Homo sapiens 78-85 16522732-4 2006 Insulin sensitivity (IS(HOMA)) was estimated from fasting levels of glucose and insulin and percent truncal fat was determined by dual energy absorptiometry (DEXA). Glucose 68-75 insulin Homo sapiens 0-7 16567381-1 2006 BACKGROUND: Previous studies have demonstrated that aerobic exercise training and weight loss have independent effects on insulin-stimulated glucose disposal (ISGD). Glucose 141-148 insulin Homo sapiens 122-129 16426829-3 2006 The phenomenon of "insulin resistance" or the impaired ability to normalize plasma glucose levels has formed the core of these pathways, but other mechanisms have also been advanced. Glucose 83-90 insulin Homo sapiens 19-26 16426829-4 2006 Obesity-induced insulin resistance leads to elevated levels of plasma insulin, glucose and fatty acids. Glucose 79-86 insulin Homo sapiens 16-23 16607927-1 2006 OBJECTIVES: To evaluate insulin sensitivity from data obtained from baseline values and from an oral glucose tolerance test (OGTT) in normal and obese children and adolescents. Glucose 101-108 insulin Homo sapiens 24-31 16517950-1 2006 BACKGROUND: Glutamine interacts with insulin-mediated glucose disposal, which is a component of the increase in energy expenditure (EE) after a meal. Glucose 54-61 insulin Homo sapiens 37-44 16711601-4 2006 Oleate-treated fat cells also showed exaggerated basal lipolysis and weak response to insulin in both lipolysis regulation and glucose uptake. Glucose 127-134 insulin Homo sapiens 86-93 16483873-13 2006 In addition, troglitazone improved insulin-stimulated glucose uptake in differentiated fat cells. Glucose 54-61 insulin Homo sapiens 35-42 16540829-2 2006 Therefore, we examined the influence of moderate-intensity (50% of VO2max) exercise training (MI) versus high-intensity (75% of VO2max) exercise training (HI) on insulin-stimulated glucose disposal (ISGD) in elderly individuals. Glucose 181-188 insulin Homo sapiens 162-169 25696601-0 2006 Glucose and potassium derangements by glucose-insulin-potassium infusion in acute myocardial infarction. Glucose 0-7 insulin Homo sapiens 46-53 25696601-0 2006 Glucose and potassium derangements by glucose-insulin-potassium infusion in acute myocardial infarction. Glucose 38-45 insulin Homo sapiens 46-53 25696601-1 2006 BACKGROUND: High-dose glucose-insulin-potassium infusion (GIK) has been suggested to be beneficial in acute myocardial infarction (MI). Glucose 22-29 insulin Homo sapiens 30-37 16530126-3 2006 Glucagon excess counteracts the action of insulin on glucose metabolism by stimulating glycogenolysis and gluconeogenesis. Glucose 53-60 insulin Homo sapiens 42-49 16639388-1 2006 Altered glucose metabolism in obese youth is associated with defects in insulin sensitivity and insulin secretion. Glucose 8-15 insulin Homo sapiens 72-79 16639388-5 2006 Altered glucose metabolism in obese youth represents an element of the "insulin resistance syndrome", comprising obesity, dyslipidemia and hypertension. Glucose 8-15 insulin Homo sapiens 72-79 16461467-9 2006 These results reveal a MAP4K4/NIK-dependent signaling pathway that potently inhibits PPARgamma-responsive gene expression, adipogenesis, and insulin-stimulated glucose transport. Glucose 160-167 insulin Homo sapiens 141-148 16246375-6 2006 This effect was independent on insulin concentration, which was similar to that of metformin and was different from that of troglitazone, whose glucose-lowering effect was insulin-dependent. Glucose 144-151 insulin Homo sapiens 172-179 16246375-10 2006 The results indicate that ecdysterone is able to exert the glucose-lowering effect in hepatocytes which is insulin-independent, but has no effect on insulin release. Glucose 59-66 insulin Homo sapiens 107-114 16131513-7 2006 VAT area was inversely related with whole body glucose disposal, insulin sensitivity, and muscle glucose uptake during insulin stimulation. Glucose 97-104 insulin Homo sapiens 119-126 16139881-0 2006 Glucose-responsive UV polymerised dextran-concanavalin A acrylic derivatised mixtures for closed-loop insulin delivery. Glucose 0-7 insulin Homo sapiens 102-109 16139881-7 2006 Insulin delivery in response to glucose in the physiologically relevant glucose concentration range was demonstrated using the novel polymerised mixture at 37 degrees C. The performance of this covalently cross-linked glucose-responsive biomaterial has been improved in terms of increased mixture stability with reduced component leaching. Glucose 32-39 insulin Homo sapiens 0-7 16139881-7 2006 Insulin delivery in response to glucose in the physiologically relevant glucose concentration range was demonstrated using the novel polymerised mixture at 37 degrees C. The performance of this covalently cross-linked glucose-responsive biomaterial has been improved in terms of increased mixture stability with reduced component leaching. Glucose 72-79 insulin Homo sapiens 0-7 16139881-7 2006 Insulin delivery in response to glucose in the physiologically relevant glucose concentration range was demonstrated using the novel polymerised mixture at 37 degrees C. The performance of this covalently cross-linked glucose-responsive biomaterial has been improved in terms of increased mixture stability with reduced component leaching. Glucose 72-79 insulin Homo sapiens 0-7 16483886-0 2006 Interactions between energy surplus and short-term exercise on glucose and insulin responses in healthy people with induced, mild insulin insensitivity. Glucose 63-70 insulin Homo sapiens 130-137 16483886-8 2006 A single exercise bout, opposed by a concurrent energy surplus, decreased the insulin response to a glucose challenge, but only partially restored the insulin AUC to baseline and had no impact on C-ISI or fasting insulin concentrations. Glucose 100-107 insulin Homo sapiens 78-85 16530130-1 2006 The glucose-stimulus/insulin-secretion-coupling by the pancreatic beta-cell, which guarantees the maintenance of glucose homeostasis in man, is regulated by a sophisticated interplay between glucose and a plethora of additional factors. Glucose 4-11 insulin Homo sapiens 21-28 16530130-1 2006 The glucose-stimulus/insulin-secretion-coupling by the pancreatic beta-cell, which guarantees the maintenance of glucose homeostasis in man, is regulated by a sophisticated interplay between glucose and a plethora of additional factors. Glucose 113-120 insulin Homo sapiens 21-28 16555754-1 2006 Intensive insulin therapy (IIT) for the management of high blood glucose can reduce mortality and morbidity in the critically ill. Glucose 65-72 insulin Homo sapiens 10-17 16633326-6 2006 Insulin resistance results in abnormalities of glucose metabolism, with reduced peripheral disposal of glucose in muscle and increased hepatic glucose output in the fasting state. Glucose 47-54 insulin Homo sapiens 0-7 16633331-3 2006 The impairment in fat and glucose metabolism that ensues once insulin resistance occurs leads to similar biochemical and clinical abnormalities in patients with NAFLD. Glucose 26-33 insulin Homo sapiens 62-69 16703228-3 2006 It is suggested to check fasting glucose levels in patients scheduled for cardiovascular surgery and to give intensive insulin therapy perioperatively if fasting glucose levels are greater than 7.0 mmol/L (126 mg/dL). Glucose 162-169 insulin Homo sapiens 119-126 16549165-9 2006 Insulin resistance was calculated by the homeostasis model assessment (HOMA) method using the values of fasting blood glucose (FBG) and insulin levels. Glucose 118-125 insulin Homo sapiens 0-7 16428559-2 2006 We describe a patient who developed cardiac asystole while being given a concentrated glucose solution to treat severe hypoglycemia after administration of insulin. Glucose 86-93 insulin Homo sapiens 156-163 16754199-5 2006 In consequence, TNF-alpha-induced insulin resistance on glucose uptake was completely alleviated. Glucose 56-63 insulin Homo sapiens 34-41 16462893-10 2006 In conclusion, this study suggests that insulin and estradiol are able to contain the deleterious effect of high concentrations of glucose on BMSC-derived osteoblast proliferation and function. Glucose 131-138 insulin Homo sapiens 40-47 16459313-1 2006 Glucose stimulates the exocytosis of insulin secretory granules of pancreatic beta cells. Glucose 0-7 insulin Homo sapiens 37-44 16459313-5 2006 Glucagon-like peptide 1 (GLP-1) potentiates glucose-stimulated insulin gene expression and secretion by increasing cAMP levels in beta cells. Glucose 44-51 insulin Homo sapiens 63-70 16430711-13 2006 Both these determinants of mortality can exert their effects by insulin-independent uptake of glucose with subsequent toxic intracellular effects. Glucose 94-101 insulin Homo sapiens 64-71 16424718-11 2006 At day 4, insulin-mediated glucose disposal was higher in group AG (2.4 +/- 0.7 mg x kg(-1) x min(-1) glucose), with significant difference from group C (1.9 +/- 0.6 mg x kg(-1) x min(-1), p = .044). Glucose 27-34 insulin Homo sapiens 10-17 16424718-11 2006 At day 4, insulin-mediated glucose disposal was higher in group AG (2.4 +/- 0.7 mg x kg(-1) x min(-1) glucose), with significant difference from group C (1.9 +/- 0.6 mg x kg(-1) x min(-1), p = .044). Glucose 102-109 insulin Homo sapiens 10-17 16469124-12 2006 CONCLUSION: Studies using a dynamic scale protocol combining a tight glucose target and the last two blood glucose values to determine the insulin infusion rate yielded the best results in terms of glycaemic control and reported low frequencies of hypoglycaemic episodes. Glucose 107-114 insulin Homo sapiens 139-146 18220618-1 2006 Insulin mediates its own access and that of glucose to muscle by capillary recruitment and an increase in bulk blood flow. Glucose 44-51 insulin Homo sapiens 0-7 16026886-8 2006 Insulin resistance was significantly associated with the progression of glycemic metabolism (HOMA-IR of subjects with normal fasting glucose, IFG, and DM were 1.12+/-1.24, 1.88+/-1.64, 4.47+/-5.12, P<0.001). Glucose 133-140 insulin Homo sapiens 0-7 16105705-3 2006 The average glucose infusion rates (GIR) before and during exercise were regarded as an index of the insulin action in peripheral tissues by the euglycemic clamp. Glucose 12-19 insulin Homo sapiens 101-108 16105705-9 2006 In elder diabetic patients, mechanical horseback riding enhances the insulin-induced glucose uptake. Glucose 85-92 insulin Homo sapiens 69-76 16226857-11 2006 CONCLUSIONS: In the largest study of normal 7-day-old children to date we have shown insulin concentrations are low compared to adults and vary with glucose, time from feed, and type of feed. Glucose 149-156 insulin Homo sapiens 85-92 16369774-6 2006 RESULTS: Insulin resistance of glucose and protein metabolism occurred in obese and elderly subjects. Glucose 31-38 insulin Homo sapiens 9-16 16385385-8 2006 CONCLUSIONS/INTERPRETATION: The expression of genes encoding inhibitors of IL-1 signalling is upregulated in the WAT of mice with diet-induced obesity, and IL-1Ra reduces insulin sensitivity in rats through a muscle-specific decrease in glucose uptake. Glucose 237-244 insulin Homo sapiens 171-178 16395615-3 2006 Moreover, such lipid effects may improve insulin sensitivity and insulin-stimulated glucose uptake. Glucose 84-91 insulin Homo sapiens 65-72 16443774-0 2006 Contrasting insulin sensitivity of endogenous glucose production rate in subjects with hepatocyte nuclear factor-1beta and -1alpha mutations. Glucose 46-53 insulin Homo sapiens 12-19 16443774-10 2006 Insulin-stimulated glucose uptake and suppression of lipolysis were similar in all groups at low- and high-dose insulin. Glucose 19-26 insulin Homo sapiens 0-7 16443774-11 2006 Subjects with HNF-1beta mutations have reduced insulin sensitivity of endogenous glucose production but normal peripheral insulin sensitivity. Glucose 81-88 insulin Homo sapiens 47-54 16443776-1 2006 Phosphatidylinositol 3-kinase (PI3 kinase) inhibition disrupts the ability of insulin to stimulate GLUT1 and GLUT4 translocation into the cell membrane and thus glucose transport. Glucose 161-168 insulin Homo sapiens 78-85 16443778-3 2006 In islets from the diabetic patients, insulin responses to 8.3 and 16.7 mmol/l glucose were markedly reduced compared with control islets (4.7 +/- 0.3 and 8.4 +/- 1.8 vs. 17.5 +/- 0.1 and 24.3 +/- 1.2 microU . Glucose 79-86 insulin Homo sapiens 38-45 16443858-1 2006 OBJECTIVE: To study the effect of the short-acting insulin secretagogue nateglinide in patients with maturity-onset diabetes of the young type 3 (MODY3), which is characterized by a defective insulin response to glucose and hypersensitivity to sulfonylureas. Glucose 212-219 insulin Homo sapiens 192-199 16443887-0 2006 Impact of differences in fasting glucose and glucose tolerance on the hyperbolic relationship between insulin sensitivity and insulin responses. Glucose 33-40 insulin Homo sapiens 102-109 16443887-0 2006 Impact of differences in fasting glucose and glucose tolerance on the hyperbolic relationship between insulin sensitivity and insulin responses. Glucose 33-40 insulin Homo sapiens 126-133 16443887-0 2006 Impact of differences in fasting glucose and glucose tolerance on the hyperbolic relationship between insulin sensitivity and insulin responses. Glucose 45-52 insulin Homo sapiens 102-109 16443887-0 2006 Impact of differences in fasting glucose and glucose tolerance on the hyperbolic relationship between insulin sensitivity and insulin responses. Glucose 45-52 insulin Homo sapiens 126-133 16443887-1 2006 OBJECTIVE: To determine whether the hyperbolic relationship between insulin sensitivity and the acute insulin response to glucose (AIRg) exists in subjects with impaired fasting glucose (IFG) or decreased glucose tolerance. Glucose 122-129 insulin Homo sapiens 68-75 16443887-1 2006 OBJECTIVE: To determine whether the hyperbolic relationship between insulin sensitivity and the acute insulin response to glucose (AIRg) exists in subjects with impaired fasting glucose (IFG) or decreased glucose tolerance. Glucose 122-129 insulin Homo sapiens 102-109 16443887-1 2006 OBJECTIVE: To determine whether the hyperbolic relationship between insulin sensitivity and the acute insulin response to glucose (AIRg) exists in subjects with impaired fasting glucose (IFG) or decreased glucose tolerance. Glucose 178-185 insulin Homo sapiens 68-75 16443887-10 2006 CONCLUSIONS: The inverse relationship between insulin sensitivity and AIRg is consistent with a hyperbola not only in subjects with normal glucose tolerance but also with mild IFG or decreased Kg. Glucose 139-146 insulin Homo sapiens 46-53 16472054-6 2006 Peak insulin levels were generally attained in 15-20 min and remained elevated for approximately 1 h; the resultant effect upon glucose peaked at 40 min and waned 1.5-2 h post-dosing. Glucose 128-135 insulin Homo sapiens 5-12 16472060-6 2006 The diabetes/insulin tutorial is currently composed of four sections: the first two cover in considerable depth insulin injection regimens and insulin dosage adjustment; the third section introduces the principles of carbohydrate counting and, specifically, matching insulin doses to carbohydrate intake; and the fourth section illustrates the relationship between blood glucose levels and renal excretion of glucose. Glucose 371-378 insulin Homo sapiens 13-20 16622294-4 2006 Weight loss and thiazolidinediones (TZDs) improve glucose disposal, in part, by increasing insulin-stimulated insulin receptor and IRS-1 tyrosine phosphorylation and PI 3-kinase activity. Glucose 50-57 insulin Homo sapiens 91-98 16622294-4 2006 Weight loss and thiazolidinediones (TZDs) improve glucose disposal, in part, by increasing insulin-stimulated insulin receptor and IRS-1 tyrosine phosphorylation and PI 3-kinase activity. Glucose 50-57 insulin Homo sapiens 110-117 16622294-7 2006 A different strategy to increase muscle glucose disposal is by stimulating insulin-independent glucose transport. Glucose 40-47 insulin Homo sapiens 75-82 16622304-7 2006 Furthermore, group IV showed significantly higher 2-h insulin levels after glucose loading compared to group I (p < 0.001). Glucose 75-82 insulin Homo sapiens 54-61 16177820-5 2006 Cotransfection of GLUT 2 with insulin permitted the diabetic rats to regulate their blood glucose levels upon exogenous glucose loading in a physiologically appropriate manner and improved postprandial glucose levels. Glucose 90-97 insulin Homo sapiens 30-37 16177820-5 2006 Cotransfection of GLUT 2 with insulin permitted the diabetic rats to regulate their blood glucose levels upon exogenous glucose loading in a physiologically appropriate manner and improved postprandial glucose levels. Glucose 120-127 insulin Homo sapiens 30-37 16177820-5 2006 Cotransfection of GLUT 2 with insulin permitted the diabetic rats to regulate their blood glucose levels upon exogenous glucose loading in a physiologically appropriate manner and improved postprandial glucose levels. Glucose 120-127 insulin Homo sapiens 30-37 16177820-6 2006 Moreover, cotransfection with insulin and GLUT 2 genes led to in vitro glucose-stimulated insulin secretion that involved the closure of K(ATP) channels. Glucose 71-78 insulin Homo sapiens 30-37 16177820-7 2006 The present study represents a new way to efficiently deliver insulin gene in vivo that is regulated by ambient glucose level with prolonged gene expression. Glucose 112-119 insulin Homo sapiens 62-69 16420480-0 2006 Prohibitin attenuates insulin-stimulated glucose and fatty acid oxidation in adipose tissue by inhibition of pyruvate carboxylase. Glucose 41-48 insulin Homo sapiens 22-29 16420480-5 2006 As a consequence, it can modulate insulin-stimulated glucose and fatty acid oxidation. Glucose 53-60 insulin Homo sapiens 34-41 15985560-8 2006 It diminished plasma insulin during duodenal glucose and significantly reduced the incretin effect by approximately 50%. Glucose 45-52 insulin Homo sapiens 21-28 16505579-4 2006 The mechanisms underlying the metabolic syndrome are not fully known; however resistance to insulin stimulated glucose uptake seems to modify biochemical responses in a way that predisposes to metabolic risk factors. Glucose 111-118 insulin Homo sapiens 92-99 16523410-5 2006 Thus, a paradoxical lowering of the insulinogenic index, i. e. the paired ratio between plasma insulin and glucose concentration, was recorded during the oral glucose tolerance test in rats fed either standard or OO diet. Glucose 107-114 insulin Homo sapiens 36-43 16523410-5 2006 Thus, a paradoxical lowering of the insulinogenic index, i. e. the paired ratio between plasma insulin and glucose concentration, was recorded during the oral glucose tolerance test in rats fed either standard or OO diet. Glucose 159-166 insulin Homo sapiens 36-43 16213777-3 2006 Akt mediates insulin-dependent glucose uptake in insulin-sensitive tissues. Glucose 31-38 insulin Homo sapiens 13-20 16213777-3 2006 Akt mediates insulin-dependent glucose uptake in insulin-sensitive tissues. Glucose 31-38 insulin Homo sapiens 49-56 16291705-6 2006 First-phase insulin release was evaluated after iv glucose stimulation. Glucose 51-58 insulin Homo sapiens 12-19 16291705-11 2006 Three patients showed an exaggerated insulin response under graded glucose infusion and preserved secretion under arginine stimulation. Glucose 67-74 insulin Homo sapiens 37-44 16291705-12 2006 Three other patients, with elevated fasting plasma glucose levels, demonstrated a very low insulin response under glucose stimulation and a low insulin response under arginine stimulation. Glucose 51-58 insulin Homo sapiens 91-98 16291705-12 2006 Three other patients, with elevated fasting plasma glucose levels, demonstrated a very low insulin response under glucose stimulation and a low insulin response under arginine stimulation. Glucose 51-58 insulin Homo sapiens 144-151 16291705-12 2006 Three other patients, with elevated fasting plasma glucose levels, demonstrated a very low insulin response under glucose stimulation and a low insulin response under arginine stimulation. Glucose 114-121 insulin Homo sapiens 91-98 16291707-1 2006 CONTEXT: Insulin-stimulated glucose uptake in skeletal muscle is mediated through translocation of the insulin-sensitive glucose transporter 4 (GLUT4)-containing vesicles to the plasma membrane. Glucose 28-35 insulin Homo sapiens 9-16 16291707-1 2006 CONTEXT: Insulin-stimulated glucose uptake in skeletal muscle is mediated through translocation of the insulin-sensitive glucose transporter 4 (GLUT4)-containing vesicles to the plasma membrane. Glucose 28-35 insulin Homo sapiens 103-110 16291707-9 2006 Both basal and insulin-stimulated expressions of GLUT4 were independently and significantly related to whole-body in vivo insulin action, nonoxidative glucose metabolism, and glucose oxidation. Glucose 151-158 insulin Homo sapiens 15-22 16317063-12 2006 CONCLUSIONS: Injection of Lispro insulin with meals produces more physiological insulin patterns, better glucose control, and improved leptin and ghrelin regulation than R+N. Glucose 105-112 insulin Homo sapiens 33-40 16510859-1 2006 BACKGROUND: Although insulin resistance of glucose is often reported with aging, that of protein metabolism is still debated. Glucose 43-50 insulin Homo sapiens 21-28 16510859-6 2006 Thus, the net anabolic (protein balance) response to hyperinsulinemia was lower in elderly versus young participants (p =.007) and was highly correlated with the clamp glucose rate of disposal (r = 0.671, p <.001), indicating insulin resistance of protein concurrent with that of glucose. Glucose 168-175 insulin Homo sapiens 58-65 16510859-6 2006 Thus, the net anabolic (protein balance) response to hyperinsulinemia was lower in elderly versus young participants (p =.007) and was highly correlated with the clamp glucose rate of disposal (r = 0.671, p <.001), indicating insulin resistance of protein concurrent with that of glucose. Glucose 283-290 insulin Homo sapiens 58-65 16301737-6 2006 Basal glucose transport and oxidation (CO2) were increased 2-fold after EPA, and insulin (100 nM) stimulated glucose transport and oxidation similarly in control and EPA-treated myotubes, whereas these responses to insulin were abolished after OA treatment. Glucose 6-13 insulin Homo sapiens 215-222 16301737-6 2006 Basal glucose transport and oxidation (CO2) were increased 2-fold after EPA, and insulin (100 nM) stimulated glucose transport and oxidation similarly in control and EPA-treated myotubes, whereas these responses to insulin were abolished after OA treatment. Glucose 109-116 insulin Homo sapiens 81-88 16492429-1 2006 OBJECTIVE: To determine whether stabilizing serum glucose, via introduction of an insulin pump, improves classroom attention among children with type-1 diabetes mellitus. Glucose 50-57 insulin Homo sapiens 82-89 16562586-2 2006 In order to further assess beta-cell function in DM2, we measured insulin and C-peptide responses to oral glucose in adolescents with DM2 in comparison to non-diabetic obese and lean adolescents. Glucose 106-113 insulin Homo sapiens 78-87 16423619-8 2006 These are the only indexes characterized by units of measure consistent with the definition of insulin sensitivity as the ability of insulin to enhance glucose effectiveness. Glucose 152-159 insulin Homo sapiens 95-102 16423619-8 2006 These are the only indexes characterized by units of measure consistent with the definition of insulin sensitivity as the ability of insulin to enhance glucose effectiveness. Glucose 152-159 insulin Homo sapiens 133-140 16423624-2 2006 The aim of this study was to find out whether insulin resistance and high-sensitivity C-reactive protein (hsCRP), a nontraditional cardiovascular risk factor, were related to the fasting glucose level, even in normoglycemic range that was categorized by the newly recommended criteria by the American Diabetes Association. Glucose 187-194 insulin Homo sapiens 46-53 16423624-9 2006 In conclusion, the insulin resistance indexes and hsCRP increased gradually even in the normal fasting glucose range, as categorized by the newly recommended criteria for abnormal fasting glucose levels, supporting the rationale for expanding the range of fasting hyperglycemia. Glucose 103-110 insulin Homo sapiens 19-26 16423624-9 2006 In conclusion, the insulin resistance indexes and hsCRP increased gradually even in the normal fasting glucose range, as categorized by the newly recommended criteria for abnormal fasting glucose levels, supporting the rationale for expanding the range of fasting hyperglycemia. Glucose 188-195 insulin Homo sapiens 19-26 16423632-5 2006 Insulin resistance was calculated using the homeostasis assessment model using the formula: fasting insulin (microIU/mL) x fasting glucose (mmol/L)/22.5. Glucose 131-138 insulin Homo sapiens 0-7 16531895-0 2006 Effects of increasing insulin secretion on acute postexercise blood glucose disposal. Glucose 68-75 insulin Homo sapiens 22-29 16489976-4 2006 The following review describes the various physiological and metabolic factors which occur both during exercise and during sport while describing specific recommendations to control glucose excursions by proper insulin management and diet. Glucose 182-189 insulin Homo sapiens 211-218 15703952-0 2006 Body mass index and blood glucose: correlations with serum insulin, growth hormone, and insulin-like growth factor-1 levels in patients with diffuse idiopathic skeletal hyperostosis (DISH). Glucose 26-33 insulin Homo sapiens 59-66 16446701-8 2006 Insulin produced a dose-dependent increase in FGF-2 in RPE cells and decrease in GFAP in Muller cells grown in 15 mM glucose. Glucose 117-124 insulin Homo sapiens 0-7 16446701-10 2006 Physiological levels of insulin inhibited changes induced by 15 mM glucose. Glucose 67-74 insulin Homo sapiens 24-31 15964160-8 2006 Pretreatment SHBG showed significant negative correlations to BMI and to variables that may reflect a certain degree of insulin resistance, the most pronounced being fasting glucose. Glucose 174-181 insulin Homo sapiens 120-127 16497175-9 2006 The actual physiological roles of resistin and TNF-alpha in altering muscle lipid metabolism are more controversial, but each has been shown to directly impair insulin signalling and consequently, insulin stimulated glucose uptake in muscle. Glucose 216-223 insulin Homo sapiens 197-204 17239301-4 2006 Application of this formula is possible, when the reference values of the area under curve of glucose (GLU(AUC)) and insulin (INS(AUC)) concentration during oral glucose tolerance test (OGTT) are available for the studied population. Glucose 162-169 insulin Homo sapiens 117-124 16461467-2 2006 Here we report an RNA interference-based screen of protein kinases expressed in adipocytes and identify four negative regulators of insulin-responsive glucose transport: the protein kinases PCTAIRE-1 (PCTK1), PFTAIRE-1 (PFTK1), IkappaB kinase alpha, and MAP4K4/NIK. Glucose 151-158 insulin Homo sapiens 132-139 17162544-3 2006 This review aims to explain the rationale for providing intensive control of serum glucose levels in the ICCU, especially using intensive insulin therapy and summarizes the available clinical evidence suggesting its effectiveness. Glucose 83-90 insulin Homo sapiens 138-145 17163094-2 2006 In virtually all studies, whether of cardiac ischemia or bypass surgery, cerebrovascular recovery from ischemia or head injury, or surgical critical illness, intensive insulin therapy with tight glucose control has resulted in improved clinical outcomes by decreasing both morbidity and mortality. Glucose 195-202 insulin Homo sapiens 168-175 17357293-6 2006 The glucose monitoring with the use of CGMS lasted 48 hours and was conducted on the second and on the third day of intensive insulin therapy. Glucose 4-11 insulin Homo sapiens 126-133 16400048-0 2006 Body mass index and waist circumference both contribute to differences in insulin-mediated glucose disposal in nondiabetic adults. Glucose 91-98 insulin Homo sapiens 74-81 16400048-3 2006 OBJECTIVE: This study quantified insulin-mediated glucose uptake (IMGU) in 330 apparently healthy volunteers and compared the relation between this value and measurements of WC and BMI. Glucose 50-57 insulin Homo sapiens 33-40 16461199-1 2006 BACKGROUND: This study examined the relative role of age and hypertension in deterioration of insulin-dependent (insulin sensitivity, S(I)) and insulin-independent (glucose effectiveness, S(G)) actions on glucose tolerance. Glucose 205-212 insulin Homo sapiens 94-101 16126809-2 2006 Nitric oxide-dependent vasodilator actions of insulin may augment glucose disposal. Glucose 66-73 insulin Homo sapiens 46-53 16144811-4 2006 The models were identified on insulin-modified intravenous glucose tolerance test (IM-IVGTT) data of 20 healthy subjects. Glucose 59-66 insulin Homo sapiens 30-37 16174656-4 2006 Compared with placebo, trimetazidine induced 1) an increase in insulin-induced forearm glucose uptake and glucose oxidation accompanied by a reduction in forearm lipid oxidation and citrate release and 2) a decrease of endothelin-1 release paralleled by a significant increase in forearm cGMP release. Glucose 87-94 insulin Homo sapiens 63-70 16174656-4 2006 Compared with placebo, trimetazidine induced 1) an increase in insulin-induced forearm glucose uptake and glucose oxidation accompanied by a reduction in forearm lipid oxidation and citrate release and 2) a decrease of endothelin-1 release paralleled by a significant increase in forearm cGMP release. Glucose 106-113 insulin Homo sapiens 63-70 16174656-6 2006 In conclusion, for the first time, we demonstrated that insulin-induced forearm glucose oxidation and forearm cGMP release were increased whereas forearm endothelin-1 release was decreased during trimetazidine treatment. Glucose 80-87 insulin Homo sapiens 56-63 16389017-5 2006 RESULTS: The kinetic decline in glucose after insulin (kITT) as a marker of IR was the most frequently abnormal test (abnormal in 81%), with QUICKI, HOMA, and a modification of the Matsuda-DeFronzo index (ISIM) abnormal in 76, 73, and 68%, respectively. Glucose 32-39 insulin Homo sapiens 46-53 16373994-4 2006 Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR) derived from fasting glucose and insulin concentrations. Glucose 96-103 insulin Homo sapiens 0-7 16448988-2 2006 In pathophysiological terms, insulin resistance (of glucose metabolism) and the attendant compensatory hyperinsulinaemia are causally related to each of glucose intolerance, dyslipidaemia, high blood pressure and vascular dysfunction. Glucose 52-59 insulin Homo sapiens 29-36 17008303-1 2006 Skeletal muscle constitutes the largest insulin-sensitive tissue in the body and is the primary site for insulin-stimulated glucose utilization. Glucose 124-131 insulin Homo sapiens 40-47 17008303-1 2006 Skeletal muscle constitutes the largest insulin-sensitive tissue in the body and is the primary site for insulin-stimulated glucose utilization. Glucose 124-131 insulin Homo sapiens 105-112 17008303-3 2006 The inability to efficiently take up and store fuel, and to transition from fat to glucose as the primary source of fuel during times of caloric abundance (high insulin) or scarcity (low insulin) has been termed metabolic inflexibility which contributes to a whole body metabolic dysregulation and cardiovascular risk. Glucose 83-90 insulin Homo sapiens 161-168 16704347-8 2006 The usual increase in insulin resistance seen in late pregnancy is enhanced in obese mothers, causing marked postprandial increases in glucose, lipids, and amino acids and excessive fetal exposure to fuel sources, which in turn increases fetal size, fat stores, and risk for disease postnatally. Glucose 135-142 insulin Homo sapiens 22-29 16848718-5 2006 In addition, tight blood glucose control with insulin is advised in fed critically ill patients because overall metabolic control appears to surpass any outcome benefit attributed to the route of feeding. Glucose 25-32 insulin Homo sapiens 46-53 17302378-7 2006 There were small increases in fasting glycaemia and insulin resistance estimated by the homeostasis model assessment, but insulin resistance measures from the 2-h oral glucose tolerance test only transiently worsened. Glucose 168-175 insulin Homo sapiens 122-129 16399498-0 2006 A missing sugar prevents glucose entry: a new twist on insulin secretion. Glucose 25-32 insulin Homo sapiens 55-62 16399498-1 2006 The signaling pathway that regulates glucose-stimulated insulin secretion depends on glucose metabolism, which is itself controlled by glucokinase. Glucose 37-44 insulin Homo sapiens 56-63 16399498-1 2006 The signaling pathway that regulates glucose-stimulated insulin secretion depends on glucose metabolism, which is itself controlled by glucokinase. Glucose 85-92 insulin Homo sapiens 56-63 16399498-2 2006 In a recent issue of Cell, show that altering N-glycosylation of the GLUT2 glucose transporter prevents its anchoring and retention at the cell surface; this impairs glucose uptake and insulin secretion. Glucose 75-82 insulin Homo sapiens 185-192 16399504-3 2006 The intra-islet action of insulin is essential to exert the effect of glucose on the alpha cells since, in the absence of insulin, glucose is not able to suppress glucagon release in vivo. Glucose 70-77 insulin Homo sapiens 26-33 16399504-3 2006 The intra-islet action of insulin is essential to exert the effect of glucose on the alpha cells since, in the absence of insulin, glucose is not able to suppress glucagon release in vivo. Glucose 131-138 insulin Homo sapiens 26-33 16898226-5 2006 Morphology, viability, and glucose-responding insulin secretion were analyzed in the coculture system. Glucose 27-34 insulin Homo sapiens 46-53 16776626-0 2006 Comparability of indices for insulin resistance and insulin secretion determined during oral glucose tolerance tests. Glucose 93-100 insulin Homo sapiens 29-59 17947036-0 2006 Neural network based glucose - insulin metabolism models for children with Type 1 diabetes. Glucose 21-28 insulin Homo sapiens 31-38 17065814-4 2006 Hyposmotic stimulation of insulin secretion is independent from the extra- and intracellular Ca(2+), does not involve other intracellular mediators of glucose stimulation, and could not be inhibited by noradrenaline. Glucose 151-158 insulin Homo sapiens 26-33 16475928-2 2006 In pancreatic beta cells the K(ATP) channels, which are formed by 4 ion channels (Kir6.2) and 4 regulatory sulfonylurea receptors (SUR1), control the glucose stimulated release of insulin. Glucose 150-157 insulin Homo sapiens 180-187 16475928-9 2006 NN414 has been shown to be a potent and Kir6.2/SUR1 selective K(ATP) channels opener, which inhibits glucose stimulated insulin release in vitro and in vivo and which has beneficial effects on glucose homeostasis in preclinical and clinical studies. Glucose 101-108 insulin Homo sapiens 120-127 16914073-2 2006 Glucose-lowering drug therapies that target insulin resistance can therefore utilize different mechanistic approaches. Glucose 0-7 insulin Homo sapiens 44-51 16914073-6 2006 FINDINGS: The different insulin-sensitizing mechanisms of metformin and the thiazolidinediones are manifest in partially distinct effects on hepatic and peripheral glucose homeostasis, and clinical studies show improved glucose control with combination therapy. Glucose 164-171 insulin Homo sapiens 24-31 17168709-5 2006 Thiazolidinediones (TZD) are ligands for PPARgamma used therapeutically to enhance insulin-mediated glucose uptake in persons with type 2 diabetes. Glucose 100-107 insulin Homo sapiens 83-90 16533167-5 2006 Furthermore, naloxone and naltrexone significantly reduce the insulin response to glucose load only in hyperinsulinemic PCOS patients. Glucose 82-89 insulin Homo sapiens 62-69 16323003-7 2006 RESULTS: Both interventions increased insulin-stimulated glucose disposal and reduced plasma oleate concentrations during the insulin clamp. Glucose 57-64 insulin Homo sapiens 38-45 16362283-7 2006 RESULTS: Insulin sensitivity was normally distributed, with a mean of 73.2+/-29.3 (SD) nmol glucose kg(-1) min(-1)/pmol insulin l(-1). Glucose 92-99 insulin Homo sapiens 9-16 16362283-8 2006 When relating the variables obtained from the arginine test to insulin sensitivity, insulin resistance was associated with increased AGR and with increased suppression of glucagon levels by glucose. Glucose 190-197 insulin Homo sapiens 84-91 16362283-9 2006 For example, the regression between insulin sensitivity and AGR(2) was r=-0.38 (p<0.001) and between insulin sensitivity and suppression of glucagon levels by 14.8 mmol/l glucose r=0.36 (p<0.001). Glucose 174-181 insulin Homo sapiens 104-111 16362283-11 2006 CONCLUSIONS/INTERPRETATION: The body adapts to insulin resistance by increasing the glucagon response to arginine and by increasing the suppression of glucagon levels by glucose. Glucose 170-177 insulin Homo sapiens 47-54 16367880-12 2006 Postprandial glucose lowering is one of several metabolic effects of PIO in addition to decreasing insulin resistance and improving some lipids components. Glucose 13-20 insulin Homo sapiens 99-106 16367888-8 2006 CONCLUSIONS: These results demonstrate that various glucose-lowering therapies and oleic acid reduce resistin gene expression in isolated adipocytes, and that resistin impairs insulin-stimulated glucose uptake in skeletal muscle-derived cells. Glucose 195-202 insulin Homo sapiens 176-183 16373894-15 2006 CONCLUSIONS: We conclude that real-time continuous glucose monitoring for periods up to 72 h is accurate and safe in insulin-requiring subjects with type 1 and type 2 diabetes. Glucose 51-58 insulin Homo sapiens 117-124 16373903-13 2006 CONCLUSIONS: Insulin analog partially reversed myocardial perfusion abnormalities observed in postprandial state by improving glucose control. Glucose 126-133 insulin Homo sapiens 13-20 16380496-11 2006 In subjects with glucose intolerance, BPI was also linked to BMI, waist-to-hip ratio, and age- and BMI-adjusted insulin sensitivity. Glucose 17-24 insulin Homo sapiens 112-119 16409572-5 2006 glucose values for insulin dosage calculation directly (i.v.-s.c. route). Glucose 0-7 insulin Homo sapiens 19-26 16706558-1 2006 Insulin glulisine is a rapid-acting human insulin analogue that has a faster onset of action and shorter duration of action than regular human insulin (RHI) in patients with type 1 or 2 diabetes mellitus and is efficacious in controlling prandial blood glucose levels in these patients. Glucose 253-260 insulin Homo sapiens 0-7 16706558-3 2006 Pre-meal insulin glulisine was also more effective than RHI at controlling 2-hour post-prandial glucose excursions in patients with type 1 or 2 diabetes over a period of 12 weeks. Glucose 96-103 insulin Homo sapiens 9-16 16740022-2 2006 This formulation of insulin has a more rapid onset, but similar duration, of glucose-lowering activity compared with subcutaneously administered regular human insulin. Glucose 77-84 insulin Homo sapiens 20-27 17100408-3 2006 This allows for increased insulin sensitivity, decreased glucagon secretion and improved beta-cell function in a glucose-dependent manner. Glucose 113-120 insulin Homo sapiens 26-33 16627374-9 2006 In acute coronary syndromes, lowering of glucose levels to the near-normal range by administration of insulin is highly beneficial. Glucose 41-48 insulin Homo sapiens 102-109 16627392-3 2006 RESULTS: Rapid-acting insulin analogues provide better and safer postprandial glucose coverage than does human regular insulin. Glucose 78-85 insulin Homo sapiens 22-29 17239309-7 2006 insulin therapy fluctuations in glucose levels persisted. Glucose 32-39 insulin Homo sapiens 0-7 17239309-10 2006 Already on the 3rd day of such treatment, the daily insulin dose could be decreased from 0.7 unit/kg/24 hrs down to 0.5 unit/kg/24 hrs, and glucose levels normalized. Glucose 140-147 insulin Homo sapiens 52-59 16381992-13 2006 CONCLUSIONS: A relevant association between postprandial insulin-mediated glucose metabolism and ghrelin secretion in children with different levels of overweight was found. Glucose 74-81 insulin Homo sapiens 57-64 17144879-4 2006 Hence, insulin-stimulated GLUT4 translocation to the cell surface is impaired, and therefore, the rate of glucose removal from the circulation into muscle is delayed. Glucose 106-113 insulin Homo sapiens 7-14 17144881-4 2006 Strength training has been shown to improve insulin-stimulated glucose uptake in both healthy elderly individuals and patients with manifest diabetes, and likewise to improve muscle strength in both elderly healthy individuals and in elderly individuals with chronic disease. Glucose 63-70 insulin Homo sapiens 44-51 17144887-3 2006 Microvascular dysfunction may increase not only peripheral vascular resistance and blood pressure, but may also decrease insulin-mediated glucose uptake in muscle. Glucose 138-145 insulin Homo sapiens 121-128 16337874-1 2006 One hallmark of the insulin-resistant state of prediabetes and overt type 2 diabetes is an impaired ability of insulin to activate glucose transport in skeletal muscle, due to defects in IRS-1-dependent signaling. Glucose 131-138 insulin Homo sapiens 20-27 16394814-1 2006 Resistance training can improve glucose transport in both normal and insulin-resistant skeletal muscle by enhancing the activation of the insulin signaling cascade and increasing GLUT-4 protein concentration. Glucose 32-39 insulin Homo sapiens 69-76 16394814-1 2006 Resistance training can improve glucose transport in both normal and insulin-resistant skeletal muscle by enhancing the activation of the insulin signaling cascade and increasing GLUT-4 protein concentration. Glucose 32-39 insulin Homo sapiens 138-145 16337874-6 2006 Recent investigations have demonstrated that the combination of exercise training and antioxidant treatment using ALA in an animal model of obesity-associated insulin resistance provides a unique interactive effect resulting in a greater improvement in insulin action on skeletal muscle glucose transport than either intervention individually. Glucose 287-294 insulin Homo sapiens 159-166 16337874-6 2006 Recent investigations have demonstrated that the combination of exercise training and antioxidant treatment using ALA in an animal model of obesity-associated insulin resistance provides a unique interactive effect resulting in a greater improvement in insulin action on skeletal muscle glucose transport than either intervention individually. Glucose 287-294 insulin Homo sapiens 253-260 16251897-8 2006 This haplotype also marks nearly two-fold lower 120 min insulin (P=0.004) as well as low baseline insulin (-11.02 pmol/l, P=0.043) and low 30 min insulin (-64.44 pmol/l, P=0.072) in a glucose tolerance test. Glucose 184-191 insulin Homo sapiens 56-63 16251897-8 2006 This haplotype also marks nearly two-fold lower 120 min insulin (P=0.004) as well as low baseline insulin (-11.02 pmol/l, P=0.043) and low 30 min insulin (-64.44 pmol/l, P=0.072) in a glucose tolerance test. Glucose 184-191 insulin Homo sapiens 98-105 16251897-8 2006 This haplotype also marks nearly two-fold lower 120 min insulin (P=0.004) as well as low baseline insulin (-11.02 pmol/l, P=0.043) and low 30 min insulin (-64.44 pmol/l, P=0.072) in a glucose tolerance test. Glucose 184-191 insulin Homo sapiens 98-105 16251897-10 2006 Our results, taken together with other data on IGFII levels and TH activity, point to the importance of (*)5 as an integrated polygenic haplotype relevant to obesity and insulin response to glucose in men. Glucose 190-197 insulin Homo sapiens 170-177 16337874-1 2006 One hallmark of the insulin-resistant state of prediabetes and overt type 2 diabetes is an impaired ability of insulin to activate glucose transport in skeletal muscle, due to defects in IRS-1-dependent signaling. Glucose 131-138 insulin Homo sapiens 111-118 16337874-4 2006 Numerous studies have demonstrated that treatment of insulin-resistant animals and type 2 diabetic humans with antioxidants, including alpha-lipoic acid (ALA), is associated with improvements in skeletal muscle glucose transport activity and whole-body glucose tolerance. Glucose 211-218 insulin Homo sapiens 53-60 16337874-4 2006 Numerous studies have demonstrated that treatment of insulin-resistant animals and type 2 diabetic humans with antioxidants, including alpha-lipoic acid (ALA), is associated with improvements in skeletal muscle glucose transport activity and whole-body glucose tolerance. Glucose 253-260 insulin Homo sapiens 53-60 16199428-5 2006 Rosiglitazone reduced insulin, IR indices [homeostasis model assessment (HOMA) and quantitative sensitivity check index (QUICKI)] and the insulin area under the curve in response to an oral glucose tolerance test (OGTT), but had limited effect on lipids, androgens and hirsutism. Glucose 190-197 insulin Homo sapiens 138-145 16612127-7 2006 In addition, we found a significantly decreased insulin secretion rate during oral glucose ingestion after correction for insulin action (disposition index), a paradoxical enhanced insulin suppression of hepatic glucose production and lower fasting plasma glycerol levels, suggesting impaired lipolysis. Glucose 83-90 insulin Homo sapiens 48-55 16549934-3 2006 METHODS: The insulin sensitivity index was calculated from the frequently sampled intravenous glucose tolerance test with tolbutamide. Glucose 94-101 insulin Homo sapiens 13-20 16444062-10 2006 Careful monitoring of glucose levels and ensuring adequate hydration in patients "at risk" of HHNS, including those receiving medications that interfere with the secretion or effectiveness of insulin should decrease the risk of HHNS. Glucose 22-29 insulin Homo sapiens 192-199 16374259-4 2006 We analyzed the plasma insulin response in a 75-g oral glucose tolerance test. Glucose 55-62 insulin Homo sapiens 23-30 16202636-2 2006 The first recognized and most important action of GLP-1 is the potentiation of glucose-stimulated insulin secretion in beta-cells, mediated by activation of its seven transmembrane domain G-protein-coupled receptor. Glucose 79-86 insulin Homo sapiens 98-105 16242377-1 2006 Glucagon-like peptide-1 is an insulinotropic hormone with antidiabetic potential due to its spectrum of effects, which include glucose-dependent stimulation of insulin and inhibition of glucagon secretion, tropic effects on the pancreatic beta-cells, inhibition of gastric emptying and the reduction of appetite. Glucose 127-134 insulin Homo sapiens 30-37 16487789-3 2006 Acute exposure of the pancreatic beta cell to both high glucose concentrations and saturated FFA results in a substantial increase of insulin release, whereas a chronic exposure results in desensitization and suppression of secretion. Glucose 56-63 insulin Homo sapiens 134-141 16459127-3 2006 The elevated blood glucose levels in diabetes mellitus are caused by a defect in production and/or secretion of the polypeptide hormone insulin, which normally promotes glucose-uptake in cells. Glucose 19-26 insulin Homo sapiens 136-143 16459127-3 2006 The elevated blood glucose levels in diabetes mellitus are caused by a defect in production and/or secretion of the polypeptide hormone insulin, which normally promotes glucose-uptake in cells. Glucose 169-176 insulin Homo sapiens 136-143 16431150-8 2006 Furthermore, the secretion of insulin and C-peptide from the islet-like cell clusters responds to glucose and other stimuli, indicating that the differentiated cells not only resemble beta-cells but also possess the unique biological function of beta-cells. Glucose 98-105 insulin Homo sapiens 30-37 16431150-8 2006 Furthermore, the secretion of insulin and C-peptide from the islet-like cell clusters responds to glucose and other stimuli, indicating that the differentiated cells not only resemble beta-cells but also possess the unique biological function of beta-cells. Glucose 98-105 insulin Homo sapiens 42-51 16487789-4 2006 Reduction of plasma FFA levels in fasted rats or humans severely impairs glucose-induced insulin release but palmitate can augment insulin release in the presence of nonstimulatory concentrations of glucose. Glucose 73-80 insulin Homo sapiens 89-96 16487789-6 2006 Although it is widely accepted that fatty acid (FA) metabolism (notably FA synthesis and/or formation of LC-acyl-CoA) is necessary for stimulation of insulin secretion, the key regulatory molecular mechanisms controlling the interplay between glucose and fatty acid metabolism and thus insulin secretion are not well understood but are now described in detail in this review. Glucose 243-250 insulin Homo sapiens 150-157 16263830-7 2006 The acute insulin response to iv glucose was comparable in the T2DM and LN groups (P < 0.05 for the OB vs. LN and T2DM), but insulin secretion adjusted for insulin resistance, the disposition index, was severely impaired in the diabetic subjects (P < 0.05 for the T2DM vs. LN and OB). Glucose 33-40 insulin Homo sapiens 10-17 16377491-2 2006 The purpose of this study was to determine the efficacy and safety of nurse-driven insulin infusion protocols in lowering blood glucose (BG) in critical illness. Glucose 128-135 insulin Homo sapiens 83-90 16219719-9 2006 Among women with normal glucose tolerance, insulin levels were significantly higher in those at high vs. low OSA risk, independently of body mass index. Glucose 24-31 insulin Homo sapiens 43-50 17139123-3 2006 He was administered insulin immediately, however, his fasting plasma glucose level remained unstable despite the insulin treatment. Glucose 69-76 insulin Homo sapiens 20-27 17139123-9 2006 Postprandial plasma glucose levels were relatively improved by lispro insulin. Glucose 20-27 insulin Homo sapiens 70-77 16141382-6 2006 The rate of insulin-stimulated glucose utilization as well as the suppression of lipolysis were determined approximately 72 h after the final exercise bout by using a two-step euglycemic-hyperinsulinemic clamp. Glucose 31-38 insulin Homo sapiens 12-19 16141382-7 2006 We observed improved glucose utilization at the higher insulin dose with training, but these improvements were statistically significant only in the T(H) (21%; P = 0.02) compared with the T(M) (16%; P = 0.17) and C(TB) (8%; P = 0.37) groups and were observed without changes in either body composition or V(O2)peak. Glucose 21-28 insulin Homo sapiens 55-62 16249279-6 2006 MAIN OUTCOME MEASURES: Insulin sensitivity was derived from a 2-h, 75-g oral glucose tolerance test (IS(OGTT)). Glucose 77-84 insulin Homo sapiens 23-30 16249285-6 2006 MAIN OUTCOME MEASURE: Insulin sensitivity was measured using the oral glucose tolerance test (IS(OGTT)) index of M. Matsuda and R. DeFronzo, previously validated in pregnancy. Glucose 70-77 insulin Homo sapiens 22-29 16234307-0 2006 Plasma adiponectin level is associated with insulin-stimulated nonoxidative glucose disposal. Glucose 76-83 insulin Homo sapiens 44-51 16234307-1 2006 CONTEXT: Impaired nonoxidative glucose disposal and decrease in mitochondrial glucose oxidation both contribute to insulin resistance in diabetic subjects. Glucose 31-38 insulin Homo sapiens 115-122 16263830-11 2006 However, the adolescent diabetic subjects retained a first-phase insulin response to glucose that was comparable to lean controls and did not have hyperproinsulinemia or hyperglucagonemia. Glucose 85-92 insulin Homo sapiens 65-72 16234307-1 2006 CONTEXT: Impaired nonoxidative glucose disposal and decrease in mitochondrial glucose oxidation both contribute to insulin resistance in diabetic subjects. Glucose 78-85 insulin Homo sapiens 115-122 17675899-2 2006 Of these, skeletal muscle is the most abundant insulin-sensitive tissue, handling > 40% of the postprandial glucose uptake, while consuming 20% of the body"s energy. Glucose 111-118 insulin Homo sapiens 47-54 16333523-9 2006 The present study indicates that the hOGG1 gene Cys/Cys variant is associated with a significant decrease in insulin sensitivity in subjects with normal glucose tolerance. Glucose 153-160 insulin Homo sapiens 109-116 16423593-1 2006 OBJECTIVE: To assess the use of oral glucose tolerance testing (OGTT) to predict efficacy of insulin sensitization (metformin) or suppression (octreotide) because insulin resistance and insulin hypersecretion may impact pharmacotherapeutic efficacy in obese children. Glucose 37-44 insulin Homo sapiens 93-100 16719233-12 2006 CONCLUSION: Results indicate significant improvement of glucose utilisation as a consequence of reduced insulin resistance in the RG group. Glucose 56-63 insulin Homo sapiens 104-111 16472699-0 2006 TC10 and insulin-stimulated glucose transport. Glucose 28-35 insulin Homo sapiens 9-16 16472699-1 2006 Insulin stimulates glucose uptake in insulin-responsive tissues by means of the translocation of the glucose transporter GLUT4 from intracellular sites to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 16472699-1 2006 Insulin stimulates glucose uptake in insulin-responsive tissues by means of the translocation of the glucose transporter GLUT4 from intracellular sites to the plasma membrane. Glucose 19-26 insulin Homo sapiens 37-44 16472699-5 2006 We describe experimental approaches using the insulin-responsive cell line 3T3-L1 adipocytes to study the role of TC10 in insulin-stimulated glucose transport. Glucose 141-148 insulin Homo sapiens 122-129 16563225-1 2006 The release of neurotransmitters at the nerve terminal for neurotransmission, release of insulin from beta-cells of the endocrine pancreas for regulating blood glucose levels, the release of growth hormone from GH cells of the pituitary gland to regulate body growth, or the expulsion of zymogen from exocrine pancreas to digest food, are only a few examples of key physiological processes made possible by cell secretion. Glucose 160-167 insulin Homo sapiens 89-96 16456195-8 2006 This difference in circulating glucose was associated with insulin responses whereby young, but not aged men experienced a postexercise spike. Glucose 31-38 insulin Homo sapiens 59-66 16396496-1 2006 The insulin-regulated glucose transporter (GLUT4) translocates to the plasma membrane in response to insulin in order to facilitate the postprandial uptake of glucose into fat and muscle cells. Glucose 22-29 insulin Homo sapiens 4-11 16396496-1 2006 The insulin-regulated glucose transporter (GLUT4) translocates to the plasma membrane in response to insulin in order to facilitate the postprandial uptake of glucose into fat and muscle cells. Glucose 22-29 insulin Homo sapiens 101-108 16399292-1 2006 OBJECTIVE: We sought to assess the role of glucose-insulin-potassium in providing myocardial protection in nondiabetic patients undergoing coronary artery surgery with cardiopulmonary bypass. Glucose 43-50 insulin Homo sapiens 51-58 16399292-8 2006 RESULTS: The glucose-insulin-potassium group experienced higher cardiac indices (P < .001) throughout infusion and reduced vascular resistance (P < .001). Glucose 13-20 insulin Homo sapiens 21-28 16399292-9 2006 The incidence of low cardiac output episodes was 15.9% (22/138) in the glucose-insulin-potassium group and 27.5% (39/142) in the placebo group (P = .021). Glucose 71-78 insulin Homo sapiens 79-86 16399292-10 2006 Inotropes were required in 18.8% (26/138) of the glucose-insulin-potassium group and 40.8% (58/142) of the placebo group (P < .001). Glucose 49-56 insulin Homo sapiens 57-64 16399292-11 2006 Fewer patients in the glucose-insulin-potassium group (12.3% [16/133]) versus those in the placebo group (23.4% [32/137]) had significant myocardial injury (P = .017). Glucose 22-29 insulin Homo sapiens 30-37 16710197-2 2006 Clamp test made it possible to follow dynamics of insulin and other hormones in the process of regulation of glucose level. Glucose 109-116 insulin Homo sapiens 50-57 16309850-2 2006 cAMP is the primary mediator of these effects, and has been shown to potentiate glucose-stimulated insulin secretion, promote proper beta cells differentiation by increasing expression of the crucial transcription factor PDX-1, and prevent beta cell apoptosis. Glucose 80-87 insulin Homo sapiens 99-106 16309850-4 2006 An increase in plasma glucose boosts beta cell production of cGMP, which acts as a feed-forward mediator to enhance glucose-stimulated insulin secretion. Glucose 22-29 insulin Homo sapiens 135-142 16309850-4 2006 An increase in plasma glucose boosts beta cell production of cGMP, which acts as a feed-forward mediator to enhance glucose-stimulated insulin secretion. Glucose 116-123 insulin Homo sapiens 135-142 16846037-5 2006 The differentiated cells release insulin in response to high glucose concentrations. Glucose 61-68 insulin Homo sapiens 33-40 17675899-3 2006 The inability to efficiently take up and store fuel, and to transition from fat to glucose as the primary source of fuel during times of plenty (increased insulin), has been termed metabolic inflexibility. Glucose 83-90 insulin Homo sapiens 155-162 17675900-1 2006 The regulation of blood glucose levels involves a finely tuned relationship between insulin sensitivity, hepatic glucose output, and production of insulin. Glucose 24-31 insulin Homo sapiens 84-91 17675900-1 2006 The regulation of blood glucose levels involves a finely tuned relationship between insulin sensitivity, hepatic glucose output, and production of insulin. Glucose 24-31 insulin Homo sapiens 147-154 17099262-4 2006 Experimental data suggest that elevated blood glucose may directly contribute to infarct expansion through a number of maladaptive metabolic pathways, and that treatment with insulin may attenuate these adverse effects. Glucose 46-53 insulin Homo sapiens 175-182 16820737-6 2006 Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. Glucose 88-95 insulin Homo sapiens 34-41 16493121-10 2006 Increases in glucose, insulin, and leptin following a glucose challenge were also blunted. Glucose 54-61 insulin Homo sapiens 22-29 16399495-0 2006 A new model to fit glucose concentration during the insulin tolerance test improving the predictive capability to estimate insulin sensitivity. Glucose 19-26 insulin Homo sapiens 52-59 17167239-5 2006 With respect to this, it is well known that glucose excites B cells (which secrete insulin) and inhibits A cells (which secrete glucagon), which in turn excites D cells (which secrete somatostatin). Glucose 44-51 insulin Homo sapiens 83-90 17167239-12 2006 That is the disorder seen in the so-called "hyperinsulinism", in which raised plasma levels of glucose, insulin and glucagon coexist. Glucose 95-102 insulin Homo sapiens 49-56 17192720-5 2006 RESULTS: The global test for the haplotype effect on insulin levels was significant (p < 0.0001), adjusting for age, education, apolipoprotein epsilon4 status and fasting glucose. Glucose 171-178 insulin Homo sapiens 53-60 16408441-5 2006 Age-related glucose intolerance in humans is often accompanied by insulin resistance. Glucose 12-19 insulin Homo sapiens 66-73 16408447-1 2006 Several studies have shown that fasting blood glucose rises about 1-2 mg/dl/decade and post-prandial glucose by about 15 mg/dl/decade, leading to mild glucose intolerance with insulin resistance associated with aging. Glucose 46-53 insulin Homo sapiens 176-183 16408447-1 2006 Several studies have shown that fasting blood glucose rises about 1-2 mg/dl/decade and post-prandial glucose by about 15 mg/dl/decade, leading to mild glucose intolerance with insulin resistance associated with aging. Glucose 101-108 insulin Homo sapiens 176-183 16408447-1 2006 Several studies have shown that fasting blood glucose rises about 1-2 mg/dl/decade and post-prandial glucose by about 15 mg/dl/decade, leading to mild glucose intolerance with insulin resistance associated with aging. Glucose 101-108 insulin Homo sapiens 176-183 16399495-0 2006 A new model to fit glucose concentration during the insulin tolerance test improving the predictive capability to estimate insulin sensitivity. Glucose 19-26 insulin Homo sapiens 123-130 16019120-7 2006 A maximally stimulating insulin concentration (100 nM) accelerated glucose transport 10- to 15-fold in 3T3-L1 adipocytes, and the half-maximally stimulating insulin dose was 0.4 nM. Glucose 67-74 insulin Homo sapiens 24-31 16876572-10 2006 Activation of the sympatico-adrenal system inhibits glucose uptake by peripheral tissues by inhibiting insulin release and inducing insulin resistance and increases hepatic glucose production. Glucose 52-59 insulin Homo sapiens 103-110 16876572-10 2006 Activation of the sympatico-adrenal system inhibits glucose uptake by peripheral tissues by inhibiting insulin release and inducing insulin resistance and increases hepatic glucose production. Glucose 52-59 insulin Homo sapiens 132-139 16876586-2 2006 In insulin deficient - T1DM and advanced T2DM - diabetes hypoglycemia is the result of the interplay of therapeutic insulin excess and compromised physiological (defective glucose counterregulation) and behavioral (hypoglycemia unawareness) defenses against falling plasma glucose concentrations. Glucose 172-179 insulin Homo sapiens 3-10 16876586-2 2006 In insulin deficient - T1DM and advanced T2DM - diabetes hypoglycemia is the result of the interplay of therapeutic insulin excess and compromised physiological (defective glucose counterregulation) and behavioral (hypoglycemia unawareness) defenses against falling plasma glucose concentrations. Glucose 273-280 insulin Homo sapiens 3-10 16876586-5 2006 Loss of the glucagon response, a key feature of defective glucose counterregulation, is plausibly attributed to insulin deficiency, specifically loss of the decrement in intraislet insulin that normally signals glucagon secretion as glucose levels fall. Glucose 58-65 insulin Homo sapiens 112-119 16876586-5 2006 Loss of the glucagon response, a key feature of defective glucose counterregulation, is plausibly attributed to insulin deficiency, specifically loss of the decrement in intraislet insulin that normally signals glucagon secretion as glucose levels fall. Glucose 233-240 insulin Homo sapiens 112-119 16472075-1 2006 A novel chemically-modified insulin, epsilon-N(B29)-lipoyl insulin, was selectively prepared by the covalent linkage of alpha-lipoic acid (LA) to the epsilon-amino group of Lys(B29) of insulin without any protecting agent and analyzed by PAGE, HPLC, MALDI-TOF-MS. Monolipoyl- insulin maintained the glucose-lowering effect as well as native insulin and showed a longer duration of action than native insulin and an inhibitory effect towards trypsin degradation. Glucose 299-306 insulin Homo sapiens 28-35 16472075-1 2006 A novel chemically-modified insulin, epsilon-N(B29)-lipoyl insulin, was selectively prepared by the covalent linkage of alpha-lipoic acid (LA) to the epsilon-amino group of Lys(B29) of insulin without any protecting agent and analyzed by PAGE, HPLC, MALDI-TOF-MS. Monolipoyl- insulin maintained the glucose-lowering effect as well as native insulin and showed a longer duration of action than native insulin and an inhibitory effect towards trypsin degradation. Glucose 299-306 insulin Homo sapiens 59-66 16472075-1 2006 A novel chemically-modified insulin, epsilon-N(B29)-lipoyl insulin, was selectively prepared by the covalent linkage of alpha-lipoic acid (LA) to the epsilon-amino group of Lys(B29) of insulin without any protecting agent and analyzed by PAGE, HPLC, MALDI-TOF-MS. Monolipoyl- insulin maintained the glucose-lowering effect as well as native insulin and showed a longer duration of action than native insulin and an inhibitory effect towards trypsin degradation. Glucose 299-306 insulin Homo sapiens 59-66 16472075-1 2006 A novel chemically-modified insulin, epsilon-N(B29)-lipoyl insulin, was selectively prepared by the covalent linkage of alpha-lipoic acid (LA) to the epsilon-amino group of Lys(B29) of insulin without any protecting agent and analyzed by PAGE, HPLC, MALDI-TOF-MS. Monolipoyl- insulin maintained the glucose-lowering effect as well as native insulin and showed a longer duration of action than native insulin and an inhibitory effect towards trypsin degradation. Glucose 299-306 insulin Homo sapiens 59-66 16472075-1 2006 A novel chemically-modified insulin, epsilon-N(B29)-lipoyl insulin, was selectively prepared by the covalent linkage of alpha-lipoic acid (LA) to the epsilon-amino group of Lys(B29) of insulin without any protecting agent and analyzed by PAGE, HPLC, MALDI-TOF-MS. Monolipoyl- insulin maintained the glucose-lowering effect as well as native insulin and showed a longer duration of action than native insulin and an inhibitory effect towards trypsin degradation. Glucose 299-306 insulin Homo sapiens 59-66 16472075-1 2006 A novel chemically-modified insulin, epsilon-N(B29)-lipoyl insulin, was selectively prepared by the covalent linkage of alpha-lipoic acid (LA) to the epsilon-amino group of Lys(B29) of insulin without any protecting agent and analyzed by PAGE, HPLC, MALDI-TOF-MS. Monolipoyl- insulin maintained the glucose-lowering effect as well as native insulin and showed a longer duration of action than native insulin and an inhibitory effect towards trypsin degradation. Glucose 299-306 insulin Homo sapiens 59-66 17479872-10 2006 It is particularly important when glucose concentrations decide on immediate physician"s action, e.g. change in insulin dosage or compensation of hypoglycemia. Glucose 34-41 insulin Homo sapiens 112-119 16402351-5 2006 The estimates of glucose effectiveness and insulin sensitivity were 2-3 times higher than those obtained in similar populations using the conventional protocol of the frequently sampled intravenous glucose tolerance test, and this appeared to be related to the kinetics of transport of glucose from accessible to remote pools. Glucose 198-205 insulin Homo sapiens 43-50 16216406-6 2006 If insulin is administered to the hypothermic patient, intensive monitoring of blood glucose is essential due to the increase in endogenous insulin secretion on rewarming. Glucose 85-92 insulin Homo sapiens 3-10 17224874-4 2006 Hyperglycemia induced by infusions of a fixed dose of insulin with high rates of glucose may neutralize the benefit of insulin, and such regimens should be replaced by infusion of insulin to restore and maintain euglycemia. Glucose 81-88 insulin Homo sapiens 54-61 17224874-4 2006 Hyperglycemia induced by infusions of a fixed dose of insulin with high rates of glucose may neutralize the benefit of insulin, and such regimens should be replaced by infusion of insulin to restore and maintain euglycemia. Glucose 81-88 insulin Homo sapiens 119-126 17224874-4 2006 Hyperglycemia induced by infusions of a fixed dose of insulin with high rates of glucose may neutralize the benefit of insulin, and such regimens should be replaced by infusion of insulin to restore and maintain euglycemia. Glucose 81-88 insulin Homo sapiens 119-126 17236290-1 2006 We studied the plasma levels of some aminoacids and immunoreactive insulin in chronic liver diseases with impaired glucose tolerance during oral glucose tolerance test (OGTT). Glucose 115-122 insulin Homo sapiens 67-74 17395025-4 2006 The regimes that infuse fixed doses of insulin with high rates of glucose are usually associated with hyperglycemia. Glucose 66-73 insulin Homo sapiens 39-46 17395027-4 2006 Mechanistic studies exploring the molecular pathways involved suggest that intensive insulin therapy exerts its beneficial effects mainly through the maintenance of normal blood glucose levels. Glucose 178-185 insulin Homo sapiens 85-92 17395031-3 2006 At Providence St. Vincent Hospital in Portland, Oregon, we have been using postoperative insulin infusions under study protocol since 1992 and have been using intravenous insulin to control intraoperative glucose levels since 1995. Glucose 205-212 insulin Homo sapiens 171-178 17395033-2 2006 Clinical trial data has demonstrated that controlling hyperglycemia with insulin infusions guided by frequent blood glucose monitoring can reduce this morbidity and mortality. Glucose 116-123 insulin Homo sapiens 73-80 17215967-2 2006 We compared the effect upon glucose control of continuous insulin infusion with that of glucometer-guided insulin injection after coronary artery bypass. Glucose 28-35 insulin Homo sapiens 58-65 16677059-10 2006 Current research has shown that the use of diabetes mellitus management practices aimed at reducing insulin resistance and hyperinsulinemia (such as weight reduction and the administration of oral antidiabetic drugs) can not only reverse testosterone and luteinizing hormone abnormalities and restore menstrual cycles, but can also improve glucose, insulin, proinflammatory cytokine, and lipid profiles.Clinical treatment with troglitazone, a member of the thiazolidinedione family, for the management of PCOS complications such as insulin resistance, hyperandrogenism, and anovulation was found to have beneficial effects; however, it was taken off the market over concerns of hepatotoxicity. Glucose 340-347 insulin Homo sapiens 100-107 16677059-10 2006 Current research has shown that the use of diabetes mellitus management practices aimed at reducing insulin resistance and hyperinsulinemia (such as weight reduction and the administration of oral antidiabetic drugs) can not only reverse testosterone and luteinizing hormone abnormalities and restore menstrual cycles, but can also improve glucose, insulin, proinflammatory cytokine, and lipid profiles.Clinical treatment with troglitazone, a member of the thiazolidinedione family, for the management of PCOS complications such as insulin resistance, hyperandrogenism, and anovulation was found to have beneficial effects; however, it was taken off the market over concerns of hepatotoxicity. Glucose 340-347 insulin Homo sapiens 128-135 16677059-10 2006 Current research has shown that the use of diabetes mellitus management practices aimed at reducing insulin resistance and hyperinsulinemia (such as weight reduction and the administration of oral antidiabetic drugs) can not only reverse testosterone and luteinizing hormone abnormalities and restore menstrual cycles, but can also improve glucose, insulin, proinflammatory cytokine, and lipid profiles.Clinical treatment with troglitazone, a member of the thiazolidinedione family, for the management of PCOS complications such as insulin resistance, hyperandrogenism, and anovulation was found to have beneficial effects; however, it was taken off the market over concerns of hepatotoxicity. Glucose 340-347 insulin Homo sapiens 128-135 17002493-2 2006 This formulation of insulin has a more rapid onset, but similar duration, of glucose-lowering activity compared with subcutaneously administered regular human insulin.Preprandial inhaled human insulin provided glycemic control that was comparable to preprandial subcutaneous regular insulin when added to long- or intermediate-acting subcutaneous basal insulin in patients with type 1 diabetes. Glucose 77-84 insulin Homo sapiens 20-27 18528484-1 2006 Fetal glucose metabolism depends on additive effects of fetal plasma glucose and insulin. Glucose 6-13 insulin Homo sapiens 81-88 18528484-2 2006 Glucose-stimulated insulin secretion increases over gestation, is down-regulated by constant hyperglycemia, but enhanced by pulsatile hyperglycemia. Glucose 0-7 insulin Homo sapiens 19-26 17319471-4 2006 Currently approved in the US as an injectable adjunct to metformin and/or sulfonylurea therapy, exenatide improves glycemic control through multiple mechanisms of action including: glucose-dependent enhancement of insulin secretion that potentially reduces the risk of hypoglycemia compared with insulin secretagogues; restoration of first-phase insulin secretion typically deficient in patients with type 2 diabetes; suppression of inappropriately elevated glucagon secretion to reduce postprandial hepatic output; and slowing the rate of gastric emptying to regulate glucose appearance into the circulation. Glucose 181-188 insulin Homo sapiens 214-221 16284741-0 2006 Cellular location of insulin-triggered signals and implications for glucose uptake. Glucose 68-75 insulin Homo sapiens 21-28 16284741-1 2006 Insulin stimulation of glucose uptake into muscle and fat cells requires movement of GLUT4-containing vesicles from intracellular compartments to the plasma membrane. Glucose 23-30 insulin Homo sapiens 0-7 16239226-1 2005 Although the cytoskeletal network is important for insulin-induced glucose uptake, several studies have assessed the effects of microtubule disruption on glucose transport with divergent results. Glucose 67-74 insulin Homo sapiens 51-58 16600084-10 2006 The correlation analysis indicated that the negative correlation was found between the level of serum insulin and the level of blood cadmium, as well as between the level of the serum insulin and the level of the urinary cadmium; the positive correlation was found between the level of blood glucose and the level of insulin, as well as between the level of blood glucose and the level of C peptide in serum. Glucose 292-299 insulin Homo sapiens 184-191 16600084-10 2006 The correlation analysis indicated that the negative correlation was found between the level of serum insulin and the level of blood cadmium, as well as between the level of the serum insulin and the level of the urinary cadmium; the positive correlation was found between the level of blood glucose and the level of insulin, as well as between the level of blood glucose and the level of C peptide in serum. Glucose 292-299 insulin Homo sapiens 184-191 16600084-10 2006 The correlation analysis indicated that the negative correlation was found between the level of serum insulin and the level of blood cadmium, as well as between the level of the serum insulin and the level of the urinary cadmium; the positive correlation was found between the level of blood glucose and the level of insulin, as well as between the level of blood glucose and the level of C peptide in serum. Glucose 364-371 insulin Homo sapiens 184-191 16600084-10 2006 The correlation analysis indicated that the negative correlation was found between the level of serum insulin and the level of blood cadmium, as well as between the level of the serum insulin and the level of the urinary cadmium; the positive correlation was found between the level of blood glucose and the level of insulin, as well as between the level of blood glucose and the level of C peptide in serum. Glucose 364-371 insulin Homo sapiens 184-191 16266372-9 2005 The decreased interstitial glucose concentration may serve to limit the rate of post-exercise muscle glucose uptake to a rate compatible with normal blood glucose levels and may also be speculated to have a positive long-term health implication by augmenting muscle insulin sensitivity. Glucose 27-34 insulin Homo sapiens 266-273 16014353-0 2005 Insulin sensitivity by oral glucose minimal models: validation against clamp. Glucose 28-35 insulin Homo sapiens 0-7 16014353-1 2005 Measuring insulin sensitivity in the presence of physiological changes in glucose and insulin concentrations, e.g., during a meal or OGTT, is important to better understand insulin resistance in a variety of metabolic conditions. Glucose 74-81 insulin Homo sapiens 10-17 16364837-5 2005 Insulin sensitivity was determined with the steady-state plasma glucose (SSPG) method. Glucose 64-71 insulin Homo sapiens 0-7 16325606-5 2005 RESULTS: Basal and insulin-stimulated glucose uptake into adipose tissue was not impaired in pregnancy or gestational diabetes mellitus compared with control subjects. Glucose 38-45 insulin Homo sapiens 19-26 16332653-0 2005 Independent association of insulin resistance with larger amounts of intermuscular adipose tissue and a greater acute insulin response to glucose in African American than in white nondiabetic women. Glucose 138-145 insulin Homo sapiens 27-34 16332653-0 2005 Independent association of insulin resistance with larger amounts of intermuscular adipose tissue and a greater acute insulin response to glucose in African American than in white nondiabetic women. Glucose 138-145 insulin Homo sapiens 118-125 16332653-8 2005 AAs had a 163% greater acute insulin response to glucose than did whites; this difference was significant even after adjustment for insulin sensivitity index, weight, height, and any magnetic resonance imaging measures. Glucose 49-56 insulin Homo sapiens 29-36 16332653-10 2005 CONCLUSIONS: Premenopausal AA women had significantly higher insulin resistance and acute insulin response to glucose than did their white counterparts. Glucose 110-117 insulin Homo sapiens 90-97 16332653-11 2005 Whereas the difference in insulin resistance was partially accounted for by a greater SM volume in the AAs than in the whites, the difference in the acute insulin response to glucose was independent of any AT and SM measures and was disproportionately larger than expected according to the difference in insulin resistance. Glucose 175-182 insulin Homo sapiens 155-162 16332653-11 2005 Whereas the difference in insulin resistance was partially accounted for by a greater SM volume in the AAs than in the whites, the difference in the acute insulin response to glucose was independent of any AT and SM measures and was disproportionately larger than expected according to the difference in insulin resistance. Glucose 175-182 insulin Homo sapiens 155-162 16399898-6 2005 Yet with "glycemic load" and the endocrine effect of glucose (the stimulation of insulin secretion), reactive oxygen species are formed in multiple sites, including adipose tissue. Glucose 53-60 insulin Homo sapiens 81-88 16128672-1 2005 Reduced insulin-mediated glucose transport in skeletal muscle is a hallmark of the pathophysiology of T2DM (Type II diabetes mellitus). Glucose 25-32 insulin Homo sapiens 8-15 16311221-5 2005 An alternative hypothesis is that increased concentrations of plasma FFA induce insulin resistance in humans through inhibition of glucose transport activity, which appears to be a consequence of decreased insulin receptor substrate-1-associated phosphatidyl inositol 3 kinase activity. Glucose 131-138 insulin Homo sapiens 80-87 16327166-7 2005 Nonetheless, plasma glucose levels in normal rats were significantly lowered after sublingual administration of insulin with an enhancer compared with those without an enhancer at the same time-point. Glucose 20-27 insulin Homo sapiens 112-119 16253402-4 2005 The body mass index was significantly higher in elderly volunteers compared to the younger ones (P<0.05) whereas insulin sensitivity was lower as shown by either the M value (P<0.05) or the glucose disposal rate (GDR)/insulinemia ratio (P<0.05). Glucose 196-203 insulin Homo sapiens 116-123 16352960-2 2005 Titration and monitoring of insulin infusions involve frequent blood glucose measurement to achieve target glucose ranges and prevent adverse events related to hypoglycemia. Glucose 69-76 insulin Homo sapiens 28-35 16352960-2 2005 Titration and monitoring of insulin infusions involve frequent blood glucose measurement to achieve target glucose ranges and prevent adverse events related to hypoglycemia. Glucose 107-114 insulin Homo sapiens 28-35 16352960-4 2005 OBJECTIVE: To determine the accuracy and clinical impact of three common methods of bedside point-of-care testing for glucose measurements in critically ill patients receiving insulin infusions. Glucose 118-125 insulin Homo sapiens 176-183 16352960-13 2005 CONCLUSIONS: The magnitude of the differences in the glucose values offered by the four different methods of glucose measurement led to frequent clinical disagreements regarding insulin dose titration in the context of an insulin infusion protocol for aggressive glucose control. Glucose 53-60 insulin Homo sapiens 178-185 16352960-13 2005 CONCLUSIONS: The magnitude of the differences in the glucose values offered by the four different methods of glucose measurement led to frequent clinical disagreements regarding insulin dose titration in the context of an insulin infusion protocol for aggressive glucose control. Glucose 53-60 insulin Homo sapiens 222-229 16352960-13 2005 CONCLUSIONS: The magnitude of the differences in the glucose values offered by the four different methods of glucose measurement led to frequent clinical disagreements regarding insulin dose titration in the context of an insulin infusion protocol for aggressive glucose control. Glucose 109-116 insulin Homo sapiens 178-185 16352960-13 2005 CONCLUSIONS: The magnitude of the differences in the glucose values offered by the four different methods of glucose measurement led to frequent clinical disagreements regarding insulin dose titration in the context of an insulin infusion protocol for aggressive glucose control. Glucose 109-116 insulin Homo sapiens 222-229 16352960-13 2005 CONCLUSIONS: The magnitude of the differences in the glucose values offered by the four different methods of glucose measurement led to frequent clinical disagreements regarding insulin dose titration in the context of an insulin infusion protocol for aggressive glucose control. Glucose 109-116 insulin Homo sapiens 178-185 16352960-13 2005 CONCLUSIONS: The magnitude of the differences in the glucose values offered by the four different methods of glucose measurement led to frequent clinical disagreements regarding insulin dose titration in the context of an insulin infusion protocol for aggressive glucose control. Glucose 109-116 insulin Homo sapiens 222-229 16375695-6 2005 Thus, defining a molecular mechanism for insulin inhibition of PEPCK gene transcription has been a major goal of research in several labs, because it would allow the development of drugs to prevent episodic increases in circulating glucose in diabetics. Glucose 232-239 insulin Homo sapiens 41-48 16464160-8 2005 Endogenous peptides that responded to oral glucose challenge were detected by DPD of pre-and post-challenge plasma samples from 16 healthy volunteers and subsequently identified by nESI-qTOF MS. Two of the 15 MS peaks that were significantly modulated by glucose challenge were subsequently identified as insulin and C-peptide. Glucose 43-50 insulin Homo sapiens 305-312 16464160-8 2005 Endogenous peptides that responded to oral glucose challenge were detected by DPD of pre-and post-challenge plasma samples from 16 healthy volunteers and subsequently identified by nESI-qTOF MS. Two of the 15 MS peaks that were significantly modulated by glucose challenge were subsequently identified as insulin and C-peptide. Glucose 43-50 insulin Homo sapiens 317-326 16464160-8 2005 Endogenous peptides that responded to oral glucose challenge were detected by DPD of pre-and post-challenge plasma samples from 16 healthy volunteers and subsequently identified by nESI-qTOF MS. Two of the 15 MS peaks that were significantly modulated by glucose challenge were subsequently identified as insulin and C-peptide. Glucose 255-262 insulin Homo sapiens 305-312 16464160-8 2005 Endogenous peptides that responded to oral glucose challenge were detected by DPD of pre-and post-challenge plasma samples from 16 healthy volunteers and subsequently identified by nESI-qTOF MS. Two of the 15 MS peaks that were significantly modulated by glucose challenge were subsequently identified as insulin and C-peptide. Glucose 255-262 insulin Homo sapiens 317-326 16306332-7 2005 Analysis of data from the glucose tolerance tests showed that both sexes had evidence of higher insulin and glucose concentrations in people who were small at birth or during infancy. Glucose 26-33 insulin Homo sapiens 96-103 16306364-1 2005 More than 40% of HIV-infected patients on highly active antiretroviral therapy (HAART) experience fat redistribution (lipodystrophy), a syndrome associated with insulin resistance primarily affecting insulin-stimulated nonoxidative glucose metabolism (NOGM(ins)). Glucose 232-239 insulin Homo sapiens 161-168 16306364-1 2005 More than 40% of HIV-infected patients on highly active antiretroviral therapy (HAART) experience fat redistribution (lipodystrophy), a syndrome associated with insulin resistance primarily affecting insulin-stimulated nonoxidative glucose metabolism (NOGM(ins)). Glucose 232-239 insulin Homo sapiens 200-207 16306371-0 2005 Rho guanosine diphosphate-dissociation inhibitor plays a negative modulatory role in glucose-stimulated insulin secretion. Glucose 85-92 insulin Homo sapiens 104-111 16306371-5 2005 Furthermore, glucose-stimulated insulin secretion (GSIS) was significantly increased in INS cells in which expression of GDI was inhibited via the small interfering RNA-mediated knockdown approach. Glucose 13-20 insulin Homo sapiens 32-39 16306379-6 2005 A 10-fold decrease in the fasting glucose-to-insulin ratio and a 4-fold decrease in whole-body insulin sensitivity index were observed. Glucose 34-41 insulin Homo sapiens 45-52 16306381-6 2005 [18F]FDG-PET scanning indicated that SNPs of PPARD primarily affected insulin sensitivity by modifying glucose uptake in skeletal muscle but not in adipose tissue. Glucose 103-110 insulin Homo sapiens 70-77 16306382-9 2005 Loss of the glucagon secretory response, a key feature of defective glucose counterregulation, is plausibly explained by insulin deficiency, specifically loss of the decrement in intraislet insulin that normally signals glucagon secretion as glucose levels fall. Glucose 68-75 insulin Homo sapiens 121-128 16306382-9 2005 Loss of the glucagon secretory response, a key feature of defective glucose counterregulation, is plausibly explained by insulin deficiency, specifically loss of the decrement in intraislet insulin that normally signals glucagon secretion as glucose levels fall. Glucose 242-249 insulin Homo sapiens 121-128 16401322-9 2005 After 6 months of follow-up, subjects in the off-insulin group had significantly lower mean HbA(1c), higher mean C-peptide-to-glucose ratio and had more clinic visits per year. Glucose 126-133 insulin Homo sapiens 49-56 16401322-11 2005 CONCLUSIONS: In subjects with ketosis-prone Type 2 diabetes, the best predictors of insulin discontinuation are having new-onset diabetes, and higher beta-cell functional reserve (as measured by the C-peptide-to-glucose ratio). Glucose 212-219 insulin Homo sapiens 84-91 16257499-4 2005 The understanding of interactions between leptin and insulin and their roles in glucose and body weight regulation provides clues towards mechanisms underlying altered appetite regulation and increased risk of type 2 diabetes in low birth weight individuals. Glucose 80-87 insulin Homo sapiens 53-60 16261312-5 2005 RESULTS: Patients with type 1 diabetes showed a reduced insulin-stimulated metabolic clearance rate of glucose (4.3+/-1.3 ml kg(-1) min(-1)) in comparison with normal subjects (6.0+/-1.6 ml kg(-1) min(-1); p<0.001). Glucose 103-110 insulin Homo sapiens 56-63 16261312-6 2005 Endogenous glucose production was higher in diabetic patients (p=0.001) and its suppression was impaired during insulin administration (66+/-30 vs 92+/-8%; p=0.047) in comparison with normal subjects. Glucose 11-18 insulin Homo sapiens 112-119 16357799-0 2005 Is non-insulin dependent glucose uptake a therapeutic alternative? Glucose 25-32 insulin Homo sapiens 7-14 16357799-10 2005 In conclusion a precise evaluation suggests that, although non-insulin dependent glucose uptake represents (3/4) of whole body glucose transport, it is difficult to consider such mechanisms able to generate a new treatment fulfilling the unavoidable request of combined efficacy and tolerability. Glucose 81-88 insulin Homo sapiens 63-70 16386093-0 2005 Insulin pump therapy in preschool children with type 1 diabetes mellitus improves glycemic control and decreases glucose excursions and the risk of hypoglycemia. Glucose 113-120 insulin Homo sapiens 0-7 16410659-7 2005 Plasma glucose at 30-120 minutes and serum insulin level at 120 minutes after glucose load are potentially significant predictors of progression from NGT to IGT even in subjects who do not show increase of body weight. Glucose 78-85 insulin Homo sapiens 43-50 16415762-6 2005 Insulin resistance develops with aging, classically involving changes in glucose tolerance. Glucose 73-80 insulin Homo sapiens 0-7 16415763-5 2005 Several abnormalities in islet beta-cell and insulin secretion were also pointed out in elderly people such as increased amyloid deposition and decreased amylin secretion, impaired insulin secretion pulsatility, decreased insulin sensitivity of pancreatic beta-cells to insulinotropic gut hormones and diminished insulin response to non-glucose stimuli such as arginine. Glucose 337-344 insulin Homo sapiens 45-52 16415763-7 2005 However, insulin secretion appears to decrease with age, with significantly diminished beta-cell sensitivity and acute insulin response to glucose, provided it is analyzed relative to concomitant decreased insulin sensitivity. Glucose 139-146 insulin Homo sapiens 9-16 16415763-8 2005 Thus, there is an interplay between decreased insulin secretion and increased insulin resistance that largely explains the abnormal glucose metabolism seen in elderly. Glucose 132-139 insulin Homo sapiens 46-53 16322388-6 2005 However, insulin sensitivity for stimulation of glucose transport in the isolated adipocytes was indistinguishable from a non-PCOS, non-diabetic control group, while the maximal insulin effect on glucose uptake was significantly lower (2.2 +/- 0.2- and 3.8 +/- 0.8-fold respectively, P = 0.02). Glucose 48-55 insulin Homo sapiens 9-16 16322388-6 2005 However, insulin sensitivity for stimulation of glucose transport in the isolated adipocytes was indistinguishable from a non-PCOS, non-diabetic control group, while the maximal insulin effect on glucose uptake was significantly lower (2.2 +/- 0.2- and 3.8 +/- 0.8-fold respectively, P = 0.02). Glucose 196-203 insulin Homo sapiens 178-185 16339749-2 2005 Here we show that C2C12 myotubes produce levodopa and that insulin-stimulated glucose transport is enhanced when endogenous levodopa is depleted. Glucose 78-85 insulin Homo sapiens 59-66 16339749-3 2005 Exogenous levodopa prevented the stimulation of glucose transport by insulin (P < 0.05) and increased cAMP concentrations (P < 0.05). Glucose 48-55 insulin Homo sapiens 69-76 16339749-4 2005 The decrease in insulin-stimulated glucose transport caused by levodopa was attenuated by propranolol (a beta-adrenergic antagonist) and prevented by NSD-1015 (NSD), an inhibitor of DOPA decarboxylase (DDC; converts levodopa to dopamine). Glucose 35-42 insulin Homo sapiens 16-23 16313276-2 2005 The pancreatic beta-cell responds to an increase in circulating glucose levels by a cascade of metabolic and electrophysiological events leading to the secretion of insulin. Glucose 64-71 insulin Homo sapiens 165-172 16313276-4 2005 Hence, drugs which stimulate or enhance insulin secretion will reduce plasma glucose concentrations; this lowering of hyperglycemia will, in turn, reduce the occurrence of long-term complications. Glucose 77-84 insulin Homo sapiens 40-47 16313276-5 2005 K(ATP) channels play a critical role in insulin secretion and can be considered as transducers of glucose-induced metabolic changes into biophysical events leading to the exocytosis of insulin granules. Glucose 98-105 insulin Homo sapiens 40-47 16313276-5 2005 K(ATP) channels play a critical role in insulin secretion and can be considered as transducers of glucose-induced metabolic changes into biophysical events leading to the exocytosis of insulin granules. Glucose 98-105 insulin Homo sapiens 185-192 16313276-10 2005 Here, we overview the existing and novel approaches targeting the beta-cell to enhance the release of insulin, with special emphasis on new ways of amplifying insulin secretion in a glucose-dependent manner. Glucose 182-189 insulin Homo sapiens 159-166 16019120-4 2006 A possible interaction of these drugs with glucose transporters has been proposed: peripheral insulin resistance may develop if these drugs inhibited glucose transport in cells which express the insulin responsive glucose transporter, GLUT4, i.e., muscle and adipocytes. Glucose 43-50 insulin Homo sapiens 94-101 16019120-4 2006 A possible interaction of these drugs with glucose transporters has been proposed: peripheral insulin resistance may develop if these drugs inhibited glucose transport in cells which express the insulin responsive glucose transporter, GLUT4, i.e., muscle and adipocytes. Glucose 43-50 insulin Homo sapiens 195-202 16372226-7 2005 Finally, insulin-stimulated glucose transport did not show any changes that could be attributed to the type of diet. Glucose 28-35 insulin Homo sapiens 9-16 16044174-4 2005 Insulin sensitivity was assessed with the euglycemic hyperinsulinemic clamp, insulin secretion with the intravenous glucose tolerance test and energy expenditure with indirect calorimetry. Glucose 116-123 insulin Homo sapiens 0-7 15902194-3 2005 In this model, intravenous insulin is used to reduce plasma glucose to 30 to 35 mg/dL for 75 mins. Glucose 60-67 insulin Homo sapiens 27-34 16280693-9 2005 The in vivo potency of PIs to impair peripheral glucose disposal acutely correlates with the degree of insulin resistance observed in HIV-infected patients receiving these drugs. Glucose 48-55 insulin Homo sapiens 103-110 16340083-2 2005 Glucose utilization and energy metabolism are regulated by insulin and insulin-like growth factor I (IGF-I), and correspondingly, studies have shown that cognitive impairment may be improved by glucose or insulin administration. Glucose 0-7 insulin Homo sapiens 59-66 16051710-9 2005 Insulin-mediated whole body glucose uptake rates increased from 6.3 +/- 0.6 to 7.3 +/- 0.3 mg.kg(-1).min(-1) (P = 0.03), and insulin-induced inhibition of adipose tissue lipolysis was more prominent after than before the intervention (P = 0.05). Glucose 28-35 insulin Homo sapiens 0-7 16051710-11 2005 This experiment is the first in humans to show that intermittent fasting increases insulin-mediated glucose uptake rates, and the findings are compatible with the thrifty gene concept. Glucose 100-107 insulin Homo sapiens 83-90 16336420-9 2005 In acute coronary syndromes, lowering glucose levels to the near-normal range with insulin is highly beneficial. Glucose 38-45 insulin Homo sapiens 83-90 16284649-2 2005 The rate of insulin-stimulated muscle glucose uptake was approximately 60% lower in the IR offspring than the control subjects and was associated with an approximately 60% increase in the intramyocellular lipid content as assessed by H magnetic resonance spectroscopy. Glucose 38-45 insulin Homo sapiens 12-19 16502647-2 2005 Based on a finite element model for insulin response to a glucose load in the presence of various oxygen supplies, the present study aimed at pointing out the major parameters influencing this secretion. Glucose 58-65 insulin Homo sapiens 36-43 16427537-4 2005 This case demonstrates that changes in insulin therapy warrant not only close monitoring of blood glucose, but also of serum potassium. Glucose 98-105 insulin Homo sapiens 39-46 16311100-11 2005 These data show that a single meal enriched with C18:1trans-fatty acids can significantly increase insulin resistance, and that in the presence of the FABP2 Thr54 allele, may contribute to increased partitioning of glucose to triacylglycerols and insulin resistance. Glucose 215-222 insulin Homo sapiens 247-254 16311091-3 2005 Plasma glucose and serum insulin concentrations were measured for 3 hours postprandially, and the insulinogenic index (the ratio of incremental serum insulin to plasma glucose concentration during the first 30 minutes after meal) was calculated. Glucose 168-175 insulin Homo sapiens 98-105 16311091-8 2005 In the NGT group the postprandial plasma glucose concentration upon thorough mastication of meal was significantly lower, most probably because of the potentiation of early-phase insulin secretion. Glucose 41-48 insulin Homo sapiens 179-186 16311102-5 2005 Insulin-stimulated glucose disposal did not change. Glucose 19-26 insulin Homo sapiens 0-7 16311104-0 2005 Continually high insulin levels impair Akt phosphorylation and glucose transport in human myoblasts. Glucose 63-70 insulin Homo sapiens 17-24 16311104-2 2005 This study analyzes the effect of long-term exposure to high insulin levels on the insulin-signaling pathway and glucose transport in cultured human myoblasts. Glucose 113-120 insulin Homo sapiens 61-68 16598900-3 2005 The defects in insulin action on target tissues are characterized by a decreased in muscle glucose uptake and by an increased hepatic glucose production. Glucose 91-98 insulin Homo sapiens 15-22 16311104-10 2005 Moreover, the impairment of the insulin-signaling steps between PI3K and Akt is concomitant with the desensitization of glucose transport. Glucose 120-127 insulin Homo sapiens 32-39 16598904-3 2005 Although the beta cell secretary response is mainly controlled by blood glucose levels, gut hormones secreted in response to food intake have an important role in potentiating glucose-stimulated insulin secretion. Glucose 176-183 insulin Homo sapiens 195-202 16300674-0 2005 Insulin induces a positive relationship between the rates of ATP and glycogen changes in isolated rat liver in presence of glucose; a 31P and 13C NMR study. Glucose 123-130 insulin Homo sapiens 0-7 16412956-2 2005 These cells are responsible for insulin production and secretion in response to increases in circulating concentrations of nutrients, such as glucose, fatty acids and amino acids. Glucose 142-149 insulin Homo sapiens 32-39 16179348-4 2005 AGN194204 had no effect on peripheral glucose utilization, whereas troglitazone increased insulin-stimulated glucose utilization by 50%, glucose uptake into skeletal muscle by 85%, and de novo skeletal muscle glycogen synthesis by 300%. Glucose 109-116 insulin Homo sapiens 90-97 16179348-4 2005 AGN194204 had no effect on peripheral glucose utilization, whereas troglitazone increased insulin-stimulated glucose utilization by 50%, glucose uptake into skeletal muscle by 85%, and de novo skeletal muscle glycogen synthesis by 300%. Glucose 109-116 insulin Homo sapiens 90-97 16300674-7 2005 With insulin + glucose, both glycogen and ATP rates were strongly related to the glucose concentration; the magnitude of net glycogen flux was linearly correlated to the magnitude of net ATP flux: flux(glycogen) = 72.543(fluxATP) + 172.08, R2 = 0.98. Glucose 81-88 insulin Homo sapiens 5-12 16155293-6 2005 Trans-10, cis-12 CLA suppression of insulin-stimulated glucose uptake at 24 h was associated with decreased total and plasma membrane glucose transporter 4 proteins. Glucose 55-62 insulin Homo sapiens 36-43 16278328-4 2005 Pramlintide complements the effects of insulin in postprandial glucose regulation by decreasing glucagon secretion. Glucose 63-70 insulin Homo sapiens 39-46 16150793-1 2005 While caffeine impedes insulin-mediated glucose disposal in humans, its effect on endo-genous glucose production (EGP) remains unknown. Glucose 40-47 insulin Homo sapiens 23-30 16129678-4 2005 Studying the function of this phosphorylation, we found that replacing Ser(318) by alanine completely prevented both the attenuation of insulin-stimulated Akt/protein kinase B Ser(473) phosphorylation and glucose uptake after 60 min of insulin stimulation. Glucose 205-212 insulin Homo sapiens 136-143 16129678-6 2005 Furthermore, replacing Ser(318) by glutamate, i.e. mimicking phosphorylation, improved glucose uptake after acute insulin stimulation. Glucose 87-94 insulin Homo sapiens 114-121 16129680-5 2005 Dopamine (10 microM) and the D2-like receptor agonist quinpirole (5 microM) inhibited glucose-stimulated insulin secretion tested in several models, i.e. INS-1E beta cells, fluorescence-activated cell-sorted primary rat beta cells, and pancreatic islets of rat, mouse, and human origin. Glucose 86-93 insulin Homo sapiens 105-112 16129680-10 2005 Dopamine inhibited glucose-stimulated insulin secretion, an effect that could be ascribed to D2-like receptors. Glucose 19-26 insulin Homo sapiens 38-45 16280432-11 2005 However, only glucose triggered an early rise in insulin concentrations. Glucose 14-21 insulin Homo sapiens 49-56 15972269-0 2005 Measurement of selective effect of insulin on glucose disposal from labeled glucose oral test minimal model. Glucose 46-53 insulin Homo sapiens 35-42 15972269-0 2005 Measurement of selective effect of insulin on glucose disposal from labeled glucose oral test minimal model. Glucose 76-83 insulin Homo sapiens 35-42 15972269-1 2005 The oral glucose minimal model (OMM) measures insulin sensitivity (S(I)) and the glucose rate of appearance (R(a)) of ingested glucose in the presence of physiological changes of insulin and glucose concentrations. Glucose 9-16 insulin Homo sapiens 46-53 15972269-1 2005 The oral glucose minimal model (OMM) measures insulin sensitivity (S(I)) and the glucose rate of appearance (R(a)) of ingested glucose in the presence of physiological changes of insulin and glucose concentrations. Glucose 9-16 insulin Homo sapiens 179-186 15972269-2 2005 However, S(I) of OMM measures the overall effect of insulin on glucose utilization and glucose production. Glucose 63-70 insulin Homo sapiens 52-59 15972269-2 2005 However, S(I) of OMM measures the overall effect of insulin on glucose utilization and glucose production. Glucose 87-94 insulin Homo sapiens 52-59 16292231-4 2005 These are glucose which leads to glyoxal and to methylglyoxal which in turn reacts with innumerable targets in the organism (including insulin) unless prevented from doing so by detoxifying mechanisms (e.g., glyoxalases). Glucose 10-17 insulin Homo sapiens 135-142 16246040-6 2005 One potential confounding factor with these data, however, is the need for co-administration of glucose with the insulin to maintain euglycaemia as glucose itself can facilitate memory function. Glucose 148-155 insulin Homo sapiens 113-120 16246040-7 2005 Administration of insulin via the intranasal route is scientifically (and therapeutically) more attractive because the insulin goes directly to the cerebrospinal fluid, with minimal systemic absorption; this obviates the need for a glucose infusion. Glucose 232-239 insulin Homo sapiens 18-25 16271533-3 2005 Here, we show that, in parallel with their effects on glucose output, CREB and TORC2 also enhance insulin signaling in liver by stimulating expression of the insulin receptor substrate 2 (IRS2) gene. Glucose 54-61 insulin Homo sapiens 98-105 16249463-4 2005 Significant positive correlations between glucose and insulin resistance with calcium were found in both sexes, whereas an inverse correlation between beta-cell function and calcium was found only in women. Glucose 42-49 insulin Homo sapiens 54-61 16188578-10 2005 Minimal model analysis of a frequently sampled intravenous glucose tolerance test revealed severe insulin resistance, despite the absence of obesity. Glucose 59-66 insulin Homo sapiens 98-105 16193292-4 2005 Short-term supraphysiological oestrogen administration has an adverse effect on glucose tolerance, resulting from suppression of first-phase insulin secretion and increased insulin resistance. Glucose 80-87 insulin Homo sapiens 141-148 16195866-0 2005 Human proinsulin C-peptide prevents proliferation of rat aortic smooth muscle cells cultured in high-glucose conditions. Glucose 101-108 insulin Homo sapiens 6-16 16195866-0 2005 Human proinsulin C-peptide prevents proliferation of rat aortic smooth muscle cells cultured in high-glucose conditions. Glucose 101-108 insulin Homo sapiens 17-26 16219007-2 2005 Thiazolidinediones such as rosiglitazone and pioglitazone enhance insulin-mediated glucose disposal, leading to reduced plasma insulin concentrations. Glucose 83-90 insulin Homo sapiens 66-73 16219007-2 2005 Thiazolidinediones such as rosiglitazone and pioglitazone enhance insulin-mediated glucose disposal, leading to reduced plasma insulin concentrations. Glucose 83-90 insulin Homo sapiens 127-134 16219007-5 2005 The thiazolidinediones in combination with insulin have also been effective in lowering blood glucose levels and total daily insulin dose. Glucose 94-101 insulin Homo sapiens 43-50 16249544-14 2005 Instead, in pregnant women, increased insulin resistance is associated with decreased proinsulin-to-C-peptide ratio, independently of glucose tolerance status. Glucose 134-141 insulin Homo sapiens 38-45 16357785-0 2005 Is non-insulin dependent glucose uptake a therapeutic alternative? Glucose 25-32 insulin Homo sapiens 7-14 16357785-1 2005 Part 1: physiology, mechanisms and role of non insulin-dependent glucose uptake in type 2 diabetes. Glucose 65-72 insulin Homo sapiens 47-54 16357785-5 2005 Although poorly explored, insulin-independent glucose uptake might nevertheless represent a therapeutic target, as an alternative to the clear limits of actual drug treatments. Glucose 46-53 insulin Homo sapiens 26-33 16143325-6 2005 In the presence of lipopolysaccharide (LPS) and 25 mM glucose, the TCB f-Mphi differentiated to express insulin mRNA, C-peptide, and insulin. Glucose 54-61 insulin Homo sapiens 104-111 16143325-6 2005 In the presence of lipopolysaccharide (LPS) and 25 mM glucose, the TCB f-Mphi differentiated to express insulin mRNA, C-peptide, and insulin. Glucose 54-61 insulin Homo sapiens 133-140 16143325-7 2005 In vitro functional analysis demonstrated that these insulin-positive cells could release insulin in response to glucose and other secretagogues. Glucose 113-120 insulin Homo sapiens 53-60 16143325-7 2005 In vitro functional analysis demonstrated that these insulin-positive cells could release insulin in response to glucose and other secretagogues. Glucose 113-120 insulin Homo sapiens 90-97 16257476-3 2005 We report that older adults with insulin resistance show remarkably similar deficits in cognitive function and respond to glucose ingestion in a comparable manner to rodents fed a high-fat diet, suggesting that insulin resistance is a probable mediator of these diet-induced deficits. Glucose 122-129 insulin Homo sapiens 33-40 16489319-1 2005 Insulin-mediated glucose disposal varies widely in apparently healthy human beings, and the more insulin resistant an individual, the more insulin they must secrete in order to prevent the development of type 2 diabetes. Glucose 17-24 insulin Homo sapiens 0-7 16489319-1 2005 Insulin-mediated glucose disposal varies widely in apparently healthy human beings, and the more insulin resistant an individual, the more insulin they must secrete in order to prevent the development of type 2 diabetes. Glucose 17-24 insulin Homo sapiens 97-104 16489319-1 2005 Insulin-mediated glucose disposal varies widely in apparently healthy human beings, and the more insulin resistant an individual, the more insulin they must secrete in order to prevent the development of type 2 diabetes. Glucose 17-24 insulin Homo sapiens 139-146 16313839-10 2005 A glucose-stimulated insulin secretion test was performed to detect the effects of Sertoli cells on allogeneic islets" function when they were co-cultured for 21 days in vitro. Glucose 2-9 insulin Homo sapiens 21-28 16288655-12 2005 Glucose is the major insulin secretagogue and insulin resistance has been tied to the hyperinsulinemic state or the effect of such a state on lipid metabolism. Glucose 0-7 insulin Homo sapiens 21-53 15935387-2 2005 In beta-cells this is accompanied by sustained oscillations of concentration of insulin, which helps to keep the blood glucose level within optimum limits. Glucose 119-126 insulin Homo sapiens 80-87 16239416-4 2005 Insulin infusions were underutilized and were often not started until capillary blood glucose concentrations were greater than 350 mg/dL for 12 or more hours. Glucose 86-93 insulin Homo sapiens 0-7 16239416-6 2005 A preliminary protocol was drafted allowing adjustments in insulin administration to be based on changes in capillary blood glucose values since the previous blood glucose measurement. Glucose 124-131 insulin Homo sapiens 59-66 16239416-6 2005 A preliminary protocol was drafted allowing adjustments in insulin administration to be based on changes in capillary blood glucose values since the previous blood glucose measurement. Glucose 164-171 insulin Homo sapiens 59-66 16356119-4 2005 This activation is accompanied by a down-regulation of the cellular response to insulin, leading to a reduced ability of insulin to promote glucose uptake, and glycogen and protein synthesis. Glucose 140-147 insulin Homo sapiens 80-87 16356119-4 2005 This activation is accompanied by a down-regulation of the cellular response to insulin, leading to a reduced ability of insulin to promote glucose uptake, and glycogen and protein synthesis. Glucose 140-147 insulin Homo sapiens 121-128 16168963-1 2005 The novel insulin receptor substrate protein APS is highly expressed in insulin-sensitive tissues and plays an important role in insulin-mediated glucose uptake and GLUT4 translocation via the Cbl/CAP pathway. Glucose 146-153 insulin Homo sapiens 10-17 16168963-1 2005 The novel insulin receptor substrate protein APS is highly expressed in insulin-sensitive tissues and plays an important role in insulin-mediated glucose uptake and GLUT4 translocation via the Cbl/CAP pathway. Glucose 146-153 insulin Homo sapiens 72-79 16168963-1 2005 The novel insulin receptor substrate protein APS is highly expressed in insulin-sensitive tissues and plays an important role in insulin-mediated glucose uptake and GLUT4 translocation via the Cbl/CAP pathway. Glucose 146-153 insulin Homo sapiens 72-79 16160865-4 2005 First-phase insulin response to a glucose infusion test was estimated as an incremental 5- or 10-min (DeltaI5 or DeltaI10) value, and as insulinogenic indices (DeltaI5/DeltaG5 or DeltaI10/DeltaG10) adjusted for insulin sensitivity determined by homeostasis model assessment for insulin resistance ([DeltaI5/DeltaG5]/HOMA-IR). Glucose 34-41 insulin Homo sapiens 12-19 16160865-10 2005 CONCLUSIONS/INTERPRETATION: In 267 non-obese healthy subjects, initial K-value and first-phase insulin response to glucose adjusted for insulin sensitivity, but not insulin sensitivity itself, were strong predictors of the outcome of an OGTT performed 25 years later. Glucose 115-122 insulin Homo sapiens 95-102 16195866-7 2005 C-peptide suppressed hyperproliferation activities that were induced by high glucose. Glucose 77-84 insulin Homo sapiens 0-9 16195866-9 2005 C-peptide (10 and 100 nmol/l) inhibited the increased protein expression of PDGF-beta receptor and the phosphorylation of p42/p44 MAP kinases that had been induced by high glucose (p<0.05). Glucose 172-179 insulin Homo sapiens 0-9 16195866-10 2005 Furthermore, 100 nmol/l of C-peptide augmented the impaired glucose uptake in the high-glucose conditions. Glucose 60-67 insulin Homo sapiens 27-36 16195866-10 2005 Furthermore, 100 nmol/l of C-peptide augmented the impaired glucose uptake in the high-glucose conditions. Glucose 87-94 insulin Homo sapiens 27-36 16195866-11 2005 CONCLUSIONS/INTERPRETATION: These observations suggest that C-peptide could prevent diabetic macroangiopathy by inhibiting smooth muscle cell growth and ameliorating glucose utilisation in smooth muscle cells. Glucose 166-173 insulin Homo sapiens 60-69 16249431-3 2005 Here, we report using novel conditionally immortalized human podocytes in vitro and human glomeruli ex vivo that the podocyte, the principal cell responsible for prevention of urinary protein loss, is insulin responsive and able to approximately double its glucose uptake within 15 min of insulin stimulation. Glucose 257-264 insulin Homo sapiens 201-208 16249438-5 2005 After acipimox, insulin-stimulated Rd increased from 3.3 +/- 0.4 to 4.4 +/- 0.4 mg x kg(-1) x min(-1) (P < 0.03), whereas suppression of endogenous glucose production (EGP) was similar and virtually complete during both insulin clamp studies (0.16 +/- 0.10 vs. 0.14 +/- 0.10 mg x kg(-1) x min(-1); P > 0.05). Glucose 151-158 insulin Homo sapiens 16-23 16249439-0 2005 The stimulatory effect of globular adiponectin on insulin-stimulated glucose uptake and fatty acid oxidation is impaired in skeletal muscle from obese subjects. Glucose 69-76 insulin Homo sapiens 50-57 16249439-7 2005 Combined exposure of insulin and gAcrp30 demonstrated an additive effect on glucose uptake in lean and obese individuals, but this effect was reduced by 50% in obese muscle (P < 0.05). Glucose 76-83 insulin Homo sapiens 21-28 16821211-8 2005 In a multiple regression analysis adjusting for age and adiposity, in the female group plasma glucose and insulin levels 2-h after glucose load were the best predictors of fasting plasma leptin (r=-0.49, p<.005 and r=0.34, p<.05; respectively). Glucose 131-138 insulin Homo sapiens 106-113 16821211-9 2005 In boys, plasma insulin level 2-h after glucose load was the independent determinant of leptin (r=0.36, p<.05). Glucose 40-47 insulin Homo sapiens 16-23 16227462-3 2005 In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated. Glucose 118-125 insulin Homo sapiens 179-186 16144950-4 2005 DESIGN: Fasted subjects received iv insulin infusion to reach plasma glucose 4.4-5.6 mmol/liter. Glucose 69-76 insulin Homo sapiens 36-43 16118336-9 2005 High-density lipoproteins and the area under curve for glucose/area under curve for insulin ratio also significantly (P < 0.001) increased, whereas low-density lipoproteins and plasma endothelin-1 levels were significantly (P < 0.001) reduced. Glucose 55-62 insulin Homo sapiens 84-91 16144950-13 2005 CONCLUSIONS: Short-term exposure to exenatide can restore the insulin secretory pattern in response to acute rises in glucose concentrations in DM2 patients who, in the absence of exenatide, do not display a first phase of insulin secretion. Glucose 118-125 insulin Homo sapiens 62-69 16278631-9 2005 The need for intensive insulin therapy, even by means of continuous infusion of insulin, to obtain the normalization of blood glucose levels, appears essential. Glucose 126-133 insulin Homo sapiens 23-30 16269383-4 2005 Insulin sensitivity was determined by frequently sampled intravenous glucose tolerance testing at the same time points. Glucose 69-76 insulin Homo sapiens 0-7 16385293-8 2005 Children receiving intensive insulin therapy had glucose levels of 90 to 120 mg/dL more consistently than those in the conventional insulin therapy group. Glucose 49-56 insulin Homo sapiens 29-36 16260353-6 2005 RESULTS: In volunteers submitted to the clamp at 4.1 mmol/l above the baseline of glucose level, the insulin secretion in the early phase was 212.4+/-55.8 pmol/l in the placebo test versus 338.4+/-124.8 pmol/l in the nateglinide test (P<.05), whereas in the group submitted at 6.9 mmol/l over the baseline, no significant differences were observed. Glucose 82-89 insulin Homo sapiens 101-108 16278631-9 2005 The need for intensive insulin therapy, even by means of continuous infusion of insulin, to obtain the normalization of blood glucose levels, appears essential. Glucose 126-133 insulin Homo sapiens 80-87 16411528-12 2005 PET glucose levels [D0/D2 glu: 0.40 (0.37 - 0.45) vs 0.50 (0.48 - 0.51), p = 0.03; D0/D4 glu: 0.36 (0.26 - 0.38) vs 0.44 (0.38 - 0.48), p = 0.04] were lower in diabetic patients receiving IP insulin who had HSS than in those who did not have HSS. Glucose 4-11 insulin Homo sapiens 191-198 15994203-3 2005 We have also reported that chronic endothelin-1 (ET-1) treatment leads to heterologous desensitization of insulin signaling with decreased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and Galphaq/11, and decreased insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 251-258 insulin Homo sapiens 106-113 15994203-3 2005 We have also reported that chronic endothelin-1 (ET-1) treatment leads to heterologous desensitization of insulin signaling with decreased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and Galphaq/11, and decreased insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 251-258 insulin Homo sapiens 167-174 16339117-5 2005 With age, sex, and study center as covariates, we detected linkage of the glucose/insulin/obesity factor to chromosome 4 (robust logarithm of the odds (LOD) = 2.2), the dyslipidemia factor to chromosome 12 (robust LOD = 2.7), and the blood pressure factor to chromosome 1 (robust LOD = 1.6). Glucose 74-81 insulin Homo sapiens 82-89 16183812-10 2005 Selective inhibition of downstream components of insulin signaling allows fetuses to adapt to nutritional stress by decreasing the anabolic response to insulin and other growth factors, so that more amino acids can be used as oxidative substrate to compensate for shortage of energy due to reduced glucose supply. Glucose 298-305 insulin Homo sapiens 49-56 16183812-10 2005 Selective inhibition of downstream components of insulin signaling allows fetuses to adapt to nutritional stress by decreasing the anabolic response to insulin and other growth factors, so that more amino acids can be used as oxidative substrate to compensate for shortage of energy due to reduced glucose supply. Glucose 298-305 insulin Homo sapiens 152-159 16137651-2 2005 We recently reported the insulin-like glucose transport stimulatory activity of tannic acid (TA) in 3T3-L1 adipocytes. Glucose 38-45 insulin Homo sapiens 25-32 16137651-4 2005 Mechanistic studies in adipocytes with alpha-PGG, the more potent of the two anomers, reveal that inhibitors that block the insulin-mediated glucose transport, including one that inhibits the insulin receptor (IR), also completely abolish the glucose transport activated by alpha-PGG. Glucose 141-148 insulin Homo sapiens 124-131 16137651-4 2005 Mechanistic studies in adipocytes with alpha-PGG, the more potent of the two anomers, reveal that inhibitors that block the insulin-mediated glucose transport, including one that inhibits the insulin receptor (IR), also completely abolish the glucose transport activated by alpha-PGG. Glucose 243-250 insulin Homo sapiens 124-131 15928020-8 2005 AMPK- and insulin-stimulated glucose uptake were similarly suppressed by wortmannin (P < 0.05-0.01). Glucose 29-36 insulin Homo sapiens 10-17 16230722-1 2005 BACKGROUND: Physicians may use either insulin or exenatide injections for patients with type 2 diabetes mellitus who have poor glycemic control despite taking oral blood glucose-lowering drugs. Glucose 170-177 insulin Homo sapiens 38-45 16230722-10 2005 Exenatide reduced postprandial glucose excursions more than insulin glargine, while insulin glargine reduced fasting glucose concentrations more than exenatide. Glucose 117-124 insulin Homo sapiens 84-91 16240848-1 2005 Continuous subcutaneous insulin infusion (CSII) was initiated in 3 patients with diabetes mellitus type I who experienced difficulties with their glucose regulation: a woman aged 26 years and two men aged 56 and 41 years. Glucose 146-153 insulin Homo sapiens 24-31 16183425-6 2005 RESULTS: In HD patients and controls, serum insulin levels increased to a similar magnitude in parallel with increased serum glucose levels, but serum potassium levels decreased significantly only in HD patients. Glucose 125-132 insulin Homo sapiens 44-51 16183425-8 2005 In HD patients, the decrease in serum potassium levels was dependent on the increase in serum insulin levels and was more prominent when 150 g of glucose was administered. Glucose 146-153 insulin Homo sapiens 94-101 16183425-10 2005 CONCLUSION: Endogenous production of physiological concentrations of insulin in response to exogenous glucose administration decreases serum potassium levels only in HD patients, independently of plasma aldosterone and epinephrine levels. Glucose 102-109 insulin Homo sapiens 69-76 15972000-0 2005 The selective recruitment of mRNA to the ER and an increase in initiation are important for glucose-stimulated proinsulin synthesis in pancreatic beta-cells. Glucose 92-99 insulin Homo sapiens 111-121 15972000-1 2005 Glucose acutely stimulates proinsulin synthesis in pancreatic beta-cells through a poorly understood post-transcriptional mechanism. Glucose 0-7 insulin Homo sapiens 27-37 15972000-2 2005 In the present study, we demonstrate in pancreatic beta-cells that glucose stimulates the recruitment of ribosome-associated proinsulin mRNA, located in the cytoplasm, to the ER (endoplasmic reticulum), the site of proinsulin synthesis, and that this plays an important role in glucose-stimulated proinsulin synthesis. Glucose 67-74 insulin Homo sapiens 125-135 15972000-2 2005 In the present study, we demonstrate in pancreatic beta-cells that glucose stimulates the recruitment of ribosome-associated proinsulin mRNA, located in the cytoplasm, to the ER (endoplasmic reticulum), the site of proinsulin synthesis, and that this plays an important role in glucose-stimulated proinsulin synthesis. Glucose 67-74 insulin Homo sapiens 215-225 15972000-2 2005 In the present study, we demonstrate in pancreatic beta-cells that glucose stimulates the recruitment of ribosome-associated proinsulin mRNA, located in the cytoplasm, to the ER (endoplasmic reticulum), the site of proinsulin synthesis, and that this plays an important role in glucose-stimulated proinsulin synthesis. Glucose 67-74 insulin Homo sapiens 215-225 15972000-2 2005 In the present study, we demonstrate in pancreatic beta-cells that glucose stimulates the recruitment of ribosome-associated proinsulin mRNA, located in the cytoplasm, to the ER (endoplasmic reticulum), the site of proinsulin synthesis, and that this plays an important role in glucose-stimulated proinsulin synthesis. Glucose 278-285 insulin Homo sapiens 125-135 15972000-3 2005 Interestingly, glucose has greater stimulatory effect on the recruitment of proinsulin mRNA to the ER compared with other mRNAs encoding secretory proteins. Glucose 15-22 insulin Homo sapiens 76-86 15972000-5 2005 Contrary to previous reports, and importantly in understanding the mechanism by which glucose stimulates proinsulin synthesis, we demonstrate that there is no large pool of "free" proinsulin mRNA in the cytoplasm and that glucose does not increase the rate of de novo initiation on the proinsulin mRNA. Glucose 86-93 insulin Homo sapiens 105-115 15972000-6 2005 However, we show that glucose does stimulate the rate of ribosome recruitment on to ribosome-associated proinsulin mRNA. Glucose 22-29 insulin Homo sapiens 104-114 15972000-7 2005 In conclusion, our results provide evidence that the selective recruitment of proinsulin mRNA to the ER, together with increases in the rate of initiation are important mediators of glucose-stimulated proinsulin synthesis in pancreatic beta-cells. Glucose 182-189 insulin Homo sapiens 78-88 15972000-7 2005 In conclusion, our results provide evidence that the selective recruitment of proinsulin mRNA to the ER, together with increases in the rate of initiation are important mediators of glucose-stimulated proinsulin synthesis in pancreatic beta-cells. Glucose 182-189 insulin Homo sapiens 201-211 16230533-1 2005 The insulin signaling pathway, which is conserved in evolution from flies to humans, evolved to allow a fast response to changes in nutrient availability while keeping glucose concentration constant in serum. Glucose 168-175 insulin Homo sapiens 4-11 15914506-0 2005 Adrenergic receptor stimulation attenuates insulin-stimulated glucose uptake in 3T3-L1 adipocytes by inhibiting GLUT4 translocation. Glucose 62-69 insulin Homo sapiens 43-50 15914506-1 2005 Activation of the sympathetic nervous system inhibits insulin-stimulated glucose uptake. Glucose 73-80 insulin Homo sapiens 54-61 15914506-3 2005 Therefore, we studied the effects of catecholamines on insulin-stimulated glucose uptake and insulin-stimulated translocation of GLUT4 to the plasma membrane in 3T3-L1 adipocytes. Glucose 74-81 insulin Homo sapiens 55-62 15914506-5 2005 The beta-adrenoceptor antagonist propranolol (0.3 microM) completely antagonized the inhibitory effect of epinephrine on insulin-stimulated glucose uptake, whereas the alpha-adrenoceptor antagonist phentolamine (10 microM) had no effect. Glucose 140-147 insulin Homo sapiens 121-128 15914506-8 2005 Combination of ICI-118551 and SR-59230A, as well as combination of all three selective beta-adrenoceptor antagonists, abolished the effect of epinephrine on insulin-stimulated glucose uptake. Glucose 176-183 insulin Homo sapiens 157-164 15914506-11 2005 These results show that beta-adrenergic (but not alpha-adrenergic) stimulation inhibits insulin-induced glucose uptake in 3T3-L1 adipocytes, most likely via the beta(2)- and beta(3)-adrenoceptor by interfering with GLUT4 translocation from intracellular vesicles to the plasma membrane. Glucose 104-111 insulin Homo sapiens 88-95 15928020-9 2005 In addition, SB-203580 also significantly prevented the enhancement of glucose uptake induced by AMPK and insulin (P < 0.05). Glucose 71-78 insulin Homo sapiens 106-113 16013082-1 2005 OBJECTIVE: To determine the feasibility of differentiating the glucose-stimulated plasma insulin response between lean and obese children using a new PK/PD model that specifically considers the insulin-glucose physiology of beta cells. Glucose 63-70 insulin Homo sapiens 89-96 16204961-3 2005 In addition, the enhanced level of blood glucose in STZ-treated embryos reduced by injection of human insulin. Glucose 41-48 insulin Homo sapiens 102-109 16188168-1 2005 Insulin resistance is a characteristic biological abnormality associated with type 2 diabetes, and is a key component of the metabolic syndrome, a condition in which an altered glucose control is associated with dyslipidemia, hypertension, and obesity. Glucose 177-184 insulin Homo sapiens 0-7 16181237-8 2005 RESULTS: Lipid infusion increased FFAs (5.41 +/- 1.00 vs. 0.48 +/- 0.20 mmol/l; P < 0.005) and significantly increased insulin resistance [glucose infusion rate (GIR) 6.02 +/- 2.60 vs. 4.08 +/- 2.15 mg/kg/min; P < 0.005]. Glucose 142-149 insulin Homo sapiens 122-129 16081057-8 2005 Multivariate regression analyses showed that insulin was positively associated with glucose, triglycerides and apoB in boys but not in girls, and negatively associated with FFA in both genders. Glucose 84-91 insulin Homo sapiens 45-52 16186273-3 2005 RESEARCH DESIGN AND METHODS: A computer-directed algorithm for advice on the delivery of intravenous insulin that is flexible in blood glucose timing and advises insulin dosing in a graduated manner has been developed. Glucose 135-142 insulin Homo sapiens 101-108 16132961-1 2005 AIMS/HYPOTHESIS: The aim of the study was to investigate the potential of human pancreatic non-endocrine cells to transdifferentiate into endocrine cells that would be capable of secreting insulin in response to glucose and ameliorating insulin-deficient diabetes after transplantation. Glucose 212-219 insulin Homo sapiens 189-196 16132961-8 2005 CONCLUSIONS/INTERPRETATION: Human pancreatic cells are a potential source of new glucose-responsive insulin-producing cells that may be developed further for clinical use. Glucose 81-88 insulin Homo sapiens 100-107 16176204-2 2005 The present study was undertaken to explore a possible influence of the oral prandial glucose regulator, repaglinide, on first-phase insulin secretion and high-frequency insulin pulsatility in Type 2 diabetes. Glucose 86-93 insulin Homo sapiens 133-140 16176204-6 2005 Entrainment of insulin secretion was assessed utilizing 1-min glucose bolus exposure (6 mg/kg body weight every 10 min) for 60 min during (A) baseline conditions, i.e. 12 h after the last repaglinide/placebo administration, and (B) 30 min after an oral dose of 0.5 mg repaglinide/placebo with subsequent application of time-series analyses. Glucose 62-69 insulin Homo sapiens 15-22 16176204-13 2005 CONCLUSION/INTERPRETATION: Repaglinide augments first-phase insulin secretion as well as high-frequency insulin secretory burst mass and amplitude during glucose entrainment in patients with Type 2 diabetes, while regularity of the insulin release process was unaltered. Glucose 154-161 insulin Homo sapiens 104-111 16176204-13 2005 CONCLUSION/INTERPRETATION: Repaglinide augments first-phase insulin secretion as well as high-frequency insulin secretory burst mass and amplitude during glucose entrainment in patients with Type 2 diabetes, while regularity of the insulin release process was unaltered. Glucose 154-161 insulin Homo sapiens 104-111 16094530-14 2005 Insulin at 10(-9)-10(-7) mol/l had no effect on DNA synthesis, but increased glucose accumulation at 10(-7) mol/l. Glucose 77-84 insulin Homo sapiens 0-7 16160866-7 2005 Insulin-mediated whole-body glucose uptake significantly (p<0.0001) increased from 21.2+/-4.1 to 52.8+/-5.9 micromol kg fat-free mass(-1) min(-1) and glucose oxidation rose from 11.1+/-2.1 to 37.7+/-4.7 micromol kg fat-free mass(-1) min(-1) (p<0.0001). Glucose 28-35 insulin Homo sapiens 0-7 16160866-7 2005 Insulin-mediated whole-body glucose uptake significantly (p<0.0001) increased from 21.2+/-4.1 to 52.8+/-5.9 micromol kg fat-free mass(-1) min(-1) and glucose oxidation rose from 11.1+/-2.1 to 37.7+/-4.7 micromol kg fat-free mass(-1) min(-1) (p<0.0001). Glucose 153-160 insulin Homo sapiens 0-7 16248779-2 2005 There is increasing evidence to suggest that chronic activation of the endothelin-1 system can lead to heterologous desensitization of the glucose-regulatory and mitogenic actions of insulin with subsequent development of glucose intolerance, hyperinsulinemia, impaired endothelial function and exacerbation of cardiovascular disease. Glucose 139-146 insulin Homo sapiens 183-190 16186396-4 2005 TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. Glucose 27-34 insulin Homo sapiens 69-76 16186396-6 2005 These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. Glucose 203-210 insulin Homo sapiens 142-149 16284426-10 2005 Insulin suppression test using 50 microg of octreotide improved plasma glucose and IRI levels, suggesting the usefulness of the treatment, and a monthly administration of 20 mg of long-acting octreotide has successfully controlled her symptoms of hypoglycemia for 10 months. Glucose 71-78 insulin Homo sapiens 0-7 16334591-1 2005 The ability of insulin to mediate glucose disposal varies more than six-fold in an apparently healthy population, and approximately one third of the most insulin-resistant of these individuals are at increased risk to develop cardiovascular disease. Glucose 34-41 insulin Homo sapiens 15-22 16334591-6 2005 Finally, there appears to be a comparable relationship between insulin-mediated glucose disposal and amount of visceral fat, subcutaneous fat, and total fat as quantified by various imaging techniques, and the magnitude of these relationships is no greater than that between insulin action and simple measure of body mass index. Glucose 80-87 insulin Homo sapiens 63-70 16284429-14 2005 Furthermore, insulin response to intravenous glucose was higher in IFG than in CGI (p<0.05). Glucose 45-52 insulin Homo sapiens 13-20 16284429-0 2005 The effect of defective early phase insulin secretion on postload glucose intolerance in impaired fasting glucose. Glucose 66-73 insulin Homo sapiens 36-43 16284429-0 2005 The effect of defective early phase insulin secretion on postload glucose intolerance in impaired fasting glucose. Glucose 106-113 insulin Homo sapiens 36-43 16284429-6 2005 A 75-g oral glucose tolerance test (OGTT) with insulin response was done and subjects were classified according to the WHO criteria. Glucose 12-19 insulin Homo sapiens 47-54 16284429-9 2005 Early phase insulin secretion was measured by intravenous glucose tolerance test (IVGTT) and OGTT. Glucose 58-65 insulin Homo sapiens 12-19 16179727-1 2005 Glucose transport into muscle is the initial process in glucose clearance and is uniformly defective in insulin-resistant conditions of obesity, metabolic syndrome, and Type II diabetes mellitus. Glucose 0-7 insulin Homo sapiens 104-111 16179727-2 2005 Insulin regulates glucose transport by activating insulin receptor substrate-1 (IRS-1)-dependent phosphatidylinositol 3-kinase (PI3K) which, via increases in PI-3,4,5-triphosphate (PIP(3)), activates atypical protein kinase C (aPKC) and protein kinase B (PKB/Akt). Glucose 18-25 insulin Homo sapiens 0-7 16179727-3 2005 Here, we review (i) the evidence that both aPKC and PKB are required for insulin-stimulated glucose transport, (ii) abnormalities in muscle aPKC/PKB activation seen in obesity and diabetes, and (iii) mechanisms for impaired aPKC activation in insulin-resistant conditions. Glucose 92-99 insulin Homo sapiens 73-80 16235156-6 2005 However, multivariate linear regression analysis identified insulin sensitivity as determined by glucose infusion rate during the steady state of an euglycemic-hyperinsulinemic clamp as the strongest predictor of adiponectin, CRP, IL-6, and IL-10 plasma concentrations. Glucose 97-104 insulin Homo sapiens 60-67 16198620-27 2005 As a result, monocyte glucose uptake by GLUT4 increases glucose disposal from blood and reduced need for insulin. Glucose 22-29 insulin Homo sapiens 105-112 16198620-29 2005 Insulin resistance is usually evaluated by fasting insulin levels, Quantitative Insulin Check Index (QUICKI) and Homeostasis Model Assessment of Insulin Resistance (HOMA), C-peptid/insulin ratio oral glucose tolerance test and hyper insulinemic euglycemic clamp. Glucose 200-207 insulin Homo sapiens 0-7 16278783-4 2005 In addition, insulin action on glucose disposal rate was measured using the glucose-insulin index, the product of the areas under the curve of glucose, and insulin during the intraperitoneal glucose tolerance test. Glucose 31-38 insulin Homo sapiens 13-20 16202646-11 2005 Insulin resistance observed in the core gene transgenic mice was chiefly due to the shortage of insulin action on the suppression of glucose production in the liver. Glucose 133-140 insulin Homo sapiens 0-7 16278783-4 2005 In addition, insulin action on glucose disposal rate was measured using the glucose-insulin index, the product of the areas under the curve of glucose, and insulin during the intraperitoneal glucose tolerance test. Glucose 76-83 insulin Homo sapiens 13-20 16202646-11 2005 Insulin resistance observed in the core gene transgenic mice was chiefly due to the shortage of insulin action on the suppression of glucose production in the liver. Glucose 133-140 insulin Homo sapiens 96-103 16278783-4 2005 In addition, insulin action on glucose disposal rate was measured using the glucose-insulin index, the product of the areas under the curve of glucose, and insulin during the intraperitoneal glucose tolerance test. Glucose 76-83 insulin Homo sapiens 84-91 16202646-12 2005 Thus, the ability of insulin to lower the plasma glucose level in the HCV transgenic mice was impaired, as observed in chronic hepatitis C patients. Glucose 49-56 insulin Homo sapiens 21-28 16278783-4 2005 In addition, insulin action on glucose disposal rate was measured using the glucose-insulin index, the product of the areas under the curve of glucose, and insulin during the intraperitoneal glucose tolerance test. Glucose 76-83 insulin Homo sapiens 13-20 16278783-4 2005 In addition, insulin action on glucose disposal rate was measured using the glucose-insulin index, the product of the areas under the curve of glucose, and insulin during the intraperitoneal glucose tolerance test. Glucose 76-83 insulin Homo sapiens 84-91 16219952-10 2005 About 60% of patients who screened positive for insulin resistance had normal fasting serum glucose levels. Glucose 92-99 insulin Homo sapiens 48-55 16278783-7 2005 The plasma glucose-lowering activity of tolbutamide was introduced to account for varying levels of endogenous insulin secretion, and is widely used as the indicator of insulin resistance development. Glucose 11-18 insulin Homo sapiens 111-118 16219952-11 2005 The same proportion who had full screening for insulin resistance by oral glucose tolerance tests and fasting serum glucose to insulin ratios had discordant results of these two tests. Glucose 74-81 insulin Homo sapiens 47-54 16219952-13 2005 Early detection of insulin resistance in patients with polycystic ovarian syndrome can be ensured by performing an oral glucose tolerance test combined with measurement of fasting serum glucose to insulin ratio. Glucose 120-127 insulin Homo sapiens 19-26 16219952-13 2005 Early detection of insulin resistance in patients with polycystic ovarian syndrome can be ensured by performing an oral glucose tolerance test combined with measurement of fasting serum glucose to insulin ratio. Glucose 186-193 insulin Homo sapiens 19-26 16278783-7 2005 The plasma glucose-lowering activity of tolbutamide was introduced to account for varying levels of endogenous insulin secretion, and is widely used as the indicator of insulin resistance development. Glucose 11-18 insulin Homo sapiens 169-176 15922648-2 2005 It accounts for >30% of energy expenditure, is the primary tissue of insulin stimulated glucose uptake, disposal, and storage. Glucose 91-98 insulin Homo sapiens 72-79 16278783-9 2005 Increased insulin sensitivity by stevioside administration was further identified using the plasma glucose-lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Glucose 99-106 insulin Homo sapiens 10-17 16278783-9 2005 Increased insulin sensitivity by stevioside administration was further identified using the plasma glucose-lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Glucose 99-106 insulin Homo sapiens 136-143 16091496-1 2005 CONTEXT: Normal glucose homeostasis is maintained despite reductions in insulin sensitivity by increasing insulin secretion. Glucose 16-23 insulin Homo sapiens 106-113 16178991-2 2005 Nateglinide, a d-phenylalanine derivative, restores postprandial early phase insulin secretion in a transient and glucose-sensitive manner without affecting basal insulin levels. Glucose 114-121 insulin Homo sapiens 77-84 16186282-11 2005 Using median splits of indexes of insulin resistance and insulin secretion (insulin-to-glucose ratio), participants with greater insulin resistance had a more adverse CVD risk-factor profile, whereas insulin secretion had little influence on risk factors. Glucose 87-94 insulin Homo sapiens 57-64 16214532-6 2005 Boluses of insulin were given during cardiopulmonary bypass when the glucose level exceeded 15 mmol/L, when the serum potassium level exceeded 6.0 mmol/L, or both. Glucose 69-76 insulin Homo sapiens 11-18 16186282-11 2005 Using median splits of indexes of insulin resistance and insulin secretion (insulin-to-glucose ratio), participants with greater insulin resistance had a more adverse CVD risk-factor profile, whereas insulin secretion had little influence on risk factors. Glucose 87-94 insulin Homo sapiens 57-64 16186290-4 2005 Insulin sensitivity (S(i)), the acute insulin response to glucose (AIRg), and the disposition index (DI; an index of beta-cell function) were determined using the insulin-modified intravenous glucose tolerance test and minimal modeling. Glucose 192-199 insulin Homo sapiens 163-170 15906397-11 2005 The enhancement of PEI on rAAV-mediated insulin gene therapy was further confirmed by glucose challenge and a 10-h fasting blood glucose test. Glucose 86-93 insulin Homo sapiens 40-47 15906397-11 2005 The enhancement of PEI on rAAV-mediated insulin gene therapy was further confirmed by glucose challenge and a 10-h fasting blood glucose test. Glucose 129-136 insulin Homo sapiens 40-47 16194983-0 2005 Insulin sensitivity derived from oral glucose tolerance testing in athletes: disagreement between available indices. Glucose 38-45 insulin Homo sapiens 0-7 16194983-1 2005 The aims of the present study were to determine whether available "fasting" and oral glucose tolerance test-derived insulin sensitivity indices could effectively discriminate between individuals with higher than normal insulin sensitivity, and whether they would all provide similar information in clinical practice. Glucose 85-92 insulin Homo sapiens 116-123 16154442-8 2005 Both groups experienced a similar decrease in insulin-stimulated glucose disposal in response to lipid infusion (approximately 15%; P < .05), which was mainly accounted for by reduced glucose oxidation (approximately 30%; P < .001). Glucose 65-72 insulin Homo sapiens 46-53 16154431-0 2005 Body mass index and waist circumference correlate to the same degree with insulin-mediated glucose uptake. Glucose 91-98 insulin Homo sapiens 74-81 16154431-1 2005 To compare the relationship between insulin-mediated glucose uptake (IMGU) and excess adiposity as determined by measurement of either body mass index (BMI) or waist circumference (WC), IMGU was quantified by determining the steady-state plasma glucose (SSPG) concentration with the insulin suppression test and the relationship between the SSPG concentration and BMI or WC evaluated in a study of 208 healthy individuals (128 women/80 men). Glucose 53-60 insulin Homo sapiens 36-43 16030168-10 2005 Insulin, glulisine, and IGF-I were equipotent in the stimulation of glucose uptake. Glucose 68-75 insulin Homo sapiens 0-7 16154442-8 2005 Both groups experienced a similar decrease in insulin-stimulated glucose disposal in response to lipid infusion (approximately 15%; P < .05), which was mainly accounted for by reduced glucose oxidation (approximately 30%; P < .001). Glucose 187-194 insulin Homo sapiens 46-53 16049004-3 2005 Here we report the PKB-mediated glucose uptake by platelets by agents that do (thrombin) or do not (insulin) induce alpha-granule translocation to the plasma membrane. Glucose 32-39 insulin Homo sapiens 100-107 16316071-3 2005 Simultaneous oral ingestion of ethanol (10 g) significantly enhanced the early increase in plasma insulin concentration at 30 min after ingestion of glucose (100 g) in subjects with normal ALDH2 phenotype, while the increase in early insulin response due to alcohol was slight and not significant in those with atypical ALDH2. Glucose 149-156 insulin Homo sapiens 98-105 16296343-5 2005 By contrast, Ubc9 gene silencing with siRNA caused a marked decrease in the GLUT4 level, whereas overexpression of the catalytically inactive mutant of Ubc9 increased GLUT4 and insulin-stimulated glucose transport to the level comparable to that with wild-type Ubc9. Glucose 196-203 insulin Homo sapiens 177-184 16296343-7 2005 Thus, Ubc9 plays an indispensable role in the expression and maintenance of the insulin-sensitive glucose transport system in adipocytes. Glucose 98-105 insulin Homo sapiens 80-87 16341336-2 2005 Insulin is rarely prescribed despite its being indicated for type 2 diabetic patients with inadequate metabolic control on maximum oral glucose-lowering agent (OGLA) therapy. Glucose 136-143 insulin Homo sapiens 0-7 16358671-3 2005 Indeed, in patients with type 1 or type 2 diabetes mellitus, insulin detemir has a more predictable, protracted and consistent effect, with less intrapatient variability in glycaemic control (particularly fasting plasma glucose levels), compared with NPH (Neutral Protamine Hagedorn) insulin. Glucose 220-227 insulin Homo sapiens 61-68 16255885-0 2005 [The relation between fasting plasma glucose concentrations and insulin resistance]. Glucose 37-44 insulin Homo sapiens 64-71 16255885-3 2005 Insulin resistance of the subjects was measured by using hyperinsulin-euglycemic clamp in which the glucose infusion rate (GIR) was the major index. Glucose 100-107 insulin Homo sapiens 0-7 16353976-3 2005 The in vivo efficacy of insulin gel administered intranasally was assessed by measuring the blood glucose levels and serum insulin levels at specified time intervals in rats and humans. Glucose 98-105 insulin Homo sapiens 24-31 16007182-2 2005 It is also involved in mediating the effects of insulin, such as lipogenesis, glucose uptake and conversion of glucose into fatty acids and cholesterol. Glucose 78-85 insulin Homo sapiens 48-55 16007182-2 2005 It is also involved in mediating the effects of insulin, such as lipogenesis, glucose uptake and conversion of glucose into fatty acids and cholesterol. Glucose 111-118 insulin Homo sapiens 48-55 16182371-5 2005 By this technique, it was found that insulin lost its physiological effects on cells in vitro meanwhile some other anti-diabetic drugs facilitated the cell glucose uptake rates with mechanisms which likely to be different from those of insulin or those that were generally accepted of each drug. Glucose 156-163 insulin Homo sapiens 37-44 16099589-4 2005 However, both 0.2 nM insulin and 200 nM insulin led to a transient increase in accessible cellular insulin content under conditions that glucose did not. Glucose 137-144 insulin Homo sapiens 21-28 16099589-4 2005 However, both 0.2 nM insulin and 200 nM insulin led to a transient increase in accessible cellular insulin content under conditions that glucose did not. Glucose 137-144 insulin Homo sapiens 40-47 16099589-4 2005 However, both 0.2 nM insulin and 200 nM insulin led to a transient increase in accessible cellular insulin content under conditions that glucose did not. Glucose 137-144 insulin Homo sapiens 40-47 16165130-6 2005 Insulin release in response to glucose or tolbutamide was strongly inhibited in Syt 9 deficient islets, whereas exocytosis potentiated by raising cAMP levels, was unaltered. Glucose 31-38 insulin Homo sapiens 0-7 16049004-1 2005 In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. Glucose 96-103 insulin Homo sapiens 3-10 16049004-1 2005 In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. Glucose 96-103 insulin Homo sapiens 31-38 16084832-6 2005 We propose that activation of T-cells with development of insulin receptors in hyperglycemic conditions may serve as a mechanism for control of glucose entry into these cells, thus, protecting them against glucose toxicity. Glucose 144-151 insulin Homo sapiens 58-65 16049004-5 2005 Inhibition of PKB by the pharmacological inhibitor ML-9 decreases thrombin-induced alpha-granule release and thrombin- and insulin-induced glucose uptake. Glucose 139-146 insulin Homo sapiens 123-130 16049004-6 2005 At low glucose (0.1 mm), both agents stimulate glucose uptake by lowering the Km for glucose (thrombin and insulin) and increasing Vmax (thrombin). Glucose 47-54 insulin Homo sapiens 107-114 16049004-6 2005 At low glucose (0.1 mm), both agents stimulate glucose uptake by lowering the Km for glucose (thrombin and insulin) and increasing Vmax (thrombin). Glucose 47-54 insulin Homo sapiens 107-114 16049004-7 2005 At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. Glucose 8-15 insulin Homo sapiens 57-64 16049004-7 2005 At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. Glucose 39-46 insulin Homo sapiens 57-64 16049004-7 2005 At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. Glucose 39-46 insulin Homo sapiens 57-64 16321271-12 2005 CONCLUSION: In newly diagnosed type 2 diabetic patients with short term insulin pump therapy, the use of insulin aspart was more effective and faster with less doses of insulin in acquiring good glucose control compared with humulin R. Glucose 195-202 insulin Homo sapiens 105-112 16168285-6 2005 Insulin sensitivity was assessed from glucose and insulin dynamic profiles during an intravenous glucose tolerance test using the minimal model technique. Glucose 38-45 insulin Homo sapiens 0-7 16168285-6 2005 Insulin sensitivity was assessed from glucose and insulin dynamic profiles during an intravenous glucose tolerance test using the minimal model technique. Glucose 97-104 insulin Homo sapiens 0-7 15935394-6 2005 Our findings, thus strongly suggest, that the increased levels of basal insulin secretion involved in glucose sensing, insulin producing and insulin secreting induced by high levels of FFAs may cause hyperinsulinemia in patients with type 2 diabetes, and thus long-term hyperinsulinemia could desensitize insulin receptors. Glucose 102-109 insulin Homo sapiens 72-79 16157560-4 2005 Furthermore, signaling pathways upon which G alpha(z) impacts are intact in beta-cells, and G alpha(z) activation inhibits both cAMP production and glucose-stimulated insulin secretion in the Ins-1(832/13) beta-cell-derived line. Glucose 148-155 insulin Homo sapiens 167-174 15983036-3 2005 Murine resistin reduced insulin-stimulated glucose uptake, establishing the heart as a resistin target tissue. Glucose 43-50 insulin Homo sapiens 24-31 16157560-5 2005 Inhibition of glucose-stimulated insulin secretion by prostaglandin E (PGE1) is pertussis-toxin insensitive, indicating that other G alpha(i) family members are not involved in this process in this beta-cell line. Glucose 14-21 insulin Homo sapiens 33-40 16157560-6 2005 Indeed, overexpression of a selective deactivator of G alpha(z), the RGS domain of RGSZ1, blocks the inhibitory effect of PGE1 on glucose-stimulated insulin secretion. Glucose 130-137 insulin Homo sapiens 149-156 16157560-7 2005 Finally, the inhibition of glucose-stimulated insulin secretion by PGE1 is substantially blunted by small interfering RNA-mediated knockdown of G alpha(z) expression. Glucose 27-34 insulin Homo sapiens 46-53 16128592-10 2005 Since the hallmark of lipotoxicity is the accumulation of fatty acids and their acyl-CoA metabolites in excess of a cell"s ability to appropriately metabolize them, these results identify a novel mechanism potentially contributing to the insulin resistance, reduced glucose utilization, and maladaptive metabolic alterations underlying the lipotoxic state. Glucose 266-273 insulin Homo sapiens 238-245 16200335-12 2005 This improvement in insulin secretion could be clearly demonstrated when the sums of insulin concentrations after oral glucose tolerance test were compared: 548-/+13 to 345-/+11.8 mIU/l in the rosiglitazone group (37% decrease, p<0.01) and from 552-/+15 to 420-/+12 mIU/l in the metformin group (24% decrease, p<0.01). Glucose 119-126 insulin Homo sapiens 20-27 16155268-4 2005 RESULTS: When assessed by euglycemic-hyperinsulinemic clamp, insulin sensitivity was higher after resistant starch supplementation than after placebo treatment (9.7 and 8.5 x 10(-2) mg glucose x kg(-1) x min(-1) x (mU insulin/L)(-1), respectively; P = 0.03); insulin sensitivity during the meal tolerance test (MTT) was 33% higher (P = 0.05). Glucose 185-192 insulin Homo sapiens 61-68 16155268-4 2005 RESULTS: When assessed by euglycemic-hyperinsulinemic clamp, insulin sensitivity was higher after resistant starch supplementation than after placebo treatment (9.7 and 8.5 x 10(-2) mg glucose x kg(-1) x min(-1) x (mU insulin/L)(-1), respectively; P = 0.03); insulin sensitivity during the meal tolerance test (MTT) was 33% higher (P = 0.05). Glucose 185-192 insulin Homo sapiens 61-68 16122452-3 2005 METHODS: An interdisciplinary team used an insulin protocol to achieve tight glucose control of cardiac surgery patients in the operating room and intensive care unit as part of an effort to reduce sternal wound infections. Glucose 77-84 insulin Homo sapiens 43-50 15975822-1 2005 Fibroin has been shown to enhance insulin-stimulated glucose uptake in 3T3-L1 adipocytes, and the mechanism underlying the fibroin effect focused on phosphatidylinositol 3-kinase (PI 3-K) pathway has been reported. Glucose 53-60 insulin Homo sapiens 34-41 15975822-3 2005 Cultivation of Hirc-B cells in high-glucose medium for 6 days led to an insulin-resistant state in which insulin-stimulated DNA synthesis was blocked completely. Glucose 36-43 insulin Homo sapiens 72-79 15975822-3 2005 Cultivation of Hirc-B cells in high-glucose medium for 6 days led to an insulin-resistant state in which insulin-stimulated DNA synthesis was blocked completely. Glucose 36-43 insulin Homo sapiens 105-112 15886226-0 2005 Initially more rapid small intestinal glucose delivery increases plasma insulin, GIP, and GLP-1 but does not improve overall glycemia in healthy subjects. Glucose 38-45 insulin Homo sapiens 72-79 15886226-4 2005 We have evaluated the hypothesis that increased stimulation of incretin hormones and insulin by a more rapid initial rate of small intestinal glucose delivery would reduce the overall glycemic response to a standardized enteral glucose load. Glucose 142-149 insulin Homo sapiens 85-92 15886226-4 2005 We have evaluated the hypothesis that increased stimulation of incretin hormones and insulin by a more rapid initial rate of small intestinal glucose delivery would reduce the overall glycemic response to a standardized enteral glucose load. Glucose 228-235 insulin Homo sapiens 85-92 15886226-11 2005 We conclude that stimulation of incretin hormone and insulin release by a more rapid initial rate of id glucose delivery does not lead to an overall reduction in glycemia in healthy subjects. Glucose 104-111 insulin Homo sapiens 53-60 16168194-0 2005 The glucose response to an oral fat tolerance test in young men with a paternal history of premature myocardial infarction: possible early indication of insulin resistance. Glucose 4-11 insulin Homo sapiens 153-160 16122452-9 2005 The factor most highly predictive of glucose being well controlled was the protocol with the 110 mg/dL trigger for insulin (p < 0.001). Glucose 37-44 insulin Homo sapiens 115-122 16168194-11 2005 This combination of findings suggests that insulin-stimulated glucose uptake was reduced in the cases. Glucose 62-69 insulin Homo sapiens 43-50 16154097-1 2005 Insulin regulates glucose transport in muscle and fat cells by stimulating the translocation of GLUT4 from intracellular vesicles to the plasma membrane. Glucose 18-25 insulin Homo sapiens 0-7 16117810-13 2005 Those metabolic changes were accompanied by a significant improvement in insulin-mediated glucose uptake (P<0.001), substrate oxidation and degree of inflammation. Glucose 90-97 insulin Homo sapiens 73-80 16172212-1 2005 Compelling evidence from epidemiologic studies indicates that elevated circulating insulin-like growth factor (IGF)-I, insulin resistance, and associated complications, such as elevated fasting plasma insulin, glucose and free fatty acids, glucose intolerance, increased body mass index, and visceral adiposity, are linked with increased risk of colorectal cancer. Glucose 210-217 insulin Homo sapiens 83-90 16172212-1 2005 Compelling evidence from epidemiologic studies indicates that elevated circulating insulin-like growth factor (IGF)-I, insulin resistance, and associated complications, such as elevated fasting plasma insulin, glucose and free fatty acids, glucose intolerance, increased body mass index, and visceral adiposity, are linked with increased risk of colorectal cancer. Glucose 240-247 insulin Homo sapiens 83-90 16187688-5 2005 It enhances glucose tolerance, insulin-stimulated glucose disposal, lipid catabolism, energy expenditure, cholesterol efflux and oxygen consumption. Glucose 50-57 insulin Homo sapiens 31-38 16079624-1 2005 PURPOSE OF REVIEW: In healthy individuals, upregulation of insulin secretion compensates for insulin resistance so that normal glucose tolerance is maintained. Glucose 127-134 insulin Homo sapiens 59-66 16001232-0 2005 Interstitial fluid glucose dynamics during insulin-induced hypoglycaemia. Glucose 19-26 insulin Homo sapiens 43-50 16010522-13 2005 RESULTS: Following oral glucose ingestion, plasma glucose, insulin and C-peptide concentrations increased to higher levels in the women with pGDM than in the control women (p<0.05). Glucose 24-31 insulin Homo sapiens 59-66 16010522-13 2005 RESULTS: Following oral glucose ingestion, plasma glucose, insulin and C-peptide concentrations increased to higher levels in the women with pGDM than in the control women (p<0.05). Glucose 24-31 insulin Homo sapiens 71-80 16003531-9 2005 Insulin sensitivity (the rate of whole-body glucose uptake divided by the steady-state insulin level x 100) was lower among the offspring strongly positive for the urinary protein than among the offspring negative for the protein (11.3 vs 15.8 micromol kg(-1)min(-1)pmol(-1)l(-1), p=0.008). Glucose 44-51 insulin Homo sapiens 0-7 16010522-21 2005 The inverse relationship between insulin resistance and the insulin secretory response to glucose or GIP suggests that beta cell secretory function in response to different stimuli increases adaptively when insulin sensitivity is diminished. Glucose 90-97 insulin Homo sapiens 33-40 16010522-21 2005 The inverse relationship between insulin resistance and the insulin secretory response to glucose or GIP suggests that beta cell secretory function in response to different stimuli increases adaptively when insulin sensitivity is diminished. Glucose 90-97 insulin Homo sapiens 60-67 16010522-21 2005 The inverse relationship between insulin resistance and the insulin secretory response to glucose or GIP suggests that beta cell secretory function in response to different stimuli increases adaptively when insulin sensitivity is diminished. Glucose 90-97 insulin Homo sapiens 60-67 16108848-3 2005 A closely related compound, sulfated lactosylceramide (sulf-lac-cer), is present in the islets during fetal and neonatal life when, as in Type 2 diabetes, insulin is secreted autonomically without the usual first phase response to glucose. Glucose 231-238 insulin Homo sapiens 155-162 16050945-0 2005 Subcutaneous microdialysis before and after an oral glucose tolerance test: a method to determine insulin resistance in the subcutaneous adipose tissue in diabetes mellitus. Glucose 52-59 insulin Homo sapiens 98-105 16123357-12 2005 In conclusion, amino acids impair 1) insulin-mediated suppression of glucose production and 2) insulin-stimulated glucose disposal in skeletal muscle. Glucose 69-76 insulin Homo sapiens 37-44 16123344-10 2005 The cells were shown to contain human C-peptide and release insulin in response to physiological glucose levels. Glucose 97-104 insulin Homo sapiens 60-67 16123473-6 2005 Postprandial glucose excursions after insulin glulisine were lower than after RHI (glucose AUC(0-6h) 641 vs. 801 mg.h(-1).dl(-1), P < 0.05). Glucose 13-20 insulin Homo sapiens 38-45 16123484-1 2005 OBJECTIVE: To assess the impact of the development of high- or low-affinity insulin antibodies (IABs) on postprandial glucose tolerance, duration of insulin action, and clinical safety in patients with type 1 diabetes receiving inhaled insulin (Exubera). Glucose 118-125 insulin Homo sapiens 76-83 16123357-12 2005 In conclusion, amino acids impair 1) insulin-mediated suppression of glucose production and 2) insulin-stimulated glucose disposal in skeletal muscle. Glucose 114-121 insulin Homo sapiens 95-102 16123362-15 2005 We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men. Glucose 61-68 insulin Homo sapiens 42-49 16123362-15 2005 We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men. Glucose 61-68 insulin Homo sapiens 297-304 16123362-15 2005 We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men. Glucose 61-68 insulin Homo sapiens 297-304 16123362-15 2005 We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men. Glucose 61-68 insulin Homo sapiens 297-304 16341288-3 2005 Exenatide mirrors many of the effects of GLP-1, improving glycemic control through a combination of mechanisms, which include glucose-dependent stimulation of insulin secretion, suppression of glucagon secretion, slowing of gastric emptying, reduced appetite and enhanced beta-cell function. Glucose 126-133 insulin Homo sapiens 159-166 16123362-15 2005 We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men. Glucose 459-466 insulin Homo sapiens 42-49 16341288-4 2005 As stimulation of insulin secretion occurs only in the presence of elevated blood glucose concentrations, the risk of hypoglycemia should be greatly reduced with exenatide. Glucose 82-89 insulin Homo sapiens 18-25 16123368-9 2005 In addition, higher acute insulin response to glucose explained lower adiponectin among African-American children. Glucose 46-53 insulin Homo sapiens 26-33 16123371-2 2005 Energy expenditure induces the endothelial NO synthase (eNOS) gene, providing a mechanism for insulin-independent glucose disposal. Glucose 114-121 insulin Homo sapiens 94-101 16389894-1 2005 The therapeutic goal in insulin-treated diabetic patients is to maintain on the long-term a tight glucose control (HbA1, < 6.5-7% or less) through an insulin regimen which "mimic" the physiological insulin profile: a basal insulin secretion to maintain glucose homeostasis and an acute post-prandial secretion in response to meal intake. Glucose 98-105 insulin Homo sapiens 24-31 15947002-0 2005 Reduction of insulin-stimulated glucose uptake in L6 myotubes by the protein kinase inhibitor SB203580 is independent of p38MAPK activity. Glucose 32-39 insulin Homo sapiens 13-20 16389896-9 2005 In patients with type 1 diabetes the combination of insulin detemir with mealtime insulin aspart, a fast-acting insulin analog, provides a smoother and more stable profile with lower post-prandial plasma glucose levels that the combination of NPH insulin with regular human insulin before each meal. Glucose 204-211 insulin Homo sapiens 52-59 16389896-9 2005 In patients with type 1 diabetes the combination of insulin detemir with mealtime insulin aspart, a fast-acting insulin analog, provides a smoother and more stable profile with lower post-prandial plasma glucose levels that the combination of NPH insulin with regular human insulin before each meal. Glucose 204-211 insulin Homo sapiens 82-89 16155260-5 2005 Insulin sensitivity was determined on the basis of the fasting insulin resistance index and with an oral-glucose-tolerance test. Glucose 105-112 insulin Homo sapiens 0-7 15947002-1 2005 Insulin increases glucose uptake through translocation of the glucose transporter GLUT4 to the plasma membrane. Glucose 18-25 insulin Homo sapiens 0-7 15947002-2 2005 We previously showed that insulin activates p38MAPK, and inhibitors of p38MAPKalpha and p38MAPKbeta (e.g. SB203580) reduce insulin-stimulated glucose uptake without affecting GLUT4 translocation. Glucose 142-149 insulin Homo sapiens 26-33 15947002-2 2005 We previously showed that insulin activates p38MAPK, and inhibitors of p38MAPKalpha and p38MAPKbeta (e.g. SB203580) reduce insulin-stimulated glucose uptake without affecting GLUT4 translocation. Glucose 142-149 insulin Homo sapiens 123-130 15947002-5 2005 SB203580 reduced insulin stimulation of glucose uptake in L6 myotubes overexpressing an SB203580-resistant p38alpha (drug-resistant p38alpha) but barely affected phosphorylation of the p38 substrate MAPK-activated protein kinase-2. Glucose 40-47 insulin Homo sapiens 17-24 16191492-6 2005 Subsequent glucose tolerance testing suggested the presence of insulin resistance. Glucose 11-18 insulin Homo sapiens 63-70 16131605-10 2005 Porcine insulin was detected in three patients" sera following glucose stimulation up to 4 years post transplant. Glucose 63-70 insulin Homo sapiens 8-15 15947002-7 2005 Gene silencing via isoform-specific small interfering RNAs reduced expression of p38alpha or p38beta by 60-70% without diminishing insulin-stimulated glucose uptake. Glucose 150-157 insulin Homo sapiens 131-138 15947002-9 2005 Unless low levels of p38MAPK suffice to regulate glucose uptake, these results suggest that the inhibition of insulin-stimulated glucose transport by SB203580 is likely not mediated by p38MAPK. Glucose 129-136 insulin Homo sapiens 110-117 16151974-5 2005 Glucose uptake was strongly induced by insulin stimulation. Glucose 0-7 insulin Homo sapiens 39-46 16151974-9 2005 However, on the functional level insulin-induced glucose uptake remained unchanged by beta (3)-adrenoceptor stimulation. Glucose 49-56 insulin Homo sapiens 33-40 16151977-6 2005 Fractional glucose infusion rate (GIR)-area under curves (AUC) of the GIR curve and maximum GIR were greater for insulin glulisine and insulin lispro versus regular human insulin. Glucose 11-18 insulin Homo sapiens 113-120 16151977-6 2005 Fractional glucose infusion rate (GIR)-area under curves (AUC) of the GIR curve and maximum GIR were greater for insulin glulisine and insulin lispro versus regular human insulin. Glucose 11-18 insulin Homo sapiens 135-142 16151977-6 2005 Fractional glucose infusion rate (GIR)-area under curves (AUC) of the GIR curve and maximum GIR were greater for insulin glulisine and insulin lispro versus regular human insulin. Glucose 11-18 insulin Homo sapiens 135-142 16151977-7 2005 Total glucose disposal was slightly greater with insulin glulisine than with regular human insulin, and was comparable to insulin lispro, although it decreased with increasing insulin resistance (HOMA index) with all insulins. Glucose 6-13 insulin Homo sapiens 49-56 15970567-0 2005 Oxidation by reactive oxygen species (ROS) alters the structure of human insulin and decreases the insulin-dependent D-glucose-C14 utilization by human adipose tissue. Glucose 117-126 insulin Homo sapiens 99-106 16151977-7 2005 Total glucose disposal was slightly greater with insulin glulisine than with regular human insulin, and was comparable to insulin lispro, although it decreased with increasing insulin resistance (HOMA index) with all insulins. Glucose 6-13 insulin Homo sapiens 91-98 16151977-7 2005 Total glucose disposal was slightly greater with insulin glulisine than with regular human insulin, and was comparable to insulin lispro, although it decreased with increasing insulin resistance (HOMA index) with all insulins. Glucose 6-13 insulin Homo sapiens 91-98 16151977-7 2005 Total glucose disposal was slightly greater with insulin glulisine than with regular human insulin, and was comparable to insulin lispro, although it decreased with increasing insulin resistance (HOMA index) with all insulins. Glucose 6-13 insulin Homo sapiens 91-98 16151977-8 2005 Time to 20 % (early glucose disposal) and 80 % (bulk of activity) of total GIR-AUC were shorter for insulin glulisine and insulin lispro versus regular human insulin. Glucose 20-27 insulin Homo sapiens 100-107 16151977-8 2005 Time to 20 % (early glucose disposal) and 80 % (bulk of activity) of total GIR-AUC were shorter for insulin glulisine and insulin lispro versus regular human insulin. Glucose 20-27 insulin Homo sapiens 122-129 16151977-8 2005 Time to 20 % (early glucose disposal) and 80 % (bulk of activity) of total GIR-AUC were shorter for insulin glulisine and insulin lispro versus regular human insulin. Glucose 20-27 insulin Homo sapiens 122-129 15970567-8 2005 The recombinant human insulin oxidized for 5 minutes only increased the glucose oxidation by 25 %. Glucose 72-79 insulin Homo sapiens 22-29 16272767-0 2005 Insulin response to oral glucose loading and coronary artery disease in nondiabetics. Glucose 25-32 insulin Homo sapiens 0-7 16385750-4 2005 Among the central mechanisms mediating the effect of physical activity are (a) increased insulin sensitivity, (b) a non-insulin-dependent glucose uptake, which causes lower insulin release, (c) an improved ratio between HDL and LDL cholesterol because of increased activity of lipoprotein lipase, and d) improved function of other metabolic hormones and enzymes for fat metabolism. Glucose 138-145 insulin Homo sapiens 120-127 15860681-1 2005 Sensitivity of glucose transport to stimulation by insulin has been shown to occur concomitant with activation of the AMP-activated protein kinase (AMPK) in skeletal muscle, suggesting a role of AMPK in regulation of insulin action. Glucose 15-22 insulin Homo sapiens 51-58 15860681-1 2005 Sensitivity of glucose transport to stimulation by insulin has been shown to occur concomitant with activation of the AMP-activated protein kinase (AMPK) in skeletal muscle, suggesting a role of AMPK in regulation of insulin action. Glucose 15-22 insulin Homo sapiens 217-224 15860681-3 2005 The experimental model involved insulin-responsive C2C12 myotubes that exhibit a twofold increase in glucose transport in the presence of insulin. Glucose 101-108 insulin Homo sapiens 32-39 15860681-4 2005 Treatment of myotubes with the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), followed by a 2-h recovery, augmented the ability of insulin to stimulate glucose transport. Glucose 184-191 insulin Homo sapiens 163-170 15860681-5 2005 Similarly, incubation in hyperosmotic medium, another AMPK-activating treatment, acted synergistically with insulin to stimulate glucose transport. Glucose 129-136 insulin Homo sapiens 108-115 15860681-7 2005 In addition, iodotubercidin, a general kinase inhibitor that is effective against AMPK, also prevented the combined effects of insulin and hyperosmotic stress on glucose transport. Glucose 162-169 insulin Homo sapiens 127-134 16817145-8 2005 In a multiple regression analysis adjusting for age and adiposity, in the female group plasma glucose and insulin levels 2-h after glucose load were the best predictors of fasting plasma leptin (r=-0.49, p<.005 and r=0.34, p<.05; respectively). Glucose 131-138 insulin Homo sapiens 106-113 16817145-9 2005 In boys, plasma insulin level 2-h after glucose load was the independent determinant of leptin (r=0.36, p<.05). Glucose 40-47 insulin Homo sapiens 16-23 15956083-7 2005 Insulin increased glucose uptake, but pancreastatin did not antagonize this action. Glucose 18-25 insulin Homo sapiens 0-7 15985479-6 2005 MAIN OUTCOME MEASURES: Insulin sensitivity (IS) was derived from a 2-h 75-g oral glucose tolerance test (IS(OGTT)). Glucose 81-88 insulin Homo sapiens 23-30 16385750-4 2005 Among the central mechanisms mediating the effect of physical activity are (a) increased insulin sensitivity, (b) a non-insulin-dependent glucose uptake, which causes lower insulin release, (c) an improved ratio between HDL and LDL cholesterol because of increased activity of lipoprotein lipase, and d) improved function of other metabolic hormones and enzymes for fat metabolism. Glucose 138-145 insulin Homo sapiens 120-127 16024167-1 2005 The GLUT4 gene transcriptional activity has a profound impact on the insulin-mediated glucose disposal and it is, therefore, important to understand the mechanisms underlying it. Glucose 86-93 insulin Homo sapiens 69-76 16279365-10 2005 CIPA suggests for the first time that the NGF-TrkA pathway may play a role in insulin secretion in response to glucose challenge in humans. Glucose 111-118 insulin Homo sapiens 78-85 16145319-1 2005 OBJECTIVE: Menopause is associated with a decline in insulin response to glucose and with insulin resistance. Glucose 73-80 insulin Homo sapiens 53-60 16208303-3 2005 Insulin resistance (IR) could occur with any of the effects of insulin, even though it usually refers to its ability to stimulate glucose uptake in insulin-sensitive peripheral tissues such as fat and muscle. Glucose 130-137 insulin Homo sapiens 0-7 16208303-3 2005 Insulin resistance (IR) could occur with any of the effects of insulin, even though it usually refers to its ability to stimulate glucose uptake in insulin-sensitive peripheral tissues such as fat and muscle. Glucose 130-137 insulin Homo sapiens 63-70 16208303-3 2005 Insulin resistance (IR) could occur with any of the effects of insulin, even though it usually refers to its ability to stimulate glucose uptake in insulin-sensitive peripheral tissues such as fat and muscle. Glucose 130-137 insulin Homo sapiens 148-155 16392197-2 2005 Glucose posprandial determinations two hours after food intake is advisable in patients that need insulin administration, which avoids determinations four times a day. Glucose 0-7 insulin Homo sapiens 98-105 16392197-4 2005 The combination of ultra-rapid acting insulin associate to ultra-slow acting insulin for application as a unique dose per day has been successfully used, but it is still necessary to determine the best diet for an adequate control of glucose. Glucose 234-241 insulin Homo sapiens 38-45 16392197-4 2005 The combination of ultra-rapid acting insulin associate to ultra-slow acting insulin for application as a unique dose per day has been successfully used, but it is still necessary to determine the best diet for an adequate control of glucose. Glucose 234-241 insulin Homo sapiens 77-84 16395988-9 2005 Patients in the insulin glargine plus OAD group controlled their blood glucose level at endpoint with a median of 60 test strips per month and those in the conventional insulin therapy group with a median of 80 strips per month (p = 0.000000739). Glucose 71-78 insulin Homo sapiens 16-23 15955810-1 2005 Insulin increases glucose uptake into muscle via glucose transporter-4 (GLUT4) translocation to the cell membrane, but the regulated events in GLUT4 traffic are unknown. Glucose 18-25 insulin Homo sapiens 0-7 16086844-0 2005 Endothelial cell injury by high glucose and heparanase is prevented by insulin, heparin and basic fibroblast growth factor. Glucose 32-39 insulin Homo sapiens 71-78 16086844-11 2005 Insulin and/or heparin and/or bFGF prevented these changes and thus protected cells from injury by high glucose or heparinase I. Glucose 104-111 insulin Homo sapiens 0-7 16086844-13 2005 CONCLUSION: Endothelial cells injured by high glucose or heparinase I are protected by a combination of insulin, heparin and bFGF, although protection by heparin and/or bFGF was variable. Glucose 46-53 insulin Homo sapiens 104-111 15955806-1 2005 The mechanisms involved in glucose regulation of insulin secretion by ATP-sensitive (K(ATP)) and calcium-activated (K(CA)) potassium channels have been extensively studied, but less is known about the role of voltage-gated (K(V)) potassium channels in pancreatic beta-cells. Glucose 27-34 insulin Homo sapiens 49-56 16026421-6 2005 These new findings are integrated into the proposal that, in its "evolutionary adaptive" role to spare glucose for rapid rebuilding of the fat stores, suppressed thermogenesis in skeletal muscle - via inhibition of substrate cycling between de novo lipogenesis and lipid oxidation - confers to the phase of weight recovery/catch-up growth its high sensitivity towards the development of insulin resistance and hyperinsulinaemia, and hence towards diseases that are clustered around the insulin resistance syndrome. Glucose 103-110 insulin Homo sapiens 387-394 15769794-1 2005 Insulin"s action to stimulate glucose utilization is determined by the insulin concentration in interstitial fluid (ISF) of insulin-sensitive tissues. Glucose 30-37 insulin Homo sapiens 0-7 15769794-1 2005 Insulin"s action to stimulate glucose utilization is determined by the insulin concentration in interstitial fluid (ISF) of insulin-sensitive tissues. Glucose 30-37 insulin Homo sapiens 71-78 15769794-1 2005 Insulin"s action to stimulate glucose utilization is determined by the insulin concentration in interstitial fluid (ISF) of insulin-sensitive tissues. Glucose 30-37 insulin Homo sapiens 124-131 16014355-1 2005 The prevalent view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by the interplay of the glucose-lowering action of insulin and the glucose-raising action of glucagon. Glucose 53-60 insulin Homo sapiens 171-178 16014355-6 2005 The alternative view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by insulin alone, specifically regulated increments and decrements in insulin, and the resulting decrements and increments in endogenous glucose production, respectively, and glucagon becomes relevant only when glucose levels drift below the physiological range. Glucose 259-266 insulin Homo sapiens 125-132 16014979-4 2005 Several studies have reported the generation of insulin-secreting cells from embryonic and adult stem cells that normalized blood glucose values when transplanted into diabetic animal models. Glucose 130-137 insulin Homo sapiens 48-55 16054467-2 2005 For this purpose, insulin resistance was quantified by determining the steady-state plasma glucose concentration during the insulin suppression test in 449 apparently healthy patients. Glucose 91-98 insulin Homo sapiens 18-25 16087979-1 2005 BACKGROUND: Obesity is associated with insulin resistance of glucose and lipid metabolism. Glucose 61-68 insulin Homo sapiens 39-46 16087979-9 2005 CONCLUSION: Obese women show a blunted protein anabolic response to hyperinsulinemia that is consistent with resistance to the action of insulin on protein concurrent with that on glucose and lipid metabolism. Glucose 180-187 insulin Homo sapiens 73-80 16039195-8 2005 The average glucose uptake in the insulin group was 7.1 g/kg in 24 hours (28 kcal.kg(-1).day(-1)). Glucose 12-19 insulin Homo sapiens 34-41 16039195-9 2005 CONCLUSIONS: The high-dose insulin treatment was associated with lower blood glucose levels, better preserved myocardial contractile function, and less need for inotropic support, and hence led to lower lactate levels postoperatively. Glucose 77-84 insulin Homo sapiens 27-34 15963471-1 2005 Thiazolidinediones are a new class of anti-diabetic agents which increase insulin sensitivity by binding to the peroxisome proliferator-activated receptor gamma (PPAR(gamma)) and stimulating the expression of insulin-responsive genes involved in glucose and lipid metabolism. Glucose 246-253 insulin Homo sapiens 74-81 15612881-5 2005 Mono-DHC-insulin maintained the glucose-lowering effect as strongly as native insulin, showed a significantly slower disappearance due to an increase of its receptor-binding potency and retained approx. Glucose 32-39 insulin Homo sapiens 9-16 16079488-6 2005 Significant insulin sensitizing activity was observed in 3T3-L1 adipocytes which were given 50 microM berberine plus 0.2 nM insulin to reach a glucose uptake level increased by 10 nM of insulin alone. Glucose 143-150 insulin Homo sapiens 12-19 16079488-6 2005 Significant insulin sensitizing activity was observed in 3T3-L1 adipocytes which were given 50 microM berberine plus 0.2 nM insulin to reach a glucose uptake level increased by 10 nM of insulin alone. Glucose 143-150 insulin Homo sapiens 124-131 16079488-6 2005 Significant insulin sensitizing activity was observed in 3T3-L1 adipocytes which were given 50 microM berberine plus 0.2 nM insulin to reach a glucose uptake level increased by 10 nM of insulin alone. Glucose 143-150 insulin Homo sapiens 124-131 16079488-8 2005 Berberine also increased glucose-stimulated insulin secretion and proliferation in Min6 cells via an enhanced insulin/insulin-like growth factor-1 signaling cascade. Glucose 25-32 insulin Homo sapiens 44-51 16079488-8 2005 Berberine also increased glucose-stimulated insulin secretion and proliferation in Min6 cells via an enhanced insulin/insulin-like growth factor-1 signaling cascade. Glucose 25-32 insulin Homo sapiens 110-117 16079488-8 2005 Berberine also increased glucose-stimulated insulin secretion and proliferation in Min6 cells via an enhanced insulin/insulin-like growth factor-1 signaling cascade. Glucose 25-32 insulin Homo sapiens 110-117 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 18-25 insulin Homo sapiens 0-7 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 18-25 insulin Homo sapiens 71-78 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 18-25 insulin Homo sapiens 140-147 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 0-7 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 71-78 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 0-7 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 71-78 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 0-7 16120192-4 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, the product from areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 71-78 16120192-11 2005 An increase in insulin sensitivity following the administration of this herb was further identified using the plasma glucose-lowering action of exogenous insulin in streptozotocin (STZ)-diabetic rats. Glucose 117-124 insulin Homo sapiens 15-22 16120192-11 2005 An increase in insulin sensitivity following the administration of this herb was further identified using the plasma glucose-lowering action of exogenous insulin in streptozotocin (STZ)-diabetic rats. Glucose 117-124 insulin Homo sapiens 154-161 16199240-12 2005 CONCLUSIONS: Premixed insulin analogues have a more physiologic time-action profile, can be administered closer to mealtime, and produce greater reductions in the magnitude of postprandial glucose excursions than human insulin 70/30. Glucose 189-196 insulin Homo sapiens 22-29 15990590-2 2005 Insulin resistance is thought to be an underlying feature of the metabolic syndrome and in the last few years efforts have been performed to assess the effects of ectopic fat accumulation on whole-body glucose metabolism and on the pathogenesis of insulin resistance. Glucose 202-209 insulin Homo sapiens 0-7 16015105-5 2005 Controlling glucose concentrations with insulin has been shown to also improve protein balance and fat metabolism. Glucose 12-19 insulin Homo sapiens 40-47 18220598-3 2005 The "glucose homeostasis" model is described by insulin sensitivity, glucose effectiveness, acute insulin response to glucose, and disposition index (DI). Glucose 5-12 insulin Homo sapiens 48-55 18220598-3 2005 The "glucose homeostasis" model is described by insulin sensitivity, glucose effectiveness, acute insulin response to glucose, and disposition index (DI). Glucose 5-12 insulin Homo sapiens 98-105 15988578-9 2005 Additionally, surgical resection of the implants, in which the insulin secretion was immunologically confirmed after transplantation, diminished the glucose-lowering effect, suggesting that in vivo expression could be eliminated if necessary. Glucose 149-156 insulin Homo sapiens 63-70 16043735-7 2005 Insulin secretion (postmeal suprabasal area under the 0- to 30-min C-peptide curve divided by the 30-min increase in glucose) was increased in the VM group but was reduced in the PM group (difference +0.011 +/- 0.03 pmol/l 30 min/mmol/l, P = 0.018; baseline 0.036 +/- 0.02). Glucose 117-124 insulin Homo sapiens 0-7 16046301-1 2005 Insulin resistance is predominantly characterized by decreased insulin-stimulated glucose uptake into skeletal muscle. Glucose 82-89 insulin Homo sapiens 0-7 16046301-1 2005 Insulin resistance is predominantly characterized by decreased insulin-stimulated glucose uptake into skeletal muscle. Glucose 82-89 insulin Homo sapiens 63-70 16046301-3 2005 We found a highly significant inverse correlation between in vivo insulin sensitivity (as measured by the glucose infusion rate) and increased protein expression of p85/55/50, protein kinase C (PKC)-theta activity, levels of pSer307 insulin receptor substrate (IRS)-1 and p-Jun NH2-terminal kinase (JNK)-1, and myosin heavy chain IIx fibers. Glucose 106-113 insulin Homo sapiens 66-73 16046305-4 2005 Insulin secretion was reconstructed from C-peptide levels by deconvolution and related to concurrent glucose levels through a mathematical model incorporating key features of beta-cell function: rate sensitivity, beta-cell glucose sensitivity, and potentiation. Glucose 101-108 insulin Homo sapiens 0-7 16046305-4 2005 Insulin secretion was reconstructed from C-peptide levels by deconvolution and related to concurrent glucose levels through a mathematical model incorporating key features of beta-cell function: rate sensitivity, beta-cell glucose sensitivity, and potentiation. Glucose 223-230 insulin Homo sapiens 0-7 16120042-1 2005 The "incretin effect" describes the enhanced insulin response from orally ingested glucose compared with intravenous glucose leading to identical postprandial plasma glucose excursions. Glucose 83-90 insulin Homo sapiens 45-52 16020439-3 2005 An inability of insulin to stimulate glucose uptake, i.e., insulin resistance, appears to be a common link between diabetes and obesity. Glucose 37-44 insulin Homo sapiens 16-23 15886245-4 2005 RESULTS: Vildagliptin significantly increased the insulin secretory rate at 7 mmol/liter glucose (secretory tone), calculated from the dose response; the difference in least squares mean (deltaLSM) was 101 +/- 51 pmol.min(-1).m(-2) (P = 0.002). Glucose 89-96 insulin Homo sapiens 50-57 15899957-6 2005 Insulin secretion in response to changes in glucose concentration ("beta-cell responsiveness") during the meal test was similar in LBW and NBW but inappropriate in LBW relative to insulin sensitivity. Glucose 44-51 insulin Homo sapiens 0-7 16075050-5 2005 The reduction in the mediators of inflammation may thus be responsible for the impressive improvement in clinical outcomes following insulin therapy, and the results suggest a new paradigm in which glucose and insulin are related not only through their metabolic actions but also through their opposite effects on inflammatory mechanisms. Glucose 198-205 insulin Homo sapiens 133-140 16079261-1 2005 Glucagon-like peptide-1 (GLP-1) is a peptide hormone secreted from the enteroendocrine L-cells of the gut and which acts primarily to potentiate the effects of glucose on insulin secretion from pancreatic beta-cells. Glucose 160-167 insulin Homo sapiens 171-178 23570224-2 2005 SUMMARY: Type 2 diabetes represents the failure of the pancreas to maintain adequate insulin secretion in response to insulin resistance, which causes impedance to glucose membrane transport. Glucose 164-171 insulin Homo sapiens 85-92 16200849-6 2005 The injection of 0.05 U/kg insulin induced a significantly (p < 0.0001) lower percent decrease of serum glucose than 0.1 U/kg. Glucose 107-114 insulin Homo sapiens 27-34 15998426-8 2005 In addition, a significant decrease of steady-state plasma glucose in insulin suppression test was noted in responders (13.6+/-1.8-11.7+/-1.2 mmol/l, P=0.03), but not in non-responders (12.3+/-1.1-11.0+/-1.0 mmol/l, P=0.20), after IFN-alpha therapy. Glucose 59-66 insulin Homo sapiens 70-77 15774496-9 2005 Formation of small insulin-responsive Glut4-containing vesicles and insulin-stimulated glucose uptake in these cells were markedly impaired. Glucose 87-94 insulin Homo sapiens 68-75 16103515-8 2005 The administration of glucose caused an increase in the circulating concentration of insulin (P < 0.05) resulting in a lower glucagon/insulin quotient than in the control group (P < 0.05). Glucose 22-29 insulin Homo sapiens 85-92 16103515-8 2005 The administration of glucose caused an increase in the circulating concentration of insulin (P < 0.05) resulting in a lower glucagon/insulin quotient than in the control group (P < 0.05). Glucose 22-29 insulin Homo sapiens 137-144 16103523-3 2005 Approximately 90% of diabetes cases are the non-insulin-dependent phenotype, which is characterized by a progressive deterioration in insulin-mediated glucose disposal, particularly by peripheral tissues. Glucose 151-158 insulin Homo sapiens 48-55 16103523-3 2005 Approximately 90% of diabetes cases are the non-insulin-dependent phenotype, which is characterized by a progressive deterioration in insulin-mediated glucose disposal, particularly by peripheral tissues. Glucose 151-158 insulin Homo sapiens 134-141 16055589-1 2005 OBJECTIVE: Our purpose was to determine glucose tolerance in pregnant women with cystic fibrosis (CF) and to relate glucose tolerance to insulin sensitivity, hepatic glucose production, and protein turnover. Glucose 116-123 insulin Homo sapiens 137-144 16055589-1 2005 OBJECTIVE: Our purpose was to determine glucose tolerance in pregnant women with cystic fibrosis (CF) and to relate glucose tolerance to insulin sensitivity, hepatic glucose production, and protein turnover. Glucose 116-123 insulin Homo sapiens 137-144 16014355-1 2005 The prevalent view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by the interplay of the glucose-lowering action of insulin and the glucose-raising action of glucagon. Glucose 144-151 insulin Homo sapiens 171-178 16014355-1 2005 The prevalent view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by the interplay of the glucose-lowering action of insulin and the glucose-raising action of glucagon. Glucose 144-151 insulin Homo sapiens 171-178 16014355-6 2005 The alternative view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by insulin alone, specifically regulated increments and decrements in insulin, and the resulting decrements and increments in endogenous glucose production, respectively, and glucagon becomes relevant only when glucose levels drift below the physiological range. Glucose 55-62 insulin Homo sapiens 125-132 16014355-6 2005 The alternative view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by insulin alone, specifically regulated increments and decrements in insulin, and the resulting decrements and increments in endogenous glucose production, respectively, and glucagon becomes relevant only when glucose levels drift below the physiological range. Glucose 55-62 insulin Homo sapiens 192-199 16014355-6 2005 The alternative view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by insulin alone, specifically regulated increments and decrements in insulin, and the resulting decrements and increments in endogenous glucose production, respectively, and glucagon becomes relevant only when glucose levels drift below the physiological range. Glucose 259-266 insulin Homo sapiens 125-132 15878854-1 2005 Glucose stimulates insulin secretion from pancreatic beta cells by inducing the recruitment and fusion of insulin vesicles to the plasma membrane. Glucose 0-7 insulin Homo sapiens 19-26 16024515-1 2005 Insulin stimulation of glucose uptake into skeletal muscle and adipose tissues is achieved by accelerating glucose transporter GLUT4 exocytosis from intracellular compartments to the plasma membrane and minimally reducing its endocytosis. Glucose 23-30 insulin Homo sapiens 0-7 16160802-4 2005 In the women with diabetes, strict adjustments of fasting glucose levels to 90 mg/dl and 130 mg/dl postprandially were achieved with insulin administration. Glucose 58-65 insulin Homo sapiens 133-140 21162204-5 2005 High insulin and high glucose and NE group showed a further increase compared with high glucose and NE group. Glucose 88-95 insulin Homo sapiens 5-12 16006430-6 2005 Amino acids and glucose were given with insulin to prevent hypoaminoacidemia and hypoglycemia. Glucose 16-23 insulin Homo sapiens 40-47 16049616-6 2005 She was treated with intravenous calcium chloride and insulin with 50% dextrose. Glucose 71-79 insulin Homo sapiens 54-61 15878854-1 2005 Glucose stimulates insulin secretion from pancreatic beta cells by inducing the recruitment and fusion of insulin vesicles to the plasma membrane. Glucose 0-7 insulin Homo sapiens 106-113 15878854-3 2005 Here, we examined the role of the SEC6-SEC8 (exocyst) complex, implicated in trafficking of secretory vesicles to fusion sites in the plasma membrane in yeast and in regulating glucose-stimulated insulin secretion from pancreatic MIN6 beta cells. Glucose 177-184 insulin Homo sapiens 196-203 16002803-13 2005 The increased insulin response stimulates plasma glucose disposal and reduces postprandial glucose concentrations. Glucose 49-56 insulin Homo sapiens 14-21 16002803-13 2005 The increased insulin response stimulates plasma glucose disposal and reduces postprandial glucose concentrations. Glucose 91-98 insulin Homo sapiens 14-21 16002813-8 2005 Insulin concentrations were higher in PI-treated than in NNRTI-treated patients [22.6 (13.1-29.8) and 11.8 (7.1-19.1) microU/mL; P = 0.01] and increased in both groups in response to each meal, whereas glucose concentrations increased only after breakfast. Glucose 202-209 insulin Homo sapiens 0-7 15741239-8 2005 Interestingly, these five amino acids potently increased basal and insulin-stimulated leptin secretion in the presence of glucose. Glucose 122-129 insulin Homo sapiens 67-74 15998257-1 2005 Oxidants, including hydrogen peroxide (H2O2), have been recognized for years to mimic insulin action on glucose transport in adipose cells. Glucose 104-111 insulin Homo sapiens 86-93 15998258-3 2005 It is suggested that alpha-lipoic acid through its prooxidant properties acutely stimulates the insulin-signaling cascade, thereby increasing glucose uptake in muscle and fat cells. Glucose 142-149 insulin Homo sapiens 96-103 16212119-5 2005 Insulin resistance was assessed using the homeostasis model assessment for insulin resistance formula derived from fasting insulin and glucose levels. Glucose 135-142 insulin Homo sapiens 0-7 15939066-1 2005 We sought to evaluate the effect of the new definition of impaired fasting glucose (IFG = fasting glucose concentration 100-125 mg/dL among people without diabetes) on the ability to identify insulin resistance, as well as the prevalence of the metabolic syndrome in apparently healthy individuals. Glucose 75-82 insulin Homo sapiens 192-199 15834002-6 2005 We also demonstrate that islets can synchronize by mutually entraining each other by their effects on a simple model "liver," which responds to the level of insulin secretion by adjusting the blood glucose concentration in an appropriate way. Glucose 198-205 insulin Homo sapiens 157-164 16029032-3 2005 HSA-Fmoc-insulin is water-soluble and, upon incubation in aqueous buffers reflecting normal human serum conditions, slowly, spontaneously, and homogeneously hydrolyzes to release unmodified insulin with a t 1/2 of 25 +/- 2 h. A single subcutaneous or intraperitoneal administration of HSA-Fmoc-insulin to diabetic rodents lowers circulating glucose levels for about 4 times longer than an equipotent dose of Zn2+-free insulin. Glucose 341-348 insulin Homo sapiens 9-16 16029032-4 2005 Following subcutaneous administration, onset of the glucose-lowering effect is delayed 0.5-1 h and persists for 12 h. Thus, we present a prototype insulin formulation possessing three desirable parameters: high aqueous solubility, delayed action following subcutaneous administration, and prolonged therapeutic effect. Glucose 52-59 insulin Homo sapiens 147-154 15930959-2 2005 Alterations in the body"s sensitivity to insulin cause a series of metabolic abnormalities representing essentially the metabolic syndrome (i.e. high fasting plasma triglyceride and glucose and low HDL-cholesterol concentrations, hypertension, abdominal obesity) and type 2 diabetes. Glucose 182-189 insulin Homo sapiens 41-48 15930970-7 2005 The increased endogenous glucose production caused by enhanced gluconeogenesis and glycogenolysis, reduced insulin sensitivity, mainly caused by acquired defects of glucose transport and phosphorylation, and the impairment of insulin secretion all together contribute to maintain a chronic status of hyperglycaemia. Glucose 25-32 insulin Homo sapiens 107-114 15930971-4 2005 This is reflected in the modulation of lipolysis/lipogenesis, local insulin sensitivity of glucose and fatty acid uptake, the expression levels of several adipokines in adipose tissue, and the modulation of fat cell number. Glucose 91-98 insulin Homo sapiens 68-75 15930973-2 2005 In addition to the inhibitory effects of insulin on endogenous glucose production, rising glucose levels have important direct effects on glucose homeostasis. Glucose 63-70 insulin Homo sapiens 41-48 15930974-3 2005 RECENT FINDINGS: Increased plasma amino acid availability in both animals and humans has been shown to cause enhanced translation initiation and protein synthesis and the inhibition of insulin-stimulated glucose transport in skeletal muscle. Glucose 204-211 insulin Homo sapiens 185-192 15992544-4 2005 Forced expression of Glut4 prior to induction of sortilin leads to rapid degradation of the transporter, whereas overexpression of sortilin increases formation of GSVs and stimulates insulin-regulated glucose uptake. Glucose 201-208 insulin Homo sapiens 183-190 16136823-7 2005 In contrast, insulin treatment in diabetic patients may also lead to a hypoglycemia, the sudden drop in blood glucose, at any moment. Glucose 110-117 insulin Homo sapiens 13-20 15724236-5 2005 First-phase insulin secretion was assessed by an intravenous glucose tolerance test (300 mg kg(-1) body weight) and insulin sensitivity by a hyperinsulinaemic euglycaemic clamp (40 mU m(-2) min(-1)). Glucose 61-68 insulin Homo sapiens 12-19 15955117-6 2005 MODY2 is characterized by glucose sensing defects, leading to an increase in insulin secretion threshold. Glucose 26-33 insulin Homo sapiens 77-84 15955381-2 2005 In this study, to establish some index to select suitable therapy for each patient, we evaluated insulin sensitivity and insulin secretion with euglycemic hyperinsulinemic clamp and hyperglycemic clamp tests, respectively, and found that specific GIR index (GIRxIRI (90)) could be a useful marker to select suitable therapy for each type 2 diabetic patient (GIR: glucose infusion rate in euglycemic hyperinsulinemic clamp test; IRI (90): plasma insulin level 90 min after starting the hyperglycemic clamp test). Glucose 363-370 insulin Homo sapiens 97-104 15975113-1 2005 AIMS: This study aimed to investigate if the previously observed association between the GLUT10 Ala206Thr polymorphism and variation in fasting and oral glucose-induced serum insulin concentrations could be replicated in a large-scale population-based cohort of Danish whites. Glucose 153-160 insulin Homo sapiens 175-182 15983190-1 2005 The quantitative insulin-sensitivity check index (QUICKI) has an excellent linear correlation with the glucose clamp index of insulin sensitivity (SI(Clamp)) that is better than that of many other surrogate indexes. Glucose 103-110 insulin Homo sapiens 17-24 15983190-1 2005 The quantitative insulin-sensitivity check index (QUICKI) has an excellent linear correlation with the glucose clamp index of insulin sensitivity (SI(Clamp)) that is better than that of many other surrogate indexes. Glucose 103-110 insulin Homo sapiens 126-133 15983215-3 2005 In pancreatic beta-cells, glucose acutely raised the NADPH-to-NADP+ ratio and stimulated insulin release in parallel. Glucose 26-33 insulin Homo sapiens 89-96 15983224-1 2005 Glucagon-like peptide 1 (GLP-1) has been proposed to act as an incretin hormone due to its ability to enhance glucose-stimulated insulin secretion. Glucose 110-117 insulin Homo sapiens 129-136 15983232-0 2005 Delayed transcapillary delivery of insulin to muscle interstitial fluid after oral glucose load in obese subjects. Glucose 83-90 insulin Homo sapiens 35-42 16193096-6 2005 Insulin glulisine effectively controls postprandial glucose excursions in both type 1 and type 2 diabetic patients without increasing the risk of hypoglycemia. Glucose 52-59 insulin Homo sapiens 0-7 16193096-7 2005 One unit of insulin glulisine has the same glucose-lowering effect as one unit of regular human insulin. Glucose 43-50 insulin Homo sapiens 12-19 15856295-7 2005 The fasting insulin and triglyceride levels strongly predicted the 2 h glucose level during the OGTT ( P < 0.05). Glucose 71-78 insulin Homo sapiens 12-19 16034720-6 2005 Furthermore, aldosterone dose-dependently impaired insulin-induced glucose uptake by about 25% (p < 0.01). Glucose 67-74 insulin Homo sapiens 51-58 16440850-9 2005 However, the serum insulin level 0.5 h after the post-asana oral 75 g-glucose challenge was higher (P<0.05) in Set IV than the 0.5 h postprandial insulin level in the pre-study OGTT; the same trend was observed in other sets as well although statistically not significant. Glucose 70-77 insulin Homo sapiens 19-26 16036906-9 2005 Further research is needed because full elucidation of an insulin-independent signal leading to glucose transport would be a promising pharmacological target for the treatment of Type 2 diabetes. Glucose 96-103 insulin Homo sapiens 58-65 15827099-10 2005 Conversely, octreotide produced an additional decrease in fasting (P = 0.018) and glucose-stimulated (P = 0.038) insulin levels, an increase in IGFBP-2 (P = 0.042) and IGFBP-3 (P = 0.047), and an improvement in hirsutism (P = 0.004). Glucose 82-89 insulin Homo sapiens 113-120 15855254-7 2005 Insulin sensitivity was estimated from a 75-g oral glucose tolerance test. Glucose 51-58 insulin Homo sapiens 0-7 16079210-4 2005 Metabolic Insulin Sensitivity Index (S(I)) was determined from a frequently sampled insulin-assisted intravenous glucose tolerance test. Glucose 113-120 insulin Homo sapiens 10-17 16079210-4 2005 Metabolic Insulin Sensitivity Index (S(I)) was determined from a frequently sampled insulin-assisted intravenous glucose tolerance test. Glucose 113-120 insulin Homo sapiens 84-91 15834118-6 2005 Also, adiponectin increased insulin"s ability to maximally stimulate glucose uptake by 78% through increased glucose transporter 4 (GLUT4) gene expression and increased GLUT4 recruitment to the plasma membrane. Glucose 69-76 insulin Homo sapiens 28-35 15979544-1 2005 OBJECTIVE: To test the hypothesis that gravidas who have an abnormal response to glucose loading have dysfunctional adipose tissue cells that produce more insulin resistance-inducing and proinflammatory adipokines but less insulin-sensitizing adipokines. Glucose 81-88 insulin Homo sapiens 155-162 15979544-1 2005 OBJECTIVE: To test the hypothesis that gravidas who have an abnormal response to glucose loading have dysfunctional adipose tissue cells that produce more insulin resistance-inducing and proinflammatory adipokines but less insulin-sensitizing adipokines. Glucose 81-88 insulin Homo sapiens 223-230 16255433-1 2005 Hypoglycaemia (blood glucose level below 3.8 mmol l(-1)) is the most common complication in the treatment of diabetes with insulin and can cause a number of problems. Glucose 21-28 insulin Homo sapiens 123-130 15988698-0 2005 Pharmacological inhibition of p38 MAP kinase results in improved glucose uptake in insulin-resistant 3T3-L1 adipocytes. Glucose 65-72 insulin Homo sapiens 83-90 15988698-4 2005 Treatment with the specific p38 inhibitor, A304000, during the development of insulin resistance increased basal glucose uptake as well as glucose uptake in response to a subsequent insulin stimulation. Glucose 113-120 insulin Homo sapiens 78-85 15988698-4 2005 Treatment with the specific p38 inhibitor, A304000, during the development of insulin resistance increased basal glucose uptake as well as glucose uptake in response to a subsequent insulin stimulation. Glucose 139-146 insulin Homo sapiens 78-85 15988698-7 2005 Rapamycin, an inhibitor or mTOR, could partially improve insulin-stimulated glucose uptake through maintaining IRS-1 protein levels. Glucose 76-83 insulin Homo sapiens 57-64 15988700-8 2005 The Ala12 allele was also significantly associated with a decreased risk of incident insulin resistance syndrome in each race (OR = 0.44, P = .04 in African Americans; OR = 0.61, P = .01 in whites) and lower mean 15-year levels of fasting insulin ( P = .02), glucose ( P = .02), and homeostasis model assessment ( P = .01) in African Americans but not in whites. Glucose 259-266 insulin Homo sapiens 85-92 15988703-13 2005 CONCLUSIONS: Insulin administered via the buccal spray formulation is as effective as the subcutaneous route in lowering blood glucose levels. Glucose 127-134 insulin Homo sapiens 13-20 15988708-2 2005 The purpose of the present study was to determine the mechanism by which improvements in glucose tolerance occur in obese African Americans with insulin resistance and abnormal glucose tolerance. Glucose 89-96 insulin Homo sapiens 145-152 15988708-8 2005 CONCLUSIONS: These results suggest that the improvements in glucose tolerance with a modest lifestyle intervention were attributable to an improvement in insulin action, and provide evidence that despite persistent obesity (body mass index, 34.7 +/- 2.4 kg/m 2 ), long-term benefits can be achieved with relatively small weight loss in obese African Americans. Glucose 60-67 insulin Homo sapiens 154-161 15988709-1 2005 OBJECTIVE: This study was undertaken to further analyze the response of the cardiovascular autonomic nervous system (ANS) to changes in plasma insulin concentration induced by an oral glucose load. Glucose 184-191 insulin Homo sapiens 143-150 16093575-5 2005 RESULTS: Obese subjects were insulin resistant (decreased glucose infusion rate (GIR) during euglycaemic hyperinsulinaemic clamp) and had higher plasma levels of hsCRP, IL-6, leptin, tPA, and PAI-1 compared with lean subjects. Glucose 58-65 insulin Homo sapiens 29-36 15995020-5 2005 Insulin resistance was assessed using the insulin/glucose ratio (I/G ratio) and homeostasis model assessment (HOMA). Glucose 50-57 insulin Homo sapiens 0-7 17491680-1 2005 Orally ingested glucose leads to a greater insulin response compared to intravenously administered glucose leading to identical postprandial plasma glucose excursions, a phenomenon referred to as the "incretin effect". Glucose 16-23 insulin Homo sapiens 43-50 16444867-9 2005 Inhibition of NOS reduces the microvascular delivery of nutrients and blunts insulin-stimulated glucose uptake in skeletal muscle. Glucose 96-103 insulin Homo sapiens 77-84 15894466-1 2005 In myotubes established from patients with type 2 diabetes (T2D), lipid oxidation and insulin-mediated glucose oxidation are reduced, whereas in myotubes from obese non-diabetic subjects, exposure to palmitate impairs insulin-mediated glucose oxidation. Glucose 103-110 insulin Homo sapiens 86-93 15894466-1 2005 In myotubes established from patients with type 2 diabetes (T2D), lipid oxidation and insulin-mediated glucose oxidation are reduced, whereas in myotubes from obese non-diabetic subjects, exposure to palmitate impairs insulin-mediated glucose oxidation. Glucose 235-242 insulin Homo sapiens 218-225 16000870-1 2005 We investigated glucose uptake and the translocation of Akt and caveolin-3 in response to insulin in H9c2 cardiomyoblasts exposed to an experimental insulin resistance condition of 100 nM insulin in a 25 mM glucose containing media for 24 h. The cells under the insulin resistance condition exhibited a decrease in insulin-stimulated 2-deoxy[(3)H]glucose uptake as compared to control cells grown in 5 mM glucose media. Glucose 16-23 insulin Homo sapiens 90-97 16000870-7 2005 We conclude that the insulin resistance condition induced the retardation of their translocation to caveolae and in turn caused an attenuation in insulin signaling, namely activation of Akt in caveolae for glucose uptake into H9c2 cardiomyoblasts. Glucose 206-213 insulin Homo sapiens 21-28 16000870-7 2005 We conclude that the insulin resistance condition induced the retardation of their translocation to caveolae and in turn caused an attenuation in insulin signaling, namely activation of Akt in caveolae for glucose uptake into H9c2 cardiomyoblasts. Glucose 206-213 insulin Homo sapiens 146-153 15883051-0 2005 A novel role for myosin II in insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Glucose 49-56 insulin Homo sapiens 30-37 15883051-1 2005 Insulin-stimulated glucose uptake requires the activation of several signaling pathways to mediate the translocation and fusion of GLUT4 vesicles from an intracellular pool to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 15780427-4 2005 However, after the development of the radio-immunoassay, the incretin-concept has been revived in 1964, showing that significantly more insulin was released after ingestion of glucose than after intravenous injection. Glucose 176-183 insulin Homo sapiens 136-143 16061021-3 2005 The rate of insulin-mediated glucose disposal (Rd) during the steady state of glucose clamp was used to assess the peripheral tissue insulin sensitivity. Glucose 29-36 insulin Homo sapiens 12-19 16061021-3 2005 The rate of insulin-mediated glucose disposal (Rd) during the steady state of glucose clamp was used to assess the peripheral tissue insulin sensitivity. Glucose 78-85 insulin Homo sapiens 12-19 15911045-9 2005 In animal studies, PEG-insulin microspheres administered subcutaneously as a single injection produced < 1% release of insulin in the first day but then lowered the serum glucose levels of diabetic rats to values < 200 mg/dL for approximately 9 days. Glucose 174-181 insulin Homo sapiens 23-30 15637182-0 2005 Contribution of defects in glucose uptake to carbohydrate intolerance in liver cirrhosis: assessment during physiological glucose and insulin concentrations. Glucose 27-34 insulin Homo sapiens 134-141 15637182-1 2005 It is well established that subjects with liver cirrhosis are insulin resistant, but the contribution of defects in insulin secretion and/or action to glucose intolerance remains unresolved. Glucose 151-158 insulin Homo sapiens 116-123 15637182-10 2005 In conclusion, carbohydrate intolerance in liver cirrhosis is determined by insulin resistance and the ability of glucose to stimulate insulin secretion. Glucose 114-121 insulin Homo sapiens 135-142 15637182-12 2005 Although insulin secretion ameliorates glucose intolerance, impaired glucose uptake during physiological glucose and insulin concentrations produces marked and sustained hyperglycemia, despite concurrent abnormalities in glucose production or insulin secretion. Glucose 39-46 insulin Homo sapiens 9-16 15671078-3 2005 Therefore, we determined if selective GSK3 inhibition in vitro leads to an improvement in insulin action on glucose transport activity in isolated skeletal muscle of insulin-resistant, prediabetic obese Zucker rats and if these effects of GSK3 inhibition are associated with enhanced insulin signaling. Glucose 108-115 insulin Homo sapiens 90-97 15671078-5 2005 Maximal insulin stimulation (5 mU/ml) of glucose transport activity, glycogen synthase activity, and selected insulin-signaling factors [tyrosine phosphorylation of insulin receptor (IR) and IRS-1, IRS-1 associated with p85 subunit of phosphatidylinositol 3-kinase, and serine phosphorylation of Akt and GSK3] were assessed. Glucose 41-48 insulin Homo sapiens 8-15 15671078-6 2005 GSK3 inhibition enhanced (P <0.05) basal glycogen synthase activity and insulin-stimulated glucose transport in obese epitrochlearis (81 and 24%) and soleus (108 and 20%) muscles. Glucose 94-101 insulin Homo sapiens 75-82 15691867-10 2005 The fall in BP, increase in HR, and stimulation of insulin secretion by oral glucose in older subjects were mediated by NO mechanisms by an effect unrelated to GE or changes in incretin hormones. Glucose 77-84 insulin Homo sapiens 51-58 15924525-14 2005 Although late gestation is associated with insulin resistance, the results show that insulin plays a regulatory role both in lipolysis and glucose production. Glucose 139-146 insulin Homo sapiens 85-92 16129894-9 2005 Insulin-stimulated hepatic glucose uptake is increased following exercise by an undefined mechanism that is independent of liver glycogen content. Glucose 27-34 insulin Homo sapiens 0-7 16129895-2 2005 In the postmeal absorptive state, 50-60% of the glucose storage action of insulin is accounted for by the actions of HISS released from the liver and acting on skeletal muscle. Glucose 48-55 insulin Homo sapiens 74-81 15746300-1 2005 Values for insulin-mediated glucose disposal vary continuously throughout a population of apparently healthy individuals, with at least a sixfold variation between the most insulin sensitive and most insulin resistant of these individuals. Glucose 28-35 insulin Homo sapiens 11-18 15746300-1 2005 Values for insulin-mediated glucose disposal vary continuously throughout a population of apparently healthy individuals, with at least a sixfold variation between the most insulin sensitive and most insulin resistant of these individuals. Glucose 28-35 insulin Homo sapiens 173-180 15746300-1 2005 Values for insulin-mediated glucose disposal vary continuously throughout a population of apparently healthy individuals, with at least a sixfold variation between the most insulin sensitive and most insulin resistant of these individuals. Glucose 28-35 insulin Homo sapiens 173-180 15929863-2 2005 Magnetic resonance spectroscopy studies in humans suggest that a defect in insulin-stimulated glucose transport in skeletal muscle is the primary metabolic abnormality in insulin-resistant patients with type 2 diabetes. Glucose 94-101 insulin Homo sapiens 75-82 15929863-2 2005 Magnetic resonance spectroscopy studies in humans suggest that a defect in insulin-stimulated glucose transport in skeletal muscle is the primary metabolic abnormality in insulin-resistant patients with type 2 diabetes. Glucose 94-101 insulin Homo sapiens 171-178 15929863-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associated phosphatidylinositol 3-kinase activity. Glucose 43-50 insulin Homo sapiens 75-82 15929863-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associated phosphatidylinositol 3-kinase activity. Glucose 43-50 insulin Homo sapiens 122-129 15919795-2 2005 The aims of this study were to define the role of insulin secretion and proinsulin processing in glucose regulation in obese youth. Glucose 97-104 insulin Homo sapiens 72-82 15746249-9 2005 Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. Glucose 220-227 insulin Homo sapiens 68-75 15919784-1 2005 The dose-response relationship between elevated plasma free fatty acid (FFA) levels and impaired insulin-mediated glucose disposal and insulin signaling was examined in 21 lean, healthy, normal glucose-tolerant subjects. Glucose 114-121 insulin Homo sapiens 97-104 15919784-5 2005 Basal plasma FFA concentration ( approximately 440 micromol/l) was increased to 695, 1,251, and 1,688 micromol/l after 4 h of Liposyn infusion and resulted in a dose-dependent reduction in insulin-stimulated glucose disposal (R(d)) by 22, 30, and 34%, respectively (all P < 0.05 vs. saline control). Glucose 208-215 insulin Homo sapiens 189-196 15919784-8 2005 However, about two-thirds of the maximal inhibition of insulin-stimulated glucose disposal already occurred at the rather modest increase in plasma FFA induced by the low-dose (30-ml/h) lipid infusion. Glucose 74-81 insulin Homo sapiens 55-62 15919784-9 2005 Insulin-stimulated glucose disposal was inversely correlated with both the plasma FFA concentration after 4 h of lipid infusion (r = -0.50, P = 0.001) and the plasma FFA level during the last 30 min of the insulin clamp (r = -0.54, P < 0.001). Glucose 19-26 insulin Homo sapiens 0-7 15919784-9 2005 Insulin-stimulated glucose disposal was inversely correlated with both the plasma FFA concentration after 4 h of lipid infusion (r = -0.50, P = 0.001) and the plasma FFA level during the last 30 min of the insulin clamp (r = -0.54, P < 0.001). Glucose 19-26 insulin Homo sapiens 206-213 15919784-10 2005 PI 3-kinase activity associated with IRS-1 correlated with insulin-stimulated glucose disposal (r = 0.45, P < 0.01) and inversely with both the plasma FFA concentration after 4 h of lipid infusion (r = -0.39, P = 0.01) and during the last 30 min of the insulin clamp (r = -0.43, P < 0.01). Glucose 78-85 insulin Homo sapiens 59-66 15919784-11 2005 In summary, in skeletal muscle of lean, healthy subjects, a progressive increase in plasma FFA causes a dose-dependent inhibition of insulin-stimulated glucose disposal and insulin signaling. Glucose 152-159 insulin Homo sapiens 133-140 15919785-14 2005 Likewise, insulin and C-peptide concentrations increased during glucose infusion (P < 0.05). Glucose 64-71 insulin Homo sapiens 10-17 15919785-19 2005 Insulin secretory-burst mass rose during glucose infusion (P < 0.05), whereas the interburst interval remained unchanged (4.4 +/- 0.2 vs. 4.5 +/- 0.3 min; P = 0.36). Glucose 41-48 insulin Homo sapiens 0-7 15919791-1 2005 Phosphatidylinositol (PI) 4,5-bisphosphate (PIP(2)) plays a pivotal role in insulin-stimulated glucose transport as an important precursor to PI 3,4,5-trisphosphate (PIP(3)) and a key regulator of actin polymerization. Glucose 95-102 insulin Homo sapiens 76-83 15920059-6 2005 RESULTS: Insulin-mediated glucose disposal was decreased by BR-HF condition (-24 +/- 6%, P < 0.05) but did not change with BR-HCHO (+19 +/- 10%, NS). Glucose 26-33 insulin Homo sapiens 9-16 15920059-8 2005 Although the increase in IMCL levels with PA-HF (+31 +/- 19%, P = 0.12) was similar to that during BR-HF, insulin-mediated glucose disposal (-7 +/- 9%, NS) was not decreased. Glucose 123-130 insulin Homo sapiens 106-113 16142014-1 2005 Incretin hormones are defined as intestinal hormones released in response to nutrient ingestion, which potentiate the glucose-induced insulin response. Glucose 118-125 insulin Homo sapiens 134-141 16142016-7 2005 Analysis of the insulin and glucose concentrations throughout the meal test revealed that AUC for glucose (758 +/- 19 vs 780 +/- 28 mg/Lxmin; P = 0.02) was significantly lower after repaglinide than glimepiride administration despite similar AUC for insulin (2327 +/- 269 vs 2148 +/- 292 mU/Lxmin; P = 0.105). Glucose 98-105 insulin Homo sapiens 16-23 15741239-3 2005 Insulin doubled leptin secretion in the presence of glucose (5 mM), but not in its absence. Glucose 52-59 insulin Homo sapiens 0-7 15741239-7 2005 On the other hand, insulin stimulated leptin secretion when glucose was replaced by L-aspartate, L-valine, L-methionine, or L-phenylalanine, but not by L-leucine (all 5 mM). Glucose 60-67 insulin Homo sapiens 19-26 15948676-3 2005 Type 2 diabetes is characterised by inappropriate regulation of hepatic glucose production, which is due, at least in part, to an imbalance in the bihormonal relationship between plasma levels of glucagon and insulin. Glucose 72-79 insulin Homo sapiens 209-216 15992544-5 2005 Knockdown of sortilin decreases both formation of GSVs and insulin-regulated glucose uptake. Glucose 77-84 insulin Homo sapiens 59-66 16020878-9 2005 RESULTS: The 12 patients showed the presence of a cluster of insulin resistance factors: higher blood pressure, higher body mass index, higher fasting plasma glucose, higher fasting serum insulin, and higher HOMA-IR than controls. Glucose 158-165 insulin Homo sapiens 61-68 15755857-5 2005 Insulin sensitivity [mean (95% confidence intervals); PCOS 4.0 (2.8-5.1) vs. controls 4.5 (3.5-5.4) 10(-4) min(-1)/microU.ml], and insulin secretion, expressed as the acute insulin response to glucose [PCOS 3.7 (3.3-4.2) vs. controls 3.7 (3.4-4.0) microU/ml] were similar in the two groups. Glucose 193-200 insulin Homo sapiens 0-7 15769987-9 2005 In summary, we found that 2 wk of diet and exercise decreased IMCL and increased muscle insulin-mediated glucose uptake, whereas diet with or without exercise decreased IHL. Glucose 105-112 insulin Homo sapiens 88-95 15797948-7 2005 Adiponectin was negatively correlated with insulin-suppressed endogenous glucose production during the clamp (P = 0.011). Glucose 73-80 insulin Homo sapiens 43-50 15797955-1 2005 There is a wide interindividual variation in peripheral insulin sensitivity at any given body mass index or percent body fat among obese adolescents with normal glucose tolerance. Glucose 161-168 insulin Homo sapiens 56-63 15774531-1 2005 Insulin-mediated glucose clearance (GC) is diminished in type 2 diabetes. Glucose 17-24 insulin Homo sapiens 0-7 15894763-5 2005 However, the insulin concentration at 60 minutes or 120 minutes after glucose challenge, insulin area, and the ratio of insulin to glucose area were significantly higher in patients with significant coronary stenosis and with previous MI. Glucose 70-77 insulin Homo sapiens 13-20 15894763-9 2005 The insulin response to the glucose challenge test requires further investigation as a potential risk factor for CAD and a potential target for intervention. Glucose 28-35 insulin Homo sapiens 4-11 15635658-1 2005 Derivatization of insulin with phenylboronic acids is described, thereby equipping insulin with novel glucose sensing ability. Glucose 102-109 insulin Homo sapiens 18-25 15635658-1 2005 Derivatization of insulin with phenylboronic acids is described, thereby equipping insulin with novel glucose sensing ability. Glucose 102-109 insulin Homo sapiens 83-90 15635658-6 2005 The dose-responsive glucose-mediated release of the novel insulins was demonstrated using glucamine-derived polyethylene glycol polyacrylamide (PEGA) as a model, and it was shown that Zn(II) hexamer formulation of the boronated insulins resulted in steeper glucose sensitivity relative to monomeric insulin formulation. Glucose 20-27 insulin Homo sapiens 58-65 15635658-6 2005 The dose-responsive glucose-mediated release of the novel insulins was demonstrated using glucamine-derived polyethylene glycol polyacrylamide (PEGA) as a model, and it was shown that Zn(II) hexamer formulation of the boronated insulins resulted in steeper glucose sensitivity relative to monomeric insulin formulation. Glucose 257-264 insulin Homo sapiens 58-65 15774531-11 2005 In conclusion, this study shows that glucose clearance is higher in arm than leg muscles, regardless of insulin resistance, which may indicate better preserved insulin sensitivity in arm than leg muscle in type 2 diabetes. Glucose 37-44 insulin Homo sapiens 160-167 15999958-4 2005 Continuous intravenous insulin was used if glucose values were >200 mg/dl on two successive occasions. Glucose 43-50 insulin Homo sapiens 23-30 15772157-1 2005 Insulin stimulates glucose uptake in fat and muscle by mobilizing Glut4 glucose transporters from intracellular membrane storage sites to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 15931613-5 2005 Insulin sensitivity in vivo was evaluated by measurement of the glucose infusion rate during a hyperinsulinemic-euglycemic clamp and of the homeostasis model of assessment-insulin resistance index. Glucose 64-71 insulin Homo sapiens 0-7 15931603-8 2005 Insulin-stimulated whole body glucose disposal did not improve, nor did insulin suppressibility of EGP and lipolysis. Glucose 30-37 insulin Homo sapiens 0-7 15931614-2 2005 We found that isolated adipocytes from omental fat of nondiabetic women expressed significantly more of the insulin-regulated glucose transporter glucose transporter 4 protein and exhibited a higher basal and insulin-stimulated rate of glucose transport, at all concentrations of insulin, than subcutaneous adipocytes from the same individuals. Glucose 126-133 insulin Homo sapiens 108-115 15931614-3 2005 In contrast, dose-response relationships for insulin stimulation of glucose transport demonstrated identical sensitivity to insulin in adipocytes from the 2 locations. Glucose 68-75 insulin Homo sapiens 45-52 15931614-3 2005 In contrast, dose-response relationships for insulin stimulation of glucose transport demonstrated identical sensitivity to insulin in adipocytes from the 2 locations. Glucose 68-75 insulin Homo sapiens 124-131 25696497-0 2005 Potential beneficial mechanisms of insulin (glucose-potassium) in acute myocardial infarction. Glucose 44-51 insulin Homo sapiens 35-42 16004598-1 2005 The incretin effect is a phenomenon in which enteral glucose administration provokes greater insulin secretion than intravenous administration. Glucose 53-60 insulin Homo sapiens 93-100 16036525-6 2005 A pronounced increase in plasma insulin levels occurred on the day after chemotherapy accompanied by a modest increase in plasma glucose concentrations. Glucose 129-136 insulin Homo sapiens 32-39 25696497-10 2005 However, systemic infusion of insulin stimulates the uptake of glucose in many celltypes, which may result in hypoglycaemic episodes. Glucose 63-70 insulin Homo sapiens 30-37 25696497-12 2005 Interventions in the glucose metabolism in the clinical arena, whether or not used to correct acute hyperglycaemia, encompass three potentially effective elements: glucose, insulin and potassium. Glucose 21-28 insulin Homo sapiens 173-180 15889321-8 2005 With postprandial aspart insulin, however, 84 % of the blood glucose levels measured one hour after breakfast exceeded > 10 mmol/l in comparison to 38 % with preprandial aspart insulin (p < 0.05). Glucose 61-68 insulin Homo sapiens 25-32 15924982-8 2005 After a 75 g oral glucose tolerance test, participants exposed to betamethasone had higher plasma insulin concentrations at 30 min (60.5 vs 52.0 mIU/L; ratio of geometric means 1.16 [95% CI 1.03 to 1.31], p=0.02) and lower glucose concentrations at 120 min (4.8 vs 5.1 mmol/L; difference -0.26 mmol/L [-0.53 to 0.00], p=0.05) than did those exposed to placebo. Glucose 18-25 insulin Homo sapiens 98-105 15883206-13 2005 These nongenomic functional effects of insulin may be of clinical relevance, eg, during insulin-glucose-potassium infusions. Glucose 96-103 insulin Homo sapiens 39-46 15883206-13 2005 These nongenomic functional effects of insulin may be of clinical relevance, eg, during insulin-glucose-potassium infusions. Glucose 96-103 insulin Homo sapiens 88-95 15764603-0 2005 Differential contribution of insulin receptor substrates 1 versus 2 to insulin signaling and glucose uptake in l6 myotubes. Glucose 93-100 insulin Homo sapiens 29-36 15774472-8 2005 419, 101-109), long-chain saturated FFAs inhibited insulin stimulation of Akt/protein kinase B, a central regulator of glucose uptake and anabolic metabolism. Glucose 119-126 insulin Homo sapiens 51-58 15892894-7 2005 Following treatment, plasma glucose and insulin were reduced during the oral glucose tolerance test by telmisartan, but not by losartan. Glucose 77-84 insulin Homo sapiens 40-47 15764603-7 2005 In contrast, siIRS-1 treatment caused a marked reduction in insulin-induced actin remodeling, glucose uptake, and GLUT4 translocation, and siIRS-2 was without effect on these responses. Glucose 94-101 insulin Homo sapiens 60-67 15764603-9 2005 We conclude that insulin-stimulated Akt1 phosphorylation, actin remodeling, GLUT4 translocation, and glucose uptake are regulated mainly by IRS-1, whereas IRS-2 contributes selectively to ERK signaling, and Akt2 and p38MAPK lie downstream of both IRS in muscle cells. Glucose 101-108 insulin Homo sapiens 17-24 15887451-9 2005 Once fluid replacement has been initiated, insulin should be given as an initial bolus of 0.15 U per kg intravenously, followed by a drip of 0.1 U per kg per hour until the blood glucose level falls to between 250 and 300 mg per dL. Glucose 179-186 insulin Homo sapiens 43-50 15866422-5 2005 However, the dominant-negative mutant reduced the efficiency of insulin to promote glucose uptake and GLUT4 translocation in both cardiac and skeletal muscle cells to about one half. Glucose 83-90 insulin Homo sapiens 64-71 20496449-3 2005 Sulfonylureas are a class of oral hypoglycemics that reduce blood glucose levels by stimulating insulin secretion. Glucose 66-73 insulin Homo sapiens 96-103 15644452-10 2005 These results indicate that a short but severe nutritional stress can significantly alter the fetal anabolic response to insulin even when both glucose and amino acid substrate supplies are restored. Glucose 144-151 insulin Homo sapiens 121-128 15613682-3 2005 Basal and insulin-stimulated glucose transport and GLUT1 abundance were significantly increased in cultured myotubes from women with PCOS. Glucose 29-36 insulin Homo sapiens 10-17 15613682-8 2005 In summary, decreased insulin-stimulated glucose uptake in PCOS skeletal muscle in vivo is an acquired defect. Glucose 41-48 insulin Homo sapiens 22-29 15632105-3 2005 Am J Physiol Endocrinol Metab 276: E285-E294, 1999), in which insulin-modified [6,6-2H2]glucose-labeled IVGTTs (0.33 g/kg glucose) were performed in 10 normal subjects. Glucose 88-95 insulin Homo sapiens 62-69 15811898-1 2005 OBJECTIVE: To evaluate the evidence for using high-dose insulin therapy with supplemental dextrose and potassium in calcium-channel blocker (CCB) overdose. Glucose 90-98 insulin Homo sapiens 56-63 15811898-2 2005 DATA SOURCES: Evidence of efficacy for high-dose insulin therapy with supplemental dextrose and potassium was sought by performing a search of MEDLINE and Toxline between 1966 and July 2004 using combinations of the terms calcium-channel blocker, overdose, poisoning, antidote, and insulin. Glucose 83-91 insulin Homo sapiens 49-56 15811898-6 2005 DATA SYNTHESIS: Animal models of CCB overdose demonstrate that high-dose insulin with supplemental dextrose and potassium was a more effective therapy than calcium, glucagon, or catecholamines. Glucose 99-107 insulin Homo sapiens 73-80 15925016-3 2005 New approaches using novel insulin analogs and routes of administration, attempting to replicate physiological insulin secretion in diabetic patients, are improving the profiles of glucose levels and, thus, the quality of life. Glucose 181-188 insulin Homo sapiens 27-34 15898729-9 2005 When the insulin conjugates were intravenously administered (0.33 IU/kg) to streptozotocin (STZ)-induced diabetic rats, the conjugates showed sustained biological activity for a longer period with the similar lowest blood glucose level (glucose nadir), compared to native insulin. Glucose 222-229 insulin Homo sapiens 9-16 15898729-9 2005 When the insulin conjugates were intravenously administered (0.33 IU/kg) to streptozotocin (STZ)-induced diabetic rats, the conjugates showed sustained biological activity for a longer period with the similar lowest blood glucose level (glucose nadir), compared to native insulin. Glucose 237-244 insulin Homo sapiens 9-16 15842553-1 2005 AIMS: To assess the effects due to an uncomplicated acute upper respiratory tract infection (URTI) on the pharmacokinetics and glucose response of insulin when delivered by oral pulmonary absorption. Glucose 127-134 insulin Homo sapiens 147-154 15975173-6 2005 C-peptide and insulin responses to intravenous glucose tended (P<0.08) to or decreased (P<0.03) with B2 while no effect was observed on glucose. Glucose 47-54 insulin Homo sapiens 14-21 15820475-7 2005 Also, plasma insulin levels during oral glucose tolerance test tended to be higher in the former than in the latter. Glucose 40-47 insulin Homo sapiens 13-20 15892653-2 2005 Physical exercise/muscle contraction elicits an insulin-independent increase in glucose transport and perturbation of this pathway may bypass defective insulin signaling. Glucose 80-87 insulin Homo sapiens 48-55 15892646-4 2005 Also, we review recent progress in relation to a model for the pathogenesis of the various stages of abnormal glucose regulation based on the concepts of thrifty genes of metabolism and pro-inflammation and genes responsible for the appearance of impaired pancreatic beta-cell function and insulin signalling under the pressure of a westernized environment. Glucose 110-117 insulin Homo sapiens 290-297 15892647-2 2005 Evidences for the islet dysfunction in type 2 diabetes are a)impaired insulin response to various challenges such as glucose, arginine and isoproterenol, b)defective dynamic of insulin secretion resulting in preferential reduction on first phase insulin secretion and irregular oscillations of plasma insulin and c)defective conversion of proinsulin to insulin leading to elevated proinsulin to insulin ratio. Glucose 117-124 insulin Homo sapiens 70-77 18220592-5 2005 At the cellular level, glucose transport into skeletal muscle is the rate-limiting step for whole body glucose uptake and a primary site of insulin resistance in Type 2 diabetes. Glucose 23-30 insulin Homo sapiens 140-147 18220593-3 2005 In addition, PGC-1alpha has been shown to increase the percentage of oxidative type I muscle fibres, with the latter responsible for the majority of insulin stimulated glucose uptake. Glucose 168-175 insulin Homo sapiens 149-156 18220597-2 2005 Normally, continuous and variable basal insulin release provides partial suppression of hepatic glucose production to maintain euglycemia during the fasting period. Glucose 96-103 insulin Homo sapiens 40-47 18220597-3 2005 With meals, additional insulin is released in a biphasic pattern to further suppress hepatic glucose production and to increase glucose transport into muscle, fat and liver. Glucose 93-100 insulin Homo sapiens 23-30 18220597-3 2005 With meals, additional insulin is released in a biphasic pattern to further suppress hepatic glucose production and to increase glucose transport into muscle, fat and liver. Glucose 128-135 insulin Homo sapiens 23-30 18220597-11 2005 Daily consecutive intensive glucose evaluations using a continuous glucose monitoring system and corresponding dosage adjustments may offer an even better tool for insulin dosing selection. Glucose 28-35 insulin Homo sapiens 164-171 18220597-11 2005 Daily consecutive intensive glucose evaluations using a continuous glucose monitoring system and corresponding dosage adjustments may offer an even better tool for insulin dosing selection. Glucose 67-74 insulin Homo sapiens 164-171 15811139-2 2005 METHODS: The Insulin Resistance Atherosclerosis Study (IRAS) estimated S(I) (x10(-4)/min.microU/ml) directly using a frequently sampled intravenous glucose tolerance test with minimal model analysis in 504 normoglycaemic subjects. Glucose 148-155 insulin Homo sapiens 13-20 15811141-5 2005 Beyond HOMA-r, another insulin resistance index (IRIp) was calculated by means of the formula: peak of blood glucose after oral glucose load x plasma insulin level/10(4). Glucose 109-116 insulin Homo sapiens 23-30 15855309-5 2005 These considerations implicate insulin action in the brain, an organ previously considered to be insulin independent, as a key determinant of both glucose and energy homeostasis. Glucose 147-154 insulin Homo sapiens 31-38 15855309-5 2005 These considerations implicate insulin action in the brain, an organ previously considered to be insulin independent, as a key determinant of both glucose and energy homeostasis. Glucose 147-154 insulin Homo sapiens 97-104 15855314-3 2005 After 7 days of physiological or supraphysiological hyperadiponectinemia, the animals displayed enhanced insulin sensitivity during the glucose tolerance and insulin tolerance tests. Glucose 136-143 insulin Homo sapiens 105-112 15855314-4 2005 Glucose clamp studies performed at submaximal and maximal insulin infusion rates (4 and 25 mU x kg(-1) x min(-1), respectively) also demonstrated increased insulin sensitivity in Adv-Adipo animals, with the insulin-stimulated glucose disposal rate being increased by 20-67%. Glucose 0-7 insulin Homo sapiens 58-65 15855314-4 2005 Glucose clamp studies performed at submaximal and maximal insulin infusion rates (4 and 25 mU x kg(-1) x min(-1), respectively) also demonstrated increased insulin sensitivity in Adv-Adipo animals, with the insulin-stimulated glucose disposal rate being increased by 20-67%. Glucose 0-7 insulin Homo sapiens 156-163 15855314-4 2005 Glucose clamp studies performed at submaximal and maximal insulin infusion rates (4 and 25 mU x kg(-1) x min(-1), respectively) also demonstrated increased insulin sensitivity in Adv-Adipo animals, with the insulin-stimulated glucose disposal rate being increased by 20-67%. Glucose 0-7 insulin Homo sapiens 156-163 15855334-3 2005 Insulin-mediated whole-body and leg muscle glucose uptake was enhanced 36 and 32%, respectively, after rosiglitazone (P < 0.01) but not after metformin or placebo treatment. Glucose 43-50 insulin Homo sapiens 0-7 15855334-7 2005 Low-intensity acute exercise increased insulin-mediated glucose uptake but was without effect on insulin signaling. Glucose 56-63 insulin Homo sapiens 39-46 15855345-2 2005 Because these events may be a consequence of their ability to directly alter insulin secretion from pancreatic beta-cells, we determined the effects of several antipsychotics on cholinergic- and glucose-stimulated insulin secretion from isolated rat islets. Glucose 195-202 insulin Homo sapiens 214-221 15855345-3 2005 At concentrations encompassing therapeutically relevant levels, olanzapine and clozapine reduced insulin secretion stimulated by 10 micromol/l carbachol plus 7 mmol/l glucose. Glucose 167-174 insulin Homo sapiens 97-104 15855574-5 2005 Lower between-subject variability was observed for insulin detemir on duration of action (0.4 units/kg insulin detemir vs. 0.3 IU/kg NPH, P < 0.05) and GIR(max) (maximal glucose infusion rate) (0.2 and 0.4 units/kg insulin detemir vs. 0.3 IU/kg NPH, both P < 0.05). Glucose 173-180 insulin Homo sapiens 51-58 15860236-6 2005 Use of Q seems to be useful to improve hyperglycemia in patients with a poor glucose profile under conventional insulin treatment with using R. The choice of insulin regimens with using Q in consideration of the blood glucose profile as well as lifestyles may lead to better glycemic control. Glucose 218-225 insulin Homo sapiens 158-165 15761746-3 2005 Insulin sensitivity index was calculated by the decline in arterial blood glucose concentration following intravenous administration of a single bolus of human insulin (0.075 IU.kg(-1) fat free mass). Glucose 74-81 insulin Homo sapiens 0-7 15824195-2 2005 Magnetic resonance spectroscopy studies in humans suggest that a defect in insulin-stimulated glucose transport in skeletal muscle is the primary metabolic abnormality in insulin-resistant type 2 diabetics. Glucose 94-101 insulin Homo sapiens 75-82 15971158-7 2005 However, taking all above listed factors into account, glucose-clamp assessed insulin sensitivity was not correlated with IMT. Glucose 55-62 insulin Homo sapiens 78-85 15824195-2 2005 Magnetic resonance spectroscopy studies in humans suggest that a defect in insulin-stimulated glucose transport in skeletal muscle is the primary metabolic abnormality in insulin-resistant type 2 diabetics. Glucose 94-101 insulin Homo sapiens 171-178 15879567-1 2005 Patients with type 2 diabetes mellitus are usually treated initially with oral antidiabetic agents, but as the disease progresses, most patients eventually require insulin to maintain glucose control. Glucose 184-191 insulin Homo sapiens 164-171 15713702-4 2005 Insulin sensitivity, expressed as the M value (milligrams per kilograms(-1) per minute(-1)), was calculated from the glucose disposal rate during the final 30 min of the clamp. Glucose 117-124 insulin Homo sapiens 0-7 15879567-3 2005 This article discusses the role of insulin therapy in patients with type 2 diabetes, emphasizing long-acting insulin agents designed to approximate physiologic basal insulin secretion and provide control over fasting plasma glucose. Glucose 224-231 insulin Homo sapiens 109-116 15877289-3 2005 To study the association of obesity with defects in insulin action, we investigated insulin stimulation of both insulin receptor (IR) autophosphorylation and subsequent glucose transport in primary skeletal muscle cell cultures obtained from both nonobese and obese nondiabetic subjects. Glucose 169-176 insulin Homo sapiens 84-91 15650027-0 2005 Elevated glucose attenuates human insulin gene promoter activity in INS-1 pancreatic beta-cells via reduced nuclear factor binding to the A5/core and Z element. Glucose 9-16 insulin Homo sapiens 34-41 15650027-3 2005 At issue, however, was that MafA also markedly stimulated an insulin reporter gene (-230 to +30 bp) that was only marginally suppressed by glucose, suggesting that glucose-mediated suppression of the insulin promoter involved elements upstream of -230. Glucose 164-171 insulin Homo sapiens 61-68 15650027-3 2005 At issue, however, was that MafA also markedly stimulated an insulin reporter gene (-230 to +30 bp) that was only marginally suppressed by glucose, suggesting that glucose-mediated suppression of the insulin promoter involved elements upstream of -230. Glucose 164-171 insulin Homo sapiens 200-207 15650027-4 2005 Using serial truncations and mini-enhancer constructs of the human insulin promoter, the majority of glucose suppression was localized to regulatory elements between -327 and -261. Glucose 101-108 insulin Homo sapiens 67-74 15650027-10 2005 These data indicate that glucose suppression of human insulin promoter activity in INS-1 cells involves reduced binding of MafA to the A5/core. Glucose 25-32 insulin Homo sapiens 54-61 15862281-5 2005 Changes in insulin-stimulated glucose uptake and glycogen synthesis in response to the calpain inhibitors ALLN and ALLM were measured. Glucose 30-37 insulin Homo sapiens 11-18 15862281-7 2005 Insulin-stimulated glucose uptake was significantly decreased following preincubation with ALLN [404+/-40 vs 505+/-55 (mean+/-SEM)pmol/mg/min; with vs without ALLN: p = 0.04] and ALLM [455+/-38 vs 550+/-50 pmol/mg/min; with vs without ALLM: p = 0.025] in day 7 fused myotubes, but not in myoblasts. Glucose 19-26 insulin Homo sapiens 0-7 15862281-9 2005 These studies confirm calpain 10 expression in cultured human muscle cells and support a role for calpains in insulin-stimulated glucose uptake in human skeletal muscle cells that may be relevant to the pathogenesis of the peripheral insulin resistance in type 2 diabetes. Glucose 129-136 insulin Homo sapiens 110-117 15862281-9 2005 These studies confirm calpain 10 expression in cultured human muscle cells and support a role for calpains in insulin-stimulated glucose uptake in human skeletal muscle cells that may be relevant to the pathogenesis of the peripheral insulin resistance in type 2 diabetes. Glucose 129-136 insulin Homo sapiens 234-241 15694116-10 2005 What more in girls with anorexia the integrated output of insulin was significantly lower in oral glucose tolerance test than after the meal (p<0.001). Glucose 98-105 insulin Homo sapiens 58-65 15694116-14 2005 Highly significant correlation was found between glucose concentration and the concentrations of insulin, cholecystokinin, and gastric inhibitory peptide in both tests and for the both groups. Glucose 49-56 insulin Homo sapiens 97-104 15749139-6 2005 Insulin sensitivity was significantly lower in the jSD group than that in the jLD group, as indicated by the area under the curves of insulin and glucose following a 75-g oral glucose load. Glucose 146-153 insulin Homo sapiens 0-7 16035288-2 2005 The most appropriate insulin scheme comprises the injection of a short-acting insulin before each meal, to control postprandial hyperglycaemia, and one (or possibly two) injection of a long-acting insulin, to maintain adequate plasma glucose levels between meals and at night. Glucose 234-241 insulin Homo sapiens 21-28 16035295-9 2005 Resistance to insulin action is located in the liver (increased hepatic glucose production), in the skeletal muscle (decreased muscular glucose uptake) and in the adipose tissue (exaggerated lipolysis with elevated plasma free fatty acids). Glucose 72-79 insulin Homo sapiens 14-21 16035301-5 2005 Amongst the different glucose-lowering agents, two kinds of insulin secretagogues may be used: sulphonylureas or, more recently, glinides (meglitinide derivatives). Glucose 22-29 insulin Homo sapiens 60-67 15931874-1 2005 OBJECTIVE: To detect the relationship between peripheral insulin resistance and beta-cell function in obese subjects with normal blood glucose, and to explore the role of free fatty acids (FFAs) in the pathogenesis of type 2 DM. Glucose 135-142 insulin Homo sapiens 57-64 15951871-15 2005 CONCLUSION: The CAPD treatment may lead to insulin insensitivity in non-diabetic end-stage renal disease patients and the high glucose content of CAPD solutions may be responsible for insulin resistance in CAPD patients. Glucose 127-134 insulin Homo sapiens 184-191 15860415-3 2005 Studies in mammalian cells reveal that FoxO proteins regulate cell cycle progression and promote resistance to oxidative stress; both in vivo and cell culture studies support the concept that FoxO proteins have an important role in mediating the effects of insulin on metabolism, including its effects on hepatic glucose production. Glucose 313-320 insulin Homo sapiens 257-264 15860416-1 2005 Insulin-like growth factor I (IGF-I) has many potential therapeutic uses because of its varied effects--growth promotion, insulin-like influence on glucose metabolism, and neuroprotection resulting from cell-proliferative and antiapoptotic properties--but they have not been investigated systematically in clinical situations. Glucose 148-155 insulin Homo sapiens 122-129 16220784-3 2005 The sensitivity to insulin in the cells was estimated by the measurement of insulin-induced glucose-uptake. Glucose 92-99 insulin Homo sapiens 19-26 16220784-3 2005 The sensitivity to insulin in the cells was estimated by the measurement of insulin-induced glucose-uptake. Glucose 92-99 insulin Homo sapiens 76-83 16220784-5 2005 RESULTS: With the administration of 25 nmol x L(-1) long-action insulin in HIRe cells for 36 hours, the GFAT activity increased by 47% and the insulin-induced glucose-uptake decreased by 21%. Glucose 159-166 insulin Homo sapiens 64-71 16220784-5 2005 RESULTS: With the administration of 25 nmol x L(-1) long-action insulin in HIRe cells for 36 hours, the GFAT activity increased by 47% and the insulin-induced glucose-uptake decreased by 21%. Glucose 159-166 insulin Homo sapiens 143-150 15851721-1 2005 OBJECTIVE: To investigate the effectiveness of maintaining blood glucose levels below 6.1 mmol/L with insulin as prevention of secondary injury to the central and peripheral nervous systems of intensive care patients. Glucose 65-72 insulin Homo sapiens 102-109 15824195-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1 associated phosphatidylinositol 3-kinase activity. Glucose 43-50 insulin Homo sapiens 75-82 15824195-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1 associated phosphatidylinositol 3-kinase activity. Glucose 43-50 insulin Homo sapiens 122-129 15766572-4 2005 Furthermore, we show that l-arginine at low levels of glucose significantly stimulates the release of insulin from these cells, compared to exposure to high concentration of glucose. Glucose 54-61 insulin Homo sapiens 102-109 15851721-6 2005 Of all metabolic and clinical effects of insulin therapy, and corrected for known risk factors, the level of glycemic control independently explained this benefit (OR for CIPNP 1.26 [1.09 to 1.46] per mmol blood glucose, p = 0.002). Glucose 212-219 insulin Homo sapiens 41-48 15752775-2 2005 When insulin-treated adipocytes were exposed to 2mM GlcN, glucose uptake was rapidly reduced by approximately 60% with a T(1/2) of 2 min. Glucose 58-65 insulin Homo sapiens 5-12 15752775-5 2005 Although the acute inhibitory action of GlcN could be completely reversed by removing extracellular GlcN, a slow and progressive decrease in insulin-stimulated glucose transport was observed with longer treatment times (T(1/2) of 45 min, 62% loss by 5h). Glucose 160-167 insulin Homo sapiens 141-148 15868990-3 2005 Microvascular dysfunction leads not only to increased peripheral vascular resistance and blood pressure, but may also decrease the insulin-mediated glucose uptake in muscles. Glucose 148-155 insulin Homo sapiens 131-138 15792832-0 2005 Insulin and nitric oxide stimulates glucose transport in human placenta. Glucose 36-43 insulin Homo sapiens 0-7 15792832-1 2005 The present work examines whether insulin and NO can act as regulators of glucose transport in placenta. Glucose 74-81 insulin Homo sapiens 34-41 15792832-2 2005 Glucose uptake (2-deoxy D-[(3)H]glucose) was measured in the absence (control or basal values) and in the presence of insulin (1200 microU/ml) or SNP (20 microM) in isolated perfused cotyledons and tissue slices preparations of human placenta. Glucose 0-7 insulin Homo sapiens 118-125 15792832-3 2005 Both insulin and NO significantly increased glucose uptake by 20 and 27 per cent, respectively. Glucose 44-51 insulin Homo sapiens 5-12 15792832-4 2005 Insulin decreased the Km of glucose transport from 42.5 +/- 2.69 to 35.1 +/- 2.58 mM. Glucose 28-35 insulin Homo sapiens 0-7 15705646-11 2005 Furthermore, oral glucose loading during recovery increased plasma insulin markedly more in F (+46.80 microU ml(-1)) than in CHO (+14.63 microU ml(-1), P = 0.02). Glucose 18-25 insulin Homo sapiens 67-74 15792832-7 2005 Taken together, these findings indicate that insulin and NO stimulate glucose uptake in human placenta and suggest that both potential regulators of glucose transport use different signaling pathways. Glucose 70-77 insulin Homo sapiens 45-52 15792832-7 2005 Taken together, these findings indicate that insulin and NO stimulate glucose uptake in human placenta and suggest that both potential regulators of glucose transport use different signaling pathways. Glucose 149-156 insulin Homo sapiens 45-52 15585585-2 2005 There is evidence suggesting that activation of p38 MAP kinase (p38) is involved in the stimulation of glucose transport by insulin and contractions. Glucose 103-110 insulin Homo sapiens 124-131 15799771-5 2005 RESULTS: The insulin-mediated glucose disposal rate (M-value) for the steady-state period (60-120 min) of the clamp, tended to be lower following arm work than for both cycling and resting regimes. Glucose 30-37 insulin Homo sapiens 13-20 15578231-1 2005 This paper presents a developed and validated dynamic simulation model of type 1 diabetes, that simulates the progression of the disease and the two term controller that is responsible for the insulin released to stabilize the glucose level. Glucose 227-234 insulin Homo sapiens 193-200 15787601-3 2005 Insulin resistance in combination with defective insulin secretion from the pancreas results in the elevated blood glucose levels that are characteristic of diabetes mellitus. Glucose 115-122 insulin Homo sapiens 0-7 15787601-3 2005 Insulin resistance in combination with defective insulin secretion from the pancreas results in the elevated blood glucose levels that are characteristic of diabetes mellitus. Glucose 115-122 insulin Homo sapiens 49-56 15787603-0 2005 Role of protein kinase B in insulin-regulated glucose uptake. Glucose 46-53 insulin Homo sapiens 28-35 15787603-1 2005 The activation of protein kinase B (or Akt) plays a central role in the stimulation of glucose uptake by insulin. Glucose 87-94 insulin Homo sapiens 105-112 15787604-1 2005 It now seems clear that aPKC (atypical protein kinase C) isoforms are required for insulin-stimulated glucose transport in muscle and adipocytes. Glucose 102-109 insulin Homo sapiens 83-90 15787605-3 2005 75% of whole body insulin-stimulated glucose uptake, defects in this tissue play a major role in the impaired glucose homoeostasis in Type II diabetic patients. Glucose 37-44 insulin Homo sapiens 18-25 15787605-5 2005 This review will describe the effects of insulin on glucose transport and other metabolic events in skeletal muscle that are mediated by intracellular signalling cascades. Glucose 52-59 insulin Homo sapiens 41-48 15578231-7 2005 It was found that the controller designed predicts an adequate amount of insulin that should be delivered into the body to obtain a normalization of the elevated glucose level. Glucose 162-169 insulin Homo sapiens 73-80 15578231-8 2005 This helps to achieve the main objective of insulin therapy: to obtain an accurate estimate of the amount of insulin to be delivered in order to compensate for the increase in glucose concentration. Glucose 176-183 insulin Homo sapiens 44-51 15578231-8 2005 This helps to achieve the main objective of insulin therapy: to obtain an accurate estimate of the amount of insulin to be delivered in order to compensate for the increase in glucose concentration. Glucose 176-183 insulin Homo sapiens 109-116 15748541-1 2005 High glucose activates a myriad of signaling and gene expression pathways in non-insulin-dependent target cells causing diabetes complications. Glucose 5-12 insulin Homo sapiens 81-88 15887790-0 2005 Insulin responses to glucose and isoproterenol decrease with age. Glucose 21-28 insulin Homo sapiens 0-7 15887790-1 2005 BACKGROUND: Older trauma patients are less tolerant of glucose loads than are young patients, in part as a result of diminished insulin response. Glucose 55-62 insulin Homo sapiens 128-135 15887790-9 2005 CONCLUSIONS: Heart rate and serum insulin responses to combined isoproterenol infusion and glucose loading were both lower in healthy older subjects than in the young. Glucose 91-98 insulin Homo sapiens 34-41 15810996-2 2005 In the 80+ years since insulin"s discovery, an enormous amount of literature has accumulated relating to its actions on body fat, glucose and protein metabolism. Glucose 130-137 insulin Homo sapiens 23-30 15810996-3 2005 In particular, skeletal muscle has been extensively studied because of its major role as a site of insulin-mediated glucose disposal. Glucose 116-123 insulin Homo sapiens 99-106 15810996-17 2005 Even so, there is now sufficient evidence to indicate that insulin"s vascular action within skeletal muscle is a major regulatory locus for its insulin mediated glucose disposal. Glucose 161-168 insulin Homo sapiens 59-66 15810996-17 2005 Even so, there is now sufficient evidence to indicate that insulin"s vascular action within skeletal muscle is a major regulatory locus for its insulin mediated glucose disposal. Glucose 161-168 insulin Homo sapiens 144-151 15665038-0 2005 The p38 mitogen-activated protein kinase inhibitor SB203580 reduces glucose turnover by the glucose transporter-4 of 3T3-L1 adipocytes in the insulin-stimulated state. Glucose 68-75 insulin Homo sapiens 142-149 15853732-9 2005 However, there is no regulatory system that results in the expression and release of insulin in response to glucose with satisfactory kinetics. Glucose 108-115 insulin Homo sapiens 85-92 15665038-1 2005 Insulin induces a profound increase in glucose uptake in 3T3-L1 adipocytes through the activity of the glucose transporter-4 (GLUT4). Glucose 39-46 insulin Homo sapiens 0-7 15665038-2 2005 Apart from GLUT4 translocation toward the plasma membrane, there is also an insulin-induced p38 MAPK-dependent step involved in the regulation of glucose uptake. Glucose 146-153 insulin Homo sapiens 76-83 15665038-3 2005 Consequently, treatment with the p38 MAPK inhibitor SB203580 reduces insulin-induced glucose uptake by approximately 30%. Glucose 85-92 insulin Homo sapiens 69-76 15747109-5 2005 Insulin-stimulated tyrosine phosphorylation of IRS-1, and IRS-1- and IRS-2-associated phosphatidylinositol 3-kinase (PI3K) activity were not impaired by TGRLs, suggesting that these steps were not involved in the lipoprotein-induced effects on glucose metabolism. Glucose 244-251 insulin Homo sapiens 0-7 15765221-0 2005 High normal 2-hour plasma glucose is associated with insulin sensitivity and secretion that may predispose to type 2 diabetes. Glucose 26-33 insulin Homo sapiens 53-60 15787664-2 2005 The present study was undertaken to compare the plasma insulin responses to glucose and tolbutamide in HNF-1alpha mutation carriers with those of healthy control subjects. Glucose 76-83 insulin Homo sapiens 55-62 15787664-5 2005 RESULTS: The plasma insulin response to intravenous glucose was reduced in the HNF-1alpha mutation carriers compared to the control subjects, with an area under the curve (median (interquartile range)) of 812 min pmol/l (421, 1647) and 1933 min pmol/l (1521, 2908), respectively (P = 0.03). Glucose 52-59 insulin Homo sapiens 20-27 15787672-6 2005 Insulin infusion for three hours, which restored near normoglycaemia (arterial glucose 7.6 +/- 0.7 mm), reduced renal tissue glucose uptake toward normal (258 +/- 41 micromol/min, P = 0.006) without altering renal blood flow (1557 +/- 110, P = 0.63) or renal tissue glucose fractional extraction (2.1 +/- 0.3%, P = 0.35). Glucose 79-86 insulin Homo sapiens 0-7 15787672-6 2005 Insulin infusion for three hours, which restored near normoglycaemia (arterial glucose 7.6 +/- 0.7 mm), reduced renal tissue glucose uptake toward normal (258 +/- 41 micromol/min, P = 0.006) without altering renal blood flow (1557 +/- 110, P = 0.63) or renal tissue glucose fractional extraction (2.1 +/- 0.3%, P = 0.35). Glucose 125-132 insulin Homo sapiens 0-7 15787672-6 2005 Insulin infusion for three hours, which restored near normoglycaemia (arterial glucose 7.6 +/- 0.7 mm), reduced renal tissue glucose uptake toward normal (258 +/- 41 micromol/min, P = 0.006) without altering renal blood flow (1557 +/- 110, P = 0.63) or renal tissue glucose fractional extraction (2.1 +/- 0.3%, P = 0.35). Glucose 125-132 insulin Homo sapiens 0-7 15787672-7 2005 Renal and hepatic glucose release, which had been increased (419 +/- 49 and 960 +/- 54 vs. 204 +/- 9 and 734 +/- 32 micromol/min, both P < 0.001), were suppressed by insulin to 138 +/- 22 and 520 +/- 53 micromol/min, respectively (both P < 0.001). Glucose 18-25 insulin Homo sapiens 169-176 15793186-10 2005 CONCLUSIONS: Fasting proinsulin was associated with all-cause and CVD mortality, independent of glucose tolerance status and insulin resistance and largely independent of other CVD risk factors. Glucose 96-103 insulin Homo sapiens 21-31 15793186-10 2005 CONCLUSIONS: Fasting proinsulin was associated with all-cause and CVD mortality, independent of glucose tolerance status and insulin resistance and largely independent of other CVD risk factors. Glucose 96-103 insulin Homo sapiens 24-31 15793193-8 2005 Changes in insulin sensitivity, strongly related to weight change, had a significant impact on the 2-h glucose level on the follow-up study. Glucose 103-110 insulin Homo sapiens 11-18 15793256-8 2005 Preincubation of myotubes with the p38 MAPK inhibitor SB203580 reduced insulin- and PPARdelta-mediated increase in glucose uptake, whereas the mitogen-activated protein kinase kinase inhibitor PD98059 was without effect. Glucose 115-122 insulin Homo sapiens 71-78 15857224-0 2005 Optimal insulin pump dosing and postprandial glycemia following a pizza meal using the continuous glucose monitoring system. Glucose 98-105 insulin Homo sapiens 8-15 15857228-13 2005 CONCLUSIONS: A new GUI that incorporates a novel glucose predicting engine is intended for all insulin-treated patients with diabetes. Glucose 49-56 insulin Homo sapiens 95-102 15857232-1 2005 BACKGROUND: The Bergman Minimal Model enables estimation of two key indices of glucose/ insulin dynamics: glucose effectiveness and insulin sensitivity. Glucose 79-86 insulin Homo sapiens 88-95 15857232-1 2005 BACKGROUND: The Bergman Minimal Model enables estimation of two key indices of glucose/ insulin dynamics: glucose effectiveness and insulin sensitivity. Glucose 79-86 insulin Homo sapiens 132-139 15857232-1 2005 BACKGROUND: The Bergman Minimal Model enables estimation of two key indices of glucose/ insulin dynamics: glucose effectiveness and insulin sensitivity. Glucose 106-113 insulin Homo sapiens 88-95 15863957-0 2005 Quantitative insulin sensitivity check index is a useful indicator of insulin resistance in Japanese metabolically obese, normal-weight subjects with normal glucose tolerance. Glucose 157-164 insulin Homo sapiens 13-20 15863957-0 2005 Quantitative insulin sensitivity check index is a useful indicator of insulin resistance in Japanese metabolically obese, normal-weight subjects with normal glucose tolerance. Glucose 157-164 insulin Homo sapiens 70-77 15728645-2 2005 In the first DIGAMI study, an insulin-based glucose management improved survival. Glucose 44-51 insulin Homo sapiens 30-37 15728645-3 2005 In DIGAMI 2, three treatment strategies were compared: group 1, acute insulin-glucose infusion followed by insulin-based long-term glucose control; group 2, insulin-glucose infusion followed by standard glucose control; and group 3, routine metabolic management according to local practice. Glucose 78-85 insulin Homo sapiens 70-77 15808380-9 2005 The 4 h glucose level, but not the 3 h glucose level, was significantly correlated with insulin resistance indices, such as fasting insulin level, HOMA-IR, Quicky index, and FIRI in the RH group. Glucose 8-15 insulin Homo sapiens 88-95 15665038-7 2005 These data suggest that SB203580 affects glucose turnover by the insulin-responsive GLUT4 transporter in 3T3-L1 adipocytes. Glucose 41-48 insulin Homo sapiens 65-72 15808380-9 2005 The 4 h glucose level, but not the 3 h glucose level, was significantly correlated with insulin resistance indices, such as fasting insulin level, HOMA-IR, Quicky index, and FIRI in the RH group. Glucose 8-15 insulin Homo sapiens 132-139 15934890-4 2005 When injected immediately premeal, insulin glulisine provides superior postprandial blood glucose control compared with regular human insulin (RHI) injected 30 min premeal. Glucose 90-97 insulin Homo sapiens 35-42 15744532-0 2005 Comparative evaluation of simple insulin sensitivity methods based on the oral glucose tolerance test. Glucose 79-86 insulin Homo sapiens 33-40 15853859-0 2005 Beta-cell function and insulin sensitivity contribute to the shape of plasma glucose curve during an oral glucose tolerance test in non-diabetic individuals. Glucose 77-84 insulin Homo sapiens 23-30 15703765-1 2005 We describe the durable correction of streptozotocin-induced murine diabetes by in vivo implantation of primary mouse hepatocytes electroporated ex vivo with a human proinsulin cDNA plasmid construct controlled by glucose and zinc regulatory elements. Glucose 214-221 insulin Homo sapiens 166-176 15703765-2 2005 Transfected hepatocytes increased insulin transgene transcription and secretion within 10-20 min of exposure to 25 mM glucose or 60 microM zinc. Glucose 118-125 insulin Homo sapiens 34-41 15853859-0 2005 Beta-cell function and insulin sensitivity contribute to the shape of plasma glucose curve during an oral glucose tolerance test in non-diabetic individuals. Glucose 106-113 insulin Homo sapiens 23-30 15853859-8 2005 In conclusion, both impaired insulin secretion and insulin resistance may contribute to the underlying mechanisms of the shape of plasma glucose curve in Japanese subjects. Glucose 137-144 insulin Homo sapiens 29-36 15868529-14 2005 CONCLUSION: Adequate glycemic control can be achieved in most diabetics during cardiac surgery using a modified insulin clamp technique provided initial glucose is <300 mg/dL. Glucose 153-160 insulin Homo sapiens 112-119 15821100-9 2005 Steady-state plasma glucose (SSPG) concentrations (a measure of insulin sensitivity) were significantly higher in men carriers of the -514T allele after the consumption of the SFA diet than after the CHO diet and the Mediterranean diet. Glucose 20-27 insulin Homo sapiens 64-71 15604115-1 2005 Phosphoenolpyruvate carboxykinase (PEPCK) transcription is induced by cAMP/protein kinase A (PKA) and glucocorticoids [dexamethasone (Dex)] and is inhibited by insulin to regulate blood glucose. Glucose 186-193 insulin Homo sapiens 160-167 16022189-6 2005 In contrast, the ingestion of 15 g of glucose significantly increased blood glucose and insulin levels, while no hydrogen was detected in the breath. Glucose 38-45 insulin Homo sapiens 88-95 15748626-1 2005 The aim of this study was to investigate the local effect of the insulin-mimetic agent vanadate on glucose metabolism in human skeletal muscle in vivo. Glucose 99-106 insulin Homo sapiens 65-72 15650020-8 2005 These data implicate two insulin-regulated steps in GLUT4 translocation: 1) redistribution of GLUT4 vesicles toward the cell cortex-this process is Akt-independent and is not blocked at 19 C; and 2) docking and/or fusion of GLUT4 vesicles with the PM-this process may be the major Akt-dependent step in the insulin regulation of glucose transport. Glucose 329-336 insulin Homo sapiens 25-32 15809555-3 2005 RESULTS: The myotubes exhibited a dose response for glucose uptake with increasing insulin concentrations; maximal glucose uptake was approximately 1.5-fold over basal. Glucose 52-59 insulin Homo sapiens 83-90 15809555-3 2005 RESULTS: The myotubes exhibited a dose response for glucose uptake with increasing insulin concentrations; maximal glucose uptake was approximately 1.5-fold over basal. Glucose 115-122 insulin Homo sapiens 83-90 15809555-5 2005 This difference persisted at insulin concentrations of 10 and 1000 etaM, although the relative increase in insulin-mediated glucose uptake (fold increase over basal) did not differ between the sedentary and endurance-trained cells. Glucose 124-131 insulin Homo sapiens 107-114 15897476-8 2005 During the oral glucose tolerance test, plasma insulin rose considerably more in ObS than in controls; PDHa and PDP1 activity also increased but remained significantly below normal, and PDHt was unvaried in both groups. Glucose 16-23 insulin Homo sapiens 47-54 15839736-3 2005 METHODS AND FINDINGS: Here we show that brain-derived human neural progenitor cells, exposed to a series of signals that regulate in vivo pancreatic islet development, form clusters of glucose-responsive insulin-producing cells (IPCs). Glucose 185-192 insulin Homo sapiens 204-211 15741351-2 2005 The aim of this study was to compare the HOMA, FGIR, and QUICKI methods for measuring insulin resistance, expressed by oral glucose tolerance test (OGTT) results, among obese children and adolescents. Glucose 124-131 insulin Homo sapiens 86-93 15839736-5 2005 Following transplantation into immunocompromised mice, IPCs released insulin C-peptide upon glucose challenge, remained differentiated, and did not form detectable tumors. Glucose 92-99 insulin Homo sapiens 69-76 15912796-6 2005 In a 75 g oral glucose tolerance test, plasma glucose level at 120 min dropped from 203.3 +/- 41.7 mg/dl to 153.9 +/- 39.5 mg/dl (p = 0.04); the area under the insulin curve up to 120 min (sigma IRI) dropped from 236.9 +/- 170.2 microU x hr/ml to 169.6 +/- 81.3 microU x hr/ml (p = 0.12). Glucose 15-22 insulin Homo sapiens 160-167 15912796-6 2005 In a 75 g oral glucose tolerance test, plasma glucose level at 120 min dropped from 203.3 +/- 41.7 mg/dl to 153.9 +/- 39.5 mg/dl (p = 0.04); the area under the insulin curve up to 120 min (sigma IRI) dropped from 236.9 +/- 170.2 microU x hr/ml to 169.6 +/- 81.3 microU x hr/ml (p = 0.12). Glucose 46-53 insulin Homo sapiens 160-167 15664668-5 2005 GLP-1, Ex-4 and Ex-9, like insulin, stimulated glucose uptake; wortmannin blocked the action of GLP-1, insulin and Ex-9, and reduced that of Ex-4; PD98059 abolished the effect of all peptides/hormones, while rapamycin blocked that of insulin and partially prevented that of GLP-1. Glucose 47-54 insulin Homo sapiens 27-34 15664668-7 2005 In conclusion, GLP-1, like insulin, stimulates glucose uptake, and this involves activation of PI3K/PKB, p44/42 MAPKs, partially p70s6k, and possibly PKC; Ex-4 and Ex-9 both have GLP-1-like effect upon glucose transport, in which both share with GLP-1 an activation of PI3K/PKB--partially in the case of Ex-4--and p44/42 MAPKs but not p70s6k. Glucose 47-54 insulin Homo sapiens 27-34 15774581-8 2005 In addition, subjects carrying the Gln62Arg allele show decreased plasma insulin after an oral glucose challenge. Glucose 95-102 insulin Homo sapiens 73-80 15774581-3 2005 Here, we report, for the first time, to our knowledge, the characterization of KLF11 as a glucose-inducible regulator of the insulin gene. Glucose 90-97 insulin Homo sapiens 125-132 15598661-4 2005 Lipid infusion increased plasma FFA concentration from 0.48 +/- 0.02 to 1.73 +/- 0.43 mm and decreased insulin-stimulated glucose disposal from 8.82 +/- 0.69 to 6.67 +/- 0.66 mg/kg.min, both with p < 0.05. Glucose 122-129 insulin Homo sapiens 103-110 15766512-2 2005 Adiponectin stimulates fatty acids oxidation, reduces plasma triglycerides, and improves glucose metabolism by increasing the insulin sensitivity. Glucose 89-96 insulin Homo sapiens 126-133 15932724-3 2005 Glucose-stimulated insulin secretion during subsequent static incubation was measured using the human insulin ELISA kit. Glucose 0-7 insulin Homo sapiens 19-26 15932724-3 2005 Glucose-stimulated insulin secretion during subsequent static incubation was measured using the human insulin ELISA kit. Glucose 0-7 insulin Homo sapiens 102-109 15932724-4 2005 RESULTS: Glucose-stimulated insulin secretion from human islet cells was significantly reduced after exposed to high concentrations of MMF and FK506 (both P < 0.05). Glucose 9-16 insulin Homo sapiens 28-35 15694391-4 2005 Glucose increases L-glutamate contents and promotes insulin secretion from INS-1E cells. Glucose 0-7 insulin Homo sapiens 52-59 16302580-5 2005 Insulin resistance was estimated by using the homeostasis model assessment (HOMA-IR) score, calculated as fasting insulin (microU/mL) x fasting glucose (mmol/L)/22.5. Glucose 144-151 insulin Homo sapiens 0-7 15670747-2 2005 We observed that the glucose- or interleukin-1beta-induced increase in insulin mRNA was paralleled by an increase in PTB mRNA. Glucose 21-28 insulin Homo sapiens 71-78 15544573-3 2005 Mitochondrial metabolism is crucial for the coupling of amino acid and glucose recognition to the exocytosis of the insulin granules. Glucose 71-78 insulin Homo sapiens 116-123 15713351-9 2005 The mean post-prandial blood glucose concentration at 90 min from self-monitored results was lower with insulin aspart than with human insulin (7.9 +/- 0.4 mmol/l versus 9.3 +/- 0.4 mmol/l, P = 0.011) as was study day post-prandial blood glucose at 90 min (8.4 +/- 0.5 mmol/l versus 9.2 +/- 0.6 mmol/l, P = 0.046). Glucose 29-36 insulin Homo sapiens 104-111 15688355-0 2005 Evaluation of glucose transport and its regulation by insulin in human monocytes using flow cytometry. Glucose 14-21 insulin Homo sapiens 54-61 15688355-1 2005 BACKGROUND: We investigated the effects of insulin on glucose transport in human monocytes using flow cytometry, a method with several advantages over previously used techniques. Glucose 54-61 insulin Homo sapiens 43-50 15688355-10 2005 CONCLUSIONS: Monocytes may be a valid model system to study the effects of insulin on glucose transport. Glucose 86-93 insulin Homo sapiens 75-82 15715891-3 2005 RESULTS: Reductions in visceral fat, liver fat, skeletal muscle fat and homeostasis model assessment (HOMA)-R due to weight loss were associated with increased Delta insulin 30 min/Delta glucose 30 min (DeltaI30/DeltaG30), and reduced area under the curve (AUC) for plasma glucose as seen in OGTT results. Glucose 187-194 insulin Homo sapiens 166-173 15715891-7 2005 CONCLUSION: Insulin response to nateglinide after glucose loading varied greatly in conjunction with weight loss. Glucose 50-57 insulin Homo sapiens 12-19 15717887-14 2005 Metformin improved hyperglycemia through increased insulin-independent glucose uptake in peripheral muscle. Glucose 71-78 insulin Homo sapiens 51-58 15729572-5 2005 PSARL gene expression in human skeletal muscle was correlated with insulin sensitivity as assessed by glucose disposal during a hyperinsulinaemic-euglycaemic clamp. Glucose 102-109 insulin Homo sapiens 67-74 15734833-1 2005 To examine the mechanism by which moderate weight reduction improves basal and insulin-stimulated rates of glucose metabolism in patients with type 2 diabetes, we used (1)H magnetic resonance spectroscopy to assess intrahepatic lipid (IHL) and intramyocellular lipid (IMCL) content in conjunction with hyperinsulinemic-euglycemic clamps using [6,6-(2)H(2)]glucose to assess rates of glucose production and insulin-stimulated peripheral glucose uptake. Glucose 107-114 insulin Homo sapiens 79-86 15734833-6 2005 These improvements in basal and insulin-stimulated hepatic glucose metabolism were associated with an 81 +/- 4% reduction in IHL (P = 0.0009) but no significant change in insulin-stimulated peripheral glucose uptake or IMCL (2.0 +/- 0.3 vs. 1.9 +/- 0.3%; P = 0.21). Glucose 59-66 insulin Homo sapiens 32-39 15734849-2 2005 Glucose-stimulated insulin secretion from type 2 diabetic islets was significantly lower than from control islets, whereas arginine- and glibenclamide-stimulated insulin release was less markedly affected. Glucose 0-7 insulin Homo sapiens 19-26 15734849-6 2005 Nitrotyrosine and 8-hydroxy-2"-deoxyguanosine concentrations, markers of oxidative stress, were significantly higher in type 2 diabetic than control islets, and they were correlated with the degree of glucose-stimulated insulin release impairment. Glucose 201-208 insulin Homo sapiens 220-227 15734849-7 2005 Accordingly, 24-h exposure to glutathione significantly improved glucose-stimulated insulin release and decreased nitrotyrosine concentration, with partial recovery of insulin mRNA expression. Glucose 65-72 insulin Homo sapiens 84-91 15734853-1 2005 The intraislet insulin hypothesis for the signaling of the glucagon secretory response to hypoglycemia states that a decrease in arterial glucose --> a decrease in beta-cell insulin secretion --> a decrease in tonic alpha-cell inhibition by insulin --> an increase in alpha-cell glucagon secretion. Glucose 138-145 insulin Homo sapiens 15-22 15734853-1 2005 The intraislet insulin hypothesis for the signaling of the glucagon secretory response to hypoglycemia states that a decrease in arterial glucose --> a decrease in beta-cell insulin secretion --> a decrease in tonic alpha-cell inhibition by insulin --> an increase in alpha-cell glucagon secretion. Glucose 138-145 insulin Homo sapiens 177-184 15734854-7 2005 The average amount of glucose needed to maintain similar blood glucose levels while infusing the same insulin dosages was higher during DHEA administration (358 +/- 24.7 vs. 320 +/- 24.6 mg/min; P < 0.05), whereas endogenous glucose production was similar. Glucose 22-29 insulin Homo sapiens 102-109 15734868-4 2005 These changes were accompanied by a 13% increase in total body fat oxidation, a 20% decrease in plasma free fatty acid levels, and a 46% increase in insulin-stimulated glucose uptake. Glucose 168-175 insulin Homo sapiens 149-156 15735189-8 2005 CONCLUSIONS: Caffeine consumption is associated with a substantial reduction in insulin-mediated glucose uptake independent of obesity, type 2 diabetes, and chronic exercise. Glucose 97-104 insulin Homo sapiens 80-87 15735201-15 2005 The glucose disposition index (GDI = insulin sensitivity x FPIS) was approximately 86% lower in type 2 diabetic patients than in obese control subjects. Glucose 4-11 insulin Homo sapiens 37-44 15735216-0 2005 Metabolic syndrome and insulin resistance in normal glucose tolerant brazilian adolescents with family history of type 2 diabetes. Glucose 52-59 insulin Homo sapiens 23-30 15739118-6 2005 RESULTS: The administration of 21, 30 and 42 U/kg (based on insulin activity) of insulin/DCK formulation reduced plasma glucose levels by up to 33.0% (median; range 30.6-70.2%), 78.5% (39.4-86.8%) and 75.2% (67.0-87.4%), respectively, compared with baseline levels. Glucose 120-127 insulin Homo sapiens 60-67 15739118-6 2005 RESULTS: The administration of 21, 30 and 42 U/kg (based on insulin activity) of insulin/DCK formulation reduced plasma glucose levels by up to 33.0% (median; range 30.6-70.2%), 78.5% (39.4-86.8%) and 75.2% (67.0-87.4%), respectively, compared with baseline levels. Glucose 120-127 insulin Homo sapiens 81-88 15739118-8 2005 In the OGTT, the insulin/DCK formulation reduced the AUC0-240 for glucose by 30.8% (22.3-54.9%) (p<0.01), and stabilized glycaemia for up to 4 h. CONCLUSIONS/INTERPRETATION: The results of this study demonstrate that the insulin/DCK formulation can be absorbed in the intestine and that it is biologically efficacious. Glucose 66-73 insulin Homo sapiens 17-24 15576463-0 2005 Activation of the mammalian target of rapamycin pathway acutely inhibits insulin signaling to Akt and glucose transport in 3T3-L1 and human adipocytes. Glucose 102-109 insulin Homo sapiens 73-80 15576463-4 2005 Inhibition of mTOR/S6K1 by rapamycin increased insulin-stimulated glucose transport by as much as 45% in 3T3-L1 adipocytes. Glucose 66-73 insulin Homo sapiens 47-54 15576463-8 2005 As in murine cells, rapamycin treatment of human adipocytes inhibited S6K1, blunted Ser636/639 phosphorylation of IRS-1, leading to increased Akt activation and glucose uptake by insulin. Glucose 161-168 insulin Homo sapiens 179-186 15576463-12 2005 Taken together, these results indicate that the mTOR pathway is an important modulator of the signals involved in the acute regulation of insulin-stimulated glucose transport in 3T3-L1 and human adipocytes. Glucose 157-164 insulin Homo sapiens 138-145 15752921-1 2005 The ability of insulin to stimulate glucose disposal varies sixfold to eightfold among apparently healthy individuals. Glucose 36-43 insulin Homo sapiens 15-22 15752921-3 2005 The greater the magnitude of muscle and adipose tissue insulin resistance, the more insulin must be secreted to maintain normal or near-normal glucose tolerance. Glucose 143-150 insulin Homo sapiens 55-62 15752921-3 2005 The greater the magnitude of muscle and adipose tissue insulin resistance, the more insulin must be secreted to maintain normal or near-normal glucose tolerance. Glucose 143-150 insulin Homo sapiens 84-91 16147578-5 2005 All patients admitted with SAH were treated with insulin to control plasma glucose with a target range of 5.0-7.0 mmol/l. Glucose 75-82 insulin Homo sapiens 49-56 15974246-4 2005 METHODS: Rat hepatocytes were transduced with adenovirus expressing a glucose-responsive human insulin transgene and cultured in high-glucose and high-insulin conditions. Glucose 70-77 insulin Homo sapiens 95-102 16296759-1 2005 Closed-loop insulin delivery in individuals with diabetes can potentially lead to near-normal glucose profiles. Glucose 94-101 insulin Homo sapiens 12-19 15772782-1 2005 Coronary vasomotor response to acetylcholine infusion was studied in a 69-year-old currently smoking man with enhanced insulin response to oral glucose load. Glucose 144-151 insulin Homo sapiens 119-126 15824968-2 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 18-25 insulin Homo sapiens 0-7 15824968-2 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 18-25 insulin Homo sapiens 71-78 15824968-2 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 0-7 15824968-2 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 71-78 15824968-2 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 0-7 15824968-2 2005 Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Glucose 63-70 insulin Homo sapiens 71-78 15824968-6 2005 The plasma glucose-lowering activity of tolbutamide is believed to depend on the secretion of endogenous insulin, which is widely used as an indicator of insulin resistance development. Glucose 11-18 insulin Homo sapiens 105-112 15598698-0 2005 Assessment of insulin sensitivity from measurements in the fasting state and during an oral glucose tolerance test in polycystic ovary syndrome and menopausal patients. Glucose 92-99 insulin Homo sapiens 14-21 15613423-1 2005 Insulin-stimulated glucose transport in skeletal muscle is regarded as a key determinant of insulin sensitivity, yet isolation of this step for quantification in human studies is a methodological challenge. Glucose 19-26 insulin Homo sapiens 0-7 15613423-1 2005 Insulin-stimulated glucose transport in skeletal muscle is regarded as a key determinant of insulin sensitivity, yet isolation of this step for quantification in human studies is a methodological challenge. Glucose 19-26 insulin Homo sapiens 92-99 15613423-9 2005 However, during insulin infusion, a robust and highly significant increase was observed in the kinetics of inward glucose transport; this and the estimated tissue distribution volume for [(11)C]3-OMG increased 6-fold compared with basal conditions. Glucose 114-121 insulin Homo sapiens 16-23 15804854-2 2005 This control scheme is based on fuzzy logic control theory to maintain a normoglycaemic average of 4.5 mmol 1(-1) and the normal conditions for free plasma insulin concentration in severe initial state; in particular, when the diabetic patient is subjected to a glucose meal disturbance or fluctuations in the measured glucose level due to error in the measuring instrument. Glucose 262-269 insulin Homo sapiens 156-163 15736105-2 2005 Recent studies suggest that GPR40 is highly expressed in pancreatic beta cells and insulin-secreting cell lines, and that fatty acids increase intracellular calcium concentration and amplify glucose-stimulated insulin secretion by activating GPR40. Glucose 191-198 insulin Homo sapiens 210-217 15736107-7 2005 In contrast, insulin-mediated whole body glucose disposal improved by 43% after red wine consumption (from 2.79 +/- 0.4 to 4.02 +/- 0.5 mg/kg of lean body mass per minute, P = .02), but did not change in the control group. Glucose 41-48 insulin Homo sapiens 13-20 15736115-1 2005 The metabolic syndrome is characterized by a blunted insulin-mediated glucose uptake in various cell types. Glucose 70-77 insulin Homo sapiens 53-60 15736115-7 2005 Baseline Glut-mediated and Glut-mediated insulin-stimulated glucose uptake by lymphoblasts from the HBP group were significantly lower than by lymphoblasts from the LBP group (cellular insulin resistance). Glucose 60-67 insulin Homo sapiens 41-48 15736115-8 2005 The net increment in Glut-mediated glucose uptake by insulin was inversely correlated with HOMA-R. Glucose 35-42 insulin Homo sapiens 53-60 15736115-10 2005 The net increment in Glut-mediated glucose uptake by insulin in lymphoblasts may be a useful intermediate phenotype to study genetic aspects of the metabolic syndrome. Glucose 35-42 insulin Homo sapiens 53-60 15736120-0 2005 Insulin sensitivity indices of glucose and free fatty acid metabolism in obese children and adolescents in relation to serum lipids. Glucose 31-38 insulin Homo sapiens 0-7 15745783-6 2005 According to a 14-mmol/l (250 mg/dl) threshold glucose level for intervention, rapid insulin was required in 27 of 27 (100%) and 24 of 53 (45%) patients with glycosylated hemoglobin levels higher than 8% and up to 8%, respectively. Glucose 47-54 insulin Homo sapiens 85-92 15741354-11 2005 There was a trend toward a higher incidence of insulin resistance, defined as a fasting glucose/insulin ratio of <7, in the LGA/GDM group at 11 years. Glucose 88-95 insulin Homo sapiens 47-54 15843282-0 2005 Validation of an insulin infusion nomogram for intensive glucose control in critically ill patients. Glucose 57-64 insulin Homo sapiens 17-24 15843282-6 2005 MEASUREMENTS AND MAIN RESULTS: Insulin infusion in the prospective patient group was titrated by the bedside nurse based on a predefined nomogram to attain the target blood glucose level. Glucose 173-180 insulin Homo sapiens 31-38 15649634-3 2005 Mercury exposure causes a modest (compared to insulin) 1.8-fold increase in glucose transport. Glucose 76-83 insulin Homo sapiens 46-53 15649634-7 2005 Activation of p38 and an increase in glucose transport corresponding to an increase in GLUT 1 are indicative the induction of a stress response, which can contribute to the induction of insulin resistance in adipocytes. Glucose 37-44 insulin Homo sapiens 186-193 15649634-9 2005 While the magnitude of the action of mercury is modest, its effects were sustained over many days of exposure and impacted subsequent insulin-mediated glucose transport. Glucose 151-158 insulin Homo sapiens 134-141 15649634-10 2005 Pre-treatment with HgCl2 decreased insulin-mediated glucose transport 1.3-fold suggesting that exposure to mercury may contribute to pathologies associated with glucose homeostasis. Glucose 52-59 insulin Homo sapiens 35-42 15813164-5 2005 The pharmacokinetic properties of the new insulin analogs (eg, insulin lispro, insulin aspart, insulin glargine) offer significant advantages, such as improved control of nocturnal hypoglycemia with basal insulin glargine, and improved postprandial glucose control, with insulin lispro or insulin aspart. Glucose 249-256 insulin Homo sapiens 42-49 15813164-5 2005 The pharmacokinetic properties of the new insulin analogs (eg, insulin lispro, insulin aspart, insulin glargine) offer significant advantages, such as improved control of nocturnal hypoglycemia with basal insulin glargine, and improved postprandial glucose control, with insulin lispro or insulin aspart. Glucose 249-256 insulin Homo sapiens 63-70 15813164-5 2005 The pharmacokinetic properties of the new insulin analogs (eg, insulin lispro, insulin aspart, insulin glargine) offer significant advantages, such as improved control of nocturnal hypoglycemia with basal insulin glargine, and improved postprandial glucose control, with insulin lispro or insulin aspart. Glucose 249-256 insulin Homo sapiens 63-70 15813164-5 2005 The pharmacokinetic properties of the new insulin analogs (eg, insulin lispro, insulin aspart, insulin glargine) offer significant advantages, such as improved control of nocturnal hypoglycemia with basal insulin glargine, and improved postprandial glucose control, with insulin lispro or insulin aspart. Glucose 249-256 insulin Homo sapiens 63-70 15813164-5 2005 The pharmacokinetic properties of the new insulin analogs (eg, insulin lispro, insulin aspart, insulin glargine) offer significant advantages, such as improved control of nocturnal hypoglycemia with basal insulin glargine, and improved postprandial glucose control, with insulin lispro or insulin aspart. Glucose 249-256 insulin Homo sapiens 63-70 15813164-5 2005 The pharmacokinetic properties of the new insulin analogs (eg, insulin lispro, insulin aspart, insulin glargine) offer significant advantages, such as improved control of nocturnal hypoglycemia with basal insulin glargine, and improved postprandial glucose control, with insulin lispro or insulin aspart. Glucose 249-256 insulin Homo sapiens 63-70 15717249-5 2005 The oral glucose tolerance test revealed a noticeable insulin secretion with a pathologically increased insulin/glucose index. Glucose 9-16 insulin Homo sapiens 54-61 15557332-1 2005 Stimulations of glucose transport produced by insulin action, contraction, or through a change in cell energy status are mediated by separate signaling pathways. Glucose 16-23 insulin Homo sapiens 46-53 15557332-3 2005 Electrical stimulation of cardiomyocytes produced a rapid, insulin-like, wortmannin-sensitive stimulation of glucose transport activity, but this occurred without extensive activation of Akt. Glucose 109-116 insulin Homo sapiens 59-66 15550383-1 2005 Insulin stimulates glucose transport in adipocytes and muscle by inducing the redistribution of Glut4 from intracellular locations to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 15550383-7 2005 We further show that adenoviral-mediated overexpression of either rsec6 or rsec8 increases the magnitude of insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 127-134 insulin Homo sapiens 108-115 15550383-9 2005 Collectively, our data support a role for the exocyst in insulin-stimulated glucose transport and suggest a model by which insulin-dependent relocation of the exocyst to the plasma membrane may contribute to the specificity of Glut4 vesicle docking and fusion with the adipocyte plasma membrane. Glucose 76-83 insulin Homo sapiens 57-64 15550383-9 2005 Collectively, our data support a role for the exocyst in insulin-stimulated glucose transport and suggest a model by which insulin-dependent relocation of the exocyst to the plasma membrane may contribute to the specificity of Glut4 vesicle docking and fusion with the adipocyte plasma membrane. Glucose 76-83 insulin Homo sapiens 123-130 15699230-3 2005 OBJECTIVE: We hypothesized that CFRD is associated with increased whole-body protein breakdown, which results in negative protein balance, and that correction of the glucose intolerance with insulin therapy would normalize whole-body protein metabolism. Glucose 166-173 insulin Homo sapiens 191-198 15752952-9 2005 In the insulin-sensitive group regardless of BMI, plasma leptin levels decreased after glucose loading. Glucose 87-94 insulin Homo sapiens 7-14 15752952-10 2005 Plasma glucose, insulin, NE, and BP levels increased in nonobese insulin-sensitive subjects after glucose loading, whereas in obese insulin-sensitive subjects, plasma NE and BP did not change in response to glucose. Glucose 98-105 insulin Homo sapiens 65-72 15752952-10 2005 Plasma glucose, insulin, NE, and BP levels increased in nonobese insulin-sensitive subjects after glucose loading, whereas in obese insulin-sensitive subjects, plasma NE and BP did not change in response to glucose. Glucose 98-105 insulin Homo sapiens 65-72 15454397-5 2005 When rat beta-cells were cultured for 24 h with nontoxic interleukin (IL)-1beta concentrations that suppressed glucose-induced insulin release, cellular GABA content was not decreased and GABA release increased by 90% in the period 8-24 h. These data indicate that a reduction in cellular and medium GABA levels is more sensitive than insulin as a marker for the presence of dead beta-cells in isolated preparations. Glucose 111-118 insulin Homo sapiens 127-134 15479952-0 2005 Tacrolimus suppresses glucose-induced insulin release from pancreatic islets by reducing glucokinase activity. Glucose 22-29 insulin Homo sapiens 38-45 15479952-4 2005 Twenty-four-hour exposure to 3 nM tacrolimus reduced high glucose (16.7 mM)-induced insulin secretion (control 2.14 +/- 0.08 vs. tacrolimus 1.75 +/- 0.02 ng.islet(-1).30 min(-1), P < 0.01) without affecting insulin content. Glucose 58-65 insulin Homo sapiens 84-91 15479952-9 2005 These results indicate that glucose-stimulated insulin release is decreased by chronic exposure to tacrolimus due to reduced ATP production and glycolysis derived from reduced glucokinase activity. Glucose 28-35 insulin Homo sapiens 47-54 15479954-4 2005 Acute insulin response (AIR) to glucose and arginine were, surprisingly, normal in obese (0.3 g/kg glucose: AIR = 246 +/- 119 vs. 255 +/- 61 pM in control; 67 mg/kg arginine: AIR = 230 +/- 124 vs. 214 +/- 85 pM in control) but reduced in obese-STZ animals (0.3 g/kg glucose: AIR = 22 +/- 36, P < 0.01; arginine: AIR = 87 +/- 92 pM, P < 0.05 vs. control). Glucose 32-39 insulin Homo sapiens 6-13 15681946-13 2005 In diabetic patients, the insulin/glucagon ratio increased during glucose infusion to a lesser extent than in the nondiabetic group (P = 0.0014). Glucose 66-73 insulin Homo sapiens 26-33 15700135-6 2005 Adipocytes from db/db mice exhibited a stronger impairment of insulin-stimulated glucose uptake than non-obese and HFD-induced obese mice. Glucose 81-88 insulin Homo sapiens 62-69 15677795-5 2005 Area under the insulin curve (AUC) assessed the cumulative insulin response to oral glucose. Glucose 84-91 insulin Homo sapiens 15-22 15811484-2 2005 In clinical trials, exenatide exhibited glucoregulatory effects (glucose-dependent stimulation of insulin secretion, suppression of inappropriately elevated glucagon secretion, slowing of gastric emptying) in patients with type 2 diabetes mellitus (DM). Glucose 65-72 insulin Homo sapiens 98-105 15677489-2 2005 To identify insulin-resistant patients, we developed decision rules from measurements of obesity, fasting glucose, insulin, lipids, and blood pressure and family history in 2,321 (2,138 nondiabetic) individuals studied with the euglycemic insulin clamp technique at 17 European sites; San Antonio, Texas; and the Pima Indian reservation. Glucose 106-113 insulin Homo sapiens 12-19 15677489-3 2005 The distribution of whole-body glucose disposal appeared to be bimodal, with an optimal insulin resistance cutoff of <28 micromol/min . Glucose 31-38 insulin Homo sapiens 88-95 15667334-1 2005 The enzyme GK (glucokinase), which phosphorylates glucose to form glucose 6-phosphate, serves as the glucose sensor of insulin-producing beta-cells. Glucose 50-57 insulin Homo sapiens 119-126 15667334-1 2005 The enzyme GK (glucokinase), which phosphorylates glucose to form glucose 6-phosphate, serves as the glucose sensor of insulin-producing beta-cells. Glucose 66-73 insulin Homo sapiens 119-126 15667334-3 2005 GK operates in tandem with the K(+) and Ca(2+) channels of the beta-cell membrane, resulting in a threshold for glucose-stimulated insulin release of approx. Glucose 112-119 insulin Homo sapiens 131-138 15677795-5 2005 Area under the insulin curve (AUC) assessed the cumulative insulin response to oral glucose. Glucose 84-91 insulin Homo sapiens 59-66 15677795-6 2005 Acute insulin response to glucose (AIR) was determined by an intravenous glucose tolerance test. Glucose 26-33 insulin Homo sapiens 6-13 15738703-4 2005 During the final phases, the algorithm was used to suggest preprandial insulin doses, with a goal of bringing the postprandial glucose into a predetermined target range within 3-7 days. Glucose 127-134 insulin Homo sapiens 71-78 15677795-6 2005 Acute insulin response to glucose (AIR) was determined by an intravenous glucose tolerance test. Glucose 73-80 insulin Homo sapiens 6-13 15738710-6 2005 At 25 IU (n = 11 doses; eight subjects with three replicates), there was a mean fall in plasma glucose of 20.49%; a greater fall in plasma glucose was seen with higher insulin doses. Glucose 139-146 insulin Homo sapiens 168-175 15688205-3 2005 RESULTS: Insulin therapy significantly reduced plasma glucose [-6.0 (4.3) mmol/l], improved [HbA(1)c [-1.9 (1.8)%], and reversed the BWt lost [3.3 (1.8) kg] before treatment. Glucose 54-61 insulin Homo sapiens 9-16 15738713-8 2005 To evaluate if silicon nanopore membranes changed insulin response patterns for glucose-stimulated islets, macrocapsules were constructed with nanopore membranes and filled with pancreatic islets, and dynamic perifusion studies were performed. Glucose 80-87 insulin Homo sapiens 50-57 15550513-9 2005 Insulin secretion by spermatozoa may provide an autocrine regulation of glucose metabolism based on their energetic needs independent of systemic insulin. Glucose 72-79 insulin Homo sapiens 0-7 15803115-5 2005 The test measured the efficacy of insulin in promoting disposal of the infused glucose load, in which the steady state plasma glucose (SSPG) during the 150-180 min of the test was used as an index of IR. Glucose 79-86 insulin Homo sapiens 34-41 15550506-6 2005 Cirazoline- or insulin-mediated glucose uptake was inhibited by the phosphatidylinositol-3 kinase inhibitor LY294002, suggesting a possible interaction between the alpha1-adrenoceptor and insulin pathways. Glucose 32-39 insulin Homo sapiens 15-22 15550506-6 2005 Cirazoline- or insulin-mediated glucose uptake was inhibited by the phosphatidylinositol-3 kinase inhibitor LY294002, suggesting a possible interaction between the alpha1-adrenoceptor and insulin pathways. Glucose 32-39 insulin Homo sapiens 188-195 15550506-8 2005 Both cirazoline- and insulin-mediated glucose uptake were inhibited by protein kinase C (PKC), phospholipase C, and p38 kinase inhibitors, but not by Erk1/2 inhibitors (despite both treatments being able to phosphorylate Erk1/2). Glucose 38-45 insulin Homo sapiens 21-28 15550513-5 2005 Insulin had an oscillatory secretory pattern involving glucose dose-dependent increases and significant decreases during the blockage of an insulin autocrine effect. Glucose 55-62 insulin Homo sapiens 0-7 15550513-7 2005 Then we evaluated the autocrine effect of sperm insulin on glucose metabolism by studying the activity of glucose-6-phosphate dehydrogenase, the key rate-limiting enzyme in the pentose phosphate pathway. Glucose 59-66 insulin Homo sapiens 48-55 15677494-0 2005 Increased hepatic levels of the insulin receptor inhibitor, PC-1/NPP1, induce insulin resistance and glucose intolerance. Glucose 101-108 insulin Homo sapiens 32-39 15693785-8 2005 Myocardial utilization of glucose as a substrate is variable, depending, among other factors, on serum levels of glucose and insulin. Glucose 26-33 insulin Homo sapiens 125-132 15701568-6 2005 A potent glucose lowering effect is typically observed after IGF-I administration, with improved insulin sensitivity with marked lowering of circulating insulin concentrations, whereas GH therapy is associated with mild compensatory hyperinsulinemia, a reflection of relative insulin resistance. Glucose 9-16 insulin Homo sapiens 97-104 15701568-6 2005 A potent glucose lowering effect is typically observed after IGF-I administration, with improved insulin sensitivity with marked lowering of circulating insulin concentrations, whereas GH therapy is associated with mild compensatory hyperinsulinemia, a reflection of relative insulin resistance. Glucose 9-16 insulin Homo sapiens 153-160 15701568-6 2005 A potent glucose lowering effect is typically observed after IGF-I administration, with improved insulin sensitivity with marked lowering of circulating insulin concentrations, whereas GH therapy is associated with mild compensatory hyperinsulinemia, a reflection of relative insulin resistance. Glucose 9-16 insulin Homo sapiens 153-160 15778928-1 2005 BACKGROUND: Minimal model analysis of the intravenous glucose tolerance test (IVGTT) has been used successfully to demonstrate that patients with chronic heart failure (CHF) are insulin-resistant. Glucose 54-61 insulin Homo sapiens 178-185 15778928-8 2005 CONCLUSION: In studies of patients with CHF, greater precision and discriminatory power of insulin sensitivity estimates is obtained when the basal glucose concentration is taken as the plasma glucose concentration 180 minutes after the start of the IVGTT. Glucose 148-155 insulin Homo sapiens 91-98 15778928-8 2005 CONCLUSION: In studies of patients with CHF, greater precision and discriminatory power of insulin sensitivity estimates is obtained when the basal glucose concentration is taken as the plasma glucose concentration 180 minutes after the start of the IVGTT. Glucose 193-200 insulin Homo sapiens 91-98 23923576-0 2005 Amino acids differentially regulate insulin receptor tyrosine kinase and phosphatidyl inositol-3-OH-kinase activities in human monocytes exposed to high glucose concentration. Glucose 153-160 insulin Homo sapiens 36-43 23923576-2 2005 Since insulin signaling pathway has been shown to be regulated by nutritional supplements, in the present study, we investigated the possible effects of free amino acids, such as lysine, arginine and alanine and their mixture in modulating the insulin receptor tyrosine kinase (IRTK) and phosphatidyl inositol-3-OH-kinase (PI3K) activities and on the changes in actin dynamics in monocytes (MC), exposed to high glucose concentration (25 mM). Glucose 412-419 insulin Homo sapiens 244-251 23923576-13 2005 In summary, our findings suggest that the amino acids apart from their antiglycating property can also modulate/influence the activities of pivotal enzymes that are upstream in the insulin-mediated signal transduction pathway and bring down glucose. Glucose 241-248 insulin Homo sapiens 181-188 15522932-9 2005 These data translated to an unfavorable (leftward) shift in the insulin feedback system for increasing 2-h glucose level (P < 0.005). Glucose 107-114 insulin Homo sapiens 64-71 15528266-4 2005 The effects of insulin (300 ng/ml, 1 h) on glucose uptake were studied in villous fragments. Glucose 43-50 insulin Homo sapiens 15-38 15536160-15 2005 The present data clearly show that PS for glucose is subnormal during steady-state hyperinsulinemia in insulin-resistant type 2 diabetic subjects. Glucose 42-49 insulin Homo sapiens 88-95 15562034-4 2005 In diabetics, insulin-stimulated glucose disposal (Rd) was reduced by 50%, compared with controls (5.4 +/- 0.3 vs. 10.4 +/- 0.5 mg/kg.min, P < 0.01). Glucose 33-40 insulin Homo sapiens 14-21 15759820-5 2005 An oral glucose tolerance test revealed high serum levels of total insulin associated with relatively low levels of free insulin, but not of C-peptide, suggesting binding of the released insulin to autoantibodies. Glucose 8-15 insulin Homo sapiens 67-74 15572432-6 2005 Insulin sensitivity was estimated by homeostasis model assessment index (HOMA(IR)) derived from fasting glucose and insulin concentrations. Glucose 104-111 insulin Homo sapiens 0-7 15690322-7 2005 Insulin resistance (SI) was determined based on the frequently sampled intravenous glucose tolerance test and the MINMOD program. Glucose 83-90 insulin Homo sapiens 0-7 15695109-8 2005 RESULTS: Fasting insulin levels (33.5 +/- 3.8 microU/mL; P <.001) and insulin area under the curve (AUC) during OGTT (536.2 +/- 70.5 microU/mL; P <.01) were higher in women with PCOS, while glucose levels were similar to controls. Glucose 196-203 insulin Homo sapiens 73-80 15690314-5 2005 Insulin-induced hypoglycemia produced a nadir serum glucose value of 36 mg/dL without adequate serum cortisol stimulation, confirming presence of adrenal insufficiency. Glucose 52-59 insulin Homo sapiens 0-7 15690315-1 2005 Homeostasis model assessment of insulin resistance (HOMA-IR) is a less invasive, inexpensive, and less labor-intensive method to measure insulin resistance (IR) as compared with the glucose clamp test. Glucose 182-189 insulin Homo sapiens 32-39 15615809-1 2005 BACKGROUND: Insulin resistance (IR) contributes to the development of glucose intolerance (post-transplant diabetes mellitus or impaired glucose tolerance) following renal transplantation. Glucose 70-77 insulin Homo sapiens 12-19 15655035-8 2005 The primary mechanisms by which adiponectin enhance insulin sensitivity appears to be through increased fatty acid oxidation and inhibition of hepatic glucose production. Glucose 151-158 insulin Homo sapiens 52-59 15792925-6 2005 Upon glucose administration, the increase in serum insulin was greater in angiotensin II-treated mice, 38.8+/-6.5 pmol/l, compared to saline-treated mice, 21.8+/-2.9 pmol/l, but only at 4 weeks of angiotensin II treatment while no difference was observed at 2 weeks of angiotensin II administration. Glucose 5-12 insulin Homo sapiens 51-58 15528266-8 2005 Insulin increased glucose uptake by 182% (n=6, P<0.05) in first trimester fragments, but not in term fragments. Glucose 18-25 insulin Homo sapiens 0-7 15528266-9 2005 CONCLUSIONS: The insulin-regulatable GLUT4 is expressed in the cytosol of first trimester ST compatible with a role for GLUT4 in placental glucose transport in early pregnancy. Glucose 139-146 insulin Homo sapiens 17-24 15539436-2 2005 The hypothesis to be tested in this study is that insulin resistance in the ovary is confined to the metabolic effects of insulin (i.e. glucose uptake and metabolism), whereas the steroidogenic action of insulin remains intact. Glucose 136-143 insulin Homo sapiens 50-57 15539436-2 2005 The hypothesis to be tested in this study is that insulin resistance in the ovary is confined to the metabolic effects of insulin (i.e. glucose uptake and metabolism), whereas the steroidogenic action of insulin remains intact. Glucose 136-143 insulin Homo sapiens 122-129 15539436-2 2005 The hypothesis to be tested in this study is that insulin resistance in the ovary is confined to the metabolic effects of insulin (i.e. glucose uptake and metabolism), whereas the steroidogenic action of insulin remains intact. Glucose 136-143 insulin Homo sapiens 122-129 15539436-7 2005 RESULTS: Insulin-stimulated glucose uptake by cells from anovPCO was attenuated at higher doses of insulin (100 and 1000 ng/ml) compared with that by cells from either ovPCO (P=0.02) or controls (P=0.02). Glucose 28-35 insulin Homo sapiens 9-16 15539436-7 2005 RESULTS: Insulin-stimulated glucose uptake by cells from anovPCO was attenuated at higher doses of insulin (100 and 1000 ng/ml) compared with that by cells from either ovPCO (P=0.02) or controls (P=0.02). Glucose 28-35 insulin Homo sapiens 99-106 15539436-10 2005 CONCLUSIONS: Granulosa-lutein cells from women with anovPCOS are relatively resistant to the effects of insulin-stimulated glucose uptake and utilization compared with those from normal and ovPCO, whilst maintaining normal steroidogenic output in response to physiological doses of insulin. Glucose 123-130 insulin Homo sapiens 104-111 15565284-1 2005 The ATP-sensitive potassium (KATP) channel couples membrane excitability to cellular metabolism and is a critical mediator in the process of glucose-stimulated insulin secretion. Glucose 141-148 insulin Homo sapiens 160-167 15762090-4 2005 In addition, glutamine may also improve glucose metabolism by reducing insulin resistance. Glucose 40-47 insulin Homo sapiens 71-78 15779360-0 2005 [Insulin secretion and insulin sensitivity in subjects with impaired fasting glucose]. Glucose 77-84 insulin Homo sapiens 1-8 15779360-0 2005 [Insulin secretion and insulin sensitivity in subjects with impaired fasting glucose]. Glucose 77-84 insulin Homo sapiens 23-30 15702735-4 2005 A further improvement of glucose control would provisionally seem possible only by using short-acting insulin analogues. Glucose 25-32 insulin Homo sapiens 102-109 15664450-3 2005 Overexpression of FL-Grb10 inhibited insulin-stimulated receptor autophosphorylation and glucose uptake. Glucose 89-96 insulin Homo sapiens 37-44 15662004-1 2005 Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic beta cells. Glucose 28-35 insulin Homo sapiens 86-93 15662004-1 2005 Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic beta cells. Glucose 28-35 insulin Homo sapiens 161-168 15662004-1 2005 Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic beta cells. Glucose 142-149 insulin Homo sapiens 161-168 20641537-9 2004 GLUT4 and HKII are the major transporter and HK isoform in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. Glucose 128-135 insulin Homo sapiens 111-118 15631504-5 2005 Our results indicated that 1 and 2 were the most effective insulin secretagogues among the anthocyanins and anthocyanidins tested at 4 and 10 mM glucose concentrations. Glucose 145-152 insulin Homo sapiens 59-66 15654919-2 2005 GLUT4 expression is exquisitely regulated in muscle and this seems important in the regulation of insulin-stimulated glucose uptake by this tissues. Glucose 117-124 insulin Homo sapiens 98-105 15588682-1 2005 Insulin action is impaired in diabetic patients, which leads to increased hepatic glucose production. Glucose 82-89 insulin Homo sapiens 0-7 15588682-4 2005 In a recent study, several herbs and spices were found to increase glucose uptake into adipocytes, an insulin-like effect. Glucose 67-74 insulin Homo sapiens 102-109 15654919-8 2005 The nature of the intracellular signals that mediate the stimulation of glucose transport in response to insulin or exercise is also reviewed. Glucose 72-79 insulin Homo sapiens 105-112 15654920-7 2005 Acute insulin treatment stimulates glucose transport largely by mediating translocation of GLUT4 to the plasma membrane, involving the activation of IRS-2/PI3K, and the downstream targets Akt and protein kinase C zeta. Glucose 35-42 insulin Homo sapiens 6-13 16492545-14 2005 1, that amylin and insulin secreted in response to meals shut down endogenous production as a source of glucose, in favor of that derived from the meal. Glucose 104-111 insulin Homo sapiens 19-26 16492545-15 2005 Amylin and insulin secreted in response to nutrients already absorbed act as a feedback switch for glucose sourcing. Glucose 99-106 insulin Homo sapiens 11-18 15619409-4 2005 Our data suggest that insulin resistance, defined as a high ratio of triglyceride to high-density lipoprotein, is associated with blunted diurnal blood pressure variation (odds ratio 6.3, 95% confidence interval 2.6 to 16.4, p <0.0001) before the development of abnormal levels of fasting blood glucose. Glucose 298-305 insulin Homo sapiens 22-29 15339744-2 2005 The aim of this study was to assess the impact of GH on insulin-stimulated glucose metabolism and insulin signaling in human skeletal muscle. Glucose 75-82 insulin Homo sapiens 56-63 15339745-3 2005 After oral diazoxide, plasma insulin appeared to decline, as did C-peptide, again associated with dose-related increments in plasma glucose (P < 0.0001) and serum nonesterified fatty acids (P = 0.0141). Glucose 132-139 insulin Homo sapiens 29-36 15339745-7 2005 Thus selective suppression of insulin secretion, without stimulation of glucagon secretion, raised plasma glucose and serum nonesterified fatty acid concentrations. Glucose 106-113 insulin Homo sapiens 30-37 15585595-2 2005 In glucose-induced insulin secretion, the rate of pyruvate carboxylation is very high and correlates more strongly with the glucose concentration the beta-cell is exposed to (and thus with insulin release) than does pyruvate decarboxylation, which produces acetyl-CoA for metabolism in the citric acid cycle to produce ATP. Glucose 3-10 insulin Homo sapiens 19-26 16028335-5 2005 In the HERITAGE cohort, the His111 allele was associated with a lower insulin sensitivity index (P = 0.018) and a higher acute insulin response to glucose (P = 0.0098) in Whites. Glucose 147-154 insulin Homo sapiens 127-134 16011472-1 2005 The ability of insulin to stimulate glucose disposal varies at least sixfold in apparently healthy individuals, and approximately one-third of the population that is most resistant to this action of insulin is at greatly increased risk to develop a number of adverse clinical outcomes. Glucose 36-43 insulin Homo sapiens 15-22 15650413-3 2005 The latter play a key role in the development of late complications of DM, as well as in mediating insulin resistance (i.e., resistance to insulin-mediated glucose uptake by some cells) and impaired insulin secretion. Glucose 156-163 insulin Homo sapiens 99-106 15650413-3 2005 The latter play a key role in the development of late complications of DM, as well as in mediating insulin resistance (i.e., resistance to insulin-mediated glucose uptake by some cells) and impaired insulin secretion. Glucose 156-163 insulin Homo sapiens 139-146 15691219-3 2005 Insulin detemir has a more predictable, protracted, and consistent effect on blood glucose than neutral protamine Hagedorn (NPH) insulin, with less intrapatient variability in glycemic control than NPH insulin or insulin glargine. Glucose 83-90 insulin Homo sapiens 0-7 15695923-1 2005 BACKGROUND: The inability of the newborn to inhibit gluconeogenesis in response to a glucose infusion leading to insulin resistance has been postulated as an important cause of hyperglycaemia observed in premature infants. Glucose 85-92 insulin Homo sapiens 113-120 15695923-2 2005 AIM: The aim of this study was to determine the efficiency and rate of response to continuous insulin infusion in improving glucose tolerance in hyperglycaemic extremely-low-birth-weight (ELBW) neonates (< or =1,000 g) compared to neonates with birth weight >1,000 g (LBW). Glucose 124-131 insulin Homo sapiens 94-101 15695923-6 2005 RESULTS: The duration (hours) of insulin infusion required to normalise blood glucose level was significantly longer in the ELBW group compared to LBW group (p < 0.0001). Glucose 78-85 insulin Homo sapiens 33-40 15486008-4 2005 The insulin resistance was measured by a glucose clamp, and it was compared with daily bioimpedance analyses, which indicated the hydration of the intra/extracellular body fluid spaces. Glucose 41-48 insulin Homo sapiens 4-11 15816204-12 2005 In conclusion, proinsulin may play an important role in glucose control in SU-treated type 2 diabetes, but the effect is reduced in SUf patients. Glucose 56-63 insulin Homo sapiens 15-25 16141714-12 2005 The homeostasis model assessment index (HOMA-R) was calculated as an estimate of insulin resistance from the fasting glucose and insulin serum levels. Glucose 117-124 insulin Homo sapiens 81-88 16454348-5 2005 The cell clusters, when tested in vitro, release insulin in response to glucose and other secretagogues. Glucose 72-79 insulin Homo sapiens 49-56 15654920-8 2005 Tumour necrosis factor (TNF-alpha) caused insulin resistance on glucose uptake by impairing insulin signalling at the level of IRS-2. Glucose 64-71 insulin Homo sapiens 42-49 15654920-8 2005 Tumour necrosis factor (TNF-alpha) caused insulin resistance on glucose uptake by impairing insulin signalling at the level of IRS-2. Glucose 64-71 insulin Homo sapiens 92-99 15654920-11 2005 Rosiglitazone ameliorates insulin resistance provoked by TNF-alpha, completely restoring insulin-stimulated glucose uptake in parallel to the insulin signalling cascade. Glucose 108-115 insulin Homo sapiens 89-96 15654920-11 2005 Rosiglitazone ameliorates insulin resistance provoked by TNF-alpha, completely restoring insulin-stimulated glucose uptake in parallel to the insulin signalling cascade. Glucose 108-115 insulin Homo sapiens 89-96 15654921-3 2005 Acute inhibition of GLUT4-mediated glucose transport, and defective insulin signalling induced by chronic exposure to nelfinavir, are described as cellular mechanisms of insulin resistance. Glucose 35-42 insulin Homo sapiens 170-177 16276080-6 2005 Glucose-potassium-insulin infusion or adjusted insulin infusions each have their proponents: both are effective but both carry a small risk of hypoglycaemia. Glucose 0-7 insulin Homo sapiens 18-25 15638870-2 2005 Glucagon-like peptide-1 (GLP-1) potentiates the insulin response to oral glucose, and its secretion is diminished in Type 2 diabetes. Glucose 73-80 insulin Homo sapiens 48-55 16207130-2 2005 Insulin action, as evaluated by glucose disposal, the insulin sensitivity index, and fasting post-hepatic insulin delivery rate were established. Glucose 32-39 insulin Homo sapiens 0-7 15638874-4 2005 Insulin action was assessed by glucose disappearance (Kg) and insulin sensitivity (SI); insulin secretion by first phase insulin release (FPIR) and disposition index (DI). Glucose 31-38 insulin Homo sapiens 0-7 24790303-7 2005 In some cases, combination therapy with metformin and sulfonylureas or use of insulin is more effective for stabilization of blood glucose values. Glucose 131-138 insulin Homo sapiens 78-85 15586000-6 2005 Recent studies related insulin resistance to glucose metabolism to accelerated fat oxidation and described the reversibility of such alterations after surgical or pharmacologic therapy. Glucose 45-52 insulin Homo sapiens 23-30 16356235-5 2005 However, these antidotal approaches are associated with several shortcomings, including further exacerbation of insulin release by glucose and glucagon, leading only to a temporary beneficial effect and later relapse into hypoglycaemia, as well as the adverse effects of both glucagon and diazoxide. Glucose 131-138 insulin Homo sapiens 112-119 16375734-7 2005 It is relevant to recognize the strong association of the insulin resistance syndrome (IRS) (abdominal obesity, dyslipidaemia, hypertension, raised serum insulin levels and glucose intolerance) with hyperuricaemia. Glucose 173-180 insulin Homo sapiens 58-65 16022672-7 2005 Such cells are significantly different than vascular cells, in which glucose uptake is mostly imparted by insulin-independent mechanisms. Glucose 69-76 insulin Homo sapiens 106-113 17632991-13 2005 Normal serum level glucose was rapidly obtained with insulin treatment. Glucose 19-26 insulin Homo sapiens 53-60 15602651-8 2005 The later marker of insulin resistance was associated with glucose tolerance status. Glucose 59-66 insulin Homo sapiens 20-27 15616016-4 2005 A glucose-potentiated arginine test, performed only in insulin-independent transplant subjects (n = 5), demonstrated significant impairments in the glucose-potentiation slope (P < 0.05) and the maximal response to arginine (AR(max); P < 0.05), a measure of beta-cell secretory capacity. Glucose 2-9 insulin Homo sapiens 55-62 15616016-4 2005 A glucose-potentiated arginine test, performed only in insulin-independent transplant subjects (n = 5), demonstrated significant impairments in the glucose-potentiation slope (P < 0.05) and the maximal response to arginine (AR(max); P < 0.05), a measure of beta-cell secretory capacity. Glucose 148-155 insulin Homo sapiens 55-62 15616023-0 2005 Delayed transcapillary delivery of insulin to muscle interstitial fluid after oral glucose load in obese subjects. Glucose 83-90 insulin Homo sapiens 35-42 15616023-1 2005 Obese subjects exhibit a delay in insulin action and delivery of insulin to muscle interstitial fluid during glucose/insulin infusion. Glucose 109-116 insulin Homo sapiens 65-72 15616023-1 2005 Obese subjects exhibit a delay in insulin action and delivery of insulin to muscle interstitial fluid during glucose/insulin infusion. Glucose 109-116 insulin Homo sapiens 65-72 15616023-7 2005 Obese subjects had a significantly higher plasma insulin level at 90-120 min after oral glucose (398 +/- 57 vs. 224 +/- 37 pmol/l in control subjects; P < 0.05). Glucose 88-95 insulin Homo sapiens 49-56 15616036-7 2005 A further reduction in glucose levels was achieved by administering a recombinant human insulin a few hours after Albulin injection in mice, indicating the potential for Albulin therapy in combination with available fast-acting insulin derivatives. Glucose 23-30 insulin Homo sapiens 88-95 15616036-7 2005 A further reduction in glucose levels was achieved by administering a recombinant human insulin a few hours after Albulin injection in mice, indicating the potential for Albulin therapy in combination with available fast-acting insulin derivatives. Glucose 23-30 insulin Homo sapiens 228-235 15616041-0 2005 A genome scan for fasting insulin and fasting glucose identifies a quantitative trait locus on chromosome 17p: the insulin resistance atherosclerosis study (IRAS) family study. Glucose 46-53 insulin Homo sapiens 115-122 15616242-9 2005 The acute insulin response to glucose, a measure of insulin secretion, increased by 7% in the quartile with the lowest baseline glucose tolerance and decreased by 14% in the quartile with the highest baseline glucose tolerance (P < 0.001). Glucose 30-37 insulin Homo sapiens 10-17 15616242-9 2005 The acute insulin response to glucose, a measure of insulin secretion, increased by 7% in the quartile with the lowest baseline glucose tolerance and decreased by 14% in the quartile with the highest baseline glucose tolerance (P < 0.001). Glucose 30-37 insulin Homo sapiens 52-59 15616242-9 2005 The acute insulin response to glucose, a measure of insulin secretion, increased by 7% in the quartile with the lowest baseline glucose tolerance and decreased by 14% in the quartile with the highest baseline glucose tolerance (P < 0.001). Glucose 128-135 insulin Homo sapiens 10-17 15616242-9 2005 The acute insulin response to glucose, a measure of insulin secretion, increased by 7% in the quartile with the lowest baseline glucose tolerance and decreased by 14% in the quartile with the highest baseline glucose tolerance (P < 0.001). Glucose 128-135 insulin Homo sapiens 10-17 17282316-2 2005 It is being used to assist biomedical and chemical engineering students in visualizing the dynamic variations in blood glucose concentration in response to external variations such as food consumption and insulin administration. Glucose 119-126 insulin Homo sapiens 205-212 15616243-3 2005 beta-Cell compensation for insulin sensitivity was calculated as the product of insulin sensitivity x first-phase insulin secretion, termed glucose disposition index (GDI). Glucose 140-147 insulin Homo sapiens 27-34 15642070-1 2005 Insulin sensitivity and insulin secretion are reciprocally related such that insulin resistance is adapted by increased insulin secretion to maintain normal glucose and lipid homeostasis. Glucose 157-164 insulin Homo sapiens 0-7 15642070-1 2005 Insulin sensitivity and insulin secretion are reciprocally related such that insulin resistance is adapted by increased insulin secretion to maintain normal glucose and lipid homeostasis. Glucose 157-164 insulin Homo sapiens 24-31 15642070-3 2005 Several potential mediators have been suggested to be signals for the beta cells to respond to insulin resistance such as glucose, free fatty acids, autonomic nerves, fat-derived hormones and the gut hormone glucagon-like peptide-1 (GLP-1). Glucose 122-129 insulin Homo sapiens 95-102 15616805-6 2005 As a measure of insulin sensitivity we used estimated glucose disposal rate. Glucose 54-61 insulin Homo sapiens 16-23 15459112-7 2005 Treatment of human islets with a combination of IL-1beta and IFN-gamma (IL-1beta+IFN-gamma), for 48 h and 5 d, resulted in an increase of NO production and the impairment of glucose-stimulated insulin secretion, respectively. Glucose 174-181 insulin Homo sapiens 193-200 16403952-1 2005 Among the putative candidate genes for insulin resistance, the peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) is a transcriptional coactivator of PPARgamma and alpha, regulating a wide range of processes involved in energy production and utilization, such as thermogenesis, liver gluconeogenesis, glucose uptake in muscle. Glucose 331-338 insulin Homo sapiens 39-46 15996336-2 2005 UNLABELLED: Insulin resistance or the impairment of insulin capability to decrease blood glucose levels is seen in approximately 25% of girls with Turner syndrome (TS). Glucose 89-96 insulin Homo sapiens 12-19 15996341-2 2005 Observation of pubertal insulin resistance showed that insulin-stimulated glucose metabolism was approximately 30% lower in a sample of children at Tanner stages II-IV compared with children at Tanner stage I or adults. Glucose 74-81 insulin Homo sapiens 24-31 15996341-2 2005 Observation of pubertal insulin resistance showed that insulin-stimulated glucose metabolism was approximately 30% lower in a sample of children at Tanner stages II-IV compared with children at Tanner stage I or adults. Glucose 74-81 insulin Homo sapiens 55-62 15762190-6 2005 Basal and insulin-stimulated total energy expenditure and rates of protein, lipid and glucose oxidation were unaffected by DHEA. Glucose 86-93 insulin Homo sapiens 10-17 16353672-0 2005 The effect of testosterone supplement on insulin sensitivity, glucose effectiveness, and acute insulin response after glucose load in male type 2 diabetics. Glucose 118-125 insulin Homo sapiens 95-102 16353673-9 2005 Correction of hyperglycemia with 3-month insulin therapy may improve metabolic effect instead of insulin sensitivity, glucose sensitivity, and acute insulin response to glucose load in severe type 2 diabetic patients. Glucose 118-125 insulin Homo sapiens 41-48 16353673-9 2005 Correction of hyperglycemia with 3-month insulin therapy may improve metabolic effect instead of insulin sensitivity, glucose sensitivity, and acute insulin response to glucose load in severe type 2 diabetic patients. Glucose 169-176 insulin Homo sapiens 41-48 15762193-8 2005 Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAIVE, indicating an impaired adaptation of beta-cell function to insulin resistance in LIPO. Glucose 68-75 insulin Homo sapiens 36-43 15664732-3 2005 After the glucose administration to old monkeys, a larger area under the curve of the plasma glucose response, a reduced glucose "disappearance" rate, and a reduced insulin peak (5 min after the glucose administration) were observed in comparison with young animals in similar experiments. Glucose 10-17 insulin Homo sapiens 165-172 16439839-2 2005 Despite (or because of) its simplicity it continues to be used today - both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes mellitus. Glucose 198-205 insulin Homo sapiens 153-182 16439841-3 2005 Alternative indirect measures of insulin sensitivity have been developed that utilize fasting glucose and insulin data in algorithms or computer programs. Glucose 94-101 insulin Homo sapiens 33-40 16439844-3 2005 Research has shown that GH induces insulin resistance by the stimulation of lipolysis and a concomitant switch from oxidation of glucose to oxidation of lipids, during both acute and chronic treatment. Glucose 129-136 insulin Homo sapiens 35-42 15591302-7 2005 Insulin action improved, as evidenced by a 29% increase in glucose disposal rate relative to insulin concentration during the hyperglycemic clamp. Glucose 59-66 insulin Homo sapiens 0-7 15483082-2 2005 To define more precisely the impact of PI therapy on glucose homeostasis in this population, we performed the insulin-modified frequent-sampling iv glucose tolerance test on 33 PI-treated and 15 PI-naive HIV-infected children. Glucose 148-155 insulin Homo sapiens 110-117 15483086-3 2005 Main determinants of beta-cell function on the oral glucose tolerance test were derived from a mathematical model featuring the following: 1) glucose concentration-insulin secretion dose response (glucose sensitivity), 2) a secretion component proportional to the derivative of plasma glucose concentration (rate sensitivity); and 3) a potentiation factor. Glucose 142-149 insulin Homo sapiens 164-171 15483086-3 2005 Main determinants of beta-cell function on the oral glucose tolerance test were derived from a mathematical model featuring the following: 1) glucose concentration-insulin secretion dose response (glucose sensitivity), 2) a secretion component proportional to the derivative of plasma glucose concentration (rate sensitivity); and 3) a potentiation factor. Glucose 142-149 insulin Homo sapiens 164-171 15483086-3 2005 Main determinants of beta-cell function on the oral glucose tolerance test were derived from a mathematical model featuring the following: 1) glucose concentration-insulin secretion dose response (glucose sensitivity), 2) a secretion component proportional to the derivative of plasma glucose concentration (rate sensitivity); and 3) a potentiation factor. Glucose 142-149 insulin Homo sapiens 164-171 15483086-4 2005 When NGT and T2DM were subgrouped by 2-h plasma glucose concentrations, insulin secretion rate revealed an inverted U-shaped pattern, rising through NGT up to IGT and falling off thereafter. Glucose 48-55 insulin Homo sapiens 72-79 15483086-9 2005 In the whole data set, insulin sensitivity and the dynamic parameters of beta-cell function explained 89% of the variability of 2-h plasma glucose levels. Glucose 139-146 insulin Homo sapiens 23-30 16114276-10 2005 It is also plausible that the long-term beneficial effects of GH on body composition will balance the insulin antagonistic effects on glucose metabolism. Glucose 134-141 insulin Homo sapiens 102-109 15937580-0 2005 Insulin responses to the oral glucose tolerance test in women of different ethnicity with polycystic ovary syndrome. Glucose 30-37 insulin Homo sapiens 0-7 15937580-1 2005 OBJECTIVE: To evaluate insulin responses to the oral glucose tolerance test (OGTT) in women of different ethnic origins diagnosed with polycystic ovary syndrome (PCOS). Glucose 53-60 insulin Homo sapiens 23-30 15541479-3 2005 The steroid was also found to diminish the insulin responsiveness of the cells in terms of cell survival, DNA synthesis, glucose transport, and glucose oxidation, this last effect possibly involving reduced phosphatidylinositol 3-kinase (PI3-kinase) activity. Glucose 121-128 insulin Homo sapiens 43-50 15541479-3 2005 The steroid was also found to diminish the insulin responsiveness of the cells in terms of cell survival, DNA synthesis, glucose transport, and glucose oxidation, this last effect possibly involving reduced phosphatidylinositol 3-kinase (PI3-kinase) activity. Glucose 144-151 insulin Homo sapiens 43-50 16125867-4 2005 Specific corrective actions are to stimulate ventilation to improve oxygen availability or to induce insulin resistance to raise blood glucose levels. Glucose 135-142 insulin Homo sapiens 101-108 15562387-0 2005 Endurance training-induced changes in the insulin response to oral glucose are associated with the peroxisome proliferator-activated receptor-gamma2 Pro12Ala genotype in men but not in women. Glucose 67-74 insulin Homo sapiens 42-49 15562387-7 2005 In conclusion, these findings suggest that sedentary men with the PPARgamma2 Pro12Ala variant have lower insulin action on glucose disposal as compared with their counterparts. Glucose 123-130 insulin Homo sapiens 105-112 15947493-3 2005 We assessed insulin sensitivity using the homeostasis model assessment (HOMA): HOMA = (FPGSI x FPI)/22.5, where FPGSI refers to fasting plasma glucose (mmol/l) and FPI refers to fasting plasma insulin (microU/l). Glucose 143-150 insulin Homo sapiens 12-19 16433317-4 2005 Insulin resistance was defined as the cutoff values for the population with normal glucose tolerance and with BMI < 25 kg/m2. Glucose 83-90 insulin Homo sapiens 0-7 16433317-6 2005 The risk of insulin resistance, increased with the category of glucose tolerance, and was the highest when Matsuda index was used. Glucose 63-70 insulin Homo sapiens 12-19 15831061-6 2005 Insulin is regulated by blood glucose and amino acid levels. Glucose 30-37 insulin Homo sapiens 0-7 15649100-3 2005 Adequate control of GH excess by surgery or pharmacologic interventions is associated with decreased insulin resistance, reflected in decreased plasma insulin levels and fasting glucose levels or improved glucose tolerance. Glucose 178-185 insulin Homo sapiens 101-108 15792925-1 2005 OBJECTIVE AND DESIGN: Insulin action was determined in a mouse model of human hypertension via chronic angiotensin II administration followed by a glucose tolerance test. Glucose 147-154 insulin Homo sapiens 22-29 15640720-2 2005 Recent research has highlighted that insulin causes similar changes, but these are absent in insulin resistance, resulting in impaired insulin-mediated muscle glucose uptake. Glucose 159-166 insulin Homo sapiens 37-44 15640720-2 2005 Recent research has highlighted that insulin causes similar changes, but these are absent in insulin resistance, resulting in impaired insulin-mediated muscle glucose uptake. Glucose 159-166 insulin Homo sapiens 93-100 16596816-2 2005 At the cellular level, insulin resistance is defined as a reduced insulin action, which can affect not only glucose uptake, but also gene regulation. Glucose 108-115 insulin Homo sapiens 23-30 16596816-2 2005 At the cellular level, insulin resistance is defined as a reduced insulin action, which can affect not only glucose uptake, but also gene regulation. Glucose 108-115 insulin Homo sapiens 66-73 15702438-0 2005 Acute insulin responses to intravenous glucose and GLP-1 are independent of preceding high-frequency insulin pulse-defects induced by glucose entrainment in healthy humans. Glucose 39-46 insulin Homo sapiens 6-13 15702438-1 2005 The objective of this study was to test the hypothesis that high-frequency oscillations in insulin release is a part of the mechanistic basis of a prompt and adequate insulin response to iv-glucose and GLP-1 exposure. Glucose 190-197 insulin Homo sapiens 91-98 15702438-1 2005 The objective of this study was to test the hypothesis that high-frequency oscillations in insulin release is a part of the mechanistic basis of a prompt and adequate insulin response to iv-glucose and GLP-1 exposure. Glucose 190-197 insulin Homo sapiens 167-174 15702438-5 2005 By frequent blood sampling and analysis of insulin concentration, glucose-induced entrainment was evident in all protocols except in the constant infusion and the very fast-pulse protocol. Glucose 66-73 insulin Homo sapiens 43-50 15702438-6 2005 The first-phase insulin release to glucose and GLP-1-induced insulin release were, however, comparable in the protocols. Glucose 35-42 insulin Homo sapiens 16-23 16366418-2 2005 The aim of this study was to determine insulin response to intravenous glucose load and insulin sensitivity in patients with ankylosing spondylitis (AS). Glucose 71-78 insulin Homo sapiens 39-46 15483099-2 2005 Basal and insulin-stimulated glucose uptakes were measured. Glucose 29-36 insulin Homo sapiens 10-17 15483106-9 2005 There was a highly significant (r = 0.881, P < 0.0001) positive correlation between insulin response during oral glucose tolerance test and basal total testosterone levels. Glucose 116-123 insulin Homo sapiens 87-94 15642492-2 2005 This study assessed the insulin content, glucose-stimulated insulin release, islet cell apoptosis, and mRNA expression of insulin and GLUT-1 in isolated human islets cultured in the presence of therapeutical concentrations of glimepiride (10 microM), glibenclamide (10 microM), or chlorpropamide (600 microM). Glucose 41-48 insulin Homo sapiens 60-67 15642492-2 2005 This study assessed the insulin content, glucose-stimulated insulin release, islet cell apoptosis, and mRNA expression of insulin and GLUT-1 in isolated human islets cultured in the presence of therapeutical concentrations of glimepiride (10 microM), glibenclamide (10 microM), or chlorpropamide (600 microM). Glucose 41-48 insulin Homo sapiens 60-67 15642492-5 2005 In response to an acute challenge with 3.3 and 16.7 mM glucose, insulin release from the control islets accounted for 1.9 +/- 0.5% and 4.9 +/- 1.7% of total insulin content (P<.01), respectively. Glucose 55-62 insulin Homo sapiens 64-71 15642492-5 2005 In response to an acute challenge with 3.3 and 16.7 mM glucose, insulin release from the control islets accounted for 1.9 +/- 0.5% and 4.9 +/- 1.7% of total insulin content (P<.01), respectively. Glucose 55-62 insulin Homo sapiens 157-164 16117426-7 2005 The study revealed a correlation between high insulin level in patients with hyperglycemia, disorder of tolerance to glucose, and type II diabetes, on the one hand, and lipid peroxidation level and dislipidemia, on the other. Glucose 117-124 insulin Homo sapiens 46-53 15603999-5 2005 A two-compartment glucose-insulin system model that accounts for time-varying insulin sensitivity and endogenous glucose removal, along with two different saturation kinetics, is developed and tested in preliminary proof-of-concept clinical trials for adaptive control of blood glucose levels. Glucose 18-25 insulin Homo sapiens 26-33 15603999-7 2005 The bolus-based insulin administration provides a safe approach to glucose level management. Glucose 67-74 insulin Homo sapiens 16-23 18370704-8 2005 This results in a moderate increase in blood pressure, and an acute increase in insulin-mediated glucose disposal. Glucose 97-104 insulin Homo sapiens 80-87 15496505-7 2005 Most prominently, adenoviral gene expression of a dominant-negative PKD isoform, PKD3, primarily inhibits basal glucose uptake and, to a lesser extent, insulin-stimulated glucose uptake, whereas overexpression of wild-type PKD3 significantly enhances basal glucose uptake. Glucose 171-178 insulin Homo sapiens 152-159 15496505-7 2005 Most prominently, adenoviral gene expression of a dominant-negative PKD isoform, PKD3, primarily inhibits basal glucose uptake and, to a lesser extent, insulin-stimulated glucose uptake, whereas overexpression of wild-type PKD3 significantly enhances basal glucose uptake. Glucose 171-178 insulin Homo sapiens 152-159 15496505-9 2005 Taken together, our results indicate that PKD, specifically PKD3, directly contributes to insulin-independent basal glucose uptake in L6 skeletal muscle cells. Glucose 116-123 insulin Homo sapiens 90-97 15619630-2 2005 Gut polypeptides secreted in response to food intake, such as glucagon-like peptide-1 (GLP-1), are potent incretin hormones that enhance the glucose-dependent secretion of insulin from pancreatic beta cells. Glucose 141-148 insulin Homo sapiens 172-179 15809512-6 2005 A hyperinsulinemic- euglycemic clamp technique was applied to keep the blood glucose concentrations normal during insulin infusion. Glucose 77-84 insulin Homo sapiens 7-14 15604945-1 2005 OBJECTIVE: Skeletal muscle glucose utilization (SMGU) can be measured by 18F-FDG PET to characterize insulin resistance. Glucose 27-34 insulin Homo sapiens 101-108 15747323-3 2005 Therapeutics developed to treat non-insulin-dependent diabetes mellitus act as releasing factors of endogenously produced insulin or improve its efficiency mediating the glucose uptake into insulin-dependent tissues. Glucose 170-177 insulin Homo sapiens 36-43 15747323-3 2005 Therapeutics developed to treat non-insulin-dependent diabetes mellitus act as releasing factors of endogenously produced insulin or improve its efficiency mediating the glucose uptake into insulin-dependent tissues. Glucose 170-177 insulin Homo sapiens 122-129 16112958-5 2005 Prevention of insulin resistance by weight loss, diet and exercise is very effective in reducing the progression from glucose intolerance to type 2 diabetes in obese subjects. Glucose 118-125 insulin Homo sapiens 14-21 16026171-4 2005 In large part, exercise-induced changes in the pancreatic secretion of glucagon and insulin are primarily responsible for the stimulation of glucose R(a) during moderate exercise. Glucose 141-148 insulin Homo sapiens 84-91 15898818-13 2005 Further advantages of inhaled insulins are the more rapid onset of insulin action and a mitigation of postprandial glucose excursions. Glucose 115-122 insulin Homo sapiens 30-37 16318400-2 2005 Historically, diabetes has been considered an inadequate insulin response leading to elevated plasma glucose levels with morbidities attributable to hyperglycemia. Glucose 101-108 insulin Homo sapiens 57-64 16318402-1 2005 The "incretin effect" describes the phenomenon of an enhanced insulin response following oral ingestion of glucose compared with that after intravenous administration of glucose, leading to identical postprandial plasma glucose excursions. Glucose 107-114 insulin Homo sapiens 62-69 15727288-4 2005 Increasing plasma insulin concentration was considered to induce acceleration of glucose utilization in leukocytes of fattening steers. Glucose 81-88 insulin Homo sapiens 18-25 15774170-11 2005 So, it is necessary to use insulin to strict control the glucose levels in human sepsis. Glucose 57-64 insulin Homo sapiens 27-34 15504741-0 2004 On the mechanism for neomycin reversal of wortmannin inhibition of insulin stimulation of glucose uptake. Glucose 90-97 insulin Homo sapiens 67-74 15504741-1 2004 Although a number of studies and approaches have indicated that activation of the Ser/Thr kinase called Akt/protein kinase B is critical for the insulin-stimulated increase of glucose uptake in adipocytes, other studies have indicated that this enzyme may play an ancillary role. Glucose 176-183 insulin Homo sapiens 145-152 15504741-6 2004 As previously reported, treatment of 3T3-L1 adipocytes with neomycin prevented the wortmannin inhibition of insulin-stimulated glucose transport. Glucose 127-134 insulin Homo sapiens 108-115 15485876-8 2004 IL-1 beta significantly decreased glucose-stimulated insulin secretion (control, 123.8 +/- 17.7; IL-1 beta, 40.2 +/- 3.9 microunits/ml insulin/islet). Glucose 34-41 insulin Homo sapiens 53-60 15581361-0 2004 Requirements for pYXXM motifs in Cbl for binding to the p85 subunit of phosphatidylinositol 3-kinase and Crk, and activation of atypical protein kinase C and glucose transport during insulin action in 3T3/L1 adipocytes. Glucose 158-165 insulin Homo sapiens 183-190 15581361-1 2004 Cbl is phosphorylated by the insulin receptor and reportedly functions within the flotillin/CAP/Cbl/Crk/C3G/TC10 complex during insulin-stimulated glucose transport in 3T3/L1 adipocytes. Glucose 147-154 insulin Homo sapiens 29-36 15581361-5 2004 Interestingly, these mutants inhibited insulin-induced increases in (a) binding of Cbl to both Crk and the p85 subunit of PI 3-kinase, (b) activation of Cbl-dependent PI 3-kinase, (c) activation and translocation of aPKC to the plasma membrane, (d) translocation of Glut4 to the plasma membrane, (e) and glucose transport. Glucose 304-311 insulin Homo sapiens 39-46 15581361-8 2004 Our findings suggest that (a) Cbl uses pYXXM motifs to simultaneously activate PI 3-kinase and Crk/C3G/TC10 pathways and (b) Cbl, along with IRS-1, functions upstream of PI 3-kinase and aPKCs during insulin-stimulated glucose transport in 3T3/L1 adipocytes. Glucose 218-225 insulin Homo sapiens 199-206 15501029-1 2004 2-(4-Methoxyphenoxy)-5-nitro-N-(4-sulfamoylphenyl)benzamide and close analogues inhibit glucose stimulated insulin release through activation of Kir6.2/SUR1 K(ATP) channels of beta cells. Glucose 88-95 insulin Homo sapiens 107-114 15660196-5 2004 Insulin secretion was estimated during intravenous glucose tolerance test; insulin resistance was assessed by the HOMA index. Glucose 51-58 insulin Homo sapiens 0-7 15753146-1 2004 The many studies on oxidative stress, antioxidant treatment, and diabetic complications have shown that oxidative stress is increased and may accelerate the development of complications through the metabolism of excessive glucose and free fatty acids in diabetic and insulin-resistant states. Glucose 222-229 insulin Homo sapiens 267-274 15460549-1 2004 Diabetes mellitus is now classified as either "type 1" (failure of endogenous insulin production) or "type 2" ("insulin resistance") and can be diagnosed if fasting blood glucose is >6.1 mmol/l (110mg/dl) on two separate occasions or there is unequivocal hyperglycaemia with acute metabolic decompensation or obvious symptoms. Glucose 171-178 insulin Homo sapiens 78-85 15460549-1 2004 Diabetes mellitus is now classified as either "type 1" (failure of endogenous insulin production) or "type 2" ("insulin resistance") and can be diagnosed if fasting blood glucose is >6.1 mmol/l (110mg/dl) on two separate occasions or there is unequivocal hyperglycaemia with acute metabolic decompensation or obvious symptoms. Glucose 171-178 insulin Homo sapiens 112-119 15533774-3 2004 GLP-1 enhances glucose-stimulated insulin secretion and inhibits glucagon secretion, gastric emptying and feeding. Glucose 15-22 insulin Homo sapiens 34-41 15533777-4 2004 Later it was found that GIP is capable of augmenting glucose-stimulated insulin secretion, and subsequent studies provided evidence that, in humans, the peptide predominantly acts as an incretin hormone. Glucose 53-60 insulin Homo sapiens 72-79 15589065-6 2004 Third, the serum fasting insulin level as well as the insulin level after a glucose load, was higher among Japanese-Americans, even when the serum glucose levels were not statistically different as compared to native Japanese. Glucose 76-83 insulin Homo sapiens 54-61 15589065-6 2004 Third, the serum fasting insulin level as well as the insulin level after a glucose load, was higher among Japanese-Americans, even when the serum glucose levels were not statistically different as compared to native Japanese. Glucose 147-154 insulin Homo sapiens 25-32 15589065-8 2004 However, the initial insulin response after a glucose load was low, which was more similar to Japanese people than to Caucasians. Glucose 46-53 insulin Homo sapiens 21-28 15613251-1 2004 To assess the effects of acute dietary saturated fat intake on glucose-induced insulin secretion rate (ISR), measured by the C-peptide deconvolution method, and on insulin clearance and sensitivity, five obese and five normal-weight women (controls) were studied after either a 100 g oral butter load or a 100 ml water load. Glucose 63-70 insulin Homo sapiens 79-86 15613251-6 2004 The data are consistent with the hypothesis that acute excess lipid availability may lead to a compensatory elevation in glucose-induced insulin secretion as a result of the decline in insulin sensitivity and a reduced insulin clearance. Glucose 121-128 insulin Homo sapiens 137-144 15613251-6 2004 The data are consistent with the hypothesis that acute excess lipid availability may lead to a compensatory elevation in glucose-induced insulin secretion as a result of the decline in insulin sensitivity and a reduced insulin clearance. Glucose 121-128 insulin Homo sapiens 185-192 15459091-6 2004 QUICKI and OGIS indicated severe insulin resistance in all individuals with type 2 diabetes and impaired glucose tolerance compared with glucose-tolerant individuals: QUICKI, glucose tolerant, 0.302 (0.002); glucose intolerant, 0.290 (0.002); type 2 diabetes, 0.281 (0.005); P <0.001; OGIS (mL . Glucose 105-112 insulin Homo sapiens 33-40 15823759-9 2004 In addition to strong evidence concerning the effect of adiposity on insulin sensitivity in nonpsychiatric populations, increased adiposity in patients with schizophrenia has been associated with decreases in insulin sensitivity; this and other effects may contribute to increases in plasma glucose concentrations and lipid levels. Glucose 291-298 insulin Homo sapiens 209-216 15823772-16 2004 CONCLUSIONS: In this study in a small, selected population of healthy male subjects under euglycemic conditions, oral insulin spray was associated with a higher C(max), shorter T(max), and faster time to peak glucose uptake compared with SC insulin. Glucose 209-216 insulin Homo sapiens 118-125 15561898-1 2004 Closure of ATP-sensitive K+ channels (KATP channels) is a key step in glucose-stimulated insulin secretion. Glucose 70-77 insulin Homo sapiens 89-96 15561905-3 2004 This stage is characterized by maintenance of differentiated function with intact acute glucose-stimulated insulin secretion (GSIS). Glucose 88-95 insulin Homo sapiens 107-114 15561910-1 2004 The incretin effect denominates the phenomenon that oral glucose elicits a higher insulin response than does intravenous glucose. Glucose 57-64 insulin Homo sapiens 82-89 15561918-3 2004 Both fasting insulin secretion and the total insulin response to oral glucose have the following characteristics: 1) they increase with BMI in an approximately linear fashion, 2) both fat-free and fat mass are significant positive correlates, and 3) BMI exerts a positive effect separate from that of insulin resistance (i.e., obesity may be a state of primary insulin hypersecretion). Glucose 70-77 insulin Homo sapiens 45-52 15561918-3 2004 Both fasting insulin secretion and the total insulin response to oral glucose have the following characteristics: 1) they increase with BMI in an approximately linear fashion, 2) both fat-free and fat mass are significant positive correlates, and 3) BMI exerts a positive effect separate from that of insulin resistance (i.e., obesity may be a state of primary insulin hypersecretion). Glucose 70-77 insulin Homo sapiens 45-52 15561921-2 2004 By closing ATP-sensitive K+ channels (KATP channels) in the plasma membrane, glucose and other metabolized nutrients depolarize beta-cells, stimulate Ca2+ influx, and increase the cytosolic concentration of free Ca2+ ([Ca2+]i), which constitutes the indispensable triggering signal to induce exocytosis of insulin granules. Glucose 77-84 insulin Homo sapiens 306-313 15561944-8 2004 In isolated islets, GH secretagogue receptor blockade and antiserum against acylated ghrelin markedly enhanced glucose-induced increases in insulin release and intracellular Ca2+ concentration ([Ca2+]i), whereas ghrelin at a relatively high concentration (10 nmol/l) suppressed insulin release. Glucose 111-118 insulin Homo sapiens 140-147 15561944-8 2004 In isolated islets, GH secretagogue receptor blockade and antiserum against acylated ghrelin markedly enhanced glucose-induced increases in insulin release and intracellular Ca2+ concentration ([Ca2+]i), whereas ghrelin at a relatively high concentration (10 nmol/l) suppressed insulin release. Glucose 111-118 insulin Homo sapiens 278-285 15561944-11 2004 These findings reveal that endogenous ghrelin in islets acts on beta-cells to restrict glucose-induced insulin release at least partly via attenuation of Ca2+ signaling, and that this insulinostatic action may be implicated in the upward control of blood glucose. Glucose 87-94 insulin Homo sapiens 103-110 15561950-5 2004 The lower fasting insulin concentration was accompanied by a decreased early insulin response to oral glucose. Glucose 102-109 insulin Homo sapiens 18-25 15561950-5 2004 The lower fasting insulin concentration was accompanied by a decreased early insulin response to oral glucose. Glucose 102-109 insulin Homo sapiens 77-84 15562199-1 2004 OBJECTIVE: 1) To evaluate the effect of a single oral dose of hexyl-insulin monoconjugate 2 (HIM2) on the rate of whole-body glucose disposal (Rd) and endogenous glucose production (EGP) in healthy nondiabetic subjects, 2) to examine the reproducibility of HIM2 on glucose metabolism, and 3) to compare the results obtained with HIM2 with those using a bioequivalent dose of subcutaneous lispro insulin. Glucose 125-132 insulin Homo sapiens 68-75 15563976-3 2004 We used a recombinant adeno-associated virus (rAAV) that expresses a single-chain insulin analogue (SIA), which possesses biologically active insulin activity without enzymatic conversion, under the control of hepatocyte-specific l-type pyruvate kinase (LPK) promoter, which regulates SIA expression in response to blood glucose levels. Glucose 321-328 insulin Homo sapiens 82-89 15563978-0 2004 Insulin secretion capacity in the development from normal glucose tolerance to type 2 diabetes. Glucose 58-65 insulin Homo sapiens 0-7 15563978-3 2004 The decline of insulin secretion capacity was significant throughout the development of glucose intolerance from NGT via IGT to DM. Glucose 88-95 insulin Homo sapiens 15-22 15569129-0 2004 Enhancement of insulin-stimulated myocardial glucose uptake in patients with Type 2 diabetes treated with rosiglitazone. Glucose 45-52 insulin Homo sapiens 15-22 15569129-10 2004 RESULTS: Rosiglitazone increased insulin-stimulated myocardial glucose uptake by 38% (from 38.7 +/- 3.4 to 53.3 +/- 3.6 micromol 100 g(-1) min(-1), P = 0.004) and whole body glucose uptake by 36% (P = 0.01), while metformin treatment had no significant effect on myocardial (40.5 +/- 3.5 vs. 36.6 +/- 5.2, NS) or whole body glucose uptake. Glucose 63-70 insulin Homo sapiens 33-40 15569129-10 2004 RESULTS: Rosiglitazone increased insulin-stimulated myocardial glucose uptake by 38% (from 38.7 +/- 3.4 to 53.3 +/- 3.6 micromol 100 g(-1) min(-1), P = 0.004) and whole body glucose uptake by 36% (P = 0.01), while metformin treatment had no significant effect on myocardial (40.5 +/- 3.5 vs. 36.6 +/- 5.2, NS) or whole body glucose uptake. Glucose 174-181 insulin Homo sapiens 33-40 15569129-10 2004 RESULTS: Rosiglitazone increased insulin-stimulated myocardial glucose uptake by 38% (from 38.7 +/- 3.4 to 53.3 +/- 3.6 micromol 100 g(-1) min(-1), P = 0.004) and whole body glucose uptake by 36% (P = 0.01), while metformin treatment had no significant effect on myocardial (40.5 +/- 3.5 vs. 36.6 +/- 5.2, NS) or whole body glucose uptake. Glucose 174-181 insulin Homo sapiens 33-40 15569129-15 2004 CONCLUSIONS: In addition to the improvement in whole body insulin sensitivity, rosiglitazone treatment enhances insulin stimulated myocardial glucose uptake in patients with Type 2 diabetes, most probably due to its suppression of the serum FFAs. Glucose 142-149 insulin Homo sapiens 112-119 15569134-2 2004 An Ala/Val polymorphism at codon 98 of the hepatocyte nuclear factor-1alpha (HNF-1alpha) gene has been associated with decreased serum insulin and C-peptide responses during an oral glucose tolerance test (OGTT) in glucose-tolerant subjects. Glucose 182-189 insulin Homo sapiens 135-142 15569134-2 2004 An Ala/Val polymorphism at codon 98 of the hepatocyte nuclear factor-1alpha (HNF-1alpha) gene has been associated with decreased serum insulin and C-peptide responses during an oral glucose tolerance test (OGTT) in glucose-tolerant subjects. Glucose 182-189 insulin Homo sapiens 147-156 15569134-2 2004 An Ala/Val polymorphism at codon 98 of the hepatocyte nuclear factor-1alpha (HNF-1alpha) gene has been associated with decreased serum insulin and C-peptide responses during an oral glucose tolerance test (OGTT) in glucose-tolerant subjects. Glucose 215-222 insulin Homo sapiens 135-142 15569134-3 2004 The aims of the present study were to evaluate the influence of the polymorphism on the serum insulin and C-peptide responses to an OGTT in glucose-tolerant women with and without previous GDM and to investigate if this polymorphism is associated with GDM. Glucose 140-147 insulin Homo sapiens 94-101 15569134-3 2004 The aims of the present study were to evaluate the influence of the polymorphism on the serum insulin and C-peptide responses to an OGTT in glucose-tolerant women with and without previous GDM and to investigate if this polymorphism is associated with GDM. Glucose 140-147 insulin Homo sapiens 106-115 15569134-6 2004 Among 117 glucose-tolerant women with previous GDM, 10 carriers of the Ala/Val98 polymorphism had a non-significant 27% and 22% reduction in serum C-peptide and insulin levels, respectively, at 30 min during an OGTT. Glucose 10-17 insulin Homo sapiens 147-156 15569134-6 2004 Among 117 glucose-tolerant women with previous GDM, 10 carriers of the Ala/Val98 polymorphism had a non-significant 27% and 22% reduction in serum C-peptide and insulin levels, respectively, at 30 min during an OGTT. Glucose 10-17 insulin Homo sapiens 161-168 15569134-9 2004 However, the codon 98 variant is associated with a significant impairment of serum insulin and C-peptide responses during an OGTT in glucose-tolerant women without previous GDM. Glucose 133-140 insulin Homo sapiens 95-104 15662548-9 2004 Alone, D: -glucose did not relax PCA, but did augment the effect of insulin on NO release and vasodilation. Glucose 11-18 insulin Homo sapiens 68-75 15662548-11 2004 This mechanism may be responsible for glucose-enhanced, insulin-dependent increases in tissue perfusion (including coronary blood-flow), thus accelerating glucose extraction from the blood circulation to limit the adverse vascular effects of prolonged hyperglycaemia. Glucose 38-45 insulin Homo sapiens 56-63 15662548-11 2004 This mechanism may be responsible for glucose-enhanced, insulin-dependent increases in tissue perfusion (including coronary blood-flow), thus accelerating glucose extraction from the blood circulation to limit the adverse vascular effects of prolonged hyperglycaemia. Glucose 155-162 insulin Homo sapiens 56-63 15758246-9 2004 These results suggest that, in a clinical setting, the early insulin response is closely associated with both postprandial glucose and postprandial lipid metabolism in Japanese patients with type 2 diabetes. Glucose 123-130 insulin Homo sapiens 61-68 15841797-2 2004 The aim of this study was to answer the question if insulin sensitivity indices (ISI) calculated from standard 3-sampled oral glucose tolerance test (3SoGTT) provide adequate information compared to the outcome when calculated from frequently sampled oral glucose tolerance test (FSoGTT). Glucose 126-133 insulin Homo sapiens 52-59 15841797-4 2004 Selected indices of insulin sensitivity were calculated using plasma glucose and insulin concentrations from FSoGTT and from samples obtained in 0, 60 and 120 min of the oGTT (3SoGTT). Glucose 69-76 insulin Homo sapiens 20-27 15543161-11 2004 Moreover, fasting insulin decreased from 30.0+/-20.4 to 8.6+/-2.9 microUI/ml (P<0.001) after 3 y, while insulin levels after (120 min) oral glucose load decreased from 105.5+/-61.5 to 12.0+/-6.0 microUI/ml (P<0.001). Glucose 143-150 insulin Homo sapiens 107-114 15561346-3 2004 Using factor analysis, metabolic syndrome and sub-clinical inflammation scores were derived from baseline measurements, which included an oral glucose tolerance test-derived measure of insulin resistance. Glucose 143-150 insulin Homo sapiens 185-192 15592487-4 2004 This interrupts the insulin signalling pathway leading to the stimulation of glucose transport. Glucose 77-84 insulin Homo sapiens 20-27 15592487-6 2004 Long-term exposure to free fatty acids (FFA) leads to an increased basal and blunted glucose-stimulated insulin secretion by affecting gene expression, increase in K(ATP) channel activity, and uncoupling of the mitochondria. Glucose 85-92 insulin Homo sapiens 104-111 15602695-4 2004 Cells of islet-like clusters show glucose-dependent insulin release at terminal stage. Glucose 34-41 insulin Homo sapiens 52-59 15565072-8 2004 Insulin concentrations peaked at 40 minutes in the glucose drink group (285.5+/-18.3 pmol) and was similar in all but the peanuts group (130.5+/-14.3 pmol) ( P <.05). Glucose 51-58 insulin Homo sapiens 0-7 15258132-0 2004 Levodopa with carbidopa diminishes glycogen concentration, glycogen synthase activity, and insulin-stimulated glucose transport in rat skeletal muscle. Glucose 110-117 insulin Homo sapiens 91-98 15258132-2 2004 We examined the effects of levodopa-carbidopa on glycogen concentration, glycogen synthase activity, and insulin-stimulated glucose transport in skeletal muscle, the predominant insulin-responsive tissue. Glucose 124-131 insulin Homo sapiens 105-112 15258132-3 2004 In isolated muscle, levodopa-carbidopa completely prevented insulin-stimulated glycogen accumulation and glucose transport. Glucose 105-112 insulin Homo sapiens 60-67 15546921-1 2004 Insulin-stimulated glucose uptake involves the recruitment of the glucose transporter 4 isoform (GLUT4) from an intracellular location to the plasma membrane of fat and muscle cells. Glucose 19-26 insulin Homo sapiens 0-7 15578099-1 2004 A critical defect in type 2 diabetes is impaired insulin-stimulated glucose transport and metabolism in muscle and adipocytes. Glucose 68-75 insulin Homo sapiens 49-56 15578099-7 2004 While insulin action on hepatic glucose production and gluconeogenic enzymes is impaired, hepatic glucokinase expression, incorporation of 14C-glucose into lipids, and hepatic VLDL-triglyceride release are increased. Glucose 32-39 insulin Homo sapiens 6-13 15579753-1 2004 Responses of whole body glucose disposal (GDR) and protein breakdown (PB) to physiological insulin levels are altered in nondiabetic elderly subjects. Glucose 24-31 insulin Homo sapiens 91-98 15579787-4 2004 Insulin sensitivity was determined by euglycemic hyperinsulinemic clamp and expressed as glucose infusion rate (GIR). Glucose 89-96 insulin Homo sapiens 0-7 15579799-7 2004 glucose tolerance test, and insulin secretion was measured as the acute insulin response to glucose and to a glucagon stimulation test. Glucose 92-99 insulin Homo sapiens 28-35 15579799-9 2004 Both acute insulin response to glucose and the C peptide response to glucagon stimulation test improved by 3 wk (P = 0.02 vs. baseline), and improvements were maintained at 3 months (P = 0.02 vs. baseline). Glucose 31-38 insulin Homo sapiens 11-18 15698938-2 2004 Diabetes is primarily caused by pancreatic damage, which reduces insulin secretion, but glucose tolerance is also modified by factors that alter insulin resistance, such as intercurrent illness and infection. Glucose 88-95 insulin Homo sapiens 145-152 15590971-2 2004 Here we investigated the long-term effects of HIV-1 protease inhibitors on glucose-stimulated insulin secretion from beta cells and explored whether altered insulin secretion might be related to altered insulin signaling. Glucose 75-82 insulin Homo sapiens 94-101 15590971-8 2004 In conclusion, certain HIV-1 protease inhibitors, such as ritonavir, nelfinavir and saquinavir, not only induce peripheral insulin resistance, but also impair glucose-stimulated insulin secretion from beta cells. Glucose 159-166 insulin Homo sapiens 178-185 15754730-0 2004 Human resistin gene polymorphism is associated with visceral obesity and fasting and oral glucose stimulated C-peptide in the Quebec Family Study. Glucose 90-97 insulin Homo sapiens 109-118 15754730-10 2004 These results suggest that in men, the human resistin gene is associated with reduced amount of visceral obesity and lower insulin secretory responses to a glucose load. Glucose 156-163 insulin Homo sapiens 123-130 15591035-0 2004 Transcriptional regulation of glucose-6-phosphatase catalytic subunit promoter by insulin and glucose in the carnivorous fish, Sparus aurata. Glucose 30-37 insulin Homo sapiens 82-89 15591035-8 2004 Transfection experiments in HepG2 cells showed that insulin repressed S. aurata G6pc under high-glucose conditions. Glucose 96-103 insulin Homo sapiens 52-59 23570175-7 2004 New research into the pathophysiology of diabetes indicates that multiple hormones--not just insulin and glucagon but amylin, GLP-1 (a glucagon-like peptide), and others--are involved in the regulation of plasma glucose levels, providing insight into why even insulin is often ineffective in helping patient with diabetes achieve their glycemic goals. Glucose 212-219 insulin Homo sapiens 260-267 15563754-6 2004 This review discusses the possibility of targeting cAMP mechanisms in the treatment of type 2 diabetes mellitus, in which insulin release in response to glucose is impaired. Glucose 153-160 insulin Homo sapiens 122-129 15645698-2 2004 The insulin dosage calculations, however, involve ratios of insulin to carbohydrate and corrections for high blood glucose values, and are labor-intensive and prone to error. Glucose 115-122 insulin Homo sapiens 4-11 16754138-1 2004 Implantable insulin delivery pumps are a response to the search for an insulin therapy that would be more physiological, more comfortable and, finally, better adapted to instantaneous insulin needs by their connection to a long term glucose sensor. Glucose 233-240 insulin Homo sapiens 12-19 16754138-1 2004 Implantable insulin delivery pumps are a response to the search for an insulin therapy that would be more physiological, more comfortable and, finally, better adapted to instantaneous insulin needs by their connection to a long term glucose sensor. Glucose 233-240 insulin Homo sapiens 71-78 16754138-3 2004 The forthcoming availability on the market of the specific insulin formulation they require and the present development of glucose sensors are two favourable conditions for the diffusion of this technology aiming at an improved diabetes treatment. Glucose 123-130 insulin Homo sapiens 59-66 15572494-1 2004 OBJECTIVE: Fetal insulin concentrations reflect the intrauterine glucose load given the fetus by the mother. Glucose 65-72 insulin Homo sapiens 17-24 15853117-10 2004 Insulin resistance was estimated on the basis of fasting glucose and insulin, using the glucose homeostasis model (HOMA scores). Glucose 57-64 insulin Homo sapiens 0-7 15853117-10 2004 Insulin resistance was estimated on the basis of fasting glucose and insulin, using the glucose homeostasis model (HOMA scores). Glucose 88-95 insulin Homo sapiens 0-7 15853121-2 2004 Several formulae developed from measurements in the fasting state and during the oral glucose tolerance test (OGTT) have been proposed to assess insulin sensitivity. Glucose 86-93 insulin Homo sapiens 145-152 15590582-10 2004 In the insulin-treated group, fasting blood glucose was a significant predictor of cataract. Glucose 44-51 insulin Homo sapiens 7-14 15660867-2 2004 To determine the optimal dose of insulin, the authors designed algorithms based on self-monitored blood glucose levels. Glucose 104-111 insulin Homo sapiens 33-40 15660867-3 2004 METHODS: Each dose of insulin was composed of two components: a basal dose determined on the basis of blood glucose levels over the previous two days and an additional dose determined on the basis of blood glucose level just before insulin injection. Glucose 108-115 insulin Homo sapiens 22-29 15660867-3 2004 METHODS: Each dose of insulin was composed of two components: a basal dose determined on the basis of blood glucose levels over the previous two days and an additional dose determined on the basis of blood glucose level just before insulin injection. Glucose 206-213 insulin Homo sapiens 22-29 15660867-10 2004 CONCLUSIONS: Algorithms developed on the basis of self-monitored blood glucose levels are useful in determining the optimal dose of insulin and can improve glycemic control and lipid metabolism. Glucose 71-78 insulin Homo sapiens 132-139 15733404-3 2004 RESULTS: Basal rates were similar, but there were significant decreases in insulin-stimulated glucose incorporation into glycogen in PCOS cells, a metabolic action of insulin. Glucose 94-101 insulin Homo sapiens 75-82 15733404-3 2004 RESULTS: Basal rates were similar, but there were significant decreases in insulin-stimulated glucose incorporation into glycogen in PCOS cells, a metabolic action of insulin. Glucose 94-101 insulin Homo sapiens 167-174 16114550-3 2004 RESULTS: After being induced by insulin or glucose for 24 h and 48 h, GPI-PLD activities and rate of CDC killing in the insulin, insulin + glucose groups significantly increased. Glucose 43-50 insulin Homo sapiens 120-127 16114550-3 2004 RESULTS: After being induced by insulin or glucose for 24 h and 48 h, GPI-PLD activities and rate of CDC killing in the insulin, insulin + glucose groups significantly increased. Glucose 43-50 insulin Homo sapiens 120-127 16114550-3 2004 RESULTS: After being induced by insulin or glucose for 24 h and 48 h, GPI-PLD activities and rate of CDC killing in the insulin, insulin + glucose groups significantly increased. Glucose 139-146 insulin Homo sapiens 32-39 15364916-1 2004 Leptin and insulin share some hypothalamic signaling molecules, but their central administration induces different effects on hepatic glucose fluxes. Glucose 134-141 insulin Homo sapiens 11-18 15364916-2 2004 Acute insulin infusion in the third cerebral ventricle inhibits endogenous glucose production (GP), whereas acute leptin infusion stimulates gluconeogenesis but does not alter GP because of a compensatory decrease in glycogenolysis. Glucose 75-82 insulin Homo sapiens 6-13 15548778-4 2004 Insulin sensitivity was measured with the use of paired insulin and glucose data obtained by frequent measurements during intravenous glucose-tolerance tests. Glucose 68-75 insulin Homo sapiens 0-7 15548778-4 2004 Insulin sensitivity was measured with the use of paired insulin and glucose data obtained by frequent measurements during intravenous glucose-tolerance tests. Glucose 134-141 insulin Homo sapiens 0-7 15491793-5 2004 Insulin secretion was stimulated significantly more by oral as compared to intravenous glucose in both groups (p<0.0001). Glucose 87-94 insulin Homo sapiens 0-7 15339920-10 2004 Moreover, chronic CT-1 treatment resulted in the development of insulin resistance as judged by a decrease in insulin-stimulated glucose uptake. Glucose 129-136 insulin Homo sapiens 110-117 15776968-2 2005 The joker glucose function, determined by individual balance between the mentioned functions, can be an important modifier of human pathology and, at the same time, a target for correcting measures implying the combination of insulin-sensitizing and antigenotoxic measures. Glucose 10-17 insulin Homo sapiens 226-233 15371448-7 2004 An insulin-resistant state was induced by exposing cells to 30 mm glucose as indicated by decreased phosphorylation of Akt and its downstream effector, glycogen synthase kinase 3alpha/beta. Glucose 66-73 insulin Homo sapiens 3-10 15371448-12 2004 Inhibition of AMPK may contribute to lipid accumulation induced by high concentrations of glucose associated with insulin resistance. Glucose 90-97 insulin Homo sapiens 114-121 15762190-9 2005 Insulin sensitivity as expressed by the glucose infusion rate during the euglycemic clamp was similar after placebo and DHEA. Glucose 40-47 insulin Homo sapiens 0-7 15568633-0 2004 [Long acting insulin analogs: possibly more stable glucose regulation]. Glucose 51-58 insulin Homo sapiens 13-20 15538371-4 2004 Here we show that overexpression of miR-375 suppressed glucose-induced insulin secretion, and conversely, inhibition of endogenous miR-375 function enhanced insulin secretion. Glucose 55-62 insulin Homo sapiens 71-78 15538371-7 2004 Inhibition of Mtpn by small interfering (si)RNA mimicked the effects of miR-375 on glucose-stimulated insulin secretion and exocytosis. Glucose 83-90 insulin Homo sapiens 102-109 15577646-5 2004 RESULTS: The mean insulin-stimulated glucose disposal (mg/min per kg body weight) per unit insulin (microU/ml) (M/I) was 9.88, 9.80 and 7.52 for placebo, ATV and LPV/r, respectively (SEM, 0.84 for all). Glucose 37-44 insulin Homo sapiens 91-98 15573890-6 2004 Insulin-induced endothelium-dependent dilation of these arterioles is inhibited by high glucose and triglyceride levels preventing metabolic effect of insulin on the parenchymal cells surrounded by nutritive capillaries and leading this way to insulin resistance. Glucose 88-95 insulin Homo sapiens 0-7 15573890-6 2004 Insulin-induced endothelium-dependent dilation of these arterioles is inhibited by high glucose and triglyceride levels preventing metabolic effect of insulin on the parenchymal cells surrounded by nutritive capillaries and leading this way to insulin resistance. Glucose 88-95 insulin Homo sapiens 151-158 15573890-6 2004 Insulin-induced endothelium-dependent dilation of these arterioles is inhibited by high glucose and triglyceride levels preventing metabolic effect of insulin on the parenchymal cells surrounded by nutritive capillaries and leading this way to insulin resistance. Glucose 88-95 insulin Homo sapiens 244-251 15577646-3 2004 METHODS: Randomized, double-blind, crossover study of the effect of 5 days of administering ATV, lopinavir/ritonavir (LPV/r) or placebo on insulin-stimulated glucose disposal in 30 healthy HIV-negative subjects. Glucose 158-165 insulin Homo sapiens 139-146 15577646-5 2004 RESULTS: The mean insulin-stimulated glucose disposal (mg/min per kg body weight) per unit insulin (microU/ml) (M/I) was 9.88, 9.80 and 7.52 for placebo, ATV and LPV/r, respectively (SEM, 0.84 for all). Glucose 37-44 insulin Homo sapiens 18-25 15059773-15 2004 These findings provide a novel mechanism by which insulin may determine blood flow and glucose disposal in skeletal muscle. Glucose 87-94 insulin Homo sapiens 50-57 15530168-3 2004 Exceeding the CVATT may result in a number of metabolic disturbances such as insulin resistance to glucose uptake by cells. Glucose 99-106 insulin Homo sapiens 77-84 15631772-5 2004 RESULTS: Decreasing glucose tolerance was associated with insulin resistance, beta cell function and DI. Glucose 20-27 insulin Homo sapiens 58-65 15198936-7 2004 Normalization of JNK activity in hepatocytes isolated from HSD rats improved insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS) proteins and insulin suppression of glucose release. Glucose 193-200 insulin Homo sapiens 77-84 15509521-9 2004 Furthermore, HCV core suppressed insulin-induced phosphorylation of p85 subunit of phosphatidylinositol 3-kinase and Akt, activation of 6-phosphofructo-2-kinase, and glucose uptake. Glucose 166-173 insulin Homo sapiens 33-40 15479216-12 2004 In humans, acute and prolonged effects of FAs on glucose-stimulated insulin secretion have been widely investigated as well as the effect of high-fat diets on insulin sensitivity and secretion and on the development of type 2 diabetes. Glucose 49-56 insulin Homo sapiens 68-75 15479774-6 2004 This article reviews the current insulin analogs available on the market and insulin regimens that are designed to mimic the pancreatic beta-cells" response to a glucose load. Glucose 162-169 insulin Homo sapiens 77-84 15591007-9 2004 In conclusion, both L-carnitine and ALC are effective in improving insulin-mediated glucose disposal either in healthy subjects or in type 2 diabetic patients. Glucose 84-91 insulin Homo sapiens 67-74 15531149-3 2004 MATERIAL AND METHODS: A virtual environment comprising a model of the carbohydrate metabolism and models of the insulin pump and the glucose sensor is employed to simulate individual glucose excursions in subjects with type 1 diabetes. Glucose 183-190 insulin Homo sapiens 112-119 15504967-3 2004 The insulin sensitivity index (S(i)) and the acute insulin response to glucose (AIRg) were determined, and from these beta-cell function was estimated as the disposition index (S(i) x AIRg). Glucose 71-78 insulin Homo sapiens 51-58 15498083-8 2004 CONCLUSIONS: The rise in blood glucose levels during the early morning hours in women with GDM and chronic hypertension could reflect greater insulin resistance and sympathetic overactivity. Glucose 31-38 insulin Homo sapiens 142-149 15498094-9 2004 CONCLUSIONS: The availability of compounds that simultaneously decrease hyperglycaemia, restore insulin resistance and inhibit pathways activated by high glucose producing oxidative stress signals a promising approach. Glucose 154-161 insulin Homo sapiens 96-103 15504985-5 2004 All 20 SNPs with minor allele frequencies >0.1 in a single haplotype block covering the PTPN1 genomic sequence show significant association with the insulin sensitivity index (S(i)) (P = 0.044-0.003) and fasting glucose (P = 0.029 to <0.001). Glucose 215-222 insulin Homo sapiens 152-159 15504990-8 2004 After 6 months, at the end of the study, there was a significant improvement in acute insulin response to glucose in the rosiglitazone group (+15.3 microIU x ml(-1) x 10 min(-1); P < 0.001) that led to an increase in the disposition index from 0.18 at baseline to 4.18 at 6 months (P = 0.02). Glucose 106-113 insulin Homo sapiens 86-93 15533580-7 2004 We calculated insulin-mediated glucose uptake by the liver and peripheral tissues using euglycemic hyperinsulinemic clamp combined with an oral glucose load before and after buformin treatment or diet therapy for 2 weeks. Glucose 31-38 insulin Homo sapiens 14-21 15533580-7 2004 We calculated insulin-mediated glucose uptake by the liver and peripheral tissues using euglycemic hyperinsulinemic clamp combined with an oral glucose load before and after buformin treatment or diet therapy for 2 weeks. Glucose 144-151 insulin Homo sapiens 14-21 15533580-9 2004 However, the glucose infusion rate thought to express insulin sensitivity in peripheral tissue, TNF-alpha, sTNFR1, fasting plasma insulin, C-peptide, and NEFA levels did not change significantly in both the groups after treatment. Glucose 13-20 insulin Homo sapiens 54-61 15565374-7 2004 AUC(glucose) was increased in the beta-cell-reduced animals (1383+/-385 vs 853+/-113 mmol.l(-1).min in control minipigs, p<0.01), as was the insulin response to oral glucose per unit of beta cell mass (123+/-84 vs 56+/-24 pmol.l(-1).min.mg(-1), p<0.05). Glucose 4-11 insulin Homo sapiens 144-151 15565374-8 2004 Total in vitro insulin secretion was increased per unit of beta cell mass in nicotinamide + streptozotocin pancreata compared to controls (83.7+/-45.9 vs 34.6+/-14.4 nmol/mg beta cells, p<0.05) with responses to glucose and glucagon-like peptide-1 showing a partial compensation for reduced beta cell mass, whereas no compensation was seen in response to arginine. Glucose 215-222 insulin Homo sapiens 15-22 15465374-10 2004 When corrected for factors associated with insulin resistance and surgical stress, post-operative glucose levels were found to be an independent risk factor for post-operative infections (odds ratio top quartile versus lowest quartile: 5.1; 95% confidence interval: 1.6-17.1; P=0.007). Glucose 98-105 insulin Homo sapiens 43-50 15525480-5 2004 For type 1 diabetes patients, insulin glargine appears to be more effective than neutral protamine Hagedorn (NPH) in reducing fasting blood glucose (FBG) but not in reducing glycosylated haemoglobin (HbA1c) and there is some evidence that both insulins are as effective as each other in both FBG and HbA1c control. Glucose 140-147 insulin Homo sapiens 30-37 15655720-1 2004 Glucose-dependent insulinotropic polypeptide (GIP) is released from K-cells in the gut after meal ingestion, and acts in concert with glucagon-like peptide 1 (GLP-1) to augment glucose-stimulated insulin secretion. Glucose 177-184 insulin Homo sapiens 18-25 15682351-2 2004 METHOD: We measured plasma lipid and lipoprotein subfractions using Vertical Auto Profile-II methodology and directly measured insulin-mediated glucose disposal in 45 protease inhibitor (PI)-treated and non-PI-treated HIV-infected patients. Glucose 144-151 insulin Homo sapiens 127-134 15534457-10 2004 Plasma insulin and plasma glucose levels were significantly elevated in burn patients and the insulin:glucose ratio was dramatically increased compared with control subjects. Glucose 102-109 insulin Homo sapiens 94-101 15534457-12 2004 This decrease may be the result of marked insulin resistance, as suggested by the elevated insulin to glucose ratio in burn patients. Glucose 102-109 insulin Homo sapiens 42-49 15534457-12 2004 This decrease may be the result of marked insulin resistance, as suggested by the elevated insulin to glucose ratio in burn patients. Glucose 102-109 insulin Homo sapiens 91-98 15531485-0 2004 Intensive insulin treatment in critically ill trauma patients normalizes glucose by reducing endogenous glucose production. Glucose 73-80 insulin Homo sapiens 10-17 15531485-0 2004 Intensive insulin treatment in critically ill trauma patients normalizes glucose by reducing endogenous glucose production. Glucose 104-111 insulin Homo sapiens 10-17 15531485-2 2004 Intensive insulin treatment to normalize blood glucose during feeding has been shown to improve morbidity and mortality in patients in intensive care. Glucose 47-54 insulin Homo sapiens 10-17 15531485-3 2004 The mechanisms behind the glucose-controlling effects of insulin in stress are not well understood. Glucose 26-33 insulin Homo sapiens 57-64 15531485-15 2004 In contrast to controls, normalization of glucose concentration during TPN needs high insulin infusion rates and is accounted for by a reduction in EGP, whereas WGD is not increased. Glucose 42-49 insulin Homo sapiens 86-93 15531518-7 2004 Glucose (117 +/- 14 vs. 98 +/- 5 mg/dl) and insulin (49.5 +/- 10 vs. 23 +/- 5 muU/ml) levels were significantly elevated during the 48-h glucose infusion compared with those during saline treatment. Glucose 137-144 insulin Homo sapiens 44-51 15531518-8 2004 Forty-eight-hour glucose infusions increased insulin and C-peptide levels during the FSIGT. Glucose 17-24 insulin Homo sapiens 45-52 15531518-8 2004 Forty-eight-hour glucose infusions increased insulin and C-peptide levels during the FSIGT. Glucose 17-24 insulin Homo sapiens 57-66 15531518-9 2004 When the FSIGT was conducted in the presence of atropine after glucose infusion, C-peptide levels were significantly attenuated during the period of endogenous insulin secretion (0-20 min; 31.8 +/- 13 vs. 39.2 +/- 11.9, atropine vs. no atropine) and exogenous insulin administration [20-40 min; 18.8 +/- 10.8 vs. 31.6 +/- 12.9., atropine vs. no atropine; F(3,9) = 4.99; P < 0.026]. Glucose 63-70 insulin Homo sapiens 81-90 15531518-10 2004 A significant negative correlation was found between the repression of C-peptide by muscarinic blockade and the magnitude of the C-peptide response to the glucose infusion (r = 0.60; P < 0.045). Glucose 155-162 insulin Homo sapiens 71-80 15531518-10 2004 A significant negative correlation was found between the repression of C-peptide by muscarinic blockade and the magnitude of the C-peptide response to the glucose infusion (r = 0.60; P < 0.045). Glucose 155-162 insulin Homo sapiens 129-138 15531537-6 2004 The I allele was associated with lower glucose at 120 min (P = 0.04) and a greater insulin response (P = 0.03 for insulin at 30 min and P = 0.06 for insulin area under the curve) to a standard oral glucose tolerance test. Glucose 198-205 insulin Homo sapiens 83-90 15531537-6 2004 The I allele was associated with lower glucose at 120 min (P = 0.04) and a greater insulin response (P = 0.03 for insulin at 30 min and P = 0.06 for insulin area under the curve) to a standard oral glucose tolerance test. Glucose 198-205 insulin Homo sapiens 114-121 15531537-6 2004 The I allele was associated with lower glucose at 120 min (P = 0.04) and a greater insulin response (P = 0.03 for insulin at 30 min and P = 0.06 for insulin area under the curve) to a standard oral glucose tolerance test. Glucose 198-205 insulin Homo sapiens 114-121 15504990-10 2004 CONCLUSIONS: Rosiglitazone, but not insulin, induced a recovery of pancreatic beta-cell function, as evidenced by the restoration of the first-phase insulin response to glucose, improvement in the disposition index, and a decrease in the proinsulin-to-insulin ratio in subjects with type 2 diabetes in whom oral antihyperglycemic therapy failed. Glucose 169-176 insulin Homo sapiens 149-156 15504990-10 2004 CONCLUSIONS: Rosiglitazone, but not insulin, induced a recovery of pancreatic beta-cell function, as evidenced by the restoration of the first-phase insulin response to glucose, improvement in the disposition index, and a decrease in the proinsulin-to-insulin ratio in subjects with type 2 diabetes in whom oral antihyperglycemic therapy failed. Glucose 169-176 insulin Homo sapiens 149-156 15505002-6 2004 RESULTS: The insulin resistance score of relatives was positively correlated with the albumin excretion rate (P = 0.0009) and fasting plasma glucose (P = 0.0003) and HbA(1c) (P < 0.0001) concentrations. Glucose 141-148 insulin Homo sapiens 13-20 15505010-7 2004 These results demonstrate that in humans, a primary in vivo impairment of insulin action affects glucose and fatty acid metabolism as previously shown and also protein/amino acid metabolism. Glucose 97-104 insulin Homo sapiens 74-81 15505016-0 2004 Effects of mixing glargine and short-acting insulin analogs on glucose control. Glucose 63-70 insulin Homo sapiens 44-51 15551048-2 2004 Insulin secretion from pancreatic islet beta cells is a tightly regulated process, under the close control of blood glucose concentrations, neural inputs and circulating hormones. Glucose 116-123 insulin Homo sapiens 0-7 15551048-6 2004 Combined with classical biochemistry, these techniques show that the beta cell is uniquely poised, thanks to the expression of low levels of lactate dehydrogenase and plasma membrane lactate/monocarboxylate transporters, to channel glucose carbons towards oxidative metabolism, ATP synthesis and inhibition of AMP-activated protein kinase, a newly defined regulator of insulin release. Glucose 232-239 insulin Homo sapiens 369-376 15551341-8 2004 CONCLUSIONS: Experimental preliminary evidences suggest that this new technology could be applied in the clinical setting to help the physician to identify mainly nocturnal hypoglycaemic events, otherwise not revealed by traditional self blood-glucose monitoring, even in those patients who are not treated by conventional insulin therapy. Glucose 244-251 insulin Homo sapiens 323-330 15565374-5 2004 Insulin responses were evaluated in vivo using the mixed meal tolerance test (2 g/kg oral glucose) and in the isolated perfused pancreata from the same animals by stimulation with glucose, glucagon-like peptide-1 or arginine. Glucose 90-97 insulin Homo sapiens 0-7 15538935-3 2004 Body fat accumulation was measured by computed tomography (CT) and insulin resistance by the glucose infusion rate (GIR) during an euglycemic hyperinsulinemic clamp study. Glucose 93-100 insulin Homo sapiens 67-74 21432309-5 2004 Although high serum insulin was significantly related to all of the CRFs in all nondrinkers, moderate drinkers consuming up to 59 ml of alcohol per day and excessive drinkers consuming more, the means of SBP, serum glucose and HDLc were significantly higher and serum LDLc was lower in drinkers than in nondrinkers at any level of serum insulin, indicating that the good and bad profiles of CRFs in alcohol consumers are independent of their low fasting serum insulin. Glucose 215-222 insulin Homo sapiens 20-27 15655702-2 2004 They amplify glucose-induced insulin release. Glucose 13-20 insulin Homo sapiens 29-36 15655702-3 2004 By raising circulating incretin levels, oral glucose provokes a higher insulin response than that resulting from intravenous glucose. Glucose 45-52 insulin Homo sapiens 71-78 15655708-12 2004 Because of the reduction of the insulin:glucagon molar ratio basal endogenous glucose concentration will be higher causing fasting hyperglycemia, while the hepatic glucose output will not be efficiently suppressed after the ingestion of a meal, contributing to excessive post-prandial glucose rise. Glucose 78-85 insulin Homo sapiens 32-39 15655708-12 2004 Because of the reduction of the insulin:glucagon molar ratio basal endogenous glucose concentration will be higher causing fasting hyperglycemia, while the hepatic glucose output will not be efficiently suppressed after the ingestion of a meal, contributing to excessive post-prandial glucose rise. Glucose 164-171 insulin Homo sapiens 32-39 15655710-0 2004 New insights concerning the glucose-dependent insulin secretagogue action of glucagon-like peptide-1 in pancreatic beta-cells. Glucose 28-35 insulin Homo sapiens 46-53 15326467-16 2004 CONCLUSION: Physical activity is inversely associated with fasting insulin in the nondiabetic range of fasting glucose. Glucose 111-118 insulin Homo sapiens 67-74 15545992-3 2004 They regulate adaptive thermogenesis as well as glucose and fat oxidation in muscle and fat tissue, gluconeogenesis in liver, and even glucose-regulated insulin secretion in beta cells. Glucose 135-142 insulin Homo sapiens 153-160 15580048-0 2004 Glucose control by insulin for critically ill surgical patients. Glucose 0-7 insulin Homo sapiens 19-26 15546003-7 2004 Whereas expression of PGC-1alpha in muscle was positively related to insulin-stimulated glucose uptake and oxidation, PGC-1beta expression was positively related to fat oxidation and nonoxidative glucose metabolism. Glucose 88-95 insulin Homo sapiens 69-76 15199095-1 2004 The purpose of this study is to ascertain the pharmacodynamic properties of exendin-4, a glucose-dependent insulinotropic agent, from plasma glucose and insulin concentration-time profiles following a 60-min intravenous infusion in healthy and type 2 diabetic subjects. Glucose 89-96 insulin Homo sapiens 107-114 15199095-5 2004 Because drug concentrations were unavailable, hypothetical pharmacokinetic driving functions were approximated during the modeling process and used to enhance a proportionality constant relating elevated glucose and the rate of second-phase insulin release. Glucose 204-211 insulin Homo sapiens 241-248 15646130-2 2004 A slowed utilization of glucose, triglycerides and of free fatty acids due to an intensified insulin concentration was detected, which essentially affects, in persons with excessive weight, the nature of the mentioned changes and belongs to the risk category of diabetes mellitus and ischemic heart disease. Glucose 24-31 insulin Homo sapiens 93-100 15536602-4 2004 Acute insulin response (AIRg) was calculated as the secretion of insulin during the first 10 minutes following a glucose bolus. Glucose 113-120 insulin Homo sapiens 6-13 15536602-4 2004 Acute insulin response (AIRg) was calculated as the secretion of insulin during the first 10 minutes following a glucose bolus. Glucose 113-120 insulin Homo sapiens 65-72 15536602-5 2004 IS x AIRg was used as an index of insulin-mediated glucose uptake (IMGU). Glucose 51-58 insulin Homo sapiens 34-41 15536603-8 2004 This quantitative difference in lipolysis may account for inadequate insulin-induced suppression of hepatic glucose production in CF, and may be a metabolic adaptation to increased energy needs. Glucose 108-115 insulin Homo sapiens 69-76 15536606-6 2004 The best model included zero order (constant) glucose disposal from the interstitial fluid (ISF) and insulin-stimulated glucose transfer from plasma to the ISF. Glucose 120-127 insulin Homo sapiens 101-108 15502400-2 2004 Insulin is released from pancreatic beta-cells in response to changes in blood glucose, the defect of which leads to impaired insulin secretion and diabetes mellitus. Glucose 79-86 insulin Homo sapiens 0-7 15536600-0 2004 Preserved circadian rhythm of serum insulin concentration at low plasma glucose during fasting in lean and overweight humans. Glucose 72-79 insulin Homo sapiens 36-43 15647708-4 2004 With the advent of insulin and treatment programs to improve glucose control, the diabetic woman now has an opportunity to lead a near-normal life. Glucose 61-68 insulin Homo sapiens 19-26 19667675-3 2004 Premixed insulin formulations of human regular and NPH insulin are commonly used to control blood glucose levels throughout the day, but because these preparations do not mimic the physiologic profile of insulin release, hypo- and hyperglycemia may ensue. Glucose 98-105 insulin Homo sapiens 9-16 19667675-3 2004 Premixed insulin formulations of human regular and NPH insulin are commonly used to control blood glucose levels throughout the day, but because these preparations do not mimic the physiologic profile of insulin release, hypo- and hyperglycemia may ensue. Glucose 98-105 insulin Homo sapiens 55-62 19667675-4 2004 Using human regular insulin to control mealtime hyperglycemia is similarly problematic, and thus recently developed rapid-acting insulin analogues, such as lispro and aspart, are now preferred for prandial glucose control. Glucose 206-213 insulin Homo sapiens 129-136 15684669-7 2004 Basal (50 G) and glucose-stimulated (300 G) levels of insulin secretion confirmed a see-saw pattern in which the VAPG gradually decreased insulin secretion from encapsulated islets and then fell below the insulin level secreted from microcapsules containing GLP-1/Zn(2+) crystal. Glucose 17-24 insulin Homo sapiens 54-61 15501490-1 2004 Insulin is mainly known for its peripheral effects on the metabolism of glucose, fats, and proteins. Glucose 72-79 insulin Homo sapiens 0-7 15464833-8 2004 The oral administration of insulin and NaTC incorporated liposomes significantly decreased blood glucose levels. Glucose 97-104 insulin Homo sapiens 27-34 15491498-2 2004 Adiponectin possesses insulin sensitizing properties, and predicts insulin sensitivity of both glucose and lipid metabolism. Glucose 95-102 insulin Homo sapiens 67-74 15369805-5 2004 We conclude, (i) that insulin induces a time-dependent inflammatory and pro-angiogenic transcriptional response in cultured human myotubes, (ii) that myotubes in vitro retain a gene expression pattern specific for type 2 diabetes and sharing five genes with that of type 2 diabetic skeletal muscle in vivo, and (iii) that insulin, despite similar metabolic effects of glucose uptake and glycogen synthesis, regulates different pools of genes in skeletal muscle during in vivo and in vitro conditions. Glucose 368-375 insulin Homo sapiens 22-29 15380928-2 2004 The dose-response curves for glucose-stimulated insulin and C-peptide release from isolated islets were practically identical: 0.05-0.1 nmol/l insulin stimulated, 1-100 nmol/l had no effect, whereas concentrations >/=250 nmol/l ("high insulin"), inhibited C-peptide release. Glucose 29-36 insulin Homo sapiens 48-55 15477435-8 2004 In subgroup analyses, insulin therapy decreased mortality in the surgical intensive care unit (RR, 0.58; 95% CI, 0.22-0.62), when the aim of therapy was glucose control (RR, 0.71; 95% CI, 0.54-0.93), and in patients with diabetes mellitus (RR, 0.73; 95% CI, 0.58-0.90). Glucose 153-160 insulin Homo sapiens 22-29 15149949-5 2004 Thirty minutes before start of the clamp, a bolus of glucose was injected intravenously to stimulate endogenous insulin secretion. Glucose 53-60 insulin Homo sapiens 112-119 15172888-0 2004 MEK inhibitors impair insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Glucose 41-48 insulin Homo sapiens 22-29 15172888-2 2004 Although PI3K and Cbl mediate insulin-stimulated glucose uptake by promoting the translocation of the insulin-responsive glucose transporter (GLUT4) to the plasma membrane, the MAPK pathway does not have an established role in insulin-stimulated glucose uptake. Glucose 49-56 insulin Homo sapiens 30-37 15172888-2 2004 Although PI3K and Cbl mediate insulin-stimulated glucose uptake by promoting the translocation of the insulin-responsive glucose transporter (GLUT4) to the plasma membrane, the MAPK pathway does not have an established role in insulin-stimulated glucose uptake. Glucose 121-128 insulin Homo sapiens 30-37 15172888-2 2004 Although PI3K and Cbl mediate insulin-stimulated glucose uptake by promoting the translocation of the insulin-responsive glucose transporter (GLUT4) to the plasma membrane, the MAPK pathway does not have an established role in insulin-stimulated glucose uptake. Glucose 121-128 insulin Homo sapiens 102-109 15172888-2 2004 Although PI3K and Cbl mediate insulin-stimulated glucose uptake by promoting the translocation of the insulin-responsive glucose transporter (GLUT4) to the plasma membrane, the MAPK pathway does not have an established role in insulin-stimulated glucose uptake. Glucose 121-128 insulin Homo sapiens 102-109 15172888-4 2004 To investigate the role of the MAPK pathway separately from that of the PI3K pathway in insulin-stimulated glucose uptake, we used two specific inhibitors of MAPK kinase (MEK) activity, PD-98059 and U-0126, which reduced insulin-stimulated glucose uptake by approximately 33 and 50%, respectively. Glucose 107-114 insulin Homo sapiens 88-95 15172888-8 2004 Importantly, the presence of MEK inhibitors only at the time of the transport assay markedly impaired both insulin-stimulated glucose uptake and MAPK signaling. Glucose 126-133 insulin Homo sapiens 107-114 15198934-5 2004 There was a strong inverse relation between adipose FOXC2 mRNA and insulin sensitivity, using the frequently sampled intravenous glucose tolerance test (r = -0.78, P < 0.001). Glucose 129-136 insulin Homo sapiens 67-74 15385347-2 2004 However, anesthesia-related increases in blood glucose can induce insulin secretion, making it difficult to interpret ASVS test data. Glucose 47-54 insulin Homo sapiens 66-73 15382139-3 2004 In this review, we will describe the special morphology of islet capillaries and its role in the physiologic function of islets: secretion of insulin in response to blood glucose levels. Glucose 171-178 insulin Homo sapiens 142-149 15516700-3 2004 To study the effect of these metal ions on insulin signaling proteins, cultured mouse skeletal muscle cells was used as an in vitro model, as the tissue accounts for more than 80% of insulin-stimulated glucose disposal in the body. Glucose 202-209 insulin Homo sapiens 183-190 15516700-11 2004 The ions could also enhance the insulin-stimulated glucose uptake into the cells. Glucose 51-58 insulin Homo sapiens 32-39 15516700-12 2004 Therefore, both Zn and Cr seem to have a positive effect on insulin signaling leading to glucose uptake. Glucose 89-96 insulin Homo sapiens 60-67 15573142-3 2004 We have found that pancreatic islets, beta-cells, and glucose-responsive insulinoma cells express an iPLA2beta that participates in glucose-stimulated insulin secretion but is not involved in membrane phospholipid remodeling. Glucose 54-61 insulin Homo sapiens 73-80 15498377-8 2004 Moreover, timely insulin treatment noticeably improved the insulin content of beta cells, with an increase of 10.2% (P < 0.05), despite a slight reduction in fasting blood glucose (FBG), triglyceride (TG), and free fatty acid (FFA) levels, as compared to an untreated diabetic group. Glucose 175-182 insulin Homo sapiens 17-24 15473886-6 2004 MEASUREMENTS: Insulin sensitivity was determined by an oral glucose tolerance test (OGTT) based on the insulin sensitivity index (ISI) formula, serum paraoxonase activity was determined with a spectrophotometric method. Glucose 60-67 insulin Homo sapiens 14-21 15461898-4 2004 An understanding of the role of basal insulin in the regulation of glucose and the development of strategies to implement basal insulin therapy can provide a transition that is rational and highly effective in most patients. Glucose 67-74 insulin Homo sapiens 38-45 15544472-2 2004 Among the GLUT family isoforms, GLUT4 is particularly important for maintaining glucose metabolism homeostasis since it is involved in insulin or exercise-induced glucose transport into muscle and adipose tissues via movement from intracellular sites to the plasma membrane in response to stimulation. Glucose 80-87 insulin Homo sapiens 135-142 15384955-2 2004 Studies suggest that both African-Americans and Pima Indians are more insulin resistant and have higher acute insulin secretory responses to glucose than Caucasians; however, a direct comparison between these three populations is lacking. Glucose 141-148 insulin Homo sapiens 110-117 15384955-3 2004 METHODS: We measured insulin secretory responses to intravenous glucose (acute insulin response, AIR, 25 g ivGTT); insulin action at physiological (M-low) and supra-physiological (M-high) levels of hyperinsulinaemia (2-step hyperinsulinaemic clamp); basal and insulin-suppressed endogenous glucose production in 30 African-Americans, 30 Pima Indians and 30 Caucasians with normal glucose tolerance who were carefully matched for age, sex, and body fat (hydrodensitometry or DEXA). Glucose 64-71 insulin Homo sapiens 21-28 15384955-7 2004 Insulin-suppressed endogenous glucose production during the clamp was not different among the groups (all P > 0.40). Glucose 30-37 insulin Homo sapiens 0-7 15384965-7 2004 RESULTS: Multiple regression analysis revealed fasting blood glucose, BMI, triglycerides and HDL as the most powerful predictors of insulin resistance which were used for further computation of the IRIS II score. Glucose 61-68 insulin Homo sapiens 132-139 15448090-4 2004 Furthermore, we find variable insulin release from these cells upon glucose addition, but C-peptide release is never detected. Glucose 68-75 insulin Homo sapiens 30-37 15448091-3 2004 A 72-h culture of islets in the presence of palmitate or oleate resulted in a marked decrease in glucose-induced insulin release assessed in 1-h static incubations. Glucose 97-104 insulin Homo sapiens 113-120 15448106-11 2004 An oral glucose tolerance test performed in one subject revealed that glucose-stimulated insulin release was restored. Glucose 8-15 insulin Homo sapiens 89-96 15448106-11 2004 An oral glucose tolerance test performed in one subject revealed that glucose-stimulated insulin release was restored. Glucose 70-77 insulin Homo sapiens 89-96 15451899-4 2004 The primary outcome was beta-cell function measured as first-phase insulin response (FPIR) to intravenous glucose at 0, 6, and 12 months and then yearly; the secondary outcome was immunity to islet antigens, measured monthly for 12 months. Glucose 106-113 insulin Homo sapiens 67-74 15480539-6 2004 Insulin secretion was measured as first-phase insulin response (FPIR) to intravenous glucose. Glucose 85-92 insulin Homo sapiens 0-7 15480539-6 2004 Insulin secretion was measured as first-phase insulin response (FPIR) to intravenous glucose. Glucose 85-92 insulin Homo sapiens 46-53 15628821-6 2004 The proposed glucose clamp technique makes possible the quantitative study of the pharmacokinetic and pharmacodynamic properties of insulin preparations under comparative and reproducible conditions. Glucose 13-20 insulin Homo sapiens 132-139 16304726-1 2004 Individuals with insulin resistance are at increased risk of glucose intolerance, dyslipidaemia and essential hypertension. Glucose 61-68 insulin Homo sapiens 17-24 15487981-6 2004 The output from continuous glucose monitoring devices will assist accurate insulin replacement, which is difficult using point-estimates of blood glucose. Glucose 27-34 insulin Homo sapiens 75-82 15337733-5 2004 On a separate day, baseline and insulin-regulated glucose ([3-3H]glucose) and FFA ([9,10-3H]palmitate) turnover were measured. Glucose 50-57 insulin Homo sapiens 32-39 15337733-8 2004 Basal and insulin-mediated glucose disposal was significantly reduced and FFA turnover significantly increased in viscerally obese men. Glucose 27-34 insulin Homo sapiens 10-17 15523593-1 2004 Class I alpha phosphatidylinositol (PI) 3-kinase is an important enzyme in the early insulin signaling cascade, and plays a key role in insulin-mediated glucose transport. Glucose 153-160 insulin Homo sapiens 136-143 15314628-5 2004 Six subjects lost significant weight (>10%) and BMI (>-3 kg/m(2)) with a 34% decline in leptin and a 46% decrease in insulin area under the curve (IAUC) to oral glucose tolerance testing. Glucose 167-174 insulin Homo sapiens 123-130 15252018-7 2004 Most importantly, NFkappaB SN50, a cell-permeable peptide that inhibits NFkappaB nuclear translocation downstream of IKK, was sufficient to prevent palmitate-induced reductions in insulin-stimulated glucose uptake. Glucose 199-206 insulin Homo sapiens 180-187 15277525-1 2004 Insulin modulates glucose uptake into adipocytes by regulating the trafficking of the GLUT4 glucose transporter. Glucose 18-25 insulin Homo sapiens 0-7 15319424-6 2004 TIRF images of single insulin granule motion during a 15-min stimulation by 22 mm glucose in IL-1beta-treated beta-cells showed a marked reduction in the fusion events from previously docked granules during the first phase insulin release. Glucose 82-89 insulin Homo sapiens 22-29 15319424-6 2004 TIRF images of single insulin granule motion during a 15-min stimulation by 22 mm glucose in IL-1beta-treated beta-cells showed a marked reduction in the fusion events from previously docked granules during the first phase insulin release. Glucose 82-89 insulin Homo sapiens 223-230 15319424-8 2004 The present observations indicate that IL-1beta, but not IFN-gamma, has a preferential inhibitory effect on the first phase of glucose-induced insulin release, mostly via an action on previously docked granules. Glucose 127-134 insulin Homo sapiens 143-150 15472206-4 2004 IL-1beta and 600 mg/dl glucose increased beta-cell apoptosis and abolished short-term glucose-stimulated insulin secretion. Glucose 23-30 insulin Homo sapiens 105-112 15472206-4 2004 IL-1beta and 600 mg/dl glucose increased beta-cell apoptosis and abolished short-term glucose-stimulated insulin secretion. Glucose 86-93 insulin Homo sapiens 105-112 15472206-5 2004 Both drugs protected partially against loss of glucose-stimulated insulin secretion and prevented completely increased apoptosis caused by IL-1beta or 600 mg/dl glucose. Glucose 47-54 insulin Homo sapiens 66-73 15648547-3 2004 Despite the ability of tumor cells to turn off insulin secretion in response to low plasma glucose during 72 h of fasting, hyperinsulinemic hypoglycemia occurred in both patients in response to stimulation by classical secretagogues. Glucose 91-98 insulin Homo sapiens 47-54 15138152-1 2004 Measuring insulin sensitivity during the physiological milieu of oral glucose perturbation, e.g., a meal or an oral glucose tolerance test, would be extremely valuable but difficult since the rate of appearance of absorbed glucose is unknown. Glucose 70-77 insulin Homo sapiens 10-17 15138152-1 2004 Measuring insulin sensitivity during the physiological milieu of oral glucose perturbation, e.g., a meal or an oral glucose tolerance test, would be extremely valuable but difficult since the rate of appearance of absorbed glucose is unknown. Glucose 116-123 insulin Homo sapiens 10-17 15138152-1 2004 Measuring insulin sensitivity during the physiological milieu of oral glucose perturbation, e.g., a meal or an oral glucose tolerance test, would be extremely valuable but difficult since the rate of appearance of absorbed glucose is unknown. Glucose 116-123 insulin Homo sapiens 10-17 15465742-1 2004 Caffeine ingestion negatively affects insulin sensitivity during an oral glucose tolerance test (OGTT) in lean and obese men, but this has not been studied in individuals with type 2 diabetes. Glucose 73-80 insulin Homo sapiens 38-45 15361774-4 2004 Insulin-adjusted glucose disposal rate (GDR/I) was measured with a 90-min hyperinsulinaemic glucose clamp and fitness by peak oxygen uptake (VO2peak) during a treadmill test. Glucose 17-24 insulin Homo sapiens 0-7 15887827-0 2004 Insulin therapy--role beyond glucose control. Glucose 29-36 insulin Homo sapiens 0-7 15542356-9 2004 We found that glucose levels were lower in the group that was supplemented with insulin only (group 2, 61.4 mg/dL +/- 2.8,mean +/- SD) and in the group that was supplemented with DHA only (group 3, 61.1 mg/dL +/- 2.0) compared to controls (group 1, 71 mg/dL +/- 6.9, P < 0.0001). Glucose 14-21 insulin Homo sapiens 80-87 15481723-8 2004 CONCLUSIONS: These results in rats indicate that if insulin is used following ischemia, blood glucose levels should be maintained at approximately 6 to 7 mM. Glucose 94-101 insulin Homo sapiens 52-59 15542356-10 2004 Supplementation of both insulin and docosahexaenoic acid (group 4) resulted in significantly lower glucose levels (56.4 mg/dL +/- 2.6) compared to those in groups 2 and 3 (P < 0.01). Glucose 99-106 insulin Homo sapiens 24-31 15542356-12 2004 We conclude that adding insulin or docosahexaenoic acid to the diet of weaned Balb C mice reduces glucose blood levels. Glucose 98-105 insulin Homo sapiens 24-31 15542356-14 2004 The presence of insulin and docosahexaenoic acid in human milk may be the cause for reduced glucose levels in breast-fed infants, in addition to the known effects of DHA on insulin sensitivity. Glucose 92-99 insulin Homo sapiens 16-23 15375778-12 2004 After the administration of insulin, plasma glucose decreased from 4.8 +/- 0.5 to 2.7 +/- 0.5 mmol/L, mean +/- SD (P < .0001). Glucose 44-51 insulin Homo sapiens 28-35 18370691-4 2004 The insulin sensitivity was estimated by means of the total glucose metabolism, which was obtained with the euglycemic- hyperinsulinemic clamp technique before the randomized assignment and on the following day for the corresponding patch. Glucose 60-67 insulin Homo sapiens 4-11 18370692-1 2004 Insulin resistance causes hyperglycemia by disturbing glucose uptake in the tissues and increasing hepatic glucose production. Glucose 54-61 insulin Homo sapiens 0-7 18370692-1 2004 Insulin resistance causes hyperglycemia by disturbing glucose uptake in the tissues and increasing hepatic glucose production. Glucose 107-114 insulin Homo sapiens 0-7 15458595-11 2004 Insulin therapy significantly reduced blood glucose concentration from a median (interquartile range) of 11.9 mmol/L (range, 11.4-13.6 mmol/L) to 8.8 mmol/L (range, 7.3-9.6 mmol/L; P < 0.001). Glucose 44-51 insulin Homo sapiens 0-7 15571230-2 2004 Insulin hypersecretion, as elicited by the oral glucose tolerance test (OGTT), increased a mean of 5-fold in 12 essential hypertensive patients. Glucose 48-55 insulin Homo sapiens 0-7 15673056-7 2004 Insulin resistance was estimated on the basis of fasting glucose and insulin, using the glucose homeostasis model (HOMA scores). Glucose 57-64 insulin Homo sapiens 0-7 15673056-7 2004 Insulin resistance was estimated on the basis of fasting glucose and insulin, using the glucose homeostasis model (HOMA scores). Glucose 88-95 insulin Homo sapiens 0-7 15474880-7 2004 In HW carriers, a delay in the maximal response of insulin secretion was observed, with a decrease of 26.7% in insulin concentrations 30 to 60 min after the 50-g glucose load. Glucose 162-169 insulin Homo sapiens 51-58 15476949-5 2004 Furthermore, in the subjects with normal glucose tolerance, 89N was associated with significantly higher insulin levels on oral glucose tolerance test, suggesting reduced insulin sensitivity in subjects with 89N. Glucose 128-135 insulin Homo sapiens 105-112 15355512-1 2004 The insulin-sensitive glucose transporter GLUT4 mediates the uptake of glucose into adipocytes and muscle cells. Glucose 22-29 insulin Homo sapiens 4-11 15651146-3 2004 Many changes will influence diabetology in next years: inhalation and bucal application of insulin, development of drugs functioning in all components of metabolic syndrome, automatisation of insulin dosing (closing of feedback from glucose level to insulin dosing), experiments with embryonic and stem cells in diabetology, preventive gene vaccination in both types of diabetes. Glucose 233-240 insulin Homo sapiens 192-199 15334413-6 2004 In this study, we present the concept of a hybrid pancreatic substitute consisting of such cells sequestered in a material exhibiting glucose-dependent changes of its permeability to insulin. Glucose 134-141 insulin Homo sapiens 183-190 15334413-11 2004 The experimental and modeling studies indicate that a hybrid pancreatic substitute consisting of constitutively secreting cells and glucose-responsive material has the potential to provide a more physiologic regulation of insulin release than the cells by themselves or in an inert material. Glucose 132-139 insulin Homo sapiens 222-229 15515877-5 2004 The primary endpoint was the efficacy of the low-dose insulin regimen to decrease serum glucose concentrations; the secondary endpoint was its influence on protein catabolism. Glucose 88-95 insulin Homo sapiens 54-61 15247266-1 2004 Insulin stimulates glucose transport in muscle and adipose tissues by recruiting intracellular membrane vesicles containing the glucose transporter GLUT4 to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 15277534-3 2004 Given that cortical filamentous actin (F-actin) represents an essential aspect of insulin regulated glucose transport, we tested to see whether cortical F-actin structure was compromised during chronic insulin treatment. Glucose 100-107 insulin Homo sapiens 82-89 15277534-4 2004 The acute effect of insulin on GLUT4 translocation and glucose uptake was diminished in 3T3-L1 adipocytes exposed to a physiological level of insulin (5 nm) for 12 h. This insulin-induced loss of insulin responsiveness was apparent under both low (5.5 mm) and high (25 mm) glucose concentrations. Glucose 55-62 insulin Homo sapiens 20-27 15277534-4 2004 The acute effect of insulin on GLUT4 translocation and glucose uptake was diminished in 3T3-L1 adipocytes exposed to a physiological level of insulin (5 nm) for 12 h. This insulin-induced loss of insulin responsiveness was apparent under both low (5.5 mm) and high (25 mm) glucose concentrations. Glucose 55-62 insulin Homo sapiens 142-149 15277534-4 2004 The acute effect of insulin on GLUT4 translocation and glucose uptake was diminished in 3T3-L1 adipocytes exposed to a physiological level of insulin (5 nm) for 12 h. This insulin-induced loss of insulin responsiveness was apparent under both low (5.5 mm) and high (25 mm) glucose concentrations. Glucose 55-62 insulin Homo sapiens 142-149 15277534-4 2004 The acute effect of insulin on GLUT4 translocation and glucose uptake was diminished in 3T3-L1 adipocytes exposed to a physiological level of insulin (5 nm) for 12 h. This insulin-induced loss of insulin responsiveness was apparent under both low (5.5 mm) and high (25 mm) glucose concentrations. Glucose 273-280 insulin Homo sapiens 20-27 15277534-4 2004 The acute effect of insulin on GLUT4 translocation and glucose uptake was diminished in 3T3-L1 adipocytes exposed to a physiological level of insulin (5 nm) for 12 h. This insulin-induced loss of insulin responsiveness was apparent under both low (5.5 mm) and high (25 mm) glucose concentrations. Glucose 273-280 insulin Homo sapiens 142-149 15277534-4 2004 The acute effect of insulin on GLUT4 translocation and glucose uptake was diminished in 3T3-L1 adipocytes exposed to a physiological level of insulin (5 nm) for 12 h. This insulin-induced loss of insulin responsiveness was apparent under both low (5.5 mm) and high (25 mm) glucose concentrations. Glucose 273-280 insulin Homo sapiens 142-149 15306821-5 2004 However on a high fat diet, levels of glucose and free fatty acids still rise in S6K1-deficient mice, resulting in insulin receptor desensitization. Glucose 38-45 insulin Homo sapiens 115-122 15375793-0 2004 Population and individual minimal modeling of the frequently sampled insulin-modified intravenous glucose tolerance test. Glucose 98-105 insulin Homo sapiens 69-76 15166000-3 2004 Here, we report that incubation of 3T3-L1 adipocytes with specific inhibitors of V-type ATPase, concanamycin A and bafilomycin A1, inhibits insulin-regulated glucose transport and results in accumulation of GLUT4 in heavy, rapidly sedimenting intracellular membranes. Glucose 158-165 insulin Homo sapiens 140-147 15337174-0 2004 The reduced insulin-mediated glucose oxidation in skeletal muscle from type 2 diabetic subjects may be of genetic origin--evidence from cultured myotubes. Glucose 29-36 insulin Homo sapiens 12-19 15337174-1 2004 Several defects in response to insulin have been described in vivo and in vitro in type 2 diabetes: a decreased glucose transport, defective glucose oxidation and altered glycogen synthesis. Glucose 112-119 insulin Homo sapiens 31-38 15337174-3 2004 The aim of this study was to evaluate whether myotubes established from type 2 diabetic subjects express a primarily or a FFA-induced reduced insulin-mediated glucose oxidation. Glucose 159-166 insulin Homo sapiens 142-149 15337174-5 2004 We found that myotubes established from type 2 diabetic subjects express a reduced insulin-stimulated increase in glucose oxidation. Glucose 114-121 insulin Homo sapiens 83-90 15337174-6 2004 Moreover, an acute exposure to FFA reduces insulin-mediated glucose oxidation without alterations in glucose uptake and glycogen synthesis. Glucose 60-67 insulin Homo sapiens 43-50 15337174-7 2004 Thus, we conclude that the diminished increase in insulin-stimulated glucose oxidation seen in type 2 diabetic subjects in vivo may be of genetic origin. Glucose 69-76 insulin Homo sapiens 50-57 15149951-3 2004 Our goal was to determine whether preincubation of primary human skeletal muscle cells with human serum and AICAR (Serum+AICAR) would also induce a subsequent elevation in insulin-stimulated glucose uptake. Glucose 191-198 insulin Homo sapiens 172-179 15149951-11 2004 In contrast to results with isolated rat skeletal muscle, increasing the pAMPK and pACC in human myocytes via preincubation with Serum+AICAR was insufficient to lead to a subsequent enhancement in insulin-stimulated glucose uptake. Glucose 216-223 insulin Homo sapiens 197-204 15308461-0 2004 Hypothesis: one rate-limiting step controls the magnitude of both phases of glucose-stimulated insulin secretion. Glucose 76-83 insulin Homo sapiens 95-102 15308473-2 2004 To fulfill its preeminent function of regulating glucose metabolism, insulin secretion must not only be quantitatively appropriate but also have qualitative, dynamic properties that optimize insulin action on target tissues. Glucose 49-56 insulin Homo sapiens 69-76 15308473-3 2004 This review focuses on the importance of the first-phase insulin secretion to glucose metabolism and attempts to illustrate the relationships between the first-phase insulin response to an intravenous glucose challenge and the early insulin response following glucose ingestion. Glucose 201-208 insulin Homo sapiens 166-173 15308473-5 2004 In contrast, peripheral insulin concentration following glucose ingestion does not bear any clear sign of biphasic shape. Glucose 56-63 insulin Homo sapiens 24-31 15308473-6 2004 Coupling data from the literature with the results of a beta-cell model simulation, a close relationship between the first-phase insulin response to intravenous glucose and the early insulin response to glucose ingestion emerges. Glucose 161-168 insulin Homo sapiens 129-136 15350994-7 2004 Glucose level indicating insulin therapy and the initial insulin doses were quite variable according to the different units (respectively 7-16.5 mmol/l and 0.01-0.1 U/kg/h). Glucose 0-7 insulin Homo sapiens 25-32 15308473-6 2004 Coupling data from the literature with the results of a beta-cell model simulation, a close relationship between the first-phase insulin response to intravenous glucose and the early insulin response to glucose ingestion emerges. Glucose 161-168 insulin Homo sapiens 183-190 15308473-6 2004 Coupling data from the literature with the results of a beta-cell model simulation, a close relationship between the first-phase insulin response to intravenous glucose and the early insulin response to glucose ingestion emerges. Glucose 203-210 insulin Homo sapiens 129-136 15308473-6 2004 Coupling data from the literature with the results of a beta-cell model simulation, a close relationship between the first-phase insulin response to intravenous glucose and the early insulin response to glucose ingestion emerges. Glucose 203-210 insulin Homo sapiens 183-190 15308473-8 2004 This early insulin response to glucose is enhanced by the concomitant action of incretins and neural responses to nutrient ingestion. Glucose 31-38 insulin Homo sapiens 11-18 15308473-11 2004 Thus, even though the classical first phase does not exist under physiological conditions, the oscillatory behavior identified at the portal level does serve the purpose of rapidly exposing the liver to elevated insulin levels that, also in virtue of their up-and-down pattern, are particularly effective in restraining hepatic glucose production. Glucose 328-335 insulin Homo sapiens 212-219 15383184-6 2004 Insulin sensitivity was assessed by plasma glucose and insulin concentrations obtained at fasting or during a 75 g oral glucose tolerance test. Glucose 43-50 insulin Homo sapiens 0-7 15294427-1 2004 Insulin-secreting beta-cells, located within the pancreatic islets of Langerhans, are excitable cells that produce regular bursts of action potentials when stimulated by glucose. Glucose 170-177 insulin Homo sapiens 0-7 15531011-2 2004 In theory, postprandial injection of rapid-acting insulin analogues could prove more effective in achieving glucose control at such times because this treatment strategy could allow adjustment of insulin dose for the actual size of the meal consumed rather than being based on an estimate of what will be consumed. Glucose 108-115 insulin Homo sapiens 50-57 15531011-2 2004 In theory, postprandial injection of rapid-acting insulin analogues could prove more effective in achieving glucose control at such times because this treatment strategy could allow adjustment of insulin dose for the actual size of the meal consumed rather than being based on an estimate of what will be consumed. Glucose 108-115 insulin Homo sapiens 196-203 15531011-11 2004 Total glucose AUC during the meal test was 22% less when insulin aspart was injected immediately before the study meal (mean [SE], 23,014 [1832] mg/dL.min) than when injected immediately after the meal (mean [SE], 29,535 [2243] mg/dL.min) (P < 0.001), but baseline-adjusted AUC was similar. Glucose 6-13 insulin Homo sapiens 57-64 15531011-15 2004 Adjustment of postprandial insulin aspart dose for the actual meal size consumed maintained postprandial glucose concentrations within currently recommended treatment guidelines. Glucose 105-112 insulin Homo sapiens 27-34 15531011-16 2004 CONCLUSIONS: Preprandial insulin aspart injection produced a better glucose profile and is preferred when conditions permit. Glucose 68-75 insulin Homo sapiens 25-32 15531011-17 2004 However, both preprandial and postprandial insulin aspart administration achieved postprandial glucose concentrations within currently recommended treatment guidelines. Glucose 95-102 insulin Homo sapiens 43-50 15331551-18 2004 In the presence of exenatide, there was a preserved, glucose-dependent insulin secretory response and counterregulatory response during hypoglycemia. Glucose 53-60 insulin Homo sapiens 71-78 15333480-6 2004 RESULTS: Athletes showed increased Vo(2max) (P < 0.0001), insulin-mediated glucose disposal (M value, 61 +/- 4 vs. 46 +/- 3 micromol. Glucose 78-85 insulin Homo sapiens 61-68 15333480-14 2004 CONCLUSIONS: We conclude that endurance training promotes insulin-mediated glucose and FFA disposal in skeletal muscle, while lowering hepatic FFA uptake. Glucose 75-82 insulin Homo sapiens 58-65 15333485-0 2004 Contribution of insulin-stimulated glucose uptake and basal hepatic insulin sensitivity to surrogate measures of insulin sensitivity. Glucose 35-42 insulin Homo sapiens 16-23 15331205-6 2004 Serum insulin levels at baseline and 2 h after OGTT showed a characteristic pattern for each category of glucose tolerance, resulting from the different insulin responses. Glucose 105-112 insulin Homo sapiens 6-13 15331205-6 2004 Serum insulin levels at baseline and 2 h after OGTT showed a characteristic pattern for each category of glucose tolerance, resulting from the different insulin responses. Glucose 105-112 insulin Homo sapiens 153-160 15343584-6 2004 However, during the past decade significant progress has been made towards an understanding of the molecular basis underlying the beneficial effects of exercise training in stimulating the entry of glucose into insulin-sensitive tissues. Glucose 198-205 insulin Homo sapiens 211-218 15343584-9 2004 In contrast, exercise training will be shown to significantly reduce the risk of developing insulin resistance by improving glucose tolerance and insulin action in individuals predisposed to develop type 2 diabetes. Glucose 124-131 insulin Homo sapiens 92-99 15626056-0 2004 Plasma insulin response to oral glucose tolerance test in type-2 Nigerian diabetics. Glucose 32-39 insulin Homo sapiens 7-14 15626056-1 2004 OBJECTIVE: To study the plasma insulin pattern in type 2 diabetic Nigerians both in the fasting state and in response to a standard oral glucose tolerance test. Glucose 137-144 insulin Homo sapiens 31-38 15626056-10 2004 Similarly, plasma insulin levels following oral glucose challenge were significantly lower in the type 2 diabetic population. Glucose 48-55 insulin Homo sapiens 18-25 15330741-4 2004 Inhibition of the enzyme, therefore, is thought to increase levels of the active forms of both incretin hormones, culminating in an increase in insulin release after a meal, in a fully glucose-dependent manner. Glucose 185-192 insulin Homo sapiens 144-151 15521214-4 2004 Treatment with insulin resulted in a decrease in serum glucose value from 913 +/- 197 mg/dL to 170 +/- 78 mg/dL, an increase in serum sodium level from 125 +/- 5 to 136 +/- 5 mmol/L, and a fall in calculated serum tonicity value from 300 +/- 13 to 282 +/- 11 mmol/kg (all at p < 0.001). Glucose 55-62 insulin Homo sapiens 15-22 15306831-3 2004 In type II diabetes, a diminished or absent first-phase insulin release is the earliest metabolic defect, which is accompanied by lack of prandial suppression of hepatic glucose production, increased postprandial glucose excursions and late insulin hypersecretion. Glucose 213-220 insulin Homo sapiens 56-63 15306831-7 2004 By then, patients require insulin administration to maintain glucose control. Glucose 61-68 insulin Homo sapiens 26-33 15306832-6 2004 Consequently, it is logical to suppose that insulin regimens that control both fasting plasma glucose and postprandial glucose excursions should also achieve the best macrovascular risk outcomes and there are some data that suggest this. Glucose 94-101 insulin Homo sapiens 44-51 15306832-6 2004 Consequently, it is logical to suppose that insulin regimens that control both fasting plasma glucose and postprandial glucose excursions should also achieve the best macrovascular risk outcomes and there are some data that suggest this. Glucose 119-126 insulin Homo sapiens 44-51 15497510-4 2004 The dosages of both types of insulin were adjusted to attain preprandial glucose levels of <6.1 mmol/l within 1 week with similar rates of glucose decline. Glucose 73-80 insulin Homo sapiens 29-36 15356061-10 2004 The mechanism accounting for the reduced dextrose requirement during hypoglycemia likely involves a markedly decreased insulin secretory response to the agents during hypoglycemia and suggests that at modest hypoglycemia, low glucose or other metabolite(s) or altered counterregulatory hormone levels are sufficient to inhibit insulin release in response to potent insulin secretagogues. Glucose 41-49 insulin Homo sapiens 119-126 15356061-10 2004 The mechanism accounting for the reduced dextrose requirement during hypoglycemia likely involves a markedly decreased insulin secretory response to the agents during hypoglycemia and suggests that at modest hypoglycemia, low glucose or other metabolite(s) or altered counterregulatory hormone levels are sufficient to inhibit insulin release in response to potent insulin secretagogues. Glucose 41-49 insulin Homo sapiens 327-334 15356061-10 2004 The mechanism accounting for the reduced dextrose requirement during hypoglycemia likely involves a markedly decreased insulin secretory response to the agents during hypoglycemia and suggests that at modest hypoglycemia, low glucose or other metabolite(s) or altered counterregulatory hormone levels are sufficient to inhibit insulin release in response to potent insulin secretagogues. Glucose 41-49 insulin Homo sapiens 327-334 15612449-3 2004 These abnormalities in hormone secretion, coupled with impaired insulin-induced suppression of glucose production and stimulation of splanchnic glucose uptake, likely account in large part for the excessive amounts of glucose that reach the systemic circulation for disposal by peripheral tissues following food ingestion. Glucose 95-102 insulin Homo sapiens 64-71 15612449-3 2004 These abnormalities in hormone secretion, coupled with impaired insulin-induced suppression of glucose production and stimulation of splanchnic glucose uptake, likely account in large part for the excessive amounts of glucose that reach the systemic circulation for disposal by peripheral tissues following food ingestion. Glucose 144-151 insulin Homo sapiens 64-71 15334372-6 2004 Total glucose requirement during moderate exercise (sum of alimentary and extracellular source) was correlated (r = 0.739, P <.001) to plasma insulin concentration, but not with fitness level. Glucose 6-13 insulin Homo sapiens 145-152 15334374-9 2004 In all subjects, the women with the Arg64 allele (n = 76) had significantly higher level of insulin secretion (the ratio of Deltainsulin(60)/Deltaglucose(60)) during OGTT than those without (n = 223) (P =.03) despite similar plasma levels of glucose and insulin in both genotypes. Glucose 146-153 insulin Homo sapiens 92-99 15166251-0 2004 Glucose regulation of insulin gene expression requires the recruitment of p300 by the beta-cell-specific transcription factor Pdx-1. Glucose 0-7 insulin Homo sapiens 22-29 15166251-1 2004 Regulation of insulin gene expression in response to increases in blood glucose levels is essential for maintaining normal glucose homeostasis; however, the exact mechanisms by which glucose stimulates insulin gene transcription are not known. Glucose 72-79 insulin Homo sapiens 14-21 15166251-1 2004 Regulation of insulin gene expression in response to increases in blood glucose levels is essential for maintaining normal glucose homeostasis; however, the exact mechanisms by which glucose stimulates insulin gene transcription are not known. Glucose 123-130 insulin Homo sapiens 14-21 15166251-1 2004 Regulation of insulin gene expression in response to increases in blood glucose levels is essential for maintaining normal glucose homeostasis; however, the exact mechanisms by which glucose stimulates insulin gene transcription are not known. Glucose 123-130 insulin Homo sapiens 14-21 15166251-2 2004 We have shown previously that glucose stimulates insulin gene expression by causing the hyperacetylation of histone H4 at the insulin promoter. Glucose 30-37 insulin Homo sapiens 49-56 15166251-2 2004 We have shown previously that glucose stimulates insulin gene expression by causing the hyperacetylation of histone H4 at the insulin promoter. Glucose 30-37 insulin Homo sapiens 126-133 15166251-3 2004 We demonstrate that the histone acetyltransferase p300 is recruited to the insulin promoter only at high concentrations of glucose via its interaction with the beta-cell-specific transcription factor Pdx-1. Glucose 123-130 insulin Homo sapiens 75-82 15166251-4 2004 Disruption of the function of the endogenous Pdx-1 abolishes the recruitment of p300 to the insulin gene promoter at high concentrations of glucose and results in decreased histone H4 acetylation and insulin gene expression. Glucose 140-147 insulin Homo sapiens 92-99 15166251-6 2004 Based on these data, we conclude that hyperacetylation of histone H4 at the insulin gene promoter in response to high concentrations of glucose depends on the beta-cell-specific transcription factor Pdx-1, which is required for the recruitment of the histone acetyltransferase p300 to the insulin gene promoter. Glucose 136-143 insulin Homo sapiens 76-83 15166251-6 2004 Based on these data, we conclude that hyperacetylation of histone H4 at the insulin gene promoter in response to high concentrations of glucose depends on the beta-cell-specific transcription factor Pdx-1, which is required for the recruitment of the histone acetyltransferase p300 to the insulin gene promoter. Glucose 136-143 insulin Homo sapiens 289-296 15166255-2 2004 To address this problem, we recently created clonal insulin-producing cell lines from the INS-1 insulinoma line, which exhibit glucose responsiveness ranging from poor to robust. Glucose 127-134 insulin Homo sapiens 52-59 15450006-1 2004 BACKGROUND: Homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) are measures of insulin resistance and insulin sensitivity derived from fasting glucose (FG) and insulin levels. Glucose 186-193 insulin Homo sapiens 122-129 15450006-1 2004 BACKGROUND: Homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) are measures of insulin resistance and insulin sensitivity derived from fasting glucose (FG) and insulin levels. Glucose 186-193 insulin Homo sapiens 122-129 15450006-1 2004 BACKGROUND: Homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) are measures of insulin resistance and insulin sensitivity derived from fasting glucose (FG) and insulin levels. Glucose 186-193 insulin Homo sapiens 122-129 15450006-4 2004 Total body insulin sensitivity (SI) was calculated using the minimal model and total glucose concentrations. Glucose 85-92 insulin Homo sapiens 11-18 15450006-5 2004 Peripheral insulin sensitivity (SI*) was calculated from labeled glucose concentrations. Glucose 65-72 insulin Homo sapiens 11-18 15450006-6 2004 Hepatic insulin resistance (HIR) was calculated by multiplying glucose production over the last hour by the average insulin level. Glucose 63-70 insulin Homo sapiens 8-15 15454864-2 2004 Dietary regulation of blood glucose level (via ingestion of food with a low glycemic index ensuring a low insulin level) improves the quality and duration of intellectual performance, if only because at rest the adult brain consumes 50 p. 100 of dietary carbohydrates, 80 p. 100 of them for energy purposes. Glucose 28-35 insulin Homo sapiens 106-113 15559444-4 2004 DIGAMI-2, by comparing three groups of subjects receiving various interventions, aimed at determining the relative benefit resulting from the insulin-glucose infusion in the acute phase and that attributable to long-term intensive insulin therapy in a similar population of type 2 diabetic patients. Glucose 150-157 insulin Homo sapiens 142-149 15498182-6 2004 (2) The blood sugar and insulin levels of fasting, 30 min, 60 min, 120 min after glucose loading in obese PCOS (BMI >/= 25 kg/m(2)) were significantly higher than those in the non-obese PCOS (BMI < 25 kg/m(2)). Glucose 81-88 insulin Homo sapiens 24-31 15317941-2 2004 Extracellular glucose stimulates insulin secretion from islet beta cells through an increase in redox state, which can be measured by NAD(P)H autofluorescence. Glucose 14-21 insulin Homo sapiens 33-40 15647716-4 2004 Progressive deterioration in beta-cell function as demonstrated in the United Kingdom Prospective Diabetes Study (UKPDS) and/or worsening of insulin resistance leads to deterioration in glucose tolerance and to secondary failure of oral antidiabetic drugs. Glucose 186-193 insulin Homo sapiens 141-148 15450302-6 2004 The proposed microcapsules provide a new mode for injection-type self-regulated drug delivery systems having the capability of adapting the release rate of drugs such as insulin in response to changes in glucose concentration, which is highly attractive for diabetes therapy. Glucose 204-211 insulin Homo sapiens 170-177 15277147-10 2004 C-peptide and insulin, as expressed by their areas under the curves, were raised not only during the early response to the glucose load but also in the postabsorptive state. Glucose 123-130 insulin Homo sapiens 14-21 15277150-13 2004 CONCLUSIONS: Energy restriction and vigorous exercise independently and additively reduce glucose and insulin concentrations in response to an oral-glucose-tolerance test. Glucose 148-155 insulin Homo sapiens 102-109 15277156-3 2004 OBJECTIVE: The aim was to dissect out insulin action with respect to whole-body energy homeostasis and glucose, protein, and lipid metabolism in patients with DM1 to assess the relevance of insulin resistance to the heterogeneous clinical manifestations of this syndrome. Glucose 103-110 insulin Homo sapiens 38-45 14665448-12 2004 The accelerated deterioration in glucose tolerance in PCOS may result, in part, from a relative attenuation in the response of the beta-cell to the demand placed on it by factors exacerbating insulin resistance. Glucose 33-40 insulin Homo sapiens 192-199 15117727-6 2004 Exercise training reduced glucose-stimulated hyperinsulinemia (before: 13.65 +/- 2.6 vs. 9.84 +/- 1.5 mU.ml(-1).min; P = 0.04) and insulin resistance. Glucose 26-33 insulin Homo sapiens 50-57 15271748-3 2004 For every 1 to 50-mg/dL increase in blood glucose concentration more than 100 mg/dL, 1 U of insulin was added to the injection port of a 100-mL measured volume set containing 5% dextrose in water. Glucose 178-186 insulin Homo sapiens 92-99 15226630-3 2004 An insulin resistance index was estimated using the homeostasis model assessment (HOMA-IR) of fasting insulin - glucose interactions. Glucose 112-119 insulin Homo sapiens 3-10 19003248-1 2004 Insulin is involved in a number of cellular functions, including the stimulation of cell growth, cell cycle progression and glucose uptake and is a common protein supplement in serum-free mammalian cell culture media. Glucose 124-131 insulin Homo sapiens 0-7 15322863-3 2004 RESULTS: The frequency of insulin resistance syndrome counted on the basis of fasting plasma glucose and insulin concentrations according to Duncan et al. Glucose 93-100 insulin Homo sapiens 26-33 15531002-1 2004 BACKGROUND: Thiazolidinediones (TZDs) are widely used oral antihyperglycemic drugs that facilitate insulin action and increase insulin-stimulated glucose metabolism, thereby decreasing insulin resistance. Glucose 146-153 insulin Homo sapiens 127-134 15531002-1 2004 BACKGROUND: Thiazolidinediones (TZDs) are widely used oral antihyperglycemic drugs that facilitate insulin action and increase insulin-stimulated glucose metabolism, thereby decreasing insulin resistance. Glucose 146-153 insulin Homo sapiens 127-134 15331532-4 2004 SOCS-3 mRNA levels were significantly increased in the skeletal muscle of type 2 diabetic patients compared with control subjects and correlated with reduced insulin-stimulated glucose uptake. Glucose 177-184 insulin Homo sapiens 158-165 15331545-5 2004 Metabolic and hormonal characteristics of the GI group included significantly higher fasting and glucose-stimulated insulin levels, more severe insulin resistance, hyperandrogenemia, and significantly higher cortisol and androstenedione responses to 1-24 ACTH stimulation. Glucose 97-104 insulin Homo sapiens 116-123 15333490-9 2004 After further adjustment for insulin resistance, determined by the frequently sampled intravenous glucose tolerance test and waist circumference, each additional CVD RF increased the risk of type 2 diabetes significantly (OR 1.81, 95% CI 1.49-2.20). Glucose 98-105 insulin Homo sapiens 29-36 15349727-5 2004 MCP-1 decreases insulin-stimulated glucose uptake into adipocytes. Glucose 35-42 insulin Homo sapiens 16-23 15054439-10 2004 neither during the IVGTT, nor in insulin-stimulated glucose disposal during the clamp. Glucose 52-59 insulin Homo sapiens 33-40 15356026-8 2004 During the insulin clamp, endogenous (hepatic) glucose production decreased (Delta = -2.67 micromol/fat-free mass.min, P < 0.05 vs. placebo), whereas metabolic clearance rate of glucose (MCR) increased (Delta = 0.58 ml/fat-free mass.min, P < 0.05 vs. placebo) after PIO. Glucose 47-54 insulin Homo sapiens 11-18 15356069-7 2004 Moreover, basal and insulin-induced glucose transport were two times higher in weaned than in adult rats. Glucose 36-43 insulin Homo sapiens 20-27 15356082-10 2004 This may be explained by a glucose-mediated potentiation of the antilipolytic effectiveness of insulin. Glucose 27-34 insulin Homo sapiens 95-102 15352073-1 2004 BACKGROUND: Cell-based therapies for treating insulin-dependent diabetes (IDD) can provide a more physiologic regulation of blood glucose levels in a less invasive fashion than insulin injections. Glucose 130-137 insulin Homo sapiens 46-53 15231849-1 2004 Nitric oxide (NO) is involved in adipose tissue biology by influencing adipogenesis, insulin-stimulated glucose uptake, and lipolysis. Glucose 104-111 insulin Homo sapiens 85-92 15370997-1 2004 In this manuscript, the well-known Bergman nonlinear mathematical model of the plasma glucose/insulin interaction is adopted and a semi closed-loop optimal technique is proposed for the correction of hyperglycemia in diabetic subjects. Glucose 86-93 insulin Homo sapiens 94-101 15334366-0 2004 Effects of weight loss in obese subjects with normal fasting plasma glucose or impaired glucose tolerance on insulin release and insulin resistance according to a minimal model analysis. Glucose 68-75 insulin Homo sapiens 109-116 15334366-7 2004 Capacity for insulin release in response to glucose increased in all subjects (first-phase insulin secretion [CS1], 4.66 +/- 4.05 v 6.81 +/- 4.57 ng/mL/5 min, P <.05), but the insulin sensitivity index (S(i)) did not change significantly. Glucose 44-51 insulin Homo sapiens 13-20 15334366-7 2004 Capacity for insulin release in response to glucose increased in all subjects (first-phase insulin secretion [CS1], 4.66 +/- 4.05 v 6.81 +/- 4.57 ng/mL/5 min, P <.05), but the insulin sensitivity index (S(i)) did not change significantly. Glucose 44-51 insulin Homo sapiens 91-98 15334366-7 2004 Capacity for insulin release in response to glucose increased in all subjects (first-phase insulin secretion [CS1], 4.66 +/- 4.05 v 6.81 +/- 4.57 ng/mL/5 min, P <.05), but the insulin sensitivity index (S(i)) did not change significantly. Glucose 44-51 insulin Homo sapiens 91-98 15334368-0 2004 Correlation of oral glucose tolerance test-derived estimates of insulin sensitivity with insulin clamp measurements in an African-American cohort. Glucose 20-27 insulin Homo sapiens 64-71 15334368-1 2004 The purpose of this study was to determine which measures obtained from an oral glucose tolerance test (OGTT) are the best estimates of insulin sensitivity measured directly using the euglycemic hyperinsulinemic clamp procedure. Glucose 80-87 insulin Homo sapiens 136-143 15334368-8 2004 These data indicate that fasting and OGTT-derived plasma insulin and glucose concentrations can be used to estimate insulin sensitivity in young adult African-Americans when it is not feasible to conduct the insulin clamp procedure. Glucose 69-76 insulin Homo sapiens 116-123 15334368-8 2004 These data indicate that fasting and OGTT-derived plasma insulin and glucose concentrations can be used to estimate insulin sensitivity in young adult African-Americans when it is not feasible to conduct the insulin clamp procedure. Glucose 69-76 insulin Homo sapiens 116-123 15314166-1 2004 GLUT4 (glucose transporter 4) plays a pivotal role in insulin-induced glucose uptake to maintain normal blood glucose levels. Glucose 7-14 insulin Homo sapiens 54-61 15314166-1 2004 GLUT4 (glucose transporter 4) plays a pivotal role in insulin-induced glucose uptake to maintain normal blood glucose levels. Glucose 70-77 insulin Homo sapiens 54-61 15314166-4 2004 GLUT4 activation can occur at the plasma membrane, since insulin was able to increase glucose uptake with a shorter time lag when inactive GLUT4 was first translocated to the plasma membrane by pretreating the cells with this peptide. Glucose 86-93 insulin Homo sapiens 57-64 15314166-5 2004 Inhibition of phosphatidylinositol (PI) 3-kinase activity failed to inhibit GLUT4 translocation by the peptide but did inhibit glucose uptake when insulin was added following peptide treatment. Glucose 127-134 insulin Homo sapiens 147-154 15258843-8 2004 Insulin resistance, estimated from values of plasma glucose ( r=0.70, P =0.03), plasma insulin ( r=0.59, P =0.02), and HOMA index ( r=0.62, P =0.01), was also directly related to the intake of monounsaturated fatty acids. Glucose 52-59 insulin Homo sapiens 0-7 15490412-13 2004 Many studies showed that carnitine allowed mitochondrial fatty acid usage to link to the rate of glucose usage, thus improving insulin resistance. Glucose 97-104 insulin Homo sapiens 127-134 15453119-0 2004 [Long acting insulin analogs: possibly more stable glucose regulation]. Glucose 51-58 insulin Homo sapiens 13-20 15258906-2 2004 These adverse effects of PI treatment result to a large extent from their inhibition of insulin-stimulated glucose transport. Glucose 107-114 insulin Homo sapiens 88-95 15317436-8 2004 Bolus (or mealtime) insulin, using short-acting or rapid-acting insulins (i.e., regular, aspart, lispro) covers mealtime carbohydrates and corrects the current glucose level. Glucose 160-167 insulin Homo sapiens 20-27 15317436-14 2004 Insulin aspart and insulin lispro provide similar A1C levels and quality of life, but lower postprandial glucose levels than regular insulin. Glucose 105-112 insulin Homo sapiens 0-7 15317436-14 2004 Insulin aspart and insulin lispro provide similar A1C levels and quality of life, but lower postprandial glucose levels than regular insulin. Glucose 105-112 insulin Homo sapiens 19-26 15271645-1 2004 The available evidence suggests that about two-thirds of the insulin response to an oral glucose load is due to the potentiating effect of gut-derived incretin hormones. Glucose 89-96 insulin Homo sapiens 61-68 15068394-1 2004 The aim of the present study was to investigate the impact of an oral glucose load on circulating insulin and glucose levels and arterial function in healthy non-diabetic subjects. Glucose 70-77 insulin Homo sapiens 98-105 15297112-9 2004 RESULTS: Endogenous glucose release during insulin infusion increased after surgery in the placebo group. Glucose 20-27 insulin Homo sapiens 43-50 15297112-11 2004 CONCLUSIONS: While insulin resistance in the first day after surgery has previously been characterised by reduced glucose disposal, enhanced endogenous glucose release was the main component of postoperative insulin resistance on the third postoperative day. Glucose 114-121 insulin Homo sapiens 19-26 15297113-0 2004 Insulin stimulated glucose disposal in peripheral tissues studied with microdialysis and stable isotope tracers. Glucose 19-26 insulin Homo sapiens 0-7 15312202-3 2004 Increased doses of exogenous insulin caused preferential use of glucose as a metabolic substrate, while total energy expenditure remained constant. Glucose 64-71 insulin Homo sapiens 29-36 15142986-9 2004 Moreover, beta/H1beta-KO islets had increased HNF1alpha and Pdx-1, decreased HNF4 mRNA levels, and reduced glucose-stimulated insulin release. Glucose 107-114 insulin Homo sapiens 126-133 15277384-0 2004 Insulin dose-response curves for stimulation of splanchnic glucose uptake and suppression of endogenous glucose production differ in nondiabetic humans and are abnormal in people with type 2 diabetes. Glucose 59-66 insulin Homo sapiens 0-7 15277384-1 2004 To determine whether the insulin dose-response curves for suppression of endogenous glucose production (EGP) and stimulation of splanchnic glucose uptake (SGU) differ in nondiabetic humans and are abnormal in type 2 diabetes, 14 nondiabetic and 12 diabetic subjects were studied. Glucose 84-91 insulin Homo sapiens 25-32 15277390-10 2004 Of the NCEP criteria, waist circumference and triglycerides may best identify insulin resistance and visceral adiposity in individuals with a fasting plasma glucose <6.4 mmol/l. Glucose 157-164 insulin Homo sapiens 78-85 15277403-9 2004 Insulin-stimulated glucose uptake increased significantly with rosiglitazone but not with metformin. Glucose 19-26 insulin Homo sapiens 0-7 15277420-2 2004 RESEARCH DESIGN AND METHODS: We analyzed basal and longitudinal changes of serum C-peptide levels during a 75-g oral glucose tolerance test (OGTT) in 125 consecutively recruited patients with type 1 diabetes including fulminant type 1 diabetes (n = 25) and acute-onset type 1 diabetes (n = 100). Glucose 117-124 insulin Homo sapiens 81-90 15277425-5 2004 We compared the phenotypic characteristics of those with and without the variant by diagnostic status and determined the insulin secretory response to intravenous glucose and tolbutamide among nondiabetic family members. Glucose 163-170 insulin Homo sapiens 121-128 15277430-1 2004 OBJECTIVE: To evaluate the role of adiposity in the relationship between specific and surrogate estimates of insulin-mediated glucose uptake (IMGU) in a large nondiabetic population. Glucose 126-133 insulin Homo sapiens 109-116 15277436-5 2004 Insulin sensitivity (glucose infusion rate [GIR]) was measured by the euglycemic-hyperinsulinemic clamp. Glucose 21-28 insulin Homo sapiens 0-7 15309295-4 2004 RESULTS: Exposure of myotubes to 20 mmol/l glucose for 4 days reduced insulin-stimulated glucose uptake and glycogen synthesis to 57+/-5% (p<0.0001) and 56+/-5% (p<0.0001) of normoglycaemic (5.5 mmol/l glucose) controls respectively. Glucose 43-50 insulin Homo sapiens 70-77 15309295-4 2004 RESULTS: Exposure of myotubes to 20 mmol/l glucose for 4 days reduced insulin-stimulated glucose uptake and glycogen synthesis to 57+/-5% (p<0.0001) and 56+/-5% (p<0.0001) of normoglycaemic (5.5 mmol/l glucose) controls respectively. Glucose 89-96 insulin Homo sapiens 70-77 15309295-4 2004 RESULTS: Exposure of myotubes to 20 mmol/l glucose for 4 days reduced insulin-stimulated glucose uptake and glycogen synthesis to 57+/-5% (p<0.0001) and 56+/-5% (p<0.0001) of normoglycaemic (5.5 mmol/l glucose) controls respectively. Glucose 89-96 insulin Homo sapiens 70-77 15321011-11 2004 Normalization of the fasting blood glucose, through whatever strategy, minimizes glucotoxicity and insulin resistance, profoundly influences daytime glycemic control, and profoundly reduces the risk of the complications of diabetes. Glucose 35-42 insulin Homo sapiens 99-106 15296476-10 2004 RESULTS: Glucose-stimulated insulin release was significantly lower after exposure to PK11195 than after exposure to Ro5-4864. Glucose 9-16 insulin Homo sapiens 28-35 15262911-4 2004 Insulin secretion was measured by deconvolution of C-peptide data obtained during an oral glucose tolerance test, and dynamic indices of beta-cell function were calculated by mathematical modeling. Glucose 90-97 insulin Homo sapiens 0-7 15311441-1 2004 Insulin glargine is a biosynthetic human insulin analogue that controls blood glucose levels over 24 hours without a pronounced peak. Glucose 78-85 insulin Homo sapiens 0-7 15311441-1 2004 Insulin glargine is a biosynthetic human insulin analogue that controls blood glucose levels over 24 hours without a pronounced peak. Glucose 78-85 insulin Homo sapiens 41-48 15318731-1 2004 Peripheral insulin resistance is the failure of proper cellular glucose uptake in response to insulin. Glucose 64-71 insulin Homo sapiens 11-18 15318731-1 2004 Peripheral insulin resistance is the failure of proper cellular glucose uptake in response to insulin. Glucose 64-71 insulin Homo sapiens 94-101 15292352-2 2004 The observation that insulin stimulates glucose oxidation in endometrial cells led us to investigate the presence of GLUT4 in this tissue and whether a defect of GLUT4 is present at the endometrial level in PCOSs. Glucose 40-47 insulin Homo sapiens 21-28 15292314-4 2004 Administration of pioglitazone resulted in a remarkable decline in both fasting serum insulin levels (P < 0.02) and the area under the insulin response curve after an oral glucose load (P < 0.02). Glucose 175-182 insulin Homo sapiens 138-145 15292339-1 2004 Insulin resistance in obesity is partly due to diminished glucose transport in myocytes and adipocytes, but underlying mechanisms are uncertain. Glucose 58-65 insulin Homo sapiens 0-7 15292339-2 2004 Insulin-stimulated glucose transport requires activation of phosphatidylinositol (PI) 3-kinase (3K), operating downstream of insulin receptor substrate-1. Glucose 19-26 insulin Homo sapiens 0-7 15292339-5 2004 Presently, we examined insulin activation of glucose transport and signaling factors in cultured adipocytes derived from preadipocytes harvested during elective liposuction in lean and obese women. Glucose 45-52 insulin Homo sapiens 23-30 15292339-9 2004 These findings suggest the presence of defects in PI3K and aPKC activation that persist in cultured cells and limit insulin-stimulated glucose transport in adipocytes and myocytes of obese subjects. Glucose 135-142 insulin Homo sapiens 116-123 15390330-16 2004 The peripheral insulin resistance in cirrhosis is characterized by a decrease in nonoxidative glucose disposal that is improved, but not normalized, after OLT. Glucose 94-101 insulin Homo sapiens 15-22 15277999-2 2004 The gold standard in measuring insulin resistance is glucose clamp, but this method is difficult to apply in large studies. Glucose 53-60 insulin Homo sapiens 31-38 15281001-3 2004 The abnormal glucose-stimulated insulin secretion in MODY1 subjects may be due to reduced glucose transport and glycolysis. Glucose 13-20 insulin Homo sapiens 32-39 15281004-9 2004 Insulin sensitivity, evaluated as glucose infusion rate using the hyperinsulinemic euglycemic clamp technique, in the MHN-01 group was higher than that in the SBF group. Glucose 34-41 insulin Homo sapiens 0-7 15308130-1 2004 Increased glucose metabolism through the hexosamine pathway may result in insulin resistance, impaired insulin secretion, and diabetic nephropathy. Glucose 10-17 insulin Homo sapiens 74-81 15257102-4 2004 In acute incubations with glucose-responsive BRIN-BD11 cells, fractions 39-40 (band 1) and fractions 43-46 (band 2) significantly stimulated insulin release by 1.5 to 2.5-fold. Glucose 26-33 insulin Homo sapiens 141-148 15340119-6 2004 The insulin sensitivity index (SI) was determined from the minimal model using data obtained from the frequently sampled intravenous glucose tolerance test. Glucose 133-140 insulin Homo sapiens 4-11 15675270-14 2004 Short-term intensive insulin therapy by MDI, CSII and IVII gives good glycemic control and significantly reduces mean daily glucose values, but this aim can be achieved most quickly using CSII and IVII. Glucose 124-131 insulin Homo sapiens 21-28 15276423-0 2004 Inhibition of insulin-dependent glucose uptake by trivalent arsenicals: possible mechanism of arsenic-induced diabetes. Glucose 32-39 insulin Homo sapiens 14-21 15276423-5 2004 In contrast, trivalent arsenicals, arsenite (iAs(III)), methylarsine oxide (MAs(III)O), and iododimethylarsine (DMAs(III)O) inhibited insulin-stimulated glucose uptake in a concentration-dependent manner. Glucose 153-160 insulin Homo sapiens 134-141 15276423-6 2004 Subtoxic concentrations of iAs(III) (20 microM), MAs(III)O (1 microM), or DMAs(III)I (2 microM) decreased insulin-stimulated glucose uptake by 35-45%. Glucose 125-132 insulin Homo sapiens 106-113 15276423-10 2004 These results suggest that trivalent arsenicals inhibit insulin-stimulated glucose uptake by interfering with the PKB/Akt-dependent mobilization of GLUT4 transporters in adipocytes. Glucose 75-82 insulin Homo sapiens 56-63 16134594-5 2004 Multiple stepwise linear regression model of insulin resistance was measured using C-peptide x blood glucose as independent variables and Homa-IR was used as the dependent variable, while the model of islet beta cell function was determined using C-peptide/(fasting blood glucose - 3.5) as the independent variable and Homaislet as the dependent variable. Glucose 101-108 insulin Homo sapiens 45-52 16134594-5 2004 Multiple stepwise linear regression model of insulin resistance was measured using C-peptide x blood glucose as independent variables and Homa-IR was used as the dependent variable, while the model of islet beta cell function was determined using C-peptide/(fasting blood glucose - 3.5) as the independent variable and Homaislet as the dependent variable. Glucose 272-279 insulin Homo sapiens 45-52 15166230-1 2004 Insulin stimulates glucose uptake into muscle and fat cells by translocating glucose transporter 4 (GLUT4) to the cell surface, with input from phosphatidylinositol (PI) 3-kinase and its downstream effector Akt/protein kinase B. Glucose 19-26 insulin Homo sapiens 0-7 15241473-0 2004 GRK2 is an endogenous protein inhibitor of the insulin signaling pathway for glucose transport stimulation. Glucose 77-84 insulin Homo sapiens 47-54 15241473-2 2004 Recently, we have reported that the heterotrimeric G protein alpha-subunit, Galphaq/11, can mediate insulin-stimulated glucose transport. Glucose 119-126 insulin Homo sapiens 100-107 15241473-4 2004 Therefore, we postulated that GRK2 could be an inhibitor of the insulin signaling cascade leading to glucose transport in 3T3-L1 adipocytes. Glucose 101-108 insulin Homo sapiens 64-71 15241473-7 2004 Taken together, these results indicate that through its RGS domain endogenous GRK2 functions as a negative regulator of insulin-stimulated glucose transport by interfering with Galphaq/11 signaling to GLUT4 translocation. Glucose 139-146 insulin Homo sapiens 120-127 15193996-6 2004 In prediabetic monkeys, the reduction of hyperinsulinaemia and improvement of insulin-stimulated glucose uptake rate indicated amelioration of insulin resistance. Glucose 97-104 insulin Homo sapiens 78-85 15332693-6 2004 The American Diabetes Association recommends starting insulin therapy when MNT fails to maintain plasma glucose concentrations at < or = 105 mg/dL during fasting, < or = 155 mg/dL one hour after eating, or < or = 130 mg/dL two hours after eating. Glucose 104-111 insulin Homo sapiens 54-61 15181163-3 2004 Such plasticity of the insulin secretory competence would imply that glucose and incretins not only act during the present meal, but also help to prepare the beta cells to function during the subsequent meal. Glucose 69-76 insulin Homo sapiens 23-30 15257035-8 2004 Pretransplant homeostasis model assessment for insulin resistance (HOMA-IR) index was calculated from fasting plasma glucose and insulin. Glucose 117-124 insulin Homo sapiens 47-54 15234411-6 2004 RESULTS: Plasma glucose responses were higher during the oral glucose tolerance tests in patients with IDCM (p < 0.01), associated with significantly higher plasma insulin concentrations following the oral glucose challenge (p < 0.01). Glucose 16-23 insulin Homo sapiens 167-174 15234411-6 2004 RESULTS: Plasma glucose responses were higher during the oral glucose tolerance tests in patients with IDCM (p < 0.01), associated with significantly higher plasma insulin concentrations following the oral glucose challenge (p < 0.01). Glucose 62-69 insulin Homo sapiens 167-174 15234411-6 2004 RESULTS: Plasma glucose responses were higher during the oral glucose tolerance tests in patients with IDCM (p < 0.01), associated with significantly higher plasma insulin concentrations following the oral glucose challenge (p < 0.01). Glucose 62-69 insulin Homo sapiens 167-174 15123681-9 2004 When IRS-2 Ser/Thr-Pro motif phosphorylation was examined, chronic insulin + high glucose resulted in a 92% increase in IRS-2 Ser/Thr-Pro motif phosphorylation without a change in IRS-2 mass. Glucose 82-89 insulin Homo sapiens 67-74 15123681-10 2004 Pretreatment of matured U937 cells with rapamycin blocked chronic insulin + high glucose-dependent IRS-2 Ser/Thr-Pro motif phosphorylation and restored IL-4-dependent IRS-2-associated PI3-kinase activity. Glucose 81-88 insulin Homo sapiens 66-73 15211435-7 2004 Plasma total homocysteine and insulin levels at 2 hours after a 75-g glucose tolerance test correlated significantly with lacunae. Glucose 69-76 insulin Homo sapiens 30-37 15213023-0 2004 Caffeine ingestion increases the insulin response to an oral-glucose-tolerance test in obese men before and after weight loss. Glucose 61-68 insulin Homo sapiens 33-40 15213023-1 2004 BACKGROUND: Caffeine ingestion decreases the insulin sensitivity index (ISI) for an oral-glucose-tolerance test (OGTT) and decreases insulin-induced glucose disposal in lean male subjects during a hyperinsulinemic clamp. Glucose 89-96 insulin Homo sapiens 45-52 14998785-8 2004 After antecedent hypoglycemia, endogenous glucose production (EGP) was significantly reduced in men only, paralleling a reduction in the glucagon-to-insulin ratio and catecholamine responses. Glucose 42-49 insulin Homo sapiens 149-156 14998786-0 2004 Loss of entrainment of high-frequency plasma insulin oscillations in type 2 diabetes is likely a glucose-specific beta-cell defect. Glucose 97-104 insulin Homo sapiens 45-52 14998786-1 2004 Spontaneous high-frequency insulin oscillations are easily entrainable to exogenous glucose in vitro and in vivo, but this property is lost in type 2 diabetes (2-DM). Glucose 84-91 insulin Homo sapiens 27-34 14998786-12 2004 We conclude that loss of entrainment of spontaneous high-frequency insulin oscillations in 2-DM is likely a glucose-specific manifestation of beta-cell secretory dysfunction. Glucose 108-115 insulin Homo sapiens 67-74 15150382-3 2004 OBJECTIVE: To examine and report on the performance of an insulin infusion protocol to maintain TGC, defined as a blood glucose level of 80-150 mg/dL, in critically ill cardiothoracic surgical patients. Glucose 120-127 insulin Homo sapiens 58-65 15187219-10 2004 Glucose levels in critically ill patients should be controlled through implementation of insulin protocols with the goal to achieve normoglycemia, regardless of a history of diabetes. Glucose 0-7 insulin Homo sapiens 89-96 15210671-2 2004 METHODS: The standard intravenous glucose tolerance test (IVGTT) was used to measure the first phase insulin response (FPIR) cumulatively at one and three minutes. Glucose 34-41 insulin Homo sapiens 101-108 15210671-6 2004 RESULTS: One child had a subnormal insulin secretory response to intravenous glucose that remained abnormal two and four years later. Glucose 77-84 insulin Homo sapiens 35-42 15210671-10 2004 Measures of insulin response to intravenous glucose loading are often normal but suggest future recurrence if profoundly abnormal. Glucose 44-51 insulin Homo sapiens 12-19 15192439-7 2004 Moreover, the same pattern of gene expression is also observed in insulin resistant "prediabetic" individuals with normal glucose tolerance. Glucose 122-129 insulin Homo sapiens 66-73 15171754-2 2004 AIM: This study examines the effect of glucosamine on glucose uptake by cultured L6 muscle cells as a model of insulin resistance. Glucose 54-61 insulin Homo sapiens 111-118 15171754-3 2004 METHODS: Glucose uptake by L6 myotubes was measured using the non-metabolized glucose analogue 2-deoxy-d-glucose after incubation with glucosamine for 4 and 24 h, with and without insulin and several other agents (metformin, peroxovanadium and d-pinitol) that improve glucose uptake in diabetic states. Glucose 9-16 insulin Homo sapiens 180-187 15171754-4 2004 RESULTS: After 4 h, high concentrations of glucosamine (5 x 10(-3) and 10(-2) M) reduced basal and insulin-stimulated glucose uptake by up to 50%. Glucose 118-125 insulin Homo sapiens 99-106 15171754-9 2004 CONCLUSION: Glucosamine decreased insulin-stimulated glucose uptake by L6 muscle cells, providing a potential model of insulin resistance with similarities to glucose toxicity. Glucose 53-60 insulin Homo sapiens 34-41 15220248-6 2004 In the former group, there was also a significant positive correlation between the augmented plasma intact and total GIP levels and both fasting and post-oral glucose load plasma insulin levels. Glucose 159-166 insulin Homo sapiens 179-186 15220249-4 2004 Insulin sensitivity was determined as M/I, the amount of glucose metabolized per unit of plasma insulin (I). Glucose 57-64 insulin Homo sapiens 0-7 15220249-4 2004 Insulin sensitivity was determined as M/I, the amount of glucose metabolized per unit of plasma insulin (I). Glucose 57-64 insulin Homo sapiens 96-103 15243703-0 2004 Non-esterified fatty acids impair insulin-mediated glucose uptake and disposition in the liver. Glucose 51-58 insulin Homo sapiens 34-41 15243703-1 2004 AIMS/HYPOTHESIS: We investigated the effect of elevated circulating NEFA on insulin-mediated hepatic glucose uptake (HGU) and whole-body glucose disposal (M) in eight healthy male subjects. Glucose 101-108 insulin Homo sapiens 76-83 15249997-8 2004 The sensitivity of late-phase insulin secretion to glucose declined at FPG concentrations above 6.0 mmol/l. Glucose 51-58 insulin Homo sapiens 30-37 15252707-10 2004 During the first year of follow-up, changes in fasting glucose and insulin indicated a significant fall in insulin resistance in actively treated women compared to the control subjects (Year 1 to baseline between-group difference -0.22+/-0.10, p=0.03). Glucose 55-62 insulin Homo sapiens 107-114 15248820-1 2004 OBJECTIVE: Modest elevations in circulating IGF-I levels have been suggested to protect against the development of glucose intolerance in insulin-resistant subjects. Glucose 115-122 insulin Homo sapiens 138-145 15194655-5 2004 Insulin resistance was estimated from plasma insulin and glucose as the homeostasis model assessment index. Glucose 57-64 insulin Homo sapiens 0-7 15240640-4 2004 Glucose-stimulated insulin secretion was lower in TS; e.g. the initial insulin response (DeltaI/DeltaG(30)) was decreased by 60% compared with POF (P < 0.0001). Glucose 0-7 insulin Homo sapiens 19-26 15240640-4 2004 Glucose-stimulated insulin secretion was lower in TS; e.g. the initial insulin response (DeltaI/DeltaG(30)) was decreased by 60% compared with POF (P < 0.0001). Glucose 0-7 insulin Homo sapiens 71-78 15240640-5 2004 We also compared responses to a standard iv glucose tolerance test in women with TS and in age- and body mass index-matched normal women and found that the insulin area under the curve was 50% lower in women with TS (P = 0.003). Glucose 44-51 insulin Homo sapiens 156-163 15505998-5 2004 In cultured rat pancreatic islets, the human autoantibodies inhibit glucose-induced insulin release, whereas, in human pancreatic islets CD38 autoantibodies stimulate glucose-mediated insulin secretion. Glucose 68-75 insulin Homo sapiens 84-91 15505998-8 2004 Transgenic mice overexpressing CD38 show enhanced glucose-induced insulin release, whereas, conversely, CD38 knockout mice display a severe impairment in beta-cell function. Glucose 50-57 insulin Homo sapiens 66-73 15246219-6 2004 HOMA-R [insulin 0xglucose 0/22.5] was greater in patients with both impaired glucose tolerance and DM than in those with normal glucose tolerance (P<0.01). Glucose 18-25 insulin Homo sapiens 8-15 15246219-9 2004 CONCLUSIONS: Both insulin resistance and beta-cell dysfunction contribute to glucose intolerance in CHC patients. Glucose 77-84 insulin Homo sapiens 18-25 15232309-13 2004 In 2 patients who were able to maintain extremely high endogenous insulin production, the fasting blood glucose remained normal even though post-glucose-challenge levels were elevated. Glucose 104-111 insulin Homo sapiens 66-73 15232309-13 2004 In 2 patients who were able to maintain extremely high endogenous insulin production, the fasting blood glucose remained normal even though post-glucose-challenge levels were elevated. Glucose 145-152 insulin Homo sapiens 66-73 15235323-3 2004 However, during the past decade major advances have been made in our understanding of the molecular and cellular mechanisms regulating the entry of glucose into insulin-sensitive tissues. Glucose 148-155 insulin Homo sapiens 161-168 15235325-3 2004 This review examines the premise that an oversupply and/or accumulation of lipid directly inhibits insulin action on glucose metabolism via changes at the level of substrate competition, enzyme regulation, intracellular signaling, and/or gene transcription. Glucose 117-124 insulin Homo sapiens 99-106 15235328-1 2004 The molecular signaling mechanisms by which insulin leads to increased glucose transport and metabolism and gene expression are not completely elucidated. Glucose 71-78 insulin Homo sapiens 44-51 15235328-5 2004 Current work is focused on mechanisms behind insulin-dependent and insulin-independent regulation of glucose uptake. Glucose 101-108 insulin Homo sapiens 45-74 15235328-6 2004 We have recently determined the independent effects of insulin and hypoxia/AICAR exposure on glucose transport and cell surface GLUT4 content in skeletal muscle from nondiabetic and Type 2 diabetic subjects. Glucose 93-100 insulin Homo sapiens 55-62 15235328-10 2004 Our studies highlight important AMPK-dependent and independent pathways in the regulation of GLUT4 and glucose transport activity in insulin resistant skeletal muscle. Glucose 103-110 insulin Homo sapiens 133-140 15462099-8 2004 Insulin/glucose ratio (I/G) was calculated as marker of insulin resistance. Glucose 8-15 insulin Homo sapiens 56-63 15462099-14 2004 Significant decrease in HbA1c with stable insulin concentration may indicate positive impact of intravenous 1,25(OH)2D3 therapy on long-term glucose metabolism. Glucose 141-148 insulin Homo sapiens 42-49 15227734-1 2004 Central obesity with visceral fat accumulation and the amount of skeletal muscle mass may influence insulin sensitivity via its capacity for glucose load uptake. Glucose 141-148 insulin Homo sapiens 100-107 15105415-0 2004 Increased beta-oxidation in muscle cells enhances insulin-stimulated glucose metabolism and protects against fatty acid-induced insulin resistance despite intramyocellular lipid accumulation. Glucose 69-76 insulin Homo sapiens 50-57 15105415-4 2004 Two to 3-fold overexpression of L-CPT I, the endogenous isoform in L6 cells, proportionally increased oxidation of the long-chain fatty acids palmitate and oleate and increased insulin stimulation of [(14)C]glucose incorporation into glycogen by 60% while enhancing insulin-stimulated phosphorylation of p38MAPK. Glucose 207-214 insulin Homo sapiens 177-184 15105415-5 2004 Incubation of control cells with 0.2 mm palmitate for 18 h caused accumulation of triacylglycerol, diacylglycerol, and ceramide (but not long-chain acyl-CoA) and decreased insulin-stimulated [(14)C]glucose incorporation into glycogen (60%), [(3)H]deoxyglucose uptake (60%), and protein kinase B phosphorylation (20%). Glucose 198-205 insulin Homo sapiens 172-179 15147975-1 2004 Insulin controls or alters glucose, protein, and fat metabolism as well as other cellular functions. Glucose 27-34 insulin Homo sapiens 0-7 15147975-2 2004 Insulin binds to a specific receptor on the cell membrane initiating a protein phosphorylation cascade that controls glucose uptake and metabolism and long-term effects such as mitogenesis. Glucose 117-124 insulin Homo sapiens 0-7 15147975-10 2004 This supports a biologically important effect of insulin metabolism and insulin degradation products on insulin action on non-glucose pathways. Glucose 126-133 insulin Homo sapiens 49-56 15220201-4 2004 This study includes information on directly measured insulin sensitivity (S(i)) from the frequently sampled intravenous glucose tolerance test among African-American, Hispanic, and non-Hispanic white subjects aged 40-69 years. Glucose 120-127 insulin Homo sapiens 53-60 15238996-9 2004 On glucose challenge, insulin release from transfected islets was comparable to nontransfected islets. Glucose 3-10 insulin Homo sapiens 22-29 15170466-8 2004 RESULTS: In all age-sex groups, adiposity indices, blood pressure (BP), plasma glucose and triglycerides (TG) increased significantly with increasing insulin quartiles while HDL cholesterol (HDL-C) decreased. Glucose 79-86 insulin Homo sapiens 150-157 15240627-5 2004 Between t = 0-180 min blood glucose, plasma insulin and plasma glucose-dependent insulin-releasing polypeptide were greater with the variable, compared with the constant, infusion. Glucose 63-70 insulin Homo sapiens 81-88 15240627-7 2004 We conclude that modest variations in the initial rate of duodenal glucose entry may have profound effects on subsequent glycemic, insulin, and incretin responses. Glucose 67-74 insulin Homo sapiens 131-138 15240629-0 2004 Cultured muscle cells from insulin-resistant type 2 diabetes patients have impaired insulin, but normal 5-amino-4-imidazolecarboxamide riboside-stimulated, glucose uptake. Glucose 156-163 insulin Homo sapiens 27-34 15240629-4 2004 Insulin-stimulated glucose uptake (100 nm; P < 0.05) and insulin-stimulated glycogen synthesis (1 nm; P < 0.01) were significantly impaired in the diabetic vs. control cultures. Glucose 19-26 insulin Homo sapiens 0-7 15240633-2 2004 Exendin-4 and tGLP-1 can reduce blood glucose levels by stimulating insulin secretion, inhibiting glucagon secretion, and delaying gastric emptying. Glucose 38-45 insulin Homo sapiens 68-75 15225135-8 2004 The islets generated within 3-4 weeks exhibited a mixed population of large- and small-sized islets with clear cut dichotomy in the pattern of their insulin secretion in response to L-arginine and glucose. Glucose 197-204 insulin Homo sapiens 149-156 15254872-0 2004 Insulin secretion and insulin sensitivity at different stages of glucose tolerance: a cross-sectional study of Japanese type 2 diabetes. Glucose 65-72 insulin Homo sapiens 0-7 15254872-0 2004 Insulin secretion and insulin sensitivity at different stages of glucose tolerance: a cross-sectional study of Japanese type 2 diabetes. Glucose 65-72 insulin Homo sapiens 22-29 15308383-4 2004 However, at the late stage of disease,most patients require exogenous insulin therapy to achieve optimal glucose control. Glucose 105-112 insulin Homo sapiens 70-77 15308392-2 2004 As patients approach the insulin-deficient end of the spectrum of type 2, hypoglycemia results from the interplay of therapeutic insulin excess and compromised physiologic and behavioral defenses against falling plasma glucose concentrations. Glucose 219-226 insulin Homo sapiens 25-32 16307172-1 2004 Gaps remain in our understanding of the precise molecular mechanisms by which insulin regulates glucose uptake in fat and muscle cells. Glucose 96-103 insulin Homo sapiens 78-85 15087463-7 2004 It was further established that PLD activity was required for both the first and the second phase of glucose-stimulated insulin release, suggesting a role in the very distal steps of exocytosis, beyond granule recruitment into a readily releasable pool. Glucose 101-108 insulin Homo sapiens 120-127 15264753-11 2004 CONCLUSIONS: The continuous glucose monitoring results provide useful information for the diabetologist in order to modify insulin treatment. Glucose 28-35 insulin Homo sapiens 123-130 15264753-12 2004 Continuous glucose monitoring-based changes in insulin treatment are reported to result in better long term metabolic control. Glucose 11-18 insulin Homo sapiens 47-54 15264753-13 2004 Continuous glucose monitoring in the near future will obviously play a primary role in insulin pump therapy where it will provide glucose result for the pump. Glucose 11-18 insulin Homo sapiens 87-94 15264753-13 2004 Continuous glucose monitoring in the near future will obviously play a primary role in insulin pump therapy where it will provide glucose result for the pump. Glucose 130-137 insulin Homo sapiens 87-94 15031294-6 2004 Insulin stimulation of protein kinase C (PKC)lambda/zeta activity, which is required for glucose transport, was impaired in muscle of PTP1B-overexpressing mice compared with controls, showing that PTP1B overexpression impairs activation of these PKC isoforms. Glucose 89-96 insulin Homo sapiens 0-7 15224208-0 2004 Evaluation of insulin release and insulin sensitivity through oral glucose tolerance test: differences between NGT, IFG, IGT, and type 2 diabetes mellitus. Glucose 67-74 insulin Homo sapiens 14-21 15224208-4 2004 In preliminary experiments, 1/HOMA correlated with glucose infusion rate (GIR) at euglycaemic insulin clamp (r=0.495) and with insulin sensitivity index (ISI) at LDIGIT (r=0.714). Glucose 51-58 insulin Homo sapiens 94-101 15383184-6 2004 Insulin sensitivity was assessed by plasma glucose and insulin concentrations obtained at fasting or during a 75 g oral glucose tolerance test. Glucose 120-127 insulin Homo sapiens 0-7 15180566-1 2004 The pattern of insulin release is crucial for regulation of glucose and lipid haemostasis. Glucose 60-67 insulin Homo sapiens 15-22 15636088-1 2004 The aim of this study was to determine possible insulin-mimetic effects of vanadate on amino acid transport, glycogen synthesis and glucose production in hepatocytes cultured in vitro. Glucose 132-139 insulin Homo sapiens 48-55 15636088-5 2004 Vanadate and insulin given together reduced more strongly the basal glucose production (68%) and also effectively prevented the glucagon-stimulated effect on glucose production. Glucose 68-75 insulin Homo sapiens 13-20 15636088-5 2004 Vanadate and insulin given together reduced more strongly the basal glucose production (68%) and also effectively prevented the glucagon-stimulated effect on glucose production. Glucose 158-165 insulin Homo sapiens 13-20 15636088-7 2004 Our results clearly demonstrated that non-insulin-like effects of vanadate could have a beneficial influence on the therapy of diabetes type 2 causing a decrease of glucose production from the liver. Glucose 165-172 insulin Homo sapiens 42-49 16566693-0 2004 Safety and feasibility of an insulin adjustment protocol to maintain blood glucose concentrations within a narrow range in critically ill patients in an Australian level III adult intensive care unit. Glucose 75-82 insulin Homo sapiens 29-36 16566693-10 2004 CONCLUSIONS: The insulin adjustment protocol with a constant caloric source and frequent blood glucose level monitoring was found to be safe and feasible in maintaining blood glucose concentrations within a narrow range in a mixed adult intensive care unit population. Glucose 95-102 insulin Homo sapiens 17-24 16566693-10 2004 CONCLUSIONS: The insulin adjustment protocol with a constant caloric source and frequent blood glucose level monitoring was found to be safe and feasible in maintaining blood glucose concentrations within a narrow range in a mixed adult intensive care unit population. Glucose 175-182 insulin Homo sapiens 17-24 15144884-4 2004 Insulin secretion is regulated in vivo by the sequential events triggered by the increase of intracellular Ca(2+)-concentration in response to high glucose concentration. Glucose 148-155 insulin Homo sapiens 0-7 14871885-0 2004 Metformin, but not leptin, regulates AMP-activated protein kinase in pancreatic islets: impact on glucose-stimulated insulin secretion. Glucose 98-105 insulin Homo sapiens 117-124 15136071-4 2004 We measured Pr-LPL mass, insulin sensitivity (Si), and acute insulin release in response to a glucose bolus (AIRg) in subjects with normal glucose tolerance (NGT; n = 23), impaired glucose tolerance (IGT; n = 10), and Type II diabetes mellitus (DM; n = 48). Glucose 94-101 insulin Homo sapiens 61-68 15153144-0 2004 Maintenance of glucose-sensitive insulin secretion of cryopreserved human islets with University of Wisconsin solution and ascorbic acid-2 glucoside. Glucose 15-22 insulin Homo sapiens 33-40 15153144-8 2004 Following three months of cryopreservation, the islets were thawed and analyzed for viability, glucose-sensitive insulin secretion, proinsulin gene expression profile, and in vivo engraftment. Glucose 95-102 insulin Homo sapiens 113-120 15153144-10 2004 The viability, morphology, glucose-sensitive insulin secretion, proinsulin gene expression, and monolayer formation efficiency of the thawed cryopreserved islets are significantly better maintained by the use of UW solution. Glucose 27-34 insulin Homo sapiens 45-52 15187412-7 2004 It is established that insulin"s dramatic effect on glucose disposal is mediated through its action on GLUT4. Glucose 52-59 insulin Homo sapiens 23-30 14976144-0 2004 Glucose-induced expression of the cyclin-dependent protein kinase 5 activator p35 involved in Alzheimer"s disease regulates insulin gene transcription in pancreatic beta-cells. Glucose 0-7 insulin Homo sapiens 124-131 14976144-11 2004 Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene. Glucose 164-171 insulin Homo sapiens 61-68 14976144-11 2004 Our findings indicate that the expression of p35 and CDK5 in insulin-producing beta-cells ensembles a new signaling pathway, the activity of which is controlled by glucose, and its functional role may comprise the regulation of various biological processes in beta-cells, such as is the case for expression of the insulin gene. Glucose 164-171 insulin Homo sapiens 314-321 15001544-6 2004 RIN beta-cells exposed to high glucose exhibited increased c-Jun N-terminal kinase (JNK) and ERK1/2 activity, which was associated with increased IRS-1 phosphorylation at serine (Ser)(307) and Ser(612), respectively, that inhibits coupling of IRS-1 to the insulin receptor and is upstream of the inhibition of IRS-1 tyrosine phosphorylation. Glucose 31-38 insulin Homo sapiens 256-263 15001544-4 2004 Exposure of human pancreatic islets and RIN beta-cells to glucosamine resulted in reduction in glucose- and insulin-stimulated insulin biosynthesis, which in RIN beta-cells was associated with impairment in insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation at Tyr(608) and Tyr(628), which are essential for engaging phosphatidylinositol 3-kinase (PI 3-kinase). Glucose 95-102 insulin Homo sapiens 127-134 15001544-4 2004 Exposure of human pancreatic islets and RIN beta-cells to glucosamine resulted in reduction in glucose- and insulin-stimulated insulin biosynthesis, which in RIN beta-cells was associated with impairment in insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation at Tyr(608) and Tyr(628), which are essential for engaging phosphatidylinositol 3-kinase (PI 3-kinase). Glucose 95-102 insulin Homo sapiens 127-134 15156315-7 2004 Among subjects with normal glucose tolerance, SNP1 (n=127) and SNP5 (n=159) were associated with insulin-mediated glucose uptake rates (p=0.03 and p=0.04), and SNP1 was further associated with fasting, 30-min, and 2-h plasma insulin concentrations (p=0.002, p=0.002 and p=0.03). Glucose 27-34 insulin Homo sapiens 97-104 15126010-1 2004 Previous studies have established that impaired glucose tolerance (IGT) patients with fasting hyperglycemia (IGT/FH: fasting plasma glucose (FPG) level 6.1-7.0 mmol/l and 2 h PG level of 7.8-11.1 mmol/l) exhibit higher insulin resistance than those with isolated IGT (FPG level <6.1 mmol/l and 2 h PG level of 7.8-11.1 mmol/l), but the association with microalbuminuria has not been determined. Glucose 48-55 insulin Homo sapiens 219-226 15156315-7 2004 Among subjects with normal glucose tolerance, SNP1 (n=127) and SNP5 (n=159) were associated with insulin-mediated glucose uptake rates (p=0.03 and p=0.04), and SNP1 was further associated with fasting, 30-min, and 2-h plasma insulin concentrations (p=0.002, p=0.002 and p=0.03). Glucose 114-121 insulin Homo sapiens 97-104 15156315-7 2004 Among subjects with normal glucose tolerance, SNP1 (n=127) and SNP5 (n=159) were associated with insulin-mediated glucose uptake rates (p=0.03 and p=0.04), and SNP1 was further associated with fasting, 30-min, and 2-h plasma insulin concentrations (p=0.002, p=0.002 and p=0.03). Glucose 114-121 insulin Homo sapiens 225-232 15161754-3 2004 The current studies address aspects of glucose-regulated transcription: 1) the number and characteristics of these genes, 2) if depolarization is the major mechanism, and 3) if glucose-stimulated insulin secretion is responsible, because insulin per se can activate transcription. Glucose 39-46 insulin Homo sapiens 238-245 15161747-2 2004 Here we show that insulin-stimulated glucose transport is increased in the skeletal muscle and white adipose tissue (WAT) of chow-fed DGAT1-deficient mice. Glucose 37-44 insulin Homo sapiens 18-25 15161747-3 2004 This increase in glucose transport correlated with enhanced insulin-stimulated activities of phosphatidylinositol 3-kinase, protein kinase B (or Akt), and protein kinase Clambda (PKC-lambda), three key molecules in the insulin-signaling pathway, and was associated with decreased levels of serine-phosphorylated insulin receptor substrate 1 (IRS-1), a molecule implicated in insulin resistance. Glucose 17-24 insulin Homo sapiens 60-67 15161754-3 2004 The current studies address aspects of glucose-regulated transcription: 1) the number and characteristics of these genes, 2) if depolarization is the major mechanism, and 3) if glucose-stimulated insulin secretion is responsible, because insulin per se can activate transcription. Glucose 177-184 insulin Homo sapiens 196-203 15161771-9 2004 Maximal insulin stimulation ( approximately 400 microU/ml) revealed pioglitazone-associated increases in glucose uptake (P+ = 10.5 +/- 0.9 vs. P- = 8.9 +/- 0.8 mg. kg(-1). Glucose 105-112 insulin Homo sapiens 8-15 15161754-4 2004 Here, the expression profiles of glucose-responsive insulinoma cells 45 min after the addition of glucose, KCl to induce depolarization, or insulin were assessed by endocrine pancreas cDNA microarrays. Glucose 33-40 insulin Homo sapiens 52-59 15161754-10 2004 This is consistent with glucose activation of gene transcription either directly or indirectly through a paracrine/autocrine effect via insulin release. Glucose 24-31 insulin Homo sapiens 136-143 15161760-8 2004 The relation of insulin resistance to glucose tolerance category was consistently seen in women and men and across the three ethnic groups of the IRAS (non-Hispanic whites, African Americans, and Hispanics). Glucose 38-45 insulin Homo sapiens 16-23 15161770-1 2004 The aim of this randomized double-blind study was to compare the within-subject variability of the glucose-lowering effect of a novel insulin analog, insulin detemir, with that of insulin glargine and NPH insulin in people with type 1 diabetes. Glucose 99-106 insulin Homo sapiens 134-141 15170498-2 2004 It has also been suggested, although inconsistently, that the class III allele plays a role in glucose-induced insulin response among NGT individuals. Glucose 95-102 insulin Homo sapiens 111-118 15198833-1 2004 The objective of the project Advanced Insulin Infusion using a Control Loop (ADICOL) was to develop a treatment system that continuously measures and controls the glucose concentration in subjects with type 1 diabetes. Glucose 163-170 insulin Homo sapiens 38-45 15334790-9 2004 Additional reduction of postprandial blood glucose by acarbose modifies the stimulation of insulin release. Glucose 43-50 insulin Homo sapiens 91-98 15191347-1 2004 BACKGROUND AND AIMS: The metabolic response to fasting involves an increase in circulating levels of growth hormone (GH) and free fatty acids, and resistance to insulin"s actions on glucose metabolism. Glucose 182-189 insulin Homo sapiens 161-168 15191347-3 2004 The present study was designed to test the degree to which the insulin antagonistic effects of GH on glucose metabolism are mediated through stimulation of lipolysis during fasting. Glucose 101-108 insulin Homo sapiens 63-70 15191347-11 2004 iii); P<0.01), whereas insulin-stimulated glucose uptake was significantly increased (glucose infusion rate (M-value) (mg/kg/min): 1.66+/-0.22 (expt. Glucose 45-52 insulin Homo sapiens 26-33 15191347-11 2004 iii); P<0.01), whereas insulin-stimulated glucose uptake was significantly increased (glucose infusion rate (M-value) (mg/kg/min): 1.66+/-0.22 (expt. Glucose 89-96 insulin Homo sapiens 26-33 15191347-16 2004 CONCLUSION: Thus, the present data provide strong evidence that the insulin antagonistic effects of GH on fasting glucose metabolism are causally linked to concomitant stimulation of lipolysis. Glucose 114-121 insulin Homo sapiens 68-75 15123571-3 2004 Insulin sensitivity was measured with a frequently sampled intravenous glucose tolerance test with minimal model analysis. Glucose 71-78 insulin Homo sapiens 0-7 15181045-4 2004 The acute insulin response to glucose (AIRg) and the maximal glucose-potentiated insulin response (AIRmax) were determined and then adjusted for SI (SI x AIRg and SI x AIRmax), thus providing measures of beta-cell function. Glucose 30-37 insulin Homo sapiens 10-17 15181051-8 2004 The presence of insulin resistance was investigated by using basal insulin levels, the oral glucose tolerance test, the i.v. Glucose 92-99 insulin Homo sapiens 16-23 15181085-1 2004 Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Glucose 81-88 insulin Homo sapiens 64-71 15181089-2 2004 This study explores the metabolic differences between s.c. and visceral fat depots with respect to effects in vitro of glucocorticoids and insulin on glucose uptake. Glucose 150-157 insulin Homo sapiens 139-146 15181089-6 2004 Omental adipocytes had an approximately 2-fold higher rate of insulin-stimulated glucose uptake compared with s.c. adipocytes (P < 0.01). Glucose 81-88 insulin Homo sapiens 62-69 15181089-7 2004 Dexamethasone treatment markedly inhibited (by approximately 50%; P < 0.05) both basal and insulin-stimulated glucose uptake in omental adipocytes but had no consistent effect in s.c. adipocytes. Glucose 113-120 insulin Homo sapiens 94-101 15147528-10 2004 In women, but not obviously in men, with normal glucose tolerance, coffee consumption was associated with a reduced risk of insulin resistance. Glucose 48-55 insulin Homo sapiens 124-131 15470319-7 2004 Fasting insulin resistance index (FIRI) was calculated from insulin and glucose plasma levels. Glucose 72-79 insulin Homo sapiens 8-15 15167329-8 2004 Metaanalysis of studies using home glucose records in insulin dose adjustment documented a mean decrease in glycated hemoglobin of.14 mmol/L (95% confidence interval [CI], 0.11-0.16) and a decrease in blood glucose of.33 mmol/L (95% CI, 0.28-0.39). Glucose 35-42 insulin Homo sapiens 54-61 15167329-8 2004 Metaanalysis of studies using home glucose records in insulin dose adjustment documented a mean decrease in glycated hemoglobin of.14 mmol/L (95% confidence interval [CI], 0.11-0.16) and a decrease in blood glucose of.33 mmol/L (95% CI, 0.28-0.39). Glucose 207-214 insulin Homo sapiens 54-61 15167329-11 2004 Prompting follow-up procedures, computerized insulin therapy adjustment using home glucose records, remote feedback, and counseling have documented benefits in improving diabetes-related outcomes. Glucose 83-90 insulin Homo sapiens 45-52 15787207-10 2004 In the OGTT performed in two patients, normal fasting glucose and insulin plasma levels were observed after 8 weeks; however, the plasma insulin concentrations were highly elevated after glucose intake, which may suggest the presence of insulin resistance. Glucose 187-194 insulin Homo sapiens 137-144 15787207-10 2004 In the OGTT performed in two patients, normal fasting glucose and insulin plasma levels were observed after 8 weeks; however, the plasma insulin concentrations were highly elevated after glucose intake, which may suggest the presence of insulin resistance. Glucose 187-194 insulin Homo sapiens 137-144 15189492-5 2004 We treated 26 subjects who were confirmed to have islet cell antibodies (ICAs) and a low first-phase insulin response (FPIR) to intravenous glucose. Glucose 140-147 insulin Homo sapiens 101-108 15193912-8 2004 CONCLUSIONS: The data suggest that moderate, short-term exercise without concomitant mass loss is effective in improving glucose tolerance and insulin response to a glucose load in obese males with abnormal glucose tolerance. Glucose 165-172 insulin Homo sapiens 143-150 15125897-5 2004 Whilst there are many published claims to success in converting ES cells into insulin secreting, glucose responsive cells, all require careful reinterpretation in the light of findings that cells can adsorb insulin present in growth media. Glucose 97-104 insulin Homo sapiens 207-214 15024008-1 2004 Insulin stimulates the movement of the facilitative glucose transporter glucose transporter-4 (Glut4) from an intracellular compartment to the plasma membrane in adipocytes and muscle cells, resulting in an increased rate of glucose uptake. Glucose 52-59 insulin Homo sapiens 0-7 15024008-2 2004 Insulin-stimulated Glut4 translocation and glucose transport are abolished by wortmannin, a specific inhibitor of phosphatidylinositol 3"-kinase (PI3K). Glucose 43-50 insulin Homo sapiens 0-7 15133852-9 2004 Up to 22.7% of the cells induced by glucose were positive for insulin immunoreactivity, and less than 3.8% of the cells were positive for glucagon immunoreactivity in pancreatic islet-like structures. Glucose 36-43 insulin Homo sapiens 62-69 15133852-10 2004 The positive ratio of immunoreactive staining was dependent on the concentration of glucose, and it was observed that the 17.8 mmol/L glucose stimulated effectively to produce insulin- and glucagons-producing cells. Glucose 84-91 insulin Homo sapiens 176-183 15133852-10 2004 The positive ratio of immunoreactive staining was dependent on the concentration of glucose, and it was observed that the 17.8 mmol/L glucose stimulated effectively to produce insulin- and glucagons-producing cells. Glucose 134-141 insulin Homo sapiens 176-183 15112185-3 2004 By measuring glucose levels during the peak period of glucose absorption, as determined by a peritoneal equilibrium test, such differences can be measured and accounted for when determining doses of intraperitoneal insulin. Glucose 13-20 insulin Homo sapiens 215-222 15112185-3 2004 By measuring glucose levels during the peak period of glucose absorption, as determined by a peritoneal equilibrium test, such differences can be measured and accounted for when determining doses of intraperitoneal insulin. Glucose 54-61 insulin Homo sapiens 215-222 15107927-4 2004 Analysis of the data for the group as a whole (patients and healthy individuals) showed that the estimate of insulin resistance by HOMA was correlated with data obtained in the forearm metabolic studies (glucose uptake: r = -0.16, P = 0.04; non-oxidative glucose metabolism: r = -0.20. Glucose 204-211 insulin Homo sapiens 109-116 15107927-4 2004 Analysis of the data for the group as a whole (patients and healthy individuals) showed that the estimate of insulin resistance by HOMA was correlated with data obtained in the forearm metabolic studies (glucose uptake: r = -0.16, P = 0.04; non-oxidative glucose metabolism: r = -0.20. Glucose 255-262 insulin Homo sapiens 109-116 15107927-7 2004 The HOMA and QUICKI are good estimates of insulin sensitivity as data derived from forearm metabolic studies involving direct measurements of insulin action on muscle glucose metabolism. Glucose 167-174 insulin Homo sapiens 142-149 15111768-2 2004 In this report, we show that the grapefruit flava-none naringenin inhibited insulin-stimulated glucose uptake in proliferating and growth-arrested MCF-7 breast cancer cells. Glucose 95-102 insulin Homo sapiens 76-83 15111768-5 2004 Inhibition of the MAPK pathway with PD98059, a MAPK kinase inhibitor, reduced insulin-stimulated glucose uptake by approximately 60%. Glucose 97-104 insulin Homo sapiens 78-85 15111768-6 2004 The MAPK pathway therefore appears to contribute significantly to insulin-stimulated glucose uptake in breast cancer cells. Glucose 85-92 insulin Homo sapiens 66-73 15111768-9 2004 Because a physiologically attainable dose of 10 micro M naringenin reduced insulin-stimulated glucose uptake by nearly 25% and also reduced cell proliferation, naringenin may possess therapeutic potential as an anti-proliferative agent. Glucose 94-101 insulin Homo sapiens 75-82 15105990-1 2004 The importance of both insulin resistance and beta cell dysfunction in the pathogenesis of glucose intolerance is widely recognised. Glucose 91-98 insulin Homo sapiens 23-30 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15111508-3 2004 A significant linkage signal (logarithm of odds [LOD] = 2.98) affecting corrected insulin response to glucose was detected on chromosome 13q between D13787 and D13S252, in the region where the MODY-4 gene has previously been mapped. Glucose 102-109 insulin Homo sapiens 82-89 15111508-5 2004 Significant linkage (LOD = 3.09) for insulin response to glucose was found on chromosome 8 between D8S1130 and D8S1106, near the lipoprotein lipase and macrophage scavenger receptor genes. Glucose 57-64 insulin Homo sapiens 37-44 15111508-8 2004 These results indicate that chromosomal locations on 8p and 13q might harbor genes that affect a variety of insulin- and glucose-related phenotypes that contribute to the observed variations in these important risk factors for diabetes in Mexican Americans. Glucose 121-128 insulin Homo sapiens 108-115 15111514-9 2004 Postprandial blood glucose decreased in the insulin aspart group: 0.44 mmol/l to >1.67 mmol/l compared with HI and 1.1 mmol/l to >1.67 mmol/l compared with MIX. Glucose 19-26 insulin Homo sapiens 44-51 15111514-13 2004 Insulin aspart treatment resulted in improved HbA1c and postprandial blood glucose. Glucose 75-82 insulin Homo sapiens 0-7 15111515-4 2004 The current study attempts to identify any characteristics of patients with newly diagnosed type 2 diabetes (fasting glucose >11.0 mmol/l) who would have a long-term benefit, in terms of glycemic control, from a brief course of insulin therapy. Glucose 117-124 insulin Homo sapiens 231-238 15111515-7 2004 The insulin area under the curve for the posttreatment oral glucose tolerance test also improved (8,251 +/- 1,880 before therapy, 18,404 +/- 4,040 directly after insulin therapy, and 42,368 +/- 8,517 pmol.min at the 1-year follow-up). Glucose 60-67 insulin Homo sapiens 4-11 15111515-10 2004 CONCLUSIONS: These results demonstrate that in newly diagnosed type 2 diabetes with elevated fasting glucose levels, a 2- to 3-week course of intensive insulin therapy can successfully lay a foundation for prolonged good glycemic control. Glucose 101-108 insulin Homo sapiens 152-159 15111515-11 2004 The ease with which normoglycemia is achieved on insulin may predict those patients who can later succeed in controlling glucose levels with attention to diet alone. Glucose 121-128 insulin Homo sapiens 49-56 15033925-11 2004 Unexpectedly, stimulation of insulin secretion by ryanodine occurs independently of glucose and by two mechanisms, including a novel cytosolic Ca2+-independent mechanism likely involving changes in Ca2+ within the lumens of non-ER organelles, such as endosomes. Glucose 84-91 insulin Homo sapiens 29-36 15099855-2 2004 The aim of this study was to examine whether it had an enhancing effect on glucose uptake, an essential process of insulin action. Glucose 75-82 insulin Homo sapiens 115-122 15099855-4 2004 The extract significantly potentiated insulin-stimulated glucose uptake with a dose-dependent manner at a concentration range from 0.02 to 0.5 mg/ml. Glucose 57-64 insulin Homo sapiens 38-45 15086511-3 2004 However, during insulin-induced hypoglycaemia, where brain glucose availability is limited, glycogen content falls first in areas with the highest metabolic rate, suggesting that glycogen provides fuel to support brain function during pathological hypoglycaemia. Glucose 59-66 insulin Homo sapiens 16-23 15135155-8 2004 The inhibition of activation of JNK as a possible mechanism whereby DMAP affects insulin-induced antilipolysis, lipogenesis, and glucose uptake, was investigated using the JNK inhibitor SP600125. Glucose 129-136 insulin Homo sapiens 81-88 15135155-9 2004 At 100 micromol/L, SP600125 completely reversed the antilipolytic effect of insulin, as well as partially inhibited insulin-induced lipogenesis and glucose-uptake, indicating that JNK may be involved in mediating these actions of insulin. Glucose 148-155 insulin Homo sapiens 116-123 15135155-9 2004 At 100 micromol/L, SP600125 completely reversed the antilipolytic effect of insulin, as well as partially inhibited insulin-induced lipogenesis and glucose-uptake, indicating that JNK may be involved in mediating these actions of insulin. Glucose 148-155 insulin Homo sapiens 116-123 15142338-1 2004 A new glucose-responsive polymeric composite membrane that provided pulsatile insulin release was developed in our laboratory previously. Glucose 6-13 insulin Homo sapiens 78-85 15141406-12 2004 Dextrose infusion increased the plasma insulin concentrations to the same extent in both groups (p < .05). Glucose 0-8 insulin Homo sapiens 39-46 15503794-3 2004 Major messengers which mediate glucose action for insulin release are Ca2+, adenosine triphosphate (ATP) and diacylglycerol (DAG). Glucose 31-38 insulin Homo sapiens 50-57 15161747-3 2004 This increase in glucose transport correlated with enhanced insulin-stimulated activities of phosphatidylinositol 3-kinase, protein kinase B (or Akt), and protein kinase Clambda (PKC-lambda), three key molecules in the insulin-signaling pathway, and was associated with decreased levels of serine-phosphorylated insulin receptor substrate 1 (IRS-1), a molecule implicated in insulin resistance. Glucose 17-24 insulin Homo sapiens 219-226 15161747-3 2004 This increase in glucose transport correlated with enhanced insulin-stimulated activities of phosphatidylinositol 3-kinase, protein kinase B (or Akt), and protein kinase Clambda (PKC-lambda), three key molecules in the insulin-signaling pathway, and was associated with decreased levels of serine-phosphorylated insulin receptor substrate 1 (IRS-1), a molecule implicated in insulin resistance. Glucose 17-24 insulin Homo sapiens 219-226 15161807-3 2004 This article summarizes the physiological basis of HOMA, a structural model of steady-state insulin and glucose domains, constructed from physiological dose responses of glucose uptake and insulin production. Glucose 104-111 insulin Homo sapiens 189-196 15161807-3 2004 This article summarizes the physiological basis of HOMA, a structural model of steady-state insulin and glucose domains, constructed from physiological dose responses of glucose uptake and insulin production. Glucose 170-177 insulin Homo sapiens 92-99 15161807-4 2004 Hepatic and peripheral glucose efflux and uptake were modeled to be dependent on plasma glucose and insulin concentrations. Glucose 23-30 insulin Homo sapiens 100-107 15200492-2 2004 These properties can be predicted to result in higher glucose levels during the night and lower glucose levels after dinner following bedtime injection of insulin glargine compared with an equal dose of NPH insulin injected at bedtime. Glucose 96-103 insulin Homo sapiens 155-162 15052278-4 2004 Reciprocal changes were observed between postglucose acute insulin secretion and insulin-mediated glucose disposal so that the so-called disposition index (product of these two variables) remained unchanged after vs before gastroplasty in those individuals with normal glucose tolerance. Glucose 45-52 insulin Homo sapiens 59-66 15181024-2 2004 Excess adipose tissue, especially in certain compartments, leads to reduced insulin sensitivity in metabolically responsive tissues, which is frequently associated with a set of cardiovascular risk factors, including hyperinsulinemia, hypertension, dyslipidemia, and glucose intolerance. Glucose 267-274 insulin Homo sapiens 76-83 15181024-4 2004 This brief review will summarize recent work on the vascular actions of adiponectin, which complements the growing body of information on its insulin-sensitizing effects in glucose and lipid metabolism. Glucose 173-180 insulin Homo sapiens 142-149 15181067-0 2004 Pharmacological treatment of insulin resistance at two different stages in the evolution of type 2 diabetes: impact on glucose tolerance and beta-cell function. Glucose 119-126 insulin Homo sapiens 29-36 15181067-1 2004 The purpose of this study was to compare the impact of treating insulin resistance with a thiazolidinedione drug before vs. at the onset of diabetes on glucose levels and beta-cell function. Glucose 152-159 insulin Homo sapiens 64-71 15164224-4 2004 The effect of insulin on the glucose disappearance is investigated by artificially maintaining a blood glucose concentration close to the normal fasting level. Glucose 29-36 insulin Homo sapiens 14-21 15164224-4 2004 The effect of insulin on the glucose disappearance is investigated by artificially maintaining a blood glucose concentration close to the normal fasting level. Glucose 103-110 insulin Homo sapiens 14-21 15449754-9 2004 RESULTS: At the starting point (time zero) the mean of insulin concentrations among four PVC bottles was 213.79 microunit per each milliliter of 5 percent dextrose solution. Glucose 155-163 insulin Homo sapiens 55-62 15212158-7 2004 Microneedles increased skin permeability to insulin, which rapidly and steadily reduced blood glucose levels to an extent similar to 0.05-0.5 U insulin injected subcutaneously. Glucose 94-101 insulin Homo sapiens 44-51 15212158-9 2004 Higher donor solution insulin concentration, shorter insertion time, and fewer repeated insertions resulted in larger drops in blood glucose level and larger plasma insulin concentrations. Glucose 133-140 insulin Homo sapiens 22-29 15148392-0 2004 Involvement of Per-Arnt-Sim (PAS) kinase in the stimulation of preproinsulin and pancreatic duodenum homeobox 1 gene expression by glucose. Glucose 131-138 insulin Homo sapiens 63-76 15148392-4 2004 Demonstrating a physiological role for PASK activation, comicroinjection into clonal beta cells of cDNA encoding wild-type PASK, or PASK protein itself, mimics the induction of preproinsulin promoter activity by high glucose concentrations. Glucose 217-224 insulin Homo sapiens 177-190 15148392-5 2004 Conversely, anti-PASK antibodies block promoter activation by the sugar, and the silencing of PASK expression by RNA interference suppresses the up-regulation by glucose of preproinsulin and pancreatic duodenum homeobox 1 gene expression, without affecting glucose-induced changes in the levels of mRNAs encoding glucokinase or uncoupling protein 2. Glucose 162-169 insulin Homo sapiens 173-186 15251377-6 2004 Islet mass was determined according to standard criteria: purity by light microscopy, viability by dye exclusion and Insulin secretory response to static glucose incubation. Glucose 154-161 insulin Homo sapiens 117-124 15147803-7 2004 For the proposed gating membrane with a PAAC grafting yield of 1.55%, the insulin permeation coefficient after the glucose addition (0.2 mol/l) was about 9.37 times that in the absence of glucose, presenting an exciting result on glucose-sensitive self-regulated insulin permeation. Glucose 115-122 insulin Homo sapiens 74-81 15147803-7 2004 For the proposed gating membrane with a PAAC grafting yield of 1.55%, the insulin permeation coefficient after the glucose addition (0.2 mol/l) was about 9.37 times that in the absence of glucose, presenting an exciting result on glucose-sensitive self-regulated insulin permeation. Glucose 115-122 insulin Homo sapiens 263-270 15103621-0 2004 Investigation of glucose binding sites on insulin. Glucose 17-24 insulin Homo sapiens 42-49 15103621-1 2004 Possible insulin binding sites for D-glucose have been investigated theoretically by docking and molecular dynamics (MD) simulations. Glucose 35-44 insulin Homo sapiens 9-16 15103621-9 2004 The motions of the bound glucose during molecular dynamics simulations are correlated with the motions of the insulin side chains that are in contact with it and with larger scale insulin motions. Glucose 25-32 insulin Homo sapiens 110-117 15103621-9 2004 The motions of the bound glucose during molecular dynamics simulations are correlated with the motions of the insulin side chains that are in contact with it and with larger scale insulin motions. Glucose 25-32 insulin Homo sapiens 180-187 15103621-10 2004 These results raise the question of whether glucose binding to insulin could play a role in its activity. Glucose 44-51 insulin Homo sapiens 63-70 15143456-3 2004 INVESTIGATIONS: An oral glucose tolerance test performed over 210 minutes showed normal baseline glucose levels, markedly elevated levels of serum insulin and slightly elevated C-peptide concentrations. Glucose 24-31 insulin Homo sapiens 147-154 15143456-5 2004 The tentative diagnosis of an insulinoma was raised and a 72 h fasting test performed, throughout which the insulin-glucose-ratio was pathologically elevated, whereas C-peptide levels were only slightly elevated. Glucose 116-123 insulin Homo sapiens 30-37 15123530-8 2004 Insulin resistance, quantified by the glucose area under the curve (AUC) during an oral glucose tolerance test, correlated with MFAUp (r=0.55, P<0.005), MFAU (r=0.62, P<0.001), and MFAO (r=0.58, P<0.005). Glucose 38-45 insulin Homo sapiens 0-7 15123530-8 2004 Insulin resistance, quantified by the glucose area under the curve (AUC) during an oral glucose tolerance test, correlated with MFAUp (r=0.55, P<0.005), MFAU (r=0.62, P<0.001), and MFAO (r=0.58, P<0.005). Glucose 88-95 insulin Homo sapiens 0-7 15126253-8 2004 MEASUREMENTS: Glucose infusion rate in response to insulin infusion was used to define insulin resistance (glucose infusion rate < or = 4.00 mg/kg of body weight per minute [range, 0.90 to 3.96 mg/kg per minute]) and insulin sensitivity (glucose infusion rate > or = 7.50 mg/kg per minute [range, 7.52 to 13.92 mg/kg per minute]). Glucose 14-21 insulin Homo sapiens 87-94 15126253-8 2004 MEASUREMENTS: Glucose infusion rate in response to insulin infusion was used to define insulin resistance (glucose infusion rate < or = 4.00 mg/kg of body weight per minute [range, 0.90 to 3.96 mg/kg per minute]) and insulin sensitivity (glucose infusion rate > or = 7.50 mg/kg per minute [range, 7.52 to 13.92 mg/kg per minute]). Glucose 14-21 insulin Homo sapiens 87-94 15126253-8 2004 MEASUREMENTS: Glucose infusion rate in response to insulin infusion was used to define insulin resistance (glucose infusion rate < or = 4.00 mg/kg of body weight per minute [range, 0.90 to 3.96 mg/kg per minute]) and insulin sensitivity (glucose infusion rate > or = 7.50 mg/kg per minute [range, 7.52 to 13.92 mg/kg per minute]). Glucose 107-114 insulin Homo sapiens 87-94 15126253-8 2004 MEASUREMENTS: Glucose infusion rate in response to insulin infusion was used to define insulin resistance (glucose infusion rate < or = 4.00 mg/kg of body weight per minute [range, 0.90 to 3.96 mg/kg per minute]) and insulin sensitivity (glucose infusion rate > or = 7.50 mg/kg per minute [range, 7.52 to 13.92 mg/kg per minute]). Glucose 107-114 insulin Homo sapiens 87-94 15078585-7 2004 Insulin resistance in heart failure can be detrimental, because transcriptional shifts in metabolic gene expression favor glucose over fat as a substrate for high-energy phosphate production. Glucose 122-129 insulin Homo sapiens 0-7 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15105990-5 2004 Next we discuss the hyperbola paradigm used to describe the reciprocal relation of beta cell function to insulin sensitivity and suggest that: (i) insulin responses reflecting the basal beta cell tone are indeed inversely related to insulin action across degrees of glucose intolerance; (ii) modes of beta cell function that selectively reflect the dynamic response to acutely changing glucose concentrations are largely independent of insulin action; and (iii) when measured by experiment or resolved by modelling, quantitatively the most important of these dynamic secretion parameters is the glucose dose-response curve (glucose sensitivity). Glucose 386-393 insulin Homo sapiens 147-154 15108304-9 2004 In addition, insulin secretion from these beta cells responded to glucose stimulation. Glucose 66-73 insulin Homo sapiens 13-20 15111485-11 2004 The disposition index (peak insulin concentration after intravenous bolus of glucose multiplied by insulin sensitivity as assessed by homeostasis model assessment) almost doubled during liraglutide treatment (P < 0.01). Glucose 77-84 insulin Homo sapiens 28-35 15111487-1 2004 Modeling analysis of glucose, insulin, and C-peptide following a meal has been proposed as a means to estimate insulin sensitivity (S(i)) and beta-cell function from a single test. Glucose 21-28 insulin Homo sapiens 111-118 15111572-0 2004 Diagnosing insulin resistance by simple quantitative methods in subjects with normal glucose metabolism. Glucose 85-92 insulin Homo sapiens 11-18 15114470-1 2004 AIMS/HYPOTHESIS: The aim of the study was to evaluate the relationship between insulin sensitivity, beta cell function and glucose tolerance, and its dependence on variants in the newly identified Type 2 diabetes susceptibility gene, calpain-10 ( CAPN10). Glucose 123-130 insulin Homo sapiens 79-86 15114470-8 2004 However, AIR adjusted for insulin sensitivity (disposition index) showed a linear decrease with increasing glucose concentrations ( r=-0.563; p<0.001) starting already in subjects with normal glucose tolerance. Glucose 107-114 insulin Homo sapiens 26-33 15114470-8 2004 However, AIR adjusted for insulin sensitivity (disposition index) showed a linear decrease with increasing glucose concentrations ( r=-0.563; p<0.001) starting already in subjects with normal glucose tolerance. Glucose 195-202 insulin Homo sapiens 26-33 15114470-10 2004 Subjects with the genotype combination of CAPN10 consisting of SNP44 TT and SNP43 GG genotypes had significantly lower insulin-stimulated glucose uptake than carriers of the other genotype combinations (5.3+/-0.4 vs 7.2+/-0.4 mg.ffm kg(-1).min(-1).mU.l(-1); p<0.005). Glucose 138-145 insulin Homo sapiens 119-126 15133754-9 2004 The reductions in glucose excursions were accompanied by significant (p < 0.05) increases in the insulin response, suggesting an improvement in meal-related insulin secretion. Glucose 18-25 insulin Homo sapiens 100-107 15132728-10 2004 The increased demand on insulin induced by ED, due to both a stimulatory effect on pancreatic beta cells and increased insulin metabolism, may explain the slightly detrimental effect on glucose tolerance with this treatment. Glucose 186-193 insulin Homo sapiens 24-31 15125825-6 2004 Insulin doses were adjusted to obtain fasting glucose <7.0 mmol/L and postprandial glucose <10.0 mmol/L. Glucose 46-53 insulin Homo sapiens 0-7 15125825-6 2004 Insulin doses were adjusted to obtain fasting glucose <7.0 mmol/L and postprandial glucose <10.0 mmol/L. Glucose 86-93 insulin Homo sapiens 0-7 15113941-4 2004 Lipogenesis, as assessed by glucose incorporation into lipids, was increased by insulin and more so by the combination of insulin and dexamethasone (Dex, a potent glucocorticoid analogue). Glucose 28-35 insulin Homo sapiens 80-87 15113941-4 2004 Lipogenesis, as assessed by glucose incorporation into lipids, was increased by insulin and more so by the combination of insulin and dexamethasone (Dex, a potent glucocorticoid analogue). Glucose 28-35 insulin Homo sapiens 122-129 14976222-0 2004 Partitioning-defective protein 6 regulates insulin-dependent glycogen synthesis via atypical protein kinase C. The atypical isoforms of protein kinase C (aPKCs) play an important role in insulin signaling and are involved in insulin-stimulated glucose uptake in different cell systems. Glucose 244-251 insulin Homo sapiens 43-50 15131768-0 2004 Insulin secretion and incretin hormones after oral glucose in non-obese subjects with impaired glucose tolerance. Glucose 51-58 insulin Homo sapiens 0-7 15228086-6 2004 The treatment of cells with p38 MAPK inhibitor, SB203580, blocked the insulin stimulated glucose uptake in sensitive as well as resistant cells and it also prevented the activation of p38 by insulin. Glucose 89-96 insulin Homo sapiens 70-77 15228086-6 2004 The treatment of cells with p38 MAPK inhibitor, SB203580, blocked the insulin stimulated glucose uptake in sensitive as well as resistant cells and it also prevented the activation of p38 by insulin. Glucose 89-96 insulin Homo sapiens 191-198 15166296-3 2004 Insulin sensitivity (IS) was determined by glucose clamp. Glucose 43-50 insulin Homo sapiens 0-7 15135009-1 2004 We examined whether the effects of intravenously injected insulin and glucose (the physiological endogenous insulin production stimulus) could be classically conditioned in healthy humans. Glucose 70-77 insulin Homo sapiens 108-115 15135009-2 2004 We expected a conditioned blood glucose decrease to a conditioned stimulus (CS) previously paired with insulin and an, albeit lower, blood glucose decrease to a CS paired with glucose injection. Glucose 32-39 insulin Homo sapiens 103-110 15135009-11 2004 In correspondence with the lower intensity of the unconditioned stimulus (US), conditioning effects with glucose-and, thus, endogenously produced insulin-are weaker but also reflect the actions of central insulin. Glucose 105-112 insulin Homo sapiens 146-153 15294035-1 2004 Exercise training improves glucose homeostasis through enhanced insulin sensitivity in skeletal muscle. Glucose 27-34 insulin Homo sapiens 64-71 15194342-2 2004 Because glycemia >150 mg/dL may harm pancreatic graft beta cells, early glucose control using insulin administration is recommended during transplantation. Glucose 75-82 insulin Homo sapiens 97-104 15194361-1 2004 Various brief metabolic tests have been proposed as surrogate measures of insulin secretory reserve, which is normally determined by the more complicated and labor-intensive method of glucose potentiation of arginine-induced insulin secretion (GPAIS). Glucose 184-191 insulin Homo sapiens 74-81 15194397-7 2004 Function was assessed by determining glucose-stimulated release of insulin, which was measured by radioimmunoassay. Glucose 37-44 insulin Homo sapiens 67-74 15194407-8 2004 Glucose-stimulated release of human insulin was measured by radioimmunoassay (Linco, St. Charles, Missouri). Glucose 0-7 insulin Homo sapiens 36-43 15586530-5 2004 A dextrose-insulin-bicarbonate infusion was required to correct the hyperkalemia. Glucose 2-10 insulin Homo sapiens 11-18 15115830-3 2004 Because ATP-sensitive potassium (K(ATP)) channels mediate glucose-stimulated insulin secretion from the pancreatic beta cells, we hypothesized that activating mutations in the gene encoding the Kir6.2 subunit of this channel (KCNJ11) cause neonatal diabetes. Glucose 58-65 insulin Homo sapiens 77-84 15094070-6 2004 In addition, we will discuss the regulation, activity and insulin-stimulated trafficking of GLUTs in the CNS, especially in relation to the centrally mediated actions of insulin and glucose. Glucose 182-189 insulin Homo sapiens 58-65 15094071-4 2004 IGF1 acts in an autocrine and/or paracrine manner to promote glucose utilization, using phosphatidylinositol 3 kinase (PI3K)/Akt, also known as protein kinase B (PKB)/glycogen synthase kinase 3beta (GSK3beta) pathways similar to insulin signaling in peripheral tissues. Glucose 61-68 insulin Homo sapiens 229-236 15094073-8 2004 Single meals as well as glucose and serotonin are able to regulate insulin release directly in the hypothalamus and may be of importance for its biological effects. Glucose 24-31 insulin Homo sapiens 67-74 15094073-9 2004 Central mechanisms operating in glucose-induced insulin release show some analogy with the mechanisms operating in the pancreas. Glucose 32-39 insulin Homo sapiens 48-55 15094074-2 2004 In the central nervous system (CNS), insulin and the insulin receptor are found in specific brain regions where they show evidence of participation in a variety of region-specific functions through mechanisms that are different from its direct glucose regulation in the periphery. Glucose 244-251 insulin Homo sapiens 37-44 15094077-5 2004 Interestingly, glucose effects on memory appear to be modulated by insulin sensitivity (efficiency of insulin-mediated glucose disposal). Glucose 15-22 insulin Homo sapiens 67-74 15094077-5 2004 Interestingly, glucose effects on memory appear to be modulated by insulin sensitivity (efficiency of insulin-mediated glucose disposal). Glucose 15-22 insulin Homo sapiens 102-109 15094077-5 2004 Interestingly, glucose effects on memory appear to be modulated by insulin sensitivity (efficiency of insulin-mediated glucose disposal). Glucose 119-126 insulin Homo sapiens 67-74 15094077-5 2004 Interestingly, glucose effects on memory appear to be modulated by insulin sensitivity (efficiency of insulin-mediated glucose disposal). Glucose 119-126 insulin Homo sapiens 102-109 15094077-10 2004 Clinical studies have corroborated findings that patients with Alzheimer"s disease are more likely than healthy older adults to have reduced insulin sensitivity, and further suggest that apolipoprotein E genotype may modulate the effects of insulin on glucose disposal, memory facilitation, and amyloid precursor protein processing. Glucose 252-259 insulin Homo sapiens 241-248 15026002-1 2004 The incretins, glucose-dependent insulinotropic peptide (GIP(1-42)) and glucagon-like peptide 1 (GLP-1(7-36)), are involved in regulation of gastric emptying, glucose homeostasis, body fat regulation and the glucose-induced insulin secretion from the endocrine pancreas. Glucose 15-22 insulin Homo sapiens 33-40 15026002-1 2004 The incretins, glucose-dependent insulinotropic peptide (GIP(1-42)) and glucagon-like peptide 1 (GLP-1(7-36)), are involved in regulation of gastric emptying, glucose homeostasis, body fat regulation and the glucose-induced insulin secretion from the endocrine pancreas. Glucose 159-166 insulin Homo sapiens 33-40 15033485-1 2004 In human type 2 diabetes, loss of glucose-stimulated insulin exocytosis from the pancreatic beta-cell is an early pathogenetic event. Glucose 34-41 insulin Homo sapiens 53-60 15033485-5 2004 Thus, an increase in cellular phosphorylation state, through inhibition of protein dephosphorylation by InsP(6), may be a novel regulatory mechanism linking glucose-stimulated polyphosphoinositide formation to insulin exocytosis in insulin-secreting cells. Glucose 157-164 insulin Homo sapiens 210-217 15033485-5 2004 Thus, an increase in cellular phosphorylation state, through inhibition of protein dephosphorylation by InsP(6), may be a novel regulatory mechanism linking glucose-stimulated polyphosphoinositide formation to insulin exocytosis in insulin-secreting cells. Glucose 157-164 insulin Homo sapiens 232-239 14656717-1 2004 Insulin stimulates muscle glucose disposal via both glycolysis and glycogen synthesis. Glucose 26-33 insulin Homo sapiens 0-7 14736887-10 2004 In normal islets, methionine sulfoximine, a glutamine synthetase inhibitor, suppressed insulin release in response to a glucose ramp. Glucose 120-127 insulin Homo sapiens 87-94 14625208-10 2004 Exposure to FFA caused inhibition of insulin mRNA expression, glucose-stimulated insulin release, and reduction of islet insulin content. Glucose 62-69 insulin Homo sapiens 81-88 14625208-10 2004 Exposure to FFA caused inhibition of insulin mRNA expression, glucose-stimulated insulin release, and reduction of islet insulin content. Glucose 62-69 insulin Homo sapiens 81-88 14625208-12 2004 In conclusion, this study shows that PPARgamma mRNA is expressed in human pancreatic islets, with predominance of PPARgamma(2); exposure to FFA downregulates PPARgamma(2) and insulin mRNA expression and inhibits glucose-stimulated insulin secretion; exposure to PPARgamma agonists can prevent these effects. Glucose 212-219 insulin Homo sapiens 175-182 14665444-5 2004 Insulin administration increased femoral venous concentration of insulin (P < 0.01) but with only a 4% (insignificant) decrease in the arterial glucose concentration and a 7% (insignificant) decrease in the arterial concentration of phenylalanine. Glucose 147-154 insulin Homo sapiens 0-7 14656717-9 2004 In contrast, a pharmacological dose of insulin significantly increased whole body glucose disposal, p70(S6K), GSK-3 phosphorylation, and GS activity. Glucose 82-89 insulin Homo sapiens 39-46 15078172-2 2004 Recently, free fatty acids as well as amino acids were shown to induce insulin resistance by decreasing glucose transport/phosphorylation with subsequent impairment of glycogen synthesis in human skeletal muscle. Glucose 104-111 insulin Homo sapiens 71-78 15033662-2 2004 However, elevated levels of glucose and insulin elicited by consumption of high amounts of refined carbohydrates may stimulate mitogenic and cancer-promoting insulin-like growth factors (IGF). Glucose 28-35 insulin Homo sapiens 158-165 15153417-4 2004 Later, it becomes restricted primarily to beta cells where it regulates the expression of beta cell-specific genes, and, most importantly, mediates the glucose effect on insulin gene transcription. Glucose 152-159 insulin Homo sapiens 170-177 15153417-5 2004 Although exposure of beta cells to high glucose concentrations for relatively short periods stimulates insulin gene expression, chronic exposure has adverse effects on many beta-cell functions, including insulin gene transcription. Glucose 40-47 insulin Homo sapiens 103-110 15153423-3 2004 Glucose phosphorylation in beta-cells has been viewed as a key regulatory event in coupling insulin secretion to extracellular glucose concentrations. Glucose 0-7 insulin Homo sapiens 92-99 15153423-3 2004 Glucose phosphorylation in beta-cells has been viewed as a key regulatory event in coupling insulin secretion to extracellular glucose concentrations. Glucose 127-134 insulin Homo sapiens 92-99 15153423-4 2004 Work with transformed rodent beta-cell lines as well as recent findings from human progenitor cells induced to differentiate into insulin-producing cells has provided new insights into the role of glucose phosphorylating enzymes in the regulation of insulin secretion. Glucose 197-204 insulin Homo sapiens 130-137 15153423-4 2004 Work with transformed rodent beta-cell lines as well as recent findings from human progenitor cells induced to differentiate into insulin-producing cells has provided new insights into the role of glucose phosphorylating enzymes in the regulation of insulin secretion. Glucose 197-204 insulin Homo sapiens 250-257 15049959-1 2004 OBJECTIVE: Glucose variability can be a significant barrier to glycaemic control for diabetic patients on insulin. Glucose 11-18 insulin Homo sapiens 106-113 15049959-13 2004 Multivariate analysis showed that treatment duration, sugar consumption, medication compliance and insulin dose were independently associated with glucose variation. Glucose 147-154 insulin Homo sapiens 99-106 15047609-6 2004 The retrieved islets, irrespective of whether they had resided in diabetic or nondiabetic recipients, had a markedly lower insulin content and glucose-stimulated insulin release when compared with isolated endogenous islets. Glucose 143-150 insulin Homo sapiens 162-169 15047659-5 2004 RESULTS: Insulin resistance was associated with increased waist circumference, fasting glucose, blood pressure, triglycerides, and decreased levels of HDL cholesterol. Glucose 87-94 insulin Homo sapiens 9-16 15047659-8 2004 The larger number of subjects who were insulin resistant but did not meet ATP III criteria were found to have an adverse cardiovascular disease risk profile, including higher BMI, waist circumference, fasting glucose, triglycerides, and an unfavorable lipoprotein subclass profile determined by nuclear magnetic resonance compared with insulin-sensitive individuals (i.e., increased large VLDL, increased small LDL, and decreased large HDL particle concentrations). Glucose 209-216 insulin Homo sapiens 39-46 15049938-6 2004 Plasma C-peptide levels were suppressed by the lowered glucose levels achieved concurrent with the increasing amount of exogenous insulin absorbed, indicating that the secretion of endogenous hormone was partially abolished. Glucose 55-62 insulin Homo sapiens 7-16 15082519-3 2004 With respect to glucose homeostasis, these include the function of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and adipose tissues, the latter resulting from the translocation of the glucose transporter 4 (GLUT4) to the cell surface membrane. Glucose 16-23 insulin Homo sapiens 67-74 15082519-3 2004 With respect to glucose homeostasis, these include the function of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and adipose tissues, the latter resulting from the translocation of the glucose transporter 4 (GLUT4) to the cell surface membrane. Glucose 95-102 insulin Homo sapiens 67-74 15117581-0 2004 Relating glucose clamp profiles to reduction of blood glucose after insulin administration. Glucose 9-16 insulin Homo sapiens 68-75 15117582-1 2004 The objective is to demonstrate the effectiveness of a simple automated insulin infusion for controlling the rise and duration of blood glucose excursion following a glucose challenge in critically ill patients with impaired glucose tolerance. Glucose 136-143 insulin Homo sapiens 72-79 15117582-1 2004 The objective is to demonstrate the effectiveness of a simple automated insulin infusion for controlling the rise and duration of blood glucose excursion following a glucose challenge in critically ill patients with impaired glucose tolerance. Glucose 166-173 insulin Homo sapiens 72-79 15298338-5 2004 Within-person day-to-day variation in plasma glucose was lower with insulin detemir/insulin aspart than with NPH insulin/regular human insulin (SD: 2.88 vs 3.12 mmol/l; p<0.001). Glucose 45-52 insulin Homo sapiens 68-75 15066462-7 2004 Insulin sensitivity was calculated as total body glucose utilization. Glucose 49-56 insulin Homo sapiens 0-7 15066462-8 2004 RESULT(S): Naltrexone reduced fasting and stimulated insulin response to the glucose load while inducing a significant improvement of the hepatic extraction, only in the hyperinsulinemic patients. Glucose 77-84 insulin Homo sapiens 53-60 15083319-10 2004 Insulin-stimulated glucose uptake and insulin binding of adipocytes were significantly reduced, and the glucose transporter IV content of adipocytes also decreased. Glucose 19-26 insulin Homo sapiens 0-7 15127887-5 2004 The area under the curve of insulin (AUCI) was substantially greater in fructose-fed rats in the intravenous glucose tolerance test, and olmesartan treatment significantly reduced the AUCI. Glucose 109-116 insulin Homo sapiens 28-35 15010821-7 2004 Our microarray analysis showed that most differentially expressed genes in ovarian cancer are linked to glucose/insulin metabolism, providing a possible molecular link between the glucose/insulin signaling pathway and the neoplasms of ovarian cancer. Glucose 104-111 insulin Homo sapiens 112-119 15101025-3 2004 Myocardial perfusion, biventricular oxidative metabolism, and insulin-stimulated glucose uptake were measured using positron emission tomography and [(15)O]H(2)O, [(11)C]acetate, and [(18)F]FDG. Glucose 81-88 insulin Homo sapiens 62-69 15117549-2 2004 In the present study, we examined the effect of ethanol on insulin actions such as glucose uptake, DNA synthesis, and c-Jun gene expression. Glucose 83-90 insulin Homo sapiens 59-66 15117549-8 2004 These results suggest that ethanol specifically inhibits the association of the insulin receptor and IRS-1 with the p85 subunit of PI3-kinase, which is required for increased glucose uptake, DNA synthesis, and c-Jun expression by insulin. Glucose 175-182 insulin Homo sapiens 80-87 15117561-4 2004 Elevation of insulin and C-peptide was significantly higher after dextrose than after honey. Glucose 66-74 insulin Homo sapiens 13-20 15260080-0 2004 Indexes of insulin resistance using the oral glucose tolerance test (O-GTT) in Japanese children and adolescents. Glucose 45-52 insulin Homo sapiens 11-18 15045685-19 2004 Our study demonstrated that GITS appears to prime beta cells to intravenous glucose stimulation resulting in restoration of physiologic acute first- and second-phase insulin secretion in African Americans with IGT. Glucose 76-83 insulin Homo sapiens 166-173 15045694-8 2004 The insulin sensitivity index (glucose infusion rate/serum insulin) was significantly lower in the offspring during both clamps. Glucose 31-38 insulin Homo sapiens 4-11 15045698-2 2004 Given the increased prevalence of obesity in the US population, we thought it important to define the relationship between degree of obesity and insulin-mediated glucose disposal in the population at large, as well as the relationship between obesity, insulin resistance, and CVD risk in these individuals. Glucose 162-169 insulin Homo sapiens 145-152 15045698-3 2004 To do this we quantified insulin-mediated glucose disposal in 465 healthy volunteers by determining the steady-state plasma glucose (SSPG) concentrations at the end of a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 42-49 insulin Homo sapiens 25-32 15045698-3 2004 To do this we quantified insulin-mediated glucose disposal in 465 healthy volunteers by determining the steady-state plasma glucose (SSPG) concentrations at the end of a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 124-131 insulin Homo sapiens 25-32 15045698-3 2004 To do this we quantified insulin-mediated glucose disposal in 465 healthy volunteers by determining the steady-state plasma glucose (SSPG) concentrations at the end of a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 124-131 insulin Homo sapiens 25-32 15045700-6 2004 Insulin sensitivity (S(I)) was determined from a frequently sampled intravenous glucose tolerance test. Glucose 80-87 insulin Homo sapiens 0-7 18370676-2 2004 Atypical protein kinase C and protein kinase B, operating downstream of phosphatidylinositol 3-kinase, mediate insulin effects on glucose transport, but their importance in these syndromes is poorly understood. Glucose 130-137 insulin Homo sapiens 111-118 18370676-5 2004 In obese subjects and obese subjects who had evidence of the polycystic ovary syndrome, insulin-stimulated glucose disposal and atypical protein kinase C activation were diminished, whereas activation of insulin receptor substrate-1-dependent phosphatidylinositol 3-kinase and protein kinase B trended lower, but not significantly. Glucose 107-114 insulin Homo sapiens 88-95 14752056-2 2004 Insulin stimulates the protein kinase C beta (PKCbeta) isozymes and preferentially switches the expression to PKCbetaII isozyme, which is shown to have a crucial role in glucose uptake, cellular proliferation, and differentiation. Glucose 170-177 insulin Homo sapiens 0-7 15272244-3 2004 Most patients receive subcutaneous insulin injections to reduce blood glucose levels. Glucose 70-77 insulin Homo sapiens 35-42 15272244-4 2004 However, strict glucose control by multiple insulin injections is associated with an increased risk of hypoglycemia and weight gain, while a less strict glucose control is insufficient to prevent chronic complications such as nephropathy, neuropathy and retinopathy. Glucose 16-23 insulin Homo sapiens 44-51 15090628-17 2004 In obese subjects with insulin resistance, the alpha1-adrenergic receptor may provide an important alternative pathway for glucose uptake. Glucose 123-130 insulin Homo sapiens 23-30 15090637-4 2004 Insulin sensitivity was determined from serum glucose and insulin levels according to the homeostatic model of assessment for insulin resistance (HOMA IR). Glucose 46-53 insulin Homo sapiens 0-7 16215099-9 2004 Studies testing which insulin infusion safely achieves tight glucose control are limited. Glucose 61-68 insulin Homo sapiens 22-29 16215100-6 2004 Close monitoring and judicious use of insulin are key in maintaining glucose control and avoiding complications. Glucose 69-76 insulin Homo sapiens 38-45 15157920-6 2004 To circumvent this need, three alternative approaches are being intensively investigated: (1) the production of surrogate cells by genetically modifying non-endocrine cells to secrete insulin in response to glucose challenge; (2) the trans-differentiation of non-endocrine stem/progenitor cells or mature cells to glucose-responsive adult tissue; and (3) the regulated differentiation of islet stem/progenitor cells to produce large numbers of mature, functional islets. Glucose 207-214 insulin Homo sapiens 184-191 14711829-1 2004 Neuregulin-1, a growth factor that potentiates myogenesis induces glucose transport through translocation of glucose transporters, in an additive manner to insulin, in muscle cells. Glucose 66-73 insulin Homo sapiens 156-163 15017354-7 2004 SUMMARY: Although results have not always been consistent, gene variants affecting primary insulin action or dyslipidaemia, and particularly their interaction with the environment, are important modulators of glucose and lipoprotein metabolism. Glucose 209-216 insulin Homo sapiens 91-98 14711829-6 2004 TPCK, an inhibitor of PDK1, abolished both HRG- and insulin-induced glucose transport. Glucose 68-75 insulin Homo sapiens 52-59 14711829-8 2004 Dominant negative PKB reduced PKB activity and insulin-stimulated glucose transport but not HRG-induced glucose transport. Glucose 66-73 insulin Homo sapiens 47-54 14711829-9 2004 In contrast, transduction of L6E9 myotubes with adenoviruses encoding a dominant negative kinase-inactive PKCzeta abolished both HRG- and insulin-stimulated glucose uptake. Glucose 157-164 insulin Homo sapiens 138-145 15028121-4 2004 Here, we hypothesize that sympathetic activation may cause peripheral insulin resistance defined as partial blocking of insulin effects on glucose uptake. Glucose 139-146 insulin Homo sapiens 70-77 15028121-4 2004 Here, we hypothesize that sympathetic activation may cause peripheral insulin resistance defined as partial blocking of insulin effects on glucose uptake. Glucose 139-146 insulin Homo sapiens 120-127 15019860-4 2004 Secretagogues and alpha-glucosidase inhibitors effectively lower plasma glucose levels only, whereas insulin sensitizers reduce several important cardiac risk factors in addition to reducing plasma glucose levels. Glucose 198-205 insulin Homo sapiens 101-108 15102335-8 2004 In addition, the parameters of glucose assimilation were significantly decreased as compared with placebo in the subgroup of 7 subjects with plasma clonazepam concentrations higher than 6.0 ng ml-1 (median and lower limit of effective therapeutic concentrations): 1.37 +/- 0.3 versus 2.84 +/- 0.60 x 10(-2)min-1 (P = 0.028) for the coefficient of glucose tolerance (Kg), 2.18 +/- 0.29 versus 3.71 +/- 0.89 x 10(-4)microUml-1min-1 (P = 0.018) for insulin sensitivity (Si) and 1.80 +/- 0.39 versus 3.59 +/- 0.71 x 10(-2)min-1 (P = 0.028) for glucose effectiveness at basal insulin (Sg). Glucose 31-38 insulin Homo sapiens 446-453 15090769-7 2004 Fasting glucose, insulin, and insulin-mediated glucose disposal were unchanged, but on a 2 h oral glucose tolerance test glucose and insulin increased. Glucose 47-54 insulin Homo sapiens 30-37 15090769-7 2004 Fasting glucose, insulin, and insulin-mediated glucose disposal were unchanged, but on a 2 h oral glucose tolerance test glucose and insulin increased. Glucose 47-54 insulin Homo sapiens 30-37 15090769-7 2004 Fasting glucose, insulin, and insulin-mediated glucose disposal were unchanged, but on a 2 h oral glucose tolerance test glucose and insulin increased. Glucose 47-54 insulin Homo sapiens 30-37 15090769-7 2004 Fasting glucose, insulin, and insulin-mediated glucose disposal were unchanged, but on a 2 h oral glucose tolerance test glucose and insulin increased. Glucose 47-54 insulin Homo sapiens 30-37 15001196-8 2004 Insulin sensitivity was measured according to the steady-state plasma glucose (SSPG) method. Glucose 70-77 insulin Homo sapiens 0-7 14983513-16 2004 The labeled clone was subjected to directed lineage induction in vitro, resulting in the formation of islet-like structures (ILSs) that secreted insulin in response to a glucose challenge. Glucose 170-177 insulin Homo sapiens 145-152 15005922-3 2004 In this series of studies, the locus of insulin resistance in the septic patient was shown to lie within the metabolic pathways of glucose storage (glycogen synthesis) within skeletal muscle, was noted to be unrelated to the actions of hormone mediators such as leptin and was shown not to be associated with altered nutrient-induced thermogenesis during total parenteral nutrition (TPN). Glucose 131-138 insulin Homo sapiens 40-47 15204362-0 2004 Relationship between body mass index and insulin measured during oral glucose tolerance testing in severely obese children and adolescents. Glucose 70-77 insulin Homo sapiens 41-48 15005922-6 2004 These studies demonstrated that insulin resistance develops within 7 h of an inflammatory stimulus and, as in clinical sepsis, is characterised by selective impairment of glucose storage. Glucose 171-178 insulin Homo sapiens 32-39 14988241-4 2004 Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration in response to an infusion of octreotide, glucose, and insulin, and degree of adiposity was assessed by BMI. Glucose 73-80 insulin Homo sapiens 0-7 15106750-3 2004 Because of the importance of insulin in the regulation of myocardial metabolism, chronic insulin deficiency or resistance results in a marked reduction in cardiac glucose utilization such that the heart relies almost exclusively on fatty acids to generate energy. Glucose 163-170 insulin Homo sapiens 29-36 15009005-9 2004 Ghrelin levels after a glucose load were lower over time in subjects with more pronounced insulin resistance (P < 0.0001). Glucose 23-30 insulin Homo sapiens 90-97 15641325-6 2004 In the early stages of the disease, glucose can be controlled with appropriate therapeutic lifestyle changes aimed at lowering insulin resistance. Glucose 36-43 insulin Homo sapiens 127-134 16563103-3 2004 As the patient remained inotrope dependent the insulin dose was increased to 25 U/hr with an infusion of 50% dextrose to maintain the blood glucose levels between 6-8 mmol/L. Glucose 109-117 insulin Homo sapiens 47-54 15032648-2 2004 The insulin resistance syndrome encompasses more than a subnormal response to insulin-mediated glucose disposal. Glucose 95-102 insulin Homo sapiens 4-11 14968296-2 2004 This effect, which is called the incretin effect and is estimated to be responsible for 50 to 70% of the insulin response to glucose, is caused mainly by the two intestinal insulin-stimulating hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Glucose 125-132 insulin Homo sapiens 105-112 14968296-2 2004 This effect, which is called the incretin effect and is estimated to be responsible for 50 to 70% of the insulin response to glucose, is caused mainly by the two intestinal insulin-stimulating hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Glucose 125-132 insulin Homo sapiens 173-180 14968298-4 2004 After 48 h, glucose-stimulated insulin secretion, insulin content, triglyceride content and expression of different genes were evaluated. Glucose 12-19 insulin Homo sapiens 31-38 14968298-5 2004 RESULTS: Non-esterified fatty acids decreased glucose-stimulated insulin secretion, insulin content and increased triglyceride content of human isolated islets, independently from the deleterious effect of glucose. Glucose 46-53 insulin Homo sapiens 65-72 14968298-6 2004 Increased glucose concentrations also decreased glucose-stimulated insulin secretion and insulin content, but had no influence on triglyceride content. Glucose 10-17 insulin Homo sapiens 67-74 14968298-6 2004 Increased glucose concentrations also decreased glucose-stimulated insulin secretion and insulin content, but had no influence on triglyceride content. Glucose 10-17 insulin Homo sapiens 89-96 14968298-6 2004 Increased glucose concentrations also decreased glucose-stimulated insulin secretion and insulin content, but had no influence on triglyceride content. Glucose 48-55 insulin Homo sapiens 67-74 14968298-7 2004 Glucose-stimulated insulin secretion of islets appeared to be significantly correlated with their triglyceride content. Glucose 0-7 insulin Homo sapiens 19-26 14968298-9 2004 CONCLUSION/INTERPRETATION: In our model of isolated human islets, increased glucose and non-esterified fatty acids separately reproduced the two major beta-cell alterations observed in vivo, i.e. loss of glucose-stimulated insulin secretion and reduction in islet insulin content. Glucose 76-83 insulin Homo sapiens 223-230 14968298-9 2004 CONCLUSION/INTERPRETATION: In our model of isolated human islets, increased glucose and non-esterified fatty acids separately reproduced the two major beta-cell alterations observed in vivo, i.e. loss of glucose-stimulated insulin secretion and reduction in islet insulin content. Glucose 76-83 insulin Homo sapiens 264-271 14968298-9 2004 CONCLUSION/INTERPRETATION: In our model of isolated human islets, increased glucose and non-esterified fatty acids separately reproduced the two major beta-cell alterations observed in vivo, i.e. loss of glucose-stimulated insulin secretion and reduction in islet insulin content. Glucose 204-211 insulin Homo sapiens 223-230 14988247-6 2004 1) Is the usual reciprocal relationship between the acute insulin response to intravenous glucose (AIR(gluc)) and the level of fasting plasma glucose (FPG) maintained in pancreas transplant recipients? Glucose 90-97 insulin Homo sapiens 58-65 14988247-6 2004 1) Is the usual reciprocal relationship between the acute insulin response to intravenous glucose (AIR(gluc)) and the level of fasting plasma glucose (FPG) maintained in pancreas transplant recipients? Glucose 142-149 insulin Homo sapiens 58-65 14988241-4 2004 Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration in response to an infusion of octreotide, glucose, and insulin, and degree of adiposity was assessed by BMI. Glucose 73-80 insulin Homo sapiens 157-164 14988241-4 2004 Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration in response to an infusion of octreotide, glucose, and insulin, and degree of adiposity was assessed by BMI. Glucose 144-151 insulin Homo sapiens 0-7 14988243-2 2004 In pancreatic beta-cells, prolongation of the action potential by block of delayed rectifier potassium channels would be expected to increase intracellular free calcium and to promote insulin release in a glucose-dependent manner. Glucose 205-212 insulin Homo sapiens 184-191 15251635-5 2004 Furthermore, a close correlation was noted between high blood glucose level at admission and mortality among the patients in the control group; this relationship was attenuated by intensive insulin treatment. Glucose 62-69 insulin Homo sapiens 190-197 14988302-1 2004 OBJECTIVE: The aim of this study was to evaluate whether low insulin sensitivity (Si) measured using a modified frequently sampled intravenous glucose tolerance test with minimal model analysis is associated with coronary artery disease (CAD) independent of other cardiovascular risk factors. Glucose 143-150 insulin Homo sapiens 61-68 14566568-1 2004 Ingestion of glucose before exercise results in a transient increase in plasma insulin concentrations. Glucose 13-20 insulin Homo sapiens 79-86 14566568-2 2004 We hypothesized that if glucose was also ingested during the exercise period the elevated plasma insulin concentration could increase exogenous glucose oxidation. Glucose 24-31 insulin Homo sapiens 97-104 14566568-4 2004 Ingestion of glucose before exercise significantly increased plasma insulin concentration [from 196 (45) to 415 (57) pmol l(-1)] but the value returned to pre-exercise level within the first 30 min of exercise in spite of a continuous increase in plasma glucose concentration. Glucose 13-20 insulin Homo sapiens 68-75 15251642-4 2004 Insulin therapy improves glucose and lipid homeostasis, both of which are deleterious to the tissues, especially during severe stress. Glucose 25-32 insulin Homo sapiens 0-7 15251644-6 2004 Three protocols for IV insulin infusion are described that maintain blood glucose levels safely below the upper limit of their respective target ranges without substantial risk of hypoglycemia. Glucose 74-81 insulin Homo sapiens 23-30 15251639-3 2004 In the case of women with insulin-requiring gestational diabetes, no additional insulin is needed with the onset of labor; sufficient glucose should be infused to keep such women from becoming ketotic from the pronged period of starvation. Glucose 134-141 insulin Homo sapiens 26-33 15251639-4 2004 Likewise, protocols derived from glucose-controlled insulin infusion studies reveal that women with type 1 diabetes require no more subcutaneously administered insulin on the morning of an induction of labor or at the onset of spontaneous labor. Glucose 33-40 insulin Homo sapiens 52-59 14687913-2 2004 The beta-cell synthesizes and secretes the hormone insulin mainly in response to glucose but also in response to several nutrients, hormones and nervous stimuli. Glucose 81-88 insulin Homo sapiens 51-58 14988838-9 2004 CONCLUSIONS: The ability of insulin to lower the plasma glucose level in the HCV transgenic mice was impaired, as observed in chronic hepatitis C patients. Glucose 56-63 insulin Homo sapiens 28-35 15255279-5 2004 Fasting insulin resistance index (FIRI) was calculated from insulin and glucose concentrations. Glucose 72-79 insulin Homo sapiens 8-15 15001621-5 2004 A short iv glucose tolerance test was carried out to assess fasting insulin sensitivity and glucose-stimulated insulin secretion. Glucose 92-99 insulin Homo sapiens 111-118 14993868-4 2004 About 30% of these children were identified as hyperinsulinemic, using an insulin-to-glucose ratio of > or =33% or a serum insulin > or =25 microU/mL. Glucose 85-92 insulin Homo sapiens 52-59 15001593-0 2004 Validation of insulin sensitivity indices from oral glucose tolerance test parameters in obese children and adolescents. Glucose 52-59 insulin Homo sapiens 14-21 15001593-2 2004 The purpose of this study was validation of two surrogate indexes of insulin sensitivity determined from the oral glucose tolerance test (OGTT): the composite whole body insulin sensitivity index (WBISI) and the insulin sensitivity index (ISI). Glucose 114-121 insulin Homo sapiens 69-76 15001593-6 2004 Both the WBISI and ISI represented good estimates (r = 0.78 and 0.74; P < 0.0005) for clamp-derived insulin sensitivity (glucose disposed, M-value), respectively. Glucose 124-131 insulin Homo sapiens 103-110 15001593-9 2004 Insulin sensitivity can be estimated using plasma glucose and insulin responses derived from the OGTT in obese youth with normal and impaired glucose tolerance. Glucose 50-57 insulin Homo sapiens 0-7 15001621-12 2004 In addition, fasting and postload insulin secretion during the short iv glucose tolerance test correlated significantly with early postnatal growth rates, independently of birth weight SD scores. Glucose 72-79 insulin Homo sapiens 34-41 15001634-6 2004 Among nonobese, nondiabetic subjects, the insulin response of KQ (P = 0.027) and QQ (P = 0.031) subjects was greater during the oral glucose tolerance test than that of KK subjects, whereas plasma glucose profiles were comparable. Glucose 133-140 insulin Homo sapiens 42-49 15001626-4 2004 Insulin-stimulated glucose disposal decreased approximately 25% after short- and long-term fat infusion in both IGT relatives and controls. Glucose 19-26 insulin Homo sapiens 0-7 15001626-6 2004 Insulin-stimulated glucose oxidation was higher after long-term as compared with short-term fat infusion in control subjects. Glucose 19-26 insulin Homo sapiens 0-7 15001651-0 2004 Quantitative insulin sensitivity check index and the reciprocal index of homeostasis model assessment are useful indexes of insulin resistance in type 2 diabetic patients with wide range of fasting plasma glucose. Glucose 205-212 insulin Homo sapiens 13-20 15001651-0 2004 Quantitative insulin sensitivity check index and the reciprocal index of homeostasis model assessment are useful indexes of insulin resistance in type 2 diabetic patients with wide range of fasting plasma glucose. Glucose 205-212 insulin Homo sapiens 124-131 15015148-7 2004 In both trials, glucose(AUC) was significantly greater (13%, P <.05) in OC(+). Glucose 16-23 insulin Homo sapiens 24-27 14657199-1 2004 Type 2 diabetes has been associated with high synthesis and low absorption of cholesterol independent of weight, indicating that insulin resistance may be a link between glucose and cholesterol metabolism. Glucose 170-177 insulin Homo sapiens 129-136 14657199-4 2004 In bivariate analysis, cholesterol synthesis markers correlated with fasting insulin (r = 0.36-0.46, P < 0.01) and the rates of insulin-stimulated whole-body glucose uptake (WBGU; r = -0.37-0.40, P < 0.01). Glucose 161-168 insulin Homo sapiens 131-138 15134308-13 2004 GH therapy induced considerably higher fasting and glucose-stimulated insulin levels. Glucose 51-58 insulin Homo sapiens 70-77 15134308-20 2004 However, as has been reported in other patient groups, GH induced higher fasting and glucose-stimulated insulin levels, indicating insulin resistance. Glucose 85-92 insulin Homo sapiens 104-111 15015138-1 2004 The objective of the study was to evaluate the effects of acute and chronic resistance training on glucose and insulin responses to a glucose load in women with type 2 diabetes. Glucose 134-141 insulin Homo sapiens 111-118 15015154-0 2004 Resistance training enhances insulin-mediated glucose disposal with minimal effect on the tumor necrosis factor-alpha system in older hypertensives. Glucose 46-53 insulin Homo sapiens 29-36 15015154-5 2004 Insulin-mediated glucose disposal, assessed by the hyperinsulinemic euglycemic clamp procedure, significantly increased following RT (P =.026). Glucose 17-24 insulin Homo sapiens 0-7 15015154-7 2004 In conclusion, a 4-month RT program significantly increased insulin-mediated glucose disposal and LBM without a significant reduction in plasma levels of TNF-alpha, sTNF R1, and sTNF R2 in older hypertensive subjects. Glucose 77-84 insulin Homo sapiens 60-67 15039777-1 2004 Pancreatic beta-cells store insulin in secretory granules that undergo exocytosis upon glucose stimulation. Glucose 87-94 insulin Homo sapiens 28-35 15148744-1 2004 Insulin therapy is an effective measure of improving glucose control even in elderly patients with type 2 diabetes. Glucose 53-60 insulin Homo sapiens 0-7 14993546-10 2004 During and after insulin infusion in hyperglycemic neonates, plasma glucose concentration fell and proinsulin and C-peptide levels were lowered (18.4 +/- 7.6 and 20.7 +/- 4.5 pmol/L, respectively). Glucose 68-75 insulin Homo sapiens 17-24 15148744-9 2004 Using rapid or ultrarapid insulin injections three times daily, good glucose control achieved the goal of plasma glucose level of < 140 mg/dl before meals and at bedtime. Glucose 69-76 insulin Homo sapiens 26-33 15148744-9 2004 Using rapid or ultrarapid insulin injections three times daily, good glucose control achieved the goal of plasma glucose level of < 140 mg/dl before meals and at bedtime. Glucose 113-120 insulin Homo sapiens 26-33 15077478-4 2004 Diabetic patients with an order of magnitude less expression of 72 kDa heat shock gene have lower insulin stimulated glucose uptake,--storage and--oxidation and the lipid oxidation is less sensitive to the insulin effect. Glucose 117-124 insulin Homo sapiens 98-105 16437024-3 2004 In particular, FFA decrease insulin-mediated glucose transport/ phosphorylation in skeletal muscle and impair suppression of glucose production by the liver, indicating insulin resistance. Glucose 45-52 insulin Homo sapiens 28-35 15077478-5 2004 Both the expression of the 72 kDa heat shock gene and the insulin stimulated glucose uptake are lower in twins with type-2 diabetes even before the manifestation of the disease suggesting the pathological role of this gene. Glucose 77-84 insulin Homo sapiens 58-65 14751249-2 2004 GLUT2 is well known as the main glucose transporter in pancreatic islets and could highly regulate glucose-stimulated insulin secretion by B-cells as a glucose sensor. Glucose 32-39 insulin Homo sapiens 118-125 14751249-2 2004 GLUT2 is well known as the main glucose transporter in pancreatic islets and could highly regulate glucose-stimulated insulin secretion by B-cells as a glucose sensor. Glucose 99-106 insulin Homo sapiens 118-125 14975702-2 2004 Y-26763 was able to inhibit both glucose- and tolbutamide-induced insulin secretion from islets as assessed by radioimmunoassay. Glucose 33-40 insulin Homo sapiens 66-73 14700743-2 2004 Evidence suggests that these agents use a combination of mechanisms which may include glucose-dependent stimulation of insulin secretion, suppression of glucagon secretion, enhancement of beta-cell mass, slowing of gastric emptying, inhibition of food intake, and modulation of glucose trafficking in peripheral tissues. Glucose 86-93 insulin Homo sapiens 119-126 14657411-0 2004 INS VNTR is a QTL for the insulin response to oral glucose in obese children. Glucose 51-58 insulin Homo sapiens 26-33 14657411-1 2004 We performed a genotype-phenotype association study to examine whether the insulin VNTR (INS VNTR) polymorphism located in the insulin gene promoter was associated with changes in insulin response to oral glucose. Glucose 205-212 insulin Homo sapiens 75-82 14741112-0 2004 Closed-loop insulin delivery-the path to physiological glucose control. Glucose 55-62 insulin Homo sapiens 12-19 14741112-3 2004 Algorithms are evaluated for their ability to deliver insulin as to recreate, as closely as possible, glucose and insulin profiles observed in healthy individuals. Glucose 102-109 insulin Homo sapiens 54-61 14657411-1 2004 We performed a genotype-phenotype association study to examine whether the insulin VNTR (INS VNTR) polymorphism located in the insulin gene promoter was associated with changes in insulin response to oral glucose. Glucose 205-212 insulin Homo sapiens 127-134 14741113-4 2004 The most complex of these systems utilizes a very small hydrogel based on phenylboronic acid to control the flow of an insulin solution in response to changes in glucose concentration. Glucose 162-169 insulin Homo sapiens 119-126 14657411-1 2004 We performed a genotype-phenotype association study to examine whether the insulin VNTR (INS VNTR) polymorphism located in the insulin gene promoter was associated with changes in insulin response to oral glucose. Glucose 205-212 insulin Homo sapiens 127-134 14657411-6 2004 The INS VNTR can therefore be considered a quantitative trait locus influencing glucose-stimulated insulin physiology in obese juveniles. Glucose 80-87 insulin Homo sapiens 99-106 14960743-6 2004 RESULTS: The insulin-stimulated rate of glucose uptake by muscle was approximately 60 percent lower in the insulin-resistant subjects than in the insulin-sensitive control subjects (P<0.001) and was associated with an increase of approximately 80 percent in the intramyocellular lipid content (P=0.005). Glucose 40-47 insulin Homo sapiens 13-20 14960743-6 2004 RESULTS: The insulin-stimulated rate of glucose uptake by muscle was approximately 60 percent lower in the insulin-resistant subjects than in the insulin-sensitive control subjects (P<0.001) and was associated with an increase of approximately 80 percent in the intramyocellular lipid content (P=0.005). Glucose 40-47 insulin Homo sapiens 107-114 14960743-6 2004 RESULTS: The insulin-stimulated rate of glucose uptake by muscle was approximately 60 percent lower in the insulin-resistant subjects than in the insulin-sensitive control subjects (P<0.001) and was associated with an increase of approximately 80 percent in the intramyocellular lipid content (P=0.005). Glucose 40-47 insulin Homo sapiens 107-114 15013454-8 2004 Although the traditional approach has been to introduce insulin therapy only after very high glucose values have persisted, despite prolonged use of oral agents alone, a more desirable strategy would be to prevent patients from ever experiencing the loss of glycemic control associated with hemoglobin A(1c) (HbA(1c)) elevations >7%. Glucose 93-100 insulin Homo sapiens 56-63 15013456-4 2004 Rapid-acting insulin has been shown to provide superior postprandial glucose control compared with regular insulin. Glucose 69-76 insulin Homo sapiens 13-20 15017466-9 2004 Longitudinal glucose values of 75-g GTT improve during third trimester in triplet pregnancies, suggesting that fetoplacental fuel drain may counterbalance maternal insulin resistance. Glucose 13-20 insulin Homo sapiens 164-171 15122091-2 2004 Insulin resistance is characterised by a decrease in insulin effect on glucose transport in muscle and adipose tIssue. Glucose 71-78 insulin Homo sapiens 0-7 15122091-2 2004 Insulin resistance is characterised by a decrease in insulin effect on glucose transport in muscle and adipose tIssue. Glucose 71-78 insulin Homo sapiens 53-60 15122091-3 2004 Tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) and its binding to phosphatidylinositol 3-kinase (PI 3-kinase) are critical events in the insulin signalling cascade leading to insulin-stimulated glucose transport. Glucose 212-219 insulin Homo sapiens 28-35 15122091-3 2004 Tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) and its binding to phosphatidylinositol 3-kinase (PI 3-kinase) are critical events in the insulin signalling cascade leading to insulin-stimulated glucose transport. Glucose 212-219 insulin Homo sapiens 155-162 15163922-1 2004 Insulin resistance is characterized by a peripheral resistance to insulin-mediated glucose uptake, and an hepatic resistance of glucose production to insulin. Glucose 83-90 insulin Homo sapiens 0-7 15163922-1 2004 Insulin resistance is characterized by a peripheral resistance to insulin-mediated glucose uptake, and an hepatic resistance of glucose production to insulin. Glucose 83-90 insulin Homo sapiens 66-73 15163922-1 2004 Insulin resistance is characterized by a peripheral resistance to insulin-mediated glucose uptake, and an hepatic resistance of glucose production to insulin. Glucose 128-135 insulin Homo sapiens 0-7 15163922-5 2004 Adiponectin improves insulin sensitivity in skeletal muscle and liver, through a stimulation of fatty acid oxidation and glucose utilization. Glucose 121-128 insulin Homo sapiens 21-28 15163922-8 2004 Adiponectin, clearly, is a major modulator of glucose and lipid metabolism in insulin-sensitive tIssue and/or regulator of insulin-sensitivity, in obese and/or glucose intolerant subjects, as well as in type 2 diabetes mellitus. Glucose 46-53 insulin Homo sapiens 78-85 14656737-7 2004 Glargine and human regular insulin similarly stimulated whole-body glucose metabolism and suppressed serum free-fatty acid (FFA) concentrations. Glucose 67-74 insulin Homo sapiens 27-34 15052336-6 2004 The consequence of these hormonal alterations with respect to both glucose and lipid metabolism in insulin target tissues is just beginning to be understood. Glucose 67-74 insulin Homo sapiens 99-106 17021526-0 2004 New perspectives for an old cure: a glucose-insulin-potassium revival in cardiac surgery? Glucose 36-43 insulin Homo sapiens 44-51 14722654-8 2004 Understanding how the mechanism by which molecular insulin action is modulated by these factors will potentially provide new targets for pharmacological agents, to enable the control of altered glucose and lipid metabolism and diabetes. Glucose 194-201 insulin Homo sapiens 51-58 14747211-5 2004 Insulin sensitivity was measured at baseline and at 6 months using the frequently sampled intravenous glucose tolerance test with minimal model analysis. Glucose 102-109 insulin Homo sapiens 0-7 14747226-5 2004 RESULTS: There was a strong correlation between the [(13)C]glucose breath test result and the glucose disposal rate (r = 0.69, P < 0.0001) and insulin sensitivity index (r = 0.69, P < 0.0001) from the insulin clamp. Glucose 59-66 insulin Homo sapiens 207-214 14747229-2 2004 In that study, the insulin infusion protocol (IIP) used to normalize blood glucose levels provided valuable guidelines for adjusting insulin therapy. Glucose 75-82 insulin Homo sapiens 19-26 14747229-2 2004 In that study, the insulin infusion protocol (IIP) used to normalize blood glucose levels provided valuable guidelines for adjusting insulin therapy. Glucose 75-82 insulin Homo sapiens 133-140 14747241-3 2004 Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated using the following formula (fasting plasma insulin x plasma glucose)/22.5. Glucose 137-144 insulin Homo sapiens 32-39 14747278-0 2004 Strength training increases insulin-mediated glucose uptake, GLUT4 content, and insulin signaling in skeletal muscle in patients with type 2 diabetes. Glucose 45-52 insulin Homo sapiens 28-35 14747294-9 2004 There was a significant correlation between the total insulin secretory response and control of glucose, measured by HbA(1c) (P = 0.003). Glucose 96-103 insulin Homo sapiens 54-61 14749262-4 2004 We have analyzed glucose-stimulated insulin secretion using hyperglycemic clamps in carriers of a CA repeat in the IGF-I promoter and an ApaI polymorphism in the IGF-II gene. Glucose 17-24 insulin Homo sapiens 36-43 14749267-3 2004 The improved insulin sensitivity may be achieved either by systemic insulin sensitization or by direct action of peroxisome proliferator-activated receptor (PPAR)-gamma on the transcription of genes involved in glucose disposal. Glucose 211-218 insulin Homo sapiens 13-20 14749267-4 2004 Evidence supporting the direct action of PPAR-gamma on glucose metabolism is observed in the genes involved in insulin-stimulated glucose disposal. Glucose 55-62 insulin Homo sapiens 111-118 14749267-4 2004 Evidence supporting the direct action of PPAR-gamma on glucose metabolism is observed in the genes involved in insulin-stimulated glucose disposal. Glucose 130-137 insulin Homo sapiens 111-118 14749269-0 2004 Potential role of peroxisome proliferator-activated receptor-alpha in the modulation of glucose-stimulated insulin secretion. Glucose 88-95 insulin Homo sapiens 107-114 14749269-5 2004 Thus, augmented insulin secretion may reflect a requirement for lipid lowering as well as for increased glucose disposal and is perceived to aim to compensate for impaired suppression of islet lipid delivery by insulin. Glucose 104-111 insulin Homo sapiens 16-23 14749274-6 2004 Carriers of the A3243G mutation show during a hyperglycemic clamp at 10 mmol/l glucose a marked reduction in first- and second-phase insulin secretion compared with noncarriers. Glucose 79-86 insulin Homo sapiens 133-140 14749274-7 2004 The molecular mechanism by which the A3243G mutation affects insulin secretion may involve an attenuation of cytosolic ADP/ATP levels leading to a resetting of the glucose sensor in the pancreatic beta-cell, such as in maturity-onset diabetes of the young (MODY)-2 patients with mutations in glucokinase. Glucose 164-171 insulin Homo sapiens 61-68 14749275-3 2004 Mitochondrial radical production associated with hyperglycemia will also disrupt glucose-stimulated insulin secretion by pancreatic beta-cells, because pancreatic beta-cells are particularly susceptible to oxidative damage. Glucose 81-88 insulin Homo sapiens 100-107 14749285-3 2004 Our studies indicate that iPLA(2)beta is expressed in beta-cells and participates in glucose-stimulated insulin secretion but is not involved in membrane phospholipid remodeling. Glucose 85-92 insulin Homo sapiens 104-111 14749285-4 2004 If iPLA(2)beta plays a signaling role in glucose-stimulated insulin secretion, then conditions that impair iPLA(2)beta functions might contribute to the diminished capacity of beta-cells to secrete insulin in response to glucose, which is a prominent characteristic of type 2 diabetes. Glucose 41-48 insulin Homo sapiens 60-67 14749285-4 2004 If iPLA(2)beta plays a signaling role in glucose-stimulated insulin secretion, then conditions that impair iPLA(2)beta functions might contribute to the diminished capacity of beta-cells to secrete insulin in response to glucose, which is a prominent characteristic of type 2 diabetes. Glucose 41-48 insulin Homo sapiens 198-205 14749285-4 2004 If iPLA(2)beta plays a signaling role in glucose-stimulated insulin secretion, then conditions that impair iPLA(2)beta functions might contribute to the diminished capacity of beta-cells to secrete insulin in response to glucose, which is a prominent characteristic of type 2 diabetes. Glucose 221-228 insulin Homo sapiens 198-205 14763919-5 2004 Insulin-stimulated glucose uptake (ISGU) was determined by a hyperinsulinemic clamp and maximal aerobic work capacity (VO2 max) by a bicycle ergometer test. Glucose 19-26 insulin Homo sapiens 0-7 15000763-11 2004 This study results demonstrated that Oralin could be used as meal insulin as an add-on therapy in combination with failing OHAs treatment in subjects with type 2 diabetes to regulate postprandial glucose levels. Glucose 196-203 insulin Homo sapiens 66-73 15034192-9 2004 Taken together, our results are in line with the hypothesis that in glucosamine-treated adipocytes UDP-hexosamines influence insulin-stimulated glucose uptake. Glucose 144-151 insulin Homo sapiens 125-132 15034192-4 2004 In glucosamine-treated 3T3-L1 adipocytes, inhibition of insulin-stimulated glucose uptake was highly correlated with UDP-hexosamine levels (r = -0.992; p < 0.0001 for UDP-GlcNAc and r = -0.996; p < 0.0001 for UDP-GalNAc). Glucose 75-82 insulin Homo sapiens 56-63 15034192-5 2004 Incubation of 3T3-L1 adipocytes with 0.1 microM insulin for 24 h in medium containing 1 and 5 mM glucose increased the rate of glucose uptake by 365% and 175% compared to untreated cells, respectively. Glucose 97-104 insulin Homo sapiens 48-55 15031772-5 2004 OGTT demonstrated that insulin secretion was severely impaired: basal insulin was 3.7 uU/ml and 60 min after an oral glucose load plasma insulin peaked only threefold to 10.7 uU/ml. Glucose 117-124 insulin Homo sapiens 23-30 15034192-5 2004 Incubation of 3T3-L1 adipocytes with 0.1 microM insulin for 24 h in medium containing 1 and 5 mM glucose increased the rate of glucose uptake by 365% and 175% compared to untreated cells, respectively. Glucose 127-134 insulin Homo sapiens 48-55 15034192-7 2004 However, treatment of cells with insulin and 1, 5, 10, or 25 mM glucose resulted in similar increases in levels of UDP-GlcNAc and UDP-GalNAc that always amounted to approx 30-40% above baseline values. Glucose 64-71 insulin Homo sapiens 33-40 14767998-8 2004 In conclusion, these findings suggest that bile acids and insulin may cooperate to regulate glucose storage in hepatocytes. Glucose 92-99 insulin Homo sapiens 58-65 14700554-2 2004 Glucose metabolism was measured in the fasting state by the homeostatic model assessment (HOMA) insulin resistance index and during a standard oral glucose tolerance test (OGTT). Glucose 0-7 insulin Homo sapiens 96-103 14747186-8 2004 Glucose:insulin ratio as a marker for insulin resistance was not associated with an increased risk for oligomenorrhoea. Glucose 0-7 insulin Homo sapiens 38-45 14764802-6 2004 The insulin sensitivity index during oral glucose tolerance test was lower in women with PCOS compared with normal women throughout the first trimester (P < 0.0001). Glucose 42-49 insulin Homo sapiens 4-11 14764797-6 2004 Integrated incremental insulin determined by FSIVGTT, the area under the curve for insulin, and fasting and 2 h glucose load insulin levels determined by an oral glucose tolerance test in both HF groups were higher (P < 0.01-0.0001) than those in normal females with normal or high BMI. Glucose 112-119 insulin Homo sapiens 83-109 14764804-9 2004 In patients with diabetes, the degradation of insulin by wound fluid correlated with glucose control (hemoglobin A(1c); r(2) = 0.5353; P < 0.001), and patients with worse outcomes (i.e. amputation) had higher wound fluid insulin degradation. Glucose 85-92 insulin Homo sapiens 46-53 14764797-6 2004 Integrated incremental insulin determined by FSIVGTT, the area under the curve for insulin, and fasting and 2 h glucose load insulin levels determined by an oral glucose tolerance test in both HF groups were higher (P < 0.01-0.0001) than those in normal females with normal or high BMI. Glucose 162-169 insulin Homo sapiens 83-109 14764798-11 2004 Static incubation at 11 and 16 vs. 4 mM glucose for 96 h decreased islet insulin stores by approximately 80% and 85% (P < 0.0001, respectively). Glucose 40-47 insulin Homo sapiens 73-80 14764798-14 2004 The orderliness of insulin secretion was significantly reduced after chronic incubation of human islets at 11 mM glucose (P = 0.04), but induction of beta-cell rest at 11 mM failed to normalize the regularity of insulin secretion during subsequent perifusion. Glucose 113-120 insulin Homo sapiens 19-26 14764798-18 2004 Impaired glucose-regulated insulin secretion in TTDM may, however, partially involve mechanisms that are distinct from insulin stores and insulin secretion rates. Glucose 9-16 insulin Homo sapiens 27-34 14759805-9 2004 In addition, insulin-induced glucose uptake was not affected by the procedure. Glucose 29-36 insulin Homo sapiens 13-20 14764799-5 2004 The insulin sensitivity index was calculated from glucose and insulin concentrations during an oral glucose tolerance test. Glucose 50-57 insulin Homo sapiens 4-11 14764799-5 2004 The insulin sensitivity index was calculated from glucose and insulin concentrations during an oral glucose tolerance test. Glucose 100-107 insulin Homo sapiens 4-11 14764791-1 2004 Increased flux of glucose through the hexosamine biosynthetic pathway has been implicated in insulin resistance, altered insulin secretion, and diabetic nephropathy. Glucose 18-25 insulin Homo sapiens 93-100 14717908-6 2004 RESULTS: For the non-stone former population, low insulin sensitivity measured as glucose disposal rate significantly correlated with low 24-hour urinary pH (r= 0. Glucose 82-89 insulin Homo sapiens 50-57 14717908-8 2004 In addition to the previously described acidic urine pH and hypouricosuria, patients with recurrent uric acid nephrolithiasis were found to be severely insulin resistant (glucose disposal rate: uric acid stone-formers vs. normals; 4.1 +/- 1.3 vs. 6.9 +/- 2.1 mg/min/kg of lean body mass, P= 0.008). Glucose 171-178 insulin Homo sapiens 152-159 14767878-2 2004 In subjects with type 2 diabetes, when protein is ingested with glucose, insulin is further increased and the glucose rise is less than when glucose is ingested alone. Glucose 64-71 insulin Homo sapiens 73-80 15112902-8 2004 The pharmacokinetic properties of insulin glargine allow an easier titration of basal insulin dose, which should facilitate adequate blood glucose control while decreasing the risk of hypoglycaemia, especially during night time. Glucose 139-146 insulin Homo sapiens 34-41 15112902-8 2004 The pharmacokinetic properties of insulin glargine allow an easier titration of basal insulin dose, which should facilitate adequate blood glucose control while decreasing the risk of hypoglycaemia, especially during night time. Glucose 139-146 insulin Homo sapiens 86-93 15102494-1 2004 Type 2 diabetes is characterized by high concentrations of glucose in the blood, which is caused by decreased secretion of insulin from the pancreas and decreased insulin action. Glucose 59-66 insulin Homo sapiens 123-130 13129856-3 2004 Insulin release was measured (radioimmunoassay) in islets incubated with 3.3 or 16.7 mM glucose with or without 75, 150, and 300 nM wortmannin. Glucose 88-95 insulin Homo sapiens 0-7 14746909-3 2004 To induce the promoter constructs by endogenous insulin released from the pancreatic beta-cells, transgenic mice were given repeated intraperitoneal injections of D-glucose. Glucose 163-172 insulin Homo sapiens 48-55 14964022-1 2004 Persistent hyperinsulinemic hypoglycaemia in infancy (PHHI) presents a diagnostic and therapeutic challenge for the treating physician: increased glucose requirements, detectable insulin levels at the point of hypoglycaemia, inappropriately low blood levels of free fatty acids and ketone bodies are characteristic of this condition. Glucose 146-153 insulin Homo sapiens 16-23 14767364-1 2004 Alterations in glucose metabolism, including hyperglycemia associated with insulin resistance, occur in critical illness. Glucose 15-22 insulin Homo sapiens 75-82 14767364-8 2004 This article reviews alterations in glucose metabolism which occur in critically ill patients and discusses potential mechanisms and mediators (e.g., hormones, cytokines) that may play a key role in hyperglycemia and insulin resistance during acute and prolonged phases of severe illness. Glucose 36-43 insulin Homo sapiens 217-224 12965873-14 2004 These results suggest that cortisol excess impairs glucose tolerance by decreasing both insulin action and glucose effectiveness. Glucose 51-58 insulin Homo sapiens 88-95 14968298-9 2004 CONCLUSION/INTERPRETATION: In our model of isolated human islets, increased glucose and non-esterified fatty acids separately reproduced the two major beta-cell alterations observed in vivo, i.e. loss of glucose-stimulated insulin secretion and reduction in islet insulin content. Glucose 204-211 insulin Homo sapiens 264-271 13129856-4 2004 Insulin significantly enhanced 14CO2 and 3H2O production with 3.3 mM glucose but not with 0.6, 8.3, or 16.7 mM glucose. Glucose 69-76 insulin Homo sapiens 0-7 13129856-5 2004 Addition of anti-insulin serum to the medium with 8.3 and 16.7 mM glucose decreased 14CO2 and 3H2O production significantly. Glucose 66-73 insulin Homo sapiens 17-24 13129856-10 2004 Addition of wortmannin significantly decreased insulin release induced by 16.7 mM glucose in a dose-dependent manner. Glucose 82-89 insulin Homo sapiens 47-54 13129856-11 2004 Our results suggest that insulin exerts a physiological autocrine stimulatory effect on glucose metabolism in intact islets as well as on glucose-induced insulin release. Glucose 88-95 insulin Homo sapiens 25-32 13129856-11 2004 Our results suggest that insulin exerts a physiological autocrine stimulatory effect on glucose metabolism in intact islets as well as on glucose-induced insulin release. Glucose 138-145 insulin Homo sapiens 25-32 13129856-11 2004 Our results suggest that insulin exerts a physiological autocrine stimulatory effect on glucose metabolism in intact islets as well as on glucose-induced insulin release. Glucose 138-145 insulin Homo sapiens 154-161 15646368-1 2004 The aim of the present study was to evaluate several long-acting insulin preparations for their ability to normalize the blood glucose profile of rats and mice with streptozocin-induced diabetes mellitus. Glucose 127-134 insulin Homo sapiens 65-72 15283380-1 2004 The aim of pancreas and islet transplantation is to establish the same status of glucose control that is provided by endogenous secretion of insulin from a healthy native pancreas in order to improve the quality of life and ameliorate secondary diabetic complications in patients with type I insulin-dependent diabetes mellitus (IDDM). Glucose 81-88 insulin Homo sapiens 141-148 15646368-2 2004 The single injection of a long-acting zinc insulin (CAS 8049-62-5) suspension or insulin glargine (CAS 160337-95-1) in both species induced a steep to moderate fall in blood glucose concentration. Glucose 174-181 insulin Homo sapiens 43-50 15646368-2 2004 The single injection of a long-acting zinc insulin (CAS 8049-62-5) suspension or insulin glargine (CAS 160337-95-1) in both species induced a steep to moderate fall in blood glucose concentration. Glucose 174-181 insulin Homo sapiens 81-88 15646368-4 2004 In contrast, implants produced with a mixture of human insulin and palmitic acid micro-crystals normalized blood glucose profile over 24 h in both species at least 30 days after implantation. Glucose 113-120 insulin Homo sapiens 55-62 15646368-5 2004 Therefore, these implants with a sustained release of insulin are suitable to control the blood glucose in diabetic rats and mice. Glucose 96-103 insulin Homo sapiens 54-61 14695465-0 2004 Insulin resistance and fasting hyperinsulinemia are risk factors for new cardiovascular events in patients with prior coronary artery disease and normal glucose tolerance. Glucose 153-160 insulin Homo sapiens 0-7 15628572-8 2004 The training induced an increase in insulin sensitivity (glucose disposal M: 3.0 vs 4.0 M - mg/min/kg, p<0,01). Glucose 57-64 insulin Homo sapiens 36-43 15289640-2 2004 Genetic engineering of nonpancreatic cells into glucose-sensitive insulin-producing cells; 2. Glucose 48-55 insulin Homo sapiens 66-73 15289640-3 2004 Transforming stem cells, pancreatic ductal cells, or pancreatic endocrine cell lines into glucose-sensitive insulin-producing cells; and 3. Glucose 90-97 insulin Homo sapiens 108-115 15289651-6 2004 We have focused on two important aspects of beta-cell biology in our studies: beta-cell function, specifically the metabolic regulatory mechanisms involved in glucose-stimulated insulin secretion, and beta-cell resistance to immune attack, with emphasis on resistance to inflammatory cytokines and reactive oxygen species. Glucose 159-166 insulin Homo sapiens 178-185 15289656-1 2004 Insulin receptor signal transduction plays a critical role in regulating pancreatic beta-cell function, notably the acute first-phase insulin release in response to glucose. Glucose 165-172 insulin Homo sapiens 134-141 15289656-6 2004 Manipulations aimed at reducing expression of physiologically relevant PTPases acting at a step proximal to the insulin receptor are accompanied by normalization of blood glucose levels and improved insulin sensitivity in both normal and diabetic animals. Glucose 171-178 insulin Homo sapiens 112-119 14675555-5 2004 If glucose metabolism through the glycolytic pathway is impaired, as in insulin resistance, there will be a build-up of glyceraldehyde, glyceraldehyde-3-phosphate and dihydroxyacetone phosphate with further metabolism to methylglyoxal, a highly reactive ketoaldehyde. Glucose 3-10 insulin Homo sapiens 72-79 15083641-22 2004 Patients with clinical prostate cancer may have the same metabolic abnormality of a defective insulin-stimulated glucose uptake and secondary hyperinsulinaemia as patients with the metabolic syndrome. Glucose 113-120 insulin Homo sapiens 94-101 15777067-2 2004 Insulin resistance detection by the fasting plasma insulin and glucose determination enables early detection, follow-up, treatment and the search for accelerating factors in kidney disease patients threatened by atherosclerosis. Glucose 63-70 insulin Homo sapiens 0-7 15777067-3 2004 PATIENTS AND METHODS: Insulin resistance was evaluated by the Quantitative Insulin Sensitivity Check Index from fasting glucose and insulin plasma concentrations in 66 kidney disease patients with a mild to moderate decrease in kidney function. Glucose 120-127 insulin Homo sapiens 22-29 15777067-3 2004 PATIENTS AND METHODS: Insulin resistance was evaluated by the Quantitative Insulin Sensitivity Check Index from fasting glucose and insulin plasma concentrations in 66 kidney disease patients with a mild to moderate decrease in kidney function. Glucose 120-127 insulin Homo sapiens 75-82 15777067-6 2004 However, patients with insulin resistance suffered from increased BMI (p < 0.001), fasting plasma glucose (p < 0.01), insulin (p < 0.001) and triglyceride (p < 0.01) concentrations. Glucose 101-108 insulin Homo sapiens 23-30 15481632-8 2004 In a large cross-sectional study with 4270 orally treated patients, elevation of fasting intact proinsulin was very closely related to insulin resistance, as assessed by iv glucose tolerance test in a subgroup, and by HOMA analysis in the entire patient population. Glucose 173-180 insulin Homo sapiens 96-106 15552273-9 2004 Significant factors affecting insulin were age, gender, body mass index and glucose, in addition to alanine aminotransferase and high-density lipoprotein cholesterol in men, triglycerides and oral contraceptive use in women, and alkaline phosphatase in girls. Glucose 76-83 insulin Homo sapiens 30-37 15258364-4 2004 While the healthy skeletal muscle has substantial metabolic flexibility and is able to switch from predominantly lipid o oxidation during fasting or endurance exercise to increased glucose oxidation in conditions of insulin stimulation, obese individuals and those with type 2 diabetes manifest higher lipid oxidation during insulin-stimulated conditions despite lower rates of lipid oxidation during fasting or prolonged exercise. Glucose 181-188 insulin Homo sapiens 216-223 15481632-8 2004 In a large cross-sectional study with 4270 orally treated patients, elevation of fasting intact proinsulin was very closely related to insulin resistance, as assessed by iv glucose tolerance test in a subgroup, and by HOMA analysis in the entire patient population. Glucose 173-180 insulin Homo sapiens 99-106 17271786-1 2004 For suppressing the development of diabetes mellitus and the onset of complications, an insulin therapy has been used for suppressing and normalizing the change of a blood glucose. Glucose 172-179 insulin Homo sapiens 88-95 14741069-1 2004 The primary aim of insulin therapy is to replace endogenous insulin secretion in patients with type 1 or type 2 diabetes in a physiologically sound manner, mimicking normal secretion patterns to adequately regulate glucose metabolism. Glucose 215-222 insulin Homo sapiens 19-26 17271786-5 2004 By local fuzzy reconstruction method, we can predict the fasting blood glucose in the short term and then we can estimate the appropriate amount of insulin shot based on the measured bedtime blood glucose. Glucose 71-78 insulin Homo sapiens 148-155 17271786-5 2004 By local fuzzy reconstruction method, we can predict the fasting blood glucose in the short term and then we can estimate the appropriate amount of insulin shot based on the measured bedtime blood glucose. Glucose 197-204 insulin Homo sapiens 148-155 17271786-6 2004 Using the system, the change of blood glucose can be suppressed and normalized and the number of the insulin dosage a day can be reduced to once. Glucose 38-45 insulin Homo sapiens 101-108 17271794-6 2004 A new minimal model of glucose and insulin concentrations in plasma, which incorporates both the pulsatile and biphasic aspect of insulin production into existing minimal models, has been developed. Glucose 23-30 insulin Homo sapiens 130-137 14673523-12 2004 Furthermore, the islets isolated by magnetic retraction stained strongly positive for insulin during the entire observation period in vitro, and produced high amounts of insulin upon a challenge with glucose. Glucose 200-207 insulin Homo sapiens 170-177 15078145-6 2004 Many potent and selective small molecule inhibitors of GSK3 have now been identified, and used in vitro to modulate glycogen metabolism and gene transcription, increase glycogen synthase activity and enhance insulin-stimulated glucose transport. Glucose 227-234 insulin Homo sapiens 208-215 14666364-1 2004 AIMS/HYPOTHESIS: Both insulin resistance and beta-cell dysfunction play a role in the transition from normal glucose tolerance (NGT) to Type 2 diabetes (T2DM) through impaired glucose tolerance (IGT). Glucose 109-116 insulin Homo sapiens 22-29 14686957-2 2004 We used a method to allow us to evaluate the possible difference of insulin sensibility with regard to the insulin action on glycaemia and blood FFA, both in the basal state and during oral glucose tolerance test (OGTT). Glucose 190-197 insulin Homo sapiens 68-75 14666364-4 2004 In all subjects the insulin secretion/insulin resistance index (DeltaI/DeltaG/IR) was calculated as the ratio of the increment in plasma insulin to the increment in plasma glucose during the OGTT divided by insulin resistance, as measured during the clamp. Glucose 172-179 insulin Homo sapiens 20-27 14666364-4 2004 In all subjects the insulin secretion/insulin resistance index (DeltaI/DeltaG/IR) was calculated as the ratio of the increment in plasma insulin to the increment in plasma glucose during the OGTT divided by insulin resistance, as measured during the clamp. Glucose 172-179 insulin Homo sapiens 38-45 14666364-8 2004 CONCLUSION/INTERPRETATION: When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in "normal" glucose tolerant individuals. Glucose 68-75 insulin Homo sapiens 43-50 14666364-8 2004 CONCLUSION/INTERPRETATION: When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in "normal" glucose tolerant individuals. Glucose 68-75 insulin Homo sapiens 129-136 14693408-3 2004 We used minimal model analysis of the frequently sampled insulin-modified intravenous glucose tolerance test (FSIGT) and polymerase chain reaction (PCR)-restriction fragment length polymorphism to examine differences of insulin secretion and insulin resistance among three genotypes. Glucose 86-93 insulin Homo sapiens 57-64 14686957-2 2004 We used a method to allow us to evaluate the possible difference of insulin sensibility with regard to the insulin action on glycaemia and blood FFA, both in the basal state and during oral glucose tolerance test (OGTT). Glucose 190-197 insulin Homo sapiens 107-114 14693710-10 2004 We conclude that, within a 3-year time frame, the onset of diabetes is very often rapid rather than gradual and is in part explained by a fall in glucose-stimulated insulin response. Glucose 146-153 insulin Homo sapiens 165-172 14693694-11 2004 This twofold increase in ceramide may be involved in the decrease in Akt phosphorylation observed after insulin infusion and could theoretically play a role in the reduced ability of insulin to stimulate glucose uptake in skeletal muscle from obese subjects. Glucose 204-211 insulin Homo sapiens 183-190 14693981-11 2004 Insulin-stimulated glucose disposal increased in the troglitazone group (from 208.3 +/- 23.7 to 263.5 +/- 30.4 vs. 197.1 +/- 20.0 to 200.8 +/- 20.8 mg. m(-2). Glucose 19-26 insulin Homo sapiens 0-7 14693981-14 2004 CONCLUSIONS: In glucose-tolerant first-degree relatives, treatment with troglitazone improved insulin sensitivity almost 50%, primarily due to increased glucose storage. Glucose 153-160 insulin Homo sapiens 94-101 14693718-5 2004 LPL haplotypes showed linkage to the glucose infusion rate (GINF), a direct physiologic measurement of insulin sensitivity (P = 0.034). Glucose 37-44 insulin Homo sapiens 103-110 14737741-0 2004 The vasodilatory actions of insulin on resistance and terminal arterioles and their impact on muscle glucose uptake. Glucose 101-108 insulin Homo sapiens 28-35 14706055-3 2004 METHODS: We measured insulin sensitivity using the euglycaemic glucose clamp technique and insulin response to oral glucose in 10 unfit (did not participate in routine physical exercise) offspring of T2DM parents and 10 unfit control subjects, and compared them with six fit (routinely swam for 3 h/day 5 days/week) offspring of T2DM parents and six fit controls with no family history of T2DM. Glucose 116-123 insulin Homo sapiens 91-98 14706055-6 2004 The corresponding insulin response of unfit offspring was significantly higher at 60 min in the oral glucose tolerance test (OGTT) that that of fit offspring or fit controls. Glucose 101-108 insulin Homo sapiens 18-25 14737741-1 2004 Whether a discrete vascular action of insulin in skeletal muscle integrally participates in insulin-mediated glucose disposal has been extensively examined but remains a contentious issue. Glucose 109-116 insulin Homo sapiens 38-45 14737741-1 2004 Whether a discrete vascular action of insulin in skeletal muscle integrally participates in insulin-mediated glucose disposal has been extensively examined but remains a contentious issue. Glucose 109-116 insulin Homo sapiens 92-99 14737741-2 2004 Here, we review some of the data both supporting and questioning the role of insulin-mediated increases in limb blood flow in glucose metabolism. Glucose 126-133 insulin Homo sapiens 77-84 14737741-5 2004 We also advance the hypothesis that an action on the precapillary arteriole may play the dominant role in mediating perfusion-dependent effects of insulin on glucose metabolism in muscle. Glucose 158-165 insulin Homo sapiens 147-154 15212558-12 2004 If the postprandial glucose level is elevated, pre-meal rapid-acting insulin should be prescribed, beginning with a dose of 1U per 10g of carbohydrates in the meal. Glucose 20-27 insulin Homo sapiens 69-76 15212559-4 2004 These actions, in conjunction with the glucose cellular uptake function of insulin, help normalise fluctuations in circulating glucose levels to a greater degree than is possible with insulin treatment alone. Glucose 39-46 insulin Homo sapiens 75-82 15212559-4 2004 These actions, in conjunction with the glucose cellular uptake function of insulin, help normalise fluctuations in circulating glucose levels to a greater degree than is possible with insulin treatment alone. Glucose 127-134 insulin Homo sapiens 75-82 15212559-4 2004 These actions, in conjunction with the glucose cellular uptake function of insulin, help normalise fluctuations in circulating glucose levels to a greater degree than is possible with insulin treatment alone. Glucose 127-134 insulin Homo sapiens 184-191 15251616-4 2004 RESULTS: A greater mean decrease in fasting blood glucose (FBG) was achieved at endpoint with insulin glargine than with NPH insulin (-21 mg/dL versus -10 mg/dL [-1.17 mmol/L versus -0.56 mmol/L]; P = 0.015), and a greater percentage of patients treated with insulin glargine reached the target FBG (32.6% versus 21.3%; P = 0.015). Glucose 50-57 insulin Homo sapiens 94-101 15516153-7 2004 Almost half of the studies with ACE inhibitors in hypertensive nondiabetic individuals demonstrated a slight but significant increase in insulin sensitivity as assessed by insulin-stimulated glucose disposal during a euglycaemic hyperinsulinaemic clamp, while the other half failed to reveal any significant change. Glucose 191-198 insulin Homo sapiens 137-144 15516153-7 2004 Almost half of the studies with ACE inhibitors in hypertensive nondiabetic individuals demonstrated a slight but significant increase in insulin sensitivity as assessed by insulin-stimulated glucose disposal during a euglycaemic hyperinsulinaemic clamp, while the other half failed to reveal any significant change. Glucose 191-198 insulin Homo sapiens 172-179 15516153-10 2004 They may include improvement of blood flow and microcirculation in skeletal muscles and, thereby, enhancement of insulin and glucose delivery to the insulin-sensitive tissues, facilitating insulin signalling at the cellular level and improvement of insulin secretion by the beta cells. Glucose 125-132 insulin Homo sapiens 149-156 15516153-10 2004 They may include improvement of blood flow and microcirculation in skeletal muscles and, thereby, enhancement of insulin and glucose delivery to the insulin-sensitive tissues, facilitating insulin signalling at the cellular level and improvement of insulin secretion by the beta cells. Glucose 125-132 insulin Homo sapiens 149-156 15516153-10 2004 They may include improvement of blood flow and microcirculation in skeletal muscles and, thereby, enhancement of insulin and glucose delivery to the insulin-sensitive tissues, facilitating insulin signalling at the cellular level and improvement of insulin secretion by the beta cells. Glucose 125-132 insulin Homo sapiens 149-156 15516157-3 2004 Insulin detemir has a more predictable, protracted and consistent effect on blood glucose than neutral protamine Hagedorn (NPH) insulin, with less intrapatient variability in glycaemic control, compared with NPH insulin or insulin glargine. Glucose 82-89 insulin Homo sapiens 0-7 14766360-13 2004 While this is also true in skeletal muscle, because many muscles are often at rest, insulin mediated GLUT4 translocation represents a quantitatively more important mechanism regulating skeletal muscle glucose uptake than is the case in the heart. Glucose 201-208 insulin Homo sapiens 84-91 15198372-5 2004 However, it has now been shown to have a number of insulin-like glucose-independent effects. Glucose 64-71 insulin Homo sapiens 51-58 14711553-10 2004 Insulin sensitivity, expressed as the glucose-to-insulin ratio, was significantly improved under glucose load after 6 months of treatment. Glucose 38-45 insulin Homo sapiens 0-7 14711553-10 2004 Insulin sensitivity, expressed as the glucose-to-insulin ratio, was significantly improved under glucose load after 6 months of treatment. Glucose 97-104 insulin Homo sapiens 0-7 14711553-10 2004 Insulin sensitivity, expressed as the glucose-to-insulin ratio, was significantly improved under glucose load after 6 months of treatment. Glucose 97-104 insulin Homo sapiens 49-56 14711554-5 2004 MAIN OUTCOME MEASURE(S): Insulin-modified frequently sampled intravenous glucose tolerance testing and an acute 60-minute ACTH-(1-24) stimulation test. Glucose 73-80 insulin Homo sapiens 25-32 15761237-2 2004 IGF-I has been shown to bind to insulin receptors to stimulate glucose transport in fat and muscle, to inhibit hepatic glucose output and to lower blood glucose while simultaneously suppressing insulin secretion. Glucose 63-70 insulin Homo sapiens 32-39 14752836-5 2004 Although subjects were on average only moderately overweight, insulin sensitivity, measured both in the fasting state and in response to oral glucose, was lower. Glucose 142-149 insulin Homo sapiens 62-69 15539818-5 2004 GH therapy induced higher fasting and glucose-stimulated insulin levels after 1 and 6 years, but 6 months after GH stop, all levels returned to normal. Glucose 38-45 insulin Homo sapiens 57-64 15761237-2 2004 IGF-I has been shown to bind to insulin receptors to stimulate glucose transport in fat and muscle, to inhibit hepatic glucose output and to lower blood glucose while simultaneously suppressing insulin secretion. Glucose 119-126 insulin Homo sapiens 32-39 14715853-2 2004 This study of 363 patients, requiring intensive care for more than 7 d and randomly assigned to either conventional or intensive insulin therapy, examines the effects of intensive insulin therapy on glucose and lipid homeostasis and their respective impact on the improved outcome. Glucose 199-206 insulin Homo sapiens 180-187 15229371-1 2004 Diabetes mellitus is a heterogeneous group of diseases characterized by high blood glucose levels due to defects in insulin secretion, insulin action, or both. Glucose 83-90 insulin Homo sapiens 116-123 15229379-2 2004 As a result, the patient requires exogenous insulin to maintain normal blood glucose levels. Glucose 77-84 insulin Homo sapiens 44-51 15356380-5 2004 An oral glucose tolerance test (OGTT) showed hyperinsulinemia with a high basal level and a glucagon infusion test showed an abnormally high insulin level. Glucose 8-15 insulin Homo sapiens 50-57 14715857-4 2004 After treatment, the mean (+/-SE) area under the curve (AUC) during the oral glucose tolerance test of insulin (AUC(insulin)) decreased significantly more in the metformin group, compared with the placebo group [-3574 +/- 962 vs. +1367 +/- 1021 micro IU/min.ml (-26 +/- 7 vs. +10 +/- 7 nmol/min.liter), P = 0.003], but the AUC of DCI-IPG (AUC(DCI-IPG)) decreased similarly in both groups (-1452 +/- 968 vs. -2207 +/- 1021%/min, P = 0.60). Glucose 77-84 insulin Homo sapiens 116-123 12972442-6 2004 Insulin action was measured with an insulin sensitivity index (SI) from an intravenous glucose tolerance test. Glucose 87-94 insulin Homo sapiens 0-7 14715831-5 2004 Insulin sensitivity was measured by 40-min iv glucose tolerance test. Glucose 46-53 insulin Homo sapiens 0-7 14715836-5 2004 Insulin sensitivity was determined by the frequently sampled iv glucose tolerance test and minimal modeling. Glucose 64-71 insulin Homo sapiens 0-7 14715853-3 2004 Intensive insulin therapy effectively normalized blood glucose levels within 24 h, both in survivors and nonsurvivors. Glucose 55-62 insulin Homo sapiens 10-17 14715853-7 2004 In conclusion, our data suggest that intensive insulin therapy normalizes blood glucose levels through stimulation of peripheral glucose uptake and concomitantly partially restores the abnormalities in the serum lipid profile, which may have contributed significantly to the improved outcome of protracted critical illness. Glucose 80-87 insulin Homo sapiens 47-54 14715853-7 2004 In conclusion, our data suggest that intensive insulin therapy normalizes blood glucose levels through stimulation of peripheral glucose uptake and concomitantly partially restores the abnormalities in the serum lipid profile, which may have contributed significantly to the improved outcome of protracted critical illness. Glucose 129-136 insulin Homo sapiens 47-54 14715857-4 2004 After treatment, the mean (+/-SE) area under the curve (AUC) during the oral glucose tolerance test of insulin (AUC(insulin)) decreased significantly more in the metformin group, compared with the placebo group [-3574 +/- 962 vs. +1367 +/- 1021 micro IU/min.ml (-26 +/- 7 vs. +10 +/- 7 nmol/min.liter), P = 0.003], but the AUC of DCI-IPG (AUC(DCI-IPG)) decreased similarly in both groups (-1452 +/- 968 vs. -2207 +/- 1021%/min, P = 0.60). Glucose 77-84 insulin Homo sapiens 103-110 14681842-2 2004 This phase I/II clinical trial was the first to investigate the safety and effectiveness of a single oral dose of a modified human insulin in controlling postprandial plasma glucose levels in patients with type 1 diabetes mellitus who were receiving basal continuous subcutaneous insulin infusion (CSII) therapy. Glucose 174-181 insulin Homo sapiens 131-138 14726631-0 2004 Insulin-stimulated myocardial glucose uptake and the relation to perfusion and the nitric oxide system. Glucose 30-37 insulin Homo sapiens 0-7 14726631-2 2004 Insulin also enhances myocardial glucose uptake, but it is unknown whether vasodilation participates in the underlying mechanism. Glucose 33-40 insulin Homo sapiens 0-7 14726631-3 2004 We studied whether insulin-stimulated myocardial glucose uptake (MGU) is associated with perfusion changes and whether MGU is EDNO dependent. Glucose 49-56 insulin Homo sapiens 19-26 14681834-5 2004 Whole body insulin-mediated glucose disposal (6,6 (2)H(2)glucose), glucose oxidation (indirect calorimetry), lipolysis ((2)H(5) glycerol), and subcutaneous adipose lipolysis (microdialysis) were evaluated during a 3-step hyperinsulinemic euglycemic clamp. Glucose 28-35 insulin Homo sapiens 11-18 14722518-6 2004 CONCLUSIONS: Simple estimates of insulin sensitivity and pancreatic beta-cell function using fasting insulin and glucose levels serve as surrogate measures of insulin sensitivity and secretion in nondiabetic youths. Glucose 113-120 insulin Homo sapiens 33-40 14681845-9 2004 The insulinogenic index (AUC(i,insulin)/AUC(i,glucose)) was increased by approximately 40% by stevioside compared to control (P <.001). Glucose 46-53 insulin Homo sapiens 4-11 14728986-8 2004 No variant was associated with type 2 diabetes in Caucasian or African-American studies, but a single SNP in intron 3 (SNP 17) was associated with a reduced disposition index (insulin sensitivity x acute insulin response to glucose) in interaction with family membership in 126 members of 26 Caucasian families. Glucose 224-231 insulin Homo sapiens 176-183 14728986-8 2004 No variant was associated with type 2 diabetes in Caucasian or African-American studies, but a single SNP in intron 3 (SNP 17) was associated with a reduced disposition index (insulin sensitivity x acute insulin response to glucose) in interaction with family membership in 126 members of 26 Caucasian families. Glucose 224-231 insulin Homo sapiens 204-211 15601378-2 2004 Stem cells offer the potential for use as renewable sources of glucose-responsive, insulin-secreting cells. Glucose 63-70 insulin Homo sapiens 83-90 14992271-2 2004 They are therefore speculated to be part of the cerebral glucose sensing system and may also respond to insulin with alterations in their glucose uptake rate. Glucose 57-64 insulin Homo sapiens 104-111 14992271-2 2004 They are therefore speculated to be part of the cerebral glucose sensing system and may also respond to insulin with alterations in their glucose uptake rate. Glucose 138-145 insulin Homo sapiens 104-111 14992271-6 2004 Insulin-like growth factor (IGF-1) was at least 10 times more potent than insulin in stimulating the rate of ependymal 2-DG uptake, suggesting that IGF-1, rather than insulin, is the physiological agonist regulating glucose transport in ependymal cells. Glucose 216-223 insulin Homo sapiens 0-7 14642866-0 2004 Effect of insulin and contraction up on glucose transport in skeletal muscle. Glucose 40-47 insulin Homo sapiens 10-17 15099124-2 2004 The drug lowers postprandial glucose excursions by targeting early-phase insulin release, an effect thought to be important in reducing long-term cardiovascular complications of diabetes. Glucose 29-36 insulin Homo sapiens 73-80 15099124-26 2004 Repaglinide, a meglitinide analogue, is an oral insulin secretagogue that reduces postprandial glucose excursions by targeting postprandial insulin release. Glucose 95-102 insulin Homo sapiens 48-55 15046562-4 2004 A small but significant increase of insulin sensitivity (decrease in fasting insulin and blood glucose) was observed, but no changes in lipoprotein parameters were demonstrated. Glucose 95-102 insulin Homo sapiens 36-43 14642866-11 2004 Since during exercise the muscle may utilize insulin-independent mechanisms to increase glucose uptake, the mechanisms involved should provide important knowledge to the understanding and managing peripheral insulin resistance. Glucose 88-95 insulin Homo sapiens 45-52 14642866-11 2004 Since during exercise the muscle may utilize insulin-independent mechanisms to increase glucose uptake, the mechanisms involved should provide important knowledge to the understanding and managing peripheral insulin resistance. Glucose 88-95 insulin Homo sapiens 208-215 15231066-2 2004 In addition, we investigated the effect of insulin on ROS production induced by high glucose concentration. Glucose 85-92 insulin Homo sapiens 43-50 14749503-1 2004 The ability of insulin to stimulate glucose disposal varies more than six-fold in apparently healthy individuals. Glucose 36-43 insulin Homo sapiens 15-22 14749503-9 2004 Furthermore, the cluster of abnormalities associated with insulin resistance - namely, glucose intolerance, hyperinsulinemia, dyslipidemia, and elevated plasma C-reactive protein concentrations -- is limited to the subset of overweight/obese individuals that are also insulin resistant. Glucose 87-94 insulin Homo sapiens 58-65 15231066-5 2004 Intracellular ROS production in cells exposed to 3 h of high glucose concentration was increased significantly by the presence of a physiological concentration of insulin. Glucose 61-68 insulin Homo sapiens 163-170 15231066-6 2004 However, after a 1-h exposure to high glucose levels, ROS generation in cells incubated with insulin was only about 80% of that measured in cells incubated without insulin. Glucose 38-45 insulin Homo sapiens 93-100 15231066-6 2004 However, after a 1-h exposure to high glucose levels, ROS generation in cells incubated with insulin was only about 80% of that measured in cells incubated without insulin. Glucose 38-45 insulin Homo sapiens 164-171 15379056-7 2004 Both fulfilled diagnostic criteria, with high serum insulin levels in the presence of a blood glucose of less than 45 mg/dl. Glucose 94-101 insulin Homo sapiens 52-59 14987787-3 2004 Recent studies suggest that hyperglycaemia and insulin resistance are harmful and that correcting blood glucose to normal levels with insulin might improve the prognosis significantly. Glucose 104-111 insulin Homo sapiens 134-141 14987787-8 2004 This included the infusion of insulin based on a blood glucose level >215 mg/dl and the maintenance of the glucose level between 180 and 200 mg/dl. Glucose 55-62 insulin Homo sapiens 30-37 14987787-13 2004 The inadequacy of the insulin treatment is shown by the mean glucose values, which exceeded 200 mg/dl in 27% of the patients. Glucose 61-68 insulin Homo sapiens 22-29 15743105-4 2004 Hypoglycemia in type 1 diabetes indicates an imbalance between caloric supply and glucose use in response to insulin or exercise. Glucose 82-89 insulin Homo sapiens 109-116 14758385-7 2004 Although serum glucose and glycosylated hemoglobin decreased insulin levels were not changed. Glucose 15-22 insulin Homo sapiens 61-68 16026109-5 2004 Traditionally, insulin therapy has been considered the gold standard for management because of its efficacy in achieving tight glucose control and the fact that it does not cross the placenta. Glucose 127-134 insulin Homo sapiens 15-22 15743111-16 2004 Patients need to know how to adjust insulin to maintain glucose levels in the range of 70-120 mg/dL (3.9-6.7 mmol/L) before meals. Glucose 56-63 insulin Homo sapiens 36-43 16026109-13 2004 Both the insulin- and glyburide-treated women were able to achieve satisfactory glucose control and had similar perinatal outcomes. Glucose 80-87 insulin Homo sapiens 9-16 14660022-4 2003 The effects of harmane and pinoline were dose-dependent (EC(50): 5 and 25 microM, respectively) and these agents also blocked the inhibitory effects of the potassium channel agonist, diazoxide, on glucose-induced insulin release. Glucose 197-204 insulin Homo sapiens 213-220 14530283-2 2003 These genes continued to respond normally to insulin even though the adipocytes themselves were metabolically insulin-resistant, i.e. they displayed a significantly decreased rate of insulin-stimulated glucose uptake. Glucose 202-209 insulin Homo sapiens 45-52 14530283-2 2003 These genes continued to respond normally to insulin even though the adipocytes themselves were metabolically insulin-resistant, i.e. they displayed a significantly decreased rate of insulin-stimulated glucose uptake. Glucose 202-209 insulin Homo sapiens 110-117 14530283-2 2003 These genes continued to respond normally to insulin even though the adipocytes themselves were metabolically insulin-resistant, i.e. they displayed a significantly decreased rate of insulin-stimulated glucose uptake. Glucose 202-209 insulin Homo sapiens 110-117 14660022-5 2003 Stimulation of insulin secretion by harmane was glucose-dependent but, unlike the imidazoline I(3) receptor agonist efaroxan, it increased the rate of insulin release beyond that elicited by 20 mM glucose (20 mM glucose alone: 253+/-34% vs. basal; 20 mM glucose plus 100 microM harmane: 327+/-15%; P<0.01). Glucose 48-55 insulin Homo sapiens 15-22 14630949-1 2003 The GLUT4 gene is subject to complex tissue-specific and metabolic regulation, with a profound impact on insulin-mediated glucose disposal. Glucose 122-129 insulin Homo sapiens 105-112 14678869-2 2003 In patients with insulin resistance or type 2 diabetes mellitus, a set of metabolic insults--namely high plasma levels of glucose and free fatty acids, increased inflammation, dyslipidemia, and hypertension--cause endothelial dysfunction and a transition from an antiatherogenic endothelium to a proatherogenic endothelium. Glucose 122-129 insulin Homo sapiens 17-24 12954593-5 2003 FH+ subjects were more insulin resistant, as seen from a higher HOMA-IR index (P = 0.006) and a lower rate of insulin-stimulated glucose uptake (P = 0.001) and had more features of the metabolic syndrome (P = 0.02, P = 0.0002) compared with FH- subjects. Glucose 129-136 insulin Homo sapiens 110-117 14704873-3 2003 The relationship between abnormal circulating glucose levels and the development of long-term diabetic complications became apparent 70 years ago, soon after the introduction of insulin and the prevention of early death due to ketoacidosis. Glucose 46-53 insulin Homo sapiens 178-185 12933352-5 2003 T1DM and T2DM patients showed reduced insulin-stimulated glucose metabolic clearance rate (MCR: 5.1 +/- 0.6 and 3.2 +/- 0.8 ml x kg(-1) min(-1)) similar to OFF (5.3 +/- 0.4 ml x kg(-1) x min(-1)) compared with NOR (8.5 +/- 0.5 ml x kg(-1) min(-1), P < 0.001). Glucose 57-64 insulin Homo sapiens 38-45 12954593-7 2003 Relatives of diabetic probands with a high WHR had reduced insulin-mediated glucose uptake compared with relatives of probands with a low WHR (P = 0.04). Glucose 76-83 insulin Homo sapiens 59-66 14641015-2 2003 Insulin resistance is characterized by a decrease in the insulin effect on glucose transport in muscle and adipose tissue. Glucose 75-82 insulin Homo sapiens 0-7 14615391-0 2003 Insulin stimulates glucose transport via nitric oxide/cyclic GMP pathway in human vascular smooth muscle cells. Glucose 19-26 insulin Homo sapiens 0-7 14615391-2 2003 The aim of the present study was to determine whether in these cells the insulin-stimulated NO/cyclic GMP pathway plays a role in the regulation of glucose uptake. Glucose 148-155 insulin Homo sapiens 73-80 14615391-4 2003 Insulin-stimulated glucose transport and GLUT4 recruitment were blocked by an inhibitor of NO synthesis and mimicked by NO-releasing drugs. Glucose 19-26 insulin Homo sapiens 0-7 14615391-5 2003 Insulin- and NO-elicited glucose uptake were blocked by inhibitors of soluble guanylate cyclase and cyclic GMP-dependent protein kinase; furthermore, glucose transport was stimulated by an analog of cyclic GMP. Glucose 25-32 insulin Homo sapiens 0-7 14615391-5 2003 Insulin- and NO-elicited glucose uptake were blocked by inhibitors of soluble guanylate cyclase and cyclic GMP-dependent protein kinase; furthermore, glucose transport was stimulated by an analog of cyclic GMP. Glucose 150-157 insulin Homo sapiens 0-7 14615391-6 2003 CONCLUSIONS: Our results suggest that insulin-elicited glucose transport (and the corresponding GLUT4 recruitment into the plasma membrane) in human vascular smooth muscle cells is mediated by an increased synthesis of NO, which stimulates the production of cyclic GMP and the subsequent activation of a cyclic GMP-dependent protein kinase. Glucose 55-62 insulin Homo sapiens 38-45 14641007-5 2003 These include stimulation of hepatic glucose output by fatty acids, potentiation of glucose-stimulated insulin secretion by fatty acids, and the cellular mechanism whereby high glucose and insulin concentrations inhibit fatty acid oxidation via malonyl-CoA regulation of carnitine palmitoyltransferase-1. Glucose 84-91 insulin Homo sapiens 103-110 14641007-5 2003 These include stimulation of hepatic glucose output by fatty acids, potentiation of glucose-stimulated insulin secretion by fatty acids, and the cellular mechanism whereby high glucose and insulin concentrations inhibit fatty acid oxidation via malonyl-CoA regulation of carnitine palmitoyltransferase-1. Glucose 84-91 insulin Homo sapiens 189-196 14728986-1 2004 Impaired glucose stimulated insulin secretion is a prominent, early defect in type 2 diabetes. Glucose 9-16 insulin Homo sapiens 28-35 14568435-1 2003 The purpose of this study is to ascertain the applicable possibility of H(2)O(2) degradable hydrogel for fabrication of insulin release system synchronized with the change in the glucose concentration in the medium. Glucose 179-186 insulin Homo sapiens 120-127 14641015-2 2003 Insulin resistance is characterized by a decrease in the insulin effect on glucose transport in muscle and adipose tissue. Glucose 75-82 insulin Homo sapiens 57-64 14641015-3 2003 Tyrosine phosphorylation of IRS-1 (insulin receptor substrate 1) and its binding to PI 3-kinase (phosphoinositide 3-kinase) are critical events in the insulin signalling cascade leading to insulin-stimulated glucose transport. Glucose 208-215 insulin Homo sapiens 35-42 14641015-3 2003 Tyrosine phosphorylation of IRS-1 (insulin receptor substrate 1) and its binding to PI 3-kinase (phosphoinositide 3-kinase) are critical events in the insulin signalling cascade leading to insulin-stimulated glucose transport. Glucose 208-215 insulin Homo sapiens 151-158 14641015-5 2003 Elevated plasma fatty acid concentrations are associated with reduced insulin-stimulated glucose transport activity as a consequence of altered insulin signalling through PI 3-kinase. Glucose 89-96 insulin Homo sapiens 70-77 14683460-4 2003 Inhibition of PI3K activity results in a blockade of insulin signaling including glucose uptake and glyocogen synthesis. Glucose 81-88 insulin Homo sapiens 53-60 14613756-5 2003 The mean glucose infusion rate during insulin treatment was 20.3+/-1.7 g/kg/day; lipid was 4.6+/-1.1 g/kg/day and non-protein caloric intake 121.7+/-16.5 kcal/kg/day. Glucose 9-16 insulin Homo sapiens 38-45 14613756-9 2003 In conclusion, continuous insulin infusion can rapidly and safely improve intravenous glucose tolerance, allowing higher caloric intake and growth in very-low-birth-weight infants who develop hyperglycaemia during total parenteral nutrition. Glucose 86-93 insulin Homo sapiens 26-33 14633821-0 2003 Diagnosing insulin resistance by simple quantitative methods in subjects with normal glucose metabolism. Glucose 85-92 insulin Homo sapiens 11-18 14633819-4 2003 RESEARCH DESIGN AND METHODS: Insulin was infused (2 IU/h) in 5% dextrose (100 ml/h) and KCl (8 mmol/h) into 10 fasting, obese, nondiabetic subjects for 4 h. Subjects were also infused with 5% dextrose without insulin and with saline on two separate occasions. Glucose 64-72 insulin Homo sapiens 29-36 14633819-4 2003 RESEARCH DESIGN AND METHODS: Insulin was infused (2 IU/h) in 5% dextrose (100 ml/h) and KCl (8 mmol/h) into 10 fasting, obese, nondiabetic subjects for 4 h. Subjects were also infused with 5% dextrose without insulin and with saline on two separate occasions. Glucose 192-200 insulin Homo sapiens 29-36 14707885-8 2003 Understanding how osmotic stress induces glucose transport or mediates insulin resistance may provide novel targets for strategies to enhance glucose transport or to prevent insulin resistance. Glucose 142-149 insulin Homo sapiens 71-78 14640991-7 2003 This resulted in a non-significant decrease in insulin-stimulated glucose uptakes (16.61+/-8.03 vs 12.74+/-5.50 micromol/kg per min (s.d. Glucose 66-73 insulin Homo sapiens 47-54 14640991-9 2003 The rates of insulin-stimulated glucose uptake correlated negatively with the FFA concentrations (r=-0.638, P<0.0001). Glucose 32-39 insulin Homo sapiens 13-20 14640991-10 2003 However, acipimox caused a significant improvement in insulin-stimulated glucose uptake in the GH-treated patients (17.35+/-5.65 vs 12.74+/-5.50 micromol/kg per min, P=0.012 for C vs B). Glucose 73-80 insulin Homo sapiens 54-61 14714271-14 2003 CONCLUSION: Early insulin signaling cascade, essential for normal glucose metabolism, is not affected by therapeutic doses of saquinavir. Glucose 66-73 insulin Homo sapiens 18-25 14656059-1 2003 Models describing plasma glucose and insulin concentration of an intravenous glucose tolerance test (IVGTT) allow a noninvasive cost-effective approach to estimate important indexes characterizing the efficiency of glucose-insulin control system, i.e., glucose effectiveness (S(G)) and insulin sensitivity (S(I)). Glucose 25-32 insulin Homo sapiens 223-230 14656059-1 2003 Models describing plasma glucose and insulin concentration of an intravenous glucose tolerance test (IVGTT) allow a noninvasive cost-effective approach to estimate important indexes characterizing the efficiency of glucose-insulin control system, i.e., glucose effectiveness (S(G)) and insulin sensitivity (S(I)). Glucose 77-84 insulin Homo sapiens 37-44 14656059-1 2003 Models describing plasma glucose and insulin concentration of an intravenous glucose tolerance test (IVGTT) allow a noninvasive cost-effective approach to estimate important indexes characterizing the efficiency of glucose-insulin control system, i.e., glucose effectiveness (S(G)) and insulin sensitivity (S(I)). Glucose 77-84 insulin Homo sapiens 223-230 15244200-6 2003 INSULIN RESISTANCE: Fasting insulin value (microU/mL) x Fasting blood glucose value (mmol/L)/22.5 Liver echogenity was measured by a 3.75 mHz ultrasound probe and was graded by comparison with renal cortical paranchymal echogenity in both groups. Glucose 70-77 insulin Homo sapiens 0-7 14640991-11 2003 The acipimox-induced enhancement of insulin-stimulated glucose uptake was mainly due to an enhanced rate of glucose oxidation (8.32+/-3.00 vs 5.88+/-2.39 micromol/kg per min, P=0.07 for C vs B). Glucose 55-62 insulin Homo sapiens 36-43 14640991-11 2003 The acipimox-induced enhancement of insulin-stimulated glucose uptake was mainly due to an enhanced rate of glucose oxidation (8.32+/-3.00 vs 5.88+/-2.39 micromol/kg per min, P=0.07 for C vs B). Glucose 108-115 insulin Homo sapiens 36-43 14640992-1 2003 AIM AND METHOD: Insulin resistance leading, in some cases, to glucose intolerance is an important contributory factor to the cardiovascular morbidity and mortality associated with acromegaly. Glucose 62-69 insulin Homo sapiens 16-23 14671204-2 2003 We investigated the effect of dexamethasone on insulin-stimulated glucose disposal and vasodilation in healthy males to test the hypothesis that a reduction in glucose disposal would be accompanied by a reduction in insulin action in the vasculature. Glucose 66-73 insulin Homo sapiens 47-54 14612956-6 2003 Insulin concentrations were measured by radio-immunoassay, and the ratio between the insulin responses to high and low glucose was calculated (insulin stimulation index, ISI). Glucose 119-126 insulin Homo sapiens 85-92 14612956-6 2003 Insulin concentrations were measured by radio-immunoassay, and the ratio between the insulin responses to high and low glucose was calculated (insulin stimulation index, ISI). Glucose 119-126 insulin Homo sapiens 143-150 14704736-5 2003 Using (13)C/(31)P magnetic resonance spectroscopy (MRS), we demonstrate that a defect in insulin-stimulated muscle glucose transport activity is the rate-controlling defect. Glucose 115-122 insulin Homo sapiens 89-96 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 167-174 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 167-174 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 167-174 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 346-353 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 346-353 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 346-353 insulin Homo sapiens 141-148 14704736-7 2003 Furthermore, we have recently proposed that this defect in insulin-stimulated muscle glucose transport activity may be due to the activation of a serine kinase cascade involving protein kinase C theta and IKK-beta, which are key downstream mediators of tissue inflammation. Glucose 85-92 insulin Homo sapiens 59-66 14671192-4 2003 A significantly higher insulin area under the curve during oral glucose tolerance testing (P < 0.0001) and lower insulin sensitivity during hyperinsulinemic-euglycemic clamps (P = 0.04) were found in Asian Indians with PC-1 121Q variant compared with Asian Indians with wild-type PC-1 and with Caucasians with or without the polymorphism. Glucose 64-71 insulin Homo sapiens 23-30 14679178-1 2003 Failure to secrete adequate amounts of insulin in response to increasing concentrations of glucose is an important feature of type 2 diabetes. Glucose 91-98 insulin Homo sapiens 39-46 14679173-2 2003 Hyperglycemia itself causes further decreases in glucose-stimulated insulin secretion. Glucose 49-56 insulin Homo sapiens 68-75 14679178-3 2003 Uncoupling protein 2 (UCP2), by virtue of its mitochondrial proton leak activity and consequent negative effect on ATP production, impairs glucose-stimulated insulin secretion. Glucose 139-146 insulin Homo sapiens 158-165 14679178-6 2003 This study demonstrates that endogenously produced mitochondrial superoxide activates UCP2-mediated proton leak, thus lowering ATP levels and impairing glucose-stimulated insulin secretion. Glucose 152-159 insulin Homo sapiens 171-178 14728104-4 2003 RESULTS: Fasting serum glucose and fasting serum insulin increased significantly in the olanzapine-treated patients (p =.008 for glucose and p =.006 for insulin). Glucose 129-136 insulin Homo sapiens 49-56 14728104-8 2003 CONCLUSION: This study indicates that the disturbances in glucose homeostasis during antipsychotic treatment with olanzapine are mainly due to insulin resistance. Glucose 58-65 insulin Homo sapiens 143-150 14728104-4 2003 RESULTS: Fasting serum glucose and fasting serum insulin increased significantly in the olanzapine-treated patients (p =.008 for glucose and p =.006 for insulin). Glucose 23-30 insulin Homo sapiens 153-160 12951360-6 2003 Men with HVFA showed higher TG, glucose, and insulin responses following fat and oral glucose tolerance tests respectively higher plasma concentrations of MDA (P < 0.001), urinary PGF2alpha (P < 0.05), and lymphocytes deoxyribonucleic acid tail moments (P < 0.01). Glucose 86-93 insulin Homo sapiens 45-52 14657818-9 2003 CONCLUSION: Insulin glargine therapy can reduce hypoglycemic episodes in children and adolescents with suboptimal glucose control without jeopardizing glycemic control. Glucose 114-121 insulin Homo sapiens 12-19 14603493-6 2003 Insulin absorption was estimated from the change in plasma glucose level. Glucose 59-66 insulin Homo sapiens 0-7 14603493-7 2003 The blood glucose level after administration of the insulin powder without citric acid prepared by the SCF process (MI SCF) decreased rapidly, and a significant difference was observed for areas under the curve of change in plasma glucose concentration versus time (AUCs) between MI SCF and the insulin powder without citric acid prepared by the SD process (MI SD). Glucose 10-17 insulin Homo sapiens 52-59 14603493-7 2003 The blood glucose level after administration of the insulin powder without citric acid prepared by the SCF process (MI SCF) decreased rapidly, and a significant difference was observed for areas under the curve of change in plasma glucose concentration versus time (AUCs) between MI SCF and the insulin powder without citric acid prepared by the SD process (MI SD). Glucose 231-238 insulin Homo sapiens 52-59 14974818-11 2003 (3) Serial concentrations of insulin significantly counteracted the inhibitory effects of glucose on the yields of DHT (n = 6; P < 0.01). Glucose 90-97 insulin Homo sapiens 29-36 14974818-12 2003 (4) The independent inhibitory effects of nicotine and glucose on metabolic yields of DHT were marginally more pronounced in combination but significantly overcome in the presence of insulin. Glucose 55-62 insulin Homo sapiens 183-190 14974818-13 2003 CONCLUSION: Human gingival fibroblasts obtained from chronically inflamed tissue of nondiabetic patients demonstrated that the inhibitory effects of glucose and nicotine on androgen metabolism can be overcome by insulin, in varying degrees. Glucose 149-156 insulin Homo sapiens 212-219 14688680-3 2003 The purpose of this study was to elucidate potential mechanisms underlying the hyperoxic-induced hyperglycemia by examining glucagon, insulin, and epinephrine, which are important in glucose regulation and skeletal and cardiac glucose transporters (GLUT1 and GLUT4), which facilitate glucose entry. Glucose 183-190 insulin Homo sapiens 134-141 14669159-9 2003 Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). Glucose 151-158 insulin Homo sapiens 11-18 14669159-9 2003 Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). Glucose 151-158 insulin Homo sapiens 23-32 14669159-9 2003 Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). Glucose 151-158 insulin Homo sapiens 113-120 14669159-9 2003 Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). Glucose 151-158 insulin Homo sapiens 125-134 14669159-9 2003 Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). Glucose 151-158 insulin Homo sapiens 113-120 14669159-9 2003 Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). Glucose 151-158 insulin Homo sapiens 125-134 18370651-4 2003 Insulin resistance was assessed by fasting glucose/insulin ratio and IMT by the Doppler system with electrical linear transducer midfrequency of 12 MHz. Glucose 43-50 insulin Homo sapiens 0-7 18370651-5 2003 Women with PCOS had higher fasting insulin levels (36.58 +/- 17.81 muU/mL, vs. 16.60 +/- 3.22 muU/mL in controls; p < 0.001), higher insulin resistance (glucose/insulin ratio 2.81 +/- 1.47 vs. 5.47 +/- 1.46 in controls; p < 0.001), and greater IMT (0.53 +/- 0.14 mm vs. 0.39 +/- 0.06 mm in controls; p < 0.001). Glucose 156-163 insulin Homo sapiens 35-42 14694214-4 2003 RESULTS: The obese patients were insulin resistant (whole-body glucose use = 19.7 +/- 1.5 vs. 51.5 +/- 2.4 micromol/min per kilogram fat-free mass, p < 0.0001) and hyperinsulinemic in the fasting state (332 +/- 86 vs. 85 +/- 5 pM, p < 0.0001) and during the oral glucose tolerance test compared with the lean subjects. Glucose 63-70 insulin Homo sapiens 33-40 14694214-7 2003 Insulin-induced glucose oxidation and nonoxidative glucose disposal were lower in the obese compared with the lean group (all p < 0.05). Glucose 16-23 insulin Homo sapiens 0-7 14733163-4 2003 The use of exogenous insulin to maintain blood glucose at a level no higher than 110 mg per deciliter, known as intensive insulin therapy, has reduced morbidity and mortality among critically ill patients. Glucose 47-54 insulin Homo sapiens 21-28 14733163-4 2003 The use of exogenous insulin to maintain blood glucose at a level no higher than 110 mg per deciliter, known as intensive insulin therapy, has reduced morbidity and mortality among critically ill patients. Glucose 47-54 insulin Homo sapiens 122-129 19087394-1 2003 Insulin resistance leads to the inability of insulin to control the utilization and storage of glucose. Glucose 95-102 insulin Homo sapiens 0-7 14651545-11 2003 (2) Insulin resistance based on fasting plasma insulin concentrations was seen in significantly more children with AN than in children without AN, even in age and percentage obesity-matched subjects with normal glucose tolerance during OGTT. Glucose 211-218 insulin Homo sapiens 4-11 16437014-3 2003 In the future, patients with type 1 diabetes will receive insulin in optimal quantities (because of more information about blood glucose values) at optimal times (because of better integration of blood glucose values with appropriate insulin dosages) by way of optimal routes into the body (because of needle-free routes of administration) in order to achieve optimal blood glucose control. Glucose 129-136 insulin Homo sapiens 58-65 12970360-0 2003 Human glycated albumin affects glucose metabolism in L6 skeletal muscle cells by impairing insulin-induced insulin receptor substrate (IRS) signaling through a protein kinase C alpha-mediated mechanism. Glucose 31-38 insulin Homo sapiens 91-98 12970360-0 2003 Human glycated albumin affects glucose metabolism in L6 skeletal muscle cells by impairing insulin-induced insulin receptor substrate (IRS) signaling through a protein kinase C alpha-mediated mechanism. Glucose 31-38 insulin Homo sapiens 107-114 12970360-4 2003 Exposure of these cells to HGA inhibited insulin-stimulated glucose uptake and glycogen synthase activity by 95 and 80%, respectively. Glucose 60-67 insulin Homo sapiens 41-48 12970360-13 2003 Simultaneously, BDM rescued insulin-stimulation of glucose uptake and glycogen synthase activity in cells exposed to HGA. Glucose 51-58 insulin Homo sapiens 28-35 12970360-15 2003 In summary, in L6 skeletal muscle cells, exposure to HGA leads to insulin resistance selectively in glucose metabolism with no effect on growth-related pathways regulated by the hormone. Glucose 100-107 insulin Homo sapiens 66-73 14504291-4 2003 These cells have a 50% decrease in PI 3-kinase activity and a 30% decrease in Akt activity, leading to decreased insulin-induced glucose uptake and anti-apoptosis. Glucose 129-136 insulin Homo sapiens 113-120 14703429-9 2003 CONCLUSION: Obese patients with different glucose tolerance have similar degrees of insulin resistance. Glucose 42-49 insulin Homo sapiens 84-91 14743578-2 2003 Defects in the action and/or secretion of insulin are the two major abnormalities leading to development of glucose intolerance. Glucose 108-115 insulin Homo sapiens 42-49 14557006-9 2003 In women with GDM, the use of insulin lispro enabled the attainment of near-normal glucose levels at the 1h post-prandial time point and was associated with normal anthropometric characteristics; the use of regular insulin was not able to blunt the 1h peak post-prandial response to a near-normal extent and resulted in infants with a tendency toward the disproportionate growth. Glucose 83-90 insulin Homo sapiens 30-37 14623617-7 2003 MEASUREMENTS: Body mass index; fasting glucose, insulin, lipid and lipoprotein concentrations; and insulin-mediated glucose disposal as quantified by the steady-state plasma glucose concentration during the insulin suppression test. Glucose 116-123 insulin Homo sapiens 99-106 14623617-7 2003 MEASUREMENTS: Body mass index; fasting glucose, insulin, lipid and lipoprotein concentrations; and insulin-mediated glucose disposal as quantified by the steady-state plasma glucose concentration during the insulin suppression test. Glucose 116-123 insulin Homo sapiens 99-106 14623617-7 2003 MEASUREMENTS: Body mass index; fasting glucose, insulin, lipid and lipoprotein concentrations; and insulin-mediated glucose disposal as quantified by the steady-state plasma glucose concentration during the insulin suppression test. Glucose 116-123 insulin Homo sapiens 99-106 14623617-7 2003 MEASUREMENTS: Body mass index; fasting glucose, insulin, lipid and lipoprotein concentrations; and insulin-mediated glucose disposal as quantified by the steady-state plasma glucose concentration during the insulin suppression test. Glucose 116-123 insulin Homo sapiens 99-106 14623617-8 2003 Overweight was defined as body mass index of 25 kg/m2 or greater, and insulin resistance was defined as being in the top tertile of steady-state plasma glucose concentrations. Glucose 152-159 insulin Homo sapiens 70-77 12952969-7 2003 Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. Glucose 60-67 insulin Homo sapiens 41-48 12941947-1 2003 Glucose-dependent exocytosis of insulin requires activation of protein kinase C (PKC). Glucose 0-7 insulin Homo sapiens 32-39 12941947-13 2003 These results suggest that association of PKC-epsilon with insulin granule membranes represents an important component of the secretory network because it is essential for insulin exocytosis in response to glucose. Glucose 206-213 insulin Homo sapiens 59-66 15058753-4 2003 After glucose loading, insulin levels increased significantly at 30, 60, 90, and 120 minutes after the patients took nateglinide, along with insulinogenic indices, the total area under the insulin curve, the area under the 0- to 90-minute insulin curve, and the area under the 90- to 180-minute insulin curve. Glucose 6-13 insulin Homo sapiens 23-30 14559391-7 2003 For P(MAA-co-MEG) hydrogels, the biological activity of insulin decreased when the pendent glucose content increased. Glucose 91-98 insulin Homo sapiens 56-63 14631475-1 2003 BACKGROUND: The use of an insulin infusion following myocardial infarction, and its consequent lowering of glucose, significantly improves mortality. Glucose 107-114 insulin Homo sapiens 26-33 14634486-1 2003 BACKGROUND: Rodent studies have highlighted the possibility that alcohol may promote a significant decrease in the level of glucose-stimulated plasma insulin concentration. Glucose 124-131 insulin Homo sapiens 150-157 14679068-0 2003 Glucose-responsive expression of the human insulin promoter in HepG2 human hepatoma cells. Glucose 0-7 insulin Homo sapiens 43-50 14679068-4 2003 Our results suggest that the human insulin promoter represents a strong candidate as a robust, glucose-responsive promoter for regulated hepatic insulin production. Glucose 95-102 insulin Homo sapiens 35-42 16119083-6 2003 After therapy we observed decrease of insulin responses during oral glucose tolerance test, (p<0.05). Glucose 68-75 insulin Homo sapiens 38-45 14702004-5 2003 Insulin dysregulation may contribute to AD pathology through several mechanisms including decreased cortical glucose utilization particularly in the hippocampus and entorhinal cortex; increased oxidative stress through the formation of advanced glycation end-products; increased Tau phosphorylation and neurofibrillary tangle formation; increased b-amyloid aggregation through inhibition of insulin-degrading enzyme. Glucose 109-116 insulin Homo sapiens 0-7 14640466-5 2003 RESULTS: There was a strong correlation between maximal oxygen uptake and insulin-stimulated glucose uptake (r = 0.7, p = 0.001), and maximal oxygen uptake was the only factor of importance for determining insulin sensitivity in a model, which also included the presence of diabetes and ischemic heart disease. Glucose 93-100 insulin Homo sapiens 74-81 14530861-0 2003 The FOXC2 -512C>T variant is associated with hypertriglyceridaemia and increased serum C-peptide in Danish Caucasian glucose-tolerant subjects. Glucose 120-127 insulin Homo sapiens 90-99 14978454-8 2003 The further study of the effects of medications on glucose metabolism and their mechanisms, therefore, is essential to developing better treatment regimens that minimize insulin resistance and avoid associated health risks such as obesity and diabetes. Glucose 51-58 insulin Homo sapiens 170-177 14530861-5 2003 Among the glucose-tolerant subjects, the T-allele carriers had higher fasting serum triglyceride ( p=0.03), fasting serum C-peptide concentrations ( p=0.009) and insulinogenic index ( p=0.04). Glucose 10-17 insulin Homo sapiens 122-131 14530861-8 2003 However, among glucose-tolerant subjects the variant is associated with hypertriglyceridaemia and increased fasting serum C-peptide. Glucose 15-22 insulin Homo sapiens 122-131 14585085-3 2003 glucose between healthy subjects and type 2 diabetic (T2DM) subjects, in whom the early insulin response to i.v. Glucose 0-7 insulin Homo sapiens 88-95 14576983-1 2003 AIMS/HYPOTHESIS: Whole body insulin resistance results largely from impaired insulin-stimulated glucose disposal into skeletal muscle. Glucose 96-103 insulin Homo sapiens 28-35 14576983-1 2003 AIMS/HYPOTHESIS: Whole body insulin resistance results largely from impaired insulin-stimulated glucose disposal into skeletal muscle. Glucose 96-103 insulin Homo sapiens 77-84 14576983-6 2003 Multiple regression analyses indicated that whole body insulin-mediated glucose disposal rates of the subjects, independent of age, sex, and percent body fat, were negatively correlated with mRNA concentrations of an EST (DD23; r=-0.38, p=0.007), ATP1A2 (r=-0.27, p=0.05), MAP2K4 (r=-0.34, p=0.02), and PRPSAP1 (r=-0.37, p=0.008). Glucose 72-79 insulin Homo sapiens 55-62 14617224-7 2003 All factors exhibited good values for construct reliability and variance extracted except for the insulin resistance factor, which was measured with the variables of fasting insulin and fasting glucose levels. Glucose 194-201 insulin Homo sapiens 98-105 14617224-9 2003 Insulin resistance was not well defined using the variables of fasting insulin and fasting glucose levels. Glucose 91-98 insulin Homo sapiens 0-7 14625173-3 2003 The dose of insulin was adjusted according to blood glucose level of the patients after the operation. Glucose 52-59 insulin Homo sapiens 12-19 14696503-8 2003 One patient with diabetes in the oral glucose tolerance test had a preexisting type II diabetes requiring insulin therapy since the onset of acute pancreatitis. Glucose 38-45 insulin Homo sapiens 106-113 14602787-4 2003 Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P < 0.05) than in OLD, YOUNG, and TRAINED. Glucose 30-37 insulin Homo sapiens 11-18 14723485-8 2003 Mean fasting and post-glucose load insulin levels (microU/ml) were 2.78 +/- 2.23 and 3.28 +/- 2.04 in Group 1, 1.67 +/- 1.20 and 2.60 +/- 2.32 in Group 2 and 3.37 +/- 2.08 and 4.40 +/- 3.05 in Group 3 and fasting C-peptide levels (microg/ml) were 0.296 +/- 0.22, 0.208 +/- 0.09 and 0.327 +/- 0.23 respectively. Glucose 22-29 insulin Homo sapiens 35-42 14723485-10 2003 A significant inverse quadratic correlation (U-shaped curve) of body weight with insulin (fasting and post-glucose) and C-peptide levels was observed (P < 0.05). Glucose 107-114 insulin Homo sapiens 81-88 14723485-11 2003 INTERPRETATION & CONCLUSION: Both low and high birth weight term neonates have high fasting and post-glucose insulin levels. Glucose 105-112 insulin Homo sapiens 113-120 14741039-3 2003 Glucose uptake by way of 2-deoxyglucose and GLUT-1 and GLUT-4 transporter protein content was measured in basal and insulin-stimulated myooids that were engineered from soleus muscles of female Sprague-Dawley rats. Glucose 0-7 insulin Homo sapiens 116-123 14626260-2 2003 Some trials show that in patients with type 1 diabetes mellitus, insulin glargine offers an advantage in blood glucose control compared with NPH insulin. Glucose 111-118 insulin Homo sapiens 65-72 14708365-0 2003 [The use of insulin-modified intravenous glucose tolerance test in the diagnosis of insulin resistance in patients with metabolic syndrome]. Glucose 41-48 insulin Homo sapiens 12-19 14708365-0 2003 [The use of insulin-modified intravenous glucose tolerance test in the diagnosis of insulin resistance in patients with metabolic syndrome]. Glucose 41-48 insulin Homo sapiens 84-91 14635635-0 2003 Assessment of insulin sensitivity and secretion indices from oral glucose tolerance testing in subjects with fasting euglycemia but impaired 2-hour plasma glucose. Glucose 66-73 insulin Homo sapiens 14-21 14635635-0 2003 Assessment of insulin sensitivity and secretion indices from oral glucose tolerance testing in subjects with fasting euglycemia but impaired 2-hour plasma glucose. Glucose 155-162 insulin Homo sapiens 14-21 14561494-9 2003 The Pi-3 kinase is the intracellular insulin signal linking the glucose homeostasis to the K(ATP) channel. Glucose 64-71 insulin Homo sapiens 37-44 14607060-7 2003 The use of medications that impair glucose tolerance, for example, corticosteroids, may have a synergistic effect in aggravating insulin resistance. Glucose 35-42 insulin Homo sapiens 129-136 14627749-4 2003 RESULTS: Relationships between insulin-stimulated glucose disposal and regional body fat depots appeared more appropriately described by nonlinear than linear models. Glucose 50-57 insulin Homo sapiens 31-38 14627749-5 2003 When the group was subdivided using median total body fat as the cut-point, insulin-stimulated glucose disposal correlated negatively to all regional body fat measures (all p < or = 0.004), serum triglycerides and free fatty acids (p < 0.02), and both soleus intramyocellular lipid (p = 0.003) and vastus lateralis triglyceride (p = 0.04) in the normal/less overweight group. Glucose 95-102 insulin Homo sapiens 76-83 14627749-6 2003 In contrast, only visceral abdominal fat showed significant negative correlation with insulin-stimulated glucose disposal in more overweight men (r = -0.576, p = 0.01), some of whom surprisingly had lower than expected myocyte lipid levels. Glucose 105-112 insulin Homo sapiens 86-93 14604750-3 2003 Multiple insulin secretory defects are present, including loss of basal pulsatility, lack of early phase of insulin secretion after intravenous glucose administration, decreased basal and stimulated plasma insulin concentrations, excess in prohormone secretion, and progressive decrease in insulin secretory capacity with time. Glucose 144-151 insulin Homo sapiens 9-16 14604750-6 2003 For the same plasma insulin levels, peripheral glucose uptake and hepatic glucose production suppressibility are lower in diabetic patients than in controls. Glucose 47-54 insulin Homo sapiens 20-27 14604750-6 2003 For the same plasma insulin levels, peripheral glucose uptake and hepatic glucose production suppressibility are lower in diabetic patients than in controls. Glucose 74-81 insulin Homo sapiens 20-27 14604750-9 2003 In subjects with normal beta-cell function, increase in insulin needs secondary to insulin resistance is compensated by an increase in insulin secretion adjusted to maintain plasma glucose levels to normal. Glucose 181-188 insulin Homo sapiens 56-63 14580758-3 2003 First, there is the evidence that resistance to insulin-stimulated glucose metabolism is not a primary event in obesity, but is secondary to lipid accumulation resulting from full responsiveness to insulin-stimulated lipogenic activity. Glucose 67-74 insulin Homo sapiens 48-55 14580758-4 2003 Second, resistance to insulin-stimulated glucose metabolism, now considered detrimental to health, might be a protective mechanism that reduces lipid-induced damage to tissue by excluding glucose from cells, thus decreasing glucose-derived lipogenesis. Glucose 41-48 insulin Homo sapiens 22-29 14580758-4 2003 Second, resistance to insulin-stimulated glucose metabolism, now considered detrimental to health, might be a protective mechanism that reduces lipid-induced damage to tissue by excluding glucose from cells, thus decreasing glucose-derived lipogenesis. Glucose 188-195 insulin Homo sapiens 22-29 14580758-4 2003 Second, resistance to insulin-stimulated glucose metabolism, now considered detrimental to health, might be a protective mechanism that reduces lipid-induced damage to tissue by excluding glucose from cells, thus decreasing glucose-derived lipogenesis. Glucose 188-195 insulin Homo sapiens 22-29 14617354-1 2003 Although the effects of insulin on glucose and lipid metabolism are well documented, gaps remain in our understanding of the precise molecular mechanisms of signal transduction. Glucose 35-42 insulin Homo sapiens 24-31 14728854-9 2003 CONCLUSION: It is necessary to monitor and control the blood glucose level by low dose constant insulin during labor in pregnant women with abnormal glucose metabolism. Glucose 61-68 insulin Homo sapiens 96-103 14515346-5 2003 This experimental evidence supports the proposal that brain glycogen may be involved in the development of diabetes complications, specifically impaired glucose sensing (hypoglycemia unawareness) observed clinically in some diabetes patients under insulin treatment. Glucose 153-160 insulin Homo sapiens 248-255 14708365-2 2003 The peroral glucose-tolerance and insulin-modified intravenous glucose-tolerance tests were used in the diagnosis of insulin-resistance. Glucose 63-70 insulin Homo sapiens 34-41 12928442-0 2003 Glucose-induced translational control of proinsulin biosynthesis is proportional to preproinsulin mRNA levels in islet beta-cells but not regulated via a positive feedback of secreted insulin. Glucose 0-7 insulin Homo sapiens 41-51 12928442-0 2003 Glucose-induced translational control of proinsulin biosynthesis is proportional to preproinsulin mRNA levels in islet beta-cells but not regulated via a positive feedback of secreted insulin. Glucose 0-7 insulin Homo sapiens 84-97 12928442-1 2003 Proinsulin biosynthesis is regulated in response to nutrients, most notably glucose. Glucose 76-83 insulin Homo sapiens 0-10 12928442-3 2003 However, prolonging glucose stimulation (24 h) also increases preproinsulin mRNA levels. Glucose 20-27 insulin Homo sapiens 62-75 12928442-7 2003 The results showed that proinsulin biosynthesis is regulated, in the short term (1 h), solely at the level of translation, through an approximately 6-fold increase in response to glucose (2.8 mm versus 16.7 mm glucose). Glucose 179-186 insulin Homo sapiens 24-34 12928442-7 2003 The results showed that proinsulin biosynthesis is regulated, in the short term (1 h), solely at the level of translation, through an approximately 6-fold increase in response to glucose (2.8 mm versus 16.7 mm glucose). Glucose 210-217 insulin Homo sapiens 24-34 12928442-8 2003 In the longer term, when preproinsulin mRNA levels have increased approximately 2-fold, a corresponding increase was observed in the fold response of proinsulin translation to a stimulatory glucose concentration (>/=10-fold). Glucose 190-197 insulin Homo sapiens 25-38 12928442-8 2003 In the longer term, when preproinsulin mRNA levels have increased approximately 2-fold, a corresponding increase was observed in the fold response of proinsulin translation to a stimulatory glucose concentration (>/=10-fold). Glucose 190-197 insulin Homo sapiens 28-38 12928442-10 2003 The results presented here indicate that long term nutritional state sets the preproinsulin mRNA level in the beta-cell at which translation control regulates short term changes in rates of proinsulin biosynthesis in response to glucose, but this is not mediated by any autocrine effect of insulin. Glucose 229-236 insulin Homo sapiens 78-91 12928442-10 2003 The results presented here indicate that long term nutritional state sets the preproinsulin mRNA level in the beta-cell at which translation control regulates short term changes in rates of proinsulin biosynthesis in response to glucose, but this is not mediated by any autocrine effect of insulin. Glucose 229-236 insulin Homo sapiens 81-91 12928442-10 2003 The results presented here indicate that long term nutritional state sets the preproinsulin mRNA level in the beta-cell at which translation control regulates short term changes in rates of proinsulin biosynthesis in response to glucose, but this is not mediated by any autocrine effect of insulin. Glucose 229-236 insulin Homo sapiens 84-91 12910539-2 2003 One example is a glucose-sensitive system for insulin-controlled release based on pH-sensitive hydrogel. Glucose 17-24 insulin Homo sapiens 46-53 14530204-0 2003 Tumor necrosis factor-alpha inhibits insulin"s stimulating effect on glucose uptake and endothelium-dependent vasodilation in humans. Glucose 69-76 insulin Homo sapiens 37-44 14530204-2 2003 Therefore, we aimed at examining whether the proinflammatory cytokine tumor necrosis factor (TNF)-alpha inhibits insulin-stimulated glucose uptake and insulin-stimulated endothelial function in humans. Glucose 132-139 insulin Homo sapiens 113-120 14530204-6 2003 During infusion of insulin alone for 20 minutes, forearm glucose uptake increased by 220+/-44%. Glucose 57-64 insulin Homo sapiens 19-26 14559958-11 2003 Multivariable logistic regression demonstrated that increased administration of insulin was positively and significantly associated with ICU mortality (odds ratio, 1.02 [95% confidence interval, 1.01-1.04] at a prevailing glucose level of 111-144 mg/dL [6.1-8.0 mmol/L] for a 1-IU/d increase), suggesting that mortality benefits are attributable to glycemic control rather than increased administration of insulin. Glucose 222-229 insulin Homo sapiens 80-87 14559958-13 2003 CONCLUSIONS: Increased insulin administration is positively associated with death in the ICU regardless of the prevailing blood glucose level. Glucose 128-135 insulin Homo sapiens 23-30 14559958-14 2003 Thus, control of glucose levels rather than of absolute levels of exogenous insulin appear to account for the mortality benefit associated with intensive insulin therapy demonstrated by others. Glucose 17-24 insulin Homo sapiens 154-161 15764080-4 2003 Insulin-induced hypoglycemia was adjusted to 2.7 mmol/l for 15 min by glucose infusion. Glucose 70-77 insulin Homo sapiens 0-7 14618447-6 2003 The carnitine system is shown to be determinant in insulin regulation of fat and glucose metabolic rate in skeletal muscle, this being critical in determining body composition and relevant raised levels of risk factors for cardiovascular disease, obesity, hypertension, and type 2 diabetes. Glucose 81-88 insulin Homo sapiens 51-58 14520628-3 2003 The aim of the study is to investigate the effects of rosiglitazone (ROS), an insulin sensitizer, on glucose metabolism in CAPD patients without diabetes. Glucose 101-108 insulin Homo sapiens 78-85 15040468-1 2003 Two formulations of insulin suppositories were prepared to contain different amounts of sodium salicylate and sodium cholate as absorption promoters and also of insulin with the purpose of obtaining the most effective formulation in reducing plasma glucose levels after rectal administration to diabetic patients. Glucose 249-256 insulin Homo sapiens 20-27 15040468-1 2003 Two formulations of insulin suppositories were prepared to contain different amounts of sodium salicylate and sodium cholate as absorption promoters and also of insulin with the purpose of obtaining the most effective formulation in reducing plasma glucose levels after rectal administration to diabetic patients. Glucose 249-256 insulin Homo sapiens 161-168 12928771-7 2003 As a measure of insulin sensitivity we used estimated glucose disposal rate. Glucose 54-61 insulin Homo sapiens 16-23 12917009-1 2003 In this issue of Clinical Science, Fugmann and co-workers demonstrate a highly integrated cardiovascular response to changes in plasma concentrations of glucose, triacylglycerols (triglycerides), fatty acids and insulin. Glucose 153-160 insulin Homo sapiens 212-219 14613756-1 2003 Continuous infusion of insulin was used to improve glucose tolerance in 30 premature (26.4+/-1.4 weeks) very-low-birth-weight (750+/-211.3 g) hyperglycaemic infants receiving parenteral nutrition. Glucose 51-58 insulin Homo sapiens 23-30 12937895-2 2003 However, recent evidence implicates a role for p38 MAPK in the regulation of glucose transport; a site of insulin resistance in Type 2 diabetes. Glucose 77-84 insulin Homo sapiens 106-113 14514588-12 2003 Infusion of GLP-1 enhanced glucose-induced insulin secretion (pre: 119 +/- 21; post: 202 +/- 51 pmol/l; P < 0.05) and insulin-mediated glucose disposal (pre: 29.8 +/- 3.3; post: 35.9 +/- 2.3 micromol x kg(-1 x min(-1); P < 0.01). Glucose 27-34 insulin Homo sapiens 43-50 14514588-12 2003 Infusion of GLP-1 enhanced glucose-induced insulin secretion (pre: 119 +/- 21; post: 202 +/- 51 pmol/l; P < 0.05) and insulin-mediated glucose disposal (pre: 29.8 +/- 3.3; post: 35.9 +/- 2.3 micromol x kg(-1 x min(-1); P < 0.01). Glucose 138-145 insulin Homo sapiens 121-128 14514628-6 2003 Insulin secretion in response to glucose was assessed with a +125 mg/dl hyperglycemic clamp on day 3. Glucose 33-40 insulin Homo sapiens 0-7 14514589-3 2003 Glucose infusion rates (GIRs) and serum insulin concentrations were monitored over the following 8 h. RESULTS: Inhaled insulin exhibited significantly shorter time-to-peak insulin levels (T(max) 77 +/- 66 vs. 193 +/- 104 min, P < 0.001) and time-to-peak metabolic effects (T(GIRmax) 240 +/- 94 vs. 353 +/- 60 min, P < 0.001) compared with subcutaneously injected insulin. Glucose 0-7 insulin Homo sapiens 119-126 14514589-3 2003 Glucose infusion rates (GIRs) and serum insulin concentrations were monitored over the following 8 h. RESULTS: Inhaled insulin exhibited significantly shorter time-to-peak insulin levels (T(max) 77 +/- 66 vs. 193 +/- 104 min, P < 0.001) and time-to-peak metabolic effects (T(GIRmax) 240 +/- 94 vs. 353 +/- 60 min, P < 0.001) compared with subcutaneously injected insulin. Glucose 0-7 insulin Homo sapiens 119-126 14514589-3 2003 Glucose infusion rates (GIRs) and serum insulin concentrations were monitored over the following 8 h. RESULTS: Inhaled insulin exhibited significantly shorter time-to-peak insulin levels (T(max) 77 +/- 66 vs. 193 +/- 104 min, P < 0.001) and time-to-peak metabolic effects (T(GIRmax) 240 +/- 94 vs. 353 +/- 60 min, P < 0.001) compared with subcutaneously injected insulin. Glucose 0-7 insulin Homo sapiens 119-126 14514592-7 2003 GLP-1 increased the dose-response relationship between glucose concentration and insulin secretion (70 +/- 26 with GLP-1 versus 38 +/- 16 pmol insulin. Glucose 55-62 insulin Homo sapiens 81-88 14514628-12 2003 When the ISR was adjusted for insulin resistance (ISRRd = ISR / [1/Rd], where Rd is the rate of insulin-stimulated glucose disposal), the inadequate beta-cell response in the FH+ group was even more evident. Glucose 115-122 insulin Homo sapiens 96-103 14514592-7 2003 GLP-1 increased the dose-response relationship between glucose concentration and insulin secretion (70 +/- 26 with GLP-1 versus 38 +/- 16 pmol insulin. Glucose 55-62 insulin Homo sapiens 143-150 14514592-13 2003 CONCLUSIONS: Administration of GLP-1 along with ingestion of a meal augments insulin secretion in humans by a dose-dependent potentiation of the dose-response relationship between plasma glucose and insulin secretion. Glucose 187-194 insulin Homo sapiens 199-206 14620622-6 2003 Euglycemia was maintained by a variable glucose infusion, a measure of tissue insulin sensitivity. Glucose 40-47 insulin Homo sapiens 78-85 14620622-11 2003 Differences were maintained after adjustment for steady-state insulin, and correlated with reduced tissue sensitivity to glucose. Glucose 121-128 insulin Homo sapiens 62-69 14511371-8 2003 Both arsenite and insulin-induced glucose uptake were inhibited partially by the p38 MAP kinase inhibitor, SB203580. Glucose 34-41 insulin Homo sapiens 18-25 14511371-10 2003 Arsenite- and insulin-induced glucose uptake responded in a remarkably similar dose-dependent fashion to a range of pharmacological- and peptide-inhibitors for atypical PKC-lambda, a downstream target of PI-3" kinase signalling in insulin-induced glucose uptake. Glucose 30-37 insulin Homo sapiens 14-21 14511371-10 2003 Arsenite- and insulin-induced glucose uptake responded in a remarkably similar dose-dependent fashion to a range of pharmacological- and peptide-inhibitors for atypical PKC-lambda, a downstream target of PI-3" kinase signalling in insulin-induced glucose uptake. Glucose 30-37 insulin Homo sapiens 231-238 14511371-10 2003 Arsenite- and insulin-induced glucose uptake responded in a remarkably similar dose-dependent fashion to a range of pharmacological- and peptide-inhibitors for atypical PKC-lambda, a downstream target of PI-3" kinase signalling in insulin-induced glucose uptake. Glucose 247-254 insulin Homo sapiens 14-21 14511371-11 2003 These data show that in 3T3-L1 adipocytes both arsenite- and insulin-induced signalling pathways project towards a similar cellular response, namely GLUT1 and GLUT4 translocation and glucose uptake. Glucose 183-190 insulin Homo sapiens 61-68 14511356-0 2003 Insulin therapy improves insulin actions on glucose metabolism and aortic wave reflection in type 2 diabetic patients. Glucose 44-51 insulin Homo sapiens 0-7 14511356-0 2003 Insulin therapy improves insulin actions on glucose metabolism and aortic wave reflection in type 2 diabetic patients. Glucose 44-51 insulin Homo sapiens 25-32 14511356-2 2003 This action of insulin and insulin action on glucose metabolism is impaired in insulin-resistant and type 2 diabetic subjects. Glucose 45-52 insulin Homo sapiens 15-22 14514347-12 2003 The effect seems to be associated with an increased insulin-induced glucose uptake. Glucose 68-75 insulin Homo sapiens 52-59 14511356-3 2003 We determined whether 6 months of insulin therapy affects insulin actions on glucose metabolism and vascular function. Glucose 77-84 insulin Homo sapiens 58-65 14514348-4 2003 Insulin resistance was assessed using the homeostasis model assessment ratio (HOMA-R) formula derived from fasting insulin and glucose levels. Glucose 127-134 insulin Homo sapiens 0-7 14511356-8 2003 RESULTS: Insulin therapy increased whole body glucose disposal by 35% from 5.1 +/- 0.7 to 6.8 +/- 0.6 mg kg ffm(-1) min(-1) (P<0.001 for 0 vs. 60 months). Glucose 46-53 insulin Homo sapiens 9-16 14556818-7 2003 RESULT(S): There were significant decreases in insulin-stimulated glucose incorporation into glycogen in PCOS cells, which is a metabolic action of insulin. Glucose 66-73 insulin Homo sapiens 47-54 14556818-7 2003 RESULT(S): There were significant decreases in insulin-stimulated glucose incorporation into glycogen in PCOS cells, which is a metabolic action of insulin. Glucose 66-73 insulin Homo sapiens 148-155 14556827-1 2003 OBJECTIVE: To examine the ability to use parameters obtainable from an oral glucose tolerance test to predict insulin action as determined under hyperinsulinemic, hyperglycemic conditions. Glucose 76-83 insulin Homo sapiens 110-117 14556827-7 2003 RESULT(S): Among individuals with normal glucose tolerance, as assessed by an oral glucose tolerance test, the fasting insulin level is the glucose tolerance test parameter that correlates best with insulin action during a hyperglycemic clamp. Glucose 41-48 insulin Homo sapiens 119-126 14556827-7 2003 RESULT(S): Among individuals with normal glucose tolerance, as assessed by an oral glucose tolerance test, the fasting insulin level is the glucose tolerance test parameter that correlates best with insulin action during a hyperglycemic clamp. Glucose 83-90 insulin Homo sapiens 119-126 14556827-7 2003 RESULT(S): Among individuals with normal glucose tolerance, as assessed by an oral glucose tolerance test, the fasting insulin level is the glucose tolerance test parameter that correlates best with insulin action during a hyperglycemic clamp. Glucose 83-90 insulin Homo sapiens 199-206 14556827-7 2003 RESULT(S): Among individuals with normal glucose tolerance, as assessed by an oral glucose tolerance test, the fasting insulin level is the glucose tolerance test parameter that correlates best with insulin action during a hyperglycemic clamp. Glucose 83-90 insulin Homo sapiens 119-126 14556827-7 2003 RESULT(S): Among individuals with normal glucose tolerance, as assessed by an oral glucose tolerance test, the fasting insulin level is the glucose tolerance test parameter that correlates best with insulin action during a hyperglycemic clamp. Glucose 83-90 insulin Homo sapiens 199-206 14556827-8 2003 CONCLUSION(S): Measurement of fasting serum insulin levels in conjunction with an oral glucose tolerance test improves the ability to assess insulin action. Glucose 87-94 insulin Homo sapiens 141-148 12920574-2 2003 PTGS2 generates prostaglandins, which negatively modulate glucose-stimulated insulin secretion, and functions as a mediator of the inflammatory response, which is associated with decreased insulin sensitivity. Glucose 58-65 insulin Homo sapiens 77-84 14557422-4 2003 During one-step hyperinsulinemic clamp (plasma insulin, 1.962 pmol/liter), PS for glucose increased from 0.2 +/- 0.1 to 2.3 +/- 0.9 ml/min.100 g (P < 0.05), and glucose uptake increased from 0.6 +/- 0.2 to 5.0 +/- 1.4 micro mol/min.100 g (P < 0.05). Glucose 82-89 insulin Homo sapiens 21-28 14557441-7 2003 The insulin response to the oral glucose tolerance test was measured by the insulin area under the curve (I(AUC120)). Glucose 33-40 insulin Homo sapiens 4-11 14557428-3 2003 Therefore, we examined the impact of different levels of HbA1c on insulin sensitivity (Si), non-insulin-dependent glucose disposal, and blood pressure (BP), as well as lipids and lipoproteins in nondiabetic, first-degree relatives of African-American patients with type 2 diabetes. Glucose 114-121 insulin Homo sapiens 96-103 14557441-7 2003 The insulin response to the oral glucose tolerance test was measured by the insulin area under the curve (I(AUC120)). Glucose 33-40 insulin Homo sapiens 76-83 14557471-0 2003 The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. Glucose 105-112 insulin Homo sapiens 85-92 14557441-8 2003 Measures of insulin sensitivity were calculated as the fasting glucose to insulin ratio, quantitative insulin sensitivity check index, and composite insulin sensitivity index. Glucose 63-70 insulin Homo sapiens 12-19 14557471-1 2003 The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. Glucose 274-281 insulin Homo sapiens 18-25 14557471-5 2003 The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. Glucose 110-117 insulin Homo sapiens 34-41 14557471-8 2003 In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. Glucose 86-93 insulin Homo sapiens 66-73 14570866-7 2003 RESULTS: Participants who consumed alcohol daily had significantly lower fasting and 2-hour postglucose serum insulin concentrations compared with those who abstained from alcohol intake, when adjusted using linear logistic regression models for serum glucose concentration, gender, ethnicity, age, and body mass index. Glucose 96-103 insulin Homo sapiens 110-117 14993457-1 2003 The hormones glucagon and insulin delicately regulate the concentration of blood glucose. Glucose 81-88 insulin Homo sapiens 26-33 12974877-7 2003 RESULTS: By the end of follow-up, men with an abnormal hormone secretion pattern (n = 73) had elevated mean arterial pressure (P = 0.003), fasting insulin (P = 0.009) and insulin : glucose ratio (P = 0.005) compared with men with a normal secretion pattern (n = 68). Glucose 181-188 insulin Homo sapiens 171-178 14604166-7 2003 The stunting-wasting cases had the lowest intraerythrocytic potassium and early insulin response to intravenous glucose administration. Glucose 112-119 insulin Homo sapiens 80-87 14607014-5 2003 Maximal transdermal insulin concentrations in the lymph nodes were observed with both 140 IU (5 mg: 43.0 +/- 18.0 microIU mg(-1) (mean +/- s.e.m., n = 4)) and 280 IU (10 mg: 48.0 +/- 19.6 microIU mg(-1) (mean +/- s.e.m., n = 4)) doses of recombinant insulin at t = 73 h. The level of insulin in the lymph nodes after subcutaneous injection of 1 mg insulin at the peak blood glucose response was 35.8 microIU mg(-1) (n = 2), before falling to 0.35 microIU mg(-1) by t = 48 h (n = 2). Glucose 374-381 insulin Homo sapiens 20-27 14993457-2 2003 When patients become resistant to the effects of insulin or produce too little of it to properly regulate glucose concentrations, then diabetes can result. Glucose 106-113 insulin Homo sapiens 49-56 14974363-6 2003 Insulin resistance ratio (IRI/G) was calculated as an insulin: glucose ratio. Glucose 63-70 insulin Homo sapiens 0-7 12954455-8 2003 Furthermore, the strong association between glucose and insulin in the diurnal lifestyle group after meals was damaged in the nocturnal lifestyle group. Glucose 44-51 insulin Homo sapiens 56-63 12855681-3 2003 Overexpression of the full-length Synip protein (Synip/wild type) inhibited VAMP2 association with syntaxin 4 and decreased glucose-stimulated insulin secretion. Glucose 124-131 insulin Homo sapiens 143-150 14508355-12 2003 Insulin secretion elicited by oral, but not intravenous glucose, is significantly reduced in both groups of patients. Glucose 56-63 insulin Homo sapiens 0-7 12842890-0 2003 The roles of Cbl-b and c-Cbl in insulin-stimulated glucose transport. Glucose 51-58 insulin Homo sapiens 32-39 12842890-1 2003 Previous studies suggest that the stimulation of glucose transport by insulin involves the tyrosine phosphorylation of c-Cbl and the translocation of the c-Cbl/CAP complex to lipid raft subdomains of the plasma membrane. Glucose 49-56 insulin Homo sapiens 70-77 12855681-5 2003 Consistent with a functional role of syntaxin 4 in this process, expression of syntaxin 4/DeltaTM also inhibited glucose-stimulated insulin secretion. Glucose 113-120 insulin Homo sapiens 132-139 12855681-7 2003 In contrast, overexpression of Synip resulted in an inhibition of both the first and second phase of glucose-stimulated insulin secretion. Glucose 101-108 insulin Homo sapiens 120-127 14605966-1 2003 Insulin-mediated vasodilation has been suggested to be of importance for glucose uptake during normoglycemic hyperinsulinemia. Glucose 73-80 insulin Homo sapiens 0-7 12897182-3 2003 We studied the effect of cessation of resistance training in young, healthy subjects by taking muscle biopsies and measuring insulin-mediated whole body and leg glucose uptake rates after 90 days of heavy resistance training (T) and again after 90 days of de-training (dT). Glucose 161-168 insulin Homo sapiens 125-132 12897182-10 2003 We have thus shown that 90 days after the termination of heavy resistance training, insulin-mediated glucose uptake rates per unit of skeletal muscle have decreased significantly. Glucose 101-108 insulin Homo sapiens 84-91 12943888-0 2003 Usefulness of plasma glucose and insulin concentrations in identifying patients with insulin resistance. Glucose 21-28 insulin Homo sapiens 85-92 12943888-1 2003 In this study, a specific measurement of insulin-mediated glucose disposal was used in 490 healthy volunteers to classify subjects as being insulin resistant. Glucose 58-65 insulin Homo sapiens 41-48 12943888-1 2003 In this study, a specific measurement of insulin-mediated glucose disposal was used in 490 healthy volunteers to classify subjects as being insulin resistant. Glucose 58-65 insulin Homo sapiens 140-147 12746213-2 2003 We evaluated fatty acid and VLDL-TG kinetics during basal conditions and during a glucose infusion that resulted in typical postprandial plasma glucose and insulin concentrations in six men with HIV-dyslipidemia [body mass index (BMI): 28 +/- 2 kg/m2] and six healthy men (BMI: 26 +/- 2 kg/m2). Glucose 82-89 insulin Homo sapiens 156-163 12760905-0 2003 Glucose regulates the cortical actin network through modulation of Cdc42 cycling to stimulate insulin secretion. Glucose 0-7 insulin Homo sapiens 94-101 15040468-8 2003 This formulation of suppositories studied in 7 insulin dependent diabetic patients was found to abolish the 2-h post-prandial significant rise in plasma glucose levels after meal. Glucose 153-160 insulin Homo sapiens 47-54 12760905-1 2003 Glucose-stimulated insulin granule exocytosis in pancreatic beta-cells involves cortical actin remodeling that results in the transient disruption of the interaction between polymerized actin with the plasma membrane t-SNARE (target membrane soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex. Glucose 0-7 insulin Homo sapiens 19-26 12760905-3 2003 Confocal immunofluorescent microscopy revealed that cortical actin remodeling was required for glucose-stimulated insulin secretion. Glucose 95-102 insulin Homo sapiens 114-121 12760905-6 2003 Moreover, expression of the constitutively active form of Cdc42 (Q61L) inhibited glucose-stimulated insulin secretion, whereas the dominant negative form (T17N) was without effect, suggesting that glucose-stimulated insulin secretion requires Cdc42 cycling to the GDP-bound state. Glucose 81-88 insulin Homo sapiens 100-107 12773307-2 2003 Although insulin is the primary regulator of glucose transport in adipose, endothelin-1, a vasoconstrictor peptide that signals through the heterotrimeric G proteins Galphaq/11, potently stimulates glucose uptake in 3T3-L1 adipocytes by a mechanism independent of phosphatidylinositol (PI) 3-kinase. Glucose 45-52 insulin Homo sapiens 9-16 12760905-6 2003 Moreover, expression of the constitutively active form of Cdc42 (Q61L) inhibited glucose-stimulated insulin secretion, whereas the dominant negative form (T17N) was without effect, suggesting that glucose-stimulated insulin secretion requires Cdc42 cycling to the GDP-bound state. Glucose 197-204 insulin Homo sapiens 216-223 12962690-5 2003 Exercise stimulates insulin-dependent and -independent muscle glucose uptake, as well as the liver"s ability to take up glucose. Glucose 62-69 insulin Homo sapiens 20-27 12962691-7 2003 These patients also exhibit augmented intracellular lipid accumulation which could hint at a link between deranged glucose and lipid metabolism in insulin-resistant states. Glucose 115-122 insulin Homo sapiens 147-154 12962692-3 2003 Glucose transport into skeletal muscle is a rate-limiting step for glucose utilization under physiological conditions and a site of insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 0-7 insulin Homo sapiens 132-139 14598859-3 2003 Over the last two decades a central role in the origin of insulin resistance has emerged for defects in the intracellular insulin signaling cascade leading to glucose uptake. Glucose 159-166 insulin Homo sapiens 58-65 12962693-7 2003 In beta-cells, FFAs potentiate glucose-stimulated insulin secretion acutely and chronically. Glucose 31-38 insulin Homo sapiens 50-57 12962696-2 2003 Insulin resistance in type 2 diabetes is mainly linked to glucose disposal in skeletal muscle, i.e. reduced glycogen synthesis. Glucose 58-65 insulin Homo sapiens 0-7 14535354-2 2003 Early work reported decreasing glucose tolerance in the evening and at night with evidence for insulin resistance at night. Glucose 31-38 insulin Homo sapiens 95-102 12919151-3 2003 PATIENTS AND MEASUREMENTS: We performed an insulin-modified, frequently sampled intravenous glucose tolerance test (FSIVGTT) in 34 normoglycaemic European women with previous GDM and 44 European control women, deriving measures of insulin sensitivity, glucose effectiveness, glucose disappearance rate and acute insulin response to glucose. Glucose 92-99 insulin Homo sapiens 43-50 14598859-3 2003 Over the last two decades a central role in the origin of insulin resistance has emerged for defects in the intracellular insulin signaling cascade leading to glucose uptake. Glucose 159-166 insulin Homo sapiens 122-129 14598859-4 2003 Herein, we will 1) review insulin signaling pathways leading to glucose uptake, 2) review mouse models of insulin resistance that demonstrate the pathophysiologic importance of specific defects of these pathways and 3) discuss the molecular basis for insulin resistance in some human disease states known to be associated with insulin resistance. Glucose 64-71 insulin Homo sapiens 26-33 12941774-8 2003 These data demonstrate that genes involved in providing cellular protection against oxidative stress are defective in patients with type 2 diabetes and correlate with insulin-stimulated glucose disposal and markers of muscle oxidative capacity. Glucose 186-193 insulin Homo sapiens 167-174 12941759-1 2003 To determine the mechanism(s) by which insulin inhibits endogenous glucose production (EGP) in nondiabetic humans, insulin was infused at rates of 0.25, 0.375, or 0.5 mU. Glucose 67-74 insulin Homo sapiens 39-46 12933652-1 2003 Insulin is unique among growth factors and hormones in its ability to control metabolic functions such as the stimulation of glucose uptake and glucose transporter (GLUT4) translocation in physiological target tissues, such as muscle and adipose cells. Glucose 125-132 insulin Homo sapiens 0-7 12856128-7 2003 In obese non-diabetic subjects, the two promoter polymorphisms were associated with higher fasting glucose concentrations (p=0.006 and p=0.0004, for -765 4G/5G and -844 A>G, respectively) and insulin (p=0.05 and p=0.008, for -765 4G/5G and -844 A>G, respectively). Glucose 99-106 insulin Homo sapiens 195-202 12879253-6 2003 CONCLUSION/INTERPRETATION: In IGT the defect in glucose sensitivity of insulin release quantitatively predominates over insulin resistance in the genesis of the reduced tolerance to oral glucose. Glucose 48-55 insulin Homo sapiens 71-78 12879253-6 2003 CONCLUSION/INTERPRETATION: In IGT the defect in glucose sensitivity of insulin release quantitatively predominates over insulin resistance in the genesis of the reduced tolerance to oral glucose. Glucose 187-194 insulin Homo sapiens 71-78 12879253-6 2003 CONCLUSION/INTERPRETATION: In IGT the defect in glucose sensitivity of insulin release quantitatively predominates over insulin resistance in the genesis of the reduced tolerance to oral glucose. Glucose 187-194 insulin Homo sapiens 120-127 12933652-8 2003 These data demonstrate that 1) the basis of insulin-specific glucose transport in cultured adipocytes is the low level of receptors for other growth factors and 2) in the presence of adequate receptors, PDGF is fully capable of activating glucose transport in a manner requiring PI3K and subsequent phosphatidylinositol-3,4,5-trisphosphate accumulation but independent of insulin, insulin receptor, and IRS proteins. Glucose 61-68 insulin Homo sapiens 44-51 12933670-3 2003 We substituted a small amount (7%) of dietary lipid with long-chain omega-3 fatty acids during 4 wk of high-saturated fat feeding to investigate the relationship between amelioration of insulin resistance and glucose-stimulated insulin secretion (GSIS). Glucose 209-216 insulin Homo sapiens 228-235 12933670-4 2003 We demonstrate that, despite dietary delivery of saturated fat throughout, this manipulation prevents high-saturated fat feeding-induced insulin resistance with respect to peripheral glucose disposal and reverses insulin hypersecretion in response to glucose in vivo. Glucose 183-190 insulin Homo sapiens 137-144 12933652-8 2003 These data demonstrate that 1) the basis of insulin-specific glucose transport in cultured adipocytes is the low level of receptors for other growth factors and 2) in the presence of adequate receptors, PDGF is fully capable of activating glucose transport in a manner requiring PI3K and subsequent phosphatidylinositol-3,4,5-trisphosphate accumulation but independent of insulin, insulin receptor, and IRS proteins. Glucose 239-246 insulin Homo sapiens 44-51 12933670-4 2003 We demonstrate that, despite dietary delivery of saturated fat throughout, this manipulation prevents high-saturated fat feeding-induced insulin resistance with respect to peripheral glucose disposal and reverses insulin hypersecretion in response to glucose in vivo. Glucose 251-258 insulin Homo sapiens 213-220 12933670-7 2003 Our data demonstrate that the insulin response to glucose is suppressed to a greater extent than whole-body insulin sensitivity is enhanced by enrichment of a high-saturated fat diet with long-chain omega-3 fatty acids. Glucose 50-57 insulin Homo sapiens 30-37 12951645-14 2003 CONCLUSIONS: C-peptide in the presence of insulin exerts synergistic effects on cell proliferation, neurite outgrowth and has in the presence of insulin an antiapoptotic effect on high glucose-induced apoptosis but less so on hyperosmolar-induced apoptosis. Glucose 185-192 insulin Homo sapiens 145-152 12941783-10 2003 Further, postclamp cathepsin L mRNA levels were correlated with insulin-mediated glucose uptake (r = 0.37, P = 0.03), particularly, with glucose oxidation (r = 0.37, P = 0.03), and fasting glucose concentrations (r = -0.45, P < 0.01) across all three study groups. Glucose 81-88 insulin Homo sapiens 64-71 12941788-7 2003 However, the codon 206 polymorphism may be related to the interindividual variation in fasting and oral glucose-induced serum insulin levels. Glucose 104-111 insulin Homo sapiens 126-133 12951646-4 2003 The insulin resistance was evaluated by insulin and glucose concentrations after a night of fasting. Glucose 52-59 insulin Homo sapiens 4-11 14502098-2 2003 Metformin, the most widely-prescribed insulin-sensitizing agent in current clinical use, improves blood glucose control mainly by improving insulin-mediated suppression of hepatic glucose production, and by enhancing insulin-stimulated glucose disposal in skeletal muscle. Glucose 104-111 insulin Homo sapiens 38-45 14986725-3 2003 Various indices of insulin sensitivity/resistance using the data from an oral glucose tolerance test were proposed in last 20 years. Glucose 78-85 insulin Homo sapiens 19-26 14502098-2 2003 Metformin, the most widely-prescribed insulin-sensitizing agent in current clinical use, improves blood glucose control mainly by improving insulin-mediated suppression of hepatic glucose production, and by enhancing insulin-stimulated glucose disposal in skeletal muscle. Glucose 180-187 insulin Homo sapiens 140-147 14502098-2 2003 Metformin, the most widely-prescribed insulin-sensitizing agent in current clinical use, improves blood glucose control mainly by improving insulin-mediated suppression of hepatic glucose production, and by enhancing insulin-stimulated glucose disposal in skeletal muscle. Glucose 180-187 insulin Homo sapiens 140-147 12943520-6 2003 Insulin sensitivity was determined by an oral glucose tolerance test based on a formula named the insulin sensitivity index (ISI composite). Glucose 46-53 insulin Homo sapiens 0-7 12943520-6 2003 Insulin sensitivity was determined by an oral glucose tolerance test based on a formula named the insulin sensitivity index (ISI composite). Glucose 46-53 insulin Homo sapiens 98-105 12943525-8 2003 Non-diabetic rats treated with insulin from day 21 to 100 showed normal glucose tolerance and no sign of insulitis at 160 days of age. Glucose 72-79 insulin Homo sapiens 31-38 12950267-2 2003 Li also mimics insulin"s ability to stimulate glucose transport (GT), an observation that has led to the suggestion that GSK3 may coordinate hormonal increases in GT and glycogen synthesis. Glucose 46-53 insulin Homo sapiens 15-22 12957810-2 2003 Both insulin and exercise increase glucose transport into myofibers through glucose transporter (GLUT) proteins. Glucose 35-42 insulin Homo sapiens 5-12 12958175-0 2003 ATP-sensitive potassium channels induced in liver cells after transfection with insulin cDNA and the GLUT 2 transporter regulate glucose-stimulated insulin secretion. Glucose 129-136 insulin Homo sapiens 80-87 12958175-8 2003 Diazoxide (150 microM) completely inhibited glucose-stimulated insulin release. Glucose 44-51 insulin Homo sapiens 63-70 12958175-11 2003 We used confocal microscopy to confirm that glucose (20 mM) stimulated the release of insulin from the fluorescently labeled secretion granules in the cells. Glucose 44-51 insulin Homo sapiens 86-93 12958175-0 2003 ATP-sensitive potassium channels induced in liver cells after transfection with insulin cDNA and the GLUT 2 transporter regulate glucose-stimulated insulin secretion. Glucose 129-136 insulin Homo sapiens 148-155 12958175-7 2003 Using radioimmunoassay techniques, we report that exposure of the cells to tolbutamide (100 microM) resulted in an increase in insulin secretion from 0.3 +/- 0.05 to 1.8 +/- 0.2 pmol insulin/10(6) cells and glibenclamide (20 microM) from 0.4 +/- 0.06 to 2.1 +/- 0.3 (n=4), similar to what is seen on glucose (20 mM) stimulation. Glucose 300-307 insulin Homo sapiens 127-134 14503930-11 2003 The concomitant administration of intravenous glucose and insulin permits the administration of higher insulin doses that can result in improved outcome due to its nonglycemic-related benefits. Glucose 46-53 insulin Homo sapiens 103-110 12923570-1 2003 Glucagon-like peptide 1 (GLP-1) is released from neuroendocrine cells in the intestine in the postprandial state and augments glucose-stimulated insulin secretion from pancreatic beta cells. Glucose 126-133 insulin Homo sapiens 145-152 12923570-9 2003 After transplantation of pituitary cells coexpressing human insulin and GLP-1 receptor into mice, enteral glucose stimulated insulin secretion. Glucose 106-113 insulin Homo sapiens 60-86 12923570-9 2003 After transplantation of pituitary cells coexpressing human insulin and GLP-1 receptor into mice, enteral glucose stimulated insulin secretion. Glucose 106-113 insulin Homo sapiens 60-67 14517773-15 2003 Glucose was eliminated faster (p < 0.0001), with an enhanced negative rebound (p = 0.014), and insulin and C-peptide increments were greater after intravenous glucose administration (p < 0.0001) if GLP-1 was administered during the injection of the glucose bolus, but not if GLP-1 had been administered until 120 or 30 min before the glucose load. Glucose 162-169 insulin Homo sapiens 98-105 14517773-15 2003 Glucose was eliminated faster (p < 0.0001), with an enhanced negative rebound (p = 0.014), and insulin and C-peptide increments were greater after intravenous glucose administration (p < 0.0001) if GLP-1 was administered during the injection of the glucose bolus, but not if GLP-1 had been administered until 120 or 30 min before the glucose load. Glucose 162-169 insulin Homo sapiens 110-119 14517773-16 2003 There was a trend towards higher insulin concentrations (p = 0.056) five minutes after glucose with GLP-1 administered until - 30 min before the glucose load. Glucose 87-94 insulin Homo sapiens 33-40 14517773-16 2003 There was a trend towards higher insulin concentrations (p = 0.056) five minutes after glucose with GLP-1 administered until - 30 min before the glucose load. Glucose 145-152 insulin Homo sapiens 33-40 12923410-5 2003 Insulin sensitivity was expressed as insulin resistance index (IRI), calculated as the ratio of the area under the curve (AUC) for glucose to that for insulin. Glucose 131-138 insulin Homo sapiens 0-7 12967337-0 2003 Interferon-alpha reduces insulin resistance and beta-cell secretion in responders among patients with chronic hepatitis B and C. This study aimed at elucidating the effects of interferon (IFN)-alpha on glucose metabolism in patients with chronic hepatitis B and C infections. Glucose 202-209 insulin Homo sapiens 25-32 12967337-4 2003 Steady-state plasma glucose of the insulin suppression test decreased significantly in responders (13.32+/-1.48 (S.E.M.) Glucose 20-27 insulin Homo sapiens 35-42 14526271-0 2003 Hepatic expression of the human insulin gene reduces glucose levels in vivo in diabetic mice model. Glucose 53-60 insulin Homo sapiens 32-39 14526271-4 2003 RESULTS: We found significant reduction in glucose levels in both experimental systems, giving evidence that prolonged constitutive systemic secretion of bioactive human (pro)insulin has been attained in non-neuroendocrine cell line in vitro and in mice following intra-liver plasmid injection. Glucose 43-50 insulin Homo sapiens 175-182 14669930-2 2003 Studies have also found that the co-ingestion of carbohydrate along with creatine increases muscle creatine uptake by a process related to insulin-stimulated glucose disposal. Glucose 158-165 insulin Homo sapiens 139-146 12923410-5 2003 Insulin sensitivity was expressed as insulin resistance index (IRI), calculated as the ratio of the area under the curve (AUC) for glucose to that for insulin. Glucose 131-138 insulin Homo sapiens 37-44 12824443-8 2003 Additionally, in subjects in the upper glucose quintile, fasting triglyceride correlated with fasting insulin (r = 0.59, P < 0.001) and with the fasting insulin resistance index (r = 0.49, P < 0.009), and plasma levels of cholesterol and 2-h glucose were also correlated (r = 0.40, P < 0.05). Glucose 39-46 insulin Homo sapiens 102-109 14569237-0 2003 Exercise training improves insulin-stimulated myocardial glucose uptake in patients with dilated cardiomyopathy. Glucose 57-64 insulin Homo sapiens 27-34 14569237-5 2003 After the training period, insulin-stimulated myocardial fractional [F-18]FDG uptake and glucose uptake rates were significantly increased in the anterior, lateral, and septal walls (P <.01) in the trained subjects but remained unchanged in the nontrained subjects. Glucose 89-96 insulin Homo sapiens 27-34 14569237-6 2003 In the trained patients, whole-body insulin-stimulated glucose uptake was enhanced and serum free fatty acid levels were suppressed during hyperinsulinemia compared with the baseline study (P <.05). Glucose 55-62 insulin Homo sapiens 36-43 14569237-8 2003 CONCLUSIONS: These results indicate that exercise training in patients with dilated cardiomyopathy improves insulin-stimulated myocardial glucose uptake. Glucose 138-145 insulin Homo sapiens 108-115 12824443-8 2003 Additionally, in subjects in the upper glucose quintile, fasting triglyceride correlated with fasting insulin (r = 0.59, P < 0.001) and with the fasting insulin resistance index (r = 0.49, P < 0.009), and plasma levels of cholesterol and 2-h glucose were also correlated (r = 0.40, P < 0.05). Glucose 39-46 insulin Homo sapiens 156-163 12901855-1 2003 Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone, released postprandially into the circulation in response to feeding, producing a glucose-dependent stimulation of insulin secretion. Glucose 159-166 insulin Homo sapiens 18-25 12972683-3 2003 Insulin sensitivity (M) was determined by milligrams glucose uptake per kilogram per minute and expressed as M/lean body mass (Mlbm). Glucose 53-60 insulin Homo sapiens 0-7 14655269-4 2003 The insulin-sensitivity index derived by the minimal model (SIMM) was calculated by the minimal model with plasma glucose and insulin data from a 90-min frequently sampled intravenous glucose test with tolbutamide. Glucose 114-121 insulin Homo sapiens 4-11 14655269-4 2003 The insulin-sensitivity index derived by the minimal model (SIMM) was calculated by the minimal model with plasma glucose and insulin data from a 90-min frequently sampled intravenous glucose test with tolbutamide. Glucose 184-191 insulin Homo sapiens 4-11 14506621-10 2003 Suppression of postabsorptive endogenous glucose production by insulin was also unchanged by treatment (doxazosin 65.6% +/- 7.5% suppression; placebo 68.3% +/- 11.2% suppression, P >.05). Glucose 41-48 insulin Homo sapiens 63-70 14506625-6 2003 A hyperglycemic clamp (8 mmol/L) coupled with stable isotope infusion ([6,6(2)H]glucose) was performed before and after treatment to assess whole-body insulin sensitivity; defined as the glucose rate of disappearance (Rd) or rate of infusion (GRIF) scaled to the steady-state insulin concentration (I). Glucose 187-194 insulin Homo sapiens 151-158 14506629-0 2003 The impact of an insulin sensitizer, troglitazone, on glucose metabolism in African Americans at risk for type 2 diabetes mellitus: a placebo-controlled, 24-month randomized study. Glucose 54-61 insulin Homo sapiens 17-24 14506629-2 2003 The objective of this study was to examine the impact of chronic use of an insulin sensitizer on glucose metabolism in normal glucose tolerant AA at risk for DM (previous gestational diabetes mellitus [GDM] or first-degree relative with DM). Glucose 97-104 insulin Homo sapiens 75-82 14506629-2 2003 The objective of this study was to examine the impact of chronic use of an insulin sensitizer on glucose metabolism in normal glucose tolerant AA at risk for DM (previous gestational diabetes mellitus [GDM] or first-degree relative with DM). Glucose 126-133 insulin Homo sapiens 75-82 14506629-13 2003 Based on our current data, the treatment of normal glucose tolerant high-risk AA with thiazolidinedione (TZD) may be beneficial to "reset" and protect glucose metabolism by improving insulin responses. Glucose 51-58 insulin Homo sapiens 183-190 14506629-13 2003 Based on our current data, the treatment of normal glucose tolerant high-risk AA with thiazolidinedione (TZD) may be beneficial to "reset" and protect glucose metabolism by improving insulin responses. Glucose 151-158 insulin Homo sapiens 183-190 14692201-3 2003 Careful attention to management of diabetes in the hospitalized patient decreases the risk of ketoacidosis, fluid and electrolyte abnormalities, and infection; in critically ill postoperative patients, tight glucose control with insulin administration decreases the risk of death. Glucose 208-215 insulin Homo sapiens 229-236 12957321-4 2003 Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligands promote the balance of these substances to enhance insulin-mediated glucose uptake and decrease inflammation. Glucose 138-145 insulin Homo sapiens 121-128 12957323-6 2003 The Insulin Resistance Atherosclerosis Study found that insulin resistance, as determined by a frequently sampled glucose tolerance test, is significantly related to higher CRP levels, higher fibrinogen, and higher plasminogen activator inhibitor-1 (PAI-1) levels. Glucose 114-121 insulin Homo sapiens 4-11 12957323-6 2003 The Insulin Resistance Atherosclerosis Study found that insulin resistance, as determined by a frequently sampled glucose tolerance test, is significantly related to higher CRP levels, higher fibrinogen, and higher plasminogen activator inhibitor-1 (PAI-1) levels. Glucose 114-121 insulin Homo sapiens 56-63 12907343-1 2003 OBJECTIVES: Insulin resistance is nearly universal in patients with nonalcoholic steatohepatitis (NASH) when tested by glucose tolerance tests or clamp methods. Glucose 119-126 insulin Homo sapiens 12-19 12864742-8 2003 In rodents there are similarities in the pattern of muscle lipid accumulation/PKC translocation/altered insulin signalling/insulin resistance inducible by 3-5-h acute free fatty acid elevation, 1-4 days intravenous glucose infusion or several weeks of high-fat feeding. Glucose 215-222 insulin Homo sapiens 104-111 12864742-8 2003 In rodents there are similarities in the pattern of muscle lipid accumulation/PKC translocation/altered insulin signalling/insulin resistance inducible by 3-5-h acute free fatty acid elevation, 1-4 days intravenous glucose infusion or several weeks of high-fat feeding. Glucose 215-222 insulin Homo sapiens 123-130 12644449-4 2003 Glutamate dimethyl ester (GME), a plasma membrane-permeable analog of glutamate, potentiated glucose-stimulated insulin secretion at 5 mM without changing cellular ATP content or cytosolic Ca2+ concentration ([Ca2+]). Glucose 93-100 insulin Homo sapiens 112-119 12882946-3 2003 Intake of whole grain was examined for associations with BMI and insulin sensitivity (measured as milligrams of glucose uptake per kilogram of lean body mass (M(lbm)) per minute). Glucose 112-119 insulin Homo sapiens 65-72 12902805-4 2003 Fasting glucose significantly increased along with a significant increase in homeostatic model assessment values, reflecting an increase in insulin resistance. Glucose 8-15 insulin Homo sapiens 140-147 12864736-5 2003 Here we focus on the influence of a single bout of exercise on the action of insulin on processes such as glucose uptake and glucose storage in skeletal muscle. Glucose 106-113 insulin Homo sapiens 77-84 12864736-5 2003 Here we focus on the influence of a single bout of exercise on the action of insulin on processes such as glucose uptake and glucose storage in skeletal muscle. Glucose 125-132 insulin Homo sapiens 77-84 12864737-1 2003 Exercise-induced glucose uptake in skeletal muscle is mediated by an insulin-independent mechanism. Glucose 17-24 insulin Homo sapiens 69-76 12684221-1 2003 To test the hypothesis that estrogens alter insulin action, we evaluated the effects of intravenous conjugated estrogens (CE) on insulin-stimulated steady-state glucose infusion rate (SSGIR) and suppression of plasma glycerol in postmenopausal women (mean +/- SD; 56 +/- 4 yr; n = 12) not using hormone replacement. Glucose 161-168 insulin Homo sapiens 129-136 12684221-8 2003 With adjustment for differences in insulin concentration between conditions, stage 2 glucose disposals were significantly higher (8.63 vs. 7.20 mg. kg-1. Glucose 85-92 insulin Homo sapiens 35-42 12866664-7 2003 In activated T-lymphocytes, insulin stimulates glucose uptake, glucose oxidation, pyruvate flux and pyruvate dehydrogenase activity, amino acid transport, lipid metabolism and protein synthesis. Glucose 47-54 insulin Homo sapiens 28-35 12774192-12 2003 Islets preincubated with 5 mg/l alpha-amanitin showed a pattern of glucose-stimulated insulin release similar to controls, whereas islets preincubated with 50 mg/l alpha-amanitin showed an increased basal release with a reduced response to glucose stimulation. Glucose 67-74 insulin Homo sapiens 86-93 12866989-2 2003 Insulin-stimulated production of nitric oxide in vascular endothelium results in capillary recruitment and vasodilation that diverts and increases blood flow to skeletal muscle and consequently increases glucose disposal. Glucose 204-211 insulin Homo sapiens 0-7 12866989-5 2003 Moreover, the time course and dose response for capillary recruitment in response to physiologic concentrations of insulin parallels that of insulin-mediated glucose uptake in vivo. Glucose 158-165 insulin Homo sapiens 115-122 12866989-5 2003 Moreover, the time course and dose response for capillary recruitment in response to physiologic concentrations of insulin parallels that of insulin-mediated glucose uptake in vivo. Glucose 158-165 insulin Homo sapiens 141-148 12866664-7 2003 In activated T-lymphocytes, insulin stimulates glucose uptake, glucose oxidation, pyruvate flux and pyruvate dehydrogenase activity, amino acid transport, lipid metabolism and protein synthesis. Glucose 63-70 insulin Homo sapiens 28-35 12866995-6 2003 This results in reduction of tyrosine phosphorylation of the insulin receptor substrate-1 and inhibits activation of phosphoinositol-3 kinase, an enzyme that is essential for normal insulin-stimulated glucose uptake. Glucose 201-208 insulin Homo sapiens 61-68 12882906-1 2003 Stimulation of glucose transport by insulin involves tyrosine phosphorylation of the insulin receptor (IR) and IR substrates (IRSs). Glucose 15-22 insulin Homo sapiens 36-43 12882902-3 2003 Insulin sensitivity, measured by intravenous glucose tolerance test, decreased with age (r = -0.32) and was related to abdominal fat content (r = -0.65). Glucose 45-52 insulin Homo sapiens 0-7 12882909-7 2003 In control and type 2 diabetic subjects, TGD/nonoxidative glucose disposal correlated positively with the insulin-stimulated increments in IRS-1 tyrosine phosphorylation (r = 0.52/r = 0.57, P < 0.01) and inversely with the plasma FFA concentration during the insulin clamp (r = -0.55/r = -0.53, P < 0.01). Glucose 58-65 insulin Homo sapiens 106-113 12882909-7 2003 In control and type 2 diabetic subjects, TGD/nonoxidative glucose disposal correlated positively with the insulin-stimulated increments in IRS-1 tyrosine phosphorylation (r = 0.52/r = 0.57, P < 0.01) and inversely with the plasma FFA concentration during the insulin clamp (r = -0.55/r = -0.53, P < 0.01). Glucose 58-65 insulin Homo sapiens 262-269 12882907-7 2003 The insulin sensitizer rosiglitazone improved insulin-stimulated IRS-1-dependent PI 3-kinase and aPKC activation, as well as glucose disposal rates. Glucose 125-132 insulin Homo sapiens 4-11 12882917-7 2003 The in vitro-generated islet buds released insulin in response to glucose nearly as efficiently as native islets. Glucose 66-73 insulin Homo sapiens 43-50 12864780-1 2003 BACKGROUND: Different time-concentration profiles of plasma insulin following insulin modification of a frequently sampled intravenous glucose-tolerance-test (FSIVGTT) were observed in a study investigating maternal metabolism and fetal macrosomia. Glucose 135-142 insulin Homo sapiens 60-67 12919921-0 2003 [Relationship between plasma glucose level and insulin secretion in type 2 diabetic patients]. Glucose 29-36 insulin Homo sapiens 47-54 12919921-1 2003 OBJECTIVE: To investigate the association between insulin secretion and plasma glucose levels, and the potential effect of plasma glucose concentration on insulin secretion stimulated by glucose in patients with type 2 diabetes. Glucose 79-86 insulin Homo sapiens 50-57 12919921-1 2003 OBJECTIVE: To investigate the association between insulin secretion and plasma glucose levels, and the potential effect of plasma glucose concentration on insulin secretion stimulated by glucose in patients with type 2 diabetes. Glucose 130-137 insulin Homo sapiens 155-162 12919921-1 2003 OBJECTIVE: To investigate the association between insulin secretion and plasma glucose levels, and the potential effect of plasma glucose concentration on insulin secretion stimulated by glucose in patients with type 2 diabetes. Glucose 130-137 insulin Homo sapiens 155-162 12919921-4 2003 RESULTS: Correlation test demonstrated that there was a significant inverse correlation between fasting blood glucose and the insulin levels measured at all the time points of IRT. Glucose 110-117 insulin Homo sapiens 126-133 12919921-5 2003 The plasma glucose levels during OGTT were inversely correlated with plasma insulin levels during IRT (instead of basal insulin level), and the relations were especially significant of all the glucose levels at 5 time points during OGTT with the insulin levels at 1, 2 h, the maximal insulin level (Imax) and the maximal-to-basal insulin level ratio (M/Bi). Glucose 11-18 insulin Homo sapiens 76-83 12919921-5 2003 The plasma glucose levels during OGTT were inversely correlated with plasma insulin levels during IRT (instead of basal insulin level), and the relations were especially significant of all the glucose levels at 5 time points during OGTT with the insulin levels at 1, 2 h, the maximal insulin level (Imax) and the maximal-to-basal insulin level ratio (M/Bi). Glucose 11-18 insulin Homo sapiens 120-127 12919921-5 2003 The plasma glucose levels during OGTT were inversely correlated with plasma insulin levels during IRT (instead of basal insulin level), and the relations were especially significant of all the glucose levels at 5 time points during OGTT with the insulin levels at 1, 2 h, the maximal insulin level (Imax) and the maximal-to-basal insulin level ratio (M/Bi). Glucose 11-18 insulin Homo sapiens 120-127 12919921-5 2003 The plasma glucose levels during OGTT were inversely correlated with plasma insulin levels during IRT (instead of basal insulin level), and the relations were especially significant of all the glucose levels at 5 time points during OGTT with the insulin levels at 1, 2 h, the maximal insulin level (Imax) and the maximal-to-basal insulin level ratio (M/Bi). Glucose 11-18 insulin Homo sapiens 120-127 12919921-5 2003 The plasma glucose levels during OGTT were inversely correlated with plasma insulin levels during IRT (instead of basal insulin level), and the relations were especially significant of all the glucose levels at 5 time points during OGTT with the insulin levels at 1, 2 h, the maximal insulin level (Imax) and the maximal-to-basal insulin level ratio (M/Bi). Glucose 11-18 insulin Homo sapiens 120-127 12919921-6 2003 The ratio of maximal glucose to fasting glucose was positively correlated with the insulin levels at the 5 time points and Imax. Glucose 21-28 insulin Homo sapiens 83-90 12864780-1 2003 BACKGROUND: Different time-concentration profiles of plasma insulin following insulin modification of a frequently sampled intravenous glucose-tolerance-test (FSIVGTT) were observed in a study investigating maternal metabolism and fetal macrosomia. Glucose 135-142 insulin Homo sapiens 78-85 12919921-6 2003 The ratio of maximal glucose to fasting glucose was positively correlated with the insulin levels at the 5 time points and Imax. Glucose 40-47 insulin Homo sapiens 83-90 12919921-8 2003 CONCLUSION: Hyperglycemia (fasting or postprandial glucose) of type-2 diabetic patients has considerably destructive effect on dynamic insulin secretion. Glucose 51-58 insulin Homo sapiens 135-142 14535628-9 2003 Insulin sensitivity was determined by using euglycemic hyperinsulinemic clamp technique [40 microU/m2/min insulin infusion rate; glucose disposal rate (M)= mg/kg/min] before and after treatment. Glucose 129-136 insulin Homo sapiens 0-7 12951276-4 2003 Over the next 2 months, the dosage of insulin required to achieve reasonable blood glucose control was reduced, with the HbA1c level decreasing significantly to 6.8%. Glucose 83-90 insulin Homo sapiens 38-45 12865318-0 2003 Diazoxide attenuates glucose-induced defects in first-phase insulin release and pulsatile insulin secretion in human islets. Glucose 21-28 insulin Homo sapiens 60-67 12865318-4 2003 whether human islets cultured at a glucose concentration of approximately 11 mM (comparable to TTDM) recapitulates impaired insulin secretion in TTDM, specifically impaired FPIR and insulin pulse mass with an increased proinsulin/insulin (PI/I) secretion ratio; and 2). Glucose 35-42 insulin Homo sapiens 124-131 12865318-4 2003 whether human islets cultured at a glucose concentration of approximately 11 mM (comparable to TTDM) recapitulates impaired insulin secretion in TTDM, specifically impaired FPIR and insulin pulse mass with an increased proinsulin/insulin (PI/I) secretion ratio; and 2). Glucose 35-42 insulin Homo sapiens 219-229 12865318-6 2003 Islets cultured with 11 mM glucose for 96 h had 75% depleted insulin stores (P < 0.05), decreased FPIR and insulin pulse mass (P < 0.05), and an approximately 3-fold increase in the ratio of PI/I islet content and in secretion ratio (P < 0.05). Glucose 27-34 insulin Homo sapiens 61-68 12865318-6 2003 Islets cultured with 11 mM glucose for 96 h had 75% depleted insulin stores (P < 0.05), decreased FPIR and insulin pulse mass (P < 0.05), and an approximately 3-fold increase in the ratio of PI/I islet content and in secretion ratio (P < 0.05). Glucose 27-34 insulin Homo sapiens 110-117 12865318-10 2003 In conclusion, the pattern of defects of insulin secretion present in TTDM (impaired FPIR and pulsatile insulin secretion, increased PI/I ratio) can be recapitulated in human islets cultured with 11 mM glucose for 96 h. These defects can be at least partially offset by concurrent inhibition of insulin secretion by diazoxide, which also preserves insulin stores. Glucose 202-209 insulin Homo sapiens 41-48 12865318-10 2003 In conclusion, the pattern of defects of insulin secretion present in TTDM (impaired FPIR and pulsatile insulin secretion, increased PI/I ratio) can be recapitulated in human islets cultured with 11 mM glucose for 96 h. These defects can be at least partially offset by concurrent inhibition of insulin secretion by diazoxide, which also preserves insulin stores. Glucose 202-209 insulin Homo sapiens 104-111 12914720-3 2003 When the capacity of GH to increase lipolysis is blocked, the protein-retaining and insulin-antagonistic effects of GH on glucose metabolism are either abolished or weakened dramatically, compatible with a key role for lipolysis in orchestrating the metabolic actions of GH. Glucose 122-129 insulin Homo sapiens 84-91 13680549-0 2003 Exercise training improves insulin stimulated skeletal muscle glucose uptake independent of changes in perfusion in patients with dilated cardiomyopathy. Glucose 62-69 insulin Homo sapiens 27-34 12861231-4 2003 MEASUREMENTS: Insulin sensitivity of glucose uptake was determined by the euglycemic insulin clamp technique. Glucose 37-44 insulin Homo sapiens 14-21 12861231-4 2003 MEASUREMENTS: Insulin sensitivity of glucose uptake was determined by the euglycemic insulin clamp technique. Glucose 37-44 insulin Homo sapiens 85-92 12915645-5 2003 Glucose utilization dependent [insulin sensitivity (SI)] or independent (Sg) of insulin was investigated by the minimal model method applied to a frequently sampled iv glucose tolerance test. Glucose 0-7 insulin Homo sapiens 31-38 12915645-5 2003 Glucose utilization dependent [insulin sensitivity (SI)] or independent (Sg) of insulin was investigated by the minimal model method applied to a frequently sampled iv glucose tolerance test. Glucose 0-7 insulin Homo sapiens 80-87 12915646-8 2003 As expected, glucose disposal correlated negatively with BMI (P = 0.01), WHR (P = 0.01), and fasting insulin level (P = 0.003). Glucose 13-20 insulin Homo sapiens 101-108 13680549-9 2003 Whole body insulin-stimulated glucose uptake enhanced by 23% (P<.05) and muscle glucose uptake by 53% (P<.05) in the trained group but tended to decrease in the untrained group. Glucose 30-37 insulin Homo sapiens 11-18 13680549-13 2003 The improved insulin sensitivity is not explained by changes in muscle perfusion suggesting enhanced cellular glucose extraction. Glucose 110-117 insulin Homo sapiens 13-20 12895270-3 2003 RESULTS: The levels of plasma immunoreactive insulin (IRI), HOMA-IR, and HOMA-beta were significantly correlated with fasting plasma glucose (FPG) levels. Glucose 133-140 insulin Homo sapiens 45-52 12914525-7 2003 Insulin content was decreased at 5.6 mM glucose but increased at 16.7 mM glucose by the presence of troglitazone (P<or=0.05). Glucose 40-47 insulin Homo sapiens 0-7 12914525-7 2003 Insulin content was decreased at 5.6 mM glucose but increased at 16.7 mM glucose by the presence of troglitazone (P<or=0.05). Glucose 73-80 insulin Homo sapiens 0-7 12914525-8 2003 Newly synthesized insulin mRNA and preproinsulin mRNA decreased by about 20% at standard glucose levels (P<or=0.05). Glucose 89-96 insulin Homo sapiens 18-25 12914525-11 2003 The reduced insulin secretion and biosynthesis at standard glucose levels can be interpreted as an insulin-sparing effect. Glucose 59-66 insulin Homo sapiens 12-19 12898472-3 2003 Basal or near basal insulin administration by pulsatile infusion augments hypoglycemic effect and improves insulin-mediated glucose uptake compared with insulin by continuous infusion. Glucose 124-131 insulin Homo sapiens 20-27 14593612-5 2003 Thiazolidinediones (TZD) or glitazones by increasing insulin sensitivity decrease plasma glucose levels in diabetic patients. Glucose 89-96 insulin Homo sapiens 53-60 12898472-3 2003 Basal or near basal insulin administration by pulsatile infusion augments hypoglycemic effect and improves insulin-mediated glucose uptake compared with insulin by continuous infusion. Glucose 124-131 insulin Homo sapiens 107-114 12898472-3 2003 Basal or near basal insulin administration by pulsatile infusion augments hypoglycemic effect and improves insulin-mediated glucose uptake compared with insulin by continuous infusion. Glucose 124-131 insulin Homo sapiens 107-114 12900683-2 2003 The amino acid, arginine, is known to stimulate insulin release and enhance glucose-stimulated insulin release. Glucose 76-83 insulin Homo sapiens 95-102 14593613-2 2003 The defects in insulin action on target tissues are characterized by a decreased in muscle glucose uptake and by an increased hepatic glucose production. Glucose 91-98 insulin Homo sapiens 15-22 14593618-3 2003 Although the beta cell secretory response is mainly controlled by blood glucose levels, gut hormones secreted in response to food intake have an important role in potentiating glucose-stimulated insulin secretion. Glucose 176-183 insulin Homo sapiens 195-202 12939679-3 2003 Persistent hyperinsulinemic hypoglycemia of infancy was diagnosed on the basis of high intravenous glucose requirement, high insulin to glucose ratio, negative urinary ketones and normal tandem mass spectrometry. Glucose 99-106 insulin Homo sapiens 16-23 12939679-3 2003 Persistent hyperinsulinemic hypoglycemia of infancy was diagnosed on the basis of high intravenous glucose requirement, high insulin to glucose ratio, negative urinary ketones and normal tandem mass spectrometry. Glucose 136-143 insulin Homo sapiens 16-23 12918129-3 2003 We assessed the role of glucose in the regulation of circulating levels of insulin, glucagon, cortisol, IL-6 and TNF-alpha in human sepsis with normal or impaired glucose tolerance. Glucose 24-31 insulin Homo sapiens 75-82 12853008-5 2003 The purpose of this study was to systematically review the evidence for the link between SDB, glucose intolerance, and insulin resistance. Glucose 94-101 insulin Homo sapiens 119-126 12911866-12 2003 10% dextrose inhalation caused mild reduction of plasma insulin and C-peptide and unremarkable changes in blood glucose level. Glucose 4-12 insulin Homo sapiens 56-63 12832099-7 2003 Glucose+saline infusions induced only minor increases in insulin concentrations. Glucose 0-7 insulin Homo sapiens 57-64 12714600-12 2003 Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. Glucose 41-48 insulin Homo sapiens 25-32 12829623-3 2003 The adipocyte secreted hormone resistin has been proposed as a link between the adipocyte and insulin resistance by inhibition of insulin-stimulated glucose uptake and/or blocking adipocyte differentiation. Glucose 149-156 insulin Homo sapiens 94-101 12841822-5 2003 DATA SYNTHESIS: Clinical trials have demonstrated that amylin in combination with insulin controls postprandial glucose levels by decreasing food intake, slowing gastric emptying, and suppressing glucagon secretion. Glucose 112-119 insulin Homo sapiens 82-89 12897817-12 2003 These effects were attributed to attenuation of pregnancy-induced insulin resistance (as reflected by insulin/glucose ratio) by physical conditioning. Glucose 110-117 insulin Homo sapiens 66-73 12915668-6 2003 Asian Indians had higher insulin areas under the curve during oral glucose tolerance tests, indicating a greater insulin resistance. Glucose 67-74 insulin Homo sapiens 25-32 12915668-6 2003 Asian Indians had higher insulin areas under the curve during oral glucose tolerance tests, indicating a greater insulin resistance. Glucose 67-74 insulin Homo sapiens 113-120 12823235-3 2003 Insulin was titrated to aim for fasting blood glucose (FBG) values between 4 and 7 mmol/l. Glucose 46-53 insulin Homo sapiens 0-7 12823237-1 2003 AIMS: To examine the efficacy of a continuous glucose monitoring (CGM) system for treatment adjustment in patients with diabetic pregnancy treated with insulin. Glucose 46-53 insulin Homo sapiens 152-159 12829623-3 2003 The adipocyte secreted hormone resistin has been proposed as a link between the adipocyte and insulin resistance by inhibition of insulin-stimulated glucose uptake and/or blocking adipocyte differentiation. Glucose 149-156 insulin Homo sapiens 130-137 12832319-0 2003 Association between insulin sensitivity and post-glucose challenge plasma insulin values in overweight Latino youth. Glucose 49-56 insulin Homo sapiens 74-81 12830381-6 2003 Furthermore, in the subjects with normal glucose tolerance, 89N was associated with higher insulin concentrations on oral glucose tolerance test, suggesting reduced insulin sensitivity in subjects with 89N. Glucose 122-129 insulin Homo sapiens 91-98 12824866-4 2003 Insulin sensitivity (IS) at both tests was assessed on the basis of insulin and glucose levels both in the fasting state and during OGTTs. Glucose 80-87 insulin Homo sapiens 0-7 12824867-0 2003 Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes. Glucose 24-31 insulin Homo sapiens 50-57 12824867-8 2003 Dexamethasone reduced both insulin- and SNP-stimulated glucose uptake with impairment of GLUT4 translocation. Glucose 55-62 insulin Homo sapiens 27-34 12738810-4 2003 Furthermore, we find that alterations in insulin expression and secretion caused by chronic exposure to high glucose are paralleled by decreased insulin receptor expression and increased relative abundance of the Ex11+ isoform in both human islets and RIN beta-cells. Glucose 109-116 insulin Homo sapiens 41-48 12832307-3 2003 Their plasma glucose was normalized overnight by intravenous infusion of insulin. Glucose 13-20 insulin Homo sapiens 73-80 12738810-7 2003 Re-expression in RIN beta-cells chronically exposed to high glucose of the Ex11-, but not the Ex11+, isoform restored insulin mRNA expression. Glucose 60-67 insulin Homo sapiens 118-125 12849814-1 2003 OBJECTIVE: Because the metabolic actions of insulin are more impaired than the mitogenic pathways in polycystic ovary syndrome (PCOS), genes coding for proteins involved in insulin-mediated glucose transport can be considered as candidate genes. Glucose 190-197 insulin Homo sapiens 44-51 12849814-1 2003 OBJECTIVE: Because the metabolic actions of insulin are more impaired than the mitogenic pathways in polycystic ovary syndrome (PCOS), genes coding for proteins involved in insulin-mediated glucose transport can be considered as candidate genes. Glucose 190-197 insulin Homo sapiens 173-180 12849814-2 2003 The sorbin and SH3-domain-containing-1 (SORBS1) gene codes for c-Cbl-associated protein (CAP) involved in insulin-mediated glucose uptake. Glucose 123-130 insulin Homo sapiens 106-113 12882466-3 2003 Insulin sensitivity was evaluated by the ratio of fasting glucose to fasting insulin. Glucose 58-65 insulin Homo sapiens 0-7 12687350-1 2003 In order to understand the role of the insulin receptor substrate-2 (IRS2) gene (chromosome region: 13q34) in obesity, a complex disorder associated with insulin resistance and glucose intolerance, we determined single nucleotide polymorphims (SNPs) and complex haplotypes in women with morbid obesity and a body mass index (BMI) of 41+/-0.8 kg/m2 ( n=99) compared with controls having a BMI of 23.8+/-0.1 kg/m2 ( n=92). Glucose 177-184 insulin Homo sapiens 39-46 14523905-1 2003 Diabetes mellitus is a group of diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both. Glucose 79-86 insulin Homo sapiens 113-120 14523905-1 2003 Diabetes mellitus is a group of diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both. Glucose 79-86 insulin Homo sapiens 133-140 12931275-8 2003 The slower absorption of insulin glargine correlated with the fall in plasma glucose levels over a 24 h period compared with the faster insulin absorption and more rapid decrease in plasma glucose levels observed in response to NPH insulin. Glucose 77-84 insulin Homo sapiens 25-32 14523905-10 2003 The principal therapeutic innovation of the past ten years is represented by the tight and flexible control of glucose plasma level obtained by using the insulin analogues produced by recombinant DNA technology. Glucose 111-118 insulin Homo sapiens 154-161 12843192-5 2003 We previously reported that insulin-induced stimulation of progesterone and inhibition of IGFBP-1 production in the human ovary are mediated by signaling pathways that are independent of phosphatidylinositol 3-kinase, the enzyme whose activation is crucial for glucose transport. Glucose 261-268 insulin Homo sapiens 28-35 12767053-5 2003 At the cellular level, ACE inhibitors acutely enhance glucose uptake in insulin-resistant skeletal muscle via two mechanisms. Glucose 54-61 insulin Homo sapiens 72-79 12767053-8 2003 The acute actions of ACE inhibitors on skeletal muscle glucose transport are associated with upregulation of insulin signaling, including enhanced IRS-1 tyrosine phosphorylation and phosphatidylinositol-3-kinase activity, and ultimately with increased cell-surface GLUT-4 glucose transporter protein. Glucose 55-62 insulin Homo sapiens 109-116 12767053-10 2003 These data support the concept that ACE inhibitors can beneficially modulate glucose control in insulin-resistant states, possibly through a NO-dependent effect of bradykinin and/or antagonism of ATII action on skeletal muscle. Glucose 77-84 insulin Homo sapiens 96-103 12843172-2 2003 To analyze the separate impact of ethnicity, Mexican-American vs. Caucasian, and FHD on the physiological determinants of glucose tolerance, we measured insulin sensitivity of glucose uptake (IS(GU)) (by the clamp technique), endogenous glucose production (by 3-[(3)H]glucose infusion), and insulin secretory response (to oral glucose) in 172 Mexican-Americans and 60 Caucasians with normal glucose tolerance (NGT) or DM. Glucose 176-183 insulin Homo sapiens 153-160 12843200-2 2003 Insulin sensitivity was measured from fasting plasma glucose and insulin values and those during a 75-g oral glucose tolerance test by five formulas: the homeostasis model assessment of insulin resistance (HOMA-R), the quantitative insulin sensitivity check index (QUICKI), the oral glucose insulin sensitivity (OGIS) index, and two insulin sensitivity indexes (ISI-composite and ISI-stumvoll). Glucose 53-60 insulin Homo sapiens 0-7 12843172-2 2003 To analyze the separate impact of ethnicity, Mexican-American vs. Caucasian, and FHD on the physiological determinants of glucose tolerance, we measured insulin sensitivity of glucose uptake (IS(GU)) (by the clamp technique), endogenous glucose production (by 3-[(3)H]glucose infusion), and insulin secretory response (to oral glucose) in 172 Mexican-Americans and 60 Caucasians with normal glucose tolerance (NGT) or DM. Glucose 176-183 insulin Homo sapiens 153-160 12843172-2 2003 To analyze the separate impact of ethnicity, Mexican-American vs. Caucasian, and FHD on the physiological determinants of glucose tolerance, we measured insulin sensitivity of glucose uptake (IS(GU)) (by the clamp technique), endogenous glucose production (by 3-[(3)H]glucose infusion), and insulin secretory response (to oral glucose) in 172 Mexican-Americans and 60 Caucasians with normal glucose tolerance (NGT) or DM. Glucose 176-183 insulin Homo sapiens 153-160 12817187-1 2003 OBJECTIVES: Metabolic syndrome is a cluster of risk factors, such as central obesity, dyslipidemia, glucose intolerance, hypertension, related to insulin resistance. Glucose 100-107 insulin Homo sapiens 146-153 12750819-8 2003 Finally, we observed that the expression levels of adiponectin affected insulin-stimulated glucose uptake in differentiated 3T3-L1 adipocytes. Glucose 91-98 insulin Homo sapiens 72-79 12840207-1 2003 Delayed glucose clearance after hyperglycemia may contribute to insulin resistance. Glucose 8-15 insulin Homo sapiens 64-71 12840207-11 2003 In conclusion, modest increases in abdominal adiposity and circulating lipids are associated with abnormal glucose clearance in clinically healthy older men; this may be a precursor to the development of insulin resistance and related complications that arise from prolonged postprandial hyperglycemia. Glucose 107-114 insulin Homo sapiens 204-211 12740426-4 2003 Whole-body insulin-stimulated glucose uptake was determined by the euglycaemic hyperinsulinaemic clamp technique and skeletal muscle biopsy samples were obtained before and after the insulin infusion for insulin signalling measurements. Glucose 30-37 insulin Homo sapiens 11-18 12740426-5 2003 Insulin-stimulated glucose uptake was 20 % lower in CHF patients versus healthy subjects. Glucose 19-26 insulin Homo sapiens 0-7 12740426-7 2003 Insulin-mediated glucose uptake was not altered in patients after standard care, whereas exercise training elicited a 25 % increase in glucose uptake. Glucose 17-24 insulin Homo sapiens 0-7 12870168-11 2003 It may be speculated on if the increased insulin sensitivity and reduced counterregulation to hypoglycemia could predispose to low plasma glucose concentrations. Glucose 138-145 insulin Homo sapiens 41-48 12843172-2 2003 To analyze the separate impact of ethnicity, Mexican-American vs. Caucasian, and FHD on the physiological determinants of glucose tolerance, we measured insulin sensitivity of glucose uptake (IS(GU)) (by the clamp technique), endogenous glucose production (by 3-[(3)H]glucose infusion), and insulin secretory response (to oral glucose) in 172 Mexican-Americans and 60 Caucasians with normal glucose tolerance (NGT) or DM. Glucose 176-183 insulin Homo sapiens 153-160 12843172-2 2003 To analyze the separate impact of ethnicity, Mexican-American vs. Caucasian, and FHD on the physiological determinants of glucose tolerance, we measured insulin sensitivity of glucose uptake (IS(GU)) (by the clamp technique), endogenous glucose production (by 3-[(3)H]glucose infusion), and insulin secretory response (to oral glucose) in 172 Mexican-Americans and 60 Caucasians with normal glucose tolerance (NGT) or DM. Glucose 176-183 insulin Homo sapiens 153-160 12843172-5 2003 Insulin resistance of glucose production was increased in diabetics (14 +/- 1 mmol.min(-1). Glucose 22-29 insulin Homo sapiens 0-7 12843172-8 2003 We conclude that the primary physiological target of the propensity to diabetes of Mexican-Americans is insulin resistance of glucose uptake. Glucose 126-133 insulin Homo sapiens 104-111 12842202-3 2003 RESULTS: The area under the curve of immunoreactive insulin in plasma during the OGTT was higher in patients with BRVO than in control subjects without BRVO, both when comparing individuals with normal glucose tolerance (P=.013) and when comparing individuals with impaired glucose tolerance (P<.005). Glucose 202-209 insulin Homo sapiens 52-59 12808101-1 2003 Insulin stimulates glucose uptake by recruiting glucose transporter 4 (GLUT4) from an intracellular pool to the cell surface through a mechanism that is dependent on phosphatidylinositol (PI) 3-kinase (PI3-K) and cortical actin remodeling. Glucose 19-26 insulin Homo sapiens 0-7 12808457-5 2003 Expression of these genes is high at sites of insulin-mediated glucose disposal, activated by PGC-1alpha and correlated with total-body aerobic capacity. Glucose 63-70 insulin Homo sapiens 46-53 14581728-1 2003 Physiological level of insulin showed more prominent inhibiting effect on the activation of hepatic glucose production and glycogenolysis promoted by cAMP than physiological levels of leptin. Glucose 100-107 insulin Homo sapiens 23-30 12814351-1 2003 Insulin improves development of mammalian preimplantation embryos and, in addition to the regulation of glucose transport, it exerts mitogenic and anti-apoptotic activities. Glucose 104-111 insulin Homo sapiens 0-7 12814870-2 2003 The protein hormone, resistin, secreted specifically by the adipose tissues, is found to antagonize insulin action upon glucose uptake and may serve as an important role between human obesity and insulin resistance. Glucose 120-127 insulin Homo sapiens 100-107 12829260-9 2003 After subcutaneous injection of intact insulin (0.3 units per mouse), blood glucose levels were reduced to nadir values at 1 h to return to normal at 3 h. In contrast, blood glucose levels in animals injected with polysialylated insulin (0.3 units or protein equivalence for polysialylated insulin), having attained nadir values also at 1 h, returned to normal levels after 6 h (39 kDa) and 9 h (22 kDa CA-insulin). Glucose 76-83 insulin Homo sapiens 39-46 12829260-9 2003 After subcutaneous injection of intact insulin (0.3 units per mouse), blood glucose levels were reduced to nadir values at 1 h to return to normal at 3 h. In contrast, blood glucose levels in animals injected with polysialylated insulin (0.3 units or protein equivalence for polysialylated insulin), having attained nadir values also at 1 h, returned to normal levels after 6 h (39 kDa) and 9 h (22 kDa CA-insulin). Glucose 174-181 insulin Homo sapiens 39-46 12829260-9 2003 After subcutaneous injection of intact insulin (0.3 units per mouse), blood glucose levels were reduced to nadir values at 1 h to return to normal at 3 h. In contrast, blood glucose levels in animals injected with polysialylated insulin (0.3 units or protein equivalence for polysialylated insulin), having attained nadir values also at 1 h, returned to normal levels after 6 h (39 kDa) and 9 h (22 kDa CA-insulin). Glucose 174-181 insulin Homo sapiens 229-236 12829260-9 2003 After subcutaneous injection of intact insulin (0.3 units per mouse), blood glucose levels were reduced to nadir values at 1 h to return to normal at 3 h. In contrast, blood glucose levels in animals injected with polysialylated insulin (0.3 units or protein equivalence for polysialylated insulin), having attained nadir values also at 1 h, returned to normal levels after 6 h (39 kDa) and 9 h (22 kDa CA-insulin). Glucose 174-181 insulin Homo sapiens 229-236 12829260-9 2003 After subcutaneous injection of intact insulin (0.3 units per mouse), blood glucose levels were reduced to nadir values at 1 h to return to normal at 3 h. In contrast, blood glucose levels in animals injected with polysialylated insulin (0.3 units or protein equivalence for polysialylated insulin), having attained nadir values also at 1 h, returned to normal levels after 6 h (39 kDa) and 9 h (22 kDa CA-insulin). Glucose 174-181 insulin Homo sapiens 229-236 12809451-8 2003 The insulin dose was titrated by using a predefined regimen to achieve fasting blood glucose levels of 5.56 mmol/L or lower (< or =100 mg/dL). Glucose 85-92 insulin Homo sapiens 4-11 12756298-6 2003 Immortalized FH cells expressing Pdx1 activated multiple beta-cell genes, produced and stored considerable amounts of insulin, and released insulin in a regulated manner in response to glucose. Glucose 185-192 insulin Homo sapiens 140-147 12861408-7 2003 Multiple regression analysis showed significant correlations between serum sialic acid and 2-h post-load glucose levels and insulin sensitivity. Glucose 105-112 insulin Homo sapiens 124-131 12582008-2 2003 In vitro and in vivo, chronic elevation of NEFA decreases glucose-stimulated insulin secretion. Glucose 58-65 insulin Homo sapiens 77-84 12582008-3 2003 We hypothesized that high fasting plasma NEFA would increase the risk of type 2 diabetes by inducing a worsening of glucose-stimulated insulin secretion in Pima Indians. Glucose 116-123 insulin Homo sapiens 135-142 12641495-3 2003 As a consequence, exposure of brown adipocytes to dexamethasone and insulin results in a dramatic increase of glucose uptake (12-fold). Glucose 110-117 insulin Homo sapiens 68-75 12829634-10 2003 We conclude that although glucagon response to arginine and insulin response to glucose and arginine are diminished after hemi-pancreatectomy, no deficiency in glucagon responses were detected during hypoglycemia. Glucose 80-87 insulin Homo sapiens 60-67 12829635-0 2003 HIV protease inhibitors acutely impair glucose-stimulated insulin release. Glucose 39-46 insulin Homo sapiens 58-65 12829635-3 2003 To determine whether beta-cell function is acutely affected by PIs, we assayed glucose-stimulated insulin secretion in rodent islets and the insulinoma cell line MIN6. Glucose 79-86 insulin Homo sapiens 98-105 12829635-7 2003 Insulin secretogogues acting downstream of glucose transport mostly reversed the indinavir-mediated inhibition of insulin release in MIN6 cells. Glucose 43-50 insulin Homo sapiens 0-7 12829635-7 2003 Insulin secretogogues acting downstream of glucose transport mostly reversed the indinavir-mediated inhibition of insulin release in MIN6 cells. Glucose 43-50 insulin Homo sapiens 114-121 12829641-4 2003 Insulin action (Si), measured with the meal and intravenous glucose tolerance test models, was highly correlated (r = 0.72; P < 0.001) and lower (P <or= 0.002) in the elderly than in the young participants. Glucose 60-67 insulin Homo sapiens 0-7 12829641-9 2003 We conclude that the deterioration in glucose tolerance that occurs in healthy elderly subjects is due to a decrease in both insulin secretion and action with the severity of the defect in insulin action being explained by the degree of fatness rather than age per se. Glucose 38-45 insulin Homo sapiens 125-132 12641495-6 2003 Our results show that the synergism between insulin and glucocorticoids on glucose uptake is a consequence of the activation of the GLUT4 promoter by the transcription factor C/EBPalpha. Glucose 75-82 insulin Homo sapiens 44-51 12762965-0 2003 Insulin-mediated capillary recruitment in skeletal muscle: is this a mediator of insulin action on glucose metabolism? Glucose 99-106 insulin Homo sapiens 0-7 12808614-7 2003 There was a higher incidence of insulin resistance in the tacrolimus group (post-transplant diabetes mellitus, glucose tolerance testing) but this was not statistically significant. Glucose 111-118 insulin Homo sapiens 32-39 12780756-2 2003 To study this further, we examined 10 healthy, nonobese subjects under standardized conditions for 24 h with and without an intravenous infusion of glucose, the latter in order to augment insulin sensitivity. Glucose 148-155 insulin Homo sapiens 188-195 12780756-5 2003 RESULTS: Glucose infusion resulted in mild hyperglycaemia (P < 0.0001), a reduction in IGFBP-1 by approximately 40% (P < 0.0003), and increased insulin and C-peptide levels (P < 0.0001). Glucose 9-16 insulin Homo sapiens 150-157 12780756-6 2003 Glucose infusion also increased insulin sensitivity (P < 0.003). Glucose 0-7 insulin Homo sapiens 32-39 12870160-6 2003 Insulin sensitivity index (ISI=glucose disposal per kg fat-free mass [FFM] divided by steady-state insulin concentration) did not differ between the elderly and Y1, but was higher in Y2 (0.10+/-0.01, 0.12+/-0.01, and 0.17+/-0.02, P=.0011 by analysis of variance [ANOVA]). Glucose 31-38 insulin Homo sapiens 0-7 12762965-0 2003 Insulin-mediated capillary recruitment in skeletal muscle: is this a mediator of insulin action on glucose metabolism? Glucose 99-106 insulin Homo sapiens 81-88 12765949-7 2003 Despite that, insulin-mediated glucose disposal and storage were reduced and activation of GS was virtually absent in type 2 diabetic subjects. Glucose 31-38 insulin Homo sapiens 14-21 12860494-13 2003 Insulin T(max) was shorter after nateglinide administration at -30 or -10 minutes, which was associated with lower glucose C(max) values (-30 minutes, P < 0.05) and a tendency for lower glucose AUC(0-5) values (-10 minutes, P = NS). Glucose 115-122 insulin Homo sapiens 0-7 12860494-13 2003 Insulin T(max) was shorter after nateglinide administration at -30 or -10 minutes, which was associated with lower glucose C(max) values (-30 minutes, P < 0.05) and a tendency for lower glucose AUC(0-5) values (-10 minutes, P = NS). Glucose 189-196 insulin Homo sapiens 0-7 12765949-9 2003 This phosphorylation abnormality likely caused the impaired GS activation and glucose storage, thereby contributing to skeletal muscle insulin resistance, and may therefore play a pathophysiological role in type 2 diabetes. Glucose 78-85 insulin Homo sapiens 135-142 12766131-6 2003 Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counterregulatory factors that normally prevent or rapidly correct hypoglycemia. Glucose 138-145 insulin Homo sapiens 14-21 12765961-0 2003 Free fatty acid-mediated impairment of glucose-stimulated insulin secretion in nondiabetic Oji-Cree individuals from the Sandy Lake community of Ontario, Canada: a population at very high risk for developing type 2 diabetes. Glucose 39-46 insulin Homo sapiens 58-65 12765961-5 2003 Total insulin secretory response to the graded glucose infusion did not change after a 48-h FFA elevation versus saline control in Caucasians and increased by approximately 30% in Oji-Cree individuals (P = 0.04 for difference between the two groups). Glucose 47-54 insulin Homo sapiens 6-13 12802496-6 2003 At this time, glucose-stimulated insulin secretion was evaluated by glucose stimulation tests in rats bearing the transplants. Glucose 14-21 insulin Homo sapiens 33-40 12766098-3 2003 RESULTS: Mean whole body insulin-stimulated glucose uptake and basal fat oxidation rate increased 16 and 41%, respectively, after two to four bouts of exercise, without further increase at program end. Glucose 44-51 insulin Homo sapiens 25-32 12766098-5 2003 Posttraining increases in insulin-stimulated glucose uptake were predicted by increase in aerobic capacity (r = 0.726, P = 0.001) and magnitude of reduction in visceral fat (r = -0.544, P = 0.02) and not by changes in myocyte lipid or LCAC levels. Glucose 45-52 insulin Homo sapiens 26-33 12766131-7 2003 In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation. Glucose 182-189 insulin Homo sapiens 3-10 12766131-16 2003 Pending the prevention and cure of diabetes or the development of methods that provide glucose-regulated insulin replacement or secretion, we need to learn to replace insulin in a much more physiological fashion, to prevent, correct, or compensate for compromised glucose counterregulation, or both if we are to achieve near-euglycemia safely in most people with diabetes. Glucose 87-94 insulin Homo sapiens 105-112 12766131-16 2003 Pending the prevention and cure of diabetes or the development of methods that provide glucose-regulated insulin replacement or secretion, we need to learn to replace insulin in a much more physiological fashion, to prevent, correct, or compensate for compromised glucose counterregulation, or both if we are to achieve near-euglycemia safely in most people with diabetes. Glucose 87-94 insulin Homo sapiens 167-174 12802496-6 2003 At this time, glucose-stimulated insulin secretion was evaluated by glucose stimulation tests in rats bearing the transplants. Glucose 68-75 insulin Homo sapiens 33-40 12786675-7 2003 Insulin sensitivity in CF is much debated and may depend upon the degree of glucose intolerance. Glucose 76-83 insulin Homo sapiens 0-7 12845556-6 2003 Defects at the level of glucose uptake/phosphorylation characterize insulin resistance in skeletal muscle of type 2 diabetic patients. Glucose 24-31 insulin Homo sapiens 68-75 14635734-3 2003 We compared demographics, blood pressure, body mass index, waist circumference, lipid profile, fasting and post-prandial glucose-insulin levels between CAD patients and the control group. Glucose 121-128 insulin Homo sapiens 129-136 12845561-3 2003 Plasma glucose concentrations were controlled by permanent intravenous administration of insulin. Glucose 7-14 insulin Homo sapiens 89-96 12743012-8 2003 In offspring of type 2 diabetic patients with normal glucose tolerance and normal blood pressure values, insulin resistance is associated with abnormal control of blood pressure and sympathetic activation. Glucose 53-60 insulin Homo sapiens 105-112 12857432-4 2003 However, vanadate treatment reverted the effect of high glucose on basal and insulin-stimulated insulin receptor and IRS1 phosphorylation. Glucose 56-63 insulin Homo sapiens 77-84 12857432-4 2003 However, vanadate treatment reverted the effect of high glucose on basal and insulin-stimulated insulin receptor and IRS1 phosphorylation. Glucose 56-63 insulin Homo sapiens 96-103 14515662-4 2003 We used the HOMA procedure (18) for diagnosis of insulin resistance (glucose nmol/L (18 x insulin mIU/mL (22.5 = > 5.2. Glucose 69-76 insulin Homo sapiens 49-56 12788850-10 2003 Glucose disposition index (insulin sensitivity x first phase insulin) was lower in high VAT vs. low VAT BOA, but not in WOA. Glucose 0-7 insulin Homo sapiens 27-34 14515662-4 2003 We used the HOMA procedure (18) for diagnosis of insulin resistance (glucose nmol/L (18 x insulin mIU/mL (22.5 = > 5.2. Glucose 69-76 insulin Homo sapiens 90-97 12788876-14 2003 Whether the lower glucose levels are attributable to an early phase of augmented insulin sensitivity, as previously reported in animal models, has to be established. Glucose 18-25 insulin Homo sapiens 81-88 12788850-10 2003 Glucose disposition index (insulin sensitivity x first phase insulin) was lower in high VAT vs. low VAT BOA, but not in WOA. Glucose 0-7 insulin Homo sapiens 61-68 12788859-2 2003 These subjects are thought to exhibit autonomic dysregulation of the beta-cell, with insulin hypersecretion in response to oral glucose tolerance testing (OGTT). Glucose 128-135 insulin Homo sapiens 85-92 12700337-1 2003 Fatty acids inhibit insulin-mediated glucose metabolism in skeletal muscle, an effect largely attributed to defects in insulin-mediated glucose transport. Glucose 37-44 insulin Homo sapiens 20-27 12700337-4 2003 Munc18c has been previously demonstrated to impair insulin-mediated glucose transport in mammalian cells in vitro. Glucose 68-75 insulin Homo sapiens 51-58 12717005-9 2003 Our synthesis of the information pertaining to the glucose homeostat that has accumulated in the literature predicts that disruption of the flip-flop mechanism by the accumulation of amyloid in the pancreatic islets in type 2 diabetes mellitus will lead to hyperglucagonaemia, hyperinsulinaemia, insulin resistance, glucose intolerance and impaired insulin responsiveness to elevated blood glucose levels. Glucose 51-58 insulin Homo sapiens 282-289 12791813-10 2003 Fifteen of 34 patients with diabetes had a plasma glucose level > 9 mmol/L, which was lowered successfully in all patients with additional insulin. Glucose 50-57 insulin Homo sapiens 142-149 12800089-8 2003 Finally, treatment of L6 cells with subtherapeutic amounts of vanadyl sulfate and rapamycin induced a synergistic 3-fold increase in insulin-induced glucose uptake at 2 hours. Glucose 149-156 insulin Homo sapiens 133-140 14571692-1 2003 The preferred approach to determine the pharmacokinetic (PK) and pharmacodynamic (PD) properties of insulin analogues is the euglycemic glucose clamp. Glucose 136-143 insulin Homo sapiens 100-107 12806595-9 2003 Whole body insulin sensitivity was measured by a formula derived from an oral glucose tolerance test and named as the insulin sensitivity index (ISI). Glucose 78-85 insulin Homo sapiens 11-18 12800089-0 2003 Vanadate and rapamycin synergistically enhance insulin-stimulated glucose uptake. Glucose 66-73 insulin Homo sapiens 47-54 12761338-7 2003 The human insulin promoter directed transcription in pancreatic islets and conferred a normal, physiological glucose response to reporter gene expression in isolated islets. Glucose 109-116 insulin Homo sapiens 10-17 12800089-2 2003 Here we show that simultaneous inhibition of IRS-1 tyrosine dephosphorylation and proteasomal degradation synergistically augments insulin-responsive glucose uptake. Glucose 150-157 insulin Homo sapiens 131-138 12800089-4 2003 Pretreatment of L6 cells with sodium orthovanadate (Na(3)VO(4)) plus the mTOR inhibitor rapamycin caused a 5-fold increase in insulin-responsive glucose uptake at 2 hours when compared to insulin alone. Glucose 145-152 insulin Homo sapiens 126-133 12800089-4 2003 Pretreatment of L6 cells with sodium orthovanadate (Na(3)VO(4)) plus the mTOR inhibitor rapamycin caused a 5-fold increase in insulin-responsive glucose uptake at 2 hours when compared to insulin alone. Glucose 145-152 insulin Homo sapiens 188-195 12800094-5 2003 Insulin sensitivity (glucose infusion rate [GIR]) was determined pre- and post-NA by euglycemic-hyperinsulinemic clamp. Glucose 21-28 insulin Homo sapiens 0-7 12800095-0 2003 Protein-tyrosine phosphatase activity in human adipocytes is strongly correlated with insulin-stimulated glucose uptake and is a target of insulin-induced oxidative inhibition. Glucose 105-112 insulin Homo sapiens 86-93 12800095-6 2003 The endogenous total PTPase activity also strongly correlated with insulin-stimulated glucose uptake (R =.89, P <.0001); however, the activity of PTP1B was unrelated to the level of glucose uptake. Glucose 86-93 insulin Homo sapiens 67-74 12800095-8 2003 Cellular treatment with diphenyleneiodonium (DPI), an NADPH oxidase inhibitor that blocks the cellular generation of H(2)O(2) and reduces the insulin-induced reduction of cellular PTPase activity, also diminished insulin-stimulated glucose uptake by 82% (P =.001). Glucose 232-239 insulin Homo sapiens 142-149 12800095-8 2003 Cellular treatment with diphenyleneiodonium (DPI), an NADPH oxidase inhibitor that blocks the cellular generation of H(2)O(2) and reduces the insulin-induced reduction of cellular PTPase activity, also diminished insulin-stimulated glucose uptake by 82% (P =.001). Glucose 232-239 insulin Homo sapiens 213-220 12800095-9 2003 These data suggest that total cellular PTPase activity, but not the activity of PTP1B, is higher in more obese subjects and is negatively associated with insulin-stimulated glucose transport. Glucose 173-180 insulin Homo sapiens 154-161 12800095-10 2003 The insulin-stimulated oxidative inhibition of PTPases may also have an important permissive role in the transmission of the insulin signal to glucose transport in human adipocytes. Glucose 143-150 insulin Homo sapiens 4-11 12800095-10 2003 The insulin-stimulated oxidative inhibition of PTPases may also have an important permissive role in the transmission of the insulin signal to glucose transport in human adipocytes. Glucose 143-150 insulin Homo sapiens 125-132 12800106-2 2003 Although increased insulin sensitivity of glucose disposal and lipolysis has been reported, the exact mechanism by which the risk reduction is conferred is not clear. Glucose 42-49 insulin Homo sapiens 19-26 12761338-8 2003 After stimulation with glucose, human insulin promoter-mediated gene expression was inhibited in normal, mature islet cells by both tacrolimus and cyclosporin A to a large extent (approximately 70%) and with high potency at concentrations that are known to inhibit calcineurin phosphatase activity (IC50 values of 1 and 35 nM, respectively). Glucose 23-30 insulin Homo sapiens 38-45 12948164-6 2003 The proteins that are involved in glucose and fat metabolism and hence can influence insulin resistance are discussed in this paper. Glucose 34-41 insulin Homo sapiens 85-92 12761338-9 2003 Furthermore, glucose stimulated calcineurin phosphatase activity in mouse pancreatic islets, further supporting the view that calcineurin phosphatase activity is an essential part of glucose signaling to the human insulin gene. Glucose 13-20 insulin Homo sapiens 214-221 12761338-9 2003 Furthermore, glucose stimulated calcineurin phosphatase activity in mouse pancreatic islets, further supporting the view that calcineurin phosphatase activity is an essential part of glucose signaling to the human insulin gene. Glucose 183-190 insulin Homo sapiens 214-221 12728367-6 2003 Amplitude and frequency-dependent adaptations of PTH and insulin outflow fail in CRF, as assessed under steady-state conditions and during metabolic drive (i.e., calcium for PTH and glucose for insulin). Glucose 182-189 insulin Homo sapiens 194-201 12637564-1 2003 Insulin stimulates glucose uptake in skeletal muscle cells and fat cells by promoting the rapid translocation of GLUT4 glucose transporters to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 12881876-1 2003 OBJECTIVE: To explore the dynamic change of serum cortisol and insulin levels, and their relation with blood glucose concentration in asphyxiated neonates. Glucose 109-116 insulin Homo sapiens 63-70 12644458-0 2003 High glucose inhibits insulin-stimulated nitric oxide production without reducing endothelial nitric-oxide synthase Ser1177 phosphorylation in human aortic endothelial cells. Glucose 5-12 insulin Homo sapiens 22-29 12644458-2 2003 Because hyperglycemia contributes to endothelial dysfunction and decreased NO availability in types 1 and 2 diabetes mellitus, we have studied the effects of high glucose (25 mM, 48 h) on insulin signaling pathways that regulate NO production in human aortic endothelial cells. Glucose 163-170 insulin Homo sapiens 188-195 12644458-3 2003 High glucose inhibited insulin-stimulated NO synthesis but was without effect on NO synthesis stimulated by increasing intracellular Ca2+ concentration. Glucose 5-12 insulin Homo sapiens 23-30 12644458-5 2003 Inhibition of insulin-stimulated NO synthesis by high glucose was unaffected by an inhibitor of PKC. Glucose 54-61 insulin Homo sapiens 14-21 12644458-6 2003 Furthermore, high glucose down-regulated the expression of CAP and Cbl, and insulin-stimulated Cbl phosphorylation, components of an insulin signaling cascade previously characterized in adipocytes. Glucose 18-25 insulin Homo sapiens 133-140 12644458-7 2003 These data suggest that high glucose specifically inhibits insulin-stimulated NO synthesis and down-regulates some aspects of insulin signaling, including the CAP-Cbl signaling pathway, yet this is not a result of reduced PKB-mediated eNOS phosphorylation at Ser1177. Glucose 29-36 insulin Homo sapiens 59-66 12644458-7 2003 These data suggest that high glucose specifically inhibits insulin-stimulated NO synthesis and down-regulates some aspects of insulin signaling, including the CAP-Cbl signaling pathway, yet this is not a result of reduced PKB-mediated eNOS phosphorylation at Ser1177. Glucose 29-36 insulin Homo sapiens 126-133 12761365-7 2003 Both diets significantly decreased diastolic blood pressure and the insulin response to an oral glucose load. Glucose 96-103 insulin Homo sapiens 68-75 12637564-4 2003 In L6 myotubes expressing GLUT4 that carries an exofacial myc-epitope (L6-GLUT4myc), insulin-stimulated GLUT4myc translocation equals in magnitude the glucose uptake response. Glucose 151-158 insulin Homo sapiens 85-92 12637564-5 2003 Inhibition of p38 MAPK with SB203580 reduces insulin-stimulated glucose uptake without affecting GLUT4myc translocation. Glucose 64-71 insulin Homo sapiens 45-52 12719278-2 2003 METHODS AND RESULTS: Insulin resistance was measured with a frequently sampled intravenous glucose tolerance test in the Insulin Resistance Atherosclerosis Study (IRAS), and PAI-1 4G/5G promoter genotype was established by allele-specific polymerase chain reaction amplification of genomic DNA. Glucose 91-98 insulin Homo sapiens 21-28 12637564-6 2003 In contrast, in myoblasts, the magnitude of insulin-stimulated glucose uptake is significantly lower than that of GLUT4myc translocation and is insensitive to SB203580. Glucose 63-70 insulin Homo sapiens 44-51 12743033-1 2003 Insulin stimulates glucose uptake in muscle and adipose cells by mobilizing intracellular membrane vesicles containing GLUT4 glucose transporter proteins to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 12743229-4 2003 Impaired insulin sensitivity was defined by a value of < or =2.5 on the Composite Insulin Sensitivity Index derived from insulin and glucose values during the test. Glucose 136-143 insulin Homo sapiens 9-16 12686458-8 2003 PACAP significantly potentiated glucose-stimulated insulin release in isolated islets of normal but not of GK rats. Glucose 32-39 insulin Homo sapiens 51-58 12743229-4 2003 Impaired insulin sensitivity was defined by a value of < or =2.5 on the Composite Insulin Sensitivity Index derived from insulin and glucose values during the test. Glucose 136-143 insulin Homo sapiens 85-92 12747853-1 2003 Insulin secretion is thought principally to be regulated by blood glucose concentration. Glucose 66-73 insulin Homo sapiens 0-7 12766740-3 2003 METHODS: Different indices of insulin sensitivity were obtained by an oral glucose tolerance test (OGTT) in 13 young women with syncope and HUT+ (age 26.8 +/- 9.1 years, body mass index 20.4 +/- 2.1), 8 patients with HUT- (age 26 +/- 5.6 years, body mass index 21.9 +/- 2.4), and 13 control subjects without syncope and HUT- (age 28.9 +/- 8.8 years, body mass index 23.1 +/- 1.7). Glucose 75-82 insulin Homo sapiens 30-37 12711303-4 2003 Among the subtypes, DCAPL3 shows significant homology with CAP, an essential component of glucose transport in insulin signal. Glucose 90-97 insulin Homo sapiens 111-118 12529176-7 2003 By reverse transcriptase PCR, immunohistochemistry and RIA, it is shown that stable transfected cells are able to form embryod bodies that produce insulin in response to glucose stimulation. Glucose 170-177 insulin Homo sapiens 147-154 12540375-0 2003 Aberrant insulin-induced GLUT4 translocation predicts glucose intolerance in the offspring of a diabetic mother. Glucose 54-61 insulin Homo sapiens 9-16 12751831-2 2003 In order to obtain a more physiological replacement therapy different approaches have been pursued since the early 70s to create an artificial wearable pancreas able to deliver insulin according to the blood glucose values as determined by continuous monitoring. Glucose 208-215 insulin Homo sapiens 177-184 12827286-1 2003 In mature human skeletal muscle, insulin-stimulated glucose transport is mediated primarily via the GLUT4 glucose transporter. Glucose 52-59 insulin Homo sapiens 33-40 12827286-4 2003 We demonstrate that insulin-stimulated glucose transport in cultured human skeletal muscle is mediated by GLUT4, as no effect on GLUT1 appearance at the plasma membrane was noted. Glucose 39-46 insulin Homo sapiens 20-27 12827286-6 2003 Incubation of differentiated human skeletal muscle cells with a non-peptide insulin mimetic significantly (p < 0.05) increased glucose uptake and glycogen synthesis. Glucose 130-137 insulin Homo sapiens 76-83 12706316-5 2003 In men, insulin sensitivity, as determined by glucose infusion rate during euglycemic hyperinsulinemic clamp, was inversely correlated with total body fat, abdominal fat, BMI and waist circumference, whereas only total body fat, but not abdominal fat, BW and hip circumference were inversely correlated with insulin sensitivity in women. Glucose 46-53 insulin Homo sapiens 8-15 12697158-3 2003 Conventional medical and nursing practitioners often incorrectly assume that they are used to control blood glucose levels, e.g. using herbal medicines to increase insulin production or reduce insulin resistance. Glucose 108-115 insulin Homo sapiens 164-171 12716734-4 2003 Insulin and AICAR increased glucose transport and cell-surface GLUT4 content to a similar extent in control subjects. Glucose 28-35 insulin Homo sapiens 0-7 12716734-5 2003 In contrast, insulin- and AICAR-stimulated responses on glucose transport and cell-surface GLUT4 content were impaired in subjects with type 2 diabetes. Glucose 56-63 insulin Homo sapiens 13-20 12716734-6 2003 Importantly, exposure of type 2 diabetic skeletal muscle to a combination of insulin and AICAR increased glucose transport and cell-surface GLUT4 content to levels achieved in control subjects. Glucose 105-112 insulin Homo sapiens 77-84 12716734-8 2003 Our studies highlight the potential importance of AMPK-dependent pathways in the regulation of GLUT4 and glucose transport activity in insulin-resistant skeletal muscle. Glucose 105-112 insulin Homo sapiens 135-142 12706316-5 2003 In men, insulin sensitivity, as determined by glucose infusion rate during euglycemic hyperinsulinemic clamp, was inversely correlated with total body fat, abdominal fat, BMI and waist circumference, whereas only total body fat, but not abdominal fat, BW and hip circumference were inversely correlated with insulin sensitivity in women. Glucose 46-53 insulin Homo sapiens 91-98 12706317-3 2003 Insulin secretion was estimated by means of HOMA(beta-cell), DeltaI(30-0)/DeltaG(30-0) ratio and the insulin concentration at 30 min post-glucose load (I(30)). Glucose 138-145 insulin Homo sapiens 0-7 12716762-4 2003 Insulin resistance was measured by the homeostasis model assessment of insulin resistance (HOMA-IR) using fasting insulin and glucose. Glucose 126-133 insulin Homo sapiens 0-7 12716734-9 2003 Activation of AMPK is an attractive strategy to enhance glucose transport through increased cell surface GLUT4 content in insulin-resistant skeletal muscle. Glucose 56-63 insulin Homo sapiens 122-129 12716738-0 2003 Restoration of euglycemia and normal acute insulin response to glucose in obese subjects with type 2 diabetes following bariatric surgery. Glucose 63-70 insulin Homo sapiens 43-50 12716738-1 2003 Insulin resistance and loss of glucose-stimulated acute insulin response (AIR) are the two major and earliest defects in the course of type 2 diabetes. Glucose 31-38 insulin Homo sapiens 56-63 12716762-4 2003 Insulin resistance was measured by the homeostasis model assessment of insulin resistance (HOMA-IR) using fasting insulin and glucose. Glucose 126-133 insulin Homo sapiens 71-78 12716767-8 2003 Children carrying the G171A variant had higher 30-min insulin responses to a glucose load (P = 0.03). Glucose 77-84 insulin Homo sapiens 54-61 12716746-5 2003 However, plasma insulin levels in transgenic mice were higher after glucose loading. Glucose 68-75 insulin Homo sapiens 16-23 12752487-7 2003 Insulin requirement during pregnancy and a diagnosis of gestational diabetes prior to 20 weeks of pregnancy were predictive for persistent postpartum glucose intolerance amongst Indo-Asians. Glucose 150-157 insulin Homo sapiens 0-7 12716794-1 2003 OBJECTIVE: Insulin lispro (Humalog), a human insulin analog, has a more rapid onset, earlier peak, and shorter duration of glucose lowering activity than regular human insulin. Glucose 123-130 insulin Homo sapiens 11-18 12716795-3 2003 RESEARCH DESIGN AND METHODS: The Botnia clamp measures the first-phase insulin response (FPIR) to 0.3g/kg glucose i.v. Glucose 106-113 insulin Homo sapiens 71-78 12716795-4 2003 and insulin sensitivity (M-value) from a 2-h euglycemic clamp begun 60 min after the glucose bolus. Glucose 85-92 insulin Homo sapiens 4-11 12917066-5 2003 The patient required large doses of insulin to control plasma glucose, and further work-up confirmed the presence of Cushing"s syndrome caused by ectopic production of corticotropin from a metastatic gastrinoma. Glucose 62-69 insulin Homo sapiens 36-43 12700065-1 2003 Fusion of GLUT4 vesicles with the plasma membrane is a key terminal step in insulin-regulated glucose transport. Glucose 94-101 insulin Homo sapiens 76-83 12626433-2 2003 Much information has been gathered on the homeostasis mechanisms of glucose regulation by insulin-producing pancreatic beta cells. Glucose 68-75 insulin Homo sapiens 90-97 12700065-5 2003 We review here insulin-mediated signaling of glucose transport, and particularly the role played by SNAREs and their accessory proteins. Glucose 45-52 insulin Homo sapiens 15-22 12784183-2 2003 They do this by inhibiting insulin-stimulated glucose uptake and glycogen synthesis. Glucose 46-53 insulin Homo sapiens 27-34 12739988-3 2003 Improving insulin sensitivity with lifestyle modifications or medications usually improves glucose and lipid levels in patients with diabetes and hyperlipidaemia. Glucose 91-98 insulin Homo sapiens 10-17 12739988-4 2003 Improving insulin sensitivity is expected to improve the liver disease but in many diabetic/hyperlipidaemic patients with NAFLD, the appropriate control of glucose and lipid levels is not always accompanied by improvement of the liver condition. Glucose 156-163 insulin Homo sapiens 10-17 12714010-3 2003 This protein is characterized by its ability to interact with anti-insulin antibodies and by mimicking insulin actions as the stimulation of glucose oxidation to CO(2) and lipogenesis in isolated rat adipocytes. Glucose 141-148 insulin Homo sapiens 103-110 12727005-5 2003 RESULTS: Compared to that in control subjects, plasma high-density lipoprotein was reduced (P<0.001) and insulin to glucose ratio increased (P=0.02) in CAD patients. Glucose 119-126 insulin Homo sapiens 108-115 12848074-3 2003 Insulin, in fact, exerts a direct effect on biological properties of myocytes by increasing the transmembrane glucose transport through glucose-specific insulin-regulated receptors, whose gene expression is down-regulated since the initial stages of myocyte hypertrophy. Glucose 110-117 insulin Homo sapiens 0-7 12792353-0 2003 Quantification of insulin-mediated glucose disposal in HIV-infected individuals: comparison of patients treated and untreated with protease inhibitors. Glucose 35-42 insulin Homo sapiens 18-25 12848074-3 2003 Insulin, in fact, exerts a direct effect on biological properties of myocytes by increasing the transmembrane glucose transport through glucose-specific insulin-regulated receptors, whose gene expression is down-regulated since the initial stages of myocyte hypertrophy. Glucose 110-117 insulin Homo sapiens 153-160 12792353-6 2003 PI-treated patients also had significantly higher plasma glucose (p =.001) and insulin (p =.03) responses to the oral glucose challenge. Glucose 118-125 insulin Homo sapiens 79-86 12727954-0 2003 Insulin-mediated hepatic glucose uptake is impaired in type 2 diabetes: evidence for a relationship with glycemic control. Glucose 25-32 insulin Homo sapiens 0-7 12682906-3 2003 PPARgamma is a member of the ligand-activated nuclear receptor superfamily that promotes adipogenesis and enhances insulin sensitivity by controlling the expression of genes in glucose and lipid metabolism. Glucose 177-184 insulin Homo sapiens 115-122 12686440-4 2003 However, the non-significant increase of serum glucose at 1 h of khat chewing corresponded with a significant increase of serum C-peptide (22%) levels. Glucose 47-54 insulin Homo sapiens 128-137 12740013-4 2003 Insulin release in response to increasing glucose concentrations in the incubation medium (2-16 mM glucose) did not increase in pancreata from either C or S offspring. Glucose 42-49 insulin Homo sapiens 0-7 12740013-4 2003 Insulin release in response to increasing glucose concentrations in the incubation medium (2-16 mM glucose) did not increase in pancreata from either C or S offspring. Glucose 99-106 insulin Homo sapiens 0-7 12771873-3 2003 We hypothesized that strict glucose control with a continuous insulin infusion in the perioperative period would reduce hospital mortality. Glucose 28-35 insulin Homo sapiens 62-69 12730484-8 2003 The relationship between decreased maternal insulin sensitivity and fetal overgrowth particularly in obese women and women with gestational diabetes may help explain the increased incidence of adolescent obesity and related glucose intolerance in the offspring of these women. Glucose 224-231 insulin Homo sapiens 44-51 12771873-13 2003 The protective effect of continuous insulin infusion may stem from the effective metabolic use of excess glucose to favorably alter pathways of myocardial adenosine triphosphate production. Glucose 105-112 insulin Homo sapiens 36-43 12759893-11 2003 In conclusion, this study shows an association between high levels of circulating TG and insulin resistance in patients with normal glucose tolerance seen in an atherosclerosis prevention clinic. Glucose 132-139 insulin Homo sapiens 89-96 12759893-0 2003 Hypertriglyceridemia is associated with increased insulin resistance in subjects with normal glucose tolerance: evaluation in a large cohort of subjects assessed with the 1999 World Health Organization criteria for the classification of diabetes. Glucose 93-100 insulin Homo sapiens 50-57 12759893-5 2003 Insulin resistance was calculated by a homeostasis model assessment (HOMA(IR) = fasting serum insulin [mU/mL] x fasting blood glucose [mmol/L]/22.5). Glucose 126-133 insulin Homo sapiens 0-7 12765847-7 2003 During a low dose insulin infusion, non-diabetic individuals with the variant genotype had a lower mean glucose oxidation (1.9+/-0.11 vs. 2.0+/-0.03 mg/kgEMBS/min; p=0.04) and total glucose turnover rate (2.5+/-0.22 vs. 2.6+/-0.06 mg/kgEMBS/min; p=0.01) compared to subjects with the wild-type genotype. Glucose 104-111 insulin Homo sapiens 18-25 12740452-1 2003 OBJECTIVE: Insulin resistance is observed in individuals with normal glucose tolerance. Glucose 69-76 insulin Homo sapiens 11-18 12740452-6 2003 Insulin sensitivity was assessed from the ratio of whole-body glucose use (6,6 (2)H(2) glucose) to plasma insulin concentrations. Glucose 62-69 insulin Homo sapiens 0-7 12740452-6 2003 Insulin sensitivity was assessed from the ratio of whole-body glucose use (6,6 (2)H(2) glucose) to plasma insulin concentrations. Glucose 87-94 insulin Homo sapiens 0-7 12828193-6 2003 Food structure plays an important role in determining the accessibility of starch to digestion, thus influencing the postprandial blood glucose response, which modulates plasma insulin and lipid levels. Glucose 136-143 insulin Homo sapiens 177-184 12702748-6 2003 In contrast, hepatic glucose production was fully suppressed by insulin in diabetic subjects. Glucose 21-28 insulin Homo sapiens 64-71 12707306-1 2003 Glucokinase (GK) activity plays a key role in glucose-stimulated insulin secretion from pancreatic beta cells. Glucose 46-53 insulin Homo sapiens 65-72 12700357-1 2003 Insulin secretion is controlled by the beta cell"s metabolic state, and the ability of the secretory granules to undergo exocytosis increases during glucose stimulation in a membrane potential-independent fashion. Glucose 149-156 insulin Homo sapiens 0-7 12721671-5 2003 PATHOPHYSIOLOGY: Glucocorticoids antagonize the insulin-mediated inhibition of hepatic glucose release, decrease glucose utilisation in muscle, and reduce the binding affinity of insulin receptors. Glucose 87-94 insulin Homo sapiens 48-55 12721671-5 2003 PATHOPHYSIOLOGY: Glucocorticoids antagonize the insulin-mediated inhibition of hepatic glucose release, decrease glucose utilisation in muscle, and reduce the binding affinity of insulin receptors. Glucose 113-120 insulin Homo sapiens 48-55 12721672-1 2003 BACKGROUND: HIV protease inhibitors improve the morbidity and mortality of HIV infection, however, this therapy also initiates insulin resistance that is associated with an increasing development of disturbances in glucose and lipid metabolism. Glucose 215-222 insulin Homo sapiens 127-134 12721674-2 2003 A major pathophysiological event in this process is an increased glucose production of the liver on the basis of glucocorticoid-induced insulin resistance resulting in an increment in hepatic gluconeogenesis. Glucose 65-72 insulin Homo sapiens 136-143 12566459-0 2003 Cdc42 is a Rho GTPase family member that can mediate insulin signaling to glucose transport in 3T3-L1 adipocytes. Glucose 74-81 insulin Homo sapiens 53-60 12566459-1 2003 We investigated the role of cdc42, a Rho GTPase family member, in insulin-induced glucose transport in 3T3-L1 adipocytes. Glucose 82-89 insulin Homo sapiens 66-73 12697301-1 2003 Variation in the insulin responsive element (IRE) of the APOC3 promoter has been shown to be associated with insulin and glucose concentrations after an oral glucose tolerance test (OGTT) in young healthy men. Glucose 121-128 insulin Homo sapiens 17-24 12697301-1 2003 Variation in the insulin responsive element (IRE) of the APOC3 promoter has been shown to be associated with insulin and glucose concentrations after an oral glucose tolerance test (OGTT) in young healthy men. Glucose 158-165 insulin Homo sapiens 17-24 12697301-1 2003 Variation in the insulin responsive element (IRE) of the APOC3 promoter has been shown to be associated with insulin and glucose concentrations after an oral glucose tolerance test (OGTT) in young healthy men. Glucose 158-165 insulin Homo sapiens 109-116 12639698-2 2003 However, in some tissues, studies have shown that troglitazone also has an acute insulin-independent effect on glucose uptake. Glucose 111-118 insulin Homo sapiens 81-88 12687004-1 2003 Insulin stimulates glucose transport by promoting exocytosis of the glucose transporter Glut4 (refs 1, 2). Glucose 19-26 insulin Homo sapiens 0-7 12687004-6 2003 Overexpression of an Exo70 mutant blocked insulin-stimulated glucose uptake, but not the trafficking of Glut4 to the plasma membrane. Glucose 61-68 insulin Homo sapiens 42-49 12569623-3 2003 Our main objective was to characterize the diffusion of model proteins (insulin, lysozyme, and BSA) through the membrane, in response to changes in environmental glucose concentrations. Glucose 162-169 insulin Homo sapiens 72-79 12569623-8 2003 Changes in the transport properties of the membranes in response to glucose were explored and it was found that, while 0.1M D-glucose caused a substantial, but saturateable, increase in the rates of diffusion of both insulin and lysozyme, controls using glycerol or L-glucose (0.1M) had no significant effect. Glucose 68-75 insulin Homo sapiens 217-224 12569623-8 2003 Changes in the transport properties of the membranes in response to glucose were explored and it was found that, while 0.1M D-glucose caused a substantial, but saturateable, increase in the rates of diffusion of both insulin and lysozyme, controls using glycerol or L-glucose (0.1M) had no significant effect. Glucose 124-133 insulin Homo sapiens 217-224 12659868-1 2003 Cell-based therapies for treating insulin-dependent diabetes (IDD) can provide a more physiologic regulation of blood glucose levels in a less invasive fashion than daily insulin injections. Glucose 118-125 insulin Homo sapiens 34-41 12700357-2 2003 Here, we demonstrate that exocytosis of insulin-containing secretory granules depends on phosphatidylinositol 4-kinase (PI 4-kinase) activity and that inhibition of this enzyme suppresses glucose-stimulated insulin secretion. Glucose 188-195 insulin Homo sapiens 40-47 12700357-2 2003 Here, we demonstrate that exocytosis of insulin-containing secretory granules depends on phosphatidylinositol 4-kinase (PI 4-kinase) activity and that inhibition of this enzyme suppresses glucose-stimulated insulin secretion. Glucose 188-195 insulin Homo sapiens 207-214 12466146-4 2003 Insulin sensitivity was restored to 321.7 +/- 44.7 mg glucose/kg after administration of an NO donor, intraportal SIN-1 (5 mg/kg), which promotes GSH nitrosation, but not after intraportal sodium nitroprusside (20 nmol x kg(-1) x min(-1)), which does not nitrosate GSH. Glucose 54-61 insulin Homo sapiens 0-7 12388147-2 2003 The effects of acromegaly and of its surgical cure on the insulin sensitivity of glucose and amino acid/protein metabolism were evaluated by infusing [6,6-(2)H(2)]glucose, [1-(13)C]leucine, and [2-(15)N]glutamine during a euglycemic insulin (1 mU x kg(-1) x min(-1)) clamp in 12 acromegalic patients, six studied again 6 mo after successful adenomectomy, and eight healthy controls. Glucose 81-88 insulin Homo sapiens 58-65 12388147-2 2003 The effects of acromegaly and of its surgical cure on the insulin sensitivity of glucose and amino acid/protein metabolism were evaluated by infusing [6,6-(2)H(2)]glucose, [1-(13)C]leucine, and [2-(15)N]glutamine during a euglycemic insulin (1 mU x kg(-1) x min(-1)) clamp in 12 acromegalic patients, six studied again 6 mo after successful adenomectomy, and eight healthy controls. Glucose 163-170 insulin Homo sapiens 58-65 12388147-6 2003 Within 6 mo, surgery reverses insulin resistance for glucose but not for protein metabolism. Glucose 53-60 insulin Homo sapiens 30-37 12672678-3 2003 Baseline insulin sensitivity (S(I)) was measured by means of a 12-sample, insulin-enhanced, frequently sampled intravenous glucose tolerance test. Glucose 123-130 insulin Homo sapiens 74-81 12672678-4 2003 Insulin secretion was assessed in terms of acute insulin response and disposition index, both obtained from the frequently sampled intravenous glucose tolerance test. Glucose 143-150 insulin Homo sapiens 0-7 12747594-9 2003 The A/G variation at position -308 in the promoter region of the TNF-alpha gene could be an important genetic factor predisposing to insulin resistance in obese women and increased levels of glucose, triglyceride, and free fatty acids in men. Glucose 191-198 insulin Homo sapiens 133-140 12716078-2 2003 Glucose infusion rate (GIR) derived from the clamp study was used as an index of insulin resistance. Glucose 0-7 insulin Homo sapiens 81-88 12663568-8 2003 By adjusting this shape index for glucose(AUC) (as continuous measure of glucose tolerance), correlations with age, BMI, WHR, HbA(1c), and insulin(AUC) were completely abolished. Glucose 34-41 insulin Homo sapiens 42-45 12663461-13 2003 The present study indicates that protease inhibitor-containing regimens impair glucose tolerance in HIV-infected patients by two mechanisms: 1) inducement of peripheral insulin resistance in skeletal muscle and adipose tissue and 2) impairment of the ability of the beta-cell to compensate. Glucose 79-86 insulin Homo sapiens 169-176 12663464-1 2003 Recent evidence has shown that activation of phosphatidyinositol-3-kinase (PI3K) and Akt, necessary for insulin stimulation of glucose transport, is impaired in insulin resistance. Glucose 127-134 insulin Homo sapiens 104-111 12663464-1 2003 Recent evidence has shown that activation of phosphatidyinositol-3-kinase (PI3K) and Akt, necessary for insulin stimulation of glucose transport, is impaired in insulin resistance. Glucose 127-134 insulin Homo sapiens 161-168 12663568-8 2003 By adjusting this shape index for glucose(AUC) (as continuous measure of glucose tolerance), correlations with age, BMI, WHR, HbA(1c), and insulin(AUC) were completely abolished. Glucose 34-41 insulin Homo sapiens 147-150 12663464-3 2003 Additionally, related growth factors (epidermal or platelet-derived vascular) also stimulate PI3K, but it is unknown whether production of 3,4,5 phosphatidyinositol is sufficient to stimulate glucose transport in insulin-resistant muscle. Glucose 192-199 insulin Homo sapiens 213-220 12663568-8 2003 By adjusting this shape index for glucose(AUC) (as continuous measure of glucose tolerance), correlations with age, BMI, WHR, HbA(1c), and insulin(AUC) were completely abolished. Glucose 73-80 insulin Homo sapiens 42-45 12663464-9 2003 These results show that a defect in the ability of insulin to activate Akt-2 and -3 may explain the impaired insulin-stimulated glucose transport in insulin resistance. Glucose 128-135 insulin Homo sapiens 51-58 12663464-9 2003 These results show that a defect in the ability of insulin to activate Akt-2 and -3 may explain the impaired insulin-stimulated glucose transport in insulin resistance. Glucose 128-135 insulin Homo sapiens 109-116 12663568-8 2003 By adjusting this shape index for glucose(AUC) (as continuous measure of glucose tolerance), correlations with age, BMI, WHR, HbA(1c), and insulin(AUC) were completely abolished. Glucose 73-80 insulin Homo sapiens 147-150 12663464-9 2003 These results show that a defect in the ability of insulin to activate Akt-2 and -3 may explain the impaired insulin-stimulated glucose transport in insulin resistance. Glucose 128-135 insulin Homo sapiens 109-116 12746615-5 2003 In glucose intolerant subjects, insulin secretion is more consistently altered, specially acute insulin response to glucose. Glucose 3-10 insulin Homo sapiens 32-39 12663620-0 2003 Glucose response to intense aerobic exercise in type 1 diabetes: maintenance of near euglycemia despite a drastic decrease in insulin dose. Glucose 0-7 insulin Homo sapiens 126-133 12675646-7 2003 Post-prandial glucose values were lower and the area under the 24-h self-monitored blood glucose curve above 7.0 mmol/l was 28% smaller with insulin aspart (35.2 +/- 3.2 vs. 48.9 +/- 3.1 mmol/l h, P = 0.0015). Glucose 14-21 insulin Homo sapiens 141-148 12675646-7 2003 Post-prandial glucose values were lower and the area under the 24-h self-monitored blood glucose curve above 7.0 mmol/l was 28% smaller with insulin aspart (35.2 +/- 3.2 vs. 48.9 +/- 3.1 mmol/l h, P = 0.0015). Glucose 89-96 insulin Homo sapiens 141-148 12746615-5 2003 In glucose intolerant subjects, insulin secretion is more consistently altered, specially acute insulin response to glucose. Glucose 116-123 insulin Homo sapiens 32-39 12746615-8 2003 The markers of the transition to glucose intolerance are both insulin resistance and acute insulin response. Glucose 33-40 insulin Homo sapiens 62-69 12746615-8 2003 The markers of the transition to glucose intolerance are both insulin resistance and acute insulin response. Glucose 33-40 insulin Homo sapiens 91-98 12746632-6 2003 Insulin-mediated glucose disposal, stimulation of glucose oxidation and suppression of endogenous glucose production were identical after metformin and placebo. Glucose 17-24 insulin Homo sapiens 0-7 12746628-13 2003 Pump control by the sensor signal is conceivable if it corresponds to a direct, continuous, real time measurement of blood glucose, and subject to a simultaneous improvement of insulin infusion modes. Glucose 123-130 insulin Homo sapiens 177-184 12803245-5 2003 An insulin-modified intravenous glucose tolerance test was performed before and at 16 h and 1 week after the last training session to determine SI using a minimal-model approach. Glucose 32-39 insulin Homo sapiens 3-10 12662161-5 2003 RESULTS: In multivariate analysis, insulin-mediated glucose uptake was positively [standardized beta, 0.21 (P = 0.05)] associated with the carotid artery compliance coefficient, and the use of alcohol was negatively associated with the femoral artery compliance coefficient [standardized beta, -0.25 (P = 0.03)]. Glucose 52-59 insulin Homo sapiens 35-42 12715971-2 2003 This review will address the hypothesis that exercise training and the antioxidant R-(+)-lipoic acid interact at the level of insulin signaling to enhance glucose transport in insulin-resistant skeletal muscle. Glucose 155-162 insulin Homo sapiens 126-133 12715971-2 2003 This review will address the hypothesis that exercise training and the antioxidant R-(+)-lipoic acid interact at the level of insulin signaling to enhance glucose transport in insulin-resistant skeletal muscle. Glucose 155-162 insulin Homo sapiens 176-183 12737675-3 2003 Insulin resistance and beta-cell function were evaluated using the continuous infusion of glucose with model assessment (CIGMA) method, which aims to give a near-physiological stimulus and to evaluate the endogenous insulin and glucose response. Glucose 90-97 insulin Homo sapiens 216-223 12744226-7 2003 Also, a strong negative correlation between PAI-1 activity and insulin/glucose index was found. Glucose 71-78 insulin Homo sapiens 63-70 12660262-6 2003 RESULTS: Insulin resistance was found in the majority of PCOS patients: -53.5% (83/155), 60.6% (94/155) and 65.8% (102/155), when defined by fasting insulin, glucose:insulin ratio, or logHOMA respectively. Glucose 158-165 insulin Homo sapiens 9-16 12842410-12 2003 It has been previously proposed that the insulin resistance of pregnancy is an important adaptation to divert maternal glucose to meet the needs of the foetus. Glucose 119-126 insulin Homo sapiens 41-48 12686467-1 2003 Since the C-peptide/insulin ratio is reduced after oral glucose ingestion, the incretin hormone gastric inhibitory polypeptide (GIP) has been assumed to decrease hepatic insulin extraction. Glucose 56-63 insulin Homo sapiens 10-19 12686467-7 2003 The rise in insulin after oral glucose and after intravenous GIP administration significantly exceeded the rise in C-peptide (p<0.0001). Glucose 31-38 insulin Homo sapiens 12-19 12686467-8 2003 Estimating insulin extraction from the total integrated insulin and C-peptide concentrations (AUCs), only the oral glucose load (p<0.0001), but not the intravenous GIP administration (p=0.18) significantly reduced insulin clearance. Glucose 115-122 insulin Homo sapiens 11-18 12686467-9 2003 Therefore, insulin clearance is reduced after an oral glucose load. Glucose 54-61 insulin Homo sapiens 11-18 12698955-6 2003 Insulin-induced glucose uptake was markedly reduced in obese patients (19.5+/-1.9 micromol/min kg FFM) and improved with weight loss, but in the third study, it was still lower than that observed in controls (35.9+/-4.0 vs 52.9+/-2.2 micromol/min kg FFM). Glucose 16-23 insulin Homo sapiens 0-7 12698955-8 2003 CONCLUSION: Weight loss in severe obesity improved insulin-induced glucose uptake, and completely normalized the insulin inhibition on its own secretion. Glucose 67-74 insulin Homo sapiens 51-58 12714201-9 2003 CONCLUSION: Our data demonstrate that postprandial hyperinsulinemia is independently associated with coronary artery disease, irrespective of fasting glucose, postprandial glucose, and fasting insulin levels in nondiabetic women with clusterings of factors of metabolic syndrome. Glucose 172-179 insulin Homo sapiens 56-63 12679468-1 2003 The aim of the present study was to examine the effects of anorexia nervosa (AN) on adipocytokines (leptin and adiponectin) plasma concentrations and insulin-stimulated glucose disposal in adolescent and young adult women. Glucose 169-176 insulin Homo sapiens 150-157 12679468-2 2003 Adiponectin and leptin plasma levels, along with insulin-stimulated glucose disposal (as measured by the euglycemic-hyperinsulinemic glucose clamp) and oxidative and nonoxidative glucose metabolism (as measured by indirect calorimetry during the last 60 min of the insulin clamp), were measured in 11 anorectic patients and 26 normal-weight healthy female controls. Glucose 68-75 insulin Homo sapiens 49-56 12679468-5 2003 Likewise, insulin-stimulated glucose disposal and nonoxidative glucose metabolism were significantly lower in AN patients. Glucose 29-36 insulin Homo sapiens 10-17 12679468-6 2003 In conclusion, our study shows that young women affected by AN have higher adiponectin plasma levels than healthy female controls of similar age, despite the presence of an impairment of insulin-stimulated glucose disposal, with a prevalent failure of nonoxidative glucose metabolism. Glucose 206-213 insulin Homo sapiens 187-194 12679472-8 2003 Compared with control studies, both GLP-1-(7-36)NH(2) and GLP-1-(7-37) significantly increased acute insulin response to glucose, glucose disappearance constant, glucose effectiveness, and glucose effectiveness at zero insulin, but did not change the insulin sensitivity index. Glucose 121-128 insulin Homo sapiens 101-108 12679472-10 2003 In a second set of experiments, 10 healthy subjects had glucose-stimulated insulin secretion measured during an infusion of GLP-1-(7-36)NH(2) alone or with a simultaneous infusion of GLP-1-(9-36)NH(2) that increased plasma levels approximately 10-fold over those produced by unmetabolized GLP-1. Glucose 56-63 insulin Homo sapiens 75-82 12679472-11 2003 Augmentation of glucose-stimulated insulin secretion by GLP-1-(7-36)NH(2) was not altered by the coadministration of GLP-1-(9-36)NH(2). Glucose 16-23 insulin Homo sapiens 35-42 12854872-9 2003 However, the effect of milrinone on glucose concentration was detectable only in 25 micromol/kg group, and the plasma insulin levels were significantly elevated in the 5 and 25 micromol/kg milrinone groups, indicating that there was a dose-response relationship between milrinone and insulin and glucose levels. Glucose 296-303 insulin Homo sapiens 118-125 12854872-11 2003 CONCLUSIONS: These data suggest that milrinone impaired the abilities of insulin to suppress lipolysis and insulin-mediated glucose utilization in peripheral tissue, despite having a slight increase in insulin secretion. Glucose 124-131 insulin Homo sapiens 73-80 12854872-11 2003 CONCLUSIONS: These data suggest that milrinone impaired the abilities of insulin to suppress lipolysis and insulin-mediated glucose utilization in peripheral tissue, despite having a slight increase in insulin secretion. Glucose 124-131 insulin Homo sapiens 107-114 12663234-4 2003 Insulin sensitivity was measured using fasting insulin and glucose levels and liver fat content was estimated by CT imaging. Glucose 59-66 insulin Homo sapiens 0-7 12683697-8 2003 Superimposition of insulin resistance on a beta cell that cannot appropriately compensate leads to deterioration in glucose tolerance. Glucose 116-123 insulin Homo sapiens 19-26 12701051-0 2003 Influence of nervous blockade on insulin-mediated glucose uptake in the human forearm. Glucose 50-57 insulin Homo sapiens 33-40 12701051-9 2003 Furthermore, insulin induced vasodilation in the blocked arm, but delayed the ability of insulin to promote glucose extraction, suggesting that the well-documented increase in skeletal muscle sympathetic nerve activity seen during acute hyperinsulinemia has metabolic rather than hemodynamic consequences. Glucose 108-115 insulin Homo sapiens 13-20 12701051-9 2003 Furthermore, insulin induced vasodilation in the blocked arm, but delayed the ability of insulin to promote glucose extraction, suggesting that the well-documented increase in skeletal muscle sympathetic nerve activity seen during acute hyperinsulinemia has metabolic rather than hemodynamic consequences. Glucose 108-115 insulin Homo sapiens 89-96 12701062-8 2003 In conclusion, both impaired insulin secretion and insulin resistance may contribute to the underlying mechanisms of glucose intolerance in Japanese subjects. Glucose 117-124 insulin Homo sapiens 29-36 12640462-2 2003 Glucose stimulates insulin secretion from beta-cells but suppresses the release of glucagon, a hormone that raises blood glucose, from alpha-cells. Glucose 0-7 insulin Homo sapiens 19-26 12671116-7 2003 CONCLUSIONS: In early postnatal life, SGA infants display an increased insulin sensitivity with respect to glucose disposal but not with respect to suppression of lipolysis, ketogenesis, and hepatic production of IGFBP-1. Glucose 107-114 insulin Homo sapiens 71-78 12931487-10 2003 We showed significant differences in insulin sensitivity between the studied groups, an index of the whole-body glucose uptake was decreased in both obese groups in comparison to controls, and it was also lower in IGT than in obese NGT group. Glucose 112-119 insulin Homo sapiens 37-44 12609749-6 2003 Hence, low concentrations of IAPP brought about a modest increase of basal insulin secretion at 7 mM glucose and also of insulin release stimulated by carbachol. Glucose 101-108 insulin Homo sapiens 75-82 12704745-2 2003 The aim of this study was to investigate if, with good glucose control achieved with continuous subcutaneous insulin infusion, normal blood flow within the fetal heart can be achieved. Glucose 55-62 insulin Homo sapiens 109-116 12609749-7 2003 High concentrations of IAPP, however, inhibited insulin release stimulated by glucose (10 and 16.7 mM), IBMX, carbachol and L-arginine. Glucose 78-85 insulin Homo sapiens 48-55 12730030-5 2003 Insulin-stimulated glucose disposal was analysed by euglycemic-hyperinsulinemic clamp. Glucose 19-26 insulin Homo sapiens 0-7 12663403-10 2003 A significant interaction existed between proinsulin concentration (a marker of insulin resistance) at baseline and antihypertensive treatment on increase in blood glucose. Glucose 164-171 insulin Homo sapiens 42-52 12663403-10 2003 A significant interaction existed between proinsulin concentration (a marker of insulin resistance) at baseline and antihypertensive treatment on increase in blood glucose. Glucose 164-171 insulin Homo sapiens 45-52 12730030-7 2003 Furthermore, insulin-stimulated glucose disposal was virtually independent of genotype. Glucose 32-39 insulin Homo sapiens 13-20 12623203-7 2003 The glucose permeation studies showed that permeation of insulin increased in the presence of NaCl due to ion induced convective flow. Glucose 4-11 insulin Homo sapiens 57-64 12460121-4 2003 [(14)C]Glucose incorporation into glycogen was decreased and unaffected by insulin in Qc cells, whereas insulin stimulated glucose incorporation by approximately 50% in G3 cells. Glucose 123-130 insulin Homo sapiens 104-111 12510058-1 2003 We have investigated the mechanism by which high concentrations of glucose inhibit insulin stimulation of glycogen synthase. Glucose 67-74 insulin Homo sapiens 83-90 12496259-1 2003 It is well established that insulin stimulation of glucose uptake requires the translocation of intracellular localized GLUT4 protein to the cell surface membrane. Glucose 51-58 insulin Homo sapiens 28-35 12591951-6 2003 The acute insulin response to glucose was not predictive of the development of diabetes when considered independently or when assessed as a function of S(I), i.e., the glucose disposition index. Glucose 30-37 insulin Homo sapiens 10-17 12587101-6 2003 We assessed the feasibility of adaptive stratification in the context of a clinical trial of insulin to control plasma glucose level following acute stroke. Glucose 119-126 insulin Homo sapiens 93-100 12629551-2 2003 Insulin is secreted from pancreatic beta cells in response to elevated plasma glucose, with various factors modifying its secretion. Glucose 78-85 insulin Homo sapiens 0-7 12618274-3 2003 The measurement of in vivo insulin sensitivity was performed using the minimal model analysis of the frequently sampled intravenous glucose tolerance test (FSIVGTT). Glucose 132-139 insulin Homo sapiens 27-34 12556346-3 2003 Among the last are the additive effects of insulin and contractions on glucose transport and GLUT4 translocation and the increases in muscle insulin sensitivity and responsiveness induced by exercise. Glucose 71-78 insulin Homo sapiens 43-50 12556352-2 2003 The insulin response to arginine at fasting (AIR(1)), at 14 mmol/l, and at >25 mmol/l glucose was reduced by 37-50% after 15 and 25% WR (P <or= 0.05). Glucose 89-96 insulin Homo sapiens 4-11 12556352-3 2003 Insulin sensitivity was determined as the amount of glucose infused to reach 14 mmol/l divided by the insulin level (M/I), a measure showing a linear correlation with insulin sensitivity during euglycemic hyperinsulinemic clamps (r = 0.74, P < 0.001) and a hyperbolic relation to AIR(1) (r = -0.63, P < 0.001) in 169 healthy subjects. Glucose 52-59 insulin Homo sapiens 0-7 12556352-3 2003 Insulin sensitivity was determined as the amount of glucose infused to reach 14 mmol/l divided by the insulin level (M/I), a measure showing a linear correlation with insulin sensitivity during euglycemic hyperinsulinemic clamps (r = 0.74, P < 0.001) and a hyperbolic relation to AIR(1) (r = -0.63, P < 0.001) in 169 healthy subjects. Glucose 52-59 insulin Homo sapiens 167-174 12614095-5 2003 Consequently, it is important to identify which overweight persons are most likely to be insulin resistant by considering their family history; blood pressure; and plasma glucose, triglyceride, and high-density lipoprotein cholesterol concentrations. Glucose 171-178 insulin Homo sapiens 89-96 12590018-6 2003 Glucose intolerance of the mothers was associated with an early middle-aged onset of diabetes, reduction in the insulin secretory capacity, early requirement of insulin therapy, and increases in the daily insulin dose. Glucose 0-7 insulin Homo sapiens 112-119 12594693-0 2003 Increased secretion of insulin during oral glucose tolerance test can be a predictor of stent restenosis in nondiabetic patients. Glucose 43-50 insulin Homo sapiens 23-30 12594693-9 2003 By multiple logistic regression analysis, insulin area during oral glucose tolerance test was found to be an independent predictor of stent restenosis (OR = 1.12; 95% CI = 1.01-1.25; P = 0.031). Glucose 67-74 insulin Homo sapiens 42-49 12608939-9 2003 Patients with the poorest growth exhibit low serum insulin concentration responses to glucose load, GH insensitivity and higher mean 24-h plasma cortisol levels when compared to those patients who were better grown. Glucose 86-93 insulin Homo sapiens 51-58 12606519-2 2003 If pancreatic K(ATP) channels localize to the insulin secretory granule, they would be well positioned to transduce changes in glucose metabolism into changes in granule transport and exocytosis. Glucose 127-134 insulin Homo sapiens 46-53 12640493-6 2003 Insulin sensitivity index (ISI) was the mean glucose infusion rate in the third hour of the clamp experiment divided by the mean plasma insulin concentration during the same period of time. Glucose 45-52 insulin Homo sapiens 0-7 12531425-0 2003 Mechanism of inhibition of insulin-stimulated glucose transport by 4-bromocrotonic acid in 3T3-L1 adipocytes. Glucose 46-53 insulin Homo sapiens 27-34 12531425-1 2003 We have demonstrated previously that 4-bromocrotonic acid (Br-C4) inhibited insulin-stimulated glucose transport by interfering with GLUT4 translocation. Glucose 95-102 insulin Homo sapiens 76-83 12531425-4 2003 However, time-course studies showed that only the inhibition of PKB activation correlated with the inhibition of insulin-stimulated glucose transport. Glucose 132-139 insulin Homo sapiens 113-120 12531425-8 2003 Taken together, these results support the notion that PKB is involved in insulin-stimulated glucose transport. Glucose 92-99 insulin Homo sapiens 73-80 12531425-9 2003 In addition, Br-C4 seems to inhibit insulin-stimulated glucose transport via inhibiting insulin activation of PKB, probably by interfering with insulin activation of an upstream kinase responsible for the phosphorylation of Ser(473/474) residue. Glucose 55-62 insulin Homo sapiens 36-43 12852706-2 2003 The synergistic effects of combining glipizide with metformin on glucose control may be realized by treating the primary effects of type 2 DM, impaired insulin secretion, and insulin resistance. Glucose 65-72 insulin Homo sapiens 152-159 12610035-10 2003 CONCLUSIONS: After inhaling insulin using the AERx iDMS, asthmatic subjects absorbed less insulin than healthy subjects, resulting in less reduction of serum glucose. Glucose 158-165 insulin Homo sapiens 28-35 12590018-6 2003 Glucose intolerance of the mothers was associated with an early middle-aged onset of diabetes, reduction in the insulin secretory capacity, early requirement of insulin therapy, and increases in the daily insulin dose. Glucose 0-7 insulin Homo sapiens 161-168 12610035-10 2003 CONCLUSIONS: After inhaling insulin using the AERx iDMS, asthmatic subjects absorbed less insulin than healthy subjects, resulting in less reduction of serum glucose. Glucose 158-165 insulin Homo sapiens 90-97 12590018-6 2003 Glucose intolerance of the mothers was associated with an early middle-aged onset of diabetes, reduction in the insulin secretory capacity, early requirement of insulin therapy, and increases in the daily insulin dose. Glucose 0-7 insulin Homo sapiens 161-168 12610039-19 2003 CONCLUSIONS: Extended administration of GLP-1 not only augments glucose-stimulated insulin secretion, but also shifts the dynamics of the insulin response to earlier release in both diabetic and nondiabetic humans. Glucose 64-71 insulin Homo sapiens 83-90 12590018-9 2003 Thus, this study has revealed that: (1) diabetes mellitus with the 3243 mutation is a subtype of diabetes mellitus with mitochondria-related complications; and (2) insulin secretory ability is more severely impaired in the patients whose mothers were glucose intolerance. Glucose 251-258 insulin Homo sapiens 164-171 12610040-8 2003 Total insulin dose required to achieve target blood glucose control was lower on LIS/GLAR (1.16 IU/kg) compared with R/NPH therapy (1.26 IU/kg, P < 0.005), but there was no significant difference in HbA(1c) levels (LIS/GLAR versus R/NPH: 8.7 vs. 9.1%, P = 0.13). Glucose 52-59 insulin Homo sapiens 6-13 12606497-0 2003 Selective glycogen synthase kinase 3 inhibitors potentiate insulin activation of glucose transport and utilization in vitro and in vivo. Glucose 81-88 insulin Homo sapiens 59-66 12610046-0 2003 Effect of glucagon-like peptide 1 (7-36 amide) on insulin-mediated glucose uptake in patients with type 1 diabetes. Glucose 67-74 insulin Homo sapiens 50-57 12610051-0 2003 Insulin secretion and insulin sensitivity pattern is different in isolated impaired glucose tolerance and impaired fasting glucose: the risk factor in Impaired Glucose Tolerance for Atherosclerosis and Diabetes study. Glucose 84-91 insulin Homo sapiens 0-7 12630938-7 2003 Fasting insulin and glucose levels contain sufficient information to assess insulin sensitivity over a wide range in a diverse population. Glucose 20-27 insulin Homo sapiens 76-83 12610051-0 2003 Insulin secretion and insulin sensitivity pattern is different in isolated impaired glucose tolerance and impaired fasting glucose: the risk factor in Impaired Glucose Tolerance for Atherosclerosis and Diabetes study. Glucose 84-91 insulin Homo sapiens 22-29 12606497-6 2003 It is interesting that these GSK-3 inhibitors enhanced insulin-stimulated glucose transport in type 1 skeletal muscle from the insulin-resistant ZDF rats but not from insulin-sensitive lean Zucker rats. Glucose 74-81 insulin Homo sapiens 55-62 12606497-6 2003 It is interesting that these GSK-3 inhibitors enhanced insulin-stimulated glucose transport in type 1 skeletal muscle from the insulin-resistant ZDF rats but not from insulin-sensitive lean Zucker rats. Glucose 74-81 insulin Homo sapiens 127-134 12652352-6 2003 The rapid increase in portal insulin concentration and the avid binding of the hormone to its receptor on liver cell membranes, account for a prompt suppression of endogenous glucose production and reduction of the rate of increase in plasma glucose concentrations. Glucose 175-182 insulin Homo sapiens 29-36 12606497-6 2003 It is interesting that these GSK-3 inhibitors enhanced insulin-stimulated glucose transport in type 1 skeletal muscle from the insulin-resistant ZDF rats but not from insulin-sensitive lean Zucker rats. Glucose 74-81 insulin Homo sapiens 127-134 12652352-6 2003 The rapid increase in portal insulin concentration and the avid binding of the hormone to its receptor on liver cell membranes, account for a prompt suppression of endogenous glucose production and reduction of the rate of increase in plasma glucose concentrations. Glucose 242-249 insulin Homo sapiens 29-36 12655415-0 2003 Insulin sensitivity and beta-cell secretion in thalassaemia major with secondary haemochromatosis: assessment by oral glucose tolerance test. Glucose 118-125 insulin Homo sapiens 0-7 12652352-9 2003 The critical role of the early-phase insulin response in determining postprandial hyperglycaemia, is supported by an amelioration of glucose tolerance by restoring the acute rise in plasma insulin concentrations after the ingestion of both glucose and a mixed meal. Glucose 133-140 insulin Homo sapiens 189-196 12652352-9 2003 The critical role of the early-phase insulin response in determining postprandial hyperglycaemia, is supported by an amelioration of glucose tolerance by restoring the acute rise in plasma insulin concentrations after the ingestion of both glucose and a mixed meal. Glucose 240-247 insulin Homo sapiens 37-44 12611609-9 2003 Concentrations of plasma adiponectin have been shown to correlate negatively with glucose, insulin, triglyceride levels and body mass index, and positively with high-density lipoprotein-cholesterol levels and insulin-stimulated glucose disposal. Glucose 228-235 insulin Homo sapiens 209-216 12673780-6 2003 The total daily insulin dosage given to normalize blood glucose levels reached a maximum dosage at 7.3 +/- 1.2 days and gradually decreased in all subjects. Glucose 56-63 insulin Homo sapiens 16-23 12687337-7 2003 RESULTS: Ad-Ins-transduced islets produced two to three times more insulin than normal islets or those infected with Ad-lacz, as assessed by in vitro perifusion tests of glucose stimulated insulin release. Glucose 170-177 insulin Homo sapiens 189-196 12655415-11 2003 In addition, a significant decrease in patients with normal glucose tolerance was shown by two insulin sensitivity indices (all P<0.05). Glucose 60-67 insulin Homo sapiens 95-102 12629079-0 2003 Novel insulin sensitivity index derived from oral glucose tolerance test. Glucose 50-57 insulin Homo sapiens 6-13 12620438-13 2003 In the active treatment groups, a significant reduction of fasting glucose and/or fasting insulin was encountered in women with higher basal fasting levels (fasting glucose >4.2 mmol/L or log-fasting insulin >0.87). Glucose 67-74 insulin Homo sapiens 203-210 12620438-13 2003 In the active treatment groups, a significant reduction of fasting glucose and/or fasting insulin was encountered in women with higher basal fasting levels (fasting glucose >4.2 mmol/L or log-fasting insulin >0.87). Glucose 165-172 insulin Homo sapiens 90-97 12629115-0 2003 Normal insulin-stimulated endothelial function and impaired insulin-stimulated muscle glucose uptake in young adults with low birth weight. Glucose 86-93 insulin Homo sapiens 7-14 12629115-0 2003 Normal insulin-stimulated endothelial function and impaired insulin-stimulated muscle glucose uptake in young adults with low birth weight. Glucose 86-93 insulin Homo sapiens 60-67 12620428-0 2003 Testosterone levels in pregnant women correlate with the insulin response during the glucose tolerance test. Glucose 85-92 insulin Homo sapiens 57-64 12749246-7 2003 RESULTS: The amount of glucose infused which is required to keep euglycemia (M value) was markedly low in the study group than in the controls (2.24 +/- 0.33 mg/kg/min and 7.45 +/- 0.82 mg/kg/min, respectively p < 0.0001) suggesting insulin resistance (M value < 4 mg/kg/min). Glucose 23-30 insulin Homo sapiens 236-243 12614971-1 2003 There are different equations to estimate insulin sensitivity by using OGTT with a reasonable approximation to whole body sensitivity obtained with the glucose clamp. Glucose 152-159 insulin Homo sapiens 42-49 12629115-4 2003 Glucose uptake was measured during intraarterial insulin infusion. Glucose 0-7 insulin Homo sapiens 49-56 12629079-3 2003 The oral glucose tolerance test (OGTT), the most commonly used method for evaluating whole body glucose tolerance, has often been used to assess insulin sensitivity. Glucose 9-16 insulin Homo sapiens 145-152 12629115-8 2003 Insulin infusion increased glucose uptake significantly in the normal birth weight group, compared with the low birth weight group: 0.40 +/- 0.09 to 1.00 +/- 0.16 vs. 0.44 +/- 0.09 to 0.59 +/- 0.1 [ micro mol glucose x (100 ml forearm)(-1) x min(-1)], P = 0.04. Glucose 27-34 insulin Homo sapiens 0-7 12629115-8 2003 Insulin infusion increased glucose uptake significantly in the normal birth weight group, compared with the low birth weight group: 0.40 +/- 0.09 to 1.00 +/- 0.16 vs. 0.44 +/- 0.09 to 0.59 +/- 0.1 [ micro mol glucose x (100 ml forearm)(-1) x min(-1)], P = 0.04. Glucose 209-216 insulin Homo sapiens 0-7 12629134-3 2003 Insulin sensitivity was estimated by the fasting glucose/insulin ratio (G/I). Glucose 49-56 insulin Homo sapiens 0-7 12629079-12 2003 In conclusion, the ISI(OGTT) derived from our equation is more suitable than others in assessing insulin sensitivity in subjects with normal glucose tolerance. Glucose 141-148 insulin Homo sapiens 97-104 12629115-9 2003 Young men with low birth weight have normal insulin-stimulated endothelial function and impaired insulin-stimulated forearm glucose uptake. Glucose 124-131 insulin Homo sapiens 97-104 12629118-5 2003 In comparison with the classic model, the skeletal muscle-specific model reveals more clearly definable effects of insulin on transmembrane glucose transport and an impairment of this response in obesity. Glucose 140-147 insulin Homo sapiens 115-122 12639991-9 2003 In the human, alleles located in the VNTR region flanking the insulin gene control beta cell response to glucose and proinsulin expression in the thymus and are key determinants of diabetes susceptibility. Glucose 105-112 insulin Homo sapiens 62-69 12629089-12 2003 Although insulin resistance, measured as insulin area under the curve by oral glucose tolerance test was higher in Asian Indians and correlated significantly with homocysteine, it did not explain inter-ethnic differences in plasma homocysteine in a multivariate analysis. Glucose 78-85 insulin Homo sapiens 41-48 12629118-6 2003 Compared with the classic model for assessment of (18)F-FDG metabolism, both the skeletal muscle-specific and the classic model indicate that, with respect to distribution of control, glucose phosphorylation has an important effect at low to moderate levels of insulin stimulation in both lean and obese subjects. Glucose 184-191 insulin Homo sapiens 261-268 12647266-12 2003 The insulin, glucose and beta-HBA data indicated the presence of insulin hypersensitivity in the recovered subjects. Glucose 13-20 insulin Homo sapiens 65-72 12647262-7 2003 There was also an increased threonine kinase B (AKT) phosphorylation in captopril-treated cells followed by enhanced basal and insulin-stimulated glucose uptake. Glucose 146-153 insulin Homo sapiens 127-134 12705369-14 2003 CONCLUSIONS: In the post-weaning period, oral insulin supplementation had a significant effect on plasma glucose levels and lipid profile, as well as on liver weight and protein content in Balb/c mice. Glucose 105-112 insulin Homo sapiens 46-53 12604916-0 2003 Impaired insulin action on phosphatidylinositol 3-kinase activity and glucose transport in skeletal muscle of pancreatic cancer patients. Glucose 70-77 insulin Homo sapiens 9-16 12701181-2 2003 However, while normal pancreatic beta-cells continually adjust insulin secretion in response to varying blood glucose levels, insulin administration cannot maintain blood glucose levels within a physiological range that protects from the development of various diabetic complications. Glucose 110-117 insulin Homo sapiens 63-70 12604916-4 2003 AIM: To characterize basal and insulin-stimulated glucose transport, phosphatidylinositol (PI) 3-kinase activity, and glucose transporter 4 (GLUT4) in skeletal muscles of PC patients. Glucose 50-57 insulin Homo sapiens 31-38 12604916-8 2003 RESULTS: In the presence of physiologic concentrations of insulin, glucose transport and PI 3-kinase activity were significantly decreased in the PC group compared with controls. Glucose 67-74 insulin Homo sapiens 58-65 12604916-9 2003 At supraphysiologic insulin concentrations, glucose transport was significantly decreased but PI 3-kinase activity was normalized. Glucose 44-51 insulin Homo sapiens 20-27 12604916-12 2003 CONCLUSION: Defects in insulin-mediated PI 3-kinase activity and glucose transport contribute to the insulin resistance in patients with PC. Glucose 65-72 insulin Homo sapiens 101-108 12615955-2 2003 The beta-cell, the insulin-secreting cell in the islet, can detect subtle increases in circulating glucose levels and a cascade of molecular events spanning the initial depolarization of the beta-cell membrane culminates in exocytosis and optimal insulin secretion. Glucose 99-106 insulin Homo sapiens 19-26 12388140-2 2003 It has been reported that a derived 2CMM parameter describing the proportional effect of glucose on insulin-independent glucose disposal can take physiologically unplausible negative values. Glucose 89-96 insulin Homo sapiens 100-107 12723510-3 2003 After a brief description of the devices presently commercialized, we will discuss their indications and their limitations, as well as their future prospects in a possible "closed loop" insulin delivery according to blood glucose level. Glucose 222-229 insulin Homo sapiens 186-193 12582199-1 2003 Insulin stimulates glucose transport in its target cells by translocation of the glucose transporter isoform 4 (Glut4) from an intracellular storage pool to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 12573222-4 2003 Here we show that glucose also increases [Ca(2+)](i) via the novel Ca(2+)-mobilizing agent nicotinic acid adenine dinucleotide phosphate (NAADP) in the insulin-secreting beta-cell line MIN6. Glucose 18-25 insulin Homo sapiens 152-159 12606056-1 2003 Cell-based therapies for treating insulin-dependent diabetes (IDD) can provide a more physiologic regulation of blood glucose levels in a less invasive fashion than daily insulin injections. Glucose 118-125 insulin Homo sapiens 34-41 12410639-1 2003 In muscle, insulin enhances influx of glucose and its conversion to glucose 6-phosphate (G6P) by hexokinase (HK). Glucose 38-45 insulin Homo sapiens 11-18 12410639-2 2003 While effects of insulin on glucose transport have been demonstrated, its effect on the activity of HK of cells has not. Glucose 28-35 insulin Homo sapiens 17-24 12410639-3 2003 In L6 myotubes treated for 24 h with insulin there was increased expression of the HK isoform, HKII, and increased glucose phosphorylation without a concomitant increase in glucose transport, indirectly suggesting that phosphorylation of glucose was a target of insulin action [Osawa, Printz, Whitesell and Granner (1995) Diabetes 44, 1426-1432]. Glucose 115-122 insulin Homo sapiens 37-44 12410639-3 2003 In L6 myotubes treated for 24 h with insulin there was increased expression of the HK isoform, HKII, and increased glucose phosphorylation without a concomitant increase in glucose transport, indirectly suggesting that phosphorylation of glucose was a target of insulin action [Osawa, Printz, Whitesell and Granner (1995) Diabetes 44, 1426-1432]. Glucose 173-180 insulin Homo sapiens 37-44 12410639-3 2003 In L6 myotubes treated for 24 h with insulin there was increased expression of the HK isoform, HKII, and increased glucose phosphorylation without a concomitant increase in glucose transport, indirectly suggesting that phosphorylation of glucose was a target of insulin action [Osawa, Printz, Whitesell and Granner (1995) Diabetes 44, 1426-1432]. Glucose 173-180 insulin Homo sapiens 37-44 12410639-7 2003 Specificity of the glucose phosphorylation of the cells increased with addition of insulin and when extracellular glucose was raised. Glucose 19-26 insulin Homo sapiens 83-90 12410639-13 2003 Insulin activation of glucose phosphorylation might then result from stimulation of these transporters together with HK recruitment or relief from inhibition by G6P. Glucose 22-29 insulin Homo sapiens 0-7 12388140-2 2003 It has been reported that a derived 2CMM parameter describing the proportional effect of glucose on insulin-independent glucose disposal can take physiologically unplausible negative values. Glucose 120-127 insulin Homo sapiens 100-107 12388140-4 2003 Here we resolve the above issues by presenting an improved version of 2CMM that relies on a new assumption on the constant component R(d0) of insulin-independent glucose disposal. Glucose 162-169 insulin Homo sapiens 142-149 12540385-1 2003 BACKGROUND: Insulin responses to the oral-glucose-tolerance test (OGTT) in anorexia nervosa (AN) are related to body weight and show various patterns. Glucose 42-49 insulin Homo sapiens 12-19 12388140-7 2003 A more reliable insulin-independent glucose disposal portrait is obtained while that of insulin action remains unchanged. Glucose 36-43 insulin Homo sapiens 16-23 12559679-6 2003 Insulin resistance was evaluated by determining the steady-state of plasma glucose (SSPG) concentration. Glucose 75-82 insulin Homo sapiens 0-7 12535750-11 2003 Adipose tissue LPL activity was related to insulin action in vitro on adipocyte glucose transport, but not to HOMA-IR. Glucose 80-87 insulin Homo sapiens 43-50 12588774-7 2003 CONCLUSIONS: These data suggest the possibility that the presence of higher insulin resistance could be a risk factor for carotid arteriosclerosis in subjects with normal fasting glucose and normal glucose tolerance. Glucose 179-186 insulin Homo sapiens 76-83 12546685-2 2003 (i) Excesses of glucose and free fatty acids cause insulin resistance in skeletal muscle and damage to the endothelial cell by a similar mechanism. Glucose 16-23 insulin Homo sapiens 51-58 12588774-7 2003 CONCLUSIONS: These data suggest the possibility that the presence of higher insulin resistance could be a risk factor for carotid arteriosclerosis in subjects with normal fasting glucose and normal glucose tolerance. Glucose 198-205 insulin Homo sapiens 76-83 12566104-9 2003 On the other hand, in contrast to these acute beneficial effect of insulin, epidemiological studies have indentified chronic hyperinsulinemia, a common feature in subjects with insulin resistance to glucose uptake, as an independent risk factor for coronary artery disease. Glucose 199-206 insulin Homo sapiens 130-137 12701881-10 2003 Glucose and serotonin regulate insulin directly in the hypothalamus and may be of importance for its biological effects. Glucose 0-7 insulin Homo sapiens 31-38 12678487-8 2003 We have recently directly tested this model in adipocytes by examining the effect of elevated levels of O-GlcNAc on insulin-stimulated glucose uptake. Glucose 135-142 insulin Homo sapiens 116-123 12553944-4 2003 In contrast to its sodium retaining properties in normal, obese and diabetic subjects, insulin-glucose-potassium therapy may induce a sodium diuresis in catabolic patients with salt and water overload and in patients with congestive heart failure in whom haemodynamic improvement has also been observed. Glucose 95-102 insulin Homo sapiens 87-94 12540592-0 2003 Plasma adiponectin concentrations predict insulin sensitivity of both glucose and lipid metabolism. Glucose 70-77 insulin Homo sapiens 42-49 12576937-13 2003 Multivariate logistic regression analysis indicated that the lowered blood glucose level rather than the insulin dose was related to reduced mortality (p <.0001), critical illness polyneuropathy (p <.0001), bacteremia (p =.02), and inflammation (p =.0006) but not to prevention of acute renal failure, for which the insulin dose was an independent determinant (p =.03). Glucose 75-82 insulin Homo sapiens 322-329 12540592-7 2003 Most notable, these relationships remained significant after adjusting for insulin sensitivity of glucose disposal in addition to sex and percentage of body fat (all P < 0.05). Glucose 98-105 insulin Homo sapiens 75-82 12540611-0 2003 The influence of GLP-1 on glucose-stimulated insulin secretion: effects on beta-cell sensitivity in type 2 and nondiabetic subjects. Glucose 26-33 insulin Homo sapiens 45-52 12540592-9 2003 This relationship is independent of low body fat mass and affects not only insulin-stimulated glucose disposal but also lipoprotein metabolism and insulin-mediated suppression of postprandial FFA release. Glucose 94-101 insulin Homo sapiens 75-82 12540598-3 2003 monotherapy for 26 weeks on adipose tissue insulin-stimulated glucose uptake in patients (n = 41) with type 2 diabetes. Glucose 62-69 insulin Homo sapiens 43-50 12540598-5 2003 Rosiglitazone improved insulin-stimulated whole-body glucose uptake by 44% (P < 0.01 vs. placebo). Glucose 53-60 insulin Homo sapiens 23-30 12540611-1 2003 The intestinally derived hormone glucagon-like peptide 1 (GLP-1) (7-36 amide) has potent effects on glucose-mediated insulin secretion, insulin gene expression, and beta-cell growth and differentiation. Glucose 100-107 insulin Homo sapiens 117-124 12540625-1 2003 To study effects of sex on free fatty acid (FFA)-induced insulin resistance, we have examined the effects of acute elevations of plasma FFA levels on insulin-stimulated total body glucose uptake in nine healthy young women. Glucose 180-187 insulin Homo sapiens 150-157 12540625-4 2003 These data showed that acute increases in plasma FFA levels inhibited the actions of insulin on glucose uptake, glycogen synthesis, and EGP in women to a degree similar to that previously reported in men. Glucose 96-103 insulin Homo sapiens 85-92 12540626-7 2003 At the lower dose, the exogenous glucose infusion rates required to maintain euglycemia during steady state were significantly lower with glycated insulin (P < 0.01) and approximately 70% more glycated insulin was required to induce a similar rate of insulin-mediated glucose uptake. Glucose 33-40 insulin Homo sapiens 147-154 12540611-3 2003 However, the dose-response relationship between GLP-1 and basal and glucose-stimulated prehepatic insulin secretion rate (ISR) is currently not known. Glucose 68-75 insulin Homo sapiens 98-105 12540626-7 2003 At the lower dose, the exogenous glucose infusion rates required to maintain euglycemia during steady state were significantly lower with glycated insulin (P < 0.01) and approximately 70% more glycated insulin was required to induce a similar rate of insulin-mediated glucose uptake. Glucose 33-40 insulin Homo sapiens 205-212 12540626-7 2003 At the lower dose, the exogenous glucose infusion rates required to maintain euglycemia during steady state were significantly lower with glycated insulin (P < 0.01) and approximately 70% more glycated insulin was required to induce a similar rate of insulin-mediated glucose uptake. Glucose 33-40 insulin Homo sapiens 205-212 12547881-3 2003 The first-phase insulin secretion was determined by the intravenous glucose tolerance test (IVGTT) in a separate sample of 295 normoglycemic subjects (group II). Glucose 68-75 insulin Homo sapiens 16-23 12540626-11 2003 The present demonstration of glycated insulin in human plasma and related impairment of physiological insulin-mediated glucose uptake suggests a role for glycated insulin in glucose toxicity and impaired insulin action in type 2 diabetes. Glucose 119-126 insulin Homo sapiens 38-45 12540626-11 2003 The present demonstration of glycated insulin in human plasma and related impairment of physiological insulin-mediated glucose uptake suggests a role for glycated insulin in glucose toxicity and impaired insulin action in type 2 diabetes. Glucose 119-126 insulin Homo sapiens 102-109 12540638-7 2003 In conclusion, the widespread E23K polymorphism may have a diabetogenic effect by impairing glucose-induced insulin release and increasing BMI. Glucose 92-99 insulin Homo sapiens 108-115 12631049-1 2003 BACKGROUND: Surgery is succeeded by long-lasting state of relative peripheral insulin resistance, which is reduced by giving glucose infusion or oral carbohydrate-rich drinks immediate before operating instead of fasting. Glucose 125-132 insulin Homo sapiens 78-85 12547889-7 2003 Postprandial blood glucose maximum concentration (278 +/- 16 vs. 240 +/- 16 mg/dl, P < 0.01) and area under the curve (79,381 +/- 19,237 vs. 72,810 +/- 16,211 mg/dl per min, P < 0,05) were significantly lower after insulin lispro than after regular insulin injection, respectively, despite comparable postprandial insulin profiles. Glucose 19-26 insulin Homo sapiens 221-228 12630945-4 2003 Insulin secretion increased 2.4-fold upon glucose stimulation, and 38-fold when 10 mm theophylline was added, showing the responsiveness of the neonatal beta cells. Glucose 42-49 insulin Homo sapiens 0-7 12547889-7 2003 Postprandial blood glucose maximum concentration (278 +/- 16 vs. 240 +/- 16 mg/dl, P < 0.01) and area under the curve (79,381 +/- 19,237 vs. 72,810 +/- 16,211 mg/dl per min, P < 0,05) were significantly lower after insulin lispro than after regular insulin injection, respectively, despite comparable postprandial insulin profiles. Glucose 19-26 insulin Homo sapiens 255-262 12547889-7 2003 Postprandial blood glucose maximum concentration (278 +/- 16 vs. 240 +/- 16 mg/dl, P < 0.01) and area under the curve (79,381 +/- 19,237 vs. 72,810 +/- 16,211 mg/dl per min, P < 0,05) were significantly lower after insulin lispro than after regular insulin injection, respectively, despite comparable postprandial insulin profiles. Glucose 19-26 insulin Homo sapiens 255-262 12574208-12 2003 In conclusion, glucose stimulates pulsatile insulin secretion from isolated human islets by amplification of insulin pulse mass without altering pulse interval. Glucose 15-22 insulin Homo sapiens 44-51 12588288-3 2003 MATERIALS AND METHODS: In the present study we set out to characterize transcapillary insulin transfer by measuring insulin concentrations in plasma and interstitial space fluid of skeletal muscle during an oral glucose tolerance test and euglycaemic hyperinsulinaemic clamp conditions, respectively. Glucose 212-219 insulin Homo sapiens 86-93 12588288-8 2003 CONCLUSION: In summary there is a substantial transcapillary insulin gradient in healthy human skeletal muscle under baseline and glucose-stimulated conditions. Glucose 130-137 insulin Homo sapiens 61-68 12562309-2 2003 Effective glucose control usually requires multiple daily injections of subcutaneous insulin. Glucose 10-17 insulin Homo sapiens 85-92 12562309-6 2003 In fact, clinical trials in the last few years have shown that intrapulmonary insulin was as good as subcutaneous insulin in controlling glucose levels in patients with both Type 1 and 2 diabetes mellitus. Glucose 137-144 insulin Homo sapiens 78-85 12627878-2 2003 Insulin affects not only glucose metabolism, but also protein synthesis and cell growth. Glucose 25-32 insulin Homo sapiens 0-7 12569234-4 2003 Reports consistently suggest that the acute affects of alcohol induce a state of insulin resistance following either an oral and/or intravenous glucose load. Glucose 144-151 insulin Homo sapiens 81-88 12574183-9 2003 In PCOS compared with OBW, insulin stimulated glucose disposal (52.7 +/- 6.6 vs. 85.5 +/- 4.4 micromol/kg fat-free mass x min; P < 0.0005) and vasodilation (increase in LBF, 22 +/- 14% vs. 59 +/- 15%; P < 0.05) were significantly improved after Tgz treatment to 68.8 +/- 7.2 micromol/kg fat-free mass x min (P < 0.0001) and 101 +/- 48% (P < 0.03), respectively. Glucose 46-53 insulin Homo sapiens 27-34 12574208-14 2003 These data imply that transplanted human islets should be able to reproduce glucose-regulated insulin secretion as observed in the intact human pancreas. Glucose 76-83 insulin Homo sapiens 94-101 12553872-8 2003 An intraperitoneal injection of insulin (0.75 mU insulin/g) caused a continuous decline in blood glucose levels in wild-type mice whereas ArKO males at 18 weeks and older exhibited a rebound increase in glucose levels 30 min after insulin injection. Glucose 97-104 insulin Homo sapiens 32-39 12588878-0 2003 Insulin"s effect on glucose production: direct or indirect? Glucose 20-27 insulin Homo sapiens 0-7 12682423-1 2003 Insulin resistance is characterized by impaired glucose utilization in the peripheral tissues, accelerated muscle protein degradation, impaired antioxidant defences and extensive cell death. Glucose 48-55 insulin Homo sapiens 0-7 12553872-8 2003 An intraperitoneal injection of insulin (0.75 mU insulin/g) caused a continuous decline in blood glucose levels in wild-type mice whereas ArKO males at 18 weeks and older exhibited a rebound increase in glucose levels 30 min after insulin injection. Glucose 97-104 insulin Homo sapiens 49-56 12553872-8 2003 An intraperitoneal injection of insulin (0.75 mU insulin/g) caused a continuous decline in blood glucose levels in wild-type mice whereas ArKO males at 18 weeks and older exhibited a rebound increase in glucose levels 30 min after insulin injection. Glucose 97-104 insulin Homo sapiens 49-56 12553872-8 2003 An intraperitoneal injection of insulin (0.75 mU insulin/g) caused a continuous decline in blood glucose levels in wild-type mice whereas ArKO males at 18 weeks and older exhibited a rebound increase in glucose levels 30 min after insulin injection. Glucose 203-210 insulin Homo sapiens 32-39 12713249-3 2003 One of the main errors was (is) to speculate that there exists a direct linear correlation between the injection of x units of insulin and the utilization of y grams of glucose. Glucose 169-176 insulin Homo sapiens 127-134 12574208-3 2003 We posed the hypothesis that glucose stimulates insulin secretion from isolated human islets by an amplification of insulin pulse mass with no change in pulse frequency and that the glucose dose-response curve for the regulation of insulin pulse mass mirrors that recognized in vivo. Glucose 29-36 insulin Homo sapiens 48-55 12574208-3 2003 We posed the hypothesis that glucose stimulates insulin secretion from isolated human islets by an amplification of insulin pulse mass with no change in pulse frequency and that the glucose dose-response curve for the regulation of insulin pulse mass mirrors that recognized in vivo. Glucose 29-36 insulin Homo sapiens 116-123 12574208-3 2003 We posed the hypothesis that glucose stimulates insulin secretion from isolated human islets by an amplification of insulin pulse mass with no change in pulse frequency and that the glucose dose-response curve for the regulation of insulin pulse mass mirrors that recognized in vivo. Glucose 29-36 insulin Homo sapiens 116-123 12713249-17 2003 The use of fast-acting insulin analogs in the basal-prandial regimen improves post-prandial glycemia at the expense of an increase in pre-prandial glucose levels, if the period between two meals, and therefore two injections, exceeds 3-4 hours, because of the short duration of action. Glucose 147-154 insulin Homo sapiens 23-30 12537988-5 2003 Intracellular Mg concentration has also been shown to be effective in modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli. Glucose 114-121 insulin Homo sapiens 81-88 12537988-8 2003 By contrast, in NIDDM patients daily Mg administration, restoring a more appropriate intracellular Mg concentration, contributes to improve insulin-mediated glucose uptake. Glucose 157-164 insulin Homo sapiens 140-147 12601307-4 2003 Adiponectin stimulates fatty acids oxidation, decreases plasma triglycerides, and improves glucose metabolism by increasing insulin sensitivity. Glucose 91-98 insulin Homo sapiens 124-131 12601639-1 2003 Elevation of plasma nonesterified fatty acid (NEFA) levels has been shown to impair the actions of insulin on peripheral glucose uptake and suppression of hepatic glucose output (HGO). Glucose 121-128 insulin Homo sapiens 99-106 12601639-3 2003 We therefore set out to test the hypothesis that obese subjects, because they are already insulin-resistant, are less susceptible than lean subjects to the inhibitory effects of elevated NEFA on insulin-stimulated glucose disposal. Glucose 214-221 insulin Homo sapiens 195-202 12601640-4 2003 Insulin action in vitro was studied by measurements of glucose uptake both directly after cell isolation and following a 24-hour incubation at a physiological glucose level (6 mmol/L). Glucose 55-62 insulin Homo sapiens 0-7 12601640-4 2003 Insulin action in vitro was studied by measurements of glucose uptake both directly after cell isolation and following a 24-hour incubation at a physiological glucose level (6 mmol/L). Glucose 159-166 insulin Homo sapiens 0-7 12601640-6 2003 Freshly isolated fat cells from type 2 diabetes patients with poor metabolic control had approximately 55% lower maximal insulin response (1,000 microU/mL) on glucose uptake (P <.05) compared to C. Cells from P were more insulin-resistant (P <.05) than cells from G at a low (5 microU/mL) but not at a high (1,000 microU/mL) insulin concentration, suggesting insulin insensitivity. Glucose 159-166 insulin Homo sapiens 121-128 12601640-7 2003 However, following 24 hours of incubation at physiological glucose levels, insulin resistance was completely reversed in the diabetes cells and no differences in insulin-stimulated glucose uptake were found among the 3 groups. Glucose 59-66 insulin Homo sapiens 75-82 12601640-8 2003 Insulin sensitivity in vivo assessed with hyperinsulinemic, euglycemic clamp (M-value) was significantly associated with insulin action on glucose uptake in fresh adipocytes in vitro (r = 0.50, P <.01). Glucose 139-146 insulin Homo sapiens 0-7 12601640-8 2003 Insulin sensitivity in vivo assessed with hyperinsulinemic, euglycemic clamp (M-value) was significantly associated with insulin action on glucose uptake in fresh adipocytes in vitro (r = 0.50, P <.01). Glucose 139-146 insulin Homo sapiens 47-54 12601640-10 2003 In the in vivo situation, fasting blood glucose, HbA(1c), and serum insulin were all negatively correlated to insulin sensitivity (M-value; r = -0.62, P<.001, r= -0.61, P<.001, and r = -0.56, p <.01, respectively). Glucose 40-47 insulin Homo sapiens 110-117 12601640-13 2003 Furthermore, insulin sensitivity in vivo could be predicted by fasting blood glucose and serum insulin levels. Glucose 77-84 insulin Homo sapiens 13-20 12601640-14 2003 We conclude that insulin resistance in fat cells from type 2 diabetes patients is fully reversible following incubation at physiological glucose concentrations. Glucose 137-144 insulin Homo sapiens 17-24 12601641-1 2003 Genetic factors play a role in the regulation of glucose metabolism-related traits such as insulin sensitivity (S(I)), insulin secretion, and glucose effectiveness (S(G)). Glucose 49-56 insulin Homo sapiens 91-98 12601641-5 2003 In addition to S(I) and S(G), we also considered acute insulin response to a glucose challenge (AIR(Glucose)), which is an index for insulin secretion, and disposition index (DI, product of S(I) and AIR(Glucose)), which is a measure of the activity of pancreatic beta cells corrected for insulin resistance. Glucose 77-84 insulin Homo sapiens 133-140 12582222-0 2003 Insulin- and exercise-stimulated skeletal muscle blood flow and glucose uptake in obese men. Glucose 64-71 insulin Homo sapiens 0-7 12582222-1 2003 OBJECTIVE: Insulin resistance in obese subjects results in the impaired use of glucose by insulin-sensitive tissues, e.g., skeletal muscle. Glucose 79-86 insulin Homo sapiens 11-18 12582222-1 2003 OBJECTIVE: Insulin resistance in obese subjects results in the impaired use of glucose by insulin-sensitive tissues, e.g., skeletal muscle. Glucose 79-86 insulin Homo sapiens 90-97 12582222-2 2003 In the present study, we determined whether insulin resistance in obesity is associated with an impaired ability of exercise to stimulate muscle blood flow, oxygen delivery, or glucose uptake. Glucose 177-184 insulin Homo sapiens 44-51 12582222-5 2003 RESULTS: The obese subjects exhibited resistance to insulin stimulation of glucose uptake in resting muscle, regardless of whether glucose uptake was expressed per kilogram of femoral muscle mass (p = 0.001) or per the total mass of quadriceps femoris muscle. Glucose 75-82 insulin Homo sapiens 52-59 12582222-7 2003 DISCUSSION: We conclude that obesity is characterized by insulin resistance of glucose uptake in resting skeletal muscle regardless of how glucose uptake is expressed. Glucose 79-86 insulin Homo sapiens 57-64 12453902-8 2002 In the SGA group, fasting insulin-to-glucose ratios were significantly higher in the TNF/-308A (P = 0.03), the PPAR/Ala12 (P = 0.01), and the ADRB3/+250G (P = 0.02) carriers than in the noncarriers. Glucose 37-44 insulin Homo sapiens 26-33 12537988-10 2003 In conclusion, a growing body of studies suggest that intracellular Mg may play a key role in modulating insulin-mediated glucose uptake and vascular tone. Glucose 122-129 insulin Homo sapiens 105-112 12559865-7 2003 Furthermore, these heterozygous people had a substantial reduction in maximum glucose-stimulated insulin secretion during hyperglycemic clamp (carriers without diabetes 422 pmol/L; carriers with diabetes 97 pmol/L). Glucose 78-85 insulin Homo sapiens 97-104 12478066-1 2003 OBJECTIVE: To test agent and cell-type specificity in insulin resistance induced by prolonged exposure to HIV protease inhibitors (HPI), and to assess its relation to the direct, short-term inhibition of insulin-stimulated glucose uptake. Glucose 223-230 insulin Homo sapiens 204-211 12478066-2 2003 METHODS: Following prolonged (18 h) and short (5-10 min) exposure to HPI, insulin-stimulated glucose transport, protein kinase B (PKB) phosphorylation, and GLUT4 translocation were evaluated in 3T3-L1 adipocytes, fibroblasts, L6 myotubes, and L6 cells overexpressing a myc tag on the first exofacial loop of GLUT4 or GLUT1. Glucose 93-100 insulin Homo sapiens 74-81 12478066-3 2003 RESULTS: Prolonged exposure of 3T3-L1 adipocytes to nelfinavir, but not to indinavir or saquinavir, resulted in increased basal lipolysis but decreased insulin-stimulated glucose transport and PKB phosphorylation. Glucose 171-178 insulin Homo sapiens 152-159 12478066-4 2003 In addition, impaired insulin-stimulated glucose uptake and PKB phosphorylation were also observed in the skeletal muscle cell line L6, and in 3T3-L1 fibroblasts. Glucose 41-48 insulin Homo sapiens 22-29 12478066-6 2003 In contrast to these unique effects of nelfinavir, the mere presence of any of the agents in the 5 min transport assay inhibited insulin-stimulated glucose-uptake activity. Glucose 148-155 insulin Homo sapiens 129-136 12675249-3 2003 It also induces satiety and promotes tissue deposition of ingested glucose by stimulating insulin secretion. Glucose 67-74 insulin Homo sapiens 90-97 12971416-6 2003 The higher plasma glucose and insulin levels were noted during the oral glucose tolerance test in space flight and also in the post flight period. Glucose 72-79 insulin Homo sapiens 30-37 14577361-1 2003 The aim of the study was to compare the information provided by both fasting and stimulated during a standard oral glucose tolerance test (oGTT) levels of glucose and insulin as regards glucose tolerance and insulin resistance in women with PCOS. Glucose 155-162 insulin Homo sapiens 208-215 14577361-1 2003 The aim of the study was to compare the information provided by both fasting and stimulated during a standard oral glucose tolerance test (oGTT) levels of glucose and insulin as regards glucose tolerance and insulin resistance in women with PCOS. Glucose 155-162 insulin Homo sapiens 208-215 14507228-3 2003 Insulin therapy is associated with important cutaneous adverse effects, which can affect insulin absorption kinetics causing glycemic excursions above and below target levels for blood glucose. Glucose 185-192 insulin Homo sapiens 0-7 14507228-3 2003 Insulin therapy is associated with important cutaneous adverse effects, which can affect insulin absorption kinetics causing glycemic excursions above and below target levels for blood glucose. Glucose 185-192 insulin Homo sapiens 89-96 14507228-7 2003 However, the absorption of insulin from lipoatrophic areas is erratic leading to frequent difficulties in achieving ideal blood glucose control. Glucose 128-135 insulin Homo sapiens 27-34 12485807-2 2003 Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. Glucose 12-19 insulin Homo sapiens 66-73 12485810-3 2003 Glucose-stimulated insulin secretion was monitored during hyperglycemic clamps for 120 min. Glucose 0-7 insulin Homo sapiens 19-26 12488297-1 2003 BACKGROUND: Dietary carbohydrates vary in their ability to raise blood glucose and insulin levels, which, in turn, influence levels of sex hormones and insulin-like growth factors. Glucose 71-78 insulin Homo sapiens 152-159 12532236-4 2003 Among the ethanol groups, only the 3% ethanol group showed an increase in insulin sensitivity based on the increase of the plasma glucose disappearance rate in the IVITT (30%, P<0.05). Glucose 130-137 insulin Homo sapiens 74-81 12532236-6 2003 Insulin sensitivity was confirmed in 3% ethanol rats based on the reduction of insulin secretion in the IVGTT (35%, P<0.05), despite the same glucose profile. Glucose 145-152 insulin Homo sapiens 0-7 15146605-4 2003 Future, widespread clinical application of islet transplantation will depend on the availability of an unlimited source of glucose sensitive, insulin-secreting tissue and less toxic immunosuppressors. Glucose 123-130 insulin Homo sapiens 142-149 12911131-4 2003 In the laminin group, the insulin accumulation was maintained at a significantly higher level than in the control group at 4 weeks of culture, and glucose-stimulated insulin secretion and the insulin-positive rate were also higher than in the control group. Glucose 147-154 insulin Homo sapiens 166-173 14608941-6 2003 Current approaches include stimulation of embryonic or adult stem cell proliferation and differentiation into beta-cells, beta-cell proliferation, transdifferentiation of non-islet cells into glucose-sensitive insulin-producing cells and xenotransplantation. Glucose 192-199 insulin Homo sapiens 210-217 12514365-3 2003 Resistance to insulin was suggested by an oral glucose tolerance test in the mother, whereas the test was normal in the index patient at the age of 2 years 2 months. Glucose 47-54 insulin Homo sapiens 14-21 12942379-1 2003 Abnormalities of glucose regulation, including impaired glucose tolerance and insulin resistance, are often seen among human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy. Glucose 17-24 insulin Homo sapiens 78-85 12942379-2 2003 Insulin resistance in this population may result from antiviral medication directly impairing glucose uptake in the muscle, effects of HIV per se, or indirect effects, such as fat redistribution. Glucose 94-101 insulin Homo sapiens 0-7 14986905-3 2003 This article describes some of the physiologic changes that occur when hyperglycemia and insulin resistance develop in patients with type 2 diabetes and discusses therapies, including insulin, that normalize glucose and reduce insulin resistance, thereby potentially reducing cardiovascular risk. Glucose 208-215 insulin Homo sapiens 89-96 14986905-3 2003 This article describes some of the physiologic changes that occur when hyperglycemia and insulin resistance develop in patients with type 2 diabetes and discusses therapies, including insulin, that normalize glucose and reduce insulin resistance, thereby potentially reducing cardiovascular risk. Glucose 208-215 insulin Homo sapiens 184-191 14986905-3 2003 This article describes some of the physiologic changes that occur when hyperglycemia and insulin resistance develop in patients with type 2 diabetes and discusses therapies, including insulin, that normalize glucose and reduce insulin resistance, thereby potentially reducing cardiovascular risk. Glucose 208-215 insulin Homo sapiens 184-191 19002958-8 2003 The deleterious effect on proinsulin secretion observed upon co-expression of the glucose sensing genes may have implications for applications requiring multigene expression in BHK21 cells. Glucose 82-89 insulin Homo sapiens 26-36 12532159-5 2003 The rate of total body insulin-mediated glucose disposal (Rd; 40 mU/m(2) min euglycemic insulin clamp in combination with (3)H-glucose) was reduced in T2DM (102+/-3 mg/m(2) min) compared with NGT (177+/-10) and IGT (151+/-14; both P<0.01). Glucose 40-47 insulin Homo sapiens 23-30 12532159-5 2003 The rate of total body insulin-mediated glucose disposal (Rd; 40 mU/m(2) min euglycemic insulin clamp in combination with (3)H-glucose) was reduced in T2DM (102+/-3 mg/m(2) min) compared with NGT (177+/-10) and IGT (151+/-14; both P<0.01). Glucose 40-47 insulin Homo sapiens 88-95 12621164-9 2003 Insulin resistance was measured by determining the plasma immunoreactive insulin concentration at the 120 min time point (IRI 120) of a 75 g oral glucose tolerance test. Glucose 146-153 insulin Homo sapiens 0-7 12456717-0 2003 An insulin-related peptide expressed in 3T3L1 adipocytes is localized in GLUT4 vesicles and secreted in response to exogenous insulin, which augments the insulin-stimulated glucose uptake. Glucose 173-180 insulin Homo sapiens 3-10 12456717-0 2003 An insulin-related peptide expressed in 3T3L1 adipocytes is localized in GLUT4 vesicles and secreted in response to exogenous insulin, which augments the insulin-stimulated glucose uptake. Glucose 173-180 insulin Homo sapiens 126-133 12456717-0 2003 An insulin-related peptide expressed in 3T3L1 adipocytes is localized in GLUT4 vesicles and secreted in response to exogenous insulin, which augments the insulin-stimulated glucose uptake. Glucose 173-180 insulin Homo sapiens 126-133 12456717-10 2003 Finally, we examined the insulin-stimulated glucose uptake by these cells. Glucose 44-51 insulin Homo sapiens 25-32 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 40-47 insulin Homo sapiens 21-28 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 40-47 insulin Homo sapiens 144-151 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 40-47 insulin Homo sapiens 144-151 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 40-47 insulin Homo sapiens 144-151 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 223-230 insulin Homo sapiens 21-28 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 223-230 insulin Homo sapiens 144-151 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 223-230 insulin Homo sapiens 144-151 12456717-11 2003 The data showed that insulin-stimulated glucose uptake increased to about 150% of that of control cells in response to exogenously administered insulin, indicating that the insulin released augmented the insulin-stimulated glucose uptake in an autocrine manner. Glucose 223-230 insulin Homo sapiens 144-151 14711103-1 2003 The aim of this study was to compare glucose transport and utilization in human placentae from pregnancies affected by insulin-treated GDM with and without macrosomia, and from non-diabetic control pregnancies. Glucose 37-44 insulin Homo sapiens 119-126 14711103-6 2003 Insulin-treated GDM group without macrosomia had reduced glucose utilization compared to the control group while the insulin-treated GDM group with macrosomia did not. Glucose 57-64 insulin Homo sapiens 0-7 14711103-8 2003 In conclusion, placental glucose utilization is different between insulin-treated GDM placentae with and without fetal macrosomia. Glucose 25-32 insulin Homo sapiens 66-73 12424750-2 2003 HISS action accounts for 50-60% of the glucose disposal produced by a wide range of insulin doses (5-100 mU/kg). Glucose 39-46 insulin Homo sapiens 84-91 12499920-7 2003 Moreover, although the insulin response to high glucose and potassium loading was maintained, the magnitude of the responses to both stimuli was attenuated in the late period of culture. Glucose 48-55 insulin Homo sapiens 23-30 15529582-6 2003 Recent evidence suggests that insulin signalling for glucose transport in classical target tissues (muscle and adipose tissue) and upregulation of NO production in the endothelium utilises the same postreceptor pathway. Glucose 53-60 insulin Homo sapiens 30-37 15871555-6 2003 Biphasic insulin aspart (30% soluble [rapid-acting] and 70% protamine-bound insulin aspart [BIAsp30]) [NovoLog Mix 70/30, NovoMix 30(2)] generally provided significantly better postprandial glucose control than a similar mixture of biphasic regular human insulin (BHI30) in a randomized, nonblind trial in patients with type 1 or 2 diabetes mellitus. Glucose 190-197 insulin Homo sapiens 9-16 12757656-3 2003 Insulin sensitivity was calculated from fasting plasma glucose (FPG) and insulin (FINS) with the formula insulin sensitivity index (ISI) = 1/(FPG x FINS) and insulin resistance index (Homa-IR) = (FPG x FINS)/22.5. Glucose 55-62 insulin Homo sapiens 0-7 12368292-0 2002 MafA is a glucose-regulated and pancreatic beta-cell-specific transcriptional activator for the insulin gene. Glucose 10-17 insulin Homo sapiens 96-103 12368292-1 2002 The insulin gene is specifically expressed in beta-cells of the Langerhans islets of the pancreas, and its transcription is regulated by the circulating glucose level. Glucose 153-160 insulin Homo sapiens 4-11 12601453-18 2003 In the group of patients with elevated fasting serum glucose level (who only got insulin but no glucose loading) the M/B activity ratio 90 min p. i. was clearly inferior compared with diabetic patients after oral glucose loading and insulin administration (M/B 2.71 +/- 0.19 versus 2.16 +/- 0.07). Glucose 53-60 insulin Homo sapiens 81-88 12879777-4 2003 SUR1 also enhances a physiological secretion of insulin induced by an increase of glucose concentration. Glucose 82-89 insulin Homo sapiens 48-55 12537172-3 2003 Frequent self-monitoring of glucose levels is important in the week before surgery so that insulin regimens can be adjusted as needed. Glucose 28-35 insulin Homo sapiens 91-98 12537172-5 2003 The usual regimen of sliding scale subcutaneous insulin for perioperative glycemic control may be a less preferable method because it can have unreliable absorption and lead to erratic blood glucose levels. Glucose 191-198 insulin Homo sapiens 48-55 12388450-7 2003 The insulin-to-glucose ratio throughout the IVGTT was increased in low compared with medium (P < 0.01) or high (P < 0.05) birth weight males. Glucose 15-22 insulin Homo sapiens 4-11 12870284-4 2003 The doses of insulin have to be defined preoperatively with respect of the metabolic needs of the patients in the days preceding the operation, and must be able meanwhile to reduce blood glucose among the physiologic values, in absence on any urinary glucose, to restore a correct metabolism. Glucose 187-194 insulin Homo sapiens 13-20 12680624-7 2003 Serum concentrations of insulin-related molecules released in response to a standard glucose challenge test were compared between the groups. Glucose 85-92 insulin Homo sapiens 24-31 14579930-3 2003 The present study investigates factors influencing the glucose-induced insulin response of encapsulated islets in vitro. Glucose 55-62 insulin Homo sapiens 71-78 14579930-5 2003 (i) Small islets (90-120 microm) showed a similar instead of a lower glucose-induced insulin response, suggesting that inclusion of only small islets, which are associated with lower protrusion and failing rates, has no consequences for the functional performance of the graft. Glucose 69-76 insulin Homo sapiens 85-92 14579930-6 2003 (ii) A capsule diameter of 800 microm showed identical rather than lower glucose-induced insulin responses as smaller, 500-microm capsules. Glucose 73-80 insulin Homo sapiens 89-96 14579930-9 2003 We conclude that capsules containing small islets (90-120 microm) and a membrane with a lower permeability than routinely applied is preferred in order to obtain a graft with adequate glucose-induced insulin responses. Glucose 184-191 insulin Homo sapiens 200-207 12520154-5 2003 Multiple regression analysis including the insulin concentrations during an OGTT revealed that the 120-min plasma glucose concentration after glucose load significantly correlated with late loss (p=0.0018) and the degree of stenosis (p=0.0100) at follow-up. Glucose 114-121 insulin Homo sapiens 43-50 12520154-5 2003 Multiple regression analysis including the insulin concentrations during an OGTT revealed that the 120-min plasma glucose concentration after glucose load significantly correlated with late loss (p=0.0018) and the degree of stenosis (p=0.0100) at follow-up. Glucose 142-149 insulin Homo sapiens 43-50 12519414-3 2003 MEASUREMENTS AND STUDY SUBJECTS: Body composition (DEXA) and measurements of fasting plasma levels of glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptides (GLPs), insulin, C-peptide, glucose, leptin and lipids were performed in 25 hypopituitary patients (15 obese, 10 normal weight) and 26 BMI and age-matched healthy controls (16 obese, 10 normal weight). Glucose 102-109 insulin Homo sapiens 120-127 14651328-7 2003 Insulin resistance was calculated from the fasting insulin and glucose values by means of the HOMA analysis. Glucose 63-70 insulin Homo sapiens 0-7 12467491-5 2003 It has recently been demonstrated that insulin-sensitive glucose transporters are localised to the same regions supporting memory and that insulin plays a role in memory functions. Glucose 57-64 insulin Homo sapiens 39-46 12467491-5 2003 It has recently been demonstrated that insulin-sensitive glucose transporters are localised to the same regions supporting memory and that insulin plays a role in memory functions. Glucose 57-64 insulin Homo sapiens 139-146 12519082-1 2003 We have examined insulin action on glucose metabolism in six hypothyroid patients before and after regular thyroid hormone treatment, and in six healthy volunteers before and after transient induction of moderate hyperthyroidism. Glucose 35-42 insulin Homo sapiens 17-24 12519082-9 2003 Insulin, in conjunction with glucose and amino acids, significantly stimulated glucose disposal (P <0.05) under all conditions. Glucose 79-86 insulin Homo sapiens 0-7 12519082-11 2003 However, the ratio of the incremental increase in glucose disposal to the increase in plasma insulin was significantly improved after thyroid hormone treatment in hypothyroid patients (P <0.05). Glucose 50-57 insulin Homo sapiens 93-100 12519082-13 2003 We conclude that thyroid hormones improve the ability of insulin to stimulate glucose disposal related to insulinaemia. Glucose 78-85 insulin Homo sapiens 57-64 12502486-6 2003 In addition, there is evidence that in type 2 diabetes, the activation of these same pathways by elevations in glucose and free fatty acid (FFA) levels leads to both insulin resistance and impaired insulin secretion. Glucose 111-118 insulin Homo sapiens 166-173 12502488-6 2003 Elevated glucose concentrations increased circulating insulin to 612 +/- 85 pmol/l (P < 0.01), but they did not affect ghrelin concentrations. Glucose 9-16 insulin Homo sapiens 54-61 12502503-1 2003 To determine whether insulin induces acute changes in endogenous glucose production (EGP) via changes in gluconeogenesis (GNG), glycogenolysis (GL), or both, we measured GNG (with (2)H(2)O) and GL (EGP-GNG) in nine patients with type 1 diabetes during acute insulin excess produced by subcutaneous injection of insulin and during insulin deficiency which developed between 5 and 8 h after insulin injection. Glucose 65-72 insulin Homo sapiens 21-28 12502512-6 2003 Independent of the polymorphisms, we observed a significant impact of zygosity status per se on the plasma insulin profile after oral glucose ingestion, with the MZ twins being more hyperinsulinemic, indicating insulin resistance, than the DZ twins. Glucose 134-141 insulin Homo sapiens 107-114 12502667-8 2003 Insulin resistance (P < 0.0001), impaired insulin secretion (P < 0.0001), and diastolic blood pressure (BP) (P < 0.05) were significantly and independently related to 2-h postload glucose values. Glucose 189-196 insulin Homo sapiens 0-7 12502677-1 2003 OBJECTIVE: Phosphatidylinositol (PI) 3-kinase activity is required for insulin-stimulated translocation of GLUT4 transporters and glucose uptake and utilization. Glucose 130-137 insulin Homo sapiens 71-78 12502677-6 2003 Insulin secretion was evaluated by intravenous glucose tolerance test and insulin sensitivity by hyperinsulinemic-euglycemic clamp. Glucose 47-54 insulin Homo sapiens 0-7 12502678-4 2003 RESULTS: The peak insulin concentration was higher and the peak glucose and C-peptide concentrations were lower with both insulin preparations than with no exogenous insulin. Glucose 64-71 insulin Homo sapiens 122-129 12502678-4 2003 RESULTS: The peak insulin concentration was higher and the peak glucose and C-peptide concentrations were lower with both insulin preparations than with no exogenous insulin. Glucose 64-71 insulin Homo sapiens 122-129 12502678-5 2003 Glucose areas under the curve above baseline were significantly lower with insulin aspart (180-min area, 7.1 mg. h. dl(-1); P = 0.018), but not with regular insulin (30.2 mg. h. dl(-1); P = 0.997), than with no insulin (29.4 mg. h. dl(-1)). Glucose 0-7 insulin Homo sapiens 75-82 12502679-5 2003 Insulin sensitivity (M(LBM)) was determined by glucose uptake per kg lean body mass (LBM), and parents reported birth weight. Glucose 47-54 insulin Homo sapiens 0-7 12502684-5 2003 Of eight studies that performed sequential oral glucose tolerance tests (OGTTs) after at least 6 months of Depo-Provera or Norplant use, seven found significant elevations (approximate doubling) of insulin at 2 or 3 h after glucose challenge; the effects on fasting, half-hour, or 1-h postchallenge insulin values were less consistent. Glucose 48-55 insulin Homo sapiens 198-205 12502684-5 2003 Of eight studies that performed sequential oral glucose tolerance tests (OGTTs) after at least 6 months of Depo-Provera or Norplant use, seven found significant elevations (approximate doubling) of insulin at 2 or 3 h after glucose challenge; the effects on fasting, half-hour, or 1-h postchallenge insulin values were less consistent. Glucose 224-231 insulin Homo sapiens 198-205 12502684-6 2003 The three studies that performed sequential intravenous glucose tolerance tests (IVGTTs) on injection users all found an increased early-phase insulin response. Glucose 56-63 insulin Homo sapiens 143-150 12502684-7 2003 One study used sequential hyperglycemic-hyperinsulinemic clamps to demonstrate reduced total-body glucose uptake per unit of insulin after 8 weeks of Norplant use. Glucose 98-105 insulin Homo sapiens 45-52 12519314-2 2003 There is increasing evidence that the growth hormone (GH)-insulin-like growth factor (IGF) axis may play an important role in glucose metabolism. Glucose 126-133 insulin Homo sapiens 58-65 12519314-4 2003 In contrast, IGF-I has insulin-like actions, which are, in the case of glucose metabolism, opposite to those of GH. Glucose 71-78 insulin Homo sapiens 23-30 12519318-3 2003 Insulin sensitivity was determined by the euglycaemic hyperinsulinaemic glucose clamp technique as the glucose disposal rate relative to the insulin level obtained (GDRI), and also estimated with the homeostasis model assessment (HOMA-S). Glucose 72-79 insulin Homo sapiens 0-7 12637978-10 2003 Intact proinsulin (OR, 1.57, CI, 1.16-2.14), and 32-33 split proinsulin (OR, 1.70, CI, 1.20-2.39) were associated with development of Type 2 diabetes, independent of AIR, adjusted for BMI and fasting glucose, whereas specific insulin was not (OR, 1.31, CI, 0.98-1.77), nor was IRI (OR, 1.25, CI, 0.96-1.63). Glucose 200-207 insulin Homo sapiens 61-71 12725708-1 2003 The altered pharmacokinetics of new rapid-acting insulin analogs make them very effective in controlling blood glucose peaks after meals. Glucose 111-118 insulin Homo sapiens 49-56 12828818-1 2003 Accurate bolus insulin doses require calculations based on (1) current blood glucose, (2) target blood glucose, (3) carbohydrate-to-insulin ratios, (4) total grams of carbohydrate in meals, and (5) insulin sensitivity factors. Glucose 77-84 insulin Homo sapiens 15-22 12828818-1 2003 Accurate bolus insulin doses require calculations based on (1) current blood glucose, (2) target blood glucose, (3) carbohydrate-to-insulin ratios, (4) total grams of carbohydrate in meals, and (5) insulin sensitivity factors. Glucose 103-110 insulin Homo sapiens 15-22 12828818-12 2003 These results confirm that bolus insulin doses computed by a bolus calculator, compared with standard bolus techniques, achieve target postprandial blood glucose but with fewer correction boluses and supplemental carbohydrate. Glucose 154-161 insulin Homo sapiens 33-40 14511424-3 2003 In addition, the calculation of the correct insulin dose is complex because it requires considering anticipated carbohydrate consumption and exercise in addition to the current blood glucose level. Glucose 183-190 insulin Homo sapiens 44-51 14609346-6 2003 The accumulation of hepatic steatosis is thought to occur initially, primarily through hepatic and peripheral insulin resistance, which leads to altered glucose and free fatty acid metabolism. Glucose 153-160 insulin Homo sapiens 110-117 14709197-1 2003 Glucose sensing and insulin delivery technology can potentially be linked to form a closed-loop insulin delivery system. Glucose 0-7 insulin Homo sapiens 96-103 14709204-0 2003 MINMOD Millennium: a computer program to calculate glucose effectiveness and insulin sensitivity from the frequently sampled intravenous glucose tolerance test. Glucose 137-144 insulin Homo sapiens 77-84 14709204-1 2003 The Bergman Minimal Model enables estimation of two key indices of glucose/insulin dynamics: glucose effectiveness and insulin sensitivity. Glucose 67-74 insulin Homo sapiens 75-82 12699398-4 2003 Defects in the action and/or secretion of insulin are the two major abnormalities leading to development of glucose intolerance. Glucose 108-115 insulin Homo sapiens 42-49 14575619-5 2003 The insulin-receptor complex stimulates the cellular uptake of glucose. Glucose 63-70 insulin Homo sapiens 4-11 12527976-2 2003 The purpose of the present study was to examine the effects of ingesting differing amounts of glucose pre-exercise on the glucose and insulin responses during exercise and on time-trial (TT) performance. Glucose 94-101 insulin Homo sapiens 134-141 12527977-11 2003 Altering the timing of the ingestion of carbohydrate before exercise resulted in differences in plasma glucose/insulin responses which disappeared within 10 min of exercise and which had no effect on performance. Glucose 103-110 insulin Homo sapiens 111-118 12527978-7 2003 This was accompanied by a more than twofold greater rise in plasma insulin concentration in GLU compared to GAL and TRE (118% and 145%, respectively). Glucose 92-95 insulin Homo sapiens 67-74 12517256-1 2003 Incretins are peptide hormones, exemplified by glucose-dependent insulinotropic peptide and glucagon-like peptide 1 that are released from the gut in response to nutrient ingestion and enhance glucose-stimulated insulin secretion. Glucose 47-54 insulin Homo sapiens 65-72 12517256-1 2003 Incretins are peptide hormones, exemplified by glucose-dependent insulinotropic peptide and glucagon-like peptide 1 that are released from the gut in response to nutrient ingestion and enhance glucose-stimulated insulin secretion. Glucose 193-200 insulin Homo sapiens 65-72 12669265-4 2003 All of the patients underwent a frequently sampled intravenous glucose tolerance test (FSIGTT), and the minimal model of glucose was used for the estimation of insulin sensitivity (IS MINIMAL ). Glucose 121-128 insulin Homo sapiens 160-167 14671407-14 2003 GH therapy induced considerably higher fasting and glucose-stimulated insulin levels after 1 and 6 years, regardless of GH dosage. Glucose 51-58 insulin Homo sapiens 70-77 14671407-16 2003 Six months after discontinuation of GH, glucose levels remained normal, whereas fasting and glucose-stimulated insulin returned to levels comparable to those of healthy peers. Glucose 92-99 insulin Homo sapiens 111-118 14671407-26 2003 However, as has been reported in other patient groups, GH induced higher fasting and glucose-stimulated insulin levels, indicating insulin resistance. Glucose 85-92 insulin Homo sapiens 104-111 17003005-4 2003 Preoperative localization of focal insulin hypersecretion by percutaneous pancreatic venous sampling allowed excision of only a small pancreatic portion which was followed by normalization of blood glucose levels. Glucose 198-205 insulin Homo sapiens 35-42 12511541-3 2003 Among them, insulin uses an inhibitory G protein-sensitive mechanism that is involved in metabolic and vascular events, leading to enhanced glucose transport and vasodilation. Glucose 140-147 insulin Homo sapiens 12-19 12532150-5 2003 Insulin sensitivity, assessed by the inhibition of glycerol release, was measured in the abdominal subcutaneous adipose tissue during a standard oral glucose tolerance test (OGTT) in six HIV-infected children under multi-therapy with abdominal lipohypertrophy (supra-iliac skinfold thickness >97th percentile) (HIV/LH+), in six obese children (obese group) and in eight HIV-infected children without lipodystrophy (HIV/LH-). Glucose 150-157 insulin Homo sapiens 0-7 12447984-5 2003 Reduction of plasma FFA levels in fasted rats or humans severely impairs glucose-induced insulin release. Glucose 73-80 insulin Homo sapiens 89-96 12519846-8 2003 Acute insulin response to iv glucose tolerance test significantly increased in 12 of 14 subjects after the first 6 months of gluten deprivation (P = 0.04) and decreased in 10 of 13 subjects during the following 6-month period of normal diet (P = 0.07). Glucose 29-36 insulin Homo sapiens 6-13 12519851-6 2003 Insulin sensitivity (S(I)) and the acute insulin response to glucose (AIR) were determined by an iv glucose tolerance test and minimal modeling, and body composition was determined by dual-energy x-ray absorptiometry. Glucose 61-68 insulin Homo sapiens 41-48 12531878-0 2003 Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production. Glucose 106-113 insulin Homo sapiens 88-95 12531878-4 2003 The effects of resistin and RELMbeta on in vivo insulin action were completely accounted for by a marked increase in the rate of glucose production. Glucose 129-136 insulin Homo sapiens 48-55 12525257-9 2003 This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. Glucose 14-21 insulin Homo sapiens 109-116 12644726-8 2003 However, insulin-stimulated whole body glucose uptake values were similar between the groups during both insulin infusions. Glucose 39-46 insulin Homo sapiens 9-16 12822388-6 2003 Glimepiride reduces glucose levels blood by stimulating insulin release from functional pancreatic beta cells in response to glucose. Glucose 125-132 insulin Homo sapiens 56-63 12858660-3 2003 Three hormones--amylin, glucagon and insulin--are a critical part of postmeal glucose regulation. Glucose 78-85 insulin Homo sapiens 37-46 12710591-4 2003 Such functional organization may account for systemic features such as the biphasic time course of glucose-stimulated insulin secretion. Glucose 99-106 insulin Homo sapiens 118-125 14668698-2 2003 Two fundamental abnormalities are involved in the pathogenesis of type 2 diabetes: Resistance to the biologic activities of insulin in glucose and lipid metabolism and inadequate insulin secretion from the pancreatic B cells. Glucose 135-142 insulin Homo sapiens 124-131 12751691-7 2003 Although there were no significant differences in the incremental areas under glucose or insulin curves (AUC) between relatives of ALB+ and ALB- in the OGTT, the insulin secretory response to the rise in plasma glucose was impaired in relatives of patients with ALB+ (insulin AUC/glucose AUC: 7.1 [1.1-30.8] vs. 9.8 [3.6-52.2], p=0.039). Glucose 211-218 insulin Homo sapiens 162-169 12499898-1 2002 BACKGROUND: A gene-therapy-based treatment of type 1 diabetes mellitus requires the development of a surrogate beta cell that can synthesize and secrete functionally active insulin in response to physiologically relevant changes in ambient glucose levels. Glucose 240-247 insulin Homo sapiens 173-180 12499898-3 2002 The authors" strategy for achieving glucose-dependent insulin secretion relies on glucose-responsive transcription of insulin mRNA and the constitutive secretory pathway of liver cells. Glucose 36-43 insulin Homo sapiens 54-61 12499898-6 2002 All detectable insulin produced by transduced hepatocytes in vitro was secreted, and the amount was dependent on the concentration of glucose and the duration of glucose stimulation. Glucose 134-141 insulin Homo sapiens 15-22 12499898-6 2002 All detectable insulin produced by transduced hepatocytes in vitro was secreted, and the amount was dependent on the concentration of glucose and the duration of glucose stimulation. Glucose 162-169 insulin Homo sapiens 15-22 12499898-7 2002 Analysis of in vivo functional efficacy of insulin gene therapy in streptozotocin-treated diabetic rats revealed the following: (1) fasting blood glucose levels were reduced to normal; (2) blood glucose levels of rats fed ad libitum were significantly reduced; and (3) peak blood glucose levels during oral glucose tolerance tests were significantly reduced. Glucose 146-153 insulin Homo sapiens 43-50 12499898-7 2002 Analysis of in vivo functional efficacy of insulin gene therapy in streptozotocin-treated diabetic rats revealed the following: (1) fasting blood glucose levels were reduced to normal; (2) blood glucose levels of rats fed ad libitum were significantly reduced; and (3) peak blood glucose levels during oral glucose tolerance tests were significantly reduced. Glucose 195-202 insulin Homo sapiens 43-50 12499898-7 2002 Analysis of in vivo functional efficacy of insulin gene therapy in streptozotocin-treated diabetic rats revealed the following: (1) fasting blood glucose levels were reduced to normal; (2) blood glucose levels of rats fed ad libitum were significantly reduced; and (3) peak blood glucose levels during oral glucose tolerance tests were significantly reduced. Glucose 195-202 insulin Homo sapiens 43-50 12499898-8 2002 CONCLUSIONS: These studies demonstrate in vivo glucose-regulated insulin secretion from an autologous non-beta cell leading to fasting euglycemia and an improved glucose tolerance, thereby supporting the feasibility of hepatocyte-based insulin gene-therapy for treatment of type 1 diabetes mellitus. Glucose 47-54 insulin Homo sapiens 65-72 12499898-8 2002 CONCLUSIONS: These studies demonstrate in vivo glucose-regulated insulin secretion from an autologous non-beta cell leading to fasting euglycemia and an improved glucose tolerance, thereby supporting the feasibility of hepatocyte-based insulin gene-therapy for treatment of type 1 diabetes mellitus. Glucose 47-54 insulin Homo sapiens 236-243 12499898-8 2002 CONCLUSIONS: These studies demonstrate in vivo glucose-regulated insulin secretion from an autologous non-beta cell leading to fasting euglycemia and an improved glucose tolerance, thereby supporting the feasibility of hepatocyte-based insulin gene-therapy for treatment of type 1 diabetes mellitus. Glucose 162-169 insulin Homo sapiens 65-72 12490950-1 2002 Insulin stimulates glucose uptake in muscle and adipocytes by signalling the translocation of GLUT4 glucose transporters from intracellular membranes to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 12393900-10 2002 Fusion of these vesicles with the plasma membrane may be largely responsible for the primary effect of insulin on glucose transport in fat tissue. Glucose 114-121 insulin Homo sapiens 103-110 12466058-4 2002 Insulin resistance was identified using the loss of tolbutamide (10 mg/kg) or electroacupuncture (EA)-induced plasma glucose lowering action. Glucose 117-124 insulin Homo sapiens 0-7 12466058-9 2002 Similar treatment with die-huang-wan at an effective dose (26.0 mg/kg) also increased the plasma glucose lowering action of exogenous insulin at 10 d later. Glucose 97-104 insulin Homo sapiens 134-141 12486493-4 2002 Insulin-mediated turnover of glucose and the clearance of insulin were measured in 7 control piglets (+D) and in 10 piglets with inherited calcitriol deficiency (-D). Glucose 29-36 insulin Homo sapiens 0-7 12486493-10 2002 The relationship between insulin concentration in plasma and glucose turnover (measured with [3-(3)H]glucose) was not influenced by the calcemic and vitamin D status of the piglets. Glucose 61-68 insulin Homo sapiens 25-32 12486493-10 2002 The relationship between insulin concentration in plasma and glucose turnover (measured with [3-(3)H]glucose) was not influenced by the calcemic and vitamin D status of the piglets. Glucose 101-108 insulin Homo sapiens 25-32 12486493-11 2002 This indicated that the peripheral action of insulin on glucose metabolism was not influenced by the extracellular calcium concentration and vitamin D status. Glucose 56-63 insulin Homo sapiens 45-52 12388133-0 2002 Insulin-stimulated cytosol alkalinization facilitates optimal activation of glucose transport in cardiomyocytes. Glucose 76-83 insulin Homo sapiens 0-7 12388133-2 2002 We have therefore investigated the dependence of insulin-stimulated glucose transport on cytosolic pH in cardiomyocytes. Glucose 68-75 insulin Homo sapiens 49-56 12388151-7 2002 The potentiation factor was found to be related to plasma glucose-dependent insulin-releasing polypeptide concentrations (r = 0.49, P < 0.0001). Glucose 58-65 insulin Homo sapiens 76-83 12388151-8 2002 Among beta-cell function parameters, only insulin secretion at 5 mM glucose from MT correlated inversely with insulin sensitivity (24-h MT: r = -0.74, P < 0.001; 2-h MT: r = -0.52, P < 0.05), whereas the dose-response slope and the OGTT parameters did not. Glucose 68-75 insulin Homo sapiens 42-49 12424101-2 2002 Inputs from glucose and cell surface receptors act together to initiate the beta-cell stimulus-response coupling that ultimately leads to the release of insulin. Glucose 12-19 insulin Homo sapiens 153-160 12450897-11 2002 The dynamics of the insulin response after the ingestion of glycine plus glucose were modestly different from those after the ingestion of glucose alone, but the area response was not significantly different. Glucose 73-80 insulin Homo sapiens 20-27 12450897-12 2002 CONCLUSION: The data are compatible with the hypothesis that oral glycine stimulates the secretion of a gut hormone that potentiates the effect of insulin on glucose removal from the circulation. Glucose 158-165 insulin Homo sapiens 147-154 12466139-7 2002 On normalization of their blood glucose and ketone body levels by exogenous insulin, their sVAP-1 concentration rapidly decreased to control levels. Glucose 32-39 insulin Homo sapiens 76-83 12489380-4 2002 Diabetes may develop in insulin-resistant persons with inherited secretory and glucose-sensing defects in beta cells. Glucose 79-86 insulin Homo sapiens 24-31 12489380-13 2002 Diabetes may develop in insulin-resistant persons with inherited secretory and glucose-sensing defects in beta cells. Glucose 79-86 insulin Homo sapiens 24-31 12392946-7 2002 When insulin was co-loaded with glucose oxidase into these "bio-smart" devices, there was a twofold increase in insulin release rate when the devices were immersed in glucose solutions. Glucose 32-39 insulin Homo sapiens 5-12 12392946-7 2002 When insulin was co-loaded with glucose oxidase into these "bio-smart" devices, there was a twofold increase in insulin release rate when the devices were immersed in glucose solutions. Glucose 32-39 insulin Homo sapiens 112-119 12392956-2 2002 The availability of long term functional implantable biosensors for continuous glucose measurings is a basic prerequisite for the individualized optimum insulin treatment of diabetics. Glucose 79-86 insulin Homo sapiens 153-160 12460323-18 2002 CONCLUSIONS: Our observations of an increased glucose requirement during the clamp as well as a decrease in haemoglobin A1c demonstrate improved insulin sensitivity in the adolescent girls with diabetes following pirenzepine therapy. Glucose 46-53 insulin Homo sapiens 145-152 12419178-1 2002 Insulin resistance and/or compensatory hyperinsulinemia are associated with hypertension, obesity, dyslipidemia, and glucose intolerance. Glucose 117-124 insulin Homo sapiens 0-7 12437616-0 2002 The impact of impaired insulin release and insulin resistance on glucose intolerance after renal transplantation. Glucose 65-72 insulin Homo sapiens 23-30 12437616-10 2002 The presence of defects in insulin release, rather than insulin action, indicates a poor prognosis regarding later normalization of glucose tolerance. Glucose 132-139 insulin Homo sapiens 27-34 12453915-1 2002 Type 2 diabetes is a heterogeneous disorder of glucose metabolism characterized by insulin resistance, beta-cell dysfunction, and increased glucose production by the liver. Glucose 47-54 insulin Homo sapiens 83-90 12453949-6 2002 CONCLUSIONS: Incubation of cultured human skeletal muscle cells derived from glucose-tolerant subjects with glimepiride caused a dose-dependent increase of insulin-stimulated glycogen synthesis using therapeutic glimepiride concentrations. Glucose 77-84 insulin Homo sapiens 156-163 12475787-0 2002 The multiple actions of GLP-1 on the process of glucose-stimulated insulin secretion. Glucose 48-55 insulin Homo sapiens 67-74 12475787-5 2002 In the pancreas, GLP-1 is now known to induce expansion of insulin-secreting beta-cell mass, in addition to its most well-characterized effect: the augmentation of glucose-stimulated insulin secretion. Glucose 164-171 insulin Homo sapiens 183-190 12482735-0 2002 Implantable closed-loop glucose-sensing and insulin delivery: the future for insulin pump therapy. Glucose 24-31 insulin Homo sapiens 77-84 12488953-1 2002 AIMS/HYPOTHESIS: A reduced first-phase insulin response to intravenous glucose is perceived as a sign of far-advanced deterioration of beta-cell function during the development of Type I (insulin-dependent) diabetes mellitus, but data on insulin responses at the onset of diabetes-related autoimmunity are lacking. Glucose 71-78 insulin Homo sapiens 39-46 12488953-1 2002 AIMS/HYPOTHESIS: A reduced first-phase insulin response to intravenous glucose is perceived as a sign of far-advanced deterioration of beta-cell function during the development of Type I (insulin-dependent) diabetes mellitus, but data on insulin responses at the onset of diabetes-related autoimmunity are lacking. Glucose 71-78 insulin Homo sapiens 188-195 12488954-5 2002 Younger monozygotic twins had a slightly higher insulin-stimulated glucose uptake (M) than younger dizygotic twins. Glucose 67-74 insulin Homo sapiens 48-55 12488954-6 2002 In contrast, elderly monozygotic twins had a lower insulin-stimulated glucose uptake value compared with elderly dizygotic twins. Glucose 70-77 insulin Homo sapiens 51-58 12522324-10 2002 Previous treatment with diazoxide was associated with a moderate 1.9 +/- 0.6 fold rise in insulin response to intravenous glucose (p=0.04) and 1.6 +/- 0.4 fold increased glucose potentiation of arginine-induced insulin secretion (GPAIS) (p=0.04). Glucose 122-129 insulin Homo sapiens 90-97 12522327-8 2002 After the oral glucose load, early and total insulin release, in relation to glucose levels, were respectively, 43 and 67% lower in the IGT individuals. Glucose 15-22 insulin Homo sapiens 45-52 12522327-8 2002 After the oral glucose load, early and total insulin release, in relation to glucose levels, were respectively, 43 and 67% lower in the IGT individuals. Glucose 77-84 insulin Homo sapiens 45-52 12647841-6 2002 Soluble insulin was given prior to each feed with isophane insulin at 2200 h. Average duration of feed was 13 +/- 8 days with an achieved glucose level of 8.7 +/- 2.5 (mean +/- SD) mmol/l associated with 0.8 episodes of biochemical hypoglycaemia (< 3 mmol/l) each week. Glucose 138-145 insulin Homo sapiens 8-15 12647845-7 2002 RESULTS: Injection of insulin lispro resulted in a significant reduction in the before-dinner blood glucose compared with the untreated control group (10.4 +/- 3.8 mmol/l vs. 14.7 +/- 3.9 mmol/l, respectively). Glucose 100-107 insulin Homo sapiens 22-29 12647845-8 2002 The number of days on which the blood glucose was > 10 mmol/l was reduced by half in the insulin lispro group. Glucose 38-45 insulin Homo sapiens 92-99 12647845-13 2002 CONCLUSIONS: We conclude that an injection of insulin lispro before the afternoon meal can effectively lower the before-dinner blood glucose, and in boys also lowers the HbA1c. Glucose 133-140 insulin Homo sapiens 46-53 12688632-0 2002 Insulin secretion induced by palmitate--a process fully dependent on glucose concentration. Glucose 69-76 insulin Homo sapiens 0-7 12688633-0 2002 Beta-cell crosstalk: a further dimension in the stimulus-secretion coupling of glucose-induced insulin release. Glucose 79-86 insulin Homo sapiens 95-102 12688635-3 2002 The pancreatic beta-cell provides a highly favourable environment for the intracellular glycation of insulin which is a relatively rapid, glucose-dependent process. Glucose 138-145 insulin Homo sapiens 101-108 12702002-8 2002 Application of repeated minimal glucose infusions has further improved the discrimination between insulin release in health and diabetes, suggesting that this method may be suitable for smaller prospective studies of the development of diabetes. Glucose 32-39 insulin Homo sapiens 98-105 12702004-5 2002 In experiments with exogenous insulin interventions, peak post-prandial blood glucose increments were curtailed without undue increases in total insulin exposure. Glucose 78-85 insulin Homo sapiens 30-37 12703060-1 2002 Insulin secretion from the beta-cells in the islets of Langerhans is mainly regulated by glucose entry via its transporter. Glucose 89-96 insulin Homo sapiens 0-7 12446586-2 2002 Glucose is the cardinal physiological stimulator of insulin secretion from the pancreatic beta-cell, but the mechanisms involved in glucose sensing are not fully understood. Glucose 0-7 insulin Homo sapiens 52-59 12446602-9 2002 When introduced into 3T3-L1 adipocytes, curcumin markedly inhibited insulin-induced GLUT4 translocation and glucose transport. Glucose 108-115 insulin Homo sapiens 68-75 12534451-1 2002 BACKGROUND: Protein phosphatase 2A (PP2A) acts on a number of enzymes involved in the insulin regulation of glucose uptake and glycogen synthesis. Glucose 108-115 insulin Homo sapiens 86-93 12534451-5 2002 RESULTS: In type 2 diabetic subjects insulin-mediated glucose disposal, glucose oxidation and nonoxidative glucose metabolism were reduced, whereas lipid oxidation was increased (all P < 0.05). Glucose 54-61 insulin Homo sapiens 37-44 12534451-7 2002 In the control subjects, the insulin-mediated decrease in PP2A-C alpha correlated with the insulin-mediated increase in glucose disposal, glucose oxidation, nonoxidative glucose metabolism (all P < 0.05) and decrease in lipid oxidation (P < 0.01). Glucose 120-127 insulin Homo sapiens 29-36 12534451-7 2002 In the control subjects, the insulin-mediated decrease in PP2A-C alpha correlated with the insulin-mediated increase in glucose disposal, glucose oxidation, nonoxidative glucose metabolism (all P < 0.05) and decrease in lipid oxidation (P < 0.01). Glucose 120-127 insulin Homo sapiens 91-98 12534451-7 2002 In the control subjects, the insulin-mediated decrease in PP2A-C alpha correlated with the insulin-mediated increase in glucose disposal, glucose oxidation, nonoxidative glucose metabolism (all P < 0.05) and decrease in lipid oxidation (P < 0.01). Glucose 138-145 insulin Homo sapiens 29-36 12534451-7 2002 In the control subjects, the insulin-mediated decrease in PP2A-C alpha correlated with the insulin-mediated increase in glucose disposal, glucose oxidation, nonoxidative glucose metabolism (all P < 0.05) and decrease in lipid oxidation (P < 0.01). Glucose 138-145 insulin Homo sapiens 91-98 12534451-9 2002 CONCLUSIONS: Down-regulation of PP2A-C alpha expression by insulin in skeletal muscle seems to be associated with a normal insulin action on glucose storage, glucose and lipid oxidation. Glucose 158-165 insulin Homo sapiens 59-66 12458394-0 2002 Variability of insulin-stimulated myocardial glucose uptake in healthy elderly subjects. Glucose 45-52 insulin Homo sapiens 15-22 12458394-1 2002 The aim of this study was to assess regional and global variability of insulin-stimulated myocardial glucose uptake in healthy elderly subjects and to evaluate potentially responsible factors. Glucose 101-108 insulin Homo sapiens 71-78 12458394-3 2002 Whole-body insulin sensitivity and insulin-stimulated myocardial glucose uptake were measured during hyperinsulinaemic euglycaemic glucose clamp with fluorine-18 fluorodeoxyglucose, and myocardial rest and hyperaemic blood flow during dipyridamole infusion were measured with nitrogen-13 ammonia and positron emission tomography in 16 left ventricular myocardial segments. Glucose 65-72 insulin Homo sapiens 35-42 12458394-4 2002 Intra-individual and inter-individual variability of insulin-stimulated myocardial glucose uptake [relative dispersion = (standard deviation/mean)] was 13% and 29% respectively. Glucose 83-90 insulin Homo sapiens 53-60 12458394-6 2002 Regional and global insulin-stimulated myocardial glucose uptake correlated linearly with whole-body insulin sensitivity ( r=0.51, P<0.05 and r=0.56, P<0.01). Glucose 50-57 insulin Homo sapiens 20-27 12458394-6 2002 Regional and global insulin-stimulated myocardial glucose uptake correlated linearly with whole-body insulin sensitivity ( r=0.51, P<0.05 and r=0.56, P<0.01). Glucose 50-57 insulin Homo sapiens 101-108 12458394-8 2002 We conclude that in healthy elderly subjects, insulin-stimulated myocardial glucose uptake is homogeneous throughout the left ventricle, but has moderate inter-individual variability. Glucose 76-83 insulin Homo sapiens 46-53 12458394-9 2002 Inter-individual variability of insulin-stimulated myocardial glucose uptake is primarily explained by variability in coronary vascular reactivity and tissue insulin sensitivity. Glucose 62-69 insulin Homo sapiens 32-39 12458394-9 2002 Inter-individual variability of insulin-stimulated myocardial glucose uptake is primarily explained by variability in coronary vascular reactivity and tissue insulin sensitivity. Glucose 62-69 insulin Homo sapiens 158-165 12477517-11 2002 RESULT(S): Metformin treatment was associated with significant reduction in basal free testosterone plasma levels, insulin plasma levels, and insulin response to oral glucose tolerance testing. Glucose 167-174 insulin Homo sapiens 142-149 12427792-1 2002 AIMS: Human liver cirrhosis is commonly associated with increased fasting and glucose induced insulin concentrations. Glucose 78-85 insulin Homo sapiens 94-101 12427792-11 2002 Insulin sensitivity, markedly reduced in cirrhosis (157 (10) versus 296 (30) ml/min/m(2), p<0.002), was strongly inversely correlated (r=0.89, p<0.002) in these patients with insulin secretion at 5 mM glucose. Glucose 207-214 insulin Homo sapiens 0-7 12500984-7 2002 An oral glucose tolerance test was performed to obtain an index of insulin sensitivity (ISI). Glucose 8-15 insulin Homo sapiens 67-74 12391128-2 2002 An index of whole body insulin sensitivity (ISI), obtained from minimal model analysis of insulin and glucose concentrations during a frequently sampled intravenous glucose tolerance test, was determined in 126 healthy adults: 25 young [27 +/- 1 (SE) yr; 13 men/12 women] and 43 older (59 +/- 1 yr; 20/13) sedentary and 25 young (29 +/- 1 yr; 12/13) and 33 older (60 +/- 1 yr; 20/13) endurance trained. Glucose 102-109 insulin Homo sapiens 23-30 12466340-15 2002 Area under the curve of insulin, C-peptide, and blood glucose levels during oral glucose tolerance test decreased after 6 months (insulin: 277 vs. 139 micro U/ml.h; C-peptide 52 vs. 15 ng/m.h; area under the curve glucose: 17316 vs. 12780 mg/d.min). Glucose 81-88 insulin Homo sapiens 130-137 12466340-15 2002 Area under the curve of insulin, C-peptide, and blood glucose levels during oral glucose tolerance test decreased after 6 months (insulin: 277 vs. 139 micro U/ml.h; C-peptide 52 vs. 15 ng/m.h; area under the curve glucose: 17316 vs. 12780 mg/d.min). Glucose 81-88 insulin Homo sapiens 130-137 12466359-9 2002 Measures of insulin sensitivity were calculated as the fasting glucose to insulin ratio, quantitative insulin sensitivity check index, and composite insulin sensitivity index. Glucose 63-70 insulin Homo sapiens 12-19 12466363-6 2002 In both groups, the markers of insulin resistance in fasting and stimulated conditions (glucose/insulin ratio, homeostasis model insulin resistance index, homeostasis model applied to the oral glucose tolerance test) demonstrated decreased insulin sensitivity. Glucose 88-95 insulin Homo sapiens 31-38 12409500-2 2002 The mechanism of action of sulfonylureas is to release insulin from pancreatic cells and they have been proposed to act on insulin-sensitive tissues to enhance glucose uptake. Glucose 160-167 insulin Homo sapiens 123-130 12522466-3 2002 This study looked at the DLF response to hyperinsulinemia, achieved by an oral glucose tolerance test (OGTT), in the setting of a naturally occurring and self-resolving state of human insulin resistance, during third-trimester pregnancy. Glucose 79-86 insulin Homo sapiens 46-53 12522466-10 2002 These findings showed that the increment of insulin induced by oral glucose during pregnancy caused a more rapid rise in circulating DLF levels than it did during the nonpregnant state. Glucose 68-75 insulin Homo sapiens 44-51 12472910-9 2002 MAIN OUTCOME MEASURE: Insulin levels and insulin to plasma glucose ratios in insulinoma patients and in individuals without insulin-secreting tumours at termination of the fast and at plasma glucose levels </=2.5 mmol L-1, prior to the occurrence of neuroglycopenic symptoms. Glucose 59-66 insulin Homo sapiens 41-48 12472910-15 2002 Prior to the occurrence of neuroglycopenic symptoms and at venous plasma glucose </=2.5 mmol L-1, insulin to plasma glucose ratios dropped in insulinoma patients to values within the normal range on several occasions. Glucose 73-80 insulin Homo sapiens 101-108 12472910-15 2002 Prior to the occurrence of neuroglycopenic symptoms and at venous plasma glucose </=2.5 mmol L-1, insulin to plasma glucose ratios dropped in insulinoma patients to values within the normal range on several occasions. Glucose 119-126 insulin Homo sapiens 101-108 12472919-0 2002 Bezafibrate-induced improvement in glucose uptake and endothelial function in protease inhibitor-associated insulin resistance. Glucose 35-42 insulin Homo sapiens 108-115 12445506-2 2002 Based on the available evidence from molecular biology, the pivotal regulatory role of T(3) in major metabolic pathways and glycemic control can be delineated by mapping the specific action sites of T(3) and insulin on the metabolic pathways of the glucose-lipid cycle. Glucose 249-256 insulin Homo sapiens 208-215 12460725-2 2002 A control method for the automation of insulin infusion that utilizes emerging technologies in blood glucose biosensors is presented. Glucose 101-108 insulin Homo sapiens 39-46 12426561-1 2002 Circulating insulin inhibits endogenous glucose production. Glucose 40-47 insulin Homo sapiens 12-19 12426561-3 2002 The infusion of either insulin or a small-molecule insulin mimetic in the third cerebral ventricle suppressed glucose production independent of circulating levels of insulin and of other glucoregulatory hormones. Glucose 110-117 insulin Homo sapiens 23-30 12426561-3 2002 The infusion of either insulin or a small-molecule insulin mimetic in the third cerebral ventricle suppressed glucose production independent of circulating levels of insulin and of other glucoregulatory hormones. Glucose 110-117 insulin Homo sapiens 51-58 12426561-3 2002 The infusion of either insulin or a small-molecule insulin mimetic in the third cerebral ventricle suppressed glucose production independent of circulating levels of insulin and of other glucoregulatory hormones. Glucose 110-117 insulin Homo sapiens 51-58 12426561-4 2002 Conversely, central antagonism of insulin signaling impaired the ability of circulating insulin to inhibit glucose production. Glucose 107-114 insulin Homo sapiens 34-41 12426561-4 2002 Conversely, central antagonism of insulin signaling impaired the ability of circulating insulin to inhibit glucose production. Glucose 107-114 insulin Homo sapiens 88-95 12426561-6 2002 These results reveal a new site of action of insulin on glucose production and suggest that hypothalamic insulin resistance can contribute to hyperglycemia in type 2 diabetes mellitus. Glucose 56-63 insulin Homo sapiens 45-52 12577084-5 2002 and decrease in the hepatic sensitivity to insulin action in suppressing glucose output have received more attention. Glucose 73-80 insulin Homo sapiens 43-50 12490664-1 2002 OBJECTIVE: Lower lipid and insulin levels are found during a glucose-tolerance test in obese black than obese white South African women. Glucose 61-68 insulin Homo sapiens 27-34 12490664-9 2002 DISCUSSION: The higher 30-minute insulin response in OBW may reflect a higher insulinotropic effect of FFAs or glucose. Glucose 111-118 insulin Homo sapiens 33-40 12434122-4 2002 These genetic variants result in an attenuated secretion of insulin in response to glucose stimulation. Glucose 83-90 insulin Homo sapiens 60-67 12435589-3 2002 In the present experiments we demonstrate that higher insulin receptor and insulin receptor substrates-1 and -2 (IRS1 and IRS2) concentrations are predominantly encountered in cells of the periphery of rat pancreatic islets, as compared to centrally located cells, and that partial blockade of IRS1 protein expression by antisense oligonucleotide treatment leads to improved insulin secretion induced by glucose overload, which is accompanied by lower steady-state glucagon secretion and blunted glucose-induced glucagon fall. Glucose 496-503 insulin Homo sapiens 54-61 12393900-0 2002 Translocation of small preformed vesicles is responsible for the insulin activation of glucose transport in adipose cells. Glucose 87-94 insulin Homo sapiens 65-72 12435589-3 2002 In the present experiments we demonstrate that higher insulin receptor and insulin receptor substrates-1 and -2 (IRS1 and IRS2) concentrations are predominantly encountered in cells of the periphery of rat pancreatic islets, as compared to centrally located cells, and that partial blockade of IRS1 protein expression by antisense oligonucleotide treatment leads to improved insulin secretion induced by glucose overload, which is accompanied by lower steady-state glucagon secretion and blunted glucose-induced glucagon fall. Glucose 404-411 insulin Homo sapiens 54-61 12435589-3 2002 In the present experiments we demonstrate that higher insulin receptor and insulin receptor substrates-1 and -2 (IRS1 and IRS2) concentrations are predominantly encountered in cells of the periphery of rat pancreatic islets, as compared to centrally located cells, and that partial blockade of IRS1 protein expression by antisense oligonucleotide treatment leads to improved insulin secretion induced by glucose overload, which is accompanied by lower steady-state glucagon secretion and blunted glucose-induced glucagon fall. Glucose 404-411 insulin Homo sapiens 75-82 12435589-3 2002 In the present experiments we demonstrate that higher insulin receptor and insulin receptor substrates-1 and -2 (IRS1 and IRS2) concentrations are predominantly encountered in cells of the periphery of rat pancreatic islets, as compared to centrally located cells, and that partial blockade of IRS1 protein expression by antisense oligonucleotide treatment leads to improved insulin secretion induced by glucose overload, which is accompanied by lower steady-state glucagon secretion and blunted glucose-induced glucagon fall. Glucose 496-503 insulin Homo sapiens 75-82 12393301-1 2002 Type 2 diabetes is associated with insulin resistance in peripheral tissues, such as muscle and fat, impaired glucose-stimulated insulin secretion from pancreatic beta-cells and elevated hepatic gluconeogenesis. Glucose 110-117 insulin Homo sapiens 129-136 12213804-7 2002 In 3T3-L1 adipocytes, 5 microm TLK19780 enhanced insulin-stimulated glucose transport, increasing both the sensitivity and maximal responsiveness to insulin. Glucose 68-75 insulin Homo sapiens 49-56 12393301-3 2002 Thus, novel targets are being explored that enhance insulin action at target tissues, stimulate carbohydrate and fat catabolism, decrease endogenous glucose production and increase pancreatic beta-cell neogenesis and glucose-dependent insulin secretion. Glucose 149-156 insulin Homo sapiens 52-59 12441210-4 2002 Insulin sensitivity was evaluated from the steady-state plasma glucose (SSPG) level measured at the steady-state insulin level (20 to 30 microU/mL) using a modification of the SSPG method previously reported. Glucose 63-70 insulin Homo sapiens 0-7 12520825-6 2002 Thiazolidinediones constitute a new class of insulin sensitizers that work predominantly in improving glucose uptake by the adipose tissues and skeletal muscles. Glucose 102-109 insulin Homo sapiens 45-52 12376328-1 2002 In our previous studies in nondiabetic dogs and humans, insulin suppressed glucose production (GP) by both an indirect extrahepatic and a direct hepatic effect. Glucose 75-82 insulin Homo sapiens 56-63 12505096-5 2002 Insulin resistance (IR) was defined as belonging to the first quartile of fasting glucose/insulin ratio (G/IR) distribution or fourth quartile of IR (HOMA). Glucose 82-89 insulin Homo sapiens 0-7 12530515-1 2002 Mitochondrial metabolism is crucial for the coupling of glucose recognition to the exocytosis of the insulin granules. Glucose 56-63 insulin Homo sapiens 101-108 12433712-1 2002 There is some evidence that glucose and other factors related to glucose metabolism, such as insulin and insulin-like growth-factors (IGFs) may contribute to breast cancer development. Glucose 28-35 insulin Homo sapiens 93-100 12433712-1 2002 There is some evidence that glucose and other factors related to glucose metabolism, such as insulin and insulin-like growth-factors (IGFs) may contribute to breast cancer development. Glucose 28-35 insulin Homo sapiens 105-112 12430784-7 2002 The insulin resistance index (IR) was determined from fasting plasma glucose and insulin concentrations, using the homeostasis model assessment (HOMA). Glucose 69-76 insulin Homo sapiens 4-11 12213349-7 2002 In addition, the area under the insulin curve for the oral glucose tolerance test showed a significant increase from 27,438+/-4,488 to 41,946+/-6,048 pmol/l (P<0.05). Glucose 59-66 insulin Homo sapiens 32-39 12213349-11 2002 The insulin-sensitizing drug also produced a marked increase in endogenous insulin secretion in response to glucose, lower total and LDL cholesterol, and decreased fasting leptin despite weight gain. Glucose 108-115 insulin Homo sapiens 4-11 12213350-9 2002 Interestingly, we determined higher levels of insulin and C-peptide in PC patients having abnormal glucose tolerance than patients having normal glucose tolerance. Glucose 99-106 insulin Homo sapiens 46-53 12401706-3 2002 Regional fat, intramyocellular lipid (by (1)H-magnetic resonance spectroscopy), serum lipids, and insulin-stimulated glucose disposal (by hyperinsulinemic-euglycemic clamp) were quantified in 10 men who had HIV-1 infection with moderate to severe lipodystrophy and a control group of 10 nonlipodystrophic men who had HIV-1 infection and were naive to protease inhibitors to examine the effects of lipodystrophy on glucose and lipid metabolism. Glucose 117-124 insulin Homo sapiens 98-105 12379175-3 2002 Thiazolidinediones (TZDs) are a new class of insulin-sensitizing agents that activate the nuclear receptor peroxisome proliferator-activated receptor-g. TZDs may improve not only glucose levels but also other metabolic parameters associated with insulin resistance. Glucose 179-186 insulin Homo sapiens 45-52 12401706-4 2002 Lipodystrophic subjects showed lower insulin-stimulated glucose disposal than control subjects (P = 0.001) and had increased serum triglycerides (P = 0.03), less limb fat (P = 0.02), increased visceral fat as a proportion of total abdominal fat (P = 0.003), and increased intramyocellular lipid (1.90 +/- 0.15 vs. 1.23 +/- 0.16% of water resonance peak area; P = 0.007). Glucose 56-63 insulin Homo sapiens 37-44 12401706-5 2002 In both groups combined, visceral fat related strongly to intramyocellular lipid (r = 0.83, P < 0.0001) and intramyocellular lipid related negatively to insulin-stimulated glucose disposal (r = -0.71, P = 0.0005). Glucose 175-182 insulin Homo sapiens 156-163 12401760-0 2002 Indices of insulin action, disposal, and secretion derived from fasting samples and clamps in normal glucose-tolerant black and white children. Glucose 101-108 insulin Homo sapiens 11-18 12401727-4 2002 On the other hand, studies in animal and cell culture models identified pancreatic beta-cell UCP2 expression as a main determinant of the insulin secretory response to glucose. Glucose 168-175 insulin Homo sapiens 138-145 12401756-1 2002 OBJECTIVE: Both rapid-acting insulin analogs, insulin aspart and lispro, attenuate prandial glucose excursion compared with human soluble insulin. Glucose 92-99 insulin Homo sapiens 29-36 12401756-1 2002 OBJECTIVE: Both rapid-acting insulin analogs, insulin aspart and lispro, attenuate prandial glucose excursion compared with human soluble insulin. Glucose 92-99 insulin Homo sapiens 46-53 12401756-9 2002 CONCLUSIONS: These data suggest that in type 1 diabetic patients, both insulin analogs are equally effective for control of postprandial blood glucose excursions. Glucose 143-150 insulin Homo sapiens 71-78 12401758-0 2002 Acute effect of glimepiride on insulin-stimulated glucose metabolism in glucose-tolerant insulin-resistant offspring of patients with type 2 diabetes. Glucose 50-57 insulin Homo sapiens 31-38 12436337-2 2002 Our aim was to investigate differential effects of acutely increased plasma monounsaturated, polyunsaturated and saturated fatty acids on glucose-stimulated insulin secretion in healthy humans. Glucose 138-145 insulin Homo sapiens 157-164 12421431-6 2002 Adding insulin sensitivity to the multivariate models further weakened the relationship of CRP to 2-h glucose (r = 0.07, P < 0.05). Glucose 102-109 insulin Homo sapiens 7-14 12436329-0 2002 Insulin regulation of glucose uptake: a complex interplay of intracellular signalling pathways. Glucose 22-29 insulin Homo sapiens 0-7 12477252-6 2002 Although limited success has been made to control insulin gene expression in ectopic cells using hormone/glucose-regulated expression systems, these transcriptionally regulated systems are relatively slow in the "on-" and "off"-kinetics of insulin production, raising a serious safety concern for clinical application. Glucose 105-112 insulin Homo sapiens 50-57 12436329-1 2002 Insulin-stimulated glucose uptake in adipose tissue and striated muscle is critical for reducing post-prandial blood glucose concentrations and the dysregulation of this process is one hallmark of Type II (non-insulin-dependent) diabetes mellitus. Glucose 19-26 insulin Homo sapiens 0-7 12436337-9 2002 CONCLUSION/INTERPRETATION: Increasing plasma NEFA concentrations by oral fat feeding with heparin infusion augments glucose-stimulated insulin secretion with the greatest effect for monounsaturated fatty acids and the lowest effect for saturated fatty acids. Glucose 116-123 insulin Homo sapiens 135-142 12436329-1 2002 Insulin-stimulated glucose uptake in adipose tissue and striated muscle is critical for reducing post-prandial blood glucose concentrations and the dysregulation of this process is one hallmark of Type II (non-insulin-dependent) diabetes mellitus. Glucose 117-124 insulin Homo sapiens 0-7 12441751-11 2002 This suggests a possible link between resistance of muscle to the action of insulin for both glucose clearance and muscle protein catabolism. Glucose 93-100 insulin Homo sapiens 76-83 12518254-6 2002 RESULTS: The patient was insulin resistant before surgery (glucose infusion 4.6 mg. kg (-1). Glucose 59-66 insulin Homo sapiens 25-32 12469357-3 2002 It also induces satiety and promotes tissue deposition of ingested glucose by stimulating insulin secretion. Glucose 67-74 insulin Homo sapiens 90-97 12469357-10 2002 In addition, insulin sensitivity doubled and insulin responses to glucose were greatly improved. Glucose 66-73 insulin Homo sapiens 45-52 12469358-4 2002 If a source of stem cells capable of yielding glucose-responsive insulin-producing (GRIP) cells can be identified, then transplantation-based treatment for type 1 diabetes may become widely available. Glucose 46-53 insulin Homo sapiens 65-72 12469359-7 2002 Activation of the KATP channel-dependent pathway results in exocytosis of an immediately releasable pool that is responsible for the first phase of glucose-stimulated insulin release. Glucose 148-155 insulin Homo sapiens 167-174 15251831-5 2002 RESULTS: In the 10 women given D-chiro-inositol, the mean (+/- standard error) area under the plasma insulin curve after oral administration of glucose decreased significantly from 8,343 +/- 1,149 mU/mL per min to 5,335 +/- 1,792 mU/mL per min in comparison with no significant change in the placebo group (P = 0.03 for difference between groups). Glucose 144-151 insulin Homo sapiens 101-108 19003111-0 2002 Fermented milk, Kefram-Kefir enhances glucose uptake into insulin-responsive muscle cells. Glucose 38-45 insulin Homo sapiens 58-65 19003111-3 2002 Water-soluble or chloroform/methanol-extracted fractions from Kefram-Kefir were examined to evaluate the glucose uptake ability of L6 myotubes.As a result, the water-soluble fraction augmented the uptake of glucose in L6 myotubes both in the presence and absence of insulin stimulation. Glucose 207-214 insulin Homo sapiens 266-273 19003111-5 2002 Especially, glucose uptake was augmented up to six times with the addition of water-soluble fraction in the insulin-stimulated L6 myotubes. Glucose 12-19 insulin Homo sapiens 108-115 19003111-8 2002 Considering together with the reports that PI 3-kinase is locatedin the insulin signaling pathway and the participation in the translocation of glucose transporter 4 to the cell membrane, it is suggested that the water-soluble fraction of Kefram-Kefir activates PI 3-kinase or other upstream molecules in the insulin signaling pathway, which resulted in the augmentation of glucose uptake and its specific inhibition by wortmannin. Glucose 144-151 insulin Homo sapiens 309-316 12518254-12 2002 Insulin and C-peptide responses after oral glucose and intravenous glucagon increased into the normal range from 6 months after surgery onwards and oral glucose tolerance remained non-diabetic (IGT). Glucose 43-50 insulin Homo sapiens 0-7 12518254-12 2002 Insulin and C-peptide responses after oral glucose and intravenous glucagon increased into the normal range from 6 months after surgery onwards and oral glucose tolerance remained non-diabetic (IGT). Glucose 43-50 insulin Homo sapiens 12-21 12660874-6 2002 Furthermore, insulin-induced glucose uptake as a hallmark of adipocyte function was not altered by ghrelin pre-treatment. Glucose 29-36 insulin Homo sapiens 13-20 12450355-0 2002 Estimation of plasma insulin from plasma glucose. Glucose 41-48 insulin Homo sapiens 21-28 12397772-8 2002 Mean insulin values fasting and 30, 60 and 90 min after administration of 75 g glucose were significantly lower in patients after acute pancreatitis than in controls (p < 0.001). Glucose 79-86 insulin Homo sapiens 5-12 12397772-11 2002 CONCLUSIONS: Pancreatic endocrine function impairment following acute pancreatitis is associated with the decreased plasma insulin levels fasting and after glucose stimulus. Glucose 156-163 insulin Homo sapiens 123-130 12189153-9 2002 IRS-1 phosphorylation and glucose transport stimulated by insulin in mature adipocytes were also unaffected by RELMalpha. Glucose 26-33 insulin Homo sapiens 58-65 12439654-16 2002 After adjustment for age and indices of global and regional obesity (ie BMI and WC), insulin-resistant individuals showed higher apolipoprotein B, triglyceride, fasting (FPG) and 2 h post-load plasma glucose (2hPG) but lower HDL and LDL size. Glucose 200-207 insulin Homo sapiens 85-92 12356920-1 2002 Recruitment of secretory vesicles to the cell surface is essential for the sustained secretion of insulin in response to glucose. Glucose 121-128 insulin Homo sapiens 98-105 12356920-8 2002 These data therefore provide evidence for a novel mechanism whereby glucose may enhance insulin release. Glucose 68-75 insulin Homo sapiens 88-95 12417562-7 2002 Insulin-mediated glucose and FFA uptake were reduced by 33% and 36%, respectively, whereas the activity of the catabolic enzyme hormone-sensitive lipase increased by 51%. Glucose 17-24 insulin Homo sapiens 0-7 12414888-4 2002 Changing from a L(CHO)/H(F) to H(CHO)/L(F) diet resulted in increased insulin sensitivity (stable labeled iv glucose tolerance test) in adolescents [from 3.2 +/- 0.7 x 10(-4) to 5.0 +/- 1.4 x 10(-4) (min(-1))/( micro U.ml(-1)) (mean +/- SE)] but not in prepubertal children [9.4 +/- 2.5 x 10(-4) to 9.9 +/- 1.5 x 10(-4) (min(-1))/( micro U.ml(-1))], whereas beta-cell sensitivity was unaffected in both groups. Glucose 109-116 insulin Homo sapiens 70-77 12414888-8 2002 In the adolescents, the high carbohydrate diet resulted in increased insulin sensitivity, thus facilitating insulin-mediated glucose uptake. Glucose 125-132 insulin Homo sapiens 69-76 12414888-8 2002 In the adolescents, the high carbohydrate diet resulted in increased insulin sensitivity, thus facilitating insulin-mediated glucose uptake. Glucose 125-132 insulin Homo sapiens 108-115 12414889-6 2002 After euglycemia, insulin resistance improved, as demonstrated by an increase in the glucose infusion rate during the clamp from 12.7 +/- 5.6 to 22.4 +/- 8.8 micro mol/kg.min (P < 0.0005) and a decrease in insulin requirement from 1.7 +/- 0.9 to 1.1 +/- 0.6 U/kg.d (P < 0.005), whereas metabolic control improved. Glucose 85-92 insulin Homo sapiens 18-25 12414889-6 2002 After euglycemia, insulin resistance improved, as demonstrated by an increase in the glucose infusion rate during the clamp from 12.7 +/- 5.6 to 22.4 +/- 8.8 micro mol/kg.min (P < 0.0005) and a decrease in insulin requirement from 1.7 +/- 0.9 to 1.1 +/- 0.6 U/kg.d (P < 0.005), whereas metabolic control improved. Glucose 85-92 insulin Homo sapiens 209-216 12417571-0 2002 Impaired glucose phosphorylation and transport in skeletal muscle cause insulin resistance in HIV-1-infected patients with lipodystrophy. Glucose 9-16 insulin Homo sapiens 72-79 12417571-10 2002 Insulin-stimulated whole-body oxidative and nonoxidative glucose disposal was significantly lower in the treated group, as was suppressive insulin action on lipolysis. Glucose 57-64 insulin Homo sapiens 0-7 12417571-11 2002 To our knowledge, this is the first report providing in vivo evidence that, in lipodystrophic HIV patients, impaired glucose transport and phosphorylation cause reduced insulin-mediated glucose uptake. Glucose 117-124 insulin Homo sapiens 169-176 12414839-2 2002 BPDZ 154, an analog of diazoxide, inhibited both glucose-induced insulin secretion from isolated perifused islets and the secretion of insulin induced by glucose and tolbutamide. Glucose 49-56 insulin Homo sapiens 65-72 12404206-7 2002 Despite the increased glucose delivery during insulin plus IA PHEN and IV PHEN, FGU did not differ between study sessions at any time during the insulin infusion. Glucose 22-29 insulin Homo sapiens 46-53 12495548-0 2002 Covalent coupling of concanavalin A to a Carbopol 934P and 941P carrier in glucose-sensitive gels for delivery of insulin. Glucose 75-82 insulin Homo sapiens 114-121 12495548-8 2002 In addition, insulin delivery in response to glucose in the physiologically relevant glucose concentration range has been demonstrated using the carbomer-stabilised gels at 37 degrees C. The performance of this self-regulating drug delivery system has been improved in terms of increased gel stability with reduced component leaching. Glucose 45-52 insulin Homo sapiens 13-20 12495548-8 2002 In addition, insulin delivery in response to glucose in the physiologically relevant glucose concentration range has been demonstrated using the carbomer-stabilised gels at 37 degrees C. The performance of this self-regulating drug delivery system has been improved in terms of increased gel stability with reduced component leaching. Glucose 85-92 insulin Homo sapiens 13-20 12404188-5 2002 Insulin sensitivity, as assessed by the insulin-assisted frequently sampled intravenous glucose tolerance test (FSIVGTT), increased significantly following AEX (P =.007). Glucose 88-95 insulin Homo sapiens 0-7 12404188-5 2002 Insulin sensitivity, as assessed by the insulin-assisted frequently sampled intravenous glucose tolerance test (FSIVGTT), increased significantly following AEX (P =.007). Glucose 88-95 insulin Homo sapiens 40-47 12404195-7 2002 The effect was not dependent on insulin concentration, which was similar to that of metformin and was different from that of TZD, whose glucose-lowering effect is insulin dependent. Glucose 136-143 insulin Homo sapiens 163-170 12587504-3 2002 The glucose clamp technique is the standard method for the measurement of insulin resistance. Glucose 4-11 insulin Homo sapiens 74-81 12388790-2 2002 Insulin sensitivity index (S(I)), assessed by the frequently sampled intravenous glucose tolerance test, was significantly (P = 0.0001) increased following AEX. Glucose 81-88 insulin Homo sapiens 0-7 12388790-5 2002 Similarly, there was a significant (P = 0.036) decrease in the acute insulin response to glucose (AIR(G)) and a significant (P = 0.05) interaction between AEX and ACE genotype. Glucose 89-96 insulin Homo sapiens 69-76 12408421-4 2002 Hyperkalemia can be temporarily improved by the intravenous administration of an insulin-dextrose combination or bicarbonate, and polystyrene binding resins or dialysis can remove excess stores of potassium. Glucose 89-97 insulin Homo sapiens 81-88 12270556-5 2002 Significant positive linear correlation was calculated among TNF-alpha, Cp, Cp/blood glucose ratio (indirect parameters of insulin resistance) and body mass indexes (BMIs) of pregnant women (P<0.01). Glucose 85-92 insulin Homo sapiens 123-130 12360163-4 2002 Furthermore, heart rate recovery after exercise was related to insulin sensitivity at the hyperinsulinemic eugleucemic clamp (r = 0.28, P <.03), and to high-density lipoprotein cholesterol and exercise capacity, and inversely to obesity and insulin and glucose levels 2 hours after an oral glucose load (P <.05 for all). Glucose 256-263 insulin Homo sapiens 63-70 12360163-4 2002 Furthermore, heart rate recovery after exercise was related to insulin sensitivity at the hyperinsulinemic eugleucemic clamp (r = 0.28, P <.03), and to high-density lipoprotein cholesterol and exercise capacity, and inversely to obesity and insulin and glucose levels 2 hours after an oral glucose load (P <.05 for all). Glucose 293-300 insulin Homo sapiens 63-70 12242483-7 2002 Insulin secretion studies demonstrated that these cells secrete insulin in a glucose-responsive fashion, although do not respond to secretagogues such as IBMX and arginine as do mature beta cells. Glucose 77-84 insulin Homo sapiens 0-7 12242483-7 2002 Insulin secretion studies demonstrated that these cells secrete insulin in a glucose-responsive fashion, although do not respond to secretagogues such as IBMX and arginine as do mature beta cells. Glucose 77-84 insulin Homo sapiens 64-71 12351442-4 2002 Baseline blood flow ((15)O-water) and insulin-stimulated glucose uptake ((18)F-fluoro-deoxyglucose) during euglycemic (5.6 mmol/l), physiological hyperinsulinemia (40 mU x min(-1) x m(-2) insulin clamp) were measured by positron emission tomography in skeletal muscle and normally contracting myocardium. Glucose 57-64 insulin Homo sapiens 38-45 12351442-6 2002 In regions with normal baseline perfusion, insulin-mediated myocardial glucose uptake was reduced in non-CAD type 2 diabetic (0.36 +/- 0.14 micro mol x min(-1). Glucose 71-78 insulin Homo sapiens 43-50 12351443-7 2002 In conclusion, these results indicate that IMCLs relate to insulin resistance in type 2 diabetic patients at baseline and that insulin-mediated near-normoglycemia for approximately 3 days reduces fasting glucose production but stimulates lipid accumulation in liver and muscle without affecting insulin sensitivity. Glucose 204-211 insulin Homo sapiens 127-134 12351443-7 2002 In conclusion, these results indicate that IMCLs relate to insulin resistance in type 2 diabetic patients at baseline and that insulin-mediated near-normoglycemia for approximately 3 days reduces fasting glucose production but stimulates lipid accumulation in liver and muscle without affecting insulin sensitivity. Glucose 204-211 insulin Homo sapiens 127-134 12378381-0 2002 Mismatch between insulin-mediated glucose uptake and blood flow in the heart of patients with Type II diabetes. Glucose 34-41 insulin Homo sapiens 17-24 12378381-9 2002 During hyperinsulinaemia, the regional distribution of myocardial blood flow and glucose uptake showed higher values in the septum and anterolateral wall (short axis) and in the mid-ventricle (long axis) in control subjects, and insulin action was circumscribed to these regions. Glucose 81-88 insulin Homo sapiens 12-19 12378381-10 2002 In diabetic patients, the regional distribution of glucose uptake was similar; however, insulin-induced increase of myocardial blood flow was mainly directed to the postero-inferior areas (short axis) and to the base (long axis) of the heart, thus cancelling the predominance of the anterior wall observed before insulin administration. Glucose 51-58 insulin Homo sapiens 88-95 12378381-12 2002 In contrast, the regional re-distribution of myocardial blood flow induced by insulin is directed to different target areas when compared with healthy subjects, thereby resulting in a mismatch between blood flow and glucose metabolism. Glucose 216-223 insulin Homo sapiens 78-85 12378382-2 2002 METHODS: We evaluated the ability of exendin-4, a GLP-1 analogue resistant to degradation by dipeptidyl peptidase IV, to modulate insulin-induced stimulation of glucose uptake and suppression of glucose production in eight healthy subjects during infusion of GLP-1 (1.2 pmol.kg(-1).min(-1)), exendin-4 (0.12 pmol.kg(-1).min(-1)), or saline. Glucose 161-168 insulin Homo sapiens 130-137 12378382-2 2002 METHODS: We evaluated the ability of exendin-4, a GLP-1 analogue resistant to degradation by dipeptidyl peptidase IV, to modulate insulin-induced stimulation of glucose uptake and suppression of glucose production in eight healthy subjects during infusion of GLP-1 (1.2 pmol.kg(-1).min(-1)), exendin-4 (0.12 pmol.kg(-1).min(-1)), or saline. Glucose 195-202 insulin Homo sapiens 130-137 12378382-7 2002 While insulin-induced stimulation of glucose disappearance at the highest insulin concentrations tended to be greater and insulin-induced suppression of glucose production lower in the presence of exendin-4 or GLP-1 than saline, the differences were not significant. Glucose 37-44 insulin Homo sapiens 6-13 12378382-7 2002 While insulin-induced stimulation of glucose disappearance at the highest insulin concentrations tended to be greater and insulin-induced suppression of glucose production lower in the presence of exendin-4 or GLP-1 than saline, the differences were not significant. Glucose 37-44 insulin Homo sapiens 74-81 12378382-7 2002 While insulin-induced stimulation of glucose disappearance at the highest insulin concentrations tended to be greater and insulin-induced suppression of glucose production lower in the presence of exendin-4 or GLP-1 than saline, the differences were not significant. Glucose 37-44 insulin Homo sapiens 74-81 12372842-3 2002 In addition, in type 2 diabetes, there is evidence that the activation of these same stress pathways by glucose and possibly FFA leads to both insulin resistance and impaired insulin secretion. Glucose 104-111 insulin Homo sapiens 143-150 12477138-1 2002 OBJECTIVE: 1) Determine in a sample of American Indians (AI) how well insulin sensitivity (SI) measured by the frequently sampled intravenous glucose test (FSIGT) correlates with a simpler measure of insulin resistance (IR) measured by the homeostasis assessment (HOMA) model; (2) compare insulin sensitivity in a sample of diabetic and non-diabetic Al in the Strong Heart Study (SHS) with that of White, Black, and Hispanic Americans in the Insulin Resistance Atherosclerosis Study (IRAS). Glucose 142-149 insulin Homo sapiens 70-77 12364442-4 2002 Insulin sensitivity was assessed by homeostasis model assessment (HOMA) and continuous infusion of glucose with model assessment (CIGMA) in all patients. Glucose 99-106 insulin Homo sapiens 0-7 12364450-3 2002 The objective of this study was to examine whether ethnic differences in glucose homeostasis (C-peptide/insulin/glucose dynamics) are present in nondiabetic pregnant women. Glucose 73-80 insulin Homo sapiens 104-111 12366603-5 2002 Insulin-mediated glucose uptake was determined by euglycaemic hyperinsulinaemic clamp as a measure of insulin sensitivity. Glucose 17-24 insulin Homo sapiens 0-7 12366603-5 2002 Insulin-mediated glucose uptake was determined by euglycaemic hyperinsulinaemic clamp as a measure of insulin sensitivity. Glucose 17-24 insulin Homo sapiens 67-74 12242347-1 2002 The GTPase TC10 plays a critical role in insulin-stimulated glucose transport. Glucose 60-67 insulin Homo sapiens 41-48 12242347-6 2002 These data suggest that CIP4/2 may play an important role in insulin-stimulated glucose transport as a downstream effector of TC10. Glucose 80-87 insulin Homo sapiens 61-68 12905776-2 2002 Normal glucose tolerance could be maintained when there is a balance between insulin sensitivity and beta-cells function. Glucose 7-14 insulin Homo sapiens 77-84 12138086-1 2002 The ability of the growth factors epidermal growth factor (EGF), transforming growth factor alpha, and platelet-derived growth factor to exert insulin-like effects on glucose transport and lipolysis were examined in human and rat fat cells. Glucose 167-174 insulin Homo sapiens 143-150 12349850-1 2002 BACKGROUND AND PURPOSE: Resistance to insulin-mediated glucose uptake by peripheral tissues is a cardinal defect in type 2 diabetes mellitus. Glucose 55-62 insulin Homo sapiens 38-45 12101177-0 2002 A functional link between glucokinase binding to insulin granules and conformational alterations in response to glucose and insulin. Glucose 112-119 insulin Homo sapiens 49-56 12101177-1 2002 Glucokinase (GK) activity is essential for the physiological regulation of insulin secretion by glucose. Glucose 96-103 insulin Homo sapiens 75-82 12101177-2 2002 Because the enzyme exerts nearly total control over glucose metabolism in the beta-cell, even small changes in GK activity exert effects on glucose-stimulated insulin secretion and, consequently, the blood glucose concentration. Glucose 140-147 insulin Homo sapiens 159-166 12101177-2 2002 Because the enzyme exerts nearly total control over glucose metabolism in the beta-cell, even small changes in GK activity exert effects on glucose-stimulated insulin secretion and, consequently, the blood glucose concentration. Glucose 140-147 insulin Homo sapiens 159-166 12207909-1 2002 Insulin rapidly stimulates the tyrosine kinase activity of its receptor, resulting in the phosphorylation of insulin receptor substrates (IRS), which in turn associates and activates PI 3-kinase, leading to an increase in glucose uptake. Glucose 222-229 insulin Homo sapiens 0-7 12207909-1 2002 Insulin rapidly stimulates the tyrosine kinase activity of its receptor, resulting in the phosphorylation of insulin receptor substrates (IRS), which in turn associates and activates PI 3-kinase, leading to an increase in glucose uptake. Glucose 222-229 insulin Homo sapiens 109-116 12207909-5 2002 Interestingly, lactacystin also preserved PKB activation and insulin-induced glucose uptake. Glucose 77-84 insulin Homo sapiens 61-68 12207909-8 2002 In conclusion, proteasome inhibitors can regulate the tyrosine phosphorylation of IRS-1 and the downstream insulin signaling pathway, leading to glucose transport. Glucose 145-152 insulin Homo sapiens 107-114 12503852-4 2002 Glucose, the main physiological regulator of insulin secretion, also regulates insulin gene transcription through PDX-1. Glucose 0-7 insulin Homo sapiens 45-52 12503852-5 2002 While acute exposure to high glucose concentrations causes an increase in PDX-1 binding, and consequently in insulin mRNA levels, chronic hyperglycemia (toxic to the beta-cell) leads to a decrease in PDX-1 and insulin levels. Glucose 29-36 insulin Homo sapiens 109-116 12404204-0 2002 Exogenous insulin replacement in type 2 diabetes reverses excessive hepatic glucose release, but not excessive renal glucose release and impaired free fatty acid clearance. Glucose 76-83 insulin Homo sapiens 10-17 12404204-2 2002 Restoration of normoglycemia by exogenous insulin replacement normalizes overall glucose release and plasma FFA concentrations. Glucose 81-88 insulin Homo sapiens 42-49 12404204-5 2002 Insulin infusion normalized plasma glucose (5.3 +/- 0.1 v 5.2 +/- 0.1 mmol/L in NV) and overall glucose release (10.1 +/- 0.7 v 10.6 +/- 0.4 micromol x kg(-1) x min(-1) in NV), (both P >.9). Glucose 35-42 insulin Homo sapiens 0-7 12404204-5 2002 Insulin infusion normalized plasma glucose (5.3 +/- 0.1 v 5.2 +/- 0.1 mmol/L in NV) and overall glucose release (10.1 +/- 0.7 v 10.6 +/- 0.4 micromol x kg(-1) x min(-1) in NV), (both P >.9). Glucose 96-103 insulin Homo sapiens 0-7 12592900-6 2002 A course intake of mineral water raised tissue sensitivity to insulin at early stages of glucose test and lowered basal level of insulin and hydrocortisone. Glucose 89-96 insulin Homo sapiens 62-69 12370460-10 2002 Plasma glucose and insulin were consistently elevated during exercise by oral and IV glucose vs placebo, but plasma glucose was higher and insulin lower in IV vs oral glucose studies in patients (p = 0.02). Glucose 85-92 insulin Homo sapiens 19-26 12370460-10 2002 Plasma glucose and insulin were consistently elevated during exercise by oral and IV glucose vs placebo, but plasma glucose was higher and insulin lower in IV vs oral glucose studies in patients (p = 0.02). Glucose 85-92 insulin Homo sapiens 19-26 12370460-10 2002 Plasma glucose and insulin were consistently elevated during exercise by oral and IV glucose vs placebo, but plasma glucose was higher and insulin lower in IV vs oral glucose studies in patients (p = 0.02). Glucose 85-92 insulin Homo sapiens 19-26 12217899-14 2002 The higher basal EGP and greater EGP overshoot in trained middle-aged men appear to compensate for the increased insulin-independent (S(2*)(G)) and -dependent (S(2*)(I)) glucose uptake to maintain glucose homeostasis. Glucose 170-177 insulin Homo sapiens 113-120 12204806-2 2002 In FCHL and DM2 in vivo insulin mediated muscle glucose uptake and inhibition of lipolysis were studied by euglycemic hyperinsulinemic clamp. Glucose 48-55 insulin Homo sapiens 24-31 12204806-3 2002 Insulin mediated glucose uptake was impaired to the same extent in both FCHL and DM2. Glucose 17-24 insulin Homo sapiens 0-7 12204806-10 2002 In conclusion, FCHL as well as DM2 subjects exhibited in vivo insulin resistance to glucose disposal, which occurs mainly in muscle. Glucose 84-91 insulin Homo sapiens 62-69 12237252-9 2002 5 Insulin-stimulated glucose uptake was impaired in chronically insulin-treated myotubes. Glucose 21-28 insulin Homo sapiens 2-9 12237252-14 2002 7 Treatment of cells with p38 inhibitor, SB203580, blocked insulin- and metformin-stimulated glucose uptake as well as p38 activation. Glucose 93-100 insulin Homo sapiens 59-66 12381332-1 2002 Chronic disease in general induces insulin resistance on glucose metabolism on hepatic and peripheral levels. Glucose 57-64 insulin Homo sapiens 35-42 12381332-5 2002 In this literature review the available data on glucose metabolism in COPD and cystic fibrosis are discussed in relation to this potential unique feature of increased peripheral insulin sensitivity despite the existence of chronic disease. Glucose 48-55 insulin Homo sapiens 178-185 12351459-3 2002 We have examined glucose-stimulated insulin secretion in relation to this KIR6.2 gene variant in two independent Dutch cohorts. Glucose 17-24 insulin Homo sapiens 36-43 12351462-5 2002 Insulin dose was titrated at the clinician"s discretion, aiming for a fasting blood glucose (FBG) < or =6.0 mmol/l. Glucose 84-91 insulin Homo sapiens 0-7 12351505-0 2002 A new index of insulin sensitivity obtained from the oral glucose tolerance test applicable to advanced type 2 diabetes. Glucose 58-65 insulin Homo sapiens 15-22 12384133-3 2002 METHODS: Insulin sensitivity (S(I)) was calculated from an intravenous glucose tolerance test in 23 type 2 albuminuric (AER+), 11 type 2 normoalbuminuric (AER-), and 17 control subjects. Glucose 71-78 insulin Homo sapiens 9-16 12364450-8 2002 There were ethnic differences in insulin production and resistance in both fasting and glucose-stimulated conditions in normal young nondiabetic pregnant women. Glucose 87-94 insulin Homo sapiens 33-40 12364473-5 2002 We also tested the effects of exendin 4 in the glucose-induced insulin secretion of human ICCs transplanted under the kidney capsule of athymic rats. Glucose 47-54 insulin Homo sapiens 63-70 12364473-6 2002 In the exendin 4-treated rats (given ip during 10 d) 8 wk after the beginning of the treatment, insulin was released in response to glucose as detected by the measurement of circulating human C-peptide. Glucose 132-139 insulin Homo sapiens 96-103 12364473-6 2002 In the exendin 4-treated rats (given ip during 10 d) 8 wk after the beginning of the treatment, insulin was released in response to glucose as detected by the measurement of circulating human C-peptide. Glucose 132-139 insulin Homo sapiens 192-201 12364473-12 2002 It also accelerates the functional maturation of fetal beta-cells as evidenced by their glucose-stimulated insulin secretion. Glucose 88-95 insulin Homo sapiens 107-114 12500431-5 2002 In fact, PPAR gamma agonists increase peripheral insulin sensitivity by increasing the transcription of genes, which, in turn, increase glucose uptake, also improving insulin-stimulated glucose disposal in muscle. Glucose 136-143 insulin Homo sapiens 49-56 12360255-2 2002 Prospective clinical studies have proven the benefits of tighter glucose control in reducing the frequency and severity of complications of the disease, leading to the advocation of earlier and more aggressive use of insulin therapy. Glucose 65-72 insulin Homo sapiens 217-224 12397689-1 2002 Impairment of insulin-dependent glucose uptake in skeletal muscles plays a major role in the pathogenesis of diabetes mellitus. Glucose 32-39 insulin Homo sapiens 14-21 12376581-4 2002 RESULTS: There was a significant improvement in glycemic control (glycosylated hemoglobin -0.7 +/- 0.7%, p < or = 0.05) and an 86% increase in insulin sensitivity in the RSG group (glucose-disposal rate change from baseline: 17.5 +/- 14.5 micro mol glucose/min/kg free fat mass, p < 0.05), but no significant change in the placebo group compared with baseline. Glucose 184-191 insulin Homo sapiens 146-153 12376581-4 2002 RESULTS: There was a significant improvement in glycemic control (glycosylated hemoglobin -0.7 +/- 0.7%, p < or = 0.05) and an 86% increase in insulin sensitivity in the RSG group (glucose-disposal rate change from baseline: 17.5 +/- 14.5 micro mol glucose/min/kg free fat mass, p < 0.05), but no significant change in the placebo group compared with baseline. Glucose 252-259 insulin Homo sapiens 146-153 12382366-2 2002 If the fasting blood glucose level is > 10 mmol/l and the postprandial values are not much higher than the fasting ones, then the patient can be started on 8-12 IU of an intermediate-acting insulin before going to sleep. Glucose 21-28 insulin Homo sapiens 193-200 12382366-3 2002 In the case of blood glucose levels which increase during the day or if a single insulin dose has insufficient effect, the patient can be started on a twice-daily administration of a premixed insulin. Glucose 21-28 insulin Homo sapiens 192-199 12382366-4 2002 If more than 40 IU of insulin per injection are needed to regulate the blood glucose levels, it might be necessary to switch to administering insulin 4 times per day. Glucose 77-84 insulin Homo sapiens 22-29 12382366-4 2002 If more than 40 IU of insulin per injection are needed to regulate the blood glucose levels, it might be necessary to switch to administering insulin 4 times per day. Glucose 77-84 insulin Homo sapiens 142-149 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 426-433 insulin Homo sapiens 238-245 12101177-3 2002 Using quantitative imaging of multicolor fluorescent proteins fused to GK, we found that the association of GK with insulin granules is regulated by glucose in the beta-cell. Glucose 149-156 insulin Homo sapiens 116-123 12101177-4 2002 Glucose stimulation increased the rate of fluorescence recovery after photobleaching of GK to insulin granules, indicating that GK is released into the cytoplasm after glucose stimulation. Glucose 0-7 insulin Homo sapiens 94-101 12101177-6 2002 Furthermore, glucose-stimulated changes in GK regulation were blocked by two inhibitors of insulin secretion. Glucose 13-20 insulin Homo sapiens 91-98 12225719-3 2002 METHODS: Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration during the last 30 min of a 180-min infusion of octreotide, glucose, and insulin. Glucose 82-89 insulin Homo sapiens 9-16 12225719-3 2002 METHODS: Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration during the last 30 min of a 180-min infusion of octreotide, glucose, and insulin. Glucose 171-178 insulin Homo sapiens 9-16 12225298-4 2002 In the first cohort the increments of insulin dose were based on the level of blood glucose obtained. Glucose 84-91 insulin Homo sapiens 38-45 12225298-6 2002 In the second cohort (n = 8) the insulin dose was increased by up to 40%, according to the algorithm, starting immediately after glucocorticoid treatment; prior to a detectable increase in blood glucose. Glucose 195-202 insulin Homo sapiens 33-40 12751567-6 2002 Further multiple regressional analysis showed that the differences in fasting plasma insulin and 2-hour post glucose load insulin observed were only accounted for by the presence of a parental history of diabetes and were not influenced significantly by BMI, waist and hip circumferences. Glucose 109-116 insulin Homo sapiens 122-129 12203819-7 2002 Fasting insulin is available for only a subset of the data and separate analysis shows that it groups with glucose. Glucose 107-114 insulin Homo sapiens 8-15 12361817-1 2002 Management of type 1 and type 2 diabetes mellitus with intensive insulin therapy usually includes an intermediate- or long-acting basal component for between-meal and nocturnal glycemic control, together with preprandial bolus injections of a short-acting insulin for control of meal-stimulated increases in serum glucose levels. Glucose 314-321 insulin Homo sapiens 65-72 12361817-4 2002 In clinical trials, postprandial increases in blood glucose levels were significantly less after treatment with insulin lispro or insulin aspart than with premeal regular insulin. Glucose 52-59 insulin Homo sapiens 112-119 12361817-4 2002 In clinical trials, postprandial increases in blood glucose levels were significantly less after treatment with insulin lispro or insulin aspart than with premeal regular insulin. Glucose 52-59 insulin Homo sapiens 130-137 12361817-4 2002 In clinical trials, postprandial increases in blood glucose levels were significantly less after treatment with insulin lispro or insulin aspart than with premeal regular insulin. Glucose 52-59 insulin Homo sapiens 130-137 12061893-4 2002 Here we review the role of the transcription factors forkhead and sterol regulatory element binding protein-1c in the inductive and repressive effects of insulin on hepatic gene expression, and the pathway that leads from glucose to gene regulation with the recently discovered carbohydrate response element binding protein. Glucose 222-229 insulin Homo sapiens 154-161 12207841-1 2002 The fasting concentration of non-esterified fatty acids (NEFA) and the degree to which it declines during an oral glucose tolerance test are closely associated with insulin resistance and glucose intolerance. Glucose 114-121 insulin Homo sapiens 165-172 12207841-8 2002 These results suggest that the area under the NEFA curve in the oral glucose tolerance test, a measure of insulin sensitivity, is strongly associated with the habitual level of physical activity. Glucose 69-76 insulin Homo sapiens 106-113 12481381-6 2002 The combination of insulin capsules and doanil tablets produced only 16% lowering in plasma glucose levels by 6h and significantly (P < 0.001) lower AUC and RH compared to the combination of glucophage + doanil. Glucose 92-99 insulin Homo sapiens 19-26 12481381-7 2002 The combination of insulin capsules and glucophage tablets produced about 38% reduction in plasma glucose levels and significantly (P < 0.001) higher AUC and RH compared to either glucophage, doanil tablets or enteric coated insulin capsules alone. Glucose 98-105 insulin Homo sapiens 19-26 12125101-2 2002 In the present extension of our studies, we demonstrate that this inhibition by aldosterone had no effects on basal glucose transport or on basal thymidine incorporation into DNA, while the cell responsiveness reflected by the maximal response to insulin was decreased by 23% for glucose transport and by 31% for DNA synthesis after the aldosterone treatment. Glucose 280-287 insulin Homo sapiens 247-254 12411107-10 2002 There was a negative linear correlation between FT and TG, TC, LDL-C, PAI-1, FPA, fasting insulin and glucose, 2-hour insulin and glucose (r = -0.311, -0.384, -0.385, -0.339, -0.353, -0.381, -0.303, -0.460 and -0.395, respectively; P < 0.05). Glucose 102-109 insulin Homo sapiens 90-97 12172477-3 2002 RECENT FINDINGS: Intensive insulin therapy titrated to maintain blood glucose level between 4.4 and 6.1 mmol/l during intensive care unit stay has recently been shown to significantly decrease mortality, septic morbidity, sepsis-related organ failure, transfusion requirements and polyneuropathies. Glucose 70-77 insulin Homo sapiens 27-34 12172479-8 2002 In the beta cells, FFAs potentiate glucose-stimulated insulin secretion. Glucose 35-42 insulin Homo sapiens 54-61 12171564-7 2002 Emerging knowledge regarding the underlying mechanisms that impair glucose-stimulated insulin secretion and the action of insulin on its target tissues has grown tremendously over the last two decades. Glucose 67-74 insulin Homo sapiens 86-93 12196433-0 2002 Intravenous glargine and regular insulin have similar effects on endogenous glucose output and peripheral activation/deactivation kinetic profiles. Glucose 76-83 insulin Homo sapiens 33-40 12196433-1 2002 OBJECTIVE: To compare the effects of intravenously administered long-acting insulin analog glargine and regular human insulin on activation and deactivation of endogenous glucose output (EGO) and peripheral glucose uptake. Glucose 171-178 insulin Homo sapiens 76-83 12196433-1 2002 OBJECTIVE: To compare the effects of intravenously administered long-acting insulin analog glargine and regular human insulin on activation and deactivation of endogenous glucose output (EGO) and peripheral glucose uptake. Glucose 171-178 insulin Homo sapiens 118-125 12196433-1 2002 OBJECTIVE: To compare the effects of intravenously administered long-acting insulin analog glargine and regular human insulin on activation and deactivation of endogenous glucose output (EGO) and peripheral glucose uptake. Glucose 207-214 insulin Homo sapiens 76-83 12196433-9 2002 The mean time required for 50% suppression of incremental glucose disposal rate (GDR), defined as the time required for activation from the basal glucose disappearance rate (R(d)) to half-maximum insulin-stimulated R(d), was 32 +/- 5 and 42 +/- 10 min for regular insulin and insulin glargine, respectively (NS). Glucose 58-65 insulin Homo sapiens 196-203 12196460-7 2002 After troglitazone treatment, insulin-stimulated glucose disposal was increased compared with pretreatment and placebo (279 +/- 37 vs. 211 +/- 26 and 200 +/- 25 mg. m(-2). Glucose 49-56 insulin Homo sapiens 30-37 12196461-1 2002 Published models of mammalian whole-body glucose metabolism generally assume that glucose uptake is proportional to circulating glucose concentration at constant insulin concentration. Glucose 82-89 insulin Homo sapiens 162-169 12196461-1 2002 Published models of mammalian whole-body glucose metabolism generally assume that glucose uptake is proportional to circulating glucose concentration at constant insulin concentration. Glucose 82-89 insulin Homo sapiens 162-169 12231074-4 2002 Results from recent studies using nuclear magnetic resonance (NMR) spectroscopy implicate intracellular defects in glucose transport as the rate-controlling step for insulin-mediated glucose uptake in muscle. Glucose 115-122 insulin Homo sapiens 166-173 12231074-4 2002 Results from recent studies using nuclear magnetic resonance (NMR) spectroscopy implicate intracellular defects in glucose transport as the rate-controlling step for insulin-mediated glucose uptake in muscle. Glucose 183-190 insulin Homo sapiens 166-173 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 21-28 insulin Homo sapiens 156-163 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 21-28 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 21-28 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 21-28 insulin Homo sapiens 238-245 12324984-10 2002 The availability of new insulin preparations that mimic the normal mealtime bursts of insulin, and another that provides a sustained insulin supply similar to basal insulin secretion in an individual without diabetes has the potential to significantly improve long-term control over blood glucose in patients with type 2 diabetes. Glucose 289-296 insulin Homo sapiens 24-31 12324987-3 2002 As would be expected for a more satisfactory basal insulin, clinical trials comparing insulin glargine with NPH insulin show less nocturnal hypoglycaemia, improved pre-breakfast blood glucose levels, or both. Glucose 184-191 insulin Homo sapiens 86-93 12324990-8 2002 Results from a recent comparative study indicate that insulin glargine plus oral therapy may provide better post-dinner glucose control as well as less symptomatic and nocturnal hypoglycemia than oral therapy combined with NPH insulin. Glucose 120-127 insulin Homo sapiens 54-61 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 426-433 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Glucose 426-433 insulin Homo sapiens 238-245 12378965-7 2002 Quite recently, glucose-sensitive hydrogels that are responsive to glucose concentration have been developed to monitor the release of insulin. Glucose 16-23 insulin Homo sapiens 135-142 12378965-7 2002 Quite recently, glucose-sensitive hydrogels that are responsive to glucose concentration have been developed to monitor the release of insulin. Glucose 67-74 insulin Homo sapiens 135-142 12231074-6 2002 The thiazolidinedione class of antidiabetic agents directly targets insulin resistance in skeletal muscle by improving glucose transport activity and insulin-stimulated muscle glycogen synthesis. Glucose 119-126 insulin Homo sapiens 68-75 12397577-2 2002 This occurs through the ability of insulin to markedly stimulate both glucose uptake and lipogenesis. Glucose 70-77 insulin Homo sapiens 35-42 12442060-1 2002 The project to finalize a "closed loop" insulin delivery according to blood glucose level, i.e. an implanted artificial beta cell, is born from the development of the first miniaturized portable insulin pumps during the 1970s. Glucose 76-83 insulin Homo sapiens 40-47 12193567-9 2002 This was further suggested by a significant increase of the glucose-dependent binding of IDX-1 to the insulin promoter in RIP/GLP-1 cells but not in CMV/GLP-1 cells or control cells. Glucose 60-67 insulin Homo sapiens 102-109 12215322-7 2002 MAIN OUTCOME MEASURE(S): Insulin resistance was defined as a fasting insulin level >20 microU/mL or a fasting glucose to insulin ratio of <4.5. Glucose 113-120 insulin Homo sapiens 25-32 12209381-10 2002 Insulin response and AUC were significantly lower after the 60 and 70% amylose starch breads than after the glucose or the other breads. Glucose 108-115 insulin Homo sapiens 0-7 12384822-7 2002 This insulin-sensitizing effect appears to be mostly attributable to enhanced suppression of glucose production, but beneficial effects on muscle cannot be excluded. Glucose 93-100 insulin Homo sapiens 5-12 12384827-1 2002 AIMS: Amylin is a second beta-cell hormone that is normally co-secreted with insulin in response to meals; it complements the effects of insulin in postprandial glucose control, in part by suppressing glucagon secretion. Glucose 161-168 insulin Homo sapiens 137-144 12207807-2 2002 The latter are usually taken as a surrogate measure of insulin resistance of whole-body glucose disposal. Glucose 88-95 insulin Homo sapiens 55-62 12207807-7 2002 Thus, subjects with "pure" insulin resistance had a more central fat distribution and presented evidence of excessive lipolysis and endogenous glucose production. Glucose 143-150 insulin Homo sapiens 27-34 12207807-8 2002 In contrast, subjects with "pure" hyperinsulinaemia had suppressed lipolysis, endogenous glucose production and insulin clearance, higher values of systolic blood pressure and lower values of serum HDL-cholesterol concentrations. Glucose 89-96 insulin Homo sapiens 39-46 12124779-8 2002 Like K-cells in vivo, the GIP/insulin-producing cells express the critical glucose sensing enzyme, glucokinase. Glucose 75-82 insulin Homo sapiens 30-37 12174317-10 2002 Use of insulin infusion to control glucose levels in ICU patients, at least in populations similar to those in our study, can be expected to achieve clinically welcome improvements in outcome. Glucose 35-42 insulin Homo sapiens 7-14 12174318-8 2002 Rapid-acting insulin analogues, used as the prandial component insulin replacement therapy and short-acting insulin secretagogues, targeting postprandial glucose control, may have a useful new role to play in the management of diabetes mellitus. Glucose 154-161 insulin Homo sapiens 13-20 12174320-10 2002 In this context, the use of premixed insulin analogues in combination with OHAs allows effective postprandial glucose control, a twice-daily injection regimen and a short meal-injection interval. Glucose 110-117 insulin Homo sapiens 37-44 12174321-5 2002 Human insulin has a slow onset of action, thus patients are advised to inject about 30 min before a meal, ensuring peak insulin concentrations coincide with postprandial glucose excursions. Glucose 170-177 insulin Homo sapiens 6-13 12213907-7 2002 Among Sicilians, subjects carrying allele 3 had a lower fasting insulin and insulin resistance index (homeostasis model assessment of insulin resistance; P < 0.001 for both) and glucose (P = 0.025) and insulin (P = 0.002) levels during the oral glucose tolerance test. Glucose 245-252 insulin Homo sapiens 64-71 12213869-5 2002 When the subjects were studied in relation to their insulin secretion in response to the glucose load, the patients, classified as hyperinsulinemic, showed the most significant response to the raloxifene treatment. Glucose 89-96 insulin Homo sapiens 52-59 12213907-7 2002 Among Sicilians, subjects carrying allele 3 had a lower fasting insulin and insulin resistance index (homeostasis model assessment of insulin resistance; P < 0.001 for both) and glucose (P = 0.025) and insulin (P = 0.002) levels during the oral glucose tolerance test. Glucose 245-252 insulin Homo sapiens 76-83 12213907-7 2002 Among Sicilians, subjects carrying allele 3 had a lower fasting insulin and insulin resistance index (homeostasis model assessment of insulin resistance; P < 0.001 for both) and glucose (P = 0.025) and insulin (P = 0.002) levels during the oral glucose tolerance test. Glucose 245-252 insulin Homo sapiens 76-83 12200761-10 2002 Since acute insulin secretion in response to glucose was markedly impaired and insulin resistance was varied in the patients carrying the homozygous mutations in the NeuroD1 and Pax4 genes, the mutations are ones of the factors involved in the beta-cell dysfunction and do not relate to the insulin resistance. Glucose 45-52 insulin Homo sapiens 12-19 12387512-1 2002 Metformin lowers blood glucose by reducing hepatic glucose output and improving insulin sensitivity without requiring an increase in circulating insulin concentration. Glucose 23-30 insulin Homo sapiens 80-87 12200763-2 2002 Insulin stimulated glucose uptake with comparable sensitivity in ND (EC(50) = 2.0 +/- 0.7 nmol/L) and diabetic (1.3 +/- 0.4) cells. Glucose 19-26 insulin Homo sapiens 0-7 12200763-4 2002 In ND cells, insulin and IGF-1 were equally potent for stimulation of glucose uptake and glycogen synthase (GS) activity. Glucose 70-77 insulin Homo sapiens 13-20 12070172-0 2002 Insulin inhibits hepatocellular glucose production by utilizing liver-enriched transcriptional inhibitory protein to disrupt the association of CREB-binding protein and RNA polymerase II with the phosphoenolpyruvate carboxykinase gene promoter. Glucose 32-39 insulin Homo sapiens 0-7 12470401-8 2002 Twelve patients received high dose insulin with glucose, potassium and amino acids. Glucose 48-55 insulin Homo sapiens 35-42 12422437-6 2002 If the insulin dosage is too high, the increase in muscular assimilation, combined with the shutdown of liver glucose production, may result in a severe hypoglycaemia. Glucose 110-117 insulin Homo sapiens 7-14 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 163-170 insulin Homo sapiens 14-21 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 163-170 insulin Homo sapiens 68-75 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 163-170 insulin Homo sapiens 68-75 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 186-193 insulin Homo sapiens 14-21 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 186-193 insulin Homo sapiens 68-75 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 186-193 insulin Homo sapiens 68-75 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 186-193 insulin Homo sapiens 14-21 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 186-193 insulin Homo sapiens 68-75 16737129-5 2002 The effect of insulin was assessed by the method of the 3-hour hyperinsulin euglycaemic clamp (insulin level 75 microU/ml, blood sugar level 5 mmol/l) acording to glucose consumption as glucose Mglu, glucose clearance MCRglu and insulin sensitivity index SI. Glucose 186-193 insulin Homo sapiens 68-75 12110540-8 2002 Glucose transport activity in the insulin-stimulated state was increased by the expression of PKC-delta but not of PKC-alpha. Glucose 0-7 insulin Homo sapiens 34-41 12242036-2 2002 Whereas pancreatic beta-cells normally respond to glucose challenge by rapid insulin release (first phase insulin secretion), there is a loss of this acute response in virtually all of the type 2 diabetes patients with significant fasting hyperglycemia. Glucose 50-57 insulin Homo sapiens 77-84 12242036-2 2002 Whereas pancreatic beta-cells normally respond to glucose challenge by rapid insulin release (first phase insulin secretion), there is a loss of this acute response in virtually all of the type 2 diabetes patients with significant fasting hyperglycemia. Glucose 50-57 insulin Homo sapiens 106-113 12242036-5 2002 In contrast, transgenic mice with down-regulated glucose to glucosamine metabolism in beta-cells exhibited an enhanced insulin secretion capacity. Glucose 49-56 insulin Homo sapiens 119-126 12070148-3 2002 As expected, both NAD(P)H and insulin secretion showed sustained increases in response to glucose stimulation. Glucose 90-97 insulin Homo sapiens 30-37 12070148-11 2002 These data support a model in which glycolysis plays a dominant role in glucose-stimulated insulin secretion. Glucose 72-79 insulin Homo sapiens 91-98 12070148-12 2002 Based on these data, we propose a mechanism for glucose-stimulated insulin secretion that includes allosteric inhibition of tricarboxylic acid cycle enzymes and pH dependence of mitochondrial pyruvate transport. Glucose 48-55 insulin Homo sapiens 67-74 12169270-0 2002 PLCgamma participates in insulin stimulation of glucose uptake through activation of PKCzeta in brown adipocytes. Glucose 48-55 insulin Homo sapiens 25-32 12169270-4 2002 Inhibition of PLCgamma activity either with the chemical compound U73122 or with an inhibitor peptide precluded insulin stimulation of glucose uptake, GLUT4 translocation, and actin reorganization, as wortmannin did. Glucose 135-142 insulin Homo sapiens 112-119 12169270-10 2002 In summary, these data indicate that PLCgamma, activated at least partially by PI3-kinase, is a link between insulin receptor and PKCzeta through the production of PA and could mediate insulin-induced glucose uptake and GLUT4 translocation. Glucose 201-208 insulin Homo sapiens 109-116 12110540-9 2002 These findings demonstrate that both conventional and novel PKC isoforms are involved in PMA-stimulated glucose transport and that other novel PKC isoforms could participate in PMA-stimulated and insulin-stimulated glucose transport. Glucose 215-222 insulin Homo sapiens 196-203 12145023-5 2002 Multivariate modeling was performed to determine the effects of body composition on fasting insulin and insulin area under the curve (AUC) during standard glucose tolerance testing. Glucose 155-162 insulin Homo sapiens 104-111 12110541-0 2002 Free fatty acid-induced peripheral insulin resistance augments splanchnic glucose uptake in healthy humans. Glucose 74-81 insulin Homo sapiens 35-42 12145150-2 2002 In contrast, a dissociation of insulin effect on glucose and amino acid metabolism has been reported in type 2 diabetes. Glucose 49-56 insulin Homo sapiens 31-38 12185578-0 2002 PDMS-chemistry of angiotensin II and insulin in glucose glass thin films. Glucose 48-55 insulin Homo sapiens 37-44 12185578-1 2002 A plasma desorption mass spectrometry study was made on the properties of glucose and glucose/glucuronic acid thin films as matrices for amino acids, small and large peptides and insulin. Glucose 74-81 insulin Homo sapiens 179-186 12185578-1 2002 A plasma desorption mass spectrometry study was made on the properties of glucose and glucose/glucuronic acid thin films as matrices for amino acids, small and large peptides and insulin. Glucose 86-93 insulin Homo sapiens 179-186 12185578-7 2002 The spectrum of insulin in glucuronic acid/glucose consists mainly of positive ions with a fragmentation pattern from the B-chain. Glucose 43-50 insulin Homo sapiens 16-23 12185578-8 2002 The spectrum of reduced insulin using a nitrocellulose matrix gives B-chain ions but glucose/glucuronic acid gives A-chain ions in both the positive and negative ion spectra. Glucose 85-92 insulin Homo sapiens 24-31 12643193-1 2002 The quest for tight glucose control has led to the development of insulin analogues (insulin lispro, insulin aspart, insulin glargine) designed to optimize glucose control while minimizing the impact of insulin therapy on daily life. Glucose 20-27 insulin Homo sapiens 66-73 12643193-1 2002 The quest for tight glucose control has led to the development of insulin analogues (insulin lispro, insulin aspart, insulin glargine) designed to optimize glucose control while minimizing the impact of insulin therapy on daily life. Glucose 20-27 insulin Homo sapiens 85-92 12643193-1 2002 The quest for tight glucose control has led to the development of insulin analogues (insulin lispro, insulin aspart, insulin glargine) designed to optimize glucose control while minimizing the impact of insulin therapy on daily life. Glucose 20-27 insulin Homo sapiens 85-92 12643193-1 2002 The quest for tight glucose control has led to the development of insulin analogues (insulin lispro, insulin aspart, insulin glargine) designed to optimize glucose control while minimizing the impact of insulin therapy on daily life. Glucose 156-163 insulin Homo sapiens 66-73 12643193-1 2002 The quest for tight glucose control has led to the development of insulin analogues (insulin lispro, insulin aspart, insulin glargine) designed to optimize glucose control while minimizing the impact of insulin therapy on daily life. Glucose 156-163 insulin Homo sapiens 85-92 12643193-1 2002 The quest for tight glucose control has led to the development of insulin analogues (insulin lispro, insulin aspart, insulin glargine) designed to optimize glucose control while minimizing the impact of insulin therapy on daily life. Glucose 156-163 insulin Homo sapiens 85-92 12062851-1 2002 The patient was an infant with transient hyperglycemia and decreased endogenous insulin secretion on intravenous glucose tolerance test (IVGTT) with the appearance of IA-2 autoantibodies (IA-2Ab), and we speculated that he was in the prediabetes stage. Glucose 113-120 insulin Homo sapiens 80-87 12145182-5 2002 This study includes information on the directly measured insulin sensitivity index (S(I)) from intravenous glucose tolerance testing among African-American, Hispanic, and non-Hispanic white subjects aged 40-69 years at various stages of glucose tolerance. Glucose 107-114 insulin Homo sapiens 57-64 12145159-4 2002 Determinants of insulin sensitivity based on nonesterified fatty acid (NEFA) suppression after oral glucose administration [ISI(NEFA)] were higher in the top tertile ATBF response group (1.29 +/- 0.09 vs. 0.90 +/- 0.08 in the lower tertiles, P = 0.01). Glucose 100-107 insulin Homo sapiens 16-23 12145232-13 2002 This correlation did not change after further adjustment for serum glucose and HbA(1c), which may suggest that in the elderly subjects, impaired fibrinolysis is probably associated with insulin resistance. Glucose 67-74 insulin Homo sapiens 186-193 12173011-6 2002 Glucose uptake in normokinetic PET-normal myocardium was found to be higher in patients with normal whole-body insulin sensitivity ( P < 0.001), whereas in patients with low whole-body insulin sensitivity more segments displayed a pattern of reduced glucose uptake in normoperfused myocardium (PET-reverse mismatch) ( P < 0.05). Glucose 0-7 insulin Homo sapiens 111-118 12189441-0 2002 Defective amplification of the late phase insulin response to glucose by GIP in obese Type II diabetic patients. Glucose 62-69 insulin Homo sapiens 42-49 12189441-8 2002 Protocol 2, "Early phase" (0-20 min) insulin response to glucose was delayed and reduced in the patients, but enhanced slightly and similarly by GIP and GLP-1. Glucose 57-64 insulin Homo sapiens 37-44 12189441-12 2002 CONCLUSION/INTERPRETATION: Lack of GIP amplification of the late phase insulin response to glucose, which contrasts markedly to the normalising effect of GLP-1, could be a key defect in insulin secretion in Type II diabetic patients. Glucose 91-98 insulin Homo sapiens 71-78 12189443-1 2002 AIM/HYPOTHESIS: We examined insulin signal transduction at the level of insulin receptor substrates (IRS) 1 and 2, phosphatidylinositol (PI) 3-kinase and glucose transport in isolated subcutaneous adipocytes from obese and lean women. Glucose 154-161 insulin Homo sapiens 28-35 12189443-3 2002 RESULTS: Insulin sensitivity of glucose transport was reduced in adipocytes from obese women (p<0.05), with further reductions in basal and maximal insulin-stimulated glucose transport after a very low calorie diet (p<0.05). Glucose 32-39 insulin Homo sapiens 9-16 12189443-3 2002 RESULTS: Insulin sensitivity of glucose transport was reduced in adipocytes from obese women (p<0.05), with further reductions in basal and maximal insulin-stimulated glucose transport after a very low calorie diet (p<0.05). Glucose 170-177 insulin Homo sapiens 9-16 12189443-3 2002 RESULTS: Insulin sensitivity of glucose transport was reduced in adipocytes from obese women (p<0.05), with further reductions in basal and maximal insulin-stimulated glucose transport after a very low calorie diet (p<0.05). Glucose 170-177 insulin Homo sapiens 151-158 12153746-4 2002 RESULTS: Free insulin concentrations were lower in the patients than in the controls (4.3+/-2.3 mU/l compared with 6.5+/-3.1 mU/l, P<0.001), and there was an inverse correlation between free insulin and fasting blood glucose in the boys with diabetes (r=-0.53, P<0.001), whereas a positive correlation was observed between free insulin and leptin concentrations in the girls with diabetes (r=0.30, P=0.020). Glucose 220-227 insulin Homo sapiens 14-21 12173011-6 2002 Glucose uptake in normokinetic PET-normal myocardium was found to be higher in patients with normal whole-body insulin sensitivity ( P < 0.001), whereas in patients with low whole-body insulin sensitivity more segments displayed a pattern of reduced glucose uptake in normoperfused myocardium (PET-reverse mismatch) ( P < 0.05). Glucose 0-7 insulin Homo sapiens 188-195 12148083-8 2002 GLUT 4, carrying glucose across the membranes of muscle and fat cells, depends on insulin. Glucose 17-24 insulin Homo sapiens 82-89 12148083-19 2002 The concept of glucose allocation, however, would predict that weight gain - with abundance of glucose in muscle and fat - increases feedback to the brain (via hyperleptinemia) which in turn results in HPA-axis and SNS overdrive, impaired insulin secretion, and insulin resistance. Glucose 15-22 insulin Homo sapiens 239-246 12133890-1 2002 Over the past 30 years, a considerable body of evidence has revealed that a prior bout of exercise can increase the ability of insulin to stimulate glucose transport and glycogen synthesis in skeletal muscle. Glucose 148-155 insulin Homo sapiens 127-134 12119578-9 2002 The insulin resistance index was calculated from fasting plasma insulin and glucose values. Glucose 76-83 insulin Homo sapiens 4-11 12133891-5 2002 The molecular mechanism for enhanced insulin-stimulated glucose uptake after exercise training may be partly related to increased expression and activity of key proteins known to regulate glucose metabolism in skeletal muscle. Glucose 56-63 insulin Homo sapiens 37-44 12154416-1 2002 OBJECTIVE: To determine whether attempted glucose control through intraoperative insulin therapy reduces the need for inotropic or antiarrhythmic therapy after cardiopulmonary bypass (CPB). Glucose 42-49 insulin Homo sapiens 81-88 12133893-1 2002 Insulin resistance of skeletal muscle glucose transport is a key defect in the development of impaired glucose tolerance and Type 2 diabetes. Glucose 38-45 insulin Homo sapiens 0-7 12133893-6 2002 A well-established adaptive response to exercise training in conditions of insulin resistance is improved glucose tolerance and enhanced skeletal muscle insulin sensitivity of glucose transport. Glucose 106-113 insulin Homo sapiens 75-82 12133893-6 2002 A well-established adaptive response to exercise training in conditions of insulin resistance is improved glucose tolerance and enhanced skeletal muscle insulin sensitivity of glucose transport. Glucose 176-183 insulin Homo sapiens 75-82 12133893-7 2002 This training-induced enhancement of insulin action is associated with upregulation of specific components of the glucose transport system in insulin-resistant muscle and includes increased protein expression of GLUT-4 and insulin receptor substrate-1. Glucose 114-121 insulin Homo sapiens 37-44 12133893-7 2002 This training-induced enhancement of insulin action is associated with upregulation of specific components of the glucose transport system in insulin-resistant muscle and includes increased protein expression of GLUT-4 and insulin receptor substrate-1. Glucose 114-121 insulin Homo sapiens 142-149 12133893-8 2002 It is clear that further investigations are needed to further elucidate the specific molecular mechanisms underlying the beneficial effects of acute exercise and exercise training on the glucose transport system in insulin-resistant mammalian skeletal muscle. Glucose 187-194 insulin Homo sapiens 215-222 12161508-0 2002 Glucagon-like peptide-1 augments insulin-mediated glucose uptake in the obese state. Glucose 50-57 insulin Homo sapiens 33-40 12421023-2 2002 DESIGN: Minimal model analysis of a frequently sampled intravenous glucose tolerance test to assess insulin sensitivity. Glucose 67-74 insulin Homo sapiens 100-107 12161530-4 2002 In both groups, insulin stimulated glucose uptake per kilogram fat was significantly higher in visceral fat depots than in sc regions (P < 0.01). Glucose 35-42 insulin Homo sapiens 16-23 12161508-14 2002 In response to the GLP-1 infusion, with maintenance of plasma glucose level clamped at fasting level, significant increases in plasma insulin occurred in all subjects (P < 0.001). Glucose 62-69 insulin Homo sapiens 134-141 12161530-8 2002 In conclusion, insulin-stimulated glucose uptake per kilogram fat is higher in visceral than in sc adipose tissue. Glucose 34-41 insulin Homo sapiens 15-22 12161508-16 2002 The rate of disappearance of glucose (insulin-mediated glucose uptake) progressively increased in response to both the GLP-1 and insulin infusion. Glucose 29-36 insulin Homo sapiens 38-45 12161508-16 2002 The rate of disappearance of glucose (insulin-mediated glucose uptake) progressively increased in response to both the GLP-1 and insulin infusion. Glucose 29-36 insulin Homo sapiens 129-136 12161508-16 2002 The rate of disappearance of glucose (insulin-mediated glucose uptake) progressively increased in response to both the GLP-1 and insulin infusion. Glucose 55-62 insulin Homo sapiens 38-45 12161508-16 2002 The rate of disappearance of glucose (insulin-mediated glucose uptake) progressively increased in response to both the GLP-1 and insulin infusion. Glucose 55-62 insulin Homo sapiens 129-136 12145777-1 2002 We previously have reported that protein, on a weight basis, is just as potent as glucose in increasing the insulin concentration in people with type 2 diabetes. Glucose 82-89 insulin Homo sapiens 108-115 12163658-10 2002 The combined administration of glucose and peptide hydrolysates stimulates a synergistic release of insulin, regardless of the protein source. Glucose 31-38 insulin Homo sapiens 100-107 12145777-3 2002 In the present study, we tested the hypothesis that the increased insulin responsiveness to protein in people with type 2 diabetes is due to the elevated plasma glucose concentration in these individuals. Glucose 161-168 insulin Homo sapiens 66-73 12145780-10 2002 Non-insulin-mediated glucose uptakes (NIMGU) and insulin-mediated glucose uptakes (IMGU) were calculated for the basal (F) and insulin-stimulated states at 11.1 mmol/L of glucose (11.1). Glucose 21-28 insulin Homo sapiens 4-11 12145780-10 2002 Non-insulin-mediated glucose uptakes (NIMGU) and insulin-mediated glucose uptakes (IMGU) were calculated for the basal (F) and insulin-stimulated states at 11.1 mmol/L of glucose (11.1). Glucose 66-73 insulin Homo sapiens 49-56 12145777-10 2002 Thus, the greater insulin response to ingested protein is not likely to be due merely to a higher initial glucose concentration. Glucose 106-113 insulin Homo sapiens 18-25 12145780-10 2002 Non-insulin-mediated glucose uptakes (NIMGU) and insulin-mediated glucose uptakes (IMGU) were calculated for the basal (F) and insulin-stimulated states at 11.1 mmol/L of glucose (11.1). Glucose 66-73 insulin Homo sapiens 49-56 12145780-10 2002 Non-insulin-mediated glucose uptakes (NIMGU) and insulin-mediated glucose uptakes (IMGU) were calculated for the basal (F) and insulin-stimulated states at 11.1 mmol/L of glucose (11.1). Glucose 66-73 insulin Homo sapiens 49-56 12165748-3 2002 Since insulin uses G-sensitive mechanisms to enhance tissue glucose uptake and vasodilatation, the GNB3 gene may be a candidate gene in type 2 diabetes. Glucose 60-67 insulin Homo sapiens 6-13 12145780-10 2002 Non-insulin-mediated glucose uptakes (NIMGU) and insulin-mediated glucose uptakes (IMGU) were calculated for the basal (F) and insulin-stimulated states at 11.1 mmol/L of glucose (11.1). Glucose 66-73 insulin Homo sapiens 49-56 12145780-11 2002 The beta-cell function was calculated via the acute insulin response to glucose (AIRg). Glucose 72-79 insulin Homo sapiens 52-59 12145783-3 2002 Glucose uptake, estimated by intramuscular (IM) injection of 2-deoxy[1,2-3H]glucose with or without insulin, was maximally increased at 10(-6) mol/L for HI and X2 and 10(-7) mol/L for H2. Glucose 0-7 insulin Homo sapiens 100-107 12164475-7 2002 Fasting glucose, insulin, total and high-density lipoprotein cholesterol and triglycerides were linked to the glucose and insulin responses during glucose tolerance tests. Glucose 8-15 insulin Homo sapiens 122-129 12164475-7 2002 Fasting glucose, insulin, total and high-density lipoprotein cholesterol and triglycerides were linked to the glucose and insulin responses during glucose tolerance tests. Glucose 110-117 insulin Homo sapiens 17-24 12164475-7 2002 Fasting glucose, insulin, total and high-density lipoprotein cholesterol and triglycerides were linked to the glucose and insulin responses during glucose tolerance tests. Glucose 110-117 insulin Homo sapiens 17-24 12142740-12 2002 Together with the enhanced insulin secretion observed in the in vivo experiment, the level of free fatty acids in blood decreased and, surprisingly, glucose concentration was significantly elevated. Glucose 149-156 insulin Homo sapiens 27-34 12181379-8 2002 Furthermore, we suggest that the influences of total adiposity, central fat, and insulin resistance, main determinants of PAI-1 concentrations, are different according to the degree of glucose tolerance. Glucose 185-192 insulin Homo sapiens 81-88 12230794-7 2002 When patients about to undergo elective surgery have been treated with glucose intravenously or a carbohydrate-rich drink instead of overnight fasting, insulin resistance was reduced by about half. Glucose 71-78 insulin Homo sapiens 152-159 12219032-5 2002 The treatment group was given continuous intravenous insulin at a rate of at least 1.5 microU/kg/min to maintain serum glucose levels between 100 to 140 mg/dL. Glucose 119-126 insulin Homo sapiens 53-60 12011082-3 2002 Glucose (8-10 mm) induced dose-dependent and kinetically similar patterns of C-peptide and insulin secretion. Glucose 0-7 insulin Homo sapiens 91-98 12235732-8 2002 Bedtime insulin may be discontinued when fasting glucose concentrations remain in the desired range and no rise of glucose concentrations occurs during the night. Glucose 49-56 insulin Homo sapiens 8-15 12016216-4 2002 However, we presented evidence for another factor, carbohydrate response factor, which is also involved in this response, and we proposed a model wherein SREBP-1c and carbohydrate response factor are independent transcription factors that act in response to insulin and glucose, respectively. Glucose 270-277 insulin Homo sapiens 258-265 12011082-7 2002 Perifusion studies using pharmacologic inhibitors (genistein and wortmannin) of the kinases thought to be involved in insulin signaling potentiated 10 mm glucose-induced secretion. Glucose 154-161 insulin Homo sapiens 118-125 12069734-1 2002 OBJECTIVE: The hypothesis was that fasting C-peptide and insulin values, during an oral glucose tolerance test (OGTT), might allow an estimation of the increased risk for gestational hypertension (GH) and fetal macrosomia. Glucose 88-95 insulin Homo sapiens 57-64 12083786-0 2002 The mif gene is transcriptionally regulated by glucose in insulin-secreting cells. Glucose 47-54 insulin Homo sapiens 58-65 12083786-4 2002 Herein, we report that incubating the differentiated insulin-secreting cell line INS-1 in high glucose concentration increases MIF transcriptional activity as well as the reporter gene activity driven by the -1033 to +63 bp fragment of the MIF promoter. Glucose 95-102 insulin Homo sapiens 53-60 12089327-1 2002 Glucose, the principal regulator of endocrine pancreas, has several effects on pancreatic beta cells, including the regulation of insulin release, cell proliferation, apoptosis, differentiation, and gene expression. Glucose 0-7 insulin Homo sapiens 130-137 12083786-8 2002 In conclusion, we identified a minimal region of the MIF promoter which contributes to the glucose stimulation of the mif gene in insulin-secreting cells. Glucose 91-98 insulin Homo sapiens 130-137 11978799-3 2002 Elevation of glucose leads to increases in cytosolic [Ca2+]i and biphasic release of insulin from both a readily releasable and a storage pool of beta-granules. Glucose 13-20 insulin Homo sapiens 85-92 11983706-3 2002 In contrast, at 25 mm glucose (HG), proliferation and thymidine incorporation were stimulated by insulin, serum, epidermal growth factor, and insulin-like growth factor 1 to a comparable extent, whereas basal levels were 25% lower than those in LG. Glucose 22-29 insulin Homo sapiens 97-104 11983706-0 2002 Glucose regulates insulin mitogenic effect by modulating SHP-2 activation and localization in JAr cells. Glucose 0-7 insulin Homo sapiens 18-25 11983706-2 2002 When JAr cells were cultured in the presence of 6 mm glucose (LG), proliferation and thymidine incorporation were induced by serum, epidermal growth factor, and insulin-like growth factor 1 but not by insulin. Glucose 53-60 insulin Homo sapiens 161-168 11983706-12 2002 Thus, in JAr cells, glucose modulates insulin mitogenic action by modulating SHP-2 activity and intracellular localization. Glucose 20-27 insulin Homo sapiens 38-45 12055099-7 2002 The data strongly suggest, but do not definitely prove, that glucose indeed has the ability to stimulate both cNOS and iNOS in the islets and that NO might serve as a negative feedback inhibitor of glucose-stimulated insulin release. Glucose 198-205 insulin Homo sapiens 217-224 12055099-0 2002 Role of nitric oxide synthase isoforms in glucose-stimulated insulin release. Glucose 42-49 insulin Homo sapiens 61-68 12055099-2 2002 By measuring enzyme activities and protein expression of NOS isoforms [i.e., cNOS and inducible NOS (iNOS)] in islets of Langerhans cells in relation to insulin secretion, we show that glucose dose-dependently stimulates islet activities of both cNOS and iNOS, that cNOS-derived nitric oxide (NO) strongly inhibits glucose-stimulated insulin release, and that short-term hyperglycemia in mice induces islet iNOS activity. Glucose 185-192 insulin Homo sapiens 153-160 12055099-2 2002 By measuring enzyme activities and protein expression of NOS isoforms [i.e., cNOS and inducible NOS (iNOS)] in islets of Langerhans cells in relation to insulin secretion, we show that glucose dose-dependently stimulates islet activities of both cNOS and iNOS, that cNOS-derived nitric oxide (NO) strongly inhibits glucose-stimulated insulin release, and that short-term hyperglycemia in mice induces islet iNOS activity. Glucose 185-192 insulin Homo sapiens 334-341 12055099-3 2002 Moreover, addition of NO gas or an NO donor inhibited glucose-stimulated insulin release, and different NOS inhibitors effected a potentiation. Glucose 54-61 insulin Homo sapiens 73-80 12081851-4 2002 In animals and in short-term human studies, a high intake of carbohydrates with a high glycemic index (a relative measure of the incremental glucose response per gram of carbohydrate) produced greater insulin resistance than did the intake of low-glycemic-index carbohydrates. Glucose 141-148 insulin Homo sapiens 201-208 12145143-6 2002 Both decreased release of insulin-desensitizing free fatty acids, tumor necrosis factor-alpha, and resistin and increased release of the insulin-sensitizing hormone adiponectin result in secondary improvement of insulin sensitivity of glucose uptake and suppression of glucose production. Glucose 235-242 insulin Homo sapiens 137-144 12145143-6 2002 Both decreased release of insulin-desensitizing free fatty acids, tumor necrosis factor-alpha, and resistin and increased release of the insulin-sensitizing hormone adiponectin result in secondary improvement of insulin sensitivity of glucose uptake and suppression of glucose production. Glucose 235-242 insulin Homo sapiens 137-144 12145143-6 2002 Both decreased release of insulin-desensitizing free fatty acids, tumor necrosis factor-alpha, and resistin and increased release of the insulin-sensitizing hormone adiponectin result in secondary improvement of insulin sensitivity of glucose uptake and suppression of glucose production. Glucose 269-276 insulin Homo sapiens 137-144 12145143-6 2002 Both decreased release of insulin-desensitizing free fatty acids, tumor necrosis factor-alpha, and resistin and increased release of the insulin-sensitizing hormone adiponectin result in secondary improvement of insulin sensitivity of glucose uptake and suppression of glucose production. Glucose 269-276 insulin Homo sapiens 137-144 12055099-8 2002 The results also suggest that hyperglycemia-evoked islet NOS activity might be one of multiple factors involved in the impairment of glucose-stimulated insulin release in type II diabetes mellitus. Glucose 133-140 insulin Homo sapiens 152-159 12067846-10 2002 In particular, at the liver site, this hormone deeply affects, in a time-dependent fashion, the inhibitory effect of insulin on glucose release. Glucose 128-135 insulin Homo sapiens 117-124 12067836-0 2002 Function and dysfunction of aPKC isoforms for glucose transport in insulin-sensitive and insulin-resistant states. Glucose 46-53 insulin Homo sapiens 67-74 12067836-0 2002 Function and dysfunction of aPKC isoforms for glucose transport in insulin-sensitive and insulin-resistant states. Glucose 46-53 insulin Homo sapiens 89-96 12067836-1 2002 Considerable evidence suggests that atypical protein kinase C isoforms (aPKCs), serving downstream of insulin receptor substrates and phosphatidylinositol (PI) 3-kinase, are required for insulin-stimulated glucose transport in skeletal muscle and adipocytes. Glucose 206-213 insulin Homo sapiens 102-109 12067837-1 2002 Free fatty acids (FFA) have been shown to inhibit insulin suppression of endogenous glucose production (EGP). Glucose 84-91 insulin Homo sapiens 50-57 11983507-4 2002 The data clearly showed that analogue 3 mimics insulin effects on DNA synthesis, glucose uptake and glycogen synthesis without loss of potency as compared to insulin. Glucose 81-88 insulin Homo sapiens 47-54 12067846-0 2002 Epinephrine effects on insulin-glucose dynamics: the labeled IVGTT two-compartment minimal model approach. Glucose 31-38 insulin Homo sapiens 23-30 12067846-3 2002 In six normal control subjects, we used the labeled intravenous glucose tolerance test (IVGTT) interpreted with the two-compartment minimal model, which provides not only glucose effectiveness (S(G)(2*)), insulin sensitivity (S(I)(2*)), and plasma clearance rate (PCR) at basal state, but also the time course of EGP. Glucose 64-71 insulin Homo sapiens 205-212 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 31-38 insulin Homo sapiens 57-64 12095410-5 2002 Six obese adolescents and six normal-weight controls underwent a 4 h frequently sampled intravenous glucose test with minimal model analysis, to bring about a sharp rise in blood insulin and provide a reliable index of insulin sensitivity (S(I)). Glucose 100-107 insulin Homo sapiens 179-186 12086926-2 2002 In keeping with previous reports, rates of insulin-stimulated glucose disappearance (G(Rd)) were normal after 2 h but were reduced by 43% (from 52.7 +/- 8.2 to 30.0 +/- 5.3 micromol. Glucose 62-69 insulin Homo sapiens 43-50 12087010-11 2002 The improvement of insulin resistance might have beneficial effects not only on glucose control but also on CVD in patients with type 2 diabetes. Glucose 80-87 insulin Homo sapiens 19-26 12087022-7 2002 Early-phase insulin secretion (insulinogenic index [Delta I/Delta G(30-0), where I is insulin and G is glucose]; P < 0.0007) was significantly higher in both lean and obese PCOS subjects than in healthy women. Glucose 103-110 insulin Homo sapiens 12-19 12087022-7 2002 Early-phase insulin secretion (insulinogenic index [Delta I/Delta G(30-0), where I is insulin and G is glucose]; P < 0.0007) was significantly higher in both lean and obese PCOS subjects than in healthy women. Glucose 103-110 insulin Homo sapiens 31-38 12007726-11 2002 Compared with regular human insulin, insulin lispro induces a more rapid and greater decrease in plasma glucose concentration during exercise because of its faster absorption. Glucose 104-111 insulin Homo sapiens 37-44 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 31-38 insulin Homo sapiens 57-64 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 79-86 insulin Homo sapiens 43-50 12099955-4 2002 RESULTS: In the 45 patients undergoing glucose clamp studies, insulin-mediated total glucose disposal (TGD) was independently and negatively associated with systolic blood pressure (standardized beta coefficient = -0.407, P = 0.003), plasma triglycerides (beta= -0.355, P = 0.007), and HbA1c (beta= -0.350, P = 0.008). Glucose 39-46 insulin Homo sapiens 62-69 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 79-86 insulin Homo sapiens 57-64 12099955-4 2002 RESULTS: In the 45 patients undergoing glucose clamp studies, insulin-mediated total glucose disposal (TGD) was independently and negatively associated with systolic blood pressure (standardized beta coefficient = -0.407, P = 0.003), plasma triglycerides (beta= -0.355, P = 0.007), and HbA1c (beta= -0.350, P = 0.008). Glucose 85-92 insulin Homo sapiens 62-69 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 79-86 insulin Homo sapiens 57-64 12099959-0 2002 Diminution of early insulin response to glucose in subjects with normal but minimally elevated fasting plasma glucose. Glucose 40-47 insulin Homo sapiens 20-27 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 79-86 insulin Homo sapiens 43-50 12099959-0 2002 Diminution of early insulin response to glucose in subjects with normal but minimally elevated fasting plasma glucose. Glucose 110-117 insulin Homo sapiens 20-27 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 79-86 insulin Homo sapiens 57-64 12099959-7 2002 In contrast, the ratio of change in insulin to change in glucose from 0 to 30 min during the glucose tolerance test was greatest in the 1st group and progressively declined in the groups with higher fasting glycaemia. Glucose 57-64 insulin Homo sapiens 36-43 12099959-7 2002 In contrast, the ratio of change in insulin to change in glucose from 0 to 30 min during the glucose tolerance test was greatest in the 1st group and progressively declined in the groups with higher fasting glycaemia. Glucose 93-100 insulin Homo sapiens 36-43 12086937-2 2002 In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Glucose 79-86 insulin Homo sapiens 57-64 12099959-9 2002 Distribution of the insulin to glucose ratio of subjects with normal glucose tolerance significantly overlapped with that of untreated patients with diabetes. Glucose 69-76 insulin Homo sapiens 20-27 12086937-4 2002 Preincubation for 24 h with high glucose and insulin (high Glc/Ins) reduced insulin-stimulated GLUT4 translocation by 50%, without affecting GLUT4 expression. Glucose 33-40 insulin Homo sapiens 76-83 12086937-5 2002 Insulin receptor and insulin receptor substrate-1 tyrosine phosphorylation, phosphatidylinositol 3-kinase activation, and Akt phosphorylation also diminished, as did insulin-mediated glucose uptake. Glucose 183-190 insulin Homo sapiens 0-7 12086937-5 2002 Insulin receptor and insulin receptor substrate-1 tyrosine phosphorylation, phosphatidylinositol 3-kinase activation, and Akt phosphorylation also diminished, as did insulin-mediated glucose uptake. Glucose 183-190 insulin Homo sapiens 166-173 12086945-14 2002 The acute insulin response to arginine correlated better with transplanted islet mass than acute insulin response to glucose (AIR(g)) and area under the curve for insulin (AUC(i)), but the AIR(g) and AUC(i) were more closely related to glycemic control. Glucose 117-124 insulin Homo sapiens 97-104 12086947-6 2002 Decreasing glucose tolerance was associated with increasing insulin resistance (HOMA: NGT 12.01 +/- 0.54 pmol/mmol; IFG/IGT 16.14 +/- 0.84; diabetes 26.99 +/- 2.62; P < 0.001) and decreasing beta-cell function (DeltaI(30)/DeltaG(30): NGT 157.7 +/- 9.7 pmol/mmol; IFG/IGT 100.4 +/- 5.4; diabetes 57.5 +/- 7.3; P < 0.001). Glucose 11-18 insulin Homo sapiens 60-67 12166545-3 2002 In patients with type 1 and type 2 diabetes, once-daily insulin glargine achieves equivalent glycaemic control to NPH insulin given once or twice daily In patients with type 1 diabetes, it is associated with significantly lower fasting blood glucose (FBG) levels, especially in those patients previously on twice-daily NPH insulin. Glucose 242-249 insulin Homo sapiens 56-63 12088922-5 2002 During the glucose clamp study, the serum levels of insulin significantly increased (from 33.0+/-3.6 to 1344.6+/-67.8 pmol/ml, P<0.001), as did the plasma levels of AM (from 12.8+/-0.7 to 14.2+/-0.9 fmol/ml, P<0.03) only in patients with type 2 diabetes mellitus. Glucose 11-18 insulin Homo sapiens 52-59 12166545-7 2002 Insulin glargine provides the opportunity to achieve target blood glucose levels more effectively and safely compared with NPH insulin, due to the reduced risk of hypoglycaemia, especially nocturnal hypoglycaemia. Glucose 66-73 insulin Homo sapiens 0-7 12070228-2 2002 The increased insulin action has been shown to involve glucose transport, glycogen synthesis, and glycogen synthase (GS) activation as well as amino acid transport. Glucose 55-62 insulin Homo sapiens 14-21 12080441-0 2002 Impaired ("diabetic") insulin signaling and action occur in fat cells long before glucose intolerance--is insulin resistance initiated in the adipose tissue? Glucose 82-89 insulin Homo sapiens 22-29 12080441-4 2002 However, insulin-stimulated glucose transport and glycogen synthesis are markedly reduced. Glucose 28-35 insulin Homo sapiens 9-16 12458657-4 2002 The 72-hour fast significantly increased plasma glucose (1.5- to 2-fold) and insulin (2- to 4-fold) after glucose ingestion versus the values after the overnight fast, indicating the manifestation of peripheral insulin resistance. Glucose 106-113 insulin Homo sapiens 77-84 12089386-5 2002 Insulin resistance was evaluated by the homeostasis model assessment method (HOMA-IR) using fasting glucose and insulin levels at baseline, and the cohort was followed for a mean period of 67 mo. Glucose 100-107 insulin Homo sapiens 0-7 12150359-8 2002 Insulin regimens should be designed to mimic the body"s natural physiologic secretion of insulin, including the basal amounts released continuously by the pancreas and the insulin surges produced in response to glucose loads. Glucose 211-218 insulin Homo sapiens 0-7 12150359-8 2002 Insulin regimens should be designed to mimic the body"s natural physiologic secretion of insulin, including the basal amounts released continuously by the pancreas and the insulin surges produced in response to glucose loads. Glucose 211-218 insulin Homo sapiens 172-179 12107194-7 2002 Insulin stimulation of glucose Rd were comparable in the men with high LFAT (141 +/- 12 mg/m(2).min) and those with low LFAT (156 +/- 14 mg/m(2).min; P = NS). Glucose 23-30 insulin Homo sapiens 0-7 12077725-5 2002 Coingestion of glucose and galactose at 33 micromol x kg(-1) x min(-1) each resulted in (1) decreased plasma galactose (0.3 +/- 0.1 mmol/L) and galactose Ra (6.4 +/- 1.8 micromol x kg(-1) x min(-1)); (2) increased plasma glucose and insulin; (3) doubling of splanchnic extraction of galactose; and (4) decreased contribution of galactose to glucose Ra (11% +/- 4%). Glucose 15-22 insulin Homo sapiens 233-240 12120259-2 2002 However, restoring normal glucose levels in diabetic patients through administering insulin by subcutaneous injection has proved virtually impossible. Glucose 26-33 insulin Homo sapiens 84-91 12105286-10 2002 Insulin sensitivity, assessed by a frequently sampled intravenous glucose-tolerance test, improved significantly (p < 0.02). Glucose 66-73 insulin Homo sapiens 0-7 12086947-10 2002 Insulin sensitivity and AUCg were linearly related so that insulin resistance was associated with poorer glucose disposal (r(2) = 0.084, P < 0.001). Glucose 105-112 insulin Homo sapiens 0-7 12086947-10 2002 Insulin sensitivity and AUCg were linearly related so that insulin resistance was associated with poorer glucose disposal (r(2) = 0.084, P < 0.001). Glucose 105-112 insulin Homo sapiens 59-66 12086947-11 2002 In contrast, there was a strong inverse curvilinear relationship between beta-cell function and AUCg such that poorer insulin release was associated with poorer glucose disposal (log[DeltaI(30)/DeltaG(30)]: r(2) = 0.29, P < 0.001; log[(DeltaI(30)/DeltaG(30))/HOMA-IR]: r(2) = 0.45, P < 0.001). Glucose 161-168 insulin Homo sapiens 118-125 12086947-13 2002 Both insulin resistance and impaired beta-cell function are associated with impaired glucose metabolism in all ethnic groups, with beta-cell function seeming to be more important in determining glucose disposal. Glucose 85-92 insulin Homo sapiens 5-12 12086949-8 2002 While prolonged (6-24 h) insulin exposure led to desensitization of GS, INH continued to activate GS FV for at least 24 h. Insulin and LiCl acutely activated glucose uptake, whereas INH stimulation of glucose uptake required more prolonged exposure, starting at 6 h and continuing to 24 h. Chronic (4-day) treatment with INH increased both basal (154 +/- 32% of control) and insulin-stimulated (219 +/- 74%) glucose uptake. Glucose 158-165 insulin Homo sapiens 123-130 12086949-11 2002 Together with the INH-induced increase in insulin-stimulated glucose uptake, there was an approximately 3.5-fold increase (P < 0.05) in insulin receptor substrate (IRS)-1 protein abundance. Glucose 61-68 insulin Homo sapiens 42-49 12124987-7 2002 RESULTS: Transfected Chang cells secreted 5-8 pmol proinsulin/10(6) cells per 24 h in continuous passage for at least a year in response to 5-25 mM glucose and 10-90 microM zinc in vitro. Glucose 148-155 insulin Homo sapiens 51-61 12124987-8 2002 Glucose and zinc synergistically increased proinsulin production by up to 30-fold. Glucose 0-7 insulin Homo sapiens 43-53 12124987-12 2002 Serum proinsulin levels were further increased 1.3-fold (p<0.05) after glucose and 1.4- to 1.6-fold (p<0.005) after zinc administration in vivo. Glucose 74-81 insulin Homo sapiens 6-16 12134080-1 2002 Insulin regulates glucose uptake into fat and muscle by modulating the distribution of the GLUT4 glucose transporter between the surface and interior of cells. Glucose 18-25 insulin Homo sapiens 0-7 12238047-0 2002 [Role of NADH shuttle system in glucose-stimulated insulin secretion]. Glucose 32-39 insulin Homo sapiens 51-58 12131777-0 2002 Effect of stimulators such as GLP-1, PACAP, and nicotinamide on glucose-stimulated insulin secretion from porcine pancreatic endocrine cells in long-term culture. Glucose 64-71 insulin Homo sapiens 83-90 12131777-1 2002 INTRODUCTION: Transplantation of glucose-responsive insulin-secreting cells has the potential to result in a cure for diabetes. Glucose 33-40 insulin Homo sapiens 52-59 12131777-2 2002 AIM: To report the development of a model of adult porcine pancreatic endocrine cells (PE cells) exhibiting glucose-stimulated insulin secretion during a long-term culture period, in vitro. Glucose 108-115 insulin Homo sapiens 127-134 12070228-3 2002 A major mechanism involved in increased insulin stimulation of glucose uptake after exercise seems to be the exercise-associated decrease in muscle glycogen content. Glucose 63-70 insulin Homo sapiens 40-47 12136270-7 2002 When glycolytic ATP production was reduced, initial but not sustained glucose-stimulated insulin release was observed. Glucose 70-77 insulin Homo sapiens 89-96 12661110-6 2002 The glucose clamp test confirmed insulin resistance. Glucose 4-11 insulin Homo sapiens 33-40 12136270-11 2002 In conclusion, glucose-induced enhancement of insulin release was only seen when the rise of the sugar concentration triggered a rapid and sustained increase of mitochondrial metabolism. Glucose 15-22 insulin Homo sapiens 46-53 12180549-6 2002 Luciferase activities, driven by the insulin gene promoter, in the rAAV-transduced hepatoma cells responded to milli molars of glucose. Glucose 127-134 insulin Homo sapiens 37-44 12126540-0 2002 [Associations of insulin resistance and pancreatic beta-cell function with plasma glucose level in type 2 diabetes]. Glucose 82-89 insulin Homo sapiens 17-24 12497978-11 2002 The present data confirm previous studies showing that quinine depresses plasma glucose through stimulation of insulin secretion. Glucose 80-87 insulin Homo sapiens 111-118 12422580-5 2002 According to multiple regression analysis insulin sensitivity, expressed as insulin stimulated glucose disposal rate, during euglycemic clamp (r = -0.81, p < 0.05 and r = -0.89; p < 0.01) and basal estradiol level (r = -0.54; p < 0.05 and r = -0.56; p < 0.05) appeared significant negative predictors of the number of fertilized oocytes and embryos, respectively. Glucose 95-102 insulin Homo sapiens 42-49 12422580-5 2002 According to multiple regression analysis insulin sensitivity, expressed as insulin stimulated glucose disposal rate, during euglycemic clamp (r = -0.81, p < 0.05 and r = -0.89; p < 0.01) and basal estradiol level (r = -0.54; p < 0.05 and r = -0.56; p < 0.05) appeared significant negative predictors of the number of fertilized oocytes and embryos, respectively. Glucose 95-102 insulin Homo sapiens 76-83 12126540-1 2002 OBJECTIVE: To investigate the influence of insulin resistance and pancreatic beta-cell function on plasma glucose level in type 2 diabetes so as to provide theoretical basis for reasonable selection of hypoglycemic agents. Glucose 106-113 insulin Homo sapiens 43-50 12115127-7 2002 Insulin secretion by the islet was thus computed as a response to glucose signal. Glucose 66-73 insulin Homo sapiens 0-7 12006356-6 2002 The insulin-stimulated glucose utilization and the insulin-stimulated increase in glycogen synthase activity during the clamp were significantly lower in the patients than in controls (51.3 +/- 6.0 vs. 72.6 +/- 13.1 micromol x min(-1) x kg lean body mass(-1), P < 0.05, and 53 +/- 15 vs. 79 +/- 9%, P < 0.05, n = 6, respectively). Glucose 23-30 insulin Homo sapiens 4-11 12006356-10 2002 In conclusion, these data show that patients with McArdle"s glycogen storage disease are insulin resistant in terms of glucose uptake, glycogen synthase activation, and alterations in fuel oxidation. Glucose 119-126 insulin Homo sapiens 89-96 12006367-2 2002 The insulin and IGF-I infusion rates were chosen to augment glucose disposal (R(d)) to a similar extent in control subjects. Glucose 60-67 insulin Homo sapiens 4-11 12006367-4 2002 In control subjects, insulin was more effective than IGF-I in suppressing endogenous glucose production (EGP) during both clamp steps. Glucose 85-92 insulin Homo sapiens 21-28 12006370-9 2002 These findings suggest the presence of a signaling pathway for insulin-stimulated glucose transport in which PDK1 to PKB or aPKC is not involved. Glucose 82-89 insulin Homo sapiens 63-70 12079834-2 2002 In rat extensor digitorum longus (EDL) muscle preparations preincubated for 2-4 h in a hyperglycemic medium (25 mM vs. 0 mM glucose), we have shown that the ability of insulin to stimulate glucose incorporation into glycogen is impaired. Glucose 124-131 insulin Homo sapiens 168-175 12079834-2 2002 In rat extensor digitorum longus (EDL) muscle preparations preincubated for 2-4 h in a hyperglycemic medium (25 mM vs. 0 mM glucose), we have shown that the ability of insulin to stimulate glucose incorporation into glycogen is impaired. Glucose 189-196 insulin Homo sapiens 168-175 12079842-4 2002 Intense efforts are under way to define the molecular mechanisms that regulate glucose metabolism and gene expression in insulin-sensitive tissues. Glucose 79-86 insulin Homo sapiens 121-128 12079842-7 2002 This review will present our current understanding of potential defects in insulin signal transduction pathways, with an emphasis on mechanisms regulating glucose transport in skeletal muscle from people with type II diabetes mellitus. Glucose 155-162 insulin Homo sapiens 75-82 12079846-1 2002 This article highlights current understanding on the mechanism of PKC-induced insulin resistance in skeletal muscle, a major target site for insulin-mediated glucose disposal. Glucose 158-165 insulin Homo sapiens 78-85 12079848-2 2002 In animals, this is true of genetic models of obesity and nutritional models of insulin resistance generated by high-fat feeding, infusion of lipid, or infusion of glucose. Glucose 164-171 insulin Homo sapiens 80-87 12079849-4 2002 Exposure of cardiomyocytes to esculetin or NDGA, two structurally different LO inhibitors, induced a complete inhibition of insulin-stimulated glucose uptake, whereas control cells showed a threefold stimulation by insulin. Glucose 143-150 insulin Homo sapiens 124-131 12079855-3 2002 METHODS: We selected genes that were implicated in the development of insulin resistance, including genes involved in insulin signaling; glucose uptake, oxidation, and storage; fat uptake, oxidation, and storage; cytoskeletal components; and transcription factors. Glucose 137-144 insulin Homo sapiens 70-77 12079869-7 2002 Insulin responses to intravenous glucose were increased (6741 +/- 2538 vs. 3938 +/- 771 pM 3 min, p = 0.050), while glucose clearance was not changed by HFD vs. CD, thus indicating insulin resistance. Glucose 33-40 insulin Homo sapiens 0-7 12079881-3 2002 These myotubes manifested both basal and insulin-stimulated (1-100 nM) glucose transport and glycogen synthesis. Glucose 71-78 insulin Homo sapiens 41-48 12079881-7 2002 Treatment with high glucose concentrations (10-20 mM) for 2-8 days reduced both basal and insulin-stimulated glucose uptake. Glucose 20-27 insulin Homo sapiens 90-97 12079881-7 2002 Treatment with high glucose concentrations (10-20 mM) for 2-8 days reduced both basal and insulin-stimulated glucose uptake. Glucose 109-116 insulin Homo sapiens 90-97 12079881-9 2002 Baseline glucose uptake and glycogen synthesis were reduced by 35%, insulin-stimulated glucose uptake by 25%, and insulin-stimulated glycogen synthesis by 39%. Glucose 87-94 insulin Homo sapiens 68-75 12079881-11 2002 The insulin-stimulated glucose uptake in hyperglycemia-treated cells was improved by electrical stimulation of the cells. Glucose 23-30 insulin Homo sapiens 4-11 12079885-4 2002 We studied the effect of an acute elevation of NEFA during lipid-heparin infusion compared to a glycerol-only control on glucose-stimulated insulin secretion and clearance during a 120-min hyperglycemic (10 mM) clamp in 7 healthy normoglucose-tolerant volunteers. Glucose 121-128 insulin Homo sapiens 140-147 12079270-6 2002 Compared with injected human insulin, they improve post-prandial glucose control and reduce late post-meal and night-time hypoglycaemic episodes. Glucose 65-72 insulin Homo sapiens 29-36 12079270-7 2002 Two basal insulin analogues, insulin glargine and insulin detemir, have also shown beneficial profiles with regard to night-time hypoglycaemia.Some, but not all, studies with the two rapid-acting insulins have shown improvement in overall glucose control, as assessed by HbA(1c), in comparison to human insulin. Glucose 239-246 insulin Homo sapiens 10-17 12079270-7 2002 Two basal insulin analogues, insulin glargine and insulin detemir, have also shown beneficial profiles with regard to night-time hypoglycaemia.Some, but not all, studies with the two rapid-acting insulins have shown improvement in overall glucose control, as assessed by HbA(1c), in comparison to human insulin. Glucose 239-246 insulin Homo sapiens 29-36 12643178-5 2002 5) The slightly increased HGP values throughout the 24-hour period together with reduced metabolic clearance rate (peripheral insulin resistance) and increased carbohydrate intake is responsible for the increase in fasting plasma glucose values. Glucose 230-237 insulin Homo sapiens 126-133 12643178-7 2002 If insulin-mediated glucose uptake in skeletal muscle is reduced, plasma glucose will increase due to the "nonsuppressed" HGP values. Glucose 20-27 insulin Homo sapiens 3-10 12643178-7 2002 If insulin-mediated glucose uptake in skeletal muscle is reduced, plasma glucose will increase due to the "nonsuppressed" HGP values. Glucose 73-80 insulin Homo sapiens 3-10 12643178-8 2002 Plasma glucose continues to rise until glucose-mediated glucose uptake compensates completely for the reduction in insulin-mediated glucose uptake. Glucose 39-46 insulin Homo sapiens 115-122 12643178-8 2002 Plasma glucose continues to rise until glucose-mediated glucose uptake compensates completely for the reduction in insulin-mediated glucose uptake. Glucose 39-46 insulin Homo sapiens 115-122 12643178-8 2002 Plasma glucose continues to rise until glucose-mediated glucose uptake compensates completely for the reduction in insulin-mediated glucose uptake. Glucose 39-46 insulin Homo sapiens 115-122 16573417-9 2002 Apart from treatment of the underlying cause (e.g sepsis), there is no specific treatment, although a 44% reduction in the incidence of critical illness polyneuropathy has been described in mechanically ventilated critically ill patients who received intensive insulin therapy to maintain the blood glucose level between 4.4-6.1 mmol/L. Glucose 299-306 insulin Homo sapiens 261-268 17019225-6 2002 RECENT FINDINGS: Maintenance of euglycemia and physiologic control of insulin responses to changes in glucose levels have been shown to prolong life and reduce complications from diabetes mellitus. Glucose 102-109 insulin Homo sapiens 70-77 11947963-8 2002 Consistent with these results, the basal and insulin-induced glucose uptakes in adipocytes from troglitazone-treated OLETF rats were significantly increased (1.5-fold, P<0.05) compared with untreated OLETF rats. Glucose 61-68 insulin Homo sapiens 45-52 12031957-8 2002 The enhanced rate of entry of glucose-derived pyruvate into the tricarboxylic acid (TCA) cycle in the presence of alanine may have stimulated rates of generation of key metabolites, including ATP, which affect the insulin secretory process. Glucose 30-37 insulin Homo sapiens 214-221 12031975-2 2002 The aim of the present study was to address whether direct measures of peripheral tissue insulin sensitivity with regard to FFAs and glucose in the fasting state are good predictors of postabsorptive VLDL triglyceride secretion rate (VLDL-TG ASR) in humans, independent of obesity. Glucose 133-140 insulin Homo sapiens 89-96 12031977-4 2002 Fasting plasma adiponectin concentration, body composition (hydrodensitometry or dual energy X-ray absorptiometry), insulin sensitivity (insulin-stimulated glucose disposal, hyperinsulinemic clamp), and glucose tolerance (75-g oral glucose tolerance test) were measured in 55 Pima Indians (47 men and 8 women, aged 31 +/- 8 years, body fat 29 +/- 8% [mean +/- SD]; 50 with normal glucose tolerance, 3 with impaired glucose tolerance, and 2 with diabetes). Glucose 156-163 insulin Homo sapiens 137-144 12031977-7 2002 Group 2 (38 subjects) had follow-up measurements of insulin-stimulated glucose disposal. Glucose 71-78 insulin Homo sapiens 52-59 12031977-8 2002 Cross-sectionally, plasma adiponectin concentration was positively associated with insulin-stimulated glucose disposal (r = 0.58, P < 0.0001) and negatively associated with percent body fat (r = -0.62, P < 0.0001) in the whole group. Glucose 102-109 insulin Homo sapiens 83-90 12031980-5 2002 Here, we report that a fourfold elevation in plasma FFA concentration induced a 40% reduction in the insulin-stimulated glucose disposal rate, a 30% decline in insulin-stimulated skeletal muscle insulin substrate receptor-1 (IRS-1) phosphorylation, a 48% decrease in IRS-1-associated phosphatidylinositol (PI) 3-kinase activity, and a 50% reduction in muscle FAT/CD36 protein expression in male rats. Glucose 120-127 insulin Homo sapiens 101-108 12031981-7 2002 Insulin sensitivity (SI) was measured using an intravenous glucose tolerance test. Glucose 59-66 insulin Homo sapiens 0-7 12032098-4 2002 A rapid increase in BG was induced by oral administration of glucose, and subsequently, a rapid decrease in glucose was induced by intravenous administration of insulin. Glucose 108-115 insulin Homo sapiens 161-168 12032122-0 2002 Effect of C-peptide on glucose metabolism in patients with type 1 diabetes. Glucose 23-30 insulin Homo sapiens 10-19 12107725-10 2002 Alterations responsible for the reduced glucose disposal could be located downstream of the investigated steps or in alternative insulin signalling pathways. Glucose 40-47 insulin Homo sapiens 129-136 12149597-9 2002 Body weight, resting energy expenditure and insulin-mediated glucose disposal [oxidative and non oxidative] were not modified after training. Glucose 61-68 insulin Homo sapiens 44-51 12149600-9 2002 In the control group, muscle Mg content correlated positively with insulin stimulated glucose disposal rate (r=0.77, p<0.01) and negatively with two hour plasma glucose concentration during an oral glucose tolerance test (OGTT) (r=- 0.64, p<0.05). Glucose 86-93 insulin Homo sapiens 67-74 12149601-7 2002 CONCLUSIONS: Insulin secretion rates, but not insulin sensitivity, assessed during graded infusion of glucose were mildly decreased in nondiabetic relatives of type 2 diabetic subjects, who carry the at risk T-allele of exon 18 variant of the SUR1 gene. Glucose 102-109 insulin Homo sapiens 13-20 12173727-5 2002 Infusion of insulin (0.5 mU/kg/min) increased insulin levels (p<0.01) to identical levels in both groups (218+/-16 vs 222+/-19), but the glucose infusion required to maintain euglycemia was higher (p<0.01) in nondiabetic than in diabetic subjects, indicating insulin resistance to glucose disposal in the diabetic subjects. Glucose 140-147 insulin Homo sapiens 12-19 12039705-13 2002 Conversely, the administration of a pulse of insulin and glucose, in the absence of dexamethasone, prevented the drop in serum leptin observed during fasting, regardless of the insulin dose or the serum glucose elevation. Glucose 203-210 insulin Homo sapiens 45-52 12028371-6 2002 Elevated FFA and intracellular lipid appear to inhibit insulin signalling, leading to a reduction in insulin-stimulated muscle glucose transport that may be mediated by a decrease in GLUT-4 translocation. Glucose 127-134 insulin Homo sapiens 55-62 12028371-6 2002 Elevated FFA and intracellular lipid appear to inhibit insulin signalling, leading to a reduction in insulin-stimulated muscle glucose transport that may be mediated by a decrease in GLUT-4 translocation. Glucose 127-134 insulin Homo sapiens 101-108 12028371-8 2002 In the liver, elevated FFA may contribute to hyperglycaemia by antagonizing the effects of insulin on endogenous glucose production. Glucose 113-120 insulin Homo sapiens 91-98 12032649-7 2002 Insulin concentration 120 min after the oral glucose load (a measure of insulin resistance) was inversely related to length at birth (P<0.005). Glucose 45-52 insulin Homo sapiens 0-7 12032649-7 2002 Insulin concentration 120 min after the oral glucose load (a measure of insulin resistance) was inversely related to length at birth (P<0.005). Glucose 45-52 insulin Homo sapiens 72-79 12067822-3 2002 RESULTS: Insulin therapy resulted in a significant decrease in fasting glucose levels by 26%; glycated hemoglobin decreased by 17% and fructosamine values by 19%. Glucose 71-78 insulin Homo sapiens 9-16 12131777-6 2002 The ability of the cells to respond to glucose-stimulated insulin secretion was also observed with and without stimulators. Glucose 39-46 insulin Homo sapiens 58-65 12207556-6 2002 Indices of insulin sensitivity and secretion were calculated from plasma glucose and insulin concentrations using the formulas proposed by Matthews et al. Glucose 73-80 insulin Homo sapiens 11-18 12207556-15 2002 CONCLUSIONS: The easiest way to predict the insulin sensitivity and to control the development of insulin resistance in a subject with yet normal glucose tolerance, but at high risk of development of overt Type 2 diabetes is to calculate an index from glucose and insulin concentrations during an oGTT. Glucose 146-153 insulin Homo sapiens 44-51 12207556-15 2002 CONCLUSIONS: The easiest way to predict the insulin sensitivity and to control the development of insulin resistance in a subject with yet normal glucose tolerance, but at high risk of development of overt Type 2 diabetes is to calculate an index from glucose and insulin concentrations during an oGTT. Glucose 146-153 insulin Homo sapiens 98-105 12207556-15 2002 CONCLUSIONS: The easiest way to predict the insulin sensitivity and to control the development of insulin resistance in a subject with yet normal glucose tolerance, but at high risk of development of overt Type 2 diabetes is to calculate an index from glucose and insulin concentrations during an oGTT. Glucose 146-153 insulin Homo sapiens 98-105 12207556-15 2002 CONCLUSIONS: The easiest way to predict the insulin sensitivity and to control the development of insulin resistance in a subject with yet normal glucose tolerance, but at high risk of development of overt Type 2 diabetes is to calculate an index from glucose and insulin concentrations during an oGTT. Glucose 252-259 insulin Homo sapiens 44-51 12207556-15 2002 CONCLUSIONS: The easiest way to predict the insulin sensitivity and to control the development of insulin resistance in a subject with yet normal glucose tolerance, but at high risk of development of overt Type 2 diabetes is to calculate an index from glucose and insulin concentrations during an oGTT. Glucose 252-259 insulin Homo sapiens 98-105 12207556-15 2002 CONCLUSIONS: The easiest way to predict the insulin sensitivity and to control the development of insulin resistance in a subject with yet normal glucose tolerance, but at high risk of development of overt Type 2 diabetes is to calculate an index from glucose and insulin concentrations during an oGTT. Glucose 252-259 insulin Homo sapiens 98-105 12039870-7 2002 4) Single beta cells secreted nearly two times more insulin in response to 5.6 or 15.6 mM glucose. Glucose 90-97 insulin Homo sapiens 52-59 12050208-2 2002 Recently, a new adipocyte hormone, resistin, was identified, shown to reduce insulin-mediated glucose uptake, and shown to be increased in obese mice. Glucose 94-101 insulin Homo sapiens 77-84 12050208-7 2002 No SNP was associated with type 2 diabetes, but the SNP in the promoter region was a significant determinant of insulin sensitivity index (P = 0.04) among nondiabetic family members who had undergone iv glucose tolerance tests. Glucose 203-210 insulin Homo sapiens 112-119 12050251-7 2002 In the postabsorptive state, hepatic insulin resistance [basal endogenous glucose production (EGP) x basal plasma insulin concentration] decreased from 41 +/- 7 to 25 +/- 3 mg/kg fat-free mass (FFM).min x microU/ml; P < 0.05) and suppression of EGP during the first insulin clamp step (1.1 +/- 0.1 to 0.6 +/- 0.2 mg/kg FFM.min; P < 0.05) improved after pioglitazone treatment. Glucose 74-81 insulin Homo sapiens 37-44 12050251-8 2002 The total body glucose MCR during the first and second insulin clamp steps increased after pioglitazone treatment [first MCR, 3.5 +/- 0.5 to 4.4 +/- 0.4 ml/kg FFM.min (P < 0.05); second MCR, 8.7 +/- 1.0 to 11.3 +/- 1.1 ml/kg FFM(. Glucose 15-22 insulin Homo sapiens 55-62 12050272-8 2002 Insulin responses to glucose and insulin sensitivity were not different among patients with different genotypes. Glucose 21-28 insulin Homo sapiens 0-7 12065236-1 2002 Glucagon-like peptide-1 (GLP-1) has been shown to have insulin-like effects upon the metabolism of glucose in rat liver, muscle and fat, and on that of lipids in rat and human adipocytes. Glucose 99-106 insulin Homo sapiens 55-62 12072869-9 2002 CONCLUSION: Prepubertal African American children have higher baseline and glucose-stimulated insulin and C-peptide levels, as well as reduced insulin sensitivity that is not entirely explained by differences in adiposity. Glucose 75-82 insulin Homo sapiens 94-101 12037728-8 2002 Insulin resistance was evaluated by the homeostasis model assessment (HOMA) and insulin secretion by HOMA and by insulin areas under curve in an oral glucose tolerance test (OGTT), insulin increment at 30 mnutes of OGTT, and insulin increment/glucose increment at 30 minutes of OGTT. Glucose 150-157 insulin Homo sapiens 0-7 12037728-8 2002 Insulin resistance was evaluated by the homeostasis model assessment (HOMA) and insulin secretion by HOMA and by insulin areas under curve in an oral glucose tolerance test (OGTT), insulin increment at 30 mnutes of OGTT, and insulin increment/glucose increment at 30 minutes of OGTT. Glucose 243-250 insulin Homo sapiens 0-7 12037730-9 2002 This protein-sparing effect of LCT appears to be dissociated from fatty acid effects on glucose metabolism; both MCT and LCT diminished insulin"s ability to increase glucose disappearance and to decrease hepatic glucose production. Glucose 166-173 insulin Homo sapiens 136-143 12323111-3 2002 The failure of glucose-stimulated insulin secretion (GSIS) in beta cells helps to sustain the elevations of serum glucose and free fatty acids, which in turn reinforce the failure of GSIS, possibly by inhibiting expression of the transcription factor IDX-1; NIDDM thus represents a vicious cycle that is not easily broken. Glucose 15-22 insulin Homo sapiens 34-41 12323111-3 2002 The failure of glucose-stimulated insulin secretion (GSIS) in beta cells helps to sustain the elevations of serum glucose and free fatty acids, which in turn reinforce the failure of GSIS, possibly by inhibiting expression of the transcription factor IDX-1; NIDDM thus represents a vicious cycle that is not easily broken. Glucose 114-121 insulin Homo sapiens 34-41 12099307-4 2002 An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat free mass and endogenous glucose production measured using [6,6(-2)H2]-glucose. Glucose 85-92 insulin Homo sapiens 12-19 12099307-4 2002 An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat free mass and endogenous glucose production measured using [6,6(-2)H2]-glucose. Glucose 160-167 insulin Homo sapiens 12-19 12099307-4 2002 An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat free mass and endogenous glucose production measured using [6,6(-2)H2]-glucose. Glucose 160-167 insulin Homo sapiens 12-19 12020984-7 2002 Insulin sensitivity was assessed by frequent intravenous glucose tolerance test. Glucose 57-64 insulin Homo sapiens 0-7 12148078-3 2002 The insulin resistance of obese people and subjects with type 2 diabetes is characterised by defects at many levels, affecting insulin receptor concentration, glucose transport mechanisms and the activities of intracellular enzymes. Glucose 159-166 insulin Homo sapiens 4-11 11809746-3 2002 In control untransfected (NON) and vector (CMV2)- and WT-transfected cells, insulin stimulated an expected 54 +/- 13, 37 +/- 4, and 47 +/- 12 increase in [U-(14)C]glucose incorporation into glycogen, respectively. Glucose 163-170 insulin Homo sapiens 76-83 12009471-4 2002 While the pretreatment of membrane with 20 mU l(-1) of insulin evoked slight increase of the current with unchanged course of the dependence of peak current on glucose, the decrease of conductance was observed above 10(5) mU l(-1) of insulin. Glucose 160-167 insulin Homo sapiens 55-62 12011435-1 2002 Of the three critical enhancer elements that mediate beta-cell-specific and glucose-responsive expression of the insulin gene, only the identity of the transcription factor binding to the RIPE3b element (RIPE3b1) has remained elusive. Glucose 76-83 insulin Homo sapiens 113-120 12023624-9 2002 The cultured islet cells secreted insulin in response to glucose challenge in a dose-dependent manner. Glucose 57-64 insulin Homo sapiens 34-41 12051762-4 2002 Chronic insulin stimulation caused a reduction of GLUT-4 and IRS-1 proteins with a correlated decrease in acute insulin-induced PKB and MAPK phosphorylations as well as a reduction in insulin-stimulated glucose transport. Glucose 203-210 insulin Homo sapiens 8-15 12212367-4 2002 RESULTS: Both fasting and glucose-induced insulin levels were higher in women with pure abdominal obesity than in the controls (p < 0.001) and in those with lower-body obesity (P < 0.01). Glucose 26-33 insulin Homo sapiens 42-49 12133483-14 2002 In addition, T2DM subjects with UCSNP44 TT genotype had lower CP levels after glucose challenge than those with non-TT genotype. Glucose 78-85 insulin Homo sapiens 62-64 11978587-7 2002 In multiple regression analysis, fasting levels of proinsulin and proinsulin/insulin ratios were positively associated both with the 2-hour glucose level (as a continuous variable) and with obesity, whereas a negative association was found with birth weight. Glucose 140-147 insulin Homo sapiens 51-61 11978587-7 2002 In multiple regression analysis, fasting levels of proinsulin and proinsulin/insulin ratios were positively associated both with the 2-hour glucose level (as a continuous variable) and with obesity, whereas a negative association was found with birth weight. Glucose 140-147 insulin Homo sapiens 66-76 11978587-7 2002 In multiple regression analysis, fasting levels of proinsulin and proinsulin/insulin ratios were positively associated both with the 2-hour glucose level (as a continuous variable) and with obesity, whereas a negative association was found with birth weight. Glucose 140-147 insulin Homo sapiens 54-61 12018664-11 2002 By exam 2, those with abnormal glucose tolerance had worse cardiovascular risk profiles and increased insulin resistance (P < 0.001). Glucose 31-38 insulin Homo sapiens 102-109 12018664-13 2002 Deterioration in glucose tolerance may be preceded by higher systolic blood pressure and is accompanied by worsening of other cardiovascular risk factors and insulin resistance. Glucose 17-24 insulin Homo sapiens 158-165 12022245-2 2002 METHODS: The relationship of insulin resistance, estimated by steady-state plasma glucose (SSPG) with the B-mode ultrasound-measured carotid intima-medial thickness (IMT) and the M-mode echocardiographically determined left ventricular mass (LVM), was examined in 82 Chinese patients with hypertension. Glucose 82-89 insulin Homo sapiens 29-36 12022245-3 2002 RESULTS: Insulin-resistant patients with obesity, glucose intolerance, dyslipidemia, and hypofibrinolysis show no significantly greater LVM index and carotid IMT than nonresistant individuals. Glucose 50-57 insulin Homo sapiens 9-16 11934663-1 2002 We have separated the effect of insulin on glucose distribution/transport, glucose disposal, and endogenous production (EGP) during an intravenous glucose tolerance test (IVGTT) by use of a dual-tracer dilution methodology. Glucose 43-50 insulin Homo sapiens 32-39 11934663-3 2002 A new model described the kinetics of the two glucose tracers and native glucose with the use of a two-compartment structure for glucose and a one-compartment structure for insulin effects. Glucose 46-53 insulin Homo sapiens 173-180 11934663-3 2002 A new model described the kinetics of the two glucose tracers and native glucose with the use of a two-compartment structure for glucose and a one-compartment structure for insulin effects. Glucose 73-80 insulin Homo sapiens 173-180 11934663-3 2002 A new model described the kinetics of the two glucose tracers and native glucose with the use of a two-compartment structure for glucose and a one-compartment structure for insulin effects. Glucose 73-80 insulin Homo sapiens 173-180 11934663-7 2002 EGP was suppressed by 70% (52-82%) (95% confidence interval relative to basal) within 60 min of the IVGTT; glucose distribution/transport was least responsive to insulin and was maximally activated by 62% (34-96%) above basal at 80 min compared with maximum 279% (116-565%) activation of glucose disposal at 20 min. Glucose 107-114 insulin Homo sapiens 162-169 11934663-10 2002 We conclude that, in healthy subjects during an IVGTT, the two peripheral insulin effects account jointly for approximately one-half of the overall insulin-stimulated glucose lowering, each effect contributing equally. Glucose 167-174 insulin Homo sapiens 74-81 11934663-10 2002 We conclude that, in healthy subjects during an IVGTT, the two peripheral insulin effects account jointly for approximately one-half of the overall insulin-stimulated glucose lowering, each effect contributing equally. Glucose 167-174 insulin Homo sapiens 148-155 11934666-3 2002 Four primary markers of insulin resistance and dyslipidemia were assessed: 1) area under the curve for the insulin (INS(AUC)) response to an oral glucose tolerance test (OGTT), 2) product of the OGTT glucose and insulin areas (INS(AUC)xGLU(AUC)), 3) serum triglycerides (TG), and 4) high-density lipoprotein (HDL)-cholesterol. Glucose 146-153 insulin Homo sapiens 107-114 11934672-4 2002 The response resembles that of the first phase of glucose-stimulated insulin release. Glucose 50-57 insulin Homo sapiens 69-76 11973171-2 2002 These data suggested that hyperglycemia impairs neutrophil function, and because nondiabetic patients also experience hyperglycemia during cardiac surgery, we hypothesized that a continuous insulin infusion would improve glucose control and neutrophil function in nondiabetic cardiac surgical patients. Glucose 221-228 insulin Homo sapiens 190-197 11973171-8 2002 IMPLICATIONS: IV insulin, as used in this study, had effects on blood glucose only after cardiac surgery, when it was associated with an increased neutrophil count and a greater total capacity of peripheral blood neutrophils to ingest foreign particles. Glucose 70-77 insulin Homo sapiens 17-24 11932032-0 2002 Insulin sensitivity in type 2 diabetes: univariate and multivariate techniques to derive estimates of insulin sensitivity from the insulin modified intravenous glucose tolerance test (FSIGT). Glucose 160-167 insulin Homo sapiens 102-109 11932032-0 2002 Insulin sensitivity in type 2 diabetes: univariate and multivariate techniques to derive estimates of insulin sensitivity from the insulin modified intravenous glucose tolerance test (FSIGT). Glucose 160-167 insulin Homo sapiens 131-138 11978642-0 2002 A potent and highly selective VPAC2 agonist enhances glucose-induced insulin release and glucose disposal: a potential therapy for type 2 diabetes. Glucose 53-60 insulin Homo sapiens 69-76 11978650-1 2002 It has been proposed that insulin-mediated changes in muscle perfusion modulate insulin-mediated glucose uptake. Glucose 97-104 insulin Homo sapiens 26-33 11978650-1 2002 It has been proposed that insulin-mediated changes in muscle perfusion modulate insulin-mediated glucose uptake. Glucose 97-104 insulin Homo sapiens 80-87 11978683-3 2002 Such inhibitors improve glucose tolerance in insulin-resistant rats and mice. Glucose 24-31 insulin Homo sapiens 45-52 11978686-2 2002 The objective of the present study was to examine whether the relationship between plasma and interstitial fluid glucose is altered by changes in plasma glucose and insulin levels and how such alterations might influence CGMS performance. Glucose 113-120 insulin Homo sapiens 165-172 11978686-5 2002 min(-1) stepped euglycemic-hypoglycemic-hyperglycemic (plasma glucose approximately 5, 3.1, and 8.6 mmol/l, respectively) insulin clamp that raised plasma insulin to approximately 360-390 pmol/l. Glucose 62-69 insulin Homo sapiens 155-162 11978686-10 2002 CONCLUSIONS: Although hyperinsulinemia may contribute to modest discrepancies between plasma and sensor glucose levels, the CGMS is able to accurately track acute changes in plasma glucose when calibrated across a range of plasma glucose and insulin levels. Glucose 104-111 insulin Homo sapiens 27-34 12047398-2 2002 We examined the effect of acute misoprostol (PGE1) administration on whole body insulin-mediated glucose disposal, as well as the major intracellular pathways of glucose metabolism in type 2 diabetic (n = 10) and non-diabetic (n = 4) subjects. Glucose 97-104 insulin Homo sapiens 80-87 12047398-5 2002 Insulin-mediated total body glucose disposal, glycolysis, glycogenesis and glucose oxidation were similar during the insulin clamp studies performed without and with misoprostol in both the diabetic and non-diabetic groups. Glucose 28-35 insulin Homo sapiens 0-7 12107742-8 2002 Raised non-esterified fatty acids impair insulin"s effect on glucose uptake in skeletal muscle and the vascular endothelium and thus could have detrimental effects on the vasculature, leading to premature cardiovascular disease. Glucose 61-68 insulin Homo sapiens 41-48 12107743-10 2002 CONCLUSION/INTERPRETATION: A minor increase in plasma glucose in non-diabetic sibling pairs of Type II (non-insulin-dependent) diabetic patients was associated with reduced insulin sensitivity, increased central adiposity and a doubling of PAI-1 antigen concentration, suggesting impaired fibrinolysis. Glucose 54-61 insulin Homo sapiens 108-115 12107743-10 2002 CONCLUSION/INTERPRETATION: A minor increase in plasma glucose in non-diabetic sibling pairs of Type II (non-insulin-dependent) diabetic patients was associated with reduced insulin sensitivity, increased central adiposity and a doubling of PAI-1 antigen concentration, suggesting impaired fibrinolysis. Glucose 54-61 insulin Homo sapiens 173-180 12107745-0 2002 Insulin sensitivity of glucose disposal and lipolysis: no influence of common genetic variants in IRS-1 and CAPN10. Glucose 23-30 insulin Homo sapiens 0-7 12107745-4 2002 RESULTS: We observed a significant correlation between insulin sensitivity of glucose disposal and insulin sensitivity of lipolysis ( r = -0.39, p < 0.001) which was retained, albeit weaker, after adjusting for BMI ( r = -0.27, p = 0.002). Glucose 78-85 insulin Homo sapiens 55-62 12107745-4 2002 RESULTS: We observed a significant correlation between insulin sensitivity of glucose disposal and insulin sensitivity of lipolysis ( r = -0.39, p < 0.001) which was retained, albeit weaker, after adjusting for BMI ( r = -0.27, p = 0.002). Glucose 78-85 insulin Homo sapiens 99-106 12107745-6 2002 CONCLUSION/INTERPRETATION: Insulin sensitivity of lipolysis has a considerable variation in healthy human beings and independently explains about 10% of the variation in insulin sensitivity of glucose disposal (or vice versa). Glucose 193-200 insulin Homo sapiens 27-34 12107745-6 2002 CONCLUSION/INTERPRETATION: Insulin sensitivity of lipolysis has a considerable variation in healthy human beings and independently explains about 10% of the variation in insulin sensitivity of glucose disposal (or vice versa). Glucose 193-200 insulin Homo sapiens 170-177 12107745-7 2002 It is possible that mediated through NEFAs, insulin resistance of glucose disposal is secondary to that of lipolysis. Glucose 66-73 insulin Homo sapiens 44-51 12207556-1 2002 OBJECTIVE: Several indices have been published to quantify insulin sensitivity from fasting plasma glucose and fasting plasma insulin levels as well as from the data obtained by the oral glucose tolerance test (oGTT). Glucose 99-106 insulin Homo sapiens 59-66 12039705-15 2002 A single pulse of insulin with glucose can prevent the drop in serum leptin normally observed during fasting. Glucose 31-38 insulin Homo sapiens 18-25 12019281-4 2002 Insulin-induced vasodilatation was assessed from peak forearm blood flow during the intravenous glucose tolerance test. Glucose 96-103 insulin Homo sapiens 0-7 11968092-1 2002 Adenylate cyclase activating polypeptide 1 (ADCYAP1) is a pancreatic neuropeptide and modulates glucose-stimulated insulin secretion. Glucose 96-103 insulin Homo sapiens 115-122 12002173-0 2002 The oral glucose minimal model: estimation of insulin sensitivity from a meal test. Glucose 9-16 insulin Homo sapiens 46-53 12019281-5 2002 Cardiac output (4.9+/-0.3 versus 5.3+/-0.4 L/min, mean+/-SEM) and insulin sensitivity (the glucose disappearance rate over insulin area under the curve: 0.91+/-0.07 versus 1.38+/-0.25 min(-1)/[pmol. Glucose 91-98 insulin Homo sapiens 66-73 12002173-1 2002 Recently, a new approach has been proposed to estimate insulin sensitivity (S(I)) from an oral glucose tolerance test or a meal using an "integral equation". Glucose 95-102 insulin Homo sapiens 55-62 12186116-8 2002 Comparing groups A and B, we found that the dose of insulin (IU/kg/day) required to achieve acceptable fasting blood glucose (FBG) did not differ significantly. Glucose 117-124 insulin Homo sapiens 52-59 12032756-6 2002 RESULTS: Pubertal insulin resistance was suggested by greater (P<0.001) fasting serum insulin concentrations in the late-pubertal than pre- and mid-pubertal groups while serum glucose concentrations were unchanged and greater (P<0.001) HOMA values in late-pubertal than pre- and mid-pubertal youth. Glucose 179-186 insulin Homo sapiens 18-25 11994326-7 2002 However, patients showed a 2.5-fold increase of insulin elimination half-life, reduced frequency of both rapid (6.1 +/- 0.4 vs. 7.1 +/- 0.2 h(-1), P < 0.001) and slow oscillations of insulin release (0.54 +/- 0.11 vs. 0.71 +/- 0.1 h(-1), P < 0.001), lack of acceleration and paradoxically more orderly slow insulin and glucose pulses after meals, and increased temporal coupling between insulin and glucose patterns (cross-ApEn: 0.58 +/- 0.13 vs. 1.37 +/- 0.23, P < 0.001). Glucose 325-332 insulin Homo sapiens 48-55 11994345-0 2002 Adipose tissue IL-6 content correlates with resistance to insulin activation of glucose uptake both in vivo and in vitro. Glucose 80-87 insulin Homo sapiens 58-65 11994326-7 2002 However, patients showed a 2.5-fold increase of insulin elimination half-life, reduced frequency of both rapid (6.1 +/- 0.4 vs. 7.1 +/- 0.2 h(-1), P < 0.001) and slow oscillations of insulin release (0.54 +/- 0.11 vs. 0.71 +/- 0.1 h(-1), P < 0.001), lack of acceleration and paradoxically more orderly slow insulin and glucose pulses after meals, and increased temporal coupling between insulin and glucose patterns (cross-ApEn: 0.58 +/- 0.13 vs. 1.37 +/- 0.23, P < 0.001). Glucose 405-412 insulin Homo sapiens 48-55 11994326-8 2002 Postprandial glucose intolerance was inferable by prolonged and amplified blood glucose excursions despite exaggerated insulin bursts of almost 3-fold higher area. Glucose 13-20 insulin Homo sapiens 119-126 11994367-0 2002 Contribution of insulin secretion and clearance to glucose-induced insulin concentration in african-american and caucasian children. Glucose 51-58 insulin Homo sapiens 16-23 11994367-0 2002 Contribution of insulin secretion and clearance to glucose-induced insulin concentration in african-american and caucasian children. Glucose 51-58 insulin Homo sapiens 67-74 11994367-1 2002 Relative to Caucasians (C), African-American (AA) children and adults have lower indices of insulin sensitivity (S(i)) and a higher acute insulin response to glucose (AIR(g)). Glucose 158-165 insulin Homo sapiens 138-145 12021247-7 2002 Aspirin treatment also resulted in a approximately 20% reduction in basal rates of hepatic glucose production and a approximately 20% improvement in insulin-stimulated peripheral glucose uptake under matched plasma insulin concentrations during the clamp. Glucose 179-186 insulin Homo sapiens 149-156 12021250-3 2002 Here we show that chronic leptin treatment improves insulin-stimulated hepatic and peripheral glucose metabolism in severely insulin-resistant lipodystrophic patients. Glucose 94-101 insulin Homo sapiens 52-59 11986393-7 2002 In the second, similar plasma concentrations of insulin and glucose were achieved by dynamic intravenous infusions of insulin and glucose. Glucose 60-67 insulin Homo sapiens 118-125 11986393-7 2002 In the second, similar plasma concentrations of insulin and glucose were achieved by dynamic intravenous infusions of insulin and glucose. Glucose 130-137 insulin Homo sapiens 48-55 11979384-1 2002 The purpose of the present work was to have a closer view on the changes in the regulation of glycogen synthase (GS) activity by insulin in relationship with the impairment of nonoxidative glucose disposal in human obesity. Glucose 189-196 insulin Homo sapiens 129-136 11979384-5 2002 Total GS activity was significantly decreased (P <.05), while its percent activation by insulin was still normal in the obese glucose-tolerant group, and nonoxidative glucose disposal was decreased by 56% (P <.001) and glucose oxidation still normal. Glucose 129-136 insulin Homo sapiens 91-98 11979402-2 2002 Changes in insulin and glucagon are important for controlling blood glucose levels under conditions in which metabolic rate is elevated, such as during and following exercise. Glucose 68-75 insulin Homo sapiens 11-18 11979384-7 2002 In conclusion, our data show that insulin-stimulated nonoxidative glucose disposal and total glycogen synthase are very early defects observed in obese patients. Glucose 66-73 insulin Homo sapiens 34-41 12038076-2 2002 METHODS AND RESULTS: During prednison treatment, we found typical signs of insulin resistance manifestation: HOMAIR 3.55 (5.13), blood insulin/glucose ratio 3.8 (5.84), QUICKI 0.61 (0.124). Glucose 143-150 insulin Homo sapiens 75-82 20046314-2 2002 The complex endocrine and metabolic changes of obesity and insulin resistance in adolescents result in hyperinsulinemia, dyslipidemia, hypertension, steatohepatitis, glucose intolerance, type 2 diabetes, acanthosis nigricans and ovarian hyperandrogenemia, commonly known as polycystic ovarian syndrome (PCOS). Glucose 166-173 insulin Homo sapiens 59-66 12108171-1 2002 OBJECTIVE: To assess insulin sensitivity and beta cell secretion in indigenous Ghanaian subjects with a spectrum of glucose intolerance. Glucose 116-123 insulin Homo sapiens 21-28 12108171-10 2002 However, mean serum insulin and C-peptide responses after oral glucose load were significantly greater in group 2 than in the group 1 healthy controls. Glucose 63-70 insulin Homo sapiens 20-27 12108171-18 2002 Mean glucose effectiveness at basal insulin level (Sg) was not significantly different among the relatives in group 2 (2.38 +/- 0.50), the healthy controls in group 1 (2.66 +/- 0.38) and the diabetic patients in group 3 (2.27 +/- 0.49 x 10(-2)/min). Glucose 5-12 insulin Homo sapiens 36-43 11943396-7 2002 The rate of insulin permeation through the membrane was modulated by glucose concentration due to shrinking or swelling of the embedded pH-sensitive nanoparticles. Glucose 69-76 insulin Homo sapiens 12-19 11943396-8 2002 The response of insulin permeability to the change in the glucose concentration could be detected within 5-15 min. Glucose 58-65 insulin Homo sapiens 16-23 11943396-0 2002 Modulated insulin permeation across a glucose-sensitive polymeric composite membrane. Glucose 38-45 insulin Homo sapiens 10-17 11943396-9 2002 The permeability of insulin increased more than 3-fold as the glucose concentration was raised from 50 to 200 mg/dl. Glucose 62-69 insulin Homo sapiens 20-27 11943396-10 2002 The average insulin permeability at 400 mg/dl of glucose was 8-fold that at 50 mg/dl in a continuous test in saline and was 6-fold in a three-cycle discontinuous test in pH 7.4 buffer. Glucose 49-56 insulin Homo sapiens 12-19 12041635-4 2002 There is level II evidence that in patients with inadequate glycaemic control both drugs reduce the level of HbA1c and fasting plasma glucose (FPG) when used as monotherapy and in combination with sulfonylurea or metformin or insulin; and both drugs increase levels of HDL and LDL and lower free fatty acid levels, but only pioglitazone significantly lowers triglyceride levels. Glucose 134-141 insulin Homo sapiens 226-233 12062111-1 2002 Insulin stimulates glucose transport by translocation of the membrane glucose transporter GLUT4 from intracellular vesicles to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 11799123-4 2002 Adenovirus-mediated c-Myc overexpression suppressed both insulin gene transcription and glucose-stimulated insulin secretion. Glucose 88-95 insulin Homo sapiens 107-114 12007541-2 2002 Its major physiological effect lies in a strongly glucose-dependent stimulation of insulin secretion from pancreatic B-cells. Glucose 50-57 insulin Homo sapiens 83-90 11969032-6 2002 In future studies the challenge will be to demonstrate the specific effects of improved postprandial blood-glucose control, and to separate these out from the general effects of intensive therapy with oral medication and insulin on glucose control. Glucose 232-239 insulin Homo sapiens 221-228 11989054-2 2002 Clinical insulin resistance is usually defined by reduced insulin-mediated uptake of glucose in skeletal muscle. Glucose 85-92 insulin Homo sapiens 9-16 11944604-10 2002 Insulin glargine should be considered for patients who continue to have elevated morning blood glucose levels and problems with nocturnal hypoglycemia despite receiving NPH insulin at bedtime. Glucose 95-102 insulin Homo sapiens 0-7 11989054-2 2002 Clinical insulin resistance is usually defined by reduced insulin-mediated uptake of glucose in skeletal muscle. Glucose 85-92 insulin Homo sapiens 58-65 11989054-10 2002 The mechanism by which FFA and triglyceride, together with the peptides mentioned, may induce insulin resistance at a cellular level, resulting in reduced glucose transport and intracellular glucose processing, is still being discussed. Glucose 155-162 insulin Homo sapiens 94-101 11989054-10 2002 The mechanism by which FFA and triglyceride, together with the peptides mentioned, may induce insulin resistance at a cellular level, resulting in reduced glucose transport and intracellular glucose processing, is still being discussed. Glucose 191-198 insulin Homo sapiens 94-101 11916760-2 2002 Continuous subcutaneous insulin infusion (CSII) provides a suitable amount of insulin to overcome insulin deficiency and achieve near-normal blood glucose concentrations. Glucose 147-154 insulin Homo sapiens 24-31 11944604-13 2002 Insulin glargine is a new long-acting formulation that can provide prolonged basal glucose control in patients with diabetes mellitus. Glucose 83-90 insulin Homo sapiens 0-7 12021084-3 2002 In vitro-generated islets exhibit temporal changes in mRNA transcripts for islet-associated markers as well as regulated insulin responses following glucose challenge. Glucose 149-156 insulin Homo sapiens 121-128 11991212-6 2002 Plasma glucose and insulin levels 2 h after a 75-g oral glucose load, reflected insulin resistance. Glucose 7-14 insulin Homo sapiens 80-87 11991212-6 2002 Plasma glucose and insulin levels 2 h after a 75-g oral glucose load, reflected insulin resistance. Glucose 56-63 insulin Homo sapiens 19-26 11991212-6 2002 Plasma glucose and insulin levels 2 h after a 75-g oral glucose load, reflected insulin resistance. Glucose 56-63 insulin Homo sapiens 80-87 11991212-9 2002 Eighty percent of EH patients showed significantly higher plasma insulin levels after glucose load. Glucose 86-93 insulin Homo sapiens 65-72 11991213-4 2002 Insulin sensitivity was measured by the fasting plasma insulin/glucose ratio and the homeostatic assessment model algorithm (HOMA) index. Glucose 63-70 insulin Homo sapiens 0-7 12037503-4 2002 Glucose clamp studies have clearly shown a 30% improvement of insulin-induced glucose utilisation in skeletal muscle. Glucose 0-7 insulin Homo sapiens 62-69 12037503-4 2002 Glucose clamp studies have clearly shown a 30% improvement of insulin-induced glucose utilisation in skeletal muscle. Glucose 78-85 insulin Homo sapiens 62-69 11916461-4 2002 Factors contributing to insulin resistance at these sites include perturbations in free fatty acids, glucose, and hormone-signalling, some of which may be linked to various genetic polymorphisms. Glucose 101-108 insulin Homo sapiens 24-31 12037503-8 2002 In human, skeletal muscles are responsible for more than 80% of glucose uptake in response to insulin and skeletal muscles contain only a limited amount of PPARgamma! Glucose 64-71 insulin Homo sapiens 94-101 12023871-2 2002 However, an increasing body of evidence shows that insulin gene transcription is affected by signals, such as incretins, glucose metabolites, intracellular Ca2+, and by insulin secreted from pancreatic beta-cells, all supporting the concept of an immediate response resulting in insulin gene transcription following food-uptake. Glucose 121-128 insulin Homo sapiens 51-58 12023871-3 2002 The present review aims to summarize the current view on the mechanisms underlying the up-regulation of insulin gene transcription in response to glucose, the major nutrient factor in insulin secretion and biosynthesis. Glucose 146-153 insulin Homo sapiens 104-111 12023874-1 2002 Glucose stimulates the release of insulin in part by activating the recruitment of secretory vesicles to the cell surface. Glucose 0-7 insulin Homo sapiens 34-41 12124639-1 2002 Long-term treatment with glucocorticoids led to the development of insulin resistance in experimental animals, which was confirmed by a progressive increase in blood insulin level and decrease in the glucose/insulin index. Glucose 200-207 insulin Homo sapiens 67-74 12179956-0 2002 Exercise- and insulin-stimulated muscle glucose transport: distinct mechanisms of regulation. Glucose 40-47 insulin Homo sapiens 14-21 12184210-0 2002 The putative roles of adenosine in insulin- and exercise-mediated regulation of glucose transport and glycogen metabolism in skeletal muscle. Glucose 80-87 insulin Homo sapiens 35-42 11914108-1 2002 The aim of this present investigation was to study the relationship between the reduction in insulin sensitivity accompanying 5 days of treatment with growth hormone (GH; 0.05 mg.24 h(-1).kg(-1)) and intracellular substrate oxidation rates in six healthy subjects, while maintaining glucose flux by a constant glucose infusion and adjusting insulin infusion rates to achieve normoglycaemia (feedback clamp). Glucose 283-290 insulin Homo sapiens 93-100 12184210-3 2002 While it is known that both insulin and contraction stimulate muscle glucose uptake and glycogen metabolism, the post-receptor mechanisms are not completely understood. Glucose 69-76 insulin Homo sapiens 28-35 11914108-1 2002 The aim of this present investigation was to study the relationship between the reduction in insulin sensitivity accompanying 5 days of treatment with growth hormone (GH; 0.05 mg.24 h(-1).kg(-1)) and intracellular substrate oxidation rates in six healthy subjects, while maintaining glucose flux by a constant glucose infusion and adjusting insulin infusion rates to achieve normoglycaemia (feedback clamp). Glucose 310-317 insulin Homo sapiens 93-100 11914108-5 2002 The ratio between glucose infusion rate and serum insulin levels decreased by 34% at the two levels of glucose infusion tested (P<0.05). Glucose 103-110 insulin Homo sapiens 50-57 12184210-5 2002 While adenosine has clearly been shown to potentiate insulin-stimulated glucose transport in adipocytes and heart muscle, its role in carbohydrate metabolism in skeletal muscle is less clear, with numerous diverging findings published to date. Glucose 72-79 insulin Homo sapiens 53-60 11914108-10 2002 In conclusion, when glucose flux was normalized by compensatory hyperinsulinaemia under conditions of GH-induced insulin resistance, intracellular rates of oxidation of glucose and fat remained unchanged. Glucose 20-27 insulin Homo sapiens 69-76 12017398-9 2002 The mean daily prandial glucose excursion was significantly lower for BIAsp 30 (16.2 mmol x h x L(-1)) than BHI 30 (17.9 mmol x h x L(-1)). Glucose 24-31 insulin Homo sapiens 108-114 12017398-10 2002 Postprandial 4-hour glucose excursions were significantly lower with BIAsp 30 than with BHI 30 after dinner and breakfast, but were significantly greater after lunch. Glucose 20-27 insulin Homo sapiens 88-94 12017407-1 2002 BACKGROUND: Although insulin lispro (insulin LP) has been shown to improve postprandial blood glucose (BG) control and reduce hypoglycemic episodes in adult patients with type I diabetes, there appear to have been few clinical studies focusing on its use in adolescents. Glucose 94-101 insulin Homo sapiens 21-28 12017407-1 2002 BACKGROUND: Although insulin lispro (insulin LP) has been shown to improve postprandial blood glucose (BG) control and reduce hypoglycemic episodes in adult patients with type I diabetes, there appear to have been few clinical studies focusing on its use in adolescents. Glucose 94-101 insulin Homo sapiens 37-44 11916916-5 2002 Insulin release at 3 mmol/l glucose was 10.5 +/- 4.5 pmol.g(-1).s(-1) and pulsatile (0.26 +/- 0.05 min(-1)). Glucose 28-35 insulin Homo sapiens 0-7 12477297-12 2002 Physiologically, both amylin and glucagon-like peptide (GLP)-1, along with insulin, are involved in a coordinated and concerted interplay between hormones acting both centrally and peripherally to provide meticulous control over the rate of appearance of exogenous and endogenous glucose and to match that rate to the rate of glucose disappearance. Glucose 280-287 insulin Homo sapiens 75-82 12477297-12 2002 Physiologically, both amylin and glucagon-like peptide (GLP)-1, along with insulin, are involved in a coordinated and concerted interplay between hormones acting both centrally and peripherally to provide meticulous control over the rate of appearance of exogenous and endogenous glucose and to match that rate to the rate of glucose disappearance. Glucose 326-333 insulin Homo sapiens 75-82 11916908-6 2002 Moreover, increasing insulin concentrations could compensate for the reduced GS activity to a certain extent, whereas chronic supraphysiological insulin concentrations induced insulin resistance in GS and glucose transport activity. Glucose 205-212 insulin Homo sapiens 145-152 11916908-6 2002 Moreover, increasing insulin concentrations could compensate for the reduced GS activity to a certain extent, whereas chronic supraphysiological insulin concentrations induced insulin resistance in GS and glucose transport activity. Glucose 205-212 insulin Homo sapiens 145-152 11916908-7 2002 Our data suggest that insulin resistance in patients with type 2 diabetes comprises at least two important defects under physiological insulin concentrations: a reduced glucose transport under basal conditions and a reduced GS activity under acute insulin stimulation, implicating a reduced glucose uptake in the fasting state and a diminished insulin-mediated storage of glucose as glycogen after a meal. Glucose 169-176 insulin Homo sapiens 22-29 11916908-7 2002 Our data suggest that insulin resistance in patients with type 2 diabetes comprises at least two important defects under physiological insulin concentrations: a reduced glucose transport under basal conditions and a reduced GS activity under acute insulin stimulation, implicating a reduced glucose uptake in the fasting state and a diminished insulin-mediated storage of glucose as glycogen after a meal. Glucose 291-298 insulin Homo sapiens 22-29 11916908-7 2002 Our data suggest that insulin resistance in patients with type 2 diabetes comprises at least two important defects under physiological insulin concentrations: a reduced glucose transport under basal conditions and a reduced GS activity under acute insulin stimulation, implicating a reduced glucose uptake in the fasting state and a diminished insulin-mediated storage of glucose as glycogen after a meal. Glucose 291-298 insulin Homo sapiens 22-29 11916916-6 2002 In islets from one subject, 11 mmol/l glucose transiently increased insulin release by augmentation of the insulin pulses without affecting the frequency. Glucose 38-45 insulin Homo sapiens 68-75 11916916-6 2002 In islets from one subject, 11 mmol/l glucose transiently increased insulin release by augmentation of the insulin pulses without affecting the frequency. Glucose 38-45 insulin Homo sapiens 107-114 11916916-10 2002 Insulin release from four normal subjects at 3 mmol/l glucose was 4.3 +/- 0.8 pmol.g(-1).s(-1) and pulsatile (0.23 +/- 0.03 min(-1)). Glucose 54-61 insulin Homo sapiens 0-7 11916916-11 2002 At 11 mmol/l glucose, insulin release increased in islets from all subjects. Glucose 13-20 insulin Homo sapiens 22-29 11916925-5 2002 Myotubes in culture from patients with IGT had insulin-induced glucose uptake that was roughly 30-50% less than that from control subjects. Glucose 63-70 insulin Homo sapiens 47-54 11916912-6 2002 Specifically, the first-phase insulin response was lower in diabetic subjects (329.1 +/- 39.6 vs. 91.3 +/- 34.1 pmol/l; P < 0.001), as was the slope of glucose potentiation of the insulin response to arginine (102 +/- 18.7 vs. 30.2 +/- 6.1 pmol/l per mmol/l; P = 0.005) and the maximum insulin response to arginine (2,524 +/- 413 vs. 629 +/- 159 pmol/l; P = 0.001). Glucose 155-162 insulin Homo sapiens 30-37 11916927-3 2002 We have analyzed GRalpha and 11beta-HSD1 expression in skeletal myoblasts from men (n = 14) with contrasting levels of insulin sensitivity (euglycemic clamp measurements of insulin-dependent glucose disposal rate), blood pressure, and adiposity. Glucose 191-198 insulin Homo sapiens 173-180 11916935-10 2002 In addition, hyperemic myocardial blood flow responses during insulin stimulation were positively correlated with whole-body glucose uptake. Glucose 125-132 insulin Homo sapiens 62-69 11916949-8 2002 Analysis of patients with varying degrees of renal function impairment demonstrated increased plasma glucose and insulin response to oral glucose load, decreased fasting glucose-to-insulin ratio, and reduced sensitivity to insulin only in those patients with creatinine clearance < 50 ml.min(-1).1.73 m(-2). Glucose 138-145 insulin Homo sapiens 113-120 11916949-8 2002 Analysis of patients with varying degrees of renal function impairment demonstrated increased plasma glucose and insulin response to oral glucose load, decreased fasting glucose-to-insulin ratio, and reduced sensitivity to insulin only in those patients with creatinine clearance < 50 ml.min(-1).1.73 m(-2). Glucose 138-145 insulin Homo sapiens 113-120 11916951-4 2002 His BMI was 34 kg/m(2), and his fasting blood glucose ranged from 2.1 to 2.7 mmol/l, associated with inappropriately high serum levels of insulin, C-peptide, and proinsulin. Glucose 46-53 insulin Homo sapiens 138-145 11919134-7 2002 CONCLUSIONS: High plasma glucose excursions over morning periods seem to be a permanent failure in non-insulin-using patients with type 2 diabetes, whatever the clinical (BMI), biological (HbA(1c)), therapeutic, and pathophysiological (residual beta-cell function) status. Glucose 25-32 insulin Homo sapiens 103-110 11916951-4 2002 His BMI was 34 kg/m(2), and his fasting blood glucose ranged from 2.1 to 2.7 mmol/l, associated with inappropriately high serum levels of insulin, C-peptide, and proinsulin. Glucose 46-53 insulin Homo sapiens 162-172 11916951-8 2002 Increases in serum insulin, C-peptide, and proinsulin in response to an OGTT suggested a lower threshold for glucose-stimulated insulin release (GSIR). Glucose 109-116 insulin Homo sapiens 19-26 11943004-6 2002 When the dual or square-wave methods of insulin administration were used, subjects had significantly lower glucose levels after 4 h in comparison with when the single or double boluses were used (P = 0.04). Glucose 107-114 insulin Homo sapiens 40-47 11916951-8 2002 Increases in serum insulin, C-peptide, and proinsulin in response to an OGTT suggested a lower threshold for glucose-stimulated insulin release (GSIR). Glucose 109-116 insulin Homo sapiens 43-53 11943743-9 2002 Recent evidence suggests that some of the biochemical mechanisms whereby glucose and fat exert adverse effects in insulin-sensitive and insulin-producing tissues are shared, thus implicating a diabetogenic role for energy excess as a whole. Glucose 73-80 insulin Homo sapiens 114-121 11916951-8 2002 Increases in serum insulin, C-peptide, and proinsulin in response to an OGTT suggested a lower threshold for glucose-stimulated insulin release (GSIR). Glucose 109-116 insulin Homo sapiens 46-53 11943743-9 2002 Recent evidence suggests that some of the biochemical mechanisms whereby glucose and fat exert adverse effects in insulin-sensitive and insulin-producing tissues are shared, thus implicating a diabetogenic role for energy excess as a whole. Glucose 73-80 insulin Homo sapiens 136-143 11916955-3 2002 Insulin secretion was examined during an oral and intravenous glucose tolerance test. Glucose 62-69 insulin Homo sapiens 0-7 11916955-7 2002 Nevertheless, basal and insulin-stimulated rates of whole-body peripheral glucose disposal, glucose oxidation, lipid oxidation, exogenous glucose storage, and nonoxidative glucose metabolism were similar in the two groups. Glucose 74-81 insulin Homo sapiens 24-31 11976560-0 2002 Molecular mechanisms of insulin-stimulated glucose uptake in adipocytes. Glucose 43-50 insulin Homo sapiens 24-31 11976560-1 2002 The stimulation of muscle and adipose tissue glucose metabolism, which is ultimately responsible for bringing about post-absorptive blood glucose clearance, is the primary clinically relevant action of insulin. Glucose 45-52 insulin Homo sapiens 202-209 11916955-7 2002 Nevertheless, basal and insulin-stimulated rates of whole-body peripheral glucose disposal, glucose oxidation, lipid oxidation, exogenous glucose storage, and nonoxidative glucose metabolism were similar in the two groups. Glucose 92-99 insulin Homo sapiens 24-31 11916955-7 2002 Nevertheless, basal and insulin-stimulated rates of whole-body peripheral glucose disposal, glucose oxidation, lipid oxidation, exogenous glucose storage, and nonoxidative glucose metabolism were similar in the two groups. Glucose 92-99 insulin Homo sapiens 24-31 11919130-1 2002 OBJECTIVE: This study was performed to evaluate whether an additional dose of NPH insulin at lunchtime might overcome the deleterious effects of waning basal insulinemia on pre-dinner and evening glucose values during insulin lispro intensive therapy with once daily basal insulin at night. Glucose 196-203 insulin Homo sapiens 82-89 12032625-3 2002 This study aimed to examine the effects of insulin on glucose transport and changes in insulin receptor tyrosine phosphorylation, IRS-1 and PC-1. Glucose 54-61 insulin Homo sapiens 43-50 11976560-2 2002 Insulin acts on many steps of glucose metabolism, but one of the most important effects is its ability to increase the rate of cellular glucose transport. Glucose 30-37 insulin Homo sapiens 0-7 11976563-8 2002 Fasting plasma glucose modified the relation between alcohol and insulin in men: while the negative relation alcohol-insulin was strong for fasting plasma glucose<6.0 mmol/l (p<0.0001), there was no association above 6.0 mmol/l (p=0.4). Glucose 15-22 insulin Homo sapiens 65-72 12032625-5 2002 RESULTS: Insulin stimulated glucose transport was reduced by 50% in women with gestational diabetes mellitus and 70% in pregnant women with Type II diabetes, compared to the non-pregnant control subjects. Glucose 28-35 insulin Homo sapiens 9-16 12032627-8 2002 RESULTS: During the course of glucose loading, the mice which had 3T3-L1 cells implanted into mesenteric area but not into subcutaneous fat area showed remarkably increased serum insulin and TMF-alpha concentrations, compared to the control mice. Glucose 30-37 insulin Homo sapiens 179-186 12059098-1 2002 Lispro insulin has been demonstrated to be effective in reducing post-prandial blood glucose levels. Glucose 85-92 insulin Homo sapiens 7-14 11910345-5 2002 However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). Glucose 87-94 insulin Homo sapiens 113-120 12081229-0 2002 Regulation of the insulin gene transcription by glucose. Glucose 48-55 insulin Homo sapiens 18-25 11937112-7 2002 Insulin resistance was estimated from fasting glucose and insulin levels by using the homeostatic model assessment. Glucose 46-53 insulin Homo sapiens 0-7 11991543-2 2002 Recent discoveries in the molecular and cellular regulation of insulin-mediated glucose metabolism in skeletal muscle have provided a deeper understanding of how exercise modulates insulin action. Glucose 80-87 insulin Homo sapiens 63-70 11991543-2 2002 Recent discoveries in the molecular and cellular regulation of insulin-mediated glucose metabolism in skeletal muscle have provided a deeper understanding of how exercise modulates insulin action. Glucose 80-87 insulin Homo sapiens 181-188 11959387-6 2002 Insulin sensitivity was assessed by intravenous glucose tolerance testing using the minimal model approach; catecholamines, TNFalpha and soluble TNF receptors 1 and 2 were also measured. Glucose 48-55 insulin Homo sapiens 0-7 11993791-0 2002 Chylomicronemia caused by lipoprotein lipase gene mutation related to a hyper-response of insulin secretion to glucose. Glucose 111-118 insulin Homo sapiens 90-97 11932281-9 2002 Insulin-stimulated glucose disposal increased (21.5 +/- 2.2 vs. 25.0 +/- 2.2 micromol/kg.min; P = 0.041). Glucose 19-26 insulin Homo sapiens 0-7 11932285-5 2002 After ingestion of glucose, insulin concentrations increased from 76.8 +/- 21.5 pM to a maximum of 520.2 +/- 118.4 pM (P < 0.01) in FCHL and from 38.0 +/- 5.0 to 221.7 +/- 25.1 pM (P < 0.01) in controls. Glucose 19-26 insulin Homo sapiens 28-35 11932299-12 2002 However, nondiabetic African-Americans with the 112/121-haplotype combination had significantly higher insulin levels, in response to an oral glucose challenge, as reflected in the area under the insulin curve (257,021 +/- 95,384 vs. 136,240 +/- 11,468 pmol/min; P = 0.03), compared with those with other haplotypes. Glucose 142-149 insulin Homo sapiens 103-110 11932299-12 2002 However, nondiabetic African-Americans with the 112/121-haplotype combination had significantly higher insulin levels, in response to an oral glucose challenge, as reflected in the area under the insulin curve (257,021 +/- 95,384 vs. 136,240 +/- 11,468 pmol/min; P = 0.03), compared with those with other haplotypes. Glucose 142-149 insulin Homo sapiens 196-203 11978262-8 2002 In the oat cereal group, a trend was observed for a lower total insulin response to a glucose load, suggesting improved insulin sensitivity. Glucose 86-93 insulin Homo sapiens 64-71 11978262-8 2002 In the oat cereal group, a trend was observed for a lower total insulin response to a glucose load, suggesting improved insulin sensitivity. Glucose 86-93 insulin Homo sapiens 120-127 12009347-13 2002 Fasting glucose-to-insulin ratio improved in women with insulin resistance. Glucose 8-15 insulin Homo sapiens 19-26 12009347-13 2002 Fasting glucose-to-insulin ratio improved in women with insulin resistance. Glucose 8-15 insulin Homo sapiens 56-63 12075574-10 2002 No association was found between any measures of adiposity and glucose concentrations, although insulin concentration in relation to glucose concentration (glucose-insulin ratio) was significantly negatively correlated with all measures of adiposity. Glucose 133-140 insulin Homo sapiens 96-103 12075578-2 2002 However, increasing evidence suggests that insulin-mediated glucose uptake rather than insulin per se regulates circulating leptin concentration. Glucose 60-67 insulin Homo sapiens 43-50 12075578-3 2002 Here, we hypothesised that a reduction of insulin sensitivity, ie insulin resistance, will diminish the stimulatory effect of insulin on leptin secretion as a consequence of decreased insulin-mediated glucose uptake. Glucose 201-208 insulin Homo sapiens 42-49 12075578-3 2002 Here, we hypothesised that a reduction of insulin sensitivity, ie insulin resistance, will diminish the stimulatory effect of insulin on leptin secretion as a consequence of decreased insulin-mediated glucose uptake. Glucose 201-208 insulin Homo sapiens 66-73 12075578-3 2002 Here, we hypothesised that a reduction of insulin sensitivity, ie insulin resistance, will diminish the stimulatory effect of insulin on leptin secretion as a consequence of decreased insulin-mediated glucose uptake. Glucose 201-208 insulin Homo sapiens 66-73 12075578-3 2002 Here, we hypothesised that a reduction of insulin sensitivity, ie insulin resistance, will diminish the stimulatory effect of insulin on leptin secretion as a consequence of decreased insulin-mediated glucose uptake. Glucose 201-208 insulin Homo sapiens 66-73 11927386-6 2002 Fatty acids (0.5 mM) acutely stimulated insulin release from rat islets of Langerhans in static incubations in a glucose-dependent manner. Glucose 113-120 insulin Homo sapiens 40-47 11943832-6 2002 An indirect index of insulin resistance was calculated using the log-transformed fasting insulin and glucose product. Glucose 101-108 insulin Homo sapiens 21-28 12017222-4 2002 Adults with T2DM have a diminished first phase response to intravenous glucose and a delayed early insulin response to oral glucose. Glucose 124-131 insulin Homo sapiens 99-106 11994746-1 2002 In muscle and fat cells, insulin stimulates the delivery of the glucose transporter GLUT4 from an intracellular location to the cell surface, where it facilitates the reduction of plasma glucose levels. Glucose 64-71 insulin Homo sapiens 25-32 11906162-1 2002 In 3T3-L1 adipocytes, we previously reported that glucosamine impairs insulin stimulation of glucose transport, which is accompanied by impaired insulin stimulation of serine/threonine kinase Akt. Glucose 93-100 insulin Homo sapiens 70-77 11964551-0 2002 Indinavir acutely inhibits insulin-stimulated glucose disposal in humans: a randomized, placebo-controlled study. Glucose 46-53 insulin Homo sapiens 27-34 11964551-4 2002 We hypothesized that a single dose of the PI indinavir resulting in therapeutic plasma concentrations would acutely decrease insulin-stimulated glucose disposal in healthy human volunteers. Glucose 144-151 insulin Homo sapiens 125-132 11964551-5 2002 METHODS: Randomized, double-blind, cross-over study comparing the effect of 1200 mg of orally administered indinavir and placebo on insulin-stimulated glucose disposal during a 180-min euglycemic, hyperinsulinemic clamp. Glucose 151-158 insulin Homo sapiens 132-139 11964551-10 2002 Insulin-stimulated glucose disposal per unit of insulin (M/I) decreased in all subjects from 14.1 +/- 1.2 to 9.2 +/- 0.8 mg/kg.min per microUI/ml (95% confidence interval for change, 3.7-6.1; P < 0.001) on indinavir (average decrease, 34.1 +/- 9.2%). Glucose 19-26 insulin Homo sapiens 0-7 11964551-10 2002 Insulin-stimulated glucose disposal per unit of insulin (M/I) decreased in all subjects from 14.1 +/- 1.2 to 9.2 +/- 0.8 mg/kg.min per microUI/ml (95% confidence interval for change, 3.7-6.1; P < 0.001) on indinavir (average decrease, 34.1 +/- 9.2%). Glucose 19-26 insulin Homo sapiens 48-55 11964551-13 2002 CONCLUSIONS: A single dose of indinavir acutely decreases total and non-oxidative insulin-stimulated glucose disposal during a euglycemic, hyperinsulinemic clamp. Glucose 101-108 insulin Homo sapiens 82-89 11909787-6 2002 RESULTS: Mean blood glucose concentration was lower in people receiving continuous subcutaneous insulin infusion compared with those receiving insulin injections (standardised mean difference 0.56, 95% confidence interval 0.35 to 0.77), equivalent to a difference of 1.0 mmol/l. Glucose 20-27 insulin Homo sapiens 96-103 11895820-8 2002 Mean insulin concentrations were higher in South Asian children (percentage difference was 53%, 14% to 106%, after fasting and 54%, 19% to 99%, after glucose load), though glucose concentrations were similar. Glucose 150-157 insulin Homo sapiens 5-12 11893791-7 2002 Insulin and C-peptide levels were markedly elevated after the glucose-tolerance test in subjects with impaired glucose tolerance but not in adolescents with diabetes, who had a reduced ratio of the 30-minute change in the insulin level to the 30-minute change in the glucose level. Glucose 62-69 insulin Homo sapiens 0-7 11893791-7 2002 Insulin and C-peptide levels were markedly elevated after the glucose-tolerance test in subjects with impaired glucose tolerance but not in adolescents with diabetes, who had a reduced ratio of the 30-minute change in the insulin level to the 30-minute change in the glucose level. Glucose 62-69 insulin Homo sapiens 222-229 11893791-7 2002 Insulin and C-peptide levels were markedly elevated after the glucose-tolerance test in subjects with impaired glucose tolerance but not in adolescents with diabetes, who had a reduced ratio of the 30-minute change in the insulin level to the 30-minute change in the glucose level. Glucose 111-118 insulin Homo sapiens 0-7 11832350-1 2002 UNLABELLED: 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high glucose or glucosamine, provided insulin (0.6 nM) is present during preincubation. Glucose 56-63 insulin Homo sapiens 38-45 11832350-1 2002 UNLABELLED: 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high glucose or glucosamine, provided insulin (0.6 nM) is present during preincubation. Glucose 56-63 insulin Homo sapiens 136-143 11832350-1 2002 UNLABELLED: 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high glucose or glucosamine, provided insulin (0.6 nM) is present during preincubation. Glucose 103-110 insulin Homo sapiens 38-45 11832350-1 2002 UNLABELLED: 3T3-L1 adipocytes develop insulin-resistant glucose transport upon preincubation with high glucose or glucosamine, provided insulin (0.6 nM) is present during preincubation. Glucose 103-110 insulin Homo sapiens 136-143 11832350-5 2002 Upon acute 100 nM insulin stimulation, plasma membrane (PM)-associated phospho-Akt was highest in cells preincubated in low glucose with no insulin, less in high glucose with no insulin, even less in low glucose+insulin, and lowest in high glucose+insulin. Glucose 124-131 insulin Homo sapiens 18-25 11832350-5 2002 Upon acute 100 nM insulin stimulation, plasma membrane (PM)-associated phospho-Akt was highest in cells preincubated in low glucose with no insulin, less in high glucose with no insulin, even less in low glucose+insulin, and lowest in high glucose+insulin. Glucose 162-169 insulin Homo sapiens 18-25 11832350-5 2002 Upon acute 100 nM insulin stimulation, plasma membrane (PM)-associated phospho-Akt was highest in cells preincubated in low glucose with no insulin, less in high glucose with no insulin, even less in low glucose+insulin, and lowest in high glucose+insulin. Glucose 162-169 insulin Homo sapiens 18-25 11832350-6 2002 Only high glucose+insulin caused insulin-resistant glucose transport. Glucose 10-17 insulin Homo sapiens 33-40 11832350-6 2002 Only high glucose+insulin caused insulin-resistant glucose transport. Glucose 51-58 insulin Homo sapiens 18-25 11832350-6 2002 Only high glucose+insulin caused insulin-resistant glucose transport. Glucose 51-58 insulin Homo sapiens 33-40 11832350-7 2002 Acute insulin stimulation increased total PM-Akt about twofold after preincubation without insulin in low or high glucose. Glucose 114-121 insulin Homo sapiens 6-13 11832350-8 2002 Preincubation with 0.6 nM insulin decreased Akt PM translocation by approximately 25% in low and approximately 50% in high glucose. Glucose 123-130 insulin Homo sapiens 26-33 11832350-10 2002 CONCLUSIONS: chronic exposure to high glucose or insulin downregulates acute insulin-stimulated Akt activation, acting synergistically distal to PI 3-kinase. Glucose 38-45 insulin Homo sapiens 77-84 11832350-11 2002 Maximal insulin activates more Akt than required for maximal glucose transport stimulation. Glucose 61-68 insulin Homo sapiens 8-15 11832350-13 2002 High glucose and glucosamine cause insulin resistance by different mechanisms in 3T3-L1 adipocytes. Glucose 5-12 insulin Homo sapiens 35-42 11832379-4 2002 GLUT-12 was identified in MCF-7 breast cancer cells by homology to the insulin-regulatable glucose transporter GLUT-4. Glucose 91-98 insulin Homo sapiens 71-78 11904616-8 2002 Insulin sensitivity was markedly decreased in the transgenic mice, as demonstrated by an insignificant decline in glucose levels after insulin injection compared with the control mice, which demonstrated more than a 65% reduction in glucose levels (P <.001). Glucose 233-240 insulin Homo sapiens 0-7 11906162-4 2002 After one hour, insulin stimulated-glucose transport was significantly increased and continued to increase up to 6-24 h. Insulin stimulation of Akt, however, did not increase after 1-3 h and began to slightly increase after 6 h. Next, we investigated effects of osmotic shock and vanadate on glucose transport in glucosamine-treated cells and found that glucosamine completely inhibited their actions in these cells. Glucose 35-42 insulin Homo sapiens 16-23 11911852-1 2002 The insulinotropic agent, exendin-4, is a long-acting analogue of glucagon-like peptide-1 (GLP-1) which improves glucose tolerance in humans and animals with diabetes, but the underlying mechanisms and the effects of exendin-4 on peripheral (muscle/fat) insulin action are unclear. Glucose 113-120 insulin Homo sapiens 4-11 11953558-1 2002 OBJECTIVE: The objective of the study was to determine the effects of short-term exercise on glucose tolerance and insulin response to a glucose load in centrally obese individuals. Glucose 137-144 insulin Homo sapiens 115-122 11872966-6 2002 When risk factor clustering is associated with glucose intolerance, obesity, and dyslipidemia, it may be attributed to insulin resistance promoted by abdominal obesity. Glucose 47-54 insulin Homo sapiens 119-126 11869176-5 2002 Insulin-mediated glucose uptake (euglycaemic hyperinsulinaemic clamp) was measured in a subgroup of these subjects (n=104). Glucose 17-24 insulin Homo sapiens 0-7 11869176-8 2002 Furthermore, alcohol consumption was positively associated with insulin-mediated glucose uptake (r=0.20, P<0.05). Glucose 81-88 insulin Homo sapiens 64-71 11869176-9 2002 In multiple regression analyses, body mass index, alcohol consumption and serum triacylglycerols were independent co-variates to insulin-mediated glucose uptake. Glucose 146-153 insulin Homo sapiens 129-136 11953558-13 2002 CONCLUSIONS: These data suggest that short-term exercise may improve glucose tolerance and insulin response to a glucose load in centrally obese men. Glucose 113-120 insulin Homo sapiens 91-98 11869176-11 2002 In a subgroup of 104 subjects, alcohol consumption was independently and positively associated with insulin-mediated glucose uptake. Glucose 117-124 insulin Homo sapiens 100-107 11850099-0 2002 Validation of simple indices to assess insulin sensitivity based on the oral glucose tolerance test in the Japanese population. Glucose 77-84 insulin Homo sapiens 39-46 12005156-4 2002 It also increases insulin-mediated glucose disposal, an effect presumably related to vasodilation. Glucose 35-42 insulin Homo sapiens 18-25 12005156-6 2002 Mental stress decreased systemic vascular resistances by 21.9% and increased insulin-mediated glucose disposal by 2 8.4% without dexamethasone pretreatment. Glucose 94-101 insulin Homo sapiens 77-84 11850099-2 2002 Insulin sensitivity indices calculated from plasma glucose and plasma insulin concentrations after an oral glucose tolerant test (OGTT) have been proposed, but have not been validated in the Japanese population. Glucose 51-58 insulin Homo sapiens 0-7 12005156-7 2002 After 2 days of dexamethasone treatment, whole body insulin-mediated glucose disposal was decreased by 40.8%. Glucose 69-76 insulin Homo sapiens 52-59 12005156-9 2002 Mental stress acutely increased insulin-mediated glucose disposal by 28.0%. Glucose 49-56 insulin Homo sapiens 32-39 11850099-2 2002 Insulin sensitivity indices calculated from plasma glucose and plasma insulin concentrations after an oral glucose tolerant test (OGTT) have been proposed, but have not been validated in the Japanese population. Glucose 107-114 insulin Homo sapiens 0-7 11872654-12 2002 We conclude that 1) caffeine impairs insulin-stimulated glucose uptake and GS activity in rested and exercised human skeletal muscle; 2) caffeine-induced impairment of insulin-stimulated muscle glucose uptake and downregulation of GS activity are not accompanied by alterations in IRTK, PI 3-kinase, PKB/Akt, or GSK-3alpha but may be associated with increases in epinephrine and intramuscular cAMP concentrations; and 3) exercise reduces the detrimental effects of caffeine on insulin action in muscle. Glucose 194-201 insulin Homo sapiens 168-175 11856912-3 2002 The receptors function as transcription factors to regulate the expression of genes involved in lipid metabolism, cell growth and migration as well as insulin-mediated skeletal muscle glucose uptake. Glucose 184-191 insulin Homo sapiens 151-158 11872671-9 2002 Interestingly, insulin secretion is also exaggerated significantly at low glucose concentrations (2 and 5 mmol/l) but not at higher glucose concentrations (8--25 mmol/l). Glucose 74-81 insulin Homo sapiens 15-22 11872654-5 2002 In accordance, the total area under the curve over 100 min (AUC(0--100 min)) for insulin-stimulated glucose uptake in caffeine was reduced (P < 0.05) by approximately 50% in rested and exercised muscle. Glucose 100-107 insulin Homo sapiens 81-88 11872654-7 2002 Exercise increased insulin sensitivity of leg glucose uptake in both caffeine and placebo. Glucose 46-53 insulin Homo sapiens 19-26 11872654-12 2002 We conclude that 1) caffeine impairs insulin-stimulated glucose uptake and GS activity in rested and exercised human skeletal muscle; 2) caffeine-induced impairment of insulin-stimulated muscle glucose uptake and downregulation of GS activity are not accompanied by alterations in IRTK, PI 3-kinase, PKB/Akt, or GSK-3alpha but may be associated with increases in epinephrine and intramuscular cAMP concentrations; and 3) exercise reduces the detrimental effects of caffeine on insulin action in muscle. Glucose 56-63 insulin Homo sapiens 37-44 11872677-1 2002 NN304 [Lys(B29)-tetradecanoyl des(B30) human insulin] is a potentially therapeutic insulin analog designed to exhibit protracted glucose-lowering action. Glucose 129-136 insulin Homo sapiens 45-52 11872677-1 2002 NN304 [Lys(B29)-tetradecanoyl des(B30) human insulin] is a potentially therapeutic insulin analog designed to exhibit protracted glucose-lowering action. Glucose 129-136 insulin Homo sapiens 83-90 11872682-4 2002 Rosiglitazone treatment resulted in a 68% (P < 0.002) and a 20% (P < 0.016) improvement in insulin-stimulated glucose metabolism during the low- and high- dosage-insulin clamps, respectively, which was associated with approximately 40% reductions in plasma fatty acid concentration (P < 0.05) and hepatic triglyceride content (P < 0.05). Glucose 116-123 insulin Homo sapiens 97-104 11874937-1 2002 OBJECTIVE: To examine the associations between estrogen use and levels of insulin and glucose as well as the effect of estrogen use on the risk of type 2 diabetes. Glucose 86-93 insulin Homo sapiens 74-81 11874938-10 2002 Insulin secretion by sequential glucose tolerance testing remained normal in four multiple d-aab subjects not developing diabetes. Glucose 32-39 insulin Homo sapiens 0-7 11874940-7 2002 The insulinogenic index (delta area under the curve [AUC] insulin/deltaAUC glucose) during the OGTT increased significantly in the 30- and 45-mg/day pioglitazone groups (0.13 +/- 0.03 to 0.27 +/- 0.05, P < 0.05). Glucose 75-82 insulin Homo sapiens 4-11 11874942-5 2002 RESULTS: Tx had postabsorptive and insulin-stimulated glucose, leucine, and free fatty acid metabolism, as well as IMCL content, similar to that of CON. Glucose 54-61 insulin Homo sapiens 35-42 11874942-8 2002 CONCLUSIONS: Heart transplantation, notwithstanding the immunosuppressive therapy, was characterized by a normal postabsorptive and insulin-stimulated glucose, leucine, and free fatty acid metabolism in Tx. Glucose 151-158 insulin Homo sapiens 132-139 11874942-9 2002 In contrast, insulin resistance with respect to glucose, free fatty acids, and protein metabolism was present in D-Tx regardless of whether diabetes was preexisting or consequent to heart transplantation. Glucose 48-55 insulin Homo sapiens 13-20 11914752-1 2002 AIMS/HYPOTHESIS: A patient with (insulin-dependent) diabetes mellitus receives at least one subcutaneous insulin injection a day to maintain low serum glucose concentrations. Glucose 151-158 insulin Homo sapiens 33-40 11914752-8 2002 The serum glucose concentration was controlled for more than 6 h after oral insulin administration but returned to the basal concentration in 3 h when 1 IU/kg of insulin was injected intravenously. Glucose 10-17 insulin Homo sapiens 76-83 11914752-8 2002 The serum glucose concentration was controlled for more than 6 h after oral insulin administration but returned to the basal concentration in 3 h when 1 IU/kg of insulin was injected intravenously. Glucose 10-17 insulin Homo sapiens 162-169 11963922-5 2002 Extended 180-min OGTTs, with frequent plasma glucose and insulin sampling, were also undertaken in 24 CF patients and eight normal healthy controls to determine glucose-induced insulin response. Glucose 161-168 insulin Homo sapiens 177-184 11963922-11 2002 Within the CF group, there was a progressive decline in glucose-induced insulin release with worsening glycaemic status. Glucose 56-63 insulin Homo sapiens 72-79 11888847-7 2002 Interestingly, the GLP-1 response to oral glucose correlated with the insulin response in patients but not in controls whereas, in controls, the insulin response closely correlated with the GIP response. Glucose 42-49 insulin Homo sapiens 70-77 11888847-9 2002 CONCLUSIONS: This study showed that the GLP-1 and ACTH/cortisol responses to oral glucose are abnormal in insulin-resistant DM1 patients and that CTG triplet repeats are linked to GIP release. Glucose 82-89 insulin Homo sapiens 106-113 11896492-6 2002 RESULTS: The apnea/hypopnea index (AHI) was positively correlated with plasma soluble leptin receptor (0.76; P<0.001) and negatively with the degree of insulin-mediated glucose uptake (r=-0.73; P<0.001). Glucose 172-179 insulin Homo sapiens 155-162 11896492-7 2002 In a multivariate analysis AHI was associated with plasma soluble leptin receptor and insulin mediated glucose uptake independently of age, gender, BMI, plasma leptin levels and PaCO(2). Glucose 103-110 insulin Homo sapiens 86-93 11889151-12 2002 We calculated the whole-body insulin sensitivity index derived from the oral glucose tolerance test that was significantly reduced in the patients (4.3 +/- 1.7 vs. 5.7 +/- 2.5, P = 0.01). Glucose 77-84 insulin Homo sapiens 29-36 11889181-9 2002 Insulin sensitivity was estimated by the fasting glucose/insulin (G/I) ratio. Glucose 49-56 insulin Homo sapiens 0-7 11889183-5 2002 The acute insulin response to arginine was lower in GADab+ than in GADab- thyroiditis subjects at glucose concentration of 14 and >25 mmol/liter (AIR(14): 76.8 +/- 52.0 vs. 158.2 +/- 118.2 mU/liter, P = 0.040; AIR(>25): 84.3 +/- 64.4 vs. 167.9 +/- 101.5 mU/liter, P = 0.035). Glucose 98-105 insulin Homo sapiens 10-17 11872698-2 2002 Recently, it has been reported that the Gly(972)Arg variant in IRS-1 was associated with reduced insulin secretion during hyperglycemic clamps in German subjects with normal glucose tolerance. Glucose 174-181 insulin Homo sapiens 97-104 11872698-3 2002 We have examined glucose-stimulated insulin secretion in relation to gene variants in the IRS-1 (Gly(972)Arg) and IRS-2 (Gly(1057)Asp) genes in two Dutch cohorts. Glucose 17-24 insulin Homo sapiens 36-43 11914741-0 2002 Prolonged glucose infusion into conscious rats inhibits early steps in insulin signalling and induces translocation of GLUT4 and protein kinase C in skeletal muscle. Glucose 10-17 insulin Homo sapiens 71-78 11914741-4 2002 In this animal model, rats accommodate systemic glucose oversupply and rapidly develop insulin resistance. Glucose 48-55 insulin Homo sapiens 87-94 11914741-5 2002 RESULTS: Glucose infusion increased both plasma glucose and insulin concentrations to peak after one day. Glucose 9-16 insulin Homo sapiens 60-67 11921434-5 2002 In clinical trials, all three TZDs effectively lower blood glucose levels as monotherapy and in combination therapy with sulfonylureas, metformin and insulin. Glucose 59-66 insulin Homo sapiens 150-157 11856812-1 2002 Growth hormone (GH) counteracts insulin action on lipid and glucose metabolism. Glucose 60-67 insulin Homo sapiens 32-39 11895468-5 2002 RESULTS: Relatives exhibited decreased insulin sensitivity (index of metabolic clearance rate of glucose; MCRI) but when genders were analysed separately, this difference was significant only in males (11.3 +/- 1.3 vs. 15.0 +/- 1.5 units, means +/- SEM, P = 0.030). Glucose 97-104 insulin Homo sapiens 39-46 11965520-2 2002 The metabolic compensatory response to insulin resistance is hyperinsulinaemia, the primary purpose of which is to maintain normal glucose tolerance. Glucose 131-138 insulin Homo sapiens 39-46 11870117-1 2002 BACKGROUND: To evaluate the effects of long-term acipimox administration on glucose-induced insulin secretion and peripheral insulin sensitivity in polycystic ovarian syndrome (PCOS), 20 PCOS subjects (eight lean and 12 obese) and 14 body mass index-matched controls (seven lean and seven obese) were investigated. Glucose 76-83 insulin Homo sapiens 92-99 17656880-5 2002 An intravenous Insulin Tolerance Test (ITT) was performed with measurement of Glucose Disposal Rate (GDR). Glucose 78-85 insulin Homo sapiens 15-22 11889193-0 2002 Glucose tolerance during moderate alcohol intake: insights on insulin action from glucose/lactate dynamics. Glucose 82-89 insulin Homo sapiens 62-69 11889219-3 2002 Insulin was infused at the rate of 2 IU/h in 5% dextrose (100 mL/h) and KCI (8 mmol/h) for 4 h in the fasting state in ten obese subjects. Glucose 48-56 insulin Homo sapiens 0-7 11986895-1 2002 Reduced insulin-mediated glucose disposal, indicative of insulin resistance, has been demonstrated in lean male hypertensives both with the hyperinsulinaemic euglycaemic clamp and the insulin suppression test. Glucose 25-32 insulin Homo sapiens 8-15 11874713-0 2002 Delays in insulin signaling towards glucose disposal in human skeletal muscle. Glucose 36-43 insulin Homo sapiens 10-17 11875319-4 2002 Insulin sensitivity (Mlbm) is defined as the amount of glucose required to maintain euglycemia (mg glucose infused/kg lean body mass (LBM)/min. Glucose 55-62 insulin Homo sapiens 0-7 11875319-4 2002 Insulin sensitivity (Mlbm) is defined as the amount of glucose required to maintain euglycemia (mg glucose infused/kg lean body mass (LBM)/min. Glucose 99-106 insulin Homo sapiens 0-7 11986895-1 2002 Reduced insulin-mediated glucose disposal, indicative of insulin resistance, has been demonstrated in lean male hypertensives both with the hyperinsulinaemic euglycaemic clamp and the insulin suppression test. Glucose 25-32 insulin Homo sapiens 57-64 11986895-2 2002 In lean hypertensives, insulin resistance was not accompanied by increases in fasting plasma insulin and glucose levels; but with modest hyperglycaemia and hyperinsulinaemia after a glucose load. Glucose 182-189 insulin Homo sapiens 23-30 11986895-9 2002 Because of the strong association between insulin resistance, hyperglycaemia and endothelial dysfunction, and the clustering of risk factors in these subjects, we propose the lowering of high normal glucose levels as part of the therapeutic strategy to prevent cardiovascular and metabolic disease. Glucose 199-206 insulin Homo sapiens 42-49 11986911-5 2002 Both oral glucose and L-arginine induced greater increases in plasma insulin in obese hypertensives than in lean normotensives. Glucose 10-17 insulin Homo sapiens 69-76 11986911-6 2002 Endothelial dysfunction which accompanies the insulin resistant state of obesity, glucose intolerance and hypertension, may account for the different BP effects induced by glucose and L-arginine in obese hypertensives and lean normotensives. Glucose 172-179 insulin Homo sapiens 46-53 11887163-0 2002 Interaction between glucose metabolism and endogenous insulin release in hypertension. Glucose 20-27 insulin Homo sapiens 54-61 11887163-1 2002 The minimal model approach was applied to examine the dynamic interaction between glucose metabolism and endogenous insulin release during an intravenous glucose tolerance test (IVGTT) in a group of hypertensive patients (H group) compared with a group of normotensive subjects (N group). Glucose 154-161 insulin Homo sapiens 116-123 11915058-9 2002 Similarly, plasma concentrations of glucose and insulin increased significantly following feeding with dextrose in both groups. Glucose 103-111 insulin Homo sapiens 48-55 11751846-1 2002 Preincubation of 3T3-L1 adipocytes in high glucose or glucosamine decreases acute insulin (100 nm)-stimulated glucose transport provided that insulin (0.6 nm) is included during preincubation. Glucose 43-50 insulin Homo sapiens 82-89 11751846-1 2002 Preincubation of 3T3-L1 adipocytes in high glucose or glucosamine decreases acute insulin (100 nm)-stimulated glucose transport provided that insulin (0.6 nm) is included during preincubation. Glucose 110-117 insulin Homo sapiens 82-89 11751846-7 2002 Under each condition except high glucose + insulin preincubation, acute insulin increased Munc18-c (50-200%) in TS-PM and decreased Munc18-c (60%) in TI-LDM. Glucose 33-40 insulin Homo sapiens 72-79 11849661-1 2002 Insulin resistance, through numerous related disturbances in glucose and lipoprotein-lipid metabolism, is associated with an increased risk of ischemic heart disease (IHD). Glucose 61-68 insulin Homo sapiens 0-7 11925664-5 2002 In diabetics, the metabolic clearance rates of glucose at either insulin level (MCRglusubmax and MCRglumax) were significantly reduced in comparison with HS (MCRglusubmax--DMN: 5.35 +/- 2.7 ml.kg-1.min-1; DMH: 5.38 +/- 2.17 ml.kg-1.min-1; DMD: 5.48 +/- 2.35 ml.kg-1.min-1; HS: 10.9 +/- 3.3 ml.kg-1.min-1; p < 0.01; and MCRglumax--DMN: 13.3 +/- 3.3 ml.kg-1.min-1; DMH: 12.5 +/- 3.0 ml.kg-1.min-1; DMD: 13.3 +/- 3.0 ml.kg-1.min-1; HS: 17.4 +/- 3.8 ml.kg-1.min-1; p < 0.05). Glucose 47-54 insulin Homo sapiens 65-72 12643127-1 2002 Insulin resistance, defined as the decreased ability of insulin to perform its biological functions, is likely to represent the primary physiologic defect underlying the insulin resistance syndrome (IRS), which includes insulin resistance/hyperinsulinemia, glucose intolerance and/or type 2 diabetes mellitus, visceral obesity, hypertension, and dyslipidemia. Glucose 257-264 insulin Homo sapiens 0-7 12643127-1 2002 Insulin resistance, defined as the decreased ability of insulin to perform its biological functions, is likely to represent the primary physiologic defect underlying the insulin resistance syndrome (IRS), which includes insulin resistance/hyperinsulinemia, glucose intolerance and/or type 2 diabetes mellitus, visceral obesity, hypertension, and dyslipidemia. Glucose 257-264 insulin Homo sapiens 56-63 11812745-14 2002 Our data militate against a primary developmental pancreatic abnormality in human IUGR, leaving peripheral insulin resistance as the most likely mechanism of glucose intolerance in adults born with IUGR. Glucose 158-165 insulin Homo sapiens 107-114 11812753-4 2002 Insulin action on whole-body glucose disposal rate (GDR) was determined before and after treatment using the hyperinsulinemic (300 mU x m(-2) x min(-1)) euglycemic (5.0-5.5 mmol/l) clamp technique. Glucose 29-36 insulin Homo sapiens 0-7 11889158-3 2002 Insulin sensitivity (glucose infusion rate during euglycemic-hyperinsulinemic clamp) was significantly less in the type 1 diabetes group than in controls (49.3 +/- 14.8 vs. 73.2 +/- 21.6 micromol/min x kg fat free mass, respectively, P = 0.01). Glucose 21-28 insulin Homo sapiens 0-7 11956956-5 2002 This abnormality along with a reduction in brain insulin concentration is assumed to induce a cascade-like process of disturbances including cellular glucose, acetylcholine, cholesterol, and ATP associated with abnormalities in membrane pathology and the formation of both amyloidogenic derivatives and hyperphosphorylated tau protein. Glucose 150-157 insulin Homo sapiens 49-56 11887165-5 2002 Over the first hour following ingestion of the glucose load, plasma glucose and insulin concentrations were higher in HIV patients than in controls, both before (approximately 15% and approximately 29%, respectively) and after (approximately 32% and approximately 43%, respectively) PI therapy. Glucose 47-54 insulin Homo sapiens 80-87 11886934-8 2002 DISCUSSION: Our data indicate that both obese non-diabetic and obese type 2 diabetic patients have a blunted suppressive action of insulin on glucose production, indicating hepatic and renal insulin resistance. Glucose 142-149 insulin Homo sapiens 131-138 12017763-11 2002 If there are significantly increased postprandial blood glucose values (due to an early-insulin-secretion deficiency or severe insulin resistance), the use of alpha-glucosidase-inhibitors, metformin, sulphonylureas or glinides is indicated. Glucose 56-63 insulin Homo sapiens 88-95 11904148-8 2002 Leptin decreased UCP-2 expression by up to 75%, and maximally inhibited insulin release by 47%, at 22 mmol/l glucose. Glucose 109-116 insulin Homo sapiens 72-79 11884934-12 2002 Tapering and eventual withdrawal of insulin should be attempted once blood glucose levels normalize. Glucose 75-82 insulin Homo sapiens 36-43 11817952-5 2002 FluoZin-3 was used to monitor Zn2+ that was co-secreted with insulin from pancreatic beta-cells by exocytosis following stimulation with glucose. Glucose 137-144 insulin Homo sapiens 61-68 11841956-6 2002 A fasting glucose-to-insulin ratio of < 7 is a useful index of insulin resistance in adolescents. Glucose 10-17 insulin Homo sapiens 21-28 11841956-6 2002 A fasting glucose-to-insulin ratio of < 7 is a useful index of insulin resistance in adolescents. Glucose 10-17 insulin Homo sapiens 66-73 11854636-0 2002 Does insulin secretion in patients with one abnormal glucose tolerance test value mimic gestational diabetes mellitus? Glucose 53-60 insulin Homo sapiens 5-12 11854636-1 2002 OBJECTIVE: The purpose of this study was to investigate the insulin response to a 3-hour oral glucose tolerance test and to compare the insulin levels in the gestational diabetes mellitus and single abnormal test value groups with a nondiabetic control group. Glucose 94-101 insulin Homo sapiens 60-67 11854636-6 2002 Total insulin secretion was assessed by mean insulin level during the oral glucose tolerance test; insulin resistance was assessed by fasting insulin concentration and by the use of the homeostasis model. Glucose 75-82 insulin Homo sapiens 6-13 11854636-8 2002 RESULTS: The fasting insulin levels of patients with normal oral glucose tolerance test results were significantly lower than those of patients with gestational diabetes mellitus and a single value abnormality (P <.001 and P <.005, respectively). Glucose 65-72 insulin Homo sapiens 21-28 11854636-9 2002 The insulinogenic index as a marker of early-phase insulin secretion was significantly lower in gestational diabetes mellitus, compared with that of patients with normal oral glucose tolerance test results (P <.05). Glucose 175-182 insulin Homo sapiens 4-11 11834144-8 2002 Whole-body insulin-mediated glucose uptake and forearm glucose uptake did not differ between the sexes, and the ability of insulin to enhance endothelium-dependent vasodilatation (+19%; P<0.01) was similar in men and women. Glucose 28-35 insulin Homo sapiens 11-18 11834144-10 2002 However, no differences between the sexes were seen with regard to insulin-mediated glucose uptake and the ability of insulin to enhance endothelium-dependent vasodilatation. Glucose 84-91 insulin Homo sapiens 67-74 11815454-3 2002 In the presence of 250 micromol/l diazoxide, simultaneous application of forskolin and 16.7 mmol/l glucose strongly stimulated insulin release: fourfold and eightfold increases with 1 and 30 micromol/l forskolin, respectively. Glucose 99-106 insulin Homo sapiens 127-134 11815456-1 2002 The beta-cell mitochondria are known to generate metabolic coupling factors, or messengers, that mediate plasma membrane depolarization and the increase in cytosolic Ca(2+), the triggering event in glucose-stimulated insulin secretion. Glucose 198-205 insulin Homo sapiens 217-224 11815459-0 2002 Modeling phasic insulin release: immediate and time-dependent effects of glucose. Glucose 73-80 insulin Homo sapiens 16-23 11815459-3 2002 The insulin response of perifused islets of rats, perfused rat pancreas, or that of a human, to a square-wave glucose stimulus is biphasic, a transient first-phase response of 4- to 10-min duration followed by a gradual rise in secretion rates (second-phase response). Glucose 110-117 insulin Homo sapiens 4-11 11815459-9 2002 In contrast, prolonged stimulations with glucose (and other nutrients) lead to the amplification of the insulin response to subsequent stimuli; this can be demonstrated in the perfused rat pancreas, in perifused islets from several rodents, and in humans. Glucose 41-48 insulin Homo sapiens 104-111 11986914-9 2002 The mean serum insulin: plasma glucose ratio for hypertensive women was significantly higher than that for normotensives after 15 min (0.596 +/- 0.46 vs. 0.359 +/- 0.20 microU/mg), 60 min (0.406 +/- 0.30 vs. 0.329 +/- 0.25 microU/mg) and 120 min (0.436 +/- 0.35 vs. 0.205 +/- 0.26 microU/mg) (P < 0.05 for all three comparisons). Glucose 31-38 insulin Homo sapiens 15-22 11815461-0 2002 Beta-cell protein kinases and the dynamics of the insulin response to glucose. Glucose 70-77 insulin Homo sapiens 50-57 11815459-12 2002 Of major interest is the observation that, while the acute insulin response to glucose is severely reduced in glucose-intolerant animals and humans, TDP seems to be intact. Glucose 79-86 insulin Homo sapiens 59-66 11815472-10 2002 Addition of metformin to high-FFA media prevented impairment in glucose-mediated insulin release, decline of first-phase insulin secretion, and reduction of glucose utilization and oxidation without significantly affecting islet triglyceride accumulation. Glucose 64-71 insulin Homo sapiens 81-88 11815466-1 2002 It is intriguing that the kinetics of glucose-stimulated insulin secretion from the in situ perfused pancreas differ between the rat and the mouse. Glucose 38-45 insulin Homo sapiens 57-64 11815466-2 2002 Here we confirm that insulin release in the rat is clearly biphasic, whereas in the mouse glucose essentially elicits a transient monophasic insulin release. Glucose 90-97 insulin Homo sapiens 141-148 11815466-7 2002 These results are compatible with a role for glucose-derived glutamate principally in the sustained phase of nutrient-stimulated insulin secretion. Glucose 45-52 insulin Homo sapiens 129-136 11815467-1 2002 The dose-response relationship between the hepatic sinusoidal insulin level and glucose production by the liver is such that a half-maximally effective concentration is at or slightly below the hormone levels seen basally after an overnight fast. Glucose 80-87 insulin Homo sapiens 62-69 11815467-4 2002 Thus, the speed with which insulin works and the sensitivity of the liver to it predict that first-phase insulin release should have a significant effect in quickly suppressing hepatic glucose production. Glucose 185-192 insulin Homo sapiens 27-34 11815467-4 2002 Thus, the speed with which insulin works and the sensitivity of the liver to it predict that first-phase insulin release should have a significant effect in quickly suppressing hepatic glucose production. Glucose 185-192 insulin Homo sapiens 105-112 11815467-8 2002 In addition, they confirmed the ability of second-phase insulin release to have significant effects on both glucose production and utilization. Glucose 108-115 insulin Homo sapiens 56-63 11815468-7 2002 After glucose challenge, a specific alteration of acute insulin release is an early and progressive defect. Glucose 6-13 insulin Homo sapiens 56-63 11815469-1 2002 Insulin is released from the pancreas in a biphasic manner in response to a square-wave increase in arterial glucose concentration. Glucose 109-116 insulin Homo sapiens 0-7 11815471-1 2002 First-phase insulin response to intravenous glucose is impaired both in type 2 diabetic patients and in subjects at risk for the disease. Glucose 44-51 insulin Homo sapiens 12-19 11815471-7 2002 In contrast, second-phase insulin secretion was related to the prevailing glucose levels across the three hyperglycemic steps in a direct quasilinear manner. Glucose 74-81 insulin Homo sapiens 26-33 11815472-2 2002 Insulin secretion was then assessed in response to glucose (16.7 mmol/l), arginine (20 mmol/l), and glyburide (200 micromol/l) during static incubation or by perifusion. Glucose 51-58 insulin Homo sapiens 0-7 11815490-2 2002 Diabetic Pima Indians are metabolically prototypic, with obesity, insulin resistance, a reduced acute insulin response to glucose, and increased endogenous glucose production. Glucose 122-129 insulin Homo sapiens 102-109 11815490-3 2002 Cross-sectional studies show that the acute insulin response is absent in diabetic subjects and lower in impaired than in normal glucose-tolerant subjects. Glucose 129-136 insulin Homo sapiens 44-51 11815490-5 2002 Longitudinal studies show that glucose tolerance deteriorates as the degree of obesity increases due to worsening insulin resistance and decreases in early insulin secretion. Glucose 31-38 insulin Homo sapiens 114-121 11815505-6 2002 However, for patients randomized to an intensive policy with sulfonylurea (n = 339), insulin was added automatically if the fasting plasma glucose remained >108 mg/dl (6.0 mmol/l) despite maximal sulfonylurea doses. Glucose 139-146 insulin Homo sapiens 85-92 11815511-4 2002 We hypothesized that caffeine reduces insulin sensitivity, either due to catecholamines and/or as a result of blocking adenosine-mediated stimulation of peripheral glucose uptake. Glucose 164-171 insulin Homo sapiens 38-45 11815511-8 2002 Insulin sensitivity was calculated as whole-body glucose uptake corrected for the insulin concentration. Glucose 49-56 insulin Homo sapiens 0-7 11935160-1 2002 AIMS/HYPOTHESIS: A common G to A polymorphism ( UCSNP-43) in the Calpain 10 gene was recently found to be associated with Type II (non-insulin-dependent) diabetes mellitus and variations in post-absorptive and insulin stimulated glucose metabolism in vivo. Glucose 229-236 insulin Homo sapiens 135-142 11938022-7 2002 Metabolic studies showed a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Glucose 74-81 insulin Homo sapiens 44-51 11938022-7 2002 Metabolic studies showed a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Glucose 134-141 insulin Homo sapiens 44-51 11895454-5 2002 METHODS: For this study, 26 adult nondiabetic individuals (12 women and 14 men) with a wide range of whole-body insulin-mediated glucose uptake (as assessed with an insulin suppression test) were studied. Glucose 129-136 insulin Homo sapiens 112-119 11895454-8 2002 Steady-state plasma glucose (SSPG) concentrations during the insulin suppression test, a reflection of the degree of insulin resistance, were also negatively correlated to adipose tissue LPL mRNA (rho = -0.50, P < 0.02) and activity (rho = -0.56, P < 0.01). Glucose 20-27 insulin Homo sapiens 61-68 12017950-4 2002 Forty percent of all studied patients had a fasting glucose/insulin ratio below 4.5, which corresponds to insulin resistance. Glucose 52-59 insulin Homo sapiens 106-113 11815477-5 2002 The frequency of the rapid oscillatory ionic activities is regulated by glucose and allows the beta-cell to respond in an analogous way, with gradual changes in [Ca(2+)](i) and insulin release in response to the alterations in glucose concentration. Glucose 72-79 insulin Homo sapiens 177-184 11815477-5 2002 The frequency of the rapid oscillatory ionic activities is regulated by glucose and allows the beta-cell to respond in an analogous way, with gradual changes in [Ca(2+)](i) and insulin release in response to the alterations in glucose concentration. Glucose 227-234 insulin Homo sapiens 177-184 11815479-1 2002 Nonselective cation channels may play a role in insulin secretion by regulating pancreatic beta-cell plasma membrane potential, Ca(2+) homeostasis, and thereby glucose signaling. Glucose 160-167 insulin Homo sapiens 48-55 11815481-6 2002 Finally, surrogate insulin sensitivity measures quantified from OGTT and the glucose-dependent arginine-stimulation test only weakly correlated to M/I(clamp) (R(2) approx equal to 0.25). Glucose 77-84 insulin Homo sapiens 19-26 11815481-7 2002 Thus, 1) insulin secretion is adaptively increased when insulin sensitivity is low in nondiabetic postmenopausal women; 2) beta-cell exocytotic ability shows more efficient adaptation than beta-cell glucose recognition to low insulin sensitivity; 3) impaired beta-cell adaptation (i.e., low DI) is associated with higher 2-h glucose values during OGTT, although other regulatory mechanisms also exist; and 4) indirect surrogate measures of insulin sensitivity only weakly correlate to insulin sensitivity as determined by the euglycemic-hyperinsulinemic clamp. Glucose 325-332 insulin Homo sapiens 9-16 11815482-3 2002 Shifts in insulin sensitivity are accompanied by compensatory alterations in beta-cell sensitivity to glucose. Glucose 102-109 insulin Homo sapiens 10-17 11815482-4 2002 Insulin-sensitive subjects do not require a massive insulin response to exogenous glucose to maintain a normal blood glucose. Glucose 117-124 insulin Homo sapiens 0-7 11815482-8 2002 Separate major issues remain, however: the causes of insulin resistance, the causes of the failure of adequate beta-cell compensation in type 2 diabetes, and the nature of the signal(s) from insulin-resistant tissues that fail to elicit the appropriate beta-cell increment in sensitivity to glucose and other stimuli. Glucose 291-298 insulin Homo sapiens 191-198 11815483-1 2002 We developed a mathematical model of the glucose control of insulin secretion capable of quantifying beta-cell function from a physiological meal test. Glucose 41-48 insulin Homo sapiens 60-67 11815483-6 2002 In diabetic patients, the dose-response function was shifted to the right (glucose concentration at a reference insulin secretion of 300 pmol.min(-1).m(-2) was 11.7 +/- 1.1 vs. 7.2 +/- 0.7 mmol/l; P < 0.05), and decreased in slope (53 +/- 15 vs. 148 +/- 38 pmol.min(-1).m(-2).mmol(-1).l; P < 0.05) and the parameter of the dynamic control was decreased (220 +/- 67 vs. 908 +/- 276 pmol.m(-2).mmol(-1).l; P < 0.05) compared with the nondiabetic control subjects. Glucose 75-82 insulin Homo sapiens 112-119 11815484-0 2002 Insulin release in impaired glucose tolerance: oral minimal model predicts normal sensitivity to glucose but defective response times. Glucose 28-35 insulin Homo sapiens 0-7 11815484-6 2002 An index of insulin sensitivity was also obtained for each subject from minimal model analysis of glucose and insulin levels achieved during the test. Glucose 98-105 insulin Homo sapiens 12-19 11972295-1 2002 This study aimed to evaluate a simplified minimal model protocol for measuring insulin sensitivity in mild and severe type 2 diabetes, considering that changes in serum insulin during an insulin-modified intravenous glucose tolerance test almost only reflect the insulin injection. Glucose 216-223 insulin Homo sapiens 79-86 11972295-1 2002 This study aimed to evaluate a simplified minimal model protocol for measuring insulin sensitivity in mild and severe type 2 diabetes, considering that changes in serum insulin during an insulin-modified intravenous glucose tolerance test almost only reflect the insulin injection. Glucose 216-223 insulin Homo sapiens 169-176 11972295-1 2002 This study aimed to evaluate a simplified minimal model protocol for measuring insulin sensitivity in mild and severe type 2 diabetes, considering that changes in serum insulin during an insulin-modified intravenous glucose tolerance test almost only reflect the insulin injection. Glucose 216-223 insulin Homo sapiens 169-176 11972295-1 2002 This study aimed to evaluate a simplified minimal model protocol for measuring insulin sensitivity in mild and severe type 2 diabetes, considering that changes in serum insulin during an insulin-modified intravenous glucose tolerance test almost only reflect the insulin injection. Glucose 216-223 insulin Homo sapiens 169-176 11786928-1 2002 Cytochalasin B is known to enhance insulin release evoked by nutrient and non-nutrient secretagogues, including D-glucose, despite inhibiting D-glucose uptake and metabolism in pancreatic islets. Glucose 112-121 insulin Homo sapiens 35-42 11786928-5 2002 Nevertheless, even in the presence of forskolin, cytochalasin B was more efficient than cytochalasin D in augmenting glucose-stimulated insulin secretion. Glucose 117-124 insulin Homo sapiens 136-143 11868613-3 2002 In addition to the central role of pancreatic beta-cell K(ATP) channels in glucose-mediated insulin secretion, several lines of evidence support the hypothesis that K(ATP) channels modulate glucose transport in the insulin target tissues. Glucose 75-82 insulin Homo sapiens 92-99 11796678-0 2002 Role of kallikrein-kininogen system in insulin-stimulated glucose transport after muscle contractions. Glucose 58-65 insulin Homo sapiens 39-46 11796678-1 2002 Serum proteins [molecular weight (MW) > 10,000] are essential for increased insulin-stimulated glucose transport after in vitro muscle contractions. Glucose 98-105 insulin Homo sapiens 79-86 11836310-0 2002 PKC-zeta mediates insulin effects on glucose transport in cultured preadipocyte-derived human adipocytes. Glucose 37-44 insulin Homo sapiens 18-25 12017950-0 2002 [Insulin-glucose ratio and body fat composition in patients with chronic anovulation and sterility]. Glucose 9-16 insulin Homo sapiens 1-8 11836295-5 2002 injection of 0.1 U of human insulin per kg of body weight in the patients or 0.15 U in healthy subjects, the plasma glucose concentrations decreased to similar minimum levels within 30 min in all three groups. Glucose 116-123 insulin Homo sapiens 28-35 11836299-12 2002 The reduction in insulin sensitivity was confirmed by analysis of the subset of individuals who underwent iv glucose tolerance tests, where SNP-19 significantly altered the insulin sensitivity index. Glucose 109-116 insulin Homo sapiens 17-24 11836299-12 2002 The reduction in insulin sensitivity was confirmed by analysis of the subset of individuals who underwent iv glucose tolerance tests, where SNP-19 significantly altered the insulin sensitivity index. Glucose 109-116 insulin Homo sapiens 173-180 11836301-9 2002 The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate). Glucose 194-201 insulin Homo sapiens 174-181 11836345-2 2002 However, insulin-mediated glucose disposal decreased transiently after one month of GH therapy. Glucose 26-33 insulin Homo sapiens 9-16 11833043-1 2002 Type 2 diabetes mellitus is characterized by insulin-resistant glucose and lipid metabolism. Glucose 63-70 insulin Homo sapiens 45-52 11833043-2 2002 Thiazolidinediones (TZDs) enhance insulin-mediated glucose disposal, but their effects on lipid kinetics are unknown. Glucose 51-58 insulin Homo sapiens 34-41 11833046-4 2002 Early phase insulin secretion (insulinogenic index) declined with worsening glucose intolerance in non-obese (tau = -.216, P <.001; Kendall"s correlation coefficient) and obese subjects (tau = -.392, P <.001). Glucose 76-83 insulin Homo sapiens 12-19 11833057-5 2002 Estimated glucose disposal rate (eGDR), a measure of insulin resistance, was calculated from glycosylated hemoglobin (HbA(1)), waist-to-hip ratio (WHR), and hypertension using an equation previously validated with hyperinsulinemic euglycemic clamp studies. Glucose 10-17 insulin Homo sapiens 53-60 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Glucose 17-24 insulin Homo sapiens 0-7 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Glucose 17-24 insulin Homo sapiens 56-63 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Glucose 130-137 insulin Homo sapiens 0-7 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Glucose 130-137 insulin Homo sapiens 56-63 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Glucose 130-137 insulin Homo sapiens 0-7 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Glucose 130-137 insulin Homo sapiens 56-63 11833059-0 2002 Elevated concentrations of free fatty acids are associated with increased insulin response to standard glucose challenge in human immunodeficiency virus-infected subjects with fat redistribution. Glucose 103-110 insulin Homo sapiens 74-81 11818508-11 2002 In summary, these data demonstrate a positive role for intracellular Ca(2+) in distal insulin signaling events, including initiation/maintenance of Akt phosphorylation, insulin-responsive glucose transporter isoform translocation, and glucose transport. Glucose 188-195 insulin Homo sapiens 86-93 11818508-11 2002 In summary, these data demonstrate a positive role for intracellular Ca(2+) in distal insulin signaling events, including initiation/maintenance of Akt phosphorylation, insulin-responsive glucose transporter isoform translocation, and glucose transport. Glucose 188-195 insulin Homo sapiens 169-176 11812756-0 2002 Normalization of plasma glucose concentration by insulin therapy improves insulin-stimulated glycogen synthesis in type 2 diabetes. Glucose 24-31 insulin Homo sapiens 49-56 11812756-0 2002 Normalization of plasma glucose concentration by insulin therapy improves insulin-stimulated glycogen synthesis in type 2 diabetes. Glucose 24-31 insulin Homo sapiens 74-81 11812756-4 2002 The purpose of the present study was to determine the biochemical mechanisms responsible for increased insulin-stimulated glucose disposal after the achievement of tight glycemic control with a mixed-split regimen. Glucose 122-129 insulin Homo sapiens 103-110 11812756-6 2002 Improved glycemic control increased insulin-stimulated glucose disposal (5.16 +/- 0.32 vs. 3.69 +/- 0.33 mg x kg(-1) x min(-1); P < 0.01); nonoxidative glucose disposal, which primarily reflects glycogen synthesis (2.11 +/- 0.26 vs. 0.90 +/- 0.16 mg x kg(-1) x min(-1); P < 0.01); and glycogen synthase fractional velocity (0.094 +/- 0.017 vs. 0.045 +/- 0.007; P < 0.05). Glucose 55-62 insulin Homo sapiens 36-43 11812756-6 2002 Improved glycemic control increased insulin-stimulated glucose disposal (5.16 +/- 0.32 vs. 3.69 +/- 0.33 mg x kg(-1) x min(-1); P < 0.01); nonoxidative glucose disposal, which primarily reflects glycogen synthesis (2.11 +/- 0.26 vs. 0.90 +/- 0.16 mg x kg(-1) x min(-1); P < 0.01); and glycogen synthase fractional velocity (0.094 +/- 0.017 vs. 0.045 +/- 0.007; P < 0.05). Glucose 155-162 insulin Homo sapiens 36-43 11812756-8 2002 All of the increase in insulin-stimulated glucose disposal could be accounted for by increased glycogen synthesis, which is likely attributable to increased activation of glycogen synthase by insulin. Glucose 42-49 insulin Homo sapiens 23-30 11812756-8 2002 All of the increase in insulin-stimulated glucose disposal could be accounted for by increased glycogen synthesis, which is likely attributable to increased activation of glycogen synthase by insulin. Glucose 42-49 insulin Homo sapiens 192-199 11833054-3 2002 The results of this analysis showed that estimates of insulin resistance derived from use of QUICKI were significantly correlated (r = -.60, P <.001) with direct measures of insulin-mediated glucose in the 490 subjects studied. Glucose 194-201 insulin Homo sapiens 54-61 11833054-3 2002 The results of this analysis showed that estimates of insulin resistance derived from use of QUICKI were significantly correlated (r = -.60, P <.001) with direct measures of insulin-mediated glucose in the 490 subjects studied. Glucose 194-201 insulin Homo sapiens 177-184 11833054-5 2002 On the other hand, the correlation between all 3 of the surrogate methods for estimating insulin resistance and the direct assessment of insulin-mediated glucose disposal was relatively weak, i.e., r =.61, r =.64, and r = -.60) for fasting insulin concentration, HOMA-IR, and QUICKI, respectively. Glucose 154-161 insulin Homo sapiens 137-144 11833054-5 2002 On the other hand, the correlation between all 3 of the surrogate methods for estimating insulin resistance and the direct assessment of insulin-mediated glucose disposal was relatively weak, i.e., r =.61, r =.64, and r = -.60) for fasting insulin concentration, HOMA-IR, and QUICKI, respectively. Glucose 154-161 insulin Homo sapiens 137-144 11833054-7 2002 Furthermore, none of the 3 surrogate estimates can account for more than approximately 40% of the variability of the difference in insulin-mediated glucose disposal measured directly in 490 healthy, nondiabetic volunteers. Glucose 148-155 insulin Homo sapiens 131-138 11836310-1 2002 Insulin-stimulated glucose transport is impaired in the early phases of type 2 diabetes mellitus. Glucose 19-26 insulin Homo sapiens 0-7 11836310-8 2002 Our findings provide convincing evidence that aPKCs and upstream activators, PI 3-kinase and PDK-1, play important roles in insulin-stimulated glucose transport in preadipocyte-derived human adipocytes. Glucose 143-150 insulin Homo sapiens 124-131 11836319-2 2002 Insulin resistance, a key component in the pathogenesis of PCOS and glucose intolerance, is ameliorated by the thiazolidinediones, synthetic ligands for the PPARgamma. Glucose 68-75 insulin Homo sapiens 0-7 11815271-3 2002 However, this approach has been hampered by the absence of (1) an appropriate glucose-sensing system to regulate insulin gene transcription; (2) enzymes that process proinsulin to insulin; and (3) glucose-regulatable exocytosis in the target cells. Glucose 78-85 insulin Homo sapiens 113-120 11818508-10 2002 Insulin-stimulated insulin-responsive glucose transporter isoform translocation and glucose uptake were both inhibited by calcium depletion. Glucose 38-45 insulin Homo sapiens 0-7 11818508-10 2002 Insulin-stimulated insulin-responsive glucose transporter isoform translocation and glucose uptake were both inhibited by calcium depletion. Glucose 38-45 insulin Homo sapiens 19-26 11739088-0 2002 Rapid effects of glucose on the insulin signaling of endothelial NO generation and epithelial Na transport. Glucose 17-24 insulin Homo sapiens 32-39 11739088-3 2002 Generation of endothelial-derived vasodilator nitric oxide (NO), estimated after a 2-h period of insulin stimulation, was inhibited in the presence of high glucose. Glucose 156-163 insulin Homo sapiens 97-104 11739088-5 2002 The enzymatic complexes did not form when the endothelial insulin stimulation occurred in the presence of high glucose concentrations. Glucose 111-118 insulin Homo sapiens 58-65 11739092-0 2002 Effects of fatty acids on exercise plus insulin-induced glucose utilization in trained and sedentary subjects. Glucose 56-63 insulin Homo sapiens 40-47 11739092-1 2002 Fatty acids are known to decrease insulin-mediated glucose utilization in humans, both at rest and during exercise. Glucose 51-58 insulin Homo sapiens 34-41 11739095-5 2002 With exercise, the glucose infusion rate increased (P < 0.001) by 33%, indicating enhanced insulin action (mean +/- SE, 6.6 +/- 0.6 vs. 8.7 +/- 0.8 mg x kg(-1) x min(-1)). Glucose 19-26 insulin Homo sapiens 94-101 12523496-1 2002 Glucose transport, the rate limiting step in glucose metabolism in skeletal muscle, is mediated by insulin-sensitive glucose transporter 4 (GLUT4) and can be activated in skeletal muscle by two separate and distinct signalling pathways: one stimulated by insulin and the second by muscle contractions. Glucose 0-7 insulin Homo sapiens 99-106 12523496-1 2002 Glucose transport, the rate limiting step in glucose metabolism in skeletal muscle, is mediated by insulin-sensitive glucose transporter 4 (GLUT4) and can be activated in skeletal muscle by two separate and distinct signalling pathways: one stimulated by insulin and the second by muscle contractions. Glucose 0-7 insulin Homo sapiens 255-262 12523496-2 2002 Skeletal muscle is the principal tissue responsible for insulin-stimulated glucose disposal and thus the major site of peripheral insulin resistance. Glucose 75-82 insulin Homo sapiens 56-63 12523500-2 2002 Defects in peripheral insulin action precede the development of glucose intolerance, as the pancreas compensates for insulin resistance by increasing insulin production and secretion. Glucose 64-71 insulin Homo sapiens 117-124 12898939-5 2002 The insulin resistance index showed significant correlations with fasting plasma insulin and glucose concentrations and HbA1C level in both groups. Glucose 93-100 insulin Homo sapiens 4-11 12898939-6 2002 In the group with normal glucose tolerance we showed significant correlations between insulin resistance index and anthropometric parameters (waist circumference, BMI, body weight, WHR). Glucose 25-32 insulin Homo sapiens 86-93 12440698-2 2002 Insulin-stimulated glucose uptake is primarily mediated by the transporter isoform GLUT4, which is predominantly expressed in mature skeletal muscle and fat tissues. Glucose 19-26 insulin Homo sapiens 0-7 11744037-1 2002 OBJECTIVES: The associations between hypertension, insulin resistance and glucose intolerance are poorly understood. Glucose 74-81 insulin Homo sapiens 51-58 11756319-4 2002 Metformin treatment increased insulin-stimulated whole-body glucose disposal rates by 20% (P < 0.05); the response to troglitazone was greater (44% increase, P < 0.01 vs. baseline, P < 0.05 vs. metformin). Glucose 60-67 insulin Homo sapiens 30-37 11756319-12 2002 We conclude that the ability of troglitazone to upregulate adipocyte glucose transport, GLUT4 expression, and insulin signaling can contribute to its greater effect on whole-body glucose disposal. Glucose 179-186 insulin Homo sapiens 110-117 11772913-18 2002 M/I, the amount of glucose metabolized per unit of plasma insulin (I), an index of insulin sensitivity, was 36% lower in women taking estrogen compared with matched women not on HRT (P < 0.05) and 28% lower in women taking estrogen plus progesterone compared with matched women not on HRT (P < 0.05). Glucose 19-26 insulin Homo sapiens 58-65 11845226-6 2002 Of importance for patient management, an assessment of fasting blood glucose and proinsulin values following overnight withdrawal of insulin administration one month after transplantation was a potent predictor of insulin independence, and could be used to decide patients who should have further islet preparations. Glucose 69-76 insulin Homo sapiens 133-140 11869298-5 2002 RESULTS: The codon 2488 polymorphism influenced fasting triglyceride levels, as well as insulin, as measured at 120 min in an oral glucose tolerance test. Glucose 131-138 insulin Homo sapiens 88-95 11869303-4 2002 At the SITT insulin sensitivity was measured from the slope of arterialized blood glucose concentrations determined for 16 min after an intravenous bolus injection of short-acting insulin, 0.1 U/kg body weight, and expressed as glucose disappearance rate (KITT). Glucose 82-89 insulin Homo sapiens 12-19 11874440-14 2002 Significant positive correlations were observed between the levels of plasma insulin and plasma glucose with plasma lipid peroxides. Glucose 96-103 insulin Homo sapiens 77-84 12396740-1 2002 This study was designed to determine plasma glucose and insulin levels after administration of three escalating doses of the oral insulin product hexyl-insulin monoconjugate 2 (HIM2) in fasting, insulin-deprived adult patients with type 1 diabetes. Glucose 44-51 insulin Homo sapiens 130-137 12396740-1 2002 This study was designed to determine plasma glucose and insulin levels after administration of three escalating doses of the oral insulin product hexyl-insulin monoconjugate 2 (HIM2) in fasting, insulin-deprived adult patients with type 1 diabetes. Glucose 44-51 insulin Homo sapiens 130-137 12396740-1 2002 This study was designed to determine plasma glucose and insulin levels after administration of three escalating doses of the oral insulin product hexyl-insulin monoconjugate 2 (HIM2) in fasting, insulin-deprived adult patients with type 1 diabetes. Glucose 44-51 insulin Homo sapiens 130-137 12396740-14 2002 Also, plasma glucose area under the concentration-time curves (AUCs) were inversely correlated with plasma insulin AUCs. Glucose 13-20 insulin Homo sapiens 107-114 12396740-16 2002 Thus, HIM2 prevented the expected rise in plasma glucose concentrations in insulin-deprived adult patients with type 1 diabetes. Glucose 49-56 insulin Homo sapiens 75-82 12396742-9 2002 Insulin bioavailability from the transdermal Biphasix-insulin patches was 21.5 +/- 6.9% (mean +/- SEM, n = 13) based on serum insulin and 39.5 +/- 8.5% (mean +/- SEM, n = 25) based on the pharmacodynamic blood glucose-lowering effects. Glucose 210-217 insulin Homo sapiens 0-7 12396742-10 2002 The Biphasix system successfully delivered insulin transdermally, as evidenced by a significant sustained decrease in blood glucose in diabetic rats, with a corresponding increase in serum insulin. Glucose 124-131 insulin Homo sapiens 43-50 11945115-9 2002 A rise in serum insulin (fasting, or post-glucose load) was reported in all studies in which it was measured. Glucose 42-49 insulin Homo sapiens 16-23 11779602-0 2002 Menopause-related differences in inflammation markers and their relationship to body fat distribution and insulin-stimulated glucose disposal. Glucose 125-132 insulin Homo sapiens 106-113 11779602-1 2002 OBJECTIVE: To determine whether postmenopausal status is associated with elevated plasma inflammation markers compared to premenopausal status, and how this explains differences in fat distribution and insulin-stimulated glucose disposal. Glucose 221-228 insulin Homo sapiens 202-209 11779602-8 2002 Insulin-stimulated glucose disposal was measured by euglycemic clamp. Glucose 19-26 insulin Homo sapiens 0-7 11779602-12 2002 The CRP was related to intraabdominal fat only in postmenopausal women and was negatively related to insulin-stimulated glucose disposal in both premenopausal and postmenopausal women. Glucose 120-127 insulin Homo sapiens 101-108 11779602-15 2002 Higher CRP is associated with lower insulin-stimulated glucose disposal in both premenopausal and postmenopausal women. Glucose 55-62 insulin Homo sapiens 36-43 12566751-7 2002 Insulin resistance prior to pregnancy, determined by continuous infusion of glucose with model assessment (CIGMA) test, did not further increase the frequency of GDM. Glucose 76-83 insulin Homo sapiens 0-7 11791142-1 2002 OBJECTIVE: To examine and compare in vitro basal and insulin-stimulated glucose uptake in human omental and subcutaneous adipose tissue derived from lean, overweight or obese individuals, and in those with central or peripheral obesity. Glucose 72-79 insulin Homo sapiens 53-60 11791152-1 2002 Insulin sensitivity and secretion in resulting subcategories of glucose tolerance. Glucose 64-71 insulin Homo sapiens 0-7 12560587-2 2002 Insulin resistance predisposes the development of glucose intolerance, hyperlipidemia, and hypertension; the cluster of these abnormalities is referred to as multiple risk factor syndrome and it increases the risk of atherosclerosis. Glucose 50-57 insulin Homo sapiens 0-7 16222593-1 2002 Insulin resistance of muscle has been attributed to impairment of elements of insulin signaling, glucose transport, and/or metabolism within the muscle cells. Glucose 97-104 insulin Homo sapiens 0-7 16222593-2 2002 This article explores the notion that a component of insulin resistance in vivo may result from impaired hemodynamic effects of this hormone to facilitate access to the muscle cells for itself and other nutrients, including glucose. Glucose 224-231 insulin Homo sapiens 53-60 16222593-5 2002 This microvascular effect of insulin correlates closely with muscle glucose uptake, is independent of increases in bulk blood flow, and is impaired in obese insulin-resistant patients. Glucose 68-75 insulin Homo sapiens 29-36 11781146-1 2002 Long-term exposure of the pancreatic beta cells to free fatty acid (FFA) reportedly inhibits glucose-stimulated insulin secretion. Glucose 93-100 insulin Homo sapiens 112-119 11781146-9 2002 The malic enzyme inhibitor alone inhibited insulin response to glucose. Glucose 63-70 insulin Homo sapiens 43-50 11781146-10 2002 In conclusion, long-term exposure of FFA to beta cells inhibits glucose-stimulated insulin secretion via the decreased NADPH contents due to the inhibition of pyruvate carboxylase and malate pyruvate shuttle flux. Glucose 64-71 insulin Homo sapiens 83-90 14727995-11 2002 Thiazolidinediones, a new class of compound for treating patients with type 2 DM, primarily exert their glucose-lowering effect by increasing insulin sensitivity at the level of skeletal muscle, and to a lesser extent, at the liver by decreasing hepatic glucose output. Glucose 104-111 insulin Homo sapiens 142-149 11739076-5 2002 Direct interactions between resident raft proteins (caveolins and flotillin-1) and insulin-signaling molecules may organize these molecules in space and time to ensure faithful transduction of the insulin signal, at least with respect to the glucose-dependent actions of insulin in adipocytes. Glucose 242-249 insulin Homo sapiens 83-90 11739076-5 2002 Direct interactions between resident raft proteins (caveolins and flotillin-1) and insulin-signaling molecules may organize these molecules in space and time to ensure faithful transduction of the insulin signal, at least with respect to the glucose-dependent actions of insulin in adipocytes. Glucose 242-249 insulin Homo sapiens 197-204 11739076-5 2002 Direct interactions between resident raft proteins (caveolins and flotillin-1) and insulin-signaling molecules may organize these molecules in space and time to ensure faithful transduction of the insulin signal, at least with respect to the glucose-dependent actions of insulin in adipocytes. Glucose 242-249 insulin Homo sapiens 197-204 11788478-7 2002 Insulin action on glucose metabolism was 69% lower in the obese subjects (1.6+/-0.2 mg. kg(-1). Glucose 18-25 insulin Homo sapiens 0-7 12102644-4 2002 This disease is a disorder of glucose homeostasis, either due to the immune-mediated eradication of pancreatic beta cells in the islets of Langerhans (type 1 diabetes) or resulting from insulin resistance and obesity syndromes where the insulin-producing capability of the beta cell is ultimately exhausted in the face of insensitivity to the effects of insulin in the peripheral glucose-utilising tissues (type 2 diabetes). Glucose 30-37 insulin Homo sapiens 186-193 12102644-4 2002 This disease is a disorder of glucose homeostasis, either due to the immune-mediated eradication of pancreatic beta cells in the islets of Langerhans (type 1 diabetes) or resulting from insulin resistance and obesity syndromes where the insulin-producing capability of the beta cell is ultimately exhausted in the face of insensitivity to the effects of insulin in the peripheral glucose-utilising tissues (type 2 diabetes). Glucose 30-37 insulin Homo sapiens 237-244 12102644-4 2002 This disease is a disorder of glucose homeostasis, either due to the immune-mediated eradication of pancreatic beta cells in the islets of Langerhans (type 1 diabetes) or resulting from insulin resistance and obesity syndromes where the insulin-producing capability of the beta cell is ultimately exhausted in the face of insensitivity to the effects of insulin in the peripheral glucose-utilising tissues (type 2 diabetes). Glucose 30-37 insulin Homo sapiens 237-244 12403642-11 2002 As with insulin lispro itself, the rapid action of insulin lispro within the insulin lispro mixtures also results in a smaller increase in blood glucose levels after meals than with comparable human insulin mixtures. Glucose 145-152 insulin Homo sapiens 51-58 12403642-11 2002 As with insulin lispro itself, the rapid action of insulin lispro within the insulin lispro mixtures also results in a smaller increase in blood glucose levels after meals than with comparable human insulin mixtures. Glucose 145-152 insulin Homo sapiens 51-58 12403642-11 2002 As with insulin lispro itself, the rapid action of insulin lispro within the insulin lispro mixtures also results in a smaller increase in blood glucose levels after meals than with comparable human insulin mixtures. Glucose 145-152 insulin Homo sapiens 51-58 12365818-4 2002 These demonstrate faster absorption and reach higher concentrations after s.c. injection compared to conventional human insulin and this more physiological action reduces post-prandial glucose to a greater extent. Glucose 185-192 insulin Homo sapiens 120-127 11756334-10 2002 We conclude that lipid deprivation selectively depletes intramyocellular lipid stores and induces a normal metabolic state (in terms of insulin-mediated whole-body glucose disposal, intracellular insulin signaling, and circulating leptin levels) despite a persistent excess of total body fat mass. Glucose 164-171 insulin Homo sapiens 136-143 11843950-2 2002 Syndrome X--a cluster of abnormalities associated with resistance to insulin-mediated glucose uptake that have been implicated in accelerating atherogenesis--provides a useful clinical concept to prevent CHD in patients with type 2 diabetes. Glucose 86-93 insulin Homo sapiens 69-76 11921426-10 2002 Insulin glargine is a peakless insulin and studies in both type 1 and type 2 diabetic patients indicate that glargine improves fasting blood glucose control and reduces the incidence of nocturnal hypoglycaemia. Glucose 141-148 insulin Homo sapiens 0-7 11921427-3 2002 NOBEX has applied this technology to insulin, creating an orally absorbed, bioactive conjugate which is safe and rapidly absorbed and which demonstrates dose-dependent, glucose-lowering effects in animal models, healthy volunteers and type 1 diabetic patients. Glucose 169-176 insulin Homo sapiens 37-44 11921428-8 2002 A simplified means for prandial insulin delivery, such as that offered by this technique, will significantly reduce the incidence of key complications by allowing increased patient compliance for consistent drug administration in order to regulate patients" blood glucose levels. Glucose 264-271 insulin Homo sapiens 32-39 12079619-2 2002 Preliminary studies have shown inhaled insulin to be effective in lowering blood glucose and HbA(1c) levels. Glucose 81-88 insulin Homo sapiens 39-46 12079621-2 2002 Among the barriers to achieving tight long-term glycemic control with insulin in both type 1 and type 2 diabetes are an increased risk of hypoglycemia, undesired weight gain, and a failure to normalize postprandial hyperglycemia and excessive unpredictable diurnal glucose fluctuations. Glucose 265-272 insulin Homo sapiens 70-77 12079621-4 2002 Preclinical studies indicate that amylin acts as a neuroendocrine hormone that complements the effects of insulin in postprandial glucose regulation by suppressing postprandial glucagon secretion and slowing the rate of nutrient delivery from the stomach to the small intestine. Glucose 130-137 insulin Homo sapiens 106-113 12450449-2 2002 In pancreatic beta cells, it is linked to the transduction mechanism that mediates glucose-stimulated insulin secretion. Glucose 83-90 insulin Homo sapiens 102-109 12450450-15 2002 In a glucose-clamp study with healthy subjects the inhalation of an identical insulin dose on three study days led to an intra-individual variability that was comparable to that after s.c. injection of regular insulin. Glucose 5-12 insulin Homo sapiens 78-85 12450450-16 2002 In a dose-response study with patients with type 1 diabetes the intra-individual CV was 34% for the area under the curve of the glucose infusion rate for 0-10 h. Studies with patients with type 2 diabetes have shown that the intra-individual CVs were within the range seen after s.c. insulin administration or even lower. Glucose 128-135 insulin Homo sapiens 284-291 12215068-6 2002 Biphasic insulin aspart [30% soluble (rapid-acting) and 70% protamine-bound insulin aspart (BIAsp30)] generally provided significantly better postprandial glucose control than a similar mixture of biphasic regular human insulin (BHI30) in a randomised, nonblind trial in patients with type 1 or 2 diabetes mellitus. Glucose 155-162 insulin Homo sapiens 9-16 11979022-3 2002 The continuous glucose monitoring system offers a new option for tailoring treatment with insulin analogues to achieve optimal glycaemia. Glucose 15-22 insulin Homo sapiens 90-97 11979031-8 2002 Currently, glucose sensors are mainly used as glycaemic holters to help in the management of insulin therapy. Glucose 11-18 insulin Homo sapiens 93-100 12006718-3 2002 A fasting serum glucose (mg/dl) to plasma insulin (microU/ml) ratio (FGIR) of < 7 was recently suggested as a screening tool for IR in certain pediatric patients. Glucose 16-23 insulin Homo sapiens 42-49 11900279-1 2002 In this review we discuss the biological significance of D-chiro-inositol, originally discovered as a component of a putative mediator of intracellular insulin action, where as a putative mediator, it accelerates the dephosphorylation of glycogen synthase and pyruvate dehydrogenase, rate limiting enzymes of non-oxidative and oxidative glucose disposal. Glucose 337-344 insulin Homo sapiens 152-159 11891852-0 2002 Nigericin inhibits insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 38-45 insulin Homo sapiens 19-26 11891852-2 2002 Our results showed that nigericin increased basal but decreased insulin-stimulated glucose uptake in a time- and dose-dependent manner. Glucose 83-90 insulin Homo sapiens 64-71 11815271-3 2002 However, this approach has been hampered by the absence of (1) an appropriate glucose-sensing system to regulate insulin gene transcription; (2) enzymes that process proinsulin to insulin; and (3) glucose-regulatable exocytosis in the target cells. Glucose 197-204 insulin Homo sapiens 169-176 11815271-4 2002 Recent attempts to solve these problems have sought new methods for effective gene transfer and have addressed issues such as the expression and release of insulin in response to the physiological stimulus of glucose, the production of biologically active insulin, and the selection of an ideal target cell for the expression of the insulin gene. Glucose 209-216 insulin Homo sapiens 156-163 11788626-7 2002 After adjustment for age, sex, C-peptide concentration, per cent body fat, and waist circumference, proinsulin was found to be significantly elevated in diabetic subjects, relative to subjects with both impaired and normal glucose tolerance (both P < 0.0001); and the concentration in those with IGT was higher, compared with normals (P < 0.0001). Glucose 223-230 insulin Homo sapiens 100-110 11788637-9 2002 The insulin sensitivity index, glucose effectiveness, and acute insulin response to glucose, derived from the insulin-modified, frequently sampled, iv glucose tolerance test using the Bergman minimal model, did not change significantly at any dose. Glucose 84-91 insulin Homo sapiens 64-71 11788637-9 2002 The insulin sensitivity index, glucose effectiveness, and acute insulin response to glucose, derived from the insulin-modified, frequently sampled, iv glucose tolerance test using the Bergman minimal model, did not change significantly at any dose. Glucose 84-91 insulin Homo sapiens 64-71 11788637-9 2002 The insulin sensitivity index, glucose effectiveness, and acute insulin response to glucose, derived from the insulin-modified, frequently sampled, iv glucose tolerance test using the Bergman minimal model, did not change significantly at any dose. Glucose 84-91 insulin Homo sapiens 64-71 11788637-9 2002 The insulin sensitivity index, glucose effectiveness, and acute insulin response to glucose, derived from the insulin-modified, frequently sampled, iv glucose tolerance test using the Bergman minimal model, did not change significantly at any dose. Glucose 84-91 insulin Homo sapiens 64-71 11788647-0 2002 Associations of glucose control with insulin sensitivity and pancreatic beta-cell responsiveness in newly presenting type 2 diabetes. Glucose 16-23 insulin Homo sapiens 37-44 11788647-5 2002 All measures of pancreatic beta-cell responsiveness (M(0), M(I), and first-phase insulin secretion) were negatively correlated with fasting plasma glucose (P < 0.01) and positively correlated with fasting plasma insulin (FPI) and insulin responses to MTT (P < 0.05). Glucose 147-154 insulin Homo sapiens 81-88 11788647-10 2002 Indices of insulin sensitivity and pancreatic beta-cell responsiveness explain fasting glucose and HbA(1C) well but fail to explain postprandial glucose. Glucose 87-94 insulin Homo sapiens 11-18 11788649-9 2002 Analysis of single human islets showed that enhanced insulin secretion by increased glucose concentrations in the perfusate is achieved by enhancing insulin pulse mass with no change in pulse frequency. Glucose 84-91 insulin Homo sapiens 53-60 11788649-9 2002 Analysis of single human islets showed that enhanced insulin secretion by increased glucose concentrations in the perfusate is achieved by enhancing insulin pulse mass with no change in pulse frequency. Glucose 84-91 insulin Homo sapiens 149-156 11788651-2 2002 A NEFA-induced defect in the activation of PI3K, which plays a key role in insulin"s stimulation of glucose transport, has been invoked. Glucose 100-107 insulin Homo sapiens 75-82 11788651-7 2002 Elevated plasma NEFA reduced whole-body insulin-stimulated glucose disposal by 24% (42.1 +/- 4.0 vs. 54.8 +/- 3.6 micromol/kg x min; P < 0.001). Glucose 59-66 insulin Homo sapiens 40-47 11788651-13 2002 The percentage reduction in PI3K activation correlated with the reduction in insulin-stimulated glucose disappearance rate that was induced by elevated NEFA (r = 0.70; P < 0.05). Glucose 96-103 insulin Homo sapiens 77-84 11788655-2 2002 Insulin-stimulated glucose uptake was decreased both in the diabetic and nondiabetic twin, compared with healthy control subjects (5.2 +/- 0.7 and 8.5 +/- 0.8 vs. 11.4 +/- 0.9 mg/kg x min(-1); P < 0.01 and P < 0.02, respectively). Glucose 19-26 insulin Homo sapiens 0-7 11786383-9 2002 Saquinavir increased the basal glucose transport threefold and decreased insulin-stimulated glucose transport by 35%. Glucose 92-99 insulin Homo sapiens 73-80 11872362-1 2002 Hypertriglyceridemia and reduced plasma levels of high-density lipoprotein cholesterol (HDL-c) are the most frequent forms of dyslipidemia observed in insulin-resistant states, such as obesity, impaired fasting glucose, and Type 2 diabetes, and are highly atherogenic in these settings. Glucose 211-218 insulin Homo sapiens 151-158 11872372-1 2002 High concentrations of glucose induce insulin resistance, impair insulin secretion, and affect hepatic glucose production in a manner that mirrors Type 2 diabetes, and hexosamines mimic many of these effects. Glucose 23-30 insulin Homo sapiens 38-45 11872375-4 2002 Indeed, insulin resistant states, which by definition, exhibit diminished insulin-mediated glucose uptake into peripheral tissues also display impaired insulin mediated vasodilation as well as impaired endothelium dependent vasolidation to the muscarinic receptor agonist acetylcholine. Glucose 91-98 insulin Homo sapiens 8-15 11872375-4 2002 Indeed, insulin resistant states, which by definition, exhibit diminished insulin-mediated glucose uptake into peripheral tissues also display impaired insulin mediated vasodilation as well as impaired endothelium dependent vasolidation to the muscarinic receptor agonist acetylcholine. Glucose 91-98 insulin Homo sapiens 74-81 12674774-1 2002 The insulin sensitivity in hypertensive patients with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (DM) and the insulin resistance (IR) under the disorder of glucose metabolism and hypertension were studied. Glucose 61-68 insulin Homo sapiens 4-11 11822582-14 2002 The apparently normal serum C-peptide levels measured after glucagon challenge in these children with type 2 DM reflect their higher glucose levels. Glucose 133-140 insulin Homo sapiens 28-37 11884763-6 2002 MAIN OUTCOME MEASURES: A classification plot which introduces two discriminant parameters for the C-peptide suppression test: the ratio of [blood glucose]/[C-peptide] at the lowest C-peptide concentration and mean glycemia during insulin infusion. Glucose 146-153 insulin Homo sapiens 98-107 12518533-3 2002 On base of insulin response to stimulation by glucose (alpha index of stimulation) we have classified the patients in three groups: I group--index of stimulation > or = 2.5; II group--index of stimulation < or = 2.5 > 1.5; III group--index of stimulation < 1.5. Glucose 46-53 insulin Homo sapiens 11-18 12518533-5 2002 After six-month treatment by medicaments selected on base of endogenous insulin reserves and BMI, the considerable fall has been achieved of medium values of glucose on empty stomach, postprandial glucose, HbA1C, triglycerides, HDL-cholesterol (p < 0.0001), total cholesterol, systolic blood pressure and diastolic blood pressure (p < 0.05) in relation to the values of these parameters of metabolic checking before the start of therapy. Glucose 158-165 insulin Homo sapiens 72-79 11782867-0 2002 Improvement of glucose tolerance by nateglinide occurs through enhancement of early phase insulin secretion. Glucose 15-22 insulin Homo sapiens 90-97 11782882-0 2002 Relative contribution of insulin sensitivity and beta-cell function to plasma glucose and insulin concentrations during the oral glucose tolerance test. Glucose 78-85 insulin Homo sapiens 25-32 11782882-1 2002 Plasma glucose and insulin concentrations have been used in genetic studies as quantitative phenotypic traits and also as surrogates for insulin sensitivity and beta-cell function. Glucose 7-14 insulin Homo sapiens 137-144 11782882-3 2002 We examined how insulin sensitivity and beta-cell function affected plasma glucose and insulin concentrations during the oral glucose tolerance test (OGTT). Glucose 75-82 insulin Homo sapiens 16-23 12425238-1 2002 OBJECTIVES: Despite evidence documenting their ineffectiveness, sliding scale insulin is a commonly used regimen for glucose management for hospitalized patients with diabetes mellitus. Glucose 117-124 insulin Homo sapiens 78-85 12425238-2 2002 At the Veterans Affairs Puget Sound Medical Center, where computer order entry has been mandated, we tested the hypothesis that an evidence-based minimal intervention order (supplemental insulin only when fasting serum glucoses exceeded 400 mg/dl) would decrease the use of sliding scale insulin orders. Glucose 219-227 insulin Homo sapiens 187-194 12372963-4 2002 Insulin sensitivity were assessed by homeostasis model assessment of insulin resistance (HOMA-IR) and plasma glucose and insulin concentrations obtained at fasting or during a 75-gram oral glucose tolerance test (insulin sensitivity index), and pancreatic beta-cell function were assessed by insulinogenic index, first-phase insulin secretion index, and area under the response curve for plasma insulin (insulin-AUC(0-180)). Glucose 109-116 insulin Homo sapiens 0-7 12372963-4 2002 Insulin sensitivity were assessed by homeostasis model assessment of insulin resistance (HOMA-IR) and plasma glucose and insulin concentrations obtained at fasting or during a 75-gram oral glucose tolerance test (insulin sensitivity index), and pancreatic beta-cell function were assessed by insulinogenic index, first-phase insulin secretion index, and area under the response curve for plasma insulin (insulin-AUC(0-180)). Glucose 189-196 insulin Homo sapiens 0-7 12401936-3 2002 Once an urgent situation has being handled with intravenous push of a 10% calcium salt, the initiation of short-term measures can be launched by either a single or combined regimen of the three agents that cause a transcellular shift of potassium - insulin with glucose, beta(2)-agonist (albuterol), and NaHCO(3). Glucose 262-269 insulin Homo sapiens 249-256 11855690-8 2002 The glucose intolerance of ageing may be due, in part, to decreased insulin sensitivity of pancreatic / cells to insulinotropic gut hormones (GLP1/GIP) and in part to alterations of hepatic glucose production. Glucose 4-11 insulin Homo sapiens 68-75 11849582-7 2002 The insulin : glucose ratio was 1.6 (normal < 0.4). Glucose 14-21 insulin Homo sapiens 4-11 11966407-4 2002 TZD lower blood glucose levels, partly by influencing glucose transporters and the insulin-signaling pathway. Glucose 16-23 insulin Homo sapiens 83-90 12036379-5 2002 As a consequence of insulin resistance, type 2 diabetes is characterised by decreased glucose transport and utilisation at the level of muscle and adipose tissue and increased glucose production by the liver. Glucose 86-93 insulin Homo sapiens 20-27 12071295-5 2002 We evaluated the metabolic clearance rate of glucose (MCR(G), ml x kg(-1) x min(-1)) as the most important indicator of insulin action by isoglycemic clamp. Glucose 45-52 insulin Homo sapiens 120-127 12071295-7 2002 We found following predictors of insulin resistance expressed in the relationship with MCR(G): BMI (r = -0.68, p<0.001), plasma glucose concentration (r = -0.66, p<0.001), cholesterol (r=-0.55, p<0.001), triglycerides (r = -0.54, p<0.001) and mean blood pressure (r = -0.38, p<0.01). Glucose 131-138 insulin Homo sapiens 33-40 12071296-6 2002 Steady-state plasma glucose concentrations at the end of the test period provided a quantitative measure of insulin resistance. Glucose 20-27 insulin Homo sapiens 108-115 12071296-10 2002 Subjects with the highest tertile of steady-state plasma glucose showed a significantly higher body mass index, blood pressure, fasting plasma triglyceride levels, plasminogen activator inhibitor-1 and lower HDL-cholesterol, i.e. an insulin resistance pattern. Glucose 57-64 insulin Homo sapiens 233-240 12511185-9 2002 The mean sum of insulin needed to metabolize the same glucose load correlated positively with tErMg (r=0.545, p<0.01) and bErMg (r=0.560, p<0.01) in the IR patients. Glucose 54-61 insulin Homo sapiens 16-23 12812310-4 2002 This leads to reduced sensitivity to insulin in the periphery in stimulating peripheral glucose uptake and to increased resistance to insulin"s ability to suppress gluconeogenesis. Glucose 88-95 insulin Homo sapiens 37-44 12812310-5 2002 Furthermore growth hormone excess leads to mobilization of free fatty acids which inhibit insulin stimulated glucose oxidation by acting as a competitive energy source thus leading to further worsening of insulin resistance. Glucose 109-116 insulin Homo sapiens 90-97 12812310-5 2002 Furthermore growth hormone excess leads to mobilization of free fatty acids which inhibit insulin stimulated glucose oxidation by acting as a competitive energy source thus leading to further worsening of insulin resistance. Glucose 109-116 insulin Homo sapiens 205-212 12715715-8 2002 RESULTS: Homozygous and heterozygous carriers of the A allele in position -308 of the TNF-alpha gene promoter showed higher plasma insulin levels at 120 min OGTT versus GG carriers (44.77 microliters/ml; SD 40.4 vs. 26.82; SD 19.9; p = 0.04) and a higher ratio of the 30 min increment in insulin to the 30 min increment in glucose (35.4; SD 21.5 vs. 22.6: SD 21.5; p = 0.03). Glucose 323-330 insulin Homo sapiens 131-138 12391573-12 2002 The parameter relating to insulin-assisted glucose disposal, S*i, was found to be the same in the two techniques, but this was not the case for the non-insulin-dependent parameter S*g. Glucose 43-50 insulin Homo sapiens 26-33 11792882-4 2002 RESULTS: The rate of glucose disappearance after insulin administration (k(ITT)) fell from 3.6%/min before the epidural to 1.9%/min 24 h afterwards (P=0.001) and returned to pretreatment values by 1 week. Glucose 21-28 insulin Homo sapiens 49-56 11941902-6 2002 Insulin resistance based on the homeostasis model assessment (HOMA) was calculated as: [fasting insulin (microU/ml) x fasting glucose (mmol/l)]: 22.5. Glucose 126-133 insulin Homo sapiens 0-7 11843026-7 2002 Simultaneously, insulin-stimulated glucose transport and glycogen synthesis in skeletal muscle were analyzed in vitro. Glucose 35-42 insulin Homo sapiens 16-23 12448933-0 2002 Insulin lispro improves postprandial glucose control in patients with diabetes mellitus. Glucose 37-44 insulin Homo sapiens 0-7 12448933-8 2002 Therapy with insulin lispro was therefore associated with a significant improvement in postprandial blood glucose excursion control when compared with regular human insulin, without an increase in rate of hypoglycaemia. Glucose 106-113 insulin Homo sapiens 13-20 12476925-7 2002 Insulin sensitivity as assessed by the amount of infused glucose and its ratio to insulin was enhanced by Intralipid after an overnight fast, but was decreased after a 58 h fast. Glucose 57-64 insulin Homo sapiens 0-7 12564620-4 2002 The oral glucose tolerance test (OGTT) for estimating insulin sensitivity and secretion is increasingly used, e.g. in intervention trials. Glucose 9-16 insulin Homo sapiens 54-61 11839071-3 2002 Clinical investigations with 18F-deoxy-glucose, combined with other radiotracers of the myocardium"s substrate metabolism, showed the dependency of the heart"s substrate selection on circulating levels of glucose, free fatty acid and insulin, and the operation of Randle"s cycle in the human myocardium. Glucose 39-46 insulin Homo sapiens 234-241 15460663-4 2002 After the alcohol is metabolised, hepatic insulin sensitivity is increased, leading to the restoration of glycogen stores and reduction in blood glucose levels, and 4. consequently, after several hours, glycogen stores and insulin sensitivity return to normal. Glucose 145-152 insulin Homo sapiens 42-49 15460748-1 2002 The Minimal Model method of determining Insulin Sensitivity from the Intravenous glucose Tolerance Test is a valuable tool for the Diabetes research community. Glucose 81-88 insulin Homo sapiens 40-47 15765621-5 2002 Fasting plasma glucose and fasting blood glucose levels generally improved to a greater extent in patients with type 1 diabetes mellitus receiving insulin glargine than patients who administered Neutral Protamine Hagedorn (NPH) insulin. Glucose 15-22 insulin Homo sapiens 147-154 12043244-1 2002 AIM: To clarify informative value of secretory ability of pancreatic beta-cells and correspondence of insulin values to glycemia in the course of standard glucose tolerance test (GTT) in detection of insulin-resistance in patients with arterial hypertension (AH) to verify metabolic syndrome (MS). Glucose 155-162 insulin Homo sapiens 200-207 12683326-2 2002 Glucose exerts its effects on virtually all of the steps of insulin production: transcription of insulin gene, mRNA stability, translation, proinsulin processing, and insulin release via a highly regulated secretory pathway. Glucose 0-7 insulin Homo sapiens 60-67 12683326-2 2002 Glucose exerts its effects on virtually all of the steps of insulin production: transcription of insulin gene, mRNA stability, translation, proinsulin processing, and insulin release via a highly regulated secretory pathway. Glucose 0-7 insulin Homo sapiens 97-104 15765621-5 2002 Fasting plasma glucose and fasting blood glucose levels generally improved to a greater extent in patients with type 1 diabetes mellitus receiving insulin glargine than patients who administered Neutral Protamine Hagedorn (NPH) insulin. Glucose 41-48 insulin Homo sapiens 147-154 12683326-2 2002 Glucose exerts its effects on virtually all of the steps of insulin production: transcription of insulin gene, mRNA stability, translation, proinsulin processing, and insulin release via a highly regulated secretory pathway. Glucose 0-7 insulin Homo sapiens 140-150 11728659-4 2001 Insulin resistance and glucose tolerance were determined by measuring insulin and glucose concentrations following a 75 g oral glucose tolerance test (OGTT). Glucose 82-89 insulin Homo sapiens 0-7 12683326-2 2002 Glucose exerts its effects on virtually all of the steps of insulin production: transcription of insulin gene, mRNA stability, translation, proinsulin processing, and insulin release via a highly regulated secretory pathway. Glucose 0-7 insulin Homo sapiens 97-104 12683326-8 2002 The attempts to reproduce regulated glucose-dependent transcription of insulin gene in transduced cells could not reproduce so far the same complex and refined regulation of insulin production and release as that provided by B cells. Glucose 36-43 insulin Homo sapiens 71-78 12715356-14 2002 Peripheral insulin resistance is central to this process by limiting insulin-mediated glucose uptake in skeletal muscles. Glucose 86-93 insulin Homo sapiens 11-18 12715356-14 2002 Peripheral insulin resistance is central to this process by limiting insulin-mediated glucose uptake in skeletal muscles. Glucose 86-93 insulin Homo sapiens 69-76 11598110-8 2001 Preventing oxidant generation with DPI also blocked insulin-stimulated glucose uptake and GLUT4 translocation to the plasma membrane, providing further evidence for an oxidant signal in the regulation of the distal insulin-signaling cascade. Glucose 71-78 insulin Homo sapiens 52-59 11598110-10 2001 Overall, these data provide insight into the physiological role of insulin-dependent H(2)O(2) generation, which is not only involved in the regulation of tyrosine phosphorylation events in the early insulin signaling cascade but also has important effects on the regulation of downstream insulin signaling, involving the activation of PI 3"-kinase, Akt, and ultimately cellular glucose transport in response to insulin. Glucose 378-385 insulin Homo sapiens 67-74 11741341-6 2001 Compared to the C rats, the F rats had a clearly reduced insulin-stimulated glucose transport. Glucose 76-83 insulin Homo sapiens 57-64 11728659-4 2001 Insulin resistance and glucose tolerance were determined by measuring insulin and glucose concentrations following a 75 g oral glucose tolerance test (OGTT). Glucose 82-89 insulin Homo sapiens 0-7 11598141-2 2001 Recent evidence suggests that the full stimulation of glucose uptake by insulin also requires activation of GLUT4, possibly via a p38 mitogen-activated protein kinase (p38 MAPK)-dependent pathway. Glucose 54-61 insulin Homo sapiens 72-79 11742415-3 2001 Emerging knowledge of key pathogenic mechanisms, such as the impairment of glucose-stimulated insulin secretion and the role of "lipotoxicity" as a probable cause of hepatic and muscle resistance to insulin"s effects on glucose metabolism, has led to a host of new molecular drug targets. Glucose 75-82 insulin Homo sapiens 94-101 11742415-3 2001 Emerging knowledge of key pathogenic mechanisms, such as the impairment of glucose-stimulated insulin secretion and the role of "lipotoxicity" as a probable cause of hepatic and muscle resistance to insulin"s effects on glucose metabolism, has led to a host of new molecular drug targets. Glucose 220-227 insulin Homo sapiens 199-206 11598141-5 2001 Wortmannin inhibited insulin-stimulated glucose uptake with an IC(50) of 3 nm. Glucose 40-47 insulin Homo sapiens 21-28 11598141-7 2001 This dissociation between insulin-stimulated glucose uptake and GLUT4myc translocation was not observed with LY294002 (IC(50) = 8 and 10 microm, respectively). Glucose 45-52 insulin Homo sapiens 26-33 11742860-3 2001 Thiazolidinediones (TZDs) are oral insulin sensitizers in broad clinical use that enhance insulin-stimulated glucose uptake into skeletal muscle. Glucose 109-116 insulin Homo sapiens 35-42 11701435-4 2001 Cardiomyocytes were cultured with the ketone body beta-hydroxybutyrate (beta-OHB) for 4 or 16 h, and insulin-stimulated glucose uptake was evaluated. Glucose 120-127 insulin Homo sapiens 101-108 11701435-5 2001 Although short-term exposure to ketone bodies was not associated with any change in insulin action, our data demonstrated that preincubation with beta-OHB for 16 h markedly reduced insulin-stimulated glucose uptake in cardiomyocytes. Glucose 200-207 insulin Homo sapiens 181-188 11701439-1 2001 The interaction of insulin with metformin on muscle glucose metabolism was examined in the perfused rat hindquarter. Glucose 52-59 insulin Homo sapiens 19-26 11701439-9 2001 This increases interstitial insulin (and, in a closed system, perfusate insulin), which acts on cell surface receptors to increase glucose uptake. Glucose 131-138 insulin Homo sapiens 28-35 11701440-1 2001 Insulin stimulates muscle and adipose tissue to absorb glucose through a signaling cascade that is incompletely understood. Glucose 55-62 insulin Homo sapiens 0-7 11701440-2 2001 Insulin resistance, the inability of insulin to appropriately stimulate glucose uptake, is a hallmark of type 2 diabetes mellitus. Glucose 72-79 insulin Homo sapiens 0-7 11701440-6 2001 Adipocytes isolated from insulin-resistant male mice display 65% less insulin-stimulated glucose uptake compared with insulin-sensitive female mice. Glucose 89-96 insulin Homo sapiens 25-32 11701440-6 2001 Adipocytes isolated from insulin-resistant male mice display 65% less insulin-stimulated glucose uptake compared with insulin-sensitive female mice. Glucose 89-96 insulin Homo sapiens 70-77 11701440-6 2001 Adipocytes isolated from insulin-resistant male mice display 65% less insulin-stimulated glucose uptake compared with insulin-sensitive female mice. Glucose 89-96 insulin Homo sapiens 70-77 11719335-4 2001 Their insulin response to an oral glucose tolerance test was assessed. Glucose 34-41 insulin Homo sapiens 6-13 11742884-10 2001 The association between insulin resistance and coronary calcification persists with impaired glucose tolerance and normal fasting serum glucose. Glucose 93-100 insulin Homo sapiens 24-31 11742886-5 2001 The areas under the curve for insulin and glucose during the oral glucose tolerance test were also decreased. Glucose 66-73 insulin Homo sapiens 30-37 11742860-3 2001 Thiazolidinediones (TZDs) are oral insulin sensitizers in broad clinical use that enhance insulin-stimulated glucose uptake into skeletal muscle. Glucose 109-116 insulin Homo sapiens 90-97 11843389-7 2001 Insulin resistance was indirectly assessed by the insulin and glucose concentrations and diet-induced thermogenesis. Glucose 62-69 insulin Homo sapiens 0-7 11723050-1 2001 Despite intensive study, the relation between insulin"s action on blood flow and glucose metabolism remains unclear. Glucose 81-88 insulin Homo sapiens 46-53 11723050-15 2001 In protocol 1 subjects, insulin increased muscle glucose uptake (180%, P < 0.05) and MBV (54%, P < 0.01) and decreased MFV (-42%, P = 0.07) in the absence of significant changes in total forearm blood flow. Glucose 49-56 insulin Homo sapiens 24-31 11723050-16 2001 In protocol 2 subjects, insulin increased glucose uptake (220%, P < 0.01) and microvascular volume (45%, P < 0.05) with an associated moderate increase in total forearm blood flow (P < 0.05). Glucose 42-49 insulin Homo sapiens 24-31 11723077-12 2001 CONCLUSIONS: These results suggest that 1) the majority of non-insulin-treated type 2 diabetic patients have exaggerated plasma/blood glucose excursions with meals, and many of them have higher-than-recommended glucose concentrations 2 h after the meals; 2) plasma/blood glucose levels throughout the day are not as strongly interrelated as one might believe; and 3) HbA(1c) is more related to preprandial than postprandial plasma/blood glucose levels. Glucose 134-141 insulin Homo sapiens 63-70 11723077-12 2001 CONCLUSIONS: These results suggest that 1) the majority of non-insulin-treated type 2 diabetic patients have exaggerated plasma/blood glucose excursions with meals, and many of them have higher-than-recommended glucose concentrations 2 h after the meals; 2) plasma/blood glucose levels throughout the day are not as strongly interrelated as one might believe; and 3) HbA(1c) is more related to preprandial than postprandial plasma/blood glucose levels. Glucose 211-218 insulin Homo sapiens 63-70 11723077-12 2001 CONCLUSIONS: These results suggest that 1) the majority of non-insulin-treated type 2 diabetic patients have exaggerated plasma/blood glucose excursions with meals, and many of them have higher-than-recommended glucose concentrations 2 h after the meals; 2) plasma/blood glucose levels throughout the day are not as strongly interrelated as one might believe; and 3) HbA(1c) is more related to preprandial than postprandial plasma/blood glucose levels. Glucose 211-218 insulin Homo sapiens 63-70 11723077-12 2001 CONCLUSIONS: These results suggest that 1) the majority of non-insulin-treated type 2 diabetic patients have exaggerated plasma/blood glucose excursions with meals, and many of them have higher-than-recommended glucose concentrations 2 h after the meals; 2) plasma/blood glucose levels throughout the day are not as strongly interrelated as one might believe; and 3) HbA(1c) is more related to preprandial than postprandial plasma/blood glucose levels. Glucose 211-218 insulin Homo sapiens 63-70 11733106-1 2001 Insulin resistance syndrome (IRS) is a cluster of prevalent conditions including glucose intolerance, hypertension and dyslipidemia, which commonly predispose to cardiovascular disease. Glucose 81-88 insulin Homo sapiens 0-7 11903420-1 2001 AIM: The effect of the angiotensin II receptor antagonist losartan on renal haemodynamics and insulin-mediated glucose disposal was examined in normotensive, normoalbuminuric type 1 diabetic patients using a double-blind, placebo-controlled, cross-over design. Glucose 111-118 insulin Homo sapiens 94-101 11903420-8 2001 However, the glucose oxidation rate increased significantly after losartan vs. placebo in the basal state (1.72 +/- 0.34 vs. 1.33 +/- 0.18, mg/kg/min, p < 0.01) and during insulin stimulation (2.89 +/- 0.75 vs. 2.40 +/- 0.62 mg/kg/min, p < 0.03). Glucose 13-20 insulin Homo sapiens 175-182 11903420-9 2001 Basal and insulin-stimulated non-oxidative glucose disposal tended to decrease after losartan; however, this was not significant. Glucose 43-50 insulin Homo sapiens 10-17 11903420-12 2001 CONCLUSIONS: Losartan reduces blood pressure, glomerular hyperfiltration and FF, and improves basal and insulin-stimulated glucose oxidation in normotensive, normoalbuminuric type 1 diabetic patients. Glucose 123-130 insulin Homo sapiens 104-111 11727406-16 2001 Intraperitoneal insulin delivery systems hold considerable promise in type 2 diabetes because of their more physiologic delivery of insulin and their ability to inhibit hepatic glucose production selectively, with less peripheral insulinemia than with subcutaneous insulin injections. Glucose 177-184 insulin Homo sapiens 16-23 11793017-2 2001 We hypothesized that insulin response to glucose-insulin-potassium infusion might lead to vasodilation in ischemia/reperfusion (I/R). Glucose 41-48 insulin Homo sapiens 21-28 11793017-2 2001 We hypothesized that insulin response to glucose-insulin-potassium infusion might lead to vasodilation in ischemia/reperfusion (I/R). Glucose 41-48 insulin Homo sapiens 49-56 11793017-5 2001 METHODS: The control (I/R), glucose-insulin-potassium groups with and without dipyridamole were treated with saline, 300 g/l, 50 U/l insulin and 80 meq/l KCl infused at 0.2 ml. Glucose 28-35 insulin Homo sapiens 36-43 11793017-11 2001 Adhering leukocytes to venules decreased by 56 and 86 % while platelets adhering to microvessels was reduced by 52 and 72 % at reperfusion in glucose-insulin-potassium groups with and without dipyridamole, respectively. Glucose 142-149 insulin Homo sapiens 150-157 11720897-8 2001 Insulin sensitivity was assessed by an intravenous glucose tolerance test using the minimal model approach. Glucose 51-58 insulin Homo sapiens 0-7 11743131-12 2001 Transcription of the leptin gene and leptin secretion are regulated by insulin-mediated increases of glucose utilization and appear to require aerobic metabolism of glucose beyond pyruvate. Glucose 101-108 insulin Homo sapiens 71-78 11787271-6 2001 The coexistence of obesity and family history of diabetes provoked a decrease in the basal insulin levels as well as in the insulin response to glucose. Glucose 144-151 insulin Homo sapiens 124-131 11895076-1 2001 Insulin has a marked effect to stimulate the transport and metabolism of glucose in skeletal muscle in healthy individuals, whereas an impaired response, termed insulin resistance, is a major risk factor for diabetes mellitus and other metabolic diseases. Glucose 73-80 insulin Homo sapiens 0-7 11895076-2 2001 Studies of the molecular physiology of insulin action in skeletal muscle indicate that a principal loci of control resides within the proximal steps of glucose transport and phosphorylation. Glucose 152-159 insulin Homo sapiens 39-46 11895076-3 2001 Deoxyglucose, the metabolism of which is limited to these proximal steps, is widely used for in vitro studies of insulin action on glucose transport. Glucose 5-12 insulin Homo sapiens 113-120 11739448-5 2001 In diabetic muscle cells, the final responsiveness of glucose uptake was greatest for IGF-I and equivalent for human insulin and insulin glargine; sensitivities were the same as those for nondiabetic cells. Glucose 54-61 insulin Homo sapiens 117-145 11739444-5 2001 Acipimox increased insulin-stimulated total glucose uptake by 36% (P = 0.021) compared with placebo, which mainly was due to a 47% (P = 0.015) increase in glucose oxidation. Glucose 44-51 insulin Homo sapiens 19-26 11739446-6 2001 Both nateglinide and glyburide enhanced glucose-induced insulin release, compared with placebo (area under the curve -15-300 min: nateglinide 23,595 +/- 11,212 pM/min, glyburide 54,556 +/- 15,253 pM/min, placebo 10,242 +/- 2,414 pM/min). Glucose 40-47 insulin Homo sapiens 56-63 11739446-9 2001 The enhancement of insulin release by glyburide resulted in a lower minimal glucose concentration with glyburide (3.8 +/- 0.2 mM), compared with nateglinide (5.0 +/- 0.2 mM) and placebo (5.9 +/- 0.2 mM). Glucose 76-83 insulin Homo sapiens 19-26 11735085-0 2001 Magnesium reduces insulin-stimulated glucose uptake and serum lipid concentrations in type 1 diabetes. Glucose 37-44 insulin Homo sapiens 18-25 11735085-6 2001 Insulin-stimulated glucose uptake decreased by 35% after 24 weeks of oral MgO supplementation. Glucose 19-26 insulin Homo sapiens 0-7 11735085-10 2001 Mg repletion was associated with a decrease in atherogenic lipid fractions and a reduced insulin-stimulated glucose uptake. Glucose 108-115 insulin Homo sapiens 89-96 11890977-1 2001 Insulin secretion from pancreatic islet beta-cells is a tightly regulated process, under the close control of blood glucose concentrations, and several hormones and neurotransmitters. Glucose 116-123 insulin Homo sapiens 0-7 11890977-2 2001 Defects in glucose-triggered insulin secretion are ultimately responsible for the development of type II diabetes, a condition in which the total beta-cell mass is essentially unaltered, but beta-cells become progressively "glucose blind" and unable to meet the enhanced demand for insulin resulting for peripheral insulin resistance. Glucose 11-18 insulin Homo sapiens 29-36 11890977-2 2001 Defects in glucose-triggered insulin secretion are ultimately responsible for the development of type II diabetes, a condition in which the total beta-cell mass is essentially unaltered, but beta-cells become progressively "glucose blind" and unable to meet the enhanced demand for insulin resulting for peripheral insulin resistance. Glucose 11-18 insulin Homo sapiens 282-289 11890977-2 2001 Defects in glucose-triggered insulin secretion are ultimately responsible for the development of type II diabetes, a condition in which the total beta-cell mass is essentially unaltered, but beta-cells become progressively "glucose blind" and unable to meet the enhanced demand for insulin resulting for peripheral insulin resistance. Glucose 11-18 insulin Homo sapiens 282-289 11890977-2 2001 Defects in glucose-triggered insulin secretion are ultimately responsible for the development of type II diabetes, a condition in which the total beta-cell mass is essentially unaltered, but beta-cells become progressively "glucose blind" and unable to meet the enhanced demand for insulin resulting for peripheral insulin resistance. Glucose 224-231 insulin Homo sapiens 29-36 11778914-4 2001 The capacity of extremely low birth weight infants to oxidize glucose at higher rates, and the positive effect that insulin may have in glucose utilization and tolerance, support the use of insulin in the prevention and treatment of hyperglycemia. Glucose 62-69 insulin Homo sapiens 190-197 11778914-4 2001 The capacity of extremely low birth weight infants to oxidize glucose at higher rates, and the positive effect that insulin may have in glucose utilization and tolerance, support the use of insulin in the prevention and treatment of hyperglycemia. Glucose 136-143 insulin Homo sapiens 116-123 11546805-1 2001 The insulin and the endothelin type A (ETA) receptor both can couple into the heterotrimeric G protein alpha(q/11) (Galpha(q/11)), leading to Galpha(q/11) tyrosine phosphorylation, phosphatidylinositol 3-kinase activation, and subsequent stimulation of glucose transport. Glucose 253-260 insulin Homo sapiens 4-11 11684928-2 2001 This is associated with insulin resistance concerning glucose uptake. Glucose 54-61 insulin Homo sapiens 24-31 11684928-9 2001 RESULTS: At post-absorptive insulin concentrations, glucose production was 47% higher in HIV+LD than controls (P = 0.025). Glucose 52-59 insulin Homo sapiens 28-35 11687655-1 2001 Insulin stimulates glucose transport by promoting translocation of the insulin-sensitive glucose transporter isoform 4 (GLUT4) from an intracellular compartment to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 11710784-6 2001 This association was modulated by insulin resistance status, measured by the homeostasis model assessment of insulin resistance (HOMA IR) using fasting insulin and glucose. Glucose 164-171 insulin Homo sapiens 34-41 11710784-6 2001 This association was modulated by insulin resistance status, measured by the homeostasis model assessment of insulin resistance (HOMA IR) using fasting insulin and glucose. Glucose 164-171 insulin Homo sapiens 109-116 11710784-6 2001 This association was modulated by insulin resistance status, measured by the homeostasis model assessment of insulin resistance (HOMA IR) using fasting insulin and glucose. Glucose 164-171 insulin Homo sapiens 109-116 11591239-1 2001 The efficacy of insulin in stimulating whole-body glucose disposal (insulin sensitivity) was quantified using direct methodology in thirty lacto-ovo vegetarians and in thirty meat-eaters. Glucose 50-57 insulin Homo sapiens 16-23 11591239-1 2001 The efficacy of insulin in stimulating whole-body glucose disposal (insulin sensitivity) was quantified using direct methodology in thirty lacto-ovo vegetarians and in thirty meat-eaters. Glucose 50-57 insulin Homo sapiens 68-75 11678825-5 2001 Insulin sensitivity was estimated from fasting glucose and insulin levels using the homeostasis model. Glucose 47-54 insulin Homo sapiens 0-7 11574396-4 2001 In particular, insulin is normally secreted in a well-regulated fashion in rapid response to the metabolic needs of the individual and most specifically (but not exclusively) to changes in circulating levels of glucose. Glucose 211-218 insulin Homo sapiens 15-22 11574399-0 2001 The effect of insulin on in vivo cerebral glucose concentrations and rates of glucose transport/metabolism in humans. Glucose 42-49 insulin Homo sapiens 14-21 11574399-3 2001 In this study, we sought to directly examine the effect of insulin on glucose concentrations and rates of glucose transport/metabolism in human brain using (1)H-magnetic resonance spectroscopy at 4 Tesla. Glucose 70-77 insulin Homo sapiens 59-66 11574399-3 2001 In this study, we sought to directly examine the effect of insulin on glucose concentrations and rates of glucose transport/metabolism in human brain using (1)H-magnetic resonance spectroscopy at 4 Tesla. Glucose 106-113 insulin Homo sapiens 59-66 11574399-11 2001 These data support the hypothesis that the majority of cerebral glucose uptake/metabolism is an insulin-independent process in humans. Glucose 64-71 insulin Homo sapiens 96-103 11574419-1 2001 The purpose of this investigation was to examine the effect of caffeine (an adenosine receptor antagonist) on whole-body insulin-mediated glucose disposal in resting humans. Glucose 138-145 insulin Homo sapiens 121-128 11574430-0 2001 Insulin and glucose excursion following premeal insulin lispro or repaglinide in cystic fibrosis-related diabetes. Glucose 12-19 insulin Homo sapiens 48-55 11574430-1 2001 OBJECTIVE: Insulin and glucose levels in response to premeal insulin lispro or repaglinide were evaluated in adult patients with cystic fibrosis-related diabetes (CFRD) without fasting hyperglycemia. Glucose 23-30 insulin Homo sapiens 61-68 11776473-6 2001 These insulin-producing cells normalize blood glucose when transplanted into streptozotocin-diabetic mice. Glucose 46-53 insulin Homo sapiens 6-13 11737223-1 2001 BACKGROUND: It is unclear if insulin-mediated vasodilatation is altered by ageing and if this affects insulin-mediated glucose uptake. Glucose 119-126 insulin Homo sapiens 102-109 11600540-2 2001 Excellent methods exist for the assessment of insulin sensitivity in the laboratory setting, such as the glucose clamp. Glucose 105-112 insulin Homo sapiens 46-53 11679606-12 2001 Since insulin receptor substrate-1 is expressed both in the spinal ligament and in the tissues regulating glucose metabolism, we speculate that some other molecules related to insulin signaling that are impaired only in the tissues regulating glucose metabolism may be responsible for the progression of ossification. Glucose 106-113 insulin Homo sapiens 6-13 11679606-12 2001 Since insulin receptor substrate-1 is expressed both in the spinal ligament and in the tissues regulating glucose metabolism, we speculate that some other molecules related to insulin signaling that are impaired only in the tissues regulating glucose metabolism may be responsible for the progression of ossification. Glucose 243-250 insulin Homo sapiens 6-13 11679606-15 2001 This study may serve as a stimulus for evaluation of the use of various drugs that may improve the response to insulin in the tissues regulating glucose metabolism to prevent the progression of ossification. Glucose 145-152 insulin Homo sapiens 111-118 11891852-9 2002 Taken together, it appears that nigericin may inhibit insulin-stimulated glucose transport mainly by interfering with GLUT4 translocation, probably by a mechanism not related to changes in cytosolic pH. Glucose 73-80 insulin Homo sapiens 54-61 11735096-5 2001 In diabetics, the metabolic clearance rates of glucose at both insulin levels (MCR(glu)submax and MCR(glu)max) were significantly reduced compared with HS (MCR(glu)submax DMN, 5.35 +/- 2.7 mL x kg(-1) x min(-1), DMH, 5.38 +/- 2.17 mL x kg(-1) x min(-1); DMD, 5.48 +/- 2.35 mL x kg(-1) x min(-1) v HS, 10.9 +/- 3.3 mL x kg(-1) x min(-1); P <.01; MCR(glu)max DMN, 13.3 +/- 3.3 mL x kg(-1) x min(-1); DMH, 12.5 +/- 3.0 mL x kg(-1) x min(-1); DMD, 13.3 +/- 3.0 mL x kg(-1) x min(-1) v HS, 17.4 +/- 3.8 mL x kg(-1) x min(-1); P <.05). Glucose 47-54 insulin Homo sapiens 63-70 11890977-3 2001 At present, the mechanisms by which glucose (and other nutrients including certain amino acids) trigger insulin secretion in healthy individuals are understood only in part. Glucose 36-43 insulin Homo sapiens 104-111 11890977-6 2001 However, recent data indicate that glucose also enhances insulin secretion through mechanisms which do not involve a change in K(ATP) channel activity, and seem likely to underlie the second, sustained phase of glucose-stimulated insulin secretion. Glucose 35-42 insulin Homo sapiens 57-64 11890977-6 2001 However, recent data indicate that glucose also enhances insulin secretion through mechanisms which do not involve a change in K(ATP) channel activity, and seem likely to underlie the second, sustained phase of glucose-stimulated insulin secretion. Glucose 35-42 insulin Homo sapiens 230-237 11890977-6 2001 However, recent data indicate that glucose also enhances insulin secretion through mechanisms which do not involve a change in K(ATP) channel activity, and seem likely to underlie the second, sustained phase of glucose-stimulated insulin secretion. Glucose 211-218 insulin Homo sapiens 230-237 11743060-10 2001 Weight loss after bariatric surgery induced an improvement in metabolic fitness, related to the reduction in insulin resistance over a range of glucose tolerance statuses from normal to diabetic. Glucose 144-151 insulin Homo sapiens 109-116 15016187-3 2001 Although routine insulin injections can provide diabetic patients their daily insulin requirements, non-compliance commonly results in blood glucose excursions that eventually lead to microvascular and macrovascular complications and early death. Glucose 141-148 insulin Homo sapiens 17-24 11701342-5 2001 However, to achieve adequately regulated insulin production in response to changes in blood glucose concentrations remains a major hurdle. Glucose 92-99 insulin Homo sapiens 41-48 11571289-0 2001 Nocodazole inhibits insulin-stimulated glucose transport in 3T3-L1 adipocytes via a microtubule-independent mechanism. Glucose 39-46 insulin Homo sapiens 20-27 11571289-1 2001 Insulin stimulates glucose transport in adipocytes and muscle cells by triggering redistribution of the GLUT4 glucose transporter from an intracellular perinuclear location to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 11571289-2 2001 Recent reports have shown that the microtubule-depolymerizing agent nocodazole inhibits insulin-stimulated glucose transport, implicating an important role for microtubules in this process. Glucose 107-114 insulin Homo sapiens 88-95 11571289-5 2001 Consistent with previous studies, higher concentrations of nocodazole (10-33 microm) significantly inhibited basal and insulin-stimulated glucose uptake in adipocytes. Glucose 138-145 insulin Homo sapiens 119-126 11571289-7 2001 Despite the decrease in insulin-stimulated glucose transport with 33 microm nocodazole we did not observe inhibition of insulin-stimulated GLUT4 translocation to the cell surface under these conditions. Glucose 43-50 insulin Homo sapiens 24-31 11779345-5 2001 The effect of PIs on insulin-induced lipogenesis was monitored by [(14)C)]glucose incorporation into lipids, which was suppressed by 21-86% in a concentration-dependent manner. Glucose 74-81 insulin Homo sapiens 21-28 11697884-1 2001 Insulin increases glucose transport into cells of target tissues, primarily striated muscle and adipose. Glucose 18-25 insulin Homo sapiens 0-7 11707743-10 2001 After 7 days (and even after only 2 days) of coculture with baboon (n=8) or human (n=18) PBMCs, basal and glucose-stimulated insulin secretions from PICs were almost completely abolished (P<0.0001). Glucose 106-113 insulin Homo sapiens 125-132 11684928-12 2001 Consequently, insulin-stimulated total glucose disposal was lower in HIV+LD patients (P = 0.006). Glucose 39-46 insulin Homo sapiens 14-21 11684928-16 2001 Moreover, both the ability of insulin to suppress endogenous glucose production and lipolysis, and to stimulate peripheral glucose uptake and its metabolic pathways is reduced, indicating severe resistance concerning multiple effects of insulin. Glucose 61-68 insulin Homo sapiens 30-37 11687655-1 2001 Insulin stimulates glucose transport by promoting translocation of the insulin-sensitive glucose transporter isoform 4 (GLUT4) from an intracellular compartment to the cell surface. Glucose 19-26 insulin Homo sapiens 71-78 11689258-0 2001 Modulated insulin delivery from glucose-sensitive hydrogel dosage forms. Glucose 32-39 insulin Homo sapiens 10-17 11689258-6 2001 Insulin release through the glucose-sensitive hydrogel membrane and from the glucose-sensitive hydrogel matrix was dependent on the glucose concentration in the receptor chamber. Glucose 28-35 insulin Homo sapiens 0-7 11689258-6 2001 Insulin release through the glucose-sensitive hydrogel membrane and from the glucose-sensitive hydrogel matrix was dependent on the glucose concentration in the receptor chamber. Glucose 77-84 insulin Homo sapiens 0-7 11689258-6 2001 Insulin release through the glucose-sensitive hydrogel membrane and from the glucose-sensitive hydrogel matrix was dependent on the glucose concentration in the receptor chamber. Glucose 77-84 insulin Homo sapiens 0-7 11689258-8 2001 The insulin release rate decreased as the glucose concentration was reduced to 1 mg/ml. Glucose 42-49 insulin Homo sapiens 4-11 11689258-9 2001 Modulated insulin release was achieved using the glucose-sensitive membrane and matrix systems. Glucose 49-56 insulin Homo sapiens 10-17 11794168-2 2001 Whether the normalization of blood glucose levels with insulin therapy improves the prognosis for such patients is not known. Glucose 35-42 insulin Homo sapiens 55-62 11696371-2 2001 These changes in protein expression were associated with a marked inhibition of insulin-stimulated glucose transport. Glucose 99-106 insulin Homo sapiens 80-87 11684526-2 2001 Studies have shown that plasma concentrations of remnant lipoproteins (RLPs) are elevated in patients with CAD and that increases in plasma RLP concentrations may be related to variations in insulin-mediated glucose disposal. Glucose 208-215 insulin Homo sapiens 191-198 11684526-6 2001 RESULTS: By selection, insulin-resistant women had higher steady state plasma glucose concentrations than did insulin-sensitive women (10.8 +/- 0.5 compared with 4.1 +/- 5 mmol/L, respectively; P < 0.001), associated with higher fasting triacylglycerol (1.58 +/- 0.04 compared with 1.00 +/- 0.03 mmol/L; P = 0.01) and lower HDL-cholesterol (1.06 +/- 0.08 compared with 1.34 +/- 0.05; P = 0.01) concentrations. Glucose 78-85 insulin Homo sapiens 23-30 11595666-0 2001 Chronic exposure to high leucine impairs glucose-induced insulin release by lowering the ATP-to-ADP ratio. Glucose 41-48 insulin Homo sapiens 57-64 11595666-1 2001 Exposure of rat pancreatic islets to 20 mM leucine for 24 h reduced insulin release in response to glucose (16.7 and 22.2 mM). Glucose 99-106 insulin Homo sapiens 68-75 11595666-5 2001 Also, the ATP-sensitive K(+) channel-independent pathway of glucose-stimulated insulin release, studied in the presence of 30 mM K(+) and 250 microM diazoxide, was normal. Glucose 60-67 insulin Homo sapiens 79-86 11595666-8 2001 In conclusion, prolonged exposure of pancreatic islets to high leucine levels selectively impairs glucose-induced insulin release. Glucose 98-105 insulin Homo sapiens 114-121 11724088-5 2001 Euglycemic clamp study demonstrated insulin resistance manifested by a glucose disposal rate of approximately 55% of mean normal values. Glucose 71-78 insulin Homo sapiens 36-43 11797687-3 2001 The need for alternatives to continuous immunosuppression, and an unlimited source of glucose-sensitive, insulin-secreting tissue, is emerging. Glucose 86-93 insulin Homo sapiens 105-112 11561895-10 2001 After 5 months implantation, insulin was infused into the devices from external pumps and rapid insulin absorption was observed in conjunction with dramatic lowering of blood glucose levels. Glucose 175-182 insulin Homo sapiens 29-36 11672439-0 2001 GLUT4 translocation precedes the stimulation of glucose uptake by insulin in muscle cells: potential activation of GLUT4 via p38 mitogen-activated protein kinase. Glucose 48-55 insulin Homo sapiens 66-73 11672439-1 2001 We previously reported that SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), attenuates insulin-stimulated glucose uptake without altering GLUT4 translocation. Glucose 133-140 insulin Homo sapiens 114-121 11672439-5 2001 This segregation of glucose uptake from GLUT4 translocation became more apparent when the two parameters were measured at 22 degrees C. Preincubation with the p38 MAPK inhibitors SB202190 and SB203580 reduced insulin-stimulated transport of either 2-deoxyglucose or 3-O-methylglucose by 40-60%. Glucose 20-27 insulin Homo sapiens 209-216 11672439-10 2001 These results suggest that activation of GLUT4 follows GLUT4 translocation and that both mechanisms contribute to the full stimulation of glucose uptake by insulin. Glucose 138-145 insulin Homo sapiens 156-163 11703405-9 2001 With weekly doses to the mother, there is restricted fetal growth, delayed myelination of the central nervous system, altered blood pressure soon after birth and increased insulin response to glucose challenge in early adulthood. Glucose 192-199 insulin Homo sapiens 172-179 11703405-11 2001 Increased insulin response to glucose challenge occurs in early adulthood with glucocorticoid by either route and is independent of growth restriction. Glucose 30-37 insulin Homo sapiens 10-17 11640998-0 2001 Use of the insulin sensitivity index obtained from oral glucose tolerance test in Japanese subjects. Glucose 56-63 insulin Homo sapiens 11-18 11679435-1 2001 Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. Glucose 63-70 insulin Homo sapiens 41-48 11679435-3 2001 A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4. Glucose 84-91 insulin Homo sapiens 65-72 11679436-4 2001 The FH(+) group had decreased insulin-stimulated glucose disposal (6.64 +/- 0.52 vs. 8.45 +/- 0.54 mg. kg(-1) fat-free mass. Glucose 49-56 insulin Homo sapiens 30-37 11679438-6 2001 Moreover, whole-body, as well as skeletal muscle, insulin-mediated glucose uptake did not differ between LPL-overexpressing and wild-type mice. Glucose 67-74 insulin Homo sapiens 50-57 11679448-2 2001 Therefore, we tested the hypothesis that short-term (4 weeks) moderate energy restriction (-750 kcal/day) would result in a significant increase in insulin-stimulated glucose disposal (40 mU x m(-2) x min(-1) hyperinsulinemic-euglycemic clamp) in moderately overweight postmenopausal women and that when combined with resistance training (RT) an even greater effect would be seen. Glucose 167-174 insulin Homo sapiens 148-155 11679463-0 2001 Effect of glucagon-like peptide 1 on non-insulin-mediated glucose uptake in the elderly patient with diabetes. Glucose 58-65 insulin Homo sapiens 41-48 11679463-1 2001 An important cause of elevated glucose levels in elderly patients with diabetes is an alteration in non-insulin-mediated glucose uptake (NIMGU). Glucose 31-38 insulin Homo sapiens 104-111 11679463-1 2001 An important cause of elevated glucose levels in elderly patients with diabetes is an alteration in non-insulin-mediated glucose uptake (NIMGU). Glucose 121-128 insulin Homo sapiens 104-111 11679468-5 2001 Insulin secretion during the OGTT was determined by (I(30 min) - I(0 min))/(G(30 min) - G(0 min)) and during the FSIGT by the acute insulin response to glucose (AIRg). Glucose 152-159 insulin Homo sapiens 0-7 11679468-5 2001 Insulin secretion during the OGTT was determined by (I(30 min) - I(0 min))/(G(30 min) - G(0 min)) and during the FSIGT by the acute insulin response to glucose (AIRg). Glucose 152-159 insulin Homo sapiens 132-139 11719829-1 2001 AIMS/HYPOTHESIS: We have shown previously that the increase of plasma non-esterified fatty acids for 48 h results in decreased glucose-stimulated insulin secretion in lean and non-diabetic obese subjects. Glucose 127-134 insulin Homo sapiens 146-153 11719836-9 2001 In addition, there was an inverse correlation between the mean glucose of the steady state plasma glucose period and logarithmic values of basal (r = -0.34; p = 0.003) and insulin stimulated glucose uptake in monocytes (r = -0.32; p = 0.006). Glucose 63-70 insulin Homo sapiens 172-179 11719836-9 2001 In addition, there was an inverse correlation between the mean glucose of the steady state plasma glucose period and logarithmic values of basal (r = -0.34; p = 0.003) and insulin stimulated glucose uptake in monocytes (r = -0.32; p = 0.006). Glucose 98-105 insulin Homo sapiens 172-179 11719836-9 2001 In addition, there was an inverse correlation between the mean glucose of the steady state plasma glucose period and logarithmic values of basal (r = -0.34; p = 0.003) and insulin stimulated glucose uptake in monocytes (r = -0.32; p = 0.006). Glucose 98-105 insulin Homo sapiens 172-179 11757080-6 2001 Insulin resistance (HOMA-IR) was calculated using the fasting plasma insulin and glucose values. Glucose 81-88 insulin Homo sapiens 0-7 11910982-9 2001 Glucose--insulin--potassium infusion in acute myocardial infarction leads to a significant reduction in the mortality relative risk in diabetic patients (ECLA and DIGAMI studies). Glucose 0-7 insulin Homo sapiens 9-16 11704136-6 2001 MAIN OUTCOME MEASURE(S): Insulin sensitivity by steady-state plasma glucose technique; serum androgens, progesterone, and hCG; and pelvic ultrasound images. Glucose 68-75 insulin Homo sapiens 25-32 11825324-3 2001 Pharmacodynamic studies have demonstrated a prolonged metabolic profile without a pronounced peak and with a duration of action of 20 - 30 h. In clinical studies in people with Type 1 and Type 2 diabetes, insulin glargine has demonstrated improved pre-breakfast blood glucose control and a reduction in the frequency of hypoglycaemia, especially nocturnal hypoglycaemia, in comparison with neutral protamine hagedorn (NPH) insulin. Glucose 268-275 insulin Homo sapiens 205-212 11733868-4 2001 Our aim was to evaluate whether this stimulatory effect on glucose production is solely attributable to inhibition of insulin secretion. Glucose 59-66 insulin Homo sapiens 118-125 11733868-6 2001 Endogenous glucose production was measured 3 hours after the start of the somatostatin, insulin and glucagon infusion, for 4 hours after administration of placebo/indomethacin, by primed, continuous infusion of [6,6-(2)H(2)] glucose. Glucose 11-18 insulin Homo sapiens 88-95 11733868-13 2001 We conclude that indomethacin stimulates endogenous glucose production in patients with type 2 diabetes mellitus by inhibition of insulin secretion. Glucose 52-59 insulin Homo sapiens 130-137 11684113-8 2001 The fasting insulin and testosterone levels were significantly higher in DM than IGT and normal glucose tolerance (NGT) subgroups. Glucose 96-103 insulin Homo sapiens 12-19 11701689-7 2001 A blunted decrease in the AgI was significantly associated with a low rate of insulin-stimulated glucose uptake, but not with the other actions of insulin. Glucose 97-104 insulin Homo sapiens 78-85 11701689-11 2001 It is correlated with insulin stimulation of glucose uptake and is blunted by known causes of insulin resistance, including overall and abdominal obesity. Glucose 45-52 insulin Homo sapiens 22-29 11701703-12 2001 Endogenous glucose production in the fasting state was also unchanged following GH (11.8 +/- 0.7 vs.12.3 +/- 0.9 micromol/kg x min, P = 0.5) and suppressed to a similar extent following insulin (4.4 +/- 0.8 vs. 5.5 +/- 0.8 micromol/kg x min, P = 0.3). Glucose 11-18 insulin Homo sapiens 186-193 11701721-1 2001 Insulin resistance in type 2 diabetes is due to impaired stimulation of the glucose transport system in muscle and fat. Glucose 76-83 insulin Homo sapiens 0-7 11701731-0 2001 Evidence for spatial heterogeneity in insulin- and exercise-induced increases in glucose uptake: studies in normal subjects and patients with type 1 diabetes. Glucose 81-88 insulin Homo sapiens 38-45 11701731-5 2001 At rest insulin-stimulated glucose uptake was significantly lower in the type 1 diabetic patients (42 +/- 7 micromol/kg per min) than in the normal subjects (78 +/- 9 micromol/kg per min, P < 0.001), while muscle blood flows were similar (26 +/- 1 vs. 31 +/- 3 ml/kg muscle per min, respectively). Glucose 27-34 insulin Homo sapiens 8-15 11701731-7 2001 Heterogeneity of glucose uptake but not of blood flow was greater in the insulin-resistant type 1 diabetic patients both at rest (RD(g) 31 +/- 1 vs. 25 +/- 2%, patients with type 1 diabetes vs. normal subjects, P < 0.05) and during exercise, compared with normal subjects (27 +/- 1 vs. 21 +/- 2%, respectively, P < 0.05). Glucose 17-24 insulin Homo sapiens 73-80 11701731-9 2001 Heterogeneity of RD(g), was inversely associated with total glucose uptake (r = -0.54, P < 0.001, pooled data) and was highest in the most insulin-resistant patients. Glucose 60-67 insulin Homo sapiens 142-149 11712861-6 2001 The cytokines had no adverse effect for the first six days on insulin secretion, content and mRNA levels of the HEP G2ins/g cells and insulin secretion in response to 1-h exposure to 20 mM glucose was enhanced 14-fold. Glucose 189-196 insulin Homo sapiens 134-141 11868861-0 2001 Comparison of aminophylline and insulin-dextrose infusions in acute therapy of hyperkalemia in end-stage renal disease patients. Glucose 40-48 insulin Homo sapiens 32-39 11868861-1 2001 OBJECTIVE: This study was performed to compare the efficacy of aminophylline and insulin-dextrose infusion as acute treatment modality of hyperkalemia in patients with end-stage renal disease (ESRD). Glucose 89-97 insulin Homo sapiens 81-88 11868861-7 2001 Whereas, intravenous infusion of insulin-dextrose decreased plasma potassium from 6.59 +/- 0.31 mEq/L to 5.76 +/- 0.32 mEq/L (p < 0.001 Vs basal) and 5.84 +/- 0.21 mEq/L (p < 0.001 Vs basal). Glucose 41-49 insulin Homo sapiens 33-40 11868861-10 2001 There was one episode of hypoglycemia (blood sugar < 60 mg%) in insulin-dextrose infusion group. Glucose 75-83 insulin Homo sapiens 67-74 11682575-0 2001 Glucagon-like peptide-1 (7-37) augments insulin-mediated glucose uptake in elderly patients with diabetes. Glucose 57-64 insulin Homo sapiens 40-47 11682575-2 2001 It has also been proposed that a substantial component of the glucose-lowering effects of GLP-1 occurs because this hormone enhances insulin-mediated glucose disposal. Glucose 62-69 insulin Homo sapiens 133-140 11682575-2 2001 It has also been proposed that a substantial component of the glucose-lowering effects of GLP-1 occurs because this hormone enhances insulin-mediated glucose disposal. Glucose 150-157 insulin Homo sapiens 133-140 11682575-4 2001 This study determines the effect of GLP-1 on insulin-mediated glucose disposal in elderly patients with type 2 diabetes. Glucose 62-69 insulin Homo sapiens 45-52 11687922-0 2001 Insulin sensitivity with respect to glucose metabolism in hypertension-prone men did not predict the blood pressure increase in 5 years. Glucose 36-43 insulin Homo sapiens 0-7 11687922-1 2001 OBJECTIVES: To evaluate peripheral insulin stimulated glucose uptake as a predictor for increase in blood pressure in hypertension-prone men. Glucose 54-61 insulin Homo sapiens 35-42 11714847-1 2001 Free fatty acids released during triglyceride lipolysis play an important role in obesity-associated insulin resistance of glucose disposal. Glucose 123-130 insulin Homo sapiens 101-108 11713450-4 2001 Insulin sensitivity (M(lbm)) is defined as the amount of glucose required to maintain euglycemia (milligrams of glucose infused per kilogram lean body mass per minute). Glucose 57-64 insulin Homo sapiens 0-7 11713450-4 2001 Insulin sensitivity (M(lbm)) is defined as the amount of glucose required to maintain euglycemia (milligrams of glucose infused per kilogram lean body mass per minute). Glucose 112-119 insulin Homo sapiens 0-7 11740232-13 2001 The glucose/insulin ratio, an indirect index of insulin sensitivity, was significantly increased with IGF-1 treatment compared with placebo ( P < 0.02). Glucose 4-11 insulin Homo sapiens 48-55 11740232-16 2001 However, the glucose/insulin ratio was increased without changing blood glucose levels with IGF-1 treatment suggesting increased insulin sensitivity. Glucose 13-20 insulin Homo sapiens 129-136 11783602-25 2001 In conclusion, our findings seem to suggest that amelioration of blood glucose control is attained both by insulin and metformin intensive treatment, but only insulin decreases and maintains HbA1c levels below 7.5%. Glucose 71-78 insulin Homo sapiens 107-114 11712393-6 2001 Plasma insulin levels usually decrease together with plasma glucose. Glucose 60-67 insulin Homo sapiens 7-14 11712395-2 2001 The mechanisms why hepatic glucose production, muscle and adipose tissue glucose uptake, and hepatic glucose uptake after meal intake are regulated with subcutaneous insulin administration, should be clarified. Glucose 27-34 insulin Homo sapiens 166-173 11712395-2 2001 The mechanisms why hepatic glucose production, muscle and adipose tissue glucose uptake, and hepatic glucose uptake after meal intake are regulated with subcutaneous insulin administration, should be clarified. Glucose 73-80 insulin Homo sapiens 166-173 11712396-4 2001 Lys.Pro insulin and insulin aspart, rapid-acting insulin analogues, have demonstrated improved post-prandial glucose control in comparison with regular insulin, even although they are usually administered immediately prior to the meal. Glucose 109-116 insulin Homo sapiens 8-15 11712396-4 2001 Lys.Pro insulin and insulin aspart, rapid-acting insulin analogues, have demonstrated improved post-prandial glucose control in comparison with regular insulin, even although they are usually administered immediately prior to the meal. Glucose 109-116 insulin Homo sapiens 20-27 11712398-4 2001 Long-term multicenter, randomized, comparative, parallel, open-label study to diabetic patients of both type 1 and type 2 by multiple injection method showed that insulin lispro resulted in the significant improvement of 2 hour-postprandial blood glucose level 12 and 24 weeks after the initiation of treatment. Glucose 247-254 insulin Homo sapiens 163-170 11712399-3 2001 As a result, insulin aspart provides significantly better postprandial glucose control than human insulin. Glucose 71-78 insulin Homo sapiens 13-20 11712399-4 2001 As mealtime insulin in a basal-bolus regimen, insulin aspart gives stable 24-hour blood glucose control, with lower maximum glucose levels during daytime than with human insulin. Glucose 88-95 insulin Homo sapiens 46-53 11712399-4 2001 As mealtime insulin in a basal-bolus regimen, insulin aspart gives stable 24-hour blood glucose control, with lower maximum glucose levels during daytime than with human insulin. Glucose 88-95 insulin Homo sapiens 46-53 11712399-4 2001 As mealtime insulin in a basal-bolus regimen, insulin aspart gives stable 24-hour blood glucose control, with lower maximum glucose levels during daytime than with human insulin. Glucose 124-131 insulin Homo sapiens 46-53 11712399-4 2001 As mealtime insulin in a basal-bolus regimen, insulin aspart gives stable 24-hour blood glucose control, with lower maximum glucose levels during daytime than with human insulin. Glucose 124-131 insulin Homo sapiens 46-53 11712411-1 2001 Hyperglycemia in patients with type 2 diabetes mellitus is caused by peripheral insulin resistance, which results in decreased insulin-mediated glucose disposal and increased endogenous glucose production, and inadequate insulin secretion. Glucose 144-151 insulin Homo sapiens 80-87 11712411-1 2001 Hyperglycemia in patients with type 2 diabetes mellitus is caused by peripheral insulin resistance, which results in decreased insulin-mediated glucose disposal and increased endogenous glucose production, and inadequate insulin secretion. Glucose 144-151 insulin Homo sapiens 127-134 11712411-1 2001 Hyperglycemia in patients with type 2 diabetes mellitus is caused by peripheral insulin resistance, which results in decreased insulin-mediated glucose disposal and increased endogenous glucose production, and inadequate insulin secretion. Glucose 186-193 insulin Homo sapiens 80-87 11712411-3 2001 As clinical difference between biguanides and thiazolidinediones in reducing blood glucose, the former primarily lowers endogenous glucose production presumably at the level of liver, whereas the latter increases insulin-mediated peripheral glucose disposal, which occurs predominantly in skeletal muscle. Glucose 83-90 insulin Homo sapiens 213-220 11694699-0 2001 Insulin lispro lowers postprandial glucose in prepubertal children with diabetes. Glucose 35-42 insulin Homo sapiens 0-7 11694699-1 2001 OBJECTIVE: This study compared the glucose-lowering effect of insulin lispro, given before or after meals, with regular human insulin given before meals in prepubertal children with diabetes. Glucose 35-42 insulin Homo sapiens 62-69 11694699-6 2001 RESULTS: Treatment with insulin lispro before breakfast resulted in lower 2-hour postprandial glucose values than regular human insulin (11.7 +/- 4.4 mmol/L vs 15.0 +/- 5.4 mmol/L). Glucose 94-101 insulin Homo sapiens 24-31 11694699-7 2001 Similarly, insulin lispro given before dinner resulted in lower blood glucose values 2 hours postprandially (8.8 +/- 5.0 mmol/L vs 10.8 +/- 5.4 mmol/L) than regular human insulin. Glucose 70-77 insulin Homo sapiens 11-18 11694699-8 2001 When insulin lispro was administered after meals, the 2-hour glucose levels were between those seen with either insulin lispro or regular human insulin given before meals. Glucose 61-68 insulin Homo sapiens 5-12 11694699-10 2001 CONCLUSIONS: In prepubertal children, insulin lispro given before meals is safe and significantly lowers postprandial glucose levels after breakfast and dinner compared with regular human insulin, and insulin lispro given after the meal provides similar benefits as regular human insulin before the meal. Glucose 118-125 insulin Homo sapiens 38-45 11589968-0 2001 Spectroscopic and molecular dynamics simulation studies of the interaction of insulin with glucose. Glucose 91-98 insulin Homo sapiens 78-85 11589968-2 2001 CD spectra indicate that D-glucose interacts with monomeric insulin whereas D-galactose, D-mannose and 2-deoxy-D-glucose have a lower effect. Glucose 25-34 insulin Homo sapiens 60-67 11589968-5 2001 Transfer nuclear Overhauser enhancement NMR experiments indicate the existence of dipolar interactions at short interatomic distances between C-1 proton of D-glucose in the beta form and the monomeric insulin. Glucose 156-165 insulin Homo sapiens 201-208 11589968-8 2001 Molecular dynamics simulations and modeling studies, based on the dynamic fluctuations of potential binding moiety sidechains, argued from results of NMR spectroscopy, provide additional informations to locate the putative binding sites of D-glucose to insulin. Glucose 240-249 insulin Homo sapiens 253-260 11533044-7 2001 Thus, the characterization of the Akt1 knockout mice and its comparison to the previously reported Akt2 deficiency phenotype reveals the non-redundant functions of Akt1 and Akt2 genes with respect to organismal growth and insulin-regulated glucose metabolism. Glucose 240-247 insulin Homo sapiens 222-229 11590090-4 2001 The model of insulin metabolic syndrome used 12 measures assessing body mass, insulin, glucose, and lipid metabolism. Glucose 87-94 insulin Homo sapiens 13-20 11498541-3 2001 The involvement of this pathway in the regulation of insulin-stimulated glucose transport was investigated in the present study. Glucose 72-79 insulin Homo sapiens 53-60 11498541-4 2001 Acute exposure (1 h) to a balanced mixture of amino acids reduced insulin-stimulated glucose transport by as much as 55% in L6 muscle cells. Glucose 85-92 insulin Homo sapiens 66-73 11498541-11 2001 These results identify the mTOR/p70 S6 kinase signaling pathway as a novel modulator of insulin-stimulated glucose transport in skeletal muscle cells. Glucose 107-114 insulin Homo sapiens 88-95 11551849-9 2001 We propose that, in catabolic, postoperative patients, increased levels of insulin from exogenous or, possibly, endogenous sources (nutritionally induced) may be a signal to increase IGF-I bioavailability by increased expression of IGFBP-3-PA to counteract further deterioration in glucose metabolism. Glucose 282-289 insulin Homo sapiens 75-82 11574295-4 2001 The degree of decrease in plasma glucose following insulin injection was similar in both breeds at each stage of growth. Glucose 33-40 insulin Homo sapiens 51-58 11574405-2 2001 It also regulates the expression of the insulin gene in response to changes in glucose and insulin concentrations. Glucose 79-86 insulin Homo sapiens 40-47 11574412-1 2001 Stimulation of lipolysis and the induction of resistance to insulin"s actions on glucose metabolism are well-recognized effects of growth hormone (GH). Glucose 81-88 insulin Homo sapiens 60-67 11574412-8 2001 Insulin-stimulated rates of total glucose turnover were significantly lower with GH alone as compared with all other conditions (P = 0.004). Glucose 34-41 insulin Homo sapiens 0-7 11574412-9 2001 Insulin sensitivity as assessed by the M value (rate of glucose infusion) was reduced with GH alone as compared with all other conditions (M value in mg. kg(-1). Glucose 56-63 insulin Homo sapiens 0-7 11574412-12 2001 From our results, we reached the following conclusions: 1) Our data strongly suggest that the insulin antagonistic actions of GH on glucose metabolism are causally linked to the concomitant activation of lipolysis. Glucose 132-139 insulin Homo sapiens 94-101 11574417-0 2001 Intramyocellular lipid is associated with resistance to in vivo insulin actions on glucose uptake, antilipolysis, and early insulin signaling pathways in human skeletal muscle. Glucose 83-90 insulin Homo sapiens 64-71 11574417-10 2001 Whole-body insulin-stimulated glucose uptake was lower in the HiIMCL group (3.0 +/- 0.4 mg. kg(-1). Glucose 30-37 insulin Homo sapiens 11-18 11574430-5 2001 Insulin lispro significantly decreased the peak glucose level (P = 0.0004) and the 2-h (P = 0.001) and 5-h (P < 0.0001) glucose area under the curve (AUC). Glucose 48-55 insulin Homo sapiens 0-7 11574430-5 2001 Insulin lispro significantly decreased the peak glucose level (P = 0.0004) and the 2-h (P = 0.001) and 5-h (P < 0.0001) glucose area under the curve (AUC). Glucose 123-130 insulin Homo sapiens 0-7 11574430-9 2001 CONCLUSIONS: In response to subcutaneous insulin lispro, postprandial glucose excursion was significantly diminished and insulin secretion was enhanced compared with a control meal in which no medication was given to patients with CFRD. Glucose 70-77 insulin Homo sapiens 41-48 11574430-12 2001 Placebo-controlled longitudinal studies comparing the effectiveness of repaglinide and insulin on glucose metabolic control as well as overall nutrition and body weight are needed to help determine optimal medical treatment of CFRD. Glucose 98-105 insulin Homo sapiens 87-94 11574439-5 2001 Insulin sensitivity was determined using the homeostasis model assessment (HOMA) estimates, which used fasting insulin and glucose measurements obtained at the same time as the MA urine sample. Glucose 123-130 insulin Homo sapiens 0-7 11588141-12 2001 The paper also discusses the mechanisms explaining the glucose dependence of the effects of ACh on insulin release. Glucose 55-62 insulin Homo sapiens 99-106 11711776-5 2001 Glucose, insulin and C-peptide levels were measured every 30 min for 2 h. Fasting insulin resistance index (FIRI) was calculated according to the formula: FIRI = (fasting glucose x fasting insulin)/25. Glucose 171-178 insulin Homo sapiens 82-89 11816527-7 2001 On the other hand, maternal hyperglycemia leads to beta-cell hyperplasia in the fetus, by a constant stimulus over the insulin production which stimulates the use of glucose as nutrients, leading to the increase in fetal weight and determining genetic changes. Glucose 166-173 insulin Homo sapiens 119-126 11572798-4 2001 Because both insulin and IGF-I elicit decreases in glucose and amino acid concentrations, the concentrations of these substrates were clamped during the hormone infusions. Glucose 51-58 insulin Homo sapiens 13-20 11572798-10 2001 Intravenous infusion of insulin inhibited hepatic IGFBP-1 gene expression when amino acids and glucose were clamped. Glucose 95-102 insulin Homo sapiens 24-31 11600513-1 2001 The purpose of this study was to determine whether the fasting glucose/insulin ratio is a useful screening test for insulin resistance in prepubertal girls with premature adrenarche. Glucose 63-70 insulin Homo sapiens 116-123 11600513-6 2001 Insulin sensitivity correlated significantly with the glucose/insulin ratio (0.76; P < 0.001), fasting insulin (0.75; P < 0.001), and IGF-binding protein-1 (0.59; P < 0.005). Glucose 54-61 insulin Homo sapiens 0-7 11600513-7 2001 Stepwise regression analysis with the insulin sensitivity index as the dependent variable showed that the fasting glucose/insulin ratio was significantly predictive of the insulin sensitivity index (P < 0.002). Glucose 114-121 insulin Homo sapiens 38-45 11600513-7 2001 Stepwise regression analysis with the insulin sensitivity index as the dependent variable showed that the fasting glucose/insulin ratio was significantly predictive of the insulin sensitivity index (P < 0.002). Glucose 114-121 insulin Homo sapiens 122-129 11600513-7 2001 Stepwise regression analysis with the insulin sensitivity index as the dependent variable showed that the fasting glucose/insulin ratio was significantly predictive of the insulin sensitivity index (P < 0.002). Glucose 114-121 insulin Homo sapiens 122-129 11600513-9 2001 Furthermore, those girls with a low glucose/insulin ratio (<7) had higher body mass index, fasting insulin, free T, and ACTH-stimulated 17-hydroxypregnenolone and lower fasting IGF-binding protein-1 and SHBG than those girls with a glucose/insulin ratio greater than 7. Glucose 36-43 insulin Homo sapiens 102-109 11600513-10 2001 The fasting glucose/insulin ratio is a useful screening test for insulin resistance in prepubertal Caribbean Hispanic and African American girls with premature adrenarche. Glucose 12-19 insulin Homo sapiens 65-72 11739459-5 2001 Although subjects were nondiabetic by selection criteria, plasma insulin concentrations during oral glucose tolerance test were higher (P < 0.05) in Q allele-carrying subjects (K121Q or Q121Q genotypes), compared with K121K individuals, in both the nonobese and obese groups. Glucose 100-107 insulin Homo sapiens 65-72 11739459-6 2001 Insulin sensitivity, measured by euglycemic clamp in a representative subgroup of 131 of 431 randomly selected subjects, progressively decreased (P < 0.001) from nonobese K121K [n = 61; glucose disposal (M) = 34.9 +/- 1.1 micromol/kg/min] to nonobese Q (n = 21; M = 29.9 +/- 2.0), obese K121K (n = 31, M = 18.5 +/- 1.2), and obese Q (n = 18, M = 15.5 +/- 1.2) carriers. Glucose 189-196 insulin Homo sapiens 0-7 11564599-8 2001 Furthermore, while transfection with the wild-type beta(3)AR preserved the glucose-dependent secretion of insulin, expression of the variant receptor rendered the host cells significantly less responsive to glucose. Glucose 75-82 insulin Homo sapiens 106-113 11641528-0 2001 Insulin secretion and sensitivity during oral glucose tolerance test in Korean lean elderly women. Glucose 46-53 insulin Homo sapiens 0-7 11697551-5 2001 A single band specific to phosphorylated PKB was found on the Western blots, indicating that the active conformation of insulin was retained when spray dried in combination with lactose and with xanthan gum over the spray-drying inlet temperature range of 110-170 degrees C. Evidence of inactivation/denaturation was observed when insulin was spray dried at an inlet temperature of 200 degrees C. The assay may be of use as a more rapid and economic means to screen insulin formulations for inhalation and other purposes as opposed to conventional monitoring of blood glucose levels in animals. Glucose 568-575 insulin Homo sapiens 120-127 11562451-2 2001 In the present article we show that 2 to 5 microM CsA diminishes glucose-induced insulin secretion of isolated mouse pancreatic islets in vitro by inhibiting glucose-stimulated oscillations of the cytoplasmic free-Ca(2+) concentration [Ca(2+)](c). Glucose 65-72 insulin Homo sapiens 81-88 11562451-2 2001 In the present article we show that 2 to 5 microM CsA diminishes glucose-induced insulin secretion of isolated mouse pancreatic islets in vitro by inhibiting glucose-stimulated oscillations of the cytoplasmic free-Ca(2+) concentration [Ca(2+)](c). Glucose 158-165 insulin Homo sapiens 81-88 11586489-8 2001 We suggest that 60- to 90-minute glucose clamps may provide information about the relationship between insulin sensitivity and various cardiovascular risk factors in borderline hypertensive young caucasian men. Glucose 33-40 insulin Homo sapiens 103-110 11579205-1 2001 Pharmacological agonists for the nuclear receptor PPAR gamma enhance glucose disposal in a variety of insulin-resistant states in humans and animals. Glucose 69-76 insulin Homo sapiens 102-109 11579205-5 2001 Rosiglitazone treatment for 48 h significantly increased basal and insulin-stimulated glucose uptake and markedly increased the cellular expression of GLUT1 but not GLUT4. Glucose 86-93 insulin Homo sapiens 67-74 11780754-2 2001 The GLUT4 intracellularly sequestered in resting adipocytes and muscle cells becomes exposed on their surface in response to an increase in insulin levels and muscle contraction, where it facilitates glucose uptake. Glucose 200-207 insulin Homo sapiens 140-147 11586502-4 2001 Acute insulin response to glucose (AIRg) correlated significantly with serum CBG concentrations at time 0 (r = -.38, P =.029), 22 minutes (r = -.41, P =.01), 50 minutes (r = -.41, P =.01), and 180 minutes (r = -.39, P =.02). Glucose 26-33 insulin Homo sapiens 6-13 11590327-6 2001 At 11.5 mM glucose concentration, SS-Ab stimulated insulin secretion, IN-Ab stimulated glucagon and inhibited somatostatin secretion, and GN-Ab stimulated insulin secretion. Glucose 11-18 insulin Homo sapiens 51-58 11575527-6 2001 RESULTS: Pain reduced whole-body insulin-stimulated glucose uptake from 6.37+/-1.87 mg x kg(-1) x min(-1) (mean +/- SD) in study C to 4.97+/-1.38 mg x kg(-1) x min(-1) in study P (P < 0.01) because of a decrease in nonoxidative glucose disposal, as determined by indirect calorimetry (2.47+/-0.88 mg x kg(-1) x min(-1) in study P vs. 3.41+/-1.03 mg x kg(-1) x min(-1) in study C; P < 0.05). Glucose 52-59 insulin Homo sapiens 33-40 11775342-13 2001 Post glucose serum insulin was over 60 uIU/ml in 40 and 63% of prepuberal and puberal children, respectively. Glucose 5-12 insulin Homo sapiens 19-26 11744937-5 2001 Plasma glucose concentration one-hour postprandially is strikingly abnormal amongst native Saudis and interestingly, is associated with insulin resistance and features of syndrome X. Glucose 7-14 insulin Homo sapiens 136-143 11729704-13 2001 A higher glucose infusion rate should be maintained to prevent hypoglycemia following insulin treatment. Glucose 9-16 insulin Homo sapiens 86-93 11591170-3 2001 Whereas treatment adjuncts to insulin may address carbohydrate metabolism from glucose absorption to insulin receptor function, success may depend on the type of diabetes present in the patient. Glucose 79-86 insulin Homo sapiens 30-37 11575527-6 2001 RESULTS: Pain reduced whole-body insulin-stimulated glucose uptake from 6.37+/-1.87 mg x kg(-1) x min(-1) (mean +/- SD) in study C to 4.97+/-1.38 mg x kg(-1) x min(-1) in study P (P < 0.01) because of a decrease in nonoxidative glucose disposal, as determined by indirect calorimetry (2.47+/-0.88 mg x kg(-1) x min(-1) in study P vs. 3.41+/-1.03 mg x kg(-1) x min(-1) in study C; P < 0.05). Glucose 231-238 insulin Homo sapiens 33-40 11514398-9 2001 Those with T3394C showed a mild defect in glucose-stimulated insulin secretion, and hyperglycemia appeared after adding such factors as aging or obesity. Glucose 42-49 insulin Homo sapiens 61-68 11500192-5 2001 In addition, the HindIII polymorphism as well as the HindIII and S447X markers combination influenced the insulin area under the curve during an oral glucose tolerance test. Glucose 150-157 insulin Homo sapiens 106-113 11589678-1 2001 OBJECTIVE: High non-esterified fatty acid (NEFA) levels impair glucose-stimulated insulin secretion from islets derived from non-diabetic Zucker rats that are genetically predisposed to diabetes. Glucose 63-70 insulin Homo sapiens 82-89 11555563-3 2001 Recent studies in human volunteers have shown that when aerosolized insulin is effectively delivered to the alveolar region of the lung, absorption rates and decreases in glucose levels are similar to those achieved with SC-delivered insulin during the fasting state. Glucose 171-178 insulin Homo sapiens 68-75 11555563-4 2001 Other human trials have shown that inhaled insulin also effectively controls postprandial glucose levels. Glucose 90-97 insulin Homo sapiens 43-50 11555563-8 2001 It is likely that the treatment of diabetes with aerosolized insulin will provide an effective alternative means for controlling plasma glucose levels in diabetic individuals. Glucose 136-143 insulin Homo sapiens 61-68 11546970-6 2001 The intervention group was treated using a dosing nomogram that allowed the nurse to adjust the insulin infusion rate based on current glucose concentration and concurrent insulin infusion rates. Glucose 135-142 insulin Homo sapiens 96-103 11546970-9 2001 Effectiveness of glucose control was determined retrospectively by measuring the area under the curve of blood concentrations >11.5 mmol/L versus time of insulin infusion, divided by total duration of insulin infusion. Glucose 17-24 insulin Homo sapiens 157-164 11546970-9 2001 Effectiveness of glucose control was determined retrospectively by measuring the area under the curve of blood concentrations >11.5 mmol/L versus time of insulin infusion, divided by total duration of insulin infusion. Glucose 17-24 insulin Homo sapiens 204-211 11546970-12 2001 CONCLUSION: Use of an insulin nomogram in critically ill patients improves control of blood glucose concentrations and is safe. Glucose 92-99 insulin Homo sapiens 22-29 11472273-3 2001 Experimental studies show that amylin acts as a neuroendocrine hormone that complements the effects of insulin in postprandial glucose regulation through several centrally mediated effects. Glucose 127-134 insulin Homo sapiens 103-110 11483229-12 2001 Twice-daily meal-related insulin secretagogue therapy with repaglinide, a new short and rapid-acting prandial glucose regulator, is capable of improving all measures of glycaemic control without increased hypoglycaemia or fasting hyperinsulinaemia. Glucose 110-117 insulin Homo sapiens 25-32 11522673-9 2001 Glucose transport increased in response to insulin in the lean and obese groups (P < 0.05), but did not increase significantly in the type 2 diabetic group. Glucose 0-7 insulin Homo sapiens 43-50 11522673-10 2001 A dose-responsive pattern of stimulation of glucose phosphorylation was observed in all groups of subjects (P < 0.05); however, glucose phosphorylation was lower in both the obese and type 2 diabetic groups compared with the lean group at the moderate insulin dose (P < 0.05). Glucose 44-51 insulin Homo sapiens 255-262 11522673-10 2001 A dose-responsive pattern of stimulation of glucose phosphorylation was observed in all groups of subjects (P < 0.05); however, glucose phosphorylation was lower in both the obese and type 2 diabetic groups compared with the lean group at the moderate insulin dose (P < 0.05). Glucose 131-138 insulin Homo sapiens 255-262 11522683-0 2001 Skeletal muscle of stroke-prone spontaneously hypertensive rats exhibits reduced insulin-stimulated glucose transport and elevated levels of caveolin and flotillin. Glucose 100-107 insulin Homo sapiens 81-88 11522683-5 2001 We show that skeletal muscle from SHRSP animals exhibits a marked decrease in insulin-stimulated glucose transport compared with WKY animals (fold increase in response to insulin: 1.4 +/- 0.15 in SHRSP, 2.29 +/- 0.22 in WKY; n = 4, P = 0.02), but the stimulation of glucose transport in response to activation of AMP-activated protein kinase was similar between the two strains. Glucose 97-104 insulin Homo sapiens 78-85 11522683-6 2001 Similar reductions in insulin-stimulated glucose transport were also evident in myoblast cultures from SHRSP compared with WKY cultures. Glucose 41-48 insulin Homo sapiens 22-29 11522683-11 2001 Taken together, these data suggest that the insulin resistance observed in the SHRSP is manifest at the level of skeletal muscle, that muscle cell glucose transport exhibits a blunted response to insulin but unchanged responses to activation of AMP-activated protein kinase, that alterations in key molecules in both GLUT4 trafficking and insulin signal compartmentalization may underlie these defects in insulin action, and that the insulin resistance of these muscles appears to be of genetic origin rather than a paracrine or autocrine effect, since the insulin resistance is also observed in cultured myoblasts over several passages. Glucose 147-154 insulin Homo sapiens 196-203 11522683-11 2001 Taken together, these data suggest that the insulin resistance observed in the SHRSP is manifest at the level of skeletal muscle, that muscle cell glucose transport exhibits a blunted response to insulin but unchanged responses to activation of AMP-activated protein kinase, that alterations in key molecules in both GLUT4 trafficking and insulin signal compartmentalization may underlie these defects in insulin action, and that the insulin resistance of these muscles appears to be of genetic origin rather than a paracrine or autocrine effect, since the insulin resistance is also observed in cultured myoblasts over several passages. Glucose 147-154 insulin Homo sapiens 196-203 11522683-11 2001 Taken together, these data suggest that the insulin resistance observed in the SHRSP is manifest at the level of skeletal muscle, that muscle cell glucose transport exhibits a blunted response to insulin but unchanged responses to activation of AMP-activated protein kinase, that alterations in key molecules in both GLUT4 trafficking and insulin signal compartmentalization may underlie these defects in insulin action, and that the insulin resistance of these muscles appears to be of genetic origin rather than a paracrine or autocrine effect, since the insulin resistance is also observed in cultured myoblasts over several passages. Glucose 147-154 insulin Homo sapiens 196-203 11522683-11 2001 Taken together, these data suggest that the insulin resistance observed in the SHRSP is manifest at the level of skeletal muscle, that muscle cell glucose transport exhibits a blunted response to insulin but unchanged responses to activation of AMP-activated protein kinase, that alterations in key molecules in both GLUT4 trafficking and insulin signal compartmentalization may underlie these defects in insulin action, and that the insulin resistance of these muscles appears to be of genetic origin rather than a paracrine or autocrine effect, since the insulin resistance is also observed in cultured myoblasts over several passages. Glucose 147-154 insulin Homo sapiens 196-203 11522706-0 2001 Clinically useful estimates of insulin sensitivity during pregnancy: validation studies in women with normal glucose tolerance and gestational diabetes mellitus. Glucose 109-116 insulin Homo sapiens 31-38 11522706-5 2001 An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat-free mass and endogenous glucose production measured using [6,6(-2)H(2)]glucose. Glucose 85-92 insulin Homo sapiens 12-19 11522706-5 2001 An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat-free mass and endogenous glucose production measured using [6,6(-2)H(2)]glucose. Glucose 160-167 insulin Homo sapiens 12-19 11522706-5 2001 An index of insulin sensitivity derived from the clamp (IS(CLAMP)) was obtained from glucose infusion rates adjusted for change in fat-free mass and endogenous glucose production measured using [6,6(-2)H(2)]glucose. Glucose 160-167 insulin Homo sapiens 12-19 11522726-0 2001 Remnant-like particle cholesterol and insulin resistance in nonobese nonhypertensive Japanese glucose-tolerant relatives of type 2 diabetic patients. Glucose 94-101 insulin Homo sapiens 38-45 11547215-7 2001 Other interesting therapeutic perspectives to treat insulin resistance lie in the development of inhibitors of protein tyrosine phosphatases and in the promotion of non insulin-dependent contraction-like muscle glucose uptake via stimulation of AMP protein kinase (AMPK). Glucose 211-218 insulin Homo sapiens 52-59 11547215-7 2001 Other interesting therapeutic perspectives to treat insulin resistance lie in the development of inhibitors of protein tyrosine phosphatases and in the promotion of non insulin-dependent contraction-like muscle glucose uptake via stimulation of AMP protein kinase (AMPK). Glucose 211-218 insulin Homo sapiens 169-176 11547222-4 2001 RESULTS: The 2-h blood glucose excursion after the post-sunset meal was significantly (p=0.026) lower with insulin lispro (2.50 +/- 0.46 mmol/l) than with regular human insulin (3.47 +/- 0.49 mmol/l). Glucose 23-30 insulin Homo sapiens 107-114 11596668-0 2001 Placental glucose transport and utilisation is altered at term in insulin-treated, gestational-diabetic patients. Glucose 10-17 insulin Homo sapiens 66-73 11596668-2 2001 To assess the placental glucose handling characteristics of women with gestational diabetes mellitus receiving insulin, we examined glucose transport and utilisation in placentae from three groups of women after term delivery: those with gestational diabetes mellitus and receiving insulin (n = 9, insulin group); those with gestational diabetes mellitus and not receiving insulin (n = 10, no insulin group); and those with normal, non-diabetic pregnancies (n = 9, control group). Glucose 24-31 insulin Homo sapiens 111-118 11596668-7 2001 RESULTS: Glucose uptake from the maternal perfusate (insulin group 0.57, no insulin group 0.30) and net glucose transfer to the fetal effluent (insulin group 0.41, no insulin group 0.20) both increased in the placentae of women receiving insulin compared with the diabetic group not receiving insulin. Glucose 9-16 insulin Homo sapiens 53-60 11596668-9 2001 CONCLUSION/INTERPRETATION: These results suggest that materno-fetal glucose transport increases in the placentae of women with gestational diabetes mellitus who receive insulin compared with those women who do not receive insulin. Glucose 68-75 insulin Homo sapiens 169-176 11596668-9 2001 CONCLUSION/INTERPRETATION: These results suggest that materno-fetal glucose transport increases in the placentae of women with gestational diabetes mellitus who receive insulin compared with those women who do not receive insulin. Glucose 68-75 insulin Homo sapiens 222-229 11517149-1 2001 We examined whether low-dose dexamethasone administration during late pregnancy modifies hepatic and/or peripheral insulin action or glucose-stimulated insulin secretion. Glucose 133-140 insulin Homo sapiens 152-159 11517149-4 2001 Insulin secretion and glucose tolerance was assessed after iv glucose, and insulin action examined during insulin infusion at euglycemia. Glucose 62-69 insulin Homo sapiens 0-7 11517149-7 2001 Suppression of endogenous glucose production by insulin was enhanced by dexamethasone treatment, but insulin"s ability to promote glucose clearance was diminished. Glucose 26-33 insulin Homo sapiens 48-55 11517149-7 2001 Suppression of endogenous glucose production by insulin was enhanced by dexamethasone treatment, but insulin"s ability to promote glucose clearance was diminished. Glucose 130-137 insulin Homo sapiens 101-108 11517149-8 2001 We demonstrate that excess maternal glucocorticoids during late pregnancy impairs glucose-stimulated insulin secretion and insulin-simulated glucose clearance but enhances insulin"s ability to suppress endogenous glucose production. Glucose 82-89 insulin Homo sapiens 101-108 11517149-8 2001 We demonstrate that excess maternal glucocorticoids during late pregnancy impairs glucose-stimulated insulin secretion and insulin-simulated glucose clearance but enhances insulin"s ability to suppress endogenous glucose production. Glucose 141-148 insulin Homo sapiens 123-130 11517149-8 2001 We demonstrate that excess maternal glucocorticoids during late pregnancy impairs glucose-stimulated insulin secretion and insulin-simulated glucose clearance but enhances insulin"s ability to suppress endogenous glucose production. Glucose 141-148 insulin Homo sapiens 123-130 11517149-8 2001 We demonstrate that excess maternal glucocorticoids during late pregnancy impairs glucose-stimulated insulin secretion and insulin-simulated glucose clearance but enhances insulin"s ability to suppress endogenous glucose production. Glucose 141-148 insulin Homo sapiens 123-130 11517149-8 2001 We demonstrate that excess maternal glucocorticoids during late pregnancy impairs glucose-stimulated insulin secretion and insulin-simulated glucose clearance but enhances insulin"s ability to suppress endogenous glucose production. Glucose 141-148 insulin Homo sapiens 123-130 11517176-10 2001 Phosphatidylinositol 3-kinase- dependent protein kinase B activation is not sufficient to stimulate glucose transport and glycogen synthesis, highlighting the placenta as a nonclassic target of insulin for the regulation of glucose metabolism. Glucose 224-231 insulin Homo sapiens 194-201 11517007-9 2001 The decrease in sTNFR2 was significantly related to the increase in insulin sensitivity; that relationship remained significant after adjustment for the concurrent changes in BMI, waist circumference, percentage of body fat, plasma glucose, insulin and free fatty acids. Glucose 232-239 insulin Homo sapiens 68-75 11517008-1 2001 OBJECTIVE: To determine the correlation between insulin sensitivity (S(I)) obtained by the minimal model method applied to a frequently sampled (n=33) intravenous glucose tolerance test (FSIGT(33)), and values obtained by reduced FSIGTs, oral glucose tolerance test (OGTT), or fasting. Glucose 163-170 insulin Homo sapiens 48-55 11532474-7 2001 Insulin sensitivity was evaluated by a standard 75-g oral glucose tolerance test and area-under-curve insulin analysis. Glucose 58-65 insulin Homo sapiens 0-7 11594246-1 2001 Insulin resistance is a core defect in Type 2 diabetes, occurring in peripheral organs (skeletal muscle and adipose tissue) leading to decreased glucose uptake and utilisation and in liver leading to increased hepatic glucose production. Glucose 145-152 insulin Homo sapiens 0-7 11594246-1 2001 Insulin resistance is a core defect in Type 2 diabetes, occurring in peripheral organs (skeletal muscle and adipose tissue) leading to decreased glucose uptake and utilisation and in liver leading to increased hepatic glucose production. Glucose 218-225 insulin Homo sapiens 0-7 11594292-7 2001 Rapid-acting insulin analogues have a greater effect on postprandial glucose levels than regular human insulin. Glucose 69-76 insulin Homo sapiens 13-20 11594298-10 2001 These may form the basis of an alert to hypoglycaemic levels or ultimately be connected directly to continuous insulin infusion, particularly with rapid-acting insulin analogues, to maintain glucose within normal physiological limits. Glucose 191-198 insulin Homo sapiens 111-118 11594299-5 2001 Lower postprandial glucose peaks and improved HbA1c levels were seen with insulin lispro by CSII. Glucose 19-26 insulin Homo sapiens 74-81 11511859-5 2001 Hyperinsulinemia seems to be an important extrinsic factor in many cases of PCOS; it results from resistance to the effects of insulin on glucose metabolism. Glucose 138-145 insulin Homo sapiens 5-12 11549635-1 2001 A novel index of insulin sensitivity, the quick insulin sensitivity check index, termed QUICKI (1/[log (insulin) + log (glucose)]), was recently developed. Glucose 120-127 insulin Homo sapiens 17-24 11549635-1 2001 A novel index of insulin sensitivity, the quick insulin sensitivity check index, termed QUICKI (1/[log (insulin) + log (glucose)]), was recently developed. Glucose 120-127 insulin Homo sapiens 48-55 11549635-1 2001 A novel index of insulin sensitivity, the quick insulin sensitivity check index, termed QUICKI (1/[log (insulin) + log (glucose)]), was recently developed. Glucose 120-127 insulin Homo sapiens 48-55 11522495-1 2001 The aim of this study was to compare the metabolic effects of a single equimolar subcutaneous injection of hepatic directed vesicle-insulin (HDV-insulin) and regular insulin on glucose levels and intermediary metabolism during a 75-g oral glucose tolerance test (OGTT). Glucose 177-184 insulin Homo sapiens 132-139 11522495-11 2001 We conclude that HDV-insulin can significantly lower plasma glucose excursions compared to an equivalent dose of regular insulin during an OGTT in Type 1 diabetic patients. Glucose 60-67 insulin Homo sapiens 21-28 11564984-7 2001 RESULTS: Plasma insulin levels and insulin-mediated glucose uptake did not differ between both groups. Glucose 52-59 insulin Homo sapiens 35-42 11588809-1 2001 Insulin resistance (IRI) applies to abnormalities of insulin-stimulated glucose metabolism. Glucose 72-79 insulin Homo sapiens 0-7 11533125-5 2001 Furthermore, the possible mechanisms behind the well-described improvement of insulin action on glucose uptake and glycogen synthase activity in the post-exercise period is discussed. Glucose 96-103 insulin Homo sapiens 78-85 11592573-12 2001 The number of patients with an abnormal insulin: glucose ratio (>1:4) increased with age. Glucose 49-56 insulin Homo sapiens 40-47 11565495-6 2001 Intravenous insulin (always R) may be limited to administration in the ICU because of the need for frequent blood glucose monitoring and rapidity of glucose response to intravenous insulin. Glucose 114-121 insulin Homo sapiens 12-19 11565495-14 2001 Sulfonylureas and other insulin secretagogues (e.g., meglitinide, nateglinide) lower glucoses acutely. Glucose 85-93 insulin Homo sapiens 24-31 11555840-0 2001 alpha-Lipoic acid prevents the development of glucose-induced insulin resistance in 3T3-L1 adipocytes and accelerates the decline in immunoreactive insulin during cell incubation. Glucose 46-53 insulin Homo sapiens 62-69 11555840-2 2001 We tested the hypothesis that certain antioxidants may prevent insulin-resistant glucose transport that develops in adipocytes after sustained exposure to high glucose, provided insulin is present. Glucose 81-88 insulin Homo sapiens 63-70 11555840-2 2001 We tested the hypothesis that certain antioxidants may prevent insulin-resistant glucose transport that develops in adipocytes after sustained exposure to high glucose, provided insulin is present. Glucose 81-88 insulin Homo sapiens 178-185 11555840-2 2001 We tested the hypothesis that certain antioxidants may prevent insulin-resistant glucose transport that develops in adipocytes after sustained exposure to high glucose, provided insulin is present. Glucose 160-167 insulin Homo sapiens 63-70 11555840-5 2001 After extensive re-equilibration in insulin and antioxidant-free media, basal and maximally insulin-stimulated (100 nmol/L) glucose transport was measured. Glucose 124-131 insulin Homo sapiens 92-99 11555840-8 2001 Preincubation in high glucose without antioxidants inhibited acutely insulin-stimulated glucose transport by 40% to 50% compared with low glucose. Glucose 22-29 insulin Homo sapiens 69-76 11555840-8 2001 Preincubation in high glucose without antioxidants inhibited acutely insulin-stimulated glucose transport by 40% to 50% compared with low glucose. Glucose 88-95 insulin Homo sapiens 69-76 11555840-8 2001 Preincubation in high glucose without antioxidants inhibited acutely insulin-stimulated glucose transport by 40% to 50% compared with low glucose. Glucose 88-95 insulin Homo sapiens 69-76 11928588-2 2001 Depending on a contribution of the primary risk factors of type 2 Diabetes Mellitus (2-DM) mainly genetic factors and obesity--an independent cause of insulin receptor resistance--glucose intolerance and 2-DM may overlap the Syndrome X. Glucose 180-187 insulin Homo sapiens 151-158 12536716-0 2001 [The molecular mechanism of high glucose-induced insulin resistance in 3T3-L1 adipocytes]. Glucose 33-40 insulin Homo sapiens 49-56 12536716-2 2001 Results showed that adipocytes treated with different high glucose (10, 15 and 25 mmol.L-1) for 24 hours showed to impair the basal and insulin-induced increase in glucose uptake in a dose-dependent manner and decreased significantly IRS1 tyrosine phosphorylation. Glucose 59-66 insulin Homo sapiens 136-143 12536716-5 2001 Chronic exposure to high glucose can inhibit glucose uptake and induce insulin resistance. Glucose 25-32 insulin Homo sapiens 71-78 11573448-4 2001 In this review the impairments of the Na(+)-pump and the Ca(2+)-transport mechanisms as well as the insulin-dependent glucose transporter GLUT4 will be discussed in diabetes. Glucose 118-125 insulin Homo sapiens 100-107 11573448-8 2001 Therefore the uptake of K+ and glucose into these tissues will increase significantly under the acute influence of insulin. Glucose 31-38 insulin Homo sapiens 115-122 11532984-1 2001 In the mouse, the SH3P12 or the c-Cbl-associated protein (CAP) has been shown as an important signaling molecule in insulin-stimulated glucose uptake. Glucose 135-142 insulin Homo sapiens 116-123 11554413-2 2001 The gastrointestinal peptide glucose-dependent insulinotropic polypeptide (GIP1-42) is one of the incretin hormones regulating glucose-induced insulin secretion from the endocrine pancreas. Glucose 29-36 insulin Homo sapiens 47-54 11554413-2 2001 The gastrointestinal peptide glucose-dependent insulinotropic polypeptide (GIP1-42) is one of the incretin hormones regulating glucose-induced insulin secretion from the endocrine pancreas. Glucose 127-134 insulin Homo sapiens 47-54 11529531-1 2001 UNLABELLED: In patients with cystic fibrosis (CF), glucose intolerance preceding diabetes (prediabetes) may have adverse effects on nutritional status and respiratory function, which are reversible after the start of insulin therapy. Glucose 51-58 insulin Homo sapiens 217-224 11440896-3 2001 Induction of fetal hyperinsulinemia by direct infusion of insulin into the fetus and by either fetal or maternal infusions of glucose resulted in significant increases in the activity of FTase and the amounts of farnesylated p21 Ras in fetal liver, skeletal muscle, fat, and white blood cells. Glucose 126-133 insulin Homo sapiens 24-31 11440917-5 2001 Steady-state insulin levels did not differ, but insulin-mediated glucose disposal was significantly decreased in PCOS women (P < 0.05). Glucose 65-72 insulin Homo sapiens 48-55 11513189-11 2001 The simultaneous disorder of iron and glucose and/or lipid metabolism, in most of the cases associated with insulin resistance, is responsible for persistent hyperferritinemia and identifies patients at risk for NASH. Glucose 38-45 insulin Homo sapiens 108-115 11556725-0 2001 Insulin secretion rate during glucose stimuli: alternative analyses of C-peptide data. Glucose 30-37 insulin Homo sapiens 0-7 11493160-8 2001 Insulin treatment of hyperglycemic animals was found to have a beneficial effect in focal and global brain ischemia, which may be mediated by the glucose-reduction effect or by a direct neuroprotection. Glucose 146-153 insulin Homo sapiens 0-7 11463364-10 2001 In conclusion, this is the first report that Ang II regulates adipocyte FAS gene transcription via insulin response sequences in a glucose-dependent manner and that this regulation is mediated at least in part via the ADD1 transcription factor. Glucose 131-138 insulin Homo sapiens 99-106 11498025-8 2001 With eIF2B and eEF2, both amino acids and glucose must be provided for insulin to regulate their activities. Glucose 42-49 insulin Homo sapiens 71-78 11498025-9 2001 In contrast, insulin-stimulation of the formation of eIF4F complexes requires glucose but not amino acids. Glucose 78-85 insulin Homo sapiens 13-20 11498026-2 2001 When the diet is rich in carbohydrates, secreted insulin stimulates the expression of genes for enzymes involved in glucose utilization (glucokinase, L-type pyruvate kinase and lipogenic enzymes) and inhibits genes for enzymes involved in glucose production (phosphenolpyruvate carboxykinase). Glucose 116-123 insulin Homo sapiens 49-56 11498026-2 2001 When the diet is rich in carbohydrates, secreted insulin stimulates the expression of genes for enzymes involved in glucose utilization (glucokinase, L-type pyruvate kinase and lipogenic enzymes) and inhibits genes for enzymes involved in glucose production (phosphenolpyruvate carboxykinase). Glucose 239-246 insulin Homo sapiens 49-56 11570119-9 2001 At the opposite end of the glucose spectrum, hypoglycemia can result from excess glucose uptake due to either increased insulin concentrations, enhanced insulin action or impaired carbohydrate absorption. Glucose 27-34 insulin Homo sapiens 120-127 11570119-9 2001 At the opposite end of the glucose spectrum, hypoglycemia can result from excess glucose uptake due to either increased insulin concentrations, enhanced insulin action or impaired carbohydrate absorption. Glucose 27-34 insulin Homo sapiens 153-160 11570119-9 2001 At the opposite end of the glucose spectrum, hypoglycemia can result from excess glucose uptake due to either increased insulin concentrations, enhanced insulin action or impaired carbohydrate absorption. Glucose 81-88 insulin Homo sapiens 120-127 11570119-9 2001 At the opposite end of the glucose spectrum, hypoglycemia can result from excess glucose uptake due to either increased insulin concentrations, enhanced insulin action or impaired carbohydrate absorption. Glucose 81-88 insulin Homo sapiens 153-160 11678027-8 2001 In all subjects with insulitis, the first phase insulin response (FPIR) was determined by the intravenous glucose tolerance test. Glucose 106-113 insulin Homo sapiens 48-55 11445062-2 2001 The fundamental abnormality leading to the manifestations that comprise syndrome X is resistance to insulin regulation of muscle glucose uptake and adipose tissue lipolysis. Glucose 129-136 insulin Homo sapiens 100-107 11473038-6 2001 Insulin pulsatility was assessed by 1-min interval blood sampling for 75 min 1) under baseline conditions (baseline), 2) 3 h after the first dose (80 mg) of gliclazide (acute) with the plasma glucose concentration clamped at the baseline value, 3) after 5 weeks of treatment (5 weeks), and 4) after 5 weeks of treatment with the plasma glucose concentration clamped during the sampling at the value of the baseline assessment (5 weeks-elevated). Glucose 192-199 insulin Homo sapiens 0-7 11473042-2 2001 In experimental animals, insulin at high doses decreases the incorporation of labeled GNG precursors into plasma glucose. Glucose 113-120 insulin Homo sapiens 25-32 11473045-4 2001 In 104 normal glucose-tolerant subjects, acute insulin secretory response (AIR) to a 25-g intravenous glucose challenge correlated with the age at onset of diabetes in the mother (r = 0.23, P = 0.03) and, in multiple regression analyses, the age at onset of diabetes in the father (P = 0.02), after adjusting for maternal age at onset and after allowing for an interaction between these terms. Glucose 14-21 insulin Homo sapiens 47-54 11473045-4 2001 In 104 normal glucose-tolerant subjects, acute insulin secretory response (AIR) to a 25-g intravenous glucose challenge correlated with the age at onset of diabetes in the mother (r = 0.23, P = 0.03) and, in multiple regression analyses, the age at onset of diabetes in the father (P = 0.02), after adjusting for maternal age at onset and after allowing for an interaction between these terms. Glucose 102-109 insulin Homo sapiens 47-54 11473051-0 2001 Small increases in insulin inhibit hepatic glucose production solely caused by an effect on glycogen metabolism. Glucose 43-50 insulin Homo sapiens 19-26 11473070-4 2001 RESULTS: In response to a glucose challenge, girls and older and heavier children produced significantly more insulin. Glucose 26-33 insulin Homo sapiens 110-117 11520309-5 2001 Glucose-stimulated plasma immunoreactive insulin concentrations in the tacrolimus-treatment group were significantly higher than in the cyclosporin group (p < 0.05) and the controls (p < 0.001). Glucose 0-7 insulin Homo sapiens 41-48 11520309-7 2001 The raised insulin concentrations with normal or increased blood glucose concentrations after renal transplantation suggests that insulin resistance was more marked in patients receiving tacrolimus-based immunosuppression. Glucose 65-72 insulin Homo sapiens 130-137 11553200-10 2001 Insulin/glucose ratio at birth was raised in infants with an AUCI in the upper tertile, accompanied by a positive correlation between insulin/glucose ratio at birth and AUCI (P = 0.02). Glucose 8-15 insulin Homo sapiens 0-7 11553200-10 2001 Insulin/glucose ratio at birth was raised in infants with an AUCI in the upper tertile, accompanied by a positive correlation between insulin/glucose ratio at birth and AUCI (P = 0.02). Glucose 8-15 insulin Homo sapiens 134-141 11553200-10 2001 Insulin/glucose ratio at birth was raised in infants with an AUCI in the upper tertile, accompanied by a positive correlation between insulin/glucose ratio at birth and AUCI (P = 0.02). Glucose 142-149 insulin Homo sapiens 0-7 12762962-5 2001 Human regular insulin peaks at 2 to 3 hours after injection; thus, checking blood glucose at the 2-hour point is a relic of strategies to prevent hypoglycemia. Glucose 82-89 insulin Homo sapiens 14-21 11484070-5 2001 Cross-sectional analyses show that acute insulin secretory responses (AIR) to intravenous glucose are lower in subjects with impaired glucose tolerance and those at high risk for developing diabetes. Glucose 90-97 insulin Homo sapiens 41-48 11499733-3 2001 Because glucose utilization by cardiomyocytes is an insulin-mediated process, we hypothesized that diabetes would have a more adverse impact on mortality and progression of heart failure in ischemic compared with nonischemic cardiomyopathy. Glucose 8-15 insulin Homo sapiens 52-59 11489930-1 2001 Insulin stimulates glucose uptake by recruiting glucose transporter 4 (GLUT4) from an intracellular compartment to the cell surface; this phenomenon is defective in type 2 diabetes. Glucose 19-26 insulin Homo sapiens 0-7 11489930-8 2001 Insulin resistance generated by prolonged (24 hours) exposure of myotubes to high glucose and insulin diminished the acute insulin-dependent remodeling of cortical actin and GLUT4myc translocation, reminiscent of the effect of swinholide-A. Glucose 82-89 insulin Homo sapiens 0-7 11489930-8 2001 Insulin resistance generated by prolonged (24 hours) exposure of myotubes to high glucose and insulin diminished the acute insulin-dependent remodeling of cortical actin and GLUT4myc translocation, reminiscent of the effect of swinholide-A. Glucose 82-89 insulin Homo sapiens 123-130 11502767-10 2001 Insulin-mediated glucose disposal, measured by a euglycemic hyperinsulinemic clamp, declined at month 1 (49.7 +/- 27.5 to 25.6 +/- 6.6 nmol/kg(LBM).min/pmol(INSULIN)/liter, P = 0.04); values improved at month 6 (49.2 +/- 22.6, P = 0.03, compared with month 1) and did not differ significantly from baseline. Glucose 17-24 insulin Homo sapiens 0-7 11502801-1 2001 To elucidate the causes of the diminished incretin effect in type 2 diabetes mellitus we investigated the secretion of the incretin hormones, glucagon-like peptide-1 and glucose- dependent insulinotropic polypeptide and measured nonesterified fatty acids, and plasma concentrations of insulin, C peptide, pancreatic polypeptide, and glucose during a 4-h mixed meal test in 54 heterogeneous type 2 diabetic patients, 33 matched control subjects with normal glucose tolerance, and 15 unmatched subjects with impaired glucose tolerance. Glucose 170-177 insulin Homo sapiens 189-196 11502802-8 2001 High blood glucose suppressed their abnormal baseline acute insulin responses to leucine of 180, 98, 47, and 28 microU/ml to 73, 0, 6, and 19 microU/ml, respectively. Glucose 11-18 insulin Homo sapiens 60-67 11518851-5 2001 Atenolol was associated with an approximately 20% reduction in insulin sensitivity (insulin-induced glucose disposal rate/mean insulin concentration ratio, P < 0.01) and an approximately 10% reduction in glucose disappearance rate (K-value, P < 0.05), whereas these variables were not significantly modified with nebivolol. Glucose 100-107 insulin Homo sapiens 84-91 11518851-5 2001 Atenolol was associated with an approximately 20% reduction in insulin sensitivity (insulin-induced glucose disposal rate/mean insulin concentration ratio, P < 0.01) and an approximately 10% reduction in glucose disappearance rate (K-value, P < 0.05), whereas these variables were not significantly modified with nebivolol. Glucose 100-107 insulin Homo sapiens 84-91 11531149-1 2001 OBJECTIVE: To study the effect of two insulin-meal intervals on short-term glucose fluctuations in tightly controlled gestational diabetes mellitus (GDM). Glucose 75-82 insulin Homo sapiens 38-45 11481396-4 2001 Due to the quantitative importance of muscle as a site for insulin-sensitive glucose metabolism, these effects may initiate the metabolic vicious cycle that results in the development of the metabolic syndrome, well in advance of overt obesity or the diagnosis of type-2 diabetes. Glucose 77-84 insulin Homo sapiens 59-66 11431640-4 2001 METHODS: The presence of insulin-resistance and hyperinsulinemia, in 15 women aged between 20 and 30 with BMI >26 kg/m2, has been verified with test loaded with glucose; 500 mg of metformin have been given to these women three times a day before meals for 12 weeks. Glucose 164-171 insulin Homo sapiens 25-32 11431640-8 2001 As well as the reproductive function, this insulin-sensitizing agent has the further <<theoretical>> advantage of a possible favourable effect also on the complications of the polycystic ovary syndrome specifically connected with: glucose-intolerance, dislipidemia, arteriosclerosis and hypertension. Glucose 243-250 insulin Homo sapiens 43-50 11474322-7 2001 RESULTS: Insulin-stimulated glucose uptake rates increased after intensive training (from 4.9 +/- 0.5 mg x min(-1) x kg(-1) to 6.2 +/- 0.6 mg x min(-1) x kg(-1) (P < 0.008) (step 1) and from 9.0 +/- 0.8 mg x min(-1) x kg(-1) to 10.6 +/- 0.8 mg x min(-1) x kg(-1) (P = 0.103) (step 2)). Glucose 28-35 insulin Homo sapiens 9-16 11474324-9 2001 Because glucose utilization increased similarly during exercise in both conditions, the higher insulin levels after the meal might have blunted glucose production, creating an imbalance between total glucose production and total peripheral utilization in the fed state in contrast to the fasted state. Glucose 8-15 insulin Homo sapiens 95-102 11474324-9 2001 Because glucose utilization increased similarly during exercise in both conditions, the higher insulin levels after the meal might have blunted glucose production, creating an imbalance between total glucose production and total peripheral utilization in the fed state in contrast to the fasted state. Glucose 144-151 insulin Homo sapiens 95-102 11474324-9 2001 Because glucose utilization increased similarly during exercise in both conditions, the higher insulin levels after the meal might have blunted glucose production, creating an imbalance between total glucose production and total peripheral utilization in the fed state in contrast to the fasted state. Glucose 144-151 insulin Homo sapiens 95-102 11474471-4 2001 In these patients, most of the insulin extracted from a 24-hour urine collection and from urine collected after stimulation of insulin secretion by glucose or glucagon was normal insulin, whereas 90% of serum insulin is structurally abnormal (Leu-A3 insulin). Glucose 148-155 insulin Homo sapiens 127-134 11474471-4 2001 In these patients, most of the insulin extracted from a 24-hour urine collection and from urine collected after stimulation of insulin secretion by glucose or glucagon was normal insulin, whereas 90% of serum insulin is structurally abnormal (Leu-A3 insulin). Glucose 148-155 insulin Homo sapiens 127-134 11474471-4 2001 In these patients, most of the insulin extracted from a 24-hour urine collection and from urine collected after stimulation of insulin secretion by glucose or glucagon was normal insulin, whereas 90% of serum insulin is structurally abnormal (Leu-A3 insulin). Glucose 148-155 insulin Homo sapiens 127-134 11474471-4 2001 In these patients, most of the insulin extracted from a 24-hour urine collection and from urine collected after stimulation of insulin secretion by glucose or glucagon was normal insulin, whereas 90% of serum insulin is structurally abnormal (Leu-A3 insulin). Glucose 148-155 insulin Homo sapiens 127-134 11438661-4 2001 Since rapamycin but not lactacystin enhances insulin-stimulated 2-deoxyglucose (2-DOG) uptake, IRS-1-associated PI 3-kinase localized at the LDM was suggested to be important in the regulation of glucose transport. Glucose 71-78 insulin Homo sapiens 45-52 11438661-8 2001 We propose that subcellular redistribution of IRS-1, regulated by the mTOR-dependent pathway, facilitates proteasomal degradation of IRS-1, thereby down-regulating Akt, and that the pathway also negatively regulates insulin-stimulated glucose transport, probably through the redistribution of IRS-1. Glucose 235-242 insulin Homo sapiens 216-223 11438681-0 2001 ADP-ribosylation factor 6 delineates separate pathways used by endothelin 1 and insulin for stimulating glucose uptake in 3T3-L1 adipocytes. Glucose 104-111 insulin Homo sapiens 80-87 11438681-1 2001 In 3T3-L1 adipocytes, both insulin and endothelin 1 stimulate glucose transport via translocation of the GLUT4 glucose carrier from an intracellular compartment to the cell surface. Glucose 62-69 insulin Homo sapiens 27-34 11438681-1 2001 In 3T3-L1 adipocytes, both insulin and endothelin 1 stimulate glucose transport via translocation of the GLUT4 glucose carrier from an intracellular compartment to the cell surface. Glucose 111-118 insulin Homo sapiens 27-34 11425552-0 2001 Phenylcyanoguanidines as inhibitors of glucose-induced insulin secretion from beta cells. Glucose 39-46 insulin Homo sapiens 55-62 11404224-6 2001 Whereas the predominant effect of insulin in human skeletal muscle cells is to enhance glucose transport, phosphorylation, and steps beyond, it also determines the overall rate of glucose metabolism. Glucose 87-94 insulin Homo sapiens 34-41 11408252-1 2001 In response to insulin, a hormone [hepatic insulin sensitizing substance (HISS)] is released from the liver to stimulate glucose uptake in skeletal muscle but not liver or gut. Glucose 121-128 insulin Homo sapiens 15-22 11408252-3 2001 Insulin action was assessed by the rapid insulin sensitivity test, where the index is the glucose required (mg/kg) to maintain euglycemia after a bolus of insulin. Glucose 90-97 insulin Homo sapiens 0-7 11408252-3 2001 Insulin action was assessed by the rapid insulin sensitivity test, where the index is the glucose required (mg/kg) to maintain euglycemia after a bolus of insulin. Glucose 90-97 insulin Homo sapiens 41-48 11462311-10 2001 In patients starting insulin therapy, mean HbA1c and fasting blood glucose level decreased from 9.5% to 7.6%, and from 12.0 mmol to 8.4 mmol, respectively (P < 0.001). Glucose 67-74 insulin Homo sapiens 21-28 11462311-14 2001 After 12 weeks, patients directly referred to insulin therapy showed a statistically significant improvement in HbA1c and fasting glucose level, in contrast to patients with enhanced compliance. Glucose 130-137 insulin Homo sapiens 46-53 11453956-7 2001 Rate of log glucose disappearance in the first 15 minutes was calculated as a direct measure of insulin sensitivity. Glucose 12-19 insulin Homo sapiens 96-103 11410108-1 2001 Minimal model analysis of glucose and insulin concentrations in the intravenous glucose tolerance test (IVGTT) has been widely used to obtain a measure of insulin sensitivity in humans. Glucose 26-33 insulin Homo sapiens 155-162 11410108-1 2001 Minimal model analysis of glucose and insulin concentrations in the intravenous glucose tolerance test (IVGTT) has been widely used to obtain a measure of insulin sensitivity in humans. Glucose 80-87 insulin Homo sapiens 38-45 11410108-1 2001 Minimal model analysis of glucose and insulin concentrations in the intravenous glucose tolerance test (IVGTT) has been widely used to obtain a measure of insulin sensitivity in humans. Glucose 80-87 insulin Homo sapiens 155-162 11410108-6 2001 Variation in basal glucose assignment significantly affected the magnitude of estimates of insulin sensitivity. Glucose 19-26 insulin Homo sapiens 91-98 11410112-0 2001 Effects of high-dose glucose-insulin-potassium on myocardial metabolism after coronary surgery in patients with Type II diabetes. Glucose 21-28 insulin Homo sapiens 29-36 11423485-10 2001 Interestingly, lack of IR expression in IR-null keratinocytes abolished insulin-induced glucose uptake and partially decreased insulin- and IGF-I-induced proliferation, demonstrating the direct involvement of the IR in these processes. Glucose 88-95 insulin Homo sapiens 72-79 11508266-7 2001 RESULTS: Insulin-stimulated total glucose disposal rate was lower in the Type II diabetic subjects compared with the obese normoglycaemic subjects (4.96 +/- 049 vs 10.35 +/- 0.89 mg.min(-1).kg ffm(-1), p < 0.001) as was glucose storage (2.03 +/- 0.50 vs 6.59 +/- 0.83, p < 0.001). Glucose 34-41 insulin Homo sapiens 9-16 11508266-7 2001 RESULTS: Insulin-stimulated total glucose disposal rate was lower in the Type II diabetic subjects compared with the obese normoglycaemic subjects (4.96 +/- 049 vs 10.35 +/- 0.89 mg.min(-1).kg ffm(-1), p < 0.001) as was glucose storage (2.03 +/- 0.50 vs 6.59 +/- 0.83, p < 0.001). Glucose 223-230 insulin Homo sapiens 9-16 11553181-9 2001 After correction for covariates according to differences between investigators and subject characteristics including BMI (multiple regression analysis), insulin-stimulated glucose disposal was lower in FH+ compared with FH- (P < 0.00001). Glucose 172-179 insulin Homo sapiens 153-160 11553181-10 2001 Insulin-stimulated glucose oxidation was slightly increased in FH+ compared with FH-, and insulin-stimulated non-oxidative glucose metabolism was consequently markedly reduced in FH+ compared with FH- (P < 0.0005). Glucose 19-26 insulin Homo sapiens 0-7 11553181-10 2001 Insulin-stimulated glucose oxidation was slightly increased in FH+ compared with FH-, and insulin-stimulated non-oxidative glucose metabolism was consequently markedly reduced in FH+ compared with FH- (P < 0.0005). Glucose 123-130 insulin Homo sapiens 90-97 11553181-12 2001 The insulin resistance is independent of degree of obesity and is restricted solely to the pathway of non-oxidative glucose metabolism. Glucose 116-123 insulin Homo sapiens 4-11 11553186-7 2001 Glucose infusion rate (GIR) curves showed clear separation 20 min after injection and were significantly greater for insulin lispro during the 40-60, 60-80 and 80-100-minute time intervals. Glucose 0-7 insulin Homo sapiens 117-124 11553186-8 2001 Total glucose infused was only approximately 5% larger with insulin lispro during the 6-h follow-up, due to lower insulinaemia at later time points. Glucose 6-13 insulin Homo sapiens 60-67 11553190-2 2001 The goal of this study was to evaluate if HOMA, a modelized plasma insulin/glucose ratio allowing simple evaluation of residual insulin secretion and sensitivity, is a better predictor of the insulin requiring stage than clinical indices. Glucose 75-82 insulin Homo sapiens 128-135 11497476-16 2001 CONCLUSION: A 1-hour postmeal blood glucose level is helpful for deciding the withdrawal of insulin therapy in overweight, insulin-treated patients with type 2 diabetes. Glucose 36-43 insulin Homo sapiens 123-130 11497481-11 2001 CONCLUSION: Current evidence suggests that the use of insulin-sensitizing agents in patients with polycystic ovary syndrome not only improves their sensitivity to the effects of insulin on glucose and lipid metabolism but also ameliorates clinical and biochemical manifestations of hyperandrogenism and increases rates of ovulation. Glucose 189-196 insulin Homo sapiens 54-61 11497481-11 2001 CONCLUSION: Current evidence suggests that the use of insulin-sensitizing agents in patients with polycystic ovary syndrome not only improves their sensitivity to the effects of insulin on glucose and lipid metabolism but also ameliorates clinical and biochemical manifestations of hyperandrogenism and increases rates of ovulation. Glucose 189-196 insulin Homo sapiens 178-185 11443175-16 2001 These findings suggest that activation of PI-3 kinase, an enzyme crucial for insulin-stimulated glucose transport, is not necessary for the above effects of insulin in the ovary. Glucose 96-103 insulin Homo sapiens 77-84 11436180-1 2001 Multiple isoforms of glucose transporters are found in muscle, the tissue that normally accounts for 85% of insulin-stimulated glucose uptake. Glucose 21-28 insulin Homo sapiens 108-115 11436184-2 2001 Because this view seems to have gained widespread support in the general population, we thought it important to perform the current study testing the hypothesis that differences in insulin-mediated glucose disposal do not affect weight loss in response to calorie-restricted diets. Glucose 198-205 insulin Homo sapiens 181-188 11681786-0 2001 Intracellular signalling mechanisms regulating glucose transport in insulin-sensitive tissues (review). Glucose 47-54 insulin Homo sapiens 68-75 11681786-2 2001 The events that mediate the action of insulin on glucose transport, which is by far the best characterized paradigm for glucose transport regulation, are discussed. Glucose 49-56 insulin Homo sapiens 38-45 11681786-2 2001 The events that mediate the action of insulin on glucose transport, which is by far the best characterized paradigm for glucose transport regulation, are discussed. Glucose 120-127 insulin Homo sapiens 38-45 11681788-1 2001 Insulin increases the rate of glucose transport into fat and muscle cells by stimulating the translocation of intracellular Glut 4-containing vesicles to the plasma membrane. Glucose 30-37 insulin Homo sapiens 0-7 11283022-5 2001 When antisense oligonucleotides targeted to a putative SRp40-binding sequence in the betaII-betaI intron were transfected into L6 cells, insulin effects on splicing and glucose uptake were blocked. Glucose 169-176 insulin Homo sapiens 137-144 11283022-7 2001 This switch in PKC isozyme expression is important for increases in the glucose transport effect of insulin. Glucose 72-79 insulin Homo sapiens 100-107 11433662-4 2001 The main defect in these patients seems to be a reduced secretion of insulin by the pancreas in response to glucose stimulation. Glucose 108-115 insulin Homo sapiens 69-76 11279172-8 2001 Rather, p38 MAPK activation leads to a marked down-regulation of insulin-induced glucose uptake via GLUT4, which may underlie cellular stress-induced insulin resistance caused by tumor necrosis factor alpha and other factors. Glucose 81-88 insulin Homo sapiens 65-72 11279172-8 2001 Rather, p38 MAPK activation leads to a marked down-regulation of insulin-induced glucose uptake via GLUT4, which may underlie cellular stress-induced insulin resistance caused by tumor necrosis factor alpha and other factors. Glucose 81-88 insulin Homo sapiens 150-157 11422115-14 2001 Adrenocortical adenoma may be one of the risk factors for insulin resistance that is believed to induce disturbed glucose tolerance and/or hypertension. Glucose 114-121 insulin Homo sapiens 58-65 11600556-7 2001 The impact on the glucose profile was consistent with the enhanced insulin profiles after nateglinide, resulting in higher peak plasma insulin concentrations compared with placebo (P < 0.01). Glucose 18-25 insulin Homo sapiens 67-74 11600556-7 2001 The impact on the glucose profile was consistent with the enhanced insulin profiles after nateglinide, resulting in higher peak plasma insulin concentrations compared with placebo (P < 0.01). Glucose 18-25 insulin Homo sapiens 135-142 11600557-2 2001 This insulin resistance is manifested by lower rates of insulin-stimulated glucose metabolism and compensatory hyperinsulinemia in pubertal compared with prepubertal children. Glucose 75-82 insulin Homo sapiens 5-12 11600557-2 2001 This insulin resistance is manifested by lower rates of insulin-stimulated glucose metabolism and compensatory hyperinsulinemia in pubertal compared with prepubertal children. Glucose 75-82 insulin Homo sapiens 56-63 11600557-8 2001 Insulin-stimulated glucose metabolism was measured during a 3-h hyperinsulinemic (40 mU/m(2).min)-euglycemic clamp procedure. Glucose 19-26 insulin Homo sapiens 0-7 11600559-2 2001 We investigated temporal and dose-response relationships of plasma leptin in response to physiological changes in insulin/glucose. Glucose 122-129 insulin Homo sapiens 114-121 11600560-7 2001 In response to glucose loading, insulin and C-peptide plasma concentrations were higher in lipid compared with saline infusion (plasma insulin: 600 +/- 98 vs. 310 +/- 45 pM, P < 0.05; plasma C-peptide 3.5 +/- 0.2 vs. 1.7 +/- 0.2 nM, P < 0.05). Glucose 15-22 insulin Homo sapiens 32-39 11600560-7 2001 In response to glucose loading, insulin and C-peptide plasma concentrations were higher in lipid compared with saline infusion (plasma insulin: 600 +/- 98 vs. 310 +/- 45 pM, P < 0.05; plasma C-peptide 3.5 +/- 0.2 vs. 1.7 +/- 0.2 nM, P < 0.05). Glucose 15-22 insulin Homo sapiens 135-142 11551598-4 2001 Insulin formulations, treatment strategies, and methods and routes of delivery have changed much, with more and more options for monitoring the effect on blood glucose concentrations. Glucose 160-167 insulin Homo sapiens 0-7 11551598-6 2001 Parallel developments in glucose-sensing technologies are welcomed as an integral part of safe and optimum implementation of insulin replacement therapy. Glucose 25-32 insulin Homo sapiens 125-132 11555840-12 2001 Because insulin and high glucose are synergistic in inducing insulin resistance in this model, the reduction in immunoreactive insulin probably contributed to the protective effect of the antioxidants. Glucose 25-32 insulin Homo sapiens 61-68 11555840-12 2001 Because insulin and high glucose are synergistic in inducing insulin resistance in this model, the reduction in immunoreactive insulin probably contributed to the protective effect of the antioxidants. Glucose 25-32 insulin Homo sapiens 61-68 11478588-0 2001 Caffeine ingestion elevates plasma insulin response in humans during an oral glucose tolerance test. Glucose 77-84 insulin Homo sapiens 35-42 11531966-6 2001 DI, derived as the product of SI and AIR(Glucose), is a measure of the activity of the B-cells adjusted for insulin resistance. Glucose 41-48 insulin Homo sapiens 108-115 11458018-3 2001 Low intracellular glucose and glucose-6-phosphate concentrations indicate that decreased glucose transport is mainly responsible for common insulin resistance. Glucose 18-25 insulin Homo sapiens 140-147 11458018-3 2001 Low intracellular glucose and glucose-6-phosphate concentrations indicate that decreased glucose transport is mainly responsible for common insulin resistance. Glucose 30-37 insulin Homo sapiens 140-147 11458019-7 2001 The production of glucose by the small intestine may be acutely blunted upon insulin infusion. Glucose 18-25 insulin Homo sapiens 77-84 11423511-0 2001 Diminished insulin secretory response to glucose but normal insulin and glucagon secretory responses to arginine in a family with maternally inherited diabetes and deafness caused by mitochondrial tRNA(LEU(UUR)) gene mutation. Glucose 41-48 insulin Homo sapiens 11-18 11423511-3 2001 Insulin and C-peptide responses were evaluated by intravenous glucagon application, intravenous arginine stimulation test, and intravenous glucose tolerance test. Glucose 139-146 insulin Homo sapiens 12-21 11423511-8 2001 CONCLUSIONS: This study shows impaired insulin and C-peptide secretion in response to a glucose challenge and to glucagon stimulation in diabetic patients with mitochondrial tRNA Leu(UUR) gene mutation, although insulin and glucagon secretory responses to arginine were normal. Glucose 88-95 insulin Homo sapiens 51-60 11423511-8 2001 CONCLUSIONS: This study shows impaired insulin and C-peptide secretion in response to a glucose challenge and to glucagon stimulation in diabetic patients with mitochondrial tRNA Leu(UUR) gene mutation, although insulin and glucagon secretory responses to arginine were normal. Glucose 88-95 insulin Homo sapiens 39-46 11508276-12 2001 The lack of correlation between the molecular severity of glucokinase mutations, insulin secretion at intravenous glucose tolerance test and differences in glucose tolerance suggests that factors outside the beta cell are also involved in determining post-load glucose concentrations in these subjects. Glucose 114-121 insulin Homo sapiens 81-88 11508279-6 2001 Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. Glucose 88-95 insulin Homo sapiens 34-41 11415999-15 2001 These observations suggest a glucose- and STAT5-independent pathway by which PRL may induce insulin gene transcription. Glucose 29-36 insulin Homo sapiens 92-99 11497476-5 2001 If the postmeal glucose level was < or = 10 mmol/L, the insulin therapy was discontinued. Glucose 16-23 insulin Homo sapiens 59-66 11497476-16 2001 CONCLUSION: A 1-hour postmeal blood glucose level is helpful for deciding the withdrawal of insulin therapy in overweight, insulin-treated patients with type 2 diabetes. Glucose 36-43 insulin Homo sapiens 92-99 11431740-7 2001 During the insulin infusion, the mean total peripheral glucose uptake (area under the curve [AUC]) was 1,422 (SD, 1,253), 2,244 (SD, 1,392), and 4,500 (SD, 1,120) micromol/kg on days 0, 7, and 14, respectively. Glucose 55-62 insulin Homo sapiens 11-18 11443163-3 2001 The parameters evaluated were as follows: glucose, insulin, and C-peptide (Cp) response to an oral glucose load. Glucose 99-106 insulin Homo sapiens 64-73 11443193-2 2001 Leptin inhibits especially the glucose-stimulated insulin secretion from pancreatic cells. Glucose 31-38 insulin Homo sapiens 50-57 11443199-1 2001 The aim of this study was to investigate whether insulin resistance-associated in utero undernutrition was related to changes in insulin action on gene expression of molecules involved in the insulin signaling pathway and peripheral glucose metabolism in muscle and adipose tissue. Glucose 233-240 insulin Homo sapiens 49-56 11443199-1 2001 The aim of this study was to investigate whether insulin resistance-associated in utero undernutrition was related to changes in insulin action on gene expression of molecules involved in the insulin signaling pathway and peripheral glucose metabolism in muscle and adipose tissue. Glucose 233-240 insulin Homo sapiens 129-136 11443199-1 2001 The aim of this study was to investigate whether insulin resistance-associated in utero undernutrition was related to changes in insulin action on gene expression of molecules involved in the insulin signaling pathway and peripheral glucose metabolism in muscle and adipose tissue. Glucose 233-240 insulin Homo sapiens 129-136 11443199-5 2001 Insulin-stimulated glucose uptake was significantly lower in IUGR-born subjects than in controls (36.9 +/- 12, 7 vs. 53.9 +/- 12.7 micromol/kg.min; P = 0.007), affecting both the glucose oxidation rate and the nonoxidative glucose disposal rate. Glucose 19-26 insulin Homo sapiens 0-7 11443199-5 2001 Insulin-stimulated glucose uptake was significantly lower in IUGR-born subjects than in controls (36.9 +/- 12, 7 vs. 53.9 +/- 12.7 micromol/kg.min; P = 0.007), affecting both the glucose oxidation rate and the nonoxidative glucose disposal rate. Glucose 179-186 insulin Homo sapiens 0-7 11443199-12 2001 Our data provide additional information about the mechanism of insulin resistance associated with in utero undernutrition and strengthen the role of glucose transport in the control of insulin sensitivity. Glucose 149-156 insulin Homo sapiens 185-192 11443204-9 2001 During the oral glucose tolerance test, glucose levels were elevated in DW, with higher insulin levels [0 h: DW, 207 +/- 8.6; OW, 100 +/- 7.2 pmol/L (P < 0.01); 1 h: DW, 410 +/- 15.2; OW, 320 +/- 10.9 pmol/L (P < 0.05)], but with a flat Cpeptide response (1 h: DW, 932 +/- 40; OW, 1764 +/- 40 pmol/L; P < 0.05). Glucose 40-47 insulin Homo sapiens 88-95 12521823-1 2001 Insulin lispro (IL) possesses characteristics (decreased hypoglycaemia, greater convenience in timing of administration and better post-prandial glucose control) which may favour its use in women with diabetes. Glucose 145-152 insulin Homo sapiens 0-7 11436184-10 2001 Weight loss in the insulin-resistant group was also associated with a significant decrease in SSPG concentration (219 +/- 7 to 144 +/- 14 mg/dL), associated with significantly lower fasting TG concentrations (P <.001) and day-long concentrations of plasma glucose and insulin (P <.005). Glucose 259-266 insulin Homo sapiens 19-26 11436188-1 2001 The relationship between insulin-mediated glucose disposal and daylong free fatty acid (FFA) concentrations before and after sibutramine-assisted weight loss was investigated in 24 healthy, normotensive, nondiabetic, obese women (body mass index [BMI] >30.0 kg/m(2)). Glucose 42-49 insulin Homo sapiens 25-32 11436188-7 2001 The improvement in insulin sensitivity in the IR group after weight loss was associated with a significant decline in daylong plasma glucose (P >.001) and insulin (P =.02) concentrations, without a weight-loss-associated decrease in daylong plasma FFA responses. Glucose 133-140 insulin Homo sapiens 19-26 11448578-3 2001 Insulin sensitivity often was reduced in patients with cancer; however, the amount of glucose metabolized was not related to tumor site or stage. Glucose 86-93 insulin Homo sapiens 0-7 11394907-1 2001 Insulin and acute exercise stimulate glucose transport in skeletal muscle by translocating GLUT4 glucose transporters to the cell surface. Glucose 37-44 insulin Homo sapiens 0-7 11440092-1 2001 UNLABELLED: Although hyperglycaemia is relatively frequent in the course of severe illnesses and may be looked upon as the possible result of an uncoordinated insulin response to the increased glucose that the body may need during periods of stress, it is generally agreed that it does not constitute a prediabetic condition. Glucose 193-200 insulin Homo sapiens 159-166 11411733-3 2001 Initially (90 to 95 min), there was a decrease in blood glucose (P = .016) that correlated negatively with glucose disposal rate corrected for insulin (r = -0.55, P = .040) and positively with fasting insulin (r = 0.55). Glucose 56-63 insulin Homo sapiens 143-150 11411733-3 2001 Initially (90 to 95 min), there was a decrease in blood glucose (P = .016) that correlated negatively with glucose disposal rate corrected for insulin (r = -0.55, P = .040) and positively with fasting insulin (r = 0.55). Glucose 56-63 insulin Homo sapiens 201-208 11411733-5 2001 The glucose increase (90 to 140 min) correlated positively with fasting insulin (r = 0.55), systolic blood pressure (r = 0.57), delta epinephrine 90 to 120 min (r = 0.59), and baseline epinephrine (r = 0.57). Glucose 4-11 insulin Homo sapiens 72-79 11411733-8 2001 The initial dip in glucose was more pronounced with higher insulin sensitivity, corresponding to previous observations during mental stress test. Glucose 19-26 insulin Homo sapiens 59-66 11411733-9 2001 The following increment in blood glucose was positively related to insulin, systolic blood pressure, and epinephrine levels. Glucose 33-40 insulin Homo sapiens 67-74 11462780-6 2001 Insulin operates by lowering glucose levels to the normal range in focal ischemia. Glucose 29-36 insulin Homo sapiens 0-7 11395034-2 2001 Insulin resistance was measured using an insulin modified frequently sampled intravenous glucose tolerance test. Glucose 89-96 insulin Homo sapiens 0-7 11678042-6 2001 The patients had high BMI values, with 32% of men and 30% of women overweight, and 2% and 14%, respectively, obese, with higher glucose, cholesterol and triglyceride values reflecting enhanced insulin resistance and lipid abnormalities. Glucose 128-135 insulin Homo sapiens 193-200 11375335-3 2001 We compared the effects of elevated plasma NEFA levels on basal and insulin-stimulated glucose metabolism in 8 normal women (age 42 +/- 8 years [mean +/- SD], BMI 25 +/- 3 kg/m(2)) and 10 normal men (35 +/- 6 years, 24 +/- 3 kg/m(2)). Glucose 87-94 insulin Homo sapiens 68-75 11375335-8 2001 In the control studies, the men and women had similar insulin-stimulated glucose disposal rates (R(d)) and substrate oxidation rates. Glucose 73-80 insulin Homo sapiens 54-61 11375335-9 2001 In the men, elevated NEFA levels decreased insulin-stimulated glucose R(d) during the final 40 min of the clamp by 23% (P < 0.001). Glucose 62-69 insulin Homo sapiens 43-50 11375335-15 2001 During the last 40 min of the high-insulin dose clamps with elevated NEFA, glucose oxidation was decreased by 33% in the men (P < 0.001) and by 23% in the women (P < 0.02). Glucose 75-82 insulin Homo sapiens 35-42 11375337-5 2001 In the diabetic patients, plasma glucose levels were normalized overnight before the studies by low-dose insulin infusion. Glucose 33-40 insulin Homo sapiens 105-112 11375338-0 2001 Resistance to exercise-induced increase in glucose uptake during hyperinsulinemia in insulin-resistant skeletal muscle of patients with type 1 diabetes. Glucose 43-50 insulin Homo sapiens 70-77 11375338-1 2001 Insulin and exercise have been shown to activate glucose transport at least in part via different signaling pathways. Glucose 49-56 insulin Homo sapiens 0-7 11375338-23 2001 We conclude that the ability of exercise to increase insulin-stimulated glucose uptake in vivo is blunted in patients with insulin-resistant type 1 diabetes compared with normal subjects. Glucose 72-79 insulin Homo sapiens 53-60 11375338-23 2001 We conclude that the ability of exercise to increase insulin-stimulated glucose uptake in vivo is blunted in patients with insulin-resistant type 1 diabetes compared with normal subjects. Glucose 72-79 insulin Homo sapiens 123-130 11375349-3 2001 In both cell types, insulin-stimulated glucose uptake is reduced by inhibitors of p38 mitogen-activated protein kinase (MAPK). Glucose 39-46 insulin Homo sapiens 20-27 11431595-2 2001 They have proven efficacy for reducing plasma glucose levels of type 2 diabetic patients treated with diet alone, sulphonylureas, metformin or insulin. Glucose 46-53 insulin Homo sapiens 143-150 11440373-1 2001 (2000) assessment of insulin sensitivity and beta-cell function from measurements in the fasting state and during an oral glucose tolerance test. Glucose 122-129 insulin Homo sapiens 21-28 11476359-7 2001 Post-prandial blood glucose levels were lower with insulin lispro after breakfast (p<0.001), lunch (p<0.005) and dinner (p<0.001). Glucose 20-27 insulin Homo sapiens 51-58 11523909-1 2001 Several lines of evidence suggest that ATP-sensitive potassium (KATP) channels are involved in glucose uptake by insulin target tissues. Glucose 95-102 insulin Homo sapiens 113-120 11523909-3 2001 We used potassium channel openers PCO-400 and nicorandil alone or in combination with channel blockers glibenclamide and gliclazide to examine their effects on insulin- or high glucose concentration-induced glucose uptake using 2-deoxy-D-3H-glucose or 3-O-methyl-D-3H-glucose as tracer, respectively. Glucose 207-214 insulin Homo sapiens 160-167 11523909-5 2001 PCO-400 and nicorandil dose-dependently inhibited insulin-stimulated glucose uptake, and their inhibitory effects were reversed by glibenclamide or gliclazide. Glucose 69-76 insulin Homo sapiens 50-57 11523909-8 2001 PMA (phorbol 12-myristate 13-acetate) dose-dependently reversed the PCO-400-induced suppression of insulin-stimulated glucose uptake. Glucose 118-125 insulin Homo sapiens 99-106 11523909-10 2001 From these results we conclude that KATP channels modulate the basal and insulin-or high glucose level-stimulated glucose transport in skeletal muscle through a mechanism independent of PKC. Glucose 114-121 insulin Homo sapiens 73-80 11588809-1 2001 Insulin resistance (IRI) applies to abnormalities of insulin-stimulated glucose metabolism. Glucose 72-79 insulin Homo sapiens 53-60 11697442-10 2001 In contrast, insulin-mediated whole-body glucose uptake was lower in middle-aged subjects (6.6 +/- 1.4 mg/ kg x min) with respect to young individuals (8.1+/-1.7 mg/kg min, p < 0.05). Glucose 41-48 insulin Homo sapiens 13-20 11697442-14 2001 In conclusion, the data provide evidence for a normal regulation of protein anabolism and an early dissociation between the metabolic effects of insulin on glucose uptake and proteolysis in middle-aged subjects. Glucose 156-163 insulin Homo sapiens 145-152 11588809-3 2001 A simple method to quantify insulin resistance was assessed through the measurement of glucose and insulin (fasting glucose [mmol/L] x fasting insulin [mU/L]/22.5) in patients (n = 50) attending our clinic of human reproduction, including controls (n = 10) and diabetics either unstable or under control (n = 5). Glucose 87-94 insulin Homo sapiens 28-35 11387273-2 2001 Insulin sensitivity was measured by the continuous infusion of glucose with model assessment (CIGMA) test. Glucose 63-70 insulin Homo sapiens 0-7 11447730-0 2001 Simplification of continuous infusion of glucose with model assessment in the evaluation of insulin resistance in women with PCOS. Glucose 41-48 insulin Homo sapiens 92-99 11447730-3 2001 Using insulin and glucose values at 60 min only, a new insulin resistance index (IR2) was obtained using the same mathematical method. Glucose 18-25 insulin Homo sapiens 55-62 11447730-7 2001 In conclusion, the simplified CIGMA test, using insulin and glucose concentration at 60 min of glucose infusion only, is a highly sensitive and specific measure of insulin sensitivity in women with PCOS. Glucose 60-67 insulin Homo sapiens 164-171 11447730-7 2001 In conclusion, the simplified CIGMA test, using insulin and glucose concentration at 60 min of glucose infusion only, is a highly sensitive and specific measure of insulin sensitivity in women with PCOS. Glucose 95-102 insulin Homo sapiens 164-171 11404534-6 2001 Insulin secretion by the acute insulin response to intravenous glucose did not change (baseline 822 +/- 283 microU/ml x min, week 8 880 +/- 289; p = 0.4), and the insulin response to oral glucose (30 minute insulin:glucose ratio) fell from 1.69 +/- 0.54 microU/ml per mg/dl at baseline to 1.18 +/- 0.34 at week 8 (p =.05). Glucose 63-70 insulin Homo sapiens 0-7 11408400-8 2001 Insulin-stimulated glucose transport was similar in the 3 groups of patients with diabetes. Glucose 19-26 insulin Homo sapiens 0-7 11439290-8 2001 Blood was sampled for analysis of hormones (GLP-1, GLP-2, glucose-dependent insulinotropic polypeptide (GIP), insulin, glucagon), and substrates (glucose, lactate, non-esterified fatty acids (NEFA), triacylglycerol (TAG)). Glucose 58-65 insulin Homo sapiens 76-83 11404534-6 2001 Insulin secretion by the acute insulin response to intravenous glucose did not change (baseline 822 +/- 283 microU/ml x min, week 8 880 +/- 289; p = 0.4), and the insulin response to oral glucose (30 minute insulin:glucose ratio) fell from 1.69 +/- 0.54 microU/ml per mg/dl at baseline to 1.18 +/- 0.34 at week 8 (p =.05). Glucose 63-70 insulin Homo sapiens 31-38 11439291-11 2001 For the obese group, markers of insulin resistance (fasting plasma glucose, HbA1c, fasting plasma insulin and C-peptide) all rose significantly with increasing BMI. Glucose 67-74 insulin Homo sapiens 32-39 11397859-5 2001 Women with previous GDM showed a lowered early phase insulin response to glucose and impaired insulin sensitivity, which was accounted for mainly by decreased glucose nonoxidation. Glucose 73-80 insulin Homo sapiens 53-60 11397859-9 2001 They are insulin resistant as a result of lowered glucose nonoxidation and show inappropriately low insulin responses to glucose, reflecting impaired beta-cell function. Glucose 50-57 insulin Homo sapiens 9-16 11397901-3 2001 Recently, in prepubertal girls with PA, a fasting glucose to insulin ratio (FGIR) of less than 7 was found to be predictive of insulin resistance as determined by the frequently sampled iv glucose tolerance test. Glucose 50-57 insulin Homo sapiens 61-68 11422660-7 2001 MAIN OUTCOME MEASURE: Insulin sensitivity (rate of glucose infusion per kg fat free body mass and minute), nicotine and free fatty acid (FFA) levels, pulse rate and blood pressure. Glucose 51-58 insulin Homo sapiens 22-29 11397901-10 2001 We conclude that the FGIR and QUICKI are highly correlated with oral glucose tolerance test measures of insulin sensitivity. Glucose 69-76 insulin Homo sapiens 104-111 11397906-7 2001 These variants were found, however, marginally associated with insulin and glucose levels during oral glucose tolerance testing in normoglycemic subjects. Glucose 102-109 insulin Homo sapiens 63-70 11435055-0 2001 Comparison of a continuous glucose-insulin-potassium infusion versus intermittent bolus application of insulin on perioperative glucose control and hormone status in insulin-treated type 2 diabetics. Glucose 27-34 insulin Homo sapiens 35-42 11435055-0 2001 Comparison of a continuous glucose-insulin-potassium infusion versus intermittent bolus application of insulin on perioperative glucose control and hormone status in insulin-treated type 2 diabetics. Glucose 128-135 insulin Homo sapiens 103-110 11435055-0 2001 Comparison of a continuous glucose-insulin-potassium infusion versus intermittent bolus application of insulin on perioperative glucose control and hormone status in insulin-treated type 2 diabetics. Glucose 128-135 insulin Homo sapiens 103-110 11435055-6 2001 Group A and C patients were treated with a continuous modified glucose-insulin-potassium infusion according to blood glucose levels after intubation. Glucose 63-70 insulin Homo sapiens 71-78 11356916-1 2001 Insulin secretion from MIN6 cells (a pancreatic beta-cell line) induced by high glucose (greater than 16.8 mM) was potentiated by a novel hypoglycemic agent [trans-4-(4-methylcyclohexyl)-4-oxobutyric acid (JTT-608)] (but not glibenclamide, a sulfonylurea). Glucose 80-87 insulin Homo sapiens 0-7 11398136-1 2001 We have sequenced the insulin gene in 72 unrelated Japanese subjects (52 with type 2 diabetes mellitus and 20 with normal glucose tolerance). Glucose 122-129 insulin Homo sapiens 22-29 11590907-6 2001 RESULTS: In the intraperitoneal glucose tolerance test studies, plasma glucose levels of STZ-induced non-insulin dependent diabetic rats were significantly higher and plasma insulin levels significantly lower than those of age-matched control rats in the age of six months. Glucose 71-78 insulin Homo sapiens 105-112 11479436-13 2001 However, in any case, insulin therapy should aim to near - normalise not only mean blood glucose and glycated hemoglobin values but also postprandial blood glucose level which represent an independent risk factor an for diabetic complications. Glucose 89-96 insulin Homo sapiens 22-29 11479436-13 2001 However, in any case, insulin therapy should aim to near - normalise not only mean blood glucose and glycated hemoglobin values but also postprandial blood glucose level which represent an independent risk factor an for diabetic complications. Glucose 156-163 insulin Homo sapiens 22-29 16120270-3 2001 The mtDNA content was significantly correlated with the area under the curve of insulin during an oral glucose tolerance test (r = -0.622), the homeostasis model assessment for insulin resistance (r = -0.616), the ratio of fasting glucose to insulin concentration (r = 0.586) and the fasting insulin level (r = -0.552). Glucose 103-110 insulin Homo sapiens 80-87 11590992-1 2001 BACKGROUND AND AIM: While lispro insulin has been reported to lower postprandial blood glucose concentrations, less consistent effects have been shown for glycosylated hemoglobin (HbA1c) levels. Glucose 87-94 insulin Homo sapiens 33-40 11510210-6 2001 Insulin resistance with normal glucose levels, glucose intolerance and clinical diabetes are the three recognized stages in the development of type 2 diabetes. Glucose 31-38 insulin Homo sapiens 0-7 11399973-5 2001 RESULTS: Fasting glucose (4.9 +/- 0.1 versus 5.2 +/- 0.2 mmol/l; P = 0.05) insulin concentrations (61.7 +/- 12.2 versus 83.9 +/- 12.2 pmol/l; P < 0.05), insulin : glucose ratio (12.6 +/- 1.7 versus 15.9 +/- 1.9 pmol/mmol; P < 0.05) and insulin resistance index by homeostasis model assessment (1.9 +/- 0.3 versus 2.8 +/- 0.5;P < 0.05) all increased significantly. Glucose 17-24 insulin Homo sapiens 75-82 11399973-7 2001 Insulin-mediated glucose disposal decreased significantly (10.4 +/- 1.4 versus 8.6 +/- 1.2 mg/kg x min per microU/ml insulin; 95% confidence interval 0.6--.0;P < 0.01). Glucose 17-24 insulin Homo sapiens 0-7 11399973-7 2001 Insulin-mediated glucose disposal decreased significantly (10.4 +/- 1.4 versus 8.6 +/- 1.2 mg/kg x min per microU/ml insulin; 95% confidence interval 0.6--.0;P < 0.01). Glucose 17-24 insulin Homo sapiens 117-124 11430712-8 2001 During an oral glucose tolerance test in the morning, glucagon and insulin were lower following evening E2 administration (ANOVA: glucagon, p = 0.03; insulin, p = 0.04), as well as insulin resistance tended to be lower (p = 0.09). Glucose 15-22 insulin Homo sapiens 67-74 11484512-0 2001 New insights into insulin resistance pathophysiology: how it affects glucose and lipid metabolism. Glucose 69-76 insulin Homo sapiens 18-25 11283790-3 2001 Insulin resistance, as assessed by the homeostasis model using fasting glucose and specific insulin (FSI) values, was also strongly linked (LOD score 3.5, empirical P<.0001) with this region. Glucose 71-78 insulin Homo sapiens 0-7 11287357-3 2001 Insulin sensitivity (S(I)) was determined by an intravenous glucose tolerance test with minimal-model analysis. Glucose 60-67 insulin Homo sapiens 0-7 11453277-6 2001 Insulin resistance was indirectly assessed by glucose and insulin concentration and DIT. Glucose 46-53 insulin Homo sapiens 0-7 11381287-3 2001 The majority of insulin-mediated glucose uptake occurs in skeletal muscle. Glucose 33-40 insulin Homo sapiens 16-23 11381287-5 2001 The authors" investigations of the relation between skeletal muscle blood flow and insulin-mediated glucose uptake in healthy elderly and young subjects are reviewed. Glucose 100-107 insulin Homo sapiens 83-90 11337252-3 2001 Northern blot analysis of isolated adult porcine islets demonstrated an increase in steady-state insulin mRNA levels in response to high concentrations of glucose. Glucose 155-162 insulin Homo sapiens 97-104 11868695-1 2001 The critically ill patient"s response to stress is to increase production of glucose; his can lead to hyperglycemia as insulin releasing factors become overloaded. Glucose 77-84 insulin Homo sapiens 119-126 11899076-7 2001 Thus, an important next step in developing curative treatments for type I diabetes will be the generation of a replenishable source of glucose-responsive, insulin-secreting cells that can be used for beta cell replacement. Glucose 135-142 insulin Homo sapiens 155-162 11334405-5 2001 This reduction at 25-60 min in glucose levels correlated significantly to the 10-min insulin response (r = 0.65, P = 0.024). Glucose 31-38 insulin Homo sapiens 85-92 11334405-8 2001 In conclusion, 1) the early preabsorptive insulin response to meal ingestion in humans can be largely attributed to autonomic activation mediated by noncholinergic and cholinergic mechanisms, 2) this cephalic insulin response is required for a normal postprandial glucose tolerance, and 3) GIP and GLP-1 do not contribute to the preabsorptive cephalic phase insulin response to meal ingestion. Glucose 264-271 insulin Homo sapiens 42-49 11334413-3 2001 Herein, we examined the effects of an insulin-sensitizing drug, troglitazone (TGZ), on glucose uptake and the translocation of GLUT4 in L6 myotubes. Glucose 87-94 insulin Homo sapiens 38-45 11334414-2 2001 Additionally, the relationship of effects on glucose metabolism to changes in the insulin signaling pathway cannot be assumed. Glucose 45-52 insulin Homo sapiens 82-89 11375342-2 2001 Despite similar plasma glucose and C-peptide levels, KPT-S (n = 9) had an approximate twofold elevation of fasting and intravenous glucose-stimulated plasma insulin levels compared with both KPT-P (n = 7) and healthy control subjects (n = 15). Glucose 131-138 insulin Homo sapiens 157-164 11375344-5 2001 Impaired insulin stimulation of glucose up take occurred at nelfinavir concentrations >10 micromol/l (EC(50) = 20 micromol/l) and could be attributed to impaired GLUT4 translocation. Glucose 32-39 insulin Homo sapiens 9-16 11375347-0 2001 Insulin sensitivity of suppression of endogenous glucose production is the single most important determinant of glucose tolerance. Glucose 49-56 insulin Homo sapiens 0-7 11375347-0 2001 Insulin sensitivity of suppression of endogenous glucose production is the single most important determinant of glucose tolerance. Glucose 112-119 insulin Homo sapiens 0-7 11375347-8 2001 During low-insulin infusion, the rate of endogenous glucose production (EGP) decreased more in subjects with NGT than in subjects with IGT or diabetes (delta rate of appearance [R(a)] 1.25 +/- 0.10 vs. 0.75 +/- 0.14 vs. 0.58 +/- 0.09 mg. kg(-1). Glucose 52-59 insulin Homo sapiens 11-18 11375347-12 2001 A total of 56% of the variation in glucose area under the curve (AUC) during OGTT (glucose AUC) was mainly explained by delta R(a) (increase in multiple R(2) 0.42) but also by delta R(d) (rate of disappearance) (increase in multiple R(2) 0.05), and the early insulin response during OGTT contributed significantly (increase in multiple R(2) 0.07). Glucose 35-42 insulin Homo sapiens 259-266 11375347-13 2001 When M value was included in the model, reflecting extrahepatic insulin sensitivity, it contributed to 20% of the variation in glucose AUC, and together with the incremental insulin response (increase in multiple R(2) 0.21), it explained 45% of the variation. Glucose 127-134 insulin Homo sapiens 64-71 11375347-14 2001 In conclusion, insulin sensitivity of suppression of EGP plays the most important role in the determination of blood glucose response during OGTT. Glucose 117-124 insulin Homo sapiens 15-22 11334415-4 2001 Interestingly, LID mice show a fourfold increase in serum insulin levels (2.2 vs. 0.6 ng/ml in control mice) and abnormal glucose clearance after insulin injection. Glucose 122-129 insulin Homo sapiens 146-153 11334442-8 2001 In cultured human islets, anti-CD38-positive sera exhibiting [Ca2+]i-mobilizing activity in Jurkat T-cells (n = 6) significantly stimulated insulin release at 3.3 mmol/l glucose (median [interquartile range] 738 microU/ml [234], P = 0.0001 vs. 320 [52] microU/ml of control), whereas 6 anti-CD38-positive sera without [Ca2+]i-mobilizing activity and 10 anti-CD38-negative did not. Glucose 170-177 insulin Homo sapiens 140-147 11334442-9 2001 In further incubations, the five anti-CD38-positive sera displaying [Ca2+]i-mobilizing activity in dispersed islet cells significantly stimulated insulin release at both 3.3 mmol/l glucose (2.2 +/- 0.3% of insulin islet content, P < 0.002 vs. 1.2 +/- 0.1% of control) and 16.7 mmol/l glucose (3.7 +/- 0.3 vs. 2.3 +/- 0.3%, P < 0.002). Glucose 181-188 insulin Homo sapiens 146-153 11334442-9 2001 In further incubations, the five anti-CD38-positive sera displaying [Ca2+]i-mobilizing activity in dispersed islet cells significantly stimulated insulin release at both 3.3 mmol/l glucose (2.2 +/- 0.3% of insulin islet content, P < 0.002 vs. 1.2 +/- 0.1% of control) and 16.7 mmol/l glucose (3.7 +/- 0.3 vs. 2.3 +/- 0.3%, P < 0.002). Glucose 287-294 insulin Homo sapiens 146-153 11347736-1 2001 OBJECTIVE: To assess insulin sensitivity and beta-cell function associated with lower maternal fasting plasma glucose levels at high altitude compared with sea level. Glucose 110-117 insulin Homo sapiens 21-28 11347736-7 2001 CONCLUSIONS: Maternal fasting plasma glucose that is lower at high altitude than at sea level in the presence of similar insulin secretion is associated with higher peripheral insulin sensitivity. Glucose 37-44 insulin Homo sapiens 121-128 11347736-7 2001 CONCLUSIONS: Maternal fasting plasma glucose that is lower at high altitude than at sea level in the presence of similar insulin secretion is associated with higher peripheral insulin sensitivity. Glucose 37-44 insulin Homo sapiens 176-183 11334414-12 2001 These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. Glucose 120-127 insulin Homo sapiens 81-88 11472449-5 2001 RESULTS: Following an oral glucose load we found significantly higher blood glucose levels at 90 min and 120 min and significantly higher insulin levels at 120 min and 180 min in non-diabetic subjects with the mutation but no difference in the insulinogenic indices at 30 min and 180 min. Glucose 27-34 insulin Homo sapiens 138-145 11424230-6 2001 Insulin resistance is present in hyperparathyroidism and probably arises from a raised intracellular free calcium concentration which, by decreasing normal insulin-stimulated glucose transport, increases the requirement for insulin: if this insulin resistance progresses, impaired glucose tolerance and diabetes mellitus would result. Glucose 175-182 insulin Homo sapiens 0-7 11424230-6 2001 Insulin resistance is present in hyperparathyroidism and probably arises from a raised intracellular free calcium concentration which, by decreasing normal insulin-stimulated glucose transport, increases the requirement for insulin: if this insulin resistance progresses, impaired glucose tolerance and diabetes mellitus would result. Glucose 175-182 insulin Homo sapiens 156-163 11424231-3 2001 Chronically elevated blood glucose concentrations determine the progression of the disease by further exacerbating insulin resistance and causing beta-cell exhaustion in addition to decreasing their responsiveness to glucose. Glucose 27-34 insulin Homo sapiens 115-122 11334920-7 2001 Insulin resistance was estimated from fasting glucose and insulin levels, using the homeostasis model assessment. Glucose 46-53 insulin Homo sapiens 0-7 11409642-7 2001 Serum glucose level increased after local anesthesia (control vs. local anesthesia: 5.16+/-0.11 vs. 5.62+/-0.10 mmol/l; p<0.01); however, plasma insulin concentrations did not change significantly. Glucose 6-13 insulin Homo sapiens 148-155 11344200-1 2001 Glucose-dependent insulinotropic hormone (GIP) is an intestinal hormone considered to be an important mediator of the incretin effect, i.e. the augmented insulin release observed in response to orally, compared with iv, administered glucose, despite isoglycemic glucose profiles. Glucose 233-240 insulin Homo sapiens 18-25 11344200-1 2001 Glucose-dependent insulinotropic hormone (GIP) is an intestinal hormone considered to be an important mediator of the incretin effect, i.e. the augmented insulin release observed in response to orally, compared with iv, administered glucose, despite isoglycemic glucose profiles. Glucose 262-269 insulin Homo sapiens 18-25 11344200-2 2001 Stimulation of beta-cell secretion of insulin by GIP is seen both in vitro and in vivo at permissive extracellular glucose concentrations (> 6 mmol/L). Glucose 115-122 insulin Homo sapiens 38-45 11344200-5 2001 The increased plasma insulin levels necessitated extra glucose infusion to maintain euglycemia, demonstrating the biological significance of the elevated insulin levels. Glucose 55-62 insulin Homo sapiens 21-28 11344200-5 2001 The increased plasma insulin levels necessitated extra glucose infusion to maintain euglycemia, demonstrating the biological significance of the elevated insulin levels. Glucose 55-62 insulin Homo sapiens 154-161 11344209-5 2001 During insulin infusion, total glucose disposal was significantly reduced in hypertensive diabetic subjects, compared with their normotensive counterparts (18.7 +/- 1.0 vs. 28.6 +/- 3.0 micromol/min.kg lean body mass; P < 0.01). Glucose 31-38 insulin Homo sapiens 7-14 11340092-0 2001 Zinc has an insulin-like effect on glucose transport mediated by phosphoinositol-3-kinase and Akt in 3T3-L1 fibroblasts and adipocytes. Glucose 35-42 insulin Homo sapiens 12-19 11340092-7 2001 Cytochalasin D, which disrupts actin filaments, attenuated the increase of glucose transport induced by zinc or insulin (P < 0.05). Glucose 75-82 insulin Homo sapiens 112-119 11340092-14 2001 Hence, it appears that zinc can induce an increase in glucose transport into cells and potentiate insulin-induced glucose transport, likely acting through the insulin-signaling pathway. Glucose 54-61 insulin Homo sapiens 159-166 11340092-14 2001 Hence, it appears that zinc can induce an increase in glucose transport into cells and potentiate insulin-induced glucose transport, likely acting through the insulin-signaling pathway. Glucose 114-121 insulin Homo sapiens 98-105 11340092-14 2001 Hence, it appears that zinc can induce an increase in glucose transport into cells and potentiate insulin-induced glucose transport, likely acting through the insulin-signaling pathway. Glucose 114-121 insulin Homo sapiens 159-166 11319711-2 2001 These estimates, however, are influenced by the degree to which the dose of exogenous insulin is greater than the physiologic response to a glucose load. Glucose 140-147 insulin Homo sapiens 86-93 11319723-2 2001 To define the impact of wide variations in dietary cholesterol intake on plasma total and low-density lipoprotein (LDL) cholesterol concentrations, as well as testing the hypothesis that resistance to insulin-mediated glucose disposal would accentuate the increase in plasma total and LDL cholesterol concentrations in response to a given increment in dietary cholesterol intake, we performed a prospective, randomized study comparing diets varying in cholesterol content in 65 healthy, postmenopausal women, 31 defined as insulin-resistant and 34 as insulin-sensitive. Glucose 218-225 insulin Homo sapiens 201-208 11377135-2 2001 Therefore, the glucose-insulin-potassium regimen might be beneficial in acute myocardial infarction and useful in the management of patients with septicemia, septic shock, and other inflammatory diseases in which tumor necrosis factor-alpha and macrophage migration-inhibitory factor have important roles. Glucose 15-22 insulin Homo sapiens 23-30 11420097-7 2001 After insulin treatment, blood-glucose levels dropped to approximately 40-60% of control levels and this HG was accompanied by decreased SMA. Glucose 31-38 insulin Homo sapiens 6-13 11475343-6 2001 MAIN OUTCOME MEASURES: Relation between reduction in the total amount of intraperitoneal infused glucose and parameters of glucose (plasma glucose, insulin, and HbA1C) and lipid metabolism [free fatty acids, plasma lipids, lipoproteins, and low density lipoprotein (LDL) subfraction profile]. Glucose 97-104 insulin Homo sapiens 148-155 11475924-2 2001 From a pathophysiological point of view, regular physical activity enhances insulin sensitivity, thus contributing to improve blood glucose control and to reduce cardiovascular risk factors associated to diabetes mellitus. Glucose 132-139 insulin Homo sapiens 76-83 11797459-7 2001 Insulin sensitivity (Si) was assessed by minimal model test (MINMOD) using frequently sampled intravenous glucose tolerance test in 0 week and after 12 weeks of treatment. Glucose 106-113 insulin Homo sapiens 0-7 11309621-1 2001 The stimulation of glucose uptake by insulin in muscle and adipose tissue requires translocation of the GLUT4 glucose transporter protein from intracellular storage sites to the cell surface. Glucose 19-26 insulin Homo sapiens 37-44 11309621-9 2001 The activation of TC10 is essential for insulin-stimulated glucose uptake and GLUT4 translocation. Glucose 59-66 insulin Homo sapiens 40-47 11311245-0 2001 Akt mediates insulin induction of glucose uptake and up-regulation of GLUT4 gene expression in brown adipocytes. Glucose 34-41 insulin Homo sapiens 13-20 11311245-1 2001 Insulin acutely stimulated glucose uptake in rat primary brown adipocytes in a PI3-kinase-dependent but p70S6-kinase-independent manner. Glucose 27-34 insulin Homo sapiens 0-7 11311245-2 2001 Since Akt represents an intermediate step between these kinases, this study investigated the contribution of Akt to insulin-induced glucose uptake by the use of a chemical compound, ML-9, as well as by transfection with a dominant-negative form of Akt (DeltaAkt). Glucose 132-139 insulin Homo sapiens 116-123 11311245-5 2001 In consequence, ML-9 precluded insulin stimulation of glucose uptake and GLUT4 translocation to plasma membrane (determined by Western blot), without any effect on the basal glucose uptake. Glucose 54-61 insulin Homo sapiens 31-38 11311245-9 2001 Our results indicate that activation of Akt may be an essential requirement for insulin regulation of glucose uptake and GLUT4 gene expression in brown adipocytes. Glucose 102-109 insulin Homo sapiens 80-87 11374224-11 2001 In patients with high-renin or low-renin hypertension, the glucose consumption during clamping was lower than that of healthy controls (M, glucose disposal rate: 23.7 +/- 4.8 and 19.5 +/- 3.4 versus 33.0 +/- 5.7 mumol.kg.-1.min-1, p < 0.001), increase of the metabolic glucose clearance (MCRG: 5.1 +/- 1.5 and 3.9 +/- 0.7 versus 7.9 +/- 1.4 ml.kg-1.min-1, p < 0.001) and tissue insulin sensitivity index (M/I: 24.3 +/- 10.1 and 26.4 +/- 8.3 versus 38.4 +/- 10.1 mumol.kg-1.min-1 to mU.l-1 x 100, p < 0.001). Glucose 59-66 insulin Homo sapiens 384-391 11145966-1 2001 Insulin regulates glucose uptake in adipocytes and muscle by stimulating the movement of sequestered glucose transporter 4 (GLUT4) proteins from intracellular membranes to the cell surface. Glucose 18-25 insulin Homo sapiens 0-7 11412606-0 2001 [Insulin secretion and insulin sensitivity in relation to glucose tolerance in a group of subjects at a high risk for type 2 diabetes mellitus]. Glucose 58-65 insulin Homo sapiens 1-8 11412606-0 2001 [Insulin secretion and insulin sensitivity in relation to glucose tolerance in a group of subjects at a high risk for type 2 diabetes mellitus]. Glucose 58-65 insulin Homo sapiens 23-30 11282903-8 2001 Intracoronary insulin infusion produced an approximately 3-fold increase in fractional extraction and net uptake of glucose across the heart in both groups (to 3.7+/-0.4% and 18.3+/-3.5 micromol. Glucose 116-123 insulin Homo sapiens 14-21 11254464-6 2001 In both groups, the major mechanism of insulin resistance was an inhibition of insulin-induced nonoxidative glucose disposal after surgery. Glucose 108-115 insulin Homo sapiens 39-46 11254464-6 2001 In both groups, the major mechanism of insulin resistance was an inhibition of insulin-induced nonoxidative glucose disposal after surgery. Glucose 108-115 insulin Homo sapiens 79-86 11254464-7 2001 The better preservation of insulin sensitivity in the treatment group was attributable to a less reduced glucose disposal in peripheral tissues and increased glucose oxidation rates. Glucose 105-112 insulin Homo sapiens 27-34 11254464-7 2001 The better preservation of insulin sensitivity in the treatment group was attributable to a less reduced glucose disposal in peripheral tissues and increased glucose oxidation rates. Glucose 158-165 insulin Homo sapiens 27-34 11256986-6 2001 There was also a significant correlation between SLC and insulin sensitivity measured as insulin-mediated glucose uptake (P < 0.01). Glucose 106-113 insulin Homo sapiens 57-64 11256986-6 2001 There was also a significant correlation between SLC and insulin sensitivity measured as insulin-mediated glucose uptake (P < 0.01). Glucose 106-113 insulin Homo sapiens 89-96 11256986-8 2001 The subjects with a SLC value in the highest tertile had a 6-fold higher prevalence of insulin resistance (low-insulin-mediated glucose uptake) as compared with those with a SLC value in the lowest tertile. Glucose 128-135 insulin Homo sapiens 87-94 11256986-8 2001 The subjects with a SLC value in the highest tertile had a 6-fold higher prevalence of insulin resistance (low-insulin-mediated glucose uptake) as compared with those with a SLC value in the lowest tertile. Glucose 128-135 insulin Homo sapiens 111-118 11259736-1 2001 AIM: To evaluate the relationship between the changes in gastrin and insulin serum concentrations after oral glucose loading in pregnant and non-pregnant women. Glucose 109-116 insulin Homo sapiens 69-76 11259736-9 2001 The insulin release due to the oral glucose loading markedly increased at t2 and t3 (Friedman"s test, p < 0.001), whereas glucagon release decreased irrespective of pregnancy. Glucose 36-43 insulin Homo sapiens 4-11 11259736-11 2001 Changes in insulin and glucagon levels induced by oral glucose loading, particularly after 60 minutes, could not be associated with changes in gastrin release. Glucose 55-62 insulin Homo sapiens 11-18 11472449-7 2001 Insulin-independent glucose disposal was increased in subjects with lower insulin sensitivity and declined with increasing age in subjects with the mutation but not in controls. Glucose 20-27 insulin Homo sapiens 0-7 11472449-7 2001 Insulin-independent glucose disposal was increased in subjects with lower insulin sensitivity and declined with increasing age in subjects with the mutation but not in controls. Glucose 20-27 insulin Homo sapiens 74-81 11289034-4 2001 Subsequent reincubation with physiological concentrations of glucose led to a dramatic increase in the rate of glycogen synthesis and in the fractional activity of GS, an effect which was both time- and glucose concentration-dependent and essentially additive with the effects of insulin. Glucose 61-68 insulin Homo sapiens 280-287 11289043-9 2001 Secretion of insulin was also induced in a parallel manner, and it was regulated by the concentration of glucose in the culture medium. Glucose 105-112 insulin Homo sapiens 13-20 11289055-9 2001 The insulin sensitivity index (ISI) of glucose disposal was 0.095+/-0.006 micromol x kg(-1) x min(-1) x pmol(-1) x l(-1) in the control group and 0.129+/-0.008 micromol x kg(-1) x min(-1) x pmol(-1) x l(-1) in the X/Ala group (P = 0.003). Glucose 39-46 insulin Homo sapiens 4-11 11289055-12 2001 In conclusion, in lean subjects, the Pro12Ala polymorphism is associated with increased insulin sensitivity of glucose disposal and suppression of lipolysis. Glucose 111-118 insulin Homo sapiens 88-95 11289055-13 2001 This result suggests that an altered transcriptional activity of PPAR-gamma2 in X/Ala subjects either causes a more efficient suppression of lipolysis in adipose tissue, which in turn results in improved insulin-stimulated glucose disposal in muscle, or, alternatively, beneficially affects insulin signaling in both tissues independently of one another. Glucose 223-230 insulin Homo sapiens 204-211 11289056-2 2001 Previously, transfection of IRS-1 with this polymorphism into insulin-secreting cells resulted in a marked reduction of glucose-stimulated insulin secretion compared with the wild-type transfected cells. Glucose 120-127 insulin Homo sapiens 62-69 11289056-6 2001 In summary, our results suggest that the Gly972Arg polymorphism in IRS-1 is associated with decreased insulin secretion in response to glucose but not with insulin sensitivity. Glucose 135-142 insulin Homo sapiens 102-109 11298729-2 2001 These studies were designed to demonstrate the importance of early insulin release on the control of meal-induced glucose excursions by capitalizing on the significant pharmacodynamic differences between several oral insulin secreting agents. Glucose 114-121 insulin Homo sapiens 67-74 11298729-9 2001 CONCLUSION: These data support the impact of early and rapid insulin release in the control of prandial and post-meal glycaemia and demonstrate that a short anticipatory burst of insulin, restricted to the beginning of a meal, provides a clear metabolic advantage and prevents post-meal hypoglycaemic episodes when compared to a greater but reactive insulin exposure that follows a meal-induced increase in glucose excursion. Glucose 407-414 insulin Homo sapiens 179-186 11298729-9 2001 CONCLUSION: These data support the impact of early and rapid insulin release in the control of prandial and post-meal glycaemia and demonstrate that a short anticipatory burst of insulin, restricted to the beginning of a meal, provides a clear metabolic advantage and prevents post-meal hypoglycaemic episodes when compared to a greater but reactive insulin exposure that follows a meal-induced increase in glucose excursion. Glucose 407-414 insulin Homo sapiens 179-186 11298734-6 2001 RESULTS: Insulin-mediated glucose disposal was similar after carbohydrate depletion (65.2 +/- 1.9 micromol/kg/min) and loading (66.9 +/- 2.8 micromol/kg/min). Glucose 26-33 insulin Homo sapiens 9-16 11315820-5 2001 At 25% VO2max for 60 min, a 50% reduction in the premeal insulin dose resulted in plasma glucose of -0.62 mmol/l compared with baseline at the end of exercise. Glucose 89-96 insulin Homo sapiens 57-64 11315820-6 2001 At 50% VO2max for 30 and 60 min, 50 and 75% reductions of the premeal insulin dose were associated with plasma glucose of -0.39 and +0.49 mmol/l, respectively, at the end of the exercise. Glucose 111-118 insulin Homo sapiens 70-77 11315820-7 2001 At 75% VO2max, a 75% reduction of the premeal insulin dose was required to achieve appropriate postexercise plasma glucose (+0.71 mmol/l). Glucose 115-122 insulin Homo sapiens 46-53 11315836-7 2001 EGP during the first insulin clamp step was significantly decreased after pioglitazone treatment (P < 0.05) whereas insulin-stimulated total and nonoxidative glucose disposal during the second insulin clamp was increased (P < 0.01). Glucose 161-168 insulin Homo sapiens 119-126 11315836-7 2001 EGP during the first insulin clamp step was significantly decreased after pioglitazone treatment (P < 0.05) whereas insulin-stimulated total and nonoxidative glucose disposal during the second insulin clamp was increased (P < 0.01). Glucose 161-168 insulin Homo sapiens 119-126 11315836-9 2001 The change in mean plasma glucose concentration during the OGGTT was strongly related to the change in total body glucose disposl during the second insulin clamp step. Glucose 26-33 insulin Homo sapiens 148-155 11315836-10 2001 CONCLUSIONS: These results suggest that pioglitazone therapy in type 2 diabetic patients decreases lasting and postprandial plasma glucose levels by improving hepatic and peripheral (muscle) tissue sensitivity to insulin. Glucose 131-138 insulin Homo sapiens 213-220 11315841-8 2001 and glucosed-induced increase in CP (expressed as log [postprandial CP/fasting CP]) were 2.0 (95% CI 1.3-3.3), 1.8 (CI 1.2-2.7), and 2.3 (CI 1.1-4.9) respectively. Glucose 4-12 insulin Homo sapiens 33-35 11327119-3 2001 A few candidate genes, encoding proteins of glucose, insulin and lipid metabolism, lipolytic cascade, fatty acid intestinal absorption, glucocorticoid metabolism, haemostasis and blood pressure, have been associated with a clustering of metabolic abnormalities, although the functional significance of these associations remains to be established. Glucose 44-51 insulin Homo sapiens 53-60 11222284-1 2001 In response to glucose application, beta-cells forming pancreatic islets of Langerhans start bursting oscillations of the membrane potential and intracellular calcium concentration, inducing insulin secretion by the cells. Glucose 15-22 insulin Homo sapiens 191-198 11222284-9 2001 We point to the possible role of the observed waves as signals controlling the insulin secretion inside the islets of Langerhans, in particular, in the regions that cannot be reached by any external stimuli such as high glucose concentration outside the islets. Glucose 220-227 insulin Homo sapiens 79-86 11332627-6 2001 Tilapia islets appear to be appropriately glucose responsive with high insulin output, can be cryopreserved, and are much more resistant to hypoxia than mammalian islets. Glucose 42-49 insulin Homo sapiens 71-78 11222114-1 2001 Insulin-mediated increases in limb blood flow are thought to enhance glucose uptake by skeletal muscle. Glucose 69-76 insulin Homo sapiens 0-7 11222114-7 2001 By 1 h, insulin had increased the glucose infusion rate from 0 to 128 micromol.min(-1) x kg(-1) and the scanning LDF had increased by 62+/-8% (P<0.05), but FBF was unaffected. Glucose 34-41 insulin Homo sapiens 8-15 11298086-6 2001 In another nine women insulin-dependent (Si) and -independent (Sg) glucose utilization was tested by a frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 67-74 insulin Homo sapiens 22-29 11318075-1 2001 BACKGROUND: Many patients with diabetes use mixtures of fast-acting (regular human) insulin and intermediate-acting (neutral protamine Hagedorn [NPH]) insulin to control their blood glucose levels. Glucose 182-189 insulin Homo sapiens 151-158 11321936-2 2001 The metabolic manifestations of insulin resistance include (1) reduced insulin-stimulated glucose uptake, (2) reduced insulin-suppression of endogenous glucose production, and (3) reduced antilipolysis. Glucose 90-97 insulin Homo sapiens 32-39 11321936-2 2001 The metabolic manifestations of insulin resistance include (1) reduced insulin-stimulated glucose uptake, (2) reduced insulin-suppression of endogenous glucose production, and (3) reduced antilipolysis. Glucose 90-97 insulin Homo sapiens 71-78 11321936-2 2001 The metabolic manifestations of insulin resistance include (1) reduced insulin-stimulated glucose uptake, (2) reduced insulin-suppression of endogenous glucose production, and (3) reduced antilipolysis. Glucose 90-97 insulin Homo sapiens 71-78 11321936-2 2001 The metabolic manifestations of insulin resistance include (1) reduced insulin-stimulated glucose uptake, (2) reduced insulin-suppression of endogenous glucose production, and (3) reduced antilipolysis. Glucose 153-160 insulin Homo sapiens 32-39 11224662-1 2001 In target organs, insulin switches substrate utilization from free fatty acids to glucose, a change that: (i) is oxygen-efficient; (ii) repletes glycogen stores; (iii) removes potentially toxic fatty acids; and (iv) restores intracellular potassium. Glucose 82-89 insulin Homo sapiens 18-25 11246876-9 2001 GLP-1 also impaired (P < 0.05) insulin-induced suppression of endogenous glucose production (6.9 +/- 2.9 vs. 1.3 +/- 1.4 micromol.kg(-1).min(-1)), but caused a time-dependent increase (P < 0.01) in glucose disappearance (93.7 +/- 10.0 vs. 69.3 +/- 6.3 micromol.kg(-1).min(-1); P < 0.01) that was evident only during the final hour of study. Glucose 76-83 insulin Homo sapiens 34-41 11246876-9 2001 GLP-1 also impaired (P < 0.05) insulin-induced suppression of endogenous glucose production (6.9 +/- 2.9 vs. 1.3 +/- 1.4 micromol.kg(-1).min(-1)), but caused a time-dependent increase (P < 0.01) in glucose disappearance (93.7 +/- 10.0 vs. 69.3 +/- 6.3 micromol.kg(-1).min(-1); P < 0.01) that was evident only during the final hour of study. Glucose 204-211 insulin Homo sapiens 34-41 11246877-5 2001 Hyperinsulinemic-euglycemic clamp study revealed a 52.7% decrease in the glucose infusion rate and a 196% increase in hepatic glucose production in high salt-fed rats, which also showed a 66.4% decrease in 2-deoxyglucose uptake into isolated skeletal muscle and a 44.5% decrease in insulin-induced glycogen synthase activation in liver, as compared with controls. Glucose 73-80 insulin Homo sapiens 5-12 11246877-5 2001 Hyperinsulinemic-euglycemic clamp study revealed a 52.7% decrease in the glucose infusion rate and a 196% increase in hepatic glucose production in high salt-fed rats, which also showed a 66.4% decrease in 2-deoxyglucose uptake into isolated skeletal muscle and a 44.5% decrease in insulin-induced glycogen synthase activation in liver, as compared with controls. Glucose 126-133 insulin Homo sapiens 5-12 11246895-0 2001 Decreased fasting and oral glucose stimulated C-peptide in nondiabetic subjects with sequence variants in the sulfonylurea receptor 1 gene. Glucose 27-34 insulin Homo sapiens 46-55 11269891-10 2001 The SSPG levels, no matter from which method, correlated positively with the 2-h insulin after oral glucose challenge. Glucose 100-107 insulin Homo sapiens 81-88 11289470-1 2001 OBJECTIVE: We have demonstrated high heritability of insulin secretion measured as acute insulin response to glucose times insulin sensitivity (disposition index). Glucose 109-116 insulin Homo sapiens 53-60 11289470-1 2001 OBJECTIVE: We have demonstrated high heritability of insulin secretion measured as acute insulin response to glucose times insulin sensitivity (disposition index). Glucose 109-116 insulin Homo sapiens 89-96 11289470-1 2001 OBJECTIVE: We have demonstrated high heritability of insulin secretion measured as acute insulin response to glucose times insulin sensitivity (disposition index). Glucose 109-116 insulin Homo sapiens 89-96 11289470-6 2001 We used minimal model analysis to calculate the insulin sensitivity index (S1) and glucose effectiveness (SG), and acute insulin response to glucose was calculated as the mean insulin excursion above baseline during the first 10 min after the glucose bolus. Glucose 141-148 insulin Homo sapiens 121-128 11289470-6 2001 We used minimal model analysis to calculate the insulin sensitivity index (S1) and glucose effectiveness (SG), and acute insulin response to glucose was calculated as the mean insulin excursion above baseline during the first 10 min after the glucose bolus. Glucose 141-148 insulin Homo sapiens 121-128 11289482-0 2001 A model-based method for assessing insulin sensitivity from the oral glucose tolerance test. Glucose 69-76 insulin Homo sapiens 35-42 11289482-1 2001 OBJECTIVE: Available insulin sensitivity (IS) methods based on the oral glucose tolerance test (OGTT) are empirical. Glucose 72-79 insulin Homo sapiens 21-28 11307176-3 2001 Continuous glucose monitoring in particular should supply the diabetic patient with all the information required to optimize insulin therapy and metabolic control. Glucose 11-18 insulin Homo sapiens 125-132 11307179-2 2001 METHODS: A frequently sampled intravenous glucose tolerance test (FSIGT) was used to assess acute insulin response to glucose (AIR) and insulin sensitivity (S(I)) among adult participants (n=675 with normal, NGT; n=332 with impaired glucose tolerance, IGT) in the Insulin Resistance Atherosclerosis Study (IRAS). Glucose 118-125 insulin Homo sapiens 98-105 11317660-7 2001 Time to maximum insulin concentration (Tmax-Ins) and time to maximum glucose infusion rate (TGIRmax) were shorter with inhaled insulin than with subcutaneous administration. Glucose 69-76 insulin Homo sapiens 127-134 11318844-6 2001 Reductions in blood glucose levels resulted in improvement in insulin sensitivity (diet KITT 2.40 +/- 0.26-3.09 +/- 0.36, P < 0.01; sulphonylurea 2.24 +/- 0.16-2.94 +/- 0.18, P < 0.01; insulin 1.68 +/- 0.27-2.16 +/- 0.22%/min, P < 0.05), and decrease in sE-selectin levels (diet 88.4 +/- 14.9-66.2 +/- 10.8, P < 0.05; sulphonylurea 85.1 +/- 11.6-59.8 +/- 7.8, P < 0.01; insulin 84.4 +/- 8.7-66.8 +/- 7.4 ng/ml, P < 0.01), but no change in sVCAM-1 levels. Glucose 20-27 insulin Homo sapiens 62-69 11318844-6 2001 Reductions in blood glucose levels resulted in improvement in insulin sensitivity (diet KITT 2.40 +/- 0.26-3.09 +/- 0.36, P < 0.01; sulphonylurea 2.24 +/- 0.16-2.94 +/- 0.18, P < 0.01; insulin 1.68 +/- 0.27-2.16 +/- 0.22%/min, P < 0.05), and decrease in sE-selectin levels (diet 88.4 +/- 14.9-66.2 +/- 10.8, P < 0.05; sulphonylurea 85.1 +/- 11.6-59.8 +/- 7.8, P < 0.01; insulin 84.4 +/- 8.7-66.8 +/- 7.4 ng/ml, P < 0.01), but no change in sVCAM-1 levels. Glucose 20-27 insulin Homo sapiens 191-198 11318844-6 2001 Reductions in blood glucose levels resulted in improvement in insulin sensitivity (diet KITT 2.40 +/- 0.26-3.09 +/- 0.36, P < 0.01; sulphonylurea 2.24 +/- 0.16-2.94 +/- 0.18, P < 0.01; insulin 1.68 +/- 0.27-2.16 +/- 0.22%/min, P < 0.05), and decrease in sE-selectin levels (diet 88.4 +/- 14.9-66.2 +/- 10.8, P < 0.05; sulphonylurea 85.1 +/- 11.6-59.8 +/- 7.8, P < 0.01; insulin 84.4 +/- 8.7-66.8 +/- 7.4 ng/ml, P < 0.01), but no change in sVCAM-1 levels. Glucose 20-27 insulin Homo sapiens 191-198 11381801-2 2001 The first step for glucose uptake is insulin receptor-binding. Glucose 19-26 insulin Homo sapiens 37-44 11181804-4 2001 PD with dextrose+AA versus PD with dextrose induced (1) similarly high insulin levels but with a significant increase in total arterial AA (+30 to 110%), mainly valine; (2) a reduced release of AA from muscle (P<0.05); and (3) a decrease in the negative NB observed during PD with dextrose, owing to an increase (approximately 20%) in muscle PS, without any further effect on muscle PB. Glucose 8-16 insulin Homo sapiens 71-78 11181804-4 2001 PD with dextrose+AA versus PD with dextrose induced (1) similarly high insulin levels but with a significant increase in total arterial AA (+30 to 110%), mainly valine; (2) a reduced release of AA from muscle (P<0.05); and (3) a decrease in the negative NB observed during PD with dextrose, owing to an increase (approximately 20%) in muscle PS, without any further effect on muscle PB. Glucose 35-43 insulin Homo sapiens 71-78 11181804-4 2001 PD with dextrose+AA versus PD with dextrose induced (1) similarly high insulin levels but with a significant increase in total arterial AA (+30 to 110%), mainly valine; (2) a reduced release of AA from muscle (P<0.05); and (3) a decrease in the negative NB observed during PD with dextrose, owing to an increase (approximately 20%) in muscle PS, without any further effect on muscle PB. Glucose 35-43 insulin Homo sapiens 71-78 11181804-6 2001 Conversely, the combined use of dextrose and AA results in a cumulative effect, because of the suppression of endogenous muscle PB (induced by insulin) and the stimulation of muscle PS (induced by AA availability). Glucose 32-40 insulin Homo sapiens 143-150 11181807-15 2001 During tacrolimus administration, k(G) decreased in almost all patients as a result of a diminished insulin secretion response to a glucose load, whereas insulin resistance did not change. Glucose 132-139 insulin Homo sapiens 100-107 11300234-8 2001 Insulin sensitivity was estimated from the relationship of glucose utilization (M) to the concentration of insulin (I) during the last 30 minutes of 3-hour hyperinsulinemic-euglycenic clamps (240 pmol x min(-2) x min(-1)) (M/I) before and after RT. Glucose 59-66 insulin Homo sapiens 0-7 11238471-5 2001 Among the latter, Akt (a product of the akt protooncogene) and atypical protein kinase C isoforms are thought to be involved in insulin regulation of glucose transport and oxidation; glycogen, lipid, and protein synthesis; and modulation of gene expression. Glucose 150-157 insulin Homo sapiens 128-135 11238496-6 2001 In the metformin group, the mean (+/-SE) area under the serum insulin curve after glucose administration decreased from 62 +/- 6 to 19 +/- 2 nmol/L.min (P < 0.001). Glucose 82-89 insulin Homo sapiens 62-69 11238514-7 2001 In response to glucose, the minimum PI/I ratio was significantly higher in IGT (3.4 +/- 0.6%) than in NGT (1.4 +/- 0.5%; P = 0.02), suggesting defective proinsulin processing in this condition. Glucose 15-22 insulin Homo sapiens 153-163 11479436-5 2001 Fast-acting analogues restore prandial insulin peaks while multiple doses of NPH restore basal insulin levels for the control of fasting blood glucose levels. Glucose 143-150 insulin Homo sapiens 95-102 11452211-1 2001 Insulin resistance is common and cluster with glucose intolerance, dyslipidaemia and high blood pressure,. Glucose 46-53 insulin Homo sapiens 0-7 11452218-1 2001 The ability of insulin to stimulate muscle glucose disposal and inhibit adipose tissue lipolysis is impaired in patients with type 2 diabetes. Glucose 43-50 insulin Homo sapiens 15-22 11452218-2 2001 The progression from normal glucose tolerance and/or impaired glucose tolerance to type 2 diabetes only occurs when insulin secretory function declines to a degree that circulating insulin concentrations are no longer able to overcome muscle and adipose tissue insulin resistance. Glucose 28-35 insulin Homo sapiens 116-123 11452219-4 2001 We emphasize on the non-insulin dependent glucose transport induced by muscular contraction, which involves AMP-activated protein kinase. Glucose 42-49 insulin Homo sapiens 24-31 11452221-4 2001 Glucose clamp studies have clearly shown an improvement of insulin-induced glucose utilization (in skeletal muscle). Glucose 0-7 insulin Homo sapiens 59-66 11452221-4 2001 Glucose clamp studies have clearly shown an improvement of insulin-induced glucose utilization (in skeletal muscle). Glucose 75-82 insulin Homo sapiens 59-66 11452221-5 2001 In contrast, the inhibition of glucose production in response to insulin was much less reproducible. Glucose 31-38 insulin Homo sapiens 65-72 11452221-11 2001 In human, skeletal muscles are responsible for more than 80% of glucose uptake in response to insulin. Glucose 64-71 insulin Homo sapiens 94-101 11469701-2 2001 Indeed, conventional subcutaneous insulin administration produces slowly changing blood insulin levels and suboptimal hepatocyte insulinization resulting in impaired hepatic capacity for processing incoming dietary glucose. Glucose 215-222 insulin Homo sapiens 34-41 11469714-14 2001 This could assist rational optimization of insulin therapy in cases of persistently poor glucose control. Glucose 89-96 insulin Homo sapiens 43-50 11455994-6 2001 Mean serum insulin and c-peptide responses after oral glucose tolerance test at t = 60, 90 and 120 minutes (P<.05) were significantly greater in the relatives than in the healthy controls. Glucose 54-61 insulin Homo sapiens 11-18 11455994-6 2001 Mean serum insulin and c-peptide responses after oral glucose tolerance test at t = 60, 90 and 120 minutes (P<.05) were significantly greater in the relatives than in the healthy controls. Glucose 54-61 insulin Homo sapiens 23-32 11455994-10 2001 In addition, the glucose effectiveness at basal insulin level (Sg) was not significantly different in the relatives and healthy controls. Glucose 17-24 insulin Homo sapiens 48-55 11292681-0 2001 Insulin resistance with low cellular IRS-1 expression is also associated with low GLUT4 expression and impaired insulin-stimulated glucose transport. Glucose 131-138 insulin Homo sapiens 0-7 11292681-0 2001 Insulin resistance with low cellular IRS-1 expression is also associated with low GLUT4 expression and impaired insulin-stimulated glucose transport. Glucose 131-138 insulin Homo sapiens 112-119 11336617-3 2001 It is a direct insulin secretagogue; indirectly, it also increases insulin secretion in response to fuels such as glucose. Glucose 114-121 insulin Homo sapiens 15-22 11336617-3 2001 It is a direct insulin secretagogue; indirectly, it also increases insulin secretion in response to fuels such as glucose. Glucose 114-121 insulin Homo sapiens 67-74 11368419-2 2001 Insulin provokes rapid changes in phospholipid metabolism and thereby generates biologically active lipids that serve as intracellular signaling factors that regulate glucose transport and glycogen synthesis. Glucose 167-174 insulin Homo sapiens 0-7 11368419-4 2001 Recent findings suggest that atypical PKCs and PKB serve as important positive regulators of insulin-stimulated glucose metabolism, whereas mechanisms that result in the activation of DAG-sensitive PKCs serve mainly as negative regulators of insulin signaling through PI3K. Glucose 112-119 insulin Homo sapiens 93-100 11368419-7 2001 Atypical PKCs and perhaps PKB appear to be required for insulin-induced translocation of the GLUT 4 glucose transporter to the plasma membrane and subsequent glucose transport. Glucose 100-107 insulin Homo sapiens 56-63 11368419-9 2001 Together, atypical PKCs and PKB serve as a potent, integrated PI3K/PDK-1-directed signaling system that is used by insulin to regulate glucose metabolism. Glucose 135-142 insulin Homo sapiens 115-122 11266382-7 2001 RESULTS: NASH and fatty liver were both associated with insulin resistance, with mean glucose infusion rates (normal/fatty liver/NASH) of step 1, 4.5/1.6/0.9; step 2, 9.5/7.7/4.5 (P < 0.03 for both steps). Glucose 86-93 insulin Homo sapiens 56-63 11319659-6 2001 Leptin decrease after 3 months of GH administration was correlated inversely with the increase in first phase insulin response to intravenous glucose tolerance test (IVGTT) (r2=-0.595, P<0.001). Glucose 142-149 insulin Homo sapiens 110-117 11319659-9 2001 CONCLUSION: The high insulin response to glucose load seen in GH-treated subjects was appropriate to their glucose concentration and the insulin sensitivity index was unchanged relative to the pretreatment period. Glucose 41-48 insulin Homo sapiens 21-28 11319659-9 2001 CONCLUSION: The high insulin response to glucose load seen in GH-treated subjects was appropriate to their glucose concentration and the insulin sensitivity index was unchanged relative to the pretreatment period. Glucose 107-114 insulin Homo sapiens 21-28 11297594-8 2001 We conclude that although the estimated indices of insulin sensitivity and beta cell function from the oral glucose tolerance test correlated with the measured ones in a wide spectrum of healthy, glucose-tolerant, and normotensive subjects, they were much less likely to detect the differences than measured ones among the ethnic groups. Glucose 108-115 insulin Homo sapiens 51-58 11509918-11 2001 Intravenous glucose infusion, leading to increased serum insulin concentration, did not modify any hemodynamic parameter. Glucose 12-19 insulin Homo sapiens 57-64 11295708-6 2001 Independent of race, children with AN had greater body weight and body fat mass (P < .001); greater basal and glucose-stimulated insulin levels during oral glucose tolerance test (P < .001); greater first-phase, second-phase, and steady-state insulin levels (P < .001); and lower insulin sensitivity (P < .001) during the hyperglycemic clamp. Glucose 113-120 insulin Homo sapiens 132-139 27407313-11 2001 There was loss of first phase insulin response to the glucose load during the IVGTT, which was blunted at all stages and the difference was statistically significant at 0 and 3 minutes. Glucose 54-61 insulin Homo sapiens 30-37 27407313-12 2001 Loss of first phase insulin response to IV glucose suggests that there is evidence of beta-cell dysfunction. Glucose 43-50 insulin Homo sapiens 20-27 27407313-14 2001 Therefore flat glucose tolerance curve can be explained by absence of insulin priming effect leading to decreased glucose absorption followed by increased glucose disposal because of higher insulin levels following OGTT and increased glucose disposal caused by increased insulin sensitivity. Glucose 15-22 insulin Homo sapiens 190-197 27407313-14 2001 Therefore flat glucose tolerance curve can be explained by absence of insulin priming effect leading to decreased glucose absorption followed by increased glucose disposal because of higher insulin levels following OGTT and increased glucose disposal caused by increased insulin sensitivity. Glucose 15-22 insulin Homo sapiens 190-197 27407313-14 2001 Therefore flat glucose tolerance curve can be explained by absence of insulin priming effect leading to decreased glucose absorption followed by increased glucose disposal because of higher insulin levels following OGTT and increased glucose disposal caused by increased insulin sensitivity. Glucose 114-121 insulin Homo sapiens 70-77 11288031-0 2001 Effects of insulin on glucose uptake and leg blood flow in patients with sickle cell disease and normal subjects. Glucose 22-29 insulin Homo sapiens 11-18 11288031-1 2001 The hemodynamic concept of insulin resistance assumes that vasodilatory effects of insulin determine glucose uptake. Glucose 101-108 insulin Homo sapiens 27-34 11288031-1 2001 The hemodynamic concept of insulin resistance assumes that vasodilatory effects of insulin determine glucose uptake. Glucose 101-108 insulin Homo sapiens 83-90 11288031-3 2001 Therefore, we hypothesized that patients with SCD have a reduced insulin-mediated glucose uptake. Glucose 82-89 insulin Homo sapiens 65-72 11288031-4 2001 In 8 patients with SCD and 8 matched normal controls, we studied the effects of a 4-hour insulin infusion (50 mU/kg/h) on glucose uptake and leg blood flow (LBF) using the euglycemic clamp technique and venous occlusion plethysmography. Glucose 122-129 insulin Homo sapiens 89-96 11288031-6 2001 Insulin-mediated glucose uptake (M value, mg/kg/min) did not differ between patients with SCD and control subjects during the second (6.3 +/- 4.6 and 7.6 +/- 2.6, P =.5), third (7.5 +/- 4.6 and 9.3 +/- 3.4, P =.4) and fourth hour (8.6 +/- 4.7 and 11.0 +/- 2.9, P =.2) of the clamp. Glucose 17-24 insulin Homo sapiens 0-7 11288031-9 2001 Respectively, 56% and 24% of the changes in glucose uptake could be explained from changes in LBF in the course of the insulin infusion in the patients with SCD and controls. Glucose 44-51 insulin Homo sapiens 119-126 11288041-0 2001 Alcohol and glucose counterregulation during acute insulin-induced hypoglycemia in type 2 diabetic subjects. Glucose 12-19 insulin Homo sapiens 51-58 11291934-5 2001 The determination of the islet peptide contents and the mRNA levels revealed a several-fold increase in the IAPP/insulin molar ratio of islets cultured in high glucose concentrations. Glucose 160-167 insulin Homo sapiens 113-120 11291934-6 2001 Thus, prolonged exposure of human islets to high concentrations of glucose results in an increase in the synthesis of IAPP with respect to insulin. Glucose 67-74 insulin Homo sapiens 139-146 11331427-5 2001 RESULTS: Fasting glucose was normalized in the diabetic subjects with insulin from day 9 of VLED onward. Glucose 17-24 insulin Homo sapiens 70-77 11335776-19 2001 Insulin sensitivity, as assessed by the ratio of fasting insulin to glucose concentrations and the quantitative insulin sensitivity check index (1/[log fasting insulin + log fasting glucose]) and homeostasis model assessment insulin resistance index (fasting insulin x fasting glucose/22.5) indices, increased slightly in the metformin-treated participants. Glucose 68-75 insulin Homo sapiens 0-7 11335776-25 2001 Early detection and therapy of the obese adolescent with a family history of type 2 diabetes may interrupt the cycle of weight gain and insulin resistance that leads to glucose intolerance in adulthood. Glucose 169-176 insulin Homo sapiens 136-143 11317469-2 2001 Excess fat, excess glucose, or both act on diverse cells and tissues to counteract insulin-mediated glucose uptake, hepatic regulation of glucose output, and insulin secretion. Glucose 19-26 insulin Homo sapiens 83-90 11317469-2 2001 Excess fat, excess glucose, or both act on diverse cells and tissues to counteract insulin-mediated glucose uptake, hepatic regulation of glucose output, and insulin secretion. Glucose 100-107 insulin Homo sapiens 83-90 11317469-2 2001 Excess fat, excess glucose, or both act on diverse cells and tissues to counteract insulin-mediated glucose uptake, hepatic regulation of glucose output, and insulin secretion. Glucose 100-107 insulin Homo sapiens 83-90 11344398-4 2001 Hepatic insulin resistance with persistent endogenous glucose production and enhanced peripheral insulin sensitivity result in a brittle form of diabetes which can be difficult to manage. Glucose 54-61 insulin Homo sapiens 8-15 11274399-1 2001 Muscle tissue is the major site for insulin-stimulated glucose uptake in vivo, due primarily to the recruitment of the insulin-sensitive glucose transporter (GLUT4) to the plasma membrane. Glucose 55-62 insulin Homo sapiens 36-43 11274399-1 2001 Muscle tissue is the major site for insulin-stimulated glucose uptake in vivo, due primarily to the recruitment of the insulin-sensitive glucose transporter (GLUT4) to the plasma membrane. Glucose 55-62 insulin Homo sapiens 119-126 11124961-2 2001 Exposure of insulin-sensitive tissues to free fatty acids can impair glucose disposal through inhibition of carbohydrate oxidation and glucose transport. Glucose 69-76 insulin Homo sapiens 12-19 11124961-2 2001 Exposure of insulin-sensitive tissues to free fatty acids can impair glucose disposal through inhibition of carbohydrate oxidation and glucose transport. Glucose 135-142 insulin Homo sapiens 12-19 11124961-4 2001 To clarify the effects of externally delivered fatty acids on glucose uptake in an insulin-responsive cell type, we systematically examined the effects of a range of fatty acids on glucose uptake in 3T3-L1 adipocytes. Glucose 62-69 insulin Homo sapiens 83-90 11124961-5 2001 Of the fatty acids examined, arachidonic acid (AA) had the greatest positive effects, significantly increasing basal and insulin-stimulated glucose uptake by 1.8- and 2-fold, respectively, with effects being maximal at 4 h at which time membrane phospholipid content of AA was markedly increased. Glucose 140-147 insulin Homo sapiens 121-128 11124961-10 2001 Thus, AA potentiates basal and insulin-stimulated glucose uptake in 3T3-L1 adipocytes by a cyclooxygenase-independent mechanism that increases the levels of both GLUT1 and GLUT4 at the plasma membrane. Glucose 50-57 insulin Homo sapiens 31-38 11257494-2 2001 There is also convincing evidence that PKB plays a role in the insulin-mediated regulation of glucose transport. Glucose 94-101 insulin Homo sapiens 63-70 11257494-3 2001 Furthermore, states of cellular insulin resistance have been shown to involve impaired PKB activation, and this usually coincides with a loss of glucose transport activation. Glucose 145-152 insulin Homo sapiens 32-39 11113153-1 2001 The long-chain acyl-CoA (LC-CoA) model of glucose-stimulated insulin secretion (GSIS) holds that secretion is linked to a glucose-induced increase in malonyl-CoA level and accumulation of LC-CoA in the cytosol. Glucose 42-49 insulin Homo sapiens 61-68 11113153-1 2001 The long-chain acyl-CoA (LC-CoA) model of glucose-stimulated insulin secretion (GSIS) holds that secretion is linked to a glucose-induced increase in malonyl-CoA level and accumulation of LC-CoA in the cytosol. Glucose 122-129 insulin Homo sapiens 61-68 11222622-1 2001 In adipose and muscle, insulin stimulates glucose uptake and glycogen synthase activity. Glucose 42-49 insulin Homo sapiens 23-30 11222622-4 2001 In 3T3-L1 adipocytes, overexpression of a dominant negative CAP mutant (CAP Delta SH3) completely blocked the insulin-stimulated glucose transport and glycogen synthesis but only partially inhibited glycogen synthase activation. Glucose 129-136 insulin Homo sapiens 110-117 11222622-7 2001 These results indicate blockade of the c-Cbl/CAP pathway directly inhibits insulin-stimulated glucose uptake, which results in secondary inhibition of glycogen synthase activation and glycogen synthesis. Glucose 94-101 insulin Homo sapiens 75-82 11412137-0 2001 Intracellular mechanisms underlying increases in glucose uptake in response to insulin or exercise in skeletal muscle. Glucose 49-56 insulin Homo sapiens 79-86 11412137-2 2001 Glucose transport, the rate limiting step in glucose metabolism, is mediated by glucose transporter 4 (GLUT4) and can be activated in skeletal muscle by two separate and distinct signalling pathways; one stimulated by insulin and the second by muscle contractions. Glucose 0-7 insulin Homo sapiens 218-225 11412137-3 2001 Impaired insulin action on whole body glucose uptake is a hallmark feature of type II (non-insulin-dependent) diabetes mellitus. Glucose 38-45 insulin Homo sapiens 9-16 11412137-3 2001 Impaired insulin action on whole body glucose uptake is a hallmark feature of type II (non-insulin-dependent) diabetes mellitus. Glucose 38-45 insulin Homo sapiens 91-98 11412137-4 2001 Defects in insulin signal transduction through the insulin-receptor substrate-1/phosphatidylinositol 3-kinase pathway are associated with reduced insulin-stimulated glucose transporter 4 translocation and glucose transport activity in skeletal muscle from type II diabetic patients. Glucose 165-172 insulin Homo sapiens 11-18 11412137-4 2001 Defects in insulin signal transduction through the insulin-receptor substrate-1/phosphatidylinositol 3-kinase pathway are associated with reduced insulin-stimulated glucose transporter 4 translocation and glucose transport activity in skeletal muscle from type II diabetic patients. Glucose 165-172 insulin Homo sapiens 51-58 11171597-5 2001 In cells with a severe 40% ATP depletion, basal glucose transport was similarly elevated, and insulin-stimulated glucose transport was similar in cells with 15% ATP depletion. Glucose 113-120 insulin Homo sapiens 94-101 11171597-7 2001 These data suggest that cellular ATP depletion by glucosamine, NaN3, and DNP exerts differential effects on basal and insulin-stimulated glucose transport and that ATP depletion per se does not induce insulin resistance in 3T3-L1 adipocytes. Glucose 137-144 insulin Homo sapiens 118-125 11237926-8 2001 These alterations in glucose metabolism are associated with a blunted decline in circulating concentrations of both insulin and leptin, which may explain some of the differences in the metabolic response to fasting observed between lean and abdominally obese persons. Glucose 21-28 insulin Homo sapiens 116-123 11237931-0 2001 Dietary fat content alters insulin-mediated glucose metabolism in healthy men. Glucose 44-51 insulin Homo sapiens 27-34 11237931-7 2001 In contrast, insulin-stimulated, nonoxidative glucose disposal tended to increase in relation to an increase in the ratio of fat to carbohydrate, from 14.8 +/- 5.1 to 20.6 +/- 1.9 to 26.2 +/- 2.9 micromol x kg(-1) x min(-1) (P < 0.074 between the 3 diets). Glucose 46-53 insulin Homo sapiens 13-20 11237931-8 2001 Insulin-stimulated glucose oxidation was significantly lower after the HFLC diet than after the IFIC and LFHC diets: 1.7 +/- 0.8 compared with 13.4 +/- 2.1 and 19.0 +/- 2.1 micromol x kg(-1) x min(-1), respectively (P < 0.05). Glucose 19-26 insulin Homo sapiens 0-7 11237931-10 2001 CONCLUSION: A high-fat, low-carbohydrate intake reduces the ability of insulin to suppress endogenous glucose production and alters the relation between oxidative and nonoxidative glucose disposal in a way that favors storage of glucose. Glucose 102-109 insulin Homo sapiens 71-78 11237931-10 2001 CONCLUSION: A high-fat, low-carbohydrate intake reduces the ability of insulin to suppress endogenous glucose production and alters the relation between oxidative and nonoxidative glucose disposal in a way that favors storage of glucose. Glucose 180-187 insulin Homo sapiens 71-78 11237931-10 2001 CONCLUSION: A high-fat, low-carbohydrate intake reduces the ability of insulin to suppress endogenous glucose production and alters the relation between oxidative and nonoxidative glucose disposal in a way that favors storage of glucose. Glucose 180-187 insulin Homo sapiens 71-78 11238539-2 2001 Insulin action on whole-body glucose uptake (M-value) and heart rate variability were measured in 21 normal men. Glucose 29-36 insulin Homo sapiens 0-7 11274904-1 2001 Conventional algorithms for regulating insulin infusion rates in those critical diabetic patients submitted to parenteral glucose and insulin infusions do not allow to approach near normal blood glucose (BG) levels since traditional control systems are not fully effective in complex nonlinear systems as BG control is. Glucose 122-129 insulin Homo sapiens 39-46 11274904-2 2001 Thus, we applied fuzzy logic principles and neural network techniques to modify intravenous insulin administration rates during glucose infusion. Glucose 128-135 insulin Homo sapiens 92-99 11288762-11 2001 Finally, the patient demonstrated an incremental increase in insulin concentration in response to minimal increases in plasma glucose during a sequential, stepped infusion of 10% dextrose. Glucose 126-133 insulin Homo sapiens 61-68 11288762-11 2001 Finally, the patient demonstrated an incremental increase in insulin concentration in response to minimal increases in plasma glucose during a sequential, stepped infusion of 10% dextrose. Glucose 179-187 insulin Homo sapiens 61-68 11230788-7 2001 Plasma glucose and serum insulin levels were significantly lower after glucose loading, and glucose oxidation increased. Glucose 71-78 insulin Homo sapiens 25-32 11230790-0 2001 Insulin and non-insulin-dependent glucose disposal in middle-aged and young athletes versus sedentary men. Glucose 34-41 insulin Homo sapiens 16-23 11230790-9 2001 These data suggest that the higher glucose uptake in endurance-trained male cyclists was mostly attributable to an increase in non-insulin-dependent glucose uptake in the young men and to an increase in its insulin-dependent component in the middle-aged men. Glucose 35-42 insulin Homo sapiens 131-138 11230790-9 2001 These data suggest that the higher glucose uptake in endurance-trained male cyclists was mostly attributable to an increase in non-insulin-dependent glucose uptake in the young men and to an increase in its insulin-dependent component in the middle-aged men. Glucose 35-42 insulin Homo sapiens 207-214 11230790-9 2001 These data suggest that the higher glucose uptake in endurance-trained male cyclists was mostly attributable to an increase in non-insulin-dependent glucose uptake in the young men and to an increase in its insulin-dependent component in the middle-aged men. Glucose 149-156 insulin Homo sapiens 131-138 11359348-7 2001 Insulin also can inhibit gluconeogenesis, both proximally and distally, and can potentiate hypoglycemia by promoting muscle glucose uptake; thus, coinfusion of high-dose insulin and of glycerol may represent an alternative viable strategy. Glucose 124-131 insulin Homo sapiens 0-7 11293003-9 2001 With increasing evidence that insulin resistance constitutes a key metabolic element, it seems logical that improving insulin sensitivity and glucose disposal might wholly, or partially, reverse certain features of PCOS, including anovulation. Glucose 142-149 insulin Homo sapiens 30-37 11249067-5 2001 With high glucose, insulin release was markedly potentiated by forskolin, glucagon, glucagon-like peptide-1, and arginine and inhibited by somatostatin, the Ca2+ channel blocker nitrendipine, and the ATP-sensitive K+ channel opener diazoxide. Glucose 10-17 insulin Homo sapiens 19-26 11268922-2 2001 The newly developed insulin secretagogues and quick-acting insulin analogues are pharmacological options to reduce the amplitude of glucose fluctuations, thereby reducing acute glucose toxicity. Glucose 132-139 insulin Homo sapiens 20-27 11268922-2 2001 The newly developed insulin secretagogues and quick-acting insulin analogues are pharmacological options to reduce the amplitude of glucose fluctuations, thereby reducing acute glucose toxicity. Glucose 132-139 insulin Homo sapiens 59-66 11305519-7 2001 RESULTS: Glibenclamide (i.e. glibenclamide plus glucose) significantly increased plasma insulin concentrations and glycemia while placebo (i.e. glucose alone) significantly increased glycemia but did not change plasma insulin levels. Glucose 48-55 insulin Homo sapiens 88-95 11223177-11 2001 We conclude that protein restriction from conception to adulthood followed by high-fat feeding sensitizes the acute leptin response to insulin, an adaptation associated with enhanced glucose utilisation by adipose tissue. Glucose 183-190 insulin Homo sapiens 135-142 11252980-8 2001 Slow-release insulin at bedtime should be added to the oral hypoglycemiants if fasting glucose exceeds 1.60 or 1.80 g/l, even if the HbA1c remains below 8%. Glucose 87-94 insulin Homo sapiens 13-20 11248902-8 2001 The combination microsensor holds great promise for real-time measurements of the insulin/glucose ratio and for improved management of diabetes. Glucose 90-97 insulin Homo sapiens 82-89 11383230-6 2001 Insulin and GLP-1 levels increased much less, to peak levels of 375 pmol/l and 75 pmol/l respectively, after one hour when plasma glucose was 6.8 mmol/l. Glucose 130-137 insulin Homo sapiens 0-7 11158925-0 2001 DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells. Glucose 80-87 insulin Homo sapiens 57-64 11158925-2 2001 This work examined the interaction of saturated and unsaturated fatty acids (FA) with insulin stimulation of glucose uptake and its relation to the FA incorporation into different lipid pools in cultured human muscle. Glucose 109-116 insulin Homo sapiens 86-93 11158925-3 2001 It is shown that basal or insulin-stimulated 2-deoxyglucose uptake was unaltered in cells preincubated with oleate, whereas basal glucose uptake was increased and insulin response was impaired in palmitate- and stearate-loaded cells. Glucose 52-59 insulin Homo sapiens 26-33 11228505-8 2001 Although low amniotic fluid insulin levels were correlated significantly with 1-hour glucose levels of the first and second oral glucose tolerance tests, high insulin levels were no longer correlated with the second oral glucose tolerance test. Glucose 85-92 insulin Homo sapiens 28-35 11228505-8 2001 Although low amniotic fluid insulin levels were correlated significantly with 1-hour glucose levels of the first and second oral glucose tolerance tests, high insulin levels were no longer correlated with the second oral glucose tolerance test. Glucose 129-136 insulin Homo sapiens 28-35 11228505-8 2001 Although low amniotic fluid insulin levels were correlated significantly with 1-hour glucose levels of the first and second oral glucose tolerance tests, high insulin levels were no longer correlated with the second oral glucose tolerance test. Glucose 129-136 insulin Homo sapiens 28-35 11315841-8 2001 and glucosed-induced increase in CP (expressed as log [postprandial CP/fasting CP]) were 2.0 (95% CI 1.3-3.3), 1.8 (CI 1.2-2.7), and 2.3 (CI 1.1-4.9) respectively. Glucose 4-12 insulin Homo sapiens 68-70 11315841-8 2001 and glucosed-induced increase in CP (expressed as log [postprandial CP/fasting CP]) were 2.0 (95% CI 1.3-3.3), 1.8 (CI 1.2-2.7), and 2.3 (CI 1.1-4.9) respectively. Glucose 4-12 insulin Homo sapiens 68-70 11315841-10 2001 CONCLUSIONS: Mid-pregnancy tasting and postoral glucose CP levels are associated with subsequent development of PIH, independent of maternal obesity and midpregnancy baseline blood pressure. Glucose 48-55 insulin Homo sapiens 56-58 11315860-0 2001 Oral glucose tolerance test indexes for insulin sensitivity and secretion based on various availabilities of sampling times. Glucose 5-12 insulin Homo sapiens 40-47 11207640-10 2001 In contrast to the effects on glucose levels, GH treatment induced considerably higher fasting insulin levels and glucose-stimulated insulin levels. Glucose 114-121 insulin Homo sapiens 133-140 11159768-0 2001 Quality specifications for glucose meters: assessment by simulation modeling of errors in insulin dose. Glucose 27-34 insulin Homo sapiens 90-97 11159768-2 2001 Because meters are used as aids in the adjustment of insulin doses, we aimed to characterize the quantitative effect of meter error on the ability to identify the insulin dose appropriate for the true glucose concentration. Glucose 201-208 insulin Homo sapiens 163-170 11159768-11 2001 To provide the intended insulin dosage 95% of the time required that both the bias and the CV of the glucose meter be <1% or <2%, depending on mean glucose concentrations and the rules for insulin dosing. Glucose 101-108 insulin Homo sapiens 24-31 11159768-11 2001 To provide the intended insulin dosage 95% of the time required that both the bias and the CV of the glucose meter be <1% or <2%, depending on mean glucose concentrations and the rules for insulin dosing. Glucose 154-161 insulin Homo sapiens 24-31 11159768-12 2001 CONCLUSIONS: Glucose meters that meet current quality specifications allow a large fraction of administered insulin doses to differ from the intended doses. Glucose 13-20 insulin Homo sapiens 108-115 11207640-12 2001 As a result, the 30- and 120-min ratios of insulin to glucose were higher during GH treatment compared to the start of treatment. Glucose 54-61 insulin Homo sapiens 43-50 11207640-16 2001 However, as has been reported in other patient groups, GH treatment induces higher fasting insulin levels and glucose-stimulated insulin levels, indicating relative insulin resistance. Glucose 110-117 insulin Homo sapiens 129-136 11207640-16 2001 However, as has been reported in other patient groups, GH treatment induces higher fasting insulin levels and glucose-stimulated insulin levels, indicating relative insulin resistance. Glucose 110-117 insulin Homo sapiens 129-136 11165689-5 2001 Glucose utilisation increased after octreotide (insulin 0.5 mU kg(-1) min(-1) clamp 3.09+/-0.23 vs. 4.19+/-0.19 mg kg(-1) min(-1); 1 mU kg(-1) min(-1) clamp 5.64+/-0.61 vs. 7.93+/-0.57 mg kg(-1) min(-1); both P<0.05) and endogenous glucose production was similarly suppressed. Glucose 0-7 insulin Homo sapiens 48-55 11272182-0 2001 A model for glucose control of insulin secretion during 24 h of free living. Glucose 12-19 insulin Homo sapiens 31-38 11272182-1 2001 The aim of this work was to develop a mathematical model describing the functional dependence of insulin secretion on plasma glucose concentrations during 24 h of free living. Glucose 125-132 insulin Homo sapiens 97-104 11272182-4 2001 The relationship between insulin release and plasma glucose concentrations was modeled as the sum of three components: a static component (describing the dependence on plasma glucose concentration itself, with an embedded circadian oscillation), a dynamic component (modeling the dependence on glucose rate of change), and a residual component (including the fraction of insulin secretion not explained by glucose levels). Glucose 52-59 insulin Homo sapiens 25-32 11272182-4 2001 The relationship between insulin release and plasma glucose concentrations was modeled as the sum of three components: a static component (describing the dependence on plasma glucose concentration itself, with an embedded circadian oscillation), a dynamic component (modeling the dependence on glucose rate of change), and a residual component (including the fraction of insulin secretion not explained by glucose levels). Glucose 175-182 insulin Homo sapiens 25-32 11272182-4 2001 The relationship between insulin release and plasma glucose concentrations was modeled as the sum of three components: a static component (describing the dependence on plasma glucose concentration itself, with an embedded circadian oscillation), a dynamic component (modeling the dependence on glucose rate of change), and a residual component (including the fraction of insulin secretion not explained by glucose levels). Glucose 175-182 insulin Homo sapiens 25-32 11272182-4 2001 The relationship between insulin release and plasma glucose concentrations was modeled as the sum of three components: a static component (describing the dependence on plasma glucose concentration itself, with an embedded circadian oscillation), a dynamic component (modeling the dependence on glucose rate of change), and a residual component (including the fraction of insulin secretion not explained by glucose levels). Glucose 175-182 insulin Homo sapiens 25-32 11272182-6 2001 The static component yielded a dose-response function in which insulin release increased quasi-linearly (from 40 to 400 pmol/min on average) over the range of 4-9 mmol/l glucose. Glucose 170-177 insulin Homo sapiens 63-70 11272182-8 2001 The circadian oscillation and the residual component accounted for the day/night difference in the ability of glucose to stimulate insulin release. Glucose 110-117 insulin Homo sapiens 131-138 11272182-11 2001 The model proposed here provides a detailed robust description of glucose-related insulin release during free-living conditions. Glucose 66-73 insulin Homo sapiens 82-89 11272182-12 2001 In nondiabetic subjects, non-glucose-dependent insulin release is a small fraction of total insulin secretion. Glucose 29-36 insulin Homo sapiens 47-54 11272196-1 2001 PDX-1 was shown to be expressed early during development in cells of both exocrine and endocrine origin; later it becomes restricted primarily to beta-cells where it regulates the expression of beta-cell-specific genes and mediates the glucose effect on insulin gene transcription. Glucose 236-243 insulin Homo sapiens 254-261 11213882-5 2001 The intrasubject variation in fasting blood glucose during the last 4 days of treatment was lower for insulin detemir compared with NPH (P < 0.001). Glucose 44-51 insulin Homo sapiens 102-109 11213882-9 2001 The results indicate that insulin detemir may provide more predictable fasting blood glucose with lower intrasubject variation and reduced risk of hypoglycemia compared with NPH. Glucose 85-92 insulin Homo sapiens 26-33 11213887-2 2001 RESEARCH DESIGN AND METHODS: Because glucose toxicity per se leads to insulin resistance, the determination of the primary metabolic alterations leading to insulin resistance is best accomplished in individuals who are at an increased risk to develop type 2 diabetes. Glucose 37-44 insulin Homo sapiens 70-77 11270672-6 2001 Basal insulin release was higher (p < 0.05) in women with gestational diabetes compared with the pregnant women with normal glucose tolerance. Glucose 127-134 insulin Homo sapiens 6-13 11270673-4 2001 RESULTS: Incubation of L6 muscle cells with ceramide (100 micromol/l) for 2 h led to a complete loss of insulin-stimulated glucose transport and glycogen synthesis. Glucose 123-130 insulin Homo sapiens 104-111 11165689-7 2001 Endogenous glucose production was more effectively suppressed at the two lower insulin infusion rates (P>0.05). Glucose 11-18 insulin Homo sapiens 79-86 11272131-8 2001 Our data indicate that an increase in metabolic flow to triglyceride synthesis can inhibit NEFA release, increase NEFA uptake, and promote insulin-mediated glucose utilization in 3T3-L1 adipocytes. Glucose 156-163 insulin Homo sapiens 139-146 11270684-1 2001 AIMS/HYPOTHESIS: The apolipoprotein C3-482C> T variant modulates insulin and glucose concentrations after an oral glucose tolerance test (OGTT) in young healthy white men. Glucose 117-124 insulin Homo sapiens 68-75 11270684-7 2001 Higher triglyceride concentrations (p = 0.004 and p = 0.007 in the two models) but not glucose concentrations were also associated with -482C > T. In black subjects, decreased fasting insulin (p = 0.04) and fasting glucose (p = 0.004) were associated with -482C > T. No relation was observed between genotype and any post-load measured. Glucose 218-225 insulin Homo sapiens 187-194 11272131-5 2001 In myotubes, overexpression of AGAT-alpha did not affect total [14C]glucose uptake in the presence or absence of insulin, whereas insulin-stimulated [14C]glucose conversion to cellular lipids increased significantly (33%, P = 0.004) with a concomitant decrease (-30%, P = 0.005) in glycogen formation. Glucose 154-161 insulin Homo sapiens 130-137 11272132-5 2001 Wortmannin completely inhibited insulin-stimulated glucose transport and only slightly inhibited SNP-stimulated 2-deoxyglucose uptake, whereas L-NMMA did not inhibit contraction-stimulated 2-deoxyglucose uptake. Glucose 51-58 insulin Homo sapiens 32-39 11272131-7 2001 AGAT-alpha overexpression in adipocytes increased basal (130%, P = 0.04) and insulin-stimulated (27%, P = 0.01) [3H]OA uptake, increased insulin-stimulated glucose uptake (56%, P = 0.04) and conversion to cellular lipids (85%, P = 0.007), and suppressed basal (-44%, P = 0.01) and isoproterenol-stimulated OA release (-45%, P = 0.03) but not glycerol release. Glucose 156-163 insulin Homo sapiens 137-144 11272137-12 2001 During insulin infusion, the metabolic clearance rate of glucose was defective in the NF group versus in the other groups (P < 0.01). Glucose 57-64 insulin Homo sapiens 7-14 11272143-5 2001 There was positive, albeit significantly blunted, acute insulin response to intravenous dextrose in the patients with diffuse hyperinsulinism. Glucose 88-96 insulin Homo sapiens 56-63 11171554-3 2001 Since skeletal muscle is considered the major organ responsible for glucose uptake under insulin-stimulated conditions, defects in this target tissue are likely to contribute to metabolic disregulation in Type II diabetes mellitus. Glucose 68-75 insulin Homo sapiens 89-96 11272143-6 2001 Graded infusions of glucose, to raise and then lower plasma glucose concentrations over 4 h, caused similar rises in blood glucose but lower peak insulin levels in the hyperinsulinemic patients. Glucose 20-27 insulin Homo sapiens 146-153 11272143-6 2001 Graded infusions of glucose, to raise and then lower plasma glucose concentrations over 4 h, caused similar rises in blood glucose but lower peak insulin levels in the hyperinsulinemic patients. Glucose 60-67 insulin Homo sapiens 146-153 11272143-6 2001 Graded infusions of glucose, to raise and then lower plasma glucose concentrations over 4 h, caused similar rises in blood glucose but lower peak insulin levels in the hyperinsulinemic patients. Glucose 60-67 insulin Homo sapiens 146-153 11171554-4 2001 Defects in insulin signal transduction through the insulin-receptor substrate-1/phosphatidylinositol 3-kinase pathway is associated with reduced insulin-stimulated glucose transport activity in skeletal muscle from Type II diabetic patients. Glucose 164-171 insulin Homo sapiens 11-18 11171554-4 2001 Defects in insulin signal transduction through the insulin-receptor substrate-1/phosphatidylinositol 3-kinase pathway is associated with reduced insulin-stimulated glucose transport activity in skeletal muscle from Type II diabetic patients. Glucose 164-171 insulin Homo sapiens 51-58 11171554-5 2001 Glucose transport, the rate limiting step in glucose metabolism, is mediated by glucose transporter 4 (GLUT4) translocation and can be activated in skeletal muscle by two separate and distinct signaling pathways; one stimulated by insulin and the second by muscle contractions. Glucose 0-7 insulin Homo sapiens 231-238 11158011-5 2001 In the mixed families, the insulin response to oral glucose load was impaired in patients who had HLA class II risk haplotypes, either DR3(17)-DQA1*0501-DQB1*02 or DR4*0401/4-DQA1*0301-DQB1*0302, compared with patients without such haplotypes (P = 0.016). Glucose 52-59 insulin Homo sapiens 27-34 11171554-7 2001 Understanding the molecular mechanism for the activation of signal transduction pathways by which insulin and muscle contraction increase glucose transport will provide a link to defining new strategies to enhance glucose metabolism in the diabetic patient. Glucose 138-145 insulin Homo sapiens 98-105 11294490-7 2001 Increase of RLP cholesterol after the fat meal load only significantly correlated with increase of insulin during the first 30 min after a 75 g oral glucose tolerance test, but not fasting lipid, insulinogenic index and HOMA-R (homeostasis model) in all subjects. Glucose 149-156 insulin Homo sapiens 99-106 11238540-8 2001 Vanadyl sulfate also caused a modest increase in insulin-mediated glucose disposal (from 4.3 +/- 0.4 to 5.1 +/- 0.6 mg/kg lean body mass x min; P< 0.03), although the improvement in insulin sensitivity did not correlate with the decline in FPG after treatment (r = -0.16; P = NS). Glucose 66-73 insulin Homo sapiens 49-56 11158013-7 2001 We conclude that although these results were obtained from an acute study, and long-term administration of pegvisomant could render different results, blockade of the GHR in the nonfasting state induces tissue-specific changes in insulin sensitivity, resulting in an increase in glucose and insulin levels (indicating insulin resistance of liver/muscle), but probably also in an increase in lipogenesis (indicating normal insulin sensitivity of adipose tissue). Glucose 279-286 insulin Homo sapiens 230-237 11158022-0 2001 Differential insulin sensitivities of glucose, amino acid, and albumin metabolism in elderly men and women. Glucose 38-45 insulin Homo sapiens 13-20 11158022-2 2001 Insulin dose responses of whole body glucose, leucine, and albumin metabolism have been investigated using isotopic dilution of D-[6, 6-(2)H(2)]glucose and L-[1-(13)C]leucine in 14 young (Y; 24.0 +/- 0.9 yr; mean +/- SEM, 20.5 +/- 0.4 kg/m(2)) and 12 healthy elderly subjects (E; 69.4 +/- 0.6 yr; 24.6 +/- 0.8 kg/m(2)) using a euglycemic and euaminoacidemic hyperinsulinemic clamp at two insulin infusion rates of 0.2 and 0.5 mU/kg.min (CL1 and CL2, respectively). Glucose 37-44 insulin Homo sapiens 0-7 11158022-3 2001 Despite significantly higher plasma insulin in E than in Y, the glucose disposal rate was lower in E than in Y at both insulin levels, whereas glucose production was normally suppressed. Glucose 64-71 insulin Homo sapiens 119-126 11160869-7 2001 Glimepiride increased the effects of insulin on glucose incorporation into glycogen by enhancing both sensitivity and maximal efficacy of insulin. Glucose 48-55 insulin Homo sapiens 37-44 11174623-0 2001 First-phase insulin release during the intravenous glucose tolerance test as a risk factor for type 1 diabetes. Glucose 51-58 insulin Homo sapiens 12-19 11174623-1 2001 OBJECTIVE: To determine the relationship between first-phase (1 minute + 3 minutes) insulin production during the intravenous glucose tolerance test (IV-GTT) and risk factors for developing type 1 diabetes. Glucose 126-133 insulin Homo sapiens 84-91 11229419-8 2001 The insulin resistance index was estimated by the calculated product of fasting plasma insulin and glucose concentrations. Glucose 99-106 insulin Homo sapiens 4-11 11160869-7 2001 Glimepiride increased the effects of insulin on glucose incorporation into glycogen by enhancing both sensitivity and maximal efficacy of insulin. Glucose 48-55 insulin Homo sapiens 138-145 11240333-10 2001 In conclusion, lipolysis rates are increased after abdominal surgery and glucose administration, most likely due to insulin resistance, and fail to inhibit stimulated whole-body lipolysis. Glucose 73-80 insulin Homo sapiens 116-123 12143835-4 2001 Use of insulin to enhance glucose tolerance in LBW infants, and thereby maximize growth, is a management modality that can be initiated early in the infant"s course and is facilitated by implementation of clear and consistent policies and procedures. Glucose 26-33 insulin Homo sapiens 7-14 11240333-9 2001 The hyperglycemic response to glucose infusion was significantly more pronounced (P < 0.05) in patients (10.7 +/- 0.7 mmol/L) than in volunteers (7.1 +/- 0.4 mmol/L), whereas the plasma insulin increased to the same extent in the two groups (P < 0.001). Glucose 30-37 insulin Homo sapiens 189-196 11158022-6 2001 In conclusion, decreased insulin action on glucose disposal is associated with a reduced insulin sensitivity for protein breakdown in healthy elderly subjects at low insulin concentrations. Glucose 43-50 insulin Homo sapiens 25-32 11235038-0 2001 Insulin secretion in glucose-tolerant offspring of type 2 diabetes patients in Trinidad, West Indies. Glucose 21-28 insulin Homo sapiens 0-7 11213069-10 2001 All patients required s.c. insulin for glucose control. Glucose 39-46 insulin Homo sapiens 27-34 11300605-3 2001 Diabetic and non-diabetic subjects were divided in equal groups of eight subjects with low or high insulin sensitivity, which was documented as the glucose infusion rate (M-value) during the last hour of a 3-h euglycaemic hyperinsulinaemic clamp (150 mU kg(-1) h(-1), blood glucose target 4.6 mmol L(-1)). Glucose 148-155 insulin Homo sapiens 99-106 11665324-1 2001 The insulin resistance syndrome (IRS) is characterized by a combination of interrelated coronary heart disease risk factors, including low high-density lipoprotein cholesterol (HDLC) levels, obesity and increases in triglyceride (TG), systolic and diastolic blood pressure (BP), small low-density lipoprotein particles (LDL-size), and fasting and postload plasma insulin and glucose. Glucose 375-382 insulin Homo sapiens 4-11 11206679-4 2001 Clamp-derived insulin sensitivity was calculated as the glucose disposal rate over steady-state plasma insulin concentration. Glucose 56-63 insulin Homo sapiens 14-21 11211190-4 2001 RESULTS: After 24-hr exposure, a marked decrease of glucose-stimulated insulin secretion was observed with human, but not with bovine islets. Glucose 52-59 insulin Homo sapiens 71-78 11024035-1 2001 Transcription factors binding the insulin enhancer region, RIPE3b, mediate beta-cell type-specific and glucose-responsive expression of the insulin gene. Glucose 103-110 insulin Homo sapiens 34-41 11024035-12 2001 In addition, RIPE3b1- and A2-specific activators respond differently to glucose, suggesting that their overlapping binding specificity and functional cooperation may play an important role in regulating insulin gene expression. Glucose 72-79 insulin Homo sapiens 203-210 11172324-4 2001 (2) After the start of hemodialysis therapy, insulin therapy must be adjusted and respect impaired glucose use and prolongation of insulin half-life. Glucose 99-106 insulin Homo sapiens 45-52 11665817-1 2001 Several reports have shown that nitric oxide (NO) stimulates glucose-induced insulin secretion in the pancreas of normal rat but the effect of L-arginine (a NO donor) on insulin secretion from the pancreas of diabetic pancreas is unknown. Glucose 61-68 insulin Homo sapiens 77-84 11120673-9 2001 These data suggest that this method is sufficiently sensitive to detect differences in insulin-stimulated glucose uptake; thus the use of radioactive stereoisomers in conjunction with the microdialysis technique provides a novel and useful technique for determining tissue-specific glucose flux and insulin sensitivity. Glucose 106-113 insulin Homo sapiens 87-94 11120673-9 2001 These data suggest that this method is sufficiently sensitive to detect differences in insulin-stimulated glucose uptake; thus the use of radioactive stereoisomers in conjunction with the microdialysis technique provides a novel and useful technique for determining tissue-specific glucose flux and insulin sensitivity. Glucose 282-289 insulin Homo sapiens 87-94 11455676-1 2001 To clarify the diversity in hypoglycemic actions of sulfonylureas, chronic effects of three sulfonylureas were compared on in vivo insulin-induced glucose uptake in peripheral tissues. Glucose 147-154 insulin Homo sapiens 131-138 11226623-0 2001 Modeling insulin kinetics: responses to a single oral glucose administration or ambulatory-fed conditions. Glucose 54-61 insulin Homo sapiens 9-16 11838327-1 2001 Insulin has been available for therapeutic use for more than 75 years and remains a powerful pharmacologic tool with nearly unlimited potential to lower plasma glucose levels in patients with diabetes. Glucose 160-167 insulin Homo sapiens 0-7 11299043-0 2001 The A54T polymorphism at the intestinal fatty acid binding protein 2 is associated with insulin resistance in glucose tolerant Caucasians. Glucose 110-117 insulin Homo sapiens 88-95 11227029-7 2001 The glucose and insulin responses to a gastric bolus of glucose were lower, and the post-bolus decrease of glucose was slower, in F28 than in F56 piglets (P < 0.0001). Glucose 56-63 insulin Homo sapiens 16-23 11227029-7 2001 The glucose and insulin responses to a gastric bolus of glucose were lower, and the post-bolus decrease of glucose was slower, in F28 than in F56 piglets (P < 0.0001). Glucose 56-63 insulin Homo sapiens 16-23 11892791-1 2001 Insulin is a potent metabolic hormone essential for the maintenance of normal circulating blood glucose level in mammals. Glucose 96-103 insulin Homo sapiens 0-7 11892791-4 2001 In particular, glucose transport into skeletal muscle and adipose tissue is the rate-limiting step in glucose metabolism and reduction in the efficiency of this process (insulin resistance) is one of the earliest predictors for the development of Type II diabetes. Glucose 15-22 insulin Homo sapiens 170-177 11892791-6 2001 In this review, we have focused on recent developments in our understanding of the molecular mechanisms and signal transduction pathways that insulin utilizes to specifically regulate glucose uptake. Glucose 184-191 insulin Homo sapiens 142-149 11814112-5 2001 Functionality of the transfected islets was measured by insulin response to glucose solutions. Glucose 76-83 insulin Homo sapiens 56-63 11167930-7 2001 It was also inversely related to the glucose and insulin levels during an oral glucose tolerance test (- 0.24 < r < - 0.40), serum oestradiol (r = - 0.26), and physical activity (r = - 0.24). Glucose 79-86 insulin Homo sapiens 49-56 11838327-3 2001 Attainment and maintenance of near-normal glycemic control can be achieved with the use of insulin replacement strategies designed to simulate the physiologic, nondiabetic patterns of insulin secretion in response to 24-hour postabsorptive and postprandial glucose profiles. Glucose 257-264 insulin Homo sapiens 91-98 11147777-2 2001 To further explore the interaction between these two elements in the rat, we used two strategies to promote the storage of lipids in skeletal muscle and then evaluated subsequent changes in insulin-mediated glucose disposal. Glucose 207-214 insulin Homo sapiens 190-197 11605714-6 2001 Pharmacodynamic studies show a smaller excursion of postprandial glucose with insulin aspart injected subcutaneously just before the meal compared with soluble human insulin injected 30 minutes before the meal in patients with type 1 diabetes mellitus, and an equivalent control in patients with type 2 diabetes displaying residual insulin production. Glucose 65-72 insulin Homo sapiens 78-85 11605714-7 2001 In a treatment study, glucose excursions evaluated from 24-hour glucose profiles showed less variability with insulin aspart compared with human insulin. Glucose 22-29 insulin Homo sapiens 110-117 11605714-7 2001 In a treatment study, glucose excursions evaluated from 24-hour glucose profiles showed less variability with insulin aspart compared with human insulin. Glucose 64-71 insulin Homo sapiens 110-117 11605714-9 2001 The available data suggest that subcutaneous injections of insulin aspart just before meals better mimic the endogenous insulin profile in blood compared with human insulin, resulting in improved glucose control in a meal-related insulin regimen. Glucose 196-203 insulin Homo sapiens 59-66 11759183-10 2001 Circulating immunoreactive insulin was elevated in active smokers and former smokers as compared to non-smokers after an oral glucose load (p < 0.05 for the area under the insulin time curve), despite a similar glucose response. Glucose 126-133 insulin Homo sapiens 27-34 11147777-6 2001 Insulin-mediated glucose disposal (IMGD) fell from 12.57 +/- 0.72 in the low-fat group to 9.79 +/- 0.59, 8.96 +/- 0.38, and 7.32 +/- 0.28 micromol x min(-1) x 100 g(-1) in the low-fat + etoxomir, lard, and lard + etoxomir groups, respectively. Glucose 17-24 insulin Homo sapiens 0-7 11147793-8 2001 As a group, they maintained stable insulin secretory reserve, but insulin responses to glucose tended to decrease over time in three patients. Glucose 87-94 insulin Homo sapiens 66-73 11147781-0 2001 Oral glucose tolerance test minimal model indexes of beta-cell function and insulin sensitivity. Glucose 5-12 insulin Homo sapiens 76-83 11147795-9 2001 Because the acute addition of FFAs also increases glucose-stimulated insulin secretion, these data suggest that the incretin function of GLP-1 may involve a major role for lipolysis in cAMP-mediated potentiation of secretion. Glucose 50-57 insulin Homo sapiens 69-76 11194244-4 2001 RESULTS: Insulin aspart and buffered regular human insulin were both effective in controlling average daily blood glucose levels (8.2 +/- 1.9 and 8.5 +/- 2.1 mmol/l, respectively) (mean +/- SD) and maintaining serum fructosamine (343 +/- 25.7 and 336 +/- 27.4 micromol/l) and HbA1c (6.9 +/- 0.6 and 7.1 +/- 0.6%) levels. Glucose 114-121 insulin Homo sapiens 9-16 11168335-11 2001 Plasma C-peptide response to oral glucose was initially (< 14 days) suppressed in all subjects and subsequently increased. Glucose 34-41 insulin Homo sapiens 7-16 11168335-15 2001 Remission was associated with a greater recovery of glucose-stimulated insulin secretion suggesting that therapies directed at promoting beta cell recovery and preservation are potentially useful approaches to the treatment of Type 2 diabetes mellitus. Glucose 52-59 insulin Homo sapiens 71-78 11168336-8 2001 The acute insulin response was markedly reduced in the subjects with diabetes (1.8 (0.60-3.1) pmol insulin/ mmol glucose), compared with the control group (31.4 (8.0-54) pmol/l insulin/mmol glucose), P<0.005. Glucose 113-120 insulin Homo sapiens 10-17 11168336-8 2001 The acute insulin response was markedly reduced in the subjects with diabetes (1.8 (0.60-3.1) pmol insulin/ mmol glucose), compared with the control group (31.4 (8.0-54) pmol/l insulin/mmol glucose), P<0.005. Glucose 190-197 insulin Homo sapiens 10-17 11194244-4 2001 RESULTS: Insulin aspart and buffered regular human insulin were both effective in controlling average daily blood glucose levels (8.2 +/- 1.9 and 8.5 +/- 2.1 mmol/l, respectively) (mean +/- SD) and maintaining serum fructosamine (343 +/- 25.7 and 336 +/- 27.4 micromol/l) and HbA1c (6.9 +/- 0.6 and 7.1 +/- 0.6%) levels. Glucose 114-121 insulin Homo sapiens 51-58 11194248-0 2001 Insulin resistance and insulin secretory dysfunction are independent predictors of worsening of glucose tolerance during each stage of type 2 diabetes development. Glucose 96-103 insulin Homo sapiens 0-7 11194248-3 2001 RESEARCH DESIGN AND METHODS: Insulin-stimulated glucose disposal (M) (hyperinsulinemic clamp), acute insulin secretory response (AIR) (25-g intravenous glucose tolerance test), and body composition (hydrodensitometry or dual-energy X-ray absorptiometry) were measured in 254 Pima Indians with NGT and in 145 Pima Indians with IGT, who were then followed for 0.5-13 years. Glucose 48-55 insulin Homo sapiens 29-36 11194248-6 2001 CONCLUSIONS: During each stage of the development of type 2 diabetes, insulin resistance and insulin secretory dysfunction are independent predictors of worsening glucose tolerance and are, therefore, both targets for the primary prevention of the disease. Glucose 163-170 insulin Homo sapiens 70-77 11577797-5 2001 Fasting plasma glucose and fasting blood glucose levels generally improved to a greater extent in patients with type 1 diabetes mellitus receiving insulin glargine than patients who administered Neutral Protamine Hagedorn (NPH) insulin. Glucose 15-22 insulin Homo sapiens 147-154 11577797-5 2001 Fasting plasma glucose and fasting blood glucose levels generally improved to a greater extent in patients with type 1 diabetes mellitus receiving insulin glargine than patients who administered Neutral Protamine Hagedorn (NPH) insulin. Glucose 41-48 insulin Homo sapiens 147-154 11735645-4 2001 They have proven efficacy for reducing plasma glucose levels in patients with type 2 diabetes mellitus treated with diet alone, sulphonylureas, metformin or insulin. Glucose 46-53 insulin Homo sapiens 157-164 11174836-6 2001 Suppression of endogenous glucose production by insulin was blunted in MODY3 patients (3.3+/-1.2 micromol/kg per min) and in patients with NIDDM (4.4+/-0.6 micromol/kg per min) compared with controls (1.7+/-0.5 micromol/kg per min, P<0.05 compared with both MODY3 patients and patients with NIDDM). Glucose 26-33 insulin Homo sapiens 48-55 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 185-192 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 185-192 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 185-192 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 216-223 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 216-223 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 216-223 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 216-223 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 216-223 insulin Homo sapiens 166-173 11250769-5 2001 Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. Glucose 216-223 insulin Homo sapiens 166-173 11453039-9 2001 While causal relationships are still to be clearly established, there are now quite plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic Randle glucose-fatty acid cycle. Glucose 205-212 insulin Homo sapiens 150-157 11368233-2 2001 Specifically, the biologic response most studied is insulin-stimulated glucose disposal, yet the precise cellular mechanism responsible is not yet known. Glucose 71-78 insulin Homo sapiens 52-59 11460564-0 2001 Integration of biochemical and physiologic effects of insulin on glucose metabolism. Glucose 65-72 insulin Homo sapiens 54-61 11460573-2 2001 The rates of insulin-stimulated glucose disposal in peripheral tissues in hyperthyroidism have been found, in general, either normal or increased. Glucose 32-39 insulin Homo sapiens 13-20 11460564-1 2001 The major effects of insulin on tissues are: (1) Carbohydrate metabolism: (a) It increases the rate of transport of glucose across the cell membrane in adipose tissue and muscle, (b) it increases the rate of glycolysis in muscle and adipose tissue, (c) it stimulates the rate of glycogen synthesis in a number of tissues, including adipose tissue, muscle, and liver. Glucose 116-123 insulin Homo sapiens 21-28 11460573-3 2001 Skeletal muscle is the most important tissue for the disposal of glucose in response to insulin. Glucose 65-72 insulin Homo sapiens 88-95 11460573-5 2001 Studies examining insulin-stimulated glucose metabolism in skeletal muscle have suggested that, in the hyperthyroid state, it may be of primary importance to increase the rates of glycolysis and lactate formation relative to glucose oxidation in this tissue in order to provide substrate for gluconeogenesis (increase Cori cycle activity). Glucose 37-44 insulin Homo sapiens 18-25 11460565-1 2001 Insulin resistance is defined clinically as the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization in an individual as much as it does in a normal population. Glucose 125-132 insulin Homo sapiens 0-7 11460583-1 2001 Continuous glucose monitoring, providing more detailed information on glucose excursions than single spot measurements, should help to improve the therapy in diabetic patients and is also required for feedback-controlled insulin delivery. Glucose 11-18 insulin Homo sapiens 221-228 11460565-1 2001 Insulin resistance is defined clinically as the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization in an individual as much as it does in a normal population. Glucose 125-132 insulin Homo sapiens 105-112 11460583-10 2001 Further work is needed to optimize continuous tissue glucose monitoring systems and to develop a closed loop system for insulin application based on continuously measured tissue glucose concentrations. Glucose 178-185 insulin Homo sapiens 120-127 11460588-4 2001 Relative or absolute insulin excess occurs when insulin doses are excessive, ill-timed or of the wrong type, when exogenous glucose delivery, endogenous glucose production or insulin clearance are decreased or when insulin-independent glucose utilization or sensitivity to insulin are increased. Glucose 153-160 insulin Homo sapiens 21-28 11460588-4 2001 Relative or absolute insulin excess occurs when insulin doses are excessive, ill-timed or of the wrong type, when exogenous glucose delivery, endogenous glucose production or insulin clearance are decreased or when insulin-independent glucose utilization or sensitivity to insulin are increased. Glucose 124-131 insulin Homo sapiens 21-28 11460588-4 2001 Relative or absolute insulin excess occurs when insulin doses are excessive, ill-timed or of the wrong type, when exogenous glucose delivery, endogenous glucose production or insulin clearance are decreased or when insulin-independent glucose utilization or sensitivity to insulin are increased. Glucose 153-160 insulin Homo sapiens 21-28 11684868-3 2001 The mechanism of obesity-related insulin resistance involves the release of factors from adipocytes which exert a negative effect on glucose metabolism: free fatty acids, tumour necrosis factor-alpha and the recently discovered hormone, resistin. Glucose 133-140 insulin Homo sapiens 33-40 11223703-8 2001 The GDM patients showed impaired insulin secretion to glucose stimuli, with low plasma insulin levels (at 30 min) and reduced insulin/glucose ratios (at 30 and 60 min) early in the 75-gram OGTT. Glucose 54-61 insulin Homo sapiens 33-40 11280715-12 2001 CONCLUSIONS: Collectively, these data show that older, moderately overweight, non-diabetic men and women with gender-related differences in glucose-stimulated C-peptide AUC, an indirect indicator of insulin secretion, also display differences in the urinary excretion of myo-inositol, D-chiro-inositol, L-chiro-inositol, and pinitol. Glucose 140-147 insulin Homo sapiens 159-168 11684868-9 2001 In non-diabetic Pima Indians, this polymorphism was associated with insulin resistance of glucose disposal. Glucose 90-97 insulin Homo sapiens 68-75 11231988-1 2001 Mental stress is known to decrease systemic vascular resistance and increase muscle blood flow and to acutely enhance insulin-mediated glucose disposal in healthy humans. Glucose 135-142 insulin Homo sapiens 118-125 11910199-8 2001 RESULTS: The insulin response at 30 min after glucose load was significantly higher (p < 0.001) in pre- and post-pubertal girls and boys formerly SGA than in controls. Glucose 46-53 insulin Homo sapiens 13-20 11910199-10 2001 Mean serum insulin (MSI), the area under the insulin curve during the glucose challenge, was statistically increased in pre- and post-pubertal boys and girls born SGA when compared to controls. Glucose 70-77 insulin Homo sapiens 11-18 11910199-11 2001 CONCLUSION: The presence of high insulin levels after an oral glucose challenge in children and adolescents born SGA might be considered as an early marker of subsequent insulin resistance in adulthood. Glucose 62-69 insulin Homo sapiens 33-40 11910199-11 2001 CONCLUSION: The presence of high insulin levels after an oral glucose challenge in children and adolescents born SGA might be considered as an early marker of subsequent insulin resistance in adulthood. Glucose 62-69 insulin Homo sapiens 170-177 11211569-4 2001 At molecular level insulin resistance appears to occur at the level of G-protein, kinase activation, glucose carriers (GLUT) and gene expression. Glucose 101-108 insulin Homo sapiens 19-26 11231980-2 2001 Hepatic glucose production and insulin-stimulated glucose disposal were measured using [6,6-(2)H(2)]glucose and a 3-h hyperinsulinemic (80 mu/m(2).min)-euglycemic clamp. Glucose 50-57 insulin Homo sapiens 31-38 11231980-2 2001 Hepatic glucose production and insulin-stimulated glucose disposal were measured using [6,6-(2)H(2)]glucose and a 3-h hyperinsulinemic (80 mu/m(2).min)-euglycemic clamp. Glucose 50-57 insulin Homo sapiens 31-38 11231980-6 2001 Insulin-stimulated glucose disposal was not different between the two groups. Glucose 19-26 insulin Homo sapiens 0-7 11231988-7 2001 During lipid infusion, the increase in heart rate was not affected, but the increase in cardiac index, the decrease in systemic vascular resistance, and the increase in insulin-mediated glucose disposal were all inhibited. Glucose 186-193 insulin Homo sapiens 169-176 11231980-8 2001 The glucose disposition index (product of insulin sensitivity x first phase insulin) was lower in IGT vs. NGT (278 +/- 40 vs. 567 +/- 119 mg/kg.min; P = 0.023; 1546 +/- 223 vs. 3249 +/- 663 micromol/kg.min). Glucose 4-11 insulin Homo sapiens 42-49 11231980-8 2001 The glucose disposition index (product of insulin sensitivity x first phase insulin) was lower in IGT vs. NGT (278 +/- 40 vs. 567 +/- 119 mg/kg.min; P = 0.023; 1546 +/- 223 vs. 3249 +/- 663 micromol/kg.min). Glucose 4-11 insulin Homo sapiens 76-83 11806485-5 2001 Recent controlled studies suggest that antipsychotics can impair glucose regulation by decreasing insulin action, although effects on insulin secretion are not ruled out. Glucose 65-72 insulin Homo sapiens 98-105 11231996-15 2001 The mean insulin (107.1 +/- 21.9 and 36.8 +/- 7.2 pmol/L), but not glucose (4.0 +/- 0.3 and 4.1 +/- 0.1 mmol/L), levels calculated over 270 min, were higher (P = 0.005) in OB than in NW; rhIGF-I administration did not modify insulin and glucose levels in either group. Glucose 237-244 insulin Homo sapiens 9-16 11204289-4 2001 The changes in serum potassium and magnesium were both inversely related to the insulin-mediated glucose uptake (r= -0.62, P< 0.0001; r= -0.31, P< 0.05, respectively). Glucose 97-104 insulin Homo sapiens 80-87 11168785-3 2001 DESIGN: A random selection of subjects from the general population were divided into quintiles of a body mass index/blood glucose score that was shown to be a valid and reproducible index of the degree of insulin sensitivity as assessed by the clamp technique. Glucose 122-129 insulin Homo sapiens 205-212 11204289-5 2001 Both body mass index (BMI) and insulin-mediated glucose disposal were significantly correlated to the changes in serum aldosterone concentration during hyperinsulinemia (r = 0.41, P < 0.01; r = -0.40, P < 0.01, respectively). Glucose 48-55 insulin Homo sapiens 31-38 11148510-10 2001 Insulin sensitivity correlated negatively with fasting insulin (r = -0.71, P =.0002) and positively with the fasting glucose to insulin ratio (r = 0.79, P<.0001). Glucose 117-124 insulin Homo sapiens 0-7 11148510-10 2001 Insulin sensitivity correlated negatively with fasting insulin (r = -0.71, P =.0002) and positively with the fasting glucose to insulin ratio (r = 0.79, P<.0001). Glucose 117-124 insulin Homo sapiens 128-135 11172485-7 2001 In a traditional multiple regression analysis, LDL peak particle size was independently associated not with insulin-mediated glucose uptake but with circulating triglycerides and HDL cholesterol, which together explained 67% of the variability in LDL particle size (P = .000). Glucose 125-132 insulin Homo sapiens 108-115 11833461-7 2001 In the liver, when the diet is rich in carbohydrates, insulin is secreted and stimulates the expression of genes involved in glucose utilization (glucokinase, L-pyruvate kinase, lipogenic enzymes) and inhibits genes involved in glucose production (phosphenolpyruvate carboxykinase). Glucose 125-132 insulin Homo sapiens 54-61 11833461-7 2001 In the liver, when the diet is rich in carbohydrates, insulin is secreted and stimulates the expression of genes involved in glucose utilization (glucokinase, L-pyruvate kinase, lipogenic enzymes) and inhibits genes involved in glucose production (phosphenolpyruvate carboxykinase). Glucose 228-235 insulin Homo sapiens 54-61 11172469-10 2001 We conclude that upper body obesity is associated with a slower rate of activation of insulin action on glucose metabolism, whereas total body adiposity selectively affects the maximal, steady-state insulin effect. Glucose 104-111 insulin Homo sapiens 86-93 11160828-5 2001 In nontransfected adipocytes, impairment of microtubule and actin filament function inhibited insulin-stimulated glucose transport by 70 and 50%, respectively. Glucose 113-120 insulin Homo sapiens 94-101 11160828-6 2001 When both filament systems were impaired insulin-stimulated glucose transport was completely inhibited. Glucose 60-67 insulin Homo sapiens 41-48 11237212-10 2001 As postprandial glucose levels rise, the subsequent increase in circulating insulin activates intracellular signaling cascades that ultimately result in the translocation of the GLUT4 storage compartments to the plasma membrane. Glucose 16-23 insulin Homo sapiens 76-83 11843266-8 2001 The elevation of CHP in those with a decrease in this estimate of HIC (obese) is interesting as the greater insulin response seen in normal persons after oral glucose compared to intravenous glucose has been postulated to be due to a decrease in HIC by some gut factor. Glucose 159-166 insulin Homo sapiens 108-115 11769387-1 2001 Insulin enhances glucose disposal, storage and oxidation in muscles. Glucose 17-24 insulin Homo sapiens 0-7 11769387-4 2001 Glucose normally provides energy sources for tissues of the body, its uptake by muscle requires a secretion of insulin. Glucose 0-7 insulin Homo sapiens 111-118 11237212-15 2001 This chapter will focus on recently elucidated insulin signal transduction pathways and GLUT4 vesicle trafficking components that are necessary for insulin-stimulated glucose uptake and GLUT4 translocation in adipocytes. Glucose 167-174 insulin Homo sapiens 47-54 11769387-7 2001 The insulin-receptor complex stimulates the cellular uptake of glucose. Glucose 63-70 insulin Homo sapiens 4-11 11237212-15 2001 This chapter will focus on recently elucidated insulin signal transduction pathways and GLUT4 vesicle trafficking components that are necessary for insulin-stimulated glucose uptake and GLUT4 translocation in adipocytes. Glucose 167-174 insulin Homo sapiens 148-155 11237217-1 2001 Insulin resistance is a change in physiologic regulation such that a fixed dose of insulin causes less of an effect on glucose metabolism than occurs in normal individuals. Glucose 119-126 insulin Homo sapiens 0-7 11237222-3 2001 Glucagon-like peptide-1 (GLP-1) is a potent insulin secretagogue that has multiple synergetic effects on the glucose-dependent insulin secretion pathways of the beta-cell. Glucose 109-116 insulin Homo sapiens 44-51 11237217-1 2001 Insulin resistance is a change in physiologic regulation such that a fixed dose of insulin causes less of an effect on glucose metabolism than occurs in normal individuals. Glucose 119-126 insulin Homo sapiens 83-90 11237217-3 2001 If the hyperinsulinemia is sufficient to overcome the insulin resistance, glucose regulation remains normal; if not, type 2 diabetes ensues. Glucose 74-81 insulin Homo sapiens 12-19 11208163-2 2001 In response to insulin, GLUT4 moves from intracellular storage areas to the plasma membrane, thus increasing cellular glucose uptake. Glucose 118-125 insulin Homo sapiens 15-22 11208163-4 2001 J Biol Chem 1980;255: 4758-4762 and Suzuki K, Kono T. Proc Natl Acad Sci 1980;77: 2542-2545) has increased our understanding of insulin-regulated glucose transport, a number of fundamental questions remain unanswered. Glucose 146-153 insulin Homo sapiens 128-135 11436686-5 2001 MODY blood glucose is primarily due to beta-cell defects resulting in inadequate insulin secretion for a given level. Glucose 11-18 insulin Homo sapiens 81-88 11013239-5 2000 Additionally, enhanced glucose transport and incorporation into lipid in response to insulin were unaffected. Glucose 23-30 insulin Homo sapiens 85-92 11013239-7 2000 Removal of extracellular glucose during the recovery period blocked the increase in glycogen levels, and restored insulin-induced glycogen synthase activation. Glucose 25-32 insulin Homo sapiens 114-121 11158022-6 2001 In conclusion, decreased insulin action on glucose disposal is associated with a reduced insulin sensitivity for protein breakdown in healthy elderly subjects at low insulin concentrations. Glucose 43-50 insulin Homo sapiens 89-96 11158022-6 2001 In conclusion, decreased insulin action on glucose disposal is associated with a reduced insulin sensitivity for protein breakdown in healthy elderly subjects at low insulin concentrations. Glucose 43-50 insulin Homo sapiens 89-96 11158023-0 2001 Oral glucose augments the counterregulatory hormone response during insulin-induced hypoglycemia in humans. Glucose 5-12 insulin Homo sapiens 68-75 11118820-4 2000 Hyperinsulinemia is secondary to impaired insulin stimulated glucose metabolism at the level of skeletal muscle (insulin resistance) and is seen in about one third of glucose tolerant humans following dietary carbohydrate intake. Glucose 61-68 insulin Homo sapiens 5-12 11093810-6 2000 Functionally, adipocyte-like LiSa-2 cells show increased insulin-dependent glucose uptake and lipid synthesis and are sensitive to lipolytic agents. Glucose 75-82 insulin Homo sapiens 57-64 11118820-4 2000 Hyperinsulinemia is secondary to impaired insulin stimulated glucose metabolism at the level of skeletal muscle (insulin resistance) and is seen in about one third of glucose tolerant humans following dietary carbohydrate intake. Glucose 167-174 insulin Homo sapiens 5-12 11085918-0 2000 Role for the microtubule cytoskeleton in GLUT4 vesicle trafficking and in the regulation of insulin-stimulated glucose uptake. Glucose 111-118 insulin Homo sapiens 92-99 11082306-4 2000 If this release is operating near an upper limit, an oscillatory insulin supply will be more efficient in lowering the blood glucose level than a constant supply. Glucose 125-132 insulin Homo sapiens 65-72 11082306-5 2000 If the insulin level is high enough for the hepatic release of glucose to nearly vanish, the opposite effect is observed. Glucose 63-70 insulin Homo sapiens 7-14 11093913-1 2000 We hypothesized that the vasodilation observed during insulin stimulation is closely coupled to the rate of glucose metabolism. Glucose 108-115 insulin Homo sapiens 54-61 11132530-4 2000 Patients with unsatisfactory glucose control, frequent hypoglycaemic events, and otherwise uncontrollable morning rises of blood glucose may in particular benefit from insulin pump therapy. Glucose 29-36 insulin Homo sapiens 168-175 11132530-4 2000 Patients with unsatisfactory glucose control, frequent hypoglycaemic events, and otherwise uncontrollable morning rises of blood glucose may in particular benefit from insulin pump therapy. Glucose 129-136 insulin Homo sapiens 168-175 11132530-5 2000 Glucose control can even be improved in CSII if insulin lispro is used instead of regular human insulin, as demonstrated in many clinical investigations. Glucose 0-7 insulin Homo sapiens 48-55 11144701-9 2000 When administered immediately prior to a meal, insulin aspart is at least as effective as regular human insulin in control of postprandial blood glucose concentrations. Glucose 145-152 insulin Homo sapiens 47-54 11144701-9 2000 When administered immediately prior to a meal, insulin aspart is at least as effective as regular human insulin in control of postprandial blood glucose concentrations. Glucose 145-152 insulin Homo sapiens 104-111 11144701-12 2000 Furthermore, due to favorable pharmacokinetics, insulin aspart controls postprandial blood glucose concentrations at least as well as regular human insulin and contributes to improved quality of life. Glucose 91-98 insulin Homo sapiens 48-55 11085918-1 2000 Insulin stimulates glucose uptake into adipocytes by promoting the translocation of the glucose transporter isoform 4 (GLUT4) from intracellular vesicles to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 11085918-7 2000 Upon further examination, microtubule depolymerization inhibited insulin-stimulated glucose uptake and GLUT4 translocation to the plasma membrane by approx. Glucose 84-91 insulin Homo sapiens 65-72 11215514-1 2000 Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. Glucose 101-108 insulin Homo sapiens 0-7 11192103-3 2000 RESULTS: In women with elevated amniotic fluid insulin levels the mean (SD) capillary blood glucose values at 0, 1, and 2 hours were 5.2 mmol/L (1.0) [94 mg/dL (18)], 10.5 mmol/L (1.4) [189 mg/dL (25)] and 8.2 mmol/L (2.0) [147 mg/dL (36)], respectively. Glucose 92-99 insulin Homo sapiens 47-54 11177197-7 2000 Total GD was similar in each group, although the insulin-dependent GD was substantially lower in the ileostomists (0.46 v. 0.13 mg glucose/min per pmol, P = 0.015). Glucose 131-138 insulin Homo sapiens 49-56 11215514-1 2000 Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. Glucose 101-108 insulin Homo sapiens 45-52 11215514-1 2000 Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. Glucose 132-139 insulin Homo sapiens 0-7 11215514-1 2000 Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. Glucose 132-139 insulin Homo sapiens 45-52 11215514-3 2000 These insulin-like actions include stimulating glucose uptake and regulating metabolic processes such as glycolysis, gluconeogenesis, fatty acid synthesis and the pentose phosphate pathway. Glucose 47-54 insulin Homo sapiens 6-13 11118028-7 2000 The individuals with diabetes in the seven most strongly linked families had high serum insulin levels during fasting and 2-h post-glucose load periods. Glucose 131-138 insulin Homo sapiens 88-95 11128348-3 2000 Early insulin secretion was calculated using the ratio of the 0- to 30-min incremental insulin values to the 0- to 30-min incremental glucose. Glucose 134-141 insulin Homo sapiens 6-13 11118012-3 2000 In 319 Pima Indians with normal glucose tolerance, fasting plasma insulin concentration and insulin-stimulated glucose disposal (M) (hyperinsulinemic clamp) were inversely related, but at any given M, there was substantial variation, with some subjects being hyperinsulinemic and others being hypoinsulinemic relative to their degree of insulin sensitivity. Glucose 111-118 insulin Homo sapiens 92-99 11118012-3 2000 In 319 Pima Indians with normal glucose tolerance, fasting plasma insulin concentration and insulin-stimulated glucose disposal (M) (hyperinsulinemic clamp) were inversely related, but at any given M, there was substantial variation, with some subjects being hyperinsulinemic and others being hypoinsulinemic relative to their degree of insulin sensitivity. Glucose 111-118 insulin Homo sapiens 92-99 11118012-4 2000 In 262 of the 319 subjects followed prospectively over 6.4 +/- 3.9 years, a high fasting plasma insulin concentration was a significant independent predictor of diabetes, in addition to low M and low acute insulin response (AIR) (intravenous glucose challenge). Glucose 242-249 insulin Homo sapiens 96-103 11173721-5 2000 During the postoperative course, the insulin doses required to maintain normal glucose levels progressively decreased, and insulin became completely unnecessary by the 29(th) postoperative day. Glucose 79-86 insulin Homo sapiens 37-44 11128372-0 2000 A retrospective study on 435 women with gestational diabetes: fasting plasma glucose is not sensitive enough for screening but predicts a need for insulin treatment. Glucose 77-84 insulin Homo sapiens 147-154 11151756-7 2000 The 2-h glucose values inversely correlated with insulin sensitivity in subjects with GADA (r = -0.447, p < 0.001) and subjects from Type II diabetic families (r = -0.426, p < 0.001), whereas no such relation was observed in subjects with MODY mutations (r = 0.151, p = NS). Glucose 8-15 insulin Homo sapiens 49-56 11151756-10 2000 Enhanced insulin sensitivity is the most likely explanation for the normal glucose tolerance. Glucose 75-82 insulin Homo sapiens 9-16 11173721-6 2000 After insulin was stopped, glucose levels remained within normal ranges for the 5-year-long follow-up, despite the worsening of a preexisting diabetic nephropathy and the occurrence of a diabetic retinopathy. Glucose 27-34 insulin Homo sapiens 6-13 11225967-11 2000 CONCLUSIONS: We conclude that insulin glargine and regular human insulin elicit comparable symptomatic and counter-regulatory hormonal responses during hypoglycaemia in healthy or diabetic subjects, and induce similar rates of glucose disposal. Glucose 227-234 insulin Homo sapiens 30-37 11225967-11 2000 CONCLUSIONS: We conclude that insulin glargine and regular human insulin elicit comparable symptomatic and counter-regulatory hormonal responses during hypoglycaemia in healthy or diabetic subjects, and induce similar rates of glucose disposal. Glucose 227-234 insulin Homo sapiens 65-72 11108280-0 2000 Insulin-mediated cellular insulin resistance decreases osmotic shock-induced glucose transport in 3T3-L1 adipocytes. Glucose 77-84 insulin Homo sapiens 0-7 11108280-0 2000 Insulin-mediated cellular insulin resistance decreases osmotic shock-induced glucose transport in 3T3-L1 adipocytes. Glucose 77-84 insulin Homo sapiens 26-33 11108280-2 2000 In our study, we evaluated the effect of chronic insulin treatment on the osmotic shock signaling pathway leading to GLUT4 translocation and glucose uptake. Glucose 141-148 insulin Homo sapiens 49-56 11108280-3 2000 We found that chronic administration of insulin to the adipocytes induced cellular resistance to osmotic shock-stimulated GLUT4 translocation and glucose transport. Glucose 146-153 insulin Homo sapiens 40-47 11108294-6 2000 Insulin-stimulated glucose uptake, an event regulated via the IGF-1 receptor, is decreased upon exposure to excess IGF-1, suggesting decreased function of the receptor. Glucose 19-26 insulin Homo sapiens 0-7 11200306-6 2000 A few trials suggest that oral estrogen therapy reduces postmenopausal insulin resistance, as suggested by reductions in fasting insulin and glucose levels and an increase in glucose metabolism rates, whereas most studies do not show an adverse effect upon carbohydrate metabolism. Glucose 141-148 insulin Homo sapiens 71-78 11228051-4 2000 In patients with Type 2 diabetes, both proinsulin/C-peptide ratio and proinsulin/IRI ratio were significantly positively correlated with fasting plasma glucose level (FPG) and HbA1c. Glucose 152-159 insulin Homo sapiens 39-49 11228051-4 2000 In patients with Type 2 diabetes, both proinsulin/C-peptide ratio and proinsulin/IRI ratio were significantly positively correlated with fasting plasma glucose level (FPG) and HbA1c. Glucose 152-159 insulin Homo sapiens 50-80 11113614-6 2000 This abnormality along with a reduction in insulin concentration is assumed to induce a cascade-like process of disturbances including decreases in cellular glucose, acetylcholine, cholesterol, and ATP, associated with changes in the metabolism of amino acids and fatty acids. Glucose 157-164 insulin Homo sapiens 43-50 11122324-6 2000 RESULTS: Whole-body glucose uptake amounted to 4.9 +/- 2.1 and 11.0 +/- 2.4 mg kg(-1) min(-1) in the insulin-resistant and to 12.7 +/- 2.3 and 17.4 +/- 2.6 mg kg(-1) min(-1) in the insulin-sensitive subjects during physiological and supraphysiological hyperinsulinaemia, respectively. Glucose 20-27 insulin Homo sapiens 101-108 11122324-6 2000 RESULTS: Whole-body glucose uptake amounted to 4.9 +/- 2.1 and 11.0 +/- 2.4 mg kg(-1) min(-1) in the insulin-resistant and to 12.7 +/- 2.3 and 17.4 +/- 2.6 mg kg(-1) min(-1) in the insulin-sensitive subjects during physiological and supraphysiological hyperinsulinaemia, respectively. Glucose 20-27 insulin Homo sapiens 181-188 11122324-10 2000 In the combined group, we found a positive correlation between insulin-mediated glucose uptake and changes in RPF during physiological hyperinsulinaemia (r = 0.57, P = 0.009), whereas insulin-mediated glucose uptake correlated with changes in leg blood flow during supraphysiological hyperinsulinaemia (r = 0.54. Glucose 80-87 insulin Homo sapiens 63-70 11122324-10 2000 In the combined group, we found a positive correlation between insulin-mediated glucose uptake and changes in RPF during physiological hyperinsulinaemia (r = 0.57, P = 0.009), whereas insulin-mediated glucose uptake correlated with changes in leg blood flow during supraphysiological hyperinsulinaemia (r = 0.54. Glucose 80-87 insulin Homo sapiens 140-147 11249478-1 2000 Repaglinide is a novel insulin secretagogue that was developed as a prandial glucose regulator for the treatment of people with Type 2 diabetes mellitus. Glucose 77-84 insulin Homo sapiens 23-30 11161963-1 2000 Hyperglycaemia and increased variability of blood glucose in pubertal children with type 1 diabetes may be related to increased growth hormone (GH) secretion and insulin resistance. Glucose 50-57 insulin Homo sapiens 162-169 11119744-6 2000 MAIN OUTCOME MEASURE(S): Insulin and glucose levels during a standard oral glucose tolerance test. Glucose 75-82 insulin Homo sapiens 25-32 11118017-0 2000 Prandial glucose effectiveness and fasting gluconeogenesis in insulin-resistant first-degree relatives of patients with type 2 diabetes. Glucose 9-16 insulin Homo sapiens 62-69 11118017-1 2000 Impaired glucose effectiveness (i.e., a diminished ability of glucose per se to facilitate its own metabolism), increased gluconeogenesis, and endogenous glucose release are, together with insulin resistance and beta-cell abnormalities, established features of type 2 diabetes. Glucose 9-16 insulin Homo sapiens 189-196 11118017-1 2000 Impaired glucose effectiveness (i.e., a diminished ability of glucose per se to facilitate its own metabolism), increased gluconeogenesis, and endogenous glucose release are, together with insulin resistance and beta-cell abnormalities, established features of type 2 diabetes. Glucose 62-69 insulin Homo sapiens 189-196 11127459-5 2000 RESULTS: Increases in plasma glucose and insulin after glucose loading were unaffected by vitamin coadministration. Glucose 55-62 insulin Homo sapiens 41-48 11145111-4 2000 In this study, we examined the involvement of insulin resistance (assessed as fasting insulin-glucose product, FIGP) and general and central obesity as potential links in the development of hypertension in 413 normoglycemic Hong Kong Chinese (56.9% hypertensive) subjects. Glucose 94-101 insulin Homo sapiens 86-93 11242807-7 2000 Proinsulin level was correlated with fasting C-peptide(r = 0.43, p = 0.002), postprandial 2 hour blood glucose(r = 0.213, p = 0.05) and triglyceride(r = 0.28, p = 0.022). Glucose 103-110 insulin Homo sapiens 0-10 11242807-8 2000 Proinsulin/insulin ratio was positively correlated with fasting C-peptide(r = 0.236, p = 0.031), fasting blood glucose (r = 0.264, p = 0.015), postprandial 2 hour blood glucose(r = 0.277, p = 0.001) and triglyceride(r = 0.428, p < 0.001). Glucose 111-118 insulin Homo sapiens 0-10 11242807-8 2000 Proinsulin/insulin ratio was positively correlated with fasting C-peptide(r = 0.236, p = 0.031), fasting blood glucose (r = 0.264, p = 0.015), postprandial 2 hour blood glucose(r = 0.277, p = 0.001) and triglyceride(r = 0.428, p < 0.001). Glucose 111-118 insulin Homo sapiens 3-10 11242807-8 2000 Proinsulin/insulin ratio was positively correlated with fasting C-peptide(r = 0.236, p = 0.031), fasting blood glucose (r = 0.264, p = 0.015), postprandial 2 hour blood glucose(r = 0.277, p = 0.001) and triglyceride(r = 0.428, p < 0.001). Glucose 169-176 insulin Homo sapiens 0-10 11242807-8 2000 Proinsulin/insulin ratio was positively correlated with fasting C-peptide(r = 0.236, p = 0.031), fasting blood glucose (r = 0.264, p = 0.015), postprandial 2 hour blood glucose(r = 0.277, p = 0.001) and triglyceride(r = 0.428, p < 0.001). Glucose 169-176 insulin Homo sapiens 3-10 11145118-9 2000 Glucose appearing in the peripheral circulation as a result of ingestion of 50 g fructose was calculated to be 9.8 +/- 2.4 g. Following the ingestion of fructose, there was a small increase in glucagon but a 2-fold increase in insulin concentration. Glucose 0-7 insulin Homo sapiens 227-234 11145118-14 2000 The increase in glucose production occurred even in the presence of an increase in the insulin concentration and an unchanged glucagon concentration. Glucose 16-23 insulin Homo sapiens 87-94 11117522-8 2000 In addition, when cotransfected together with the GAL4-substituted insulin enhancer reporter gene in glucose-responsive MIN-6 beta-cells, glucose-induced activation is observed with GAL4:PDX-1 but not with fusions of the heterologous activation domains from herpes virus VP16 or adenovirus-5 E1A proteins. Glucose 101-108 insulin Homo sapiens 67-74 11145123-11 2000 After glucose ingestion, both serum C-peptide and glucagon-like peptide-1 (GLP-1) increased (C-peptide from 1.1 +/- 0.05 to 1.4 +/- 0.05 nmol/L and GLP-1 from 3.2 +/- 0.8 to 18.1 +/- 3.3 pmol/L), in contrast to the situation without oral glucose (P < .05). Glucose 6-13 insulin Homo sapiens 36-45 11145123-11 2000 After glucose ingestion, both serum C-peptide and glucagon-like peptide-1 (GLP-1) increased (C-peptide from 1.1 +/- 0.05 to 1.4 +/- 0.05 nmol/L and GLP-1 from 3.2 +/- 0.8 to 18.1 +/- 3.3 pmol/L), in contrast to the situation without oral glucose (P < .05). Glucose 6-13 insulin Homo sapiens 93-102 11145123-11 2000 After glucose ingestion, both serum C-peptide and glucagon-like peptide-1 (GLP-1) increased (C-peptide from 1.1 +/- 0.05 to 1.4 +/- 0.05 nmol/L and GLP-1 from 3.2 +/- 0.8 to 18.1 +/- 3.3 pmol/L), in contrast to the situation without oral glucose (P < .05). Glucose 238-245 insulin Homo sapiens 36-45 11145124-1 2000 Basal, "insulin-independent" glucose uptake into skeletal muscle is provided by glucose transporters positioned at the plasma membrane. Glucose 29-36 insulin Homo sapiens 8-15 11117522-8 2000 In addition, when cotransfected together with the GAL4-substituted insulin enhancer reporter gene in glucose-responsive MIN-6 beta-cells, glucose-induced activation is observed with GAL4:PDX-1 but not with fusions of the heterologous activation domains from herpes virus VP16 or adenovirus-5 E1A proteins. Glucose 138-145 insulin Homo sapiens 67-74 15016214-0 2000 Impaired insulin-mediated glucose uptake in monocytes of short children with intrauterine growth retardation. Glucose 26-33 insulin Homo sapiens 9-16 11118610-2 2000 The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. Glucose 129-136 insulin Homo sapiens 15-22 11118610-5 2000 Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Glucose 157-164 insulin Homo sapiens 24-54 15016214-5 2000 Insulin-stimulated glucose uptake was determined in two ways: 6 nm insulin concentration minus baseline (6-0 nm) and the regression slope of glucose uptake over the range of log insulin concentrations (slope value). Glucose 19-26 insulin Homo sapiens 0-7 15016214-5 2000 Insulin-stimulated glucose uptake was determined in two ways: 6 nm insulin concentration minus baseline (6-0 nm) and the regression slope of glucose uptake over the range of log insulin concentrations (slope value). Glucose 19-26 insulin Homo sapiens 67-74 15016214-5 2000 Insulin-stimulated glucose uptake was determined in two ways: 6 nm insulin concentration minus baseline (6-0 nm) and the regression slope of glucose uptake over the range of log insulin concentrations (slope value). Glucose 141-148 insulin Homo sapiens 0-7 15016214-6 2000 Insulin sensitivity was determined from a 90-min frequently sampled intravenous glucose tolerance test with the minimal model. Glucose 80-87 insulin Homo sapiens 0-7 15016214-9 2000 In the five subjects with IUGR that were evaluated, the in vivo insulin sensitivity index and glucose effectiveness were found to be positively correlated with insulin-mediated glucose uptake in monocytes (r = 0.54) and baseline glucose uptake in monocytes, respectively (r = 0.69). Glucose 94-101 insulin Homo sapiens 160-167 15016214-9 2000 In the five subjects with IUGR that were evaluated, the in vivo insulin sensitivity index and glucose effectiveness were found to be positively correlated with insulin-mediated glucose uptake in monocytes (r = 0.54) and baseline glucose uptake in monocytes, respectively (r = 0.69). Glucose 177-184 insulin Homo sapiens 64-71 15016214-9 2000 In the five subjects with IUGR that were evaluated, the in vivo insulin sensitivity index and glucose effectiveness were found to be positively correlated with insulin-mediated glucose uptake in monocytes (r = 0.54) and baseline glucose uptake in monocytes, respectively (r = 0.69). Glucose 177-184 insulin Homo sapiens 160-167 15016214-11 2000 Our hitherto limited data indicate that insulin-mediated glucose uptake in monocytes is correlated with in vivo assessment of insulin sensitivity in children with IUGR. Glucose 57-64 insulin Homo sapiens 40-47 15016214-11 2000 Our hitherto limited data indicate that insulin-mediated glucose uptake in monocytes is correlated with in vivo assessment of insulin sensitivity in children with IUGR. Glucose 57-64 insulin Homo sapiens 126-133 11132123-17 2000 When glucose is ingested at the beginning of moderate exercise, plasma glucose levels are higher in children than in adults, but this may be caused by decreased insulin sensitivity during the peripubertal period (as shown by glucose: insulin ratios). Glucose 5-12 insulin Homo sapiens 161-168 11132123-17 2000 When glucose is ingested at the beginning of moderate exercise, plasma glucose levels are higher in children than in adults, but this may be caused by decreased insulin sensitivity during the peripubertal period (as shown by glucose: insulin ratios). Glucose 5-12 insulin Homo sapiens 234-241 11286024-0 2000 [Insulin secretion and resistance during pregnancy in women with glucose intolerance]. Glucose 65-72 insulin Homo sapiens 1-8 11798541-0 2000 [The clinical significance of true insulin and proinsulin levels in subjects with different glucose tolerance]. Glucose 92-99 insulin Homo sapiens 35-42 11798542-6 2000 CONCLUSION: PI and TI, whether fasting or post-glucose loading, may not be independently related to CAD. Glucose 47-54 insulin Homo sapiens 12-14 11798541-1 2000 OBJECTIVE: To examine the levels of serum true insulin (TI) and proinsulin (PI) in individuals with different glucose tolerance and to assess its clinical significance. Glucose 110-117 insulin Homo sapiens 47-54 11798542-5 2000 RESULTS: Fasting and post-glucose loading PI and TI levels in both CAD and non-CAD groups significantly increased when compared with the control group (P < 0.05), after adjustment for age, body mass index and waist hip ratio, all statistically significant associations weakened or disappeared among three groups; but there was no significant difference of all the above variables between CAD group and non-CAD group (P > 0.05). Glucose 26-33 insulin Homo sapiens 42-44 11100731-5 2000 We used a recombinant adeno-associated virus (rAAV) that expresses a single-chain insulin analogue (SIA), which possesses biologically active insulin activity without enzymatic conversion, under the control of hepatocyte-specific L-type pyruvate kinase (LPK) promoter, which regulates SIA expression in response to blood glucose levels. Glucose 321-328 insulin Homo sapiens 82-89 10967116-7 2000 In a streptozotocin-induced diabetic mouse model, compound 2 potentiated the glucose-lowering effect of insulin. Glucose 77-84 insulin Homo sapiens 104-111 10967116-8 2000 In normal rats, compound 2 improved oral glucose tolerance with significant reduction in insulin release following glucose challenge. Glucose 115-122 insulin Homo sapiens 89-96 11052965-1 2000 Previous measurement of insulin in human muscle has shown that interstitial muscle insulin and glucose concentrations are approximately 30-50% lower than in plasma during hyperinsulinemia in normal subjects. Glucose 95-102 insulin Homo sapiens 24-31 10967090-2 2000 Glucose, leucine, succinic acid methyl ester, and alpha-ketoisocaproic acid all markedly stimulate insulin release but do not increase glutamate levels in pancreatic islets. Glucose 0-7 insulin Homo sapiens 99-106 10967090-4 2000 When leucine, in addition to glutamine, is applied to islets, insulin release is almost as high as with glucose alone. Glucose 104-111 insulin Homo sapiens 62-69 11032784-7 2000 In nondiabetic individuals, the strongest results were observed on chromosomes 10 (acute insulin response: MLS = 3.11 at 21.0 cM), 13 (2-h insulin: MLS = 2.86 at 65.5 cM), and 17 (fasting insulin/glucose ratio: MLS = 3.20 at 9.0 cM). Glucose 196-203 insulin Homo sapiens 89-96 11187397-7 2000 Fast-acting insulins and the newer classes of insulin secretagogues, which target postprandial glucose, may pose distinct therapeutic advantages in this regard. Glucose 95-102 insulin Homo sapiens 12-19 11049901-12 2000 The myocardial glucose uptake is stimulated not only by catecholamine, but also by insulin, protein kinase C, and increase of intracellular calcium. Glucose 15-22 insulin Homo sapiens 83-90 11052965-15 2000 It is suggested that decreased glucose uptake in type 2 diabetes is caused by insulin resistance at the cellular level rather than by a deficient access of insulin and glucose surrounding the muscle cell. Glucose 31-38 insulin Homo sapiens 78-85 11073844-14 2000 Insulin stimulated whole-body glucose disposal to 20+/-2 micromol. Glucose 30-37 insulin Homo sapiens 0-7 11110261-2 2000 This system is designed to predict glucose level changes in advance, considering delayed response time and the administered doses of insulin. Glucose 35-42 insulin Homo sapiens 133-140 11110261-5 2000 The model predictive control method resulted in a significant reduction of mean insulin infusion rate compared with the conventional PD controller (0.71 mU/kg per min vs. 1.81 mU/kg per min, p = 0.0005), when the glucose level in both methods reached the planned target level (100 mg/dl). Glucose 213-220 insulin Homo sapiens 80-87 11202571-9 2000 Similar results were obtained using either glucose-stimulated insulin release or graft insulin content as a measure of graft survival. Glucose 43-50 insulin Homo sapiens 62-69 11134088-11 2000 Nevertheless, most methods used in the assessment of insulin sensitivity examine the response to insulin of a single metabolite, glucose, primarily in the muscle and liver, and under fasting conditions and should, therefore, demonstrate insulin sensitivity that is comparable among methods. Glucose 129-136 insulin Homo sapiens 53-60 11134088-11 2000 Nevertheless, most methods used in the assessment of insulin sensitivity examine the response to insulin of a single metabolite, glucose, primarily in the muscle and liver, and under fasting conditions and should, therefore, demonstrate insulin sensitivity that is comparable among methods. Glucose 129-136 insulin Homo sapiens 97-104 11134088-11 2000 Nevertheless, most methods used in the assessment of insulin sensitivity examine the response to insulin of a single metabolite, glucose, primarily in the muscle and liver, and under fasting conditions and should, therefore, demonstrate insulin sensitivity that is comparable among methods. Glucose 129-136 insulin Homo sapiens 97-104 11134101-10 2000 Of the 9 subjects with improved glucose tolerance during the OGTT+F, 5 had smaller insulin AUC during the OGTT+F than the OGTT-F. Glucose 32-39 insulin Homo sapiens 83-90 11154073-4 2000 It was found that wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase, prevented insulin-induced, as well as cyclic PIP-induced activation of glucose transport, indicating that PI 3-kinase action on glucose transport involves downstream signaling of both insulin and cyclic PIP. Glucose 156-163 insulin Homo sapiens 269-276 11154073-4 2000 It was found that wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase, prevented insulin-induced, as well as cyclic PIP-induced activation of glucose transport, indicating that PI 3-kinase action on glucose transport involves downstream signaling of both insulin and cyclic PIP. Glucose 213-220 insulin Homo sapiens 269-276 11202571-5 2000 In some mice, insulin production following intraperitoneal glucose injection was determined in serum. Glucose 59-66 insulin Homo sapiens 14-21 11105797-5 2000 Insulin sensitivity was estimated by the glucose infusion rate (M value) during euglycemic hyperinsulinemic clamping for 60 to 120 min. Glucose 41-48 insulin Homo sapiens 0-7 11078441-1 2000 There are strong correlations between impaired insulin-stimulated glucose metabolism and increased intramuscular lipid pools; however, the mechanism by which lipids interact with glucose metabolism is not completely understood. Glucose 179-186 insulin Homo sapiens 47-54 11078440-0 2000 Triggering and amplifying pathways of regulation of insulin secretion by glucose. Glucose 73-80 insulin Homo sapiens 52-59 11073844-17 2000 Forearm glucose uptake was similarly stimulated after 80 minutes of insulin infusion (to 2.11+/-0.42 and 2.06+/-0.43 micromol. Glucose 8-15 insulin Homo sapiens 68-75 11078450-4 2000 Culture with 27 mmol/l glucose obliterated postculture insulin responses to 27 mmol/l glucose. Glucose 23-30 insulin Homo sapiens 55-62 11092282-6 2000 The difference was accounted for by higher evening glucose levels with ultralente insulin (fasting 8.2 +/- 0.3 vs. 8.2 +/- 0.3 mmol/l, 6:00 P.M. 11.5 +/- 0.4 vs. 10.6 +/- 0.4 mmol/l). Glucose 51-58 insulin Homo sapiens 82-89 11078450-4 2000 Culture with 27 mmol/l glucose obliterated postculture insulin responses to 27 mmol/l glucose. Glucose 86-93 insulin Homo sapiens 55-62 11078450-9 2000 Coculture with diazoxide and 27 mmol/l glucose significantly (P < 0.05) restored postculture insulin responses to glucose and lowered basal [Ca2+]i and normalized glucose-induced oscillatory activity. Glucose 39-46 insulin Homo sapiens 96-103 11078450-9 2000 Coculture with diazoxide and 27 mmol/l glucose significantly (P < 0.05) restored postculture insulin responses to glucose and lowered basal [Ca2+]i and normalized glucose-induced oscillatory activity. Glucose 117-124 insulin Homo sapiens 96-103 11078450-9 2000 Coculture with diazoxide and 27 mmol/l glucose significantly (P < 0.05) restored postculture insulin responses to glucose and lowered basal [Ca2+]i and normalized glucose-induced oscillatory activity. Glucose 117-124 insulin Homo sapiens 96-103 11078452-2 2000 IPF-1 is required for the development of the pancreas and mediates glucose-responsive stimulation of insulin gene transcription. Glucose 67-74 insulin Homo sapiens 101-108 11092290-4 2000 These differences were evident early and persisted throughout the study More patients in the insulin glargine group (29.6%) than in the NPH group (16.8%) reached a target fasting blood glucose of 119 mg/dl (< 6.6 mmol/l). Glucose 185-192 insulin Homo sapiens 93-100 11092290-6 2000 Insulin glargine treatment was also associated with a significant decrease in the variability of fasting blood glucose values (P = 0.0124). Glucose 111-118 insulin Homo sapiens 0-7 11119017-5 2000 Insulin-mediated glucose disposal and suppression of endogenous glucose production at euglycemia were unchanged in MODY2 patients, but were blunted in type 2 diabetes. Glucose 17-24 insulin Homo sapiens 0-7 11078993-0 2000 In middle-aged siblings of patients with type 2 diabetes mellitus normal glucose tolerance is associated with insulin resistance and with increased insulin secretion. Glucose 73-80 insulin Homo sapiens 110-117 11122785-1 2000 Syndrome X is a cluster of abnormalities, associated with resistance to insulin-mediated glucose uptake, that increases risk of coronary heart disease. Glucose 89-96 insulin Homo sapiens 72-79 11126405-3 2000 RESULTS: Treatment of these cells with each of these sex hormones resulted in a statistically significant reduction in the ability of insulin to stimulate glucose transport independently of a reduction in total cellular GLUT-4 content. Glucose 155-162 insulin Homo sapiens 134-141 11126405-4 2000 This diminished ability of insulin to stimulate glucose transport was accompanied by a reduction in the total cellular content of insulin receptor substrates -1 and -2 and the p85alpha subunit of phosphatidylinositol 3"-kinase. Glucose 48-55 insulin Homo sapiens 27-34 11130936-10 2000 Newer methods of insulin delivery, such as continuous subcutaneous infusion, have greatly improved glucose control, given greater freedom to patients, and reduced the risks of hypoglycemia. Glucose 99-106 insulin Homo sapiens 17-24 11110411-0 2000 Glucose-stimulated and self-limiting insulin production by glucose 6-phosphatase promoter driven insulin expression in hepatoma cells. Glucose 0-7 insulin Homo sapiens 37-44 11110411-0 2000 Glucose-stimulated and self-limiting insulin production by glucose 6-phosphatase promoter driven insulin expression in hepatoma cells. Glucose 0-7 insulin Homo sapiens 97-104 11110411-6 2000 At the physiologic glucose level of 5.5 mM glucose, vector-transduced hepatoma cells produced a self-limited level of insulin at approximately 0.2-0.3 ng/ml, which is within the range of fasting levels of insulin in normal animals. Glucose 43-50 insulin Homo sapiens 118-125 11078441-1 2000 There are strong correlations between impaired insulin-stimulated glucose metabolism and increased intramuscular lipid pools; however, the mechanism by which lipids interact with glucose metabolism is not completely understood. Glucose 66-73 insulin Homo sapiens 47-54 11078441-8 2000 This inhibition of skeletal muscle hexokinase by long-chain acyl CoA suggests that increases in intramuscular lipid metabolites could interact directly with insulin-mediated glucose metabolism in vivo by decreasing the rate of glucose phosphorylation and decreasing glucose-6-phosphate concentrations. Glucose 174-181 insulin Homo sapiens 157-164 11078441-8 2000 This inhibition of skeletal muscle hexokinase by long-chain acyl CoA suggests that increases in intramuscular lipid metabolites could interact directly with insulin-mediated glucose metabolism in vivo by decreasing the rate of glucose phosphorylation and decreasing glucose-6-phosphate concentrations. Glucose 227-234 insulin Homo sapiens 157-164 11126245-4 2000 Surgical removal of selected VF provided direct evidence of improved in vivo insulin action on hepatic glucose production (HGP) by over 2-fold vs sham-operated control. Glucose 103-110 insulin Homo sapiens 77-84 11126246-2 2000 Critical to these functions is the capacity of the fat cell to respond to insulin with a significant increase in glucose uptake. Glucose 113-120 insulin Homo sapiens 74-81 11126246-4 2000 Nonetheless, the precise signaling pathways which mediate the insulin-stimulated increase in glucose transport remain uncertain. Glucose 93-100 insulin Homo sapiens 62-69 11126246-6 2000 Considerable current effort is being directed at trying to definitively establish whether Akt/PKB is an important intermediate in insulin signaling to glucose transport in muscle and fat. Glucose 151-158 insulin Homo sapiens 130-137 11058093-2 2000 Insulin regulation of GLUT4 trafficking in these cells underlies the role that adipose tissue and muscle play in the maintenance of whole body glucose homeostasis. Glucose 143-150 insulin Homo sapiens 0-7 11095426-0 2000 Insulin response to glucose is lower in individuals homozygous for the Arg 64 variant of the beta-3-adrenergic receptor. Glucose 20-27 insulin Homo sapiens 0-7 11095452-8 2000 In conclusion, sc insulin therapy, independently of glucose control and even in the presence of quite low plasma triglyceride levels, is able to reduce small LDL particles in type 2 diabetic patients. Glucose 52-59 insulin Homo sapiens 18-25 11095485-1 2000 In this report a new approach is introduced that allows estimation of insulin sensitivity (S(I)) from orally ingested glucose during an oral glucose tolerance test (OGTT) or a meal glucose tolerance test (MGTT) in normal subjects. Glucose 118-125 insulin Homo sapiens 70-77 11095485-1 2000 In this report a new approach is introduced that allows estimation of insulin sensitivity (S(I)) from orally ingested glucose during an oral glucose tolerance test (OGTT) or a meal glucose tolerance test (MGTT) in normal subjects. Glucose 141-148 insulin Homo sapiens 70-77 11095485-1 2000 In this report a new approach is introduced that allows estimation of insulin sensitivity (S(I)) from orally ingested glucose during an oral glucose tolerance test (OGTT) or a meal glucose tolerance test (MGTT) in normal subjects. Glucose 141-148 insulin Homo sapiens 70-77 11117432-6 2000 Similarly, a significant correlation of insulin concentrations with BG 60 min after glucose intake was observed in PW with T/T genotype (r=0.5, p<0.0001) and T/G genotype (r=0.24, p<0.03) but not in PW with G/G genotype (r=0.01, p=0.9). Glucose 84-91 insulin Homo sapiens 40-47 11117432-7 2000 From our data we conclude that in PW with the alanine substitution in the NBF-2 region, the insulin response of the pancreatic beta-cell after glucose intake is enhanced and does not correlate with actual BG levels. Glucose 143-150 insulin Homo sapiens 92-99 11147570-6 2000 I conclude: (I) The blood glucose decrease provoked by Amaryl can be explained by a combination of stimulation of insulin release from the pancreas and direct enhancement, as well as potentiation of the insulin response of glucose utilization in peripheral tissues only. Glucose 26-33 insulin Homo sapiens 114-121 11103847-1 2000 Insulin resistance, a reduction in the rate of glucose disposal elicited by a given insulin concentration, is present in individuals who are obese, and those with diabetes mellitus, and may develop with aging. Glucose 47-54 insulin Homo sapiens 0-7 11103847-1 2000 Insulin resistance, a reduction in the rate of glucose disposal elicited by a given insulin concentration, is present in individuals who are obese, and those with diabetes mellitus, and may develop with aging. Glucose 47-54 insulin Homo sapiens 84-91 11103847-2 2000 Methods which are utilised to measure insulin sensitivity include the hyperinsulinaemic-euglycaemic and hyperglycaemic clamps and the intravenous glucose tolerance tests. Glucose 146-153 insulin Homo sapiens 38-45 11042465-0 2000 GLUT4 and company: SNAREing roles in insulin-regulated glucose uptake. Glucose 55-62 insulin Homo sapiens 37-44 11042465-2 2000 This is accomplished through the inhibition of gluconeogenesis in the liver and the stimulation of glucose uptake into insulin-sensitive tissues, such as adipose tissue, skeletal muscle and cardiac muscle. Glucose 99-106 insulin Homo sapiens 119-126 11042465-3 2000 The ability of insulin to stimulate glucose uptake relies on a complex signaling cascade that leads to the translocation of glucose transporter protein 4 (GLUT4) from an intracellular compartment to the plasma membrane, which results in increased glucose uptake. Glucose 36-43 insulin Homo sapiens 15-22 11042465-3 2000 The ability of insulin to stimulate glucose uptake relies on a complex signaling cascade that leads to the translocation of glucose transporter protein 4 (GLUT4) from an intracellular compartment to the plasma membrane, which results in increased glucose uptake. Glucose 124-131 insulin Homo sapiens 15-22 11042465-5 2000 To design effective treatments for diabetes, there have been major efforts to understand the insulin-regulated mechanisms that govern glucose uptake. Glucose 134-141 insulin Homo sapiens 93-100 11069096-1 2000 Insulin resistance, the hallmark of non-insulin dependent diabetes mellitus, is characterized by the failure of tissues to take up and store glucose in response to insulin. Glucose 141-148 insulin Homo sapiens 0-7 11110411-2 2000 We hypothesize that insulin production regulated by both glucose and insulin may be achieved using the promoter of the glucose 6-phosphatase gene (G6Pase), the expression of which in the liver is induced by glucose and suppressed by insulin. Glucose 57-64 insulin Homo sapiens 20-27 11110411-4 2000 Glucose-stimulated as well as self-limiting insulin production was achieved in vector-transduced hepatoma cells in which expression of the insulin gene was controlled by the G6Pase promoter. Glucose 0-7 insulin Homo sapiens 139-146 11110411-5 2000 While insulin strongly inhibited the G6Pase promoter activity under low glucose conditions, its inhibitory capacity was attenuated when glucose levels were elevated. Glucose 72-79 insulin Homo sapiens 6-13 11013117-3 2000 Existing mathematical models of glucose regulation incorporate only glucose and/or insulin dynamics. Glucose 32-39 insulin Homo sapiens 83-90 11013117-4 2000 Here we develop a novel model of beta -cell mass, insulin, and glucose dynamics, which consists of a system of three nonlinear ordinary differential equations, where glucose and insulin dynamics are fast relative to beta-cell mass dynamics. Glucose 63-70 insulin Homo sapiens 178-185 11110411-5 2000 While insulin strongly inhibited the G6Pase promoter activity under low glucose conditions, its inhibitory capacity was attenuated when glucose levels were elevated. Glucose 136-143 insulin Homo sapiens 6-13 11065164-8 2000 In addition, troglitazone has potent antioxidant effect, and suppresses both L-type and receptor operated Ca2+ channel and protein kinase C. Thus since TZD class of insulin sensitizers has many kind of therapeutic effect in addition to lowering blood glucose, these agents expect to have therapeutic potential beyond diabetes. Glucose 251-258 insulin Homo sapiens 165-172 11045639-12 2000 Cell viability, and insulin production in presence of high glucose concentration, were not affected by donor age. Glucose 59-66 insulin Homo sapiens 20-27 11030756-10 2000 Conversely, among overweight patients there was a parallel increase in fasting plasma glucose (P for trend = 0.037) and fasting C-peptide according to the dosage of the D1057 allele, suggesting that higher insulin resistance and relative beta cell failure contributed to the increased risk of type 2 diabetes in overweight carriers of this allele. Glucose 86-93 insulin Homo sapiens 206-213 11033179-7 2000 When insulin was added to the perfusate, the concentration of glucose was significantly reduced, indicating that insulin diffuses across the dialysis membrane and has cellular effects that can be simultaneously recorded. Glucose 62-69 insulin Homo sapiens 5-12 11033179-7 2000 When insulin was added to the perfusate, the concentration of glucose was significantly reduced, indicating that insulin diffuses across the dialysis membrane and has cellular effects that can be simultaneously recorded. Glucose 62-69 insulin Homo sapiens 113-120 10995595-2 2000 TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. Glucose 35-42 insulin Homo sapiens 18-25 11001761-0 2000 Effects of mental stress on insulin-mediated glucose metabolism and energy expenditure in lean and obese women. Glucose 45-52 insulin Homo sapiens 28-35 11001775-1 2000 Hepatic and extrahepatic insulin sensitivity was assessed in six healthy humans from the insulin infusion required to maintain an 8 mmol/l glucose concentration during hyperglycemic pancreatic clamp with or without infusion of 16.7 micromol. Glucose 139-146 insulin Homo sapiens 89-96 11001775-6 2000 Fructose infusion increased insulin requirements 2.3-fold to maintain blood glucose. Glucose 76-83 insulin Homo sapiens 28-35 11077984-5 2000 The observations that the glucose-lowering effect of vanadium depends on the presence of endogenous insulin whereas metabolic homeostasis in control animals appears not to be affected, suggest that vanadium does not act completely independently in vivo, but augments tissue sensitivity to low levels of plasma insulin. Glucose 26-33 insulin Homo sapiens 100-107 11080610-1 2000 A reduced capacity for insulin to elicit increases in glucose uptake and metabolism in target tissues such as skeletal muscle is a common feature of obesity and diabetes. Glucose 54-61 insulin Homo sapiens 23-30 11080610-8 2000 Thus lipids can inhibit glucose disposal by causing interference with insulin signal transduction, and most likely by more than one pathway depending on the prevalent species of fatty acids. Glucose 24-31 insulin Homo sapiens 70-77 10995598-6 2000 Endogenous glucose production was completely suppressed in control subjects by the first insulin infusion (0.4 m-unit x min(-1) x kg(-1)), but was only suppressed during infusion at 1 m-unit x min(-1) x kg(-1) insulin in patients with sepsis. Glucose 11-18 insulin Homo sapiens 89-96 10995598-6 2000 Endogenous glucose production was completely suppressed in control subjects by the first insulin infusion (0.4 m-unit x min(-1) x kg(-1)), but was only suppressed during infusion at 1 m-unit x min(-1) x kg(-1) insulin in patients with sepsis. Glucose 11-18 insulin Homo sapiens 210-217 10995598-7 2000 The glucose utilization rate increased significantly with exogenous insulin infusion in control subjects, but did not increase in patients with sepsis. Glucose 4-11 insulin Homo sapiens 68-75 10995598-9 2000 In conclusion, sepsis impaired to a varying extent the action of insulin on endogenous glucose production, glucose utilization, lipolysis and ketogenesis. Glucose 87-94 insulin Homo sapiens 65-72 10995595-6 2000 Dose-response curves for glucose uptake were fitted to a quadratic function to derive C(I-150) values (concentration of insulin required to increase glucose uptake by 50%). Glucose 25-32 insulin Homo sapiens 120-127 10995598-9 2000 In conclusion, sepsis impaired to a varying extent the action of insulin on endogenous glucose production, glucose utilization, lipolysis and ketogenesis. Glucose 107-114 insulin Homo sapiens 65-72 10995598-11 2000 Suppression of endogenous glucose production and lipolysis could only be achieved with higher doses of insulin than those required in normal subjects. Glucose 26-33 insulin Homo sapiens 103-110 11110228-7 2000 Four to 8 mg/d of rosiglitazone given alone or in combination with metformin, sulfonylureas, or insulin has produced reductions in baseline fasting plasma glucose and glycosylated hemoglobin in studies of up to 1 year"s duration. Glucose 155-162 insulin Homo sapiens 96-103 10995595-6 2000 Dose-response curves for glucose uptake were fitted to a quadratic function to derive C(I-150) values (concentration of insulin required to increase glucose uptake by 50%). Glucose 149-156 insulin Homo sapiens 120-127 10995598-0 2000 Insulin sensitivity of glucose and fat metabolism in severe sepsis. Glucose 23-30 insulin Homo sapiens 0-7 11016448-0 2000 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) inhibits insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 82-89 insulin Homo sapiens 63-70 10960722-0 2000 Parallel changes of proinsulin and islet amyloid polypeptide in glucose intolerance. Glucose 64-71 insulin Homo sapiens 20-30 11016459-1 2000 Phosphatidylinositol (PI) 3-kinase is a key signaling molecule in insulin-stimulated glucose transport. Glucose 85-92 insulin Homo sapiens 66-73 11023159-0 2000 Insulin sensitivity indexes calculated from oral glucose tolerance test data. Glucose 49-56 insulin Homo sapiens 0-7 11024579-8 2000 In recent years, the data from a 75-g oral glucose tolerance test of 2121 clients showed that insulinogenic index of clients with impaired glucose tolerance was similar to that of a normal glucose tolerance group and that the area under the insulin curve (AUC) was high in younger diabetics. Glucose 43-50 insulin Homo sapiens 94-101 11024579-8 2000 In recent years, the data from a 75-g oral glucose tolerance test of 2121 clients showed that insulinogenic index of clients with impaired glucose tolerance was similar to that of a normal glucose tolerance group and that the area under the insulin curve (AUC) was high in younger diabetics. Glucose 139-146 insulin Homo sapiens 94-101 11079744-7 2000 RESULTS: Glucose-stimulated insulin secretion was increased in the high protein group (516 +/- 45 pmol/l vs 305 +/- 32, p = 0.012) due to reduced glucose threshold of the endocrine beta cells (4.2 +/- 0.5 mmol/l vs 4.9 +/- 0.3, p = 0.031). Glucose 9-16 insulin Homo sapiens 28-35 11079744-8 2000 Endogeneous glucose output was increased by 12% (p = 0.009) at 40 pmol/l plasma insulin in the high protein group, but not at higher insulin concentration whereas overall glucose disposal was reduced. Glucose 12-19 insulin Homo sapiens 80-87 11467343-5 2000 infusion of LA increases insulin-mediated glucose disposal, whereas oral administration of LA has only marginal effects. Glucose 42-49 insulin Homo sapiens 25-32 11467346-1 2000 A considerable amount of data have accumulated showing that contraction of muscle has an acute insulin-like effect, triggering the uptake of glucose. Glucose 141-148 insulin Homo sapiens 95-102 11467346-2 2000 Chronic muscle contraction, as seen in endurance training has effects on insulin sensitivity, enhancing the effect of insulin on glucose uptake. Glucose 129-136 insulin Homo sapiens 118-125 11200947-0 2000 Impairment of early insulin response after glucose load, rather than insulin resistance, is responsible for postprandial hyperglycemia seen in obese type 2 diabetes: assessment using nateglinide, a new insulin secretagogue. Glucose 43-50 insulin Homo sapiens 20-27 11200947-1 2000 The insulin secretory pattern as a phenotype of type 2 diabetes is an impairment in the rapid, pulsatile secretion of insulin in response to a rise in blood glucose after meal-intake. Glucose 157-164 insulin Homo sapiens 4-11 11200947-1 2000 The insulin secretory pattern as a phenotype of type 2 diabetes is an impairment in the rapid, pulsatile secretion of insulin in response to a rise in blood glucose after meal-intake. Glucose 157-164 insulin Homo sapiens 118-125 11200947-2 2000 The restoration of endogenous rapid insulin secretion after oral glucose load was established for the first time by using nateglinide, which is a newly developed insulin secretagogue, in obese patients with type 2 diabetes mellitus. Glucose 65-72 insulin Homo sapiens 36-43 11200947-4 2000 Therefore, the lack of rapid, pulsatile secretion of insulin in response to glycemic rise after oral glucose load, rather than insulin resistance, is responsible for postprandial glycemic response in obese type 2 diabetes patients. Glucose 101-108 insulin Homo sapiens 53-60 11083496-2 2000 We have created a liver-targeted insulin transgene by engineering glucose responsive elements into a hepatic promoter containing an inhibitory insulin response sequence. Glucose 66-73 insulin Homo sapiens 33-40 11083496-9 2000 Treatment with the insulin transgene enabled diabetic animals to reduce blood sugars following a glucose load, and to maintain blood sugar levels during a 10-h fast. Glucose 97-104 insulin Homo sapiens 19-26 11069206-9 2000 In conclusion, these data suggest that the PPARgamma2-Pro12Ala mutation is associated with better insulin sensitivity of glucose disposal and possibly, also of antilipolysis. Glucose 121-128 insulin Homo sapiens 98-105 11965833-2 2000 Insulin resistance occurs in peripheral organs (muscle and fat), leading to decreased glucose uptake and utilisation, and in liver, leading to increased hepatic glucose production. Glucose 86-93 insulin Homo sapiens 0-7 11965833-2 2000 Insulin resistance occurs in peripheral organs (muscle and fat), leading to decreased glucose uptake and utilisation, and in liver, leading to increased hepatic glucose production. Glucose 161-168 insulin Homo sapiens 0-7 11061533-6 2000 For each compartment there were significant correlations between the EC50 and the insulin sensitivity index for glucose disposal (r > 0.67; P < 0.05). Glucose 112-119 insulin Homo sapiens 82-89 11057434-0 2000 Glucose modifies the cross-talk between insulin and the beta-adrenergic signalling system in vascular smooth muscle cells. Glucose 0-7 insulin Homo sapiens 40-47 11057434-2 2000 OBJECTIVE: To investigate the role of glucose in the interaction of insulin and beta-adrenergic signalling systems in vascular smooth muscle cells (VSMC). Glucose 38-45 insulin Homo sapiens 68-75 11079812-1 2000 A high proportion of patients with depression develop glucose intolerance accompanied by hyperinsulinemia, suggestive of reduced insulin sensitivity (insulin resistance). Glucose 54-61 insulin Homo sapiens 129-136 11079812-4 2000 Metabolic indices measuring glucose effectiveness at basal insulin (SG) and insulin sensitivity (SI) were derived from minimal model analysis. Glucose 28-35 insulin Homo sapiens 59-66 11079822-4 2000 Beta-Cell function and insulin sensitivity accounted for one fourth of the variability in glucose tolerance. Glucose 90-97 insulin Homo sapiens 23-30 11079822-5 2000 Fasting plasma glucose in subjects with NGT (n = 185) was a function of both phases of insulin secretion and of insulin sensitivity (all, P < .05), whereas, in IGT subjects (n = 98), it was a function of first phase insulin secretion and insulin sensitivity (P < .01). Glucose 15-22 insulin Homo sapiens 87-94 11068099-4 2000 administration of diglycated insulin to mice alone or in combination with glucose (7 nmol/kg) resulted in a 43-61% and 11-34% reduction in glucose lowering activity, respectively, compared with native insulin. Glucose 74-81 insulin Homo sapiens 201-208 11068099-4 2000 administration of diglycated insulin to mice alone or in combination with glucose (7 nmol/kg) resulted in a 43-61% and 11-34% reduction in glucose lowering activity, respectively, compared with native insulin. Glucose 139-146 insulin Homo sapiens 29-36 11068099-5 2000 Consistent with these findings, diglycated insulin (10(-9) to 10(-7) mol/liter) was 22-38% less effective (P < 0.001) than native insulin in stimulating glucose uptake, glucose oxidation and glycogen production in isolated mouse abdominal muscle. Glucose 156-163 insulin Homo sapiens 43-50 11068099-5 2000 Consistent with these findings, diglycated insulin (10(-9) to 10(-7) mol/liter) was 22-38% less effective (P < 0.001) than native insulin in stimulating glucose uptake, glucose oxidation and glycogen production in isolated mouse abdominal muscle. Glucose 156-163 insulin Homo sapiens 133-140 11068099-5 2000 Consistent with these findings, diglycated insulin (10(-9) to 10(-7) mol/liter) was 22-38% less effective (P < 0.001) than native insulin in stimulating glucose uptake, glucose oxidation and glycogen production in isolated mouse abdominal muscle. Glucose 172-179 insulin Homo sapiens 43-50 10913151-0 2000 Glucose-stimulated insulin biosynthesis depends on insulin-stimulated insulin gene transcription. Glucose 0-7 insulin Homo sapiens 19-26 10913151-0 2000 Glucose-stimulated insulin biosynthesis depends on insulin-stimulated insulin gene transcription. Glucose 0-7 insulin Homo sapiens 51-58 10913151-0 2000 Glucose-stimulated insulin biosynthesis depends on insulin-stimulated insulin gene transcription. Glucose 0-7 insulin Homo sapiens 51-58 10913151-1 2000 Glucose stimulation of pancreatic beta-cells leads to insulin secretion as well as up-regulation of insulin biosynthesis. Glucose 0-7 insulin Homo sapiens 54-61 10913151-3 2000 Glucose-stimulated insulin gene transcription is believed to be a long term effect and should therefore not contribute to the acute elevation in pro-insulin levels. Glucose 0-7 insulin Homo sapiens 19-26 10913151-4 2000 We have recently shown that glucose activates insulin gene transcription within minutes and that secreted insulin is one of the key factors triggering this process in an autocrine manner. Glucose 28-35 insulin Homo sapiens 46-53 10913151-5 2000 We now provide evidence that 50% of the glucose-stimulated, acute pro-insulin biosynthesis within 30 min results from up-regulated insulin gene transcription. Glucose 40-47 insulin Homo sapiens 70-77 10913151-5 2000 We now provide evidence that 50% of the glucose-stimulated, acute pro-insulin biosynthesis within 30 min results from up-regulated insulin gene transcription. Glucose 40-47 insulin Homo sapiens 131-138 10913151-6 2000 Our data led us to propose that glucose elevates pro-insulin levels by stimulating both transcriptional and post-transcriptional/post-translational events to an equal extent. Glucose 32-39 insulin Homo sapiens 53-60 10913151-7 2000 Whereas the stimulatory effect on transcription is mediated by insulin secreted in response to glucose, glucose directly stimulates the post-transcriptional/post-translational processes. Glucose 95-102 insulin Homo sapiens 63-70 10966758-3 2000 We improve our earlier model for the control of glucose by insulin and glucagon by relaxing the condition necessary for it to operate. Glucose 48-55 insulin Homo sapiens 59-66 11032558-4 2000 flies in the face of the notion that insulin is involved solely in glucose storage, its conversion to fat, and weight gain. Glucose 67-74 insulin Homo sapiens 37-44 11001060-0 2000 CAP defines a second signalling pathway required for insulin-stimulated glucose transport. Glucose 72-79 insulin Homo sapiens 53-60 11001060-1 2000 Insulin stimulates the transport of glucose into fat and muscle cells. Glucose 36-43 insulin Homo sapiens 0-7 11001060-8 2000 Expression of the N-terminal domain of CAP in 3T3-L1 adipocytes blocks the stimulation of glucose transport by insulin, without affecting signalling events that depend on phosphatidylinositol-3-OH kinase. Glucose 90-97 insulin Homo sapiens 111-118 10966898-8 2000 These findings suggest that total plasma lipid peroxidation is increased in insulin-resistant individuals at an early, preclinical stage, ie, well before the development of glucose intolerance and type 2 diabetes. Glucose 173-180 insulin Homo sapiens 76-83 10950819-9 2000 Thus we hypothesize that GLUT-4 also mediates basal glucose transport in muscle fibers, possibly through constant exposure to tonal contraction and basal insulin levels. Glucose 52-59 insulin Homo sapiens 154-161 10950823-1 2000 Elevated plasma lipid and nonesterified fatty acid concentrations reduce insulin-mediated glucose disposal in skeletal muscle. Glucose 90-97 insulin Homo sapiens 73-80 10950838-7 2000 Pancreas perfusion experiments suggest that GABA generated by GAD65 may function as a negative regulator of first-phase insulin secretion in response to glucose by affecting a step proximal to or at the K(ATP)(+) channel. Glucose 153-160 insulin Homo sapiens 120-127 10996356-0 2000 The relationship between plasma glucose and insulin responses to oral glucose, LDL oxidation, and soluble intercellular adhesion molecule-1 in healthy volunteers. Glucose 32-39 insulin Homo sapiens 44-51 10996356-0 2000 The relationship between plasma glucose and insulin responses to oral glucose, LDL oxidation, and soluble intercellular adhesion molecule-1 in healthy volunteers. Glucose 70-77 insulin Homo sapiens 44-51 10996356-1 2000 This study was initiated to describe the relationships between plasma glucose and insulin responses to oral glucose and the concentrations of partially oxidized low density lipoprotein (poxLDL) and soluble intercellular adhesion molecule-1 (sICAM-1) in 23 healthy, non-diabetic volunteers. Glucose 70-77 insulin Homo sapiens 82-89 10996356-1 2000 This study was initiated to describe the relationships between plasma glucose and insulin responses to oral glucose and the concentrations of partially oxidized low density lipoprotein (poxLDL) and soluble intercellular adhesion molecule-1 (sICAM-1) in 23 healthy, non-diabetic volunteers. Glucose 108-115 insulin Homo sapiens 82-89 10996356-2 2000 Results demonstrated that plasma glucose (r=0.65, P<0.002) and insulin (r=0.58, P<0.007) responses to a 75-g oral glucose challenge were highly correlated to poxLDL concentrations. Glucose 120-127 insulin Homo sapiens 66-73 11092145-2 2000 Various conventional therapies including intravenous sodium bicarbonate, insulin with glucose and several beta-2 agonists are commonly employed as transient measures to enhance shift of potassium from the extracellular to the intracellular compartment. Glucose 86-93 insulin Homo sapiens 73-80 11122771-1 2000 The common syndrome of insulin resistance is frequently seen in obese individuals, and is characterized by glucose intolerance, dyslipidemia, high blood pressure, and an increased risk of coronary heart disease. Glucose 107-114 insulin Homo sapiens 23-30 10969839-1 2000 In response to hypoglycemia, healthy individuals rapidly antagonize insulin action on glucose and lipid metabolism, but the effects on protein metabolism are unclear. Glucose 86-93 insulin Homo sapiens 68-75 10969839-4 2000 As expected, hypoglycemia antagonized the insulin suppression of glucose production achieved in euglycemia (from 21 +/- 15 to 116 +/- 12% of basal, P < 0.001), the stimulation of glucose uptake (from 207 +/- 28 to 103 +/- 7% of basal, P < 0.01) and the suppression of circulating free fatty acids (from 30 +/- 5 to 80 +/- 17% of basal, P < 0.001). Glucose 65-72 insulin Homo sapiens 42-49 10977012-9 2000 However, when insulin lispro was used to focus on postprandial blood glucose, there was a greater impact on overall metabolic control. Glucose 69-76 insulin Homo sapiens 14-21 10977030-5 2000 The maximal glucose infusion rate after inhalation of insulin was comparable to that after subcutaneous insulin injection (9.2+/-2.6 vs. 8.8+/-2.8 mg x kg(-1) x min(-1), NS). Glucose 12-19 insulin Homo sapiens 54-61 10977053-0 2000 Assessment of insulin sensitivity and insulin secretion from the oral glucose tolerance test in nonobese Japanese type 2 diabetic patients: comparison with minimal-model approach. Glucose 70-77 insulin Homo sapiens 14-21 10977053-0 2000 Assessment of insulin sensitivity and insulin secretion from the oral glucose tolerance test in nonobese Japanese type 2 diabetic patients: comparison with minimal-model approach. Glucose 70-77 insulin Homo sapiens 38-45 10977054-0 2000 Assessment of insulin secretion from the oral glucose tolerance test in white patients with type 2 diabetes. Glucose 46-53 insulin Homo sapiens 14-21 11011218-13 2000 Although peripheral glucose uptake by insulin-dependent tissues is altered in type 2 diabetic patients, it does not appear to be the major cause of the PPHG as there are patients with insulin resistance but without post-prandial hyperglycemia. Glucose 20-27 insulin Homo sapiens 38-45 11011219-8 2000 Furthermore, the proportionally constant participation of PI to insulin secretion observed in various stages of glucose intolerance suggests that the results obtained in the past with non specific insulin radioimmunoassays remain valid. Glucose 112-119 insulin Homo sapiens 58-60 11043855-6 2000 RESULTS: Treatment with sulphonylureas and insulin resulted in similar improvements in glycaemic control (glycated haemoglobin, baseline: 11.8 [(SD 2.2)%; after sulphonylureas: 8.6 (1.2)%,p < 0.001; after insulin: 8.6 (1.2)%, p < 0.001] and in insulin sensitivity ?metabolic clearance rate of glucose, baseline: median 1.75 [interquartile (IQ) range 1.41, 2.27] ml x kg(-1) x min(-1); after sulphonylureas: 2.41 (1.82, 3.01) ml x kg(-1) x min(-1), p = 0.001; after insulin: 2.23 (1.92, 2.75) ml x kg(-1) min(-1), p = 0.027?. Glucose 299-306 insulin Homo sapiens 43-50 11043858-5 2000 RESULTS: Men with impaired glucose tolerance had more visceral adipose tissue and higher concentrations of plasma glucose and insulin in the fasting state and following a 75-g oral glucose load than men with a normal glucose tolerance. Glucose 27-34 insulin Homo sapiens 126-133 11043858-8 2000 Although men with impaired glucose tolerance still had higher fasting plasma glucose and insulin concentrations after the adjustment for visceral adipose tissue, differences in all the variables of the lipid-lipoprotein profile were eliminated. Glucose 27-34 insulin Homo sapiens 89-96 10965900-0 2000 A link between insulin resistance and hyperinsulinemia: inhibitors of phosphatidylinositol 3-kinase augment glucose-induced insulin secretion from islets of lean, but not obese, rats. Glucose 108-115 insulin Homo sapiens 15-22 10965900-3 2000 Wortmannin amplified insulin release induced by the combination of 6-8 mM glucose plus 1 microM carbachol; however, it had no effect on phorbol ester- or alpha-ketoisocaproate-induced insulin secretion. Glucose 74-81 insulin Homo sapiens 21-28 10965900-7 2000 These findings support the concept that the same biochemical process, inhibition ofphosphatidyinositol 3-kinase, that causes peripheral tissue insulin resistance enhances beta-cell sensitivity to glucose and produces a compensatory increase in insulin secretion from these cells. Glucose 196-203 insulin Homo sapiens 143-150 10973659-0 2000 Effects of laparoscopic ovarian drilling on serum vascular endothelial growth factor and on insulin responses to the oral glucose tolerance test in women with polycystic ovary syndrome. Glucose 122-129 insulin Homo sapiens 92-99 11063281-3 2000 Therefore, insulin secretagogue therapy, particularly when focused on prandial glucose regulation, is a logical approach to treatment because it addresses one of the most fundamental pathophysiological aspects of the disease. Glucose 79-86 insulin Homo sapiens 11-18 11063282-5 2000 The pathology of excessive prandial glucose excursions and continual daytime hyperglycaemia can be normalised, at least in part, if early-phase insulin availability is restored through pharmacologic intervention. Glucose 36-43 insulin Homo sapiens 144-151 11063282-7 2000 More recently, the availability of the rapid or early augmentor of insulin secretion--repaglinide--provides a means for restoring prandial glucose regulation with oral therapy. Glucose 139-146 insulin Homo sapiens 67-74 11063282-9 2000 Prandial glucose regulation with repaglinide has also been demonstrated to provide synergies when used as combination therapy with insulin sensitising agents. Glucose 9-16 insulin Homo sapiens 131-138 10983904-0 2000 Aerobic exercise training-induced reductions in abdominal fat and glucose-stimulated insulin responses in middle-aged and older men. Glucose 66-73 insulin Homo sapiens 85-92 10983904-1 2000 OBJECTIVE: To test the effects of aerobic exercise training on glucose-stimulated insulin responses in middle-aged and older individuals. Glucose 63-70 insulin Homo sapiens 82-89 10983904-12 2000 CONCLUSIONS: The decrease in glucose-stimulated insulin secretion with aerobic exercise training in middle-aged and older men appears to be mediated, at least in part, by reductions in the amount of abdominal fat. Glucose 29-36 insulin Homo sapiens 48-55 10999789-6 2000 Basal endogenous glucose production decreased from 3.2 +/- 0.2 to 2.7 +/- 0.2 mg/kg lean body mass x min (P < 0.03) despite a concomitant decline in the fasting plasma insulin concentration from 13 +/- 5 to 5 +/- 1 microU/mL (P < 0.01). Glucose 17-24 insulin Homo sapiens 171-178 10999789-8 2000 Whole body insulin-stimulated glucose disposal increased by 27% (from 5.6 +/- 0.8 to 7.1 +/- 0.8 mg/kg lean body mass x min; P < 0.01), but remained well below that observed in age- and weight-matched healthy subjects. Glucose 30-37 insulin Homo sapiens 11-18 10999809-5 2000 In contrast, insulin-stimulated forearm glucose uptake was markedly lower in acromegalic patients (2.3 +/- 0.4 mg x L(-1) x min(-1)) than in control subjects (7.9 +/- 1.3 mg x L(-1) x min(-1), P < 0.001), indicating the presence of severe insulin resistance involving glucose metabolism. Glucose 40-47 insulin Homo sapiens 13-20 10999809-5 2000 In contrast, insulin-stimulated forearm glucose uptake was markedly lower in acromegalic patients (2.3 +/- 0.4 mg x L(-1) x min(-1)) than in control subjects (7.9 +/- 1.3 mg x L(-1) x min(-1), P < 0.001), indicating the presence of severe insulin resistance involving glucose metabolism. Glucose 271-278 insulin Homo sapiens 13-20 10999821-8 2000 Insulin-stimulated glucose uptake increased by 41% (P < 0.01), which was accounted for by a significant increase in nonoxidative glucose disposal (P = 0.003). Glucose 19-26 insulin Homo sapiens 0-7 10999821-8 2000 Insulin-stimulated glucose uptake increased by 41% (P < 0.01), which was accounted for by a significant increase in nonoxidative glucose disposal (P = 0.003). Glucose 132-139 insulin Homo sapiens 0-7 11132581-8 2000 Significant differences in mean postprandial plasma glucose levels were found between the no-treatment and insulin groups on days 1 and 2. Glucose 52-59 insulin Homo sapiens 107-114 11031747-10 2000 Nateglinide is a highly physiologic mealtime glucose regulator, which rapidly increases insulin secretion when taken before meals, mimicking early-phase insulin release lost in patients with Type 2 diabetes. Glucose 45-52 insulin Homo sapiens 88-95 15016224-10 2000 The higher 3 am blood glucose levels in those on insulin lispro could translate to reduced nocturnal hypoglycaemia in some individuals. Glucose 22-29 insulin Homo sapiens 49-56 11087036-8 2000 CONCLUSIONS: Delivery of the insulin gene promoter via rAAV was shown in this study to result in glucose-dependent control of the reporter gene expression. Glucose 97-104 insulin Homo sapiens 29-36 10944108-7 2000 As predicted from this altered gene expression profile, HNF1 alpha-P291fsinsC also inhibits insulin secretory responses to glucose and leucine, correlated with impaired nutrient-evoked mitochondrial ATP production and mitochondrial membrane hyperpolarization. Glucose 123-130 insulin Homo sapiens 92-99 10949203-6 2000 A low insulin response after glucagon was associated with significantly lower 120-min glucose concentrations (P=0.043) and a lower integrated incremental insulin response after oral glucose (P=0.006). Glucose 86-93 insulin Homo sapiens 6-13 10949203-6 2000 A low insulin response after glucagon was associated with significantly lower 120-min glucose concentrations (P=0.043) and a lower integrated incremental insulin response after oral glucose (P=0.006). Glucose 182-189 insulin Homo sapiens 6-13 10949203-7 2000 CONCLUSIONS: In pancreas-kidney transplant recipients, a low insulin response after intravenous glucagon predicts a reduced insulin response after oral glucose and an impaired oral glucose tolerance. Glucose 152-159 insulin Homo sapiens 61-68 10949203-7 2000 CONCLUSIONS: In pancreas-kidney transplant recipients, a low insulin response after intravenous glucagon predicts a reduced insulin response after oral glucose and an impaired oral glucose tolerance. Glucose 152-159 insulin Homo sapiens 124-131 10801824-2 2000 Insulin regulates glucose metabolism in adipocytes via a phosphatidylinositide 3-kinase (PI3K)-dependent pathway that appears to involve protein phosphorylation. Glucose 18-25 insulin Homo sapiens 0-7 10801824-3 2000 However, the generation of phosphoinositides is not sufficient for insulin action, and it has been suggested that insulin regulation of glucose metabolism may involve both PI3K-dependent and -independent pathways, the latter being insulin specific. Glucose 136-143 insulin Homo sapiens 114-121 10801824-3 2000 However, the generation of phosphoinositides is not sufficient for insulin action, and it has been suggested that insulin regulation of glucose metabolism may involve both PI3K-dependent and -independent pathways, the latter being insulin specific. Glucose 136-143 insulin Homo sapiens 114-121 10913038-0 2000 Effect of training on insulin sensitivity of glucose uptake and lipolysis in human adipose tissue. Glucose 45-52 insulin Homo sapiens 22-29 10913038-9 2000 In conclusion, training enhances insulin sensitivity of glucose uptake in subcutaneous adipose tissue and in skeletal muscle. Glucose 56-63 insulin Homo sapiens 33-40 10945722-3 2000 Thiazolidinediones, which are recently introduced insulin sensitizing agents, have been shown to be effective not only in reducing elevated glucose levels, but also in improving the other metabolic abnormalities that are associated with insulin resistance. Glucose 140-147 insulin Homo sapiens 50-57 10923634-7 2000 During glucose entrainment, spectral density peaks (SP) and autocorrelation coefficients (AC) increased significantly (P < 0.001), and ApEn decreased (P < 0.01), indicating more regular insulin time-series in the healthy volunteers. Glucose 7-14 insulin Homo sapiens 192-199 10923634-9 2000 Furthermore, in spite of identical absolute glucose excursions (approximately 0.3 mmol/l) glucose pulse entrainment led to a complete (SP: 4.76 +/- 0.62 [range 2.08-7.60] vs. 17.24 +/- 0.93 [11.70-20.58], P < 0.001; AC: 0.01 +/- 0.05 [0.33-0.24] vs. 0.64 +/- 0.05 [0.35-0.83], P < 0.001) or almost complete (ApEn: 1.59 +/- 0.02 [1.48-1.67] vs. 1.42 +/- 0.05 [1.26-1.74], P < 0.005) separation of the insulin time-series in diabetic and control subjects. Glucose 90-97 insulin Homo sapiens 409-416 10937511-9 2000 RESULTS: At study end point, insulin glargine-pooled groups had significantly lower fasting plasma glucose (FPG) levels than the NPH insulin group, with adjusted mean FPG levels reduced by 2.2 mmol/l (P = 0.0001). Glucose 99-106 insulin Homo sapiens 29-36 10937511-16 2000 CONCLUSIONS: Basal insulin glargine administered once daily for 4 weeks as part of a basal-bolus multiple daily insulin regimen was safe and more effective in lowering fasting plasma glucose levels than NPH in patients with type 1 diabetes. Glucose 183-190 insulin Homo sapiens 19-26 10937514-16 2000 The bromocriptine-induced improvement in glycemic control is associated with enhanced maximally stimulated insulin-mediated glucose disposal. Glucose 124-131 insulin Homo sapiens 107-114 10937517-3 2000 RESULTS: Thalidomide reduced insulin-stimulated glucose uptake by 31% (from 27.7 to 19.2 pmol x kg(-1) x min(-1), P < 0.05) compared with the prestudy and by 21% (from 24.2 to 19.2 pmol x kg(-1) x min(-1), P < 0.05) compared with placebo. Glucose 48-55 insulin Homo sapiens 29-36 10990074-9 2000 Poor fetal followed by higher postnatal growth results in low beta-cell numbers and reduced whole-body glucose uptake which leads to reduced efficiency in the processing of proinsulin. Glucose 103-110 insulin Homo sapiens 173-183 10990079-0 2000 Glucagon receptors on human islet cells contribute to glucose competence of insulin release. Glucose 54-61 insulin Homo sapiens 76-83 10990079-1 2000 AIMS/HYPOTHESIS: Synergism between glucose and cAMP in the stimulation of insulin secretion has been suggested to regulate beta cells. Glucose 35-42 insulin Homo sapiens 74-81 10990079-2 2000 This study assessed the importance of an interaction between glucose and cAMP in the stimulation of insulin secretion from human islet cells by investigating expression and functional activity of receptors recognising glucagon, glucagon-like peptide-1 (7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Glucose 61-68 insulin Homo sapiens 100-107 11075718-3 2000 In these optimal conditions the stimulatory effect of 1,25-dihydroxyvitamin D3 was accompanied by increases in both IR capacity, and insulin responsiveness for glucose transport in these cells. Glucose 160-167 insulin Homo sapiens 133-140 11075718-5 2000 These results provide evidence of 1,25-dihydroxyvitamin D3 acting as genomic stimulator of the insulin response in the control of glucose transport. Glucose 130-137 insulin Homo sapiens 95-102 10952826-18 2000 Diabetes mellitus and hyperglycaemia or hyperlinsulinaemia in non-diabetic patients were related to worse symptomatic status but not worsening left ventricular ejection fraction compared to patients with normal glucose and insulin levels. Glucose 211-218 insulin Homo sapiens 46-53 11016448-6 2000 The effects of AICAR on insulin-stimulated glucose transport are not mediated by either adenosine receptors or nitric oxide synthase and are mediated downstream of phosphatidylinositol 3"-kinase stimulation. Glucose 43-50 insulin Homo sapiens 24-31 11016448-7 2000 We propose that in contrast to skeletal muscle, in which AMPK stimulation promotes glucose transport to provide ATP as a fuel, AMPK stimulation inhibits insulin-stimulated glucose transport in adipocytes, inhibiting triacylglycerol synthesis, to conserve ATP under conditions of cellular stress. Glucose 172-179 insulin Homo sapiens 153-160 11016454-0 2000 Dexamethasone-induced insulin resistance in 3T3-L1 adipocytes is due to inhibition of glucose transport rather than insulin signal transduction. Glucose 86-93 insulin Homo sapiens 22-29 11016454-2 2000 In this study, we investigated the mechanism of glucocorticoid-induced insulin resistance using 3T3-L1 adipocytes in which treatment with dexamethasone has been shown to impair the insulin-induced increase in glucose uptake. Glucose 209-216 insulin Homo sapiens 181-188 11016454-4 2000 On the other hand, dexamethasone treatment did not alter the amount of GLUT4 protein in total cell lysates but decreased the insulin-stimulated GLUT4 translocation to the plasma membrane, which possibly caused decreased insulin-stimulated glucose uptake. Glucose 239-246 insulin Homo sapiens 125-132 11016454-4 2000 On the other hand, dexamethasone treatment did not alter the amount of GLUT4 protein in total cell lysates but decreased the insulin-stimulated GLUT4 translocation to the plasma membrane, which possibly caused decreased insulin-stimulated glucose uptake. Glucose 239-246 insulin Homo sapiens 220-227 11079745-7 2000 Although inversely related to one another (r = -0.41, p < 0.0001), peripheral insulin sensitivity and fasting plasma insulin were both independently associated with endogenous glucose output in an inverse fashion (with partial r"s of 0.19 and 0.21, respectively, after adjusting for lean body mass and centre, p < 0.0001 for both). Glucose 179-186 insulin Homo sapiens 81-88 11079745-7 2000 Although inversely related to one another (r = -0.41, p < 0.0001), peripheral insulin sensitivity and fasting plasma insulin were both independently associated with endogenous glucose output in an inverse fashion (with partial r"s of 0.19 and 0.21, respectively, after adjusting for lean body mass and centre, p < 0.0001 for both). Glucose 179-186 insulin Homo sapiens 120-127 11079745-9 2000 Independently of the amount of lean mass, peripheral insulin resistance is associated with a higher endogenous glucose output independently of fasting plasma insulin concentration, suggesting coupled regulation of insulin action in peripheral tissues and the liver. Glucose 111-118 insulin Homo sapiens 53-60 11079746-0 2000 Long-term insulin treatment of 3T3-L1 adipocytes results in mis-targeting of GLUT4: implications for insulin-stimulated glucose transport. Glucose 120-127 insulin Homo sapiens 10-17 11079746-0 2000 Long-term insulin treatment of 3T3-L1 adipocytes results in mis-targeting of GLUT4: implications for insulin-stimulated glucose transport. Glucose 120-127 insulin Homo sapiens 101-108 11079746-1 2000 AIMS/HYPOTHESIS: Insulin stimulates glucose transport in adipose and muscle tissue by the translocation of a specialised pool of intracellular GLUT4-containing vesicles to the cell surface. Glucose 36-43 insulin Homo sapiens 17-24 11029601-6 2000 Fasting serum insulin levels and insulin response (area under the curve) after oral glucose load were significantly reduced by 26.8% and 18.7%, respectively, indicating an improvement of insulin sensitivity. Glucose 84-91 insulin Homo sapiens 14-21 11029601-6 2000 Fasting serum insulin levels and insulin response (area under the curve) after oral glucose load were significantly reduced by 26.8% and 18.7%, respectively, indicating an improvement of insulin sensitivity. Glucose 84-91 insulin Homo sapiens 33-40 11029601-6 2000 Fasting serum insulin levels and insulin response (area under the curve) after oral glucose load were significantly reduced by 26.8% and 18.7%, respectively, indicating an improvement of insulin sensitivity. Glucose 84-91 insulin Homo sapiens 33-40 11109972-2 2000 Insulin sensitivity was assessed by continuous infusion of glucose with model assessment test (CIGMA). Glucose 59-66 insulin Homo sapiens 0-7 11126262-6 2000 The incidence of both glucose intolerance requiring insulin (0 % vs. 18 %, P = 0.006) and cystic periventricular leukomalacia (2 % vs. 18%, P = 0.03) was lower among methylprednisolone-treated infants. Glucose 22-29 insulin Homo sapiens 52-59 11018080-5 2000 However, Pima Indians with normal glucose tolerance, who have a G/G genotype at UCSNP-43, were found to have decreased rates of postabsorptive and insulin-stimulated glucose turnover that appear to result from decreased rates of glucose oxidation. Glucose 166-173 insulin Homo sapiens 147-154 11061548-5 2000 Glycemic levels after an oral glucose tolerance test showed a diabetic profile at 1 yr, a normal profile at 2 yr, and an impaired glucose tolerance profile at 3 yr. Intravenous glucose tolerance test-induced first phase insulin release, present at 1 and 2 yr, disappeared at 3 yr. Diabetes-related autoantibodies (islet cell antibodies, glutamic acid decarboxylase antibodies, and tyrosine phosphatase-like protein antibodies) were undetectable before transplantation and remained so during the entire follow-up. Glucose 30-37 insulin Homo sapiens 220-227 11061548-5 2000 Glycemic levels after an oral glucose tolerance test showed a diabetic profile at 1 yr, a normal profile at 2 yr, and an impaired glucose tolerance profile at 3 yr. Intravenous glucose tolerance test-induced first phase insulin release, present at 1 and 2 yr, disappeared at 3 yr. Diabetes-related autoantibodies (islet cell antibodies, glutamic acid decarboxylase antibodies, and tyrosine phosphatase-like protein antibodies) were undetectable before transplantation and remained so during the entire follow-up. Glucose 130-137 insulin Homo sapiens 220-227 11057434-5 2000 RESULTS: In the presence of low glucose concentrations (5 mmol/l), insulin enhanced isoproterenol-, forskolin- and cholera toxin-stimulated adenylyl cyclase activities. Glucose 32-39 insulin Homo sapiens 67-74 11057434-7 2000 In contrast, in the presence of high glucose concentrations (25 mmol/l), insulin attenuated isoproterenol-stimulated activity but not cholera toxin- or forskolin-stimulated activity. Glucose 37-44 insulin Homo sapiens 73-80 11057434-8 2000 Insulin-stimulated activities of IRS-1 and PI3-K, but not MAPK activity, were also attenuated in the presence of high concentrations of glucose. Glucose 136-143 insulin Homo sapiens 0-7 11057434-11 2000 CONCLUSIONS: In the presence of low glucose concentrations, insulin stimulates the beta-adrenergic signalling system through the IRS-1/PI3-K pathway. Glucose 36-43 insulin Homo sapiens 60-67 11057434-12 2000 However, in the presence of high glucose concentrations, the effect of insulin is switched to an inhibitory one, through the MAPK pathway. Glucose 33-40 insulin Homo sapiens 71-78 11057434-13 2000 Our finding suggests that high glucose concentrations modify the cross-talk between insulin and the beta-adrenergic signalling systems in VSMC. Glucose 31-38 insulin Homo sapiens 84-91 11039477-7 2000 Insulin significantly enhanced glucose utilization of pancreatic cancer cells before it enhanced cell proliferation. Glucose 31-38 insulin Homo sapiens 0-7 11039477-8 2000 The MAPK kinase inhibitor PD 098059 abolished insulin-stimulated DNA synthesis and partially reduced insulin-stimulated glucose uptake. Glucose 120-127 insulin Homo sapiens 101-108 11039477-9 2000 In contrast, the PI3 kinase inhibitor wortmannin substantially inhibited insulin-induced glucose uptake and partially blocked thymidine incorporation. Glucose 89-96 insulin Homo sapiens 73-80 11039477-10 2000 Furthermore, after 24-hour treatment with insulin, GLUT-I expression in pancreatic cancer cells was markedly increased, indicating that insulin enhances glucose utilization partly through increasing glucose transport. Glucose 153-160 insulin Homo sapiens 42-49 11039477-10 2000 Furthermore, after 24-hour treatment with insulin, GLUT-I expression in pancreatic cancer cells was markedly increased, indicating that insulin enhances glucose utilization partly through increasing glucose transport. Glucose 153-160 insulin Homo sapiens 136-143 11039477-10 2000 Furthermore, after 24-hour treatment with insulin, GLUT-I expression in pancreatic cancer cells was markedly increased, indicating that insulin enhances glucose utilization partly through increasing glucose transport. Glucose 199-206 insulin Homo sapiens 42-49 11039477-10 2000 Furthermore, after 24-hour treatment with insulin, GLUT-I expression in pancreatic cancer cells was markedly increased, indicating that insulin enhances glucose utilization partly through increasing glucose transport. Glucose 199-206 insulin Homo sapiens 136-143 11039477-11 2000 These findings suggest that insulin stimulates proliferation and glucose utilization in pancreatic cancer cells by two distinct pathways. Glucose 65-72 insulin Homo sapiens 28-35 11039477-12 2000 Insulin augments DNA synthesis mainly by MAP kinase activation and glucose uptake mainly by PI3 kinase activation and enhancement of GLUT-I expression. Glucose 67-74 insulin Homo sapiens 0-7 11107928-1 2000 Insulin secretion is finely tuned to tissue requirements by tight links to prevailing blood glucose levels. Glucose 92-99 insulin Homo sapiens 0-7 11027500-5 2000 In conclusion, insulin appears to induce an early inhibition of leptin secretion by the adipose cell, followed later by a stimulatory effect secondary to the metabolic changes triggered by the insulin-induced increase in glucose uptake. Glucose 221-228 insulin Homo sapiens 15-22 11027500-5 2000 In conclusion, insulin appears to induce an early inhibition of leptin secretion by the adipose cell, followed later by a stimulatory effect secondary to the metabolic changes triggered by the insulin-induced increase in glucose uptake. Glucose 221-228 insulin Homo sapiens 193-200 10966898-2 2000 OBJECTIVE: The goal of this study was to define the relation between resistance to insulin-mediated glucose disposal and plasma concentrations of lipid hydroperoxides and liposoluble antioxidant vitamins in healthy volunteers. Glucose 100-107 insulin Homo sapiens 83-90 10966898-3 2000 DESIGN: Insulin-mediated glucose disposal was determined in 36 healthy, nondiabetic volunteers by measuring their steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a 180-min constant infusion of octreotide, insulin, and glucose. Glucose 25-32 insulin Homo sapiens 8-15 10966898-3 2000 DESIGN: Insulin-mediated glucose disposal was determined in 36 healthy, nondiabetic volunteers by measuring their steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a 180-min constant infusion of octreotide, insulin, and glucose. Glucose 153-160 insulin Homo sapiens 8-15 10966898-3 2000 DESIGN: Insulin-mediated glucose disposal was determined in 36 healthy, nondiabetic volunteers by measuring their steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a 180-min constant infusion of octreotide, insulin, and glucose. Glucose 153-160 insulin Homo sapiens 8-15 10966898-7 2000 CONCLUSIONS: Variations in insulin-mediated glucose disposal in healthy individuals are significantly related to plasma concentrations of lipid hydroperoxides and liposoluble antioxidant vitamins. Glucose 44-51 insulin Homo sapiens 27-34 10937504-3 2000 Area under the insulin response curve (AUC insulin) during an oral glucose tolerance test was used to reflect plasma insulin levels. Glucose 67-74 insulin Homo sapiens 15-22 10937510-0 2000 Less nocturnal hypoglycemia and better post-dinner glucose control with bedtime insulin glargine compared with bedtime NPH insulin during insulin combination therapy in type 2 diabetes. Glucose 51-58 insulin Homo sapiens 80-87 10937510-11 2000 CONCLUSIONS: Use of insulin glargine compared with NPH is associated with less nocturnal hypoglycemia and lower post-dinner glucose levels. Glucose 124-131 insulin Homo sapiens 20-27 10937510-13 2000 Achievement of acceptable average glucose control requires titration of the insulin dose to an FBG target < or =6.7 mmol/l. Glucose 34-41 insulin Homo sapiens 76-83 10963820-6 2000 Administration of IFN was stopped and insulin treatment was started, but plasma glucose level was not controlled well. Glucose 80-87 insulin Homo sapiens 38-45 10963823-5 2000 The time to the minimal level of glucose after insulin aspart was significantly shorter compared with human insulin (P<0.05 for 0.025 U/kg BW and P<0.01 for 0.05 U/kg BW). Glucose 33-40 insulin Homo sapiens 47-54 10963823-6 2000 The Delta change in blood glucose induced by insulin aspart was larger than that observed for human insulin at any dose (P<0.001). Glucose 26-33 insulin Homo sapiens 45-52 10990079-4 2000 Functional activity of these receptors was assessed by the effects of peptides (agonists and antagonists) on glucose-induced insulin release. Glucose 109-116 insulin Homo sapiens 125-132 10990079-6 2000 Glucose (10 mmol/l) stimulated insulin release 4.5 +/- 0.6-fold over basal (2.5 mmol/l). Glucose 0-7 insulin Homo sapiens 31-38 10990079-9 2000 The glucagon-receptor antagonist also suppressed the potentiation of glucose-induced insulin release by addition of 10 nmol/l glucagon. Glucose 69-76 insulin Homo sapiens 85-92 11073183-9 2000 CONCLUSIONS: In conclusion, the offspring of Type 2 diabetic patients with normal glucose tolerance display an increased insulin secretion; however, they are not resistant to the haemodynamic effects of insulin, as suggested by the reduction of diastolic blood pressure. Glucose 82-89 insulin Homo sapiens 121-128 11009049-8 2000 CONCLUSIONS: The improved absorption properties of soluble insulin aspart in its premixed formulation provide a basis for a more efficient meal-related glucose control and immediate pre-meal delivery when compared with a similar human premixed insulin in the treatment of diabetes mellitus. Glucose 152-159 insulin Homo sapiens 59-66 10948084-3 2000 In the presence of 1 nmol/L of insulin, 1 micromol/L of enalaprilat enhanced insulin-induced glucose uptake from 89.2+/-8. Glucose 93-100 insulin Homo sapiens 31-38 10948084-3 2000 In the presence of 1 nmol/L of insulin, 1 micromol/L of enalaprilat enhanced insulin-induced glucose uptake from 89.2+/-8. Glucose 93-100 insulin Homo sapiens 77-84 10948084-6 2000 In the presence of 1 nmol/L of insulin, exposure to 10 micromol/L BK stimulated glucose uptake from 89.2+/-8.1 to 171.6+/-10.1 pmol/h per mg protein. Glucose 80-87 insulin Homo sapiens 31-38 10948084-12 2000 Angiotensin-converting enzyme inhibitors enhanced insulin-induced glucose uptake via the BK B2 receptor. Glucose 66-73 insulin Homo sapiens 50-57 10930434-0 2000 Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. Glucose 84-91 insulin Homo sapiens 21-28 10946879-18 2000 Fasting insulin significantly decreased in both PCOS women and controls, regardless of treatment, whereas glucose-stimulated insulin significantly decreased only in PCOS women and controls treated with metformin. Glucose 106-113 insulin Homo sapiens 125-132 10954026-13 2000 In a multiple regression model controlling for the BMI in the female subgroup, circulating insulin and glucose concentrations 2 hours after the 75-g glucose load were good predictors of fasting plasma leptin (r = +.38, P = .02 and r = -.70, P < .001, respectively). Glucose 149-156 insulin Homo sapiens 91-98 10896818-5 2000 It appears that insulin causes increased availability of glucose and energy-producing substrates. Glucose 57-64 insulin Homo sapiens 16-23 10954010-4 2000 The quartile with the greatest insulin response also had a significantly higher plasma glucose response to oral glucose, faster heart rate, higher blood pressure, and the combination of higher triglyceride and lower high-density lipoprotein (HDL) cholesterol concentrations. Glucose 87-94 insulin Homo sapiens 31-38 10997652-9 2000 Based on in vitro studies, the effect of insulin to stimulate leptin production appears to involve increased glucose metabolism. Glucose 109-116 insulin Homo sapiens 41-48 10954010-4 2000 The quartile with the greatest insulin response also had a significantly higher plasma glucose response to oral glucose, faster heart rate, higher blood pressure, and the combination of higher triglyceride and lower high-density lipoprotein (HDL) cholesterol concentrations. Glucose 112-119 insulin Homo sapiens 31-38 10954011-10 2000 The insulin responsiveness of glucose uptake was abolished by antisense ODN treatment. Glucose 30-37 insulin Homo sapiens 4-11 11055555-6 2000 Addition of 30 mM glucose caused a decrease in phosphorylase "a" activity in the absence of insulin and this effect was additive with insulin up to 10 nM concentration. Glucose 18-25 insulin Homo sapiens 92-99 11055555-6 2000 Addition of 30 mM glucose caused a decrease in phosphorylase "a" activity in the absence of insulin and this effect was additive with insulin up to 10 nM concentration. Glucose 18-25 insulin Homo sapiens 134-141 10997652-12 2000 Alterations in insulin-mediated glucose metabolism in adipose tissue are likely to mediate the effects of energy restriction to decrease, and refeeding to increase, circulating leptin levels. Glucose 32-39 insulin Homo sapiens 15-22 11003253-1 2000 UNLABELLED: Our objective was to investigate the usefulness of human ultralente insulin as basal substitution overnight in patients with Type 1 diabetes treated with multiple insulin injection therapy by evaluating the free insulin and glucose profiles, the day-to-day variability and the impact of the time of injection. Glucose 236-243 insulin Homo sapiens 80-87 10966860-3 2000 Metabolic signals derived from glucose can also stimulate insulin release independent of their effects on ATP-sensitive K(+)-channels. Glucose 31-38 insulin Homo sapiens 58-65 11789189-4 2000 RESULTS: After treatment for three months with metformin or TGF, fasting and the integrated insulin response to the glucose load decreased. Glucose 116-123 insulin Homo sapiens 92-99 11208153-6 2000 BFA increased the half time of reversal of insulin-stimulated glucose transport from 17 to 30 min but did not prevent complete reversal. Glucose 62-69 insulin Homo sapiens 43-50 11208153-7 2000 Furthermore, following reversal restimulation of glucose transport activity by insulin was not compromised. Glucose 49-56 insulin Homo sapiens 79-86 10916505-1 2000 When oral agents alone can no longer provide adequate glycemic control, the combination of a single bedtime injection of insulin with two daily doses of metformin will often normalize blood glucoses levels without the weight gain and hypoglycemia that may occur with other combined regimens. Glucose 190-198 insulin Homo sapiens 121-128 10911003-6 2000 However, plasma insulin concentrations, at fasting and 30, 60, and 120 min following a 75 g glucose load, were significantly higher in the group with high blood TCDD levels. Glucose 92-99 insulin Homo sapiens 16-23 10873662-2 2000 Transfection of human insulin vector resulted in a transient decrease in serum glucose in streptozotocin (SZT)-induced diabetic mice, accompanied by the detection of human insulin in the liver and spleen. Glucose 79-86 insulin Homo sapiens 22-29 10891367-7 2000 The present work describes the development and comparison of two methods for inducing insulin resistance, by treating 3T3-L1 adipocytes overnight using either 25 mM glucose/5 nM insulin or 2 mM glucosamine. Glucose 165-172 insulin Homo sapiens 86-93 10891367-9 2000 Insulin-stimulated 2-deoxyglucose uptake, however, was reduced by approximately 45% in response to both high glucose/insulin and glucosamine treatment, relative to control cells. Glucose 26-33 insulin Homo sapiens 0-7 10891367-9 2000 Insulin-stimulated 2-deoxyglucose uptake, however, was reduced by approximately 45% in response to both high glucose/insulin and glucosamine treatment, relative to control cells. Glucose 26-33 insulin Homo sapiens 117-124 10891367-16 2000 Thus, 3T3-L1 adipocytes can be used as a model system for studying insulin resistance induced by increased influx of glucose. Glucose 117-124 insulin Homo sapiens 67-74 10806189-3 2000 We demonstrate that the HIV protease inhibitor, indinavir, dramatically inhibits insulin-stimulated glucose uptake in 3T3-L1 adipocytes in a dose-dependent manner (63% inhibition observed with 100 micrometer indinavir). Glucose 100-107 insulin Homo sapiens 81-88 10880413-6 2000 Insulin sensitivity (S(I)) was measured by a frequently sampled intravenous glucose tolerance test, and CRP was measured by a highly sensitive competitive immunoassay. Glucose 76-83 insulin Homo sapiens 0-7 10764799-1 2000 The effects of a high concentration of glucose on the insulin receptor-down signaling were investigated in human hepatoma (HepG2) cells in vitro to delineate the molecular mechanism of insulin resistance under glucose toxicity. Glucose 39-46 insulin Homo sapiens 54-61 10764799-4 2000 The high glucose treatment attenuated insulin-induced association of IRS-1 and phosphatidylinositol 3-kinase and insulin-stimulated phosphorylation of Akt. Glucose 9-16 insulin Homo sapiens 38-45 10764799-4 2000 The high glucose treatment attenuated insulin-induced association of IRS-1 and phosphatidylinositol 3-kinase and insulin-stimulated phosphorylation of Akt. Glucose 9-16 insulin Homo sapiens 113-120 10764799-9 2000 We conclude that a high concentration of glucose causes phosphorylation of IRS-1, leading to selective attenuation of metabolic signaling of insulin. Glucose 41-48 insulin Homo sapiens 141-148 10873662-3 2000 In accordance with the decreased glucose, plasma immunoreactive insulin could be detected up to 14 days after a single transfection in mice transfected with insulin vector. Glucose 33-40 insulin Homo sapiens 64-71 10893317-7 2000 The stimulatory action of insulin was mitigated by high-glucose concentration and abolished by cotreatment of cells with glucagon. Glucose 56-63 insulin Homo sapiens 26-33 10894818-2 2000 Therefore, in this study, the relationship of the G-250A promoter variant of the HL gene to the rates of insulin-stimulated glucose uptake measured by the hyperinsulinemic euglycemic clamp was investigated in 110 control subjects (82 men and 28 women, aged 50.7+/-7.6 [mean+/-SD] years, body mass index 26. Glucose 124-131 insulin Homo sapiens 105-112 10894818-4 2000 The A-250 allele of the HL promoter was associated with low rates of insulin-stimulated whole-body nonoxidative glucose disposal in control subjects (41.1+/-12.7 micromol. Glucose 112-119 insulin Homo sapiens 69-76 10893341-10 2000 In summary, the physiological stress associated with muscle damage impairs insulin stimulation of IRS-1, PI 3-kinase, and Akt-kinase, presumably leading to decreased insulin-mediated glucose uptake. Glucose 183-190 insulin Homo sapiens 75-82 10894818-10 2000 min(-1) in subjects with the A-250A genotype; P=0.012 adjusted for age and sex) and with low rates of insulin-stimulated whole-body glucose oxidation in FCHL family members (16.7+/-4.2 versus 15.0+/-4. Glucose 132-139 insulin Homo sapiens 102-109 10873662-3 2000 In accordance with the decreased glucose, plasma immunoreactive insulin could be detected up to 14 days after a single transfection in mice transfected with insulin vector. Glucose 33-40 insulin Homo sapiens 157-164 10873662-4 2000 Repeated intravenous injection of human insulin vector every week resulted in a sustained decrease in serum glucose over a 4-week period, accompanied by the detection of C-peptide fragments and a significant decrease in BUN and creatinine. Glucose 108-115 insulin Homo sapiens 40-47 10909962-2 2000 We determined whether a high rate of insulin-stimulated glucose uptake (good insulin sensitivity) is associated with an enhanced ability of exercise to increase glucose uptake in vivo in humans. Glucose 161-168 insulin Homo sapiens 37-44 10939754-14 2000 Patients with an initial plasma glucose of 5.5 mmol/l (100 mg/dl) or less who are hemodialyzed and who do not eat during dialysis may be particularly at risk, especially if they are on insulin or taking glucose-lowering medication. Glucose 32-39 insulin Homo sapiens 185-192 10909962-7 2000 The exercise-induced increase in glucose uptake was due to marked increases in blood flow (36 +/- 5 ml x kg(-1) muscle x min(-1) [insulin] vs. 262 +/- 20 ml x kg(-1) muscle x min(-1) [insulin and exercise], P < 0.001) rather than glucose extraction, which decreased from 2.0 +/- 0.2 mmol/l (insulin) to 1.0 +/- 0.1 mmol/1 (insulin and exercise) (P < 0.001). Glucose 33-40 insulin Homo sapiens 130-137 10909962-0 2000 Enhanced stimulation of glucose uptake by insulin increases exercise-stimulated glucose uptake in skeletal muscle in humans: studies using [15O]O2, [15O]H2O, [18F]fluoro-deoxy-glucose, and positron emission tomography. Glucose 24-31 insulin Homo sapiens 42-49 10909962-0 2000 Enhanced stimulation of glucose uptake by insulin increases exercise-stimulated glucose uptake in skeletal muscle in humans: studies using [15O]O2, [15O]H2O, [18F]fluoro-deoxy-glucose, and positron emission tomography. Glucose 80-87 insulin Homo sapiens 42-49 10909962-1 2000 In vitro studies have shown that insulin and exercise stimulate glucose uptake in part via distinct mechanisms. Glucose 64-71 insulin Homo sapiens 33-40 10909962-2 2000 We determined whether a high rate of insulin-stimulated glucose uptake (good insulin sensitivity) is associated with an enhanced ability of exercise to increase glucose uptake in vivo in humans. Glucose 56-63 insulin Homo sapiens 37-44 10909962-2 2000 We determined whether a high rate of insulin-stimulated glucose uptake (good insulin sensitivity) is associated with an enhanced ability of exercise to increase glucose uptake in vivo in humans. Glucose 56-63 insulin Homo sapiens 77-84 10909980-5 2000 In conclusion, in insulin-resistant relatives of DM2 patients, whole-body glucose-mediated glucose disposal is increased by GE enhancement of the muscle nonoxidative glucose pathway and by GE enhancement of the suppression of HGP. Glucose 91-98 insulin Homo sapiens 18-25 10909980-5 2000 In conclusion, in insulin-resistant relatives of DM2 patients, whole-body glucose-mediated glucose disposal is increased by GE enhancement of the muscle nonoxidative glucose pathway and by GE enhancement of the suppression of HGP. Glucose 91-98 insulin Homo sapiens 18-25 10909983-1 2000 The effect and time course of free fatty acid (FFA) elevation on insulin-mediated vasodilation (IMV) and the relationship of FFA elevation to changes in insulin-mediated glucose uptake was studied. Glucose 170-177 insulin Homo sapiens 153-160 10909980-5 2000 In conclusion, in insulin-resistant relatives of DM2 patients, whole-body glucose-mediated glucose disposal is increased by GE enhancement of the muscle nonoxidative glucose pathway and by GE enhancement of the suppression of HGP. Glucose 74-81 insulin Homo sapiens 18-25 10909971-6 2000 Furthermore, when transfected into rat primary cultured islets, ATF-2 enhanced glucose-induced insulin promoter activity, whereas cAMP response element-binding protein (CREB) repressed it. Glucose 79-86 insulin Homo sapiens 95-102 10909975-2 2000 Insulin stimulation of glucose uptake and glycogen synthesis was maximal in myoblasts. Glucose 23-30 insulin Homo sapiens 0-7 10909975-3 2000 Insulin-stimulated glucose uptake (fold-stimulation over basal uptake) was decreased in relative compared with control myoblasts at 0.001 micromol/l (0.93 +/- 0.05 [mean +/- SE] vs. 1.15 +/- 0.06, P < 0.05) and 0.1 micromol/l (1.38 +/- 0.10 vs. 1.69 +/- 0.08, P = 0.025) insulin. Glucose 19-26 insulin Homo sapiens 0-7 10909975-3 2000 Insulin-stimulated glucose uptake (fold-stimulation over basal uptake) was decreased in relative compared with control myoblasts at 0.001 micromol/l (0.93 +/- 0.05 [mean +/- SE] vs. 1.15 +/- 0.06, P < 0.05) and 0.1 micromol/l (1.38 +/- 0.10 vs. 1.69 +/- 0.08, P = 0.025) insulin. Glucose 19-26 insulin Homo sapiens 274-281 10909978-1 2000 In patients harboring the IR1152 mutant insulin receptor, hepatic glucose production was normally suppressed by insulin. Glucose 66-73 insulin Homo sapiens 40-47 10909980-0 2000 Glucose-mediated glucose disposal in insulin-resistant normoglycemic relatives of type 2 diabetic patients. Glucose 0-7 insulin Homo sapiens 37-44 10909980-0 2000 Glucose-mediated glucose disposal in insulin-resistant normoglycemic relatives of type 2 diabetic patients. Glucose 17-24 insulin Homo sapiens 37-44 10909980-1 2000 With the aim of investigating glucose-mediated glucose disposal (glucose effectiveness [GE]) in 15 (3 female and 12 male subjects) insulin-resistant normoglycemic relatives of patients with type 2 diabetes (DM2), and 15 age-, sex-, and BMI-matched control subjects without a family history of DM2, we performed 2 studies: 1) a 5-h euglycemic near-normoinsulinemic pancreatic clamp with somatostatin (360 microg/h), insulin (0.25 mU x kg(-1) x min(-1)), glucagon (0.5 ng x kg(-1) x min(-1)), growth hormone (6 ng x kg(-1) x min(-1)), and tritiated glucose infusion and indirect calorimetry; and 2) on a separate day, an identical 5-h clamp but at hyperglycemia (approximately 12 mmol/l) over the last 2 h. Fasting plasma insulin (PI) concentrations were elevated in the relatives compared with control subjects (49 +/- 6 vs. 32 +/- 5 pmol/l, P < 0.04), whereas plasma glucose (PG) was not (5.6 +/- 0.1 vs. 5.5 +/-0.1 mmol/l). Glucose 30-37 insulin Homo sapiens 131-138 10934454-3 2000 The primary objective was to compare the blood glucose threshold for autonomic activation during hypoglycaemia induced by insulin aspart and soluble human insulin. Glucose 47-54 insulin Homo sapiens 122-129 10909983-7 2000 Importantly, throughout all groups, FFA-induced changes in whole-body glucose uptake correlated significantly with FFA-induced changes in insulin-mediated increases in LBF (r = 0.706, P < 0.001), which indicates coupling of metabolic and vascular effects. Glucose 70-77 insulin Homo sapiens 138-145 10934457-7 2000 RESULTS: The insulin secretion results demonstrated that, compared to the control islets, the islets previously exposed to either 44 or 430 pmol/l glucagon exhibited changes in insulin release in response to glucose, consisting of augmented secretion at low glucose challenge, and no further significant increase at high glucose stimulation, similar to the effects observed with islets pre-cultured with high glucose. Glucose 208-215 insulin Homo sapiens 13-20 10909962-7 2000 The exercise-induced increase in glucose uptake was due to marked increases in blood flow (36 +/- 5 ml x kg(-1) muscle x min(-1) [insulin] vs. 262 +/- 20 ml x kg(-1) muscle x min(-1) [insulin and exercise], P < 0.001) rather than glucose extraction, which decreased from 2.0 +/- 0.2 mmol/l (insulin) to 1.0 +/- 0.1 mmol/1 (insulin and exercise) (P < 0.001). Glucose 33-40 insulin Homo sapiens 184-191 10909962-7 2000 The exercise-induced increase in glucose uptake was due to marked increases in blood flow (36 +/- 5 ml x kg(-1) muscle x min(-1) [insulin] vs. 262 +/- 20 ml x kg(-1) muscle x min(-1) [insulin and exercise], P < 0.001) rather than glucose extraction, which decreased from 2.0 +/- 0.2 mmol/l (insulin) to 1.0 +/- 0.1 mmol/1 (insulin and exercise) (P < 0.001). Glucose 33-40 insulin Homo sapiens 184-191 10909962-7 2000 The exercise-induced increase in glucose uptake was due to marked increases in blood flow (36 +/- 5 ml x kg(-1) muscle x min(-1) [insulin] vs. 262 +/- 20 ml x kg(-1) muscle x min(-1) [insulin and exercise], P < 0.001) rather than glucose extraction, which decreased from 2.0 +/- 0.2 mmol/l (insulin) to 1.0 +/- 0.1 mmol/1 (insulin and exercise) (P < 0.001). Glucose 33-40 insulin Homo sapiens 184-191 10909962-8 2000 The subjects were classified according to their mean rate of whole-body insulin-stimulated glucose uptake into those with high (49 +/- 3 micromol x kg(-1) x min(-1)) and normal (27 +/- 2 micromol x kg(-1) x min(-1)) rates of insulin-stimulated glucose uptake. Glucose 91-98 insulin Homo sapiens 72-79 10909962-10 2000 Exercise increased glucose uptake more in the group with high insulin sensitivity (195 +/- 25 pmol x kg(-1) muscle x min(-1)) than in the group with normal insulin sensitivity (125 +/- 19 micromol x kg(-1) muscle x min(-1)) (P < 0.05). Glucose 19-26 insulin Homo sapiens 62-69 11469258-1 2000 BACKGROUND: Orally inhaled insulin may provide a convenient and effective therapy for prandial glucose control in patients with diabetes. Glucose 95-102 insulin Homo sapiens 27-34 11469258-5 2000 RESULTS: Time to maximum insulin concentration in serum (Tmax) after SC dosing occurred approximately 50-60 minutes with the time to minimum plasma glucose concentration (i.e., maximum hypoglycemic effect), (TGmin), occurring later, at around 100-120 minutes. Glucose 148-155 insulin Homo sapiens 25-32 10909962-12 2000 Glucose extraction remained higher in the group with high insulin sensitivity (1.2 +/- 0.2 mmol/l) than in the group with normal insulin sensitivity (0.7 +/- 0.1 mmol/l, P < 0.05). Glucose 0-7 insulin Homo sapiens 58-65 10902785-5 2000 We obtained correlations between indexes of insulin sensitivity from glucose clamp studies (SI(Clamp)) and minimal model analysis (SI(MM)) that were comparable to previous reports (r = 0.57). Glucose 69-76 insulin Homo sapiens 44-51 11242605-5 2000 In addition, plasma glucose was effectively controlled with twice-daily mixed NPH and regular insulin in conjunction with metformin or a thiazolidinedione (or both) in 22 patients and with twice-daily mixed NPH and regular insulin alone in 17. Glucose 20-27 insulin Homo sapiens 94-101 11242605-5 2000 In addition, plasma glucose was effectively controlled with twice-daily mixed NPH and regular insulin in conjunction with metformin or a thiazolidinedione (or both) in 22 patients and with twice-daily mixed NPH and regular insulin alone in 17. Glucose 20-27 insulin Homo sapiens 223-230 10899497-7 2000 The glucose/insulin ratio was calculated as a measure of insulin resistance (normal value, > or =4.5). Glucose 4-11 insulin Homo sapiens 57-64 10861277-9 2000 RESULTS: In individuals with no clinical diagnosis of diabetes and serum glucose <7 mmol/l, insulin was associated with gall stones. Glucose 73-80 insulin Homo sapiens 95-102 10904008-6 2000 Blood samples were collected for the measurement of plasma catecholamines, leptin, and the insulin response to an oral glucose load. Glucose 119-126 insulin Homo sapiens 91-98 10902787-1 2000 In this study, we have compared resistance to insulin-mediated glucose disposal and plasma concentrations of nitric oxide (NO) and cyclic-GMP in healthy volunteers with (n = 35) or without (n = 27) at least one sibling and one parent with type 2 diabetes. Glucose 63-70 insulin Homo sapiens 46-53 10902787-3 2000 Insulin-mediated glucose disposal was quantified by determining the insulin sensitivity index (ISI) in response to a low-dose, constant infusion of insulin (25 mU/kg x h) and glucose (4 mg/kg x min) for 150 min. Glucose 17-24 insulin Homo sapiens 0-7 10751417-11 2000 Our results suggest that: 1) insulin stimulation of glucose transport in adipocytes requires </=45% of maximal tyrosyl phosphorylation of IR or IRS-1 and <50% of maximal activation of PI3K, 2) a novel PI3K-independent pathway may play a role in insulin-induced glucose transport in adipocytes, and 3) overexpression of PTP1B alone in adipocytes does not impair glucose transport. Glucose 267-274 insulin Homo sapiens 29-36 10902787-3 2000 Insulin-mediated glucose disposal was quantified by determining the insulin sensitivity index (ISI) in response to a low-dose, constant infusion of insulin (25 mU/kg x h) and glucose (4 mg/kg x min) for 150 min. Glucose 17-24 insulin Homo sapiens 68-75 10902787-3 2000 Insulin-mediated glucose disposal was quantified by determining the insulin sensitivity index (ISI) in response to a low-dose, constant infusion of insulin (25 mU/kg x h) and glucose (4 mg/kg x min) for 150 min. Glucose 17-24 insulin Homo sapiens 148-155 10902787-3 2000 Insulin-mediated glucose disposal was quantified by determining the insulin sensitivity index (ISI) in response to a low-dose, constant infusion of insulin (25 mU/kg x h) and glucose (4 mg/kg x min) for 150 min. Glucose 175-182 insulin Homo sapiens 0-7 10902794-5 2000 When the glucose disposal rate was expressed per kg fat-free mass (FFM), the improved insulin sensitivity persisted in endurance-trained (pre, 10.5 +/- 2.7; post, 12.1 +/- 3.3 mg/min x kg FFM; P < 0.05), but not in resistance-trained (pre, 9.7 +/- 1.9; post, 10.2 +/- 1.8 mg/min x kg FFM; P = NS) women. Glucose 9-16 insulin Homo sapiens 86-93 11253257-0 2000 Gender differences in the relationship between insulin-mediated glucose utilization and sex hormones in young African-Americans. Glucose 64-71 insulin Homo sapiens 47-54 11253257-1 2000 OBJECTIVE: To determine whether there are gender differences in insulin-mediated glucose utilization and if sex hormones correlate with measures of insulin sensitivity in young adult African-Americans. Glucose 81-88 insulin Homo sapiens 64-71 11253257-9 2000 When insulin-mediated glucose utilization was corrected for body fat, there was no gender difference in insulin sensitivity. Glucose 22-29 insulin Homo sapiens 5-12 10909995-5 2000 The insulin sensitivity index (SI determined from an intravenous glucose tolerance test (IVGTT) improved significantly (P < .05) in both the young group (4.8 +/- 0.6 v6.9 +/- 0.8 x 10(-4)/ min (microU/mL) and the older group (3.2 +/- 0.6 v 5.9 +/- 1.0 x 10(-4)/min (microU/mL)). Glucose 65-72 insulin Homo sapiens 4-11 10910002-8 2000 In conclusion, nonstationary and disorderly insulin secretion patterns during glucose stimulation and a low acute-phase serum insulin response associated with significant insulin resistance suggest early beta-cell regulatory dysfunction in individuals genetically predisposed to type 2 diabetes mellitus prior to any evident alterations in insulin secretory burst frequency or mass. Glucose 78-85 insulin Homo sapiens 44-51 10764780-1 2000 Osmotic shock can cause insulin resistance in 3T3-L1 adipocytes by inhibiting insulin activation of glucose transport, p70S6 kinase, glycogen synthesis, and lipogenesis. Glucose 100-107 insulin Homo sapiens 24-31 10764780-1 2000 Osmotic shock can cause insulin resistance in 3T3-L1 adipocytes by inhibiting insulin activation of glucose transport, p70S6 kinase, glycogen synthesis, and lipogenesis. Glucose 100-107 insulin Homo sapiens 78-85 10856891-18 2000 As expected, glucose levels declined within 10 min of the insulin injection and rose after 3 min following both adrenaline and glucagon injections. Glucose 13-20 insulin Homo sapiens 58-65 10968480-10 2000 However, in the pubertal group an inverse correlation was found between insulin and cortisol (p=0.03), and between insulin and glucose after control for adiposity. Glucose 127-134 insulin Homo sapiens 115-122 10888677-1 2000 Like neuronal synaptic vesicles, intracellular GLUT4-containing vesicles must dock and fuse with the plasma membrane, thereby facilitating insulin-regulated glucose uptake into muscle and fat cells. Glucose 157-164 insulin Homo sapiens 139-146 10862997-0 2000 Effects of glucose and insulin levels on adipose tissue glucose measurement by microdialysis probes retained for three weeks in Type 1 diabetic patients. Glucose 56-63 insulin Homo sapiens 23-30 10751417-11 2000 Our results suggest that: 1) insulin stimulation of glucose transport in adipocytes requires </=45% of maximal tyrosyl phosphorylation of IR or IRS-1 and <50% of maximal activation of PI3K, 2) a novel PI3K-independent pathway may play a role in insulin-induced glucose transport in adipocytes, and 3) overexpression of PTP1B alone in adipocytes does not impair glucose transport. Glucose 52-59 insulin Homo sapiens 29-36 10751417-11 2000 Our results suggest that: 1) insulin stimulation of glucose transport in adipocytes requires </=45% of maximal tyrosyl phosphorylation of IR or IRS-1 and <50% of maximal activation of PI3K, 2) a novel PI3K-independent pathway may play a role in insulin-induced glucose transport in adipocytes, and 3) overexpression of PTP1B alone in adipocytes does not impair glucose transport. Glucose 52-59 insulin Homo sapiens 251-258 10751417-11 2000 Our results suggest that: 1) insulin stimulation of glucose transport in adipocytes requires </=45% of maximal tyrosyl phosphorylation of IR or IRS-1 and <50% of maximal activation of PI3K, 2) a novel PI3K-independent pathway may play a role in insulin-induced glucose transport in adipocytes, and 3) overexpression of PTP1B alone in adipocytes does not impair glucose transport. Glucose 267-274 insulin Homo sapiens 29-36 10837281-6 2000 Serum insulin and glucose concentrations during the oral-glucose-tolerance test increased significantly after weight gain in obese subjects. Glucose 57-64 insulin Homo sapiens 6-13 10860996-0 2000 GLUT8 is a glucose transporter responsible for insulin-stimulated glucose uptake in the blastocyst. Glucose 11-18 insulin Homo sapiens 47-54 10860996-1 2000 Mammalian preimplantation blastocysts exhibit insulin-stimulated glucose uptake despite the absence of the only known insulin-regulated transporter, GLUT4. Glucose 65-72 insulin Homo sapiens 46-53 10860996-3 2000 Insulin induces a change in the intracellular localization of this protein, which translates into increased glucose uptake into the blastocyst, a process that is inhibited by antisense oligoprobes. Glucose 108-115 insulin Homo sapiens 0-7 10860996-5 2000 Moreover, the existence of an alternative transporter may explain examples in other tissues of insulin-regulated glucose transport in the absence of GLUT4. Glucose 113-120 insulin Homo sapiens 95-102 10856515-3 2000 This impairment is associated with decreased basal and insulin-stimulated glucose metabolism. Glucose 74-81 insulin Homo sapiens 55-62 10827000-1 2000 Insulin and exercise potently stimulate glucose metabolism and gene transcription in vivo in skeletal muscle. Glucose 40-47 insulin Homo sapiens 0-7 10827000-2 2000 A single bout of exercise increases the rate of insulin-stimulated glucose uptake and metabolism in skeletal muscle in the postexercise period. Glucose 67-74 insulin Homo sapiens 48-55 10827003-1 2000 Skeletal muscle denervation decreases insulin-sensitive glucose uptake into this tissue as a result of marked GLUT-4 protein downregulation ( approximately 20% of controls). Glucose 56-63 insulin Homo sapiens 38-45 10827003-2 2000 The process of insulin-stimulated glucose transport in muscle requires the movement or translocation of intracellular GLUT-4-rich vesicles to the cell surface, and it is accompanied by the translocation of several additional vesicular cargo proteins. Glucose 34-41 insulin Homo sapiens 15-22 10827008-2 2000 To examine whether the insulin antagonistic effect of growth hormone (GH) acts upon the heart, we compared insulin-stimulated whole body and myocardial glucose uptake with and without GH administration during a 3.5-h euglycemic-hyperinsulinemic clamp in eight healthy males. Glucose 152-159 insulin Homo sapiens 107-114 10827008-6 2000 GH decreased whole body insulin-stimulated glucose disposal by 26% (48.0 +/- 12.1 vs. control 62.8 +/- 6.1 micromol. Glucose 43-50 insulin Homo sapiens 24-31 10827008-10 2000 Insulin-stimulated myocardial glucose uptake was similar in the presence and in the absence of GH (0.34 +/- 0.05 and 0.31 +/- 0.03 micromol. Glucose 30-37 insulin Homo sapiens 0-7 10921528-5 2000 Sympathetically mediated vasoconstriction in skeletal muscle vascular beds reduces the uptake of glucose by muscle, and is thus a basis for insulin resistance and consequent hyperinsulinemia. Glucose 97-104 insulin Homo sapiens 140-147 10856528-4 2000 Insulin sensitivity was quantified by the minimal model procedure over a 180-min intravenous glucose tolerance test with iterative sampling. Glucose 93-100 insulin Homo sapiens 0-7 10915018-4 2000 All eight patients with adrenocortical adenoma exhibited insulin resistance as estimated by the steady-state plasma glucose (SSPG). Glucose 116-123 insulin Homo sapiens 57-64 10802311-1 2000 This paper describes the neural basis and the role of Pavlovian conditioning in the modification of blood glucose and related endocrine parameters after repeated insulin and glucose administration. Glucose 106-113 insulin Homo sapiens 162-169 10841000-0 2000 Effect of menopausal status on insulin-stimulated glucose disposal: comparison of middle-aged premenopausal and early postmenopausal women. Glucose 50-57 insulin Homo sapiens 31-38 10911773-5 2000 After an oral glucose load, the glucose disposal of R+ cockerels was faster despite lower glucose-induced plasma insulin concentration. Glucose 14-21 insulin Homo sapiens 113-120 10914635-5 2000 In the presence of 16.7 mM glucose, tetracaine transiently increased the insulin secretion from islets perfused in the absence and presence of external Ca2+. Glucose 27-34 insulin Homo sapiens 73-80 10894496-2 2000 Insulin secretion was found to be significantly lower in B6 than in C3H/He (C3H) mice (analysis of variance, P < 0.05) at 10, 20, and 30 minutes during the intraperitoneal glucose tolerance test (IPGTT: 1.5 g glucose/kg of body weight). Glucose 175-182 insulin Homo sapiens 0-7 10894496-2 2000 Insulin secretion was found to be significantly lower in B6 than in C3H/He (C3H) mice (analysis of variance, P < 0.05) at 10, 20, and 30 minutes during the intraperitoneal glucose tolerance test (IPGTT: 1.5 g glucose/kg of body weight). Glucose 212-219 insulin Homo sapiens 0-7 10840996-4 2000 Subjects were characterized for body composition dual-energy X-ray absorptiometry, insulin action (insulin-stimulated glucose disposal [M], hyperinsulinemic glucose clamp), and glucose tolerance (75-g oral glucose tolerance test). Glucose 118-125 insulin Homo sapiens 99-106 10830281-0 2000 Long-chain acyl CoA regulation of protein kinase C and fatty acid potentiation of glucose-stimulated insulin secretion in clonal beta-cells. Glucose 82-89 insulin Homo sapiens 101-108 10830281-4 2000 Down-regulation of PKC by phorbol esters was confirmed by Western blotting and resulted in the complete loss of cPKC activity, partial loss of nPKC activity and preservation of aPKC activity and glucose-stimulated insulin secretion. Glucose 195-202 insulin Homo sapiens 214-221 10830281-9 2000 The addition of exogenous oleate or palmitate potentiated glucose-stimulated insulin secretion 2-fold and was unaffected by PMA-induced down-regulation. Glucose 58-65 insulin Homo sapiens 77-84 10841000-5 2000 RESEARCH DESIGN AND METHODS: Insulin-stimulated glucose disposal was measured in 43 middle-aged premenopausal women (47 +/- 3 years of age) during the luteal phase of the menstrual cycle and 40 early postmenopausal women (51 +/- 4 years; time since menopause, 21 +/- 13 months) using the hyperinsulinemic-euglycemic clamp technique. Glucose 48-55 insulin Homo sapiens 29-36 10841001-5 2000 Finally, we compared the insulin response to glucose plus GLP-1 stimulation with that observed during a hyperglycemic arginine clamp (30 mmol/l) in 8 patients and 8 control subjects. Glucose 45-52 insulin Homo sapiens 25-32 10945154-9 2000 Thus fast-acting insulin analogs feature interesting characteristics, noteworthy immediate premeal injection and a better postprandial glucose control. Glucose 135-142 insulin Homo sapiens 17-24 10866050-0 2000 Insulin secretion and insulin sensitivity in relation to glucose tolerance: lessons from the Botnia Study. Glucose 57-64 insulin Homo sapiens 0-7 10866050-0 2000 Insulin secretion and insulin sensitivity in relation to glucose tolerance: lessons from the Botnia Study. Glucose 57-64 insulin Homo sapiens 22-29 10866050-3 2000 To address this question, we estimated insulin secretion (by measuring both insulin levels and the ratio of insulin-to-glucose levels in 30-min intervals) and insulin sensitivity (by using the homeostasis model assessment [HOMA] index) from an oral glucose tolerance test (OGTT) in 5,396 individuals from the Botnia Study who had varying degrees of glucose tolerance. Glucose 249-256 insulin Homo sapiens 39-46 10866050-3 2000 To address this question, we estimated insulin secretion (by measuring both insulin levels and the ratio of insulin-to-glucose levels in 30-min intervals) and insulin sensitivity (by using the homeostasis model assessment [HOMA] index) from an oral glucose tolerance test (OGTT) in 5,396 individuals from the Botnia Study who had varying degrees of glucose tolerance. Glucose 249-256 insulin Homo sapiens 39-46 10866050-6 2000 Compared with subjects with IFG, subjects with IGT had a lower incremental 30-min insulin-to-glucose area during an OGTT (13.8 +/- 1.7 vs. 21.7 +/- 1.7, P = 0.0008). Glucose 93-100 insulin Homo sapiens 82-89 10866051-0 2000 High glucose and glucosamine induce insulin resistance via different mechanisms in 3T3-L1 adipocytes. Glucose 5-12 insulin Homo sapiens 36-43 10866051-2 2000 Glucosamine (GlcN) has been extensively used to model the role of the hexosamine synthesis pathway (HSP) in glucose-induced insulin resistance. Glucose 108-115 insulin Homo sapiens 124-131 10866051-4 2000 Basal and acute insulin-stimulated (100 nmol/l) glucose transport was measured after re-equilibration in serum and insulin-free media. Glucose 48-55 insulin Homo sapiens 16-23 10866051-5 2000 Preincubation with high glucose or GlcN (1-2.5 mmol/l) inhibited basal and acute insulin-stimulated glucose transport only if insulin was present during preincubation. Glucose 24-31 insulin Homo sapiens 81-88 10866051-5 2000 Preincubation with high glucose or GlcN (1-2.5 mmol/l) inhibited basal and acute insulin-stimulated glucose transport only if insulin was present during preincubation. Glucose 24-31 insulin Homo sapiens 126-133 10866051-5 2000 Preincubation with high glucose or GlcN (1-2.5 mmol/l) inhibited basal and acute insulin-stimulated glucose transport only if insulin was present during preincubation. Glucose 100-107 insulin Homo sapiens 81-88 10866051-5 2000 Preincubation with high glucose or GlcN (1-2.5 mmol/l) inhibited basal and acute insulin-stimulated glucose transport only if insulin was present during preincubation. Glucose 100-107 insulin Homo sapiens 126-133 10866051-17 2000 1) Chronic exposure to high glucose or GlcN in the presence of low insulin caused insulin resistance of glucose transport by different mechanisms. Glucose 28-35 insulin Homo sapiens 67-74 10866051-17 2000 1) Chronic exposure to high glucose or GlcN in the presence of low insulin caused insulin resistance of glucose transport by different mechanisms. Glucose 104-111 insulin Homo sapiens 67-74 10866052-3 2000 In these cells, insulin stimulation of glucose uptake, glycogen synthesis, insulin receptor (IR) kinase activity, and insulin receptor substrate 1-associated phosphatidylinositol 3-kinase (PI 3-kinase) activity were measured. Glucose 39-46 insulin Homo sapiens 16-23 10975045-4 2000 Last, regarding metabolic monitoring, taking postprandial blood glucose into account leads to increasing insulin dosage, improving final term HbA1c and, finally, a lower average birth weight. Glucose 64-71 insulin Homo sapiens 105-112 10975046-8 2000 Finally, insulin sensitizing agents are being investigated as a way to improve postprandial glucose efflux by potentiating insulin effects. Glucose 92-99 insulin Homo sapiens 9-16 11036871-4 2000 Gel chromatographic analysis of the plasma in combination with sensitive enzyme immunoassay of insulin revealed that the ratio of proinsulin to total immunoreactive insulin was elevated at fasting (12.9%), and was decreased to 8.9% at 60 min after glucose administration. Glucose 248-255 insulin Homo sapiens 130-140 10975046-8 2000 Finally, insulin sensitizing agents are being investigated as a way to improve postprandial glucose efflux by potentiating insulin effects. Glucose 92-99 insulin Homo sapiens 123-130 10975211-1 2000 AIMS: Use of the oral glucose tolerance test (OGTT) to define glucose intolerance in the general population may bias towards selection of those with insulin resistance. Glucose 22-29 insulin Homo sapiens 149-156 10975211-1 2000 AIMS: Use of the oral glucose tolerance test (OGTT) to define glucose intolerance in the general population may bias towards selection of those with insulin resistance. Glucose 62-69 insulin Homo sapiens 149-156 10975211-8 2000 In all, 192 subjects" 30-min insulin concentration and incremental insulin response showed only a significantly negative correlation with fasting glucose concentration. Glucose 146-153 insulin Homo sapiens 29-36 10975211-8 2000 In all, 192 subjects" 30-min insulin concentration and incremental insulin response showed only a significantly negative correlation with fasting glucose concentration. Glucose 146-153 insulin Homo sapiens 67-74 10975211-9 2000 In a linear regression analysis, a low 30-min insulin-glucose ratio was only a significant factor in the fasting glucose model. Glucose 54-61 insulin Homo sapiens 46-53 10975211-9 2000 In a linear regression analysis, a low 30-min insulin-glucose ratio was only a significant factor in the fasting glucose model. Glucose 113-120 insulin Homo sapiens 46-53 11036871-4 2000 Gel chromatographic analysis of the plasma in combination with sensitive enzyme immunoassay of insulin revealed that the ratio of proinsulin to total immunoreactive insulin was elevated at fasting (12.9%), and was decreased to 8.9% at 60 min after glucose administration. Glucose 248-255 insulin Homo sapiens 133-140 11036871-5 2000 These findings may indicate that biologically active authentic insulin was predominantly secreted after glucose administration in the present case. Glucose 104-111 insulin Homo sapiens 63-70 10806013-2 2000 METHODS AND RESULTS: Insulin resistance was calculated from fasting plasma glucose and insulin concentration using homeostasis model assessment in 40 patients suspected of having ischaemic heart disease, but without angiographic evidence of atherosclerotic coronary artery disease defined as a discrete stenosis or intimal irregularity. Glucose 75-82 insulin Homo sapiens 21-28 10834933-5 2000 The expression of GLUT4 protein and the maximal insulin-stimulated glucose transport was 50% decreased in adipocytes from all three groups. Glucose 67-74 insulin Homo sapiens 48-55 11036875-0 2000 Characterization of an early decline in baseline plasma glucose concentration after acute insulin elevation during euglycemic hyperinsulinemic clamp in patients with type 2 diabetes mellitus. Glucose 56-63 insulin Homo sapiens 90-97 11036875-5 2000 Their insulin resistance (GIR) substantially recovered concomitant with an increase in slope "a" after pretreatment with somatostatin analogue in two cases studied, suggesting possible suppression of hepatic glucose production through lowering of plasma glucagon concentrations. Glucose 208-215 insulin Homo sapiens 6-13 10834933-12 2000 However, the insulin signaling cascade has sufficient plasticity to accommodate significant changes in specific components without further reducing glucose uptake. Glucose 148-155 insulin Homo sapiens 13-20 10834933-13 2000 Furthermore, the data indicate that the cellular content of GLUT4 is the rate-limiting factor in mediating maximal insulin-stimulated glucose uptake in GLUT4(+/-) adipocytes. Glucose 134-141 insulin Homo sapiens 115-122 10875604-2 2000 The inability of the body to maintain normal glucose levels or to require excessive levels of insulin to do so has been called glucose intolerance, impaired glucose tolerance and insulin resistance. Glucose 127-134 insulin Homo sapiens 94-101 12515147-5 2000 The results showed the levels of serum FFA, PG and insulin of fasting and after glucose load in the patients were significantly increased and their insulin-sensitive (ISI) was remarkably decreased as compared with those in 30 normal controls, P < 0.05. Glucose 80-87 insulin Homo sapiens 51-58 11006892-3 2000 Insulin resistance and its components for children and adolescents, especially obesity and dyslipidemia, are generators of hypertension, glucose intolerance and complications of atherosclerosis in adulthood. Glucose 137-144 insulin Homo sapiens 0-7 10872559-5 2000 Insulin action was measured using the glucose clamp technique combined with isotope dilution methodology. Glucose 38-45 insulin Homo sapiens 0-7 10872559-7 2000 RESULTS: Insulin sensitivity index (glucose infusion rate/ serum insulin) was lower in the hypertensive patients (P= 0.01) and fasting insulin was increased (P= 0.008) compared to controls. Glucose 36-43 insulin Homo sapiens 9-16 10838535-7 2000 Insulin"s effect was independent of the ambient glucose concentration. Glucose 48-55 insulin Homo sapiens 0-7 10827212-6 2000 The plasma glucose response to a fixed exogenous insulin bolus did not differ at the end of the two periods. Glucose 11-18 insulin Homo sapiens 49-56 11014617-2 2000 Acute administration of high glucose concentrations to pancreatic beta-cells stimulates insulin secretion. Glucose 29-36 insulin Homo sapiens 88-95 10879332-4 2000 Regular insulin was given intravenously with an infusion pump to maintain the plasma glucose concentration between 60 and 90 mg/dl. Glucose 85-92 insulin Homo sapiens 8-15 11014617-3 2000 In addition, short term exposure of this cell type to dietary fatty acids potentiates glucose-induced insulin release. Glucose 86-93 insulin Homo sapiens 102-109 11967809-4 2000 The stimulatory effect of glucose (25 mM) was blocked by insulin and tolrestat (an inhibitor of aldose reductase). Glucose 26-33 insulin Homo sapiens 57-64 11967809-6 2000 While insulin did not affect the cellular DAG and PKC activity, it did block the stimulatory effect of high glucose (25 mM) and PMA on the expression of the fusion gene. Glucose 108-115 insulin Homo sapiens 6-13 10872801-3 2000 274, 33866-33869, 1999) that the expression of the catalytic subunit (p36) and putative glucose 6-phosphate translocase (p46) of the liver glucose 6-phosphatase system was stimulated by cyclic AMP and glucose and repressed by insulin. Glucose 88-95 insulin Homo sapiens 226-233 10748179-1 2000 The role of glycogen-synthase kinase 3 (GSK3) in insulin-stimulated glucose transport and glycogen synthase activation was investigated in 3T3-L1 adipocytes. Glucose 68-75 insulin Homo sapiens 49-56 10811900-1 2000 Pancreatic beta cells respond to changes in blood glucose by secreting insulin and increasing insulin synthesis. Glucose 50-57 insulin Homo sapiens 71-78 10811900-1 2000 Pancreatic beta cells respond to changes in blood glucose by secreting insulin and increasing insulin synthesis. Glucose 50-57 insulin Homo sapiens 94-101 10872292-6 2000 Among the stimulators of insulin secretion are the sulfonylureas (e.g. glibenclamide, glibonuride, glisoxepid, glimepiride), and the so-called prandial glucose regulators, such as repaglinide, which differ from the sulfonylureas both chemically and in their pharmacodynamic properties. Glucose 152-159 insulin Homo sapiens 25-32 10878324-3 2000 Serum insulin levels rose and serum glucose levels decreased in an insulin dose-related fashion. Glucose 36-43 insulin Homo sapiens 67-74 10878324-6 2000 In the in vivo rectal absorption experiment using emulsions incorporating 2% DHA, 5 IU/kg of insulin emulsion produced a rapid, transitory increase in serum insulin levels and strong reduction of serum glucose levels. Glucose 202-209 insulin Homo sapiens 93-100 10748090-3 2000 The promoters of both genes share similar cis-acting sequence elements, and both bind the homeodomain transcription factor PDX1, which plays an important role in the regulation of the insulin promoter and insulin mRNA levels by glucose. Glucose 228-235 insulin Homo sapiens 184-191 10748090-7 2000 We have previously used these cells to show that glucose regulation of the insulin gene is dependent on PDX1, but not calcium. Glucose 49-56 insulin Homo sapiens 75-82 10748090-3 2000 The promoters of both genes share similar cis-acting sequence elements, and both bind the homeodomain transcription factor PDX1, which plays an important role in the regulation of the insulin promoter and insulin mRNA levels by glucose. Glucose 228-235 insulin Homo sapiens 205-212 10792038-3 2000 However, because glucose-stimulated insulin secretion involves both glycolytic and Kreb"s cycle metabolism, islets were cultured on extracellular matrix that promotes cell spreading and allows spatial resolution of the NAD(P)H signals from the cytoplasm and mitochondria. Glucose 17-24 insulin Homo sapiens 36-43 10799399-3 2000 The hyperinsulinemic-euglycemic glucose clamp technique and intravenous-glucose-tolerance test have indicated that insulin action in late normal pregnancy is 50-70% lower than in nonpregnant women. Glucose 32-39 insulin Homo sapiens 9-16 10799399-8 2000 Endogenous hepatic glucose production was shown to remain sensitive to increased insulin concentration in normal pregnancy (96% suppression), but is less sensitive in GDM (80%). Glucose 19-26 insulin Homo sapiens 81-88 10780952-4 2000 Among 47 lean and obese glucose-tolerant men and women, insulin-stimulated glucose utilization, measured by euglycemic clamp, was strongly correlated with both VAT and deep SAT (r = -0.61 and -0.64, respectively; both P < 0.001), but not with superficial SAT (r = -0.29, not significant). Glucose 24-31 insulin Homo sapiens 56-63 10780934-0 2000 Dose-response characteristics of insulin action on glucose metabolism: a non-steady-state approach. Glucose 51-58 insulin Homo sapiens 33-40 10817253-9 2000 These results are consistent with the notion that decreased insulin sensitivity and pancreatic beta-cell dysfunction may predispose the elderly to glucose intolerance. Glucose 147-154 insulin Homo sapiens 60-67 10780934-2 2000 This curve is typically characterized by a maximally insulin-stimulated glucose clearance (Cl(max)) and an insulin concentration at half-maximal response (EC(50)). Glucose 72-79 insulin Homo sapiens 53-60 10780934-4 2000 The effect of insulin on plasma glucose clearance was calculated from non-steady-state data by use of a circulatory model of glucose kinetics and a model of insulin action in which glucose clearance is represented as a Michaelis-Menten function of insulin concentration with a delay (t(1/2)). Glucose 32-39 insulin Homo sapiens 14-21 10780934-10 2000 We conclude that the test here presented, based on a more elaborate representation of glucose kinetics and insulin action, allows a reliable quantitation of the insulin dose-response curve for whole body glucose utilization in a single session of relatively short duration. Glucose 86-93 insulin Homo sapiens 161-168 10780934-10 2000 We conclude that the test here presented, based on a more elaborate representation of glucose kinetics and insulin action, allows a reliable quantitation of the insulin dose-response curve for whole body glucose utilization in a single session of relatively short duration. Glucose 204-211 insulin Homo sapiens 107-114 10780934-10 2000 We conclude that the test here presented, based on a more elaborate representation of glucose kinetics and insulin action, allows a reliable quantitation of the insulin dose-response curve for whole body glucose utilization in a single session of relatively short duration. Glucose 204-211 insulin Homo sapiens 161-168 10780948-2 2000 Furthermore, the dependency of insulin-stimulated glucose uptake on fiber type distribution was investigated. Glucose 50-57 insulin Homo sapiens 31-38 10780948-7 2000 Insulin-stimulated glucose uptake rates measured by hyperinsulinemic, euglycemic clamp were not correlated with the fraction of slow fibers in the young (r = -0.45, P > 0.25) or in the elderly (r = 0. Glucose 19-26 insulin Homo sapiens 0-7 10792333-0 2000 Impaired beta-cell function in the presence of reduced insulin sensitivity determines glucose tolerance status in acromegalic patients. Glucose 86-93 insulin Homo sapiens 55-62 10928124-5 2000 As expected, administration of a bolus of glucose resulted in a more rapid clearance of blood glucose than was observed in 5 control subjects, indicating the presence of insulin hypersensitivity in the patient. Glucose 42-49 insulin Homo sapiens 170-177 10781647-9 2000 Men with coronary artery disease had an enhanced insulin response during the intravenous glucose tolerance test (P<0.03) particularly in the low fat phase. Glucose 89-96 insulin Homo sapiens 49-56 10792333-11 2000 CONCLUSIONS: We conclude that insulin sensitivity is reduced to a similar extent in acromegalic patients with normal glucose tolerance and those with impaired glucose tolerance or diabetes. Glucose 117-124 insulin Homo sapiens 30-37 10792333-12 2000 Compensatory hyperfunction of beta-cells appears to counterbalance the reduced insulin sensitivity in the acromegalic patients with normal glucose tolerance but not in those with impaired glucose tolerance or diabetes. Glucose 139-146 insulin Homo sapiens 79-86 10834425-1 2000 OBJECTIVE: To characterize in detail the association between insulin sensitivity and islet function in relation to glucose tolerance in nondiabetic subjects. Glucose 115-122 insulin Homo sapiens 61-68 10826072-7 2000 Phase III clinical trials are in progress of a long-acting basal insulin without peak actions to simulate the low dose continuous production of the insulin which normally inhibits hepatic glucose production. Glucose 188-195 insulin Homo sapiens 148-155 10834420-3 2000 RESEARCH DESIGN AND METHODS: Insulin sensitivity (S(I)) and the acute insulin response (AIR) to glucose were assessed by a frequently sampled intravenous glucose tolerance test and related to resting heart rate in the tri-ethnic nondiabetic population (n = 1,000) of the Insulin Resistance Atherosclerosis Study. Glucose 96-103 insulin Homo sapiens 70-77 10834441-0 2000 Interesting insulin response to oral glucose load in young Japanese subjects with impaired glucose tolerance. Glucose 37-44 insulin Homo sapiens 12-19 10834423-9 2000 After the 1-month titration phase, significantly fewer subjects receiving insulin glargine experienced symptomatic hypoglycemia (39.9 vs. 49.2%, P = 0.0219) or nocturnal hypoglycemia (18.2 vs. 27.1%, P = 0.0116) with a blood glucose level <2.0 mmol/l compared with subjects receiving NPH insulin. Glucose 225-232 insulin Homo sapiens 74-81 10905474-0 2000 Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. Glucose 91-98 insulin Homo sapiens 72-79 10880895-0 2000 Glucose profiles in a type 1 diabetic patient successively treated with CSII using regular insulin, lispro and an implantable insulin pump. Glucose 0-7 insulin Homo sapiens 91-98 10880895-0 2000 Glucose profiles in a type 1 diabetic patient successively treated with CSII using regular insulin, lispro and an implantable insulin pump. Glucose 0-7 insulin Homo sapiens 126-133 10905474-4 2000 We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). Glucose 105-112 insulin Homo sapiens 86-93 10905472-4 2000 However, results obtained with rodent or human systems that more directly examined muscle fuel selection have found that skeletal muscle in insulin resistance is accompanied by increased, rather than decreased, muscle glucose oxidation under basal conditions and decreased glucose oxidation under insulin-stimulated circumstances, producing a state of "metabolic inflexibility." Glucose 218-225 insulin Homo sapiens 140-147 10905474-5 2000 As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. Glucose 60-67 insulin Homo sapiens 41-48 10905483-4 2000 The amount of insulin absorbed, measured as either free or total insulin, was significantly correlated with its ability to suppress FFAs and stimulate glucose metabolism but not with the insulin dose per se. Glucose 151-158 insulin Homo sapiens 14-21 10905474-7 2000 Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). Glucose 177-184 insulin Homo sapiens 158-165 10905483-4 2000 The amount of insulin absorbed, measured as either free or total insulin, was significantly correlated with its ability to suppress FFAs and stimulate glucose metabolism but not with the insulin dose per se. Glucose 151-158 insulin Homo sapiens 65-72 10905483-4 2000 The amount of insulin absorbed, measured as either free or total insulin, was significantly correlated with its ability to suppress FFAs and stimulate glucose metabolism but not with the insulin dose per se. Glucose 151-158 insulin Homo sapiens 65-72 10905474-8 2000 In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. Glucose 149-156 insulin Homo sapiens 128-135 10905483-8 2000 The percent hepatic fat was also significantly correlated with the ability of intravenous insulin to suppress endogenous glucose production (r = 0.72, P < 0.005). Glucose 121-128 insulin Homo sapiens 90-97 10905483-10 2000 Variation in hepatic fat content may influence insulin requirements via an effect on the sensitivity of endogenous glucose production to insulin. Glucose 115-122 insulin Homo sapiens 47-54 10905483-0 2000 Hepatic fat content and insulin action on free fatty acids and glucose metabolism rather than insulin absorption are associated with insulin requirements during insulin therapy in type 2 diabetic patients. Glucose 63-70 insulin Homo sapiens 24-31 10905483-10 2000 Variation in hepatic fat content may influence insulin requirements via an effect on the sensitivity of endogenous glucose production to insulin. Glucose 115-122 insulin Homo sapiens 137-144 10905485-0 2000 Interaction between insulin sensitivity and muscle perfusion on glucose uptake in human skeletal muscle: evidence for capillary recruitment. Glucose 64-71 insulin Homo sapiens 20-27 10905485-1 2000 Insulin and glucose delivery (muscle perfusion) can modulate insulin-mediated glucose uptake. Glucose 12-19 insulin Homo sapiens 61-68 10905485-1 2000 Insulin and glucose delivery (muscle perfusion) can modulate insulin-mediated glucose uptake. Glucose 78-85 insulin Homo sapiens 0-7 10905485-1 2000 Insulin and glucose delivery (muscle perfusion) can modulate insulin-mediated glucose uptake. Glucose 78-85 insulin Homo sapiens 61-68 10905485-2 2000 This study was undertaken to determine 1) to what extent insulin sensitivity modulates the effect of perfusion on glucose uptake and 2) whether this effect is achieved via capillary recruitment. Glucose 114-121 insulin Homo sapiens 57-64 10905485-10 2000 Together, the data indicate that 1) muscle perfusion becomes more rate limiting to glucose uptake as insulin sensitivity increases and 2) insulin-mediated increments in muscle perfusion are accompanied by capillary recruitment. Glucose 83-90 insulin Homo sapiens 101-108 10905485-10 2000 Together, the data indicate that 1) muscle perfusion becomes more rate limiting to glucose uptake as insulin sensitivity increases and 2) insulin-mediated increments in muscle perfusion are accompanied by capillary recruitment. Glucose 83-90 insulin Homo sapiens 138-145 10905485-11 2000 Thus, insulin-stimulated glucose uptake displays both permeability- and perfusion-limited glucose exchange properties. Glucose 25-32 insulin Homo sapiens 6-13 10905485-11 2000 Thus, insulin-stimulated glucose uptake displays both permeability- and perfusion-limited glucose exchange properties. Glucose 90-97 insulin Homo sapiens 6-13 10905483-2 2000 Insulin absorption (increase in free and total insulin over 8 h after a subcutaneous dose of regular insulin) and actions of intravenous (6-h 0.3 mU x kg(-1) x min(-1) euglycemic insulin clamp combined with [3-3H]glucose) and subcutaneous (glucose infusion rate required to maintain isoglycemia and suppression of free fatty acids [FFAs]) insulin, liver fat content (proton spectroscopy), visceral fat (magnetic resonance imaging), weight, and body composition were determined. Glucose 213-220 insulin Homo sapiens 0-7 10905487-3 2000 Insulin sensitivity was assessed by minimal model analysis, and beta-cell insulin release was assessed as acute insulin responses to glucose (AIRg) and tolbutamide (AIRt) during FSIGTs and as the 30-min incremental insulin response (30-min dINS) during OGTTs. Glucose 133-140 insulin Homo sapiens 74-81 10905487-3 2000 Insulin sensitivity was assessed by minimal model analysis, and beta-cell insulin release was assessed as acute insulin responses to glucose (AIRg) and tolbutamide (AIRt) during FSIGTs and as the 30-min incremental insulin response (30-min dINS) during OGTTs. Glucose 133-140 insulin Homo sapiens 112-119 10905483-2 2000 Insulin absorption (increase in free and total insulin over 8 h after a subcutaneous dose of regular insulin) and actions of intravenous (6-h 0.3 mU x kg(-1) x min(-1) euglycemic insulin clamp combined with [3-3H]glucose) and subcutaneous (glucose infusion rate required to maintain isoglycemia and suppression of free fatty acids [FFAs]) insulin, liver fat content (proton spectroscopy), visceral fat (magnetic resonance imaging), weight, and body composition were determined. Glucose 240-247 insulin Homo sapiens 0-7 10905487-11 2000 The predominant response of beta-cells to improved insulin sensitivity in women at high risk for type 2 diabetes was a reduction in insulin release to maintain nearly constant glucose tolerance. Glucose 176-183 insulin Homo sapiens 51-58 10809901-8 2000 On a third occasion 6 subjects additionally received an arginine bolus at > 25 mM blood glucose, a test hitherto claimed to provoke maximal insulin secretion. Glucose 91-98 insulin Homo sapiens 143-150 10905487-11 2000 The predominant response of beta-cells to improved insulin sensitivity in women at high risk for type 2 diabetes was a reduction in insulin release to maintain nearly constant glucose tolerance. Glucose 176-183 insulin Homo sapiens 132-139 10905488-8 2000 Basal glucose kinetics were unchanged, but an increase in insulin-stimulated peripheral glucose disposal was observed after IGF-I therapy (37+/-6 vs. 52+/-10 micromol x kg(-1) x min(-1), P < 0.05). Glucose 88-95 insulin Homo sapiens 58-65 10905488-11 2000 These findings demonstrated that IGF-I replacement resulted in significant alterations in glucose and protein metabolism in the basal and insulin-stimulated states. Glucose 90-97 insulin Homo sapiens 138-145 10905493-2 2000 The rate-controlling steps of insulin-stimulated muscle glucose metabolism were assessed using 31P-NMR spectroscopic measurement of intramuscular glucose-6-phosphate (G-6-P) combined with a novel 13C-NMR method to assess intracellular glucose concentrations. Glucose 56-63 insulin Homo sapiens 30-37 10809900-4 2000 In study 2, CON further increased the glucose uptake via an increment in prehepatic insulin secretion that stimulated insulin sensitivity without changes in peripheral insulin and glucose concentrations. Glucose 38-45 insulin Homo sapiens 84-91 10809901-6 2000 We determined glucose-induced first and second-phase insulin secretion, GLP-1-stimulated insulin secretion, arginine-stimulated insulin response (increase above prestimulus, DeltaIarg) and the maximal, i. e. highest absolute, insulin concentration (Imax). Glucose 14-21 insulin Homo sapiens 53-60 10809901-12 2000 The insulin concentration after the arginine bolus at > 25 mM glucose (n = 6) was 2773 +/- 855 pM vs. 7562 +/- 1168 pM for Imax (P = 0.003). Glucose 65-72 insulin Homo sapiens 4-11 10809901-13 2000 CONCLUSION: This novel insulin secretion test elicits a distinct pattern of plasma insulin concentrations in response to the secretagogues glucose, GLP-1 and arginine and is highly reproducible and can be used for differential characterization of islet function. Glucose 139-146 insulin Homo sapiens 23-30 10748179-4 2000 LiCl- and insulin-stimulated glucose transport were abolished by the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, wortmannin; however, LiCl stimulation of glycogen synthase was not. Glucose 29-36 insulin Homo sapiens 10-17 10809901-13 2000 CONCLUSION: This novel insulin secretion test elicits a distinct pattern of plasma insulin concentrations in response to the secretagogues glucose, GLP-1 and arginine and is highly reproducible and can be used for differential characterization of islet function. Glucose 139-146 insulin Homo sapiens 83-90 10748179-5 2000 In contrast to the rapid stimulation of glucose transport by insulin, transport stimulated by LiCl increased gradually over 3-5 h reaching 40% of the maximal insulin-stimulated level. Glucose 40-47 insulin Homo sapiens 61-68 10818070-0 2000 Aldose reductase inhibitor improves insulin-mediated glucose uptake and prevents migration of human coronary artery smooth muscle cells induced by high glucose. Glucose 53-60 insulin Homo sapiens 36-43 10783157-3 2000 Our findings show that insulin promotes APP metabolism by a glucose-independent mechanism. Glucose 60-67 insulin Homo sapiens 23-30 10877006-11 2000 CONCLUSIONS: Nateglinide produced rapid, short-lived, dose-related increases in plasma insulin that significantly lowered mealtime glucose excursions compared with placebo with no incidence of hypoglycemia. Glucose 131-138 insulin Homo sapiens 87-94 11421538-1 2000 OBJECTIVE: To investigate, in a clinical setting, the effect of implementation of continuous subcutaneous insulin infusion (CSII) on control of plasma glucose and to identify factors associated with improved glycemic control in patients with type 1 diabetes mellitus. Glucose 151-158 insulin Homo sapiens 106-113 10818070-7 2000 High glucose-induced suppression of insulin-mediated [(3)H]-deoxyglucose uptake, which was blocked by both calphostin C (100 nmol/L) and chelerythrine (1 micromol/L), was decreased by epalrestat (100 nmol/L). Glucose 5-12 insulin Homo sapiens 36-43 10810293-3 2000 As nitric oxide (NO) has been found to be a potent inhibitor of glucose-stimulated insulin secretion, we have now investigated a possible influence of exogenous NO and inhibition of endogenous NO production on islet acid glucan-1,4-alpha-glucosidase activity in relation to insulin release stimulated by glucose and l-arginine. Glucose 64-71 insulin Homo sapiens 83-90 10902570-0 2000 What couples glycolysis to mitochondrial signal generation in glucose-stimulated insulin secretion? Glucose 62-69 insulin Homo sapiens 81-88 10902577-5 2000 Furthermore, NO had an insulin-like effect in stimulating glucose transport and glucose oxidation in muscle, a major site for insulin action. Glucose 58-65 insulin Homo sapiens 23-30 10902577-5 2000 Furthermore, NO had an insulin-like effect in stimulating glucose transport and glucose oxidation in muscle, a major site for insulin action. Glucose 80-87 insulin Homo sapiens 23-30 10902577-6 2000 Addition of NAME to the reaction mixture completely blocked the stimulatory effect of insulin by inhibiting both NO production and glucose metabolism, without affecting the hormone-stimulated tyrosine or phosphatidyl-inositol 3-kinases of the membrane preparation. Glucose 131-138 insulin Homo sapiens 86-93 10902577-7 2000 Injection of NO in alloxan-induced diabetic mice mimicked the effect of insulin in the control of hyperglycemia (i.e., lowered the glucose content in plasma). Glucose 131-138 insulin Homo sapiens 72-79 10843180-0 2000 Variations in vitamin D-binding protein (group-specific component protein) are associated with fasting plasma insulin levels in Japanese with normal glucose tolerance. Glucose 149-156 insulin Homo sapiens 110-117 10843180-8 2000 In conclusion, genetic variations of DBP are associated with insulin resistance in Japanese with normal glucose tolerance, which might contribute to the development of type 2 diabetes. Glucose 104-111 insulin Homo sapiens 61-68 10810293-9 2000 We propose that an important inhibitory effect of NO on the insulin secretory processes stimulated by glucose and l-arginine is exerted via inactivation of islet acid glucan-1,4-alpha-glucosidase, a putative key enzyme in nutrient-stimulated insulin release. Glucose 102-109 insulin Homo sapiens 60-67 10810293-7 2000 Finally, in the presence of the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester, insulin release from isolated islets stimulated by glucose or l-arginine was markedly potentiated in parallel with an accompanying increase in the activities of acid glucan-1,4-alpha-glucosidase and acid alpha-glucosidase. Glucose 141-148 insulin Homo sapiens 90-97 10698091-1 2000 BACKGROUND: It has been shown that insulin resistance syndrome, including glucose intolerance, dyslipidemia, and hypertension, is frequently associated with coronary artery disease (CAD). Glucose 74-81 insulin Homo sapiens 35-42 10831183-7 2000 These data indicate that the rapid suppression of endogenous glucose production by insulin reflects primarily a decrease in hepatic glucose release, most likely due to inhibition of net glycogenolysis, combined with suppression of renal gluconeogenesis. Glucose 61-68 insulin Homo sapiens 83-90 10831183-7 2000 These data indicate that the rapid suppression of endogenous glucose production by insulin reflects primarily a decrease in hepatic glucose release, most likely due to inhibition of net glycogenolysis, combined with suppression of renal gluconeogenesis. Glucose 132-139 insulin Homo sapiens 83-90 10831183-9 2000 We conclude that peripheral insulin, in addition to its inhibition of glycogen degradation, regulates endogenous glucose production, in part, by modifying the splanchnic and renal substrate supply. Glucose 113-120 insulin Homo sapiens 28-35 10781824-1 2000 In the present study we have investigated the effect of increased serine/threonine phosphorylation of insulin receptor substrates-1 and -2 (IRS-1 and IRS-2) by okadaic acid pretreatment on brown adipocyte insulin signalling leading to glucose transport, an important metabolic effect of insulin in brown adipose tissue. Glucose 235-242 insulin Homo sapiens 102-109 10781824-4 2000 Furthermore, insulin-induced glucose uptake was totally abolished by the inhibitor in parallel with a total inhibition of insulin-induced protein kinase C (PKC) zeta activity. Glucose 29-36 insulin Homo sapiens 13-20 10781824-4 2000 Furthermore, insulin-induced glucose uptake was totally abolished by the inhibitor in parallel with a total inhibition of insulin-induced protein kinase C (PKC) zeta activity. Glucose 29-36 insulin Homo sapiens 122-129 10781824-6 2000 Our results suggest that downstream of PI 3-kinase, insulin signalling diverges into at least two independent pathways through Akt/PKB and PKC zeta, the PKC zeta pathway contributing to glucose transport induced by insulin in fetal brown adipocytes. Glucose 186-193 insulin Homo sapiens 52-59 10781824-6 2000 Our results suggest that downstream of PI 3-kinase, insulin signalling diverges into at least two independent pathways through Akt/PKB and PKC zeta, the PKC zeta pathway contributing to glucose transport induced by insulin in fetal brown adipocytes. Glucose 186-193 insulin Homo sapiens 215-222 10798747-0 2000 Insulin secretion and sensitivity after simultaneous pancreas-kidney transplantation estimated by continuous infusion of glucose with model assessment. Glucose 121-128 insulin Homo sapiens 0-7 10760274-1 2000 Elevated glucose concentrations stimulate the transcription of the pre-proinsulin (PPI), L-type pyruvate kinase (L-PK), and other genes in islet beta cells. Glucose 9-16 insulin Homo sapiens 71-81 10751207-4 2000 We propose that this is due to the effect of endogenous insulin on peripheral glucose uptake. Glucose 78-85 insulin Homo sapiens 56-63 10751207-5 2000 Second, during the spontaneous secondary decrease in plasma glucose after the glucose load, interstitial glucose decreased faster than plasma glucose, which may also be due to the effect of insulin on peripheral glucose uptake. Glucose 60-67 insulin Homo sapiens 190-197 10751207-5 2000 Second, during the spontaneous secondary decrease in plasma glucose after the glucose load, interstitial glucose decreased faster than plasma glucose, which may also be due to the effect of insulin on peripheral glucose uptake. Glucose 78-85 insulin Homo sapiens 190-197 10751207-5 2000 Second, during the spontaneous secondary decrease in plasma glucose after the glucose load, interstitial glucose decreased faster than plasma glucose, which may also be due to the effect of insulin on peripheral glucose uptake. Glucose 78-85 insulin Homo sapiens 190-197 10751207-5 2000 Second, during the spontaneous secondary decrease in plasma glucose after the glucose load, interstitial glucose decreased faster than plasma glucose, which may also be due to the effect of insulin on peripheral glucose uptake. Glucose 78-85 insulin Homo sapiens 190-197 10751207-5 2000 Second, during the spontaneous secondary decrease in plasma glucose after the glucose load, interstitial glucose decreased faster than plasma glucose, which may also be due to the effect of insulin on peripheral glucose uptake. Glucose 78-85 insulin Homo sapiens 190-197 10751207-6 2000 Third, during insulin-induced hypoglycemia, the decrease in interstitial glucose was less marked than that of plasma glucose, suggesting that hypoglycemia suppressed transfer of glucose into the interstitial tissue; subsequently, interstitial glucose remained lower than plasma glucose during its return to basal value, suggesting that the stimulatory effect of insulin on peripheral glucose uptake was protracted. Glucose 73-80 insulin Homo sapiens 14-21 10751207-6 2000 Third, during insulin-induced hypoglycemia, the decrease in interstitial glucose was less marked than that of plasma glucose, suggesting that hypoglycemia suppressed transfer of glucose into the interstitial tissue; subsequently, interstitial glucose remained lower than plasma glucose during its return to basal value, suggesting that the stimulatory effect of insulin on peripheral glucose uptake was protracted. Glucose 117-124 insulin Homo sapiens 14-21 10751207-6 2000 Third, during insulin-induced hypoglycemia, the decrease in interstitial glucose was less marked than that of plasma glucose, suggesting that hypoglycemia suppressed transfer of glucose into the interstitial tissue; subsequently, interstitial glucose remained lower than plasma glucose during its return to basal value, suggesting that the stimulatory effect of insulin on peripheral glucose uptake was protracted. Glucose 117-124 insulin Homo sapiens 14-21 10751207-6 2000 Third, during insulin-induced hypoglycemia, the decrease in interstitial glucose was less marked than that of plasma glucose, suggesting that hypoglycemia suppressed transfer of glucose into the interstitial tissue; subsequently, interstitial glucose remained lower than plasma glucose during its return to basal value, suggesting that the stimulatory effect of insulin on peripheral glucose uptake was protracted. Glucose 117-124 insulin Homo sapiens 14-21 10751207-6 2000 Third, during insulin-induced hypoglycemia, the decrease in interstitial glucose was less marked than that of plasma glucose, suggesting that hypoglycemia suppressed transfer of glucose into the interstitial tissue; subsequently, interstitial glucose remained lower than plasma glucose during its return to basal value, suggesting that the stimulatory effect of insulin on peripheral glucose uptake was protracted. Glucose 117-124 insulin Homo sapiens 14-21 10751207-6 2000 Third, during insulin-induced hypoglycemia, the decrease in interstitial glucose was less marked than that of plasma glucose, suggesting that hypoglycemia suppressed transfer of glucose into the interstitial tissue; subsequently, interstitial glucose remained lower than plasma glucose during its return to basal value, suggesting that the stimulatory effect of insulin on peripheral glucose uptake was protracted. Glucose 117-124 insulin Homo sapiens 14-21 10744911-8 2000 Conversely, supplementation of insulin during the preabsorptive time period improves glucose tolerance in certain clinical populations. Glucose 85-92 insulin Homo sapiens 31-38 10731469-11 2000 If prolonged, it results in a delayed increase in non-oxidative glucose disposal, which is most pronounced in subjects with low insulin sensitivity. Glucose 64-71 insulin Homo sapiens 128-135 10731472-11 2000 Over the 4 h feeding period, changes in insulin and glucose concentrations in cancer patients suggested relative glucose intolerance. Glucose 113-120 insulin Homo sapiens 40-47 10819247-3 2000 We investigated whether these gene variants associate with changes in the pattern of glucose-stimulated insulin secretion. Glucose 85-92 insulin Homo sapiens 104-111 10871199-8 2000 During both the basal and prandial insulin infusions, glucose disappearance promptly increased after initiation of the glucose infusion to rates that did not differ on the GLP-1 and saline study days. Glucose 54-61 insulin Homo sapiens 35-42 10871199-8 2000 During both the basal and prandial insulin infusions, glucose disappearance promptly increased after initiation of the glucose infusion to rates that did not differ on the GLP-1 and saline study days. Glucose 119-126 insulin Homo sapiens 35-42 11467326-1 2000 Implantation of glucose-responsive, insulin-secreting cells is promising in providing a treatment for type I diabetes, which is more effective, less invasive, and potentially less costly than conventional insulin injections. Glucose 16-23 insulin Homo sapiens 36-43 11467326-1 2000 Implantation of glucose-responsive, insulin-secreting cells is promising in providing a treatment for type I diabetes, which is more effective, less invasive, and potentially less costly than conventional insulin injections. Glucose 16-23 insulin Homo sapiens 205-212 11060717-2 2000 Prandial glucose regulation is aimed at restoring the first-phase insulin response that follows consumption of a meal, which is missing in patients with Type 2 diabetes. Glucose 9-16 insulin Homo sapiens 66-73 11060717-6 2000 Rapid elimination ensures that postprandial insulin levels quickly return to preprandial levels as the high prandial glucose level subsides. Glucose 117-124 insulin Homo sapiens 44-51 10770173-1 2000 In a case-control study that investigated the effect of intrauterine growth retardation (IUGR) on glucose homeostasis, 20-yr-old adults born with IUGR were shown to be hyperinsulinemic in an oral glucose tolerance test, suggestive of insulin resistance. Glucose 98-105 insulin Homo sapiens 173-180 10770173-1 2000 In a case-control study that investigated the effect of intrauterine growth retardation (IUGR) on glucose homeostasis, 20-yr-old adults born with IUGR were shown to be hyperinsulinemic in an oral glucose tolerance test, suggestive of insulin resistance. Glucose 196-203 insulin Homo sapiens 173-180 10770173-3 2000 We studied 26 IUGR-born subjects and 25 controls, aged 25 yr. Insulin sensitivity was assessed by peripheral glucose uptake and monitoring free fatty acid (FFA) concentrations under euglycemic hyperinsulinemic clamp. Glucose 109-116 insulin Homo sapiens 62-69 10770173-5 2000 Insulin-stimulated glucose uptake was significantly lower in IUGR-born subjects than in controls (6.7 +/- 2.9 vs. 8.0 +/- 1.9 mg/kg fat-free mass x min; P = 0.05), and the difference remained significant after adjustment for body mass index, total body fat, or waist to hip ratio. Glucose 19-26 insulin Homo sapiens 0-7 10770173-6 2000 In IUGR-born subjects, insulin-stimulated FFA suppression correlated significantly with peripheral glucose uptake (r2 = 0.23; P = 0.02). Glucose 99-106 insulin Homo sapiens 23-30 10770173-8 2000 In conclusion, IUGR subjects have decreased insulin-stimulated glucose uptake as early as 25 yr of age without major impairment of insulin secretion. Glucose 63-70 insulin Homo sapiens 44-51 10770173-9 2000 Low glucose uptake is associated with a lesser degree of FFA suppression in adipose tissue, which suggests a role of adipose tissue at an early stage of insulin resistance in these subjects. Glucose 4-11 insulin Homo sapiens 153-160 10770174-11 2000 Baseline reduction in Si was accompanied by elevated acute insulin response to glucose, which also fell in a dose-dependent manner. Glucose 79-86 insulin Homo sapiens 59-66 10770175-7 2000 Frequently sampled iv glucose tolerance tests revealed an increased responsivity of the acute insulin secretion (P = 0.04) and a nonsignificant trend toward improved insulin sensitivity. Glucose 22-29 insulin Homo sapiens 94-101 10792555-3 2000 Such abnormalities in endothelial function could represent the impact of subclinical disturbance of metabolism or alternatively the presence of a common cellular defect that influences both nitric oxide bioavailability and insulin mediated glucose disposal. Glucose 240-247 insulin Homo sapiens 223-230 10736369-4 2000 We review here our recent work on the effects of insulin, glucagon and epinephrine on plasma glutamine kinetics and its conversion to glucose by liver and kidney. Glucose 134-141 insulin Homo sapiens 49-56 10778867-5 2000 Insulin secretion was assessed immediately after completion of the 10-hour infusion by an intravenous glucose tolerance test. Glucose 102-109 insulin Homo sapiens 0-7 10778870-1 2000 The triglyceride content of skeletal muscle samples determined by lipid extraction correlates with the severity of insulin-resistant glucose metabolism in muscle. Glucose 133-140 insulin Homo sapiens 115-122 11390882-1 2000 Glucose-stimulated insulin secretion consists of a transient first phase followed by a sustained second phase. Glucose 0-7 insulin Homo sapiens 19-26 10861107-4 2000 RESULTS: The insulin level in fatty liver group was significantly higher than that in normal control group at 60 min, 120 min and 180 min after glucose intake (P<0.01) with the postpond peak. Glucose 144-151 insulin Homo sapiens 13-20 10928235-8 2000 Immediate pre-meal administration of the rapid-acting insulin analogue Aspart in patients with type 2 diabetes resulted in an improved postprandial glucose control compared to Actrapid injected immediately before the meal, but showed similar control compared to Actrapid injected 30 minutes before the meal. Glucose 148-155 insulin Homo sapiens 54-61 10928235-9 2000 These results indicate that the improved glucose control previously demonstrated with insulin Aspart compared to human insulin in healthy subjects and type 1 diabetic patients also applies to insulin-treated type 2 diabetic patients. Glucose 41-48 insulin Homo sapiens 86-93 10710341-5 2000 Coronary insulin infusion increased glucose extraction to 5 +/- 3% (P < 0.01 vs. basal) without changing plasma FFA or heart FFA extraction. Glucose 36-43 insulin Homo sapiens 9-16 10710341-8 2000 This suggests the increase in myocardial glucose extraction observed in response to an increment in systemic insulin concentration is mediated equally by a reduction in circulating FFA and by direct insulin action on the heart itself. Glucose 41-48 insulin Homo sapiens 109-116 10710341-8 2000 This suggests the increase in myocardial glucose extraction observed in response to an increment in systemic insulin concentration is mediated equally by a reduction in circulating FFA and by direct insulin action on the heart itself. Glucose 41-48 insulin Homo sapiens 199-206 10710341-9 2000 Coronary insulin infusion increased myocardial lactate extraction as well (from 20 +/- 10% to 29 +/- 9%, P < 0.05), suggesting the local action may include stimulation of a metabolic step distal to glucose transport and glycolysis. Glucose 201-208 insulin Homo sapiens 9-16 10710505-3 2000 Plasma glucose, insulin, and C-peptide concentrations were significantly (P < 0.01) higher in obese women in response to the graded intravenous glucose infusion, associated with a 40% (P < 0.005) greater insulin secretory response. Glucose 147-154 insulin Homo sapiens 210-217 10710505-7 2000 It is concluded that 1) obesity is associated with a shift to the left in the glucose-stimulated insulin secretory dose-response curve as well as a decrease in insulin clearance and 2) changes in insulin secretion and insulin clearance in obese women are more a function of insulin resistance than obesity. Glucose 78-85 insulin Homo sapiens 97-104 10710511-2 2000 Therefore, the present study determined the effects of PKC activation/inhibition on insulin-mediated glucose transport in incubated human skeletal muscle and primary adipocytes to discern a potential role for PKC in insulin action. Glucose 101-108 insulin Homo sapiens 84-91 10710511-10 2000 These data demonstrate that certain PKC inhibitors augment insulin-mediated glucose uptake and suggest that PKC may modulate insulin action in human skeletal muscle. Glucose 76-83 insulin Homo sapiens 59-66 10889799-1 2000 The metabolic syndrome represents a vicious cycle whereby insulin resistance leads to compensatory hyperinsulinaemia, which maintains normal plasma glucose but may exacerbate insulin resistance. Glucose 148-155 insulin Homo sapiens 58-65 10889799-1 2000 The metabolic syndrome represents a vicious cycle whereby insulin resistance leads to compensatory hyperinsulinaemia, which maintains normal plasma glucose but may exacerbate insulin resistance. Glucose 148-155 insulin Homo sapiens 104-111 10889799-2 2000 Excess insulin secretion may eventually reduce beta-cell function due to amyloid deposition, leading to raised blood glucose and further deterioration of beta-cell function and insulin sensitivity via glucose toxicity. Glucose 117-124 insulin Homo sapiens 7-14 10823244-1 2000 Insulin secretion is finely tuned to the requirements of tissues by tight coupling to prevailing blood glucose levels. Glucose 103-110 insulin Homo sapiens 0-7 12899390-0 2000 Responsibility of insulin to the change of glucose level in newborn small for gestational age infants. Glucose 43-50 insulin Homo sapiens 18-25 10741566-1 2000 The purpose of this study was to explore possible calculations using oral glucose tolerance test (OGTT) values in order to develop a simple measure of insulin sensitivity. Glucose 74-81 insulin Homo sapiens 151-158 10741566-2 2000 We devised a formula for an insulin sensitivity index, ISI(0,120), that uses the fasting (0 min) and 120 min post-oral glucose (OGTT) insulin and glucose concentrations. Glucose 119-126 insulin Homo sapiens 28-35 10741566-2 2000 We devised a formula for an insulin sensitivity index, ISI(0,120), that uses the fasting (0 min) and 120 min post-oral glucose (OGTT) insulin and glucose concentrations. Glucose 146-153 insulin Homo sapiens 28-35 10768093-1 2000 AIMS/HYPOTHESIS: Phosphoinositide 3-kinase (PI 3K) plays a central part in the mediation of insulin-stimulated glucose disposal. Glucose 111-118 insulin Homo sapiens 92-99 10784225-12 2000 CONCLUSIONS: Substitution of insulin lispro for soluble insulin in a multiple injection regimen improved post-prandial glucose control at the expense of an increase in fasting and pre-prandial glucose levels. Glucose 119-126 insulin Homo sapiens 29-36 10784225-12 2000 CONCLUSIONS: Substitution of insulin lispro for soluble insulin in a multiple injection regimen improved post-prandial glucose control at the expense of an increase in fasting and pre-prandial glucose levels. Glucose 119-126 insulin Homo sapiens 56-63 10868952-2 2000 Four hours before the clamp, the subjects performed one-legged exercise for 1 h. In the exercised leg, insulin more rapidly activated glucose uptake (half activation time [t1/2] = 11 vs. 34 min) and glycogen synthase activity (t1/2 = 8 vs. 17 min), and the magnitude of increase was two- to fourfold higher compared with the rested leg. Glucose 134-141 insulin Homo sapiens 103-110 10698169-6 2000 In betaTC3 cells, expression of GRK2 or beta-arrestin-1 attenuated GIP-induced insulin release and cAMP production, whereas glucose-stimulated insulin secretion was not affected. Glucose 124-131 insulin Homo sapiens 143-150 10786930-3 2000 METHODS: The insulin sensitivity was investigated by 75 g oral glucose tolerance test (OGTT) and modified insulin suppression test. Glucose 63-70 insulin Homo sapiens 13-20 10786930-7 2000 With the modified insulin suppression test, the steady-state plasma glucose levels (SSPG) were higher in the offspring of parents with essential hypertension (138+/-43 mg/dl) than in the control group (95+/-26 mg/dl). Glucose 68-75 insulin Homo sapiens 18-25 10697112-0 2000 Engineering cells for glucose-sensitive production of insulin: toward genetic reconstruction. Glucose 22-29 insulin Homo sapiens 54-61 10669654-3 2000 Areas under the glucose and insulin response curves (AUC glucose and AUC insulin) were used to reflect glucose and insulin levels during oral glucose tolerance tests. Glucose 57-64 insulin Homo sapiens 28-35 10669654-3 2000 Areas under the glucose and insulin response curves (AUC glucose and AUC insulin) were used to reflect glucose and insulin levels during oral glucose tolerance tests. Glucose 57-64 insulin Homo sapiens 28-35 10851805-1 2000 The role of pancreatic beta-cells is fundamental in the control endocrine system, maintaining the blood glucose homeostais in a physiological regime, via the glucose-induced release of insulin. Glucose 104-111 insulin Homo sapiens 185-192 10833328-6 2000 03) and fasting plasma glucose concentrations (r = 0.57, P = 0.02) and were negatively correlated to glucose disposal at physiologic insulin concentrations (750 +/- 40 pmol/L) during the clamp (r = -0. Glucose 101-108 insulin Homo sapiens 133-140 10813588-1 2000 Insulin secretion rates are greater after oral glucose than after parenteral administration of an equivalent glucose load. Glucose 47-54 insulin Homo sapiens 0-7 10813588-1 2000 Insulin secretion rates are greater after oral glucose than after parenteral administration of an equivalent glucose load. Glucose 109-116 insulin Homo sapiens 0-7 10813588-10 2000 After oral glucose, plasma insulin, C-peptide, and insulin secretion rates further increased in all four groups. Glucose 11-18 insulin Homo sapiens 27-34 10772913-0 2000 Quantification of SNARE protein levels in 3T3-L1 adipocytes: implications for insulin-stimulated glucose transport. Glucose 97-104 insulin Homo sapiens 78-85 10772913-1 2000 Insulin-stimulates glucose transport in peripheral tissues by stimulating the movement ("translocation") of a pool of intracellular vesicles containing the glucose transporter Glut4 to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 10781824-0 2000 Okadaic acid inhibits insulin-induced glucose transport in fetal brown adipocytes in an Akt-independent and protein kinase C zeta-dependent manner. Glucose 38-45 insulin Homo sapiens 22-29 10764845-2 2000 Insulin resistance is a state of reduced insulin sensitivity, an inability of insulin to lower plasma glucose levels through suppression of hepatic glucose production and stimulation of glucose utilization in skeletal muscle and adipose tissue. Glucose 102-109 insulin Homo sapiens 0-7 10764845-2 2000 Insulin resistance is a state of reduced insulin sensitivity, an inability of insulin to lower plasma glucose levels through suppression of hepatic glucose production and stimulation of glucose utilization in skeletal muscle and adipose tissue. Glucose 148-155 insulin Homo sapiens 0-7 10764845-2 2000 Insulin resistance is a state of reduced insulin sensitivity, an inability of insulin to lower plasma glucose levels through suppression of hepatic glucose production and stimulation of glucose utilization in skeletal muscle and adipose tissue. Glucose 148-155 insulin Homo sapiens 0-7 10776065-5 2000 An increase is seen in maximal oxygen consumption, in the insulin stimulated glucose uptake and in the muscular mass and bone mineral content of the lower extremities. Glucose 77-84 insulin Homo sapiens 58-65 10767564-4 2000 The insulin absorption enhancement effect was not increased in proportion to the amount of DHA in the emulsion, the mean T(max) value of the serum glucose-time curve could be extended to twice that of the emulsion without PF 127. Glucose 147-154 insulin Homo sapiens 4-11 10751195-7 2000 Insulin, which increases glucose uptake by these cells, increased the cell lactate content and the lactate-to-pyruvate ratio (LPR) by 81 and 97%, respectively (both P < 0.05), indicating that the hormone increased aerobic glycolysis and the redox potential. Glucose 25-32 insulin Homo sapiens 0-7 10751195-8 2000 The effects of insulin on LPR and cGMP production were blocked by removing glucose or by adding 2-deoxyglucose to the incubation media and were duplicated by the reducing substrate, beta-hydroxybutyrate. Glucose 75-82 insulin Homo sapiens 15-22 10818510-0 2000 Insulin effects on glucose metabolism, memory, and plasma amyloid precursor protein in Alzheimer"s disease differ according to apolipoprotein-E genotype. Glucose 19-26 insulin Homo sapiens 0-7 10818510-3 2000 We examined the effects of intravenous insulin administration while maintaining euglycemia on insulin-mediated glucose disposal, memory, and plasma APP in patients with AD and normal adults of varying ApoE genotypes. Glucose 111-118 insulin Homo sapiens 94-101 10818510-4 2000 AD subjects without an epsilon 4 allele had significantly lower insulin-mediated glucose disposal rates than did AD patients with an epsilon 4 allele (p < 0.03) or than did normal adults without an epsilon 4 allele (p < 0.02). Glucose 81-88 insulin Homo sapiens 64-71 10762282-4 2000 Insulin sensitivity was assessed by measurement of whole body glucose uptake (M-value) during a 3-4 h euglycaemic clamp, directly after the 24 h insulin infusion and compared to the M-value on a control day, at least 1 week apart from the 24 h insulin infusion. Glucose 62-69 insulin Homo sapiens 0-7 10871195-14 2000 Assessment of C-peptide kinetics with and without infusion of somatostatin results in nearly identical secretion rates for insulin during an oral glucose tolerance test. Glucose 146-153 insulin Homo sapiens 123-130 10898126-5 2000 Basal insulin release is increased as a result of an increase of the low-Km component of glucose phosphorylation. Glucose 89-96 insulin Homo sapiens 6-13 10898130-0 2000 Evaluation of insulin response in glucose tolerance test in a patient with Werner"s syndrome: a 16-year follow-up study. Glucose 34-41 insulin Homo sapiens 14-21 10775552-6 2000 Insulin sensitivity was measured according to the steady-state plasma glucose (SSPG) method on the seventh day of each diet. Glucose 70-77 insulin Homo sapiens 0-7 10853708-7 2000 In absence of activin A, 8.3 mM and 16.7 mM glucose significantly increased insulin secretion, with a dose-dependent pattern. Glucose 44-51 insulin Homo sapiens 76-83 10853708-8 2000 In presence of a non stimulatory concentration of glucose (3.3 mM), activin A significantly increased insulin secretion starting from low concentration (0.1 nM). Glucose 50-57 insulin Homo sapiens 102-109 10853708-10 2000 The present data could support a role for activin A in human endocrine pancreas in modulating insulin response to different glucose concentrations. Glucose 124-131 insulin Homo sapiens 94-101 10854077-4 2000 In hypertension we find insulin resistance mainly in skeletal muscle involving the conversion of glucose to glycogen independently of blood flow. Glucose 97-104 insulin Homo sapiens 24-31 10778883-1 2000 This study tested the hypothesis that the integrated plasma insulin response to oral glucose is a more sensitive predictor of the fasting plasma leptin concentration than the body mass index (BMI) or waist to hip ratio (WHR). Glucose 85-92 insulin Homo sapiens 60-67 10778883-3 2000 The results demonstrated that fasting plasma leptin concentrations were significantly correlated with both the BMI (r = .64, P < .001) and the plasma insulin response to glucose (r = .61, P < .001), but not with the WHR (r = .27). Glucose 173-180 insulin Homo sapiens 153-160 10778883-9 2000 These results indicate that while both the plasma insulin response to glucose and the BMI are significantly associated with the fasting plasma leptin concentration, the plasma insulin response appears more closely associated with the plasma leptin concentration. Glucose 70-77 insulin Homo sapiens 50-57 10710341-0 2000 Comparison of local and systemic effects of insulin on myocardial glucose extraction in ischemic heart disease. Glucose 66-73 insulin Homo sapiens 44-51 10710496-1 2000 It has been suggested that insulin-induced suppression of endogenous glucose production (EGP) may be counteracted independently of increased epinephrine (Epi) or glucagon during moderate hypoglycemia. Glucose 69-76 insulin Homo sapiens 27-34 10710505-2 2000 Measurements were also made of insulin clearance, resistance to insulin-mediated glucose, uptake, and the plasma glucose, insulin, and C-peptide concentrations at hourly intervals from 8:00 AM to 4:00 PM in response to breakfast and lunch. Glucose 81-88 insulin Homo sapiens 64-71 10710505-2 2000 Measurements were also made of insulin clearance, resistance to insulin-mediated glucose, uptake, and the plasma glucose, insulin, and C-peptide concentrations at hourly intervals from 8:00 AM to 4:00 PM in response to breakfast and lunch. Glucose 81-88 insulin Homo sapiens 64-71 10710505-3 2000 Plasma glucose, insulin, and C-peptide concentrations were significantly (P < 0.01) higher in obese women in response to the graded intravenous glucose infusion, associated with a 40% (P < 0.005) greater insulin secretory response. Glucose 147-154 insulin Homo sapiens 16-23 10694991-3 2000 The resistance to insulin-mediated glucose transport appears to be greater in skeletal muscle from GDM subjects than from pregnancy alone. Glucose 35-42 insulin Homo sapiens 18-25 10768089-5 2000 Insulin-stimulated glucose uptake showed a more modest correlation between monozygotic twins (r = 0.46; p = 0.015). Glucose 19-26 insulin Homo sapiens 0-7 10768089-9 2000 In the current study, genetic variance accounted almost 60% for the variance in glucose-stimulated insulin secretion and almost 40% for the variance in insulin-stimulated glucose uptake. Glucose 80-87 insulin Homo sapiens 99-106 10768090-0 2000 Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes. Glucose 66-73 insulin Homo sapiens 18-25 10868854-0 2000 Use of the oral glucose tolerance test to assess insulin release and insulin sensitivity. Glucose 16-23 insulin Homo sapiens 49-56 10868854-1 2000 OBJECTIVE: The oral glucose tolerance test (OGTT) has often been used to evaluate apparent insulin release and insulin resistance in various clinical settings. Glucose 20-27 insulin Homo sapiens 91-98 10868854-1 2000 OBJECTIVE: The oral glucose tolerance test (OGTT) has often been used to evaluate apparent insulin release and insulin resistance in various clinical settings. Glucose 20-27 insulin Homo sapiens 111-118 10868963-0 2000 Glucose modulation of insulin mRNA levels is dependent on transcription factor PDX-1 and occurs independently of changes in intracellular Ca2+. Glucose 0-7 insulin Homo sapiens 22-29 10868963-1 2000 Glucose regulates insulin production in pancreatic beta-cells in the long term by stimulating insulin gene transcription. Glucose 0-7 insulin Homo sapiens 18-25 10868963-1 2000 Glucose regulates insulin production in pancreatic beta-cells in the long term by stimulating insulin gene transcription. Glucose 0-7 insulin Homo sapiens 94-101 10868963-3 2000 The availability of a human beta-like cell line, NES2Y, which lacks PDX-1 but expresses the insulin gene, allowed us to determine whether PDX-1 was essential for the stimulatory effect of glucose on insulin mRNA levels. Glucose 188-195 insulin Homo sapiens 199-206 10868963-5 2000 However, in NES2Y cells stably transfected with PDX-1 (NES-PDX-1), glucose exhibited a marked stimulatory effect on both the insulin promoter (5+/-0.2-fold, n = 6) and insulin mRNA levels (4.8+/-0.5-fold, n = 4). Glucose 67-74 insulin Homo sapiens 125-132 10868963-5 2000 However, in NES2Y cells stably transfected with PDX-1 (NES-PDX-1), glucose exhibited a marked stimulatory effect on both the insulin promoter (5+/-0.2-fold, n = 6) and insulin mRNA levels (4.8+/-0.5-fold, n = 4). Glucose 67-74 insulin Homo sapiens 168-175 10868963-7 2000 Despite the loss of control of Ca2+ channel activity, NES-PDX-1 cells maintained normal glucose-responsive insulin gene regulation. Glucose 88-95 insulin Homo sapiens 107-114 10868963-8 2000 These results demonstrate that glucose modulation of insulin mRNA levels is dependent on the activity of PDX-1 and that these effects are independent of changes in intracellular Ca2+ concentrations. Glucose 31-38 insulin Homo sapiens 53-60 10793398-9 2000 Multiple regression analysis showed that obesity, as reflected by either the body mass index or waist circumference, had a closer association than plasma insulin with the fasting plasma glucose concentration, blood pressure, and high-density lipoprotein-cholesterol and triglyceride concentrations. Glucose 186-193 insulin Homo sapiens 154-161 10720029-7 2000 Compared with ov-NAO, 31% of ov-PAO women had reduced glucose responses after insulin (K(itt)), suggesting mild insulin resistance, and 35% had high density lipoprotein levels below 35 mg/dL, a level considered to represent significant cardiovascular risk. Glucose 54-61 insulin Homo sapiens 78-85 10720071-1 2000 This study was initiated to see if defects in the ability of physiological hyperinsulinemia (approximately 60 microU/mL) to stimulate glucose uptake in healthy, nondiabetic volunteers are associated with increases in concentrations of plasma glucose and free fatty acid (FFA) when measured at basal insulin concentrations (approximately 10 microU/mL). Glucose 134-141 insulin Homo sapiens 80-87 10720071-1 2000 This study was initiated to see if defects in the ability of physiological hyperinsulinemia (approximately 60 microU/mL) to stimulate glucose uptake in healthy, nondiabetic volunteers are associated with increases in concentrations of plasma glucose and free fatty acid (FFA) when measured at basal insulin concentrations (approximately 10 microU/mL). Glucose 242-249 insulin Homo sapiens 80-87 10720071-3 2000 Resistance to insulin-mediated glucose disposal during physiological hyperinsulinemia was determined by suppressing endogenous insulin and determining the steady-state plasma glucose (SSPG) and steady-state plasma insulin (SSPI) concentrations at the end of a 3-h infusion, period during which glucose (267 mg/m2 x min) and insulin (32 mU/m2 x min) were infused at a constant rate. Glucose 31-38 insulin Homo sapiens 14-21 10720071-3 2000 Resistance to insulin-mediated glucose disposal during physiological hyperinsulinemia was determined by suppressing endogenous insulin and determining the steady-state plasma glucose (SSPG) and steady-state plasma insulin (SSPI) concentrations at the end of a 3-h infusion, period during which glucose (267 mg/m2 x min) and insulin (32 mU/m2 x min) were infused at a constant rate. Glucose 31-38 insulin Homo sapiens 74-81 10720071-3 2000 Resistance to insulin-mediated glucose disposal during physiological hyperinsulinemia was determined by suppressing endogenous insulin and determining the steady-state plasma glucose (SSPG) and steady-state plasma insulin (SSPI) concentrations at the end of a 3-h infusion, period during which glucose (267 mg/m2 x min) and insulin (32 mU/m2 x min) were infused at a constant rate. Glucose 31-38 insulin Homo sapiens 74-81 10720071-3 2000 Resistance to insulin-mediated glucose disposal during physiological hyperinsulinemia was determined by suppressing endogenous insulin and determining the steady-state plasma glucose (SSPG) and steady-state plasma insulin (SSPI) concentrations at the end of a 3-h infusion, period during which glucose (267 mg/m2 x min) and insulin (32 mU/m2 x min) were infused at a constant rate. Glucose 31-38 insulin Homo sapiens 74-81 10720071-10 2000 The results presented demonstrate that individual differences in the ability of elevated insulin concentrations to stimulate muscle glucose disposal are significantly correlated with variations in insulin regulation of plasma glucose and FFA concentrations at basal insulin concentrations. Glucose 132-139 insulin Homo sapiens 89-96 10720071-10 2000 The results presented demonstrate that individual differences in the ability of elevated insulin concentrations to stimulate muscle glucose disposal are significantly correlated with variations in insulin regulation of plasma glucose and FFA concentrations at basal insulin concentrations. Glucose 132-139 insulin Homo sapiens 197-204 10720071-10 2000 The results presented demonstrate that individual differences in the ability of elevated insulin concentrations to stimulate muscle glucose disposal are significantly correlated with variations in insulin regulation of plasma glucose and FFA concentrations at basal insulin concentrations. Glucose 132-139 insulin Homo sapiens 197-204 10720071-10 2000 The results presented demonstrate that individual differences in the ability of elevated insulin concentrations to stimulate muscle glucose disposal are significantly correlated with variations in insulin regulation of plasma glucose and FFA concentrations at basal insulin concentrations. Glucose 226-233 insulin Homo sapiens 89-96 10720071-10 2000 The results presented demonstrate that individual differences in the ability of elevated insulin concentrations to stimulate muscle glucose disposal are significantly correlated with variations in insulin regulation of plasma glucose and FFA concentrations at basal insulin concentrations. Glucose 226-233 insulin Homo sapiens 197-204 10720071-10 2000 The results presented demonstrate that individual differences in the ability of elevated insulin concentrations to stimulate muscle glucose disposal are significantly correlated with variations in insulin regulation of plasma glucose and FFA concentrations at basal insulin concentrations. Glucose 226-233 insulin Homo sapiens 197-204 10720074-9 2000 However, when the total amount of dextrose infused during the clamp (grams of dextrose per kg BW) was included into the regression model, this variable was significantly related to the changes in serum leptin (P = 0.001), whereas circulating insulin and glucose had no additional effect. Glucose 34-42 insulin Homo sapiens 242-249 10720082-7 2000 Insulin-mediated glucose disposal (2.23 +/- 0.74 vs. 2.38 +/- 0.99 mg/kg(-1) x min(-1)) and glucose metabolic clearance rate (2.28 +/- 0.85 vs. 2.48 +/- 1.03 mL/kg(-1) x min(-1)) were similar after placebo and after the drug. Glucose 17-24 insulin Homo sapiens 0-7 11229109-3 2000 Post-oral glucose load serum insulin level (2 hrs) was determined and this was used as a marker for insulin resistance. Glucose 10-17 insulin Homo sapiens 29-36 11229109-9 2000 The post oral glucose load serum insulin levels in the study ranged from 57.65 to 210.81 microU/ml. Glucose 14-21 insulin Homo sapiens 33-40 11229109-11 2000 The correlation coefficient ("r" value) between post oral glucose load serum insulin levels and left ventricular mass and left ventricular mass index were calculated. Glucose 58-65 insulin Homo sapiens 77-84 11229109-12 2000 CONCLUSION: A strong positive correlation was observed between the post oral glucose load serum insulin levels and left ventricular mass ("r" = +0.750). Glucose 77-84 insulin Homo sapiens 96-103 11229109-13 2000 A strong positive correlation between post oral glucose load serum insulin levels and left ventricular mass index ("r" = +0.757) was also observed. Glucose 48-55 insulin Homo sapiens 67-74 10930100-8 2000 Elevated glucose consumption within the tumor might be addressed as one of the reasons for hypoglycemia, not due to the elevated serum levels of insulin or IGF, but due to the closely related blood glucose level. Glucose 9-16 insulin Homo sapiens 145-152 10714756-4 2000 Oral glucose tolerance test (OGTT) was performed with simultaneous measurement of insulin and serum trypsin. Glucose 5-12 insulin Homo sapiens 82-89 10756492-4 2000 Whereas 24-hour LH inversely correlated with body mass index (r = .37, P = .04), 24-hour hormone profile, and basal or glucose-stimulated serum insulin levels did not correlate in group P-1. Glucose 119-126 insulin Homo sapiens 144-151 10726916-2 2000 Insulin sensitivity and glucose effectiveness were determined by analyzing glucose and insulin data from the FSIGTT with Bergman"s minimal model technique for glucose. Glucose 75-82 insulin Homo sapiens 0-7 10726916-2 2000 Insulin sensitivity and glucose effectiveness were determined by analyzing glucose and insulin data from the FSIGTT with Bergman"s minimal model technique for glucose. Glucose 75-82 insulin Homo sapiens 0-7 10726923-0 2000 Insulin-mediated glucose disposal is decreased in normal subjects with relatively low plasma magnesium concentrations. Glucose 17-24 insulin Homo sapiens 0-7 10726923-6 2000 These results indicate that variations in the plasma Mg concentration have a relatively modest but significant effect on insulin-mediated glucose disposal in healthy subjects, with lower plasma Mg concentrations associated with increased insulin resistance. Glucose 138-145 insulin Homo sapiens 121-128 10812932-6 2000 Familial components also appear to account for approximately 50% of the variation and insulin action (as commonly defined by glucose metabolic effects). Glucose 125-132 insulin Homo sapiens 86-93 11236238-2 2000 Insulin resistance is characterised by an impaired insulin-mediated glucose uptake. Glucose 68-75 insulin Homo sapiens 0-7 10751238-5 2000 Insulin resistance (IR) was calculated using the homeostasis model assessment (HOMA) based on a product of fasting plasma glucose and insulin concentrations. Glucose 122-129 insulin Homo sapiens 0-7 10684630-1 2000 Previously, we have described significant effects of human insulin on glucose metabolism in the yeast Saccharomyces cerevisiae under conditions of growth limitation. Glucose 70-77 insulin Homo sapiens 59-66 10684630-5 2000 In addition, glycosyl-phosphatidylinositol-specific phospholipase C (GPI-PLC), which in isolated rat adipocytes is activated by insulin, was stimulated to up to 5-fold by glucose and 10-fold by glucose plus insulin in both yeast spheroplasts and intact cells leading to a concentration-dependent leftward shift of the glucose-response curve for activation of the GPI-PLC. Glucose 171-178 insulin Homo sapiens 128-135 10684630-5 2000 In addition, glycosyl-phosphatidylinositol-specific phospholipase C (GPI-PLC), which in isolated rat adipocytes is activated by insulin, was stimulated to up to 5-fold by glucose and 10-fold by glucose plus insulin in both yeast spheroplasts and intact cells leading to a concentration-dependent leftward shift of the glucose-response curve for activation of the GPI-PLC. Glucose 194-201 insulin Homo sapiens 128-135 10684630-8 2000 As the GPI-PLC reaction is rate limiting, the efficiency of the two-step anchor cleavage was significantly increased when insulin was present together with glucose as compared to glucose alone. Glucose 156-163 insulin Homo sapiens 122-129 10684630-8 2000 As the GPI-PLC reaction is rate limiting, the efficiency of the two-step anchor cleavage was significantly increased when insulin was present together with glucose as compared to glucose alone. Glucose 179-186 insulin Homo sapiens 122-129 10671942-6 2000 Insulin sensitivity and secretion were determined through a frequently sampled intravenous glucose tolerance test with minimal model analysis. Glucose 91-98 insulin Homo sapiens 0-7 10753041-6 2000 When related to the 3-year follow-up, the baseline product of AIR at 14 mmol/l glucose times insulin sensitivity, insulin effect index (IE) (r = -0.40, p < 0.001) and the arginine-induced glucagon response at 14 mmol/l glucose (AGR, r = 0.28, p = 0.009) both correlated with follow-up 2-h glucose. Glucose 79-86 insulin Homo sapiens 93-100 10753041-9 2000 In a multiple regression, alterations in 2-h glucose over the 3 years were independently determined by changes in fasting insulin and glucagon secretion (r = 0.424, p < 0.001). Glucose 45-52 insulin Homo sapiens 122-129 10753041-10 2000 CONCLUSION/INTERPRETATION: Low insulin secretion, when judged in relation to insulin sensitivity, and high glucagon secretion, determine glucose tolerance over time in the individual subject. Glucose 137-144 insulin Homo sapiens 31-38 10811296-3 2000 Glucose infusion rate (GIR) was measured as a reverse index for insulin resistance by euglycemic glucose clamp study using an artificial pancreas in 20 of 102 diabetic patients. Glucose 0-7 insulin Homo sapiens 64-71 10868826-9 2000 Fasting insulin concentration accounted for approximately one-third of the variability in insulin-mediated glucose disposal, and the use of fasting plasma glucose and insulin concentrations to calculate more sophisticated estimates of insulin resistance appears to offer little advantage over the fasting plasma insulin concentration. Glucose 107-114 insulin Homo sapiens 90-97 10868826-9 2000 Fasting insulin concentration accounted for approximately one-third of the variability in insulin-mediated glucose disposal, and the use of fasting plasma glucose and insulin concentrations to calculate more sophisticated estimates of insulin resistance appears to offer little advantage over the fasting plasma insulin concentration. Glucose 107-114 insulin Homo sapiens 90-97 10868835-2 2000 We used a pedigree-based approach to test the hypothesis that beta-cell compensation to the insulin resistance associated with obesity is defective among individuals predisposed to diabetes by virtue of a strong family history of type 2 diabetes before the development of diabetes or glucose intolerance. Glucose 284-291 insulin Homo sapiens 92-99 10868835-5 2000 The acute insulin response to glucose (AIRglucose) was determined and insulin sensitivity (S(I)) estimated by minimal model analysis of FSIGT data. Glucose 30-37 insulin Homo sapiens 10-17 10868933-1 2000 Insulin and contraction increase glucose transport in an additive fashion in skeletal muscle. Glucose 33-40 insulin Homo sapiens 0-7 10766028-1 2000 Proinsulin C-peptide ameliorates renal and autonomic nerve function and increases skeletal muscle blood flow, oxygen uptake and glucose transport in patients with insulin-dependent diabetes mellitus. Glucose 128-135 insulin Homo sapiens 0-10 10766028-1 2000 Proinsulin C-peptide ameliorates renal and autonomic nerve function and increases skeletal muscle blood flow, oxygen uptake and glucose transport in patients with insulin-dependent diabetes mellitus. Glucose 128-135 insulin Homo sapiens 11-20 10657266-7 2000 In a multivariate linear stepwise analysis (n=72), a model including body fat, waist/hip ratio, fasting plasma glucose concentration and insulin-mediated glucose uptake explained 47% of the variability of the change in the LF/HF ratio, with body fat (t=-3.11; P<0.01) and insulin-mediated glucose uptake (t=-3.48; P<0. Glucose 154-161 insulin Homo sapiens 137-144 10657266-7 2000 In a multivariate linear stepwise analysis (n=72), a model including body fat, waist/hip ratio, fasting plasma glucose concentration and insulin-mediated glucose uptake explained 47% of the variability of the change in the LF/HF ratio, with body fat (t=-3.11; P<0.01) and insulin-mediated glucose uptake (t=-3.48; P<0. Glucose 154-161 insulin Homo sapiens 137-144 10730548-6 2000 In 3 large comparative trials, insulin glargine decreased glycosylated haemoglobin and/or fasting blood glucose levels to a similar extent to that seen with NPH insulin in patients with insulin-dependent or non-insulin-dependent type 2 diabetes mellitus, either as monotherapy or in combination with oral hypoglycaemic agents. Glucose 104-111 insulin Homo sapiens 31-38 10746482-3 2000 Insulin sensitivity (Si) was estimated as the rate of glucose disappearance divided by the area under the insulin curve during an intravenous glucose tolerance test. Glucose 54-61 insulin Homo sapiens 0-7 10746482-3 2000 Insulin sensitivity (Si) was estimated as the rate of glucose disappearance divided by the area under the insulin curve during an intravenous glucose tolerance test. Glucose 142-149 insulin Homo sapiens 0-7 10746484-2 2000 METHODS: Insulin sensitivity was assessed after an acute dose (day 3) and 19 days continuous treatment (days 3-21) using the isoglycaemic, hyperinsulinaemic glucose clamp with D[3-3H] labelled glucose, a variable D[3-3H] priming dose and a "hot" glucose infusion. Glucose 157-164 insulin Homo sapiens 9-16 10746484-2 2000 METHODS: Insulin sensitivity was assessed after an acute dose (day 3) and 19 days continuous treatment (days 3-21) using the isoglycaemic, hyperinsulinaemic glucose clamp with D[3-3H] labelled glucose, a variable D[3-3H] priming dose and a "hot" glucose infusion. Glucose 193-200 insulin Homo sapiens 9-16 10868943-7 2000 GSK-3 expression was related to in vivo insulin action, as GSK-3 protein was negatively correlated with maximal insulin-stimulated glucose disposal rates. Glucose 131-138 insulin Homo sapiens 40-47 10868945-5 2000 Impaired glucose transport activity was noted at all insulin concentrations (0.6-60 nmol/l). Glucose 9-16 insulin Homo sapiens 53-60 10868943-7 2000 GSK-3 expression was related to in vivo insulin action, as GSK-3 protein was negatively correlated with maximal insulin-stimulated glucose disposal rates. Glucose 131-138 insulin Homo sapiens 112-119 10868943-8 2000 In summary, GSK-3 protein levels and total activities are 1) elevated in type 2 diabetic muscle independent of obesity and 2) inversely correlated with both GS activity and maximally insulin-stimulated glucose disposal. Glucose 202-209 insulin Homo sapiens 183-190 10868944-2 2000 To determine whether insulin-induced stimulation of splanchnic glucose uptake (SGU) is also impaired, we simultaneously measured leg glucose uptake (LGU) and SGU in 14 nondiabetic subjects and 16 subjects with type 2 diabetes using a combined organ catheterization-tracer infusion technique. Glucose 63-70 insulin Homo sapiens 21-28 10868944-5 2000 Total body glucose disappearance was lower (P < 0.01) and glucose production higher (P < 0.01) during both insulin infusions in the diabetic compared with the nondiabetic subjects, indicating insulin resistance. Glucose 11-18 insulin Homo sapiens 113-120 10651836-0 2000 Assessment of human muscle glycogen synthesis and total glucose content by in vivo 13C MRS. BACKGROUND: Obesity is often accompanied by a decreased ability of insulin to stimulate glucose uptake and glycogenesis in skeletal muscle. Glucose 180-187 insulin Homo sapiens 159-166 10868945-8 2000 Impaired insulin signal transduction in skeletal muscle from type 2 diabetic patients may partly account for reduced insulin-stimulated glucose transport; however, additional defects are likely to play a role. Glucose 136-143 insulin Homo sapiens 9-16 10651836-1 2000 The aim of this study was to investigate the rate of glycogen formation and of muscular glucose content in relation to insulin sensitivity under euglycemic conditions. Glucose 88-95 insulin Homo sapiens 119-126 10868945-8 2000 Impaired insulin signal transduction in skeletal muscle from type 2 diabetic patients may partly account for reduced insulin-stimulated glucose transport; however, additional defects are likely to play a role. Glucose 136-143 insulin Homo sapiens 117-124 10685525-6 2000 Insulin resistance was estimated by continuous infusion of glucose with model assessment in the early follicular phase. Glucose 59-66 insulin Homo sapiens 0-7 10694797-0 2000 Glucose regulated production of human insulin in rat hepatocytes. Glucose 0-7 insulin Homo sapiens 38-45 10694797-2 2000 To this end, we have developed an insulin transgene whose transcription is stimulated by glucose and inhibited by insulin. Glucose 89-96 insulin Homo sapiens 34-41 10694797-3 2000 Glucose- and insulin-sensitive promoters were constructed by inserting glucose-responsive elements (GlREs) from the rat L-pyruvate kinase (L-PK) gene into the insulin-sensitive, liver-specific, rat insulin-like growth factor binding protein-1 (IGFBP-1) promoter. Glucose 0-7 insulin Homo sapiens 159-166 10694797-3 2000 Glucose- and insulin-sensitive promoters were constructed by inserting glucose-responsive elements (GlREs) from the rat L-pyruvate kinase (L-PK) gene into the insulin-sensitive, liver-specific, rat insulin-like growth factor binding protein-1 (IGFBP-1) promoter. Glucose 71-78 insulin Homo sapiens 13-20 10694797-3 2000 Glucose- and insulin-sensitive promoters were constructed by inserting glucose-responsive elements (GlREs) from the rat L-pyruvate kinase (L-PK) gene into the insulin-sensitive, liver-specific, rat insulin-like growth factor binding protein-1 (IGFBP-1) promoter. Glucose 71-78 insulin Homo sapiens 159-166 10658053-20 2000 We conclude that regular exercise leads to greater insulin-stimulated IRS-1-associated PI3-kinase activation in human skeletal muscle, thus facilitating enhanced insulin-mediated glucose uptake. Glucose 179-186 insulin Homo sapiens 162-169 10694797-9 2000 In both H4IIE hepatoma cells stably transfected with this construct, and normal rat hepatocytes (GlRE)3BP-1 2xfur-mediated insulin secretion increased in response to stimulation by glucose. Glucose 181-188 insulin Homo sapiens 123-130 10694797-10 2000 Moreover, a capacity to decrease insulin production in response to diminishing glucose exposure was also demonstrated. Glucose 79-86 insulin Homo sapiens 33-40 10694797-11 2000 We conclude that the transcriptional regulation of insulin production using these glucose- and insulin-sensitive constructs meets the requirements for application in a rodent model of insulin gene therapy. Glucose 82-89 insulin Homo sapiens 51-58 10658053-14 2000 Insulin-mediated glucose disposal rates (GDR) were greater (P < 0.05) in the exercise-trained compared with the sedentary control group (9.22 +/- 0.95 vs. 6.36 +/- 0.57 mg. kg fat-free mass(-1). Glucose 17-24 insulin Homo sapiens 0-7 10658053-20 2000 We conclude that regular exercise leads to greater insulin-stimulated IRS-1-associated PI3-kinase activation in human skeletal muscle, thus facilitating enhanced insulin-mediated glucose uptake. Glucose 179-186 insulin Homo sapiens 51-58 11229149-7 2000 CONCLUSIONS: Our observations suggest that the insulin secretory response in fasting and 30 minutes after oral glucose load was earliest metabolic abnormality in subjects at high risk for developing hypertension i.e. offspring of hypertensive parents. Glucose 111-118 insulin Homo sapiens 47-54 10676673-10 2000 Insulin levels correlated with blood glucose (r = 0.56, p = 0.0003), but were not independently associated with either PDT, platelet aggregation or P-selectin expression. Glucose 37-44 insulin Homo sapiens 0-7 10664920-1 2000 Repaglinide is a novel insulin secretagogue developed in response to the need for a fast-acting, oral prandial glucose regulator for the treatment of type 2 (non-insulin-dependent) diabetes mellitus. Glucose 111-118 insulin Homo sapiens 23-30 10690909-1 2000 The purpose of this study was to examine the molecular mechanism responsible for the defective insulin-stimulated glucose transport in cultured fibroblasts from a patient (VH) with clinical features of Werner syndrome and severe insulin resistance. Glucose 114-121 insulin Homo sapiens 95-102 10675357-1 2000 The broad nature of insulin resistant glucose metabolism in skeletal muscle of patients with type 2 diabetes suggests a defect in the proximal part of the insulin signaling network. Glucose 38-45 insulin Homo sapiens 20-27 10675357-1 2000 The broad nature of insulin resistant glucose metabolism in skeletal muscle of patients with type 2 diabetes suggests a defect in the proximal part of the insulin signaling network. Glucose 38-45 insulin Homo sapiens 155-162 10675357-6 2000 Insulin stimulation of glucose-disposal correlated with association of p85 with IRS-1. Glucose 23-30 insulin Homo sapiens 0-7 10690889-7 2000 Seven-year data for group C1 showed that glucose levels did not significantly change during GH treatment, whereas fasting insulin levels as well as glucose-induced insulin levels increased significantly. Glucose 148-155 insulin Homo sapiens 164-171 10690909-1 2000 The purpose of this study was to examine the molecular mechanism responsible for the defective insulin-stimulated glucose transport in cultured fibroblasts from a patient (VH) with clinical features of Werner syndrome and severe insulin resistance. Glucose 114-121 insulin Homo sapiens 229-236 10743599-2 2000 The minimal model, which is the model currently mostly used in physiological research on the metabolism of glucose, was proposed in the early eighties for the interpretation of the glucose and insulin plasma concentrations following the intravenous glucose tolerance test. Glucose 107-114 insulin Homo sapiens 193-200 10657854-11 2000 The effect of T(3) on glucose uptake induced by insulin can also be explained by the high expression of both glucose transporters. Glucose 22-29 insulin Homo sapiens 48-55 10692093-2 2000 This study was aimed at determining whether any relationship between plasma insulin and glucose levels and total plasma homocysteine (tHcy) concentrations exists in a population based survey performed 10 years apart. Glucose 88-95 insulin Homo sapiens 76-83 10743599-3 2000 It is composed of two parts: the first consists of two differential equations and describes the glucose plasma concentration time-course treating insulin plasma concentration as a known forcing function; the second consists of a single equation and describes the time course of plasma insulin concentration treating glucose plasma concentration as a known forcing function. Glucose 316-323 insulin Homo sapiens 285-292 10743599-3 2000 It is composed of two parts: the first consists of two differential equations and describes the glucose plasma concentration time-course treating insulin plasma concentration as a known forcing function; the second consists of a single equation and describes the time course of plasma insulin concentration treating glucose plasma concentration as a known forcing function. Glucose 96-103 insulin Homo sapiens 146-153 10690948-8 2000 In conclusion, not only the MTG concentration but also the FFA pattern seems to affect insulin-mediated glucose uptake. Glucose 104-111 insulin Homo sapiens 87-94 10711656-3 2000 Since whole body glucose utilization depends mainly on controlled changes in glucose transport in these tissues, this review focuses on the role of glucose transporters in the regulation of insulin-stimulated glucose transport activity. Glucose 17-24 insulin Homo sapiens 190-197 10711656-3 2000 Since whole body glucose utilization depends mainly on controlled changes in glucose transport in these tissues, this review focuses on the role of glucose transporters in the regulation of insulin-stimulated glucose transport activity. Glucose 77-84 insulin Homo sapiens 190-197 10711656-3 2000 Since whole body glucose utilization depends mainly on controlled changes in glucose transport in these tissues, this review focuses on the role of glucose transporters in the regulation of insulin-stimulated glucose transport activity. Glucose 77-84 insulin Homo sapiens 190-197 10711656-4 2000 The molecular mechanisms by which several inducers of insulin resistance inhibit insulin action on glucose uptake are also discussed. Glucose 99-106 insulin Homo sapiens 54-61 10711656-4 2000 The molecular mechanisms by which several inducers of insulin resistance inhibit insulin action on glucose uptake are also discussed. Glucose 99-106 insulin Homo sapiens 81-88 10690944-10 2000 This finding may be attributable to a relative insulin resistance induced by epinephrine, resulting in a decreased rate of glucose clearance by cells. Glucose 123-130 insulin Homo sapiens 47-54 10707550-1 2000 Insulin stimulates glucose transport in muscle and adipose tissue by promoting the appearance of GLUT4, the main glucose transporter isoform in these tissues, on the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 10707550-2 2000 Insulin resistance is instrumental in pathogenesis of type 2 diabetes mellitus and involves decreased glucose transport activity in these tissues. Glucose 102-109 insulin Homo sapiens 0-7 10707557-4 2000 Increased HGO and decreased PGU, suggesting insulin resistances bring increased fasting blood glucose. Glucose 94-101 insulin Homo sapiens 44-51 10707566-2 2000 Insulin resistance is diagnosed clinically by fasting hyperinsulinemia, steady state plasma glucose (SSPG) method, insulin tolerance test and glucose clamp study. Glucose 92-99 insulin Homo sapiens 0-7 10707557-6 2000 The regulation of hepatic glucose uptake(HGU) occurs by way of the hormonal milieu(insulin and glucagon), the glucose level, and the rote of glucose delivery. Glucose 26-33 insulin Homo sapiens 83-90 10707566-2 2000 Insulin resistance is diagnosed clinically by fasting hyperinsulinemia, steady state plasma glucose (SSPG) method, insulin tolerance test and glucose clamp study. Glucose 142-149 insulin Homo sapiens 0-7 10707568-1 2000 Insulin resistance syndrome is the theory that glucose intolerance, hyperinsulinemia, increased very low density lipoprotein triglyceride level, decreased high density lipoprotein cholesterol level, and hypertension are proposed consequences of insulin resistance. Glucose 47-54 insulin Homo sapiens 0-7 10707557-8 2000 Hepatic insulin resistance(increased HGO and decreased HGU) and peripheral insulin resistance(decreased PGU) are the characters of glucose intolerance. Glucose 131-138 insulin Homo sapiens 8-15 10654615-2 2000 In insulin resistant obese mouse models, neutralization of TNF-alpha in circulation has been demonstrated to restore insulin-mediated glucose uptake. Glucose 134-141 insulin Homo sapiens 117-124 10707574-1 2000 Insulin resistance (reduced insulin action to stimulate glycogen synthesis in muscle and occasionally to inhibit glucose output in liver) is well known to be frequently present in patients with chronic liver diseases, especially cirrhosis. Glucose 113-120 insulin Homo sapiens 0-7 10700478-4 2000 Insulin-mediated glucose transport was measured in isolated adipocytes. Glucose 17-24 insulin Homo sapiens 0-7 10655495-8 2000 The mUbc9 sentrin-conjugating enzyme represents a novel regulator of GLUT1 and GLUT4 protein levels with potential importance as a determinant of basal and insulin-stimulated glucose uptake in normal and pathophysiological states. Glucose 175-182 insulin Homo sapiens 156-163 10700478-8 2000 Insulin-stimulated (1 ng/ml) glucose transport was significantly greater on the oleic- acid-rich diet (0.56+/-0.17 vs. 0.29+/-0.14 nmol/10(5) cells/3 min, p<0.0001). Glucose 29-36 insulin Homo sapiens 0-7 10700478-10 2000 There was a significant correlation between adipocyte membrane oleic/linoleic acid and insulin-mediated glucose transport (p<0.001) but no relationship between insulin-stimulated glucose transport and change in endothelium-dependent FMD. Glucose 104-111 insulin Homo sapiens 87-94 10670626-18 2000 The acute insulin response to glucose indicated no significant reduction of functional islet mass. Glucose 30-37 insulin Homo sapiens 10-17 10868826-0 2000 Relationship between several surrogate estimates of insulin resistance and quantification of insulin-mediated glucose disposal in 490 healthy nondiabetic volunteers. Glucose 110-117 insulin Homo sapiens 93-100 10868826-1 2000 OBJECTIVE: The goal of this study was to define the relationship between a quantitative measure of the ability of physiological hyperinsulinemia to stimulate glucose disposal and several surrogate measures of insulin resistance. Glucose 158-165 insulin Homo sapiens 133-140 10868826-2 2000 RESEARCH DESIGN AND METHODS: Insulin-mediated glucose disposal was quantified in 490 healthy nondiabetic volunteers by determining the steady-state plasma glucose (SSPG) concentration in response to a continuous infusion of somatostatin, insulin, and glucose. Glucose 46-53 insulin Homo sapiens 29-36 10868826-2 2000 RESEARCH DESIGN AND METHODS: Insulin-mediated glucose disposal was quantified in 490 healthy nondiabetic volunteers by determining the steady-state plasma glucose (SSPG) concentration in response to a continuous infusion of somatostatin, insulin, and glucose. Glucose 155-162 insulin Homo sapiens 29-36 10868826-2 2000 RESEARCH DESIGN AND METHODS: Insulin-mediated glucose disposal was quantified in 490 healthy nondiabetic volunteers by determining the steady-state plasma glucose (SSPG) concentration in response to a continuous infusion of somatostatin, insulin, and glucose. Glucose 155-162 insulin Homo sapiens 29-36 10868826-3 2000 Because the steady-state plasma insulin concentration was similar in all subjects during the infusion (approximately 60 microU/ml), the SSPG concentration provided a direct estimate of insulin-mediated glucose disposal. Glucose 202-209 insulin Homo sapiens 185-192 10868826-5 2000 RESULTS: The surrogate measure of insulin resistance most closely related to the direct determination of insulin action was the total integrated insulin response to a 75-g oral glucose challenge with correlation coefficients (r) varying from 0.67 to 0.79. Glucose 177-184 insulin Homo sapiens 34-41 10868826-5 2000 RESULTS: The surrogate measure of insulin resistance most closely related to the direct determination of insulin action was the total integrated insulin response to a 75-g oral glucose challenge with correlation coefficients (r) varying from 0.67 to 0.79. Glucose 177-184 insulin Homo sapiens 105-112 10868826-5 2000 RESULTS: The surrogate measure of insulin resistance most closely related to the direct determination of insulin action was the total integrated insulin response to a 75-g oral glucose challenge with correlation coefficients (r) varying from 0.67 to 0.79. Glucose 177-184 insulin Homo sapiens 105-112 10868826-8 2000 CONCLUSIONS: The total integrated insulin response to oral glucose is the best surrogate measure of insulin resistance, accounting for approximately two-thirds of the variability in insulin-mediated glucose disposal. Glucose 59-66 insulin Homo sapiens 34-41 10868826-8 2000 CONCLUSIONS: The total integrated insulin response to oral glucose is the best surrogate measure of insulin resistance, accounting for approximately two-thirds of the variability in insulin-mediated glucose disposal. Glucose 59-66 insulin Homo sapiens 100-107 10868826-8 2000 CONCLUSIONS: The total integrated insulin response to oral glucose is the best surrogate measure of insulin resistance, accounting for approximately two-thirds of the variability in insulin-mediated glucose disposal. Glucose 59-66 insulin Homo sapiens 100-107 10868826-8 2000 CONCLUSIONS: The total integrated insulin response to oral glucose is the best surrogate measure of insulin resistance, accounting for approximately two-thirds of the variability in insulin-mediated glucose disposal. Glucose 199-206 insulin Homo sapiens 34-41 10868826-8 2000 CONCLUSIONS: The total integrated insulin response to oral glucose is the best surrogate measure of insulin resistance, accounting for approximately two-thirds of the variability in insulin-mediated glucose disposal. Glucose 199-206 insulin Homo sapiens 100-107 10868826-8 2000 CONCLUSIONS: The total integrated insulin response to oral glucose is the best surrogate measure of insulin resistance, accounting for approximately two-thirds of the variability in insulin-mediated glucose disposal. Glucose 199-206 insulin Homo sapiens 100-107 10868826-9 2000 Fasting insulin concentration accounted for approximately one-third of the variability in insulin-mediated glucose disposal, and the use of fasting plasma glucose and insulin concentrations to calculate more sophisticated estimates of insulin resistance appears to offer little advantage over the fasting plasma insulin concentration. Glucose 107-114 insulin Homo sapiens 90-97 10868826-9 2000 Fasting insulin concentration accounted for approximately one-third of the variability in insulin-mediated glucose disposal, and the use of fasting plasma glucose and insulin concentrations to calculate more sophisticated estimates of insulin resistance appears to offer little advantage over the fasting plasma insulin concentration. Glucose 107-114 insulin Homo sapiens 90-97 10955370-6 2000 Insulin also increased myocardial uptake of glucose (from 6+/-1 to 17+/-6 mmol/min) and lactate (from 8+/-2 to 12+/-5 mmol/min), resulting in approximately 30% increase in total oxidative substrate uptake, but without increasing myocardial oxygen consumption (7.0+/-0.7 vs. 7.1+/-0.8 ml/min). Glucose 44-51 insulin Homo sapiens 0-7 10645822-7 2000 Corrected insulin response (I120/(G120 x (G120 - 70))) was modestly correlated with insulin secretion as measured by an intravenous glucose tolerance test (r = 0.35). Glucose 132-139 insulin Homo sapiens 10-17 10645822-7 2000 Corrected insulin response (I120/(G120 x (G120 - 70))) was modestly correlated with insulin secretion as measured by an intravenous glucose tolerance test (r = 0.35). Glucose 132-139 insulin Homo sapiens 84-91 14564604-7 2000 Immunoreactive insulin levels increased in the groups receiving 0.2 or 0.3 g.kg(-1).h(-1) of glucose infusion. Glucose 93-100 insulin Homo sapiens 15-22 10672916-3 2000 A number of physiological alterations of glucose metabolism including hepatic overproduction of glucose, and reduced glucose utilization by peripheral tissues as a result of insulin resistance contribute to the development of the metabolic manifestations of this disease. Glucose 41-48 insulin Homo sapiens 174-181 11450502-1 2000 We studied a patient with systemic lupus erythematosus and type B insulin resistance who showed almost complete normalization of postprandial plasma glucose in 3 months and a transient occurrence of fasting hypoglycemia from day 35 (i.e. the 35th day of hospitalization) to day 77. Glucose 149-156 insulin Homo sapiens 66-73 10634338-11 2000 Among subjects with glucose intolerance, levels of PAI-1 and tPA antigen in men and women (P<.01 for trend) and vWF antigen in men (P<.05 for trend) increased significantly across insulin quintiles, but levels of factor VII antigen, fibrinogen, and plasma viscosity did not increase. Glucose 20-27 insulin Homo sapiens 186-193 10634338-12 2000 CONCLUSIONS: Elevated levels of fasting insulin are associated with impaired fibrinolysis and hypercoagulability in subjects with normal glucose tolerance. Glucose 137-144 insulin Homo sapiens 40-47 10644543-5 2000 Inhibition of insulin-stimulated glucose transport was correlated with that of Akt activity. Glucose 33-40 insulin Homo sapiens 14-21 11078259-0 2000 Insulin-mediated glucose uptake in congestive heart failure. Glucose 17-24 insulin Homo sapiens 0-7 10644551-6 2000 The smaller glucose dose induced insulin pulses at lower significance levels and with considerable breakthrough insulin release. Glucose 12-19 insulin Homo sapiens 112-119 10644551-6 2000 The smaller glucose dose induced insulin pulses at lower significance levels and with considerable breakthrough insulin release. Glucose 12-19 insulin Homo sapiens 33-40 10644551-8 2000 The orderliness of insulin release as estimated by approximate entropy (1.459 +/- 0.009 vs. 1.549 +/- 0.027, P = 0.016) was significantly improved by glucose pulse induction (n = 6; 6 mg x kg(-1) x min(-1)) compared with unstimulated insulin profiles (n = 7). Glucose 150-157 insulin Homo sapiens 19-26 10644551-9 2000 We conclude that rapid in vivo oscillations in glucose may be an important regulator of pulsatile insulin secretion in humans and that the use of an intermittent pulsed glucose induction to evoke defined and recurrent insulin secretory signals may be a useful tool to unveil more subtle defects in beta-cell glucose sensitivity. Glucose 47-54 insulin Homo sapiens 98-105 10634813-12 2000 min(-1), P<0.001) had lower rates of insulin-stimulated glucose oxidation than did controls (19.4+/-4.7 micromol. Glucose 59-66 insulin Homo sapiens 40-47 11193829-2 2000 Insulin, insulin-like growth factor (IGF-1), and glucagon-like peptide-1 (GLP-1) act as glucose-dependent growth factors for pancreatic beta-cells. Glucose 88-95 insulin Homo sapiens 0-7 11193829-2 2000 Insulin, insulin-like growth factor (IGF-1), and glucagon-like peptide-1 (GLP-1) act as glucose-dependent growth factors for pancreatic beta-cells. Glucose 88-95 insulin Homo sapiens 9-16 11193829-4 2000 Insulin, IGF-1, and GLP-1 induced distinctive time dependent, dose dependent, and glucose dependent phosphorylation of PKB/Akt. Glucose 82-89 insulin Homo sapiens 0-7 10638900-8 2000 Dextrose infusion significantly increased glucose clearance and plasma concentrations of glucose and insulin, while endogenous glucose production and lipolysis decreased to a similar degree in both groups. Glucose 0-8 insulin Homo sapiens 101-108 10634813-16 2000 In contrast, subjects with hypercholesterolemia and control subjects had similar rates of insulin-stimulated glucose uptake. Glucose 109-116 insulin Homo sapiens 90-97 10784063-12 2000 Islets retained their functionality when cultured on hydrogels, as judged by insulin secretion in response to glucose challenge (16.0 mM). Glucose 110-117 insulin Homo sapiens 77-84 10855737-11 2000 However, the action of insulin on peripheral glucose uptake was influenced by endothelial dysfunction (delayed transcapillary insulin transport) and by changes in and/or redistribution of blood flow suggesting a link between vascular function and insulin sensitivity. Glucose 45-52 insulin Homo sapiens 23-30 10855737-11 2000 However, the action of insulin on peripheral glucose uptake was influenced by endothelial dysfunction (delayed transcapillary insulin transport) and by changes in and/or redistribution of blood flow suggesting a link between vascular function and insulin sensitivity. Glucose 45-52 insulin Homo sapiens 126-133 10855737-11 2000 However, the action of insulin on peripheral glucose uptake was influenced by endothelial dysfunction (delayed transcapillary insulin transport) and by changes in and/or redistribution of blood flow suggesting a link between vascular function and insulin sensitivity. Glucose 45-52 insulin Homo sapiens 126-133 10663214-4 2000 RESULTS: There was a linear negative relation between changes in body weight and changes in insulin-stimulated glucose disposal in subjects with normal glucose tolerance (r = -0.51, p < 0.0001) and impaired glucose tolerance (r = -0.54, p < 0.0001). Glucose 111-118 insulin Homo sapiens 92-99 10615953-6 2000 Thus, Gck mutations in beta-cells may impair insulin response to glucose and alter intrauterine growth as well as glucose metabolism after birth. Glucose 65-72 insulin Homo sapiens 45-52 10631198-5 2000 RESULTS: A statistically significant decrease was found in the blood glucose level, from 111.2 +/- 4.2 to 97.8 +/- 3.5 mg/dL (p < 0.01); this decrease was not accompanied by significant insulin concentration changes. Glucose 69-76 insulin Homo sapiens 189-196 10663214-4 2000 RESULTS: There was a linear negative relation between changes in body weight and changes in insulin-stimulated glucose disposal in subjects with normal glucose tolerance (r = -0.51, p < 0.0001) and impaired glucose tolerance (r = -0.54, p < 0.0001). Glucose 152-159 insulin Homo sapiens 92-99 10663214-5 2000 In contrast, changes in the acute insulin response were positively related to weight changes in subjects with normal glucose tolerance (r = +0.26, p < 0.005) but negatively in those with impaired glucose tolerance (r = -0.51, p < 0.0001). Glucose 117-124 insulin Homo sapiens 34-41 10899726-9 2000 CONCLUSIONS: HCV-infected patients with normal glucose tolerance are insulin and glucose resistant. Glucose 47-54 insulin Homo sapiens 69-76 10663218-3 2000 RESULTS: The early insulin response during the first 10 min of an intravenous glucose tolerance test was about 40% lower in the LADA-offspring than in the control group (p = 0.008). Glucose 78-85 insulin Homo sapiens 19-26 10620000-0 2000 Effect of transdermal nitroglycerin on glucose-stimulated insulin release in healthy male volunteers. Glucose 39-46 insulin Homo sapiens 58-65 10610742-3 2000 We hypothesized that the insulin response to an intravenous glucose challenge during the intravenous glucose tolerance test might lead to increases in forearm blood flow in healthy individuals, and that such a response might be altered in patients with coronary heart disease. Glucose 60-67 insulin Homo sapiens 25-32 10610742-3 2000 We hypothesized that the insulin response to an intravenous glucose challenge during the intravenous glucose tolerance test might lead to increases in forearm blood flow in healthy individuals, and that such a response might be altered in patients with coronary heart disease. Glucose 101-108 insulin Homo sapiens 25-32 10552272-8 2000 A linear relationship between glucose and insulin concentrations was found only for women during exercise (r = 0.615, P < 0.0001). Glucose 30-37 insulin Homo sapiens 42-49 10552272-10 2000 In conclusion, this study postulates that an oral glucose load given at the onset of a prolonged and moderate exercise bout induced lesser plasma glucose and greater insulin concentrations in women as compared to men. Glucose 50-57 insulin Homo sapiens 166-173 10552278-10 2000 Plasma glucose levels were slightly reduced only in those children with the highest insulin levels whose VO(2max) improved (P < 0.0506). Glucose 7-14 insulin Homo sapiens 84-91 10620000-2 2000 We studied whether transdermal application of nitroglycerin, another NO donor widely used for angina prophylaxis, influenced glucose-stimulated insulin release in healthy, young, male volunteers. Glucose 125-132 insulin Homo sapiens 144-151 10620000-6 2000 Glucose-stimulated maximum increase in plasma insulin immunoreactivity were 36.3 +/- 5 and 78.8 +/- 6.1 mU mL-1 (P < 0.05) in the presence of active and placebo patches, respectively. Glucose 0-7 insulin Homo sapiens 46-53 10620000-9 2000 CONCLUSION: We conclude that inhibition of glucose-stimulated insulin release by transdermal nitroglycerin without causing hyperglycaemia may serve as a novel component of the antianginal mechanism of action of nitrates. Glucose 43-50 insulin Homo sapiens 62-69 10663449-11 2000 RESULTS: When glucose was administered orally without Gb, Chinese patients had higher plasma glucose increases at 10 min (7.6 mmol/l x min vs 2.6 mmol/l x min) and higher increases of plasma insulin levels than Caucasians at both 10 min (198 pmol/l x min vs 54 pmol/l x min) and 30 min (2286 pmol/l x min vs 1198 pmol/l x min). Glucose 14-21 insulin Homo sapiens 191-198 10620001-10 2000 Non-esterified fatty acids at steady state were positively correlated with fasting markers of insulin resistance: fasting plasma glucose (P < 0.05), fasting plasma insulin (P < 0.005) and negatively correlated with the M-value (P < 0.0005). Glucose 129-136 insulin Homo sapiens 94-101 10663449-19 2000 CONCLUSION: In summary, following oral glucose administration without Gb, Chinese type-2 diabetic patients had higher plasma insulin levels but also higher plasma glucose levels during the first 10 min, which might reflect reduced insulin sensitivity or more rapid glucose absorption. Glucose 39-46 insulin Homo sapiens 125-132 10663449-19 2000 CONCLUSION: In summary, following oral glucose administration without Gb, Chinese type-2 diabetic patients had higher plasma insulin levels but also higher plasma glucose levels during the first 10 min, which might reflect reduced insulin sensitivity or more rapid glucose absorption. Glucose 39-46 insulin Homo sapiens 231-238 10620001-14 2000 All these associations were independent of obesity and geographical location CONCLUSION: The results in this large cohort of healthy European subjects suggest that triglyceride concentrations depend upon both insulin"s gluco-regulation (estimated by glucose uptake) and antilipolytic insulin action (measured by NEFA levels) during an euglycaemic clamp. Glucose 250-257 insulin Homo sapiens 209-216 10663449-20 2000 Gb augmented glucose-induced release of both insulin and proinsulin in both ethnic groups; the effect on insulin secretion was more pronounced. Glucose 13-20 insulin Homo sapiens 45-52 10633217-2 2000 As this latter tissue is the main target for insulin-estimulated glucose disposal, we hypothesized that the muscular and fat-free mass (FFM) compartments might influence serum leptin levels in humans through increased insulin resistance. Glucose 65-72 insulin Homo sapiens 45-52 10663449-20 2000 Gb augmented glucose-induced release of both insulin and proinsulin in both ethnic groups; the effect on insulin secretion was more pronounced. Glucose 13-20 insulin Homo sapiens 57-67 10826516-8 2000 This study demonstrates that the principle of protracted insulin action of NN304 by reversible binding to albumin is effective in humans albeit at a much lower rate of glucose utilisation when compared to NPH insulin. Glucose 168-175 insulin Homo sapiens 57-64 10989952-5 2000 It generates insulin-like signals for glucose transport and glycogen synthesis via leptin receptors and the PI3-kinase and could, therefore, play a role as a mediator of obesity-related insulin resistance. Glucose 38-45 insulin Homo sapiens 13-20 11341594-4 2000 METHODS: The basal and glucose stimulated secretion of insulin was compared with and without immunoneutralization of somatostatin using a somatostatin antibody in an isolated perfused rat pancreas model. Glucose 23-30 insulin Homo sapiens 55-62 10989952-5 2000 It generates insulin-like signals for glucose transport and glycogen synthesis via leptin receptors and the PI3-kinase and could, therefore, play a role as a mediator of obesity-related insulin resistance. Glucose 38-45 insulin Homo sapiens 186-193 10611182-7 2000 The administration of metformin was associated with a decrease in area under the curve for insulin during a 2h, 75g oral glucose tolerance test, in plasma free testosterone concentrations and an increase in plasma sex hormone binding globulin concentration. Glucose 121-128 insulin Homo sapiens 91-98 10642350-1 2000 A primary defect in the vascular action of insulin may be a key intermediate mechanism that links endothelial dysfunction with reduced insulin-mediated cellular glucose uptake in metabolic and cardiovascular disorders. Glucose 161-168 insulin Homo sapiens 43-50 10642350-1 2000 A primary defect in the vascular action of insulin may be a key intermediate mechanism that links endothelial dysfunction with reduced insulin-mediated cellular glucose uptake in metabolic and cardiovascular disorders. Glucose 161-168 insulin Homo sapiens 135-142 11467407-10 2000 Infection by this strain also caused functional impairment that significantly affected insulin response to high glucose at 48 hours post infection (p<0.001). Glucose 112-119 insulin Homo sapiens 87-94 10736756-1 2000 Insulin resistance syndrome is the theory that glucose intolerance, hyperinsulinemia, increased very low density lipoprotein triglyceride level, decreased high density lipoprotein cholesterol level, and hypertension are proposed consequences of insulin resistance. Glucose 47-54 insulin Homo sapiens 0-7 10683091-3 2000 Up to two hours after exercise, glucose uptake is in part elevated due to insulin independent mechanisms, probably involving a contraction-induced increase in the amount of GLUT4 associated with the plasma membrane and T-tubules. Glucose 32-39 insulin Homo sapiens 74-81 10683091-7 2000 Physical training potentiates the effect of exercise on insulin sensitivity through multiple adaptations in glucose transport and metabolism. Glucose 108-115 insulin Homo sapiens 56-63 11341594-8 2000 Immunoneutralization during glucose stimulated insulin secretion produced a significant rise in insulin secretion compared to the control group of 2,678 +/- 187% vs. 535 +/- 39% (p < 0.05). Glucose 28-35 insulin Homo sapiens 47-54 10634367-2 2000 The acute insulin response to arginine was impaired in LADA vs. type 2 diabetes at all glucose levels, with the greatest impairment in the maximally stimulated insulin concentrations (P<0.04). Glucose 87-94 insulin Homo sapiens 10-17 10634378-7 2000 Area under the curve for insulin (AUCins) during oral glucose tolerance test was calculated. Glucose 54-61 insulin Homo sapiens 25-32 10925065-2 2000 Insulin sensitivity was measured by steady-state plasma glucose method or euglycemic glucose clamp method. Glucose 56-63 insulin Homo sapiens 0-7 10659969-9 2000 During insulin clamp treatments, the mammary gland was able to support the increased milk protein yields by increasing extraction efficiency of essential amino acids, mammary blood flow, and glucose uptake. Glucose 191-198 insulin Homo sapiens 7-14 10925065-2 2000 Insulin sensitivity was measured by steady-state plasma glucose method or euglycemic glucose clamp method. Glucose 85-92 insulin Homo sapiens 0-7 10925065-5 2000 Insulin sensitivity expressed as glucose utilization and glucose clearance was significantly (p<0.05) lower in diabetic subjects with retinopathy (without nephropathy) compared with subjects without the microangiopathies after adjustment for age, body mass index (BMI), fasting blood glucose (FBS), and diabetic duration. Glucose 33-40 insulin Homo sapiens 0-7 10925065-5 2000 Insulin sensitivity expressed as glucose utilization and glucose clearance was significantly (p<0.05) lower in diabetic subjects with retinopathy (without nephropathy) compared with subjects without the microangiopathies after adjustment for age, body mass index (BMI), fasting blood glucose (FBS), and diabetic duration. Glucose 57-64 insulin Homo sapiens 0-7 10925065-5 2000 Insulin sensitivity expressed as glucose utilization and glucose clearance was significantly (p<0.05) lower in diabetic subjects with retinopathy (without nephropathy) compared with subjects without the microangiopathies after adjustment for age, body mass index (BMI), fasting blood glucose (FBS), and diabetic duration. Glucose 57-64 insulin Homo sapiens 0-7 10925068-4 2000 Therefore, the study of insulin pharmacokinetics after insulin overdose may be useful to know the necessary duration of exogenous glucose administration required to manage the medical emergency of severe insulin intoxication in future cases. Glucose 130-137 insulin Homo sapiens 24-31 10757434-8 2000 Ideally, insulin pump therapy should be initiated prior to pregnancy so that glucose control can be normalized, thereby reducing the risk for spontaneous abortion and fetal malformations. Glucose 77-84 insulin Homo sapiens 9-16 10673732-8 2000 The results were that pre-menopausal women showed a higher insulin-mediated glucose disposal (7.6 vs5.8 mg/kg/min; P < 0. Glucose 76-83 insulin Homo sapiens 59-66 10757434-10 2000 The published experience with the insulin pump has demonstrated that this therapy can achieve glucose control and perinatal outcomes comparable to that obtained with multiple-dose insulin injection therapy. Glucose 94-101 insulin Homo sapiens 34-41 11210345-5 2000 Increased need in glucose as a main energy substrate during ischemia and therefore in insulin leads to disturbed carbohydrate metabolism in 33% of patients recorded 3-5 years after MI. Glucose 18-25 insulin Homo sapiens 86-93 10998755-1 2000 We investigated the relationship between changes in insulin resistance and blood coagulation-fibrinolysis following institution of a glucose clamp (GC) in patients with type 2 diabetes mellitus. Glucose 133-140 insulin Homo sapiens 52-59 10998755-4 2000 The degree of insulin resistance was determined from the glucose infusion rate (GIR) calculated from the GC technique. Glucose 57-64 insulin Homo sapiens 14-21 11117667-4 2000 Furthermore, those girls with the more marked hyperandrogenism have been noted to have insulin resistance as assessed by the frequently sampled intravenous glucose tolerance test. Glucose 156-163 insulin Homo sapiens 87-94 11117672-3 2000 Insulin resistance in PCOS adipocytes was manifested as a reduction in insulin sensitivities for stimulation of glucose transport and suppression of catecholamine-activated lipolysis with no impact on final hormone responsiveness. Glucose 112-119 insulin Homo sapiens 0-7 11117672-3 2000 Insulin resistance in PCOS adipocytes was manifested as a reduction in insulin sensitivities for stimulation of glucose transport and suppression of catecholamine-activated lipolysis with no impact on final hormone responsiveness. Glucose 112-119 insulin Homo sapiens 71-78 11117673-2 2000 We review studies indicating that the IPG signaling system transduces insulin"s stimulation of human thecal androgen biosynthesis, thus offering a mechanism by which insulin can stimulate ovarian androgen production even in women with PCOS whose tissues are resistant to insulin"s stimulation of glucose metabolism. Glucose 296-303 insulin Homo sapiens 70-77 11117673-2 2000 We review studies indicating that the IPG signaling system transduces insulin"s stimulation of human thecal androgen biosynthesis, thus offering a mechanism by which insulin can stimulate ovarian androgen production even in women with PCOS whose tissues are resistant to insulin"s stimulation of glucose metabolism. Glucose 296-303 insulin Homo sapiens 166-173 11117673-2 2000 We review studies indicating that the IPG signaling system transduces insulin"s stimulation of human thecal androgen biosynthesis, thus offering a mechanism by which insulin can stimulate ovarian androgen production even in women with PCOS whose tissues are resistant to insulin"s stimulation of glucose metabolism. Glucose 296-303 insulin Homo sapiens 166-173 10666005-6 2000 Accordingly, it was later renamed glucose-dependent insulinotropic polypeptide because its action on insulin release depends upon an increase in circulating levels of glucose. Glucose 34-41 insulin Homo sapiens 52-59 10647071-4 2000 Since small amounts of regular insulin, which were found to decrease plasma glucose more than the amino acids, did not decrease the plasma concentration of uridine, these results suggest that plasma uridine was decreased by a direct effect of the branched-chain amino acids on the cellular uptake and/or release of uridine. Glucose 76-83 insulin Homo sapiens 31-38 10647056-3 2000 Our aim was to determine the relationships between insulin sensitivity (assessed by euglycemic-hyperinsulinemic clamp) and postprandial glucose, insulin, C-peptide, and glucagon responses to a 75-g protein meal and a 75-g glucose load. Glucose 136-143 insulin Homo sapiens 51-58 10647056-3 2000 Our aim was to determine the relationships between insulin sensitivity (assessed by euglycemic-hyperinsulinemic clamp) and postprandial glucose, insulin, C-peptide, and glucagon responses to a 75-g protein meal and a 75-g glucose load. Glucose 222-229 insulin Homo sapiens 51-58 10647056-6 2000 Insulin sensitivity (M value) was 1.1 to 3.9 mmol/L/m2 min in the subjects and correlated inversely with the plasma glucose response to the protein meal (r = -.58, P = .03), ie, the most insulin-sensitive subjects showed the greatest decline in plasma glucose. Glucose 116-123 insulin Homo sapiens 0-7 10953550-13 2000 Decrease in renal glucose production would lead to a decrease in glucose appearance in circulation and decrease of insulin sensitivity. Glucose 18-25 insulin Homo sapiens 115-122 10953550-15 2000 It is now recognized that insulin-stimulated glucose transport in skeletal muscles and in other peripheral tissues is reduced. Glucose 45-52 insulin Homo sapiens 26-33 10647056-6 2000 Insulin sensitivity (M value) was 1.1 to 3.9 mmol/L/m2 min in the subjects and correlated inversely with the plasma glucose response to the protein meal (r = -.58, P = .03), ie, the most insulin-sensitive subjects showed the greatest decline in plasma glucose. Glucose 252-259 insulin Homo sapiens 0-7 10697389-10 2000 Insulin sensitivity on glucose metabolism is usually normal in the aged, despite subtle impairments in insulin secretion, hepatic uptake, and onset of action. Glucose 23-30 insulin Homo sapiens 0-7 10647056-8 2000 Our study suggests that the net effect of insulin and glucagon secretion on postprandial glucose levels after a protein meal might depend on the individual"s degree of insulin sensitivity. Glucose 89-96 insulin Homo sapiens 42-49 10647056-8 2000 Our study suggests that the net effect of insulin and glucagon secretion on postprandial glucose levels after a protein meal might depend on the individual"s degree of insulin sensitivity. Glucose 89-96 insulin Homo sapiens 168-175 10647056-9 2000 Gluconeogenesis in the liver may be less susceptible to inhibition by insulin in the more highly resistant subjects, thereby counteracting a decline in plasma glucose. Glucose 159-166 insulin Homo sapiens 70-77 10607769-6 2000 The glucose disposal rate (GDR mg/kg/min) was used as an index of insulin sensitivity during the clamp technique. Glucose 4-11 insulin Homo sapiens 66-73 10670439-3 2000 Recent research suggests that there is a correlation between plasma insulin and glucose concentrations and memory performance in Alzheimer"s disease sufferers. Glucose 80-87 insulin Homo sapiens 68-75 10670439-10 2000 We conclude that glucose ingestion, and the subsequent elevation of plasma levels of glucose and insulin leads to a decrease in plasma amyloid precursor protein concentration. Glucose 17-24 insulin Homo sapiens 97-104 10770899-5 2000 AIM: In alcoholics with minimal hepatic lesions to evaluate the seric insulin and glucose levels after stimulus with intravenous glucose. Glucose 129-136 insulin Homo sapiens 70-77 10965515-3 2000 Most recently, McKeown-Eyssen and Giovannucci noted the similarity of the risk factors for colorectal cancer and those for insulin resistance and suggested that insulin resistance leads to colorectal cancer through the growth-promoting effect of elevated levels of insulin, glucose, or triglycerides. Glucose 274-281 insulin Homo sapiens 123-130 10965515-3 2000 Most recently, McKeown-Eyssen and Giovannucci noted the similarity of the risk factors for colorectal cancer and those for insulin resistance and suggested that insulin resistance leads to colorectal cancer through the growth-promoting effect of elevated levels of insulin, glucose, or triglycerides. Glucose 274-281 insulin Homo sapiens 161-168 10965515-3 2000 Most recently, McKeown-Eyssen and Giovannucci noted the similarity of the risk factors for colorectal cancer and those for insulin resistance and suggested that insulin resistance leads to colorectal cancer through the growth-promoting effect of elevated levels of insulin, glucose, or triglycerides. Glucose 274-281 insulin Homo sapiens 161-168 11201820-0 2000 [Dynamics of changes in levels of insulin, glucagon, and C-peptide during glucose tolerance test in patients with coronary atherosclerosis]. Glucose 74-81 insulin Homo sapiens 34-41 10752774-0 2000 The effects of intraoperative glucose infusion on portal blood insulin concentration and hepatic mitochondrial redox state during surgery: comparison of short-term and continuous infusions. Glucose 30-37 insulin Homo sapiens 63-70 11201820-0 2000 [Dynamics of changes in levels of insulin, glucagon, and C-peptide during glucose tolerance test in patients with coronary atherosclerosis]. Glucose 74-81 insulin Homo sapiens 57-66 11201820-1 2000 AIM: To study velocity characteristics of changes in the levels of insulin, glucagon and C-peptide in the course of the intravenous glucose tolerance test (IGTT). Glucose 132-139 insulin Homo sapiens 67-74 11201820-1 2000 AIM: To study velocity characteristics of changes in the levels of insulin, glucagon and C-peptide in the course of the intravenous glucose tolerance test (IGTT). Glucose 132-139 insulin Homo sapiens 89-98 11217433-3 2000 The permanent high blood glucose stimulates the beta-cells of the islet transplants to permanent maximal synthesis and secretion of insulin which causes hyper-insulinemia in the liver acini downstream of the transplants. Glucose 25-32 insulin Homo sapiens 132-139 10593919-3 1999 Measurement of glucose transport and glycogen synthesis in L6 myotubes showed that insulin stimulated both processes, by 2- and 5-fold, respectively. Glucose 15-22 insulin Homo sapiens 83-90 11798736-6 2000 Insulin sensitivity index (SI) was calculated according to minimal model technique about glucose in FSIVGTT. Glucose 89-96 insulin Homo sapiens 0-7 11798736-13 2000 CONCLUSIONS: There are obvious impaired first phase insulin secretion after glucose challenge in non-insulin-dependent diabetic subjects from MDP. Glucose 76-83 insulin Homo sapiens 52-59 10593919-9 1999 However, of the kinases assayed, only p38 MAP kinase was activated at H(2)O(2) concentrations (50 microM) that caused an inhibition of insulin-stimulated glucose transport and glycogen synthesis. Glucose 154-161 insulin Homo sapiens 135-142 10593919-11 1999 Our data indicate that activation of the p38 MAP kinase pathway plays a central role in the oxidant-induced inhibition of insulin-regulated glucose transport, and unveils an important biochemical link between the classical stress-activated and insulin signaling pathways in skeletal muscle. Glucose 140-147 insulin Homo sapiens 122-129 10593919-11 1999 Our data indicate that activation of the p38 MAP kinase pathway plays a central role in the oxidant-induced inhibition of insulin-regulated glucose transport, and unveils an important biochemical link between the classical stress-activated and insulin signaling pathways in skeletal muscle. Glucose 140-147 insulin Homo sapiens 244-251 10585868-1 1999 Pancreatic-duodenal homoeobox factor-1 (PDX1) is a homoeodomain transcription factor that plays an important role in linking glucose metabolism in pancreatic beta cells to the regulation of insulin gene transcription. Glucose 125-132 insulin Homo sapiens 190-197 10585868-2 1999 Our previous results indicated that glucose activates PDX1 DNA-binding activity and insulin promoter activity via a stress-activated signalling pathway involving phosphatidylinositol 3-kinase (PtdIns 3-kinase) and stress-activated protein kinase 2 (SAPK2/p38). Glucose 36-43 insulin Homo sapiens 84-91 10604477-2 1999 In the consensus model of glucose-stimulated insulin secretion, ATP is generated by mitochondrial metabolism, promoting closure of ATP-sensitive potassium (KATP) channels, which depolarizes the plasma membrane. Glucose 26-33 insulin Homo sapiens 45-52 10601502-8 1999 SNP infusion increased skeletal muscle blood flow by 86 % (P < 0.01), but skeletal muscle flow distribution and insulin-stimulated glucose uptake (61.4 +/- 7. Glucose 134-141 insulin Homo sapiens 115-122 10619584-2 1999 Oral glucose tolerance tests and hyperglycemic clamps were performed for measurements of insulin action on glucose disposal and suppression of nonesterified fatty acids (NEFA). Glucose 107-114 insulin Homo sapiens 89-96 10591291-2 1999 Increasing plasma glucose levels also increases endogenous insulin levels, raising the question of whether memory improvement is due to changes in insulin, independent of hyperglycemia. Glucose 18-25 insulin Homo sapiens 59-66 10605995-3 1999 Acarbose, metformin, miglitol, pioglitazone, rosiglitazone and troglitazone help the patient"s own insulin control glucose levels and allow early treatment with little risk of hypoglycemia. Glucose 115-122 insulin Homo sapiens 99-106 10567235-1 1999 The activation of phosphatidylinositol 3-kinase (PI 3-kinase) and production of PtdIns(3,4,5)P(3) is crucial in the actions of numerous extracellular stimuli, including insulin-stimulated glucose uptake. Glucose 188-195 insulin Homo sapiens 169-176 10567226-2 1999 Here, we demonstrate that their activation by insulin requires the presence, in the medium in which the cells are maintained, of both amino acids and glucose: insulin only induced activation of eIF2B and the dephosphorylation of eEF2 when cells were exposed to both types of nutrient. Glucose 150-157 insulin Homo sapiens 46-53 10567235-7 1999 The results suggest that the greater ability of insulin to stimulate glucose uptake may be the result of its ability to generate significantly more plasma-membrane PtdIns(3, 4,5)P(3) than PDGF. Glucose 69-76 insulin Homo sapiens 48-55 10567226-2 1999 Here, we demonstrate that their activation by insulin requires the presence, in the medium in which the cells are maintained, of both amino acids and glucose: insulin only induced activation of eIF2B and the dephosphorylation of eEF2 when cells were exposed to both types of nutrient. Glucose 150-157 insulin Homo sapiens 159-166 10567226-3 1999 Other translational regulators, e.g. the 70 kDa ribosomal protein S6 kinase (p70 S6 kinase) and the eIF4E binding protein 1, 4E-BP1, are also regulated by insulin but their control does not require glucose, only amino acids. Glucose 198-205 insulin Homo sapiens 155-162 10567238-1 1999 Insulin stimulates glucose transport in adipose and muscle tissue by stimulating the movement ("translocation") of an intracellular pool of glucose transporters (the Glut4 isoform) to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 10567226-6 1999 These data show that activation by insulin of p70 S6 kinase, which modulates the translation of specific mRNAs, depends on the availability of amino acids whereas regulation of factors involved in overall activation of translation (eIF2B, eEF2) requires both amino acids and glucose. Glucose 275-282 insulin Homo sapiens 35-42 10624789-1 1999 There is evidence that intracellular insulin may carry out some insulin mediated actions, including glucose transport. Glucose 100-107 insulin Homo sapiens 37-44 10580414-0 1999 Evidence for glucose/hexosamine in vivo regulation of insulin/IGF-I hybrid receptor assembly. Glucose 13-20 insulin Homo sapiens 54-61 10580418-8 1999 The anti-CD38+ sera potentiated insulin release both at low [95 (64) vs. 23 (12) microU/ml of control incubations, respectively, P < 0.0001] and high [271 (336) vs. a control of 55 (37) microU/ml, respectively, P = 0.001] medium glucose concentrations, whereas the anti-CD38- sera did not. Glucose 232-239 insulin Homo sapiens 32-39 10624789-1 1999 There is evidence that intracellular insulin may carry out some insulin mediated actions, including glucose transport. Glucose 100-107 insulin Homo sapiens 64-71 10601964-14 1999 Secondary insulin resistance might contribute to the chronic hyperglycemia of MODY3 patients and modulate their glucose tolerance. Glucose 112-119 insulin Homo sapiens 10-17 11387965-6 1999 Two hours after administration of glucose, the level of plasma glucose(2hPG) and plasma insulin(2hPI)increased(the latter, P < 0.05). Glucose 34-41 insulin Homo sapiens 88-95 10601077-2 1999 Hyperinsulinaemia was determined by measuring the insulin response after oral glucose tolerance test (OGTT). Glucose 78-85 insulin Homo sapiens 5-12 10668912-5 1999 Recent studies demonstrated that TNF directly interferes with the insulin signaling cascade at early steps and, thus, impairs insulin-stimulated glucose transport. Glucose 145-152 insulin Homo sapiens 66-73 10668912-5 1999 Recent studies demonstrated that TNF directly interferes with the insulin signaling cascade at early steps and, thus, impairs insulin-stimulated glucose transport. Glucose 145-152 insulin Homo sapiens 126-133 10668913-1 1999 Thioctic acid (alpha-lipoic acid) has been shown to improve insulin-regulated glucose disposal in animal models of insulin resistance and type 2 diabetic patients. Glucose 78-85 insulin Homo sapiens 60-67 10668913-1 1999 Thioctic acid (alpha-lipoic acid) has been shown to improve insulin-regulated glucose disposal in animal models of insulin resistance and type 2 diabetic patients. Glucose 78-85 insulin Homo sapiens 115-122 11387965-9 1999 So we advise patients with Type II B hyperlipemia treated by statin to limit their glucose intake in case of hyperinsulinemia and insulin resistance. Glucose 83-90 insulin Homo sapiens 114-121 10601150-0 1999 Glucose clearance in aged trained skeletal muscle during maximal insulin with superimposed exercise. Glucose 0-7 insulin Homo sapiens 65-72 10643681-5 1999 Insulin was measured at fasting, and 30 and 120 min post-glucose load using a highly specific assay. Glucose 57-64 insulin Homo sapiens 0-7 10643689-0 1999 Effect of obesity and insulin resistance on resting and glucose-induced thermogenesis in man. Glucose 56-63 insulin Homo sapiens 22-29 10643689-2 1999 OBJECTIVE: To assess the impact of obesity and insulin sensitivity on resting (REE) and glucose-induced thermogenesis (GIT). Glucose 88-95 insulin Homo sapiens 47-54 10643689-9 1999 Furthermore, both of the main components of insulin-mediated glucose disposal (glucose oxidation and glycogen synthesis) correlated with GIT independently of one another. Glucose 61-68 insulin Homo sapiens 44-51 10643689-9 1999 Furthermore, both of the main components of insulin-mediated glucose disposal (glucose oxidation and glycogen synthesis) correlated with GIT independently of one another. Glucose 79-86 insulin Homo sapiens 44-51 10643689-13 1999 In contrast, insulin sensitivity and, to a lesser extent, abdominal obesity are the principal factors controlling glucose-induced thermogenesis. Glucose 114-121 insulin Homo sapiens 13-20 10660869-9 1999 Plasma insulin concentrations measured 2 hrs after glucose ingestion were lower in trained girls. Glucose 51-58 insulin Homo sapiens 7-14 10601150-1 1999 Insulin and muscle contractions are major stimuli for glucose uptake in skeletal muscle and have in young healthy people been shown to be additive. Glucose 54-61 insulin Homo sapiens 0-7 10601150-9 1999 From these results it can be concluded that, in both diabetic and healthy aged muscle, exercise adds to a maximally insulin-stimulated glucose clearance and that glucose extraction and clearance are both enhanced by training. Glucose 135-142 insulin Homo sapiens 116-123 11225212-4 1999 METHODS: In a case control design insulin mediated glucose disposal assessed by HECS at insulin infusion rate of 40 mU/m2 during steady state of 60-120 minutes. Glucose 51-58 insulin Homo sapiens 34-41 11225212-4 1999 METHODS: In a case control design insulin mediated glucose disposal assessed by HECS at insulin infusion rate of 40 mU/m2 during steady state of 60-120 minutes. Glucose 51-58 insulin Homo sapiens 88-95 11225212-7 1999 RESULTS: Insulin mediated glucose disposal was measured in MRDM and compared with ketosis prone diabetes of young (IDDM) by HECS. Glucose 26-33 insulin Homo sapiens 9-16 10620096-8 1999 Insulin-mediated glucose disposal was related to body mass index (BMI) (r = -0.49, P = 0. Glucose 17-24 insulin Homo sapiens 0-7 10588827-10 1999 These results show that insulin and glucose act together to influence ovarian function directly and suggest that the effects of short-term nutrition on ovulation rate may be mediated by a direct ovarian action of insulin and glucose. Glucose 36-43 insulin Homo sapiens 213-220 10588827-10 1999 These results show that insulin and glucose act together to influence ovarian function directly and suggest that the effects of short-term nutrition on ovulation rate may be mediated by a direct ovarian action of insulin and glucose. Glucose 225-232 insulin Homo sapiens 24-31 10658938-5 1999 METHODS: The waist:hip ratio was used as measure of central obesity, and insulin-stimulated glucose disposal during a hyperinsulinaemic euglycaemic clamp was used as measure of insulin sensitivity. Glucose 92-99 insulin Homo sapiens 73-80 10638500-5 1999 In contrast, PZI and neutral protamine Hagedorn (NPH) insulin given twice daily provided glucose values comparable to those in controls, whereas glucose values were modestly higher in response to a 70% human insulin isophane suspension and 30% soluble human insulin solution (70/ 30 insulin) given twice daily. Glucose 89-96 insulin Homo sapiens 54-61 10542398-3 1999 We will discuss examples of recent findings, suggesting that spatial compartmentalization and protein translocation might be the keys to understanding the specificity of insulin in the regulation of glucose metabolism. Glucose 199-206 insulin Homo sapiens 170-177 10598202-10 1999 Improved glucose control was most significant in patients whose condition was managed with oral hypoglycemics (P = .05) or insulin (P = .03). Glucose 9-16 insulin Homo sapiens 123-130 10589951-7 1999 RESULTS: Insulin sensitivity (total glucose disposal) was statistically lower in patients treated with FK-506 and CsA (5.05+/-0.47 and 5.05+/-0.42 mg/kg/min) as compared to controls (6.62+/-0.38 mg/kg/min) (P<0.02), with a significantly higher nonoxidative glucose disposal for the control group (P<0.01), and lower free fatty acid levels (P<0.05). Glucose 36-43 insulin Homo sapiens 9-16 10567373-0 1999 Engineering a glucose-responsive human insulin-secreting cell line from islets of Langerhans isolated from a patient with persistent hyperinsulinemic hypoglycemia of infancy. Glucose 14-21 insulin Homo sapiens 39-46 10567373-6 1999 One selected clonal cell line (NISK9) had normal K(ATP) channel activity, and as a result of changes in intracellular Ca(2+) homeostasis ([Ca(2+)](i)) secreted insulin within the physiological range of glucose concentrations. Glucose 202-209 insulin Homo sapiens 160-167 10589951-7 1999 RESULTS: Insulin sensitivity (total glucose disposal) was statistically lower in patients treated with FK-506 and CsA (5.05+/-0.47 and 5.05+/-0.42 mg/kg/min) as compared to controls (6.62+/-0.38 mg/kg/min) (P<0.02), with a significantly higher nonoxidative glucose disposal for the control group (P<0.01), and lower free fatty acid levels (P<0.05). Glucose 260-267 insulin Homo sapiens 9-16 10567702-3 1999 PDX-1 has been suggested to be involved in the glucose-dependent regulation of insulin gene transcription. Glucose 47-54 insulin Homo sapiens 79-86 10842651-1 1999 Insulin-mediated glucose disposal varies approximately 10-fold in apparently healthy human beings. Glucose 17-24 insulin Homo sapiens 0-7 10842651-2 1999 Insulin (I)-resistant individuals can remain glucose tolerant if the pancreas compensates for this defect by secreting large amounts of I. Glucose 45-52 insulin Homo sapiens 0-7 10842657-1 1999 Adipose tissue only accounts for a relatively small proportion (< 10%) of the peripheral glucose utilization in response to insulin. Glucose 92-99 insulin Homo sapiens 127-134 10842654-4 1999 Because insulin-mediated glucose uptake in central hypothalamic neurons regulates SNS activity in response to dietary intake, a hypothesis was developed that links the hyperinsulinemia of obesity to sympathetic stimulation, the latter exerting a prohypertensive effect mediated by the kidney, the heart, and the vasculature. Glucose 25-32 insulin Homo sapiens 8-15 10842662-0 1999 Signaling pathways mediating insulin-stimulated glucose transport. Glucose 48-55 insulin Homo sapiens 29-36 10842663-3 1999 The infusion of amino acids or fatty acids decreases insulin-stimulated glucose disposal in vivo; sustained hyperglycemia also induces insulin resistance. Glucose 72-79 insulin Homo sapiens 53-60 10593324-3 1999 Factors such as onset, peak and duration of action can influence the ability of a particular insulin regimen to help control glucose levels. Glucose 125-132 insulin Homo sapiens 93-100 10593324-6 1999 The premeal dose of insulin lispro can be adjusted based on the content of the meal and the patient"s blood glucose level. Glucose 108-115 insulin Homo sapiens 20-27 10609251-12 1999 These patients had reduced basal but increased glucose stimulated insulin levels. Glucose 47-54 insulin Homo sapiens 66-73 10567007-1 1999 The effects of fasting on the pathways of insulin-stimulated glucose disposal were explored in three groups of seven normal subjects. Glucose 61-68 insulin Homo sapiens 42-49 10567007-5 1999 Results were similar in group 3 in which the clamp glucose disposal was restored by a pharmacological elevation of insulin ( approximately 2,800 microU/ml), but in this case, both glycogen synthesis and nonoxidative glycolysis participated in the rise in nonoxidative glucose disposal. Glucose 51-58 insulin Homo sapiens 115-122 10567007-5 1999 Results were similar in group 3 in which the clamp glucose disposal was restored by a pharmacological elevation of insulin ( approximately 2,800 microU/ml), but in this case, both glycogen synthesis and nonoxidative glycolysis participated in the rise in nonoxidative glucose disposal. Glucose 268-275 insulin Homo sapiens 115-122 10672386-6 1999 The serum insulin at the second hour of the OGTT fell from 100.79 +/- 42.79 mU/l to 54.56 +/- 25.43 mU/l (P < 0.0005) even though there was no change in the blood glucose level at this point. Glucose 166-173 insulin Homo sapiens 10-17 10559032-1 1999 The primary goal of this investigation was to see whether plasminogen activator inhibitor-1 (PAI-1) concentrations varied as a function of differences in insulin-mediated glucose disposal in 2 groups of healthy women matched for every other variable that might play a role in regulation of PAI-1. Glucose 171-178 insulin Homo sapiens 154-161 10687763-5 1999 Changes to diet and the introduction and adjustment of insulin therapy were designed to maintain postprandial glucose levels below these targets. Glucose 110-117 insulin Homo sapiens 55-62 10574416-5 1999 As for oral glucose tolerance test, the area under the curve of insulin diminished significantly after benidipine treatment. Glucose 12-19 insulin Homo sapiens 64-71 10535452-10 1999 In summary, we found that FDRs with normal glucose tolerance had defects in insulin action and secretion. Glucose 43-50 insulin Homo sapiens 76-83 10535452-11 1999 The newly recognized insulin secretory defect consisted of disruption of the normal circadian ISR cycle, which resulted in reduced insulin secretion (and glucose uptake) during the ascending part of the 24 h ISR cycle. Glucose 154-161 insulin Homo sapiens 21-28 10535454-4 1999 Compared with the NFG/NGT group, individuals with IFG/NGT had lower maximal insulin-stimulated glucose disposal (M; -20%, P < 0.01), a lower acute insulin response (AIR) to intravenous glucose (-33%, P < 0.05), and higher EGO (8%, P = 0.055). Glucose 95-102 insulin Homo sapiens 76-83 10634968-3 1999 A summary of recent reviews on the pathogenesis of systemic insulin resistance indicates that major factors are decreased insulin effects on muscular glycogen synthase or preceding steps in the insulin signalling cascade, on endogenous glucose production and on circulating free fatty acids (FFA) from adipose tissue lipolysis. Glucose 236-243 insulin Homo sapiens 60-67 10634968-3 1999 A summary of recent reviews on the pathogenesis of systemic insulin resistance indicates that major factors are decreased insulin effects on muscular glycogen synthase or preceding steps in the insulin signalling cascade, on endogenous glucose production and on circulating free fatty acids (FFA) from adipose tissue lipolysis. Glucose 236-243 insulin Homo sapiens 122-129 10634968-9 1999 Cortisol counteracts the insulin activation of glycogen synthase in muscle, the insulin inhibition of hepatic glucose production and the insulin inhibition of lipolysis in adipose tissue, leading to the well-established systemic insulin resistance caused by excess cortisol. Glucose 110-117 insulin Homo sapiens 80-87 10634968-9 1999 Cortisol counteracts the insulin activation of glycogen synthase in muscle, the insulin inhibition of hepatic glucose production and the insulin inhibition of lipolysis in adipose tissue, leading to the well-established systemic insulin resistance caused by excess cortisol. Glucose 110-117 insulin Homo sapiens 80-87 15251651-5 1999 Basal and glucose-stimulated C-peptide levels as well as stimulated glucose values were contrasted in the responder versus nonresponder groups. Glucose 10-17 insulin Homo sapiens 29-38 15251651-9 1999 In a comparison of the non-insulin-requiring responder and insulin-requiring nonresponder groups, the responder group had significantly higher glucose-stimulated C-peptide levels and much lower stimulated glucose levels. Glucose 143-150 insulin Homo sapiens 59-66 15251651-9 1999 In a comparison of the non-insulin-requiring responder and insulin-requiring nonresponder groups, the responder group had significantly higher glucose-stimulated C-peptide levels and much lower stimulated glucose levels. Glucose 143-150 insulin Homo sapiens 162-171 15251651-9 1999 In a comparison of the non-insulin-requiring responder and insulin-requiring nonresponder groups, the responder group had significantly higher glucose-stimulated C-peptide levels and much lower stimulated glucose levels. Glucose 205-212 insulin Homo sapiens 59-66 15251651-11 1999 Combination treatment with metformin and troglitazone for 12 weeks resulted in a significant reduction in the C-peptide response and glucose variables after the glucose load. Glucose 161-168 insulin Homo sapiens 110-119 15251651-13 1999 Inability to normalize glucose intolerance after restoring insulin resistance with insulin sensitizers is supportive of the presence of both disturbed beta-cell function and insulin resistance in patients with type 2 diabetes. Glucose 23-30 insulin Homo sapiens 59-66 10542046-0 1999 Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. Glucose 203-210 insulin Homo sapiens 44-51 10542046-3 1999 We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. Glucose 276-283 insulin Homo sapiens 46-53 10542046-5 1999 In contrast, the nonesterified fatty acid palmitate inhibited insulin-induced signalling cascades not only at the level of IR and IRS-1 phosphorylation, but also at the level protein kinase B (PKB/Akt), which is thought to be directly involved in the insulin-induced translocation of GLUT4, and inhibited insulin-induced glucose uptake. Glucose 321-328 insulin Homo sapiens 62-69 10551692-9 1999 Glucose infusion rate was significantly lower in CSX and MSx groups than in normal controls (p < 0.01), suggesting that in both CSX and MSX groups insulin resistance is present. Glucose 0-7 insulin Homo sapiens 150-157 10573439-0 1999 Low plasma insulin-like growth factor-1 concentrations predict worsening of insulin-mediated glucose uptake in older people. Glucose 93-100 insulin Homo sapiens 11-18 10573439-2 1999 To gain further insight, the predictive role that low plasma IGF-1 concentration may have on insulin- mediated glucose uptake in older persons was investigated. Glucose 111-118 insulin Homo sapiens 93-100 10573439-5 1999 MEASUREMENTS: At baseline and at the end of the follow-up, insulin-mediated glucose uptake was assessed by euglycemic glucose clamp and plasma total IGF-1 and IGF-binding protein 3 (IGF-BP-3) in each subject, and concentrations were determined. Glucose 76-83 insulin Homo sapiens 59-66 10573439-5 1999 MEASUREMENTS: At baseline and at the end of the follow-up, insulin-mediated glucose uptake was assessed by euglycemic glucose clamp and plasma total IGF-1 and IGF-binding protein 3 (IGF-BP-3) in each subject, and concentrations were determined. Glucose 118-125 insulin Homo sapiens 59-66 10573439-6 1999 RESULTS: At baseline, plasma IGF-1 concentrations correlated with whole body glucose uptake (WBGD) (r = 0.39, P < .003), insulin-stimulated glucose oxidation (GOX) (r = 0.35, P < .009), and non-oxidative glucose metabolism (r = 0.37, P < .007). Glucose 143-150 insulin Homo sapiens 124-131 10573439-6 1999 RESULTS: At baseline, plasma IGF-1 concentrations correlated with whole body glucose uptake (WBGD) (r = 0.39, P < .003), insulin-stimulated glucose oxidation (GOX) (r = 0.35, P < .009), and non-oxidative glucose metabolism (r = 0.37, P < .007). Glucose 143-150 insulin Homo sapiens 124-131 10583718-6 1999 MAIN OUTCOME MEASURES: Insulin-mediated glucose disposal (hyperinsulinaemic euglycaemic clamp) adjusted for lean body mass and fibrinogen, von Willebrand factor, prothrombin fragment 1 + 2, thrombin/antithrombin complex and plasminogen activator inhibitor activity were determined. Glucose 40-47 insulin Homo sapiens 23-30 10583718-7 1999 RESULTS: Insulin-mediated glucose disposal adjusted for lean body mass was significantly lower in the high-risk group than in the low-risk group. Glucose 26-33 insulin Homo sapiens 9-16 10583718-14 1999 The negative relationship between von Willebrand factor levels and glucose disposal in the low-risk group may indicate that insulin resistance can induce an endothelial dysfunction even in non-diabetic subjects. Glucose 67-74 insulin Homo sapiens 124-131 10608589-15 1999 This may be because serum insulin levels are not increased by acipimox, and insulin is instrumental in enhancing the joint transport of glucose and TI-201 into myocytes. Glucose 136-143 insulin Homo sapiens 76-83 10582546-6 1999 However, the acute insulin response to intravenous (IV) glucose (AIR(G)) and IV glucagon at euglycemia and hyperglycemia did not change with rhGH therapy and were similar to the control group values. Glucose 56-63 insulin Homo sapiens 19-26 10582559-1 1999 The increase in leg and forearm blood flow induced by insulin could be secondary to its metabolic effect on glucose uptake. Glucose 108-115 insulin Homo sapiens 54-61 10547194-7 1999 An alteration of the IAPP/insulin secretory ratio is seen in response to infusion of exogenous glucose or in response to the neutralization of intraislet somatostatin. Glucose 95-102 insulin Homo sapiens 26-33 10578247-21 1999 By stepwise regression analyses, higher peak serum glucose concentrations were associated with increased total body %fat, highest level of lesion (complete Tetra vs other neurological subgroups), older age at time of injury, and male gender; higher peak plasma insulin was associated with increased total body %fat and male gender. Glucose 51-58 insulin Homo sapiens 261-268 10535992-7 1999 Hepatic fatty acid synthase and Spot-14 are insulin/glucose-dependent genes. Glucose 52-59 insulin Homo sapiens 44-51 10534468-12 1999 CONCLUSIONS: These data indicate that insulin and IGF-1 are powerful independent determinants of LV mass and geometry in untreated subjects with essential hypertension and normal glucose tolerance. Glucose 179-186 insulin Homo sapiens 38-45 10572531-12 1999 Glucose was administered initially, but transient intravenous insulin infusion became necessary to counteract hyperglycaemia. Glucose 0-7 insulin Homo sapiens 62-69 10551191-0 1999 Insulin adjustment by a diabetes nurse educator improves glucose control in insulin-requiring diabetic patients: a randomized trial. Glucose 57-64 insulin Homo sapiens 0-7 10551191-0 1999 Insulin adjustment by a diabetes nurse educator improves glucose control in insulin-requiring diabetic patients: a randomized trial. Glucose 57-64 insulin Homo sapiens 76-83 10551191-1 1999 BACKGROUND: Diabetic patients taking insulin often have suboptimal glucose control, and standard methods of health care delivery are ineffective in improving such control. Glucose 67-74 insulin Homo sapiens 37-44 10551191-2 1999 This study was undertaken to determine if insulin adjustment according to advice provided by telephone by a diabetes nurse educator could lead to better glucose control, as indicated by level of glycated hemoglobin (HbA1c). Glucose 153-160 insulin Homo sapiens 42-49 10551191-3 1999 METHODS: The authors conducted a prospective randomized trial involving 46 insulin-requiring diabetic patients who had poor glucose control (HbA1c of 0.085 or more). Glucose 124-131 insulin Homo sapiens 75-82 10551191-9 1999 INTERPRETATION: Insulin adjustment according to advice from a diabetes nurse educator is an effective method of improving glucose control in insulin-requiring diabetic patients. Glucose 122-129 insulin Homo sapiens 16-23 10551191-9 1999 INTERPRETATION: Insulin adjustment according to advice from a diabetes nurse educator is an effective method of improving glucose control in insulin-requiring diabetic patients. Glucose 122-129 insulin Homo sapiens 141-148 10641582-7 1999 As in previous reports, patients demonstrated higher plasma glucose and insulin concentrations than controls in response to fixed glucose dosing. Glucose 130-137 insulin Homo sapiens 72-79 10532502-3 1999 We used Bergman"s minimal model to analyze the insulin response to intravenous glucose in 21 subjects: 8 patients with previous (>3 months) acute coronary syndrome but no effort-related angina; 6 patients with stable effort angina but no prior acute event; and 7 healthy controls. Glucose 79-86 insulin Homo sapiens 47-54 10532502-10 1999 In contrast, patients with previous acute onset of ischemia had significantly greater 180-minute integrated insulinemia (p = 0.04) and reduced insulin sensitivity (p = 0.05) after the glucose challenge than did the stable angina group. Glucose 184-191 insulin Homo sapiens 108-115 10523787-1 1999 Insulin has diverse effects on cells, including stimulation of glucose transport, gene expression, and alterations of cell morphology. Glucose 63-70 insulin Homo sapiens 0-7 10523787-8 1999 In both muscle and adipose cells, actin disassembly inhibited early insulin-induced events such as recruitment of glucose transporters to the cell surface and enhanced glucose transport. Glucose 114-121 insulin Homo sapiens 68-75 10603743-2 1999 The aim was to assess glucose and insulin responses to oral glucose loading in 9 prepubertal and 11 pubertal patients with Turner syndrome. Glucose 60-67 insulin Homo sapiens 34-41 10516134-1 1999 Studies in rodents have established that GLUT-4 translocation is the major mechanism by which insulin and exercise increase glucose uptake in skeletal muscle. Glucose 124-131 insulin Homo sapiens 94-101 10516134-8 1999 Compared with insulin treatment alone, glucose infusion rates were significantly increased during the postexercise clamp for the periods 0-30 min, 30-60 min, and 60-90 min, but not during the last 30 min of the clamp. Glucose 39-46 insulin Homo sapiens 14-21 10554661-2 1999 As a result of influences on insulin signalling, glucose transport, hepatic glucose metabolism and modulation of the peroxisome proliferator activating receptor (PPAR-gamma), TZDs augment the effect of insulin in insulin-sensitive target tissues. Glucose 49-56 insulin Homo sapiens 202-209 10554661-2 1999 As a result of influences on insulin signalling, glucose transport, hepatic glucose metabolism and modulation of the peroxisome proliferator activating receptor (PPAR-gamma), TZDs augment the effect of insulin in insulin-sensitive target tissues. Glucose 49-56 insulin Homo sapiens 202-209 10491343-0 1999 Splanchnic and extrasplanchnic extraction of insulin following oral and intravenous glucose loads. Glucose 84-91 insulin Homo sapiens 45-52 10491343-7 1999 Extrasplanchnic extraction of insulin fell from 90-100% in the basal state to a minimum of 3+/-6% (P<0.001) after oral glucose; during the first 5 min of intravenous glucose infusion it fell in relative but not in absolute terms. Glucose 122-129 insulin Homo sapiens 30-37 10491343-7 1999 Extrasplanchnic extraction of insulin fell from 90-100% in the basal state to a minimum of 3+/-6% (P<0.001) after oral glucose; during the first 5 min of intravenous glucose infusion it fell in relative but not in absolute terms. Glucose 169-176 insulin Homo sapiens 30-37 10525657-3 1999 Therefore a database of kinetic variables of wild-type and 20 missense mutants of glucokinase was developed and used in mathematical modelling to predict the thresholds for glucose-stimulated insulin release. Glucose 173-180 insulin Homo sapiens 192-199 10525657-7 1999 A mathematical model predicting the threshold for glucose-stimulated insulin release was constructed. Glucose 50-57 insulin Homo sapiens 69-76 10525657-11 1999 Glucokinase flux at threshold for glucose-stimulated insulin release was about 25 % of total phosphorylating potential in the normal beta-cell and this was used to predict thresholds for the mutant heterozygotes. Glucose 34-41 insulin Homo sapiens 53-60 10525657-16 1999 The mathematical model to calculate the threshold for glucose-stimulated insulin release predicts fasting blood glucose between 3 and 7 mmol/l in subjects with glucokinase gene mutations. Glucose 54-61 insulin Homo sapiens 73-80 10525657-16 1999 The mathematical model to calculate the threshold for glucose-stimulated insulin release predicts fasting blood glucose between 3 and 7 mmol/l in subjects with glucokinase gene mutations. Glucose 112-119 insulin Homo sapiens 73-80 10525666-2 1999 The sarco(endo)plasmic reticulum Ca(2+)-transport ATPase (SERCA) plays an important part in the glucose-activated beta-cell Ca(2+) signalling that regulates insulin secretion. Glucose 96-103 insulin Homo sapiens 157-164 10525667-9 1999 Glucose tolerant middle-aged subjects homozygous for the polymorphism (n = 31), however, had on average a 25 % decrease in fasting serum insulin concentrations (p = 0.009) and 28 % (p = 0.01) and 34 % (p = 0.003) reductions in serum insulin concentrations at 30 and 60 min, respectively, during an OGTT compared with wildtype carriers (n = 107). Glucose 0-7 insulin Homo sapiens 137-144 10525667-9 1999 Glucose tolerant middle-aged subjects homozygous for the polymorphism (n = 31), however, had on average a 25 % decrease in fasting serum insulin concentrations (p = 0.009) and 28 % (p = 0.01) and 34 % (p = 0.003) reductions in serum insulin concentrations at 30 and 60 min, respectively, during an OGTT compared with wildtype carriers (n = 107). Glucose 0-7 insulin Homo sapiens 233-240 10526729-12 1999 The interaction reflects an increased inhibition by glibenclamide-enhanced insulin levels of hepatic glucose production when hepatic glucose production is accelerated by exercise. Glucose 101-108 insulin Homo sapiens 75-82 10526729-12 1999 The interaction reflects an increased inhibition by glibenclamide-enhanced insulin levels of hepatic glucose production when hepatic glucose production is accelerated by exercise. Glucose 133-140 insulin Homo sapiens 75-82 10547214-7 1999 The rise in blood glucose after the main meal after sunset was 3.0+/-0.4 mmol/l after 1 h in the insulin lispro treatment group compared to 4.3+/-0.4 mmol/l in the soluble insulin treatment group (P<0.01), and 2.6+/-0.4 mmol/l after 2h with insulin lispro compared to 4.0+/-0.5 mmol/l with soluble insulin (P<0.008). Glucose 18-25 insulin Homo sapiens 97-104 11475277-12 1999 Studies comparing sequentially administered subcutaneous and inhaled regular insulins have demonstrated significantly reproducible glucose-lowering effects of inhaled insulin. Glucose 131-138 insulin Homo sapiens 77-84 10583426-2 1999 The classical action of insulin is the control of glucose metabolism through the dual feedback loop linking plasma insulin with plasma glucose concentrations. Glucose 50-57 insulin Homo sapiens 24-31 10583426-2 1999 The classical action of insulin is the control of glucose metabolism through the dual feedback loop linking plasma insulin with plasma glucose concentrations. Glucose 50-57 insulin Homo sapiens 115-122 10583426-2 1999 The classical action of insulin is the control of glucose metabolism through the dual feedback loop linking plasma insulin with plasma glucose concentrations. Glucose 135-142 insulin Homo sapiens 24-31 10583426-2 1999 The classical action of insulin is the control of glucose metabolism through the dual feedback loop linking plasma insulin with plasma glucose concentrations. Glucose 135-142 insulin Homo sapiens 115-122 10583426-3 1999 This canon has been revised to incorporate the impact of insulin resistance or insulin deficiency, both of which alter glucose homeostasis through maladaptive responses (namely, chronic hyperinsulinaemia and glucose toxicity). Glucose 119-126 insulin Homo sapiens 57-64 10583426-4 1999 A large body of knowledge is available on the physiology, cellular biology and molecular genetics of insulin action on glucose production and uptake. Glucose 119-126 insulin Homo sapiens 101-108 10615805-18 1999 Body weight of children from insulin treated GDM mothers is connected with fasting and 2-hour 75OGTT glucose level. Glucose 101-108 insulin Homo sapiens 29-36 10490558-10 1999 CONCLUSIONS: A simple index of insulin resistance measured on patients admitted with myocardial infarction provides an important predictive measure of poor outcome and is superior to admission glucose measurement. Glucose 193-200 insulin Homo sapiens 31-38 10523330-6 1999 In contrast, fasting insulin concentrations and the insulin response (insulin area under the curve) to glucose challenge were unchanged. Glucose 103-110 insulin Homo sapiens 52-59 10523330-6 1999 In contrast, fasting insulin concentrations and the insulin response (insulin area under the curve) to glucose challenge were unchanged. Glucose 103-110 insulin Homo sapiens 52-59 10523330-7 1999 Insulin sensitivity (defined as the rate of glucose disappearance per unit of insulin increase during the period 0 to 40 minutes after the glucose load) was significantly higher on the low-fat diet. Glucose 44-51 insulin Homo sapiens 0-7 10523330-7 1999 Insulin sensitivity (defined as the rate of glucose disappearance per unit of insulin increase during the period 0 to 40 minutes after the glucose load) was significantly higher on the low-fat diet. Glucose 44-51 insulin Homo sapiens 78-85 10523330-7 1999 Insulin sensitivity (defined as the rate of glucose disappearance per unit of insulin increase during the period 0 to 40 minutes after the glucose load) was significantly higher on the low-fat diet. Glucose 139-146 insulin Homo sapiens 0-7 10557022-7 1999 Leptin concentration also correlated with fasting insulin (r=0.41) and with glucose and insulin concentrations 2 h after a glucose load (r=0.19 and 0.49). Glucose 123-130 insulin Homo sapiens 88-95 10579679-0 1999 Insulin delivery governed by covalently modified lectin-glycogen gels sensitive to glucose. Glucose 83-90 insulin Homo sapiens 0-7 10579679-7 1999 Insulin delivery was demonstrated using this covalently modified system in conditions of repeated glucose triggering at 20 degrees C and 37 degrees C. The magnitude of the response was less variable than for the dextran-based gels studied previously. Glucose 98-105 insulin Homo sapiens 0-7 10490615-0 1999 G alpha-q/11 protein plays a key role in insulin-induced glucose transport in 3T3-L1 adipocytes. Glucose 57-64 insulin Homo sapiens 41-48 10490615-3 1999 Galphaq/11 antibody and RGS2 inhibited insulin-induced GLUT4 translocation by 60 or 75%, respectively, indicating that activated Galphaq is important for insulin-induced glucose transport. Glucose 170-177 insulin Homo sapiens 39-46 10490615-3 1999 Galphaq/11 antibody and RGS2 inhibited insulin-induced GLUT4 translocation by 60 or 75%, respectively, indicating that activated Galphaq is important for insulin-induced glucose transport. Glucose 170-177 insulin Homo sapiens 154-161 10540872-6 1999 Biotin-induced enhancement of glucose-induced insulin release was evident within the first few minutes of perfusion. Glucose 30-37 insulin Homo sapiens 46-53 10488084-0 1999 The role of glucose metabolites in the activation and translocation of glycogen synthase by insulin in 3T3-L1 adipocytes. Glucose 12-19 insulin Homo sapiens 92-99 10488084-1 1999 The role of increased glucose transport in the hormonal regulation of glycogen synthase by insulin was investigated in 3T3-L1 adipocytes. Glucose 22-29 insulin Homo sapiens 91-98 10488084-11 1999 These results indicate that glucose metabolites have an impact on the regulation of glycogen synthase activation and localization by insulin. Glucose 28-35 insulin Homo sapiens 133-140 10625950-7 1999 The fact that some InsP6 is localised to membranes, so being topographically disposed to regulate ion channels as well as exocytosis, and that it has a rapid rate of turnover in glucose-stimulated insulin-secreting cells, suggest novel functions for InsP6 in the insulin secretory process. Glucose 178-185 insulin Homo sapiens 197-204 10480508-7 1999 Insulin resistance index was estimated as a product of fasting plasma insulin and glucose concentrations. Glucose 82-89 insulin Homo sapiens 0-7 10480510-0 1999 Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Glucose 47-54 insulin Homo sapiens 0-7 10480595-0 1999 Identification of the docked granule pool responsible for the first phase of glucose-stimulated insulin secretion. Glucose 77-84 insulin Homo sapiens 96-103 10480595-1 1999 The mechanisms underlying the first phase of glucose-stimulated insulin release, the deterioration of which marks the early stages of both type 1 and type 2 diabetes, are essentially unknown. Glucose 45-52 insulin Homo sapiens 64-71 10480595-6 1999 Using co-immunoprecipitation as a marker for docked granules, we found that the docked pool was rapidly discharged during the first phase of glucose-stimulated insulin release and refilled during the second phase. Glucose 141-148 insulin Homo sapiens 160-167 10480612-10 1999 These data indicate that insulin resistance to glucose transport during pregnancy is uniquely associated with a decrease in IRS-1 tyrosine phosphorylation, primarily due to decreased expression of IRS-1 protein. Glucose 47-54 insulin Homo sapiens 25-32 10480612-11 1999 However, in GDM subjects, a decrease in tyrosine phosphorylation of the insulin receptor beta-subunit is associated with further decreases in glucose transport activity. Glucose 142-149 insulin Homo sapiens 72-79 10480616-7 1999 Insulin-stimulated glucose uptake during euglycemic-hyperinsulinemic clamping was more than twofold higher after Acipimox than after placebo. Glucose 19-26 insulin Homo sapiens 0-7 10480625-1 1999 Because overexpression of the glucose-6-phosphatase catalytic subunit (G-6-Pase) in both type 1 and type 2 diabetes may contribute to the characteristic increased rate of hepatic glucose production, we have investigated whether the insulin response unit (IRU) identified in the mouse G-6-Pase promoter is conserved in the human promoter. Glucose 30-37 insulin Homo sapiens 232-239 10469164-5 1999 Such changes are combined with a decline in plasma DHEAS and IGF-I concentration and a rise in plasma TNF-alpha concentrations and oxidative stress, which, in turn, may interact with the anthropometric changes determining the worsening in insulin-mediated glucose uptake. Glucose 256-263 insulin Homo sapiens 239-246 10480298-3 1999 Hyperinsulinemia was defined as a serum insulin level of > or = 60.4 IU/l at 120 minutes after 75 g oral glucose challenge. Glucose 108-115 insulin Homo sapiens 5-12 10491408-3 1999 Insulin-stimulated glucose disposal was reduced 31% in obese subjects and 63% in diabetic subjects, compared with lean subjects. Glucose 19-26 insulin Homo sapiens 0-7 10491408-12 1999 In lean subjects only, insulin-stimulated Akt1/2 activity correlated with glucose disposal rate. Glucose 74-81 insulin Homo sapiens 23-30 10610071-4 1999 Dietary carbohydrate promotes its own oxidation by an insulin-mediated stimulation of glucose oxidation. Glucose 86-93 insulin Homo sapiens 54-61 10610074-2 1999 The defects most likely to explain the insulin resistance of the insulin resistance syndrome include: 1) the glucose transport system of skeletal muscle (GLUT-4) and its different signalling proteins and enzymes; 2) glucose phosphorylation by hexokinase; 3) glycogen synthase activity and 4) competition between glucose and fatty acid oxidation (glucose-fatty acid cycle). Glucose 109-116 insulin Homo sapiens 39-46 10610074-2 1999 The defects most likely to explain the insulin resistance of the insulin resistance syndrome include: 1) the glucose transport system of skeletal muscle (GLUT-4) and its different signalling proteins and enzymes; 2) glucose phosphorylation by hexokinase; 3) glycogen synthase activity and 4) competition between glucose and fatty acid oxidation (glucose-fatty acid cycle). Glucose 216-223 insulin Homo sapiens 39-46 10610074-2 1999 The defects most likely to explain the insulin resistance of the insulin resistance syndrome include: 1) the glucose transport system of skeletal muscle (GLUT-4) and its different signalling proteins and enzymes; 2) glucose phosphorylation by hexokinase; 3) glycogen synthase activity and 4) competition between glucose and fatty acid oxidation (glucose-fatty acid cycle). Glucose 216-223 insulin Homo sapiens 39-46 10446150-2 1999 This accounts for the unique capability of insulin (and possibly insulin-like growth factor-1), but not other growth factors, to stimulate glucose uptake and anabolic metabolism in heart, skeletal muscle, and adipose tissue. Glucose 139-146 insulin Homo sapiens 43-93 10446150-4 1999 The serine/threonine protein kinases Akt1 and Akt2, which have been implicated as mediators of insulin-stimulated glucose uptake, as well as glycogen, lipid, and protein synthesis, were shown to mirror this selectivity in this tissue culture system. Glucose 114-121 insulin Homo sapiens 95-102 10487270-0 1999 Insulin-like growth factor-1 receptors mediate infragenicular vascular smooth muscle cell proliferation in response to glucose and insulin not by insulin receptors. Glucose 119-126 insulin Homo sapiens 0-7 10487270-5 1999 By using monoclonal antibodies directed against insulin (IRA) and IGF-1 (IGF-1RA) receptors, we attempt to further delineate the mechanism for the proliferation of VSMC in response to insulin and glucose. Glucose 196-203 insulin Homo sapiens 48-55 11261605-9 2000 The mouse islets maintained a 2- to 3-fold insulin response at both time points when challenged high glucose. Glucose 101-108 insulin Homo sapiens 43-50 10615832-4 1999 After adjusting for age, gender, and body mass index, and using identical laboratory methods, we found significantly lower insulin levels among Eskimo compared with Indian participants with normal glucose tolerance. Glucose 197-204 insulin Homo sapiens 123-130 10526906-6 1999 In addition, they had greater serum insulin (59 +/- 31 versus 43 +/- 12 pmol/l) despite there being no differences in plasma glucose, resulting in a reduction of the ratio of glucose to insulin (x 10(6)) (107 +/- 43 versus 126 +/-, which is an estimate of insulin sensitivity in a nondiabetic population. Glucose 175-182 insulin Homo sapiens 36-43 10490615-9 1999 In summary, (i) Galphaq appears to play a necessary role in insulin-stimulated glucose transport, (ii) Galphaq action in the insulin signaling pathway is upstream of and dependent upon PI3-kinase, and (iii) Galphaq can transmit signals from the insulin receptor to the p110alpha subunit of PI3-kinase, which leads to GLUT4 translocation. Glucose 79-86 insulin Homo sapiens 60-67 10490615-9 1999 In summary, (i) Galphaq appears to play a necessary role in insulin-stimulated glucose transport, (ii) Galphaq action in the insulin signaling pathway is upstream of and dependent upon PI3-kinase, and (iii) Galphaq can transmit signals from the insulin receptor to the p110alpha subunit of PI3-kinase, which leads to GLUT4 translocation. Glucose 79-86 insulin Homo sapiens 125-132 10535386-4 1999 Oral administration of imidapril improved insulin sensitivity based on the results of an oral glucose tolerance test (OGTT) and a decrease in urinary glucose secretion. Glucose 94-101 insulin Homo sapiens 42-49 10540872-5 1999 In control rats as well as biotin-deficient rats, the insulin response to glucose stimulation was enhanced by the addition of 1 mM biotin to the perfusate. Glucose 74-81 insulin Homo sapiens 54-61 10656171-2 1999 This study aimed to provide insight on insulin behavior and its relationship with glucose metabolism by investigating insulin secretion and hepatic clearance in non-steady-state conditions in borderline hypertensive patients. Glucose 82-89 insulin Homo sapiens 39-46 10656171-6 1999 glucose tolerance factor KG (2.0 +/- 0.2 vs 2.2 +/- 0.1% min-1), SG (0.035 +/- 0.004 vs 0.032 +/- 0.007 min-1) and S1 [3.5 +/- 0.5 vs 3.8 +/- 0.3 10(4) min-1 (microU/mL)] were similar, both basal insulin and C-peptide exhibited a marked increase (87 +/- 8 vs 46 +/- 6 pmol/L, p = 0.0003; 637 +/- 62 vs 381 +/- 76 pmol/L, p < 0.03) demonstrating insulin resistance in basal conditions. Glucose 0-7 insulin Homo sapiens 196-203 10498157-0 1999 Insulin-mediated glucose uptake in congestive heart failure. Glucose 17-24 insulin Homo sapiens 0-7 10464254-6 1999 Our results suggest the existence of at least two distinct pathways that undergo insulin-stimulated exocytosis in 3T3-L1 adipocytes, one for adipsin release and one for glucose transporter translocation. Glucose 169-176 insulin Homo sapiens 81-88 10469863-5 1999 Insulin-treated patients also had greater plasma albumin levels and body weights and lower fasting serum C-peptide levels (2.81 +/- 1.77 v 3.12 +/- 2.04 ng/mL; analysis of variance, P = 0.007 adjusted for fasting glucose concentration). Glucose 213-220 insulin Homo sapiens 0-7 10484354-4 1999 Glucose stimulation of the migration was additively enhanced by 100 nM insulin, and the insulin effect was found to be unaffected by either PD-98059 or wortmannin, a mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase inhibitor and a phosphatidylinositol 3-kinase inhibitor, respectively. Glucose 0-7 insulin Homo sapiens 71-78 10469012-9 1999 During the insulin infusion, insulin concentration increased from 78 +/- 12 to 660 +/- 30 pmol/l, resulting in a complete inhibition of splanchnic glucose production after 40 min of infusion. Glucose 147-154 insulin Homo sapiens 11-18 10469012-9 1999 During the insulin infusion, insulin concentration increased from 78 +/- 12 to 660 +/- 30 pmol/l, resulting in a complete inhibition of splanchnic glucose production after 40 min of infusion. Glucose 147-154 insulin Homo sapiens 29-36 10447516-8 1999 Fasting glucose correlated positively with intact proinsulin (r(s) = 0.34) and the intact proinsulin:insulin ratio (r(s) = 0.24, p < 0. Glucose 8-15 insulin Homo sapiens 50-60 10447516-8 1999 Fasting glucose correlated positively with intact proinsulin (r(s) = 0.34) and the intact proinsulin:insulin ratio (r(s) = 0.24, p < 0. Glucose 8-15 insulin Homo sapiens 90-100 10447516-8 1999 Fasting glucose correlated positively with intact proinsulin (r(s) = 0.34) and the intact proinsulin:insulin ratio (r(s) = 0.24, p < 0. Glucose 8-15 insulin Homo sapiens 53-60 10447516-13 1999 In contrast, both low AIR and high fasting glucose concentrations were associated with a disproportionate increase in proinsulin concentration. Glucose 43-50 insulin Homo sapiens 118-128 10447521-11 1999 By suppressing cell proliferation and insulin biosynthesis, the p21 induction is likely to be implicated in the beta-cell glucose toxicity. Glucose 122-129 insulin Homo sapiens 38-45 10480510-1 1999 OBJECTIVE: Several methods have been proposed to evaluate insulin sensitivity from the data obtained from the oral glucose tolerance test (OGTT). Glucose 115-122 insulin Homo sapiens 58-65 10480510-8 1999 From the OGTT, we developed an index of whole-body insulin sensitivity (10,000/square root of [fasting glucose x fasting insulin] x [mean glucose x mean insulin during OGTT]), which is highly correlated (r = 0.73, P < 0.0001) with the rate of whole-body glucose disposal during the euglycemic insulin clamp. Glucose 103-110 insulin Homo sapiens 51-58 10480510-8 1999 From the OGTT, we developed an index of whole-body insulin sensitivity (10,000/square root of [fasting glucose x fasting insulin] x [mean glucose x mean insulin during OGTT]), which is highly correlated (r = 0.73, P < 0.0001) with the rate of whole-body glucose disposal during the euglycemic insulin clamp. Glucose 138-145 insulin Homo sapiens 51-58 10480510-8 1999 From the OGTT, we developed an index of whole-body insulin sensitivity (10,000/square root of [fasting glucose x fasting insulin] x [mean glucose x mean insulin during OGTT]), which is highly correlated (r = 0.73, P < 0.0001) with the rate of whole-body glucose disposal during the euglycemic insulin clamp. Glucose 138-145 insulin Homo sapiens 51-58 10480510-9 1999 CONCLUSIONS: Previous methods used to derive an index of insulin sensitivity from the OGTT have relied on the ratio of plasma glucose to insulin concentration during the OGTT. Glucose 126-133 insulin Homo sapiens 57-64 10480520-6 1999 Insulin sensitivity was measured by glucose decrement during the first 15 min of an intravenous insulin tolerance test. Glucose 36-43 insulin Homo sapiens 0-7 10480602-7 1999 They had intact acute insulin responses to intravenous pulses of glucose and to arginine and insulin secretory reserve. Glucose 65-72 insulin Homo sapiens 22-29 10480602-8 1999 Glucose potentiation of arginine-induced insulin secretion, the measure of insulin secretory reserve, correlated significantly (r = 0.095, P < 0.001) with the acute insulin response to intravenous glucose, rendering the latter a much simpler and valid measure of functional beta-cell mass. Glucose 0-7 insulin Homo sapiens 41-48 10480602-8 1999 Glucose potentiation of arginine-induced insulin secretion, the measure of insulin secretory reserve, correlated significantly (r = 0.095, P < 0.001) with the acute insulin response to intravenous glucose, rendering the latter a much simpler and valid measure of functional beta-cell mass. Glucose 0-7 insulin Homo sapiens 75-82 10480602-8 1999 Glucose potentiation of arginine-induced insulin secretion, the measure of insulin secretory reserve, correlated significantly (r = 0.095, P < 0.001) with the acute insulin response to intravenous glucose, rendering the latter a much simpler and valid measure of functional beta-cell mass. Glucose 200-207 insulin Homo sapiens 41-48 10480602-8 1999 Glucose potentiation of arginine-induced insulin secretion, the measure of insulin secretory reserve, correlated significantly (r = 0.095, P < 0.001) with the acute insulin response to intravenous glucose, rendering the latter a much simpler and valid measure of functional beta-cell mass. Glucose 200-207 insulin Homo sapiens 75-82 10499192-1 1999 Elevated free fatty acid concentrations are known to decrease insulin-mediated glucose uptake, glucose oxidation and glycogen synthesis. Glucose 79-86 insulin Homo sapiens 62-69 10465266-1 1999 Chronic exposure (48 h) to glucosamine resulted in a dose-dependent reduction of basal and insulin-stimulated glucose uptake activities in human skeletal muscle cell cultures from nondiabetic and type 2 diabetic subjects. Glucose 110-117 insulin Homo sapiens 91-98 10519617-5 1999 INTERVENTION(S): Variable hyperglycemic-hyperinsulinemic infusions replicated physiological increases in circulating glucose and insulin levels before and after 3-month GnRH-a administration. Glucose 117-124 insulin Homo sapiens 45-52 10462370-5 1999 The improved insulin-mediated glucose uptake was the result of a normalization of nonoxidative glucose disposal. Glucose 30-37 insulin Homo sapiens 13-20 10462370-5 1999 The improved insulin-mediated glucose uptake was the result of a normalization of nonoxidative glucose disposal. Glucose 95-102 insulin Homo sapiens 13-20 10462370-7 1999 The glucose-induced increase of insulin concentration, which was higher before LT, showed a significant reduction, although the first phase of beta-cell secretion remained significantly higher compared with that of controls. Glucose 4-11 insulin Homo sapiens 32-39 10462370-11 1999 An increased first-phase beta-cell insulin secretion in response to high glucose levels persists, suggesting that a memory of previous insulin resistance is maintained. Glucose 73-80 insulin Homo sapiens 35-42 10487672-1 1999 Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenemia that is amplified by insulin in the presence of resistance to insulin"s action to stimulate glucose uptake in muscle and fat. Glucose 163-170 insulin Homo sapiens 133-140 10487672-4 1999 Basal rates were similar, but there were significant decreases in insulin-stimulated (control, 51.8 +/- 7.0; PCOS, 29.5 +/- 2.9 nmol/10(6) cells x 2 h at 1,000,000 pmol/L; P < 0.005) and IGF-I-stimulated (control, 48.9 +/- 6.7; PCOS, 33.0 +/- 3.2 PCOS nmol/10(6) cells x 2 h at 100,000 pmol/L IGF-I; P < 0.05) glucose incorporation into glycogen in PCOS fibroblasts, a metabolic action of insulin. Glucose 316-323 insulin Homo sapiens 66-73 10491414-4 1999 Transition from NGT to IGT was associated with an increase in body weight, a decline in insulin-stimulated glucose disposal, and a decline in the acute insulin secretory response (AIR) to intravenous glucose, but no change in EGO. Glucose 107-114 insulin Homo sapiens 88-95 10491414-4 1999 Transition from NGT to IGT was associated with an increase in body weight, a decline in insulin-stimulated glucose disposal, and a decline in the acute insulin secretory response (AIR) to intravenous glucose, but no change in EGO. Glucose 200-207 insulin Homo sapiens 152-159 10491414-5 1999 Progression from IGT to diabetes was accompanied by a further increase in body weight, further decreases in insulin-stimulated glucose disposal and AIR, and an increase in basal EGO. Glucose 127-134 insulin Homo sapiens 108-115 10491414-6 1999 Thirty-one subjects who retained NGT over a similar period also gained weight, but their AIR increased with decreasing insulin-stimulated glucose disposal. Glucose 138-145 insulin Homo sapiens 119-126 10496480-3 1999 Insulin resistance was assessed by a 75-g oral glucose tolerance test and homeostasis model assessment (HOMA). Glucose 47-54 insulin Homo sapiens 0-7 10484052-10 1999 We postulate that the insulin resistance induced by dex in first-degree relatives of type 2 diabetic patients is associated with a preferential channeling of glucose into the glycolytic pathway (increased glucose oxidation and lactate production), probably associated with a preexisting downregulation of the glycosen synthase pathway. Glucose 158-165 insulin Homo sapiens 22-29 10484052-10 1999 We postulate that the insulin resistance induced by dex in first-degree relatives of type 2 diabetic patients is associated with a preferential channeling of glucose into the glycolytic pathway (increased glucose oxidation and lactate production), probably associated with a preexisting downregulation of the glycosen synthase pathway. Glucose 205-212 insulin Homo sapiens 22-29 10553576-1 1999 Glucose induces an increase in the intracellular Ca2+ concentration in pancreatic beta-cells to secrete insulin. Glucose 0-7 insulin Homo sapiens 104-111 10455135-1 1999 DissociationoOf insulin-stimulated glucose uptake and glut4 translocation. Glucose 35-42 insulin Homo sapiens 16-23 10455135-2 1999 The current studies investigated the contribution of phosphatidylinositol 3-kinase (PI3-kinase) isoforms to insulin-stimulated glucose uptake and glucose transporter 4 (GLUT4) translocation. Glucose 127-134 insulin Homo sapiens 108-115 10455135-5 1999 Interestingly, wortmannin inhibited insulin-stimulated glucose uptake at much lower doses, suggesting the existence of a second, higher affinity target of the drug. Glucose 55-62 insulin Homo sapiens 36-43 10468524-5 1999 A significant relationship also existed between insulin resistance (estimated by the steady-state plasma glucose concentration during the insulin suppression test) and mononuclear cell binding in both the normotensive (r=0.86, P<0.001) and hypertensive (r=0.74, P<0. Glucose 105-112 insulin Homo sapiens 48-55 10468524-5 1999 A significant relationship also existed between insulin resistance (estimated by the steady-state plasma glucose concentration during the insulin suppression test) and mononuclear cell binding in both the normotensive (r=0.86, P<0.001) and hypertensive (r=0.74, P<0. Glucose 105-112 insulin Homo sapiens 138-145 10454950-2 1999 An elevated rate of basal hepatic glucose production in the presence of hyperinsulinemia is the primary cause of fasting hyperglycemia; after a meal, impaired suppression of hepatic glucose production by insulin and decreased insulin-mediated glucose uptake by muscle contribute almost equally to postprandial hyperglycemia. Glucose 182-189 insulin Homo sapiens 77-84 10454950-2 1999 An elevated rate of basal hepatic glucose production in the presence of hyperinsulinemia is the primary cause of fasting hyperglycemia; after a meal, impaired suppression of hepatic glucose production by insulin and decreased insulin-mediated glucose uptake by muscle contribute almost equally to postprandial hyperglycemia. Glucose 182-189 insulin Homo sapiens 204-211 10509803-1 1999 Nutrient stimulation of pancreatic beta-cells increases the cellular reduced pyridine nucleotide content, but the specific role of cytosolic redox state in glucose-induced insulin release (GIIR) remains undetermined. Glucose 156-163 insulin Homo sapiens 172-179 10509803-2 1999 The role of cytosolic redox state has been assessed (as reflected by the lactate/pyruvate ratio) in nutrient- and non-nutrient-induced insulin release using a recently established glucose-sensitive clonal beta-cell line (BRIN-BD11). Glucose 180-187 insulin Homo sapiens 135-142 10515671-7 1999 The insulin response to an oral glucose load diminished by 30% with hormone replacement therapy (102.3+/-32.8 mmicro/l versus 71.4+/-20.0 mmicro/l). Glucose 32-39 insulin Homo sapiens 4-11 10444433-0 1999 Insulin regulation of glucose transport and phosphorylation in skeletal muscle assessed by PET. Glucose 22-29 insulin Homo sapiens 0-7 10444433-1 1999 The current study examined in vivo insulin regulation of glucose transport and phosphorylation in skeletal muscle of healthy, lean volunteers. Glucose 57-64 insulin Homo sapiens 35-42 10444433-5 1999 On the basis of compartmental modeling, the fraction of glucose undergoing phosphorylation (PF) increased in a dose-responsive manner from 11% during basal conditions to 74% at the highest insulin infusion rate (P < 0.001). Glucose 56-63 insulin Homo sapiens 189-196 10444433-9 1999 These findings indicate an important interaction between transport and phosphorylation in the control of insulin-stimulated glucose metabolism in skeletal muscle. Glucose 124-131 insulin Homo sapiens 105-112 10480466-9 1999 There was a significant negative correlation of total dietary magnesium intake with the sum of insulin levels measured during an oral glucose tolerance test (OGTT) (r = -0.13, P < .05). Glucose 134-141 insulin Homo sapiens 95-102 10430643-3 1999 In the diabetic subjects, plasma glucose was regulated throughout the night by a constant infusion of insulin and a variable infusion of 24% glucose. Glucose 33-40 insulin Homo sapiens 102-109 10842654-5 1999 Evidence in support of this hypothesis has been obtained from the Normative Aging Study (NAS) in which a relationship between insulin (and glucose) and the SNS, and between insulin and SNS activity and blood pressure was demonstrated. Glucose 139-146 insulin Homo sapiens 126-133 10543718-2 1999 Postprandial elevation in insulin levels activates a hepatic parasympathetic reflex release of a putative hepatic insulin-sensitizing substance (HISS), which activates glucose uptake at skeletal muscle. Glucose 168-175 insulin Homo sapiens 26-33 10543718-2 1999 Postprandial elevation in insulin levels activates a hepatic parasympathetic reflex release of a putative hepatic insulin-sensitizing substance (HISS), which activates glucose uptake at skeletal muscle. Glucose 168-175 insulin Homo sapiens 114-121 10426375-5 1999 During the clamp, the insulin sensitivity index for glucose disposal was lower (P < 0.03) in relatives than in control subjects (low 12.0 +/- 1.6 vs. 18.1 +/- 1.4; high 9.4 +/- 0.8 vs. 12.9 +/- 0.6 [100 x mg x l x kg(-1) x mU(-1) x min(-1)]). Glucose 52-59 insulin Homo sapiens 22-29 10430816-9 1999 Insulin resistance is associated with a cluster of metabolic abnormalities that include glucose intolerance, hypertension, a unique dyslipidemia, a procoagulant state, and an increase in macrovascular disease. Glucose 88-95 insulin Homo sapiens 0-7 10468995-10 1999 Metformin therapy improved menstrual disturbances in 25% of the women with PCOS and also resulted in some improvement in insulin sensitivity and reduced basal and post glucose load insulin levels. Glucose 168-175 insulin Homo sapiens 181-188 10468995-13 1999 These abnormalities explain the increased prevalence of glucose intolerance in women with PCOS and metformin has beneficial effects on insulin sensitivity in women with PCOS. Glucose 56-63 insulin Homo sapiens 135-142 10426366-0 1999 Insulin-regulated mitochondrial gene expression is associated with glucose flux in human skeletal muscle. Glucose 67-74 insulin Homo sapiens 0-7 10426366-4 1999 The ND1 response to insulin correlated with glucose uptake (r = 0.46, P = 0.002). Glucose 44-51 insulin Homo sapiens 20-27 10433517-9 1999 In this review we discuss recent advances in the elucidation of specific metabolic insulin signalling pathways related to glucose transport, one of the most distinctive biological actions of insulin. Glucose 122-129 insulin Homo sapiens 83-90 10433517-9 1999 In this review we discuss recent advances in the elucidation of specific metabolic insulin signalling pathways related to glucose transport, one of the most distinctive biological actions of insulin. Glucose 122-129 insulin Homo sapiens 191-198 10426382-7 1999 Only in nonmodulators were the following cardiovascular risk factors significantly increased: fasting insulin (P < 0.01); increment in post-glucose load insulin (P < 0.01); total, LDL, and VLDL cholesterol and triglyceride levels (P < 0.05); and erythrocyte Na+/Li+ countertransport activity (P < 0.001). Glucose 143-150 insulin Homo sapiens 156-163 10426366-5 1999 Although the rate of insulin-mediated glucose uptake was decreased in the diabetic versus the nondiabetic twins (5.2 +/- 0.7 vs. 8.5 +/- 0.8 mg x kg(-1) fat-free mass x min(-1), P < 0.01), insulin-stimulated ND1 expression was not significantly different between them (2.4 +/- 0.5 vs. 2.7 +/- 0.5 relative units). Glucose 38-45 insulin Homo sapiens 21-28 10426375-9 1999 In contrast, in vitro experiments with isolated subcutaneous adipocytes displayed similar effects of insulin in relatives and control subjects with respect to both glucose uptake and antilipolysis. Glucose 164-171 insulin Homo sapiens 101-108 10426367-6 1999 Total body fat was determined by dual-energy X-ray absorptiometry, visceral fat by computed tomography, and insulin sensitivity by the tolbutamide-modified, frequently sampled intravenous glucose tolerance test with minimal modeling. Glucose 188-195 insulin Homo sapiens 108-115 10426375-10 1999 In conclusion, insulin action in vivo on both lipolysis and glucose uptake is impaired early in the development of type 2 diabetes. Glucose 60-67 insulin Homo sapiens 15-22 10491753-4 1999 Five women had high insulin sensitivity as shown by euglycaemic, hyperinsulinaemic clamp (99 +/- 12 nmol glucose.kg body weight-1.min-1/pmol insulin.l-1; means +/- SD) whereas five women had low insulin sensitivity (34 +/- 15 nmol glucose.kg body weight-1.min-1/pmol insulin.l-1). Glucose 105-112 insulin Homo sapiens 20-27 10491753-6 1999 Fasting insulin concentration increased by dexamethasone in high insulin sensitivity (72 +/- 10 vs 49 +/- 9 pmol/l, p = 0.043) but not in low insulin sensitivity (148 +/- 63 vs 145 +/- 78 pmol/l) whereas the fasting glucose concentration increased in low insulin sensitivity (6.5 +/- 0.8 vs 5.8 +/- 0.6 mmol/l, p = 0.043) but not in high insulin sensitivity (5.3 +/- 0.8 vs 5.3 +/- 0.6 mmol/l). Glucose 216-223 insulin Homo sapiens 8-15 10477209-6 1999 Basal and insulin-stimulated glucose oxidation were comparable in the placebo and metformin-treated groups at the end of each treatment period, as was the SSPG concentration. Glucose 29-36 insulin Homo sapiens 10-17 10477209-8 1999 CONCLUSIONS: These results indicate that metformin administration to patients with IGT is associated with enhanced glucose disposal at baseline insulin concentrations and a fall in blood pressure. Glucose 115-122 insulin Homo sapiens 144-151 10477209-1 1999 AIMS: This study was initiated to test the hypothesis that metformin treatment leads to enhanced glucose disposal at ambient insulin concentrations. Glucose 97-104 insulin Homo sapiens 125-132 10477209-3 1999 Insulin secretion and insulin resistance were quantified using the homeostasis model assessment (HOMA) and insulin-stimulated glucose disposal were measured by determining the steady-state plasma glucose (SSPG). Glucose 126-133 insulin Homo sapiens 107-114 10491755-4 1999 RESULTS: These conditions resulted in a 50-70% reduction in insulin-stimulated glucose transport activity associated with a decrease in reduced glutathione content from 37.4 +/- 3.1 to 26.4 +/- 4.9 nmol/mg protein, (p < 0.005). Glucose 79-86 insulin Homo sapiens 60-67 10491755-5 1999 Lipoic acid pretreatment increased insulin-stimulated glucose transport following oxidative stress, reaching 84.8 +/- 4.4% of the control, associated with an increase in reduced glutathione content. Glucose 54-61 insulin Homo sapiens 35-42 10499882-8 1999 PC-1 activity of the patients with insulin resistance (glucose infusion rate < 3.0 mg/kg per min, n = 7) was elevated to 99.9 +/- 31.9 nmol/mg per min, while that of the other patients (n = 4) was 55.3 +/- 7.5 nmol/mg per min (P = 0.003). Glucose 55-62 insulin Homo sapiens 35-42 10491753-8 1999 Plasma insulin concentrations after raising glucose to 14 and more than 25 mmol/l and the insulin response to arginine at more than 25 mmol/l glucose were increased by dexamethasone in high insulin sensitivity (p < 0.05) but not changed by dexamethasone in low insulin sensitivity. Glucose 44-51 insulin Homo sapiens 7-14 10491753-8 1999 Plasma insulin concentrations after raising glucose to 14 and more than 25 mmol/l and the insulin response to arginine at more than 25 mmol/l glucose were increased by dexamethasone in high insulin sensitivity (p < 0.05) but not changed by dexamethasone in low insulin sensitivity. Glucose 142-149 insulin Homo sapiens 90-97 10491753-8 1999 Plasma insulin concentrations after raising glucose to 14 and more than 25 mmol/l and the insulin response to arginine at more than 25 mmol/l glucose were increased by dexamethasone in high insulin sensitivity (p < 0.05) but not changed by dexamethasone in low insulin sensitivity. Glucose 142-149 insulin Homo sapiens 90-97 10782752-8 1999 Only in the non-obese patients with gestational diabetes, is there an absolute defect of early insulin response to the glucose load, as it is seen in T2DM. Glucose 119-126 insulin Homo sapiens 95-102 10580744-3 1999 Insulin sensitivity was measured by the steady state plasma glucose method. Glucose 60-67 insulin Homo sapiens 0-7 10433221-11 1999 This is in contrast to the processing of proinsulin to insulin in the pancreatic beta-cell, which is up-regulated by glucose stimulation of PC1 and PC2 synthesis. Glucose 117-124 insulin Homo sapiens 41-51 10433221-11 1999 This is in contrast to the processing of proinsulin to insulin in the pancreatic beta-cell, which is up-regulated by glucose stimulation of PC1 and PC2 synthesis. Glucose 117-124 insulin Homo sapiens 44-51 10457152-2 1999 DESIGN: In this study of seven volunteers, global blood-brain barrier permeability to glucose and phenylalanine was measured by means of the intracarotid double-indicator method before, during, and after an insulin-glucose clamp. Glucose 215-222 insulin Homo sapiens 207-214 10457152-4 1999 RESULTS: The permeability-surface area product (PS) for glucose transport from the blood into the brain, PS1, was 0.145 (0.102-0.211) (median and quartiles), 0.146 (0.113-0.259), and 0.157 (0.133-0.181) ml g-1 min-1 before, during, and after insulin challenge, respectively. Glucose 56-63 insulin Homo sapiens 242-249 10457152-5 1999 In six of the subjects, PS for transport from brain to blood over the brain glucose distribution volume, PS2/Ve decreased under hyperinsulinemia, from a baseline value of 6.56 (3.0-14.9) to 3.86 (1.41-5.32), and restored to a value of 3.8 (2.8-12.1) min-1 after insulin challenge. Glucose 76-83 insulin Homo sapiens 133-140 10457152-6 1999 This decrease in PS2/Ve is probably due to an increase in the brain glucose distribution volume induced by an insulin induced increased intracellular glucose uptake during the experiment. Glucose 68-75 insulin Homo sapiens 110-117 10457152-6 1999 This decrease in PS2/Ve is probably due to an increase in the brain glucose distribution volume induced by an insulin induced increased intracellular glucose uptake during the experiment. Glucose 150-157 insulin Homo sapiens 110-117 10457152-10 1999 It seems, however, that high plasma insulin levels induce an increase in the movement of D-glucose and L-phenylalanine from the brain interstitial fluid into the intracellular compartment. Glucose 89-98 insulin Homo sapiens 36-43 10580755-15 1999 It remains necessary to elucidate what kinds of effects of the long-lasting increased levels of insulin and triglyceride, even if reversible, would have on glucose and lipid metabolism. Glucose 156-163 insulin Homo sapiens 96-103 10580744-5 1999 Steady state plasma glucose was significantly higher in hypertensive subjects indicating insulin resistance compared with control subjects. Glucose 20-27 insulin Homo sapiens 89-96 10580744-7 1999 Fasting serum DHEAS levels were inversely correlated with steady state plasma glucose significantly (p=0.0008), indicating a close association between DHEAS levels and insulin resistance. Glucose 78-85 insulin Homo sapiens 168-175 10668648-8 1999 The results suggest that NO and hydroperoxide inhibit glucose-stimulated insulin release by perturbing Ca2+ fluxes and probably acting through S-nitrosylation (NO) or oxidation (hydroperoxide) of thiol groups critical to the secretory process. Glucose 54-61 insulin Homo sapiens 73-80 10668648-2 1999 Both donors dose dependently inhibited glucose-stimulated insulin release and induced modest (hydroxylamine) or profound (tertbutylhydroperoxide) suppression of 45Ca2+-efflux from perifused islets. Glucose 39-46 insulin Homo sapiens 58-65 10668648-5 1999 Insulin and glucagon release stimulated by activation of the cAMP system through isobutylmethylxanthine (IBMX) at basal glucose was modestly potentiated by low concentrations of both donors. Glucose 120-127 insulin Homo sapiens 0-7 10494871-6 1999 The lower (p = 0.03) insulin area under curve on oral glucose tolerance test in presence of portal systemic shunting (7.40 (0.95) vs. 10.83 (1.15) U/L-min) indicated that lower extraction of insulin by the liver leads to a lower requirements in the periphery. Glucose 54-61 insulin Homo sapiens 21-28 10468203-9 1999 When compared to placebo, significantly more subjects had an increase in insulin-stimulated glucose disposal (MCR) after ALA treatment in each group. Glucose 92-99 insulin Homo sapiens 73-80 10443650-9 1999 However, the slope of the regression and the predicted insulin level at zero glucose decreased with increasing age. Glucose 77-84 insulin Homo sapiens 55-62 10490784-9 1999 They also indicate that the impaired CIT sometimes observed returns to normal after weight reduction suggesting that it is secondary to a decrease in glucose uptake induced by obesity-associated insulin resistance. Glucose 150-157 insulin Homo sapiens 195-202 10443650-10 1999 When insulin levels were normalized for the plasma glucose concentrations, an exponential decrease in the insulin/glucose ratio was observed (r2 = 0.92; P < 0.01), with most of the decline occurring before 2 yr of age. Glucose 51-58 insulin Homo sapiens 106-113 10443650-10 1999 When insulin levels were normalized for the plasma glucose concentrations, an exponential decrease in the insulin/glucose ratio was observed (r2 = 0.92; P < 0.01), with most of the decline occurring before 2 yr of age. Glucose 114-121 insulin Homo sapiens 5-12 10443650-10 1999 When insulin levels were normalized for the plasma glucose concentrations, an exponential decrease in the insulin/glucose ratio was observed (r2 = 0.92; P < 0.01), with most of the decline occurring before 2 yr of age. Glucose 114-121 insulin Homo sapiens 106-113 10466471-4 1999 Insulin resistance was evaluated by the insulin suppression test by use of the steady-state plasma glucose (SSPG) level. Glucose 99-106 insulin Homo sapiens 0-7 10480766-8 1999 Protocol 3: With rapid-acting insulin, there was a significant increase in the percentage of blood glucose levels within the target range (1 month, P = 0.04; at 3 months, P = 0.03). Glucose 99-106 insulin Homo sapiens 30-37 10466471-4 1999 Insulin resistance was evaluated by the insulin suppression test by use of the steady-state plasma glucose (SSPG) level. Glucose 99-106 insulin Homo sapiens 40-47 10480778-9 1999 These children manifest important metabolic alterations, including impaired insulin-stimulated total and nonoxidative glucose disposal early in the first decade of life. Glucose 118-125 insulin Homo sapiens 76-83 10657503-3 1999 An insulin injection decreased the plasma glucose level, which followed a prompt rise in plasma ACTH level and an increase in serum CINC level. Glucose 42-49 insulin Homo sapiens 3-10 10489096-7 1999 Insulin response was measured during intravenous glucose tolerance test. Glucose 49-56 insulin Homo sapiens 0-7 10489096-11 1999 In the predefined insulin-resistant subgroup with M/I ratio < 3.6 at baseline, glucose infusion rate and insulin sensitivity index increased by 21% whereas values in the placebo group remained unchanged. Glucose 82-89 insulin Homo sapiens 18-25 10489096-14 1999 The insulin secretion in response to glucose stimulation was unaffected in insulin-resistant as well as in insulin-sensitive hypertensive patients. Glucose 37-44 insulin Homo sapiens 4-11 10489096-16 1999 Insulin response to glucose stimulation was unaffected. Glucose 20-27 insulin Homo sapiens 0-7 10459560-1 1999 Postprandial insulin responses (integrated area under the curve) to an oral glucose load after a period of aerobic exercise and no exercise (control) were compared in sedentary normoglycemic Mexican American and non-Hispanic women pair-matched (n = 9) on total body fat mass (21.8 +/- 3.5 kg). Glucose 76-83 insulin Homo sapiens 13-20 10459561-5 1999 The acute insulin response to glucose (AIRg) was calculated as the area under the insulin curve above the basal level between 0 and 10 minutes, and the suprabasal insulin effect was determined by the product of S(I) times AIRg. Glucose 30-37 insulin Homo sapiens 10-17 10459563-1 1999 The study was initiated to evaluate the ability of hyperinsulinemia (as a surrogate measure of insulin resistance) to predict the development in a previously healthy population of three putative outcomes of this abnormality--glucose intolerance, hypertension, and coronary heart disease (CHD). Glucose 225-232 insulin Homo sapiens 56-63 10459563-3 1999 The study population consisted of approximately 90% of the subjects evaluated in 1981, divided into quartiles on the basis of the plasma insulin response to a glucose challenge as determined in 1981. Glucose 159-166 insulin Homo sapiens 137-144 10461029-4 1999 AD subjects without an epsilon4 allele had significantly lower insulin-mediated glucose disposal rates than AD patients with an epsilon4 allele (p < 0.03), or than normal adults without an epsilon4 allele (p < 0.02). Glucose 80-87 insulin Homo sapiens 63-70 10461029-5 1999 Female AD subjects showed lower insulin-mediated glucose disposal rates than did male AD subjects (p < 0.02). Glucose 49-56 insulin Homo sapiens 32-39 10406747-8 1999 During the oral glucose tolerance test, monozygotic twins had a higher incremental plasma insulin area under the curve than dizygotic twins (10.05 (SD 0.68) v 9.89 (0.72) pmol/lxminutes, P<0.01) indicating insulin resistance. Glucose 16-23 insulin Homo sapiens 90-97 10452283-8 1999 The deterioration of glucose tolerance was correlated with a decreased early phase of insulin secretion, estimated from the plasma insulin level at 30 min of the OGTT, while there was no evidence of insulin resistance. Glucose 21-28 insulin Homo sapiens 86-93 10452283-8 1999 The deterioration of glucose tolerance was correlated with a decreased early phase of insulin secretion, estimated from the plasma insulin level at 30 min of the OGTT, while there was no evidence of insulin resistance. Glucose 21-28 insulin Homo sapiens 131-138 10452283-8 1999 The deterioration of glucose tolerance was correlated with a decreased early phase of insulin secretion, estimated from the plasma insulin level at 30 min of the OGTT, while there was no evidence of insulin resistance. Glucose 21-28 insulin Homo sapiens 131-138 10467625-6 1999 Adjustments in insulin can be done both in anticipation of the glucocorticoid effect and based on home glucose monitoring. Glucose 103-110 insulin Homo sapiens 15-22 10413736-0 1999 Impaired glucose transport as a cause of decreased insulin-stimulated muscle glycogen synthesis in type 2 diabetes. Glucose 9-16 insulin Homo sapiens 51-58 10413736-9 1999 CONCLUSIONS: Impaired insulin-stimulated glucose transport is responsible for the reduced rate of insulin-stimulated muscle glycogen synthesis in patients with type 2 diabetes mellitus. Glucose 41-48 insulin Homo sapiens 22-29 10413736-9 1999 CONCLUSIONS: Impaired insulin-stimulated glucose transport is responsible for the reduced rate of insulin-stimulated muscle glycogen synthesis in patients with type 2 diabetes mellitus. Glucose 41-48 insulin Homo sapiens 98-105 10604198-3 1999 The ability of insulin to regulate glucose production and disposal varies between individuals. Glucose 35-42 insulin Homo sapiens 15-22 10406747-10 1999 CONCLUSION: Zygosity influences both plasma glucose and plasma insulin concentrations during an oral glucose tolerance test. Glucose 101-108 insulin Homo sapiens 63-70 10416516-15 1999 Fasting concentrations and secretion response of insulin, proinsulin, and C-peptide to glucose ingestion was significantly increased in the PI-treated group suggesting a beta-cell dysfunction in addition to peripheral insulin resistance. Glucose 87-94 insulin Homo sapiens 49-56 10393723-9 1999 Glucose and insulin levels 2 hours after oral glucose challenge also exhibited statistically significant associations with colorectal cancer (2-hour glucose levels: RR = 2.4 [95% CI = 1.2-4. Glucose 46-53 insulin Homo sapiens 12-19 10393723-9 1999 Glucose and insulin levels 2 hours after oral glucose challenge also exhibited statistically significant associations with colorectal cancer (2-hour glucose levels: RR = 2.4 [95% CI = 1.2-4. Glucose 149-156 insulin Homo sapiens 12-19 10448935-7 1999 These results suggest that metformin combined with insulin can maintain glucose homeostasis by increasing the catalytic activity of some hexose carriers or by improving the affinity of GLUT4 for glucose. Glucose 72-79 insulin Homo sapiens 51-58 10409274-6 1999 Blood samples were taken for 3.5 h. Insulin infusion had no effect on postprandial insulin levels in either population but significantly reduced postprandial glucose in the obese subjects (P < 0.05). Glucose 158-165 insulin Homo sapiens 36-43 10383432-2 1999 To define the effect of platelet-derived growth factor (PDGF) on glucose transport in 3T3-L1 adipocytes, we investigated the PDGF- and insulin-induced glucose uptake, translocation of glucose transporters, and phosphatidylinositol (PI) 3-kinase activity in 3T3-L1, 3T3-L1GLUT4MYC, and 3T3-L1GLUT1MYC adipocytes. Glucose 151-158 insulin Homo sapiens 135-142 10383432-3 1999 Insulin and PDGF stimulated glucose uptake by 9-10- and 5.5-6.5-fold, respectively, in both 3T3-L1 and 3T3-L1GLUT4MYC adipocytes. Glucose 28-35 insulin Homo sapiens 0-7 10408765-7 1999 Oral glucose tolerance test revealed impaired glucose tolerance and hyperresponse of insulin. Glucose 5-12 insulin Homo sapiens 85-92 10409274-7 1999 Obese subjects with elevated postprandial glucose levels in the presence of muscarinic blockade exhibited a decline in glucose with insulin supplementation. Glucose 42-49 insulin Homo sapiens 132-139 10409274-7 1999 Obese subjects with elevated postprandial glucose levels in the presence of muscarinic blockade exhibited a decline in glucose with insulin supplementation. Glucose 119-126 insulin Homo sapiens 132-139 10451792-5 1999 Plasma insulin increased when glucose was provided, whereas insulin-like growth factor (IGF) I was unchanged during all infusions. Glucose 30-37 insulin Homo sapiens 7-14 10454248-6 1999 In cancer patients with insulin resistance, decreased glucose uptake was closely associated with a rapid decrease in glucose storage, an increase in fat oxidation and a mild decrease in glucose oxidation, suggesting that insulin resistance was connected with the alterations of substrate utilization which may induce host depletion. Glucose 54-61 insulin Homo sapiens 24-31 10454248-6 1999 In cancer patients with insulin resistance, decreased glucose uptake was closely associated with a rapid decrease in glucose storage, an increase in fat oxidation and a mild decrease in glucose oxidation, suggesting that insulin resistance was connected with the alterations of substrate utilization which may induce host depletion. Glucose 54-61 insulin Homo sapiens 221-228 10454248-6 1999 In cancer patients with insulin resistance, decreased glucose uptake was closely associated with a rapid decrease in glucose storage, an increase in fat oxidation and a mild decrease in glucose oxidation, suggesting that insulin resistance was connected with the alterations of substrate utilization which may induce host depletion. Glucose 117-124 insulin Homo sapiens 24-31 10454248-6 1999 In cancer patients with insulin resistance, decreased glucose uptake was closely associated with a rapid decrease in glucose storage, an increase in fat oxidation and a mild decrease in glucose oxidation, suggesting that insulin resistance was connected with the alterations of substrate utilization which may induce host depletion. Glucose 117-124 insulin Homo sapiens 221-228 10389846-0 1999 Enhancing effects of long-term elevated glucose and palmitate on stored and secreted proinsulin-to-insulin ratios in human pancreatic islets. Glucose 40-47 insulin Homo sapiens 85-95 10388973-3 1999 We examined the relationship between the rate of insulin-mediated glucose uptake and serum leptin concentrations among nondiabetic men and women. Glucose 66-73 insulin Homo sapiens 49-56 10389846-0 1999 Enhancing effects of long-term elevated glucose and palmitate on stored and secreted proinsulin-to-insulin ratios in human pancreatic islets. Glucose 40-47 insulin Homo sapiens 88-95 10388973-6 1999 RESULTS: The rate of insulin-mediated glucose uptake (M in milligrams per kilogram per minute) was significantly associated with leptin concentrations in both men (r = -0.83; P < 0.001) and women (r = -0.59; P < 0.001). Glucose 38-45 insulin Homo sapiens 21-28 10389846-3 1999 A 48-h culture period with 27 mmol/l glucose increased the intraislet proinsulin-to-insulin (PI/I) ratio 5.0-fold, owing to preferential decrease of insulin. Glucose 37-44 insulin Homo sapiens 70-80 10389846-3 1999 A 48-h culture period with 27 mmol/l glucose increased the intraislet proinsulin-to-insulin (PI/I) ratio 5.0-fold, owing to preferential decrease of insulin. Glucose 37-44 insulin Homo sapiens 73-80 10389846-12 1999 Culture with palmitate together with 27 mmol/l glucose decreased islet contents of proinsulin and insulin and further enhanced intraislet PI/I ratios (from 9.3 +/- 1.1 to 13.4 +/- 2.5%, P < 0.05). Glucose 47-54 insulin Homo sapiens 83-93 10389846-12 1999 Culture with palmitate together with 27 mmol/l glucose decreased islet contents of proinsulin and insulin and further enhanced intraislet PI/I ratios (from 9.3 +/- 1.1 to 13.4 +/- 2.5%, P < 0.05). Glucose 47-54 insulin Homo sapiens 86-93 10389846-15 1999 We conclude that 1) long-term exposure of human islets to elevated glucose leads to preferential secretion of proinsulin, and this effect persists also after glucose normalization; 2) the glucose effect appears secondary to depletion of mature insulin granules; and 3) elevated fatty acids influence PI/I ratios of secretion by mechanisms that are, in part, incongruous with an over-stimulation effect. Glucose 67-74 insulin Homo sapiens 110-120 10389846-3 1999 A 48-h culture period with 27 mmol/l glucose increased the intraislet proinsulin-to-insulin (PI/I) ratio 5.0-fold, owing to preferential decrease of insulin. Glucose 37-44 insulin Homo sapiens 84-91 10389846-15 1999 We conclude that 1) long-term exposure of human islets to elevated glucose leads to preferential secretion of proinsulin, and this effect persists also after glucose normalization; 2) the glucose effect appears secondary to depletion of mature insulin granules; and 3) elevated fatty acids influence PI/I ratios of secretion by mechanisms that are, in part, incongruous with an over-stimulation effect. Glucose 67-74 insulin Homo sapiens 113-120 10389846-10 1999 Culture with 0.2 mmol/l palmitate and 5.5 mmol/l glucose decreased islet contents of proinsulin and insulin and increased the secreted products in culture media without affecting PI/I ratios. Glucose 49-56 insulin Homo sapiens 85-95 10389846-10 1999 Culture with 0.2 mmol/l palmitate and 5.5 mmol/l glucose decreased islet contents of proinsulin and insulin and increased the secreted products in culture media without affecting PI/I ratios. Glucose 49-56 insulin Homo sapiens 88-95 10440123-0 1999 Impaired glucose transport and protein kinase B activation by insulin, but not okadaic acid, in adipocytes from subjects with Type II diabetes mellitus. Glucose 9-16 insulin Homo sapiens 62-69 10440123-1 1999 AIMS/HYPOTHESIS: To study the effects of insulin and okadaic acid, a serine/threonine phosphatase inhibitor which does not increase PI3-kinase activity, on the rate of glucose transport and protein kinase B activation in adipocytes from healthy subjects and subjects with Type II (non-insulin-dependent) diabetes mellitus. Glucose 168-175 insulin Homo sapiens 41-48 10495475-5 1999 Because glucose transport across these barriers is mediated exclusively by the sodium-independent glucose transporter GLUT1, changes in endothelial glucose transport and GLUT1 abundance in the barriers of the brain and retina may have profound consequences on glucose delivery to these tissues and major implications in the development of two major diabetic complications, namely insulin-induced hypoglycemia and diabetic retinopathy. Glucose 8-15 insulin Homo sapiens 380-387 11228758-12 1999 Meal-stimulated glucose (net AUC) decreased after treatment only in those with low baseline proinsulin levels. Glucose 16-23 insulin Homo sapiens 92-102 10440123-3 1999 RESULTS: Insulin and okadaic acid alone increased glucose uptake to a similar degree in adipocytes from healthy subjects and, when combined, exerted a partial additive effect. Glucose 50-57 insulin Homo sapiens 9-16 11228758-14 1999 High proinsulin levels are associated with an atherogenic-risk marker profile and an impaired therapeutic postprandial glucose response after treatment in patients with type 2 diabetes. Glucose 119-126 insulin Homo sapiens 5-15 10404835-2 1999 In human mature adipocytes isolated from omental (OM) and s.c. tissue, we found that leptin (10 and 100 ng/mL) significantly reduced insulin-mediated glucose uptake by 40% (P<0.05). Glucose 150-157 insulin Homo sapiens 133-140 10487323-5 1999 Insulin sensitivity in terms of the glucose disposal rate was not significantly different among the three ACE genotypes, although there was a tendency for insulin sensitivity to decrease in the order of II, ID and DD, DD being the lowest. Glucose 36-43 insulin Homo sapiens 0-7 10418851-1 1999 Carbon nuclear magnetic resonance (13C NMR) spectroscopy and phosphorus (31p) NMR spectroscopy have been used to help define the contribution of insulin-stimulated muscle glycogen synthesis to whole-body insulin-stimulated glucose metabolism in normal individuals and the extent to which this process is defective in patients with type 2 (non-insulin-dependent) diabetes. Glucose 223-230 insulin Homo sapiens 204-211 10418851-1 1999 Carbon nuclear magnetic resonance (13C NMR) spectroscopy and phosphorus (31p) NMR spectroscopy have been used to help define the contribution of insulin-stimulated muscle glycogen synthesis to whole-body insulin-stimulated glucose metabolism in normal individuals and the extent to which this process is defective in patients with type 2 (non-insulin-dependent) diabetes. Glucose 223-230 insulin Homo sapiens 204-211 10418851-3 1999 Studies of the mechanisms by which free fatty acids (FFA) cause insulin resistance in humans indicate that increased FFA levels inhibit glucose transport, which may be a consequence of decreased insulin receptor substrate (IRS-1)-associated phosphatidylinositol 3-kinase activity. Glucose 136-143 insulin Homo sapiens 64-71 10418851-3 1999 Studies of the mechanisms by which free fatty acids (FFA) cause insulin resistance in humans indicate that increased FFA levels inhibit glucose transport, which may be a consequence of decreased insulin receptor substrate (IRS-1)-associated phosphatidylinositol 3-kinase activity. Glucose 136-143 insulin Homo sapiens 195-202 10418854-6 1999 Thus, 1 of the 2 major pathways of insulin action is the phosphatidylinositol 3-kinase pathway, which is important for glucose transport in skeletal muscle, as well as endothelial NO production and insulin-induced vasodilation. Glucose 119-126 insulin Homo sapiens 35-42 10418855-2 1999 The ability of insulin to cause endothelium-derived nitric oxide (NO)-dependent vasodilation amplifies its overall effect of stimulating skeletal muscle glucose uptake and modulating vascular tone. Glucose 153-160 insulin Homo sapiens 15-22 10418855-3 1999 The dose-dependent physiologic increase in skeletal muscle blood flow in response to insulin, which is highly associated with the rate of glucose metabolism, is impaired in insulin-resistant states. Glucose 138-145 insulin Homo sapiens 85-92 10418855-3 1999 The dose-dependent physiologic increase in skeletal muscle blood flow in response to insulin, which is highly associated with the rate of glucose metabolism, is impaired in insulin-resistant states. Glucose 138-145 insulin Homo sapiens 173-180 10778592-6 1999 Insulin response to glucose and correlation between basal insulin secretion and urinary sodium excretion were evaluated. Glucose 20-27 insulin Homo sapiens 0-7 10404835-10 1999 The autocrine effects of leptin to inhibit insulin-stimulated glucose uptake and subsequent lipogenesis in adipose tissue may, therefore, be less in OM adipocytes and may play a role in determining visceral obesity. Glucose 62-69 insulin Homo sapiens 43-50 10643214-2 1999 This case report describes an obese African-American woman who was treated with subcutaneous injections of lispro insulin every 2 hours with resultant decrease of mean daily blood glucose from 264.7 mg/dL to 111 mg/dL and in insulin requirement from 479 U/24 hours to 60 U/24 hours. Glucose 180-187 insulin Homo sapiens 114-121 10396024-13 1999 bolus of insulin the group receiving GH+MP had a significantly (P<0.007) higher level of circulating glucose compared with controls (6.5+/-0.3 mM vs 4.4+/-0.7 mM). Glucose 104-111 insulin Homo sapiens 9-16 10396024-15 1999 In conclusion this study shows that a combined administration of GH and MP decreases the potency by which insulin decreases circulating glucose levels, but that peripheral tissues are not primarily involved in this insulin resistance. Glucose 136-143 insulin Homo sapiens 106-113 10405129-8 1999 CONCLUSION: Both heart and skeletal muscle glucose utilization were related to insulin resistance in hypertriglyceridemics. Glucose 43-50 insulin Homo sapiens 79-86 10421231-13 1999 In addition, insulin actions on glucose metabolism and on the endothelial mediators appear dissociated. Glucose 32-39 insulin Homo sapiens 13-20 10416561-2 1999 Moreover, exercise training or a prior bout of exercise increases insulin-stimulated glucose uptake in resting skeletal muscle. Glucose 85-92 insulin Homo sapiens 66-73 10373517-1 1999 We have previously reported that insulin and osmotic shock stimulate an increase in glucose transport activity and translocation of the insulin-responsive glucose transporter isoform GLUT4 to the plasma membrane through distinct pathways in 3T3L1 adipocytes (D. Chen, J. S. Elmendorf, A. L. Olson, X. Li, H. S. Earp, and J. E. Pessin, J. Biol. Glucose 84-91 insulin Homo sapiens 33-40 10421232-2 1999 We measured insulin sensitivity by the minimal model technique between 29 and 39 weeks of gestation in 22 preeclamptic and 16 control women, whose glucose tolerance was first confirmed as normal by an oral glucose tolerance test. Glucose 147-154 insulin Homo sapiens 12-19 10421232-2 1999 We measured insulin sensitivity by the minimal model technique between 29 and 39 weeks of gestation in 22 preeclamptic and 16 control women, whose glucose tolerance was first confirmed as normal by an oral glucose tolerance test. Glucose 206-213 insulin Homo sapiens 12-19 10421232-4 1999 Preeclamptic women showed a higher insulin response (P = .001) during the oral glucose tolerance test than the controls. Glucose 79-86 insulin Homo sapiens 35-42 10422091-2 1999 Although alcohol can lead to severe hypoglycemia, alcoholics are usually glucose intolerant, probably due to a inhibition of glucose-stimulated insulin secretion. Glucose 73-80 insulin Homo sapiens 144-151 10422091-2 1999 Although alcohol can lead to severe hypoglycemia, alcoholics are usually glucose intolerant, probably due to a inhibition of glucose-stimulated insulin secretion. Glucose 125-132 insulin Homo sapiens 144-151 10437638-3 1999 Simulation of a simple mass balance model for insulin and proinsulin concentrations during an oral glucose tolerance test predicts that the ratio (R) of RIA to IMX insulin measurements of [insulin] should transiently decrease, pass through a minimum, increase past the initial value, pass through a maximum and eventually return to the initial value. Glucose 99-106 insulin Homo sapiens 46-53 10364216-8 1999 These data suggest that aldolase functions as a scaffolding protein for GLUT4 and that glucose metabolism may provide a negative feedback signal for the regulation of glucose transport by insulin. Glucose 87-94 insulin Homo sapiens 188-195 10438116-7 1999 RESULTS: Following an oral glucose load the SCI group demonstrated normal glucose tolerance but impaired insulin sensitivity with a maximum insulin value of 83 mU x l(-1) in SCI compared to 50 in siblings, while adipose tissue metabolism was normal compared to siblings. Glucose 27-34 insulin Homo sapiens 105-112 10437638-3 1999 Simulation of a simple mass balance model for insulin and proinsulin concentrations during an oral glucose tolerance test predicts that the ratio (R) of RIA to IMX insulin measurements of [insulin] should transiently decrease, pass through a minimum, increase past the initial value, pass through a maximum and eventually return to the initial value. Glucose 99-106 insulin Homo sapiens 58-68 10437638-3 1999 Simulation of a simple mass balance model for insulin and proinsulin concentrations during an oral glucose tolerance test predicts that the ratio (R) of RIA to IMX insulin measurements of [insulin] should transiently decrease, pass through a minimum, increase past the initial value, pass through a maximum and eventually return to the initial value. Glucose 99-106 insulin Homo sapiens 61-68 10437638-3 1999 Simulation of a simple mass balance model for insulin and proinsulin concentrations during an oral glucose tolerance test predicts that the ratio (R) of RIA to IMX insulin measurements of [insulin] should transiently decrease, pass through a minimum, increase past the initial value, pass through a maximum and eventually return to the initial value. Glucose 99-106 insulin Homo sapiens 61-68 10362630-3 1999 The hot model provides, from hot IVGTT data, indexes of glucose effectiveness (SG*) and insulin sensitivity (SI*) that, respectively, measure the effects of glucose and insulin on glucose disappearance only. Glucose 56-63 insulin Homo sapiens 169-176 10359389-2 1999 CONTEXT: Treatment with diet alone, insulin, sulfonylurea, or metformin is known to improve glycemia in patients with type 2 diabetes mellitus, but which treatment most frequently attains target fasting plasma glucose (FPG) concentration of less than 7.8 mmol/L (140 mg/dL) or glycosylated hemoglobin A1c (HbA1c) below 7% is unknown. Glucose 210-217 insulin Homo sapiens 36-43 10420493-1 1999 In healthy persons insulin secreting beta-cells of the pancreas regulate blood glucose levels within a narrow physiological range. Glucose 79-86 insulin Homo sapiens 19-26 11910673-5 1999 CONCLUSIONS: During a 2-year treatment with oral estradiol and cyclical dydrogesterone, a direct progesterone derivative, tolerance to glucose was unchanged, fasting plasma insulin and insulin response to repeated glucose loads were decreased, and C-peptide levels remained unchanged, indicating a potential improvement in insulin sensitivity and clearance, as in younger women; additionally, a slightly enhanced antilipolytic activity of insulin was observed. Glucose 214-221 insulin Homo sapiens 185-192 16211669-5 1999 Water flow over the dam is analogous to glucose leaving the blood for tissues, which is controlled by insulin. Glucose 40-47 insulin Homo sapiens 102-109 10371376-4 1999 Systemic insulin resistance as assessed by the fasting plasma glucose-to-insulin ratio was aggravated by dietary sodium restriction (normal sodium: 1.2 +/- 0.1 mmol/mIU; low sodium 0.6 +/- 0.1, P < .05). Glucose 62-69 insulin Homo sapiens 9-16 10403543-0 1999 Glucose uptake in the human gastric cancer cell line, MKN28, is increased by insulin stimulation. Glucose 0-7 insulin Homo sapiens 77-84 10403543-4 1999 Insulin stimulation of MKN28 cells resulted in a 22% increase in glucose uptake over that found under basal conditions (0.60 +/- 0.05 fmol/cell per min after insulin stimulation versus 0.53 +/- 0.07 fmol/cell per 3 min at basal). Glucose 65-72 insulin Homo sapiens 0-7 10403543-7 1999 The greater expression of this transporter in MKN28 cells is likely responsible for the cell"s ability to increase glucose uptake with insulin stimulation. Glucose 115-122 insulin Homo sapiens 135-142 10421979-15 1999 However, shortly after the withdrawal of the intravenous insulin infusion, the plasma glucose concentration increased spontaneously in the NIDDM patients. Glucose 86-93 insulin Homo sapiens 57-64 11910673-5 1999 CONCLUSIONS: During a 2-year treatment with oral estradiol and cyclical dydrogesterone, a direct progesterone derivative, tolerance to glucose was unchanged, fasting plasma insulin and insulin response to repeated glucose loads were decreased, and C-peptide levels remained unchanged, indicating a potential improvement in insulin sensitivity and clearance, as in younger women; additionally, a slightly enhanced antilipolytic activity of insulin was observed. Glucose 214-221 insulin Homo sapiens 185-192 11910673-5 1999 CONCLUSIONS: During a 2-year treatment with oral estradiol and cyclical dydrogesterone, a direct progesterone derivative, tolerance to glucose was unchanged, fasting plasma insulin and insulin response to repeated glucose loads were decreased, and C-peptide levels remained unchanged, indicating a potential improvement in insulin sensitivity and clearance, as in younger women; additionally, a slightly enhanced antilipolytic activity of insulin was observed. Glucose 214-221 insulin Homo sapiens 185-192 10390156-0 1999 Regulation of the insulin gene by glucose: stimulation of trans-activation potency of human PDX-1 N-terminal domain. Glucose 34-41 insulin Homo sapiens 18-25 10342809-7 1999 We conclude that cultured human islets are sensitive to the deleterious effect of high glucose concentrations at multiple functional levels, and that such mechanisms may play an important role in the decreased insulin production and secretion of type 2 diabetic patients. Glucose 87-94 insulin Homo sapiens 210-217 10342813-10 1999 Concurrently, fasting plasma glucose levels fell from 17 to 5 mmol/l (with no therapy), while insulin-stimulated glucose uptake, oxidation, and storage were all markedly improved. Glucose 113-120 insulin Homo sapiens 94-101 10352919-12 1999 The hyperinsulinemia that is compensatory for resistance to the glucose-metabolic effect of insulin seems to have a role in many cases. Glucose 64-71 insulin Homo sapiens 9-16 10342809-1 1999 In type 2 diabetes, chronic hyperglycemia has been suggested to be detrimental to beta-cell function, causing reduced glucose-stimulated insulin secretion and disproportionately elevated proinsulin. Glucose 118-125 insulin Homo sapiens 137-144 10342809-3 1999 Islets exposed to high glucose levels (33 mmol/l) for 4 and 9 days showed dramatic decreases in glucose-induced insulin release and in islet insulin content, with increased proportion of proinsulin-like peptides relative to insulin. Glucose 23-30 insulin Homo sapiens 112-119 10342809-3 1999 Islets exposed to high glucose levels (33 mmol/l) for 4 and 9 days showed dramatic decreases in glucose-induced insulin release and in islet insulin content, with increased proportion of proinsulin-like peptides relative to insulin. Glucose 23-30 insulin Homo sapiens 187-197 10342809-3 1999 Islets exposed to high glucose levels (33 mmol/l) for 4 and 9 days showed dramatic decreases in glucose-induced insulin release and in islet insulin content, with increased proportion of proinsulin-like peptides relative to insulin. Glucose 23-30 insulin Homo sapiens 141-148 10400405-6 1999 Addition of rosiglitazone 2 to 8 mg/day to existing sulphonylurea, metformin or insulin therapy achieved further reductions in fasting plasma glucose and HbA1c. Glucose 142-149 insulin Homo sapiens 80-87 10443327-1 1999 The present study aimed at investigating the influence of the time interval between injection of regular insulin and meal ingestion on postprandial glucose changes and overall blood glucose control in patients with type 1 diabetes on intensive insulin therapy. Glucose 148-155 insulin Homo sapiens 105-112 10390156-2 1999 The pancreatic and duodenal homeobox-1 (PDX-1) plays a major role in glucose-induced insulin transcription. Glucose 69-76 insulin Homo sapiens 85-92 10443327-5 1999 Only a tendency to a greater 90-minutes postprandial increase in blood glucose levels was observed when regular insulin was injected 5 minutes rather than 30 minutes before meal. Glucose 71-78 insulin Homo sapiens 112-119 10554902-8 1999 Data provided strong evidence that acarbose prevents the marked increase in postprandial glucose level normally observed when insulin is administered with a meal. Glucose 89-96 insulin Homo sapiens 126-133 10462139-8 1999 The glucose response to an insulin-infusion test appeared reproducible among the patients with recurrent attacks of severe hypoglycaemia. Glucose 4-11 insulin Homo sapiens 27-34 10378101-4 1999 Choline incorporation was significantly lower after a 4-hour pulse in low glucose (+/- insulin) than under continuing high glucose (+/- insulin) conditions (P < .01). Glucose 74-81 insulin Homo sapiens 87-94 10378391-2 1999 In CF patients, a fast postprandial rise in plasma glucose is typically followed by a delayed but prolonged insulin response. Glucose 51-58 insulin Homo sapiens 108-115 10431702-2 1999 The liver as a sensory organ detects a glucose concentration gradient between the hepatic artery and the portal vein by intrahepatic sensory-effector nerves, generating a cholinergic signal for an insulin-dependent net hepatic glucose uptake. Glucose 39-46 insulin Homo sapiens 197-204 10431702-2 1999 The liver as a sensory organ detects a glucose concentration gradient between the hepatic artery and the portal vein by intrahepatic sensory-effector nerves, generating a cholinergic signal for an insulin-dependent net hepatic glucose uptake. Glucose 227-234 insulin Homo sapiens 197-204 10431702-3 1999 The liver senses the insulin concentration by hepatoenteral sensory-effector nerves, generating a cholinergic signal to increase glucose absorption in the intestine and thus its coordinated utilization in liver, muscle and adipose tissue. Glucose 129-136 insulin Homo sapiens 21-28 10390951-7 1999 None of the relatives had glucose intolerance, however, the glucose-stimulated insulin response was elevated at all points in men as well as in women. Glucose 60-67 insulin Homo sapiens 79-86 10368369-5 1999 Despite these differences, increases in whole body insulin action (insulin sensitivity index, determined with an intravenous glucose tolerance test and minimal-model analysis) with training were similar regardless of age, in both the women and men (mean increase of 2.2 +/- 0.3-fold). Glucose 125-132 insulin Homo sapiens 51-58 10372689-6 1999 Insulin and the insulin-to-glucose ratio were most significantly elevated among patients with increased truncal adiposity (insulin, 28.2 +/- 3.2 microU/mL, P < 0.001 vs. control; insulin/ glucose, 0.32 +/- 0.04, P < 0.001 vs. control). Glucose 27-34 insulin Homo sapiens 16-23 10372689-5 1999 Insulin and the insulin-to-glucose ratio were increased, even among HIV-infected patients with low body weight (<90% of ideal body weight) (insulin, 13.3 +/- 2.8 microU/mL, P < 0.01 vs. control; insulin/glucose, 0.2 +/- 0.04, P < 0.01 vs. control). Glucose 209-216 insulin Homo sapiens 0-7 10372689-6 1999 Insulin and the insulin-to-glucose ratio were most significantly elevated among patients with increased truncal adiposity (insulin, 28.2 +/- 3.2 microU/mL, P < 0.001 vs. control; insulin/ glucose, 0.32 +/- 0.04, P < 0.001 vs. control). Glucose 191-198 insulin Homo sapiens 0-7 10372689-6 1999 Insulin and the insulin-to-glucose ratio were most significantly elevated among patients with increased truncal adiposity (insulin, 28.2 +/- 3.2 microU/mL, P < 0.001 vs. control; insulin/ glucose, 0.32 +/- 0.04, P < 0.001 vs. control). Glucose 191-198 insulin Homo sapiens 123-130 10372689-6 1999 Insulin and the insulin-to-glucose ratio were most significantly elevated among patients with increased truncal adiposity (insulin, 28.2 +/- 3.2 microU/mL, P < 0.001 vs. control; insulin/ glucose, 0.32 +/- 0.04, P < 0.001 vs. control). Glucose 191-198 insulin Homo sapiens 123-130 10999153-1 1999 OBJECTIVE: To study the relationship between serum leptin and circulating insulin under basal and in response to oral glucose administration in hyperinsulinemic patients with or without obesity. Glucose 118-125 insulin Homo sapiens 74-81 10372690-0 1999 Disruption of the pulsatile and entropic modes of insulin release during an unvarying glucose stimulus in elderly individuals. Glucose 86-93 insulin Homo sapiens 50-57 10372690-11 1999 We conclude that in response to a sustained (10-h) glucose infusion, normal aging is characterized by a reduction in mass and amplitude of rapid insulin pulses and a decrease in the frequency, amplitude, and regularity of ultradian pulses. Glucose 51-58 insulin Homo sapiens 145-152 10389964-2 1999 However, with cases of persistent hypoglycemia or cases refractory to IV glucose supplementation, attempts to inhibit insulin secretion should be considered. Glucose 73-80 insulin Homo sapiens 118-125 10330141-14 1999 These results outline an important role for PKBalpha/Akt1 in the stimulation of glucose transport by insulin in muscle cells in culture. Glucose 80-87 insulin Homo sapiens 101-108 10394363-1 1999 Insulin-stimulated glucose transport and GLUT4 translocation require regulated interactions between the v-SNARE, VAMP2, and the t-SNARE, syntaxin 4. Glucose 19-26 insulin Homo sapiens 0-7 10394363-5 1999 These data implicate Synip as an insulin-regulated syntaxin 4-binding protein directly involved in the control of glucose transport and GLUT4 vesicle translocation. Glucose 114-121 insulin Homo sapiens 33-40 10362166-8 1999 In those with fasting glucose above 95 mg/dL, insulin may be prescribed after 1 week of dietary therapy, or at diagnosis. Glucose 22-29 insulin Homo sapiens 46-53 10444811-8 1999 However, most recent studies have shown that prolonged reduction of hyperinsulinemia in cirrhosis normalize insulin-mediated glucose uptake and glycogen synthesis in muscle. Glucose 125-132 insulin Homo sapiens 73-80 10444814-1 1999 Glucocorticoid excess causes insulin resistance i.e. a reduced effectiveness of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and fat tissue. Glucose 108-115 insulin Homo sapiens 29-36 10444814-1 1999 Glucocorticoid excess causes insulin resistance i.e. a reduced effectiveness of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and fat tissue. Glucose 108-115 insulin Homo sapiens 80-87 10444814-1 1999 Glucocorticoid excess causes insulin resistance i.e. a reduced effectiveness of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and fat tissue. Glucose 143-150 insulin Homo sapiens 29-36 10444814-1 1999 Glucocorticoid excess causes insulin resistance i.e. a reduced effectiveness of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and fat tissue. Glucose 143-150 insulin Homo sapiens 80-87 10411329-4 1999 Both excess glucose and excess fat can cause insulin resistance in muscle and fat tissue, while excess fat can cause impaired suppression of endogenous glucose production. Glucose 12-19 insulin Homo sapiens 45-52 10348008-6 1999 Insulin secreted by the fetal pancreas in response to maternal glucose concentrations is a key growth factor. Glucose 63-70 insulin Homo sapiens 0-7 10318828-5 1999 Expression of many genes important for glucose-induced insulin release decreased progressively with increasing hyperglycemia, in parallel with a reduction of several islet transcription factors involved in beta cell development and differentiation. Glucose 39-46 insulin Homo sapiens 55-62 11230804-4 1999 Glucose-stimulated insulin secretion in human islets incubated for 1 hr at 20 mM glucose, and in islets cultured for 24 hr at a near-physiological (6.1 mM) glucose concentration, was inhibited (<50% of the control) by SSTR5-specific analogs and by SS14 and SS28. Glucose 0-7 insulin Homo sapiens 19-26 11230804-4 1999 Glucose-stimulated insulin secretion in human islets incubated for 1 hr at 20 mM glucose, and in islets cultured for 24 hr at a near-physiological (6.1 mM) glucose concentration, was inhibited (<50% of the control) by SSTR5-specific analogs and by SS14 and SS28. Glucose 81-88 insulin Homo sapiens 19-26 10318852-1 1999 Phosphatidylinositol (PI) 3-kinase plays an important role in various insulin-stimulated biological responses including glucose transport, glycogen synthesis, and protein synthesis. Glucose 120-127 insulin Homo sapiens 70-77 10235092-0 1999 Prognostic importance of insulin-mediated glucose uptake in aged patients with congestive heart failure secondary to mitral and/or aortic valve disease. Glucose 42-49 insulin Homo sapiens 25-32 10382582-4 1999 There is convincing evidence that insulin increases leptin synthesis and secretion, probably through an insulin-dependent effect on glucose metabolism. Glucose 132-139 insulin Homo sapiens 34-41 10235092-2 1999 We tested the hypothesis that insulin-mediated glucose uptake (IMGU) is a prognostic factor in CHF in aged patients. Glucose 47-54 insulin Homo sapiens 30-37 10329959-4 1999 Introduction of recombinant SNAP23 into chemically permeabilized cells also enhanced insulin-stimulated glucose transport. Glucose 104-111 insulin Homo sapiens 85-92 10329994-7 1999 In the present study, to determine whether decreased IR function is a primary trait of muscle, and not secondary to an altered in vivo environment, we cultured myoblasts from 17 nondiabetic Pima Indians in whom insulin-stimulated glucose disposal (M) was measured during hyperinsulinemic-euglycemic glucose clamps. Glucose 230-237 insulin Homo sapiens 211-218 10329959-0 1999 SNAP23 promotes insulin-dependent glucose uptake in 3T3-L1 adipocytes: possible interaction with cytoskeleton. Glucose 34-41 insulin Homo sapiens 16-23 10329959-1 1999 The acute stimulation of glucose uptake by insulin in fat and muscle cells is primarily the result of translocation of facilitative glucose transporter 4 (GLUT-4) from an internal compartment to the plasma membrane. Glucose 25-32 insulin Homo sapiens 43-50 10329975-10 1999 During moderate-intensity exercise, the very small elevation in plasma insulin concentration (approximately 3 microU/ml; P < 0.05) during the second hour of exercise when subjects were fed vs. when they were fasted slightly attenuated lipolysis (P < 0.05) but did not increase Rd Glc or suppress fat oxidation. Glucose 286-289 insulin Homo sapiens 71-78 10331349-5 1999 IV calcium-based therapy and infusion of insulin with glucose represent the mainstays of immediate therapy, and sodium bicarbonate therapy should be given only when severe acidemia is present. Glucose 54-61 insulin Homo sapiens 41-48 10326169-4 1999 Insulin sensitivity was assessed by an insulin-enhanced, frequently sampled intravenous glucose tolerance test with minimal model analysis. Glucose 88-95 insulin Homo sapiens 0-7 10326169-4 1999 Insulin sensitivity was assessed by an insulin-enhanced, frequently sampled intravenous glucose tolerance test with minimal model analysis. Glucose 88-95 insulin Homo sapiens 39-46 10468921-7 1999 Insulin levels, both fasting and after oral glucose were higher in patients than in controls, and insulin sensitivity was lower in patients than in controls. Glucose 44-51 insulin Homo sapiens 0-7 10331417-12 1999 sTNFR2 levels were also associated with the insulin sensitivity index (S(I)), calculated from an oral glucose tolerance test (OGTT) according to the method by Cederholm and Wibell (r = -0.43, P = 0.006). Glucose 102-109 insulin Homo sapiens 44-51 10331418-6 1999 Insulin sensitivity was determined by the hyperinsulinemic-euglycemic clamp method (for insulin-resistant subjects, glucose metabolic clearance rate [MCR] was 5.77+/-0.28 ml x kg(-1) x min(-1) [mean +/- SE]; for insulin-sensitive subjects, MCR was 10.15+/-0.7 ml x kg(-1) x min(-1); P<0.002). Glucose 116-123 insulin Homo sapiens 0-7 10331418-10 1999 These results indicate that increased IMCL represents an early abnormality in the pathogenesis of insulin resistance and suggest that increased IMCL may contribute to the defective glucose uptake in skeletal muscle in insulin-resistant subjects. Glucose 181-188 insulin Homo sapiens 218-225 10332666-13 1999 Because changes in glucose and insulin were related to reductions in visceral and abdominal subcutaneous AT, we conclude that reduction in abdominal obesity consequent to diet and exercise-induced weight loss is important for attaining improvements in plasma insulin levels, observations that strengthen the concept that abdominal obesity has an important role in mediating insulin resistance. Glucose 19-26 insulin Homo sapiens 259-266 10332666-13 1999 Because changes in glucose and insulin were related to reductions in visceral and abdominal subcutaneous AT, we conclude that reduction in abdominal obesity consequent to diet and exercise-induced weight loss is important for attaining improvements in plasma insulin levels, observations that strengthen the concept that abdominal obesity has an important role in mediating insulin resistance. Glucose 19-26 insulin Homo sapiens 259-266 10332682-10 1999 In addition, the 1-h and 2-h postprandial rises in blood glucose were significantly lower (P < 0.001 for each meal) with insulin lispro, resulting in smoother daily glucose profiles as compared with regular human insulin. Glucose 57-64 insulin Homo sapiens 124-131 10332682-10 1999 In addition, the 1-h and 2-h postprandial rises in blood glucose were significantly lower (P < 0.001 for each meal) with insulin lispro, resulting in smoother daily glucose profiles as compared with regular human insulin. Glucose 57-64 insulin Homo sapiens 216-223 10332682-10 1999 In addition, the 1-h and 2-h postprandial rises in blood glucose were significantly lower (P < 0.001 for each meal) with insulin lispro, resulting in smoother daily glucose profiles as compared with regular human insulin. Glucose 168-175 insulin Homo sapiens 124-131 10332682-14 1999 CONCLUSIONS: Insulin lispro is a suitable and very convenient pump insulin that may result in an improvement of long-term glucose control during CSII treatment. Glucose 122-129 insulin Homo sapiens 13-20 10332682-14 1999 CONCLUSIONS: Insulin lispro is a suitable and very convenient pump insulin that may result in an improvement of long-term glucose control during CSII treatment. Glucose 122-129 insulin Homo sapiens 67-74 10332684-1 1999 OBJECTIVE: To quantitate the contribution of postprandial blood glucose, which improves with the short-acting insulin analog lispro [Lys(B28),Pro(B29)] in type 1 diabetes, to the overall 24-h blood glucose concentration and the long-term HbA1c concentration under conditions of different postabsorptive blood glucose. Glucose 64-71 insulin Homo sapiens 110-117 10332685-3 1999 This study was performed to compare the postprandial serum glucose control after administration of insulin aspart with that of unmodified human insulin. Glucose 59-66 insulin Homo sapiens 99-106 10332685-6 1999 RESULTS: The postprandial glucose control as assessed by the excursion of serum glucose was superior with insulin aspart as compared with that with human insulin injected immediately before or 30 min before a meal (891 +/- 521 vs. 1,311 +/- 512 vs. 1,106 +/- 571 mmol.l-1.min-1, P < 0.0001 and P < 0.02). Glucose 26-33 insulin Homo sapiens 106-113 10332685-7 1999 This was accompanied by a significantly lower glucose maximum concentration [Cmax(SG)] for insulin aspart than for human insulin injected immediately before the meal (13.5 +/- 3.5 vs. 16.4 +/- 3.4 mmol/l, P < 0.001). Glucose 46-53 insulin Homo sapiens 91-98 10332685-11 1999 CONCLUSIONS: This study demonstrates the ability of insulin aspart to improve postprandial glucose control when compared with human insulin. Glucose 91-98 insulin Homo sapiens 52-59 10332710-0 1999 Insulin response to intravenous glucose correlates with plasma levels of the tumor necrosis factor receptor-1. Glucose 32-39 insulin Homo sapiens 0-7 10531859-5 1999 RESULTS: Amylin appears to work with insulin to regulate plasma glucose concentrations in the bloodstream, suppressing the postprandial secretion of glucagon and restraining the rate of gastric emptying. Glucose 64-71 insulin Homo sapiens 37-44 10531859-7 1999 CONCLUSIONS: While insulin replacement therapy is a cornerstone of diabetes treatment, replacement of the function of both amylin and insulin may allow a more complete restoration of the normal physiology of glucose control. Glucose 208-215 insulin Homo sapiens 134-141 11220283-6 1999 Impaired insulin-stimulated glucose metabolism (particularly non-oxidative) in skeletal muscle represents a key feature of type 2 diabetes and is observed early in the pre-diabetic state. Glucose 28-35 insulin Homo sapiens 9-16 11220289-5 1999 The term "insulin resistance" denotes resistance to insulin-mediated glucose uptake into skeletal muscle, which can be measured by the glucose clamp technique. Glucose 69-76 insulin Homo sapiens 10-17 11220289-5 1999 The term "insulin resistance" denotes resistance to insulin-mediated glucose uptake into skeletal muscle, which can be measured by the glucose clamp technique. Glucose 69-76 insulin Homo sapiens 52-59 11220289-5 1999 The term "insulin resistance" denotes resistance to insulin-mediated glucose uptake into skeletal muscle, which can be measured by the glucose clamp technique. Glucose 135-142 insulin Homo sapiens 10-17 11220289-5 1999 The term "insulin resistance" denotes resistance to insulin-mediated glucose uptake into skeletal muscle, which can be measured by the glucose clamp technique. Glucose 135-142 insulin Homo sapiens 52-59 11220295-1 1999 AIM: Rosiglitazone is the most potent of the thiazolidinediones, a novel class of oral antidiabetic agents that reduce blood glucose levels by sensitizing peripheral tissues to insulin. Glucose 125-132 insulin Homo sapiens 177-184 10375055-0 1999 Assessment of insulin sensitivity from plasma insulin and glucose in the fasting or post oral glucose-load state. Glucose 94-101 insulin Homo sapiens 14-21 10624065-12 1999 Elevated serum insulin values at 90 minutes during oral glucose tolerance test could differentiate among both groups and subgroups, except IB versus IIB. Glucose 56-63 insulin Homo sapiens 15-22 10232692-0 1999 Effects of insulin and amino acids on glucose and leucine metabolism in CAPD patients. Glucose 38-45 insulin Homo sapiens 11-18 10232692-1 1999 This study investigates the basal and insulin-stimulated glucose metabolism, substrate utilization, and protein turnover in eight patients maintained on continuous ambulatory peritoneal dialysis (CAPD) (mean age 39+/-5 yr, body mass index [BMI] 108+/-6) and 14 control subjects (mean age 33+/-4 yr, BMI 103+/-3). Glucose 57-64 insulin Homo sapiens 38-45 10232692-5 1999 Both insulin-stimulated glucose oxidation (2.53+/-0.27 versus 2.64+/-0.37 mg/kg per min) and glucose storage (3.70+/-0.48 versus 3.90+/-0.58 mg/kg per min) were similar in CAPD and control subjects. Glucose 24-31 insulin Homo sapiens 5-12 10232692-12 1999 In summary, in CAPD patients: (1) basal glucose oxidation is increased; (2) basal lipid oxidation is decreased; (3) insulin-mediated glucose oxidation and storage are normal; (4) basal leucine flux is reduced; (5) the antiproteolitic action of insulin is normal; and (6) the anabolic response to insulin plus amino acid administration is normal. Glucose 133-140 insulin Homo sapiens 116-123 10323381-0 1999 Measurements of insulin-mediated glucose disposal are stable over time. Glucose 33-40 insulin Homo sapiens 16-23 10323381-1 1999 To evaluate the stability of insulin-mediated glucose disposal, over time, we measured the steady-state plasma insulin (SSPI) and steady-state plasma glucose (SSPG) concentrations in response to a continuous infusion of SRIF (5 microg/min), insulin (25 microU/m2 x min), and dextrose (240 microg/m2 x min). Glucose 46-53 insulin Homo sapiens 29-36 10323381-4 1999 Given the similarity of both SSPI and SSPG concentrations at baseline and follow-up, it can be concluded that insulin-mediated glucose disposal was stable in these 15 individuals over an interval of approximately 4 yr. Glucose 127-134 insulin Homo sapiens 110-117 10210726-2 1999 Further, the effect of iontophoresis of monomeric human insulin analogue (r-DNA origin) on the plasma glucose level (PGL) of diabetic rats was studied. Glucose 102-109 insulin Homo sapiens 56-63 10331492-2 1999 This study was performed to test whether the inhibitory effect of elevated D-glucose concentrations on insulin-stimulated chemokinesis in normal human neutrophils is mediated by increase in protein kinase C (PKC) activity. Glucose 75-84 insulin Homo sapiens 103-110 10331492-6 1999 These results therefore suggest that glucose-induced PKC activation may mediate the inhibitory effects of high glucose levels on insulin-stimulated chemokinesis in normal human neutrophils. Glucose 37-44 insulin Homo sapiens 129-136 10331492-6 1999 These results therefore suggest that glucose-induced PKC activation may mediate the inhibitory effects of high glucose levels on insulin-stimulated chemokinesis in normal human neutrophils. Glucose 111-118 insulin Homo sapiens 129-136 10337851-7 1999 Collectively, these data suggest that RT decreases the insulin response following an oral glucose challenge in older moderately overweight men and women without affecting glucose tolerance. Glucose 90-97 insulin Homo sapiens 55-62 10337869-4 1999 Plasma glucose and insulin responses to a 75-g oral glucose tolerance test and insulin resistance measured by the insulin suppression test, were determined in 58 (42%) patients with CHD and 121 (64%) controls. Glucose 52-59 insulin Homo sapiens 19-26 10416940-4 1999 Finally, loss of renal tissue as a consumer of glucose could explain the insulin resistance of uremia. Glucose 47-54 insulin Homo sapiens 73-80 10416946-1 1999 A stimulus to mitochondrial respiratory activity is a crucial component of the signal transduction mechanism whereby increased plasma glucose evokes insulin secretion by beta-cells. Glucose 134-141 insulin Homo sapiens 149-156 10416947-2 1999 Efficient GK activity is required for normal glucose-stimulated insulin secretion, postprandial hepatic glucose uptake, and the appropriate suppression of hepatic glucose output and gluconeogenesis by elevated plasma glucose. Glucose 45-52 insulin Homo sapiens 64-71 10231837-3 1999 Similar synergistic effects on insulin gene transcription were previously reported for other key insulin regulators, cyclic adenosine monophosphate (cAMP) and glucose. Glucose 159-166 insulin Homo sapiens 31-38 10231848-4 1999 After infusion of glucose, the plasma insulin and C-peptide levels were significantly increased and remained at high levels during 30-min experiments, intravenous administration of secretin and CCK resulted in significant increases of pancreatic secretion including volume, bicarbonate, and protein output. Glucose 18-25 insulin Homo sapiens 38-45 10354364-2 1999 Plasma FFA levels are elevated in most obese subjects, and physiological elevations of plasma FFA inhibit insulin-stimulated glucose uptake into muscle. Glucose 125-132 insulin Homo sapiens 106-113 10354364-3 1999 This peripheral insulin resistance is caused by an FFA-induced defect, which develops 3-4 hr after raising plasma FFA, in insulin-stimulated glucose transport or phosphorylation, or both. Glucose 141-148 insulin Homo sapiens 16-23 10354364-3 1999 This peripheral insulin resistance is caused by an FFA-induced defect, which develops 3-4 hr after raising plasma FFA, in insulin-stimulated glucose transport or phosphorylation, or both. Glucose 141-148 insulin Homo sapiens 122-129 10354364-5 1999 Whether elevated plasma FFA levels inhibit insulin action on endogenous glucose production (EGP), that is, cause central insulin resistance, is more difficult to demonstrate. Glucose 72-79 insulin Homo sapiens 43-50 10354364-5 1999 Whether elevated plasma FFA levels inhibit insulin action on endogenous glucose production (EGP), that is, cause central insulin resistance, is more difficult to demonstrate. Glucose 72-79 insulin Homo sapiens 121-128 10354364-8 1999 In addition, elevated plasma FFA levels potentiate glucose-stimulated insulin secretion acutely and during prolonged exposure (48 hr). Glucose 51-58 insulin Homo sapiens 70-77 10394242-5 1999 In case of diet failure to obtain good glucose control, insulin therapy should be proposed. Glucose 39-46 insulin Homo sapiens 56-63 10219066-5 1999 RESULTS: In the 22 women given D-chiro-inositol, the mean (+/-SD) area under the plasma insulin curve after the oral administration of glucose decreased from 13,417+/-11,572 to 5158+/-6714 microU per milliliter per minute (81+/-69 to 31+/-40 nmol per liter per minute) (P=0.007; P=0.07 for the comparison of this change with the change in the placebo group); glucose tolerance did not change significantly. Glucose 135-142 insulin Homo sapiens 88-95 10219066-5 1999 RESULTS: In the 22 women given D-chiro-inositol, the mean (+/-SD) area under the plasma insulin curve after the oral administration of glucose decreased from 13,417+/-11,572 to 5158+/-6714 microU per milliliter per minute (81+/-69 to 31+/-40 nmol per liter per minute) (P=0.007; P=0.07 for the comparison of this change with the change in the placebo group); glucose tolerance did not change significantly. Glucose 359-366 insulin Homo sapiens 88-95 10339922-5 1999 Intensified conventional insulin treatment (ICT) using the short-acting insulin, Lispro, facilitates the calculation of insulin requirements and helps to avoid large fluctuations in blood glucose levels. Glucose 188-195 insulin Homo sapiens 25-32 10339922-5 1999 Intensified conventional insulin treatment (ICT) using the short-acting insulin, Lispro, facilitates the calculation of insulin requirements and helps to avoid large fluctuations in blood glucose levels. Glucose 188-195 insulin Homo sapiens 72-79 10339922-5 1999 Intensified conventional insulin treatment (ICT) using the short-acting insulin, Lispro, facilitates the calculation of insulin requirements and helps to avoid large fluctuations in blood glucose levels. Glucose 188-195 insulin Homo sapiens 72-79 10370204-3 1999 The in vivo data suggests that there is a direct relationship between blood glucose lowering and the rate of release of insulin from the device. Glucose 76-83 insulin Homo sapiens 120-127 10353113-12 1999 Furthermore, insulin response after oral glucose is independently associated with serum leptin level only in men. Glucose 41-48 insulin Homo sapiens 13-20 10187787-0 1999 An inhibitor of p38 mitogen-activated protein kinase prevents insulin-stimulated glucose transport but not glucose transporter translocation in 3T3-L1 adipocytes and L6 myotubes. Glucose 81-88 insulin Homo sapiens 62-69 10187787-1 1999 The precise mechanisms underlying insulin-stimulated glucose transport still require investigation. Glucose 53-60 insulin Homo sapiens 34-41 10187787-2 1999 Here we assessed the effect of SB203580, an inhibitor of the p38 MAP kinase family, on insulin-stimulated glucose transport in 3T3-L1 adipocytes and L6 myotubes. Glucose 106-113 insulin Homo sapiens 87-94 10187787-3 1999 We found that SB203580, but not its inactive analogue (SB202474), prevented insulin-stimulated glucose transport in both cell types with an IC50 similar to that for inhibition of p38 MAP kinase (0.6 microM). Glucose 95-102 insulin Homo sapiens 76-83 10187787-10 1999 In conclusion, in the presence of SB203580, insulin caused normal translocation and cell surface membrane insertion of glucose transporters without stimulating glucose transport. Glucose 119-126 insulin Homo sapiens 44-51 10187787-11 1999 We propose that insulin stimulates two independent signals contributing to stimulation of glucose transport: phosphatidylinositol 3-kinase leads to glucose transporter translocation and a pathway involving p38 MAP kinase leads to activation of the recruited glucose transporter at the membrane. Glucose 90-97 insulin Homo sapiens 16-23 10342535-5 1999 Insulin secretion during oral glucose tolerance tests (OGTT) deteriorated over time in both groups, whereas a progressive deterioration of glucose tolerance was only evident in the patients who developed diabetes and increased baseline glucose areas were the only predictive parameter of diabetes onset. Glucose 30-37 insulin Homo sapiens 0-7 10203659-3 1999 Insulin response was estimated as the area under the curve during the intravenous glucose tolerance test. Glucose 82-89 insulin Homo sapiens 0-7 10203659-4 1999 Basal endogenous glucose production was estimated from isotope tracer dilution during steady state with [6,6 (2)H2 ]glucose and suppression during insulin infusion. Glucose 17-24 insulin Homo sapiens 147-154 10203659-5 1999 Insulin sensitivity to glucose was defined as the glucose infusion rate required to maintain euglycemia during steady-state insulin infusion. Glucose 23-30 insulin Homo sapiens 0-7 10203659-5 1999 Insulin sensitivity to glucose was defined as the glucose infusion rate required to maintain euglycemia during steady-state insulin infusion. Glucose 23-30 insulin Homo sapiens 124-131 10203659-5 1999 Insulin sensitivity to glucose was defined as the glucose infusion rate required to maintain euglycemia during steady-state insulin infusion. Glucose 50-57 insulin Homo sapiens 0-7 10198307-0 1999 Insulin action on heart and skeletal muscle glucose uptake in weight lifters and endurance athletes. Glucose 44-51 insulin Homo sapiens 0-7 10198307-15 1999 Despite this, cardiac changes are remarkably similar in weight lifters and endurance athletes and are characterized by an increase in left ventricular mass and diminished insulin-stimulated glucose uptake per heart mass. Glucose 190-197 insulin Homo sapiens 171-178 10198313-0 1999 Surgery-induced insulin resistance in human patients: relation to glucose transport and utilization. Glucose 66-73 insulin Homo sapiens 16-23 10198313-4 1999 Surgery reduced insulin-stimulated glucose disposal (P < 0.05) without altering the insulin-stimulated increase in glucose oxidation or suppression of endogenous glucose production. Glucose 35-42 insulin Homo sapiens 16-23 10198313-7 1999 These findings demonstrate that peripheral insulin resistance develops immediately postoperatively and that this condition might be associated with perturbations in insulin-stimulated GLUT-4 translocation as well as nonoxidative glucose disposal, presumably at the level of glycogen synthesis. Glucose 229-236 insulin Homo sapiens 43-50 10200749-6 1999 There was, however, an association between the magnitude of the fasting insulin level and abnormal movements after the authors controlled for fasting glucose level. Glucose 150-157 insulin Homo sapiens 72-79 10340097-2 1999 A pancreatic insulin-secreting neoplasm (insulinoma) was diagnosed on the basis of clinical signs, serum glucose levels, serum insulin levels, abdominal ultrasonography, and exploratory laparotomy with histologic evaluation of neoplastic tissue. Glucose 105-112 insulin Homo sapiens 13-20 10331397-12 1999 The insulin stimulatory effects on inward alanine transport and glucose uptake were three times greater during the postexercise recovery than at rest (P<0.05). Glucose 64-71 insulin Homo sapiens 4-11 10331397-14 1999 In conclusion, the ability of insulin to stimulate glucose uptake and alanine transport and to suppress protein degradation in skeletal muscle is increased after resistance exercise. Glucose 51-58 insulin Homo sapiens 30-37 10342337-1 1999 AIMS: To evaluate the long-term effectiveness of Humalog insulin in lowering post meal glucose excursions. Glucose 87-94 insulin Homo sapiens 57-64 10342337-8 1999 CONCLUSIONS: We conclude that Humalog insulin is effective in lowering postprandial glucose excursions even after up to 5.4 years of treatment. Glucose 84-91 insulin Homo sapiens 38-45 10342341-5 1999 An index of insulin secretion was derived as the ratio of incremental insulin at 30 min divided by 30 minute plasma glucose (delta I/G). Glucose 116-123 insulin Homo sapiens 12-19 10342341-7 1999 Fasting and 2 h insulin secretion showed bell shaped curves with increasing plasma glucose. Glucose 83-90 insulin Homo sapiens 16-23 10342341-11 1999 CONCLUSIONS: Evaluation of insulin resistance and beta-cell function in different stages of glucose tolerance indicate that insulin resistance is manifested in the early stage of glucose intolerance in South Indians, i.e. IGT. Glucose 92-99 insulin Homo sapiens 27-34 10342341-11 1999 CONCLUSIONS: Evaluation of insulin resistance and beta-cell function in different stages of glucose tolerance indicate that insulin resistance is manifested in the early stage of glucose intolerance in South Indians, i.e. IGT. Glucose 92-99 insulin Homo sapiens 124-131 10353301-4 1999 In healthy individuals undergoing euglycaemic glucose clamp testing, glucose infusion rates were higher and reached maximum concentrations significantly earlier after insulin aspart than after human insulin. Glucose 69-76 insulin Homo sapiens 167-174 10353301-4 1999 In healthy individuals undergoing euglycaemic glucose clamp testing, glucose infusion rates were higher and reached maximum concentrations significantly earlier after insulin aspart than after human insulin. Glucose 69-76 insulin Homo sapiens 199-206 10353301-6 1999 In patients with type 1 diabetes postprandial glucose excursions were less pronounced with insulin aspart than human insulin. Glucose 46-53 insulin Homo sapiens 91-98 10408737-15 1999 A single bedtime dose of neutral protamine Hagedorn (NPH) insulin, with or without continuation of daytime oral agents, may control fasting blood glucose. Glucose 146-153 insulin Homo sapiens 58-65 10102699-9 1999 Percent fat (r = 0.86, P < 0.0001) and whole-body glucose uptake (r = -0.72, P < 0.01) correlated with the change in the augmentation index by insulin. Glucose 53-60 insulin Homo sapiens 149-156 10347805-1 1999 Glucokinase (GCK) is an enzyme that regulates insulin secretion, keeping glucose levels within a narrow range. Glucose 73-80 insulin Homo sapiens 46-53 10102691-2 1999 The injection of GLP-1 produces a lengthening of the active phase with respect to the silent phase, leading to a stimulation of insulin release, which produces a secondary decrease in blood glucose concentration and eventually, to the hyperpolarization of the membrane at a blood glucose level of approximately 5 mmol/l. Glucose 190-197 insulin Homo sapiens 128-135 10102691-2 1999 The injection of GLP-1 produces a lengthening of the active phase with respect to the silent phase, leading to a stimulation of insulin release, which produces a secondary decrease in blood glucose concentration and eventually, to the hyperpolarization of the membrane at a blood glucose level of approximately 5 mmol/l. Glucose 280-287 insulin Homo sapiens 128-135 10102699-13 1999 The degree of impairment in this novel vascular action of insulin is closely correlated with the degree of obesity and insulin action on glucose uptake. Glucose 137-144 insulin Homo sapiens 58-65 10102699-13 1999 The degree of impairment in this novel vascular action of insulin is closely correlated with the degree of obesity and insulin action on glucose uptake. Glucose 137-144 insulin Homo sapiens 119-126 10102702-9 1999 Rates of insulin-stimulated nonoxidative glucose disposal accounted for the majority of this improvement (3.00 +/- 0.3 to 4.3 +/- 0.4 mg x FFM(-1) x min(-1)). Glucose 41-48 insulin Homo sapiens 9-16 10189532-4 1999 RESEARCH DESIGN AND METHODS: To examine this issue, we determined insulin sensitivity (SI) in 479 type 2 diabetic subjects by minimal model analyses of frequently sampled intravenous glucose tolerance tests in the Insulin Resistance Atherosclerosis Study (IRAS), a large multicenter study of insulin sensitivity and cardiovascular disease in African-Americans, Hispanics, and non-Hispanic whites. Glucose 183-190 insulin Homo sapiens 66-73 10414937-9 1999 An inverse relationship was found between MDA concentration and insulin sensitivity expressed by glucose disposal rate (r = -0.73). Glucose 97-104 insulin Homo sapiens 64-71 10189532-7 1999 RESULTS: After adjustment for age, sex, ethnicity, and clinic, insulin resistance was significantly correlated with total triglycerides, VLDL cholesterol, VLDL triglyceride, fibrinogen, PAI-1, and fasting glucose, and was inversely correlated with HDL cholesterol level and LDL size. Glucose 205-212 insulin Homo sapiens 63-70 10189539-16 1999 However, in patients who require a second injection of basal insulin, NPH insulin appears to provide lower prebreakfast and prelunch glucose levels compared with UL insulin. Glucose 133-140 insulin Homo sapiens 74-81 10220211-7 1999 Insulin was given at rates of 8 to 14 U/h, with 10% or 20% glucose infusion to maintain the blood glucose above 5 mmol/l; despite this it was not until the fifth day that her serum bicarbonate became normal. Glucose 98-105 insulin Homo sapiens 0-7 10097254-7 1999 Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. Glucose 51-58 insulin Homo sapiens 0-7 10373342-10 1999 The non-insulin-dependent glucose uptake (glucose effectiveness SG did not change (before GH 0.017 +/- 0.005 and after 0.015 +/- 0.006 min-1, NS). Glucose 26-33 insulin Homo sapiens 8-15 10365991-3 1999 The general stress response involves a disruption in normal glucoregulation, in that hepatic glucose production is accelerated and the normal blood glucose lowering action of insulin is diminished. Glucose 148-155 insulin Homo sapiens 175-182 10373342-11 1999 Insulin secretion was enhanced during GH therapy, but insufficiently to match the changes in SI, resulting in a higher blood glucose level during an OGTT. Glucose 125-132 insulin Homo sapiens 0-7 10205239-3 1999 Insulin resistance was assessed by the steady-state plasma glucose concentration at the end of a 3-hour insulin suppression test. Glucose 59-66 insulin Homo sapiens 0-7 10363663-4 1999 CONCLUSIONS: The rapid glycaemic and insulin responses to an oral glucose load may be a result of accelerated gastric emptying. Glucose 66-73 insulin Homo sapiens 37-44 10194529-4 1999 Results showed that CM cells from an early-passage express specific beta-cell genes in response to glucose stimulation, in particular the insulin and GLUT genes. Glucose 99-106 insulin Homo sapiens 138-145 10199783-0 1999 Prolonged exposure of human beta-cells to high glucose increases their release of proinsulin during acute stimulation with glucose or arginine. Glucose 47-54 insulin Homo sapiens 82-92 10199783-0 1999 Prolonged exposure of human beta-cells to high glucose increases their release of proinsulin during acute stimulation with glucose or arginine. Glucose 123-130 insulin Homo sapiens 82-92 10199783-2 1999 This study examines the effect of a 10- to 13-day exposure to 20 mmol/L glucose on subsequent proinsulin and insulin release by human islets isolated from nondiabetic donors. Glucose 72-79 insulin Homo sapiens 94-104 10199783-2 1999 This study examines the effect of a 10- to 13-day exposure to 20 mmol/L glucose on subsequent proinsulin and insulin release by human islets isolated from nondiabetic donors. Glucose 72-79 insulin Homo sapiens 97-104 10199783-3 1999 Compared to control preparations kept at 6 mmol/L glucose, the high glucose cultured beta-cells released more proinsulin and less insulin during perifusion at 5, 10, or 20 mmol/L glucose. Glucose 68-75 insulin Homo sapiens 110-120 10199783-3 1999 Compared to control preparations kept at 6 mmol/L glucose, the high glucose cultured beta-cells released more proinsulin and less insulin during perifusion at 5, 10, or 20 mmol/L glucose. Glucose 68-75 insulin Homo sapiens 113-120 10199783-3 1999 Compared to control preparations kept at 6 mmol/L glucose, the high glucose cultured beta-cells released more proinsulin and less insulin during perifusion at 5, 10, or 20 mmol/L glucose. Glucose 68-75 insulin Homo sapiens 110-120 10199783-3 1999 Compared to control preparations kept at 6 mmol/L glucose, the high glucose cultured beta-cells released more proinsulin and less insulin during perifusion at 5, 10, or 20 mmol/L glucose. Glucose 68-75 insulin Homo sapiens 113-120 10199783-5 1999 The higher amount of secreted proinsulin is attributed to the sustained state of cellular activation that is known to occur after prolonged exposure to high glucose levels. Glucose 157-164 insulin Homo sapiens 30-40 10199783-6 1999 This activated state of the beta-cell population is also held responsible for its higher secretory responsiveness to 5 mmol/L arginine at a submaximal (5 mmol/L) glucose concentration (8-fold higher proinsulin levels than in the control population). Glucose 162-169 insulin Homo sapiens 199-209 10199783-7 1999 It results, together with the reduction in cellular insulin content, in 7- to 10-fold higher proinsulin over insulin ratios in the medium; at 5 mmol/L glucose, this extracellular ratio is similar to that in the cells. Glucose 151-158 insulin Homo sapiens 93-103 10199785-3 1999 glucose tolerance test to determine the insulin sensitivity index (S(I)) and acute insulin response to glucose (AIRglucose). Glucose 103-110 insulin Homo sapiens 83-90 10194529-8 1999 In conclusion, these data show that the human insulinoma cell line CM, at both early-passage and late-passage, posseses a functional glucose-signalling pathway and insulin mRNA expression similar to normal beta-cells, representing, therefore, a good model for studies concerning the signalling and expression of beta-cells. Glucose 133-140 insulin Homo sapiens 46-53 10066918-3 1999 Nevertheless, they also play subtle roles in glucose homeostasis, acting as the sensor for substrate supply in the transduction pathway that promotes insulin secretion by the pancreatic -cell and that modulates the excitability of the hypothalamic glucose-sensitive neurons involved in appetite control. Glucose 45-52 insulin Homo sapiens 150-157 10187881-6 1999 Insulin concentration in the GKI was altered according to BM glucose values. Glucose 61-68 insulin Homo sapiens 0-7 10206433-0 1999 Adenosine triphosphate-sensitive potassium channels are involved in insulin-mediated glucose transport in humans. Glucose 85-92 insulin Homo sapiens 68-75 10206433-9 1999 Since the therapeutic dose of nicorandil did not affect pancreatic B-cell function but caused insulin resistance in both healthy and NIDDM subjects, we conclude that K-ATP channels play a regulatory role in insulin-mediated glucose transport in humans. Glucose 224-231 insulin Homo sapiens 207-214 10203749-2 1999 To accomplish this, there must be mechanisms to sense the amount of blood glucose coupled to rapid release of the right amount of insulin. Glucose 74-81 insulin Homo sapiens 130-137 10420477-3 1999 Analysis of the time course of electrophysiological processes coursing in them, showed appreciable changes in the time of the channel closing, which led to deceleration of insulin secretin starting from the moment of exposure to glucose or sulfonylurea agents till exocytosis of insulin quantum. Glucose 229-236 insulin Homo sapiens 172-179 10420477-3 1999 Analysis of the time course of electrophysiological processes coursing in them, showed appreciable changes in the time of the channel closing, which led to deceleration of insulin secretin starting from the moment of exposure to glucose or sulfonylurea agents till exocytosis of insulin quantum. Glucose 229-236 insulin Homo sapiens 279-286 10080951-6 1999 These results suggest that physiological human leptin concentration is able to importantly affect glucose (but not arginine) stimulated insulin release from human islets only after prolonged exposure. Glucose 98-105 insulin Homo sapiens 136-143 10102010-6 1999 INVESTIGATIONS: In the course of an oGTT (75 g glucose) the basal insulin concentration (146 pmol/l) had risen to 1663 pmol/l at 30 min. Glucose 47-54 insulin Homo sapiens 66-73 10074959-7 1999 Baseline plasma insulin and insulin-to-glucose ratio were associated with an increased risk of hypertension in both the African Americans and the whites. Glucose 39-46 insulin Homo sapiens 28-35 10068412-8 1999 Patients were taught to adjust the bedtime insulin dose on the basis of fasting glucose measurements. Glucose 80-87 insulin Homo sapiens 43-50 11220296-0 1999 Glucose and fatty acid metabolism in type 2 diabetes mellitus: an assessment using low-dose insulin infusion and the hyperinsulinaemic euglycaemic clamp. Glucose 0-7 insulin Homo sapiens 92-99 11220296-5 1999 RESULTS: Using the low-dose insulin infusion there were significant correlations between measures of insulin sensitivity for glucose metabolism and those for NEFA (r = 0.82, p < 0.01) and glycerol (r = 0.73, p < 0.01). Glucose 125-132 insulin Homo sapiens 28-35 11220296-5 1999 RESULTS: Using the low-dose insulin infusion there were significant correlations between measures of insulin sensitivity for glucose metabolism and those for NEFA (r = 0.82, p < 0.01) and glycerol (r = 0.73, p < 0.01). Glucose 125-132 insulin Homo sapiens 101-108 11220296-9 1999 CONCLUSIONS: At low insulin concentrations, insulin"s effects on glucose metabolism (mainly suppression of hepatic glucose output) mirror those on inhibition of lipolysis. Glucose 65-72 insulin Homo sapiens 44-51 11220296-10 1999 At the high insulin concentrations seen during the clamp, stimulation of glucose uptake provides a measure of maximal insulin action which does not parallel its physiological effects shown at lower concentrations. Glucose 73-80 insulin Homo sapiens 12-19 11220296-10 1999 At the high insulin concentrations seen during the clamp, stimulation of glucose uptake provides a measure of maximal insulin action which does not parallel its physiological effects shown at lower concentrations. Glucose 73-80 insulin Homo sapiens 118-125 10070142-4 1999 We conclude that fetal glucose transporters are subject to a time-dependent and tissue- and isoform-specific differential regulation in response to altered circulating glucose and/or insulin concentrations. Glucose 23-30 insulin Homo sapiens 183-190 12482292-5 1999 The use of insulin to keep young diabetic subjects alive, albeit with elevated glucose levels, lead to the discovery of the association of retinopathy and elevated plasma glucose. Glucose 79-86 insulin Homo sapiens 11-18 10088567-14 1999 Serum glucose levels decreased significantly when insulin was administered (5.8+/-0.4 mmol/L [104.6+/-7.2 mg/dL] vs 7.7+/-0.4 mmol/L [138.1+/-7.4 mg/dL; P =.004). Glucose 6-13 insulin Homo sapiens 50-57 10192233-10 1999 The clamp-derived insulin sensitivity index (that corrects for steady-state insulin levels and glucose levels during the clamp) increased similarly in both groups: from 1.15 +/- 0.11 to 1.39 +/- 0.13 with amlodipine (P = .03) and from 1.25 +/- 0.13 to 1.49 +/- 0.16 with enalapril (P = .01). Glucose 95-102 insulin Homo sapiens 18-25 12482292-5 1999 The use of insulin to keep young diabetic subjects alive, albeit with elevated glucose levels, lead to the discovery of the association of retinopathy and elevated plasma glucose. Glucose 171-178 insulin Homo sapiens 11-18 10078556-2 1999 In humans, direct central nervous effects of insulin are difficult to distinguish from alterations in neuronal functions because of insulin-induced decrease in blood glucose levels. Glucose 166-173 insulin Homo sapiens 132-139 10078574-4 1999 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose 29-36 insulin Homo sapiens 39-46 10078557-10 1999 Alpha-met5HT infusion had no effect on hindlimb glucose uptake but markedly inhibited the insulin stimulation of glucose uptake (P < 0.05) and was associated with decreased glucose infusion rates to maintain euglycemia (P < 0.05). Glucose 113-120 insulin Homo sapiens 90-97 10078574-4 1999 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose 29-36 insulin Homo sapiens 98-105 10078574-4 1999 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose 130-137 insulin Homo sapiens 39-46 10078574-4 1999 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose 130-137 insulin Homo sapiens 98-105 10097909-8 1999 Studies of insulin sensitivity in normal and preeclamptic pregnancy by minimal-model analysis of a frequently sampled intravenous glucose tolerance test and of glycosylated hemoglobin in a large survey of nondiabetic pregnancy indicate that the pregnant state may unmask an increase in insulin resistance, causing both pregnancy-induced hyperglycemia and pregnancy-induced hypertension. Glucose 130-137 insulin Homo sapiens 11-18 10078557-10 1999 Alpha-met5HT infusion had no effect on hindlimb glucose uptake but markedly inhibited the insulin stimulation of glucose uptake (P < 0.05) and was associated with decreased glucose infusion rates to maintain euglycemia (P < 0.05). Glucose 113-120 insulin Homo sapiens 90-97 10097926-9 1999 Among individuals with normal glucose levels, having more syndrome traits was significantly related (P < or = 0.05) to higher fasting insulin levels after adjusting for age and measures of adiposity, although associations were attenuated with adjustment for either BMI or waist circumference. Glucose 30-37 insulin Homo sapiens 137-144 10078574-4 1999 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose 130-137 insulin Homo sapiens 39-46 10078574-4 1999 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose 130-137 insulin Homo sapiens 98-105 10097929-9 1999 RESULTS: The peak rise in serum glucose was lower after Mix25 (76 +/- 7 mg/dl) than after 30/70 (94 +/- 5 mg/dl, P < 0.05) or NPH (113 +/- 4 mg/dl, P < 0.005) insulin. Glucose 32-39 insulin Homo sapiens 165-172 10078574-7 1999 Preincubation for 4 h with 25 mmol/l glucose in the absence of insulin produced a similar although somewhat smaller decrease in insulin-stimulated glycogen synthesis; however, it did not alter 2-DG uptake, glucose oxidation to CO2, or incorporation into lipids. Glucose 37-44 insulin Homo sapiens 128-135 10097929-10 1999 The incremental area under the serum glucose curve was 36% smaller after Mix25 than after 30/70 (P < 0.01) and 56% smaller than after NPH (P < 0.005) insulin. Glucose 37-44 insulin Homo sapiens 156-163 10097929-13 1999 After Mix25 injection, there was an inverse correlation between the glucose response to a meal and insulin dose (r = -0.56, P < 0.01) or the incremental area under the serum insulin curve (r = -0.39, P < 0.05). Glucose 68-75 insulin Homo sapiens 99-106 10227568-11 1999 CONCLUSIONS: The use of acarbose in combination with insulin reduces postprandial plasma glucose levels in Type 1 diabetic patients who are not satisfactorily controlled with insulin alone but without significant effect on HbA1c. Glucose 89-96 insulin Homo sapiens 53-60 10078558-0 1999 Resistance to insulin"s acute direct hepatic effect in suppressing steady-state glucose production in individuals with type 2 diabetes. Glucose 80-87 insulin Homo sapiens 14-21 10078558-1 1999 We and others have shown that insulin acutely suppresses glucose production in fasting nondiabetic humans and dogs, by both a direct hepatic effect and an indirect (extrahepatic) effect, and in diabetic dogs by an indirect effect alone. Glucose 57-64 insulin Homo sapiens 30-37 10078558-2 1999 In type 2 diabetes, there is resistance to insulin"s ability to suppress hepatic glucose production, but it has not previously been determined whether the resistance is primarily at the level of the hepatocyte or the peripheral tissues. Glucose 81-88 insulin Homo sapiens 43-50 10078558-12 1999 In conclusion, this is the first study in patients with type 2 diabetes to characterize insulin resistance to the acute direct suppressive effect of insulin on hepatic glucose production. Glucose 168-175 insulin Homo sapiens 88-95 10078558-12 1999 In conclusion, this is the first study in patients with type 2 diabetes to characterize insulin resistance to the acute direct suppressive effect of insulin on hepatic glucose production. Glucose 168-175 insulin Homo sapiens 149-156 10036338-1 1999 Previous investigations have reported that soluble fiber reduces the plasma glucose and insulin changes after an oral glucose load. Glucose 118-125 insulin Homo sapiens 88-95 10216518-1 1999 OBJECTIVE: The present study was undertaken to examine the association of a glucose-stimulated insulin response with the fasting insulin-like growth factor-binding protein (IGFBP)-1 concentration in prepubertal obese children. Glucose 76-83 insulin Homo sapiens 95-102 15992080-11 1999 It thus appears that insulin glargine is a genuinely new addition to the insulin family, and with further clinical experience it may well be possible to achieve better basal blood glucose control (without enhanced risk of hypoglycaemia), particularly at night or in conjunction with rapid-acting insulin analogues. Glucose 180-187 insulin Homo sapiens 21-28 10220236-1 1999 BACKGROUND: Factitious hypoglycemia is a deliberate attempt to induce a low serum glucose level using either insulin or oral hypoglycemic agents. Glucose 82-89 insulin Homo sapiens 109-116 10076585-6 1999 Because many patients use insulin to reduce blood glucose and glycated hemoglobin (HbA1c) to acceptable levels, management should combine diet therapy with insulin and/or 1 or 2 oral antidiabetic agents to help minimize the dose of exogenous insulin needed for glucose control. Glucose 50-57 insulin Homo sapiens 26-33 10331647-1 1999 Glucose induces an increase in the intracellular Ca2+ concentration in pancreatic beta-cells to secrete insulin. Glucose 0-7 insulin Homo sapiens 104-111 10084563-0 1999 Can changes in plasma insulin concentration explain the variability in leptin response to weight loss in obese women with normal glucose tolerance? Glucose 129-136 insulin Homo sapiens 22-29 10362277-4 1999 In the brain, increased levels of insulin result in increased glucose utilization and over-stimulation of the autonomic nervous system (ANS), while the inhibition of insulin secretion results in decreased glucose utilization and dysregulation of the hypothalamo-pituitary-adrenal (HPA) axis. Glucose 62-69 insulin Homo sapiens 34-41 10066387-6 1999 The ratio of the splice variants was positively correlated with fasting plasma insulin concentration (r = 0.757; P = 0.0001), 2-h plasma insulin concentration following an oral glucose tolerance test (r = 0.614; P = 0.01, n = 16), and percentage of body fat (r = 0.746; P = 0.0001). Glucose 177-184 insulin Homo sapiens 137-144 10362277-4 1999 In the brain, increased levels of insulin result in increased glucose utilization and over-stimulation of the autonomic nervous system (ANS), while the inhibition of insulin secretion results in decreased glucose utilization and dysregulation of the hypothalamo-pituitary-adrenal (HPA) axis. Glucose 205-212 insulin Homo sapiens 166-173 10362277-6 1999 It is hypothesized that insulin regulates rCBF either directly, or indirectly via GLUT4 in the hypothalamus now considered the glucose-sensing, insulin-sensing mechanism of the brain and the body. Glucose 127-134 insulin Homo sapiens 24-31 10199158-7 1999 These rapid absorbed insulin analogues significantly inhibited the postprandial plasma glucose excursion more effectively even injected just before each meal in type 1 diabetic patients. Glucose 87-94 insulin Homo sapiens 21-28 10198911-2 1999 Carbohydrate that is malabsorbed and fermented in the colon has been demonstrated to decrease insulin response to a glucose load and improve other risk factors associated with coronary heart disease, although the mechanism remains unclear. Glucose 116-123 insulin Homo sapiens 94-101 10090412-1 1999 As a major counterregulatory hormone of insulin, glucagon plays an important role in regulating glucose homeostasis through its binding to the glucagon receptor. Glucose 96-103 insulin Homo sapiens 40-47 10189006-4 1999 Insulin was positively associated with the female sex, height, body mass index, waist-to-hip ratio, serum triglyceride, total cholesterol, uric acid, and fasting plasma glucose, and was negatively associated with age, smoking, and high-density lipoprotein cholesterol. Glucose 169-176 insulin Homo sapiens 0-7 10189006-7 1999 In conclusion, both fasting serum insulin and C-peptide are quantitatively associated with cardiovascular risk factors in this homogeneous Chinese population with normal glucose tolerance. Glucose 170-177 insulin Homo sapiens 34-41 10189006-7 1999 In conclusion, both fasting serum insulin and C-peptide are quantitatively associated with cardiovascular risk factors in this homogeneous Chinese population with normal glucose tolerance. Glucose 170-177 insulin Homo sapiens 46-55 10358994-6 1999 65 patients with dumping-syndrome following a course of drinking mineral water demonstrated improvement in clinical symptoms of the disease and changed hormonal response to glucose which manifested with activation of insulin secretion early phase and reduced rise of hydrocortisone levels. Glucose 173-180 insulin Homo sapiens 217-224 10837699-1 1999 Inhalation of regular insulin for meal time glucose control has been found to be safe, efficacious and reliable in Type I and Type II diabetics. Glucose 44-51 insulin Homo sapiens 22-29 10837699-9 1999 A potential advantage of aerosol insulin is that it is more rapidly absorbed (serum peak at 5-60 min) and cleared than SC injection (peak at 60-150 min), which provides a more relevant and convenient therapy for meal time glucose control. Glucose 222-229 insulin Homo sapiens 33-40 10023638-7 1999 Patients with a glucose disposal rate less than the mean rate were considered to have a high degree of insulin resistance (n = 36). Glucose 16-23 insulin Homo sapiens 103-110 9895282-5 1999 In consequence, insulin treatment for 24 h increased by 3-fold the basal glucose uptake. Glucose 73-80 insulin Homo sapiens 16-23 9895282-6 1999 Inhibition of phosphoinositide (PI) 3-kinase activity with chemical agents such as wortmannin or LY294002 partially blocked insulin-induced GLUT4 mRNA accumulation, insulin-induced GLUT4 protein content, GLUT4-CAT transactivation and glucose uptake. Glucose 234-241 insulin Homo sapiens 124-131 10064099-8 1999 We concluded that prolonged in vitro exposure of beta cells to raised glucose concentrations increases the relative proportion of islet amyloid polypeptide over insulin, as well as of its precursors over the mature form of islet amyloid polypeptide. Glucose 70-77 insulin Homo sapiens 161-168 10064107-12 1999 Thus we suggest that electroacupuncture stimulation at the Zhongwan acupoint induces secretion of endogenous beta-endorphin which reduces plasma glucose concentration in an insulin-dependent manner. Glucose 145-152 insulin Homo sapiens 173-180 10081651-0 1999 Studies of gene expression and activity of hexokinase, phosphofructokinase and glycogen synthase in human skeletal muscle in states of altered insulin-stimulated glucose metabolism. Glucose 162-169 insulin Homo sapiens 143-150 10081651-1 1999 When whole body insulin-stimulated glucose disposal rate is measured in man applying the euglycaemic, hyperinsulinaemic clamp technique it has been shown that approximately 75% of glucose is taken up by skeletal muscle. Glucose 35-42 insulin Homo sapiens 16-23 10081651-1 1999 When whole body insulin-stimulated glucose disposal rate is measured in man applying the euglycaemic, hyperinsulinaemic clamp technique it has been shown that approximately 75% of glucose is taken up by skeletal muscle. Glucose 180-187 insulin Homo sapiens 16-23 10229308-12 1999 CONCLUSIONS: In South Asian subjects treated with gliclazide the reduction in fasting glucose concentrations appears to be due to an improvement in insulin sensitivity as well as in beta-cell function. Glucose 86-93 insulin Homo sapiens 148-155 10333956-8 1999 African-American children and youth have greater insulin responses during glucose tolerance testing and during hyperglycemic clamp study than do whites. Glucose 74-81 insulin Homo sapiens 49-56 10334321-1 1999 The finding of a reduced insulin-stimulated glucose uptake and glycogen synthesis in the skeletal muscle of glucose-tolerant first-degree relatives of patients with NIDDM, as well as in cultured fibroblasts and skeletal muscle cells isolated from NIDDM patients, has been interpreted as evidence for a genetic involvement in the disease. Glucose 44-51 insulin Homo sapiens 25-32 10334321-1 1999 The finding of a reduced insulin-stimulated glucose uptake and glycogen synthesis in the skeletal muscle of glucose-tolerant first-degree relatives of patients with NIDDM, as well as in cultured fibroblasts and skeletal muscle cells isolated from NIDDM patients, has been interpreted as evidence for a genetic involvement in the disease. Glucose 108-115 insulin Homo sapiens 25-32 10426567-0 1999 Possible involvement of atypical protein kinase C (PKC) in glucose-sensitive expression of the human insulin gene: DNA-binding activity and transcriptional activity of pancreatic and duodenal homeobox gene-1 (PDX-1) are enhanced via calphostin C-sensitive but phorbol 12-myristate 13-acetate (PMA) and Go 6976-insensitive pathway. Glucose 59-66 insulin Homo sapiens 101-108 10426567-2 1999 In this study, we tried to elucidate the role of PDX-1 in the glucose-induced transcriptional activation of the human insulin gene promoter in MIN6 cells. Glucose 62-69 insulin Homo sapiens 118-125 10069661-2 1999 Insulin secretion in response to an oral glucose tolerance test (OGTT) and a GH stimulation test by L-dopa, growth hormone-binding protein (GHBP) and IGF-I were measured. Glucose 41-48 insulin Homo sapiens 0-7 10193857-7 1999 Insulin resistance was calculated from fasting glucose and insulin concentrations. Glucose 47-54 insulin Homo sapiens 0-7 10067662-1 1999 OBJECTIVE: Aim of the present study is to evaluate the effects of L-carnitine on insulin-mediated glucose uptake and oxidation in type II diabetic patients and compare the results with those in healthy controls. Glucose 98-105 insulin Homo sapiens 81-88 10022419-3 1999 Resistance to insulin-mediated glucose disposal was assessed by determining their steady state plasma insulin and glucose concentration during the last 30 min of a 180-min infusion of somatostatin, insulin, and glucose. Glucose 31-38 insulin Homo sapiens 14-21 10022446-5 1999 Positive relationships were also found between the lipolytic sensitivity of s.c. abdominal adipocytes and plasma insulin concentrations measured in the fasting state and after an oral glucose load. Glucose 184-191 insulin Homo sapiens 113-120 10024074-1 1999 We have recently found that in nondiabetic dogs and humans, suppression of glucose production (GP) is mediated by both peripheral and hepatic effects of insulin. Glucose 75-82 insulin Homo sapiens 153-160 10069357-6 1999 Improved insulin sensitivity through lifestyle modifications or pharmacologic therapy (troglitazone and metformin) will lower both insulin and glucose levels as well as diminish dyslipidemia and hypertension. Glucose 143-150 insulin Homo sapiens 9-16 10069357-7 1999 In contrast, sulfonylurea agents lower glucose by increasing insulin levels and may increase the risk of cardiovascular events. Glucose 39-46 insulin Homo sapiens 61-68 10079680-1 1999 OBJECTIVE: To assess which factors influence or predict the efficacy of insulin therapy in subjects with type 2 diabetes, who were poorly controlled despite maximal doses of oral glucose lowering agents. Glucose 179-186 insulin Homo sapiens 72-79 10079680-5 1999 RESULTS: During insulin therapy, HbA1c levels decreased from 10.9 +/- 1.3 to 8.2 +/- 1.1% (p < 0.001), and fasting blood glucose levels decreased from 14.0 +/- 2.3 to 8.2 +/- 2.1 mmol/l (p < 0.001). Glucose 124-131 insulin Homo sapiens 16-23 10200135-6 1999 In siblings the first phase insulin release (FPIR) during an intravenous glucose tolerance test was 128.5 +/- 96.6 (above the 50th percentile) and stimulated insulin release (SIR) was 103.8 +/- 92.5 (above 25th percentile). Glucose 73-80 insulin Homo sapiens 28-35 9890934-0 1999 Insulin-stimulated glucose transport minireview series. Glucose 19-26 insulin Homo sapiens 0-7 9921815-3 1999 RESULTS: Exposure to GLP-1 and PACAP significantly potentiated glucose-induced insulin release and improved the sensitivity to glucose as a secretagogue. Glucose 63-70 insulin Homo sapiens 79-86 9878763-2 1999 Pharmacological doses of glucose analog, 2-deoxyglucose (2DG), is an alternative glucoprivic agent that in contrast to insulin, directly inhibits glycolysis and glucose utilization. Glucose 25-32 insulin Homo sapiens 119-126 9878763-2 1999 Pharmacological doses of glucose analog, 2-deoxyglucose (2DG), is an alternative glucoprivic agent that in contrast to insulin, directly inhibits glycolysis and glucose utilization. Glucose 48-55 insulin Homo sapiens 119-126 9873045-1 1999 One of the mechanisms whereby glucose stimulates insulin gene transcription in pancreatic beta-cells involves activation of the homeodomain transcription factor PDX1 (pancreatic/duodenal homeobox-1) via a stress-activated pathway involving stress-activated protein kinase 2 (SAPK2, also termed RK/p38, CSBP, and Mxi2). Glucose 30-37 insulin Homo sapiens 49-56 10513036-7 1999 The different factors that may impair insulin action and alter glucose uptake in skeletal muscle are: lower blood flow to muscle, produced by either decreased vasodilation or by increased sympathetic nerve activity; augmented diffusion distance from capillaries to muscle due to a decrease in capillary number or to enlarged muscle cells; decrease of insulin receptors; change in the fatty acid profile of major membrane structural phospholipids; decrease in glucose transporters (GLUT 4) and/or hexokinase; impairment in metabolic routes of glucose in muscle as reduction in glycogen synthase. Glucose 63-70 insulin Homo sapiens 351-358 10513036-7 1999 The different factors that may impair insulin action and alter glucose uptake in skeletal muscle are: lower blood flow to muscle, produced by either decreased vasodilation or by increased sympathetic nerve activity; augmented diffusion distance from capillaries to muscle due to a decrease in capillary number or to enlarged muscle cells; decrease of insulin receptors; change in the fatty acid profile of major membrane structural phospholipids; decrease in glucose transporters (GLUT 4) and/or hexokinase; impairment in metabolic routes of glucose in muscle as reduction in glycogen synthase. Glucose 459-466 insulin Homo sapiens 38-45 11107313-3 1999 The perfusion pressure, the perfusion flow, the response to noradrenergic stimuli, the glucose consumption influenced by insulin dosage and the absorption of estradiol were investigated. Glucose 87-94 insulin Homo sapiens 121-128 11107313-5 1999 Moreover, in the legs treated with insulin, a glucose consumption was detected. Glucose 46-53 insulin Homo sapiens 35-42 11533949-5 1999 The results indicate that obese adolescent girls have the following characteristics: 1) insulin resistance with major defects in oxidative and nonoxidative glucose metabolism; 2) hyperinsulinemia in the fasting state and in response to intravenous glucose; and 3) impaired suppression of total body lipid oxidation and plasma FFA concentrations in response to insulin. Glucose 156-163 insulin Homo sapiens 88-95 11533949-5 1999 The results indicate that obese adolescent girls have the following characteristics: 1) insulin resistance with major defects in oxidative and nonoxidative glucose metabolism; 2) hyperinsulinemia in the fasting state and in response to intravenous glucose; and 3) impaired suppression of total body lipid oxidation and plasma FFA concentrations in response to insulin. Glucose 248-255 insulin Homo sapiens 184-191 10774766-7 1999 Serum insulin concentrations followed the glucose response with the peak at the 60-min time point and a significantly lower concentration at the 180-min time point in the SF than in the MUFA group. Glucose 42-49 insulin Homo sapiens 6-13 11701486-2 1999 In the near future, subcutaneously implanted electrochemical glucose sensors will be available to provide frequent or continuous information on which timely treatment decisions, such as insulin injection or glucose source intake, can be based, as well as timely alarm signals. Glucose 61-68 insulin Homo sapiens 186-193 10448535-4 1999 Included are studies on the use of these vectors for gaining insights into the biochemical mechanisms that regulate glucose-stimulated insulin secretion from pancreatic islet beta-cells. Glucose 116-123 insulin Homo sapiens 135-142 10325757-6 1999 After insulin injection, glucose in both plasma and dialysate fell in parallel. Glucose 25-32 insulin Homo sapiens 6-13 10028376-0 1999 Effect of carbohydrate intake on serum 3,5,3"-triiodothyronine-response to glucose ingestion and its relation to glucose tolerance in lean non-insulin-dependent diabetic patients. Glucose 75-82 insulin Homo sapiens 143-150 10412880-14 1999 The results also suggest that BPH is a component of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinaemia, as patients with the metabolic syndrome. Glucose 170-177 insulin Homo sapiens 153-160 10347771-0 1999 Specific insulin and proinsulin in normal glucose tolerant first-degree relatives of NIDDM patients. Glucose 42-49 insulin Homo sapiens 9-16 10347771-0 1999 Specific insulin and proinsulin in normal glucose tolerant first-degree relatives of NIDDM patients. Glucose 42-49 insulin Homo sapiens 21-31 10071593-12 1999 Twenty of 735 (27%) high values triggered a therapeutic response that most commonly required administration of insulin for elevated serum glucose in 17 of 197 occasions in five diabetic PTs. Glucose 138-145 insulin Homo sapiens 111-118 10068865-0 1999 Controlled oral glucose tolerance test: evaluation of insulin resistance with an insulin infusion algorithm that forces the OGTT glycaemic curve within the normal range. Glucose 16-23 insulin Homo sapiens 81-88 10068865-2 1999 This is a technical study to show the feasibility of a computer-controlled oral glucose tolerance test (OGTT) using a specific algorithm, consisting of an OGTT carried out while insulin is infused as required to keep glycaemia within the normal range (National Diabetes Data Group 1979 criteria). Glucose 80-87 insulin Homo sapiens 178-185 9892228-2 1999 The fast-acting insulin analog lispro provides a therapeutic tool for assessing the metabolic outcome of restoration of an early rise in plasma insulin levels after the ingestion of an oral glucose load. Glucose 190-197 insulin Homo sapiens 16-23 9892228-2 1999 The fast-acting insulin analog lispro provides a therapeutic tool for assessing the metabolic outcome of restoration of an early rise in plasma insulin levels after the ingestion of an oral glucose load. Glucose 190-197 insulin Homo sapiens 144-151 10027574-4 1999 Insulin action was measured as glucose disposal during a two-step hyperinsulinaemic-euglycaemic glucose clamp and insulin secretion was assessed in response to oral and intravenous glucose tolerance tests. Glucose 31-38 insulin Homo sapiens 0-7 10027574-4 1999 Insulin action was measured as glucose disposal during a two-step hyperinsulinaemic-euglycaemic glucose clamp and insulin secretion was assessed in response to oral and intravenous glucose tolerance tests. Glucose 96-103 insulin Homo sapiens 0-7 10027574-7 1999 Plasma insulin concentrations were higher in Pimas than Caucasians in the fasting state (27+/-6 vs 11+/-2 mU/ml; p < 0.01) and after a 75-g oral glucose load (area under the curve 19975+/-2626 vs 9293+/-1847 mU x l(-1) x 180 min(-1); p < 0.005). Glucose 148-155 insulin Homo sapiens 7-14 10398545-4 1999 The overriding question is: How can we learn to replace insulin more perfectly, prevent, correct or compensate for compromised glucose counterregulation, or both? Glucose 127-134 insulin Homo sapiens 56-63 11221809-12 1999 Bedtime insulin significantly decreased fasting plasma glucose (13.1 +/- 2.9 vs. 8.2 +/- 2.3 mmol/l, p < 0.01), HbA1c (11.7 +/- 2.9 vs. 9.4 +/- 2.7%, p < 0.01) and plasma cholesterol. Glucose 55-62 insulin Homo sapiens 8-15 11474834-2 1999 Thirty obese subjects participated in an insulin-modified frequently sampled intravenous glucose tolerance test. Glucose 89-96 insulin Homo sapiens 41-48 10364784-8 1999 Capillary glycemia was measured every 6 hours and insulin given if glucose levels rose above 180 mg/dL. Glucose 67-74 insulin Homo sapiens 50-57 10364784-12 1999 In pneumonia, tolerance was similar with both intakes; glycemia was kept at the same level in both, but the amount of insulin given was significantly more in those patients fed on glucose (p < 0.05). Glucose 180-187 insulin Homo sapiens 118-125 10609294-4 1999 The primary reaction of organism on chromium (III) deficiency, is the lowered tolerance of glucose, which is the consequence of changes in insulin affinity to its receptors on cells. Glucose 91-98 insulin Homo sapiens 139-146 10049759-7 1999 Chronic IGF-I treatment caused an increase in both acute insulin-stimulated dGlc uptake and acute IGF-I-stimulated dGlc uptake. Glucose 76-80 insulin Homo sapiens 57-64 10049759-8 1999 Chronic insulin treatment caused a decrease in both acute insulin-stimulated dGlc uptake and acute IGF-I-stimulated dGlc uptake. Glucose 77-81 insulin Homo sapiens 8-15 10049759-8 1999 Chronic insulin treatment caused a decrease in both acute insulin-stimulated dGlc uptake and acute IGF-I-stimulated dGlc uptake. Glucose 116-120 insulin Homo sapiens 8-15 10036770-3 1999 The production of the insulin fusion proteins were carried out in high-cell density fed-batch cultures using a synthetic medium with glucose as sole carbon and energy source. Glucose 133-140 insulin Homo sapiens 22-29 10036770-7 1999 The metabolic burden imposed on the recombinant cells during temperature-induced production of insulin fusion proteins in high-cell density cultures is reflected in an increased respiratory activity and a reduction of the biomass yield coefficient with respect to glucose. Glucose 264-271 insulin Homo sapiens 95-102 9950801-1 1999 Insulin-stimulated glucose uptake is defective in patients with type 2 diabetes. Glucose 19-26 insulin Homo sapiens 0-7 10197653-7 1999 RESULTS: Compared with subcutaneous insulin injections, continuous intravenous insulin infusion induced a significant reduction in perioperative blood glucose levels, which led to a significant reduction in the incidence of deep sternal wound infection in the continuous intravenous insulin infusion group (0.8% [12 of 1,499]) versus the intermittent subcutaneous insulin injection group (2.0% [19 of 968], p = 0.01 by the chi2 test). Glucose 151-158 insulin Homo sapiens 79-86 10197653-7 1999 RESULTS: Compared with subcutaneous insulin injections, continuous intravenous insulin infusion induced a significant reduction in perioperative blood glucose levels, which led to a significant reduction in the incidence of deep sternal wound infection in the continuous intravenous insulin infusion group (0.8% [12 of 1,499]) versus the intermittent subcutaneous insulin injection group (2.0% [19 of 968], p = 0.01 by the chi2 test). Glucose 151-158 insulin Homo sapiens 79-86 10197653-7 1999 RESULTS: Compared with subcutaneous insulin injections, continuous intravenous insulin infusion induced a significant reduction in perioperative blood glucose levels, which led to a significant reduction in the incidence of deep sternal wound infection in the continuous intravenous insulin infusion group (0.8% [12 of 1,499]) versus the intermittent subcutaneous insulin injection group (2.0% [19 of 968], p = 0.01 by the chi2 test). Glucose 151-158 insulin Homo sapiens 79-86 10064097-0 1999 Hyperproinsulinaemia in impaired glucose tolerance is associated with a delayed insulin response to glucose. Glucose 33-40 insulin Homo sapiens 8-15 10064099-4 1999 After 6 days stimulation with 20 mmol/l glucose the cellular content of insulin but not islet amyloid polypeptide was decreased leading to an increase in the ratio of the latter over insulin (3.0 +/- 0.6 vs 1.8 +/- 0.3 after 6 mmol/l glucose culture, p < 0.05). Glucose 40-47 insulin Homo sapiens 72-79 10064099-4 1999 After 6 days stimulation with 20 mmol/l glucose the cellular content of insulin but not islet amyloid polypeptide was decreased leading to an increase in the ratio of the latter over insulin (3.0 +/- 0.6 vs 1.8 +/- 0.3 after 6 mmol/l glucose culture, p < 0.05). Glucose 40-47 insulin Homo sapiens 183-190 10064099-4 1999 After 6 days stimulation with 20 mmol/l glucose the cellular content of insulin but not islet amyloid polypeptide was decreased leading to an increase in the ratio of the latter over insulin (3.0 +/- 0.6 vs 1.8 +/- 0.3 after 6 mmol/l glucose culture, p < 0.05). Glucose 234-241 insulin Homo sapiens 72-79 10081651-11 1999 Endurance training in young healthy subjects results in improved insulin-stimulated glucose disposal rates, predominantly due to an increased glycogen synthesis rate in muscle, which is paralleled by an increased total GS activity, increased GS mRNA levels and enhanced insulin-stimulated activation of GS. Glucose 84-91 insulin Homo sapiens 65-72 10081651-13 1999 Likewise, one-legged exercise training has been reported to increase the basal concentration of muscle GS mRNA in NIDDM patients to a level similar to that seen in control subjects although insulin-stimulated glucose disposal rates remain reduced in NIDDM patients. Glucose 209-216 insulin Homo sapiens 190-197 10081651-14 1999 In the insulin resistant states examined so far, basal and insulin-stimulated glucose oxidation rate at the whole body level and PFK activity in muscle are normal. Glucose 78-85 insulin Homo sapiens 59-66 10081651-16 1999 In endurance trained subjects insulin-stimulated whole body glucose oxidation rate is often increased. Glucose 60-67 insulin Homo sapiens 30-37 10334310-5 1999 We have reported that adipocyte glucose utilization is involved in insulin-induced leptin secretion in vitro. Glucose 32-39 insulin Homo sapiens 67-74 10426567-9 1999 These results suggest that high glucose increased DNA-binding activity of PDX-1 by activating atypical PKC including PKC zeta, resulting in transcriptional activation of the human insulin gene promoter. Glucose 32-39 insulin Homo sapiens 180-187 10517305-6 1999 These results suggested that VK may play an important role on the acute insulin response in glucose tolerance. Glucose 92-99 insulin Homo sapiens 72-79 10022419-10 1999 In summary, insulin-mediated glucose disposal varied widely in nondiabetic, obese women, and there was no relationship between baseline insulin resistance or total integrated insulin response and weight loss. Glucose 29-36 insulin Homo sapiens 12-19 10022436-7 1999 Leptin also reduced proinsulin messenger ribonucleic acid levels that were increased in islets by treatment with 10 nM glucagon-like peptide-1 in the presence of either 5.6 or 11.1 mM glucose. Glucose 184-191 insulin Homo sapiens 20-30 10100062-1 1999 To better understand the links between circulating insulin and albuminuria in essential hypertension, the plasma insulin response t alpha a 75 gram glucose load and albuminuria were evaluated in 53 glucose-tolerant essential hypertensives and 12 controls. Glucose 148-155 insulin Homo sapiens 113-120 10024089-6 1999 Basal and insulin-stimulated femoral muscle blood flow was measured using [(15)O]H2O and insulin-stimulated muscle glucose uptake using [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET). Glucose 115-122 insulin Homo sapiens 89-96 10024089-12 1999 The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects. Glucose 73-80 insulin Homo sapiens 54-61 10024089-12 1999 The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects. Glucose 73-80 insulin Homo sapiens 54-61 10024089-12 1999 The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects. Glucose 73-80 insulin Homo sapiens 54-61 10376388-3 1999 The author presents a review on candidate genes of proteins involved in the metabolism of glucose, lipids and other metabolites (glucose carriers, insulin receptors, proinsulin, glucokinase, amyline, glycogen synthase). Glucose 90-97 insulin Homo sapiens 166-176 9873045-8 1999 These results demonstrate that glucose regulates the insulin gene promoter through activation and nuclear translocation of PDX1 via the SAPK2 pathway. Glucose 31-38 insulin Homo sapiens 53-60 9932725-6 1999 In the presence of metformin, the islets fully maintained the ability to significantly increase their insulin release in response to glucose, even when previously exposed to 22.2 mmol/l glucose. Glucose 133-140 insulin Homo sapiens 102-109 9878708-3 1999 Oral glucose tolerance test revealed that during 40-48 weeks of age, NIDDM became very severe with advancing insulin resistance in OLETF rats. Glucose 5-12 insulin Homo sapiens 109-116 10072095-9 1999 Administration of C-peptide increased basal blood flow by 25 +/- 6%, to 46.3 +/- 3.5 mL min(-1) L(-1) tissue (P < 0.01) and forearm glucose uptake by 76 +/- 34% (P < 0.05). Glucose 135-142 insulin Homo sapiens 18-27 10797845-4 1999 Oral glucose load caused an increase in plasma glucose and insulin levels, which was accompanied by a significant increase in left ventricular shortening (from 35.2 +/- 0.7% at baseline, to 38.5 +/- 0.6% and 39 +/- 0.9% at 30 and 60 minutes post glucose load, respectively [P < 0.05 vs baseline]; ejection fraction rose from 0.73% +/- 0.01 to 0.77% +/- 0.01 (P < 0.05); pressure rate product increased from 7.29 +/- 0.2 to 8.31 +/- 0.3 mmHg x beats per min (P < 0.007) and heart rate enhanced from 68.3 +/- 1.9 to 74 +/- 1.6 (P < 0.034) and 75.3 +/- 1.5 beats per min (P < 0.008) at 60 and 90 minutes after glucose, respectively. Glucose 5-12 insulin Homo sapiens 59-66 10797845-6 1999 These results indicate a significant change in the myocardial contractile response to an oral glucose load, probably related to baroreceptor reflex response as well as an overridden by a potent vasodilator action of insulin. Glucose 94-101 insulin Homo sapiens 216-223 9886953-29 1999 We conclude that glucose production and utilization by the kidney are important insulin-responsive components of glucose metabolism in humans. Glucose 17-24 insulin Homo sapiens 80-87 9886953-29 1999 We conclude that glucose production and utilization by the kidney are important insulin-responsive components of glucose metabolism in humans. Glucose 113-120 insulin Homo sapiens 80-87 9923795-2 1999 SUMMARY BACKGROUND DATA: The authors previously showed that a maximal dose of insulin administered to patients with severe burns promoted skeletal muscle glucose uptake and net protein synthesis. Glucose 154-161 insulin Homo sapiens 78-85 10073278-3 1999 13C NMR spectroscopy has shown that muscle glycogen synthesis accounts for the majority of insulin-stimulated muscle glucose uptake in normal volunteers and that defects in this process are chiefly responsible for insulin resistance in type 1 and type 2 diabetes mellitus, as well as in other insulin resistant states (obesity, insulin-resistant offspring of type 2 diabetic parents, elevation of plasma FFA concentrations). Glucose 117-124 insulin Homo sapiens 91-98 10073278-4 1999 Furthermore, using 31P NMR spectroscopy to measure intracellular glucose-6-phosphate, it has been shown that defects in insulin-stimulated glucose transport/phosphorylation activity are primarily responsible for the insulin resistance in these states. Glucose 65-72 insulin Homo sapiens 120-127 10073278-4 1999 Furthermore, using 31P NMR spectroscopy to measure intracellular glucose-6-phosphate, it has been shown that defects in insulin-stimulated glucose transport/phosphorylation activity are primarily responsible for the insulin resistance in these states. Glucose 65-72 insulin Homo sapiens 216-223 10697303-2 1999 The aim of the present study was therefore to examine the effect of the isoglycemic hyperinsulinemic glucose clamp procedure on FBF and to relate the increase to the glucose disposal rate (GDR), i.e. insulin sensitivity. Glucose 101-108 insulin Homo sapiens 89-96 10803485-2 1999 It seems that in hypertensive patients, two major functions of insulin are impaired: there is insulin resistance of peripheral glucose uptake (primarily skeletal muscle) and insulin resistance of insulin-stimulated vasodilation. Glucose 127-134 insulin Homo sapiens 63-70 10803485-2 1999 It seems that in hypertensive patients, two major functions of insulin are impaired: there is insulin resistance of peripheral glucose uptake (primarily skeletal muscle) and insulin resistance of insulin-stimulated vasodilation. Glucose 127-134 insulin Homo sapiens 94-101 10803485-2 1999 It seems that in hypertensive patients, two major functions of insulin are impaired: there is insulin resistance of peripheral glucose uptake (primarily skeletal muscle) and insulin resistance of insulin-stimulated vasodilation. Glucose 127-134 insulin Homo sapiens 94-101 10803485-2 1999 It seems that in hypertensive patients, two major functions of insulin are impaired: there is insulin resistance of peripheral glucose uptake (primarily skeletal muscle) and insulin resistance of insulin-stimulated vasodilation. Glucose 127-134 insulin Homo sapiens 94-101 10453333-7 1999 The main sites for insulin resistance seem to be extrahepatic tissues, probably skeletal muscle, where preliminary data suggest that the glucose transporting system is involved. Glucose 137-144 insulin Homo sapiens 19-26 9892228-10 1999 After the ingestion of the oral glucose load, plasma glucose concentration increased by 78% at 80-100 min with regular insulin and by 62% with lispro (P < 0.05) and remained lower for the ensuing 3 h. The incremental area under the curve was 46% lower with lispro (715 +/- 109 vs. 389 +/- 109 pmol/300 min; P < 0.01). Glucose 32-39 insulin Homo sapiens 119-126 9892228-10 1999 After the ingestion of the oral glucose load, plasma glucose concentration increased by 78% at 80-100 min with regular insulin and by 62% with lispro (P < 0.05) and remained lower for the ensuing 3 h. The incremental area under the curve was 46% lower with lispro (715 +/- 109 vs. 389 +/- 109 pmol/300 min; P < 0.01). Glucose 53-60 insulin Homo sapiens 119-126 9892228-13 1999 These results show that an early rise in plasma insulin levels after the ingestion of a glucose load is associated with a significant improvement in glucose tolerance due to a prompter, though short-lived, suppression of endogenous glucose production. Glucose 88-95 insulin Homo sapiens 48-55 9892228-13 1999 These results show that an early rise in plasma insulin levels after the ingestion of a glucose load is associated with a significant improvement in glucose tolerance due to a prompter, though short-lived, suppression of endogenous glucose production. Glucose 149-156 insulin Homo sapiens 48-55 9892239-5 1999 When either the initial absolute acute insulin response to glucose (AIRg) or the AIR percentile, which accounts for the individual"s insulin sensitivity, was below the 10th percentile of normal subjects, the risk of diabetes approached 50% at 5 years. Glucose 59-66 insulin Homo sapiens 39-46 10333899-8 1999 RESULTS: After insulin lispro administration, glucose levels were significantly lower between the evening meal and the bedtime snack (analysis of variance [ANOVA] P = 0.02), and four hypoglycemic episodes were recorded. Glucose 46-53 insulin Homo sapiens 15-22 10333906-3 1999 Sensitivity to insulin as a glucoregulatory hormone was determined by M/FFM, where M is the mean glucose infusion rate during the second hour of the clamp and FFM is fat-free mass. Glucose 97-104 insulin Homo sapiens 15-22 10333911-12 1999 CONCLUSIONS: We conclude that type 2 diabetes in obese middle-aged subjects is characterized by impaired glucose-induced insulin release, altered regulation of hepatic glucose output, and resistance to insulin-mediated glucose disposal. Glucose 105-112 insulin Homo sapiens 121-128 10333911-13 1999 In contrast, the primary defect in elderly obese patients with type 2 diabetes is resistance to insulin-mediated glucose disposal. Glucose 113-120 insulin Homo sapiens 96-103 10333914-3 1999 In contrast to normoglycemic patients with diabetes, we hypothesized that injection of lispro insulin 15-30 min before meal ingestion would improve postprandial glucose excursion in hyperglycemic diabetic subjects. Glucose 161-168 insulin Homo sapiens 94-101 10333914-7 1999 RESULTS: Results demonstrated that postprandial glucose excursion was reduced when lispro insulin was administered 15 or 30 min before the meal compared with lispro insulin injected at the meal (P < 0.002). Glucose 48-55 insulin Homo sapiens 90-97 10576516-3 1999 Model assessment methods are also available for the measurement of insulin sensitivity at steady-state plasma glucose and insulin levels or after a standardised glucose infusion. Glucose 110-117 insulin Homo sapiens 67-74 10576516-3 1999 Model assessment methods are also available for the measurement of insulin sensitivity at steady-state plasma glucose and insulin levels or after a standardised glucose infusion. Glucose 161-168 insulin Homo sapiens 67-74 10576523-6 1999 Insulin-stimulated glucose uptake into skeletal muscle is enhanced by metformin. Glucose 19-26 insulin Homo sapiens 0-7 10576523-10 1999 Other effects involved in the blood glucose-lowering effect of metformin include an insulin-independent suppression of fatty acid oxidation and a reduction in hypertriglyceridaemia. Glucose 36-43 insulin Homo sapiens 84-91 10037253-6 1999 Insulin sensitivity was measured by the rate of endogenous glucose disposal after i.v. Glucose 59-66 insulin Homo sapiens 0-7 10037253-12 1999 Metformin therapy resulted in some improvement in insulin sensitivity and reduced the basal and post-glucose load insulin levels. Glucose 101-108 insulin Homo sapiens 114-121 10320055-0 1999 Insulin action and secretion in healthy, glucose tolerant first degree relatives of patients with type 2 diabetes mellitus. Glucose 41-48 insulin Homo sapiens 0-7 10320055-9 1999 Insulin secretion after oral glucose was significantly increased in insulin resistant first degree relatives of patients with type 2 diabetes compared to insulin sensitive first degree relatives of patients with type 2 diabetes. Glucose 29-36 insulin Homo sapiens 0-7 10320055-9 1999 Insulin secretion after oral glucose was significantly increased in insulin resistant first degree relatives of patients with type 2 diabetes compared to insulin sensitive first degree relatives of patients with type 2 diabetes. Glucose 29-36 insulin Homo sapiens 68-75 10433062-2 1999 In a detailed evaluation of the data accumulated for 493 type 2 diabetics who participated in the KID Study, pre- and postprandial C-peptide was correlated with blood glucose level, HbA1, body mass index (BMI), duration of disease and age. Glucose 167-174 insulin Homo sapiens 131-140 10482045-6 1999 Despite identical fasting plasma glucose, carriers of the polymorphism showed a slightly lower fasting serum insulin and lower insulin response to an oral glucose load but higher glucose concentrations. Glucose 33-40 insulin Homo sapiens 109-116 10482045-6 1999 Despite identical fasting plasma glucose, carriers of the polymorphism showed a slightly lower fasting serum insulin and lower insulin response to an oral glucose load but higher glucose concentrations. Glucose 33-40 insulin Homo sapiens 127-134 10482045-6 1999 Despite identical fasting plasma glucose, carriers of the polymorphism showed a slightly lower fasting serum insulin and lower insulin response to an oral glucose load but higher glucose concentrations. Glucose 155-162 insulin Homo sapiens 109-116 10482045-6 1999 Despite identical fasting plasma glucose, carriers of the polymorphism showed a slightly lower fasting serum insulin and lower insulin response to an oral glucose load but higher glucose concentrations. Glucose 155-162 insulin Homo sapiens 127-134 10482045-6 1999 Despite identical fasting plasma glucose, carriers of the polymorphism showed a slightly lower fasting serum insulin and lower insulin response to an oral glucose load but higher glucose concentrations. Glucose 155-162 insulin Homo sapiens 109-116 10482045-6 1999 Despite identical fasting plasma glucose, carriers of the polymorphism showed a slightly lower fasting serum insulin and lower insulin response to an oral glucose load but higher glucose concentrations. Glucose 155-162 insulin Homo sapiens 127-134 10522836-1 1999 Patients with overt Type 2 diabetes consistently have alterations in insulin secretion, including reduced insulin secretory responses to glucose, delayed and blunted meal-induced insulin secretion, increased pro-insulin and abnormal insulin secretory oscillations. Glucose 137-144 insulin Homo sapiens 69-76 10522836-1 1999 Patients with overt Type 2 diabetes consistently have alterations in insulin secretion, including reduced insulin secretory responses to glucose, delayed and blunted meal-induced insulin secretion, increased pro-insulin and abnormal insulin secretory oscillations. Glucose 137-144 insulin Homo sapiens 106-113 10522837-2 1999 Various degrees of peripheral insulin resistance and inadequate glucose-induced insulin secretory profiles are seen in Type 2 diabetes. Glucose 64-71 insulin Homo sapiens 80-87 10543410-5 1999 In the morning following the last r-INF-alpha injection four months later, insulin sensitivity improved significantly in hepatitis C virus-infected patients with normal glucose tolerance (2.17 +/- 0.37 vs. 6.18 +/- 0.94 10(-4) min(-1) per microU/ml, p < 0.001) and with diabetes mellitus (0.86 to 2.61; 0.46 to 1.06 10(-4) min(-1) per microU/ml). Glucose 169-176 insulin Homo sapiens 75-82 10595596-0 1999 Proinsulin in pregnant women with normal glucose tolerance or mild gestational diabetes mellitus. Glucose 41-48 insulin Homo sapiens 0-10 10199159-2 1999 With either a miniaturized extracorporeal glucose monitoring system based on microdialysis sampling method or a ferrocene-mediated needle-type glucose sensor covered with highly biocompatible membrane, and with subcutaneous insulin infusion algorithm using short-acting insulin analogue, long-term physiological glycemic control could be obtained by wearable artificial endocrine pancreas. Glucose 143-150 insulin Homo sapiens 224-231 10207722-8 1999 A submodel of the general bivariate model suggested that the covariance between glucose and insulin has a unique environmental basis, whereas for the reciprocal causation model both causal paths were needed to explain the phenotypic correlation between insulin and glucose and estimates of the reciprocal paths were of opposite sign, an indication for the expected negative feedback loop. Glucose 80-87 insulin Homo sapiens 92-99 9852383-6 1999 The mean insulin values in response to oral glucose load in patients with upper body segment obesity were significantly higher than those corresponding to women with lower body segment obesity. Glucose 44-51 insulin Homo sapiens 9-16 10207722-8 1999 A submodel of the general bivariate model suggested that the covariance between glucose and insulin has a unique environmental basis, whereas for the reciprocal causation model both causal paths were needed to explain the phenotypic correlation between insulin and glucose and estimates of the reciprocal paths were of opposite sign, an indication for the expected negative feedback loop. Glucose 265-272 insulin Homo sapiens 253-260 9931164-1 1999 Intra-arterial infusion of insulin in physiological doses causes forearm vasodilation which is augmented by co-infusion of D-glucose, leading us to speculate that local insulin-mediated vasodilation may depend on insulin-mediated glucose uptake. Glucose 123-132 insulin Homo sapiens 27-34 10844412-5 1999 Both groups showed almost the same levels of insulin sensitivity (glucose infusion rate, GIR = 50.2 +/- 3.0 vs. 51.3 +/- 12.1 micromol/kg/min). Glucose 66-73 insulin Homo sapiens 45-52 9931164-1 1999 Intra-arterial infusion of insulin in physiological doses causes forearm vasodilation which is augmented by co-infusion of D-glucose, leading us to speculate that local insulin-mediated vasodilation may depend on insulin-mediated glucose uptake. Glucose 123-132 insulin Homo sapiens 169-176 9931164-1 1999 Intra-arterial infusion of insulin in physiological doses causes forearm vasodilation which is augmented by co-infusion of D-glucose, leading us to speculate that local insulin-mediated vasodilation may depend on insulin-mediated glucose uptake. Glucose 123-132 insulin Homo sapiens 169-176 10338089-7 1999 Inadequately high insulin secretion in one family with an autosomal dominant mode of inheritance is caused by a mutation in the glucokinase gene, resulting in increased affinity of the enzyme for glucose. Glucose 196-203 insulin Homo sapiens 18-25 9931164-1 1999 Intra-arterial infusion of insulin in physiological doses causes forearm vasodilation which is augmented by co-infusion of D-glucose, leading us to speculate that local insulin-mediated vasodilation may depend on insulin-mediated glucose uptake. Glucose 125-132 insulin Homo sapiens 27-34 9931164-1 1999 Intra-arterial infusion of insulin in physiological doses causes forearm vasodilation which is augmented by co-infusion of D-glucose, leading us to speculate that local insulin-mediated vasodilation may depend on insulin-mediated glucose uptake. Glucose 125-132 insulin Homo sapiens 169-176 9931164-1 1999 Intra-arterial infusion of insulin in physiological doses causes forearm vasodilation which is augmented by co-infusion of D-glucose, leading us to speculate that local insulin-mediated vasodilation may depend on insulin-mediated glucose uptake. Glucose 125-132 insulin Homo sapiens 169-176 9931164-2 1999 We have examined the relationship between whole-body insulin sensitivity and forearm vasodilation in response to local infusion of insulin/glucose, thus avoiding any confounding effects of sympathetic stimulation on peripheral blood flow. Glucose 139-146 insulin Homo sapiens 53-60 9931164-4 1999 Insulin-mediated glucose uptake (M) for the group (mean+/-SD) was 10.0+/-2.2 mg. kg-1. Glucose 17-24 insulin Homo sapiens 0-7 10091930-8 1999 Rat islets entrapped by the polymer also released higher quantities of insulin more rapidly in response to changes in concentrations of glucose and other stimulants than rat islets entrapped in an alginate control. Glucose 136-143 insulin Homo sapiens 71-78 11938735-3 1999 While post-glucose load the serum insulin and glucose level after glucose load were much higher (P < 0.01) in the test group than that in controls. Glucose 11-18 insulin Homo sapiens 34-41 9916137-3 1999 Rates of insulin stimulated whole-body glucose uptake. Glucose 39-46 insulin Homo sapiens 9-16 9916137-7 1999 Taken together, these data suggest that increased concentrations of plasma FFA induce insulin resistance in humans through inhibition of glucose transport activity; this may be a consequence of decreased IRS-1-associated PI 3-kinase activity. Glucose 137-144 insulin Homo sapiens 86-93 9920074-3 1999 To test whether insulin action was related to total or regional adiposity and to explore the potential role of plasma leptin and lipids, we measured insulin-mediated glucose disposal by the euglycemic insulin clamp, adipose distribution and muscle volume using computed axial tomography, and fasting serum leptin and lipid levels in 20 healthy Asian Indian male volunteers (age, 36 +/- 10 yr). Glucose 166-173 insulin Homo sapiens 149-156 9920114-0 1999 Comment on glucose-to-insulin ratio as a measure of insulin sensitivity in women with PCOS. Glucose 11-18 insulin Homo sapiens 22-29 9920074-3 1999 To test whether insulin action was related to total or regional adiposity and to explore the potential role of plasma leptin and lipids, we measured insulin-mediated glucose disposal by the euglycemic insulin clamp, adipose distribution and muscle volume using computed axial tomography, and fasting serum leptin and lipid levels in 20 healthy Asian Indian male volunteers (age, 36 +/- 10 yr). Glucose 166-173 insulin Homo sapiens 149-156 9920114-0 1999 Comment on glucose-to-insulin ratio as a measure of insulin sensitivity in women with PCOS. Glucose 11-18 insulin Homo sapiens 52-59 9920095-12 1999 We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. Glucose 173-180 insulin Homo sapiens 133-140 10727044-0 1999 The predictive role of insulin-like growth factor-I on insulin-mediated glucose uptake in the elderly. Glucose 72-79 insulin Homo sapiens 23-30 10442567-5 1999 Insulin-induced muscle hexokinase activity appears also to be attenuated in GH-deficient adults with raised intramuscular cellular glucose and normal-reduced concentrations of glucose-6-phosphate. Glucose 131-138 insulin Homo sapiens 0-7 9930972-6 1999 Special problems associated with the use of non-B-cell somatic cells include the processing of proinsulin to insulin, and the conferment of sensitivity to glucose-stimulated proinsulin biosynthesis and regulated insulin release. Glucose 155-162 insulin Homo sapiens 174-184 10095815-9 1999 An extended peak of free insulin was reached 30 min after the insulin injection with a slow decrease to the fasting level after 5 h. After the insulin injection a significant decrease in blood glucose occurred within 30-45 min. Glucose 193-200 insulin Homo sapiens 25-32 10503183-6 1999 The activation of large groups of muscles allow for an improved glucose utilization by simultaneously increasing insulin sensitivity. Glucose 64-71 insulin Homo sapiens 113-120 10392343-1 1999 Although intensified insulin therapy regimens enable normalization of blood glucose levels and related metabolic parameters, these regimens are associated with an increased incidence of hypoglycemic episodes. Glucose 76-83 insulin Homo sapiens 21-28 10419100-8 1999 By contrast, treating the 3T3-L1 adipocytes for 2-24 h with C2-ceramide diminished insulin-stimulated glucose uptake by decreasing the insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. Glucose 102-109 insulin Homo sapiens 83-90 9987735-2 1999 OBJECTIVE: To evaluate insulin secretion detected on oral glucose tolerance testing in relation to clomiphene citrate (CC) responses in women with polycystic ovary syndrome (PCOS). Glucose 58-65 insulin Homo sapiens 23-30 10419100-8 1999 By contrast, treating the 3T3-L1 adipocytes for 2-24 h with C2-ceramide diminished insulin-stimulated glucose uptake by decreasing the insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. Glucose 102-109 insulin Homo sapiens 135-142 10419100-10 1999 Our work provides further mechanisms whereby TNF-alpha and ceramides produce insulin resistance and decrease the effectiveness of insulin in stimulating glucose disposal from the blood. Glucose 153-160 insulin Homo sapiens 130-137 10638680-1 1999 Insulin is known to increase blood flow in parallel to glucose uptake in skeletal muscle. Glucose 55-62 insulin Homo sapiens 0-7 10465505-7 1999 Whereas glucose and fructose both increased plasma glucose, insulin and GLP-1 (P < 0.000)] for all), the response to glucose was much greater (P < 0.005 for all). Glucose 8-15 insulin Homo sapiens 60-67 9893168-0 1999 The I/D polymorphism of angiotensin-converting enzyme gene but not the angiotensinogen gene is associated with insulin response to oral glucose in Japanese. Glucose 136-143 insulin Homo sapiens 111-118 10396583-4 1999 The insulin sensitivity index was calculated by the formula: insulin sensitivity index = (glucose infusion rate/steady state plasma glucose concentrations) x 10(3). Glucose 90-97 insulin Homo sapiens 4-11 10396583-4 1999 The insulin sensitivity index was calculated by the formula: insulin sensitivity index = (glucose infusion rate/steady state plasma glucose concentrations) x 10(3). Glucose 90-97 insulin Homo sapiens 61-68 10396583-4 1999 The insulin sensitivity index was calculated by the formula: insulin sensitivity index = (glucose infusion rate/steady state plasma glucose concentrations) x 10(3). Glucose 132-139 insulin Homo sapiens 4-11 10396583-4 1999 The insulin sensitivity index was calculated by the formula: insulin sensitivity index = (glucose infusion rate/steady state plasma glucose concentrations) x 10(3). Glucose 132-139 insulin Homo sapiens 61-68 9893168-3 1999 The insulin response to the 75-g oral glucose tolerance test (OGTT) was significantly lower in subjects with the ACE D/D genotype compared to those with the I allele (I/D and I/I genotypes) in both nondiabetic (P < 0.05) and NIDDM subjects (P < 0.005). Glucose 38-45 insulin Homo sapiens 4-11 9893168-6 1999 From a viewpoint that insulin response to oral glucose is significantly correlated with insulin sensitivity, these results suggest that polymorphic variations at the ACE gene, but not the AGT gene, may be involved in the genetic regulation of insulin sensitivity in both nondiabetic and NIDDM Japanese subjects. Glucose 47-54 insulin Homo sapiens 22-29 9893168-6 1999 From a viewpoint that insulin response to oral glucose is significantly correlated with insulin sensitivity, these results suggest that polymorphic variations at the ACE gene, but not the AGT gene, may be involved in the genetic regulation of insulin sensitivity in both nondiabetic and NIDDM Japanese subjects. Glucose 47-54 insulin Homo sapiens 88-95 10554572-2 1999 Tests used for estimation of insulin sensitivity in vivo can be divided into indirect tests measuring action of endogenous insulin, usually in response to a glucose stimulus, and direct tests measuring glucose metabolism in response to exogenous insulin. Glucose 157-164 insulin Homo sapiens 123-130 9893168-6 1999 From a viewpoint that insulin response to oral glucose is significantly correlated with insulin sensitivity, these results suggest that polymorphic variations at the ACE gene, but not the AGT gene, may be involved in the genetic regulation of insulin sensitivity in both nondiabetic and NIDDM Japanese subjects. Glucose 47-54 insulin Homo sapiens 88-95 10554572-2 1999 Tests used for estimation of insulin sensitivity in vivo can be divided into indirect tests measuring action of endogenous insulin, usually in response to a glucose stimulus, and direct tests measuring glucose metabolism in response to exogenous insulin. Glucose 157-164 insulin Homo sapiens 123-130 9926712-2 1999 The defects in insulin action on target tissues are characterized by a decreased in muscle glucose uptake and by an increased hepatic glucose production. Glucose 91-98 insulin Homo sapiens 15-22 12136196-3 1999 Over-high concentration of glucose suppressed the expression of leptin and the effect of insulin. Glucose 27-34 insulin Homo sapiens 89-96 10528363-3 1999 In early pregnancy, glucose-stimulated insulin secretion is increased, insulin sensitivity is unchanged or enhanced, and glucose tolerance is normal or slightly improved. Glucose 20-27 insulin Homo sapiens 39-46 10486878-0 1999 [Changes in insulin-glucose quotients in a glucose tolerance test in the third trimester]. Glucose 20-27 insulin Homo sapiens 12-19 10335123-5 1999 The highest glucose levels were in insulin treated group--174.17 +/- 40.31 mg%, and were significantly higher from the values observed in oral antidiabetic agents treated group (169.89 +/- 41.34 mg%), and in diet treated group, where glucose levels were the lowest--134.57 +/- 25.06 mg%. Glucose 12-19 insulin Homo sapiens 35-42 10335123-5 1999 The highest glucose levels were in insulin treated group--174.17 +/- 40.31 mg%, and were significantly higher from the values observed in oral antidiabetic agents treated group (169.89 +/- 41.34 mg%), and in diet treated group, where glucose levels were the lowest--134.57 +/- 25.06 mg%. Glucose 234-241 insulin Homo sapiens 35-42 10486878-0 1999 [Changes in insulin-glucose quotients in a glucose tolerance test in the third trimester]. Glucose 43-50 insulin Homo sapiens 12-19 10486878-1 1999 OBJECTIVE: In comparison a higher insulin-glucose-index is usually associated with an increased insulin resistance. Glucose 42-49 insulin Homo sapiens 34-41 10486878-1 1999 OBJECTIVE: In comparison a higher insulin-glucose-index is usually associated with an increased insulin resistance. Glucose 42-49 insulin Homo sapiens 96-103 10486878-2 1999 In the present study changes in insulin-glucose-indices were examined in relation to a defined glucose tolerance in the last trimester of pregnancy. Glucose 40-47 insulin Homo sapiens 32-39 10486878-2 1999 In the present study changes in insulin-glucose-indices were examined in relation to a defined glucose tolerance in the last trimester of pregnancy. Glucose 95-102 insulin Homo sapiens 32-39 10486878-7 1999 Pregnant women with gestational diabetes were shown to have significantly lower insulin-glucose-indices in the early and intermediate phase of the challenge test while the indices were higher in the final phase of the test. Glucose 88-95 insulin Homo sapiens 80-87 10486878-8 1999 CONCLUSIONS: Women with gestational diabetes demonstrated an initial delay in insulin secretion in combination with a higher insulin-glucose-index, corresponding to an increased insulin resistance, only in the end of the test. Glucose 133-140 insulin Homo sapiens 125-132 10522373-9 1999 There was a tendency of positive correlations between high GADA-levels and higher concentrations of insulin as well as an increased insulin-glucose-index. Glucose 140-147 insulin Homo sapiens 132-139 9843733-3 1998 Glucose transport was increased by insulin (100 nM) and IGF-I (5 nM) by approximately 60%. Glucose 0-7 insulin Homo sapiens 35-42 10025037-1 1998 Disturbances of glucose metabolism with hyperinsulinism and peripheral insulin resistance are frequently observed in patients with hyperparathyroidism. Glucose 16-23 insulin Homo sapiens 45-52 9934819-1 1998 Insulin-mediated stimulation of blood flow to skeletal muscle has been proposed to be of major importance for insulin-mediated glucose uptake. Glucose 127-134 insulin Homo sapiens 0-7 9934819-1 1998 Insulin-mediated stimulation of blood flow to skeletal muscle has been proposed to be of major importance for insulin-mediated glucose uptake. Glucose 127-134 insulin Homo sapiens 110-117 9934819-2 1998 The aim of this study was to investigate the relative importance of blood flow and glucose extraction as determinants of insulin-mediated glucose uptake in the human forearm. Glucose 83-90 insulin Homo sapiens 121-128 9934819-2 1998 The aim of this study was to investigate the relative importance of blood flow and glucose extraction as determinants of insulin-mediated glucose uptake in the human forearm. Glucose 138-145 insulin Homo sapiens 121-128 9934819-12 1998 In conclusion, the early course of insulin-mediated glucose uptake in the human forearm was mainly due to an increase in glucose extraction. Glucose 52-59 insulin Homo sapiens 35-42 9934819-12 1998 In conclusion, the early course of insulin-mediated glucose uptake in the human forearm was mainly due to an increase in glucose extraction. Glucose 121-128 insulin Homo sapiens 35-42 9934819-13 1998 However, with time the insulin-mediated increase in blood flow increased in importance and after 100 min of hyperinsulinaemia FBF was the major determinant of glucose uptake. Glucose 159-166 insulin Homo sapiens 23-30 9843746-0 1998 Overestimation of minimal model glucose effectiveness in presence of insulin response is due to undermodeling. Glucose 32-39 insulin Homo sapiens 69-76 9843746-9 1998 Results suggest that minimal model overestimation is due to single-compartment representation of glucose kinetics that results in a critical oversimplification in the presence of increasingly dynamic insulin secretion patterns. Glucose 97-104 insulin Homo sapiens 200-207 9855615-5 1998 This insulin resistance occurs mostly in the peripheral tissues (muscle and fat cells), and results in increased pancreatic insulin secretion to maintain normal glucose levels. Glucose 161-168 insulin Homo sapiens 5-12 9843908-4 1998 Infusion of insulin suppressed systemic glucose release and glutamine gluconeogenesis by approximately 50% during the last hour of the insulin infusion (P < 0.001). Glucose 40-47 insulin Homo sapiens 12-19 10576516-2 1999 Techniques available for the determination of insulin sensitivity include the glucose clamp, insulin tolerance test, insulin suppression test, the frequently sampled intravenous glucose tolerance test and the regional artero-venous balance. Glucose 78-85 insulin Homo sapiens 46-53 9880120-9 1998 The results of this study demonstrate that AEX and WL are effective nonpharmacologic therapies to lower BP and alter glucose and insulin responses to an oral glucose challenge. Glucose 158-165 insulin Homo sapiens 129-136 9886762-8 1998 MCC-555 treatment also enhanced insulin-induced suppression of hepatic glucose production in ZDF rats as measured using infusions of [6-3H]-glucose under clamp conditions. Glucose 71-78 insulin Homo sapiens 32-39 9886766-6 1998 In both models, JTT-501 improved metabolic abnormalities by enhancing insulin action during the glucose tolerance test and the euglycaemic-hyperinsulinaemic clamp study. Glucose 96-103 insulin Homo sapiens 70-77 9886766-7 1998 In ex vivo assays, JTT-501 ameliorated the impaired insulin-sensitive glucose oxidation and lipid synthesis in peripheral tissues. Glucose 70-77 insulin Homo sapiens 52-59 9836524-0 1998 Alterations in non-insulin-mediated glucose uptake in the elderly patient with diabetes. Glucose 36-43 insulin Homo sapiens 19-26 9837698-8 1998 The insulin response to intravenous glucose tolerance test in two patients with autoantibodies was found to be normal. Glucose 36-43 insulin Homo sapiens 4-11 9832415-9 1998 Increased skeletal muscle glucose uptake in conditions of TNF alpha excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes. Glucose 26-33 insulin Homo sapiens 120-127 9872209-0 1998 The lung as an alternative route of delivery for insulin in controlling postprandial glucose levels in patients with diabetes. Glucose 85-92 insulin Homo sapiens 49-56 9872209-1 1998 STUDY OBJECTIVES: To determine the efficacy of the lung as an alternative route of delivery for insulin in controlling glucose below diabetic levels (11.2 mmol/L) 2 h after the ingestion of a meal in patients with type 2 diabetes mellitus. Glucose 119-126 insulin Homo sapiens 96-103 9872209-10 1998 During the postprandial period, glucose levels were significantly lower at 20 min (5.12+/-1.08 mmol/L), 1 h (7.87+/-0.73 mmol/L), 2 h (8.05+/-1.24 mmol/L) and 3 h (7.50+/-1.43 mmol/L) following inhalation of insulin than when the placebo was used. Glucose 32-39 insulin Homo sapiens 208-215 9872209-12 1998 On the insulin visit, glucose levels were < 11.2 mmol/L 2 h after the meal in six of seven patients. Glucose 22-29 insulin Homo sapiens 7-14 9872209-14 1998 In addition, glucose levels were within the normal postprandial range of < 7.84 mmol/L in four of seven patients 2 h after eating on the insulin visit. Glucose 13-20 insulin Homo sapiens 140-147 9872209-15 1998 CONCLUSIONS: These results suggest that, once plasma glucose levels are normalized, postprandial glucose levels can be maintained below diabetic levels by delivering 1.5 U/kg insulin into the lungs 5 min before the ingestion of a meal. Glucose 53-60 insulin Homo sapiens 175-182 9872209-15 1998 CONCLUSIONS: These results suggest that, once plasma glucose levels are normalized, postprandial glucose levels can be maintained below diabetic levels by delivering 1.5 U/kg insulin into the lungs 5 min before the ingestion of a meal. Glucose 97-104 insulin Homo sapiens 175-182 9836524-1 1998 It is increasingly recognized that alterations in non-insulin-mediated glucose uptake (NIMGU) play an important pathogenic role in disorders of carbohydrate metabolism. Glucose 71-78 insulin Homo sapiens 54-61 9867217-8 1998 Insulin secretion stimulated by glibenclamide, KCl or CRF was further enhanced by the addition of 25 mmol/l glucose in AtT20HI-GLUT2-GK-6 cells but not in AtT20HI cells. Glucose 108-115 insulin Homo sapiens 0-7 9867217-3 1998 Other cell lines transfected with insulin and GLUT2 genes (AtT20HI-GLUT2-3) or with insulin and GK genes (AtT20HI-GK-1) secreted insulin in response to glucose concentrations of only less than 1 mmol/l. Glucose 152-159 insulin Homo sapiens 84-91 9867217-3 1998 Other cell lines transfected with insulin and GLUT2 genes (AtT20HI-GLUT2-3) or with insulin and GK genes (AtT20HI-GK-1) secreted insulin in response to glucose concentrations of only less than 1 mmol/l. Glucose 152-159 insulin Homo sapiens 84-91 9867221-1 1998 Recent studies have shown that cytokines and endotoxins impair insulin-stimulated glucose transport by activating the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in skeletal muscle cells. Glucose 82-89 insulin Homo sapiens 63-70 9868972-3 1998 We examined insulin-stimulated glucose uptake in adipocytes and in vivo insulin sensitivity using the fasting insulin resistance index (FIRI) in 60 subjects (45 Caucasian and 15 Asian) with CHD and 30 Caucasian subjects without CHD. Glucose 31-38 insulin Homo sapiens 12-19 9868972-4 1998 In 25 CHD subjects (18 Caucasian and 7 Asian), the relationship between adipocyte insulin sensitivity and non-esterified fatty acid (NEFA) suppression to oral glucose was examined. Glucose 159-166 insulin Homo sapiens 82-89 9868972-7 1998 Insulin-stimulated glucose uptake in adipocytes was lower in the CHD than control subjects [56 (50 to 62) vs 115 (75 to 132) attomol min(-1).mm2, p < 0.05], being most reduced among the Asians. Glucose 19-26 insulin Homo sapiens 0-7 9868979-8 1998 Our results indicate that in former GDM patients, who are japanese and non-obese, impairment of the acute insulin response to glucose and a decrease in tissue glucose sensitivity rather than insulin sensitivity are the primary pathogenic factors involved. Glucose 126-133 insulin Homo sapiens 106-113 9886724-6 1998 All patients underwent a metabolic assessment, which provided a measure of insulin sensitivity (intravenous glucose tolerance tests and minimal modelling analysis). Glucose 108-115 insulin Homo sapiens 75-82 9932219-0 1998 Effects of regular insulin or insulin LISPRO on glucose metabolism after an oral glucose load in patients with type 2 diabetes mellitus. Glucose 48-55 insulin Homo sapiens 30-37 9932219-4 1998 Suppression of endogenous glucose production was similar with both types of insulin. Glucose 26-33 insulin Homo sapiens 76-83 9925352-4 1998 Therapy was directed primarily at decreasing insulin resistance and thereby improving glucose intolerance by the administration of troglitazone, which increases insulin sensitivity. Glucose 86-93 insulin Homo sapiens 161-168 10095997-10 1998 Longer term exposure of islet beta-cells to fatty acids impairs the insulin secretory response to glucose and mechanisms are known. Glucose 98-105 insulin Homo sapiens 68-75 10395234-8 1998 Serum insulin response at 60 min and the sum of serum insulin in the glucose challenge were greater in the former subjects than those in the latter subjects (P=0.041 and 0.076, respectively). Glucose 69-76 insulin Homo sapiens 54-61 9874192-4 1998 This regulator participates in the stimulation of heart glycolysis in response to glucose, workload, insulin and adrenaline, and it decreases the glycolytic flux when alternative fuels are oxidized. Glucose 82-89 insulin Homo sapiens 101-108 9837860-3 1998 Physical training (seven ESLC sessions/wk for 8 wk) increased whole body insulin-stimulated glucose uptake by 33+/-13%, concomitant with a 2.1-fold increase in insulin-stimulated (100 microU/ml) 3-O-methylglucose transport in isolated vastus lateralis muscle. Glucose 92-99 insulin Homo sapiens 73-80 9837860-7 1998 In conclusion, muscle contraction improves insulin action on whole body and cellular glucose uptake in cervical cord-injured persons through a major increase in protein expression of key genes involved in the regulation of glucose metabolism. Glucose 85-92 insulin Homo sapiens 43-50 9837860-7 1998 In conclusion, muscle contraction improves insulin action on whole body and cellular glucose uptake in cervical cord-injured persons through a major increase in protein expression of key genes involved in the regulation of glucose metabolism. Glucose 223-230 insulin Homo sapiens 43-50 9837860-8 1998 Furthermore, improvements in insulin action on glucose metabolism are independent of changes in muscle fiber type distribution. Glucose 47-54 insulin Homo sapiens 29-36 9837864-5 1998 In addition, insulin-stimulated rates of glucose disposal (Rd) were measured under euglycemic hyperinsulinemic conditions. Glucose 41-48 insulin Homo sapiens 13-20 9851788-8 1998 The ratio of glucose uptake per unit of insulin was also significantly reduced from a control study value of 14.3+/-1.4 to 9.4+/-1.3 mg/kg/min per microU/mL x 100 during methyltestosterone administration. Glucose 13-20 insulin Homo sapiens 40-47 9881888-1 1998 OBJECTIVE: To determine the plasma glucose and insulin responses of various doses of glucose, sucrose, fructose and white bread in normal human subjects. Glucose 85-92 insulin Homo sapiens 47-54 9851800-2 1998 Recently, we demonstrated an association between a prevalent polymorphism at codon 98, Ala/Val98, of this gene and a 20% decreased insulin release during an oral glucose tolerance test (OGTT) in middle-aged glucose-tolerant Danish Caucasian subjects. Glucose 162-169 insulin Homo sapiens 131-138 9851800-2 1998 Recently, we demonstrated an association between a prevalent polymorphism at codon 98, Ala/Val98, of this gene and a 20% decreased insulin release during an oral glucose tolerance test (OGTT) in middle-aged glucose-tolerant Danish Caucasian subjects. Glucose 207-214 insulin Homo sapiens 131-138 9850487-6 1998 Interim efficacy analyses revealed that the intensive policies with sulfonylurea, insulin, and metformin were equally effective in reducing fasting plasma glucose concentrations. Glucose 155-162 insulin Homo sapiens 82-89 9851765-3 1998 The insulin sensitivity index (SI) was quantitatively determined from the frequently sampled iv glucose tolerance test. Glucose 96-103 insulin Homo sapiens 4-11 9851788-10 1998 During low-dose insulin infusion, rates of endogenous hepatic glucose production were equivalently suppressed from basal values of 2.37+/-0.29 and 2.40+/-0.27 mg/kg/min to 0.88+/-0.25 and 0.77+/-0.26 mg/kg/min in the methyltestesterone and control studies respectively. Glucose 62-69 insulin Homo sapiens 16-23 9851788-11 1998 Whole body glucose uptake during low-dose insulin infusion was minimally affected. Glucose 11-18 insulin Homo sapiens 42-49 9851788-12 1998 During the high-dose insulin infusion, endogenous hepatic glucose production was nearly totally suppressed in both groups. Glucose 58-65 insulin Homo sapiens 21-28 9869012-5 1998 During the first 2 h of the clamp, mean glucose infusion rate, the traditional approach to assessing insulin sensitivity, was lower in the hypertensive than in the normotensive obese patients (2.04+/-0.13 versus 3.29+/-0.41 mg/kg per min, respectively; P < 0.05). Glucose 40-47 insulin Homo sapiens 101-108 9869012-8 1998 CONCLUSION: In obesity, hypertension was associated with a slower rate of activation of the insulin effect on glucose metabolism, whereas the maximal steady-state insulin effects were not altered by elevated blood pressure. Glucose 110-117 insulin Homo sapiens 92-99 9845654-3 1998 Insulin and glucose stimulate VSMC proliferation and are elevated in patients with non-insulin-dependent DM. Glucose 12-19 insulin Homo sapiens 87-94 9868173-7 1998 To assess the putative action of leptin and leptin receptors on insulin-mediated glucose transport, muscles from SHR and SHROB were incubated in vitro with recombinant human leptin. Glucose 81-88 insulin Homo sapiens 64-71 9868173-8 1998 Leptin directly suppressed insulin-mediated glucose transport by 50% in skeletal muscle from SHR but not in obese SHROB rats lacking all forms of the leptin receptor. Glucose 44-51 insulin Homo sapiens 27-34 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-8 1998 Glucose stimulated VSMC proliferation up to a concentration of 0.2% (42% and 117% higher growth at 0.1% and 0.2% glucose, respectively, compared with the baseline, P <.05), regardless of the insulin concentration in the media. Glucose 0-7 insulin Homo sapiens 194-201 9878302-9 1998 CONCLUSION: Morbidly obese patients have an increased glucose-stimulated response of beta-endorphin, insulin, and glucose which is partially corrected with weight loss following vertical banded gastroplasty. Glucose 54-61 insulin Homo sapiens 101-108 9923727-2 1998 Skeletal muscle glucose uptake and metabolism are major determinants of whole body glucose metabolism in response to exercise and insulin stimulation. Glucose 16-23 insulin Homo sapiens 130-137 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9923727-2 1998 Skeletal muscle glucose uptake and metabolism are major determinants of whole body glucose metabolism in response to exercise and insulin stimulation. Glucose 83-90 insulin Homo sapiens 130-137 9923727-3 1998 An understanding of the mechanisms responsible for increased muscle glucose uptake under these conditions is crucial for identifying strategies that enhance insulin action and exercise performance. Glucose 68-75 insulin Homo sapiens 157-164 9923727-4 1998 Regular exercise, by favourably influencing the intramuscular determinants of glucose uptake, enhances insulin action. Glucose 78-85 insulin Homo sapiens 103-110 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 43-50 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9845654-7 1998 RESULTS: Insulin stimulated VSMC growth at glucose concentrations more than 0.2% (0.4% glucose with no added insulin resulted in 13,073 +/- 336 cells/mL, 0.4% glucose with 100 ng/mL insulin resulted in 16,536 +/- 1175 cells/mL, 0.4% glucose with 1000 ng/mL insulin resulted in 17,500 +/- 808 cells/mL, 0.6% glucose with no added insulin resulted in 14,167 +/- 1062 cells/mL, 0.6% glucose with 100 ng/mL insulin resulted in 18,984 +/- 1265 cells/mL, 0.6% glucose with 1000 ng/mL insulin resulted in 20,450 +/- 1523 cells/mL, 0.8% glucose with no added insulin resulted in 15, 853 +/- 1650 cells/mL, 0.8% glucose with 1000 ng/mL insulin resulted in 26,302 +/- 1919 cells/mL; P <.05 compared with glucose with no added insulin). Glucose 87-94 insulin Homo sapiens 9-16 9822613-6 1998 Loss of HNF-1alpha function leads to severe defects in insulin secretory responses to glucose and leucine, resulting from impaired glucose utilization and mitochondrial oxidation. Glucose 86-93 insulin Homo sapiens 55-62 9867071-4 1998 We found that the basal ACTH level during the OGTT was positively associated with the cortisol response to ACTH at 60 minutes, the fasting insulin level, and the insulin to glucose ratio among exhausted and high DB men, while the reverse was true for nonexhausted and low DB men. Glucose 173-180 insulin Homo sapiens 162-169 9858970-1 1998 POSSIBLE INTERACTIONS: Converting enzyme inhibitors (CEI) can intensify the glucose lowering effect of insulin or sulfonureas. Glucose 76-83 insulin Homo sapiens 103-110 9858970-8 1998 AN INDIRECT MECHANISM: Captopril, and to a lesser extent enalapril, indirectly increases insulin sensitivity by increasing circulating kinine which leads to vasodilatation in the muscles and increased glucose uptake in muscle tissue. Glucose 201-208 insulin Homo sapiens 89-96 9822613-6 1998 Loss of HNF-1alpha function leads to severe defects in insulin secretory responses to glucose and leucine, resulting from impaired glucose utilization and mitochondrial oxidation. Glucose 131-138 insulin Homo sapiens 55-62 9832102-5 1998 Amputees had higher plasma insulin levels (during fasting and in response to oral glucose loading) and increased blood coagulation activity. Glucose 82-89 insulin Homo sapiens 27-34 9825733-7 1998 An acute inhibitory effect by 10 nM leptin was observed on the ratio of IAPP/insulin release at 5.6-11.1 mM glucose, but this was overcome by 16.7 mM glucose. Glucose 108-115 insulin Homo sapiens 77-84 9861912-5 1998 Recent research has shown that the application of diabetes management techniques aimed at reducing insulin resistance and hyperinsulinaemia (such as weight reduction and the administration of oral hypoglycaemic agents) can not only reverse testosterone and luteinising hormone abnormalities and infertility, but can also improve glucose, insulin and lipid profiles. Glucose 329-336 insulin Homo sapiens 99-106 9861912-5 1998 Recent research has shown that the application of diabetes management techniques aimed at reducing insulin resistance and hyperinsulinaemia (such as weight reduction and the administration of oral hypoglycaemic agents) can not only reverse testosterone and luteinising hormone abnormalities and infertility, but can also improve glucose, insulin and lipid profiles. Glucose 329-336 insulin Homo sapiens 127-134 9839062-7 1998 Although most older studies showed no change in glycosylated hemoglobin (HbA1c) levels, a few recent studies involving refinements, such as continuous subcutaneous insulin infusion or basal insulin to reduce preprandial glucose levels, have found small but significant improvements. Glucose 220-227 insulin Homo sapiens 164-171 9844728-0 1998 Arachidonic acid and protein synthesis inhibitor act synergistically to suppress insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 100-107 insulin Homo sapiens 81-88 9844728-1 1998 The effect of arachidonic acid (AA) on insulin-stimulated glucose transport by 3T3-L1 adipocytes was examined in the presence of cycloheximide. Glucose 58-65 insulin Homo sapiens 39-46 9844728-2 1998 We found that AA acted synergistically with cycloheximide to suppress insulin-stimulated glucose transport, although it alone was without effect. Glucose 89-96 insulin Homo sapiens 70-77 9813142-8 1998 This suggests that endogenous NO has an inhibitory role on insulin release induced by glucose and that its underlying mechanism is the suppression of phosphofructokinase activity in glycolysis. Glucose 86-93 insulin Homo sapiens 59-66 9832174-5 1998 We measured blood pressure (BP), heart rate (HR), muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow, and insulin sensitivity (total glucose uptake determined by an euglycemic/hyperinsulinemic clamp using stable isotope tracer infusion), and calculated forearm vascular resistance (FVR). Glucose 161-168 insulin Homo sapiens 134-141 9839062-7 1998 Although most older studies showed no change in glycosylated hemoglobin (HbA1c) levels, a few recent studies involving refinements, such as continuous subcutaneous insulin infusion or basal insulin to reduce preprandial glucose levels, have found small but significant improvements. Glucose 220-227 insulin Homo sapiens 190-197 9792543-7 1998 In the nondiabetic subjects, an increase in glucose concentration from 95 to 130 to 165 mg/dl resulted in a progressive increase in glucose disappearance during both the low (19.9 +/- 1.8 to 23.6 +/- 1.8 to 25.4 +/- 1.6 micromol x kg(-1) x min(-1); P = 0.003 by ANOVA) and high (36.4 +/- 3.1 to 47.6 +/- 4.5 to 61.1 +/- 7.0 micromol x kg(-1) x min(-1); P = 0.001 by ANOVA) insulin infusions. Glucose 44-51 insulin Homo sapiens 373-380 20957827-2 1998 The motivation for this work is to understand the role of electrical coupling in promoting the synchronization of bursting electrical activity (BEA) observed in the -cells of the islet of Langerhans, which secrete insulin in response to glucose. Glucose 237-244 insulin Homo sapiens 214-221 9850811-22 1998 Thus the present review has shown that even nonobese glucose tolerant women with previous GDM are characterized by the metabolic profile of NIDDM i.e. insulin resistance and impaired insulin secretion. Glucose 53-60 insulin Homo sapiens 151-158 9792543-7 1998 In the nondiabetic subjects, an increase in glucose concentration from 95 to 130 to 165 mg/dl resulted in a progressive increase in glucose disappearance during both the low (19.9 +/- 1.8 to 23.6 +/- 1.8 to 25.4 +/- 1.6 micromol x kg(-1) x min(-1); P = 0.003 by ANOVA) and high (36.4 +/- 3.1 to 47.6 +/- 4.5 to 61.1 +/- 7.0 micromol x kg(-1) x min(-1); P = 0.001 by ANOVA) insulin infusions. Glucose 132-139 insulin Homo sapiens 373-380 9792543-8 1998 In contrast, in the diabetic subjects, whereas an increase in glucose from 95 to 130 mg/dl resulted in an increase in glucose disappearance during both the low (P = 0.001) and high (P = 0.01) dose insulin infusions, a further increase in glucose concentration to 165 mg/dl had no further effect (P = 0.41 and 0.38) on disappearance at either insulin dose (low: 14.2 +/- 0.8 to 18.2 +/- 1.1 to 18.7 +/- 2.4 micromol x kg(-1) x min(-1); high: 21.0 +/- 3.2 to 33.9 +/- 6.4 to 32.5 +/- 8.0 micromol x kg(-1) x min(-1) for 95, 130, and 165 mg/dl, respectively). Glucose 62-69 insulin Homo sapiens 197-204 9792543-8 1998 In contrast, in the diabetic subjects, whereas an increase in glucose from 95 to 130 mg/dl resulted in an increase in glucose disappearance during both the low (P = 0.001) and high (P = 0.01) dose insulin infusions, a further increase in glucose concentration to 165 mg/dl had no further effect (P = 0.41 and 0.38) on disappearance at either insulin dose (low: 14.2 +/- 0.8 to 18.2 +/- 1.1 to 18.7 +/- 2.4 micromol x kg(-1) x min(-1); high: 21.0 +/- 3.2 to 33.9 +/- 6.4 to 32.5 +/- 8.0 micromol x kg(-1) x min(-1) for 95, 130, and 165 mg/dl, respectively). Glucose 62-69 insulin Homo sapiens 342-349 9792543-8 1998 In contrast, in the diabetic subjects, whereas an increase in glucose from 95 to 130 mg/dl resulted in an increase in glucose disappearance during both the low (P = 0.001) and high (P = 0.01) dose insulin infusions, a further increase in glucose concentration to 165 mg/dl had no further effect (P = 0.41 and 0.38) on disappearance at either insulin dose (low: 14.2 +/- 0.8 to 18.2 +/- 1.1 to 18.7 +/- 2.4 micromol x kg(-1) x min(-1); high: 21.0 +/- 3.2 to 33.9 +/- 6.4 to 32.5 +/- 8.0 micromol x kg(-1) x min(-1) for 95, 130, and 165 mg/dl, respectively). Glucose 118-125 insulin Homo sapiens 197-204 9802741-6 1998 RESULTS: The 24-h plasma glucose control obtained with insulin aspart, as assessed by excursions of blood glucose outside a predefined normal range (4.0-7.0 mmo/l), was superior (22% reduction in excursion, P < 0.01). Glucose 25-32 insulin Homo sapiens 55-62 9802741-6 1998 RESULTS: The 24-h plasma glucose control obtained with insulin aspart, as assessed by excursions of blood glucose outside a predefined normal range (4.0-7.0 mmo/l), was superior (22% reduction in excursion, P < 0.01). Glucose 106-113 insulin Homo sapiens 55-62 9802742-4 1998 Glucose infusion rates necessary to neutralize the blood glucose-lowering effect of the administered insulin were registered during euglycemic glucose clamps (blood glucose 5.0 mmol/l; basal intravenous insulin infusion 0.15 mU x kg(-1) x min(-1) over the subsequent 600 min. Glucose 0-7 insulin Homo sapiens 101-108 9802742-4 1998 Glucose infusion rates necessary to neutralize the blood glucose-lowering effect of the administered insulin were registered during euglycemic glucose clamps (blood glucose 5.0 mmol/l; basal intravenous insulin infusion 0.15 mU x kg(-1) x min(-1) over the subsequent 600 min. Glucose 0-7 insulin Homo sapiens 203-210 9802742-4 1998 Glucose infusion rates necessary to neutralize the blood glucose-lowering effect of the administered insulin were registered during euglycemic glucose clamps (blood glucose 5.0 mmol/l; basal intravenous insulin infusion 0.15 mU x kg(-1) x min(-1) over the subsequent 600 min. Glucose 57-64 insulin Homo sapiens 101-108 9833947-7 1998 In contrast, the insulin response to gastric glucose (150 mg/mouse) was reduced and the glucose elimination was inhibited in both male and female transgenic mice. Glucose 45-52 insulin Homo sapiens 17-24 9825953-20 1998 The management of the hypoglycaemic drugs (insulin and sulphonylureas) is based primarily on restoring and maintaining euglycaemia via intravenous dextrose supplementation. Glucose 147-155 insulin Homo sapiens 43-50 9825953-23 1998 The management focus is on restoring acid-base balance with hyperventilation and the use of insulin to shift the utilisation of glucose from the nonoxidative pathway to the oxidative pathway. Glucose 128-135 insulin Homo sapiens 92-99 9827846-5 1998 The insulin-induced glucose disposal rate (Kitt) was calculated from the slope of the regression line of the logarithm of blood glucose against time during the first 3-15 min. Glucose 20-27 insulin Homo sapiens 4-11 9827853-8 1998 These observations indicate that in well-controlled Type 1 diabetic subjects on intensive insulin therapy, major alterations in the GI and fibre content of meals induce small but significant changes in glucose profile. Glucose 202-209 insulin Homo sapiens 90-97 9881243-7 1998 In the insulin-treated group, the 5 patients with progression had higher initial fasting blood-glucose levels than other patients in the group (15.8 vs 13.1 mmol/L, p < 0.05). Glucose 95-102 insulin Homo sapiens 7-14 9792543-8 1998 In contrast, in the diabetic subjects, whereas an increase in glucose from 95 to 130 mg/dl resulted in an increase in glucose disappearance during both the low (P = 0.001) and high (P = 0.01) dose insulin infusions, a further increase in glucose concentration to 165 mg/dl had no further effect (P = 0.41 and 0.38) on disappearance at either insulin dose (low: 14.2 +/- 0.8 to 18.2 +/- 1.1 to 18.7 +/- 2.4 micromol x kg(-1) x min(-1); high: 21.0 +/- 3.2 to 33.9 +/- 6.4 to 32.5 +/- 8.0 micromol x kg(-1) x min(-1) for 95, 130, and 165 mg/dl, respectively). Glucose 118-125 insulin Homo sapiens 342-349 9886745-3 1998 Insulin insensitivity is also a feature of the insulin resistance syndrome, which describes the epidemiological association of glucose intolerance, upper body obesity, hyperinsulinaemia, hypertension, increased triglyceride levels and decreased high-density-lipoprotein (HDL)-cholesterol concentrations. Glucose 127-134 insulin Homo sapiens 0-7 15251717-5 1998 RESULTS: Insulin is used in patients with NIDDM when adequate plasma glucose control can no longer be maintained by orally administered agents. Glucose 69-76 insulin Homo sapiens 9-16 9792543-8 1998 In contrast, in the diabetic subjects, whereas an increase in glucose from 95 to 130 mg/dl resulted in an increase in glucose disappearance during both the low (P = 0.001) and high (P = 0.01) dose insulin infusions, a further increase in glucose concentration to 165 mg/dl had no further effect (P = 0.41 and 0.38) on disappearance at either insulin dose (low: 14.2 +/- 0.8 to 18.2 +/- 1.1 to 18.7 +/- 2.4 micromol x kg(-1) x min(-1); high: 21.0 +/- 3.2 to 33.9 +/- 6.4 to 32.5 +/- 8.0 micromol x kg(-1) x min(-1) for 95, 130, and 165 mg/dl, respectively). Glucose 118-125 insulin Homo sapiens 197-204 9792543-8 1998 In contrast, in the diabetic subjects, whereas an increase in glucose from 95 to 130 mg/dl resulted in an increase in glucose disappearance during both the low (P = 0.001) and high (P = 0.01) dose insulin infusions, a further increase in glucose concentration to 165 mg/dl had no further effect (P = 0.41 and 0.38) on disappearance at either insulin dose (low: 14.2 +/- 0.8 to 18.2 +/- 1.1 to 18.7 +/- 2.4 micromol x kg(-1) x min(-1); high: 21.0 +/- 3.2 to 33.9 +/- 6.4 to 32.5 +/- 8.0 micromol x kg(-1) x min(-1) for 95, 130, and 165 mg/dl, respectively). Glucose 118-125 insulin Homo sapiens 342-349 9792543-10 1998 The abnormality in uptake occurs in the presence of both basal and high insulin concentrations and is evident at glucose concentrations above but not below 130 mg/dl, implying a defect in a glucose-responsive step. Glucose 190-197 insulin Homo sapiens 72-79 9809466-2 1998 Skeletal muscle is a major glucose-utilizing tissue in the absorptive state and alterations in muscle insulin-stimulated glucose uptake lead to derangements in whole body glucose disposal. Glucose 121-128 insulin Homo sapiens 102-109 9809466-2 1998 Skeletal muscle is a major glucose-utilizing tissue in the absorptive state and alterations in muscle insulin-stimulated glucose uptake lead to derangements in whole body glucose disposal. Glucose 121-128 insulin Homo sapiens 102-109 9824974-6 1998 The insulin-sensitizing drug troglitazone enhances insulin-mediated glucose disposal. Glucose 68-75 insulin Homo sapiens 4-11 9822441-4 1998 Insulin sensitivity measured as glucose disposal rate (GDR) correlated with MFBF (r=0.55, P=0.003), MFVR (r=-0.58, P=0. Glucose 32-39 insulin Homo sapiens 0-7 9824974-6 1998 The insulin-sensitizing drug troglitazone enhances insulin-mediated glucose disposal. Glucose 68-75 insulin Homo sapiens 51-58 9864685-3 1998 Insulin resistance was estimated by plasma insulin level at 120 min after the 75g oral glucose tolerance test. Glucose 87-94 insulin Homo sapiens 0-7 9918388-5 1998 S.c. injection of 0.15 U/kg of regular insulin induced a fourfold increase in insulinemia on both study days as well as a mean decline in blood glucose by 1.6 mmol/l to a minimum of 2.8 mmol/l within 60 min after injection. Glucose 144-151 insulin Homo sapiens 39-46 9814481-1 1998 The objective of the present study was to investigate whether the frequent amino acid polymorphisms, Ile/Leu27 and Ser/Asn487, of the hepatocyte nuclear factor-1alpha gene were associated with alterations in glucose-induced serum C-peptide and serum insulin responses among glucose-tolerant first-degree relatives of type 2 diabetic patients. Glucose 208-215 insulin Homo sapiens 250-257 9864685-12 1998 These results suggest that insulin resistance is an important risk factor for coronary artery disease in patients with normal glucose tolerance, and is related to the severity and multiplicity of coronary atherosclerosis as in patients with diabetes. Glucose 126-133 insulin Homo sapiens 27-34 9844629-5 1998 Thus, insulin resistance in muscle contributes to the altered fat metabolism associated with type 2 diabetes, but tissues other than muscle appear to be more involved in insulin-regulated glucose disposal than previously recognized. Glucose 188-195 insulin Homo sapiens 170-177 9826207-5 1998 Integrated proinsulin concentrations during the oral glucose load were also higher in pancreas-kidney recipients (1.4 [1.1 to 1.8] nmol/L x min) and kidney recipients (1.5 [1.2 to 2.0] nmol/L x min) versus normal subjects (0.8 [0.7 to 0.9] nmol/L x min). Glucose 53-60 insulin Homo sapiens 11-21 9829612-3 1998 Insulin secretion was measured during an IV glucose tolerance test (IVGTT; 0.5 g/kg) followed by a hyperglycemic clamp (plasma glucose at 10 mmol/L). Glucose 44-51 insulin Homo sapiens 0-7 9829612-3 1998 Insulin secretion was measured during an IV glucose tolerance test (IVGTT; 0.5 g/kg) followed by a hyperglycemic clamp (plasma glucose at 10 mmol/L). Glucose 127-134 insulin Homo sapiens 0-7 9829612-5 1998 RESULTS: Patients with normal glucose tolerance receiving TPN had an insulin response to IVGTT similar to that of normal children of the same age. Glucose 30-37 insulin Homo sapiens 69-76 9829612-10 1998 CONCLUSIONS: The insulin response to sustained hyperglycemia was stronger in children with normal glucose tolerance on cyclic TPN. Glucose 98-105 insulin Homo sapiens 17-24 9829612-11 1998 Patients with a limited capacity to release insulin, either constitutional or acquired, may not be able to produce enough insulin in these conditions and develop glucose intolerance during TPN. Glucose 162-169 insulin Homo sapiens 44-51 10070221-7 1998 Bezafibrate lowered slightly the insulin level but did not affect peptide C. A correlation of changes in fibrinogen levels and the 60 min insulin concentration in the glucose tolerance test was higher in the bezafibrate group (r = 0.61) than in the placebo group (r = 0.23). Glucose 167-174 insulin Homo sapiens 138-145 9874082-3 1998 Integrated response of insulin to the glucose load was calculated as the area under the curve of insulin (AUC-I) and glucose (AUC-G). Glucose 38-45 insulin Homo sapiens 23-30 9874082-3 1998 Integrated response of insulin to the glucose load was calculated as the area under the curve of insulin (AUC-I) and glucose (AUC-G). Glucose 38-45 insulin Homo sapiens 97-111 9874082-3 1998 Integrated response of insulin to the glucose load was calculated as the area under the curve of insulin (AUC-I) and glucose (AUC-G). Glucose 117-124 insulin Homo sapiens 23-30 9851571-7 1998 Neural vasoconstriction in skeletal muscle has metabolic effects by impairing glucose delivery, which is a basis for insulin resistance and hyperinsulinemia. Glucose 78-85 insulin Homo sapiens 117-124 9774438-3 1998 We previously reported that amino acids are required for glucose or exogenous insulin to stimulate phosphorylation of PHAS-I (phosphorylated heat- and acid-stable protein regulated by insulin), a recently discovered regulator of translation initiation during cell mitogenesis. Glucose 57-64 insulin Homo sapiens 184-191 9801136-0 1998 Insulin-independent glucose transport regulates insulin sensitivity. Glucose 20-27 insulin Homo sapiens 0-7 9801136-0 1998 Insulin-independent glucose transport regulates insulin sensitivity. Glucose 20-27 insulin Homo sapiens 48-55 9801136-1 1998 The glucose transport proteins (GLUT1 and GLUT4) facilitate glucose transport into insulin-sensitive cells. Glucose 4-11 insulin Homo sapiens 83-90 9801136-3 1998 GLUT4 is insulin-dependent and is responsible for the majority of glucose transport into muscle and adipose cells in anabolic conditions. Glucose 66-73 insulin Homo sapiens 9-16 9801136-4 1998 We suggest the hypothesis that insulin resistance is dependent on whether glucose is entering through GLUT1 or GLUT4 and on the two functional compartments of glucose 6-phosphate formation within the cell. Glucose 74-81 insulin Homo sapiens 31-38 9801136-7 1998 Hexosamines have a negative feedback effect on GLUT4, and reduced GLUT4 activity decreases insulin-mediated glucose uptake. Glucose 108-115 insulin Homo sapiens 91-98 9801136-8 1998 Thus, insulin-independent glucose transport through GLUT1 can meet the basal needs of the muscle cell. Glucose 26-33 insulin Homo sapiens 6-13 9801136-9 1998 If glucose entrance through GLUT1 and the activation of the hexosamine pathway is abundant, it can decrease the insulin-mediated glucose transport through GLUT4 leading to insulin resistance. Glucose 3-10 insulin Homo sapiens 112-119 9801136-9 1998 If glucose entrance through GLUT1 and the activation of the hexosamine pathway is abundant, it can decrease the insulin-mediated glucose transport through GLUT4 leading to insulin resistance. Glucose 3-10 insulin Homo sapiens 172-179 9801136-9 1998 If glucose entrance through GLUT1 and the activation of the hexosamine pathway is abundant, it can decrease the insulin-mediated glucose transport through GLUT4 leading to insulin resistance. Glucose 129-136 insulin Homo sapiens 112-119 9801136-9 1998 If glucose entrance through GLUT1 and the activation of the hexosamine pathway is abundant, it can decrease the insulin-mediated glucose transport through GLUT4 leading to insulin resistance. Glucose 129-136 insulin Homo sapiens 172-179 9809695-0 1998 Insulin action and insulin resistance: diseases involving defects in insulin receptors, signal transduction, and the glucose transport effector system. Glucose 117-124 insulin Homo sapiens 0-7 9822197-1 1998 Day-to-day variations in diet and physical exercise, large variations in the glucose response to small changes in insulin doses, and high insulin sensitivity are characteristic of preschool children with diabetes. Glucose 77-84 insulin Homo sapiens 114-121 9809695-0 1998 Insulin action and insulin resistance: diseases involving defects in insulin receptors, signal transduction, and the glucose transport effector system. Glucose 117-124 insulin Homo sapiens 19-26 9800933-2 1998 DESIGN: Minimal model analysis of a frequently sampled intravenous glucose tolerance test to assess insulin sensitivity. Glucose 67-74 insulin Homo sapiens 100-107 9755083-3 1998 During the lipid infusion, plasma glucose and insulin levels were higher, showing some insulin resistance. Glucose 34-41 insulin Homo sapiens 87-94 9783646-0 1998 Enhanced insulin response to oral glucose load in patients with angina pectoris associated with ST segment elevation in the absence of epicardial coronary arterial obstruction. Glucose 34-41 insulin Homo sapiens 9-16 9783646-11 1998 Enhanced insulin response to oral glucose loading may also contribute to the pathogenesis of MVA. Glucose 34-41 insulin Homo sapiens 9-16 9773716-8 1998 The impact of hormone therapy on insulin and glucose depended on baseline levels of fasting insulin and 1-h glucose (P < 0.05). Glucose 45-52 insulin Homo sapiens 92-99 9753292-4 1998 Insulin-mediated glucose disposal (IMGD), nonoxidative glucose disposal (NOGD), oxidative glucose disposal (OGD) (indirect calorimetry), and splanchnic glucose output (SGO; beta3-[H3]glucose) were determined during a 100-min hyperinsulinemic-euglycemic glucose clamp (40 mU x m(-2) x min(-1)) before and after 4 and 8 weeks of treatment. Glucose 17-24 insulin Homo sapiens 0-7 9753293-2 1998 In this study, we further characterized the mechanisms by which oxidative stress impairs insulin stimulation of glucose transport activity. Glucose 112-119 insulin Homo sapiens 89-96 9753300-3 1998 NA treatment resulted in a fall in basal insulin concentrations of 35 and 45% and in the area under the insulin response curve (area under the curve [AUC]) to glucose of 47 and 42% in the 24- and 48-h fasted individuals, respectively. Glucose 159-166 insulin Homo sapiens 104-111 9753300-7 1998 The insulin AUC in response to glucose was unaffected by lowering of the FFA level in nonobese subjects, but fell by 29% in the obese group. Glucose 31-38 insulin Homo sapiens 4-11 9773721-7 1998 However, plasma glucose increased to 9.2+/-1.1 mmo/l after lispro insulin compared with 7.1+/-0.9 mmol/l after regular insulin (P < 0.01), and the rise in HGP was 5.7 +/-2.8 micromol x kg(-1) x min(-1) after lispro insulin versus 3.1+/-2.9 micromol x kg(-1) x min(-1) after regular insulin treatment (P=0.02). Glucose 16-23 insulin Homo sapiens 66-73 9773716-8 1998 The impact of hormone therapy on insulin and glucose depended on baseline levels of fasting insulin and 1-h glucose (P < 0.05). Glucose 108-115 insulin Homo sapiens 33-40 9796880-2 1998 MODY3 is characterized by a defective glucose-stimulated insulin secretion. Glucose 38-45 insulin Homo sapiens 57-64 9794097-6 1998 The difference in the acute insulin response persisted, even after adjustment for the 2-h plasma glucose concentration, insulin-mediated glucose uptake, the fasting plasma glucagon concentration and the growth hormone concentration (p < 0.05). Glucose 97-104 insulin Homo sapiens 28-35 9794097-6 1998 The difference in the acute insulin response persisted, even after adjustment for the 2-h plasma glucose concentration, insulin-mediated glucose uptake, the fasting plasma glucagon concentration and the growth hormone concentration (p < 0.05). Glucose 137-144 insulin Homo sapiens 28-35 9794097-6 1998 The difference in the acute insulin response persisted, even after adjustment for the 2-h plasma glucose concentration, insulin-mediated glucose uptake, the fasting plasma glucagon concentration and the growth hormone concentration (p < 0.05). Glucose 137-144 insulin Homo sapiens 120-127 9794097-8 1998 The acute insulin response (44 +/- 5.1 vs 71 +/- 5.3 mU/l, p < 0.01) and the insulin-mediated glucose uptake (27.4 +/- 0.4 vs 36.7 +/- 0.5 mumol/kg fat free mass per min, p < 0.003) were lower with acipimox plus intralipid treatment than with acipimox alone. Glucose 97-104 insulin Homo sapiens 80-87 9794097-9 1998 It is concluded that long term acipimox treatment lowers the plasma fasting free fatty acid concentration and improves the acute insulin response and the insulin mediated glucose uptake. Glucose 171-178 insulin Homo sapiens 154-161 9794098-0 1998 Glucose tolerance and resistance to insulin-stimulated glucose uptake in men aged 70 years in relation to size at birth. Glucose 55-62 insulin Homo sapiens 36-43 9794098-8 1998 These results confirm that the association between reduced fetal growth and glucose intolerance is mediated through insulin resistance and depends upon an interaction with obesity in adult life. Glucose 76-83 insulin Homo sapiens 116-123 9794102-4 1998 Oral glucose tolerance tests (OGTTs) were carried out on 152 subjects and inverse correlations were found between birth weight and the total amount of insulin secreted during the first 30 min (r = -0.19, p = 0.04) and last 90 min (r = -0.19, p = 0.04) of the oral glucose tolerance test and also between birth weight and the 30 min glucose concentrations (r = -0.20, p = 0.02). Glucose 5-12 insulin Homo sapiens 151-158 9794102-4 1998 Oral glucose tolerance tests (OGTTs) were carried out on 152 subjects and inverse correlations were found between birth weight and the total amount of insulin secreted during the first 30 min (r = -0.19, p = 0.04) and last 90 min (r = -0.19, p = 0.04) of the oral glucose tolerance test and also between birth weight and the 30 min glucose concentrations (r = -0.20, p = 0.02). Glucose 264-271 insulin Homo sapiens 151-158 9794102-4 1998 Oral glucose tolerance tests (OGTTs) were carried out on 152 subjects and inverse correlations were found between birth weight and the total amount of insulin secreted during the first 30 min (r = -0.19, p = 0.04) and last 90 min (r = -0.19, p = 0.04) of the oral glucose tolerance test and also between birth weight and the 30 min glucose concentrations (r = -0.20, p = 0.02). Glucose 264-271 insulin Homo sapiens 151-158 9751494-8 1998 In addition, we measured insulin-stimulated glucose transport in adipose cells cultured with conditioned medium from the transfected cells as well as in freshly isolated adipose cells treated with purified human alpha2-HSG. Glucose 44-51 insulin Homo sapiens 25-32 9774373-1 1998 Insulin-mediated vasodilation has been proposed as an important determinant of whole-body insulin-stimulated glucose disposal. Glucose 109-116 insulin Homo sapiens 0-7 9751501-2 1998 It plays an important role in insulin secretion from beta-cells and glucose metabolism in hepatocytes. Glucose 68-75 insulin Homo sapiens 30-37 9774373-1 1998 Insulin-mediated vasodilation has been proposed as an important determinant of whole-body insulin-stimulated glucose disposal. Glucose 109-116 insulin Homo sapiens 90-97 9760308-6 1998 Prior exercise resulted in greater cell surface GLUT-4 labeling in response to submaximal insulin treatment (5.36 +/- 0.45 dpm x 10(3)/g in exercised vs. 3.00 +/- 0.38 dpm x 10(3)/g in sedentary group; n = 10/group) that closely mirrored the increase in glucose transport activity. Glucose 254-261 insulin Homo sapiens 90-97 10186961-5 1998 Ratios were related to glucose responses after inhalation of insulin. Glucose 23-30 insulin Homo sapiens 61-68 10186961-10 1998 Linear regression analysis revealed that the maximum percentage of decrease in glucose after insulin inhalation was significantly related to the A:B ratio such that percentage decrease in glucose was greater in patients who demonstrated a lower A:B ratio (P = 0.003). Glucose 79-86 insulin Homo sapiens 93-100 10186961-10 1998 Linear regression analysis revealed that the maximum percentage of decrease in glucose after insulin inhalation was significantly related to the A:B ratio such that percentage decrease in glucose was greater in patients who demonstrated a lower A:B ratio (P = 0.003). Glucose 188-195 insulin Homo sapiens 93-100 9760308-8 1998 We conclude that the increase in muscle insulin sensitivity of glucose transport after exercise is due to translocation of more GLUT-4 to the cell surface and that this effect is not due to potentiation of insulin-stimulated tyrosine phosphorylation. Glucose 63-70 insulin Homo sapiens 40-47 10186961-12 1998 These results indicate that the bioavailability of nebulized insulin inhaled by mouth is approximately 20% when calculated in terms of drug deposited and suggest that increasing the distribution of insulin aerosol to the base of the lung enhances the glucose response in patients with NIDDM during the fasting state. Glucose 251-258 insulin Homo sapiens 61-68 10186961-12 1998 These results indicate that the bioavailability of nebulized insulin inhaled by mouth is approximately 20% when calculated in terms of drug deposited and suggest that increasing the distribution of insulin aerosol to the base of the lung enhances the glucose response in patients with NIDDM during the fasting state. Glucose 251-258 insulin Homo sapiens 198-205 9773947-6 1998 Low serum glucose was associated with low insulin levels and high levels of hormones (i.e., glucagon and IGF-II) that are functionally opposite to insulin. Glucose 10-17 insulin Homo sapiens 42-49 9768653-7 1998 Consequently, we conclude that 6-fold differences in plasma insulin responses to glucose do not predict weight gain in a healthy, nonobese population. Glucose 81-88 insulin Homo sapiens 60-67 9773947-6 1998 Low serum glucose was associated with low insulin levels and high levels of hormones (i.e., glucagon and IGF-II) that are functionally opposite to insulin. Glucose 10-17 insulin Homo sapiens 147-154 9856413-5 1998 Conversely, major increases in androgen levels may induce muscular changes leading to reduced insulin-mediated glucose uptake. Glucose 111-118 insulin Homo sapiens 94-101 9814618-10 1998 Furthermore, the insulin response to an oral glucose load was significantly related to both plasma angiotensinogen (r=0.22, P< 0.05) and plasma leptin (r=0.47, P< 0.001). Glucose 45-52 insulin Homo sapiens 17-24 9781617-5 1998 The results show a consistent relationship between insulin-mediated glucose disposal and dyslipidemia in African American, Hispanic, and non-Hispanic white men and women. Glucose 68-75 insulin Homo sapiens 51-58 9776793-5 1998 The improvement in glucose tolerance involves the insulin sensitivity of endogenous glucose production, glucose oxidative disposal, and its nonoxidative disposal. Glucose 19-26 insulin Homo sapiens 50-57 9776793-5 1998 The improvement in glucose tolerance involves the insulin sensitivity of endogenous glucose production, glucose oxidative disposal, and its nonoxidative disposal. Glucose 84-91 insulin Homo sapiens 50-57 9781619-9 1998 Furthermore, fasting insulin and the insulin to glucose ratio correlated positively and high-density lipoprotein (HDL) cholesterol correlated negatively with BMI, WHR, and D in the total study population and in the subgroups. Glucose 48-55 insulin Homo sapiens 37-44 9781629-4 1998 Insulin-stimulated glucose uptake in isolated subcutaneous and omental adipocytes obtained during elective surgery was measured in 61 premenopausal women, 24 with a parental history (PH) of CHD. Glucose 19-26 insulin Homo sapiens 0-7 9781629-7 1998 On the habitual diet, in vitro insulin-stimulated glucose uptake in adipocytes as a percentage increase over basal was less in women with PH-CHD than in those without it (presented as the median with 95% confidence limits: subcutaneous, 28% (17% to 39%) v 96% (70% to 120%), P < .01); omental, 40% (28% to 52%) v 113% (83% to 143%), P < .01). Glucose 50-57 insulin Homo sapiens 31-38 9774494-2 1998 In the 1.0-10-microM range, this agent augmented, in a concentration-related manner, the release of insulin from islets incubated at intermediate concentrations of d-glucose (4.0-7.0 mm), this enhancing action fading out at both lower a nd higher d-glucose levels. Glucose 164-173 insulin Homo sapiens 100-107 9787110-4 1998 PDK2 and PDK4 mRNAs were positively correlated with fasting plasma insulin concentration, 2-h plasma insulin concentration in response to oral glucose, and percentage body fat, whereas both isoforms were negatively correlated with insulin-mediated glucose uptake rates. Glucose 143-150 insulin Homo sapiens 101-108 9787110-4 1998 PDK2 and PDK4 mRNAs were positively correlated with fasting plasma insulin concentration, 2-h plasma insulin concentration in response to oral glucose, and percentage body fat, whereas both isoforms were negatively correlated with insulin-mediated glucose uptake rates. Glucose 143-150 insulin Homo sapiens 101-108 9774494-2 1998 In the 1.0-10-microM range, this agent augmented, in a concentration-related manner, the release of insulin from islets incubated at intermediate concentrations of d-glucose (4.0-7.0 mm), this enhancing action fading out at both lower a nd higher d-glucose levels. Glucose 247-256 insulin Homo sapiens 100-107 9774494-3 1998 When the concentration of RX 871024 was raised to 1.0 mm, severe inhibition of glucose-stimulated insulin output was observed. Glucose 79-86 insulin Homo sapiens 98-105 9751707-0 1998 A novel glucose-responsive element in the human insulin gene functions uniquely in primary cultured islets. Glucose 8-15 insulin Homo sapiens 48-55 9738018-9 1998 Insulin-stimulated glucose transport was unaffected by any construct. Glucose 19-26 insulin Homo sapiens 0-7 9778431-6 1998 This allows us to explain why patients with untreated Type I diabetes mellitus have high blood glucose levels even under conditions of low glucose input, and why it is difficult to maintain the normal level of 5 mmol/1 in patients who are being treated with insulin. Glucose 95-102 insulin Homo sapiens 258-265 9778431-6 1998 This allows us to explain why patients with untreated Type I diabetes mellitus have high blood glucose levels even under conditions of low glucose input, and why it is difficult to maintain the normal level of 5 mmol/1 in patients who are being treated with insulin. Glucose 139-146 insulin Homo sapiens 258-265 9753008-6 1998 The odds of high (> or =30.0 mU/liter) fasting insulin levels in subjects with impaired glucose tolerance were 6.9 (95% CI 0.6-74.2) and 21.0 (95% CI 2.1-206.4) for short and long durations of obesity, respectively. Glucose 91-98 insulin Homo sapiens 50-57 9753619-7 1998 In a transgenic rescue experiment, using an insulin-promoter human-IAPP fusion gene, insulin responses and blood glucose elimination were reversed in IAPP-deficient males, whereas the female phenotype appeared unaffected. Glucose 113-120 insulin Homo sapiens 44-51 9734735-5 1998 Intraduodenal glucose infusion resulted in a further increase in plasma insulin to a peak of 779.4 +/- 114.0 pmol/L, caused an early increase in plasma GIP and a later increase in GLP-1 concentrations (P < 0.01), suppressed appetite (P < 0.05), and reduced energy intake (P < 0.01) compared with intraduodenal infusion of saline. Glucose 14-21 insulin Homo sapiens 72-79 9730851-7 1998 The desired blood glucose level was approached after approximately 60 min of insulin infusion. Glucose 18-25 insulin Homo sapiens 77-84 9972287-2 1998 Glucose, mannose, fructose, glyceraldehyde and dihydroxyacetone all at 8 mM, significantly enhanced the release of insulin elicited by basal concentrations of these carbohydrates (2 mM). Glucose 0-7 insulin Homo sapiens 115-122 9972287-6 1998 At 8 mM, the D-glucose alpha-anomer significantly increased insulin release, while this effect was not observed using the beta-anomer. Glucose 13-22 insulin Homo sapiens 60-67 10205355-1 1998 The Diabetes Control and Complications Trial (DCCT) ended decades of controversy regarding the necessity of tight glycemic control for type 1 diabetes by demonstrating that glucose control using intensive insulin therapy significantly reduced long-term microvascular complications. Glucose 173-180 insulin Homo sapiens 205-212 9726235-7 1998 Insulin-stimulated glucose utilization and oxidation measured during the hyperinsulinemic clamp (at approximately 200 pmol/l insulin) were identical in MODY3 patients and in healthy control subjects, indicating that peripheral insulin sensitivity was not altered. Glucose 19-26 insulin Homo sapiens 0-7 9726246-5 1998 In the NIDDM patients, a positive correlation between UCP-3 expression and whole-body insulin-mediated glucose utilization rate was also noted. Glucose 103-110 insulin Homo sapiens 86-93 9727891-5 1998 Insulin dose was reduced 25% based on a study-specific algorithm whenever fasting blood glucose was reduced 5% from baseline. Glucose 88-95 insulin Homo sapiens 0-7 9727896-7 1998 Total glucose disposal at euglycemic-hyperinsulinemic clamp increased significantly in the metformin group by 25% at high insulin level (259 +/- 31 vs. 207 +/- 21 mg x m(-2) x min(-1), P < 0.05). Glucose 6-13 insulin Homo sapiens 42-49 9754815-0 1998 The direct and indirect effects of insulin on hepatic glucose production in vivo. Glucose 54-61 insulin Homo sapiens 35-42 9754821-0 1998 Assessment of insulin sensitivity and secretion with the labelled intravenous glucose tolerance test: improved modelling analysis. Glucose 78-85 insulin Homo sapiens 14-21 9754821-7 1998 Glucose clearance was assumed to depend linearly on plasma insulin concentration delayed. Glucose 0-7 insulin Homo sapiens 59-66 9805407-9 1998 The three intravenous insulin infusion regimens produced similar control of arterial whole blood glucose concentrations. Glucose 97-104 insulin Homo sapiens 22-29 9805407-10 1998 Patients with high initial glucose concentrations (greater than 400 mg/dL) (22.2 mmol/L) required intravenous insulin therapy for ten or more hours before attaining the target range of 151-250 mg/dL (8.3-13.9 mmol/L). Glucose 27-34 insulin Homo sapiens 110-117 9805407-11 1998 CONCLUSIONS: Constant-rate intravenous insulin therapy is effective in lowering arterial whole blood glucose concentrations in postoperative coronary artery bypass graft patients. Glucose 101-108 insulin Homo sapiens 39-46 9805407-12 1998 Initiation of intravenous insulin therapy at lower glucose values reduces the time necessary for the infusion. Glucose 51-58 insulin Homo sapiens 26-33 9777320-12 1998 Thus, in obesity, higher insulin levels are necessary to maintain glucose tolerance, leading to increased stress on the beta-cells. Glucose 66-73 insulin Homo sapiens 25-32 9735562-1 1998 A neural predictive controller for closed-loop control of glucose using subcutaneous (s.c.) tissue glucose measurement and s.c. infusion of monomeric insulin analogs was developed and evaluated in a simulation study. Glucose 58-65 insulin Homo sapiens 150-157 9756248-17 1998 Both groups sustained a reduction in the insulin to glucose (I/G) ratio and systolic and diastolic blood pressure for three months after medication was ceased, while those on d-fen initially also maintained a reduction in total and LDL cholesterol. Glucose 52-59 insulin Homo sapiens 41-48 9855697-1 1998 Skeletal muscle is a major glucose-utilizing tissue in the absorptive state and alterations in muscle insulin-stimulated glucose uptake lead to derangements in whole body glucose disposal. Glucose 121-128 insulin Homo sapiens 102-109 9855697-1 1998 Skeletal muscle is a major glucose-utilizing tissue in the absorptive state and alterations in muscle insulin-stimulated glucose uptake lead to derangements in whole body glucose disposal. Glucose 121-128 insulin Homo sapiens 102-109 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9746115-4 1998 Using dynamic assessment by the minimal model approach with the modified frequent sampling intravenous glucose tolerance test (FSIGT) the following and other parameters were measured: insulin sensitivity; acute insulin response to glucose (AIR(G)) calculated as the average of the three peak values between 2 and 5 min after injection of glucose from which the basal insulin levels were subtracted; the initial area under the curve (AUC(1-19)) from insulin values between time 0 and 19 min and the first-phase insulin secretion (phi1) from insulin kinetics parameters. Glucose 231-238 insulin Homo sapiens 211-218 9731791-13 1998 Intracellular adenosine triphosphate was improved by 75% in cells exposed to high glucose concentrations in the presence of insulin. Glucose 82-89 insulin Homo sapiens 124-131 9710629-3 1998 In the present series of studies, the short-chain ceramide analog C2-ceramide inhibited insulin-stimulated glucose transport by approximately 50% in 3T3-L1 adipocytes, with similar reductions in hormone-stimulated translocation of the insulin-responsive glucose transporter (GLUT4) and insulin-responsive aminopeptidase. Glucose 107-114 insulin Homo sapiens 88-95 9758309-1 1998 Insulin resistance is characterized by impaired responsiveness to endogenous or exogenous insulin and often results in the insulin resistance syndrome, a clustering of cardiovascular risk factors that includes abdominal obesity, hypertension, dyslipidemia, glucose intolerance, and hyperinsulinemia. Glucose 257-264 insulin Homo sapiens 0-7 9758309-1 1998 Insulin resistance is characterized by impaired responsiveness to endogenous or exogenous insulin and often results in the insulin resistance syndrome, a clustering of cardiovascular risk factors that includes abdominal obesity, hypertension, dyslipidemia, glucose intolerance, and hyperinsulinemia. Glucose 257-264 insulin Homo sapiens 90-97 9758309-2 1998 Although the mechanism responsible for insulin resistance has not been completely defined, it is likely due to defective insulin receptor signaling and results in decreased use of glucose. Glucose 180-187 insulin Homo sapiens 39-46 9758309-2 1998 Although the mechanism responsible for insulin resistance has not been completely defined, it is likely due to defective insulin receptor signaling and results in decreased use of glucose. Glucose 180-187 insulin Homo sapiens 121-128 9758309-3 1998 Troglitazone, the first in a new class of drugs, directly decreases insulin resistance by improving insulin-mediated glucose disposal and reduces plasma insulin concentrations. Glucose 117-124 insulin Homo sapiens 68-75 9758309-3 1998 Troglitazone, the first in a new class of drugs, directly decreases insulin resistance by improving insulin-mediated glucose disposal and reduces plasma insulin concentrations. Glucose 117-124 insulin Homo sapiens 100-107 9758309-3 1998 Troglitazone, the first in a new class of drugs, directly decreases insulin resistance by improving insulin-mediated glucose disposal and reduces plasma insulin concentrations. Glucose 117-124 insulin Homo sapiens 100-107 9949668-11 1998 Only glucose decreased in the insulin subgroup. Glucose 5-12 insulin Homo sapiens 30-37 9731609-5 1998 Area under the insulin response curve during oral glucose tolerance test was used as a composite variable reflecting plasma insulin levels. Glucose 50-57 insulin Homo sapiens 15-22 9731609-5 1998 Area under the insulin response curve during oral glucose tolerance test was used as a composite variable reflecting plasma insulin levels. Glucose 50-57 insulin Homo sapiens 124-131 9861371-6 1998 This might reflect increased non-insulin-mediated glucose uptake in falciparum malaria and/or impaired gluconeogenesis in enteric fever, and may have implications for metabolic complications and their clinical management in both infections. Glucose 50-57 insulin Homo sapiens 33-40 9921039-4 1998 This 24-h variation is due to coordinated changes in insulin-dependent and non-insulin dependent glucose utilization (e.g. by the brain), in insulin sensitivity and in insulin secretion. Glucose 97-104 insulin Homo sapiens 53-60 9921039-4 1998 This 24-h variation is due to coordinated changes in insulin-dependent and non-insulin dependent glucose utilization (e.g. by the brain), in insulin sensitivity and in insulin secretion. Glucose 97-104 insulin Homo sapiens 79-86 9921039-4 1998 This 24-h variation is due to coordinated changes in insulin-dependent and non-insulin dependent glucose utilization (e.g. by the brain), in insulin sensitivity and in insulin secretion. Glucose 97-104 insulin Homo sapiens 79-86 9764732-0 1998 Modulation of LDL particle size after an oral glucose load is associated with insulin levels. Glucose 46-53 insulin Homo sapiens 78-85 9764732-8 1998 These results suggest that plasma insulin levels during glucose load modulate LDL particle size. Glucose 56-63 insulin Homo sapiens 34-41 9710443-3 1998 Overnight low-dose insulin was used to normalize the plasma glucose levels in DM2 before initiation of the study protocol. Glucose 60-67 insulin Homo sapiens 19-26 9685425-1 1998 Glucosamine, which enters the hexosamine pathway downstream of the rate-limiting step, has been routinely used to mimic the insulin resistance caused by high glucose and insulin. Glucose 158-165 insulin Homo sapiens 124-131 9685425-2 1998 We investigated the effect of glucosamine on insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 64-71 insulin Homo sapiens 45-52 9689076-0 1998 Short-term regulation of insulin gene transcription by glucose. Glucose 55-62 insulin Homo sapiens 25-32 9689076-3 1998 By studying the dynamics of newly synthesized (prepro)insulin RNA and by employing on-line monitoring of gene expression in single, insulin-producing cells, we were able to provide convincing evidence that insulin gene transcription indeed is affected by glucose within minutes. Glucose 255-262 insulin Homo sapiens 54-61 9689076-3 1998 By studying the dynamics of newly synthesized (prepro)insulin RNA and by employing on-line monitoring of gene expression in single, insulin-producing cells, we were able to provide convincing evidence that insulin gene transcription indeed is affected by glucose within minutes. Glucose 255-262 insulin Homo sapiens 132-139 9689076-3 1998 By studying the dynamics of newly synthesized (prepro)insulin RNA and by employing on-line monitoring of gene expression in single, insulin-producing cells, we were able to provide convincing evidence that insulin gene transcription indeed is affected by glucose within minutes. Glucose 255-262 insulin Homo sapiens 132-139 9689076-4 1998 Exposure of insulinoma cells and isolated pancreatic islets to elevated glucose for only 15 min resulted in a 2- to 5-fold elevation in (prepro)insulin mRNA levels within 60-90 min. Glucose 72-79 insulin Homo sapiens 12-19 9689076-5 1998 Similarly, insulin promoter-driven green fluorescent protein expression in single insulin-producing cells was significantly enhanced after transient glucose stimulation. Glucose 149-156 insulin Homo sapiens 11-18 9689076-5 1998 Similarly, insulin promoter-driven green fluorescent protein expression in single insulin-producing cells was significantly enhanced after transient glucose stimulation. Glucose 149-156 insulin Homo sapiens 82-89 9736233-1 1998 Maturity-onset diabetes of the young (MODY) is a form of diabetes mellitus characterized by autosomal dominant inheritance, onset usually before 25 y of age and a primary defect in glucose-stimulated insulin secretion. Glucose 181-188 insulin Homo sapiens 200-207 9789584-5 1998 Assuming unchanged rate constant for loss of labelled CO2 at normo- and hyperglycaemia the oxidative metabolic rate of glucose was found to be slightly larger at combined hyperglycaemia and hypersulinemia (0.30 +/- 0.01 mmol mL-1 min-1) than at normal glucose and insulin levels (0.25 +/- 0.01 mmol mL-1 min-1). Glucose 119-126 insulin Homo sapiens 264-271 9701199-0 1998 The SstI polymorphism of the apolipoprotein C-III gene determines the insulin response to an oral-glucose-tolerance test after consumption of a diet rich in saturated fats. Glucose 98-105 insulin Homo sapiens 70-77 9715789-3 1998 Insulin sensitivity was calculated using the M value from the infusion rate of glucose with hyperinsulinemia using the glucose clamp method. Glucose 79-86 insulin Homo sapiens 0-7 9715789-3 1998 Insulin sensitivity was calculated using the M value from the infusion rate of glucose with hyperinsulinemia using the glucose clamp method. Glucose 119-126 insulin Homo sapiens 0-7 9688638-1 1998 Decreased insulin-mediated muscle glucose uptake is a characteristic feature of non-insulin-dependent diabetes mellitus and other insulin-resistant states. Glucose 34-41 insulin Homo sapiens 10-17 9688638-1 1998 Decreased insulin-mediated muscle glucose uptake is a characteristic feature of non-insulin-dependent diabetes mellitus and other insulin-resistant states. Glucose 34-41 insulin Homo sapiens 84-91 9688638-2 1998 It has been suggested that an impairment in the ability of insulin to augment limb blood flow, resulting in diminished glucose delivery to muscle, may contribute to this abnormality. Glucose 119-126 insulin Homo sapiens 59-66 9716418-1 1998 Skeletal muscle is the major tissue responsible for insulin-stimulated glucose uptake and incorporation into glycogen. Glucose 71-78 insulin Homo sapiens 52-59 9716418-7 1998 Both insulin and the insulin-mimetic compound pervanadate activate L6 cell glucose incorporation in dose-responsive manners. Glucose 75-82 insulin Homo sapiens 5-12 9716418-7 1998 Both insulin and the insulin-mimetic compound pervanadate activate L6 cell glucose incorporation in dose-responsive manners. Glucose 75-82 insulin Homo sapiens 21-28 9780420-3 1998 In the isolated adipocytes we studied the interaction of insulin with its receptor and the glucose transport. Glucose 91-98 insulin Homo sapiens 57-64 9677303-3 1998 It is now apparent that the activation of class 1a phosphoinositide 3-kinase (PI 3-kinase) is necessary and in some cases sufficient to elicit many of insulin"s effects on glucose and lipid metabolism. Glucose 172-179 insulin Homo sapiens 151-158 9714125-2 1998 TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. Glucose 38-45 insulin Homo sapiens 20-27 9714125-2 1998 TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. Glucose 38-45 insulin Homo sapiens 94-101 9714125-2 1998 TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. Glucose 38-45 insulin Homo sapiens 94-101 9780839-2 1998 Its main action is to stimulate insulin secretion through potentiating the insulinotropic action of glucose. Glucose 100-107 insulin Homo sapiens 32-39 9725782-7 1998 (2) After treatment with benazepril for ten weeks, the blood glucose and serum insulin concentrations after glucose load and AUCG, AUCINS values in the uremic patients were significantly lower than before treatment, but were still significantly higher than in the controls. Glucose 108-115 insulin Homo sapiens 79-86 9702429-7 1998 Insulin-modified frequently sampled intravenous glucose tolerance (FSIGT) test was performed in each subject. Glucose 48-55 insulin Homo sapiens 0-7 9702429-18 1998 Mean glucose effectiveness at zero insulin concentrations (GEZI) was significantly lower in the HGDM subjects when compared with the NHGDM and healthy control subjects. Glucose 5-12 insulin Homo sapiens 35-42 9703329-1 1998 The serine/threonine kinase Akt (PKB/Rac) has been implicated as playing a role in the insulin-signaling pathway to glucose transport. Glucose 116-123 insulin Homo sapiens 87-94 9703329-4 1998 Whole-body insulin sensitivity, assessed by the euglycemic-hyperinsulinemic clamp, was significantly lower in NIDDM subjects (P < 0.001), and this was accompanied by impaired in vitro insulin-stimulated glucose transport in skeletal muscle. Glucose 206-213 insulin Homo sapiens 11-18 9703329-8 1998 These parallel defects in insulin-stimulated Akt kinase activity and glucose transport in diabetic skeletal muscle suggest that reduced Akt kinase activity may play a role in the development of insulin resistance in NIDDM. Glucose 69-76 insulin Homo sapiens 194-201 9703331-8 1998 The present study shows that microdialysis is a useful tool to obtain tissue-specific information about the effect of insulin on blood flow and glucose extraction in human skeletal muscle and adipose tissue. Glucose 144-151 insulin Homo sapiens 118-125 9703338-5 1998 Insulin-mediated glucose disposal was not affected by sodium dietary content, but it was lower in microalbuminuric (P < 0.05) than in normoalbuminuric IDDM patients. Glucose 17-24 insulin Homo sapiens 0-7 9704223-4 1998 Insulin secretion during an oral glucose tolerance test (OGTT) or a meal is substantially increased in women with GDM compared with the same women postpartum. Glucose 33-40 insulin Homo sapiens 0-7 9704223-6 1998 Peak insulin concentrations during an OGTT occur later in women with GDM, and following intravenous glucose, a reduced first-phase insulin response is also seen in these women. Glucose 100-107 insulin Homo sapiens 131-138 9704234-7 1998 Obese women or those with fasting plasma glucose > 95 mg/dl on the OGTT should be referred to insulin therapy in order to minimize exposure of the fetus to a hyperglycemic environment. Glucose 41-48 insulin Homo sapiens 97-104 9681494-7 1998 Both peptides produced concentration-dependent increases in insulin release from glucose-responsive rat insulinoma-derived BRIN-BD11 cells. Glucose 81-88 insulin Homo sapiens 60-67 9715376-19 1998 In fact, subtle defects in the beta-cell response to glucose may be widespread in the population (108, 125) and only cause frank hyperglycemia when obesity/insulin resistance stress the secretory machinery. Glucose 53-60 insulin Homo sapiens 156-163 9756275-5 1998 Clinically the anovulatory women differed from the ovulating in two aspects: more profound essential fatty acid deficiency (EFAD) and higher peak/basal insulin response during an oral glucose tolerance test. Glucose 184-191 insulin Homo sapiens 152-159 9709933-5 1998 glucose tolerance test (FSIGT) to assess whether there is a simple screening test for insulin resistance in PCOS. Glucose 0-7 insulin Homo sapiens 86-93 9709933-7 1998 The insulin sensitivity index (S(I)) was calculated by application of the minimal model of glucose kinetics to the dynamics of plasma glucose and insulin levels during the FSIGT. Glucose 91-98 insulin Homo sapiens 4-11 9709933-7 1998 The insulin sensitivity index (S(I)) was calculated by application of the minimal model of glucose kinetics to the dynamics of plasma glucose and insulin levels during the FSIGT. Glucose 134-141 insulin Homo sapiens 4-11 9709967-2 1998 We have undertaken this study to investigate whether serum TNFalpha concentrations are elevated in obese subjects, whether they fall after weight loss, and whether this fall parallels the fall in insulin release after glucose challenge. Glucose 218-225 insulin Homo sapiens 196-203 9709967-6 1998 The magnitude of insulin release after glucose (75 g) challenge (area under the curve) also fell significantly (P < 0.01) after weight loss. Glucose 39-46 insulin Homo sapiens 17-24 9709971-2 1998 An important mechanism underlying the glucose intolerance of aging is an impairment in glucose-induced insulin release. Glucose 38-45 insulin Homo sapiens 103-110 9709971-2 1998 An important mechanism underlying the glucose intolerance of aging is an impairment in glucose-induced insulin release. Glucose 87-94 insulin Homo sapiens 103-110 9709971-12 1998 In response to the GIP infusions, significant increases in insulin occurred in young and old at both glucose levels (P < 0.01). Glucose 101-108 insulin Homo sapiens 59-66 9709971-16 1998 We conclude that normal aging is characterized by a decreased beta-cell sensitivity to GIP during modest hyperglycemia, which may explain, in part, the age-related impairment in glucose-induced insulin release. Glucose 178-185 insulin Homo sapiens 194-201 9747063-5 1998 Insulin resistance was evaluated by two methods: the total area under the curve (AUC) and the incremental AUC of serum insulin concentrations in response to a 75-g oral glucose load, and the insulin suppression test. Glucose 169-176 insulin Homo sapiens 0-7 9711989-1 1998 Insulin resistance in polycystic ovary syndrome (PCOS) is characterized by a novel defect in insulin signal transduction expressed in isolated human adipocytes as impaired insulin sensitivity for glucose transport and antilipolysis. Glucose 196-203 insulin Homo sapiens 0-7 9711989-1 1998 Insulin resistance in polycystic ovary syndrome (PCOS) is characterized by a novel defect in insulin signal transduction expressed in isolated human adipocytes as impaired insulin sensitivity for glucose transport and antilipolysis. Glucose 196-203 insulin Homo sapiens 93-100 9711989-5 1998 Fibroblasts from NC (4.9- +/- 0.5-fold stimulation) and PCOS (4.6- +/- 0.3-fold) subjects were equally responsive to insulin for stimulation of glucose incorporation into glycogen. Glucose 144-151 insulin Homo sapiens 117-124 9664081-3 1998 Insulin secretion from pancreatic islets by glucose is significantly inhibited by the addition of the NIDDM sera with anti-CD38 antibodies (P </= 0.04-0.0001), and the inhibition of insulin secretion is abolished by the addition of recombinant CD38 (P </= 0.02). Glucose 44-51 insulin Homo sapiens 0-7 9675108-0 1998 Effect of high glucose concentration on proinsulin biosynthesis and conversion by human islets. Glucose 15-22 insulin Homo sapiens 40-50 9675108-1 1998 In the present study we investigate whether glucose concentration could have an effect on proinsulin biosynthesis and processing. Glucose 44-51 insulin Homo sapiens 90-100 9675108-5 1998 We have found an accelerated rate of proinsulin conversion by those islets exposed to high glucose concentration (at 24.4 mM of glucose), but not by those islets cultured at low glucose concentration (at 5.5 mM of glucose). Glucose 91-98 insulin Homo sapiens 37-47 9675108-5 1998 We have found an accelerated rate of proinsulin conversion by those islets exposed to high glucose concentration (at 24.4 mM of glucose), but not by those islets cultured at low glucose concentration (at 5.5 mM of glucose). Glucose 128-135 insulin Homo sapiens 37-47 9675108-5 1998 We have found an accelerated rate of proinsulin conversion by those islets exposed to high glucose concentration (at 24.4 mM of glucose), but not by those islets cultured at low glucose concentration (at 5.5 mM of glucose). Glucose 128-135 insulin Homo sapiens 37-47 9675108-5 1998 We have found an accelerated rate of proinsulin conversion by those islets exposed to high glucose concentration (at 24.4 mM of glucose), but not by those islets cultured at low glucose concentration (at 5.5 mM of glucose). Glucose 128-135 insulin Homo sapiens 37-47 9665229-5 1998 Nevertheless, compared with individuals with homozygotes T174, subjects with heterozygotes T174M were associated with greater glucose and insulin response to the oral glucose tolerance test and insulin resistance indicated by higher steady state plasma glucose concentrations in patients with CHD (14.7+/-0.9 vs 11.3+/-0.7 mmol/L, p < 0.04). Glucose 167-174 insulin Homo sapiens 138-145 9665229-5 1998 Nevertheless, compared with individuals with homozygotes T174, subjects with heterozygotes T174M were associated with greater glucose and insulin response to the oral glucose tolerance test and insulin resistance indicated by higher steady state plasma glucose concentrations in patients with CHD (14.7+/-0.9 vs 11.3+/-0.7 mmol/L, p < 0.04). Glucose 167-174 insulin Homo sapiens 138-145 9688885-0 1998 Perioperative insulin and glucose infusion maintains normal insulin sensitivity after surgery. Glucose 26-33 insulin Homo sapiens 60-67 9688885-8 1998 We conclude that perioperative insulin and glucose infusions minimize the endocrine stress response and normalize postoperative insulin sensitivity and substrate utilization. Glucose 43-50 insulin Homo sapiens 128-135 9688888-0 1998 Role of free fatty acids and glucagon in the peripheral effect of insulin on glucose production in humans. Glucose 77-84 insulin Homo sapiens 66-73 9688888-1 1998 We have shown previously that the greater suppression of endogenous glucose production (GP) with equimolar peripheral vs. portal insulin cannot be detected or is minimally reversed when the insulin-induced suppression of either free fatty acids (FFA) or glucagon alone is prevented. Glucose 68-75 insulin Homo sapiens 129-136 9688888-1 1998 We have shown previously that the greater suppression of endogenous glucose production (GP) with equimolar peripheral vs. portal insulin cannot be detected or is minimally reversed when the insulin-induced suppression of either free fatty acids (FFA) or glucagon alone is prevented. Glucose 68-75 insulin Homo sapiens 190-197 9754276-5 1998 The two most widely used methods for quantifying insulin sensitivity are the euglycaemic hyperinsulinaemic clamp and the intravenous glucose tolerance test with minimal model analysis. Glucose 133-140 insulin Homo sapiens 49-56 9663332-6 1998 To investigate this lack of effect, we examined whether transfection of GLUT2 cDNA, which is ordinarily not expressed in CHO-INS cells, would confer glucose-stimulated insulin secretion. Glucose 149-156 insulin Homo sapiens 168-175 9663332-7 1998 Consequently, we have demonstrated that glucose regulated insulin release occurs in the CHO-INS-GLUT2 cell line and that glucose potentiates the insulin secretory response to non-glucose secretagogues. Glucose 40-47 insulin Homo sapiens 58-65 9663332-7 1998 Consequently, we have demonstrated that glucose regulated insulin release occurs in the CHO-INS-GLUT2 cell line and that glucose potentiates the insulin secretory response to non-glucose secretagogues. Glucose 121-128 insulin Homo sapiens 145-152 9663332-7 1998 Consequently, we have demonstrated that glucose regulated insulin release occurs in the CHO-INS-GLUT2 cell line and that glucose potentiates the insulin secretory response to non-glucose secretagogues. Glucose 121-128 insulin Homo sapiens 145-152 9672061-0 1998 Abdominal obesity, impaired nonesterified fatty acid suppression, and insulin-mediated glucose disposal are early metabolic abnormalities in families with premature myocardial infarction. Glucose 87-94 insulin Homo sapiens 70-77 9692417-6 1998 Insulin resistance was measured by the glucose infusion rate required to maintain the plasma glucose at 4.5 mmol/l. Glucose 39-46 insulin Homo sapiens 0-7 9692417-6 1998 Insulin resistance was measured by the glucose infusion rate required to maintain the plasma glucose at 4.5 mmol/l. Glucose 93-100 insulin Homo sapiens 0-7 9710309-10 1998 Glucose stimulation during in vitro incubation induced significant insulin release from isolated breeder porcine islets. Glucose 0-7 insulin Homo sapiens 67-74 9741674-3 1998 Insulin sensitivity was assessed with the minimal model procedure, over a 180 min intravenous glucose tolerance test with iterative sampling. Glucose 94-101 insulin Homo sapiens 0-7 9741674-5 1998 The insulin sensitivity index SI (i.e., the slope of the dose-response relationship between insulin increased above baseline and glucose disposal) ranged from 0.0009 to 16 x 10(-4) min(-1)/(microU/ml), with a mean value of 4.76+/-0.73 x 10(-4). Glucose 129-136 insulin Homo sapiens 4-11 9797852-12 1998 The subgroup of women without PCO or NIDDM had the highest insulin sensitivity (189.1 +/- 46.4 mumol glucose/l/min, mean +/- SD) and the women with both PCO and NIDDM had the lowest insulin sensitivity (80.5 +/- 30.9 mumol glucose/l/min). Glucose 101-108 insulin Homo sapiens 59-66 9797852-14 1998 The effects of NIDDM and PCO on insulin sensitivity were independent; the effect of PCO on insulin sensitivity was -60 mumol glucose/l/min (95% confidence interval -100 to -21, P = 0.004) and the effect of NIDDM was -68 mumol glucose/l/min (95% confidence interval -105 to -31, P < 0.001). Glucose 125-132 insulin Homo sapiens 91-98 9648821-1 1998 Phosphatidylinositol 3-kinase (PI 3-kinase) has been implicated in the regulation of numerous cellular processes, including the insulin-induced regulation of glycogen synthase kinase 3 (GSK-3) and glucose transport. Glucose 197-204 insulin Homo sapiens 128-135 9648821-5 1998 Both wtPKBalpha and mPKBalpha expression led to a significant increase in the basal uptake of glucose and methyl-aminoisobutyric acid (a substrate for the system A amino acid transporter), at least to a level seen in control cells treated with insulin. Glucose 94-101 insulin Homo sapiens 244-251 9648835-1 1998 Impaired muscle glucose phosphorylation to glucose-6-phosphate by hexokinases (HKs)-I and -II may contribute to insulin resistance in NIDDM and obesity. Glucose 16-23 insulin Homo sapiens 112-119 9653592-6 1998 A 5-h intermediate attempt with human regular insulin in CSII, however, increased blood glucose concentrations from 6.0 to 28.8 mmol/l, despite identical basal rates and additional injection of 16 U of human regular insulin. Glucose 88-95 insulin Homo sapiens 46-53 9653608-0 1998 Usefulness of revised fasting plasma glucose criterion and characteristics of the insulin response to an oral glucose load in newly diagnosed Japanese diabetic subjects. Glucose 110-117 insulin Homo sapiens 82-89 9653613-11 1998 CONCLUSIONS: With lower mealtime and higher basal bedtime insulin doses, patients using insulin lispro may be able to gain an overall improvement in evening blood glucose control without deteriorated nighttime glucose levels. Glucose 163-170 insulin Homo sapiens 88-95 9768373-0 1998 The effect of low intensity bicycle exercise on the insulin-induced glucose uptake in obese patients with type 2 diabetes. Glucose 68-75 insulin Homo sapiens 52-59 9768373-1 1998 OBJECTIVE: The present study was undertaken to reveal the effect of low intensity bicycle exercise on the insulin-induced glucose uptake in obese patients. Glucose 122-129 insulin Homo sapiens 106-113 9768373-8 1998 CONCLUSION: These results indicated that in obese Type 2 diabetes, 30 min of low intensity bicycle exercise significantly enhances the lower level of insulin-induced glucose uptake shortly after exercise and might be useful for the treatment of post-prandial hyperglycemia. Glucose 166-173 insulin Homo sapiens 150-157 15251737-3 1998 RESULTS: Although the precise mode of action of troglitazone, a thiazolidinedione, is unknown, this agent is an insulin sensitizer that has been shown to decrease fasting insulin, fasting plasma glucose, and blood pressure levels in humans. Glucose 195-202 insulin Homo sapiens 112-119 9726033-5 1998 RESULTS: Patients with CAD who had increased serum insulin or C-peptide (fasting and after glucose load) were predominantly heterozygous for TNF-beta (72% vs. 47%) and less frequently homozygous for TNF-beta *2 (22% vs. 43%, P = 0 x 0.03). Glucose 91-98 insulin Homo sapiens 51-58 9726033-5 1998 RESULTS: Patients with CAD who had increased serum insulin or C-peptide (fasting and after glucose load) were predominantly heterozygous for TNF-beta (72% vs. 47%) and less frequently homozygous for TNF-beta *2 (22% vs. 43%, P = 0 x 0.03). Glucose 91-98 insulin Homo sapiens 62-71 9657106-5 1998 During the baseline (pre-octreotide) study, patients demonstrated a significant decrease in insulin-mediated glucose uptake compared with controls (5.75 +/- 0.21 vs. 7.98 +/- 0.84 mg/kg/min; P < .03), which was entirely accounted for by an impairment in non-oxidative glucose disposal (P < .04). Glucose 109-116 insulin Homo sapiens 92-99 9657106-5 1998 During the baseline (pre-octreotide) study, patients demonstrated a significant decrease in insulin-mediated glucose uptake compared with controls (5.75 +/- 0.21 vs. 7.98 +/- 0.84 mg/kg/min; P < .03), which was entirely accounted for by an impairment in non-oxidative glucose disposal (P < .04). Glucose 271-278 insulin Homo sapiens 92-99 9657106-7 1998 Restoration of insulin-mediated glucose utilization was entirely caused by normalization of non-oxidative glucose disposal; 4) was associated with a considerably more pronounced stimulation by insulin of the fractional glycogen synthase in muscle compared with pre-octreotide results (increment above baseline pre: 0.035 +/- 0.010 vs. post: 0.060 +/- 0.023 nmol/min/mg protein; P < .04). Glucose 32-39 insulin Homo sapiens 15-22 9657106-7 1998 Restoration of insulin-mediated glucose utilization was entirely caused by normalization of non-oxidative glucose disposal; 4) was associated with a considerably more pronounced stimulation by insulin of the fractional glycogen synthase in muscle compared with pre-octreotide results (increment above baseline pre: 0.035 +/- 0.010 vs. post: 0.060 +/- 0.023 nmol/min/mg protein; P < .04). Glucose 106-113 insulin Homo sapiens 15-22 9657106-8 1998 Fractional glycogen activity significantly correlated with non-oxidative glucose disposal during insulin infusion (r = .69; P < .03). Glucose 73-80 insulin Homo sapiens 97-104 9657106-9 1998 Prolonged reduction of hyperinsulinemia for 96 hours in cirrhotic patients normalizes insulin-mediated glucose uptake and glycogen synthesis in muscle. Glucose 103-110 insulin Homo sapiens 28-35 9674647-1 1998 The insulin resistance syndrome has been characterized by hypertension, upper body obesity, insulin resistance, hyperinsulinemia, glucose intolerance, and hypertriglyceridemia. Glucose 130-137 insulin Homo sapiens 4-11 9705022-11 1998 However, when subjects without medication affecting insulin or glucose levels were considered, serum insulin levels were found to be lower in the heterozygous carriers of the insertion allele (15.1 +/- 9.2 mU/l) than in the subjects homozygous for the deletion allele (21.8 +/- 13.7 mU/l, P = 0.0035). Glucose 63-70 insulin Homo sapiens 101-108 23105185-1 1998 Diabetes has been classified as a disease of glucose overproduction by tissues, mainly liver and glucose underutilization by insulin requiring tissues like liver, adipose and muscle due to lack of insulin. Glucose 45-52 insulin Homo sapiens 125-132 23105185-1 1998 Diabetes has been classified as a disease of glucose overproduction by tissues, mainly liver and glucose underutilization by insulin requiring tissues like liver, adipose and muscle due to lack of insulin. Glucose 97-104 insulin Homo sapiens 125-132 9649577-1 1998 The homeodomain transcription factor insulin promoter factor-1 (IPF-1) is required for development of the pancreas and also mediates glucose-responsive stimulation of insulin gene transcription. Glucose 133-140 insulin Homo sapiens 37-44 9649577-1 1998 The homeodomain transcription factor insulin promoter factor-1 (IPF-1) is required for development of the pancreas and also mediates glucose-responsive stimulation of insulin gene transcription. Glucose 133-140 insulin Homo sapiens 167-174 9661605-1 1998 The purpose of this study was to determine whether elevation of plasma free fatty acids (FFA) in early pregnancy would cause alterations in insulin-stimulated glucose disposal similar to those occurring in late gestation. Glucose 159-166 insulin Homo sapiens 140-147 9661605-6 1998 L/H infusion inhibited insulin stimulation of total body glucose disposal by 28% compared with S/G infusion (from 6.7 +/- 0.7 to 4.9 +/- 0.6 mg/kg.min; P < 0.01). Glucose 57-64 insulin Homo sapiens 23-30 9661629-4 1998 Insulin-induced stimulation of glucose uptake (to 34.9 +/- 6.8 vs. 28.8 +/- 3.4 mumol/kg.min; P = 0.2) and inhibition of free fatty acids (to 0.13 +/- 0.03 vs. 0.12 +/- 0.04 mmol/L; P = 0.6) did not differ after overnight saline and overnight insulin. Glucose 31-38 insulin Homo sapiens 0-7 9661629-5 1998 In contrast, endogenous glucose production during the final hour of the hyperinsulinemic clamps (i.e. when glucose concentrations were the same) remained higher (P = 0.05) after overnight saline than after overnight insulin (5.5 +/- 1.5 vs. 0.02 +/- 1.4 mumol/kg.min). Glucose 24-31 insulin Homo sapiens 77-84 9753305-7 1998 The prevalence of insulin resistance in subjects with the combination of glucose intolerance (IGT or NIDDM), dyslipidemia (hypercholesterolemia and/or hypertriglyceridemia and/or low HDL cholesterol), hyperuricemia, and hypertension (n = 21) was 95.2%. Glucose 73-80 insulin Homo sapiens 18-25 9743587-0 1998 H-ras induces glucose uptake in brown adipocytes in an insulin- and phosphatidylinositol 3-kinase-independent manner. Glucose 14-21 insulin Homo sapiens 55-62 9743587-2 1998 At physiological doses, insulin stimulation for 15 min increased 3-fold glucose uptake and doubled the amount of Glut4 protein located at the plasma membrane. Glucose 72-79 insulin Homo sapiens 24-31 9743587-3 1998 Moreover, phosphatidylinositol (PI) 3-kinase activity was induced by the presence of insulin in those cells, glucose uptake being precluded by PI 3-kinase inhibitors such as wortmannin or LY294002. Glucose 109-116 insulin Homo sapiens 85-92 9743587-8 1998 Our results indicate that activated Ras induces brown adipocyte glucose transport in an insulin-independent manner, this induction not involving PI 3-kinase activation. Glucose 64-71 insulin Homo sapiens 88-95 9742977-2 1998 BACKGROUND: In patients with type 2 diabetes, intensive blood-glucose control with insulin or sulphonylurea therapy decreases progression of microvascular disease and may also reduce the risk of heart attacks. Glucose 62-69 insulin Homo sapiens 83-90 9734735-7 1998 Infusion of octreotide to suppress the release of gastrointestinal hormones prevented the rise in insulin, GIP, and GLP-1 induced by intraduodenal glucose infusion and reversed the suppression of appetite and reduction in energy intake. Glucose 147-154 insulin Homo sapiens 98-105 9726226-1 1998 Insulin resistance, as is found in skeletal muscle of individuals with obesity and NIDDM, appears to involve a reduced capacity of the hormone to stimulate glucose uptake and/or phosphorylation. Glucose 156-163 insulin Homo sapiens 0-7 9726231-1 1998 Islets undergo a number of upregulatory changes to meet the increased demand for insulin during pregnancy, including an increase in glucose-stimulated insulin secretion with a reduction in the stimulation threshold. Glucose 132-139 insulin Homo sapiens 81-88 9726231-5 1998 Insulin secretion increased by 2.1-, 5.0-, and 5.9-fold at the suprathreshold glucose concentration and by 1.6-, 2.3-, and 2.9-fold at the higher glucose concentration after 1, 3, and 5 days of PRL treatment, respectively. Glucose 78-85 insulin Homo sapiens 0-7 9726231-5 1998 Insulin secretion increased by 2.1-, 5.0-, and 5.9-fold at the suprathreshold glucose concentration and by 1.6-, 2.3-, and 2.9-fold at the higher glucose concentration after 1, 3, and 5 days of PRL treatment, respectively. Glucose 146-153 insulin Homo sapiens 0-7 9726231-9 1998 Under all conditions (differing glucose concentrations and time periods), the increase in insulin release was directly proportional to the increase in cAMP. Glucose 32-39 insulin Homo sapiens 90-97 9727896-13 1998 The added effect of metformin to that of a hypocaloric diet in improving insulin-stimulated glucose utilization is marginal when blood glucose reduction is obtained by weight loss. Glucose 92-99 insulin Homo sapiens 73-80 9727913-0 1998 A novel missense mutation in the homeodomain of the hepatocyte nuclear factor-1alpha/maturity-onset diabetes of the young 3 in a Japanese early-onset type 2 diabetic patient and time-course of glucose-stimulated insulin secretion. Glucose 193-200 insulin Homo sapiens 212-219 9737810-3 1998 A very high glucose transport in adipocytes (basal: 176 and insulin stimulated glucose transport 10(-7) mol l(-1): 335 fl cell(-1) s(-1)) was found when compared with reference laboratory diabetic patients (basal: 59 +/- 10 and insulin 10(-7) mol l(-1): 106 +/- 7 fl cell(-1) s(-1), mean +/- SE) and with reference laboratory of non-diabetic subjects (basal: 106 +/- 6 and insulin 10(-7) mol l(-1): 188 +/- 15 fl cell(-1) s(-1)). Glucose 12-19 insulin Homo sapiens 60-67 9737810-3 1998 A very high glucose transport in adipocytes (basal: 176 and insulin stimulated glucose transport 10(-7) mol l(-1): 335 fl cell(-1) s(-1)) was found when compared with reference laboratory diabetic patients (basal: 59 +/- 10 and insulin 10(-7) mol l(-1): 106 +/- 7 fl cell(-1) s(-1), mean +/- SE) and with reference laboratory of non-diabetic subjects (basal: 106 +/- 6 and insulin 10(-7) mol l(-1): 188 +/- 15 fl cell(-1) s(-1)). Glucose 12-19 insulin Homo sapiens 228-235 9737810-3 1998 A very high glucose transport in adipocytes (basal: 176 and insulin stimulated glucose transport 10(-7) mol l(-1): 335 fl cell(-1) s(-1)) was found when compared with reference laboratory diabetic patients (basal: 59 +/- 10 and insulin 10(-7) mol l(-1): 106 +/- 7 fl cell(-1) s(-1), mean +/- SE) and with reference laboratory of non-diabetic subjects (basal: 106 +/- 6 and insulin 10(-7) mol l(-1): 188 +/- 15 fl cell(-1) s(-1)). Glucose 12-19 insulin Homo sapiens 228-235 9737810-3 1998 A very high glucose transport in adipocytes (basal: 176 and insulin stimulated glucose transport 10(-7) mol l(-1): 335 fl cell(-1) s(-1)) was found when compared with reference laboratory diabetic patients (basal: 59 +/- 10 and insulin 10(-7) mol l(-1): 106 +/- 7 fl cell(-1) s(-1), mean +/- SE) and with reference laboratory of non-diabetic subjects (basal: 106 +/- 6 and insulin 10(-7) mol l(-1): 188 +/- 15 fl cell(-1) s(-1)). Glucose 79-86 insulin Homo sapiens 60-67 9754821-13 1998 Hepatic insulin resistance was however present as basal glucose and insulin were higher. Glucose 56-63 insulin Homo sapiens 8-15 9816472-9 1998 Reduced NO availability may not only be of relevance to the development of atherosclerotic complications in diabetes but may also interfere with insulin-mediated postprandial glucose disposal and possibly contribute to the development of insulin resistance. Glucose 175-182 insulin Homo sapiens 145-152 9789794-8 1998 The affinity of receptors for insulin seems to depend mainly on glucose concentrations. Glucose 64-71 insulin Homo sapiens 30-37 9739026-7 1998 RESULTS: The amino acid infusions elevated plasma amino acid levels, and the glucose infusions increased both glucose and insulin concentrations. Glucose 77-84 insulin Homo sapiens 122-129 9710629-9 1998 These studies demonstrate ceramide"s capacity to inhibit activation of Akt and imply that this is a mechanism of antagonism of insulin-dependent physiological events, such as the peripheral activation of glucose transport and the suppression of apoptosis. Glucose 204-211 insulin Homo sapiens 127-134 9744832-3 1998 Two kinds of mechanisms may be involved: one in which insulin interacts directly with brain tissue and one in which insulin acts indirectly by reducing peripheral blood glucose levels. Glucose 169-176 insulin Homo sapiens 116-123 9744832-6 1998 In focal ischemia, unlike global ischemia, the effect of insulin is predominantly via peripheral hypoglycemia, because neuroprotection is largely annulled by co-administration of glucose. Glucose 179-186 insulin Homo sapiens 57-64 9710443-14 1998 The abilities of glucose at basal insulin to both increase the flux through glucokinase and to inhibit the flux through glucose-6-phosphatase are impaired in DM2. Glucose 17-24 insulin Homo sapiens 34-41 9719049-8 1998 Obese hypertensive patients are resistant to the effects of insulin with regard to both glucose uptake and vasodilatation. Glucose 88-95 insulin Homo sapiens 60-67 9691088-4 1998 The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. Glucose 164-171 insulin Homo sapiens 183-190 9709945-0 1998 Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease. Glucose 31-38 insulin Homo sapiens 14-21 9709945-1 1998 Resistance to insulin-mediated glucose disposal has been postulated to predispose individuals to a cluster of associated abnormalities (Syndrome X) known to increase risk of cardiovascular disease (CVD). Glucose 31-38 insulin Homo sapiens 14-21 9709945-3 1998 Therefore, this study was initiated to evaluate the hypothesis that resistance to insulin-mediated glucose disposal would predict the development of CVD in healthy volunteers. Glucose 99-106 insulin Homo sapiens 82-89 9709945-4 1998 To accomplish this goal, 147 normal, healthy, nonobese, volunteers were evaluated [4.7 +/- 0.1 yr (mean +/- SEM)] after baseline measurements of steady state plasma glucose concentration (an estimate of insulin-mediated glucose disposal), as well as other CVD risk factors. Glucose 220-227 insulin Homo sapiens 203-210 9709945-8 1998 SSPG was also related significantly to diastolic blood pressure, triglyceride, and low-density lipoprotein and high-density lipoprotein cholesterol concentrations, and the glucose and insulin responses to oral glucose. Glucose 210-217 insulin Homo sapiens 184-191 9771464-0 1998 Long-term in vitro exposure to high glucose increases proinsulin-like-molecules release by isolated human islets. Glucose 36-43 insulin Homo sapiens 54-64 9771464-1 1998 The aim of this study was to determine the effect of long-term in vitro exposure to high glucose on the release and content of proinsulin and insulin in human islets. Glucose 89-96 insulin Homo sapiens 127-137 9771464-1 1998 The aim of this study was to determine the effect of long-term in vitro exposure to high glucose on the release and content of proinsulin and insulin in human islets. Glucose 89-96 insulin Homo sapiens 130-137 9881813-3 1998 According to this hypothesis, insulin resistance leads to inadequate intracellular glucose, which in turn leads to insufficient amounts of adenosine triphosphate needed for ion transfer, and to drive energy-requiring reactions. Glucose 83-90 insulin Homo sapiens 30-37 11038806-5 1998 RESULTS: In nondiabetic first-degree relatives, SGI and ISI were significantly decreased (P < 0.01), and plasma insulin was increased at 0, 30, 60, 120 minutes after administration of oral glucose load (P < 0.05 and P < 0.01), as compared with the controls, in matched age, body mass index (BMI) and proportion of sex. Glucose 192-199 insulin Homo sapiens 115-122 9668074-6 1998 Mutation of this motif abolished not only the induction of the promoter by insulin but also abrogated its suppression by glucose. Glucose 121-128 insulin Homo sapiens 75-82 9660823-6 1998 This resulted in inhibition of insulin-stimulated glucose transport, glycogen synthase activity and DNA synthesis. Glucose 50-57 insulin Homo sapiens 31-38 9660823-8 1998 However, co-expression of a membrane-targeted p110(C) with the p85N-SH2 protein rescued glucose transport, supporting our argument that the p85N-SH2 protein specifically blocks insulin-mediated PI 3-kinase activity, and, that the signaling pathways downstream of PI 3-kinase are intact. Glucose 88-95 insulin Homo sapiens 177-184 9697823-0 1998 Role of tissue-specific blood flow and tissue recruitment in insulin-mediated glucose uptake of human skeletal muscle. Glucose 78-85 insulin Homo sapiens 61-68 9697823-1 1998 BACKGROUND: Conflicting evidence exists concerning whether insulin-induced vasodilation plays a mechanistic role in the regulation of limb glucose uptake. Glucose 139-146 insulin Homo sapiens 59-66 9697823-2 1998 It can be predicted that if insulin augments blood flow by causing tissue recruitment, this mechanism would enhance limb glucose uptake. Glucose 121-128 insulin Homo sapiens 28-35 9697823-9 1998 The amount of tissue newly recruited by insulin was strongly correlated to the concomitant increase in tissue glucose uptake (r=0.789, P<0.01). Glucose 110-117 insulin Homo sapiens 40-47 9670003-6 1998 Transfection of PED/PEA-15 in differentiating L6 skeletal muscle cells increases the content of Glut1 transporters on the plasma membrane and inhibits insulin-stimulated glucose transport and cell-surface recruitment of Glut4, the major insulin-sensitive glucose transporter. Glucose 170-177 insulin Homo sapiens 151-158 9670003-8 1998 Overexpression of the PED/PEA-15 gene may contribute to insulin resistance in glucose uptake in type 2 diabetes. Glucose 78-85 insulin Homo sapiens 56-63 9702932-12 1998 CONCLUSION: Our results suggest that hyperinsulinaemia/insulin resistance in hypertensives becomes identifiable by using simple measurements of BMI, WHR, serum triglycerides and HDL cholesterol as well as the oral glucose tolerance test as means. Glucose 214-221 insulin Homo sapiens 42-49 9794728-1 1998 Insulin resistance is common in the general population and tends to cluster with glucose intolerance, dyslipidaemia and high blood pressure. Glucose 81-88 insulin Homo sapiens 0-7 11542308-5 1998 Our previous study showed, that after three days of bed rest the plasma insulin response to a glucose load markedly increases both in untrained and in endurance-trained subjects; but the blood glucose (BG) response was less affected in athletes. Glucose 94-101 insulin Homo sapiens 72-79 11542308-6 1998 The present investigation was designed to compare an effect of three day bed rest on BG and plasma insulin responses to oral glucose in untrained subjects, and in endurance or strength trained athletes. Glucose 125-132 insulin Homo sapiens 99-106 9751707-1 1998 Insulin gene transcription is limited to the beta cells within the mammalian pancreas and, like insulin secretion, is regulated by glucose. Glucose 131-138 insulin Homo sapiens 0-7 9751707-2 1998 Our previous studies in primary cultured beta cells suggested the presence of a strong glucose-responsive enhancer element between base pairs -341 and -260 of the human insulin promoter, the same region in which a transcriptional repressor had been identified in beta-cell tumor lines. Glucose 87-94 insulin Homo sapiens 169-176 9751707-6 1998 These data demonstrate a critical role for the Z element in human insulin gene transcription and its regulation by glucose. Glucose 115-122 insulin Homo sapiens 66-73 9667221-16 1998 Troglitazone could block the insulin antagonistic effects of GH on hepatic glucose output and peripheral glucose utilization. Glucose 75-82 insulin Homo sapiens 29-36 9667230-2 1998 Insulin resistance was defined as the steady-state plasma glucose (SSPG) concentration at the end of a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 58-65 insulin Homo sapiens 0-7 9667230-2 1998 Insulin resistance was defined as the steady-state plasma glucose (SSPG) concentration at the end of a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 153-160 insulin Homo sapiens 0-7 9667230-6 1998 When multiple regression analysis was used to evaluate these relationships, the only variables that were consistently found to be associated with Hct and Hgb were insulin resistance and plasma insulin response to oral glucose. Glucose 218-225 insulin Homo sapiens 193-200 9628730-2 1998 Stimulation of glucose metabolism and Snf1 kinase by human insulin. Glucose 15-22 insulin Homo sapiens 59-66 9637806-7 1998 Among the 21 women given metformin plus clomiphene, the mean (+/-SE) area under the serum insulin curve after oral glucose administration decreased from 6745+/-2021 to 3479+/-455 microU per milliliter per minute (40.5+/-12.1 to 20.9+/-2.7 nmol per liter per minute, P=0.03), but it did not change significantly in the 25 women given placebo plus clomiphene. Glucose 115-122 insulin Homo sapiens 90-97 9628730-3 1998 Effects of human insulin on glucose metabolism in the yeast Saccharomyces cerevisiae were studied in this report. Glucose 28-35 insulin Homo sapiens 17-24 9628730-4 1998 Under two conditions of growth limitation (glucose-grown cells during transition to stationary phase or spheroplasts during incubation in synthetic glucose medium), human insulin (10 and 1 microM, respectively) enhanced glycogen accumulation and glycogen synthase activity by 40-60% compared to control cells. Glucose 43-50 insulin Homo sapiens 171-178 9628730-4 1998 Under two conditions of growth limitation (glucose-grown cells during transition to stationary phase or spheroplasts during incubation in synthetic glucose medium), human insulin (10 and 1 microM, respectively) enhanced glycogen accumulation and glycogen synthase activity by 40-60% compared to control cells. Glucose 148-155 insulin Homo sapiens 171-178 9628730-7 1998 In glucose-induced spheroplasts, insulin (1 microM), in addition to glycogen accumulation, led to about 2-fold increases of the rates of ethanol production and glucose oxidation compared to control cells, and the maximal concentration of hexose 6-phosphate was increased by 30-40%. Glucose 3-10 insulin Homo sapiens 33-40 9628730-10 1998 Snf1 kinase activity was elevated 5-10-fold in response to insulin both during glucose induction of yeast spheroplasts and during transition to stationary phase of glucose-grown cells. Glucose 79-86 insulin Homo sapiens 59-66 9628730-10 1998 Snf1 kinase activity was elevated 5-10-fold in response to insulin both during glucose induction of yeast spheroplasts and during transition to stationary phase of glucose-grown cells. Glucose 164-171 insulin Homo sapiens 59-66 9628730-11 1998 We conclude that Saccharomyces cerevisiae and insulin-sensitive mammalian cells share some parts of the signaling cascades regulating oxidative and nonoxidative glucose metabolism in response to glucose and insulin. Glucose 161-168 insulin Homo sapiens 46-53 9628730-11 1998 We conclude that Saccharomyces cerevisiae and insulin-sensitive mammalian cells share some parts of the signaling cascades regulating oxidative and nonoxidative glucose metabolism in response to glucose and insulin. Glucose 161-168 insulin Homo sapiens 207-214 9628730-11 1998 We conclude that Saccharomyces cerevisiae and insulin-sensitive mammalian cells share some parts of the signaling cascades regulating oxidative and nonoxidative glucose metabolism in response to glucose and insulin. Glucose 195-202 insulin Homo sapiens 46-53 9628731-4 1998 The binding affinities of various mutant insulin analogues correlated well with their capacities to activate glycogen synthase and SNF1 kinase in glucose-induced yeast spheroplasts, the ranking of their relative efficacies in yeast and in isolated rat adipocytes being similar. Glucose 146-153 insulin Homo sapiens 41-48 9570069-4 1998 When the tubular PVA bioartificial pancreas was perifused in a small chamber with RPMI-1640 medium containing glucose at concentrations of 5.6-16.6 mmol/L, insulin release began to increase without delay. Glucose 110-117 insulin Homo sapiens 156-163 9614064-1 1998 Insulin and muscle contraction potently stimulate glucose uptake in mammalian skeletal muscle. Glucose 50-57 insulin Homo sapiens 0-7 9614064-5 1998 Either insulin or in vitro muscle contraction significantly elevated glucose transport in isolated rat epitrochlearis and soleus muscles. Glucose 69-76 insulin Homo sapiens 7-14 9614064-7 1998 Moreover, wortmannin, an inhibitor of PI 3"-kinase, completely blocked the insulin-stimulated increase in Akt activity and glucose transport but did not alter either of these parameters in contracting muscles. Glucose 123-130 insulin Homo sapiens 75-82 9677011-6 1998 In clinical trials with insulin lispro, the postprandial rise of blood glucose is smaller, the rate of hypoglycaemia is lower particularly at night-time, the need for snacks is smaller and the patient preference is better than with human insulin. Glucose 71-78 insulin Homo sapiens 24-31 9626175-4 1998 Insulin-stimulated whole body glucose uptake was significantly decreased in the hypertensive men (41 +/- 4 mumol/kg per minute) compared with the normotensive (59 +/- 4 mumol/kg per minute, P < 0.005) men. Glucose 30-37 insulin Homo sapiens 0-7 9854458-11 1998 Octreotide completely abolished the immediate insulin response to glucose in all subjects (both P < 0.0001) and caused a delayed and significantly increased glycaemic response in both groups (P < 0.0001). Glucose 66-73 insulin Homo sapiens 46-53 9690914-8 1998 Insulin resistance was defined as the ratio of area under curve for insulin/area under curve for glucose. Glucose 97-104 insulin Homo sapiens 0-7 9698815-3 1998 It has been shown that the OB protein interferes with insulin secretion from pancreatic islets, reduces insulin-stimulated glucose transport in adipocytes, and increases glucose transport, glycogen synthesis and fatty acid oxidation in skeletal muscle. Glucose 123-130 insulin Homo sapiens 104-111 9604880-10 1998 The group receiving nicotinamide exhibited decreased first-phase insulin secretion in response to intravenous glucose (P = 0.03). Glucose 110-117 insulin Homo sapiens 65-72 9690051-8 1998 The main problem is that although it is possible to determine the viability of isolated islets by measuring specific cellular functions such as glucose-stimulated insulin release, it is impossible to compare this with the same function performed by islets within the native pancreas. Glucose 144-151 insulin Homo sapiens 163-170 9632121-4 1998 SHBG was positively correlated (r = 0.41, p < 0.01) to hepatic insulin sensitivity derived from mathematical modelling of fasting glucose and insulin data using the homeostasis assessment model (HOMA). Glucose 133-140 insulin Homo sapiens 66-73 9632121-10 1998 Further studies in 15 of the diabetic patients (11 men), showed a significant positive correlation (r = 0.52, p < 0.05) between SHBG and peripheral insulin sensitivity derived by continuous infusion of glucose with model assessment (CIGMA) but not between SHBG and CIGMA-modelled beta-cell function. Glucose 205-212 insulin Homo sapiens 151-158 9662054-7 1998 Fasting plasma glucose was found to be significantly positively correlated to intima media thickness, body mass index, waist to hip ratio, haemoglobin A1c, insulin, C-peptide, triglycerides, plasminogen activator inhibitor and significantly negatively correlated to high density lipoprotein cholesterol. Glucose 15-22 insulin Homo sapiens 156-163 9690052-7 1998 Insulin secretion increased in a glucose dose-dependent manner (p < 0.001): SI: 3.1 +/- 0.3 and 3.6 +/- 0.2 with 11.0 mmol/l and 22.0 mmol/l glucose, which showed a satisfactory magnitude with reference to human islets. Glucose 33-40 insulin Homo sapiens 0-7 9662054-7 1998 Fasting plasma glucose was found to be significantly positively correlated to intima media thickness, body mass index, waist to hip ratio, haemoglobin A1c, insulin, C-peptide, triglycerides, plasminogen activator inhibitor and significantly negatively correlated to high density lipoprotein cholesterol. Glucose 15-22 insulin Homo sapiens 165-174 9662057-0 1998 Does insulin-induced increase in the amount of plasma membrane GLUTs quantitatively account for insulin-induced increase in glucose uptake? Glucose 124-131 insulin Homo sapiens 5-12 9690052-7 1998 Insulin secretion increased in a glucose dose-dependent manner (p < 0.001): SI: 3.1 +/- 0.3 and 3.6 +/- 0.2 with 11.0 mmol/l and 22.0 mmol/l glucose, which showed a satisfactory magnitude with reference to human islets. Glucose 144-151 insulin Homo sapiens 0-7 9662057-0 1998 Does insulin-induced increase in the amount of plasma membrane GLUTs quantitatively account for insulin-induced increase in glucose uptake? Glucose 124-131 insulin Homo sapiens 96-103 9716921-10 1998 Changes in the waking time and the subsequent delay in the first insulin bolus on Sunday may alter blood glucose control in patients on MDI, but CSII allows such changes without any glycemic side effects. Glucose 105-112 insulin Homo sapiens 65-72 9716924-4 1998 The functional significance of IAA was assessed in 46 of them by first phase (sum of +1 and +3 min) insulin response to intravenous glucose (IVGTT) and an oral glucose tolerance test (OGTT) undertaken before commencement of the carbimazole therapy. Glucose 132-139 insulin Homo sapiens 100-107 9679397-6 1998 The insulin/glucose ratio was obtained as the coefficient of insulin/glucose. Glucose 12-19 insulin Homo sapiens 61-68 9667398-2 1998 We report here three members of a two-generation Caucasian family in whom this syndrome was identified by unexplained hyperinsulinism associated with normal glucose tolerance and normal insulin sensitivity. Glucose 157-164 insulin Homo sapiens 123-130 9679397-1 1998 The purpose of this investigation was to determine the baseline insulin level in sera during fasting and after an oral glucose load in patients with mild preeclampsia and compare these values with those obtained from pregnant women with normal arterial pressure during the third trimester of their pregnancy. Glucose 119-126 insulin Homo sapiens 64-71 9679397-6 1998 The insulin/glucose ratio was obtained as the coefficient of insulin/glucose. Glucose 69-76 insulin Homo sapiens 4-11 9679397-9 1998 Insulin fasting levels were lower in the preeclampsia group compared with the normotensive one (7.1 +/- 3.8 vs 10.6 +/- 8.7 microU/mL, p = 0.02), however there was no difference in either group after the glucose load was administered (66.8 +/- 46.5 vs 71.0 +/- 51.9, p = N.S.). Glucose 204-211 insulin Homo sapiens 0-7 9616209-2 1998 While insulin resistance involves decreased glucose transport activity in skeletal muscle, its molecular basis is unknown. Glucose 44-51 insulin Homo sapiens 6-13 9627620-3 1998 Insulin dosage and glucose levels after fasting and at 80 and 110 minutes after eating (by measuring capillary blood glucose concentrations and glycated hemoglobin [HbA1c] values) are described for women with type 1 diabetes. Glucose 117-124 insulin Homo sapiens 0-7 11273248-0 1998 Estimation of fasting and post oral glucose serum insulin levels in hypertensive and obese subjects. Glucose 36-43 insulin Homo sapiens 50-57 9626150-0 1998 The vasodilating effect of insulin is dependent on local glucose uptake: a double blind, placebo-controlled study. Glucose 57-64 insulin Homo sapiens 27-34 9626150-9 1998 These data suggest that local uptake of D-glucose by insulin-sensitive tissues is an important determinant of insulin-mediated vasodilation. Glucose 40-49 insulin Homo sapiens 53-60 9626150-9 1998 These data suggest that local uptake of D-glucose by insulin-sensitive tissues is an important determinant of insulin-mediated vasodilation. Glucose 40-49 insulin Homo sapiens 110-117 11273248-2 1998 Fasting and post oral glucose serum insulin levels serve as reliable markers of the state of insulin resistance. Glucose 22-29 insulin Homo sapiens 36-43 11273248-2 1998 Fasting and post oral glucose serum insulin levels serve as reliable markers of the state of insulin resistance. Glucose 22-29 insulin Homo sapiens 93-100 11273248-4 1998 While, post-oral glucose load serum insulin levels increased more in hypertensive individuals than those with obesity alone. Glucose 17-24 insulin Homo sapiens 36-43 11273248-5 1998 In subjects who had obesity and hypertension together, the fasting serum insulin levels did not show much change while post oral glucose load serum insulin levels greatly increased suggesting a compounding effect. Glucose 129-136 insulin Homo sapiens 148-155 9627584-1 1998 OBJECTIVE: To determine the effect of a continuous insulin infusion on protein and glucose metabolism in extremely low birth weight (ELBW) infants. Glucose 83-90 insulin Homo sapiens 51-58 9663927-3 1998 Preliminary results have shown that tissue availability of insulin-like growth factor I is a determinant of glucose regulation in essential hypertension OBJECTIVE: To investigate whether the tissue availability of circulating insulin-like growth factor I in patients with essential hypertension is related to insulin resistance and whether chronic angiotensin converting enzyme inhibition influences tissue availability of the factor and insulin resistance in these patients. Glucose 108-115 insulin Homo sapiens 59-66 9627584-6 1998 Glucose utilization doubled (from 8 +/- 0.9 to 15.7 +/- 1.1 mg/kg/min; p = 0.0003) and plasma lactate concentrations tripled (from 2.1 +/- 0.5 to 5.7 +/- 1.0 mmol/L; p < 0.05) during the insulin infusion. Glucose 0-7 insulin Homo sapiens 190-197 9627584-7 1998 CONCLUSIONS: During an infusion of glucose alone, pharmacologic concentrations of insulin in ELBW infants produced no net protein anabolic effect. Glucose 35-42 insulin Homo sapiens 82-89 9680777-9 1998 Two hours after the oral glucose load, serum insulin levels increased significantly in malnourished children but fell well short of the control values. Glucose 25-32 insulin Homo sapiens 45-52 9659817-3 1998 Using the method of vector autoregressive modeling (VAR) analysis of frequently sampled oral glucose tolerance test (OGTT) results, we evaluated abnormalities in the feedback relationships between plasma glucose and insulin in gastrectomized patients to assess insulin secretion capacity and insulin resistance following gastrectomy. Glucose 204-211 insulin Homo sapiens 216-223 9659817-5 1998 After gastrectomy, the predicted response of insulin to a glucose challenge was excessive in normal subjects and those with slightly impaired glucose tolerance. Glucose 58-65 insulin Homo sapiens 45-52 9659817-6 1998 Furthermore, the glucose response to insulin was clearly positive in gastrectomized subjects with moderately to severely impaired glucose tolerance, i.e., diabetics, indicating strong insulin resistance. Glucose 17-24 insulin Homo sapiens 37-44 9659817-6 1998 Furthermore, the glucose response to insulin was clearly positive in gastrectomized subjects with moderately to severely impaired glucose tolerance, i.e., diabetics, indicating strong insulin resistance. Glucose 17-24 insulin Homo sapiens 184-191 9659817-8 1998 Our results suggest that the lowered glucose tolerance which follows gastrectomy results from disturbance of the hormonal relationship between pancreas and intestine (entero-insular axis), which causes increased intestinal glucose absorption, and the insulin resistance which occurs in response to hyperinsulinemia in patients with normal fasting plasma glucose. Glucose 37-44 insulin Homo sapiens 251-258 9680777-10 1998 The insulin:glucose ratio was consistently low in all cases but was more marked in PEM patients, both in the basal state as well as oral glucose loading Glucose 12-19 insulin Homo sapiens 4-11 9680777-10 1998 The insulin:glucose ratio was consistently low in all cases but was more marked in PEM patients, both in the basal state as well as oral glucose loading Glucose 137-144 insulin Homo sapiens 4-11 9627359-6 1998 On SU therapy, subjects had higher fasting and post-glucose load levels of intact proinsulin compared with B1 and I (fasting, 13.9 x/divided by 2.6 v 9.5 x/divided by 2.2 (P = .004) and 9.1 x/divided by 2.4 pmol x L(-1) (P = .01), respectively). Glucose 52-59 insulin Homo sapiens 82-92 9678192-10 1998 CONCLUSIONS: The improvement in glucose metabolism seen after JIB may be due to reduced insulin resistance after weight loss and/or increased levels of the incretin hormones GIP and GLP-1. Glucose 32-39 insulin Homo sapiens 88-95 9610534-7 1998 Total body glucose uptake also increased significantly (+60.8 +/- 12.0%, P<.05), indicating an increase in insulin sensitivity. Glucose 11-18 insulin Homo sapiens 110-117 9630814-5 1998 glucose production by the human kidney is stimulated by epinephrine and inhibited by insulin. Glucose 0-7 insulin Homo sapiens 85-92 9727207-11 1998 In patients with primary hyperaldosteronism the authors observed, as compared with healthy controls, a lower glucose consumption during the clamping (glucose disposal rate 18.7 +/- 4.8 vs 29.3 +/- 3.7 mumol/kg/min, p < 0.01), a rise of the metabolic glucose clearance (3.8 +/- 1.5 vs. 7.0 +/- 1.1 ml/kg/min, p < 0.01 and an index of tissue sensitivity for insulin) 23.7 +/- 9.8 vs. 37.5 +/- 11.6 mumol/kg/min per mU/l x 100, p < 0.02). Glucose 109-116 insulin Homo sapiens 362-369 9593781-0 1998 Postabsorptive respiratory quotient and insulin-stimulated glucose storage rate in nondiabetic pima indians are related To glycogen synthase fractional activity in cultured myoblasts. Glucose 59-66 insulin Homo sapiens 40-47 9593781-2 1998 Skeletal muscle accounts for a major fraction of total body lipid oxidation and is the principle site for reduced glucose storage in insulin-resistant subjects. Glucose 114-121 insulin Homo sapiens 133-140 9593781-6 1998 Basal GSFA in cultured muscle cells is inversely correlated with postabsorptive respiratory quotient of the muscle donors (r = -0.66, P = 0.001) and with in vivo high dose insulin-stimulated glucose storage rates (r = 0.47, P = 0.04). Glucose 191-198 insulin Homo sapiens 172-179 9593781-7 1998 These results indicate that the postabsorptive respiratory quotients and insulin-mediated glucose storage rates in vivo share a common regulatory mechanism with GSFA in cultured myoblasts. Glucose 90-97 insulin Homo sapiens 73-80 9573413-2 1998 Patients with insulin-dependent diabetes mellitus (IDDM) who practice conventional insulin therapy are at risk of developing hypoglycemia (low levels of blood glucose), which can lead to severe dysfunction of the central nervous system. Glucose 159-166 insulin Homo sapiens 14-21 9573413-5 1998 Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. Glucose 191-198 insulin Homo sapiens 34-41 9573413-5 1998 Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. Glucose 191-198 insulin Homo sapiens 295-302 9573413-5 1998 Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. Glucose 238-245 insulin Homo sapiens 34-41 9573413-5 1998 Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. Glucose 238-245 insulin Homo sapiens 295-302 9573413-5 1998 Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. Glucose 238-245 insulin Homo sapiens 34-41 9573413-5 1998 Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. Glucose 238-245 insulin Homo sapiens 295-302 9609581-10 1998 There was a 28% decrease in insulin sensitivity as measured by the glucose infusion rate during the euglycemic clamp plus residual hepatic glucose turnover (5.78 +/- 1.91 vs 4.16 +/- 1.49 mg/kg fat-free mass/min, p = 0.005). Glucose 67-74 insulin Homo sapiens 28-35 9591763-8 1998 In these subjects, the systemic serum insulin levels increased significantly during the dextrose infusion (P<.001). Glucose 88-96 insulin Homo sapiens 38-45 9609581-13 1998 CONCLUSION: Decreased peripheral insulin sensitivity, and to a lesser degree increased endogenous glucose production, may represent the pathophysiology of abnormal glucose tolerance observed in many women treated with oral terbutaline. Glucose 164-171 insulin Homo sapiens 33-40 9560323-1 1998 Insulin stimulates the rate of glucose uptake into muscle and adipose cells by translocation of glucose transporters from an intracellular storage pool to the plasma membrane. Glucose 31-38 insulin Homo sapiens 0-7 9560323-6 1998 Cytochalasin D, and the chemically unrelated latrunculin B, which also inhibits actin filament reassembly, prevented the insulin stimulation of glucose transport by approx. Glucose 144-151 insulin Homo sapiens 121-128 9588447-5 1998 Stimulation of insulin release by tolbutamide, which inhibits the K(ATP) channel and depolarizes the beta-cell, and inhibition of glucose-stimulated release by diazoxide, which activates the channel and repolarizes the beta-cell, confirm the involvement of the K(ATP) channel-dependent pathway in glucose signaling. Glucose 297-304 insulin Homo sapiens 15-22 9598835-1 1998 This study was performed in 36 healthy volunteers to define the relationship between plasma concentrations of partially oxidized low density lipoprotein (poxLDL), plasma glucose and insulin responses to oral glucose, and steady-state plasma glucose (SSPG) concentrations after a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 208-215 insulin Homo sapiens 182-189 9598835-1 1998 This study was performed in 36 healthy volunteers to define the relationship between plasma concentrations of partially oxidized low density lipoprotein (poxLDL), plasma glucose and insulin responses to oral glucose, and steady-state plasma glucose (SSPG) concentrations after a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 208-215 insulin Homo sapiens 182-189 9598835-1 1998 This study was performed in 36 healthy volunteers to define the relationship between plasma concentrations of partially oxidized low density lipoprotein (poxLDL), plasma glucose and insulin responses to oral glucose, and steady-state plasma glucose (SSPG) concentrations after a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 208-215 insulin Homo sapiens 182-189 9707263-5 1998 More aggressive screening, using fasting plasma glucose (FPG) concentrations of > or = 110 mg/dL as a marker of insulin resistance, should help identify not only patients with hyperglycemia but also those with insulin resistance without significant hyperglycemia. Glucose 48-55 insulin Homo sapiens 115-122 9707263-5 1998 More aggressive screening, using fasting plasma glucose (FPG) concentrations of > or = 110 mg/dL as a marker of insulin resistance, should help identify not only patients with hyperglycemia but also those with insulin resistance without significant hyperglycemia. Glucose 48-55 insulin Homo sapiens 213-220 9707264-1 1998 Millions of Americans are at risk for cardiovascular morbidity and mortality related to disorders of glucose intolerance--particularly type 2 diabetes and prediabetic conditions, including the insulin resistance, or "cardiovascular dysmetabolic," syndrome. Glucose 101-108 insulin Homo sapiens 193-200 9588447-6 1998 The participation of the K(ATP) channel-independent pathway in the stimulation of insulin release by glucose was demonstrated for the first time in human islets. Glucose 101-108 insulin Homo sapiens 82-89 9588447-9 1998 Under these conditions, glucose stimulated insulin release. Glucose 24-31 insulin Homo sapiens 43-50 9588447-11 1998 Again, with no possibility of further action on the K(ATP) channel, glucose stimulated insulin release. Glucose 68-75 insulin Homo sapiens 87-94 9589246-6 1998 RESULTS: Both sulfonylurea and insulin therapy reduced basal glucose concentrations compared with diet alone, but neither reduced the increased postprandial glucose increments. Glucose 61-68 insulin Homo sapiens 31-38 9588447-12 1998 In a final series of experiments, glucose-stimulated insulin release was profoundly inhibited by somatostatin, clonidine, and prostaglandin E2, but not by galanin. Glucose 34-41 insulin Homo sapiens 53-60 9589247-7 1998 Plasma glucose concentrations rose to 13.8 +/- 1.9 and 16.0 +/- 1.7 mmol/l in the regular insulin- and insulin lispro-treated groups, respectively. Glucose 7-14 insulin Homo sapiens 90-97 9609356-2 1998 This review examines the evidence that elevated plasma NEFA can inhibit glucose-stimulated insulin secretion by pancreatic beta-cells and impair glucose- and insulin-stimulated glucose disposal by peripheral tissues. Glucose 72-79 insulin Homo sapiens 91-98 9589247-7 1998 Plasma glucose concentrations rose to 13.8 +/- 1.9 and 16.0 +/- 1.7 mmol/l in the regular insulin- and insulin lispro-treated groups, respectively. Glucose 7-14 insulin Homo sapiens 103-110 9589247-10 1998 In association with this, plasma glucose decreased to a lower nadir after lispro insulin (9.7 +/- 0.4 vs. 13.7 +/- 0.7 mmol/l, lispro- vs. regular-treated groups at 120 min after insulin administration, P < 0.01). Glucose 33-40 insulin Homo sapiens 81-88 9589247-10 1998 In association with this, plasma glucose decreased to a lower nadir after lispro insulin (9.7 +/- 0.4 vs. 13.7 +/- 0.7 mmol/l, lispro- vs. regular-treated groups at 120 min after insulin administration, P < 0.01). Glucose 33-40 insulin Homo sapiens 179-186 9609368-4 1998 With insulin therapy and cessation of IFN-gamma, fasting blood glucose concentration returned to 6.2 mmol l(-1), and insulin therapy was discontinued. Glucose 63-70 insulin Homo sapiens 5-12 9681274-4 1998 In 15 healthy men, hypoglycaemia was induced by an intravenous infusion of insulin (2.5 mU/kg per min) to a blood glucose of 2.2 +/- 0.3 mmol/l (mean +/- S.D.) Glucose 114-121 insulin Homo sapiens 75-82 9628273-0 1998 Insulin resistance characterizes glucose uptake in skeletal muscle but not in the heart in NIDDM. Glucose 33-40 insulin Homo sapiens 0-7 9628273-6 1998 Insulin-stimulated femoral muscle glucose uptake was significantly lower in the patients with NIDDM (71+/-6 micromol/kg muscle x min) than in the normal subjects (96+/-5 micromol/kg muscle x min, p < 0.01). Glucose 34-41 insulin Homo sapiens 0-7 9700428-1 1998 A novel strategy for closed-loop control of glucose using subcutaneous (s.c.) tissue glucose measurement and s.c. infusion of monomeric insulin analogues was developed and evaluated in a simulation study. Glucose 44-51 insulin Homo sapiens 136-143 9700428-8 1998 In conclusion, the simulation results suggest that closed-loop control of glucose will be achievable using s.c. glucose measurement and s.c. insulin administration. Glucose 74-81 insulin Homo sapiens 141-148 9700430-1 1998 The Diabetes Advisory System (DIAS) is a model of human glucose metabolism which predicts hourly blood glucose concentrations and provides advice on insulin dose. Glucose 56-63 insulin Homo sapiens 149-156 9700431-2 1998 DIAS is based on a model of the human carbohydrate metabolism and is designed an interactive clinical tool, which can be used to predict the effects of changes in insulin dose or food intake on the blood glucose concentration in patients with insulin dependent diabetes. Glucose 204-211 insulin Homo sapiens 163-170 9625361-6 1998 RESULTS: With low glucose concentrations, at which glucose transport is rate-limiting, maximal insulin-induced lipogenesis was increased by 120% after GH treatment (P < 0.05), but the sensitivity to insulin (half-maximum effective hormone concentration) was unchanged. Glucose 18-25 insulin Homo sapiens 95-102 9650743-8 1998 Following training fasting plasma glucose and fasting plasma insulin were significantly reduced [Glucose: 5.9 (0.2) mmol x l(-1) vs. 5.3 (0.22) mmol x l(-1) (p < 0.05); Insulin 264.3 (53.8) rho x mol x l(-1) vs. 200.9 (30.1) rho x mol x l(-1), p=0.05]. Glucose 97-104 insulin Homo sapiens 61-68 9625361-6 1998 RESULTS: With low glucose concentrations, at which glucose transport is rate-limiting, maximal insulin-induced lipogenesis was increased by 120% after GH treatment (P < 0.05), but the sensitivity to insulin (half-maximum effective hormone concentration) was unchanged. Glucose 51-58 insulin Homo sapiens 95-102 15010702-8 1998 The insulin sensitivity effects of glimepiride have been demonstrated in vivo by increased glucose disposal rates in euglycemic clamp studies and in vitro by increased sensitivity and responsiveness of insulin-induced glucose uptake. Glucose 91-98 insulin Homo sapiens 4-11 15010702-8 1998 The insulin sensitivity effects of glimepiride have been demonstrated in vivo by increased glucose disposal rates in euglycemic clamp studies and in vitro by increased sensitivity and responsiveness of insulin-induced glucose uptake. Glucose 218-225 insulin Homo sapiens 4-11 15010702-8 1998 The insulin sensitivity effects of glimepiride have been demonstrated in vivo by increased glucose disposal rates in euglycemic clamp studies and in vitro by increased sensitivity and responsiveness of insulin-induced glucose uptake. Glucose 218-225 insulin Homo sapiens 202-209 15010702-9 1998 Moreover, glimepiride might stimulate insulin-mediated glucose utilization in hepatocytes. Glucose 55-62 insulin Homo sapiens 38-45 9660090-6 1998 The presence of hyperinsulinemia both basally and after glucose stimulation, with normal glycemia, in phosphate-depleted individuals suggests that this condition is associated with reduced insulin sensitivity. Glucose 56-63 insulin Homo sapiens 21-28 9622342-1 1998 OBJECTIVE: In differentiating human preadipocytes glucose uptake in the presence of insulin is a prerequisite for lipid accumulation. Glucose 50-57 insulin Homo sapiens 84-91 10771998-4 1998 In the non-diabetic children we investigated the early phase of insulin release after intravenous bolus of glucose and evaluated tolerance to oral glucose (OGTT). Glucose 107-114 insulin Homo sapiens 64-71 9622342-2 1998 The aim of this study was to characterize the insulin-regulated glucose transport system during and after differentiation. Glucose 64-71 insulin Homo sapiens 46-53 9622342-6 1998 On day 16, when cells have acquired the adipocyte phenotype, there was a 3-4-fold stimulation of glucose transport by insulin compared to basal rates, whereas basal glucose uptake was dramatically diminished. Glucose 97-104 insulin Homo sapiens 118-125 11273280-4 1998 Insulin release to glucose (IRG-insulinogenic index) in control group was 352 +/- 42 mu U/mg. Glucose 19-26 insulin Homo sapiens 0-7 9589675-6 1998 Although rates of baseline hepatic glucose production, GF, and GS were unchanged, the insulin-stimulated increment (delta) in Rd, GF, and GS remained markedly attenuated in the long-term rhGH-treated GHD adults [pretreatment: delta Rd 16.6 +/- 3.4, delta GF 3.0 +/- 1.2, delta GS 13.6 +/- 3.0 vs. 24 months of rhGH: delta Rd 17.2 +/- 3.3, delta GF 3.1 +/- 0.9, delta GS 14.1 +/- 2.5 vs. controls: delta Rd 42.6 +/- 4.3, delta GF 9.2 +/- 1.9, delta GS 35.9 +/- 4.5 mumol/kg fat free mass.min; P < 0.05-0.01 vs. controls]. Glucose 35-42 insulin Homo sapiens 86-93 9589675-7 1998 Additionally, there was a sustained reduction in the insulin-stimulated skeletal muscle glycogen synthase fractional velocity (pretreatment: 0.29 +/- 0.03 vs. 24 months of rhGH: 0.24 +/- 0.03 vs. controls: 0.48 +/- 0.04; both P < 0.05 vs. controls), which was accompanied by a sustained 44% decrease in baseline glycogen content and a 70% increase in baseline im glucose concentrations in the presence of low-to-normal glucose 6-phosphate levels and persisting euglycemia. Glucose 366-373 insulin Homo sapiens 53-60 9591749-2 1998 Glucosamine, a product of glucose flux through the hexosamine biosynthetic pathway (HBP), causes insulin resistance in peripheral tissues and has been shown to cause abnormal glucose-insulin secretion coupling, and thus has been implicated in the pathogenesis of glucose toxicity. Glucose 26-33 insulin Homo sapiens 97-104 9591739-1 1998 The presence of insulin resistance in 20 male nondiabetic patients with familial combined hyperlipidemia (FCH) and 20 controls of similar age and body mass index (BMI) was investigated using the minimal model method modified by the administration of insulin and an oral glucose tolerance test. Glucose 270-277 insulin Homo sapiens 16-23 9609124-2 1998 The decrease in insulin-mediated peripheral glucose uptake in NIDDM patients can be localized to defects in insulin action on glucose transport in skeletal muscle. Glucose 44-51 insulin Homo sapiens 16-23 9609124-2 1998 The decrease in insulin-mediated peripheral glucose uptake in NIDDM patients can be localized to defects in insulin action on glucose transport in skeletal muscle. Glucose 44-51 insulin Homo sapiens 108-115 9609124-2 1998 The decrease in insulin-mediated peripheral glucose uptake in NIDDM patients can be localized to defects in insulin action on glucose transport in skeletal muscle. Glucose 126-133 insulin Homo sapiens 16-23 9609124-2 1998 The decrease in insulin-mediated peripheral glucose uptake in NIDDM patients can be localized to defects in insulin action on glucose transport in skeletal muscle. Glucose 126-133 insulin Homo sapiens 108-115 9660977-1 1998 The control of glucose homeostasis by insulin requires, in addition to the glucose-induced insulin release, a highly dynamic control of insulin biosynthesis. Glucose 15-22 insulin Homo sapiens 38-45 9609124-5 1998 Impaired insulin-stimulated GLUT4 translocation and glucose transport in NIDDM skeletal muscle is associated with reduced insulin-stimulated IRS-1 tyrosine phosphorylation and PI3-kinase activity. Glucose 52-59 insulin Homo sapiens 122-129 9660977-2 1998 Although elevated glucose concentrations have been shown to trigger insulin biosynthesis at the levels of transcription and translation, the molecular mechanisms underlying the immediate transcriptional control are poorly understood. Glucose 18-25 insulin Homo sapiens 68-75 9609124-7 1998 Altered glycemia may contribute to decreased insulin-mediated glucose transport in skeletal muscle from NIDDM patients. Glucose 62-69 insulin Homo sapiens 45-52 9660977-3 1998 By investigating signal transduction pathways involved in the "glucose-dependent" transcriptional control, thereby analyzing endogenous (prepro)insulin mRNA levels and monitoring on-line insulin promoter-driven GFP expression, we provide, for the first time, evidence that physiologically stimulated insulin secretion from the pancreatic beta cell promotes insulin biosynthesis by enhancing insulin gene transcription in an autocrine manner. Glucose 63-70 insulin Homo sapiens 144-151 9660977-3 1998 By investigating signal transduction pathways involved in the "glucose-dependent" transcriptional control, thereby analyzing endogenous (prepro)insulin mRNA levels and monitoring on-line insulin promoter-driven GFP expression, we provide, for the first time, evidence that physiologically stimulated insulin secretion from the pancreatic beta cell promotes insulin biosynthesis by enhancing insulin gene transcription in an autocrine manner. Glucose 63-70 insulin Homo sapiens 187-194 9660977-3 1998 By investigating signal transduction pathways involved in the "glucose-dependent" transcriptional control, thereby analyzing endogenous (prepro)insulin mRNA levels and monitoring on-line insulin promoter-driven GFP expression, we provide, for the first time, evidence that physiologically stimulated insulin secretion from the pancreatic beta cell promotes insulin biosynthesis by enhancing insulin gene transcription in an autocrine manner. Glucose 63-70 insulin Homo sapiens 187-194 9660977-3 1998 By investigating signal transduction pathways involved in the "glucose-dependent" transcriptional control, thereby analyzing endogenous (prepro)insulin mRNA levels and monitoring on-line insulin promoter-driven GFP expression, we provide, for the first time, evidence that physiologically stimulated insulin secretion from the pancreatic beta cell promotes insulin biosynthesis by enhancing insulin gene transcription in an autocrine manner. Glucose 63-70 insulin Homo sapiens 187-194 9660977-3 1998 By investigating signal transduction pathways involved in the "glucose-dependent" transcriptional control, thereby analyzing endogenous (prepro)insulin mRNA levels and monitoring on-line insulin promoter-driven GFP expression, we provide, for the first time, evidence that physiologically stimulated insulin secretion from the pancreatic beta cell promotes insulin biosynthesis by enhancing insulin gene transcription in an autocrine manner. Glucose 63-70 insulin Homo sapiens 187-194 9609124-8 1998 We have shown that insulin-stimulated glucose transport is normalized in vitro in the presence of euglycemia, but not in the presence of hyperglycemia. Glucose 38-45 insulin Homo sapiens 19-26 9609124-9 1998 Thus, the circulating level of glucose may independently regulate insulin stimulated glucose transport in skeletal muscle from NIDDM patients via a down regulation of the insulin signaling cascade. Glucose 31-38 insulin Homo sapiens 66-73 9609124-9 1998 Thus, the circulating level of glucose may independently regulate insulin stimulated glucose transport in skeletal muscle from NIDDM patients via a down regulation of the insulin signaling cascade. Glucose 31-38 insulin Homo sapiens 171-178 9609124-9 1998 Thus, the circulating level of glucose may independently regulate insulin stimulated glucose transport in skeletal muscle from NIDDM patients via a down regulation of the insulin signaling cascade. Glucose 85-92 insulin Homo sapiens 66-73 9609124-9 1998 Thus, the circulating level of glucose may independently regulate insulin stimulated glucose transport in skeletal muscle from NIDDM patients via a down regulation of the insulin signaling cascade. Glucose 85-92 insulin Homo sapiens 171-178 9609127-6 1998 Studies in muscle, the primary site for insulin-mediated glucose disposal, have shown that the levels of PC-1 in this tissue are inversely correlated to insulin action both in vivo and in vitro. Glucose 57-64 insulin Homo sapiens 40-47 9642681-1 1998 Phosphoinositolglycan molecules isolated from insulin-sensitive mammalian tissues have been demonstrated in numerous in vitro studies to exert partial insulin-mimetic activity on glucose and lipid metabolism in insulin-sensitive cells. Glucose 179-186 insulin Homo sapiens 46-53 9642681-1 1998 Phosphoinositolglycan molecules isolated from insulin-sensitive mammalian tissues have been demonstrated in numerous in vitro studies to exert partial insulin-mimetic activity on glucose and lipid metabolism in insulin-sensitive cells. Glucose 179-186 insulin Homo sapiens 151-158 9642681-1 1998 Phosphoinositolglycan molecules isolated from insulin-sensitive mammalian tissues have been demonstrated in numerous in vitro studies to exert partial insulin-mimetic activity on glucose and lipid metabolism in insulin-sensitive cells. Glucose 179-186 insulin Homo sapiens 151-158 9575818-1 1998 The minimal model is widely used to evaluate insulin action on glucose disappearance from frequently sampled intravenous glucose tolerance tests (FSIGT). Glucose 63-70 insulin Homo sapiens 45-52 9785419-0 1998 [Effects of the hormonal activity of the thyroid gland and insulin system on the glucose level in man in the North]. Glucose 81-88 insulin Homo sapiens 59-66 9583592-8 1998 In three cases glucose tolerance test was performed revealing a high level of insulin between the first and third hour of loading. Glucose 15-22 insulin Homo sapiens 78-85 9571809-4 1998 The insulinotropic effect of GLP-1 is preserved in patients with non insulin-dependent diabetes mellitus (NIDDM) and, because GLP-1 also inhibits glucagon secretion, it effectively lowers blood glucose in such, and given as an intravenous infusion it may completely normalise blood glucose. Glucose 194-201 insulin Homo sapiens 4-11 9571809-4 1998 The insulinotropic effect of GLP-1 is preserved in patients with non insulin-dependent diabetes mellitus (NIDDM) and, because GLP-1 also inhibits glucagon secretion, it effectively lowers blood glucose in such, and given as an intravenous infusion it may completely normalise blood glucose. Glucose 282-289 insulin Homo sapiens 4-11 9571809-5 1998 Furthermore, because its actions on insulin and glucagon secretion are dependent on the blood glucose levels it will not cause hypoglycemia. Glucose 94-101 insulin Homo sapiens 36-43 9588451-2 1998 Insulin response to a 75-g oral glucose load was evaluated in healthy nondiabetic Caucasians with first-degree family history of diabetes (relatives, n = 55) and those without family history (nonrelatives, n = 33). Glucose 32-39 insulin Homo sapiens 0-7 9588452-5 1998 Therefore, we examined, cross-sectionally, the relationship of insulin sensitivity (S(I) x 10(-4) min x microU(-1) x ml(-1)), estimated by a frequently sampled intravenous glucose tolerance test and the minimal model and fasting plasma insulin concentration, to microalbuminuria (albumin-to-creatinine ratio > or = 2 mg/mmol) in 982 nondiabetic subjects aged 40-69 years. Glucose 172-179 insulin Homo sapiens 63-70 9588452-11 1998 Our results suggest a relationship between insulin resistance and microalbuminuria in nondiabetic subjects that is partially dependent on blood pressure, glucose levels, and obesity. Glucose 154-161 insulin Homo sapiens 43-50 9589225-3 1998 Body composition changes were assessed by dual energy x-ray absorptiometry and insulin secretory changes were measured by insulin response to intravenous glucose before and after weight loss. Glucose 154-161 insulin Homo sapiens 79-86 9589225-3 1998 Body composition changes were assessed by dual energy x-ray absorptiometry and insulin secretory changes were measured by insulin response to intravenous glucose before and after weight loss. Glucose 154-161 insulin Homo sapiens 122-129 9575818-1 1998 The minimal model is widely used to evaluate insulin action on glucose disappearance from frequently sampled intravenous glucose tolerance tests (FSIGT). Glucose 121-128 insulin Homo sapiens 45-52 9518395-11 1998 INTERVENTIONS: 1) Intensive therapy with 3 or more insulin injections daily or continuous subcutaneous infusion of insulin, guided by 4 or more glucose tests per day or 2) conventional therapy with 1 or 2 insulin injections daily. Glucose 144-151 insulin Homo sapiens 115-122 9579452-12 1998 This is due to elevated insulin resistance shown by a low insulin/glucose quotient at 1 hour. Glucose 66-73 insulin Homo sapiens 24-31 9607376-2 1998 Alterations in insulin-mediated glucose disposal were assessed by means of the insulin suppression test. Glucose 32-39 insulin Homo sapiens 15-22 9607376-6 1998 The insulin suppression test revealed the existence of marked differences in insulin-mediated glucose uptake between salt sensitive and salt resistant hypertensives. Glucose 94-101 insulin Homo sapiens 4-11 9607376-6 1998 The insulin suppression test revealed the existence of marked differences in insulin-mediated glucose uptake between salt sensitive and salt resistant hypertensives. Glucose 94-101 insulin Homo sapiens 77-84 9607376-7 1998 Much higher steady-state glucose values (nanomoles of glucose/ liter) were obtained during the insulin suppression test in salt sensitive than in salt-resistant hypertensives (7.4+/-1.6 v 3.5+/-0.1 under low salt; and 12.5+/-1.1 v 4.3+/-0.1 under high salt intake). Glucose 25-32 insulin Homo sapiens 95-102 9607376-7 1998 Much higher steady-state glucose values (nanomoles of glucose/ liter) were obtained during the insulin suppression test in salt sensitive than in salt-resistant hypertensives (7.4+/-1.6 v 3.5+/-0.1 under low salt; and 12.5+/-1.1 v 4.3+/-0.1 under high salt intake). Glucose 54-61 insulin Homo sapiens 95-102 9607376-8 1998 The product of glucose times insulin obtained at steady state during low and high salt intakes were 2.5 and 5 times greater, respectively, in salt sensitive than in salt resistant hypertensives. Glucose 15-22 insulin Homo sapiens 29-36 9607376-9 1998 Therefore, the impairment in insulin-mediated glucose disposal observed in salt sensitive hypertensives was present both under low salt (60 to 70 mEq/day) and high salt intake (300 mEq/day). Glucose 46-53 insulin Homo sapiens 29-36 9607376-11 1998 These results suggest that untreated salt sensitive hypertensives have a considerable impairment in insulin-mediated glucose disposal because of a state of insulin resistance. Glucose 117-124 insulin Homo sapiens 100-107 9607376-11 1998 These results suggest that untreated salt sensitive hypertensives have a considerable impairment in insulin-mediated glucose disposal because of a state of insulin resistance. Glucose 117-124 insulin Homo sapiens 156-163 10205319-7 1998 Endogenous glucose production was higher after surgery and the difference was significant during low insulin infusion rates in both groups (P < 0.05). Glucose 11-18 insulin Homo sapiens 101-108 10205319-8 1998 The supressibility of endogenous glucose production by the two step insulin infusion was similar pre-and postoperatively in both groups. Glucose 33-40 insulin Homo sapiens 68-75 10205319-9 1998 At the high insulin infusion rate postoperatively, whole body glucose disposal was more reduced in the fasted group (-49 +/- 6% vs -26 +/- 8%, P < 0.05 vs drink). Glucose 62-69 insulin Homo sapiens 12-19 10205319-10 1998 Furthermore, during high insulin infusion rates, glucose oxidation decreased postoperatively only in the fasted group (P < 0. Glucose 49-56 insulin Homo sapiens 25-32 9568681-8 1998 The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. Glucose 125-132 insulin Homo sapiens 18-25 9568681-8 1998 The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. Glucose 125-132 insulin Homo sapiens 106-113 9571331-7 1998 RESULTS: Fasting plasma glucose was a significant indicator of HbA1c > 8.0%, both in the whole group and in subgroups for diet, sulfonylureas, and insulin; the corresponding areas under the ROC curve were 0.87, 0.90, 0.87, and 0.84, respectively (all P < 0.0001). Glucose 24-31 insulin Homo sapiens 150-157 9571331-9 1998 Random plasma glucose was also a good indicator of HbA1c > 8.0%, both in the whole group and in subgroups for diet, sulfonylureas, and insulin; the corresponding areas under the ROC curve were 0.85, 0.91, 0.85, and 0.77, respectively (all P < 0.0001). Glucose 14-21 insulin Homo sapiens 138-145 9592635-8 1998 The correction of weight excess after successful gastroplasty fully reverses the abnormalities of insulin secretion, clearance and action on glucose metabolism present in markedly obese non-diabetic patients, and allows interruption or reduction of insulin therapy and antidiabetic oral agents in most obese diabetic patients. Glucose 141-148 insulin Homo sapiens 98-105 9615904-0 1998 Relationship between insulin"s haemodynamic effects and insulin-mediated glucose uptake. Glucose 73-80 insulin Homo sapiens 21-28 9615904-0 1998 Relationship between insulin"s haemodynamic effects and insulin-mediated glucose uptake. Glucose 73-80 insulin Homo sapiens 56-63 9615904-3 1998 METHODS: We investigated, using the euglycaemic clamp technique, the relationship between insulin-mediated glucose uptake and insulin-induced changes in leg blood flow and cardiac index in 13 healthy subjects. Glucose 107-114 insulin Homo sapiens 90-97 9615904-3 1998 METHODS: We investigated, using the euglycaemic clamp technique, the relationship between insulin-mediated glucose uptake and insulin-induced changes in leg blood flow and cardiac index in 13 healthy subjects. Glucose 107-114 insulin Homo sapiens 126-133 9615904-8 1998 The insulin-mediated glucose disposal and the increases in leg blood flow were not correlated during the second hour (r = 0.21, P = 0.51) but showed a strong correlation during the fourth hour of the clamp (r = 0.88, P < 0.001). Glucose 21-28 insulin Homo sapiens 4-11 9615904-9 1998 Insulin-mediated glucose disposal was not correlated with the increases in cardiac index. Glucose 17-24 insulin Homo sapiens 0-7 9615904-10 1998 CONCLUSION: Thus, insulin-mediated muscle blood flow may be an important contributor to glucose uptake during sustained exogenous hyperinsulinaemia aiming at physiological insulin levels. Glucose 88-95 insulin Homo sapiens 18-25 9615904-10 1998 CONCLUSION: Thus, insulin-mediated muscle blood flow may be an important contributor to glucose uptake during sustained exogenous hyperinsulinaemia aiming at physiological insulin levels. Glucose 88-95 insulin Homo sapiens 135-142 9700469-2 1998 We examined patients with NIDDM to find whether maintaining plasma FFA levels in the fasting range with a euglycemic hyperinsulinemic clamp combined with an oral glucose load (clamp OGL) would affect insulin-mediated peripheral glucose uptake (PGU) and splanchnic glucose uptake (SGU). Glucose 228-235 insulin Homo sapiens 122-129 9570959-1 1998 Glucokinase plays an important role in regulating insulin secretion in response to changes in blood glucose levels. Glucose 100-107 insulin Homo sapiens 50-57 9623635-4 1998 Glucose tolerance was normal in all, but insulin-stimulated glucose uptake (Rd) was diminished in the relatives (p < 0.001). Glucose 60-67 insulin Homo sapiens 41-48 9623638-4 1998 In order to assess the role of glucose changes on calciuric response to insulin and oxalate excretion, hypoglycemia induced by insulin (hypo) and hyperglycemia induced by oral glucose load (hyper) were studied in 7 healthy subjects on two separate days. Glucose 31-38 insulin Homo sapiens 72-79 9684435-1 1998 In Type I diabetes, conclusive evidence exists that intensive insulin strategies can achieve normal or near normal blood glucose levels and, as a result, reduce the risk of major complications and produce major benefits in years of life, years of sight, and years free from end-stage renal disease and amputation. Glucose 121-128 insulin Homo sapiens 62-69 9543131-7 1998 glucose tolerance test) for their degree of insulin resistance (euglycemic hyperinsulinemic clamp) compared with controls (P < 0.05). Glucose 0-7 insulin Homo sapiens 44-51 9543147-0 1998 Effect of glucose on production and release of proinsulin conversion products by cultured human islets. Glucose 10-17 insulin Homo sapiens 47-57 9543147-3 1998 During the first hour following labeling of newly synthesized proteins, PI represented the main newly formed hormonal peptide in the medium; its release was stimulated 2-fold over the basal level by 20 mmol/L glucose. Glucose 209-216 insulin Homo sapiens 72-74 9543147-4 1998 During the second hour, newly synthesized hormone was mainly released as insulin, with 10- to 20-fold higher rates at 20 mmol/L glucose. Glucose 128-135 insulin Homo sapiens 73-80 9543147-5 1998 Prolonged preculture of the islets at 20 mmol/L glucose did not delay PI conversion, but markedly increased the release of newly formed PI, des(31,32)-PI, and insulin at both low and high glucose levels. Glucose 48-55 insulin Homo sapiens 136-138 9543147-5 1998 Prolonged preculture of the islets at 20 mmol/L glucose did not delay PI conversion, but markedly increased the release of newly formed PI, des(31,32)-PI, and insulin at both low and high glucose levels. Glucose 48-55 insulin Homo sapiens 136-138 9543147-5 1998 Prolonged preculture of the islets at 20 mmol/L glucose did not delay PI conversion, but markedly increased the release of newly formed PI, des(31,32)-PI, and insulin at both low and high glucose levels. Glucose 48-55 insulin Homo sapiens 159-166 9607696-4 1998 Insulin sensitivity index values (glucose disposal/serum insulin concentration during the clamp) were lower in the familial hypertension group than in the control group, but the two groups did not differ in Na+-Li+-countertransport, or in the platelet cytosolic free Ca2+ concentration which was correlated to the waist: hip circumference ratio in both groups (r = 0.38 and r = 0.49, respectively). Glucose 34-41 insulin Homo sapiens 0-7 9607697-3 1998 Multiple logistic regression analysis adjusted for glucose tolerance status, serum lipids, exercise behaviour and alcohol consumption shows that the odds ratios of one unit (mU/l) increase in the baseline fasting insulin concentration were 1.13 (95% confidence interval 1.00-1.28) for the 2-year incidence of hypertension in subjects with IGT at baseline. Glucose 51-58 insulin Homo sapiens 213-220 9627143-11 1998 Patients with a high TC/HDL-C ratio were also significantly (P < 0.05-0.001) more insulin resistant, glucose intolerant with a greater plasma insulin response to oral glucose, and hypertriglyceridemic. Glucose 104-111 insulin Homo sapiens 145-152 9642928-8 1998 We are using FDG to evaluate insulin resistance during insulin clamp in patients with diabetes mellitus by measuring glucose utilization rate of myocardium and skeletal muscle. Glucose 117-124 insulin Homo sapiens 29-36 9642928-8 1998 We are using FDG to evaluate insulin resistance during insulin clamp in patients with diabetes mellitus by measuring glucose utilization rate of myocardium and skeletal muscle. Glucose 117-124 insulin Homo sapiens 55-62 9550539-7 1998 Insulin and the insulin to glucose ratio increased with age in obese children, whereas there were slight changes in non-obese children. Glucose 27-34 insulin Homo sapiens 16-23 29508806-2 1998 Fasting blood glucose was found to be low on multiple occasions along with raised insulin levels. Glucose 14-21 insulin Homo sapiens 82-89 9540949-8 1998 Fewer subjects in the low-carbohydrate group required the addition of insulin for glucose control (P < .047; relative risk [RR] 0.14; 95% confidence interval [CI] 0.02, 1.00). Glucose 82-89 insulin Homo sapiens 70-77 9730393-5 1998 Insulin sensitivity in the two treated subjects, as well as in 24 healthy volunteers constituting the control group, was assessed by euglycemic hyperinsulinemic clamp and indirect calorimetry, obtaining total end-clamp glucose uptake (M) and end-clamp glucose oxidation (ECGO) rates. Glucose 219-226 insulin Homo sapiens 0-7 9730393-5 1998 Insulin sensitivity in the two treated subjects, as well as in 24 healthy volunteers constituting the control group, was assessed by euglycemic hyperinsulinemic clamp and indirect calorimetry, obtaining total end-clamp glucose uptake (M) and end-clamp glucose oxidation (ECGO) rates. Glucose 252-259 insulin Homo sapiens 0-7 9730393-7 1998 Fasting plasma glucose levels had decreased from above 300 (under daily repeated subcutaneous injections of insulin) to 80-100 mg/dl (without administration of insulin or oral hypoglycemic agents). Glucose 15-22 insulin Homo sapiens 108-115 9820107-8 1998 Eleven subjects were obese, four patients suffered from hypertension, another six from systolic hypertension, in eight patients a significantly elevated C-peptide level on fasting was found, in the majority of patients an elevated, or protracted response of C-peptide and insulin to orally administered glucose was found. Glucose 303-310 insulin Homo sapiens 153-162 9549368-1 1998 Long-term intensified insulin therapy composing of multiple insulin injection and self-blood glucose monitoring enables glycemic control of insulin-requiring diabetics. Glucose 93-100 insulin Homo sapiens 22-29 9510144-10 1998 Insulin secretion in response to square-wave increases in glucose concentration to 11 mM was inhibited dose dependently by CGRP; at 10(-8) M the insulin output decreased by 72+/-9% (n = 6). Glucose 58-65 insulin Homo sapiens 0-7 9510144-10 1998 Insulin secretion in response to square-wave increases in glucose concentration to 11 mM was inhibited dose dependently by CGRP; at 10(-8) M the insulin output decreased by 72+/-9% (n = 6). Glucose 58-65 insulin Homo sapiens 145-152 12496910-11 1998 The results suggest that BPH is a facet of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinemia as patients with the metabolic syndrome. Glucose 161-168 insulin Homo sapiens 144-151 9473490-2 1998 Introduction of IGF-II during perifusion of the cells with 20 mM glucose abolished glucose-induced insulin release. Glucose 83-90 insulin Homo sapiens 99-106 9473490-3 1998 Concomitant addition of IGF-II with 20 mM glucose caused a complete inhibition of insulin release. Glucose 42-49 insulin Homo sapiens 82-89 9519717-5 1998 In the isolated perfused pancreas, insulin response to glucose elevation (5-11 mmol/l) was clearly present, although significantly reduced with respect to controls (P < 0.01). Glucose 55-62 insulin Homo sapiens 35-42 9519720-1 1998 The aim of this study was to test the hypothesis that plasma leptin concentrations contributed to the pathophysiology of NIDDM by decreasing both insulin-mediated glucose disposal and glucose-stimulated insulin secretion. Glucose 163-170 insulin Homo sapiens 146-153 9519720-1 1998 The aim of this study was to test the hypothesis that plasma leptin concentrations contributed to the pathophysiology of NIDDM by decreasing both insulin-mediated glucose disposal and glucose-stimulated insulin secretion. Glucose 184-191 insulin Homo sapiens 203-210 9519720-3 1998 Differences in insulin-mediated glucose disposal were determined by comparing the steady-state plasma glucose (SSPG) concentrations attained at the end of a 180-min constant infusion of somatostatin, glucose, and insulin, while comparisons of glucose-stimulated insulin secretion were based on the incremental increase in insulin concentration 30 min after an oral glucose challenge (deltaIns) as compared with the fasting value. Glucose 32-39 insulin Homo sapiens 15-22 9539996-0 1998 Insulin secretion in normal glucose-tolerant relatives of type 2 diabetic subjects. Glucose 28-35 insulin Homo sapiens 0-7 9539996-11 1998 CONCLUSIONS: Normal glucose-tolerant first-degree relatives of type 2 diabetic subjects have a decreased second-phase insulin release, compared with matched control subjects. Glucose 20-27 insulin Homo sapiens 118-125 9597380-0 1998 Non-insulin-mediated glucose uptake in several insulin-resistant states in the postabsortive period. Glucose 21-28 insulin Homo sapiens 4-11 9597380-0 1998 Non-insulin-mediated glucose uptake in several insulin-resistant states in the postabsortive period. Glucose 21-28 insulin Homo sapiens 47-54 9575839-9 1998 These observations may explain inconsistencies between the results of tolbutamide and insulin injection in the frequently sampled intravenous glucose tolerance test and call for further study of insulin- vs. tolbutamide-modified frequently sampled intravenous glucose tolerance tests in the assessment of the insulin sensitivity and glucose effectiveness indexes. Glucose 142-149 insulin Homo sapiens 86-93 9527077-0 1998 Usefulness of enhanced insulin secretion during an oral glucose tolerance test as a predictor of restenosis after direct percutaneous transluminal coronary angioplasty during acute myocardial infarction in patients without diabetes mellitus. Glucose 56-63 insulin Homo sapiens 23-30 9527077-4 1998 These results suggest that enhanced insulin secretion in response to glucose plays an important role in the development of restenosis after direct PTCA in non-diabetic patients, which may be through the direct action of insulin on smooth muscle cells of the coronary artery. Glucose 69-76 insulin Homo sapiens 36-43 9527077-4 1998 These results suggest that enhanced insulin secretion in response to glucose plays an important role in the development of restenosis after direct PTCA in non-diabetic patients, which may be through the direct action of insulin on smooth muscle cells of the coronary artery. Glucose 69-76 insulin Homo sapiens 220-227 9497382-2 1998 Protein kinase B/Akt (PKB/Akt), a member of the PKA/PKC serine/threonine kinase family, functions downstream from phosphatidylinositol 3"-kinase (PI3K) in mediating effects of insulin on glucose transport and glycogen synthesis. Glucose 187-194 insulin Homo sapiens 176-183 9514876-0 1998 4-Bromocrotonic acid enhances basal but inhibits insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 68-75 insulin Homo sapiens 49-56 9514876-5 1998 Thus these results seem to suggest that Br-C4 has opposite effect on basal and insulin-stimulated glucose transport by a mechanism other than its inhibition of fatty acid oxidation. Glucose 98-105 insulin Homo sapiens 79-86 9531829-1 1998 Maturity-onset diabetes of the young (MODY) is a clinically and genetically heterogenous disorder characterized by autosomal dominant inheritance with onset usually before 25 years of age, and a primary defect in glucose-stimulated insulin secretion. Glucose 213-220 insulin Homo sapiens 232-239 9496984-6 1998 MAIN OUTCOME MEASURE: Insulin sensitivity as measured by an intravenous glucose tolerance test. Glucose 72-79 insulin Homo sapiens 22-29 9497160-1 1998 It is widely held that although obesity and type 2 diabetes are polygenic in origin, the primary defect causing both conditions is insulin resistance, which in turn gives rise to a constellation of other abnormalities, including hyperinsulinemia, dyslipidemia, glucose intolerance, and (in the genetically predisposed) frank hyperglycemia. Glucose 261-268 insulin Homo sapiens 131-138 9525530-1 1998 Factor analysis has previously identified four independent factors that characterize the insulin resistance syndrome in women, interpreted as 1) weight/waist, 2) lipids, 3) insulin/glucose, and 4) systolic and diastolic blood pressure. Glucose 181-188 insulin Homo sapiens 89-96 9530121-2 1998 Insulin sensitivity was assessed by a frequently sampled intravenous glucose tolerance test to determine the insulin sensitivity index (SI) after 1 wk each of low- (20 mmol.l-1.day-1) and high- (200 mmol.l-1.day-1) sodium diets in 21 older (63 +/- 2 yr) hypertensives. Glucose 69-76 insulin Homo sapiens 0-7 9530129-1 1998 An important signal involved in glucose-stimulated insulin secretion is transduced through the action of a lysosomal acid, glucan 1,4-alpha-glucosidase. Glucose 32-39 insulin Homo sapiens 51-58 9530129-9 1998 Hence, Ca(2+)-induced changes in acid glucan 1,4-alpha-glucosidase activity were intimately coupled to similar changes in Ca(2+)-glucose-induced insulin release. Glucose 129-136 insulin Homo sapiens 145-152 9558446-4 1998 However, proinsulin in hypothyroid patients was only rarely reported, and the difference was only demonstrated after glucose stimulation-there was a greater response of proinsulin secretion after thyroxine therapy-and the basal fasting proinsulin level was not different after therapy. Glucose 117-124 insulin Homo sapiens 169-179 9558446-4 1998 However, proinsulin in hypothyroid patients was only rarely reported, and the difference was only demonstrated after glucose stimulation-there was a greater response of proinsulin secretion after thyroxine therapy-and the basal fasting proinsulin level was not different after therapy. Glucose 117-124 insulin Homo sapiens 169-179 9514414-5 1998 Hyperinsulinemia, defined as a fasting insulin > or =95th percentile among nonobese men with normal glucose tolerance and no diabetic history or medication use, was observed in 22% of the population. Glucose 103-110 insulin Homo sapiens 5-12 9578818-4 1998 MEASUREMENTS: In the whole group of subjects plasma sex hormones, leptin and insulin concentrations were determined, body fat content assessed by bioimpedance analysis, body fat distribution evaluated and insulin-mediated glucose uptake measured by euglycemic hyperinsulinemic glucose. Glucose 222-229 insulin Homo sapiens 205-212 9590566-9 1998 There is evidence both for and against the existence of a functional relationship between insulin-mediated glucose uptake (insulin sensitivity) and insulin-mediated vasodilation (which can be regarded as a surrogate measure for endothelial function). Glucose 107-114 insulin Homo sapiens 90-97 9590566-9 1998 There is evidence both for and against the existence of a functional relationship between insulin-mediated glucose uptake (insulin sensitivity) and insulin-mediated vasodilation (which can be regarded as a surrogate measure for endothelial function). Glucose 107-114 insulin Homo sapiens 123-130 9590566-9 1998 There is evidence both for and against the existence of a functional relationship between insulin-mediated glucose uptake (insulin sensitivity) and insulin-mediated vasodilation (which can be regarded as a surrogate measure for endothelial function). Glucose 107-114 insulin Homo sapiens 123-130 9590566-11 1998 If substrate delivery is the rate-limiting step for insulin-mediated glucose uptake (in other words, if skeletal muscle blood flow is a determinant of glucose uptake), then endothelial dysfunction, resulting in a relative inability of mediators, including insulin, to stimulate muscle blood flow, may be the underlying mechanism accounting for the association of atherosclerosis and other cardiovascular disorders with insulin resistance. Glucose 69-76 insulin Homo sapiens 52-59 9590566-11 1998 If substrate delivery is the rate-limiting step for insulin-mediated glucose uptake (in other words, if skeletal muscle blood flow is a determinant of glucose uptake), then endothelial dysfunction, resulting in a relative inability of mediators, including insulin, to stimulate muscle blood flow, may be the underlying mechanism accounting for the association of atherosclerosis and other cardiovascular disorders with insulin resistance. Glucose 151-158 insulin Homo sapiens 52-59 9590566-18 1998 A complex interaction between endothelial dysfunction, abnormal skeletal muscle blood flow and reduced insulin-mediated glucose uptake may be central to the link between insulin resistance, blood pressure, impaired glucose tolerance and the risk of cardiovascular disease. Glucose 120-127 insulin Homo sapiens 103-110 9590566-18 1998 A complex interaction between endothelial dysfunction, abnormal skeletal muscle blood flow and reduced insulin-mediated glucose uptake may be central to the link between insulin resistance, blood pressure, impaired glucose tolerance and the risk of cardiovascular disease. Glucose 120-127 insulin Homo sapiens 170-177 9519735-6 1998 Acute insulin responses to arginine, glucose, and GPAIS were significantly reduced after islet transplantation in both study groups. Glucose 37-44 insulin Homo sapiens 6-13 9519739-0 1998 Palmitate and myristate selectively mimic the effect of glucose in augmenting insulin release in the absence of extracellular Ca2+. Glucose 56-63 insulin Homo sapiens 78-85 9519739-1 1998 Under Ca2+-free conditions, activation of the pancreatic beta-cell with forskolin and 12-O-tetradecanoylphorbol 13-acetate (TPA) is permissive for the augmentation of insulin release by glucose and other nutrients. Glucose 186-193 insulin Homo sapiens 167-174 9519739-2 1998 The ability of fatty acids to mimic the effect of glucose and thereby augment insulin secretion in the absence of extracellular Ca2+ is the focus of the present study. Glucose 50-57 insulin Homo sapiens 78-85 9519739-8 1998 The results suggest that the mechanism underlying the Ca2+-independent augmentation of insulin release by glucose and other nutrients involves the proposed malonyl-CoA/long-chain acyl-CoA pathway with specificity for myristoyl- and palmitoyl-CoA esters and/or their derivatives. Glucose 106-113 insulin Homo sapiens 87-94 9519743-4 1998 We conclude that insulin resistance in obesity can be mostly attributed to impairment of insulin-stimulated muscle glycogen synthesis due to a defect in glucose transport and/or phosphorylation activity. Glucose 153-160 insulin Homo sapiens 17-24 9519744-1 1998 NIDDM and obesity are characterized by decreased insulin-stimulated glucose uptake in muscle. Glucose 68-75 insulin Homo sapiens 49-56 9519744-8 1998 In response to 240 mU insulin, leg glucose uptake was similar in all of the groups. Glucose 35-42 insulin Homo sapiens 22-29 9519756-9 1998 Consistent with this observation, the relationship between the ACE polymorphism and the insulin response to a glucose load was significantly heterogeneous between the AGA and SGA groups (P < 0.05); this was due to a tendency for ACE II individuals in the SGA group to exhibit increased 30-min plasma insulin levels (P < 0.05). Glucose 110-117 insulin Homo sapiens 88-95 9519756-9 1998 Consistent with this observation, the relationship between the ACE polymorphism and the insulin response to a glucose load was significantly heterogeneous between the AGA and SGA groups (P < 0.05); this was due to a tendency for ACE II individuals in the SGA group to exhibit increased 30-min plasma insulin levels (P < 0.05). Glucose 110-117 insulin Homo sapiens 303-310 9545125-0 1998 Reproducibility and comparability of insulin sensitivity indices measured by stable-label intravenous glucose tolerance test. Glucose 102-109 insulin Homo sapiens 37-44 9617535-6 1998 Recent developments in atherosclerosis research support the introduction of progestogens such as desogestrel that allow the estrogenic increase in high density lipoprotein levels to persist and that may cause less of an elevation in plasma insulin responses to glucose. Glucose 261-268 insulin Homo sapiens 240-247 9649951-11 1998 CONCLUSION: The addition of a sulfonylurea (glipizide) to insulin therapy in patients with insulin-requiring type 2 diabetes mellitus taking large doses of insulin results in a rapid and substantial improvement in glucose control despite a significant reduction in insulin dose. Glucose 214-221 insulin Homo sapiens 58-65 9649951-11 1998 CONCLUSION: The addition of a sulfonylurea (glipizide) to insulin therapy in patients with insulin-requiring type 2 diabetes mellitus taking large doses of insulin results in a rapid and substantial improvement in glucose control despite a significant reduction in insulin dose. Glucose 214-221 insulin Homo sapiens 91-98 9649951-11 1998 CONCLUSION: The addition of a sulfonylurea (glipizide) to insulin therapy in patients with insulin-requiring type 2 diabetes mellitus taking large doses of insulin results in a rapid and substantial improvement in glucose control despite a significant reduction in insulin dose. Glucose 214-221 insulin Homo sapiens 91-98 9649951-11 1998 CONCLUSION: The addition of a sulfonylurea (glipizide) to insulin therapy in patients with insulin-requiring type 2 diabetes mellitus taking large doses of insulin results in a rapid and substantial improvement in glucose control despite a significant reduction in insulin dose. Glucose 214-221 insulin Homo sapiens 91-98 9492058-4 1998 Moreover, TNF-alpha caused an insulin resistance on the insulin-induced glucose uptake in brown adipocytes. Glucose 72-79 insulin Homo sapiens 30-37 9492058-4 1998 Moreover, TNF-alpha caused an insulin resistance on the insulin-induced glucose uptake in brown adipocytes. Glucose 72-79 insulin Homo sapiens 56-63 9539300-3 1998 Compared with baseline values, glucose utilization was markedly enhanced at 6 months using the two-step euglycaemic-hyperinsulinaemic clamp to measure changes in insulin sensitivity (2.56 +/- 0.32 vs 4.68 +/- 0.49 mg/kg per min, P = 0.0001, when 40 mU insulin/m2 per min was infused, and 6.48 +/- 0.58 vs 9.84 +/- 0.72 mg/kg per min, P = 0.0002, when 400 mU insulin insulin/m2 per min was infused). Glucose 31-38 insulin Homo sapiens 121-128 9539300-3 1998 Compared with baseline values, glucose utilization was markedly enhanced at 6 months using the two-step euglycaemic-hyperinsulinaemic clamp to measure changes in insulin sensitivity (2.56 +/- 0.32 vs 4.68 +/- 0.49 mg/kg per min, P = 0.0001, when 40 mU insulin/m2 per min was infused, and 6.48 +/- 0.58 vs 9.84 +/- 0.72 mg/kg per min, P = 0.0002, when 400 mU insulin insulin/m2 per min was infused). Glucose 31-38 insulin Homo sapiens 162-169 9551792-1 1998 An automated on-line competitive immunoassay based on capillary electrophoresis (CE) was utilized to monitor secretion of insulin from single islets of Langerhans stimulated by glucose and tolbutamide. Glucose 177-184 insulin Homo sapiens 122-129 9568452-2 1998 AIM: Patients with heart failure have a reduced sensitivity to insulin"s actions on glucose metabolism and a compensatory increase in endogenous plasma insulin levels. Glucose 84-91 insulin Homo sapiens 63-70 15251753-4 1998 RESULTS: An inverse relationship was found between both serum insulin and C peptide levels and serum glucose level. Glucose 101-108 insulin Homo sapiens 62-69 9566856-3 1998 Non-esterified fatty acids and insulin response to a 75 g oral glucose tolerance test were higher in abdominal obesity. Glucose 63-70 insulin Homo sapiens 31-38 9566856-8 1998 Variation of triglyceride concentrations in obesity is dependent on both fasting and 120 min non-esterified fatty acids as well as on insulin sensitivity to glucose utilization. Glucose 157-164 insulin Homo sapiens 134-141 9582109-3 1998 Insulin sensitivity was evaluated by GC and expressed as metabolic clearance rate of glucose (M value, mg/m2/min). Glucose 85-92 insulin Homo sapiens 0-7 9582109-14 1998 These results suggest that disturbances of glucose and lipid metabolism in EHT may be related to both insulin resistance and compensatory hyperinsulinemia, and that EHT-R may have more risk factors for arteriosclerotic complications than EHT-N. Glucose 43-50 insulin Homo sapiens 102-109 9539195-5 1998 RESULTS: The obese group presented hyperinsulinaemia in the basal state and after glucose loading (insulin area = 58+/-5 vs 33+/-3 nmol x I[-1] x 2 h, P = 0.005), insulin resistance (M value = 37.4+/-4.8 vs 50.6+/-2.6 micromol x min[-1] x kg FFM[-1], P = 0.002), and insulin hypersecretion (61.9+/-6.0 vs 33.9 +/- 4.0 nmol x 2 h, P = 0.007); endogenous glucose production was similar in the two groups. Glucose 82-89 insulin Homo sapiens 40-47 9539195-5 1998 RESULTS: The obese group presented hyperinsulinaemia in the basal state and after glucose loading (insulin area = 58+/-5 vs 33+/-3 nmol x I[-1] x 2 h, P = 0.005), insulin resistance (M value = 37.4+/-4.8 vs 50.6+/-2.6 micromol x min[-1] x kg FFM[-1], P = 0.002), and insulin hypersecretion (61.9+/-6.0 vs 33.9 +/- 4.0 nmol x 2 h, P = 0.007); endogenous glucose production was similar in the two groups. Glucose 82-89 insulin Homo sapiens 99-106 9539195-5 1998 RESULTS: The obese group presented hyperinsulinaemia in the basal state and after glucose loading (insulin area = 58+/-5 vs 33+/-3 nmol x I[-1] x 2 h, P = 0.005), insulin resistance (M value = 37.4+/-4.8 vs 50.6+/-2.6 micromol x min[-1] x kg FFM[-1], P = 0.002), and insulin hypersecretion (61.9+/-6.0 vs 33.9 +/- 4.0 nmol x 2 h, P = 0.007); endogenous glucose production was similar in the two groups. Glucose 82-89 insulin Homo sapiens 99-106 9539195-6 1998 In the whole dataset, insulin resistance was directly related to BMI, the waist-to-hip ratio (WHR), endogenous glucose production, insulin secretion, and fasting serum triglycerides and uric acid concentrations. Glucose 111-118 insulin Homo sapiens 22-29 9486987-0 1998 Insulin resistance of glucose uptake in skeletal muscle cannot be ameliorated by enhancing endothelium-dependent blood flow in obesity. Glucose 22-29 insulin Homo sapiens 0-7 9486987-1 1998 We tested the hypothesis that endothelium-dependent vasodilatation is a determinant of insulin resistance of skeletal muscle glucose uptake in human obesity. Glucose 125-132 insulin Homo sapiens 87-94 9486987-5 1998 Whole body insulin-stimulated glucose uptake was lower in the obese (507+/-47 mumol/m2 . Glucose 30-37 insulin Homo sapiens 11-18 9486987-8 1998 Muscle glucose uptake in the insulin-infused leg was 66% lower in the obese (19+/-4 micromol/kg muscle . Glucose 7-14 insulin Homo sapiens 29-36 9486987-18 1998 Despite this, insulin-stimulated glucose uptake remained unchanged in the bradykinin and insulin-infused leg (18+/-4 mumol/kg . Glucose 33-40 insulin Homo sapiens 14-21 9486987-21 1998 Insulin-stimulated glucose uptake also was unaffected by bradykinin in the normal subjects (58+/-10 vs. 56+/-9 micromol/kg . Glucose 19-26 insulin Homo sapiens 0-7 9486987-23 1998 These data demonstrate that obesity is characterized by two distinct defects in skeletal muscle: insulin resistance of cellular glucose extraction and impaired endothelium-dependent vasodilatation. Glucose 128-135 insulin Homo sapiens 97-104 9506740-2 1998 We evaluated the relationship of TNF-alpha levels with the visceral, subcutaneous, and total fat areas measured by computed tomography (CT), and with insulin resistance evaluated by the glucose infusion rate (GIR) observed during an euglycemic hyperinsulinemic clamp study. Glucose 186-193 insulin Homo sapiens 150-157 9506746-14 1998 This inhibition was observed in both lean and obese subjects, whereas the expected stimulation of insulin on glucose metabolism and the accumulation of mRNA species for the insulin-sensitive transporter GLUT4 and glyceraldehyde-3-phosphate dehydrogenase occurred in lean patients only. Glucose 109-116 insulin Homo sapiens 98-105 9520910-5 1998 This decline in insulin-mediated glucose uptake was accounted for by a decrease in whole body glycolytic rate with no change in the rate of glycogen synthesis. Glucose 33-40 insulin Homo sapiens 16-23 9557929-7 1998 Fasting plasma insulin levels, the insulin-production response to administration of glucose (insulin area under the curve) and resting clinic and night-time systolic blood pressures were all significantly reduced on the low-fat diet, but only in non-users. Glucose 84-91 insulin Homo sapiens 35-42 9557929-7 1998 Fasting plasma insulin levels, the insulin-production response to administration of glucose (insulin area under the curve) and resting clinic and night-time systolic blood pressures were all significantly reduced on the low-fat diet, but only in non-users. Glucose 84-91 insulin Homo sapiens 35-42 9557929-11 1998 CONCLUSIONS: These results confirm that oral contraceptive pills have the potential to cause adverse effects on blood pressure, cardiovascular reactivity and the insulin-production response to administration of glucose and suggest that some of the beneficial effects of a low-fat diet on these parameters may be negated in women taking oral contraceptive pills. Glucose 211-218 insulin Homo sapiens 162-169 9529278-1 1998 UNLABELLED: This study was performed to evaluate the effect of insulin on myocardial kinetics of 18F-fluorodeoxyglucose (FDG) and glucose in patients with ischemic heart disease. Glucose 112-119 insulin Homo sapiens 63-70 9529278-8 1998 RESULTS: Euglycemic insulin infusion lowered arterial concentrations of free fatty acids, reducing myocardial extraction of free fatty acids by 85% and stimulated uptake of glucose and FDG. Glucose 173-180 insulin Homo sapiens 20-27 9560529-3 1998 To elucidate abnormalities in the feedback relationships between plasma glucose and plasma insulin levels in diabetic patients, we have introduced the vector autoregressive modeling method as a new for tool feedback analysis. Glucose 72-79 insulin Homo sapiens 91-98 9560529-6 1998 We were able to predict the degree of the plasma glucose response occurring after an impulse-like increase in plasma insulin at 1 mU/mL, as well as the plasma insulin response triggered by an impulse-like increase in plasma glucose at 1 mg/dL, in the form of "impulse response curves". Glucose 49-56 insulin Homo sapiens 117-124 9560529-6 1998 We were able to predict the degree of the plasma glucose response occurring after an impulse-like increase in plasma insulin at 1 mU/mL, as well as the plasma insulin response triggered by an impulse-like increase in plasma glucose at 1 mg/dL, in the form of "impulse response curves". Glucose 224-231 insulin Homo sapiens 159-166 9560529-7 1998 The predicted impulse response curve of glucose to insulin gradually changed from negative to positive with incremental changes in the fasting plasma glucose level, reflecting increased insulin resistance. Glucose 40-47 insulin Homo sapiens 51-58 9560529-7 1998 The predicted impulse response curve of glucose to insulin gradually changed from negative to positive with incremental changes in the fasting plasma glucose level, reflecting increased insulin resistance. Glucose 40-47 insulin Homo sapiens 186-193 9560529-7 1998 The predicted impulse response curve of glucose to insulin gradually changed from negative to positive with incremental changes in the fasting plasma glucose level, reflecting increased insulin resistance. Glucose 150-157 insulin Homo sapiens 51-58 9560529-7 1998 The predicted impulse response curve of glucose to insulin gradually changed from negative to positive with incremental changes in the fasting plasma glucose level, reflecting increased insulin resistance. Glucose 150-157 insulin Homo sapiens 186-193 9500569-0 1998 Both a reduced acute insulin response to glucose and lower glucose effectiveness are responsible for the worsening of intravenous glucose tolerance in healthy subjects independently of the degree of obesity. Glucose 41-48 insulin Homo sapiens 21-28 9500569-10 1998 In conclusion, although the main factors that determine intravenous glucose tolerance are the suprabasal insulin effect and GEZI, worsening of the KG index depends on inadequate insulin secretion for the degree of insulin sensitivity and lower non-insulin-mediated glucose uptake. Glucose 68-75 insulin Homo sapiens 105-112 9500569-11 1998 Age seems to be another factor in the worsening of intravenous glucose tolerance through a lower suprabasal insulin effect. Glucose 63-70 insulin Homo sapiens 108-115 9500570-16 1998 However, a potentiating effect of endogenous insulin on the satiating effect of high blood glucose levels cannot be excluded. Glucose 91-98 insulin Homo sapiens 45-52 9608544-0 1998 Response of insulin, glucagon, lactate, and nonesterified fatty acids to glucose in visceral obesity with and without NIDDM: relationship to hypertension. Glucose 73-80 insulin Homo sapiens 12-19 9478990-0 1998 Potential role of protein kinase B in insulin-induced glucose transport, glycogen synthesis, and protein synthesis. Glucose 54-61 insulin Homo sapiens 38-45 9478990-1 1998 Various biological responses stimulated by insulin have been thought to be regulated by phosphatidylinositol 3-kinase, including glucose transport, glycogen synthesis, and protein synthesis. Glucose 129-136 insulin Homo sapiens 43-50 9508068-5 1998 It is presumed that a selective defect in insulin-stimulated glucose uptake, with preservation of anabolic effect, was one of the causes of his "overgrowth without growth hormone," at least in the last 12 months of life after severe brain damage. Glucose 61-68 insulin Homo sapiens 42-49 9511732-2 1998 Furthermore, insulin caused the integration of these microvilli into the plasma membrane, suggesting that insulin-induced stimulation of glucose uptake may be due to the destruction of the cytoskeletal diffusion barrier formed by the actin filament bundle of the microvillar shaft regions [Lange et al. Glucose 137-144 insulin Homo sapiens 13-20 9511732-2 1998 Furthermore, insulin caused the integration of these microvilli into the plasma membrane, suggesting that insulin-induced stimulation of glucose uptake may be due to the destruction of the cytoskeletal diffusion barrier formed by the actin filament bundle of the microvillar shaft regions [Lange et al. Glucose 137-144 insulin Homo sapiens 106-113 9511732-22 1998 The observations presented strengthen the previously postulated diffusion-barrier concept of glucose- and ion-uptake regulation and provide a mechanistic basis for explaining the action of insulin and other growth factors on transport processes across the plasma membrane. Glucose 93-100 insulin Homo sapiens 189-196 9468502-0 1998 Insulin mediates glucose-stimulated phosphorylation of PHAS-I by pancreatic beta cells. Glucose 17-24 insulin Homo sapiens 0-7 9468502-9 1998 These results indicate that glucose stimulates PHAS-I phosphorylation via insulin interacting with its own receptor on the beta cell which may serve as an important mechanism for autoregulation of protein synthesis by translation. Glucose 28-35 insulin Homo sapiens 74-81 9450985-3 1998 Second, physiological elevations of plasma FFA inhibit acutely as well as chronically insulin stimulated glucose uptake in a dose dependent fashion. Glucose 105-112 insulin Homo sapiens 86-93 9450985-6 1998 Elevated plasma FFA levels also modestly increase insulin suppressed endogenous glucose production (EGP) although this effect has not been found by all investigators. Glucose 80-87 insulin Homo sapiens 50-57 9452481-5 1998 The 52% decrease in islet TG was accompanied by >30- and 2-fold improvements in glucose- and arginine-stimulated insulin secretion, respectively. Glucose 83-90 insulin Homo sapiens 116-123 9473490-1 1998 We have investigated the effect of IGF-II on glucose-induced insulin release in the pancreatic beta-cell. Glucose 45-52 insulin Homo sapiens 61-68 9473490-2 1998 Introduction of IGF-II during perifusion of the cells with 20 mM glucose abolished glucose-induced insulin release. Glucose 65-72 insulin Homo sapiens 99-106 9473513-1 1998 To investigate the possible involvement of some intracellular metabolic signaling other than the ATP derived from glucose metabolism under protein kinase A (PKA) activation, we measured the insulin secretory capacity stimulated by glucose and other fuel secretagogues using diazoxide-treated pancreatic islets. Glucose 231-238 insulin Homo sapiens 190-197 9459367-6 1998 Insulin increment and the area under the insulin curve during an intravenous glucose tolerance test were inversely correlated with iMg++ [r = -0.56 (P < 0.01) and r = -0.64 (P < 0.0005), respectively], but were not significantly correlated with tMg. Glucose 77-84 insulin Homo sapiens 0-7 9459367-6 1998 Insulin increment and the area under the insulin curve during an intravenous glucose tolerance test were inversely correlated with iMg++ [r = -0.56 (P < 0.01) and r = -0.64 (P < 0.0005), respectively], but were not significantly correlated with tMg. Glucose 77-84 insulin Homo sapiens 41-48 9459367-7 1998 Insulin-mediated glucose uptake and the insulin sensitivity index during the hyperinsulinemic euglycemic clamp test were not significantly correlated with tMg (r = 0.05 and 0.12, respectively; NS) nor with iMg++ (r = 0.23 and 0.31, respectively; NS). Glucose 17-24 insulin Homo sapiens 0-7 9486162-1 1998 A single bout of exercise increases the rate of insulin-stimulated glucose uptake and metabolism in skeletal muscle. Glucose 67-74 insulin Homo sapiens 48-55 9486162-12 1998 The increase in HK II activity after moderate exercise in healthy subjects could be one factor responsible for the enhanced rate of insulin-stimulated glucose uptake seen after exercise. Glucose 151-158 insulin Homo sapiens 132-139 9454524-10 1998 At 6 years, patients allocated to insulin had lower fasting plasma glucose levels than did patients allocated to oral agents, but hemoglobin A1c concentrations were similar. Glucose 67-74 insulin Homo sapiens 34-41 9454525-17 1998 CONCLUSION: Troglitazone monotherapy decreased fasting and postprandial glucose levels in patients with type 2 diabetes, primarily by augmenting insulin-mediated glucose disposal. Glucose 162-169 insulin Homo sapiens 145-152 9541719-4 1998 Troglitazone mainly elicits the following actions: Enhancement of insulin-mediated glucose disposal in patients with insulin resistance, impaired glucose tolerance and NIDDM, reduction of hyperglycaemia (blood glucose; HbA1c) and concomitant hyperinsulinaemia, improvement of dyslipidaemia in NIDDM. Glucose 83-90 insulin Homo sapiens 66-73 9541719-4 1998 Troglitazone mainly elicits the following actions: Enhancement of insulin-mediated glucose disposal in patients with insulin resistance, impaired glucose tolerance and NIDDM, reduction of hyperglycaemia (blood glucose; HbA1c) and concomitant hyperinsulinaemia, improvement of dyslipidaemia in NIDDM. Glucose 83-90 insulin Homo sapiens 117-124 9541719-4 1998 Troglitazone mainly elicits the following actions: Enhancement of insulin-mediated glucose disposal in patients with insulin resistance, impaired glucose tolerance and NIDDM, reduction of hyperglycaemia (blood glucose; HbA1c) and concomitant hyperinsulinaemia, improvement of dyslipidaemia in NIDDM. Glucose 146-153 insulin Homo sapiens 66-73 9653515-2 1998 We found that glucose-induced insulin release was potentiated by L-NAME in the absence or presence of diazoxide, a potent K+ATP channel opener, as well as in the presence of diazoxide plus a depolarizing concentration of K+. Glucose 14-21 insulin Homo sapiens 30-37 9519730-3 1998 We hypothesized that induction of increased insulin accompanied by increased glucose and triglycerides would increase PAI-1. Glucose 77-84 insulin Homo sapiens 44-51 9534004-1 1998 Glucose-stimulated insulin release from pancreatic beta cells involves a complex series of signalling pathways. Glucose 0-7 insulin Homo sapiens 19-26 9534007-1 1998 Stimulation of insulin release by glucose and other nutrients has been attributed to a rise of cytoplasmic Ca2+([Ca2+]i). Glucose 34-41 insulin Homo sapiens 15-22 9669085-4 1998 Insulin secretion in response to glucose and arginine injection was not affected by heat exposure. Glucose 33-40 insulin Homo sapiens 0-7 9518395-11 1998 INTERVENTIONS: 1) Intensive therapy with 3 or more insulin injections daily or continuous subcutaneous infusion of insulin, guided by 4 or more glucose tests per day or 2) conventional therapy with 1 or 2 insulin injections daily. Glucose 144-151 insulin Homo sapiens 115-122 9449624-3 1998 To investigate the role of insulin-stimulated glucose metabolism in the regulation of leptin secretion, we examined the effects of insulin and inhibitors of glucose transport and metabolism on leptin secretion from rat adipocytes in primary culture. Glucose 46-53 insulin Homo sapiens 27-34 9449686-6 1998 The obese controls and NIDDM patients were insulin resistant with glucose disposal rates during the last 30 min of the clamp that were 67 and 31%, respectively, of those found in the lean controls. Glucose 66-73 insulin Homo sapiens 43-50 9449624-4 1998 Insulin (0.16-16 nM) increased leptin secretion over 96 h; however, the increase in leptin was more closely related to the amount of glucose taken up by the adipocytes (r = 0.64; P < 0.0001) than to the insulin concentration per se (r = 0.20; P < 0.28), suggesting a role for glucose transport and/or metabolism in regulating leptin secretion. Glucose 133-140 insulin Homo sapiens 0-7 9449624-4 1998 Insulin (0.16-16 nM) increased leptin secretion over 96 h; however, the increase in leptin was more closely related to the amount of glucose taken up by the adipocytes (r = 0.64; P < 0.0001) than to the insulin concentration per se (r = 0.20; P < 0.28), suggesting a role for glucose transport and/or metabolism in regulating leptin secretion. Glucose 282-289 insulin Homo sapiens 0-7 9449624-5 1998 2-Deoxy-D-glucose (2-DG), a competitive inhibitor of glucose transport and phosphorylation, caused a concentration-dependent (2-50 mg/dl) inhibition of leptin release in the presence of 1.6 nM insulin. Glucose 10-17 insulin Homo sapiens 193-200 9449624-11 1998 We conclude that glucose transport and metabolism are important factors in the regulation of leptin expression and secretion and that the effect of insulin to increase adipocyte glucose utilization is likely to contribute to insulin-stimulated leptin secretion. Glucose 17-24 insulin Homo sapiens 225-232 9449624-11 1998 We conclude that glucose transport and metabolism are important factors in the regulation of leptin expression and secretion and that the effect of insulin to increase adipocyte glucose utilization is likely to contribute to insulin-stimulated leptin secretion. Glucose 178-185 insulin Homo sapiens 148-155 9449624-11 1998 We conclude that glucose transport and metabolism are important factors in the regulation of leptin expression and secretion and that the effect of insulin to increase adipocyte glucose utilization is likely to contribute to insulin-stimulated leptin secretion. Glucose 178-185 insulin Homo sapiens 225-232 9461233-6 1998 During insulin administration, tissue glucose extraction rose from 2+/-1% to 21+/-4% (P<.001) in the control forearm and from 2+/-1% to 8+/-3% in the infused forearm (P<.02 versus baseline for both); the calculated net glucose uptake reached similar plateaus in the two forearms (3.5+/-0.7 versus 3.7+/-0.6 micromol x min(-1) x kg(-1), control versus infused, P=.6). Glucose 38-45 insulin Homo sapiens 7-14 9461233-6 1998 During insulin administration, tissue glucose extraction rose from 2+/-1% to 21+/-4% (P<.001) in the control forearm and from 2+/-1% to 8+/-3% in the infused forearm (P<.02 versus baseline for both); the calculated net glucose uptake reached similar plateaus in the two forearms (3.5+/-0.7 versus 3.7+/-0.6 micromol x min(-1) x kg(-1), control versus infused, P=.6). Glucose 225-232 insulin Homo sapiens 7-14 9514530-2 1998 Nevertheless, interferon therapy worsened insulin-mediated glucose uptake in the peripheral tissues by 17% from 44.4+/-3.2 to 37.3+/-3.0 micromol x kg(-1) x min(-1) (p<0.05). Glucose 59-66 insulin Homo sapiens 42-49 9816552-10 1998 The mean serum insulin: plasma glucose ratio for men in the low BMI group was significantly higher than that for normotensives after 60 min and 120 min (P < 0.05 for both comparisons). Glucose 31-38 insulin Homo sapiens 15-22 9514541-6 1998 C-peptide levels at t=35 min of the clamp increased more with glucose concentration in non-diabetic cirrhotic patients than controls; there was little increase in diabetic cirrhotic patients. Glucose 62-69 insulin Homo sapiens 0-9 9468278-0 1998 Insulin-stimulated chemokinesis in normal human neutrophils is dependent on D-glucose concentration and sensitive to inhibitors of tyrosine kinase and phosphatidylinositol 3-kinase. Glucose 76-85 insulin Homo sapiens 0-7 9468278-2 1998 A stimulatory chemokinetic effect of insulin was present at 40-160 microU/mL insulin but only in the presence of 5 mM, and not at 15 mM, D-glucose. Glucose 137-146 insulin Homo sapiens 37-44 9468278-5 1998 The tyrosine kinase inhibitor, genistein, or the phosphatidylinositol 3-kinase inhibitor, wortmannin, abolished the chemokinetic effect of 160 microU/mL insulin in the presence of 5 mM D-glucose. Glucose 185-194 insulin Homo sapiens 153-160 9513084-1 1998 The importance of the glucose transporter isoform, GLUT2, in the construction of glucose-sensitive surrogate insulin-secreting cells was evaluated using murine pituitary AtT20 cells. Glucose 22-29 insulin Homo sapiens 109-116 9513084-4 1998 Increasing glucose concentrations in the subphysiological range up to 50 microM increased insulin release, but greater glucose concentrations did not further increase insulin release. Glucose 11-18 insulin Homo sapiens 90-97 9513084-5 1998 Suppression of the low-K(m) glucose-phosphorylating enzyme, hexokinase, with 2-deoxy-D-glucose increased glucose-stimulated insulin release by two- to threefold in the presence of subphysiological and physiological glucose concentrations up to 10 mM. Glucose 28-35 insulin Homo sapiens 124-131 9513084-5 1998 Suppression of the low-K(m) glucose-phosphorylating enzyme, hexokinase, with 2-deoxy-D-glucose increased glucose-stimulated insulin release by two- to threefold in the presence of subphysiological and physiological glucose concentrations up to 10 mM. Glucose 87-94 insulin Homo sapiens 124-131 9513084-5 1998 Suppression of the low-K(m) glucose-phosphorylating enzyme, hexokinase, with 2-deoxy-D-glucose increased glucose-stimulated insulin release by two- to threefold in the presence of subphysiological and physiological glucose concentrations up to 10 mM. Glucose 87-94 insulin Homo sapiens 124-131 9513084-10 1998 Expression of GLUT2 enables glucose to enter the cell at high K(m), but high-K(m) glucose phosphorylation is also required to signal glucose-stimulated genes affecting insulin release. Glucose 82-89 insulin Homo sapiens 168-175 9513084-10 1998 Expression of GLUT2 enables glucose to enter the cell at high K(m), but high-K(m) glucose phosphorylation is also required to signal glucose-stimulated genes affecting insulin release. Glucose 82-89 insulin Homo sapiens 168-175 9482663-2 1998 We now report that culturing the highly differentiated rat insulinoma cell line, INS-1, in glucose concentrations above 8.0 mM caused a marked decrease in insulin mRNA levels within 24 h. The decrease in insulin mRNA levels was reversed by further incubation of the cells in 4.0 mM glucose. Glucose 91-98 insulin Homo sapiens 59-66 9498508-5 1998 Patients receiving insulin received dextrose 50 at 20 to 50 mL/h, titrated to maintain euglycemia. Glucose 36-44 insulin Homo sapiens 19-26 9482663-2 1998 We now report that culturing the highly differentiated rat insulinoma cell line, INS-1, in glucose concentrations above 8.0 mM caused a marked decrease in insulin mRNA levels within 24 h. The decrease in insulin mRNA levels was reversed by further incubation of the cells in 4.0 mM glucose. Glucose 91-98 insulin Homo sapiens 155-162 9482663-2 1998 We now report that culturing the highly differentiated rat insulinoma cell line, INS-1, in glucose concentrations above 8.0 mM caused a marked decrease in insulin mRNA levels within 24 h. The decrease in insulin mRNA levels was reversed by further incubation of the cells in 4.0 mM glucose. Glucose 282-289 insulin Homo sapiens 59-66 9482663-2 1998 We now report that culturing the highly differentiated rat insulinoma cell line, INS-1, in glucose concentrations above 8.0 mM caused a marked decrease in insulin mRNA levels within 24 h. The decrease in insulin mRNA levels was reversed by further incubation of the cells in 4.0 mM glucose. Glucose 282-289 insulin Homo sapiens 155-162 9482663-4 1998 The decrease in insulin gene promoter activity was associated with reductions in the binding activities of both STF-1 and C1 activator, and these were partially reversed by lowering the glucose concentration. Glucose 186-193 insulin Homo sapiens 16-23 9482663-7 1998 We conclude that physiologically relevent elevations in glucose can reversibly diminish insulin gene transcription by reducing the expression and/or binding activity of two critical beta-cell transcription factors. Glucose 56-63 insulin Homo sapiens 88-95 9562967-0 1998 Insulin sensitivity indices calculated from basal and OGTT-induced insulin, glucose, and FFA levels. Glucose 76-83 insulin Homo sapiens 0-7 9509457-6 1998 Insulin response was calculated from the increase in serum insulin concentration during the oral glucose tolerance test. Glucose 97-104 insulin Homo sapiens 0-7 9565989-9 1998 The length of the expansion of the CTG repeats correlated negatively with the CMRGlu (r2 = 0.63, P = 0.003) and positively with the area under the curve for insulin changes over time after oral glucose (r2 = 0.49, P = 0.016). Glucose 194-201 insulin Homo sapiens 157-164 9597380-1 1998 The aim of our work was to study non-insulin-mediated glucose uptake (NIMGU), in the postabsorptive state, in several pathologies characterized by peripheral insulin resistance, namely, obesity (n = 10), NIDDM (n = 7), acromegaly (n = 7) and Cushing"s disease (n = 6). Glucose 54-61 insulin Homo sapiens 37-44 9597380-6 1998 In conclusion, our data show that, in the postabsorptive period, non-insulin mediated glucose uptake is a major determinant of glucose disposal and is similar in the different pathologies studied; on the other hand, although absolute rates of basal insulin-mediated glucose uptake are reduced in insulin-resistant states, they did not achieve statistical value compared with control subjects because of compensatory hyperinsulinaemia. Glucose 86-93 insulin Homo sapiens 69-76 9597380-6 1998 In conclusion, our data show that, in the postabsorptive period, non-insulin mediated glucose uptake is a major determinant of glucose disposal and is similar in the different pathologies studied; on the other hand, although absolute rates of basal insulin-mediated glucose uptake are reduced in insulin-resistant states, they did not achieve statistical value compared with control subjects because of compensatory hyperinsulinaemia. Glucose 86-93 insulin Homo sapiens 249-256 9597380-6 1998 In conclusion, our data show that, in the postabsorptive period, non-insulin mediated glucose uptake is a major determinant of glucose disposal and is similar in the different pathologies studied; on the other hand, although absolute rates of basal insulin-mediated glucose uptake are reduced in insulin-resistant states, they did not achieve statistical value compared with control subjects because of compensatory hyperinsulinaemia. Glucose 86-93 insulin Homo sapiens 249-256 9597380-6 1998 In conclusion, our data show that, in the postabsorptive period, non-insulin mediated glucose uptake is a major determinant of glucose disposal and is similar in the different pathologies studied; on the other hand, although absolute rates of basal insulin-mediated glucose uptake are reduced in insulin-resistant states, they did not achieve statistical value compared with control subjects because of compensatory hyperinsulinaemia. Glucose 127-134 insulin Homo sapiens 69-76 9597383-0 1998 Minimal model of glucose metabolism: modified equations and its application in the study of insulin sensitivity in obese subjects. Glucose 17-24 insulin Homo sapiens 92-99 9509457-6 1998 Insulin response was calculated from the increase in serum insulin concentration during the oral glucose tolerance test. Glucose 97-104 insulin Homo sapiens 59-66 9509457-9 1998 The impaired glucose tolerance and post-transplant diabetes mellitus groups showed a significant reduction in insulin-stimulated glucose disposal rate (mg/kg.min) compared to the normal glucose tolerance group (4.6 +/- 1.6 and 3.4 +/- 1.3 respectively vs 7.1 +/- 2.4, P < 0.05). Glucose 13-20 insulin Homo sapiens 110-117 9509457-9 1998 The impaired glucose tolerance and post-transplant diabetes mellitus groups showed a significant reduction in insulin-stimulated glucose disposal rate (mg/kg.min) compared to the normal glucose tolerance group (4.6 +/- 1.6 and 3.4 +/- 1.3 respectively vs 7.1 +/- 2.4, P < 0.05). Glucose 129-136 insulin Homo sapiens 110-117 9509457-10 1998 The insulin response (picomol/l) was not different between the normal glucose tolerance and impaired glucose tolerance groups but was significantly reduced in the post-transplant diabetes mellitus group (448 +/- 310 and 450 +/- 291 respectively vs 170 +/- 128, P < 0.05). Glucose 70-77 insulin Homo sapiens 4-11 9513368-0 1998 [Improvement of insulin sensitivity after renal transplantation measured by a glucose clamp technique]. Glucose 78-85 insulin Homo sapiens 16-23 9513368-5 1998 The clamp was applied for 120 minutes and the average of the glucose disposal rates measured from 90 to 120 minutes was regarded as insulin sensitivity. Glucose 61-68 insulin Homo sapiens 132-139 9430708-0 1998 A high affinity glutamate/aspartate transport system in pancreatic islets of Langerhans modulates glucose-stimulated insulin secretion. Glucose 98-105 insulin Homo sapiens 117-124 9775125-1 1998 UNLABELLED: OBJECTIVES AND JUSTIFICATION: To describe facilitated diffusion glucose transporters (GLUT) in humans, and particularly the regulation of GLUT4 expression since it is predominantly responsible for insulin-mediated glucose transport in muscle and adipose tissue, and plays a crucial role in whole-body glucose homeostasis. Glucose 76-83 insulin Homo sapiens 209-216 9557035-8 1998 In carriers of the MIDD mutation the insulin secretion by the pancreas in response to stimulation by glucose is impaired. Glucose 101-108 insulin Homo sapiens 37-44 9430708-11 1998 Furthermore, 6-cyano-7-nitroquinoxaline-2,3-dione alone inhibited glucose-stimulated insulin secretion in isolated islets by 15.9 +/- 5.9% (n = 3). Glucose 66-73 insulin Homo sapiens 85-92 9430708-12 1998 Taken together these data suggest that a high affinity glutamate transport system exists in pancreatic islets and that this system contributes to a glutamatergic signaling pathway that can modulate glucose-inducible insulin secretion. Glucose 198-205 insulin Homo sapiens 216-223 9492712-10 1998 The incremental area under the curve for the glucose (p = 0.001) and insulin (p = 0.02) responses to oral glucose tolerance test showed higher values for preeclampsia as compared to women with normal pregnancy. Glucose 106-113 insulin Homo sapiens 69-76 9446815-0 1998 Identification and characterization of a glucose-responsiveness region upstream of human insulin gene in transfected HIT-T 15 cells. Glucose 41-48 insulin Homo sapiens 89-96 9782622-5 1998 The treatment was well tolerated except for mild insulinoresistance, which could be easily corrected by slightly increasing the insulin added to glucose solutions. Glucose 145-152 insulin Homo sapiens 49-56 9439595-0 1998 The importance of nitric oxide in the cytokine-induced inhibition of glucose formation by cultured hepatocytes incubated with insulin, dexamethasone, and glucagon. Glucose 69-76 insulin Homo sapiens 126-133 9781315-3 1998 Intense interest is now focused on whether reduced insulin-mediated glucose transport in muscle from NIDDM patients results from alterations in the insulin signal transduction pathway or from alterations in traffic and/or translocation of GLUT4 to the plasma membrane. Glucose 68-75 insulin Homo sapiens 51-58 9781315-3 1998 Intense interest is now focused on whether reduced insulin-mediated glucose transport in muscle from NIDDM patients results from alterations in the insulin signal transduction pathway or from alterations in traffic and/or translocation of GLUT4 to the plasma membrane. Glucose 68-75 insulin Homo sapiens 148-155 9781317-4 1998 The studies presented here demonstrate that endogenous adenosine via A1-adenosine receptors is able to directly stimulate insulin-mediated glucose transport in oxidative muscle cells during contractions. Glucose 139-146 insulin Homo sapiens 122-129 9781317-5 1998 In addition, adenosine may further contribute to stimulation of muscle glucose uptake during contractions by increasing blood flow and thereby targetting glucose and insulin delivery to active muscle fibres. Glucose 71-78 insulin Homo sapiens 166-173 9781319-6 1998 A decline in plasma insulin is important for the rise in glucose production during exercise in a variety of species, whereas an increase in plasma glucagon is probably more important in other species than man, where glucagon plays a role only in prolonged exercise. Glucose 57-64 insulin Homo sapiens 20-27 9781320-2 1998 Since skeletal muscle plays a major role in insulin-stimulated glucose uptake and whole-body energy expenditure, it is a central player in carbohydrate and lipid metabolism, and hence in the balance between health and disease. Glucose 63-70 insulin Homo sapiens 44-51 9869897-3 1998 Our data clearly demonstrate that islet cell viability, as determined by glucose-stimulated insulin secretion, is directly correlated with reduced expression of microsomal cytochrome P-450IIIA. Glucose 73-80 insulin Homo sapiens 92-99 9895418-7 1998 Increased insulin sensitivity and increased free fatty acid oxidation by exercise may facilitate the conversion of glucose to glycogen in muscle. Glucose 115-122 insulin Homo sapiens 10-17 9895418-8 1998 On the other hand, insulin secretion expressed as the ratio of plasma levels of insulin to glucose after the meal was significantly decreased in the exercise experiment (p < 0.05). Glucose 91-98 insulin Homo sapiens 19-26 9449362-0 1998 Structure of cubic insulin crystals in glucose solutions. Glucose 39-46 insulin Homo sapiens 19-26 9449362-1 1998 X-ray structures of cubic insulin crystals in high concentrations of glucose at different pH levels and temperatures have been refined to high resolution. Glucose 69-76 insulin Homo sapiens 26-33 9493563-8 1998 Peripheral insulin resistance (impaired insulin-mediated glucose uptake, primarily of an acute glucose load in skeletal muscle) also present in obesity hypertension, but now reported in lean essential hypertension as well, is linked most notably to impaired insulin-mediated skeletal muscle vasodilation. Glucose 57-64 insulin Homo sapiens 11-18 9493563-8 1998 Peripheral insulin resistance (impaired insulin-mediated glucose uptake, primarily of an acute glucose load in skeletal muscle) also present in obesity hypertension, but now reported in lean essential hypertension as well, is linked most notably to impaired insulin-mediated skeletal muscle vasodilation. Glucose 95-102 insulin Homo sapiens 11-18 9522110-0 1998 Stimulation of glucose and amino acid transport and activation of the insulin signaling pathways by insulin lispro in L6 skeletal muscle cells. Glucose 15-22 insulin Homo sapiens 100-107 9522110-6 1998 (1) Insulin lispro stimulated glucose and amino acid transport into L6 myotubes with a dose dependency and time course virtually identical to those of human regular insulin. Glucose 30-37 insulin Homo sapiens 4-11 9522110-9 1998 (4) As with human regular insulin, 100 nmol of the fungal metabolite wortmannin completely inhibited insulin lispro stimulation of glucose uptake. Glucose 131-138 insulin Homo sapiens 26-33 9522110-9 1998 (4) As with human regular insulin, 100 nmol of the fungal metabolite wortmannin completely inhibited insulin lispro stimulation of glucose uptake. Glucose 131-138 insulin Homo sapiens 101-108 9421370-4 1998 This together with increased GLUT1 (but not GLUT4) synthesis explains the increase in non-insulin-dependent glucose uptake. Glucose 108-115 insulin Homo sapiens 90-97 9421370-5 1998 C2-ceramide inhibited insulin-stimulated glucose uptake after 2 h by decreasing insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. Glucose 41-48 insulin Homo sapiens 22-29 9421370-5 1998 C2-ceramide inhibited insulin-stimulated glucose uptake after 2 h by decreasing insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. Glucose 41-48 insulin Homo sapiens 80-87 9421370-9 1998 We identified a site for inhibiting insulin-stimulated glucose uptake that is downstream of PI 3-kinase. Glucose 55-62 insulin Homo sapiens 36-43 9421370-10 1998 Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo. Glucose 116-123 insulin Homo sapiens 98-105 9498639-7 1998 The IDDM patients had lower insulin stimulated whole body total (-25%, p < 0.001), oxidative (-18%, p < 0.01) and non-oxidative glucose disposal rates (-43%, p < 0.001), whereas lipid oxidation rate was higher in the basal state (+ 44%, p < 0.01) and during hyperinsulinaemia (+283%, p < 0.05). Glucose 134-141 insulin Homo sapiens 28-35 9498639-8 1998 mTG concentrations did not change significantly during the clamp or correlate with insulin stimulated glucose disposal. Glucose 102-109 insulin Homo sapiens 83-90 9597374-6 1998 Insulin resistance, assessed as the insulin area/glucose area ratio during OGTT decreased by 24% (P = 0.028) in the whole group and by 30% in obese subjects (P = 0.049). Glucose 49-56 insulin Homo sapiens 0-7 9868985-8 1998 Relative or absolute excess insulin occurs when: insulin (or insulin secretagogue) doses are excessive, ill-timed or of the wrong type; the influx of exogenous glucose, endogenous glucose production or insulin clearance are decreased; and insulin-independent glucose utilization or insulin sensitivity are increased. Glucose 160-167 insulin Homo sapiens 28-35 10079026-0 1998 Reduced insulin-mediated glucose uptake by euglycemic clamp in offspring of patients with type 2 diabetes. Glucose 25-32 insulin Homo sapiens 8-15 10079027-4 1998 It is possible, based on these findings, that the glucose intolerance was due to increased insulin resistance. Glucose 50-57 insulin Homo sapiens 91-98 9628238-3 1998 It is well established that insulin regulates glycemic control by promoting glucose disposal. Glucose 76-83 insulin Homo sapiens 28-35 9565141-3 1998 Cord C-peptide (p = 0.001) and insulin (p = 0.008) concentrations were significantly higher in patients with GIGT in comparison to those with normal glucose tolerance. Glucose 149-156 insulin Homo sapiens 5-14 9503037-10 1998 Circuit-type resistance training increased insulin sensitivity (glucose disposal) by 23% (p < 0.05), primarily due to a 27% increase in non-oxidative glucose metabolism. Glucose 64-71 insulin Homo sapiens 43-50 9503042-3 1998 However, several recent studies during the last five years have demonstrated that administration of C-peptide in physiological amounts to type 1 diabetes (IDDM) patients on a short term basis (1-3h) results in decreased glomerular hyperfiltration, augmented glucose utilization and improved autonomic nerve function. Glucose 258-265 insulin Homo sapiens 100-109 9550122-3 1998 Treatment of impaired glucose tolerance with troglitazone, a thiazolidinedione that improves insulin sensitivity, leads to an improvement in the ability of the beta-cell to sense and respond to a glucose stimulus restoring the ability of glucose to entrain the ultradian oscillations. Glucose 22-29 insulin Homo sapiens 93-100 9550122-3 1998 Treatment of impaired glucose tolerance with troglitazone, a thiazolidinedione that improves insulin sensitivity, leads to an improvement in the ability of the beta-cell to sense and respond to a glucose stimulus restoring the ability of glucose to entrain the ultradian oscillations. Glucose 196-203 insulin Homo sapiens 93-100 9852229-2 1998 Previous studies have demonstrated that 12-LO, but not 5- or 15-lipoxygenase (5-LO, 15-LO respectively), is specifically expressed in pancreatic -cells and is involved in regulating glucose-stimulated insulin secretion. Glucose 182-189 insulin Homo sapiens 201-208 9852229-9 1998 In this review, we present an overview of the 12-LO pathway in regulating glucose-stimulated insulin secretion in beta-cells as well as more recent data which supports the hypothesis that the 12-LO pathway participates in cytokine mediated beta-cell dysfunction and cytotoxicity. Glucose 74-81 insulin Homo sapiens 93-100 10212828-1 1998 We have achieved significant progress in understanding the central role of the insulin receptor in an increasingly complicated web of intracellular signal transduction leading to the ultimate biological actions of insulin on glucose, lipid, and other metabolic pathways. Glucose 225-232 insulin Homo sapiens 79-86 10212830-9 1998 Thus, the pathophysiology in the chiro-inositol system related to insulin resistance and its reversal by chiro-inositol administration, in addition to the basic work, argues strongly for the physiological significance of this novel signaling system in the control of glucose metabolism. Glucose 267-274 insulin Homo sapiens 66-73 10212832-1 1998 Insulin stimulates glucose transport in skeletal muscle, heart, and adipose tissue by promoting the appearance of GLUT4, the major glucose transporter isoform present in these tissues, on the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 10212832-1 1998 Insulin stimulates glucose transport in skeletal muscle, heart, and adipose tissue by promoting the appearance of GLUT4, the major glucose transporter isoform present in these tissues, on the cell surface. Glucose 131-138 insulin Homo sapiens 0-7 10212832-3 1998 Ligands which activate the heterotrimeric GTP-binding proteins Gs and Gi appear to modulate insulin-stimulated glucose transport through effects on the fusion of docked GLUT4-containing vesicles with the plasma membrane. Glucose 111-118 insulin Homo sapiens 92-99 10212832-4 1998 In insulin resistance states, reduced cellular GLUT4 levels in adipose cells fully account for the decreased glucose transport response to insulin in these cells. Glucose 109-116 insulin Homo sapiens 139-146 10212832-12 1998 Furthermore, recent studies have demonstrated that VAMP2/3, syntaxin 4, SNAP-23, and NSF are functionally involved in insulin-stimulated GLUT4 translocation in adipose cells and thus are likely to be involved in the Gs- and Gi-mediated modulation of the glucose transport response to insulin as well. Glucose 254-261 insulin Homo sapiens 118-125 9421470-5 1998 The IS-group had lower insulin-glucose response at 30 min in the oral glucose tolerance test (85.2+/-10.0 pmol insulin per mmol glucose) than the control group (136.4+/-23.1 pmol insulin per mmol glucose; P < 0.05) and the IR-group (115.6+/-11.8 pmol insulin per mmol glucose; P = 0.05). Glucose 31-38 insulin Homo sapiens 23-30 9421470-5 1998 The IS-group had lower insulin-glucose response at 30 min in the oral glucose tolerance test (85.2+/-10.0 pmol insulin per mmol glucose) than the control group (136.4+/-23.1 pmol insulin per mmol glucose; P < 0.05) and the IR-group (115.6+/-11.8 pmol insulin per mmol glucose; P = 0.05). Glucose 70-77 insulin Homo sapiens 23-30 9421470-5 1998 The IS-group had lower insulin-glucose response at 30 min in the oral glucose tolerance test (85.2+/-10.0 pmol insulin per mmol glucose) than the control group (136.4+/-23.1 pmol insulin per mmol glucose; P < 0.05) and the IR-group (115.6+/-11.8 pmol insulin per mmol glucose; P = 0.05). Glucose 70-77 insulin Homo sapiens 23-30 9421470-5 1998 The IS-group had lower insulin-glucose response at 30 min in the oral glucose tolerance test (85.2+/-10.0 pmol insulin per mmol glucose) than the control group (136.4+/-23.1 pmol insulin per mmol glucose; P < 0.05) and the IR-group (115.6+/-11.8 pmol insulin per mmol glucose; P = 0.05). Glucose 70-77 insulin Homo sapiens 23-30 9421470-6 1998 Furthermore, the acute insulin response during the first 10 min of an intravenous glucose tolerance test was lower in the IS-group than in the IR-group. Glucose 82-89 insulin Homo sapiens 23-30 9533423-13 1998 Suppression of glucose production by insulin was similar with both treatments. Glucose 15-22 insulin Homo sapiens 37-44 9481683-0 1998 Elevated D-glucose induces insulin insensitivity in human umbilical endothelial cells isolated from gestational diabetic pregnancies. Glucose 9-18 insulin Homo sapiens 27-34 9481683-13 1998 Elevated D-glucose abolished the stimulatory effect of human insulin (1 nM, 8 h) on L-[3H]leucine incorporation in diabetic endothelial cells cultured in 5 mM D-glucose. Glucose 9-18 insulin Homo sapiens 61-68 9481683-13 1998 Elevated D-glucose abolished the stimulatory effect of human insulin (1 nM, 8 h) on L-[3H]leucine incorporation in diabetic endothelial cells cultured in 5 mM D-glucose. Glucose 159-168 insulin Homo sapiens 61-68 9481683-15 1998 Human insulin reduced the elevated rates of L-arginine transport and cGMP accumulation in diabetic cells cultured in 5 mM D-glucose but failed to reduce increased rates of transport or NO production in cells exposed to 25 mM D-glucose or cycloheximide. Glucose 122-131 insulin Homo sapiens 6-13 10214471-5 1998 Considerably higher insulinaemia and C-peptidemia values accompanied by impaired metabolic clearance of insulin and lowered glucose utilization in children with significant accumulation of adipose tissue in the abdominal area (waist/hip ratio p > 0.95), may constitute a possible predictor for diet-controlled diabetes mellitus and cardiovascular system diseases in adult age. Glucose 124-131 insulin Homo sapiens 20-27 9440471-3 1998 Both fasting and glucose-induced insulin levels were higher in women with upper-body obesity than in controls (P < .001) and those with lower-body obesity (P < .001). Glucose 17-24 insulin Homo sapiens 33-40 9440471-8 1998 The duration of obesity exaggerated the glucose-induced insulin level and cumulative insulin response independently of the degree of obesity and obesity type. Glucose 40-47 insulin Homo sapiens 56-63 9513457-0 1998 [Estimation of insulin sensitivity in vivo using glucose clamp and minimal model]. Glucose 49-56 insulin Homo sapiens 15-22 27406021-6 1998 We have shown that cyclo(His-Pro) augments the insulin response to oral glucose in rat by decreasing hepatic insulin clearance. Glucose 72-79 insulin Homo sapiens 47-54 9502570-10 1998 Conversely, serum insulin was higher with the glucose-charged dialysate (38 +/- 17 mU/l) than the glucose-free dialysate (19 +/- 9 mU/l). Glucose 46-53 insulin Homo sapiens 18-25 9502570-10 1998 Conversely, serum insulin was higher with the glucose-charged dialysate (38 +/- 17 mU/l) than the glucose-free dialysate (19 +/- 9 mU/l). Glucose 98-105 insulin Homo sapiens 18-25 9949859-4 1998 Insulin resistance is established as the characteristic pathologic feature of patients with glucose intolerance and NIDDM describing a state in which insulin stimulated glucose uptake and utilisation in liver, skeletal muscle and adipose tissue is impaired and coupled to impaired suppression of hepatic glucose output. Glucose 92-99 insulin Homo sapiens 0-7 9949859-4 1998 Insulin resistance is established as the characteristic pathologic feature of patients with glucose intolerance and NIDDM describing a state in which insulin stimulated glucose uptake and utilisation in liver, skeletal muscle and adipose tissue is impaired and coupled to impaired suppression of hepatic glucose output. Glucose 92-99 insulin Homo sapiens 150-157 9949859-4 1998 Insulin resistance is established as the characteristic pathologic feature of patients with glucose intolerance and NIDDM describing a state in which insulin stimulated glucose uptake and utilisation in liver, skeletal muscle and adipose tissue is impaired and coupled to impaired suppression of hepatic glucose output. Glucose 169-176 insulin Homo sapiens 0-7 9949859-4 1998 Insulin resistance is established as the characteristic pathologic feature of patients with glucose intolerance and NIDDM describing a state in which insulin stimulated glucose uptake and utilisation in liver, skeletal muscle and adipose tissue is impaired and coupled to impaired suppression of hepatic glucose output. Glucose 169-176 insulin Homo sapiens 150-157 10660973-7 1998 In patients previously receiving insulin treatment, therapy with lispro insulin significantly reduced postprandial glucose values. Glucose 115-122 insulin Homo sapiens 72-79 9654606-3 1998 Women with preeclampsia had higher fasting insulin levels, but also exaggerated hyperinsulinemia, in response to an oral glucose tolerance test, which is consistent with increased insulin resistance in preeclampsia. Glucose 121-128 insulin Homo sapiens 43-50 9654606-3 1998 Women with preeclampsia had higher fasting insulin levels, but also exaggerated hyperinsulinemia, in response to an oral glucose tolerance test, which is consistent with increased insulin resistance in preeclampsia. Glucose 121-128 insulin Homo sapiens 85-92 9458525-5 1998 Physical activity exerts pronounced effects on substrate utilisation and insulin sensitivity, which in turn potentially lowers blood glucose and lipid levels. Glucose 133-140 insulin Homo sapiens 73-80 9616712-7 1997 Glucose-stimulated insulin secretion by encapsulated pancreatic islets did not differ as capsule permeability was decreased from a molecular exclusion limit of 230 kD to 120 kD. Glucose 0-7 insulin Homo sapiens 19-26 9399959-0 1997 Indirect effect of insulin to suppress endogenous glucose production is dominant, even with hyperglucagonemia. Glucose 50-57 insulin Homo sapiens 19-26 9399959-1 1997 Suppression of endogenous glucose production (EGP) is one of insulin"s primary metabolic effects and failure of this action is a major contributor to fasting hyperglycemia of type 2 diabetes mellitus. Glucose 26-33 insulin Homo sapiens 61-68 9449378-7 1997 Insulin produced by FTOInsm cells was biologically active because it blocked endogenous PEPCK gene expression and induced glucose uptake and lactate production. Glucose 122-129 insulin Homo sapiens 0-7 9506190-13 1998 In selected patients, combination therapy consisting of bedtime intermediate-acting insulin in addition to daytime oral antidiabetic agent(s) can be an effective method to normalize glucose control without the need for rigorous insulin regimens. Glucose 182-189 insulin Homo sapiens 84-91 9509261-4 1998 Exercise and insulin utilize different signaling pathways, both of which lead to the activation of glucose transport, which perhaps explains why humans with insulin resistance can increase muscle glucose transport in response to an acute bout of exercise. Glucose 99-106 insulin Homo sapiens 13-20 9509261-4 1998 Exercise and insulin utilize different signaling pathways, both of which lead to the activation of glucose transport, which perhaps explains why humans with insulin resistance can increase muscle glucose transport in response to an acute bout of exercise. Glucose 99-106 insulin Homo sapiens 157-164 10321450-6 1998 Moxonidine has been shown to improve glucose tolerance in man, probably by two different mechanisms, i.e. by augmenting insulin sensitivity in peripheral tissues and by enhancing glucose-stimulated insulin release from the pancreas. Glucose 179-186 insulin Homo sapiens 198-205 9421379-11 1998 Increased abundance of hybrid receptors was positively correlated with insulin levels (r = -0.82, P < 0.0009) and inversely correlated with insulin-mediated glucose uptake (r = -0.80, P < 0.01). Glucose 160-167 insulin Homo sapiens 143-150 9472863-4 1998 Specific serum insulin 2 h after ingestion of 75 g glucose (2hI), also measured on two occasions, was analysed in this same subgroup after excluding 59 subjects with fasting plasma glucose >7 mmol l(-1) (n = 481, sub-sample 3). Glucose 51-58 insulin Homo sapiens 15-22 9538973-17 1998 In diabetic subjects, the insulin-to-glucose ratio, C-peptide-to-glucose ratio, and delta I/G were significantly low compared with all other groups (P < 0.005). Glucose 37-44 insulin Homo sapiens 26-33 9538982-11 1998 In healthy control subjects and in obese subjects, the insulin:glucose ratio, used as an indirect measure of insulin sensitivity, was positively correlated to GTN IC50 (r = 0.530, P = 0.008), further suggesting that the sensitivity to NO is reduced in the presence of insulin resistance. Glucose 63-70 insulin Homo sapiens 55-62 9538983-4 1998 Insulin secretion was assessed using ratio of increment (0 to 30 min) in insulin to glucose concentrations during an oral glucose tolerance test (OGTT). Glucose 84-91 insulin Homo sapiens 0-7 9538983-4 1998 Insulin secretion was assessed using ratio of increment (0 to 30 min) in insulin to glucose concentrations during an oral glucose tolerance test (OGTT). Glucose 122-129 insulin Homo sapiens 0-7 9868985-8 1998 Relative or absolute excess insulin occurs when: insulin (or insulin secretagogue) doses are excessive, ill-timed or of the wrong type; the influx of exogenous glucose, endogenous glucose production or insulin clearance are decreased; and insulin-independent glucose utilization or insulin sensitivity are increased. Glucose 180-187 insulin Homo sapiens 28-35 9868985-8 1998 Relative or absolute excess insulin occurs when: insulin (or insulin secretagogue) doses are excessive, ill-timed or of the wrong type; the influx of exogenous glucose, endogenous glucose production or insulin clearance are decreased; and insulin-independent glucose utilization or insulin sensitivity are increased. Glucose 180-187 insulin Homo sapiens 28-35 9868986-10 1998 In principle, insulin therapy should always be able to lower glucose levels; improved glycaemic control is achieved in most patients, followed by amelioration of hyperglycaemic symptoms and improvements in quality of life. Glucose 61-68 insulin Homo sapiens 14-21 9868989-3 1998 The mealtime insulin response in patients with Type 2 diabetes is blunted and delayed, whereas basal levels often remain within the normal range (albeit at elevated fasting glucose levels). Glucose 173-180 insulin Homo sapiens 13-20 9868989-4 1998 Restoration of the insulin secretion pattern at mealtimes (prandial phase)--without stimulating insulin secretion in the "postabsorptive" phase--is the rationale for the development of "prandial glucose regulators", drugs that are characterized by a very rapid onset and short duration of action in stimulating insulin secretion. Glucose 195-202 insulin Homo sapiens 19-26 9710357-7 1998 In conclusion, these findings indicate that hP-16 attenuates the elevation of blood glucose and insulin levels after an oral glucose load in non-diabetic humans. Glucose 125-132 insulin Homo sapiens 96-103 9792458-3 1998 Thus, during short-term substitution of C-peptide (1-3 h) decreased glomerular hyperfiltration, augmented whole body and skeletal muscle glucose utilisation, improved autonomic nerve function and a redistribution of microvascular skin blood flow could be observed. Glucose 137-144 insulin Homo sapiens 40-49 10658358-10 1998 The baseline levels of plasma immunoreactive insulin showed a tendency towards increase in the patients with uremia as compared with the controls (7.2 +/- 1.1 IU/ml versus 6.4 +/- 0.7 IU/ml) whereas no significant difference was found at the 1st, 2nd or 3rd hour following the ingestion of glucose as compared with the healthy controls. Glucose 290-297 insulin Homo sapiens 45-52 9449401-1 1998 Insulin sensitivity was assessed using a glucose-insulin infusion test in 15 newly diagnosed non-obese hypertensive black Tanzanians with normal glucose tolerance and in 15 normotensive control subjects matched for age, sex, and body mass index. Glucose 41-48 insulin Homo sapiens 0-7 9449401-6 1998 These data indicate a strong association between insulin mediated glucose uptake and blood pressure in this population of normal weight untreated urban Africans. Glucose 66-73 insulin Homo sapiens 49-56 9583287-6 1998 At 60 minutes during oral glucose tolerance test, higher insulin levels were seen in Groups I and II as compared to controls (p = NS). Glucose 26-33 insulin Homo sapiens 57-64 16250706-2 1998 In Session I each of our 40 healthy male volunteers received a bolus injection of human insulin (0.05 IU/kg) resulting in plasma glucose nadirs of below 2.8 mmo/L. Glucose 129-136 insulin Homo sapiens 88-95 9434671-5 1998 This value was then divided by the average plasma glucose value to give glucose clearance per plasma insulin concentration. Glucose 72-79 insulin Homo sapiens 101-108 10212834-4 1998 For example, it would be instructive to determine simultaneously the effects of insulin on glucose disposal and testosterone biosynthesis in isolated thecal cells. Glucose 91-98 insulin Homo sapiens 80-87 10212834-7 1998 There is substantial evidence to suggest that some IPGs may also be responsible in part for mediating insulin"s stimulation of glucose disposal (see paper by Dr. Joseph Larner in this issue)--this raises the question as to whether specific forms of IPGs are responsible for glucose metabolism in vivo, whereas other IPGs are responsible for mediating insulin"s effects on steroidogenesis. Glucose 127-134 insulin Homo sapiens 102-109 10212835-5 1998 Interestingly, the transport of insulin across the endothelial barrier not only limits the rate of insulin to stimulate glucose uptake by skeletal muscle, but appears also to determine the rate at which insulin suppresses liver glucose output. Glucose 120-127 insulin Homo sapiens 32-39 10212835-5 1998 Interestingly, the transport of insulin across the endothelial barrier not only limits the rate of insulin to stimulate glucose uptake by skeletal muscle, but appears also to determine the rate at which insulin suppresses liver glucose output. Glucose 120-127 insulin Homo sapiens 99-106 10212835-5 1998 Interestingly, the transport of insulin across the endothelial barrier not only limits the rate of insulin to stimulate glucose uptake by skeletal muscle, but appears also to determine the rate at which insulin suppresses liver glucose output. Glucose 120-127 insulin Homo sapiens 99-106 10212835-11 1998 3) If FFA are reduced independent of insulin administration, glucose output is reduced. Glucose 61-68 insulin Homo sapiens 37-44 10212835-12 1998 These three points support the concept that insulin, by regulating adipocyte lipolysis, controls liver glucose production. Glucose 103-110 insulin Homo sapiens 44-51 10212835-15 1998 Insulin resistance at the fat cell may be an important component of the overall regulation of glycemia because of the relationships between FFA and glucose production, glucose uptake, and insulin release. Glucose 148-155 insulin Homo sapiens 0-7 10212835-15 1998 Insulin resistance at the fat cell may be an important component of the overall regulation of glycemia because of the relationships between FFA and glucose production, glucose uptake, and insulin release. Glucose 168-175 insulin Homo sapiens 0-7 10212836-5 1998 However, in addition to abnormalities of phosphorylation processes, it appears that alterations in cellular cation metabolism contribute to diminished cellular actions of insulin (i.e., glucose transport and hemodynamic actions). Glucose 186-193 insulin Homo sapiens 171-178 10212838-0 1998 Mechanisms of insulin resistance in non-oxidative glucose metabolism: the role of glycogen synthase. Glucose 50-57 insulin Homo sapiens 14-21 10212838-1 1998 Insulin-mediated non-oxidative glucose metabolism is more or less identical to glycogen synthesis in skeletal muscle and that is why this pathway is specifically discussed in this paper. Glucose 31-38 insulin Homo sapiens 0-7 10212838-2 1998 All three major steps in non-oxidative glucose processing--glucose transport, phosphorylation and glycogen synthesis--are found to be reduced in response to insulin in insulin-resistant type 2 diabetic subjects compared with controls. Glucose 39-46 insulin Homo sapiens 157-164 10212838-2 1998 All three major steps in non-oxidative glucose processing--glucose transport, phosphorylation and glycogen synthesis--are found to be reduced in response to insulin in insulin-resistant type 2 diabetic subjects compared with controls. Glucose 39-46 insulin Homo sapiens 168-175 10212838-5 1998 The most pronounced finding in our studies is reduced glycogen synthase activation by insulin which is found in prediabetic subjects with normal glucose tolerance as well as in type 2 diabetics, but more severely. Glucose 145-152 insulin Homo sapiens 86-93 9470007-11 1998 Furthermore, weight at age 14 years is significantly negatively correlated with measures of insulin-stimulated glucose use, indicating that obese adolescents may be at greater risk than nonobese adolescents for development of non-insulin dependent diabetes in adulthood. Glucose 111-118 insulin Homo sapiens 92-99 9470007-13 1998 However, we did find evidence that somatic growth (body weight and body mass index) is significantly related to obesity and attenuated insulin-stimulated glucose utilization in adulthood. Glucose 154-161 insulin Homo sapiens 135-142 9595364-5 1998 Insulin therapy was added for women with a mean serum glucose value > 100 mg/dl on a 24 hour glucose profile. Glucose 54-61 insulin Homo sapiens 0-7 9595364-5 1998 Insulin therapy was added for women with a mean serum glucose value > 100 mg/dl on a 24 hour glucose profile. Glucose 96-103 insulin Homo sapiens 0-7 9870417-12 1998 As insulin resistance worsens, glucose levels increase, with the appearance of glucose intolerance and, finally, of NIDDM, when insulin response cannot compensate for insulin resistance. Glucose 31-38 insulin Homo sapiens 3-10 9870417-12 1998 As insulin resistance worsens, glucose levels increase, with the appearance of glucose intolerance and, finally, of NIDDM, when insulin response cannot compensate for insulin resistance. Glucose 31-38 insulin Homo sapiens 128-135 9870417-12 1998 As insulin resistance worsens, glucose levels increase, with the appearance of glucose intolerance and, finally, of NIDDM, when insulin response cannot compensate for insulin resistance. Glucose 31-38 insulin Homo sapiens 128-135 9870417-12 1998 As insulin resistance worsens, glucose levels increase, with the appearance of glucose intolerance and, finally, of NIDDM, when insulin response cannot compensate for insulin resistance. Glucose 79-86 insulin Homo sapiens 3-10 9481140-2 1998 Insulin resistance results, with the wound in the skin receiving increased glucose, presumably to be used for wound healing and fighting invasion by foreign organisms. Glucose 75-82 insulin Homo sapiens 0-7 10342486-4 1998 Insulin secretory response to glucose, insulin content, DNA strand breakage, and early-to-late stage apoptosis were recorded in each experiment. Glucose 30-37 insulin Homo sapiens 0-7 9403636-3 1997 On the other hand, this interest has been stimulated by experimental evidence suggesting that the vascular actions of insulin may play a role in its main action, namely the promotion of glucose uptake in skeletal muscle tissue. Glucose 186-193 insulin Homo sapiens 118-125 9398143-1 1997 The ability of insulin to stimulate glucose disposal by muscle varies widely within the population at large. Glucose 36-43 insulin Homo sapiens 15-22 9451467-4 1997 Here, we demonstrate that leptin acts as an inhibitor of glucose-induced (20 mM) insulin secretion from isolated human islets. Glucose 57-64 insulin Homo sapiens 81-88 9451470-1 1997 Bovine insulin was glycated by in vitro incubation with 20-220 mM D-glucose for 1-48 h. The percentage of glycation was dependent on time, glucose concentration, temperature and pH, attaining values up to 28%. Glucose 66-75 insulin Homo sapiens 7-14 9451470-1 1997 Bovine insulin was glycated by in vitro incubation with 20-220 mM D-glucose for 1-48 h. The percentage of glycation was dependent on time, glucose concentration, temperature and pH, attaining values up to 28%. Glucose 68-75 insulin Homo sapiens 7-14 9451470-2 1997 Glucose-lowering activities of glycated and control (non-glycated) insulin preparations were assessed in mice by intraperitoneal injection in a 39% (w/v) glucose solution (2 g/kg body weight) at doses of 0.05 and 0.25 units/kg body weight. Glucose 0-7 insulin Homo sapiens 67-74 9451470-4 1997 Simultaneous administration of non-glycated insulin with glucose significantly decreased the 30-min glycaemic excursion (P < 0.001) in a dose-dependent manner. Glucose 57-64 insulin Homo sapiens 44-51 9451470-5 1997 Glycated insulin exhibited a significant reduction (P < 0.001) in glucose-lowering activity under these conditions. Glucose 69-76 insulin Homo sapiens 9-16 9451470-6 1997 The relationship between the extent of insulin glycation and glucose-lowering activity at 0.25 units/kg was assessed using five different insulin preparations glycated between 6%-28%. Glucose 61-68 insulin Homo sapiens 39-46 9451470-7 1997 The insulin-induced decrease in plasma glucose at 30 min was inversely related to the extent of glycation (r = 0.99). Glucose 39-46 insulin Homo sapiens 4-11 9451470-8 1997 Glycated insulin (10(-8) and 10(-6) M) also exhibited a significantly reduced (P < 0.05) ability to stimulate glucose oxidation in isolated mouse diaphragm muscle compared with non-glycated insulin. Glucose 113-120 insulin Homo sapiens 9-16 9435517-2 1997 This effect of exercise is similar to the action of insulin on glucose uptake, and the mechanism through which both stimuli increase skeletal muscle glucose uptake involves the translocation of GLUT-4 glucose transporters to the plasma membrane and transverse tubules. Glucose 63-70 insulin Homo sapiens 52-59 9435517-2 1997 This effect of exercise is similar to the action of insulin on glucose uptake, and the mechanism through which both stimuli increase skeletal muscle glucose uptake involves the translocation of GLUT-4 glucose transporters to the plasma membrane and transverse tubules. Glucose 149-156 insulin Homo sapiens 52-59 9435517-2 1997 This effect of exercise is similar to the action of insulin on glucose uptake, and the mechanism through which both stimuli increase skeletal muscle glucose uptake involves the translocation of GLUT-4 glucose transporters to the plasma membrane and transverse tubules. Glucose 149-156 insulin Homo sapiens 52-59 9435517-7 1997 The ability of exercise to utilize insulin-independent mechanisms to increase glucose uptake in skeletal muscle has important clinical implications, especially for patients with diseases that are associated with peripheral insulin resistance, such as non-insulin-dependent diabetes mellitus. Glucose 78-85 insulin Homo sapiens 35-42 9435517-7 1997 The ability of exercise to utilize insulin-independent mechanisms to increase glucose uptake in skeletal muscle has important clinical implications, especially for patients with diseases that are associated with peripheral insulin resistance, such as non-insulin-dependent diabetes mellitus. Glucose 78-85 insulin Homo sapiens 223-230 9441869-1 1997 The mitochondrial enzyme FAD-linked glycerophosphate dehydrogenase (mGDH) plays a key role in the recognition of glucose as a stimulus for insulin release from the pancreatic islet B-cell. Glucose 113-120 insulin Homo sapiens 139-146 9392476-0 1997 Augmentation of insulin release by glucose in the absence of extracellular Ca2+: new insights into stimulus-secretion coupling. Glucose 35-42 insulin Homo sapiens 16-23 9589775-4 1997 Somewhat paradoxically, the ability of insulin to stimulate glucose uptake is diminished, so that hyperglycaemia is often evident during nutritional intake. Glucose 60-67 insulin Homo sapiens 39-46 9415826-0 1997 Mechanisms by which insulin and muscle contraction stimulate glucose transport. Glucose 61-68 insulin Homo sapiens 20-27 9415826-4 1997 The contraction signaling pathway is distinct from the insulin pathway because the effect of insulin and contractions on glucose uptake are additive, and contractions do not increase insulin receptor kinase or PI 3-kinase activity. Glucose 121-128 insulin Homo sapiens 93-100 9415826-4 1997 The contraction signaling pathway is distinct from the insulin pathway because the effect of insulin and contractions on glucose uptake are additive, and contractions do not increase insulin receptor kinase or PI 3-kinase activity. Glucose 121-128 insulin Homo sapiens 93-100 9415826-5 1997 In contrast, studies indicating that contractions cause the translocation of GLUT4 and that both contractions and insulin-stimulated glucose transport can be blocked by calcium channel blockers suggest that the two pathways may converge. Glucose 133-140 insulin Homo sapiens 114-121 9392476-5 1997 These mechanisms are in accord with the belief that glucose-stimulated insulin secretion has an essential requirement for extracellular Ca2+ and increased [Ca2+]i. Glucose 52-59 insulin Homo sapiens 71-78 9392476-6 1997 However, when protein kinases A and C are activated simultaneously, a large effect of glucose to augment insulin release can be seen in the absence of extracellular Ca2+, under conditions in which [Ca2+]i is not increased, and even when [Ca2+]i is decreased to low levels by intracellular chelation with BAPTA. Glucose 86-93 insulin Homo sapiens 105-112 9502570-3 1998 In adult patients, this induces, over the dialysis session, a significant uptake of glucose, with some benefits, i.e., avoidance of caloric loss, but also with some metabolic risks, i.e. decreased dialytic potassium removal secondary to an insulin-dependent intracellular potassium shift. Glucose 84-91 insulin Homo sapiens 240-247 9392476-11 1997 The augmentation pathways are likely responsible for time-dependent potentiation of secretion and for the second phase of glucose-stimulated insulin release. Glucose 122-129 insulin Homo sapiens 141-148 9392481-1 1997 Insulin-stimulated glucose transport across the skeletal muscle cell membrane is a major regulatory step in postprandial glucose disposal. Glucose 19-26 insulin Homo sapiens 0-7 9392481-1 1997 Insulin-stimulated glucose transport across the skeletal muscle cell membrane is a major regulatory step in postprandial glucose disposal. Glucose 121-128 insulin Homo sapiens 0-7 9392481-7 1997 In conclusion, maximal in vitro insulin stimulation of vastus lateralis muscle strips from healthy subjects resulted in a twofold rise in glucose transport as well as in cell surface content, whereas the turnover rate of GLUT4 was unaffected by insulin under the chosen experimental conditions. Glucose 138-145 insulin Homo sapiens 32-39 9447955-1 1997 Hexokinase II (HKII) plays an important role in facilitating glucose uptake by skeletal muscle, heart, and adipose tissue in response to insulin. Glucose 61-68 insulin Homo sapiens 137-144 9389497-9 1997 Despite the low levels of insulin-induced PLC activity, insulin-stimulated glucose transport activity was similarly inhibited by U73122 (55.9 +/- 13.1% inhibition). Glucose 75-82 insulin Homo sapiens 56-63 9405901-9 1997 Meal-related glucose excursions were significantly lower with insulin lispro compared with regular insulin (mean -0.8 +/- 1.7 vs. 1.1 +/- 1.6 mmol/l, P < 0.001), as was the within-day variability (M value 27.7 +/- 19.7 vs. 30.2 +/- 23.1, P = 0.007). Glucose 13-20 insulin Homo sapiens 62-69 9405906-1 1997 OBJECTIVE: The interrelations between obesity, glucose intolerance, hypertension, dyslipidemia, and insulin resistance are well recognized. Glucose 47-54 insulin Homo sapiens 100-107 9389497-10 1997 Inhibition of PLC activation did not impair either EGF- or insulin-induced activation of glycogen synthase or incorporation of glucose into lipid, supporting the hypothesis that both EGF- and insulin-induced glucose disposal can be independent of GLUT4-mediated glucose transport. Glucose 208-215 insulin Homo sapiens 192-199 9389497-10 1997 Inhibition of PLC activation did not impair either EGF- or insulin-induced activation of glycogen synthase or incorporation of glucose into lipid, supporting the hypothesis that both EGF- and insulin-induced glucose disposal can be independent of GLUT4-mediated glucose transport. Glucose 208-215 insulin Homo sapiens 192-199 9389497-11 1997 The diminution of glucose transport secondary to inhibition of PLC activity was reflected by a decrease in GLUT4 translocation to the plasma membrane upon either EGF or insulin stimulation. Glucose 18-25 insulin Homo sapiens 169-176 9403581-3 1997 Insulin-assisted frequently-sampled intravenous glucose tolerance tests were performed at baseline and 14 to 18 hours after the 7th exercise session. Glucose 48-55 insulin Homo sapiens 0-7 9408743-10 1997 Indeed, the defect in insulin action appears to be selective, affecting glucose metabolism but not cell growth. Glucose 72-79 insulin Homo sapiens 22-29 9527493-1 1997 Whole body glucose homeostasis is dependent on the action of insulin. Glucose 11-18 insulin Homo sapiens 61-68 9527493-2 1997 In muscle and adipose tissues, insulin stimulates glucose uptake by inducing the translocation of vesicles containing the glucose transporter GLUT4 to the cell surface. Glucose 50-57 insulin Homo sapiens 31-38 9470869-6 1997 Mean serum insulin at 0, 1, and 2 hours after 75 g oral glucose was higher among the sedentary population (17.1 v 11.6, 88.2 v 62.1, and 57.9 v 36.2 microU/ml, respectively (all p < 0.0001). Glucose 56-63 insulin Homo sapiens 11-18 9403581-6 1997 Fasting (73+/-9 to 50+/-9 pmol/L, P=.02) and glucose-stimulated (332+/-58 to 261+/-45 pmol/L, P=.05) plasma insulin levels decreased. Glucose 45-52 insulin Homo sapiens 108-115 9403583-0 1997 Antihypertensive agent moxonidine enhances muscle glucose transport in insulin-resistant rats. Glucose 50-57 insulin Homo sapiens 71-78 9403583-7 1997 Moreover, glucose transport activity in the isolated epitrochlearis muscle stimulated by a maximally effective insulin dose (13.3 nmol/L) was 39% and 70% greater in the 6 and 10 mg/kg moxonidine-treated groups, respectively (P<.05 for all effects). Glucose 10-17 insulin Homo sapiens 111-118 9400562-9 1997 In centenarians, insulin-mediated glucose uptake was greater (34.6 +/- 0.5 vs 23.3 +/- .05 mumol/Kg FFM x min P < .010) than in aged subjects and correlated with fasting plasma triglycerides, FFA, LDL, and HDL cholesterol, Apo B, and Apo A1 concentrations. Glucose 34-41 insulin Homo sapiens 17-24 9426377-0 1997 Cholinergic enhancement by pyridostigmine increases the insulin response to glucose load in obese patients but not in normal subjects. Glucose 76-83 insulin Homo sapiens 56-63 9426381-3 1997 OBJECTIVE: To investigate whether these alterations characterize circulating lymphocytes of individuals with insulin resistance in whom derangements of glucose homeostasis are absent (obese subjects with normal glucose tolerance), or present but still controllable (nonobese and obese newly diagnosed NIDDM patients on an appropriate diet). Glucose 152-159 insulin Homo sapiens 109-116 9398716-4 1997 In the 19 women given metformin, the mean (+/- SE) area under the serum insulin curve after oral glucose administration decreased from 44 +/- 5 to 24 +/- 3 nmol/L.min (P = 0.003). Glucose 97-104 insulin Homo sapiens 72-79 9389749-12 1997 PFK1-M deficiency causes impaired insulin secretion in response to glucose, demonstrating its participation in islet glucose metabolism, and peripheral insulin resistance. Glucose 67-74 insulin Homo sapiens 34-41 9504888-3 1997 The aim of this study was to evaluate the effect of cisapride on plasma concentrations of glucose, insulin and C-peptide in response to oral and intravenous glucose loads. Glucose 157-164 insulin Homo sapiens 111-120 9504888-7 1997 After the intravenous glucose load, plasma concentrations of C-peptide were higher (P< 0.01) on cisapride when compared with placebo (e.g. peak C-peptide 2.08+/-0.25 nmol/L vs 1.78+/-0.22 nmol/L, P< 0.01) while there was no significant difference in plasma glucose or insulin. Glucose 263-270 insulin Homo sapiens 61-70 9504888-9 1997 Mean plasma concentrations of insulin and C-peptide were higher after oral glucose on cisapride than placebo, but these differences were not significantly different. Glucose 75-82 insulin Homo sapiens 30-37 9504888-9 1997 Mean plasma concentrations of insulin and C-peptide were higher after oral glucose on cisapride than placebo, but these differences were not significantly different. Glucose 75-82 insulin Homo sapiens 42-51 9504888-10 1997 These observations indicate that cisapride may increase glucose-stimulated insulin secretion. Glucose 56-63 insulin Homo sapiens 75-82 9431856-8 1997 CONCLUSIONS: This study showed that essential hypertensive patients with high NaCl sensitivities were relatively insulin resistant compared with those with low NaCl sensitivities, independently of confounding factors such as age, obesity and glucose intolerance. Glucose 242-249 insulin Homo sapiens 113-120 9458276-8 1997 Chronic exogenous insulin administration resulted in a 11.5 (1.73%/h) and 11.0 (1.65%/h)-fold increase over baseline in the synthesis of newly made VLDL-TG palmitate in the glucose and fructose groups, respectively. Glucose 173-180 insulin Homo sapiens 18-25 9444629-0 1997 The influence of oral glucose intake on binding and degradation of 125I-insulin by receptors on erythrocytes as well as on insulin and C-peptide serum levels in patients after myocardial infarction and healthy individuals. Glucose 22-29 insulin Homo sapiens 72-79 9444629-1 1997 In this study, we investigated the influence of glucose administration on binding and degradation of 125I-insulin by receptors on erythrocytes as well as on insulin and C-peptide serum levels in 15 patients after myocardial infarction and in 15 age-matched healthy persons. Glucose 48-55 insulin Homo sapiens 106-113 9444629-7 1997 Impaired degradation of 125I-insulin during the oral glucose tolerance test in the patients after myocardial infarction indicates that insulin resistance is located at the receptor level. Glucose 53-60 insulin Homo sapiens 29-36 9372969-14 1997 These results indicate a bifurcation or subcompartmentalization of the insulin signalling pathway whereby some targets of PI 3-K (i.e., p70s6k) are dependent on IRS-1-associated PI 3-K and other targets (i.e., AKT and glucose transport) are not. Glucose 218-225 insulin Homo sapiens 71-78 9439539-1 1997 Basal plasma glucose is usually increased in uncomplicated malaria, implying insulin resistance. Glucose 13-20 insulin Homo sapiens 77-84 9439543-2 1997 After 17 or 18 weeks of treatment, the glucose infusion rate (GIR) in the euglycemic insulin-glucose clamp test only showed a significant increase in EPA-E-treated rats compared with control rats given distilled water alone as the vehicle. Glucose 39-46 insulin Homo sapiens 85-92 9439543-2 1997 After 17 or 18 weeks of treatment, the glucose infusion rate (GIR) in the euglycemic insulin-glucose clamp test only showed a significant increase in EPA-E-treated rats compared with control rats given distilled water alone as the vehicle. Glucose 93-100 insulin Homo sapiens 85-92 9439547-7 1997 In a multivariate analysis controlling for the influence of the body mass index, we found that circulating leptin correlated significantly to fasting insulin (r = .38, P = .002), and to circulating insulin at 14 mmol/L glucose levels (r = .29, P = .0019) and 28 mmol/L glucose (r = .32, P = .009), as well as to the insulin response to arginine at all three glucose levels (r > .30, P < .013). Glucose 219-226 insulin Homo sapiens 198-205 9439547-7 1997 In a multivariate analysis controlling for the influence of the body mass index, we found that circulating leptin correlated significantly to fasting insulin (r = .38, P = .002), and to circulating insulin at 14 mmol/L glucose levels (r = .29, P = .0019) and 28 mmol/L glucose (r = .32, P = .009), as well as to the insulin response to arginine at all three glucose levels (r > .30, P < .013). Glucose 219-226 insulin Homo sapiens 198-205 9439548-3 1997 We found that previously untreated girls with Turner"s syndrome had a normal insulin activity on glucose metabolism. Glucose 97-104 insulin Homo sapiens 77-84 9439548-12 1997 In conclusion, we found that insulin-stimulated glucose turnover was normal in girls with Turner"s syndrome before therapy. Glucose 48-55 insulin Homo sapiens 29-36 9374566-1 1997 OBJECTIVE: The purpose of this study was to determine whether postprandial administration of the new rapid-acting insulin analog Humalog could effectively reduce glucose excursions in children <5 years old. Glucose 162-169 insulin Homo sapiens 114-121 9404899-6 1997 We discuss the mechanisms responsible for the defects in insulin-mediated glucose utilization, as well as the relation of insulin resistance to obesity, hypertension, and dyslipidemia. Glucose 74-81 insulin Homo sapiens 57-64 9453242-4 1997 To directly evaluate the role of GFAT in modulating insulin-stimulated glucose transport, we co-transfected primary cultures of rat adipose cells with expression vectors for human GFAT as well as an epitope-tagged GLUT4 and examined the effect of overexpressed GFAT on insulin-stimulated translocation of GLUT4. Glucose 71-78 insulin Homo sapiens 52-59 9453242-7 1997 Interestingly, for short incubation times (4 h) we observed a decrease in both basal and insulin-stimulated glucose transport without a detectable effect on insulin-stimulated translocation of GLUT4. Glucose 108-115 insulin Homo sapiens 89-96 9388085-11 1997 After adjusting for age, sex, race, socioeconomic status, disease duration, and severity of diabetes and comorbidities, insulin users had slightly more laboratory tests performed, 2.4 more outpatient visits per year, and almost 300 more fingersticks for home glucose testing per year compared with sulfonylurea users (all P<.01). Glucose 259-266 insulin Homo sapiens 120-127 9424548-5 1997 An increase in the blood glucose level triggers a chain of events in insulin-secreting cells and K(ATP) channel closure which is a prerequisite for insulin secretion. Glucose 25-32 insulin Homo sapiens 69-76 9402775-9 1997 Short adult stature was associated with raised concentrations of glucose and insulin 2 hours after a glucose load-independently of siege exposure. Glucose 101-108 insulin Homo sapiens 77-84 9399641-1 1997 The binding of insulin to its receptor initiates multiple signal transduction pathways regulating such diverse processes as proliferation, differentiation, glucose transport, and glycogen metabolism. Glucose 156-163 insulin Homo sapiens 15-22 9356542-4 1997 Insulin sensitivity was measured by minimal model analysis of a 12-sample, insulin-modified, frequently sampled intravenous glucose tolerance test. Glucose 124-131 insulin Homo sapiens 0-7 9356542-4 1997 Insulin sensitivity was measured by minimal model analysis of a 12-sample, insulin-modified, frequently sampled intravenous glucose tolerance test. Glucose 124-131 insulin Homo sapiens 75-82 9397243-4 1997 Insulin resistance was evaluated by means of constant glucose infusion rate (M value) during euglycemic-hyperinsulinemic glucose clamp test. Glucose 54-61 insulin Homo sapiens 0-7 9374676-6 1997 We conclude that in vivo insulin secretion in humans during nominal glucose stimulation consists of a series of punctuated insulin secretory bursts accounting for > or = 75% of total insulin secretion. Glucose 68-75 insulin Homo sapiens 25-32 9374676-6 1997 We conclude that in vivo insulin secretion in humans during nominal glucose stimulation consists of a series of punctuated insulin secretory bursts accounting for > or = 75% of total insulin secretion. Glucose 68-75 insulin Homo sapiens 123-130 9374676-6 1997 We conclude that in vivo insulin secretion in humans during nominal glucose stimulation consists of a series of punctuated insulin secretory bursts accounting for > or = 75% of total insulin secretion. Glucose 68-75 insulin Homo sapiens 123-130 9460526-4 1997 An oral glucose tolerance test (OGTT) was performed to find the best time for FDG injection and 3 hours after loading, the serum insulin concentration was increased significantly. Glucose 8-15 insulin Homo sapiens 129-136 9409209-3 1997 This cluster is referred to as the insulin resistance syndrome, and the risk factors commonly include dyslipidemia, elevated blood pressure, an android pattern of body fat distribution, and glucose intolerance. Glucose 190-197 insulin Homo sapiens 35-42 9409209-7 1997 Factor 1 consisted of positive loadings for uric acid, systolic and diastolic blood pressure, triglyceride concentration, and waist girth and negative loadings for HDL cholesterol and the rate of insulin-mediated glucose disposal (M, in milligrams per kilogram of body weight per minute). Glucose 213-220 insulin Homo sapiens 196-203 9409326-7 1997 The steady-state plasma glucose level in the vasospastic angina group was about twofold higher than that of the control group, confirming the presence of insulin resistance in patients with vasospastic angina. Glucose 24-31 insulin Homo sapiens 154-161 9581537-1 1997 Insulin stimulates glucose uptake into its target cells by a process which involves the translocation of the GLUT4 isoform of glucose transporter from an intracellular vesicular compartment(s) to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 9389896-3 1997 The aim of the present study was to investigate the effect of C12 infusion on insulin-stimulated glucose uptake in patients with non-insulin-dependent diabetes mellitus (NIDDM) compared with healthy volunteers. Glucose 97-104 insulin Homo sapiens 78-85 9389896-14 1997 Thus, it might be a useful alternative substrate in enteral or parenteral nutrition, sparing glucose utilization and increasing glycogen stores, in those clinical conditions, like NIDDM, where reduced insulin-induced glucose uptake and oxidation are observed. Glucose 217-224 insulin Homo sapiens 201-208 9425398-0 1997 Lower cortisol levels after oral glucose in subjects with insulin resistance and abdominal obesity. Glucose 33-40 insulin Homo sapiens 58-65 9425398-12 1997 This maximal cortisol suppression correlated weakly with the maximal insulin response after oral glucose (r = 0.49, P = 0.07). Glucose 97-104 insulin Homo sapiens 69-76 9444449-4 1997 In practice, patients often inject regular human insulin closer to mealtime, causing a higher post-prandial serum glucose level and an increased potential for hypoglycemia in the postabsorptive period. Glucose 114-121 insulin Homo sapiens 49-56 9444449-8 1997 Treatment with insulin lispro resulted in lower postprandial glucose levels and smaller increases in glucose level after the morning and evening meals compared with treatment with regular human insulin. Glucose 61-68 insulin Homo sapiens 15-22 9444449-8 1997 Treatment with insulin lispro resulted in lower postprandial glucose levels and smaller increases in glucose level after the morning and evening meals compared with treatment with regular human insulin. Glucose 101-108 insulin Homo sapiens 15-22 9472456-6 1997 RESULTS: There was a significant correlation between elevated "true" fasting serum insulin level and various constituents of the insulin resistance syndrome, such as obesity, dyslipidemia (hypertriglyceridemia, increased apolipoprotein B and decreased high-density lipoprotein cholesterol and apolipoprotein A1 concentrations), increased serum glucose, uric acid levels, and plasminogen activator inhibitor type I concentration, as well as increased frequency of diabetes. Glucose 344-351 insulin Homo sapiens 83-90 9353606-4 1997 The insulin area under the curve (AUC) in response to a standard 75-g oral glucose tolerance test (OGTT) was used as an indicator of hyperinsulinemia/insulin resistance. Glucose 75-82 insulin Homo sapiens 4-11 9353606-4 1997 The insulin area under the curve (AUC) in response to a standard 75-g oral glucose tolerance test (OGTT) was used as an indicator of hyperinsulinemia/insulin resistance. Glucose 75-82 insulin Homo sapiens 138-145 9353615-7 1997 beta-cell sensitivity to glucose for insulin release was decreased in subjects with GDM versus pregnant women with NGT as well as nonpregnant women by 40-50% (P < 0.01). Glucose 25-32 insulin Homo sapiens 37-44 9356025-2 1997 Concomitant insulin stimulation (three- to six-fold [P < 0.05]) of thigh glucose clearance, muscle insulin receptor tyrosine kinase (IRTK), insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, and IRS-1-associated phosphatidylinositol 3-kinase (PI 3-kinase) was observed in the rested leg. Glucose 76-83 insulin Homo sapiens 12-19 9356025-4 1997 A twofold higher insulin-stimulated glucose clearance in the exercised compared with the rested thigh was accompanied by unaltered maximal IRTK activation and IRS-1 tyrosine phosphorylation, and by a decreased (approximately 50%, P < 0.05) maximal IRS-1 associated PI 3-kinase activation. Glucose 36-43 insulin Homo sapiens 17-24 9356025-5 1997 Prior exercise caused significantly faster insulin-stimulated tyrosine phosphorylation of IRS-1, PI 3-kinase activity, and glucose clearance compared with those in the rested thigh. Glucose 123-130 insulin Homo sapiens 43-50 9356025-9 1997 Thus, the activity of IRS-1-associated PI 3-kinase and glucose uptake may not always be tightly coupled during insulin stimulation in human muscle. Glucose 55-62 insulin Homo sapiens 111-118 9356031-1 1997 Minimal model analysis with the frequently sampled intravenous glucose tolerance test provides an effective way to measure two important metabolic parameters in vivo under non-steady-state conditions: glucose effectiveness (SG) and insulin sensitivity (SI). Glucose 63-70 insulin Homo sapiens 232-239 9389425-9 1997 When the insulin infusion was stopped, the increases in adipose tissue and muscle glucose concentrations were delayed by approximately 25 and 45 min, respectively, as compared to the increase in plasma glucose. Glucose 82-89 insulin Homo sapiens 9-16 9389425-9 1997 When the insulin infusion was stopped, the increases in adipose tissue and muscle glucose concentrations were delayed by approximately 25 and 45 min, respectively, as compared to the increase in plasma glucose. Glucose 202-209 insulin Homo sapiens 9-16 9463021-2 1997 Upper body obesity, which can be found in 85% of these subjects, can increase muscular insulin resistance through several mechanisms, the best known being a free fatty acid-induced decrease in intracellular free CoA/acylCoA that inhibits the stimulatory effect of insulin on glycolysis, glucose transport across cell membrane, and glycogen storage. Glucose 287-294 insulin Homo sapiens 87-94 9463022-5 1997 Studies of insulin sensitivity during a hyperinsulinaemic hyperglycaemic clamp (a supraphysiological experimental condition) indicated that: i) insulin-induced glucose utilization is decreased in the morning according to a circadian rhythm; ii) this change results from an increase in hepatic glucose production but not from a decrease in glucose uptake; and iii) a circadian rhythm is also observed for plasma free fatty acids and cortisol concentrations, which could account in part for the circadian changes in insulin sensitivity. Glucose 160-167 insulin Homo sapiens 11-18 9463023-10 1997 As a function of their action period and possibly of intrinsic properties, some sulfonamides more than others (e.g. glibenclamide) affect fasting hepatic glucose production, which is particularly increased early in the day in non-insulin-dependent diabetic patients because of a circadian drop in insulin sensitivity (dawn phenomenon). Glucose 154-161 insulin Homo sapiens 230-237 9483371-3 1997 However, insulin stimulated global glucose uptake remained unchanged. Glucose 35-42 insulin Homo sapiens 9-16 15251769-5 1997 RESULTS: The magnitude of the 1.5- and 2-hour postprandial glucose excursion was reduced with 70/30 insulin in comparison with NPH insulin, and patients treated with 70/30 insulin experienced fewer hypoglycemic events than with NPH insulin. Glucose 59-66 insulin Homo sapiens 100-107 15251776-5 1997 Although insulin replacement therapy is well known to be both the best and the most cost-effective way to control glucose levels in patients with type 1 diabetes, studies have no shown that those with type 2 diabetes can likewise benefit from appropriate insulin therapy. Glucose 114-121 insulin Homo sapiens 9-16 9425444-2 1997 We have previously shown that the stable transfection of the full-length insulin cDNA into the human liver cell line, (HEP G2ins) resulted in synthesis, storage and acute regulated release of insulin to analogues of cAMP, but not to the physiological stimulus glucose. Glucose 260-267 insulin Homo sapiens 73-80 9425444-2 1997 We have previously shown that the stable transfection of the full-length insulin cDNA into the human liver cell line, (HEP G2ins) resulted in synthesis, storage and acute regulated release of insulin to analogues of cAMP, but not to the physiological stimulus glucose. Glucose 260-267 insulin Homo sapiens 192-199 9368834-3 1997 DESIGN: We have studied the insulin response to an oral glucose tolerance test (OGTT) and the GH response to GHRH before and after prolonged treatment with Naltrexone (NTX). Glucose 56-63 insulin Homo sapiens 28-35 9360516-2 1997 Insulin and C-peptide responses to oral glucose load were significantly higher in smokers than nonsmokers, whereas glucose levels were not substantially different. Glucose 40-47 insulin Homo sapiens 0-7 9360516-2 1997 Insulin and C-peptide responses to oral glucose load were significantly higher in smokers than nonsmokers, whereas glucose levels were not substantially different. Glucose 40-47 insulin Homo sapiens 12-21 9360541-0 1997 Effect of variations in plasma magnesium concentration on resistance to insulin-mediated glucose disposal in nondiabetic subjects. Glucose 89-96 insulin Homo sapiens 72-79 9360541-4 1997 The low Mg group had significantly higher plasma glucose (P < 0.001) and insulin (P < 0.002) concentrations after the oral glucose challenge. Glucose 129-136 insulin Homo sapiens 76-83 9365878-8 1997 In contrast to microalbuminuria, which is a reflection of renal injury, insulin resistance is a genetically determined problem that directly relates to peripheral glucose utilization. Glucose 163-170 insulin Homo sapiens 72-79 9438920-4 1997 Aim of the present study was to verify the GH response to GHRH and the ability of glucose load to inhibit it in patients with essential hypertension in whom hyperinsulinism and insulin resistance are frequently present. Glucose 82-89 insulin Homo sapiens 162-169 9438920-14 1997 In conclusion, this study demonstrates that, like in normal subjects but differently from in obese patients the GH response to GHRH is normal in patients with essential hypertension and it is normally inhibited by oral glucose load even when these patients show high insulin levels. Glucose 219-226 insulin Homo sapiens 267-274 9459136-1 1997 Insulin resistance is characterized principally by impaired insulin-mediated glucose uptake which provokes a compensatory increase in pancreatic beta-cell secretory activity. Glucose 77-84 insulin Homo sapiens 0-7 9442446-4 1997 OBJECTIVES: In this study, we examined the relationship between insulin secretion in response to an oral glucose load, circadian variation of blood pressure, and evidence of vascular damage, measured by the thickness of the carotid artery and urinary albumin excretion. Glucose 105-112 insulin Homo sapiens 64-71 9361681-5 1997 Insulin-stimulated glucose uptake and insulin binding of adipocytes were significantly reduced. Glucose 19-26 insulin Homo sapiens 0-7 9361681-7 1997 beta-Cell function as shown by plasma glucose and insulin responses to oral glucose remained intact in group F and group O. Glucose 76-83 insulin Homo sapiens 50-57 9361683-3 1997 The relationship between physical activity and insulin resistance could be mediated, in part, by direct effects on skeletal muscle, a significant site for insulin-mediated glucose disposal. Glucose 172-179 insulin Homo sapiens 47-54 9361683-3 1997 The relationship between physical activity and insulin resistance could be mediated, in part, by direct effects on skeletal muscle, a significant site for insulin-mediated glucose disposal. Glucose 172-179 insulin Homo sapiens 155-162 9361685-5 1997 An insulin sensitivity index (Si) was determined from a frequently sampled intravenous glucose tolerance test using a minimal modeling method. Glucose 87-94 insulin Homo sapiens 3-10 9368278-4 1997 It has been found that older individuals who vigorously train on a regular basis exhibit a greater glucose tolerance and a lower insulin response to a glucose challenge than sedentary individuals of similar age and weight. Glucose 151-158 insulin Homo sapiens 129-136 10889869-2 1997 Insulin is anabolic, increasing storage of glucose, fatty acids and amino acids, while glucagon namely stimulates hepatic glycogenolysis, gluconeogenesis, and ketogenesis. Glucose 43-50 insulin Homo sapiens 0-7 9368278-13 1997 Several months of weight training has been found to significantly lower the insulin response to a glucose challenge without affecting glucose tolerance, and to increase the rate of glucose clearance during a euglycaemic clamp. Glucose 98-105 insulin Homo sapiens 76-83 9368278-15 1997 While it has been known for many years that insulin will accelerate blood glucose extraction by insulin-sensitive peripheral tissues, recent evidence suggests that it can also acutely vasodilate skeletal muscle and increase muscle blood flow in a dose-dependent manner. Glucose 74-81 insulin Homo sapiens 44-51 9368278-15 1997 While it has been known for many years that insulin will accelerate blood glucose extraction by insulin-sensitive peripheral tissues, recent evidence suggests that it can also acutely vasodilate skeletal muscle and increase muscle blood flow in a dose-dependent manner. Glucose 74-81 insulin Homo sapiens 96-103 9550126-2 1997 We evaluated the effect of pioglitazone, a thiazolidinedione compound, on insulin-stimulated glucose disposal (Rd) and its efficacy on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 93-100 insulin Homo sapiens 74-81 9368278-18 1997 Improvements in insulin resistance and glucose tolerance with exercise training are highly related to an increased skeletal muscle insulin action. Glucose 39-46 insulin Homo sapiens 131-138 9368278-19 1997 This increased insulin action is associated with an increase in the insulin-regulatable glucose transporters, GLUT4, and enzymes responsible for the phosphorylation, storage and oxidation of glucose. Glucose 88-95 insulin Homo sapiens 15-22 9368278-19 1997 This increased insulin action is associated with an increase in the insulin-regulatable glucose transporters, GLUT4, and enzymes responsible for the phosphorylation, storage and oxidation of glucose. Glucose 88-95 insulin Homo sapiens 68-75 9355825-6 1997 Upon exposure to high glucose, the islet batches that did retain the ability to respond to glucose were shown to have secreted an average of 1220+/-73 pM/24 hr/islet of insulin as compared with 1528+/-118 pM/24 hr/islet for fresh islets. Glucose 22-29 insulin Homo sapiens 169-176 9353126-1 1997 In mammals, insulin signalling regulates glucose transport together with the expression and activity of various metabolic enzymes. Glucose 41-48 insulin Homo sapiens 12-19 9341192-3 1997 However, although the insulin stimulation of GLUT4 translocation and glucose transport activity was completely inhibited by wortmannin, activation by osmotic shock was wortmannin-insensitive. Glucose 69-76 insulin Homo sapiens 22-29 9355825-6 1997 Upon exposure to high glucose, the islet batches that did retain the ability to respond to glucose were shown to have secreted an average of 1220+/-73 pM/24 hr/islet of insulin as compared with 1528+/-118 pM/24 hr/islet for fresh islets. Glucose 91-98 insulin Homo sapiens 169-176 9334237-1 1997 Insulin production by the pancreatic islet is tightly coupled to the concentration of blood glucose. Glucose 92-99 insulin Homo sapiens 0-7 9334237-2 1997 The mechanism by which glucose controls proinsulin biosynthesis in beta cells is poorly understood. Glucose 23-30 insulin Homo sapiens 40-50 9329954-6 1997 Whole body insulin-stimulated glucose uptake was decreased in the patients (15.6+/-2.1 vs. 23.1+/-2.0 micromol x kg-1 x min-1). Glucose 30-37 insulin Homo sapiens 11-18 9329954-7 1997 Insulin-stimulated glucose uptake in the forearm and the cardiac muscle was equally reduced in the patients (46+/-5 and 48+/-5%). Glucose 19-26 insulin Homo sapiens 0-7 9329954-11 1997 In patients with syndrome X, insulin-stimulated glucose uptake is independent from myocardial blood flow. Glucose 48-55 insulin Homo sapiens 29-36 9404359-2 1997 Recent interventional trials in both insulin-dependent and non-insulin-dependent patients have helped identify this target glucose level. Glucose 123-130 insulin Homo sapiens 37-44 9366261-5 1997 Results demonstrate that whereas the effects of vanadate and hypoxia were additive with insulin stimulated glucose transport, the effect of vanadate plus hypoxia was not. Glucose 107-114 insulin Homo sapiens 88-95 9404359-2 1997 Recent interventional trials in both insulin-dependent and non-insulin-dependent patients have helped identify this target glucose level. Glucose 123-130 insulin Homo sapiens 63-70 9350889-3 1997 Investigations included an intravenous glucose tolerance test, insulin response to the glucose load in plasma and insulin secretion rate. Glucose 87-94 insulin Homo sapiens 63-70 9366964-4 1997 The endothelin-1 infusion reduced insulin sensitivity as demonstrated by a 31 +/- 7% decrease in whole-body glucose uptake (P < 0.05) and a 26 +/- 11% fall in leg glucose uptake (P < 0.05) compared with the control protocol. Glucose 108-115 insulin Homo sapiens 34-41 9314631-0 1997 Modification of postprandial hyperglycemia with insulin lispro improves glucose control in patients with type 2 diabetes. Glucose 72-79 insulin Homo sapiens 48-55 9366964-7 1997 In summary, exogenous endothelin-1 induced insulin resistance in healthy humans by reducing insulin-dependent glucose uptake in skeletal muscle without decreasing skeletal muscle blood flow. Glucose 110-117 insulin Homo sapiens 92-99 9357798-0 1997 Impaired adaptation of first-phase insulin secretion in postmenopausal women with glucose intolerance. Glucose 82-89 insulin Homo sapiens 35-42 9453278-4 1997 Patients with GH deficiency tend to be obese, and obesity per se is also associated with insulin resistance which plays a key role in a cluster of metabolic derangements including glucose intolerance, hypertension, lipid abnormalities and atherosclerotic cardiovascular disease. Glucose 180-187 insulin Homo sapiens 89-96 9361613-6 1997 Patients with sepsis had an attenuated plasma insulin response to glucose administration compared with control subjects (P < 0.001) and less marked suppression of plasma fatty acid and glycerol concentrations (P < 0.001). Glucose 66-73 insulin Homo sapiens 46-53 9361934-5 1997 Late insulin release in brain-dead patients was not lower, but was higher than controls and was accompanied by a decrease in the glucose disappearance rate. Glucose 129-136 insulin Homo sapiens 5-12 9313749-6 1997 Both sulfonylurea and insulin therapy substantially reduced fasting plasma glucose and glycosylated hemoglobin (HbA1e) concentrations, compared with diet therapy alone. Glucose 75-82 insulin Homo sapiens 22-29 9313753-5 1997 Insulin sensitivity was measured using the glucose clamp technique (40 mU.m-2.min-1), in conjunction with [3-3H]glucose isotope dilution. Glucose 43-50 insulin Homo sapiens 0-7 9313753-7 1997 Insulin-stimulated glucose disposal (Rd) ranged from 3.03 to 16.83 mg.min-1.kg-1 FFM. Glucose 19-26 insulin Homo sapiens 0-7 9313755-2 1997 Insulin resistance has been hypothesized to unify the clustering of hypertension, glucose intolerance, hyperinsulinemia, increased levels of triglyceride and decreased HDL cholesterol, and central and overall obesity. Glucose 82-89 insulin Homo sapiens 0-7 9314631-1 1997 OBJECTIVE: Insulin lispro is a rapid-acting analog of human insulin that can be used to target the postprandial rise in plasma glucose. Glucose 127-134 insulin Homo sapiens 11-18 9314631-1 1997 OBJECTIVE: Insulin lispro is a rapid-acting analog of human insulin that can be used to target the postprandial rise in plasma glucose. Glucose 127-134 insulin Homo sapiens 60-67 9314631-8 1997 RESULTS: Insulin lispro in combination with sulfonylurea therapy significantly reduced 2-h postprandial glucose concentrations compared with sulfonylureas alone, from 18.6 to 14.2 mmol/l (P < 0.0001), and incremental postprandial glucose area from 617.8 to 472.9 mmol.min.1-1 (P < 0.0007). Glucose 104-111 insulin Homo sapiens 9-16 9314631-8 1997 RESULTS: Insulin lispro in combination with sulfonylurea therapy significantly reduced 2-h postprandial glucose concentrations compared with sulfonylureas alone, from 18.6 to 14.2 mmol/l (P < 0.0001), and incremental postprandial glucose area from 617.8 to 472.9 mmol.min.1-1 (P < 0.0007). Glucose 233-240 insulin Homo sapiens 9-16 9349600-10 1997 In conclusion, we have identified several metabolic abnormalities in the normal glucose tolerant relatives, and propose that the decreased hepatic insulin clearance helps to maintain normoglycaemia in the face of combined insulin resistance and decreased insulin secretion. Glucose 80-87 insulin Homo sapiens 147-154 9349602-8 1997 2) Both insulin and bpV(pic) decrease lipolysis and enhance glucose uptake in control as well as NIDDM adipocytes. Glucose 60-67 insulin Homo sapiens 8-15 9349602-10 1997 3) Peroxovanadate does not improve sensitivity and responsiveness to insulin in NIDDM adipocytes, showing that insulin-resistant glucose uptake in NIDDM is not overcome by phosphotyrosine-phosphatase inhibition and, thus, probably is not caused by impaired tyrosine phosphorylation events alone. Glucose 129-136 insulin Homo sapiens 111-118 9314631-15 1997 We have now shown that the treatment of postprandial hyperglycemia with insulin lispro markedly improves overall glucose control and some lipid parameters in patients with type 2 diabetes. Glucose 113-120 insulin Homo sapiens 72-79 9314636-4 1997 Early-phase insulin secretion was assessed by the insulinogenic index (the ratio of the increment of insulin to that of plasma glucose [PG] 30 min after a glucose load [delta IRI0-30 min/delta PG0-30 min]). Glucose 127-134 insulin Homo sapiens 12-19 9314636-4 1997 Early-phase insulin secretion was assessed by the insulinogenic index (the ratio of the increment of insulin to that of plasma glucose [PG] 30 min after a glucose load [delta IRI0-30 min/delta PG0-30 min]). Glucose 127-134 insulin Homo sapiens 50-57 9314636-4 1997 Early-phase insulin secretion was assessed by the insulinogenic index (the ratio of the increment of insulin to that of plasma glucose [PG] 30 min after a glucose load [delta IRI0-30 min/delta PG0-30 min]). Glucose 155-162 insulin Homo sapiens 12-19 9314636-4 1997 Early-phase insulin secretion was assessed by the insulinogenic index (the ratio of the increment of insulin to that of plasma glucose [PG] 30 min after a glucose load [delta IRI0-30 min/delta PG0-30 min]). Glucose 155-162 insulin Homo sapiens 50-57 9371478-11 1997 A delay in insulin response to glucose was noted in many of the offspring as indicated by a low deltaI/deltaG at 30". Glucose 31-38 insulin Homo sapiens 11-18 9371478-13 1997 The relatively high plasma glucose values in the presence of normal insulin secretion in both groups of offspring of diabetic parents suggest the presence of insulin resistance. Glucose 27-34 insulin Homo sapiens 158-165 9314636-9 1997 When the fasting glucose (FPG) exceeded 100 mg/dl, early-phase insulin decreased progressively. Glucose 17-24 insulin Homo sapiens 63-70 9314636-14 1997 We suggest that impaired early-phase insulin secretion may be the initial abnormality in the development of glucose intolerance in Japanese people. Glucose 108-115 insulin Homo sapiens 37-44 9337803-5 1997 If monotherapy does not maintain near-normoglycemia, combined oral antidiabetic medication or insulin may bring glucose levels into the therapeutic range. Glucose 112-119 insulin Homo sapiens 94-101 9440253-1 1997 We investigated the influence of ouabain on glucose-induced insulin release from toad pancreatic minces in the same nanomolar range as that of an ouabain-like compound found in human blood. Glucose 44-51 insulin Homo sapiens 60-67 9440253-5 1997 Acetylcholine at 8 microM augmented insulin release at both levels of glucose, and ouabain potentiated this effect synergistically at high, but not low glucose. Glucose 70-77 insulin Homo sapiens 36-43 9339963-5 1997 Available clinical trials are well designed and results suggest that 1- and 2-hour postprandial blood glucose levels with insulin lispro are similar to or lower than those with human regular insulin; 1- and 2-hourpostprandial glucose excursions are similar to or less pronounced than those with human regular insulin. Glucose 102-109 insulin Homo sapiens 122-129 9339963-7 1997 Continuous subcutaneous insulin infusion was associated with greater improvements in postprandial blood glucose levels and glycated haemoglobin A1 values with insulin lispro than with human regular insulin. Glucose 104-111 insulin Homo sapiens 24-31 9328322-5 1997 During euglycemic hyperinsulinemia, insulin-mediated glucose disposal was significantly reduced in cirrhotic patients (3.43 +/- 0.26 vs. 7.36 +/- 0.48 mg/kg/min, P < .01). Glucose 53-60 insulin Homo sapiens 23-30 9347408-7 1997 In the whole series of hypertensive subjects, plasma insulin and insulin/glucose ratio at fasting and after glucose correlated significantly with BMI, triceps skinfold and waist and hip cicumferences. Glucose 73-80 insulin Homo sapiens 65-72 9385530-3 1997 Leptin was determined using Linco Research radio-immunoassay while insulin sensitivity was calculated from intravenous glucose tolerance tests with frequent blood sampling using MINMOD analysis. Glucose 119-126 insulin Homo sapiens 67-74 9336379-2 1997 Insulin could act directly on smooth muscle altering intracellular calcium levels that mediate contraction and glucose transport or could induce the secretion of endothelin by the endothelial cells lining the vessels. Glucose 111-118 insulin Homo sapiens 0-7 9397146-4 1997 GLP-1 and gastric inhibitory peptide (GIP) which has also been termed glucose-dependent insulinotropic peptide appear to account for most of the incretin effect in the augmentation of glucose-stimulated insulin secretion. Glucose 70-77 insulin Homo sapiens 88-95 9347408-7 1997 In the whole series of hypertensive subjects, plasma insulin and insulin/glucose ratio at fasting and after glucose correlated significantly with BMI, triceps skinfold and waist and hip cicumferences. Glucose 108-115 insulin Homo sapiens 65-72 9397146-4 1997 GLP-1 and gastric inhibitory peptide (GIP) which has also been termed glucose-dependent insulinotropic peptide appear to account for most of the incretin effect in the augmentation of glucose-stimulated insulin secretion. Glucose 184-191 insulin Homo sapiens 88-95 9347408-8 1997 After exclusion of the subjects with BMI > 22 kg/m2, compared with the controls, plasma insulin and insulin/glucose ratio were significantly higher in the whole hypertensive group and separately in hypertensive men and women. Glucose 111-118 insulin Homo sapiens 103-110 9347408-9 1997 The logistic regression analyses have shown that plasma insulin and insulin/glucose ratio at fasting and after glucose were significantly associated with hypertension, independently of gender, BMI and waist circumference. Glucose 76-83 insulin Homo sapiens 68-75 9347408-9 1997 The logistic regression analyses have shown that plasma insulin and insulin/glucose ratio at fasting and after glucose were significantly associated with hypertension, independently of gender, BMI and waist circumference. Glucose 111-118 insulin Homo sapiens 56-63 9347408-9 1997 The logistic regression analyses have shown that plasma insulin and insulin/glucose ratio at fasting and after glucose were significantly associated with hypertension, independently of gender, BMI and waist circumference. Glucose 111-118 insulin Homo sapiens 68-75 9336582-2 1997 Insulin adjustments and carbohydrate supplementation can be used independently or in conjunction to maintain target-range blood glucose levels during activity. Glucose 128-135 insulin Homo sapiens 0-7 9329342-2 1997 In addition, insulin-mediated glucose disposal was estimated by determining the steady state plasma glucose (SSPG) concentration after a 180-min iv infusion of somatostatin, insulin, and glucose. Glucose 30-37 insulin Homo sapiens 13-20 9322186-5 1997 In aging, similar to diabetes, the elevation in circulating glucose and other reducing sugars secondary to age-induced insulin resistance can react nonenzymatically with proteins and nucleic acids to form products that affect function and diminish tissue elasticity. Glucose 60-67 insulin Homo sapiens 119-126 9329342-2 1997 In addition, insulin-mediated glucose disposal was estimated by determining the steady state plasma glucose (SSPG) concentration after a 180-min iv infusion of somatostatin, insulin, and glucose. Glucose 100-107 insulin Homo sapiens 13-20 9329342-2 1997 In addition, insulin-mediated glucose disposal was estimated by determining the steady state plasma glucose (SSPG) concentration after a 180-min iv infusion of somatostatin, insulin, and glucose. Glucose 100-107 insulin Homo sapiens 13-20 9329374-6 1997 Insulin sensitivity was assessed by the reduction in endogenous glucose concentration after exogenous insulin; the insulin, glucose, and fatty acid responses to oral glucose; and the fasting insulin concentration. Glucose 64-71 insulin Homo sapiens 0-7 9329374-6 1997 Insulin sensitivity was assessed by the reduction in endogenous glucose concentration after exogenous insulin; the insulin, glucose, and fatty acid responses to oral glucose; and the fasting insulin concentration. Glucose 124-131 insulin Homo sapiens 0-7 9329374-6 1997 Insulin sensitivity was assessed by the reduction in endogenous glucose concentration after exogenous insulin; the insulin, glucose, and fatty acid responses to oral glucose; and the fasting insulin concentration. Glucose 124-131 insulin Homo sapiens 0-7 9329374-12 1997 Although in PCOS, correlations were obtained between the free androgen index and cholesterol, triglyceride, and apoB levels and between the integrated glucose and insulin responses after oral glucose and fasting fatty acid and triglyceride levels, when age and adiposity were included as covariates only fatty acids and the integrated glucose response remained significantly correlated. Glucose 192-199 insulin Homo sapiens 163-170 9329374-12 1997 Although in PCOS, correlations were obtained between the free androgen index and cholesterol, triglyceride, and apoB levels and between the integrated glucose and insulin responses after oral glucose and fasting fatty acid and triglyceride levels, when age and adiposity were included as covariates only fatty acids and the integrated glucose response remained significantly correlated. Glucose 192-199 insulin Homo sapiens 163-170 9335414-2 1997 Increased insulin/glucose ratios (IGR) suggestive of insulin resistance were found in half of our patients. Glucose 18-25 insulin Homo sapiens 53-60 9350634-2 1997 Exposure to altitude hypoxia elicits changes in glucose homeostasis with increases in glucose and insulin concentrations within the first few days at altitude. Glucose 48-55 insulin Homo sapiens 98-105 9350634-4 1997 Insulin action on glucose uptake has never been investigated during altitude hypoxia. Glucose 18-25 insulin Homo sapiens 0-7 9350634-9 1997 Insulin-stimulated glucose uptake rate was halved on day two compared with sea level (4.5 +/- 0.6 and 9.8 +/- 1.1 mg min-1 kg-1, respectively; P < 0.05), and was partly restored on day 7 (7.4 +/- 1.4 mg min-1 kg-1; P < 0.05 vs. day two and sea level). Glucose 19-26 insulin Homo sapiens 0-7 9322797-4 1997 The imidazoline-derivative alpha 2-adrenoceptor agonists clonidine and oxymetazoline at concentrations as low as 10(-8) mol/L significantly inhibited glucose-stimulated insulin secretion by 63% and 65%, respectively (P < .01 for both). Glucose 150-157 insulin Homo sapiens 169-176 9322799-0 1997 Hyperamylinemia is associated with hyperinsulinemia in the glucose-tolerant, insulin-resistant offspring of two Mexican-American non-insulin-dependent diabetic parents. Glucose 59-66 insulin Homo sapiens 40-47 9334720-1 1997 GLUT4, the insulin-responsive glucose transporter, plays an important role in postprandial glucose disposal. Glucose 30-37 insulin Homo sapiens 11-18 9455124-6 1997 The glucose and insulin responses in both the GTT and OGTT showed that there was a slight decrease in the initial response of insulin in the immobilized patients and was in the controls compared with adolescent controls. Glucose 4-11 insulin Homo sapiens 126-133 9430382-1 1997 Muscle plays a major role in insulin-stimulated glucose disposal. Glucose 48-55 insulin Homo sapiens 29-36 10173306-2 1997 They offered patients an alternative to using insulin to lower their blood glucose. Glucose 75-82 insulin Homo sapiens 46-53 9380379-7 1997 This was the case in people with "diabetoid" glucose responses too, suggesting an early failure of glucose tolerance and/or insulin secretion. Glucose 45-52 insulin Homo sapiens 124-131 9392489-5 1997 Insulin-stimulated whole-body glucose uptake was significantly lower in the patients with IDDM (45 +/- 15 micromol x kg(-1) x min[-1]) than in the normal subjects (62 +/- 14 micromol x kg(-1) x min[-1]) (P < 0.05). Glucose 30-37 insulin Homo sapiens 0-7 10322887-5 1997 Before and after treatment standard steamed bread meal test was performed to measure the insulin peripheral sensitivity, insulin release to glucose and insulin sensitivity index. Glucose 140-147 insulin Homo sapiens 121-128 10322887-5 1997 Before and after treatment standard steamed bread meal test was performed to measure the insulin peripheral sensitivity, insulin release to glucose and insulin sensitivity index. Glucose 140-147 insulin Homo sapiens 121-128 9381045-6 1997 Exogen insulin substitution ameliorates typical abnormalities in type II diabetes, such as increased hepatic glucose production, reduced peripheral glucose utilization, reduced function of beta-cells and dyslipidemia. Glucose 109-116 insulin Homo sapiens 7-14 9381045-6 1997 Exogen insulin substitution ameliorates typical abnormalities in type II diabetes, such as increased hepatic glucose production, reduced peripheral glucose utilization, reduced function of beta-cells and dyslipidemia. Glucose 148-155 insulin Homo sapiens 7-14 9294105-6 1997 Subjects with the R154X mutation exhibited a diminished insulin secretory response to oral glucose. Glucose 91-98 insulin Homo sapiens 56-63 9324100-1 1997 Increased dietary sodium intake has been associated with an increase in blood pressure as well as a decrease in insulin-mediated glucose disposal in young healthy adults. Glucose 129-136 insulin Homo sapiens 112-119 9294129-11 1997 These data indicate that gamma subunits of trimeric G-proteins undergo a glucose- and calcium-regulated methylation-demethylation cycle in insulin-secreting cells, findings that may imply an important role in beta cell function. Glucose 73-80 insulin Homo sapiens 139-146 24394760-13 1997 Higher glucose levels, despite elevated insulin levels, suggested insulin resistance. Glucose 7-14 insulin Homo sapiens 66-73 24394763-2 1997 Recently a simple index of insulin resistance referred to as the Fasting Insulin Resistance Index (FIRI) was proposed by Duncan et al, for use in clinical practice and epidemiologic investigations of disease FIRI is estimated as the product of fasting plasma glucose and fasting plasma insulin divided by 25 (FIRI = (glucose x insulin/25). Glucose 259-266 insulin Homo sapiens 27-34 24394763-2 1997 Recently a simple index of insulin resistance referred to as the Fasting Insulin Resistance Index (FIRI) was proposed by Duncan et al, for use in clinical practice and epidemiologic investigations of disease FIRI is estimated as the product of fasting plasma glucose and fasting plasma insulin divided by 25 (FIRI = (glucose x insulin/25). Glucose 259-266 insulin Homo sapiens 73-80 9283783-9 1997 Fasting insulin and C-peptide concentrations were independently associated with glucose intolerance, high triglyceride levels, and low HDL cholesterol levels. Glucose 80-87 insulin Homo sapiens 20-29 9283804-0 1997 Insulin responses to oral glucose during 4-year treatment with nifedipine retard in hypertensive patients with and without NIDDM. Glucose 26-33 insulin Homo sapiens 0-7 9287037-6 1997 The drug induces a large increase of glucose utilization in adipose tissue, where it stimulates the expression of genes involved in lipid metabolism such as the insulin-responsive GLUT, fatty acid synthase, and phosphoenolpyruvate carboxykinase genes, but decreases the expression of the ob gene. Glucose 37-44 insulin Homo sapiens 161-168 9300235-0 1997 From receptor to transporter: insulin signalling to glucose transport. Glucose 52-59 insulin Homo sapiens 30-37 9287048-9 1997 The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). Glucose 105-112 insulin Homo sapiens 45-52 9300247-7 1997 Furthermore, insulin/glucose ratio in childhood showed a positive correlation to insulin (p < 0.01) and insulin/glucose ratio at birth (p < 0.005). Glucose 115-122 insulin Homo sapiens 13-20 9306037-0 1997 Differential effects of ambient blood glucose level and degree of obesity on basal serum C-peptide level and the C-peptide response to glucose and glucagon in non-insulin-dependent diabetes mellitus. Glucose 38-45 insulin Homo sapiens 89-98 9300238-5 1997 This enhanced oxidative metabolism may explain the increased insulin release at a low glucose level but is clearly dissociated from the blunted insulin secretion at high glucose concentrations. Glucose 86-93 insulin Homo sapiens 61-68 9300238-6 1997 We conclude that a reduction of oxidative metabolism in pancreatic beta cells is unlikely to be the cause of the dramatic effect that high levels of non-esterified fatty acids have on glucose-induced insulin release. Glucose 184-191 insulin Homo sapiens 200-207 9300247-7 1997 Furthermore, insulin/glucose ratio in childhood showed a positive correlation to insulin (p < 0.01) and insulin/glucose ratio at birth (p < 0.005). Glucose 21-28 insulin Homo sapiens 13-20 9300247-7 1997 Furthermore, insulin/glucose ratio in childhood showed a positive correlation to insulin (p < 0.01) and insulin/glucose ratio at birth (p < 0.005). Glucose 21-28 insulin Homo sapiens 81-88 9306037-0 1997 Differential effects of ambient blood glucose level and degree of obesity on basal serum C-peptide level and the C-peptide response to glucose and glucagon in non-insulin-dependent diabetes mellitus. Glucose 135-142 insulin Homo sapiens 113-122 9300247-7 1997 Furthermore, insulin/glucose ratio in childhood showed a positive correlation to insulin (p < 0.01) and insulin/glucose ratio at birth (p < 0.005). Glucose 21-28 insulin Homo sapiens 81-88 9306037-3 1997 C-peptide response to glucose, but not basal serum C-peptide and C-peptide response to glucagon, was significantly lower in NIDDM than in controls (P < 0.001). Glucose 22-29 insulin Homo sapiens 0-9 9306037-4 1997 FBS was inversely correlated with C-peptide response to glucose in NIDDM patients (r = -0.67, P < 0.001), but not with basal C-peptide level and C-peptide response to glucagon. Glucose 56-63 insulin Homo sapiens 34-43 9306037-7 1997 C-peptide response to glucose significantly increase, but not to a level in control subjects, after glycemic control. Glucose 22-29 insulin Homo sapiens 0-9 9330585-3 1997 Insulin-stimulated glucose uptake (hyperinsulinemic, euglycemic clamp, insulin infusion rate 1.5 mU/kg per min) was markedly reduced following fasting (M-value 5.96 +/- 0.74 vs 2.79 +/- 0.23 mg/kg per min, P < 0.0001). Glucose 19-26 insulin Homo sapiens 0-7 9342537-2 1997 In terms of physiology, emphasis is placed on new information concerning the role of glucokinase and the identity of coupling factors in the process of glucose-stimulated insulin release. Glucose 152-159 insulin Homo sapiens 171-178 9314017-10 1997 Closing the loop with a continuous glucose sensor will be the only way to achieve truly normal blood glucose homeostasis by directing insulin delivery automatically on demand. Glucose 35-42 insulin Homo sapiens 134-141 9330585-3 1997 Insulin-stimulated glucose uptake (hyperinsulinemic, euglycemic clamp, insulin infusion rate 1.5 mU/kg per min) was markedly reduced following fasting (M-value 5.96 +/- 0.74 vs 2.79 +/- 0.23 mg/kg per min, P < 0.0001). Glucose 19-26 insulin Homo sapiens 40-47 9313101-0 1997 Trp64Arg mutation of beta 3-adrenergic receptor and insulin sensitivity in subjects with glucose intolerance. Glucose 89-96 insulin Homo sapiens 52-59 9630759-6 1997 Insulin stimulated glucose utilization, expressed as M-value, was significantly decreased in both PCO groups compared to normal ovulatory women (p < 0.005). Glucose 19-26 insulin Homo sapiens 0-7 9284750-6 1997 The peak insulin after bolus glucose was 797 +/- 232 pmol/L during PACAP27 infusion vs. 559 +/- 164 pmol/L during saline infusion (P = 0.018). Glucose 29-36 insulin Homo sapiens 9-16 9284716-7 1997 The subjects with insulinomas had lower mean plasma glucose and higher insulin concentrations than controls, 3.6 +/- 0.3 mmol/L (P = 0.01) and 150 +/- 42 pmol/L (P = 0.01), respectively. Glucose 52-59 insulin Homo sapiens 18-25 9284716-9 1997 The insulin pulses were irregular, and interpeak intervals varied between 4-54 min in different subjects; in some subjects, the amplitude was also variable, with sudden spontaneous pulses as high as 565 pmol/L, with an associated glucose decrement. Glucose 230-237 insulin Homo sapiens 4-11 9284756-0 1997 The effect of oral glucose on serum free insulin-like growth factor-I and -II in health adults. Glucose 19-26 insulin Homo sapiens 41-48 9284756-1 1997 Insulin-like growth factor (IGF) binding protein-I (IGFBP-1) has been suggested to regulate the availability of free IGF and the glucose lowering activity of the IGF-system in relation to fuel supply. Glucose 129-136 insulin Homo sapiens 0-7 9284756-11 1997 Insulin, but not free IGF-I, correlated significantly with serum glucose (P < 0.05). Glucose 65-72 insulin Homo sapiens 0-7 9364250-6 1997 There was negative correlation between glucose, insulin, C-peptide, and erythrocyte GSH levels after glucose loading (p < 0.005). Glucose 101-108 insulin Homo sapiens 57-66 9303923-4 1997 We measured insulin sensitivity (as the whole-body insulin-mediated glucose uptake) and fasting posthepatic insulin delivery rate (IDR) with the use of the euglycemic insulin clamp technique in a large group of obese subjects in the database of the European Group for the Study of Insulin Resistance (1,146 nondiabetic, normotensive Caucasian men and women aged 18-85 yr, with a body mass index (BMI) ranging from 15 to 55 kg.m-2). Glucose 68-75 insulin Homo sapiens 51-58 9303923-4 1997 We measured insulin sensitivity (as the whole-body insulin-mediated glucose uptake) and fasting posthepatic insulin delivery rate (IDR) with the use of the euglycemic insulin clamp technique in a large group of obese subjects in the database of the European Group for the Study of Insulin Resistance (1,146 nondiabetic, normotensive Caucasian men and women aged 18-85 yr, with a body mass index (BMI) ranging from 15 to 55 kg.m-2). Glucose 68-75 insulin Homo sapiens 51-58 9303923-4 1997 We measured insulin sensitivity (as the whole-body insulin-mediated glucose uptake) and fasting posthepatic insulin delivery rate (IDR) with the use of the euglycemic insulin clamp technique in a large group of obese subjects in the database of the European Group for the Study of Insulin Resistance (1,146 nondiabetic, normotensive Caucasian men and women aged 18-85 yr, with a body mass index (BMI) ranging from 15 to 55 kg.m-2). Glucose 68-75 insulin Homo sapiens 51-58 9462418-8 1997 Multiple regression analysis revealed that not only BMI, but also the plasma glucose and insulin response during the 75 g glucose loading test independently correlated with mean blood pressure. Glucose 122-129 insulin Homo sapiens 89-96 9348735-4 1997 The glucose uptake in insulin-treated human corneal endothelial cells also exhibited a similar declining effect in high glucose media from 0.30 (5 mM), 0.11 (10 mM), 0.08 (20 mM) to 0.05 (25 mM). Glucose 4-11 insulin Homo sapiens 22-29 9284890-4 1997 In the glucose tolerance test, nine patients (75.0%) showed lower C-peptide reactivity (CPR) than normal at 30 minutes, suggesting blunted insulin secretion. Glucose 7-14 insulin Homo sapiens 66-75 9348735-4 1997 The glucose uptake in insulin-treated human corneal endothelial cells also exhibited a similar declining effect in high glucose media from 0.30 (5 mM), 0.11 (10 mM), 0.08 (20 mM) to 0.05 (25 mM). Glucose 120-127 insulin Homo sapiens 22-29 9348735-6 1997 It was indicated that the cAMP concentrations of pmole/well in both insulin-treated and non-insulin treated cells were also decreased after increasing the glucose concentration in the media from 73 (5 mM) to 20 (25 mM) and 101 (5 mM) respectively. Glucose 155-162 insulin Homo sapiens 68-75 9348735-6 1997 It was indicated that the cAMP concentrations of pmole/well in both insulin-treated and non-insulin treated cells were also decreased after increasing the glucose concentration in the media from 73 (5 mM) to 20 (25 mM) and 101 (5 mM) respectively. Glucose 155-162 insulin Homo sapiens 92-99 9284894-8 1997 In two transfectants expressing the largest amount of human IAPP, insulin secretion was increased in response to glucose stimulation; however, the magnitude of the insulin response in cells transfected with human IAPP was smaller than in control clones. Glucose 113-120 insulin Homo sapiens 66-73 9284890-8 1997 The glucose metabolized (M value) was negatively correlated with 24-hour urinary C-peptide excretion (r = .696, P < .05). Glucose 4-11 insulin Homo sapiens 81-90 9284898-13 1997 Nitric oxide (NO), the metabolic mediator for L-arginine, potentiates insulin-mediated glucose uptake through the increase in blood flow. Glucose 87-94 insulin Homo sapiens 70-77 9284898-0 1997 L-arginine but not D-arginine stimulates insulin-mediated glucose uptake. Glucose 58-65 insulin Homo sapiens 41-48 9284898-1 1997 Our study aims at investigating a possible role for L-arginine and D-arginine in insulin-mediated glucose uptake. Glucose 98-105 insulin Homo sapiens 81-88 9284898-12 1997 In conclusion, L-arginine but not D-arginine stimulates insulin-mediated glucose uptake. Glucose 73-80 insulin Homo sapiens 56-63 9280070-2 1997 Infection with a virus encoding a mutant regulatory subunit of phosphoinositide (PI) 3-kinase that does not bind the 110-kDa catalytic subunit (delta p85) inhibited the insulin-induced increase in PI 3-kinase activity co-precipitated by antibodies to phosphotyrosine and glucose uptake in a virus dose-dependent manner. Glucose 271-278 insulin Homo sapiens 169-176 9280070-3 1997 Overexpression of a dominant negative RAS mutant in which Asp57 is replaced with tyrosine (RAS57Y) or of a dominant negative SOS mutant that lacks guanine nucleotide exchange activity (delta SOS) abolished the insulin-induced increase in mitogen-activated protein kinase activity, but had no effect on PI 3-kinase activity or glucose uptake. Glucose 326-333 insulin Homo sapiens 210-217 9280070-7 1997 A serine/threonine kinase Akt, a constitutively active mutant of which was previously shown to stimulate glucose uptake, is activated by insulin, GH, and hyperosmolarity to approximately 4-fold, approximately 2.1-fold, and approximately 2.3-fold over basal level, respectively. Glucose 105-112 insulin Homo sapiens 137-144 16501482-6 1997 RESULTS: Plasma glucose level in basal condition, after oral glucose tolerance test, intravenous glucose tolerance test and glucagone challenge test, shows that insulin secretion and/or its effectiveness is not impaired after PPPD. Glucose 16-23 insulin Homo sapiens 161-168 9290109-8 1997 This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. Glucose 78-85 insulin Homo sapiens 35-42 9360409-8 1997 After a mean weight loss of 7.7 +/- 4.9 kg, the time-integrated insulin response to an oral glucose load was significantly lower but the leptin response remained unchanged. Glucose 92-99 insulin Homo sapiens 64-71 9290109-8 1997 This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. Glucose 78-85 insulin Homo sapiens 191-198 9290109-8 1997 This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. Glucose 107-114 insulin Homo sapiens 35-42 9290109-8 1997 This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. Glucose 107-114 insulin Homo sapiens 191-198 9280302-3 1997 The present study investigated potential defects in the regulation of the insulin gene by glucose in a beta-cell line (NES 2Y) derived from a patient with PHHI. Glucose 90-97 insulin Homo sapiens 74-81 9277650-10 1997 Fasting (P < .001) and the integrated insulin response to the glucose load decreased (P < .001) after 8 weeks of metformin treatment. Glucose 65-72 insulin Homo sapiens 41-48 9595787-2 1997 glucose tolerance test are the most frequently used methods to assess insulin resistance. Glucose 0-7 insulin Homo sapiens 70-77 9595787-8 1997 Insulin sensitivity was calculated as the blood glucose slope in the ITT and with the minimal model of Bergman in the IVGTT. Glucose 48-55 insulin Homo sapiens 0-7 9270410-4 1997 Therefore, the authors examined the association of insulin sensitivity estimated by means of a frequently sampled intravenous glucose tolerance test and the minimal model with the number of metabolic disorders (dyslipidemia [high triglyceride level or low HDL cholesterol level or both], hypertension, and IGT according to the World Health Organization criteria). Glucose 126-133 insulin Homo sapiens 51-58 9280302-5 1997 Because IUF1 is involved not only in linking glucose metabolism to the control of the insulin, but is also a major regulator of beta-cell differentiation during embryogenesis, we propose that impaired expression of IUF1 contributes to beta-cell dysfunction in PHHI by leading to abnormal beta-cell differentiation. Glucose 45-52 insulin Homo sapiens 86-93 9252422-0 1997 The p38/reactivating kinase mitogen-activated protein kinase cascade mediates the activation of the transcription factor insulin upstream factor 1 and insulin gene transcription by high glucose in pancreatic beta-cells. Glucose 186-193 insulin Homo sapiens 121-128 9381016-8 1997 In our opinion the c-peptide/glucose-quotient serves as simple, cost-effective and non-invasive method in the assessment of beta-cell capacity. Glucose 29-36 insulin Homo sapiens 19-28 9259575-1 1997 We tested the hypothesis that defects in insulin stimulation of skeletal muscle blood flow, flow dispersion, and coupling between flow and glucose uptake contribute to insulin resistance of glucose uptake in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 139-146 insulin Homo sapiens 41-48 9259575-8 1997 Furthermore, insulin redirects flow to areas where it stimulates glucose uptake. Glucose 65-72 insulin Homo sapiens 13-20 9259575-1 1997 We tested the hypothesis that defects in insulin stimulation of skeletal muscle blood flow, flow dispersion, and coupling between flow and glucose uptake contribute to insulin resistance of glucose uptake in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 139-146 insulin Homo sapiens 168-175 9259575-1 1997 We tested the hypothesis that defects in insulin stimulation of skeletal muscle blood flow, flow dispersion, and coupling between flow and glucose uptake contribute to insulin resistance of glucose uptake in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 190-197 insulin Homo sapiens 41-48 9259575-1 1997 We tested the hypothesis that defects in insulin stimulation of skeletal muscle blood flow, flow dispersion, and coupling between flow and glucose uptake contribute to insulin resistance of glucose uptake in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 190-197 insulin Homo sapiens 168-175 9259575-6 1997 In both groups, insulin increased absolute but not relative dispersion of flow, and insulin-stimulated but not basal blood flow colocalized with glucose uptake. Glucose 145-152 insulin Homo sapiens 84-91 9264492-7 1997 During the clamp, insulin sensitive patients tended to have greater increments in forearm blood flow when compared to their insulin resistant counterparts (+53+/-21 versus +9+/-7%, P=.06); in the whole group, clamp-induced vasodilatation was weakly related to insulin-mediated glucose uptake (r=.44, P<.02) as well as to the slope of the acetylcholine dose-response curve (r=.40, P<.04). Glucose 277-284 insulin Homo sapiens 18-25 9238070-2 1997 It is closed by glucose metabolism, which stimulates secretion, and opened by the drug diazoxide, which inhibits insulin release. Glucose 16-23 insulin Homo sapiens 113-120 9313602-5 1997 Insulin sensitivity (SI) was assessed by the minimal model analysis of the intravenous glucose tolerance test. Glucose 87-94 insulin Homo sapiens 0-7 9277397-1 1997 To determine the interrelationship among insulin action, total or regional adiposity, and sex, we measured insulin-mediated glucose disposal by the euglycemic insulin clamp and adipose distribution using computed axial tomography (22 scans) in 32 black men and 20 black women with non-insulin-dependent diabetes mellitus (age 48 +/- 9 and 54 +/- 9 yr, body mass index 26.3 +/- 2.3 and 27.2 +/- 2.6 kg/m2, respectively). Glucose 124-131 insulin Homo sapiens 107-114 9338524-0 1997 Glucagon-like peptide-1 reduces hepatic glucose production indirectly through insulin and glucagon in humans. Glucose 40-47 insulin Homo sapiens 78-85 9277377-2 1997 The cells were washed, and the rate of glucose transport (2-deoxy-[3H]glucose uptake) was measured after incubation with various concentrations of insulin for 45 min. Glucose 39-46 insulin Homo sapiens 147-154 9277397-1 1997 To determine the interrelationship among insulin action, total or regional adiposity, and sex, we measured insulin-mediated glucose disposal by the euglycemic insulin clamp and adipose distribution using computed axial tomography (22 scans) in 32 black men and 20 black women with non-insulin-dependent diabetes mellitus (age 48 +/- 9 and 54 +/- 9 yr, body mass index 26.3 +/- 2.3 and 27.2 +/- 2.6 kg/m2, respectively). Glucose 124-131 insulin Homo sapiens 107-114 9277377-8 1997 This decrease in tyrosine kinase activity of the receptor may account for the decrease in insulin sensitivity of glucose transport but cannot account for the complete loss of antilipolysis. Glucose 113-120 insulin Homo sapiens 90-97 9277380-5 1997 Maximal in vitro insulin stimulation of insulin receptor autophosphorylation strongly correlated with both low (Mlow)- and high (Mhigh)-dose insulin-stimulated glucose disposal (r = 0.62 and 0.51, P < 0.002 and 0.011, respectively). Glucose 160-167 insulin Homo sapiens 17-24 9277397-5 1997 Visceral fat explained a significant portion (34%) of variance in insulin-mediated glucose disposal, whereas total or subcutaneous fat and sex did not. Glucose 83-90 insulin Homo sapiens 66-73 9284856-6 1997 This was the result of small improvements in whole-body insulin sensitivity (steady-state plasma glucose during the insulin suppression test: from 11.09 +/- 1.1 to 10.3 +/- 0.8 mmol/L versus 13.8 +/- 1.0 to 10.0 +/- 0.9 mmol/L, placebo versus troglitazone; p = 0.01) and EGP (from 103% +/- 3% versus 96% +/- 2% of baseline, placebo versus troglitazone; p = 0.09). Glucose 97-104 insulin Homo sapiens 56-63 9388584-2 1997 The study of the nature and biogenesis of this compartment will provide important insight into the mechanism by which insulin stimulates glucose transport. Glucose 137-144 insulin Homo sapiens 118-125 9388585-2 1997 However, there is a strong body of evidence to suggest class-1 PI 3-kinase activity is necessary for insulin stimulation of glucose transport and a growing body of evidence to suggest that insulin stimulation of this class of PI 3-kinase is sufficient to stimulate glucose transport. Glucose 124-131 insulin Homo sapiens 101-108 9388585-2 1997 However, there is a strong body of evidence to suggest class-1 PI 3-kinase activity is necessary for insulin stimulation of glucose transport and a growing body of evidence to suggest that insulin stimulation of this class of PI 3-kinase is sufficient to stimulate glucose transport. Glucose 265-272 insulin Homo sapiens 189-196 9388586-0 1997 A role for the serine/threonine kinase, Akt, in insulin-stimulated glucose uptake. Glucose 67-74 insulin Homo sapiens 48-55 9284856-6 1997 This was the result of small improvements in whole-body insulin sensitivity (steady-state plasma glucose during the insulin suppression test: from 11.09 +/- 1.1 to 10.3 +/- 0.8 mmol/L versus 13.8 +/- 1.0 to 10.0 +/- 0.9 mmol/L, placebo versus troglitazone; p = 0.01) and EGP (from 103% +/- 3% versus 96% +/- 2% of baseline, placebo versus troglitazone; p = 0.09). Glucose 97-104 insulin Homo sapiens 116-123 9301428-19 1997 In conclusion, impaired glucose tolerance develops after surgery as a result of decreased insulin-stimulated whole-body glucose disposal as well as increased endogenous glucose release. Glucose 24-31 insulin Homo sapiens 90-97 9301428-19 1997 In conclusion, impaired glucose tolerance develops after surgery as a result of decreased insulin-stimulated whole-body glucose disposal as well as increased endogenous glucose release. Glucose 120-127 insulin Homo sapiens 90-97 9284856-7 1997 The time course of insulin action showed an early (first week of treatment) decrease in EGP in the troglitazone group that was maintained throughout, whereas steady-state plasma glucose levels began to diverge toward the end of treatment. Glucose 178-185 insulin Homo sapiens 19-26 9301428-20 1997 Despite the increase in endogenous glucose production, the reduction in endogenous glucose production with each elevation of insulin was unaffected by surgery. Glucose 83-90 insulin Homo sapiens 125-132 9301428-21 1997 Perioperative bed rest and/or hypocaloric nutrition contribute to the decrease in insulin-stimulated whole-body glucose disposal in the post-operative state, whereas these factors have no effects on endogenous glucose production. Glucose 112-119 insulin Homo sapiens 82-89 9231649-6 1997 In conclusion, GLP-I exerts insulin-like effects on D-glucose metabolism in both muscle and liver tissue in IDDM or NIDDM animal models, and present observations reinforce the view that GLP-I may represent a most promising tool in the treatment of diabetic patients. Glucose 52-61 insulin Homo sapiens 28-35 9231649-2 1997 This work confirms the previously reported insulin-like effects of GLP-I on glucose metabolism in both muscle and liver tissue from normal rats (control). Glucose 76-83 insulin Homo sapiens 43-50 9267983-4 1997 However, the dose response curve of insulin-stimulated glucose transport was right-shifted. Glucose 55-62 insulin Homo sapiens 36-43 9267983-8 1997 In conclusion, the mechanism of saturated non-esterified fatty acid induced insulin resistance in glucose uptake may reside at post PI3-kinase or Shc steps, including the level of MAP kinase activation. Glucose 98-105 insulin Homo sapiens 76-83 9272591-6 1997 The decrease of blood glucose was faster and more pronounced during C-peptide infusion, yielding a significantly lower AUC 0-180 min of blood glucose (38.5 +/- 1.6 vs 44.4 +/- 2.2 mmol l(-1)h(-1); p = 0.032). Glucose 22-29 insulin Homo sapiens 68-77 9272591-6 1997 The decrease of blood glucose was faster and more pronounced during C-peptide infusion, yielding a significantly lower AUC 0-180 min of blood glucose (38.5 +/- 1.6 vs 44.4 +/- 2.2 mmol l(-1)h(-1); p = 0.032). Glucose 142-149 insulin Homo sapiens 68-77 9272607-3 1997 Data from patients in the Study to Prevent NIDDM show that patients with impaired glucose tolerance (IGT) have higher fasting levels of triglycerides, and higher fasting and postprandial levels of pro-insulin, insulin, and C-peptide levels, compared with those who have normal glucose tolerance (NGT). Glucose 82-89 insulin Homo sapiens 197-232 9272609-3 1997 In non-diabetic individuals, an oral glucose load triggers a rapid insulin secretory response. Glucose 37-44 insulin Homo sapiens 67-74 9272609-4 1997 Insulin suppresses hepatic glucose release and stimulates peripheral glucose uptake, thereby limiting the postprandial rise in plasma glucose concentration. Glucose 27-34 insulin Homo sapiens 0-7 9272609-4 1997 Insulin suppresses hepatic glucose release and stimulates peripheral glucose uptake, thereby limiting the postprandial rise in plasma glucose concentration. Glucose 69-76 insulin Homo sapiens 0-7 9272609-4 1997 Insulin suppresses hepatic glucose release and stimulates peripheral glucose uptake, thereby limiting the postprandial rise in plasma glucose concentration. Glucose 69-76 insulin Homo sapiens 0-7 9272611-5 1997 These defects in insulin action may themselves have evolved to protect insulin-sensitive tissues from excessive glucose utilization during hyperglycaemia. Glucose 112-119 insulin Homo sapiens 17-24 9272611-5 1997 These defects in insulin action may themselves have evolved to protect insulin-sensitive tissues from excessive glucose utilization during hyperglycaemia. Glucose 112-119 insulin Homo sapiens 71-78 9231763-7 1997 The rhythmic activity in the glucose-stimulated beta-cell had its counterpart in pulsatile insulin release when single islets were perifused with a Sr2+-containing medium. Glucose 29-36 insulin Homo sapiens 91-98 9487416-20 1997 Repeated administration of glucose with insulin may not be safe because of the hypoglycaemic effect. Glucose 27-34 insulin Homo sapiens 40-47 9288574-2 1997 To examine mechanisms involved, we induced IR induced IR in H-411 E cells with graded doses of TNF-alpha and measured the ability of insulin (INS) to stimulate both calmodulin (CaM) mRNA and glucose utilization. Glucose 191-198 insulin Homo sapiens 133-140 9288577-2 1997 Using the frequently sampled intravenous glucose tolerance test and the minimal model analyses we have therefore determined the early insulin response to glucose (EIR) and insulin sensitivity (Si), in women with GDM of different severity (n = 14) and in normal women (n = 10). Glucose 154-161 insulin Homo sapiens 134-141 9288577-6 1997 The insulin treated GDM group only had higher fasting glucose level than controls (5.2 vs 4.2 mmol/l, p < 0.001). Glucose 54-61 insulin Homo sapiens 4-11 9288577-10 1997 These results suggest that glucose intolerance in GDM patients in the last trimester of pregnancy is characterized by both an impaired insulin secretion and an increased resistance to insulin. Glucose 27-34 insulin Homo sapiens 135-142 9283038-3 1997 Glycaemic and insulinemic indexes can be used to semi-quantitatively classify types of food as a function of their power to raise glucose and insulin levels. Glucose 130-137 insulin Homo sapiens 14-21 9247528-5 1997 Insulin sensitivity was estimated by minimal modeling analysis of the glucose and insulin and profiles during a 0.5 g/kg body weight intravenous glucose tolerance test. Glucose 70-77 insulin Homo sapiens 0-7 9247528-5 1997 Insulin sensitivity was estimated by minimal modeling analysis of the glucose and insulin and profiles during a 0.5 g/kg body weight intravenous glucose tolerance test. Glucose 145-152 insulin Homo sapiens 0-7 9263055-14 1997 Liver glucose release decreased in response to insulin; Rmin (mmol glucose.h-1.kg liver-1) was higher for younger (36.0 +/- 6.9) than for older (24.7 +/- 3.2) steers. Glucose 6-13 insulin Homo sapiens 47-54 9263055-14 1997 Liver glucose release decreased in response to insulin; Rmin (mmol glucose.h-1.kg liver-1) was higher for younger (36.0 +/- 6.9) than for older (24.7 +/- 3.2) steers. Glucose 67-74 insulin Homo sapiens 47-54 9239399-2 1997 Troglitazone, an insulin sensitizing agent, reduces glucose concentrations in subjects with NIDDM and IGT but is not known to affect insulin secretion. Glucose 52-59 insulin Homo sapiens 17-24 9239399-6 1997 Troglitazone reduced integrated glucose and insulin responses to oral glucose by 10% (P = 0.03) and 39% (P = 0.003), respectively. Glucose 70-77 insulin Homo sapiens 44-51 9239399-8 1997 Average insulin secretion rates adjusted for SI over the glucose interval 5-11 mmol/liter were increased by 52% (P = 0.02), and the ability of the beta cell to entrain to an exogenous oscillatory glucose infusion, as evaluated by analysis of spectral power, was improved by 49% (P = 0.04). Glucose 57-64 insulin Homo sapiens 8-15 9239399-8 1997 Average insulin secretion rates adjusted for SI over the glucose interval 5-11 mmol/liter were increased by 52% (P = 0.02), and the ability of the beta cell to entrain to an exogenous oscillatory glucose infusion, as evaluated by analysis of spectral power, was improved by 49% (P = 0.04). Glucose 196-203 insulin Homo sapiens 8-15 9253350-0 1997 Mechanisms of defective glucose-induced insulin release in human pancreatic islets transplanted to diabetic nude mice. Glucose 24-31 insulin Homo sapiens 40-47 9253350-1 1997 We have previously observed that human islets, transplanted under the kidney capsule of hyperglycemic nude mice, show a longlasting impairment in glucose-induced insulin release. Glucose 146-153 insulin Homo sapiens 162-169 9253350-4 1997 Four to 6 weeks of hyperglycemia induced a severe impairment of glucose- and arginine-induced insulin release, as demonstrated by perfusion of the graft-bearing kidney. Glucose 64-71 insulin Homo sapiens 94-101 9253350-7 1997 This, and the similar inhibition of glucose- and arginine-induced insulin release, suggest that prolonged hyperglycemia may exert its deleterious effect on insulin release at a step distal to closure of ATP-sensitive K-channels. Glucose 36-43 insulin Homo sapiens 66-73 9253350-7 1997 This, and the similar inhibition of glucose- and arginine-induced insulin release, suggest that prolonged hyperglycemia may exert its deleterious effect on insulin release at a step distal to closure of ATP-sensitive K-channels. Glucose 36-43 insulin Homo sapiens 156-163 9321736-5 1997 Also alpha-adrenergic stimulation can cause insulin resistance through vasoconstriction and the consequent decrease in the delivery of glucose and insulin to the muscles. Glucose 135-142 insulin Homo sapiens 44-51 9264009-8 1997 Insulin sensitivity was assessed by a short insulin tolerance test to derive the first-order rate constant for the disappearance of glucose (Kitt) and mononuclear leukocyte membrane fluidity was measured by fluorescence anisotropy. Glucose 132-139 insulin Homo sapiens 0-7 9284010-6 1997 Glucose-independent parameters were used to evaluate insulin response, insulin activity and glucose tolerance in fasting and postglucose ingestion states. Glucose 0-7 insulin Homo sapiens 53-60 9284010-6 1997 Glucose-independent parameters were used to evaluate insulin response, insulin activity and glucose tolerance in fasting and postglucose ingestion states. Glucose 0-7 insulin Homo sapiens 71-78 9284010-12 1997 In the postglucose ingestion state, insulin activity and glucose tolerance was lower in gestational hypertension than in preeclampsia. Glucose 11-18 insulin Homo sapiens 36-43 9258268-0 1997 Decreased glucose effectiveness but not insulin resistance in glucose-tolerant offspring of Japanese non-insulin-dependent diabetic patients: a minimal-model analysis. Glucose 10-17 insulin Homo sapiens 105-112 9258268-8 1997 The acute insulin response to glucose (AIRglucose) estimated by intravenous glucose tolerance testing was significantly lower in the offspring than in the normal controls (2,139 +/- 265 v 3,438 +/- 318 pmol/L.min, P < .05). Glucose 30-37 insulin Homo sapiens 10-17 9258268-8 1997 The acute insulin response to glucose (AIRglucose) estimated by intravenous glucose tolerance testing was significantly lower in the offspring than in the normal controls (2,139 +/- 265 v 3,438 +/- 318 pmol/L.min, P < .05). Glucose 42-49 insulin Homo sapiens 10-17 9258268-10 1997 Thus, glucose-tolerant Japanese NIDDM offspring with normal insulin sensitivity are characterized by a reduced AIRglucose and diminished SG. Glucose 6-13 insulin Homo sapiens 60-67 9268955-3 1997 Chromium picolinate supplementation resulted in significant weight gain in this population, while exercise training combined with chromium nicotinate supplementation resulted in significant weight loss and lowered the insulin response to an oral glucose load. Glucose 246-253 insulin Homo sapiens 218-225 9404147-3 1997 Insulin treatment during one month decreased her postprandial plasma glucose level from more than 400mg/dl to about 200mg/dl. Glucose 69-76 insulin Homo sapiens 0-7 9280885-5 1997 Postoperatively, the patient had complete relief of the abdominal pain, and the insulin-independent condition remained with normal fasting blood glucose, and hemoglobin A1c for 11 months. Glucose 145-152 insulin Homo sapiens 80-87 9234903-10 1997 Finally, the glucose-sensitive range can be adjusted by selection of the sugar structure and extent of labeling of the insulin. Glucose 13-20 insulin Homo sapiens 119-126 9244225-5 1997 Subjects with high BP, irrespective of parental BP, were heavier (P=.003) and fatter (P=.002) and had a greater rise in plasma insulin (P=.003) following glucose than those with low BP. Glucose 154-161 insulin Homo sapiens 127-134 9329342-4 1997 Fasting and postglucose load insulin concentrations were similar in the normal glucose-tolerant insulin-resistant and IGT groups, but were significantly higher (P < 0.02- < 0.001) than those in normal glucose-tolerant insulin-sensitive individuals. Glucose 16-23 insulin Homo sapiens 29-36 9329342-4 1997 Fasting and postglucose load insulin concentrations were similar in the normal glucose-tolerant insulin-resistant and IGT groups, but were significantly higher (P < 0.02- < 0.001) than those in normal glucose-tolerant insulin-sensitive individuals. Glucose 79-86 insulin Homo sapiens 29-36 9329342-5 1997 Fasting proinsulin concentrations were also higher (P < 0.002) in the normal glucose-tolerant insulin-resistant (15.1 +/- 1.5 pmol/L) and IGT (15.8 +/- 1.8 pmol/L) groups compared to those in normal glucose-tolerant insulin-sensitive volunteers (9.3 +/- 1.2 pmol/ L). Glucose 80-87 insulin Homo sapiens 8-18 9329342-5 1997 Fasting proinsulin concentrations were also higher (P < 0.002) in the normal glucose-tolerant insulin-resistant (15.1 +/- 1.5 pmol/L) and IGT (15.8 +/- 1.8 pmol/L) groups compared to those in normal glucose-tolerant insulin-sensitive volunteers (9.3 +/- 1.2 pmol/ L). Glucose 80-87 insulin Homo sapiens 11-18 9329342-5 1997 Fasting proinsulin concentrations were also higher (P < 0.002) in the normal glucose-tolerant insulin-resistant (15.1 +/- 1.5 pmol/L) and IGT (15.8 +/- 1.8 pmol/L) groups compared to those in normal glucose-tolerant insulin-sensitive volunteers (9.3 +/- 1.2 pmol/ L). Glucose 80-87 insulin Homo sapiens 97-104 9329342-5 1997 Fasting proinsulin concentrations were also higher (P < 0.002) in the normal glucose-tolerant insulin-resistant (15.1 +/- 1.5 pmol/L) and IGT (15.8 +/- 1.8 pmol/L) groups compared to those in normal glucose-tolerant insulin-sensitive volunteers (9.3 +/- 1.2 pmol/ L). Glucose 202-209 insulin Homo sapiens 8-18 9329342-5 1997 Fasting proinsulin concentrations were also higher (P < 0.002) in the normal glucose-tolerant insulin-resistant (15.1 +/- 1.5 pmol/L) and IGT (15.8 +/- 1.8 pmol/L) groups compared to those in normal glucose-tolerant insulin-sensitive volunteers (9.3 +/- 1.2 pmol/ L). Glucose 202-209 insulin Homo sapiens 11-18 9329345-8 1997 Even in the face of higher mean plasma insulin levels after GH treatment, the rate of insulin-stimulated glucose metabolism did not differ during the last 60 min of both studies. Glucose 105-112 insulin Homo sapiens 86-93 9329345-9 1997 Hence, the rate of insulin-stimulated glucose metabolism/mean plasma insulin ratio (an index of insulin sensitivity) was sharply reduced after GH treatment (P < 0.01). Glucose 38-45 insulin Homo sapiens 19-26 9329345-11 1997 We conclude that glucose-stimulated insulin responses are increased in short children treated with GH and that such hyperinsulinemic responses compensate for reductions in insulin sensitivity. Glucose 17-24 insulin Homo sapiens 36-43 9329345-11 1997 We conclude that glucose-stimulated insulin responses are increased in short children treated with GH and that such hyperinsulinemic responses compensate for reductions in insulin sensitivity. Glucose 17-24 insulin Homo sapiens 121-128 9252495-0 1997 Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Glucose 53-60 insulin Homo sapiens 75-82 9252478-2 1997 Adipocytes isolated from low-protein offspring had significantly higher basal and insulin-stimulated glucose uptakes than controls. Glucose 101-108 insulin Homo sapiens 82-89 9252495-1 1997 The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. Glucose 91-98 insulin Homo sapiens 72-79 9252495-1 1997 The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. Glucose 91-98 insulin Homo sapiens 113-120 9252495-11 1997 Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer. Glucose 93-100 insulin Homo sapiens 74-81 9200644-0 1997 Fatty acids mediate the acute extrahepatic effects of insulin on hepatic glucose production in humans. Glucose 73-80 insulin Homo sapiens 54-61 9261281-8 1997 In addition, the glucose uptake per unit insulin (I) was lower in FCH patients (insulin sensitivity index [M/I], 7.46 +/- 0.50 versus 9.51 +/- 0.53; P = .009). Glucose 17-24 insulin Homo sapiens 41-48 9261281-8 1997 In addition, the glucose uptake per unit insulin (I) was lower in FCH patients (insulin sensitivity index [M/I], 7.46 +/- 0.50 versus 9.51 +/- 0.53; P = .009). Glucose 17-24 insulin Homo sapiens 80-87 9203442-3 1997 The homeostasis model assessment (HOMA) has been suggested as a method to assess insulin resistance and secretion from the fasting glucose and insulin concentrations. Glucose 131-138 insulin Homo sapiens 81-88 9200644-1 1997 We have shown previously in humans that insulin partly suppresses hepatic glucose production (HGP) by an extrahepatic (indirect) mechanism. Glucose 74-81 insulin Homo sapiens 40-47 9223392-4 1997 Pramlintide infusion in the insulin-treated patients resulted in statistically significant reductions in mean glucose, insulin, C-peptide, and lactate concentrations during the 4-h period after the Sustacal test meal. Glucose 110-117 insulin Homo sapiens 28-35 9223393-4 1997 insulin infusion to stabilize fasting blood glucose levels at 4.0 mmol l(-1)). Glucose 44-51 insulin Homo sapiens 0-7 9200644-15 1997 This suggests that other mechanisms, most likely hepatic, dominate the acute insulin-induced suppression of glucose production. Glucose 108-115 insulin Homo sapiens 77-84 9200652-1 1997 The insulin-modified frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis (MINMOD) was compared with the tolbutamide protocol and the glucose clamp in 35 nondiabetic subjects (age 38 +/- 2 years [mean +/- SE], BMI 27.2 +/- 0.9 kg/m2). Glucose 52-59 insulin Homo sapiens 4-11 9211083-1 1997 Troglitazone decreases insulin resistance (improves insulin sensitivity), which results in reduced plasma glucose and insulin levels in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 106-113 insulin Homo sapiens 23-30 9248699-1 1997 The knowledge of the mechanism whereby glucose and other fuel stimuli promote the release of insulin by the pancreatic beta cell remains fragmentary. Glucose 39-46 insulin Homo sapiens 93-100 9248700-4 1997 This article seeks to provide a brief summary of the current status of this growing field, with a particular emphasis on progress in producing cell lines with appropriate glucose-stimulated insulin secretion. Glucose 171-178 insulin Homo sapiens 190-197 9243094-5 1997 Moreover, these studies indicate that glucose production by the human kidney is stimulated by epinephrine, inhibited by insulin and is excessive in diabetes mellitus. Glucose 38-45 insulin Homo sapiens 120-127 9243107-6 1997 The oestrogen treated group demonstrated a significant decrease of HbA1c and in the normotriglyceridaemic group a significantly increased suppression of hepatic glucose production by insulin. Glucose 161-168 insulin Homo sapiens 183-190 9243108-0 1997 Relationship between insulin-mediated glucose disposal and regulation of plasma and adipose tissue lipoprotein lipase. Glucose 38-45 insulin Homo sapiens 21-28 9243108-1 1997 The relationship between insulin-mediated glucose disposal and fasting insulin and triglyceride (TG) concentrations, plasma post-heparin lipoprotein lipase (PH-LPL) activity and mass, and adipose tissue LPL activity, mass, and mRNA content was defined in 19 non-diabetic men. Glucose 42-49 insulin Homo sapiens 25-32 9243108-1 1997 The relationship between insulin-mediated glucose disposal and fasting insulin and triglyceride (TG) concentrations, plasma post-heparin lipoprotein lipase (PH-LPL) activity and mass, and adipose tissue LPL activity, mass, and mRNA content was defined in 19 non-diabetic men. Glucose 42-49 insulin Homo sapiens 71-78 9233793-1 1997 In the pancreatic beta-cell, insulin secretion is stimulated by glucose metabolism resulting in membrane potential-dependent elevation of cytosolic Ca2+ ([Ca2+]c). Glucose 64-71 insulin Homo sapiens 29-36 9211083-1 1997 Troglitazone decreases insulin resistance (improves insulin sensitivity), which results in reduced plasma glucose and insulin levels in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 106-113 insulin Homo sapiens 52-59 9211083-3 1997 In clinical trials, troglitazone 200 to 800 mg daily (alone or in combination with other oral antidiabetic agents or insulin) reduced plasma or serum glucose levels and glycosylated haemoglobin compared with both baseline and placebo in patients with NIDDM refractory to other oral antidiabetic agents (usually sulphonylureas). Glucose 150-157 insulin Homo sapiens 117-124 9207262-4 1997 Using an insulin-glucose clamp, the blood glucose concentration was stabilized at 4 and 8 mmol/L on 2 separate days. Glucose 17-24 insulin Homo sapiens 9-16 9263752-7 1997 Insulin-mediated glucose uptake, i.e. insulin sensitivity, was assessed using the euglycaemic clamp technique. Glucose 17-24 insulin Homo sapiens 0-7 9263752-7 1997 Insulin-mediated glucose uptake, i.e. insulin sensitivity, was assessed using the euglycaemic clamp technique. Glucose 17-24 insulin Homo sapiens 38-45 9263753-3 1997 In the whole group, insulin sensitivity (as the ratio of insulin-mediated glucose clearance to steady-state plasma insulin concentrations) was inversely related to the haematocrit (r = 0.50, P < 0.01). Glucose 74-81 insulin Homo sapiens 20-27 9263753-3 1997 In the whole group, insulin sensitivity (as the ratio of insulin-mediated glucose clearance to steady-state plasma insulin concentrations) was inversely related to the haematocrit (r = 0.50, P < 0.01). Glucose 74-81 insulin Homo sapiens 57-64 9263753-3 1997 In the whole group, insulin sensitivity (as the ratio of insulin-mediated glucose clearance to steady-state plasma insulin concentrations) was inversely related to the haematocrit (r = 0.50, P < 0.01). Glucose 74-81 insulin Homo sapiens 57-64 9207262-4 1997 Using an insulin-glucose clamp, the blood glucose concentration was stabilized at 4 and 8 mmol/L on 2 separate days. Glucose 42-49 insulin Homo sapiens 9-16 9226489-14 1997 Significant correlations were found between visceral fat area and the sum of the glucose and insulin concentration during an oral glucose tolerance test. Glucose 130-137 insulin Homo sapiens 93-100 9288564-3 1997 PET has allowed study of the factors regulating heart glucose uptake in normal subjects and in subjects with alterations in skeletal muscle insulin sensitivity, and has provided evidence that insulin stimulated rates of blood flow and glucose uptake do not co-localize within muscle tissues. Glucose 235-242 insulin Homo sapiens 192-199 9215291-7 1997 Serum insulin reached a first peak after glucose injection and a second, higher peak after exogenous insulin administration. Glucose 41-48 insulin Homo sapiens 6-13 9276675-3 1997 The effects of insulin and BRL37344 were completely additive, suggesting that these two agents enhance glucose uptake by L6 myocytes through different mechanisms. Glucose 103-110 insulin Homo sapiens 15-22 9215295-4 1997 In all subjects, fasting plasma IGF-I, IGF-binding protein-3 (IGFBP-3), leptin, and lipid concentrations were determined; body composition was assessed by bioimpedance analysis; and insulin-mediated glucose up-take was evaluated by euglycemic hyperinsulinemic glucose clamp. Glucose 199-206 insulin Homo sapiens 182-189 9215311-3 1997 Basal insulin secretion rates, the glucose-stimulated early insulin secretion rates, as well as beta-cell responsiveness were markedly reduced in IPx than in the glucose-tolerant transplant subjects. Glucose 35-42 insulin Homo sapiens 60-67 9377730-2 1997 Hypertensive patients with microalbuminuria manifest abnormal circadian variation of blood pressure, increased serum levels of LDL-cholesterol and lipoprotein(a), a greater rise of serum insulin in response to an oral glucose tolerance test, and greater thickness of the carotid artery than patients without microalbuminuria. Glucose 218-225 insulin Homo sapiens 187-194 9225841-2 1997 This alteration has been attributed to a defective insulin-mediated glucose uptake in peripheral tissue, where nonoxidative glucose disposal seems to be chiefly impaired. Glucose 68-75 insulin Homo sapiens 51-58 9225841-2 1997 This alteration has been attributed to a defective insulin-mediated glucose uptake in peripheral tissue, where nonoxidative glucose disposal seems to be chiefly impaired. Glucose 124-131 insulin Homo sapiens 51-58 9225836-3 1997 On 1 day, insulin sensitivity was assessed as the steady-state plasma glucose (SSPG) level achieved during intravenous infusion of glucose insulin, and somatostatin. Glucose 70-77 insulin Homo sapiens 10-17 9225841-6 1997 By increasing insulin to pharmacological levels, glucose disposal increased in both groups. Glucose 49-56 insulin Homo sapiens 14-21 9225841-10 1997 In conclusion, in liver cirrhosis a reduced insulin sensitivity is associated with a reduced insulin responsiveness that is mainly caused by defective nonoxidative glucose disposal. Glucose 164-171 insulin Homo sapiens 44-51 9210493-11 1997 Microencapsulated porcine ICC also had a marked reduction in their insulin secretion in response to stimulation with glucose or glucose + theophylline both on days 1 and 6 in tissue culture. Glucose 117-124 insulin Homo sapiens 67-74 9249764-14 1997 Consequently, extremely elevated serum leptin may play a role in reducing glucose-stimulated insulin secretion and glucose intolerance in CRF. Glucose 74-81 insulin Homo sapiens 93-100 9301221-0 1997 [Effects of aerobic capacity and body fat accumulation on the insulin response after an oral glucose load]. Glucose 93-100 insulin Homo sapiens 62-69 9301221-1 1997 The effects of aerobic capacity and body fat accumulation on the insulin response after an oral glucose load were investigated in 21 college students. Glucose 96-103 insulin Homo sapiens 65-72 9301221-6 1997 These results suggest that an inactive life style, decreased aerobic capacity and increased body fat accumulation all appear to result in an increased insulin response after a glucose load. Glucose 176-183 insulin Homo sapiens 151-158 9210493-11 1997 Microencapsulated porcine ICC also had a marked reduction in their insulin secretion in response to stimulation with glucose or glucose + theophylline both on days 1 and 6 in tissue culture. Glucose 128-135 insulin Homo sapiens 67-74 9210493-16 1997 CONCLUSIONS: Pancreatic islets isolated from human, rat, and mouse donors show a glucose-stimulated insulin release in vitro after microencapsulation and repeated transports between laboratories. Glucose 81-88 insulin Homo sapiens 100-107 9220027-0 1997 Overexpression of glucagon-like peptide-1 receptor in an insulin-secreting cell line enhances glucose responsiveness. Glucose 94-101 insulin Homo sapiens 57-64 9188534-3 1997 Inhalation of large porous insulin particles resulted in elevated systemic levels of insulin and suppressed systemic glucose levels for 96 hours, whereas small nonporous insulin particles had this effect for only 4 hours. Glucose 117-124 insulin Homo sapiens 27-34 9220027-4 1997 In GLP-1 receptor transfected cells, glucose (0.5 mM)-mediated insulin release was increased compared with parental cells (4.52 +/- 0.79 pmol insulin/l per mg protein x h vs. 2.21 +/- 0.36 pmol insulin/l per mg protein x h; mean +/- S.E., n = 6, P = 0.015, in transfected vs. parental cells, respectively). Glucose 37-44 insulin Homo sapiens 63-70 9220027-4 1997 In GLP-1 receptor transfected cells, glucose (0.5 mM)-mediated insulin release was increased compared with parental cells (4.52 +/- 0.79 pmol insulin/l per mg protein x h vs. 2.21 +/- 0.36 pmol insulin/l per mg protein x h; mean +/- S.E., n = 6, P = 0.015, in transfected vs. parental cells, respectively). Glucose 37-44 insulin Homo sapiens 142-149 9220027-4 1997 In GLP-1 receptor transfected cells, glucose (0.5 mM)-mediated insulin release was increased compared with parental cells (4.52 +/- 0.79 pmol insulin/l per mg protein x h vs. 2.21 +/- 0.36 pmol insulin/l per mg protein x h; mean +/- S.E., n = 6, P = 0.015, in transfected vs. parental cells, respectively). Glucose 37-44 insulin Homo sapiens 142-149 9200389-7 1997 In conclusion, we demonstrated frequent disturbances in glucose metabolism indicating insulin resistance in patients with ischemic heart disease without a history of diabetes, but we could not demonstrate a relation between these disturbances and degree of coronary atherosclerosis. Glucose 56-63 insulin Homo sapiens 86-93 9183237-8 1997 RESULTS: Throughout the study, the postprandial rise in serum glucose levels was significantly lower during insulin lispro than human regular insulin treatment. Glucose 62-69 insulin Homo sapiens 108-115 9183237-8 1997 RESULTS: Throughout the study, the postprandial rise in serum glucose levels was significantly lower during insulin lispro than human regular insulin treatment. Glucose 62-69 insulin Homo sapiens 142-149 9183237-9 1997 At end point the rise (mean +/- SEM) in serum glucose levels was 30% lower at 1 hour (2.6 +/- 0.1 mmol/L [46.8 +/- 1.8 mg/ dL] for lispro vs 3.7 +/- 0.1 mmol/L [66.6 +/- 1.8 mg/dL] for human regular insulin) and 53% lower 2 hours after the test meal (1.4 +/- 0.1 mmol/L [25.2 +/- 1.8 mg/dL] for lispro vs 3.0 +/- 0.1 mmol/L [54.0 +/- 1.8 mg/dL] for human regular insulin) with insulin lispro compared with human regular insulin therapy (P < .001 for both intervals). Glucose 46-53 insulin Homo sapiens 199-206 9183237-9 1997 At end point the rise (mean +/- SEM) in serum glucose levels was 30% lower at 1 hour (2.6 +/- 0.1 mmol/L [46.8 +/- 1.8 mg/ dL] for lispro vs 3.7 +/- 0.1 mmol/L [66.6 +/- 1.8 mg/dL] for human regular insulin) and 53% lower 2 hours after the test meal (1.4 +/- 0.1 mmol/L [25.2 +/- 1.8 mg/dL] for lispro vs 3.0 +/- 0.1 mmol/L [54.0 +/- 1.8 mg/dL] for human regular insulin) with insulin lispro compared with human regular insulin therapy (P < .001 for both intervals). Glucose 46-53 insulin Homo sapiens 363-370 9183237-9 1997 At end point the rise (mean +/- SEM) in serum glucose levels was 30% lower at 1 hour (2.6 +/- 0.1 mmol/L [46.8 +/- 1.8 mg/ dL] for lispro vs 3.7 +/- 0.1 mmol/L [66.6 +/- 1.8 mg/dL] for human regular insulin) and 53% lower 2 hours after the test meal (1.4 +/- 0.1 mmol/L [25.2 +/- 1.8 mg/dL] for lispro vs 3.0 +/- 0.1 mmol/L [54.0 +/- 1.8 mg/dL] for human regular insulin) with insulin lispro compared with human regular insulin therapy (P < .001 for both intervals). Glucose 46-53 insulin Homo sapiens 363-370 9194511-3 1997 The drinking water contained 10% glucose to prevent hypoglycemia in the insulin-injected rats. Glucose 33-40 insulin Homo sapiens 72-79 9194511-6 1997 The blood glucose levels were higher at the end of the experiment, in both the placebo- (saline)-injected and the insulin-injected rats. Glucose 10-17 insulin Homo sapiens 114-121 9184703-11 1997 Insulin concentrations increased more during the postprandial glucose peaks than when subjects were fasting. Glucose 62-69 insulin Homo sapiens 0-7 9177859-2 1997 The main goal of this study was to characterize the release of model proteins (insulin and lysozyme) through the hydrogel membrane as the free glucose concentration in the environment was changed. Glucose 143-150 insulin Homo sapiens 63-99 9177859-8 1997 This study demonstrated the possibility that the glucose-sensitive phase-reversible hydrogels can be used to regulate the insulin release as a function of the free glucose concentration in the environment. Glucose 49-56 insulin Homo sapiens 122-129 9177859-8 1997 This study demonstrated the possibility that the glucose-sensitive phase-reversible hydrogels can be used to regulate the insulin release as a function of the free glucose concentration in the environment. Glucose 164-171 insulin Homo sapiens 122-129 9296913-4 1997 Insulin induced changes in the dehydroepiandrosterone level during the intravenous glucose tolerance test were described. Glucose 83-90 insulin Homo sapiens 0-7 9222649-10 1997 IN CONCLUSION: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. Glucose 59-66 insulin Homo sapiens 101-108 9222649-10 1997 IN CONCLUSION: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. Glucose 125-132 insulin Homo sapiens 101-108 9222649-10 1997 IN CONCLUSION: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. Glucose 125-132 insulin Homo sapiens 101-108 9222649-10 1997 IN CONCLUSION: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. Glucose 125-132 insulin Homo sapiens 101-108 9222649-10 1997 IN CONCLUSION: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. Glucose 125-132 insulin Homo sapiens 101-108 9222651-7 1997 Oral glucose tolerance tests performed in 392 subjects without fasting hyperglycaemia showed higher 2-h insulin concentrations in individuals homozygous for the Thr54 allele when compared with heterozygotes or homozygotes for the Ala54 allele. Glucose 5-12 insulin Homo sapiens 104-111 9212078-4 1997 However, insulin released as a result of elevated blood glucose stimulates the translocation of specific glucose transporters to the cell membrane, increases the uptake of glucose, and causes the covalent, dephosphorylation-mediated activation of glycogen synthase. Glucose 56-63 insulin Homo sapiens 9-16 9212078-4 1997 However, insulin released as a result of elevated blood glucose stimulates the translocation of specific glucose transporters to the cell membrane, increases the uptake of glucose, and causes the covalent, dephosphorylation-mediated activation of glycogen synthase. Glucose 105-112 insulin Homo sapiens 9-16 9212078-7 1997 We show that the stimulated glucose uptake and phosphorylation appear to play a major role in the control by insulin of the enzymes involved in glycogen synthesis. Glucose 28-35 insulin Homo sapiens 109-116 9177369-1 1997 Counterregulation and awareness of hypoglycemia begins at lower plasma glucose levels in insulin-dependent diabetes mellitus (IDDM) subjects given intensive insulin treatment. Glucose 71-78 insulin Homo sapiens 89-96 9177391-4 1997 The nocturnal glucose infusion resulted in higher (P < 0.05) plasma glucose (6.0 +/- 0.1 vs. 5.1 +/- 0.1 mmol/L) and insulin (127 +/- 38 vs. 49 +/- 9 pmol/L) concentrations, and lower (P < 0.05) plasma glucagon concentrations (74 +/- 11 vs. 97 +/- 20 pg/mL) than did saline infusion. Glucose 14-21 insulin Homo sapiens 120-127 9177391-6 1997 After discontinuation of the glucose infusion, glucose and insulin concentrations fell to levels that no longer differed from those observed during the saline infusion. Glucose 29-36 insulin Homo sapiens 59-66 9177391-9 1997 On the other hand, when differences in basal rates were taken into account, insulin-induced suppression of both EGP and incorporation of 14CO2 into glucose did not differ on the two occasions. Glucose 148-155 insulin Homo sapiens 76-83 9177392-0 1997 Alterations in the glucose-stimulated insulin secretory dose-response curve and in insulin clearance in nondiabetic insulin-resistant individuals. Glucose 19-26 insulin Homo sapiens 38-45 9177392-3 1997 Resistance to insulin-mediated glucose disposal was measured using the insulin suppression test, and the women studied were chosen to represent the highest and lowest quartiles of insulin resistance seen in the normal population. Glucose 31-38 insulin Homo sapiens 14-21 9177392-8 1997 When expressed as a function of the molar increments in plasma glucose achieved during the glucose infusion studies, the insulin-resistant women had a 90% higher (684 +/- 55 vs. 360 +/- 36 pmol/L x mmol/L; P < 0.001) total integrated plasma insulin response as the glucose concentration was increased from 5 to 9 mmol/L. Glucose 63-70 insulin Homo sapiens 121-128 9177392-8 1997 When expressed as a function of the molar increments in plasma glucose achieved during the glucose infusion studies, the insulin-resistant women had a 90% higher (684 +/- 55 vs. 360 +/- 36 pmol/L x mmol/L; P < 0.001) total integrated plasma insulin response as the glucose concentration was increased from 5 to 9 mmol/L. Glucose 63-70 insulin Homo sapiens 244-251 9177392-8 1997 When expressed as a function of the molar increments in plasma glucose achieved during the glucose infusion studies, the insulin-resistant women had a 90% higher (684 +/- 55 vs. 360 +/- 36 pmol/L x mmol/L; P < 0.001) total integrated plasma insulin response as the glucose concentration was increased from 5 to 9 mmol/L. Glucose 91-98 insulin Homo sapiens 121-128 9177392-8 1997 When expressed as a function of the molar increments in plasma glucose achieved during the glucose infusion studies, the insulin-resistant women had a 90% higher (684 +/- 55 vs. 360 +/- 36 pmol/L x mmol/L; P < 0.001) total integrated plasma insulin response as the glucose concentration was increased from 5 to 9 mmol/L. Glucose 91-98 insulin Homo sapiens 121-128 9177392-11 1997 These results show that the hyperinsulinemia of insulin resistance results from an increase in insulin secretion secondary to a shift to the left of the glucose-stimulated insulin response curve as well as a decrease in insulin clearance. Glucose 153-160 insulin Homo sapiens 33-40 9177392-11 1997 These results show that the hyperinsulinemia of insulin resistance results from an increase in insulin secretion secondary to a shift to the left of the glucose-stimulated insulin response curve as well as a decrease in insulin clearance. Glucose 153-160 insulin Homo sapiens 48-55 10497620-5 1997 MAIN OUTCOME MEASURES: Insulin sensitivity was assessed by the oral glucose tolerance test (OGTT). Glucose 68-75 insulin Homo sapiens 23-30 9202618-11 1997 When each subgroup was compared separately with control subjects, all subgroups were statistically insulin resistant (glucose disposal rate, patients with CF and normal glucose tolerance = 10.8; those with impaired glucose tolerance = 8.4; those with DM = 10.1 mg/kg per minute), and the patients with CF with impaired glucose tolerance were the most insulin resistant. Glucose 118-125 insulin Homo sapiens 99-106 9202618-12 1997 When plotted versus glucose disposal rate, a striking positive correlation between worsened clinical status and insulin resistance (r = 0.85) is demonstrated. Glucose 20-27 insulin Homo sapiens 112-119 9186304-6 1997 Intramuscular (IM) injection of insulin (600 nmol/L) stimulated in situ protein synthesis similarly in 4-day unweighted (+56%) and weight-bearing (+90%) soleus, even though unweighted muscle showed a greater in situ response of 2-deoxy-[3H]glucose uptake to IM injection of either insulin (133 nmol/L) or insulin-like growth factor-I (IGF-I) (200 nmol/L) than control muscle. Glucose 240-247 insulin Homo sapiens 32-39 9186311-6 1997 Insulin infusion with 250 microU/mL obtained half-maximal effects, causing a 2.8-fold increase in glucose uptake and a 1.5-fold increase in lactate and pyruvate release. Glucose 98-105 insulin Homo sapiens 0-7 9186311-7 1997 When 20 mumol/L troglitazone was infused for 30 minutes together with 250 microU/mL insulin, insulin-induced glucose uptake significantly increased 30 minutes after troglitazone infusion, and this increase was further augmented after withdrawal of troglitazone. Glucose 109-116 insulin Homo sapiens 84-91 9186311-7 1997 When 20 mumol/L troglitazone was infused for 30 minutes together with 250 microU/mL insulin, insulin-induced glucose uptake significantly increased 30 minutes after troglitazone infusion, and this increase was further augmented after withdrawal of troglitazone. Glucose 109-116 insulin Homo sapiens 93-100 9186311-10 1997 In the presence of insulin, troglitazone increases insulin-induced glucose uptake, and this increase is further augmented after troglitazone removal. Glucose 67-74 insulin Homo sapiens 19-26 9186311-10 1997 In the presence of insulin, troglitazone increases insulin-induced glucose uptake, and this increase is further augmented after troglitazone removal. Glucose 67-74 insulin Homo sapiens 51-58 9186311-12 1997 This decrease in muscle glycogen content may trigger an enhancement of insulin-induced glucose uptake similar to that observed during muscle contraction or epinephrine treatment. Glucose 87-94 insulin Homo sapiens 71-78 9171835-4 1997 The spontaneously hypertensive rat (SHR), a widely used animal model of essential hypertension, has a global defect in insulin action on glucose metabolism and shows reduced catecholamine action on lipolysis in fat cells. Glucose 137-144 insulin Homo sapiens 119-126 9200568-2 1997 At a physiological level of [Ca2+]o, tetracaine (0.1-5 mM) dose-dependently inhibited insulin secretion induced by 22 mM glucose. Glucose 121-128 insulin Homo sapiens 86-93 9153412-0 1997 Botulinum neurotoxin B inhibits insulin-stimulated glucose uptake into 3T3-L1 adipocytes and cleaves cellubrevin unlike type A toxin which failed to proteolyze the SNAP-23 present. Glucose 51-58 insulin Homo sapiens 32-39 9153412-3 1997 In this study, exposure of cultured 3T3-L1 adipocytes to BoNT/B in a low-ionic strength medium was found to block insulin-evoked glucose uptake by up to 64%. Glucose 129-136 insulin Homo sapiens 114-121 9188084-7 1997 In the celiac-preserved group, the glucagon stimulated glucose-related C-peptide ratio (x 10(-3) was 0.5 +/- 0.7 before the nerve manipulation and 3.5 +/- 3.0 after it, a significant difference (p < 0.01). Glucose 55-62 insulin Homo sapiens 71-80 9129485-0 1997 A low-protein diet improves insulin sensitivity of endogenous glucose production in predialytic uremic patients. Glucose 62-69 insulin Homo sapiens 28-35 9129485-2 1997 We used the glucose clamp technique at a low (0.25 mU.kg-1.min-1) level of hyperinsulinemia associated with the infusion of D[6,6-2H2] glucose to assess the insulin sensitivity of endogenous glucose production (EGP). Glucose 12-19 insulin Homo sapiens 80-87 9176195-1 1997 Insulin sensitivity is frequently assessed with the minimal model (MM) and the insulin-modified intravenous glucose tolerance test (MIVGTT). Glucose 108-115 insulin Homo sapiens 0-7 9176195-1 1997 Insulin sensitivity is frequently assessed with the minimal model (MM) and the insulin-modified intravenous glucose tolerance test (MIVGTT). Glucose 108-115 insulin Homo sapiens 79-86 9176196-6 1997 Basal lipogenesis activity was significantly enhanced by GO, but acute insulin stimulation resulted in significantly reduced lipogenesis activity (29 +/- 4 vs. 11 +/- 1 nmol glucose/well for control and 50 mU/ml GO, respectively, P = 0.001). Glucose 174-181 insulin Homo sapiens 71-78 9283635-3 1997 Phenobarbital, a hepatic enzyme inducer, has been used in the treatment of patients with non-insulin-dependent diabetes mellitus (NIDDM), increasing the insulin-mediated glucose disposal. Glucose 170-177 insulin Homo sapiens 93-100 9283637-0 1997 Monosodium glutamate (MSG)-obese rats develop glucose intolerance and insulin resistance to peripheral glucose uptake. Glucose 103-110 insulin Homo sapiens 70-77 9283637-10 1997 The mean post-glucose area increase of insulin was 111% higher in MSG-obese than in control rats. Glucose 14-21 insulin Homo sapiens 39-46 9283637-13 1997 These data demonstrate that MSG-obese rats develop insulin resistance to peripheral glucose uptake. Glucose 84-91 insulin Homo sapiens 51-58 9231061-7 1997 A dose-dependent inhibition of glucagon release by insulin was however, observed at low glucose concentration. Glucose 88-95 insulin Homo sapiens 51-58 9133547-6 1997 Regular human insulin was infused (0.28 pmol x m(-2) x min(-1)) with a variable rate glucose infusion to lower the plasma glucose from 4.9 +/- 0.2 to 2.6 +/- 0.2 mmol/l in the control study and from 4.9 +/- 0.2 to 2.5 +/- 0.2 mmol/l in the trimethaphan study. Glucose 122-129 insulin Homo sapiens 14-21 9133564-0 1997 A prevalent amino acid polymorphism at codon 98 in the hepatocyte nuclear factor-1alpha gene is associated with reduced serum C-peptide and insulin responses to an oral glucose challenge. Glucose 169-176 insulin Homo sapiens 140-147 9133564-10 1997 Val 98 homozygotes may exhibit a more severe defect in the early glucose-induced insulin response. Glucose 65-72 insulin Homo sapiens 81-88 9215486-2 1997 In this study, a systems analysis approach was used to study glucose homeostasis which is considered as the dynamic balance between glucose release by the liver and its uptake by the peripheral tissues as regulated by insulin and glucagon. Glucose 61-68 insulin Homo sapiens 218-225 9215486-5 1997 When peripheral cellular insulin receptors which regulate glucose uptake were reduced to 25% of normal, the steady state plasma insulin concentration showed little change from the basal level of 8 microU/ml. Glucose 58-65 insulin Homo sapiens 25-32 9215486-8 1997 Hence, this study suggests that the liver and its release of glucose, as controlled by insulin and glucagon, plays a central role in the development of a steady-state insulin resistance and hyperinsulinemia. Glucose 61-68 insulin Homo sapiens 87-94 9215486-8 1997 Hence, this study suggests that the liver and its release of glucose, as controlled by insulin and glucagon, plays a central role in the development of a steady-state insulin resistance and hyperinsulinemia. Glucose 61-68 insulin Homo sapiens 167-174 9135944-3 1997 RESEARCH DESIGN AND METHODS: Serum insulin was measured 2 h after an oral glucose load, while global cognitive function was assessed by the Mini Mental State Examination in 5,510 subjects, aged 55 years and over. Glucose 74-81 insulin Homo sapiens 35-42 9165215-2 1997 During the last 30 years, a combination of biochemical and ultrastructural approaches has resulted in dramatic progress in the understanding of the processes by which glucose and other nutrients modulate the release of insulin. Glucose 167-174 insulin Homo sapiens 219-226 9165224-0 1997 Insulin mediators in man: effects of glucose ingestion and insulin resistance. Glucose 37-44 insulin Homo sapiens 0-7 9165224-8 1997 These data suggest that the pH 2.0 IPG plays an important role in mediating insulin"s effect on peripheral glucose utilization in man under physiological conditions. Glucose 107-114 insulin Homo sapiens 76-83 9165229-3 1997 The stimulatory effect of insulin on glucose transport and the ability of the hormone to inhibit lipolysis were determined in adipocytes isolated from these three adipose depots. Glucose 37-44 insulin Homo sapiens 26-33 9165229-4 1997 Insulin stimulated glucose transport 2-3 times over basal rates in all adipocytes. Glucose 19-26 insulin Homo sapiens 0-7 9165229-7 1997 We also investigated whether regional differences in fat cell insulin-stimulated glucose transport were linked to a differential expression of the GLUT4 glucose transporter. Glucose 81-88 insulin Homo sapiens 62-69 9165229-12 1997 The greater insulin effect on glucose transport in round ligament adipocytes was associated with a higher expression of GLUT4 when compared to subcutaneous abdominal and omental fat cells. Glucose 30-37 insulin Homo sapiens 12-19 9186267-7 1997 IN CONCLUSION: 2 weeks of high-dose rhIGF-I therapy in insulin-treated patients with severe insulin resistance has a marked lowering effect on fasting plasma glucose and serum insulin levels whereas the metabolic and glycaemic effects of 10 weeks of treatment with low-dose rhIGF-I may be modest and transient. Glucose 158-165 insulin Homo sapiens 55-62 9186267-7 1997 IN CONCLUSION: 2 weeks of high-dose rhIGF-I therapy in insulin-treated patients with severe insulin resistance has a marked lowering effect on fasting plasma glucose and serum insulin levels whereas the metabolic and glycaemic effects of 10 weeks of treatment with low-dose rhIGF-I may be modest and transient. Glucose 158-165 insulin Homo sapiens 92-99 9183237-9 1997 At end point the rise (mean +/- SEM) in serum glucose levels was 30% lower at 1 hour (2.6 +/- 0.1 mmol/L [46.8 +/- 1.8 mg/ dL] for lispro vs 3.7 +/- 0.1 mmol/L [66.6 +/- 1.8 mg/dL] for human regular insulin) and 53% lower 2 hours after the test meal (1.4 +/- 0.1 mmol/L [25.2 +/- 1.8 mg/dL] for lispro vs 3.0 +/- 0.1 mmol/L [54.0 +/- 1.8 mg/dL] for human regular insulin) with insulin lispro compared with human regular insulin therapy (P < .001 for both intervals). Glucose 46-53 insulin Homo sapiens 363-370 9191458-5 1997 Dietary measures are used initially in the management of gestational diabetes, with the addition of insulin therapy if glucose levels exceed 105 mg per dL (5.8 mmol per L) in a fasting state or 120 mg per dL (6.7 mmol per L) two hours postprandial. Glucose 119-126 insulin Homo sapiens 100-107 9189306-3 1997 With GLU, serum insulin was significantly increased prior to exercise. Glucose 5-8 insulin Homo sapiens 16-23 9274705-5 1997 DESIGN: Insulin action was assessed using the euglycaemic glucose clamp at insulin infusion rates of 0.4 and 2.0 mU/kg/min combined with a simultaneous infusion of [2(3)H]- and [6(3)-H]-glucose. Glucose 58-65 insulin Homo sapiens 8-15 9274705-5 1997 DESIGN: Insulin action was assessed using the euglycaemic glucose clamp at insulin infusion rates of 0.4 and 2.0 mU/kg/min combined with a simultaneous infusion of [2(3)H]- and [6(3)-H]-glucose. Glucose 186-193 insulin Homo sapiens 8-15 9274705-7 1997 MEASUREMENTS AND RESULTS: Exogenous glucose infusion rates required to maintain euglycaemia were significantly lower in Cushing"s patients compared to controls, during the 0.4 mU/kg/min (7.8 +/- 1.2 vs 15.7 +/- 0.5 mumol/kg/min, P < 0.001) and the 2.0 mU/ kg/min insulin infusions (26.2 +/- 2.8 vs 51.5 +/- 3.5 mumol/ kg/min, P < 0.001). Glucose 36-43 insulin Homo sapiens 266-273 9274705-12 1997 During hyperinsulinaemia G/G6P cycle activity was increased but insulin resistance was predominantly due to reduced peripheral glucose uptake. Glucose 127-134 insulin Homo sapiens 12-19 9166667-5 1997 As a result, betaG 49/206 and betaG 40/110 cells exhibit potent insulin-secretory responses to glucose alone (6.1- and 7.6-fold, respectively) or to glucose plus isobutylmethylxanthine (10.8- and 15.1-fold, respectively) that are clearly larger than the corresponding responses of betaG I/17 or parental RIN 1046-38 cells. Glucose 95-102 insulin Homo sapiens 64-71 9166667-5 1997 As a result, betaG 49/206 and betaG 40/110 cells exhibit potent insulin-secretory responses to glucose alone (6.1- and 7.6-fold, respectively) or to glucose plus isobutylmethylxanthine (10.8- and 15.1-fold, respectively) that are clearly larger than the corresponding responses of betaG I/17 or parental RIN 1046-38 cells. Glucose 149-156 insulin Homo sapiens 64-71 9166675-13 1997 Therefore a high first-phase insulin response to intravenous glucose is a risk factor for long-term weight gain, and this effect is particularly manifested in insulin-sensitive individuals. Glucose 61-68 insulin Homo sapiens 29-36 9166675-13 1997 Therefore a high first-phase insulin response to intravenous glucose is a risk factor for long-term weight gain, and this effect is particularly manifested in insulin-sensitive individuals. Glucose 61-68 insulin Homo sapiens 159-166 9233544-28 1997 The reduction in urea synthesis by glucose, i.e. its nitrogen sparing effect, is accomplished by two different mechanisms: A hepatic component (reduction of the hepatic nitrogen clearance) and a peripheral component (reduced substrate availability mediated by the insulin response). Glucose 35-42 insulin Homo sapiens 264-271 14655846-2 1997 We compared insulin secretion, clearance and action on glucose metabolism during an intravenous glucose tolerance test in nine women with anorexia nervosa and in nine age-matched normal-weight controls. Glucose 55-62 insulin Homo sapiens 12-19 14655846-3 1997 Insulin secretion (ISR) was derived by deconvolution of plasma C-peptide levels, insulin clearance (MCR(I)) was obtained by dividing the area under the curve (AUC(0-180 min)) of ISR by the corresponding AUC of plasma insulin levels, insulin sensitivity (S(I)) and glucose effectiveness index (S(G)) were calculated by Bergman"s minimal model. Glucose 264-271 insulin Homo sapiens 81-88 9230352-3 1997 Adaptive changes that occur in islets during normal pregnancy include: 1) increased glucose-stimulated insulin secretion with a lowered threshold for glucose-stimulated insulin secretion, 2) increased insulin synthesis, 3) increased beta-cell proliferation and islet volume, 4) increased gap-junctional coupling among beta-cells, 5) increased glucose metabolism, and 6) increased c-AMP metabolism. Glucose 84-91 insulin Homo sapiens 103-110 9230352-7 1997 The lowering of the threshold for glucose stimulated insulin secretion is the primary mechanism by which beta-cells can release significantly more insulin under normal blood glucose concentrations. Glucose 34-41 insulin Homo sapiens 53-60 9230352-7 1997 The lowering of the threshold for glucose stimulated insulin secretion is the primary mechanism by which beta-cells can release significantly more insulin under normal blood glucose concentrations. Glucose 174-181 insulin Homo sapiens 53-60 9141538-6 1997 Glucose levels also were significantly inversely related to IGFBP-1 in old and young men (r = 0.37; P = 0.02 and r = -0.49; P < 0.01), and this relationship was not accounted for by the effect of insulin. Glucose 0-7 insulin Homo sapiens 199-206 9152737-9 1997 We conclude that fasting and post-glucose stimulated plasma insulin levels are frequent findings in patients with FCH when compared with control subjects of similar age, gender and BMI. Glucose 34-41 insulin Homo sapiens 60-67 9141527-3 1997 Insulin sensitivity for glucose transport stimulation was impaired in PCOS adipocytes (EC50 = 290 +/- 42 pmol/L) compared to that in NC cells (93 +/- 14; P < 0.005). Glucose 24-31 insulin Homo sapiens 0-7 9141527-8 1997 In conclusion, our results suggest that insulin resistance in PCOS, as accessed in the adipocyte, occurs at an early step in insulin signaling that is common for glucose transport and lipolysis. Glucose 162-169 insulin Homo sapiens 40-47 9151794-7 1997 Together, these data indicate that defective glucose transport/phosphorylation is the major factor responsible for the lower rate of muscle glycogen synthesis in the poorly controlled insulin-dependent diabetic subjects. Glucose 45-52 insulin Homo sapiens 184-191 9141527-8 1997 In conclusion, our results suggest that insulin resistance in PCOS, as accessed in the adipocyte, occurs at an early step in insulin signaling that is common for glucose transport and lipolysis. Glucose 162-169 insulin Homo sapiens 125-132 9166122-0 1997 Normal pancreastatin-like and increased post-glucose insulin levels in young offspring of insulin-resistant non-obese essential hypertensive patients. Glucose 45-52 insulin Homo sapiens 53-60 9166122-8 1997 We found that after an intravenous glucose load, offspring from insulin-resistant patients were already hyperinsulinemic, although glucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were normal compared with matched controls. Glucose 35-42 insulin Homo sapiens 64-71 9166122-8 1997 We found that after an intravenous glucose load, offspring from insulin-resistant patients were already hyperinsulinemic, although glucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were normal compared with matched controls. Glucose 35-42 insulin Homo sapiens 109-116 9160821-5 1997 Chronic inhibition of opioid tone by the opioid antagonist naltrexone (NTX) is able to reduce the insulin response to an oral glucose tolerance test (OGTT) in hyperinsulinemic PCOS patients. Glucose 126-133 insulin Homo sapiens 98-105 9205938-1 1997 We investigated the possible role of losartan on insulin-mediated glucose uptake, substrate oxidation and blood flow in insulin-resistant hypertensive patients. Glucose 66-73 insulin Homo sapiens 49-56 9205938-13 1997 In conclusion losartan improves insulin-mediated glucose uptake through an increase in NOGM and blood flow in hypertensive patients. Glucose 49-56 insulin Homo sapiens 32-39 9160811-9 1997 On the other hand, glucose effectiveness at basal (SG) and zero (GEZI) insulin was significantly diminished in comparison to normal controls (SG, 0.011 +/- 0.002 v 0.024 +/- 0.002 min(-1), P < .01; GEZI, 0.008 +/- 0.002 v 0.017 +/- 0.003 min(-1), P < .01). Glucose 19-26 insulin Homo sapiens 71-78 9172168-2 1997 Risk for NIDDM was considered increased if both 2 h glucose and insulin values on oral glucose tolerance testing were higher than the median in normoglycaemic subjects, and low if the respective values were lower than the median. Glucose 87-94 insulin Homo sapiens 64-71 9160815-2 1997 The insulin sensitivity index (S[I]) was determined by the minimal modeling method of Bergman from a frequently sampled intravenous glucose tolerance test with intravenous tolbutamide. Glucose 132-139 insulin Homo sapiens 4-11 9267146-5 1997 Insulin sensitivity, as assessed by the ratio of the sum of the plasma glucose divided by the sum of the serum insulin during the test (sigma PG/sigma IRI), was significantly lower in subjects over 60 years old than in younger subjects. Glucose 71-78 insulin Homo sapiens 0-7 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Glucose 128-135 insulin Homo sapiens 44-51 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Glucose 128-135 insulin Homo sapiens 203-210 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Glucose 128-135 insulin Homo sapiens 203-210 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Glucose 238-245 insulin Homo sapiens 44-51 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Glucose 238-245 insulin Homo sapiens 203-210 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Glucose 238-245 insulin Homo sapiens 203-210 9411418-11 1997 In the majority of patients treated during pregnancy with insulin the results of oral glucose tolerance test were pathological. Glucose 86-93 insulin Homo sapiens 58-65 9142870-4 1997 During control studies, prepubertal children had lower basal fat oxidation and higher insulin-mediated glucose disposal than pubertal adolescents. Glucose 103-110 insulin Homo sapiens 86-93 9094877-9 1997 In conclusion, lactitol and xylitol cause smaller changes than does glucose in plasma glucose and insulin concentrations and thermogenic response. Glucose 68-75 insulin Homo sapiens 98-105 9142870-6 1997 Insulin-stimulated whole body glucose disposal did not change in prepubertal children (control 77.6 +/- 8.9, Intralipid 84.5 +/- 13.3 micromol x kg(-1) x min(-1)) but decreased in pubertal adolescents (control 55.0 +/- 3.6, Intralipid 46.7 +/- 3.4 micromol x kg(-1) x min(-1), P = 0.01) despite comparable decrements in glucose oxidaion. Glucose 30-37 insulin Homo sapiens 0-7 9259932-7 1997 Insulin was begun if the fasting blood glucose was > 90 mg/dL and/or the 1-hour post meal was > 120 mg/dL. Glucose 39-46 insulin Homo sapiens 0-7 9333317-2 1997 Several hormones, including insulin, glucagon, growth hormone, cortisol, and catecholamines contribute to the regulation of glucose metabolism by the liver. Glucose 124-131 insulin Homo sapiens 28-35 9108790-6 1997 During high-dose insulin infusion, insulin sensitivity for peripheral glucose disposal was reduced by 60% in FCHL patients compared with control subjects (P = .03). Glucose 70-77 insulin Homo sapiens 17-24 9108790-6 1997 During high-dose insulin infusion, insulin sensitivity for peripheral glucose disposal was reduced by 60% in FCHL patients compared with control subjects (P = .03). Glucose 70-77 insulin Homo sapiens 35-42 9108790-8 1997 In multiple regression analysis, increased upper-body fat in the patient group accounted for the impairment of insulin-mediated glucose disposal but did not influence the defect in insulin-mediated NEFA suppression in the FCHL patients. Glucose 128-135 insulin Homo sapiens 111-118 9126663-7 1997 Age trends of insulin concentrations in sexes emerged as independent of age-related changes in body weight, type of fat distribution, alcohol consumption, cigarette smoking, social status, fasting glucose, and physical activity (P < 0.001 for sex-specific difference in the regression slopes). Glucose 197-204 insulin Homo sapiens 14-21 9126663-11 1997 The analysis suggests that variations in insulin levels are a common metabolic basis for sex/age trends in fasting glucose, apolipoprotein B, total cholesterol, total cholesterol/HDL cholesterol ratio, LDL density (LDL cholesterol/apolipoprotein B), triglycerides and systolic blood pressure. Glucose 115-122 insulin Homo sapiens 41-48 9136630-5 1997 Diacylglycerol may mediate insulin"s stimulation of glucose transport over the plasma membrane. Glucose 52-59 insulin Homo sapiens 27-34 9235288-1 1997 The beta-cells of the pancreas control the blood levels of glucose and other nutrients by secreting insulin. Glucose 59-66 insulin Homo sapiens 100-107 9088667-6 1997 Insulin secretion was measured as the acute insulin response to glucose (AIRg). Glucose 64-71 insulin Homo sapiens 0-7 9088667-6 1997 Insulin secretion was measured as the acute insulin response to glucose (AIRg). Glucose 64-71 insulin Homo sapiens 44-51 9088667-17 1997 Impaired glucose tolerance resulting from insulin resistance in subjects with cirrhosis or diabetes mellitus is not affected by phlebotomy treatment. Glucose 9-16 insulin Homo sapiens 42-49 9176029-9 1997 Engineering glucose-stimulated insulin secretion in such cells has proved extremely difficult and several genes may he required. Glucose 12-19 insulin Homo sapiens 31-38 9075792-2 1997 Insulin activates both glucose transport and glycogen synthase in skeletal muscle. Glucose 23-30 insulin Homo sapiens 0-7 9075793-6 1997 The fractional glucose requirements (relative to the total amount infused) increased more rapidly for the two analogs than for insulin, with 50% of the glucose infused by 105 min for both analogs vs. 145 min for insulin. Glucose 15-22 insulin Homo sapiens 127-134 9075793-6 1997 The fractional glucose requirements (relative to the total amount infused) increased more rapidly for the two analogs than for insulin, with 50% of the glucose infused by 105 min for both analogs vs. 145 min for insulin. Glucose 152-159 insulin Homo sapiens 127-134 9075793-7 1997 The total amount of glucose required was, however, significantly less (19.7 +/- 1.5 mmol/kg) for AspB10LysB28ProB29-human insulin than for either LysB28ProB29-human insulin (25.9 +/- 3.0 mmol/kg) or human insulin (27.8 +/- 2.6 mmol/kg). Glucose 20-27 insulin Homo sapiens 122-129 9075793-7 1997 The total amount of glucose required was, however, significantly less (19.7 +/- 1.5 mmol/kg) for AspB10LysB28ProB29-human insulin than for either LysB28ProB29-human insulin (25.9 +/- 3.0 mmol/kg) or human insulin (27.8 +/- 2.6 mmol/kg). Glucose 20-27 insulin Homo sapiens 165-172 9075793-7 1997 The total amount of glucose required was, however, significantly less (19.7 +/- 1.5 mmol/kg) for AspB10LysB28ProB29-human insulin than for either LysB28ProB29-human insulin (25.9 +/- 3.0 mmol/kg) or human insulin (27.8 +/- 2.6 mmol/kg). Glucose 20-27 insulin Homo sapiens 165-172 9075793-8 1997 The glucose requirements were reflected in a lower MCR for AspB10LysB28ProB29-human insulin but equivalent decreases in the rates of glucose production. Glucose 4-11 insulin Homo sapiens 84-91 9075812-1 1997 The sulfonylurea receptor (SUR) is a key component in glucose-stimulated insulin secretion. Glucose 54-61 insulin Homo sapiens 73-80 9096992-5 1997 Insulin resistance was assessed by computing glucose disappearance rate from plasma after intravenous insulin injection (Kitt). Glucose 45-52 insulin Homo sapiens 0-7 9112018-2 1997 Site-directed mutagenesis as well as analyses of the patient"s lymphocytes revealed that this mutation causes a marked decrease in tyrosine kinase activity of the insulin receptor without any defect in insulin binding, which causes severe defects in insulin-stimulated glucose transport, glycogen synthesis and DNA synthesis. Glucose 269-276 insulin Homo sapiens 163-170 9112019-10 1997 A negative correlation was demonstrated between the magnitude of insulin-dependent glucose uptake by the fibroblasts and plasma insulin levels in vivo. Glucose 83-90 insulin Homo sapiens 65-72 9112019-10 1997 A negative correlation was demonstrated between the magnitude of insulin-dependent glucose uptake by the fibroblasts and plasma insulin levels in vivo. Glucose 83-90 insulin Homo sapiens 128-135 9187410-6 1997 PAI-1, FVII and fibrinogen levels were significantly correlated with the degree of insulin resistance estimated by the steady state plasma glucose concentration (SSPG) during the continuous infusion of glucose, insulin and octreotide. Glucose 139-146 insulin Homo sapiens 83-90 9177378-6 1997 Furthermore, a blunting of Mg(i) responses to insulin could be reproduced in normal cells that were magnesium depleted by prior treatment either with A23187 in a calcium-free medium or with high glucose concentrations (15 mmol/L). Glucose 195-202 insulin Homo sapiens 46-53 9137903-0 1997 Effect of metformin on insulin-stimulated tyrosine kinase activity of erythrocytes from obese women with normal glucose tolerance. Glucose 112-119 insulin Homo sapiens 23-30 9187410-6 1997 PAI-1, FVII and fibrinogen levels were significantly correlated with the degree of insulin resistance estimated by the steady state plasma glucose concentration (SSPG) during the continuous infusion of glucose, insulin and octreotide. Glucose 202-209 insulin Homo sapiens 83-90 9075721-8 1997 In adipocytes of nontransgenic diabetic mice, GLUT4 protein was reduced 34%, with a 46% reduction in insulin stimulated glucose transport. Glucose 120-127 insulin Homo sapiens 101-108 9075721-9 1997 In contrast, in adipocytes of transgenic diabetic mice, GLUT4 remained 21-fold overexpressed, resulting in 21-fold increased basal and 10-fold increased insulin stimulated glucose transport. Glucose 172-179 insulin Homo sapiens 153-160 9075721-12 1997 Overexpression of GLUT4 in adipocytes prevents insulin resistant glucose transport at the cellular level and improves insulin action in vivo, even with overt diabetes. Glucose 65-72 insulin Homo sapiens 47-54 9150702-3 1997 We investigated the correlation between the 17-OHP response to buserelin testing and the insulin response to oral glucose in PCOS. Glucose 114-121 insulin Homo sapiens 89-96 9150702-7 1997 The PCOS patients showed significantly higher mean post-glucose load insulin and C-peptide levels than controls (P < 0.05). Glucose 56-63 insulin Homo sapiens 69-76 9112973-5 1997 However, insulin enhanced the low glucose-induced decrease in rod-driven b-wave amplitude (P < 0.05 at 2 mM; P < 0.01 at 1 mM) without affecting the corresponding changes in the optic nerve response. Glucose 34-41 insulin Homo sapiens 9-16 9093185-10 1997 Insulin tolerance testing demonstrated a slower glucose disappearance in the polycystic appearing ovary group (Kitt glucose was 4.58% +/- 1.4%/min in the normal-appearing ovaries group versus 2.07% +/- 1.07%/min in the polycystic-appearing ovaries group). Glucose 48-55 insulin Homo sapiens 0-7 9093185-10 1997 Insulin tolerance testing demonstrated a slower glucose disappearance in the polycystic appearing ovary group (Kitt glucose was 4.58% +/- 1.4%/min in the normal-appearing ovaries group versus 2.07% +/- 1.07%/min in the polycystic-appearing ovaries group). Glucose 116-123 insulin Homo sapiens 0-7 9126490-1 1997 The rate-limiting enzyme in insulin-mediated nonoxidative glucose disposal, glycogen synthase, has reduced activity in insulin-resistant subjects at risk for developing non-insulin-dependent diabetes mellitus (NIDDM). Glucose 58-65 insulin Homo sapiens 28-35 9126490-1 1997 The rate-limiting enzyme in insulin-mediated nonoxidative glucose disposal, glycogen synthase, has reduced activity in insulin-resistant subjects at risk for developing non-insulin-dependent diabetes mellitus (NIDDM). Glucose 58-65 insulin Homo sapiens 119-126 9112973-9 1997 The differential responsiveness to insulin under low glucose of the b-wave versus the optic nerve response is thought to reflect suppression of glucose use by Muller (glial) cells rather than neuromodulation, as the neuronal optic nerve response is unaffected. Glucose 53-60 insulin Homo sapiens 35-42 9112973-9 1997 The differential responsiveness to insulin under low glucose of the b-wave versus the optic nerve response is thought to reflect suppression of glucose use by Muller (glial) cells rather than neuromodulation, as the neuronal optic nerve response is unaffected. Glucose 144-151 insulin Homo sapiens 35-42 9112973-11 1997 The electrophysiological effect of insulin under low glucose suggests its passage across the blood-retina barrier. Glucose 53-60 insulin Homo sapiens 35-42 9109844-1 1997 Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. Glucose 17-24 insulin Homo sapiens 0-7 9100595-1 1997 Persistent hyperinsulinemic hypoglycemia of infancy (PHHI), a rare disorder due to defective negative feedback regulation of insulin secretion by low glucose levels, is often familial. Glucose 150-157 insulin Homo sapiens 16-23 9083290-5 1997 Insulin-stimulated glucose oxidation (2.36 +/- 0.29 vs. 3.37 +/- 0.35 mg x kg(-1) x min(-1); P < 0.05 at first clamp step) and nonoxidative disposal (P < 0.05 at both clamp steps) increased after LPD. Glucose 19-26 insulin Homo sapiens 0-7 9221612-2 1997 The insulin response after oral doses of glucose is substantially stronger than after intravenous doses of sugar, even when identical glucose plasma levels are attained. Glucose 41-48 insulin Homo sapiens 4-11 9221612-2 1997 The insulin response after oral doses of glucose is substantially stronger than after intravenous doses of sugar, even when identical glucose plasma levels are attained. Glucose 134-141 insulin Homo sapiens 4-11 9135131-2 1997 It is closed by glucose metabolism, which stimulates insulin secretion, and opened by the drug diazoxide, which inhibits insulin release. Glucose 16-23 insulin Homo sapiens 53-60 9065437-4 1997 Under these conditions, we show that the concentration of insulin required for 50% desensitization of glucose transport activity is 100 pM; maximal desensitization could be achieved with 1 nM. Glucose 102-109 insulin Homo sapiens 58-65 9134058-2 1997 At 3.3 mmol/l glucose level, the addition of 5.0 mumol/l glibenclamide or 5.0 mumol/l glibenclamide plus 200 mumol/l metformin caused a significant increase of insulin release, compared with glucose alone. Glucose 14-21 insulin Homo sapiens 160-167 9054426-2 1997 However, insulin treatment decreased glucose consumption of the mutant cells by 20% while increasing that of the L6(WT) by 30%. Glucose 37-44 insulin Homo sapiens 9-16 9054426-3 1997 In the L6(WT), insulin elicited a significant increase in glucose transport and GLUT1 and GLUT4 plasma membrane expression, while in the L6(1152), all of these functions were constitutively activated and not further stimulated by insulin. Glucose 58-65 insulin Homo sapiens 15-22 9054426-9 1997 We conclude that, in skeletal muscle, glucose storage and oxidation are differentially impaired by the expression of IR1152, suggesting that their regulation by insulin involves divergent signaling pathways. Glucose 38-45 insulin Homo sapiens 161-168 9134058-2 1997 At 3.3 mmol/l glucose level, the addition of 5.0 mumol/l glibenclamide or 5.0 mumol/l glibenclamide plus 200 mumol/l metformin caused a significant increase of insulin release, compared with glucose alone. Glucose 191-198 insulin Homo sapiens 160-167 9056694-5 1997 Intracellular magnesium concentration has also been shown to be effective on modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli, by stimulating Ca2+-dependent K+ channels. Glucose 121-128 insulin Homo sapiens 88-95 9056694-8 1997 By contrast, in NIDDM patients daily magnesium administration, restoring a more appropriate intracellular magnesium concentration, contributes to improve insulin-mediated glucose uptake. Glucose 171-178 insulin Homo sapiens 154-161 9056694-9 1997 Similarly, in HP patients magnesium administration may be useful in decreasing arterial blood pressure and improving insulin-mediated glucose uptake. Glucose 134-141 insulin Homo sapiens 117-124 9056694-11 1997 In conclusion, a growing body of studies suggest that intracellular magnesium may play a key role on modulating insulin-mediated glucose uptake and vascular tone. Glucose 129-136 insulin Homo sapiens 112-119 9091005-11 1997 Fasting insulin concentrations fell substantially (-41.6%, 95% CI -23.4 to -59.8) with falls also being seen in insulin responses to glucose. Glucose 133-140 insulin Homo sapiens 112-119 9124541-0 1997 Glucagon enhances the direct suppressive effect of insulin on hepatic glucose production in humans. Glucose 70-77 insulin Homo sapiens 51-58 9124541-1 1997 The present study examines the role of glucagon in modulating the hepatic and extrahepatic effects of insulin on hepatic glucose production (HGP). Glucose 121-128 insulin Homo sapiens 102-109 9032109-1 1997 Signals derived from the metabolism of glucose in pancreatic beta-cells lead to insulin secretion via the closure of ATP-sensitive K+ channels (KATP). Glucose 39-46 insulin Homo sapiens 80-87 9032098-2 1997 The present studies sought to determine whether the ability of glucose to regulate its own metabolism in the presence of basal insulin concentrations is impaired. Glucose 63-70 insulin Homo sapiens 127-134 9032098-10 1997 We conclude that the ability of glucose to regulate its own metabolism in the presence of basal insulin concentrations is abnormal in people with NIDDM. Glucose 32-39 insulin Homo sapiens 96-103 9051394-6 1997 S(t) and Sg were measured by insulin-modified, frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 78-85 insulin Homo sapiens 29-36 9051394-9 1997 The mean acute first-phase insulin release after intravenous glucose was blunted also in the IGT and type II diabetic groups when compared with the NGT group. Glucose 61-68 insulin Homo sapiens 27-34 9051394-12 1997 The glucose effectiveness at theoretical zero insulin concentration (GEZI) followed similar patterns as the Sg. Glucose 4-11 insulin Homo sapiens 46-53 9088772-0 1997 Homozygosity for a common polymorphism in the islet-specific promoter of the glucokinase gene is associated with a reduced early insulin response to oral glucose in pregnant women. Glucose 154-161 insulin Homo sapiens 129-136 9088772-1 1997 A commonly occurring sequence variant in the islet-specific promoter of the glucokinase gene (-30 G to A) has been variably reported to be associated with reduced insulin secretory responses to oral glucose. Glucose 199-206 insulin Homo sapiens 163-170 9088772-8 1997 Under the conditions of increased secretory demand represented by late pregnancy, a promoter variant in the glucokinase gene may influence the early insulin secretory response to oral glucose. Glucose 184-191 insulin Homo sapiens 149-156 9088776-2 1997 Insulin dose was reduced by 20% on arrival at camp, and adjusted daily to maintain preprandial capillary glucose between 4 and 11 mmol l-1 and overnight glucose above 7 mmol l-1. Glucose 105-112 insulin Homo sapiens 0-7 9088776-2 1997 Insulin dose was reduced by 20% on arrival at camp, and adjusted daily to maintain preprandial capillary glucose between 4 and 11 mmol l-1 and overnight glucose above 7 mmol l-1. Glucose 153-160 insulin Homo sapiens 0-7 9105783-2 1997 In this review we summarise the data which unequivocally indicate that insulin response to glucose is grossly deficient in patients with impaired glucose tolerance and NIDDM. Glucose 91-98 insulin Homo sapiens 71-78 9179468-8 1997 This points towards the fluctuations in blood glucose levels experienced by IDDM patients in a setting where insulin supply is unreliable. Glucose 46-53 insulin Homo sapiens 109-116 10684071-2 1997 The beta-cell 1st phase insulin response was measured by intravenous glucose tolerance test and the 2nd phase insulin response was measured by oral glucose tolerance test. Glucose 69-76 insulin Homo sapiens 24-31 9062507-7 1997 Peak postprandial glucose was increased in the Regular insulin group compared to that in all groups that incorporated Lispro insulin (P < 0.001). Glucose 18-25 insulin Homo sapiens 55-62 9062507-13 1997 This study demonstrates that the reductions in plasma glucose effected by Lispro insulin are consistent and stable for 8 h after meal ingestion when Lispro insulin is used in combination with human Ultralente insulin. Glucose 54-61 insulin Homo sapiens 81-88 9062507-13 1997 This study demonstrates that the reductions in plasma glucose effected by Lispro insulin are consistent and stable for 8 h after meal ingestion when Lispro insulin is used in combination with human Ultralente insulin. Glucose 54-61 insulin Homo sapiens 156-163 9062507-13 1997 This study demonstrates that the reductions in plasma glucose effected by Lispro insulin are consistent and stable for 8 h after meal ingestion when Lispro insulin is used in combination with human Ultralente insulin. Glucose 54-61 insulin Homo sapiens 156-163 9087870-4 1997 Diabetes was defined as glucose intolerance requiring long-term insulin treatment more than 30 days after transplantation. Glucose 24-31 insulin Homo sapiens 64-71 9148220-4 1997 Insulinomas synthesize and secrete insulin autonomously in the presence of low blood glucose levels, causing spontaneous hypoglycemia and characteristic clinical symptoms. Glucose 85-92 insulin Homo sapiens 35-42 9112243-6 1997 Compared to the anterior compartment mass, the posterior compartment mass displayed stronger relationship with insulin-mediated glucose disposal (Rd) (r = -0.44, p = 0.009, and r = -0.76, p = 0.0001, respectively) as well as with residual hepatic glucose output during the 40 mU.m-2.min-1 insulin infusion (r = 0.39, p = 0.02, and r = 0.53, p = 0.001, respectively). Glucose 128-135 insulin Homo sapiens 111-118 9112243-6 1997 Compared to the anterior compartment mass, the posterior compartment mass displayed stronger relationship with insulin-mediated glucose disposal (Rd) (r = -0.44, p = 0.009, and r = -0.76, p = 0.0001, respectively) as well as with residual hepatic glucose output during the 40 mU.m-2.min-1 insulin infusion (r = 0.39, p = 0.02, and r = 0.53, p = 0.001, respectively). Glucose 247-254 insulin Homo sapiens 111-118 9078532-0 1997 Intracellular pathways of insulin-mediated glucose uptake before and after puberty in conscious rats. Glucose 43-50 insulin Homo sapiens 26-33 9078532-4 1997 Insulin stimulated (by insulin clamp 18 mU/kg/min) glucose uptake [rate of glucose disappearance (Rd)] was decreased by approximately 30% postpuberty (from 339 +/- 22 to 239 +/- 28 mumol/kg/min; p < 0.001). Glucose 51-58 insulin Homo sapiens 0-7 9078532-4 1997 Insulin stimulated (by insulin clamp 18 mU/kg/min) glucose uptake [rate of glucose disappearance (Rd)] was decreased by approximately 30% postpuberty (from 339 +/- 22 to 239 +/- 28 mumol/kg/min; p < 0.001). Glucose 51-58 insulin Homo sapiens 23-30 9078532-4 1997 Insulin stimulated (by insulin clamp 18 mU/kg/min) glucose uptake [rate of glucose disappearance (Rd)] was decreased by approximately 30% postpuberty (from 339 +/- 22 to 239 +/- 28 mumol/kg/min; p < 0.001). Glucose 75-82 insulin Homo sapiens 0-7 9078536-1 1997 Oral glucose induces a greater insulin response than i.v. Glucose 5-12 insulin Homo sapiens 31-38 9078536-9 1997 After oral glucose, both plasma insulin and C-peptide levels sharply increased by 45-55% above control values (p < 0.001), indicating a potentiation of insulin secretion rather than decreased hepatic extraction of insulin. Glucose 11-18 insulin Homo sapiens 32-39 9078536-9 1997 After oral glucose, both plasma insulin and C-peptide levels sharply increased by 45-55% above control values (p < 0.001), indicating a potentiation of insulin secretion rather than decreased hepatic extraction of insulin. Glucose 11-18 insulin Homo sapiens 44-53 9078536-9 1997 After oral glucose, both plasma insulin and C-peptide levels sharply increased by 45-55% above control values (p < 0.001), indicating a potentiation of insulin secretion rather than decreased hepatic extraction of insulin. Glucose 11-18 insulin Homo sapiens 155-162 9078536-9 1997 After oral glucose, both plasma insulin and C-peptide levels sharply increased by 45-55% above control values (p < 0.001), indicating a potentiation of insulin secretion rather than decreased hepatic extraction of insulin. Glucose 11-18 insulin Homo sapiens 155-162 9078536-12 1997 We conclude that the GIP response to a modest oral glucose load may play an important physiologic role in glucose-stimulated insulin secretion in healthy young subjects. Glucose 51-58 insulin Homo sapiens 125-132 9078536-12 1997 We conclude that the GIP response to a modest oral glucose load may play an important physiologic role in glucose-stimulated insulin secretion in healthy young subjects. Glucose 106-113 insulin Homo sapiens 125-132 9069587-11 1997 In summary, the NIDDM patients treated with insulin had more nephropathy, retinopathy, and neuropathy than did NIDDM patients treated with OHA, independent of duration of diabetes, fasting blood glucose, glycosylated hemoglobin, age, and blood pressure level. Glucose 195-202 insulin Homo sapiens 44-51 9032110-0 1997 Amino acid polymorphisms in the ATP-regulatable inward rectifier Kir6.2 and their relationships to glucose- and tolbutamide-induced insulin secretion, the insulin sensitivity index, and NIDDM. Glucose 99-106 insulin Homo sapiens 132-139 9032113-6 1997 The present findings couple both reduced insulin-stimulated IRS-1 tyrosine phosphorylation and PI 3-kinase activity to the impaired insulin-stimulated glucose transport in skeletal muscle from lean-to-moderately obese NIDDM subjects. Glucose 151-158 insulin Homo sapiens 41-48 10374307-8 1997 Patients with LADA should take diet, exercises, especially insulin as early as possible in order to control fasting and post prandial plasma glucose, and prevent from further destroy of residue islet B cells and reduce diabetic complications of eye, kidney and nerve. Glucose 141-148 insulin Homo sapiens 59-66 10374310-4 1997 The insulin-sensitivity index determined by the reverse of fasting plasma glucose and insulin product. Glucose 74-81 insulin Homo sapiens 4-11 9032113-6 1997 The present findings couple both reduced insulin-stimulated IRS-1 tyrosine phosphorylation and PI 3-kinase activity to the impaired insulin-stimulated glucose transport in skeletal muscle from lean-to-moderately obese NIDDM subjects. Glucose 151-158 insulin Homo sapiens 132-139 9045872-13 1997 LTx-26 had normal basal and insulin-modulated endogenous glucose production. Glucose 57-64 insulin Homo sapiens 28-35 9030547-0 1997 The tissue concentration of UDP-N-acetylglucosamine modulates the stimulatory effect of insulin on skeletal muscle glucose uptake. Glucose 115-122 insulin Homo sapiens 88-95 9030547-7 1997 The decrease in insulin action on peripheral glucose uptake was highly correlated with the increase in skeletal muscle UDP-GlcNAc levels. Glucose 45-52 insulin Homo sapiens 16-23 9078265-6 1997 SNP stimulated the insulin-stimulated rates of net and [14C]lactate release and glucose oxidation in a concentration-dependent manner. Glucose 80-87 insulin Homo sapiens 19-26 9078265-22 1997 The results suggest that in rat skeletal muscle: (a) nitric oxide (from SNP or spermine NONOate) increases the rate of glucose transport and metabolism, an effect independent of insulin; (b) SNP inhibits insulin-mediated rates of glycogen synthesis; (c) SNP stimulates cGMP formation, which mediates, at least partly, the effects on glucose metabolism; (d) nitric oxide-mediated stimulation of glucose utilization might occur in fibre contraction. Glucose 333-340 insulin Homo sapiens 204-211 9078265-22 1997 The results suggest that in rat skeletal muscle: (a) nitric oxide (from SNP or spermine NONOate) increases the rate of glucose transport and metabolism, an effect independent of insulin; (b) SNP inhibits insulin-mediated rates of glycogen synthesis; (c) SNP stimulates cGMP formation, which mediates, at least partly, the effects on glucose metabolism; (d) nitric oxide-mediated stimulation of glucose utilization might occur in fibre contraction. Glucose 333-340 insulin Homo sapiens 204-211 9045872-14 1997 In conclusion, LTx have impaired insulin-stimulated glucose, FFA, and protein metabolism 5 mo after surgery. Glucose 52-59 insulin Homo sapiens 33-40 9124326-8 1997 In conclusion, this experimental and statistical model demonstrates that the stimulated insulin secretion of glucose-tolerant relatives of NIDDM patients is characterized by disorderliness. Glucose 109-116 insulin Homo sapiens 88-95 9124342-0 1997 Roles of PI 3-kinase and Ras on insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 51-58 insulin Homo sapiens 32-39 9059765-0 1997 Insulin responses to intravenous glucose, intravenous arginine and a hyperglycaemic clamp in ICA-positive subjects with different degrees of glucose tolerance. Glucose 33-40 insulin Homo sapiens 0-7 9124342-3 1997 N17Ras expression did not affect glucose transport activity, whereas delta p85alpha expression inhibited insulin-stimulated glucose transport with impairment of GLUT-4 translocation, although inhibition of glucose transport activity was less remarkable than that of PI 3-kinase activity in delta p85alpha-expressing cells. Glucose 124-131 insulin Homo sapiens 105-112 9124342-3 1997 N17Ras expression did not affect glucose transport activity, whereas delta p85alpha expression inhibited insulin-stimulated glucose transport with impairment of GLUT-4 translocation, although inhibition of glucose transport activity was less remarkable than that of PI 3-kinase activity in delta p85alpha-expressing cells. Glucose 124-131 insulin Homo sapiens 105-112 9124342-5 1997 However, a discrepancy was observed between PI 3-kinase activity and glucose transport activity, suggesting a possibility that a different pathway(s) is involved in insulin-stimulated intrinsic activity of glucose transporters. Glucose 69-76 insulin Homo sapiens 165-172 9000704-6 1997 Throughout the study, the postprandial rise in serum glucose was significantly lower during insulin lispro therapy. Glucose 53-60 insulin Homo sapiens 92-99 9000704-7 1997 At the endpoint, the postprandial rise in serum glucose was reduced at 1 h by 1.3 mmol/l and at 2 h by 2.0 mmol/l in patients treated with insulin lispro (P < 0.001). Glucose 48-55 insulin Homo sapiens 139-146 9118772-7 1997 The glucose, insulin, and C-peptide responses after a glucose load were significantly reduced at 6 and 12 weeks in the troglitazone treatment group. Glucose 54-61 insulin Homo sapiens 26-35 9059765-0 1997 Insulin responses to intravenous glucose, intravenous arginine and a hyperglycaemic clamp in ICA-positive subjects with different degrees of glucose tolerance. Glucose 141-148 insulin Homo sapiens 0-7 9059765-4 1997 Acute insulin response to IVGTT and insulin and C-peptide responses to the hyperglycaemic clamp and the arginine bolus were dramatically lower (p < 0.001) in diabetic and IGT subjects than in ICA-positive patients with normal glucose tolerance and control subjects. Glucose 229-236 insulin Homo sapiens 6-13 9127707-2 1997 Syndrome X refers to a cluster of abnormalities, associated with resistance to insulin-mediated glucose uptake that increase risk of coronary heart disease. Glucose 96-103 insulin Homo sapiens 79-86 9059765-5 1997 Insulin responses to the three tests were inversely correlated with plasma glucose levels and the area under the curve of OGTT. Glucose 75-82 insulin Homo sapiens 0-7 9059765-6 1997 The correlations between the degree of glucose tolerance and insulin responses to IVGTT, the hyperglycaemic clamp and the arginine bolus were virtually identical. Glucose 39-46 insulin Homo sapiens 61-68 9059765-7 1997 It is concluded that insulin responses to the three stimuli were severely altered in ICA-positive patients with impaired glucose tolerance or asymptomatic diabetes, normal in normotolerant ICA-positive subjects, and correlated with glucose tolerance. Glucose 121-128 insulin Homo sapiens 21-28 9116912-5 1997 Insulin-stimulated glucose uptake (M) was decreased in the relatives compared with the control subjects (4.58 +/- 0.27 versus 6.06 +/- 0.25 mg/kg per min, P < 0.001). Glucose 19-26 insulin Homo sapiens 0-7 9043962-2 1997 RESEARCH DESIGN AND METHODS: In a randomized, double-blind, placebo-controlled trial, insulin-mediated glucose disposal was measured in 12 obese patients with NIDDM on diet alone before and after four weeks of treatment with either placebo (n = 6) or fluoxetine (n = 6) at a dose level of 60 mg once a day. Glucose 103-110 insulin Homo sapiens 86-93 9147065-1 1997 Insulin stimulation of glucose transport in skeletal muscle is considered to involve translocation of the skeletal muscle/adipose tissue glucose transporter isoform, Glut 4, from cytosolic vesicles to the cell surface. Glucose 23-30 insulin Homo sapiens 0-7 9043962-3 1997 Insulin-mediated glucose disposal was assessed by the 2-step euglycemic hyperinsulinemic clamp technique. Glucose 17-24 insulin Homo sapiens 0-7 9043962-15 1997 CONCLUSION: Fluoxetine improves insulin-mediated glucose disposal in obese patients with NIDDM independently of weight loss. Glucose 49-56 insulin Homo sapiens 32-39 9022089-1 1997 Chronic exposure of HIT-T15 cells to supraphysiologic glucose concentration diminishes insulin gene expression and decreased binding of two critical insulin gene transcription factors, STF-1 and RIPE-3b1 activator. Glucose 54-61 insulin Homo sapiens 149-156 9024248-5 1997 The insulin secretory response to glucose, administered in both graded and oscillatory fashions, was likewise unaltered in response to metformin. Glucose 34-41 insulin Homo sapiens 4-11 9024239-4 1997 GLP-1 (1.5 pmol/kg per min iv) increased serum insulin levels at fasting glucose (P = 0.028), at 14 mmol/L glucose (P = 0.028), and at 28 mmol/L glucose (P = 0.028). Glucose 73-80 insulin Homo sapiens 47-54 9024239-5 1997 The acute insulin response (AIR) to 5 g iv arginine was increased by GLP-1 at 14 mmol/L glucose (P = 0.028), and the slopeAIR, i.e., the glucose potentiation of insulin secretion, was markedly increased by GLP-1 (P = 0.028). Glucose 88-95 insulin Homo sapiens 10-17 9030818-6 1997 The acute insulin response to IV glucose was reduced in normal-weight and underweight cancer patients by approximately 40% to 50% (P < .05). Glucose 33-40 insulin Homo sapiens 10-17 9030830-0 1997 Influence of moderate physical exercise on insulin-mediated and non-insulin-mediated glucose uptake in healthy subjects. Glucose 85-92 insulin Homo sapiens 68-75 9030830-4 1997 Insulin sensitivity (S(I)), glucose effectiveness at basal insulin (S(G)), insulin action [X(t)], and first-phase (phi1) and second-phase (phi2) beta-cell responsiveness to glucose were estimated using both minimal models of glucose disposal (MMg) and insulin kinetics (MMi). Glucose 28-35 insulin Homo sapiens 59-66 9030830-8 1997 Despite a significant decrease in the insulin response to glucose (AUC0-90, 21,000 +/- 2,008 v 14,340 +/- 2,596 pmol x L(-1) x min, P < .01), insulin action [X(t)] was significantly higher during the FSIGTe. Glucose 58-65 insulin Homo sapiens 38-45 9030830-8 1997 Despite a significant decrease in the insulin response to glucose (AUC0-90, 21,000 +/- 2,008 v 14,340 +/- 2,596 pmol x L(-1) x min, P < .01), insulin action [X(t)] was significantly higher during the FSIGTe. Glucose 58-65 insulin Homo sapiens 145-152 9030830-10 1997 During exercise, the insulin response to glucose was lower than at rest, but beta-cell responsiveness to glucose did not change. Glucose 41-48 insulin Homo sapiens 21-28 9106794-0 1997 Dietary regulation of glucose transport in animal models of insulin resistance. Glucose 22-29 insulin Homo sapiens 60-67 9046927-0 1997 Benefits of lispro insulin: control of postprandial glucose levels is within reach. Glucose 52-59 insulin Homo sapiens 19-26 9046928-1 1997 Insulin therapy can control glucose levels in patients with type II diabetes. Glucose 28-35 insulin Homo sapiens 0-7 9046928-5 1997 On the other hand, beta-cell failure is progressive, and with long duration of diabetes, permanent insulin therapy may be necessary to achieve satisfactory glucose control. Glucose 156-163 insulin Homo sapiens 99-106 9061763-1 1997 Associations between elevated amniotic fluid glucose and insulin levels in the second trimester and the subsequent development of gestational diabetes have been reported. Glucose 45-52 insulin Homo sapiens 57-64 9123511-0 1997 Impaired glucose tolerance in recipients of an intraperitoneally implanted microencapsulated islet allograft is caused by the slow diffusion of insulin through the peritoneal membrane. Glucose 9-16 insulin Homo sapiens 144-151 9110380-5 1997 The magnitude of the insulin gene response to glucose was smaller (1.3-fold); none of the above-mentioned agents had significant effects on insulin mRNA content. Glucose 46-53 insulin Homo sapiens 21-28 9544261-0 1997 Trans-acting factor(s) confer glucose-responsive transcriptional regulation in the insulin gene. Glucose 30-37 insulin Homo sapiens 83-90 9002529-3 1997 We examined 85 African-Americans aged 25 to 33 years with measurement of blood pressure, an oral glucose tolerance test to measure insulin response to glucose challenge, and an insulin clamp for insulin sensitivity (M). Glucose 151-158 insulin Homo sapiens 131-138 9240931-5 1997 In adipose tissue, insulin increases the expression of lipogenic enzymes indirectly by stimulating glucose uptake. Glucose 99-106 insulin Homo sapiens 19-26 9240931-6 1997 In the liver, insulin also acts indirectly by stimulating the expression of glucokinase and, hence, by increasing glucose metabolism. Glucose 114-121 insulin Homo sapiens 14-21 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 130-137 insulin Homo sapiens 5-12 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 130-137 insulin Homo sapiens 85-92 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 130-137 insulin Homo sapiens 85-92 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 130-137 insulin Homo sapiens 85-92 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 180-187 insulin Homo sapiens 5-12 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 180-187 insulin Homo sapiens 85-92 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 180-187 insulin Homo sapiens 85-92 9240937-3 1997 This insulin-mediated increase in muscle perfusion accounts for approximately 30% of insulin"s overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Glucose 180-187 insulin Homo sapiens 85-92 9012639-9 1997 In summary, elevated plasma apoB and triglyceride concentrations associated with male gender and with glucose intolerance are partly accounted for by differences in the ability of insulin to suppress FFA concentrations. Glucose 102-109 insulin Homo sapiens 180-187 9116920-5 1997 MAIN METHODS: Insulin sensitivity index was determined by the modified frequent sampling intravenous glucose tolerance test (FSIGT) and blood pressure was determined by indirect ambulatory blood pressure monitoring. Glucose 101-108 insulin Homo sapiens 14-21 9101062-1 1997 This study was designed to further characterize the role of insulin and glucagon in the regulation of glucose production and gluconeogenesis during a 2-h mild intensity exercise (40% VO2max) in 14 h fasted healthy male subjects. Glucose 102-109 insulin Homo sapiens 60-67 9101062-14 1997 It is also suggested that the lower level of insulin during exercise still exerts a restraining effect on glucagon-stimulated glucose production and gluconeogenesis, thus preventing hyperglycemia. Glucose 126-133 insulin Homo sapiens 45-52 9101063-0 1997 Glucose metabolism during exercise in man: the role of insulin in the regulation of glucose utilization. Glucose 84-91 insulin Homo sapiens 55-62 9101063-1 1997 The present study was designed to characterize further the role of insulin in the regulation of glucose utilization during a 2-h exercise at 40% VO2max in 14 h fasted, healthy subjects. Glucose 96-103 insulin Homo sapiens 67-74 9101063-7 1997 When insulin was replaced without glucagon replacement, plasma glucose was maintained at 3.85 +/- 0.06 mmol/L by dextrose infusion and Rd increased significantly (p < 0.05) from the resting value to 25.9 +/- 0.7 mumol.kg-1.min-1. Glucose 63-70 insulin Homo sapiens 5-12 9101063-7 1997 When insulin was replaced without glucagon replacement, plasma glucose was maintained at 3.85 +/- 0.06 mmol/L by dextrose infusion and Rd increased significantly (p < 0.05) from the resting value to 25.9 +/- 0.7 mumol.kg-1.min-1. Glucose 113-121 insulin Homo sapiens 5-12 9101063-8 1997 When insulin was replaced together with glucagon, the plasma glucose (4.29 +/- 0.15 mmol/L) and the Rd (32.1 +/- 0.9 mumol.kg-1.min-1, p < 0.05 versus the resting value) obtained were similar to the values from the saline exercising control. Glucose 61-68 insulin Homo sapiens 5-12 9101063-13 1997 Insulin is necessary, however, for optimal glucose utilization during prolonged mild intensity exercise. Glucose 43-50 insulin Homo sapiens 0-7 9342471-1 1997 Twenty patients with polycystic ovarian syndrome and with or without insulin resistance, and 20 healthy women (controls) underwent an oral glucose tolerance test, which resulted in a short duration but significant increase of serum insulin levels. Glucose 139-146 insulin Homo sapiens 232-239 8971073-3 1997 Second, physiological elevations in plasma FFA concentrations inhibit insulin stimulated peripheral glucose uptake in a dose-dependent manner in normal controls and in patients with NIDDM. Glucose 100-107 insulin Homo sapiens 70-77 9028716-14 1997 Our results suggest that supplements of 1,25-dihydroxyvitamin D3 influence glucose metabolism in patients with GDM probably by increasing the insulin sensitivity. Glucose 75-82 insulin Homo sapiens 142-149 9069567-5 1997 The lowest GIR was associated with higher fasting plasma insulin, increased insulin response to glucose, higher plasma triglyceride and uric acid, and lower high-density-lipoprotein cholesterol, but not with increased creatinine clearance rate in normotensive subjects. Glucose 96-103 insulin Homo sapiens 76-83 9143861-8 1997 The metabolic clearance rate of glucose at the hyper-insulinemic clamp test (adjusted for the prevailing insulin and glucose concentrations) decreased by 17%. Glucose 32-39 insulin Homo sapiens 53-60 9143861-10 1997 glucose tolerance test the insulin area under the curve was increased by 18% and the glucose area by 10%. Glucose 0-7 insulin Homo sapiens 27-34 9143862-10 1997 Insulin-stimulated glucose uptake was reduced by 46% in the whole body, from 39 to 21 mumol.kg-1.min-1 and by 59% in the femoral muscles, from 99 to 41 mumol.kg-1.min-1, with celiprolol as compared to saline. Glucose 19-26 insulin Homo sapiens 0-7 9143863-1 1997 OBJECTIVE: To investigate a long-term colchicine treatment in inhibiting normal release of insulin, in response to a glucose load. Glucose 117-124 insulin Homo sapiens 91-98 9143863-4 1997 METHODS: A standard oral glucose tolerance test (OGTT) was performed to study the effect of long-term colchicine treatment on glucose-induced insulin response. Glucose 126-133 insulin Homo sapiens 142-149 9285204-1 1997 Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone in normal humans explaining in part the augmented insulin response after oral versus intravenous glucose administration. Glucose 165-172 insulin Homo sapiens 118-125 9285204-3 1997 Therefore, GLP-1, in many aspects, opposes the Type 2-diabetic phenotype characterized by disturbed glucose-induced insulin secretory capacity, hyperglucagonaemia, moderate insulin deficiency, accelerated gastric emptying, overeating (obesity) and insulin resistance. Glucose 100-107 insulin Homo sapiens 116-123 9444512-2 1997 Principally the insulin infusion algorithm was developed as a transfer function with the first-order delay in both proportional and derivative actions to blood glucose concentrations. Glucose 160-167 insulin Homo sapiens 16-23 9444512-4 1997 By applying this algorithm with regular insulin, diabetic patients showed a 2 h postprandial hyperglycemia and a delayed hyperinsulinemia, followed by hypoglycemic episodes 4-5 h after oral glucose load, just as observed in the computer simulation study. Glucose 190-197 insulin Homo sapiens 40-47 9181354-1 1997 The insulin resistance syndrome (IRS) is characterized by a combination of interrelated coronary heart disease (CHD) risk factors, including low high-density lipoprotein cholesterol (HDL-C) levels, obesity and increases in triglyceride (TG), blood pressure, small low-density lipoprotein particles (LDL), and both fasting and postload plasma insulin and glucose. Glucose 354-361 insulin Homo sapiens 4-11 9251924-6 1997 Incubation experiments revealed that a low glucose concentration (1 mmol/l) was sufficient to increase cytosolic free calcium and to produce a maximal glucose-induced insulin release. Glucose 43-50 insulin Homo sapiens 167-174 9251924-6 1997 Incubation experiments revealed that a low glucose concentration (1 mmol/l) was sufficient to increase cytosolic free calcium and to produce a maximal glucose-induced insulin release. Glucose 151-158 insulin Homo sapiens 167-174 9251924-8 1997 The abnormal distribution of glucose transporters probably relates to the abnormal glucose sensing of insulinoma cells, and explains their sustained insulin secretion at low glucose concentrations. Glucose 29-36 insulin Homo sapiens 102-109 9251924-8 1997 The abnormal distribution of glucose transporters probably relates to the abnormal glucose sensing of insulinoma cells, and explains their sustained insulin secretion at low glucose concentrations. Glucose 83-90 insulin Homo sapiens 102-109 9039089-8 1997 Hypertensive subjects were characterized by decreased insulin sensitivity (insulin-mediated glucose uptake: 5.14 +/- 0.28 versus 7.26 +/- 0.61 mg glucose/kg fat-free mass per minute, hypertensive versus normotensive, P = .002), increased insulin levels during the insulin infusions (804 +/- 36 versus 510 +/- 38 pmol/L, hypertensive versus normotensive, P < .001), and decreased insulin metabolic clearance rate (328 +/- 15 versus 521 +/- 30 mL/min per meter squared, hypertensive versus normotensive, P < .001). Glucose 92-99 insulin Homo sapiens 75-82 9039089-8 1997 Hypertensive subjects were characterized by decreased insulin sensitivity (insulin-mediated glucose uptake: 5.14 +/- 0.28 versus 7.26 +/- 0.61 mg glucose/kg fat-free mass per minute, hypertensive versus normotensive, P = .002), increased insulin levels during the insulin infusions (804 +/- 36 versus 510 +/- 38 pmol/L, hypertensive versus normotensive, P < .001), and decreased insulin metabolic clearance rate (328 +/- 15 versus 521 +/- 30 mL/min per meter squared, hypertensive versus normotensive, P < .001). Glucose 92-99 insulin Homo sapiens 75-82 9039089-8 1997 Hypertensive subjects were characterized by decreased insulin sensitivity (insulin-mediated glucose uptake: 5.14 +/- 0.28 versus 7.26 +/- 0.61 mg glucose/kg fat-free mass per minute, hypertensive versus normotensive, P = .002), increased insulin levels during the insulin infusions (804 +/- 36 versus 510 +/- 38 pmol/L, hypertensive versus normotensive, P < .001), and decreased insulin metabolic clearance rate (328 +/- 15 versus 521 +/- 30 mL/min per meter squared, hypertensive versus normotensive, P < .001). Glucose 92-99 insulin Homo sapiens 75-82 9161866-2 1997 The regulation of fetal IGF-I in utero is primarily influenced by placental glucose transfer, which regulates fetal insulin release. Glucose 76-83 insulin Homo sapiens 116-123 9029223-12 1997 We speculate that the magnitude of insulin surge after acutely increased Glc before exercise in GD subjects may exert dissociative effects on adrenal-dependent glycogenolysis and on sympathetic responses. Glucose 73-76 insulin Homo sapiens 35-42 9142889-7 1997 These results demonstrate that, in denervated muscles, there is a clear dissociation between insulin-stimulated 2-deoxyglucose uptake and upstream events involved in insulin-stimulated glucose uptake. Glucose 119-126 insulin Homo sapiens 93-100 9142893-1 1997 In the beta-cells of the pancreas, glucose phosphorylation carried out by glucokinase is the rate-controlling step in glycolysis, and the kinetic characteristics of glucokinase govern to a high degree the dose-response relationship between glucose and insulin release. Glucose 35-42 insulin Homo sapiens 252-259 9142893-1 1997 In the beta-cells of the pancreas, glucose phosphorylation carried out by glucokinase is the rate-controlling step in glycolysis, and the kinetic characteristics of glucokinase govern to a high degree the dose-response relationship between glucose and insulin release. Glucose 240-247 insulin Homo sapiens 252-259 9142893-2 1997 Because glucose-6-phosphatase (G-6-Pase) opposes the action of glucokinase, it may have a regulatory role in the release of insulin in response to glucose if the enzyme is present in the beta-cells. Glucose 8-15 insulin Homo sapiens 124-131 9489131-5 1997 After 6 months therapy the 22 patients with an impaired glucose tolerance test (IGTT) had a significant decrease in plasma glucose and insulin values, and a tendency for increased HDL. Glucose 56-63 insulin Homo sapiens 135-142 9038984-4 1997 Insulin was used to reduce plasma glucose levels, and an inhibitor of glucose utilization, 2-deoxy-D-glucose (2-DG), was used to cause intracellular glucopenia. Glucose 34-41 insulin Homo sapiens 0-7 9038984-5 1997 Insulin injections into the dorsal lymph sac caused significant reductions of both plasma glucose levels and body temperature. Glucose 90-97 insulin Homo sapiens 0-7 9542271-2 1997 The GDM group underwent a diet containing 25 kcal/kg/24 h and insulin was started when fasting and 2 h after meals glucose levels were respectively > 95 and > 125 mg/dl. Glucose 115-122 insulin Homo sapiens 62-69 9542271-7 1997 In conclusion, triglyceride and 180" glucose levels, AUC, pregestational BMI and diagnosis week are predictive factors for insulin treatment in gestational diabetes. Glucose 37-44 insulin Homo sapiens 123-130 9580366-1 1997 An insulin-modified frequently sampled intravenous glucose tolerance test with minimal model analysis was performed in normal pregnant women between 28-32 weeks of gestation, to assess insulin sensitivity and insulin secretion. Glucose 51-58 insulin Homo sapiens 3-10 10023151-0 1997 [The effect of polarizing mixture KIG (potassium + insulin + glucose) on some metabolites of glucose transformation in patients with ischemic stroke during the earliest period of illness]. Glucose 93-100 insulin Homo sapiens 51-58 9428581-10 1997 High levels of fasting and post-glucose load insulin in women and men respectively were associated with CL. Glucose 32-39 insulin Homo sapiens 45-52 9012639-0 1997 Differences in insulin suppression of free fatty acid levels by gender and glucose tolerance status. Glucose 75-82 insulin Homo sapiens 15-22 9012639-3 1997 Most discussions of relations of insulin resistance to coronary heart disease risk factors have focused on insulin-stimulated glucose uptake, but insulin suppression of plasma free fatty acid (FFA) levels is also important in lipid and lipoprotein metabolism. Glucose 126-133 insulin Homo sapiens 33-40 9012639-3 1997 Most discussions of relations of insulin resistance to coronary heart disease risk factors have focused on insulin-stimulated glucose uptake, but insulin suppression of plasma free fatty acid (FFA) levels is also important in lipid and lipoprotein metabolism. Glucose 126-133 insulin Homo sapiens 107-114 9012639-3 1997 Most discussions of relations of insulin resistance to coronary heart disease risk factors have focused on insulin-stimulated glucose uptake, but insulin suppression of plasma free fatty acid (FFA) levels is also important in lipid and lipoprotein metabolism. Glucose 126-133 insulin Homo sapiens 107-114 9495639-1 1997 Reduced peripheral sensitivity to insulin-stimulated glucose disposal, insulin resistance, is considered to be central in the metabolic cardiovascular syndrome. Glucose 53-60 insulin Homo sapiens 34-41 9495639-1 1997 Reduced peripheral sensitivity to insulin-stimulated glucose disposal, insulin resistance, is considered to be central in the metabolic cardiovascular syndrome. Glucose 53-60 insulin Homo sapiens 71-78 9059567-8 1997 RESULTS: Basal and L-arginine or glucose induced glucagon secretions and basal and glucose stimulated insulin secretions were not altered by L-NAME administration. Glucose 83-90 insulin Homo sapiens 102-109 9083709-7 1997 The postprandial rise in serum glucose was lower in patients receiving insulin lispro than in those receiving regular human insulin therapy. Glucose 31-38 insulin Homo sapiens 71-78 9083709-7 1997 The postprandial rise in serum glucose was lower in patients receiving insulin lispro than in those receiving regular human insulin therapy. Glucose 31-38 insulin Homo sapiens 124-131 9017356-4 1997 Onset of action, assessed as glucose infusion rate, after insulin inhalation was substantially more rapid than after subcutaneous injection and half-maximal action was reached earlier (31 +/- 17 vs 54 +/- 12 min; p < 0.001). Glucose 29-36 insulin Homo sapiens 58-65 9017356-6 1997 The maximal glucose infusion rate after inhalation of insulin was lower than after subcutaneous insulin injection (6.2 +/2- 2.4 vs 9.1 +/- 2.5 mg kg-1 min-1; p < 0.001). Glucose 12-19 insulin Homo sapiens 54-61 9028721-2 1997 Increased activity of the hexosamine pathway is a putative mediator of glucose-induced insulin resistance but the mechanisms are unclear. Glucose 71-78 insulin Homo sapiens 87-94 9052056-5 1997 More insulin, less food, and more exercise each were associated with low glucose levels. Glucose 73-80 insulin Homo sapiens 5-12 8977384-0 1997 In vivo insulin-dependent glucose uptake of specific tissues is decreased during aging of mature Wistar rats. Glucose 26-33 insulin Homo sapiens 8-15 8977384-3 1997 In the present work we studied the glucose metabolic index of a number of tissues known to be insulin sensitive in 3- and 24-month-old Wistar rats by measuring 2-deoxy-D-[1-3H]glucose uptake both under euglycemic-hyperinsulinemic conditions and in the basal state. Glucose 35-42 insulin Homo sapiens 94-101 8977384-5 1997 The maximal response of glucose uptake to insulin as well as insulin sensitivity in red and white quadriceps were unaltered in old rats. Glucose 24-31 insulin Homo sapiens 42-49 9041374-4 1997 Insulin sensitivity was evaluated by means of three different methods: diurnal plasma insulin and glucose levels; glucose consumption; and insulin sensitivity index during euglycaemic clamp conditions. Glucose 98-105 insulin Homo sapiens 0-7 9041374-4 1997 Insulin sensitivity was evaluated by means of three different methods: diurnal plasma insulin and glucose levels; glucose consumption; and insulin sensitivity index during euglycaemic clamp conditions. Glucose 114-121 insulin Homo sapiens 0-7 9041374-7 1997 Consequently, the insulin sensitivity index [glucose infusion rate (GIR)/ plasma insulin] was lower after metoprolol treatment (16.1 +/- 2.6 vs. 10.2 +/- 1.2, P < 0.05), although GIR was not significantly changed. Glucose 45-52 insulin Homo sapiens 18-25 9288547-3 1997 Insulin resistance would have minimised glucose utilisation by muscles thereby facilitating the preferential utilisation of glucose by the brain, foetus and mammary gland. Glucose 40-47 insulin Homo sapiens 0-7 9288547-3 1997 Insulin resistance would have minimised glucose utilisation by muscles thereby facilitating the preferential utilisation of glucose by the brain, foetus and mammary gland. Glucose 124-131 insulin Homo sapiens 0-7 8989269-3 1997 Frequently sampled intravenous glucose tolerance test allows the calculation of insulin sensitivity and peripheral glucose use independent of insulin. Glucose 31-38 insulin Homo sapiens 80-87 9075065-3 1997 We studied the effect of 150 mg orally administered pirenzepine (PNZ), a muscarinic receptor antagonist, on the insulin response to glucose (75 g p.o. Glucose 132-139 insulin Homo sapiens 112-119 9075065-8 1997 Calculated as AUC the insulin response to oral glucose load was unaffected by PNZ (6601.5 +/- 1218.6 vs 8614.3 +/- 1095.2 mU/L.min). Glucose 47-54 insulin Homo sapiens 22-29 9075065-9 1997 Actually, the insulin rises at +30 min after oral glucose load was significantly blunted by PNZ (37.0 +/- 3.4 vs 81.6 +/- 16.9 mU/L; p < 0.03). Glucose 50-57 insulin Homo sapiens 14-21 9008670-1 1997 BACKGROUND: This study was initiated to test the hypothesis that older, healthy, nondiabetic Mexican American women would be relatively resistant to insulin-mediated glucose disposal, hyperinsulinemic, and dyslipidemic as compared to a matched group of non-Hispanic White (NHW) women. Glucose 166-173 insulin Homo sapiens 149-156 9008670-5 1997 Resistance to insulin-mediated glucose disposal was estimated by the steady-state plasma glucose (SSPG) concentration achieved at the end of a 3-hour constant infusion of glucose, insulin, and somatostatin. Glucose 31-38 insulin Homo sapiens 14-21 9008670-6 1997 RESULTS: Mexican American women had significantly greater glucose (p < .001) and insulin (p < .001) responses to the oral glucose challenge than did the NHW women. Glucose 128-135 insulin Homo sapiens 84-91 9008670-7 1997 Resistance to insulin-mediated glucose disposal was increased in Mexican American women (SSPG 195 +/- 25 mg/dl compared to 137 +/- 18 mg/dl in NHW; p < .001). Glucose 31-38 insulin Homo sapiens 14-21 9050983-13 1997 The results obtained for glucose-stimulated insulin release opposed in part those for basal insulin release, since the preincubation with moxonidine up to 10 micromol/l gave rise to an increased insulin release. Glucose 25-32 insulin Homo sapiens 44-51 9050983-13 1997 The results obtained for glucose-stimulated insulin release opposed in part those for basal insulin release, since the preincubation with moxonidine up to 10 micromol/l gave rise to an increased insulin release. Glucose 25-32 insulin Homo sapiens 92-99 9050983-13 1997 The results obtained for glucose-stimulated insulin release opposed in part those for basal insulin release, since the preincubation with moxonidine up to 10 micromol/l gave rise to an increased insulin release. Glucose 25-32 insulin Homo sapiens 92-99 9050983-14 1997 An additional direct effect of moxonidine with a marked reduction of glucose-stimulated insulin release was observed, however, when moxonidine was present during the preincubation (24 h) and the functional test at a concentration of 1 nmol/l or 1 micromol/l. Glucose 69-76 insulin Homo sapiens 88-95 9111160-7 1997 The relationship between basal endothelin and insulin values was also found in each glucose tolerance group. Glucose 84-91 insulin Homo sapiens 46-53 9111160-8 1997 At 120 min after the glucose load, mean plasma values of endothelin were significantly higher (6.66 +/- 1.31 vs 4.17 +/- 0.61 pmol/L); moreover, the per cent increase of endothelin at 120 min was positively related to the per cent increase of insulin. Glucose 21-28 insulin Homo sapiens 243-250 9266410-2 1997 While cortisol and insulin have opposing effects on glucose metabolism, desensitization of the neuronal insulin receptor results in metabolic abnormalities. Glucose 52-59 insulin Homo sapiens 19-26 9266324-0 1997 Cell biology of insulin action on glucose transport. Glucose 34-41 insulin Homo sapiens 16-23 9266328-0 1997 Molecular mechanism of insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 42-49 insulin Homo sapiens 23-30 9275010-1 1997 Alpha-lipoic acid (ALA), a potent biological antioxidant, improves insulin action of skeletal muscle glucose transport and metabolism in both human and animal models of insulin resistance. Glucose 101-108 insulin Homo sapiens 67-74 9275010-2 1997 In order to obtain further insight into the potential intracellular mechanisms for the action of ALA on insulin-stimulated glucose transport in skeletal muscle, we investigated the effects of direct incubation with ALA (2 mM) on 2-deoxyglucose (2-DG) uptake by epitrochlearis muscle from either insulin-sensitive lean (Fa/-) or insulin-resistant obese (fa/fa) Zucker rats. Glucose 123-130 insulin Homo sapiens 104-111 9275010-7 1997 Collectively, these results indicate that although a portion of ALA action on glucose transport in mammalian skeletal muscle is mediated via the insulin signal transduction pathway, the majority of the direct effect of ALA on skeletal muscle glucose transport is insulin-independent. Glucose 242-249 insulin Homo sapiens 263-270 9005961-11 1997 After adjusting for age, insulin was lower and the glucose to insulin ratio was higher in postmenopause than in premenopause. Glucose 51-58 insulin Homo sapiens 62-69 9005961-14 1997 A significant positive correlation between the glucose to insulin ratio and SHBG was present in both groups. Glucose 47-54 insulin Homo sapiens 58-65 9005969-8 1997 Following the oral glucose load, the mean serum peak and incremental integrated areas of insulin were significantly (P < .05) greater in native Ghanaians, African-Americans, and Ghanaian immigrants compared with white Americans. Glucose 19-26 insulin Homo sapiens 89-96 9030822-4 1997 Basal and glucose-stimulated insulin levels were elevated in both the OGTT and IVGTT in both patients. Glucose 10-17 insulin Homo sapiens 29-36 9030822-5 1997 The response of plasma glucose to exogenously administered insulin was decreased. Glucose 23-30 insulin Homo sapiens 59-66 9030822-9 1997 Insulin binding to abdominal adipocytes was increased in one patient whose adipocytes displayed higher glucose transport at low insulin concentrations. Glucose 103-110 insulin Homo sapiens 0-7 8994189-10 1997 Similarly, insulin and epidermal growth factor activation of total (no immunoprecipitation) PI3-kinase activity in both cytosol and total cellular membranes and insulin stimulation of glucose transport were not affected by expression of dominant negative ras. Glucose 184-191 insulin Homo sapiens 161-168 9674263-5 1997 The Area Under the Curve of insulin during a standard glucose tolerance test showed an inverse relationship with fluoremia. Glucose 54-61 insulin Homo sapiens 28-35 8972199-5 1997 While insulin increased glucose transport 15-fold, coexpression of iSH2-p110 increased transport (5.2-) +/- 0.7-fold with a parallel increase in GLUT4 translocation to the plasma membrane. Glucose 24-31 insulin Homo sapiens 6-13 9201292-1 1997 Blood insulin level was measured in 113 breast cancer (BC) patients, 18 endometrial cancer (EC) patients, and 35 women with benign breast disease (BBD), after fasting and after 120 min of oral glucose tolerance test (OGTT). Glucose 193-200 insulin Homo sapiens 6-13 9437719-11 1997 Chronic changes in levels of glucose, insulin or other hormone or neuroendocrine agents are likely to underlie the altered rate of transport of insulin across the BBB of diabetic mice. Glucose 29-36 insulin Homo sapiens 144-151 9436233-0 1997 Specific problems facing gene therapy for insulin-dependent diabetes mellitus: glucose-regulated insulin secretion from hepatocytes. Glucose 79-86 insulin Homo sapiens 42-49 9230639-1 1997 The sympathetic nervous system can modulate glucose levels through a variety of mechanisms, including inhibition of insulin release by alpha2-adrenergic receptors. Glucose 44-51 insulin Homo sapiens 116-123 9418981-6 1997 Glucose or casein increased insulin concentrations and decreased GH concentrations, but did not affect gonadotrophins or testicular growth. Glucose 0-7 insulin Homo sapiens 28-35 9238859-3 1997 Resistance to insulin"s effects on carbohydrate metabolism include diminished actions of insulin to enhance glucose uptake and suppress endogenous glucose production. Glucose 108-115 insulin Homo sapiens 14-21 9238859-3 1997 Resistance to insulin"s effects on carbohydrate metabolism include diminished actions of insulin to enhance glucose uptake and suppress endogenous glucose production. Glucose 108-115 insulin Homo sapiens 89-96 9238859-3 1997 Resistance to insulin"s effects on carbohydrate metabolism include diminished actions of insulin to enhance glucose uptake and suppress endogenous glucose production. Glucose 147-154 insulin Homo sapiens 14-21 9238859-3 1997 Resistance to insulin"s effects on carbohydrate metabolism include diminished actions of insulin to enhance glucose uptake and suppress endogenous glucose production. Glucose 147-154 insulin Homo sapiens 89-96 9238859-4 1997 This chapter introduces new concepts related to the mechanism by which insulin stimulates glucose utilization in vivo and demonstrates that these processes are mechanistically linked to glucose production. Glucose 90-97 insulin Homo sapiens 71-78 9238859-4 1997 This chapter introduces new concepts related to the mechanism by which insulin stimulates glucose utilization in vivo and demonstrates that these processes are mechanistically linked to glucose production. Glucose 186-193 insulin Homo sapiens 71-78 9238859-5 1997 Insulin acts rapidly in vitro to stimulate glucose uptake; in contrast, its effects in vivo are relatively slow in the conscious animal or human subject. Glucose 43-50 insulin Homo sapiens 0-7 9238859-10 1997 Transendothelial transport alters the in vivo patterns of insulin signaling-biphasic plasma insulin after glucose injection is reflected in a simple, rapid increase in interstitial insulin to an elevated concentration. Glucose 106-113 insulin Homo sapiens 58-65 9238859-10 1997 Transendothelial transport alters the in vivo patterns of insulin signaling-biphasic plasma insulin after glucose injection is reflected in a simple, rapid increase in interstitial insulin to an elevated concentration. Glucose 106-113 insulin Homo sapiens 92-99 9238859-11 1997 The time course of insulin"s effect to suppress endogenous glucose output is a mirror image of its effect to enhance glucose uptake; however, there is no transendothelial barrier to insulin action at the liver. Glucose 59-66 insulin Homo sapiens 19-26 9238859-11 1997 The time course of insulin"s effect to suppress endogenous glucose output is a mirror image of its effect to enhance glucose uptake; however, there is no transendothelial barrier to insulin action at the liver. Glucose 117-124 insulin Homo sapiens 19-26 9238859-12 1997 The similarity in action dynamics at periphery and liver was explained by a mechanism in which insulin crosses into peripheral tissue and alters a "second (blood-borne) signal" that, in turn, suppresses liver glucose production. Glucose 209-216 insulin Homo sapiens 95-102 9238859-14 1997 We have proposed the "single gateway hypothesis" to explain insulin"s action on carbohydrate metabolism in vivo: insulin crosses the endothelial boundary in skeletal muscle (to stimulate glucose disposal) and traverses the endothelial barrier in adipose tissue to suppress lipolysis. Glucose 187-194 insulin Homo sapiens 60-67 9238859-14 1997 We have proposed the "single gateway hypothesis" to explain insulin"s action on carbohydrate metabolism in vivo: insulin crosses the endothelial boundary in skeletal muscle (to stimulate glucose disposal) and traverses the endothelial barrier in adipose tissue to suppress lipolysis. Glucose 187-194 insulin Homo sapiens 113-120 9238859-15 1997 The declining free fatty acids are proposed to be a major factor in the insulin-mediated decline in glucose output. Glucose 100-107 insulin Homo sapiens 72-79 9238859-18 1997 These results raise the question of whether hepatic insulin resistance in Type 2 diabetes can be explained by insulin resistance at the adipocyte, which causes a failure of reduction of FFA by insulin, leading to overproduction of glucose by the liver. Glucose 231-238 insulin Homo sapiens 52-59 9238859-18 1997 These results raise the question of whether hepatic insulin resistance in Type 2 diabetes can be explained by insulin resistance at the adipocyte, which causes a failure of reduction of FFA by insulin, leading to overproduction of glucose by the liver. Glucose 231-238 insulin Homo sapiens 110-117 9281236-5 1997 A new short-acting insulin-analogue (Lispro) shows a reduced effect on blood glucose levels after 3 h as compared to regular insulin. Glucose 77-84 insulin Homo sapiens 19-26 8986763-1 1996 The beta cell-specific glucose-sensitive factor (GSF), which binds the A3 motif of the rat I and human insulin promoters, is modulated by extracellular glucose. Glucose 23-30 insulin Homo sapiens 103-110 9281232-4 1997 Intensified insulin replacement derives its strategy from knowledge about physiological insulin release and requires the patient, and this applies in particular to "Functional Insulin Therapy (FIT)", to measure his blood glucose frequently and to correct aberrant blood glucose values by additional insulin or glucose as necessary. Glucose 221-228 insulin Homo sapiens 12-19 9281232-4 1997 Intensified insulin replacement derives its strategy from knowledge about physiological insulin release and requires the patient, and this applies in particular to "Functional Insulin Therapy (FIT)", to measure his blood glucose frequently and to correct aberrant blood glucose values by additional insulin or glucose as necessary. Glucose 221-228 insulin Homo sapiens 176-183 8986763-2 1996 A single mutation in the GSF binding site of the human insulin promoter abolishes the stimulation by high glucose only in normal islets, supporting the suggested physiological role of GSF in the glucose-regulated expression of the insulin gene. Glucose 106-113 insulin Homo sapiens 55-62 8986763-2 1996 A single mutation in the GSF binding site of the human insulin promoter abolishes the stimulation by high glucose only in normal islets, supporting the suggested physiological role of GSF in the glucose-regulated expression of the insulin gene. Glucose 106-113 insulin Homo sapiens 231-238 8986763-2 1996 A single mutation in the GSF binding site of the human insulin promoter abolishes the stimulation by high glucose only in normal islets, supporting the suggested physiological role of GSF in the glucose-regulated expression of the insulin gene. Glucose 195-202 insulin Homo sapiens 55-62 8986763-2 1996 A single mutation in the GSF binding site of the human insulin promoter abolishes the stimulation by high glucose only in normal islets, supporting the suggested physiological role of GSF in the glucose-regulated expression of the insulin gene. Glucose 195-202 insulin Homo sapiens 231-238 8986763-5 1996 Its amino acid sequence, determined by microsequencing, provided direct evidence that GSF corresponds to insulin promoter factor 1 (IPF-1; also known as PDX-1) and that, in addition to its essential roles in development and differentiation of pancreatic islets and in beta cell-specific gene expression, it functions as mediator of the glucose effect on insulin gene transcription in differentiated beta cells. Glucose 336-343 insulin Homo sapiens 105-112 8986782-1 1996 A major physiological role of insulin is the regulation of glucose uptake into skeletal and cardiac muscle and adipose tissue, mediated by an insulin-stimulated translocation of GLUT4 glucose transporters from an intracellular vesicular pool to the plasma membrane. Glucose 59-66 insulin Homo sapiens 30-37 8986782-1 1996 A major physiological role of insulin is the regulation of glucose uptake into skeletal and cardiac muscle and adipose tissue, mediated by an insulin-stimulated translocation of GLUT4 glucose transporters from an intracellular vesicular pool to the plasma membrane. Glucose 59-66 insulin Homo sapiens 142-149 8986782-6 1996 These results provide evidence of a functional role for SNARE-complex proteins in insulin-stimulated glucose uptake and suggest that adipocytes utilize a mechanism of regulating vesicle docking and fusion analogous to that found in neuroendocrine tissues. Glucose 101-108 insulin Homo sapiens 82-89 8988521-0 1996 Postprandial glucose-dependent insulinotropic polypeptide and insulin responses in patients with chronic pancreatitis with and without secondary diabetes. Glucose 13-20 insulin Homo sapiens 31-38 9003374-1 1996 A key metabolic action of insulin is the stimulation of non-oxidative glucose utilization in skeletal muscle, by increasing both glucose uptake and glycogen synthesis. Glucose 70-77 insulin Homo sapiens 26-33 9003374-1 1996 A key metabolic action of insulin is the stimulation of non-oxidative glucose utilization in skeletal muscle, by increasing both glucose uptake and glycogen synthesis. Glucose 129-136 insulin Homo sapiens 26-33 8981925-6 1996 FK506 decreased HIT cell expression of the human insulin promoter-CAT reporter gene by 40% in the presence of both low (0.4 mM) at high (20 mM) glucose concentrations. Glucose 144-151 insulin Homo sapiens 49-56 8981928-8 1996 It leads to elevated basal biosynthetic (3-fold) and secretory (10-fold) activities, and, hence, to a 4-fold reduction in the beta cell insulin content and the amount of insulin released at maximal glucose stimulation. Glucose 198-205 insulin Homo sapiens 170-177 8954915-1 1996 The signal transduction pathway by which insulin stimulates glucose transport is largely unknown, but a role of PI-3-kinase and small GTP-binding proteins has been proposed. Glucose 60-67 insulin Homo sapiens 41-48 8954915-9 1996 Our data suggest that insulin might stimulate glucose uptake through inactivation of rho. Glucose 46-53 insulin Homo sapiens 22-29 8954915-2 1996 In previous studies we, among many others, excluded a role for the ras/MAP kinase pathway in insulin-mediated glucose transport. Glucose 110-117 insulin Homo sapiens 93-100 8954915-4 1996 Pretreatment of 3T3-L1 adipocytes with botulinum C3 exoenzyme (C3), which is known to ADP-ribosylate and inactivate rho, potently stimulated glucose uptake to a level similar to insulin. Glucose 141-148 insulin Homo sapiens 178-185 8954915-6 1996 Insulin stimulates glucose uptake by triggering the translocation of GLUT4, the insulin-sensitive glucose transporter isotype, from an intracellular compartment to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 8954915-6 1996 Insulin stimulates glucose uptake by triggering the translocation of GLUT4, the insulin-sensitive glucose transporter isotype, from an intracellular compartment to the plasma membrane. Glucose 19-26 insulin Homo sapiens 80-87 8972886-3 1996 Insulin resistance was evaluated by the constant glucose infusion rate (M value) during the euglycemic-hyperinsulinemic glucose clamp test. Glucose 49-56 insulin Homo sapiens 0-7 8945471-2 1996 Clinical studies have shown that prediabetic MODY subjects have normal insulin sensitivity but suffer from a defect in glucose-stimulated insulin secretion, suggesting that pancreatic beta-cell dysfunction rather than insulin resistance is the primary defect in this disorder. Glucose 119-126 insulin Homo sapiens 138-145 8945471-2 1996 Clinical studies have shown that prediabetic MODY subjects have normal insulin sensitivity but suffer from a defect in glucose-stimulated insulin secretion, suggesting that pancreatic beta-cell dysfunction rather than insulin resistance is the primary defect in this disorder. Glucose 119-126 insulin Homo sapiens 138-145 9033967-4 1996 Insulin responses to a glucose clamp (11 mM) procedure were threefold higher in the high insulin responders (HIR) than low insulin responders (LIR). Glucose 23-30 insulin Homo sapiens 0-7 9033967-4 1996 Insulin responses to a glucose clamp (11 mM) procedure were threefold higher in the high insulin responders (HIR) than low insulin responders (LIR). Glucose 23-30 insulin Homo sapiens 89-96 9039334-3 1996 DESIGN AND PATIENTS: Insulin-modified intravenous glucose tolerance tests were performed on 14 hyperthyroid women with body mass indices (BMI) ranging from 21 to 31 kg/m2. Glucose 50-57 insulin Homo sapiens 21-28 8997227-0 1996 Effect of perfusion rate on the time course of insulin-mediated skeletal muscle glucose uptake. Glucose 80-87 insulin Homo sapiens 47-54 8997227-10 1996 Thus insulin-mediated vasodilation has a modest effect in slowing the time course at which insulin stimulates glucose uptake but has a marked effect in augmenting the maximal rate of insulin-stimulated glucose uptake in skeletal muscle. Glucose 110-117 insulin Homo sapiens 5-12 8997227-10 1996 Thus insulin-mediated vasodilation has a modest effect in slowing the time course at which insulin stimulates glucose uptake but has a marked effect in augmenting the maximal rate of insulin-stimulated glucose uptake in skeletal muscle. Glucose 110-117 insulin Homo sapiens 91-98 8997227-10 1996 Thus insulin-mediated vasodilation has a modest effect in slowing the time course at which insulin stimulates glucose uptake but has a marked effect in augmenting the maximal rate of insulin-stimulated glucose uptake in skeletal muscle. Glucose 110-117 insulin Homo sapiens 91-98 8997227-10 1996 Thus insulin-mediated vasodilation has a modest effect in slowing the time course at which insulin stimulates glucose uptake but has a marked effect in augmenting the maximal rate of insulin-stimulated glucose uptake in skeletal muscle. Glucose 202-209 insulin Homo sapiens 5-12 9039334-5 1996 MEASUREMENTS: Intravenous glucose tolerance (KG), first and second-phase integrated insulin responses to glucose, the integrated glucose area under the curve (AUC), and minimal model parameters of insulin sensitivity (SI) and glucose effectiveness (SG) were determined. Glucose 105-112 insulin Homo sapiens 84-91 9039334-5 1996 MEASUREMENTS: Intravenous glucose tolerance (KG), first and second-phase integrated insulin responses to glucose, the integrated glucose area under the curve (AUC), and minimal model parameters of insulin sensitivity (SI) and glucose effectiveness (SG) were determined. Glucose 105-112 insulin Homo sapiens 84-91 9039334-11 1996 Overweight hyperthyroid patients (BMI > 25 kg/m2, n = 6) had a higher (P < 0.05) second-phase insulin response to glucose than normal weight patients, a higher glucose AUC (P < 0.05) than normal weight patients and overweight controls (n = 8), and a lower SI (P < 0.05) than normal weight patients and overweight controls. Glucose 120-127 insulin Homo sapiens 100-107 8941470-8 1996 Multivariate regression indicated the contribution of glucose to LVMI was independent of age, BMI, insulin, and blood pressure but demonstrated a significant interaction with Cai. Glucose 54-61 insulin Homo sapiens 99-106 8922349-4 1996 These agents reduce insulin resistance by increasing insulin-dependent glucose disposal and reducing hepatic glucose output. Glucose 71-78 insulin Homo sapiens 20-27 8922349-4 1996 These agents reduce insulin resistance by increasing insulin-dependent glucose disposal and reducing hepatic glucose output. Glucose 71-78 insulin Homo sapiens 53-60 8941457-4 1996 Insulin responses during the oral glucose tolerance test were similar in obese subjects (control subjects: 417 +/- 64 pmol/l; NIDDM patients: 392 +/- 47 pmol/l) but were reduced in lean NIDDM patients (control subjects: 374 +/- 34 pmol/l; NIDDM patients: 217 +/- 20 pmol/l, P < 0.01). Glucose 34-41 insulin Homo sapiens 0-7 8941457-9 1996 CONCLUSIONS: Lean elderly NIDDM patients have a profound impairment in glucose-induced insulin release but mild resistance to insulin-mediated glucose disposal. Glucose 71-78 insulin Homo sapiens 87-94 8941472-11 1996 Because it has been reported that disturbances in insulin-glucose homeostasis are more likely associated with a WC value > 1 m, in subjects matched for total adiposity, we compared the glucose and insulin area values for those with a WC above (n = 17) and below (n = 15) this value. Glucose 58-65 insulin Homo sapiens 50-57 8941457-10 1996 Obese elderly NIDDM patients have adequate circulating insulin, but marked resistance to insulin-mediated glucose disposal. Glucose 106-113 insulin Homo sapiens 89-96 8941458-4 1996 RESULTS: After 6 months of insulin treatment, fasting blood glucose of the total patient population had decreased from an average of 14.1 +/- 2.2 to 8.3 +/- 2.0 mmol/L (P < 0.001), and HbA1c fell from 11.0 +/- 1.3 to 8.3 +/- 1.2% (P < 0.001); 34 patients reached HbA1c levels below 8.0%, 25 of them even below 7.5%. Glucose 60-67 insulin Homo sapiens 27-34 8960829-0 1996 Dissociation between insulin sensitivity of glucose uptake and endothelial function in normal subjects. Glucose 44-51 insulin Homo sapiens 21-28 8941477-5 1996 At t = 120 min, glucose concentrations had decreased 1.4 mmol/l more with lispro than with regular insulin (95% confidence interval [CI] 0.6-2.3, P = 0.002). Glucose 16-23 insulin Homo sapiens 99-106 8960829-4 1996 To examine whether endothelial function and insulin sensitivity are interrelated we quantitated in vivo insulin-stimulated rates of whole body and forearm glucose uptake at a physiological insulin concentration (euglycaemic hyperinsulinaemic clamp, 1 mU.kg-1.min-1 insulin infusion for 2 h) and on another occasion, in vivo endothelial function (blood flow response to intrabrachial infusions of sodium nitroprusside, acetylcholine, and N-monomethyl-L-arginine) in 30 normal male subjects. Glucose 155-162 insulin Homo sapiens 104-111 8960829-4 1996 To examine whether endothelial function and insulin sensitivity are interrelated we quantitated in vivo insulin-stimulated rates of whole body and forearm glucose uptake at a physiological insulin concentration (euglycaemic hyperinsulinaemic clamp, 1 mU.kg-1.min-1 insulin infusion for 2 h) and on another occasion, in vivo endothelial function (blood flow response to intrabrachial infusions of sodium nitroprusside, acetylcholine, and N-monomethyl-L-arginine) in 30 normal male subjects. Glucose 155-162 insulin Homo sapiens 104-111 8960829-4 1996 To examine whether endothelial function and insulin sensitivity are interrelated we quantitated in vivo insulin-stimulated rates of whole body and forearm glucose uptake at a physiological insulin concentration (euglycaemic hyperinsulinaemic clamp, 1 mU.kg-1.min-1 insulin infusion for 2 h) and on another occasion, in vivo endothelial function (blood flow response to intrabrachial infusions of sodium nitroprusside, acetylcholine, and N-monomethyl-L-arginine) in 30 normal male subjects. Glucose 155-162 insulin Homo sapiens 104-111 8960829-7 1996 The IR group also had diminished insulin-stimulated glucose extraction (p < 0.05) compared to the IS group, while basal and insulin-stimulated forearm blood flow rates were identical. Glucose 52-59 insulin Homo sapiens 33-40 8960829-9 1996 In conclusion, the ability of insulin to stimulate glucose uptake at physiological insulin concentrations and endothelium-dependent vasodilatation are distinct phenomena and do not necessarily coexist. Glucose 51-58 insulin Homo sapiens 30-37 8960829-9 1996 In conclusion, the ability of insulin to stimulate glucose uptake at physiological insulin concentrations and endothelium-dependent vasodilatation are distinct phenomena and do not necessarily coexist. Glucose 51-58 insulin Homo sapiens 83-90 8960831-2 1996 The reason for choosing the prepubertal stage of development is that it is metabolically characterized by both a high sensitivity to insulin and low glucose stimulated insulin responses. Glucose 149-156 insulin Homo sapiens 168-175 9075603-9 1996 In conclusion, the results of the present study indicate that a failure of hyperinsulinemic suppression of C-peptide in euglycemia is not specific for insulinoma, and that suppression of C-peptide by insulin at lower plasma glucose levels (50-60 mg/dl) would be a better diagnostic test. Glucose 224-231 insulin Homo sapiens 187-196 9075607-10 1996 The mean M value reflecting insulin sensitivity in the whole body determined by euglycemic glucose clamping was increased significantly after mazindol treatment (from 4.92 +/- 0.30 mg/kg/min to 6.36 +/- 0.43 mg/kg/min). Glucose 91-98 insulin Homo sapiens 28-35 9100085-4 1996 RESULTS: Mean plasma insulin, 1 h after a 75 g oral glucose load, was higher in cases than in controls (73.6 versus 59.8 mU/l; P < 0.05). Glucose 52-59 insulin Homo sapiens 21-28 8954022-10 1996 Simultaneous 10% Intralipid (0.4 mL/min) infusion significantly enhanced plasma TBARS concentrations and inhibited insulin-stimulated whole body glucose disposal (WBGD). Glucose 145-152 insulin Homo sapiens 115-122 8954022-13 1996 In conclusion, fasting plasma FFA seems to enhances oxidative stress, which might contribute to the disruptive effects of plasma FFA on insulin-mediated glucose uptake. Glucose 153-160 insulin Homo sapiens 136-143 8986932-10 1996 RESULTS: Insulin sensitivity assessed as glucose utilization during the clamp was significantly higher following bunazosin retard compared with following atenolol administration (3.52 +/- 0.27 versus 2.86 +/- 0.19 units of metabolic clearance rate of glucose index, P < 0.05). Glucose 41-48 insulin Homo sapiens 9-16 8986932-10 1996 RESULTS: Insulin sensitivity assessed as glucose utilization during the clamp was significantly higher following bunazosin retard compared with following atenolol administration (3.52 +/- 0.27 versus 2.86 +/- 0.19 units of metabolic clearance rate of glucose index, P < 0.05). Glucose 251-258 insulin Homo sapiens 9-16 8986933-6 1996 The IST consisted of a constant infusion of glucose, insulin and somatostatin for 150 min; insulin resistance was estimated by determining the steady-state plasma glucose (SSPG) concentrations during the last 60 min of the test. Glucose 163-170 insulin Homo sapiens 91-98 8986933-7 1996 The insulin sensitivity index (ISI) was calculated by the formula ISI = (glucose infusion rate/SSPG]x10(3). Glucose 73-80 insulin Homo sapiens 4-11 9015488-5 1996 Another glucose product, glucosamine-6-phosphate, is formed when there is hexosamine flux along with insulin resistance in tissues, and is implicated in glomerulosclerosis, since it also stimulates TGF-beta transcription. Glucose 8-15 insulin Homo sapiens 101-108 9139277-5 1996 In 14 patients with essential hypertension resistant to treatment insulin level one hour after oral glucose load was significantly (p < 0.01) higher than in 16 patients with essential hypertension responsive to antihypertensive treatment. Glucose 100-107 insulin Homo sapiens 66-73 9036569-3 1996 Therefore, it is a major therapeutical aim to put the B-cell to rest and improve insulin sensitivity by a strict control of fasting blood glucose and of postprandial hyperglycemia. Glucose 138-145 insulin Homo sapiens 81-88 9300976-12 1996 Plasma levels of insulin during oral glucose tolerance test were high. Glucose 37-44 insulin Homo sapiens 17-24 8984751-4 1996 High triglyceride and low HDL cholesterol is the characteristic dyslipidaemia seen in subjects with insulin resistance, a basic abnormality in glucose- and insulin metabolism. Glucose 143-150 insulin Homo sapiens 100-107 8941162-3 1996 Achieving and maintaining that goal involves educating the patient, encouraging regular glucose determinations, and gradually adjusting the dosage and timing of insulin administration to match the patient"s glucose levels and lifestyle. Glucose 207-214 insulin Homo sapiens 161-168 8941652-5 1996 Labeled glucose was used to measure the insulin-stimulated conversion of glucose to glycogen in these cultures. Glucose 8-15 insulin Homo sapiens 40-47 8941652-5 1996 Labeled glucose was used to measure the insulin-stimulated conversion of glucose to glycogen in these cultures. Glucose 73-80 insulin Homo sapiens 40-47 9006804-6 1996 Insulin increased the uptake of 2-deoxyglucose in a dose-dependent manner, and its effect was dependent on the preincubation dose of D-glucose. Glucose 133-142 insulin Homo sapiens 0-7 9006804-7 1996 Insulin-stimulated uptake was lower in the cells pre-exposed to 25 mmol/l D-glucose than in the cells pre-exposed to concentrations of D-glucose below 5.5 mmol/l. Glucose 74-83 insulin Homo sapiens 0-7 9006804-7 1996 Insulin-stimulated uptake was lower in the cells pre-exposed to 25 mmol/l D-glucose than in the cells pre-exposed to concentrations of D-glucose below 5.5 mmol/l. Glucose 135-144 insulin Homo sapiens 0-7 9006804-8 1996 After a long-term incubation with insulin, the insulin-stimulated glucose transport was inhibited. Glucose 66-73 insulin Homo sapiens 34-41 9006804-8 1996 After a long-term incubation with insulin, the insulin-stimulated glucose transport was inhibited. Glucose 66-73 insulin Homo sapiens 47-54 9006804-13 1996 Wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3-kinase), inhibited the uptake of glucose stimulated by insulin or IGF-I in a dose-dependent manner. Glucose 96-103 insulin Homo sapiens 118-125 9006804-14 1996 Our results suggest that D-glucose regulates its own uptake independently of insulin and modulates the ability of insulin to induce insulin resistance in the cultured rat VSMCs. Glucose 25-34 insulin Homo sapiens 114-121 9006804-14 1996 Our results suggest that D-glucose regulates its own uptake independently of insulin and modulates the ability of insulin to induce insulin resistance in the cultured rat VSMCs. Glucose 25-34 insulin Homo sapiens 114-121 9006804-16 1996 Activation of wortmannin-sensitive PI3-kinase may be involved in the signaling pathways of the insulin- and IGF-I-stimulated glucose uptake in VSMCs. Glucose 125-132 insulin Homo sapiens 95-102 8932277-5 1996 At high multiplicity of infection (100:1), islet viability was normal, but insulin secretion in response to glucose stimulation was blunted by 50%. Glucose 108-115 insulin Homo sapiens 75-82 8901806-4 1996 The peripheral hypoglycemic action of insulin was diminished, as was its effectiveness in suppressing endogenous glucose production, but the intracellular capacity to oxidize glucose was not impaired. Glucose 113-120 insulin Homo sapiens 38-45 8944683-1 1996 The minimal model of glucose kinetics interprets blood glucose and insulin concentrations after an interprets blood glucose and insulin concentrations after an intravenous glucose tolerance test (IVGTT) and provides parameters describing tissue insulin sensitivity and glucose-dependent tissue glucose disposal. Glucose 21-28 insulin Homo sapiens 67-74 8944683-1 1996 The minimal model of glucose kinetics interprets blood glucose and insulin concentrations after an interprets blood glucose and insulin concentrations after an intravenous glucose tolerance test (IVGTT) and provides parameters describing tissue insulin sensitivity and glucose-dependent tissue glucose disposal. Glucose 21-28 insulin Homo sapiens 128-135 8944683-1 1996 The minimal model of glucose kinetics interprets blood glucose and insulin concentrations after an interprets blood glucose and insulin concentrations after an intravenous glucose tolerance test (IVGTT) and provides parameters describing tissue insulin sensitivity and glucose-dependent tissue glucose disposal. Glucose 21-28 insulin Homo sapiens 128-135 8913409-6 1996 DATA SYNTHESIS: The human insulin analog, insulin lispro, which is biosynthetically made by inverting the amino acid sequence of human insulin at B-28 and B-29, is more effective than regular human insulin in improving postprandial glucose control. Glucose 232-239 insulin Homo sapiens 26-33 8913409-6 1996 DATA SYNTHESIS: The human insulin analog, insulin lispro, which is biosynthetically made by inverting the amino acid sequence of human insulin at B-28 and B-29, is more effective than regular human insulin in improving postprandial glucose control. Glucose 232-239 insulin Homo sapiens 42-49 8913409-6 1996 DATA SYNTHESIS: The human insulin analog, insulin lispro, which is biosynthetically made by inverting the amino acid sequence of human insulin at B-28 and B-29, is more effective than regular human insulin in improving postprandial glucose control. Glucose 232-239 insulin Homo sapiens 42-49 8913409-15 1996 In addition, insulin lispro improves the dosing convenience for patients with diabetes and provides a more natural control of blood glucose concentrations. Glucose 132-139 insulin Homo sapiens 13-20 8978879-3 1996 Hyperinsulinemia was defined as fasting insulin > or = 95th percentile (20 microU/mL) among the subset of subjects (n = 504) who were nonobese and free of clinical diabetes and glucose intolerance. Glucose 180-187 insulin Homo sapiens 5-12 8908335-6 1996 Static glucose challenge test with microencapsulated islets revealed the insulin response to the concentration of glucose. Glucose 7-14 insulin Homo sapiens 73-80 8908335-6 1996 Static glucose challenge test with microencapsulated islets revealed the insulin response to the concentration of glucose. Glucose 114-121 insulin Homo sapiens 73-80 8912642-3 1996 Based on the combination of this novel approach with the simultaneous microfluorometric recording of cytosolic free Ca2+ concentration ([Ca2+]i), we demonstrate that glucose-stimulated islets secrete 5-HT/insulin in a pulsatile fashion under physiological conditions, and that this activity is encoded by synchronous [Ca2+]i oscillations. Glucose 166-173 insulin Homo sapiens 205-212 8922599-4 1996 The mass transfer coefficient was improved from 1.04 x 10(-4) to 2.16 x 10(-4) cm/ sec for glucose, from 2.84 x 10(-5) to 8.36 x 10(-5) cm/sec for vitamin B12 and from 1.45 x 10(-6) to 4.15 x 10(-6) cm/sec for insulin, whereas the passage of immunoglobulin G was completely prevented, indicating that these membranes could be effective in protecting islets from immunorejection. Glucose 91-98 insulin Homo sapiens 210-217 8922348-7 1996 Thus, insulin sensitivity concerning glucose metabolism increased in response to mild mental stress. Glucose 37-44 insulin Homo sapiens 6-13 9011569-7 1997 These observations suggest that protein glycation in pancreatic beta cells, which occurs in vivo under chronic hyperglycemia, suppresses insulin gene transcription and thus can explain part of the beta cell glucose toxicity. Glucose 207-214 insulin Homo sapiens 137-144 8866549-13 1996 Insulin-stimulated rates of blood flow and glucose uptake do not colocalize in the same regions of muscle tissue, suggesting that insulin"s hemodynamic and metabolic effects are differentially regulated. Glucose 43-50 insulin Homo sapiens 0-7 8866553-0 1996 Altered insulin secretory responses to glucose in diabetic and nondiabetic subjects with mutations in the diabetes susceptibility gene MODY3 on chromosome 12. Glucose 39-46 insulin Homo sapiens 8-15 8866556-0 1996 Normalization of insulin responses to glucose by overnight infusion of glucagon-like peptide 1 (7-36) amide in patients with NIDDM. Glucose 38-45 insulin Homo sapiens 17-24 8866556-2 1996 Its effects on overnight glucose concentrations and the specific phases of insulin response to glucose and nonglucose secretogogues in subjects with NIDDM are not known. Glucose 95-102 insulin Homo sapiens 75-82 8866553-4 1996 Each subject received graded intravenous glucose infusions on two occasions separated by a 42-h continuous intravenous glucose infusion designed to prime the beta-cell to secrete more insulin in response to glucose. Glucose 119-126 insulin Homo sapiens 184-191 8866553-4 1996 Each subject received graded intravenous glucose infusions on two occasions separated by a 42-h continuous intravenous glucose infusion designed to prime the beta-cell to secrete more insulin in response to glucose. Glucose 119-126 insulin Homo sapiens 184-191 8866553-10 1996 Administration of glucose by intravenous infusion for 42 h resulted in a significant increase in the amount of insulin secreted over the 5-9 mmol/l glucose concentration range in the control subjects and nondiabetic MODY3 subjects (by 38 and 35%, respectively), but no significant change was observed in the diabetic MODY3 subjects. Glucose 18-25 insulin Homo sapiens 111-118 8866556-12 1996 Reduction of overnight glucose by exogenous insulin did not improve any of the phases of stimulated beta-cell function. Glucose 23-30 insulin Homo sapiens 44-51 8866553-10 1996 Administration of glucose by intravenous infusion for 42 h resulted in a significant increase in the amount of insulin secreted over the 5-9 mmol/l glucose concentration range in the control subjects and nondiabetic MODY3 subjects (by 38 and 35%, respectively), but no significant change was observed in the diabetic MODY3 subjects. Glucose 148-155 insulin Homo sapiens 111-118 8866560-11 1996 While some ethnic variability exists, a negative relationship between abdominal obesity and insulin sensitivity was confirmed for all three ethnic groups across the spectrum of glucose tolerance. Glucose 177-184 insulin Homo sapiens 92-99 8908381-9 1996 The insulin-mediated glucose uptake was unchanged in both groups (fish oil, 4.04 +/- 0.82 mg.kg-1.min-1 at baseline and 3.96 +/- 0.50 mg.kg-1.min-1 at 6 months; placebo, 3.51 +/- 0.62 mg.kg-1.min-1 at baseline and 4.09 +/- 0.49 mg.kg-1.min-1 at 6 months). Glucose 21-28 insulin Homo sapiens 4-11 8866565-6 1996 Insulin-stimulated glucose metabolism (P = 0.002), particularly nonoxidative glucose metabolism (P = 0.009), was reduced in FH+ compared with FH- subjects, and this difference remained after adjustment for WHR. Glucose 19-26 insulin Homo sapiens 0-7 8866565-6 1996 Insulin-stimulated glucose metabolism (P = 0.002), particularly nonoxidative glucose metabolism (P = 0.009), was reduced in FH+ compared with FH- subjects, and this difference remained after adjustment for WHR. Glucose 77-84 insulin Homo sapiens 0-7 8866565-7 1996 A parental history of NIDDM influenced the insulin response to the oral glucose load, with male offspring of diabetic mothers showing the lowest insulin values (P = 0.011). Glucose 72-79 insulin Homo sapiens 43-50 8866565-7 1996 A parental history of NIDDM influenced the insulin response to the oral glucose load, with male offspring of diabetic mothers showing the lowest insulin values (P = 0.011). Glucose 72-79 insulin Homo sapiens 145-152 8933003-1 1996 The purpose of the present study was to quantitate insulin-mediated glucose disposal in normal glucose tolerant patients with angiographically documented coronary artery disease (CAD) and to define the pathways responsible for the insulin resistance. Glucose 68-75 insulin Homo sapiens 51-58 8933003-6 1996 Insulin-mediated whole body glucose disposal (27.8 +/- 3.9 vs 38.3 +/- 4.4 mumol.kg fat free mass (FFM)-1.min-1, p < 0.01) was significantly decreased in CAD subjects and this was entirely due to diminished non-oxidative glucose disposal (8.9 +/- 2.8 vs 20.0 +/- 3.3 mumol.kg FFM-1.min-1, p < 0.001). Glucose 28-35 insulin Homo sapiens 0-7 8908387-2 1996 OBJECTIVE: The objective of this study is to compare the effect of intraperitoneal versus subcutaneous insulin injection on hepatic glucose production (HGP) and systemic glucose utilization (Rd) in patients with NIDDM. Glucose 132-139 insulin Homo sapiens 103-110 8933003-6 1996 Insulin-mediated whole body glucose disposal (27.8 +/- 3.9 vs 38.3 +/- 4.4 mumol.kg fat free mass (FFM)-1.min-1, p < 0.01) was significantly decreased in CAD subjects and this was entirely due to diminished non-oxidative glucose disposal (8.9 +/- 2.8 vs 20.0 +/- 3.3 mumol.kg FFM-1.min-1, p < 0.001). Glucose 224-231 insulin Homo sapiens 0-7 8933003-8 1996 In the CAD subjects basal and insulin-mediated rates of glucose and lipid oxidation were normal and insulin caused a normal suppression of hepatic glucose production. Glucose 56-63 insulin Homo sapiens 30-37 8908387-8 1996 CONCLUSIONS: In patients with NIDDM, intraperitoneal insulin injection achieves more rapid and greater peak values for stimulation of glucose Rd than subcutaneous insulin injection. Glucose 134-141 insulin Homo sapiens 53-60 8933003-8 1996 In the CAD subjects basal and insulin-mediated rates of glucose and lipid oxidation were normal and insulin caused a normal suppression of hepatic glucose production. Glucose 147-154 insulin Homo sapiens 100-107 8895337-6 1996 To assess the metabolic consequences of troglitazone treatment, both basal and insulin-stimulated glucose uptake were monitored in treated cells. Glucose 98-105 insulin Homo sapiens 79-86 8946153-3 1996 Insulin sensitivity was estimated by modelling basal serum glucose and insulin values. Glucose 59-66 insulin Homo sapiens 0-7 8895337-9 1996 These results suggest the possibility that in vivo, the troglitazone-dependent increase in glucose disposal may be attributable in part to modification in the expression of Glut1 in insulin-responsive tissues. Glucose 91-98 insulin Homo sapiens 182-189 8912043-1 1996 OBJECTIVE: The aim of this provocation study was to examine insulin, glucose, and cortisol levels in response to a glucose load in bulimia nervosa patients and to relate this to behavior, treatment status, and depressive symptomatology. Glucose 115-122 insulin Homo sapiens 60-67 8981115-3 1996 Plasma concentrations of insulin and glucose after an oral glucose tolerance test (OGTT) were determined by immunoradiometric assay and glucose oxidase technique respectively. Glucose 59-66 insulin Homo sapiens 25-32 8903329-11 1996 In the whole dataset, a direct relationship existed between insulin-stimulated glucose uptake in heart and skeletal muscle. Glucose 79-86 insulin Homo sapiens 60-67 8937933-5 1996 Concommitantly, a decrease of serum glucose and insulin dose was observed, reflecting a higher insulin sensitivity during Lispro treatment. Glucose 36-43 insulin Homo sapiens 95-102 8923861-7 1996 The study design allowed us to evaluate the effects of metformin vs. placebo treatment on glycemic control, plasma lipid profile, HGP, insulin-mediated glucose uptake, oxidative and nonoxidative glucose metabolism, and lactate turnover. Glucose 152-159 insulin Homo sapiens 135-142 8923846-1 1996 To determine potential abnormalities in beta-cell function after pancreas transplantation, the secretory capacity of the pancreatic grafts was assessed by measuring the glucose-potentiating effect on arginine-induced insulin secretion in recipients of cadaveric segmental (SPx; n = 8) and whole organ pancreas grafts (WPx; n = 6) and compared to that in nondiabetic kidney transplant recipients (Kx; n = 6) and normal controls (Ns; n = 7). Glucose 169-176 insulin Homo sapiens 217-224 8923875-9 1996 There were trends toward increased body mass indices, waist to hip ratios, and 2-h insulin levels during oral glucose tolerance tests in Samoans with the mutation; however, the limited number of subjects available for study precluded rigorous statistical analysis. Glucose 110-117 insulin Homo sapiens 83-90 8946813-13 1996 Impaired glucose tolerance was characterised by increased insulin resistance, with a significant rise in serum insulin and C-peptide concentrations and in the insulin/glucose index during the oral glucose tolerance test at the 32nd week of gestation. Glucose 9-16 insulin Homo sapiens 58-65 8946813-13 1996 Impaired glucose tolerance was characterised by increased insulin resistance, with a significant rise in serum insulin and C-peptide concentrations and in the insulin/glucose index during the oral glucose tolerance test at the 32nd week of gestation. Glucose 9-16 insulin Homo sapiens 111-118 8946813-13 1996 Impaired glucose tolerance was characterised by increased insulin resistance, with a significant rise in serum insulin and C-peptide concentrations and in the insulin/glucose index during the oral glucose tolerance test at the 32nd week of gestation. Glucose 9-16 insulin Homo sapiens 111-118 8972407-13 1996 Those with a fasting serum glucose of > or = 140 mg/dl may begin diet therapy, glucose monitoring, and insulin as indicated. Glucose 27-34 insulin Homo sapiens 106-113 9346691-0 1996 Glucose and potassium metabolic responses to insulin during liver transplantation. Glucose 0-7 insulin Homo sapiens 45-52 9346691-1 1996 Insulin regulates glucose and potassium metabolism by acting differently upon peripheral tissues (e.g., skeletal muscle) and the splanchnic bed, including the liver. Glucose 18-25 insulin Homo sapiens 0-7 9346691-2 1996 Liver disease is accompanied by "insulin resistance" of glucose metabolism, whereby glucose intolerance occurs despite relatively increased plasma insulin concentration. Glucose 56-63 insulin Homo sapiens 33-40 9346691-5 1996 The present study evaluated the role of the liver in maximal insulin responsiveness of whole-body glucose and potassium metabolism, using a hyperinsulinemic clamp technique, to identify the mechanism(s) underlying post-reperfusion hyperglycemia and intraoperative hyperkalemia. Glucose 98-105 insulin Homo sapiens 61-68 9346691-10 1996 Insulin-stimulated exogenous glucose and potassium uptakes were determined in protocol 2 before skin incision and during the dissection, anhepatic, and neohepatic stages. Glucose 29-36 insulin Homo sapiens 0-7 9346691-16 1996 Insulin-stimulated glucose uptake, in mg . Glucose 19-26 insulin Homo sapiens 0-7 8931646-7 1996 Thus, the 12 most insulin-resistant subjects were characterized by a cluster of abnormalities (mild overweight, higher blood pressure and prevalence of hypertension, higher serum triglycerides and insulin response to oral glucose, and reduced glucose storage) that included an insulin-induced increase in [Ca2+]i (9 +/- 2 nmol/L, P < .001 v basal). Glucose 222-229 insulin Homo sapiens 18-25 8931646-7 1996 Thus, the 12 most insulin-resistant subjects were characterized by a cluster of abnormalities (mild overweight, higher blood pressure and prevalence of hypertension, higher serum triglycerides and insulin response to oral glucose, and reduced glucose storage) that included an insulin-induced increase in [Ca2+]i (9 +/- 2 nmol/L, P < .001 v basal). Glucose 243-250 insulin Homo sapiens 18-25 8987057-2 1996 Exhaustive clinical and laboratory examinations showed an association with other abnormalities: hypertrichosis, steatohepatitis, and an abnormal insulin response to the glucose loading test in the first patient. Glucose 169-176 insulin Homo sapiens 145-152 8948006-5 1996 In patients with diabetes, due to a relative or absolute lack of insulin, stress-induced increases in glucose cannot be properly metabolized. Glucose 102-109 insulin Homo sapiens 65-72 8857019-0 1996 Increased glucose transport-phosphorylation and muscle glycogen synthesis after exercise training in insulin-resistant subjects. Glucose 10-17 insulin Homo sapiens 101-108 8857019-9 1996 CONCLUSIONS: Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. Glucose 255-262 insulin Homo sapiens 32-39 8857019-9 1996 CONCLUSIONS: Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. Glucose 255-262 insulin Homo sapiens 84-91 8857019-9 1996 CONCLUSIONS: Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. Glucose 255-262 insulin Homo sapiens 84-91 8857019-9 1996 CONCLUSIONS: Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. Glucose 255-262 insulin Homo sapiens 84-91 8911919-2 1996 Hydroxylamine provoked a concentration-dependent inhibition of the glucose-induced insulin release. Glucose 67-74 insulin Homo sapiens 83-90 8911919-6 1996 Hydroxylamine decreased 45Ca outflow, [Ca2+]i and insulin output from islets exposed to 16.7 mM glucose and extracellular Ca2+. Glucose 96-103 insulin Homo sapiens 50-57 8931504-6 1996 Intensified (insulin) treatment reduced the rate of macrosomia and large-for-gestational age infants in the subgroups with intermediate and high levels of fasting plasma glucose on the oral glucose tolerance test (9.5%/14.2% and 12.2%/24.2% respectively), again not to levels of the control group (5.2%/10.8%). Glucose 170-177 insulin Homo sapiens 13-20 8931504-6 1996 Intensified (insulin) treatment reduced the rate of macrosomia and large-for-gestational age infants in the subgroups with intermediate and high levels of fasting plasma glucose on the oral glucose tolerance test (9.5%/14.2% and 12.2%/24.2% respectively), again not to levels of the control group (5.2%/10.8%). Glucose 190-197 insulin Homo sapiens 13-20 8942005-3 1996 Three months later, the control of blood glucose improved with smaller doses of insulin in four cases and milder hypoglycemia was observed compared to when using multiple injections. Glucose 41-48 insulin Homo sapiens 80-87 8942005-5 1996 Buffered regular insulin continuously injected by pumps brought a more stable nocturnal blood glucose level compared to isophane insulin injected at bedtime, the absorption of which seemed to vary considerably. Glucose 94-101 insulin Homo sapiens 17-24 9254534-4 1996 Monitoring first phase insulin release during intravenous glucose administration is a useful index of residual beta cell function that can be used to detect individuals who are close to insulin dependence. Glucose 58-65 insulin Homo sapiens 23-30 8896647-1 1996 This study was initiated to see if the presence of resistance to insulin-mediated glucose disposal, glucose intolerance, and hyperinsulinemia in healthy patients with hypertension was dependent upon the coexistence of microalbuminuria. Glucose 82-89 insulin Homo sapiens 65-72 8896647-6 1996 In addition, the steady-state plasma glucose (SSPG) concentrations at the end of a 180 min continuous infusion of somatostatin, insulin, and glucose was significantly higher in those with hypertension (156 +/- 13 v 107 +/- 10 mg/dL, P < .01). Glucose 37-44 insulin Homo sapiens 128-135 8896654-3 1996 A total of 45 normotensive, nondiabetic individuals had insulin-mediated glucose disposal quantified by the insulin suppression test. Glucose 73-80 insulin Homo sapiens 56-63 8896654-5 1996 The average heart rate (as calculated by a mean of 30,720 +/- 208 beats per subject over a monitoring time of 6.9 +/- 0.6 h) was significantly related (r = 0.61; P < .001) to insulin resistance as expressed by the steady-state plasma glucose (SSPG) response to a continuous infusion of glucose, insulin and somatostatin and to the plasma insulin response to a 75 g of oral glucose challenge (r = 0.51; P < .001). Glucose 237-244 insulin Homo sapiens 178-185 8896654-5 1996 The average heart rate (as calculated by a mean of 30,720 +/- 208 beats per subject over a monitoring time of 6.9 +/- 0.6 h) was significantly related (r = 0.61; P < .001) to insulin resistance as expressed by the steady-state plasma glucose (SSPG) response to a continuous infusion of glucose, insulin and somatostatin and to the plasma insulin response to a 75 g of oral glucose challenge (r = 0.51; P < .001). Glucose 289-296 insulin Homo sapiens 178-185 8896654-5 1996 The average heart rate (as calculated by a mean of 30,720 +/- 208 beats per subject over a monitoring time of 6.9 +/- 0.6 h) was significantly related (r = 0.61; P < .001) to insulin resistance as expressed by the steady-state plasma glucose (SSPG) response to a continuous infusion of glucose, insulin and somatostatin and to the plasma insulin response to a 75 g of oral glucose challenge (r = 0.51; P < .001). Glucose 289-296 insulin Homo sapiens 178-185 8897815-3 1996 Stimulation of insulin release evoked by glucose, phospholipase C activation with carbachol, and protein kinase C activation with phorbol ester were obtained by SIN-1, whereas the response to adenylyl cyclase activation or K(+)-induced depolarization was not affected. Glucose 41-48 insulin Homo sapiens 15-22 8897815-5 1996 Reversal of SIN-1 inhibition of glucose-stimulated insulin release by dithiothreitol suggests that NO may inhibit insulin secretion partly by S-nitrosylation of thiol residues in key proteins in the stimulus-secretion coupling. Glucose 32-39 insulin Homo sapiens 51-58 8897815-5 1996 Reversal of SIN-1 inhibition of glucose-stimulated insulin release by dithiothreitol suggests that NO may inhibit insulin secretion partly by S-nitrosylation of thiol residues in key proteins in the stimulus-secretion coupling. Glucose 32-39 insulin Homo sapiens 114-121 8897853-1 1996 The insulin-mediated vasodilator effect has been proposed as an important physiological determinant of insulin action on glucose disposal in normotensive humans. Glucose 121-128 insulin Homo sapiens 4-11 8897853-1 1996 The insulin-mediated vasodilator effect has been proposed as an important physiological determinant of insulin action on glucose disposal in normotensive humans. Glucose 121-128 insulin Homo sapiens 103-110 9181099-7 1996 New studies should be designed to identify the precise mechanisms involved in the interaction between hypertension, serum insulin-glucose levels and the magnitude of the renal tubule reabsorption abnormality. Glucose 130-137 insulin Homo sapiens 122-129 8896859-1 1996 PURPOSE: The effects of prolonged sevoflurane anaesthesia on insulin sensitivity were investigated by two successive intravenous glucose tolerance tests (IVGTT) in eight patients who underwent prolonged surgery. Glucose 129-136 insulin Homo sapiens 61-68 8896859-7 1996 The maximum insulin response to glucose (delta IRI-delta BS-1) of the second IVGTT was lower than the first IVGTT (0.124 +/- 0.092 vs 0.071 +/- 0.056, P < 0.05). Glucose 32-39 insulin Homo sapiens 12-19 8896859-9 1996 CONCLUSION: Glucose intolerance is enhanced by diminished insulin output in response to blood glucose elevation during prolonged anaesthesia and surgery. Glucose 94-101 insulin Homo sapiens 58-65 9191497-1 1996 OBJECTIVE: To study how muscle ubiquinone content (MUQ) and percentage slow twitch (%ST) of muscle fibres in the thighs of male healthy subjects with a low or high insulin response to glucose infusion tests (GIT) affected blood glucose control (BGC). Glucose 184-191 insulin Homo sapiens 164-171 8873692-3 1996 It has been appreciated that salt restriction may have adverse effects on glucose and lipid metabolism--processes regulated by insulin. Glucose 74-81 insulin Homo sapiens 127-134 8826973-2 1996 In 13 individuals who had data at three time-points and who developed NIDDM only at the final test, 2-h insulin levels followed an inverted V-shaped pattern as glucose tolerance declined to NIDDM. Glucose 160-167 insulin Homo sapiens 104-111 8826973-4 1996 Changes in glucose tolerance were accompanied by changes in mean 2-h insulin concentration that paralleled the inverted V pattern seen in the 13 individuals. Glucose 11-18 insulin Homo sapiens 69-76 8826974-0 1996 Epinephrine exerts opposite effects on peripheral glucose disposal and glucose-stimulated insulin secretion. Glucose 71-78 insulin Homo sapiens 90-97 8826974-9 1996 Furthermore, EPI enhances phi 2, the ratio between the C-peptide amount secreted during the second phase and the area under the curve of the glucose signal, indicating that the observed increase of C-peptide concentration is due not only to the augmented glucose signal but also to a specific EPI-mediated enhancement of beta-cell responsivity to glucose. Glucose 141-148 insulin Homo sapiens 198-207 8826978-10 1996 In addition, the integrated area under the curve of plasma insulin concentrations, measured in response to a 75-g oral glucose challenge, and the amount of visceral adipose tissue, measured by computed tomography, were positively associated with the LDL particle score only in (+/-) heterozygotes. Glucose 119-126 insulin Homo sapiens 59-66 8897005-0 1996 Insulin action on glucose transport and plasma membrane GLUT4 content in skeletal muscle from patients with NIDDM. Glucose 18-25 insulin Homo sapiens 0-7 8897005-1 1996 We investigated the response of the glucose transport system to insulin, in the presence of ambient glucose concentrations, in isolated skeletal muscle from seven patients with non-insulin-dependent diabetes mellitus (NIDDM) (age, 55 +/- 3 years, BMI 27.4 +/- 1.8 kg/m2) and seven healthy control subjects (age, 54 +/- 3 years, BMI 26.5 +/- 1.1 kg/m2). Glucose 36-43 insulin Homo sapiens 64-71 8897005-2 1996 Insulin-mediated whole body glucose utilization was similar between the groups when studied in the presence of ambient glucose concentrations (approximately 10 mmol/l for the NIDDM patients and 5 mmol/l for the control subjects). Glucose 28-35 insulin Homo sapiens 0-7 8897005-6 1996 Insulin-stimulated 3-O-methylglucose transport was positively correlated with whole body insulin-mediated glucose uptake in all participants (r = 0.78, p < 0.001) and negatively correlated with fasting plasma glucose levels in the NIDDM subjects (r = 0.93, p < 0.001). Glucose 29-36 insulin Homo sapiens 0-7 8897005-6 1996 Insulin-stimulated 3-O-methylglucose transport was positively correlated with whole body insulin-mediated glucose uptake in all participants (r = 0.78, p < 0.001) and negatively correlated with fasting plasma glucose levels in the NIDDM subjects (r = 0.93, p < 0.001). Glucose 29-36 insulin Homo sapiens 89-96 8897005-6 1996 Insulin-stimulated 3-O-methylglucose transport was positively correlated with whole body insulin-mediated glucose uptake in all participants (r = 0.78, p < 0.001) and negatively correlated with fasting plasma glucose levels in the NIDDM subjects (r = 0.93, p < 0.001). Glucose 106-113 insulin Homo sapiens 0-7 8897005-6 1996 Insulin-stimulated 3-O-methylglucose transport was positively correlated with whole body insulin-mediated glucose uptake in all participants (r = 0.78, p < 0.001) and negatively correlated with fasting plasma glucose levels in the NIDDM subjects (r = 0.93, p < 0.001). Glucose 106-113 insulin Homo sapiens 89-96 8897005-8 1996 Our results suggest that insulin-stimulated glucose transport in skeletal muscle from patients with NIDDM is down-regulated in the presence of hyperglycaemia. Glucose 44-51 insulin Homo sapiens 25-32 8897005-9 1996 The increased flux of glucose as a consequence of hyperglycaemia may result in resistance to any further insulin-induced gain of GLUT4 at the level of the plasma membrane. Glucose 22-29 insulin Homo sapiens 105-112 8897008-3 1996 We examined the relation of fasting serum insulin level (as a marker of insulin resistance) and change in insulin/glucose ratio (delta I30/ delta G30) over the first 30 min after glucose ingestion (as a marker of insulin secretion) as predictors of the 7-year development of IGT in 839 Mexican Americans and non-Hispanic whites with normal glucose tolerance at baseline from the San Antonio Heart Study. Glucose 179-186 insulin Homo sapiens 42-49 8897008-3 1996 We examined the relation of fasting serum insulin level (as a marker of insulin resistance) and change in insulin/glucose ratio (delta I30/ delta G30) over the first 30 min after glucose ingestion (as a marker of insulin secretion) as predictors of the 7-year development of IGT in 839 Mexican Americans and non-Hispanic whites with normal glucose tolerance at baseline from the San Antonio Heart Study. Glucose 179-186 insulin Homo sapiens 42-49 9015667-0 1996 Proinsulin and insulin levels according to glucose tolerance among Japanese-Brazilians, aged 40-79 years. Glucose 43-50 insulin Homo sapiens 0-10 9015667-0 1996 Proinsulin and insulin levels according to glucose tolerance among Japanese-Brazilians, aged 40-79 years. Glucose 43-50 insulin Homo sapiens 3-10 8940800-1 1996 More than 30% of the end stage liver cirrhosis was complicated by the impared glucose tolerance, in some of which insulin supplements may be required to control the blood glucose level. Glucose 171-178 insulin Homo sapiens 114-121 8940800-3 1996 Here, we presented a case of liver cirrhosis and hepatocellular caricnoma complicated by the severe glucose intolerance, and summarized our recent insulin therapy on the glucose intolerance of the decompensated liver cirrhosis in Fukuoka City Hospital, Department of Internal Medicine. Glucose 100-107 insulin Homo sapiens 147-154 8940800-3 1996 Here, we presented a case of liver cirrhosis and hepatocellular caricnoma complicated by the severe glucose intolerance, and summarized our recent insulin therapy on the glucose intolerance of the decompensated liver cirrhosis in Fukuoka City Hospital, Department of Internal Medicine. Glucose 170-177 insulin Homo sapiens 147-154 8843883-1 1996 It has been reported that insulin resistance is associated with essential hypertension and that an aggregation of risk factors-hypertension, dyslipidemia, and glucose intolerance-together with insulin resistance leads to the more frequent appearance of coronary artery disease. Glucose 159-166 insulin Homo sapiens 26-33 8843883-1 1996 It has been reported that insulin resistance is associated with essential hypertension and that an aggregation of risk factors-hypertension, dyslipidemia, and glucose intolerance-together with insulin resistance leads to the more frequent appearance of coronary artery disease. Glucose 159-166 insulin Homo sapiens 193-200 8843883-3 1996 Intima-media thickness and plaque formation of the carotid artery were assessed by B-mode ultrasonography, and insulin sensitivity was measured by the steady-state plasma glucose method. Glucose 171-178 insulin Homo sapiens 111-118 8910104-4 1996 MEASUREMENTS: Insulin sensitivity was calculated by an oral glucose tolerance test. Glucose 60-67 insulin Homo sapiens 14-21 8936926-7 1996 In both groups, the fasting insulin level was associated with more risk factors than the insulin level at 2 hours after administration of 75 g of oral glucose. Glucose 151-158 insulin Homo sapiens 89-96 8855826-4 1996 In contrast, during the low and high insulin clamps, glucose utilization was lower in NIDDM [14.90 +/- 1.00 vs. 17.24 +/- 0.83 (P < 0.01) and 41.37 +/- 3.05 vs. 50.54 +/- 3.61 mumol/kg BW.min (P < 0.01)]. Glucose 53-60 insulin Homo sapiens 37-44 8855826-7 1996 The insulin response to orally administered glucose as well as that to a standardized glucose infusion test (GIT) were diminished in NIDDM [average incremental insulin secretion during an oral glucose tolerance test, 88 +/- 28 vs. 251 +/- 50 pmol/L.min (P < 0.05); during first 10 min of GIT, 7 +/- 16 vs. 234 +/- 29 pmol/L.min (P < 0.001)]. Glucose 44-51 insulin Homo sapiens 4-11 8891888-8 1996 Glucose tolerance, insulin response, insulin-induced inhibition of hepatic glucose production and lipolysis, and insulin-mediated glucose uptake and oxidation were all slightly but not significantly improved after treatment, with no significant differences between pravastatin and placebo. Glucose 75-82 insulin Homo sapiens 37-44 8891888-8 1996 Glucose tolerance, insulin response, insulin-induced inhibition of hepatic glucose production and lipolysis, and insulin-mediated glucose uptake and oxidation were all slightly but not significantly improved after treatment, with no significant differences between pravastatin and placebo. Glucose 75-82 insulin Homo sapiens 37-44 8906517-8 1996 In the logistic regression model, the body mass index and age showed statistically significant effects on the fasting glucose:insulin ratio and on serum insulin levels after an oral load of glucose. Glucose 118-125 insulin Homo sapiens 126-133 8906517-8 1996 In the logistic regression model, the body mass index and age showed statistically significant effects on the fasting glucose:insulin ratio and on serum insulin levels after an oral load of glucose. Glucose 190-197 insulin Homo sapiens 126-133 8906517-8 1996 In the logistic regression model, the body mass index and age showed statistically significant effects on the fasting glucose:insulin ratio and on serum insulin levels after an oral load of glucose. Glucose 190-197 insulin Homo sapiens 153-160 8906517-10 1996 In the logistic regression analysis the body mass index was a significant predictor of the glucose:insulin ratio and serum insulin levels after an oral load of glucose, especially in men. Glucose 91-98 insulin Homo sapiens 99-106 8906517-10 1996 In the logistic regression analysis the body mass index was a significant predictor of the glucose:insulin ratio and serum insulin levels after an oral load of glucose, especially in men. Glucose 160-167 insulin Homo sapiens 123-130 8918511-12 1996 Insulin in pmol L-1 after glucose load decreased significantly in all intervention groups compared to controls (diet: -82.2 +/- 49.9 P = 0.02; exercise: -92.4 +/- 60.1 P = 0.03; diet + exercise: -179.6 +/- 46.1 P = 0.0004). Glucose 26-33 insulin Homo sapiens 0-7 8952221-4 1996 Insulin-mediated vasodilation in skeletal muscle appears to be an important mechanism to amplify insulin"s overall action to stimulate skeletal muscle glucose uptake in insulin-sensitive man. Glucose 151-158 insulin Homo sapiens 0-7 8952221-4 1996 Insulin-mediated vasodilation in skeletal muscle appears to be an important mechanism to amplify insulin"s overall action to stimulate skeletal muscle glucose uptake in insulin-sensitive man. Glucose 151-158 insulin Homo sapiens 97-104 8952221-4 1996 Insulin-mediated vasodilation in skeletal muscle appears to be an important mechanism to amplify insulin"s overall action to stimulate skeletal muscle glucose uptake in insulin-sensitive man. Glucose 151-158 insulin Homo sapiens 169-176 8936961-0 1996 Insulin and glucagon responses to provocation with glucose and arginine in prepubertal children with thalassemia major before and after long-term blood transfusion. Glucose 51-58 insulin Homo sapiens 0-7 8843179-7 1996 Peripheral insulin action was measured as absolute glucose uptake (M value) and normalized to estimated metabolic body size (EMBS). Glucose 51-58 insulin Homo sapiens 11-18 8914424-2 1996 Several studies showed decreases in the initial insulin release in response to glucose without significant changes in insulin sensitivity in IGT. Glucose 79-86 insulin Homo sapiens 48-55 8914424-5 1996 They have demonstrated that absolute day-long plasma insulin concentrations in response to glucose are not lower than normal and glucose metabolism is impaired. Glucose 91-98 insulin Homo sapiens 53-60 8914432-5 1996 The small subgroup of acromegalics(5-10%) with severe glucose intolerance requiring insulin therapy have low endogenous insulin levels and insulin responses that are markedly impaired. Glucose 54-61 insulin Homo sapiens 84-91 8914432-5 1996 The small subgroup of acromegalics(5-10%) with severe glucose intolerance requiring insulin therapy have low endogenous insulin levels and insulin responses that are markedly impaired. Glucose 54-61 insulin Homo sapiens 120-127 8914432-5 1996 The small subgroup of acromegalics(5-10%) with severe glucose intolerance requiring insulin therapy have low endogenous insulin levels and insulin responses that are markedly impaired. Glucose 54-61 insulin Homo sapiens 120-127 8914433-2 1996 Insulin resistance and impaired insulin secretion contribute to the pathogenesis of glucose intolerance. Glucose 84-91 insulin Homo sapiens 0-7 8914434-3 1996 However, recent observation using glucose clamp techniques has demonstrated that the majority of patients with cirrhosis are characterized by peripheral hyperinsulinemia and insulin resistance of muscle tissues. Glucose 34-41 insulin Homo sapiens 158-165 8914435-5 1996 In contrast, we have shown that most of the Japanese patients with NIDDM have impaired early insulin response after glucose loading and this should be important as a predictor for NIDDM. Glucose 116-123 insulin Homo sapiens 93-100 8914439-6 1996 New insulin sensitizers, such as troglitazone and pioglitazone, improve insulin-mediated glucose disposal by enhancing tissue sensitivity to the actions of insulin and reversing the insulin resistance, characteristic of NIDDM. Glucose 89-96 insulin Homo sapiens 4-11 8914439-6 1996 New insulin sensitizers, such as troglitazone and pioglitazone, improve insulin-mediated glucose disposal by enhancing tissue sensitivity to the actions of insulin and reversing the insulin resistance, characteristic of NIDDM. Glucose 89-96 insulin Homo sapiens 72-79 8914439-6 1996 New insulin sensitizers, such as troglitazone and pioglitazone, improve insulin-mediated glucose disposal by enhancing tissue sensitivity to the actions of insulin and reversing the insulin resistance, characteristic of NIDDM. Glucose 89-96 insulin Homo sapiens 72-79 8914439-6 1996 New insulin sensitizers, such as troglitazone and pioglitazone, improve insulin-mediated glucose disposal by enhancing tissue sensitivity to the actions of insulin and reversing the insulin resistance, characteristic of NIDDM. Glucose 89-96 insulin Homo sapiens 72-79 8914443-3 1996 The insulin response to glucose shows little change with age. Glucose 24-31 insulin Homo sapiens 4-11 8914443-4 1996 The primary cause results from resistance to the ability of insulin to stimulate glucose uptake. Glucose 81-88 insulin Homo sapiens 60-67 8914449-2 1996 The data of this test is composed of the blood glucose level and insulin level with 75 g glucose loading dose. Glucose 89-96 insulin Homo sapiens 65-72 9063024-0 1996 Insulin-stimulated glucose disposal: does adipose play a role? Glucose 19-26 insulin Homo sapiens 0-7 8936492-3 1996 Infusion of glucose overnight resulted in preoperative elevations of insulin and c-peptide (P < 0.05) and lower plasma levels of FFA, while the same glucose levels were found in both groups, 4.6 mmol/L. Glucose 12-19 insulin Homo sapiens 69-76 8936492-3 1996 Infusion of glucose overnight resulted in preoperative elevations of insulin and c-peptide (P < 0.05) and lower plasma levels of FFA, while the same glucose levels were found in both groups, 4.6 mmol/L. Glucose 12-19 insulin Homo sapiens 81-90 9036240-5 1996 IVGTT showed a significant decrease in acute first phase of insulin response to glucose (IRI 1 minute + 3 minute) in those with ICA > or = 20 JDF units. Glucose 80-87 insulin Homo sapiens 60-67 9592328-3 1996 Insulin sensitivity index (ISI) [-ln(FInx x fasting blood glucose)] ranked from high to low in the order of normal controls, IGT subjects, newly-diagnosed NIDDM patients and patients with known NIDDM (P < 0.01). Glucose 58-65 insulin Homo sapiens 0-7 8823152-10 1996 Increased insulin secretion (as judged by the 30-minute insulin increment) on an oral glucose tolerance test also predicted the development of hypertension. Glucose 86-93 insulin Homo sapiens 10-17 8798502-3 1996 Expression of Rad resulted in a 50-90% reduction in insulin-stimulated 2-deoxyglucose glucose uptake in C2C12 murine myotubes, L6 rat myotubes, and 3T3-L1 adipocytes and a 25% reduction in 3-O-methylglucose uptake in 3T3-L1 adipocytes. Glucose 78-85 insulin Homo sapiens 52-59 8798518-2 1996 The incretins glucose-dependent insulinotropic polypeptide (GIP1-42) and glucagon-like peptide-1-(7-36)-amide (GLP-17-36), hormones that potentiate glucose-induced insulin secretion from the endocrine pancreas, are substrates of the circulating exopeptidase dipeptidyl peptidase IV and are rendered biologically inactive upon cleavage of their N-terminal dipeptides. Glucose 14-21 insulin Homo sapiens 32-39 8843750-0 1996 Effect of overexpressing GLUT-1 and GLUT-4 on insulin- and contraction-stimulated glucose transport in muscle. Glucose 82-89 insulin Homo sapiens 46-53 8843756-3 1996 Whole body insulin-mediated glucose utilization was reduced by 43% in the quadriplegic patients compared with the controls (P < 0.001). Glucose 28-35 insulin Homo sapiens 11-18 8843756-5 1996 Despite whole body insulin resistance, in isolated vastus lateralis muscle, basal and insulin-stimulated 3-O-methylglucose transport, as well as protein expression of the insulin or exercise-regulatable glucose transporter, GLUT-4, and glycogen content were comparable between the patients and controls. Glucose 115-122 insulin Homo sapiens 86-93 8843756-5 1996 Despite whole body insulin resistance, in isolated vastus lateralis muscle, basal and insulin-stimulated 3-O-methylglucose transport, as well as protein expression of the insulin or exercise-regulatable glucose transporter, GLUT-4, and glycogen content were comparable between the patients and controls. Glucose 115-122 insulin Homo sapiens 86-93 8843756-7 1996 In conclusion, the dissociation between whole body insulin-mediated glucose uptake and skeletal muscle glucose transport in quadriplegic patients primarily reflects the decreased muscle mass. Glucose 68-75 insulin Homo sapiens 51-58 8889211-6 1996 Glucose at 16.7 mmol/L had the capacity to elicit insulin release from 3-day-old cultured islets. Glucose 0-7 insulin Homo sapiens 50-57 8889211-8 1996 Similar results were obtained following cryopreservation: glucose at 16.7 mmol/L stimulated a mean +/- SEM of 27.9 +/- 6.6, uU/mL/10 islets, of insulin in absence of, and 44.9 +/- 9.9, uU/mL/10 islets, in presence of, Sertoli cells. Glucose 58-65 insulin Homo sapiens 144-151 8889374-1 1996 Resistance to insulin-stimulated glucose uptake is associated with several cardiovascular disease risk factors, including hypertension, dyslipidemia, and alterations of the blood clotting cascade that accentuate thrombosis. Glucose 33-40 insulin Homo sapiens 14-21 8772733-0 1996 Impaired insulin-stimulated nonoxidative glucose metabolism in pancreas-kidney transplant recipients. Glucose 41-48 insulin Homo sapiens 9-16 8772733-1 1996 Dose-response effects of insulin on glucose turnover. Glucose 36-43 insulin Homo sapiens 25-32 8772733-4 1996 The overall effects of insulin on whole-body glucose metabolism, determined as the glucose infusion rates versus the corresponding steady-state serum insulin concentrations, demonstrated a rightward shift in the dose-response curves of the transplanted groups compared with those of normal subjects. Glucose 45-52 insulin Homo sapiens 23-30 8772733-4 1996 The overall effects of insulin on whole-body glucose metabolism, determined as the glucose infusion rates versus the corresponding steady-state serum insulin concentrations, demonstrated a rightward shift in the dose-response curves of the transplanted groups compared with those of normal subjects. Glucose 45-52 insulin Homo sapiens 150-157 8772733-4 1996 The overall effects of insulin on whole-body glucose metabolism, determined as the glucose infusion rates versus the corresponding steady-state serum insulin concentrations, demonstrated a rightward shift in the dose-response curves of the transplanted groups compared with those of normal subjects. Glucose 83-90 insulin Homo sapiens 23-30 8772733-14 1996 The principal site of insulin resistance was a reduced insulin-stimulated nonoxidative glucose metabolism of peripheral tissues, which resulted in decreased capacity to store glucose as glycogen. Glucose 87-94 insulin Homo sapiens 22-29 8772733-14 1996 The principal site of insulin resistance was a reduced insulin-stimulated nonoxidative glucose metabolism of peripheral tissues, which resulted in decreased capacity to store glucose as glycogen. Glucose 87-94 insulin Homo sapiens 55-62 8772733-14 1996 The principal site of insulin resistance was a reduced insulin-stimulated nonoxidative glucose metabolism of peripheral tissues, which resulted in decreased capacity to store glucose as glycogen. Glucose 175-182 insulin Homo sapiens 22-29 8772733-14 1996 The principal site of insulin resistance was a reduced insulin-stimulated nonoxidative glucose metabolism of peripheral tissues, which resulted in decreased capacity to store glucose as glycogen. Glucose 175-182 insulin Homo sapiens 55-62 8891456-3 1996 Baseline and insulin stimulated rates of glucose and lipid oxidation were similar in non-diabetic twins and controls. Glucose 41-48 insulin Homo sapiens 13-20 8891456-5 1996 Insulin stimulated glucose disposal, exogenous glucose storage (glucose disposal-exogenous glycolytic flux) and skeletal muscle glycogen synthase activity were all significantly decreased in NIDDM twins compared with both their non-diabetic co-twins and controls. Glucose 19-26 insulin Homo sapiens 0-7 8960831-6 1996 Insulin-stimulated glucose uptake measured at two physiological levels of hyperinsulinaemia (approximately 180 and 480 pmol) was reduced by 20 and 45% in all three groups of obese compared to non-obese subjects (p < 0.01). Glucose 19-26 insulin Homo sapiens 0-7 8960831-9 1996 Increases in basal and glucose-stimulated insulin levels during the hyperglycaemic clamp mirrored the reductions in glucose uptake during the insulin clamp in all obese groups. Glucose 23-30 insulin Homo sapiens 42-49 8960831-9 1996 Increases in basal and glucose-stimulated insulin levels during the hyperglycaemic clamp mirrored the reductions in glucose uptake during the insulin clamp in all obese groups. Glucose 23-30 insulin Homo sapiens 142-149 8960831-9 1996 Increases in basal and glucose-stimulated insulin levels during the hyperglycaemic clamp mirrored the reductions in glucose uptake during the insulin clamp in all obese groups. Glucose 116-123 insulin Homo sapiens 42-49 8960831-9 1996 Increases in basal and glucose-stimulated insulin levels during the hyperglycaemic clamp mirrored the reductions in glucose uptake during the insulin clamp in all obese groups. Glucose 116-123 insulin Homo sapiens 142-149 8822980-3 1996 At identical glucose and insulin levels, insulin stimulation of whole-body and forearm glucose uptake was 57% reduced in the IDDM patients compared with normal subjects (P < .001). Glucose 13-20 insulin Homo sapiens 41-48 8822980-3 1996 At identical glucose and insulin levels, insulin stimulation of whole-body and forearm glucose uptake was 57% reduced in the IDDM patients compared with normal subjects (P < .001). Glucose 87-94 insulin Homo sapiens 41-48 8822980-7 1996 CONCLUSIONS: We conclude that chronic hyperglycemia is associated with impaired endothelium-dependent vasodilatation in vivo and with a glucose extraction defect during insulin stimulation. Glucose 136-143 insulin Homo sapiens 169-176 8949614-0 1996 [Medium-level glucose control in non-insulin-dependent diabetics in Dakar]. Glucose 14-21 insulin Homo sapiens 37-44 8843732-2 1996 This insulin secretory response is paralleled by a significant five- to sixfold increase in the phospholipase C (PLC)-mediated hydrolysis of islet phosphoinositide (PI) pools by high glucose. Glucose 183-190 insulin Homo sapiens 5-12 8843732-4 1996 The minimal second-phase insulin secretory response to high glucose is accompanied by the minimal activation of PLC in mouse islets as well. Glucose 60-67 insulin Homo sapiens 25-32 8843732-6 1996 When previously exposed to high glucose, both rat and human islets respond to subsequent restimulation with an amplified insulin secretory response. Glucose 32-39 insulin Homo sapiens 121-128 8889233-7 1996 This sense-antisense regulation system may make it feasible to induce a feedback mechanism to control proinsulin based on the blood glucose concentration. Glucose 132-139 insulin Homo sapiens 102-112 8875088-13 1996 Serum insulin was mainly determined by a positive family history of diabetes, obesity, plasma glucose, and TG levels. Glucose 94-101 insulin Homo sapiens 6-13 8875092-6 1996 Patients with IA levels > or = 40% insulin binding (8 of 46) had a higher insulin requirement and lower preprandial capillary blood glucose at the beginning of pregnancy but not at term (P < 0.005), whereas they had lower HbA1c at term than did patients with low IA levels (P < 0.01). Glucose 135-142 insulin Homo sapiens 38-45 8877295-2 1996 Of the 20 women with the lowest insulin sensitivity, 11 had impaired glucose tolerance (IGT) whereas 9 had normal glucose tolerance (NGT). Glucose 69-76 insulin Homo sapiens 32-39 8894483-5 1996 The regular insulin secretory oscillations seen in the fasting stage in normal subjects are completely lost by raising the basal glucose concentration only marginally to about 6 mmol l-1. Glucose 129-136 insulin Homo sapiens 12-19 8894483-8 1996 Additional studies indicate that it is the periodicity of the insulin secretory oscillations and the rate of rise of the first phase insulin secretion in response to a glucose challenge which are the main candidates for successful signalling. Glucose 168-175 insulin Homo sapiens 62-69 8894483-8 1996 Additional studies indicate that it is the periodicity of the insulin secretory oscillations and the rate of rise of the first phase insulin secretion in response to a glucose challenge which are the main candidates for successful signalling. Glucose 168-175 insulin Homo sapiens 133-140 8894484-5 1996 Insulin response was evaluated by the insulinogenic index, the ratio of increment of serum insulin to that of plasma glucose (mg dl-1) 30 min after the oral glucose load. Glucose 117-124 insulin Homo sapiens 0-7 8894484-5 1996 Insulin response was evaluated by the insulinogenic index, the ratio of increment of serum insulin to that of plasma glucose (mg dl-1) 30 min after the oral glucose load. Glucose 157-164 insulin Homo sapiens 0-7 8894486-11 1996 This relationship, the "hyperbolic law of glucose tolerance" indicates that insulin secretion can only be assessed in terms of the ambient degree of insulin sensitivity. Glucose 42-49 insulin Homo sapiens 76-83 8894486-14 1996 The latter realization indicates that the insulin effect on lipolysis is what is critical for determination of glucose output in the fasting state, and that insulin resistance at the level of the adipocyte may determine the extent of fasting hyperglycaemia, and may be an important factor in the overall phenotype in prediabetic and NIDDM individuals. Glucose 111-118 insulin Homo sapiens 42-49 8894489-3 1996 We found that insulin-induced binding of the PI 3-kinase activity to IRS-1 generates the signal to activate glucose transport and membrane ruffling. Glucose 108-115 insulin Homo sapiens 14-21 8894494-0 1996 Insulin response to oral glucose load is consistently decreased in established non-insulin-dependent diabetes mellitus: the usefulness of decreased early insulin response as a predictor of non-insulin-dependent diabetes mellitus. Glucose 25-32 insulin Homo sapiens 0-7 8894494-0 1996 Insulin response to oral glucose load is consistently decreased in established non-insulin-dependent diabetes mellitus: the usefulness of decreased early insulin response as a predictor of non-insulin-dependent diabetes mellitus. Glucose 25-32 insulin Homo sapiens 83-90 8894494-1 1996 We studied the plasma insulin response during a 100 g oral glucose tolerance test (OGTT) in subjects with NIDDM and various other conditions associated with glucose intolerance. Glucose 59-66 insulin Homo sapiens 22-29 8894494-1 1996 We studied the plasma insulin response during a 100 g oral glucose tolerance test (OGTT) in subjects with NIDDM and various other conditions associated with glucose intolerance. Glucose 157-164 insulin Homo sapiens 22-29 8894494-5 1996 This was in contrast to other conditions which are often associated with glucose intolerance such as corticosteroid treatment, post-gastrectomy, liver diseases, in which insulin response is increased with the impairment of glucose tolerance as far as the FBG remains below 140 mg dl-1. Glucose 73-80 insulin Homo sapiens 170-177 8894494-6 1996 The low insulin response in definite diabetes can be represented by a decreased insulinogenic index, the ratio of increment of plasma insulin (muU ml-1) to that of blood glucose (mg dl-1) 30 min after the glucose load. Glucose 170-177 insulin Homo sapiens 8-15 8894494-6 1996 The low insulin response in definite diabetes can be represented by a decreased insulinogenic index, the ratio of increment of plasma insulin (muU ml-1) to that of blood glucose (mg dl-1) 30 min after the glucose load. Glucose 205-212 insulin Homo sapiens 8-15 8894494-12 1996 Fasting and 2-h insulin levels are lower in definite diabetes than in control groups with similar blood glucose levels. Glucose 104-111 insulin Homo sapiens 16-23 8894494-13 1996 The so-called inverted-U shape relationship of plasma insulin to blood glucose was not so apparent in definite diabetes. Glucose 71-78 insulin Homo sapiens 54-61 8894494-14 1996 We conclude that a low insulin response to oral glucose, as represented by a low insulinogenic index, is an important inherent characteristic in definite diabetes and probably plays a predominant role in the pathogenesis of NIDDM in most Japanese patients. Glucose 48-55 insulin Homo sapiens 23-30 8894495-4 1996 Low insulin secretory response was defined when the insulinogenic index, a ratio of increment of plasma insulin to that of plasma glucose 30 min after oral glucose load, was lower than 0.5. Glucose 130-137 insulin Homo sapiens 4-11 8894495-4 1996 Low insulin secretory response was defined when the insulinogenic index, a ratio of increment of plasma insulin to that of plasma glucose 30 min after oral glucose load, was lower than 0.5. Glucose 156-163 insulin Homo sapiens 4-11 8894495-5 1996 Cumulative incidence of diabetes with fasting blood glucose (FBG) exceeding 120 mg dl-1 was significantly higher in impaired glucose tolerance (IGT) than in non-IGT, and in each of IGT and non-IGT groups, the incidence was significantly higher for low than normal insulin responders. Glucose 52-59 insulin Homo sapiens 264-271 8894495-6 1996 The mean initial plasma insulin response in subjects who developed diabetes was significantly lower than in those who remained non-diabetic with the same category of glucose tolerance at baseline irrespective of the degree of glucose intolerance. Glucose 166-173 insulin Homo sapiens 24-31 8894497-16 1996 In the Japanese-Americans, diminished early insulin release to an oral glucose challenge and increased insulin resistance characterized by hyperinsulinaemia are suspected to be some of the important risk factors for NIDDM. Glucose 71-78 insulin Homo sapiens 44-51 8894498-6 1996 Delayed early insulin response to glucose or a meal always accompanies chronic hyperglycaemia and is not normalized by non-pharmacologic treatment. Glucose 34-41 insulin Homo sapiens 14-21 8894501-4 1996 However, as its effects on insulin secretion are glucose dependent, its effect on blood glucose in self-limiting. Glucose 49-56 insulin Homo sapiens 27-34 9363214-11 1996 The absence of the insulin-sensitive GLUT4 in the placenta is in line with the current consensus of insulin-independent glucose transport. Glucose 120-127 insulin Homo sapiens 100-107 15251510-6 1996 For a fasting plasma venous glucose level of 150 mg/dL at the time of initiation of long-term glucocorticoid therapy, 54% of respondents disagreed with immediate increase of insulin in the case of a patient already taking insulin, and 80% disagreed with immediate substitution of insulin in the case of a patient on maximal glyburide therapy (P = 0.0053 for mean change of position). Glucose 28-35 insulin Homo sapiens 174-181 15251512-1 1996 OBJECTIVE: To determine whether an initial fasting blood glucose determination will predict which pregnant women will need insulin in addition to dietary measures to maintain fasting glucose levels during gestation. Glucose 57-64 insulin Homo sapiens 123-130 15251512-3 1996 Insulin therapy was initiated if the fasting blood glucose value exceeded 5.8 mmol/L (105 mg/dL) on more than one occasion, the 2-hour postprandial glucose exceeded 8.3 mmol/L (150 mg/dL), or the 2-hour postprandial glucose exceeded 6.7 mmol/L (120 mg/dL) three times in a week. Glucose 51-58 insulin Homo sapiens 0-7 15251512-3 1996 Insulin therapy was initiated if the fasting blood glucose value exceeded 5.8 mmol/L (105 mg/dL) on more than one occasion, the 2-hour postprandial glucose exceeded 8.3 mmol/L (150 mg/dL), or the 2-hour postprandial glucose exceeded 6.7 mmol/L (120 mg/dL) three times in a week. Glucose 148-155 insulin Homo sapiens 0-7 15251512-3 1996 Insulin therapy was initiated if the fasting blood glucose value exceeded 5.8 mmol/L (105 mg/dL) on more than one occasion, the 2-hour postprandial glucose exceeded 8.3 mmol/L (150 mg/dL), or the 2-hour postprandial glucose exceeded 6.7 mmol/L (120 mg/dL) three times in a week. Glucose 148-155 insulin Homo sapiens 0-7 8889439-12 1996 Insulin-mediated skeletal muscle glucose uptake precedes this effect, but seems not to be an important determinant of the vasodilator response to insulin. Glucose 33-40 insulin Homo sapiens 0-7 8794828-2 1996 This vasodilation contributes to insulin-stimulated glucose uptake and has been found to be reduced in various insulin-resistant states. Glucose 52-59 insulin Homo sapiens 33-40 8794828-2 1996 This vasodilation contributes to insulin-stimulated glucose uptake and has been found to be reduced in various insulin-resistant states. Glucose 52-59 insulin Homo sapiens 111-118 8911974-2 1996 Its pathogenesis is multifactorial involving both genetic (e.g. impaired insulin-secretion) and acquired (e.g. insulin-resistance) factors which cause overproduction of glucose and inefficient glucose utilization. Glucose 169-176 insulin Homo sapiens 73-80 8911980-10 1996 They act as a negative feedback system to limit further glucose transport by insulin target tissue during hyperglycemia. Glucose 56-63 insulin Homo sapiens 77-84 8911980-11 1996 Lipotoxicity has previously been implicated in insulin resistance by its inhibitory effect on glucose uptake by muscle because of the Randle-fatty acid cycle. Glucose 94-101 insulin Homo sapiens 47-54 8921059-4 1996 At the time of first oral glucose tolerance testing, insulin resistance was a feature in 85% of the women in the therapy group, and 22% were hyperandrogenaemic. Glucose 26-33 insulin Homo sapiens 53-60 8889763-0 1996 Insulin resistance limits glucose utilization and exercise tolerance in myophosphorylase deficiency and NIDDM. Glucose 26-33 insulin Homo sapiens 0-7 8889763-3 1996 We hypothesized that insulin resistance would limit transport of extracellular glucose to skeletal muscle during exercise, resulting in impaired exercise performance that was reversible by insulin infusion. Glucose 79-86 insulin Homo sapiens 21-28 8889763-3 1996 We hypothesized that insulin resistance would limit transport of extracellular glucose to skeletal muscle during exercise, resulting in impaired exercise performance that was reversible by insulin infusion. Glucose 79-86 insulin Homo sapiens 189-196 8889763-5 1996 We observed that insulin infusion significantly increased the rate of systemic glucose utilization (P < 0.01) and also significantly decreased the ratio of inorganic phosphate to phosphocreatine (P < 0.001) during forearm exercise compared with the control study. Glucose 79-86 insulin Homo sapiens 17-24 8889763-7 1996 Our findings demonstrate that resistance to the biological actions of insulin, as occurs in type II diabetes mellitus, leads to a defect in glucose transport that limits the availability of extracellular glucose to exercising muscle. Glucose 140-147 insulin Homo sapiens 70-77 8889763-7 1996 Our findings demonstrate that resistance to the biological actions of insulin, as occurs in type II diabetes mellitus, leads to a defect in glucose transport that limits the availability of extracellular glucose to exercising muscle. Glucose 204-211 insulin Homo sapiens 70-77 8784086-2 1996 Additionally, we performed iv glucose tolerance tests to measure the insulin sensitivity index, glucose effectiveness at zero insulin, iv glucose tolerance, and the acute insulin response to glucose. Glucose 96-103 insulin Homo sapiens 126-133 8784086-2 1996 Additionally, we performed iv glucose tolerance tests to measure the insulin sensitivity index, glucose effectiveness at zero insulin, iv glucose tolerance, and the acute insulin response to glucose. Glucose 96-103 insulin Homo sapiens 126-133 8784086-2 1996 Additionally, we performed iv glucose tolerance tests to measure the insulin sensitivity index, glucose effectiveness at zero insulin, iv glucose tolerance, and the acute insulin response to glucose. Glucose 96-103 insulin Homo sapiens 126-133 8784086-2 1996 Additionally, we performed iv glucose tolerance tests to measure the insulin sensitivity index, glucose effectiveness at zero insulin, iv glucose tolerance, and the acute insulin response to glucose. Glucose 96-103 insulin Homo sapiens 126-133 8784086-2 1996 Additionally, we performed iv glucose tolerance tests to measure the insulin sensitivity index, glucose effectiveness at zero insulin, iv glucose tolerance, and the acute insulin response to glucose. Glucose 96-103 insulin Homo sapiens 126-133 8784086-2 1996 Additionally, we performed iv glucose tolerance tests to measure the insulin sensitivity index, glucose effectiveness at zero insulin, iv glucose tolerance, and the acute insulin response to glucose. Glucose 96-103 insulin Homo sapiens 126-133 8784087-5 1996 Fasting (P < 0.01) and 2-h post-75-g glucose load insulin levels (P < 0.05), as well as integrated insulin responses to the glucose load, decreased (P < 0.05), and insulin sensitivity assessed by a frequently sampled iv glucose tolerance test increased significantly (P < 0.001) during troglitazone treatment. Glucose 130-137 insulin Homo sapiens 105-112 8784087-5 1996 Fasting (P < 0.01) and 2-h post-75-g glucose load insulin levels (P < 0.05), as well as integrated insulin responses to the glucose load, decreased (P < 0.05), and insulin sensitivity assessed by a frequently sampled iv glucose tolerance test increased significantly (P < 0.001) during troglitazone treatment. Glucose 130-137 insulin Homo sapiens 105-112 8784087-5 1996 Fasting (P < 0.01) and 2-h post-75-g glucose load insulin levels (P < 0.05), as well as integrated insulin responses to the glucose load, decreased (P < 0.05), and insulin sensitivity assessed by a frequently sampled iv glucose tolerance test increased significantly (P < 0.001) during troglitazone treatment. Glucose 130-137 insulin Homo sapiens 105-112 8784087-5 1996 Fasting (P < 0.01) and 2-h post-75-g glucose load insulin levels (P < 0.05), as well as integrated insulin responses to the glucose load, decreased (P < 0.05), and insulin sensitivity assessed by a frequently sampled iv glucose tolerance test increased significantly (P < 0.001) during troglitazone treatment. Glucose 130-137 insulin Homo sapiens 105-112 8784087-7 1996 Stepwise regression analysis indicated that decreases in nonsex hormone-binding globulin testosterone levels were significantly correlated with decreases in integrated insulin responses to the glucose load (r2 0.44, P < 0.01). Glucose 193-200 insulin Homo sapiens 168-175 8784108-2 1996 Five normal-weight (BMI < 28, 2 males/3 females) and five obese subjects (BMI > 28, 2 males/3 females) were fasted (0 Kcal) for 52 h. Mean plasma glucose decreased from 88 +/- 3 to 63 +/- 5 mg/dl, serum insulin from 16 +/- 1 to 10 +/- 1 microU/ml, plasma beta-hydroxybutyrate increased from 0.2 +/- 0.1 to 1.8 +/- 0.4 mumol/ml. Glucose 152-159 insulin Homo sapiens 209-216 8808989-8 1996 Insulin response during the last 20 min of the 2 hr hyperglycemic clamps (7.9 mmol/L above basal plasma glucose levels) decreased after the intervention(s) in the entire group by 29% (p < .01), but decreased more in the group that lost weight (43%, p < .05) than in women who remained weight stable (16%, p = .05). Glucose 104-111 insulin Homo sapiens 0-7 8862120-1 1996 Recent studies have demonstrated that replacement of C-peptide to normal physiological concentrations in insulin-dependent diabetic (IDDM) patients on a short-term basis (1-3 h) results in decreased glomerular hyperfiltration, augmented glucose utilization and improved autonomic nervous function. Glucose 237-244 insulin Homo sapiens 53-62 8862124-6 1996 Measurements were made of the plasma glucose and insulin responses to oral glucose, fasting triglyceride (TG) and high density lipoprotein (HDL)-cholesterol concentrations, blood pressure, and UAE rates. Glucose 75-82 insulin Homo sapiens 49-56 8862124-9 1996 Finally, significant relationships were found between various measures of plasma insulin concentration and plasma glucose response to oral glucose, plasma TG and HDL-cholesterol concentrations, and mean arterial blood pressure, independent of variations in age, body mass index, ratio of waist-to-hip girth, and UAE rates. Glucose 114-121 insulin Homo sapiens 81-88 8862124-9 1996 Finally, significant relationships were found between various measures of plasma insulin concentration and plasma glucose response to oral glucose, plasma TG and HDL-cholesterol concentrations, and mean arterial blood pressure, independent of variations in age, body mass index, ratio of waist-to-hip girth, and UAE rates. Glucose 139-146 insulin Homo sapiens 81-88 8986907-1 1996 OBJECTIVE: To investigate the glucose-independent calcium-related effects of insulin from subjects with normal and hypertensive pregnancies. Glucose 30-37 insulin Homo sapiens 77-84 8781291-1 1996 The study was performed to determine the relationship between urinary albumin excretion (UAE) and resistance to insulin-mediated glucose disposal in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 129-136 insulin Homo sapiens 112-119 8781291-2 1996 Twenty-five non-obese male patients were enrolled; UAE rates were determined on two 24-hour urine collections, and resistance to insulin-mediated glucose disposal was quantified by measurement of steady-state plasma glucose (SSPG) and steady-state plasma insulin concentrations during the last 30 minutes of a 180-minute infusion of somatostatin, insulin, and glucose. Glucose 146-153 insulin Homo sapiens 129-136 8781291-6 1996 Thus, resistance to insulin-mediated glucose disposal occurs in patients with NIDDM in the absence of microalbuminuria, and we could not detect any relationship between UAE and insulin resistance in this population. Glucose 37-44 insulin Homo sapiens 20-27 8782826-1 1996 Non-insulin dependent diabetes mellitus (NIDDM) affects more than 100 million people worldwide and is associated with severe metabolic defects, including peripheral insulin resistance, elevated hepatic glucose production, and inappropriate insulin secretion. Glucose 202-209 insulin Homo sapiens 4-11 8949587-7 1996 Control of plasma glucose requires alteration of insulin doses as pregnancy proceeds. Glucose 18-25 insulin Homo sapiens 49-56 9122011-6 1996 But significant linear correlations were found between pre-follow-up glucose and insulin and changes of daily proteinuria (r = 0.632, p < 0.05; r = 0.538, 0.05 < p < 0.1) respectively. Glucose 69-76 insulin Homo sapiens 81-88 8687515-6 1996 RESULTS: In the 11 women given metformin, the mean (+/- SE) area under the serum insulin curve after oral glucose administration decreased from 9303 +/- 1603 to 4982 +/- 911 microU per milliliter per minute (56 +/- 10 to 30 +/- 6 nmol per liter per minute) (P = 0.004). Glucose 106-113 insulin Homo sapiens 81-88 8894466-4 1996 It may be concluded then that agents which delay the absorption of glucose in the postprandial period may help to improve glycaemic control in patients with diabetes by improving the match between meal-derived glucose appearance and the period of insulin availability. Glucose 67-74 insulin Homo sapiens 247-254 8894467-11 1996 The influence of glycaemia on vagal activity and gastric emptying rate probably alters the optimal time interval between insulin injections and postprandial increases in the blood glucose concentration in patients treated with short-acting insulin administered at mealtimes. Glucose 180-187 insulin Homo sapiens 240-247 8894476-5 1996 The early phase (0-10 min) insulin secretion to intravenous glucose (300 mg kg-1) was severely impaired in NIDDM patients. Glucose 60-67 insulin Homo sapiens 27-34 8761472-8 1996 In summary, these results demonstrate: (1) that PMA and insulin stimulate PtdIns(3,4,5)P3 production by distinct mechanisms in 3T3-L1 adipocytes, and (2) that stimulation of PtdIns(3,4,5)P3 production by PMA is likely to be important in signalling pathways leading from PMA stimulation to end-point responses such as glucose transport. Glucose 317-324 insulin Homo sapiens 56-63 9095709-10 1996 Individuals treated with insulin and those who underwent major surgery were more likely to have glucose levels monitored. Glucose 96-103 insulin Homo sapiens 25-32 8770859-10 1996 Since PI 3-kinase activity is required for insulin-stimulated glucose transport, our data suggest that NO is a novel effector of insulin signaling pathways that are also involved with glucose metabolism. Glucose 62-69 insulin Homo sapiens 43-50 8770859-10 1996 Since PI 3-kinase activity is required for insulin-stimulated glucose transport, our data suggest that NO is a novel effector of insulin signaling pathways that are also involved with glucose metabolism. Glucose 62-69 insulin Homo sapiens 129-136 8761452-2 1996 Insulin caused a large stimulation of glucose transport and stimulated recruitment of transferrin receptors to the plasma membrane (PM) in these cells, whereas platelet-derived growth factor (PDGF)-bb was virtually without effect on these responses. Glucose 38-45 insulin Homo sapiens 0-7 8770012-4 1996 In contrast, intraduodenal infusion of glucose suppressed hunger, increased fullness and satiety ratings, reduced energy intake, and resulted in higher plasma insulin responses compared with the intravenous glucose infusion. Glucose 39-46 insulin Homo sapiens 159-166 8770012-5 1996 Octreotide abolished the plasma insulin response to intraduodenal glucose and reversed the changes in ratings and eating behavior. Glucose 66-73 insulin Homo sapiens 32-39 8770012-6 1996 This study has shown that the effects of intestinal glucose on appetite are not mediated via an increase in blood glucose but are likely to reflect small intestinal stimulation of release of either insulin or intestinal incretins. Glucose 52-59 insulin Homo sapiens 198-205 8770017-6 1996 We concluded that normal human subjects have a circadian rhythm of insulin secretion, which becomes more apparent with rising ISR, and that circadian changes in ISR, rising during the day and falling during the night, may be one explanation for the well-established observation that glucose tolerance and insulin responses to glucose and meals are higher in the morning than at night. Glucose 283-290 insulin Homo sapiens 67-74 8770017-6 1996 We concluded that normal human subjects have a circadian rhythm of insulin secretion, which becomes more apparent with rising ISR, and that circadian changes in ISR, rising during the day and falling during the night, may be one explanation for the well-established observation that glucose tolerance and insulin responses to glucose and meals are higher in the morning than at night. Glucose 326-333 insulin Homo sapiens 67-74 8770022-1 1996 The effects of physiological increments in epinephrine and insulin on glucose production (GP), skeletal muscle glycogen metabolism, and substrate oxidation were studied in eight insulin-dependent diabetes mellitus (IDDM) and nine control subjects. Glucose 70-77 insulin Homo sapiens 59-66 8770022-3 1996 In both groups, insulin increased glucose uptake, glycogen synthesis, and whole body carbohydrate (CHO) oxidation and inhibited GP (by 70-80%) and lipid oxidation (by approximately 50%), whereas epinephrine antagonized the effect of insulin on glucose uptake and glycogen synthesis. Glucose 34-41 insulin Homo sapiens 16-23 8770022-3 1996 In both groups, insulin increased glucose uptake, glycogen synthesis, and whole body carbohydrate (CHO) oxidation and inhibited GP (by 70-80%) and lipid oxidation (by approximately 50%), whereas epinephrine antagonized the effect of insulin on glucose uptake and glycogen synthesis. Glucose 244-251 insulin Homo sapiens 16-23 8902315-3 1996 The young subjects responded to glucose intake with a pronounced increase in MSA, a response that was blunted in the elderly and weakest in the insulin-resistant subjects. Glucose 32-39 insulin Homo sapiens 144-151 8862219-3 1996 In the subjects with a positive family history of hypertension regardless of BP levels, the basal levels and changes in insulin levels after glucose ingestion were significantly greater than those in the subjects without a family history of hypertension (F = 13.32, P = .0001). Glucose 141-148 insulin Homo sapiens 120-127 8862219-6 1996 Thus, abnormal insulin and NE responses to glucose appear to aggregate in subjects with a history of familial hypertension, regardless of the level of BP. Glucose 43-50 insulin Homo sapiens 15-29 8883708-6 1996 Both the MB ratio and FDG uptake index can be used for the simple estimation of myocardial glucose metabolism not only during fasting but also during oral glucose loading and insulin clamp, although the MB ratios at 45 min and at 55 min were slightly better than MB that at 35 min and the FDG uptake index during fasting. Glucose 91-98 insulin Homo sapiens 175-182 8874984-2 1996 Following intravenous insulin (0.1 IU/kg) administration in normal minipigs, the time for the glucose level to reach nadir (tnadir) was significantly longer in the evening than the morning [(A.M.; 30.4 (+/- 2.4) vs. Glucose 94-101 insulin Homo sapiens 22-29 8858221-8 1996 These data suggest that the glucose intolerance in gestational diabetes compared to normal pregnancy is due to reduced insulin sensitivity and an impaired ability in gestational diabetes to increase insulin secretion in response to glucose. Glucose 28-35 insulin Homo sapiens 119-126 8862952-7 1996 Changes in the ratio of proinsulin-like molecules were significantly related with those in fasting plasma glucose (r1 = 0.69, p < 0.001). Glucose 106-113 insulin Homo sapiens 24-34 8699204-3 1996 The association between insulin-mediated glucose uptake (i.e., insulin sensitivity) and blood pressure was examined among 25 nondiabetic African-American and 28 white non-Hispanic persons aged 25-44 years who ranged from normal weight to obese, using the hyperinsulinemic euglycemic clamp technique. Glucose 41-48 insulin Homo sapiens 24-31 8872059-6 1996 Thus, insulin resistance in ageing appears selective on glucose utilization, inhibition of lipolysis and feedback inhibition of the B-cell secretion. Glucose 56-63 insulin Homo sapiens 6-13 8810734-0 1996 Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity. Glucose 11-18 insulin Homo sapiens 43-50 8810734-6 1996 The insulin response to glucose in HP (area under curve = 11,460.8 +/- 1407.5 mU x min x l(-1)) was not significantly different from NS (7743.7 +/- 882.9 mU x min x l(-1)) and OB (14,504.8 +/- 1659.9 mU x min x l(-1)). Glucose 24-31 insulin Homo sapiens 4-11 8810734-8 1996 Glucose and arginine had an additive effect on insulin release in HP and NS (19,769.1 +/- 3249.6 and 10,996.6 +/- 1201.0 mU x min 1(-1), respectively) and a synergistic effect in OB (28 117.3 +/- 5224.7 mU x min x l(-1)). Glucose 0-7 insulin Homo sapiens 47-54 8810734-9 1996 In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. Glucose 61-68 insulin Homo sapiens 10-17 8810734-15 1996 The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. Glucose 112-119 insulin Homo sapiens 4-11 8698860-5 1996 During glucose infusion, glucose concentration increased from 86 +/- 2 to 228 +/- 13 mg/dl and insulin concentration increased from 6.6 +/- 0.6 to 35.0 +/- 3.9 mU/liter, both P < 0.001. Glucose 7-14 insulin Homo sapiens 95-102 8768842-9 1996 An enhanced early insulin response to glucose occurs equally in obese control (P < 0.01) and obese PCOS (P < 0.05), but not in their lean counterparts. Glucose 38-45 insulin Homo sapiens 18-25 8810935-9 1996 RESULTS: After the 160 U insulin dose the blood glucose concentration (mean +/- SE) fell from 4.3 +/- 0.2 to 2.8 +/- 0.2 mmol L-1 (P < 0.001), concomitant with an increase in mean serum insulin concentrations, rising from 9.5 +/- 1.5 to 26.1 +/- 2.5 mU L-1 (P < 0.001). Glucose 48-55 insulin Homo sapiens 25-32 8854583-0 1996 Mild insulin resistance during oral glucose tolerance test (OGTT) in women with acne. Glucose 36-43 insulin Homo sapiens 5-12 8854583-1 1996 The purpose of this study was to evaluate serum levels of basal insulin and glucose-stimulated insulin, and to evaluate their correlations with androgen levels in women with acne. Glucose 76-83 insulin Homo sapiens 95-102 8869586-0 1996 Dihydropyridine-sensitive and -insensitive voltage-operated calcium channels participate in the control of glucose-induced insulin release from human pancreatic beta cells. Glucose 107-114 insulin Homo sapiens 123-130 8869586-7 1996 However, about 20% of the glucose-induced insulin release was found to be resistant to high nitrendipine concentrations. Glucose 26-33 insulin Homo sapiens 42-49 8865083-7 1996 During PEC the maximal insulin-stimulated glucose uptake over the eccentric thigh was marginally lower when compared with the control thigh, (11.9%, 64.6 +/- 10.3 vs. 73.3 +/- 10.2 mumol kg-1 min-1, P = 0.08), whereas no inter-thigh difference was observed at a submaximal insulin concentration. Glucose 42-49 insulin Homo sapiens 23-30 8865083-11 1996 The glucose infusion rate (GIR) necessary to maintain euglycaemia during maximal insulin stimulation was lower during PEC compared with CC (15.7%, 81.3 +/- 3.2 vs. 96.4 +/- 8.8 mumol kg-1 min-1, P < 0.05). Glucose 4-11 insulin Homo sapiens 81-88 8769364-7 1996 During the treatment, plasma glucose significantly increased both at fasting and after the glucose load (basal, 5.3 +/- 0.1 v 4.9 +/- 0.2 mmol/L, P < .05; area under the curve [AUC] for OGTT, 7.7 +/- 0.3 v 6.7 +/- 0.4 mmol/L min, P < .01) without any change in plasma insulin levels. Glucose 29-36 insulin Homo sapiens 274-281 8829185-5 1996 Cultured human islets responded by a 2.2-fold increase in insulin release to a glucose challenge. Glucose 79-86 insulin Homo sapiens 58-65 8829185-10 1996 Islets exposed to BHA showed an improved glucose-induced insulin release and had an increased insulin content. Glucose 41-48 insulin Homo sapiens 57-64 9196992-2 1996 BACKGROUND: Insulin tolerance test is a simple method to measure insulin resistance that has a good correlation with glucose clamp studies. Glucose 117-124 insulin Homo sapiens 12-19 9196992-2 1996 BACKGROUND: Insulin tolerance test is a simple method to measure insulin resistance that has a good correlation with glucose clamp studies. Glucose 117-124 insulin Homo sapiens 65-72 9196992-7 1996 Insulin resistance was calculated using the slope of descending blood glucose levels (SI1). Glucose 70-77 insulin Homo sapiens 0-7 9196992-13 1996 CONCLUSIONS: Insulin tolerance test is a good method to measure insulin resistance and has a good correlation with the frequently sampled intravenous glucose tolerance test. Glucose 150-157 insulin Homo sapiens 13-20 8751600-8 1996 Infusion of 16.7 mmol/L glucose significantly stimulated insulin secretion before and after NMMA infusion, but there was no significant difference seen with insulin secretion before and after NMMA infusion. Glucose 24-31 insulin Homo sapiens 57-64 8967027-15 1996 Amylin reduces in the muscle, probably by inhibition of glycogen synthase, the insulin stimulated non-oxidative utilization of glucose into muscle glycogen and conversely by stimulation of phosphorylase it stimulates glycogenolysis and thus also lactate production and gluconeogenesis in the liver which all are anti-insulin effects which intensify the insulin resistance of the main target tissues. Glucose 127-134 insulin Homo sapiens 79-86 8663361-0 1996 Okadaic acid exerts a full insulin-like effect on glucose transport and glucose transporter 4 translocation in human adipocytes. Glucose 50-57 insulin Homo sapiens 27-34 8663361-3 1996 Okadaic acid consistently produced a greater increase than insulin in the rate of glucose transport, and both agents together had a partial additive effect. Glucose 82-89 insulin Homo sapiens 59-66 8663361-5 1996 Insulin, but not okadaic acid, stimulated phosphatidylinositol 3-kinase (PI 3-kinase) activity, and wortmannin completely inhibited the effect of insulin on glucose transport. Glucose 157-164 insulin Homo sapiens 146-153 8663368-0 1996 Reversible Ca2+-dependent translocation of protein kinase C and glucose-induced insulin release. Glucose 64-71 insulin Homo sapiens 80-87 8663368-2 1996 Nevertheless, there is still controversy concerning the importance of this enzyme in glucose-induced insulin release. Glucose 85-92 insulin Homo sapiens 101-108 8663368-7 1996 Cells pretreated with TPA demonstrated increased insulin secretion in response to glucose for several hours. Glucose 82-89 insulin Homo sapiens 49-56 8663584-1 1996 To elucidate the mechanisms of phosphatidylinositol (PI) 3-kinase involvement in insulin-stimulated glucose transport activity, the epitope-tagged p110alpha subunit of PI 3-kinase was overexpressed in 3T3-L1 adipocytes using an adenovirus-mediated gene transduction system. Glucose 100-107 insulin Homo sapiens 81-88 8663584-8 1996 These findings indicate that an increment in PI 3-kinase activity induced by overexpression of p110alpha of PI 3-kinase stimulates glucose transport activity with translocation of glucose transporters, i.e., mimics the effect of insulin. Glucose 131-138 insulin Homo sapiens 229-236 8755501-4 1996 When the muscle cell is exposed to conditions which favor glycogen synthesis such as high plasma insulin and glucose concentrations the fractional activity of GSase is increased in coordination with increases in the activity of glucose transport and hexokinase. Glucose 228-235 insulin Homo sapiens 97-104 8837313-7 1996 Stimulated levels of insulin during glucose tolerance test also significantly decreased by lisinopril (peak insulin from 57 +/- 10 to 41.2 +/- 7.3 uU/ml, p < or = 0.02). Glucose 36-43 insulin Homo sapiens 21-28 8663315-3 1996 Insulin induces HKII gene transcription in L6 myotubes, and this, in turn, increases HKII mRNA and the rates of HKII protein synthesis and glucose phosphorylation in these cells. Glucose 139-146 insulin Homo sapiens 0-7 8669419-8 1996 After 112 g oral glucose, increments in energy expenditure were significantly greater during isoenergetic feeding with insulin than without (7.5 +/- 1.3% compared with 4.3 +/- 0.9% above REE) and after the VLED (10.5 +/- 1.0% above REE, P < 0.05). Glucose 17-24 insulin Homo sapiens 119-126 8669419-12 1996 Cumulative nonoxidative glucose disposal (stored glucose) was higher with insulin therapy than without (52 +/- 6 compared with 35 +/- 7 g/210 min, P < 0.05) and increased significantly to 66 +/- 6 g after the VLED (compared with the isoenergetic diet without insulin). Glucose 24-31 insulin Homo sapiens 74-81 8669419-12 1996 Cumulative nonoxidative glucose disposal (stored glucose) was higher with insulin therapy than without (52 +/- 6 compared with 35 +/- 7 g/210 min, P < 0.05) and increased significantly to 66 +/- 6 g after the VLED (compared with the isoenergetic diet without insulin). Glucose 49-56 insulin Homo sapiens 74-81 8669419-15 1996 The greater TEF was associated with a greater insulin response, which was probably responsible for the greater stored glucose. Glucose 118-125 insulin Homo sapiens 46-53 8760075-3 1996 In the case of insulin-activated glucose transport, this translocation has been proven to be the major, if not the only regulatory mechanism of this process. Glucose 33-40 insulin Homo sapiens 15-22 8760075-9 1996 In skeletal muscle, two independent populations of GLUT-4-containing vesicles are found, insulin sensitive and exercise sensitive, which explains the additive effect of insulin and exercise on glucose uptake. Glucose 193-200 insulin Homo sapiens 89-96 8760075-9 1996 In skeletal muscle, two independent populations of GLUT-4-containing vesicles are found, insulin sensitive and exercise sensitive, which explains the additive effect of insulin and exercise on glucose uptake. Glucose 193-200 insulin Homo sapiens 169-176 8760081-5 1996 Insulin-stimulated glucose transport was decreased in denervated muscles (P < 0.05). Glucose 19-26 insulin Homo sapiens 0-7 8760081-7 1996 The increase in basal glucose transport was correlated with the loss of insulin-stimulated transport (r = 0.95). Glucose 22-29 insulin Homo sapiens 72-79 8760081-8 1996 Thus the increase in GLUT-1 compensates for the loss of GLUT-4, resulting in a 56% regain of the reduced insulin-stimulated glucose transport. Glucose 124-131 insulin Homo sapiens 105-112 8680675-3 1996 In vivo insulin action with determination of steady-state plasma glucose (SSPG) and insulin was measured using simultaneous intravenous infusion of somatostatin, glucose, and insulin via a Harvard pump. Glucose 65-72 insulin Homo sapiens 8-15 8680675-3 1996 In vivo insulin action with determination of steady-state plasma glucose (SSPG) and insulin was measured using simultaneous intravenous infusion of somatostatin, glucose, and insulin via a Harvard pump. Glucose 162-169 insulin Homo sapiens 8-15 9035467-9 1996 The insulin response to glucose index increased in the Cp (0.28 vs 0.40; p < 0.05) group but not in the CLH (0.25 vs 0.42; NS) and CLN (0.07 vs 0.24). Glucose 24-31 insulin Homo sapiens 4-11 9035467-10 1996 CONCLUSION: The antihypertensive therapy with chlortalidone in essential hypertensive patients may result in reductions in the peripheral sensitivity to insulin that can be accompanied by increases in glycemic levels after oral glucose load, particularly in patients who develop hypocalemia. Glucose 228-235 insulin Homo sapiens 153-160 9035467-11 1996 Our results indicate that Cp therapy induces increments in insulin response to glucose without detectable changes in peripheral insulin sensitivity. Glucose 79-86 insulin Homo sapiens 59-66 8813781-8 1996 Thus, an infusion of glucose (and the associated physiological increase in the concentration of insulin) at doses commonly used in parenteral nutrition does not influence the rate of elimination of triglycerides from plasma in normal subjects. Glucose 21-28 insulin Homo sapiens 96-103 8832156-3 1996 In moderate and severe hyperkalemia infusion of glucose with insulin has been regarded as the standard medical treatment so far. Glucose 48-55 insulin Homo sapiens 61-68 8666137-6 1996 The percentage rate of glucose clearance per minute (KITT) during intravenous insulin sensitivity tests was identical in the CDP571 and placebo groups at baseline and also at 1 and 4 weeks after treatment (mean +/- SE; CDP571: 1.33 +/- 0.21, 1.44 +/- 0.25, 1.26 +/- 0.18; placebo: 1.38 +/- 0.15, 1.47 +/- 0.20, 1.52 +/- 0.20; P = 0.85, 0.93, and 0.36, respectively). Glucose 23-30 insulin Homo sapiens 78-85 8666140-4 1996 Expressions of insulin and PC3, but not PC2, are coordinately regulated by glucose, consistent with the important role of PC3 in regulating proinsulin processing. Glucose 75-82 insulin Homo sapiens 15-22 8666143-0 1996 Roles of glucose transport and glucose phosphorylation in muscle insulin resistance of NIDDM. Glucose 9-16 insulin Homo sapiens 65-72 8666143-0 1996 Roles of glucose transport and glucose phosphorylation in muscle insulin resistance of NIDDM. Glucose 31-38 insulin Homo sapiens 65-72 8666143-10 1996 These data suggest that when assessed in vivo, both transmembrane transport and intracellular phosphorylation of glucose are refractory to insulin action and add to each other in determining insulin resistance in skeletal muscle of NIDDM patients. Glucose 113-120 insulin Homo sapiens 191-198 8666154-6 1996 Marked alterations in plasma glucose and insulin concentrations induced by glucose and tolbutamide injection did not cause any change in plasma leptin levels. Glucose 75-82 insulin Homo sapiens 41-48 8674890-3 1996 Investigators have shown that insulin regulates VSM intracellular cation metabolism through attenuating effects on inward calcium (Ca2+) currents and by direct effects on VSM cells (VSMCs) Na+, K(+)-ATPase pump expression and activity and that insulin and IGF-I stimulate glucose uptake in VSMCs. Glucose 272-279 insulin Homo sapiens 30-37 8674891-3 1996 In subjects with nonobese and nondiabetic essential hypertension, steady-state plasma glucose (SSPG) was higher than in normotensive subjects during an insulin sensitivity test, indicating reduced insulin sensitivity to glucose metabolism in the hypertensive group. Glucose 86-93 insulin Homo sapiens 197-204 8674891-3 1996 In subjects with nonobese and nondiabetic essential hypertension, steady-state plasma glucose (SSPG) was higher than in normotensive subjects during an insulin sensitivity test, indicating reduced insulin sensitivity to glucose metabolism in the hypertensive group. Glucose 220-227 insulin Homo sapiens 197-204 8674893-6 1996 The mean insulin response during an oral glucose tolerance test was also significantly decreased (258.6 +/- 26.4 to 181.8 +/- 6.6 pmol/l, P < 0.05). Glucose 41-48 insulin Homo sapiens 9-16 8799647-0 1996 Metformin potentiates glucose-stimulated insulin secretion. Glucose 22-29 insulin Homo sapiens 41-48 8800555-7 1996 Potential use in fluorescence imaging and metabolic studies is shown with DNA synthesis, cell replication, cell substratum attachment, 32P-ATP phosphorylation, and insulin-mediated increases in glucose uptake and its suppression by antiphosphotyrosine and antiglucose transporter protein antibodies. Glucose 194-201 insulin Homo sapiens 164-171 8817110-3 1996 During insulin infusion the arterial glucose level was reduced in parallel and the hypoglycaemic nadir was almost identical in the two groups (diabetic patients 2.2 +/- 0.1 and control subjects 2.3 +/- 0.1 mmol/l). Glucose 37-44 insulin Homo sapiens 7-14 8840095-7 1996 Following the injection of insulin lispro the area under the blood glucose curve after the meal was 78% of that of regular insulin (1.76 +/- 0.34 vs 2.26 +/- 0.68 mol l-1 *240 min-1; p < 0.01). Glucose 67-74 insulin Homo sapiens 27-34 8840098-1 1996 It has been suggested that kallikrein-kinin system may influence carbohydrate metabolism via a kinin-mediated increment of insulin-mediated glucose uptake. Glucose 140-147 insulin Homo sapiens 123-130 8840098-6 1996 Thus, in spite of the suggested positive effects of kinins on insulin-mediated glucose uptake, acute inhibition of the kallikrein-kinins system resulted in a paradoxical increment of insulin sensitivity, which was probably mediated by the reduced metabolic clearance rate of insulin. Glucose 79-86 insulin Homo sapiens 62-69 8706703-2 1996 Insulin stimulates glucose uptake by induction of the translocation of vesicles that contain the glucose transporter Glut 4 to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 8706703-3 1996 Phosphatidylinositol 3-kinase (PtdIns 3-kinase), which is thought to be involved in intracellular trafficking, could play a critical role in insulin-induced glucose transport. Glucose 157-164 insulin Homo sapiens 141-148 8706703-4 1996 In 3T3-L1 adipocytes, insulin and platelet-derived-growth-factor (PDGF) stimulated glucose uptake by 5.8-fold and 2.4-fold, respectively, but PDGF had no significant effect on Glut 4 translocation. Glucose 83-90 insulin Homo sapiens 22-29 8706703-11 1996 We would like to suggest that a crucial event in the stimulation of glucose uptake by insulin could be that insulin, but not PDGF, induces activation of PtdIns 3-kinase in the cytosol and in LDM, the compartment enriched in Glut-4-containing vesicles. Glucose 68-75 insulin Homo sapiens 86-93 8706703-11 1996 We would like to suggest that a crucial event in the stimulation of glucose uptake by insulin could be that insulin, but not PDGF, induces activation of PtdIns 3-kinase in the cytosol and in LDM, the compartment enriched in Glut-4-containing vesicles. Glucose 68-75 insulin Homo sapiens 108-115 8770928-1 1996 Neurotransmitters and hormones, by binding to receptors linked to adenylate cyclase or phospholipase C (PLC), increase cytosolic free Ca2+ and potentiate glucose-induced insulin release from beta-cells. Glucose 154-161 insulin Homo sapiens 170-177 8770928-4 1996 Forskolin also potentiates AVP- or bombesin-induced insulin secretion from populations of HIT cells in the presence of elevated glucose (10 mM). Glucose 128-135 insulin Homo sapiens 52-59 8770928-6 1996 Physiologically, synergistic cross-signaling between the cAMP- and Ca2+ -phosphoinositide signaling pathway could be important for the regulation of insulin release under conditions where extracellular glucose is high and beta-cells are exposed to multiple stimuli activating adenylate cyclase or PLC at the same time. Glucose 202-209 insulin Homo sapiens 149-156 8864417-4 1996 Following glucose ingestion, patients and controls showed similar insulin and glucose responses. Glucose 10-17 insulin Homo sapiens 66-73 8864417-5 1996 Insulin infusion (7 pmol min-1 kg-1) promoted similar glucose utilization in the hypertensives and normotensives: 24.8 +/- 2.3 vs. 26.0 +/- 3.0 mumol min-1 kg-1 respectively. Glucose 54-61 insulin Homo sapiens 0-7 8858409-3 1996 Thirty min prior to exercise, they ingested 1 g.kg-1 body weight of GL, WS, RS, or PL At rest, GL elicited greater (p < 0.05) serum glucose and insulin responses than all other trials. Glucose 95-97 insulin Homo sapiens 147-154 8828680-6 1996 Oral glucose tolerance tests showed significant reductions in insulin responses in the AEX, WL, and AEX+WL groups, but the decrease in insulin response in the AEX+WL group was significantly greater than that in the other three groups. Glucose 5-12 insulin Homo sapiens 62-69 8828680-8 1996 There were significant increases in insulin-mediated glucose disposal rates as measured by the hyperinsulinemic (600 pmol.m-2.min-1) euglycemic clamps in the AEX and AEX+WL groups [1.66 +/- 0.50 and 1.76 +/- 0.41 mg.kg fat-free mass (FFM)-1.min-1, respectively] that were significantly greater than those in the WL (0.13 +/- 0.31 mg.kg FFM-1.min-1) and Con groups (-0.05 +/- 0.51 mg.kg FFM-1.min-1; n = 5). Glucose 53-60 insulin Homo sapiens 36-43 8675555-11 1996 Insulin to glucose and C peptide to glucose ratios improved maximally at 1 week, indicating rapid reversal of glucotoxicity on the beta-cell. Glucose 11-18 insulin Homo sapiens 0-7 8675570-5 1996 Insulin sensitivity was evaluated by the hyperinsulinemic euglycemic clamp technique expressed as the glucose infusion rate (GIR) before and after the treatment. Glucose 102-109 insulin Homo sapiens 0-7 8675576-0 1996 Gemfibrozil treatment of endogenous hypertriglyceridemia: effect on insulin-mediated glucose disposal and plasma insulin concentrations. Glucose 85-92 insulin Homo sapiens 68-75 8866300-15 1996 This abnormal pattern of glucose control may represent poorly regulated release of endogenous insulin. Glucose 25-32 insulin Homo sapiens 94-101 8686691-9 1996 Similar associations between insulin and coronary disease events were seen in men with and without evidence of coronary disease at screening and in men with baseline serum glucose below the 80th percentile. Glucose 172-179 insulin Homo sapiens 29-36 8675587-10 1996 Insulin sensitivity x insulin area as an estimate of insulin-dependent glucose uptake and insulin"s action to suppress hepatic glucose production decreased significantly in the high-dose group (0.588 +/- 0.112 to 0.441 +/- 0.073, P < 0.05), but did not change in the low-dose group (0.436 +/- 0.050 to 0.484 +/- 0.032, P = 0.77). Glucose 71-78 insulin Homo sapiens 0-7 8675587-10 1996 Insulin sensitivity x insulin area as an estimate of insulin-dependent glucose uptake and insulin"s action to suppress hepatic glucose production decreased significantly in the high-dose group (0.588 +/- 0.112 to 0.441 +/- 0.073, P < 0.05), but did not change in the low-dose group (0.436 +/- 0.050 to 0.484 +/- 0.032, P = 0.77). Glucose 71-78 insulin Homo sapiens 22-29 8680988-15 1996 Training increases overall insulin action on glucose clearance in skeletal muscle identically in aged and young subjects. Glucose 45-52 insulin Homo sapiens 27-34 8827527-0 1996 Hyperinsulinemia and insulin resistance are associated with multiple abnormalities of lipoprotein subclasses in glucose-tolerant relatives of NIDDM patients. Glucose 112-119 insulin Homo sapiens 5-12 8685947-6 1996 Insulin output, stimulated by oral glucose tolerance tests and assessed by the ratio of AUC insulin to AUC glucose, fell gradually after transplantation and was decreased by an elevated serum calcium level and high cyclosporine dose. Glucose 107-114 insulin Homo sapiens 0-7 8685947-7 1996 The ratio of fasting insulin to glucose, which acts as a marker of peripheral insulin resistance, fell with time after transplantation and was increased by greater body weight, higher prednisolone dose, and lower cyclosporine dose. Glucose 32-39 insulin Homo sapiens 78-85 8699204-3 1996 The association between insulin-mediated glucose uptake (i.e., insulin sensitivity) and blood pressure was examined among 25 nondiabetic African-American and 28 white non-Hispanic persons aged 25-44 years who ranged from normal weight to obese, using the hyperinsulinemic euglycemic clamp technique. Glucose 41-48 insulin Homo sapiens 63-70 8675698-5 1996 Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation. Glucose 130-137 insulin Homo sapiens 111-118 8675680-7 1996 Insulin stimulation of the rate constant for glucose phosphorylation was similar in obese and lean subjects but reduced in NIDDM. Glucose 45-52 insulin Homo sapiens 0-7 8783770-7 1996 It is concluded that patients with congenital generalized lipodystrophy may present severe insulin resistance with regard to hepatic glucose production as well as muscle glycogen synthesis and lipid oxidation. Glucose 133-140 insulin Homo sapiens 91-98 8672547-0 1996 In vitro effect of adenosine agonist GR79236 on the insulin sensitivity of glucose utilisation in rat soleus and human rectus abdominus muscle. Glucose 75-82 insulin Homo sapiens 52-59 8644691-0 1996 Relation between dietary vitamin intake and resistance to insulin-mediated glucose disposal in healthy volunteers. Glucose 75-82 insulin Homo sapiens 58-65 8644690-1 1996 We aimed to study the effects of chronic ingestion of short-chain fructooligosaccharides (FOS), an indigestible carbohydrate, on hepatic glucose production, insulin-mediated glucose metabolism, erythrocyte insulin binding, and blood lipids in healthy subjects. Glucose 174-181 insulin Homo sapiens 157-164 8644691-1 1996 The relation between the self-reported intake of various dietary constituents and insulin-mediated glucose disposal was evaluated in 52 healthy volunteers. Glucose 99-106 insulin Homo sapiens 82-89 8644691-2 1996 Insulin-mediated glucose uptake was independently associated with degree of obesity (inversely) and estimates of level of physical activity (directly). Glucose 17-24 insulin Homo sapiens 0-7 8644691-3 1996 An independent relation between increased intake of vitamin A and insulin action was shown, ie, the greater the intake of vitamin A, the more effective was insulin in stimulating glucose disposal. Glucose 179-186 insulin Homo sapiens 66-73 8644691-3 1996 An independent relation between increased intake of vitamin A and insulin action was shown, ie, the greater the intake of vitamin A, the more effective was insulin in stimulating glucose disposal. Glucose 179-186 insulin Homo sapiens 156-163 8644691-5 1996 These results suggest that vitamin A intake, but not intakes of vitamin C and E, fiber, fat, or carbohydrate is associated with enhanced insulin-mediated glucose disposal. Glucose 154-161 insulin Homo sapiens 137-144 8783787-8 1996 We conclude that preeclampsia is associated with marked hyperinsulinemia both in the fasting state and after oral glucose ingestion, suggesting that insulin resistance may play a role in pregnancy-induced hypertension. Glucose 114-121 insulin Homo sapiens 61-68 8818516-1 1996 Resistance to insulin-stimulated glucose uptake and to insulin suppression of free fatty acids is related to numerous lipid and lipoprotein abnormalities that increase risk for coronary heart disease. Glucose 33-40 insulin Homo sapiens 14-21 8712258-3 1996 The analysis is achieved by equating curves representing both the inflow and outflow of glucose from the circulation as dependent upon the serum insulin concentration. Glucose 88-95 insulin Homo sapiens 145-152 8805995-2 1996 Serum insulin was measured 2 h after a nonfasting oral glucose load in subjects not using antidiabetes medication. Glucose 55-62 insulin Homo sapiens 6-13 8635661-3 1996 The two nucleotide-binding fold (NBF) regions of SUR are known to be critical for normal glucose regulation of insulin secretion. Glucose 89-96 insulin Homo sapiens 111-118 8635647-6 1996 Subjects received a standard 2-h oral glucose tolerance test on the first day and an insulin-modified frequently sampled intravenous glucose tolerance test on the second day. Glucose 133-140 insulin Homo sapiens 85-92 8635649-7 1996 In 1993, men with the lowest glucose versus those with the highest glucose had a lower waist-to-hip ratio, plasma HbA1c, fasting and postload insulin and glucose values, and a higher insulin sensitivity index. Glucose 29-36 insulin Homo sapiens 142-149 8635649-7 1996 In 1993, men with the lowest glucose versus those with the highest glucose had a lower waist-to-hip ratio, plasma HbA1c, fasting and postload insulin and glucose values, and a higher insulin sensitivity index. Glucose 29-36 insulin Homo sapiens 183-190 8641194-3 1996 IGF-II peptide binds weakly to the insulin receptor and exerts insulin-like effects on the blood glucose level. Glucose 97-104 insulin Homo sapiens 63-70 8697303-8 1996 Glucose modulates insulin gene transcription, with multiple elements of the promoter involved in glucose responsiveness. Glucose 0-7 insulin Homo sapiens 18-25 8725857-13 1996 This was achieved with insulin concentrations three- to fivefold higher than normal, suggesting significant insulin resistance for both glucose and protein metabolism in GDM. Glucose 136-143 insulin Homo sapiens 108-115 8725869-4 1996 Proinsulin response to intravenous glucose decreased in NIDDM patients with ICAs (from 35.6 +/- 6.2 to 13.5 +/- 5.4 pmol/l, P < 0.05), but remained unchanged in those without ICAs. Glucose 35-42 insulin Homo sapiens 0-10 8725869-5 1996 At 3 years after diagnosis, fasting proinsulin (10.0 +/- 3.7 vs. 59.1 +/- 17.0 pmol/l) and proinsulin responses to intravenous glucose (13.5 +/- 5.4 vs. 103.9 +/- 35.1 pmol/l) and to intravenous glucagon (7.4 +/- 3.9 vs. 36.0 +/- 7.7 pmol/l) were much lower (P < 0.01) in NIDDM patients with ICAs than in those without ICAs. Glucose 127-134 insulin Homo sapiens 91-101 8799655-5 1996 Thirty-six percent of all study participants were making adjustments to their insulin dose in response to these changes in capillary blood glucose. Glucose 139-146 insulin Homo sapiens 78-85 8877277-4 1996 In the (h) group, but not in the (h + d) group, the drug caused reduction of the glucose-dependent increases in serum IRI and CP, more marked with respect to CP, as expressed by the decrease in the molar serum CP/IRI ratio. Glucose 81-88 insulin Homo sapiens 126-128 8877277-6 1996 In patients with type 2 diabetes, this phenomenon does not become manifest because of absence or reduction in the early glucose-dependent insulin release. Glucose 120-127 insulin Homo sapiens 138-145 8789768-1 1996 UNLABELLED: Hyperkalaemia is a life-threatening emergency and infusion of glucose with insulin has so far been regarded as the standard treatment of choice. Glucose 74-81 insulin Homo sapiens 87-94 9240760-4 1996 Insulin sensitivity was determined using glucose-clamp method or glucose, insulin, and somatostatin infusion method. Glucose 41-48 insulin Homo sapiens 0-7 9240760-4 1996 Insulin sensitivity was determined using glucose-clamp method or glucose, insulin, and somatostatin infusion method. Glucose 65-72 insulin Homo sapiens 0-7 9240760-6 1996 Insulin induced glucose clearance was significantly decreased in subjects developed hypertension (30 +/- 12 ml/kg/10 min) than in subjects remained normotensive (50 +/- 19 ml/kg/10 min). Glucose 16-23 insulin Homo sapiens 0-7 9240767-3 1996 To investigate the organ-specific insulin action on glucose homeostasis, we developed an innovative non-invasive method, using an euglycemic hyperinsulinemic clamp combined with oral glucose load. Glucose 52-59 insulin Homo sapiens 34-41 9240767-3 1996 To investigate the organ-specific insulin action on glucose homeostasis, we developed an innovative non-invasive method, using an euglycemic hyperinsulinemic clamp combined with oral glucose load. Glucose 183-190 insulin Homo sapiens 34-41 9240769-3 1996 Intra-abdominal fat area was correlated with insulin concentration at 120 min in oral glucose tolerance tests and triglyceride level in male, on the other hand, in female were HDL-cholesterol level, apolipoprotein B, glucose area under curve and insulin concentration at 60 and 120 min. Glucose 86-93 insulin Homo sapiens 45-52 8697303-8 1996 Glucose modulates insulin gene transcription, with multiple elements of the promoter involved in glucose responsiveness. Glucose 97-104 insulin Homo sapiens 18-25 8697303-9 1996 Remarkably, IPF-1 and IEF1 are involved in both beta-cell-specific expression and glucose regulation of the insulin gene. Glucose 82-89 insulin Homo sapiens 108-115 8697308-4 1996 The most notable results involved a significantly faster time-course of glucose infusion rates during the first 30 min of each insulin infusion period [analysed by calculating slopes (S1 and S2)] after ramipril than placebo administration. Glucose 72-79 insulin Homo sapiens 127-134 8964865-0 1996 Ethanol impairs insulin-mediated glucose uptake by an indirect mechanism. Glucose 33-40 insulin Homo sapiens 16-23 8964837-9 1996 Added NPY (100 nmol/L) decreased (P = 0.001) glucose-stimulated (8 mmol/L) insulin release from the human islets by 45% in a perfusion system. Glucose 45-52 insulin Homo sapiens 75-82 8807554-1 1996 The work presents the results of researches of binding and degradation of 125I-Insulin by erythrocyte receptors in the patients with essential hypertension and healthy patients after glucose intake. Glucose 183-190 insulin Homo sapiens 79-86 8637438-4 1996 Insulin-stimulated glucose uptake in isolated adipocytes harvested from a presternal fat biopsy was significantly greater following the LGI diet (P < .05). Glucose 19-26 insulin Homo sapiens 0-7 8637450-1 1996 The rate of insulin-stimulated glucose disposal is reduced in individuals with insulin resistance, and is associated with a blunted or absent increase in energy expenditure in response to a glucose load. Glucose 31-38 insulin Homo sapiens 12-19 8637450-1 1996 The rate of insulin-stimulated glucose disposal is reduced in individuals with insulin resistance, and is associated with a blunted or absent increase in energy expenditure in response to a glucose load. Glucose 31-38 insulin Homo sapiens 79-86 8637450-1 1996 The rate of insulin-stimulated glucose disposal is reduced in individuals with insulin resistance, and is associated with a blunted or absent increase in energy expenditure in response to a glucose load. Glucose 190-197 insulin Homo sapiens 12-19 9026680-5 1996 However, the addition of bed-time ultralent insulin caused a greater and significant decrease in post prandial plasma glucose. Glucose 118-125 insulin Homo sapiens 44-51 8637450-9 1996 The data indicate that the glucose effect on energy expenditure was slightly positive in the more insulin-sensitive individuals, but negative in the more insulin-resistant subjects. Glucose 27-34 insulin Homo sapiens 98-105 8637450-9 1996 The data indicate that the glucose effect on energy expenditure was slightly positive in the more insulin-sensitive individuals, but negative in the more insulin-resistant subjects. Glucose 27-34 insulin Homo sapiens 154-161 8637455-5 1996 Tissue sensitivity to insulin in the whole body was expressed as the glucose infusion rate (M value) and that divided by steady-state plasma insulin levels (M/I ratio) during the last 30 minutes of the clamp. Glucose 69-76 insulin Homo sapiens 22-29 9026680-6 1996 In contrast, the average fasting plasma glucose decrease was significantly greater after NPH insulin administration. Glucose 40-47 insulin Homo sapiens 93-100 9026680-7 1996 These results indicate that in NIDDM patients with secondary failure to glyburide bed-time ultralent insulin administration is a better tool to improve the post prandial plasma glucose. Glucose 177-184 insulin Homo sapiens 101-108 8636416-6 1996 A delayed pattern of insulin delivery (i.e., a "diabetic" insulin profile) led to higher (P < 0.05) glucose concentrations in all groups; however, the effects were transient, resulting in only a modest increase in the integrated glycemic responses. Glucose 103-110 insulin Homo sapiens 21-28 9005421-19 1996 Among them one can see subjects with normal glucose tolerance that is accompanied with high serum C-peptide and insulin concentration. Glucose 44-51 insulin Homo sapiens 112-119 8638204-4 1996 During an insulin-modified frequently sampled intravenous glucose tolerance test, the first phase of insulin release in response to the administration of glucose was blunted. Glucose 58-65 insulin Homo sapiens 10-17 8638204-4 1996 During an insulin-modified frequently sampled intravenous glucose tolerance test, the first phase of insulin release in response to the administration of glucose was blunted. Glucose 58-65 insulin Homo sapiens 101-108 8638204-4 1996 During an insulin-modified frequently sampled intravenous glucose tolerance test, the first phase of insulin release in response to the administration of glucose was blunted. Glucose 154-161 insulin Homo sapiens 10-17 8638204-4 1996 During an insulin-modified frequently sampled intravenous glucose tolerance test, the first phase of insulin release in response to the administration of glucose was blunted. Glucose 154-161 insulin Homo sapiens 101-108 8641378-0 1996 Some thoughts on the importance of insulin in the regulation of the blood glucose level. Glucose 74-81 insulin Homo sapiens 35-42 8641378-1 1996 Insulin can influence rates of glucose utilization by muscle and possibly other tissues via both direct and indirect effects. Glucose 31-38 insulin Homo sapiens 0-7 8641378-3 1996 Insulin may influence the levels of insulin-like growth factors I and II, both of which have effects on rates of glucose utilization by muscle. Glucose 113-120 insulin Homo sapiens 0-7 8641378-4 1996 The inter-tissue cycle between glucose and lactate-the Cori cycle, which is influenced by insulin-may provide another novel mechanism for control of blood glucose. Glucose 31-38 insulin Homo sapiens 90-97 8641378-4 1996 The inter-tissue cycle between glucose and lactate-the Cori cycle, which is influenced by insulin-may provide another novel mechanism for control of blood glucose. Glucose 155-162 insulin Homo sapiens 90-97 8641379-1 1996 For better comprehension of the metabolic syndrome, it is necessary to differentiate the effect of insulin on glucose metabolism on the one hand, and on other metabolic activities on the other hand. Glucose 110-117 insulin Homo sapiens 99-106 8641379-2 1996 Whereas glucose utilization is affected by insulin resistance, the effect of insulin on lipid metabolism, ion and aminoacid transport does not seem to be diminished. Glucose 8-15 insulin Homo sapiens 43-50 8641379-7 1996 The increased plasma free fatty acid level then results in insulin resistance affecting glucose metabolism. Glucose 88-95 insulin Homo sapiens 59-66 8641379-9 1996 Induction of insulin resistance results in higher glucose levels, which may cause hyperinsulinemia. Glucose 50-57 insulin Homo sapiens 13-20 8641379-11 1996 When diabetes becomes overt and elevated glucose levels prevail, the hyperinsulinism acts on the metabolic pathways which are still sensitive to insulin, namely lipid metabolism, aminoacid transport and ion transport. Glucose 41-48 insulin Homo sapiens 74-81 8626671-1 1996 Okadaic acid has been described previously as being a negative regulator of insulin signaling, as it inhibits insulin stimulation of glucose transport. Glucose 133-140 insulin Homo sapiens 76-83 8626671-1 1996 Okadaic acid has been described previously as being a negative regulator of insulin signaling, as it inhibits insulin stimulation of glucose transport. Glucose 133-140 insulin Homo sapiens 110-117 8643546-1 1996 Pancreatic beta cells exhibit oscillations in electrical activity, cytoplasmic free Ca2+ concentration ([Ca2+](i)), and insulin release upon glucose stimulation. Glucose 141-148 insulin Homo sapiens 120-127 8795087-4 1996 The levels of glucose-stimulated insulin release from NOD mouse islets increased after tissue culture, whereas it remained unchanged in NMRI mouse islets. Glucose 14-21 insulin Homo sapiens 33-40 8795087-8 1996 At a later stage of advanced insulitis (12-15 weeks) also the basal IAPP/insulin secretory ratio at low glucose tended to decline. Glucose 104-111 insulin Homo sapiens 73-80 8736826-0 1996 Effect of insulin on glucose transport in adipose tissue in lactation. Glucose 21-28 insulin Homo sapiens 10-17 8653871-8 1996 During insulin clamping, a striking increase in glucose uptake by insulin was obtained in both the dysfunctional and the normal regions (72 +/- 22 and 79 +/- 21 micromol/100 g per minute, respectively; P<.001, fasting versus clamping). Glucose 48-55 insulin Homo sapiens 7-14 8653871-8 1996 During insulin clamping, a striking increase in glucose uptake by insulin was obtained in both the dysfunctional and the normal regions (72 +/- 22 and 79 +/- 21 micromol/100 g per minute, respectively; P<.001, fasting versus clamping). Glucose 48-55 insulin Homo sapiens 66-73 8653871-9 1996 CONCLUSIONS: Contrary to previous suggestions, glucose uptake can be increased strikingly by insulin in chronically dysfunctional but viable myocardium. Glucose 47-54 insulin Homo sapiens 93-100 8653871-10 1996 This demonstrates that insulin control over glucose uptake is preserved in the dysfunctional myocardium and provides a rational basis for metabolic intervention. Glucose 44-51 insulin Homo sapiens 23-30 8621019-8 1996 Increased insulin-stimulated glycogen synthesis accounted for >80% of the increased Rd with vanadyl sulfate (P < 0.005), but plasma glucose flux via glycolysis was unchanged. Glucose 138-145 insulin Homo sapiens 10-17 8621023-5 1996 Insulin action was assessed prevailing fasting glucose levels before and after hype insulinemia (2-h insulin infusion at 2.0 mU / kg / min). Glucose 47-54 insulin Homo sapiens 0-7 8621023-8 1996 During the 2.0 mU insulin infusion, glucose clearance was lower in the diabetic subjects (3.6 +/- 0.7 vs. 6.9 +/- 0.5 ml / kg / min), P < 0.05), whereas endogenous glucose production was suppressed to a similar degree in both groups (4.5 +/- 0.8 vs. 3.6 +/- 0.7 micromol x kg(-1) x min(-1), NS). Glucose 36-43 insulin Homo sapiens 18-25 8665779-9 1996 We conclude that insulin resistance of glucose uptake observed in the forearm of obese subjects is not evident in adipose tissue. Glucose 39-46 insulin Homo sapiens 17-24 8665779-10 1996 Adipose tissue glucose uptake in obese, insulin-resistant subjects is similar to that in lean control subjects, although it occurs at elevated circulating insulin and glucose concentrations. Glucose 15-22 insulin Homo sapiens 40-47 8665779-10 1996 Adipose tissue glucose uptake in obese, insulin-resistant subjects is similar to that in lean control subjects, although it occurs at elevated circulating insulin and glucose concentrations. Glucose 15-22 insulin Homo sapiens 155-162 8665779-10 1996 Adipose tissue glucose uptake in obese, insulin-resistant subjects is similar to that in lean control subjects, although it occurs at elevated circulating insulin and glucose concentrations. Glucose 167-174 insulin Homo sapiens 40-47 8725774-2 1996 However, transformed cells are generally glucose hypersensitive, i.e. insulin secretion is near maximal at much lower than physiological glucose levels. Glucose 41-48 insulin Homo sapiens 70-77 8725774-2 1996 However, transformed cells are generally glucose hypersensitive, i.e. insulin secretion is near maximal at much lower than physiological glucose levels. Glucose 137-144 insulin Homo sapiens 70-77 8732718-4 1996 RESULTS: After glucose load, insulin increased more significantly in hypertensive subjects than in normotensive subjects at times 60 (P = 0.004) and 90 (P = 0.001) min. Glucose 15-22 insulin Homo sapiens 29-36 8732718-7 1996 CONCLUSIONS: This study indicates that significant changes in circulating ET-1 levels occur after oral glucose loading, probably due to a glucose-induced increment in endogenous insulin concentration. Glucose 103-110 insulin Homo sapiens 178-185 8732718-7 1996 CONCLUSIONS: This study indicates that significant changes in circulating ET-1 levels occur after oral glucose loading, probably due to a glucose-induced increment in endogenous insulin concentration. Glucose 138-145 insulin Homo sapiens 178-185 8737025-7 1996 After a glucose challenge (120 min), the increases in both insulin and C-peptide concentrations were significantly greater in the positive family history group (289.2 +/- 214.1 pmol l-1, 2.23 +/- 1.48 nmol l-1), respectively, than in CS (192.4 +/- 170.3 pmol l-1, p < 0.05) (1.54 +/- 0.99 nmol l-1 p < 0.01), respectively. Glucose 8-15 insulin Homo sapiens 59-66 8739915-1 1996 It has previously been shown that insulin-induced stimulation of glucose uptake and glycogen synthesis requires activation of phosphatidylinositol-3-kinase (PI3kinase). Glucose 65-72 insulin Homo sapiens 34-41 8739915-2 1996 Insulin also induces formation of RasGTP in cells and various studies have yielded inconsistent data with respect to the contribution of signalling pathways activated by RasGTP, to insulin-stimulated glucose uptake and glycogen synthesis. Glucose 200-207 insulin Homo sapiens 181-188 8739915-10 1996 We conclude that stimulation of glucose transport and glycogen synthesis by insulin occurs independently of RasGTP-mediated signalling. Glucose 32-39 insulin Homo sapiens 76-83 8739917-2 1996 At the baseline examination, physical fitness was measured in terms of lung vital capacity and oxygen uptake during ergometry; early insulin response in terms of the 40-min insulin increment during an oral glucose tolerance test (a correlate of acute insulin response to an intravenous glucose tolerance test), and late insulin response were measured in terms of the 2-h insulin value during the oral glucose tolerance test (a correlate of glucose disposal during euglycaemic clamp testing). Glucose 206-213 insulin Homo sapiens 133-140 15251537-3 1996 Basal and glucose-stimulated C-peptide levels as well as increased stimulated glucose values were contrasted in insulin- versus OHA-treated groups. Glucose 10-17 insulin Homo sapiens 29-38 15251537-3 1996 Basal and glucose-stimulated C-peptide levels as well as increased stimulated glucose values were contrasted in insulin- versus OHA-treated groups. Glucose 10-17 insulin Homo sapiens 112-119 15251537-3 1996 Basal and glucose-stimulated C-peptide levels as well as increased stimulated glucose values were contrasted in insulin- versus OHA-treated groups. Glucose 78-85 insulin Homo sapiens 112-119 15251537-4 1996 In a second protocol, basal and glucose-stimulated C-peptide reactivity and stimulated glucose levels were also measured in eight patients with diabetes, before and after glycemic control. Glucose 32-39 insulin Homo sapiens 51-60 15251537-6 1996 Similarly, for both the middle-aged and elderly patients, stimulated glucose levels and degree of glucose elevation were higher in the insulin-treated patients. Glucose 69-76 insulin Homo sapiens 135-142 15251537-6 1996 Similarly, for both the middle-aged and elderly patients, stimulated glucose levels and degree of glucose elevation were higher in the insulin-treated patients. Glucose 98-105 insulin Homo sapiens 135-142 15251537-7 1996 In the second protocol, as hyperglycemia was reduced, beta-cell secretion measured by C-peptide responses to glucose was significantly increased, in conjunction with a decrease in the stimulated glucose levels. Glucose 109-116 insulin Homo sapiens 86-95 15251537-8 1996 CONCLUSION: These results indicate that measurements of C-peptide responses to glucose stimulation are helpful to determine the decision to use insulin in both elderly and middle-aged patients with diabetes. Glucose 79-86 insulin Homo sapiens 56-65 15251537-8 1996 CONCLUSION: These results indicate that measurements of C-peptide responses to glucose stimulation are helpful to determine the decision to use insulin in both elderly and middle-aged patients with diabetes. Glucose 79-86 insulin Homo sapiens 144-151 8621203-7 1996 Similarly, in the presence of physiological concentrations of glucose (5.5 mmol/L), insulin increased lactate production from 123 +/- 6 to 175 +/- 10 nmol/min (P < .01). Glucose 62-69 insulin Homo sapiens 84-91 8621214-5 1996 The insulin sensitivity index, which is a measure of the glucose infusion rate divided by plasma insulin, increased significantly (42.6%), from 10.8 +/- 3.5 to 15.4 +/- 4.4 (mumol/m2 per minute)/(microU/mL). Glucose 57-64 insulin Homo sapiens 4-11 8797056-7 1996 Thus, we suggested that high plasma glucose and insulin due to NIDDM may induce blood-borne glucose uptake with exercise. Glucose 92-99 insulin Homo sapiens 48-55 8626958-0 1996 Impaired glucose tolerance with late hypersecretion of insulin during oral glucose tolerance test in patients with vasospastic angina. Glucose 9-16 insulin Homo sapiens 55-62 8621801-1 1996 Resistance to insulin-mediated glucose disposal is a common finding in patients with non-insulin-dependent diabetes mellitus (NIDDM), as well as in nondiabetic individuals with hypertension. Glucose 31-38 insulin Homo sapiens 14-21 8626867-0 1996 The degree/rapidity of the metabolic deterioration following interruption of a continuous subcutaneous insulin infusion is influenced by the prevailing blood glucose Level. Glucose 158-165 insulin Homo sapiens 103-110 8626867-1 1996 This study aims at investigating the influence of the prevailing blood glucose level on the metabolic deterioration that follows a nocturnal interruption of a continuous sc insulin infusion (CSII). Glucose 71-78 insulin Homo sapiens 173-180 9377371-4 1996 The insulin-producing apparatus of beta-cells tends to get low in the glucose tolerance test, which fact is evidenced by lack of the blood glucose level control. Glucose 70-77 insulin Homo sapiens 4-11 8622603-1 1996 The impact of the dynamic changes in plasma glucose and insulin levels observed during a frequently sampled intravenous (IV) glucose tolerance test (FSIGT) on whole-body glucose processing and muscle glycogen metabolism is not known. Glucose 125-132 insulin Homo sapiens 56-63 8622603-1 1996 The impact of the dynamic changes in plasma glucose and insulin levels observed during a frequently sampled intravenous (IV) glucose tolerance test (FSIGT) on whole-body glucose processing and muscle glycogen metabolism is not known. Glucose 125-132 insulin Homo sapiens 56-63 8622604-8 1996 The results showed an increased insulin-mediated glucose uptake in IRH (9.10 +/- 0.19 v 6.78 +/- 0.18 mg kg-1 . Glucose 49-56 insulin Homo sapiens 32-39 8622604-20 1996 In conclusion, in IRH: (1) increased insulin-mediated glucose disposal is due to the increase of nonoxidative glucose metabolism; and (2) glucagon secretion has been confirmed to be inadequate. Glucose 54-61 insulin Homo sapiens 37-44 8622604-20 1996 In conclusion, in IRH: (1) increased insulin-mediated glucose disposal is due to the increase of nonoxidative glucose metabolism; and (2) glucagon secretion has been confirmed to be inadequate. Glucose 110-117 insulin Homo sapiens 37-44 8622608-6 1996 Insulin sensitivity was assessed by homeostatic model assessment (HOMAS), as well as by fasting insulin and the ratio of fasting insulin to glucose. Glucose 140-147 insulin Homo sapiens 0-7 8622611-9 1996 In conclusion, the glucose intolerance of TM, like that of cirrhosis, is associated with insulin resistance, not insulin deficiency, and may be a direct or indirect consequence of hepatic damage. Glucose 19-26 insulin Homo sapiens 89-96 8784789-0 1996 Insulin-stimulated glucose uptake involves the transition of glucose transporters to a caveolae-rich fraction within the plasma membrane: implications for type II diabetes. Glucose 19-26 insulin Homo sapiens 0-7 8784789-4 1996 In type II diabetes, the cellular transport of glucose in response to insulin is impaired, partly explaining why blood-glucose levels in patients are not lowered by insulin as in normal individuals. Glucose 47-54 insulin Homo sapiens 70-77 8784789-4 1996 In type II diabetes, the cellular transport of glucose in response to insulin is impaired, partly explaining why blood-glucose levels in patients are not lowered by insulin as in normal individuals. Glucose 119-126 insulin Homo sapiens 70-77 8784789-9 1996 The insulin-stimulated appearance of transporters in the caveolae-rich fraction occurred in parallel with enhanced glucose uptake by cells. Glucose 115-122 insulin Homo sapiens 4-11 8784789-10 1996 Treatment with isoproterenol plus adenosine deaminase rapidly inhibited insulin-stimulated glucose transport by 40%, and at the same time GLUT4 disappeared from the caveolae-rich fraction and from plasma membranes as a whole. Glucose 91-98 insulin Homo sapiens 72-79 8784789-11 1996 CONCLUSIONS: Insulin stimulates glucose uptake in adipocytes by rapidly translocating GLUT4 from intracellular stores to the plasma membrane. Glucose 32-39 insulin Homo sapiens 13-20 8609843-12 1996 Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. Glucose 66-73 insulin Homo sapiens 10-17 8635260-5 1996 METHODS AND RESULTS: The Insulin Resistance Atherosclerosis Study (IRAS) evaluated insulin sensitivity (SI) by the frequently sampled intravenous glucose tolerance test with analysis by the minimal model of Bergman. Glucose 146-153 insulin Homo sapiens 83-90 8685947-6 1996 Insulin output, stimulated by oral glucose tolerance tests and assessed by the ratio of AUC insulin to AUC glucose, fell gradually after transplantation and was decreased by an elevated serum calcium level and high cyclosporine dose. Glucose 35-42 insulin Homo sapiens 0-7 8630009-5 1996 After oral glucose challenge, the homozygous A/A subjects had the highest stimulated insulin levels at 60 and 90 minutes and the highest insulin area under the curve as compared to the subjects with other genotypes, which suggested the homozygous A/A subjects were more insulin resistant. Glucose 11-18 insulin Homo sapiens 85-92 8630009-5 1996 After oral glucose challenge, the homozygous A/A subjects had the highest stimulated insulin levels at 60 and 90 minutes and the highest insulin area under the curve as compared to the subjects with other genotypes, which suggested the homozygous A/A subjects were more insulin resistant. Glucose 11-18 insulin Homo sapiens 137-144 8630009-5 1996 After oral glucose challenge, the homozygous A/A subjects had the highest stimulated insulin levels at 60 and 90 minutes and the highest insulin area under the curve as compared to the subjects with other genotypes, which suggested the homozygous A/A subjects were more insulin resistant. Glucose 11-18 insulin Homo sapiens 137-144 8623183-12 1996 Locally procured pancreases and donors with elevated minimum blood glucose levels were identified as factors that affect the insulin secretory capabilities of the isolated islets. Glucose 67-74 insulin Homo sapiens 125-132 9125300-7 1996 Furthermore, the association between high insulin and lower cholesterol was seen in normoglycemic (fasting blood glucose <6.7 mmol/l) and diabetic subjects. Glucose 113-120 insulin Homo sapiens 42-49 8623689-1 1996 The numerous benefits of exercise for patients with insulin-dependent (type I) diabetes mellitus include an increase in insulin sensitivity and a reduction of blood glucose levels. Glucose 165-172 insulin Homo sapiens 52-59 8928757-4 1996 However, whole body and net forearm glucose uptakes were more markedly stimulated by insulin (+20 and +8%, respectively) in the IGF-I period. Glucose 36-43 insulin Homo sapiens 85-92 8928761-3 1996 However, a number of defects in insulin secretion were seen in the NDX and IGT groups, including reduced first-phase insulin secretory responses in intravenous glucose in relation to the degree of insulin resistance, and reduced normalized spectral power of insulin secretion during oscillatory glucose infusion. Glucose 160-167 insulin Homo sapiens 32-39 8928761-3 1996 However, a number of defects in insulin secretion were seen in the NDX and IGT groups, including reduced first-phase insulin secretory responses in intravenous glucose in relation to the degree of insulin resistance, and reduced normalized spectral power of insulin secretion during oscillatory glucose infusion. Glucose 160-167 insulin Homo sapiens 117-124 8928761-3 1996 However, a number of defects in insulin secretion were seen in the NDX and IGT groups, including reduced first-phase insulin secretory responses in intravenous glucose in relation to the degree of insulin resistance, and reduced normalized spectral power of insulin secretion during oscillatory glucose infusion. Glucose 295-302 insulin Homo sapiens 32-39 8928761-5 1996 The ability of a low-dose glucose infusion to prime the insulin secretory response to a subsequent glucose stimulus was normal in subjects with IGT but reduced or absent in subjects with overt NIDDM. Glucose 26-33 insulin Homo sapiens 56-63 8928761-5 1996 The ability of a low-dose glucose infusion to prime the insulin secretory response to a subsequent glucose stimulus was normal in subjects with IGT but reduced or absent in subjects with overt NIDDM. Glucose 99-106 insulin Homo sapiens 56-63 8773746-9 1996 At one end of the spectrum is a large subgroup of mainly obese women with reduced insulin secretion, which appears to result from failure of the beta cells to compensate for insulin resistance in susceptible women, resulting in glucose intolerance and NIDDM. Glucose 228-235 insulin Homo sapiens 82-89 8773746-10 1996 In the insulin-resistant patients with normal glucose tolerance, most of the hyperinsulinaemia is probably due to secondarily increased insulin secretion and decreased insulin degradation. Glucose 46-53 insulin Homo sapiens 7-14 8612405-8 1996 Septic humans exhibited impaired maximal insulin-stimulated glucose utilization (39.5 +/- 2.7 mumol/kg/min), despite complete suppression of endogenous glucose production. Glucose 60-67 insulin Homo sapiens 41-48 8612405-11 1996 Maximal, whole-body, insulin-stimulated glucose utilization was 205 +/- 11 and 146 +/- 9 mumol/kg/min in control and septic rats, respectively. Glucose 40-47 insulin Homo sapiens 21-28 8612405-14 1996 Dichloroacetate reversed the impairment of insulin-stimulated myocardial glucose uptake in septic rats, but did not influence skeletal muscle glucose uptake either under basal conditions or during insulin stimulation. Glucose 73-80 insulin Homo sapiens 43-50 16844002-2 1996 Insulin sensitivity was determined employing the normoglycaemic, hyperinsulinaemic clamp at a plasma insulin concentration of 380 pmol/I and a blood glucose concentration of 4.5 mmol/I. Glucose 149-156 insulin Homo sapiens 0-7 8603759-4 1996 Increasing the media insulin concentration to 30 micromol/l during fusion at 5.5 mmol/l glucose also did not alter basal GS FV (10.61 +/- 1.69%) but completely abolished the normal insulin-stimulated increase in GS activity (to 11.63 +/- 1.55%, NS). Glucose 88-95 insulin Homo sapiens 181-188 8603761-6 1996 Insulin-stimulated glucose metabolic index (Rg") in red gastrocnemius muscle (red muscle) was reduced (P < 0.05 and P < 0.01) at 5 h and 3 days of hGH infusion, respectively (e.g., 5 h, 10.0 +/- 1.8 vs. 24.1 +/- 4.4 [controls] micromol x 100 g-1 x min-1), whereas insulin-mediated muscle glycogen synthesis was reduced (P < 0.03) only in rats infused with hGH for 3 days. Glucose 19-26 insulin Homo sapiens 0-7 8603761-6 1996 Insulin-stimulated glucose metabolic index (Rg") in red gastrocnemius muscle (red muscle) was reduced (P < 0.05 and P < 0.01) at 5 h and 3 days of hGH infusion, respectively (e.g., 5 h, 10.0 +/- 1.8 vs. 24.1 +/- 4.4 [controls] micromol x 100 g-1 x min-1), whereas insulin-mediated muscle glycogen synthesis was reduced (P < 0.03) only in rats infused with hGH for 3 days. Glucose 19-26 insulin Homo sapiens 270-277 8603767-0 1996 Hepatic glucose production is regulated both by direct hepatic and extrahepatic effects of insulin in humans. Glucose 8-15 insulin Homo sapiens 91-98 8603767-9 1996 Hepatic glucose production (HGP) was suppressed to a greater extent with the full-rate peripheral insulin infusion (69.3 +/- 7.8%, P < 0.001 vs. portal or half-rate peripheral insulin) than portal (50.3 +/- 9.8%) or half-rate peripheral insulin infusion (36.8 +/- 3.8%). Glucose 8-15 insulin Homo sapiens 98-105 8603767-9 1996 Hepatic glucose production (HGP) was suppressed to a greater extent with the full-rate peripheral insulin infusion (69.3 +/- 7.8%, P < 0.001 vs. portal or half-rate peripheral insulin) than portal (50.3 +/- 9.8%) or half-rate peripheral insulin infusion (36.8 +/- 3.8%). Glucose 8-15 insulin Homo sapiens 179-186 8603767-9 1996 Hepatic glucose production (HGP) was suppressed to a greater extent with the full-rate peripheral insulin infusion (69.3 +/- 7.8%, P < 0.001 vs. portal or half-rate peripheral insulin) than portal (50.3 +/- 9.8%) or half-rate peripheral insulin infusion (36.8 +/- 3.8%). Glucose 8-15 insulin Homo sapiens 179-186 8603770-5 1996 Insulin secretion was evaluated during two experimental protocols: the first involved the measurement of insulin secretory responses during intravenous glucose tolerance test, hyperglycemic clamp, and intravenous injection of arginine. Glucose 152-159 insulin Homo sapiens 105-112 8729157-1 1996 OBJECTIVE: The primary purpose of this study was to evaluate the acute effect of exercise of differing intensity on plasma glucose and insulin responses to an oral glucose challenge. Glucose 164-171 insulin Homo sapiens 135-142 8729171-1 1996 We have demonstrated that physiological elevations in plasma free fatty acid concentrations inhibit insulin-stimulated glucose uptake in a dose-dependent manner in normal control subjects and in patients with NIDDM. Glucose 119-126 insulin Homo sapiens 100-107 8777996-8 1996 Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Glucose 67-74 insulin Homo sapiens 8-15 8777999-6 1996 After ingestion of glucose, plasma concentrations of insulin (p < 0.05) and gastric inhibitory polypeptide (p < 0.05) were higher during the glucose-supplemented diet. Glucose 19-26 insulin Homo sapiens 53-60 8777999-6 1996 After ingestion of glucose, plasma concentrations of insulin (p < 0.05) and gastric inhibitory polypeptide (p < 0.05) were higher during the glucose-supplemented diet. Glucose 147-154 insulin Homo sapiens 53-60 8792090-1 1996 Insulin action is crucial for the regulation of glucose metabolism. Glucose 48-55 insulin Homo sapiens 0-7 8792090-2 1996 Insulin plays a key role in suppressing endogenous glucose production by the liver, both in fasting and postprandial states. Glucose 51-58 insulin Homo sapiens 0-7 8792090-3 1996 Insulin is also necessary for the maintenance of normal rates of glucose oxidation and storage in insulin-sensitive tissues and for the prevention of excessive gluconeogenic substrate production. Glucose 65-72 insulin Homo sapiens 0-7 9162608-0 1996 A higher proinsulin response to glucose loading predicts deteriorating fasting plasma glucose and worsening to diabetes in subjects with impaired glucose tolerance. Glucose 32-39 insulin Homo sapiens 9-19 9162608-0 1996 A higher proinsulin response to glucose loading predicts deteriorating fasting plasma glucose and worsening to diabetes in subjects with impaired glucose tolerance. Glucose 86-93 insulin Homo sapiens 9-19 9162608-4 1996 The present findings suggest that the proinsulin response to glucose loading might be a useful indicator for predicting worsening to diabetes in subjects with impaired glucose tolerance. Glucose 61-68 insulin Homo sapiens 38-48 8838915-9 1996 The differential effect of obesity on glucose, blood pressure, and lipid levels in the Inuit compared with non-Inuit suggests a type of selective insulin resistance, the underlying mechanism of obesity and several chronic diseases. Glucose 38-45 insulin Homo sapiens 146-153 9062808-1 1996 Insulin sensitivity was measured by insulin tolerance test using KITT as an index of insulin mediated glucose metabolism in 9 non-obese healthy offspring of conjugal diabetic parents (OCDP) and 9 non-obese NIDDM patients. Glucose 102-109 insulin Homo sapiens 0-7 9062808-1 1996 Insulin sensitivity was measured by insulin tolerance test using KITT as an index of insulin mediated glucose metabolism in 9 non-obese healthy offspring of conjugal diabetic parents (OCDP) and 9 non-obese NIDDM patients. Glucose 102-109 insulin Homo sapiens 85-92 9119554-5 1996 Insulin resistance was estimated indirectly from the fasting levels of insulin and glucose. Glucose 83-90 insulin Homo sapiens 0-7 9119566-7 1996 In diabetic men with a family history, the ratio of fasting insulin to glucose and the ratio of areas under the insulin and glucose curves during oral glucose tolerance testing were lower compared to men with normal glucose tolerance. Glucose 71-78 insulin Homo sapiens 60-67 8601640-0 1996 Role of blood flow in regulating insulin-stimulated glucose uptake in humans. Glucose 52-59 insulin Homo sapiens 33-40 8601640-11 1996 These data provide direct evidence against the hypothesis that blood flow is an independent regulator of insulin-stimulated glucose uptake in humans. Glucose 124-131 insulin Homo sapiens 105-112 8636364-9 1996 During the constant infusion of glucose, oscillations of similar periodicity (110.1 +/- 10.3 min) were observed for insulin. Glucose 32-39 insulin Homo sapiens 116-123 8636369-7 1996 Insulin-mediated glucose disposal was higher after metformin treatment (26.1 +/- 2.4 vs. 19.3 +/- 2.3 micromol/min x kg; P < 0.01), whereas hepatic glucose production was completely suppressed. Glucose 17-24 insulin Homo sapiens 0-7 8636369-12 1996 In conclusion, 1 month of metformin administration to patients with essential hypertension and normal glucose tolerance 1) reduces the basal plasma insulin concentration, 2) improves whole body insulin-mediated glucose utilization, and 3) improves plasma high density lipoprotein cholesterol levels. Glucose 211-218 insulin Homo sapiens 194-201 8636371-0 1996 Nandrolone, a 19-nortestosterone, enhances insulin-independent glucose uptake in normal men. Glucose 63-70 insulin Homo sapiens 43-50 8636371-6 1996 A tolbutamide-modified, frequently sampled, iv glucose tolerance test was used to assess insulin-dependent and insulin-independent glucose disposal. Glucose 131-138 insulin Homo sapiens 111-118 8636380-8 1996 In the basal state and after oral glucose administration, their proinsulin responses were immense, but intact insulin responses were slightly reduced. Glucose 34-41 insulin Homo sapiens 64-74 8636380-8 1996 In the basal state and after oral glucose administration, their proinsulin responses were immense, but intact insulin responses were slightly reduced. Glucose 34-41 insulin Homo sapiens 67-74 8636380-12 1996 These results suggest that this mutation in the heterozygous state per se does not affect glucose tolerance and that the biological activity of mutant proinsulin contributes to glucose homeostasis in this family. Glucose 177-184 insulin Homo sapiens 151-161 8761898-7 1996 Odds ratios (95% confidence intervals) for the future development of hypertension between the highest and the lowest tertiles of insulin levels were 4.06 (1.40-11.76) for fasting insulin, 4.25 (1.45-12.45) for 60 min post-glucose load insulin, and 3.88 (1.34-11.20) for the sum of insulin concentrations, after adjustment for age, sex, systolic blood pressure, body mass index and alcohol consumption. Glucose 222-229 insulin Homo sapiens 129-136 8761899-1 1996 BACKGROUND: Hypertensive patients frequently show resistance to insulin-stimulated glucose uptake and hyperinsulinemia. Glucose 83-90 insulin Homo sapiens 64-71 8609828-1 1996 Physical training affects carbohydrate metabolism and results in an increased insulin-stimulated glucose disposal. Glucose 97-104 insulin Homo sapiens 78-85 8609839-7 1996 Obese subjects with normal glucose tolerance had a higher insulin response to both glucose (P < or = .004) and arginine (P < or = .02) than nonobese women, and higher glucose potentiation of insulin secretion, slopeAIR (P = .05). Glucose 27-34 insulin Homo sapiens 58-65 8609839-7 1996 Obese subjects with normal glucose tolerance had a higher insulin response to both glucose (P < or = .004) and arginine (P < or = .02) than nonobese women, and higher glucose potentiation of insulin secretion, slopeAIR (P = .05). Glucose 83-90 insulin Homo sapiens 58-65 8609839-8 1996 Compared with obese subjects with normal glucose tolerance, the obese subjects with impaired glucose tolerance had a lower insulin response to glucose (P = .03) and to arginine at blood glucose levels of 14 mmol/L (P = .03), as well as a lower slopeAIR levels ( P = .03). Glucose 93-100 insulin Homo sapiens 123-130 8609839-8 1996 Compared with obese subjects with normal glucose tolerance, the obese subjects with impaired glucose tolerance had a lower insulin response to glucose (P = .03) and to arginine at blood glucose levels of 14 mmol/L (P = .03), as well as a lower slopeAIR levels ( P = .03). Glucose 93-100 insulin Homo sapiens 123-130 8609843-12 1996 Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. Glucose 184-191 insulin Homo sapiens 10-17 8609843-12 1996 Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. Glucose 184-191 insulin Homo sapiens 34-41 8609843-12 1996 Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. Glucose 184-191 insulin Homo sapiens 34-41 8609843-12 1996 Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. Glucose 184-191 insulin Homo sapiens 34-41 8644011-0 1996 Insulin metabolism after relief of obstructive jaundice: intravenous glucose tolerance test with portal blood sampling. Glucose 69-76 insulin Homo sapiens 0-7 8609843-12 1996 Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. Glucose 184-191 insulin Homo sapiens 34-41 8609843-17 1996 2, who underwent three FSIGT studies over a 16-month interval, showed transient improvement in insulin release in response to modification of diet and exercise (first-phase insulin AUC, 57 pmol/min v 287 pmol/min 10 months later; fasting insulin, 97 pmol/L v 237 pmol/L 10 months later), but by 16 months, first-phase insulin release and fasting insulin had decreased (AUC, 64 and 136 pmol/L, respectively) despite higher fasting glucose. Glucose 430-437 insulin Homo sapiens 95-102 8615332-1 1996 Involuntary weight gains worsen all elements of the cardiovascular risk profile, including dyslipidemia, hypertension, insulin-resistant glucose intolerance, left-ventricular hypertrophy, hyperuricemia, and elevated fibrinogen. Glucose 137-144 insulin Homo sapiens 119-126 8617870-10 1996 In conclusion, an adequate insulin delivery in the peripheral circulation, obtained by islet transplantation, fully restores the muscle glucose transport system to normal in streptozocin diabetic rats. Glucose 136-143 insulin Homo sapiens 27-34 8617880-9 1996 Whereas TNF-alpha did not prevent insulin-induced dephosphorylation of FAK125, 25 mM glucose blocked this insulin effect completely. Glucose 85-92 insulin Homo sapiens 106-113 8617880-11 1996 (b) Differences in modulation of the insulin receptor signaling cascade are found with TNF-alpha and high glucose: Hyperglycemia-induced insulin receptor inhibition blocks both insulin receptor-dependent tyrosine phosphorylation and dephosphorylation of insulin receptor substrate proteins. Glucose 106-113 insulin Homo sapiens 37-44 8607835-5 1996 In addition, BoNTx/B partially inhibited insulin-stimulated GLUT4 translocation and glucose transport activity. Glucose 84-91 insulin Homo sapiens 41-48 8777278-3 1996 The intravenous glucose tolerance test (IVGTT, 0.5 g/kg glucose IV) with 0.02 U/kg insulin given at the 19th min and frequent sampling over 180 min shows that PRH patients exhibit a higher glucose tolerance coefficient Kg (2.99 +/- 0.26 vs 2.19 +/- 0.12; P < 0.02), higher SI [22.9 +/- 6.4 vs 7.18 +/- 0.14 min-1/(microU/ml). Glucose 16-23 insulin Homo sapiens 83-90 8777278-9 1996 Thus, in sedentary subjects, the previously reported rise in tissue glucose assimilation is mainly explained by an increased insulin-mediated glucose disposal rather than non-insulin-mediated glucose disposal. Glucose 68-75 insulin Homo sapiens 125-132 8777278-9 1996 Thus, in sedentary subjects, the previously reported rise in tissue glucose assimilation is mainly explained by an increased insulin-mediated glucose disposal rather than non-insulin-mediated glucose disposal. Glucose 142-149 insulin Homo sapiens 125-132 8777278-9 1996 Thus, in sedentary subjects, the previously reported rise in tissue glucose assimilation is mainly explained by an increased insulin-mediated glucose disposal rather than non-insulin-mediated glucose disposal. Glucose 142-149 insulin Homo sapiens 125-132 8777287-0 1996 Heterogeneity of high-density lipoprotein particles and insulin output during oral glucose tolerance test in men with coronary artery disease. Glucose 83-90 insulin Homo sapiens 56-63 8615340-5 1996 We believe that most weight-associated health problems result from a cascade of events associated with abnormal blood concentrations of insulin, glucose, or lipids that occur when fat cells become full and insulin-insensitive, and lose their protective functions. Glucose 145-152 insulin Homo sapiens 206-213 8777287-7 1996 Our results demonstrate that even in the normoglycemic, normocholesterolemic CAD patients, a high insulin output observed during the oral glucose tolerance test may be connected with a different HDL particle pattern, which suggests changes in the reverse cholesterol transport. Glucose 138-145 insulin Homo sapiens 98-105 8785208-7 1996 The measurement of RAG in vitro provides values for direct calculation of the amount of glucose likely to be rapidly absorbed in the human small intestine and, thus, to influence blood glucose and insulin levels. Glucose 88-95 insulin Homo sapiens 197-204 8638681-1 1996 Insulin is one of the most important regulators of glucose and lipid homeostasis. Glucose 51-58 insulin Homo sapiens 0-7 8638694-8 1996 Hyperglycemia in NIDDM compensated for insulin resistance to the extent that rates of glucose metabolism were the same as those for nondiabetics studied at euglycemia. Glucose 86-93 insulin Homo sapiens 39-46 8638702-5 1996 A [6,6- 2H2] glucose-labeled insulin-modified intravenous glucose tolerance test was performed in seven NIDDM subjects. Glucose 13-20 insulin Homo sapiens 29-36 8638702-8 1996 Another advantage of the hot indexes with respect to the cold indexes is their ability to reflect glucose and insulin effect on glucose disposal only, and not also on hepatic glucose production. Glucose 128-135 insulin Homo sapiens 110-117 8638702-8 1996 Another advantage of the hot indexes with respect to the cold indexes is their ability to reflect glucose and insulin effect on glucose disposal only, and not also on hepatic glucose production. Glucose 128-135 insulin Homo sapiens 110-117 8670061-2 1996 In this study we characterized the glucose transport system in cultured brown adipocytes, which responds to noradrenaline as well as insulin, and analysed the mechanism underlying the noradrenaline-induced increase in glucose transport. Glucose 35-42 insulin Homo sapiens 133-140 8901147-1 1996 Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore, pharmacological intervention should aim to improve insulin sensitivity. Glucose 38-45 insulin Homo sapiens 0-7 8901147-1 1996 Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore, pharmacological intervention should aim to improve insulin sensitivity. Glucose 38-45 insulin Homo sapiens 167-174 8901147-6 1996 Parenteral administration of the hemodialysate markedly augmented insulin stimulated glucose disposal (glucose infusion rate and metabolic clearance rate) by more than 80% (p < 0.003 day 11 vs. day 0). Glucose 85-92 insulin Homo sapiens 66-73 8901147-6 1996 Parenteral administration of the hemodialysate markedly augmented insulin stimulated glucose disposal (glucose infusion rate and metabolic clearance rate) by more than 80% (p < 0.003 day 11 vs. day 0). Glucose 103-110 insulin Homo sapiens 66-73 8901147-8 1996 This is the first clinical study to show that parenteral administration of the tested hemodialysate results in a significant increase of insulin-stimulated glucose disposal in NIDDM. Glucose 156-163 insulin Homo sapiens 137-144 8593934-1 1996 Overactivity of the hexosamine pathway mediates glucose-induced insulin resistance in rat adipocytes. Glucose 48-55 insulin Homo sapiens 64-71 8593934-3 1996 We determined GFA activity in human skeletal muscle biopsies and rates of insulin-stimulated whole-body, oxidative, and nonoxidative glucose disposal using the euglycemic insulin clamp technique combined with indirect calorimetry (insulin infusion rate (1.5 mU x kg-1 x min-1)) in 12 male patients with NIDDM (age 54 +/- 2 years, BMI 27.5 +/- 0.9 kg/m2, fasting plasma glucose 8.5 +/- 0.6 mmol/l) and 9 matched normal men. Glucose 133-140 insulin Homo sapiens 74-81 8593939-7 1996 Glucose disposal (1 mU x kg-1 x min-1) euglycemic insulin clamp with D-[3(-3)H]glucose) was higher in the normal glucose tolerance group compared with the impaired and diabetic groups (37.8 +/- 10.2 vs. 26.1 +/- 10.7 and 26.7 +/- 12.0 micromol x kg-1 x min-1; P < 0.05) despite similar BMIs in all three groups (28.8 +/- 3.7 kg/m2). Glucose 79-86 insulin Homo sapiens 50-57 8689841-8 1996 Thus, hypoglycaemia at a blood glucose level that is common among patients treated with insulin causes clear cognitive dysfunction, although restoration of the cognitive dysfunction to normal was fast. Glucose 31-38 insulin Homo sapiens 88-95 8593942-7 1996 Pancreas transplantation normalized only insulin-mediated glucose oxidation, leaving the stimulation of non-oxidative glucose disposal still markedly defective. Glucose 58-65 insulin Homo sapiens 41-48 8593942-10 1996 Insulin-mediated glucose metabolism remained abnormal after pancreas transplantation. Glucose 17-24 insulin Homo sapiens 0-7 8593946-4 1996 Because insulin is known to stimulate sympathetic activity, we studied the association of insulin level and glucose tolerance with QTc. Glucose 108-115 insulin Homo sapiens 8-15 8721776-10 1996 In contrast to the effect on insulin-stimulated glucose transport, catecholamines do not appear to have a counter regulatory action on C-peptide-mediated glucose transport. Glucose 48-55 insulin Homo sapiens 29-36 8721773-6 1996 Intravenous bolus injections of LysB29-tetradecanoyl des-(B30) human insulin showed a protracted blood glucose lowering effect compared to that of human insulin. Glucose 103-110 insulin Homo sapiens 69-76 8721774-3 1996 In cells from normal, obese, and NIDDM subjects cultured in low glucose concentrations, exposure to 100 nmol/l insulin for 30 min at 37 degrees C reduced cell-surface 125I-insulin binding to a similar extent (82 +/- 2, 77 +/- 5, and 82 +/- 5% of initial values, respectively). Glucose 64-71 insulin Homo sapiens 111-118 8721774-5 1996 In cells cultured under both glucose conditions, and exposed to 100 nmol/l insulin for 30 min at 37 degrees C, a complete recovery of the initial 125I-insulin binding was observed in normal but not in obese and NIDDM subjects. Glucose 29-36 insulin Homo sapiens 75-82 8721774-5 1996 In cells cultured under both glucose conditions, and exposed to 100 nmol/l insulin for 30 min at 37 degrees C, a complete recovery of the initial 125I-insulin binding was observed in normal but not in obese and NIDDM subjects. Glucose 29-36 insulin Homo sapiens 151-158 8721777-1 1996 Skeletal muscle glycogen synthase (encoded by GYS1 on chromosome 19q13.3) is the rate-limiting enzyme in insulin-mediated non-oxidative glucose disposal. Glucose 136-143 insulin Homo sapiens 105-112 8721788-0 1996 Normal values of first-phase insulin response to intravenous glucose in healthy Italian children and adolescents. Glucose 61-68 insulin Homo sapiens 29-36 8720744-11 1996 The most promising target in this respect has been the control of glucose overproduction from the liver by the nocturnal administration of intermediate- or long-acting insulin with or without oral antihyperglycaemic drugs. Glucose 66-73 insulin Homo sapiens 168-175 8742584-7 1996 Steady-state plasma glucose (SSPG) level was significantly higher in patients with VFO than with SFO, suggesting that insulin resistance may be more remarkable in VFO than in SFO. Glucose 20-27 insulin Homo sapiens 118-125 8742584-14 1996 High portal FFA levels would also induce insulin resistance, thereby causing glucose intolerance, hypertension, and finally atherosclerosis. Glucose 77-84 insulin Homo sapiens 41-48 8613231-1 1996 Although resistance to insulin-mediated glucose disposal has emerged as a link between abdominal obesity and hypertension, abnormalities of nonesterified fatty acid metabolism may play a greater role. Glucose 40-47 insulin Homo sapiens 23-30 8613231-7 1996 These correlations remained significant after fasting insulin, the insulin area under the curve during an oral glucose tolerance test, and glucose disposal during the clamp were controlled for. Glucose 111-118 insulin Homo sapiens 67-74 8613231-9 1996 These correlations remained significant after insulin and an index of sensitivity to insulin-mediated glucose disposal were statistically controlled for. Glucose 102-109 insulin Homo sapiens 85-92 8772555-2 1996 We investigated this with a modified frequently sampled iv glucose tolerance test to determine acute insulin responses to glucose (AIRg) as well as insulin action by minimal model analysis in 28 women with polycystic ovary syndrome (PCOS; 15 obese and 13 nonobese) and 29 age- and weight-matched normal women (14 obese and 15 nonobese). Glucose 122-129 insulin Homo sapiens 101-108 8772551-13 1996 In this patient with a hemangiopericytoma, hypoglycemia was associated with increased circulating insulin-like activity from elevated free and big IGF-II, which stimulated glucose uptake primarily into muscle tissue. Glucose 172-179 insulin Homo sapiens 98-105 8772557-4 1996 At baseline, insulin-mediated glucose uptake was lower in hyperandrogenic women than in controls (by ANOVA, F = 14.3; P < 0.001). Glucose 30-37 insulin Homo sapiens 13-20 8772557-6 1996 After antiandrogen therapy, insulin action on glucose metabolism significantly increased for both the patients as a whole (F = 7.4; P < 0.01) and each treatment group separately. Glucose 46-53 insulin Homo sapiens 28-35 8772575-3 1996 A novel low mol wt inositol phosphoglycan antagonist of insulin action of oxidative glucose metabolism in isolated rat adipocytes was partially purified from normal human plasma and shown to be increased in type II diabetic plasma. Glucose 84-91 insulin Homo sapiens 56-63 8772592-0 1996 Resistance to insulin-mediated glucose disposal in patients with noninsulin-dependent diabetes mellitus in the absence of obesity or microalbuminuria--a Clinical Research Center study. Glucose 31-38 insulin Homo sapiens 14-21 8772592-1 1996 To challenge the view that resistance to insulin-mediated glucose uptake in noninsulin-dependent diabetes mellitus (NIDDM) is limited to patients with microalbuminuria, high blood pressure, or obesity, we compared measurements of insulin resistance in 29 normal volunteers and 31 normotensive patients with NIDDM (mean +/- SE fasting plasma glucose, 160 +/- 10 mg/dL). Glucose 58-65 insulin Homo sapiens 41-48 8772592-5 1996 Resistance to insulin-mediated glucose disposal was quantified by measurement of the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations during the last 30 min of an 180-min infusion of somatostatin (5 micrograms/min), insulin (25 mU/min-m2), and glucose (240 mg/min-m2). Glucose 31-38 insulin Homo sapiens 14-21 8772575-11 1996 Inhibition by fraction V3 of Mg(2+)-stimulated PDH phosphatase and its cloned catalytic subunit helps explain its mechanism of action to inhibit insulin-stimulated oxidative glucose metabolism in adipocytes and its potential clinical significance in insulin resistance. Glucose 174-181 insulin Homo sapiens 145-152 8772576-1 1996 Syndrome X, or the syndrome of insulin resistance, is a cluster of related metabolic abnormalities of hyperinsulinemia, glucose intolerance, increased very low density lipoprotein (VLDL), decreased high density lipoprotein (HDL), and hypertension in nonobese adults and plays an important role in the genesis of cardiovascular disease. Glucose 120-127 insulin Homo sapiens 31-38 8772576-4 1996 In vivo insulin-mediated glucose disposal (Rd) was evaluated during a 40 mu/m2. Glucose 25-32 insulin Homo sapiens 8-15 8887138-0 1996 Normal values of first-phase insulin response to intravenous glucose in healthy Italian children and adolescents. Glucose 61-68 insulin Homo sapiens 29-36 8743278-11 1996 Insulin resistance, expressed by an enhanced pancreatic sensitivity to oral glucose, is present in both the high LH and the normal LH subjects, even though the PCOS patients with elevated LH tend to be more insulin resistant and hyperandrogenic than the normal LH patients. Glucose 76-83 insulin Homo sapiens 0-7 8743287-1 1996 Neuropeptide Y (NPY) is a 36 aminoacid peptide known to inhibit glucose-stimulated insulin secretion. Glucose 64-71 insulin Homo sapiens 83-90 8723995-3 1996 METHODS: Insulin sensitivity was estimated by the minimal model from a frequently sampled intravenous glucose tolerance test. Glucose 102-109 insulin Homo sapiens 9-16 8606396-5 1996 Plasma insulin concentration increased with glucose. Glucose 44-51 insulin Homo sapiens 7-14 8606636-1 1996 Acute insulin responses to glucose (AIRG), glucagon (AIRGln), and arginine (AIRArg) were evaluated prospectively in nine subjects positive for islet-cell antibodies (ICAs) who later progressed to type I diabetes or impaired glucose tolerance (IGT) (progressors), 64 ICA-positive subjects at risk who did not develop type I diabetes, 365 ICA-negative relatives of diabetic patients who also remained free of the disease, and 89 control subjects. Glucose 27-34 insulin Homo sapiens 6-13 8729130-1 1996 Skeletal muscle plays a major role in insulin-stimulated glucose disposal. Glucose 57-64 insulin Homo sapiens 38-45 8606640-2 1996 Obesity in both humans and experimental animals is associated with a reduced number of insulin receptors and a decreased insulin-mediated glucose disposal, whereas sensitivity to insulin"s antilipolytic action is unaltered. Glucose 138-145 insulin Homo sapiens 121-128 8759412-3 1996 The prime site of insulin resistance is in the skeletal muscle affecting non oxidative glucose metabolism (glycogen synthesis). Glucose 87-94 insulin Homo sapiens 18-25 8601111-6 1996 RESULTS: There was a weak inverse correlation (r=-0.07, P=0.03) between ponderal index at birth and 60 minute insulin concentrations in the intravenous glucose tolerance test at age 50 years. Glucose 152-159 insulin Homo sapiens 110-117 8606640-2 1996 Obesity in both humans and experimental animals is associated with a reduced number of insulin receptors and a decreased insulin-mediated glucose disposal, whereas sensitivity to insulin"s antilipolytic action is unaltered. Glucose 138-145 insulin Homo sapiens 121-128 8606640-3 1996 To evaluate the antiobesity effect of diazoxide (DZ), an inhibitor of glucose-stimulated insulin release, 7-week-old Zucker obese and lean rats were studied. Glucose 70-77 insulin Homo sapiens 89-96 8606640-12 1996 This was accompanied by increased basal and insulin-stimulated glucose transport in both genotypes (P<.01). Glucose 63-70 insulin Homo sapiens 44-51 8628644-3 1996 Glucose toxicity (i.e., glucose-induced insulin resistance) explains why apparently unrelated therapeutic measures to improve glycaemic control (e.g., weight reduction, and sulphonylurea, metformin or insulin administration) all also increase insulin sensitivity. Glucose 24-31 insulin Homo sapiens 40-47 8628644-3 1996 Glucose toxicity (i.e., glucose-induced insulin resistance) explains why apparently unrelated therapeutic measures to improve glycaemic control (e.g., weight reduction, and sulphonylurea, metformin or insulin administration) all also increase insulin sensitivity. Glucose 24-31 insulin Homo sapiens 201-208 8628644-3 1996 Glucose toxicity (i.e., glucose-induced insulin resistance) explains why apparently unrelated therapeutic measures to improve glycaemic control (e.g., weight reduction, and sulphonylurea, metformin or insulin administration) all also increase insulin sensitivity. Glucose 24-31 insulin Homo sapiens 201-208 8628644-4 1996 The improvement is manifest when insulin-stimulated glucose uptake is measured at similar glucose and insulin concentrations in IDDM and NIDDM patients. Glucose 52-59 insulin Homo sapiens 33-40 8628644-4 1996 The improvement is manifest when insulin-stimulated glucose uptake is measured at similar glucose and insulin concentrations in IDDM and NIDDM patients. Glucose 52-59 insulin Homo sapiens 102-109 8628644-4 1996 The improvement is manifest when insulin-stimulated glucose uptake is measured at similar glucose and insulin concentrations in IDDM and NIDDM patients. Glucose 90-97 insulin Homo sapiens 33-40 8628644-5 1996 In daily life, however, both IDDM and NIDDM patients utilise as much glucose in insulin-sensitive tissues as do non-diabetic individuals since, due to the mass action effect of glucose, glucose uptake increases in response to hyperglycaemia. Glucose 69-76 insulin Homo sapiens 80-87 8628644-5 1996 In daily life, however, both IDDM and NIDDM patients utilise as much glucose in insulin-sensitive tissues as do non-diabetic individuals since, due to the mass action effect of glucose, glucose uptake increases in response to hyperglycaemia. Glucose 177-184 insulin Homo sapiens 80-87 8628644-5 1996 In daily life, however, both IDDM and NIDDM patients utilise as much glucose in insulin-sensitive tissues as do non-diabetic individuals since, due to the mass action effect of glucose, glucose uptake increases in response to hyperglycaemia. Glucose 177-184 insulin Homo sapiens 80-87 8684772-2 1996 In early pregnancy, insulin secretion in response to glucose is increased, peripheral insulin sensitivity is normal or increased, glucose tolerance is normal or slightly enhanced. Glucose 53-60 insulin Homo sapiens 20-27 8650968-0 1996 Release of glucagon-like peptide 1 (GLP-1 [7-36 amide]), gastric inhibitory polypeptide (GIP) and insulin in response to oral glucose after upper and lower intestinal resections. Glucose 126-133 insulin Homo sapiens 98-105 8613527-6 1996 The relative activity of a chloramphenicol acetyl transferase (CAT) reporter gene controlled by the 5" regulatory region of the human insulin gene was decreased in late passage betaTC-6 cells chronically cultured in 11.1 mM glucose, but was preserved in late passages of cells chronically cultured in 0.8 mM glucose. Glucose 224-231 insulin Homo sapiens 134-141 8554246-6 1996 INTERVENTION: Intensive therapy with 3 or more daily insulin injections or continuous subcutaneous insulin infusion, guided by 4 or more glucose tests per day, compared with conventional therapy with 1 or 2 daily insulin injections. Glucose 137-144 insulin Homo sapiens 99-106 8554246-6 1996 INTERVENTION: Intensive therapy with 3 or more daily insulin injections or continuous subcutaneous insulin infusion, guided by 4 or more glucose tests per day, compared with conventional therapy with 1 or 2 daily insulin injections. Glucose 137-144 insulin Homo sapiens 99-106 8633616-7 1996 In an unmatched multiple regression model among women from monozygous twin pairs only, log fasting insulin was independently associated with body mass index (p < 0.0001), waist/hip ratio (p = 0.02), and glucose intolerance (p = 0.04), but not with triglycerides, high density lipoprotein cholesterol, or hypertension. Glucose 206-213 insulin Homo sapiens 99-106 8613527-6 1996 The relative activity of a chloramphenicol acetyl transferase (CAT) reporter gene controlled by the 5" regulatory region of the human insulin gene was decreased in late passage betaTC-6 cells chronically cultured in 11.1 mM glucose, but was preserved in late passages of cells chronically cultured in 0.8 mM glucose. Glucose 308-315 insulin Homo sapiens 134-141 8695671-0 1996 Insulin response during the oral glucose tolerance test: the role of age, sex, body fat and the pattern of fat distribution. Glucose 33-40 insulin Homo sapiens 0-7 8695671-1 1996 To clarify their primary roles on insulin response to oral glucose, age and sex differences in body composition should be taken into account. Glucose 59-66 insulin Homo sapiens 34-41 8695671-9 1996 We conclude that the sex differences in insulin levels are explained by differences in body habitus and post-load glucose levels, but that insulin levels decline with age per se. Glucose 114-121 insulin Homo sapiens 40-47 8779949-3 1996 During both low (10 mU.m-2.min-1)- and higher (40 mU.m-2.min-1)-dose insulin clamp studies, insulin-mediated glucose uptake was reduced in obese vs. control subjects (P < 0.01). Glucose 109-116 insulin Homo sapiens 69-76 8607504-11 1996 Post-operatively, the patients had a pathological glucose tolerance with increased postprandial insulin and glucagon secretion. Glucose 50-57 insulin Homo sapiens 96-103 8623813-0 1996 Impaired insulin-stimulated nonoxidative glucose metabolism in glucose-tolerant women with previous gestational diabetes. Glucose 41-48 insulin Homo sapiens 9-16 8623813-0 1996 Impaired insulin-stimulated nonoxidative glucose metabolism in glucose-tolerant women with previous gestational diabetes. Glucose 63-70 insulin Homo sapiens 9-16 8623813-5 1996 RESULTS: Women with previous gestational diabetes had a decreased glucose disposal rate (p<0.01) because of a reduced insulin-stimulated nonoxidative glucose metabolism (6.63 +/- 0.47 vs 9.04 +/- 0.57 mg/kg fat-free mass per minute, p<0.01). Glucose 66-73 insulin Homo sapiens 121-128 8623813-7 1996 The first-phase insulin response to the intravenous glucose tolerance test was, in absolute terms, comparable in the two groups. Glucose 52-59 insulin Homo sapiens 16-23 8779949-3 1996 During both low (10 mU.m-2.min-1)- and higher (40 mU.m-2.min-1)-dose insulin clamp studies, insulin-mediated glucose uptake was reduced in obese vs. control subjects (P < 0.01). Glucose 109-116 insulin Homo sapiens 92-99 8779949-9 1996 In conclusion, insulin resistance is a common feature of both glucose and protein metabolism in obesity. Glucose 62-69 insulin Homo sapiens 15-22 8779957-7 1996 In conclusion, 1) after the marathon run, probably because of increased lipid oxidation, the insulin-stimulated glucose disposal is decreased despite muscle glycogen depletion and the activation of glycogen synthase; 2) the contribution of lipid oxidation in energy expenditure is increased in proportion to physical fitness; 3) these adaptations of fuel homeostasis may contribute to the maintenance of physical performance after prolonged exercise. Glucose 112-119 insulin Homo sapiens 93-100 8620342-7 1996 Multiple logistic regression analysis revealed that fasting insulin levels were positively correlated with body mass index and fasting glucose and factor VII activity levels, whereas they were negatively correlated with HDL cholesterol in both sexes. Glucose 135-142 insulin Homo sapiens 60-67 8731348-7 1996 There was an increase of proinsulin related to obesity and increased glucose levels, suggesting that proinsulin levels increase with insulin resistance. Glucose 69-76 insulin Homo sapiens 28-35 8549858-9 1996 In IC subjects, plasma insulin increased and glucagon was either constant (IC-2) or increased less than insulin, resulting in nonsignificant declines in the immunoreactive glucose-to-immunoreactive insulin ratio. Glucose 172-179 insulin Homo sapiens 23-30 8731348-5 1996 Serum concentration of proinsulin was analyzed in 50 subjects during an oral glucose tolerance test (10 non-obese control, 10 obese controls, 10 subjects with impaired glucose tolerance, 10 patients with type II diabetes mellitus (DM) and fasting blood glucose (FBG) < 140 mg/dl, and 10 patients with type II DM and FBG > 150 mg/dl). Glucose 77-84 insulin Homo sapiens 23-33 8731348-5 1996 Serum concentration of proinsulin was analyzed in 50 subjects during an oral glucose tolerance test (10 non-obese control, 10 obese controls, 10 subjects with impaired glucose tolerance, 10 patients with type II diabetes mellitus (DM) and fasting blood glucose (FBG) < 140 mg/dl, and 10 patients with type II DM and FBG > 150 mg/dl). Glucose 168-175 insulin Homo sapiens 23-33 8731348-7 1996 There was an increase of proinsulin related to obesity and increased glucose levels, suggesting that proinsulin levels increase with insulin resistance. Glucose 69-76 insulin Homo sapiens 25-35 8731348-7 1996 There was an increase of proinsulin related to obesity and increased glucose levels, suggesting that proinsulin levels increase with insulin resistance. Glucose 69-76 insulin Homo sapiens 101-111 8635675-5 1996 The insulinoma patients displayed a significant increase in the expression of the insulin receptor isoform containing exon 11 (75.7 +/- 2.3%) when compared with normal subjects (57.9 +/- 1.5%); furthermore, this increase was positively correlated with plasma insulin concentration and negatively correlated with in vivo insulin sensitivity (glucose clamp). Glucose 341-348 insulin Homo sapiens 4-11 8635675-5 1996 The insulinoma patients displayed a significant increase in the expression of the insulin receptor isoform containing exon 11 (75.7 +/- 2.3%) when compared with normal subjects (57.9 +/- 1.5%); furthermore, this increase was positively correlated with plasma insulin concentration and negatively correlated with in vivo insulin sensitivity (glucose clamp). Glucose 341-348 insulin Homo sapiens 82-89 8635675-5 1996 The insulinoma patients displayed a significant increase in the expression of the insulin receptor isoform containing exon 11 (75.7 +/- 2.3%) when compared with normal subjects (57.9 +/- 1.5%); furthermore, this increase was positively correlated with plasma insulin concentration and negatively correlated with in vivo insulin sensitivity (glucose clamp). Glucose 341-348 insulin Homo sapiens 82-89 8641120-3 1996 Insulin resistance was calculated from simultaneous fasting plasma glucose and insulin concentrations using the homeostasis model assessment (HOMA) method. Glucose 67-74 insulin Homo sapiens 0-7 8549858-9 1996 In IC subjects, plasma insulin increased and glucagon was either constant (IC-2) or increased less than insulin, resulting in nonsignificant declines in the immunoreactive glucose-to-immunoreactive insulin ratio. Glucose 172-179 insulin Homo sapiens 104-111 8697293-3 1996 Hypoglycaemia was induced by an intravenous infusion of insulin (100 mU.kg-1.h-1), together with a glucose clamp, to obtain an arterialised venous blood glucose level of 2.3 mmol/l. Glucose 153-160 insulin Homo sapiens 56-63 8549858-9 1996 In IC subjects, plasma insulin increased and glucagon was either constant (IC-2) or increased less than insulin, resulting in nonsignificant declines in the immunoreactive glucose-to-immunoreactive insulin ratio. Glucose 172-179 insulin Homo sapiens 104-111 8630519-6 1996 Fasting PIM/C-peptide and PIM/insulin ratios of 0.5% and 2.3% increased during the glucose clamp to levels of 1.4% and 7.6%, respectively. Glucose 83-90 insulin Homo sapiens 30-37 8867906-8 1996 Our results suggested that intensive insulin treatment reduced platelet aggregation in patients without microvascular disease when strict glycemia control was maintained and indicated that changes in platelet aggregation could directly result from changes in plasma glucose concentrations. Glucose 266-273 insulin Homo sapiens 37-44 8636258-2 1996 In this study, we sought to test the hypothesis that mutations in the PEPCK gene promoter may impair the ability of insulin to suppress hepatic glucose production, thereby contributing to both the insulin resistance and increased rate of gluconeogenesis characteristic of NIDDM. Glucose 144-151 insulin Homo sapiens 116-123 8636267-0 1996 Insulin resistance in growth hormone-deficient adults: defects in glucose utilization and glycogen synthase activity. Glucose 66-73 insulin Homo sapiens 0-7 8636292-0 1996 Insulin resistance in type I diabetes mellitus: a major role for reduced glucose extraction. Glucose 73-80 insulin Homo sapiens 0-7 8636267-2 1996 Despite similar basal rates of total glucose disposal (Rd), there was a 64% reduction in the insulin-stimulated rise (delta) in Rd in the GHD adults compared to that in controls [16.6 +/- 2.8 vs. 44.7 +/- 6.0 mumol/kg fat free mass (FFM)/min; P < 0.001], which was mainly due to a decreased glucose storage (GS) rate (delta GS, 12.6 +/- 2.9 vs. 39.5 +/- 7.5 mumol/kg FFM/min; P < 0.01). Glucose 37-44 insulin Homo sapiens 93-100 8636292-8 1996 We conclude that a defect in glucose extraction rather than blood flow characterizes insulin resistance in uncomplicated Type I diabetes. Glucose 29-36 insulin Homo sapiens 85-92 8683475-10 1996 Insulin induced a protein synthesis-dependent stimulation of L-arginine transport and increased NO and PGI2 production in cells exposed to 5 mM glucose. Glucose 144-151 insulin Homo sapiens 0-7 8683475-12 1996 In cells exposed to high glucose, insulin downregulated elevated rates of L-arginine transport and cGMP accumulation but had no effect on the depressed PGI2 production. Glucose 25-32 insulin Homo sapiens 34-41 8596502-2 1996 Compared with responses observed from control islets incubated for 3.5 hours with 5.6 mmol/L glucose alone, prior exposure to 10 mmol/L glucose, 20 mmol/L glucose, or 10 micromol/L carbachol reduced peak second-phase insulin release rates to a subsequent 20-mmol/L glucose stimulus by 63%, 81%, or 70%, respectively. Glucose 136-143 insulin Homo sapiens 217-224 8596492-1 1996 To examine the effect of the somatostatin analog, octreotide, on insulin-mediated glucose uptake, seven insulin-dependent diabetic (IDDM) subjects were studied with and without 4 days of continuous subcutaneous octreotide administration (1 mg/kg/d). Glucose 82-89 insulin Homo sapiens 65-72 8596502-2 1996 Compared with responses observed from control islets incubated for 3.5 hours with 5.6 mmol/L glucose alone, prior exposure to 10 mmol/L glucose, 20 mmol/L glucose, or 10 micromol/L carbachol reduced peak second-phase insulin release rates to a subsequent 20-mmol/L glucose stimulus by 63%, 81%, or 70%, respectively. Glucose 136-143 insulin Homo sapiens 217-224 8596492-2 1996 Insulin dosage was adjusted after frequent measurements of plasma glucose level. Glucose 66-73 insulin Homo sapiens 0-7 8596502-2 1996 Compared with responses observed from control islets incubated for 3.5 hours with 5.6 mmol/L glucose alone, prior exposure to 10 mmol/L glucose, 20 mmol/L glucose, or 10 micromol/L carbachol reduced peak second-phase insulin release rates to a subsequent 20-mmol/L glucose stimulus by 63%, 81%, or 70%, respectively. Glucose 136-143 insulin Homo sapiens 217-224 8596502-4 1996 Further addition of 10 nmol/L GLP-1 together with 20 mmol/L glucose significantly increased insulin output from desensitized islets. Glucose 60-67 insulin Homo sapiens 92-99 8596502-5 1996 Carbachol (10 micromol/L) preexposure also abolished the subsequent insulin secretory and 3H-inositol efflux responses to 8 mmol/L glucose plus 10 micromol/L carbachol. Glucose 131-138 insulin Homo sapiens 68-75 8632749-0 1996 [Effect of high concentration insulin during glucose clamp on blood amino acids and lipids]. Glucose 45-52 insulin Homo sapiens 30-37 8689277-10 1996 Increased [Ca2+]i in skeletal myocytes can either directly promote the phosphorylation of GLUT4 or prevent its dephosphorylation, both of which effectively block insulin stimulation of glucose uptake, thereby contributing to insulin resistance. Glucose 185-192 insulin Homo sapiens 162-169 8689277-9 1996 The increased basal [Ca2+]i can negatively modulate the insulin-mediated stimulation of GLUT4-dependent glucose transport despite the possibility that Ca2+i might not participate as a component in the insulin-receptor-regulated signaling pathway. Glucose 104-111 insulin Homo sapiens 56-63 8775516-6 1996 In response to this elevation in plasma glucose levels, insulin levels increase to approximately 60 microU/ml, a 2-fold increase over resting values. Glucose 40-47 insulin Homo sapiens 56-63 8865748-8 1996 From these experiments we speculate that exaggerated insulin resistance due to injected ethanol may be one of the factors influencing glucose tolerance after PEI. Glucose 134-141 insulin Homo sapiens 53-60 8567967-8 1996 The ratio of total proinsulin to immunoreactive insulin was directly correlated with fasting plasma glucose and showed a significant inverse relationship to secretory reserve capacity. Glucose 100-107 insulin Homo sapiens 19-29 8567638-1 1996 Pancreatic islet beta cells regulate the rate of insulin gene transcription in response to a number of nutrients, the most potent of which is glucose. Glucose 142-149 insulin Homo sapiens 49-56 8567638-2 1996 To test for its regulation by glucose, the promoter sequence was isolated from the human insulin gene. Glucose 30-37 insulin Homo sapiens 89-96 8567638-3 1996 When linked to chloramphenicol acetyltransferase and transfected into primary islet cultures, the human insulin promoter is activated by glucose. Glucose 137-144 insulin Homo sapiens 104-111 8567967-8 1996 The ratio of total proinsulin to immunoreactive insulin was directly correlated with fasting plasma glucose and showed a significant inverse relationship to secretory reserve capacity. Glucose 100-107 insulin Homo sapiens 22-29 8567973-2 1996 Administration of exogenous insulin during an intravenous glucose tolerance test allows the use of the minimal model technique to determine the insulin sensitivity index in subjects with reduced endogenous insulin responses. Glucose 58-65 insulin Homo sapiens 28-35 8567973-2 1996 Administration of exogenous insulin during an intravenous glucose tolerance test allows the use of the minimal model technique to determine the insulin sensitivity index in subjects with reduced endogenous insulin responses. Glucose 58-65 insulin Homo sapiens 144-151 8567973-2 1996 Administration of exogenous insulin during an intravenous glucose tolerance test allows the use of the minimal model technique to determine the insulin sensitivity index in subjects with reduced endogenous insulin responses. Glucose 58-65 insulin Homo sapiens 144-151 8550560-0 1996 Hepatic overexpression of insulin-like growth factor-II in adulthood increases basal and insulin-stimulated glucose disposal in conscious mice. Glucose 108-115 insulin Homo sapiens 26-33 8834976-7 1996 Negative correlations were found between the nocturnal serum GH AUC and the insulin-stimulated glucose metabolism (r = -0.65, p = 0.0241) and between the nocturnal urinary GH excretion and the insulin-stimulated glucose metabolism (r = -0.77, p = 0.0054). Glucose 95-102 insulin Homo sapiens 76-83 8834976-2 1996 The mean nocturnal intravenous insulin infusion required to maintain a normal constant blood glucose concentration between 24:00 and 07:00 was 53% higher during the night on placebo (p = 0.0212). Glucose 93-100 insulin Homo sapiens 31-38 8869748-7 1996 In adipose tissue, insulin increases indirectly the expression of FAS and ACC by stimulating glucose metabolism through its well-known effect on glucose transport. Glucose 93-100 insulin Homo sapiens 19-26 8869748-7 1996 In adipose tissue, insulin increases indirectly the expression of FAS and ACC by stimulating glucose metabolism through its well-known effect on glucose transport. Glucose 145-152 insulin Homo sapiens 19-26 8869748-8 1996 In the liver, the action of insulin is also indirect by allowing the expression of glucokinase and hence by increasing glucose metabolism. Glucose 119-126 insulin Homo sapiens 28-35 9219598-1 1996 A transient depression of blood-glucose level was found after streptozotocin administration, which can be explained by insulin release due to the destroying effect of streptozotocin on beta-cells of pancreas, the biliary flow was elevated, when blood sugar level was low. Glucose 32-39 insulin Homo sapiens 119-126 12893474-2 1996 Insulin is well known to play an important regulatory role in nutrient, especially glucose, uptake and utilization in skeletal muscle. Glucose 83-90 insulin Homo sapiens 0-7 8834703-11 1996 In conclusion, these studies have demonstrated that in response to an oral glucose load, salt-sensitive patients with essential hypertension manifest increased insulin secretion. Glucose 75-82 insulin Homo sapiens 160-167 12893488-1 1996 Ethanol is known to cause an acute and profound insulin resistance in man and the rat primarily via effects on glucose utilization. Glucose 111-118 insulin Homo sapiens 48-55 12893488-3 1996 We confirm that ethanol infusion causes an acute insulin resistance, the rate of glucose infusion required to maintain euglycaemia (GIR) being decreased markedly by ethanol. Glucose 81-88 insulin Homo sapiens 49-56 12893488-8 1996 The basis of the inhibitory effects of ethanol on insulin-stimulated glucose metabolism in muscle is unknown, but may involve membrane-associated impairments in insulin signalling and/or the glucose transport system. Glucose 69-76 insulin Homo sapiens 50-57 8604670-4 1996 Whole-body glucose uptake was similar with both diets at a low plasma insulin concentration (370 pmol/L) but decreased (P < 0.05) at a high insulin concentration (2.4 nmol/L) with the LGI diet compared with the HGI diet. Glucose 11-18 insulin Homo sapiens 70-77 8604670-8 1996 It is concluded that when ingesting a diet with an energy composition common in Western countries, switching the carbohydrates from high to low GI sources decreases insulin action on whole-body glucose disposal at a high but not at a physiologic plasma insulin concentration. Glucose 194-201 insulin Homo sapiens 165-172 8772471-5 1996 Larger cortisol elevations, such as occurred after hydrocortisone administration, were additionally associated with the appearance of insulin resistance, which developed 4-6 h after the cortisol elevation and persisted for > 16 h. These observations support the concept that the 24-h cortisol rhythmicity is responsible, at least in part, for the normal diurnal variation in glucose tolerance. Glucose 378-385 insulin Homo sapiens 134-141 8772490-0 1996 A model to measure insulin effects on glucose transport and phosphorylation in muscle: a three-tracer study. Glucose 38-45 insulin Homo sapiens 19-26 8554200-6 1996 Plasma glucose levels were 1.7 to 2.2 mmol/L lower in the variable-dose insulin regimen group than in the other two treatment groups. Glucose 7-14 insulin Homo sapiens 72-79 8554200-8 1996 There was a slight suggestion only from post hoc analysis that patients in both insulin treatment groups, who were defined as having good glucose control, had fewer cardiovascular events than those with fair or poor control. Glucose 138-145 insulin Homo sapiens 80-87 8554206-4 1996 RESULTS: All three modes of pharmacologic therapy in the intensively treated group-sulfonylurea, insulin, and metformin-had similar efficacy in reducing the fasting plasma glucose and glycated hemoglobin levels. Glucose 172-179 insulin Homo sapiens 97-104 8554221-7 1996 Intensive insulin therapy normalizes glycemia by decreasing hepatic glucose output and improving peripheral glucose uptake and may also improve insulin resistance and insulin secretion by reducing hyperglycemic glucotoxicity. Glucose 68-75 insulin Homo sapiens 10-17 8773736-2 1996 The stimulated insulin secretion was quantified by the frequently sampled intravenous glucose tolerance test (FSIGT; 0.3 g glucose/kg body weight), while the insulin sensitivity was determined by an euglycemic-hyperinsulinemic 5-mU clamp. Glucose 86-93 insulin Homo sapiens 15-22 8773736-2 1996 The stimulated insulin secretion was quantified by the frequently sampled intravenous glucose tolerance test (FSIGT; 0.3 g glucose/kg body weight), while the insulin sensitivity was determined by an euglycemic-hyperinsulinemic 5-mU clamp. Glucose 123-130 insulin Homo sapiens 15-22 8991103-12 1996 Endogenous insulin secretion is even potentiated at increasing blood glucose levels. Glucose 69-76 insulin Homo sapiens 11-18 9092341-4 1996 Moreover, insulin sensitivity was lower in hypertensive compared to normotensive diabetic patients (Steady State Plasma Glucose = 18.8 +/- 3 mmol/l vs 15.1 +/- 3.3 mmol/l p < 0.05) and L3 visceral fat was greater (238 +/- 70 cm2 vs 106 +/- 36 cm2 p < 0.01), although there were no differences in body mass index, L3 subcutaneous fat, waist to hip circumference ratio or age. Glucose 120-127 insulin Homo sapiens 10-17 8725404-3 1996 Receptor-mediated phosphorylation of the IRS proteins is required for the propagation of signals for mitogenesis, glucose transport, and numerous other biological and biochemical events during insulin signaling. Glucose 114-121 insulin Homo sapiens 193-200 8839927-7 1996 GLUT4 is the insulin-regulated glucose transporter found in adipose tissues, heart muscles, and skeletal muscles that is responsible for insulin-regulated glucose disposal. Glucose 31-38 insulin Homo sapiens 13-20 8839927-7 1996 GLUT4 is the insulin-regulated glucose transporter found in adipose tissues, heart muscles, and skeletal muscles that is responsible for insulin-regulated glucose disposal. Glucose 31-38 insulin Homo sapiens 137-144 8960353-9 1996 Cell-permeable ceramides decrease insulin-stimulated glucose uptake in 3T3-L1 adipocytes after 2-24 h, whereas they stimulate basal glucose uptake. Glucose 53-60 insulin Homo sapiens 34-41 9162434-3 1996 Insulin mediated glucose metabolism, in central neurons related anatomically to the ventromedial hypothalamus, mediates fasting-induced suppression, and overfeeding-induced stimulation of the SNS. Glucose 17-24 insulin Homo sapiens 0-7 8777469-7 1996 These results suggest that epinephrine when infused acutely may suppress the insulin response to raised glucose, and that the acute hypophosphatemic effect of epinephrine is related to the glucose production. Glucose 104-111 insulin Homo sapiens 77-84 9162434-7 1996 Data developed in a population based cohort (The Normative Aging Study, NAS) support this hypothesis since: obesity was associated with evidence of increased SNS activity; there was a demonstrable relationship between glucose and insulin levels and SNS activity; and blood pressure was associated with both insulin and sympathetic activity, a relationship that was noted in the population as a whole after adjustment for body mass index and body fat distribution. Glucose 218-225 insulin Homo sapiens 230-237 9162440-5 1996 Also, salt-sensitive subjects displayed a hyperinsulinaemic response to an oral glucose load and a decreased insulin-mediated glucose disposal, as assessed by the insulin suppression test. Glucose 80-87 insulin Homo sapiens 47-54 9162440-5 1996 Also, salt-sensitive subjects displayed a hyperinsulinaemic response to an oral glucose load and a decreased insulin-mediated glucose disposal, as assessed by the insulin suppression test. Glucose 126-133 insulin Homo sapiens 109-116 9162435-1 1996 The primary site of insulin resistance, as measured by the euglycaemic glucose clamp technique, is skeletal muscle. Glucose 71-78 insulin Homo sapiens 20-27 9162436-6 1996 Recent data both from our and other laboratories have clearly established that an acute activation of sympathetic nervous system is able to antagonize insulin-mediated glucose uptake in the skeletal muscle, making very real the possibility that a primary defect in insulin sensitivity in hypertension may be further aggravated by the greater sympathetic response evoked by episodic stimuli, such as postprandial hyperinsulinaemia. Glucose 168-175 insulin Homo sapiens 151-158 9162436-6 1996 Recent data both from our and other laboratories have clearly established that an acute activation of sympathetic nervous system is able to antagonize insulin-mediated glucose uptake in the skeletal muscle, making very real the possibility that a primary defect in insulin sensitivity in hypertension may be further aggravated by the greater sympathetic response evoked by episodic stimuli, such as postprandial hyperinsulinaemia. Glucose 168-175 insulin Homo sapiens 265-272 9221053-3 1996 At postreceptor steps, phosphatidylinositol 3-kinase (PI3-K) plays an important role in insulin signalling, particularly for the stimulation of glucose transport in muscle and adipocyte. Glucose 144-151 insulin Homo sapiens 88-95 8696875-8 1996 These data indicate that a sustained near-normal blood glucose control can be achieved under long-term peritoneal insulin infusion, without significant impairment of diabetic retinopathy when an initial ophthalmological evaluation, and a specific treatment if necessary, are performed. Glucose 55-62 insulin Homo sapiens 114-121 8706294-6 1996 The insulin secretion rate was calculated by the "combined model" approach, after which the insulin secretion rates and the ambient glucose levels were cross-correlated. Glucose 132-139 insulin Homo sapiens 4-11 8737618-6 1996 We matched the presence of at least one residual value in the oral glucose tolerance test above the limit used with the subsequent need for insulin treatment. Glucose 67-74 insulin Homo sapiens 140-147 8706296-12 1996 After insulin administration, glucose reached a similar nadir during beta-endorphin and normal saline (2.1 +/- 0.1 and 1.9 +/- 0.15 mmol/l, respectively) but the fall in plasma glucose was delayed during beta-endorphin (P < 0.01 by ANOVA). Glucose 30-37 insulin Homo sapiens 6-13 8706296-12 1996 After insulin administration, glucose reached a similar nadir during beta-endorphin and normal saline (2.1 +/- 0.1 and 1.9 +/- 0.15 mmol/l, respectively) but the fall in plasma glucose was delayed during beta-endorphin (P < 0.01 by ANOVA). Glucose 177-184 insulin Homo sapiens 6-13 8706299-4 1996 METHODS: Insulin sensitivity was assessed by fasting insulin measurements, as well as following oral glucose tolerance test. Glucose 101-108 insulin Homo sapiens 9-16 8706299-6 1996 insulin tolerance test was performed to measure the rate of endogenous blood glucose disposal following an i.v. Glucose 77-84 insulin Homo sapiens 0-7 8737618-9 1996 From our results, the need for more accurate monitoring and insulin treatment may be predicted by simply looking at the residual values in the glucose tolerance test. Glucose 143-150 insulin Homo sapiens 60-67 8522054-11 1996 Although these nonobese subjects with uncomplicated NIDDM showed postprandial hyperinsulinemia and resistance to the effect of insulin on glucose metabolism, this group was not resistant to the vasodilator and sympathetic stimulant effects of insulin. Glucose 138-145 insulin Homo sapiens 127-134 8522066-13 1996 The insulin sensitivity index (SI) calculated from a frequently sampled intravenous glucose tolerance test (FSIVGTT) after the method of Bergman et al. Glucose 84-91 insulin Homo sapiens 4-11 8522066-20 1996 In summary, IGF-I significantly lowered blood glucose as reflected by short-term and long-term indexes of glycemic control and increased insulin sensitivity. Glucose 46-53 insulin Homo sapiens 137-144 8529789-2 1996 Insulin-mediated glucose metabolism in skeletal muscle is associated with a commensurate increase in muscle perfusion. Glucose 17-24 insulin Homo sapiens 0-7 8529789-5 1996 This defect in insulin-mediated vasodilation may contribute to 1) enhanced pressor sensitivity and 2) reduced rates of insulin-mediated glucose uptake. Glucose 136-143 insulin Homo sapiens 15-22 8529789-5 1996 This defect in insulin-mediated vasodilation may contribute to 1) enhanced pressor sensitivity and 2) reduced rates of insulin-mediated glucose uptake. Glucose 136-143 insulin Homo sapiens 119-126 8529790-7 1996 Applying the same kallikrein inhibitor during the infusion of insulin into the brachial artery significantly reduced the effect of insulin on glucose uptake into forearm muscle. Glucose 142-149 insulin Homo sapiens 62-69 8529790-7 1996 Applying the same kallikrein inhibitor during the infusion of insulin into the brachial artery significantly reduced the effect of insulin on glucose uptake into forearm muscle. Glucose 142-149 insulin Homo sapiens 131-138 8529804-0 1996 Insulin-induced redistribution of GLUT4 glucose carriers in the muscle fiber. Glucose 40-47 insulin Homo sapiens 0-7 8529804-2 1996 Insulin rapidly stimulates glucose transport in muscle fiber. Glucose 27-34 insulin Homo sapiens 0-7 8529804-3 1996 This process controls the utilization of glucose in skeletal muscle, and it is deficient in various insulin-resistant states, such as non-insulin-dependent diabetes mellitus. Glucose 41-48 insulin Homo sapiens 100-107 8529804-4 1996 The effect of insulin on muscle glucose transport is mainly due to the recruitment of GLUT4 glucose carriers to the cell surface of the muscle fiber. Glucose 32-39 insulin Homo sapiens 14-21 8529804-4 1996 The effect of insulin on muscle glucose transport is mainly due to the recruitment of GLUT4 glucose carriers to the cell surface of the muscle fiber. Glucose 92-99 insulin Homo sapiens 14-21 8529809-4 1996 Yet contractions become a more potent stimulus of muscle glucose uptake as the plasma insulin level is increased. Glucose 57-64 insulin Homo sapiens 86-93 8529809-6 1996 Again, however, increased glucose delivery appears to be a more potent stimulus of muscle glucose uptake as the circulating insulin level is increased. Glucose 26-33 insulin Homo sapiens 124-131 8529809-6 1996 Again, however, increased glucose delivery appears to be a more potent stimulus of muscle glucose uptake as the circulating insulin level is increased. Glucose 90-97 insulin Homo sapiens 124-131 8529809-8 1996 In conclusion, the extent to which muscle glucose uptake is stimulated during exercise depends on various factors, including 1) the intensity of the contractile activity, 2) the magnitude of the exercise-associated increase in muscle blood flow, and 3) the circulating insulin level. Glucose 42-49 insulin Homo sapiens 269-276 8720524-4 1996 Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method using Sandostatin. Glucose 62-69 insulin Homo sapiens 0-7 8720525-2 1996 OBJECTIVE: To determine the secretion of insulin, C-peptide, and proinsulin after oral glucose loading in healthy elderly subjects compared with middle-aged subjects with and without obesity and with NIDDM. Glucose 87-94 insulin Homo sapiens 65-75 8720525-8 1996 Increased proinsulin was rather dominant in the OL group, especially late after glucose loading. Glucose 80-87 insulin Homo sapiens 10-20 8720531-4 1996 An index of insulin secretion was derived as a ratio of incremental insulin to incremental glucose concentrations from 0 to 30 min during an oral glucose tolerance test. Glucose 91-98 insulin Homo sapiens 12-19 8720531-4 1996 An index of insulin secretion was derived as a ratio of incremental insulin to incremental glucose concentrations from 0 to 30 min during an oral glucose tolerance test. Glucose 146-153 insulin Homo sapiens 12-19 8720531-6 1996 Asian subjects with NGT showed significant hyperinsulinemia 2 h after oral glucose load (plasma insulin median 274 pmol/l [range 26-1,505] vs. 186 pmol/l [27-720], P < 0.005) compared with whites. Glucose 75-82 insulin Homo sapiens 48-55 8720607-4 1996 Logistic regression analysis showed that in glucokinase-deficient subjects a decrease in insulin sensitivity was associated with deterioration of the glucose tolerance status. Glucose 150-157 insulin Homo sapiens 89-96 8720607-9 1996 Hepatic glucose production at 1 mU.kg body weight-1.min-1 insulin-infusion rate was significantly higher in patients than in control subjects. Glucose 8-15 insulin Homo sapiens 58-65 8720607-12 1996 Insulin resistance might also result from interactions between the unbalanced glucose metabolism and susceptibility gene(s) to low insulin sensitivity likely to be present in this population. Glucose 78-85 insulin Homo sapiens 0-7 8720607-12 1996 Insulin resistance might also result from interactions between the unbalanced glucose metabolism and susceptibility gene(s) to low insulin sensitivity likely to be present in this population. Glucose 78-85 insulin Homo sapiens 131-138 8741810-2 1996 The term "insulin resistance", when applied to human disease, is often equated with impaired whole-body insulin-mediated glucose disposal as determined using techniques such as the hyperinsulinaemic glucose "clamp" technique. Glucose 121-128 insulin Homo sapiens 10-17 8741810-2 1996 The term "insulin resistance", when applied to human disease, is often equated with impaired whole-body insulin-mediated glucose disposal as determined using techniques such as the hyperinsulinaemic glucose "clamp" technique. Glucose 121-128 insulin Homo sapiens 104-111 8741810-8 1996 Using this approach, we have identified multiple abnormalities in the regulation of carbohydrate and lipid metabolism in subjects with a diverse array of insulin-resistant states characterized by variable degrees of glucose intolerance. Glucose 216-223 insulin Homo sapiens 154-161 8741812-4 1996 The 2-h postprandial glucose excursion at 1 year was also significantly less (p < 0.05, ANOVA) in the group treated with insulin lispro. Glucose 21-28 insulin Homo sapiens 124-131 8741812-5 1996 The reductions in the total number of hypoglycaemic episodes and in the postprandial glucose excursion with use of insulin lispro may be beneficial for the long-term management of subjects with Type 1 diabetes. Glucose 85-92 insulin Homo sapiens 115-122 8940617-8 1996 Both insulin and IGF-I increased glucose metabolism during normoxia in astrocytes but not in neurons, whereas during hypoxia this increase was less pronounced. Glucose 33-40 insulin Homo sapiens 5-12 8536617-4 1996 Arginine vasopressin (AVP), bombesin, and acetylcholine potentiate glucose-induced insulin secretion and are known to raise cytosolic calcium levels through binding to cell surface receptors that activate phospholipase C. The effect of AVP on CRE-directed transcription was examined in the beta-cell line HIT. Glucose 67-74 insulin Homo sapiens 83-90 8750567-8 1996 While no differences were seen in the hemoglobin A1c values, there was a trend for a decrease in the pretest blood glucose levels and significant decreases of the 1 and 2-hour postprandial glucose excursions in the patients treated with insulin lispro. Glucose 115-122 insulin Homo sapiens 237-244 8740931-2 1996 Insulin resistance, particularly an impaired action of insulin on the glucose metabolism in skeletal muscles, has been assumed to be the primary factor in the pathophysiology of this disease and it is observed years before the precipitation of overt NIDDM. Glucose 70-77 insulin Homo sapiens 0-7 8740931-2 1996 Insulin resistance, particularly an impaired action of insulin on the glucose metabolism in skeletal muscles, has been assumed to be the primary factor in the pathophysiology of this disease and it is observed years before the precipitation of overt NIDDM. Glucose 70-77 insulin Homo sapiens 55-62 8817248-0 1996 Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Glucose 34-41 insulin Homo sapiens 15-22 8750567-8 1996 While no differences were seen in the hemoglobin A1c values, there was a trend for a decrease in the pretest blood glucose levels and significant decreases of the 1 and 2-hour postprandial glucose excursions in the patients treated with insulin lispro. Glucose 189-196 insulin Homo sapiens 237-244 8671152-4 1996 The women with PCOS had a more pronounced truncal-abdominal fat distribution (P < 0.05) and a lower insulin-mediated glucose disposal (P < 0.01) during the clamp. Glucose 120-127 insulin Homo sapiens 103-110 8817248-1 1996 Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore, pharmacological intervention should aim to improve insulin sensitivity. Glucose 38-45 insulin Homo sapiens 0-7 8817248-1 1996 Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore, pharmacological intervention should aim to improve insulin sensitivity. Glucose 38-45 insulin Homo sapiens 167-174 8817248-3 1996 It also increased insulin-stimulated glucose disposal in patients with NIDDM after acute administration. Glucose 37-44 insulin Homo sapiens 18-25 8817248-7 1996 Parenteral administration of TA resulted in a significant increase of insulin-stimulated glucose-disposal by about 30% (metabolic clearance rate for glucose, 2.5 +/- 0.3 vs. 3.2 +/- 0.4 ml/kg/min and insulin-sensitivity-index: 3.5 +/- 0.5 vs. 4.7 +/- 0.4 mg/kg/microU/ml; p < 0.05, Wilcoxon-Rank-Sum-Test). Glucose 89-96 insulin Homo sapiens 70-77 8817248-7 1996 Parenteral administration of TA resulted in a significant increase of insulin-stimulated glucose-disposal by about 30% (metabolic clearance rate for glucose, 2.5 +/- 0.3 vs. 3.2 +/- 0.4 ml/kg/min and insulin-sensitivity-index: 3.5 +/- 0.5 vs. 4.7 +/- 0.4 mg/kg/microU/ml; p < 0.05, Wilcoxon-Rank-Sum-Test). Glucose 149-156 insulin Homo sapiens 70-77 8817248-9 1996 This is the first clinical study to show that a ten day administration of TA is able to improve resistance of insulin-stimulated glucose disposal in NIDDM. Glucose 129-136 insulin Homo sapiens 110-117 8840171-6 1996 Moreover a higher glucose/ insulin ratio was significantly related to birth weight (p < 0.01). Glucose 18-25 insulin Homo sapiens 27-34 8591890-2 1996 Impaired insulin activation and altered genetic control of muscle glycogen synthase, the rate-limiting enzyme for glucose storage in skeletal muscle, could provide an explanation for this insulin resistance. Glucose 114-121 insulin Homo sapiens 188-195 8591890-6 1996 The presence of the A2 versus the A1 allele was associated with decreased rates of insulin-stimulated glucose storage in hypertensive subjects (11.2 +/- 2.3 versus 16.9 +/- 2.6 mumol/kg lean body mass per minute, P = .029) but not in normotensive subjects (28.0 +/- 4.6 versus 29.6 +/- 3.7 mumol/kg lean body mass per minute). Glucose 102-109 insulin Homo sapiens 83-90 8820989-5 1996 We found, that phentolamine precludes the effect of pinacidil on glucose induced insulin release in healthy man. Glucose 65-72 insulin Homo sapiens 81-88 8788325-1 1996 OBJECTIVE: To determine the extent to which gender differences in the rate of insulin-mediated glucose disposal are influenced by differences in body fatness. Glucose 95-102 insulin Homo sapiens 78-85 8788325-6 1996 MEASUREMENTS: All persons volunteered to undergo a hyperinsulinemic euglycemic clamp procedure to determine the rate of insulin-mediated glucose disposal (insulin sensitivity, M). Glucose 137-144 insulin Homo sapiens 120-127 8847309-6 1996 Glucose disposal rates during the last 30 min of each insulin infusion were significantly reduced after 6 days of IA, averaging 6.45 +/- 1.04 mg.kg fat-free mass (FFM)-1.min-1 before and 4.55 +/- 0.56 mg.kg FFM-1.min-1 after detraining for the LO insulin infusion rate and 13.77 +/- 0.88 mg.kg FFM-1.min-1 before and 11.81 +/- 0.60 mg.kg FFM-1.min-1 after detraining for the HI insulin infusion rate (both P < 0.05), despite the fact that plasma insulin was higher in the inactive state (LO, 19.2 +/- 0.9 microU/ml before and 23.4 +/- 1.5 microU/ml after detraining; HI, 56.0 +/- 2.0 microU/ml before and 61.6 +/- 1.6 microU/ml after detraining; P < 0.05)). Glucose 0-7 insulin Homo sapiens 54-61 8847309-6 1996 Glucose disposal rates during the last 30 min of each insulin infusion were significantly reduced after 6 days of IA, averaging 6.45 +/- 1.04 mg.kg fat-free mass (FFM)-1.min-1 before and 4.55 +/- 0.56 mg.kg FFM-1.min-1 after detraining for the LO insulin infusion rate and 13.77 +/- 0.88 mg.kg FFM-1.min-1 before and 11.81 +/- 0.60 mg.kg FFM-1.min-1 after detraining for the HI insulin infusion rate (both P < 0.05), despite the fact that plasma insulin was higher in the inactive state (LO, 19.2 +/- 0.9 microU/ml before and 23.4 +/- 1.5 microU/ml after detraining; HI, 56.0 +/- 2.0 microU/ml before and 61.6 +/- 1.6 microU/ml after detraining; P < 0.05)). Glucose 0-7 insulin Homo sapiens 247-254 8847309-6 1996 Glucose disposal rates during the last 30 min of each insulin infusion were significantly reduced after 6 days of IA, averaging 6.45 +/- 1.04 mg.kg fat-free mass (FFM)-1.min-1 before and 4.55 +/- 0.56 mg.kg FFM-1.min-1 after detraining for the LO insulin infusion rate and 13.77 +/- 0.88 mg.kg FFM-1.min-1 before and 11.81 +/- 0.60 mg.kg FFM-1.min-1 after detraining for the HI insulin infusion rate (both P < 0.05), despite the fact that plasma insulin was higher in the inactive state (LO, 19.2 +/- 0.9 microU/ml before and 23.4 +/- 1.5 microU/ml after detraining; HI, 56.0 +/- 2.0 microU/ml before and 61.6 +/- 1.6 microU/ml after detraining; P < 0.05)). Glucose 0-7 insulin Homo sapiens 247-254 8550745-1 1996 The euglycemic clamp technique is a useful tool to evaluate insulin-mediated glucose uptake. Glucose 77-84 insulin Homo sapiens 60-67 8550745-3 1996 Because insulin-dependent glucose uptake is closely related to phosphate uptake, we investigated whether modulation of plasma phosphate levels in the range observed during clamp studies influences insulin sensitivity. Glucose 26-33 insulin Homo sapiens 8-15 8550855-10 1996 Oral administration of glucose yielded higher GLP-1 and insulin releases but an equal GIP release compared with the isocaloric duodenal perfusion. Glucose 23-30 insulin Homo sapiens 56-63 8825422-9 1996 Both oleic acid and PMA potentiated glucose-induced insulin release but oleic acid, in contrast to PMA, was unable to initiate insulin release in the presence of substimulatory concentrations of glucose. Glucose 36-43 insulin Homo sapiens 52-59 8965046-3 1996 In 22 nondiabetic women (20-54 years) presenting a wide range of body mass index (from 20 to 48 kg/m2), insulin sensitivity was assessed with the minimal model procedure, over a 180 min intravenous glucose tolerance test with frequent sampling. Glucose 198-205 insulin Homo sapiens 104-111 8965046-4 1996 The insulin sensitivity index SI (i.e. the slope of the dose-response relationship between insulin increased above baseline and glucose disposal) ranges between 0.1 and 20.1 x 10(-4) min-1/microU/ml) i.e all the range of insulin sensitivity. Glucose 128-135 insulin Homo sapiens 4-11 8615385-0 1996 Decreased insulin-mediated but not non-insulin-dependent glucose disposal rates in glucose intolerance and type II diabetes in African (Ghanaian) immigrants. Glucose 83-90 insulin Homo sapiens 10-17 8615385-4 1996 Insulin sensitivity index and Sg were measured by an insulin-modified, frequently sampled intravenous glucose tolerance test. Glucose 102-109 insulin Homo sapiens 53-60 8544782-0 1996 Effects of insulin on glucose turnover rates in vivo: isotope dilution versus constant specific activity technique. Glucose 22-29 insulin Homo sapiens 11-18 8771007-13 1996 GH induced a significant increase in mean integrated plasma insulin levels during oral glucose tolerance test, without changing plasma glucose levels. Glucose 87-94 insulin Homo sapiens 60-67 9284567-1 1996 Hyperinsulinemia and insulin-resistance are metabolic disturbances associated with obesity, essential hypertension, hypertriglyceridemia, glucose intolerance, overt non-insulin dependent diabetes mellitus, polymetabolic syndrome and atherosclerotic disease. Glucose 138-145 insulin Homo sapiens 5-12 9284567-6 1996 We also measured SAI in vivo by assessing the rate of serum glucose decline induced by human cristalline insulin 0.025 U/kg IV dose after a 12-14 hours fasting period (a modified Bonora"s method or BBD) in 11 subjects. Glucose 60-67 insulin Homo sapiens 105-112 8786794-4 1996 Distributions of insulin receptors in the hippocampus and insulin-mediated increases in glucose utilization in entorhinal cortex provide potential mechanisms for such improvement. Glucose 88-95 insulin Homo sapiens 17-24 8742956-1 1996 Glucose intolerance has been shown in patients with chronic renal failure (CRF), probably associated with insulin resistance in peripheral tissues. Glucose 0-7 insulin Homo sapiens 106-113 8742956-14 1996 These data demonstrate that insulin resistance in the presence of chronic uremia is accompanied by impaired muscle glucose uptake and nonoxidative glucose metabolism, which are significantly improved by the hemodialysis treatment. Glucose 115-122 insulin Homo sapiens 28-35 8786794-4 1996 Distributions of insulin receptors in the hippocampus and insulin-mediated increases in glucose utilization in entorhinal cortex provide potential mechanisms for such improvement. Glucose 88-95 insulin Homo sapiens 58-65 8852501-2 1996 Simultaneous administration of sodium bicarbonate and insulin with glucose was compared with infusion of either bicarbonate alone or insulin and glucose. Glucose 67-74 insulin Homo sapiens 54-61 8971927-3 1996 The difference in mass (163.7 Da) from nonglycated insulin (5807.6 Da) corresponds to a single reduced glucose (glucitol) residue. Glucose 103-110 insulin Homo sapiens 51-58 8852501-6 1996 The combined infusion of bicarbonate and insulin with glucose showed the greatest decline in plasma potassium, from 6.2 +/- 0.2 to 5.2 +/- 0.1 mEq/l (p < 0.01). Glucose 54-61 insulin Homo sapiens 41-48 8852501-8 1996 Plasma insulin levels before treatment were similar in all treatment regimens, and increased markedly following the infusion of insulin with glucose, either with or without sodium bicarbonate (9 +/- 1.5 vs. 10 +/- 10 microU/ml before insulin, and 196 +/- 18.0 vs. 201 +/- 26.4 microU/ml after insulin). Glucose 141-148 insulin Homo sapiens 128-135 8852501-8 1996 Plasma insulin levels before treatment were similar in all treatment regimens, and increased markedly following the infusion of insulin with glucose, either with or without sodium bicarbonate (9 +/- 1.5 vs. 10 +/- 10 microU/ml before insulin, and 196 +/- 18.0 vs. 201 +/- 26.4 microU/ml after insulin). Glucose 141-148 insulin Homo sapiens 128-135 8852501-8 1996 Plasma insulin levels before treatment were similar in all treatment regimens, and increased markedly following the infusion of insulin with glucose, either with or without sodium bicarbonate (9 +/- 1.5 vs. 10 +/- 10 microU/ml before insulin, and 196 +/- 18.0 vs. 201 +/- 26.4 microU/ml after insulin). Glucose 141-148 insulin Homo sapiens 128-135 8893142-10 1996 After drainage and rinsing, 66.0 +/- 10 and 71.8 +/- 9.8% of the insulin instilled had disappeared after 6 h from the glucose fluid and from the Ringer solution respectively and did not differ significantly. Glucose 118-125 insulin Homo sapiens 65-72 8878357-1 1996 Insulin and glucagon levels, the mass of glucose presented to the liver and the portal signal are important regulators of the liver"s response to glucose delivery. Glucose 146-153 insulin Homo sapiens 0-7 8728209-1 1996 We evaluated in a cross-over manner the consequences of subcutaneously and intraperitoneally given insulin on glucose control, insulin sensitivity, and serum lipids in 8 type I diabetic patients on continuous ambulatory peritoneal dialysis (CAPD). Glucose 110-117 insulin Homo sapiens 99-106 8878357-4 1996 Our current understanding of the neural control of hepatic glucose metabolism includes a tonic block to the entry of glucose into the liver, probably mediated both by sympathetic neural activity and by a low insulin:glucagon ratio. Glucose 59-66 insulin Homo sapiens 208-215 8878357-7 1996 The portal signal thus relieves the sympathetic inhibition of hepatic glucose uptake and enhances hepatic glucose uptake directly by stimulating the parasympathetic innervation to the liver and indirectly by enhancing insulin release. Glucose 70-77 insulin Homo sapiens 218-225 8878357-7 1996 The portal signal thus relieves the sympathetic inhibition of hepatic glucose uptake and enhances hepatic glucose uptake directly by stimulating the parasympathetic innervation to the liver and indirectly by enhancing insulin release. Glucose 106-113 insulin Homo sapiens 218-225 8927032-1 1995 The insulin mimetic effect of vanadate in in vitro incubation of erythrocytes with high glucose concentrations showed an increase in sorbitol accumulation and glucose utilization using U-14C-glucose. Glucose 88-95 insulin Homo sapiens 4-11 8553400-5 1996 Insulin sensitivity was determined by the steady state plasma glucose method with the use of octreotide acetate. Glucose 62-69 insulin Homo sapiens 0-7 8553400-7 1996 RESULTS: Steady state plasma glucose levels were significantly higher in the atherothrombotic infarction group compared with control subjects and the other two stroke groups, indicating the presence of insulin resistance in patients with atherothrombotic infarction. Glucose 29-36 insulin Homo sapiens 202-209 8543058-5 1995 However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. Glucose 63-70 insulin Homo sapiens 79-86 8750761-3 1995 The type 1 diabetic patients were resistant to insulin-stimulated glucose disposal as estimated by a 45% lower metabolic (P < 0.01) clearance of glucose as compared with controls. Glucose 66-73 insulin Homo sapiens 47-54 7484901-3 1995 After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). Glucose 263-270 insulin Homo sapiens 65-72 8572190-8 1995 Thus decreased glucose tolerance in aging is associated with insulin resistance and also with a relative insensitivity of the beta-cell to the modulation of glucose regulation by sleep and circadian rhythmicity. Glucose 15-22 insulin Homo sapiens 61-68 7489245-5 1995 Factors most strongly correlated with insulin included measures of obesity, fat distribution, and levels of triglyceride, glucose (r = .38 to r = .50 fasting, r = .21 to r = .27 2-hour), and HDL cholesterol (r = -.41 and r = -.22, respectively). Glucose 122-129 insulin Homo sapiens 38-45 7489245-9 1995 In multiple linear regression analyses, log10 fasting insulin was positively and independently associated with body mass index, triglycerides, glucose, fibrinogen, hematocrit, heart rate, diabetes, and hypertension and negatively associated with HDL cholesterol, physical activity, and forced vital capacity. Glucose 143-150 insulin Homo sapiens 54-61 7589843-7 1995 Further, when we stratified subjects by baseline glucose tolerance, both increased fasting insulin and decreased delta I30/delta G30 significantly predicted NIDDM in subjects with both impaired and normal glucose tolerance at baseline. Glucose 49-56 insulin Homo sapiens 91-98 7589851-0 1995 Enteral enhancement of glucose disposition by both insulin-dependent and insulin-independent processes. Glucose 23-30 insulin Homo sapiens 51-58 7589851-0 1995 Enteral enhancement of glucose disposition by both insulin-dependent and insulin-independent processes. Glucose 23-30 insulin Homo sapiens 73-80 7589851-5 1995 The results of the IVGTTs were analyzed using the minimal model technique to determine the insulin sensitivity index (SI) and indexes of insulin-independent glucose disposition, glucose effectiveness at basal insulin (SG), and glucose effectiveness at zero insulin (GEZI), as well as the glucose disappearance constant (k(g)) and the acute insulin response to glucose (AIRg). Glucose 157-164 insulin Homo sapiens 137-144 8750221-9 1995 In summary, IP insulin, when compared to IV insulin at similar delivery rates, but not at similar insulinaemia, is associated with a less negative glucose balance (glucose production-glucose utilization) during hypoglycaemia. Glucose 147-154 insulin Homo sapiens 15-22 8750221-9 1995 In summary, IP insulin, when compared to IV insulin at similar delivery rates, but not at similar insulinaemia, is associated with a less negative glucose balance (glucose production-glucose utilization) during hypoglycaemia. Glucose 164-171 insulin Homo sapiens 15-22 8750221-9 1995 In summary, IP insulin, when compared to IV insulin at similar delivery rates, but not at similar insulinaemia, is associated with a less negative glucose balance (glucose production-glucose utilization) during hypoglycaemia. Glucose 164-171 insulin Homo sapiens 15-22 8786010-3 1995 The methodological difficulties in assessing the fate of glucose in many insulin-resistant states raise the possibility that defects in glycogen synthesis may not be rate-limiting for insulin action. Glucose 57-64 insulin Homo sapiens 73-80 8719935-7 1995 Glucose-stimulated insulin secretion at 60 and 120 min and the area under the curve (AUC) for insulin during the oGTT, were significantly increased after danazol treatment compared with pre-treatment values (P < 0.05), whereas glucagon secretion showed a similar decrease at both time points of investigation (NS). Glucose 0-7 insulin Homo sapiens 19-26 7589662-6 1995 Mean serum insulin levels were significantly higher in patients than in controls, whereas 24% of patients had abnormal insulin responses to glucose and/or insulin sensitivity indexes. Glucose 140-147 insulin Homo sapiens 119-126 8747309-5 1995 Insulin sensitivity was assessed as M-value, the rate at which glucose must be infused to maintain a basal blood glucose level. Glucose 63-70 insulin Homo sapiens 0-7 8747309-5 1995 Insulin sensitivity was assessed as M-value, the rate at which glucose must be infused to maintain a basal blood glucose level. Glucose 113-120 insulin Homo sapiens 0-7 8847263-1 1995 Endurance exercise training reduces glucose-stimulated insulin secretion while elevating insulin action on target tissues. Glucose 36-43 insulin Homo sapiens 55-62 8530617-3 1995 The proband"s consanguineous parents (diabetic mother and normal father) and her sister (impaired glucose tolerance), each of whom showed an exaggerated insulin response to an oral glucose load, were heterozygous for this mutation. Glucose 98-105 insulin Homo sapiens 153-160 8675629-3 1995 Reduced insulin-stimulated glucose uptake and reduced glucose-6-phosphate concentrations in muscle have been found in non-insulin-dependent diabetes mellitus (NIDDM) patients when examined during a hyperglycemic hyperinsulinemic clamp. Glucose 27-34 insulin Homo sapiens 8-15 8866908-4 1995 RESULTS: The mean value for insulin-mediated glucose uptake (M-value at clamp) in the healthy control group (8.2 mg/kg per min) -2 SD was chosen as the cutoff limit for insulin resistance (4.4 mg/kg per min). Glucose 45-52 insulin Homo sapiens 28-35 8866908-4 1995 RESULTS: The mean value for insulin-mediated glucose uptake (M-value at clamp) in the healthy control group (8.2 mg/kg per min) -2 SD was chosen as the cutoff limit for insulin resistance (4.4 mg/kg per min). Glucose 45-52 insulin Homo sapiens 169-176 8786722-7 1995 Baseline insulin levels at 2 hours after an oral glucose load correlated with baseline PAI activity (P < .001) and PAI-1 antigen levels (P < .001). Glucose 49-56 insulin Homo sapiens 9-16 8786722-12 1995 Moreover, in line with the suggestion that high PAI activity goes together with insulin resistance, a relationship between insulin concentration after a glucose load and PAI activity was found. Glucose 153-160 insulin Homo sapiens 123-130 8851476-6 1995 On separate morning, modified insulin suppression test was performed for three hours, which involved a constant infusion of insulin (25 mU/m2/min) glucose (240 mg/m2/min) and somatostatin (350 micrograms/h). Glucose 147-154 insulin Homo sapiens 124-131 7491941-1 1995 Accumulated evidence suggests that GLUT-2, in addition to its role in glucose transport, may also have other functions in glucose-stimulated insulin secretion. Glucose 122-129 insulin Homo sapiens 141-148 8594980-0 1995 A nonradioactive assay for the insulin receptor tyrosine kinase: use in monitoring receptor kinase activity after activation of overexpressed protein kinase C alpha and high glucose treatment. Glucose 174-181 insulin Homo sapiens 31-38 8535874-2 1995 Neonatal plasma insulin concentrations were high relative to blood glucose concentrations and compared with adult insulin-glucose relations. Glucose 122-129 insulin Homo sapiens 114-121 7583558-6 1995 Insulin-stimulated glucose utilization (M), determined by insulin clamp, was significantly lower in the BHt subjects compared with the Nt subjects (men, Nt 6.91 +/- 0.62 versus BHt 5.54 +/- 0.65; women, Nt 5.97 +/- 0.47 versus BHt 3.79 +/- 0.38 mg.kg-1.min-1, P = .006). Glucose 19-26 insulin Homo sapiens 0-7 7583558-6 1995 Insulin-stimulated glucose utilization (M), determined by insulin clamp, was significantly lower in the BHt subjects compared with the Nt subjects (men, Nt 6.91 +/- 0.62 versus BHt 5.54 +/- 0.65; women, Nt 5.97 +/- 0.47 versus BHt 3.79 +/- 0.38 mg.kg-1.min-1, P = .006). Glucose 19-26 insulin Homo sapiens 58-65 8701256-6 1996 The results of static incubation experiments confirmed that the insulin secretion of cryopreserved human islets in response to glucose stimulation was comparable to the response of islets that have not been frozen. Glucose 127-134 insulin Homo sapiens 64-71 8927032-1 1995 The insulin mimetic effect of vanadate in in vitro incubation of erythrocytes with high glucose concentrations showed an increase in sorbitol accumulation and glucose utilization using U-14C-glucose. Glucose 159-166 insulin Homo sapiens 4-11 8927038-9 1995 Recently, following withdrawal of vanadyl treatment up to 30 weeks, diabetic animals which had remained normoglycemic and had normalized glucose tolerance showed improvements in plasma insulin levels both in the basal state and in response to oral glucose, as compared to those which had reverted to hyperglycemia. Glucose 248-255 insulin Homo sapiens 185-192 8927042-4 1995 This increase in insulin sensitivity was primarily due to an increase in non-oxidative glucose disposal, whereas oxidative glucose disposal and both basal and insulin stimulated suppression of hepatic glucose output (HGP) were unchanged. Glucose 87-94 insulin Homo sapiens 17-24 8927046-5 1995 In 1980 it was observed that vanadate vanadyl, when added to intact rat adipocytes, mimics the biological actions of insulin in stimulating hexose uptake and glucose oxidation. Glucose 158-165 insulin Homo sapiens 117-124 8572189-8 1995 The rate of whole body glucose uptake was 53 +/- 6 mumol.kg-1.min-1 and correlated with muscle blood volume during insulin stimulation (r = 0.65, P < 0.02). Glucose 23-30 insulin Homo sapiens 115-122 8572196-5 1995 Insulin induced a 2.5-fold increase in glucose uptake in untreated cells, which was additive to the chelator"s effect. Glucose 39-46 insulin Homo sapiens 0-7 8963374-6 1995 The goal of the Low Level Module, whose characteristics can be adaptively modified by the High Level Module, is to suggest the next insulin dosage, depending on the actual blood glucose measurement and a certain pre-defined insulin delivery protocol. Glucose 178-185 insulin Homo sapiens 132-139 9156573-2 1995 In adipocytes, skeletal muscle and heart the principal regulator is the hormone insulin, which rapidly stimulates glucose uptake by bringing about the translocation of the GLUT4 glucose transporter isoform from an intracellular vesicular compartment to the cell surface. Glucose 114-121 insulin Homo sapiens 80-87 8736275-10 1995 However, the serum insulin levels after glucose ingestion were significantly higher in hyperprolactinaemic patients than in normal subjects, especially at 30 (N 283 +/- 46 vs HP 581 +/- 133 pmol/l) and 60 minutes (N 291 +/- 37 vs HP 544 +/- 61 pmol/l). Glucose 40-47 insulin Homo sapiens 19-26 7589851-5 1995 The results of the IVGTTs were analyzed using the minimal model technique to determine the insulin sensitivity index (SI) and indexes of insulin-independent glucose disposition, glucose effectiveness at basal insulin (SG), and glucose effectiveness at zero insulin (GEZI), as well as the glucose disappearance constant (k(g)) and the acute insulin response to glucose (AIRg). Glucose 157-164 insulin Homo sapiens 137-144 8586149-12 1995 In the case of IGFBP-1, whose hepatic synthesis is negatively regulated by insulin, plasma concentrations are subject to extensive nycthemeral variation, rising with fasting and dropping after feeding, which may be involved in controlling the access of free IGF-I to its cellular receptors and hence IGF-I-regulated glucose and amino acid uptake. Glucose 316-323 insulin Homo sapiens 75-82 8593919-3 1995 The introduction of insulin in the 1920s and then of oral hypoglycaemic drugs led to various studies evaluating the biochemical characteristics of carbohydrates and their effects on glucose metabolism in diabetic patients. Glucose 182-189 insulin Homo sapiens 20-27 8593924-5 1995 After surgical resection of the insulinoma, the blood glucose level rose to 0.94 +/- 0.02 g/l and EGP to 2.33 +/- 0.04 mg kg-1 min-1, whereas the insulin level fell to 6.4 +/- 0.5 mU/l. Glucose 54-61 insulin Homo sapiens 32-39 8593924-8 1995 These data suggest that chronic hyperinsulinaemia is associated with inhibition of endogenous glucose production, a rise in basal glucose clearance and a state of insulin insensitivity during the clamp. Glucose 94-101 insulin Homo sapiens 37-44 8593924-8 1995 These data suggest that chronic hyperinsulinaemia is associated with inhibition of endogenous glucose production, a rise in basal glucose clearance and a state of insulin insensitivity during the clamp. Glucose 130-137 insulin Homo sapiens 37-44 8822315-1 1995 The aims of this study were to determine the change in the rate of insulin-stimulated glucose disposal (insulin sensitivity) and the ability of insulin to inhibit its own secretion in four pancreas-kidney transplant recipients with insulin-dependent diabetes mellitus. Glucose 86-93 insulin Homo sapiens 67-74 8822315-1 1995 The aims of this study were to determine the change in the rate of insulin-stimulated glucose disposal (insulin sensitivity) and the ability of insulin to inhibit its own secretion in four pancreas-kidney transplant recipients with insulin-dependent diabetes mellitus. Glucose 86-93 insulin Homo sapiens 104-111 8822315-1 1995 The aims of this study were to determine the change in the rate of insulin-stimulated glucose disposal (insulin sensitivity) and the ability of insulin to inhibit its own secretion in four pancreas-kidney transplant recipients with insulin-dependent diabetes mellitus. Glucose 86-93 insulin Homo sapiens 104-111 8822315-2 1995 Insulin sensitivity (glucose infusion rate, GIR) was measured by a euglycemic hyperinsulinemic clamp technique before and 2, 6 and 12 months after transplantation. Glucose 21-28 insulin Homo sapiens 0-7 7498970-3 1995 We have previously shown that normotensive offspring of essential hypertensive individuals have an exaggerated insulin response to a glucose overload. Glucose 133-140 insulin Homo sapiens 111-118 7498970-4 1995 Therefore, the aim of the present study was to evaluate basal and calmodulin-activated Ca(2+)-ATPase in red blood cells and its relationship to the insulin response during an intravenous glucose tolerance test in 27 normotensive adolescents with a family history of essential hypertension (F+) (mean age, 13.9 +/- 0.5 years) and in 10 control subjects matched for age and body mass index with no family history of hypertension (F-). Glucose 187-194 insulin Homo sapiens 148-155 7498970-6 1995 The insulin area under the curve after the glucose load was 3413 +/- 1674 microU/mL per hour in F+ and 2752 +/- 928 in F- (P = NS). Glucose 43-50 insulin Homo sapiens 4-11 7498973-6 1995 During the oral glucose tolerance test the hypertensive patients compared with control subjects presented higher levels of glucose at 60 minutes (138.7 +/- 30.3 versus 108.7 +/- 35.7 mg/dL; P < .05) and 90 minutes (114.0 +/- 23.8 versus 94.8 +/- 31.1 mg/dL; P < .05) and insulin at 60 minutes (287.1 +/- 259.4 versus 142.1 +/- 83.9 pmol/L; P < .05). Glucose 123-130 insulin Homo sapiens 277-284 8929644-5 1995 The resistance to the action of insulin on glucose metabolism which was evaluated in three patients by the euglycemic hyperinsulinemic clamp study was found to be comparable to the lowest quartile level for common NIDDM patients. Glucose 43-50 insulin Homo sapiens 32-39 8530635-6 1995 However, in the presence of GLP-1, the insulin response to glucose was markedly potentiated and appeared in a biphasic manner (10-fold first phase and 3-fold second phase). Glucose 59-66 insulin Homo sapiens 39-46 8530635-8 1995 In static incubations, the relative insulin release responses to 16.7 mmol/L glucose plus 10 nmol/L GLP-1 were equal in the fetal and adult cells. Glucose 77-84 insulin Homo sapiens 36-43 8675652-2 1995 A primary human skeletal muscle culture (HSMC) system, which retains cellular integrity and insulin responsiveness for glucose transport was employed to evaluate glucose transport regulation. Glucose 119-126 insulin Homo sapiens 92-99 8675652-8 1995 In summary: (a) insulin resistance of glucose transport can be induced in HSMC of both NC and NIDDM by hyperinsulinemia and is accompanied by unaltered GLUT4 but increased GLUT1 levels; and (b) HSMC from NIDDM subjects demonstrate an increased sensitivity to impairment of glucose transport by hyperglycemia. Glucose 38-45 insulin Homo sapiens 16-23 7491541-6 1995 Furthermore, improved glucose control as shown by a decreased insulin requirement was seen in 57% (four of seven patients) of these patients. Glucose 22-29 insulin Homo sapiens 62-69 8928187-9 1995 The results suggested that, under the conditions of euglycemic hyperinsulinemia by glucose clamp technique, insulin increased the serum free Ca ion, and as a result, PTH was suppressed. Glucose 83-90 insulin Homo sapiens 68-75 7499278-1 1995 Insulin stimulates glucose transport largely by mediating translocation of the insulin-sensitive glucose transporter (GLUT4) from an intracellular compartment to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 7499278-1 1995 Insulin stimulates glucose transport largely by mediating translocation of the insulin-sensitive glucose transporter (GLUT4) from an intracellular compartment to the plasma membrane. Glucose 19-26 insulin Homo sapiens 79-86 8554729-4 1995 Furthermore, the plasma glucose and insulin responses to a 75 g oral glucose load were significantly lower (P < .001) following weight loss. Glucose 69-76 insulin Homo sapiens 36-43 8554729-5 1995 Finally, insulin resistance, as assessed by determining the steady-state plasma glucose (SSPG) concentration at the end of a 180 min infusion of somatostatin, insulin, and glucose, was also lower (P < .002) after the 8 kg weight loss in the normotensive (243 +/- 23 to 172 +/- 15 mg/dL) and hypertensive subjects (266 +/- 18 to 181 +/- 25 mg/dL). Glucose 80-87 insulin Homo sapiens 9-16 8554729-5 1995 Finally, insulin resistance, as assessed by determining the steady-state plasma glucose (SSPG) concentration at the end of a 180 min infusion of somatostatin, insulin, and glucose, was also lower (P < .002) after the 8 kg weight loss in the normotensive (243 +/- 23 to 172 +/- 15 mg/dL) and hypertensive subjects (266 +/- 18 to 181 +/- 25 mg/dL). Glucose 172-179 insulin Homo sapiens 9-16 8554729-7 1995 Thus, weight loss of 8 kg in moderately obese individuals leads to significant decreases in blood pressure and plasma glucose and insulin concentrations in response to an oral glucose challenge and degree of insulin resistance. Glucose 176-183 insulin Homo sapiens 130-137 7491941-5 1995 Furthermore, glucose-stimulated insulin secretion was not affected by over-expression of human GLUT-2. Glucose 13-20 insulin Homo sapiens 32-39 8678268-10 1995 Serum insulin activity showed significant differences as a function of carbohydrate regimen, i.e. infusion of fructose instead of glucose produced a less pronounced increase in insulin activity (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids P<0.01). Glucose 130-137 insulin Homo sapiens 177-184 8678268-10 1995 Serum insulin activity showed significant differences as a function of carbohydrate regimen, i.e. infusion of fructose instead of glucose produced a less pronounced increase in insulin activity (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids P<0.01). Glucose 219-226 insulin Homo sapiens 6-13 8678268-10 1995 Serum insulin activity showed significant differences as a function of carbohydrate regimen, i.e. infusion of fructose instead of glucose produced a less pronounced increase in insulin activity (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids P<0.01). Glucose 219-226 insulin Homo sapiens 177-184 8548941-16 1995 The relations between the dawn rise in glucose and the changes in IGFBP-1, GH and free insulin were examined by multiple linear regression analysis. Glucose 39-46 insulin Homo sapiens 87-94 8548941-22 1995 REGRESSION ANALYSIS: The change in plasma glucose between 0200 and 0700 h in both studies related to free insulin, IGFBP-1 and the sum of the GH levels over the preceding hour (log glucose = 7.87 + 5.32 log IGFBP-1 (P = 0.0001) - 5.05 log free insulin (P = 0.0001) - 1.44 log GH (P = 0.004); R2 = 72%). Glucose 42-49 insulin Homo sapiens 106-113 8548941-22 1995 REGRESSION ANALYSIS: The change in plasma glucose between 0200 and 0700 h in both studies related to free insulin, IGFBP-1 and the sum of the GH levels over the preceding hour (log glucose = 7.87 + 5.32 log IGFBP-1 (P = 0.0001) - 5.05 log free insulin (P = 0.0001) - 1.44 log GH (P = 0.004); R2 = 72%). Glucose 42-49 insulin Homo sapiens 244-251 8563700-1 1995 To determine whether ACE inhibitor other than captopril improves insulin sensitivity in patients with essential hypertension, we measured insulin sensitivity to glucose utilization using SSPG method in 10 lean hypertensive subjects before and after chronic cilazapril treatment (1.5 +/- 0.2 mg/day, 15.6 +/- 2.1 weeks). Glucose 161-168 insulin Homo sapiens 138-145 7589820-10 1995 In the first comparison, in 2,287 subjects studied for 6 years, intensive therapy with sulfonylurea and insulin similarly improved glucose control compared with conventional therapy, with median FPG at 1 year of 6.8 and 8.2 mmol/l, respectively (P < 0.0001). Glucose 131-138 insulin Homo sapiens 104-111 7589820-18 1995 Sulfonylurea, metformin, and insulin therapies were similarly effective in improving glucose control compared with a policy of diet therapy. Glucose 85-92 insulin Homo sapiens 29-36 8582122-4 1995 Assessment of the acute insulin response, through an intravenous glucose tolerance test (IVGTT), was carried out in 9 ICA+ women with previous GDM and normal oral glucose tolerance, and their results were compared to those of a control group (9 women) and a group of 12 adult ICA+ relatives. Glucose 65-72 insulin Homo sapiens 24-31 8582122-6 1995 Women with ICA at diagnosis of GDM and normal oral glucose tolerance after pregnancy showed a decreased insulin response to glucose as compared to the control group. Glucose 51-58 insulin Homo sapiens 104-111 8582122-6 1995 Women with ICA at diagnosis of GDM and normal oral glucose tolerance after pregnancy showed a decreased insulin response to glucose as compared to the control group. Glucose 124-131 insulin Homo sapiens 104-111 8582126-3 1995 Diabetes in middle-aged subjects is characterized by an impairment in glucose induced insulin release, increased fasting hepatic glucose output and resistance to insulin mediated glucose disposal. Glucose 70-77 insulin Homo sapiens 86-93 8582132-6 1995 The insulin-antagonistic effect of GH on glucose uptake was seen after 2 h and was at a maximum 4 to 5 h after the start of the GH infusion (difference in glucose infusion rate between C and 24 was 1.7 +/- 0.4 mg kg-1 min-1, p < 0.01). Glucose 41-48 insulin Homo sapiens 4-11 8582132-6 1995 The insulin-antagonistic effect of GH on glucose uptake was seen after 2 h and was at a maximum 4 to 5 h after the start of the GH infusion (difference in glucose infusion rate between C and 24 was 1.7 +/- 0.4 mg kg-1 min-1, p < 0.01). Glucose 155-162 insulin Homo sapiens 4-11 8582132-8 1995 Infusion of GH at 12 mU kg-1 min-1 induced a less pronounced insulin resistance both with regards to maximal effect (glucose infusion rate C - GH 1.4 +/- 0.5 mg kg-1 min-1, p < 0.05) and duration (3 h). Glucose 117-124 insulin Homo sapiens 61-68 8582132-9 1995 At 6 mU kg-1 min-1, a clear GH-induced insulin-antagonistic effect was only seen during the third hour of the clamp (glucose infusion rate C-GH 1.3 +/- 0.5 mg kg-1 min-1, p < 0.05). Glucose 117-124 insulin Homo sapiens 39-46 8582538-11 1995 In conclusion, our study demonstrates that short- and long-term exposures of beta cells to high plasma NEFA concentrations have opposite effects on glucose-induced insulin secretion. Glucose 148-155 insulin Homo sapiens 164-171 8722067-6 1995 RESULTS: Insulin therapy was required in 53 women (37.5%) to maintain fasting blood glucose levels at < 95 mg/dl and 2-h postprandial levels at < 120 mg/dl. Glucose 84-91 insulin Homo sapiens 9-16 8770624-4 1995 An increase in DHEA sensitivity with an enhanced glucose uptake was observed in cells exposed to 10(-7)M of human insulin. Glucose 49-56 insulin Homo sapiens 114-121 8770624-8 1995 In reciprocal plot analysis, the Km value for glucose transport was decreased by preincubation with DHEA (from 0.67 mM without DHEA, 0.56mM with 10(-5)M DHEA, and 0.25mM with 10(-4) M DHEA), although Vmax was unchanged, We conclude that DHEA increases the affinity of glucose transport in the plasma membrane of cultured rat myoblasts, leading to an enhanced glucose uptake and an increase in insulin sensitivity. Glucose 46-53 insulin Homo sapiens 393-400 7591019-3 1995 Recent evidence has shown that hypertensive patients with microalbuminuria have a hyperinsulinemic response to oral glucose, suggesting the presence of insulin resistance. Glucose 116-123 insulin Homo sapiens 87-94 7591019-7 1995 Insulin-stimulated wholebody glucose uptake was 25% lower in microalbuminuric patients (33.5 +/- 2.5 versus 25.2 +/- 2.1 mumol/min-1/kg-1, P < .02). Glucose 29-36 insulin Homo sapiens 0-7 8589781-2 1995 In this study, we considered the independent contributions of age, total body fatness, abdominal fat distribution, peak aerobic capacity, leisure time physical activity, dietary intake, and fasting glucose levels to the age-associated increase in fasting insulin levels in healthy men and women. Glucose 198-205 insulin Homo sapiens 255-262 7593419-6 1995 Carbenoxolone increased whole body insulin sensitivity (M values for dextrose infusion rates, 41.1 +/- 2.4 mumol/kg.min for placebo vs. 44.6 +/- 2.3 for carbenoxolone; P < 0.03), but had no effect on forearm insulin sensitivity. Glucose 69-77 insulin Homo sapiens 35-42 7593453-0 1995 Relationship between insulin-mediated glucose disposal by muscle and adipose tissue lipolysis in healthy volunteers. Glucose 38-45 insulin Homo sapiens 21-28 7593453-2 1995 Insulin-mediated glucose disposal was assessed by determining the steady state plasma glucose (SSPG) concentration during the insulin suppression test [180 min infusion of somatostatin (350 micrograms/h), insulin (25 mU/m2min), and glucose (240 mg/m2.min)]. Glucose 17-24 insulin Homo sapiens 0-7 7593453-2 1995 Insulin-mediated glucose disposal was assessed by determining the steady state plasma glucose (SSPG) concentration during the insulin suppression test [180 min infusion of somatostatin (350 micrograms/h), insulin (25 mU/m2min), and glucose (240 mg/m2.min)]. Glucose 17-24 insulin Homo sapiens 126-133 7593453-2 1995 Insulin-mediated glucose disposal was assessed by determining the steady state plasma glucose (SSPG) concentration during the insulin suppression test [180 min infusion of somatostatin (350 micrograms/h), insulin (25 mU/m2min), and glucose (240 mg/m2.min)]. Glucose 86-93 insulin Homo sapiens 0-7 7593453-2 1995 Insulin-mediated glucose disposal was assessed by determining the steady state plasma glucose (SSPG) concentration during the insulin suppression test [180 min infusion of somatostatin (350 micrograms/h), insulin (25 mU/m2min), and glucose (240 mg/m2.min)]. Glucose 86-93 insulin Homo sapiens 0-7 7593453-6 1995 These results demonstrate for the first time that plasma FFA and glycerol concentrations are increased commensurate with the degree of resistance to insulin-mediated glucose disposal at a basal insulin level, in response to isoproterenol stimulation, and after insulin inhibition of isoproterenol-stimulated lipolysis. Glucose 166-173 insulin Homo sapiens 149-156 8583481-2 1995 The primary site of insulin resistance, as measured by the glucose clamp technique, is skeletal muscle. Glucose 59-66 insulin Homo sapiens 20-27 7476324-9 1995 Pancreatic insulin secretion expressed as the integrated area of plasma insulin above the basal level during the first 19 minutes was significantly lower in obese subjects with IGT (3,366 +/- 1,495 pmol/L.min) than in those with normal glucose tolerance (16,400 +/- 4,509 pmol/L.min, P < .05). Glucose 236-243 insulin Homo sapiens 11-18 7476331-3 1995 PBMNC from newly diagnosed IDDM children elicited basal nonfasting hyperglycemia and in vitro inhibition of the first and second phases of glucose-stimulated insulin secretion in recipient mice. Glucose 139-146 insulin Homo sapiens 158-165 7476331-8 1995 When relapsed to their former clinical stage, injection of the cells significantly inhibited first-phase glucose-induced insulin secretion in recipients. Glucose 105-112 insulin Homo sapiens 121-128 7476337-4 1995 It was therefore hypothesized that the increased insulin resistance of NIDDM would result in an even greater defect in the response of ATLPL to insulin/glucose. Glucose 152-159 insulin Homo sapiens 49-56 7476337-4 1995 It was therefore hypothesized that the increased insulin resistance of NIDDM would result in an even greater defect in the response of ATLPL to insulin/glucose. Glucose 152-159 insulin Homo sapiens 144-151 7487889-4 1995 Cytochalasin B, a competitive inhibitor of hexose transport mediated by the GLUT1 and GLUT4 facilitative glucose transporters, completely inhibited insulin-stimulated glucose incorporation into glycogen and glucose oxidation (P < 0.01), but did not alter fructose incorporation into glycogen or fructose oxidation. Glucose 105-112 insulin Homo sapiens 148-155 7487889-5 1995 Insulin (1000 mu-units/ml) increased glucose incorporation into glycogen 2.7-fold and glucose oxidation 2.3-fold, whereas no effect on fructose incorporation into glycogen or fructose oxidation was noted. Glucose 37-44 insulin Homo sapiens 0-7 7487889-11 1995 In the presence of 5 mM glucose, physiological concentrations of fructose could account for approximately 10-30% of hexose (glucose + fructose) incorporation into glycogen under non-insulin-stimulated conditions. Glucose 24-31 insulin Homo sapiens 182-189 7487895-2 1995 Accordingly, we have now evaluated the linkage between this insulin-regulation of VSMC[Ca2+]i and classical actions of insulin (i.e. glucose transport and metabolism). Glucose 133-140 insulin Homo sapiens 60-67 7487895-2 1995 Accordingly, we have now evaluated the linkage between this insulin-regulation of VSMC[Ca2+]i and classical actions of insulin (i.e. glucose transport and metabolism). Glucose 133-140 insulin Homo sapiens 119-126 7487895-4 1995 Insulin caused an 87% increase in [Ca2+]i recovery rate after stimulation with arginine-vasopressin (P < 0.01) and caused a marked increase in Ca(2+)-ATPase mRNA and protein levels in the presence of glucose. Glucose 203-210 insulin Homo sapiens 0-7 7487991-5 1995 The presence of this mutation was also accompanied by significantly higher fasting (p = 0.000) and 2 hrs (p = 0.018) serum insulin levels during an oral glucose tolerance test. Glucose 153-160 insulin Homo sapiens 123-130 7572943-0 1995 Exploration of simple insulin sensitivity measures derived from frequently sampled intravenous glucose tolerance (FSIGT) tests. Glucose 95-102 insulin Homo sapiens 22-29 7572943-4 1995 The authors considered eight previously described measures or indices of indices of insulin sensitivity derived from the frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 152-159 insulin Homo sapiens 84-91 7572943-5 1995 Each one was evaluated by strength and consistency of association with insulin sensitivity computed from glucose clamp (SI(clamp)), across three glucose tolerance groups, including participants with normal glucose tolerance (n = 11), impaired glucose tolerance (n = 20), and non-insulin-dependent diabetes mellitus (n = 24). Glucose 105-112 insulin Homo sapiens 71-78 7572943-8 1995 (Diabetic Medicine 1990;9:921-8), defined as glucose disappearance (10-50 minutes) divided by insulin area under the curve above baseline from 0-50 minutes, performed best based on statistical criteria and time-savings. Glucose 45-52 insulin Homo sapiens 94-101 7572943-9 1995 Galvin insulin sensitivity is simple to calculate, requires only a 50-minute FSIGT, and is significantly (p < 0.001) and not inconsistently (p = 0.12 for inconsistent association) associated with SI(clamp) over a wide range of glucose tolerance. Glucose 230-237 insulin Homo sapiens 7-14 7485299-0 1995 Insulin and glucose modulate glucose transporter messenger ribonucleic acid expression and glucose uptake in trophoblasts isolated from first-trimester chorionic villi. Glucose 29-36 insulin Homo sapiens 0-7 7485299-1 1995 OBJECTIVE: Our purpose was to determine the effects of insulin and glucose on glucose transport and expression of GLUT1 glucose transporter messenger ribonucleic acid in first-trimester human trophoblast-like cells. Glucose 78-85 insulin Homo sapiens 55-62 7485299-17 1995 CONCLUSION: Although it has been assumed that the placenta has a limited role in influencing glucose transport to the fetus, our in vitro data demonstrate that both insulin and glucose can modulate glucose transport at the cellular level of the placental trophoblast. Glucose 93-100 insulin Homo sapiens 165-172 7485299-18 1995 Thus maternal insulin and glycemic status may influence the expression of GLUT1, the major trophoblast glucose transporter protein, therefore directly affecting first-trimester placental glucose transport. Glucose 103-110 insulin Homo sapiens 14-21 8562259-4 1995 Since hypertension, hypercholesterolemia, hyperglycemia and insulin resistance are frequently associated, further improvement in cardiovascular risk can be obtained only with a comprehensive approach to the hypertensive patients, including dietary and life style modifications and the use of antihypertensive drugs with beneficial effects on lipid and glucose metabolism. Glucose 352-359 insulin Homo sapiens 60-67 15251563-2 1995 The insulin infusion achieved a mean (+/-SD) overnight blood glucose concentration of 101 +/- 15 mg/dL and 24-hour glucose concentration of 118 +/- 18 mg/dL. Glucose 61-68 insulin Homo sapiens 4-11 15251563-3 1995 The intravenous insulin requirement of 81 +/- 32 U/day correlated well (P<0.001) with the subsequent subcutaneous insulin requirement of 84 +/- 43 U/day necessary to maintain preprandial glucose values of 112 +/- 15 mg/dL. Glucose 190-197 insulin Homo sapiens 117-124 8640333-17 1995 SNP alone at 3 microM was ineffective but at 30 microM substantially reduced to second phase of insulin response to glucose; however, at both concentrations the NO donor partly reversed alterations in insulin secretion caused by L-NAME (5 mM) and restored a biphasic response. Glucose 116-123 insulin Homo sapiens 96-103 8563461-1 1995 This study examined plasma insulin response to oral glucose load and autonomic nervous system activity in male lower limb amputees (n = 52) aged 50-65 years, compared to matched controls (n = 53). Glucose 52-59 insulin Homo sapiens 27-34 7671357-4 1995 Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method for nondiabetic, normotensive, nonobese subjects (16 control subjects, 16 obstructive coronary artery disease patients, and 16 VAP patients). Glucose 62-69 insulin Homo sapiens 0-7 7671357-5 1995 Compared with the control group, the 2-hour insulin area (area under the plasma insulin concentration-time curve) during a 75-g oral glucose tolerance test was significantly higher in both VAP groups with normal and impaired glucose tolerance. Glucose 133-140 insulin Homo sapiens 44-51 8789672-6 1995 Insulin level was significantly elevated in patients with microvascular angina 90 min (median: 101 versus 54 microU/ml) and 120 min (median: 88 versus 51 microU/ml) after ingestion of 100 g glucose. Glucose 190-197 insulin Homo sapiens 0-7 7671357-5 1995 Compared with the control group, the 2-hour insulin area (area under the plasma insulin concentration-time curve) during a 75-g oral glucose tolerance test was significantly higher in both VAP groups with normal and impaired glucose tolerance. Glucose 133-140 insulin Homo sapiens 80-87 7586939-12 1995 As a result of these findings, we propose that a rapidly absorbed analogue of insulin is capable of achieving better control of postprandial glucose at a more convenient injection time. Glucose 141-148 insulin Homo sapiens 78-85 7556952-1 1995 Insulin has important effects to increase skeletal muscle (leg) blood flow under euglycemic hyperinsulinemic clamp conditions and after oral glucose tolerance testing. Glucose 141-148 insulin Homo sapiens 0-7 7664650-2 1995 Wortmannin (WM), an inhibitor of PI3k, inhibits the stimulation of glucose transport by insulin and the gain of glucose transporters at the cell surface. Glucose 67-74 insulin Homo sapiens 88-95 7556964-4 1995 This decrease disappeared during the second 24 h. In summary, we found that physiologically elevated plasma FFAs 1) potentiated glucose-stimulated insulin secretion for 48 h and 2) initially caused peripheral insulin resistance that disappeared during the 2nd day, probably as a result of elevated circulating insulin levels. Glucose 128-135 insulin Homo sapiens 147-154 7664650-3 1995 However, the effect of inhibition of PI3k on the maintenance of the basal and the insulin-stimulated glucose transport and on the intracellular donor pool of glucose transporters has not been clarified. Glucose 101-108 insulin Homo sapiens 82-89 8529763-5 1995 Fasting plasma glucose concentrations decreased from 8.9 to 6.4 mmol/L after 10 weeks of metformin treatment (p < 0.001), in association with significantly lower (p < 0.001) plasma glucose and insulin concentrations in response to an oral glucose load. Glucose 15-22 insulin Homo sapiens 199-206 7664650-10 1995 We conclude that in muscle cells PI3k activity is required to maintain basal and insulin-stimulated glucose and amino acid transport, as well as to develop the stimulation of the two transport processes in response to the hormone. Glucose 100-107 insulin Homo sapiens 81-88 8690166-1 1995 Insulin-induced glucose transport stimulation, which results from the translocation of glucose transporter 4 (GLUT 4)-containing vesicles, is completely blocked after prolonged insulin treatment of 3T3-L1 adipocytes. Glucose 16-23 insulin Homo sapiens 0-7 8745206-3 1995 The glucose infusion rate (GIR, mg/kg/min), an index of whole body insulin resistance (IR), was measured by the euglycemic (80 mg/dl) hyperinsulinemic clamp technique (insulin infusion rate 1.12 mU/kg/min). Glucose 4-11 insulin Homo sapiens 67-74 8690166-1 1995 Insulin-induced glucose transport stimulation, which results from the translocation of glucose transporter 4 (GLUT 4)-containing vesicles, is completely blocked after prolonged insulin treatment of 3T3-L1 adipocytes. Glucose 16-23 insulin Homo sapiens 177-184 8846686-11 1995 The demonstrable influence on the kinetics of free insulin and glucose utilization leads to a slight increase in daily total insulin requirements. Glucose 63-70 insulin Homo sapiens 125-132 8690174-6 1995 A high fasting plasma NEFA concentration was also a risk factor for NIDDM (RR=2.3; 95% CI=1.1-4.7) independent of sex, percent body fat, waist/thigh ratio, insulin-mediated glucose uptake and fasting triglyceride concentration. Glucose 173-180 insulin Homo sapiens 156-163 8846687-0 1995 The 30 minute insulin incremental response in an oral glucose tolerance test as a measure of insulin secretion. Glucose 54-61 insulin Homo sapiens 14-21 8575727-4 1995 Since the SSPI concentrations are similar in all individuals, the SSPG concentrations provide an estimate of the ability of insulin to stimulate glucose disposal. Glucose 145-152 insulin Homo sapiens 124-131 7559871-2 1995 Highly reproducible decreases in plasma glucose (< 2.8 mmol/L) occurred on study days 1, 2, 3, 4, and 12 after iv insulin boluses (0.04 U/kg). Glucose 40-47 insulin Homo sapiens 117-124 7559882-5 1995 Insulin sensitivity was assessed by a frequent-sample iv glucose tolerance test (ivGTT, 0.3 g/kg). Glucose 57-64 insulin Homo sapiens 0-7 7559882-9 1995 Thus, hyperinsulinemia with normal fasting glucose levels in HA girls may reflect insulin resistance, as suggested by the increased ratio of insulin and glucose (P < 0.001). Glucose 43-50 insulin Homo sapiens 11-18 7559882-9 1995 Thus, hyperinsulinemia with normal fasting glucose levels in HA girls may reflect insulin resistance, as suggested by the increased ratio of insulin and glucose (P < 0.001). Glucose 153-160 insulin Homo sapiens 11-18 8573730-1 1995 This study was designed to investigate the effects of the calcium channel blocker manidipine on insulin-dependent glucose uptake (insulin sensitivity) and insulin action to renal sodium handling and pressor systems in essential hypertensive (EHT). Glucose 114-121 insulin Homo sapiens 96-103 8573730-1 1995 This study was designed to investigate the effects of the calcium channel blocker manidipine on insulin-dependent glucose uptake (insulin sensitivity) and insulin action to renal sodium handling and pressor systems in essential hypertensive (EHT). Glucose 114-121 insulin Homo sapiens 130-137 8573730-1 1995 This study was designed to investigate the effects of the calcium channel blocker manidipine on insulin-dependent glucose uptake (insulin sensitivity) and insulin action to renal sodium handling and pressor systems in essential hypertensive (EHT). Glucose 114-121 insulin Homo sapiens 130-137 8573730-3 1995 Insulin sensitivity was evaluated as M-value calculated from the infusion rate of glucose. Glucose 82-89 insulin Homo sapiens 0-7 8573730-7 1995 Thus, the calcium channel blocker improved insulin resistance as assessed by glucose clamp technique in EHT. Glucose 77-84 insulin Homo sapiens 43-50 7476300-8 1995 The fasting insulin to glucose ratio was significantly increased in IGT and new type II diabetes subjects. Glucose 23-30 insulin Homo sapiens 12-19 7476303-3 1995 Fasting plasma insulin was higher than expected for concomitant glucose levels, and several of the 20 patients who underwent an oral glucose tolerance test (OGTT) had glucose intolerance and relatively high insulin levels. Glucose 64-71 insulin Homo sapiens 15-22 7476289-1 1995 Infusion of epinephrine and norepinephrine reduces insulin-mediated glucose disposal, ie, induces insulin resistance. Glucose 68-75 insulin Homo sapiens 51-58 7476289-1 1995 Infusion of epinephrine and norepinephrine reduces insulin-mediated glucose disposal, ie, induces insulin resistance. Glucose 68-75 insulin Homo sapiens 98-105 7476289-3 1995 However, the effect of acute mental stress on insulin-mediated glucose uptake has not been examined. Glucose 63-70 insulin Homo sapiens 46-53 7476303-3 1995 Fasting plasma insulin was higher than expected for concomitant glucose levels, and several of the 20 patients who underwent an oral glucose tolerance test (OGTT) had glucose intolerance and relatively high insulin levels. Glucose 133-140 insulin Homo sapiens 207-214 7476303-3 1995 Fasting plasma insulin was higher than expected for concomitant glucose levels, and several of the 20 patients who underwent an oral glucose tolerance test (OGTT) had glucose intolerance and relatively high insulin levels. Glucose 133-140 insulin Homo sapiens 207-214 8538592-0 1995 [Contribution of insulin resistance on intracellular glucose metabolism in patients with cancer: preliminary report]. Glucose 53-60 insulin Homo sapiens 17-24 16031847-3 1995 Plasma insulin concentrations in the healthy cat increased and decreased in parallel with the plasma glucose concentration. Glucose 101-108 insulin Homo sapiens 7-14 16031847-5 1995 Reflecting these observations, the amended insulin to glucose ratios in the affected cat were much lower than those of the healthy cat, until the 4-hour sample. Glucose 54-61 insulin Homo sapiens 43-50 8522882-2 1995 Diet and/or insulin was prescribed to adjust their glucose control at fasting to < 100 mg/dl, as well as at 2 hours postprandial to < 120 mg/dl. Glucose 51-58 insulin Homo sapiens 12-19 8541012-2 1995 We have previously evaluated whole body glucose disposal and insulin sensitivity in different models of hypertensive rats, showing an increase rather than an impairment of glucose metabolism, which in turn was due to an improved ability of insulin to channel the absorbed glucose towards the nonoxidative disposal. Glucose 40-47 insulin Homo sapiens 240-247 7576535-5 1995 Intermittent additions of serum or insulin to a dual substrate (glucose and glutamine) limited fed batch culture increased the growth rate also here, and the results indicate the existence of a minimum growth rate (about 0.02 h-1) at a threshold glutamine level (0.005 mM). Glucose 64-71 insulin Homo sapiens 35-42 7576535-7 1995 The reduced concentrations of glucose and glutamine in substrate limited fed batch cultures suppressed substrate consumption rates and byproduct formation (lactate, ammonium, alanine, other amino acids) even in the serum and insulin stimulated cultures and rendered the energy metabolism much more efficient than in batch culture. Glucose 30-37 insulin Homo sapiens 225-232 7664422-6 1995 Severity of coronary atherosclerosis correlated significantly (P < .05 to P < .01) with basal proinsulin (r = .40) and the proinsulin area under the curve (AUC) (r = .34), basal insulin (r = .31), basal C peptide (r = .30), and the glucose AUC (r = .30). Glucose 238-245 insulin Homo sapiens 129-139 7677082-9 1995 In conclusion, both fasting serum insulin and C-peptide concentrations are significantly associated with BP in this homogeneous Chinese population with normal glucose tolerance. Glucose 159-166 insulin Homo sapiens 34-41 7677082-9 1995 In conclusion, both fasting serum insulin and C-peptide concentrations are significantly associated with BP in this homogeneous Chinese population with normal glucose tolerance. Glucose 159-166 insulin Homo sapiens 46-55 7481291-1 1995 Hypoglycaemia can occur if the endogenous liver glucose output is lower than the glucose uptake in insulin-sensitive and insulin-insensitive tissues. Glucose 81-88 insulin Homo sapiens 99-106 8540943-7 1995 Maternal infusion of 5% dextrose at 180 mL/h (9 g/h), compared with saline solution, produces higher glucose levels in both mother and fetus, but increased insulin concentrations only in the mother. Glucose 24-32 insulin Homo sapiens 156-163 7554137-3 1995 The oral glucose challenge significantly increased plasma glucose, plasma insulin, and the lymphocytic Na(+)-H+ exchange activity, measured as change of pHi per second (control [0 hours], 5.20 +/- 0.53 x 10(-3) dpHi/s; 1 hour after glucose administration, 8.28 +/- 1.07 x 10(-3) dpHi/s; 2 hours after glucose administration, 8.15 +/- 1.18 x 10(-3) dpHi/s; P = .002). Glucose 9-16 insulin Homo sapiens 74-81 8541012-6 1995 In conclusion, under our experimental conditions, hypertension and chronic hyperadrenergism are associated with an increased ability of insulin to stimulate glucose uptake and disposal. Glucose 157-164 insulin Homo sapiens 136-143 7677463-10 1995 In those patients with adequate follow-up, 121 of 146 patients (82.9%) with NIDDM and 150 of 152 patients (98.7%) with glucose impairment maintained normal levels of plasma glucose, glycosylated hemoglobin, and insulin. Glucose 119-126 insulin Homo sapiens 211-218 8535550-3 1995 Insulin sensitivity was determined by fasting serum insulin, glucose disposal rate (GDR) and insulin sensitivity index (GDR/I) using euglycemic hyperinsulinemic glucose clamp technique. Glucose 61-68 insulin Homo sapiens 0-7 8542740-3 1995 We have, therefore, measured fasting plasma triglyceride and NEFA, and the insulin-mediated suppression of NEFA during an oral glucose tolerance test in 93 men and women aged 50, born in Preston, whose birthweight and body size at birth had been recorded. Glucose 127-134 insulin Homo sapiens 75-82 8580884-0 1995 Insulin resistance and myocardial hypertrophy in the attenuated reduction in mean arterial pressure after a glucose load in hypertensive patients. Glucose 108-115 insulin Homo sapiens 0-7 8580884-3 1995 In the first part of the present study we characterized the reduction in blood pressure after a glucose load in hypertensive patients with and without insulin resistance. Glucose 96-103 insulin Homo sapiens 151-158 8580884-5 1995 In the hypertensive patients with insulin resistance the reduction in mean arterial pressure (MAP) after a glucose load was blunted (6.7 +/- 1.7% (N = 5)) when compared to insulin-sensitive (12.9 +/- 1.1% (N = 9)) and normal subjects (10.1 +/- 0.8%). Glucose 107-114 insulin Homo sapiens 34-41 8580884-7 1995 The glucose disappearance rate (Kitt) was lower in hypertensive patients with myocardial hypertrophy (6.0 +/- 1.0 (N = 6)) when compared to hypertensive patients without myocardial hypertrophy (8.2 +/- 1.0%/min (N = 8)), suggesting an association between this organomegaly and insulin resistance. Glucose 4-11 insulin Homo sapiens 277-284 7493430-15 1995 Hypopituitary patients with normal glucose tolerance compared with normal control subjects had a significantly lower fasting plasma glucose concentration (P < 0.01), a lower fasting insulin concentration (P < 0.006), a lower insulin-glucose ratio (P < 0.02) and a lower percentage of insulin to total insulin-like molecules [hypopituitary patients, 90% (81-96%); control subjects, 93% (78-97%); P < 0.02]. Glucose 35-42 insulin Homo sapiens 185-192 7657022-0 1995 Insulin-stimulated muscle glucose clearance in patients with NIDDM. Glucose 26-33 insulin Homo sapiens 0-7 7657022-4 1995 We studied the effect of training on insulin-mediated glucose clearance rates (GCRs) in the whole body and in leg muscle in seven patients with NIDDM and in eight healthy control subjects. Glucose 54-61 insulin Homo sapiens 37-44 7657027-7 1995 Initial sib-pair linkage analysis revealed a possible association between 2-h post-glucose challenge insulin levels and the intestinal fatty acid-binding protein (FABP2) locus located in the region of chromosome 4q28-31 (P = 0.006). Glucose 83-90 insulin Homo sapiens 101-108 8542741-7 1995 To conclude, plasma TBARS were increased in impaired glucose tolerance and in diabetes and they were related to prevailing plasma glucose and insulin levels, suggesting a role for insulin resistance in increased lipid peroxidation process. Glucose 53-60 insulin Homo sapiens 180-187 8542740-4 1995 Elevated fasting plasma triglycerides and reduced NEFA suppression during the oral glucose tolerance test were associated with the male sex, glucose intolerance, central obesity as indicated by a high waist to hip ratio and insulin resistance as measured by a short insulin tolerance test. Glucose 83-90 insulin Homo sapiens 224-231 8542740-4 1995 Elevated fasting plasma triglycerides and reduced NEFA suppression during the oral glucose tolerance test were associated with the male sex, glucose intolerance, central obesity as indicated by a high waist to hip ratio and insulin resistance as measured by a short insulin tolerance test. Glucose 83-90 insulin Homo sapiens 266-273 7657103-6 1995 The rate of entry of ingested glucose into the systemic circulation was similar, but higher postprandial glucagon and lower insulin concentrations led to greater (P < 0.01) postprandial hepatic glucose release. Glucose 197-204 insulin Homo sapiens 124-131 8591826-1 1995 We have previously demonstrated that glucose-tolerant American blacks manifest significantly higher insulin concentrations and a lower insulin sensitivity than native African blacks who reside in their respective countries. Glucose 37-44 insulin Homo sapiens 100-107 8591826-1 1995 We have previously demonstrated that glucose-tolerant American blacks manifest significantly higher insulin concentrations and a lower insulin sensitivity than native African blacks who reside in their respective countries. Glucose 37-44 insulin Homo sapiens 135-142 7584634-1 1995 The aim of this study was to determine how the insulin sensitive enzymes pyruvate dehydrogenase (PDH) complex and glycogen synthase (GS) of different tissues respond to an endogenous pulse of insulin elicited by an intravenous infusion of glucose. Glucose 239-246 insulin Homo sapiens 47-54 7584634-1 1995 The aim of this study was to determine how the insulin sensitive enzymes pyruvate dehydrogenase (PDH) complex and glycogen synthase (GS) of different tissues respond to an endogenous pulse of insulin elicited by an intravenous infusion of glucose. Glucose 239-246 insulin Homo sapiens 192-199 7584634-2 1995 An infusion of glucose (0.5 g/kg) into conscious, unrestrained animals via an indwelling cannula rapidly elevated plasma insulin concentration (to approx. Glucose 15-22 insulin Homo sapiens 121-128 8581072-3 1995 Impaired glucose tolerance is observed when insulin resistance is associated to impaired first-phase insulin response, which results in a significant increase in plasma glucose levels and a late insulin hyperresponsiveness. Glucose 9-16 insulin Homo sapiens 44-51 8581072-2 1995 In obese subjects, glucose tolerance can be maintained within the normal range by compensating for insulin resistance by peripheral hyperinsulinism, the latter resulting from both increased insulin secretion and reduced insulin clearance. Glucose 19-26 insulin Homo sapiens 99-106 7548306-6 1995 The Insulin/Glucose ratio was also higher (p < 0.01) at 0 and 120 min of OGTT, this might be indirect evidence of Insulin- Resistance. Glucose 12-19 insulin Homo sapiens 4-11 7548306-6 1995 The Insulin/Glucose ratio was also higher (p < 0.01) at 0 and 120 min of OGTT, this might be indirect evidence of Insulin- Resistance. Glucose 12-19 insulin Homo sapiens 117-124 7544796-1 1995 Insulin stimulates glucose transport in muscle and adipose tissue by triggering the movement of the glucose transporter GLUT-4 from an intracellular compartment to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 7657800-1 1995 It was the aim of this study to determine whether FFA inhibit insulin-stimulated whole body glucose uptake and utilization in patients with non-insulin-dependent diabetes. Glucose 92-99 insulin Homo sapiens 62-69 7657800-4 1995 Fat/heparin infusion did not affect basal glucose uptake, but inhibited total stimulated (insulin stimulated plus basal) glucose uptake by 40-50% in isoglycemic and in euglycemic patients at plasma FFA concentration of approximately 950 and approximately 550 microM, respectively. Glucose 121-128 insulin Homo sapiens 90-97 7657800-5 1995 In isoglycemic patients, the 40-50% inhibition of total stimulated glucose uptake was due to near complete inhibition of the insulin-stimulated part of glucose uptake. Glucose 67-74 insulin Homo sapiens 125-132 7657800-5 1995 In isoglycemic patients, the 40-50% inhibition of total stimulated glucose uptake was due to near complete inhibition of the insulin-stimulated part of glucose uptake. Glucose 152-159 insulin Homo sapiens 125-132 7657800-7 1995 In summary, fat produced proportional inhibitions of insulin-stimulated glucose uptake and of intracellular glucose utilization. Glucose 72-79 insulin Homo sapiens 53-60 8847690-2 1995 It showed that intensive insulin therapy, designed to produce "near-normal" blood glucose levels, resulted in a spectacular reduction in long-term risks of all microvascular complications of insulin dependent diabetes mellitus (IDDM) when compared with "conventional" insulin therapy. Glucose 82-89 insulin Homo sapiens 25-32 9420879-0 1995 Reciprocal variations in insulin-stimulated glucose uptake and pancreatic insulin secretion in women with normal glucose tolerance. Glucose 44-51 insulin Homo sapiens 25-32 9420879-0 1995 Reciprocal variations in insulin-stimulated glucose uptake and pancreatic insulin secretion in women with normal glucose tolerance. Glucose 113-120 insulin Homo sapiens 25-32 9420879-1 1995 OBJECTIVE: Maintenance of normal glucose tolerance is achieved in subjects with a wide range of insulin sensitivity. Glucose 33-40 insulin Homo sapiens 96-103 7666784-0 1995 Comparison of the minimal model and the hyperglycemic clamp for measuring insulin sensitivity and acute insulin response to glucose. Glucose 124-131 insulin Homo sapiens 104-111 7666784-1 1995 Glucose clamp techniques are established methods for assessment of insulin sensitivity and secretion. Glucose 0-7 insulin Homo sapiens 67-74 7666784-3 1995 To address this issue, the present study was undertaken to compare determinations of ISI and the acute insulin response to glucose (AIRg) obtained using the MMT with similar measures obtained from a hyperglycemic clamp. Glucose 123-130 insulin Homo sapiens 103-110 7666790-2 1995 To determine whether this drug could affect in vivo insulin action acutely, insulin-stimulated glucose utilization was measured with the euglycemic glucose clamp technique before, during, and after troglitazone infusion (20 micrograms/min) in normal rats. Glucose 95-102 insulin Homo sapiens 76-83 7666790-4 1995 At 18-pmol/kg/min insulin infusion rate, steady-state glucose disposal rate (GDR) was significantly increased during troglitazone infusion versus control vehicle infusion (162 +/- 6.1 v 142.3 +/- 4.4 mumol/kg/min, P < .02). Glucose 54-61 insulin Homo sapiens 18-25 7674910-2 1995 Glucose utilization rate, measured by the euglycemic clamp technique, is a direct measure of insulin sensitivity. Glucose 0-7 insulin Homo sapiens 93-100 7674910-6 1995 The increased supply of fatty substrates and their competition with glucose for oxidation constitute a component of insulin resistance in obesity. Glucose 68-75 insulin Homo sapiens 116-123 7674911-4 1995 Studies in healthy subjects have shown that increased plasma levels of nonesterified free fatty acids resulted in a decrease in peripheral insulin-induced glucose uptake. Glucose 155-162 insulin Homo sapiens 139-146 7578797-5 1995 During 8 h of incubation in the presence of 5 mM glucose, the content of glycogen increased from 1.5 to 8.1 mumol/g blot weight in the absence of insulin and to 11.4 mumol/g blot weight in the presence of 0.5 U/ml insulin. Glucose 49-56 insulin Homo sapiens 146-153 7578797-5 1995 During 8 h of incubation in the presence of 5 mM glucose, the content of glycogen increased from 1.5 to 8.1 mumol/g blot weight in the absence of insulin and to 11.4 mumol/g blot weight in the presence of 0.5 U/ml insulin. Glucose 49-56 insulin Homo sapiens 214-221 9420879-2 1995 It follows, therefore, that the body must possess a sensor mechanism that assesses the body"s sensitivity to insulin and appropriately adjusts the secretion of insulin to maintain normal glucose homeostasis. Glucose 187-194 insulin Homo sapiens 109-116 9420879-2 1995 It follows, therefore, that the body must possess a sensor mechanism that assesses the body"s sensitivity to insulin and appropriately adjusts the secretion of insulin to maintain normal glucose homeostasis. Glucose 187-194 insulin Homo sapiens 160-167 9420879-5 1995 The subjects were stratified into quartiles based upon their insulin-mediated rate of glucose uptake during the euglycemic insulin clamp. Glucose 86-93 insulin Homo sapiens 61-68 9420879-7 1995 A significant inverse relation (r = -0.50, P < .01) was noted between the rate of total body insulin-mediated glucose disposal (insulin clamp) and the total plasma insulin response during the hyperglycemic clamp. Glucose 113-120 insulin Homo sapiens 96-103 9420879-7 1995 A significant inverse relation (r = -0.50, P < .01) was noted between the rate of total body insulin-mediated glucose disposal (insulin clamp) and the total plasma insulin response during the hyperglycemic clamp. Glucose 113-120 insulin Homo sapiens 131-138 9420879-7 1995 A significant inverse relation (r = -0.50, P < .01) was noted between the rate of total body insulin-mediated glucose disposal (insulin clamp) and the total plasma insulin response during the hyperglycemic clamp. Glucose 113-120 insulin Homo sapiens 131-138 9420879-8 1995 Women in the lowest quartile of insulin sensitivity (mean glucose uptake 5.07 +/- 0.20 mg/kg.minute) had the highest plasma insulin response during the hyperglycemic clamp (109 +/- 20 microU/mL). Glucose 58-65 insulin Homo sapiens 32-39 9420879-8 1995 Women in the lowest quartile of insulin sensitivity (mean glucose uptake 5.07 +/- 0.20 mg/kg.minute) had the highest plasma insulin response during the hyperglycemic clamp (109 +/- 20 microU/mL). Glucose 58-65 insulin Homo sapiens 124-131 9420879-9 1995 In contrast, women in the highest quartile of insulin sensitivity (glucose uptake 9.90 +/- 0.38 mg/kg.minute) had the lowest plasma insulin response during the hyperglycemic clamp (55 +/- 16 microU/mL; P < .001 versus the lowest quartile). Glucose 67-74 insulin Homo sapiens 46-53 9420879-9 1995 In contrast, women in the highest quartile of insulin sensitivity (glucose uptake 9.90 +/- 0.38 mg/kg.minute) had the lowest plasma insulin response during the hyperglycemic clamp (55 +/- 16 microU/mL; P < .001 versus the lowest quartile). Glucose 67-74 insulin Homo sapiens 132-139 9420879-11 1995 Nonetheless, normal glucose tolerance is maintained because of a finely regulated balance, which couples the demand for insulin secretion by the pancreatic beta cells to the level of whole-body insulin sensitivity. Glucose 20-27 insulin Homo sapiens 120-127 8581072-3 1995 Impaired glucose tolerance is observed when insulin resistance is associated to impaired first-phase insulin response, which results in a significant increase in plasma glucose levels and a late insulin hyperresponsiveness. Glucose 9-16 insulin Homo sapiens 101-108 8714501-8 1995 It is concluded that the estimation of a two hour plasma insulin level after 75 gm of glucose load, could help differentiate CAD from normals. Glucose 86-93 insulin Homo sapiens 57-64 8674816-2 1995 In the presence of 2.7 mM glucose, and 1.25 mM calcium, activin A induced a biphasic secretory response of insulin. Glucose 26-33 insulin Homo sapiens 107-114 8581772-12 1995 Fasting insulin levels and the insulin-to-glucose ratio were more than twice as high as control levels. Glucose 42-49 insulin Homo sapiens 31-38 8581775-9 1995 Excess free fatty acids may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. Glucose 149-156 insulin Homo sapiens 100-107 8587950-4 1995 The low dose treatment prevented the characteristic rise of the insulin response to a glucose challenge during pregnancy, both in vivo and in vitro, while the high dose treatment suppressed the insulin response, as well as the pancreatic insulin content. Glucose 86-93 insulin Homo sapiens 64-71 8571308-4 1995 These results confirm the association of PAI-1 levels with the features of insulin resistance and indicate that the association between PAI-1 levels and both triglyceride and glucose is influenced by genotype in the region of PAI-1 gene promoter. Glucose 175-182 insulin Homo sapiens 75-82 7576397-7 1995 Insulin and glucose responses to an oral glucose tolerance test and the lipid profiles were not modified by quinapril treatment. Glucose 41-48 insulin Homo sapiens 0-7 7650022-2 1995 Previous studies indicated that in pancreatic islets the amount of glucose-derived pyruvate that enters mitochondrial metabolism via carboxylation is approximately equal to that entering via decarboxylation and that both carboxylation and decarboxylation are correlated with capacitation of glucose metabolism and insulin release. Glucose 67-74 insulin Homo sapiens 314-321 7646447-1 1995 D-Glyceraldehyde"s capacity to mimic the effect of D-glucose on insulin secretion has not yet been sufficiently substantiated. Glucose 51-60 insulin Homo sapiens 64-71 7646447-7 1995 The ratio of the maximum insulin responses D-glyceraldehyde and D-glucose (57%) correlated with the ratio of their respective maximum rates of oxidation (68%). Glucose 64-73 insulin Homo sapiens 25-32 7653553-4 1995 In contrast, glucose production was nearly completely suppressed (approximately 90%) during intravenous infusions of glucose provided either alone or in combination with lipid; this suppression was achieved at glucose concentrations of approximately 90 mg/dl and insulin concentrations of approximately 6 microU/ml. Glucose 13-20 insulin Homo sapiens 263-270 7653553-4 1995 In contrast, glucose production was nearly completely suppressed (approximately 90%) during intravenous infusions of glucose provided either alone or in combination with lipid; this suppression was achieved at glucose concentrations of approximately 90 mg/dl and insulin concentrations of approximately 6 microU/ml. Glucose 117-124 insulin Homo sapiens 263-270 7653553-4 1995 In contrast, glucose production was nearly completely suppressed (approximately 90%) during intravenous infusions of glucose provided either alone or in combination with lipid; this suppression was achieved at glucose concentrations of approximately 90 mg/dl and insulin concentrations of approximately 6 microU/ml. Glucose 117-124 insulin Homo sapiens 263-270 7639686-0 1995 Dissection of stress-activated glucose transport from insulin-induced glucose transport in mammalian cells using wortmannin and ML-9. Glucose 70-77 insulin Homo sapiens 54-61 7639686-2 1995 Exposure of both cell types to azide or insulin markedly increased their glucose uptake capacity (Vmax.) Glucose 73-80 insulin Homo sapiens 40-47 8815863-0 1995 The relationship between blood pressure and serum insulin response in glucose intolerant subjects. Glucose 70-77 insulin Homo sapiens 50-57 8549009-10 1995 The efficiency of glucose uptake by the peripheral tissues is also impaired due to a combination of decreased insulin secretion and defective cellular insulin action. Glucose 18-25 insulin Homo sapiens 110-117 8549011-7 1995 It is suggested that any attempt to prevent macrovascular disease in subjects with glucose intolerance should aim at decreasing insulin resistance and hyperinsulinemia. Glucose 83-90 insulin Homo sapiens 128-135 7587853-0 1995 Reproducibility of the first-phase insulin response to intravenous glucose is not improved by retrograde cannulation and arterialization or the use of a lower glucose dose. Glucose 67-74 insulin Homo sapiens 35-42 7587853-1 1995 OBJECTIVE: To determine whether the reproducibility of the first-phase insulin response (FPIR) measured during an intravenous glucose tolerance test is improved by the use of a lower glucose dose or retrograde sampling from an arterialized hand vein. Glucose 126-133 insulin Homo sapiens 71-78 7587853-6 1995 RESULTS: Responses to the mean sum of serum insulin concentrations at 1 and 3 min after intravenous glucose were significantly lower for the low-dose test (mean 94 mU/l) than for the high-dose test (mean 184 mU/l) for samples taken from the arm (P < 0.05); mean 0- to 10-min insulin areas were 367 and 596 mU/l for low- and high-dose tests, respectively (P < 0.05). Glucose 100-107 insulin Homo sapiens 44-51 7587856-10 1995 CONCLUSIONS: The two insulin regimens exert similar effect on glucose metabolism and serum lipids in NIDDM patients on combination therapy. Glucose 62-69 insulin Homo sapiens 21-28 7622002-0 1995 Insulin sensitivity accounts for glucose and lactate kinetics after intravenous glucose injection. Glucose 33-40 insulin Homo sapiens 0-7 7622002-0 1995 Insulin sensitivity accounts for glucose and lactate kinetics after intravenous glucose injection. Glucose 80-87 insulin Homo sapiens 0-7 8591697-0 1995 Elevated ratio of summed serum proinsulin to insulin response after oral glucose load in type 2 diabetes decreases following sulfonylurea treatment. Glucose 73-80 insulin Homo sapiens 31-41 8591697-0 1995 Elevated ratio of summed serum proinsulin to insulin response after oral glucose load in type 2 diabetes decreases following sulfonylurea treatment. Glucose 73-80 insulin Homo sapiens 34-41 8591697-1 1995 We showed previously that the disproportionate elevation of serum proinsulin at fasting and after glucose ingestion in Type 2 diabetes is reduced to nearly normal after improvement of glycemic control by diet therapy. Glucose 98-105 insulin Homo sapiens 66-76 7655651-4 1995 However, in rat islets the peptide induced a significant decrease in the insulin increase ratio in response to 16.7 mmol/l glucose. Glucose 123-130 insulin Homo sapiens 73-80 8567821-2 1995 The occurrence of insulin resistance was determined by measuring insulin and glucose concentrations following a standard 75 g oral glucose load. Glucose 77-84 insulin Homo sapiens 18-25 8567821-2 1995 The occurrence of insulin resistance was determined by measuring insulin and glucose concentrations following a standard 75 g oral glucose load. Glucose 131-138 insulin Homo sapiens 18-25 8567821-10 1995 The diagnosis of insulin resistance in PCOS can be easily determined by the insulin response to an oral glucose tolerance test. Glucose 104-111 insulin Homo sapiens 17-24 8567821-10 1995 The diagnosis of insulin resistance in PCOS can be easily determined by the insulin response to an oral glucose tolerance test. Glucose 104-111 insulin Homo sapiens 76-83 7543114-16 1995 The trend toward increased insulin levels after GH injections was also found during the oral glucose tolerance test (P = 0.07). Glucose 93-100 insulin Homo sapiens 27-34 7629232-8 1995 We conclude that 1) the clear improvement in glucose metabolism produced by intensive insulin therapy in NIDDM is not accompanied by changes in whole body or skeletal muscle proteolysis; 2) skeletal muscle proteolysis is reduced even though whole body proteolysis is increased in NIDDM subjects compared with controls; and 3) although a high-dose systemic infusion of insulin significantly reduces whole body proteolysis in both NIDDM and control subjects, skeletal muscle proteolysis is suppressed only in controls. Glucose 45-52 insulin Homo sapiens 86-93 7635965-5 1995 Grafts of normoglycemic recipients responded with an increased insulin release to a glucose stimulus during perfusion, whereas grafts of hyperglycemic recipients failed to respond to glucose. Glucose 84-91 insulin Homo sapiens 63-70 7635965-7 1995 Recipients initially hyperglycemic (4 wk), followed by 2 wk of normoglycemia regained a normal graft insulin content, but a decreased insulin response to glucose remained. Glucose 154-161 insulin Homo sapiens 134-141 8536147-1 1995 An important determinant of insulin sensitivity in humans, the insulin-induced glucose uptake in skeletal muscle (directed into glycogen synthesis), has been found to be markedly enhanced in endurance-trained individuals compared with sedentary controls. Glucose 79-86 insulin Homo sapiens 28-35 8536147-1 1995 An important determinant of insulin sensitivity in humans, the insulin-induced glucose uptake in skeletal muscle (directed into glycogen synthesis), has been found to be markedly enhanced in endurance-trained individuals compared with sedentary controls. Glucose 79-86 insulin Homo sapiens 63-70 8536147-2 1995 This enhanced insulin action is accompanied by a decreased insulin response during an oral glucose load. Glucose 91-98 insulin Homo sapiens 14-21 8536147-2 1995 This enhanced insulin action is accompanied by a decreased insulin response during an oral glucose load. Glucose 91-98 insulin Homo sapiens 59-66 8536152-5 1995 RESULTS: In both multivariate analyses at age 40 years and age 51 years, the BMI, the fasting glucose level and lack of physical activity showed a positive independent association with the insulin level. Glucose 94-101 insulin Homo sapiens 189-196 8536152-6 1995 In follow-up analyses over 11 years, only BMI changes and fasting glucose changes were associated with changes in insulin level. Glucose 66-73 insulin Homo sapiens 114-121 7629581-11 1995 CONCLUSION: These results confirm that continuous infusion of 201Tl with a low dose of insulin in a glucose/potassium chloride solution is safe and may enhance cellular uptake of the radiotracer in severe ischemic regions, thereby improving viable myocardium detection. Glucose 100-107 insulin Homo sapiens 87-94 7637649-3 1995 The present study was performed to evaluate the insulin secretory responses to oral and intravenous glucose and to mixed meals in women with a history of GDM, and to determine if the hyperinsulinemia present in these subjects is appropriate for the degree of insulin resistance. Glucose 100-107 insulin Homo sapiens 48-55 7637649-4 1995 To address these questions, we studied the insulin secretory responses to oral glucose over a 3-hour period and to three mixed meals over a 24-hour period, and quantified the acute insulin response to glucose (AIRglucose) and insulin sensitivity (SI) during frequently sampled intravenous glucose tolerance tests (FSIVGTTs). Glucose 201-208 insulin Homo sapiens 181-188 7637649-4 1995 To address these questions, we studied the insulin secretory responses to oral glucose over a 3-hour period and to three mixed meals over a 24-hour period, and quantified the acute insulin response to glucose (AIRglucose) and insulin sensitivity (SI) during frequently sampled intravenous glucose tolerance tests (FSIVGTTs). Glucose 201-208 insulin Homo sapiens 181-188 7637649-4 1995 To address these questions, we studied the insulin secretory responses to oral glucose over a 3-hour period and to three mixed meals over a 24-hour period, and quantified the acute insulin response to glucose (AIRglucose) and insulin sensitivity (SI) during frequently sampled intravenous glucose tolerance tests (FSIVGTTs). Glucose 201-208 insulin Homo sapiens 181-188 7637649-4 1995 To address these questions, we studied the insulin secretory responses to oral glucose over a 3-hour period and to three mixed meals over a 24-hour period, and quantified the acute insulin response to glucose (AIRglucose) and insulin sensitivity (SI) during frequently sampled intravenous glucose tolerance tests (FSIVGTTs). Glucose 201-208 insulin Homo sapiens 181-188 7637656-1 1995 Upper-body obesity (UBO) in white women is associated with increased fatty acid turnover and resistance to the effects of insulin on systemic glucose metabolism. Glucose 142-149 insulin Homo sapiens 122-129 7637656-2 1995 The present study determined whether the abilities of insulin to stimulate glucose transport and suppress lipolysis are impaired in adipocytes from white UBO (W-UBO) women. Glucose 75-82 insulin Homo sapiens 54-61 7637656-5 1995 In white women, both abdominal and gluteal fat cells from the UBO versus LBO group were less responsive to the stimulatory effects of insulin on glucose uptake and less sensitive to the antilipolytic effects of insulin and the adenosine analog, phenylisopropyladenosine (PIA). Glucose 145-152 insulin Homo sapiens 134-141 7637656-6 1995 In contrast, in black women, fat cells from UBO and LBO groups were equally sensitive to the stimulatory effects of insulin on glucose transport and the suppressive effects of insulin and PIA on lipolysis. Glucose 127-134 insulin Homo sapiens 116-123 7479680-6 1995 At 16.3 +/- 0.5 mM glucose, the insulin response was increased to 1,516 +/- 325 pM (p < 0.001), whereas the IAPP response was increased to 10.4 +/- 2.8 pM (p < 0.01) (r = 0.91, p < 0.001). Glucose 19-26 insulin Homo sapiens 32-39 7474436-1 1995 Glucose homeostasis depends upon a balance between glucose production by the liver and glucose utilization by insulin-dependent tissues, such as muscle and fat. Glucose 87-94 insulin Homo sapiens 110-117 7474436-2 1995 Insulin, secreted by the pancreatic B cell, inhibits hepatic glucose output and facilitates glucose utilization in the muscle and fat tissues. Glucose 61-68 insulin Homo sapiens 0-7 8565693-4 1995 RESULTS: There were significant increases of the peak level or AUC of insulin in PIH (61.42 +/- 48.72, 137.12 +/- 81.12 mIU/L) and in normal pregnant group (70.46 +/- 58.42, 150.37 +/- 104.76 mIU/L) compared with non-pregnant controls (17.12 +/- 11.03, 34.38 +/- 16.01 mIU/L) (P < 0.01), however, they had a similar glucose levels before or after GTT (P > 0.05). Glucose 319-326 insulin Homo sapiens 70-77 7777034-12 1995 Low serum insulin concentrations before and after the oral administration of glucose were associated with the development of polyneuropathy, regardless of the degree of glycemia. Glucose 77-84 insulin Homo sapiens 10-17 7484471-6 1995 In addition, cells isolated from intraoperative and lipectomy samples did not differ functionally, responded similarly to insulin stimulation of glucose transport and epinephrine-stimulated lipolysis, and retained the same growth pattern in culture. Glucose 145-152 insulin Homo sapiens 122-129 7546505-0 1995 Resistance to insulin-mediated glucose uptake and hyperinsulinemia in women who had preeclampsia during pregnancy. Glucose 31-38 insulin Homo sapiens 14-21 7631766-2 1995 Insulin action was assessed by a sequential two-step (8 and 40 mU,m-2.min-1) euglycemic insulin clamp in combination with [1-13C]glucose and indirect calorimetry. Glucose 129-136 insulin Homo sapiens 0-7 7631766-5 1995 In obese girls, an impairment in glucose disposal was present with both insulin doses; at the higher dose, rates of glucose uptake were reduced by 30% in nonobese girls (240 +/- 30 vs. 340 +/- 19 mg.m-2.min-1, P < 0.05) and by an additional 29% (170 +/- 17 mg.m-2.min-1, P < 0.05) in obese girls. Glucose 33-40 insulin Homo sapiens 72-79 7631766-5 1995 In obese girls, an impairment in glucose disposal was present with both insulin doses; at the higher dose, rates of glucose uptake were reduced by 30% in nonobese girls (240 +/- 30 vs. 340 +/- 19 mg.m-2.min-1, P < 0.05) and by an additional 29% (170 +/- 17 mg.m-2.min-1, P < 0.05) in obese girls. Glucose 116-123 insulin Homo sapiens 72-79 7631766-8 1995 Fasting and glucose-stimulated insulin responses were greater in obese than in nonobese adolescents, who, in turn, had greater responses than lean women. Glucose 12-19 insulin Homo sapiens 31-38 7631777-2 1995 Nonoxidative glucose metabolism was reduced by 64% in patients with NIDDM compared with control subjects and correlated with insulin-stimulated glycogen synthase activity (r = 0.55, P < 0.05). Glucose 13-20 insulin Homo sapiens 125-132 7576404-4 1995 Both plasma glucose and insulin concentrations following a 75-g oral glucose challenge were significantly higher after the high-salt diet in the salt-sensitive patients. Glucose 69-76 insulin Homo sapiens 24-31 7576404-6 1995 These data are consistent with the view that there is an association between resistance to insulin-mediated glucose disposal and salt sensitivity in patients with high blood pressure. Glucose 108-115 insulin Homo sapiens 91-98 7625352-4 1995 During a glucose clamp (216 pmol insulin/L) glucose disposal increased from 13.2 +/- 0.83 to 14.6 +/- 0.83 mumol.kg fat-free mass-1.min-1 (P < 0.05) in both groups. Glucose 9-16 insulin Homo sapiens 33-40 7625352-4 1995 During a glucose clamp (216 pmol insulin/L) glucose disposal increased from 13.2 +/- 0.83 to 14.6 +/- 0.83 mumol.kg fat-free mass-1.min-1 (P < 0.05) in both groups. Glucose 44-51 insulin Homo sapiens 33-40 7575750-1 1995 Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore pharmacological interventions should aim to improve insulin sensitivity. Glucose 38-45 insulin Homo sapiens 0-7 7575750-1 1995 Insulin resistance of skeletal muscle glucose uptake is a prominent feature of Type II diabetes (NIDDM); therefore pharmacological interventions should aim to improve insulin sensitivity. Glucose 38-45 insulin Homo sapiens 167-174 7575750-3 1995 To see whether this compound also augments insulin mediated glucose disposal in NIDDM, 13 patients received either ALA (1000 mg/Thioctacid/500 ml NaCl, n = 7) or vehicle only (500 ml NaCl, n = 6) during a glucose-clamp study. Glucose 60-67 insulin Homo sapiens 43-50 7575750-5 1995 Acute parenteral administration of ALA resulted in a significant increase of insulin-stimulated glucose disposal; metabolic clearance rate (MCR) for glucose rose by about 50% (3.76 ml/kg/min = pre vs. 5.82 ml/kg/min = post, p < 0.05), whereas the control group did not show any significant change (3.57 ml/kg/min = pre vs. 3.91 ml/kg/min = post). Glucose 96-103 insulin Homo sapiens 77-84 7575750-6 1995 This is the first clinical study to show that alpha-lipoic acid increases insulin stimulated glucose disposal in NIDDM. Glucose 93-100 insulin Homo sapiens 74-81 7639686-5 1995 Wortmannin, a selective inhibitor of phosphatidylinositol (PI) 3-kinase, did not affect stimulation of transport by azide but inhibited insulin-induced glucose transport with a Ki of < 10 nM. Glucose 152-159 insulin Homo sapiens 136-143 7639686-6 1995 ML-9, a putative mitogen-activated protein kinase inhibitor, was equipotent in its inhibition of azide- and insulin-stimulated glucose transport. Glucose 127-134 insulin Homo sapiens 108-115 8546639-0 1995 Using glucose tolerance test results to predict insulin requirement in women with gestational diabetes. Glucose 6-13 insulin Homo sapiens 48-55 8546639-3 1995 The second analysis was to test the clinical impression that the fasting glucose level was the best predictor of insulin requirement in women with gestational diabetes. Glucose 73-80 insulin Homo sapiens 113-120 8546639-6 1995 The receiver-operator characteristic curves also showed that the 2-hour postload glucose level during the 75 g load glucose tolerance test was a better predictor of insulin requirement than the fasting glucose level. Glucose 81-88 insulin Homo sapiens 165-172 8546639-6 1995 The receiver-operator characteristic curves also showed that the 2-hour postload glucose level during the 75 g load glucose tolerance test was a better predictor of insulin requirement than the fasting glucose level. Glucose 116-123 insulin Homo sapiens 165-172 8546639-6 1995 The receiver-operator characteristic curves also showed that the 2-hour postload glucose level during the 75 g load glucose tolerance test was a better predictor of insulin requirement than the fasting glucose level. Glucose 116-123 insulin Homo sapiens 165-172 8549009-6 1995 This increased rate of glucose release by the liver results in part from impaired hepatic sensitivity to insulin, but is largely due to reduced insulin secretion and increased glucagon secretion. Glucose 23-30 insulin Homo sapiens 105-112 7622000-5 1995 Acute insulin treatment (33 nmol/l) doubled glycogen synthase activity and glucose incorporation into glycogen while increasing pyruvate dehydrogenase approximately 30%. Glucose 75-82 insulin Homo sapiens 6-13 7622000-8 1995 A significant correlation (r = 0.65, P < or = 0.05) was present when maximal rates of insulin-stimulated glucose transport in cell culture from subjects were compared with their corresponding in vivo glucose disposal determined by hyperinsulinemic glucose clamp. Glucose 108-115 insulin Homo sapiens 89-96 7622000-9 1995 In summary, differentiated human skeletal muscle cultures exhibit biochemical and molecular features of insulin-stimulated glucose transport and intracellular enzyme activity comparable with the in vivo situation. Glucose 123-130 insulin Homo sapiens 104-111 7622000-10 1995 Defective insulin-stimulated glucose transport persists in muscle cultures from NIDDM subjects and resembles the reduced insulin-mediated glucose uptake present in vivo. Glucose 29-36 insulin Homo sapiens 10-17 7622000-10 1995 Defective insulin-stimulated glucose transport persists in muscle cultures from NIDDM subjects and resembles the reduced insulin-mediated glucose uptake present in vivo. Glucose 29-36 insulin Homo sapiens 121-128 7622000-10 1995 Defective insulin-stimulated glucose transport persists in muscle cultures from NIDDM subjects and resembles the reduced insulin-mediated glucose uptake present in vivo. Glucose 138-145 insulin Homo sapiens 10-17 7622000-10 1995 Defective insulin-stimulated glucose transport persists in muscle cultures from NIDDM subjects and resembles the reduced insulin-mediated glucose uptake present in vivo. Glucose 138-145 insulin Homo sapiens 121-128 8529509-5 1995 The defect in the early release of insulin may have quite an impact in post-prandial glucose homeostasis, due to inadequate suppression of hepatic glucose production. Glucose 85-92 insulin Homo sapiens 35-42 8529509-10 1995 Exogenous insulin exerts an inhibitory effect on hepatic glucose production but it does not maintain the physiologic gradient, neither can it mimic first-phase insulin secretion. Glucose 57-64 insulin Homo sapiens 10-17 8529511-2 1995 Impairment of the signal transmission from the insulin receptor to glycogen synthase and the glucose transport system was shown in insulin resistant subjects. Glucose 93-100 insulin Homo sapiens 131-138 8529512-2 1995 The dose of insulin required can be predicted from the level of the fasting plasma glucose and the degree of obesity, which provides an index of the accompanying insulin resistance. Glucose 83-90 insulin Homo sapiens 12-19 8529512-2 1995 The dose of insulin required can be predicted from the level of the fasting plasma glucose and the degree of obesity, which provides an index of the accompanying insulin resistance. Glucose 83-90 insulin Homo sapiens 162-169 7581368-6 1995 Interestingly, the Tyr905 variant was associated with altered routing of glucose: a decreased insulin stimulated non-oxidative glucose metabolism of peripheral tissues (glycogen synthesis) (p < 0.04) and an increased basal glucose oxidation rate (p < 0.04) when compared with wild type carriers. Glucose 73-80 insulin Homo sapiens 94-101 7581368-6 1995 Interestingly, the Tyr905 variant was associated with altered routing of glucose: a decreased insulin stimulated non-oxidative glucose metabolism of peripheral tissues (glycogen synthesis) (p < 0.04) and an increased basal glucose oxidation rate (p < 0.04) when compared with wild type carriers. Glucose 127-134 insulin Homo sapiens 94-101 8568110-3 1995 METHODS: A step increase in insulin administration during a euglycemic clamp protocol was used to measure insulin effects on glucose and leucine metabolism. Glucose 125-132 insulin Homo sapiens 106-113 8568110-10 1995 The insulin concentration required to stimulate half maximal glucose utilization in cancer patients was significantly increased by 58% (470 +/- 82 pM vs. 741 +/- 124 pM; p < or = 0.05). Glucose 61-68 insulin Homo sapiens 4-11 8568110-11 1995 Non-oxidative glucose utilization was reduced in the cancer patients at both lower doses of insulin infusion (6.4 +/- 2.1 mumol/kg/minute vs. 0.1 +/- 1.6 mumol/kg/minute p < or = 0.05; and 23.7 +/- 1.3 mumol/kg/minute vs. 15.1 +/- 2.0 mumol/kg/minute p < 0.01). Glucose 14-21 insulin Homo sapiens 92-99 7635936-0 1995 Insulin action on heart and skeletal muscle glucose uptake in essential hypertension. Glucose 44-51 insulin Homo sapiens 0-7 7635936-6 1995 We conclude that insulin-stimulated glucose uptake is decreased in skeletal muscle but increased in proportion to cardiac work in essential hypertension. Glucose 36-43 insulin Homo sapiens 17-24 7635973-1 1995 Whether insulin-mediated vasodilation is important in determining insulin"s overall action to stimulate glucose uptake is unknown. Glucose 104-111 insulin Homo sapiens 8-15 7635973-1 1995 Whether insulin-mediated vasodilation is important in determining insulin"s overall action to stimulate glucose uptake is unknown. Glucose 104-111 insulin Homo sapiens 66-73 7635973-5 1995 We also found a significant relationship between the rate of insulin-stimulated whole body glucose uptake and the magnitude of flow dependent glucose uptake (r = 0.57, P = 0.02). Glucose 91-98 insulin Homo sapiens 61-68 7635973-5 1995 We also found a significant relationship between the rate of insulin-stimulated whole body glucose uptake and the magnitude of flow dependent glucose uptake (r = 0.57, P = 0.02). Glucose 142-149 insulin Homo sapiens 61-68 7637643-9 1995 Insulin and glucose responses in the OGTT and estimates of insulin resistance and beta-cell function from fasting samples show that insulin resistance was the principal abnormality in IGT subjects, whereas in DM subjects, both insulin resistance and beta-cell dysfunction contributed. Glucose 12-19 insulin Homo sapiens 132-139 7637643-9 1995 Insulin and glucose responses in the OGTT and estimates of insulin resistance and beta-cell function from fasting samples show that insulin resistance was the principal abnormality in IGT subjects, whereas in DM subjects, both insulin resistance and beta-cell dysfunction contributed. Glucose 12-19 insulin Homo sapiens 132-139 7482987-5 1995 In vitro, vanadium salts mimic most effects of insulin on the main target tissues of the hormone, and in vivo they induce a sustained fall in blood glucose levels in insulin-deficient diabetic rats, and improve glucose homeostasis in obese, insulin-resistant diabetic rodents. Glucose 148-155 insulin Homo sapiens 166-173 7556777-6 1995 The daily intravenous infusion of glucose brought the fasting hypoglycemia to normal and hypothermia to normothermia in the morning, and improved no or blunt responsiveness of insulin to glucose. Glucose 34-41 insulin Homo sapiens 176-183 7556777-8 1995 infusion of glucose quickly produced moderate hyperglycemia and an increase in plasma insulin, and inhibited secretions of CRH, ACTH and cortisol. Glucose 12-19 insulin Homo sapiens 86-93 18623391-7 1995 Including insulin in the medium resulted in a higher specific glucose consumption rate, a shorter exponential growth stage, and a lower final antibody concentration. Glucose 62-69 insulin Homo sapiens 10-17 7613432-5 1995 The programming of blood pressure, insulin responses to glucose, cholesterol metabolism, blood coagulation, and hormonal settings are all areas of active research. Glucose 56-63 insulin Homo sapiens 35-42 7619042-8 1995 We conclude that insulin and dinitrophenol stimulate glucose transport by different mechanisms. Glucose 53-60 insulin Homo sapiens 17-24 7662453-5 1995 Insulin and C peptide responses to the intravenous glucose tolerance test were higher (27.6 v 19.8 microU/ml/min, P < 0.01; 101 v 72 pmol/ml/min, P < 0.05, respectively), and insulin sensitivity was lower (1.89 v 3.09 min/microU/ml, P < 0.05). Glucose 51-58 insulin Homo sapiens 0-7 8528146-9 1995 However, the degree of PI 3-kinase by these growth factors appears to be much smaller than that by insulin, consistent with smaller stimulations of glucose transport. Glucose 148-155 insulin Homo sapiens 99-106 8528146-1 1995 Activation of phosphatidylinositol 3-kinase (PI 3-kinase) appears to be part of the signaling mechanism by which insulin stimulates cellular glucose uptake. Glucose 141-148 insulin Homo sapiens 113-120 7662453-5 1995 Insulin and C peptide responses to the intravenous glucose tolerance test were higher (27.6 v 19.8 microU/ml/min, P < 0.01; 101 v 72 pmol/ml/min, P < 0.05, respectively), and insulin sensitivity was lower (1.89 v 3.09 min/microU/ml, P < 0.05). Glucose 51-58 insulin Homo sapiens 181-188 7789652-0 1995 Defective insulin action on protein and glucose metabolism during chronic hyperinsulinemia in subjects with benign insulinoma. Glucose 40-47 insulin Homo sapiens 10-17 7742741-3 1995 The model includes the kinetics of uptake of glucose by GLUT transporters, the rate of glucose metabolism within the cell, and the effect of glucose on the rate of insulin secretion. Glucose 45-52 insulin Homo sapiens 164-171 7742741-4 1995 Putative feedback by insulin on the rate of glucose transport into the cells is treated phenomenologically and leads to insulin oscillations similar to those observed experimentally in HIT cells. Glucose 44-51 insulin Homo sapiens 21-28 7555562-2 1995 RESEARCH DESIGN AND METHODS: In this report, we study the association of three major apoE phenotypes (apoE 3/2, apoE 3/3, and apoE 4/3) with indicators of insulin resistance such as fasting insulin, glucose, and lipid levels in 320 nondiabetic Mexican-Americans and non-Hispanic whites from San Antonio, TX. Glucose 199-206 insulin Homo sapiens 155-162 7556975-1 1995 Previous studies have suggested that human and porcine insulin exert identical effects on blood glucose and counter-regulatory hormones but elicit different neurophysiological reactions. Glucose 96-103 insulin Homo sapiens 55-62 8846403-8 1995 In addition, CGRP and amylin (homologous pancreatic peptide) reduce the tissue--glucose response to insulin. Glucose 80-87 insulin Homo sapiens 100-107 7556989-7 1995 Postabsorptive endogenous glucose production was higher on treatment with bendrofluazide 5.0 mg compared to 1.25 mg (11.7 +/- 0.5 vs 10.2 +/- 0.3 mumol.kg-1.min-1, p < 0.05) and suppressed to a lesser extent following insulin (4.0 +/- 0.7 vs 2.0 +/- 0.4 mumol.kg-1.min-1, p < 0.05). Glucose 26-33 insulin Homo sapiens 221-228 7556992-10 1995 Abnormal function of the re-arranged mtDNA could affect both development and function of pancreatic islet cells since glucose-stimulated insulin secretion is energy dependent. Glucose 118-125 insulin Homo sapiens 137-144 7556372-8 1995 Hypertensive patients with LVH had the lowest insulin-mediated nonoxidative glucose metabolism compared to hypertensive patients without LVH (P < 0.01) and to healthy subjects (P < 0.001). Glucose 76-83 insulin Homo sapiens 46-53 7789652-1 1995 The ability of chronic endogenous hyperinsulinemia to induce a resistance to insulin action on protein and glucose metabolism was studied in 10 subjects affected by a benign (functioning) insulinoma and 18 healthy subjects by means of infusions of [1-(14)C]leucine and [3-(3)H] glucose. Glucose 107-114 insulin Homo sapiens 39-46 7556372-9 1995 In the whole group of hypertensive patients (n = 26), partial correlations showed left ventricular mass index (LVMI) associated with fasting plasma insulin levels (r = 0.44 P < 0.005), insulin-mediated whole body glucose disposal (r = -0.41 P < 0.01) and nonoxidative glucose metabolism (r = -0.33 P < 0.04) independently of age, body weight, systolic blood pressure and plasma catecholamines levels. Glucose 216-223 insulin Homo sapiens 188-195 7556372-9 1995 In the whole group of hypertensive patients (n = 26), partial correlations showed left ventricular mass index (LVMI) associated with fasting plasma insulin levels (r = 0.44 P < 0.005), insulin-mediated whole body glucose disposal (r = -0.41 P < 0.01) and nonoxidative glucose metabolism (r = -0.33 P < 0.04) independently of age, body weight, systolic blood pressure and plasma catecholamines levels. Glucose 274-281 insulin Homo sapiens 188-195 7789653-2 1995 Parametric models of insulin secretion are used to measure indexes of beta-cell function from plasma C-peptide concentration during an intravenous glucose tolerance test (IVGTT). Glucose 147-154 insulin Homo sapiens 21-28 8593759-3 1995 The hypertensive patients without glucose intolerance showed a significantly lower insulin-mediated glucose disposal and a compensating increase in second-phase insulin secretion compared with normotensives without glucose intolerance. Glucose 34-41 insulin Homo sapiens 83-90 8593759-3 1995 The hypertensive patients without glucose intolerance showed a significantly lower insulin-mediated glucose disposal and a compensating increase in second-phase insulin secretion compared with normotensives without glucose intolerance. Glucose 100-107 insulin Homo sapiens 83-90 8593759-3 1995 The hypertensive patients without glucose intolerance showed a significantly lower insulin-mediated glucose disposal and a compensating increase in second-phase insulin secretion compared with normotensives without glucose intolerance. Glucose 100-107 insulin Homo sapiens 83-90 8593759-4 1995 In hypertensives with glucose intolerance, insulin-mediated glucose disposal was significantly lower and second-phase insulin secretion was comparable to that in normotensives without glucose intolerance. Glucose 22-29 insulin Homo sapiens 43-50 8593759-4 1995 In hypertensives with glucose intolerance, insulin-mediated glucose disposal was significantly lower and second-phase insulin secretion was comparable to that in normotensives without glucose intolerance. Glucose 60-67 insulin Homo sapiens 43-50 8593759-4 1995 In hypertensives with glucose intolerance, insulin-mediated glucose disposal was significantly lower and second-phase insulin secretion was comparable to that in normotensives without glucose intolerance. Glucose 60-67 insulin Homo sapiens 43-50 8593759-6 1995 The insulin-mediated glucose disposal significantly (P < 0.01) recovered from 6.0 +/- 0.81 to 8.0 +/- 0.71 mg/kg per min. Glucose 21-28 insulin Homo sapiens 4-11 8593759-9 1995 In hypertensives with glucose intolerance, insulin resistance might induce postprandial hyperglycemia, which leads to hyperinsulinemia because of second phase insulin secretion at a level similar to that of normotensives. Glucose 22-29 insulin Homo sapiens 43-50 7616840-1 1995 After exercise, glucose uptake in tissues increases by insulin-dependent and -independent mechanisms. Glucose 16-23 insulin Homo sapiens 55-62 7607722-6 1995 Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Glucose 8-15 insulin Homo sapiens 134-141 7607722-8 1995 Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Glucose 93-100 insulin Homo sapiens 48-55 7637188-0 1995 [Portal blood immunoreactive insulin concentration after glucose infusion in elderly patients during gastrectomy compared with younger patients]. Glucose 57-64 insulin Homo sapiens 29-36 7784031-14 1995 Patients receiving at least 100 U/day of insulin have a 100% incidence of postpartum glucose intolerance. Glucose 85-92 insulin Homo sapiens 41-48 7607722-6 1995 Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Glucose 8-15 insulin Homo sapiens 83-90 7473782-0 1995 The effect of insulin and FFA on myocardial glucose uptake. Glucose 44-51 insulin Homo sapiens 14-21 7473782-3 1995 To study the mechanism of insulin action on myocardial glucose uptake (MGU) in vivo, five patients with stable coronary artery disease were studied with positron emission tomography (PET) and [18F]FDG. Glucose 55-62 insulin Homo sapiens 26-33 7616846-1 1995 Studies in patients with microvascular angina (MA) or the cardiologic syndrome X have shown a hyperinsulinemic response to an oral glucose challenge, suggesting insulin resistance and a role for increased serum insulin in coronary microvascular dysfunction. Glucose 131-138 insulin Homo sapiens 99-106 7616846-1 1995 Studies in patients with microvascular angina (MA) or the cardiologic syndrome X have shown a hyperinsulinemic response to an oral glucose challenge, suggesting insulin resistance and a role for increased serum insulin in coronary microvascular dysfunction. Glucose 131-138 insulin Homo sapiens 161-168 7616846-8 1995 The fasting level of "true" serum insulin was significantly higher (43 +/- 6 v 22 +/- 3 pmol/L, P < .02) and the rate of insulin-stimulated glucose disposal to peripheral tissues was lower in patients with MA (13.4 +/- 1.0 v 18.2 +/- 1.4 mg.kg fat-free mass [FFM]-1.min-1, P < .02) due to a decrease in nonoxidative glucose metabolism (8.4 +/- 0.9 v 12.5 +/- 1.3 mg.kg FFM-1.min-1, P < .02). Glucose 143-150 insulin Homo sapiens 124-131 7637208-3 1995 Glucose infusion rate (GIR), as an index of insulin sensitivity, was significantly increased by 54.3% (from 3.66 +/- 2.4 to 5.5 +/- 9.3 ml/kg/min; p < 0.01). Glucose 0-7 insulin Homo sapiens 44-51 7624391-1 1995 The ability of insulin to stimulate glucose uptake varies widely from person to person, and these differences, as well as how the individual attempts to compensate for them, are of fundamental importance in the development and clinical course of what are often designated as diseases of Western civilization. Glucose 36-43 insulin Homo sapiens 15-22 7624391-5 1995 In contrast, evidence is presented supporting the view that the combination of insulin resistance and compensatory hyperinsulinemia predisposes to the development of a cluster of abnormalities, including some degree of glucose intolerance, an increase in plasma triglyceride and a decrease in high-density lipoprotein cholesterol concentrations, high blood pressure, hyperuricemia, smaller denser low-density lipoprotein particles, and higher circulating levels of plaminogen activator inhibitor 1. Glucose 219-226 insulin Homo sapiens 79-86 7763119-3 1995 Although not yet definitively established, it is likely that optimal control of plasma glucose will also assist in the prevention of such problems in type II (non-insulin-dependent) diabetes. Glucose 87-94 insulin Homo sapiens 163-170 7579540-0 1995 Relationship between insulin responses to D-glucose and to L-arginine in women with a history of gestational diabetes. Glucose 42-51 insulin Homo sapiens 21-28 7579540-1 1995 The relationship between insulin responses to glucose and to arginine was studied in non-obese women with previous gestational diabetes (PGD). Glucose 46-53 insulin Homo sapiens 25-32 7579540-7 1995 However, within each group insulin responses 0-10 min to glucose and arginine were strongly correlated: for NGT (r = 0.75, P < 0.05), for IGT (r = 0.85, P < 0.01) and for women without PGD (r = 0.69, P < 0.05). Glucose 57-64 insulin Homo sapiens 27-34 7616840-5 1995 Bergman"s minimal model of insulin action was used to analyze the two FSIVGTTs and produced the following parameters: coefficient of glucose tolerance (Kg), ie, the slope of the exponential decrease in glycemia between 4 and 19 minutes after intravenous glucose; insulin sensitivity (Sl); and glucose effectiveness at basal insulin (Sg). Glucose 133-140 insulin Homo sapiens 27-34 7773733-6 1995 However, the only statistically significant differences were between the ID and DD groups; the latter had lower values for body mass index, was more insulin sensitive, and had a lower plasma insulin response to oral glucose. Glucose 216-223 insulin Homo sapiens 191-198 7662572-4 1995 Fasting serum insulin levels were found to be significantly lower in groups III, IV and V than in groups I and II, with no significant difference between groups I and II, or between groups III, IV and V. Total insulin response following administration of glucose did not differ significantly between the groups. Glucose 255-262 insulin Homo sapiens 14-21 7611377-0 1995 Insulin-stimulated glucose uptake is enhanced in sedentary and endurance-trained low insulin responders. Glucose 19-26 insulin Homo sapiens 0-7 7611377-0 1995 Insulin-stimulated glucose uptake is enhanced in sedentary and endurance-trained low insulin responders. Glucose 19-26 insulin Homo sapiens 85-92 7611377-1 1995 The mechanisms by which healthy sedentary subjects with low insulin response (LIR; 5-min insulin response to glucose load within lowest quartile of healthy population) maintain a normal glucose tolerance are not clear. Glucose 109-116 insulin Homo sapiens 60-67 7611377-1 1995 The mechanisms by which healthy sedentary subjects with low insulin response (LIR; 5-min insulin response to glucose load within lowest quartile of healthy population) maintain a normal glucose tolerance are not clear. Glucose 109-116 insulin Homo sapiens 89-96 7611377-1 1995 The mechanisms by which healthy sedentary subjects with low insulin response (LIR; 5-min insulin response to glucose load within lowest quartile of healthy population) maintain a normal glucose tolerance are not clear. Glucose 186-193 insulin Homo sapiens 60-67 7662572-4 1995 Fasting serum insulin levels were found to be significantly lower in groups III, IV and V than in groups I and II, with no significant difference between groups I and II, or between groups III, IV and V. Total insulin response following administration of glucose did not differ significantly between the groups. Glucose 255-262 insulin Homo sapiens 210-217 7555498-8 1995 The DM-B group also had significantly lower insulin response at 30 min after oral glucose at baseline but no significant difference in intra-abdominal fat or fasting plasma insulin and C-peptide levels. Glucose 82-89 insulin Homo sapiens 44-51 7640642-7 1995 The association between blood flow and insulin stimulated glucose uptake suggests that therapeutic intervention against the development of skeletal muscle vascular resistance should occur early in individuals generally predisposed to cardiovascular pathology in order to attenuate, or avoid, insulin resistance and its sequelae. Glucose 58-65 insulin Homo sapiens 39-46 7634752-4 1995 The doses of insulin-like growth factor I and insulin were equipotent with regard to increases in glucose uptake during 8 h euglycaemic clamping. Glucose 98-105 insulin Homo sapiens 13-20 7634752-9 1995 The present results demonstrate that insulin-like growth factor I and insulin infused at doses which result in identical increases in glucose uptake during euglycaemic clamping are equipotent inhibitors of lipolysis. Glucose 134-141 insulin Homo sapiens 37-44 7648818-7 1995 The most promising new approach for enhancing insulin secretion has been suggested by the demonstration that pharmacological doses of GLP-1 (7-36 amide), a natural enteric incretin hormone, improves pancreatic beta-cell and alpha-cell sensitivity to glucose and can induce normal basal glucose levels in diabetic man. Glucose 250-257 insulin Homo sapiens 46-53 7648818-7 1995 The most promising new approach for enhancing insulin secretion has been suggested by the demonstration that pharmacological doses of GLP-1 (7-36 amide), a natural enteric incretin hormone, improves pancreatic beta-cell and alpha-cell sensitivity to glucose and can induce normal basal glucose levels in diabetic man. Glucose 286-293 insulin Homo sapiens 46-53 7648818-12 1995 When full insulin replacement therapy is not feasible, reducing the fasting blood glucose level towards normal with a single daily basal insulin supplement, either alone or in combination with oral agents, could become a more widely used therapy. Glucose 82-89 insulin Homo sapiens 10-17 7648818-12 1995 When full insulin replacement therapy is not feasible, reducing the fasting blood glucose level towards normal with a single daily basal insulin supplement, either alone or in combination with oral agents, could become a more widely used therapy. Glucose 82-89 insulin Homo sapiens 137-144 7648827-2 1995 All studies in which supplemental insulin was administered lowered the integrated glucose response above baseline versus the control study (short 76%, medium 71%, and long 56% of control, p = 0.003). Glucose 82-89 insulin Homo sapiens 34-41 7555511-13 1995 There also was an increase in the rate of exogenous glucose infused (M) (P < 0.01) and in the M/C-peptide ratio (P < 0.02), suggesting enhanced insulin sensitivity. Glucose 52-59 insulin Homo sapiens 150-157 7555513-5 1995 RESULTS: Plasma glucose reached a peak at 60 min and a nadir at 240 min for both types of insulin. Glucose 16-23 insulin Homo sapiens 90-97 7555498-11 1995 CONCLUSION--In DM-A, lower 30-min insulin response to oral glucose (an indicator of beta-cell lesion) and increased intra-abdominal fat and fasting C-peptide (indicators of insulin resistance) were the risk factors related to the development of NIDDM. Glucose 59-66 insulin Homo sapiens 34-41 7555498-12 1995 DM-B subjects had a lower 30-min insulin response to oral glucose at baseline and increased intra-abdominal fat at 5-years, when they were found to have NIDDM. Glucose 58-65 insulin Homo sapiens 33-40 7555510-11 1995 CONCLUSIONS: Basal and insulin-stimulated glucose uptakes are comparable in carefully matched normo- and microalbuminuric NIDDM patients, and glucose oxidation may be positively related to albuminuria. Glucose 42-49 insulin Homo sapiens 23-30 7656918-6 1995 During the insulin infusion glucose Ra decreased from 1.89 +/- 0.13 to 0.34 +/- 0.33 mg kg-1 min-1 (P < 0.01) and FFA from 0.546 mmol l-1 to 0.198 mmol l-1 (P < 0.01), glucose Rd increased from 1.89 +/- 0.18 to 5.41 +/- 1.47 mg kg-1 min-1 (P < 0.01) and there were no significant changes in the cardiovascular variables. Glucose 28-35 insulin Homo sapiens 11-18 7656918-6 1995 During the insulin infusion glucose Ra decreased from 1.89 +/- 0.13 to 0.34 +/- 0.33 mg kg-1 min-1 (P < 0.01) and FFA from 0.546 mmol l-1 to 0.198 mmol l-1 (P < 0.01), glucose Rd increased from 1.89 +/- 0.18 to 5.41 +/- 1.47 mg kg-1 min-1 (P < 0.01) and there were no significant changes in the cardiovascular variables. Glucose 174-181 insulin Homo sapiens 11-18 7672486-1 1995 Human adipose cells are much less responsive to insulin stimulation of glucose transport activity than are rat adipocytes. Glucose 71-78 insulin Homo sapiens 48-55 7672496-10 1995 Before glucose administration, insulin (p < 0.0001) and C-peptide (p < 0.0004) increased, whereas glucagon (p = 0.0018) and glucose (p < 0.0001) decreased in a dose-dependent manner. Glucose 7-14 insulin Homo sapiens 31-38 7672492-7 1995 First phase insulin secretion (delta 0-10 min insulin area divided by delta 0-10 min glucose area) was significantly decreased in the subjects with impaired glucose tolerance (median [range]: 1.2 [0.2-19.4] vs 9.1 [2.6-14.5] mU.mmol-1; p < 0.01). Glucose 85-92 insulin Homo sapiens 12-19 7672496-2 1995 Intravenous infusions of glucagon-like peptide 1 (GLP-1) [7-36 amide] are glucose-dependently insulinotropic and glucagonostatic and normalize plasma glucose concentrations in non-insulin-dependent diabetic patients. Glucose 74-81 insulin Homo sapiens 94-101 7672496-10 1995 Before glucose administration, insulin (p < 0.0001) and C-peptide (p < 0.0004) increased, whereas glucagon (p = 0.0018) and glucose (p < 0.0001) decreased in a dose-dependent manner. Glucose 7-14 insulin Homo sapiens 59-68 7672496-11 1995 After glucose stimulation, integrated increments in insulin (p = 0.0007) and C-peptide (p = 0.02) were augmented and kG-values increased (p < 0.0001) in a dose-related fashion. Glucose 6-13 insulin Homo sapiens 52-59 7672496-11 1995 After glucose stimulation, integrated increments in insulin (p = 0.0007) and C-peptide (p = 0.02) were augmented and kG-values increased (p < 0.0001) in a dose-related fashion. Glucose 6-13 insulin Homo sapiens 77-86 7789625-6 1995 Infusion of 1.2 pmol.kg-1.min-1 GLP-I with 20 g glucose (10% dextrose in water) injected intravenously over 60 min enhanced plasma responses of immunoreactive CP; the mean incremental areas under concentration curves (0-60 min) increased sixfold, but the glycemic excursion was not affected. Glucose 48-55 insulin Homo sapiens 159-161 7789625-6 1995 Infusion of 1.2 pmol.kg-1.min-1 GLP-I with 20 g glucose (10% dextrose in water) injected intravenously over 60 min enhanced plasma responses of immunoreactive CP; the mean incremental areas under concentration curves (0-60 min) increased sixfold, but the glycemic excursion was not affected. Glucose 61-69 insulin Homo sapiens 159-161 7789626-0 1995 Comparison of estimates of insulin sensitivity from minimal model analysis of the insulin-modified frequently sampled intravenous glucose tolerance test and the isoglycemic hyperinsulinemic clamp in subjects with NIDDM. Glucose 130-137 insulin Homo sapiens 27-34 7789626-0 1995 Comparison of estimates of insulin sensitivity from minimal model analysis of the insulin-modified frequently sampled intravenous glucose tolerance test and the isoglycemic hyperinsulinemic clamp in subjects with NIDDM. Glucose 130-137 insulin Homo sapiens 82-89 7789626-1 1995 Minimal model (MINMOD) analysis of the frequently sampled intravenous glucose tolerance test (FSIVGTT) is dependent on an adequate insulin response to the glucose load. Glucose 70-77 insulin Homo sapiens 131-138 7789626-1 1995 Minimal model (MINMOD) analysis of the frequently sampled intravenous glucose tolerance test (FSIVGTT) is dependent on an adequate insulin response to the glucose load. Glucose 155-162 insulin Homo sapiens 131-138 7789626-4 1995 We have compared estimates of insulin sensitivity derived from minimal modeling of a 4-h insulin-modified FSIVGTT and the glucose clamp in subjects with NIDDM. Glucose 122-129 insulin Homo sapiens 30-37 7789628-6 1995 These findings provide further evidence that hyperinsulinemia per se is the primary stimulus that triggers stimulation of muscle blood flow and MSNA during insulin/glucose infusion in humans and suggest that the impaired insulin-induced vasodilation in obese subjects is not related primarily to impaired stimulation of muscle carbohydrate metabolism. Glucose 164-171 insulin Homo sapiens 50-57 7789637-9 1995 These characteristics of the dose-response relationships between glucose and insulin secretion result in a more severe degree of hyperglycemia than observed in subjects with glucokinase mutations, and these subjects more frequently need insulin treatment. Glucose 65-72 insulin Homo sapiens 77-84 7557835-5 1995 All these agents exert little effect upon insulin release in nutrient-deprived islets, but markedly augment glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 127-134 7768580-6 1995 The sum of insulin levels during glucose tolerance was significantly greater in the borderline hypertensive compared with the normotensive subjects (P = .014), and insulin-stimulated glucose utilization during the clamp was significantly lower in borderline hypertensive compared with normotensive subjects (P = .016). Glucose 33-40 insulin Homo sapiens 11-18 7768580-6 1995 The sum of insulin levels during glucose tolerance was significantly greater in the borderline hypertensive compared with the normotensive subjects (P = .014), and insulin-stimulated glucose utilization during the clamp was significantly lower in borderline hypertensive compared with normotensive subjects (P = .016). Glucose 183-190 insulin Homo sapiens 164-171 7768580-9 1995 Sodium-lithium countertransport correlated with albuminuria (r = .31, P < .05) as well as significantly with insulin-stimulated glucose utilization during the clamp (r = .44, P < .001). Glucose 131-138 insulin Homo sapiens 112-119 7769096-6 1995 This improvement was due to both enhanced insulin-mediated stimulation of glucose uptake (rate of glucose disposal [Rd], +0.89 mg/kg.min) and increased inhibition of HGP (-0.74 mg/kg.min) (P < 0.0001 for both). Glucose 74-81 insulin Homo sapiens 42-49 7769096-6 1995 This improvement was due to both enhanced insulin-mediated stimulation of glucose uptake (rate of glucose disposal [Rd], +0.89 mg/kg.min) and increased inhibition of HGP (-0.74 mg/kg.min) (P < 0.0001 for both). Glucose 98-105 insulin Homo sapiens 42-49 7775622-0 1995 Glucose modulation of insulin and glucagon secretion is altered in impaired glucose tolerance. Glucose 0-7 insulin Homo sapiens 22-29 7775622-5 1995 The acute insulin response to arginine (AIR = 2-5 min postload increase) at BG 14 mmol/L, but not at fasting BG or BG 28 mmol/L, was lower in IGT than in NGT (P = 0.033), as was the glucose potentiation of AIR (slopeAIR) (P = 0.020). Glucose 182-189 insulin Homo sapiens 10-17 7775624-0 1995 Somatostatin enhances insulin-stimulated glucose uptake in the perfused human forearm. Glucose 41-48 insulin Homo sapiens 22-29 7775624-5 1995 Compared with the systemic control infusion, local forearm perfusion with somatostatin caused a 55% increase in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs. 0.47 +/- 0.19 mmol/L, P < 0.05). Glucose 139-146 insulin Homo sapiens 112-119 7775624-9 1995 Our data suggest that somatostatin increases insulin-stimulated muscle utilization of glucose through local mechanisms. Glucose 86-93 insulin Homo sapiens 45-52 7566560-6 1995 Oral contraceptive can induce deterioration in glucose tolerance that has consistently been associated with insulin excess and insulin resistance. Glucose 47-54 insulin Homo sapiens 108-115 7789631-7 1995 Insulin-mediated glucose uptake (144 +/- 11 mg.m-2.min-1), glucose oxidation (76 +/- 4 mg.m-2.min-1), and nonoxidative glucose disposal (71 +/- 6 mg.m-2.min-1) were similar in all groups before the start of antihypertensive treatment and did not change in captopril and nifedipine groups. Glucose 17-24 insulin Homo sapiens 0-7 7789635-0 1995 Hypoxia stimulates glucose transport in insulin-resistant human skeletal muscle. Glucose 19-26 insulin Homo sapiens 40-47 7789635-1 1995 Insulin and muscle contraction stimulate glucose transport into muscle cells by separate signaling pathways, and hypoxia has been shown to operate via the contraction signaling pathway. Glucose 41-48 insulin Homo sapiens 0-7 7789635-7 1995 Hypoxia + insulin significantly stimulated glucose transport in lean, obese, and diabetic muscle. Glucose 43-50 insulin Homo sapiens 10-17 7789636-0 1995 Altered insulin secretory responses to glucose in subjects with a mutation in the MODY1 gene on chromosome 20. Glucose 39-46 insulin Homo sapiens 8-15 7789636-5 1995 However, the marker-positive subjects had defective insulin secretory responses to an increase in plasma glucose concentrations. Glucose 105-112 insulin Homo sapiens 52-59 7782939-1 1995 This review examines the molecular mechanisms underlying substrate competition between glucose and lipid in starvation and in insulin-resistant states. Glucose 87-94 insulin Homo sapiens 126-133 7626505-5 1995 Serum SHBG concentrations are inversely correlated with both fasting and glucose-stimulated insulin levels, and insulin has been shown to have a direct inhibitory effect on SHBG synthesis and secretion by hepatocytes in culture. Glucose 73-80 insulin Homo sapiens 92-99 7783660-9 1995 Insulin secretion in IGT is variable and, overall, seems intact, although a subtle defect in the first-phase insulin response to glucose could not be ruled out in this study. Glucose 129-136 insulin Homo sapiens 109-116 7783664-9 1995 Relative insulin action was determined by calculation of the mean glucose infusion rate (GIR) required to sustain euglycemia over the last 60 minutes of the infusion. Glucose 66-73 insulin Homo sapiens 9-16 7611377-7 1995 In conclusion, the present study demonstrates increased insulin sensitivity in LIR and ET with respect to glucose uptake but not glucose production. Glucose 106-113 insulin Homo sapiens 56-63 7611377-7 1995 In conclusion, the present study demonstrates increased insulin sensitivity in LIR and ET with respect to glucose uptake but not glucose production. Glucose 129-136 insulin Homo sapiens 56-63 7611383-0 1995 Basal plasma insulin levels exert a qualitative but not quantitative effect on glucose-mediated glucose uptake. Glucose 79-86 insulin Homo sapiens 13-20 7611383-0 1995 Basal plasma insulin levels exert a qualitative but not quantitative effect on glucose-mediated glucose uptake. Glucose 96-103 insulin Homo sapiens 13-20 7637151-0 1995 [Portal and peripheral blood immunoreactive insulin concentrations after glucose infusion during gastrectomy]. Glucose 73-80 insulin Homo sapiens 44-51 7742317-1 1995 Insulin is a proteohormone with amphipathic three-dimensional structure and the ligand of a receptor, which itself spans the plasma membrane of glucose-metabolizing cells. Glucose 144-151 insulin Homo sapiens 0-7 7762045-0 1995 Carotid artery wall intima-media thickness is associated with insulin-mediated glucose disposal in men at high and low coronary risk. Glucose 79-86 insulin Homo sapiens 62-69 7770935-4 1995 The acute insulin response to glucose (0.3 g/kg i.v.) Glucose 30-37 insulin Homo sapiens 10-17 7762630-0 1995 Stimulation of muscle glucose disposal by insulin in humans is a function of the preexisting plasma insulin level. Glucose 22-29 insulin Homo sapiens 42-49 7662232-0 1995 Doxazosin lowers blood pressure and improves insulin responses to a glucose load with no changes in tyrosine kinase activity or insulin binding. Glucose 68-75 insulin Homo sapiens 45-52 7662232-2 1995 We evaluated the glucose and insulin responses to a glucose load and lipid profiles in 36 diabetic hypertensive patients before and after 8 weeks of doxazosin administration. Glucose 52-59 insulin Homo sapiens 29-36 7762630-0 1995 Stimulation of muscle glucose disposal by insulin in humans is a function of the preexisting plasma insulin level. Glucose 22-29 insulin Homo sapiens 100-107 7762630-6 1995 The effects of insulin to stimulate whole body glucose utilization, nonoxidative glucose disposal, and glycogen synthase activity in muscle are therefore functions of the preexisting plasma insulin concentration. Glucose 47-54 insulin Homo sapiens 15-22 7762630-6 1995 The effects of insulin to stimulate whole body glucose utilization, nonoxidative glucose disposal, and glycogen synthase activity in muscle are therefore functions of the preexisting plasma insulin concentration. Glucose 47-54 insulin Homo sapiens 190-197 7762630-6 1995 The effects of insulin to stimulate whole body glucose utilization, nonoxidative glucose disposal, and glycogen synthase activity in muscle are therefore functions of the preexisting plasma insulin concentration. Glucose 81-88 insulin Homo sapiens 190-197 7605885-4 1995 The drop in glucose concentration induced 20 minutes after a single administration of insulin can also be detected in both fluids. Glucose 12-19 insulin Homo sapiens 86-93 7672344-0 1995 Mechanisms underlying suppression of glucose oxidation in insulin-resistant states. Glucose 37-44 insulin Homo sapiens 58-65 7489839-5 1995 The tissue sensitivity to insulin, expressed by the amount of glucose infused during the last 60 min of a 120-min hyperinsulinaemia euglycaemic clamp (M-value) and the M/I ratio, was significantly lower in the patients than in the control subjects (M-value 404 +/- 118 vs 494 +/- 85 mg glucose/kg body weight, p < 0.02) (M/I ratio 1.77 +/- 0.71 vs 2.57 +/- 0.70 (mg/(kgBW.min) per pmol/l.100, p < 0.001). Glucose 62-69 insulin Homo sapiens 26-33 7772420-5 1995 Serum insulin concentrations increased 30 min after operation to coincide with the peak of the glucose increase in the non-diabetic patients who received general anaesthesia, but no insulin response was seen in the diabetic general anaesthesia patients. Glucose 95-102 insulin Homo sapiens 6-13 7621645-0 1995 Effects of glucocorticoids and sympathomimetic agents on basal and insulin-stimulated glucose metabolism. Glucose 86-93 insulin Homo sapiens 67-74 7621645-4 1995 Basal and insulin-stimulated glucose metabolism was measured in healthy human subjects during four 2-h clamp studies as follows: control (C); after taking oral dexamethasone (2 mg daily) for 2 days (D); after taking oral ephedrine sulphate (40 mg daily) for 2 days (E); and after taking dexamethasone+ephedrine (D+E). Glucose 29-36 insulin Homo sapiens 10-17 7489839-5 1995 The tissue sensitivity to insulin, expressed by the amount of glucose infused during the last 60 min of a 120-min hyperinsulinaemia euglycaemic clamp (M-value) and the M/I ratio, was significantly lower in the patients than in the control subjects (M-value 404 +/- 118 vs 494 +/- 85 mg glucose/kg body weight, p < 0.02) (M/I ratio 1.77 +/- 0.71 vs 2.57 +/- 0.70 (mg/(kgBW.min) per pmol/l.100, p < 0.001). Glucose 286-293 insulin Homo sapiens 26-33 7729608-7 1995 However, the rate of glucose infusion required to maintain hypoglycemic plateaus during hypoglycemia was lower after hyperglycemia (nondiabetic subjects 31.2 +/- 3.4 vs. 36.7 +/- 4 mumol.kg-1.min-1, IDDM patients 33 +/- 3.1 vs. 42.5 +/- 3.9 mumol.kg-1.min-1; P < 0.05) indicating greater insulin resistance induced by antecedent hyperglycemia. Glucose 21-28 insulin Homo sapiens 291-298 7601013-3 1995 It reduces blood glucose levels, predominantly by improving hepatic and peripheral tissue sensitivity to insulin without affecting the secretion of this hormone. Glucose 17-24 insulin Homo sapiens 105-112 7661312-10 1995 We also studied those 10 patients whose blood glucose improved during intensified insulin therapy. Glucose 46-53 insulin Homo sapiens 82-89 7729621-1 1995 The metabolism of glucose in insulin-secreting cells leads to closure of ATP-sensitive K+ channels (KATP), an event that initiates the insulin secretory process. Glucose 18-25 insulin Homo sapiens 29-36 7729621-1 1995 The metabolism of glucose in insulin-secreting cells leads to closure of ATP-sensitive K+ channels (KATP), an event that initiates the insulin secretory process. Glucose 18-25 insulin Homo sapiens 135-142 7737738-4 1995 Insulin levels were higher in the hypertensive subjects (11.7 +/- 1.5 microU/mL, mean +/- SEM) than in the normotensive subjects (8.2 +/- 1.2 microU/mL), but glucose levels were similar and within normal limits. Glucose 158-165 insulin Homo sapiens 0-7 7641765-7 1995 Irrespective of the degree of glucose tolerance, the insulin response to oral glucose was not reduced but delayed, up to 60 min in the CF-IGT/DM group. Glucose 78-85 insulin Homo sapiens 53-60 7641765-8 1995 First-phase insulin release (0-10 min) after i.v.-glucose was significantly lower in CF patients (29% of healthy controls; P < 0.0001), with no difference between the CF-NGT and CF-IGT/DM groups. Glucose 50-57 insulin Homo sapiens 12-19 7642171-6 1995 In vitro experiment on isolated pancreatic islets demonstrated that STZ-induced loss of insulin response to glucose was also counteracted by incubation with GHB and NA (Peak insulin response to 16.4 mM glucose: 0.69 +/- 0.31 vs 3.03 +/- 0.67 microU/islet/min), but not by GHB or NA alone. Glucose 108-115 insulin Homo sapiens 88-95 7642171-6 1995 In vitro experiment on isolated pancreatic islets demonstrated that STZ-induced loss of insulin response to glucose was also counteracted by incubation with GHB and NA (Peak insulin response to 16.4 mM glucose: 0.69 +/- 0.31 vs 3.03 +/- 0.67 microU/islet/min), but not by GHB or NA alone. Glucose 202-209 insulin Homo sapiens 88-95 7628524-0 1995 Surgical removal of insulinoma restores glucose recovery from hypoglycaemia but does not normalize insulin action. Glucose 40-47 insulin Homo sapiens 20-27 7628524-7 1995 Before the operation, insulin-mediated glucose disposal was significantly lower than in the controls (30.8 +/- 3.1 vs. 49.1 +/- 3.1 mumol kg-1 min-1). Glucose 39-46 insulin Homo sapiens 22-29 7550534-1 1995 The insulin resistance syndrome is characterized by a constellation of risk factors including obesity, central body fat distribution, hypertension, glucose intolerance, elevated plasma insulin levels, increased triglyceride and decreased high-density lipoprotein (HDL) cholesterol. Glucose 148-155 insulin Homo sapiens 4-11 7550539-5 1995 Studies of details of function and morphology in the muscles in this rat model have revealed that insulin stimulation of glucose transport, glycogen synthesis and the insulin sensitive part of the glycogen synthase is diminished at submaximal insulin concentrations. Glucose 121-128 insulin Homo sapiens 98-105 7745004-12 1995 Ten millimoles of D-beta-OHB per L inhibited the subsequently tested insulin response to 27 mmol/L glucose by 56% (P < 0.001). Glucose 99-106 insulin Homo sapiens 69-76 7537758-1 1995 To determine whether the impaired insulin-stimulated glucose uptake in obese individuals is associated with altered insulin receptor signaling, we measured both glucose uptake and early steps in the insulin action pathway in intact strips of human skeletal muscle. Glucose 53-60 insulin Homo sapiens 34-41 7537758-9 1995 We conclude that impaired insulin-stimulated glucose uptake in skeletal muscle from severely obese subjects is accompanied by a deficiency in insulin receptor signaling, which may contribute to decreased insulin action. Glucose 45-52 insulin Homo sapiens 26-33 7537758-9 1995 We conclude that impaired insulin-stimulated glucose uptake in skeletal muscle from severely obese subjects is accompanied by a deficiency in insulin receptor signaling, which may contribute to decreased insulin action. Glucose 45-52 insulin Homo sapiens 142-149 7665757-11 1995 An infusion of glucose at 5.95 +/- 0.53 mg/kg x min (97.20 +/- 0.03% of the fasting measured EPR) with 1.22 +/- 0.18 mU/kg x min insulin infusion reduced N and 3-MH loss after a time lag of 12 h. The peak decrease in body N (-36%) and 3-MH loss (-38%) was reached during the first 12 h of glucose withdrawal period. Glucose 289-296 insulin Homo sapiens 129-136 7744999-1 1995 Recent studies have focused on the link between the development of disordered vascular regulation (e.g. hypertension) and alteration in the effects of insulin to mediate glucose uptake. Glucose 170-177 insulin Homo sapiens 151-158 7744999-4 1995 However, whether the local vascular effects of insulin correlate with its systemic glucose regulatory effects remains unclear. Glucose 83-90 insulin Homo sapiens 47-54 7745002-5 1995 Insulin secretion was negatively associated with the rate of weight gain, whether assessed by the insulin response during the meal tolerance test (r = -0.35; P < 0.001), the oral glucose tolerance test (r = -0.30; P = 0.004), or the acute insulin secretory response to iv glucose (r = -0.28; P = 0.002). Glucose 182-189 insulin Homo sapiens 0-7 7745002-5 1995 Insulin secretion was negatively associated with the rate of weight gain, whether assessed by the insulin response during the meal tolerance test (r = -0.35; P < 0.001), the oral glucose tolerance test (r = -0.30; P = 0.004), or the acute insulin secretory response to iv glucose (r = -0.28; P = 0.002). Glucose 275-282 insulin Homo sapiens 0-7 7745004-2 1995 To further assess the clinical significance of these findings, we tested in human islets the effects of fatty acids on glucose-induced insulin release and biosynthesis and on pyruvate dehydrogenase (PDH) activity. Glucose 119-126 insulin Homo sapiens 135-142 7745004-4 1995 Exposure to 0.125 mmol/L palmitate or oleate for 48 h during tissue culture (RPMI-1640 and 5.5 mmol/L glucose) inhibited the postculture insulin response to 27 mmol/L glucose by 40% and 42% (P < 0.01 for difference). Glucose 102-109 insulin Homo sapiens 137-144 7745004-4 1995 Exposure to 0.125 mmol/L palmitate or oleate for 48 h during tissue culture (RPMI-1640 and 5.5 mmol/L glucose) inhibited the postculture insulin response to 27 mmol/L glucose by 40% and 42% (P < 0.01 for difference). Glucose 167-174 insulin Homo sapiens 137-144 7752906-7 1995 The rate of insulin-induced whole-body glucose disposal increased similarly both before (basal 10.8 +/- 1.8, low-dose insulin 10.5 +/- 2.1, and high-dose insulin 20.9 +/- 11.9 mumol.kg-1.min-1) and after (11.1 +/- 1.7, 10.7 +/- 1.2, and 18.6 +/- 7.9, respectively) gemfibrozil treatment. Glucose 39-46 insulin Homo sapiens 12-19 7738420-6 1995 In addition, prospective studies have indicated that NIDDM rarely develops in the most insulin-sensitive subjects, and the relatively lower insulin concentrations in patients with a known beta-cell defect--that is a glucokinase mutation--are compatible with normal glucose tolerance if ideal whole body insulin sensitivity is maintained. Glucose 265-272 insulin Homo sapiens 140-147 7738420-6 1995 In addition, prospective studies have indicated that NIDDM rarely develops in the most insulin-sensitive subjects, and the relatively lower insulin concentrations in patients with a known beta-cell defect--that is a glucokinase mutation--are compatible with normal glucose tolerance if ideal whole body insulin sensitivity is maintained. Glucose 265-272 insulin Homo sapiens 140-147 7751990-3 1995 Insulin resistance was assessed by fasting insulin level and sum of the insulin values after an oral glucose tolerance test in all 82, and were compared with data from 40 nonobese adolescents. Glucose 101-108 insulin Homo sapiens 0-7 7752913-6 1995 Stimulation of glucose oxidation and utilization by insulin was reduced in the Ivelip study, but not in the heparin study. Glucose 15-22 insulin Homo sapiens 52-59 7752913-8 1995 On the other hand, insulin-induced inhibition of glucose production was impaired in both the heparin and Ivelip studies. Glucose 49-56 insulin Homo sapiens 19-26 7713930-1 1995 Insulin stimulates glucose transport in muscle and fat cells by inducing translocation of GLUT4 glucose transporters from a storage site to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 7733278-1 1995 A glucose kinetic model is described that contains insulin-independent and insulin-dependent pathways of glucose uptake and includes a saturating flux term for glucose transport into the cells by the glucose transporters. Glucose 2-9 insulin Homo sapiens 51-58 7733278-1 1995 A glucose kinetic model is described that contains insulin-independent and insulin-dependent pathways of glucose uptake and includes a saturating flux term for glucose transport into the cells by the glucose transporters. Glucose 2-9 insulin Homo sapiens 75-82 7733278-1 1995 A glucose kinetic model is described that contains insulin-independent and insulin-dependent pathways of glucose uptake and includes a saturating flux term for glucose transport into the cells by the glucose transporters. Glucose 105-112 insulin Homo sapiens 51-58 7733278-1 1995 A glucose kinetic model is described that contains insulin-independent and insulin-dependent pathways of glucose uptake and includes a saturating flux term for glucose transport into the cells by the glucose transporters. Glucose 105-112 insulin Homo sapiens 75-82 7733278-1 1995 A glucose kinetic model is described that contains insulin-independent and insulin-dependent pathways of glucose uptake and includes a saturating flux term for glucose transport into the cells by the glucose transporters. Glucose 105-112 insulin Homo sapiens 51-58 7733278-1 1995 A glucose kinetic model is described that contains insulin-independent and insulin-dependent pathways of glucose uptake and includes a saturating flux term for glucose transport into the cells by the glucose transporters. Glucose 105-112 insulin Homo sapiens 75-82 7733278-4 1995 In addition, the model was used to simulate published results from glucose clamp experiments with a range of glycemic levels and insulin concentrations. Glucose 67-74 insulin Homo sapiens 129-136 7619649-13 1995 During D-glucose infusion, insulin was stimulated and the other hormones were inhibited. Glucose 7-16 insulin Homo sapiens 27-34 11850664-3 1995 The individual steps in the secretory pathway of insulin which is induced primarily by blood plasma glucose have now been identified. Glucose 100-107 insulin Homo sapiens 49-56 11850664-8 1995 In addition to the major effects of blood plasma glucose in the regulation of insulin secretion, a variety of hormonal and neural factors producing endocrine and paracrine effects modulate and fine-tune beta-cell insulin secretion. Glucose 49-56 insulin Homo sapiens 78-85 7497873-2 1995 RESEARCH DESIGN AND METHODS: Insulin secretion rates (ISR) in response to intravenous glucose and mixed meals were estimated by deconvolution of C-peptide levels. Glucose 86-93 insulin Homo sapiens 29-36 7497873-3 1995 RESULTS: When fasting glucose and glycosylated hemoglobin concentrations were still within the normal range, insulin secretory responses to intravenous glucose infusion were reduced, but 80- to 100-min secretory oscillations could still be detected. Glucose 152-159 insulin Homo sapiens 109-116 7600749-4 1995 Among 201 children who had been looked after on the routine postnatal wards at birth, those with lower birthweights had higher plasma glucose and insulin concentrations 30 min after an oral glucose load, independently of their current size (p = 0.01 and 0.04, respectively). Glucose 190-197 insulin Homo sapiens 146-153 7796987-6 1995 Using sib-pair linkage analyses, no evidence for linkage was found between the D2S1237 marker at this locus and fasting insulin, insulin-stimulated glucose uptake in vivo, obesity, or non-insulin-dependent diabetes mellitus. Glucose 148-155 insulin Homo sapiens 129-136 7711877-1 1995 Thyroid hormone action on insulin"s effect on glucose kinetics was investigated with the use of a physiological three compartment model. Glucose 46-53 insulin Homo sapiens 26-33 7711877-5 1995 Insulin stimulated basal plasma glucose clearance fourfold (p < 0.001) and completely suppressed basal hepatic glucose production (p < 0.001). Glucose 32-39 insulin Homo sapiens 0-7 7711877-6 1995 Concomitantly, the total distribution volume of glucose was increased by 19% (p < 0.05); this change was accompanied by about 50% expansion of the slowly exchanging glucose pool (putatively representing the insulin-dependent compartment). Glucose 48-55 insulin Homo sapiens 210-217 7711877-6 1995 Concomitantly, the total distribution volume of glucose was increased by 19% (p < 0.05); this change was accompanied by about 50% expansion of the slowly exchanging glucose pool (putatively representing the insulin-dependent compartment). Glucose 168-175 insulin Homo sapiens 210-217 7711877-8 1995 However, thyroxine treatment blunted the insulin-induced increases in total distribution volume and the slowly exchanging pool of glucose (p = NS vs the basal state). Glucose 130-137 insulin Homo sapiens 41-48 7706456-1 1995 The effects of increased GLUT4 (insulin-regulatable muscle/fat glucose transporter) expression on glucose homeostasis in a genetic model of non-insulin-dependent diabetes mellitus were determined by expressing a human GLUT4 transgene (hGLUT4) in diabetic C57BL/KsJ-db/db mice. Glucose 63-70 insulin Homo sapiens 32-39 7706500-11 1995 The impaired insulin-stimulated glucose disposal to peripheral tissues was primarily due to reduced nonoxidative glucose metabolism. Glucose 32-39 insulin Homo sapiens 13-20 7706500-11 1995 The impaired insulin-stimulated glucose disposal to peripheral tissues was primarily due to reduced nonoxidative glucose metabolism. Glucose 113-120 insulin Homo sapiens 13-20 7629403-6 1995 RESULTS: In univariate analyses the plasma insulin response after an oral glucose load, especially after 60 min, was significantly related to blood pressure level. Glucose 74-81 insulin Homo sapiens 43-50 7629403-8 1995 When adjusted for age, body mass index, plasma glucose response and alcohol consumption, plasma insulin concentrations after 30 and 60 min in the highest quartile were significantly higher than those in the lowest quartile. Glucose 47-54 insulin Homo sapiens 96-103 7629403-9 1995 CONCLUSIONS: Blood pressure was significantly and independently related to plasma insulin level after an oral glucose load in normotensive Japanese men with normal glucose tolerance. Glucose 110-117 insulin Homo sapiens 82-89 7629403-9 1995 CONCLUSIONS: Blood pressure was significantly and independently related to plasma insulin level after an oral glucose load in normotensive Japanese men with normal glucose tolerance. Glucose 164-171 insulin Homo sapiens 82-89 7723677-4 1995 Compared with control values, insulin-mediated glucose utilization in PCO women was significantly lower in lean (1.96 +/- 0.17 v 1.24 +/- 0.10, P < .01) and obese (1.23 +/- 0.18 v 1.03 +/- 0.09 mmol/m2/min, P < .01) subjects. Glucose 47-54 insulin Homo sapiens 30-37 8630745-3 1995 In concert with decrements in insulin, increments in glucagon, and in the absence of the latter increments in epinephrine, stand high in the hierarchy of redundant glucose counterregulatory factors. Glucose 164-171 insulin Homo sapiens 30-37 7796075-9 1995 It is essential to study insulin and C-peptide secretion in controlled "fasting" glucose conditions. Glucose 81-88 insulin Homo sapiens 25-32 7796075-9 1995 It is essential to study insulin and C-peptide secretion in controlled "fasting" glucose conditions. Glucose 81-88 insulin Homo sapiens 37-46 7535776-0 1995 Thiazolidine derivatives ameliorate high glucose-induced insulin resistance via the normalization of protein-tyrosine phosphatase activities. Glucose 41-48 insulin Homo sapiens 57-64 7535776-1 1995 The mechanisms for the insulin resistance induced by hyperglycemia were investigated by studying the effect of high glucose concentration (HG) and its modulation by thiazolidine derivatives, on insulin signaling using Rat 1 fibroblasts expressing human insulin receptors (HIRc). Glucose 116-123 insulin Homo sapiens 23-30 7535776-1 1995 The mechanisms for the insulin resistance induced by hyperglycemia were investigated by studying the effect of high glucose concentration (HG) and its modulation by thiazolidine derivatives, on insulin signaling using Rat 1 fibroblasts expressing human insulin receptors (HIRc). Glucose 116-123 insulin Homo sapiens 194-201 7535776-1 1995 The mechanisms for the insulin resistance induced by hyperglycemia were investigated by studying the effect of high glucose concentration (HG) and its modulation by thiazolidine derivatives, on insulin signaling using Rat 1 fibroblasts expressing human insulin receptors (HIRc). Glucose 116-123 insulin Homo sapiens 194-201 7535776-2 1995 Incubating HIRc cells in 27 mM D-glucose for 4 days impaired the insulin-stimulated phosphorylation of pp185 and receptor beta-subunits. Glucose 31-40 insulin Homo sapiens 65-72 7701583-9 1995 The kinetics of the C-peptide response to intravenously injected glucose shows a persistent abnormality of first-phase insulin release and a prolonged second phase release. Glucose 65-72 insulin Homo sapiens 119-126 7890039-1 1995 In skeletal muscle, glucose transport is stimulated by insulin, contractions and hypoxia. Glucose 20-27 insulin Homo sapiens 55-62 7890039-2 1995 In this study, we used the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin to examine whether (i) PI 3-kinase activity is necessary for stimulation of glucose transport by insulin in muscle, and (ii) PI 3-kinase mediates a step in the pathway by which contractions/hypoxia stimulate glucose transport. Glucose 168-175 insulin Homo sapiens 189-196 7890039-3 1995 Wortmannin completely blocked insulin- and insulin-like growth factor-1-stimulated glucose transport in muscle. Glucose 83-90 insulin Homo sapiens 30-37 7890039-3 1995 Wortmannin completely blocked insulin- and insulin-like growth factor-1-stimulated glucose transport in muscle. Glucose 83-90 insulin Homo sapiens 43-50 7887929-5 1995 Insulin secretagogues (28 mM glucose + 0.5 mM carbachol) caused a rapid and transient increase in PtdIns(3,4,5)P3 levels which peaked at 2-5 min, corresponding to peak early phase insulin release. Glucose 29-36 insulin Homo sapiens 0-7 7887929-5 1995 Insulin secretagogues (28 mM glucose + 0.5 mM carbachol) caused a rapid and transient increase in PtdIns(3,4,5)P3 levels which peaked at 2-5 min, corresponding to peak early phase insulin release. Glucose 29-36 insulin Homo sapiens 180-187 7612911-0 1995 Paradoxical inhibition of insulin secretion by glucose in non-insulin-dependent diabetic patients. Glucose 47-54 insulin Homo sapiens 26-33 7612911-2 1995 glucose bolus leads to an immediate increase in plasma insulin, whereas in non-insulin-dependent diabetic patients this early response is diminished, lacking or even negative. Glucose 0-7 insulin Homo sapiens 55-62 7612911-6 1995 Paradoxical responses (a decrease of two or more times the SD of the analysis within 15 min of increasing the glucose concentration) were seen in five diabetic patients for insulin (22 +/- 8%) and in nine diabetic patients for C-peptide (13 +/- 3%), but never in the healthy controls. Glucose 110-117 insulin Homo sapiens 173-180 7612920-8 1995 In normal subjects, the true and total insulin levels in the fasting state and at the time peak after glucose- or arginine-induced endogenous insulin release were well correlated at r = 0.88 and 0.89, respectively. Glucose 102-109 insulin Homo sapiens 39-46 7612920-8 1995 In normal subjects, the true and total insulin levels in the fasting state and at the time peak after glucose- or arginine-induced endogenous insulin release were well correlated at r = 0.88 and 0.89, respectively. Glucose 102-109 insulin Homo sapiens 142-149 7900781-1 1995 We explore possible kinetic mechanisms responsible for the oscillatory (pulsatile) secretion of insulin observed in vitro when pancreatic islets or islet-derived cells are perifused with glucose. Glucose 187-194 insulin Homo sapiens 96-103 7900781-2 1995 Three primary processes are included: 1) glucose stimulation of insulin secretion, controlled by glucokinase; 2) uptake of glucose through GLUT transporters; and 3) glucose metabolism. Glucose 41-48 insulin Homo sapiens 64-71 7762828-7 1995 During 5-min static incubations, 3 mM glucose elicited 0.8 +/- 0.2 ng of insulin release while 16 mM glucose elicited 3.2 +/- 0.5 ng of insulin release. Glucose 38-45 insulin Homo sapiens 73-80 7762828-7 1995 During 5-min static incubations, 3 mM glucose elicited 0.8 +/- 0.2 ng of insulin release while 16 mM glucose elicited 3.2 +/- 0.5 ng of insulin release. Glucose 101-108 insulin Homo sapiens 136-143 7605362-2 1995 Insulin sensitivity of the patients was characterized by their insulin-stimulated glucose uptake rate determined by euglycemic clamp technique. Glucose 82-89 insulin Homo sapiens 0-7 7605362-2 1995 Insulin sensitivity of the patients was characterized by their insulin-stimulated glucose uptake rate determined by euglycemic clamp technique. Glucose 82-89 insulin Homo sapiens 63-70 7605362-5 1995 To evaluate the effect of insulin resistance on LDL particle size the participants were categorized into two subgroups using the median of their insulin-stimulated glucose uptake rate (14.67 mumol/kg/min) as a cut-off point. Glucose 164-171 insulin Homo sapiens 145-152 8520522-4 1995 The glucose disappearance rate during the 15-min ITT was lower in patients with psoriasis than in controls (5.1 +/- 0.5%/min vs 7.5 +/- 0.4%/min, P < 0.05), demonstrating a state of insulin resistance. Glucose 4-11 insulin Homo sapiens 185-192 7758230-0 1995 Increased secretion of 32,33 split proinsulin after intravenous glucose in glucose-tolerant first-degree relatives of patients with non-insulin dependent diabetes of European, but not Asian, origin. Glucose 64-71 insulin Homo sapiens 35-45 7758230-0 1995 Increased secretion of 32,33 split proinsulin after intravenous glucose in glucose-tolerant first-degree relatives of patients with non-insulin dependent diabetes of European, but not Asian, origin. Glucose 75-82 insulin Homo sapiens 35-45 7758230-18 1995 CONCLUSION: First-degree relatives of European patients with NIDDM possess early signs of beta-cell dysfunction, with increased and disproportionate secretion of 32,33 split proinsulin after intravenous glucose, whilst glucose tolerance is still normal. Glucose 203-210 insulin Homo sapiens 174-184 7883122-2 1995 Since defects involving glucose transport and/or its phosphorylation to glucose-6-phosphate are present in muscle of insulin-resistant humans, HKII should be viewed as a candidate gene for inherited insulin resistance and susceptibility to non-insulin-dependent diabetes mellitus (NIDDM). Glucose 24-31 insulin Homo sapiens 117-124 7883123-2 1995 Since reduced insulin-stimulated glucose uptake and reduced glucose-6-phosphate content in muscle have been demonstrated in pre-non-insulin-dependent diabetes mellitus (pre-NIDDM) and NIDDM subjects, we have examined the coding region of the HKII gene in NIDDM patients to determine whether these patients show genetic polymorphisms that are associated with or contribute to the disease. Glucose 33-40 insulin Homo sapiens 14-21 7780493-0 1995 High fasting insulin levels associated with lower rates of weight gain in persons with normal glucose tolerance: the San Luis Valley Diabetes Study. Glucose 94-101 insulin Homo sapiens 13-20 7883976-3 1995 Pimas who were homozygous or heterozygous for the threonine-encoding allele were found to have a higher mean fasting plasma insulin concentration, a lower mean insulin-stimulated glucose uptake rate, a higher mean insulin response to oral glucose and a mixed meal, and a higher mean fat oxidation rate compared with Pimas who were homozygous for the alanine-encoding allele. Glucose 179-186 insulin Homo sapiens 160-167 7883976-3 1995 Pimas who were homozygous or heterozygous for the threonine-encoding allele were found to have a higher mean fasting plasma insulin concentration, a lower mean insulin-stimulated glucose uptake rate, a higher mean insulin response to oral glucose and a mixed meal, and a higher mean fat oxidation rate compared with Pimas who were homozygous for the alanine-encoding allele. Glucose 179-186 insulin Homo sapiens 160-167 7783102-7 1995 After adjustment for fasting plasma insulin levels and insulin-mediated glucose uptake, fasting and insulin-mediated erythrocyte magnesium accumulation were no longer different between the two groups. Glucose 72-79 insulin Homo sapiens 55-62 7783102-7 1995 After adjustment for fasting plasma insulin levels and insulin-mediated glucose uptake, fasting and insulin-mediated erythrocyte magnesium accumulation were no longer different between the two groups. Glucose 72-79 insulin Homo sapiens 55-62 7732710-9 1995 Insulin was significantly elevated in patients with microvascular angina 90 min (median: 101 vs 54 microU/ml; p < 0.01) and 120 min (median: 88 vs 51 microU/ml; p < 0.05) after ingestion of 100 g glucose. Glucose 202-209 insulin Homo sapiens 0-7 7758830-1 1995 Factors that regulate the tissue specific and developmental expression of the GLUT4 gene, whose transcribed protein is primarily responsible for mediating insulin stimulated glucose transport, are poorly defined. Glucose 174-181 insulin Homo sapiens 155-162 7864871-0 1995 Exogenous triacylglycerol inhibits insulin-stimulated glucose transport in L6 muscle cells in vitro. Glucose 54-61 insulin Homo sapiens 35-42 8583968-3 1995 It will be shown that the area of dopaminergic and serotonergic activity in the brain is intimately tied to the relative distribution of the central glucose transporters and, hence, to glucose metabolism and insulin activity. Glucose 149-156 insulin Homo sapiens 208-215 27414277-11 1995 Under hyperglycemic conditions, such as in diabetes mellitus, high levels of glucose occur in insulin-independent tissues such as the lens. Glucose 77-84 insulin Homo sapiens 94-101 7569360-6 1995 The only statistically significant difference, detected at the end of the study, was a reduction in fasting blood glucose level in the human insulin group (animal insulin 212 +/- 95.3 initial vs 193 +/- 78.3 mg/dL final, p = 0.18; human insulin 198 +/- 86.8 vs 169 +/- 71.7, p = 0.025). Glucose 114-121 insulin Homo sapiens 141-148 7569360-6 1995 The only statistically significant difference, detected at the end of the study, was a reduction in fasting blood glucose level in the human insulin group (animal insulin 212 +/- 95.3 initial vs 193 +/- 78.3 mg/dL final, p = 0.18; human insulin 198 +/- 86.8 vs 169 +/- 71.7, p = 0.025). Glucose 114-121 insulin Homo sapiens 163-170 7569360-6 1995 The only statistically significant difference, detected at the end of the study, was a reduction in fasting blood glucose level in the human insulin group (animal insulin 212 +/- 95.3 initial vs 193 +/- 78.3 mg/dL final, p = 0.18; human insulin 198 +/- 86.8 vs 169 +/- 71.7, p = 0.025). Glucose 114-121 insulin Homo sapiens 163-170 21232245-7 1995 Patients with elevated antiporter activity manifest metabolic abnormalities (for example, high fasting insulin levels, hyperlipidemia, increased total body exchangeable Na(+), and renal and cardiac hypertrophy) that are part of the syndrome characterized by resistance to insulin-stimulated body glucose disposal. Glucose 296-303 insulin Homo sapiens 272-279 7612874-5 1995 It could be demonstrated that insulin and IGF-I have similar effects on mitochondria but individual effects on cytosolic glucose metabolism. Glucose 121-128 insulin Homo sapiens 30-37 7887548-6 1995 INTERVENTION: Intensive therapy with three or more daily insulin injections or continuous subcutaneous insulin infusion guided by four or more glucose tests per day compared with conventional therapy with one or two daily insulin injections. Glucose 143-150 insulin Homo sapiens 103-110 7887548-6 1995 INTERVENTION: Intensive therapy with three or more daily insulin injections or continuous subcutaneous insulin infusion guided by four or more glucose tests per day compared with conventional therapy with one or two daily insulin injections. Glucose 143-150 insulin Homo sapiens 103-110 7784407-6 1995 The rate of dextrose infused to maintain euglycaemia is an estimate of the amount of glucose which is taken up by the tissues under the effect of a defined plasma insulin concentration. Glucose 12-20 insulin Homo sapiens 163-170 7784407-6 1995 The rate of dextrose infused to maintain euglycaemia is an estimate of the amount of glucose which is taken up by the tissues under the effect of a defined plasma insulin concentration. Glucose 85-92 insulin Homo sapiens 163-170 7784407-7 1995 Using several rates of insulin infusion allows to establish the relationship between the whole body glucose disposal and plasma insulin levels, and to discriminate between the states of decreased insulin sensitivity and/or altered maximal capacity to dispose of glucose. Glucose 100-107 insulin Homo sapiens 23-30 7784407-7 1995 Using several rates of insulin infusion allows to establish the relationship between the whole body glucose disposal and plasma insulin levels, and to discriminate between the states of decreased insulin sensitivity and/or altered maximal capacity to dispose of glucose. Glucose 100-107 insulin Homo sapiens 128-135 7784407-7 1995 Using several rates of insulin infusion allows to establish the relationship between the whole body glucose disposal and plasma insulin levels, and to discriminate between the states of decreased insulin sensitivity and/or altered maximal capacity to dispose of glucose. Glucose 100-107 insulin Homo sapiens 128-135 7784407-7 1995 Using several rates of insulin infusion allows to establish the relationship between the whole body glucose disposal and plasma insulin levels, and to discriminate between the states of decreased insulin sensitivity and/or altered maximal capacity to dispose of glucose. Glucose 262-269 insulin Homo sapiens 23-30 7784407-8 1995 The measurement of glucose fluxes, using the constant infusion of stable isotope labelled glucose, allows to differentiate the hepatic and the peripheral components of insulin resistance. Glucose 19-26 insulin Homo sapiens 168-175 7784407-8 1995 The measurement of glucose fluxes, using the constant infusion of stable isotope labelled glucose, allows to differentiate the hepatic and the peripheral components of insulin resistance. Glucose 90-97 insulin Homo sapiens 168-175 7784407-9 1995 Insulin sensitivity may be estimated using other methods, such as the minimal model which consists in a mathematical analysis of the intravenous glucose tolerance test. Glucose 145-152 insulin Homo sapiens 0-7 7733259-1 1995 Understanding the molecular mechanisms involved in the regulation of glucose transport into human muscle is necessary to unravel possible defects in glucose uptake associated with insulin resistance in humans. Glucose 69-76 insulin Homo sapiens 180-187 7733259-1 1995 Understanding the molecular mechanisms involved in the regulation of glucose transport into human muscle is necessary to unravel possible defects in glucose uptake associated with insulin resistance in humans. Glucose 149-156 insulin Homo sapiens 180-187 7900697-2 1995 The pathophysiologic state involves increased basal hepatic glucose production, decreased insulin-mediated glucose utilization in target tissues, and altered pancreatic function with decreased beta cell function and enhanced glucagon secretion. Glucose 107-114 insulin Homo sapiens 90-97 7900697-3 1995 Prospective studies indicate that insulin resistance and hyperinsulinemia exist in the prediabetic state at a time when glucose tolerance is normal. Glucose 120-127 insulin Homo sapiens 34-41 8581359-4 1995 This study thus reveals that formycin A may display cytotoxic potential in the same range of concentrations in which it causes a progressive increase of glucose-stimulated insulin secretion in normal pancreatic islets. Glucose 153-160 insulin Homo sapiens 172-179 7662596-10 1995 Glucose parameters in OGTT correlated only weakly and inversely with insulin sensitivity. Glucose 0-7 insulin Homo sapiens 69-76 7789044-9 1995 Intraperitoneal insulin resulted in an enhanced glucose disposal rate (P < 0.01) and reduced fasting hepatic glucose production (P < 0.01). Glucose 48-55 insulin Homo sapiens 16-23 7789044-9 1995 Intraperitoneal insulin resulted in an enhanced glucose disposal rate (P < 0.01) and reduced fasting hepatic glucose production (P < 0.01). Glucose 112-119 insulin Homo sapiens 16-23 7698518-5 1995 In each subject, we measured glycemic control, insulin-stimulated glucose uptake in the whole body and forearm, rates of glucose and lipid oxidation, and muscle glycogen, glycogen synthase, and glucose transport protein (GLUT4) concentrations. Glucose 66-73 insulin Homo sapiens 47-54 7698518-7 1995 The insulin-stimulated rates of whole-body and forearm glucose uptake and glucose oxidation were similar in the two groups, whereas both energy expenditure and lipid oxidation were increased in the athletes. Glucose 55-62 insulin Homo sapiens 4-11 7698518-7 1995 The insulin-stimulated rates of whole-body and forearm glucose uptake and glucose oxidation were similar in the two groups, whereas both energy expenditure and lipid oxidation were increased in the athletes. Glucose 74-81 insulin Homo sapiens 4-11 7698518-9 1995 The mean glucose arterialized venous blood-deep venous blood (A-V) difference during the insulin infusion (60-240 min) correlated with the whole-body glucose disposal throughout the insulin infusion (after 60 min, r > 0.73, P < 0.001 for all 30-min periods). Glucose 9-16 insulin Homo sapiens 89-96 7698518-9 1995 The mean glucose arterialized venous blood-deep venous blood (A-V) difference during the insulin infusion (60-240 min) correlated with the whole-body glucose disposal throughout the insulin infusion (after 60 min, r > 0.73, P < 0.001 for all 30-min periods). Glucose 9-16 insulin Homo sapiens 182-189 7890060-6 1995 MAIN OUTCOME MEASURES: Basal levels of glucose and insulin, as well as glucose-mediated insulin secretion, glucose uptake, and tissue sensitivity to insulin were assessed using the hyperglycemic hyperinsulinemic clamp technique before and after Norplant insertion. Glucose 71-78 insulin Homo sapiens 88-95 7890060-6 1995 MAIN OUTCOME MEASURES: Basal levels of glucose and insulin, as well as glucose-mediated insulin secretion, glucose uptake, and tissue sensitivity to insulin were assessed using the hyperglycemic hyperinsulinemic clamp technique before and after Norplant insertion. Glucose 71-78 insulin Homo sapiens 88-95 7890060-6 1995 MAIN OUTCOME MEASURES: Basal levels of glucose and insulin, as well as glucose-mediated insulin secretion, glucose uptake, and tissue sensitivity to insulin were assessed using the hyperglycemic hyperinsulinemic clamp technique before and after Norplant insertion. Glucose 71-78 insulin Homo sapiens 88-95 7890060-6 1995 MAIN OUTCOME MEASURES: Basal levels of glucose and insulin, as well as glucose-mediated insulin secretion, glucose uptake, and tissue sensitivity to insulin were assessed using the hyperglycemic hyperinsulinemic clamp technique before and after Norplant insertion. Glucose 71-78 insulin Homo sapiens 88-95 7890060-9 1995 In association with this increase in insulin levels after Norplant insertion, total mean body glucose uptake (M) increased from 8.08 +/- 0.91 to 9.53 +/- 0.95 mg/kg per minute. Glucose 94-101 insulin Homo sapiens 37-44 7706450-0 1995 24-hour glucose profiles during continuous or oscillatory insulin infusion. Glucose 8-15 insulin Homo sapiens 58-65 7706450-4 1995 Endogenous insulin secretion was suppressed by somatostatin, a constant intravenous glucose infusion was administered, and exogenous insulin was infused either at a constant rate or in a sinusoidal pattern with a period of 120 min. Glucose 84-91 insulin Homo sapiens 11-18 7706450-5 1995 The mean glucose level over the 28-h period was 0.72 +/- 0.31 mmol/liter lower when insulin was infused in an oscillatory pattern than when the rate of infusion was constant (P < 0.05). Glucose 9-16 insulin Homo sapiens 84-91 7706480-6 1995 On the other hand, a high glucose concentration evoked a three-fold increase in the release of insulin, suggesting that IL-1ra was released constitutively. Glucose 26-33 insulin Homo sapiens 95-102 7706491-7 1995 Visceral fat content was negatively correlated with insulin sensitivity (rates of leg glucose uptake and storage), but insulin resistance was not caused by glucose-FFA competition. Glucose 86-93 insulin Homo sapiens 52-59 7714113-4 1995 The same amount of insulin was infused on both occasions in a manner that reproduced the systemic insulin concentrations normally observed after glucose ingestion. Glucose 145-152 insulin Homo sapiens 98-105 7714113-6 1995 Glucose disappearance also was lower (P < 0.05) in the diabetic patients than that in the nondiabetic subjects, and the insulin-induced decrement in plasma magnesium was correlated (P < 0.01) with glucose disappearance. Glucose 0-7 insulin Homo sapiens 123-130 7714113-6 1995 Glucose disappearance also was lower (P < 0.05) in the diabetic patients than that in the nondiabetic subjects, and the insulin-induced decrement in plasma magnesium was correlated (P < 0.01) with glucose disappearance. Glucose 203-210 insulin Homo sapiens 123-130 7714113-8 1995 We conclude that insulin resistance in subjects with NIDDM impairs the ability of insulin to stimulate magnesium as well as glucose uptake. Glucose 124-131 insulin Homo sapiens 17-24 7714113-8 1995 We conclude that insulin resistance in subjects with NIDDM impairs the ability of insulin to stimulate magnesium as well as glucose uptake. Glucose 124-131 insulin Homo sapiens 82-89 7714114-2 1995 Magnesium accumulation is dependent upon insulin action and correlates with insulin-mediated glucose uptake. Glucose 93-100 insulin Homo sapiens 76-83 7714114-4 1995 Insulin-mediated glucose uptake was determined by a euglycemic hyperinsulinemic glucose clamp in 29 obese nondiabetic volunteers: 15 Caucasians (8 males and 7 females) and 14 Pima Indians (8 males and 6 females). Glucose 17-24 insulin Homo sapiens 0-7 7714114-6 1995 Despite higher steady state plasma insulin levels (692 +/- 260 vs. 540 +/- 70 pmol/L; P < 0.03), Pima Indians had lower insulin-mediated glucose uptake than Caucasians (108 +/- 20 vs. 244 +/- 32 mg/m2.min; P < 0.0001). Glucose 140-147 insulin Homo sapiens 123-130 7714114-9 1995 However, this increase was similar in the 2 groups when values were adjusted for insulin-mediated glucose uptake. Glucose 98-105 insulin Homo sapiens 81-88 7730693-0 1995 [Study on insulin resistance evaluated by glucose tolerance test in obese pregnant women]. Glucose 42-49 insulin Homo sapiens 10-17 7618066-1 1995 Defective insulin-regulatable glucose transport plays an important role. Glucose 30-37 insulin Homo sapiens 10-17 7623786-0 1995 Adenosine effects upon insulin action on lipolysis and glucose transport in human adipocytes. Glucose 55-62 insulin Homo sapiens 23-30 7623786-5 1995 To examine adenosine effects on the insulin signalling pathway separately from those on lipolysis, the insulin sensitivity of glucose transport was examined. Glucose 126-133 insulin Homo sapiens 103-110 7623786-6 1995 Removal of adenosine brought about a small but significant increase in the concentration of insulin required for half-maximal stimulation of glucose transport. Glucose 141-148 insulin Homo sapiens 92-99 7534449-6 1995 Additionally, after the area under curve insulin response during intravenous glucose tolerance testing was controlled for, the decline in area under curve insulin-like growth factor binding protein-1 responses was on average 66% less in both obese and nonobese women with polycystic ovarian syndrome compared with same-weight controls (95% confidence interval 110% to 270%, p = 0.04). Glucose 77-84 insulin Homo sapiens 41-48 7794576-2 1995 Insulin sensitivity (GDR/I; euglycemic glucose clamp technique) was related to BP and heart rate (HR) in different situations in 40 healthy young men: in the laboratory, during a mental arithmetic stress test, and during baseline conditions at home. Glucose 39-46 insulin Homo sapiens 0-7 7794577-8 1995 Insulin-mediated glucose uptake increased significantly after 8 and 16 weeks of monotherapy with enalapril. Glucose 17-24 insulin Homo sapiens 0-7 7900793-4 1995 Insulin-stimulated glucose transport, determined on 28 subjects, was significantly lower in both the obese (3.83 +/- 0.48 nmol.min-1.mg-1) and NIDDM (3.93 +/- 1.0 nmol.min-1.mg-1) groups vs. the control group (7.35 +/- 1.50 nmol.min-1.mg-1). Glucose 19-26 insulin Homo sapiens 0-7 7900793-5 1995 Body mass index (BMI) was inversely correlated to percent type I fibers (r = -0.50, P < 0.01) and to the insulin-stimulated glucose transport rate (r = -0.53, P < 0.01). Glucose 127-134 insulin Homo sapiens 108-115 7900793-6 1995 The percentage of type I muscle fibers was related to the insulin-stimulated glucose transport rate (r = 0.57, P < 0.01), although this relationship was not significant after adjusting for BMI. Glucose 77-84 insulin Homo sapiens 58-65 7900795-4 1995 The insulin concentration producing a half-maximal increase in glucose disposal (EC50) during a three-step hyperinsulinemic-euglycemic glucose clamp was 41% lower in the athletes than in controls (483 +/- 30 vs. 822 +/- 132 pmol/l, P < 0.05), whereas maximal responsiveness was comparable (81.0 +/- 4.4 vs. 85.5 +/- 8.3 mumol.kg fat-free mass-1.min-1, P = not significant). Glucose 63-70 insulin Homo sapiens 4-11 7703919-2 1995 The fraction of the time spent in the active phase is called the plateau fraction and appears to be strongly correlated with the rate of release of insulin from islets as glucose concentration is varied. Glucose 171-178 insulin Homo sapiens 148-155 7703919-4 1995 Experimental rates of insulin release are correlated with "effective" plateau fractions over a range of glucose concentrations. Glucose 104-111 insulin Homo sapiens 22-29 7703919-7 1995 Knowledge of the relationships between beta and glucose concentration and between experimental measurements of rates of insulin release and plateau fractions permits the determination of theoretical rates of insulin release from the model. Glucose 48-55 insulin Homo sapiens 208-215 7555472-5 1995 Insulin doses were increased incrementally, aiming at fasting plasma glucose (FPG) < 7.8 mmol/l during a stabilization period of up to 8 weeks. Glucose 69-76 insulin Homo sapiens 0-7 7555475-13 1995 CONCLUSIONS: --Intersession observations demonstrated that the intrasubject blood glucose responses to prolonged moderate-intensity exercise were reliable and repeatable when pre-exercise meal, exercise, and insulin, regimens were kept constant. Glucose 82-89 insulin Homo sapiens 208-215 7758258-3 1995 The insulin sensitivity was assessed by the insulin (0.4 mU kg-1 min-1)-glucose/(4.5 mg kg-1 min-1)-infusion test (IGIT). Glucose 72-79 insulin Homo sapiens 4-11 7758258-3 1995 The insulin sensitivity was assessed by the insulin (0.4 mU kg-1 min-1)-glucose/(4.5 mg kg-1 min-1)-infusion test (IGIT). Glucose 72-79 insulin Homo sapiens 44-51 7758260-1 1995 In both fasting normal and diabetic subjects, nasally administered insulin achieves significant falls in plasma glucose concentrations. Glucose 112-119 insulin Homo sapiens 67-74 7758260-6 1995 Intranasal insulin given at 0 min at a dose of 60 U or 120 U resulted in a 50% reduction in postprandial incremental glucose compared to placebo over the first 2 h, whereas treatment with 60 U both at 0 and 20 min lead to a 70% reduction over the 240 min postprandial period. Glucose 117-124 insulin Homo sapiens 11-18 7758880-8 1995 Insulin resistance was demonstrated during the hyperinsulinaemic clamp in the NIDDM patients with a decrease in the major peripheral pathways of intracellular glucose metabolism (oxidation, storage and muscle glycogen synthase activity), but not in the pathway of non-oxidative glycolytic flux which was not completely suppressed during insulin infusion in the NIDDM patients (0.55 +/- 0.15 mg.kg FFM-1.min-1; p < 0.05 vs 0; control subjects: 0.17 +/- 0.29; NS vs 0). Glucose 159-166 insulin Homo sapiens 0-7 7608319-6 1995 Pinacidil inhibits the first phase of insulin release after glucose administration in healthy volunteers. Glucose 60-67 insulin Homo sapiens 38-45 7885279-7 1995 Stepwise regression analysis showed that variations in body fatness accounted for the greatest variation in fasting lipid profile, blood pressure, and the insulin to glucose ratio among groups. Glucose 166-173 insulin Homo sapiens 155-162 7669426-5 1995 We evaluated their capacity of insulin secretion by the ratio of increment of serum insulin level to that of plasma glucose level 30 minutes after a 75 g oral glucose load (insulinogenic index; I.I.) Glucose 116-123 insulin Homo sapiens 31-38 7669426-5 1995 We evaluated their capacity of insulin secretion by the ratio of increment of serum insulin level to that of plasma glucose level 30 minutes after a 75 g oral glucose load (insulinogenic index; I.I.) Glucose 159-166 insulin Homo sapiens 31-38 7836438-2 1995 Both the anabolic hormone insulin and contractile activity stimulate the uptake of glucose into mammalian skeletal muscle. Glucose 83-90 insulin Homo sapiens 26-33 7752909-7 1995 Insulin sensitivity (glucose disposal rate [GDR]) was increased by 93% (P < .05). Glucose 21-28 insulin Homo sapiens 0-7 7752910-4 1995 Insulin secretion was stimulated by glucagon, arginine, and glucose on separate days. Glucose 60-67 insulin Homo sapiens 0-7 7581042-8 1995 These data show that insulin resistance occurring in patients with chronic renal failure is accompanied by impaired muscle glucose uptake and nonoxidative glucose metabolism. Glucose 123-130 insulin Homo sapiens 21-28 7864100-1 1995 The forearm perfusion technique was used 1) to quantify the muscle metabolism of glucose and gluconeogenic precursors in response to insulin-induced hypoglycemia and 2) to assess the role of catecholamines and glucose concentration, pe se. Glucose 81-88 insulin Homo sapiens 133-140 7537193-3 1995 In eight healthy subjects and eight NIDDM patients, we studied insulin action by euglycemic glucose clamp (insulin infusion rate 2 mU.kg-1.min-1) along with saline and iloprost delivery (0.7 ng.kg-1.min-1). Glucose 92-99 insulin Homo sapiens 63-70 8665539-4 1995 As compared with pretreatment values, a significant alteration of the insulin response to glucose was observed. Glucose 90-97 insulin Homo sapiens 70-77 7537193-4 1995 In the other five subjects of each group, forearm blood flow and insulin-mediated glucose uptake during saline and iloprost infusion (0.7 ng.kg-1.min-1) were investigated. Glucose 82-89 insulin Homo sapiens 65-72 7537193-5 1995 RESULTS: Iloprost infusion improved insulin-stimulated whole-body glucose uptake and oxidative and nonoxidative glucose metabolism in both study groups. Glucose 66-73 insulin Homo sapiens 36-43 7729302-6 1995 A possible unfavorable effect of ET-1 on the tissue sensitivity to insulin-stimulated glucose uptake was suggested by the presence of a negative correlation between total glucose uptake and baseline ET-1 levels (r = -0.498, P < 0.05). Glucose 86-93 insulin Homo sapiens 67-74 7599689-0 1995 High glucose condition desensitizes insulin action at the levels of receptor kinase. Glucose 5-12 insulin Homo sapiens 36-43 7599689-1 1995 The mechanisms for the insulin resistance induced by hyperglycemia were investigated by studying the in vitro effects of a high glucose concentration on insulin signaling with Rat 1 fibroblasts expressing human insulin receptors (HIRc). Glucose 128-135 insulin Homo sapiens 23-30 7599689-1 1995 The mechanisms for the insulin resistance induced by hyperglycemia were investigated by studying the in vitro effects of a high glucose concentration on insulin signaling with Rat 1 fibroblasts expressing human insulin receptors (HIRc). Glucose 128-135 insulin Homo sapiens 153-160 7599689-1 1995 The mechanisms for the insulin resistance induced by hyperglycemia were investigated by studying the in vitro effects of a high glucose concentration on insulin signaling with Rat 1 fibroblasts expressing human insulin receptors (HIRc). Glucose 128-135 insulin Homo sapiens 153-160 7599689-2 1995 Incubation of HIRc cells for 4 days in 27 mM D-glucose led to impaired insulin-stimulation of both alpha-aminoisobutyric acid uptake (AIB) and phosphorylation of pp185 and receptor beta-subunits in vivo. Glucose 45-54 insulin Homo sapiens 71-78 7599689-3 1995 In vitro autophosphorylation and tyrosine kinase activities toward poly Glu80 Tyr20 of insulin receptors from cells exposed to high glucose media (HG) were also impaired (46-48% of control), although the binding of insulin to HG cells was unchanged. Glucose 132-139 insulin Homo sapiens 87-94 7599689-7 1995 These results indicate that in cells exposed to high glucose, desensitization of insulin receptors was induced via several intracellular events, but might not be due to persistent activation of PKC in HIRc cells. Glucose 53-60 insulin Homo sapiens 81-88 7729302-6 1995 A possible unfavorable effect of ET-1 on the tissue sensitivity to insulin-stimulated glucose uptake was suggested by the presence of a negative correlation between total glucose uptake and baseline ET-1 levels (r = -0.498, P < 0.05). Glucose 171-178 insulin Homo sapiens 67-74 7599690-4 1995 Prolongation of the glucose-lowering effect of "rapid-acting" insulin frequently caused subsequent hypoglycemia in this patient, but the effect of IGF-I seemed to have disappeared within the first three hours. Glucose 20-27 insulin Homo sapiens 62-69 7729302-8 1995 The negative correlation between total glucose uptake and circulating ET-1 levels suggests that the peptide might exert negative effects on the insulin sensitivity of target tissues. Glucose 39-46 insulin Homo sapiens 144-151 7599691-4 1995 A clamp study revealed that his insulin-stimulated glucose disposal rate (2.80 mg/kg/min) was comparable to that in noninsulin-dependent diabetes mellitus (4.14 +/- 1.94 (SD) mg/kg/min, n = 23). Glucose 51-58 insulin Homo sapiens 32-39 7781840-16 1995 A probably indirect effect of amylin in muscle is to decrease insulin- (or glucose)-induced glucose uptake, which may contribute to insulin resistance. Glucose 75-82 insulin Homo sapiens 132-139 7743763-4 1995 However, compared to obese control subjects (403 +/- 65 mg m-2 min-1) both groups of diabetic patients had significantly decreased insulin-stimulated glucose disposal rates (p < 0.005). Glucose 150-157 insulin Homo sapiens 131-138 7781840-16 1995 A probably indirect effect of amylin in muscle is to decrease insulin- (or glucose)-induced glucose uptake, which may contribute to insulin resistance. Glucose 92-99 insulin Homo sapiens 62-69 7781840-16 1995 A probably indirect effect of amylin in muscle is to decrease insulin- (or glucose)-induced glucose uptake, which may contribute to insulin resistance. Glucose 92-99 insulin Homo sapiens 132-139 7781840-17 1995 Other actions include inhibition of glucose-stimulated insulin secretion and, in general, actions mimicking CGRP effects. Glucose 36-43 insulin Homo sapiens 55-62 7642026-9 1995 The pathways that could link insulin resistance, through hyperinsulinemia, with essential hypertension are based on the concept that a defect of insulin action on glucose utilization, does not imply that all other effects of insulin are equally blunted. Glucose 163-170 insulin Homo sapiens 29-36 7835273-1 1995 Insulin-stimulated glucose transport in adipocytes is mediated by the insulin receptor. Glucose 19-26 insulin Homo sapiens 0-7 7835273-12 1995 These data suggest that the insulin and EGF signaling pathways that lead to glucose transport converge in these adipocytes down-stream of the insulin receptor, and that activation of this pathway requires signaling motifs in the carboxy-terminus of the EGFR. Glucose 76-83 insulin Homo sapiens 28-35 7843771-10 1995 On the other hand, the positive correlation between glucose disposal and decrease in forearm vascular resistance in the relatives suggests that insulin-mediated vasodilation may be a limiting factor for peripheral glucose uptake in insulin-resistant individuals. Glucose 52-59 insulin Homo sapiens 144-151 7843771-1 1995 Insulin-stimulated peripheral glucose uptake and insulin-mediated forearm vasodilation were investigated in 38 normotensive men with a family history of hypertension (relatives) compared with 27 age- and body mass index-matched normotensive men with no family history of hypertension (control subjects). Glucose 30-37 insulin Homo sapiens 0-7 7843771-10 1995 On the other hand, the positive correlation between glucose disposal and decrease in forearm vascular resistance in the relatives suggests that insulin-mediated vasodilation may be a limiting factor for peripheral glucose uptake in insulin-resistant individuals. Glucose 52-59 insulin Homo sapiens 232-239 7843771-8 1995 In conclusion, impaired insulin-stimulated peripheral glucose uptake in normotensive sons from hypertensive families was accompanied by retained insulin-mediated forearm vasodilation. Glucose 54-61 insulin Homo sapiens 24-31 7843771-8 1995 In conclusion, impaired insulin-stimulated peripheral glucose uptake in normotensive sons from hypertensive families was accompanied by retained insulin-mediated forearm vasodilation. Glucose 54-61 insulin Homo sapiens 145-152 7843771-10 1995 On the other hand, the positive correlation between glucose disposal and decrease in forearm vascular resistance in the relatives suggests that insulin-mediated vasodilation may be a limiting factor for peripheral glucose uptake in insulin-resistant individuals. Glucose 214-221 insulin Homo sapiens 144-151 7843771-10 1995 On the other hand, the positive correlation between glucose disposal and decrease in forearm vascular resistance in the relatives suggests that insulin-mediated vasodilation may be a limiting factor for peripheral glucose uptake in insulin-resistant individuals. Glucose 214-221 insulin Homo sapiens 232-239 7829788-1 1995 OBJECTIVES: This study investigated whether insulin response to an oral glucose load correlates to acetylcholine-induced coronary vasoconstriction in subjects with vasospastic angina. Glucose 72-79 insulin Homo sapiens 44-51 7852494-6 1995 The insulin response to glucose was blunted in all pancreatectomized and in 2 conservatively treated patients. Glucose 24-31 insulin Homo sapiens 4-11 7852494-11 1995 These results show that children with PHHI have impaired insulin responses to glucose and lack of suppressibility of endogenous insulin secretion several years after clinical remission. Glucose 78-85 insulin Homo sapiens 57-64 7852529-7 1995 Insulin sensitivity was measured by the frequently sampled iv glucose tolerance test with tolbutamide and was assessed using the modified minimal model. Glucose 62-69 insulin Homo sapiens 0-7 7852495-5 1995 An index of insulin sensitivity was obtained by dividing the rate of decrease in blood glucose by the total amount of insulin entering the circulation (secreted+infused by the Biostator). Glucose 87-94 insulin Homo sapiens 12-19 7852495-8 1995 The insulin sensitivity index obtained from this test correlated with the glucose MCR obtained from a euglycemic glucose clamp (r = 0.816; P < 0.001; n = 12). Glucose 74-81 insulin Homo sapiens 4-11 7852532-6 1995 Diazoxide administration worsened glucose tolerance in several subjects and reduced fasting and glucose-stimulated insulin levels by approximately 50% in both control and obese subjects. Glucose 96-103 insulin Homo sapiens 115-122 7852495-8 1995 The insulin sensitivity index obtained from this test correlated with the glucose MCR obtained from a euglycemic glucose clamp (r = 0.816; P < 0.001; n = 12). Glucose 113-120 insulin Homo sapiens 4-11 7852539-12 1995 We conclude that benfluorex treatment lowers blood pressure, improves glucose tolerance, reduces the glucose-stimulated insulin response, and increases serum DHEA and DHEA sulfate in both middle-aged and elderly men. Glucose 101-108 insulin Homo sapiens 120-127 7615956-5 1995 We further measured the responses to the glucose challenge of insulin, glucagon, catecholamines and free fatty acids, as well as other factors related to insulin resistance (i.e. lipoproteins and apolipoproteins). Glucose 41-48 insulin Homo sapiens 62-69 7860750-5 1995 The nondiabetic twins were insulin resistant and had a delayed insulin and C-peptide response during oral glucose tolerance tests compared with controls. Glucose 106-113 insulin Homo sapiens 63-70 7860757-5 1995 In contrast, the rate of suppression of glucose release in response to a change in insulin did not differ in the diabetic and nondiabetic subjects during either the low (slope 30-240 min:0.02 +/- 0.01 vs 0.02 +/- 0.01) or high (0.02 +/- 0.00 vs 0.02 +/- 0.00) insulin infusions. Glucose 40-47 insulin Homo sapiens 83-90 7860757-7 1995 Both glucose release and the proportion of systemic glucose being derived from 14CO2 (an index of gluconeogenesis) was inappropriately high for the prevailing insulin concentration in the diabetic subjects. Glucose 5-12 insulin Homo sapiens 159-166 7860757-7 1995 Both glucose release and the proportion of systemic glucose being derived from 14CO2 (an index of gluconeogenesis) was inappropriately high for the prevailing insulin concentration in the diabetic subjects. Glucose 52-59 insulin Homo sapiens 159-166 7860757-8 1995 Thus non-insulin-dependent diabetes mellitus slows the rate-limiting step in insulin action in muscle but not liver and alters the relative contribution of gluconeogenesis and glycogenolysis to hepatic glucose release. Glucose 202-209 insulin Homo sapiens 9-16 7752170-4 1995 The results of 75 g oral glucose tolerance test showed a higher blood glucose at 120 minutes and a higher plasma immunoreactive insulin at baseline, 60 and 120 minutes in the subjects with hepatic steatosis, being adjusted for age, BMI and alcohol consumption. Glucose 25-32 insulin Homo sapiens 128-135 7852923-7 1995 MAIN OUTCOME MEASURES: Overnight urinary albumin excretion, insulin-mediated glucose disposal (hyperinsulinaemic euglycaemic clamp), blood glucose and plasma insulin during oral glucose tolerance test, fibrinogen, von Willebrand factor and plasminogen activator inhibitor activity. Glucose 77-84 insulin Homo sapiens 60-67 7752181-4 1995 As expected, glucose ingestion caused a significant increase in glycaemia and serum insulin; the latter rose significantly more at 60 minutes in normotensives (85 +/- 6) and essential hypertensives (83 +/- 5) than in N-NIDD (30 +/- 4) and H-NIDD (29 +/- 3). Glucose 13-20 insulin Homo sapiens 84-91 7852923-9 1995 In a randomly selected subgroup (n = 36), insulin-mediated glucose disposal was lower in microalbuminuric than in normoalbuminuric patients, and an inverse relationship between insulin sensitivity and albuminuria (r = -0.37; P = 0.028) was found. Glucose 59-66 insulin Homo sapiens 42-49 7725645-2 1995 The measurement of insulin sensitivity means to measure the insulin"s effect on glucose metabolism--on hepatic glucose production and peripheral glucose uptake. Glucose 111-118 insulin Homo sapiens 60-67 7869918-2 1995 After gemfibrozil treatment, the insulin concentration was increased during the major part of the intravenous glucose tolerance test (IVGTT) and during the hyperinsulinemic euglycemic clamp. Glucose 110-117 insulin Homo sapiens 33-40 7869924-4 1995 After oral glucose, the incremental area under the serum insulin concentration curve was 3,475 +/- 1,009 pmol.L-1.h in nondiabetic cirrhotic patients, significantly higher than in controls (761 +/- 48, P < .001) or diabetic cirrhotic patients (881 +/- 186, P < .05). Glucose 11-18 insulin Homo sapiens 57-64 7869925-3 1995 In the present study, we first examined insulin release in response to glucose in static incubation experiments. Glucose 71-78 insulin Homo sapiens 40-47 7869925-4 1995 Increasing glucose concentrations up to 8.3 mmol/L stimulated insulin release; however, this elevation was only twofold, and a paradoxical decline was observed at glucose concentrations higher than 8.3 mmol/L. Glucose 11-18 insulin Homo sapiens 62-69 7725633-4 1995 Enhanced oxidation of non-esterified fatty acids leads to inhibition of glucose oxidation and this may participate in the development of insulin resistance. Glucose 72-79 insulin Homo sapiens 137-144 7725645-2 1995 The measurement of insulin sensitivity means to measure the insulin"s effect on glucose metabolism--on hepatic glucose production and peripheral glucose uptake. Glucose 80-87 insulin Homo sapiens 19-26 7725645-2 1995 The measurement of insulin sensitivity means to measure the insulin"s effect on glucose metabolism--on hepatic glucose production and peripheral glucose uptake. Glucose 80-87 insulin Homo sapiens 60-67 7725645-2 1995 The measurement of insulin sensitivity means to measure the insulin"s effect on glucose metabolism--on hepatic glucose production and peripheral glucose uptake. Glucose 111-118 insulin Homo sapiens 19-26 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 7-14 insulin Homo sapiens 84-91 7725645-2 1995 The measurement of insulin sensitivity means to measure the insulin"s effect on glucose metabolism--on hepatic glucose production and peripheral glucose uptake. Glucose 111-118 insulin Homo sapiens 60-67 7725645-2 1995 The measurement of insulin sensitivity means to measure the insulin"s effect on glucose metabolism--on hepatic glucose production and peripheral glucose uptake. Glucose 111-118 insulin Homo sapiens 19-26 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 7-14 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 7-14 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 7-14 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-1 1995 Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Glucose 192-199 insulin Homo sapiens 107-114 7725647-2 1995 Clinically overt non-insulin-dependent diabetes mellitus (NIDDM) is characterized by abnormality of insulin secretion combined with insulin resistance in glucose metabolism of all major target tissues. Glucose 154-161 insulin Homo sapiens 21-28 7725647-3 1995 While the fasting hyperglycaemia depends primarily on decreased insulin ability to inhibit hepatic glucose production, in the postabsorptive state the main role is played by decreased insulin-stimulated glucose uptake in muscles and impaired glycogen synthesis. Glucose 99-106 insulin Homo sapiens 64-71 7725647-3 1995 While the fasting hyperglycaemia depends primarily on decreased insulin ability to inhibit hepatic glucose production, in the postabsorptive state the main role is played by decreased insulin-stimulated glucose uptake in muscles and impaired glycogen synthesis. Glucose 203-210 insulin Homo sapiens 184-191 7725647-4 1995 Because of hyperglycaemia, and increased insulin-independent glucose uptake, whole glucose utilisation is not altered in NIDDM. Glucose 61-68 insulin Homo sapiens 41-48 7811129-5 1995 In multivariate analysis, fasting insulin level was associated with very-low-density lipoprotein cholesterol level for most of the age groups in both races independently of age, sex, glucose levels, obesity, cigarette smoking, and alcohol intake. Glucose 183-190 insulin Homo sapiens 34-41 7695182-6 1995 Excess free fatty acid may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance, and hypertension and finally atherosclerosis. Glucose 148-155 insulin Homo sapiens 99-106 7810485-7 1995 In each of the subjects with normal and impaired glucose tolerance, and NIDDM, the elevation of plasma insulin concentration during both the complete test period and the early phase of an oral glucose challenge was significantly higher in the CAD than in the normal group. Glucose 49-56 insulin Homo sapiens 103-110 7660747-5 1995 glucose sensor as an input to the computer that controls the insulin pump, and (d) that stable function of sc. Glucose 0-7 insulin Homo sapiens 61-68 7833731-7 1995 RESULTS: Median fasting plasma glucose concentrations were significantly lower at three years in patients allocated to chlorpropamide, glibenclamide, or insulin rather than diet alone (7.0, 7.6, 7.4, and 9.0 mmol/l respectively; P < 0.001) with lower mean glycated haemoglobin values (6.8%, 6.9%, 7.0%, and 7.6%, respectively; P < 0.001). Glucose 31-38 insulin Homo sapiens 153-160 7840169-0 1995 Insulin-mediated changes in PD and glucose uptake after correction of acidosis in humans with CRF. Glucose 35-42 insulin Homo sapiens 0-7 9279024-0 1995 Effect of glucose-dependent insulinotropic polypeptide (GIP) on insulin response to glucose in acromegalics. Glucose 10-17 insulin Homo sapiens 28-35 7847527-2 1995 STUDY DESIGN: Plasma glucose was lowered from approximately 95 mg/dl to 45 mg/dl in decrements of 10 mg/dl every 40 minutes with the insulin clamp technique. Glucose 21-28 insulin Homo sapiens 133-140 8597497-2 1995 The glucose clamp is the reference method, well validated and easy to interpret, which allows various extensions to the basic experimental procedure in order to obtain more valuable information on the specific effects of insulin on the various aspects of glucose metabolism. Glucose 4-11 insulin Homo sapiens 221-228 8597497-2 1995 The glucose clamp is the reference method, well validated and easy to interpret, which allows various extensions to the basic experimental procedure in order to obtain more valuable information on the specific effects of insulin on the various aspects of glucose metabolism. Glucose 255-262 insulin Homo sapiens 221-228 8597498-5 1995 In non-diabetic obese subjects, insulin resistance can be demonstrated by the inhibition of glucose storage during a euglycemic, hyperinsulinemic, clamp. Glucose 92-99 insulin Homo sapiens 32-39 7778865-5 1995 For example, during moderate-intensity exercise, the glucoregulatory response resembles glucoregulation in the basal state in that under both conditions, glucose release from the liver is controlled by glucagon and insulin, and blood glucose levels are tightly controlled. Glucose 154-161 insulin Homo sapiens 215-222 8527229-0 1995 Molecular actions of insulin on glucose transport. Glucose 32-39 insulin Homo sapiens 21-28 8527229-1 1995 Low basal glucose uptake by insulin-sensitive muscle and adipose cells reflects rapid endocytic retrieval of GLUT4 glucose transporters from the cell surface and their retention in intracellular membranes. Glucose 10-17 insulin Homo sapiens 28-35 7826337-3 1995 Wortmannin (100 nM) completely blocked the ability of insulin to activate glycogen synthase in 3T3-L1 adipocytes and the ability of insulin to stimulate glucose incorporation into glycogen in 3T3-L1 fibroblasts. Glucose 153-160 insulin Homo sapiens 132-139 8555732-6 1995 The simultaneous increase of serum insulin, free-T and DHEAS coinciding with a cortisol decrease may enhance insulin anabolic effects following breakfast, but not after oral glucose alone. Glucose 174-181 insulin Homo sapiens 35-42 8555732-6 1995 The simultaneous increase of serum insulin, free-T and DHEAS coinciding with a cortisol decrease may enhance insulin anabolic effects following breakfast, but not after oral glucose alone. Glucose 174-181 insulin Homo sapiens 109-116 7767439-7 1995 The predicted insulin release in response to a square-wave and a triangular-wave glucose stimulation is given for the bioartificial pancreas of dimensions necessary for implantation in diabetic patients. Glucose 81-88 insulin Homo sapiens 14-21 7826337-6 1995 Rapamycin inhibited insulin-stimulated glucose incorporation into glycogen to a similar extent and with similar dose-dependency, while having no effect on insulin-stimulated glucose transport. Glucose 39-46 insulin Homo sapiens 20-27 7735493-1 1995 The relationship between fasting insulin as well as the insulin response to an oral glucose tolerance test and echocardiographic cardiac geometry and function was assessed in 55 never-treated lean patients with essential hypertension and normal glucose tolerance and 31 age- and gender-matched normal subjects. Glucose 84-91 insulin Homo sapiens 56-63 7579009-5 1995 The fasting and the mean OGTT plasma beta-endorphin values negatively correlated with insulin initial response to glucose, insulin and C-peptide mean OGTT values, but not with glucose OGTT mean values. Glucose 114-121 insulin Homo sapiens 86-93 7735493-4 1995 When hypertensive patients were divided into those without (n = 39) and with insulin resistance (n = 16), as defined by an elevated value of the ratio of the area under the curve of the response of insulin and glucose, it appeared that both heart rate, end-systolic wall stress to end-systolic volume index ratio and afterload-corrected fractional shortening were higher in patients with insulin resistance, whereas age, arterial pressure, left ventricular mass index, urinary electrolytes, and plasma renin activity were similar in the two groups. Glucose 210-217 insulin Homo sapiens 77-84 7533613-13 1995 Sydnonimine-1 (SIN-1), an extracellular donor of NO and superoxide, induced a modest suppression of glucose-stimulated insulin release. Glucose 100-107 insulin Homo sapiens 119-126 7533613-21 1995 Our results strongly suggest that NO is a negative modulator of insulin release induced by the nutrient secretagogues L-arginine and glucose. Glucose 133-140 insulin Homo sapiens 64-71 7648365-3 1995 At the cellular level, insulin activates glucose and amino acids transport, lipid and glycogen metabolism, protein synthesis, and transcription of specific genes. Glucose 41-48 insulin Homo sapiens 23-30 8845794-1 1995 Insulin secretion from pancreatic B-cells is tightly controlled by variations in the plasma concentration of nutrients, in particular glucose. Glucose 134-141 insulin Homo sapiens 0-7 7735282-2 1995 An increased sympathetic tone can negatively affect glucose utilization through three distinct mechanisms; a direct beta-adrenoreceptor-mediated insulin resistance, through conversion to more insulin resistant fast twitch fibers and through alpha-adrenergic vasoconstriction which may decrease the delivery of insulin and glucose to the skeletal muscle cells. Glucose 52-59 insulin Homo sapiens 145-152 7735282-2 1995 An increased sympathetic tone can negatively affect glucose utilization through three distinct mechanisms; a direct beta-adrenoreceptor-mediated insulin resistance, through conversion to more insulin resistant fast twitch fibers and through alpha-adrenergic vasoconstriction which may decrease the delivery of insulin and glucose to the skeletal muscle cells. Glucose 52-59 insulin Homo sapiens 192-199 7735282-2 1995 An increased sympathetic tone can negatively affect glucose utilization through three distinct mechanisms; a direct beta-adrenoreceptor-mediated insulin resistance, through conversion to more insulin resistant fast twitch fibers and through alpha-adrenergic vasoconstriction which may decrease the delivery of insulin and glucose to the skeletal muscle cells. Glucose 52-59 insulin Homo sapiens 192-199 7735282-5 1995 The increase of cardiac output, blood pressure and insulin resistance in the course of the defense reaction are viewed as an appropriate preparatory response to facilitate muscular exercise (through higher cardiac output and increased pressure) and preserve (through insulin resistance) the optimal supply of glucose to the brain. Glucose 309-316 insulin Homo sapiens 51-58 7735282-5 1995 The increase of cardiac output, blood pressure and insulin resistance in the course of the defense reaction are viewed as an appropriate preparatory response to facilitate muscular exercise (through higher cardiac output and increased pressure) and preserve (through insulin resistance) the optimal supply of glucose to the brain. Glucose 309-316 insulin Homo sapiens 267-274 8001390-13 1995 However, once exogenous insulin was infused during the third hour, glucose utilization increased by 55% (p < .05) when compared with the baseline (hour 1) rate. Glucose 67-74 insulin Homo sapiens 24-31 8001390-17 1995 Pharmacologic intervention with somatostatin and insulin (physiologic dose) can facilitate glucose utilization and oxidation in these patients. Glucose 91-98 insulin Homo sapiens 49-56 8561892-6 1995 The major causes of insulin resistance are the genetic deficiency of glycogen synthase activation, compounded by additional defects due to metabolic disorders, receptor downregulation, and glucose transporter abnormalities, all contributing to the impairment in muscle glucose uptake. Glucose 189-196 insulin Homo sapiens 20-27 7712705-8 1995 A negative correlation existed between the 30-min insulin and 120-min glucose concentration during the OGTT (Rho -0.328, p < 0.05). Glucose 70-77 insulin Homo sapiens 50-57 7744214-6 1995 Serum insulin or analogue concentration at the beginning of the exercise correlated closely with the fall in blood glucose during exercise (r = 0.74, p < 0.01; r = 0.73, p < 0.02, respectively). Glucose 115-122 insulin Homo sapiens 6-13 7744233-8 1995 Logistic regression analyses showed that any arterial disease was significantly associated with HbA1c, fasting and 2-h post-load plasma glucose after correction for cardiovascular risk factors (odds ratios and 95% confidence intervals 1.35; 1.10-1.65 per %, 1.20; 1.06-1.36 and 1.06; 1.01-1.12 per mmol/l, respectively), whereas it was not associated with fasting and 2-h post-load specific insulin. Glucose 136-143 insulin Homo sapiens 391-398 7744234-5 1995 The 24-h mean of serum insulin together with HbA1c concentration predicted 32% of the variation of mean blood glucose concentrations. Glucose 110-117 insulin Homo sapiens 23-30 7813811-3 1995 We compared insulin sensitivity of glucose uptake directly in muscle and heart tissues between healthy women (age 29 +/- 2 years, body mass index [BMI] 22 +/- 1 kg/m2, VO2max 39 +/- 4 ml.kg-1.min-1) and men matched for age (31 +/- 2 years), BMI (23 +/- 1 kg/m2), and VO2max (44 +/- 3 ml.kg-1.min-1) using [18F]fluoro-2-deoxy-D-glucose and positron emission tomography under hyperinsulinemic (insulin infusion rate 1 mU.kg-1.min-1) normoglycemic conditions. Glucose 35-42 insulin Homo sapiens 12-19 7813811-6 1995 Insulin-stimulated glucose uptake rates in the heart were similar in women (738 +/- 58) and men (749 +/- 62 mumol.kg muscle-1.min-1). Glucose 19-26 insulin Homo sapiens 0-7 7589041-12 1995 Insulin was stimulated and the other hormones inhibited during infusion of D-glucose. Glucose 75-84 insulin Homo sapiens 0-7 7553077-4 1995 Furthermore, defective glucose storage due to reduced insulin sensitivity predominantly of muscle tissue has been observed. Glucose 23-30 insulin Homo sapiens 54-61 7584526-12 1995 The insulin requirements in diabetic patients during surgery vary from 0.25-0.40 U per gram glucose in normal weight patients, 0.4-0.8 U per gram glucose in case of obesity, liver disease, steroid therapy or sepsis, to 0.8-1.2 U per gram glucose in patients undergoing cardiopulmonary bypass surgery. Glucose 92-99 insulin Homo sapiens 4-11 7584526-12 1995 The insulin requirements in diabetic patients during surgery vary from 0.25-0.40 U per gram glucose in normal weight patients, 0.4-0.8 U per gram glucose in case of obesity, liver disease, steroid therapy or sepsis, to 0.8-1.2 U per gram glucose in patients undergoing cardiopulmonary bypass surgery. Glucose 146-153 insulin Homo sapiens 4-11 7584526-12 1995 The insulin requirements in diabetic patients during surgery vary from 0.25-0.40 U per gram glucose in normal weight patients, 0.4-0.8 U per gram glucose in case of obesity, liver disease, steroid therapy or sepsis, to 0.8-1.2 U per gram glucose in patients undergoing cardiopulmonary bypass surgery. Glucose 146-153 insulin Homo sapiens 4-11 7805925-5 1995 MAIN OUTCOME MEASURE: Insulin and glucose in plasma after oral glucose testing. Glucose 63-70 insulin Homo sapiens 22-29 8839247-2 1995 The beta-cell has the unique capacity to "sense" the extracellular glucose concentration and to respond to cellular signals generated by the "glucose-sensor" by secreting exactly the amount of insulin required to maintain glucose homeostasis. Glucose 142-149 insulin Homo sapiens 193-200 7768322-6 1995 PACAP and its receptors are also present in the pancreas and appear to play a regulatory role in insulin secretion at extremely low concentrations in a glucose-dependent manner. Glucose 152-159 insulin Homo sapiens 97-104 8529954-1 1995 We report the glucose and insulin response to a 300-min glucose tolerance test among 17 women athletes as compared with 11 normal, nonatheletic controls. Glucose 56-63 insulin Homo sapiens 26-33 8529954-3 1995 Athletes had a more sensitive insulin response to the glucose tolerance test as compared with controls. Glucose 54-61 insulin Homo sapiens 30-37 7806165-0 1995 Insulin independent glucose uptake in cirrhosis. Glucose 20-27 insulin Homo sapiens 0-7 7590631-1 1995 Plasma glucose and insulin responses to oral glucose load were investigated and reinvestigated approximately 4 years later in 29 cystic fibrosis children and adolescents with initially normal fasting blood glucose levels. Glucose 45-52 insulin Homo sapiens 19-26 7590631-1 1995 Plasma glucose and insulin responses to oral glucose load were investigated and reinvestigated approximately 4 years later in 29 cystic fibrosis children and adolescents with initially normal fasting blood glucose levels. Glucose 45-52 insulin Homo sapiens 19-26 7843750-8 1995 Those subjects also demonstrated the greatest resistance to insulin action on glucose and plasma unesterified fatty acids. Glucose 78-85 insulin Homo sapiens 60-67 7719392-5 1995 In addition, we examined the relation between these sex steroid hormones and insulin response to an oral glucose tolerance test. Glucose 105-112 insulin Homo sapiens 77-84 10753320-1 1995 Hyperinsulinemia as determined by glucose/insulin tolerance identified an etiologic relationship to idiopathic Meniere"s disease. Glucose 34-41 insulin Homo sapiens 5-12 7713829-5 1995 Steady-state plasma glucose concentration and rate of glucose disposal per unit plasma insulin were almost identical after LO or HI; values were significantly greater than after NX. Glucose 54-61 insulin Homo sapiens 87-94 7814644-0 1995 Overexpression of Glut4 protein in muscle increases basal and insulin-stimulated whole body glucose disposal in conscious mice. Glucose 92-99 insulin Homo sapiens 62-69 7814644-4 1995 In the fed state, the rate of whole body glucose disposal was 70% higher in transgenic mice in the basal state, 81 and 54% higher during submaximal and maximal insulin stimulation. Glucose 41-48 insulin Homo sapiens 160-167 7814644-5 1995 In the fasting state, insulin-stimulated whole body glucose disposal was also higher in the transgenic mice. Glucose 52-59 insulin Homo sapiens 22-29 7814644-7 1995 Our data demonstrate that overexpression of Glut4 protein in muscle increases basal as well as insulin-stimulated whole body glucose disposal. Glucose 125-132 insulin Homo sapiens 95-102 7829636-0 1995 The continuous low dose insulin and glucose infusion test: a simplified and accurate method for the evaluation of insulin sensitivity and insulin secretion in population studies. Glucose 36-43 insulin Homo sapiens 114-121 7829636-3 1995 Insulin sensitivity was evaluated as the MCR of glucose divided by the steady state serum insulin level achieved at the end of the test. Glucose 48-55 insulin Homo sapiens 0-7 8705254-0 1995 The delivery of insulin from aqueous and non-aqueous reservoirs governed by a glucose sensitive gel membrane. Glucose 78-85 insulin Homo sapiens 16-23 7707290-10 1995 In particular, the sustained increases in insulin concentrations suggest that an increased supply of glucose to the follicle mediates nutritionally stimulated increases in ovulation rate. Glucose 101-108 insulin Homo sapiens 42-49 7854164-0 1995 Role of basal insulin in maintenance of intracellular glucose metabolic pathways in non-insulin-dependent diabetes mellitus. Glucose 54-61 insulin Homo sapiens 14-21 7854164-1 1995 Impairments of both basal and insulin-stimulated oxidative (Gox) and nonoxidative (Nox) glucose metabolism are documented to exist in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 88-95 insulin Homo sapiens 30-37 7854171-4 1995 Peripheral insulin sensitivity, ie, insulin stimulation of glucose utilization, increased approximately 30%, or by 4.3 +/- 1.7 mumol/kg.min (13.1 +/- 2.0 v 17.4 +/- 3.5 mumol/kg.min, P < .05, 0 v 4 weeks) during enalapril treatment, but remained unchanged during placebo treatment (15.4 +/- 2.8 v 15.3 +/- 2.7 mumol/kg.min, respectively). Glucose 59-66 insulin Homo sapiens 11-18 7854171-4 1995 Peripheral insulin sensitivity, ie, insulin stimulation of glucose utilization, increased approximately 30%, or by 4.3 +/- 1.7 mumol/kg.min (13.1 +/- 2.0 v 17.4 +/- 3.5 mumol/kg.min, P < .05, 0 v 4 weeks) during enalapril treatment, but remained unchanged during placebo treatment (15.4 +/- 2.8 v 15.3 +/- 2.7 mumol/kg.min, respectively). Glucose 59-66 insulin Homo sapiens 36-43 7854171-7 1995 We conclude that enalapril improves insulin sensitivity by increasing glucose storage in hypertensive patients with NIDDM. Glucose 70-77 insulin Homo sapiens 36-43 7854173-3 1995 During a 75-g oral glucose tolerance test (OGTT), no major alteration in glucose tolerance was observed and insulin area under the curve was increased. Glucose 19-26 insulin Homo sapiens 108-115 7796936-2 1995 In response to insulin this transporter moves rapidly from an intracellular storage site to the plasma membrane, thus accounting for the substantial increase in glucose uptake by these tissues following insulin stimulation. Glucose 162-169 insulin Homo sapiens 15-22 7796936-2 1995 In response to insulin this transporter moves rapidly from an intracellular storage site to the plasma membrane, thus accounting for the substantial increase in glucose uptake by these tissues following insulin stimulation. Glucose 162-169 insulin Homo sapiens 204-211 7796936-3 1995 The recent finding that GLUT 4 is also expressed in the hypothalamus suggests that this brain region, which is outside the blood-brain barrier and therefore sensitive to circulating insulin, may experience stimulation of glucose uptake in response to insulin. Glucose 221-228 insulin Homo sapiens 182-189 7796936-3 1995 The recent finding that GLUT 4 is also expressed in the hypothalamus suggests that this brain region, which is outside the blood-brain barrier and therefore sensitive to circulating insulin, may experience stimulation of glucose uptake in response to insulin. Glucose 221-228 insulin Homo sapiens 251-258 7796936-4 1995 We propose that this may allow regions of the hypothalamus to respond directly to elevated blood glucose, constituting a form of metabolic regulation by allowing circulating glucose (and therefore insulin) in concert with other mechanisms to maintain blood glucose homeostasis. Glucose 97-104 insulin Homo sapiens 197-204 7824108-3 1995 The glucose infusion increased plasma glucose levels to 170 to 182 mg/dl and serum insulin levels to 30 to 50 microU/ml, while it markedly decreased plasma free fatty acid levels. Glucose 4-11 insulin Homo sapiens 83-90 7479336-1 1995 Neuropeptide Y (NPY) is a 36 amino acid peptide known to inhibit glucose-stimulated insulin secretion. Glucose 65-72 insulin Homo sapiens 84-91 7777712-18 1995 Glucose control improved in our patient cohort the pancreatic insulin response probably due to a more adequate glycemic microenvironment and a possible enhanced exogenous and endogenous insulin function. Glucose 0-7 insulin Homo sapiens 62-69 7626185-6 1995 Twenty-four months after grafting, islet function was provoked by glucagon and glucose, which led to elevations in the C-peptide and insulin levels. Glucose 79-86 insulin Homo sapiens 133-140 7736898-1 1994 The reported glucose and immunoreactive insulin (IRI) responses to oral and intravenous glucose in subjects with Type 2 diabetes have not always been consistent. Glucose 88-95 insulin Homo sapiens 40-47 7736899-4 1994 Insulin sensitivity was reflected by the ratio of the glucose infusion rate and the mean insulin level during the last 20 min of the clamp (M/I ratio). Glucose 54-61 insulin Homo sapiens 0-7 7798198-1 1994 Glucose stimulation of beta-cell insulin secretion is initiated by membrane depolarization coupled with an elevation in intracellular Ca2+ concentration ([Ca2+]i). Glucose 0-7 insulin Homo sapiens 33-40 7705194-0 1994 Insulin response after treatment depends on fasting plasma glucose level in NIDDM. Glucose 59-66 insulin Homo sapiens 0-7 7705196-1 1994 A mathematical model was recently developed (minimal model) to estimate insulin sensitivity from the analysis of blood glucose and insulin concentration after a modified intravenous glucose tolerance test. Glucose 119-126 insulin Homo sapiens 72-79 7983006-3 1994 Our previous studies demonstrated that the expression of gp160 is also limited to fat and muscle tissues, where it is localized exclusively in GLUT4-containing vesicles, and thus, it represents a marker protein for insulin-activated glucose transport. Glucose 233-240 insulin Homo sapiens 215-222 7871973-7 1994 ), and indicate that the inhibition of the glucose transport activity recruited by insulin is the major effect of polymyxin B (100 micrograms/mL) and the inhibition of the process of insulin action is rather small. Glucose 43-50 insulin Homo sapiens 83-90 7634261-7 1994 Hyperinsulinemia is the consequence of insulin resistance, a defect in insulin-mediated glucose uptake. Glucose 88-95 insulin Homo sapiens 5-12 7634261-7 1994 Hyperinsulinemia is the consequence of insulin resistance, a defect in insulin-mediated glucose uptake. Glucose 88-95 insulin Homo sapiens 39-46 7628063-6 1994 We suggest that the stimulus for increased circulating insulin was elevated plasma glucose, rather than a direct effect of IL-6. Glucose 83-90 insulin Homo sapiens 55-62 7874862-10 1994 Fasting reduced total insulin-mediated glucose disposal rates from 42.6 +/- 2.5, to 31.0 +/- 1.8 to 21.3 +/- 1.5 mumol min-1 kg-1 body weight after 12, 36 and 72h respectively (P < 0.001). Glucose 39-46 insulin Homo sapiens 22-29 7533613-16 1995 The intracellular "hydroperoxide donor" tert-butylhydroperoxide in the concentration range of 0.03-3 mM inhibited insulin release stimulated by the nutrient secretagogues glucose and L-arginine. Glucose 171-178 insulin Homo sapiens 114-121 7836430-4 1995 Nevertheless, an effect of insulin on glucose uptake remained unaffected. Glucose 38-45 insulin Homo sapiens 27-34 7836430-5 1995 It appears that in contrast to its mitogenic action and to its effect on glycogenesis, an effect of insulin on glucose uptake does not require p21ras activation. Glucose 111-118 insulin Homo sapiens 100-107 7882808-7 1994 Finally, as seen from glucose infusion rates necessary to maintain identical plasma glucose levels, patients with hypoglycemia unawareness had increased sensitivity to insulin (P < 0.001). Glucose 22-29 insulin Homo sapiens 168-175 7882808-7 1994 Finally, as seen from glucose infusion rates necessary to maintain identical plasma glucose levels, patients with hypoglycemia unawareness had increased sensitivity to insulin (P < 0.001). Glucose 84-91 insulin Homo sapiens 168-175 7882819-5 1994 RESULTS: Fasting glucose level was reduced from 10.0 to 8.45 mmol/l, and 71% of 197 subjects taking oral hypoglycemic agents and 39% of 212 taking insulin were able to discontinue their medication. Glucose 17-24 insulin Homo sapiens 147-154 7895958-6 1994 This provides the clue that insulin resistance is the mechanism for coping with a shortage of dietary glucose. Glucose 102-109 insulin Homo sapiens 28-35 7958489-5 1994 Recent transgenic initiatives have provided important insights into 1) the mechanism of glucose-stimulated insulin secretion and the role of potential defects in this system, 2) the regulated expression of genes that control hepatic glucose production, 3) the role of specific molecules that mediate the actions of insulin, and 4) the elucidation of factors that contribute to in vivo regulation of energy balance and body composition. Glucose 88-95 insulin Homo sapiens 107-114 7958489-5 1994 Recent transgenic initiatives have provided important insights into 1) the mechanism of glucose-stimulated insulin secretion and the role of potential defects in this system, 2) the regulated expression of genes that control hepatic glucose production, 3) the role of specific molecules that mediate the actions of insulin, and 4) the elucidation of factors that contribute to in vivo regulation of energy balance and body composition. Glucose 88-95 insulin Homo sapiens 315-329 7958490-5 1994 Insulin sensitivity was assessed as the ratio between infused glucose and the insulin level (M:I) during hyperglycemic clamps. Glucose 62-69 insulin Homo sapiens 0-7 7958490-7 1994 Insulin release was reduced in response to 11 mmol/l glucose (61% of control group, P < 0.05) as well as to arginine in the presence of 11 mmol/l glucose (54% of control group, P < 0.01). Glucose 53-60 insulin Homo sapiens 0-7 7958490-7 1994 Insulin release was reduced in response to 11 mmol/l glucose (61% of control group, P < 0.05) as well as to arginine in the presence of 11 mmol/l glucose (54% of control group, P < 0.01). Glucose 149-156 insulin Homo sapiens 0-7 7958490-11 1994 Glucokinase deficiency thus affects not only insulin responses to glucose per se but also glucose potentiation of responses to non-nutrient secretagogues. Glucose 66-73 insulin Homo sapiens 45-52 7958497-7 1994 Whole body insulin sensitivity was 23.8 +/- 12.7 mumol glucose.kg-1.min-1 after placebo and 30.6 +/- 12.7 and 27.2 +/- 13.3 following low and high dose ANG II infusions, respectively (P < 0.05, analysis of variance). Glucose 55-62 insulin Homo sapiens 11-18 7958504-7 1994 The fasting proinsulin:insulin ratio was higher in 85 subjects with NIDDM compared with subjects with IGT or normal glucose tolerance (0.31, 0.09, and 0.07, respectively). Glucose 116-123 insulin Homo sapiens 12-22 7958504-7 1994 The fasting proinsulin:insulin ratio was higher in 85 subjects with NIDDM compared with subjects with IGT or normal glucose tolerance (0.31, 0.09, and 0.07, respectively). Glucose 116-123 insulin Homo sapiens 15-22 7713298-1 1994 Rapid glucose control was achieved by insulin therapy in a patient diagnosed to have gestational diabetes at 8 weeks of pregnancy. Glucose 6-13 insulin Homo sapiens 38-45 7863803-3 1994 RESULTS: The sliding-scale insulin therapy group"s glucose deviation score (167.4) was significantly higher than the deviation for the proactive (112.9) and combination (121.3) groups. Glucose 51-58 insulin Homo sapiens 27-34 7863803-4 1994 The sliding-scale insulin therapy group also had a significantly higher median glucose value (262.5) than the proactive (199.9) and combination (221.2) groups as well as a significantly higher number of nursing shifts (0.70) in which a glucose of 250 mg/dl or greater was recorded than in the proactive (0.37) and combination (0.40) groups. Glucose 79-86 insulin Homo sapiens 18-25 7863803-4 1994 The sliding-scale insulin therapy group also had a significantly higher median glucose value (262.5) than the proactive (199.9) and combination (221.2) groups as well as a significantly higher number of nursing shifts (0.70) in which a glucose of 250 mg/dl or greater was recorded than in the proactive (0.37) and combination (0.40) groups. Glucose 236-243 insulin Homo sapiens 18-25 7995624-7 1994 Insulin infusion increased venous plasma insulin to 98.4 microU/mL and increased net glucose uptake threefold. Glucose 85-92 insulin Homo sapiens 0-7 7995625-1 1994 Resistance to insulin-mediated glucose disposal has been previously shown to be increased in association with obesity, high blood pressure, and non-insulin-dependent diabetes mellitus. Glucose 31-38 insulin Homo sapiens 14-21 7995625-5 1994 Resistance to insulin-mediated glucose disposal was estimated by determining the steady-state plasma insulin and glucose concentrations during the last 30 minutes of a continuous infusion of somatostatin (5 micrograms/min), exogenous insulin (25 mU/m2 per minute), and glucose (240 mg/m2 per minute). Glucose 31-38 insulin Homo sapiens 14-21 7995625-6 1994 Since the steady-state plasma insulin concentrations are similar in all subjects, the higher the steady-state plasma glucose, the more insulin resistant the individual. Glucose 117-124 insulin Homo sapiens 30-37 7995625-6 1994 Since the steady-state plasma insulin concentrations are similar in all subjects, the higher the steady-state plasma glucose, the more insulin resistant the individual. Glucose 117-124 insulin Homo sapiens 135-142 7718969-1 1994 A patient with insulinoma had frequent hypoglycemic episodes with normal plasma insulin levels and insulin/glucose ratios. Glucose 107-114 insulin Homo sapiens 15-22 7706596-1 1994 OBJECTIVE: We have previously shown in an acute inpatient setting that dietary substitution of 77.5% of fat kcal as medium chain triglycerides (MCT) increased insulin-mediated glucose metabolism in patients with non-insulin-dependent diabetes mellitus (NIDDM), and that this effect appeared to be mediated by increases in insulin-mediated glucose disposal. Glucose 176-183 insulin Homo sapiens 159-166 7989456-0 1994 Insulin secretion, insulin action and non-insulin-dependent glucose uptake in pancreas transplant recipients. Glucose 60-67 insulin Homo sapiens 42-49 7989456-2 1994 glucose tolerance test, with frequent blood sampling and tolbutamide administration to elicit a second insulin response was used to estimate insulin sensitivity (SI) and glucose effectiveness (SG) with Bergman"s minimal model. Glucose 0-7 insulin Homo sapiens 141-148 7989456-11 1994 In conclusion, after pancreas transplantation, the overall glucose tolerance is determined by the net effect of reductions in insulin sensitivity and glucose effectiveness and in the adaptability of the beta-cells to ensure sufficient insulin secretion. Glucose 59-66 insulin Homo sapiens 126-133 7989457-9 1994 During glucose stimulation, maximal responses of IRI and C-peptide were 4-fold lower in group 1, and the time of maximal responses of IRI and C-peptide occurred later in group 1 than in group 2. Glucose 7-14 insulin Homo sapiens 57-66 7989457-9 1994 During glucose stimulation, maximal responses of IRI and C-peptide were 4-fold lower in group 1, and the time of maximal responses of IRI and C-peptide occurred later in group 1 than in group 2. Glucose 7-14 insulin Homo sapiens 142-151 7989475-10 1994 Insulin responsiveness in terms of glucose disposal measured by hyperinsulinemic euglycemic clamps improved from 11.4 +/- 6.2 to 15.1 +/- 4.6 mumol/kg.min (P < 0.05) during CPAP treatment. Glucose 35-42 insulin Homo sapiens 0-7 7989590-1 1994 Insulin concentrations in humans continuously change and typically increase only when glucose also increases such as with eating. Glucose 86-93 insulin Homo sapiens 0-7 7989590-5 1994 During euglycemia, insulin increased glucose disposal in nondiabetic but not diabetic subjects indicating marked extrahepatic resistance. Glucose 37-44 insulin Homo sapiens 19-26 7989590-6 1994 In contrast, insulin-induced suppression of glucose release was only minimally less (P < 0.05) in diabetic than nondiabetic subjects (-1.06 +/- 0.09 vs. -1.47 +/- 0.21 nmol.kg-1 per 4 h). Glucose 44-51 insulin Homo sapiens 13-20 7989610-1 1994 Insulin exerts effects on the vasculature that (a) may play a role in the regulation of blood pressure; and (b) by boosting its own delivery to target tissues, also have been proposed to play an integral part in its main action, the promotion of glucose disposal. Glucose 246-253 insulin Homo sapiens 0-7 7699364-0 1994 Nitric oxide opens ATP-sensitive K+ channels through suppression of phosphofructokinase activity and inhibits glucose-induced insulin release in pancreatic beta cells. Glucose 110-117 insulin Homo sapiens 126-133 7699364-8 1994 Furthermore, these activating effects were completely eliminated by hemoglobin, in accordance with the reversibility in inhibition of glucose-induced insulin release. Glucose 134-141 insulin Homo sapiens 150-157 7990708-7 1994 The concentration of insulin required for half-maximal stimulation of glucose uptake was 165 +/- 36 versus 32 +/- 10 pmol in PCOS and control subjects, respectively (P < .05). Glucose 70-77 insulin Homo sapiens 21-28 7970483-7 1994 Fasting glucose and insulin levels were significantly lower and the insulin response to glucose challenge was significantly blunted in all groups (P < or = .05). Glucose 88-95 insulin Homo sapiens 68-75 7712896-1 1994 Plasma glucose and serum insulin in oral glucose tolerance test (OGTT) were measured in 40 patients with pregnancy induced hypertension (PIH) and 30 normal pregnancies. Glucose 41-48 insulin Homo sapiens 25-32 7712896-4 1994 The results indicated that patients with severe PIH are insulin resistant and hyperinsulinemic after an oral glucose load. Glucose 109-116 insulin Homo sapiens 56-63 7999081-0 1994 PI 3-kinase activation is required for insulin stimulation of glucose transport into L6 myotubes. Glucose 62-69 insulin Homo sapiens 39-46 7999081-2 1994 Insulin acutely stimulates glucose transport into L6 myotubes approximately 2-fold, and activates PI 3-kinase activity 2 to 3-fold. Glucose 27-34 insulin Homo sapiens 0-7 7999081-9 1994 It is concluded that insulin activation of PI 3-kinase is necessary for stimulation of glucose transport into L6 muscle cells. Glucose 87-94 insulin Homo sapiens 21-28 7948013-10 1994 Insulin resistance in the liver results in the inability to suppress hepatic glucose production; in muscle, in impaired glucose uptake and oxidation and in adipose tissue, in the inability to suppress release of free FA. Glucose 77-84 insulin Homo sapiens 0-7 7947736-2 1994 The insulin secretagogues D-glucose and the muscarinic agonist carbachol both increase unesterified arachidonic acid accumulation in isolated islets. Glucose 26-35 insulin Homo sapiens 4-11 7947736-9 1994 RHC-80267 inhibits glucose- and carbachol-induced insulin release from intact islets in a dose-dependent manner that parallels its inhibition of diacylglycerol lipase activity. Glucose 19-26 insulin Homo sapiens 50-57 7525563-3 1994 We have now investigated the possible role of IRS-1 in mediating the effect of insulin to stimulate glucose transport in a physiologically relevant insulin target tissue. Glucose 100-107 insulin Homo sapiens 79-86 7525563-3 1994 We have now investigated the possible role of IRS-1 in mediating the effect of insulin to stimulate glucose transport in a physiologically relevant insulin target tissue. Glucose 100-107 insulin Homo sapiens 148-155 7525563-8 1994 These data provide strong support for the hypothesis that IRS-1 plays a role in insulin-stimulated glucose transport in insulin-responsive cells. Glucose 99-106 insulin Homo sapiens 80-87 7525563-8 1994 These data provide strong support for the hypothesis that IRS-1 plays a role in insulin-stimulated glucose transport in insulin-responsive cells. Glucose 99-106 insulin Homo sapiens 120-127 7973537-1 1994 Insulin secretory reserve assessed by the method of glucose potentiation of arginine induced insulin secretion is decreased in non-diabetic transplant recipients using triple immunosuppressive therapy with prednisone, cyclosporine, and azathioprine. Glucose 52-59 insulin Homo sapiens 0-7 7935656-4 1994 The insulin-sensitivity index, calculated from the results of intravenous glucose-tolerance tests, increased from 0.7 +/- 0.6 x 10(-4) to 1.6 +/- 0.9 x 10(-4) in subjects given troglitazone, and their glycemic response to oral glucose and to mixed meals decreased. Glucose 74-81 insulin Homo sapiens 4-11 7935656-3 1994 RESULTS: The mean (+/- SD) rates of glucose disposal increased from 4.7 +/- 1.7 to 6.0 +/- 1.7 mg per kilogram of body weight per minute (P = 0.004) and from 9.0 +/- 1.8 to 9.9 +/- 1.3 mg per kilogram per minute (P = 0.02) during insulin infusions of 40 and 300 mU per square meter of body-surface area per minute, respectively, in the troglitazone group. Glucose 36-43 insulin Homo sapiens 230-237 7935656-4 1994 The insulin-sensitivity index, calculated from the results of intravenous glucose-tolerance tests, increased from 0.7 +/- 0.6 x 10(-4) to 1.6 +/- 0.9 x 10(-4) in subjects given troglitazone, and their glycemic response to oral glucose and to mixed meals decreased. Glucose 227-234 insulin Homo sapiens 4-11 7935656-5 1994 The mean fasting plasma insulin concentration decreased by 48 percent (P = 0.002), and the plasma insulin response to oral glucose and mixed meals decreased by 40 and 41 percent, respectively. Glucose 123-130 insulin Homo sapiens 98-105 7848620-0 1994 Gender differences in insulin-stimulated glucose utilization among African-Americans. Glucose 41-48 insulin Homo sapiens 22-29 7848620-8 1994 The insulin clamp data also demonstrated significantly lower insulin-stimulated glucose utilization (M) in women compared to men in each BP group (N males 7.28 +/- 0.72 v N females 4.94 +/- 1.2 mg/kg-min; BH males 5.28 +/- .56 v BH females 2.59 +/- 0.50 mg/kg-min; P < .004 for gender differences). Glucose 80-87 insulin Homo sapiens 4-11 7848620-8 1994 The insulin clamp data also demonstrated significantly lower insulin-stimulated glucose utilization (M) in women compared to men in each BP group (N males 7.28 +/- 0.72 v N females 4.94 +/- 1.2 mg/kg-min; BH males 5.28 +/- .56 v BH females 2.59 +/- 0.50 mg/kg-min; P < .004 for gender differences). Glucose 80-87 insulin Homo sapiens 61-68 7942581-6 1994 These data indicate that elevated plasma AA delays the insulin response to a glucose challenge in normoglycemic adults, thereby prolonging the postprandial hyperglycemia. Glucose 77-84 insulin Homo sapiens 55-62 7818957-9 1994 Patients in all three ethnic groups had higher total insulin concentrations than their controls in the fasting state and after the glucose load. Glucose 131-138 insulin Homo sapiens 53-60 7874862-19 1994 Fasting caused a progressive resistance to the effects of insulin and glucose on oxidative glucose disposal and on forearm glucose uptake. Glucose 91-98 insulin Homo sapiens 58-65 7874862-19 1994 Fasting caused a progressive resistance to the effects of insulin and glucose on oxidative glucose disposal and on forearm glucose uptake. Glucose 91-98 insulin Homo sapiens 58-65 7874862-20 1994 Insulin-mediated glucose storage was unaffected by fasting, but the apparent cost of this storage was reduced by fasting. Glucose 17-24 insulin Homo sapiens 0-7 7867884-10 1994 The present study shows that human islets can respond to stimulation with glucose and sulphonylurea with oscillations in [Ca2+]i, which is the signal probably underlying the oscillations in plasma insulin levels observed in healthy subjects. Glucose 74-81 insulin Homo sapiens 197-204 7704946-2 1994 In addition, insulin mediated glucose uptake was measured in the NIDDM patients and the normolipidaemic subjects. Glucose 30-37 insulin Homo sapiens 13-20 7704946-6 1994 Insulin mediated glucose uptake was unrelated to plasma NCET rates in the study. Glucose 17-24 insulin Homo sapiens 0-7 7821172-5 1994 Proinsulin levels correlated with glucose levels, suggesting that hyperglycemia is the main stimulus for increased proinsulin secretion. Glucose 34-41 insulin Homo sapiens 0-10 7821172-5 1994 Proinsulin levels correlated with glucose levels, suggesting that hyperglycemia is the main stimulus for increased proinsulin secretion. Glucose 34-41 insulin Homo sapiens 115-125 7535191-1 1994 Insulin sensitivity in terms of glucose disposal rate was determined by using the hyperinsulinemic euglycemic clamp technique in seven obese hypertensive patients and nine normotensive control subjects. Glucose 32-39 insulin Homo sapiens 0-7 7713278-4 1994 Significant correlations were also found between glucose variability and patients" variations of insulin dosage (r = 0.31, p = 0.004), duration of diabetes (r = 0.22, p = 0.03), and body-mass index (r = 0.20, p = 0.04). Glucose 49-56 insulin Homo sapiens 97-104 7821172-3 1994 RESULTS: Both fasting and post-glucose levels of proinsulin were elevated in patients with diabetes, but not in the relatives with IGT or NGT. Glucose 31-38 insulin Homo sapiens 49-59 7875050-1 1994 Serum insulin 1 h post-glucose load is examined in this prospective study of 2971 Caucasoid subjects aged > 20 years in 1966 and followed to 1989. Glucose 23-30 insulin Homo sapiens 6-13 7868874-0 1994 Impaired glucose tolerance in hypertension is associated with impaired insulin release independently of changes in insulin sensitivity. Glucose 9-16 insulin Homo sapiens 71-78 7890013-5 1994 Insulin (0.3 mU kg-1 min-1) was infused for 2 h to induce mild hypoglycaemia (plasma glucose 3.2-3.5 mmol l-1) and exogenous glucose was infused as required to prevent any glucose decrease below 3.1 mmol l-1. Glucose 85-92 insulin Homo sapiens 0-7 7851833-3 1994 Using the ratio of fasting plasma glucose per insulin (IRI) as a parameter of insulin resistance, I have attempted to know how the insulin resistance would be improved concomitant to the weight reduction of obese patients who mainly suffered from musculoskeletal diseases. Glucose 34-41 insulin Homo sapiens 78-85 7851833-3 1994 Using the ratio of fasting plasma glucose per insulin (IRI) as a parameter of insulin resistance, I have attempted to know how the insulin resistance would be improved concomitant to the weight reduction of obese patients who mainly suffered from musculoskeletal diseases. Glucose 34-41 insulin Homo sapiens 78-85 7851834-4 1994 Furthermore, extreme insulin resistance was found by measuring glucose infusion rate with an euglycemic hyperinsulinemic clamp method. Glucose 63-70 insulin Homo sapiens 21-28 7875653-4 1994 The insulin level reached 30 minutes after glucose ingestion was significantly greater (p < .05) in patients with CAH. Glucose 43-50 insulin Homo sapiens 4-11 7875653-5 1994 The patients with C 21-OH had elevated androstenedione (A) and testosterone (T) and low DHEA-S and presented a 35% greater insulin response to a glucose stimulus than the control group, area under the curve (AUC) of 9457 +/- 887 vs 6989 +/- 833 microU/ml.3 hours. Glucose 145-152 insulin Homo sapiens 123-130 7875653-8 1994 The ratio of insulin response to the increment of forearm glucose uptake over a period of 3 h was significantly higher in patients with CAH (control group = 59.6 +/- 6.5 vs CAH = 98.6 +/- 19.4 microU.ml-1/mg.100 ml forearm-1, p < 0.05). Glucose 58-65 insulin Homo sapiens 13-20 7730186-8 1994 The decrease in liver glucose release in response to infusion of insulin was greater (P < .01) for older (-170 mmol/h) than younger (-106 mmol/h) steers. Glucose 22-29 insulin Homo sapiens 65-72 7730186-12 1994 We concluded that older steers tended to be less sensitive than younger steers to the effects of insulin on glucose metabolism. Glucose 108-115 insulin Homo sapiens 97-104 7926315-5 1994 Decrements in insulin, increments in glucagon, and, in the absence of the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counterregulatory factors. Glucose 149-156 insulin Homo sapiens 14-21 7835369-4 1994 Insulin sensitivity (inversely related to insulin resistance) was estimated by minimal modelling analysis of the glucose and insulin profiles. Glucose 113-120 insulin Homo sapiens 0-7 7835369-4 1994 Insulin sensitivity (inversely related to insulin resistance) was estimated by minimal modelling analysis of the glucose and insulin profiles. Glucose 113-120 insulin Homo sapiens 42-49 7875645-6 1994 Here it is shown (a) that under steady state conditions the s.c. glucose concentration is nearly identical to that in blood, (b) that s.c. inserted glucose electrodes do mirror the intracorporal glucose concentration both under hypo-, normo-, and hyperglycaemic conditions with a clinically relevant accuracy, (c) that even stable feedback control of intracorporal glucose concentration is possible employing s.c. glucosensor signal as an input to automated insulin pump controller, and (d) that stable function of s.c. sensor is usually accomplished over intervals up to one day but in some cases applications over up to ten days could be realized. Glucose 148-155 insulin Homo sapiens 458-465 7875645-6 1994 Here it is shown (a) that under steady state conditions the s.c. glucose concentration is nearly identical to that in blood, (b) that s.c. inserted glucose electrodes do mirror the intracorporal glucose concentration both under hypo-, normo-, and hyperglycaemic conditions with a clinically relevant accuracy, (c) that even stable feedback control of intracorporal glucose concentration is possible employing s.c. glucosensor signal as an input to automated insulin pump controller, and (d) that stable function of s.c. sensor is usually accomplished over intervals up to one day but in some cases applications over up to ten days could be realized. Glucose 148-155 insulin Homo sapiens 458-465 7875645-6 1994 Here it is shown (a) that under steady state conditions the s.c. glucose concentration is nearly identical to that in blood, (b) that s.c. inserted glucose electrodes do mirror the intracorporal glucose concentration both under hypo-, normo-, and hyperglycaemic conditions with a clinically relevant accuracy, (c) that even stable feedback control of intracorporal glucose concentration is possible employing s.c. glucosensor signal as an input to automated insulin pump controller, and (d) that stable function of s.c. sensor is usually accomplished over intervals up to one day but in some cases applications over up to ten days could be realized. Glucose 148-155 insulin Homo sapiens 458-465 7875646-1 1994 Continuous glucose monitoring is the conditio sine qua non to achieve total automation in glucose-controlled insulin-delivery. Glucose 11-18 insulin Homo sapiens 109-116 7875646-1 1994 Continuous glucose monitoring is the conditio sine qua non to achieve total automation in glucose-controlled insulin-delivery. Glucose 90-97 insulin Homo sapiens 109-116 7868874-11 1994 CONCLUSION: Impaired insulin release might contribute to the glucose intolerance associated with hypertension, and this can occur in the absence of insulin resistance, which is not present in all subjects with essential hypertension. Glucose 61-68 insulin Homo sapiens 21-28 7868970-5 1994 Insulin treatment normalized the glucose and triglyceride levels and diminished hepatic apoC-III mRNA levels by 59%. Glucose 33-40 insulin Homo sapiens 0-7 7868874-3 1994 RESULTS: Intravenous glucose tolerance (defined as the glucose disappearance rate constant) was significantly correlated with the minimal model parameters for insulin sensitivity, glucose effectiveness or insulin-independent glucose uptake, and first- and second-phase beta-cell responsiveness (phi 1 and phi 2). Glucose 21-28 insulin Homo sapiens 159-166 7868874-3 1994 RESULTS: Intravenous glucose tolerance (defined as the glucose disappearance rate constant) was significantly correlated with the minimal model parameters for insulin sensitivity, glucose effectiveness or insulin-independent glucose uptake, and first- and second-phase beta-cell responsiveness (phi 1 and phi 2). Glucose 21-28 insulin Homo sapiens 205-212 7868874-3 1994 RESULTS: Intravenous glucose tolerance (defined as the glucose disappearance rate constant) was significantly correlated with the minimal model parameters for insulin sensitivity, glucose effectiveness or insulin-independent glucose uptake, and first- and second-phase beta-cell responsiveness (phi 1 and phi 2). Glucose 55-62 insulin Homo sapiens 159-166 7868874-3 1994 RESULTS: Intravenous glucose tolerance (defined as the glucose disappearance rate constant) was significantly correlated with the minimal model parameters for insulin sensitivity, glucose effectiveness or insulin-independent glucose uptake, and first- and second-phase beta-cell responsiveness (phi 1 and phi 2). Glucose 55-62 insulin Homo sapiens 205-212 7868874-3 1994 RESULTS: Intravenous glucose tolerance (defined as the glucose disappearance rate constant) was significantly correlated with the minimal model parameters for insulin sensitivity, glucose effectiveness or insulin-independent glucose uptake, and first- and second-phase beta-cell responsiveness (phi 1 and phi 2). Glucose 55-62 insulin Homo sapiens 159-166 7868874-3 1994 RESULTS: Intravenous glucose tolerance (defined as the glucose disappearance rate constant) was significantly correlated with the minimal model parameters for insulin sensitivity, glucose effectiveness or insulin-independent glucose uptake, and first- and second-phase beta-cell responsiveness (phi 1 and phi 2). Glucose 55-62 insulin Homo sapiens 205-212 7868874-4 1994 First-phase insulin release, expressed either as the area under the insulin-time curve between 0 and 10 min or as the ratio of that area to total insulin area was also correlated with glucose tolerance. Glucose 184-191 insulin Homo sapiens 12-19 7868874-4 1994 First-phase insulin release, expressed either as the area under the insulin-time curve between 0 and 10 min or as the ratio of that area to total insulin area was also correlated with glucose tolerance. Glucose 184-191 insulin Homo sapiens 68-75 7868874-4 1994 First-phase insulin release, expressed either as the area under the insulin-time curve between 0 and 10 min or as the ratio of that area to total insulin area was also correlated with glucose tolerance. Glucose 184-191 insulin Homo sapiens 68-75 7877889-0 1994 Insulin responses to intravenous glucose and the hyperglycemic clamp in cystic fibrosis patients with different degrees of glucose tolerance. Glucose 33-40 insulin Homo sapiens 0-7 7966476-7 1994 Aging has a major impact on postinjury metabolism, being associated with exaggerated glucose intolerance and diminished insulin responses to glucose infusion. Glucose 141-148 insulin Homo sapiens 120-127 7659127-1 1994 Addition of mammalian insulin to Saccharomyces cerevisiae enhanced the growth of the cells in several glucose concentrations. Glucose 102-109 insulin Homo sapiens 22-29 7659127-4 1994 The effect of insulin was very similar to the increase in yeast growth observed by the addition of GTF (glucose tolerance factor) to the medium. Glucose 104-111 insulin Homo sapiens 14-21 7804792-3 1994 These responses can be specific to a particular stressor and relatively circumscribed (e.g., secretion of insulin in response to an increase in blood glucose), or can be generalized and relatively nonspecific (e.g., behavioral manifestations of severe anxiety). Glucose 150-157 insulin Homo sapiens 106-113 7703598-4 1994 After a glucose load, plasma glucose and insulin concentrations were higher in cirrhotic patients than in control subjects (p < 0.05). Glucose 8-15 insulin Homo sapiens 41-48 7877889-0 1994 Insulin responses to intravenous glucose and the hyperglycemic clamp in cystic fibrosis patients with different degrees of glucose tolerance. Glucose 123-130 insulin Homo sapiens 0-7 7877889-10 1994 Alterations in the acute phase of glucose-stimulated insulin secretion seem to be principally responsible for the early impairment in glucose tolerance. Glucose 34-41 insulin Homo sapiens 53-60 7826558-6 1994 Insulin-stimulated glucose disposal was not different between the preeclamptic (5.6 +/- 0.3 mg/kg/min) and control groups (5.7 +/- 0.7 mg/kg/min). Glucose 19-26 insulin Homo sapiens 0-7 7980500-3 1994 However, LY294002 partially inhibited insulin stimulated glucose uptake, amino acid uptake and protein synthesis, while it completely inhibited insulin stimulation of DNA synthesis and p70 S6 kinase activation. Glucose 57-64 insulin Homo sapiens 38-45 7980479-1 1994 The rate-limiting step in the uptake and metabolism of D-glucose by insulin target cells is thought to be glucose transport mediated by glucose transporters (primarily the GLUT4 isoform) localized to the plasma membrane. Glucose 55-64 insulin Homo sapiens 68-75 7980479-1 1994 The rate-limiting step in the uptake and metabolism of D-glucose by insulin target cells is thought to be glucose transport mediated by glucose transporters (primarily the GLUT4 isoform) localized to the plasma membrane. Glucose 57-64 insulin Homo sapiens 68-75 7955454-2 1994 A blunted insulin response to glucose in patients with primary aldosteronism is well known, but insulin sensitivity has not been thoroughly determined. Glucose 30-37 insulin Homo sapiens 10-17 7848543-5 1994 This effect is a predictable consequence of the principal pharmacological effect of these drugs, i.e. sensitisation of the islet beta-cell to glucose, resulting in enhanced endogenous insulin secretion. Glucose 142-149 insulin Homo sapiens 184-191 7851682-5 1994 Glucose-mediated uptake was calculated as the difference between the rates of glucose disappearance measured during a hyperglycaemic clamp performed at identical rates of insulin infusion and was also found to be similar in both donor subjects and control subjects. Glucose 0-7 insulin Homo sapiens 171-178 7859590-1 1994 Insulin (immunoreactive insulin, IRI) response during a 100 g oral glucose tolerance test was studied in a large number of patients with definite diabetes, equivocal diabetes, and other pathological states causing glucose intolerance. Glucose 67-74 insulin Homo sapiens 0-7 7859590-1 1994 Insulin (immunoreactive insulin, IRI) response during a 100 g oral glucose tolerance test was studied in a large number of patients with definite diabetes, equivocal diabetes, and other pathological states causing glucose intolerance. Glucose 214-221 insulin Homo sapiens 0-7 7859591-6 1994 Excess free fatty acid may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. Glucose 148-155 insulin Homo sapiens 99-106 7859593-2 1994 In addition, subjects with a lower insulin response to glucose show a higher risk for the development of NIDDM. Glucose 55-62 insulin Homo sapiens 35-42 7859593-3 1994 In fact, most of the subjects who later develop diabetes show a lower insulin response to glucose at the initial examination. Glucose 90-97 insulin Homo sapiens 70-77 7859594-3 1994 In addition, plasma insulin response to glucose was exaggerated in Cushing"s syndrome with glucose intolerance, but was impaired in acromegaly and pheochromocytoma with glucose intolerance. Glucose 40-47 insulin Homo sapiens 20-27 7859594-3 1994 In addition, plasma insulin response to glucose was exaggerated in Cushing"s syndrome with glucose intolerance, but was impaired in acromegaly and pheochromocytoma with glucose intolerance. Glucose 91-98 insulin Homo sapiens 20-27 7859594-3 1994 In addition, plasma insulin response to glucose was exaggerated in Cushing"s syndrome with glucose intolerance, but was impaired in acromegaly and pheochromocytoma with glucose intolerance. Glucose 91-98 insulin Homo sapiens 20-27 7859608-4 1994 Multiple regression analysis demonstrated a significant relationship of either blood pressure, plasma triglyceride or HDL cholesterol level to plasma insulin and glucose response after glucose loading. Glucose 185-192 insulin Homo sapiens 150-157 7859613-4 1994 The improvement of glucose and lipid metabolism obtained during the training program, consisting of fast walking or jogging corresponding to 40-60% of predictive VO2 max for 30-60 min daily, was suggested to be related to improved insulin sensitivity in patients with NIDDM. Glucose 19-26 insulin Homo sapiens 231-238 7859631-4 1994 The fasting and post-glucose load serum immunoreactive insulin concentrations were higher in the Japanese-Americans compared to the Hiroshima inhabitants with the same degree of obesity and glucose tolerance. Glucose 21-28 insulin Homo sapiens 55-62 7859631-4 1994 The fasting and post-glucose load serum immunoreactive insulin concentrations were higher in the Japanese-Americans compared to the Hiroshima inhabitants with the same degree of obesity and glucose tolerance. Glucose 190-197 insulin Homo sapiens 55-62 7929824-4 1994 During the insulin clamp study, serum insulin rose from 34 +/- 2 to 1084 +/- 136 pmol/liter (P = 0.0001) in men and from 40 +/- 5 to 1357 +/- 175 pmol/liter (P = 0.0003) in women, while serum glucose remained constant in both groups. Glucose 192-199 insulin Homo sapiens 38-45 7962308-4 1994 When the 1 week data were compared to baseline, there was a small but significant rise in mean (+/- SE) fasting glucose (4.62 +/- 0.17 vs. 5.1 +/- 0.15 mmol/L; P < 0.01), NEFA (0.70 +/- 0.09 vs. 1.1 +/- 0.12 mmol/L; P < 0.005), insulin (93.6 +/- 8.9 vs. 238.9 +/- 9.2 pmol/L; P < 0.0001), C-peptide (0.32 +/- 0.13 vs. 0.66 +/- 0.13 nmol/L; P < 0.005), and phi 1 (11.9 +/- 1.3 vs. 16.2 +/- 1.8 pmol/L.min/mmol.L x 10(2)) and phi 2 (1.43 +/- 0.17 vs. 3.15 +/- 0.25 pmol/L.min/mmol.L x 10(3); P < 0.05). Glucose 112-119 insulin Homo sapiens 234-241 7962308-4 1994 When the 1 week data were compared to baseline, there was a small but significant rise in mean (+/- SE) fasting glucose (4.62 +/- 0.17 vs. 5.1 +/- 0.15 mmol/L; P < 0.01), NEFA (0.70 +/- 0.09 vs. 1.1 +/- 0.12 mmol/L; P < 0.005), insulin (93.6 +/- 8.9 vs. 238.9 +/- 9.2 pmol/L; P < 0.0001), C-peptide (0.32 +/- 0.13 vs. 0.66 +/- 0.13 nmol/L; P < 0.005), and phi 1 (11.9 +/- 1.3 vs. 16.2 +/- 1.8 pmol/L.min/mmol.L x 10(2)) and phi 2 (1.43 +/- 0.17 vs. 3.15 +/- 0.25 pmol/L.min/mmol.L x 10(3); P < 0.05). Glucose 112-119 insulin Homo sapiens 298-307 7962308-5 1994 Conversely, there were associated decreases in glucose decay rate (1.83 +/- 0.26 vs. 1.28 +/- 0.12 min-1; P < 0.05) and insulin-mediated glucose disposal (0.36 +/- 0.08 vs. 0.18 +/- 0.06 min/pmol.L x 10(-4); P < 0.005). Glucose 140-147 insulin Homo sapiens 123-130 7837212-2 1994 In this study, we measured insulin sensitivity by the euglycaemic hyperinsulinaemic glucose clamp technique and ability to release insulin by 75 g oral glucose tolerance test (OGTT) in primary aldosteronism. Glucose 84-91 insulin Homo sapiens 27-34 7837212-6 1994 The mean rate of glucose infusion to maintain euglycemia for the last 30 minutes of the clamp technique was used as an indicator of insulin sensitivity (M-value). Glucose 17-24 insulin Homo sapiens 132-139 7836868-7 1994 These results indicate that it is feasible to use insulin eyedrops to lower the blood glucose in humans. Glucose 86-93 insulin Homo sapiens 50-57 7983783-1 1994 The ATP-sensitive K+ (K+ATP) channel plays a key role in secretion of insulin in response to glucose-stimulation in pancreatic beta-cells. Glucose 93-100 insulin Homo sapiens 70-77 7983786-6 1994 The insulin response to oral glucose was decreased in all other family members with the mutation. Glucose 29-36 insulin Homo sapiens 4-11 7983798-3 1994 Recent Advances are revealing the molecular mechanism how insulin is secreted in response to glucose and how insulin acts on the target tissues. Glucose 93-100 insulin Homo sapiens 58-65 7983803-5 1994 In these cases, despite having a same mutation in the insulin receptor gene, some individuals exhibited significant clinical differences (e.g. insulin resistance or glucose tolerance). Glucose 165-172 insulin Homo sapiens 54-61 7983805-1 1994 As glycogen synthase is a key enzyme of the non-oxidative pathway of glucose metabolism in the skeletal muscle, and reduced activity of this enzyme is related to insulin resistance, it seems likely that this enzyme is a candidate gene for contributing to the pathogenesis of NIDDM. Glucose 69-76 insulin Homo sapiens 162-169 7937750-5 1994 Glucose (16.7 mM)-induced insulin release by human islets was not impaired after a 30-min exposure to SZ or alloxan, at concentrations that inhibited insulin release from rat (30-80% inhibition; P < 0.001) or mouse (10-70% inhibition; P < 0.05) islets. Glucose 0-7 insulin Homo sapiens 26-33 8090784-8 1994 This animal model shows that primary alterations in the rate of liver glucose production may induce insulin resistance and NIDDM. Glucose 70-77 insulin Homo sapiens 100-107 7827780-3 1994 The tissue assumed the trabecular column-like architecture of adult islets by 3 mo, with a concomitant 3-4-fold increase in serum human C-peptide concentration after glucose challenge. Glucose 166-173 insulin Homo sapiens 136-145 7827780-7 1994 At this time, 1 yr posttransplantation, although the proportion of insulin containing cells in the graft remained unchanged from that measured at 4 mo, a reduction in the magnitude of the C-peptide response to glucose was observed; this finding coincided with a significant mononuclear infiltrate in some areas of the transplanted tissue. Glucose 210-217 insulin Homo sapiens 188-197 7827781-5 1994 Although adequate insulin responses to glucose were seen after culture in conventional or matrix media, only agarose embedded islets were consistently able to induce normoglycemia in diabetic recipients after 14 days of culture. Glucose 39-46 insulin Homo sapiens 18-25 7820976-11 1994 These effects are attributed to a specific effect of leucine on the other two BCAA and a depression of muscle proteolysis by both leucine and insulin, resulting from glucose infusion. Glucose 166-173 insulin Homo sapiens 142-149 8070607-0 1994 Differentiating glucose toxicity from glucose desensitization: a new message from the insulin gene. Glucose 16-23 insulin Homo sapiens 86-93 8070607-4 1994 With regard to the pancreatic islet beta-cell, the mechanism of action for glucose desensitization seems most likely to be expressed at the level of the insulin exocytotic apparatus or insulin stores within the beta-cell, whereas the mechanism of action for glucose toxicity may be at the level of insulin gene transcription. Glucose 75-82 insulin Homo sapiens 153-160 8070607-4 1994 With regard to the pancreatic islet beta-cell, the mechanism of action for glucose desensitization seems most likely to be expressed at the level of the insulin exocytotic apparatus or insulin stores within the beta-cell, whereas the mechanism of action for glucose toxicity may be at the level of insulin gene transcription. Glucose 75-82 insulin Homo sapiens 185-192 8070607-4 1994 With regard to the pancreatic islet beta-cell, the mechanism of action for glucose desensitization seems most likely to be expressed at the level of the insulin exocytotic apparatus or insulin stores within the beta-cell, whereas the mechanism of action for glucose toxicity may be at the level of insulin gene transcription. Glucose 75-82 insulin Homo sapiens 185-192 8070607-5 1994 This differentiation raises the possibility that exposure of patients to chronic hyperglycemia may cause glucose toxic effects on the process of insulin gene transcription and/or expression that are irreversible. Glucose 105-112 insulin Homo sapiens 145-152 8070611-0 1994 A comparison between the minimal model and the glucose clamp in the assessment of insulin sensitivity across the spectrum of glucose tolerance. Glucose 125-132 insulin Homo sapiens 82-89 8070611-2 1994 An insulin-modified frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis was compared with the glucose clamp in 11 subjects with normal glucose tolerance (NGT), 20 with impaired glucose tolerance (IGT), and 24 with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 51-58 insulin Homo sapiens 3-10 8070611-10 1994 Thus, minimal model analysis of the insulin-modified FSIGTT provides estimates of insulin sensitivity that correlate significantly with those from the glucose clamp. Glucose 151-158 insulin Homo sapiens 36-43 8070611-10 1994 Thus, minimal model analysis of the insulin-modified FSIGTT provides estimates of insulin sensitivity that correlate significantly with those from the glucose clamp. Glucose 151-158 insulin Homo sapiens 82-89 7921208-5 1994 The median insulin area under the curve 10-60 min after an intravenous glucose tolerance test increased from 480 mU.l-1.min-1 before treatment to 799 mU.l-1.min-1 (p < 0.05) after 1 year. Glucose 71-78 insulin Homo sapiens 11-18 8082943-3 1994 Insulin sensitivity (glucose metabolic clearance rate) correlated strongly with mean 24-hour ambulatory systolic blood pressure (r = -.650, P < .001). Glucose 21-28 insulin Homo sapiens 0-7 8000110-2 1994 Insulin-induced glucose metabolism markedly decreased compared with 12 healthy subjects. Glucose 16-23 insulin Homo sapiens 0-7 7521354-13 1994 Insulin inhibited splanchnic IGFBP-1 production within 120 min and glucose output within 20 min. Glucose 67-74 insulin Homo sapiens 0-7 8083360-0 1994 Increased glucose effectiveness in normoglycemic but insulin-resistant relatives of patients with non-insulin-dependent diabetes mellitus. Glucose 10-17 insulin Homo sapiens 53-60 7852750-6 1994 Insulin levels also increased more in obese patients after the glucose load. Glucose 63-70 insulin Homo sapiens 0-7 7852750-10 1994 If dynamic increases in flow are indeed important to insulin-mediated glucose disposal, then these observations raise the possibility that the greater increase of regional blood flow during an OGTT in obese hypertensives represents a component of the compensatory response for their defect in glucose metabolism. Glucose 70-77 insulin Homo sapiens 53-60 7852755-10 1994 Models investigating change in systolic or diastolic blood pressure levels found higher baseline levels of insulin area under the glucose tolerance curve predicted greater increases in systolic blood pressure in non-Hispanic Whites only. Glucose 130-137 insulin Homo sapiens 107-114 7986852-4 1994 Insulin is the only hormone which produces anabolism in all energetic substrates, but the results published about its administration with glucose and amino acids and its effects upon the nitrogen balance are controversial. Glucose 138-145 insulin Homo sapiens 0-7 7801339-5 1994 The use of continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg/hr, with supplementation of potassium as needed and maintenance of fluid electrolytes and acid-based balance, has become a routine protocol in our setting for treating the victims of scorpion envenoming. Glucose 85-92 insulin Homo sapiens 54-61 7914964-3 1994 We have noted that with insulin resistance the fasting plasma glucose is often normal and severe hyperglycaemia occurs after a glucose load. Glucose 62-69 insulin Homo sapiens 24-31 7914964-3 1994 We have noted that with insulin resistance the fasting plasma glucose is often normal and severe hyperglycaemia occurs after a glucose load. Glucose 127-134 insulin Homo sapiens 24-31 7914964-5 1994 Supportive evidence showing that beta-cell dysfunction and insulin resistance may have different effects on fasting and post-prandial glucose concentrations comes from studies of identical twins of NIDDM patients, hemi-pancreatectomised normal subjects, and insulin-resistant Asian subjects. Glucose 134-141 insulin Homo sapiens 59-66 7923327-7 1994 As compared with healthy subjects, in diabetics before treatment a reduced insulin sensitivity was found, evaluated either by the index of insulin sensitivity (24.0 +/- 0.8, as compared with 35.5 +/- 4.9 mumol/kg/min per mU/l x 100, p < 0.05) or metabolic glucose clearance (3.7 +/- 0.9, as compared with 6.3 +/- 1.0 ml/kg/min, p < 0.01) and a slightly reduced insulin bond with receptors (p < 0.05). Glucose 259-266 insulin Homo sapiens 75-82 8059770-4 1994 Insulin levels during the oral glucose tolerance test were lowest in men with the highest physical activity. Glucose 31-38 insulin Homo sapiens 0-7 8049187-4 1994 Insulin sensitivity was estimated by the minimal model from a frequently sampled intravenous glucose tolerance test. Glucose 93-100 insulin Homo sapiens 0-7 7857772-3 1994 Insulin-stimulated glucose transport was also insensitive to pertussis toxin pretreatment. Glucose 19-26 insulin Homo sapiens 0-7 7923827-5 1994 The quantity of glucose metabolized per unit of serum insulin concentration (M/I ratio) was similar in the three study groups (median approximately 145 (mumol/kg/min)/(nmol/l); range 70-252). Glucose 16-23 insulin Homo sapiens 54-61 7923827-6 1994 Insulin clearance rates were higher in cystic fibrosis patients with diabetic (24.4 (19.3-29.9) ml/kg/min) and normal (22.6 (14.9-28.4) ml/kg/min) glucose tolerance than in control subjects (17.5 (15.9-24.2) ml/kg/min). Glucose 147-154 insulin Homo sapiens 0-7 7923827-9 1994 CONCLUSIONS: Insulin sensitivity, calculated as the quantity of glucose metabolized per kg body weight per unit of serum insulin concentration, is normal in cystic fibrosis patients with normal glucose tolerance and with well controlled diabetes mellitus. Glucose 64-71 insulin Homo sapiens 13-20 7923827-9 1994 CONCLUSIONS: Insulin sensitivity, calculated as the quantity of glucose metabolized per kg body weight per unit of serum insulin concentration, is normal in cystic fibrosis patients with normal glucose tolerance and with well controlled diabetes mellitus. Glucose 194-201 insulin Homo sapiens 13-20 7923827-10 1994 The insulin clearance rate is increased in cystic fibrosis patients with diabetic and normal glucose tolerance, owing to a shorter serum half-life of insulin, whereas the apparent distribution space for insulin is normal. Glucose 93-100 insulin Homo sapiens 4-11 7988776-9 1994 During local glucose infusion there was a slight increase in the levels of insulin, C-peptide, systemic glucose, and blood pressure, compared to the placebo experiments. Glucose 13-20 insulin Homo sapiens 75-82 7988776-9 1994 During local glucose infusion there was a slight increase in the levels of insulin, C-peptide, systemic glucose, and blood pressure, compared to the placebo experiments. Glucose 13-20 insulin Homo sapiens 84-93 8039605-1 1994 To examine the hypothesis that variants in the regulatory or coding regions of the glycogen synthase (GS) and insulin-responsive glucose transporter (GLUT4) genes contribute to insulin-resistant glucose processing of muscle from non-insulin-dependent diabetes mellitus (NIDDM) patients, promoter regions and regions of importance for translation, as well as coding sequences of the two genes, were studied using single-strand conformation polymorphism (SSCP) analysis and DNA sequencing. Glucose 129-136 insulin Homo sapiens 110-117 8055951-2 1994 Glycated insulin was prepared by incubating native insulin with glucose in 67 mM sodium phosphate, pH 7.5, at 37 degrees C for 30 h. In the presence of micromolar concentrations of Cu2+, glycated insulin was oxidized and its fragmentation or aggregation was detected. Glucose 64-71 insulin Homo sapiens 9-16 8045959-6 1994 With sc administered IGF-I (up to 10 mg twice daily), insulin appeared to control patient glucose concentrations, but severe insulin resistance returned within 72 h of discontinuing IGF-I therapy. Glucose 90-97 insulin Homo sapiens 54-61 7814857-8 1994 The insulin sum and the 2-h insulin level of the oral glucose-tolerance test were more closely correlated with ambulatory blood pressure recordings than was the fasting insulin level. Glucose 54-61 insulin Homo sapiens 28-35 7814857-8 1994 The insulin sum and the 2-h insulin level of the oral glucose-tolerance test were more closely correlated with ambulatory blood pressure recordings than was the fasting insulin level. Glucose 54-61 insulin Homo sapiens 28-35 8040779-6 1994 Endogenous glucose production was correlated with plasma glucose concentration (r = 0.76; p < 0.05) and the rate of glucose disappearance (r = 0.75; p < 0.05); plasma glucose concentration was correlated with the rate of disappearance (r = 0.87; p = < 0.01) and insulin concentrations (p < 0.05). Glucose 11-18 insulin Homo sapiens 271-278 8052146-1 1994 Skeletal muscle contributes significantly to reduced insulin-stimulated glucose disposal in patients with obesity and non-insulin-dependent (type II) diabetes mellitus (NIDDM). Glucose 72-79 insulin Homo sapiens 53-60 8052146-2 1994 The biochemical basis for insulin resistance is not known but may involve reduced glucose transport and/or a defect in intracellular pathways for glucose disposal. Glucose 82-89 insulin Homo sapiens 26-33 8052146-2 1994 The biochemical basis for insulin resistance is not known but may involve reduced glucose transport and/or a defect in intracellular pathways for glucose disposal. Glucose 146-153 insulin Homo sapiens 26-33 8052146-3 1994 To address this question, we measured basal and insulin-stimulated glucose oxidation, glycogen formation, and nonoxidative glycolysis (lactate and amino acid release) in an incubated muscle preparation from nonobese and morbidly obese patients with and without NIDDM. Glucose 67-74 insulin Homo sapiens 48-55 8052146-7 1994 Under maximal insulin-stimulated conditions, rates of glycogen formation, glucose oxidation, and nonoxidized glycolysis increased 1.9-, 2.3-, and 2.2-fold over basal (P < .05) in nonobese controls. Glucose 74-81 insulin Homo sapiens 14-21 7937976-1 1994 Insulin gene transcription is a unique feature of the pancreatic beta cells and is increased in response to glucose. Glucose 108-115 insulin Homo sapiens 0-7 7980425-2 1994 Recent studies have mapped a glucose response element to a CT-like sequence in the rat insulin I gene. Glucose 29-36 insulin Homo sapiens 87-94 7980425-3 1994 The present study was therefore undertaken to ascertain the role of IUF1 in glucose-stimulated insulin gene transcription. Glucose 76-83 insulin Homo sapiens 95-102 7826552-5 1994 Using the euglycemic clamp technique, the data show a significant inverse correlation between supine plasma renin activity and insulin-mediated glucose uptake (r = -0.44; P = .027). Glucose 144-151 insulin Homo sapiens 127-134 7943097-9 1994 A significant relationship between waist/hip ratio and glucose level (r = 0.70, p < 0.004) and insulin areas (r = 0.76, p < 0.001) was present in late pregnancy in obese subjects. Glucose 55-62 insulin Homo sapiens 98-105 7943102-5 1994 The requirement of insulin for glucose control during gestation and gestational age at diagnosis were significantly associated with abnormal postpartum glucose tolerance (p < 0.0001 and p = 0.012, respectively). Glucose 31-38 insulin Homo sapiens 19-26 7943102-5 1994 The requirement of insulin for glucose control during gestation and gestational age at diagnosis were significantly associated with abnormal postpartum glucose tolerance (p < 0.0001 and p = 0.012, respectively). Glucose 152-159 insulin Homo sapiens 19-26 7943102-6 1994 Multivariate analysis showed that only a requirement for insulin for glucose control was significant (p < 0.001). Glucose 69-76 insulin Homo sapiens 57-64 7943429-0 1994 Interactions between effects of W-7, insulin, and hypoxia on glucose transport in skeletal muscle. Glucose 61-68 insulin Homo sapiens 37-44 7943429-12 1994 This study was performed to describe the interactions between the effects of W-7 and those of hypoxia and of insulin on glucose transport. Glucose 120-127 insulin Homo sapiens 109-116 7943429-16 1994 Thus these data demonstrate that W-7 selectively inhibits insulin stimulation of glucose transport. Glucose 81-88 insulin Homo sapiens 58-65 7943297-2 1994 A hyperinsulinemic (2 mU.kg-1.min-1) glucose clamp procedure was used to control glucose and insulin levels during stepwise lowering of plasma glucose. Glucose 37-44 insulin Homo sapiens 7-14 7943303-0 1994 Effect of needle biopsy from the vastus lateralis muscle on insulin-stimulated glucose metabolism in humans. Glucose 79-86 insulin Homo sapiens 60-67 7943303-2 1994 To test whether the trauma of a needle biopsy from the vastus lateralis muscle per se may influence insulin-stimulated glucose uptake, eight healthy subjects underwent two randomly sequenced hyperinsulinemic (insulin infusion rate: 0.6 mU.kg-1.min-1 for 150 min) euglycemic clamps with an interval of 4-6 wk. Glucose 119-126 insulin Homo sapiens 100-107 7943303-4 1994 Insulin-stimulated glucose uptake was significantly reduced in study B (5.36 +/- 0.96 mg.kg-1.min-1) compared with study C (6.06 +/- 0.68 mg.kg-1.min-1; P < 0.05). Glucose 19-26 insulin Homo sapiens 0-7 7943303-8 1994 In conclusion, performance of a muscle biopsy may diminish insulin sensitivity by affecting nonoxidative glucose metabolism. Glucose 105-112 insulin Homo sapiens 59-66 7918315-6 1994 Fasting insulin concentration was significantly associated with levels of glucose, triglycerides, uric acid, serum albumin, creatinine, and fibrinogen as well as resting heart rate. Glucose 74-81 insulin Homo sapiens 8-15 7857380-6 1994 Furthermore, at least one of the dyslipoproteinemias--hypertriglyceridemia--is associated with insulin resistance and therefore could aggravate glucose intolerance. Glucose 144-151 insulin Homo sapiens 95-102 7821127-3 1994 Fasting glucose, GHb, lipid and lipoprotein concentrations were determined, and resistance to insulin-mediated glucose disposal was estimated by measuring the steady-state plasma glucose (SSPG) concentration at the end of a 180-min infusion of somatostatin, glucose, and insulin. Glucose 111-118 insulin Homo sapiens 94-101 7821127-3 1994 Fasting glucose, GHb, lipid and lipoprotein concentrations were determined, and resistance to insulin-mediated glucose disposal was estimated by measuring the steady-state plasma glucose (SSPG) concentration at the end of a 180-min infusion of somatostatin, glucose, and insulin. Glucose 111-118 insulin Homo sapiens 94-101 7821127-3 1994 Fasting glucose, GHb, lipid and lipoprotein concentrations were determined, and resistance to insulin-mediated glucose disposal was estimated by measuring the steady-state plasma glucose (SSPG) concentration at the end of a 180-min infusion of somatostatin, glucose, and insulin. Glucose 111-118 insulin Homo sapiens 94-101 7821148-9 1994 It is proposed that non-insulin-dependent diabetic patients who have markers that characterize individuals at risk of type I diabetes may be suitable candidates for those same therapeutic strategies that seek to prevent progression to insulin-dependence or even to reestablish normal glucose tolerance. Glucose 284-291 insulin Homo sapiens 24-31 7851076-6 1994 Insulin losses at the injection site are frequent and, although usually small in amount, are a potential source of blood glucose variability. Glucose 121-128 insulin Homo sapiens 0-7 7851274-1 1994 To investigate whether a resistance to insulin-stimulated glucose uptake (IR) is associated with the risk factors (RF) for cardiovascular disease (CVD) in non-insulin-dependent diabetic (NIDDM) patients, we determined the degree of IR in 135 adult NIDDM patients who had no advanced diabetic complications. Glucose 58-65 insulin Homo sapiens 39-46 7851275-5 1994 The ratio of the level of serum C-peptide to that of insulin after a 75 g oral glucose tolerance test (OGTT) was augmented after 4 weeks of bezafibrate administration. Glucose 79-86 insulin Homo sapiens 53-60 7851681-4 1994 During each insulin clamp step, the defect in insulin action was accounted for by impaired non-oxidative glucose disposal (p < 0.01). Glucose 105-112 insulin Homo sapiens 12-19 7851681-4 1994 During each insulin clamp step, the defect in insulin action was accounted for by impaired non-oxidative glucose disposal (p < 0.01). Glucose 105-112 insulin Homo sapiens 46-53 7851681-8 1994 However, glucose oxidation during each insulin clamp step was significantly increased and there was a reciprocal decline in non-oxidative glucose disposal by 25-39% (p < 0.01); suppression of hepatic glucose production by insulin was unaltered by chronic hyperglycaemic hyperinsulinaemia. Glucose 9-16 insulin Homo sapiens 39-46 7851681-9 1994 Chronic glucose infusion increased the plasma insulin response to acute hyperglycaemia more than twofold. Glucose 8-15 insulin Homo sapiens 46-53 7851682-3 1994 Insulin-mediated glucose uptake was measured during sequential infusions of insulin at rates of 0.25, 1.0, and 10.0 mU.kg-1.min-1 in 12 donor subjects and 12 matched control subjects maintained at euglycaemia. Glucose 17-24 insulin Homo sapiens 0-7 7926290-7 1994 The absolute insulin secretory responses to oral glucose were significantly higher in the resistant group (83,205 +/- 17,787 pmol/l x min) than in the sensitive group (24,727 +/- 3,591 pmol/l x min, P < 0.01), whose absolute responses were similar to those of normal control subjects (24,576 +/- 2,767 pmol/l x min). Glucose 49-56 insulin Homo sapiens 13-20 7926293-4 1994 The levels of GAAs were found to be inversely related to both the levels of insulin autoantibodies and the rate of loss of intravenous glucose-stimulated insulin secretion (P < 10(-5) and P < 0.01, respectively). Glucose 135-142 insulin Homo sapiens 154-161 7926294-1 1994 Impaired insulin-stimulated glycogen synthesis of peripheral tissues is a characteristic feature of many patients with non-insulin-dependent diabetes mellitus (NIDDM) and their first-degree relatives with normal glucose tolerance, suggesting putative inherited defects in this metabolic pathway. Glucose 212-219 insulin Homo sapiens 9-16 7851871-4 1994 Insulin sensitivity measured by the short insulin tolerance test (ITT) was expressed as % disappearance of glucose per minute (KITT). Glucose 107-114 insulin Homo sapiens 0-7 7851871-4 1994 Insulin sensitivity measured by the short insulin tolerance test (ITT) was expressed as % disappearance of glucose per minute (KITT). Glucose 107-114 insulin Homo sapiens 42-49 7962273-13 1994 The finding that increasing the rate of insulin infusion restored plasma glucose to normal in IDDM subjects suggests that the postexercise increase in insulin levels observed in normal subjects is essential to return plasma glucose to resting levels. Glucose 73-80 insulin Homo sapiens 40-47 7962273-13 1994 The finding that increasing the rate of insulin infusion restored plasma glucose to normal in IDDM subjects suggests that the postexercise increase in insulin levels observed in normal subjects is essential to return plasma glucose to resting levels. Glucose 73-80 insulin Homo sapiens 151-158 7962273-13 1994 The finding that increasing the rate of insulin infusion restored plasma glucose to normal in IDDM subjects suggests that the postexercise increase in insulin levels observed in normal subjects is essential to return plasma glucose to resting levels. Glucose 224-231 insulin Homo sapiens 40-47 7962273-13 1994 The finding that increasing the rate of insulin infusion restored plasma glucose to normal in IDDM subjects suggests that the postexercise increase in insulin levels observed in normal subjects is essential to return plasma glucose to resting levels. Glucose 224-231 insulin Homo sapiens 151-158 7962275-1 1994 Insulin resistance may result from decreased muscle blood flow, impaired cellular glucose transport, or intracellular deficits of glucose metabolism. Glucose 82-89 insulin Homo sapiens 0-7 7862618-2 1994 Its mechanism of action, unknown until a few years ago, is now linked to an improved peripheral sensitivity to insulin, through a stimulated tissue glucose uptake by a transporter linked system. Glucose 148-155 insulin Homo sapiens 111-118 7827358-0 1994 Effects of non-esterified fatty acids on insulin-stimulated glucose transport in isolated skeletal muscle from patients with type 2 (non-insulin-dependent) diabetes mellitus. Glucose 60-67 insulin Homo sapiens 41-48 7819685-0 1994 Inter-relationship between serum concentrations of glucose, glucagon and insulin during the first two days of life in healthy newborns. Glucose 51-58 insulin Homo sapiens 73-80 7951170-3 1994 Modified insulin suppression test was employed to compared the insulin-stimulated glucose uptake and insulin clearance rate between two groups. Glucose 82-89 insulin Homo sapiens 9-16 7951170-3 1994 Modified insulin suppression test was employed to compared the insulin-stimulated glucose uptake and insulin clearance rate between two groups. Glucose 82-89 insulin Homo sapiens 63-70 7951170-3 1994 Modified insulin suppression test was employed to compared the insulin-stimulated glucose uptake and insulin clearance rate between two groups. Glucose 82-89 insulin Homo sapiens 63-70 7804749-2 1994 Patients with elevated antiporter activity manifest high total body exhangeable Na+ levels, renal and cardiac hypertrophy, and metabolic abnormalities which are part of the syndrome characterized by resistance to insulin-stimulated body glucose disposal. Glucose 237-244 insulin Homo sapiens 213-220 7821192-3 1994 However, the values for insulin response to glucose were significantly increased when blood was drawn from the hand site (410.1 vs. 328.7 pM, P < 0.05). Glucose 44-51 insulin Homo sapiens 24-31 7821192-6 1994 The acute insulin response to glucose obtained from samples drawn in this manner is, however, significantly increased and this should be borne in mind when comparing results from centers using these different methods. Glucose 30-37 insulin Homo sapiens 10-17 7821746-1 1994 Short-term administration of physiological amounts of C-peptide to patients with insulin-dependent diabetes was found to reduce the glomerular hyperfiltration in these patients as well as augment whole body glucose utilization. Glucose 207-214 insulin Homo sapiens 54-63 7821746-3 1994 Studies under in vitro conditions have shown that C-peptide stimulates glucose transport in skeletal muscle with its maximal effect within the physiological concentration range. Glucose 71-78 insulin Homo sapiens 50-59 8070618-7 1994 Glucose-stimulated insulin release could be demonstrated in vitro from recovered islets. Glucose 0-7 insulin Homo sapiens 19-26 7821371-11 1994 Preincubation of the cells in 25 mM glucose overnight also increased the uptake of retinal outer segments over control and reduced the effect of insulin. Glucose 36-43 insulin Homo sapiens 145-152 7959530-9 1994 In addition, hyperinsulinemia was observed during the 75g glucose tolerance test and the presence of insulin resistance was suggested. Glucose 58-65 insulin Homo sapiens 18-25 7812419-9 1994 Blood glucose and insulin both fasting and after glucose load. Glucose 49-56 insulin Homo sapiens 18-25 7836113-8 1994 Glucose infusion rates during the hyperinsulinemic-euglycemic glucose clamp increased 24% (13.5 +/- 1.7 vs. 16.7 +/- 2.2 mumol.kg FFM-1.min-1; P < 0.05) during the low (20 mU.m-2.min-1) insulin infusion and increased 22% (55.7 +/- 3.3 vs. 67.7 +/- 3.9 mumol.kg FFM-1.min-1; P < 0.05) during the high (100 mU.m-2.min-1) insulin infusion. Glucose 0-7 insulin Homo sapiens 39-46 7836113-8 1994 Glucose infusion rates during the hyperinsulinemic-euglycemic glucose clamp increased 24% (13.5 +/- 1.7 vs. 16.7 +/- 2.2 mumol.kg FFM-1.min-1; P < 0.05) during the low (20 mU.m-2.min-1) insulin infusion and increased 22% (55.7 +/- 3.3 vs. 67.7 +/- 3.9 mumol.kg FFM-1.min-1; P < 0.05) during the high (100 mU.m-2.min-1) insulin infusion. Glucose 0-7 insulin Homo sapiens 189-196 7836113-9 1994 These increases were accompanied by a 40% increase (n = 7; P < 0.08) in nonoxidative glucose metabolism during the high insulin infusion. Glucose 88-95 insulin Homo sapiens 123-130 8077883-0 1994 Insulin responses to glucose in healthy males are associated with adult height but not with birth weight. Glucose 21-28 insulin Homo sapiens 0-7 8077883-5 1994 MAIN OUTCOME MEASURES: Insulin responses were measured by standardized glucose infusion tests. Glucose 71-78 insulin Homo sapiens 23-30 8077883-11 1994 CONCLUSIONS: An early insulin response to glucose associates with postnatal growth. Glucose 42-49 insulin Homo sapiens 22-29 8077888-9 1994 The total glucose disposal rate showed a small increase in the insulin group. Glucose 10-17 insulin Homo sapiens 63-70 7815681-8 1994 Isolated adipocytes remained highly viable, as evidenced by glucose transport under both basal and maximal insulin-stimulated conditions. Glucose 60-67 insulin Homo sapiens 107-114 7885957-0 1994 [Blood insulin values after the oral glucose tolerance test (OGTT) and the body composition in 30 obese children]. Glucose 37-44 insulin Homo sapiens 7-14 7839016-17 1994 However, the ratio does not require a previous definition of a normal value as for fasting or post-oral glucose insulin levels, and thus, it can be easily calculated in daily clinical practice to establish specific therapeutic maneuvers at an early stage of the evaluation of such patients. Glucose 104-111 insulin Homo sapiens 112-119 8063743-9 1994 The transgenic serum insulin levels at 15 min after glucose administration were 2.5-3.0-fold higher than control levels. Glucose 52-59 insulin Homo sapiens 21-28 7968872-4 1994 During an oral glucose tolerance test the hypertensive subjects had higher blood glucose and serum insulin levels than the controls. Glucose 15-22 insulin Homo sapiens 99-106 7968872-8 1994 In a second glucose tolerance test carried out in 13 patients blood glucose, serum insulin and triglyceride concentrations were significantly lower compared to the pretreatment period. Glucose 12-19 insulin Homo sapiens 83-90 8074189-8 1994 Together, these results strongly suggest that insulin, insulin-like growth factors, and interferon-gamma increase the permeability across T84 cell monolayers through a common mechanism that is modulated by glucose-derived metabolites and oxidative metabolism. Glucose 206-213 insulin Homo sapiens 46-53 8074189-8 1994 Together, these results strongly suggest that insulin, insulin-like growth factors, and interferon-gamma increase the permeability across T84 cell monolayers through a common mechanism that is modulated by glucose-derived metabolites and oxidative metabolism. Glucose 206-213 insulin Homo sapiens 55-62 8074198-5 1994 Data indicate that the degree of skeletal muscle perfusion can be an important determinant of insulin-mediated glucose uptake. Glucose 111-118 insulin Homo sapiens 94-101 8074198-6 1994 Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin"s overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. Glucose 124-131 insulin Homo sapiens 31-38 8074198-6 1994 Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin"s overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. Glucose 124-131 insulin Homo sapiens 86-93 7523002-11 1994 CONCLUSION: This difference in the IGFBP-1 response in the presence of a similar glucose response suggests that in Type 1 diabetes there may be different sensitivities to the actions of exogenous insulin on IGFBP-1 regulation. Glucose 81-88 insulin Homo sapiens 196-203 7924163-0 1994 Physical fitness and insulin sensitivity in human subjects with a low insulin response to glucose. Glucose 90-97 insulin Homo sapiens 21-28 7924163-0 1994 Physical fitness and insulin sensitivity in human subjects with a low insulin response to glucose. Glucose 90-97 insulin Homo sapiens 70-77 7924163-5 1994 During glucose infusion, low insulin responders and endurance-trained subjects had acute-phase (0-10 min) insulin responses that were 26% (P < 0.001) and 31% (P < 0.001), and C-peptide responses that were 35% (P < 0.001) and 42% (P < 0.01), respectively of the responses in high insulin responders. Glucose 7-14 insulin Homo sapiens 29-36 7924163-9 1994 In conclusion, we demonstrate that low insulin responders exhibited decreased insulin and C-peptide responses to glucose, despite normal insulin sensitivity and exercise capacity. Glucose 113-120 insulin Homo sapiens 39-46 7924163-9 1994 In conclusion, we demonstrate that low insulin responders exhibited decreased insulin and C-peptide responses to glucose, despite normal insulin sensitivity and exercise capacity. Glucose 113-120 insulin Homo sapiens 90-99 7924163-9 1994 In conclusion, we demonstrate that low insulin responders exhibited decreased insulin and C-peptide responses to glucose, despite normal insulin sensitivity and exercise capacity. Glucose 113-120 insulin Homo sapiens 78-85 7924165-13 1994 Fasting plasma insulin level increased with fasting plasma glucose level (r = 0.53, P = 0.01). Glucose 59-66 insulin Homo sapiens 15-22 7956622-2 1994 We compared the acute effects of 12-h nocturnal or daytime insulin infusions on the 24-h glucose profile in 20 patients with NIDDM. Glucose 89-96 insulin Homo sapiens 59-66 7988780-4 1994 The improvement in glycaemic control was associated with increases in insulin-mediated glucose uptake (p < 0.001) and plasma post-heparin lipoprotein and hepatic lipolytic activities (p < 0.02). Glucose 87-94 insulin Homo sapiens 70-77 7988785-0 1994 Effect of metformin on insulin-stimulated glucose transport in isolated skeletal muscle obtained from patients with NIDDM. Glucose 42-49 insulin Homo sapiens 23-30 7988785-4 1994 Whole body insulin-mediated glucose utilization was decreased by 45% (p < 0.05) in the diabetic subjects when studied at 8 mmol/l glucose, compared to the healthy subjects studied at 5 mmol/l glucose. Glucose 28-35 insulin Homo sapiens 11-18 7988785-4 1994 Whole body insulin-mediated glucose utilization was decreased by 45% (p < 0.05) in the diabetic subjects when studied at 8 mmol/l glucose, compared to the healthy subjects studied at 5 mmol/l glucose. Glucose 133-140 insulin Homo sapiens 11-18 7988785-4 1994 Whole body insulin-mediated glucose utilization was decreased by 45% (p < 0.05) in the diabetic subjects when studied at 8 mmol/l glucose, compared to the healthy subjects studied at 5 mmol/l glucose. Glucose 133-140 insulin Homo sapiens 11-18 7988785-6 1994 However, the two control subjects and three patients with NIDDM which displayed a low rate of insulin-mediated glucose utilization (< 20 mumol.kg-1.min-1), as well as in vitro insulin resistance, demonstrated increased insulin-stimulated glucose transport in the presence of metformin at 0.1 mmol/l (p < 0.05). Glucose 111-118 insulin Homo sapiens 94-101 7988785-6 1994 However, the two control subjects and three patients with NIDDM which displayed a low rate of insulin-mediated glucose utilization (< 20 mumol.kg-1.min-1), as well as in vitro insulin resistance, demonstrated increased insulin-stimulated glucose transport in the presence of metformin at 0.1 mmol/l (p < 0.05). Glucose 241-248 insulin Homo sapiens 94-101 7988785-7 1994 In conclusion, the concentration of metformin resulting in a potentiating effect on insulin-stimulated glucose transport in insulin-resistant human skeletal muscle is 10-fold higher than the therapeutic concentrations administered to patients with NIDDM. Glucose 103-110 insulin Homo sapiens 84-91 7988785-7 1994 In conclusion, the concentration of metformin resulting in a potentiating effect on insulin-stimulated glucose transport in insulin-resistant human skeletal muscle is 10-fold higher than the therapeutic concentrations administered to patients with NIDDM. Glucose 103-110 insulin Homo sapiens 124-131 7988789-0 1994 Evaluation of octreotide to assess insulin-mediated glucose disposal by the insulin suppression test. Glucose 52-59 insulin Homo sapiens 35-42 7822064-4 1994 Strength training also lowered the total plasma insulin area (pmol.l-1.120 min-1) under the OGTT curve (60082 +/- 25467 vs 46727 +/- 11273, p < 0.05) as well as plasma insulin levels (pmol.l-1) at fasting (p < 0.05) and at 90 min (p < 0.01) and 120 min (p < 0.05) after glucose ingestion. Glucose 282-289 insulin Homo sapiens 48-55 7990080-5 1994 The insulin-mediated glucose disposal rate during euglycaemic clamp (M-value) was significantly lower in the hypertensive group than in normal controls (7.32 +/- 0.56 vs 8.88 +/- 0.34 mg/kg/min, P < 0.05). Glucose 21-28 insulin Homo sapiens 4-11 8048934-0 1994 Effects of wortmannin on increased glucose transport by insulin and norepinephrine in primary culture of brown adipocytes. Glucose 35-42 insulin Homo sapiens 56-63 8048939-1 1994 Specific insulin binding by the fetal lung insulin receptor is reduced in vitro by a combination of high glucose and insulin. Glucose 105-112 insulin Homo sapiens 9-16 8048934-1 1994 The effects of wortmannin, a selective inhibitor of phosphatidylinositol (PI) 3-kinase, on increases in glucose transport activity induced by insulin and norepinephrine (NE) have been studied in primary culture of brown adipocytes. Glucose 104-111 insulin Homo sapiens 142-149 8048939-1 1994 Specific insulin binding by the fetal lung insulin receptor is reduced in vitro by a combination of high glucose and insulin. Glucose 105-112 insulin Homo sapiens 43-50 8048934-5 1994 When wortmannin was added to the medium before stimulation with insulin, the increase in glucose transport and translocation of GLUT4 were completely abolished. Glucose 89-96 insulin Homo sapiens 64-71 8048939-7 1994 These data indicate that down-regulation of fetal lung insulin receptors by high glucose + insulin occurs at the pre-translational level and that glucose transport is adversely affected under these conditions. Glucose 81-88 insulin Homo sapiens 55-62 8048502-1 1994 Phenylarsine oxide (PAO) has previously been shown to inhibit insulin-stimulated glucose transport without affecting insulin binding and tyrosine kinase activity of insulin receptor (S. C. Frost and M. D. Lane. Glucose 81-88 insulin Homo sapiens 62-69 8017722-8 1994 CONCLUSIONS: Our data are compatible with the concept that continued glucose transport, mediated by the low-Km Glut 1 glucose transporter, was responsible for continued insulin release during hypoglycemia in these patients. Glucose 69-76 insulin Homo sapiens 169-176 7818648-11 1994 Postabsorptive endogenous glucose production was significantly higher with bendrofluazide 5.0 mg compared with 1.25 mg (10.9 (1.2) v 9.9 (0.8) mumol/kg/min) but was suppressed to a similar extent after insulin (bendrofluazide 5.0 mg 2.8 (1.5) mumol/kg/min v bendrofluazide 1.25 mg 2.2 (1.5) mumol/kg/min). Glucose 26-33 insulin Homo sapiens 202-209 8027028-1 1994 Glut2, the facilitative glucose transporter isoform expressed in pancreatic beta cells, is believed to play a role in glucose-stimulated insulin secretion. Glucose 24-31 insulin Homo sapiens 137-144 8017286-4 1994 Patients with a pretransplant diagnosis of ischemic heart disease had higher plasma glucose and insulin concentrations in response to oral glucose as well as higher fasting plasma triglyceride, cholesterol, and low-density lipoprotein cholesterol concentrations than did the control group (p < 0.005 to p < 0.001). Glucose 139-146 insulin Homo sapiens 96-103 7843475-0 1994 Measurement of insulin sensitivity by the minimal model method using a simplified intravenous glucose tolerance test: validity and reproducibility. Glucose 94-101 insulin Homo sapiens 15-22 7980344-2 1994 There is evidence that each of the control points of insulin on glucose metabolism are negatively influenced by lipid oversupply, a characteristic of the obese state. Glucose 64-71 insulin Homo sapiens 53-60 7981578-4 1994 In group I the insulin response to the glucose tolerance test showed hyperinsulinism and was lower than that in group II patients; stimulated C-peptide was also higher in group II than in group I and in controls; urinary C-peptide levels were parallel to those in previous data. Glucose 39-46 insulin Homo sapiens 15-22 7981578-5 1994 In all MD patients there were a negative correlation between absolute values of GH response to GHRH and insulin response to glucose tolerance test (r = -0.79, P < 0.001). Glucose 124-131 insulin Homo sapiens 104-111 7843475-1 1994 This study aimed at testing whether 12 rather than 26 plasma glucose and insulin determinations can be used to calculate the indices of insulin sensitivity and of glucose effectiveness using Bergman"s minimal model during a simple intravenous glucose tolerance test performed without tolbutamide injection. Glucose 61-68 insulin Homo sapiens 136-143 7843475-7 1994 In conclusion, in non-diabetic subjects, the insulin sensitivity index can be accurately measured during a simple intravenous glucose tolerance test, without tolbutamide injection and with only 12 blood samples. Glucose 126-133 insulin Homo sapiens 45-52 8027188-1 1994 In the beta-cells of pancreatic islets, insulin is stored as the predominant protein within storage granules that undergo regulated exocytosis in response to glucose. Glucose 158-165 insulin Homo sapiens 40-47 8013749-2 1994 Glucose was infused in a randomized fashion to maintain either a lower glucose level (6.6 +/- 0.3 mM, mean +/- SE) or hyperglycemia (11.8 +/- 0.8 mM) for 3 h. For insulin concentrations of 84 +/- 12 and 96 +/- 12 pM, hyperglycemia (11.8 +/- 0.8 mM) did not alter the plasma glycerol or lactate levels significantly but resulted in a significant (P < 0.0001) increase in plasma free fatty acid levels (0.49 +/- 0.13 vs. 0.32 +/- 0.08 mM). Glucose 0-7 insulin Homo sapiens 163-170 8013753-0 1994 Non-insulin-mediated glucose disappearance in subjects with IDDM. Glucose 21-28 insulin Homo sapiens 4-11 8013755-1 1994 Lithium is thought to have an insulin-like effect on glucose transport and metabolism in skeletal muscle and adipocytes. Glucose 53-60 insulin Homo sapiens 30-37 8013755-3 1994 Instead, lithium markedly increased the sensitivity of glucose transport to insulin, so that the increase in glucose transport activity induced by 300 pM insulin was approximately 2.5-fold greater in the presence of lithium than in its absence. Glucose 55-62 insulin Homo sapiens 76-83 8013756-2 1994 In vivo resistance to the action of insulin on glucose uptake has been documented during puberty. Glucose 47-54 insulin Homo sapiens 36-43 8013756-7 1994 The rates of insulin-stimulated glucose disposal (Rd) were measured during the clamp, whereas glucose and fat oxidation were measured by using indirect respiratory calorimetry. Glucose 32-39 insulin Homo sapiens 13-20 7982513-5 1994 During the oral glucose tolerance test glucose, C-peptide and insulin levels were measured at baseline and at 2 h. RESULTS: Insulin and C-peptide responses were significantly lower in pregnant women with impaired glucose tolerance and diabetes compared with women with normal glucose tolerance. Glucose 16-23 insulin Homo sapiens 124-131 8027228-12 1994 We conclude that sc rhIGF-I can reduce blood glucose effectively in selected patients with the type A phenotype of severe insulin resistance who have diabetes mellitus. Glucose 45-52 insulin Homo sapiens 122-129 8027230-0 1994 Insulin response to intravenous glucose in patients with anorexia nervosa showing low insulin response to oral glucose. Glucose 32-39 insulin Homo sapiens 0-7 8027230-0 1994 Insulin response to intravenous glucose in patients with anorexia nervosa showing low insulin response to oral glucose. Glucose 32-39 insulin Homo sapiens 86-93 8027230-0 1994 Insulin response to intravenous glucose in patients with anorexia nervosa showing low insulin response to oral glucose. Glucose 111-118 insulin Homo sapiens 0-7 8027230-0 1994 Insulin response to intravenous glucose in patients with anorexia nervosa showing low insulin response to oral glucose. Glucose 111-118 insulin Homo sapiens 86-93 8027230-1 1994 To investigate the cause of a low insulin secretory response to an oral glucose tolerance test (OGTT) in patients with anorexia nervosa (AN), we performed iv glucose tolerance tests (IVGTT) before and after treatment in 36 anorectic patients who showed low insulin secretion in response to the OGTT. Glucose 72-79 insulin Homo sapiens 34-41 8027230-3 1994 The results showed that the normal and flat type groups had normal glucose and insulin responses to iv glucose. Glucose 103-110 insulin Homo sapiens 79-86 8027230-6 1994 The rate of glucose disappearance for the IVGTT was lower both before and after weight gain in this subgroup compared to that in normal controls, suggesting insulin resistance. Glucose 12-19 insulin Homo sapiens 157-164 8027255-8 1994 The dextrose infusion rates required to maintain euglycemia were also higher in the insulin infusion study (0.44 +/- 0.03 vs. 0.32 +/- 0.03 mmol/kg.min; P = 0.003). Glucose 4-12 insulin Homo sapiens 84-91 8027259-3 1994 Hepatic glucose production (HGP) and insulin-stimulated glucose disposal were measured using [6,6-2H2]glucose and a stepwise hyperinsulinemic-euglycemic clamp. Glucose 56-63 insulin Homo sapiens 37-44 8027230-7 1994 In conclusion, the low insulin response to oral glucose seen in the flat type group may be due to the disturbance of gastrointestinal factors, such as motility. Glucose 48-55 insulin Homo sapiens 23-30 7913205-1 1994 The present study was designed to examine the effect of pulsatile versus continuous insulin delivery on glucose and lipid metabolism in insulin-resistant subjects. Glucose 104-111 insulin Homo sapiens 84-91 8027240-6 1994 During step 1 of each clamp, with insulin levels in the physiological range, glucose utilization decreased from 3.5 +/- 1.2 to 2.6 +/- 0.9 mmol/kg lean body mass (LBM).h in women treated with testosterone esters (P < 0.001) and from 3.2 +/- 0.7 to 2.5 +/- 0.5 mmol/kg lean body mass.h in men treated with ethinyl estradiol (P < 0.001). Glucose 77-84 insulin Homo sapiens 34-41 7521436-1 1994 A new side effect of interferon (IFN) therapy, glucose intolerance was investigated using insulin-clamp study. Glucose 47-54 insulin Homo sapiens 90-97 7521436-3 1994 Our data suggested that insulin resistance was the main reason for glucose intolerance observed during INF therapy in the patients with chronic active hepatitis C. Early detection and strict control of glucose intolerance could avoid the progress of glucose intolerance. Glucose 202-209 insulin Homo sapiens 24-31 8028511-2 1994 Its effects on glucose metabolism include suppression of glucose oxidation and may be associated with insulin resistance. Glucose 15-22 insulin Homo sapiens 102-109 8028513-1 1994 The insulin-mediated glucose disposal rate was assessed during a euglycemic hyperinsulinemic clamp in 16 normotensive men (mean age, 41 +/- 5 years) with positive family histories of hypertension and mild overweight (PFHO) and in 25 men with negative family histories of hypertension (NFH). Glucose 21-28 insulin Homo sapiens 4-11 8028513-5 1994 Insulin sensitivity, expressed as the glucose disposal rate per total body weight, was significantly (P < .01) decreased in PFHO subjects (7.7 +/- 3.0 mg/kg/min) and in NFHO subjects (7.1 +/- 3.5 mg/kg/min) as compared with NFHN subjects (11.1 +/- 4.0 mg/kg/min). Glucose 38-45 insulin Homo sapiens 0-7 8028514-4 1994 The increment in plasma glucose (AUC0-55 min) following glycerol infusion was greater during acute malaria compared with convalescence (median [range], +31.6 [-0.9 to +107.6] v +14.5 [-103 to +27.1] mmol.min-L-1, P < .05), but the insulin increments were similar (P = .9), indicating reduced tissue insulin sensitivity. Glucose 24-31 insulin Homo sapiens 234-241 7521436-3 1994 Our data suggested that insulin resistance was the main reason for glucose intolerance observed during INF therapy in the patients with chronic active hepatitis C. Early detection and strict control of glucose intolerance could avoid the progress of glucose intolerance. Glucose 67-74 insulin Homo sapiens 24-31 8028514-4 1994 The increment in plasma glucose (AUC0-55 min) following glycerol infusion was greater during acute malaria compared with convalescence (median [range], +31.6 [-0.9 to +107.6] v +14.5 [-103 to +27.1] mmol.min-L-1, P < .05), but the insulin increments were similar (P = .9), indicating reduced tissue insulin sensitivity. Glucose 24-31 insulin Homo sapiens 302-309 7521436-3 1994 Our data suggested that insulin resistance was the main reason for glucose intolerance observed during INF therapy in the patients with chronic active hepatitis C. Early detection and strict control of glucose intolerance could avoid the progress of glucose intolerance. Glucose 202-209 insulin Homo sapiens 24-31 7971909-1 1994 Studies of membrane receptor system in patients with insulin-dependent diabetes mellitus revealed that insulin resistance in pregnant patients with type I diabetes is caused by disordered cellular sensitivity to threshold physiological and submaximal insulin doses, whereas the maximal doses of the hormone normalize glucose consumption by the cells. Glucose 317-324 insulin Homo sapiens 103-110 7922295-0 1994 Insulin-mediated glucose disposal in black south Africans with essential hypertension. Glucose 17-24 insulin Homo sapiens 0-7 7949222-4 1994 After insulin therapy was re-introduced, catch-up growth and normalization of the blood glucose and IGF-I levels were noted. Glucose 88-95 insulin Homo sapiens 6-13 8202531-2 1994 We report a physiologically relevant system for dissecting the molecular mechanisms of insulin signal transduction related to glucose transport. Glucose 126-133 insulin Homo sapiens 87-94 8202531-8 1994 These results demonstrate that insulin receptor tyrosine kinase activity is essential in insulin-stimulated glucose transport in adipose cells. Glucose 108-115 insulin Homo sapiens 31-38 8202531-8 1994 These results demonstrate that insulin receptor tyrosine kinase activity is essential in insulin-stimulated glucose transport in adipose cells. Glucose 108-115 insulin Homo sapiens 89-96 8023270-3 1994 RESULTS: Glucose metabolized (milligrams per kilogram per minute), metabolic clearance rate of glucose (milliliters per kilogram per minute), and glucose metabolized per unit of insulin (milligrams per kilogram per minute/microunits per milligram) were significantly decreased in the cancer group compared with the control (4.50 +/- 1.32 vs 8.11 +/- 0.56 mg/kg/min, 5.26 +/- 2.22 vs 10.67 +/- 1.98 ml/kg/min, and 4.34 +/- 1.16 vs 8.92 +/- 1.03 mg/kg/min/uU/ml, respectively), regardless of the weight loss. Glucose 146-153 insulin Homo sapiens 178-185 8010960-0 1994 Stimulation of glucose uptake by insulin-like growth factor II in human muscle is not mediated by the insulin-like growth factor II/mannose 6-phosphate receptor. Glucose 15-22 insulin Homo sapiens 33-40 8003509-2 1994 Here we report that clonal insulin-secreting HIT beta-cells contain substantial amounts of endogenous plasmalogens and express a similar ASCI-PLA2 activity with the following properties: (1) Enzymatic activity as well as glucose-induced eicosanoid release and insulin secretion are inhibited by a mechanism-based suicide substrate directed towards ASCI-PLA2. Glucose 221-228 insulin Homo sapiens 27-34 8199182-7 1994 Resistance to insulin-stimulated glucose uptake and to insulin suppression of free fatty acid levels in Asian Indians is associated with a number of metabolic abnormalities that are demonstrated risk factors for coronary heart disease, including increased glucose, insulin, and triglyceride concentrations and decreased high-density lipoprotein cholesterol concentrations. Glucose 33-40 insulin Homo sapiens 14-21 8198053-3 1994 After the glucose clamp, insulin-mediated stimulation 2 of whole-body glucose disposal (18.4 +/- 0.5 vs 26.1 +/- 0.6 mumol.min/kg lean body mass P < 0.02) was significantly potentiated by vitamin E rather than placebo administration. Glucose 10-17 insulin Homo sapiens 25-32 8198053-3 1994 After the glucose clamp, insulin-mediated stimulation 2 of whole-body glucose disposal (18.4 +/- 0.5 vs 26.1 +/- 0.6 mumol.min/kg lean body mass P < 0.02) was significantly potentiated by vitamin E rather than placebo administration. Glucose 70-77 insulin Homo sapiens 25-32 8198053-4 1994 Furthermore, net changes in plasma vitamin E concentrations correlated with net changes in insulin-stimulated whole-body glucose disposal (r = 0.60 P < 0.003). Glucose 121-128 insulin Homo sapiens 91-98 8023918-1 1994 Insulin"s ability to stimulate glucose metabolism is reduced during normal puberty; these changes are exaggerated in adolescents with insulin-dependent diabetes mellitus (IDDM). Glucose 31-38 insulin Homo sapiens 0-7 8023918-3 1994 IDDM subjects received overnight low-dose insulin infusion to normalize fasting glucose. Glucose 80-87 insulin Homo sapiens 42-49 8023918-5 1994 Insulin-stimulated glucose metabolism was reduced by 40% in healthy adolescents vs. adults (P < 0.05) and by an additional 40% in poorly controlled IDDM (P < 0.05 vs, normal adolescents). Glucose 19-26 insulin Homo sapiens 0-7 8023918-6 1994 Although basal glucose and lipid oxidation rates (measured by indirect calorimetry) were similar in all three groups, when insulin was infused, glucose oxidation increased and lipid oxidation decreased only in the two nondiabetic groups. Glucose 144-151 insulin Homo sapiens 123-130 8023918-11 1994 We conclude that insulin resistance of puberty is selective for glucose metabolism, sparing amino acid/protein metabolism. Glucose 64-71 insulin Homo sapiens 17-24 8199182-7 1994 Resistance to insulin-stimulated glucose uptake and to insulin suppression of free fatty acid levels in Asian Indians is associated with a number of metabolic abnormalities that are demonstrated risk factors for coronary heart disease, including increased glucose, insulin, and triglyceride concentrations and decreased high-density lipoprotein cholesterol concentrations. Glucose 256-263 insulin Homo sapiens 14-21 8199182-7 1994 Resistance to insulin-stimulated glucose uptake and to insulin suppression of free fatty acid levels in Asian Indians is associated with a number of metabolic abnormalities that are demonstrated risk factors for coronary heart disease, including increased glucose, insulin, and triglyceride concentrations and decreased high-density lipoprotein cholesterol concentrations. Glucose 256-263 insulin Homo sapiens 55-62 8199182-7 1994 Resistance to insulin-stimulated glucose uptake and to insulin suppression of free fatty acid levels in Asian Indians is associated with a number of metabolic abnormalities that are demonstrated risk factors for coronary heart disease, including increased glucose, insulin, and triglyceride concentrations and decreased high-density lipoprotein cholesterol concentrations. Glucose 256-263 insulin Homo sapiens 55-62 7923256-5 1994 Body weight increased in a dose dependent manner, while atrial natriuretic peptide, serum glucose and insulin during oral glucose tolerance test, total cholesterol, HDL and LDL cholesterol, triglycerides were unaffected. Glucose 122-129 insulin Homo sapiens 102-109 8054148-3 1994 Intravenous insulin infusion monitored by hourly glucose levels was required to manage this hyperglycaemia. Glucose 49-56 insulin Homo sapiens 12-19 8062504-14 1994 Hyperketonaemia appears to prevent insulin-stimulated glucose oxidation, but does not reduce insulin-mediated glucose storage. Glucose 54-61 insulin Homo sapiens 35-42 7926344-4 1994 The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p = 0.04). Glucose 27-34 insulin Homo sapiens 67-74 7926345-1 1994 Prospective studies have shown a relationship between hyperinsulinaemia, an indirect index of insulin resistance, and IHD in men with normal glucose tolerance. Glucose 141-148 insulin Homo sapiens 59-66 8088120-7 1994 In the transient IGT group, despite similar plasma glucose levels, the insulin responses at 0, 15, 30, and 60 min (p < 0.01, p < 0.001, p < 0.001, p < 0.001, respectively) were lower than in the control group; the 30-min insulin/glucose ratio (7.1 +/- 5.1 vs 13.3 +/- 8.7, p < 0.001) and 60-min insulinogenic index (46.9 +/- 86.3 vs 123.4 +/- 206.3, p < 0.001) were also lower in the transient IGT group. Glucose 241-248 insulin Homo sapiens 71-78 8088119-0 1994 Loss of the first phase insulin response to intravenous glucose in subjects with persistent impaired glucose tolerance. Glucose 56-63 insulin Homo sapiens 24-31 8088121-10 1994 Multiple regression analysis showed that in urban population the fasting insulin was correlated to the BMI and the 2h IRI to 2 h glucose, BMI and the subscapular:triceps ratio. Glucose 129-136 insulin Homo sapiens 73-80 8088119-1 1994 Loss of the first phase insulin response to intravenous glucose is one of the earliest detectable defects of beta cell dysfunction in Type 2 diabetes mellitus. Glucose 56-63 insulin Homo sapiens 24-31 8088119-7 1994 Thus subjects with persistent impaired glucose tolerance demonstrated loss of the first phase insulin response as an early indicator of beta cell dysfunction while subjects with transient IGT had a normal insulin response to intravenous glucose. Glucose 39-46 insulin Homo sapiens 94-101 7919903-1 1994 OBJECTIVE: The goal of this study was to examine the metabolic and hemodynamic effects of a glucose-insulin-potassium infusion in elective coronary surgery, when blood cardioplegia was used for cardiac protection. Glucose 92-99 insulin Homo sapiens 100-107 8194667-5 1994 Moreover, the number of capillaries per muscle fiber and the 2-h insulin value in the oral glucose tolerance test were highly correlated (r = 0.82, P < 0.005), whereas no correlation was found among IGT subjects who remained nondiabetic and in the control group. Glucose 91-98 insulin Homo sapiens 65-72 8194667-6 1994 With body mass index and the 2-h glucose concentration included in a regression model, 68% of the variation in the number of capillaries per muscle fiber was explained (P < 0.05), with the 2-h insulin value independently accounting for 33%. Glucose 33-40 insulin Homo sapiens 196-203 8194670-5 1994 With 3.3 mM glucose (n = 17), insulin oscillations were demonstrated with a periodicity of 9.8 +/- 0.1 min (means +/- SE), mean amplitude was 16.8 +/- 1.8 pM, and overall mean insulin release was 43.8 +/- 4.2 pM. Glucose 12-19 insulin Homo sapiens 30-37 8205258-8 1994 The insulinogenic index (insulin/glucose) response to a glucose challenge decreased uniformly in octreotide-treated patients. Glucose 33-40 insulin Homo sapiens 4-11 8205258-8 1994 The insulinogenic index (insulin/glucose) response to a glucose challenge decreased uniformly in octreotide-treated patients. Glucose 56-63 insulin Homo sapiens 4-11 7927191-3 1994 The affinity of the receptor for insulin, however, was reduced in both obese subjects and patients with NIDDM as compared to non-obese subjects with normal glucose tolerance. Glucose 156-163 insulin Homo sapiens 33-40 7927191-6 1994 In contrast, insulin-stimulated tyrosine kinase activity, when normalized to insulin binding activity, was unchanged in both non-obese and obese subjects with normal glucose tolerance, but was reduced approximately 60% in the NIDDM group. Glucose 166-173 insulin Homo sapiens 13-20 8206589-6 1994 However, insulin sensitivity, defined as glucose uptake in the presence of 900 pmol/L insulin minus basal, was depressed in the high-fructose compared with the control group (1.02 +/- 0.38 to 1.77 +/- 0.57 mumol/g per hour, P < .05). Glucose 41-48 insulin Homo sapiens 9-16 7959906-5 1994 However, only KH1060 opposed the suppressive effect of IL-1 beta on islet glucose-stimulated insulin secretion and glucose oxidation rate despite the fact that KH1060 itself reduced the islet DNA and insulin content by approximately 10% and 30%, respectively. Glucose 74-81 insulin Homo sapiens 93-100 8206563-4 1994 To test this possibility, we measured the plasma insulin response to an oral glucose load in 25 patients with or without microalbuminuria and 20 normotensive control subjects. Glucose 77-84 insulin Homo sapiens 49-56 8206563-6 1994 In the hypertensive patients as a group, the plasma insulin response to glucose (evaluated as the insulin area under the curve) was significantly enhanced compared with a group of 20 normotensive healthy control subjects (46,311 +/- 3745 and 27,557 +/- 2563 pmol/L x 2 hours, P < .01). Glucose 72-79 insulin Homo sapiens 52-59 8206589-6 1994 However, insulin sensitivity, defined as glucose uptake in the presence of 900 pmol/L insulin minus basal, was depressed in the high-fructose compared with the control group (1.02 +/- 0.38 to 1.77 +/- 0.57 mumol/g per hour, P < .05). Glucose 41-48 insulin Homo sapiens 86-93 8206563-6 1994 In the hypertensive patients as a group, the plasma insulin response to glucose (evaluated as the insulin area under the curve) was significantly enhanced compared with a group of 20 normotensive healthy control subjects (46,311 +/- 3745 and 27,557 +/- 2563 pmol/L x 2 hours, P < .01). Glucose 72-79 insulin Homo sapiens 98-105 8206593-7 1994 The hypertensive patients were significantly less insulin sensitive than their normotensive counterparts, as reflected by a lower glucose utilization rate and higher mean baseline plasma insulin level (P < .05 for each). Glucose 130-137 insulin Homo sapiens 50-57 7614420-10 1994 A significant positive correlation was found between insulin levels after the glucose load and the rate-pressure product increment with exercise (60 min, r = 0.60; 120 min, r = 0.65). Glucose 78-85 insulin Homo sapiens 53-60 7921578-4 1994 There was evidence of inhibition of glucose metabolism ("insulin resistance"), but none for any particular mechanism. Glucose 36-43 insulin Homo sapiens 57-64 7928862-1 1994 Exercise adds to the effect of maximal insulin on whole body glucose uptake. Glucose 61-68 insulin Homo sapiens 39-46 7852223-2 1994 Serum insulin (IRI) and C-peptide (CP) responses to oral glucose were reevaluated three years after the initial study in 25 normoglycaemic offspring of conjugal Type 2 diabetic parents. Glucose 57-64 insulin Homo sapiens 24-33 8200993-2 1994 After 60 min of euglycemia (plasma insulin approximately 140 microU/ml), plasma glucose was lowered to 62 +/- 2 mg/dl by 120 min. Glucose 80-87 insulin Homo sapiens 35-42 8200955-6 1994 In the last 60 min of the glucose clamp, insulin-mediated glucose disappearance, total body glucose disposal (24.5 +/- 0.4 vs. 28.2 +/- 0.7 mumol/kg.min; P < 0.005), and glucose oxidation (13.0 +/- 0.4 vs. 16.3 +/- 0.8 mumol/kg.min; P < 0.01) were increased after chronic magnesium supplementation. Glucose 58-65 insulin Homo sapiens 41-48 8200955-6 1994 In the last 60 min of the glucose clamp, insulin-mediated glucose disappearance, total body glucose disposal (24.5 +/- 0.4 vs. 28.2 +/- 0.7 mumol/kg.min; P < 0.005), and glucose oxidation (13.0 +/- 0.4 vs. 16.3 +/- 0.8 mumol/kg.min; P < 0.01) were increased after chronic magnesium supplementation. Glucose 58-65 insulin Homo sapiens 41-48 8201261-4 1994 The area under the insulin curve after oral glucose tolerance fell 33% (p = 0.0001), while the ratio of insulin area to glucose area fell 22% (p = 0.006). Glucose 44-51 insulin Homo sapiens 19-26 8207367-8 1994 Within this group there was a significant correlation between insulin and triglyceride (r = 0.30; P < 0.05), high-density lipoprotein (HDL) cholesterol (r = 0.24; P < 0.05) and glucose (r = 0.30; P < 0.05). Glucose 183-190 insulin Homo sapiens 62-69 8207367-11 1994 CONCLUSIONS: There is a relationship between insulin and triglyceride, HDL cholesterol and glucose but not blood pressure, cholesterol or low-density-lipoprotein (LDL) cholesterol in a healthy population at high risk of ischaemic heart disease. Glucose 91-98 insulin Homo sapiens 45-52 7968932-6 1994 Home glucose monitoring must be used to adjust insulin doses. Glucose 5-12 insulin Homo sapiens 47-54 8201958-5 1994 Baseline blood and urine samples were obtained for several hormone and lipid determinations, and the response of glucose, insulin, and C-peptide to a glucose oral challenge (75 g) was investigated. Glucose 150-157 insulin Homo sapiens 122-129 8201958-5 1994 Baseline blood and urine samples were obtained for several hormone and lipid determinations, and the response of glucose, insulin, and C-peptide to a glucose oral challenge (75 g) was investigated. Glucose 150-157 insulin Homo sapiens 135-144 7920639-5 1994 This locus, which is important for normal glucose-regulated insulin secretion, represents a candidate gene for studies of other diseases of beta-cell dysfunction including non-insulin-dependent diabetes mellitus (NIDDM). Glucose 42-49 insulin Homo sapiens 60-67 8720766-7 1994 Serum insulin levels after glucose administration were lower when the patients were treated with felodipine than when taking hydrochlorothiazide. Glucose 27-34 insulin Homo sapiens 6-13 8720766-8 1994 A possible explanation for this observation may be an increased insulin release as a consequence of treatment with a diuretic in order to maintain normal blood glucose levels during the glucose tolerance test. Glucose 160-167 insulin Homo sapiens 64-71 8720766-8 1994 A possible explanation for this observation may be an increased insulin release as a consequence of treatment with a diuretic in order to maintain normal blood glucose levels during the glucose tolerance test. Glucose 186-193 insulin Homo sapiens 64-71 7937632-7 1994 The blood glucose level thus corresponds to hepatic production and insulin sensitivity is expressed as the amount of glucose infused in mg/kglmin. Glucose 10-17 insulin Homo sapiens 67-74 7937632-7 1994 The blood glucose level thus corresponds to hepatic production and insulin sensitivity is expressed as the amount of glucose infused in mg/kglmin. Glucose 117-124 insulin Homo sapiens 67-74 7937632-10 1994 Steady state plasma glucose relies on drugs which suppress endogenous insulin secretion. Glucose 20-27 insulin Homo sapiens 70-77 7937632-11 1994 Glucose and insulin are then infused at constant rates and the resulting glucose and insulin levels express insulin sensitivity. Glucose 73-80 insulin Homo sapiens 12-19 8197147-4 1994 Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. Glucose 103-110 insulin Homo sapiens 84-91 8060573-12 1994 As shown by the increase of CLi and (CLi-CNa/CLi, and the decrease of UNaV and CNa/CLi in the glucose clamp group, insulin decreases urinary sodium excretion by increasing distal sodium reabsorption, whereas it inhibits sodium reabsorption in the proximal tubule. Glucose 94-101 insulin Homo sapiens 115-122 8060574-4 1994 In the nondiabetic group, doxazosin treatment was associated with significant improvement in insulin-mediated glucose disposal (P < .05) and lower plasma insulin (P < .001), and triglyceride (P < .001) concentrations measured at hourly intervals from 8 AM to 4 PM (breakfast at 8 AM and lunch at noon). Glucose 110-117 insulin Homo sapiens 93-100 8060581-2 1994 The plasma glucose and insulin response to 75 g oral glucose intake was assessed on low (34 mmol/day) and high (342 mmol/day) NaCl diets in 31 patients with essential hypertension, and the area under the curve for both variables (AUCglu and AUCins) was calculated. Glucose 53-60 insulin Homo sapiens 23-30 8042763-13 1994 After determination of the fasting blood glucose level, insulin is given at a dosage of 0.5-1 U.h-1 (at gluc < 11.1 mmol.l-1), 1.5-2 U.h-1 (at gluc 11.1-16.7 mmol.l-1) or 3 U.h-1 (at gluc > 16.7 mmol.l-1). Glucose 41-48 insulin Homo sapiens 56-63 7514870-2 1994 Previous studies have shown that pretreatment of islets for 18 h with IL-1 beta results in an inhibition of glucose-stimulated insulin secretion that requires 4 days incubation in the absence of IL-1 beta to restore islet secretory function. Glucose 108-115 insulin Homo sapiens 127-134 7514870-5 1994 Inhibition of NO synthase also restores IL-1 beta-induced inhibition of mitochondrial aconitase activity in a time-dependent fashion that mimics the recovery of glucose-stimulated insulin secretion by islets. Glucose 161-168 insulin Homo sapiens 180-187 7945558-22 1994 An estimate of insulin resistance (EIR), calculated from plasma insulin and glucose in part of the study population (n = 145), was significantly higher in the subjects with a B-pattern than in those with an A-pattern (3.12 vs. 2.00, P < 0.003). Glucose 76-83 insulin Homo sapiens 15-22 7945563-7 1994 Glucose caused a concentration dependent (up to 10 mM) stimulation of LDL oxidation reaching 85% and 77% at insulin concentrations of 10(-7) M and 10(-6) M, respectively. Glucose 0-7 insulin Homo sapiens 108-115 7525376-0 1994 Tyrosine kinase inhibitors inhibit glucose-stimulated insulin secretion. Glucose 35-42 insulin Homo sapiens 54-61 8069407-4 1994 The insulin sensitivity index (glucose disposal rate divided by mean insulin concentration during clamp) increased from 7.7 +/- 4.5 to 10.1 +/- 4.1 arbitrary units (30%, p < 0.05). Glucose 31-38 insulin Homo sapiens 4-11 7947248-7 1994 The findings are consistent with the hypothesis that the plasma cell tumour was associated with excessive production of insulin-like peptides with consequent reduction in the blood glucose level. Glucose 181-188 insulin Homo sapiens 120-127 8013142-2 1994 The short insulin tolerance test is a simple and rapid method for screening large numbers of subjects when the fasting glucose level is normal. Glucose 119-126 insulin Homo sapiens 10-17 8013142-8 1994 MEASUREMENTS: Insulin sensitivity was measured in the short insulin tolerance test using the slope of arterialized blood glucose concentration from 3 to 15 minutes after an intravenous bolus of short-acting insulin, 0.05 units/kg body weight. Glucose 121-128 insulin Homo sapiens 14-21 8013142-9 1994 In the clamp study, insulin sensitivity was derived from the average amount of glucose infused at steady state (M) and the mean plasma insulin level (I). Glucose 79-86 insulin Homo sapiens 20-27 8026143-7 1994 Insulin restored near-normoglycaemia (7.4 +/- 0.8 mmole l-1) and normalized rates of glucose appearance and glucose cycling. Glucose 85-92 insulin Homo sapiens 0-7 8026143-7 1994 Insulin restored near-normoglycaemia (7.4 +/- 0.8 mmole l-1) and normalized rates of glucose appearance and glucose cycling. Glucose 108-115 insulin Homo sapiens 0-7 8168643-1 1994 Although successful pancreas transplantation in humans with type I diabetes mellitus restores glucose-induced insulin secretion, provides freedom from insulin treatment, and normalizes fasting glucose levels, much less is known about its effects on counterregulation of hypoglycemia. Glucose 94-101 insulin Homo sapiens 110-117 8168647-6 1994 Insulin sensitivity evaluated as the rate of glucose uptake during a three-step hyperinsulinemic euglycemic clamp was comparable in the obese (20 +/- 1.5 mmol.m-2.min-1) and the normal (21.7 +/- 1.5 mmol.m-2.min-1) children. Glucose 45-52 insulin Homo sapiens 0-7 8168647-7 1994 Initially higher than normal in obese children, the maximal rate of glucose uptake decreased with both obesity duration (r = -0.67, P < 0.005) and children"s age (r = -0.66, P < 0.005), indicating the progressive development of insulin resistance. Glucose 68-75 insulin Homo sapiens 234-241 8168650-1 1994 The relationship between the in vivo insulin secretory responsiveness of the pancreatic beta-cell to glucose and the flux of glucose through the enzyme glucokinase was investigated in six subjects with heterozygous glucokinase mutations and in six matched control subjects. Glucose 101-108 insulin Homo sapiens 37-44 8168650-1 1994 The relationship between the in vivo insulin secretory responsiveness of the pancreatic beta-cell to glucose and the flux of glucose through the enzyme glucokinase was investigated in six subjects with heterozygous glucokinase mutations and in six matched control subjects. Glucose 125-132 insulin Homo sapiens 37-44 7921517-0 1994 Pharmacodynamics of a continuous intravenous infusion of CGP-35126 recombinant human insulin-like growth factor-I (rhIGF-I) on glucose and insulin levels in healthy males. Glucose 127-134 insulin Homo sapiens 85-92 8061724-6 1994 Insulin concentrations were significantly increased by lipids both during infusion of glucose alone and of glucose+amino acids. Glucose 86-93 insulin Homo sapiens 0-7 8061724-6 1994 Insulin concentrations were significantly increased by lipids both during infusion of glucose alone and of glucose+amino acids. Glucose 107-114 insulin Homo sapiens 0-7 8175958-4 1994 When glucose levels were between 2.8 mmol/L (50 mg/dL) and 3.3 mmol/L (60 mg/dL) at the end of the prolonged fast, proinsulin was better than C-peptide and insulin in the diagnosis of insulinoma. Glucose 5-12 insulin Homo sapiens 115-125 8175958-4 1994 When glucose levels were between 2.8 mmol/L (50 mg/dL) and 3.3 mmol/L (60 mg/dL) at the end of the prolonged fast, proinsulin was better than C-peptide and insulin in the diagnosis of insulinoma. Glucose 5-12 insulin Homo sapiens 118-125 8175959-0 1994 Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance. Glucose 35-42 insulin Homo sapiens 15-22 8175959-0 1994 Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance. Glucose 35-42 insulin Homo sapiens 58-65 8175959-0 1994 Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance. Glucose 128-135 insulin Homo sapiens 15-22 8175959-0 1994 Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance. Glucose 128-135 insulin Homo sapiens 58-65 8175959-3 1994 Compared with control subjects, women with PCOS and normal glucose tolerance had an increased (36-56%) insulin increment, not explained by insulin resistance, and over the whole range of BMI. Glucose 59-66 insulin Homo sapiens 103-110 8175959-7 1994 It is concluded that the early insulin response to glucose was increased in women with PCOS, not accounted for by insulin resistance, closely associated to the increased androgenicity, and present also at low-normal BMI. Glucose 51-58 insulin Homo sapiens 31-38 8175987-0 1994 Amylin/insulin secretory ratios in morbidly obese man: inverse relationship with glucose disappearance rate. Glucose 81-88 insulin Homo sapiens 7-14 8175987-4 1994 Portal venous amylin and insulin concentrations peak 90 s after the initiation of a 2-min glucose infusion. Glucose 90-97 insulin Homo sapiens 25-32 8175987-7 1994 The amylin/insulin secretory ratios calculated at the time of surgery varied inversely (r = -0.89; P < 0.001) with glucose disappearance rates obtained 5-7 months later after 19- to 29-kg weight loss. Glucose 118-125 insulin Homo sapiens 11-18 8182159-0 1994 Glucagon-like peptide 1 enhances glucose tolerance both by stimulation of insulin release and by increasing insulin-independent glucose disposal. Glucose 33-40 insulin Homo sapiens 74-81 8182159-0 1994 Glucagon-like peptide 1 enhances glucose tolerance both by stimulation of insulin release and by increasing insulin-independent glucose disposal. Glucose 33-40 insulin Homo sapiens 108-115 8182159-0 1994 Glucagon-like peptide 1 enhances glucose tolerance both by stimulation of insulin release and by increasing insulin-independent glucose disposal. Glucose 128-135 insulin Homo sapiens 108-115 8182159-11 1994 Furthermore, this peptide may be useful for studying the process of insulin-independent glucose disposal, and pharmacologic analogues may be beneficial for treating patients with diabetes mellitus. Glucose 88-95 insulin Homo sapiens 68-75 8182160-0 1994 Different alterations in the insulin-stimulated glucose uptake in the athlete"s heart and skeletal muscle. Glucose 48-55 insulin Homo sapiens 29-36 8182160-10 1994 Thus, in athletes, (a) insulin-stimulated glucose uptake is enhanced in the whole body and skeletal muscles, (b) whereas myocardial glucose uptake per muscle mass is reduced possibly due to decreased wall stress and energy requirements or the use of alternative fuels, or both. Glucose 42-49 insulin Homo sapiens 23-30 8071604-4 1994 As the steady-state plasma insulin levels were essentially identical in the two groups (approximately 1000 pmol/l), these results show that whole body insulin-mediated glucose disposal was unchanged in the transgenic mice. Glucose 168-175 insulin Homo sapiens 151-158 8071604-5 1994 Finally, values for isoproterenol-stimulated lipolysis, insulin-inhibition of lipolysis, and insulin-stimulated glucose disposal were similar in adipocytes isolated from transgenic and control mice. Glucose 112-119 insulin Homo sapiens 93-100 8061905-2 1994 The model attempts to reflect the underlying (patho)physiology of insulin action and carbohydrate absorption in quantitative terms such as insulin sensitivity, volume of glucose and insulin distribution and maximal rate of gastric emptying. Glucose 170-177 insulin Homo sapiens 66-73 8177047-1 1994 We have previously shown that human circulating mononuclear cells (CMCs) respond to physiological concentrations of insulin with a rapid increase in glucose transport rate. Glucose 149-156 insulin Homo sapiens 116-123 8177047-2 1994 The responding cells were found to be the monocytes, and cells derived from individuals with insulin-dependent diabetes mellitus (IDDM) had lower basal and insulin-stimulated glucose transport rates. Glucose 175-182 insulin Homo sapiens 93-100 8177047-5 1994 The time course of insulin-stimulated glucose uptake in CMCs was rapid, reaching a plateau within 30 minutes. Glucose 38-45 insulin Homo sapiens 19-26 8177054-4 1994 Obese subjects were more resistant to insulin with respect to its effects on glucose metabolism than normal-weight controls, as calculated by the method described by Matthews. Glucose 77-84 insulin Homo sapiens 38-45 8177055-4 1994 After covariance adjusting for changes in the QI and WHR, on Metformin the area under the insulin curve (IA) during oral glucose tolerance testing decreased 35% (P = .04), and the insulin area to glucose area ratio decreased 31% (P = .03). Glucose 121-128 insulin Homo sapiens 90-97 8177055-4 1994 After covariance adjusting for changes in the QI and WHR, on Metformin the area under the insulin curve (IA) during oral glucose tolerance testing decreased 35% (P = .04), and the insulin area to glucose area ratio decreased 31% (P = .03). Glucose 196-203 insulin Homo sapiens 180-187 8190093-10 1994 Together, our data show that interaction between GLP-1 and glucose signaling pathways in beta cells may be mediated uniquely by an increase in the intracellular cAMP concentration, with the consequent activation of protein kinase A and phosphorylation of elements of the glucose-sensing apparatus or of the insulin granule exocytic machinery. Glucose 59-66 insulin Homo sapiens 307-314 8190093-10 1994 Together, our data show that interaction between GLP-1 and glucose signaling pathways in beta cells may be mediated uniquely by an increase in the intracellular cAMP concentration, with the consequent activation of protein kinase A and phosphorylation of elements of the glucose-sensing apparatus or of the insulin granule exocytic machinery. Glucose 271-278 insulin Homo sapiens 307-314 10742775-3 1994 The ratio of the area under the curve (AUC) for glucose over that of insulin was used as a measure of insulin sensitivity. Glucose 48-55 insulin Homo sapiens 102-109 10742775-9 1994 In conclusion, the present study indicates that, after a body weight reduction operation capable of almost re-establishing ideal body weight like BPD, obese individuals with a family history of obesity show a normalization of insulin response to glucose load. Glucose 246-253 insulin Homo sapiens 226-233 8036449-0 1994 Insulin and PAI-1 levels during oral glucose tolerance test in patients with coronary heart disease. Glucose 37-44 insulin Homo sapiens 0-7 8036449-3 1994 All subjects in the OGTT group were adequate responders to glucose administration, giving peak values of glucose (median 6.90 mmol l-1) and insulin (median 123 mU l-1) after 1 h. TG were unchanged throughout the test period in both groups. Glucose 59-66 insulin Homo sapiens 140-147 7909102-6 1994 The glucose fatty-acid cycle may operate in patients with severe insulin resistance and hyperlipidaemia: high serum NEFA aggravates insulin resistance and hyperglycaemia by inhibiting glucose uptake and utilisation. Glucose 4-11 insulin Homo sapiens 65-72 7909102-6 1994 The glucose fatty-acid cycle may operate in patients with severe insulin resistance and hyperlipidaemia: high serum NEFA aggravates insulin resistance and hyperglycaemia by inhibiting glucose uptake and utilisation. Glucose 4-11 insulin Homo sapiens 132-139 8159103-3 1994 Insulin-mediated glucose disposal (M) and the insulin sensitivity index (M/I) increased by 19% (P = .011) and 10% (P = .27), respectively, during dilevalol treatment, but decreased by 10% (P = .15) and 22% (P = .0025), respectively, during metoprolol treatment, giving rise to significant differences between the two treatment regimens. Glucose 17-24 insulin Homo sapiens 0-7 7930477-1 1994 The effects of glucose and insulin administration on splanchnic and leg exchange of glucose were investigated in seven patients with cirrhosis and six sex- and age-matched healthy controls using the catheter technique. Glucose 84-91 insulin Homo sapiens 27-34 8159098-0 1994 Effects of glucose and amino acid infusion on glucose turnover in insulin-resistant obese and type II diabetic patients. Glucose 46-53 insulin Homo sapiens 66-73 7511205-8 1994 In addition, insulin-mediated glucose transport was not potentiated by thrombin or EGF. Glucose 30-37 insulin Homo sapiens 13-20 7511205-9 1994 Although these results cannot exclude the possibility that p21ras and/or MAP kinase is needed in conjunction with other signaling molecules that are activated by insulin and not by thrombin or EGF, they show that the Ras/MAP kinase signaling pathway alone is not sufficient to induce insulin-mediated glucose transport. Glucose 301-308 insulin Homo sapiens 162-169 8199181-3 1994 Lipoprotein size was measured by nondenaturing polyacrylamide gradient gel electrophoresis; insulin sensitivity was assessed by using a euglycemic hyperinsulinemic clamp and [6,6(2)H]glucose tracer infusion for simultaneous measurement of hepatic glucose output and whole-body glucose utilization. Glucose 183-190 insulin Homo sapiens 92-99 8199182-0 1994 Resistance to insulin-stimulated glucose uptake and dyslipidemia in Asian Indians. Glucose 33-40 insulin Homo sapiens 14-21 8016951-7 1994 The newly-diagnosed NIDDM patients mostly suffered from diseases related to the insulin resistance syndrome, and we thus recommend measurement of non-fasting blood-glucose as a screening procedure in such patients. Glucose 164-171 insulin Homo sapiens 80-87 8036284-1 1994 Despite similar glycemic profiles, higher insulin levels are achieved following oral versus intravenous administration of glucose. Glucose 122-129 insulin Homo sapiens 42-49 8036284-8 1994 In normal subjects, at a glucose level of 10.4 mmol/l, the 90-120 min insulin response was 279 pmol/l. Glucose 25-32 insulin Homo sapiens 70-77 8036284-13 1994 The additive insulinotropic effect suggests that more than one incretin may be responsible for the greater insulin levels observed following oral administration of glucose compared to the intravenous route. Glucose 164-171 insulin Homo sapiens 13-20 8043893-3 1994 Insulin secretion was measured in an intravenous glucose tolerance test (IVGTT) and insulin sensitivity by the hyperinsulinaemic euglycaemic clamp test. Glucose 49-56 insulin Homo sapiens 0-7 8043893-4 1994 Both the early insulin response in the IVGTT (increment) and the glucose disposal rate in the clamp test (M-value) were found to be related hyperbolically to fasting glucose (r = -0.63 and -0.66, respectively; both P < 0.0001) and in a second-order polynomial manner to the glucose disappearance rate (k-value) in the IVGTT (r = 0.53 and 0.48, respectively; both P < 0.0001). Glucose 166-173 insulin Homo sapiens 15-22 8043893-4 1994 Both the early insulin response in the IVGTT (increment) and the glucose disposal rate in the clamp test (M-value) were found to be related hyperbolically to fasting glucose (r = -0.63 and -0.66, respectively; both P < 0.0001) and in a second-order polynomial manner to the glucose disappearance rate (k-value) in the IVGTT (r = 0.53 and 0.48, respectively; both P < 0.0001). Glucose 166-173 insulin Homo sapiens 15-22 8043893-5 1994 Multiple regression analysis showed the insulin increment in the IVGTT and the M-value in the clamp test to be equally important determinants of glucose tolerance, together explaining about 50% of the variation in fasting glucose and the k-value in the IVGTT. Glucose 145-152 insulin Homo sapiens 40-47 8043893-5 1994 Multiple regression analysis showed the insulin increment in the IVGTT and the M-value in the clamp test to be equally important determinants of glucose tolerance, together explaining about 50% of the variation in fasting glucose and the k-value in the IVGTT. Glucose 222-229 insulin Homo sapiens 40-47 8043893-7 1994 However, low levels of insulin increment in the IVGTT were more often associated with glucose intolerance than was a low insulin sensitivity. Glucose 86-93 insulin Homo sapiens 23-30 8043894-6 1994 Moreover, GZ resulted in a significant increase in the immunoreactive abundance of the insulin-regulatable glucose transport protein (GLUT 4) (P < 0.02). Glucose 107-114 insulin Homo sapiens 87-94 8043900-1 1994 Hypertriglyceridaemia is associated with insulin resistance of both lipid and glucose metabolism. Glucose 78-85 insulin Homo sapiens 41-48 8043900-5 1994 This was associated with impaired insulin-stimulated glucose uptake (P < 0.05), predominantly in the non-oxidative pathway (P < 0.05). Glucose 53-60 insulin Homo sapiens 34-41 8043900-8 1994 In conclusion, the insulin resistance of glucose metabolism associated with hypertriglyceridaemia is largely due to a defect in non-oxidative glucose metabolism. Glucose 41-48 insulin Homo sapiens 19-26 8043900-8 1994 In conclusion, the insulin resistance of glucose metabolism associated with hypertriglyceridaemia is largely due to a defect in non-oxidative glucose metabolism. Glucose 142-149 insulin Homo sapiens 19-26 7513957-2 1994 To resolve whether this discrepancy was due to the use of a heterologous peptide or to a true species response difference, we studied the effect of a synthetic replicate of human galanin on glucose-stimulated insulin secretion in rats, dogs, and humans. Glucose 190-197 insulin Homo sapiens 209-216 7513957-3 1994 On administration into rats, human and rat galanin significantly inhibited glucose-induced insulin responses to a similar degree. Glucose 75-82 insulin Homo sapiens 91-98 7513957-5 1994 In contrast, plasma glucose and insulin responses to glucose administration in humans were unaltered by the addition of human galanin at or above the maximum effective dose employed in dogs. Glucose 53-60 insulin Homo sapiens 32-39 8178978-1 1994 Reduced type 1 protein phosphatase (PP-1) activity in human muscle extracts may contribute to the reduced insulin-stimulated glycogen synthase activity associated with insulin resistance for glucose disposal in humans. Glucose 191-198 insulin Homo sapiens 106-113 8178978-1 1994 Reduced type 1 protein phosphatase (PP-1) activity in human muscle extracts may contribute to the reduced insulin-stimulated glycogen synthase activity associated with insulin resistance for glucose disposal in humans. Glucose 191-198 insulin Homo sapiens 168-175 8178986-5 1994 Insulin stimulated tissue glucose and net amino acid uptake across the arm and leg tissues, whereas the disposal of both tyrosine and phenylalanine (protein synthesis) was not stimulated across the arm and the leg during hyperinsulinemia. Glucose 26-33 insulin Homo sapiens 0-7 8087097-11 1994 The administration of carbohydrate, usually glucose, leads to a decrease in the serum level of inorganic phosphorus (Pi), attributed to Pi flow from the extracellular to the intracellular compartment as part of the increased glucose metabolism induced by insulin. Glucose 44-51 insulin Homo sapiens 255-262 8087097-11 1994 The administration of carbohydrate, usually glucose, leads to a decrease in the serum level of inorganic phosphorus (Pi), attributed to Pi flow from the extracellular to the intracellular compartment as part of the increased glucose metabolism induced by insulin. Glucose 225-232 insulin Homo sapiens 255-262 8087097-16 1994 The insulin resistance occurring in the presence of chronic growth hormone (GH) excess is accompanied by impaired muscle glucose uptake and nonoxidative glucose metabolism. Glucose 121-128 insulin Homo sapiens 4-11 7907998-0 1994 Regulation of human insulin gene transcription by glucose, epinephrine, and somatostatin. Glucose 50-57 insulin Homo sapiens 20-27 7907998-3 1994 HIT cell expression of this human insulin-CAT reporter gene was responsive to glucose in a concentration-dependent manner, increasing threefold as the glucose concentration increased from 0.4 to 11 mM. Glucose 78-85 insulin Homo sapiens 34-41 7907998-3 1994 HIT cell expression of this human insulin-CAT reporter gene was responsive to glucose in a concentration-dependent manner, increasing threefold as the glucose concentration increased from 0.4 to 11 mM. Glucose 151-158 insulin Homo sapiens 34-41 8026282-7 1994 Insulin therapy reduced maternal capillary (P < 0.005) and MTT (P < 0.001) glucose levels and prevented a diet-associated rise in MTT triglyceride levels (P < 0.002). Glucose 81-88 insulin Homo sapiens 0-7 8033528-1 1994 The extent to which the oral glucose tolerance test can be used to estimate insulin secretion and insulin resistance has been evaluated by comparing glucose and insulin concentrations during an oral glucose tolerance test with specific measurements of insulin secretion and insulin resistance in 85 normoglycaemic subjects and 23 subjects with impaired glucose tolerance (IGT). Glucose 29-36 insulin Homo sapiens 76-83 8033528-1 1994 The extent to which the oral glucose tolerance test can be used to estimate insulin secretion and insulin resistance has been evaluated by comparing glucose and insulin concentrations during an oral glucose tolerance test with specific measurements of insulin secretion and insulin resistance in 85 normoglycaemic subjects and 23 subjects with impaired glucose tolerance (IGT). Glucose 29-36 insulin Homo sapiens 76-105 8033528-2 1994 Insulin secretion was measured by the first phase insulin response to intravenous glucose and insulin resistance by the insulin tolerance test which measures the decline of plasma glucose after the injection of a bolus of insulin. Glucose 82-89 insulin Homo sapiens 0-7 8033528-2 1994 Insulin secretion was measured by the first phase insulin response to intravenous glucose and insulin resistance by the insulin tolerance test which measures the decline of plasma glucose after the injection of a bolus of insulin. Glucose 180-187 insulin Homo sapiens 0-7 8033528-3 1994 The best measure of insulin secretion was the ratio of the 30 min increment in insulin concentration to the 30 min increment in glucose concentration following oral glucose loading. Glucose 128-135 insulin Homo sapiens 20-27 8033528-3 1994 The best measure of insulin secretion was the ratio of the 30 min increment in insulin concentration to the 30 min increment in glucose concentration following oral glucose loading. Glucose 165-172 insulin Homo sapiens 20-27 8033528-4 1994 This correlated with the first phase insulin release following intravenous glucose (r = 0.61, p < 0.001) but not insulin resistance (r = -0.05, p > 0.05). Glucose 75-82 insulin Homo sapiens 37-44 8033528-8 1994 We conclude that the oral glucose tolerance test can be used to derive estimates of the relative roles of insulin secretion and insulin resistance in population studies of glucose tolerance. Glucose 26-33 insulin Homo sapiens 106-135 8033529-10 1994 Final fasting glucose following sulphonylurea therapy was positively correlated with the initial intact and 32/33 split proinsulin and the fasting glucose following dietary treatment. Glucose 14-21 insulin Homo sapiens 120-130 8033534-2 1994 Computing disappearance rates of glucose from its infused amounts necessary to maintain euglycaemia during 65 h after the insulin injection in analogy to experimental hyperinsulinaemic euglycaemic clamp examinations, a glucose consumption of 55.6 mumol kg-1 min-1 was found at peak serum insulin concentrations of about 14,400 pmol l-1. Glucose 33-40 insulin Homo sapiens 122-129 8033534-2 1994 Computing disappearance rates of glucose from its infused amounts necessary to maintain euglycaemia during 65 h after the insulin injection in analogy to experimental hyperinsulinaemic euglycaemic clamp examinations, a glucose consumption of 55.6 mumol kg-1 min-1 was found at peak serum insulin concentrations of about 14,400 pmol l-1. Glucose 33-40 insulin Homo sapiens 172-179 8033534-2 1994 Computing disappearance rates of glucose from its infused amounts necessary to maintain euglycaemia during 65 h after the insulin injection in analogy to experimental hyperinsulinaemic euglycaemic clamp examinations, a glucose consumption of 55.6 mumol kg-1 min-1 was found at peak serum insulin concentrations of about 14,400 pmol l-1. Glucose 219-226 insulin Homo sapiens 172-179 8033534-3 1994 The insulin-induced glucose dynamics resemble closely those seen in healthy persons and Type 1 diabetic subjects during a 10 mU kg-1 min-1 euglycaemic clamp. Glucose 20-27 insulin Homo sapiens 4-11 8039433-2 1994 Insulin stimulates glucose uptake and non-oxidative glucose metabolism (predominantly glycogen synthesis) in skeletal muscle. Glucose 19-26 insulin Homo sapiens 0-7 8039433-2 1994 Insulin stimulates glucose uptake and non-oxidative glucose metabolism (predominantly glycogen synthesis) in skeletal muscle. Glucose 52-59 insulin Homo sapiens 0-7 8039433-3 1994 Among other things, insulin resistance is characterized by a subnormal insulin-stimulated glucose disposal, and it appears to be associated with an increased risk for development of non-insulin-dependent diabetes mellitus (NIDDM). Glucose 90-97 insulin Homo sapiens 20-27 8039433-3 1994 Among other things, insulin resistance is characterized by a subnormal insulin-stimulated glucose disposal, and it appears to be associated with an increased risk for development of non-insulin-dependent diabetes mellitus (NIDDM). Glucose 90-97 insulin Homo sapiens 71-78 8039433-4 1994 The aim of the present investigation has been to elucidate the mechanism of action of insulin on non-oxidative glucose metabolism both during conditions of insulin resistance and during physiological modification of glucose metabolism. Glucose 111-118 insulin Homo sapiens 86-93 8039433-4 1994 The aim of the present investigation has been to elucidate the mechanism of action of insulin on non-oxidative glucose metabolism both during conditions of insulin resistance and during physiological modification of glucose metabolism. Glucose 111-118 insulin Homo sapiens 156-163 8039433-4 1994 The aim of the present investigation has been to elucidate the mechanism of action of insulin on non-oxidative glucose metabolism both during conditions of insulin resistance and during physiological modification of glucose metabolism. Glucose 216-223 insulin Homo sapiens 86-93 8063035-2 1994 Insulin infusions maintained plasma glucose concentrations on one study day in "tight" control (TC: 6 mmol/l) and on a separate day in "loose" control (LC: 12 mmol/l). Glucose 36-43 insulin Homo sapiens 0-7 8063042-1 1994 We examined whether insulin resistance, i.e. impaired insulin stimulated glucose uptake in NIDDM patients and their first-degree relatives is associated with alterations in the effect of insulin on the expression of the GLUT-4 gene in skeletal muscle in vivo. Glucose 73-80 insulin Homo sapiens 20-27 8063042-1 1994 We examined whether insulin resistance, i.e. impaired insulin stimulated glucose uptake in NIDDM patients and their first-degree relatives is associated with alterations in the effect of insulin on the expression of the GLUT-4 gene in skeletal muscle in vivo. Glucose 73-80 insulin Homo sapiens 54-61 8063042-3 1994 Insulin stimulated glucose uptake was decreased in the diabetic subjects (19.8 +/- 3.0 mumol.kg LBM-1.min-1, both p < 0.001) compared with control subjects (44.1 +/- 2.5 mumol.kg LBM-1.min-1) and relatives (39.9 +/- 3.3 mumol.kg LBM-1.min-1). Glucose 19-26 insulin Homo sapiens 0-7 8063045-1 1994 The purpose of these experiments was to test the hypothesis that impaired glucose-stimulated insulin secretion in NIDDM is due to mutations in the islet beta cell/liver glucose transporter (GLUT 2) gene. Glucose 74-81 insulin Homo sapiens 93-100 8138054-12 1994 When an increased demand is placed on the proinsulin-processing mechanism by a glucose-stimulated increase in proinsulin biosynthesis, there is a coordinate increase in PC3 biosynthesis (but not in PC2). Glucose 79-86 insulin Homo sapiens 42-52 8138054-12 1994 When an increased demand is placed on the proinsulin-processing mechanism by a glucose-stimulated increase in proinsulin biosynthesis, there is a coordinate increase in PC3 biosynthesis (but not in PC2). Glucose 79-86 insulin Homo sapiens 110-120 8138065-0 1994 The contribution of insulin-dependent and insulin-independent glucose uptake to intravenous glucose tolerance in healthy human subjects. Glucose 92-99 insulin Homo sapiens 20-49 8138065-4 1994 To eliminate the effect of basal insulin on SG and estimate insulin-independent glucose uptake, we calculated glucose effectiveness at zero insulin (GEZI = SG - [SI x basal insulin]). Glucose 80-87 insulin Homo sapiens 60-67 8138065-4 1994 To eliminate the effect of basal insulin on SG and estimate insulin-independent glucose uptake, we calculated glucose effectiveness at zero insulin (GEZI = SG - [SI x basal insulin]). Glucose 80-87 insulin Homo sapiens 60-67 8138065-5 1994 Insulin-dependent glucose uptake was estimated as SI x IIR0-19, because the relationship between SI and beta-cell function has been shown to be hyperbolic. Glucose 18-25 insulin Homo sapiens 0-7 8143469-15 1994 This caution is especially advised if the glucose values obtained with arterial whole blood are used in conjunction with a sliding scale of insulin, which depends on threshold concentrations of glucose. Glucose 194-201 insulin Homo sapiens 140-147 7516860-9 1994 Regular insulin is used to control the postprandial glucose excursion and a slow infusion of regular insulin by a pump or injected intermediate or long-acting insulin is used to balance fasting glucose utilisation and production. Glucose 52-59 insulin Homo sapiens 8-15 7516860-9 1994 Regular insulin is used to control the postprandial glucose excursion and a slow infusion of regular insulin by a pump or injected intermediate or long-acting insulin is used to balance fasting glucose utilisation and production. Glucose 194-201 insulin Homo sapiens 101-108 7516860-9 1994 Regular insulin is used to control the postprandial glucose excursion and a slow infusion of regular insulin by a pump or injected intermediate or long-acting insulin is used to balance fasting glucose utilisation and production. Glucose 194-201 insulin Homo sapiens 101-108 7951567-4 1994 The basal concentrations of proinsulin increased as glucose tolerance declined (P < 0.05 between NGT and NIDDM). Glucose 52-59 insulin Homo sapiens 28-38 8039489-7 1994 RESULTS: Erythritol did not increase serum levels of glucose or insulin, while the same dose of glucose increased rapidly glucose and insulin levels within 30 min. Glucose 96-103 insulin Homo sapiens 134-141 8039489-7 1994 RESULTS: Erythritol did not increase serum levels of glucose or insulin, while the same dose of glucose increased rapidly glucose and insulin levels within 30 min. Glucose 96-103 insulin Homo sapiens 134-141 8050454-6 1994 These patients showed a bimodal distribution of whole body glucose utilization rate, a parameter of peripheral insulin sensitivity. Glucose 59-66 insulin Homo sapiens 111-118 8150099-2 1994 DESIGN: Comparative study of endogenous glucose disposal and serum insulin responses to oral glucose load with endocrine parameters in PCOS. Glucose 93-100 insulin Homo sapiens 67-74 8150099-6 1994 Measurements of insulin sensitivity by rate of endogenous glucose disposal after i.v. Glucose 58-65 insulin Homo sapiens 16-23 8168691-3 1994 The former are responsible for the metabolism and storage of an important part of the ingested glucose, whereas the latter secrete insulin in response to an increase in the blood glucose level. Glucose 179-186 insulin Homo sapiens 131-138 8046011-3 1994 Enhanced body mass index (BMI kg/m2) resulted in a significant elevation of basal insulin (b-Ins), glucose-stimulated (delta) insulin (del-Ins), triglycerides (TG), very low density lipoprotein (VLDL), low density lipoprotein (LDL), and LDL/high density lipoprotein (HDL) ratio, and in a significant reduction of HDL. Glucose 99-106 insulin Homo sapiens 126-133 8082871-2 1994 To investigate the possibility that a "threshold" of obesity exists, above which glucose transport is significantly decreased, hormone (insulin, IGF-I, or IGF-II) stimulation of glucose transport was correlated with body mass index using muscle biopsies from a group of 30 lean to obese females with BMI ranging from 16 to 40. Glucose 178-185 insulin Homo sapiens 136-143 8082871-4 1994 These data suggest there is no obesity threshold for insulin resistance in skeletal muscle but a continuous decline in glucose transport below a BMI of approximately 30 kg/m2, after which insulin and the IGFs no longer stimulate glucose transport. Glucose 229-236 insulin Homo sapiens 188-195 8082873-7 1994 glucose load, due to an increased first phase of insulin secretion (phi 1), a reduced insulin sensitivity (Si) and glucose effectiveness (Sg) in respect to normal-weight subjects. Glucose 0-7 insulin Homo sapiens 49-56 8144824-0 1994 Seven consecutive days of exercise lowers plasma insulin responses to an oral glucose challenge in sedentary elderly. Glucose 78-85 insulin Homo sapiens 49-56 8144824-1 1994 OBJECTIVE: To assess the effects of 1 and 7 consecutive days of exercise on glucose and insulin responses to an oral glucose challenge. Glucose 117-124 insulin Homo sapiens 88-95 8144824-7 1994 MAIN RESULTS: Fasting plasma insulin levels and plasma insulin responses to an oral glucose challenge were reduced by 15% and 20%, respectively, with 7 consecutive days of exercise that resulted in no change in body weight or body composition. Glucose 84-91 insulin Homo sapiens 55-62 8149032-0 1994 Glucose infusion instead of preoperative fasting reduces postoperative insulin resistance. Glucose 0-7 insulin Homo sapiens 71-78 8149032-6 1994 Insulin sensitivity (M value, milligram per kilogram per minute) was determined using the hyperinsulinemic normoglycemic clamp (plasma insulin level, 65 microunits per milliliter and blood glucose level, 4.5 millimoles per liter) before and the first postoperative day. Glucose 189-196 insulin Homo sapiens 0-7 8149032-10 1994 The present results indicate that active preoperative carbohydrate preservation may improve postoperative metabolism because postoperative occurrence of insulin resistance was reduced with preoperative glucose infusion. Glucose 202-209 insulin Homo sapiens 153-160 7512573-4 1994 Insulin-resistant NIDDM patients, with high basal glucose and insulin, normal IGFBP-1, and low GH, had decreased prefasting serum IGF-I concentrations, similar to the values in fasted body mass index- and age-matched OB subjects. Glucose 50-57 insulin Homo sapiens 0-7 8144513-0 1994 A role for Raf-1 in the divergent signaling pathways mediating insulin-stimulated glucose transport. Glucose 82-89 insulin Homo sapiens 63-70 8144513-2 1994 To investigate a role for the Raf-1 protein kinase in insulin-stimulated glucose transport, a gene encoding an oncogenically activated Raf-1 mutant was introduced into 3T3-L1 fibroblasts by retroviral gene transfer. Glucose 73-80 insulin Homo sapiens 54-61 8144513-9 1994 Moreover, the differential effects of activated Raf-1 expression on the two transporter isoforms define divergent signaling pathways by which insulin regulates glucose transport in cultured adipocytes. Glucose 160-167 insulin Homo sapiens 142-149 8061353-7 1994 There was a positive correlation between mean glucose levels, duration of disease, insulin dosage, and bone-mass decrease. Glucose 46-53 insulin Homo sapiens 83-90 7511205-1 1994 The signal transduction pathway by which insulin stimulates glucose transport is largely unknown, but a role for tyrosine and serine/threonine kinases has been proposed. Glucose 60-67 insulin Homo sapiens 41-48 7511205-2 1994 Since mitogen-activated protein (MAP) kinase is activated by insulin through phosphorylation on both tyrosine and threonine residues, we investigated whether MAP kinase and its upstream regulator, p21ras, are involved in insulin-mediated glucose transport. Glucose 238-245 insulin Homo sapiens 221-228 7511205-3 1994 We did this by examining the time- and dose-dependent stimulation of glucose uptake in relation to the activation of Ras-GTP formation and MAP kinase by thrombin, epidermal growth factor (EGF), and insulin in 3T3-L1 adipocytes. Glucose 69-76 insulin Homo sapiens 198-205 8171515-0 1994 Differential effects of systemic insulin delivery and prednisone on tissue glucose and insulin sensitivity in insulin-dependent diabetes mellitus pancreas recipients. Glucose 75-82 insulin Homo sapiens 33-40 8171517-3 1994 This is accounted for by higher insulin concentrations following diversion, more than compensating for decreases in insulin sensitivity and the suppression of endogenous glucose production. Glucose 170-177 insulin Homo sapiens 32-39 8171568-0 1994 In vitro assessment of human islets for transplantation: a comparison of glucose-stimulated insulin secretion from short-term-cultured (< 48 hours) versus long-term-cultured (> 72 hours) human islets. Glucose 73-80 insulin Homo sapiens 92-99 14731734-1 1994 Insulin stimulates glucose transport in muscle and fat cells by causing the redistribution of a facilitative glucose transporter, GLUT-4, from an intracellular compartment to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 8156572-9 1994 The authors found in all groups of diabetic patients, as compared with controls, a comparable drop of the insulin effect evaluated as the metabolic glucose clearance during an hyperinsulinaemic euglycaemic (5 mmol/l) or isoglycaemic (fasting blood sugar level) clamp, the insulin level being 75 microU/ml (controls 10.9 +/- 3.3 ml/kg.min., first group 5.35 +/- 2.7 ml/kg.min., second group 5.47 +/- 2.35 ml/kg.min., third group 5.38 +/- 2.1 ml/kg.min. Glucose 148-155 insulin Homo sapiens 106-113 8156572-15 1994 In all diabetic groups, as compared with controls, higher C peptide values and insulin values (IRI) were found on fasting and a slower rise and longer persistence of higher levels after oral glucose administration, although an inadequate secretory response during the hyperglycaemic clamp in diabetics is apparent. Glucose 191-198 insulin Homo sapiens 79-86 7510884-5 1994 Insulin release in response to glucose from in situ-perfused pancreas was impaired; however, the plasma glucose and insulin levels of the mice remained normal. Glucose 31-38 insulin Homo sapiens 0-7 8159111-3 1994 Insulin sensitivity was assessed as the insulin-mediated glucose uptake rate (M value) with the hyperinsulinemic euglycemic clamp technique. Glucose 57-64 insulin Homo sapiens 0-7 8159111-3 1994 Insulin sensitivity was assessed as the insulin-mediated glucose uptake rate (M value) with the hyperinsulinemic euglycemic clamp technique. Glucose 57-64 insulin Homo sapiens 40-47 8111717-8 1994 Both basal (2.3 +/- 0.2 mumol/100 g/minute, P = 0.061) and insulin-stimulated (8.5 +/- 1.9 mumol/100 g/minute, P = 0.055) skeletal arm muscle glucose uptake rates were higher in control subjects than in patients. Glucose 142-149 insulin Homo sapiens 59-66 8010722-0 1994 Altered insulin response to glucose in weight-losing cancer patients. Glucose 28-35 insulin Homo sapiens 8-15 8010722-3 1994 The aim of this study was to investigate the insulin response in fasted, weigh-losing cancer patients following an oral glucose load (75 g). Glucose 120-127 insulin Homo sapiens 45-52 8010722-9 1994 Plasma fatty acid concentrations were increased in all cancer patients and decreased appropriately after glucose administration, indicating that lipolysis remained sensitive to the action of insulin. Glucose 105-112 insulin Homo sapiens 191-198 8019763-2 1994 Lithium salts, used in the treatment of affective disorders, may have adverse effects on glucose tolerance in man, and suppress glucose-stimulated insulin secretion in rats. Glucose 128-135 insulin Homo sapiens 147-154 8166272-1 1994 We assessed insulin effects on plasma free fatty acid (FFA) and glucose metabolism in seven elderly (71 +/- 2 yr) and in seven younger (21 +/- 1 yr) subjects matched for body weight and body mass index but not for percent body fat (32.4 +/- 3.8% in elderly vs. 20.4 +/- 3.5% in young, P < 0.05), by performing sequential euglycemic clamps at five insulin doses (0.6, 1.5, 3, 6, and 15 pmol.min-1.kg-1) in combination with indirect calorimetry and [1-14C]palmitate plus [3-3H]glucose infusion. Glucose 64-71 insulin Homo sapiens 12-19 8111717-11 1994 Although insulin sensitivity of skeletal muscle was also reduced in patients with lymphoma, the net insulin effect may counteract imbalance between glucose uptake of tumor and muscle, offering a potential means to circumvent at least some metabolic abnormalities found in cancer. Glucose 148-155 insulin Homo sapiens 100-107 8156743-11 1994 The high-dose, unmodified intravenous glucose tolerance test with minimal model analysis is a straightforward and economical clinical procedure and provides a valid measure of insulin sensitivity, in health and disease. Glucose 38-45 insulin Homo sapiens 176-183 8194212-2 1994 In women with normal glucose tolerance, there is a significant (30%) increase in basal hepatic glucose production, a progressive (60%) decrease in insulin sensitivity, and an associated 3.0-3.5-fold increase in insulin response by 34-36 weeks" gestation. Glucose 21-28 insulin Homo sapiens 211-218 8314006-3 1994 Such initiatives have included attempts to engineer glucose-stimulated insulin secretion in cell lines that might serve as surrogates for islets in IDDM. Glucose 52-59 insulin Homo sapiens 71-78 7805948-1 1994 A decreased insulin response, preferentially to glucose, has been considered a hallmark of non-insulin dependent diabetes mellitus (Type 2) in humans. Glucose 48-55 insulin Homo sapiens 12-19 7805949-6 1994 Glucose regulation of this process is manifested as alterations of the amplitudes of the insulin pulses without effects on the frequency. Glucose 0-7 insulin Homo sapiens 89-96 7805950-0 1994 Multisite control of insulin release by glucose. Glucose 40-47 insulin Homo sapiens 21-28 7805952-1 1994 Secretion of insulin from beta cells of the pancreatic islets is regulated by glucose, its anaerobic metabolism and its metabolites. Glucose 78-85 insulin Homo sapiens 13-20 7805958-4 1994 Insulin response to glucose, glucose+forskolin and leucine+glutamine was evaluated in freshly isolated and cultured islets. Glucose 20-27 insulin Homo sapiens 0-7 8174841-0 1994 Effects of glycaemia on glucose transport in isolated skeletal muscle from patients with NIDDM: in vitro reversal of muscular insulin resistance. Glucose 24-31 insulin Homo sapiens 126-133 8174841-1 1994 We investigated the influence of altered glucose levels on insulin-stimulated 3-0-methylglucose transport in isolated skeletal muscle obtained from NIDDM patients (n = 13) and non-diabetic subjects (n = 23). Glucose 41-48 insulin Homo sapiens 59-66 8174841-2 1994 Whole body insulin sensitivity was 71% lower in the NIDDM patients compared to the non-diabetic subjects (p < 0.05), whereas, insulin-mediated peripheral glucose utilization in the NIDDM patients under hyperglycaemic conditions was comparable to that of the non-diabetic subjects at euglycaemia. Glucose 157-164 insulin Homo sapiens 129-136 8174841-3 1994 Following a 30-min in vitro exposure to 4 mmol/l glucose, insulin-stimulated 3-0-methylglucose transport (600 pmol/l insulin) was 40% lower in isolated skeletal muscle strips from the NIDDM patients when compared to muscle strips from the non-diabetic subjects. Glucose 49-56 insulin Homo sapiens 58-65 7514971-2 1994 Insulin resistance is generally interpreted as the physiological state under which insulin causes a reduced glucose-lowering effect. Glucose 108-115 insulin Homo sapiens 0-7 7514971-2 1994 Insulin resistance is generally interpreted as the physiological state under which insulin causes a reduced glucose-lowering effect. Glucose 108-115 insulin Homo sapiens 83-90 7528694-1 1994 The insulin-secreting pancreatic beta cell is electrically excitable and changes in the membrane potential play an important role in coupling the metabolism of glucose (and other nutrient secretagogues) to the discharge of the insulin-containing granule. Glucose 160-167 insulin Homo sapiens 4-11 8174837-4 1994 Insulin sensitivity was estimated by an insulin (0.4 mU.kg-1 x min-1)-glucose (4.5 mg.kg-1 x min-1)-infusion test (IGIT) for 6.5 h. Mental stress evoked significant responses for adrenaline, cortisol and GH, their respective peak values being 0.27 +/- 0.05 nmol/l, 426 +/- 27 nmol/l and 7.6 +/- 1.8 micrograms/l, as well as increases in systolic and diastolic blood pressure and pulse rate The steady-state blood glucose levels, i.e. the mean blood glucose levels 3-6.5 h after the start of the IGIT, were significantly higher after stress, compared with those on the control day, 10.6 +/- 1.5 vs 8.7 +/- 1.4 mmol/l, p = 0.01, demonstrating impairment of the insulin sensitivity by mental stress. Glucose 70-77 insulin Homo sapiens 0-7 8314023-0 1994 Impaired insulin-induced glucose uptake by extrahepatic tissue is hallmark of NIDDM patients who have or will develop hypertension and microalbuminuria. Glucose 25-32 insulin Homo sapiens 9-16 8174841-3 1994 Following a 30-min in vitro exposure to 4 mmol/l glucose, insulin-stimulated 3-0-methylglucose transport (600 pmol/l insulin) was 40% lower in isolated skeletal muscle strips from the NIDDM patients when compared to muscle strips from the non-diabetic subjects. Glucose 49-56 insulin Homo sapiens 117-124 8174841-4 1994 The impaired capacity for insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle was normalized following prolonged (2h) exposure to 4 mmol/l, but not to 8 mmol/l glucose. Glucose 55-62 insulin Homo sapiens 26-33 8174841-5 1994 Insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle exposed to 8 mmol/l glucose was similar to that of the non-diabetic muscle exposed to 5 mmol/l glucose, but was decreased by 43% (p < 0.01) when compared to non-diabetic muscle exposed to 8 mmol/l glucose. Glucose 29-36 insulin Homo sapiens 0-7 8174841-5 1994 Insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle exposed to 8 mmol/l glucose was similar to that of the non-diabetic muscle exposed to 5 mmol/l glucose, but was decreased by 43% (p < 0.01) when compared to non-diabetic muscle exposed to 8 mmol/l glucose. Glucose 96-103 insulin Homo sapiens 0-7 8314023-10 1994 The results from the cross-sectional study indicate that the mean of insulin-induced whole-body glucose utilization, primarily an index of extrahepatic insulin action, was lower at all insulin infusion steps in the group of hypertensive and/or microalbuminuric patients than in the group of normotensive normoalbuminuric patients and control subjects. Glucose 96-103 insulin Homo sapiens 69-76 8314023-10 1994 The results from the cross-sectional study indicate that the mean of insulin-induced whole-body glucose utilization, primarily an index of extrahepatic insulin action, was lower at all insulin infusion steps in the group of hypertensive and/or microalbuminuric patients than in the group of normotensive normoalbuminuric patients and control subjects. Glucose 96-103 insulin Homo sapiens 152-159 8174841-5 1994 Insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle exposed to 8 mmol/l glucose was similar to that of the non-diabetic muscle exposed to 5 mmol/l glucose, but was decreased by 43% (p < 0.01) when compared to non-diabetic muscle exposed to 8 mmol/l glucose. Glucose 96-103 insulin Homo sapiens 0-7 8314011-10 1994 At the same time, the glucose infusion rate peaked in about half the time (time to maximum glucose infusion rate [TRmax], 99 vs. 179 min, A vs. C) and was slightly but not significantly higher (maximum glucose infusion rate [Rmax], 3.1 vs. 2.2 mmol/min, A vs. C) than that of human Regular insulin. Glucose 22-29 insulin Homo sapiens 290-297 8174841-7 1994 Kinetic studies revel a Km for 3-0-methylglucose transport of 9.7 and 8.8 mmol/l glucose for basal and insulin-stimulated conditions, respectively. Glucose 41-48 insulin Homo sapiens 103-110 8119686-4 1994 In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Glucose 3-10 insulin Homo sapiens 159-166 8156098-5 1994 In the 10 patients who underwent a 4-year follow-up, insulin responses to oral glucose decreased significantly, whilst insulin sensitivity did not change substantially. Glucose 79-86 insulin Homo sapiens 53-60 8156098-6 1994 Insulin sensitivity persisted unmodified even in the patients with deteriorating glucose tolerance. Glucose 81-88 insulin Homo sapiens 0-7 8119686-7 1994 In diabetic patients, insulin-mediated glucose uptake was significantly reduced, mainly because of impaired non-oxidative glucose disposal. Glucose 39-46 insulin Homo sapiens 22-29 8119686-7 1994 In diabetic patients, insulin-mediated glucose uptake was significantly reduced, mainly because of impaired non-oxidative glucose disposal. Glucose 122-129 insulin Homo sapiens 22-29 8119686-9 1994 Hepatic glucose production was significantly increased in the basal state (3.03 +/- 0.24 vs. 2.34 +/- 0.10 mg/kg min, p < 0.02) and during insulin infusion (+50 microU/ml: 0.67 +/- 0.17 vs. 0.13 +/- 0.08 mg/kg min, p < 0.05) compared with that in controls. Glucose 8-15 insulin Homo sapiens 142-149 8119686-11 1994 In conclusion, glucose intolerance in cirrhosis results from two abnormalities that occur simultaneously: (a) insulin resistance of muscle and (b) an inadequate response (even when comparable to that of controls) of the beta-cells to appropriately secrete insulin to overcome the defect in insulin action. Glucose 15-22 insulin Homo sapiens 110-117 8014072-6 1994 Following successful treatment of acute pancreatitis and hyperglycemia with gabexate mesilate and insulin, his serum glucose, lipid and pancreatic enzyme levels decreased to the normal range. Glucose 117-124 insulin Homo sapiens 98-105 8119686-4 1994 In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Glucose 43-50 insulin Homo sapiens 159-166 8119686-4 1994 In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Glucose 43-50 insulin Homo sapiens 159-166 8119686-4 1994 In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Glucose 43-50 insulin Homo sapiens 159-166 8119686-4 1994 In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Glucose 43-50 insulin Homo sapiens 159-166 7510305-7 1994 As expected, during oral glucose tolerance testing, the area under the curve of C-peptide was suppressed after an injection of IGF-I (P < 0.05), but the area under the glucose curve did not change significantly. Glucose 25-32 insulin Homo sapiens 80-89 8125556-1 1994 Insulin-stimulated peripheral glucose uptake and insulin-induced renal tubular sodium reabsorption were investigated in normotensive men with a family history of hypertension (relatives, n = 35) compared with age- and body mass index-matched normotensive men with no family history of hypertension (controls, n = 23). Glucose 30-37 insulin Homo sapiens 0-7 8125556-9 1994 In conclusion, the impaired insulin-stimulated glucose uptake in peripheral tissues in normotensive sons of hypertensive families was accompanied by retained insulin-induced tubular sodium reabsorption. Glucose 47-54 insulin Homo sapiens 28-35 8125556-9 1994 In conclusion, the impaired insulin-stimulated glucose uptake in peripheral tissues in normotensive sons of hypertensive families was accompanied by retained insulin-induced tubular sodium reabsorption. Glucose 47-54 insulin Homo sapiens 158-165 8125557-5 1994 In this population of normotensive and hypertensive men, systolic, diastolic, and mean arterial blood pressures were related to glucose disposal at these insulin infusion rates (r = -.35 to -.46, P < .05) as well as the EC50 (r = .42 to .44, P < .05). Glucose 128-135 insulin Homo sapiens 154-161 7510305-9 1994 IGFBP-1 was suppressed by 32% after oral glucose alone, whereas an injection of IGF-I plus oral glucose were associated with a more marked fall of 53% (despite suppression of C-peptide). Glucose 96-103 insulin Homo sapiens 175-184 7911838-4 1994 The metabolic clearance rate of insulin (MCRins) was calculated during a constant infusion of glucose (320 mg/m2/min) and insulin (25 mU/m2/min), under conditions where endogenous insulin secretion was suppressed by somatostatin infusion (250 micrograms/h) for four groups of age sex and weight-matched patients: normotensive volunteers, untreated hypertensives, hypertensives treated with diuretics and hypertensives treated with diuretics and beta-blockers. Glucose 94-101 insulin Homo sapiens 32-39 8132753-9 1994 However, insulin-induced stimulation of glucose uptake was blunted in older subjects (P = 0.05). Glucose 40-47 insulin Homo sapiens 9-16 8139483-8 1994 In contrast, PB administration enhanced insulin-mediated peripheral glucose utilization, as well as suppression of hepatic glucose production, in both low-dose and high-dose diabetic groups. Glucose 68-75 insulin Homo sapiens 40-47 8139489-0 1994 Insulin production following intravenous glucose, arginine, and valine: different pattern in patients with impaired glucose tolerance and non-insulin-dependent diabetes mellitus. Glucose 41-48 insulin Homo sapiens 0-7 8177058-6 1994 The practical applicability of causal probabilistic networks to real medical problems is illustrated by a model of glucose metabolism which is used to adjust insulin therapy in type I diabetic patients. Glucose 115-122 insulin Homo sapiens 158-165 8134869-6 1994 He was managed with intravenous fluids, bicarbonate infusion, calcium gluconate, and 25% dextrose with insulin. Glucose 89-97 insulin Homo sapiens 103-110 7514790-3 1994 In our study, we have evaluated the effects of DTZ (dissolved in dimethyl sulfoxide [DMSO] 1% w/v) at three different concentrations (2, 10, and 100 micrograms/ml) on insulin response to glucose in human and rat islets. Glucose 187-194 insulin Homo sapiens 167-174 7910686-6 1994 Immunoneutralization of intraislet somatostatin with CURE.S6 resulted in a significant increase in insulin secretion under both low glucose (454 +/- 162 pM) (p < 0.05) and high glucose (2,177 +/- 829 pM) (p < 0.05) conditions. Glucose 132-139 insulin Homo sapiens 99-106 7910686-6 1994 Immunoneutralization of intraislet somatostatin with CURE.S6 resulted in a significant increase in insulin secretion under both low glucose (454 +/- 162 pM) (p < 0.05) and high glucose (2,177 +/- 829 pM) (p < 0.05) conditions. Glucose 180-187 insulin Homo sapiens 99-106 7991936-4 1994 When the test was performed at the end of the period of treatment with insulin plus glipizide and 30 min after the ingestion of the last dose of 10 mg glipizide, plasma C-peptide levels were significantly increased and steady-state free insulin levels tended to be slightly higher whereas the metabolic clearance rate of glucose was not affected. Glucose 321-328 insulin Homo sapiens 71-78 8119950-7 1994 Finally, the inhibitory effect of okadaic acid on the stimulatory action of insulin on glucose transport suggests that the serine/threonine phosphorylation of IRS 1 might represent a key regulatory mechanism of insulin action. Glucose 87-94 insulin Homo sapiens 76-83 8123024-0 1994 Regulation of human insulin receptor RNA splicing in HepG2 cells: effects of glucocorticoid and low glucose concentration. Glucose 100-107 insulin Homo sapiens 20-27 8123030-0 1994 Glyburide enhances insulin gene expression and glucose-induced insulin release in isolated rat islets. Glucose 47-54 insulin Homo sapiens 63-70 8123030-5 1994 These results suggest that a high concentration of glyburide stimulates insulin release directly, while a low concentration of glyburide increases the PPI mRNA level and may thereby enhance glucose-induced insulin release. Glucose 190-197 insulin Homo sapiens 206-213 8119950-7 1994 Finally, the inhibitory effect of okadaic acid on the stimulatory action of insulin on glucose transport suggests that the serine/threonine phosphorylation of IRS 1 might represent a key regulatory mechanism of insulin action. Glucose 87-94 insulin Homo sapiens 211-218 8296701-3 1994 Plasma glucose and insulin concentrations after an oral glucose load and from 8 AM to 4PM in response to meals were higher in patients with Type IIB HLP, who also had higher steady-state plasma glucose concentrations after an infusion of somatostatin, insulin, and glucose (12.4 +/- 1 vs 5.5 +/- 0.8 mmol/L, p < 0.001). Glucose 7-14 insulin Homo sapiens 252-259 8108432-5 1994 The ratio between the splice variants changed from 74% to 48% Ex 11- RNA after initiation of insulin treatment, which considerably improved his blood glucose concentrations and insulin-stimulated glucose utilization rate. Glucose 150-157 insulin Homo sapiens 93-100 8108432-5 1994 The ratio between the splice variants changed from 74% to 48% Ex 11- RNA after initiation of insulin treatment, which considerably improved his blood glucose concentrations and insulin-stimulated glucose utilization rate. Glucose 196-203 insulin Homo sapiens 93-100 8108432-5 1994 The ratio between the splice variants changed from 74% to 48% Ex 11- RNA after initiation of insulin treatment, which considerably improved his blood glucose concentrations and insulin-stimulated glucose utilization rate. Glucose 196-203 insulin Homo sapiens 177-184 8296701-3 1994 Plasma glucose and insulin concentrations after an oral glucose load and from 8 AM to 4PM in response to meals were higher in patients with Type IIB HLP, who also had higher steady-state plasma glucose concentrations after an infusion of somatostatin, insulin, and glucose (12.4 +/- 1 vs 5.5 +/- 0.8 mmol/L, p < 0.001). Glucose 56-63 insulin Homo sapiens 19-26 8141165-2 1994 In essential hypertension, data suggest the insulin resistance pertains predominantly to nonoxidative glucose disposal, especially in skeletal muscle and adipose tissue, which contrasts with a more generalized deficit in obesity and NIDDM. Glucose 102-109 insulin Homo sapiens 44-51 8296701-3 1994 Plasma glucose and insulin concentrations after an oral glucose load and from 8 AM to 4PM in response to meals were higher in patients with Type IIB HLP, who also had higher steady-state plasma glucose concentrations after an infusion of somatostatin, insulin, and glucose (12.4 +/- 1 vs 5.5 +/- 0.8 mmol/L, p < 0.001). Glucose 56-63 insulin Homo sapiens 19-26 8116725-1 1994 OBJECTIVES: The cellular mechanism(s) of insulin resistance developed during pregnancy were studied by investigating the functionality of insulin receptors and glucose transport. Glucose 160-167 insulin Homo sapiens 41-48 8296701-3 1994 Plasma glucose and insulin concentrations after an oral glucose load and from 8 AM to 4PM in response to meals were higher in patients with Type IIB HLP, who also had higher steady-state plasma glucose concentrations after an infusion of somatostatin, insulin, and glucose (12.4 +/- 1 vs 5.5 +/- 0.8 mmol/L, p < 0.001). Glucose 56-63 insulin Homo sapiens 19-26 8116725-8 1994 Adipocytes from pregnant subjects displayed a threefold decrease in insulin sensitivity for glucose transport (median effective concentration 324 +/- 93 vs 93 +/- 14 pmol/L, p < 0.025) and a reduction in maximal insulin-stimulated glucose transport (1.58 +/- 0.15 vs 2.33 +/- 0.24 pmol/10(5) cells/10 seconds, p < 0.025). Glucose 92-99 insulin Homo sapiens 68-75 8012426-2 1994 In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. Glucose 50-57 insulin Homo sapiens 112-119 8141282-1 1994 We assessed in normal subjects the effects of an acute increase in forearm norepinephrine (NE) release, evoked by -20 mmHg lower body negative pressure (LBNP), on insulin-mediated muscle glucose uptake. Glucose 187-194 insulin Homo sapiens 163-170 8141282-4 1994 Forearm glucose uptake rose from 0.97 +/- 0.13 to 5.2 +/- 0.2 mg.l-1.min-1 in response to insulin infusion. Glucose 8-15 insulin Homo sapiens 90-97 8141282-6 1994 Under these conditions, the stimulatory effect of insulin on forearm glucose uptake was markedly reduced (from 0.78 +/- 0.10 to 3.2 +/- 0.7 mg.l-1.min-1; P < 0.02 vs. control). Glucose 69-76 insulin Homo sapiens 50-57 8141282-8 1994 These data demonstrate that an acute activation of endogenous NE release antagonizes insulin-mediated glucose uptake in forearm skeletal muscle, probably accounted for by a direct metabolic effect of NE. Glucose 102-109 insulin Homo sapiens 85-92 8141283-0 1994 Skeletal muscle blood flow independently modulates insulin-mediated glucose uptake. Glucose 68-75 insulin Homo sapiens 51-58 8141283-1 1994 Insulin-mediated glucose uptake (IMGU) occurs principally in skeletal muscle. Glucose 17-24 insulin Homo sapiens 0-7 8141285-3 1994 In both groups of subjects vitamin C-mediated increase in insulin action was mainly due to an improvement in nonoxidative glucose metabolism. Glucose 122-129 insulin Homo sapiens 58-65 8012426-2 1994 In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. Glucose 156-163 insulin Homo sapiens 203-210 8012426-2 1994 In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. Glucose 156-163 insulin Homo sapiens 203-210 8137525-8 1994 MEASUREMENTS: Metabolic evaluation including insulin secretion and insulin-mediated glucose uptake were evaluated by oral glucose tolerance test and the modification of insulin suppression test. Glucose 84-91 insulin Homo sapiens 67-74 8143426-11 1994 A rise in muscle nerve sympathetic activity takes place in the absence of an insulin response, and insulin contributes to only part of the increase after ingestion of glucose or a mixed meal. Glucose 167-174 insulin Homo sapiens 99-106 7907975-1 1994 OBJECTIVE: To test the hypothesis that insulin-mediated glucose uptake is enhanced in light-to-moderate alcohol consumption. Glucose 56-63 insulin Homo sapiens 39-46 8137680-3 1994 RESULTS: Multiple regression analysis demonstrated a significant relationship of either BP, plasma triglyceride (TG), or high-density lipoprotein (HDL) cholesterol levels to plasma insulin and glucose response after the glucose load. Glucose 220-227 insulin Homo sapiens 181-188 8137680-7 1994 CONCLUSIONS: Based on these findings, subjects with hyperinsulinemia or glucose intolerance should be carefully managed to prevent CAD, because they have more numerous and more severe risk factors than subjects with normal plasma insulin levels or subjects without glucose intolerance. Glucose 265-272 insulin Homo sapiens 57-64 8163052-4 1994 The utilization of D-[5-3H]glucose, oxidation of D-[6-14C]glucose and release of insulin evoked by D-glucose were all lower in Type 2 diabetic patients than control subjects. Glucose 99-108 insulin Homo sapiens 81-88 8163054-4 1994 Based on the insulin sensitivity index derived from the minimal model analysis of intravenous glucose tolerance test data, both the hypertensive (2.4 +/- 0.4 min-1/(microU/ml); p < 0.0005) and the obese (2.7 +/- 0.5; p < 0.001) patients demonstrated severe insulin resistance compared to control subjects (8.1 +/- 1.3). Glucose 94-101 insulin Homo sapiens 13-20 8193213-8 1994 In response to the glucose infusion, the maximum increase in plasma insulin trebled (p < 0.01) and the integrated concentrations (area under the curve) of plasma glucose, lactate and pyruvate were significantly more pronounced (p < 0.02-p < 0.001) after than before operation. Glucose 19-26 insulin Homo sapiens 68-75 8157524-13 1994 Exogenous insulin seems to increase feed intake by reducing plasma glucose rather than be affecting plasma NEFA. Glucose 67-74 insulin Homo sapiens 10-17 8169563-2 1994 Hypothyroid patients demonstrate increased serum immunoreactive insulin levels in response to oral glucose when compared with euthyroid subjects. Glucose 99-106 insulin Homo sapiens 64-71 8121304-5 1994 During the IVGTT, plasma glucose level initially increased by twofold and slowly returned to basal level thereafter, whereas insulin level responded to glucose and tolbutamide infusions in a typical biphasic manner. Glucose 152-159 insulin Homo sapiens 125-132 8194268-4 1994 Abnormal laboratory tests include hypersecretion of insulin after glucose loading, elevated levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH), and hypersecretion of LH in the LH-RH test. Glucose 66-73 insulin Homo sapiens 52-59 7507665-4 1994 Increased expression of IRS-1 occurred during differentiation simultaneously with increased insulin-responsive dGlc transport. Glucose 111-115 insulin Homo sapiens 92-99 7507665-5 1994 These data are consistent with a role of IRS-1 in insulin signaling to the glucose transport system. Glucose 75-82 insulin Homo sapiens 50-57 7905262-1 1994 Recent reports of a pertussis-toxin (Ptx)-sensitive inhibition of glucose-induced insulin release by prostaglandin E2 (PGE2) in transformed beta-cells prompted us to look for the presence of prostaglandin-regulatable GTP-binding proteins (G-proteins) on the secretory granules of normal pancreatic islets. Glucose 66-73 insulin Homo sapiens 82-89 8042526-8 1994 The insulin-response curve to glucose ingestion tended to shift to the right during bed rest. Glucose 30-37 insulin Homo sapiens 4-11 7864513-12 1994 For 7 out of 12 patients, glucose tolerance tests showed an adequate insulin secretion: the addition of the two best insulin levels were higher than 70 IU/ml. Glucose 26-33 insulin Homo sapiens 69-76 7864513-12 1994 For 7 out of 12 patients, glucose tolerance tests showed an adequate insulin secretion: the addition of the two best insulin levels were higher than 70 IU/ml. Glucose 26-33 insulin Homo sapiens 117-124 7946533-5 1994 The crucial steps in receptor-mediated stimulation-secretion coupling and their relationship to glucose-stimulated insulin release is summarized in Figure 1. Glucose 96-103 insulin Homo sapiens 115-122 8010891-9 1994 The insulin responsiveness to glucose increased significantly from 0.16 +/- 0.020 during placebo to 0.21 +/- 0.023 during enalapril. Glucose 30-37 insulin Homo sapiens 4-11 8199238-0 1994 Design and synthesis of a protein device that releases insulin in response to glucose concentration. Glucose 78-85 insulin Homo sapiens 55-62 8199238-1 1994 To synthesize a glucose-sensitive insulin-releasing protein device, insulin was esterified with methanol and connected to glucose oxidase with intervention of a disulfide compound, 5,5"-dithiobis(2-nitrobenzoic acid). Glucose 16-23 insulin Homo sapiens 34-41 8199238-1 1994 To synthesize a glucose-sensitive insulin-releasing protein device, insulin was esterified with methanol and connected to glucose oxidase with intervention of a disulfide compound, 5,5"-dithiobis(2-nitrobenzoic acid). Glucose 16-23 insulin Homo sapiens 68-75 8199238-2 1994 On adding glucose to an aqueous solution containing the hybrid enzyme, the modified insulin was released. Glucose 10-17 insulin Homo sapiens 84-91 8199238-3 1994 The amount of insulin released increased with increasing concentration of added glucose. Glucose 80-87 insulin Homo sapiens 14-21 8199238-4 1994 The insulin release from the hybrid enzyme was specific to glucose. Glucose 59-66 insulin Homo sapiens 4-11 7907975-8 1994 CONCLUSIONS: Light-to-moderate alcohol consumption in healthy men and women is associated with enhanced insulin-mediated glucose uptake, lower plasma glucose and insulin concentrations in response to oral glucose, and a higher HDL-cholesterol concentration. Glucose 121-128 insulin Homo sapiens 104-111 8163048-6 1994 Insulin resistance was measured by the insulin tolerance test which uses the rate of fall in blood glucose concentrations after intravenous injection of insulin as an index of insulin resistance. Glucose 99-106 insulin Homo sapiens 0-7 8163048-6 1994 Insulin resistance was measured by the insulin tolerance test which uses the rate of fall in blood glucose concentrations after intravenous injection of insulin as an index of insulin resistance. Glucose 99-106 insulin Homo sapiens 39-46 8163050-3 1994 The amylin used opposed insulin-mediated glucose disposal in rat soleus muscle at concentrations of 10 nmol/l. Glucose 41-48 insulin Homo sapiens 24-31 8288053-0 1994 Assessment of insulin action in NIDDM in the presence of dynamic changes in insulin and glucose concentration. Glucose 88-95 insulin Homo sapiens 14-21 7904978-7 1994 Peripheral glucose uptake, exemplified by forearm glucose uptake (0.27 +/- 0.04 vs. 1.22 +/- 0.42 mg/100 ml/min, p < 0.02), and calculated insulin sensitivity (24 +/- 8 vs. 114 +/- 20 microliters/kg/min per mU/L) were particularly diminished. Glucose 11-18 insulin Homo sapiens 142-149 8294100-6 1994 Specificity of the glucose effect was shown by the binding of insulin and transferrin to their respective receptors, which was unaffected by the high glucose concentration that increased asialoorosomucoid binding. Glucose 19-26 insulin Homo sapiens 62-69 8294688-1 1994 OBJECTIVES: This study was conducted to compare the insulin responses to an oral glucose load in healthy volunteers and patients with syndrome X and patients with coronary artery disease. Glucose 81-88 insulin Homo sapiens 52-59 8294688-5 1994 METHODS: Insulin responses to an oral glucose load (75 g) were compared in 17 patients with coronary artery disease, 17 patients with chest pain, positive exercise test findings, normal coronary arteries and impaired coronary flow reserve (syndrome X) and 17 healthy volunteers (control subjects). Glucose 38-45 insulin Homo sapiens 9-16 8294690-4 1994 RESULTS: Patients with chest pain had higher insulin responses to an intravenous glucose challenge, lower insulin sensitivity, lower high density lipoprotein (HDL) and subfraction 2 cholesterol, lower apolipoprotein AI, higher triglycerides, greater android fat and higher systolic blood pressure at rest compared with levels in healthy control subjects (p < 0.05). Glucose 81-88 insulin Homo sapiens 45-52 8153289-3 1994 We therefore measured the insulin response to a 75 g oral glucose tolerance test in five groups with normal glucose tolerance, comparing normal male controls to men with chronic stable angina, men with recent myocardial infarction (two groups, 3 weeks and 3 months post infarction), and men with chronic severe heart failure. Glucose 58-65 insulin Homo sapiens 26-33 8288558-1 1994 The effect of ascorbic acid on glucose-induced insulin release from single pancreatic islets was measured using a new, ultra-sensitive enzyme-linked immunosorbent insulin assay. Glucose 31-38 insulin Homo sapiens 47-54 8288558-1 1994 The effect of ascorbic acid on glucose-induced insulin release from single pancreatic islets was measured using a new, ultra-sensitive enzyme-linked immunosorbent insulin assay. Glucose 31-38 insulin Homo sapiens 163-170 8288558-5 1994 The inhibition of glucose-induced insulin release by ascorbic acid was associated with hyperpolarization of the pancreatic beta-cell. Glucose 18-25 insulin Homo sapiens 34-41 8136109-10 1994 Lipid metabolism, quality of diabetic control, and the insulin response to a glucose load were not affected unfavorably. Glucose 77-84 insulin Homo sapiens 55-62 8304448-8 1994 We conclude that athletes have increased whole body insulin-stimulated nonoxidative glucose metabolism associated with both pretranslational (mRNA) and posttranslational (enzyme activity) upregulation of GS. Glucose 84-91 insulin Homo sapiens 52-59 8011858-0 1994 Preparation and characterization of a glucose-responsive insulin-releasing polymer device. Glucose 38-45 insulin Homo sapiens 57-64 8011858-9 1994 This gluconic acid-modified insulin (G-Ins) was bound onto a PBA gel column, and the G-Ins release profile in response to varying glucose concentrations was investigated. Glucose 130-137 insulin Homo sapiens 28-35 8110550-12 1994 bolus of insulin 10 u. every 2 h is a simple and effective method to control blood glucose concentrations; the method can be used when an insulin infusion pump is not available. Glucose 83-90 insulin Homo sapiens 9-16 8297693-3 1994 Insulin sensitivity (inversely related to insulin resistance) was measured by minimal modelling analysis of glucose and insulin concentrations during an intravenous glucose tolerance test. Glucose 108-115 insulin Homo sapiens 0-7 8297693-3 1994 Insulin sensitivity (inversely related to insulin resistance) was measured by minimal modelling analysis of glucose and insulin concentrations during an intravenous glucose tolerance test. Glucose 108-115 insulin Homo sapiens 42-49 8297693-3 1994 Insulin sensitivity (inversely related to insulin resistance) was measured by minimal modelling analysis of glucose and insulin concentrations during an intravenous glucose tolerance test. Glucose 165-172 insulin Homo sapiens 0-7 7867022-5 1994 In the present study, we succeeded in introducing and expressing the functional gene for human insulin, and we observed the expression of this gene in mouse plasma and the reduction of plasma glucose. Glucose 192-199 insulin Homo sapiens 95-102 8187463-2 1994 The parameters of the model were based on experimental data from the literature describing insulin and carbohydrate absorption, renal loss of glucose, insulin-independent glucose utilisation and insulin-dependent glucose utilisation and production. Glucose 171-178 insulin Homo sapiens 151-158 8187463-2 1994 The parameters of the model were based on experimental data from the literature describing insulin and carbohydrate absorption, renal loss of glucose, insulin-independent glucose utilisation and insulin-dependent glucose utilisation and production. Glucose 171-178 insulin Homo sapiens 151-158 8187463-2 1994 The parameters of the model were based on experimental data from the literature describing insulin and carbohydrate absorption, renal loss of glucose, insulin-independent glucose utilisation and insulin-dependent glucose utilisation and production. Glucose 171-178 insulin Homo sapiens 151-158 8187463-2 1994 The parameters of the model were based on experimental data from the literature describing insulin and carbohydrate absorption, renal loss of glucose, insulin-independent glucose utilisation and insulin-dependent glucose utilisation and production. Glucose 171-178 insulin Homo sapiens 151-158 7512060-3 1994 Subcutaneous injections of rapid acting insulin were given at 3-h intervals to improve glycaemic control in diabetic patients (fasting plasma glucose decreased from 20.8 +/- 0.8 to 8.7 +/- 0.8 mmol/l whereas fasting serum insulin increased from 59 +/- 8 to 173 +/- 3 pmol/l). Glucose 142-149 insulin Homo sapiens 40-47 7648784-1 1994 Estimates of in vivo insulin sensitivity (S1) can be derived from minimal model analysis of a frequently sampled intravenous glucose tolerance test (FSIVGTT). Glucose 125-132 insulin Homo sapiens 21-28 8056132-11 1994 A vicious circle starts after insulin resistance to glucose uptake appears, followed by hyperglycaemia blocking the glucose storage system and by the lack of storing capacity leading to a rise in glycaemia. Glucose 52-59 insulin Homo sapiens 30-37 8112186-3 1994 Insulin sensitivity was assessed using the minimal model analysis of frequently sampled intravenous glucose tolerance tests. Glucose 100-107 insulin Homo sapiens 0-7 8181257-7 1994 The fasting glucose achieved following diet was positively correlated with the initial fasting glucose (r = 0.7) and negatively correlated with the degree of insulin deficiency at diagnosis (with the initial 30 min insulin r = -0.62). Glucose 12-19 insulin Homo sapiens 158-165 8262308-1 1994 During the infusion of insulin in vivo, the rate of activation of glucose disposal lags significantly behind the rate of increase in serum insulin levels. Glucose 66-73 insulin Homo sapiens 23-30 8262308-1 1994 During the infusion of insulin in vivo, the rate of activation of glucose disposal lags significantly behind the rate of increase in serum insulin levels. Glucose 66-73 insulin Homo sapiens 139-146 8262308-6 1994 Insulin infusion increased both IR kinase and GDR maximally approximately 10-fold, with half-maximal stimulation at approximately 3,600 and approximately 700 pM, indicating spare kinase for glucose disposal. Glucose 190-197 insulin Homo sapiens 0-7 8262308-7 1994 These results demonstrate that the delay in stimulation of glucose disposal by insulin is related to a rate-limiting step between the intravascular space and the cell-surface of skeletal muscle. Glucose 59-66 insulin Homo sapiens 79-86 8262315-7 1994 Insulin secretion was further assessed during constant glucose infusion by deconvolution of plasma C-peptide and by pulse analysis. Glucose 55-62 insulin Homo sapiens 0-7 8262315-9 1994 However, the nondiabetic marker-positive group had decreased mean plasma C-peptide concentration and reduced absolute amplitude of insulin secretory oscillations during prolonged glucose infusion. Glucose 179-186 insulin Homo sapiens 131-138 7758398-0 1994 The effect of L-carnitine, administered through intravenous infusion of glucose, on both glucose and insulin levels in healthy subjects. Glucose 72-79 insulin Homo sapiens 101-108 8162919-9 1994 In boys only, the initial glucose drop was significantly correlated to the pre-exercise insulin values. Glucose 26-33 insulin Homo sapiens 88-95 7957534-0 1994 Serum glucose, insulin and C-peptide response to oral glucose after intravenous administration of hydrocortisone and methylprednisolone in man. Glucose 54-61 insulin Homo sapiens 27-36 7957545-4 1994 Insulin action on glucose turnover was assessed directly after each treatment period with the hyperinsulinaemic euglycaemic glucose clamp technique. Glucose 18-25 insulin Homo sapiens 0-7 7957545-8 1994 In conclusion, these data suggest that short-term amiloride slightly impairs insulin sensitivity with respect to glucose uptake. Glucose 113-120 insulin Homo sapiens 77-84 8124481-1 1994 Plasma non-esterified fatty acid concentrations were elevated acutely (Intralipid+heparin infusion) in 14 normal humans in order to study the effects of fatty acids on whole-body basal and insulin-stimulated glucose metabolism, and on activities of skeletal muscle key enzymes. Glucose 208-215 insulin Homo sapiens 189-196 7867989-8 1994 In this patient we also established delayed insulin response after an intravenous glucose load. Glucose 82-89 insulin Homo sapiens 44-51 7867989-9 1994 We concluded that the disturbed insulin secretion found in the children studied is most likely the earliest manifestation of the pancreatic beta-cell insufficiency which precedes the changes in the glucose tolerance. Glucose 198-205 insulin Homo sapiens 32-39 8299887-1 1994 The beta cell of the islets of Langerhans contributes along with other factors to glucose homeostasis by sensing changes in the plasma glucose concentrations and adjusting the rate of insulin production and release. Glucose 82-89 insulin Homo sapiens 184-191 8299887-6 1994 Effects of glucose metabolism on the turnover of insulin mRNA have yet to be characterized in detail. Glucose 11-18 insulin Homo sapiens 49-56 8299887-7 1994 At the level of transcription, cis-acting DNA elements and trans-acting factors involved in the transient response of the insulin gene to changes in intracellular cAMP levels, or to signals generated as a result of glucose metabolism, have been identified. Glucose 215-222 insulin Homo sapiens 122-129 8299888-2 1994 The transcriptional effect of glucose can be indirect, being mediated in vivo by hormonal variations, especially increase in insulin and decrease in glucagon secretion. Glucose 30-37 insulin Homo sapiens 125-132 8299888-4 1994 The role of insulin in the activation of these genes seems mainly to stimulate glucokinase synthesis, and thus to permit glucose phosphorylation. Glucose 121-128 insulin Homo sapiens 12-19 8299888-6 1994 In hepatocytes, the insulin effect on the glucose-dependent activation of the L-pyruvate kinase gene can be reproduced by fructose at low concentrations. Glucose 42-49 insulin Homo sapiens 20-27 7590419-10 1994 The analysis of the first-phase insulin secretory response (the insulin response to rapidly injected glucose during the intravenous glucose tolerance test) which has been shown to be impaired very early during the development of diabetes, has demonstrated the lack of its recovery both in the spontaneous and in cyclosporin A-induced remissions. Glucose 101-108 insulin Homo sapiens 32-39 7590419-10 1994 The analysis of the first-phase insulin secretory response (the insulin response to rapidly injected glucose during the intravenous glucose tolerance test) which has been shown to be impaired very early during the development of diabetes, has demonstrated the lack of its recovery both in the spontaneous and in cyclosporin A-induced remissions. Glucose 101-108 insulin Homo sapiens 64-71 7590419-10 1994 The analysis of the first-phase insulin secretory response (the insulin response to rapidly injected glucose during the intravenous glucose tolerance test) which has been shown to be impaired very early during the development of diabetes, has demonstrated the lack of its recovery both in the spontaneous and in cyclosporin A-induced remissions. Glucose 132-139 insulin Homo sapiens 32-39 7590419-10 1994 The analysis of the first-phase insulin secretory response (the insulin response to rapidly injected glucose during the intravenous glucose tolerance test) which has been shown to be impaired very early during the development of diabetes, has demonstrated the lack of its recovery both in the spontaneous and in cyclosporin A-induced remissions. Glucose 132-139 insulin Homo sapiens 64-71 7959621-1 1994 The authors observed that there is wide variability in insulin response to an oral glucose tolerance test in women developing carbohydrate intolerance during pregnancy. Glucose 83-90 insulin Homo sapiens 55-62 8088710-5 1994 LysPro-insulin has demonstrated an improved time course of action in control of a mealtime glucose elevation. Glucose 91-98 insulin Homo sapiens 7-14 7714402-2 1994 The major regulator of glucose concentration in the blood is insulin. Glucose 23-30 insulin Homo sapiens 61-68 8282343-3 1994 Offspring of hypertensive parents presented significantly higher serum insulin levels both after an overnight fast (17.4 +/- 1.6 versus 11.6 +/- 1.6 microU/mL in control [mean +/- SEM], P < .01) and after intravenous glucose than control subjects (insulin area under the curve, 3015 +/- 310 and 2057 +/- 234 microU/mL per hour, respectively, P < .01). Glucose 220-227 insulin Homo sapiens 71-78 8282372-3 1994 The mean glucose infusion rate was used as an indicator of insulin sensitivity (M value). Glucose 9-16 insulin Homo sapiens 59-66 8282372-8 1994 These results indicate that selective insulin resistance with respect to glucose metabolism exists in essential hypertensive patients and that insulin action on renal sodium handling and pressor systems was maintained in these patients. Glucose 73-80 insulin Homo sapiens 38-45 7511740-5 1994 More obvious improvement in glucose tolerance was evident in hypertensive patients who were glucose intolerant and/or insulin resistant (GI/IR, 53.8% of all), however. Glucose 28-35 insulin Homo sapiens 118-125 7519694-2 1994 Today, insulin resistance is widely understood as a tissue- and pathway-specific defect of insulin-stimulated glucose uptake into skeletal muscle that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. Glucose 110-117 insulin Homo sapiens 7-14 7519694-2 1994 Today, insulin resistance is widely understood as a tissue- and pathway-specific defect of insulin-stimulated glucose uptake into skeletal muscle that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. Glucose 110-117 insulin Homo sapiens 91-98 7519694-4 1994 Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. Glucose 148-155 insulin Homo sapiens 113-120 7519694-4 1994 Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. Glucose 242-249 insulin Homo sapiens 113-120 7519694-4 1994 Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. Glucose 242-249 insulin Homo sapiens 181-188 7519694-5 1994 This improvement of insulin sensitivity could mean not only improvement of glucose metabolism, but also reduction of chronically elevated serum insulin and the ensuing atherogenic consequences (hyper- and dyslipidemia, sympathetic overactivity, growth of vascular smooth-muscle cells, hypertension, etc.). Glucose 75-82 insulin Homo sapiens 20-27 7700069-2 1994 The effects of insulin on plasma potassium levels and whole-body potassium content and the effect of potassium on glucose-induced insulin release identify a physiological glucose-potassium cycle. Glucose 114-121 insulin Homo sapiens 130-137 7700069-6 1994 The effects of angiotensin-converting enzyme inhibition on insulin sensitivity and glucose tolerance are reviewed in the context of the glucose-potassium cycle. Glucose 136-143 insulin Homo sapiens 59-66 8137525-10 1994 RESULTS: The plasma glucose and insulin responses during a 75-g oral glucose challenge increased significantly (P < 0.05 and P < 0.03, respectively). Glucose 69-76 insulin Homo sapiens 32-39 8137525-11 1994 The steady-state plasma glucose (SSPG) concentrations achieved during constant infusion of glucose, insulin and somatostatin increased significantly after 3 cycles of OC administration (glucose 7.5 +/- 0.8 vs 12.4 +/- 0.7 mmol/l, P < 0.001) while the steady-state plasma insulin (SSPI) concentrations were relatively similar (410 +/- 14 vs 391 +/- 7 pmol/l, NS). Glucose 24-31 insulin Homo sapiens 100-107 8282776-6 1994 In each individual, the glucose uptake closely correlated with peripheral lymphatic insulin concentrations (mean r2 = 0.95). Glucose 24-31 insulin Homo sapiens 84-91 8282776-0 1994 Interstitial insulin concentrations determine glucose uptake rates but not insulin resistance in lean and obese men. Glucose 46-53 insulin Homo sapiens 13-20 8282776-7 1994 The coupling between glucose uptake and lymph insulin (glucose uptake/pmol insulin) was much steeper in lean subjects than in the obese (P < or = 0.0001). Glucose 21-28 insulin Homo sapiens 46-53 8282776-7 1994 The coupling between glucose uptake and lymph insulin (glucose uptake/pmol insulin) was much steeper in lean subjects than in the obese (P < or = 0.0001). Glucose 55-62 insulin Homo sapiens 46-53 7986303-1 1994 Resistance to insulin-stimulated glucose uptake is a common phenomenon, occurring in approximately 25% of the population at large, and is associated with a number of conditions known to be risk factors for coronary heart disease (CHD). Glucose 33-40 insulin Homo sapiens 14-21 8288709-4 1994 In simple linear regression analysis, the serum uric acid concentration (range, 182-568 mumol/L) was inversely correlated with insulin sensitivity (rate of glucose utilization; r = -0.61; P < 0.001) and positively with serum triglycerides (r = 0.68; P < 0.001), but not with body mass index, age, or the plasma glucose concentration. Glucose 156-163 insulin Homo sapiens 127-134 8288709-4 1994 In simple linear regression analysis, the serum uric acid concentration (range, 182-568 mumol/L) was inversely correlated with insulin sensitivity (rate of glucose utilization; r = -0.61; P < 0.001) and positively with serum triglycerides (r = 0.68; P < 0.001), but not with body mass index, age, or the plasma glucose concentration. Glucose 317-324 insulin Homo sapiens 127-134 8283160-3 1994 DESIGN: This represents a case-control study, in which normal volunteers were subdivided into four equal groups based upon degree of obesity and plasma insulin response to a 74 g oral glucose challenge. Glucose 184-191 insulin Homo sapiens 152-159 8186820-0 1994 First-phase insulin response to intravenous glucose in cystic fibrosis patients with different degrees of glucose tolerance. Glucose 44-51 insulin Homo sapiens 12-19 7714412-1 1994 Animal studies have shown that insulin eyedrops containing an absorption-enhancing agent can have a significant effect on blood glucose levels. Glucose 128-135 insulin Homo sapiens 31-38 8186820-4 1994 glucose bolus to evaluate early phase insulin release. Glucose 0-7 insulin Homo sapiens 38-45 8186820-5 1994 When compared to the normal subjects, CF patients had significantly reduced basal (76 +/- 50 vs 108 +/- 30 pM/l, 2 p < 0.02) and glucose stimulated insulin levels (1 + 3 min insulin = 456 +/- 275 vs 951 +/- 170 pM/l, 2 p < 0.01). Glucose 132-139 insulin Homo sapiens 151-158 8111128-3 1994 This reduced phosphatase activity probably leads to the abnormal insulin action for glucose storage observed in insulin-resistant subjects. Glucose 84-91 insulin Homo sapiens 65-72 8289670-4 1994 In addition, fasting plasma insulin concentrations and the glucose and insulin areas under the oral glucose tolerance test (OGTT) curve were both significantly associated with systolic BP during submaximal exercise. Glucose 100-107 insulin Homo sapiens 71-78 8289671-3 1994 Prolonged (270 minutes) hyperglycemic clamps were used to assess octreotide-mediated suppression of glucose-stimulated endogenous insulin secretion. Glucose 100-107 insulin Homo sapiens 130-137 8134054-9 1994 This leads to gestational diabetes in 2 to 3 per cent of women who exhibit hyperglycemia despite an increased insulin response to oral glucose as well as an increased insulin/glucagon ratio. Glucose 135-142 insulin Homo sapiens 110-117 8199424-7 1994 After hypoglycemia, higher insulin infusion rates than in the control group were required to clamp plasma glucose concentrations at similar levels (p < 0.05). Glucose 106-113 insulin Homo sapiens 27-34 8159440-4 1994 During an overnight fast, blood glucose concentration was normalized by refract insulin injections. Glucose 32-39 insulin Homo sapiens 80-87 8165371-2 1994 Insulin was infused into the subjects for 2 hours while baseline plasma glucose concentrations were maintained. Glucose 72-79 insulin Homo sapiens 0-7 7863172-13 1994 In CPE induced by hyperglycaemia without ketosis normalization of blood glucose level with insulin therapy is concomitant with a rapid cure of epilepsy. Glucose 72-79 insulin Homo sapiens 91-98 8128180-0 1994 Insulin action on glucose transport in isolated skeletal muscle from patients with liver cirrhosis. Glucose 18-25 insulin Homo sapiens 0-7 8128180-2 1994 We used an in vitro incubation technique to determine insulin action on glucose transport in skeletal muscle obtained from seven patients with clinically stable alcoholic cirrhosis and seven healthy age- and sex-matched individuals. Glucose 72-79 insulin Homo sapiens 54-61 8128180-4 1994 Insulin-mediated peripheral glucose utilization was 40% lower (p < 0.05) in the cirrhotic patients than in the healthy individuals. Glucose 28-35 insulin Homo sapiens 0-7 8128180-10 1994 In conclusion, the present group of patients, with liver cirrhosis on an alcoholic basis, had a normal insulin-stimulated capacity for glucose transport at the cellular level irrespective of the degree of whole-body insulin resistance. Glucose 135-142 insulin Homo sapiens 103-110 7524845-5 1994 The existence of the common epitope leads to competition of insulin and apoprotein B for an insulin receptor and reduces tissue glucose uptake. Glucose 128-135 insulin Homo sapiens 60-67 7846893-2 1994 The individual components of the metabolic syndrome such as central obesity, dyslipidemia with increased triglycerides and decreased HDL-cholesterol, hyperuricemia, hypertension and progressive glucose intolerance are markers for an increased risk of atheroma and type 2 (non-insulin-dependent) diabetes. Glucose 194-201 insulin Homo sapiens 276-283 7846898-2 1994 Several studies demonstrate that body weight decreases and insulin resistance improves--as evaluated by peripheral glucose utilisation--under metformin treatment. Glucose 115-122 insulin Homo sapiens 59-66 8045181-4 1994 were used to relieve the symptoms; insulin was also administered to control the blood glucose level. Glucose 86-93 insulin Homo sapiens 35-42 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-7 1993 Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Glucose 107-114 insulin Homo sapiens 75-82 8247074-8 1993 CONCLUSIONS: Insulin resistance is a major risk factor for the development of NIDDM: A low acute insulin response to glucose is an additional but weaker risk factor. Glucose 117-124 insulin Homo sapiens 97-104 8253768-4 1993 Insulin increased glucose transport and GLUT4 translocation to the cell surface by 15- and 7-fold, respectively. Glucose 18-25 insulin Homo sapiens 0-7 8253768-6 1993 Insulin increased the glycogen synthase ratio (-Glc-6-P/+Glc-6-P) by 7.5- and 3.5-fold in the presence and absence of glucose, respectively. Glucose 48-51 insulin Homo sapiens 0-7 8253768-6 1993 Insulin increased the glycogen synthase ratio (-Glc-6-P/+Glc-6-P) by 7.5- and 3.5-fold in the presence and absence of glucose, respectively. Glucose 57-60 insulin Homo sapiens 0-7 8253768-6 1993 Insulin increased the glycogen synthase ratio (-Glc-6-P/+Glc-6-P) by 7.5- and 3.5-fold in the presence and absence of glucose, respectively. Glucose 118-125 insulin Homo sapiens 0-7 8253768-8 1993 EGF did not appear to inhibit downstream of MAP kinase, because when adipocytes were incubated with insulin plus EGF, the stimulation of glucose transport and glycogen synthase was similar to that observed with insulin alone. Glucose 137-144 insulin Homo sapiens 100-107 8280078-12 1993 The effects of glucose and fructose were rapid (t1/2 5 min) and reversible, and were potentiated by insulin and counteracted by glucagon. Glucose 15-22 insulin Homo sapiens 100-107 8257685-1 1993 Pancreatic islets, when stimulated with D-glucose, secrete insulin by processes requiring glycolytic metabolism and generation of ATP. Glucose 40-49 insulin Homo sapiens 59-66 8257685-2 1993 Hydrolysis of membrane phospholipids also occurs in glucose-stimulated islets, resulting in accumulation of nonesterified arachidonate, which facilitates Ca2+ entry and the rise in beta-cell [Ca2+] that triggers insulin secretion. Glucose 52-59 insulin Homo sapiens 212-219 8128887-0 1993 Increased insulin-stimulated glucose uptake in athletes: the importance of GLUT4 mRNA, GLUT4 protein and fibre type composition of skeletal muscle. Glucose 29-36 insulin Homo sapiens 10-17 8128887-5 1993 The rate of insulin-stimulated glucose uptake was increased in the trained subjects (17.34 +/- 0.53 vs. 13.53 +/- 0.79 mg kg-1 min-1, P < 0.01). Glucose 31-38 insulin Homo sapiens 12-19 8128887-7 1993 In the total group of participants, GLUT4 protein per DNA in the basal state and insulin-stimulated glucose uptake rate correlated positively, (r = 0.51, P = 0.05). Glucose 100-107 insulin Homo sapiens 81-88 8128887-10 1993 A significantly negative correlation was found between type 2B fibre area and insulin-stimulated glucose uptake (r = -0.63, P < 0.05). Glucose 97-104 insulin Homo sapiens 78-85 8128887-12 1993 However, factors other than GLUT4 immunoreactive protein abundance seem to be determinant for the increased insulin-stimulated whole body glucose uptake in endurance trained subjects. Glucose 138-145 insulin Homo sapiens 108-115 8279537-4 1993 Glucose rate of appearance (Ra) declined equivalently in the 49 pmol.kg-1.min-1 IGF-I and insulin clamps but remained at basal levels during the 33 pmol.kg-1 x min-1 IGF-I infusions. Glucose 0-7 insulin Homo sapiens 90-97 8279545-0 1993 Differential regulation of intracellular glucose metabolism by glucose and insulin in human muscle. Glucose 41-48 insulin Homo sapiens 75-82 8279545-1 1993 Insulin and glucose stimulate glucose uptake in human muscle by different mechanisms. Glucose 30-37 insulin Homo sapiens 0-7 8279545-2 1993 Insulin has well-known effects on glucose transport, glycogen synthesis, and glucose oxidation, but the effects of hyperglycemia on the intracellular routing of glucose are less well characterized. Glucose 34-41 insulin Homo sapiens 0-7 8279545-2 1993 Insulin has well-known effects on glucose transport, glycogen synthesis, and glucose oxidation, but the effects of hyperglycemia on the intracellular routing of glucose are less well characterized. Glucose 77-84 insulin Homo sapiens 0-7 8279550-8 1993 In conclusion, in healthy subjects, glycogen synthesis plays a greater role than glycolysis and glucose oxidation in determining insulin-mediated glucose disposal. Glucose 96-103 insulin Homo sapiens 129-136 8279550-9 1993 Part of insulin-mediated increase in glycolysis/oxidation might be secondary to the relief of the competition between fat and glucose for oxidation. Glucose 126-133 insulin Homo sapiens 8-15 8136068-3 1993 Initially, adults with very mild DAT showed memory facilitation and elevations in plasma insulin in the 225-mg/dl glucose condition relative to baseline. Glucose 114-121 insulin Homo sapiens 89-96 8141692-2 1993 AIM: To compare the impact of two different ACEIs (captopril and enalapril) on insulin mediated glucose uptake in normotensive, non-obese, insulin sensitive subjects. Glucose 96-103 insulin Homo sapiens 79-86 8141692-4 1993 Insulin mediated glucose uptake was measured by means of the euglycaemic hyperinsulinaemic clamp at the start and completion of each period of drug therapy. Glucose 17-24 insulin Homo sapiens 0-7 8141692-5 1993 RESULTS: Both drugs resulted in elevations of fasting insulin levels (mean difference +/- SEM for combined data, 2.7 +/- 1.8; p < 0.05) and a reduction in insulin mediated glucose uptake (mean difference for combined data, -0.72 +/- 0.37 mg/kg-1 minute-1; p = 0.056). Glucose 175-182 insulin Homo sapiens 158-165 8141692-7 1993 CONCLUSIONS: The increase in fasting insulin levels, and reduction in insulin mediated glucose uptake in this study are in contrast to findings in obese and hypertensive subjects, and indicate that studies of insulin sensitivity of ACEIs in non-obese, normotensive subjects are inappropriate for predicting likely effects in clinical practice. Glucose 87-94 insulin Homo sapiens 70-77 8141692-7 1993 CONCLUSIONS: The increase in fasting insulin levels, and reduction in insulin mediated glucose uptake in this study are in contrast to findings in obese and hypertensive subjects, and indicate that studies of insulin sensitivity of ACEIs in non-obese, normotensive subjects are inappropriate for predicting likely effects in clinical practice. Glucose 87-94 insulin Homo sapiens 70-77 8180882-6 1993 The variations of insulin and C-peptide exactly paralleled those observed for glucose. Glucose 78-85 insulin Homo sapiens 18-25 8111860-3 1993 Insulin is a hormone which regulates the carbohydrate and triacylglyceride metabolism through its action at several sites and facilitates the entry of glucose accumulation in the blood. Glucose 151-158 insulin Homo sapiens 0-7 8243815-8 1993 Intensive insulin therapy lowered the mean daily blood glucose concentration and HbA1 (14.8 +/- 1.6 to 7.7 +/- 0.6 mM and 12.9 +/- 0.9 to 9.6 +/- 0.6%, both P < 0.01) and almost eliminated glycosuria (428 +/- 116 to 39 +/- 22 mmol/day, P < 0.05). Glucose 55-62 insulin Homo sapiens 10-17 8243815-11 1993 The rates of glucose, glycerol, free fatty acid, and leucine turnover, triglyceride/free fatty acid cycling, and nonoxidative glucose and protein disposal were reduced in the diabetic volunteers during intensive insulin therapy. Glucose 126-133 insulin Homo sapiens 212-219 8243823-0 1993 Multiple defects in the adipocyte glucose transport system cause cellular insulin resistance in gestational diabetes. Glucose 34-41 insulin Homo sapiens 74-81 8243823-4 1993 Cellular insulin resistance was attributed to impaired stimulation of glucose transport; compared with control subjects, basal and maximally insulin-stimulated transport rates (per surface area) were reduced 38 and 60% in GDM patients, respectively. Glucose 70-77 insulin Homo sapiens 9-16 8243823-4 1993 Cellular insulin resistance was attributed to impaired stimulation of glucose transport; compared with control subjects, basal and maximally insulin-stimulated transport rates (per surface area) were reduced 38 and 60% in GDM patients, respectively. Glucose 70-77 insulin Homo sapiens 141-148 8243823-5 1993 To determine underlying mechanisms, we assessed the number, subcellular distribution, and translocation of GLUT4, the predominant insulin-responsive glucose transporter isoform. Glucose 149-156 insulin Homo sapiens 130-137 8243823-15 1993 In GDM, we conclude that insulin resistance in adipocytes involves impaired stimulation of glucose transport and arises from a heterogeneity of defects intrinsic to the glucose transport effector system. Glucose 91-98 insulin Homo sapiens 25-32 8243823-15 1993 In GDM, we conclude that insulin resistance in adipocytes involves impaired stimulation of glucose transport and arises from a heterogeneity of defects intrinsic to the glucose transport effector system. Glucose 169-176 insulin Homo sapiens 25-32 8243832-2 1993 The improvement of glucose tolerance after long-term treatment of NIDDM patients with the drug can be explained by stimulation of glucose utilization in peripheral tissues that are characterized by insulin resistance in these patients. Glucose 19-26 insulin Homo sapiens 198-205 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 87-94 insulin Homo sapiens 156-163 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 87-94 insulin Homo sapiens 156-163 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 135-142 insulin Homo sapiens 111-118 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 135-142 insulin Homo sapiens 156-163 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 135-142 insulin Homo sapiens 156-163 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 135-142 insulin Homo sapiens 111-118 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 135-142 insulin Homo sapiens 156-163 8243832-4 1993 After long-term incubation of the cells in primary culture with high concentrations of glucose, glutamine, and insulin, stimulation of glucose transport by insulin was significantly reduced both with respect to maximal responsiveness (65% decrease of Vmax) and sensitivity (2.6-fold increase of ED50) compared with adipocytes cultured in medium containing a low concentration of glucose and no insulin. Glucose 135-142 insulin Homo sapiens 156-163 8243832-5 1993 This reflects insulin resistance of glucose transport. Glucose 36-43 insulin Homo sapiens 14-21 8243832-7 1993 Glimepiride, in combination with glucose and glutamine during the primary culture, caused desensitization of the glucose transport system toward stimulation by insulin, but to a lesser degree than insulin itself (50% reduction of Vmax; ninefold increase of ED50). Glucose 113-120 insulin Homo sapiens 160-167 8243832-10 1993 The stimulation of glucose transport in insulin-resistant adipocytes by glimepiride is caused by translocation of glucose transporters from low-density microsomes to plasma membranes as demonstrated by subcellular fractionation and immunoblotting with anti-GLUT1 and anti-GLUT4 antibodies. Glucose 19-26 insulin Homo sapiens 40-47 8243833-0 1993 Different sensitivity of glucose and amino acid metabolism to insulin in NIDDM. Glucose 25-32 insulin Homo sapiens 62-69 8243833-6 1993 Insulin-mediated total body glucose uptake was significantly reduced in NIDDM during both study 1 (5.6 +/- 0.4 vs. 6.9 +/- 0.6 mg.kg-1 x min-1, P < 0.01) and study 2 (5.2 +/- 0.4 vs. 6.8 +/- 0.6, P < 0.01). Glucose 28-35 insulin Homo sapiens 0-7 8299450-6 1993 In the postprandial studies of control subjects, insulin and C-peptide levels were higher at the time of ingestion of the 50 g of glucose, but the early (1 h) insulin secretory response was less than in the fasting study. Glucose 130-137 insulin Homo sapiens 49-56 8299450-6 1993 In the postprandial studies of control subjects, insulin and C-peptide levels were higher at the time of ingestion of the 50 g of glucose, but the early (1 h) insulin secretory response was less than in the fasting study. Glucose 130-137 insulin Homo sapiens 61-70 8299450-8 1993 In contrast to the control subjects, the insulin secretory response to 50 g of oral glucose was greater in the two postprandial studies than in the fasting study. Glucose 84-91 insulin Homo sapiens 41-48 8299451-2 1993 OBJECTIVE: To ascertain whether childbearing would decrease oral glucose-stimulated insulin and C-peptide levels and increase the risk of NIDDM and impaired glucose tolerance in a population of Hispanic and non-Hispanic white women residing in the San Luis Valley of Colorado. Glucose 65-72 insulin Homo sapiens 84-91 8299455-7 1993 RESULTS: After injections of regular insulin in the abdomen, the peak postprandial increment in plasma glucose was 3.1 mM or 29% lower (P < 0.001), the peak increment in serum free insulin was 54 pM or 38% higher (P = 0.017), and the length of time required to achieve peak serum free insulin was significantly shorter than after injections of regular insulin in the thigh. Glucose 103-110 insulin Homo sapiens 37-44 8299455-7 1993 RESULTS: After injections of regular insulin in the abdomen, the peak postprandial increment in plasma glucose was 3.1 mM or 29% lower (P < 0.001), the peak increment in serum free insulin was 54 pM or 38% higher (P = 0.017), and the length of time required to achieve peak serum free insulin was significantly shorter than after injections of regular insulin in the thigh. Glucose 103-110 insulin Homo sapiens 184-191 8299455-7 1993 RESULTS: After injections of regular insulin in the abdomen, the peak postprandial increment in plasma glucose was 3.1 mM or 29% lower (P < 0.001), the peak increment in serum free insulin was 54 pM or 38% higher (P = 0.017), and the length of time required to achieve peak serum free insulin was significantly shorter than after injections of regular insulin in the thigh. Glucose 103-110 insulin Homo sapiens 184-191 8299455-7 1993 RESULTS: After injections of regular insulin in the abdomen, the peak postprandial increment in plasma glucose was 3.1 mM or 29% lower (P < 0.001), the peak increment in serum free insulin was 54 pM or 38% higher (P = 0.017), and the length of time required to achieve peak serum free insulin was significantly shorter than after injections of regular insulin in the thigh. Glucose 103-110 insulin Homo sapiens 184-191 8299455-10 1993 CONCLUSIONS: A subcutaneous injection of regular insulin in the abdomen produced a substantially greater reduction in plasma glucose than an injection of regular insulin in the thigh. Glucose 125-132 insulin Homo sapiens 49-56 8299456-0 1993 Prepregnancy weight and antepartum insulin secretion predict glucose tolerance five years after gestational diabetes mellitus. Glucose 61-68 insulin Homo sapiens 35-42 8299475-1 1993 Administration of exogenous insulin can ameliorate metabolic abnormalities in type II diabetes: It compensates for reduced endogenous insulin secretion, reduces excessive hepatic glucose production, and stimulates glucose uptake, enhancing both glucose oxidation and storage in the muscle tissue. Glucose 179-186 insulin Homo sapiens 28-35 8299475-1 1993 Administration of exogenous insulin can ameliorate metabolic abnormalities in type II diabetes: It compensates for reduced endogenous insulin secretion, reduces excessive hepatic glucose production, and stimulates glucose uptake, enhancing both glucose oxidation and storage in the muscle tissue. Glucose 214-221 insulin Homo sapiens 28-35 8299475-1 1993 Administration of exogenous insulin can ameliorate metabolic abnormalities in type II diabetes: It compensates for reduced endogenous insulin secretion, reduces excessive hepatic glucose production, and stimulates glucose uptake, enhancing both glucose oxidation and storage in the muscle tissue. Glucose 214-221 insulin Homo sapiens 28-35 8299479-4 1993 The thrifty genotype hypothesis provides a plausible basis for a better understanding of how hyperinsulinemia and insulin resistance could lead to glucose intolerance and atherosclerotic cardiovascular disease, but the detailed biochemical mechanisms remain elusive. Glucose 147-154 insulin Homo sapiens 98-105 8299480-3 1993 If the target fasting plasma glucose is the ambitious near-normoglycemia of intensive insulin therapy, intermediate-acting insulin at suppertime easily results in hypoglycemia in the early evening hours and hyperglycemia in the fasting state. Glucose 29-36 insulin Homo sapiens 86-93 8299480-3 1993 If the target fasting plasma glucose is the ambitious near-normoglycemia of intensive insulin therapy, intermediate-acting insulin at suppertime easily results in hypoglycemia in the early evening hours and hyperglycemia in the fasting state. Glucose 29-36 insulin Homo sapiens 123-130 8306591-6 1993 Inhibition of NEFA metabolism was associated with increased insulin-stimulated glucose uptake (from 3.56 +/- 0.28 to 5.14 +/- 0.67 mumol kg-1 min-1, p < 0.05), mainly due to stimulation of non-oxidative glucose disposal (from 1.74 +/- 0.23 to 3.03 +/- 0.53 mumol kg-1 min-1, p < 0.05). Glucose 79-86 insulin Homo sapiens 60-67 8306591-6 1993 Inhibition of NEFA metabolism was associated with increased insulin-stimulated glucose uptake (from 3.56 +/- 0.28 to 5.14 +/- 0.67 mumol kg-1 min-1, p < 0.05), mainly due to stimulation of non-oxidative glucose disposal (from 1.74 +/- 0.23 to 3.03 +/- 0.53 mumol kg-1 min-1, p < 0.05). Glucose 206-213 insulin Homo sapiens 60-67 8307262-7 1993 In a subgroup of 134 normal mothers with pre-pregnancy body mass index of less than 25 kg.m-2, in whom plasma insulin measurements were available, the insulin area-under-curve was inversely related to birthweight (p < 0.02) after simultaneously adjusting for physiological factors and glucose area. Glucose 288-295 insulin Homo sapiens 151-158 8143760-3 1993 Dialysate glucose levels decreased similarly by 20-30%., in patients and controls, which in the presence of unchanged local blood flow in the adipose tissue in response to insulin, is at hand with a glucose uptake into the adipocytes of similar magnitude in both groups. Glucose 10-17 insulin Homo sapiens 172-179 8143760-3 1993 Dialysate glucose levels decreased similarly by 20-30%., in patients and controls, which in the presence of unchanged local blood flow in the adipose tissue in response to insulin, is at hand with a glucose uptake into the adipocytes of similar magnitude in both groups. Glucose 199-206 insulin Homo sapiens 172-179 8243706-7 1993 The effects on circulating androgen levels of oral glucose-mediated increases in insulin levels were significantly different from those of a continuous intravenous insulin infusion. Glucose 51-58 insulin Homo sapiens 81-88 8263133-4 1993 Moreover, insulin-stimulated glucose disposal was studied by means of the euglycemic hyperinsulinemic clamp technique. Glucose 29-36 insulin Homo sapiens 10-17 8263144-10 1993 The insulin response to glucose of the human islets was about 5-fold. Glucose 24-31 insulin Homo sapiens 4-11 8148041-4 1993 After culturing for 24 h in Dulbecco"s medium containing 10 mM glucose, the AtT20MtIns-1.4 cells released human insulin at about 5 ng/10(6) cells per 24 h. Insulin release was not significantly altered by raised concentrations of glucose, potassium or calcium, but insulin release was increased by 20 mM arginine, 5 mM isomethylbutylxanthine and 90 microM zinc. Glucose 63-70 insulin Homo sapiens 112-119 8148041-4 1993 After culturing for 24 h in Dulbecco"s medium containing 10 mM glucose, the AtT20MtIns-1.4 cells released human insulin at about 5 ng/10(6) cells per 24 h. Insulin release was not significantly altered by raised concentrations of glucose, potassium or calcium, but insulin release was increased by 20 mM arginine, 5 mM isomethylbutylxanthine and 90 microM zinc. Glucose 63-70 insulin Homo sapiens 156-163 8246770-0 1993 Effects of glucose, galactose, and lactose ingestion on the plasma glucose and insulin response in persons with non-insulin-dependent diabetes mellitus. Glucose 11-18 insulin Homo sapiens 79-86 8246770-2 1993 The contribution of galactose to the increase in glucose and insulin levels following ingestion of equimolar amounts of galactose and glucose, or lactose, has not been reported in people with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 134-141 insulin Homo sapiens 61-68 8246771-3 1993 In one study (12 females, 17 males), plasma glucose level was rapidly decreased to about 57 mg/dL for 100 minutes with a 0.65-mU/kg/min insulin infusion. Glucose 44-51 insulin Homo sapiens 136-143 8246771-5 1993 In the second study (10 females, eight males), a 5.0-mU/kg/min insulin infusion was used to decrease glucose levels to 55 mg/dL for 180 minutes. Glucose 101-108 insulin Homo sapiens 63-70 8248296-5 1993 We review the mechanisms and regulation of skeletal muscle glucose transport as background for understanding how defects in this process may contribute to the underlying pathogenesis of insulin resistance. Glucose 59-66 insulin Homo sapiens 186-193 8122030-5 1993 These results indicate that insulin absorption occurred, as evidenced from a decrease in blood glucose concentration, and in the case of free insulin and erythrocyte-ghosts-insulin (EG-INS). Glucose 95-102 insulin Homo sapiens 28-35 7506454-3 1993 In the present study, we have compared the effects of CsA and FK506 on glucose-stimulated insulin release from the isolated dog pancreatic islets, which have been maintained in culture for 3 days after isolation. Glucose 71-78 insulin Homo sapiens 90-97 7506454-6 1993 CsA (100 nM), which is a therapeutically relevant concentration, significantly suppressed both the first and second phases of glucose-stimulated insulin release compared with 100 nM FK506. Glucose 126-133 insulin Homo sapiens 145-152 8279000-10 1993 Our results indicate that it is possible to generate ICCs from cryopreserved human fetal pancreas with the capacity, after transplantation, to release insulin appropriately in response to glucose. Glucose 188-195 insulin Homo sapiens 151-158 8149641-9 1993 The findings suggest that (a) higher insulin binding in HP could contribute to the improved glucose tolerance in early pregnancy and (b) the lack of increase in insulin binding during early pregnancy in gestational diabetes might be one factor leading to the manifestation of the disease in late pregnancy. Glucose 92-99 insulin Homo sapiens 37-44 8218298-2 1993 Insulin secretagogues, such as glucose and the muscarinic agonist carbachol, stimulate arachidonic acid accumulation, although the mechanisms involved are controversial: carbachol is believed to stimulate phospholipase A2, while glucose-induced arachidonic acid release is the result of diacylglycerol hydrolysis [Konrad, R. J., et al. Glucose 31-38 insulin Homo sapiens 0-7 7934624-0 1994 Different mechanism for insulin induced and contraction induced increases in skeletal muscle glucose uptake. Glucose 93-100 insulin Homo sapiens 24-31 7934624-1 1994 Glucose facilitated diffusion into cells depends on concentration gradients between intracellular and extracellular spaces and can be modified by several factors such as insulin and contractions. Glucose 0-7 insulin Homo sapiens 170-177 7934624-2 1994 Calmodulin participates in the insulin induced recruitment of vesicles containing glucose transporter molecules and its inhibition by trifluoperazine blocks insulin increases in glucose uptake. Glucose 82-89 insulin Homo sapiens 31-38 7934624-2 1994 Calmodulin participates in the insulin induced recruitment of vesicles containing glucose transporter molecules and its inhibition by trifluoperazine blocks insulin increases in glucose uptake. Glucose 82-89 insulin Homo sapiens 157-164 7934624-4 1994 Trifluoperazine does not inhibit exercise induced increases in glucose uptake; therefore, the mechanisms by which insulin and functional activity increase glucose uptake are different. Glucose 155-162 insulin Homo sapiens 114-121 7967789-4 1994 High level of blood glucose were influenced by in coordinated doses of human insulin and bad correlated food intake during the war. Glucose 20-27 insulin Homo sapiens 77-84 8187467-3 1994 The program simulates the dependences of glucose utilization, glucose production and serum insulin level as a function of glucose and insulin and displays the results as curves on the screen. Glucose 41-48 insulin Homo sapiens 91-98 8187467-3 1994 The program simulates the dependences of glucose utilization, glucose production and serum insulin level as a function of glucose and insulin and displays the results as curves on the screen. Glucose 41-48 insulin Homo sapiens 134-141 8187467-3 1994 The program simulates the dependences of glucose utilization, glucose production and serum insulin level as a function of glucose and insulin and displays the results as curves on the screen. Glucose 62-69 insulin Homo sapiens 134-141 8187467-3 1994 The program simulates the dependences of glucose utilization, glucose production and serum insulin level as a function of glucose and insulin and displays the results as curves on the screen. Glucose 62-69 insulin Homo sapiens 134-141 8187468-0 1994 A simulation study to determine optimal insulin priming during glucose clamp studies. Glucose 63-70 insulin Homo sapiens 40-47 8187468-5 1994 We conclude that priming of insulin is essential to attain steady state of glucose uptake within 90 min of HECS and that conventionally used priming regimens result in an underestimation of glucose uptake. Glucose 75-82 insulin Homo sapiens 28-35 8187470-1 1994 The discovery of the radioimmunoassay for the measurement of insulin concentration stimulated several clever studies which showed, both in vitro and in vivo, the peculiar biphasic pattern of the beta-cell response to glucose stimulation. Glucose 217-224 insulin Homo sapiens 61-68 8187470-8 1994 This model, fully identifiable, thus enables the furnishing of a personalized picture of insulin behaviour, providing insights on hormone secretion during a (frequently sampled) intravenous glucose tolerance test. Glucose 190-197 insulin Homo sapiens 89-96 8282127-4 1993 Since the mechanism of insulin-stimulated glucose uptake is mainly due to translocation of glucose transporters from an intracellular vesicle pool to the plasma membrane, PI 3-kinase activity may be involved in vesicle transport in mammalian cells. Glucose 42-49 insulin Homo sapiens 23-30 8218298-2 1993 Insulin secretagogues, such as glucose and the muscarinic agonist carbachol, stimulate arachidonic acid accumulation, although the mechanisms involved are controversial: carbachol is believed to stimulate phospholipase A2, while glucose-induced arachidonic acid release is the result of diacylglycerol hydrolysis [Konrad, R. J., et al. Glucose 229-236 insulin Homo sapiens 0-7 8237984-4 1993 In the multivariate analysis for women, glucose was related to age and exercise, and insulin was related to glucose levels, triceps skinfold thickness, and waist/hip ratios. Glucose 108-115 insulin Homo sapiens 85-92 8238081-0 1993 Insulin resistance and hypertension: glucose intolerance, hyperinsulinemia, and elevated free fatty acids in the lean spontaneously hypertensive rat. Glucose 37-44 insulin Homo sapiens 0-7 8238081-8 1993 It is concluded that SHR express insulin resistance in terms of glucose and fatty acid metabolism, and therefore are a suitable model for insulin resistance and essential hypertension in non-obese humans. Glucose 64-71 insulin Homo sapiens 33-40 8240280-2 1993 We investigated whether other insulin-sensitive tissues release glucose transport-stimulating IPOs and whether this is related to the human insulin receptor isoform-A or -B (HIR-A or HIR-B). Glucose 64-71 insulin Homo sapiens 30-37 8240280-7 1993 Using the pH 2 fraction from the supernatant of rat1-HIR fibroblasts, insulin increased the release of 3-O-methylglucose-transport-stimulating activity (HIR-A: without insulin, 22.4 +/- 5.4%; with insulin 54.0 +/- 8.4%; HIR-B: without insulin 21.6 +/- 7.5%, with insulin, 44.7 +/- 10.6%, given as a percentage of equilibrium glucose transport reached after 4 s) and lipogenesis-stimulating activity (HIR-A: without insulin, 1.24 +/- 0.17; with insulin, 4.69 +/- 0.2; HIR-B: without insulin, 1.34 +/- 0.18; with insulin, 4.98 +/- 0.31, given as nmol of [3H]glucose converted into lipids/min per 10(6) cells). Glucose 113-120 insulin Homo sapiens 70-77 8240280-7 1993 Using the pH 2 fraction from the supernatant of rat1-HIR fibroblasts, insulin increased the release of 3-O-methylglucose-transport-stimulating activity (HIR-A: without insulin, 22.4 +/- 5.4%; with insulin 54.0 +/- 8.4%; HIR-B: without insulin 21.6 +/- 7.5%, with insulin, 44.7 +/- 10.6%, given as a percentage of equilibrium glucose transport reached after 4 s) and lipogenesis-stimulating activity (HIR-A: without insulin, 1.24 +/- 0.17; with insulin, 4.69 +/- 0.2; HIR-B: without insulin, 1.34 +/- 0.18; with insulin, 4.98 +/- 0.31, given as nmol of [3H]glucose converted into lipids/min per 10(6) cells). Glucose 325-332 insulin Homo sapiens 70-77 8287639-9 1993 Hepatic glucose production was higher at baseline, and less suppressed by insulin. Glucose 8-15 insulin Homo sapiens 74-81 8287639-10 1993 Whole-body glucose disposal was impaired at all insulin doses (by 33-60%). Glucose 11-18 insulin Homo sapiens 48-55 8287639-13 1993 At all insulin levels, forearm glucose extraction was markedly depressed and forearm lactate release was in excess of concurrent glucose uptake, suggesting ongoing glycogenolysis despite insulin. Glucose 31-38 insulin Homo sapiens 7-14 8270132-2 1993 Insulin binding to cultured fibroblasts from PK was almost not detectable and insulin-induced insulin receptor autophosphorylation and glucose uptake was abolished. Glucose 135-142 insulin Homo sapiens 78-85 8270134-0 1993 Hepatic glucose production during intraperitoneal and intravenous closed-loop insulin regulation of blood glucose in type 1 (insulin-dependent) diabetic patients. Glucose 8-15 insulin Homo sapiens 78-85 8270134-2 1993 The regulation of hepatic glucose production during the intraperitoneal and intravenous infusions of insulin were compared in eight Type 1 (insulin-dependent), C-peptide-deficient diabetic patients. Glucose 26-33 insulin Homo sapiens 101-108 8270134-5 1993 The insulin infusion rates required for normal plasma glucose concentrations were essentially the same for the intravenous and intraperitoneal routes in all cases, although the variations were greater with intraperitoneal insulin. Glucose 54-61 insulin Homo sapiens 4-11 8270134-7 1993 Hepatic glucose production was significantly lower with intraperitoneal insulin during all three conditions: basal: 1.71 +/- 0.14, i.p. Glucose 8-15 insulin Homo sapiens 72-79 8270135-3 1993 Hypoglycaemia was induced by a continuous infusion of insulin (0.40 mU.kg-1.min-1 for 8 h, plasma insulin approximately 180 pmol/l) which decreased the plasma glucose concentration to approximately 3.1 mmol/l during the last 3 h of the studies. Glucose 159-166 insulin Homo sapiens 54-61 8270135-3 1993 Hypoglycaemia was induced by a continuous infusion of insulin (0.40 mU.kg-1.min-1 for 8 h, plasma insulin approximately 180 pmol/l) which decreased the plasma glucose concentration to approximately 3.1 mmol/l during the last 3 h of the studies. Glucose 159-166 insulin Homo sapiens 98-105 8221577-6 1993 Insulin infusion enhanced glucose oxidation and suppressed lipid oxidation, but such changes were at lower extent in malnourished patients. Glucose 26-33 insulin Homo sapiens 0-7 8213608-9 1993 This observation indicates that insulin resistance is likely to play an important role in the decreased glucose-induced thermogenesis of these individuals. Glucose 104-111 insulin Homo sapiens 32-39 8238089-6 1993 With DHEA + dexamethasone, the ratio of DHEAS/testosterone increased 16-fold along with a marked improvement in insulin sensitivity, as determined by a more than 30% reduction in fasting and oral glucose tolerance test insulin levels, a threefold stimulation of the rate of glucose disappearance with intravenous insulin, and a 30% increase in insulin binding. Glucose 196-203 insulin Homo sapiens 112-119 8238089-6 1993 With DHEA + dexamethasone, the ratio of DHEAS/testosterone increased 16-fold along with a marked improvement in insulin sensitivity, as determined by a more than 30% reduction in fasting and oral glucose tolerance test insulin levels, a threefold stimulation of the rate of glucose disappearance with intravenous insulin, and a 30% increase in insulin binding. Glucose 274-281 insulin Homo sapiens 112-119 8238183-7 1993 The late plasma insulin response to glucose was higher in the women who used the gestodene formulation than in those who used the desogestrel formulation. Glucose 36-43 insulin Homo sapiens 16-23 8305165-4 1993 Insulin infusion per se stimulated erythrocyte magnesium (1.83 +/- 0.04 v 1.98 +/- 0.03 mmol/L, P < .03) and calcium (4.7 +/- 0.3 v 6.2 +/- 0.4 mumol/L, P < .02) accumulation, and enhanced total body glucose disposal oxidative and nonoxidative glucose metabolisms. Glucose 206-213 insulin Homo sapiens 0-7 8305165-5 1993 Infusion of insulin and nifedipine v insulin alone reduced insulin-mediated increase in intracellular calcium (5.4 +/- 0.3 v 6.2 +/- 0.4 mumol/L, P < .02), but potentiated the insulin effect upon nonoxidative glucose (15.4 +/- 0.4 v 11.1 +/- 0.3 mumol/kg lean body mass [LBM] x min, P < .03) metabolism. Glucose 212-219 insulin Homo sapiens 12-19 8305166-4 1993 Only nitrendipine reduced glucose-stimulated insulin levels. Glucose 26-33 insulin Homo sapiens 45-52 8131999-0 1993 The involvement of protein kinase C in glucose-stimulated insulin secretion. Glucose 39-46 insulin Homo sapiens 58-65 8132007-0 1993 Insulin-stimulated glucose uptake in C2C12 myoblasts. Glucose 19-26 insulin Homo sapiens 0-7 8179540-5 1993 Women with gestational diabetes who later developed permanent diabetes mellitus had higher mean amniotic fluid insulin levels than those whose glucose tolerance remained normal on follow-up (p < or = 0.0072) and more of them had a level greater than the 97th percentile than those whose glucose tolerance remained normal (odds ratio 6.48, 95% confidence interval 1.51-27.8, p = 0.0094). Glucose 290-297 insulin Homo sapiens 111-118 8222114-2 1993 BACKGROUND: The relation between alcohol intake and insulin levels may explain, in part, the reported associations of alcohol with cardiovascular disease risk factors, including high-density lipoprotein (HDL) cholesterol, triglycerides, blood pressure, and glucose levels, each of which has been recognized as a component of the insulin resistance syndrome. Glucose 257-264 insulin Homo sapiens 52-59 8287639-21 1993 Post-surgical insulin resistance is characterized by normal sensitivity but decreased responsiveness of glucose oxidation, lipolysis and plasma free fatty acid oxidation, whereas glycogen synthesis and direct free fatty acid oxidation are virtually unresponsive. Glucose 104-111 insulin Homo sapiens 14-21 8287639-22 1993 For both glucose and lipid metabolism, the insulin resistance is particularly severe in forearm tissues, in which mild metabolic acidosis may play an additional role. Glucose 9-16 insulin Homo sapiens 43-50 8299437-0 1993 Jet-injected insulin is associated with decreased antibody production and postprandial glucose variability when compared with needle-injected insulin in gestational diabetic women. Glucose 87-94 insulin Homo sapiens 13-20 8299437-3 1993 However, the pharmacokinetics of jet-injected insulin suggest that it might be useful in controlling postprandial glucose levels. Glucose 114-121 insulin Homo sapiens 46-53 8299485-6 1993 Insulin sensitivity was assessed by means of a euglycaemic (5.1 +/- 0.1 mM) hyperinsulinaemic (516 +/- 28 pM) clamp performed in combination with [3(-3)H]glucose infusion and indirect calorimetry. Glucose 154-161 insulin Homo sapiens 0-7 8405705-0 1993 Alcohol intake impairs glucose counterregulation during acute insulin-induced hypoglycemia in IDDM patients. Glucose 23-30 insulin Homo sapiens 62-69 8405705-2 1993 In this study, we assessed the effects of alcohol intake on glucose counterregulation in response to acute insulin-induced hypoglycemia in IDDM patients and in normal control subjects. Glucose 60-67 insulin Homo sapiens 107-114 8237984-5 1993 In the multivariate analysis for men, none of the variables was related to glucose levels; insulin levels were related to glucose and waist/hip ratio. Glucose 122-129 insulin Homo sapiens 91-98 8276953-6 1993 However, the rise of insulin in plasma following an oral load of glucose (oGTT) was blunted considerably, resulting in normalization of previously elevated circulating insulin levels. Glucose 65-72 insulin Homo sapiens 21-28 8112499-2 1993 It acts in the presence of insulin to increase glucose utilization and reduce glucose production, thereby countering insulin resistance. Glucose 47-54 insulin Homo sapiens 27-34 8112499-2 1993 It acts in the presence of insulin to increase glucose utilization and reduce glucose production, thereby countering insulin resistance. Glucose 47-54 insulin Homo sapiens 117-124 8112499-2 1993 It acts in the presence of insulin to increase glucose utilization and reduce glucose production, thereby countering insulin resistance. Glucose 78-85 insulin Homo sapiens 27-34 8112499-2 1993 It acts in the presence of insulin to increase glucose utilization and reduce glucose production, thereby countering insulin resistance. Glucose 78-85 insulin Homo sapiens 117-124 8225533-1 1993 Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Glucose 30-37 insulin Homo sapiens 14-21 8225533-1 1993 Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Glucose 30-37 insulin Homo sapiens 115-122 8225533-1 1993 Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Glucose 30-37 insulin Homo sapiens 115-122 8225533-1 1993 Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Glucose 198-205 insulin Homo sapiens 14-21 8225533-1 1993 Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Glucose 198-205 insulin Homo sapiens 115-122 8225533-1 1993 Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Glucose 198-205 insulin Homo sapiens 115-122 8307092-7 1993 Free fatty acid (FFA) levels measured in the fasting state and during an oral glucose tolerance test (OGTT) were positively associated with fasting plasma insulin and triglyceride levels as well as with both glucose and insulin areas measured during the OGTT. Glucose 78-85 insulin Homo sapiens 155-162 8307092-7 1993 Free fatty acid (FFA) levels measured in the fasting state and during an oral glucose tolerance test (OGTT) were positively associated with fasting plasma insulin and triglyceride levels as well as with both glucose and insulin areas measured during the OGTT. Glucose 78-85 insulin Homo sapiens 220-227 8276953-6 1993 However, the rise of insulin in plasma following an oral load of glucose (oGTT) was blunted considerably, resulting in normalization of previously elevated circulating insulin levels. Glucose 65-72 insulin Homo sapiens 168-175 8077319-0 1993 Insulin secretion, clearance, and action on glucose metabolism in cirrhotic patients. Glucose 44-51 insulin Homo sapiens 0-7 8077319-5 1993 glucose tolerance test by a 60% greater insulin secretion rate (P < 0.05), a markedly reduced insulin sensitivity index (SI; 2.82 +/- 0.75 vs. 5.86 +/- 0.68 x 10(-4) min/mU.L; P < 0.01) and a 40% reduced insulin clearance (725 +/- 169 vs. 1165 +/- 99 mL/min.m-2; P < 0.05). Glucose 0-7 insulin Homo sapiens 40-47 8077310-3 1993 Endogenous glucose production ([6-3H]glucose) was greater after cortisol than saline in the postabsorptive state (13.3 +/- 0.5 vs. 12.2 +/- 0.5 mumol/kg.min; P < 0.05) and during 0.4-mU insulin infusion (10.5 +/- 0.7 vs. 5.0 +/- 0.8 mumol/kg.min; P < 0.005). Glucose 11-18 insulin Homo sapiens 189-196 8077310-4 1993 During 2.0-mU insulin infusion, endogenous glucose production was suppressed similarly (5.1 +/- 0.4 vs. 4.1 +/- 0.5 mumol/kg.min), but glucose disappearance was less after cortisol than saline (38.7 +/- 3.5 vs. 64.6 +/- 4.3 mumol/kg.min; P < 0.001). Glucose 43-50 insulin Homo sapiens 14-21 8308470-1 1993 Evidence in the literature suggests that the trace element chromium may have a role in glucose homeostasis through the regulation of insulin action. Glucose 87-94 insulin Homo sapiens 133-140 8077317-6 1993 Her basal insulin levels were normal (129 and 114 pmol/L), but increased markedly (peak values, 1304 and 5045 pmol/L) after iv glucose and a mixed meal. Glucose 127-134 insulin Homo sapiens 10-17 8308470-2 1993 We have previously reported a significant reduction in plasma chromium levels in healthy individuals, following a 75 g oral glucose load, and after meals and glucose-dependent uptake of chromium in insulin-dependent tissues in vitro. Glucose 158-165 insulin Homo sapiens 198-205 8229481-1 1993 Normal values for the first-phase insulin release during an intravenous glucose tolerance test are not yet well defined for children and adolescents. Glucose 72-79 insulin Homo sapiens 34-41 8227340-4 1993 IGF-I treatment led to reduced fasting and stimulated (glucose and/or L-arginine) insulin and growth hormone secretion. Glucose 55-62 insulin Homo sapiens 82-89 8227340-9 1993 Moreover, insulin-stimulated oxidative and nonoxidative glucose disposal (i.e., insulin sensitivity) were enhanced during IGF-I treatment. Glucose 56-63 insulin Homo sapiens 10-17 8227340-9 1993 Moreover, insulin-stimulated oxidative and nonoxidative glucose disposal (i.e., insulin sensitivity) were enhanced during IGF-I treatment. Glucose 56-63 insulin Homo sapiens 80-87 8227343-5 1993 In contrast, the decreased rates of glucose uptake appeared to result from a state of "physiologic" insulin resistance. Glucose 36-43 insulin Homo sapiens 100-107 8227992-2 1993 METHODS: In 60 human subjects (age range 19-78 years), insulin sensitivity, SI, was determined from glucose and insulin levels obtained during an intravenous glucose tolerance test, and plasma norepinephrine (NE) levels were measured to estimate SNS activity. Glucose 100-107 insulin Homo sapiens 55-62 8255886-1 1993 It is well known that the ability of the immature rodent fetal beta cell to release insulin in response to a glucose challenge can be enhanced by chronic exposure to a high concentration of glucose in vitro. Glucose 109-116 insulin Homo sapiens 84-91 8231840-8 1993 The glucose to insulin ratio, also known as the insulin sensitivity index, increased (1.56 +/- 0.15 v 1.95 +/- 0.12, P < .05). Glucose 4-11 insulin Homo sapiens 48-55 8231841-6 1993 GH treatment induced a marked change in insulin action evident after 6 weeks of therapy as shown by lower glucose infusion rates (GIRs) during the clamp compared with placebo treatment (2.6 +/- 0.4 v 4.1 +/- 0.7 mg.kg-1.min-1). Glucose 106-113 insulin Homo sapiens 40-47 8231841-7 1993 This change in insulin action was due to a decreased insulin effect on glucose utilization. Glucose 71-78 insulin Homo sapiens 15-22 8231841-7 1993 This change in insulin action was due to a decreased insulin effect on glucose utilization. Glucose 71-78 insulin Homo sapiens 53-60 8255886-1 1993 It is well known that the ability of the immature rodent fetal beta cell to release insulin in response to a glucose challenge can be enhanced by chronic exposure to a high concentration of glucose in vitro. Glucose 190-197 insulin Homo sapiens 84-91 16353333-3 1993 The control obese subjects showed a diurnal variation in glucose-stimulated insulin secretion, whereas the patients with hypothalamic obesity did not, suggesting that hypothalamic injury had destroyed diurnal rhythms. Glucose 57-64 insulin Homo sapiens 76-83 8124870-8 1993 These results suggest that PPH occurs at high incidence in patients with moderately severe Parkinson"s disease, and that high baseline blood pressure and abnormally high insulin response to glucose load may play a role, while medications for Parkinson"s disease may not. Glucose 190-197 insulin Homo sapiens 170-177 8233456-8 1993 The alterations are related to increased free fatty acid levels and decreased glucose uptake resulting from elevated insulin levels. Glucose 78-85 insulin Homo sapiens 117-124 7903820-0 1993 Cholecystokinin and somatostatin modulate the glucose-induced insulin secretion by different mechanisms in pancreatic islets. Glucose 46-53 insulin Homo sapiens 62-69 7903820-6 1993 Both the phospholipase C activity and the insulin secretion increased in response to 12 mmol l-1 glucose. Glucose 97-104 insulin Homo sapiens 42-49 8105311-3 1993 The aims of the study were to investigate performance of the microdialysis device and to evaluate whether consecutive 24 h glucose profiles could be used to adjust insulin therapy. Glucose 123-130 insulin Homo sapiens 164-171 8105311-7 1993 When patients" insulin therapy was adjusted on the basis of ambulatory glucose monitoring, HbA1c decreased by almost 2% (p < 0.01), and this decrease lasted for at least 9 months. Glucose 71-78 insulin Homo sapiens 15-22 8105311-9 1993 Daily glucose profiles are often reproducible and the recordings may thus be used for individual tailoring of insulin therapy to improve glycaemic control. Glucose 6-13 insulin Homo sapiens 110-117 8137657-3 1993 This difference remained to be significant even after the adjustment of age, sex, insulin and 2-hours plasma glucose. Glucose 109-116 insulin Homo sapiens 82-95 8249111-7 1993 The first sign of a reinstalled physiological axis was the decrease of the blood glucose concentration after a median duration of 40 min (range 5-90 min) and the association of the recipient"s ambient blood glucose levels with insulin release between 25 and 180 min after reperfusion. Glucose 207-214 insulin Homo sapiens 227-234 8105164-5 1993 There were also significant differences between the groups in the daily insulin dose needed for equivalent glucose control (0.76 [0.20] vs 0.65 [0.10] U/kg, p < 0.05), mean systolic blood pressure over 24 h ambulatory monitoring (134 [7] vs 127 [7] mm Hg; p < 0.05), and various plasma lipid concentrations, contributing to a more atherogenic profile in the microalbuminuric group. Glucose 107-114 insulin Homo sapiens 72-79 8408055-1 1993 We have shown that culturing HepG2 cells in Ham"s F-12 medium supplemented with calf serum, dexamethasone, and triiodothyronine causes an increase in the insulin sensitivity and responsiveness for glucose incorporation into glycogen. Glucose 197-204 insulin Homo sapiens 154-161 8267948-5 1993 We conclude that angiotensin II within physiological range stimulates insulin-mediated glucose uptake in healthy men. Glucose 87-94 insulin Homo sapiens 70-77 7901997-3 1993 However, it is unclear whether this is a direct effect of insulin or is secondary to increased insulin-mediated glucose utilization. Glucose 112-119 insulin Homo sapiens 95-102 7901997-14 1993 Changes in fetal glucose concentration may alter the pattern of utilization of essential amino acids, independent of changes in insulin and insulin-mediated glucose utilization rate. Glucose 157-164 insulin Homo sapiens 140-147 8136423-1 1993 The aim of this study was to know about the plasmatic variations of insulin and its potential origin in the obesity with or without abnormal tolerance to glucose. Glucose 154-161 insulin Homo sapiens 68-75 8136423-2 1993 Obese patients with normal tolerance to glucose showed normal and hypersecretion of insulin during fasting and after oral overdose of glucose (OOG). Glucose 40-47 insulin Homo sapiens 84-91 8379513-1 1993 The glucose responses (GR) and insulin requirements (IRs) were measured by a glucose-controlled insulin infusion system for 5 h after 12 patients with insulin-dependent diabetes mellitus consumed each of three meals: a 1890-kJ standard meal, the standard meal with 840 kJ added protein, and the standard meal with 840 kJ added fat. Glucose 77-84 insulin Homo sapiens 96-103 8222508-9 1993 Whole-body insulin sensitivity was 10.5 +/- 2 mg of glucose min-1kg-1 after placebo, and 10.5 +/- 2.2 and 10.9 +/- 3.4 mg of glucose min-1kg-1 after low and high dose angiotensin II (not significant). Glucose 52-59 insulin Homo sapiens 11-18 8136423-4 1993 Most of the obese patients with glucose intolerance showed hypersecretion of insulin during fasting and after OOG, being their basal hyperinsulinism due to insulinic secretion. Glucose 32-39 insulin Homo sapiens 77-84 8304911-1 1993 An increased supply of FFAs for oxidation leads to a reduced rate of glucose oxidation and interferes with the inhibitory action of insulin on hepatic glucose production. Glucose 151-158 insulin Homo sapiens 132-139 8304912-7 1993 It is further complicated by the frequent association of insulin resistance with a wide range of disturbances, including hypertension, dyslipidaemia and glucose intolerance--the insulin resistance "syndrome". Glucose 153-160 insulin Homo sapiens 57-64 8304912-7 1993 It is further complicated by the frequent association of insulin resistance with a wide range of disturbances, including hypertension, dyslipidaemia and glucose intolerance--the insulin resistance "syndrome". Glucose 153-160 insulin Homo sapiens 178-185 8304913-1 1993 In this presentation an effort has been made to review the impact of resistance to insulin-mediated glucose uptake and/or hyperinsulinaemia on various metabolic end-points and clinical syndromes. Glucose 100-107 insulin Homo sapiens 83-90 8304913-2 1993 Insulin resistance is present in the great majority of patients with states of glucose intolerance, but frank decompensation of glucose homoeostasis does not occur if individuals can maintain a state of compensatory hyperinsulinaemia. Glucose 79-86 insulin Homo sapiens 0-7 8304913-5 1993 Resistance to insulin-mediated glucose uptake and/or hyperinsulinaemia have been shown to be associated with high blood pressure, microvascular angina and CHD. Glucose 31-38 insulin Homo sapiens 14-21 8304913-6 1993 Thus, resistance to insulin-mediated glucose uptake is a common phenomenon, which makes a major contribution to the aetiology and clinical course of common and serious diseases. Glucose 37-44 insulin Homo sapiens 20-27 8304913-7 1993 Based on the above considerations, it is difficult to over-emphasize the health-related implication of a defect in insulin-mediated glucose uptake. Glucose 132-139 insulin Homo sapiens 115-122 8304919-5 1993 The effects of insulin on the cardiovascular system and, in particular, on skeletal muscle vasculature are physiological, specific, co-ordinated and appear to play an integral part in its overall action to promote the disposal of glucose and probably other substrates. Glucose 230-237 insulin Homo sapiens 15-22 8403289-6 1993 Insulin resistance was assessed using indices derived from Intravenous Glucose Tolerance Test (IVGTT): insulin level at baseline, insulin level at 90 minutes of IVGTT (insulin-90), insulin integration over 90 minutes of IVGTT, and rate of glucose disposal (k value). Glucose 239-246 insulin Homo sapiens 0-7 8243878-5 1993 Plasma glucose in Type 2 diabetic subjects did not reach hypoglycaemic levels but the acute glucose decrease to 4.5 +/- 0.8 mmol/l was associated with significantly lower responses of plasma glucagon and adrenaline but higher cortisol levels after insulin-like growth factor I compared to insulin (p < 0.003). Glucose 92-99 insulin Homo sapiens 248-255 7505214-4 1993 After intensified treatment with soluble insulin for 24 h the fasting plasma glucose concentration decreased from 20.8 +/- 2.3 (SD) to 8.7 +/- 2.3 mmol 1-1, whereas the fasting serum insulin level increased from 0.06 +/- 0.02 to 0.17 +/- 0.09 nmol 1-1. Glucose 77-84 insulin Homo sapiens 41-48 8269795-6 1993 The acute first- (t = 0-5 min) and second-phase (t = 10-60 min) insulin releases were calculated as the sum of incremental insulin responses to the intravenous glucose stimulation. Glucose 160-167 insulin Homo sapiens 64-71 8269795-16 1993 CONCLUSIONS: Our preliminary study demonstrates greater serum insulin responses and, perhaps, insulin resistance in glucose-tolerant African Americans than in their Nigerian counterparts, irrespective of family history of diabetes and obesity. Glucose 116-123 insulin Homo sapiens 62-69 8269795-16 1993 CONCLUSIONS: Our preliminary study demonstrates greater serum insulin responses and, perhaps, insulin resistance in glucose-tolerant African Americans than in their Nigerian counterparts, irrespective of family history of diabetes and obesity. Glucose 116-123 insulin Homo sapiens 94-101 8243858-5 1993 Isotopically determined basal and insulin-stimulated glucose disposal was similarly reduced before and during therapy in both the simvastatin (2.0 +/- 0.1 vs 1.9 +/- 0.1 (NS) and 3.1 +/- 0.6 vs 3.1 +/- 0.7 mg.kg-1 x min-1 (NS)) and the placebo group (1.9 +/- 0.1 vs 1.8 +/- 0.1 (NS) and 4.1 +/- 0.6 vs 3.8 +/- 0.2 mg.kg-1 x min-1 (NS)). Glucose 53-60 insulin Homo sapiens 34-41 8243878-0 1993 Effects of recombinant human insulin-like growth factor I and insulin on counterregulation during acute plasma glucose decrements in normal and type 2 (non-insulin-dependent) diabetic subjects. Glucose 111-118 insulin Homo sapiens 62-69 8243878-3 1993 Insulin-like growth factor I and insulin injection resulted in identical decrements of plasma glucose concentrations after 30 min but in delayed recovery after insulin-like growth factor I as compared to insulin in both groups (p < 0.05 insulin-like growth factor I vs insulin). Glucose 94-101 insulin Homo sapiens 33-40 8243878-7 1993 The present results demonstrate that insulin-like growth factor I is capable of mimicking the acute effects of insulin on metabolic substrates (plasma glucose, non-esterified fatty acids, leucine). Glucose 151-158 insulin Homo sapiens 37-44 8375585-8 1993 However, significant independent effects existed for both polycystic ovary syndrome (P < 0.01) and ethnicity (P < 0.05) that resulted in decreased insulin-mediated glucose disposal. Glucose 170-177 insulin Homo sapiens 153-160 8243878-9 1993 Counterregulatory hormone responses to plasma glucose decrements differed, however, between insulin-like growth factor I and insulin and in the diabetic and the control subjects. Glucose 46-53 insulin Homo sapiens 92-99 8375587-6 1993 These results suggest that apolipoprotein E polymorphism substantially modifies the associations between glucose tolerance, plasma insulin levels, and plasma lipoprotein concentrations. Glucose 105-112 insulin Homo sapiens 131-138 8310248-1 1993 Massive obesity is always accompanied by insulin resistance with hyperinsulinaemia in proportion to the amount of visceral fat, which has repercussions on oxidative and non-oxidative glucose metabolism. Glucose 183-190 insulin Homo sapiens 41-48 8375592-3 1993 The islet amyloid polypeptide-to-insulin molar ratios in response to 5.5 and 16.7 mM glucose were 1:16 and 1:15 respectively. Glucose 85-92 insulin Homo sapiens 33-40 8375592-5 1993 The islet amyloid polypeptide response to the 1-day culture was similar to that of the fresh islets; however, after the 7-day culture the islet amyloid polypeptide and insulin secretory responses to glucose were dissociated. Glucose 199-206 insulin Homo sapiens 168-175 8375592-6 1993 The insulin response of islets to a high-glucose stimulus was significantly (P < 0.001) increased, whereas the islet amyloid polypeptide response of islets to the same stimulus was blunted. Glucose 41-48 insulin Homo sapiens 4-11 8375592-8 1993 Northern blot analysis of each cultured condition showed an increase of both mRNA IAPP and insulin signals after exposure of islets at 16.7 mM glucose, the maximum mRNA expression being after long exposure to high-glucose concentrations. Glucose 143-150 insulin Homo sapiens 91-98 8375592-8 1993 Northern blot analysis of each cultured condition showed an increase of both mRNA IAPP and insulin signals after exposure of islets at 16.7 mM glucose, the maximum mRNA expression being after long exposure to high-glucose concentrations. Glucose 214-221 insulin Homo sapiens 91-98 8408642-3 1993 Glucose rate of disappearance (measured by [6,6-D2]-glucose infusions) increased from baseline by 239 +/- 16% during high dose IGF-I vs 197 +/- 18% during insulin (P = 0.021 vs IGF-I). Glucose 0-7 insulin Homo sapiens 155-162 8408642-4 1993 Hepatic glucose production decreased by 37 +/- 6% during high dose IGF-I vs 89 +/- 13% during insulin (P = 0.0028 vs IGF-I). Glucose 8-15 insulin Homo sapiens 94-101 8258677-1 1993 OBJECTIVE: To assess the relationship of insulin levels and glucose tolerance to blood pressure in hypertension. Glucose 60-67 insulin Homo sapiens 41-48 8258677-8 1993 Two-way analysis of variance indicated significant decreases in both glucose (P < 0.04) and insulin (P < 0.03), fasting and throughout the intravenous glucose tolerance test. Glucose 157-164 insulin Homo sapiens 95-102 8412734-1 1993 The routes by which glucose-derived pyruvate is metabolized to enter mitochondrial pathways to stimulate insulin release in the pancreatic beta cell are unknown. Glucose 20-27 insulin Homo sapiens 105-112 8412734-4 1993 Glucose and methyl succinate, which are insulin secretagogues, gave more accurate ratios than ratios estimated with pyruvate and acetate, which do not initiate insulin release. Glucose 0-7 insulin Homo sapiens 40-47 8412735-0 1993 Serum insulin distributions and reproducibility of the relationship between 2-hour insulin and plasma glucose levels in Asian Indian, Creole, and Chinese Mauritians. Glucose 102-109 insulin Homo sapiens 83-90 8412735-2 1993 The relationship of 2-hour (post-75 g oral glucose) serum insulin levels with plasma glucose levels was studied in a population-based random sample comprising 2,627 Hindu Indians, 685 Muslim Indians, 1,351 Creoles (African, European, and Indian admixture), and 415 Chinese from the Indian Ocean island of Mauritius. Glucose 43-50 insulin Homo sapiens 58-65 8412735-2 1993 The relationship of 2-hour (post-75 g oral glucose) serum insulin levels with plasma glucose levels was studied in a population-based random sample comprising 2,627 Hindu Indians, 685 Muslim Indians, 1,351 Creoles (African, European, and Indian admixture), and 415 Chinese from the Indian Ocean island of Mauritius. Glucose 85-92 insulin Homo sapiens 58-65 8405515-2 1993 DESIGN: Insulin responses during an oral glucose tolerance test (OGTT) were assessed in 25 consecutive women with PCOS and 20 control women matched for BMI. Glucose 41-48 insulin Homo sapiens 8-15 8405515-9 1993 The average differences in oral- and intravenous-glucose-induced hyperinsulinemia and in insulin sensitivity between PCOS and controls were relatively constant across the entire physiological range of BMI. Glucose 49-56 insulin Homo sapiens 70-77 8093122-3 1993 The insulin response to an oral glucose tolerance test was abnormal 3 months after discontinuation of growth hormone; 18 months later, it remained delayed but was normal quantitatively. Glucose 32-39 insulin Homo sapiens 4-11 8302399-10 1993 With mild hyperglycaemia, the metabolic effects of sulphonylurea and insulin treatment were comparable, but insulin is superior to sulphonylurea in patients who are more hyperglycaemic (fasting blood glucose > 11 mmol/l). Glucose 200-207 insulin Homo sapiens 108-115 8255675-0 1993 Postnatal glucose kinetics in newborns of tightly controlled insulin-dependent diabetic mothers. Glucose 10-17 insulin Homo sapiens 61-68 8256243-9 1993 At one month, the high dose significantly decreased serum insulin concentrations as calculated from the areas under the incremental two hours curves in the glucose tolerance test. Glucose 156-163 insulin Homo sapiens 58-65 8256243-15 1993 Paralleling the changes for insulin, the area under the incremental two hour blood glucose curve decreased significantly (medians 1.4 v 0.4 mmol/l/h, p < 0.05) during the first month of treatment. Glucose 83-90 insulin Homo sapiens 28-35 8156833-1 1993 This paper suggests a new simple insulin-sensitivity index, the reverse of fasting plasma glucose and insulin product, which is significantly correlated with the insulin-sensitivity index determined by euglycemic insulin clamp technique (insulin mediated glucose disposal rate, M value) in 320 subjects of Americans including two races (r > 0.7, P = 0.0001). Glucose 90-97 insulin Homo sapiens 33-40 8156833-1 1993 This paper suggests a new simple insulin-sensitivity index, the reverse of fasting plasma glucose and insulin product, which is significantly correlated with the insulin-sensitivity index determined by euglycemic insulin clamp technique (insulin mediated glucose disposal rate, M value) in 320 subjects of Americans including two races (r > 0.7, P = 0.0001). Glucose 255-262 insulin Homo sapiens 33-40 8156833-1 1993 This paper suggests a new simple insulin-sensitivity index, the reverse of fasting plasma glucose and insulin product, which is significantly correlated with the insulin-sensitivity index determined by euglycemic insulin clamp technique (insulin mediated glucose disposal rate, M value) in 320 subjects of Americans including two races (r > 0.7, P = 0.0001). Glucose 255-262 insulin Homo sapiens 102-109 8156833-1 1993 This paper suggests a new simple insulin-sensitivity index, the reverse of fasting plasma glucose and insulin product, which is significantly correlated with the insulin-sensitivity index determined by euglycemic insulin clamp technique (insulin mediated glucose disposal rate, M value) in 320 subjects of Americans including two races (r > 0.7, P = 0.0001). Glucose 255-262 insulin Homo sapiens 102-109 8156833-1 1993 This paper suggests a new simple insulin-sensitivity index, the reverse of fasting plasma glucose and insulin product, which is significantly correlated with the insulin-sensitivity index determined by euglycemic insulin clamp technique (insulin mediated glucose disposal rate, M value) in 320 subjects of Americans including two races (r > 0.7, P = 0.0001). Glucose 255-262 insulin Homo sapiens 102-109 8214044-0 1993 Pressor doses of angiotensin II increase insulin-mediated glucose uptake in normotensive men. Glucose 58-65 insulin Homo sapiens 41-48 8156833-1 1993 This paper suggests a new simple insulin-sensitivity index, the reverse of fasting plasma glucose and insulin product, which is significantly correlated with the insulin-sensitivity index determined by euglycemic insulin clamp technique (insulin mediated glucose disposal rate, M value) in 320 subjects of Americans including two races (r > 0.7, P = 0.0001). Glucose 255-262 insulin Homo sapiens 102-109 8156833-2 1993 The analysis of 874 cases Chinese showed that the insulin-sensitivity (IS) evaluated by this new index in Chinese was similar to that determined by insulin clamp in Americans: If the IS in subjects with normal glucose tolerance defined as 1.0, then the IS in subjects with impaired glucose tolerance in Chinese and in Americans was 0.61, 0.62 (Pima Indians), 0.71 (Caucasians) and in diabetic Chinese and Americans was 0.57 and 0.53 (Pima Indians and Caucasians) respectively. Glucose 210-217 insulin Homo sapiens 50-57 8200305-5 1993 The results indicated that the patients with essential hypertension, simple obesity and acromegaly are insulin resistant and hyperinsulinemic after an oral glucose load. Glucose 156-163 insulin Homo sapiens 103-110 8200307-2 1993 The significant positive correlation between SBP and 2-hour plasma insulin (INS 2h) after 75g glucose load was found in the BMI (body mass index) 15.9-27.0 group (n = 287) after the adjustment for age, sex, BMI, smoking and plasma cholesterol (P = 0.01). Glucose 94-101 insulin Homo sapiens 67-74 8366094-1 1993 Insulin stimulation of glucose transport involves the translocation of vesicles containing the glucose transporter Glut 4 to the plasma membrane. Glucose 23-30 insulin Homo sapiens 0-7 8366094-12 1993 We suggest that insulin and okadaic acid induce a cycling of Rab4 from a vesicular fraction containing the Glut 4 transporter to the cytosol and that this cycling may participate in the insulin stimulatory action on glucose transporter translocation. Glucose 216-223 insulin Homo sapiens 16-23 8366094-12 1993 We suggest that insulin and okadaic acid induce a cycling of Rab4 from a vesicular fraction containing the Glut 4 transporter to the cytosol and that this cycling may participate in the insulin stimulatory action on glucose transporter translocation. Glucose 216-223 insulin Homo sapiens 186-193 8214044-1 1993 The effect of pressor doses of angiotensin II infused intravenously on insulin-mediated glucose uptake was determined in normotensive men. Glucose 88-95 insulin Homo sapiens 71-78 8214044-5 1993 We conclude that angiotensin II in pressor doses increases insulin-mediated glucose disposal and oxidation. Glucose 76-83 insulin Homo sapiens 59-66 8312129-0 1993 What signals are involved in the stimulation of glucose transport by insulin in muscle cells? Glucose 48-55 insulin Homo sapiens 69-76 7693379-17 1993 There was glucose intolerance and increased insulin levels following the glucose meal preceded by the 59-hour fast when compared with the overnight fast. Glucose 73-80 insulin Homo sapiens 44-51 7693379-3 1993 In animal studies high IGFBP-1 levels increase plasma glucose levels possibly by regulating the insulin-like actions of "bio-available" plasma IGF. Glucose 54-61 insulin Homo sapiens 96-103 8269449-1 1993 Insulin sensitivity in terms of glucose disposal rate was measured by the hyperinsulinemic/euglycemic clamp technique in 10 hypertensive patients and 7 normotensive control subjects before and after 12 weeks of doxazosin therapy. Glucose 32-39 insulin Homo sapiens 0-7 8269449-6 1993 Steady-state serum insulin concentrations, as measured during the glucose clamp procedure, were 172 +/- 10.4 microU/ml before and 176 +/- 13.5 microU/ml after doxazosin treatment; these levels were significantly higher than the 137 +/- 7.0 microU/ml reading obtained in the normotensive subjects (P < 0.05). Glucose 66-73 insulin Homo sapiens 19-26 8404429-1 1993 OBJECTIVE: To ascertain whether the effect of sulfonylureas on glucose-mediated insulin release persists for years to decades in patients with maturity-onset diabetes of the young. Glucose 63-70 insulin Homo sapiens 80-87 8405753-7 1993 Patients with impaired glucose tolerance had significantly higher fasting serum immunoreactive insulin (p < 0.05), higher fasting serum fluoride (p < 0.001), and a significantly lower fasting glucose to insulin ratio than that in patients with normal glucose tolerance (p < 0.001) or control subjects (p < 0.05). Glucose 23-30 insulin Homo sapiens 95-102 8405756-5 1993 Both intravenous and oral glucose tolerance tests revealed inhibited early responses in insulin and C-peptide release, but the insulin and C-peptide response to glucagon stimulation was less affected. Glucose 26-33 insulin Homo sapiens 88-95 8405756-5 1993 Both intravenous and oral glucose tolerance tests revealed inhibited early responses in insulin and C-peptide release, but the insulin and C-peptide response to glucagon stimulation was less affected. Glucose 26-33 insulin Homo sapiens 100-109 8405756-6 1993 Aneuglycaemic insulin clamp showed normal insulin-mediated glucose disposal. Glucose 59-66 insulin Homo sapiens 14-21 8405756-6 1993 Aneuglycaemic insulin clamp showed normal insulin-mediated glucose disposal. Glucose 59-66 insulin Homo sapiens 42-49 8405756-7 1993 In vitro experiments, where isolated rat pancreatic islets were cultured with serum from the patient, showed a moderately decreased islet glucose oxidation rate and glucose-stimulated insulin release compared to islets cultured with serum from healthy subjects. Glucose 165-172 insulin Homo sapiens 184-191 8405756-9 1993 In conclusion, the observed effects show that the diabetic state in this patient was associated with an impaired glucose-stimulated insulin release but not with an increased peripheral insulin resistance. Glucose 113-120 insulin Homo sapiens 132-139 8225693-4 1993 In those pregnancies complicated by glucose intolerance reflected in hyperglycemia, insulin resistance appears to be heightened, both blood flow and transcapillary transport of insulin are compromised and insulin receptor and post receptor defects are exacerbated. Glucose 36-43 insulin Homo sapiens 177-184 8225693-4 1993 In those pregnancies complicated by glucose intolerance reflected in hyperglycemia, insulin resistance appears to be heightened, both blood flow and transcapillary transport of insulin are compromised and insulin receptor and post receptor defects are exacerbated. Glucose 36-43 insulin Homo sapiens 177-184 8104197-6 1993 Islet-like cell clusters cultured with NIC responded to glucose stimulation with a biphasic increase in insulin release (fourfold peak), whereas control cells were unresponsive to glucose. Glucose 56-63 insulin Homo sapiens 104-111 8254181-4 1993 DESIGN: In order to study the influence of subpressor doses of Ang II on insulin-mediated glucose uptake under euglycemic conditions, eight healthy volunteers were allocated in random order to sham infusion or infusion of Ang II (first 0.75 ng/kg per min and subsequently 1.5 ng/kg per min). Glucose 90-97 insulin Homo sapiens 73-80 8254181-6 1993 METHODS: Insulin-mediated glucose uptake (expressed as M value) was measured with the euglycemic clamp technique. Glucose 26-33 insulin Homo sapiens 9-16 8254181-13 1993 CONCLUSIONS: Ang II increases insulin-mediated glucose uptake: that is, it enhances insulin sensitivity by mechanisms independent of prostaglandins. Glucose 47-54 insulin Homo sapiens 30-37 8254181-13 1993 CONCLUSIONS: Ang II increases insulin-mediated glucose uptake: that is, it enhances insulin sensitivity by mechanisms independent of prostaglandins. Glucose 47-54 insulin Homo sapiens 84-91 8271219-2 1993 Physical training enhances sensitivity and responsiveness of insulin-mediated glucose uptake in human muscle. Glucose 78-85 insulin Homo sapiens 61-68 8271219-11 1993 The training-induced increase in GLUT 4 (26 +/- 11%) matched a previously reported increase in maximum insulin-stimulated leg glucose uptake (25 +/- 7%) in the same subjects, and individual values of the two variables correlated (correlation coefficient (r) = 0.84, P < 0.05). Glucose 126-133 insulin Homo sapiens 103-110 8271219-13 1993 In conclusion, in human muscle training induces a local contraction-dependent increase in GLUT 4 protein, which enhances the effect of insulin on glucose uptake. Glucose 146-153 insulin Homo sapiens 135-142 8412770-7 1993 Insulin secretion assessed by the integrated area of plasma insulin above basal level during the first 20 minutes after intravenous stimulation with glucose was significantly decreased in anorectic patients (283 +/- 69 microU.mL-1 x min) compared with control subjects (529 +/- 63 microU.mL-1 x min, P < .05). Glucose 149-156 insulin Homo sapiens 0-7 8412770-7 1993 Insulin secretion assessed by the integrated area of plasma insulin above basal level during the first 20 minutes after intravenous stimulation with glucose was significantly decreased in anorectic patients (283 +/- 69 microU.mL-1 x min) compared with control subjects (529 +/- 63 microU.mL-1 x min, P < .05). Glucose 149-156 insulin Homo sapiens 60-67 8412779-7 1993 Insulin-stimulated glucose uptake was assessed using the hyperinsulinemic euglycemic clamp technique and was increased post-metformin (3.8 +/- 0.6 v 3.1 +/- 0.7 mg.kg-1 x min-1, P < .05). Glucose 19-26 insulin Homo sapiens 0-7 8232378-1 1993 Chronic alcohol consumers may have, as judged by functional criteria, exocrine as well as endocrine pancreatic dysfunction, the latter represented by a decreased insulin response to an oral glucose load. Glucose 190-197 insulin Homo sapiens 162-169 8232378-4 1993 The total integrated response values for insulin in the alcoholic group following both glucose loads as well as C-peptide plasma concentrations were significantly lower than in the control group. Glucose 87-94 insulin Homo sapiens 41-48 8232378-5 1993 Moreover, in both groups the insulin TIR values following the oral glucose load were significantly greater than the values obtained following the intravenous glucose load, indicating an incretin effect. Glucose 67-74 insulin Homo sapiens 29-36 8232378-6 1993 These results indicate that the decreased insulin response observed in alcoholics was not caused by a dysfunction of the enteroinsular axis because it also occurred following an intravenous glucose load, but by an ethanol-induced beta-cell dysfunction because C-peptide and insulin were proportionally decreased in this group. Glucose 190-197 insulin Homo sapiens 42-49 7692419-6 1993 The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells, related to the insulin-mediated movement of glucose from the blood into cells. Glucose 203-210 insulin Homo sapiens 174-181 8102666-2 1993 We tried to reactivate the liver by long-term treatment of IDDM patients with intravenous insulin in pulses, with the aim of achieving high portal-vein concentrations during and after a glucose meal. Glucose 186-193 insulin Homo sapiens 90-97 8363584-9 1993 These data are consistent with a central role for mitochondrial oxidative phosphorylation in coupling changes in glucose concentration with the secretion of insulin. Glucose 113-120 insulin Homo sapiens 157-164 7688386-16 1993 Through these receptors, insulin and IGF-1 regulate mitogenesis and glucose metabolism, and may be important in potentiating plasma cell malignancy. Glucose 68-75 insulin Homo sapiens 25-32 8213196-5 1993 Plasma insulin and glucose decreased to very low levels during fasting and increased (P < 0.001) after refeeding (insulin, 2.5 +/- 0.7 vs. 28.9 +/- 0.7 mU l-1; glucose, 2.6 +/- 0.3 vs. 6.4 +/- 0.3 mmol l-1). Glucose 163-170 insulin Homo sapiens 7-14 8362934-1 1993 OBJECTIVE: In making decisions regarding initiation of insulin therapy in gestational diabetes, most maternal-fetal obstetricians rely more on elevated fasting glucose values than on elevated 2-hour postprandial levels. Glucose 160-167 insulin Homo sapiens 55-62 8269814-7 1993 In accordance with this, injection into the site above vs. below the umbilicus resulted in a greater area under curve for plasma insulin, 3306 +/- 493 vs. 2357 +/- 466 mU/l per min (0-180 min; P < 0.01), and a more pronounced plasma glucose-lowering effect (P < 0.05). Glucose 236-243 insulin Homo sapiens 129-136 8269814-10 1993 Thus, insulin injection into the epigastric area causes more rapid insulin absorption resulting in an enhanced plasma glucose-lowering effect than injection into the more conventional site close beneath the umbilicus. Glucose 118-125 insulin Homo sapiens 6-13 8375246-1 1993 OBJECTIVE: To characterize the ability of insulin to activate the skeletal muscle metabolic pathways of glucose storage, oxidation, and glycolysis in normal weight patients with NIDDM and nondiabetic volunteer subjects closely matched for age, sex, relative weight, and body composition. Glucose 104-111 insulin Homo sapiens 42-49 8375246-8 1993 Nondiabetic subjects and NIDDM patients who were withdrawn from sulfonylurea therapy had impaired insulin secretion during a 75-g oral glucose tolerance test, with similar basal levels as nondiabetic subjects (54 +/- 12 vs. 42 +/- 6 pM), but reduced peak insulin levels (126 +/- 30 vs. 468 +/- 102 pM, P < 0.01). Glucose 135-142 insulin Homo sapiens 98-105 8392011-3 1993 It has potent glucose-dependent insulin secretory effects and also suppresses gastric acid secretion in the stomach. Glucose 14-21 insulin Homo sapiens 32-39 8344209-2 1993 To assess the role of insulin in developing obesity, diazoxide (DZ), an inhibitor of glucose-stimulated insulin secretion, was administered for 8 weeks to 7-week-old female Zucker rats in two concentrations, 50 mg/kg.day (LD-DZ), and 100 mg/kg.day (HD-DZ). Glucose 85-92 insulin Homo sapiens 104-111 8345055-2 1993 Insulin secretion and action were quantified by application of the minimal model of glucose kinetics and the combined model of insulin and C-peptide kinetics to the FSIGT data. Glucose 84-91 insulin Homo sapiens 0-7 8345813-5 1993 These results suggest that hepatic extraction of insulin is diminished when insulin secretion is potentiated by enteroinsular mechanisms after oral glucose administration. Glucose 148-155 insulin Homo sapiens 49-56 8345815-3 1993 Subjects with previously increased fasting glucose levels were significantly more insulin resistant than a control group, taking into account BMI, age, and gender (% normal insulin sensitivity [%], 59 [50 to 79] v 87 [73 to 96]; P < .005), and previously gestationally diabetic subjects showed greater impairment of beta-cell function (% normal beta-cell function [% beta], 69 [60 to 87] v 97 [89 to 105]; P < .005). Glucose 43-50 insulin Homo sapiens 82-89 8345817-3 1993 Plasma PAI-1 antigen (Ag) correlated significantly with peripheral insulin resistance, represented by the insulin level at which peripheral glucose uptake (PGU) is half-maximal ([ED50PGU] r = .87, P < .001). Glucose 140-147 insulin Homo sapiens 106-113 8345824-2 1993 The present study was performed to investigate the relative importance of total fat mass versus localization of adipose tissue in insulin-stimulated glucose disposal (Rd) and skeletal muscle glycogen synthase (GS) activity in obese individuals. Glucose 149-156 insulin Homo sapiens 130-137 8345824-6 1993 Insulin-stimulated glucose Rd was negatively correlated with WHR (R = -.52, P < .025) whereas there were no correlations with BMI or percent fat (R = .16, NS and R = .16, NS, respectively). Glucose 19-26 insulin Homo sapiens 0-7 8356592-9 1993 An elevated C-peptide/glucose molar ratio might be considered a sign of peripheral insulin resistance. Glucose 22-29 insulin Homo sapiens 83-90 8101255-7 1993 Mean (SE) total insulin-induced glucose uptake was significantly impaired in patients compared with controls (3.9 [0.7] vs 6.4 [0.7] mg/kg per min; p < 0.01), and insulin-stimulated glucose uptake in the forearm was significantly reduced in patients (0.88 [0.10] vs 1.6 [0.30] mmol/L; p < 0.001). Glucose 32-39 insulin Homo sapiens 16-23 8101255-7 1993 Mean (SE) total insulin-induced glucose uptake was significantly impaired in patients compared with controls (3.9 [0.7] vs 6.4 [0.7] mg/kg per min; p < 0.01), and insulin-stimulated glucose uptake in the forearm was significantly reduced in patients (0.88 [0.10] vs 1.6 [0.30] mmol/L; p < 0.001). Glucose 185-192 insulin Homo sapiens 16-23 8101255-7 1993 Mean (SE) total insulin-induced glucose uptake was significantly impaired in patients compared with controls (3.9 [0.7] vs 6.4 [0.7] mg/kg per min; p < 0.01), and insulin-stimulated glucose uptake in the forearm was significantly reduced in patients (0.88 [0.10] vs 1.6 [0.30] mmol/L; p < 0.001). Glucose 185-192 insulin Homo sapiens 166-173 8517428-3 1993 Therefore, the effects of a low salt diet alone and with enalapril on blood pressure and the insulin response to an oral glucose tolerance test were studied in 9 obese (body mass index 35 +/- 2 kg/m2) men with mild hypertension. Glucose 121-128 insulin Homo sapiens 93-100 8348704-11 1993 CONCLUSIONS: Abnormal beta cell function in cystic fibrosis patients was reflected initially in a diminished 30-minute insulin response to oral glucose. Glucose 144-151 insulin Homo sapiens 119-126 8359092-6 1993 A large insulin response to oral glucose was evident, with the upper tertile of the 2-h insulin response six times higher than the lower tertile (113 +/- 43 vs. 19 +/- 8 mU/L). Glucose 33-40 insulin Homo sapiens 8-15 8359092-6 1993 A large insulin response to oral glucose was evident, with the upper tertile of the 2-h insulin response six times higher than the lower tertile (113 +/- 43 vs. 19 +/- 8 mU/L). Glucose 33-40 insulin Homo sapiens 88-95 8359105-0 1993 Acute insulin response to glucose and glucagon in subjects at risk of developing type I diabetes. Glucose 26-33 insulin Homo sapiens 6-13 8359105-3 1993 Acute response to glucose was expressed as the sum of plasma insulin at 2 and 5 min and response to glucagon as the increase in plasma insulin after 10 min. Glucose 18-25 insulin Homo sapiens 61-68 8359105-3 1993 Acute response to glucose was expressed as the sum of plasma insulin at 2 and 5 min and response to glucagon as the increase in plasma insulin after 10 min. Glucose 18-25 insulin Homo sapiens 135-142 8359105-13 1993 CONCLUSIONS: Both insulin responses to glucose and glucagon are related. Glucose 39-46 insulin Homo sapiens 18-25 8359586-4 1993 Since insulin secretion, as measured by the acute insulin response to intravenous glucose, is used to predict diabetes and to monitor therapy, the effects of nicotinamide must be established before trials in individuals at high risk of progression to Type 1 diabetes can be interpreted. Glucose 82-89 insulin Homo sapiens 6-13 8395436-1 1993 Recently, we demonstrated insulin resistance due to reduced glucose storage in young relatives of Type 2 diabetic patients. Glucose 60-67 insulin Homo sapiens 26-33 8395436-8 1993 Insulin stimulation of non-oxidative glucose metabolism correlated with "in vitro" insulin-stimulated tyrosine kinase activity (r = 0.61, p < 0.01) and also when expressed per binding capacity (r = 0.53, p < 0.025). Glucose 37-44 insulin Homo sapiens 0-7 8395436-8 1993 Insulin stimulation of non-oxidative glucose metabolism correlated with "in vitro" insulin-stimulated tyrosine kinase activity (r = 0.61, p < 0.01) and also when expressed per binding capacity (r = 0.53, p < 0.025). Glucose 37-44 insulin Homo sapiens 83-90 8224035-2 1993 Normal subjects are exquisitely sensitive to small decrements in glucose; levels within the normal range cause suppression of endogenous insulin (approximately 4.0 mM) and activation of glucagon and epinephrine (approximately 3.5 mM) secretion. Glucose 65-72 insulin Homo sapiens 137-144 8224035-3 1993 The glucose threshold for hormone release is modified by multiple factors, including age, gender, and the level of insulin per se. Glucose 4-11 insulin Homo sapiens 115-122 8224035-9 1993 Commonly, the glucose level triggering adrenergic responses is shifted downward during intensive insulin therapy of IDDM. Glucose 14-21 insulin Homo sapiens 97-104 8224036-0 1993 The effects of single and sequential insulin infusions on glucose disposal in older men. Glucose 58-65 insulin Homo sapiens 37-44 8224036-5 1993 In four subjects with impaired glucose tolerance, the EC50 (insulin concentration producing a half-maximal response) was higher and Mmax (maximal glucose disposal) lower than in subjects with normal glucose tolerance, suggesting impairments in both insulin sensitivity and responsiveness in older subjects with impaired glucose tolerance. Glucose 31-38 insulin Homo sapiens 60-67 8224036-5 1993 In four subjects with impaired glucose tolerance, the EC50 (insulin concentration producing a half-maximal response) was higher and Mmax (maximal glucose disposal) lower than in subjects with normal glucose tolerance, suggesting impairments in both insulin sensitivity and responsiveness in older subjects with impaired glucose tolerance. Glucose 31-38 insulin Homo sapiens 249-256 8224037-6 1993 Insulin-dependent glucose uptake, a measure of tissue sensitivity to insulin, was decreased in the old-impaired group at every plateau except the highest. Glucose 18-25 insulin Homo sapiens 0-7 8224037-6 1993 Insulin-dependent glucose uptake, a measure of tissue sensitivity to insulin, was decreased in the old-impaired group at every plateau except the highest. Glucose 18-25 insulin Homo sapiens 69-76 8224037-7 1993 We conclude that healthy, active older subjects showed moderate intolerance to oral and IV glucose and that the mechanism of this physiological aging process is most likely decreased insulin sensitivity. Glucose 91-98 insulin Homo sapiens 183-190 8100799-0 1993 Normal splanchnic but impaired peripheral insulin-stimulated glucose uptake in cirrhosis. Glucose 61-68 insulin Homo sapiens 42-49 8100799-12 1993 Glucose intolerance in cirrhosis is characterized by impaired peripheral insulin-stimulated non-oxidative glucose disposal. Glucose 106-113 insulin Homo sapiens 73-80 8319989-0 1993 Insulin-stimulated glucose utilization and borderline hypertension in young adult blacks. Glucose 19-26 insulin Homo sapiens 0-7 8319989-1 1993 The purpose of this investigation was to determine whether there is a relation between impaired insulin-stimulated glucose utilization, or insulin resistance, and blood pressure (BP) in a young adult black population. Glucose 115-122 insulin Homo sapiens 96-103 8406325-6 1993 The half maximally effective dose of insulin on glucose disposal was 43 +/- 3 and 69 +/- 9 uU/ml in N and HTD respectively (p < 0.05). Glucose 48-55 insulin Homo sapiens 37-44 8406325-8 1993 The concentration of insulin giving a half maximal effect on serum amino acids correlated with the half-maximally effective dose on glucose disposal rate (r = 0.72, p < 0.01). Glucose 132-139 insulin Homo sapiens 21-28 8406325-12 1993 This also confirms the association between glucose disposal and amino acids levels in a variety of insulin sensitive and resistant states. Glucose 43-50 insulin Homo sapiens 99-106 8100832-9 1993 It should be noted that the increases in hepatic glucose production and plasma glucose concentration after glucagon was added to SRIF were prevented when basal insulin levels were replaced. Glucose 49-56 insulin Homo sapiens 160-167 8325938-5 1993 A reduced insulin and augmented glucose response to oral glucose during therapy normalized after octreotide withdrawal (insulin, 527 +/- 84, 289 +/- 62, and 733 +/- 110 pmol/L; glucose, 6.2 +/- 0.3, 8.5 +/- 0.4, and 6.8 +/- 0.2 mmol/L; pre-Tx, on and off octreotide, means +/- SE). Glucose 57-64 insulin Homo sapiens 120-127 8325938-5 1993 A reduced insulin and augmented glucose response to oral glucose during therapy normalized after octreotide withdrawal (insulin, 527 +/- 84, 289 +/- 62, and 733 +/- 110 pmol/L; glucose, 6.2 +/- 0.3, 8.5 +/- 0.4, and 6.8 +/- 0.2 mmol/L; pre-Tx, on and off octreotide, means +/- SE). Glucose 57-64 insulin Homo sapiens 120-127 8325978-1 1993 Subjects characterized by a predominance of small LDL particles (pattern B) have changes in plasma triglyceride (TG) and HDL-cholesterol concentrations consistent with the presence of resistance to insulin-mediated glucose uptake. Glucose 215-222 insulin Homo sapiens 198-205 8325993-2 1993 These oscillations appear to be a function of the feedback loop linking glucose and insulin. Glucose 72-79 insulin Homo sapiens 84-91 8326013-10 1993 We conclude that transmembrane glucose transport, when assessed in vivo in skeletal muscle, is insensitive to insulin in nonobese NIDDM patients, and plays a major role in determining whole body insulin resistance. Glucose 31-38 insulin Homo sapiens 195-202 8326016-0 1993 Chronic exposure of HIT cells to high glucose concentrations paradoxically decreases insulin gene transcription and alters binding of insulin gene regulatory protein. Glucose 38-45 insulin Homo sapiens 85-92 8326016-0 1993 Chronic exposure of HIT cells to high glucose concentrations paradoxically decreases insulin gene transcription and alters binding of insulin gene regulatory protein. Glucose 38-45 insulin Homo sapiens 134-141 8326016-11 1993 The decrease in INSCAT expression in late passages of cells serially cultured in 11.1 mM glucose was associated with the inability to form a specific nuclear protein-DNA complex with the CT motifs of the human insulin promoter. Glucose 89-96 insulin Homo sapiens 210-217 8326016-14 1993 These data indicate that chronic exposure of the beta cell to high glucose concentrations can paradoxically decrease insulin gene transcription, in part, by altering the ability of a regulatory protein (GSTF) to interact with the insulin gene promoter. Glucose 67-74 insulin Homo sapiens 117-124 8326016-14 1993 These data indicate that chronic exposure of the beta cell to high glucose concentrations can paradoxically decrease insulin gene transcription, in part, by altering the ability of a regulatory protein (GSTF) to interact with the insulin gene promoter. Glucose 67-74 insulin Homo sapiens 230-237 8315223-0 1993 Relationship between glucose tolerance and glucose-stimulated insulin response in 65-year-olds. Glucose 21-28 insulin Homo sapiens 62-69 8315223-0 1993 Relationship between glucose tolerance and glucose-stimulated insulin response in 65-year-olds. Glucose 43-50 insulin Homo sapiens 62-69 8315223-6 1993 Another subgroup of older subjects with a decrease in glucose tolerance mild enough to be considered normal by the National Diabetes Group Criteria tended to have both an increase in the early insulin response and a decrease in the third hour response. Glucose 54-61 insulin Homo sapiens 193-200 8315223-8 1993 CONCLUSION: Aberrations in early and late phase glucose-stimulated insulin responses appear to be present in older subjects with even mildly decreased glucose tolerance. Glucose 48-55 insulin Homo sapiens 67-74 8315223-8 1993 CONCLUSION: Aberrations in early and late phase glucose-stimulated insulin responses appear to be present in older subjects with even mildly decreased glucose tolerance. Glucose 151-158 insulin Homo sapiens 67-74 8112479-5 1993 Comparative studies of blood insulin dynamics revealed that this new method of delivery resulted in a circadian blood glucose pattern closely approximating normal levels, the complete elimination of subjective symptoms and the normalization of basal insulin secretory patterns. Glucose 118-125 insulin Homo sapiens 29-36 8326285-9 1993 In addition, the plasma insulin response to oral glucose was increased in individuals with asymptomatic hyperuricaemia (P < 0.005) as were both systolic (136 +/- 3 vs. 126 +/- 3 mmHg, P < 0.05) and diastolic (91 +/- 1 vs. 82 +/- 1, P < 0.01) blood pressure. Glucose 49-56 insulin Homo sapiens 24-31 8397124-3 1993 MP caused a temperature-dependent and dose-related stimulation of insulin secretion from intact islets at a substimulatory concentration (2 mM) of glucose, which was not dependent upon the presence of extracellular Ca2+. Glucose 147-154 insulin Homo sapiens 66-73 8400594-6 1993 Selecting the method of insulin infusion (i.e., intermittent subcutaneous insulin therapy versus continuous intravenous or continuous subcutaneous infusion) for maximizing glucose control is an important step in the acute nutrition management of insulin-dependent diabetic patients. Glucose 172-179 insulin Homo sapiens 24-31 8400594-6 1993 Selecting the method of insulin infusion (i.e., intermittent subcutaneous insulin therapy versus continuous intravenous or continuous subcutaneous infusion) for maximizing glucose control is an important step in the acute nutrition management of insulin-dependent diabetic patients. Glucose 172-179 insulin Homo sapiens 74-81 8327595-7 1993 In four sessions, subjects were injected with 0.035 IU/kg body weight of human insulin as the unconditioned stimulus (US), which induced the expected fall in blood glucose level below 50 mg/dl (UR). Glucose 164-171 insulin Homo sapiens 79-86 8105502-2 1993 The effects of stress on glucose metabolism are mediated by a variety of "counter-regulatory" hormones that are released in response to stress and that result in elevated blood glucose levels and decreased insulin action. Glucose 25-32 insulin Homo sapiens 206-213 8378744-0 1993 The relationship between early insulin release and glucose tolerance in healthy subjects. Glucose 51-58 insulin Homo sapiens 31-38 8378744-2 1993 Whether improved glucose tolerance results from enhanced early insulin release or greater total insulin secretion is not clear. Glucose 17-24 insulin Homo sapiens 63-70 8378744-3 1993 Therefore insulin and C-peptide responses to oral glucose were measured in healthy subjects with and without a single dose of oral and intravenous glipizide. Glucose 50-57 insulin Homo sapiens 22-31 8378744-6 1993 In contrast, enhancement of the early insulin response with intravenous glipizide almost completely prevented postprandial glucose rise. Glucose 123-130 insulin Homo sapiens 38-45 8352433-5 1993 For example, glucose uptake as measured by the euglycemic clamp includes both insulin-dependent and non-insulin-dependent (SG) factors, so that the M value could be affected by changes in SG as well as in insulin action. Glucose 13-20 insulin Homo sapiens 78-85 8352433-5 1993 For example, glucose uptake as measured by the euglycemic clamp includes both insulin-dependent and non-insulin-dependent (SG) factors, so that the M value could be affected by changes in SG as well as in insulin action. Glucose 13-20 insulin Homo sapiens 104-111 8352433-5 1993 For example, glucose uptake as measured by the euglycemic clamp includes both insulin-dependent and non-insulin-dependent (SG) factors, so that the M value could be affected by changes in SG as well as in insulin action. Glucose 13-20 insulin Homo sapiens 104-111 8517876-3 1993 In the perfused rat pancreas, homologous CGRP and amylin, at 75 pM, exerted comparable inhibitory effects on the insulin response to 9 mM glucose (ca. Glucose 138-145 insulin Homo sapiens 113-120 8342781-0 1993 Failure of insulin mixing in 10% glucose. Glucose 33-40 insulin Homo sapiens 11-18 8392806-6 1993 Both insulin-stimulated glucose transport and IGF-II binding were prevented when cells were pretreated with okadaic acid. Glucose 24-31 insulin Homo sapiens 5-12 8216497-0 1993 Effects of physiological plasma insulin levels on glucose turnover parameters in familial hypercholesterolemia. Glucose 50-57 insulin Homo sapiens 32-39 8334748-11 1993 Insulin sensitivity was given by the ratio of glycaemic variation to initial blood glucose (delta G/G index). Glucose 83-90 insulin Homo sapiens 0-7 8325202-6 1993 Insulin sensitivity was even higher than normal in the remission patients, who also were characterized by the reappearance of some endogenous insulin secretion and the sustained normalization of blood glucose profiles. Glucose 201-208 insulin Homo sapiens 0-7 8325202-10 1993 The secretion of endogenous insulin, although lower than normal, was sufficient to secure a high sensitivity to insulin and the maintenance of normal blood glucose profiles, presumably because of the fact that insulin was released directly into the portal vein in these conditions. Glucose 156-163 insulin Homo sapiens 28-35 8325205-0 1993 Comparison of bolus and infusion protocols for determining acute insulin response to intravenous glucose in normal humans. Glucose 97-104 insulin Homo sapiens 65-72 8325205-6 1993 The acute insulin response to glucose was calculated as the mean of the 1" + 3", the mean of 1" to 10", or as the integrated area from 0 to 10". Glucose 30-37 insulin Homo sapiens 10-17 8325205-8 1993 RESULTS: With the infusion protocol, the 1" insulin was significantly higher, resulting in a higher acute insulin response to glucose when calculated as 1" + 3" (525 +/- 66 vs. 376 +/- 35 pM, P < 0.004). Glucose 126-133 insulin Homo sapiens 44-51 8325205-8 1993 RESULTS: With the infusion protocol, the 1" insulin was significantly higher, resulting in a higher acute insulin response to glucose when calculated as 1" + 3" (525 +/- 66 vs. 376 +/- 35 pM, P < 0.004). Glucose 126-133 insulin Homo sapiens 106-113 8325205-9 1993 When calculated over 10 min, however, the acute insulin response to glucose was not different between protocols. Glucose 68-75 insulin Homo sapiens 48-55 8334821-2 1993 After 6 months of insulin treatment, mean fasting blood glucose concentrations had decreased from 14.1 +/- 2.2 mmol l-1 to 8.4 +/- 1.8 mmol l-1 (p < 0.001), and HbA1c had fallen from 11.1 +/- 1.4% to 8.2 +/- 1.1% (p < 0.001). Glucose 56-63 insulin Homo sapiens 18-25 8404454-0 1993 Study of the rate of early glucose disappearance following insulin injection: insulin sensitivity index. Glucose 27-34 insulin Homo sapiens 59-66 8404454-0 1993 Study of the rate of early glucose disappearance following insulin injection: insulin sensitivity index. Glucose 27-34 insulin Homo sapiens 78-85 8404454-6 1993 The ITT was significantly correlated both with fasting insulin (r = -0.43, P < 0.01), and post-glucose load insulin concentration (r = -0.67, P < 0.01); each measurement expressing insulin sensitivity. Glucose 98-105 insulin Homo sapiens 111-118 8404454-6 1993 The ITT was significantly correlated both with fasting insulin (r = -0.43, P < 0.01), and post-glucose load insulin concentration (r = -0.67, P < 0.01); each measurement expressing insulin sensitivity. Glucose 98-105 insulin Homo sapiens 111-118 8344647-0 1993 The magnitude, the kinetics and the metabolic efficiency of first-phase insulin response to intravenous glucose are related. Glucose 104-111 insulin Homo sapiens 72-79 8344647-1 1993 We investigated the relationship between the kinetics, the magnitude and the metabolic efficiency of first-phase insulin response (FPIR) to intravenous glucose. Glucose 152-159 insulin Homo sapiens 113-120 8344647-3 1993 The first significant increase in plasma insulin concentrations above baseline appeared as early as the 2nd min (1 min before the end of glucose injection, fast response) in 80% of controls and 70% of relatives, and at the 3rd min or later (delayed response) in the remaining subjects. Glucose 137-144 insulin Homo sapiens 41-48 8344647-5 1993 In the controls and the relatives, the subjects with a fast insulin response had a significantly higher FPIR (controls 215.4 +/- 93.5 vs 59.7 +/- 5.6 microU/ml, p < 0.001 and relatives 143.5 +/- 61.8 vs 55.9 +/- 27.7 microU/ml, p < 0.001) and showed better glucose assimilation (controls 3.05 +/- 1.05 vs 1.64 +/- 0.16%/min, p < 0.05 and relatives 2.6 +/- 0.96 vs 1.6 +/- 0.85%/min, p < 0.01) during IVGTT than the subjects with a delayed response. Glucose 263-270 insulin Homo sapiens 60-67 8500731-8 1993 Insulin resistance is restricted to glucose, but not to amino acid metabolism. Glucose 36-43 insulin Homo sapiens 0-7 8005969-1 1993 Fifty-six patients who had been diagnosed diabetic prior to the age of 30 were evaluated to determine the C-peptide (CP) secretory response to a glucose load. Glucose 145-152 insulin Homo sapiens 106-115 8005969-1 1993 Fifty-six patients who had been diagnosed diabetic prior to the age of 30 were evaluated to determine the C-peptide (CP) secretory response to a glucose load. Glucose 145-152 insulin Homo sapiens 117-119 8349447-4 1993 However, in the Ethiopians, impaired glucose tolerance was associated with hyperinsulinemia, suggesting that similar to some other populations glucose intolerance is associated with insulin resistance. Glucose 37-44 insulin Homo sapiens 80-87 8366184-4 1993 Time courses of plasma glucose and serum insulin changes from baseline after the oral glucose tolerance test were evaluated by AUC. Glucose 86-93 insulin Homo sapiens 41-48 8501151-5 1993 We conclude that amlodipine treatment improves glucose tolerance, reduces fasting and glucose-stimulated serum insulin levels, increases serum DHEA-S and androstenedione levels, and decreases circulating cortisol. Glucose 86-93 insulin Homo sapiens 111-118 8514849-5 1993 The rate of insulin-stimulated nonoxidative glucose metabolism was decreased by 47% (P < 0.005) in NIDDM patients, whereas the glucose oxidation rate was normal. Glucose 44-51 insulin Homo sapiens 12-19 8514849-9 1993 In conclusion, qualitative but not quantitative posttranslational abnormalities of the GS protein in muscle determine the reduced insulin-stimulated nonoxidative glucose metabolism in NIDDM. Glucose 162-169 insulin Homo sapiens 130-137 8377030-7 1993 Multiple regression analysis with age, sex and obesity as confounding variables showed that insulin resistance was superior to hyperinsulinemia in the relationships with blood pressure and indices of hyperlipidemia (elevated free fatty acids, serum triglycerides and low HDL cholesterol), but both insulin sensitivity and hyperinsulinemia were significantly related to fasting glucose. Glucose 377-384 insulin Homo sapiens 92-99 8377030-8 1993 CONCLUSIONS: Insulin sensitivity was more closely related to blood pressure, serum triglycerides and HDL cholesterol than hyperinsulinemia, but both insulin sensitivity and the insulin levels were associated with fasting glucose. Glucose 221-228 insulin Homo sapiens 149-156 8377030-9 1993 Thus, insulin resistance is more important than hyperinsulinemia as a determinant of the constellation of cardiovascular risk factors comprising hypertension, glucose intolerance and hyperlipidemia. Glucose 159-166 insulin Homo sapiens 6-13 8331618-4 1993 A low-dose (0.25 mU/kg/min) insulin infusion suppressed endogenous hepatic glucose production. Glucose 75-82 insulin Homo sapiens 28-35 8499439-1 1993 D-Glucose induces insulin secretion from beta-cells of pancreatic islets by processes involving glycolytic metabolism and generation of ATP. Glucose 0-9 insulin Homo sapiens 18-25 8499439-2 1993 Glucose also induces hydrolysis of beta-cell membrane phospholipids and accumulation of nonesterified arachidonate, which facilitates Ca2+ entry and the rise in beta-cell Ca2+ concentration that is a critical signal in the induction of insulin secretion. Glucose 0-7 insulin Homo sapiens 236-243 8098525-2 1993 Insulin resistance is associated with a number of risk factors for atherosclerosis, including glucose intolerance, hypertension, and dyslipidemia. Glucose 94-101 insulin Homo sapiens 0-7 8317453-3 1993 The author measured insulin response to an oral glucose load and quantitated insulin resistance using the euglycemic hyperinsulinemic clamp technique to evaluate the correlation between insulin level and the degree of insulin resistance in individuals with varying degrees of glucose tolerance. Glucose 48-55 insulin Homo sapiens 20-27 8317453-6 1993 Correlations of insulin resistance (whole-body glucose uptake in clamp studies) with fasting or postload insulin levels were remarkably consistent, ranging from -0.58 to -0.74 (p < 0.01) in subjects with normoglycemia. Glucose 47-54 insulin Homo sapiens 16-23 8317453-6 1993 Correlations of insulin resistance (whole-body glucose uptake in clamp studies) with fasting or postload insulin levels were remarkably consistent, ranging from -0.58 to -0.74 (p < 0.01) in subjects with normoglycemia. Glucose 47-54 insulin Homo sapiens 105-112 8498392-8 1993 On a separate study day, the subjects underwent the identical protocol, with the addition of 50 g of oral glucose to the potassium load to stimulate endogenous insulin release. Glucose 106-113 insulin Homo sapiens 160-167 8498392-16 1993 CONCLUSIONS: Exogenous glucose, by stimulating endogenous secretion of insulin, enhances extrarenal disposal of a potassium load. Glucose 23-30 insulin Homo sapiens 71-78 8498413-6 1993 There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Glucose 139-146 insulin Homo sapiens 158-165 8498413-6 1993 There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Glucose 139-146 insulin Homo sapiens 225-232 8498413-6 1993 There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Glucose 139-146 insulin Homo sapiens 225-232 8498413-6 1993 There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Glucose 139-146 insulin Homo sapiens 158-165 8498413-6 1993 There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Glucose 139-146 insulin Homo sapiens 225-232 8498413-6 1993 There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Glucose 139-146 insulin Homo sapiens 225-232 8498497-9 1993 Whole body glucose uptake was quantitated by the euglycemic insulin clamp technique. Glucose 11-18 insulin Homo sapiens 60-67 8498497-10 1993 Whole body glucose uptake was approximately 31% lower in the diabetic patients (P < 0.01) than in the normal subjects, thus confirming the presence of whole body insulin resistance. Glucose 11-18 insulin Homo sapiens 165-172 8498505-5 1993 The new minimal model has two novel features: glucose kinetics are described by a two-compartment structure, and insulin exerts its action on the irreversible loss of the slowly exchanging glucose pool. Glucose 189-196 insulin Homo sapiens 113-120 8512657-1 1993 The role of angiotensin converting enzyme (ACE) inhibitors in improving insulin-mediated glucose uptake has been described. Glucose 89-96 insulin Homo sapiens 72-79 8216104-3 1993 Body habitus, serum lipid levels and the serum insulin response to a glucose load in pregnancy were compared in 15 women with normal glucose tolerance, 16 Caucasian women with GDM and 19 Asian-born women with GDM. Glucose 69-76 insulin Homo sapiens 47-54 8216104-1 1993 An analysis of racial differences in body habitus, lipid metabolism and the serum insulin response to an oral glucose load. Glucose 110-117 insulin Homo sapiens 82-89 8216104-5 1993 Both groups of GDM women had similar patterns of insulin response to oral glucose with a delayed insulin peak and an elevated 2-hour insulin level (p = 0.0021). Glucose 74-81 insulin Homo sapiens 49-56 8216104-5 1993 Both groups of GDM women had similar patterns of insulin response to oral glucose with a delayed insulin peak and an elevated 2-hour insulin level (p = 0.0021). Glucose 74-81 insulin Homo sapiens 97-104 8216104-5 1993 Both groups of GDM women had similar patterns of insulin response to oral glucose with a delayed insulin peak and an elevated 2-hour insulin level (p = 0.0021). Glucose 74-81 insulin Homo sapiens 97-104 8216104-6 1993 In addition, the insulin response per unit of glycaemic stimulus (incremental insulin area/incremental glucose area at 1 hour) was reduced in both GDM groups (p = 0.035). Glucose 103-110 insulin Homo sapiens 17-24 8257938-0 1993 Heterogenous insulin response to an oral glucose load by patients with the indeterminate clinical form of Chagas" disease. Glucose 41-48 insulin Homo sapiens 13-20 8257938-1 1993 This study was designed to investigate the behavior of serum glucose and insulin in response to an oral glucose load in chagasic patients with the indeterminate clinical form of the disease. Glucose 104-111 insulin Homo sapiens 73-80 8490596-5 1993 Plasma glucose and insulin responses to an oral glucose challenge did not change in association with nicardipine therapy. Glucose 48-55 insulin Homo sapiens 19-26 8490597-0 1993 Role of insulin in the pathogenesis of hypertension associated with glucose intolerance. Glucose 68-75 insulin Homo sapiens 8-15 8508007-8 1993 Bromocriptine led to a significant decrease in basal as well as glucose-stimulated insulin levels, and growth hormone secretion during oral glucose load was reduced in all 12 patients. Glucose 64-71 insulin Homo sapiens 83-90 7683288-7 1993 The diabetic subjects as a group had higher fasting insulin levels and lower insulin-mediated glucose uptake during a euglycemic-hyperinsulinemic clamp (P = 0.042). Glucose 94-101 insulin Homo sapiens 77-84 8314448-9 1993 All subjects with the Thr188 mutation show a decreased insulin secretory response during oral glucose tolerance testing. Glucose 94-101 insulin Homo sapiens 55-62 8314452-3 1993 In response to low-dose intravenous insulin infusion (0.3 mU.kg-1.min-1), plasma glucose fall and counterregulation in seven men and seven women had a different course (p < 0.001), with different glucose kinetics. Glucose 81-88 insulin Homo sapiens 36-43 8314453-1 1993 Type 2 (non-insulin-dependent) diabetes mellitus is associated with increased glucose, insulin, total and VLDL-triglyceride, and often total and LDL-cholesterol levels which promote vascular disease. Glucose 78-85 insulin Homo sapiens 12-19 8314453-7 1993 In conclusion, insulin-like growth factor-I lowered lipid levels in Type 2 diabetic patients directly or indirectly or both because of decreased glucose and insulin levels. Glucose 145-152 insulin Homo sapiens 15-22 8375268-2 1993 glucose tolerance test modified by exogenous insulin administration for estimation of insulin sensitivity (SI) and glucose-mediated glucose disposal (SG) with Bergman"s minimal model computer analysis of glucose kinetics. Glucose 0-7 insulin Homo sapiens 86-93 8375272-3 1993 With 0.3 U/kg of insulin, the rate of fall in glycemia and the nadir of blood glucose were made similar to those with 0.1 U/kg of insulin by glucose infusion with artificial endocrine pancreas. Glucose 78-85 insulin Homo sapiens 17-24 8482434-2 1993 Glucose metabolism in the basal state and in response to insulin was quantitated by using the euglycemic insulin (20 mU.min-1 x m-2) clamp in combination with 3-[3H]glucose infusion and indirect calorimetry in 20 obese nondiabetic subjects (10 hypertensive and 10 normotensive), 26 type II diabetic subjects (13 hypertensive and 13 normotensive), and 11 normal nondiabetic subjects. Glucose 165-172 insulin Homo sapiens 57-64 8508611-3 1993 Similar fasting insulin concentrations but lower 30-min post-glucose-load insulin concentrations were found in diabetic subjects (mean +/- SEM 143 +/- 12 pmol-1 vs 304 +/- 19 (p < 0.001). Glucose 61-68 insulin Homo sapiens 74-81 8389334-3 1993 Before training, the ratio of insulin to glucose area measured during an oral glucose tolerance test (OGTT) was significantly correlated with fat mass (r = 0.72, P < 0.05) as well as with abdominal AT-LPL activity (r = 0.69, P < 0.05). Glucose 78-85 insulin Homo sapiens 30-37 8389334-7 1993 However, changes in insulin sensitivity, as estimated by changes in the insulin area/glucose area ratio were positively correlated with changes in abdominal AT-LPL activity expressed on a per cell (r = 0.72, P < 0.05) or per surface area (r = 0.81, P < 0.01) basis. Glucose 85-92 insulin Homo sapiens 20-27 8491496-3 1993 Local hyperinsulinemia in the forearm (132 +/- 25 microunits/mL for 90 minutes) induced a significant increase in the utilization of glucose from baseline (16.4 +/- 3.1 mg.dL-1.min-1 per 100 mL forearm volume) to a plateau (85.7 +/- 15.1 mg.dL-1.min-1 per 100 mL forearm volume) between 40 and 60 minutes of insulin infusion but did not alter the utilization of oxygen. Glucose 133-140 insulin Homo sapiens 11-18 8320268-0 1993 Role of transverse tubules in insulin stimulated muscle glucose transport. Glucose 56-63 insulin Homo sapiens 30-37 8388405-5 1993 Insulin resistance was estimated by calculating the area under the curve for serum insulin levels in response to a 75 g oral glucose load. Glucose 125-132 insulin Homo sapiens 0-7 8388405-5 1993 Insulin resistance was estimated by calculating the area under the curve for serum insulin levels in response to a 75 g oral glucose load. Glucose 125-132 insulin Homo sapiens 83-90 8496333-5 1993 In spite of increased epinephrine secretion, the glucose infusion rate required to maintain glucose was 2-fold greater in the high insulin study, and there was greater suppression of lipolysis in that group. Glucose 49-56 insulin Homo sapiens 131-138 8222297-10 1993 The cortisol response was negatively correlated with insulin-stimulated glucose disposal (P < 0.01, r2 = 0.23), but not with other indices of insulin secretion/resistance (fasting insulin, oral glucose tolerance test area under the curve, index of insulin resistance) or fat distribution. Glucose 72-79 insulin Homo sapiens 53-60 8222298-9 1993 Insulin sensitivity was assessed by the decline in plasma glucose following intravenous insulin (0.05 U/kg). Glucose 58-65 insulin Homo sapiens 0-7 8222298-9 1993 Insulin sensitivity was assessed by the decline in plasma glucose following intravenous insulin (0.05 U/kg). Glucose 58-65 insulin Homo sapiens 88-95 8222298-11 1993 Insulin area median (interquartile range) in response to glucose was significantly greater in the oligomenorrhoeic group (346 (239-734) mU/l h), compared with both PCO with regular cycles (246 (148-355), P < 0.01) and controls (221 (147-277), P < 0.01). Glucose 57-64 insulin Homo sapiens 0-7 8222336-12 1993 Our data demonstrate that a defect in glucose uptake exists in erythrocytes from NIDD patients, affecting both free and stored glucose, and that this defect is reversed by Metformin treatment, indicating that this drug can increase glycogen levels even in insulin-insensitive cells. Glucose 38-45 insulin Homo sapiens 256-263 8222650-4 1993 Slight and transient variations of fasting blood glucose levels were seen in the 30 mcg EE group and in the two groups for fasting insulin levels. Glucose 49-56 insulin Homo sapiens 131-138 8403806-13 1993 We conclude that (a) insulin causes antinatriuresis, antikaliuresis and hypokalaemia under physiological conditions; (b) in hyperinsulinaemic (insulin-resistant) patients with essential hypertension, the antinatriuretic action of insulin is quantitatively preserved; and (c) clamping plasma potassium levels prevents insulin-induced antikaliuresis but not antinatriuresis, and potentiates the insulin secretory response to glucose. Glucose 423-430 insulin Homo sapiens 21-28 8349044-2 1993 We have now evaluated the role of insulin resistance in determining the plasma glucose response to oral glucose in 74 volunteer subjects with normal glucose tolerance. Glucose 79-86 insulin Homo sapiens 34-41 8349044-2 1993 We have now evaluated the role of insulin resistance in determining the plasma glucose response to oral glucose in 74 volunteer subjects with normal glucose tolerance. Glucose 104-111 insulin Homo sapiens 34-41 8349044-2 1993 We have now evaluated the role of insulin resistance in determining the plasma glucose response to oral glucose in 74 volunteer subjects with normal glucose tolerance. Glucose 104-111 insulin Homo sapiens 34-41 8349044-6 1993 These analyses indicated that both the steady-state plasma glucose and the incremental insulin response during the first 30 min after the glucose load were significant predictors of the plasma glucose response. Glucose 138-145 insulin Homo sapiens 87-94 8349044-6 1993 These analyses indicated that both the steady-state plasma glucose and the incremental insulin response during the first 30 min after the glucose load were significant predictors of the plasma glucose response. Glucose 138-145 insulin Homo sapiens 87-94 8349044-7 1993 In those individuals in whom insulin action was impaired and the 30-min plasma insulin response was decreased, plasma glucose values reached higher levels. Glucose 118-125 insulin Homo sapiens 29-36 8349044-7 1993 In those individuals in whom insulin action was impaired and the 30-min plasma insulin response was decreased, plasma glucose values reached higher levels. Glucose 118-125 insulin Homo sapiens 79-86 8349044-8 1993 When standardized regression coefficients were determined, the incremental glucose response was directly correlated with steady-state plasma glucose (r = 0.700, P < 0.001) and inversely with the insulin response during the first 30 min (r = 0.268, P = 0.023). Glucose 75-82 insulin Homo sapiens 198-205 8225693-4 1993 In those pregnancies complicated by glucose intolerance reflected in hyperglycemia, insulin resistance appears to be heightened, both blood flow and transcapillary transport of insulin are compromised and insulin receptor and post receptor defects are exacerbated. Glucose 36-43 insulin Homo sapiens 84-91 8370696-7 1993 Insulin antibodies were significantly associated with decreased early phase insulin response to iv glucose (P = 0.0003). Glucose 99-106 insulin Homo sapiens 0-7 8370696-7 1993 Insulin antibodies were significantly associated with decreased early phase insulin response to iv glucose (P = 0.0003). Glucose 99-106 insulin Homo sapiens 76-83 8277227-2 1993 In static incubation experiments, adrenaline (0.1 nmol/l to 10 mumol/l) caused a concentration-dependent inhibition of glucose-induced insulin secretion from isolated human islets. Glucose 119-126 insulin Homo sapiens 135-142 8277227-4 1993 When employed at a high concentration (1 mumol/l), adrenaline caused a sustained inhibition of glucose-induced insulin secretion, which could be relieved by the addition of the alpha 2-antagonist yohimbine (10 mumol/l). Glucose 95-102 insulin Homo sapiens 111-118 8355109-6 1993 The stimulated insulin release during an intravenous glucose tolerance test, adjusted for age, had the highest overall accuracy of prediction. Glucose 53-60 insulin Homo sapiens 15-22 8355109-11 1993 A combination of islet cell antibodies, competitive insulin autoantibodies, and stimulated insulin release levels during an intravenous glucose tolerance test can accurately distinguish children with prediabetes from those with presumed benign transient increases in plasma glucose concentrations. Glucose 136-143 insulin Homo sapiens 91-98 8355109-11 1993 A combination of islet cell antibodies, competitive insulin autoantibodies, and stimulated insulin release levels during an intravenous glucose tolerance test can accurately distinguish children with prediabetes from those with presumed benign transient increases in plasma glucose concentrations. Glucose 274-281 insulin Homo sapiens 91-98 8412759-1 1993 Plasma glucose and insulin responses to oral glucose and insulin-mediated glucose disposal were determined in 20 patients with microvascular angina and 20 normal volunteers who were similar in terms of age, gender distribution, and degree of obesity. Glucose 45-52 insulin Homo sapiens 19-26 8412759-1 1993 Plasma glucose and insulin responses to oral glucose and insulin-mediated glucose disposal were determined in 20 patients with microvascular angina and 20 normal volunteers who were similar in terms of age, gender distribution, and degree of obesity. Glucose 45-52 insulin Homo sapiens 19-26 8412759-2 1993 Plasma glucose and insulin responses to a 75-g oral glucose challenge were significantly higher in those with microvascular angina (P < .001), as were steady-state plasma glucose concentrations after a 180-minute infusion of somatostatin, glucose, and insulin (12.2 +/- 1.0 v 7.6 +/- 0.6 mmol/L, P < .001). Glucose 52-59 insulin Homo sapiens 19-26 8412759-2 1993 Plasma glucose and insulin responses to a 75-g oral glucose challenge were significantly higher in those with microvascular angina (P < .001), as were steady-state plasma glucose concentrations after a 180-minute infusion of somatostatin, glucose, and insulin (12.2 +/- 1.0 v 7.6 +/- 0.6 mmol/L, P < .001). Glucose 52-59 insulin Homo sapiens 19-26 8412759-2 1993 Plasma glucose and insulin responses to a 75-g oral glucose challenge were significantly higher in those with microvascular angina (P < .001), as were steady-state plasma glucose concentrations after a 180-minute infusion of somatostatin, glucose, and insulin (12.2 +/- 1.0 v 7.6 +/- 0.6 mmol/L, P < .001). Glucose 52-59 insulin Homo sapiens 19-26 8247911-7 1993 Some authors recommend adding more insulin to bags with a higher concentration of dextrose. Glucose 82-90 insulin Homo sapiens 35-42 8237363-2 1993 During the episodes of hypoglycemia, his serum insulin level was inappropriately high and the symptoms of hypoglycemia were dramatically ameliorated by intravenously administering glucose bolus. Glucose 180-187 insulin Homo sapiens 47-54 7690718-2 1993 Plasma glucose and insulin responses to oral administration of 75 g glucose were not changed by arotinolol treatment. Glucose 68-75 insulin Homo sapiens 19-26 7690718-4 1993 Glucose infusion rate (GIR) as an indicator of insulin sensitivity and glucose clearance rate (GCR) were not influenced by arotinolol therapy. Glucose 0-7 insulin Homo sapiens 47-54 8372281-2 1993 Before and after that description, several studies featured the central role of tissue resistance to the effects of endogenous insulin during development of diverse biological disturbances: adipositas, intolerance to glucose (or diabetes mellitus), arterial hypertension, dyslipidemia, atherosclerosis. Glucose 217-224 insulin Homo sapiens 127-134 8215955-6 1993 In vitro studies demonstrated that the isolated islets secreted insulin in response to glucose and 3-isobutyl-L-methylxanthine (IBMX) challenge for at least 4 weeks. Glucose 87-94 insulin Homo sapiens 64-71 16843315-2 1993 As compared to the postabsorptive state, fasting resulted in a 50-80% decrease in glucose disposal during the clamps, indicating insulin resistance. Glucose 82-89 insulin Homo sapiens 129-136 8403824-0 1993 The acute effect of preprandial exogenous and endogenous sulphonylurea-stimulated insulin secretion on postprandial glucose excursions in patients with type 2 diabetes. Glucose 116-123 insulin Homo sapiens 82-89 8403824-1 1993 Sulphonylureas improve glucose tolerance by stimulating insulin secretion. Glucose 23-30 insulin Homo sapiens 56-63 8403824-2 1993 Whether improved glucose tolerance results from enhanced early insulin release or greater total insulin secretion is not clear. Glucose 17-24 insulin Homo sapiens 63-70 8403824-7 1993 This allowed comparison of the effect of exogenous and endogenous insulin supply on postprandial glucose excursions. Glucose 97-104 insulin Homo sapiens 66-73 8403824-10 1993 In conclusion, the total amount of insulin secreted seems more important than the timing of the insulin release for the postprandial glucose tolerance in Type 2 diabetic subjects. Glucose 133-140 insulin Homo sapiens 35-42 8225190-7 1993 The observed dissociation of ERPF and ELPF suggests a differential response to insulin in renal vs. leg vasculature which possibly is due to increased peripheral glucose metabolism. Glucose 162-169 insulin Homo sapiens 79-86 7901065-0 1993 Insulin responses following glucose administration in menstruating women. Glucose 28-35 insulin Homo sapiens 0-7 7901065-2 1993 METHOD: Insulin responses to intravenous glucose (300 mg/kg) were assessed, for up to 3 h, in 3 groups of age- and body mass-matched non-obese sedentary Nigerian women: Group A, 7 women in the menstrual follicular phase; Group B, 7 women in the menstrual luteal phase; C, 7 men. Glucose 41-48 insulin Homo sapiens 8-15 7901065-5 1993 CONCLUSION: Black African women in the menstrual luteal phase demonstrate an exaggerated insulin response to an acute glucose load and are thus relatively insulin-insensitive. Glucose 118-125 insulin Homo sapiens 89-96 8393428-0 1993 Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal. Glucose 84-91 insulin Homo sapiens 66-73 8393428-11 1993 In conclusion, these results indicate that in hypertensive blacks, insulin-resistant glucose disposal is strongly associated with elevated red blood cell Na(+)-H+ exchange activity. Glucose 85-92 insulin Homo sapiens 67-74 8408513-0 1993 Insulin hypersecretion together with high luteinizing hormone concentration augments androgen secretion in oral glucose tolerance test in women with polycystic ovarian disease. Glucose 112-119 insulin Homo sapiens 0-7 8345050-7 1993 In this plasma glucose range these insulin surrogates provide better diagnostic accuracy than plasma insulin and C-peptide. Glucose 15-22 insulin Homo sapiens 35-42 8349811-3 1993 Second, in the presence of plasma insulin concentrations that stimulate glucose transport maximally (approximately 5,000 microU/ml), AII infusions increased whole-body glucose clearance without enhancing glucose extraction across the leg. Glucose 72-79 insulin Homo sapiens 34-41 8349811-9 1993 However, when leg glucose uptake was activated by insulin, the redistribution of flow caused a net increase in whole-body glucose utilization. Glucose 18-25 insulin Homo sapiens 50-57 8349811-9 1993 However, when leg glucose uptake was activated by insulin, the redistribution of flow caused a net increase in whole-body glucose utilization. Glucose 122-129 insulin Homo sapiens 50-57 8345810-7 1993 Change in countertransport activity was correlated with change in body mass index (BMI) in men (r = .52, P < .01) and women (r = .27, NS) and was also strongly correlated with change in fasting glucose levels in both men and women (r = .50 and r = .56, respectively; P < .01) and with change in fasting insulin levels in men (r = .42, P = .04). Glucose 197-204 insulin Homo sapiens 309-316 8345813-0 1993 Hepatic extraction of insulin after stimulation of secretion with oral glucose or parenteral nutrients. Glucose 71-78 insulin Homo sapiens 22-29 8212621-1 1993 Increased glucose release from the liver which is responsible to a considerable extent for fasting hyperglycaemia in type 2 diabetics is associated with hepatic insulin resistance. Glucose 10-17 insulin Homo sapiens 161-168 8212622-5 1993 Patients with an impaired glucose tolerance and NIDDM had significantly higher fasting insulin levels and insulin levels after two hours (the latter value was not assessed in diabetes) and unfavourable "atherogenic" lipid and lipoprotein values, as compared with subjects without glucose intolerance and the control group. Glucose 26-33 insulin Homo sapiens 87-94 8212622-5 1993 Patients with an impaired glucose tolerance and NIDDM had significantly higher fasting insulin levels and insulin levels after two hours (the latter value was not assessed in diabetes) and unfavourable "atherogenic" lipid and lipoprotein values, as compared with subjects without glucose intolerance and the control group. Glucose 26-33 insulin Homo sapiens 106-113 8343735-8 1993 Their insulin mediated glucose disposal was lower than that of controls (29.5 (6.5) v 40.1 (8.6) mumol/kg/min, p = 0.002), but, after adjustment for blood pressure, the difference was not significant (difference 6.9 (95% confidence interval -1.5 to 15.3), p = 0.10). Glucose 23-30 insulin Homo sapiens 6-13 8343735-9 1993 Insulin secretion in the first hour after injection of glucose was slightly but not significantly higher in the offspring of hypertensive patients (9320 (5484) v 6723 (3751) pmol.min/l). Glucose 55-62 insulin Homo sapiens 0-7 8397996-3 1993 The relationship between fasting insulin and glucose at baseline and longitudinal changes in blood pressure were examined. Glucose 45-52 insulin Homo sapiens 33-40 8397996-4 1993 Significantly positive correlations were observed between fasting insulin and glucose at baseline and systolic and diastolic blood pressure at follow-up in white boys and girls (r = 0.19 to 0.38, P < .01), but not in blacks. Glucose 78-85 insulin Homo sapiens 66-73 8401319-2 1993 The levels of plasma immunoreactive insulin reached maximum at 60 min with a value of 62.77 +/- 6.52 microU/ml after the glucose load and 62.62 +/- 6.52 microU/ml after the test meal. Glucose 121-128 insulin Homo sapiens 36-43 8401319-3 1993 In the case of salivary immunoreactive insulin levels, the maximum was attained at 90 min with a value of 18.47 +/- 2.68 microU/min after the glucose load and 22.40 +/- 2.01 microU/min after the test meal. Glucose 142-149 insulin Homo sapiens 39-46 8149701-2 1993 Modelling analysis of intravenous glucose tolerance test glucose and insulin concentrations can provide measures of insulin sensitivity and metabolism from a single straightforward procedure. Glucose 34-41 insulin Homo sapiens 116-123 8149701-2 1993 Modelling analysis of intravenous glucose tolerance test glucose and insulin concentrations can provide measures of insulin sensitivity and metabolism from a single straightforward procedure. Glucose 57-64 insulin Homo sapiens 116-123 8293864-0 1993 Predictive value of age-related acute insulin response to glucose in subjects at risk for type 1 diabetes: results of a 6-year follow-up study from west-France. Glucose 58-65 insulin Homo sapiens 38-45 8365089-2 1993 Subcutaneous injection of 0.15 U kg-1 body weight (range 9.5-14.3 U) of the insulin analogue or soluble human insulin resulted in half-maximal glucose infusion rates (after subtraction of mean baseline glucose infusion rates) that were reached significantly earlier after injection of B28Asp (45 +/- 11 (SD) min) as compared to human insulin (58 +/- 25 min, p < 0.05). Glucose 143-150 insulin Homo sapiens 76-83 8365089-2 1993 Subcutaneous injection of 0.15 U kg-1 body weight (range 9.5-14.3 U) of the insulin analogue or soluble human insulin resulted in half-maximal glucose infusion rates (after subtraction of mean baseline glucose infusion rates) that were reached significantly earlier after injection of B28Asp (45 +/- 11 (SD) min) as compared to human insulin (58 +/- 25 min, p < 0.05). Glucose 143-150 insulin Homo sapiens 110-117 8365089-2 1993 Subcutaneous injection of 0.15 U kg-1 body weight (range 9.5-14.3 U) of the insulin analogue or soluble human insulin resulted in half-maximal glucose infusion rates (after subtraction of mean baseline glucose infusion rates) that were reached significantly earlier after injection of B28Asp (45 +/- 11 (SD) min) as compared to human insulin (58 +/- 25 min, p < 0.05). Glucose 143-150 insulin Homo sapiens 110-117 8365089-2 1993 Subcutaneous injection of 0.15 U kg-1 body weight (range 9.5-14.3 U) of the insulin analogue or soluble human insulin resulted in half-maximal glucose infusion rates (after subtraction of mean baseline glucose infusion rates) that were reached significantly earlier after injection of B28Asp (45 +/- 11 (SD) min) as compared to human insulin (58 +/- 25 min, p < 0.05). Glucose 202-209 insulin Homo sapiens 76-83 8365089-2 1993 Subcutaneous injection of 0.15 U kg-1 body weight (range 9.5-14.3 U) of the insulin analogue or soluble human insulin resulted in half-maximal glucose infusion rates (after subtraction of mean baseline glucose infusion rates) that were reached significantly earlier after injection of B28Asp (45 +/- 11 (SD) min) as compared to human insulin (58 +/- 25 min, p < 0.05). Glucose 202-209 insulin Homo sapiens 110-117 8365089-2 1993 Subcutaneous injection of 0.15 U kg-1 body weight (range 9.5-14.3 U) of the insulin analogue or soluble human insulin resulted in half-maximal glucose infusion rates (after subtraction of mean baseline glucose infusion rates) that were reached significantly earlier after injection of B28Asp (45 +/- 11 (SD) min) as compared to human insulin (58 +/- 25 min, p < 0.05). Glucose 202-209 insulin Homo sapiens 110-117 8365089-3 1993 Forty-five and 60 min after injection of human insulin, glucose infusion rates had increased by 3.4 +/- 1.8 and 4.8 +/- 2.3 mg min-1 kg-1 above baseline glucose infusion rates, reflecting 30 +/- 15 and 42 +/- 17% of maximal action of 10.6 +/- 2.7 mg min-1 kg-1. Glucose 56-63 insulin Homo sapiens 47-54 8365089-3 1993 Forty-five and 60 min after injection of human insulin, glucose infusion rates had increased by 3.4 +/- 1.8 and 4.8 +/- 2.3 mg min-1 kg-1 above baseline glucose infusion rates, reflecting 30 +/- 15 and 42 +/- 17% of maximal action of 10.6 +/- 2.7 mg min-1 kg-1. Glucose 153-160 insulin Homo sapiens 47-54 8513959-2 1993 DESIGN: Comparison of the GH response to L-dopa with or without pyridostigmine (inhibitor of acetylcholinesterase) pretreatment and insulin response to oral glucose tolerance test in patients with PCOS and matched controls. Glucose 157-164 insulin Homo sapiens 132-139 24202501-9 1993 Binding of insulin to carp hepatocytes resulted in a significant reduction of glucose release and a significant increase of protein synthesis as of de novo fatty acid synthesis. Glucose 78-85 insulin Homo sapiens 11-18 8406325-1 1993 Insulin is known to decrease plasma levels of both glucose and amino acids. Glucose 51-58 insulin Homo sapiens 0-7 8406325-2 1993 We have designed a study to examine whether in hyperthyroidism, where insulin sensitivity is changed, correlation between glucose disposal and amino acids levels is maintained. Glucose 122-129 insulin Homo sapiens 70-77 7686914-6 1993 During an oral glucose tolerance test, the mean glucose levels at 1 and 3 h as well as the mean insulin level at 3 h were significantly higher in the endometrial cancer patients than in the controls, and the area under the glucose curve was larger in the first group. Glucose 15-22 insulin Homo sapiens 96-103 7686918-9 1993 Glucose-stimulated insulin release was not inhibited. Glucose 0-7 insulin Homo sapiens 19-26 8325952-2 1993 Insulin-stimulated glucose uptake rate in peripheral tissue was decreased by 41% (P < 0.01) in NIDDM patients compared to healthy subjects, whereas no significant differences could be shown in the abundance of total GLUT4 protein per DNA or GLUT4 messenger RNA (mRNA) per DNA among the 2 groups in muscle biopsies obtained in the basal state. Glucose 19-26 insulin Homo sapiens 0-7 8325952-4 1993 The GLUT4 protein per DNA of muscle obtained in the basal state correlated positively with the in vivo insulin-stimulated glucose uptake rate in the control group (r = 0.82, P < 0.05), whereas there was no comparable correlation in the NIDDM group (r = 0.05, P = 0.88). Glucose 122-129 insulin Homo sapiens 103-110 8325952-8 1993 Factors other than total GLUT4 protein content of muscle play a role in determining insulin-stimulated glucose uptake in human skeletal muscle. Glucose 103-110 insulin Homo sapiens 84-91 8325954-1 1993 We have characterized the insulin-dependent increase in glucose transport in human adipocytes using subcellular fractionation and antibodies specific for the two isoforms of the glucose transporter that are expressed in these cells. Glucose 56-63 insulin Homo sapiens 26-33 8325954-6 1993 These data indicate that the insulin-mediated increases in glucose transport in human fat cells is a result of the translocation of vesicles uniquely containing the muscle-fat glucose transporter isoform. Glucose 59-66 insulin Homo sapiens 29-36 8325954-6 1993 These data indicate that the insulin-mediated increases in glucose transport in human fat cells is a result of the translocation of vesicles uniquely containing the muscle-fat glucose transporter isoform. Glucose 176-183 insulin Homo sapiens 29-36 8482816-0 1993 Endurance exercise training reduces glucose-stimulated insulin levels in 60- to 70-year-old men and women. Glucose 36-43 insulin Homo sapiens 55-62 8482816-4 1993 METHODS: We evaluated the effect of 9 mo of vigorous endurance exercise training (approximately 80% of maximal heart rate) on the glucose-stimulated insulin response and glucose disposal rate, using the hyperglycemic clamp procedure, in 12 people aged 65 +/- 1 yr (mean +/- SE) with normal glucose tolerance. Glucose 130-137 insulin Homo sapiens 149-156 8377410-8 1993 Only the functional insulin therapy allows the achievement of optimal blood glucose control in about 40% of patients without increased risk of hypoglycemia. Glucose 76-83 insulin Homo sapiens 20-27 7693380-1 1993 OBJECTIVE: We determined the relationship of short-term changes in circulating insulin concentrations, resulting from an oral glucose load, to those in both sex hormone binding globulin (SHBG) and insulin-like growth factor binding protein 1 (IGFBP-1) and assessed the effect of a short-term low calorie diet on the levels of SHBG and IGFBP-1 during an oral glucose tolerance test. Glucose 126-133 insulin Homo sapiens 79-86 7693380-1 1993 OBJECTIVE: We determined the relationship of short-term changes in circulating insulin concentrations, resulting from an oral glucose load, to those in both sex hormone binding globulin (SHBG) and insulin-like growth factor binding protein 1 (IGFBP-1) and assessed the effect of a short-term low calorie diet on the levels of SHBG and IGFBP-1 during an oral glucose tolerance test. Glucose 358-365 insulin Homo sapiens 79-86 8511023-5 1993 However, insulin responses to glucose fell significantly after 3 mo of glyburide (to 52 +/- 7 nmol/min/L, p < 0.05 versus pretreatment) and were normalized after 12 mo (42 +/- 7 nmol/min/L, p = NS versus controls). Glucose 30-37 insulin Homo sapiens 9-16 8344130-6 1993 Significant linear dose-response relationships were found between plasma insulin (log) and glucose, TKB (log), NEFA, and glycerol concentrations by analysis of variance applied to regression (all P < 0.001). Glucose 91-98 insulin Homo sapiens 73-80 8511023-6 1993 The rate of insulin-stimulated glucose metabolism during euglycemic insulin clamps (40 mU/m2/min) was low in the patients before treatment (163 +/- 10 versus 215 +/- 17 mg/m2/min in controls, p < 0.05) and increased to 205 +/- 30 mg/m2/min after 3 mo of glyburide. Glucose 31-38 insulin Homo sapiens 12-19 8511023-6 1993 The rate of insulin-stimulated glucose metabolism during euglycemic insulin clamps (40 mU/m2/min) was low in the patients before treatment (163 +/- 10 versus 215 +/- 17 mg/m2/min in controls, p < 0.05) and increased to 205 +/- 30 mg/m2/min after 3 mo of glyburide. Glucose 31-38 insulin Homo sapiens 68-75 8488854-12 1993 In the responders, fasting potassium levels at baseline were directly related to the decrease in BP (p < 0.01) and to the improvement of glucose-induced insulin response (p < 0.04) achieved after treatment. Glucose 140-147 insulin Homo sapiens 156-163 8488854-13 1993 Thus, the therapeutic effect of ACE inhibition is in part related to fractional potassium excretion, which, in turn, affects glucose tolerance through the influence of potassium levels on glucose-induced insulin release. Glucose 125-132 insulin Homo sapiens 204-211 8488854-13 1993 Thus, the therapeutic effect of ACE inhibition is in part related to fractional potassium excretion, which, in turn, affects glucose tolerance through the influence of potassium levels on glucose-induced insulin release. Glucose 188-195 insulin Homo sapiens 204-211 8476125-1 1993 Insulin- and contraction-stimulated skeletal muscle glucose transport is governed largely by the GLUT-4 isoform of the glucose transporter. Glucose 52-59 insulin Homo sapiens 0-7 8324268-4 1993 When the MRPT were perfused in a small chamber with buffer containing 3.3 mmol or 16.7 mmol glucose, insulin release from the MRPT began to increase at 9 +/- 3 min, reaching a plateau at approximately 40 min after the glucose concentration in the perfusate increased from 3.3 to 16.7 mmol. Glucose 92-99 insulin Homo sapiens 101-108 8324268-4 1993 When the MRPT were perfused in a small chamber with buffer containing 3.3 mmol or 16.7 mmol glucose, insulin release from the MRPT began to increase at 9 +/- 3 min, reaching a plateau at approximately 40 min after the glucose concentration in the perfusate increased from 3.3 to 16.7 mmol. Glucose 218-225 insulin Homo sapiens 101-108 8324268-5 1993 When MRPT seeded with islets were subjected to static incubation in buffer containing 3.3 mmol or 16.7 mmol glucose, insulin release from the MRPT remained elevated for 3 hr of high glucose stimulation, the amount of secreted insulin depending upon the number of islets seeded. Glucose 108-115 insulin Homo sapiens 117-124 8324268-5 1993 When MRPT seeded with islets were subjected to static incubation in buffer containing 3.3 mmol or 16.7 mmol glucose, insulin release from the MRPT remained elevated for 3 hr of high glucose stimulation, the amount of secreted insulin depending upon the number of islets seeded. Glucose 182-189 insulin Homo sapiens 117-124 8483904-0 1993 Glucose modulates the binding of an islet-specific factor to a conserved sequence within the rat I and the human insulin promoters. Glucose 0-7 insulin Homo sapiens 113-120 8483904-1 1993 In cultured rat and human pancreatic islets, glucose stimulated transcription of the rat insulin I gene through the mini-enhancer (FF) located between residues -196 and -247. Glucose 45-52 insulin Homo sapiens 89-96 8483904-8 1993 We therefore suggest that the factor(s) involved in the C1 complex corresponds to the glucose-sensitive factor and, consequently, may play a determining role in glucose-regulated expression of the insulin gene. Glucose 86-93 insulin Homo sapiens 197-204 8483904-8 1993 We therefore suggest that the factor(s) involved in the C1 complex corresponds to the glucose-sensitive factor and, consequently, may play a determining role in glucose-regulated expression of the insulin gene. Glucose 161-168 insulin Homo sapiens 197-204 8385716-1 1993 OBJECTIVE: To maximize deposition of an aerosolized dose of insulin (mean +/- SD = 0.99 +/- 0.06 U/kg of body weight) in the lungs of subjects with non-insulin-dependent diabetes mellitus (NIDDM), and investigate its efficacy in normalizing plasma glucose levels during the fasting state. Glucose 248-255 insulin Homo sapiens 60-67 8385716-17 1993 CONCLUSIONS: These preliminary results indicate that a dose of approximately 1.0 U of aerosolized insulin per kilogram of body weight, delivered by oral inhalation and deposited predominantly within the lungs, is well tolerated and can effectively normalize plasma glucose levels in patients with NIDDM. Glucose 265-272 insulin Homo sapiens 98-105 8386456-10 1993 Our results demonstrate that the inhibition of insulin-stimulated glucose transport by amylin is independent of cAMP and may be mediated by a unique receptor that is distinct from the adenylyl cyclase-coupled CGRP receptor. Glucose 66-73 insulin Homo sapiens 47-54 8482051-0 1993 Glucose-dependent uptake of chromium in human and rat insulin-sensitive tissues. Glucose 0-7 insulin Homo sapiens 54-61 8482051-4 1993 Evidence is provided that, in the rat in vitro, a clear difference exists in chromium binding between insulin-sensitive and -insensitive tissues in that chromium binding is significantly enhanced by glucose in insulin-sensitive tissues. Glucose 199-206 insulin Homo sapiens 102-109 8482051-4 1993 Evidence is provided that, in the rat in vitro, a clear difference exists in chromium binding between insulin-sensitive and -insensitive tissues in that chromium binding is significantly enhanced by glucose in insulin-sensitive tissues. Glucose 199-206 insulin Homo sapiens 210-217 8482051-8 1993 Addition of insulin slightly increased the response to glucose in muscle and reduced the response to glucose in adipose tissue; such effects were less marked than those seen in response to glucose alone. Glucose 55-62 insulin Homo sapiens 12-19 8482051-8 1993 Addition of insulin slightly increased the response to glucose in muscle and reduced the response to glucose in adipose tissue; such effects were less marked than those seen in response to glucose alone. Glucose 101-108 insulin Homo sapiens 12-19 8482051-8 1993 Addition of insulin slightly increased the response to glucose in muscle and reduced the response to glucose in adipose tissue; such effects were less marked than those seen in response to glucose alone. Glucose 101-108 insulin Homo sapiens 12-19 8462385-12 1993 Impaired glucose tolerance occurs when insulin resistance increases further. Glucose 9-16 insulin Homo sapiens 39-46 8462388-5 1993 RESULTS: Insulin concentration varied with age, sex, glucose concentration, and relative weight. Glucose 53-60 insulin Homo sapiens 9-16 8462388-7 1993 For each sex, the mean fasting insulin concentration, controlled for age, glucose, and relative weight, was significantly higher in the Pima Indians than in the Caucasians (P < 0.001). Glucose 74-81 insulin Homo sapiens 31-38 8102540-0 1993 Interferon-alpha in the treatment of neuroendocrine tumours: effect on glucose tolerance and glucose-stimulated insulin secretion. Glucose 93-100 insulin Homo sapiens 112-119 8477882-3 1993 Insulin response to glucose and forskolin was completely absent in diabetic islets, as compared to control islets. Glucose 20-27 insulin Homo sapiens 0-7 8462385-8 1993 RESULTS: High baseline fasting insulin predicted impaired glucose tolerance regardless of weight after adjustment for age, sex, body mass index, and glucose. Glucose 58-65 insulin Homo sapiens 31-38 7903182-0 1993 Effects of acute exercise on insulin and non-insulin-dependent glucose uptake in normal and moderately obese women. Glucose 63-70 insulin Homo sapiens 45-52 8500514-9 1993 However, reduced insulin-action (insulin resistance) was closely related to abdominal fatness determined by WHR both in relation to the insulin-effect on mLPL as well as for the insulin-effect on whole-body glucose metabolism (clamp-study). Glucose 207-214 insulin Homo sapiens 17-24 8491223-8 1993 Increases in MRGlc following glucose loading were correlated with plasma glucose, insulin and free fatty acid concentrations, ratios of insulin to glucagon levels, and influx rate constants of FDG. Glucose 29-36 insulin Homo sapiens 82-89 8491223-8 1993 Increases in MRGlc following glucose loading were correlated with plasma glucose, insulin and free fatty acid concentrations, ratios of insulin to glucagon levels, and influx rate constants of FDG. Glucose 29-36 insulin Homo sapiens 136-143 8458499-4 1993 RESULTS: The three indexes measuring the insulin-induced glucose disposal during the clamp (glucose infusion rate, glucose metabolic clearance rate, and glucose infusion rate divided by plasma insulin plateau levels) were not significantly affected by Diane-35. Glucose 57-64 insulin Homo sapiens 41-48 8500514-9 1993 However, reduced insulin-action (insulin resistance) was closely related to abdominal fatness determined by WHR both in relation to the insulin-effect on mLPL as well as for the insulin-effect on whole-body glucose metabolism (clamp-study). Glucose 207-214 insulin Homo sapiens 33-40 8500514-9 1993 However, reduced insulin-action (insulin resistance) was closely related to abdominal fatness determined by WHR both in relation to the insulin-effect on mLPL as well as for the insulin-effect on whole-body glucose metabolism (clamp-study). Glucose 207-214 insulin Homo sapiens 33-40 8500514-9 1993 However, reduced insulin-action (insulin resistance) was closely related to abdominal fatness determined by WHR both in relation to the insulin-effect on mLPL as well as for the insulin-effect on whole-body glucose metabolism (clamp-study). Glucose 207-214 insulin Homo sapiens 33-40 8514239-4 1993 Basal and glucose-stimulated insulin secretion of embedded islets decreased slightly, but significantly after the first week (from 4.39 +/- 0.64 to 2.87 +/- 0.47 at normal and from 11.96 +/- 1.44 to 4.76 +/- 0.78 microU pro 24 h pro islet at elevated glucose concentration, p < 0.05 and < 0.01, resp.) and remained unchanged thereafter. Glucose 10-17 insulin Homo sapiens 29-36 8514239-4 1993 Basal and glucose-stimulated insulin secretion of embedded islets decreased slightly, but significantly after the first week (from 4.39 +/- 0.64 to 2.87 +/- 0.47 at normal and from 11.96 +/- 1.44 to 4.76 +/- 0.78 microU pro 24 h pro islet at elevated glucose concentration, p < 0.05 and < 0.01, resp.) and remained unchanged thereafter. Glucose 251-258 insulin Homo sapiens 29-36 8514239-5 1993 Glucose-stimulation resulted in significant increases in insulin secretion at all three testings (p < 0.001, < 0.01 and < 0.01). Glucose 0-7 insulin Homo sapiens 57-64 8473405-1 1993 Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1-(7-36) amide (GLP-1) are glucose-dependent insulinotropic gut hormones that may explain the greater insulin secretory response with oral compared to i.v. Glucose 90-97 insulin Homo sapiens 108-115 8270561-1 1993 As anti-inflammatory drugs such as acetylsalicylic acid are known to partially restore insulin response to glucose, the possible beneficial effect of colchicine, an anti-gout and anti-inflammatory drug, in non-insulin dependent diabetes mellitus (NIDDM) was studied. Glucose 107-114 insulin Homo sapiens 87-94 8473402-8 1993 The number of insulin pulses during saline and glucose infusions corresponded to a mean periodicity of 10 min. Glucose 47-54 insulin Homo sapiens 14-21 8473402-9 1993 The amplitude of these rapid insulin pulses increased from 17.3 +/- 2.9 to 39.8 +/- 11.8 pmol/L (P < 0.01) in response to glucose. Glucose 125-132 insulin Homo sapiens 29-36 8326279-13 1993 Diabetes was more prevalent in Asian men (10.9% v 4.4% p < 0.05), who also showed higher serum insulin concentrations after glucose loading (22.3 mU/l v 10.2 mU/l, p < 0.0001). Glucose 127-134 insulin Homo sapiens 98-105 8473402-10 1993 In contrast to the ultradian oscillations, the relative amplitude of the rapid insulin pulses decreased significantly from 28.8 +/- 3.4% during saline infusion to 13.6 +/- 1.6% during high dose glucose infusion (P < 0.01). Glucose 194-201 insulin Homo sapiens 79-86 8518455-2 1993 The role of glucose transport in insulin resistance and non-insulin-dependent diabetes mellitus (NIDDM) is discussed. Glucose 12-19 insulin Homo sapiens 33-40 8518452-5 1993 Findings in these studies suggest that the use of such analogues may provide meal-related insulin effects closer to those observed in the physiologic state by limiting excessive postprandial glucose excursions and decreasing the risk of late hypoglycemia. Glucose 191-198 insulin Homo sapiens 90-97 8518461-7 1993 The regulation of glucose transport is a primary feature of the physiologic role of insulin and is performed by a family of glucose-transporter proteins with different characteristics. Glucose 18-25 insulin Homo sapiens 84-91 8518453-6 1993 A potential therapeutic role of proinsulin in NIDDM thus has been envisioned, in that suppression of hepatic glucose output might reduce the risk of hypoglycemia caused by increased peripheral glucose uptake. Glucose 109-116 insulin Homo sapiens 32-42 8518455-0 1993 The molecular biology of glucose transport: relevance to insulin resistance and non-insulin-dependent diabetes mellitus. Glucose 25-32 insulin Homo sapiens 57-64 8518461-8 1993 One mechanism by which insulin exerts its effect on glucose transport is the stimulation of the translocation of the glucose transporter to the plasma membrane. Glucose 52-59 insulin Homo sapiens 23-30 8390516-12 1993 Microalbuminuria was significantly related to body mass index and waist:hip ratio, age and plasma insulin during oral glucose tolerance testing. Glucose 118-125 insulin Homo sapiens 98-105 8390510-4 1993 RESULTS: Insulin-induced glucose uptake was significantly impaired in subjects with positive compared with in subjects with negative family history of essential hypertension. Glucose 25-32 insulin Homo sapiens 9-16 8466262-6 1993 In children and AGA neonates, plasma immunoreactive insulin concentration was positively related to blood glucose concentration. Glucose 106-113 insulin Homo sapiens 52-59 8487675-6 1993 Postprandial forearm glucose uptake followed very closely the plasma (free) insulin concentration. Glucose 21-28 insulin Homo sapiens 76-83 8328221-6 1993 Exogenous treatment with insulin increased plasma levels of insulin (53 v 36 mU/l, P < 0.001) and decreased plasma levels of glucose (4.6 v 5.5 mmol/l, P < 0.001) in T-sows as compared to C-sows. Glucose 128-135 insulin Homo sapiens 25-32 8447358-3 1993 Studies that use curve analysis of glucose tolerance tests have demonstrated insulin resistance, rises in plasma insulin, and relative glucose intolerance in women using oral contraceptives. Glucose 35-42 insulin Homo sapiens 77-84 8447358-3 1993 Studies that use curve analysis of glucose tolerance tests have demonstrated insulin resistance, rises in plasma insulin, and relative glucose intolerance in women using oral contraceptives. Glucose 35-42 insulin Homo sapiens 113-120 8478967-0 1993 Plasma glucose and insulin responses to oral glucose loading in nonobese Nigerian subjects with essential hypertension. Glucose 45-52 insulin Homo sapiens 19-26 8478967-4 1993 These parameters suggest some impairment of glucose tolerance in the hypertensive subjects related to an inadequate insulin response to the oral glucose load. Glucose 44-51 insulin Homo sapiens 116-123 8478967-5 1993 Model analysis of the glucose and insulin data confirmed these observations in that the estimated rate of glucose uptake into peripheral tissues (M value) was lower in the hypertensive subjects (P = .02). Glucose 106-113 insulin Homo sapiens 34-41 8478967-7 1993 These results suggest that essential hypertension in Nigerian diabetic subjects is associated with a reduced insulin response to glucose loading, which is at variance with reports in whites, and deserve further investigation. Glucose 129-136 insulin Homo sapiens 109-116 8455819-4 1993 Filling the storage space from plasma glucose and triglyceride is insulin dependent. Glucose 38-45 insulin Homo sapiens 66-73 8480468-2 1993 Compared to control subjects, initial insulin and C-peptide responses to oral glucose were lower in all patient groups, and decreased with decreasing glucose tolerance. Glucose 78-85 insulin Homo sapiens 38-45 8480468-2 1993 Compared to control subjects, initial insulin and C-peptide responses to oral glucose were lower in all patient groups, and decreased with decreasing glucose tolerance. Glucose 78-85 insulin Homo sapiens 50-59 8480468-4 1993 The 6 min post-glucagon C-peptide concentration was positively correlated with the initial insulin response to oral glucose. Glucose 116-123 insulin Homo sapiens 24-33 8480468-4 1993 The 6 min post-glucagon C-peptide concentration was positively correlated with the initial insulin response to oral glucose. Glucose 116-123 insulin Homo sapiens 91-98 8480475-6 1993 Insulin-stimulated (2 mU.kg-1 x min-1) glucose disposal rate tended to be increased (18%, p = 0.10) after dexfenfluramine. Glucose 39-46 insulin Homo sapiens 0-7 8443140-3 1993 The results indicated that patients with either type IIB or IV HLP had higher plasma glucose (p < 0.05-< 0.001) and insulin (p < 0.001) responses to both oral glucose and mixed meals compared with the normal subjects and patients with type IIA HLP. Glucose 168-175 insulin Homo sapiens 122-129 8443140-4 1993 Steady-state plasma glucose concentrations (mmol/L) were also higher (p < 0.001) in patients with types IIB (13.3 +/- 0.6) and IV (12.8 +/- 1.2) HLP during a continuous infusion of somatostatin, glucose, and insulin than either the control group (volunteer subjects) (6.2 +/- 0.9) or patients with type IIA HLP (5.6 +/- 1.0). Glucose 20-27 insulin Homo sapiens 211-218 8443140-5 1993 Because the steady-state plasma insulin concentrations were similar in all four groups, patients with either type IIB or IV HLP were resistant to insulin-mediated glucose uptake. Glucose 163-170 insulin Homo sapiens 146-153 8193731-1 1993 Obesity and an enhanced insulin response to oral glucose tolerance test are associated with therapy resistance in hypertension. Glucose 49-56 insulin Homo sapiens 24-31 8466263-9 1993 A negative relationship existed between plasma glucagon and blood glucose concentrations, but there was a wide variation in plasma insulin levels at all blood glucose concentrations. Glucose 159-166 insulin Homo sapiens 131-138 8485464-3 1993 It is proposed, therefore, that a preferential stimulation by D-glucose of oxidative relative to total glycolysis represents an intrinsic attribute of insulin-producing cells, as distinct from other endocrine islet cells. Glucose 62-71 insulin Homo sapiens 151-158 8432411-4 1993 We found an inverse correlation between BMI and the glucose infusion rate necessary to maintain euglycemia during the first two of three insulin infusions (r = -0.63, P < 0.001, r = -0.57, P < 0.01, and r = -0.36, P = 0.08). Glucose 52-59 insulin Homo sapiens 137-144 8432411-2 1993 We examined the impact of obesity on insulin-mediated glucose metabolism in 25 patients with NIDDM, whose BMI ranged from 20.8 to 36.9 kg/m2, during insulin infusions of 0.4, 1.0, and 10 microU/kg min using the glucose clamp technique. Glucose 54-61 insulin Homo sapiens 37-44 8339856-4 1993 After a continuous insulin infusion of 40, 100, and 350 mU/m2/min we estimated the tissue sensitivity to insulin by the determination of Km, the glucose disposal (M), and the amount of glucose metabolized per U insulin (M/I ratio). Glucose 145-152 insulin Homo sapiens 105-112 8339856-4 1993 After a continuous insulin infusion of 40, 100, and 350 mU/m2/min we estimated the tissue sensitivity to insulin by the determination of Km, the glucose disposal (M), and the amount of glucose metabolized per U insulin (M/I ratio). Glucose 145-152 insulin Homo sapiens 105-112 8339856-4 1993 After a continuous insulin infusion of 40, 100, and 350 mU/m2/min we estimated the tissue sensitivity to insulin by the determination of Km, the glucose disposal (M), and the amount of glucose metabolized per U insulin (M/I ratio). Glucose 185-192 insulin Homo sapiens 105-112 8339856-4 1993 After a continuous insulin infusion of 40, 100, and 350 mU/m2/min we estimated the tissue sensitivity to insulin by the determination of Km, the glucose disposal (M), and the amount of glucose metabolized per U insulin (M/I ratio). Glucose 185-192 insulin Homo sapiens 105-112 8432411-5 1993 Glucose disposal was correlated with BMI during the 1.0 mU/kg min insulin infusion (r = -0.57, P < 0.05), and glucose production was correlated at the 0.4 mU/kg min infusion (r = 0.69, P < 0.01). Glucose 0-7 insulin Homo sapiens 66-73 8432415-5 1993 Insulin sensitivity was determined by measuring glucose disposal with the euglycemic insulin clamp technique with a 1 mU.kg-1.min-1 insulin infusion. Glucose 48-55 insulin Homo sapiens 0-7 8097483-1 1993 Insulin, proinsulin and C-peptide responses to intravenous glucose (glucose infusion test, GIT) and insulin sensitivity were measured in women who previously and for unexplained reasons gave birth to small-for-gestational-age infants (SGA, n = 10) or appropriate-for-gestational-age infants (AGA, n = 11). Glucose 59-66 insulin Homo sapiens 24-33 8458461-7 1993 Insulin resistance was assessed by measuring fasting glucose, fasting insulin, and nadir glucose after a 0.1 U/kg i.v. Glucose 53-60 insulin Homo sapiens 0-7 8458461-7 1993 Insulin resistance was assessed by measuring fasting glucose, fasting insulin, and nadir glucose after a 0.1 U/kg i.v. Glucose 89-96 insulin Homo sapiens 0-7 8477950-3 1993 In the presence of 16.7 mM D-glucose, however, epinephrine lowered both 86Rb and 45Ca outflow, this coinciding with suppression of insulin release. Glucose 27-36 insulin Homo sapiens 131-138 8097483-1 1993 Insulin, proinsulin and C-peptide responses to intravenous glucose (glucose infusion test, GIT) and insulin sensitivity were measured in women who previously and for unexplained reasons gave birth to small-for-gestational-age infants (SGA, n = 10) or appropriate-for-gestational-age infants (AGA, n = 11). Glucose 68-75 insulin Homo sapiens 24-33 8097483-2 1993 Insulin sensitivity was evaluated by two different methods, somatostatin-, insulin- and glucose infusion test (SIGIT) and Bergman"s minimal model method applied to the frequently samples intravenous glucose tolerance test. Glucose 88-95 insulin Homo sapiens 0-7 8478036-2 1993 Recently, a hyperinsulinemic response to an oral glucose load has been found in salt-sensitive normotensive subjects, suggesting that insulin resistance may be present in these hypertension-prone individuals before the development of hypertension. Glucose 49-56 insulin Homo sapiens 17-24 8097483-2 1993 Insulin sensitivity was evaluated by two different methods, somatostatin-, insulin- and glucose infusion test (SIGIT) and Bergman"s minimal model method applied to the frequently samples intravenous glucose tolerance test. Glucose 199-206 insulin Homo sapiens 0-7 8478036-4 1993 Insulin sensitivity was estimated by the "insulin suppression test," i.e., by measuring the plasma glucose and insulin concentrations achieved during a 180-minute infusion of somatostatin, insulin, and glucose in 18 healthy male volunteers (age, 21-28 years) given a standardized low salt diet (20 mmol/day) for 2 weeks, supplemented by either 220 mmol of NaCl per day or placebo in a single-blind randomized order for 1 week each. Glucose 99-106 insulin Homo sapiens 0-7 8478036-4 1993 Insulin sensitivity was estimated by the "insulin suppression test," i.e., by measuring the plasma glucose and insulin concentrations achieved during a 180-minute infusion of somatostatin, insulin, and glucose in 18 healthy male volunteers (age, 21-28 years) given a standardized low salt diet (20 mmol/day) for 2 weeks, supplemented by either 220 mmol of NaCl per day or placebo in a single-blind randomized order for 1 week each. Glucose 99-106 insulin Homo sapiens 42-49 8450036-4 1993 After 75 g of oral glucose, plasma glucose levels were higher in cirrhotics than controls, the curves diverging for 80 min despite markedly higher insulin levels in cirrhotics. Glucose 19-26 insulin Homo sapiens 147-154 8478036-4 1993 Insulin sensitivity was estimated by the "insulin suppression test," i.e., by measuring the plasma glucose and insulin concentrations achieved during a 180-minute infusion of somatostatin, insulin, and glucose in 18 healthy male volunteers (age, 21-28 years) given a standardized low salt diet (20 mmol/day) for 2 weeks, supplemented by either 220 mmol of NaCl per day or placebo in a single-blind randomized order for 1 week each. Glucose 202-209 insulin Homo sapiens 0-7 8450036-7 1993 Glucose metabolic clearance rate rose more slowly in cirrhotics and was significantly lower than in controls during the first 2 h after glucose ingestion (2.24 +/- 0.17 vs 3.30 +/- 0.23 ml/kg per min, P < 0.005), in keeping with their known insulin insensitivity. Glucose 136-143 insulin Homo sapiens 244-251 8450036-14 1993 Our results suggest that the higher glucose levels seen in cirrhotics after oral glucose are due initially to an increase in the amount of ingested glucose appearing in the systemic circulation, and subsequently to an impairment in glucose uptake by tissues due to insulin insensitivity. Glucose 36-43 insulin Homo sapiens 265-272 8450036-14 1993 Our results suggest that the higher glucose levels seen in cirrhotics after oral glucose are due initially to an increase in the amount of ingested glucose appearing in the systemic circulation, and subsequently to an impairment in glucose uptake by tissues due to insulin insensitivity. Glucose 81-88 insulin Homo sapiens 265-272 8450036-14 1993 Our results suggest that the higher glucose levels seen in cirrhotics after oral glucose are due initially to an increase in the amount of ingested glucose appearing in the systemic circulation, and subsequently to an impairment in glucose uptake by tissues due to insulin insensitivity. Glucose 81-88 insulin Homo sapiens 265-272 8450036-14 1993 Our results suggest that the higher glucose levels seen in cirrhotics after oral glucose are due initially to an increase in the amount of ingested glucose appearing in the systemic circulation, and subsequently to an impairment in glucose uptake by tissues due to insulin insensitivity. Glucose 81-88 insulin Homo sapiens 265-272 7682592-1 1993 We have examined the biological effects of insulin-like growth factor-binding proteins (IGFBPs) on insulin-like growth factor (IGF)-activated glucose consumption in a BALB/c 3T3 subline. Glucose 142-149 insulin Homo sapiens 43-50 7682592-1 1993 We have examined the biological effects of insulin-like growth factor-binding proteins (IGFBPs) on insulin-like growth factor (IGF)-activated glucose consumption in a BALB/c 3T3 subline. Glucose 142-149 insulin Homo sapiens 99-106 8487645-2 1993 The night before the study, diabetic patients received variable-rate intravenous insulin in an attempt to normalize fasting plasma glucose concentrations. Glucose 131-138 insulin Homo sapiens 81-88 8445035-1 1993 Emergency therapy of sulfonylurea overdoses with glucose is often unsatisfactory because glucose stimulates insulin release and initiates a need for escalating quantities of hypertonic glucose to maintain normoglycemia. Glucose 89-96 insulin Homo sapiens 108-115 8445035-6 1993 Insulin concentrations were 4-5 times greater with dextrose alone or in combination with diazoxide than with octreotide (P < 0.01). Glucose 51-59 insulin Homo sapiens 0-7 8487654-0 1993 Effect of heparin on insulin-glucose interactions measured by the minimal model technique: implications for reproducibility using this method. Glucose 29-36 insulin Homo sapiens 21-28 8487654-1 1993 The minimal model technique permits investigation of glucose and insulin interactions during a frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 126-133 insulin Homo sapiens 65-72 8487660-9 1993 Hyperglycemia for 44 hours induced insulin resistance (32% reduction of glucose infusion rate, P < .02). Glucose 72-79 insulin Homo sapiens 35-42 8487660-10 1993 In the control study, a 21% reduction (P = .064, NS) of the glucose disposal rate (Rd) was seen, suggesting that the hospitalization period per se may also reduce insulin sensitivity. Glucose 60-67 insulin Homo sapiens 163-170 8383325-11 1993 These results indicate that nitric oxide mediates the inhibitory effects of cytokines on glucose-stimulated insulin secretion by human islets and suggest that nitric oxide may participate in beta-cell dysfunction associated with insulin-dependent diabetes mellitus. Glucose 89-96 insulin Homo sapiens 108-115 8446591-5 1993 Cells expressing glucose transporter 1 do not differ significantly from control cells, but in cells expressing hexokinase I, insulin promoter activity increases, reaches a maximum by 1 mM glucose, and does not respond to changes in glucose concentration within the physiologic range. Glucose 17-24 insulin Homo sapiens 125-132 8446591-5 1993 Cells expressing glucose transporter 1 do not differ significantly from control cells, but in cells expressing hexokinase I, insulin promoter activity increases, reaches a maximum by 1 mM glucose, and does not respond to changes in glucose concentration within the physiologic range. Glucose 188-195 insulin Homo sapiens 125-132 8354090-10 1993 The results showed that serum insulin release levels after a glucose load in late pregnancy were more active than those in the non-pregnant state. Glucose 61-68 insulin Homo sapiens 30-37 8441528-5 1993 The negative correlation between glucose- and insulin-responses to glucose challenge may suggest the presence of insulin resistance. Glucose 33-40 insulin Homo sapiens 113-120 8441528-5 1993 The negative correlation between glucose- and insulin-responses to glucose challenge may suggest the presence of insulin resistance. Glucose 67-74 insulin Homo sapiens 46-53 8441528-5 1993 The negative correlation between glucose- and insulin-responses to glucose challenge may suggest the presence of insulin resistance. Glucose 67-74 insulin Homo sapiens 113-120 8427537-5 1993 In multivariate regression analyses, fasting insulin remained independently associated with blood pressure levels after controlling for glucose levels, body mass index (weight/height) and skinfold thickness in children (aged 5 to 12 years) and young adults (aged 18 to 26 years), although not in adolescents (aged 13 to 17 years). Glucose 136-143 insulin Homo sapiens 45-52 7679106-0 1993 Dissociation of pp70 ribosomal protein S6 kinase from insulin-stimulated glucose transport in 3T3-L1 adipocytes. Glucose 73-80 insulin Homo sapiens 54-61 8432232-5 1993 Oral glucose loading with 100 g increased the insulin and C-peptide swings, but not their periodicity. Glucose 5-12 insulin Homo sapiens 46-53 8432232-5 1993 Oral glucose loading with 100 g increased the insulin and C-peptide swings, but not their periodicity. Glucose 5-12 insulin Homo sapiens 58-67 8453648-1 1993 The objective of the work was to test the minimal model method based on computer evaluation of parameters (blood sugar level, insulin blood level) obtained during the intravenous glucose tolerance test with frequent collection of samples, when examining the insulin glucose homeostasis in patients in the initial stage of type II diabetes. Glucose 179-186 insulin Homo sapiens 258-265 8453648-1 1993 The objective of the work was to test the minimal model method based on computer evaluation of parameters (blood sugar level, insulin blood level) obtained during the intravenous glucose tolerance test with frequent collection of samples, when examining the insulin glucose homeostasis in patients in the initial stage of type II diabetes. Glucose 266-273 insulin Homo sapiens 126-133 8453648-1 1993 The objective of the work was to test the minimal model method based on computer evaluation of parameters (blood sugar level, insulin blood level) obtained during the intravenous glucose tolerance test with frequent collection of samples, when examining the insulin glucose homeostasis in patients in the initial stage of type II diabetes. Glucose 266-273 insulin Homo sapiens 258-265 8424516-3 1993 Plasma glucose, insulin activity, pyruvate and alanine concentrations in the glucose-receiving group increased significantly during the operation in comparison with the control group. Glucose 77-84 insulin Homo sapiens 16-23 8424516-5 1993 These results suggest that administration of glucose stimulated insulin secretion and resulted in accumulation of the substrates such as pyruvate and alanine which were utilized readily in the body. Glucose 45-52 insulin Homo sapiens 64-71 8427437-5 1993 Inability to maintain euglycemia following glucose administration suggests excessive insulin and requires further workup. Glucose 43-50 insulin Homo sapiens 85-92 8447379-2 1993 Whereas insulin is the dominant glucose-lowering factor, there are redundant glucose counterregulatory factors. Glucose 32-39 insulin Homo sapiens 8-15 8447379-4 1993 The first defense against a decrement in plasma glucose is decreased insulin secretion; this occurs with glucose decrements within the physiological range at a glycemic threshold of 4.6 +/- 0.2 mmol/l. Glucose 48-55 insulin Homo sapiens 69-76 8447379-4 1993 The first defense against a decrement in plasma glucose is decreased insulin secretion; this occurs with glucose decrements within the physiological range at a glycemic threshold of 4.6 +/- 0.2 mmol/l. Glucose 105-112 insulin Homo sapiens 69-76 8447386-3 1993 Insulin-stimulated glucose transport and GLUT-4 abundance were measured in abdominal adipocytes from obese (n = 9) and lean (n = 7) PCOS as well as obese (n = 8) and lean (n = 8) control women matched for age and weight. Glucose 19-26 insulin Homo sapiens 0-7 8447386-5 1993 The maximal insulin-stimulated increment in adipocyte glucose transport was independently decreased by obesity and by PCOS. Glucose 54-61 insulin Homo sapiens 12-19 8447386-8 1993 There was a highly significant correlation (R = 0.66, P < = 0.001) between GLUT-4 content and insulin-stimulated glucose transport in adipocytes from individual women across the study population. Glucose 116-123 insulin Homo sapiens 97-104 8095007-0 1993 Non-insulin-mediated glucose uptake in human immunodeficiency virus-infected men. Glucose 21-28 insulin Homo sapiens 4-11 8095007-2 1993 One of the metabolic features of acquired immunodeficiency syndrome is increased tissue glucose uptake documented by euglycaemic-hyperinsulinaemic clamp studies, suggesting increased insulin sensitivity. Glucose 88-95 insulin Homo sapiens 134-141 8095007-3 1993 However, these results may also be related to the confounding effect of increased non-insulin-mediated glucose uptake in acquired immunodeficiency syndrome, which will result in an erroneously presumed increased insulin sensitivity. Glucose 103-110 insulin Homo sapiens 86-93 8095007-3 1993 However, these results may also be related to the confounding effect of increased non-insulin-mediated glucose uptake in acquired immunodeficiency syndrome, which will result in an erroneously presumed increased insulin sensitivity. Glucose 103-110 insulin Homo sapiens 212-219 8095007-4 1993 To study the contribution of non-insulin-mediated glucose uptake to total tissue glucose uptake in acquired immunodeficiency syndrome, we conducted a hypoinsulinaemic clamp study in clinically stable human immunodeficiency virus-infected (Centers for Disease Control class IV) men (n = 7) and healthy subjects (n = 5). Glucose 50-57 insulin Homo sapiens 33-40 8095007-9 1993 Euglycaemic glucose uptake during somatostatin infusion, reflecting non-insulin-mediated glucose uptake, decreased to 82 +/- 3% in patients and 78 +/- 2% in control subjects (not significant). Glucose 89-96 insulin Homo sapiens 72-79 8425661-3 1993 The protocol has been modified by the addition of a bolus tolbutamide or insulin injection 20 min after glucose. Glucose 104-111 insulin Homo sapiens 73-80 8432213-3 1993 RESEARCH DESIGN AND METHODS: Insulin action was measured with the euglycemic insulin clamp with a 1 mU.kg-1.min-1 insulin infusion with [3-3H]glucose. Glucose 142-149 insulin Homo sapiens 29-36 8432213-3 1993 RESEARCH DESIGN AND METHODS: Insulin action was measured with the euglycemic insulin clamp with a 1 mU.kg-1.min-1 insulin infusion with [3-3H]glucose. Glucose 142-149 insulin Homo sapiens 114-121 8432213-4 1993 A glucose disposal of < 278 mumol.kg-1.min-1 was considered insulin resistant, and a value greater than this was considered insulin sensitive. Glucose 2-9 insulin Homo sapiens 63-70 8458523-0 1993 Contribution of glucose/glucose 6-phosphate cycle activity to insulin resistance in type 2 (non-insulin-dependent) diabetes mellitus. Glucose 16-23 insulin Homo sapiens 62-69 8458523-4 1993 Endogenous glucose production ([6-3H]glucose) was greater in diabetic than control subjects in the post-absorptive state (15.6 +/- 1.5 vs 11.3 +/- 0.4 mumol.kg-1 x min-1, p < 0.05) and during the 0.4 mU insulin infusion (10.1 +/- 1.3 vs 5.2 +/- 0.3 mumol.kg-1 x min-1, p < 0.01) indicating hepatic insulin resistance. Glucose 11-18 insulin Homo sapiens 206-213 8458523-5 1993 Glucose/glucose 6-phosphate cycling was significantly greater in diabetic than in control subjects in the post-absorptive state (2.6 +/- 0.4 vs 1.6 +/- 0.2 mumol.kg-1 x min-1, p < 0.05) but not during the 0.4 mU insulin infusion (2.0 +/- 0.4 vs 2.0 +/- 0.3 mumol.kg-1 x min-1). Glucose 0-7 insulin Homo sapiens 215-222 8458526-1 1993 In cirrhotic patients with normal fasting glucose levels both insulin insensitivity and a blunted early insulin response to oral glucose are important determinants of the degree of intolerance to oral glucose. Glucose 42-49 insulin Homo sapiens 62-69 8458526-1 1993 In cirrhotic patients with normal fasting glucose levels both insulin insensitivity and a blunted early insulin response to oral glucose are important determinants of the degree of intolerance to oral glucose. Glucose 129-136 insulin Homo sapiens 104-111 8458526-1 1993 In cirrhotic patients with normal fasting glucose levels both insulin insensitivity and a blunted early insulin response to oral glucose are important determinants of the degree of intolerance to oral glucose. Glucose 129-136 insulin Homo sapiens 104-111 8472625-8 1993 Hepatic glucose production was suppressed similarly following proinsulin and insulin zinc injection. Glucose 8-15 insulin Homo sapiens 62-72 8472625-8 1993 Hepatic glucose production was suppressed similarly following proinsulin and insulin zinc injection. Glucose 8-15 insulin Homo sapiens 65-72 8472625-9 1993 However, both proinsulin and insulin zinc had a significantly greater effect on suppression of hepatic glucose production compared to control (P = 0.01, P = 0.009, respectively). Glucose 103-110 insulin Homo sapiens 14-24 8472625-9 1993 However, both proinsulin and insulin zinc had a significantly greater effect on suppression of hepatic glucose production compared to control (P = 0.01, P = 0.009, respectively). Glucose 103-110 insulin Homo sapiens 17-24 8472625-13 1993 The conclusions were: (1) In overnight fasted hyperglycemic non-insulin-dependent subjects s.c. injections of proinsulin and insulin zinc can produce similar effects on glucose turnover, intermediary lipid and carbohydrate metabolism. Glucose 169-176 insulin Homo sapiens 110-120 8472625-13 1993 The conclusions were: (1) In overnight fasted hyperglycemic non-insulin-dependent subjects s.c. injections of proinsulin and insulin zinc can produce similar effects on glucose turnover, intermediary lipid and carbohydrate metabolism. Glucose 169-176 insulin Homo sapiens 113-120 8472630-7 1993 In case of hyperglycemia occurring in 12 of 15 patients due to the administration of steroid, insulin was used to normalize blood glucose levels (average 0.47 +/- 0.21 IU/kg/day). Glucose 130-137 insulin Homo sapiens 94-101 8454171-0 1993 Biological activity of alligator, avian, and mammalian insulin in juvenile alligators: plasma glucose and amino acids. Glucose 94-101 insulin Homo sapiens 55-62 8454171-8 1993 The decline in plasma amino acids was much more rapid than the decline in plasma glucose in response to insulin. Glucose 81-88 insulin Homo sapiens 104-111 8384175-2 1993 Glucose-Induced-Thermogenesis (GIT) was shown to be diminished in 55 obese patients particularly in the presence of insulin resistance (r = 0.44 p < 0.001) and in obese diabetic patients (3.7 +/- 0.7% vs 8.6 +/- 0.9% p < 0.001). Glucose 0-7 insulin Homo sapiens 116-123 8384179-3 1993 The combination also had pronounced effects on glucose metabolism by increasing plasma glucose, insulin and C-peptide concentrations. Glucose 47-54 insulin Homo sapiens 96-103 8384179-3 1993 The combination also had pronounced effects on glucose metabolism by increasing plasma glucose, insulin and C-peptide concentrations. Glucose 47-54 insulin Homo sapiens 108-117 8428775-9 1993 Rates of insulin-mediated glucose uptake were inversely correlated with the baseline mean arterial pressure (r = -0.62, p < 0.01). Glucose 26-33 insulin Homo sapiens 9-16 8428775-11 1993 Mean arterial pressure and insulin-mediated glucose uptake were not correlated with either age or body fat content. Glucose 44-51 insulin Homo sapiens 27-34 8432782-4 1993 After 48 h of culture in the presence of rIL-1 beta, the human islets showed an increased insulin release during short term incubations in the presence of 1.7 or 16.7 mM glucose. Glucose 170-177 insulin Homo sapiens 90-97 8432782-8 1993 Rat islets exposed for 48 h in culture to the same concentrations of rIL-1 beta, however, showed a 40-60% decrease in insulin accumulation into the medium, glucose-induced insulin release, and glucose oxidation. Glucose 156-163 insulin Homo sapiens 172-179 8432792-3 1993 Insulin sensitivity and glucose effectiveness were derived using insulin and glucose levels obtained from tolbutamide-modified iv glucose tolerance tests and analyzed with the minimal model computer program. Glucose 77-84 insulin Homo sapiens 0-7 8432792-3 1993 Insulin sensitivity and glucose effectiveness were derived using insulin and glucose levels obtained from tolbutamide-modified iv glucose tolerance tests and analyzed with the minimal model computer program. Glucose 77-84 insulin Homo sapiens 0-7 8450519-2 1993 In 40 hypertensive patients studied by oral glucose tolerance test (standard OGTT) 23 presented with pathological blood glucose and plasma insulin values. Glucose 44-51 insulin Homo sapiens 139-146 8474314-4 1993 ST also decreased insulin levels during fasting (P < .05) and at 90 and 120 minutes (P < .01) after glucose ingestion. Glucose 106-113 insulin Homo sapiens 18-25 8474314-5 1993 AT decreased insulin levels at 90 and 120 minutes (P < .01) after glucose ingestion. Glucose 69-76 insulin Homo sapiens 13-20 8446221-1 1993 In NIDDM, first-phase insulin release to glucose is (almost) absent. Glucose 41-48 insulin Homo sapiens 22-29 8446221-3 1993 This suggests that the metabolism of glucose is probably not deranged in NIDDM, since glucose leads to insulin release after it has been metabolized. Glucose 86-93 insulin Homo sapiens 103-110 8446221-5 1993 Various mechanisms have been proposed, whereby hyperglycaemia may diminish insulin release: inhibition of Ca2+ mobilization from the endoplasmic reticulum by glucose-6-phosphate, Ca2+ uptake in the ER by glucose and inhibitory effects of protein kinase C. Whatever may prove to be the underlying mechanism(s), glucose toxicity is unlikely to be the only cause of insulin secretory disturbances in NIDDM, since the glucose level would have to be elevated before it could be toxic. Glucose 204-211 insulin Homo sapiens 75-82 11538517-1 1993 It is well known that a daily positive physical activity is able to control body fat and to improve insulin action for intaking glucose in the muscles, especially under administration of nutrition in human. Glucose 128-135 insulin Homo sapiens 100-107 11538517-2 1993 Conversely, when exposed prolonged inactive condition such as bed-rest in spite of control of nutrition, the insulin action may be declined due to less glucose intake in the muscles and thus the insulin secretion may be increased to maintain blood glucose level. Glucose 152-159 insulin Homo sapiens 109-116 11538517-2 1993 Conversely, when exposed prolonged inactive condition such as bed-rest in spite of control of nutrition, the insulin action may be declined due to less glucose intake in the muscles and thus the insulin secretion may be increased to maintain blood glucose level. Glucose 248-255 insulin Homo sapiens 109-116 8303118-7 1993 This leads to a reduction in glucose disposal and increases hepatic glucose output, outlining a post receptor defect leading to insulin resistance. Glucose 29-36 insulin Homo sapiens 128-135 8381211-1 1993 Non-insulin-dependent diabetes mellitus (NIDDM, type 2 diabetes) is a disorder of glucose homeostasis characterized by hyperglycaemia, peripheral insulin resistance, impaired hepatic glucose metabolism, and diminished glucose-dependent secretion of insulin from pancreatic beta-cells. Glucose 82-89 insulin Homo sapiens 4-11 8381211-1 1993 Non-insulin-dependent diabetes mellitus (NIDDM, type 2 diabetes) is a disorder of glucose homeostasis characterized by hyperglycaemia, peripheral insulin resistance, impaired hepatic glucose metabolism, and diminished glucose-dependent secretion of insulin from pancreatic beta-cells. Glucose 82-89 insulin Homo sapiens 146-153 8381211-2 1993 Glucagon-like-peptide-1(7-37) (GLP-1) is an intestinally derived hormone that may be useful for the treatment of NIDDM because it acts in vivo to increase the level of circulating insulin, and thus lower the concentration of blood glucose. Glucose 231-238 insulin Homo sapiens 180-187 8424787-1 1993 Both insulin and contraction stimulate glucose transport in skeletal muscle. Glucose 39-46 insulin Homo sapiens 5-12 8424787-2 1993 Insulin-stimulated glucose transport is decreased in obese humans and rats. Glucose 19-26 insulin Homo sapiens 0-7 8424787-7 1993 As expected, the insulin-stimulated glucose transport rate in each of the three muscles was significantly slower (P < 0.05) in obese rats when compared with lean animals. Glucose 36-43 insulin Homo sapiens 17-24 8424787-10 1993 Prior contraction increased insulin responsiveness of glucose transport 2-5-fold in the obese rats, but had no effect on insulin responsiveness in the lean controls. Glucose 54-61 insulin Homo sapiens 28-35 8424787-11 1993 This contraction-induced improvement in insulin responsiveness could be of clinical importance to obese subjects as a way to improve insulin-stimulated glucose uptake in resistant skeletal muscle. Glucose 152-159 insulin Homo sapiens 40-47 8424787-11 1993 This contraction-induced improvement in insulin responsiveness could be of clinical importance to obese subjects as a way to improve insulin-stimulated glucose uptake in resistant skeletal muscle. Glucose 152-159 insulin Homo sapiens 133-140 8416266-6 1993 The diabetic patients with the A2 allele had a stronger family history of NIDDM (P = 0.019), a higher prevalence of hypertension (P = 0.008), and a more severe defect in insulin-stimulated glucose storage (P = 0.001) than the diabetic patients with the A1 allele. Glucose 189-196 insulin Homo sapiens 170-177 8111072-10 1993 The incremental PIM, insulin and C-peptide responses to glucose and glucagon in the relatives were not different from those in the controls. Glucose 56-63 insulin Homo sapiens 33-42 8212978-7 1993 Numerous studies have shown that a combination of insulin and sulphonylurea is more effective than insulin alone in the treatment of patients with NIDDM after secondary failure to oral drugs, leading to better glucose profiles and/or decreased insulin needs. Glucose 210-217 insulin Homo sapiens 50-57 8212978-7 1993 Numerous studies have shown that a combination of insulin and sulphonylurea is more effective than insulin alone in the treatment of patients with NIDDM after secondary failure to oral drugs, leading to better glucose profiles and/or decreased insulin needs. Glucose 210-217 insulin Homo sapiens 99-106 8212978-7 1993 Numerous studies have shown that a combination of insulin and sulphonylurea is more effective than insulin alone in the treatment of patients with NIDDM after secondary failure to oral drugs, leading to better glucose profiles and/or decreased insulin needs. Glucose 210-217 insulin Homo sapiens 99-106 8329728-10 1993 Net forearm glucose uptake (FGU) increased by a greater amount during insulin compared with proinsulin infusion: 1.44 +/- 0.02 (I) and 0.71 +/- 0.01 (P) mumol/100 ml forearm per minute (P < 0.02). Glucose 12-19 insulin Homo sapiens 70-77 8424283-9 1993 The higher insulin secretion in response to glucose infusion in the RA group compared to the GA group may indicate an increased peripheral insulin resistance after regional anesthesia or, more likely, this secretion may be beneficial in contributing to improve postoperative nitrogen balance. Glucose 44-51 insulin Homo sapiens 11-18 8424283-9 1993 The higher insulin secretion in response to glucose infusion in the RA group compared to the GA group may indicate an increased peripheral insulin resistance after regional anesthesia or, more likely, this secretion may be beneficial in contributing to improve postoperative nitrogen balance. Glucose 44-51 insulin Homo sapiens 139-146 8249680-0 1993 Indirect effects of insulin in regulating glucose fluxes. Glucose 42-49 insulin Homo sapiens 20-27 8249680-2 1993 Insulin is of utmost importance in regulating glucose metabolism by promoting glucose uptake in the insulin-sensitive tissues for energy consumption and/or storage. Glucose 46-53 insulin Homo sapiens 0-7 8249680-2 1993 Insulin is of utmost importance in regulating glucose metabolism by promoting glucose uptake in the insulin-sensitive tissues for energy consumption and/or storage. Glucose 46-53 insulin Homo sapiens 100-107 8249680-2 1993 Insulin is of utmost importance in regulating glucose metabolism by promoting glucose uptake in the insulin-sensitive tissues for energy consumption and/or storage. Glucose 78-85 insulin Homo sapiens 0-7 8249680-2 1993 Insulin is of utmost importance in regulating glucose metabolism by promoting glucose uptake in the insulin-sensitive tissues for energy consumption and/or storage. Glucose 78-85 insulin Homo sapiens 100-107 8249680-3 1993 The effects of insulin on glucose metabolism can be both direct and indirect. Glucose 26-33 insulin Homo sapiens 15-22 8249680-4 1993 Ample evidence has indicated that insulin directly stimulates glucose transport systems in the target tissues. Glucose 62-69 insulin Homo sapiens 34-41 8249680-5 1993 However, the changes in glucose fluxes can also be brought out by indirect effects of insulin which are produced secondary to the insulin-induced changes in other hormones and metabolites. Glucose 24-31 insulin Homo sapiens 86-93 8249680-5 1993 However, the changes in glucose fluxes can also be brought out by indirect effects of insulin which are produced secondary to the insulin-induced changes in other hormones and metabolites. Glucose 24-31 insulin Homo sapiens 130-137 8249680-6 1993 In this chapter, we discussed a number of examples of insulin"s indirect effects on glucose metabolism. Glucose 84-91 insulin Homo sapiens 54-61 8249680-7 1993 We demonstrated that insulin can indirectly promote muscle glucose uptake during exercise by restraining the release and oxidation of fatty acids and decrease of hyperglycemia. Glucose 59-66 insulin Homo sapiens 21-28 8249680-8 1993 We have presented some evidence for an indirect regulation of glucose cycling by insulin. Glucose 62-69 insulin Homo sapiens 81-88 8249680-9 1993 We have also demonstrated the importance of the peripheral levels of insulin for insulin-induced inhibition of hepatic glucose production. Glucose 119-126 insulin Homo sapiens 69-76 8249680-9 1993 We have also demonstrated the importance of the peripheral levels of insulin for insulin-induced inhibition of hepatic glucose production. Glucose 119-126 insulin Homo sapiens 81-88 8105958-9 1993 Insulin administration induced a decrease in glucose levels that reached a nadir at 30 minutes in both groups (1.8 +/- 0.1 mmol/L in the rHuEPO group vs 2.1 +/- 0.2 mmol/L in the control group). Glucose 45-52 insulin Homo sapiens 0-7 8418611-9 1993 The results of the glucose tolerance tests revealed marked elevation of insulin (5955 pmol/L and 7677 pmol/L) and glucose intolerance consistent with insulin resistance. Glucose 19-26 insulin Homo sapiens 72-79 8430789-4 1993 Basal endogenous glucose production increased during gestation [Ctl: P 2.74 +/- 0.23, E 2.62 +/- 0.38, and L 3.14 +/- 0.36; GDM: P 2.68 +/- 0.51, E 2.78 +/- 0.45, and L 2.98 +/- 0.48 mg.kg fat-free mass (FFM)-1 x min-1; P = 0.02], but there was resistance to suppression by insulin infusion (P = 0.03) in late gestation (GDM: 0.61 +/- 0.44 vs. Ctl: 0.16 +/- 0.17 mg.kg FFM-1 x min-1). Glucose 17-24 insulin Homo sapiens 274-281 8476236-1 1993 Resistance to insulin-mediated glucose uptake is characteristic of individuals with impaired glucose intolerance or non-insulin-dependent diabetes, and it also occurs commonly in patients with high blood pressure. Glucose 31-38 insulin Homo sapiens 14-21 8476236-2 1993 The physiological response to a decrease in insulin-mediated glucose uptake is an increase in insulin secretion, and as long as a state of compensatory hyperinsulinemia can be maintained, frank decompensation of glucose tolerance can be prevented. Glucose 61-68 insulin Homo sapiens 44-51 8476236-2 1993 The physiological response to a decrease in insulin-mediated glucose uptake is an increase in insulin secretion, and as long as a state of compensatory hyperinsulinemia can be maintained, frank decompensation of glucose tolerance can be prevented. Glucose 212-219 insulin Homo sapiens 44-51 8476236-4 1993 It seems likely that the cluster of changes associated with resistance to insulin-mediated glucose uptake comprise a syndrome, which plays an important role in the etiology and clinical course of patients with non-insulin-dependent diabetes, high blood pressure, and coronary heart disease. Glucose 91-98 insulin Homo sapiens 74-81 8424653-3 1993 Islets maintained at 1 mM glucose in tissue culture medium for 1 day lose the ability to release insulin in response to glucose and glucose metabolism is decreased 50-80%. Glucose 26-33 insulin Homo sapiens 97-104 8424653-3 1993 Islets maintained at 1 mM glucose in tissue culture medium for 1 day lose the ability to release insulin in response to glucose and glucose metabolism is decreased 50-80%. Glucose 120-127 insulin Homo sapiens 97-104 8424653-3 1993 Islets maintained at 1 mM glucose in tissue culture medium for 1 day lose the ability to release insulin in response to glucose and glucose metabolism is decreased 50-80%. Glucose 120-127 insulin Homo sapiens 97-104 8281530-6 1993 The changes in daylong plasma glucose and insulin-stimulated glucose uptake increased after hydrochlorothiazide treatment and decreased following lisinopril. Glucose 61-68 insulin Homo sapiens 42-49 7693357-2 1993 It inhibits glucose-induced insulin release, hippocampal acetylcholine release, hippocampal glutamate but not GABA release, and it lowers spinal excitability and firing of locus coeruleus neurons. Glucose 12-19 insulin Homo sapiens 28-35 8093605-2 1993 Transmembrane glucose transport plays a key role in determining insulin sensitivity. Glucose 14-21 insulin Homo sapiens 64-71 8420813-0 1993 Normal proinsulin responses to glucose in mild type II subjects with subnormal insulin response. Glucose 31-38 insulin Homo sapiens 7-17 8420813-0 1993 Normal proinsulin responses to glucose in mild type II subjects with subnormal insulin response. Glucose 31-38 insulin Homo sapiens 10-17 8420813-10 1993 The major defect in pancreatic function is an impaired insulin response to glucose, and this, rather than an increase in proinsulin secretion, gives rise to the relative increase in proinsulin. Glucose 75-82 insulin Homo sapiens 182-192 8420818-4 1993 Normal rats made hyperglycemic with 48-h glucose infusions had a raised pancreatic percentage of proinsulin. Glucose 41-48 insulin Homo sapiens 97-107 8420818-5 1993 In contrast, rats infused with enough glucose to induce compensatory hyperinsulinemia without changing the plasma glucose level had a normal percentage of proinsulin. Glucose 38-45 insulin Homo sapiens 155-165 8420819-10 1993 Ethanol reduced insulin-stimulated glucose uptake from 40.6 +/- 3.1 to 25.6 +/- 1.9 mumol.kg-1.min-1 (-37%, P < 0.05), glucose oxidation from 11.7 +/- 1.1 to 7.0 +/- 0.7 mumol.kg-1.min-1 (-33%, P < 0.01), and glucose storage from 28.7 +/- 2.4 to 18.6 +/- 1.7 mumol.kg-1.min-1 (-35%, P < 0.01). Glucose 35-42 insulin Homo sapiens 16-23 8420819-10 1993 Ethanol reduced insulin-stimulated glucose uptake from 40.6 +/- 3.1 to 25.6 +/- 1.9 mumol.kg-1.min-1 (-37%, P < 0.05), glucose oxidation from 11.7 +/- 1.1 to 7.0 +/- 0.7 mumol.kg-1.min-1 (-33%, P < 0.01), and glucose storage from 28.7 +/- 2.4 to 18.6 +/- 1.7 mumol.kg-1.min-1 (-35%, P < 0.01). Glucose 122-129 insulin Homo sapiens 16-23 8420819-10 1993 Ethanol reduced insulin-stimulated glucose uptake from 40.6 +/- 3.1 to 25.6 +/- 1.9 mumol.kg-1.min-1 (-37%, P < 0.05), glucose oxidation from 11.7 +/- 1.1 to 7.0 +/- 0.7 mumol.kg-1.min-1 (-33%, P < 0.01), and glucose storage from 28.7 +/- 2.4 to 18.6 +/- 1.7 mumol.kg-1.min-1 (-35%, P < 0.01). Glucose 122-129 insulin Homo sapiens 16-23 8422836-6 1993 Glycemic and C-peptide response to breakfast was qualitatively typical for each patient with the correlation between plasma glucose and C-peptide. Glucose 124-131 insulin Homo sapiens 13-22 8422836-6 1993 Glycemic and C-peptide response to breakfast was qualitatively typical for each patient with the correlation between plasma glucose and C-peptide. Glucose 124-131 insulin Homo sapiens 136-145 8435988-2 1993 Glucose disposal (assessed by the euglycaemic insulin clamp technique) was significantly reduced in diabetic patients compared to control subjects (4.4 +/- 0.5 vs 6.4 +/- 0.5 mg kg-1 min-1, p < 0.05), and increased after 1 and 3 months of sulphonylurea therapy to 6.8 +/- 0.6 mg kg-1 min-1 (p = 0.01) and 6.3 +/- 0.7 mg kg-1 min-1 (p = 0.04), respectively. Glucose 0-7 insulin Homo sapiens 46-53 8504885-7 1993 The mean glucose infusion rate during the clamp was low in the diabetic girls (2.29 +/- 1.35 mg kg-1 min-1), confirming the existence of insulin resistance. Glucose 9-16 insulin Homo sapiens 137-144 7512468-4 1993 Conversely, hypertension can cause insulin resistance by altering the delivery of insulin and glucose to skeletal muscle cells, resulting in impaired glucose uptake. Glucose 94-101 insulin Homo sapiens 35-42 7712683-8 1993 In diabetic patients, naloxone can improve the surviving insulin secretion with better glucose tolerance. Glucose 87-94 insulin Homo sapiens 57-64 7924144-6 1993 The ratio of metabolic clearance rate of glucose (MCRG) and Insulin (I) was used as the measure of insulin action during Eu, Hy and IGI. Glucose 41-48 insulin Homo sapiens 99-106 7924144-15 1993 In conclusion we have demonstrated that: 1) The insulin-glucose infusion test and the eu(iso)glycaemic clamp were significantly correlated in normals, obese and NIDDM subjects. Glucose 56-63 insulin Homo sapiens 48-55 8174494-3 1993 Insulin plasma levels increased rapidly after the beginning of the glucose infusion in both groups. Glucose 67-74 insulin Homo sapiens 0-7 8200184-1 1993 During constant infusion of exogenous human insulin and glucose to healthy volunteers, a rise in glycemia was still able to stimulate the B-cell as judged from the increase in C-peptide plasma concentration. Glucose 56-63 insulin Homo sapiens 176-185 8422762-4 1993 RESULTS: The increments in npRQ and CHO oxidation rates after the glucose meals in the diabetic women on insulin pump therapy were similar to those in the normal subjects. Glucose 66-73 insulin Homo sapiens 105-112 8422762-6 1993 CONCLUSIONS: This investigation demonstrated that the treatment of IDDM patients during early pregnancy by an open-loop insulin infusion system is sufficient to normalize their glucose-processing capability with respect to cellular oxidative and nonoxidative glucose metabolism in response to an oral glucose challenge, but some abnormalities in their blood profiles of glucose, lactate, and pyruvate persisted. Glucose 177-184 insulin Homo sapiens 120-127 8422762-6 1993 CONCLUSIONS: This investigation demonstrated that the treatment of IDDM patients during early pregnancy by an open-loop insulin infusion system is sufficient to normalize their glucose-processing capability with respect to cellular oxidative and nonoxidative glucose metabolism in response to an oral glucose challenge, but some abnormalities in their blood profiles of glucose, lactate, and pyruvate persisted. Glucose 259-266 insulin Homo sapiens 120-127 8422762-6 1993 CONCLUSIONS: This investigation demonstrated that the treatment of IDDM patients during early pregnancy by an open-loop insulin infusion system is sufficient to normalize their glucose-processing capability with respect to cellular oxidative and nonoxidative glucose metabolism in response to an oral glucose challenge, but some abnormalities in their blood profiles of glucose, lactate, and pyruvate persisted. Glucose 259-266 insulin Homo sapiens 120-127 8422777-11 1993 Both pre- and posttreatment glucose disposal rates correlated with the total exogenous insulin dose required to achieve glycemic control (r = -0.75 and -0.78, both P < 0.005). Glucose 28-35 insulin Homo sapiens 87-94 8436253-0 1993 Erythrocyte sodium-lithium countertransport activity and total body insulin-mediated glucose disposal in normoalbuminuric normotensive type 1 (insulin-dependent) diabetic patients. Glucose 85-92 insulin Homo sapiens 68-75 8436253-3 1993 We have therefore examined the relationship between insulin-mediated glucose disposal and erythrocyte sodium-lithium countertransport in 41 normotensive (mean blood pressure 120/74 mmHg), normoalbuminuric (mean albumin excretion 6.2 micrograms/min), normolipidaemic (mean serum cholesterol 4.3 mmol/l and mean serum triglycerides 1.0 mmol/l) Type 1 diabetic patients. Glucose 69-76 insulin Homo sapiens 52-59 8436253-7 1993 Insulin-mediated glucose disposal was evaluated during the last hour of a euglycaemic clamp (insulin 0.015 U.kg-1.h-1; blood glucose clamped at 7.0 mmol/l). Glucose 17-24 insulin Homo sapiens 0-7 8436253-9 1993 Insulin-mediated glucose disposal was on average 3.1 +/- 1.5 (range 0.8-6.8) mg.kg-1.min-1. Glucose 17-24 insulin Homo sapiens 0-7 8436259-3 1993 The area under the curve representing above-basal levels of insulin during oral glucose tolerance test increased significantly following dexamethasone treatment from 48132 +/- 9736 to 82230 +/- 14846 pmol.l-1 x 3 h-1, p < 0.05, the area under the curve of islet amyloid polypeptide increased from 1308 +/- 183 to 2448 +/- 501 pmol.l-1 x 3 h-1, p < 0.05. Glucose 80-87 insulin Homo sapiens 60-67 8436259-5 1993 During the oral glucose tolerance test the insulin/islet amyloid polypeptide ratio increased significantly from baseline to 30 min (p < 0.05), then declined towards initial values before and after dexamethasone treatment. Glucose 16-23 insulin Homo sapiens 43-50 8444124-3 1993 Surveys of clinic populations suggest a relationship between body habitus, parameters of sleep-disordered breathing, indices of oxygenation, and insulin resistance, defined by fasting serum levels of glucose and insulin. Glucose 200-207 insulin Homo sapiens 145-152 8405025-1 1993 The effect of enalapril, an angiotensin converting enzyme inhibitor, on glucose tolerance and serum insulin response to a glucose load has been evaluated in 8 non-obese patients (3 women and 5 men) with untreated essential hypertension (WHO Stage I or II) and without insulin resistance. Glucose 122-129 insulin Homo sapiens 100-107 8453955-4 1993 At six months, there was a relevant and significant improvement in glycaemic control in diabetics receiving the combined insulin-metformin treatment (decrease in glucose -4.1 mmol.l-1; glycosylated haemoglobin A1 decrease -1.84%). Glucose 162-169 insulin Homo sapiens 121-128 7607335-2 1993 The most important regulator of glucose uptake from the blood is the hormone insulin, which is produced by islet beta cells and acts on insulin receptors to promote nutrient uptake and processing. Glucose 32-39 insulin Homo sapiens 77-84 7607335-2 1993 The most important regulator of glucose uptake from the blood is the hormone insulin, which is produced by islet beta cells and acts on insulin receptors to promote nutrient uptake and processing. Glucose 32-39 insulin Homo sapiens 136-143 8157092-7 1993 An inverse relationship was found between metabolic clearance rate of glucose and of insulin (r = 0.72, p < 0.001). Glucose 70-77 insulin Homo sapiens 85-92 8299708-1 1993 Insulin secretion and sensitivity are basic characteristics determining the glucose tolerance. Glucose 76-83 insulin Homo sapiens 0-7 8299708-3 1993 The early insulin response at the intravenous glucose tolerance test (IVGTT) in 42 subjects with IGT was found to be correlated to the glucose tolerance (r = -0.38, p < 0.01 vs, fasting glucose and r = 0.35, p < 0.02, vs the k-value of IVGTT) while fasting insulin was found to be closely correlated to insulin sensitivity, measured by the euglycemic clamp method (r = -0.83, p < 0.003, n = 11). Glucose 46-53 insulin Homo sapiens 10-17 8299708-3 1993 The early insulin response at the intravenous glucose tolerance test (IVGTT) in 42 subjects with IGT was found to be correlated to the glucose tolerance (r = -0.38, p < 0.01 vs, fasting glucose and r = 0.35, p < 0.02, vs the k-value of IVGTT) while fasting insulin was found to be closely correlated to insulin sensitivity, measured by the euglycemic clamp method (r = -0.83, p < 0.003, n = 11). Glucose 46-53 insulin Homo sapiens 263-270 8299708-3 1993 The early insulin response at the intravenous glucose tolerance test (IVGTT) in 42 subjects with IGT was found to be correlated to the glucose tolerance (r = -0.38, p < 0.01 vs, fasting glucose and r = 0.35, p < 0.02, vs the k-value of IVGTT) while fasting insulin was found to be closely correlated to insulin sensitivity, measured by the euglycemic clamp method (r = -0.83, p < 0.003, n = 11). Glucose 46-53 insulin Homo sapiens 263-270 8299708-3 1993 The early insulin response at the intravenous glucose tolerance test (IVGTT) in 42 subjects with IGT was found to be correlated to the glucose tolerance (r = -0.38, p < 0.01 vs, fasting glucose and r = 0.35, p < 0.02, vs the k-value of IVGTT) while fasting insulin was found to be closely correlated to insulin sensitivity, measured by the euglycemic clamp method (r = -0.83, p < 0.003, n = 11). Glucose 135-142 insulin Homo sapiens 10-17 8299708-3 1993 The early insulin response at the intravenous glucose tolerance test (IVGTT) in 42 subjects with IGT was found to be correlated to the glucose tolerance (r = -0.38, p < 0.01 vs, fasting glucose and r = 0.35, p < 0.02, vs the k-value of IVGTT) while fasting insulin was found to be closely correlated to insulin sensitivity, measured by the euglycemic clamp method (r = -0.83, p < 0.003, n = 11). Glucose 135-142 insulin Homo sapiens 10-17 8262485-2 1993 The target organs for insulin action are the liver (restriction of glucose production), the muscle (acceleration of glucose disposal) and the adipose tissue (inhibition of free fatty acid mobilization). Glucose 67-74 insulin Homo sapiens 22-29 8262485-2 1993 The target organs for insulin action are the liver (restriction of glucose production), the muscle (acceleration of glucose disposal) and the adipose tissue (inhibition of free fatty acid mobilization). Glucose 116-123 insulin Homo sapiens 22-29 8093619-7 1993 Glucose (20 mmol/L) induced a 2- to 3-fold increase in insulin release in two clinically mild cases of PHHI, but no response at all in the four others. Glucose 0-7 insulin Homo sapiens 55-62 8093619-9 1993 Furthermore, insulin release from PHHI cells is poorly stimulated by glucose but effectively blocked by somatostatin, supporting the concept of somatostatin deficiency in PHHI. Glucose 69-76 insulin Homo sapiens 13-20 8093620-4 1993 These studies demonstrate that during insulin and glucose infusion, insulin, but neither the plasma glucose concentration nor the rate of glucose utilization, primarily regulates leucine flux (a reflection of endogenous whole body proteolysis) in normal humans. Glucose 50-57 insulin Homo sapiens 68-75 8421087-5 1993 We conclude that nitrendipine treatment is associated with improved glucose tolerance, reduced fasting and glucose-stimulated serum insulin levels, and increased circulating DHEA-S levels. Glucose 107-114 insulin Homo sapiens 132-139 8421101-7 1993 Both plasma immunoreactive insulin and C-peptide concentrations from 0800-1600 h were higher (P < 0.002-0.001) in patients with either IGT or NIDDM than in the group with normal glucose tolerance. Glucose 181-188 insulin Homo sapiens 27-34 8421101-9 1993 Plasma proinsulin concentrations were highest in patients with NIDDM (P < 0.002), lower in those with normal glucose tolerance (P < 0.002), and intermediate in patients with IGT. Glucose 112-119 insulin Homo sapiens 7-17 8421104-5 1993 Glucose and insulin concentrations were higher in the patients with Friedreich"s ataxia after an oral glucose load, consistent with the presence of insulin resistance. Glucose 0-7 insulin Homo sapiens 148-155 8421104-5 1993 Glucose and insulin concentrations were higher in the patients with Friedreich"s ataxia after an oral glucose load, consistent with the presence of insulin resistance. Glucose 102-109 insulin Homo sapiens 12-19 8421104-6 1993 The normal increase in the affinity of insulin receptors on monocytes 5 h after oral glucose was absent in the five patients with Friedreich"s ataxia. Glucose 85-92 insulin Homo sapiens 39-46 8421108-5 1993 Insulin secretory rates were also 50% higher in the hyperthyroid subjects during the hyperglycemic clamp at a time when glucose levels in both groups were comparable. Glucose 120-127 insulin Homo sapiens 0-7 8421108-8 1993 Thus, stimulated insulin secretion rates are significantly increased in thyrotoxicosis possibly reflecting an increased sensitivity of the beta-cell to glucose in subjects who are hyperthyroid. Glucose 152-159 insulin Homo sapiens 17-24 8423214-6 1993 Absent glucagon responses were associated with a blunting of the rebound increase in glucose production (P < 0.05 vs. insulin). Glucose 85-92 insulin Homo sapiens 121-128 8069546-2 1993 It has been shown that an implantable polymeric system which releases insulin in response to blood glucose levels is feasible. Glucose 99-106 insulin Homo sapiens 70-77 8433549-3 1993 Similar to other cells types that are affected by the diabetic state (such as, vascular cells and peripheral nerve), mesangial cells transport glucose by an insulin-independent, facilitated diffusion transport system. Glucose 143-150 insulin Homo sapiens 157-164 8479103-3 1993 Whereas glucose is available at increased rates, the muscle tissue is less responsive than normal to the stimulatory effect of insulin on glucose uptake. Glucose 138-145 insulin Homo sapiens 127-134 8433561-8 1993 The patients were restudied under the same experimental protocols, while receiving a continuous infusion of insulin with dextrose. Glucose 121-129 insulin Homo sapiens 108-115 8433561-10 1993 Administration of insulin with dextrose at a dose that doubled the plasma insulin levels within the physiologic range (9.3 +/- 1.1 vs. 20.2 +/- 2.3 mU/liter, P < 0.002), completely prevented the rise in plasma potassium (+0.06 +/- 0.13 mmol/liter, P = 0.64). Glucose 31-39 insulin Homo sapiens 18-25 8433561-10 1993 Administration of insulin with dextrose at a dose that doubled the plasma insulin levels within the physiologic range (9.3 +/- 1.1 vs. 20.2 +/- 2.3 mU/liter, P < 0.002), completely prevented the rise in plasma potassium (+0.06 +/- 0.13 mmol/liter, P = 0.64). Glucose 31-39 insulin Homo sapiens 74-81 8268149-6 1993 However, both serum glucose and insulin levels, after a 75 g glucose load, were significantly increased in hyperprolactinemic women, (p = 0.001, p < 0.001, respectively). Glucose 61-68 insulin Homo sapiens 32-39 8412503-2 1993 In untreated islets, alpha-D-glucose stimulated insulin secretion more efficiently than beta-D-glucose at a glucose concentration of 10 mM. Glucose 29-36 insulin Homo sapiens 48-55 8412519-5 1993 The improved glucose tolerance brought about by Benfluorex in an animal model of insulin resistance may suggest a wider therapeutic application in man, to include insulin resistant states as type II diabetes or Syndrome X. Glucose 13-20 insulin Homo sapiens 81-88 8446038-5 1993 To determine whether the relationships between sex hormone levels and insulin and glucose levels found in non-obese men also occur in obese men independent of obesity, fasting levels of these substances, as well as free testosterone (FT) and sex-hormone-binding globulin (SHBG), were measured in 55 obese men aged 21 to 70. Glucose 82-89 insulin Homo sapiens 70-77 8446044-5 1993 During the clamp studies, glucose Rd was lower in insulinoma patients (18.7 +/- 1.2 v 33.8 +/- 3.1 mumol/kg/min; P < .01) despite higher plasma insulin concentration (612 +/- 48 v 420 +/- 12 pmol/L). Glucose 26-33 insulin Homo sapiens 50-57 8446044-6 1993 Therefore, glucose Rd/I x 100 ratio (where I is plasma insulin concentration) was much lower in insulinoma patients (3.1 +/- 0.9 v 8.0 +/- 0.7; P < .01), suggesting a marked degree of insulin resistance. Glucose 11-18 insulin Homo sapiens 96-103 8446045-0 1993 Proinsulin and insulin concentrations following intravenous glucose challenges in normal, obese, and non-insulin-dependent diabetic subjects. Glucose 60-67 insulin Homo sapiens 0-10 8446045-0 1993 Proinsulin and insulin concentrations following intravenous glucose challenges in normal, obese, and non-insulin-dependent diabetic subjects. Glucose 60-67 insulin Homo sapiens 3-10 8446045-1 1993 We investigated the effects of different intravenous (IV) glucose challenges on insulin and proinsulin secretion. Glucose 58-65 insulin Homo sapiens 80-87 8446045-7 1993 In normal and obese subjects, IV glucose administration resulted in significant acute increases in insulin concentrations compared with the characteristic blunted response in NIDDM subjects. Glucose 33-40 insulin Homo sapiens 99-106 8446055-8 1993 Thus hyperglycemia, at basal insulin levels enhanced glucose utilization and suppressed glucose production in insulin-dependent diabetic patients. Glucose 53-60 insulin Homo sapiens 29-36 8446055-8 1993 Thus hyperglycemia, at basal insulin levels enhanced glucose utilization and suppressed glucose production in insulin-dependent diabetic patients. Glucose 88-95 insulin Homo sapiens 29-36 8413768-5 1993 It is concluded that psi inhibits glucose utilization at the level of Ca modulation in the insulin regulatory cascade. Glucose 34-41 insulin Homo sapiens 91-98 8443563-6 1993 Recognized physiological effects of insulin in the central nervous system (CNS) include regulation of food intake, control of glucose uptake and trophic actions on neuronal and glial cells. Glucose 126-133 insulin Homo sapiens 36-43 8457423-3 1993 The present experiments inhibited lactic acid production by lowering glucose availability using insulin-induced hypoglycemia. Glucose 69-76 insulin Homo sapiens 96-103 8419906-1 1993 Insulin response to glucose is severely impaired in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 20-27 insulin Homo sapiens 0-7 8419906-2 1993 Also in a rat model of NIDDM, neonatally streptozotocin diabetic rats (STZ), the insulin response to glucose is profoundly suppressed when studied in vivo or in the perfused pancreas. Glucose 101-108 insulin Homo sapiens 81-88 8419906-4 1993 Since alpha 2-adrenoceptor stimulation suppresses insulin secretion, catecholamines from intrapancreatic nerve terminals may be involved in the mechanism behind the marked impairment of the glucose-stimulated insulin response in the intact pancreas. Glucose 190-197 insulin Homo sapiens 50-57 8419906-4 1993 Since alpha 2-adrenoceptor stimulation suppresses insulin secretion, catecholamines from intrapancreatic nerve terminals may be involved in the mechanism behind the marked impairment of the glucose-stimulated insulin response in the intact pancreas. Glucose 190-197 insulin Homo sapiens 209-216 8419906-11 1993 After reserpine, however, glucose-induced insulin release was not enhanced in either STZ or control pancreata. Glucose 26-33 insulin Homo sapiens 42-49 8441762-1 1993 In previous investigations we have shown a striking relationship between the activity of glycogenolytic glucose producing acid hydrolases in pancreatic islet tissue and certain insulin-releasing processes. Glucose 104-111 insulin Homo sapiens 177-184 8441762-3 1993 It was observed that the nonmetabolizable glucose analogue, mannoheptulose (5 mmol/l) did induce a 2-fold increase in insulin release at low (1 mmol/l) glucose, and a total suppression of insulin release at high (16.7 mmol/l) glucose. Glucose 42-49 insulin Homo sapiens 118-125 8441762-3 1993 It was observed that the nonmetabolizable glucose analogue, mannoheptulose (5 mmol/l) did induce a 2-fold increase in insulin release at low (1 mmol/l) glucose, and a total suppression of insulin release at high (16.7 mmol/l) glucose. Glucose 42-49 insulin Homo sapiens 188-195 8441762-3 1993 It was observed that the nonmetabolizable glucose analogue, mannoheptulose (5 mmol/l) did induce a 2-fold increase in insulin release at low (1 mmol/l) glucose, and a total suppression of insulin release at high (16.7 mmol/l) glucose. Glucose 152-159 insulin Homo sapiens 118-125 8441762-3 1993 It was observed that the nonmetabolizable glucose analogue, mannoheptulose (5 mmol/l) did induce a 2-fold increase in insulin release at low (1 mmol/l) glucose, and a total suppression of insulin release at high (16.7 mmol/l) glucose. Glucose 152-159 insulin Homo sapiens 118-125 8441762-7 1993 At high glucose, however, a partial inhibition of both insulin release (approximately 50%) and acid alpha-glucosidase activity was seen. Glucose 8-15 insulin Homo sapiens 55-62 8220508-4 1993 Immunologic markers (ICA and/or AAI) of DMI and abnormalities of the first-phase insulin secretion in response to intravenous glucose also may precede by several months the most common clinical picture of type I diabetes as they were detected in this child. Glucose 126-133 insulin Homo sapiens 81-88 8009086-0 1993 [Evaluation of the participation of proinsulin in hyperinsulinism in patients with obesity and glucose intolerance]. Glucose 95-102 insulin Homo sapiens 36-46 8362105-5 1993 This prediabetic phase can be detected by the presence of autoantibodies directed against islet cells and sometimes associated with anti-insulin antibodies in children, and later on by the disappearance of the early insulin secretion peak in response to intravenous glucose. Glucose 266-273 insulin Homo sapiens 216-223 7678356-0 1993 Inhibition of glucose-stimulated insulin release from beta TC3 cells and rodent islets by an analog of FK506. Glucose 14-21 insulin Homo sapiens 33-40 8266608-4 1993 In addition, the plasma glucose and insulin levels after oral glucose load did not differ between the stone patients and control subjects and were affected by the individual degree of obesity. Glucose 62-69 insulin Homo sapiens 36-43 1291337-9 1992 From these data, it is concluded that the decrease in glucose tolerance in patients with Graves" disease can be explained by 1) the impairment of early insulin release response to rapid intestinal glucose absorption, 2) increased insulin metabolic clearance and 3) hyperglucagonemia. Glucose 54-61 insulin Homo sapiens 152-159 1291337-9 1992 From these data, it is concluded that the decrease in glucose tolerance in patients with Graves" disease can be explained by 1) the impairment of early insulin release response to rapid intestinal glucose absorption, 2) increased insulin metabolic clearance and 3) hyperglucagonemia. Glucose 54-61 insulin Homo sapiens 230-237 1291337-9 1992 From these data, it is concluded that the decrease in glucose tolerance in patients with Graves" disease can be explained by 1) the impairment of early insulin release response to rapid intestinal glucose absorption, 2) increased insulin metabolic clearance and 3) hyperglucagonemia. Glucose 197-204 insulin Homo sapiens 152-159 1472063-3 1992 In contrast, insulin stimulated glucose uptake in the control cell line and in each of the chimeric receptor-expressing lines with similar dose-response characteristics. Glucose 32-39 insulin Homo sapiens 13-20 1483614-3 1992 The underlying common cause of this syndrome appears to be insulin resistance of the skeletal muscles, which is related in particular to the non-oxidative glucose utilization on the part of the muscle. Glucose 155-162 insulin Homo sapiens 59-66 1294980-8 1992 The reduction of Glut 2 expression correlates with, and may contribute to the loss of glucose-stimulated insulin secretion. Glucose 86-93 insulin Homo sapiens 105-112 1285941-4 1992 Subjects with hypertension had higher peak serum insulin and lower plasma glucose area/insulin area ratio in response to glucose (1.8 +/- 0.2 v 2.4 +/- 0.2 mg/dL/microU/mL, P < .05) than normotensive subjects. Glucose 121-128 insulin Homo sapiens 87-94 1363049-4 1992 Hypertensive subjects had shown an increased area under the curve of glucose and insulin during the oral glucose tolerance test compared with normal controls. Glucose 105-112 insulin Homo sapiens 81-88 1456195-1 1992 Patients with noninsulin-dependent diabetes demonstrate peripheral insulin resistance that is aggravated by increased hepatic glucose production and results in elevated serum insulin and serum glucose levels. Glucose 126-133 insulin Homo sapiens 17-24 1456195-1 1992 Patients with noninsulin-dependent diabetes demonstrate peripheral insulin resistance that is aggravated by increased hepatic glucose production and results in elevated serum insulin and serum glucose levels. Glucose 126-133 insulin Homo sapiens 67-74 1456195-1 1992 Patients with noninsulin-dependent diabetes demonstrate peripheral insulin resistance that is aggravated by increased hepatic glucose production and results in elevated serum insulin and serum glucose levels. Glucose 193-200 insulin Homo sapiens 17-24 1456195-1 1992 Patients with noninsulin-dependent diabetes demonstrate peripheral insulin resistance that is aggravated by increased hepatic glucose production and results in elevated serum insulin and serum glucose levels. Glucose 193-200 insulin Homo sapiens 67-74 1456258-1 1992 OBJECTIVE: To differentiate the insulin-dependent glucose intolerance associated with cystic fibrosis from type I diabetes mellitus in patients with cystic fibrosis. Glucose 50-57 insulin Homo sapiens 32-39 1471704-9 1992 After oral glucose was given, elevated fasting insulin levels increased significantly in patients with polycystic ovary syndrome (p < 0.01), as did immunoreactive beta-endorphin levels (p < 0.05). Glucose 11-18 insulin Homo sapiens 47-54 1476187-0 1992 Effect of training on insulin-mediated glucose uptake in human muscle. Glucose 39-46 insulin Homo sapiens 22-29 1476187-1 1992 During insulin stimulation whole body glucose uptake is increased in trained compared with untrained humans. Glucose 38-45 insulin Homo sapiens 7-14 1476187-10 1992 Insulin-mediated glucose uptake was not increased after detraining or a single bout of exercise. Glucose 17-24 insulin Homo sapiens 0-7 1476187-11 1992 In conclusion, training increases sensitivity and responsiveness of insulin-mediated glucose uptake in human muscle by local mechanisms. Glucose 85-92 insulin Homo sapiens 68-75 1485943-2 1992 Insulin resistance manifested as impaired activation of glycogen synthase and thereby storage of glucose as glycogen in skeletal muscle is demonstrable early on in NIDDM relatives, suggesting that NIDDM could be an inherited muscle disease. Glucose 97-104 insulin Homo sapiens 0-7 1334411-7 1992 However, evidence for post-receptor interactions between cAMP and insulin was also found: an impairment of maximal insulin-stimulated 3-O-methylglucose transport and a delay in the rate of activation of the glucose transport system by insulin. Glucose 144-151 insulin Homo sapiens 66-73 1334411-7 1992 However, evidence for post-receptor interactions between cAMP and insulin was also found: an impairment of maximal insulin-stimulated 3-O-methylglucose transport and a delay in the rate of activation of the glucose transport system by insulin. Glucose 144-151 insulin Homo sapiens 115-122 1334411-7 1992 However, evidence for post-receptor interactions between cAMP and insulin was also found: an impairment of maximal insulin-stimulated 3-O-methylglucose transport and a delay in the rate of activation of the glucose transport system by insulin. Glucose 144-151 insulin Homo sapiens 115-122 1345629-2 1992 Although there can be insensitivity to any of insulin"s actions, insulin resistance par excellence is a decreased insulin-mediated whole-body glucose disposal rate. Glucose 142-149 insulin Homo sapiens 65-72 1446794-5 1992 The insulin response to oral glucose was significantly lower in NIDDM patients than in normal control subjects. Glucose 29-36 insulin Homo sapiens 4-11 1446794-9 1992 These results suggest that impaired insulin secretion and decreased SG are the factors responsible for glucose intolerance of Japanese NIDDM patients with normal insulin sensitivity. Glucose 103-110 insulin Homo sapiens 36-43 1446794-10 1992 Because SI and SG are the factors responsible for glucose intolerance of NIDDM patients with insulin resistance, it is conceivable that decreased SG is common in NIDDM patients regardless of their SI index. Glucose 50-57 insulin Homo sapiens 93-100 1446799-6 1992 Insulin-mediated glucose disposal (insulin clamp technique), measured at two physiological levels of hyperinsulinemia (approximately 240 and 450 pM [approximately 40 and 75 microU/ml]), was reduced by 43 and 33%, respectively. Glucose 17-24 insulin Homo sapiens 0-7 1446799-6 1992 Insulin-mediated glucose disposal (insulin clamp technique), measured at two physiological levels of hyperinsulinemia (approximately 240 and 450 pM [approximately 40 and 75 microU/ml]), was reduced by 43 and 33%, respectively. Glucose 17-24 insulin Homo sapiens 35-42 1446799-7 1992 During both the low- and high-dose insulin clamp steps, impaired nonoxidative glucose disposal, which primarily represents glycogen synthesis, was the major defect responsible for the insulin resistance. Glucose 78-85 insulin Homo sapiens 35-42 1446799-11 1992 These results indicate that the glucose-tolerant offspring of two NIDDM parents are characterized by hyperinsulinemia and manifest all of the metabolic abnormalities that characterize the fully established diabetic state, including insulin resistance, a major impairment in nonoxidative glucose disposal, a quantitatively less important defect in glucose oxidation, and a diminished insulin-mediated suppression of lipid oxidation and plasma FFA concentration. Glucose 32-39 insulin Homo sapiens 106-113 1446799-11 1992 These results indicate that the glucose-tolerant offspring of two NIDDM parents are characterized by hyperinsulinemia and manifest all of the metabolic abnormalities that characterize the fully established diabetic state, including insulin resistance, a major impairment in nonoxidative glucose disposal, a quantitatively less important defect in glucose oxidation, and a diminished insulin-mediated suppression of lipid oxidation and plasma FFA concentration. Glucose 32-39 insulin Homo sapiens 232-239 1446799-11 1992 These results indicate that the glucose-tolerant offspring of two NIDDM parents are characterized by hyperinsulinemia and manifest all of the metabolic abnormalities that characterize the fully established diabetic state, including insulin resistance, a major impairment in nonoxidative glucose disposal, a quantitatively less important defect in glucose oxidation, and a diminished insulin-mediated suppression of lipid oxidation and plasma FFA concentration. Glucose 287-294 insulin Homo sapiens 232-239 1446801-3 1992 Fasting (5.3 +/- 0.1 vs. 5.4 +/- 0.1 mM) and nadir (2.3 +/- 0.1 vs. 2.4 +/- 0.1 mM) glucose levels achieved during insulin infusion did not differ on study days 1 and 4. Glucose 84-91 insulin Homo sapiens 115-122 1478365-2 1992 The connection between hypertriglyceridaemia and insulin resistance is not clear, but could be due to substrate competition between glucose and lipids. Glucose 132-139 insulin Homo sapiens 49-56 1478365-8 1992 Stimulation of glucose disposal by insulin was reduced in hypertriglyceridaemic vs normotriglyceridaemic patients (27.0 +/- 1.3 vs 31.9 +/- 1.6 mumol.kg-1 x min-1; p < 0.05) primarily due to impaired glucose storage (9.8 +/- 1.0 vs 14.6 +/- 1.4 mumol.kg-1 x min-1; p < 0.01). Glucose 15-22 insulin Homo sapiens 35-42 1478367-9 1992 Forearm uptake of oxygen and glucose in the diabetic patients increased markedly after C-peptide administration but were unchanged after NaCl infusion. Glucose 29-36 insulin Homo sapiens 87-96 1294375-5 1992 As the plasma glucose level declined by only 203 mg dl-1 (41 mg dl-1 h-1) in the first 5 h, the insulin dose was doubled every 2 h. At hour 4, the patient developed circulatory shock which required vasopressor support and respiratory assistance. Glucose 14-21 insulin Homo sapiens 96-103 1307719-1 1992 Although closure of the ATP-sensitive K+ (K+ ATP) channel produced by glucose metabolism in the B-cell has been considered mediating the major signal for glucose-induced insulin release, evidences indicating the existence of the K+ ATP channel-independent, insulinotropic action of glucose have recently been accumulated. Glucose 70-77 insulin Homo sapiens 170-177 1307719-1 1992 Although closure of the ATP-sensitive K+ (K+ ATP) channel produced by glucose metabolism in the B-cell has been considered mediating the major signal for glucose-induced insulin release, evidences indicating the existence of the K+ ATP channel-independent, insulinotropic action of glucose have recently been accumulated. Glucose 154-161 insulin Homo sapiens 170-177 1307719-1 1992 Although closure of the ATP-sensitive K+ (K+ ATP) channel produced by glucose metabolism in the B-cell has been considered mediating the major signal for glucose-induced insulin release, evidences indicating the existence of the K+ ATP channel-independent, insulinotropic action of glucose have recently been accumulated. Glucose 154-161 insulin Homo sapiens 170-177 1307719-2 1992 Namely, glucose stimulates insulin release by the B-cell with a full inhibition of the K+ ATP channel closure by diazoxide, a K+ ATP channel opener, provided cytosolic calcium is elevated. Glucose 8-15 insulin Homo sapiens 27-34 1307719-3 1992 Glucose clearly elicits insulin release even if the K+ ATP channel is maximally inhibited by high concentration of sulfonylurea. Glucose 0-7 insulin Homo sapiens 24-31 1307719-4 1992 In this case, glucose-induced insulin release is associated with net increase, not decrease, of K+ outflow, indicating glucose is opening K+ channels. Glucose 14-21 insulin Homo sapiens 30-37 1307719-4 1992 In this case, glucose-induced insulin release is associated with net increase, not decrease, of K+ outflow, indicating glucose is opening K+ channels. Glucose 119-126 insulin Homo sapiens 30-37 1307719-7 1992 The K+ ATP channel-independent, glucose-induced insulin release shows gradually increasing monophasic pattern which temporally resembles the second phase response of glucose-induced insulin release. Glucose 32-39 insulin Homo sapiens 48-55 1307719-7 1992 The K+ ATP channel-independent, glucose-induced insulin release shows gradually increasing monophasic pattern which temporally resembles the second phase response of glucose-induced insulin release. Glucose 32-39 insulin Homo sapiens 182-189 1307719-7 1992 The K+ ATP channel-independent, glucose-induced insulin release shows gradually increasing monophasic pattern which temporally resembles the second phase response of glucose-induced insulin release. Glucose 166-173 insulin Homo sapiens 48-55 1307719-7 1992 The K+ ATP channel-independent, glucose-induced insulin release shows gradually increasing monophasic pattern which temporally resembles the second phase response of glucose-induced insulin release. Glucose 166-173 insulin Homo sapiens 182-189 1486908-1 1992 Hypertension, dyslipidaemia, glucose intolerance (associated with insulin resistance and compensatory hyperinsulinaemia) and other abnormalities are complementary coronary risk factors which often occur in association. Glucose 29-36 insulin Homo sapiens 66-73 1451969-8 1992 The long-term dextrose infusion was associated with a sustained increase, and both short-term dextrose infusions were associated with peaks in glucose, insulin, and gastric inhibitory polypeptide levels. Glucose 94-102 insulin Homo sapiens 152-159 1459257-8 1992 MAIN OUTCOME MEASURES: Pancreatic insulin secretion in response to hyperglycemia and insulin action as assessed by insulin-mediated glucose utilization using the euglycemic, hyperinsulinemic clamp technique. Glucose 132-139 insulin Homo sapiens 34-41 1459257-8 1992 MAIN OUTCOME MEASURES: Pancreatic insulin secretion in response to hyperglycemia and insulin action as assessed by insulin-mediated glucose utilization using the euglycemic, hyperinsulinemic clamp technique. Glucose 132-139 insulin Homo sapiens 85-92 1459257-10 1992 Glucose-stimulated insulin release was negatively correlated with serum T and free T throughout the normal range of these hormones. Glucose 0-7 insulin Homo sapiens 19-26 1338387-9 1992 Likewise, only the individuals with the most outspoken hepatic insulin resistance demonstrated a decrease in insulin level, at which hepatic glucose production (HGP) is completely suppressed (HGP0) (P < 0.01). Glucose 141-148 insulin Homo sapiens 63-70 1464641-4 1992 Plasma insulin concentrations were elevated in hypercholesterolemic patients vs. controls both in the fasting state (86 +/- 6 vs. 59 +/- 8 pmol/L) and 2 h after a 75-g oral glucose load (412 +/- 16 vs. 276 +/- 18 pmol/L, P < 0.02 for both). Glucose 173-180 insulin Homo sapiens 7-14 1469091-0 1992 Insulin sensitivity of protein and glucose metabolism in human forearm skeletal muscle. Glucose 35-42 insulin Homo sapiens 0-7 1469091-5 1992 Compared to saline, increasing rates of insulin infusion progressively increased net forearm glucose uptake from 0.9 mumol/min per 100 ml (saline) to 1.0, 1.8, 2.4, and 4.7 mumol/min per 100 ml forearm, respectively. Glucose 93-100 insulin Homo sapiens 40-47 1469091-11 1992 Further increments of insulin within the physiologic range augment glucose uptake but have little additional effect on phenylalanine R(a) or balance. Glucose 67-74 insulin Homo sapiens 22-29 1469091-12 1992 These results suggest that proteolysis in human skeletal muscle is more sensitive than glucose uptake to physiologic increments in insulin. Glucose 87-94 insulin Homo sapiens 131-138 1461136-4 1992 A highly reduced tissue insulin sensitivity (2.4 +/- 0.5 v 9.5 +/- 1.5 10(4).min-1/[microU/mL], P > .0005) and glucose effectiveness, ie, glucose"s ability to stimulate its own disappearance at basal insulin (16 +/- 2 v 30 +/- 3 10(3).min-1, P > .005), were found in the overweight subjects compared with the controls. Glucose 141-148 insulin Homo sapiens 24-31 1369592-2 1992 Nature and/or degree of this response to glucose was influenced by some effect, long-lived in vitro, which was correlatable to serum insulin levels. Glucose 41-48 insulin Homo sapiens 133-140 1369592-6 1992 We conclude (1) that modulation of glucose levels in vitro regulates prolactin release from pituitary mammotrophs and (2) that this glucose regulation of prolactin release is in turn coregulated with or regulated by insulin. Glucose 35-42 insulin Homo sapiens 216-223 1369592-6 1992 We conclude (1) that modulation of glucose levels in vitro regulates prolactin release from pituitary mammotrophs and (2) that this glucose regulation of prolactin release is in turn coregulated with or regulated by insulin. Glucose 132-139 insulin Homo sapiens 216-223 1494399-8 1992 Despite this difference in initial glucose concentration, normalization of plasma glucose to less than 5 mmol/l with insulin resulted in the same decrease in nitrogen excretion and improvement in glucose oxidation. Glucose 82-89 insulin Homo sapiens 117-124 1494399-8 1992 Despite this difference in initial glucose concentration, normalization of plasma glucose to less than 5 mmol/l with insulin resulted in the same decrease in nitrogen excretion and improvement in glucose oxidation. Glucose 82-89 insulin Homo sapiens 117-124 1360036-3 1992 The early insulin response to oral glucose was impaired in affected relatives, but was normal in those unaffected. Glucose 35-42 insulin Homo sapiens 10-17 1414934-5 1992 There was a significant correlation between visceral fat and triglycerides, apoprotein B and sum of glucose and insulin during glucose oral tolerance test. Glucose 127-134 insulin Homo sapiens 112-119 1414934-6 1992 Sum of insulin during glucose oral tolerance test, visceral abdominal adipose tissue area and visceral/subcutaneous abdominal adipose tissue area ratio correlated significantly with severity of CAD, as evaluated by coronary score in all subjects and in CAD patients alone. Glucose 22-29 insulin Homo sapiens 7-14 1457085-3 1992 In addition, insulin-mediated glucose uptake was significantly greater after doxazosin treatment. Glucose 30-37 insulin Homo sapiens 13-20 1471586-0 1992 C-peptide response to oral glucose. Glucose 27-34 insulin Homo sapiens 0-9 1442986-6 1992 RESULTS: Women receiving human insulin required significantly less insulin per kilogram of body weight and showed significant dampening of glucose excursions (p < 0.05 for each comparison). Glucose 139-146 insulin Homo sapiens 31-38 1442986-9 1992 Infants born to mothers receiving human insulin had a 1 hour C-peptide level after the glucose-amino acid challenge at 3 months of age of 0.21 +/- 0.13 pmol/ml compared with 0.32 +/- 0.13 pmol/ml (p = 0.01). Glucose 87-94 insulin Homo sapiens 40-47 1443115-2 1992 Following the latter combination, there were significant increases in plasma glucose concentration [4.07 +/- 0.11 (73 +/- 2 mg/dl) to 5.00 +/- 0.22 mmol/l (90 +/- 4 mg/dl); P < 0.01] and in plasma insulin concentration [72 +/- 14 (10 +/- 2 microU/ml) to 172 +/- 36 pmol/l (24 +/- 5 microU/ml); P < 0.05]. Glucose 77-84 insulin Homo sapiens 200-207 1297601-5 1992 Insulin action was monitored by the glucose needs delivered by the artificial pancreas working in euglycemic glucose clamp mode. Glucose 36-43 insulin Homo sapiens 0-7 1297601-5 1992 Insulin action was monitored by the glucose needs delivered by the artificial pancreas working in euglycemic glucose clamp mode. Glucose 109-116 insulin Homo sapiens 0-7 1397715-7 1992 However, within the Afro-Caribbean group, subjects with plasma insulin concentrations above the median (> 52 pM) had higher mean BP and glucose and triglyceride levels compared with subjects with insulin concentrations < or = 52 pM (P < 0.001). Glucose 139-146 insulin Homo sapiens 63-70 1425430-3 1992 These cells acutely respond to insulin for glucose transport. Glucose 43-50 insulin Homo sapiens 31-38 1468279-0 1992 Analysis of early-phase insulin responses in nonobese subjects with mild glucose intolerance. Glucose 73-80 insulin Homo sapiens 24-31 1468279-7 1992 CONCLUSIONS: Impaired early-phase insulin response to glucose was associated with mild glucose intolerance, suggesting the importance of impaired insulin secretion in the development of glucose intolerance in nonobese subjects. Glucose 54-61 insulin Homo sapiens 34-41 1468279-7 1992 CONCLUSIONS: Impaired early-phase insulin response to glucose was associated with mild glucose intolerance, suggesting the importance of impaired insulin secretion in the development of glucose intolerance in nonobese subjects. Glucose 87-94 insulin Homo sapiens 34-41 1468279-7 1992 CONCLUSIONS: Impaired early-phase insulin response to glucose was associated with mild glucose intolerance, suggesting the importance of impaired insulin secretion in the development of glucose intolerance in nonobese subjects. Glucose 87-94 insulin Homo sapiens 34-41 1468301-0 1992 Interaction of insulin and exercise on glucose transport in muscle. Glucose 39-46 insulin Homo sapiens 15-22 1468301-2 1992 In muscle and adipose tissue, glucose transport is acutely regulated by such factors as insulin and exercise. Glucose 30-37 insulin Homo sapiens 88-95 1468302-4 1992 Additionally, the effects of localized (regional) muscular contractions on insulin-mediated glucose disposal in previously exercised and nonexercised muscle groups will be discussed briefly. Glucose 92-99 insulin Homo sapiens 75-82 1468307-5 1992 RESULTS: Plasma glucose, initially 9.2 +/- 0.5 mmol/L (mean +/- SE) when insulin infused and 14.0 +/- 0.8 when insulin was withdrawn, fell on exercise by 3.4 +/- 1.1 mmol/L (P < 0.05) saline, 4.0 +/- 0.8 mmol/L (P < 0.01) with betaxolol, 3.8 +/- 0.7 mmol/L (P < 0.01) with atenolol, 5.0 +/- 0.6 mmol/L (P < 0.005) with propranolol, and 1.7 +/- 1.0 mmol/L (NS) when insulin was withdrawn. Glucose 16-23 insulin Homo sapiens 73-80 1468314-1 1992 In skeletal muscle, at the level of glucose transport, insulin resistance appears to be a major alteration responsible for decreased glucose disposal rates in non-insulin-dependent (type II) diabetes mellitus. Glucose 36-43 insulin Homo sapiens 55-62 1468314-1 1992 In skeletal muscle, at the level of glucose transport, insulin resistance appears to be a major alteration responsible for decreased glucose disposal rates in non-insulin-dependent (type II) diabetes mellitus. Glucose 133-140 insulin Homo sapiens 55-62 8458196-4 1993 After intramuscular injection of NPH and Ultralente human insulin (0.1 U kg-1), the lowest plasma glucose levels occurred 1 and 7 h later, respectively; the hypoglycaemic effect lasted approximately 2 and 12 h, respectively. Glucose 98-105 insulin Homo sapiens 58-65 1426762-3 1992 With insulin stimulation, glucose transport is accelerated by translocating GLUT-4 transporters from an intracellular pool out to the T-tubule and SL membranes. Glucose 26-33 insulin Homo sapiens 5-12 1426762-14 1992 After an acute bout of exercise, glucose transport in muscle increases to the same level as with maximum insulin stimulation. Glucose 33-40 insulin Homo sapiens 105-112 1478241-4 1992 Insulin-mediated glucose utilization was more severely impaired in oIGT than in oNGT with respect to the controls (621 +/- 51 vs. 897 +/- 83 vs. 1298 +/- 55 mumol m-2 min-1, P < 0.001). Glucose 17-24 insulin Homo sapiens 0-7 1430079-1 1992 The dependency of the secretory pattern of insulin and C-peptide on either oral ingestion of the energy substrates glucose and protein or gastric distension was determined in nine healthy male subjects. Glucose 115-122 insulin Homo sapiens 43-50 1430079-8 1992 When calculated by multiple regression analysis glucose, insulin and C-peptide plasma levels increased simultaneously after the challenge with either glucose or protein, suggesting a neuronal or humoral intestinal-pancreatic regulation of pancreatic hormone secretion. Glucose 150-157 insulin Homo sapiens 57-64 1430079-8 1992 When calculated by multiple regression analysis glucose, insulin and C-peptide plasma levels increased simultaneously after the challenge with either glucose or protein, suggesting a neuronal or humoral intestinal-pancreatic regulation of pancreatic hormone secretion. Glucose 150-157 insulin Homo sapiens 69-78 1430079-1 1992 The dependency of the secretory pattern of insulin and C-peptide on either oral ingestion of the energy substrates glucose and protein or gastric distension was determined in nine healthy male subjects. Glucose 115-122 insulin Homo sapiens 55-64 1430079-3 1992 After stimulation with oral glucose and protein, baseline insulin, C-peptide, and glucose levels increased in parallel, forming two or three large increases (macropulses), with a mean duration of 63.8 min. Glucose 28-35 insulin Homo sapiens 58-65 1430089-6 1992 Percentage elevation of glucose disposal was significantly increased during the insulin infusions compared to proinsulin; (I1) 132 +/- 12 (P1) 78 +/- 4 p < 0.01; (I2) 157 +/- 18 (P2) 104 +/- 14; P < 0.05; (I3) 242 +/- 23 (P3) 159 +/- 24 p = 0.02. Glucose 24-31 insulin Homo sapiens 80-87 1430089-7 1992 Dose response curve analysis demonstrated that proinsulin stimulated glucose disposal approximately or equal to 3.7% whereas suppression of HGP was congruent to 5.7% compared to insulin. Glucose 69-76 insulin Homo sapiens 47-57 1430079-3 1992 After stimulation with oral glucose and protein, baseline insulin, C-peptide, and glucose levels increased in parallel, forming two or three large increases (macropulses), with a mean duration of 63.8 min. Glucose 28-35 insulin Homo sapiens 67-76 1430089-7 1992 Dose response curve analysis demonstrated that proinsulin stimulated glucose disposal approximately or equal to 3.7% whereas suppression of HGP was congruent to 5.7% compared to insulin. Glucose 69-76 insulin Homo sapiens 50-57 1494868-2 1992 In the absolute majority of patients with IHD, as apparent from the IRI and C-peptide response after a glucose load, hyperinsulinism is present. Glucose 103-110 insulin Homo sapiens 76-85 1287226-7 1992 Studies of glucose, growth hormone, cortisol, and insulin secretion following an oral glucose load in well-nourished cancer patients are consistent with insulin resistance but no other hormonal abnormalities. Glucose 86-93 insulin Homo sapiens 50-57 1435293-0 1992 An apparently anomalous relationship between insulin and C-peptide concentrations in their initial response to intravenous glucose. Glucose 123-130 insulin Homo sapiens 45-52 1435293-0 1992 An apparently anomalous relationship between insulin and C-peptide concentrations in their initial response to intravenous glucose. Glucose 123-130 insulin Homo sapiens 57-66 1435293-2 1992 It was found that in 4% of men and 12% of women the plasma concentration of insulin exceeded that of C-peptide during the initial response to glucose. Glucose 142-149 insulin Homo sapiens 76-83 1435293-2 1992 It was found that in 4% of men and 12% of women the plasma concentration of insulin exceeded that of C-peptide during the initial response to glucose. Glucose 142-149 insulin Homo sapiens 101-110 1448045-7 1992 Moreover, plasma insulin and blood sugar in response to oral glucose test were significantly higher in patients with postgastrectomy fatty liver, compared to those in patients without fatty liver. Glucose 61-68 insulin Homo sapiens 17-24 1455155-2 1992 Insulin and C-peptide responses to 0.5 g kg-1 intravenous glucose and 1.0 mg glucagon were studied in 34 healthy subjects (age 19-78 years, mean 45). Glucose 58-65 insulin Homo sapiens 12-21 1455155-4 1992 However, the C-peptide response at 70 min (r = 0.36; p < 0.05), 80 min (r = 0.41; p < 0.05), and 90 min (r = 0.46; p < 0.01) after the glucose infusion correlated with age as well as both insulin (r = 0.42; p < 0.05) and C-peptide (r = 0.45; p < 0.05) responses to the glucagon injection. Glucose 144-151 insulin Homo sapiens 13-22 1399128-9 1992 However, the relative increase of C-peptide, C-peptide to glucose or C-peptide to fructosamine in cases was independent of BMI or WHR. Glucose 58-65 insulin Homo sapiens 45-54 1399128-9 1992 However, the relative increase of C-peptide, C-peptide to glucose or C-peptide to fructosamine in cases was independent of BMI or WHR. Glucose 58-65 insulin Homo sapiens 45-54 1470614-7 1992 The implantable artificial pancreas is still awaiting the development of long-term reliable glucose sensors, but one of its elements, the implantable insulin pump, is already operational; its safety and reliability have now been proven; its effectiveness seems to result from a better stabilization of blood glucose level variations; it will not supersede conventional injections, but it is the only alternative for patients with poor glycaemia control and notably for those at high risk of hypoglycaemia. Glucose 308-315 insulin Homo sapiens 150-157 1357346-9 1992 The development of type 2 diabetes is preceded by and predicted by defects in both insulin-dependent and insulin-independent glucose uptake; the defects are detectable when the patients are normoglycaemic and in most cases more than a decade before diagnosis of disease. Glucose 125-132 insulin Homo sapiens 105-112 1408088-2 1992 Even the most careful exogenous insulin administration can neither maintain an entirely physiological glucose metabolism nor prevent the development of the late complications. Glucose 102-109 insulin Homo sapiens 32-39 1449046-5 1992 Despite this, repeated acute Acipimox administration after the three months" treatment period enhanced total insulin-stimulated glucose disposal to the same extent as acute Acipimox administration before the treatment period (367 +/- 59 vs 392 +/- 66 mg.m-2.min-1, NS; both p < 0.05 vs placebo glucose disposal) (267 +/- 44 mg.m-2.min-1). Glucose 128-135 insulin Homo sapiens 109-116 1449046-6 1992 In conclusion, insulin resistance or tachyphylaxis towards the effects of Acipimox on insulin stimulated glucose disposal was not induced during prolonged Acipimox treatment. Glucose 105-112 insulin Homo sapiens 15-22 1449046-6 1992 In conclusion, insulin resistance or tachyphylaxis towards the effects of Acipimox on insulin stimulated glucose disposal was not induced during prolonged Acipimox treatment. Glucose 105-112 insulin Homo sapiens 86-93 1415425-1 1992 OBJECTIVE: The purpose of this study was to evaluate basal endogenous glucose production and suppression during insulin infusion in normal pregnant women. Glucose 70-77 insulin Homo sapiens 112-119 1415425-8 1992 During insulin infusion endogenous glucose production was almost completely suppressed (i.e., > 90%) throughout gestation. Glucose 35-42 insulin Homo sapiens 7-14 1415425-10 1992 However, endogenous glucose production remains sensitive to insulin infusion throughout gestation. Glucose 20-27 insulin Homo sapiens 60-67 1415443-8 1992 Studies have demonstrated insulin resistance, rises in plasma insulin, and relative glucose intolerance by means of curve analysis of glucose tolerance tests. Glucose 134-141 insulin Homo sapiens 26-33 1415700-4 1992 Although the rates of insulin-stimulated total glucose disposal and nonoxidative glucose metabolism were similar in females and males, nonoxidative glucose metabolism expressed per kilogram body weight (r = -0.64; P < 0.01) or per kilogram LBM (r = -0.46; P < 0.05) was inversely correlated with age only in males. Glucose 47-54 insulin Homo sapiens 22-29 1418831-4 1992 Furthermore, the steady state plasma glucose concentration during a constant infusion of glucose, insulin and somatostatin was significantly greater in subjects with a family history of hypertension (8.1 +/- 0.6 v 6.2 +/- 0.6 mmol/L, P < .001). Glucose 37-44 insulin Homo sapiens 98-105 1450470-3 1992 The original goal of developing a totally artificial beta-cell remains unrealized, but programmable insulin pumps that contain all of the elements of the artificial beta-cell except the glucose sensor are involved in clinical trials in the United States and are commercially available in Europe. Glucose 186-193 insulin Homo sapiens 100-107 1384465-2 1992 Treatment of pancreatic islets with interleukin 1 (IL-1) results in a time-dependent inhibition of glucose-stimulated insulin secretion which has recently been demonstrated to be dependent on the metabolism of L-arginine to nitric oxide. Glucose 99-106 insulin Homo sapiens 118-125 1384465-13 1992 These results show that IL-1 beta-induced nitric oxide formation parallels the ability of IL-1 beta to inhibit glucose-stimulated insulin secretion by islets, and that protein synthesis is required for IL-1 beta-induced nitric oxide formation. Glucose 111-118 insulin Homo sapiens 130-137 1330412-0 1992 Ageing and the response of plasma insulin, glucose and C-peptide concentrations to intravenous glucose in postmenopausal women. Glucose 95-102 insulin Homo sapiens 34-41 1330412-0 1992 Ageing and the response of plasma insulin, glucose and C-peptide concentrations to intravenous glucose in postmenopausal women. Glucose 95-102 insulin Homo sapiens 55-64 1338040-0 1992 The bioactivity of insulin analogues from in vitro receptor binding to in vivo glucose uptake. Glucose 79-86 insulin Homo sapiens 19-26 1341460-14 1992 In the other treatment groups, plasma insulin decreased or glucose disappearance rate increased in clamp measurements, suggesting improved insulin sensitivity. Glucose 59-66 insulin Homo sapiens 139-146 1397698-3 1992 PCO resulted in significant increases in the ED50 insulin for glucose utilization in vivo (P less than 0.001) and in adipocytes (P less than 0.01), without significant changes in adipocyte insulin-binding sites. Glucose 62-69 insulin Homo sapiens 50-57 1397698-4 1992 PCO also resulted in significant decreases in maximal insulin-stimulated rates of glucose utilization in vivo (P less than 0.01) and in adipocytes (P less than 0.01). Glucose 82-89 insulin Homo sapiens 54-61 1397712-12 1992 Further studies are needed to define its overall contribution to fructose and glucose transport in insulin-responsive tissues and brain. Glucose 78-85 insulin Homo sapiens 99-106 1425092-5 1992 During carefully monitored follow-up, 9 patients relapsed into a hyperglycemic state, and insulin action was restudied after acute reregulation of their plasma glucose. Glucose 160-167 insulin Homo sapiens 90-97 1425092-8 1992 A plot of frequency versus glucose disposal in those patients was compatible with a bimodal distribution (P less than 0.025): 12 of 22 patients were normally insulin sensitive (glucose disposal 6.1-9.4 mg.kg-1.min-1), and 10 were insulin resistant (glucose disposal 2.4-4.8 mg.kg-1.min-1). Glucose 177-184 insulin Homo sapiens 158-165 1425092-8 1992 A plot of frequency versus glucose disposal in those patients was compatible with a bimodal distribution (P less than 0.025): 12 of 22 patients were normally insulin sensitive (glucose disposal 6.1-9.4 mg.kg-1.min-1), and 10 were insulin resistant (glucose disposal 2.4-4.8 mg.kg-1.min-1). Glucose 177-184 insulin Homo sapiens 158-165 1425092-9 1992 Analysis of this midrange BMI group showed that in the insulin-sensitive group, an inverse relationship existed between BMI and glucose disposal (r = -0.64, P less than 0.05), whereas no such relationship was found in the insulin-resistant group. Glucose 128-135 insulin Homo sapiens 55-62 1425099-16 1992 CONCLUSIONS: The data suggest that two forms of NIDDM may exist, crudely distinguished by the clinical decision to use insulin to control blood glucose levels. Glucose 144-151 insulin Homo sapiens 119-126 1446577-7 1992 This was particularly demonstrated by four patients with apparently normal glucose tolerance by WHO criteria who subsequently required insulin therapy. Glucose 75-82 insulin Homo sapiens 135-142 1451954-4 1992 The basal rate of hepatic glucose production was higher in Type 2 diabetic patients than in control subjects (1044.0 +/- 29.9 vs 789.3 +/- 41.7 mumol/min; p less than 0.001) and decreased after insulin therapy (p less than 0.01). Glucose 26-33 insulin Homo sapiens 194-201 1478183-2 1992 The insulin dose-response curves of the glucose metabolic clearance rates (MCR) were shifted to the right and downward both in patients with LC and NIDDM, indicating a reduced sensitivity and responsiveness to insulin. Glucose 40-47 insulin Homo sapiens 4-11 1478183-2 1992 The insulin dose-response curves of the glucose metabolic clearance rates (MCR) were shifted to the right and downward both in patients with LC and NIDDM, indicating a reduced sensitivity and responsiveness to insulin. Glucose 40-47 insulin Homo sapiens 210-217 1526327-8 1992 insulin therapy is capable of maintaining near normal plasma glucose levels while reducing the peripheral hyperinsulinemia. Glucose 61-68 insulin Homo sapiens 0-7 1398891-7 1992 Plasma insulin level at 90 minutes during the glucose load was significantly higher in subjects with PFH. Glucose 46-53 insulin Homo sapiens 7-14 1398891-8 1992 In multivariate analysis, WHR was significantly related to baseline blood pressure, insulin, and cholesterol, whereas BMI was significantly associated with the insulin response to the oral glucose tolerance test. Glucose 189-196 insulin Homo sapiens 160-167 1483772-2 1992 Although the cold-induced enhancements in carbohydrate metabolism have been the focus of numerous studies, it was only recently that pieces of evidence from animal studies have suggested that cold exposure exerts an insulin-like effect on peripheral tissue glucose uptake, which appears to proceed primarily via insulin-independent pathways. Glucose 257-264 insulin Homo sapiens 216-223 1483772-2 1992 Although the cold-induced enhancements in carbohydrate metabolism have been the focus of numerous studies, it was only recently that pieces of evidence from animal studies have suggested that cold exposure exerts an insulin-like effect on peripheral tissue glucose uptake, which appears to proceed primarily via insulin-independent pathways. Glucose 257-264 insulin Homo sapiens 312-319 1450370-4 1992 Plasma insulin concentration was determined during an oral glucose tolerance test (OGTT). Glucose 59-66 insulin Homo sapiens 7-14 1457761-5 1992 Whole-body glucose utilization during euglycemic hyperinsulinemic clamp (40 mU/m2/min insulin infusion) was calculated by tracer dilution techniques (6,6 2H2 glucose tracer continuous infusion) and was significantly lower in hypertensives with microalbuminuria than in those without (H2 versus H1 versus controls: 3.41 +/- 0.51 versus 6.52 +/- 0.62 versus 7.03 +/- 0.48 mg/kg/min; mean +/- SE). Glucose 11-18 insulin Homo sapiens 54-61 1384762-0 1992 Prebypass glucose-insulin-potassium infusion in elective nondiabetic coronary artery surgery patients. Glucose 10-17 insulin Homo sapiens 18-25 1400874-2 1992 Since the response of the liver to insulin-induced hypoglycemia normally involves activation of gluconeogenesis, we measured [14C]alanine conversion to [14C]glucose (a qualitative index of gluconeogenesis) and glucose production (using [3-3H]glucose) in seven intensively treated type I diabetic subjects (hemoglobin-A1, 7.1 +/- 0.4%) during low dose infusion of insulin (0.3 mU/kg.min for 210 min). Glucose 157-164 insulin Homo sapiens 35-42 1400882-5 1992 Furthermore, in older and young men with normal OGTT matched for WHR, percent fat, or VO2max, glucose disposal was comparable at sequential 15-min intervals during the clamp and in its relationship to insulin concentrations at the tissue level (multicompartmental analysis). Glucose 94-101 insulin Homo sapiens 201-208 1401063-4 1992 However, islets cultured at 11 or 28 mM glucose showed a 45 or 60% decrease in insulin content, as compared to islets cultured at 5.6 mM glucose. Glucose 40-47 insulin Homo sapiens 79-86 1401063-5 1992 Moreover, when such islets were submitted to a 60-min stimulation with a low (1.7 mM) followed by a high (16.7 mM) concentration of glucose, the islets cultured at 5.6 mM glucose showed a higher insulin response to glucose than those of the two other groups. Glucose 132-139 insulin Homo sapiens 195-202 1401063-5 1992 Moreover, when such islets were submitted to a 60-min stimulation with a low (1.7 mM) followed by a high (16.7 mM) concentration of glucose, the islets cultured at 5.6 mM glucose showed a higher insulin response to glucose than those of the two other groups. Glucose 171-178 insulin Homo sapiens 195-202 1401063-5 1992 Moreover, when such islets were submitted to a 60-min stimulation with a low (1.7 mM) followed by a high (16.7 mM) concentration of glucose, the islets cultured at 5.6 mM glucose showed a higher insulin response to glucose than those of the two other groups. Glucose 171-178 insulin Homo sapiens 195-202 1401063-6 1992 Islets cultured at the two higher glucose concentrations showed increased rates of insulin release in the presence of low glucose, and a failure to enhance further the release in response to an elevated glucose level. Glucose 34-41 insulin Homo sapiens 83-90 1401063-6 1992 Islets cultured at the two higher glucose concentrations showed increased rates of insulin release in the presence of low glucose, and a failure to enhance further the release in response to an elevated glucose level. Glucose 122-129 insulin Homo sapiens 83-90 1401063-6 1992 Islets cultured at the two higher glucose concentrations showed increased rates of insulin release in the presence of low glucose, and a failure to enhance further the release in response to an elevated glucose level. Glucose 122-129 insulin Homo sapiens 83-90 1401063-7 1992 Islets cultured at 28 mM glucose showed an absolute decrease in insulin release after stimulation with 16.7 mM glucose, as compared to islets cultured at 5.6 mM glucose. Glucose 25-32 insulin Homo sapiens 64-71 1401063-7 1992 Islets cultured at 28 mM glucose showed an absolute decrease in insulin release after stimulation with 16.7 mM glucose, as compared to islets cultured at 5.6 mM glucose. Glucose 111-118 insulin Homo sapiens 64-71 1401063-7 1992 Islets cultured at 28 mM glucose showed an absolute decrease in insulin release after stimulation with 16.7 mM glucose, as compared to islets cultured at 5.6 mM glucose. Glucose 111-118 insulin Homo sapiens 64-71 1464889-0 1992 Association between insulin and blood pressure in a community population with normal glucose tolerance. Glucose 85-92 insulin Homo sapiens 20-27 1464889-1 1992 The purpose of this study was to examine the relationship between insulin and BP in patients with normal glucose tolerance. Glucose 105-112 insulin Homo sapiens 66-73 1406301-7 1992 When either protein was ingested with glucose, the insulin area response was greater than the sum of the individual responses, indicating a synergistic effect (glucose alone, 732 pmol/L.h; glucose with cottage cheese, 1,637 pmol/L.h; glucose with egg white, 1,213 pmol/L.h). Glucose 38-45 insulin Homo sapiens 51-58 1449039-6 1992 Total glucose uptake was impaired in the insulin-resistant subjects with impaired first-phase insulin secretion compared to controls (18.8 (13.2-22.2) vs 34.8 (24.3-62.1) mumol.kg-1 x min-1; p < 0.01). Glucose 6-13 insulin Homo sapiens 41-48 1449039-6 1992 Total glucose uptake was impaired in the insulin-resistant subjects with impaired first-phase insulin secretion compared to controls (18.8 (13.2-22.2) vs 34.8 (24.3-62.1) mumol.kg-1 x min-1; p < 0.01). Glucose 6-13 insulin Homo sapiens 94-101 1406297-2 1992 The aim of this study was to determine whether impaired intracellular glucose metabolism contributes to insulin resistance in the elderly independent of reduced glucose uptake. Glucose 70-77 insulin Homo sapiens 104-111 1455507-5 1992 This interaction gives beta-cells the ability to match the ambient concentration of glucose to an appropriate insulin secretory response, a process we refer to as the induction of glucose competence. Glucose 84-91 insulin Homo sapiens 110-117 1455507-5 1992 This interaction gives beta-cells the ability to match the ambient concentration of glucose to an appropriate insulin secretory response, a process we refer to as the induction of glucose competence. Glucose 180-187 insulin Homo sapiens 110-117 1332021-2 1992 A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension. Glucose 79-86 insulin Homo sapiens 14-21 1332021-2 1992 A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension. Glucose 127-134 insulin Homo sapiens 14-21 1332021-14 1992 In favor of this hypothesis are the observations that insulin resistance segregates in familial clusters and that the first defect found in normoglycemic relatives of insulin-resistant diabetic patients is a reduced transformation of glucose into glycogen. Glucose 234-241 insulin Homo sapiens 167-174 1332021-15 1992 Whatever is the primary defect, it is likely that a correction of insulin resistance might reduce the circulating levels of plasma insulin, possibly playing a beneficial effect on glucose tolerance, body weight, blood pressure and plasma lipid concentration. Glucose 180-187 insulin Homo sapiens 66-73 1332021-15 1992 Whatever is the primary defect, it is likely that a correction of insulin resistance might reduce the circulating levels of plasma insulin, possibly playing a beneficial effect on glucose tolerance, body weight, blood pressure and plasma lipid concentration. Glucose 180-187 insulin Homo sapiens 131-138 1438099-14 1992 This is probably related to the presence of other metabolic risk factors associated with insulin resistance: hyperinsulinemia, glucose intolerance, hypertriglyceridemia, decreased HDL cholesterol. Glucose 127-134 insulin Homo sapiens 89-96 1438100-7 1992 Can insulin resistance, characterized by a raised circulating insulin concentration in the presence of normal blood glucose, be responsible for certain "modifications" associated with essential hypertension? Glucose 116-123 insulin Homo sapiens 4-11 1438102-5 1992 Glucocorticoids and fatty acids (which are produced in response to stress) antagonise the actions of insulin in promoting glucose uptake and protein synthesis, in decreasing gluconeogenesis and protein catabolism, and promoting the clearance of intermediate density lipoprotein and low density lipoprotein from the circulation by the liver. Glucose 122-129 insulin Homo sapiens 101-108 1438104-10 1992 During the insulin clamp study, insulin-mediated glucose disposal increased after benfluorex (5.7 +/- 0.3 vs 4.8 +/- 0.2 mg/kg/min; P < 0.01). Glucose 49-56 insulin Homo sapiens 11-18 1438104-10 1992 During the insulin clamp study, insulin-mediated glucose disposal increased after benfluorex (5.7 +/- 0.3 vs 4.8 +/- 0.2 mg/kg/min; P < 0.01). Glucose 49-56 insulin Homo sapiens 32-39 1476155-5 1992 Oral glucose tolerance testing resulted in a prompt 10-fold increase in serum insulin accompanied by a mildly symptomatic and gradual fall in serum glucose to 30 mg/dl 90 minutes after glucose ingestion. Glucose 5-12 insulin Homo sapiens 78-85 1476155-6 1992 An intravenous glucose challenge caused an acute increase in serum insulin to more than 1200 microU/ml with a resulting serum glucose of 11 mg/dl 25 minutes later, associated with loss of consciousness. Glucose 15-22 insulin Homo sapiens 67-74 1476155-6 1992 An intravenous glucose challenge caused an acute increase in serum insulin to more than 1200 microU/ml with a resulting serum glucose of 11 mg/dl 25 minutes later, associated with loss of consciousness. Glucose 126-133 insulin Homo sapiens 67-74 1530038-7 1992 It was not possible to identify any cluster of women, obese or otherwise, in whom poor glucose tolerance was specifically associated with an unusually high insulin response. Glucose 87-94 insulin Homo sapiens 156-163 1415522-4 1992 In controls and diabetics, insulin infusion with a simultaneous increase in the plasma GSH/GSSG ratio significantly enhanced nonoxidative glucose disposal without affecting oxidative glucose metabolism. Glucose 138-145 insulin Homo sapiens 27-34 1323492-4 1992 In response to the glucose infusion, plasma glucose rose higher in the diabetic subjects (mean +/- 1 SD: 13.7 +/- 3.1 and 9.6 +/- 0.9 mM, P = 0.007) and plasma insulin was impaired in the diabetic compared with the nondiabetic subjects (geometric mean (1 SD range): 14 (8-26) and 34 (18-63), P less than 0.01). Glucose 19-26 insulin Homo sapiens 160-167 1323492-4 1992 In response to the glucose infusion, plasma glucose rose higher in the diabetic subjects (mean +/- 1 SD: 13.7 +/- 3.1 and 9.6 +/- 0.9 mM, P = 0.007) and plasma insulin was impaired in the diabetic compared with the nondiabetic subjects (geometric mean (1 SD range): 14 (8-26) and 34 (18-63), P less than 0.01). Glucose 44-51 insulin Homo sapiens 160-167 1425160-7 1992 Insulin therapy, while correcting the hormone deficiency and restoring glucose and protein metabolism, seems to activate the synthesis of type III procollagen in patients with NIDDM. Glucose 71-78 insulin Homo sapiens 0-7 1425156-6 1992 During 2 mg/kg.min glucose infusion, mean serum insulin and C-peptide rose to significantly (P less than 0.05-0.02) greater levels in the offspring vs. controls, while serum glucose levels were similar. Glucose 19-26 insulin Homo sapiens 48-55 1425156-6 1992 During 2 mg/kg.min glucose infusion, mean serum insulin and C-peptide rose to significantly (P less than 0.05-0.02) greater levels in the offspring vs. controls, while serum glucose levels were similar. Glucose 19-26 insulin Homo sapiens 60-69 1425156-7 1992 With the 4 mg/kg.min glucose infusion, mean serum glucose, insulin and C-peptide levels were significantly (P less than 0.02-0.001) greater in the offspring at 100-120 min. Glucose 21-28 insulin Homo sapiens 59-66 1425156-7 1992 With the 4 mg/kg.min glucose infusion, mean serum glucose, insulin and C-peptide levels were significantly (P less than 0.02-0.001) greater in the offspring at 100-120 min. Glucose 21-28 insulin Homo sapiens 71-80 1499856-6 1992 We conclude that intraportal administration of insulin via the umbilical vein at rates of 0.01-0.05 U.kg-1.hr-1 reduces plasma levels of glucose, three carbon precursors, cortisol, and growth hormone by a direct action on the liver, and the hepatic action of peripherally administered insulin is manifested only when the infusion rate is increased to 0.1-0.3 U.kg-1.hr-1. Glucose 137-144 insulin Homo sapiens 47-54 1499861-1 1992 Patients with non-insulin-dependent diabetes mellitus (NIDDM) exhibit decreased rates of skeletal muscle insulin-mediated glucose uptake (IMGU). Glucose 122-129 insulin Homo sapiens 18-25 1499866-7 1992 However, both WHR and VSR were related inversely to total, oxidative, and nonoxidative glucose disposal rates during the insulin clamp. Glucose 87-94 insulin Homo sapiens 121-128 1341607-0 1992 Insulin effects on glucose kinetics in non-insulin-dependent diabetic patients with secondary failure to hypoglycaemic agents: role of different modes and rates of delivery. Glucose 19-26 insulin Homo sapiens 0-7 1341607-1 1992 OBJECTIVES: This study aimed at investigating the effects of pulsatile and continuous insulin delivery on glucose kinetics in non-insulin-dependent (type 2) diabetic patients with secondary failure to oral hypoglycaemic agents. Glucose 106-113 insulin Homo sapiens 86-93 1341607-8 1992 RESULTS: Infusion of identical amounts of insulin (A vs C) demonstrated that pulsatile insulin delivery exerted greater metabolic effects (higher glucose infusion rate and, mainly at the beginning of the experiment, lower endogenous glucose production) than continuous infusion; furthermore pulsatile insulin delivery (C) exerted metabolic effects similar to those of a greater dose of insulin (B) infused continuously. Glucose 146-153 insulin Homo sapiens 87-94 1341607-8 1992 RESULTS: Infusion of identical amounts of insulin (A vs C) demonstrated that pulsatile insulin delivery exerted greater metabolic effects (higher glucose infusion rate and, mainly at the beginning of the experiment, lower endogenous glucose production) than continuous infusion; furthermore pulsatile insulin delivery (C) exerted metabolic effects similar to those of a greater dose of insulin (B) infused continuously. Glucose 233-240 insulin Homo sapiens 87-94 1459175-0 1992 Insulin sensitivity and secretion in healthy elderly human subjects with "abnormal" glucose tolerance. Glucose 84-91 insulin Homo sapiens 0-7 1477295-4 1992 Islet cultured with 1 g/l (5.5 mmol/l) glucose maintained normal insulin- secretion and morphology for more than two months. Glucose 39-46 insulin Homo sapiens 65-72 1521640-7 1992 Serum LH response to gonadotropin-releasing hormone (GnRH) administration and assessment of insulin resistance by the continuous infusion of glucose with model assessment (CIGMA) test. Glucose 141-148 insulin Homo sapiens 92-99 1363384-4 1992 A steady state plasma glucose (SSPG) concentration achieved during the last 30 minutes of infusion represented the measurement of insulin sensitivity. Glucose 22-29 insulin Homo sapiens 130-137 1328367-9 1992 However, plasma insulin and plasma-C-peptide decreased both in the fasting state and after 1 and 2 h of oral glucose tolerance testing. Glucose 109-116 insulin Homo sapiens 16-23 1402624-1 1992 In order to evaluate the relationship between peripheral white blood cell (WBC) count, insulin-mediated glucose uptake, and several risk factors for coronary heart disease (CHD), WBC, plasma glucose and insulin responses to a 75-g oral glucose challenge, fasting plasma cholesterol, high-density-lipoprotein (HDL)-cholesterol, and triglyceride concentration, and systolic and diastolic blood pressure were determined in 63 consecutive female volunteers with normal glucose tolerance. Glucose 104-111 insulin Homo sapiens 87-94 1402624-2 1992 The results demonstrated the presence of statistically significant correlation coefficients between WBC count and both insulin-mediated glucose disposal (r = 0.50, P less than 0.001) and insulin response to oral glucose (r = 0.50, P less than 0.001). Glucose 136-143 insulin Homo sapiens 119-126 1402624-2 1992 The results demonstrated the presence of statistically significant correlation coefficients between WBC count and both insulin-mediated glucose disposal (r = 0.50, P less than 0.001) and insulin response to oral glucose (r = 0.50, P less than 0.001). Glucose 212-219 insulin Homo sapiens 187-194 1406302-0 1992 Epinephrine directly antagonizes insulin-mediated activation of glucose uptake and inhibition of free fatty acid release in forearm tissues. Glucose 64-71 insulin Homo sapiens 33-40 1406302-4 1992 Forearm glucose uptake (FGU) increased in response to insulin alone from 0.8 +/- 0.2 mg.L-1.min-1 to 4.3 +/- 0.8. Glucose 8-15 insulin Homo sapiens 54-61 1406302-9 1992 The data demonstrate that epinephrine is able to antagonize directly insulin action on forearm tissues with respect to both stimulation of glucose uptake and inhibition of FFA mobilization. Glucose 139-146 insulin Homo sapiens 69-76 1361659-5 1992 The studies on insulin metabolism preoperatively determined by oral glucose tolerance test and postoperative control of DM revealed that diabetic patients with hepatectomy, especially hepatogenous DM, had a significantly reduced insulin uptake in the liver and exogenous insulin resistance to glucose. Glucose 68-75 insulin Homo sapiens 15-22 1433778-10 1992 Because the postprandial glucose oxidation rate was normal, the low insulin-mediated glucose uptake observed in cirrhotic patients seems to reflect a defect in the nonoxidative disposal of the glucose ingested. Glucose 85-92 insulin Homo sapiens 68-75 1433778-10 1992 Because the postprandial glucose oxidation rate was normal, the low insulin-mediated glucose uptake observed in cirrhotic patients seems to reflect a defect in the nonoxidative disposal of the glucose ingested. Glucose 85-92 insulin Homo sapiens 68-75 1361659-5 1992 The studies on insulin metabolism preoperatively determined by oral glucose tolerance test and postoperative control of DM revealed that diabetic patients with hepatectomy, especially hepatogenous DM, had a significantly reduced insulin uptake in the liver and exogenous insulin resistance to glucose. Glucose 293-300 insulin Homo sapiens 15-22 1330242-1 1992 To examine the release of insulin in response to oral glucose, intravenous glucagon and intravenous arginine, we measured the levels of plasma glucose, immuno-reactive insulin (IRI) and C-peptide levels on fasting and following an oral glucose loading (OGTT), intravenous glucagon (GON) and arginine (ARG) infusion test in nine newly diagnosed non-insulin dependent diabetics. Glucose 54-61 insulin Homo sapiens 26-33 1518704-8 1992 Furthermore, insulin levels remained significantly elevated in the obese subjects compared with the nonobese subjects throughout the glucose tolerance test (118 +/- 19 vs 49 +/- 6 microU/mL, obese vs nonobese subjects at 1-hour post-glucose tolerance test). Glucose 133-140 insulin Homo sapiens 13-20 1518704-8 1992 Furthermore, insulin levels remained significantly elevated in the obese subjects compared with the nonobese subjects throughout the glucose tolerance test (118 +/- 19 vs 49 +/- 6 microU/mL, obese vs nonobese subjects at 1-hour post-glucose tolerance test). Glucose 233-240 insulin Homo sapiens 13-20 1519166-5 1992 Insulin and glucagon levels increased in both groups; however, the rise in insulin level was greater in the glucose group, whereas glucagon increased in both groups to a similar degree. Glucose 108-115 insulin Homo sapiens 75-82 1354782-5 1992 However, beta-cell secretory response to continuous glucose stimulus during a hyperglycaemic glucose clamp was significantly reduced: mean plasma insulin values of 12 (SD 7) vs 40 (11) mU/l (p = 0.0001) and mean plasma C-peptide values 1.20 (0.30) vs 2.61 (0.37) (p = 0.0001). Glucose 52-59 insulin Homo sapiens 146-153 1354782-5 1992 However, beta-cell secretory response to continuous glucose stimulus during a hyperglycaemic glucose clamp was significantly reduced: mean plasma insulin values of 12 (SD 7) vs 40 (11) mU/l (p = 0.0001) and mean plasma C-peptide values 1.20 (0.30) vs 2.61 (0.37) (p = 0.0001). Glucose 93-100 insulin Homo sapiens 146-153 1354782-7 1992 Fasting plasma insulin and C-peptide in patients were inappropriately low in relation to concomitant plasma glucose level. Glucose 108-115 insulin Homo sapiens 15-22 1437507-5 1992 A self-regulating delivery system releasing insulin in response to glucose levels is described. Glucose 67-74 insulin Homo sapiens 44-51 1388960-5 1992 Plasma glucose and insulin responses to oral glucose and lipid concentrations were measured before, 26, and 52 weeks after starting treatment. Glucose 45-52 insulin Homo sapiens 19-26 1468314-3 1992 Muscle strips from a group of lean type II diabetic patients demonstrated a 50% decrease in insulin responsiveness for glucose transport when compared with nondiabetic subjects. Glucose 119-126 insulin Homo sapiens 92-99 1468314-6 1992 However, both regular physical exercise and insulin therapy normalized the decreased capacity for glucose transport in the diabetic rat muscles. Glucose 98-105 insulin Homo sapiens 44-51 1468314-7 1992 Therefore, it appears that regular physical exercise and, in some cases insulin therapy, would be advisable for type II diabetic patients with marked muscular insulin resistance to improve peripheral glucose disposal rates. Glucose 200-207 insulin Homo sapiens 72-79 1529656-4 1992 In NIDDM patients the rate of insulin-stimulated glucose disposal was 57% greater during hyperglycemia compared with euglycemia throughout the 4 h clamp (p less than 0.01). Glucose 49-56 insulin Homo sapiens 30-37 1514599-0 1992 Effects of epinephrine on insulin-mediated glucose uptake in whole body and leg muscle in humans: role of blood flow. Glucose 43-50 insulin Homo sapiens 26-33 1529656-9 1992 The data thus suggest that glucose metabolism in NIDDM is insulin resistant, but that the defect in insulin-stimulated glucose uptake can be overcome by increasing the glucose concentration. Glucose 27-34 insulin Homo sapiens 58-65 1529656-9 1992 The data thus suggest that glucose metabolism in NIDDM is insulin resistant, but that the defect in insulin-stimulated glucose uptake can be overcome by increasing the glucose concentration. Glucose 119-126 insulin Homo sapiens 100-107 1529656-9 1992 The data thus suggest that glucose metabolism in NIDDM is insulin resistant, but that the defect in insulin-stimulated glucose uptake can be overcome by increasing the glucose concentration. Glucose 119-126 insulin Homo sapiens 100-107 1482235-5 1992 The fasting insulin-to-glucose ratio was significantly higher in EH as compared to NT. Glucose 23-30 insulin Homo sapiens 12-19 1514599-1 1992 In vivo insulin-mediated glucose uptake (IMGU) occurs chiefly in skeletal muscle, where it is determined by the product of arteriovenous glucose difference (delta AVG) and blood flow (BF) rate into muscle. Glucose 25-32 insulin Homo sapiens 8-15 1482235-6 1992 Fasting as well as integrated serum insulin to glucose values ratio were positively correlated with heart rate (r = 0.35, p < 0.05, r = 0.38, p < 0.05) and the LV end-systolic stress to volume ratio (r = 0.48, p < 0.001, r = 0.54, p < 0.001) but not with LV mass (r = 0.02, r = 0.02) in EH. Glucose 47-54 insulin Homo sapiens 36-43 1417911-2 1992 Insulin stimulates glucose transport, glucose oxidation and lipogenesis in RPE cells. Glucose 19-26 insulin Homo sapiens 0-7 1637215-2 1992 The hemodynamic parameters measured before and after administration of the solution, after cardiopulmonary bypass, after administration of protamine, and 3 hours after leaving the operating room showed the beneficial effect of the glucose-insulin-potassium infusion on cardiac index (+23.6% after protamine infusion) and left (+16.3% 3 hours postoperatively) and right (+47.3% after cardiopulmonary bypass) ventricular workload index with a decrease in systemic vascular resistance. Glucose 231-238 insulin Homo sapiens 239-246 1637215-5 1992 Laboratory tests showed that postoperative hypoglycemia was more common in the glucose-insulin-potassium group but had no detrimental effects; it no longer occurs since we began administering the glucose infusion at 15 g/h over 8 hours. Glucose 79-86 insulin Homo sapiens 87-94 1417911-2 1992 Insulin stimulates glucose transport, glucose oxidation and lipogenesis in RPE cells. Glucose 38-45 insulin Homo sapiens 0-7 1417911-5 1992 The effects of TPA on RPE cells cannot be explained by the activation of protein kinase C. An alternative possibility is that the effects of TPA on insulin-stimulated glucose disposal in RPE cells is mediated by a change in adenosine concentration and/or the affinity/number of its receptors. Glucose 167-174 insulin Homo sapiens 148-155 1417911-3 1992 TPA at low concentrations of insulin increases the rates of glucose transport and glucose oxidation. Glucose 60-67 insulin Homo sapiens 29-36 1417911-3 1992 TPA at low concentrations of insulin increases the rates of glucose transport and glucose oxidation. Glucose 82-89 insulin Homo sapiens 29-36 1505328-7 1992 Tight plasma glucose control was achieved with an insulin regimen, and the patient delivered a healthy girl at term. Glucose 13-20 insulin Homo sapiens 50-57 1511565-1 1992 To investigate the relationship between glucose uptake and the content of the insulin regulatable glucose transporter, GLUT4, in skeletal muscle at near physiological insulin concentrations in vivo, we measured the effect of a 3h euglycemic insulin-infusion (40 mU m-2 min-1) on glucose uptake and skeletal muscle GLUT4 content in 10 healthy subjects. Glucose 40-47 insulin Homo sapiens 78-85 1511567-6 1992 Injection of magnesium insulin prior to a test breakfast in people with Type 2 diabetes resulted in significantly lower total and 0 to 120 min areas under the glucose curve, an earlier rise in exogenous insulin levels and a higher area under the insulin curve from 0 to 120 min compared with unmodified 100 U ml-1 human insulin. Glucose 159-166 insulin Homo sapiens 23-30 1511806-1 1992 Insulin resistant glucose metabolism is a key element in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus. Glucose 18-25 insulin Homo sapiens 0-7 1511565-1 1992 To investigate the relationship between glucose uptake and the content of the insulin regulatable glucose transporter, GLUT4, in skeletal muscle at near physiological insulin concentrations in vivo, we measured the effect of a 3h euglycemic insulin-infusion (40 mU m-2 min-1) on glucose uptake and skeletal muscle GLUT4 content in 10 healthy subjects. Glucose 98-105 insulin Homo sapiens 78-85 1511806-1 1992 Insulin resistant glucose metabolism is a key element in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus. Glucose 18-25 insulin Homo sapiens 89-96 1511806-6 1992 Insulin-stimulated glucose utilization improved from 110 +/- 11 to 183 +/- 23 mg.m-2.min-1 (p less than 0.03); control subjects: 219 +/- 23 mg.m-2.min-1 (p = NS, vs post-diet Type 2 diabetes). Glucose 19-26 insulin Homo sapiens 0-7 1511565-4 1992 However, when the same subjects were made insulin resistant by infusion of lipid, as evidenced by a reduction of 16 +/- 7.2% (mean +/- SE, p less than 0.05), in insulin-stimulated glucose uptake, the effect of insulin on GLUT4 content was attenuated and no change in GLUT4 content was observed. Glucose 180-187 insulin Homo sapiens 42-49 1511806-9 1992 After diet therapy the increase in insulin sensitivity correlated with reductions in fasting plasma glucose levels (r = 0.97, p less than 0.001), reductions in serum fructosamine (r = 0.77, p less than 0.05), and weight loss (r = 0.78, p less than 0.05). Glucose 100-107 insulin Homo sapiens 35-42 1511565-4 1992 However, when the same subjects were made insulin resistant by infusion of lipid, as evidenced by a reduction of 16 +/- 7.2% (mean +/- SE, p less than 0.05), in insulin-stimulated glucose uptake, the effect of insulin on GLUT4 content was attenuated and no change in GLUT4 content was observed. Glucose 180-187 insulin Homo sapiens 161-168 1511565-4 1992 However, when the same subjects were made insulin resistant by infusion of lipid, as evidenced by a reduction of 16 +/- 7.2% (mean +/- SE, p less than 0.05), in insulin-stimulated glucose uptake, the effect of insulin on GLUT4 content was attenuated and no change in GLUT4 content was observed. Glucose 180-187 insulin Homo sapiens 161-168 1511807-6 1992 In European men with normal glucose tolerance fasting insulin levels were more strongly correlated with body mass index than with waist-hip ratio. Glucose 28-35 insulin Homo sapiens 54-61 1639031-6 1992 Normal pancreases responded characteristically with a diphasic insulin release during 30-min stimulation by glucose, a response that was enhanced by subsequent forskolin. Glucose 108-115 insulin Homo sapiens 63-70 1446650-6 1992 Her parents and sister exhibited hypersecretion of insulin in response to a 75 g oral glucose tolerance test. Glucose 86-93 insulin Homo sapiens 51-58 1407245-7 1992 Furthermore, it has been shown that amylin has the potential to antagonize the action of insulin on glucose metabolism by increasing hepatic glucose production and by decreasing muscle, but not adipocyte glucose uptake. Glucose 100-107 insulin Homo sapiens 89-96 1430129-8 1992 We suggest that independent alterations in both glucose- and insulin-mediated glucose uptake occur in patients with PCOS. Glucose 78-85 insulin Homo sapiens 61-68 1639459-5 1992 On the euglycemic clamp, insulin-mediated (plasma insulin, 470 pM) whole body glucose use averaged 42.5 +/- 1.6 mumol.min-1.kg-1 before and 43.6 +/- 1.9 after ACE inhibition (p = NS). Glucose 78-85 insulin Homo sapiens 25-32 1639459-5 1992 On the euglycemic clamp, insulin-mediated (plasma insulin, 470 pM) whole body glucose use averaged 42.5 +/- 1.6 mumol.min-1.kg-1 before and 43.6 +/- 1.9 after ACE inhibition (p = NS). Glucose 78-85 insulin Homo sapiens 50-57 1639459-8 1992 The latter change was associated with enhanced (+16%, p less than 0.05) insulin responsiveness to glucose (estimated as the insulin AUC divided by the glucose AUC) throughout the 3 months of ACE inhibition. Glucose 98-105 insulin Homo sapiens 72-79 1639459-8 1992 The latter change was associated with enhanced (+16%, p less than 0.05) insulin responsiveness to glucose (estimated as the insulin AUC divided by the glucose AUC) throughout the 3 months of ACE inhibition. Glucose 98-105 insulin Homo sapiens 124-131 1639459-8 1992 The latter change was associated with enhanced (+16%, p less than 0.05) insulin responsiveness to glucose (estimated as the insulin AUC divided by the glucose AUC) throughout the 3 months of ACE inhibition. Glucose 151-158 insulin Homo sapiens 72-79 1639461-8 1992 A decline in blood pressure was noted that correlated with the whole body glucose uptake during the high insulin dose (r = 0.52, p less than 0.05). Glucose 74-81 insulin Homo sapiens 105-112 1322430-9 1992 Strikingly, there was a large rightward shift in the insulin dose-response curve for transport stimulation in PCO cells (EC50 = 87 +/- 14 pmol in NC vs. 757 +/- 138 in PCO, P less than 0.0005); 8-fold greater insulin concentrations were required to attain comparable glucose transport rates in cells from PCO against NC. Glucose 267-274 insulin Homo sapiens 53-60 1322430-10 1992 In conclusion, our results suggest that insulin resistance in PCO, as assessed in the adipocyte, is accompanied by normal function of insulin receptors, but involves a novel postreceptor defect in the insulin signal transduction chain between the receptor kinase and glucose transport. Glucose 267-274 insulin Homo sapiens 40-47 1500795-2 1992 This study investigated the temporal relationship between serum cortisol, insulin levels and metabolic changes in glucose, protein and fat following acute severe trauma. Glucose 114-121 insulin Homo sapiens 74-81 1407245-7 1992 Furthermore, it has been shown that amylin has the potential to antagonize the action of insulin on glucose metabolism by increasing hepatic glucose production and by decreasing muscle, but not adipocyte glucose uptake. Glucose 141-148 insulin Homo sapiens 89-96 1379358-2 1992 This paper reports 16 months of palliative treatment with cyproheptadine and diazoxide in a child with hyperinsulinism initially diagnosed at 6 months of age (her insulin level was 80 microU/mL while her glucose level was 38 mg/dL). Glucose 204-211 insulin Homo sapiens 108-115 1640870-2 1992 At insulin levels of approximately 200 pmol/L, glucose disposal rates were 2.9 +/- 0.4, 4.7 +/- 0.5, 6.4 +/- 0.6, and 6.5 +/- 0.8 mg/kg/min at plasma glucose concentrations of 5.55, 11.10, 13.88, and 19.43 mmol/L (or 100, 200, 250, and 350 mg/dL, respectively). Glucose 47-54 insulin Homo sapiens 3-10 1640870-3 1992 At insulin levels of approximately 750 pmol/L, glucose disposal rates were 1.7 to 2.1-fold higher: 6.2 +/- 0.7, 9.2 +/- 1.1, 11.0 +/- 1.1, and 12.3 +/- 1.4 mg/kg/min at glucose levels of 5.55, 11.10, 13.88, and 19.43 mmol/L. Glucose 47-54 insulin Homo sapiens 3-10 1640870-3 1992 At insulin levels of approximately 750 pmol/L, glucose disposal rates were 1.7 to 2.1-fold higher: 6.2 +/- 0.7, 9.2 +/- 1.1, 11.0 +/- 1.1, and 12.3 +/- 1.4 mg/kg/min at glucose levels of 5.55, 11.10, 13.88, and 19.43 mmol/L. Glucose 169-176 insulin Homo sapiens 3-10 1640870-4 1992 Thus, during both the 15- and 40-mU/m2/min insulin infusions, glucose disposal increased in a linear fashion from 5.55 to 13.88 mmol/L (r = .90) and then effectively plateaued at the same plasma glucose level. Glucose 62-69 insulin Homo sapiens 43-50 1640870-4 1992 Thus, during both the 15- and 40-mU/m2/min insulin infusions, glucose disposal increased in a linear fashion from 5.55 to 13.88 mmol/L (r = .90) and then effectively plateaued at the same plasma glucose level. Glucose 195-202 insulin Homo sapiens 43-50 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 18-25 insulin Homo sapiens 59-66 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 18-25 insulin Homo sapiens 230-237 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 18-25 insulin Homo sapiens 230-237 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 142-149 insulin Homo sapiens 59-66 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 142-149 insulin Homo sapiens 59-66 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 142-149 insulin Homo sapiens 59-66 1640870-5 1992 If the plateau of glucose disposal during the 40-mU/m2/min insulin infusion was due to saturation of the intracellular capacity to metabolize glucose, then when plasma glucose was increased from 13.88 to 19.43 mmol/L at the lower insulin level, the glucose disposal should have continued to increase and not plateau, since the rate of glucose disposal was only approximately 50% of that attained at the higher insulin infusion rate. Glucose 142-149 insulin Homo sapiens 59-66 1523247-1 1992 It has been reported that insulin concentration is altered by a hepatic vagotomy following intraperitoneal glucose injection (0.3 g/kg) resulting in supraphysiological blood glucose concentrations. Glucose 107-114 insulin Homo sapiens 26-33 1523247-1 1992 It has been reported that insulin concentration is altered by a hepatic vagotomy following intraperitoneal glucose injection (0.3 g/kg) resulting in supraphysiological blood glucose concentrations. Glucose 174-181 insulin Homo sapiens 26-33 1341259-0 1992 The effect of insulin on glucose and protein metabolism in the forearm of cancer patients. Glucose 25-32 insulin Homo sapiens 14-21 1641767-9 1992 CONCLUSIONS: r-hGH and insulin in the presence of amino acids and glucose combine to improve whole-body and skeletal muscle protein kinetics. Glucose 66-73 insulin Homo sapiens 23-30 1614463-5 1992 Islet function was assessed by measuring the plasma insulin responses to intravenous glucose and arginine and the plasma glucagon responses to hypoglycemia and arginine. Glucose 85-92 insulin Homo sapiens 52-59 1614463-9 1992 The acute plasma insulin responses to glucose and to arginine in the five patients were 23 +/- 13 and 26 +/- 10 microU per milliliter (168 +/- 94 and 184 +/- 70 pmol per liter), respectively, as compared with 58 +/- 6 and 37 +/- 8 microU per milliliter (416 +/- 44 and 267 +/- 61 pmol per liter) in the normal subjects. Glucose 38-45 insulin Homo sapiens 17-24 1322137-0 1992 Control of insulin gene expression by glucose. Glucose 38-45 insulin Homo sapiens 11-18 1322137-1 1992 Northern-blot analysis was used to demonstrate that an increase in extracellular glucose concentration increased the content of preproinsulin mRNA 2.3-fold in the beta-cell line HIT T15. Glucose 81-88 insulin Homo sapiens 128-141 1322137-7 1992 The ability of the 5" upstream region of the preproinsulin gene to mediate the effect of glucose and other metabolites on transcription was studied by using a bacterial reporter gene technique. Glucose 89-96 insulin Homo sapiens 45-58 1322137-14 1992 Both dibutyryl cyclic AMP and forskolin caused an increase in insulin promoter-driven gene expression in the presence of 1 mM-glucose, but neither agent further increased the level of expression occurring in the presence of a maximally stimulating glucose concentration. Glucose 126-133 insulin Homo sapiens 62-69 1322137-15 1992 The phorbol ester phorbol 12-myristate 13-acetate (PMA) also increased insulin promoter-driven CAT expression in the presence of 1 mM-, but not 11 mM-glucose. Glucose 150-157 insulin Homo sapiens 71-78 1322137-17 1992 We conclude that the 5" upstream region of the insulin gene contains sequences responsible for mediating the stimulatory effect of glucose on insulin-gene transcription. Glucose 131-138 insulin Homo sapiens 47-54 1617658-6 1992 Glucose disposal of CANWL and CAWL during the study period was significantly (P less than 0.05, analysis of variance) less than controls (3.91 +/- 0.6 in CANWL, 3.66 +/- 1.0 in CAWL, and 5.87 +/- 0.6 mg/kg/min in controls), suggesting resistance to insulin with respect to carbohydrate metabolism. Glucose 0-7 insulin Homo sapiens 249-256 1322137-17 1992 We conclude that the 5" upstream region of the insulin gene contains sequences responsible for mediating the stimulatory effect of glucose on insulin-gene transcription. Glucose 131-138 insulin Homo sapiens 142-149 1618850-0 1992 Differential role of insulin receptor autophosphorylation sites 1162 and 1163 in the long-term insulin stimulation of glucose transport, glycogenesis, and protein synthesis. Glucose 118-125 insulin Homo sapiens 21-28 1618850-2 1992 Previous studies showed that, when acutely stimulated by insulin, CHO-Y2 cells exhibit decreased receptor kinase activity along with decreased signaling of several pathways, including that for glucose transport, as compared with CHO-R cells. Glucose 193-200 insulin Homo sapiens 57-64 1618850-6 1992 (ii) By contrast, under similar conditions, CHO-Y2 cells exhibited a marked decrease in their response to insulin for [U-14C]glucose incorporation into glycogen (decreased sensitivity and maximal responsiveness) and for [U-14C]leucine incorporation into protein (decreased sensitivity) as compared with CHO-R cells. Glucose 125-132 insulin Homo sapiens 106-113 1618850-8 1992 These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin. Glucose 155-162 insulin Homo sapiens 32-39 1618850-8 1992 These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin. Glucose 155-162 insulin Homo sapiens 144-151 1618850-8 1992 These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin. Glucose 155-162 insulin Homo sapiens 144-151 1618850-8 1992 These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin. Glucose 155-162 insulin Homo sapiens 144-151 1618850-8 1992 These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin. Glucose 155-162 insulin Homo sapiens 144-151 1618850-8 1992 These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin. Glucose 155-162 insulin Homo sapiens 144-151 1519420-0 1992 Long-term stability of low insulin responses to glucose in non-diabetic subjects. Glucose 48-55 insulin Homo sapiens 27-34 1519420-1 1992 We investigated the stability of the insulin response to glucose in healthy subjects by making retrospective comparisons of insulin responses after two 60 min glucose infusion tests performed many years apart. Glucose 57-64 insulin Homo sapiens 37-44 1519420-9 1992 Predictable "regression toward the mean" at follow-up was moderate, hence the individual insulin response to glucose was relatively stable with time. Glucose 109-116 insulin Homo sapiens 89-96 1519420-10 1992 This finding is compatible with the hypothesis that genetic factors are of major importance for the insulin response to glucose. Glucose 120-127 insulin Homo sapiens 100-107 1637516-3 1992 Patients with hypertension and an abnormal EKG had significantly higher plasma glucose and insulin concentrations following oral glucose than did the control population. Glucose 129-136 insulin Homo sapiens 91-98 1519429-4 1992 Prior to GHRH-44 therapy the hypopituitary patient had higher insulin mediated glucose disposal rate and lower basal and stimulated insulin concentrations by more than two standard deviations from the mean of a control group. Glucose 79-86 insulin Homo sapiens 62-69 1519429-6 1992 This was manifested by decreased insulin mediated glucose disposal during the hyperinsulinemic-euglycemic clamp, and increased insulin secretion during the hyperglycemic clamp. Glucose 50-57 insulin Homo sapiens 33-40 1615879-6 1992 These results suggest that a significant amount of glucose is taken up through insulin-independent mechanisms during the intravenous glucose tolerance test (ivGTT) in these subjects. Glucose 51-58 insulin Homo sapiens 79-86 1615879-6 1992 These results suggest that a significant amount of glucose is taken up through insulin-independent mechanisms during the intravenous glucose tolerance test (ivGTT) in these subjects. Glucose 133-140 insulin Homo sapiens 79-86 1615879-7 1992 This insulin-independent glucose uptake may be an important determinant of the fate of glucose in obese females as well as normal females. Glucose 25-32 insulin Homo sapiens 5-12 1615879-7 1992 This insulin-independent glucose uptake may be an important determinant of the fate of glucose in obese females as well as normal females. Glucose 87-94 insulin Homo sapiens 5-12 1615892-7 1992 Weight loss increased glucose utilization by 26%, primarily by enhancing insulin-stimulated glucose oxidation (P less than 0.05), whereas the effect on nonoxidative glucose metabolism was less pronounced (P greater than 0.05). Glucose 22-29 insulin Homo sapiens 73-80 1637516-6 1992 Insulin-mediated glucose uptake was also measured in a subset of patients with hypertension and either a normal (n = 18) or abnormal (n = 17) EKG. Glucose 17-24 insulin Homo sapiens 0-7 1637516-8 1992 In addition, they also had higher plasma glucose and insulin responses to oral glucose, higher fasting plasma triglyceride and cholesterol concentrations, and an increase in the ratio of total to HDL cholesterol. Glucose 79-86 insulin Homo sapiens 53-60 1636695-4 1992 To address these questions, glucose turnover was measured simultaneously with [3-3H]- and [6-14C]glucose in the basal state and in presence of low (approximately 200 pM) and high (approximately 750 pM) insulin concentrations. Glucose 28-35 insulin Homo sapiens 202-209 1636698-8 1992 Hepatic glucose production was suppressed equally by proinsulin and insulin at all doses. Glucose 8-15 insulin Homo sapiens 56-63 1636698-9 1992 The metabolic clearance rate of glucose was significantly increased during the insulin infusion compared with proinsulin. Glucose 32-39 insulin Homo sapiens 79-86 1636698-10 1992 The use of [6",6"-2H2]glucose resulted in a mean underestimation of the glucose infusion rate of 10.0 +/- 4.0 and 6.0 +/- 2.5% during the two highest insulin and proinsulin doses, respectively. Glucose 22-29 insulin Homo sapiens 150-157 1636698-10 1992 The use of [6",6"-2H2]glucose resulted in a mean underestimation of the glucose infusion rate of 10.0 +/- 4.0 and 6.0 +/- 2.5% during the two highest insulin and proinsulin doses, respectively. Glucose 22-29 insulin Homo sapiens 162-172 1643801-4 1992 Hypoglycaemia was induced by insulin infusion aiming at a plasma glucose less than or equal to 2.0 mmol l-1 or hypoglycaemic symptoms. Glucose 65-72 insulin Homo sapiens 29-36 1457899-5 1992 Before scaling the HAP to human size, the dynamics of its insulin response to a perfusion glucose challenge must be better understood. Glucose 90-97 insulin Homo sapiens 58-65 1623737-16 1992 In both groups, however, the postoperative increase in blood glucose was accompanied by a similar increase in insulin, cortisol and catecholamines but glucagon was lower after hypothermic CPB. Glucose 61-68 insulin Homo sapiens 110-117 1322851-5 1992 During the insulin infusion, glucose in adipose tissue decreased by 20% (p less than 0.001), despite arterial steady-state normoglycaemia. Glucose 29-36 insulin Homo sapiens 11-18 1322851-9 1992 It is concluded that insulin action on glucose uptake and lipolysis in human adipose tissue in vivo is counteracted by beta-adrenoceptor stimulation. Glucose 39-46 insulin Homo sapiens 21-28 1322851-10 1992 In contrast, insulin and beta-adrenoceptors have synergistic effects on non-oxidative glucose metabolism in human adipose tissue in situ. Glucose 86-93 insulin Homo sapiens 13-20 1612199-1 1992 This study"s objective was to determine whether there is familial clustering of insulin sensitivity (SI) or insulin-independent glucose uptake (SG), which would be evidence that they are genetically determined traits. Glucose 128-135 insulin Homo sapiens 108-115 1484021-4 1992 The mean fasting plasma glucose in the 15 subjects with this insulin regimen was 321.28 +/- 69.32 mgm% and the insulin requirement per day was 106.87 +/- 35.77 units. Glucose 24-31 insulin Homo sapiens 61-68 1321040-1 1992 In isolated adipocytes, polymyxin B inhibited insulin-induced glucose incorporation into lipids in a dose-dependent manner, while polymyxin E, a structurally related antibiotic, was ineffective. Glucose 62-69 insulin Homo sapiens 46-53 1484021-8 1992 The subjects were switched back to conventional insulin therapy after SIPT during which period the mean fasting plasma glucose was 125.82 +/- 34.50 mgm% and this value was again significantly lower than the pre SIPT fasting plasma glucose value (P < .05). Glucose 119-126 insulin Homo sapiens 48-55 1619013-6 1992 The time course of in vivo kinase activity, plasma insulin concentrations, and insulin-mediated glucose disposal rates displayed parallel patterns, indicating close interrelationships among these variables. Glucose 96-103 insulin Homo sapiens 79-86 1618923-7 1992 Our results suggest that rat hepatocytes and HepG2 cells possess an intracellular storage pool for GLUT-2, but lack the insulin-responsive glucose transporter translocation mechanism. Glucose 139-146 insulin Homo sapiens 120-127 1619013-9 1992 We conclude that in vivo activation of the insulin receptor tyrosine kinase in human skeletal muscle is a rapid process, related to insulin action on glucose disposal, and that circulating insulin primes inactive insulin receptor molecules for subsequent tyrosine kinase activation by a mechanism that remains to be elucidated. Glucose 150-157 insulin Homo sapiens 43-50 1619033-6 1992 After oral glucose ingestion, mean incremental integrated plasma insulin areas were significantly (P less than 0.02) greater in the black than the white relatives (70 +/- 14 vs. 29 +/- 6 nM.min). Glucose 11-18 insulin Homo sapiens 65-72 1619013-9 1992 We conclude that in vivo activation of the insulin receptor tyrosine kinase in human skeletal muscle is a rapid process, related to insulin action on glucose disposal, and that circulating insulin primes inactive insulin receptor molecules for subsequent tyrosine kinase activation by a mechanism that remains to be elucidated. Glucose 150-157 insulin Homo sapiens 132-139 1634611-5 1992 Forearm glucose uptake rose to 5.1 +/- .7 mg.liter-1.min-1 in response to insulin in hypertensives and to 7.9 +/- 1.3 mg.liter-1.min-1 in normotensives (P less than 0.05). Glucose 8-15 insulin Homo sapiens 74-81 1619013-9 1992 We conclude that in vivo activation of the insulin receptor tyrosine kinase in human skeletal muscle is a rapid process, related to insulin action on glucose disposal, and that circulating insulin primes inactive insulin receptor molecules for subsequent tyrosine kinase activation by a mechanism that remains to be elucidated. Glucose 150-157 insulin Homo sapiens 132-139 1613561-4 1992 Infusion of insulin and glucose gave stable plasma-glucose and serum-insulin levels during imaging. Glucose 24-31 insulin Homo sapiens 69-76 1613561-4 1992 Infusion of insulin and glucose gave stable plasma-glucose and serum-insulin levels during imaging. Glucose 51-58 insulin Homo sapiens 12-19 1613561-5 1992 In contrast, glucose loading caused marked changes in plasma-glucose and insulin concentrations. Glucose 13-20 insulin Homo sapiens 73-80 1511777-6 1992 Insulin action, evaluated either as total glucose utilization or as [3H]thymidine incorporation into DNA, significantly increased in HEp-2 treated with androgens in comparison to control cultures. Glucose 42-49 insulin Homo sapiens 0-7 1631055-9 1992 The transgenic mice provide an experimental system for studying the role of glucose phosphorylation in regulation of insulin release in the absence of GLUT2. Glucose 76-83 insulin Homo sapiens 117-124 1619986-1 1992 A recent report suggested that the glucose-free fatty acid (FFA) cycle may contribute to steroid-induced insulin resistance in rats, and that glucose tolerance could be restored to normal when FFA levels were lowered with nicotinic acid. Glucose 35-42 insulin Homo sapiens 105-112 1619986-6 1992 The reduction in insulin-stimulated glucose uptake was mainly due to an impairment in nonoxidative glucose metabolism (primarily glucose storage as glycogen) (18.3 +/- 2.8 v 27.2 +/- 2.2 mumol/kg LBM.min, P less than .01). Glucose 36-43 insulin Homo sapiens 17-24 1619986-6 1992 The reduction in insulin-stimulated glucose uptake was mainly due to an impairment in nonoxidative glucose metabolism (primarily glucose storage as glycogen) (18.3 +/- 2.8 v 27.2 +/- 2.2 mumol/kg LBM.min, P less than .01). Glucose 99-106 insulin Homo sapiens 17-24 1619986-6 1992 The reduction in insulin-stimulated glucose uptake was mainly due to an impairment in nonoxidative glucose metabolism (primarily glucose storage as glycogen) (18.3 +/- 2.8 v 27.2 +/- 2.2 mumol/kg LBM.min, P less than .01). Glucose 99-106 insulin Homo sapiens 17-24 1619995-9 1992 Partial correlation coefficients showed a significant negative correlation between percent variation of glucose-stimulated insulin incremental areas during the naloxone study and the WHR in all women considered together (r = .544, P less than .025). Glucose 104-111 insulin Homo sapiens 123-130 1631055-6 1992 Insulin secretion studied in isolated islets and the perfused pancreas is characterized by a normal incremental response to increasing glucose concentrations. Glucose 135-142 insulin Homo sapiens 0-7 1631088-8 1992 Dex effects on insulin release during hyperglycemic clamp were negatively correlated with the glucose area during Dex OGTT (P less than 0.01). Glucose 94-101 insulin Homo sapiens 15-22 1643376-4 1992 Regular monitoring of blood glucose levels and careful insulin administration should be undertaken to prevent fluctuations in blood glucose levels. Glucose 132-139 insulin Homo sapiens 55-62 1642079-6 1992 The decrease in serum C-peptide concentration during insulin treatment correlated with the change in blood glucose. Glucose 107-114 insulin Homo sapiens 53-60 1642079-8 1992 In conclusion, insulin treatment of NIDDM patients with secondary failure to oral agents greatly reduces the insulin secretion, probably owing to the reduction in blood glucose. Glucose 169-176 insulin Homo sapiens 15-22 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 213-220 insulin Homo sapiens 242-249 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 213-220 insulin Homo sapiens 106-113 1616018-1 1992 Amino acids have been reported to increase endogenous glucose production in normal human subjects during hyperinsulinemia: however, controversy exists as to whether insulin-mediated glucose disposal is inhibited under these conditions. Glucose 54-61 insulin Homo sapiens 110-117 1524526-7 1992 His 75 g OGTT was diabetic in type and serum insulin response to glucose decreased markedly. Glucose 65-72 insulin Homo sapiens 45-52 1591229-2 1992 Subjects with IGT exhibited the highest insulin responses to an oral glucose load. Glucose 69-76 insulin Homo sapiens 40-47 1535580-4 1992 The latter however increased the glucose and insulin responses to a glucose tolerance test whereas Marvelon and Mercilon had no effect. Glucose 68-75 insulin Homo sapiens 45-52 1375175-4 1992 With whole-islet perifusion, we demonstrated that insulin secretion induced by glucose, tolbutamide, or elevated K+ is dependent on extracellular Ca2+. Glucose 79-86 insulin Homo sapiens 50-57 1425138-6 1992 The decline in plasma insulin from 03.00 to 08.00 h and mean cortisol level between 03.00 and 06.00 h were both significantly correlated with the increase in plasma glucose between 03.00 and 08.00 h. We concluded that an increase of 1.0 mmol/l or more in plasma glucose during the early morning is of clinical importance. Glucose 165-172 insulin Homo sapiens 22-29 1425142-2 1992 In 29 diabetic patients intravenous infusion of soluble insulin was started upon admission to hospital and the rate adjusted hourly on the basis of bedside capillary glucose estimations. Glucose 166-173 insulin Homo sapiens 56-63 1425455-6 1992 Glucose clamp and glucose tolerance study showed decreased sensitivity to exogenous or newly secreted insulin, prolonged half disappearance time of serum insulin, and normal disappearance of blood glucose. Glucose 0-7 insulin Homo sapiens 102-109 1425455-6 1992 Glucose clamp and glucose tolerance study showed decreased sensitivity to exogenous or newly secreted insulin, prolonged half disappearance time of serum insulin, and normal disappearance of blood glucose. Glucose 18-25 insulin Homo sapiens 102-109 1534057-4 1992 However, the molar ratio of secreted amylin to insulin in response to 16.7 mM glucose by n5STZ pancreases (6.55 +/- 0.71%) was significantly greater than that for either n2STZ (1.71 +/- 0.24%, P less than 0.05) or the control (0.60 +/- 0.03%, P less than 0.05) pancreases. Glucose 78-85 insulin Homo sapiens 47-54 1534057-6 1992 The increased amylin-insulin molar ratios of both n2STZ and n5STZ pancreases also occurred during infusions of 33.3 mM glucose and 10 mM arginine. Glucose 119-126 insulin Homo sapiens 21-28 1587393-5 1992 Studies in IDDM patients have demonstrated that good glucose control can be achieved with intraperitoneal delivery of insulin from implantable pumps with lesser glycemic fluctuations and, therefore, fewer episodes of hypoglycemia. Glucose 53-60 insulin Homo sapiens 118-125 1587393-10 1992 Furthermore, insulin resistance, which is an integral part of NIDDM, results in higher physiological levels of insulin, which are required for glucose control, and thus significant peripheral hyperinsulinemia occurs in patients receiving exogenous insulin. Glucose 143-150 insulin Homo sapiens 13-20 1587393-10 1992 Furthermore, insulin resistance, which is an integral part of NIDDM, results in higher physiological levels of insulin, which are required for glucose control, and thus significant peripheral hyperinsulinemia occurs in patients receiving exogenous insulin. Glucose 143-150 insulin Homo sapiens 111-118 1587393-10 1992 Furthermore, insulin resistance, which is an integral part of NIDDM, results in higher physiological levels of insulin, which are required for glucose control, and thus significant peripheral hyperinsulinemia occurs in patients receiving exogenous insulin. Glucose 143-150 insulin Homo sapiens 111-118 1587394-7 1992 The attenuated glucose recovery was associated with higher plasma insulin concentrations (maximum increment 1385 +/- 122 vs. 940 +/- 72 pM, P less than 0.01) and reduced glucagon responses to hypoglycemia (maximum increment 43 +/- 6 vs. 66 +/- 12 ng/L). Glucose 15-22 insulin Homo sapiens 66-73 1587397-1 1992 Skeletal muscle insulin resistance in obese patients with non-insulin-dependent diabetes mellitus (NIDDM) is characterized by decreased glucose uptake. Glucose 136-143 insulin Homo sapiens 16-23 1587397-4 1992 This study was undertaken to determine whether, under euglycemic conditions, insulin resistance for leg muscle glucose uptake in NIDDM patients is due primarily to decreased glucose storage or to oxidation. Glucose 111-118 insulin Homo sapiens 77-84 1587401-6 1992 The reduction in glucose tolerance in the normal-weight subjects was caused by diminished insulin sensitivity (parameter S1, AM 15.4 +/- 2.9, PM 10.2 +/- 1.9 x 10(-5) min-1/pM, P less than 0.01) and reduced beta-cell responsivity to glucose. Glucose 17-24 insulin Homo sapiens 90-97 1600834-3 1992 Sulfonylureas lower blood glucose concentrations primarily by stimulating insulin secretion. Glucose 26-33 insulin Homo sapiens 74-81 1600835-7 1992 In peripheral tissues metformin increases insulin-mediated glucose uptake and oxidative metabolism. Glucose 59-66 insulin Homo sapiens 42-49 1611830-3 1992 We have therefore compared the glucose disappearance rate KITT in the first 15 min of the insulin tolerance test (ITT) with the M and M/I values derived from the standard euglycaemic clamp in nine normal subjects and eight subjects with Type 2 (non-insulin dependent) diabetes mellitus and coexisting obesity. Glucose 31-38 insulin Homo sapiens 90-97 1611830-7 1992 The first order rate constant for the disappearance of glucose KITT over the period 3-15 min was taken as a measure of insulin sensitivity. Glucose 55-62 insulin Homo sapiens 119-126 1612067-1 1992 Intensive insulin therapy is suitable for individuals who want optimal glucose control and the least fluctuation in glucose levels. Glucose 71-78 insulin Homo sapiens 10-17 1612067-1 1992 Intensive insulin therapy is suitable for individuals who want optimal glucose control and the least fluctuation in glucose levels. Glucose 116-123 insulin Homo sapiens 10-17 1612073-4 1992 The major aim of treatment is to rapidly replace the major water loss that is responsible for this clinical condition and to stimulate glucose metabolism with insulin. Glucose 135-142 insulin Homo sapiens 159-166 1612226-7 1992 Body mass index-adjusted geometric mean 2-h plasma insulin was higher in subjects with abnormal glucose tolerance relative to those with normal glucose tolerance in both populations. Glucose 96-103 insulin Homo sapiens 51-58 1612226-7 1992 Body mass index-adjusted geometric mean 2-h plasma insulin was higher in subjects with abnormal glucose tolerance relative to those with normal glucose tolerance in both populations. Glucose 144-151 insulin Homo sapiens 51-58 1612228-8 1992 Of 40 individuals tested in the intravenous glucose tolerance test, three had a first phase insulin response below the first percentile of normal control subjects. Glucose 44-51 insulin Homo sapiens 92-99 1587421-1 1992 Insulin-induced glucose metabolism was investigated in 26 patients with biopsy-proven liver cirrhosis and 10 control subjects. Glucose 16-23 insulin Homo sapiens 0-7 1587421-4 1992 Simultaneously, insulin-induced increases in glucose oxidation, plasma lactate levels, and lipogenesis were normal, whereas nonoxidative glucose metabolism was reduced (-82% and -47% of controls, respectively). Glucose 45-52 insulin Homo sapiens 16-23 1639045-8 1992 However, the results suggest that the FFA/glucose interrelationship may override exercise-induced changes in insulin-stimulated glucose uptake. Glucose 42-49 insulin Homo sapiens 109-116 1639045-8 1992 However, the results suggest that the FFA/glucose interrelationship may override exercise-induced changes in insulin-stimulated glucose uptake. Glucose 128-135 insulin Homo sapiens 109-116 1592457-2 1992 Insulin resistance was assessed by fasting insulin levels and sum of insulin values after an oral glucose tolerance test in all 95 subjects and whole body glucose uptake during euglycemic hyperinsulinemia in 35 of 95 subjects. Glucose 98-105 insulin Homo sapiens 0-7 1592457-2 1992 Insulin resistance was assessed by fasting insulin levels and sum of insulin values after an oral glucose tolerance test in all 95 subjects and whole body glucose uptake during euglycemic hyperinsulinemia in 35 of 95 subjects. Glucose 155-162 insulin Homo sapiens 0-7 1629073-6 1992 Insulin-mediated glucose disposal rate was significantly impaired (P less than 0.05) during the clamp performed after eccentric exercise (3.47 +/- 0.51 mg.kg-1.min-1) compared with the clamps performed after concentric exercise (5.55 +/- 0.94 mg.kg-1.min-1) or control conditions (5.48 +/- 1.0 mg.kg-1.min-1). Glucose 17-24 insulin Homo sapiens 0-7 1592879-4 1992 Insulin-glucose interactions were assessed by measuring indices of insulin sensitivity (SI) and glucose effectiveness at zero insulin (GEZI) using Bergman"s minimal model. Glucose 8-15 insulin Homo sapiens 0-7 1592879-4 1992 Insulin-glucose interactions were assessed by measuring indices of insulin sensitivity (SI) and glucose effectiveness at zero insulin (GEZI) using Bergman"s minimal model. Glucose 8-15 insulin Homo sapiens 67-74 1592879-5 1992 B-Cell function was assessed by determining the acute insulin responses (AIR) to glucose (AIRgluc) and arginine at 3 different glucose levels: fasting, approximately 14 mM, and greater than 28 mM (AIRmax). Glucose 81-88 insulin Homo sapiens 54-61 1601986-5 1992 Beta cell reserve, as measured by glucose potentiation of arginine-induced insulin secretion, was significantly decreased in donors (maximal acute insulin response [AIRmax]: donors = 666 +/- 84 pM vs controls = 1,772 +/- 234 pM) while the PG50 (the glucose value at which the half-maximal response was observed) was the same in the two groups. Glucose 34-41 insulin Homo sapiens 75-82 1601998-1 1992 Insulin-like growth factor-I (IGF-I) and insulin interact with related receptors to lower plasma glucose and to exert mitogenic effects. Glucose 97-104 insulin Homo sapiens 41-48 1601998-5 1992 The decreased insulin/glucose-ratio presumably is caused by an enhanced tissue sensitivity to insulin. Glucose 22-29 insulin Homo sapiens 14-21 1522489-1 1992 A self-regulating insulin delivery system based on the competitive binding of glucose and p-succinylamidophenyl-alpha-D-glycopyranoside-insulin (SAPG-insulin) to crosslinked concanavalin A (Con A) microspheres (MSs) has been investigated. Glucose 78-85 insulin Homo sapiens 18-25 1522489-5 1992 This system showed a pulsatile release pattern for insulin with a short lag time in response to glucose challenges of 50-500 mg/dL. Glucose 96-103 insulin Homo sapiens 51-58 1640847-1 1992 Obesity is associated with impaired insulin action in glucose disposal, but not necessarily in other aspects of intermediary metabolism or insulin clearance. Glucose 54-61 insulin Homo sapiens 36-43 1640847-6 1992 Insulin infusion caused blood glucose to decrease less in the obese patients (1.4 +/- 0.5 v 1.9 +/- 0.5 mmol.L-1, P less than .05); hepatic glucose production was appropriately suppressed in them by hyperinsulinemia, but their insulin-mediated glucose disposal was reduced (1.67 [0.79] v 4.45 [2.13] mL.m-2.min-1/mU.L-1, P less than .01). Glucose 30-37 insulin Homo sapiens 0-7 1640854-0 1992 The effect of epinephrine on glucose-mediated and insulin-mediated glucose disposal in insulin-dependent diabetes. Glucose 67-74 insulin Homo sapiens 50-57 1321355-4 1992 In contrast, AVP and OT responses during ITT were completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. Glucose 104-111 insulin Homo sapiens 122-129 1436266-4 1992 Fasting blood glucose was the highest (13.8 +/- 2.8 mmol/l) in secondary failure and newly-diagnosed patients (12.6 +/- 3.8 mmol/l) compared to tablet-treated (8.7 +/- 3.3 mmol/l) and insulin-treated patients (9.6 +/- 3.2 mmol/l, p less than 0.05). Glucose 14-21 insulin Homo sapiens 184-191 1286587-3 1992 There was no correlation between diastole blood pressure and plasma insulin; multiple regression analysis showed that fasting plasma insulin was significantly associated with systolic blood pressure after controlling age, BMI and plasma glucose level (beta = 0.27, P = 0.0078). Glucose 237-244 insulin Homo sapiens 133-140 1529568-1 1992 The minimal model of insulin and blood sugar kinetics is a method the basis of which are two mathematical models describing the dynamic changes of plasma glucose and insulin concentration along with the beta-cell response to the rise of the blood sugar level during the intravenous glucose tolerance test with frequent collection of samples. Glucose 154-161 insulin Homo sapiens 21-28 1529568-1 1992 The minimal model of insulin and blood sugar kinetics is a method the basis of which are two mathematical models describing the dynamic changes of plasma glucose and insulin concentration along with the beta-cell response to the rise of the blood sugar level during the intravenous glucose tolerance test with frequent collection of samples. Glucose 282-289 insulin Homo sapiens 21-28 1529568-1 1992 The minimal model of insulin and blood sugar kinetics is a method the basis of which are two mathematical models describing the dynamic changes of plasma glucose and insulin concentration along with the beta-cell response to the rise of the blood sugar level during the intravenous glucose tolerance test with frequent collection of samples. Glucose 282-289 insulin Homo sapiens 166-173 1577807-1 1992 Crucial role of glucose and the hexosamine biosynthesis pathway in the expression of insulin action. Glucose 16-23 insulin Homo sapiens 85-92 1577807-6 1992 Several lines of additional evidence implicated the hexosamine biosynthesis pathway in PK regulation; therefore, it appears that the M2 isoform of pyruvate kinase represents another enzyme regulated by insulin through stimulation of glucose uptake and formation of hexosamine products. Glucose 233-240 insulin Homo sapiens 202-209 1348845-7 1992 The insulinogenic index (the ratio of insulin to glucose) increased almost 10-fold, indicating that GLIP had an insulinotropic effect. Glucose 49-56 insulin Homo sapiens 4-11 1349365-3 1992 To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Glucose 82-89 insulin Homo sapiens 65-72 1349365-6 1992 Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p less than 0.001), despite similar steady-state plasma insulin concentrations. Glucose 48-55 insulin Homo sapiens 120-127 1577744-2 1992 Compared with wild type receptors, the Y/F2 receptor exhibited markedly enhanced sensitivity to insulin-stimulated DNA synthesis with normal insulin-stimulated glucose uptake (Takata, Y., Webster, N. J. G., and Olefsky, J. M. (1991) J. Biol. Glucose 160-167 insulin Homo sapiens 141-148 1577744-6 1992 The mutant receptor showed normal sensitivity and responsiveness for insulin-stimulated glucose incorporation into glycogen. Glucose 88-95 insulin Homo sapiens 69-76 1631967-1 1992 Recent research has demonstrated that reduced insulin-stimulated glucose metabolism in skeletal muscle (insulin resistance) and hyperinsulinism are common features in widespread diseases such as essential hypertension, android obesity, non-insulin dependent diabetes mellitus, dyslipidemia (in the form of raised serum triglyceride and reduced serum high-density lipoprotein (HDL) cholesterol) and arteriosclerosis. Glucose 65-72 insulin Homo sapiens 46-53 1631967-1 1992 Recent research has demonstrated that reduced insulin-stimulated glucose metabolism in skeletal muscle (insulin resistance) and hyperinsulinism are common features in widespread diseases such as essential hypertension, android obesity, non-insulin dependent diabetes mellitus, dyslipidemia (in the form of raised serum triglyceride and reduced serum high-density lipoprotein (HDL) cholesterol) and arteriosclerosis. Glucose 65-72 insulin Homo sapiens 104-111 1631967-8 1992 For example if the beta-cells of the pancreas are unable to secrete sufficient insulin to compensate the insulin resistance on account of genetic defects, glucose intolerance will develop. Glucose 155-162 insulin Homo sapiens 79-86 1631967-8 1992 For example if the beta-cells of the pancreas are unable to secrete sufficient insulin to compensate the insulin resistance on account of genetic defects, glucose intolerance will develop. Glucose 155-162 insulin Homo sapiens 105-112 1570809-3 1992 A significant inverse relationship was found between plasma chromium and plasma insulin concentrations both over a 24-h period (P less than 0.001) and after a 75-g glucose load (P less than 0.01). Glucose 164-171 insulin Homo sapiens 80-87 1376980-3 1992 Growth hormone (GH) secretion is almost invariably depressed as is the plasma insulin response to oral glucose. Glucose 103-110 insulin Homo sapiens 78-85 1376980-6 1992 Treatment with biosynthetic GH restored IGFBP-3 to levels which were approximately equimolar to total plasma IGF concentrations, alleviated the hypoglycaemia and restored the plasma insulin responses to oral glucose. Glucose 208-215 insulin Homo sapiens 182-189 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 213-220 insulin Homo sapiens 242-249 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 213-220 insulin Homo sapiens 242-249 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 261-268 insulin Homo sapiens 242-249 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 261-268 insulin Homo sapiens 242-249 1524758-3 1992 Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. Glucose 261-268 insulin Homo sapiens 242-249 1345145-2 1992 The skeletal muscle is the major site of insulin resistance; when stimulated with insulin, the hypertensive skeletal muscles extract less glucose than the normotensive. Glucose 138-145 insulin Homo sapiens 82-89 1632860-1 1992 The insulin response to a standard oral glucose tolerance test (OGTT) and other anthropometric and biochemical risk factors for coronary heart disease (CHD) were measured in a random sample of 107 Edinburgh men, who were initially studied in 1976 when they were 40 and who were reexamined in 1988-89. Glucose 40-47 insulin Homo sapiens 4-11 1318188-1 1992 Insulin binding and the capacity of insulin to stimulate the conversion of glucose to carbon dioxide and lipid, and to activate the protein tyrosine kinase associated with the insulin receptor have been investigated in adipocytes isolated from pregnant and non-pregnant women. Glucose 75-82 insulin Homo sapiens 36-43 1389712-6 1992 Two hours after an oral glucose load Asian men had double the serum insulin concentrations of non-Asian men (p < 0.0001). Glucose 24-31 insulin Homo sapiens 68-75 1351429-2 1992 The beta-cell/liver glucose transporter gene GLUT2 represents a good candidate for the etiology of the disease, being involved in the glucose signalling for beta-cell insulin release. Glucose 20-27 insulin Homo sapiens 167-174 1521730-6 1992 Individual immunoradiometric assay insulin responses to glucose expressed in terms of obesity were subnormal in nine of ten diabetic subjects. Glucose 56-63 insulin Homo sapiens 35-42 1505651-3 1992 Computer modelling of plasma glucose, insulin and C-peptide concentrations during an intravenous glucose tolerance test enables quantification of the determinants of plasma insulin concentration. Glucose 29-36 insulin Homo sapiens 173-180 1505651-3 1992 Computer modelling of plasma glucose, insulin and C-peptide concentrations during an intravenous glucose tolerance test enables quantification of the determinants of plasma insulin concentration. Glucose 97-104 insulin Homo sapiens 38-45 1505651-3 1992 Computer modelling of plasma glucose, insulin and C-peptide concentrations during an intravenous glucose tolerance test enables quantification of the determinants of plasma insulin concentration. Glucose 97-104 insulin Homo sapiens 50-59 1505651-3 1992 Computer modelling of plasma glucose, insulin and C-peptide concentrations during an intravenous glucose tolerance test enables quantification of the determinants of plasma insulin concentration. Glucose 97-104 insulin Homo sapiens 173-180 1521732-4 1992 In parallel, insulin contents of the islets and the media were determined as well as the rates of glucose-stimulated (pro)insulin biosynthesis. Glucose 98-105 insulin Homo sapiens 122-129 1505651-5 1992 In univariate linear regression analysis of the glucose, insulin and C-peptide data, the incremental insulin area during the second phase (10-180 min.) Glucose 48-55 insulin Homo sapiens 101-108 1568535-0 1992 Dietary substitution of medium-chain triglycerides improves insulin-mediated glucose metabolism in NIDDM subjects. Glucose 77-84 insulin Homo sapiens 60-67 1521732-6 1992 Diazoxide on the other hand reduced the rate of the 64 kDa/glutamic acid decarboxylase autoantigen synthesis in parallel with an inhibition of glucose-stimulated insulin release. Glucose 143-150 insulin Homo sapiens 162-169 1568535-1 1992 Dietary medium-chain triglycerides (MCT) may improve insulin-mediated glucose metabolism. Glucose 70-77 insulin Homo sapiens 53-60 1568535-4 1992 On MCT, the amount of glucose needed to maintain euglycemia during an intravenous insulin infusion was increased in diabetic subjects by 30%, in hypertriglyceridemic subjects by 30%, and in normotriglyceridemic control subjects by 17%. Glucose 22-29 insulin Homo sapiens 82-89 1568535-5 1992 MCT increased mean +/- SE insulin-mediated glucose disposal (4.52 +/- 0.56 vs. 2.89 +/- 0.21 mg.kg-1.min-1; n = 3, P less than 0.05) but failed to alter basal glucose metabolism or insulin-mediated suppression of hepatic glucose output. Glucose 43-50 insulin Homo sapiens 26-33 1568535-9 1992 Thus, MCT-containing diets increased insulin-mediated glucose metabolism in both diabetic patients and nondiabetic subjects. Glucose 54-61 insulin Homo sapiens 37-44 1568535-10 1992 In diabetic subjects, this effect appears to be mediated by increases in insulin-mediated glucose disposal. Glucose 90-97 insulin Homo sapiens 73-80 1588781-2 1992 The model attempts to reflect the underlying (patho)physiology of insulin action and carbohydrate absorption in quantitative terms such as insulin sensitivity, volume of glucose and insulin distribution and maximal rate of gastric emptying. Glucose 170-177 insulin Homo sapiens 66-73 1534120-4 1992 In those respondents who also completed an oral glucose tolerance test (OGTT) or who were currently receiving insulin, the prevalence of disability was 25% in persons with an abnormal OGTT and 40.2% in those who were receiving insulin compared with 14.9% in those with a normal OGTT. Glucose 48-55 insulin Homo sapiens 227-234 1569149-4 1992 The improvement in glycemic control was associated with a 24% increase (P less than 0.05) in insulin-stimulated glucose uptake during glucose clamp studies and a 16% decrease in basal hepatic glucose production (P less than 0.05). Glucose 112-119 insulin Homo sapiens 93-100 1569149-4 1992 The improvement in glycemic control was associated with a 24% increase (P less than 0.05) in insulin-stimulated glucose uptake during glucose clamp studies and a 16% decrease in basal hepatic glucose production (P less than 0.05). Glucose 134-141 insulin Homo sapiens 93-100 1569151-0 1992 Very high concentrations of islet amyloid polypeptide are necessary to alter the insulin response to intravenous glucose in man. Glucose 113-120 insulin Homo sapiens 81-88 1569151-4 1992 IAPP at 25 pmol/kg.min had no effect on the plasma glucose disposal rate or the total incremental insulin response, but, in contrast, at 50 pmol/kg.min decreased the insulin response to glucose compared to the saline infusion (incremental area under the curve, 11,276 +/- 2,353 vs. 17,549 +/- 2,687 U; mean +/- SEM; P less than 0.02). Glucose 186-193 insulin Homo sapiens 166-173 1569151-7 1992 Thus, circulating IAPP concentrations greater than 90 times normal postprandial peaks were necessary to affect the insulin response to glucose. Glucose 135-142 insulin Homo sapiens 115-122 1569156-1 1992 Insulin-dependent diabetes mellitus (IDDM) is associated with insulin deficiency and insulin-resistant glucose uptake in skeletal muscle. Glucose 103-110 insulin Homo sapiens 0-7 1569156-5 1992 Euglycemic clamp studies over a range of insulin concentrations in these IDDM subjects previously showed both decreased insulin sensitivity and decreased maximally insulin stimulated glucose utilization. Glucose 183-190 insulin Homo sapiens 41-48 1569157-10 1992 In contrast, the insulin-antagonistic effect of adrenaline on glucose uptake is persistent for at least 4 h. Glucose 62-69 insulin Homo sapiens 17-24 1577853-1 1992 GLUT-4 is the major facilitative glucose transporter isoform in tissues that exhibit insulin-stimulated glucose transport. Glucose 33-40 insulin Homo sapiens 85-92 1577853-2 1992 Insulin regulates glucose transport by the rapid translocation of GLUT-4 from an intracellular compartment to the plasma membrane. Glucose 18-25 insulin Homo sapiens 0-7 1573895-5 1992 A glucose tolerance test revealed an exuberant insulin response. Glucose 2-9 insulin Homo sapiens 47-54 1573849-2 1992 IAPP, a highly conserved and carboxy-terminally amidated 37 amino acid polypeptide with approximately 45% amino acid sequence identity to CGRP, is produced by islet beta cells and is cosecreted with insulin in response to glucose and other secretagogues. Glucose 222-229 insulin Homo sapiens 199-206 1573849-4 1992 Glucose-stimulated IAPP secretion generally parallels that of insulin and, on a molar basis, IAPP represents about 1% of the amount of insulin secreted. Glucose 0-7 insulin Homo sapiens 62-69 1573849-12 1992 Evidence has been provided which indicates that IAPP can inhibit glucose-stimulated insulin secretion by beta cells, and that IAPP can also potentially contribute to the pathogenesis of type 2 diabetes by increasing hepatic glucose output and by inducing peripheral insulin resistance. Glucose 65-72 insulin Homo sapiens 84-91 1574008-1 1992 Patients with impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) are more resistant to insulin-stimulated glucose uptake than are individuals with normal glucose tolerance. Glucose 140-147 insulin Homo sapiens 55-62 1574008-2 1992 Evidence has also been published showing that first-degree relatives of patients with NIDDM are insulin resistant when compared with a matched group of relatives of subjects with normal glucose tolerance. Glucose 186-193 insulin Homo sapiens 96-103 1574008-3 1992 In addition, the ability of insulin to stimulate glucose uptake varies approximately fourfold in individuals with normal glucose tolerance, and insulin resistance of a degree comparable to that seen in patients with IGT or with Type II diabetes is present in a significant portion of the normal population. Glucose 49-56 insulin Homo sapiens 28-35 1574008-3 1992 In addition, the ability of insulin to stimulate glucose uptake varies approximately fourfold in individuals with normal glucose tolerance, and insulin resistance of a degree comparable to that seen in patients with IGT or with Type II diabetes is present in a significant portion of the normal population. Glucose 121-128 insulin Homo sapiens 28-35 1574008-4 1992 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 37-44 insulin Homo sapiens 18-25 1574008-4 1992 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 37-44 insulin Homo sapiens 97-104 1574008-4 1992 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 37-44 insulin Homo sapiens 97-104 1574008-4 1992 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 53-60 insulin Homo sapiens 18-25 1574008-4 1992 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 53-60 insulin Homo sapiens 97-104 1574008-4 1992 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 53-60 insulin Homo sapiens 97-104 1574008-5 1992 As a corollary, glucose homeostasis will decompensate when the insulin secretory response begins to decrease, and the greater the decline in insulin secretion, the larger the increase in plasma glucose concentration. Glucose 16-23 insulin Homo sapiens 63-70 1574008-6 1992 Resistance to insulin-stimulated glucose uptake and compensatory hyperinsulinemia seems to represent the basic defect in patients with NIDDM, with failure of beta-cell function and subsequent development of fasting hyperglycemia only occurring later. Glucose 33-40 insulin Homo sapiens 14-21 1574008-8 1992 The fact that an increase in ambient insulin concentration can prevent gross decompensation of glucose tolerance in an insulin-resistant individual does not mean that this compensatory response is benign. Glucose 95-102 insulin Homo sapiens 37-44 1574015-5 1992 The glucose-lowering effects are secondary to both enhanced insulin secretion and a decrease in insulin resistance. Glucose 4-11 insulin Homo sapiens 60-67 1588825-4 1992 This result could be related to insulin resistance, which was evidenced by a large increase in glucose and insulin levels after the meal intake in patients (P +/- .001). Glucose 95-102 insulin Homo sapiens 32-39 1588830-8 1992 The insulin response also was curvilinear, but the curve was opposite to that of the glucose curve. Glucose 85-92 insulin Homo sapiens 4-11 1588835-0 1992 Intravenous infusion of diarginylinsulin, an insulin analogue: effects on glucose turnover and lipid levels in insulin-treated type II diabetic patients. Glucose 74-81 insulin Homo sapiens 33-40 1588835-7 1992 In conclusion, these results indicate that diarginylinsulin is as potent as regular human insulin; it is normalizes HGO in the postabsorptive state; and its hepatic and peripheral actions on glucose and lipids are comparable to those of human insulin during an euglycemic hyperinsulinemic clamp. Glucose 191-198 insulin Homo sapiens 52-59 1608161-4 1992 However, after the administration of glucose the values decreased, and returned to the normal value with administration of insulin. Glucose 37-44 insulin Homo sapiens 123-130 10765208-3 1992 The insulin response to oral glucose at 6 months after surgery was as good as in the normal controls. Glucose 29-36 insulin Homo sapiens 4-11 1595129-2 1992 A large reserve of latent glucose transport capacity must be maintained by muscle and adipose cells that are sensitive to insulin, the primary activator of sugar uptake after feeding. Glucose 26-33 insulin Homo sapiens 122-129 1575739-1 1992 The insulin secretagogue D-glucose induces both accumulation of nonesterified arachidonic acid (35 microM) in pancreatic islets and a rise in beta cell cytosolic [Ca++]i. Glucose 25-34 insulin Homo sapiens 4-11 1315961-1 1992 The glucose/insulin response element of the L-pyruvate kinase gene is a perfect palindrome located from nt -168 to -144 with respect to the cap site. Glucose 4-11 insulin Homo sapiens 12-19 1570017-4 1992 Glucokinase is an enzyme that catalyses the formation of glucose-6-phosphate from glucose and may be involved in the regulation of insulin secretion and integration of hepatic intermediary metabolism. Glucose 57-64 insulin Homo sapiens 131-138 1570017-4 1992 Glucokinase is an enzyme that catalyses the formation of glucose-6-phosphate from glucose and may be involved in the regulation of insulin secretion and integration of hepatic intermediary metabolism. Glucose 82-89 insulin Homo sapiens 131-138 1619960-1 1992 Net effects of insulin on glucose entry, metabolism and other cellular processes have been well documented over the past 30-40 years. Glucose 26-33 insulin Homo sapiens 15-22 1619960-6 1992 It will be proposed here that the insulin binding membrane protein functions mainly to inhibit glucose transport under low physiological levels of insulin. Glucose 95-102 insulin Homo sapiens 34-41 1619960-6 1992 It will be proposed here that the insulin binding membrane protein functions mainly to inhibit glucose transport under low physiological levels of insulin. Glucose 95-102 insulin Homo sapiens 147-154 1619960-8 1992 Under metabolically sufficient conditions, enough insulin receptors are functionally active to interact with the glucose transport system in an inhibitory manner, providing membrane control of internal glucose metabolism. Glucose 113-120 insulin Homo sapiens 50-57 1619960-8 1992 Under metabolically sufficient conditions, enough insulin receptors are functionally active to interact with the glucose transport system in an inhibitory manner, providing membrane control of internal glucose metabolism. Glucose 202-209 insulin Homo sapiens 50-57 1619960-19 1992 70, 490) proposed that the internal supply of energy rich compounds limited glucose entry and that the effect of insulin was to inhibit this process which was inhibiting glucose entry. Glucose 170-177 insulin Homo sapiens 113-120 1566838-1 1992 Tissue glucose uptake occurs by insulin-dependent and insulin-independent mechanisms. Glucose 7-14 insulin Homo sapiens 32-39 1566838-1 1992 Tissue glucose uptake occurs by insulin-dependent and insulin-independent mechanisms. Glucose 7-14 insulin Homo sapiens 54-61 1566838-4 1992 Twenty-four hours of glucose infusion increased the basal plasma glucose (5.1 +/- 0.1 to 6.4 +/- 0.2 mM, P = 0.001) and insulin (79 +/- 8 to 174 +/- 31 pM, P less than 0.05) levels. Glucose 21-28 insulin Homo sapiens 120-127 1566838-8 1992 From these data we conclude that, in normal subjects, the mild hyperglycemia and hyperinsulinemia occurring during a prolonged glucose infusion improves glucose disposal in the basal state by increasing insulin secretion and insulin sensitivity but does not enhance glucose effectiveness independent of insulin. Glucose 127-134 insulin Homo sapiens 86-93 1566838-8 1992 From these data we conclude that, in normal subjects, the mild hyperglycemia and hyperinsulinemia occurring during a prolonged glucose infusion improves glucose disposal in the basal state by increasing insulin secretion and insulin sensitivity but does not enhance glucose effectiveness independent of insulin. Glucose 153-160 insulin Homo sapiens 86-93 1566838-8 1992 From these data we conclude that, in normal subjects, the mild hyperglycemia and hyperinsulinemia occurring during a prolonged glucose infusion improves glucose disposal in the basal state by increasing insulin secretion and insulin sensitivity but does not enhance glucose effectiveness independent of insulin. Glucose 153-160 insulin Homo sapiens 86-93 10078237-0 1992 Artificial connection between glucose sensing and insulin delivery: implications of peritoneal administration. Glucose 30-37 insulin Homo sapiens 50-57 10078237-1 1992 The replacement of insulinogenic function in insulin-dependent diabetes has to restore the feedback between intracorporal glucose and insulin. Glucose 122-129 insulin Homo sapiens 19-26 1637215-6 1992 The data reflect the beneficial effect associated with the action of glucose-insulin-potassium on myocardial protection during heart operations and were confirmed by the hemodynamic results. Glucose 69-76 insulin Homo sapiens 77-84 10078237-3 1992 This artificial device works on the basis of an algorithm of glucose-dependent insulin provision, compensating for the lack of other regulators, for the site of insulin administration, which is usually posthepatic, and for the kinetic properties of sensing system, e.g., a subcutaneous inserted amperometric electrode. Glucose 61-68 insulin Homo sapiens 79-86 10078237-6 1992 Feedback-controlled peritoneal insulin administration by means of an artificial beta-cell working on peripheral-venous blood glucose monitoring results in normal glycemic profiles under basal conditions and during oral glucose loads, if the pharmacodynamic properties of the peritoneal route are implemented into the insulin dosage algorithm. Glucose 125-132 insulin Homo sapiens 31-38 10078237-6 1992 Feedback-controlled peritoneal insulin administration by means of an artificial beta-cell working on peripheral-venous blood glucose monitoring results in normal glycemic profiles under basal conditions and during oral glucose loads, if the pharmacodynamic properties of the peritoneal route are implemented into the insulin dosage algorithm. Glucose 219-226 insulin Homo sapiens 31-38 1424175-10 1992 Despite similar glucose concentrations during the oral glucose tolerance test the insulin response during the first 60 minutes following oral glucose was significantly reduced in the subjects with previous gestational diabetes when compared with controls (insulin area, 0-60 minutes; 2172, range 788-4767 vs 2830, range 996-4784 pmol min/l, P less than 0.05). Glucose 55-62 insulin Homo sapiens 82-89 1424175-10 1992 Despite similar glucose concentrations during the oral glucose tolerance test the insulin response during the first 60 minutes following oral glucose was significantly reduced in the subjects with previous gestational diabetes when compared with controls (insulin area, 0-60 minutes; 2172, range 788-4767 vs 2830, range 996-4784 pmol min/l, P less than 0.05). Glucose 55-62 insulin Homo sapiens 82-89 1424175-11 1992 CONCLUSIONS: Women with a previous history of gestational diabetes, despite having normal glucose tolerance, have defective insulin release with resultant abnormalities of intermediary metabolism. Glucose 90-97 insulin Homo sapiens 124-131 1294081-4 1992 RESULTS: Mean +/- SD areas under the blood glucose response curve (above basal) over a 3-h period were 557 +/- 60, 569 +/- 74, and 565 +/- 67 mM x 180 min (NS), and areas under the insulin-response curve were 3350 +/- 448, 2815 +/- 359 and 3551 +/- 679 mU/L x 180 min (NS) on each of the three occasions. Glucose 43-50 insulin Homo sapiens 181-188 1372238-0 1992 Sensitive colorimetric bioassays for insulin-like growth factor (IGF) stimulation of cell proliferation and glucose consumption: use in studies of IGF analogs. Glucose 108-115 insulin Homo sapiens 37-44 1535055-5 1992 The maximally insulin-stimulated rate of in vivo glucose disposal, assessed with euglycemic glucose clamps, decreased 26% in obesity and 74% in NIDDM, reflecting diminished glucose uptake by muscle. Glucose 49-56 insulin Homo sapiens 14-21 1347743-2 1992 Both 6 and 30 nM synthetic somatostatin-14 affect both glyceraldehyde- and glucose-stimulated insulin secretion to a greater degree in pancreases from old animals (24-27 months) than in those from young (2-5 months). Glucose 75-82 insulin Homo sapiens 94-101 1516757-1 1992 Northern blot analysis of human tissues has demonstrated the expression of the brain-type glucose transporter isoform (GLUT 3) in liver, muscle and fat, raising the possibility that this transporter isoform may play a role in the regulation of glucose disposal in these tissues in response to insulin. Glucose 90-97 insulin Homo sapiens 293-300 1535055-5 1992 The maximally insulin-stimulated rate of in vivo glucose disposal, assessed with euglycemic glucose clamps, decreased 26% in obesity and 74% in NIDDM, reflecting diminished glucose uptake by muscle. Glucose 92-99 insulin Homo sapiens 14-21 1535055-5 1992 The maximally insulin-stimulated rate of in vivo glucose disposal, assessed with euglycemic glucose clamps, decreased 26% in obesity and 74% in NIDDM, reflecting diminished glucose uptake by muscle. Glucose 92-99 insulin Homo sapiens 14-21 1516764-0 1992 Short-term regulation of insulin-mediated glucose utilization in four-day fasted human volunteers: role of amino acid availability. Glucose 42-49 insulin Homo sapiens 25-32 1535055-9 1992 Because muscle fibers (types I and II) exhibit different capacities for insulin-mediated glucose uptake, we tested whether a change in fiber composition could cause insulin resistance without altering overall levels of GLUT4. Glucose 89-96 insulin Homo sapiens 72-79 1516764-4 1992 The infusion of amino acids produced a rightward shift in the dose-response curve of insulin"s effect on suppressing hepatic glucose production, indicating decreased sensitivity in addition to blunting of the maximal responsiveness. Glucose 125-132 insulin Homo sapiens 85-92 1516764-5 1992 Total body glucose rate of disappearance was progressively increased with escalating insulin doses, but was 22% lower at the intermediate and highest insulin doses in the group that was infused with amino acids (3.44 +/- 0.53 vs 4.82 +/- 0.71 and 7.72 +/- 1.01 vs 10.36 +/- 1.08 mg.kg-1.min-1, respectively; p less than 0.05). Glucose 11-18 insulin Homo sapiens 85-92 1607069-5 1992 Glucose uptake by forearm tissues in response to GH and insulin did not change significantly between 3 and 6 h. By 6 h, the combined infusion of GH and insulin promoted a significantly more positive net balance of phenylalanine, leucine, isoleucine, and valine (all P less than 0.05). Glucose 0-7 insulin Homo sapiens 56-63 1516764-5 1992 Total body glucose rate of disappearance was progressively increased with escalating insulin doses, but was 22% lower at the intermediate and highest insulin doses in the group that was infused with amino acids (3.44 +/- 0.53 vs 4.82 +/- 0.71 and 7.72 +/- 1.01 vs 10.36 +/- 1.08 mg.kg-1.min-1, respectively; p less than 0.05). Glucose 11-18 insulin Homo sapiens 150-157 1516764-6 1992 Forearm balance data confirmed the isotopic data, since amino acid infusions blunted the insulin-mediated increase in net forearm glucose utilization (by 50-83%). Glucose 130-137 insulin Homo sapiens 89-96 1516764-8 1992 The data indicate that the amino acid-mediated suppression of glucose utilization and carbohydrate oxidation is exerted on the responsive component of insulin action. Glucose 62-69 insulin Homo sapiens 151-158 1516766-6 1992 Glucose levels rose in control and fell in growth hormone deficient patients when insulin infusion rates were fixed at 04.00 hours. Glucose 0-7 insulin Homo sapiens 82-89 1607069-5 1992 Glucose uptake by forearm tissues in response to GH and insulin did not change significantly between 3 and 6 h. By 6 h, the combined infusion of GH and insulin promoted a significantly more positive net balance of phenylalanine, leucine, isoleucine, and valine (all P less than 0.05). Glucose 0-7 insulin Homo sapiens 152-159 1499645-9 1992 After 5 and 24-h preincubations with interferon we observed modest changes in glucose transport sensitivity to moderate concentrations of insulin (50-100 pM) with upregulation in the presence of 10(-2)-10 IU ml-1 interferon and downregulation in the presence of 10(4)-10(5) IUm ml-1 interferon (P less than 0.05). Glucose 78-85 insulin Homo sapiens 138-145 1555870-10 1992 These results support the hypothesis that abnormalities in blood pressure regulation, insulin-stimulated glucose uptake, and insulin secretion coexist. Glucose 105-112 insulin Homo sapiens 86-93 1555690-2 1992 DESIGN: Hyperinsulinemia was determined by measuring the insulin responses during a 2-hour oral glucose tolerance test (OGTT). Glucose 96-103 insulin Homo sapiens 13-20 1556356-14 1992 However, the levels of plasma C-peptide for older men or women were statistically significantly higher than levels for the young age groups of the same sex; fasting plasma glucose also was higher for older groups of both sexes, and postmeal glucose was significantly higher for older women. Glucose 241-248 insulin Homo sapiens 30-39 1556356-16 1992 In multiple regression models for men alone and women alone, that controlled for age, post-meal plasma glucose best explained plasma C-peptide levels. Glucose 103-110 insulin Homo sapiens 133-142 1556356-18 1992 For older men and both middle-aged and older women, a combination of urine C-peptide clearance and plasma glucose best predicted plasma C-peptide levels; for middle-aged men, BMI also contributed to the prediction. Glucose 106-113 insulin Homo sapiens 136-145 1452531-6 1992 In obese patients, even fasting immunoreactive insulin (IRI) value was decreased and with increasing hyperglycaemia the reduction in IRI response to glucose stimulation was of greater magnitude compared to non-obese patients. Glucose 149-156 insulin Homo sapiens 47-54 1452531-3 1992 Insulin response patterns during 2h oral glucose tolerance test were analysed in comparison with the values in weight matched control subjects and also with respect to the degree of hyperglycaemia. Glucose 41-48 insulin Homo sapiens 0-7 1556176-11 1992 Increasing insulin concentrations to insulin 8,500 pmol/liter in four NIDDM subjects restored the glucose uptake rate and G6P concentrations to normal levels. Glucose 98-105 insulin Homo sapiens 11-18 1548342-8 1992 In a second set of experiments, islets cultured in 5.5 or 16.7 mmol/L glucose showed an insulin response to a supramaximal glucose stimulation (30 mmol/L glucose plus 0.5 mmol/L isobutylmethylxanthine) that was not statistically different. Glucose 70-77 insulin Homo sapiens 88-95 1556176-11 1992 Increasing insulin concentrations to insulin 8,500 pmol/liter in four NIDDM subjects restored the glucose uptake rate and G6P concentrations to normal levels. Glucose 98-105 insulin Homo sapiens 37-44 1556542-6 1992 If insulin therapy had been adjusted according to urine glucose results rather than blood glucose readings, diabetic ketoacidosis could have been averted in this patient. Glucose 56-63 insulin Homo sapiens 3-10 1512417-1 1992 We previously reported that patients with idiopathic reactive hypoglycemia (plasma glucose concentration lower than 2.5 mmol/L 2-4 h after the ingestion of 75 g of glucose) display reduced or absent counterregulatory response of the glucagon secretion and increased insulin sensitivity. Glucose 83-90 insulin Homo sapiens 266-273 1512417-1 1992 We previously reported that patients with idiopathic reactive hypoglycemia (plasma glucose concentration lower than 2.5 mmol/L 2-4 h after the ingestion of 75 g of glucose) display reduced or absent counterregulatory response of the glucagon secretion and increased insulin sensitivity. Glucose 164-171 insulin Homo sapiens 266-273 1619503-5 1992 In turn, the renin-angiotensin-aldosterone system affects glucose tolerance by modulating plasma potassium levels, which act as a stimulus for glucose-induced insulin release. Glucose 58-65 insulin Homo sapiens 159-166 1593308-7 1992 Pollare and co-workers tested insulin sensitivity by using the glucose-clamp technique in hypertensive patients, and found a 21% decrease in insulin sensitivity during atenolol treatment. Glucose 63-70 insulin Homo sapiens 30-37 1593308-7 1992 Pollare and co-workers tested insulin sensitivity by using the glucose-clamp technique in hypertensive patients, and found a 21% decrease in insulin sensitivity during atenolol treatment. Glucose 63-70 insulin Homo sapiens 141-148 1593308-11 1992 CONCLUSIONS: ACE inhibitors may improve insulin-dependent glucose uptake, thus leading to a reduction in insulin concentrations. Glucose 58-65 insulin Homo sapiens 40-47 1593308-11 1992 CONCLUSIONS: ACE inhibitors may improve insulin-dependent glucose uptake, thus leading to a reduction in insulin concentrations. Glucose 58-65 insulin Homo sapiens 105-112 1619503-5 1992 In turn, the renin-angiotensin-aldosterone system affects glucose tolerance by modulating plasma potassium levels, which act as a stimulus for glucose-induced insulin release. Glucose 143-150 insulin Homo sapiens 159-166 1611143-11 1992 Moreover, acute insulin response to intravenous glucose was not restored in any subject. Glucose 48-55 insulin Homo sapiens 16-23 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Glucose 372-379 insulin Homo sapiens 6-13 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Glucose 182-189 insulin Homo sapiens 6-13 1556951-5 1992 Insulin (3 x 10(-10) mol/L) submaximally decreased the glucagon-stimulated glucose production to 73% (from 30.0 +/- 1.7 to 22.0 +/- 1.4 mumol/35 min/g liver; n = 7, P less than .01). Glucose 75-82 insulin Homo sapiens 0-7 1374880-3 1992 Furthermore, atrial fibrillation was inducible or spontaneously occurred only when the blood glucose level was reduced by IV insulin administration. Glucose 93-100 insulin Homo sapiens 125-132 1579999-6 1992 Dietary regulation in IDDM is thus a compensation for the defective synchronization of variations in the plasma levels of glucose and insulin in the present day forms of insulin therapy. Glucose 122-129 insulin Homo sapiens 170-177 1579999-9 1992 The condition is characterized pathophysiologically by insulin resistance in muscle, fat and liver tissue and delayed and frequently reduced glucose-stimulated secretion of insulin. Glucose 141-148 insulin Homo sapiens 173-180 1556096-6 1992 Exogenous saturated long chain fatty acids markedly potentiated glucose-induced insulin release and elevated long chain acyl-CoA esters in the clonal beta-cell line (HIT). Glucose 64-71 insulin Homo sapiens 80-87 1312081-1 1992 Unlike glucose transport, where translocation of the insulin-responsive glucose transporter (GLUT4) from an intracellular compartment to the plasma membrane is the principal mechanism underlying insulin stimulation, no consensus exists presently for the mechanism by which insulin activates the Na+/K(+)-ATPase. Glucose 7-14 insulin Homo sapiens 53-60 1511193-7 1992 The hypertonic solution consisted of a dextrose/insulin ratio of 2.2 +/- 0.6 g/IU, which delivered glucose at a rate of 0.46 +/- 0.15 g/kg/h, in addition to the pre-existing stable maintenance glucose intake. Glucose 99-106 insulin Homo sapiens 48-55 1550048-2 1992 The increase in Am:Ap resulted in a change in the shape of the glucose and insulin responses in the blood with significantly lower initial responses but a small increase for glucose and a decrease for insulin if averaged over the 6 h of the study. Glucose 174-181 insulin Homo sapiens 75-82 1575087-0 1992 C-peptide response to oral glucose and its clinical role in elderly people. Glucose 27-34 insulin Homo sapiens 0-9 1575087-1 1992 C-Peptide response to oral glucose was measured in 45 elderly diabetics, in whom final treatment was established on clinical grounds during a 16-18 months follow-up. Glucose 27-34 insulin Homo sapiens 0-9 1575087-10 1992 These findings suggest that C-peptide response to oral glucose may be a useful test in certain elderly diabetic patients whose insulin dependence is in question. Glucose 55-62 insulin Homo sapiens 28-37 1595776-4 1992 Eleven subjects using insulin plus 10 mg glyburide before breakfast had lower mean fasting glucose at 10-16 weeks than 10 subjects using insulin with placebo (mean +/- SEM; 5.9 +/- 0.3 versus 7.5 +/- 0.7 mmol/L; p less than 0.05), and had a greater decrement of glycosylated hemoglobin from baseline values (1.3 +/- 0.1 versus 0.8 +/- 0.2% A1, p less than 0.05). Glucose 91-98 insulin Homo sapiens 22-29 1590742-3 1992 Insulin resistance as assessed for the whole body arises from a reduced glucose utilization of skeletal muscle. Glucose 72-79 insulin Homo sapiens 0-7 1315620-6 1992 Arachidonic acid inhibited glucose-sensitive insulin secretion from islets (K0.5 = 24 microM) measured in static secretion assays. Glucose 27-34 insulin Homo sapiens 45-52 1563080-10 1992 Insulin infusion during the glucose clamp completely suppressed hepatic glucose production during but not before octreotide treatment (7.9 +/- 2.4 vs 0.7 +/- 2.2 mumol/kg min, P = 0.02). Glucose 28-35 insulin Homo sapiens 0-7 1563080-10 1992 Insulin infusion during the glucose clamp completely suppressed hepatic glucose production during but not before octreotide treatment (7.9 +/- 2.4 vs 0.7 +/- 2.2 mumol/kg min, P = 0.02). Glucose 72-79 insulin Homo sapiens 0-7 1563080-11 1992 Insulin-mediated stimulation of peripheral glucose uptake was unaffected by treatment. Glucose 43-50 insulin Homo sapiens 0-7 1563080-13 1992 CONCLUSIONS: Octreotide improves whole body insulin sensitivity by an increased ability of insulin to suppress hepatic glucose production without affecting the substantial impairment of peripheral insulin action. Glucose 119-126 insulin Homo sapiens 91-98 1511755-5 1992 Noteworthy however is the ability of low-dose progestogen containing oral contraceptives, such as low dose gonane or estrane oral contraceptives, to induce glucose intolerance by increasing the plasma insulin response to oral glucose. Glucose 156-163 insulin Homo sapiens 201-208 1511755-5 1992 Noteworthy however is the ability of low-dose progestogen containing oral contraceptives, such as low dose gonane or estrane oral contraceptives, to induce glucose intolerance by increasing the plasma insulin response to oral glucose. Glucose 226-233 insulin Homo sapiens 201-208 1511756-7 1992 Insulin levels reached after 100 g glucose ingestion were significantly higher than after the 50 g glucose load. Glucose 35-42 insulin Homo sapiens 0-7 1511757-8 1992 Intralipid infusion prior to the clamp protocol induced a suppression of both insulin-mediated glucose uptake (4.91 +/- 0.46 (Intralipid) vs 6.83 +/- 0.63 mg.kg-1.min-1 (saline)) and storage (1.61 +/- 0.34 vs 2.99 +/- 0.53 mg.kg-1.min-1) while beta-pyridylcarbinol infusion induced an increased insulin-mediated glucose uptake (8.58 +/- 0.37 mg.kg-1.min-1) and in glucose storage (4.29 +/- 0.31 mg.kg-1.min-1) (p less than 0.5 vs Intralipid). Glucose 95-102 insulin Homo sapiens 78-85 1532777-10 1992 In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. Glucose 87-94 insulin Homo sapiens 70-77 1532777-10 1992 In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. Glucose 144-151 insulin Homo sapiens 70-77 1532777-12 1992 In muscle many cellular defects in insulin action have been described including impaired insulin-receptor tyrosine kinase activity, diminished glucose transport, and reduced glycogen synthase and pyruvate dehydrogenase. Glucose 143-150 insulin Homo sapiens 35-42 1551490-4 1992 Overall insulin response was compared by measuring the area under the insulin curve from the glucose tolerance test. Glucose 93-100 insulin Homo sapiens 8-15 1551490-4 1992 Overall insulin response was compared by measuring the area under the insulin curve from the glucose tolerance test. Glucose 93-100 insulin Homo sapiens 70-77 1551490-10 1992 It is concluded that there is a clear difference between blacks and whites in insulin response to a glucose load early in childhood. Glucose 100-107 insulin Homo sapiens 78-85 1551495-6 1992 Insulin-stimulated glucose disposal was significantly increased by 25% after metformin compared with placebo (26.67 +/- 2.87 vs. 21.31 +/- 1.73 mumol.kg-1.min-1, P less than 0.05). Glucose 19-26 insulin Homo sapiens 0-7 1559408-6 1992 Peripheral insulin resistance is associated with decreased glucose transport activity, the likely rate-limiting step for glucose uptake in fat and muscle. Glucose 59-66 insulin Homo sapiens 11-18 1551497-5 1992 This analysis showed that the volume of distribution and kinetic parameters of C-peptide distribution and metabolism vary by less than 30% in a population highly heterogeneous in terms of age, sex, degree of obesity, and degree of glucose tolerance. Glucose 231-238 insulin Homo sapiens 79-88 1559407-3 1992 Insulin resistance primarily involves defective regulation of hepatic glucose production and the peripheral utilization of glucose. Glucose 70-77 insulin Homo sapiens 0-7 1559407-3 1992 Insulin resistance primarily involves defective regulation of hepatic glucose production and the peripheral utilization of glucose. Glucose 123-130 insulin Homo sapiens 0-7 1559409-1 1992 Skeletal muscles in patients with non-insulin-dependent diabetes mellitus (NIDDM) are resistant to insulin; i.e., the effect of insulin on glucose disposal is reduced compared with the effect in control subjects. Glucose 139-146 insulin Homo sapiens 99-106 1559409-6 1992 Insulin is postulated to stimulate glucose storage by initiating a cascade of phosphorylation and dephosphorylation events, which results in dephosphorylation and hence activation of the enzyme glycogen synthase. Glucose 35-42 insulin Homo sapiens 0-7 1559409-17 1992 Thus, insulin resistance in the nonoxidative pathway of glucose processing can be overcomed (compensated) by hyperinsulinemia and hyperglycemia. Glucose 56-63 insulin Homo sapiens 6-13 1559410-2 1992 Insulin controls hepatic glucose production and promotes glucose utilization by the skeletal muscle. Glucose 25-32 insulin Homo sapiens 0-7 1559410-2 1992 Insulin controls hepatic glucose production and promotes glucose utilization by the skeletal muscle. Glucose 57-64 insulin Homo sapiens 0-7 1563250-2 1992 Insulin was given as a bolus intravenous injection (0.125 U kg-1) and plasma glucose fell to a nadir of 1.6 (SE 0.2) mmol l-1, with all patients experiencing an acute autonomic reaction. Glucose 77-84 insulin Homo sapiens 0-7 1563585-1 1992 To define the glucose to insulin dose-response relationship before the onset of diabetes, we studied 22 non-diabetic co-twins of patients with Type 1 (insulin-dependent) diabetes mellitus and nine control subjects. Glucose 14-21 insulin Homo sapiens 25-32 1563585-5 1992 Using a curve-fitting programme, the normal glucose to insulin relationship was lost in prediabetic twins who had lower coefficient of determination (R2) than control subjects (p less than 0.01). Glucose 44-51 insulin Homo sapiens 55-62 1563585-8 1992 These observations demonstrate an altered glucose to insulin dose-response relationship and loss of maximum insulin secretory response to glucose before the onset of Type 1 diabetes. Glucose 42-49 insulin Homo sapiens 53-60 1563585-8 1992 These observations demonstrate an altered glucose to insulin dose-response relationship and loss of maximum insulin secretory response to glucose before the onset of Type 1 diabetes. Glucose 138-145 insulin Homo sapiens 108-115 1563587-4 1992 The insulin response during the oral glucose load was inversely correlated with the rate of glucose disposal measured during a euglycaemic hyperinsulinaemic clamp (r = -0.725; p less than 0.01), while no significant correlation was observed between the corresponding values for islet amyloid polypeptide and glucose disposal (r = -0.380; p = NS). Glucose 37-44 insulin Homo sapiens 4-11 1563587-4 1992 The insulin response during the oral glucose load was inversely correlated with the rate of glucose disposal measured during a euglycaemic hyperinsulinaemic clamp (r = -0.725; p less than 0.01), while no significant correlation was observed between the corresponding values for islet amyloid polypeptide and glucose disposal (r = -0.380; p = NS). Glucose 92-99 insulin Homo sapiens 4-11 1563587-4 1992 The insulin response during the oral glucose load was inversely correlated with the rate of glucose disposal measured during a euglycaemic hyperinsulinaemic clamp (r = -0.725; p less than 0.01), while no significant correlation was observed between the corresponding values for islet amyloid polypeptide and glucose disposal (r = -0.380; p = NS). Glucose 92-99 insulin Homo sapiens 4-11 1601320-7 1992 The average insulin values in response to oral glucose load of patients with upper body segment obesity were significantly higher (Mann-Whitney"s U = 0, p less than 0.02) than the corresponding cases with lower body segment obesity. Glucose 47-54 insulin Homo sapiens 12-19 1601320-8 1992 Besides, there was a significant correlation between WHR and serum insulin values at 30 minutes after the oral glucose load (Pearson"s r = 0.331, p less than 0.02). Glucose 111-118 insulin Homo sapiens 67-74 1383242-4 1992 Acetyl choline and vasopressin (VP) both potentiate the acute effects of glucose on insulin secretion by generating inositol 1,4,5-trisphosphate to release intracellular Ca2+; VP also potentiates sustained insulin secretion by effects on depolarization. Glucose 73-80 insulin Homo sapiens 84-91 1317827-0 1992 Resistance to insulin mediated glucose disposal in obese subjects: respective effect of lipid metabolism and glycemia. Glucose 31-38 insulin Homo sapiens 14-21 1577399-1 1992 Oral application of 50 mg Etomoxir caused a significant rise (33.1%) of insulin-mediated glucose uptake. Glucose 89-96 insulin Homo sapiens 72-79 1568974-4 1992 During insulin infusion, plasma glucose decreased to a mean range of 2.0-2.1 mM for the two conditions. Glucose 32-39 insulin Homo sapiens 7-14 1541672-4 1992 Insulin-stimulated glucose disposal was decreased in the relatives (9.2 +/- 0.6 vs 11.5 +/- 0.5 mg/kg fat-free mass per (FFM) min, P less than 0.02), and was due to a decreased rate of insulin-stimulated nonoxidative glucose metabolism (5.0 +/- 0.5 vs 7.5 +/- 0.4 mg/kg fat-free mass per min, P less than 0.001). Glucose 19-26 insulin Homo sapiens 0-7 1541672-4 1992 Insulin-stimulated glucose disposal was decreased in the relatives (9.2 +/- 0.6 vs 11.5 +/- 0.5 mg/kg fat-free mass per (FFM) min, P less than 0.02), and was due to a decreased rate of insulin-stimulated nonoxidative glucose metabolism (5.0 +/- 0.5 vs 7.5 +/- 0.4 mg/kg fat-free mass per min, P less than 0.001). Glucose 19-26 insulin Homo sapiens 185-192 1383242-4 1992 Acetyl choline and vasopressin (VP) both potentiate the acute effects of glucose on insulin secretion by generating inositol 1,4,5-trisphosphate to release intracellular Ca2+; VP also potentiates sustained insulin secretion by effects on depolarization. Glucose 73-80 insulin Homo sapiens 206-213 1541672-4 1992 Insulin-stimulated glucose disposal was decreased in the relatives (9.2 +/- 0.6 vs 11.5 +/- 0.5 mg/kg fat-free mass per (FFM) min, P less than 0.02), and was due to a decreased rate of insulin-stimulated nonoxidative glucose metabolism (5.0 +/- 0.5 vs 7.5 +/- 0.4 mg/kg fat-free mass per min, P less than 0.001). Glucose 217-224 insulin Homo sapiens 0-7 1541672-5 1992 The insulin-stimulated, fractional glycogen synthase activity (0.1/10 mmol liter glucose-6-phosphate) was decreased in the relatives (46.9 +/- 2.3 vs 56.4 +/- 3.2%, P less than 0.01), and there was a significant correlation between insulin-stimulated, fractional glycogen synthase activity and nonoxidative glucose metabolism in relatives (r = 0.76, P less than 0.001) and controls (r = 0.63, P less than 0.01). Glucose 81-88 insulin Homo sapiens 4-11 1400609-3 1992 Defective glucose-induced first phase insulin responses in patients with NIDDM can be partially restored by exogenous insulin treatment and by other pharmacologic therapy. Glucose 10-17 insulin Homo sapiens 38-45 1400609-3 1992 Defective glucose-induced first phase insulin responses in patients with NIDDM can be partially restored by exogenous insulin treatment and by other pharmacologic therapy. Glucose 10-17 insulin Homo sapiens 118-125 1537878-10 1992 Finally, we found that IGF-1 and insulin, probably acting through the IGF-1 receptor, increase GLUT1 expression and stimulate glucose transport activity in epidermis reconstituted in culture. Glucose 126-133 insulin Homo sapiens 33-40 1542270-5 1992 Insulin sensitivity was measured using the hyperinsulinemic, euglycemic glucose clamp technique, and an insulin-sensitivity index was calculated as the ratio of the glucose disposal rate (GDR) to the insulin concentration during clamp (GDR/I). Glucose 165-172 insulin Homo sapiens 104-111 1556520-3 1992 Plasma glucose and insulin responses to oral glucose and fasting plasma triglyceride (TG), cholesterol, and high-density-lipoprotein (HDL) cholesterol concentrations of these 41 individuals were compared with those of 41 other factor workers, with normal blood pressure, matched with the hypertensive group in terms of gender, age, degree of obesity, job in the factory, and leisure-time activity. Glucose 45-52 insulin Homo sapiens 19-26 1556520-4 1992 Patients with hypertension had significantly higher plasma glucose (P less than 0.05) and insulin (P less than 0.05) concentrations in response to oral glucose, as well as a higher plasma TG concentration (P less than 0.05). Glucose 152-159 insulin Homo sapiens 90-97 1311795-1 1992 An insulin-like growth factor II (IGF-II)-producing histiocytoma was detected in a patient presenting with the classical findings of tumor-related hypoglycemia (low serum insulin and IGF-I concentrations, glucose intolerance, and only modestly increased serum IGF-II levels). Glucose 205-212 insulin Homo sapiens 3-10 1542271-5 1992 With the 1.0 mU insulin infusion, glucose disappearance determined with (6(3)H)glucose was lower in the hypertensive group (21.8 +/- 2.4 v 29.9 +/- 2.4 mumol.kg-1.min-1, P less than .001). Glucose 34-41 insulin Homo sapiens 16-23 1542271-5 1992 With the 1.0 mU insulin infusion, glucose disappearance determined with (6(3)H)glucose was lower in the hypertensive group (21.8 +/- 2.4 v 29.9 +/- 2.4 mumol.kg-1.min-1, P less than .001). Glucose 79-86 insulin Homo sapiens 16-23 1540164-4 1992 The reduction in Gi-proteins correlated with a decrease in insulin-stimulated glucose transport. Glucose 78-85 insulin Homo sapiens 59-66 1542855-0 1992 Insulin action on glucose and branched-chain amino acid metabolism in cancer cachexia: differential effects of insulin. Glucose 18-25 insulin Homo sapiens 0-7 1542855-2 1992 We investigated insulin action on glucose turnover rates, arterial BCAA concentrations, and forearm BCAA flux in cancer cachexia. Glucose 34-41 insulin Homo sapiens 16-23 1542855-6 1992 Total body glucose uptake was decreased in patients with cancer compared with control subjects at the 0.5 mU/kg.min (2.9 +/- 0.4 vs 3.6 +/- 1.2 mg/kg.min), 1.0 mU/kg.min (5.3 +/- 0.3 vs 8.7 +/- 0.8 mg/kg.min; p less than 0.05), and 4.0 mU/kg.min (10.9 +/- 0.9 vs 13.7 +/- 1.1 mg/kg.min) insulin infusion rates, consistent with a state of insulin resistance. Glucose 11-18 insulin Homo sapiens 287-294 1542855-6 1992 Total body glucose uptake was decreased in patients with cancer compared with control subjects at the 0.5 mU/kg.min (2.9 +/- 0.4 vs 3.6 +/- 1.2 mg/kg.min), 1.0 mU/kg.min (5.3 +/- 0.3 vs 8.7 +/- 0.8 mg/kg.min; p less than 0.05), and 4.0 mU/kg.min (10.9 +/- 0.9 vs 13.7 +/- 1.1 mg/kg.min) insulin infusion rates, consistent with a state of insulin resistance. Glucose 11-18 insulin Homo sapiens 338-345 1542855-9 1992 Insulin-induced branched-chain hypoaminoacidemia is unimpaired in this group of patients manifesting resistance to insulin action on glucose metabolism, thereby providing evidence of a differential resistance to insulin action on glucose metabolism versus insulin action on BCAA concentrations in cancer cachexia. Glucose 133-140 insulin Homo sapiens 115-122 1310987-2 1992 Genistein inhibited insulin-stimulated glucose oxidation in a concentration-dependent manner with an ID50 of 25 micrograms/ml and complete inhibition at 100 micrograms/ml. Glucose 39-46 insulin Homo sapiens 20-27 1550850-0 1992 Glucose transport by cultured human fibroblasts: regulation by phorbol esters and insulin. Glucose 0-7 insulin Homo sapiens 82-89 1543016-10 1992 Further, in the model of insulin resistance described here, metformin enhanced the basal rate of glucose transport through a direct insulin-mimicking activity and/or a potentiation of the sensitivity of glucose transport to the antibody. Glucose 97-104 insulin Homo sapiens 25-32 1371193-2 1992 Data from three model systems support the hypothesis that L-arginine-derived nitrogen oxides (NOs) mediate insulin release stimulated by L-arginine in the presence of D-glucose and by the hypoglycemic drug tolbutamide. Glucose 167-176 insulin Homo sapiens 107-114 1543016-10 1992 Further, in the model of insulin resistance described here, metformin enhanced the basal rate of glucose transport through a direct insulin-mimicking activity and/or a potentiation of the sensitivity of glucose transport to the antibody. Glucose 97-104 insulin Homo sapiens 132-139 1734672-3 1992 Total glucose disposal during insulin clamp increased from 30.4 +/- 4.3 to 38.4 +/- 4.4 mumol.kg lean body mass (LBM)-1.min-1 (P less than 0.05), insulin-stimulated glucose oxidation from 14.3 +/- 4.6 to 19.1 +/- 1.4 mumol.kg LBM-1.min-1 (P less than 0.05), and non-oxidative glucose metabolism from 16.0 +/- 3.8 to 19.3 +/- 3.6 mumol.kg LBM-1.min-1 (NS). Glucose 6-13 insulin Homo sapiens 30-37 1543018-4 1992 However, compared with controls, the obese women with the polycystic ovary syndrome showed a hyperinsulinemic response to the glucose tolerance test, indicating insulin resistance. Glucose 126-133 insulin Homo sapiens 98-105 1543018-6 1992 The insulin response to an oral glucose tolerance test remained unchanged in all women, although a hypogonadotropic hypogonadal state was maintained for several weeks. Glucose 32-39 insulin Homo sapiens 4-11 1734672-3 1992 Total glucose disposal during insulin clamp increased from 30.4 +/- 4.3 to 38.4 +/- 4.4 mumol.kg lean body mass (LBM)-1.min-1 (P less than 0.05), insulin-stimulated glucose oxidation from 14.3 +/- 4.6 to 19.1 +/- 1.4 mumol.kg LBM-1.min-1 (P less than 0.05), and non-oxidative glucose metabolism from 16.0 +/- 3.8 to 19.3 +/- 3.6 mumol.kg LBM-1.min-1 (NS). Glucose 165-172 insulin Homo sapiens 146-153 1734672-3 1992 Total glucose disposal during insulin clamp increased from 30.4 +/- 4.3 to 38.4 +/- 4.4 mumol.kg lean body mass (LBM)-1.min-1 (P less than 0.05), insulin-stimulated glucose oxidation from 14.3 +/- 4.6 to 19.1 +/- 1.4 mumol.kg LBM-1.min-1 (P less than 0.05), and non-oxidative glucose metabolism from 16.0 +/- 3.8 to 19.3 +/- 3.6 mumol.kg LBM-1.min-1 (NS). Glucose 165-172 insulin Homo sapiens 146-153 1539681-0 1992 Glucose and amino acid metabolism in chronic renal failure: effect of insulin and amino acids. Glucose 0-7 insulin Homo sapiens 70-77 1539681-3 1992 In CRF patients insulin-mediated whole body glucose metabolism was reduced by 35% (4.41 +/- 0.50 vs. 6.76 +/- 0.73 mg.kg-1.min-1, P less than 0.01), primarily due to a decrease in nonoxidative glucose disposal (1.70 +/- 0.70 vs. 4.32 +/- 0.60 mg.kg-1.min-1, P less than 0.01); glucose oxidation was similar in both groups. Glucose 44-51 insulin Homo sapiens 16-23 1539681-3 1992 In CRF patients insulin-mediated whole body glucose metabolism was reduced by 35% (4.41 +/- 0.50 vs. 6.76 +/- 0.73 mg.kg-1.min-1, P less than 0.01), primarily due to a decrease in nonoxidative glucose disposal (1.70 +/- 0.70 vs. 4.32 +/- 0.60 mg.kg-1.min-1, P less than 0.01); glucose oxidation was similar in both groups. Glucose 193-200 insulin Homo sapiens 16-23 1539681-3 1992 In CRF patients insulin-mediated whole body glucose metabolism was reduced by 35% (4.41 +/- 0.50 vs. 6.76 +/- 0.73 mg.kg-1.min-1, P less than 0.01), primarily due to a decrease in nonoxidative glucose disposal (1.70 +/- 0.70 vs. 4.32 +/- 0.60 mg.kg-1.min-1, P less than 0.01); glucose oxidation was similar in both groups. Glucose 193-200 insulin Homo sapiens 16-23 1311660-10 1992 The insulin and C-peptide responses to the intravenous glucose tolerance test were increased twofold and the net decrement in glucagon concentration was increased tenfold. Glucose 55-62 insulin Homo sapiens 4-11 1311660-10 1992 The insulin and C-peptide responses to the intravenous glucose tolerance test were increased twofold and the net decrement in glucagon concentration was increased tenfold. Glucose 55-62 insulin Homo sapiens 16-25 1311661-2 1992 Experimental elevation of plasma non-esterified fatty acid concentrations has been postulated to decrease insulin-stimulated glucose oxidation and storage rates. Glucose 125-132 insulin Homo sapiens 106-113 1311661-11 1992 During the clamp with Intralipid infusion, insulin-stimulated whole-body glucose disposal decreased by 28% (from 8.53 +/- 0.77 to 6.17 +/- 0.71 mg min-1 kg-1, P less than 0.005). Glucose 73-80 insulin Homo sapiens 43-50 1547673-8 1992 RESULTS: Fasting blood glucose levels (at 06:00 and 08:00) were significantly lower after the long-acting insulin regimen (6.26 +/- 0.88 vs. 10.82 +/- 4.27 mM, P less than 0.05 and 9.26 +/- 1.02 vs. 14.03 +/- 1.08 mM, P less than 0.05, respectively). Glucose 23-30 insulin Homo sapiens 106-113 1547915-10 1992 It is concluded that short-term administration of C-peptide in physiological amounts to patients with Type 1 diabetes may reduce the glomerular filtration rate and increase whole-body glucose utilization. Glucose 184-191 insulin Homo sapiens 50-59 1547673-9 1992 Plasma-free insulin levels mirrored blood glucose concentrations because they were significantly higher at 06:00 and 08:00 after the long-acting insulin regimen (49.5 +/- 10.1 vs. 20.1 +/- 4.3 pM, P less than 0.05 and 31.6 +/- 5.0 vs. 16.5 +/- 3.4 pM, P less than 0.05, respectively). Glucose 42-49 insulin Homo sapiens 12-19 1547915-11 1992 The results suggest the possibility that short-term C-peptide administration may exert a regulatory influence on renal function and stimulate glucose utilization in Type 1 diabetic patients. Glucose 142-149 insulin Homo sapiens 52-61 1547918-2 1992 Insulin sensitivity was measured with a + 45 mU.m2(-1).min-1 euglycaemic insulin clamp in combination with indirect calorimetry and infusion of [3-3H]glucose. Glucose 150-157 insulin Homo sapiens 0-7 1547678-7 1992 CONCLUSIONS: 1) Marked heterogeneity in glucose metabolism is seen throughout the menstrual cycle in women with IDDM, 2) a subgroup of patients exhibits worsening premenstrual hyperglycemia and a decline in insulin sensitivity during the luteal phase, and 3) the deterioration in glucose uptake in this subgroup was associated with a greater increment in estradiol levels from the follicular to the luteal phase. Glucose 40-47 insulin Homo sapiens 112-119 1547918-4 1992 Both Type 2 diabetic patients and their relatives showed impaired stimulation of total-body glucose disposal by insulin compared with control subjects (29.5 +/- 2.1 and 34.0 +/- 4.8 vs 57.9 +/- 3.1 mumol.kg lean body mass-1.min-1; p less than 0.01). Glucose 92-99 insulin Homo sapiens 112-119 1547918-5 1992 This impairment in glucose disposal was primarily accounted for by a reduction in insulin-stimulated storage of glucose as glycogen (13.0 +/- 2.4 and 15.6 +/- 3.9 vs 36.9 +/- 2.2 mumol.kg lean body mass-1.min-1; p less than 0.01). Glucose 19-26 insulin Homo sapiens 82-89 1547918-5 1992 This impairment in glucose disposal was primarily accounted for by a reduction in insulin-stimulated storage of glucose as glycogen (13.0 +/- 2.4 and 15.6 +/- 3.9 vs 36.9 +/- 2.2 mumol.kg lean body mass-1.min-1; p less than 0.01). Glucose 112-119 insulin Homo sapiens 82-89 1547928-2 1992 Intravenous infusion of insulin in doses which increase plasma insulin to physiological levels, induced vascular dilatation and increased muscle sympathetic nerve activity during a euglycaemic glucose clamp. Glucose 193-200 insulin Homo sapiens 24-31 1547679-1 1992 OBJECTIVE: To develop a computer program (Macintosh) to predict changes in blood glucose after changes in insulin dose, timing, and regimen. Glucose 81-88 insulin Homo sapiens 106-113 1563326-1 1992 Werner"s syndrome is a genetic disease characterized by premature aging and is often associated with glucose intolerance due to insulin resistance. Glucose 101-108 insulin Homo sapiens 128-135 1547685-6 1992 Insulin-releasing potency of GLP-I-(7-37) was attenuated at decreased glucose levels. Glucose 70-77 insulin Homo sapiens 0-7 1563327-9 1992 These results indicate that "normoglycemia" rather than "normoinsulinemia" attained during exogenous insulin therapy, is responsible for suppressing endogenous insulin secretion against orally administered glucose. Glucose 206-213 insulin Homo sapiens 101-108 1563328-6 1992 The plasma insulin response to a glucose load in elderly subjects was not different from that in young subjects. Glucose 33-40 insulin Homo sapiens 11-18 1733815-9 1992 Duration of obesity was inversely associated with fasting serum insulin concentration through most of the range of fasting plasma glucose concentrations (P less than 0.001) and tended to be inversely associated with 2-h postload serum insulin concentration through the entire range of postload plasma glucose concentrations (P = 0.058). Glucose 130-137 insulin Homo sapiens 64-71 1563329-7 1992 In addition, the fact that diabetic patients could reduce their insulin requirement (P less than 0.05) with concomitant reduction of their daily blood glucose level implies that sensitivity to insulin was improved by slow release starct foods consumed at breakfast. Glucose 151-158 insulin Homo sapiens 193-200 1733814-0 1992 Insulin-stimulated glucose transport in circulating mononuclear cells from nondiabetic and IDDM subjects. Glucose 19-26 insulin Homo sapiens 0-7 1733814-1 1992 The objectives of this study were 1) to evaluate glucose transport and its regulation by insulin in easily accessible human cells, 2) to investigate the glucose transporter isoforms involved, and 3) to establish whether a defect in glucose transport is associated with peripheral insulin resistance, which is common in insulin-dependent diabetes mellitus (IDDM) patients. Glucose 49-56 insulin Homo sapiens 89-96 9109953-0 1992 Insulin and glucose response following oral glucose administration in well-conditioned ponies. Glucose 44-51 insulin Homo sapiens 0-7 1572594-3 1992 These data indicate that, in neonatal islet cells, the reduced insulin release in response to glucose is associated with a diminished increase in [Ca2+]i. Glucose 94-101 insulin Homo sapiens 63-70 1735589-2 1992 Increases in plasma insulin and glucose levels have been observed in thiazide-treated hypertensive patients and have been attributed to a diminished insulin sensitivity induced by diuretic therapy. Glucose 32-39 insulin Homo sapiens 149-156 1735589-6 1992 The results obtained in the HK group after chlorthalidone showed that plasma glucose and insulin values increased after the oral glucose load to levels significantly higher than those observed after placebo. Glucose 129-136 insulin Homo sapiens 89-96 1316330-12 1992 Likewise, only the individuals with the most outspoken hepatic insulin resistance demonstrated a decrease in insulin level, at which hepatic glucose production is completely suppressed (HGP0) (P less than 0.01). Glucose 141-148 insulin Homo sapiens 63-70 1555877-7 1992 In vitro, the islets inside the bioreactor perfused with glucose solutions (300 mg%) showed a rapid, high insulin secretory response, related to the glucose stimulation. Glucose 57-64 insulin Homo sapiens 106-113 1555877-7 1992 In vitro, the islets inside the bioreactor perfused with glucose solutions (300 mg%) showed a rapid, high insulin secretory response, related to the glucose stimulation. Glucose 149-156 insulin Homo sapiens 106-113 1618926-3 1992 Two of these transporters, GLUT1 and GLUT4, are present in muscle and adipose cells, tissues in which glucose transport is markedly stimulated by insulin. Glucose 102-109 insulin Homo sapiens 146-153 1569291-0 1992 The effect of various blood glucose levels on post-glucagon C-peptide secretion in type 2 (non insulin-dependent) diabetes. Glucose 28-35 insulin Homo sapiens 60-69 1569291-1 1992 We investigated how different plasma glucose concentrations could significantly modify the C-peptide response to glucagon. Glucose 37-44 insulin Homo sapiens 91-100 1569291-10 1992 In conclusion, our data confirms that blood glucose levels modulate the pancreatic insulin secretion; glycemic normalization significantly reduced both basal and post-glucagon C-peptide release. Glucose 44-51 insulin Homo sapiens 176-185 1737857-5 1992 In vivo glucose disposal during a euglycemic clamp at an insulin infusion rate of 40 mU/m2 per min was reduced to 27% of nonobese controls (P less than 0.01) and improved to 78% of normal after weight loss of 43.1 +/- 3.1 kg (P less than 0.01). Glucose 8-15 insulin Homo sapiens 57-64 1737857-6 1992 Maximal insulin-stimulated glucose transport activity in incubated muscle fibers was reduced by approximately 50% in obese patients at the time of gastric bypass surgery but increased twofold (P less than 0.01) to 88% of normal in five separate patients after similar weight reduction. Glucose 27-34 insulin Homo sapiens 8-15 1735819-1 1992 To determine whether the insulin resistance in patients with Turner syndrome, which may be exaggerated by treatment with human growth hormone, leads to excessive insulin secretion, we applied the hyperglycemic glucose-clamp technique to produce a standard hyperglycemic stimulus (6.9 mmol/L, or 125 mg/dl, greater than fasting plasma glucose level for 120 minutes) in seven patients with Turner syndrome and in seven healthy children. Glucose 210-217 insulin Homo sapiens 25-32 1735819-6 1992 Nevertheless, the rate of insulin-stimulated glucose metabolism during the last 60 minutes of the clamp procedure was similar in all three groups of studies. Glucose 45-52 insulin Homo sapiens 26-33 1735819-8 1992 We conclude that glucose-stimulated insulin response is increased in patients with Turner syndrome and that these alterations are further exaggerated by treatment with growth hormone. Glucose 17-24 insulin Homo sapiens 36-43 1736045-1 1992 Insulin-mediated glucose disposal was studied immediately prior to and following moderate hypoglycemia in nondiabetic subjects and subjects with insulin-dependent (type I) diabetes mellitus (IDDM), the latter having varying epinephrine secretory capacities. Glucose 17-24 insulin Homo sapiens 0-7 1568529-2 1992 Insulin-stimulated glucose storage (20.1 +/- 1.5 and 11.6 +/- 1.7 vs. 27.9 +/- 1.7 mumol.kg-1 lean body mass [LBM].min-1, P less than 0.01-0.001 [3.6 +/- 0.3 and 2.1 +/- 0.3 vs. 5.0 +/- 0.3 mg.kg-1 LBM.min-1] and glycogen synthase activity, measured at 0.1 mM glucose-6-phosphate concentration (11.3 +/- 1.3 and 11.6 +/- 1.3 vs. 18.3 +/- 2.0 nmol.min-1.mg-1 protein, P less than 0.01), were impaired in relatives and diabetic subjects compared with control subjects. Glucose 19-26 insulin Homo sapiens 0-7 1583801-3 1992 He had markedly increased insulin response to oral glucose but not to intravenous glucose, intravenous arginine or intravenous glucagon. Glucose 51-58 insulin Homo sapiens 26-33 1733815-9 1992 Duration of obesity was inversely associated with fasting serum insulin concentration through most of the range of fasting plasma glucose concentrations (P less than 0.001) and tended to be inversely associated with 2-h postload serum insulin concentration through the entire range of postload plasma glucose concentrations (P = 0.058). Glucose 301-308 insulin Homo sapiens 235-242 1542462-4 1992 Prolonged hypersecretion of insulin presumably leads to pancreatic exhaustion and subsequent glucose intolerance that can progress to type II diabetes. Glucose 93-100 insulin Homo sapiens 28-35 1727062-8 1992 Molar ratios of plasma insulin to plasma glucagon levels correlated inversely (r = -0.62, P less than 0.001) with the rates of systemic glucose appearance; the latter correlated positively (r = 0.72, P less than 0.0001) with peak plasma glucose concentrations. Glucose 136-143 insulin Homo sapiens 23-30 1310538-8 1992 These results suggest that glucose may regulate expression of the human insulin gene through multiple CREs and c-Jun. Glucose 27-34 insulin Homo sapiens 72-79 1727062-8 1992 Molar ratios of plasma insulin to plasma glucagon levels correlated inversely (r = -0.62, P less than 0.001) with the rates of systemic glucose appearance; the latter correlated positively (r = 0.72, P less than 0.0001) with peak plasma glucose concentrations. Glucose 237-244 insulin Homo sapiens 23-30 1315588-0 1992 Insulin resistance and endogenous digoxin-like factor in obese hypertensive patients with glucose intolerance. Glucose 90-97 insulin Homo sapiens 0-7 1733189-5 1992 Although changes in the blood glucose and plasma insulin levels at different times during the oral glucose tolerance test occurred, they were all within normal limits for normal women. Glucose 99-106 insulin Homo sapiens 49-56 1729814-4 1992 Our results show that beta-adrenergic blockade significantly enhances insulin-mediated suppression of hepatic glucose output (p less than 0.005) and increase in glucose uptake (p less than 0.01) with a concurrent improvement in New York Heart Association functional class (p less than 0.05) and the multistage exercise treadmill test score (p less than 0.05). Glucose 110-117 insulin Homo sapiens 70-77 1736653-6 1992 In response to oral glucose, each had a diabetic response, with peak insulin levels between 2870 and 22,960 pmol/L. Glucose 20-27 insulin Homo sapiens 69-76 1736653-7 1992 Insulin-stimulated glucose disposal was determined in two patients with MAD. Glucose 19-26 insulin Homo sapiens 0-7 1520903-0 1992 Comparison of the metabolic effects of mixed meal and standard oral glucose tolerance test on glucose, insulin and C-peptide response in healthy, impaired glucose tolerance, mild and severe non-insulin-dependent diabetic subjects. Glucose 68-75 insulin Homo sapiens 115-124 1520903-2 1992 This study was carried out to compare the effects of a standard meal and the oral glucose tolerance test on glucose, insulin and C-peptide plasma levels in four groups of subjects: healthy controls, subjects with impaired glucose tolerance, patients with mild non-insulin-dependent diabetes, and non-insulin-dependent diabetic patients with secondary failure to oral agents. Glucose 82-89 insulin Homo sapiens 129-138 1520903-5 1992 Insulin and C-peptide responses per unit rise in blood glucose were significantly higher after the oral glucose tolerance test than after the mixed meal both in mild non-insulin-dependent diabetics (P less than 0.05 and P less than 0.05) and in non-insulin-dependent diabetics in secondary failure (P less than 0.01 and P less than 0.05). Glucose 55-62 insulin Homo sapiens 0-7 1520903-5 1992 Insulin and C-peptide responses per unit rise in blood glucose were significantly higher after the oral glucose tolerance test than after the mixed meal both in mild non-insulin-dependent diabetics (P less than 0.05 and P less than 0.05) and in non-insulin-dependent diabetics in secondary failure (P less than 0.01 and P less than 0.05). Glucose 55-62 insulin Homo sapiens 12-21 1520903-5 1992 Insulin and C-peptide responses per unit rise in blood glucose were significantly higher after the oral glucose tolerance test than after the mixed meal both in mild non-insulin-dependent diabetics (P less than 0.05 and P less than 0.05) and in non-insulin-dependent diabetics in secondary failure (P less than 0.01 and P less than 0.05). Glucose 104-111 insulin Homo sapiens 0-7 1520903-5 1992 Insulin and C-peptide responses per unit rise in blood glucose were significantly higher after the oral glucose tolerance test than after the mixed meal both in mild non-insulin-dependent diabetics (P less than 0.05 and P less than 0.05) and in non-insulin-dependent diabetics in secondary failure (P less than 0.01 and P less than 0.05). Glucose 104-111 insulin Homo sapiens 12-21 1576354-2 1992 Insulin secretion from isolated islets was studied after consecutive stimulation with alpha-ketoisocaproic acid + glutamine, glucose, forskolin, and 12-O-tetradecanoylphorbol 13-acetate. Glucose 125-132 insulin Homo sapiens 0-7 1576354-7 1992 Proinsulin mRNA was reduced by 35% in islets from fat-fed mice, and was associated with a reduction of approximately 50% in glucose-stimulated (pro)insulin biosynthesis. Glucose 124-131 insulin Homo sapiens 3-10 1576354-8 1992 It is concluded that the insulin secretory response of islets isolated from fat-fed mice is similar to the secretory pattern known from human type 2, non-insulin-dependent diabetics, and that a defect in islet glucose recognition, resulting in decreased glucose oxidation, may be responsible for the observed insulin secretory and biosynthetic defects seen after glucose stimulation. Glucose 210-217 insulin Homo sapiens 25-32 1576354-8 1992 It is concluded that the insulin secretory response of islets isolated from fat-fed mice is similar to the secretory pattern known from human type 2, non-insulin-dependent diabetics, and that a defect in islet glucose recognition, resulting in decreased glucose oxidation, may be responsible for the observed insulin secretory and biosynthetic defects seen after glucose stimulation. Glucose 210-217 insulin Homo sapiens 154-161 1576354-8 1992 It is concluded that the insulin secretory response of islets isolated from fat-fed mice is similar to the secretory pattern known from human type 2, non-insulin-dependent diabetics, and that a defect in islet glucose recognition, resulting in decreased glucose oxidation, may be responsible for the observed insulin secretory and biosynthetic defects seen after glucose stimulation. Glucose 254-261 insulin Homo sapiens 25-32 1736653-8 1992 At an insulin infusion rate of 120 mU/m2 per minute, glucose disposal was less than 25% of that measured at similar levels of insulinemia in nondiabetic control subjects, indicating marked insulin resistance in patients with MAD. Glucose 53-60 insulin Homo sapiens 6-13 1733245-1 1992 We performed euglycemic clamp studies with labeled glucose to measure insulin"s effect on hepatic glucose output (HGO) and peripheral glucose clearance in eight conscious mobile spontaneously hypertensive rats (SHR) and eleven normotensive Wistar-Kyoto (WKY) rats age 9-10 wk. Glucose 98-105 insulin Homo sapiens 70-77 1733245-6 1992 Insulin sensitivity, calculated as the increase in glucose clearance effected by an increase in circulating insulin during higher-dose insulin infusions, did not differ significantly between SHR and WKY groups (P greater than 0.3). Glucose 51-58 insulin Homo sapiens 0-7 1733245-6 1992 Insulin sensitivity, calculated as the increase in glucose clearance effected by an increase in circulating insulin during higher-dose insulin infusions, did not differ significantly between SHR and WKY groups (P greater than 0.3). Glucose 51-58 insulin Homo sapiens 108-115 1733245-8 1992 Our data indicate that hypertension is present in SHR at an age when insulin-mediated glucose disposal is not different from age-matched WKY rats. Glucose 86-93 insulin Homo sapiens 69-76 1590641-5 1992 Our results demonstrate that basal insulin levels as well as the insulin response after an intravenous glucose challenge are higher in moderately hypertriglyceridaemic patients when compared to age and body mass index matched controls. Glucose 103-110 insulin Homo sapiens 65-72 1590654-6 1992 Hyperresponse of serum insulin to glucose also improved. Glucose 34-41 insulin Homo sapiens 23-30 1733189-6 1992 The peak blood glucose and insulin levels after insertion of the implant occurred 60 minutes after the glucose load, as opposed to 30 minutes before insertion. Glucose 103-110 insulin Homo sapiens 27-34 1292516-1 1992 A new prototype direct reading glucose electrode working with glucose oxidase and hydrogen peroxide was preliminarily tested clinically during insulin-induced hypoglycemia in eight healthy subjects, and during hyperglycemia in five dysregulated diabetic patients. Glucose 31-38 insulin Homo sapiens 143-150 1580598-4 1992 Improvements are observed in glucose recovery following insulin-induced insulin hypoglycemia, glucagon secretion during hypoglycemia, kidney structure, and both motor and sensory nerve function. Glucose 29-36 insulin Homo sapiens 56-63 1562194-1 1992 Increases in the glucose level in the absence of the portal signal or changes in insulin elicits little if any glucose uptake by the liver. Glucose 111-118 insulin Homo sapiens 81-88 1342834-2 1992 Muscle glucose uptake and oxidation before and after ingestion of 75 g of glucose were similar to control group values, although a greater insulin release (16,578 vs 6,242 +/- 1,136 microU/3 h) occurred simultaneously. Glucose 74-81 insulin Homo sapiens 139-146 1310909-0 1992 Insulin resistance and Na+/K(+)-ATPase in hypertensive women: a difference in mechanism depending on the level of glucose tolerance. Glucose 114-121 insulin Homo sapiens 0-7 1600330-5 1992 In response to nutrients, insulin secretion (IR insulin, C-peptide) was significantly stimulated by glucose, and - to a lesser degree - also by protein. Glucose 100-107 insulin Homo sapiens 26-66 1563547-10 1992 Glucose tolerance impairment may be related to lower insulin-inhibited glucose production whereas insulin-stimulated glucose peripheral utilization is unmodified. Glucose 71-78 insulin Homo sapiens 53-60 1563547-10 1992 Glucose tolerance impairment may be related to lower insulin-inhibited glucose production whereas insulin-stimulated glucose peripheral utilization is unmodified. Glucose 117-124 insulin Homo sapiens 98-105 1563555-6 1992 Insulin increases glycogen synthesis by counteracting the action of glycogenolytic hormones and by enhancing the glucose induced activation of glycogen synthase. Glucose 113-120 insulin Homo sapiens 0-7 1291406-7 1992 With glucose and protein as intraduodenal stimulus (no pancreatin added), the plasma amino acids rose significantly less (by approximately 50% of the control experiment) and the increment in insulin (but not C-peptide) concentrations was significantly reduced by loxiglumide. Glucose 5-12 insulin Homo sapiens 191-198 1541378-6 1992 The presence of human islet amyloid polypeptide at 1, 10 and 100 nmol/l decreased the effect of 100 microU/ml of insulin on glucose transport by 61% (p less than 0.05), 78% (p less than 0.05) and 76% (p less than 0.05), respectively. Glucose 124-131 insulin Homo sapiens 113-120 1541380-6 1992 "Diabetes", as diagnosed by the oral glucose tolerance test, might be the consequence of excessive alcohol consumption which could lead to insulin resistance, then to coronary heart disease, as well as to alcohol-related diseases. Glucose 37-44 insulin Homo sapiens 139-146 1541385-6 1992 Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. Glucose 31-38 insulin Homo sapiens 12-19 1541385-6 1992 Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. Glucose 50-57 insulin Homo sapiens 12-19 1541385-9 1992 A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r = 0.65, p less than 0.02 and 0.0 mmol/l glucose 6-phosphate: r = 0.91, p less than 0.0001). Glucose 67-74 insulin Homo sapiens 138-145 1541386-8 1992 The insulin-independent patient has maintained normal fasting glucose, glycosylated haemoglobin, and oral glucose tolerance at 1 year following cessation of daily insulin therapy. Glucose 62-69 insulin Homo sapiens 4-11 1541386-8 1992 The insulin-independent patient has maintained normal fasting glucose, glycosylated haemoglobin, and oral glucose tolerance at 1 year following cessation of daily insulin therapy. Glucose 106-113 insulin Homo sapiens 4-11 1280572-7 1992 Patients with insulin-dependent diabetes frequently exhibit impaired glucose counterregulation and, although its aetiology is uncertain in some patients, intensification of insulin therapy per se has been implicated. Glucose 69-76 insulin Homo sapiens 14-21 1727716-5 1992 Under hyperinsulinemic conditions, the glucose infusion rate necessary to maintain euglycemia was 30% lower in TNF-treated rats, indicating an insulin-resistant condition. Glucose 39-46 insulin Homo sapiens 11-18 1727716-6 1992 This resulted from an impaired ability of insulin to both suppress hepatic glucose production and stimulate peripheral glucose utilization in TNF-infused animals. Glucose 75-82 insulin Homo sapiens 42-49 1309325-1 1992 Glucagon-like peptide-I(7-37) [GLP-I(7-37)] is an intestinal peptide hormone that is released in response to oral nutrients and that potently augments glucose-mediated insulin secretion. Glucose 151-158 insulin Homo sapiens 168-175 1577046-7 1992 Except for another patient who dropped out, all the others had to be treated again with insulin because their fasting blood glucose exceeded 180 mg.dl-1. Glucose 124-131 insulin Homo sapiens 88-95 1577046-8 1992 It is concluded that a single subcutaneous injection of an intermediate-acting insulin at bedtime combined with glibenclamide improved fasting and post-meal blood glucose concentrations in non-insulin-dependent patients resistant to diet and oral hypoglycaemic treatment. Glucose 163-170 insulin Homo sapiens 79-86 1612082-2 1992 In contrast, physical exercise has been shown to improve glucose tolerance and blunt the insulin response to a glucose load in insulin-resistant individuals. Glucose 111-118 insulin Homo sapiens 89-96 1612082-2 1992 In contrast, physical exercise has been shown to improve glucose tolerance and blunt the insulin response to a glucose load in insulin-resistant individuals. Glucose 111-118 insulin Homo sapiens 127-134 1612082-6 1992 These results suggest that the insulin response to a glucose load is improved in late gestational women by a single bout of moderate intensity exercise. Glucose 53-60 insulin Homo sapiens 31-38 1451714-4 1992 The metabolic clearance rate of glucose increased from 2.35 to 3.37 ml.min-1.kg-1 during treatment, suggesting improved sensitivity to insulin. Glucose 32-39 insulin Homo sapiens 135-142 1292982-3 1992 Furthermore, the insulin resistance normally seen during puberty may be restricted to peripheral glucose metabolism. Glucose 97-104 insulin Homo sapiens 17-24 1292982-4 1992 In patients with Turner"s syndrome, data indicate that there is an increase in the glucose-stimulated insulin response which is exaggerated by GH treatment. Glucose 83-90 insulin Homo sapiens 102-109 1306510-7 1992 One alternative approach is the frequently sampled intravenous glucose tolerance test where the dynamic changes in plasma insulin and glucose levels are analyzed using the so-called "minimal model" method. Glucose 63-70 insulin Homo sapiens 122-129 1306510-9 1992 The insulin resistance is located at the liver site (increased glucose production) and at the peripheral tissues (decreased oxidation and, even more, defective storage of glucose in the muscles). Glucose 63-70 insulin Homo sapiens 4-11 1306510-9 1992 The insulin resistance is located at the liver site (increased glucose production) and at the peripheral tissues (decreased oxidation and, even more, defective storage of glucose in the muscles). Glucose 171-178 insulin Homo sapiens 4-11 1306511-1 1992 It is well known that excessive weight is associated with resistance to insulin-mediated glucose uptake and predisposition to the development of type II diabetes. Glucose 89-96 insulin Homo sapiens 72-79 1306512-4 1992 When hypertensive patients whether obese or of normal weight are compared with matched normotensive control subjects, an increased plasma insulin response to a glucose challenge is consistently observed. Glucose 160-167 insulin Homo sapiens 138-145 1306515-2 1992 This impairment is multifactorial including a decrease in insulin-mediated glucose uptake by peripheral tissues and a delay in insulin-induced suppression of hepatic glucose output. Glucose 75-82 insulin Homo sapiens 58-65 1490681-12 1992 Nevertheless there are certain features such as the protracted action, the stronger effect on hepatic glucose production and the lower suppression of endogenous insulin secretion which make proinsulin a promising agent in the future management of type II diabetes. Glucose 102-109 insulin Homo sapiens 190-200 1490687-5 1992 Thus a reduced velocity of glucose transport activation by insulin appears to be a further factor contributing to peripheral insulin resistance in type II diabetics. Glucose 27-34 insulin Homo sapiens 59-66 1490687-5 1992 Thus a reduced velocity of glucose transport activation by insulin appears to be a further factor contributing to peripheral insulin resistance in type II diabetics. Glucose 27-34 insulin Homo sapiens 125-132 1490689-0 1992 Effect of the infusion of p-Glu-His-Ala-OH, analog of the anorexigenic peptide, on the insulin response induced by intravenous glucose. Glucose 127-134 insulin Homo sapiens 87-94 1612555-0 1992 Peripheral glucose metabolism in patients with insulin resistance and acanthosis nigricans. Glucose 11-18 insulin Homo sapiens 47-54 1612555-9 1992 Serum insulin levels were significantly higher in acanthotic patients than in normals before and after glucose loading. Glucose 103-110 insulin Homo sapiens 6-13 1730456-4 1992 Insulin-mediated glucose metabolism within central neurons sensitive to insulin and glucose appears to be one important signal in this relation between diet and sympathetic activity. Glucose 17-24 insulin Homo sapiens 0-7 1730456-4 1992 Insulin-mediated glucose metabolism within central neurons sensitive to insulin and glucose appears to be one important signal in this relation between diet and sympathetic activity. Glucose 17-24 insulin Homo sapiens 72-79 1730456-4 1992 Insulin-mediated glucose metabolism within central neurons sensitive to insulin and glucose appears to be one important signal in this relation between diet and sympathetic activity. Glucose 84-91 insulin Homo sapiens 0-7 1283763-3 1992 A major biochemical defect in insulin resistance seems to be a defect in the intracellular nonoxidative metabolism of glucose in muscle cells. Glucose 118-125 insulin Homo sapiens 30-37 1284137-3 1992 Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. Glucose 181-188 insulin Homo sapiens 159-166 1284137-5 1992 Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. Glucose 18-25 insulin Homo sapiens 146-153 1284137-5 1992 Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. Glucose 69-76 insulin Homo sapiens 146-153 1284137-5 1992 Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. Glucose 69-76 insulin Homo sapiens 146-153 1284139-6 1992 Although considerable knowledge has accumulated as to the actual mechanisms of insulin-dependent glucose transport, the signal transduction pathway of insulin remains poorly understood. Glucose 97-104 insulin Homo sapiens 79-86 1284139-7 1992 When insulin sensitivity is measured, it is the overall glucose uptake that is quantified under controlled conditions. Glucose 56-63 insulin Homo sapiens 5-12 1284140-2 1992 According to recent estimations, not only individuals with obesity, NIDDM, and impaired glucose tolerance (IGT) but also one fourth of the "healthy" glucose tolerant and the majority of the hypertensive population are insulin resistant. Glucose 88-95 insulin Homo sapiens 218-225 1284142-1 1992 Angiotensin-converting enzyme (ACE) inhibitors are established in the treatment of hypertension and heart failure; both conditions are complicated by resistance to insulin-mediated glucose disposal. Glucose 181-188 insulin Homo sapiens 164-171 1284142-5 1992 A number of studies, both with captopril and with enalapril, have shown small increases in insulin sensitivity, and there is evidence that this is due to enhanced glucose uptake into skeletal muscle. Glucose 163-170 insulin Homo sapiens 91-98 1284142-7 1992 Overall, there probably is a modest class effect of ACE inhibitors that enhances insulin-mediated glucose disposal; the mechanism of this effect is likely to be a combination of increased muscle blood flow, local renin-angiotensin system blockade, and elevated kinin levels. Glucose 98-105 insulin Homo sapiens 81-88 1316359-4 1992 Glucose-stimulated insulin synthesis can be increased or decreased depending on the system studied. Glucose 0-7 insulin Homo sapiens 19-26 1316359-6 1992 This hypothesis suggests that glucose-desensitization is caused by an impairment in stimulation of a hypothetical potentiator singularly responsible for: 1) some of the characteristic phases of insulin secretion; 2) basal release; 3) potentiation of non-glucose stimulators; and 4) apparent "recovery" from desensitization. Glucose 30-37 insulin Homo sapiens 194-201 1316359-6 1992 This hypothesis suggests that glucose-desensitization is caused by an impairment in stimulation of a hypothetical potentiator singularly responsible for: 1) some of the characteristic phases of insulin secretion; 2) basal release; 3) potentiation of non-glucose stimulators; and 4) apparent "recovery" from desensitization. Glucose 254-261 insulin Homo sapiens 194-201 1316359-7 1992 Review of some of the pathways that regulate insulin secretion suggest that phosphoinositol metabolism and protein kinase-C production are regulated similarly to the theoretical potentiator and their impairment is a major contributor to glucose desensitization in the beta cell. Glucose 237-244 insulin Homo sapiens 45-52 1530790-1 1992 Studies of insulin employing the oral glucose tolerance test demonstrate marked differences between the effects of different oral contraceptives, but provide little insight into the underlying disturbances. Glucose 38-45 insulin Homo sapiens 11-18 1530790-10 1992 The effects of different combined oral contraceptives on glucose tolerance test glucose, insulin, and C-peptide concentration profiles appears to be due to a combination of estrogen-induced insulin resistance and progestin-associated changes in insulin half-life. Glucose 57-64 insulin Homo sapiens 190-197 1530790-10 1992 The effects of different combined oral contraceptives on glucose tolerance test glucose, insulin, and C-peptide concentration profiles appears to be due to a combination of estrogen-induced insulin resistance and progestin-associated changes in insulin half-life. Glucose 57-64 insulin Homo sapiens 190-197 1727814-7 1992 The MCR of insulin (milliliters per kg/min) at all insulin-glucose infusion rates was significantly (P less than 0.05 or less) lower in hypertensive than normotensive subjects. Glucose 59-66 insulin Homo sapiens 11-18 1727814-7 1992 The MCR of insulin (milliliters per kg/min) at all insulin-glucose infusion rates was significantly (P less than 0.05 or less) lower in hypertensive than normotensive subjects. Glucose 59-66 insulin Homo sapiens 51-58 1727814-10 1992 In addition, a defect in insulin-stimulated glucose uptake which persists at supraphysiological insulin concentrations is confirmed in this population. Glucose 44-51 insulin Homo sapiens 25-32 1727814-10 1992 In addition, a defect in insulin-stimulated glucose uptake which persists at supraphysiological insulin concentrations is confirmed in this population. Glucose 44-51 insulin Homo sapiens 96-103 1727822-6 1992 From stepwise regression analysis using multiple, additional variables only the plasma glucose concentration at 30 min made a significant, albeit small (8%), contribution to the variability in percent decrease in C-peptide at 60 min. Glucose 87-94 insulin Homo sapiens 213-222 1732395-2 1992 It has been suggested that these metabolic abnormalities are all secondary to resistance to insulin-stimulated glucose uptake. Glucose 111-118 insulin Homo sapiens 92-99 1732395-4 1992 The high group had significantly higher fasting (P less than 0.05) and post-oral glucose challenge (P less than 0.01) insulin concentrations, higher fasting TG (P less than 0.05) and lower fasting HDL-cholesterol (P less than 0.05) concentrations than the other two groups. Glucose 81-88 insulin Homo sapiens 118-125 1495234-0 1992 [Transport and transporters of glucose in different animal models of insulin resistance]. Glucose 31-38 insulin Homo sapiens 69-76 1477029-6 1992 This finding suggests that osmotic mechanisms with various degree of well known abnormal insulin secretion and resistance to insulin action in target tissues in NIDDM patients may account for these heterogeneous responses in serum potassium changes after glucose load, and normal aldosterone levels may not be sufficient to prevent glucose induced increases in serum potassium in NIDDM patients. Glucose 255-262 insulin Homo sapiens 89-96 1535403-1 1992 By the term "insulin resistance" we understand the attenuation of insulin-stimulated glucose uptake, which is mainly due to attenuated glycogen synthesis in skeletal muscle and is partially compensated with regard to plasma glucose homeostasis by hyperinsulinemia. Glucose 85-92 insulin Homo sapiens 13-20 1535403-1 1992 By the term "insulin resistance" we understand the attenuation of insulin-stimulated glucose uptake, which is mainly due to attenuated glycogen synthesis in skeletal muscle and is partially compensated with regard to plasma glucose homeostasis by hyperinsulinemia. Glucose 85-92 insulin Homo sapiens 66-73 1535403-5 1992 At the postreceptor level, the translocation and or expression of the insulin-responsive glucose carrier GluT-4 can be down-regulated via the hexosamine pathway by hyperglycemia plus hyperinsulinemia. Glucose 89-96 insulin Homo sapiens 70-77 1308266-9 1992 IN CONCLUSION: in women with normal carbohydrate tolerance the thermogenic effect of glucose depends to a large extent on insulin sensitivity and the glucose-induced activation of the sympathetic nervous system. Glucose 85-92 insulin Homo sapiens 122-129 1347143-0 1992 Regulation of glucose kinetics in trauma patients by insulin and glucagon. Glucose 14-21 insulin Homo sapiens 53-60 1347143-5 1992 Modulation of insulin and glucagon with somatostatin indicated that non-insulin-mediated glucose uptake (NIMGU) was significantly elevated in injured patients (12.2 +/- 0.94 mumol/kg/min v 7.4 +/- 0.61 mumol/kg/min). Glucose 89-96 insulin Homo sapiens 14-21 1347143-5 1992 Modulation of insulin and glucagon with somatostatin indicated that non-insulin-mediated glucose uptake (NIMGU) was significantly elevated in injured patients (12.2 +/- 0.94 mumol/kg/min v 7.4 +/- 0.61 mumol/kg/min). Glucose 89-96 insulin Homo sapiens 72-79 1371576-2 1992 GAL is also endowed with an inhibiting effect on glucose-stimulated insulin release in animals, but not in man. Glucose 49-56 insulin Homo sapiens 68-75 1538640-0 1992 Insulin resistance in obesity is associated with elevated basal lactate levels and diminished lactate appearance following intravenous glucose and insulin. Glucose 135-142 insulin Homo sapiens 0-7 1538640-3 1992 In contrast, we have recently shown a marked decrease in the capacity for acute lactate generation in obese subjects following an oral glucose load, which we postulated might be linked to altered insulin sensitivity. Glucose 135-142 insulin Homo sapiens 196-203 1538640-6 1992 Insulin sensitivity was more tightly associated with glucose, insulin, and lactate levels (both basal and integrated) than obesity per se. Glucose 53-60 insulin Homo sapiens 0-7 1734231-6 1992 Case 3, a patient with severe hyperglycemia, illustrates that insulin will only promote the oxidation of glucose at a rapid rate once the levels of fatty acids and ketoacids decline to low levels. Glucose 105-112 insulin Homo sapiens 62-69 1734231-7 1992 Accelerated transport of glucose by insulin is only a permissive action for the oxidation of glucose. Glucose 25-32 insulin Homo sapiens 36-43 1734231-7 1992 Accelerated transport of glucose by insulin is only a permissive action for the oxidation of glucose. Glucose 93-100 insulin Homo sapiens 36-43 1375749-7 1992 When exposed to varying concentrations of glucose, these cells secreted insulin. Glucose 42-49 insulin Homo sapiens 72-79 1504480-5 1992 Complex insulin programs and frequent self-monitoring of blood glucose are required to achieve acceptable glucose control in patients with insulin-dependent diabetes mellitus. Glucose 106-113 insulin Homo sapiens 8-15 1820474-0 1991 Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration. Glucose 52-59 insulin Homo sapiens 35-42 1820474-1 1991 OBJECTIVE: To define the relationship, if any, between insulin-mediated glucose disposal and serum uric acid. Glucose 72-79 insulin Homo sapiens 55-62 1750458-2 1991 There was a significant increase in the insulin/glucose ratio (p = 0.028) during the oral glucose tolerance test during gestation. Glucose 48-55 insulin Homo sapiens 40-47 1750458-2 1991 There was a significant increase in the insulin/glucose ratio (p = 0.028) during the oral glucose tolerance test during gestation. Glucose 90-97 insulin Homo sapiens 40-47 1750458-3 1991 There was also a significant 3.0- to 3.5-fold increase throughout gestation in first-phase (p = 0.001) and second-phase (p = 0.0001) insulin release during the intravenous glucose tolerance test. Glucose 172-179 insulin Homo sapiens 133-140 1750458-4 1991 Peripheral insulin sensitivity was estimated as the glucose infusion rate (in milligrams per kilogram fat-free mass per minute) during the hyperinsulinemic-euglycemic clamp. Glucose 52-59 insulin Homo sapiens 11-18 1767833-2 1991 In study 1, insulin was infused subcutaneously (15 mU.m-2.min-1 for 12 h), and plasma glucose concentration (PG) decreased from 89 +/- 2 to 50 +/- 1 mg/dl. Glucose 86-93 insulin Homo sapiens 12-19 1836305-6 1991 The maternal insulin response to streptozocin demonstrated a loss of the second-phase insulin response to the glucose load after one dose of streptozocin and loss of the first phase after two doses. Glucose 110-117 insulin Homo sapiens 13-20 1836305-6 1991 The maternal insulin response to streptozocin demonstrated a loss of the second-phase insulin response to the glucose load after one dose of streptozocin and loss of the first phase after two doses. Glucose 110-117 insulin Homo sapiens 86-93 1811442-4 1991 Insulin (0.3 units g-1 of glucose) was administered when the standard therapy failed to produce an improvement, and at the earliest sign of haemodynamic instability. Glucose 26-33 insulin Homo sapiens 0-7 1793613-1 1991 Insulin-dependent diabetes mellitus is known to be associated with impaired ability of insulin to enhance tissue glucose uptake. Glucose 113-120 insulin Homo sapiens 0-7 1793613-4 1991 Insulin-mediated glucose disposal rate was lower in IDDM compared with controls (37.4 +/- 3.2 vs 63.8 +/- 5.4 mumol/kg/min, P less than 0.001). Glucose 17-24 insulin Homo sapiens 0-7 1793613-8 1991 Similarly, the decrement in serum K+ concentration showed a positive correlation with the rate of insulin-mediated glucose disposal (r = 0.68, P = 0.02) in controls but not in diabetics. Glucose 115-122 insulin Homo sapiens 98-105 1777624-3 1991 PMAP significantly enhanced both basal and glucose-stimulated insulin release (2.2- and 4.1-fold, respectively). Glucose 43-50 insulin Homo sapiens 62-69 1769133-12 1991 However, non-insulin-mediated glucose disposal was significantly reduced in the preoperative Cushing"s disease subjects (pre: 0.55 (0.08-1.59) vs control 1.43 (0.94-2.27) per min x 10(2), P less than 0.05). Glucose 30-37 insulin Homo sapiens 13-20 1769133-13 1991 In the Cushing"s disease subjects, glucose tolerance correlated with both insulin sensitivity (rs = 0.84, P less than 0.01) and non-insulin-mediated glucose disposal (rs = 0.56, P less than 0.05). Glucose 35-42 insulin Homo sapiens 74-81 1769133-13 1991 In the Cushing"s disease subjects, glucose tolerance correlated with both insulin sensitivity (rs = 0.84, P less than 0.01) and non-insulin-mediated glucose disposal (rs = 0.56, P less than 0.05). Glucose 35-42 insulin Homo sapiens 132-139 1769133-13 1991 In the Cushing"s disease subjects, glucose tolerance correlated with both insulin sensitivity (rs = 0.84, P less than 0.01) and non-insulin-mediated glucose disposal (rs = 0.56, P less than 0.05). Glucose 149-156 insulin Homo sapiens 132-139 1769133-15 1991 CONCLUSIONS: Cushing"s disease subjects are characterized by impaired glucose tolerance due to both reduced insulin sensitivity and non-insulin-mediated glucose disposal, in the presence of enhanced insulin secretion. Glucose 70-77 insulin Homo sapiens 108-115 1756911-2 1991 Denervated muscle is generally regarded as insulin resistant because the ability of insulin to stimulate glucose transport and glycogen synthesis is impaired. Glucose 105-112 insulin Homo sapiens 84-91 1756911-7 1991 Studies of glucose disposition confirmed that the stimulation of glycogen synthesis by insulin and, to a lesser extent, 2-deoxyglucose uptake were impaired by denervation. Glucose 11-18 insulin Homo sapiens 87-94 1756911-8 1991 However, the stimulation by insulin of glucose incorporation into DAG and other lipids was two- to threefold greater in denervated than in control muscles, and conversion of glucose to lactate and pyruvate and glucose oxidation to CO2 were unchanged. Glucose 39-46 insulin Homo sapiens 28-35 1756911-8 1991 However, the stimulation by insulin of glucose incorporation into DAG and other lipids was two- to threefold greater in denervated than in control muscles, and conversion of glucose to lactate and pyruvate and glucose oxidation to CO2 were unchanged. Glucose 174-181 insulin Homo sapiens 28-35 1756911-8 1991 However, the stimulation by insulin of glucose incorporation into DAG and other lipids was two- to threefold greater in denervated than in control muscles, and conversion of glucose to lactate and pyruvate and glucose oxidation to CO2 were unchanged. Glucose 174-181 insulin Homo sapiens 28-35 1748243-1 1991 Insulin, C-peptide, and proinsulin responses to oral glucose load. Glucose 53-60 insulin Homo sapiens 0-7 1748243-1 1991 Insulin, C-peptide, and proinsulin responses to oral glucose load. Glucose 53-60 insulin Homo sapiens 24-34 1748246-5 1991 However, insulin response to oral glucose increased significantly after hormonal intake for 6 mo. Glucose 34-41 insulin Homo sapiens 9-16 1748249-2 1991 The degree of OGTT abnormality will also influence the therapeutic approach, although the insulin response to the glucose challenge seems to be of little discriminating value. Glucose 114-121 insulin Homo sapiens 90-97 1748255-3 1991 Both nondiabetic pregnant women and women with GDM exhibit much higher insulin responses to oral or intravenous administration of glucose or amino acids than found in the nonpregnant state, and the insulin responses to a protein-rich meal are also significantly enhanced in pregnancy. Glucose 130-137 insulin Homo sapiens 71-78 1748255-3 1991 Both nondiabetic pregnant women and women with GDM exhibit much higher insulin responses to oral or intravenous administration of glucose or amino acids than found in the nonpregnant state, and the insulin responses to a protein-rich meal are also significantly enhanced in pregnancy. Glucose 130-137 insulin Homo sapiens 198-205 1748255-4 1991 Both quantitative and qualitative differences in insulin secretion exist between pregnant women with normal glucose tolerance (NGT) and women with GDM. Glucose 108-115 insulin Homo sapiens 49-56 1748255-5 1991 Insulin responses to oral glucose and protein-rich meals are thus lower in pregnant women with GDM than in women with NGT, despite significantly higher mean plasma glucose concentrations in the women with GDM. Glucose 26-33 insulin Homo sapiens 0-7 1748255-5 1991 Insulin responses to oral glucose and protein-rich meals are thus lower in pregnant women with GDM than in women with NGT, despite significantly higher mean plasma glucose concentrations in the women with GDM. Glucose 164-171 insulin Homo sapiens 0-7 1748255-7 1991 Finally, a reduced first-phase insulin response to intravenous glucose can be observed in some women with GDM. Glucose 63-70 insulin Homo sapiens 31-38 1748257-1 1991 A prospective study was undertaken to test the hypothesis that insulin treatment in patients with gestational diabetes mellitus (GDM) with fasting plasma glucose (FPG) greater than 5.3 mM significantly reduces adverse perinatal outcome. Glucose 154-161 insulin Homo sapiens 63-70 1748264-1 1991 Quantitation of insulin sensitivity (SI) with the insulin suppression test, glucose clamp, or the minimal model method has been achieved in various clinical circumstances. Glucose 76-83 insulin Homo sapiens 16-23 1778109-1 1991 The variation of endogenous insulin secretion in association with fasting plasma glucose (FPG) level and the modality of treatment was assessed using serum C-peptide levels before and after breakfast and the corrected value of 24-h urinary C-peptide (24 h-UCP) in inpatients with non-insulin-dependent diabetes mellitus. Glucose 81-88 insulin Homo sapiens 28-35 1778222-2 1991 Compared with lean controls, obese patients had increased basal and glucose-stimulated plasma insulin and C-peptide concentrations and increased plasma glucose concentrations during glucose infusion. Glucose 68-75 insulin Homo sapiens 94-101 1778355-0 1991 Effect of human C-peptide on glucose transport in in vitro incubated human skeletal muscle. Glucose 29-36 insulin Homo sapiens 16-25 1778355-3 1991 Glucose transport increased 1.8-fold in the presence of 0.3 nmol/l of insulin (p less than 0.05). Glucose 0-7 insulin Homo sapiens 70-77 1954910-1 1991 Insulin stimulation of glucose transport involves the translocation of vesicles containing the glucose transporter Glut 4 to the plasma membrane. Glucose 23-30 insulin Homo sapiens 0-7 1743436-1 1991 In primary cultured adipocytes, metabolic substrates such as glucose and amino acids have profound effects on modulating insulin"s stimulatory actions on glucose uptake and protein synthesis. Glucose 61-68 insulin Homo sapiens 121-128 1743436-1 1991 In primary cultured adipocytes, metabolic substrates such as glucose and amino acids have profound effects on modulating insulin"s stimulatory actions on glucose uptake and protein synthesis. Glucose 154-161 insulin Homo sapiens 121-128 1743436-2 1991 Insights into how substrates modulate insulin action were recently obtained when we discovered that the routing of incoming glucose through the hexosamine biosynthesis pathway leads to a refractory state over a period of several hours in which the ability of insulin to stimulate glucose uptake is severely impaired--a state known as insulin resistance. Glucose 124-131 insulin Homo sapiens 38-45 1743436-2 1991 Insights into how substrates modulate insulin action were recently obtained when we discovered that the routing of incoming glucose through the hexosamine biosynthesis pathway leads to a refractory state over a period of several hours in which the ability of insulin to stimulate glucose uptake is severely impaired--a state known as insulin resistance. Glucose 124-131 insulin Homo sapiens 259-266 1743436-2 1991 Insights into how substrates modulate insulin action were recently obtained when we discovered that the routing of incoming glucose through the hexosamine biosynthesis pathway leads to a refractory state over a period of several hours in which the ability of insulin to stimulate glucose uptake is severely impaired--a state known as insulin resistance. Glucose 124-131 insulin Homo sapiens 259-266 1743436-2 1991 Insights into how substrates modulate insulin action were recently obtained when we discovered that the routing of incoming glucose through the hexosamine biosynthesis pathway leads to a refractory state over a period of several hours in which the ability of insulin to stimulate glucose uptake is severely impaired--a state known as insulin resistance. Glucose 280-287 insulin Homo sapiens 38-45 1743436-2 1991 Insights into how substrates modulate insulin action were recently obtained when we discovered that the routing of incoming glucose through the hexosamine biosynthesis pathway leads to a refractory state over a period of several hours in which the ability of insulin to stimulate glucose uptake is severely impaired--a state known as insulin resistance. Glucose 280-287 insulin Homo sapiens 259-266 1743436-2 1991 Insights into how substrates modulate insulin action were recently obtained when we discovered that the routing of incoming glucose through the hexosamine biosynthesis pathway leads to a refractory state over a period of several hours in which the ability of insulin to stimulate glucose uptake is severely impaired--a state known as insulin resistance. Glucose 280-287 insulin Homo sapiens 259-266 1778939-3 1991 Total insulin-stimulated glucose disposal (M) was corrected for residual hepatic glucose output. Glucose 25-32 insulin Homo sapiens 6-13 1955512-6 1991 During a 6.9 mmol/L hyperglycemic clamp, glucose uptake increased in every NIDD subject (113 +/- 15 to 141 +/- 12 mg/m2.min; P less than 0.001) without a change in the plasma insulin response. Glucose 41-48 insulin Homo sapiens 175-182 1955512-7 1991 During a euglycemic insulin clamp, total glucose uptake rose in obese NIDD subjects (121 +/- 10 to 146 +/- 9 mmol/m2.min; P less than 0.05), but decreased slightly in lean NIDD (121 +/- 10 to 146 +/- 0.5; P = NS). Glucose 41-48 insulin Homo sapiens 20-27 1955512-8 1991 Hepatic glucose production was suppressed by more than 80-90% in all insulin clamp studies before and after metformin treatment. Glucose 8-15 insulin Homo sapiens 69-76 1541035-1 1992 Under certain circumstances the effect of insulin to promote glucose uptake in peripheral tissues is reduced because of a resistance to insulin action. Glucose 61-68 insulin Homo sapiens 42-49 1559300-2 1992 DESIGN: A cross-sectional study was used with continuous infusion of glucose with model assessment to determine insulin sensitivity and beta-cell function. Glucose 69-76 insulin Homo sapiens 112-119 1551306-7 1992 Differences in blood glucose concentration between stress and control day for each patient showed strong correlation with differences in plasma free insulin both during (r = -0.73) and after stress (r = -0.79). Glucose 21-28 insulin Homo sapiens 149-156 1551306-10 1992 Most of the blood glucose response to stress is explained by changes in free insulin concentration. Glucose 18-25 insulin Homo sapiens 77-84 1343113-0 1992 Acute and chronic effects of dexfenfluramine on glucose and insulin response to intravenous glucose in diabetic and non-diabetic obese subjects. Glucose 92-99 insulin Homo sapiens 60-67 1345002-2 1992 While there was no significant difference in fasting blood glucose concentrations between the four groups plasma immuno-reactive insulin concentrations were elevated (p < 0.01 or less) in the obese subjects relative to the non-obese subjects within each category of glucose tolerance. Glucose 269-276 insulin Homo sapiens 129-136 1541239-3 1992 Glucose dose-dependently stimulated a biphasic release of amylin from the pancreas in parallel with that of insulin. Glucose 0-7 insulin Homo sapiens 108-115 1541239-5 1992 The amylin-insulin molar ratios induced by 22.2 mM and 33.3 mM glucose (1.11 +/- 0.05%, 1.05 +/- 0.04%, respectively) were significantly higher than that induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs 22.2 mM glucose, P less than 0.05 vs 33.3 mM glucose). Glucose 63-70 insulin Homo sapiens 11-18 1541239-5 1992 The amylin-insulin molar ratios induced by 22.2 mM and 33.3 mM glucose (1.11 +/- 0.05%, 1.05 +/- 0.04%, respectively) were significantly higher than that induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs 22.2 mM glucose, P less than 0.05 vs 33.3 mM glucose). Glucose 173-180 insulin Homo sapiens 11-18 1541239-5 1992 The amylin-insulin molar ratios induced by 22.2 mM and 33.3 mM glucose (1.11 +/- 0.05%, 1.05 +/- 0.04%, respectively) were significantly higher than that induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs 22.2 mM glucose, P less than 0.05 vs 33.3 mM glucose). Glucose 173-180 insulin Homo sapiens 11-18 1541239-5 1992 The amylin-insulin molar ratios induced by 22.2 mM and 33.3 mM glucose (1.11 +/- 0.05%, 1.05 +/- 0.04%, respectively) were significantly higher than that induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs 22.2 mM glucose, P less than 0.05 vs 33.3 mM glucose). Glucose 173-180 insulin Homo sapiens 11-18 1541239-6 1992 In the presence of 5.6 mM glucose, glucagon also stimulated the release of amylin from the perfused pancreas in parallel with that of insulin. Glucose 26-33 insulin Homo sapiens 134-141 1541240-4 1992 Our data revealed that (1) IAPP is co-secreted with insulin from islet cells of the rat pancreas by glucose and non-glucose stimuli; (2) fasting plasma IAPP levels in normal control subjects are 24.9 +/- 2.0 pg/ml and the molar ratio of IAPP/insulin is approximately 1/7; (3) fasting IAPP levels are high in obese patients and low in insulin-dependent diabetic patients, and the molar ratio of IAPP/C-peptide in NIDDM patients is lower than that in normal control subjects, suggesting the basal hyposecretion of IAPP relative to insulin in NIDDM; and (4) the obese patients who had a hyperresponsiveness of insulin relative to C-peptide had the hyperresponsiveness of IAPP relative to C-peptide during an oral glucose load, suggesting that IAPP may have some physiological effect in glucose metabolism. Glucose 100-107 insulin Homo sapiens 52-59 1818930-0 1991 Insulin response to oral glucose in essential hypertensives with increased circulating levels of insulin growth factor I. Glucose 25-32 insulin Homo sapiens 0-7 1818930-0 1991 Insulin response to oral glucose in essential hypertensives with increased circulating levels of insulin growth factor I. Glucose 25-32 insulin Homo sapiens 97-104 1310909-10 1992 We conclude that insulin resistance is correlated with high blood pressure in women with glucose intolerance and increased androgenic activity. Glucose 89-96 insulin Homo sapiens 17-24 1748860-2 1991 Thus in these patients the spontaneous blood glucose recovery after insulin-induced hypoglycaemia (0.1 U kg-1 h-1 i.v. Glucose 45-52 insulin Homo sapiens 68-75 1748860-5 1991 When the insulin infusion test was repeated 3 months after the transplantation, the blood glucose level recovered rapidly after insulin withdrawal. Glucose 90-97 insulin Homo sapiens 9-16 1748860-5 1991 When the insulin infusion test was repeated 3 months after the transplantation, the blood glucose level recovered rapidly after insulin withdrawal. Glucose 90-97 insulin Homo sapiens 128-135 1748055-1 1991 Patients with hypertension have been shown to be resistant to insulin-stimulated glucose uptake and to be both hyperinsulinemic and hypertriglyceridemic compared with matched normotensive control groups. Glucose 81-88 insulin Homo sapiens 62-69 1961126-2 1991 To explore acute metabolic effects of IGF-I on mesangial cells, uptake of glucose and amino acid was measured in the presence of IGF-I or insulin. Glucose 74-81 insulin Homo sapiens 138-145 1961128-1 1991 To determine the contribution of skeletal muscle to the insulin resistance of essential hypertension, insulin-stimulated forearm glucose uptake was quantitated in 12 control (age, 32 +/- 3 years) and 12 hypertensive subjects (age, 36 +/- 2 years) using the forearm perfusion technique. Glucose 129-136 insulin Homo sapiens 102-109 1961128-3 1991 During insulin stimulation, whole body glucose uptake was lower in hypertensive (4.5 +/- .3 mg.kg-1.min-1) than in normal subjects (5.8 +/- .4 mg.kg-1.min-1, P less than .05). Glucose 39-46 insulin Homo sapiens 7-14 1933705-7 1991 Therapy with one or two injections per day of mixed short-acting or intermediate-acting insulin preparations is a compromise between convenience and the potential for achieving target plasma glucose levels. Glucose 191-198 insulin Homo sapiens 88-95 1661655-9 1991 In order to investigate whether a high plasma glucose concentration was maintaining the plasma C-peptide concentration in the diabetic patients, six of these patients underwent a second clamp study at euglycaemia (plasma glucose concentration 5.2 mmol/l). Glucose 46-53 insulin Homo sapiens 95-104 1748055-4 1991 Furthermore, insulin-stimulated glucose uptake is lower in spontaneously hypertensive rats (SHRs) than Wistar-Kyoto rats, and this is associated with higher plasma triglyceride concentrations and blood pressure. Glucose 32-39 insulin Homo sapiens 13-20 1748055-5 1991 In addition, a defect in insulin-stimulated glucose uptake can be shown in adipocytes isolated from SHRs, and the greater the degree of in vitro insulin resistance, the higher the plasma insulin concentration and blood pressure. Glucose 44-51 insulin Homo sapiens 25-32 1748055-5 1991 In addition, a defect in insulin-stimulated glucose uptake can be shown in adipocytes isolated from SHRs, and the greater the degree of in vitro insulin resistance, the higher the plasma insulin concentration and blood pressure. Glucose 44-51 insulin Homo sapiens 145-152 1748055-5 1991 In addition, a defect in insulin-stimulated glucose uptake can be shown in adipocytes isolated from SHRs, and the greater the degree of in vitro insulin resistance, the higher the plasma insulin concentration and blood pressure. Glucose 44-51 insulin Homo sapiens 145-152 1797490-0 1991 Altering triglyceride concentrations changes insulin-glucose relationships in hypertriglyceridemic patients. Glucose 53-60 insulin Homo sapiens 45-52 1797484-3 1991 RESEARCH DESIGN AND METHODS: Fifty-two black NIDDM subjects were assessed for insulin-stimulated glucose disposal (euglycemic clamp), glycemic control (fasting plasma glucose and HbA1c), and fasting lipid profiles. Glucose 97-104 insulin Homo sapiens 78-85 1797490-10 1991 Because glucose concentration remains the same despite the reduced insulin, the triglyceride reduction may result in greater sensitivity to insulin. Glucose 8-15 insulin Homo sapiens 140-147 1797484-5 1991 Eighteen of 30 subjects (BMI 26.4 +/- 0.5 kg/m2) had insulin resistance (glucose disposal 3.21 +/- 0.24 mg.kg-1.min-1). Glucose 73-80 insulin Homo sapiens 53-60 1797484-7 1991 Twenty-one of the remaining 22 subjects (BMI 33.4 +/- 0.7 kg/m2) were insulin resistant (glucose disposal 2.88 +/- 0.21 mg.kg-1.min-1). Glucose 89-96 insulin Homo sapiens 70-77 1797509-6 1991 Insulin was given twice daily to all patients as a mixture of NPH and regular insulins in dosages aiming at optimal glucose control. Glucose 116-123 insulin Homo sapiens 0-7 1797498-12 1991 CONCLUSIONS: Compared with a mixed dose of regular and NPH, a similar dose of a mixture of regular and human ultralente insulin before supper caused a modest reduction in fasting blood glucose levels but was associated with higher blood glucose levels before the bedtime snack. Glucose 185-192 insulin Homo sapiens 120-127 1797498-12 1991 CONCLUSIONS: Compared with a mixed dose of regular and NPH, a similar dose of a mixture of regular and human ultralente insulin before supper caused a modest reduction in fasting blood glucose levels but was associated with higher blood glucose levels before the bedtime snack. Glucose 237-244 insulin Homo sapiens 120-127 1658046-4 1991 In addition, newly differentiated adipocytes from the SC region were less sensitive to the ability of insulin to stimulate glucose uptake, and maximal insulin-stimulated glucose uptake by these cells was also significantly lower (P less than 0.05) when compared to cells obtained from the two other regions. Glucose 123-130 insulin Homo sapiens 102-109 1837509-10 1991 Possible sources of these inconsistencies are an inadequate description of the glucose and/or insulin effect upon hepatic glucose production, and the assumption that glucose kinetics are monocompartmental. Glucose 122-129 insulin Homo sapiens 94-101 1837509-10 1991 Possible sources of these inconsistencies are an inadequate description of the glucose and/or insulin effect upon hepatic glucose production, and the assumption that glucose kinetics are monocompartmental. Glucose 122-129 insulin Homo sapiens 94-101 1837511-5 1991 Linear dose-response relationships (p less than 0.005) for circulating immunoreactive insulin (log) vs metabolite concentrations were demonstrated by analysis of variance for glucose, non-esterified fatty acids (NEFA), glycerol, and total ketone bodies. Glucose 175-182 insulin Homo sapiens 86-93 1757161-0 1991 An insulin-releasing system responsive to glucose: thermodynamic evaluation of permeability properties. Glucose 42-49 insulin Homo sapiens 3-10 1757161-4 1991 The polymeric membrane system, containing immobilized glucose oxidase, was synthesized for the purpose of insulin delivery in response to glucose concentration. Glucose 54-61 insulin Homo sapiens 106-113 1658046-4 1991 In addition, newly differentiated adipocytes from the SC region were less sensitive to the ability of insulin to stimulate glucose uptake, and maximal insulin-stimulated glucose uptake by these cells was also significantly lower (P less than 0.05) when compared to cells obtained from the two other regions. Glucose 170-177 insulin Homo sapiens 151-158 1939536-7 1991 In conclusion, during training adaptations in pancreas- and insulin-sensitive tissues allow the necessary increase in food intake without harmful hyperglycemia and overloading of beta-cells, but sparing of insulin secretion and reductions in glucose levels are only relative to food intake. Glucose 242-249 insulin Homo sapiens 60-67 1939378-4 1991 Insulin administered concomitantly with glucose significantly reduced the seizure rate, as well as cortical and striatal neuronal necrosis below that seen in untreated animals. Glucose 40-47 insulin Homo sapiens 0-7 1802920-1 1991 Much research has demonstrated that in late pregnancy glucose administration causes a marked increase of peripheral insulin levels. Glucose 54-61 insulin Homo sapiens 116-123 1720806-7 1991 Secretion of both insulin and growth hormone was suppressed before the operation in response to a 75 g glucose meal and to an infusion of 100 micrograms GH-releasing hormone (GHRH) respectively in comparison with studies after the operation. Glucose 103-110 insulin Homo sapiens 18-25 1802920-4 1991 Data obtained showed that both plasma insulin and C-peptide response to oral glucose is considerably higher in women at third trimester of pregnancy as compared with that observed in the same subjects after delivery and in nonpregnant women. Glucose 77-84 insulin Homo sapiens 38-45 1802920-7 1991 The increased plasma C-peptide response clearly indicates that in pregnancy oral glucose-induced hyperinsulinism is caused by increased insulin release from pancreatic B-cells. Glucose 81-88 insulin Homo sapiens 102-109 1802920-8 1991 Moreover, the marked overall decrease of the C-peptide/insulin molar ratio suggests, even if it does not definitely prove, that hyperinsulinism after glucose in late pregnancy may be a consequence not only of increased insulin secretion, but also of decreased hepatic extraction of insulin. Glucose 150-157 insulin Homo sapiens 133-140 1802920-8 1991 Moreover, the marked overall decrease of the C-peptide/insulin molar ratio suggests, even if it does not definitely prove, that hyperinsulinism after glucose in late pregnancy may be a consequence not only of increased insulin secretion, but also of decreased hepatic extraction of insulin. Glucose 150-157 insulin Homo sapiens 133-140 1802922-4 1991 Fasting and glucose-stimulated insulin levels were significantly higher in OB than NO, in OB-HA and OB-HA-AN than in OB and NO-HA, and in OB-HA-AN than in OB-HA, without any significant difference between OB and NO-HA. Glucose 12-19 insulin Homo sapiens 31-38 1802922-6 1991 Determination coefficients r2 obtained from simple regression analysis showed that the sum of insulin values during the glucose tolerance test and testosterone levels had a more significant power in determining WHR variability. Glucose 120-127 insulin Homo sapiens 94-101 1954173-3 1991 Serum concentrations of SHBG were inversely correlated with those of both fasting and glucose-stimulated insulin. Glucose 86-93 insulin Homo sapiens 105-112 1766056-2 1991 The magnitude of resistance to insulin"s antilipolytic action is usually less than the resistance to insulin"s action on glucose metabolism. Glucose 121-128 insulin Homo sapiens 101-108 1766056-1 1991 Resistance to insulin"s effect on glucose metabolism is a well-documented phenomenon. Glucose 34-41 insulin Homo sapiens 14-21 1766056-3 1991 In sepsis, resistance to the antilipolytic effect of insulin may be more prominent than resistance to insulin"s action on glucose metabolism. Glucose 122-129 insulin Homo sapiens 102-109 1766056-5 1991 During infusion of glucose alone, plasma insulin concentration in patients and control subjects were, respectively 33 +/- 7 mU/L and 23 +/- 4 mU/L. Glucose 19-26 insulin Homo sapiens 41-48 1787825-1 1991 Amylin is a proteinaceous hormone secreted form insulin-producing pancreatic beta-cells following stimulation by food molecules such as glucose and arginine. Glucose 136-143 insulin Homo sapiens 48-55 1787825-2 1991 Amylin decreases insulin-stimulated glucose uptake in skeletal muscle and counteracts the ability of insulin to suppress output of glucose from the liver. Glucose 36-43 insulin Homo sapiens 17-24 1787825-2 1991 Amylin decreases insulin-stimulated glucose uptake in skeletal muscle and counteracts the ability of insulin to suppress output of glucose from the liver. Glucose 131-138 insulin Homo sapiens 101-108 1943745-2 1991 Acute decrements of insulin secretion (AID) are observed following the early phase of insulin release on IV glucose stimulation in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 108-115 insulin Homo sapiens 20-27 1807010-6 1991 Plasma glucose and serum insulin responses to the glucose load in hypertensive subjects were identical to the respective responses in normotensive subjects, while the mean total serum cholesterol level was slightly higher (p less than 0.05) in hypertensive subjects. Glucose 50-57 insulin Homo sapiens 25-32 1810020-1 1991 Ketone bodies and non-esterified fatty acids (NEFA) inhibit insulin stimulated glucose uptake in muscle in-vitro. Glucose 79-86 insulin Homo sapiens 60-67 1810020-3 1991 The aim of this study was to examine the effect of ketone bodies on insulin mediated forearm glucose metabolism independent of the changes in the plasma NEFA levels. Glucose 93-100 insulin Homo sapiens 68-75 1719424-1 1991 Glucose-stimulated insulin secretion is associated with the appearance of electrical activity in the pancreatic beta-cell. Glucose 0-7 insulin Homo sapiens 19-26 1719424-10 1991 These observations suggest that oscillatory glucose-stimulated electrical activity, which is correlated with pulsatile release of insulin, results from the interaction between the beta-cell and intraislet hormones and neurotransmitters. Glucose 44-51 insulin Homo sapiens 130-137 1762386-0 1991 Glucose counterregulation in type 1 diabetic patients with decreased symptoms of hypoglycemia after insulin pump treatment. Glucose 0-7 insulin Homo sapiens 100-107 1792800-3 1991 In the regulation of the glucose-concentration in the plasma the content of the skeletal musculature and of the adipose tissue in GluT type 4 plays an important role: It is insulin-dependent. Glucose 25-32 insulin Homo sapiens 173-180 1681214-0 1991 Ethnic differences in fasting plasma C-peptide and insulin in relation to glucose tolerance and blood pressure. Glucose 74-81 insulin Homo sapiens 37-46 1280578-5 1992 This effect might be helpful in patients with insulin-dependent diabetes mellitus, as insulin injections do not provide complete control of rises in postprandial glucose levels, and in patients with non-insulin-dependent diabetes mellitus, because it simplifies the treatment programme. Glucose 162-169 insulin Homo sapiens 46-53 1762378-3 1991 The results were compared with the insulin responses in the intravenous glucose tolerance tests (IVGTT) and with HLA types. Glucose 72-79 insulin Homo sapiens 35-42 1681214-0 1991 Ethnic differences in fasting plasma C-peptide and insulin in relation to glucose tolerance and blood pressure. Glucose 74-81 insulin Homo sapiens 51-58 1681214-5 1991 Fasting C-peptide and insulin concentrations increased from the subgroup with normal glucose tolerance, through impaired glucose tolerance, to new NIDDM, and were lower again in subjects with known NIDDM. Glucose 85-92 insulin Homo sapiens 8-17 1681214-5 1991 Fasting C-peptide and insulin concentrations increased from the subgroup with normal glucose tolerance, through impaired glucose tolerance, to new NIDDM, and were lower again in subjects with known NIDDM. Glucose 85-92 insulin Homo sapiens 22-29 1656753-5 1991 The insulin dose response curve was shifted to the left and at plasma insulin levels of 72 microU/ml, steady-state glucose consumption was 9.6 mg/kg/min, 50% more than in normals, and nearly three times greater than that in other cirrhotics. Glucose 115-122 insulin Homo sapiens 4-11 1759920-7 1991 Insulin sensitivity, measured as total glucose utilisation during hyperinsulinaemia, increased from stage 1 (10.3 +/- 2.1 mumoL/kg/min) by 23% at stage 3 (p less than 0.05) and by 29% at stage 4 (p less than 0.02). Glucose 39-46 insulin Homo sapiens 0-7 1928061-7 1991 Furthermore, stimulation of endogenous insulin by oral glucose results in a greater intracellular translocation of potassium in uremic rats than in controls. Glucose 55-62 insulin Homo sapiens 39-46 1928777-0 1991 The effects of insulin infusion on plasma and brain glucose in hyperglycemic diabetic rats. Glucose 52-59 insulin Homo sapiens 15-22 1928777-3 1991 A possible therapy to reduce the magnitude of ischemic brain injury in diabetic subjects would be to use an insulin infusion to reduce brain glucose concentrations to values found in those who are normoglycemic and non-diabetic. Glucose 141-148 insulin Homo sapiens 108-115 1748062-6 1991 Following insulin alone a significant increase in blood glucose levels was observed after the meal. Glucose 56-63 insulin Homo sapiens 10-17 1928777-4 1991 The present study, using hyperglycemic diabetic rats, examined the effect of an insulin infusion on plasma and brain glucose concentrations to determine their relationship while plasma glucose concentrations decreased. Glucose 117-124 insulin Homo sapiens 80-87 1928777-8 1991 When an insulin infusion was used in diabetic rats to decrease plasma glucose to nondiabetic levels over approximately 2 h, the brain glucose concentration decreased. Glucose 70-77 insulin Homo sapiens 8-15 1928777-8 1991 When an insulin infusion was used in diabetic rats to decrease plasma glucose to nondiabetic levels over approximately 2 h, the brain glucose concentration decreased. Glucose 134-141 insulin Homo sapiens 8-15 1721565-12 1991 The present results demonstrate that these changes in the GH-IGF-I axis are associated with insulin resistance with respect to blood glucose and high levels of IGFBP-1 when patients are fasted. Glucose 133-140 insulin Homo sapiens 92-99 1773683-7 1991 For the patients who were in remission for greater than 1 yr, a significant improvement of glucose intolerance was observed in association with a significantly higher insulin response to oral glucose load; however, their glycemic profile still showed a significantly higher plasma glucose concentration and a prolonged continuous elevation without initial peak of the insulin-response curve in contrast to the normal pattern found in nondiabetic subjects in the CsA-treated group. Glucose 91-98 insulin Homo sapiens 167-174 1773683-7 1991 For the patients who were in remission for greater than 1 yr, a significant improvement of glucose intolerance was observed in association with a significantly higher insulin response to oral glucose load; however, their glycemic profile still showed a significantly higher plasma glucose concentration and a prolonged continuous elevation without initial peak of the insulin-response curve in contrast to the normal pattern found in nondiabetic subjects in the CsA-treated group. Glucose 91-98 insulin Homo sapiens 368-375 1748063-6 1991 In summary, hypertriglyceridemia is associated with insulin resistance as it relates to muscle glucose utilization. Glucose 95-102 insulin Homo sapiens 52-59 1773683-7 1991 For the patients who were in remission for greater than 1 yr, a significant improvement of glucose intolerance was observed in association with a significantly higher insulin response to oral glucose load; however, their glycemic profile still showed a significantly higher plasma glucose concentration and a prolonged continuous elevation without initial peak of the insulin-response curve in contrast to the normal pattern found in nondiabetic subjects in the CsA-treated group. Glucose 192-199 insulin Homo sapiens 167-174 1773683-7 1991 For the patients who were in remission for greater than 1 yr, a significant improvement of glucose intolerance was observed in association with a significantly higher insulin response to oral glucose load; however, their glycemic profile still showed a significantly higher plasma glucose concentration and a prolonged continuous elevation without initial peak of the insulin-response curve in contrast to the normal pattern found in nondiabetic subjects in the CsA-treated group. Glucose 192-199 insulin Homo sapiens 167-174 1773687-6 1991 After intravenous stimulation with glucose and tolbutamide, the mean serum insulin rose to significantly greater (P less than 0.05) levels at t = 5 and 25 min in the offspring compared with the control subjects. Glucose 35-42 insulin Homo sapiens 75-82 1773687-12 1991 CONCLUSIONS: Our study confirmed that insulin insensitivity but not a reduced glucose effectiveness exists in young glucose-tolerant offspring of patients with NIDDM. Glucose 116-123 insulin Homo sapiens 38-45 1936592-7 1991 The biological significance of insulin-dependent gly-Pl hydrolysis was demonstrated by insulin and inositol phosphoglycan regulation of glucose metabolism in intact lymphocytes. Glucose 136-143 insulin Homo sapiens 31-38 1838062-7 1991 Glucose disposal per unit circulating insulin at the maximal infusion rate was approximately half in subjects with Impaired Glucose Tolerance (0.022 +/- 0.010 vs 0.047 +/- 0.017 ml kg-1 min-1 mU-1 l, p less than 0.01). Glucose 0-7 insulin Homo sapiens 38-45 1959706-2 1991 We studied the effect of obesity on serum proinsulin with varying degrees of glucose intolerance. Glucose 77-84 insulin Homo sapiens 42-52 1752291-7 1991 Insulin sensitivity increased significantly during treatment with enalapril (with enalapril: Ins I: 11.3 +/- 3.0, Ins II: 20.0 +/- 3.4 and Ins III: 20.6 +/- 3.9 mg kg-1 min-1 glucose (mean +/- SD); without enalapril: Ins I: 8.7 +/- 2.3, Ins II: 13.7 +/- 3.0 and Ins III: 15.5 +/- 3.1 mg kg-1 min-1 glucose; P less than 0.05). Glucose 175-182 insulin Homo sapiens 0-7 1959706-5 1991 Fasting serum proinsulin and insulin and the summed values of proinsulin and insulin during oral glucose tolerance test were significantly, or tended to be, higher in obese subjects than in those without obesity in each category of glucose tolerance. Glucose 97-104 insulin Homo sapiens 62-72 1959706-5 1991 Fasting serum proinsulin and insulin and the summed values of proinsulin and insulin during oral glucose tolerance test were significantly, or tended to be, higher in obese subjects than in those without obesity in each category of glucose tolerance. Glucose 232-239 insulin Homo sapiens 62-72 1959706-7 1991 On the other hand, the proinsulin/insulin ratio increased progressively with the deterioration of glucose tolerance. Glucose 98-105 insulin Homo sapiens 23-33 1959706-7 1991 On the other hand, the proinsulin/insulin ratio increased progressively with the deterioration of glucose tolerance. Glucose 98-105 insulin Homo sapiens 26-33 1959706-8 1991 We conclude that proinsulin secretion is disproportionately increased in the presence of glucose intolerance but not by obesity itself. Glucose 89-96 insulin Homo sapiens 17-27 1959709-0 1991 Level of skeletal muscle glucose transporter protein correlates with insulin-stimulated whole body glucose disposal in man. Glucose 25-32 insulin Homo sapiens 69-76 1752291-7 1991 Insulin sensitivity increased significantly during treatment with enalapril (with enalapril: Ins I: 11.3 +/- 3.0, Ins II: 20.0 +/- 3.4 and Ins III: 20.6 +/- 3.9 mg kg-1 min-1 glucose (mean +/- SD); without enalapril: Ins I: 8.7 +/- 2.3, Ins II: 13.7 +/- 3.0 and Ins III: 15.5 +/- 3.1 mg kg-1 min-1 glucose; P less than 0.05). Glucose 298-305 insulin Homo sapiens 0-7 1752724-9 1991 After oral glucose, exaggerated rises in plasma insulin and blood glucose were observed in obese subjects but a lesser rise was seen for lactate. Glucose 11-18 insulin Homo sapiens 48-55 1917388-3 1991 Insulin-mediated stimulation of glucose uptake and lactate production was decreased significantly in the RPE cells from diabetic donors compared with those from normal controls. Glucose 32-39 insulin Homo sapiens 0-7 1832424-3 1991 Furthermore, as serum insulin increased after glucose, DHEA-S (r2 = 0.351, P less than 0.05) and delta 4A (r2 = 0.314, P less than 0.05) decreased in an inverse linear relationship with insulin. Glucose 46-53 insulin Homo sapiens 22-29 1832424-5 1991 Thus, the endogenous serum insulin response after oral glucose in normal women is associated with suppression of serum DHEA-S and delta 4A with absence of testosterone and cortisol suppression. Glucose 55-62 insulin Homo sapiens 27-34 1890150-4 1991 During infusion study I, insulin was infused in a dynamic square wave fashion to mimic the individual post-OGTT insulin levels at content euglycemic glucose levels. Glucose 149-156 insulin Homo sapiens 25-32 1890157-4 1991 During oral glucose tolerance testing, mean plasma insulin concentrations were 33% higher in the Pimas (P less than 0.0001), but these differences were largely explained by the greater insulin resistance in the Pimas. Glucose 12-19 insulin Homo sapiens 51-58 1890150-8 1991 Insulin-stimulated glucose disposal rates and total incremental glucose disposal (IGD) over 4 h during study I at euglycemia were significantly lower in obese compared to lean subjects (area under the curve, 824 +/- 166 vs. 1222 +/- 161 mmol/L.m2; P less than 0.01) despite higher post-OGTT insulin levels in obese subjects. Glucose 19-26 insulin Homo sapiens 0-7 1890157-7 1991 After accounting for differences in insulin action, plasma insulin concentrations in Pima Indians were 50% higher than those in caucasians 3-5 min after iv glucose (P less than 0.0001), 38% higher 10 min after the end of a meal (P less than 0.0001), and 20% higher 30 min after an oral glucose load (P less than 0.006). Glucose 286-293 insulin Homo sapiens 59-66 1779020-4 1991 Insulin-stimulated glucose disposal was reduced in transplanted and non-transplanted IDDM patients and nondiabetic transplanted patients versus healthy controls (6.6 +/- 0.8, 5.7 +/- 0.7, and 7.5 +/- 0.6 versus 9.3 +/- 0.6 mg/kg LBM.min; p less than 0.05). Glucose 19-26 insulin Homo sapiens 0-7 1918378-2 1991 The acute effect of the antilipolytic nicotinic acid analogue Acipimox (2 X 250 mg) on basal and insulin-stimulated (3 h, 40 mU/m2 per min) glucose metabolism was therefore studied in 12 patients with NIDDM. Glucose 140-147 insulin Homo sapiens 97-104 1918378-7 1991 Acipimox increased the insulin-stimulated glucose disposal rate (369 +/- 49 vs. 262 +/- 31 mg/m2 per min, P less than 0.01), whereas the glucose disposal rate was unaffected by Acipimox in the basal state. Glucose 42-49 insulin Homo sapiens 23-30 1918378-14 1991 The mechanism responsible for the increased insulin-stimulated nonoxidative glucose disposal may be a stimulatory effect of Acipimox on glycogen synthase activity in skeletal muscles. Glucose 76-83 insulin Homo sapiens 44-51 1918382-2 1991 Two potential candidate genes are the insulin receptor (IR) and the insulin-sensitive glucose transporter (GLUT-4). Glucose 86-93 insulin Homo sapiens 38-45 1761807-8 1991 In summary: i) intervariations in insulin dependent glucose metabolism were described in different cirrhotic groups; ii) basal hepatic glucose production and insulin clearance rate impaired in the different groups of cirrhotics; iii) the role of decreased cholesterol/phospholipid ratio on tissues glucose metabolism in cirrhotic patients should be further studied. Glucose 52-59 insulin Homo sapiens 34-41 1943725-5 1991 On both diets, the diabetic subjects had an impaired first-phase insulin response to an intravenous glucose load compared with nondiabetic subjects (high-energy diet median first-phase increment, 4.3 and 21.2 mU/L in diabetic and nondiabetic subjects, P = .0007; low-energy diet, 4.0 and 20.4 mU/L, respectively, P = .003). Glucose 100-107 insulin Homo sapiens 65-72 1919450-3 1991 Since a subcutaneous injection of Ultralente insulin exerts its peak effect between 16 and 18 hours after injection, its prebreakfast administration is likely to inhibit overnight hepatic glucose production, which is a primary modulator of fasting plasma glucose, a major determinant of diurnal glycemia in NIDDM: Moreover, the simultaneous administration of regular insulin tends to improve glycemia during the premeal and immediate postmeal period before the onset of sulfonylurea-induced insulin secretion. Glucose 188-195 insulin Homo sapiens 45-52 1919450-3 1991 Since a subcutaneous injection of Ultralente insulin exerts its peak effect between 16 and 18 hours after injection, its prebreakfast administration is likely to inhibit overnight hepatic glucose production, which is a primary modulator of fasting plasma glucose, a major determinant of diurnal glycemia in NIDDM: Moreover, the simultaneous administration of regular insulin tends to improve glycemia during the premeal and immediate postmeal period before the onset of sulfonylurea-induced insulin secretion. Glucose 188-195 insulin Homo sapiens 367-374 1919450-3 1991 Since a subcutaneous injection of Ultralente insulin exerts its peak effect between 16 and 18 hours after injection, its prebreakfast administration is likely to inhibit overnight hepatic glucose production, which is a primary modulator of fasting plasma glucose, a major determinant of diurnal glycemia in NIDDM: Moreover, the simultaneous administration of regular insulin tends to improve glycemia during the premeal and immediate postmeal period before the onset of sulfonylurea-induced insulin secretion. Glucose 255-262 insulin Homo sapiens 45-52 1919450-3 1991 Since a subcutaneous injection of Ultralente insulin exerts its peak effect between 16 and 18 hours after injection, its prebreakfast administration is likely to inhibit overnight hepatic glucose production, which is a primary modulator of fasting plasma glucose, a major determinant of diurnal glycemia in NIDDM: Moreover, the simultaneous administration of regular insulin tends to improve glycemia during the premeal and immediate postmeal period before the onset of sulfonylurea-induced insulin secretion. Glucose 255-262 insulin Homo sapiens 367-374 1685285-3 1991 The relatively simple proof of the existence of an insulinoma which is possible by the determination of insulin is performed by the recognition of a pathognomonic insulin--blood glucose--quotient in fasting state and in the fasting test, respectively. Glucose 178-185 insulin Homo sapiens 51-58 1685285-3 1991 The relatively simple proof of the existence of an insulinoma which is possible by the determination of insulin is performed by the recognition of a pathognomonic insulin--blood glucose--quotient in fasting state and in the fasting test, respectively. Glucose 178-185 insulin Homo sapiens 104-111 1799920-9 1991 Fasting glucose levels declined significantly from 202 +/- 87 mg/dl on animal-source insulin to 178 +/- 66 mg/dl on human insulin (rDNAE coli) (P less than 0.001). Glucose 8-15 insulin Homo sapiens 85-92 1887355-7 1991 Insulin estimations in response to glucose loading were normal, which largely negates the possibility of an insulin-receptor defect in this disorder. Glucose 35-42 insulin Homo sapiens 0-7 1911706-9 1991 The hepatic lipase activity was positively correlated with the insulin area under the curve of the intravenous glucose tolerance test (r = 0.35, p = 0.02). Glucose 111-118 insulin Homo sapiens 63-70 1959042-3 1991 Insulin responses and resultant glycemic changes differ following fast and slow duodenal glucose infusion. Glucose 89-96 insulin Homo sapiens 0-7 1799920-9 1991 Fasting glucose levels declined significantly from 202 +/- 87 mg/dl on animal-source insulin to 178 +/- 66 mg/dl on human insulin (rDNAE coli) (P less than 0.001). Glucose 8-15 insulin Homo sapiens 122-129 1934705-6 1991 Essential to the success of these protocols has been our ability to monitor maternal glycemia and to maintain glucose levels in the physiologic range through aggressive therapy with insulin and diet. Glucose 110-117 insulin Homo sapiens 182-189 1959482-7 1991 On insulin treatment interruption, we observed a significantly improved fasting blood glucose level and we observed decreased insulin needs. Glucose 86-93 insulin Homo sapiens 3-10 1936615-5 1991 Improvements are also observed in glucose recovery after insulin-induced hypoglycemia and in glucagon secretion during hypoglycemia. Glucose 34-41 insulin Homo sapiens 57-64 1874176-1 1991 A water-soluble quinone, coenzyme Q0 (CoQ0), was shown to stimulate insulin release, and dicumarol, an inhibitor of quinone reductase, inhibited glucose-induced insulin release in pancreatic islets. Glucose 145-152 insulin Homo sapiens 161-168 1955097-0 1991 Acute insulin response to intravenous glucose, glucagon and arginine in some subjects at risk for type 1 (insulin-dependent) diabetes mellitus. Glucose 38-45 insulin Homo sapiens 6-13 1955101-7 1991 The markedly elevated insulin and C-peptide levels fell in a parallel manner to blood glucose but not to normal levels. Glucose 86-93 insulin Homo sapiens 22-29 1955101-8 1991 The results show that recombinant human insulin-like growth factor I, presumably by reacting with the type 1 insulin-like growth factor receptor, can normalize serum glucose levels in patients with severe insulin resistance at least for several hours. Glucose 166-173 insulin Homo sapiens 40-47 1955101-8 1991 The results show that recombinant human insulin-like growth factor I, presumably by reacting with the type 1 insulin-like growth factor receptor, can normalize serum glucose levels in patients with severe insulin resistance at least for several hours. Glucose 166-173 insulin Homo sapiens 109-116 1794936-8 1991 In vitro experiments showed that visceral fat was much more sensitive to insulin in terms of glucose uptake and triglyceride synthesis than visceral fat. Glucose 93-100 insulin Homo sapiens 73-80 1874488-6 1991 Insulin-mediated glucose disposal (4.68 vs. 6.45 mg/kg-min, p less than 0.01) was significantly impaired by 30% in cirrhotic patients during both insulin clamp studies. Glucose 17-24 insulin Homo sapiens 0-7 1874488-6 1991 Insulin-mediated glucose disposal (4.68 vs. 6.45 mg/kg-min, p less than 0.01) was significantly impaired by 30% in cirrhotic patients during both insulin clamp studies. Glucose 17-24 insulin Homo sapiens 146-153 1791088-7 1991 Levels of insulin in the serum in the serum in the fasting state and during glucose load were significantly correlated with the response of blood pressure to cold and isometric exercise, but not to blood pressure at rest. Glucose 76-83 insulin Homo sapiens 10-17 1874934-0 1991 Insulin effects on glucose and potassium metabolism in vivo: evidence for selective insulin resistance in humans. Glucose 19-26 insulin Homo sapiens 0-7 1874934-1 1991 UNLABELLED: The effects of insulin on in vivo glucose use and potassium uptake in healthy humans are well documented. Glucose 46-53 insulin Homo sapiens 27-34 1874934-9 1991 These results indicate that: 1) patients with AN are resistant to insulin action on glucose use, 2) AN patients have a normal response to insulin on potassium uptake, 3) HK is a patient with normal response to insulin on glucose use, and 4) this patient is resistant to insulin action on potassium uptake. Glucose 84-91 insulin Homo sapiens 66-73 1874934-10 1991 IN CONCLUSION: 1) we have demonstrated the independence of insulin action on glucose and potassium uptake in vivo, 2) we documented the existence of selective insulin resistance in the above patients, 3) we speculate, that in patients with a normal response to insulin on one parameter of its actions, and subnormal response on another parameter, a postreceptor defect rather than a receptor abnormality must exist. Glucose 77-84 insulin Homo sapiens 59-66 1874935-4 1991 Insulin-mediated glucose disposal was determined by the euglycemic clamp technique, and neck or axillary skin biopsies were graded blind for the presence and severity of AN in lean and obese women with the polycystic ovary syndrome (PCO) and in age- and weight-matched normal ovulatory controls. Glucose 17-24 insulin Homo sapiens 0-7 1874935-7 1991 The severity of histological AN was most highly correlated with insulin-mediated glucose disposal (r = -0.61; P less than 0.001) rather than fasting (r = 0.46; P less than 0.05) or glucose-stimulated insulin levels (r = 0.48; P less than 0.01). Glucose 81-88 insulin Homo sapiens 64-71 1895963-7 1991 After loading glucose, plasma glucose and insulin levels were still significantly higher in patients than controls. Glucose 14-21 insulin Homo sapiens 42-49 1753610-3 1991 In patients with Stage I heart failure, who had normal resting hemodynamic parameters, metabolic parameters were indicative of abnormalities in carbohydrate metabolism: there was a reduction in carbohydrate tolerance and red blood cell release of insulin in response to glucose load and an increase in blood immunoreactive insulin, erythrocytic glucose-6-phosphate dehydrogenase activity and greater adrenalin- and insulin-containing erythrocytes. Glucose 270-277 insulin Homo sapiens 247-254 1753610-3 1991 In patients with Stage I heart failure, who had normal resting hemodynamic parameters, metabolic parameters were indicative of abnormalities in carbohydrate metabolism: there was a reduction in carbohydrate tolerance and red blood cell release of insulin in response to glucose load and an increase in blood immunoreactive insulin, erythrocytic glucose-6-phosphate dehydrogenase activity and greater adrenalin- and insulin-containing erythrocytes. Glucose 270-277 insulin Homo sapiens 323-330 1753610-3 1991 In patients with Stage I heart failure, who had normal resting hemodynamic parameters, metabolic parameters were indicative of abnormalities in carbohydrate metabolism: there was a reduction in carbohydrate tolerance and red blood cell release of insulin in response to glucose load and an increase in blood immunoreactive insulin, erythrocytic glucose-6-phosphate dehydrogenase activity and greater adrenalin- and insulin-containing erythrocytes. Glucose 270-277 insulin Homo sapiens 323-330 1895955-0 1991 Understanding "insulin resistance": both glucose resistance and insulin resistance are required to model human diabetes. Glucose 41-48 insulin Homo sapiens 15-22 1895955-4 1991 A defect of either glucose resistance or insulin resistance affecting both periphery and liver allowed a wider range of basal glucose and insulin concentration values, but resulted in unphysiologically low hepatic glucose output: with modeling insulin resistance, hyperglycemia suppressed glucose output, whereas with glucose resistance, raised insulin levels suppressed hepatic glucose output. Glucose 19-26 insulin Homo sapiens 138-145 1895955-4 1991 A defect of either glucose resistance or insulin resistance affecting both periphery and liver allowed a wider range of basal glucose and insulin concentration values, but resulted in unphysiologically low hepatic glucose output: with modeling insulin resistance, hyperglycemia suppressed glucose output, whereas with glucose resistance, raised insulin levels suppressed hepatic glucose output. Glucose 19-26 insulin Homo sapiens 138-145 1895963-8 1991 Euglycemic hyperinsulinemic glucose clamp produced a lower insulin-mediated inhibition of endogenous (hepatic) glucose production (HGP) and a greater increase in both glucose disappearance rate (Rd) and glucose metabolic clearance rate (gMCR) in patients than in controls during the first two insulin infusion rates (25 and 50 mU/kg/h). Glucose 28-35 insulin Homo sapiens 16-23 1895955-4 1991 A defect of either glucose resistance or insulin resistance affecting both periphery and liver allowed a wider range of basal glucose and insulin concentration values, but resulted in unphysiologically low hepatic glucose output: with modeling insulin resistance, hyperglycemia suppressed glucose output, whereas with glucose resistance, raised insulin levels suppressed hepatic glucose output. Glucose 126-133 insulin Homo sapiens 41-48 1895963-8 1991 Euglycemic hyperinsulinemic glucose clamp produced a lower insulin-mediated inhibition of endogenous (hepatic) glucose production (HGP) and a greater increase in both glucose disappearance rate (Rd) and glucose metabolic clearance rate (gMCR) in patients than in controls during the first two insulin infusion rates (25 and 50 mU/kg/h). Glucose 28-35 insulin Homo sapiens 59-66 1895955-4 1991 A defect of either glucose resistance or insulin resistance affecting both periphery and liver allowed a wider range of basal glucose and insulin concentration values, but resulted in unphysiologically low hepatic glucose output: with modeling insulin resistance, hyperglycemia suppressed glucose output, whereas with glucose resistance, raised insulin levels suppressed hepatic glucose output. Glucose 126-133 insulin Homo sapiens 41-48 1895958-0 1991 Forearm insulin- and non-insulin-mediated glucose uptake and muscle metabolism in man: role of free fatty acids and blood glucose levels. Glucose 42-49 insulin Homo sapiens 8-15 1895963-8 1991 Euglycemic hyperinsulinemic glucose clamp produced a lower insulin-mediated inhibition of endogenous (hepatic) glucose production (HGP) and a greater increase in both glucose disappearance rate (Rd) and glucose metabolic clearance rate (gMCR) in patients than in controls during the first two insulin infusion rates (25 and 50 mU/kg/h). Glucose 111-118 insulin Homo sapiens 16-23 1895958-0 1991 Forearm insulin- and non-insulin-mediated glucose uptake and muscle metabolism in man: role of free fatty acids and blood glucose levels. Glucose 42-49 insulin Homo sapiens 25-32 1895958-1 1991 Muscle can utilize glucose by two different mechanisms, one non-insulin-mediated and the other insulin-mediated. Glucose 19-26 insulin Homo sapiens 64-71 1895963-8 1991 Euglycemic hyperinsulinemic glucose clamp produced a lower insulin-mediated inhibition of endogenous (hepatic) glucose production (HGP) and a greater increase in both glucose disappearance rate (Rd) and glucose metabolic clearance rate (gMCR) in patients than in controls during the first two insulin infusion rates (25 and 50 mU/kg/h). Glucose 111-118 insulin Homo sapiens 59-66 1895958-1 1991 Muscle can utilize glucose by two different mechanisms, one non-insulin-mediated and the other insulin-mediated. Glucose 19-26 insulin Homo sapiens 95-102 1895963-8 1991 Euglycemic hyperinsulinemic glucose clamp produced a lower insulin-mediated inhibition of endogenous (hepatic) glucose production (HGP) and a greater increase in both glucose disappearance rate (Rd) and glucose metabolic clearance rate (gMCR) in patients than in controls during the first two insulin infusion rates (25 and 50 mU/kg/h). Glucose 111-118 insulin Homo sapiens 16-23 1895958-2 1991 The aim of this study was to investigate and to quantify the influence of high and low free fatty acids (FFA) levels on muscle non-insulin-mediated glucose uptake (MNIMGU) and muscle insulin-mediated glucose uptake (MIMGU) and on muscle metabolism during euglycemia and hyperglycemia. Glucose 148-155 insulin Homo sapiens 131-138 1895958-2 1991 The aim of this study was to investigate and to quantify the influence of high and low free fatty acids (FFA) levels on muscle non-insulin-mediated glucose uptake (MNIMGU) and muscle insulin-mediated glucose uptake (MIMGU) and on muscle metabolism during euglycemia and hyperglycemia. Glucose 200-207 insulin Homo sapiens 183-190 1895960-7 1991 Percentage elevation of glucose disposal was significantly increased during each of the insulin infusions compared with proinsulin: I1 107% +/- 4%, P1 87% +/- 4% (P = .03); I2 143% +/- 7%, P2 125% +/- 12% (P = .01); I3 238% +/- 38%, P3 173% +/- 22% (P = .03); I4 283% +/- 17%, P4 178% +/- 11% (P = .002). Glucose 24-31 insulin Homo sapiens 88-95 1895960-8 1991 Dose-response curve analysis demonstrated that proinsulin stimulated glucose disposal approximately 3.3% compared with insulin. Glucose 69-76 insulin Homo sapiens 47-57 1895960-8 1991 Dose-response curve analysis demonstrated that proinsulin stimulated glucose disposal approximately 3.3% compared with insulin. Glucose 69-76 insulin Homo sapiens 50-57 1895963-8 1991 Euglycemic hyperinsulinemic glucose clamp produced a lower insulin-mediated inhibition of endogenous (hepatic) glucose production (HGP) and a greater increase in both glucose disappearance rate (Rd) and glucose metabolic clearance rate (gMCR) in patients than in controls during the first two insulin infusion rates (25 and 50 mU/kg/h). Glucose 111-118 insulin Homo sapiens 59-66 1716797-13 1991 Higher doses of FK506 produced a significant delay in glucose disappearance in groups 3 and 4, and a significant inhibition of glucose-mediated C-peptide response in group 4. Glucose 127-134 insulin Homo sapiens 144-153 1944317-1 1991 The benefit of lowering blood glucose levels with intensive insulin therapy, especially with regard to the development and progression of microvascular complications, is still being investigated. Glucose 30-37 insulin Homo sapiens 60-67 1930926-3 1991 Regular physical activity increases insulin sensitivity through its effect on glucose utilisation in peripheral (muscle) tissue. Glucose 78-85 insulin Homo sapiens 36-43 1872837-3 1991 When medium glucose was less than or equal to 10 mM, the production of insulin exceeded or equaled its release. Glucose 12-19 insulin Homo sapiens 71-78 1872837-4 1991 Raising the glucose levels above 10 mM did not further increase the rate of insulin synthesis (67 +/- 10 fmol/10(3) cells/2 hour) but elevated that of insulin release up to 3-fold the production rates (181 +/- 10 fmol/10(3) cells/2 hour). Glucose 12-19 insulin Homo sapiens 151-158 1872837-6 1991 It is concluded that glucose as well as hormonal regulators of islet B cells can influence, bi-directionally, the balance between the rates of insulin synthesis and release. Glucose 21-28 insulin Homo sapiens 143-150 1860833-1 1991 At physiological glucose concentrations, isolated pancreatic islets release a minor portion of their newly synthesized insulin and precursors in a phase of secretion which is largely complete by 4 h of chase. Glucose 17-24 insulin Homo sapiens 119-126 1860833-4 1991 The stoichiometry of release of labeled C-peptide:insulin during this phase is 1:1 at high glucose concentrations. Glucose 91-98 insulin Homo sapiens 40-49 1860833-4 1991 The stoichiometry of release of labeled C-peptide:insulin during this phase is 1:1 at high glucose concentrations. Glucose 91-98 insulin Homo sapiens 50-57 1858738-4 1991 In patients with pancreatic tissue with the most severe fibrosis, of several preoperative glucose metabolism indices measured, it was found that the ratio of integrated value of change in serum insulin to that of serum glucose (sigma delta IRI:sigma delta BS) was significantly decreased. Glucose 90-97 insulin Homo sapiens 194-201 1653662-4 1991 A controlled, step-wise reduction in blood glucose concentration was achieved by adjusting the rate of glucose infusion during a primed-continuous infusion of soluble insulin (1.5 m-units min-1 kg-1 body weight, plasma insulin concentration approximately 90 m-units/l). Glucose 43-50 insulin Homo sapiens 167-174 1653663-3 1991 The insulin response to oral glucose, insulin sensitivity and fasting glucose production rates were measured by using a 75 g oral glucose tolerance test, an insulin tolerance test and a non-radioactive tracer, [6,6-2H]glucose, respectively. Glucose 29-36 insulin Homo sapiens 4-11 1653663-6 1991 After oral glucose the 60 min plasma glucose levels in the women with previous gestational diabetes were significantly higher (8.5 +/- 0.6 versus 6.7 +/- 0.8 mmol/l, P less than 0.05), whereas the plasma insulin level was significantly lower at both 30 min (median 23 m-units/l, range 4-47 m-units/l versus median 55 m-units/l, range 23-100 m-units/l, P less than 0.02) and at 60 min (median 23 m-units/l, range 4-43 m-units/l versus median 60 m-units/l, range 16-126 m-units/l, P less than 0.02). Glucose 11-18 insulin Homo sapiens 204-211 1653663-6 1991 After oral glucose the 60 min plasma glucose levels in the women with previous gestational diabetes were significantly higher (8.5 +/- 0.6 versus 6.7 +/- 0.8 mmol/l, P less than 0.05), whereas the plasma insulin level was significantly lower at both 30 min (median 23 m-units/l, range 4-47 m-units/l versus median 55 m-units/l, range 23-100 m-units/l, P less than 0.02) and at 60 min (median 23 m-units/l, range 4-43 m-units/l versus median 60 m-units/l, range 16-126 m-units/l, P less than 0.02). Glucose 37-44 insulin Homo sapiens 204-211 1680601-3 1991 The proinsulin-corrected insulin response to an intravenous glucose infusion test was significantly lower among siblings when insulin sensitivity was taken into account (1.65 (inter-quartile range 1.20-2.64) vs 2.18 (1.65-3.28) nmol mmol-1 min, p = 0.04). Glucose 60-67 insulin Homo sapiens 4-14 1653663-8 1991 Insulin sensitivity, expressed as the slope of the regression line of plasma glucose level against time after intravenous infusion of insulin (0.05 unit/kg), was similar in the women with previous gestational diabetes and the control subjects (mean slope, -0.17 +/- 0.01 versus -0.17 +/- 0.01). Glucose 77-84 insulin Homo sapiens 0-7 1680601-1 1991 Glucose-stimulated insulin and proinsulin responses, and insulin sensitivity, were studied in 30 HLA identical, 38 HLA haplo-identical, and 25 HLA non-identical, healthy islet-cell-antibody negative siblings of Type 1 diabetic patients. Glucose 0-7 insulin Homo sapiens 19-26 1680601-3 1991 The proinsulin-corrected insulin response to an intravenous glucose infusion test was significantly lower among siblings when insulin sensitivity was taken into account (1.65 (inter-quartile range 1.20-2.64) vs 2.18 (1.65-3.28) nmol mmol-1 min, p = 0.04). Glucose 60-67 insulin Homo sapiens 7-14 1680601-3 1991 The proinsulin-corrected insulin response to an intravenous glucose infusion test was significantly lower among siblings when insulin sensitivity was taken into account (1.65 (inter-quartile range 1.20-2.64) vs 2.18 (1.65-3.28) nmol mmol-1 min, p = 0.04). Glucose 60-67 insulin Homo sapiens 25-32 1860552-5 1991 However, the release of amylin induced by high concentrations of glucose was partially dissociated from that of insulin; that is, the amylin-insulin molar ratios induced by 22.2 and 33.3 mM glucose (1.11 +/- 0.05 and 1.05 +/- 0.04%, respectively) were significantly higher than those induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs. 22.2 mM glucose, P less than 0.05 vs. 33.3 mM glucose). Glucose 190-197 insulin Homo sapiens 141-148 1860552-5 1991 However, the release of amylin induced by high concentrations of glucose was partially dissociated from that of insulin; that is, the amylin-insulin molar ratios induced by 22.2 and 33.3 mM glucose (1.11 +/- 0.05 and 1.05 +/- 0.04%, respectively) were significantly higher than those induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs. 22.2 mM glucose, P less than 0.05 vs. 33.3 mM glucose). Glucose 190-197 insulin Homo sapiens 141-148 1860552-5 1991 However, the release of amylin induced by high concentrations of glucose was partially dissociated from that of insulin; that is, the amylin-insulin molar ratios induced by 22.2 and 33.3 mM glucose (1.11 +/- 0.05 and 1.05 +/- 0.04%, respectively) were significantly higher than those induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs. 22.2 mM glucose, P less than 0.05 vs. 33.3 mM glucose). Glucose 190-197 insulin Homo sapiens 141-148 1860552-5 1991 However, the release of amylin induced by high concentrations of glucose was partially dissociated from that of insulin; that is, the amylin-insulin molar ratios induced by 22.2 and 33.3 mM glucose (1.11 +/- 0.05 and 1.05 +/- 0.04%, respectively) were significantly higher than those induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs. 22.2 mM glucose, P less than 0.05 vs. 33.3 mM glucose). Glucose 190-197 insulin Homo sapiens 141-148 1860554-1 1991 Hyperinsulinemia may be an early inherited marker for a defect in insulin action that subsequently results in glucose intolerance and non-insulin-dependent diabetes mellitus (NIDDM). Glucose 110-117 insulin Homo sapiens 5-12 1914533-2 1991 One major problem encountered when treating diabetic patients with insulin is the very large inter- and intra-individual variability in subcutaneous insulin absorption, a major contributory factor in the variability of the blood glucose level. Glucose 229-236 insulin Homo sapiens 67-74 1936660-7 1991 Glucose tolerance to the additional glucose infusion stimulus improved, suggesting that the increased insulin response during hyperglycaemia was enhancing peripheral glucose uptake. Glucose 36-43 insulin Homo sapiens 102-109 1936660-7 1991 Glucose tolerance to the additional glucose infusion stimulus improved, suggesting that the increased insulin response during hyperglycaemia was enhancing peripheral glucose uptake. Glucose 166-173 insulin Homo sapiens 102-109 1936692-2 1991 Insulin-secretion was assessed by intravenous glucose tolerance test performed 24h after transplantation and oral glucose tolerance test during the follow-up. Glucose 46-53 insulin Homo sapiens 0-7 1936692-2 1991 Insulin-secretion was assessed by intravenous glucose tolerance test performed 24h after transplantation and oral glucose tolerance test during the follow-up. Glucose 114-121 insulin Homo sapiens 0-7 1936692-4 1991 Insulin levels in patients with pancreas and kidney transplantations both at the basal level and after glucose stimulation were higher than normal but not different than those observed in patients with kidney transplantation only. Glucose 103-110 insulin Homo sapiens 0-7 1936692-5 1991 Patients with both pancreas and kidney transplantations and kidney transplantation only presented a mild insulin resistance, measured by the glucose/insulin ratio. Glucose 141-148 insulin Homo sapiens 105-112 1936696-0 1991 First peak insulin release after intravenous glucose and arginine is maintained for up to 3 years after segmental pancreas transplantation. Glucose 45-52 insulin Homo sapiens 11-18 1936696-1 1991 In this study we have investigated blood glucose and serum free insulin response to glucose and to arginine orally or intravenously, 3 months and 3 years after a successful segmental, neoprene-injected, pancreas transplantation. Glucose 84-91 insulin Homo sapiens 64-71 1936697-1 1991 It has been established that successful pancreas transplantation in Type 1 (insulin-dependent) diabetic patients results in normal but exaggerated phasic glucose-induced insulin secretion, normal intravenous glucose disappearance rates, improved glucose recovery from insulin-induced hypoglycaemia, improved glucagon secretion during insulin-induced hypoglycaemia, but no alterations in pancreatic polypeptide responses to hypoglycaemia. Glucose 154-161 insulin Homo sapiens 76-83 1936697-1 1991 It has been established that successful pancreas transplantation in Type 1 (insulin-dependent) diabetic patients results in normal but exaggerated phasic glucose-induced insulin secretion, normal intravenous glucose disappearance rates, improved glucose recovery from insulin-induced hypoglycaemia, improved glucagon secretion during insulin-induced hypoglycaemia, but no alterations in pancreatic polypeptide responses to hypoglycaemia. Glucose 154-161 insulin Homo sapiens 170-177 1936697-1 1991 It has been established that successful pancreas transplantation in Type 1 (insulin-dependent) diabetic patients results in normal but exaggerated phasic glucose-induced insulin secretion, normal intravenous glucose disappearance rates, improved glucose recovery from insulin-induced hypoglycaemia, improved glucagon secretion during insulin-induced hypoglycaemia, but no alterations in pancreatic polypeptide responses to hypoglycaemia. Glucose 208-215 insulin Homo sapiens 76-83 1936697-1 1991 It has been established that successful pancreas transplantation in Type 1 (insulin-dependent) diabetic patients results in normal but exaggerated phasic glucose-induced insulin secretion, normal intravenous glucose disappearance rates, improved glucose recovery from insulin-induced hypoglycaemia, improved glucagon secretion during insulin-induced hypoglycaemia, but no alterations in pancreatic polypeptide responses to hypoglycaemia. Glucose 208-215 insulin Homo sapiens 76-83 1936698-9 1991 Biphasic insulin release was seen in patients with normal glucose tolerance. Glucose 58-65 insulin Homo sapiens 9-16 1936698-12 1991 Reduced blood glucose decline indicates insulin resistance, but glucose recovery was normal, despite markedly reduced catecholamine and glucagon release. Glucose 14-21 insulin Homo sapiens 40-47 1936700-3 1991 Using the insulin clamp technique, insulin action was expressed as the metabolic clearance rate of glucose at insulin infusion rates of 1.0 (MCRsubmax) and 10.0 (MCRmax) mU.kg-1.min-1. Glucose 99-106 insulin Homo sapiens 35-42 1936700-3 1991 Using the insulin clamp technique, insulin action was expressed as the metabolic clearance rate of glucose at insulin infusion rates of 1.0 (MCRsubmax) and 10.0 (MCRmax) mU.kg-1.min-1. Glucose 99-106 insulin Homo sapiens 35-42 1954807-2 1991 RESEARCH DESIGN AND METHODS: Determinations were made of 1- and 3-min insulin responses to glucose (0.5 g/kg i.v. Glucose 91-98 insulin Homo sapiens 70-77 1954809-3 1991 Either pork (n = 15) or human (n = 20) regular insulin was infused (0.8 mU.kg-1.min-1) to lower plasma glucose from 4.7 +/- 0.07 to 3.3 +/- 0.04 mM (both groups) over approximately 40 min. Glucose 103-110 insulin Homo sapiens 47-54 1802683-0 1991 Insulin-stimulated glucose uptake and fasting blood glucose. Glucose 19-26 insulin Homo sapiens 0-7 1802683-1 1991 Changes in insulin-stimulated glucose metabolism were studied in young and aged subjects, subjects with impaired glucose tolerance, and patients with NIDDM by means of the glucose clamp technique. Glucose 30-37 insulin Homo sapiens 11-18 1802683-1 1991 Changes in insulin-stimulated glucose metabolism were studied in young and aged subjects, subjects with impaired glucose tolerance, and patients with NIDDM by means of the glucose clamp technique. Glucose 113-120 insulin Homo sapiens 11-18 1802683-8 1991 These results suggest that in the course of developing NIDDM, a decrease in insulin-stimulated glucose uptake precedes a rise in fasting blood glucose. Glucose 95-102 insulin Homo sapiens 76-83 1802683-8 1991 These results suggest that in the course of developing NIDDM, a decrease in insulin-stimulated glucose uptake precedes a rise in fasting blood glucose. Glucose 143-150 insulin Homo sapiens 76-83 1802683-9 1991 Thus, as previously reported for Caucasian NIDDM patients, resistance to insulin-stimulated glucose uptake may be one of the basic defects in Japanese patients with NIDDM. Glucose 92-99 insulin Homo sapiens 73-80 1936110-0 1991 Insulin time-dependent effects on the leg exchange of glucose and amino acids in man. Glucose 54-61 insulin Homo sapiens 0-7 1936110-1 1991 Time-dependent effects of insulin on the leg exchange of glucose, lactate, glycerol, free fatty acids (FFA) and amino acids were measured in relation to oxygen uptake (leg and whole body) and whole body glucose assimilation including oxidation. Glucose 57-64 insulin Homo sapiens 26-33 1833115-4 1991 Early glucose-stimulated insulin output (incremental 1st-phase insulin area) was not significantly positively correlated with the fasting plasma concentration of immunoreactive insulin at any time. Glucose 6-13 insulin Homo sapiens 25-32 1794843-0 1991 Increased insulin-insensitive glucose transport in polymorphonuclear leukocytes from non-insulin-dependent diabetic patients. Glucose 30-37 insulin Homo sapiens 89-96 1833115-4 1991 Early glucose-stimulated insulin output (incremental 1st-phase insulin area) was not significantly positively correlated with the fasting plasma concentration of immunoreactive insulin at any time. Glucose 6-13 insulin Homo sapiens 63-70 1833115-4 1991 Early glucose-stimulated insulin output (incremental 1st-phase insulin area) was not significantly positively correlated with the fasting plasma concentration of immunoreactive insulin at any time. Glucose 6-13 insulin Homo sapiens 63-70 1860552-4 1991 Dose-response studies of the glucose-induced release of amylin and insulin revealed that they possessed a similar dependency on glucose. Glucose 29-36 insulin Homo sapiens 67-74 1860552-4 1991 Dose-response studies of the glucose-induced release of amylin and insulin revealed that they possessed a similar dependency on glucose. Glucose 128-135 insulin Homo sapiens 67-74 1860552-5 1991 However, the release of amylin induced by high concentrations of glucose was partially dissociated from that of insulin; that is, the amylin-insulin molar ratios induced by 22.2 and 33.3 mM glucose (1.11 +/- 0.05 and 1.05 +/- 0.04%, respectively) were significantly higher than those induced by 16.7 mM glucose (0.90 +/- 0.04%, P less than 0.01 vs. 22.2 mM glucose, P less than 0.05 vs. 33.3 mM glucose). Glucose 65-72 insulin Homo sapiens 141-148 1794843-6 1991 It can be concluded that unlike insulin-sensitive cells such as adipocytes and muscle, glucose transport in human polymorphonuclear leukocytes, which are insulin insensitive cells, is increased in patients with non-insulin-dependent diabetes mellitus. Glucose 87-94 insulin Homo sapiens 154-161 1651337-1 1991 Insulin stimulates glucose transport in adipocytes via the rapid redistribution of the GLUT1 and GLUT4 glucose transporters from intracellular membrane compartments to the cell surface. Glucose 19-26 insulin Homo sapiens 0-7 1937346-6 1991 After successful treatment of the diabetic ketoacidosis with insulin and fluid supplementation, serum cholesterol, triglyceride and pancreatic enzyme levels decreased concomitantly with stabilization of the blood glucose level. Glucose 213-220 insulin Homo sapiens 61-68 1960049-8 1991 If diet and exercise do not achieve the requisite glucose levels, insulin therapy based on body weight and gestational age is instituted. Glucose 50-57 insulin Homo sapiens 66-73 1655881-2 1991 While insulin produced a dose-dependent decrease in the rate of Li(+)-Na+ countertransport, from 0.272 mmol/l erythrocytes per h at zero insulin to 0.081 at a concentration of 50 mU/l (P less than 0.0001), alterations in ambient glucose concentration had no significant effect on the rate of countertransport. Glucose 229-236 insulin Homo sapiens 6-13 1864966-4 1991 During the two highest insulin infusion steps glucose uptake was impaired (3.33 +/- 0.31 vs. 5.06 +/- 0.40 mg/kg.min, P less than 0.01, and 6.09 +/- 0.50 vs. 7.95 +/- 0.52 mg/kg.min, P less than 0.01). Glucose 46-53 insulin Homo sapiens 23-30 1864966-5 1991 Stimulation of glucose oxidation by insulin was normal; in contrast, nonoxidative glucose disposal (i.e., glycogen synthesis) was markedly reduced. Glucose 15-22 insulin Homo sapiens 36-43 1864966-6 1991 Fasting (r = -0.553, P less than 0.01) and glucose-stimulated (r = -0.592, P less than 0.01) plasma insulin concentration correlated inversely with the severity of insulin resistance. Glucose 43-50 insulin Homo sapiens 100-107 1864966-6 1991 Fasting (r = -0.553, P less than 0.01) and glucose-stimulated (r = -0.592, P less than 0.01) plasma insulin concentration correlated inversely with the severity of insulin resistance. Glucose 43-50 insulin Homo sapiens 164-171 1864966-7 1991 Basal hepatic glucose production was normal in cirrhotics and suppressed normally with insulin. Glucose 14-21 insulin Homo sapiens 87-94 1864966-11 1991 In summary, stable cirrhotic patients with normal glucose tolerance exhibit marked insulin resistance secondary to the impaired nonoxidative glucose disposal. Glucose 141-148 insulin Homo sapiens 83-90 1867224-5 1991 In fact, there is considerable evidence that insulin resistance (abnormal nonoxidative glucose disposal), not hyperinsulinemia, is the primary insulin-related abnormality in human hypertension, and that hyperinsulinemia occurs as a response to insulin resistance. Glucose 87-94 insulin Homo sapiens 45-52 1861628-5 1991 While fasting concentrations were normal, both glucose and insulin concentrations in response to oral glucose were significantly elevated compared with controls. Glucose 102-109 insulin Homo sapiens 59-66 2067758-3 1991 Insulin resistance was measured by the frequently sampled intravenous glucose tolerance test, and inhibin was measured by a specific radioimmunoassay. Glucose 70-77 insulin Homo sapiens 0-7 1871791-7 1991 When theophylline was added, insulin secretion increased to 264.2 +/- 63.2 pM/200 IE (P less than 0.001 vs. basal secretion and P less than 0.005 vs. secretion at 16.7 mM glucose). Glucose 171-178 insulin Homo sapiens 29-36 1858830-7 1991 Univariate analysis demonstrated that serum total cholesterol, LDL cholesterol, and fasting plasma triglycerides were highly correlated with insulin-mediated glucose disposal and fasting plasma insulin. Glucose 158-165 insulin Homo sapiens 141-148 1858830-3 1991 PATIENTS AND METHODS: Twenty-two black patients with NIDDM in near-normoglycemic remission who were receiving no pharmacologic therapy for NIDDM were evaluated for insulin sensitivity by the euglycemic insulin clamp, plasma insulin levels, degree of obesity, glucose metabolism, serum total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol levels, and fasting plasma triglyceride levels. Glucose 259-266 insulin Homo sapiens 164-171 1858873-5 1991 In the recovery periods, approximately fourfold peripheral with approximately twofold portal insulin elevations prevented glucose recovery (glucose = 3.6 +/- 0.1 mM, counter-regulatory hormone levels elevated throughout). Glucose 122-129 insulin Homo sapiens 93-100 1858873-5 1991 In the recovery periods, approximately fourfold peripheral with approximately twofold portal insulin elevations prevented glucose recovery (glucose = 3.6 +/- 0.1 mM, counter-regulatory hormone levels elevated throughout). Glucose 140-147 insulin Homo sapiens 93-100 1858877-2 1991 Uremic subjects had significantly reduced rates of insulin-stimulated glucose disposal, as determined by a 3-h intravenous glucose tolerance test and using the hyperinsulinemic euglycemic clamp technique. Glucose 70-77 insulin Homo sapiens 51-58 1858877-2 1991 Uremic subjects had significantly reduced rates of insulin-stimulated glucose disposal, as determined by a 3-h intravenous glucose tolerance test and using the hyperinsulinemic euglycemic clamp technique. Glucose 123-130 insulin Homo sapiens 51-58 1858877-5 1991 However, the increase in insulin-stimulated glucose transport was significantly reduced by 50% in muscles from uremic patients (P = 0.012). Glucose 44-51 insulin Homo sapiens 25-32 1858877-9 1991 An alternative step in insulin-dependent activation of the glucose transport process may be involved. Glucose 59-66 insulin Homo sapiens 23-30 2063969-3 1991 The insulinogenic index represents the ratio of the cumulative enhancement of immunoreactive insulin (IRI) to the glucose level (delta IRI/delta glucose). Glucose 114-121 insulin Homo sapiens 4-11 2063969-3 1991 The insulinogenic index represents the ratio of the cumulative enhancement of immunoreactive insulin (IRI) to the glucose level (delta IRI/delta glucose). Glucose 145-152 insulin Homo sapiens 4-11 1952228-1 1991 The use of glucose-insulin mixture (0.5 g/(kg.h) glucose and 1 U/(kg.h) insulin) during preperfusion period in 26 cardiosurgical patients subject to cardiopulmonary bypass surgery prevented the disturbances in carbohydrate metabolism, reduced hemoglobin glycosylation, and normalized thromboxane-prostacyclin system functions, as compared to the data obtained in control groups. Glucose 11-18 insulin Homo sapiens 19-26 2065028-2 1991 Furthermore, insulin resistance measured by the euglycemic glucose clamp technique has been shown to be related to lipid and lipoprotein changes favoring atherosclerosis and to high blood pressure. Glucose 59-66 insulin Homo sapiens 13-20 2065028-11 1991 This insulin resistance is characterized by reduced whole-body and nonoxidative glucose uptake. Glucose 80-87 insulin Homo sapiens 5-12 1859747-3 1991 The resulting error signal controlled the infusion rates of a concentrated potassium chloride solution (50 or 200 mmol litre-1) and a solution of 50% glucose with insulin 200 u litre-1. Glucose 150-157 insulin Homo sapiens 163-170 1649715-5 1991 We assessed the effect of gliclazide on glucose-stimulated insulin secretion in eight healthy volunteers. Glucose 40-47 insulin Homo sapiens 59-66 1647993-7 1991 Furthermore, the percentage of phosphorylated insulin receptors stimulated by 8.3 nM insulin was significantly lower than the control subjects (mean +/- SD, 29.0 +/- 12.0 vs. 56.0 +/- 7.4%, P less than 0.01), and there was a significant inverse correlation between fasting plasma glucose levels and the percentage of phosphorylated receptors among diabetic subjects (r = 0.73, P less than 0.025). Glucose 280-287 insulin Homo sapiens 46-53 1647993-7 1991 Furthermore, the percentage of phosphorylated insulin receptors stimulated by 8.3 nM insulin was significantly lower than the control subjects (mean +/- SD, 29.0 +/- 12.0 vs. 56.0 +/- 7.4%, P less than 0.01), and there was a significant inverse correlation between fasting plasma glucose levels and the percentage of phosphorylated receptors among diabetic subjects (r = 0.73, P less than 0.025). Glucose 280-287 insulin Homo sapiens 85-92 1680759-1 1991 In searching for a genetic marker of type 2 diabetes we estimated the frequency of alleles of the Bgl II restriction fragment length polymorphism (RFLP) of the insulin receptor gene in a group of type II diabetic patients (n = 50), characterized by OGTT (glucose, insulin, C-peptide) and insulin receptor binding parameters. Glucose 255-262 insulin Homo sapiens 160-167 1832357-1 1991 Fourteen male patients with Type 2 diabetes were studied to identify relationships between insulin-mediated glucose disposal, basal and glucose-stimulated insulin secretion, fasting lipoproteins and apolipoproteins, and the activities of lipoprotein lipase and hepatic lipase. Glucose 108-115 insulin Homo sapiens 91-98 1832357-1 1991 Fourteen male patients with Type 2 diabetes were studied to identify relationships between insulin-mediated glucose disposal, basal and glucose-stimulated insulin secretion, fasting lipoproteins and apolipoproteins, and the activities of lipoprotein lipase and hepatic lipase. Glucose 136-143 insulin Homo sapiens 155-162 1832357-2 1991 Sensitivity of glucose disposal to exogenous insulin correlated positively with HDL-cholesterol (r = 0.65, p less than 0.05), HDL2-cholesterol (r = 0.59, p less than 0.05), and apolipoprotein A1 (r = 0.57, p less than 0.05) and negatively with apolipoprotein B (r = -0.53, p less than 0.05) and total: HDL-cholesterol ratio (r = -0.68, p less than 0.01). Glucose 15-22 insulin Homo sapiens 45-52 1832357-4 1991 Neither fasting plasma glucose nor the indices of stimulated insulin secretion (glucose-stimulated plasma insulin and C-peptide) were related to any of the lipoprotein measures. Glucose 80-87 insulin Homo sapiens 106-113 1914797-5 1991 Relative to soluble human insulin (100% +/- SE21), incremental areas under the glucose curve between 0 and 240 min were 79% +/- 34 (AspB10, NS), 70% +/- 29 (AspB9, GluB27, NS), and 43% +/- 23 (AspB28, P less than 0.02). Glucose 79-86 insulin Homo sapiens 26-33 1915998-4 1991 Fasting and 1 h-post glucose load serum insulin levels in both Group A and Group B patients were higher than those found out in non over-weight tolerant subjects, but there were no differences between both groups. Glucose 21-28 insulin Homo sapiens 40-47 1915998-5 1991 The serum glucose descent slope after an insulin tolerance test (ITT) was lower for group B than for group A (p less than 0.05), whereas both groups demonstrated lower descent slopes than non overweight tolerant subjects (p less than 0.05). Glucose 10-17 insulin Homo sapiens 41-48 1916053-1 1991 Insulin responses to intravenous glucose infusion and glucose utilization during hyperinsulinaemic euglycaemic clamp were determined in a large homogeneous group of 65-year-old male subjects. Glucose 33-40 insulin Homo sapiens 0-7 1916054-1 1991 The plasma insulin or C-peptide response to a 90-min constant glucose infusion 5 mg.kg ideal body weight-1.min-1 provides Beta-cell assessment comparable to more intensive methods. Glucose 62-69 insulin Homo sapiens 11-18 1916054-1 1991 The plasma insulin or C-peptide response to a 90-min constant glucose infusion 5 mg.kg ideal body weight-1.min-1 provides Beta-cell assessment comparable to more intensive methods. Glucose 62-69 insulin Homo sapiens 22-31 1916054-2 1991 In 14 diet-treated Type 2 (non-insulin-dependent) diabetic subjects and 12 non-diabetic subjects, plasma insulin and C-peptide concentrations gave near linear plots against simultaneous glucose values. Glucose 186-193 insulin Homo sapiens 105-112 1916054-2 1991 In 14 diet-treated Type 2 (non-insulin-dependent) diabetic subjects and 12 non-diabetic subjects, plasma insulin and C-peptide concentrations gave near linear plots against simultaneous glucose values. Glucose 186-193 insulin Homo sapiens 117-126 1916054-10 1991 The insulin or C-peptide response to the glucose infusion provides a direct empirical measure of the Beta-cell function, which can be interpreted in relation to obesity or to insulin resistance to assess underlying pancreatic responsiveness. Glucose 41-48 insulin Homo sapiens 4-11 1916054-10 1991 The insulin or C-peptide response to the glucose infusion provides a direct empirical measure of the Beta-cell function, which can be interpreted in relation to obesity or to insulin resistance to assess underlying pancreatic responsiveness. Glucose 41-48 insulin Homo sapiens 15-24 1916054-10 1991 The insulin or C-peptide response to the glucose infusion provides a direct empirical measure of the Beta-cell function, which can be interpreted in relation to obesity or to insulin resistance to assess underlying pancreatic responsiveness. Glucose 41-48 insulin Homo sapiens 175-182 1916055-6 1991 The insulin-antagonistic effect of growth hormone started after approximately 2 h, was maximal after 4-5 h (approximately 39% inhibition of glucose infusion rate between control and growth hormone 24 mU.kg-1.h-1) and lasted for 6-7 h after peak levels. Glucose 140-147 insulin Homo sapiens 4-11 1916055-7 1991 The resistance was due to a less pronounced insulin effect both to inhibit glucose production and to stimulate glucose utilization. Glucose 75-82 insulin Homo sapiens 44-51 1916055-7 1991 The resistance was due to a less pronounced insulin effect both to inhibit glucose production and to stimulate glucose utilization. Glucose 111-118 insulin Homo sapiens 44-51 2060716-6 1991 In a multiple logistic regression, a high fasting plasma insulin concentration and a low 2-h plasma insulin concentration after a glucose load in association with a high body mass index were independent predictors of conversion to NIDDM from impaired glucose tolerance. Glucose 130-137 insulin Homo sapiens 100-107 1916916-1 1991 There is good evidence that the long-term complications of diabetes are caused by poor control of blood sugar, even in patients where intensive glucose monitoring is used to control insulin therapy. Glucose 144-151 insulin Homo sapiens 182-189 1889898-1 1991 A new glucose clamp technique for in vivo studies of insulin sensitivity was validated clinically. Glucose 6-13 insulin Homo sapiens 53-60 1894421-15 1991 In contrast, both percent BFM and SS thickness correlated significantly (P less than 0.001) with post-glucose insulin concentrations in the relatives only. Glucose 102-109 insulin Homo sapiens 110-117 1894422-12 1991 Also, insulin resistance as reflected in GLU response was not related to SBP or DBP. Glucose 41-44 insulin Homo sapiens 6-13 1940028-2 1991 Upon oral administration of a loading dose of glucose, plasma levels of glucose, insulin and glucagon changed abnormally in all FAP patients tested. Glucose 46-53 insulin Homo sapiens 81-88 1940062-3 1991 In the PCO group, the fasting insulin levels and the insulin response to oral glucose load were higher than in the matched controls. Glucose 78-85 insulin Homo sapiens 53-60 2045466-5 1991 The decline in glucose tolerance was associated with similar insulin-mediated, but 23% lower glucose-mediated (P less than 0.001), glucose disposal, a 17% lower acute insulin response to glucose (P less than 0.03), a 9% lower beta-cell sensitivity to glucose (P less than 0.02), and similar beta-cell capacities. Glucose 15-22 insulin Homo sapiens 61-68 2045466-5 1991 The decline in glucose tolerance was associated with similar insulin-mediated, but 23% lower glucose-mediated (P less than 0.001), glucose disposal, a 17% lower acute insulin response to glucose (P less than 0.03), a 9% lower beta-cell sensitivity to glucose (P less than 0.02), and similar beta-cell capacities. Glucose 15-22 insulin Homo sapiens 167-174 2056116-5 1991 (b) The percent weight change per year correlated with glucose disposal at submaximally-(r = 0.19, P less than 0.01) and maximally-stimulating (r = 0.34, P less than 0.0001) insulin concentrations independent of sex, age, initial weight, and 24-h energy expenditure; the correlations were stronger for glucose oxidation than for glucose storage. Glucose 55-62 insulin Homo sapiens 174-181 1858869-3 1991 Glucose uptake in the basal state was greater in NIDDM [3.75 +/- 0.23 vs. 2.50 +/- 0.10 mg.kg fat-free mass (FFM)-1.min-1, P less than 0.005] but was similar at approximately 8, 12, and 26 mg.kg FFM-1.min-1 at each insulin infusion. Glucose 0-7 insulin Homo sapiens 215-222 1858869-6 1991 The dose-response relationship between serum insulin and glucose oxidation was right shifted in NIDDM with half-maximal activation at 368 +/- 91 vs. 179 +/- 27 pM in controls (P less than 0.05). Glucose 57-64 insulin Homo sapiens 45-52 1858869-7 1991 In conclusion, glucose oxidation is reduced at physiological insulin concentrations in NIDDM and cannot be explained by concomitant obesity, increased fat oxidation, or reduced glucose uptake but results from impaired sensitivity to stimulation by insulin, possibly at pyruvate dehydrogenase. Glucose 15-22 insulin Homo sapiens 61-68 1910105-1 1991 The efficiency of a continuous infusion of insulin in improving glucose tolerance was compared in two groups of very low-birth weight infants (mean +/- SEM birth weights 757 +/- 40 vs 828 +/- 80 g and gestational ages 27.6 +/- 0.7 vs. 27.2 +/- 0.5 weeks) receiving total parenteral nutrition with and without the addition of lipid emulsion to the nutrition regimen. Glucose 64-71 insulin Homo sapiens 43-50 1858869-7 1991 In conclusion, glucose oxidation is reduced at physiological insulin concentrations in NIDDM and cannot be explained by concomitant obesity, increased fat oxidation, or reduced glucose uptake but results from impaired sensitivity to stimulation by insulin, possibly at pyruvate dehydrogenase. Glucose 15-22 insulin Homo sapiens 248-255 1714534-8 1991 In conclusion, the morning levels of IGFBP-1 in healthy subjects reflect the acute beta-cell responsiveness to glucose, which may correspond to integrated diurnal insulin levels. Glucose 111-118 insulin Homo sapiens 163-170 1870422-7 1991 In conclusion, in anorexia nervosa, insulin stimulates glucose oxidation more than storage. Glucose 55-62 insulin Homo sapiens 36-43 1943865-5 1991 In this paper it is proposed that the primary abnormality is failure of hepatic gluconeogenesis to suppress adequately and that the resulting excess glucose flux results in peripheral insulin resistance and in a defect of glucose-mediated insulin secretion. Glucose 149-156 insulin Homo sapiens 184-191 1870422-8 1991 In obesity, both components of insulin-stimulated glucose metabolism are impaired. Glucose 50-57 insulin Homo sapiens 31-38 1802223-4 1991 A second determinant of obesity is related to fuel utilization and suggests that those predisposed to be obese may have an innate insulin resistance in muscle, leading to decreased uptake, oxidation, and storage of glucose in this tissue. Glucose 215-222 insulin Homo sapiens 130-137 1853403-6 1991 For the 15 patients with complete data, the major determinants of the blood glucose concentration were the cortisol, insulin, and glucagon concentrations (all p less than 0.001), which accounted for 42% of the variance. Glucose 76-83 insulin Homo sapiens 117-124 1686803-2 1991 It was found that in 3-day HK insulin production and catabolism are sharply stimulated, the glucagon and glucose content is increased, the somatostatin level is reduced, and cAMP content in the liver and kidneys is reduced. Glucose 105-112 insulin Homo sapiens 30-37 1788198-1 1991 The rate of insulin dependent utilization of glucose by tissues under the conditions of normoglycemia was assessed in 76 patients with insulin dependent diabetes mellitus (their age and period of disease varied) without clinical signs of resistance to insulin. Glucose 45-52 insulin Homo sapiens 12-19 1788198-1 1991 The rate of insulin dependent utilization of glucose by tissues under the conditions of normoglycemia was assessed in 76 patients with insulin dependent diabetes mellitus (their age and period of disease varied) without clinical signs of resistance to insulin. Glucose 45-52 insulin Homo sapiens 135-142 1788198-4 1991 A decrease in the insulin dependent rate of glucose utilization by tissues depended neither on sex and age of the patients, nor on a period of disease, body mass, daily requirement in insulin, the levels of cholesterol, triglycerides and ketone bodies. Glucose 44-51 insulin Homo sapiens 18-25 1831320-10 1991 After gliclazide therapy in both the n5-STZ gliclazide responder group and the n0-STZ group: (a) in vitro glucose-induced insulin secretion was increased three- to fivefold; (b) the response to arginine, which is increased in diabetic rats, was amplified by two- to threefold; (c) insulin release in response to gliclazide was unchanged. Glucose 106-113 insulin Homo sapiens 122-129 1950085-2 1991 The main reason for a deterioration of glucose tolerance with age is insulin resistance, primarily concerning glucose uptake of skeletal muscle. Glucose 39-46 insulin Homo sapiens 69-76 1950085-2 1991 The main reason for a deterioration of glucose tolerance with age is insulin resistance, primarily concerning glucose uptake of skeletal muscle. Glucose 110-117 insulin Homo sapiens 69-76 1872303-7 1991 This was accompanied by the appearance of a small first-phase insulin response to intravenous glucose, and significant increases in the mean-daily-insulin to mean-daily-blood-glucose ratio, as well as in the 24-hour urinary C-peptide-to-glucose ratio. Glucose 94-101 insulin Homo sapiens 62-69 1872301-1 1991 Insulin regulation of hepatic glucose production (HGP) is altered in non-insulin-dependent diabetes mellitus (NIDDM), resulting in increased glucose output by the liver; this contributes to the elevation in plasma glucose concentration observed both in the basal state and postprandially. Glucose 30-37 insulin Homo sapiens 0-7 1872303-11 1991 This was paralleled by unchanged stimulation by gliclazide of first-phase insulin response to glucose, and augmented mean 48-hour insulin-to-glucose and urinary C-peptide-to-glucose ratios. Glucose 141-148 insulin Homo sapiens 130-137 1872303-11 1991 This was paralleled by unchanged stimulation by gliclazide of first-phase insulin response to glucose, and augmented mean 48-hour insulin-to-glucose and urinary C-peptide-to-glucose ratios. Glucose 141-148 insulin Homo sapiens 130-137 1872301-1 1991 Insulin regulation of hepatic glucose production (HGP) is altered in non-insulin-dependent diabetes mellitus (NIDDM), resulting in increased glucose output by the liver; this contributes to the elevation in plasma glucose concentration observed both in the basal state and postprandially. Glucose 141-148 insulin Homo sapiens 0-7 1872309-2 1991 On the other hand, in insulin-treated NIDDM patients a progressive increase in insulin requirement can occur without significant improvement in glucose control. Glucose 144-151 insulin Homo sapiens 22-29 1872309-5 1991 Long-acting insulin, administered as a single dose at supper or bedtime, should restrain excessive overnight hepatic glucose production, thus allowing a significant reduction in fasting glucose concentrations. Glucose 117-124 insulin Homo sapiens 12-19 1872301-1 1991 Insulin regulation of hepatic glucose production (HGP) is altered in non-insulin-dependent diabetes mellitus (NIDDM), resulting in increased glucose output by the liver; this contributes to the elevation in plasma glucose concentration observed both in the basal state and postprandially. Glucose 141-148 insulin Homo sapiens 0-7 1872309-5 1991 Long-acting insulin, administered as a single dose at supper or bedtime, should restrain excessive overnight hepatic glucose production, thus allowing a significant reduction in fasting glucose concentrations. Glucose 186-193 insulin Homo sapiens 12-19 1908182-5 1991 In contrast, insulin-stimulated glucose transport and lipogenesis were both significantly enhanced (p less than 0.05). Glucose 32-39 insulin Homo sapiens 13-20 1872309-6 1991 A lower ambient glucose level should favor the stimulatory effect of sulfonylureas on insulin secretion. Glucose 16-23 insulin Homo sapiens 86-93 1872309-8 1991 Moreover, sulfonylureas might improve insulin action on its target tissue (i.e., muscle), thus increasing overall insulin-mediated glucose metabolism. Glucose 131-138 insulin Homo sapiens 38-45 1872309-8 1991 Moreover, sulfonylureas might improve insulin action on its target tissue (i.e., muscle), thus increasing overall insulin-mediated glucose metabolism. Glucose 131-138 insulin Homo sapiens 114-121 1872309-9 1991 The reduction in prevailing plasma glucose levels will reduce the toxic effect of hyperglycemia on the beta-cell and on insulin-sensitive tissues. Glucose 35-42 insulin Homo sapiens 120-127 1872310-8 1991 The efficiency of glucose uptake by the peripheral tissues is also impaired due to a combination of decreased insulin secretion and defective cellular insulin action. Glucose 18-25 insulin Homo sapiens 110-117 1908182-10 1991 In conclusion, sulfonylurea treatment of NIDDM enhances insulin-stimulated peripheral glucose utilization in part through a potentiation of insulin action on adipose tissue glucose transport and lipogenesis and skeletal muscle glycogen synthase. Glucose 86-93 insulin Homo sapiens 56-63 1872310-10 1991 Therapeutic interventions, to be effective, must reduce hepatic glucose production either by improving islet dysfunction and raising plasma insulin levels, or improving the effectiveness of insulin on the liver. Glucose 64-71 insulin Homo sapiens 140-147 2050674-10 1991 The down-regulation of GLUT4 due to the chronic-insulin treatment is associated with a marked resistance of the cells to restimulate glucose transport and particularly to recruit further GLUT4 to the cell-surface following an additional insulin treatment. Glucose 133-140 insulin Homo sapiens 48-55 1908182-10 1991 In conclusion, sulfonylurea treatment of NIDDM enhances insulin-stimulated peripheral glucose utilization in part through a potentiation of insulin action on adipose tissue glucose transport and lipogenesis and skeletal muscle glycogen synthase. Glucose 173-180 insulin Homo sapiens 56-63 1908182-10 1991 In conclusion, sulfonylurea treatment of NIDDM enhances insulin-stimulated peripheral glucose utilization in part through a potentiation of insulin action on adipose tissue glucose transport and lipogenesis and skeletal muscle glycogen synthase. Glucose 173-180 insulin Homo sapiens 140-147 1645719-7 1991 Surprisingly, cells expressing Ser1200 receptors showed increased insulin stimulation of 2-deoxyglucose uptake and glucose incorporation into glycogen compared with CHO-NEO, whereas Thr1134 receptors failed to signal these metabolic responses. Glucose 96-103 insulin Homo sapiens 66-73 1906584-0 1991 [The effects of insulin combined with glibenclamide on glucose and lipid metabolism in patients with Type II diabetes mellitus]. Glucose 55-62 insulin Homo sapiens 16-23 2037572-6 1991 When adipocytes were cultured for 18 h with 20 mM glucose, amino acids, and 25 ng/ml insulin, maximal insulin responsiveness of the GTS was reduced by greater than 70%. Glucose 50-57 insulin Homo sapiens 102-109 2068893-4 1991 Insulin-stimulated glucose utilization was reduced in both diabetic groups (lean patients: 313 +/- 35 vs 531 +/- 22 mg.m-2.min-1, p less than 0.01; obese patients: 311 +/- 28 vs 453 +/- 26 mg.m-2.min-1, p less than 0.01). Glucose 19-26 insulin Homo sapiens 0-7 1877373-2 1991 However the direct dose-response relationship between insulin and glucose transport has not yet been studied in human skeletal muscle. Glucose 66-73 insulin Homo sapiens 54-61 1877373-6 1991 Glucose transport responded to insulin in a dose-response manner in the control group, with a 2-fold increase following maximal stimulation. Glucose 0-7 insulin Homo sapiens 31-38 1827703-2 1991 Insulin concentrations, insulin binding, insulin action on glucose disposal, fatty acid metabolism, and islet function were compared in lean and obese individuals, and the relationship between insulin resistance and muscle morphology was explored. Glucose 59-66 insulin Homo sapiens 41-48 1852092-0 1991 Oat gum lowers glucose and insulin after an oral glucose load. Glucose 49-56 insulin Homo sapiens 27-34 1827703-2 1991 Insulin concentrations, insulin binding, insulin action on glucose disposal, fatty acid metabolism, and islet function were compared in lean and obese individuals, and the relationship between insulin resistance and muscle morphology was explored. Glucose 59-66 insulin Homo sapiens 41-48 2058661-7 1991 We conclude that opiate blockade augments glucoregulatory responses to insulin-induced hypoglycemia, even in IDDM patients with preexisting defects in glucose counterregulation. Glucose 151-158 insulin Homo sapiens 71-78 2025856-8 1991 Thus, increased whole body glucose utilization in the absence of insulin resistance or increased insulin-dependent glucose disposal was observed. Glucose 115-122 insulin Homo sapiens 97-104 1954714-4 1991 The insulin responses to an oral glucose load or a test meal are thus lower in gestational diabetic women than in normal pregnant women, despite significantly higher plasma glucose concentrations in the gestational diabetics. Glucose 33-40 insulin Homo sapiens 4-11 1954714-4 1991 The insulin responses to an oral glucose load or a test meal are thus lower in gestational diabetic women than in normal pregnant women, despite significantly higher plasma glucose concentrations in the gestational diabetics. Glucose 173-180 insulin Homo sapiens 4-11 1954714-5 1991 Also the insulin responses to intravenous glucose injections or infusions are abnormal in gestational diabetics when compared with normal pregnant women, a difference which is still detectable for some time after the completion of pregnancy in at least a fraction of gestational diabetic women. Glucose 42-49 insulin Homo sapiens 9-16 1720333-7 1991 Dicumarol, an inhibitor of quinone reductase, did not inhibit CoQ0-induced insulin release, but it did inhibit glucose-induced insulin release suggesting that the enzyme and quinones play a role in glucose-induced insulin release. Glucose 111-118 insulin Homo sapiens 127-134 1720333-7 1991 Dicumarol, an inhibitor of quinone reductase, did not inhibit CoQ0-induced insulin release, but it did inhibit glucose-induced insulin release suggesting that the enzyme and quinones play a role in glucose-induced insulin release. Glucose 111-118 insulin Homo sapiens 127-134 1720333-7 1991 Dicumarol, an inhibitor of quinone reductase, did not inhibit CoQ0-induced insulin release, but it did inhibit glucose-induced insulin release suggesting that the enzyme and quinones play a role in glucose-induced insulin release. Glucose 198-205 insulin Homo sapiens 127-134 1720333-7 1991 Dicumarol, an inhibitor of quinone reductase, did not inhibit CoQ0-induced insulin release, but it did inhibit glucose-induced insulin release suggesting that the enzyme and quinones play a role in glucose-induced insulin release. Glucose 198-205 insulin Homo sapiens 127-134 2025856-9 1991 These data are consistent with the concept of a localized tumor acting as a glucose drain in which case increased glucose appearance and increased insulin clearance would defend against hypoglycemia. Glucose 76-83 insulin Homo sapiens 147-154 21229036-1 1991 Tight glucose control is clearly beneficial in the pregnant insulin-dependent diabetic. Glucose 6-13 insulin Homo sapiens 60-67 1868636-4 1991 Alternatively, glucose self-monitoring (four to six times daily with institution of insulin treatment when fasting glucose exceeds some arbitrary threshold such as 90 mg/dl or postprandial values exceed a threshold such as 100 mg/dl) is likely to be equally effective with fewer patients requiring insulin injections. Glucose 15-22 insulin Homo sapiens 84-91 1868636-4 1991 Alternatively, glucose self-monitoring (four to six times daily with institution of insulin treatment when fasting glucose exceeds some arbitrary threshold such as 90 mg/dl or postprandial values exceed a threshold such as 100 mg/dl) is likely to be equally effective with fewer patients requiring insulin injections. Glucose 15-22 insulin Homo sapiens 298-305 1868636-4 1991 Alternatively, glucose self-monitoring (four to six times daily with institution of insulin treatment when fasting glucose exceeds some arbitrary threshold such as 90 mg/dl or postprandial values exceed a threshold such as 100 mg/dl) is likely to be equally effective with fewer patients requiring insulin injections. Glucose 115-122 insulin Homo sapiens 84-91 1828239-4 1991 PCO patients exhibited elevated basal and glucose-challenged insulin levels and had blunted hypoglycemic responses to IV insulin. Glucose 42-49 insulin Homo sapiens 61-68 1828239-5 1991 Conversely, AH patients had hypoglycemic responses to IV insulin significantly greater than and basal and glucose-challenged insulin levels lower than the PCO patients and weight-matched control subjects. Glucose 106-113 insulin Homo sapiens 125-132 1830533-9 1991 However, human insulin use does appear to be associated with reduced awareness of hypoglycaemia in those whose blood glucose control is relatively poor. Glucose 117-124 insulin Homo sapiens 15-22 1830535-7 1991 Multiple regression analysis demonstrated not only a highly significant association between 2-h plasma glucose and insulin concentrations (p less than 0.001), but also that for a given value of plasma insulin, 2-h plasma glucose values were lower for non-Austronesian than for Austronesian subjects (males, p less than 0.05, females, p less than 0.01). Glucose 103-110 insulin Homo sapiens 115-122 1830535-7 1991 Multiple regression analysis demonstrated not only a highly significant association between 2-h plasma glucose and insulin concentrations (p less than 0.001), but also that for a given value of plasma insulin, 2-h plasma glucose values were lower for non-Austronesian than for Austronesian subjects (males, p less than 0.05, females, p less than 0.01). Glucose 221-228 insulin Homo sapiens 201-208 1868754-6 1991 In the isolated human adipocyte it was possible to measure both insulin binding and the action of insulin on glucose transport and on the intracellular glucose processing. Glucose 109-116 insulin Homo sapiens 98-105 1884901-13 1991 The rate of glucose infusion had to be increased by 35% during the low dose C-peptide, but not during NaCl infusion in order to maintain a constant plasma glucose concentration. Glucose 12-19 insulin Homo sapiens 76-85 1909631-5 1991 After adjusting for factors (age, sex, body mass, and body fat distribution) known to affect insulin levels, a direct relationship between post-glucose plasma insulin concentrations and prevalence of hypertension was still present in both ethnic groups. Glucose 144-151 insulin Homo sapiens 159-166 1885243-8 1991 There was a direct relationship between measurement delay and amount of insulin delivered, i.e., the longer the delay the higher the insulin dose needed to control a rise in blood glucose; the closed-loop response in presence of a time delay was qualitatively impaired both during insulin delivery and blood glucose clamp studies; time delay compensation was effective in reducing the insulin dose and improving controller stability during the early phase of clamp studies. Glucose 180-187 insulin Homo sapiens 72-79 1885243-8 1991 There was a direct relationship between measurement delay and amount of insulin delivered, i.e., the longer the delay the higher the insulin dose needed to control a rise in blood glucose; the closed-loop response in presence of a time delay was qualitatively impaired both during insulin delivery and blood glucose clamp studies; time delay compensation was effective in reducing the insulin dose and improving controller stability during the early phase of clamp studies. Glucose 180-187 insulin Homo sapiens 133-140 1885243-8 1991 There was a direct relationship between measurement delay and amount of insulin delivered, i.e., the longer the delay the higher the insulin dose needed to control a rise in blood glucose; the closed-loop response in presence of a time delay was qualitatively impaired both during insulin delivery and blood glucose clamp studies; time delay compensation was effective in reducing the insulin dose and improving controller stability during the early phase of clamp studies. Glucose 308-315 insulin Homo sapiens 72-79 1885243-8 1991 There was a direct relationship between measurement delay and amount of insulin delivered, i.e., the longer the delay the higher the insulin dose needed to control a rise in blood glucose; the closed-loop response in presence of a time delay was qualitatively impaired both during insulin delivery and blood glucose clamp studies; time delay compensation was effective in reducing the insulin dose and improving controller stability during the early phase of clamp studies. Glucose 308-315 insulin Homo sapiens 133-140 1645756-1 1991 Correlation with insulin-stimulated glucose disposal during euglycemic clamp studies. Glucose 36-43 insulin Homo sapiens 17-24 2026743-0 1991 Insulin-sensitive tyrosine kinase activity changes in parallel with plasma insulin and glucose concentrations in humans. Glucose 87-94 insulin Homo sapiens 0-7 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 41-48 insulin Homo sapiens 118-125 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 41-48 insulin Homo sapiens 274-281 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 118-125 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 274-281 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 118-125 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 274-281 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 118-125 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 274-281 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 118-125 2026747-8 1991 We conclude that the interaction between glucose and FFA fuels in human forearm tissues is dependent upon the ambient insulin concentration; the increase in basal glucose uptake would be compatible with the increase need of glucose for FFA reesterification; the decrease in insulin-stimulated glucose uptake supports operation of the glucose-FFA cycle in human forearm tissues. Glucose 163-170 insulin Homo sapiens 274-281 2026760-1 1991 Although assessment of counterregulatory hormone responses to hypoglycemia relies upon insulin to lower the glucose level, it is not known if the exogenous insulin does used itself influences the magnitude of the hormone response. Glucose 108-115 insulin Homo sapiens 87-94 1904090-0 1991 A controlled trial of insulin infusion and parenteral nutrition in extremely low birth weight infants with glucose intolerance. Glucose 107-114 insulin Homo sapiens 22-29 1904090-6 1991 During the study, the 11 insulin-treated infants tolerated higher glucose infusion rates (20.1 +/- 2.5 vs 13.2 +/- 3.2 mg/kg/min (1.1 +/- 0.1 vs 0.7 +/- 0.2 mmol/L); p less than 0.01), had greater nonprotein energy intake (124.7 +/- 18 vs 86.0 +/- 6 kcal/kg/day; p less than 0.01), and had better weight gain (20.1 +/- 12.1 vs 7.8 +/- 5.1 gm/kg/day; p less than 0.01) than the 12 control infants. Glucose 66-73 insulin Homo sapiens 25-32 1904090-8 1991 We conclude that a controlled insulin infusion improves and sustains glucose tolerance, facilitates provision of calories, and enhances weight gain in glucose-intolerant premature infants. Glucose 69-76 insulin Homo sapiens 30-37 1865823-4 1991 Insulin sensitivity, expressed as the ratio of rate of glucose utilization to the mean plasma insulin concentration during the second hour of glucose clamp (M/I) was negatively correlated with BMI (r = -.91, P less than .001), waist to hip girth ratio (WHR) (r = -.80, P less than .01), subcutaneous abdominal fat area (r = -.90, P less than .001), and intra-abdominal fat area (r = -.88, P less than .01). Glucose 55-62 insulin Homo sapiens 0-7 1865823-4 1991 Insulin sensitivity, expressed as the ratio of rate of glucose utilization to the mean plasma insulin concentration during the second hour of glucose clamp (M/I) was negatively correlated with BMI (r = -.91, P less than .001), waist to hip girth ratio (WHR) (r = -.80, P less than .01), subcutaneous abdominal fat area (r = -.90, P less than .001), and intra-abdominal fat area (r = -.88, P less than .01). Glucose 142-149 insulin Homo sapiens 0-7 1865823-4 1991 Insulin sensitivity, expressed as the ratio of rate of glucose utilization to the mean plasma insulin concentration during the second hour of glucose clamp (M/I) was negatively correlated with BMI (r = -.91, P less than .001), waist to hip girth ratio (WHR) (r = -.80, P less than .01), subcutaneous abdominal fat area (r = -.90, P less than .001), and intra-abdominal fat area (r = -.88, P less than .01). Glucose 142-149 insulin Homo sapiens 94-101 1925506-0 1991 Metabolic control in diabetic subjects following myocardial infarction: difficulties in improving blood glucose levels by intravenous insulin infusion. Glucose 104-111 insulin Homo sapiens 134-141 2048191-6 1991 Human C-peptide was detectable in blood by 26 weeks, with a rise demonstrable during the oral glucose tolerance test. Glucose 94-101 insulin Homo sapiens 6-15 2048192-2 1991 Digestion times, collagenase concentrations, and culture conditions were optimized by assessing insulin release in response to low glucose (3.3 mM), high glucose (16.7 mM), and high glucose plus theophylline (10 mM). Glucose 131-138 insulin Homo sapiens 96-103 2048192-2 1991 Digestion times, collagenase concentrations, and culture conditions were optimized by assessing insulin release in response to low glucose (3.3 mM), high glucose (16.7 mM), and high glucose plus theophylline (10 mM). Glucose 154-161 insulin Homo sapiens 96-103 2048192-2 1991 Digestion times, collagenase concentrations, and culture conditions were optimized by assessing insulin release in response to low glucose (3.3 mM), high glucose (16.7 mM), and high glucose plus theophylline (10 mM). Glucose 154-161 insulin Homo sapiens 96-103 2028355-5 1991 Defects in insulin action could also arise at post-receptor events particularly glucose transport. Glucose 80-87 insulin Homo sapiens 11-18 1673496-1 1991 To test the hypothesis that there is an abnormal serum insulin response to a carbohydrate load in thyrotoxic hypokalaemic periodic paralysis (THPP), 18 men with THPP and 15 with uncomplicated thyrotoxicosis were studied during an oral glucose tolerance test. Glucose 235-242 insulin Homo sapiens 55-62 1673496-2 1991 The THPP group had significantly higher fasting insulin concentrations (27.6 [3.6] vs 13.4 [1.8] mU/l; p less than 0.005) and a higher overall insulin response to oral glucose (p less than 0.001 by ANOVA) than the thyrotoxicosis group. Glucose 168-175 insulin Homo sapiens 143-150 2028714-1 1991 The dose-response relationships between prestimulatory blood glucose concentration and the plasma C-peptide responses to stimulation with 1 mg of glucagon iv or a standard mixed meal were studied in 8 C-peptide positive patients with insulin-dependent diabetes mellitus. Glucose 61-68 insulin Homo sapiens 98-107 1943751-4 1991 With low-dose insulin infusion, despite similar free insulin levels, diabetics had a greater decrease in plasma glucose concentrations during exercise than controls. Glucose 112-119 insulin Homo sapiens 14-21 1943751-7 1991 To better compare responses, a group of normal controls exercised during an infusion of insulin, which resulted in a similar decrease in plasma glucose to that of exercising diabetics. Glucose 144-151 insulin Homo sapiens 88-95 2028714-4 1991 The glucose potentiation of the incremental plasma C-peptide area under the curve at the two levels of hyperglycemia in percent of the area at normoglycemia (median and range) was 343% (53-1053) (p less than 0.05) and 341% (267-1027) (p less than 0.05) after glucagon and 140% (76-227) (NS) and 251% (95-1700) (p less than 0.05) after the meal. Glucose 4-11 insulin Homo sapiens 51-60 2028714-5 1991 The corresponding relative glucose potentiation of plasma C-peptide 6 min after stimulation with glucagon was 124% (100-427) (p less than 0.02) and 144% (100-209) (p less than 0.05). Glucose 27-34 insulin Homo sapiens 58-67 2035626-5 1991 However, when insulin was decreased and glucagon was increased simultaneously, there was an initial increase in glucose production, and the glucose level was 4.5 +/- 0.2 mmol/l at 60 min, a value not different from that in the comparison study. Glucose 112-119 insulin Homo sapiens 14-21 1903598-3 1991 GH inhibited the insulin-stimulated glucose disposal by 27% from 4.4 +/- 0.7 to 3.3 +/- 0.4 mg.kg-1.min-1 (P less than 0.02) and raised the nonprotein energy expenditures (NPEE) from 18.7 +/- 0.5 to 20.5 +/- 0.3 kcal.kg-1.24 h-1 (P less than 0.03). Glucose 36-43 insulin Homo sapiens 17-24 2035626-5 1991 However, when insulin was decreased and glucagon was increased simultaneously, there was an initial increase in glucose production, and the glucose level was 4.5 +/- 0.2 mmol/l at 60 min, a value not different from that in the comparison study. Glucose 140-147 insulin Homo sapiens 14-21 2035626-6 1991 Thus we conclude that both decrements in insulin and increments in glucagon play important roles in the prevention of hypoglycemia during exercise and do so by signaling increments in glucose production. Glucose 184-191 insulin Homo sapiens 41-48 2035636-3 1991 To determine whether the oscillations could result from the feedback loops between insulin and glucose, a parsimonious mathematical model including the major mechanisms involved in glucose regulation was developed. Glucose 181-188 insulin Homo sapiens 83-90 2035636-4 1991 This model comprises two major negative feedback loops describing the effects of insulin on glucose utilization and glucose production, respectively, and both loops include the stimulatory effect of glucose on insulin secretion. Glucose 92-99 insulin Homo sapiens 81-88 1669512-2 1991 Patients with untreated hypertension have been shown to be resistant to insulin-stimulated glucose uptake and both hyperinsulinemic and hypertriglyceridemic when compared to matched control groups with normal blood pressure. Glucose 91-98 insulin Homo sapiens 72-79 1669512-4 1991 In addition, insulin resistance, hyperinsulinemia, and hypertriglyceridemia have been demonstrated in rat models of hypertension, including rats with spontaneous hypertension and Sprague-Dawley rats fed a fructose-enriched diet, and the defect in insulin-stimulated glucose uptake in these experimental models can also be shown at the cellular level. Glucose 266-273 insulin Homo sapiens 13-20 2035636-6 1991 The occurrence of sustained insulin and glucose oscillations was found to be dependent on two essential features: 1) a time delay of 30-45 min for the effect of insulin on glucose production and 2) a sluggish effect of insulin on glucose utilization, because insulin acts from a compartment remote from plasma. Glucose 40-47 insulin Homo sapiens 161-168 2035636-6 1991 The occurrence of sustained insulin and glucose oscillations was found to be dependent on two essential features: 1) a time delay of 30-45 min for the effect of insulin on glucose production and 2) a sluggish effect of insulin on glucose utilization, because insulin acts from a compartment remote from plasma. Glucose 40-47 insulin Homo sapiens 161-168 2035636-6 1991 The occurrence of sustained insulin and glucose oscillations was found to be dependent on two essential features: 1) a time delay of 30-45 min for the effect of insulin on glucose production and 2) a sluggish effect of insulin on glucose utilization, because insulin acts from a compartment remote from plasma. Glucose 172-179 insulin Homo sapiens 28-35 2035636-6 1991 The occurrence of sustained insulin and glucose oscillations was found to be dependent on two essential features: 1) a time delay of 30-45 min for the effect of insulin on glucose production and 2) a sluggish effect of insulin on glucose utilization, because insulin acts from a compartment remote from plasma. Glucose 172-179 insulin Homo sapiens 161-168 2035636-6 1991 The occurrence of sustained insulin and glucose oscillations was found to be dependent on two essential features: 1) a time delay of 30-45 min for the effect of insulin on glucose production and 2) a sluggish effect of insulin on glucose utilization, because insulin acts from a compartment remote from plasma. Glucose 172-179 insulin Homo sapiens 161-168 1715240-3 1991 Therefore, we examined the presence and nature of human pancreatic galanin-like immunoreactive material (GLIR) and the effects of galanin on glucose-stimulated insulin secretion from isolated human islets. Glucose 141-148 insulin Homo sapiens 160-167 1747417-3 1991 This effect of insulin is due to glucose, an indispensable participant of the complex formation between the enzyme and the mitochondrial membrane. Glucose 33-40 insulin Homo sapiens 15-22 1715240-7 1991 Moreover, synthetic porcine galanin inhibited glucose-stimulated insulin secretion from collagenase-isolated human islets at dose rates greater than 10(-8) M. Thus, (1) human pancreas is innervated by galanin-containing nerves, (2) human pancreatic GLIR is of similar size as synthetic porcine galanin, and (3) porcine galanin inhibits glucose-stimulated insulin secretion from human islets. Glucose 46-53 insulin Homo sapiens 65-72 1715240-7 1991 Moreover, synthetic porcine galanin inhibited glucose-stimulated insulin secretion from collagenase-isolated human islets at dose rates greater than 10(-8) M. Thus, (1) human pancreas is innervated by galanin-containing nerves, (2) human pancreatic GLIR is of similar size as synthetic porcine galanin, and (3) porcine galanin inhibits glucose-stimulated insulin secretion from human islets. Glucose 46-53 insulin Homo sapiens 355-362 2065473-13 1991 The expected large insulin response to rising glucose was not seen until after ADR was ceased, confirming the inhibitory effect of ADR on glucose stimulated insulin release. Glucose 46-53 insulin Homo sapiens 19-26 2065473-13 1991 The expected large insulin response to rising glucose was not seen until after ADR was ceased, confirming the inhibitory effect of ADR on glucose stimulated insulin release. Glucose 138-145 insulin Homo sapiens 19-26 2065473-13 1991 The expected large insulin response to rising glucose was not seen until after ADR was ceased, confirming the inhibitory effect of ADR on glucose stimulated insulin release. Glucose 138-145 insulin Homo sapiens 157-164 1884880-9 1991 Blunting the insulin response to glucose directly by delaying glucose absorption and indirectly through reducing GIP secretion, may be a valuable therapeutic approach in reactive hypoglycemia; nevertheless, long-term study with Miglitol are needed, due to the poor intestinal tolerance of this drug in the present acute study. Glucose 33-40 insulin Homo sapiens 13-20 1816976-1 1991 The circadian variation of basal and postprandial plasma glucose and insulin levels was analyzed in 10 healthy individuals and 10 type-1 diabetic patients treated with a glucose-controlled insulin infusion system. Glucose 170-177 insulin Homo sapiens 189-196 1834487-1 1991 Three prospective population studies on non-diabetic subjects--the Helsinki Policemen Study, the Busselton Study, and the Paris Prospective Study--have shown that high plasma insulin levels, fasting or after oral glucose load, are associated with an increased risk of coronary heart disease (CHD). Glucose 213-220 insulin Homo sapiens 175-182 1884880-9 1991 Blunting the insulin response to glucose directly by delaying glucose absorption and indirectly through reducing GIP secretion, may be a valuable therapeutic approach in reactive hypoglycemia; nevertheless, long-term study with Miglitol are needed, due to the poor intestinal tolerance of this drug in the present acute study. Glucose 62-69 insulin Homo sapiens 13-20 1936473-2 1991 Basal and insulin-mediated glucose and free-fatty acid (FFA) metabolism was evaluated in 6 non-insulin-dependent diabetic patients (NIDDM) previously treated by diet, before and after 4 week metformin treatment (850 mg twice/day). Glucose 27-34 insulin Homo sapiens 10-17 1936464-2 1991 Elevated serum insulin concentrations in the presence of normal fasting plasma glucose levels reflect the presence of insulin resistance and they have also been shown to predict deterioration to NIDDM in a number of populations. Glucose 79-86 insulin Homo sapiens 15-22 1936464-2 1991 Elevated serum insulin concentrations in the presence of normal fasting plasma glucose levels reflect the presence of insulin resistance and they have also been shown to predict deterioration to NIDDM in a number of populations. Glucose 79-86 insulin Homo sapiens 118-125 1936464-4 1991 In Nauruans and Pima subjects with normal glucose tolerance, those with higher post-load (2-hour) serum insulin at baseline were more likely to progress to either impaired glucose tolerance (IGT) or NIDDM. Glucose 42-49 insulin Homo sapiens 104-111 1936465-1 1991 Recent reports have shown that resistance to insulin-stimulated glucose uptake, increased plasma glucose and insulin response to oral glucose, and hypertriglyceridemia can be seen in first degree relatives of patients with type 2 diabetes. Glucose 64-71 insulin Homo sapiens 45-52 1936465-3 1991 Given these data, we thought it would be of interest to compare the plasma glucose and insulin response to an oral glucose challenge, plasma lipid concentrations, and blood pressure in offspring of parents with IGT as compared to offspring of parents with normal glucose tolerance. Glucose 115-122 insulin Homo sapiens 87-94 1936465-3 1991 Given these data, we thought it would be of interest to compare the plasma glucose and insulin response to an oral glucose challenge, plasma lipid concentrations, and blood pressure in offspring of parents with IGT as compared to offspring of parents with normal glucose tolerance. Glucose 115-122 insulin Homo sapiens 87-94 1936465-6 1991 Statistically significant increases in plasma insulin response to oral glucose and in systolic and diastolic blood pressure were present in the offspring of parents with IGT. Glucose 71-78 insulin Homo sapiens 46-53 1936465-7 1991 Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that individual differences in insulin metabolism and blood pressure are modulated by genetic factors and that both may be related to variations in insulin-stimulated glucose uptake and/or plasma insulin concentration. Glucose 69-76 insulin Homo sapiens 49-56 1936465-7 1991 Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that individual differences in insulin metabolism and blood pressure are modulated by genetic factors and that both may be related to variations in insulin-stimulated glucose uptake and/or plasma insulin concentration. Glucose 69-76 insulin Homo sapiens 210-217 1936465-7 1991 Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that individual differences in insulin metabolism and blood pressure are modulated by genetic factors and that both may be related to variations in insulin-stimulated glucose uptake and/or plasma insulin concentration. Glucose 69-76 insulin Homo sapiens 210-217 1936465-7 1991 Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that individual differences in insulin metabolism and blood pressure are modulated by genetic factors and that both may be related to variations in insulin-stimulated glucose uptake and/or plasma insulin concentration. Glucose 346-353 insulin Homo sapiens 49-56 1936482-2 1991 The addition of both insulin and metformin treatment significantly improved fasting plasma glucose, post-prandial plasma glucose and %HbA1. Glucose 91-98 insulin Homo sapiens 21-28 1936482-2 1991 The addition of both insulin and metformin treatment significantly improved fasting plasma glucose, post-prandial plasma glucose and %HbA1. Glucose 121-128 insulin Homo sapiens 21-28 1936484-1 1991 Resistance to insulin-stimulated glucose uptake is associated with an increased rate of synthesis and secretion of VLDL-triglycerides and, in the absence of adequate removal capacity, with hypertriglyceridemia. Glucose 33-40 insulin Homo sapiens 14-21 1936488-0 1991 Resistance to insulin-stimulated glucose uptake and hyperinsulinemia: role in non-insulin-dependent diabetes, high blood pressure, dyslipidemia and coronary heart disease. Glucose 33-40 insulin Homo sapiens 14-21 1936488-1 1991 Patients with impaired glucose tolerance (IGT) and Type 2 diabetes have been shown to be more resistant to insulin-stimulated glucose uptake than individuals with normal glucose tolerance. Glucose 23-30 insulin Homo sapiens 107-114 1936488-1 1991 Patients with impaired glucose tolerance (IGT) and Type 2 diabetes have been shown to be more resistant to insulin-stimulated glucose uptake than individuals with normal glucose tolerance. Glucose 126-133 insulin Homo sapiens 107-114 1936488-2 1991 Evidence has also been published showing that first degree relatives of patients with Type 2 diabetes are insulin resistant when compared to a matched group of relatives of subjects with normal glucose tolerance. Glucose 194-201 insulin Homo sapiens 106-113 1936488-3 1991 In addition, it has recently been shown that the ability of insulin to stimulate glucose uptake varies approximately four-fold in individuals with normal glucose tolerance, and insulin resistance of a degree comparable to that seen in patients with IGT or with Type 2 diabetes is present in a significant portion of the normal population. Glucose 81-88 insulin Homo sapiens 60-67 1936488-3 1991 In addition, it has recently been shown that the ability of insulin to stimulate glucose uptake varies approximately four-fold in individuals with normal glucose tolerance, and insulin resistance of a degree comparable to that seen in patients with IGT or with Type 2 diabetes is present in a significant portion of the normal population. Glucose 154-161 insulin Homo sapiens 60-67 1936488-4 1991 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 37-44 insulin Homo sapiens 18-25 1936488-4 1991 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 37-44 insulin Homo sapiens 97-104 1936488-4 1991 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 37-44 insulin Homo sapiens 97-104 1936488-4 1991 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 53-60 insulin Homo sapiens 18-25 1936488-4 1991 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 53-60 insulin Homo sapiens 97-104 1936488-4 1991 Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin resistant individuals continue to secrete greater than normal amounts of insulin. Glucose 53-60 insulin Homo sapiens 97-104 1936488-5 1991 As a corollary, glucose homeostasis will decompensate when the insulin secretory response begins to fall, and the greater the decline in insulin secretion, the larger the rise in plasma glucose concentration. Glucose 16-23 insulin Homo sapiens 63-70 1936488-7 1991 On the other hand, the relationship between plasma insulin and glucose concentration will be negatively correlated in patients with Type 2 diabetes and varying degrees of fasting hyperglycemia. Glucose 63-70 insulin Homo sapiens 51-58 2019259-4 1991 After 5 h, glucose and insulin alone had no chronic regulatory effects; however, in combination, these agents were able to decrease insulin sensitivity. Glucose 11-18 insulin Homo sapiens 132-139 2019259-5 1991 In cells preincubated with 50 ng/ml insulin, the insulin ED50 for acute stimulation of glucose transport was increased by 65% and 116% as medium glucose was raised to 5 and 20 mM, respectively, relative to that at 0 mM glucose. Glucose 87-94 insulin Homo sapiens 36-43 2019259-5 1991 In cells preincubated with 50 ng/ml insulin, the insulin ED50 for acute stimulation of glucose transport was increased by 65% and 116% as medium glucose was raised to 5 and 20 mM, respectively, relative to that at 0 mM glucose. Glucose 87-94 insulin Homo sapiens 49-56 2019259-5 1991 In cells preincubated with 50 ng/ml insulin, the insulin ED50 for acute stimulation of glucose transport was increased by 65% and 116% as medium glucose was raised to 5 and 20 mM, respectively, relative to that at 0 mM glucose. Glucose 145-152 insulin Homo sapiens 36-43 2019259-5 1991 In cells preincubated with 50 ng/ml insulin, the insulin ED50 for acute stimulation of glucose transport was increased by 65% and 116% as medium glucose was raised to 5 and 20 mM, respectively, relative to that at 0 mM glucose. Glucose 145-152 insulin Homo sapiens 49-56 2019259-5 1991 In cells preincubated with 50 ng/ml insulin, the insulin ED50 for acute stimulation of glucose transport was increased by 65% and 116% as medium glucose was raised to 5 and 20 mM, respectively, relative to that at 0 mM glucose. Glucose 145-152 insulin Homo sapiens 36-43 2019259-5 1991 In cells preincubated with 50 ng/ml insulin, the insulin ED50 for acute stimulation of glucose transport was increased by 65% and 116% as medium glucose was raised to 5 and 20 mM, respectively, relative to that at 0 mM glucose. Glucose 145-152 insulin Homo sapiens 49-56 2019259-8 1991 Insulin receptor down-regulation (18%) was observed after 24 h (but not 5 h) in insulin-treated cells; however, the major portion of the decrease in insulin sensitivity was due to uncoupling of occupied insulin receptors from stimulation of the glucose transport system. Glucose 245-252 insulin Homo sapiens 80-87 2019259-8 1991 Insulin receptor down-regulation (18%) was observed after 24 h (but not 5 h) in insulin-treated cells; however, the major portion of the decrease in insulin sensitivity was due to uncoupling of occupied insulin receptors from stimulation of the glucose transport system. Glucose 245-252 insulin Homo sapiens 149-156 2019259-8 1991 Insulin receptor down-regulation (18%) was observed after 24 h (but not 5 h) in insulin-treated cells; however, the major portion of the decrease in insulin sensitivity was due to uncoupling of occupied insulin receptors from stimulation of the glucose transport system. Glucose 245-252 insulin Homo sapiens 149-156 2019259-11 1991 Long term treatment (24 h) with glucose (10 mM) and insulin (50 ng/ml) markedly decreased insulin sensitivity (and receptor coupling), but did not affect insulin receptor kinase activity in any of these studies. Glucose 32-39 insulin Homo sapiens 90-97 2022304-6 1991 After bolus intravenous injections of glucose, the patients with diabetes again exhibited glucose intolerance; acute responses of immunoreactive insulin (IRI) and C-peptide were present, although grossly obtunded. Glucose 38-45 insulin Homo sapiens 145-152 2060451-6 1991 RESULTS: When insulin was given 30 min before the meal with miglitol (protocol 4) or placebo (protocol 5), plasma glucose increased from 4.94 +/- 0.16 to 5.94 +/- 0.55 mM and from 5.11 +/- 0.22 to 8.22 +/- 0.72 mM, respectively (P less than 0.01). Glucose 114-121 insulin Homo sapiens 14-21 2060451-7 1991 When insulin was given at the time of the meal with miglitol (protocol 2) or placebo (protocol 3), plasma glucose increased from 5.44 +/- 0.27 to 7.77 +/- 0.5 mM and from 5.72 +/- 0.22 to 10.83 +/- 0.77 mM, respectively (P less than 0.01). Glucose 106-113 insulin Homo sapiens 5-12 2060451-8 1991 When insulin was given 60 min before the meal (protocol 1), plasma glucose initially decreased from 5.61 +/- 0.38 to 4.33 +/- 0.33 mM and then increased to 6.94 +/- 0.66 mM after the meal. Glucose 67-74 insulin Homo sapiens 5-12 1874481-0 1991 Insulin prevents glucose induced inhibition of angiotensin II-stimulated aldosterone secretion. Glucose 17-24 insulin Homo sapiens 0-7 1874481-3 1991 The effect of insulin on glucose-induced inhibition of angiotensin II-stimulated aldosterone secretion was examined. Glucose 25-32 insulin Homo sapiens 14-21 1874481-8 1991 These results (1) demonstrate that insulin can prevent inhibition of glucose-induced angiotensin II-stimulated aldosterone secretion, possibly by preventing a glucose-induced decrease in cell volume, and (2) suggest that the suppressed plasma level of aldosterone found in individuals with diabetes mellitus may in part be due to the direct effects of hyperglycemia on the adrenal gland secretion of aldosterone. Glucose 69-76 insulin Homo sapiens 35-42 1865561-1 1991 The regulation of net hepatic glucose uptake in vivo occurs by way of the hormonal milieu (insulin and glucagon), the glucose level, and the route of glucose delivery. Glucose 30-37 insulin Homo sapiens 91-98 1865561-3 1991 Net hepatic glucose uptake is augmented in a dose-dependent manner by a rise in insulin and is further stimulated by the presence of a "portal signal." Glucose 12-19 insulin Homo sapiens 80-87 1865561-4 1991 The presence of coordinated changes in insulin, glucagon, and the glucose level in combination with the "portal signal" ensures adequate glucose uptake by the liver in response to a meal. Glucose 137-144 insulin Homo sapiens 39-46 1876486-8 1991 Since increasing glucose concentration lengthens calcium wave and burst duration without significantly affecting wave amplitude, we further propose that it is the fractional time at an enhanced Ca2+ level, rather than its amplitude, that encodes for the primary response of insulin-secreting cells to fuel secretagogues. Glucose 17-24 insulin Homo sapiens 274-281 1844297-3 1991 Insulin blood levels of 53 uU/ml and Peptide C levels of 6.5 ng/dl were shown associated to a blood glucose level of 34 mg/dl. Glucose 100-107 insulin Homo sapiens 0-7 1891638-4 1991 These facts at the receptor level could be originating a decrease in tissue response to insulin and be the base for glucose intolerance observed in patients with this pathology. Glucose 116-123 insulin Homo sapiens 88-95 1649673-0 1991 Insulin treatment improved glucose-induced insulin release in elderly non-insulin-dependent diabetes mellitus, secondary failure to oral hypoglycemic agents. Glucose 27-34 insulin Homo sapiens 0-7 1649673-0 1991 Insulin treatment improved glucose-induced insulin release in elderly non-insulin-dependent diabetes mellitus, secondary failure to oral hypoglycemic agents. Glucose 27-34 insulin Homo sapiens 43-50 1649673-5 1991 After insulin therapy for three weeks, the fasting plasma glucose levels dropped to 130 +/- 8 mg/dl (Mean +/- SEM, P less than 0.001). Glucose 58-65 insulin Homo sapiens 6-13 1649673-8 1991 These results suggested that greater C-peptide response was found in non-insulin dependent elderly diabetics following oral glucose after plasma glucose normalized with insulin therapy. Glucose 124-131 insulin Homo sapiens 37-46 1649673-8 1991 These results suggested that greater C-peptide response was found in non-insulin dependent elderly diabetics following oral glucose after plasma glucose normalized with insulin therapy. Glucose 124-131 insulin Homo sapiens 73-80 1649673-8 1991 These results suggested that greater C-peptide response was found in non-insulin dependent elderly diabetics following oral glucose after plasma glucose normalized with insulin therapy. Glucose 124-131 insulin Homo sapiens 169-176 1649673-8 1991 These results suggested that greater C-peptide response was found in non-insulin dependent elderly diabetics following oral glucose after plasma glucose normalized with insulin therapy. Glucose 145-152 insulin Homo sapiens 37-46 1649673-8 1991 These results suggested that greater C-peptide response was found in non-insulin dependent elderly diabetics following oral glucose after plasma glucose normalized with insulin therapy. Glucose 145-152 insulin Homo sapiens 169-176 2008857-1 1991 Resistance to insulin-stimulated glucose uptake and hyperinsulinemia may play a central role in the cause and clinical course of patients with non-insulin-dependent diabetes mellitus, high blood pressure, abnormalities of lipoprotein metabolism, and coronary heart disease. Glucose 33-40 insulin Homo sapiens 14-21 1819986-3 1991 Fourteen patients had active AS with ESR of 47.0 +/- 27.7 mm; they had increased insulin levels measured as area under curve (AUC) of a glucose tolerance test 107.4 +/- 44.1 cm2 vs controls 40.8 +/- 12.6 cm2 (p less than 0.03). Glucose 136-143 insulin Homo sapiens 81-88 2012520-2 1991 High fasting insulin levels (1183 pmol/L) and strikingly high insulin release in response to glucose (7892 pmol/L) were found within weeks of the onset of the illness. Glucose 93-100 insulin Homo sapiens 62-69 1873991-3 1991 With self-monitored glucose values and insulin doses collected with one of several commercially available memory meters, GLUCOJECT reconstructs an average or "typical" daily plasma glucose and insulin profile and displays them in a graph. Glucose 20-27 insulin Homo sapiens 193-200 1873991-3 1991 With self-monitored glucose values and insulin doses collected with one of several commercially available memory meters, GLUCOJECT reconstructs an average or "typical" daily plasma glucose and insulin profile and displays them in a graph. Glucose 181-188 insulin Homo sapiens 39-46 1873991-5 1991 In turn, this allows one to calculate an "ideal" plasma insulin profile required to maintain a relatively constant "ideal" plasma glucose level. Glucose 130-137 insulin Homo sapiens 56-63 1873991-7 1991 For any optimized insulin regimen, GLUCOJECT calculates and displays the predicted time course of plasma glucose. Glucose 105-112 insulin Homo sapiens 18-25 2010042-10 1991 Moreover, they have shown that specific depletion of the glucose-transporter isoform that mediates insulin-stimulated glucose transport is responsible for decreased transport activity in adipose tissue in insulin-resistant states. Glucose 57-64 insulin Homo sapiens 99-106 2010042-10 1991 Moreover, they have shown that specific depletion of the glucose-transporter isoform that mediates insulin-stimulated glucose transport is responsible for decreased transport activity in adipose tissue in insulin-resistant states. Glucose 57-64 insulin Homo sapiens 205-212 2010047-2 1991 We investigated the mechanism of peripheral insulin resistance in the adipose tissue of obese and non-insulin-dependent diabetes mellitus (NIDDM) patients at the level of the glucose-transport effector system. Glucose 175-182 insulin Homo sapiens 44-51 2010047-3 1991 Freshly isolated adipocytes from obese nondiabetic and obese NIDDM subjects had decreased insulin sensitivity and responsiveness for glucose-transport stimulation compared with control subjects, with more pronounced changes associated with obese NIDDM patients. Glucose 133-140 insulin Homo sapiens 90-97 2010051-6 1991 Insulin-stimulated glucose uptake in the diabetic patients (1.60 +/- 0.28 mumol.min-1.100 g-1, P = 0.04). Glucose 19-26 insulin Homo sapiens 0-7 2010052-3 1991 We compared fasting and glucose-stimulated insulin and C-peptide levels in a community-based sample of 464 Hispanic and 676 non-Hispanic white adult residents of the San Luis Valley of Colorado. Glucose 24-31 insulin Homo sapiens 43-50 2010052-5 1991 Mean fasting and 1- and 2-h post-glucose load insulin levels were significantly higher in Hispanics versus non-Hispanic whites (fasting 0.08 vs. 0.07 nM, P = 0.0026; 1 h 0.52 vs. 0.47 nM, P = 0.0129; 2 h 0.36 vs. 0.27 nM, P less than 0.0001), even after adjustment for age, sex, body mass index, waist-hip ratio, family history of diabetes mellitus, concurrent plasma glucose level, and fasting insulin level. Glucose 33-40 insulin Homo sapiens 46-53 2010052-5 1991 Mean fasting and 1- and 2-h post-glucose load insulin levels were significantly higher in Hispanics versus non-Hispanic whites (fasting 0.08 vs. 0.07 nM, P = 0.0026; 1 h 0.52 vs. 0.47 nM, P = 0.0129; 2 h 0.36 vs. 0.27 nM, P less than 0.0001), even after adjustment for age, sex, body mass index, waist-hip ratio, family history of diabetes mellitus, concurrent plasma glucose level, and fasting insulin level. Glucose 368-375 insulin Homo sapiens 46-53 2010052-6 1991 Mean fasting and 1- and 2-h glucose-stimulated C-peptide levels in Hispanics also significantly exceeded those in non-Hispanic whites (fasting 0.58 vs. 0.54 nM, P = 0.0119; 1 h 2.72 vs. 2.46 nM, P less than 0.0001; 2 h 2.25 vs. 1.97 nM, P less than 0.0001). Glucose 28-35 insulin Homo sapiens 47-56 2065862-8 1991 The metabolic clearance rate of glucose during the last 30 min of insulin infusion was lower in the diabetic patients (155 +/- 62 vs 320 +/- 69 ml.min-1.m-2, p less than 0.01), reflecting peripheral insulin resistance. Glucose 32-39 insulin Homo sapiens 199-206 1826009-4 1991 Androgen levels were measured before and at the conclusion of studies in which either insulin was infused exogenously at 1 mU/kg.min or endogenous insulin secretion was stimulated for 2 h by elevation of the plasma glucose concentration by 125 mg/dL above basal levels by an exogenous glucose infusion. Glucose 215-222 insulin Homo sapiens 147-154 2010535-0 1991 Reduced capacity and affinity of skeletal muscle for insulin-mediated glucose uptake in noninsulin-dependent diabetic subjects. Glucose 70-77 insulin Homo sapiens 53-60 2010535-2 1991 We have estimated the capacity and affinity of insulin-mediated glucose uptake (IMGU) in whole body and in leg muscle of obese non-insulin-dependent diabetics (NIDDM, n = 6) with severe hyperglycemia, glycohemoglobin (GHb 14.4 +/- 1.2%), lean controls (ln, n = 7) and obese nondiabetic controls (ob, n = 7). Glucose 64-71 insulin Homo sapiens 47-54 1646259-1 1991 Insulin resistance associated with a hyperinsulinemic response to oral glucose intake has been found in patients with essential hypertension and is believed to play a role in inducing hypertension by causing renal sodium and water retention. Glucose 71-78 insulin Homo sapiens 0-7 1646259-5 1991 Following the glucose load, plasma levels of both glucose and insulin were significantly higher (P less than 0.01) in the salt-sensitive (n = 10) compared with the salt-resistant subjects (n = 13) during the high-salt diet but not during the low-salt diet. Glucose 14-21 insulin Homo sapiens 62-69 2025856-3 1991 Glucose disposal rates, determined by the euglycemic clamp at three different rates of insulin infusion did not differ significantly between the two groups. Glucose 0-7 insulin Homo sapiens 87-94 2025856-5 1991 Peripheral insulin sensitivity calculated from the slope of glucose disposal versus plasma insulin concentration did not differ between the two groups. Glucose 60-67 insulin Homo sapiens 11-18 1826185-3 1991 In the first study described in this investigation, hypertensive subjects with insulin-dependent diabetes mellitus (IDDM) who had an elevated Na+/Li+ countertransport activity were found to have a lower whole body glucose utilization, a lower insulin-stimulated forearm carbohydrate oxidation, larger ultrasound kidney volume, and increased left ventricular mass index when compared with hypertensive IDDM subjects with a normal Na+/Li+ countertransport activity or normotensive IDDM subjects. Glucose 214-221 insulin Homo sapiens 79-86 2018116-5 1991 This was confirmed when glucose was infused in the absence of growth hormone to achieve glucose (and insulin) concentrations comparable to those present during growth hormone infusion. Glucose 24-31 insulin Homo sapiens 101-108 2069355-9 1991 In diabetic children, an adequate insulin therapy is required to allow the full benefit of muscular activity on glucose assimilation and to reach the same level of physical performance as the non-diabetic. Glucose 112-119 insulin Homo sapiens 34-41 2018470-0 1991 Phorbol ester only partially mimics the effects of insulin on glucose transport and glucose-transporter distribution in 3T3-L1 adipocytes. Glucose 62-69 insulin Homo sapiens 51-58 1905629-1 1991 We investigated the dose-response characteristics of glucose-induced insulin release and the influence of hyperglycaemia on arginine-induced insulin secretion in eight non-obese subjects with NIDDM and in eight non-diabetic volunteers. Glucose 53-60 insulin Homo sapiens 69-76 1905629-3 1991 The insulin secretory capacity (Vmax) for glucose-stimulated insulin release showed a trend towards a negative correlation with the fasting blood glucose in the NIDDM subjects (r = 0.68, P = 0.6); it was lower than the Vmax of non-diabetic controls (2.2 +/- 0.2 vs 4.2 +/- 0.4 nmol l-1 respectively; P less than 0.001). Glucose 42-49 insulin Homo sapiens 4-11 1905629-3 1991 The insulin secretory capacity (Vmax) for glucose-stimulated insulin release showed a trend towards a negative correlation with the fasting blood glucose in the NIDDM subjects (r = 0.68, P = 0.6); it was lower than the Vmax of non-diabetic controls (2.2 +/- 0.2 vs 4.2 +/- 0.4 nmol l-1 respectively; P less than 0.001). Glucose 42-49 insulin Homo sapiens 61-68 1905629-3 1991 The insulin secretory capacity (Vmax) for glucose-stimulated insulin release showed a trend towards a negative correlation with the fasting blood glucose in the NIDDM subjects (r = 0.68, P = 0.6); it was lower than the Vmax of non-diabetic controls (2.2 +/- 0.2 vs 4.2 +/- 0.4 nmol l-1 respectively; P less than 0.001). Glucose 146-153 insulin Homo sapiens 4-11 1905629-3 1991 The insulin secretory capacity (Vmax) for glucose-stimulated insulin release showed a trend towards a negative correlation with the fasting blood glucose in the NIDDM subjects (r = 0.68, P = 0.6); it was lower than the Vmax of non-diabetic controls (2.2 +/- 0.2 vs 4.2 +/- 0.4 nmol l-1 respectively; P less than 0.001). Glucose 146-153 insulin Homo sapiens 61-68 1905629-4 1991 The ED50 (half maximal stimulating blood glucose concentration) of the second-phase glucose-stimulated insulin release (determined from the plasma C-peptide levels at 60 min) was not significantly different from the ED50 of the controls (11.9 +/- 0.8 vs 13.3 +/- 1.9 mmol l-1 respectively; P greater than 0.2). Glucose 41-48 insulin Homo sapiens 103-110 1905629-4 1991 The ED50 (half maximal stimulating blood glucose concentration) of the second-phase glucose-stimulated insulin release (determined from the plasma C-peptide levels at 60 min) was not significantly different from the ED50 of the controls (11.9 +/- 0.8 vs 13.3 +/- 1.9 mmol l-1 respectively; P greater than 0.2). Glucose 84-91 insulin Homo sapiens 103-110 1906024-1 1991 In order to evaluate the importance of a defect in insulin mediated non-oxidative glucose metabolism and glycogen synthase activity in skeletal muscles in obese subjects with and without Type 2 (non-insulin-dependent) diabetes mellitus we studied: 10 lean and 10 obese control subjects and 12 obese diabetic patients using the euglycaemic hyperinsulinaemic clamp technique (basal, 20 mU. Glucose 82-89 insulin Homo sapiens 51-58 1906024-5 1991 We found that non-oxidative glucose metabolism could be stimulated by insulin in all three groups (p less than 0.01). Glucose 28-35 insulin Homo sapiens 70-77 1906024-9 1991 We conclude that insulin resistance in peripheral tissues in obese subjects with and without Type 2 diabetes may be partly explained by a reduced insulin mediated non-oxidative glucose metabolism and that this abnormality might be due to an absent insulin stimulation of glycogen synthase in skeletal muscles. Glucose 177-184 insulin Homo sapiens 17-24 1906024-9 1991 We conclude that insulin resistance in peripheral tissues in obese subjects with and without Type 2 diabetes may be partly explained by a reduced insulin mediated non-oxidative glucose metabolism and that this abnormality might be due to an absent insulin stimulation of glycogen synthase in skeletal muscles. Glucose 177-184 insulin Homo sapiens 146-153 1906024-9 1991 We conclude that insulin resistance in peripheral tissues in obese subjects with and without Type 2 diabetes may be partly explained by a reduced insulin mediated non-oxidative glucose metabolism and that this abnormality might be due to an absent insulin stimulation of glycogen synthase in skeletal muscles. Glucose 177-184 insulin Homo sapiens 146-153 2060435-1 1991 OBJECTIVE: To study the short-term effects of the serotoninergic anorectic drug d-fenfluramine on insulin-induced glucose disposal. Glucose 114-121 insulin Homo sapiens 98-105 2065862-8 1991 The metabolic clearance rate of glucose during the last 30 min of insulin infusion was lower in the diabetic patients (155 +/- 62 vs 320 +/- 69 ml.min-1.m-2, p less than 0.01), reflecting peripheral insulin resistance. Glucose 32-39 insulin Homo sapiens 66-73 1874475-6 1991 These results emphasize the metabolic importance of G-6-PD in the process of glucose induced insulin release. Glucose 77-84 insulin Homo sapiens 93-100 2005209-4 1991 During the euglycemic clamp, insulin-stimulated glucose metabolism was decreased in both groups of patients [group 1, 8.4 +/- 1.0 vs. 14.7 +/- 2 mM/m2.min in controls (P less than 0.05); group 2, 9 +/- 0.7 vs. 11.7 +/- 0.9 mM/m2.min in controls (P less than 0.05)]. Glucose 48-55 insulin Homo sapiens 29-36 2005209-5 1991 The impairment of insulin-stimulated glucose metabolism in patients with Turner"s syndrome was accounted for by reduced nonoxidative glucose disposal; glucose oxidation rose to a similar extent in Turner patients and normal controls. Glucose 37-44 insulin Homo sapiens 18-25 2005209-5 1991 The impairment of insulin-stimulated glucose metabolism in patients with Turner"s syndrome was accounted for by reduced nonoxidative glucose disposal; glucose oxidation rose to a similar extent in Turner patients and normal controls. Glucose 133-140 insulin Homo sapiens 18-25 2005209-5 1991 The impairment of insulin-stimulated glucose metabolism in patients with Turner"s syndrome was accounted for by reduced nonoxidative glucose disposal; glucose oxidation rose to a similar extent in Turner patients and normal controls. Glucose 133-140 insulin Homo sapiens 18-25 2005209-7 1991 Our data suggest that in patients with Turner"s syndrome, insulin resistance is a very early metabolic defect that may be restricted to nonoxidative pathways of intracellular glucose metabolism. Glucose 175-182 insulin Homo sapiens 58-65 2005215-0 1991 Insulin action kinetics in adipocytes from obese and noninsulin-dependent diabetes mellitus subjects: identification of multiple cellular defects in glucose transport. Glucose 149-156 insulin Homo sapiens 0-7 2005215-2 1991 We have measured the onset and loss of insulin action on glucose transport in adipocytes obtained from obese nondiabetic and obese NIDDM subjects to determine the contributions of obesity and diabetes to these cellular defects in insulin action. Glucose 57-64 insulin Homo sapiens 39-46 2005215-4 1991 The activation of glucose transport by insulin (4.3 nmol/L) was slower in cells from obese NIDDM patients. Glucose 18-25 insulin Homo sapiens 39-46 2005215-6 1991 Conversely, the deactivation of insulin-stimulated glucose transport upon removal of insulin was more rapid in adipocytes from the obese and obese NIDDM subjects. Glucose 51-58 insulin Homo sapiens 32-39 2005215-6 1991 Conversely, the deactivation of insulin-stimulated glucose transport upon removal of insulin was more rapid in adipocytes from the obese and obese NIDDM subjects. Glucose 51-58 insulin Homo sapiens 85-92 2005215-8 1991 In conclusion, 1) basal and insulin-stimulated rates of glucose transport are similarly reduced in adipocytes from obese and obese NIDDM subjects; and 2) adipocytes from obese and obese NIDDM subjects display defects in the kinetics of insulin action, slower activation and accelerated deactivation, that mirror the defects measured in vivo. Glucose 56-63 insulin Homo sapiens 28-35 2005219-3 1991 During a 1.7 mU/kg.min hyperinsulinemic-euglycemic clamp, the insulin-mediated glucose disposal rate was lower (26.9 +/- 2.1 vs. 47.1 +/- 3.7 mumol/kg.min; P less than 0.001), and GH levels were higher (6.5 +/- 1.2 vs. 2.9 +/- 0.8 micrograms/L; P = 0.03) in females than in males. Glucose 79-86 insulin Homo sapiens 28-35 2005219-5 1991 During insulin-induced hypoglycemia, the rate of drop in plasma glucose was faster (0.16 +/- 0.01 vs. 0.11 +/- 0.01 mmol/L.min; P = 0.001), and the rate of glucose recovery was slower in males than in females (0.04 +/- 0.01 vs. 0.06 +/- 0.01 mmol/L.min; P = 0.05). Glucose 64-71 insulin Homo sapiens 7-14 2005219-5 1991 During insulin-induced hypoglycemia, the rate of drop in plasma glucose was faster (0.16 +/- 0.01 vs. 0.11 +/- 0.01 mmol/L.min; P = 0.001), and the rate of glucose recovery was slower in males than in females (0.04 +/- 0.01 vs. 0.06 +/- 0.01 mmol/L.min; P = 0.05). Glucose 156-163 insulin Homo sapiens 7-14 2005219-6 1991 Plasma glucose concentrations were lower in males than in females (glucose nadir, 2.3 +/- 0.2 vs. 3.3 +/- 0.2 mmol/L; P = 0.002; glucose peak, 3.7 +/- 0.2 vs. 5.3 +/- 0.4 mmol/L; P = 0.002), with similar plasma free insulin concentrations. Glucose 7-14 insulin Homo sapiens 216-223 1765903-2 1991 By encapsulating the Con-A bound G- insulin in a suitable polymer membrane, which was permeable to both glucose and insulin, the insulin efflux was regulated in response to glucose influx. Glucose 104-111 insulin Homo sapiens 36-43 2008651-0 1991 The effect of graded doses of insulin on peripheral glucose uptake and lactate release in cancer cachexia. Glucose 52-59 insulin Homo sapiens 30-37 2008651-5 1991 Complete suppression of endogenous glucose production occurred at high physiologic insulin concentrations. Glucose 35-42 insulin Homo sapiens 83-90 2008651-6 1991 With progressive insulin infusion, the rate of glucose disappearance increased to 3.6 +/- 1.2, 8.7 +/- 0.8, and 13.7 +/- 1.1 mg/kg/min in control subjects and 2.9 +/- 0.4, 5.3 +/- 0.3, and 10.9 +/- 0.9 mg/kg.min in patients, significantly different from that of control subjects (p less than 0.05) during the intermediate (high physiologic) insulin infusion. Glucose 47-54 insulin Homo sapiens 17-24 2008651-12 1991 Total body glucose use was diminished in these patients, consistent with a state of insulin resistance. Glucose 11-18 insulin Homo sapiens 84-91 2008651-13 1991 This impaired insulin action on peripheral glucose use was associated with an increase in peripheral lactate release in patients. Glucose 43-50 insulin Homo sapiens 14-21 1936473-7 1991 During the insulin clamp studies, whole body glucose disposal was higher both at the lower (2.1 +/- 0.4 vs 2.8 +/- 0.4 mg/kg/min) and higher insulin plateau (4.8 +/- 0.9 vs 6.3 +/- 0.9 mg/kg/min; p less than 0.01). Glucose 45-52 insulin Homo sapiens 11-18 1936473-10 1991 In conclusion, metformin treatment induces an improvement in glucose metabolism both in the basal and insulin-stimulated state. Glucose 61-68 insulin Homo sapiens 102-109 2002019-2 1991 Based on our previous finding that desensitization of the insulin-responsive glucose transport system (GTS) requires three components, glucose, insulin, and glutamine, we postulated that the routing of incoming glucose through the hexosamine biosynthesis pathway plays a key role in the development of insulin resistance in primary cultured adipocytes. Glucose 135-142 insulin Homo sapiens 58-65 1830013-5 1991 In PCO patients, we found that basal and glucose-challenged insulin levels were significantly greater than, and hypoglycemic responses to IV insulin, significantly lower than, weight-matched control values. Glucose 41-48 insulin Homo sapiens 60-67 2002019-2 1991 Based on our previous finding that desensitization of the insulin-responsive glucose transport system (GTS) requires three components, glucose, insulin, and glutamine, we postulated that the routing of incoming glucose through the hexosamine biosynthesis pathway plays a key role in the development of insulin resistance in primary cultured adipocytes. Glucose 77-84 insulin Homo sapiens 58-65 2043298-7 1991 The changes in day-long plasma glucose and insulin responses suggested that resistance to insulin-stimulated glucose uptake had increased in association with atenolol treatment and decreased following nifedipine. Glucose 31-38 insulin Homo sapiens 90-97 2002019-2 1991 Based on our previous finding that desensitization of the insulin-responsive glucose transport system (GTS) requires three components, glucose, insulin, and glutamine, we postulated that the routing of incoming glucose through the hexosamine biosynthesis pathway plays a key role in the development of insulin resistance in primary cultured adipocytes. Glucose 77-84 insulin Homo sapiens 144-151 1900667-0 1991 Insulin resistance in normal rats infused with glucose for 72 h. Insulin resistance is accentuated during periods of poor metabolic control in human non-insulin-dependent diabetes mellitus. Glucose 47-54 insulin Homo sapiens 0-7 1900667-0 1991 Insulin resistance in normal rats infused with glucose for 72 h. Insulin resistance is accentuated during periods of poor metabolic control in human non-insulin-dependent diabetes mellitus. Glucose 47-54 insulin Homo sapiens 65-72 1900667-6 1991 Insulin-stimulated glucose uptake in vivo and in vitro (by perfused hindquarters and isolated adipocytes) were suppressed in the glucose-infused group (P less than 0.01). Glucose 19-26 insulin Homo sapiens 0-7 1900667-6 1991 Insulin-stimulated glucose uptake in vivo and in vitro (by perfused hindquarters and isolated adipocytes) were suppressed in the glucose-infused group (P less than 0.01). Glucose 129-136 insulin Homo sapiens 0-7 1900667-8 1991 Basal and isoproterenol-stimulated lipolysis were increased, whereas insulin suppression of lipolysis was blunted in adipocytes from glucose-infused animals (P less than 0.01). Glucose 133-140 insulin Homo sapiens 69-76 1872925-6 1991 Glucose stimulated plasma insulin response during a hyperglycemic clamp was not significantly influenced by fish oil both in the early phase and during steady state. Glucose 0-7 insulin Homo sapiens 26-33 1828417-2 1991 New information indicates that resistance to insulin action on glucose uptake in peripheral tissues is a common underlying mechanism in hypertension and diabetes. Glucose 63-70 insulin Homo sapiens 45-52 1999279-8 1991 Insulin is able to abolish this inhibitory action of glucose on collagen production, but the precise mechanism is unclear. Glucose 53-60 insulin Homo sapiens 0-7 2044434-4 1991 Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. Glucose 189-196 insulin Homo sapiens 167-174 2044434-6 1991 With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. Glucose 17-24 insulin Homo sapiens 146-153 2044434-6 1991 With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. Glucose 69-76 insulin Homo sapiens 146-153 2044434-6 1991 With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. Glucose 69-76 insulin Homo sapiens 146-153 2054671-4 1991 Insulin induced a long-lasting increase of up to 350% that could be reversed by glucose infusion. Glucose 80-87 insulin Homo sapiens 0-7 2008711-3 1991 The forms of treatment most commonly employed are infusion of glucose-insulin-potassium (GIK) and subcutaneous administration of insulin followed by infusion of glucose (KON). Glucose 62-69 insulin Homo sapiens 70-77 1900669-1 1991 The effect of epinephrine (E) infusion on insulin-mediated glucose metabolism in humans has been studied. Glucose 59-66 insulin Homo sapiens 42-49 1900669-9 1991 E also appears to inhibit insulin-mediated glucose utilization, at least partly, because of an increase in G-6-phosphate (which inhibits hexokinase) and enhances glycolysis by G-1,6-P2-, fructose 6-phosphate-, and F-1,6-P2-mediated activation of PFK. Glucose 43-50 insulin Homo sapiens 26-33 2003588-6 1991 EtOH-Ci reduced insulin sensitivity (-59%) and maximal insulin-dependent glucose disposal (-40%) during a sequential two-step glucose clamp protocol (phase 1: 1 mU.kg body wt-1.min-1 insulin infusion rate + euglycemia; phase 2: 4 mU.kg body wt-1.min-1 insulin infusion rate + 165 mg/dl plasma glucose concentration). Glucose 73-80 insulin Homo sapiens 55-62 2003588-6 1991 EtOH-Ci reduced insulin sensitivity (-59%) and maximal insulin-dependent glucose disposal (-40%) during a sequential two-step glucose clamp protocol (phase 1: 1 mU.kg body wt-1.min-1 insulin infusion rate + euglycemia; phase 2: 4 mU.kg body wt-1.min-1 insulin infusion rate + 165 mg/dl plasma glucose concentration). Glucose 73-80 insulin Homo sapiens 55-62 2003592-8 1991 These data demonstrate that 1) insulin action on skeletal muscle glucose disposal is mediated by a direct as well as an indirect component, and 2) the maintenance of basal FFA does not affect insulin-stimulated FGU, indicating that the indirect component of insulin action is mediated by a different mechanism. Glucose 65-72 insulin Homo sapiens 31-38 2003593-4 1991 Twelve-hour insulin infusions, in low doses adjusted over the 1st 2 h to produce plasma glucose concentrations of 3.6 mmol/l (65 mg/dl) and then fixed at that dose, resulted in significantly (P less than 0.0001) lower late plasma glucose concentrations in the patients, without and with replacement. Glucose 88-95 insulin Homo sapiens 12-19 2003593-4 1991 Twelve-hour insulin infusions, in low doses adjusted over the 1st 2 h to produce plasma glucose concentrations of 3.6 mmol/l (65 mg/dl) and then fixed at that dose, resulted in significantly (P less than 0.0001) lower late plasma glucose concentrations in the patients, without and with replacement. Glucose 230-237 insulin Homo sapiens 12-19 2003599-1 1991 We have observed that in vitro incubated human muscle fiber strips from obese patients with or without non-insulin-dependent diabetes mellitus (NIDDM) have reduced insulin-stimulated glucose transport rates compared with nonobese control patients. Glucose 183-190 insulin Homo sapiens 107-114 2003599-5 1991 These data suggest that the decreased glucose transport rate observed in muscle of these obese patients with or without NIDDM may be due, at least in part, to a decreased expression of the "insulin-sensitive" (GLUT-4) glucose transporter. Glucose 38-45 insulin Homo sapiens 190-197 2003599-5 1991 These data suggest that the decreased glucose transport rate observed in muscle of these obese patients with or without NIDDM may be due, at least in part, to a decreased expression of the "insulin-sensitive" (GLUT-4) glucose transporter. Glucose 218-225 insulin Homo sapiens 190-197 1999270-3 1991 IAPP is stored with insulin in beta-cell secretory vesicles and is cosecreted with insulin in response to glucose and several secretagogues. Glucose 106-113 insulin Homo sapiens 83-90 1999270-9 1991 A significant causal relationship between IAPP and type II diabetes is based on reports that IAPP inhibits glucose-stimulated insulin release by beta-cells and that IAPP inhibits insulin-stimulated rates of glycogen synthesis and glucose uptake by skeletal muscle cells. Glucose 107-114 insulin Homo sapiens 126-133 1999270-9 1991 A significant causal relationship between IAPP and type II diabetes is based on reports that IAPP inhibits glucose-stimulated insulin release by beta-cells and that IAPP inhibits insulin-stimulated rates of glycogen synthesis and glucose uptake by skeletal muscle cells. Glucose 230-237 insulin Homo sapiens 179-186 2043298-7 1991 The changes in day-long plasma glucose and insulin responses suggested that resistance to insulin-stimulated glucose uptake had increased in association with atenolol treatment and decreased following nifedipine. Glucose 109-116 insulin Homo sapiens 43-50 2032990-2 1991 To elucidate the mechanism, insulin action on whole body glucose uptake rate (WBGUR) and leg glucose uptake rate (LGUR) was measured by sequential euglycemic clamp technique combined with femoral arterial and venous cannulation at insulin concentrations of 10 +/- 1, 18 +/- 1, 37 +/- 2, and 360 +/- 15 microU/ml. Glucose 57-64 insulin Homo sapiens 28-35 2043298-7 1991 The changes in day-long plasma glucose and insulin responses suggested that resistance to insulin-stimulated glucose uptake had increased in association with atenolol treatment and decreased following nifedipine. Glucose 109-116 insulin Homo sapiens 90-97 2043298-8 1991 This conclusion was supported in that measurement of insulin-stimulated glucose disposal showed a decrease in atenolol-treated patients and an increase in nifedipine-treated patients. Glucose 72-79 insulin Homo sapiens 53-60 1999488-1 1991 A major portion of insulin-mediated glucose uptake occurs via the translocation of GLUT 4 glucose transporter proteins from an intracellular depot to the plasma membrane. Glucose 36-43 insulin Homo sapiens 19-26 1997515-8 1991 When compared with continuous insulin, 13-min insulin pulses induced a significantly greater inhibition of endogenous glucose production. Glucose 118-125 insulin Homo sapiens 30-37 1904953-7 1991 During this period, blood glucose level was kept in almost normal range (between 100 and 200 mg/dL) through the continuous insulin infusion of regular insulin (1.0-1.5 U/h). Glucose 26-33 insulin Homo sapiens 123-130 1997515-8 1991 When compared with continuous insulin, 13-min insulin pulses induced a significantly greater inhibition of endogenous glucose production. Glucose 118-125 insulin Homo sapiens 46-53 1997515-10 1991 We conclude that, in man, an adequate pulse frequency is required to allow the appearance of the greater inhibition of pulsatile insulin on endogenous glucose production. Glucose 151-158 insulin Homo sapiens 129-136 1997519-0 1991 Intravenous glucose tolerance test-derived insulin sensitivity changes during the menstrual cycle. Glucose 12-19 insulin Homo sapiens 43-50 1997519-4 1991 Insulin sensitivity (SI) and glucose effectiveness were derived using insulin and glucose levels obtained from tolbutamide-modified IVGTTs and analyzed with the minimal model computer program. Glucose 82-89 insulin Homo sapiens 0-7 2051553-0 1991 Amino acids enhance insulin resistance to exogenous glucose infusion in overnight-fasted humans. Glucose 52-59 insulin Homo sapiens 20-27 2051553-6 1991 When amino acids were infused, the amount of glucose required to maintain euglycemia was lower at each insulin dose used (4.5 +/- 0.3 vs 3.6 +/- 0.4, 7.6 +/- 0.5 vs 6.9 +/- 0.3, 10.4 +/- 1.0 vs 8.7 +/- 0.5, 13.3 +/- 0.8 vs 10.2 +/- 0.4, 14.7 +/- 0.8 vs 11.7 +/- 0.6, and 14.9 +/- 0.6 vs 11.8 +/- 0.8 mg/kg/min at escalating insulin doses, respectively; p less than 0.05). Glucose 45-52 insulin Homo sapiens 103-110 2051553-6 1991 When amino acids were infused, the amount of glucose required to maintain euglycemia was lower at each insulin dose used (4.5 +/- 0.3 vs 3.6 +/- 0.4, 7.6 +/- 0.5 vs 6.9 +/- 0.3, 10.4 +/- 1.0 vs 8.7 +/- 0.5, 13.3 +/- 0.8 vs 10.2 +/- 0.4, 14.7 +/- 0.8 vs 11.7 +/- 0.6, and 14.9 +/- 0.6 vs 11.8 +/- 0.8 mg/kg/min at escalating insulin doses, respectively; p less than 0.05). Glucose 45-52 insulin Homo sapiens 324-331 2071824-7 1991 These data suggest that in pheochromocytoma impaired glucose tolerance is partly due to the reduced insulin response to oral glucose load. Glucose 53-60 insulin Homo sapiens 100-107 1900343-9 1991 Muscle GS activity at the end of the euglycemic clamp correlated with glucose requirement (r = .53, P less than .001), and a similar correlation was observed between the insulin-induced change in muscle GS activity from basal and glucose requirement (r = .47, P less than .005). Glucose 230-237 insulin Homo sapiens 170-177 2026275-4 1991 Chronic exposure to insulin increased the glucose transporter protein levels to similar degrees in the cells incubated with 11.1, 22.2 and 44.4 mM glucose accompanied by increases in the glucose transport activity. Glucose 42-49 insulin Homo sapiens 20-27 2000033-6 1991 In addition, these data suggest that diabetes causes a defect in the ability of insulin and glucose to stimulate TG synthesis, as the increase in diabetic muscle TG synthesis in the presence of insulin and glucose was less than in normal muscle. Glucose 92-99 insulin Homo sapiens 194-201 2000033-6 1991 In addition, these data suggest that diabetes causes a defect in the ability of insulin and glucose to stimulate TG synthesis, as the increase in diabetic muscle TG synthesis in the presence of insulin and glucose was less than in normal muscle. Glucose 206-213 insulin Homo sapiens 80-87 2026275-4 1991 Chronic exposure to insulin increased the glucose transporter protein levels to similar degrees in the cells incubated with 11.1, 22.2 and 44.4 mM glucose accompanied by increases in the glucose transport activity. Glucose 147-154 insulin Homo sapiens 20-27 2026275-5 1991 Effects of insulin on the glucose transporter mRNA and protein levels, however, were not evident in the glucose-deprived cells. Glucose 26-33 insulin Homo sapiens 11-18 2041930-0 1991 Insulin resistance in the oral glucose tolerance test--a link with hypertension. Glucose 31-38 insulin Homo sapiens 0-7 2041930-1 1991 Insulin resistance was evaluated in 807 middle-aged subjects at a health survey, with use of an index measured in 75 g oral glucose tolerance tests. Glucose 124-131 insulin Homo sapiens 0-7 1899928-3 1991 The majority of the diabetic subjects in this pedigree has a reduced and delayed insulin-secretory response to glucose, and it has been proposed that this abnormal response is the manifestation of the basic genetic defect that leads to diabetes. Glucose 111-118 insulin Homo sapiens 81-88 2031314-2 1991 Comparisons disclosed: a) Levels of immunoreactive insulin (IRI) rose more and declined more slowly in patients with glucose intolerance than in patients with glucose tolerance. Glucose 117-124 insulin Homo sapiens 51-58 2031314-2 1991 Comparisons disclosed: a) Levels of immunoreactive insulin (IRI) rose more and declined more slowly in patients with glucose intolerance than in patients with glucose tolerance. Glucose 159-166 insulin Homo sapiens 51-58 1994722-1 1991 Patients with untreated hypertension have been shown to be resistant to insulin-stimulated glucose uptake and are more hyperinsulinemic and hypertriglyceridemic than matched groups of patients with normal blood pressure. Glucose 91-98 insulin Homo sapiens 72-79 1994722-3 1991 The defect in insulin-stimulated glucose uptake in these experimental models can also be shown at the cellular level. Glucose 33-40 insulin Homo sapiens 14-21 1990010-0 1991 Differential regulation of the GLUT-1 and GLUT-4 glucose transport systems by glucose and insulin in L6 muscle cells in culture. Glucose 49-56 insulin Homo sapiens 90-97 1990010-1 1991 The regulation by glucose and insulin of the muscle-specific facilitative glucose transport system GLUT-4 was investigated in L6 muscle cells in culture. Glucose 74-81 insulin Homo sapiens 30-37 1826998-7 1991 These observations provide further support for the view that hyperinsulinemia, presumably secondary to resistance to insulin-stimulated glucose uptake, is associated with a cluster of variables that may play important roles in the etiology and clinical course of hypertension. Glucose 136-143 insulin Homo sapiens 66-73 1990010-14 1991 It is proposed that glucose and insulin differentially regulate the two glucose transport systems in L6 muscle cells and that the rapid down-regulation of hexose transport activity by glucose is regulated by post-translational mechanisms. Glucose 72-79 insulin Homo sapiens 32-39 1990010-14 1991 It is proposed that glucose and insulin differentially regulate the two glucose transport systems in L6 muscle cells and that the rapid down-regulation of hexose transport activity by glucose is regulated by post-translational mechanisms. Glucose 72-79 insulin Homo sapiens 32-39 1709028-0 1991 Interaction among zinc, glucose, and insulin in normal individuals during glucose and tolbutamid perfusion. Glucose 74-81 insulin Homo sapiens 37-44 2036198-1 1991 A prime target of insulin action in patients with maturity onset diabetes is suppression of hepatic glucose production in both the fasting and postprandial states. Glucose 100-107 insulin Homo sapiens 18-25 1709028-3 1991 Thus, the objective of the investigation described here was to determine the relationship existing among zinc, glucose, and insulin under acute conditions. Glucose 111-118 insulin Homo sapiens 124-131 1846828-7 1991 Insulin (10(4) pM) was able to totally suppress basal glycogenolysis; insulin was also essential to reverse the action of glucagon in hepatocytes incubated with glucagon, whereas glucose alone, even at postprandial concentration, was unable to reverse glucagon action. Glucose 179-186 insulin Homo sapiens 0-7 1648521-8 1991 In the father there was a mild insulin resistance in the glucose clamp study and a borderline impaired glucose tolerance. Glucose 57-64 insulin Homo sapiens 31-38 1817807-8 1991 The post-prandial glucose excursion between 60 and 120 min was significantly lowered with insulin (p less than 0.01). Glucose 18-25 insulin Homo sapiens 90-97 1902411-4 1991 DPG but not D improved the plasma insulin response to glucose ingestion and in vivo insulin action measured by insulin tolerance test with unaltered erythrocyte 125I-insulin binding. Glucose 54-61 insulin Homo sapiens 34-41 1902411-6 1991 Improvements in in vivo insulin action and in insulin secretion after DPG closely correlated with decrease in fasting glycemia and reduction in the day-time elevation of plasma glucose levels, respectively. Glucose 177-184 insulin Homo sapiens 24-31 2065848-8 1991 This study suggests that basal hypo-secretion of islet amyloid polypeptide relative to insulin exists in non-obese Type 2 diabetes and that circulating islet amyloid polypeptide may act physiologically with insulin to modulate the glucose metabolism. Glucose 231-238 insulin Homo sapiens 207-214 1991568-4 1991 Subsequently, it was recognized that glucose not only directly regulated insulin synthesis and secretion but moderated all other islet signals, including other substrates, hormones, and neural factors. Glucose 37-44 insulin Homo sapiens 73-80 1991568-9 1991 This is because progressive islet failure is matched by rising glucose levels to maintain basal and second-phase insulin output. Glucose 63-70 insulin Homo sapiens 113-120 1991568-12 1991 Insulin resistance is also present in most patients and contributes to the hyperglycemia by augmenting the glucose levels needed for compensation. Glucose 107-114 insulin Homo sapiens 0-7 2026051-3 1991 Primarily, this has been possible by means of the glucose clamp technique which basically makes it possible to evaluate insulin sensitivity and glucose-stimulated insulin secretion. Glucose 50-57 insulin Homo sapiens 120-127 2026051-3 1991 Primarily, this has been possible by means of the glucose clamp technique which basically makes it possible to evaluate insulin sensitivity and glucose-stimulated insulin secretion. Glucose 50-57 insulin Homo sapiens 163-170 2026051-3 1991 Primarily, this has been possible by means of the glucose clamp technique which basically makes it possible to evaluate insulin sensitivity and glucose-stimulated insulin secretion. Glucose 144-151 insulin Homo sapiens 163-170 2026051-10 1991 In contrast to insulin-stimulated glucose uptake, basal glucose turnover is normal in patients with ESRF. Glucose 34-41 insulin Homo sapiens 15-22 2026051-11 1991 The ability of glucose to enhance its own uptake is difficult to measure in human studies, because even small amounts of insulin is able to modulate GIGU profoundly. Glucose 15-22 insulin Homo sapiens 121-128 2065854-0 1991 Predictive value of intravenous glucose tolerance test insulin secretion less than or greater than the first percentile in islet cell antibody positive relatives of type 1 (insulin-dependent) diabetic patients. Glucose 32-39 insulin Homo sapiens 55-62 1907557-0 1991 Increased insulin-stimulated glucose uptake by exercised human muscles one day after prolonged physical exercise. Glucose 29-36 insulin Homo sapiens 10-17 1673444-3 1991 Glucose and mannose are well-known stimuli of insulin release in mammals and fish. Glucose 0-7 insulin Homo sapiens 46-53 1991649-5 1991 After glucose ingestion (40 g/m2), normal glucose tolerance in the patients was maintained at the expense of a heightened plasma insulin response, suggesting the presence of insulin resistance. Glucose 6-13 insulin Homo sapiens 129-136 2005672-8 1991 The blood glucose levels varied less after an IP supply of insulin. Glucose 10-17 insulin Homo sapiens 59-66 1991649-5 1991 After glucose ingestion (40 g/m2), normal glucose tolerance in the patients was maintained at the expense of a heightened plasma insulin response, suggesting the presence of insulin resistance. Glucose 6-13 insulin Homo sapiens 174-181 1854502-4 1991 In the pancreatic islets the IAPP is confined to the beta-cells, co-stored with insulin in the secretory granules and apparently co-secreted with insulin on glucose stimulation. Glucose 157-164 insulin Homo sapiens 146-153 1991827-5 1991 After oral glucose the insulin concentrations in plasma were lower and the concentrations of all proglucagon products were higher in the NIDDM group compared to the control group. Glucose 11-18 insulin Homo sapiens 23-30 1991830-11 1991 These results suggest that the ultradian oscillations of insulin secretion are caused by the feedback loop linking glucose and insulin. Glucose 115-122 insulin Homo sapiens 57-64 1777653-0 1991 Effect of sulphonylurea on glucose-stimulated insulin secretion in healthy and non-insulin dependent diabetic subjects: a dose-response study. Glucose 27-34 insulin Homo sapiens 46-53 1777653-4 1991 In control subjects in the absence of glipizide, the first-phase plasma insulin response (0-10 min) increased progressively with increasing plasma glucose concentration up to 10 mmol/l, above which it tended to plateau. Glucose 147-154 insulin Homo sapiens 72-79 1991798-0 1991 Insulin resistance of puberty: a defect restricted to peripheral glucose metabolism. Glucose 65-72 insulin Homo sapiens 0-7 1991798-3 1991 The low as well as the high insulin dose stimulated peripheral glucose uptake much more effectively in prepubertal children (P less than 0.05). Glucose 63-70 insulin Homo sapiens 28-35 1991798-6 1991 Our data suggest that insulin resistance during puberty is restricted to peripheral glucose metabolism. Glucose 84-91 insulin Homo sapiens 22-29 2066661-8 1991 Both high plasma glucose and high plasma insulin in the presence of normal glucose significantly increased LPL activity within 4 hours. Glucose 75-82 insulin Homo sapiens 41-48 1988776-5 1991 An index of insulin secretion in all four tests was obtained from measurement of the acute release of insulin in response to two intravenous (IV) boluses of arginine, one given basally and the other given after raising glucose levels to approximately 150 mg/dL above the baseline. Glucose 219-226 insulin Homo sapiens 12-19 1985741-4 1991 After administration of 100 g of oral glucose, peak insulin achieved in D (60 +/- 11) was lower than in IGT (101 +/- 26) and ND (83 +/- 20), whereas peak insulin levels in IGT and ND were significantly (P less than 0.05) higher than in C (45 +/- 6). Glucose 38-45 insulin Homo sapiens 52-59 1985741-11 1991 Patients with pancreatic cancer manifest insulin resistance by virtue of a decrease in total body glucose use (M) and decreased insulin response to glucose due to either inherent beta cell dysfunction or decreased islet cell mass. Glucose 98-105 insulin Homo sapiens 41-48 1985741-11 1991 Patients with pancreatic cancer manifest insulin resistance by virtue of a decrease in total body glucose use (M) and decreased insulin response to glucose due to either inherent beta cell dysfunction or decreased islet cell mass. Glucose 148-155 insulin Homo sapiens 41-48 1992500-3 1991 The emergency treatment in patients with severe hyperkalemia consists of intravenous calcium injections, infusion of glucose with insulin and, more recently, salbutamol. Glucose 117-124 insulin Homo sapiens 130-137 1862688-4 1991 However, with increasing glucose concentration, all the three analogues potentiate the glucose stimulus for insulin release. Glucose 25-32 insulin Homo sapiens 108-115 1862688-4 1991 However, with increasing glucose concentration, all the three analogues potentiate the glucose stimulus for insulin release. Glucose 87-94 insulin Homo sapiens 108-115 1667959-4 1991 Near-normal blood glucose control obtained by continuous subcutaneous insulin infusion (CSII) significantly enhanced both normal and impaired macular recovery. Glucose 18-25 insulin Homo sapiens 70-77 1794265-2 1991 This model analyzed, during an intravenous glucose tolerance test, the response of the first and second phase of insulin secretion in relation to the variations in blood glucose (insulin secretion) and the rate of decline in the blood glucose curve in relation to the variations in insulin (insulin response). Glucose 43-50 insulin Homo sapiens 113-120 1666765-0 1991 Effects of insulin mediated plasma glucose changes on brain function. Glucose 35-42 insulin Homo sapiens 11-18 1987849-2 1991 The glucose, insulin, and C peptide responses to oral glucose post-shunt were exaggerated but comparable to preoperative values. Glucose 54-61 insulin Homo sapiens 13-20 2018414-2 1991 In order to study the capacity of the first phase insulin response (FPIR) for predicting insulin-dependent diabetes (IDDM), we have performed one or more intravenous glucose tolerance tests (IVGTT) and determined islet-cell antibodies (ICA) and HLA-types in 220 first degree relatives of IDDM patients (194 siblings, 26 offsprings) aged 2 to 29 years. Glucose 166-173 insulin Homo sapiens 50-57 1751673-1 1991 We previously developed self-regulating insulin delivery systems using concanavalin A (Con A)-bound succinyl-amidophenyl-glucopyranoside insulin (SAPG-insulin) in pouch membrane which exhibited long lag times for exchange diffusion in response to glucose changes. Glucose 247-254 insulin Homo sapiens 40-47 1751673-1 1991 We previously developed self-regulating insulin delivery systems using concanavalin A (Con A)-bound succinyl-amidophenyl-glucopyranoside insulin (SAPG-insulin) in pouch membrane which exhibited long lag times for exchange diffusion in response to glucose changes. Glucose 247-254 insulin Homo sapiens 137-144 1934023-0 1991 Rheumatoid arthritis modifies basal and insulin-mediated glucose uptake by human synoviocytes. Glucose 57-64 insulin Homo sapiens 40-47 1934023-1 1991 Basal and insulin-mediated glucose uptake were studied in human synovial cells. Glucose 27-34 insulin Homo sapiens 10-17 1790686-3 1991 A pharmacokinetic model of glucose and insulin dynamics which includes the islet insulin response to plasma glucose is used to compare the effectiveness of subcutaneous insulin injections and transplanted islets of Langerhans for the treatment of a hypothetical patient with insulin dependent diabetes mellitus. Glucose 108-115 insulin Homo sapiens 39-46 1790686-4 1991 For a patient receiving 60 U of insulin per day the results show that 500,000 human islets would be needed to obtain glucose control comparable to that obtained with insulin injections and at least 1.5 million human islets are needed to obtain normoglycemia. Glucose 117-124 insulin Homo sapiens 32-39 1794269-6 1991 This was accompanied by the appearance of a small first-phase insulin response to iv glucose and by significant increases in the mean daily insulin to mean daily blood glucose ratio and in the 24-h urinary C-peptide to glucose ratio. Glucose 168-175 insulin Homo sapiens 140-147 1794269-6 1991 This was accompanied by the appearance of a small first-phase insulin response to iv glucose and by significant increases in the mean daily insulin to mean daily blood glucose ratio and in the 24-h urinary C-peptide to glucose ratio. Glucose 168-175 insulin Homo sapiens 140-147 1794269-10 1991 This was paralleled by unchanged stimulation by gliclazide of first-phase insulin response to glucose as well as mean by 48-h insulin to glucose and urinary C-peptide to glucose ratios. Glucose 94-101 insulin Homo sapiens 74-81 1794269-10 1991 This was paralleled by unchanged stimulation by gliclazide of first-phase insulin response to glucose as well as mean by 48-h insulin to glucose and urinary C-peptide to glucose ratios. Glucose 137-144 insulin Homo sapiens 126-133 1794269-10 1991 This was paralleled by unchanged stimulation by gliclazide of first-phase insulin response to glucose as well as mean by 48-h insulin to glucose and urinary C-peptide to glucose ratios. Glucose 137-144 insulin Homo sapiens 126-133 1785708-3 1991 It has not been clearly demonstrated that the administration of exogenous insulin with glucose improves nitrogen retention. Glucose 87-94 insulin Homo sapiens 74-81 2031957-4 1991 Insulin or glucose are individually inefficient and glucagon-dependent transcriptional inhibition seems to be dominant in insulin + glucose-dependent activation. Glucose 132-139 insulin Homo sapiens 0-7 2031957-4 1991 Insulin or glucose are individually inefficient and glucagon-dependent transcriptional inhibition seems to be dominant in insulin + glucose-dependent activation. Glucose 132-139 insulin Homo sapiens 122-129 1846787-0 1991 Dose-response relationships for the effects of insulin on glucose and fat metabolism in injured patients and control subjects. Glucose 58-65 insulin Homo sapiens 47-54 1846787-9 1991 The dose-response curve for whole-body glucose infusion rate against plasma insulin concentration showed diminished sensitivity and diminished maximal response in the patients. Glucose 39-46 insulin Homo sapiens 76-83 1846787-10 1991 A similar pattern was seen for forearm glucose uptake, with a marked impairment of both sensitivity to insulin and maximal responsiveness. Glucose 39-46 insulin Homo sapiens 103-110 1846791-3 1991 As insulin activates the sympathetic nervous system, the present study was undertaken to measure the plasma noradrenaline concentration in the fasting state and after 75 g of oral glucose in simple-obese patients (n = 13), in non-insulin-dependent (type 2) diabetic patients (n = 37) and in normal control subjects (n = 12). Glucose 180-187 insulin Homo sapiens 3-10 1647334-0 1991 Basal and insulin stimulated substrate metabolism in tumour induced hypoglycaemia; evidence for increased muscle glucose uptake. Glucose 113-120 insulin Homo sapiens 10-17 1826243-4 1991 Preprandial insulin gave better control of daytime blood glucose levels but fasting plasma glucose did not differ between the two regimens (basal group 10.6 +/- 3.6, preprandial group 11.1 +/- 3.6 mmol l-1). Glucose 57-64 insulin Homo sapiens 12-19 1983828-4 1991 The ability of insulin to promote total body (primarily muscle) glucose uptake was markedly impaired, whereas its effect to suppress hepatic glucose production was normal compared with results obtained in nine healthy subjects. Glucose 64-71 insulin Homo sapiens 15-22 2173694-9 1990 These data indicate that: 1) the membrane distributions of a glucose transporter protein, which is not responsive to insulin in HepG2 cells, and both mouse GLUT1 and GLUT4 glucose transporter isoforms are regulated by insulin in mouse 3T3-L1 adipocytes, and 2) the expressed human GLUT1 appears to contribute significantly to the rate of basal uptake but not to the insulin-stimulated increase in 2-deoxyglucose uptake by 3T3-L1 fibroblasts and adipocytes. Glucose 61-68 insulin Homo sapiens 218-225 2173694-9 1990 These data indicate that: 1) the membrane distributions of a glucose transporter protein, which is not responsive to insulin in HepG2 cells, and both mouse GLUT1 and GLUT4 glucose transporter isoforms are regulated by insulin in mouse 3T3-L1 adipocytes, and 2) the expressed human GLUT1 appears to contribute significantly to the rate of basal uptake but not to the insulin-stimulated increase in 2-deoxyglucose uptake by 3T3-L1 fibroblasts and adipocytes. Glucose 61-68 insulin Homo sapiens 218-225 2136310-0 1990 Insulin and glucose concentration changes in newborn piglets after suckling the colostrum from insulin administered sows. Glucose 12-19 insulin Homo sapiens 95-102 2240211-9 1990 Hepatic glucose production and total glucose disposal showed the expected dose-dependent suppression and stimulation, respectively, by insulin. Glucose 8-15 insulin Homo sapiens 135-142 2240211-9 1990 Hepatic glucose production and total glucose disposal showed the expected dose-dependent suppression and stimulation, respectively, by insulin. Glucose 37-44 insulin Homo sapiens 135-142 2261148-3 1990 Glucose load increased serum insulin (P less than .001) and plasma norepinephrine concentrations (P = .001) in both groups and hypertensives had still higher postglucose insulin (P = .003) and norepinephrine levels (P = .003) than normotensives. Glucose 0-7 insulin Homo sapiens 29-36 2174311-8 1990 Insulin sensitivity was quantified by clamping plasma glucose concentrations at 5.6 mmol/l during 24 h of total parenteral nutrition (15% protein, 55% glucose and 30% fat, supplying 1.25 times the measured resting energy expenditure) with a variable infusion of exogenous insulin. Glucose 54-61 insulin Homo sapiens 0-7 2174311-8 1990 Insulin sensitivity was quantified by clamping plasma glucose concentrations at 5.6 mmol/l during 24 h of total parenteral nutrition (15% protein, 55% glucose and 30% fat, supplying 1.25 times the measured resting energy expenditure) with a variable infusion of exogenous insulin. Glucose 151-158 insulin Homo sapiens 0-7 2224751-3 1990 Pathophysiologically, most of the decline in glucose tolerance appears to be caused by a decrease in insulin action with aging. Glucose 45-52 insulin Homo sapiens 101-108 2224751-4 1990 Given that it has been shown that exercise increases insulin action, there is a plausible biologic mechanism explaining the observed association between physical activity and the preservation of insulin sensitivity and glucose tolerance with aging. Glucose 219-226 insulin Homo sapiens 53-60 1979763-3 1990 Both insulin preparations gave close to identical responses for glucose, glucagon, growth hormone, adrenaline, and somatostatin. Glucose 64-71 insulin Homo sapiens 5-12 2073874-3 1990 Insulin resistance and beta-cell function were estimated by a computer solved model based on fasting plasma glucose and insulin concentrations. Glucose 108-115 insulin Homo sapiens 0-7 2073874-4 1990 Insulin resistance increased with declining glucose tolerance, whereas beta-cell function was highest in subjects with impaired glucose tolerance (IGT) and lowest in those with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 44-51 insulin Homo sapiens 0-7 2076628-3 1990 However, substantial day-to-day variation in blood glucose concentration is observed when diet, exercise, emotional state, insulin dosage, and timing of insulin administration are held constant. Glucose 51-58 insulin Homo sapiens 123-130 2076628-3 1990 However, substantial day-to-day variation in blood glucose concentration is observed when diet, exercise, emotional state, insulin dosage, and timing of insulin administration are held constant. Glucose 51-58 insulin Homo sapiens 153-160 2121567-0 1990 Effect of insulin on oxidation of intracellularly and extracellularly derived glucose in patients with NIDDM. Glucose 78-85 insulin Homo sapiens 10-17 2121567-2 1990 Insulin-stimulated glucose oxidation is decreased in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 19-26 insulin Homo sapiens 0-7 2121567-4 1990 To address this issue, glucose oxidation was measured under steady-state conditions at low (approximately 270 pmol) and high (approximately 17 mumol) insulin concentrations in seven patients with NIDDM and seven healthy nondiabetic subjects matched for sex, age, and obesity. Glucose 23-30 insulin Homo sapiens 150-157 2121567-7 1990 Both techniques provided identical estimates of glucose oxidation during the high-dose insulin infusion. Glucose 48-55 insulin Homo sapiens 87-94 2121569-11 1990 Staurosporine, a protein kinase C inhibitor, blocked glyburide-, tolbutamide-, and insulin-stimulated glucose uptake. Glucose 102-109 insulin Homo sapiens 83-90 2127573-5 1990 Combining insulin and sulfonylurea agents resulted in a reduction in fasting plasma glucose (12.9 +/- 7 vs 10.4 +/- 1.2 mmol/l; p less than 0.05) and hepatic glucose production (13.9 +/- 1.1 vs 11.1 +/- 1.1 mumol.kg-1.min-1; p less than 0.05). Glucose 84-91 insulin Homo sapiens 10-17 2148133-4 1990 In vivo peripheral insulin sensitivity (euglycaemic clamp with insulin infusion of 40, 160, and 600 mU m-2 min-1, respectively) was significantly improved (glucose requirement: to 4.7 +/- 1.0 from 3.0 +/- 0.6 mg kg-1 min-1, p less than 0.05 at first insulin level; to 10.8 +/- 0.5 from 9.3 +/- 0.7 mg kg-1 min-1, p less than 0.01 at second level; to 13.3 +/- 0.6 from 11.8 +/- 0.8 mg kg-1 min-1, p less than 0.025 at third level). Glucose 156-163 insulin Homo sapiens 19-26 2086209-21 1990 The negative relationship between insulin binding and plasma glucose during malnutrition may be related to carbohydrate intolerance. Glucose 61-68 insulin Homo sapiens 34-41 1980259-5 1990 In the period 0-120 min the area under the plasma C-peptide curve was significantly higher in obese than in nonobese subjects (292 +/- 23 vs. 230 +/- 17 nmol/l x 120 min, P less than 0.05), however, in the last 20 min of the glucose infusion period without somatostatin (100-120 min) plasma C-peptide was not significantly different in the two groups (2.94 +/- 0.32 nmol/l in nonobese subjects and 3.21 +/- 0.19 nmol/l in obese patients, p = NS). Glucose 225-232 insulin Homo sapiens 50-59 2272963-0 1990 Effect of exercise on glucose disposal: response to a maximal insulin stimulus. Glucose 22-29 insulin Homo sapiens 62-69 2272963-1 1990 We used the euglycemic clamp to assess the effects of exercise on maximally insulin-stimulated glucose disposal. Glucose 95-102 insulin Homo sapiens 76-83 2272963-8 1990 Our results are compatible with the interpretations that glucose availability rather than glucose metabolism limits the rate of glucose disposal in response to a maximal insulin stimulus in resting subjects and that the increase in glucose uptake in response to superimposed exercise is primarily due to an increase in glucose availability. Glucose 57-64 insulin Homo sapiens 170-177 2096155-12 1990 These findings suggest that in cirrhotic patients the effects of insulin on both FFA and glucose metabolism are reduced. Glucose 89-96 insulin Homo sapiens 65-72 2146283-7 1990 These diabetic rosettes were slightly associated with acute insulin response to iv glucose lower than the 5th percentile of controls (immunoreactive insulin at 1 +/- 3 min, 250 pmol/L; by chi 2, P = 0.04) and with HLA DR 3/4 heterozygosity (by chi 2, P = 0.04). Glucose 83-90 insulin Homo sapiens 60-67 2146283-7 1990 These diabetic rosettes were slightly associated with acute insulin response to iv glucose lower than the 5th percentile of controls (immunoreactive insulin at 1 +/- 3 min, 250 pmol/L; by chi 2, P = 0.04) and with HLA DR 3/4 heterozygosity (by chi 2, P = 0.04). Glucose 83-90 insulin Homo sapiens 149-156 2146283-9 1990 A statistical association was detected between HLA DR 3/4 heterozygosity and a low acute insulin response to iv glucose (by chi 2, P less than 0.003). Glucose 112-119 insulin Homo sapiens 89-96 2229281-7 1990 This suggests that, although the muscle does not contribute directly to fasting hyperglycemia, it may play an indirect role through an increased delivery of glucose precursors; and 2) insulin-induced normoglycemia is maintained by mechanisms that do not involve the exchange of glucose and gluconeogenic substrates by the skeletal muscle. Glucose 278-285 insulin Homo sapiens 184-191 2229287-4 1990 Abdominal obesity was estimated by determining the ratio of waist to hip girth, fasting and postprandial plasma FFA and insulin concentrations were measured at hourly intervals from 0800-1600 h, and insulin-stimulated glucose disposal was quantified by the euglycemic hyperinsulinemic clamp technique. Glucose 218-225 insulin Homo sapiens 199-206 2229287-8 1990 However, there was a modest inverse relationship between height of circulating plasma insulin concentration and a decrease in insulin-stimulated glucose uptake (r = -0.43; P less than 0.03) in the group as a whole. Glucose 145-152 insulin Homo sapiens 86-93 2229287-8 1990 However, there was a modest inverse relationship between height of circulating plasma insulin concentration and a decrease in insulin-stimulated glucose uptake (r = -0.43; P less than 0.03) in the group as a whole. Glucose 145-152 insulin Homo sapiens 126-133 2266199-5 1990 Endogenous glucose production was less sensitive to inhibition by insulin in the animals subjected to restricted food intake, compared with those on the ad libitum regime, which suggested a major role for the plane of nutrition in adjusting the homeorhetic control of metabolism during lactation. Glucose 11-18 insulin Homo sapiens 66-73 2266671-4 1990 Following insulin with glucose, plasma glucose increased transiently. Glucose 23-30 insulin Homo sapiens 10-17 2266671-4 1990 Following insulin with glucose, plasma glucose increased transiently. Glucose 39-46 insulin Homo sapiens 10-17 2122177-7 1990 Changes of insulin-stimulated active glycogen synthase associated with glyburide treatment correlated with changes in total body glucose disposal rates (r = .70, P less than .05) during euglycemic clamps. Glucose 129-136 insulin Homo sapiens 11-18 2232625-2 1990 The patients were treated with penbutolol and placebo for a period of three days, and then were examined with the help of the glucose-controlled insulin infusion system. Glucose 126-133 insulin Homo sapiens 145-152 1700570-4 1990 At 3.3 mmol/l of glucose, 60,000 U/l of interleukin 1 beta caused an inhibition of medium insulin accumulation to 62 +/- 5% of control from 48 h to 6 days of exposure, whereas islet DNA content was unaffected. Glucose 17-24 insulin Homo sapiens 90-97 2220936-3 1990 Insulin release in response to 100 gm oral glucose administration decreased from 108.0 +/- 28.2 to 49.3 +/- 5.2 nmol.min/L (p = 0.05) after diazoxide administration. Glucose 43-50 insulin Homo sapiens 0-7 2221049-1 1990 Although starvation is known to impair insulin-stimulated glucose disposal, whether it also induces resistance to insulin"s antiproteolytic action on muscle is unknown. Glucose 58-65 insulin Homo sapiens 39-46 2221049-10 1990 We conclude that in short-term fasted humans 1) muscle amino acid output accelerates due to increased proteolysis rather than reduced protein synthesis, and 2) despite its catabolic state and a marked impairment in insulin-mediated glucose disposal, muscle remains sensitive to insulin"s antiproteolytic action. Glucose 232-239 insulin Homo sapiens 215-222 2221056-3 1990 Viable islets that lose glucose-induced insulin release gradually regain it during culture for 24 h in 20 mM glucose. Glucose 24-31 insulin Homo sapiens 40-47 2221056-3 1990 Viable islets that lose glucose-induced insulin release gradually regain it during culture for 24 h in 20 mM glucose. Glucose 109-116 insulin Homo sapiens 40-47 2055337-0 1991 The dawn phenomenon in type 1 (insulin-dependent) diabetes mellitus: magnitude, frequency, variability, and dependency on glucose counterregulation and insulin sensitivity. Glucose 122-129 insulin Homo sapiens 31-38 2055343-3 1991 Female non-obese diabetic (NOD) mice from our colony, at the age of 12-13 weeks, have a normal basal glycaemia but an impaired intravenous glucose tolerance test, insulitis and a defective insulin response to glucose. Glucose 209-216 insulin Homo sapiens 189-196 2055343-5 1991 Immediately after isolation (day 0) the NOD islets displayed a defective insulin response to an acute stimulation with 16.7 mmol/l glucose. Glucose 131-138 insulin Homo sapiens 73-80 2055343-6 1991 After seven days in culture at both 11 and 28 mmol/l glucose these islets showed an increased insulin release in response to an acute glucose stimulation. Glucose 53-60 insulin Homo sapiens 94-101 2055343-6 1991 After seven days in culture at both 11 and 28 mmol/l glucose these islets showed an increased insulin release in response to an acute glucose stimulation. Glucose 134-141 insulin Homo sapiens 94-101 2055343-8 1991 Experiments performed in parallel, using islets obtained from a non-diabetes prone strain of mice (Naval Medical Research Institute, NMRI) showed that these islets had a similar insulin release in response to glucose both on day 0 and after seven days in culture at 11 mmol/l glucose. Glucose 209-216 insulin Homo sapiens 178-185 2055343-9 1991 The insulin mRNA levels of NOD islets did not change over one week in culture at 11 or 28 mmol/l glucose, but culture at the high glucose concentration induced a decrease in the islet insulin content. Glucose 130-137 insulin Homo sapiens 184-191 1900469-7 1991 The mean insulin requirement until the dextrose infusion was initiated was 33.2 +/- 7.3 units, IV fluid requirement was 3.5 +/- 0.8 litres and mean duration of treatment 4.4 +/- 1.6 hours. Glucose 39-47 insulin Homo sapiens 9-16 1761015-4 1991 Plasma insulin concentrations attained a plateau at 596 (SEM 100) pmol.l-1 after 120 min of glucose infusion and were not affected by muscarinic blockade; plasma glucose concentrations peaked at 13.3 (SEM 0.5) mmol.l-1 at 90 min and decreased progressively thereafter; no difference was observed with or without atropine. Glucose 92-99 insulin Homo sapiens 7-14 2044540-7 1991 These observations indicated that at HA the glucose values were high for the insulin concentration observed and might have been due to increased secretion of GH by the pituitary gland. Glucose 44-51 insulin Homo sapiens 77-84 1761067-0 1991 Effect of nifedipine on glucose potentiation of the acute insulin response to arginine in non-insulin-dependent diabetics. Glucose 24-31 insulin Homo sapiens 58-65 2060542-5 1991 After simvastatin, and in the last 60 min of the glucose clamp, there was an improvement in the action of insulin as demonstrated by stronger inhibition of hepatic glucose output (2.7 vs 5.2 mumol.kg-1.min-1) and stimulation both of the glucose disappearance rate (26.3 vs 19.5 mumol.kg-1.min-1) and glucose metabolic clearance rate (4.3 vs 3.6 ml.kg-1.min-1). Glucose 49-56 insulin Homo sapiens 106-113 2060542-5 1991 After simvastatin, and in the last 60 min of the glucose clamp, there was an improvement in the action of insulin as demonstrated by stronger inhibition of hepatic glucose output (2.7 vs 5.2 mumol.kg-1.min-1) and stimulation both of the glucose disappearance rate (26.3 vs 19.5 mumol.kg-1.min-1) and glucose metabolic clearance rate (4.3 vs 3.6 ml.kg-1.min-1). Glucose 164-171 insulin Homo sapiens 106-113 2060542-5 1991 After simvastatin, and in the last 60 min of the glucose clamp, there was an improvement in the action of insulin as demonstrated by stronger inhibition of hepatic glucose output (2.7 vs 5.2 mumol.kg-1.min-1) and stimulation both of the glucose disappearance rate (26.3 vs 19.5 mumol.kg-1.min-1) and glucose metabolic clearance rate (4.3 vs 3.6 ml.kg-1.min-1). Glucose 164-171 insulin Homo sapiens 106-113 1983828-2 1991 After oral glucose ingestion, glucose tolerance remained normal; however, this occurred at the expense of a markedly hyperinsulinemic plasma response, suggesting the presence of insulin resistance. Glucose 11-18 insulin Homo sapiens 122-129 1806481-1 1991 Growth hormone (GH) counteracts in general the effects of insulin on glucose and lipid metabolism, but shares protein anabolic properties with insulin. Glucose 69-76 insulin Homo sapiens 58-65 2026432-1 1991 In this paper, a theoretical analysis of the control of plasma glucose levels in diabetic individuals is undertaken using a simple mathematical model of the dynamics of glucose and insulin interaction in the blood system. Glucose 63-70 insulin Homo sapiens 181-188 2026432-7 1991 Various insulin infusion programs for the control of plasma glucose levels following a meal are then assessed. Glucose 60-67 insulin Homo sapiens 8-15 1671016-1 1991 On the basis of normative data from non-diabetic gravidae, the daytime glucose profile (DGP) is introduced as a model for insulin management of diabetes mellitus in pregnancy. Glucose 71-78 insulin Homo sapiens 122-129 1671016-3 1991 Insulin changes are based on a simple equation applied to individual glucose value difference between the patient (P) and target (T) levels (P - T/20). Glucose 69-76 insulin Homo sapiens 0-7 1671016-4 1991 With the aid of this model, the average (+/- SD) of the daytime mean plasma glucose (DMG) levels of 22 pregnant women requiring insulin treatment (183 +/- 36 mg/dl) approached normalization (114 +/- 15 mg/dl) after 2-7 profile determinations (median = 3.5). Glucose 76-83 insulin Homo sapiens 128-135 1773890-0 1991 Effects of insulin on glucose uptake in cultured cells from the central nervous system of rodent. Glucose 22-29 insulin Homo sapiens 11-18 1773890-7 1991 The basal level and stimulatory effect by insulin on this glucose uptake observed in C6 glioma cells were dependent on the presence of calcium in the medium. Glucose 58-65 insulin Homo sapiens 42-49 1823085-6 1991 The changes in day-long plasma glucose and insulin-stimulated glucose uptake had increased in association with metoprolol treatment and decreased following nicardipine. Glucose 62-69 insulin Homo sapiens 43-50 1725797-5 1991 Glucose and insulin response to an oral carbohydrate challenge (glucose % removal rate 1.4 +/- 0.2 vs. 1.5 +/- 0.3%/min; incremental area for serum insulin 955 +/- 279 vs. 905 +/- 458 microU/ml/min), serum cholesterol (192 +/- 33 vs. 200 +/- 43 mg/dl), triglyceride (83 +/- 57 vs. 84 +/- 37 mg/dl) and high-density lipoprotein cholesterol (46 +/- 9 vs. 50 +/- 14 mg/dl) were not affected as well. Glucose 64-71 insulin Homo sapiens 12-19 1723467-6 1991 However, a slight decrease in early insulin response to glucose was observed in the nifedipine and the nitrendipine groups. Glucose 56-63 insulin Homo sapiens 36-43 1725042-2 1991 In hypertension, hyperinsulinemia probably reflects reduced insulin-stimulated glucose uptake, but the reason for this, and the contribution of hyperinsulinemia (or of resistance to insulin) to the development of hypertension and atheroma, remains unclear. Glucose 79-86 insulin Homo sapiens 22-29 1725042-2 1991 In hypertension, hyperinsulinemia probably reflects reduced insulin-stimulated glucose uptake, but the reason for this, and the contribution of hyperinsulinemia (or of resistance to insulin) to the development of hypertension and atheroma, remains unclear. Glucose 79-86 insulin Homo sapiens 60-67 1725042-9 1991 If the growth regulatory actions of insulin are also unimpaired despite limitation of insulin-stimulated glucose uptake, chronic hyperinsulinemia could lead to increased vascular smooth muscle cell growth and contribute to development of atheroma. Glucose 105-112 insulin Homo sapiens 86-93 1986018-4 1991 Islets were then perifused to study their insulin response to glucose. Glucose 62-69 insulin Homo sapiens 42-49 1986018-5 1991 Islets cultured in the high glucose medium lost glucose-induced insulin release and, when challenged with an acute fall of glucose concentration in the perifusate, showed a paradoxical insulin release. Glucose 28-35 insulin Homo sapiens 64-71 1986018-5 1991 Islets cultured in the high glucose medium lost glucose-induced insulin release and, when challenged with an acute fall of glucose concentration in the perifusate, showed a paradoxical insulin release. Glucose 48-55 insulin Homo sapiens 64-71 1986018-5 1991 Islets cultured in the high glucose medium lost glucose-induced insulin release and, when challenged with an acute fall of glucose concentration in the perifusate, showed a paradoxical insulin release. Glucose 48-55 insulin Homo sapiens 64-71 1986018-6 1991 Insulin release in response to 10 mmol/L L-arginine was preserved in these islets, suggesting a selective reduction of the insulin response to glucose. Glucose 143-150 insulin Homo sapiens 0-7 1986018-6 1991 Insulin release in response to 10 mmol/L L-arginine was preserved in these islets, suggesting a selective reduction of the insulin response to glucose. Glucose 143-150 insulin Homo sapiens 123-130 1986032-7 1991 In both obesity and NIDDM, the dose-response curve for suppression of hepatic glucose production by insulin was impaired. Glucose 78-85 insulin Homo sapiens 100-107 1986032-9 1991 The combination of obesity and NIDDM further impaired the sensitivity of liver glucose output and glucose oxidation to insulin. Glucose 79-86 insulin Homo sapiens 119-126 2037862-3 1991 Insulin was positively correlated with serum glucose, body mass index (BMI), skinfold thickness, waist/hip ratio and sucrose intake, and negatively correlated with heavy physical activity score, treadmill exercise duration, and magnesium intake (each p less than 0.01). Glucose 45-52 insulin Homo sapiens 0-7 1675225-4 1991 These findings suggest that rapid changes in plasma growth hormone concentrations, corresponding to the fluctuations seen during normal daily life, may play a role in the short time regulation of blood glucose concentration through an inhibition of insulin and glucagon secretion. Glucose 202-209 insulin Homo sapiens 249-256 1675054-1 1991 Insulin is the dominant glucoregulatory factor; by suppressing endogenous glucose production and stimulating glucose utilization, it lowers the plasma glucose concentration. Glucose 74-81 insulin Homo sapiens 0-7 1675054-1 1991 Insulin is the dominant glucoregulatory factor; by suppressing endogenous glucose production and stimulating glucose utilization, it lowers the plasma glucose concentration. Glucose 109-116 insulin Homo sapiens 0-7 1675054-1 1991 Insulin is the dominant glucoregulatory factor; by suppressing endogenous glucose production and stimulating glucose utilization, it lowers the plasma glucose concentration. Glucose 109-116 insulin Homo sapiens 0-7 1675054-4 1991 However, the regulation of systemic glucose balance normally involves a highly co-ordinated interplay between the glucose-lowering effects of insulin and the glucose-elevating actions of an array of glucose counterregulatory hormones, primarily glucagon (and epinephrine under some conditions). Glucose 36-43 insulin Homo sapiens 142-149 1675054-4 1991 However, the regulation of systemic glucose balance normally involves a highly co-ordinated interplay between the glucose-lowering effects of insulin and the glucose-elevating actions of an array of glucose counterregulatory hormones, primarily glucagon (and epinephrine under some conditions). Glucose 114-121 insulin Homo sapiens 142-149 1675054-4 1991 However, the regulation of systemic glucose balance normally involves a highly co-ordinated interplay between the glucose-lowering effects of insulin and the glucose-elevating actions of an array of glucose counterregulatory hormones, primarily glucagon (and epinephrine under some conditions). Glucose 114-121 insulin Homo sapiens 142-149 1675054-4 1991 However, the regulation of systemic glucose balance normally involves a highly co-ordinated interplay between the glucose-lowering effects of insulin and the glucose-elevating actions of an array of glucose counterregulatory hormones, primarily glucagon (and epinephrine under some conditions). Glucose 114-121 insulin Homo sapiens 142-149 1675054-11 1991 The glucose counterregulatory hormones approach parity with insulin only when plasma glucose concentrations are lowered to levels that threaten brain function. Glucose 85-92 insulin Homo sapiens 60-67 2019315-3 1991 Significant correlations were found between fasting and post-glucose integrated area of blood glucose, insulin and C-peptide concentrations versus blood pressure measures. Glucose 61-68 insulin Homo sapiens 115-124 2043219-4 1991 Due to their effects on voltage-dependent Ca2+ channels, it is suspected that calcium antagonists influence glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 127-134 2043220-3 1991 Some recent studies using the euglycaemic insulin clamp technique have indicated that the beneficial effect of captopril, the most extensively studied drug, is exerted on insulin sensitivity, a site with the potential to influence glucose and lipid metabolism. Glucose 231-238 insulin Homo sapiens 171-178 2043221-6 1991 Regulatory factors in insulin sensitivity, such as free fatty acids, counterregulatory hormones and blood glucose level, play an important role in the metabolic control and pathogenesis of insulin resistance in man. Glucose 106-113 insulin Homo sapiens 22-29 2043221-6 1991 Regulatory factors in insulin sensitivity, such as free fatty acids, counterregulatory hormones and blood glucose level, play an important role in the metabolic control and pathogenesis of insulin resistance in man. Glucose 106-113 insulin Homo sapiens 189-196 2043223-5 1991 Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. Glucose 158-165 insulin Homo sapiens 103-110 2043227-5 1991 Present experience suggests that thiazide-induced impairment of glucose tolerance is due to both reduced glucose-stimulated insulin release and increased peripheral resistance to the action of insulin. Glucose 64-71 insulin Homo sapiens 124-131 2043227-5 1991 Present experience suggests that thiazide-induced impairment of glucose tolerance is due to both reduced glucose-stimulated insulin release and increased peripheral resistance to the action of insulin. Glucose 64-71 insulin Homo sapiens 193-200 1687782-2 1991 These receptors are also present post-synaptically in the pancreatic islets were they mediate inhibition of the glucose-induced release of insulin. Glucose 112-119 insulin Homo sapiens 139-146 1905936-5 1991 The predominant abnormality in brain glucose utilization in incipient late-onset DAT may be associated with an impairment of its control mechanism(s), which are assumed to be either an influence of brain insulin action, or brain insulin receptor function, or both. Glucose 37-44 insulin Homo sapiens 204-211 1984505-6 1991 Although there were no differences in blood or CSF glucose concentrations in the two groups of patients, the glucose group had higher plasma insulin levels, with a mean +/- standard deviation of 14.8 +/- 7.3 microU/ml compared to 10.3 +/- 4.2 microU/ml in the saline group. Glucose 109-116 insulin Homo sapiens 141-148 1958579-5 1991 Under such circumstances, a high fasting insulin level, normal glycemia and a low SHBG level suggest insulin resistance in terms of glucose disposal but not in terms of SHBG inhibition. Glucose 132-139 insulin Homo sapiens 41-48 1958579-5 1991 Under such circumstances, a high fasting insulin level, normal glycemia and a low SHBG level suggest insulin resistance in terms of glucose disposal but not in terms of SHBG inhibition. Glucose 132-139 insulin Homo sapiens 101-108 2034042-2 1991 On the 8th day of culture, the ICC that had been maintained in 16.7 mM glucose contained 60% less insulin than the ICC cultured in 2.8 mM glucose. Glucose 71-78 insulin Homo sapiens 98-105 2034042-5 1991 During a 24-day culture period, the total release of insulin and glucagon was similar in all glucose concentrations. Glucose 93-100 insulin Homo sapiens 53-60 1984562-4 1991 Fasting and glucose-stimulated insulin and C-peptide levels were significantly higher in obese than in controls, and in obese with the WHR value greater than 0.97 (corresponding to the distribution median) than in those with WHR lower or equal to 0.97. Glucose 12-19 insulin Homo sapiens 31-38 1984562-6 1991 On the contrary, WHR was significantly correlated with fasting and post-glucose insulin levels (P less than .05), but not with those of sex steroids. Glucose 72-79 insulin Homo sapiens 80-87 1984568-1 1991 Although glucose utilization is impaired in insulin-dependent diabetes mellitus (IDDM), it is unclear whether this is due to reductions in insulin sensitivity (Si) and/or glucose-mediated glucose disposal (SG). Glucose 9-16 insulin Homo sapiens 44-51 1984568-4 1991 The minimal model was modified to model the effects of the exogenous insulin on glucose kinetics to estimate SI and SG. Glucose 80-87 insulin Homo sapiens 69-76 1984571-0 1991 Differential effects of insulin resistance on leucine and glucose kinetics in obesity. Glucose 58-65 insulin Homo sapiens 24-31 1984571-5 1991 Insulin-mediated glucose disposal rate was significantly slower in the obese group: 2.05 +/- 0.05 versus 3.84 +/- 0.18 mg (kg.min)-1 in controls during the 10-mU insulin clamp, and 3.80 +/- 0.23 versus 9.16 +/- 0.47 mg (kg.min)-1 during the 40-mU clamp. Glucose 17-24 insulin Homo sapiens 0-7 1984571-5 1991 Insulin-mediated glucose disposal rate was significantly slower in the obese group: 2.05 +/- 0.05 versus 3.84 +/- 0.18 mg (kg.min)-1 in controls during the 10-mU insulin clamp, and 3.80 +/- 0.23 versus 9.16 +/- 0.47 mg (kg.min)-1 during the 40-mU clamp. Glucose 17-24 insulin Homo sapiens 162-169 1984572-10 1991 We conclude that infusion of amino acids with insulin under euglycemic conditions reduces whole body glucose utilization primarily by reducing peripheral glucose disposal. Glucose 101-108 insulin Homo sapiens 46-53 1984572-10 1991 We conclude that infusion of amino acids with insulin under euglycemic conditions reduces whole body glucose utilization primarily by reducing peripheral glucose disposal. Glucose 154-161 insulin Homo sapiens 46-53 1944014-7 1991 Significantly higher levels of insulin and C-peptide, both fasting and after a oral glucose tolerance test, were also found in obese subjects. Glucose 84-91 insulin Homo sapiens 31-38 2046822-1 1991 Tissue insulin sensitivity was measured by the glucose clamp technique in 8 uremic insulin-dependent diabetic patients before and after 3 months on a low-protein diet (LPD) providing daily 35 kcal/kg body weight, 60% of the caloric supply being obtained from carbohydrates. Glucose 47-54 insulin Homo sapiens 7-14 1788391-3 1991 Insulin and thyroid hormones are controlled by the supply of glucose and oxygen, respectively, and they influence fetal growth, partly via IGF-I. Glucose 61-68 insulin Homo sapiens 0-7 2048024-3 1991 The rate of the hormonal mechanisms of carbohydrate metabolism abnormality was shown to depend on the gravity and duration of chronic pancreatitis whereas blood sugar and insulin response to intravenous injection of glucose in patients with chronic pancreatitis to have characteristic features in common to type I and II diabetes. Glucose 216-223 insulin Homo sapiens 171-178 1845144-0 1991 The role of diacylglycerol/protein kinase C signaling in insulin-stimulated glucose transport. Glucose 76-83 insulin Homo sapiens 57-64 1845144-2 1991 Considerable new evidence further suggests that DAG/PKC signaling plays an important role in insulin-stimulated glucose transport. Glucose 112-119 insulin Homo sapiens 93-100 2125218-4 1990 In addition, insulin response to intravenous glucose loading was also attenuated in ADX rats with pretreatment by IL-1. Glucose 45-52 insulin Homo sapiens 13-20 2076525-6 1990 Combined with the relationship between the fatty acid composition of lipids and insulin secretion and action, our findings suggest a common metabolic defect of atherosclerosis and Type 2 diabetes which is probably insulin resistance in glucose metabolism. Glucose 236-243 insulin Homo sapiens 80-87 2276706-4 1990 In type II diabetics, the use of insulin is indicated only when all other therapeutic measures (diet, physical activity, oral antidiabetic drugs, lipid-lowering agents and substances delaying glucose resorption) have failed. Glucose 192-199 insulin Homo sapiens 33-40 2127994-0 1990 Plasma and salivary concentrations of glucose and cortisol during insulin-induced hypoglycaemic stress in healthy Nigerians. Glucose 38-45 insulin Homo sapiens 66-73 2250023-0 1990 Insulin receptor tyrosine residues 1162 and 1163 control insulin stimulation of myristoyl-diacylglycerol generation and subsequent activation of glucose transport. Glucose 145-152 insulin Homo sapiens 57-64 2256487-2 1990 An interval of less than 3 hours after the last meal was found to be associated with a significantly greater insulin response as opposed to a fasting interval of more than 3 hours (121.3 pmol/l vs. 83.5 pmol/l, p less than .001) and a greater insulin/glucose index (0.92 vs. 0.66, p less than .001), with no difference in plasma glucose. Glucose 251-258 insulin Homo sapiens 109-116 2256487-2 1990 An interval of less than 3 hours after the last meal was found to be associated with a significantly greater insulin response as opposed to a fasting interval of more than 3 hours (121.3 pmol/l vs. 83.5 pmol/l, p less than .001) and a greater insulin/glucose index (0.92 vs. 0.66, p less than .001), with no difference in plasma glucose. Glucose 329-336 insulin Homo sapiens 109-116 2256487-4 1990 Our data suggest that the fasting interval can influence insulin response during a glucose challenge test and the aberration in insulin secretion may effect screening results, especially in the high-risk gravida with glucose abnormality. Glucose 83-90 insulin Homo sapiens 57-64 2256488-0 1990 Relationships between glucose levels and insulin secretion during a glucose challenge test. Glucose 22-29 insulin Homo sapiens 41-48 2256488-0 1990 Relationships between glucose levels and insulin secretion during a glucose challenge test. Glucose 68-75 insulin Homo sapiens 41-48 2256488-1 1990 The relationship between glucose and insulin levels was examined in a prospective study of 153 pregnant patients without diabetes who underwent a standard 50 gm glucose challenge test. Glucose 25-32 insulin Homo sapiens 37-44 2256488-4 1990 Patients with glucose levels less than 100 mg/dl had significantly lower insulin/glucose indices. Glucose 14-21 insulin Homo sapiens 73-80 2256488-4 1990 Patients with glucose levels less than 100 mg/dl had significantly lower insulin/glucose indices. Glucose 81-88 insulin Homo sapiens 73-80 2256488-6 1990 Glucose levels accounted for 52% of the insulin output and 29% of the insulin/glucose index variance. Glucose 0-7 insulin Homo sapiens 40-47 2291591-6 1990 The diagnosis of hyperinsulinism rests on four criteria: the presence of increased insulin levels in the face of hypoglycemia, the low urinary excretion of ketone bodies during hypoglycemic episodes, the need for more than 15/mg/kg/min glucose to maintain the serum glucose level above 2 mmol/l, and a positive response to glucagon. Glucose 236-243 insulin Homo sapiens 22-29 2291591-6 1990 The diagnosis of hyperinsulinism rests on four criteria: the presence of increased insulin levels in the face of hypoglycemia, the low urinary excretion of ketone bodies during hypoglycemic episodes, the need for more than 15/mg/kg/min glucose to maintain the serum glucose level above 2 mmol/l, and a positive response to glucagon. Glucose 266-273 insulin Homo sapiens 22-29 2102082-3 1990 Blood pressure, glucose but not triglyceride, were also negatively and significantly correlated with SHBG and positively with fasting insulin. Glucose 16-23 insulin Homo sapiens 134-141 1965168-0 1990 Insulin action on glucose transport in isolated cardiac myocytes: signalling pathways and diabetes-induced alterations. Glucose 18-25 insulin Homo sapiens 0-7 2088821-0 1990 Aspects of the regulation of glucose transport in insulin-sensitive tissues in normal conditions and in type-2 diabetes. Glucose 29-36 insulin Homo sapiens 50-57 1980453-4 1990 Insulin therapy improves the abnormalities of NIDDM (reduced beta-cell function, increased hepatic glucose production, reduced peripheral glucose disposal, lipid abnormalities). Glucose 99-106 insulin Homo sapiens 0-7 1980453-4 1990 Insulin therapy improves the abnormalities of NIDDM (reduced beta-cell function, increased hepatic glucose production, reduced peripheral glucose disposal, lipid abnormalities). Glucose 138-145 insulin Homo sapiens 0-7 2132403-1 1990 The reduction of elevated fasting plasma glucose levels to near normal by repeated intravenous bolus insulin doses, given according to a simple algorithm, has been studied in 17 Type I and 23 Type II, healthy diabetic patients. Glucose 41-48 insulin Homo sapiens 101-108 2132403-2 1990 Using a formula based on the patient"s plasma glucose, height and bodyweight with insulin boluses given every 30 min if the plasma glucose remained above 6 mmol/1, plasma glucose levels were reduced to less than 7.5 mmol/1 in 28 (70%) patients by 60 min at which time the mean (+/- 1 SD) plasma glucose level in the Type I diabetic patients had reduced from 18.2 +/- 4.9 to 8.9 +/- 3.5 mmol/1 and in the Type II diabetic patients from 12.3 +/- 3.1 to 5.9 +/- 1.4 mmol/1. Glucose 46-53 insulin Homo sapiens 82-89 2132403-2 1990 Using a formula based on the patient"s plasma glucose, height and bodyweight with insulin boluses given every 30 min if the plasma glucose remained above 6 mmol/1, plasma glucose levels were reduced to less than 7.5 mmol/1 in 28 (70%) patients by 60 min at which time the mean (+/- 1 SD) plasma glucose level in the Type I diabetic patients had reduced from 18.2 +/- 4.9 to 8.9 +/- 3.5 mmol/1 and in the Type II diabetic patients from 12.3 +/- 3.1 to 5.9 +/- 1.4 mmol/1. Glucose 131-138 insulin Homo sapiens 82-89 2132403-2 1990 Using a formula based on the patient"s plasma glucose, height and bodyweight with insulin boluses given every 30 min if the plasma glucose remained above 6 mmol/1, plasma glucose levels were reduced to less than 7.5 mmol/1 in 28 (70%) patients by 60 min at which time the mean (+/- 1 SD) plasma glucose level in the Type I diabetic patients had reduced from 18.2 +/- 4.9 to 8.9 +/- 3.5 mmol/1 and in the Type II diabetic patients from 12.3 +/- 3.1 to 5.9 +/- 1.4 mmol/1. Glucose 131-138 insulin Homo sapiens 82-89 2132403-2 1990 Using a formula based on the patient"s plasma glucose, height and bodyweight with insulin boluses given every 30 min if the plasma glucose remained above 6 mmol/1, plasma glucose levels were reduced to less than 7.5 mmol/1 in 28 (70%) patients by 60 min at which time the mean (+/- 1 SD) plasma glucose level in the Type I diabetic patients had reduced from 18.2 +/- 4.9 to 8.9 +/- 3.5 mmol/1 and in the Type II diabetic patients from 12.3 +/- 3.1 to 5.9 +/- 1.4 mmol/1. Glucose 131-138 insulin Homo sapiens 82-89 2245873-5 1990 Aerobic glycolysis is required for glucose-induced insulin release. Glucose 35-42 insulin Homo sapiens 51-58 2245873-10 1990 Leucine-induced insulin release is suppressed and glucose-induced insulin release is activated in islets cultured at a high concentration of glucose. Glucose 50-57 insulin Homo sapiens 66-73 2245873-10 1990 Leucine-induced insulin release is suppressed and glucose-induced insulin release is activated in islets cultured at a high concentration of glucose. Glucose 141-148 insulin Homo sapiens 66-73 2245873-11 1990 Conversely, leucine-induced insulin release is activated and glucose-induced insulin release is suppressed in islets cultured at low glucose. Glucose 61-68 insulin Homo sapiens 77-84 2245873-11 1990 Conversely, leucine-induced insulin release is activated and glucose-induced insulin release is suppressed in islets cultured at low glucose. Glucose 133-140 insulin Homo sapiens 77-84 2276309-6 1990 A key goal of insulin therapy is to normalize the fasting plasma glucose level. Glucose 65-72 insulin Homo sapiens 14-21 2282786-1 1990 The minimal model approach to analysis of intravenous glucose tolerance tests (IVGTT) yields estimates of parameters representing insulin sensitivity, glucose-mediated glucose disposal and pancreatic responsiveness. Glucose 54-61 insulin Homo sapiens 130-137 2249632-6 1990 Insulin suppresses adipsin gene expression via high affinity insulin receptors, because physiological levels of insulin produce this effect, and dose-response curves for insulin stimulation of 2-deoxyglucose uptake and glucose utilization are similar to insulin"s effect on adipsin. Glucose 200-207 insulin Homo sapiens 0-7 2246037-6 1990 Insulin-directed exogenous glucose metabolism at the same degree of steady-state hyperinsulinemia was significantly lower in the borderline hypertensive group (5.98 +/- 2.22 versus 8.22 +/- 1.96 mg/kg/min; p less than 0.01). Glucose 27-34 insulin Homo sapiens 0-7 2246037-8 1990 These data indicate that there is a relation between insulin-mediated glucose uptake and blood pressure. Glucose 70-77 insulin Homo sapiens 53-60 2086453-2 1990 Rat pancreatic islets exposed to human recombinant IL-1 beta (rIL-1 beta) for 48 h in vitro exhibit a markedly reduced glucose-stimulated insulin secretion. Glucose 119-126 insulin Homo sapiens 138-145 2086453-7 1990 In short-term incubations in the absence of rIL-1 beta after the preceding culture with the cytokine, the glucose-stimulated insulin release was reduced by 70% in islets cultured at 11.1 mM glucose and by only 40% after culture at 56 mM glucose, when compared to the corresponding control islets. Glucose 106-113 insulin Homo sapiens 125-132 2086453-7 1990 In short-term incubations in the absence of rIL-1 beta after the preceding culture with the cytokine, the glucose-stimulated insulin release was reduced by 70% in islets cultured at 11.1 mM glucose and by only 40% after culture at 56 mM glucose, when compared to the corresponding control islets. Glucose 190-197 insulin Homo sapiens 125-132 2086453-7 1990 In short-term incubations in the absence of rIL-1 beta after the preceding culture with the cytokine, the glucose-stimulated insulin release was reduced by 70% in islets cultured at 11.1 mM glucose and by only 40% after culture at 56 mM glucose, when compared to the corresponding control islets. Glucose 190-197 insulin Homo sapiens 125-132 2102480-7 1990 As with insulin-stimulated glucose uptake, the mechanism is by translocation of the glucose transporter protein from an intracellular (inactive) site to the plasma membrane. Glucose 27-34 insulin Homo sapiens 8-15 1699966-2 1990 It has not been determined, however, whether glucose-dependent suppression is due to enhancement of insulin-stimulated glucose transport, to some other insulin-mediated effect, or to a direct effect of glucose. Glucose 119-126 insulin Homo sapiens 100-107 1699966-2 1990 It has not been determined, however, whether glucose-dependent suppression is due to enhancement of insulin-stimulated glucose transport, to some other insulin-mediated effect, or to a direct effect of glucose. Glucose 119-126 insulin Homo sapiens 100-107 2121778-1 1990 The present studies were undertaken to determine whether fasting hyperglycemia can compensate for decreased insulin-stimulated glucose disposal, oxidation, and storage in noninsulin-dependent diabetes mellitus (NIDDM) as well as to determine whether hyperglycemia normalizes insulin-stimulated skeletal muscle glycogen synthase and pyruvate dehydrogenase (PDH) activities. Glucose 127-134 insulin Homo sapiens 108-115 2121778-7 1990 We conclude that prevailing fasting hyperglycemia normalizes the nonoxidative and oxidative pathways of insulin-stimulated glucose in metabolism in NIDDM and may act as a homeostatic mechanism to normalize muscle glucose metabolism. Glucose 123-130 insulin Homo sapiens 104-111 2146285-0 1990 Androgen response to endogenous insulin secretion during the frequently sampled intravenous glucose tolerance test in normal and hyperandrogenic women. Glucose 92-99 insulin Homo sapiens 32-39 2146285-3 1990 Insulin sensitivity, glucose-mediated insulin release, and glucose/insulin-stimulated androgen responses were determined during a frequently sampled iv glucose tolerance test in a group of 19 women with clinical evidence of polycystic ovary syndrome (PCOS) and 9 age- and weight-matched controls. Glucose 21-28 insulin Homo sapiens 38-45 2146285-6 1990 Insulin sensitivity (SI) was calculated by application of the minimal model of glucose kinetics. Glucose 79-86 insulin Homo sapiens 0-7 2146285-15 1990 The failure of glucose-stimulated endogenous insulin secretion to significantly depress DHEA levels in insulin-resistant women with PCOS may account in part for their androgen excess. Glucose 15-22 insulin Homo sapiens 45-52 2146285-15 1990 The failure of glucose-stimulated endogenous insulin secretion to significantly depress DHEA levels in insulin-resistant women with PCOS may account in part for their androgen excess. Glucose 15-22 insulin Homo sapiens 103-110 2229300-2 1990 The peak insulin response to the oral glucose load was progressively delayed with each of the 3 glucose tolerance categories. Glucose 38-45 insulin Homo sapiens 9-16 2229300-2 1990 The peak insulin response to the oral glucose load was progressively delayed with each of the 3 glucose tolerance categories. Glucose 96-103 insulin Homo sapiens 9-16 2229300-4 1990 Variables measuring the initial rate of insulin or C-peptide secretion (0-30 min) after oral glucose also demonstrated a progressive diminution with increasing glucose intolerance. Glucose 93-100 insulin Homo sapiens 40-47 2229300-4 1990 Variables measuring the initial rate of insulin or C-peptide secretion (0-30 min) after oral glucose also demonstrated a progressive diminution with increasing glucose intolerance. Glucose 160-167 insulin Homo sapiens 40-47 2229309-0 1990 Minimal model analysis of intravenous glucose tolerance test-derived insulin sensitivity in diabetic subjects. Glucose 38-45 insulin Homo sapiens 69-76 2229309-6 1990 Across all subjects, the level of fasting serum glucose was correlated inversely with both insulin sensitivity (r = -0.62; P less than 0.05) and acute insulin responses (r = -0.72; P less than 0.02); however, insulin sensitivity in diabetic subjects with little insulin secretion (0.6 +/- 0.2) was comparable to insulin sensitivity in diabetic subjects with near-normal responses (0.6 +/- 0.3). Glucose 48-55 insulin Homo sapiens 91-98 2229309-6 1990 Across all subjects, the level of fasting serum glucose was correlated inversely with both insulin sensitivity (r = -0.62; P less than 0.05) and acute insulin responses (r = -0.72; P less than 0.02); however, insulin sensitivity in diabetic subjects with little insulin secretion (0.6 +/- 0.2) was comparable to insulin sensitivity in diabetic subjects with near-normal responses (0.6 +/- 0.3). Glucose 48-55 insulin Homo sapiens 151-158 2229309-6 1990 Across all subjects, the level of fasting serum glucose was correlated inversely with both insulin sensitivity (r = -0.62; P less than 0.05) and acute insulin responses (r = -0.72; P less than 0.02); however, insulin sensitivity in diabetic subjects with little insulin secretion (0.6 +/- 0.2) was comparable to insulin sensitivity in diabetic subjects with near-normal responses (0.6 +/- 0.3). Glucose 48-55 insulin Homo sapiens 151-158 2229309-10 1990 Total glucose uptake was decreased in diabetic subjects (5.2 +/- 0.8 vs. 12.7 +/- 1.7 mg/min.kg in normals; P less than 0.001), insulin-dependent glucose uptake was diminished to a greater extent (1.3 +/- 0.4 vs. 6.2 +/- 1.2) than noninsulin-independent glucose uptake (3.9 +/- 0.5 vs. 6.4 +/- 0.9; both P less than 0.02). Glucose 6-13 insulin Homo sapiens 128-135 2229309-10 1990 Total glucose uptake was decreased in diabetic subjects (5.2 +/- 0.8 vs. 12.7 +/- 1.7 mg/min.kg in normals; P less than 0.001), insulin-dependent glucose uptake was diminished to a greater extent (1.3 +/- 0.4 vs. 6.2 +/- 1.2) than noninsulin-independent glucose uptake (3.9 +/- 0.5 vs. 6.4 +/- 0.9; both P less than 0.02). Glucose 146-153 insulin Homo sapiens 128-135 2229309-10 1990 Total glucose uptake was decreased in diabetic subjects (5.2 +/- 0.8 vs. 12.7 +/- 1.7 mg/min.kg in normals; P less than 0.001), insulin-dependent glucose uptake was diminished to a greater extent (1.3 +/- 0.4 vs. 6.2 +/- 1.2) than noninsulin-independent glucose uptake (3.9 +/- 0.5 vs. 6.4 +/- 0.9; both P less than 0.02). Glucose 146-153 insulin Homo sapiens 128-135 2229309-11 1990 Administration of insulin permits minimal model FSIGT analysis to be applied to diabetic as well as normal subjects, yielding information about both insulin- and noninsulin-mediated glucose uptake as well as insulin sensitivity and insulin secretion. Glucose 182-189 insulin Homo sapiens 18-25 2229317-8 1990 Further studies of the effects of insulin on brain glucose metabolism are needed. Glucose 51-58 insulin Homo sapiens 34-41 2254456-1 1990 Successful pancreas transplantation in type I diabetic patients restores normal fasting glucose levels and biphasic insulin responses to glucose. Glucose 137-144 insulin Homo sapiens 116-123 2254456-4 1990 Glucose recovery after insulin-induced hypoglycemia in pancreas recipients was significantly improved. Glucose 0-7 insulin Homo sapiens 23-30 1702170-4 1990 The findings in the three different groups could be correlated to three trends of insulin secretion of the preparations following glucose challenge: good response to the glucose challenge, continuous decrease of insulin production, and no insulin secretion. Glucose 130-137 insulin Homo sapiens 82-89 1702170-4 1990 The findings in the three different groups could be correlated to three trends of insulin secretion of the preparations following glucose challenge: good response to the glucose challenge, continuous decrease of insulin production, and no insulin secretion. Glucose 170-177 insulin Homo sapiens 82-89 1963648-1 1990 To explain mechanisms responsible for derangement of insulin release in uremia, we investigated glucose metabolism through three different tests in 14 patients with end-stage chronic renal failure. Glucose 96-103 insulin Homo sapiens 53-60 1963648-13 1990 From these data we infer that defective insulin release in uremia is due to a decrease of beta-cell glucose sensitivity rather than to their functional exhaustion. Glucose 100-107 insulin Homo sapiens 40-47 2246962-4 1990 Insulin secretion was assessed during a 75-g oral glucose tolerance test (OGTT). Glucose 50-57 insulin Homo sapiens 0-7 2246970-0 1990 Dose-response characteristics for glucose-stimulated insulin release in man and assessment of influence of glucose on arginine-stimulated insulin release. Glucose 34-41 insulin Homo sapiens 53-60 2246970-0 1990 Dose-response characteristics for glucose-stimulated insulin release in man and assessment of influence of glucose on arginine-stimulated insulin release. Glucose 107-114 insulin Homo sapiens 138-145 2246970-1 1990 Glucose potentiates arginine-induced insulin release. Glucose 0-7 insulin Homo sapiens 37-44 2246970-2 1990 We investigated the dose-response characteristics for both phases of glucose-induced insulin release in normal man, and studied the influence of hyperglycemia on arginine-induced insulin secretion. Glucose 69-76 insulin Homo sapiens 85-92 2246970-4 1990 The ED50 (half-maximally stimulating blood glucose concentration) of first-phase insulin release (determined from plasma C-peptide increments at 5 minutes) was significantly lower than the ED50 for the second phase (60 minutes; 8.4 +/- 0.8 v 14.3 +/- 1.3 mmol/L, respectively, P less than .002). Glucose 43-50 insulin Homo sapiens 81-88 2246970-6 1990 Vmax of both phases of glucose-arginine-stimulated insulin release were positively correlated (r = .75, P less than .05). Glucose 23-30 insulin Homo sapiens 51-58 2246970-7 1990 The ED50 of the influence of glucose on first-phase arginine-induced insulin release was significantly lower than the ED50 for the second phase (9.0 +/- 1.1 v 12.7 +/- 1.0 mmol/L, respectively, P less than .02). Glucose 29-36 insulin Homo sapiens 69-76 2246970-9 1990 When dose-response curves of plasma insulin increments were analyzed with the same equation, the ED50 of second-phase glucose-induced plasma insulin increments was significantly higher than the ED50 assessed from the plasma C-peptide increments (21.6 +/- 2.8 v 14.3 +/- 1.3 mmol/L, respectively, P less than .05). Glucose 118-125 insulin Homo sapiens 36-43 2246970-9 1990 When dose-response curves of plasma insulin increments were analyzed with the same equation, the ED50 of second-phase glucose-induced plasma insulin increments was significantly higher than the ED50 assessed from the plasma C-peptide increments (21.6 +/- 2.8 v 14.3 +/- 1.3 mmol/L, respectively, P less than .05). Glucose 118-125 insulin Homo sapiens 141-148 2221056-4 1990 Survival was defined as the ability to regain glucose-induced insulin release. Glucose 46-53 insulin Homo sapiens 62-69 2268141-3 1990 Plasma glucose decreased significantly in individuals receiving insulin and the time of the maximum decrease (30 min) was concurrent with the beginning of water intake. Glucose 7-14 insulin Homo sapiens 64-71 2096883-8 1990 The glucose/insulin ratio exhibited trend towards a fall after hemodialysis. Glucose 4-11 insulin Homo sapiens 12-19 1794265-2 1991 This model analyzed, during an intravenous glucose tolerance test, the response of the first and second phase of insulin secretion in relation to the variations in blood glucose (insulin secretion) and the rate of decline in the blood glucose curve in relation to the variations in insulin (insulin response). Glucose 170-177 insulin Homo sapiens 113-120 1794265-2 1991 This model analyzed, during an intravenous glucose tolerance test, the response of the first and second phase of insulin secretion in relation to the variations in blood glucose (insulin secretion) and the rate of decline in the blood glucose curve in relation to the variations in insulin (insulin response). Glucose 170-177 insulin Homo sapiens 179-186 1794265-4 1991 In healthy subjects, the glucose load after placebo induced an insulin response of 7.4 +/- 1.0 and 11.3 +/- 1.4 microU ml-1 min-1 mg-1 dl-1 for the first and second phases, respectively, and an insulin sensitivity evaluated to be 4.7 +/- 0.3 min microU-1 ml-1. Glucose 25-32 insulin Homo sapiens 63-70 1794265-4 1991 In healthy subjects, the glucose load after placebo induced an insulin response of 7.4 +/- 1.0 and 11.3 +/- 1.4 microU ml-1 min-1 mg-1 dl-1 for the first and second phases, respectively, and an insulin sensitivity evaluated to be 4.7 +/- 0.3 min microU-1 ml-1. Glucose 25-32 insulin Homo sapiens 194-201 1794265-5 1991 Following the administration of Diamicron, the insulin response to the same glucose load increased two-fold and five-fold for the first and second phases, respectively, and the insulin sensitivity also increased by a factor of 2. Glucose 76-83 insulin Homo sapiens 47-54 1794265-6 1991 In diabetic subjects the insulin response to the glucose load after placebo was markedly decreased (2.2 +/- 0.5 and 2.5 +/- 0.3 microU ml-1 min-1 mg-1 dl-1, respectively) as was the insulin sensitivity (2.5 +/- 0.3 min microU-1 ml-1). Glucose 49-56 insulin Homo sapiens 25-32 1794265-6 1991 In diabetic subjects the insulin response to the glucose load after placebo was markedly decreased (2.2 +/- 0.5 and 2.5 +/- 0.3 microU ml-1 min-1 mg-1 dl-1, respectively) as was the insulin sensitivity (2.5 +/- 0.3 min microU-1 ml-1). Glucose 49-56 insulin Homo sapiens 182-189 1794267-3 1991 Glycogen synthesis in muscle accounts for the major part of non-oxidative glucose metabolism during insulin stimulation. Glucose 74-81 insulin Homo sapiens 100-107 1794267-4 1991 Treatment with gliclazide of patients with NIDDM has been shown to be associated with a potentiation of both insulin-mediated glucose disposal and insulin-stimulated glycogen synthase activity in skeletal muscle. Glucose 126-133 insulin Homo sapiens 109-116 1794269-6 1991 This was accompanied by the appearance of a small first-phase insulin response to iv glucose and by significant increases in the mean daily insulin to mean daily blood glucose ratio and in the 24-h urinary C-peptide to glucose ratio. Glucose 85-92 insulin Homo sapiens 62-69 2170088-0 1990 Impact of glucose self-monitoring on non-insulin-treated patients with type II diabetes mellitus. Glucose 10-17 insulin Homo sapiens 41-48 2210070-8 1990 This conclusion supports the view that glucokinase is a key enzyme in the recognition of glucose as an insulin secretagogue in pancreatic islets. Glucose 89-96 insulin Homo sapiens 103-110 2210069-4 1990 Insulin release increased 10-fold in response to the higher glucose concentration, and dot-blot analysis of islet mRNA with a rat preproinsulin cDNA probe showed a concomitant increase in mRNA levels. Glucose 60-67 insulin Homo sapiens 0-7 2261853-0 1990 Insulin release and peripheral sensitivity at the oral glucose tolerance test. Glucose 55-62 insulin Homo sapiens 0-7 2210069-4 1990 Insulin release increased 10-fold in response to the higher glucose concentration, and dot-blot analysis of islet mRNA with a rat preproinsulin cDNA probe showed a concomitant increase in mRNA levels. Glucose 60-67 insulin Homo sapiens 130-143 2079316-4 1990 Similarly, correlation coefficients between body mass index and plasma glucose response, plasma insulin response, and insulin-stimulated glucose disposal were equal to or greater than the correlation coefficients between ratio of waist to hip girth and the same three variables. Glucose 137-144 insulin Homo sapiens 118-125 2257995-7 1990 Chronic hyperglycaemia may also reduce non-insulin-dependent glucose utilization, at least in rats. Glucose 61-68 insulin Homo sapiens 43-50 2257995-10 1990 At the diabetic stage, hyperglycaemia could, however, maintain a self-perpetuating cycle, where the deleterious effects of high glucose concentrations on insulin action and secretion cause further deterioration of glycaemic control. Glucose 128-135 insulin Homo sapiens 154-161 2257997-0 1990 On the determination of basal glucose production rate in patients with type 2 (non-insulin-dependent) diabetes mellitus using primed-continuous 3-3H-glucose infusion. Glucose 30-37 insulin Homo sapiens 83-90 2257997-1 1990 UNLABELLED: Using primed-continuous 3-3H-glucose infusion, basal glucose production rate has been reported to be 140% higher than normal or almost normal in hyperglycaemic patients with Type 2 (non-insulin-dependent) diabetes mellitus. Glucose 41-48 insulin Homo sapiens 198-205 2258000-5 1990 We have measured the content of the insulin regulatable glucose transporter in a vesicular fraction isolated from muscle biopsies from fasting individuals with Type 2 diabetes and control subjects, and we found that the number of the insulin regulatable glucose transporters expressed in skeletal muscle was unaffected by Type 2 diabetes (0.208 vs 0.205, arbitrary units, p greater than 0.5, control subjects and diabetic patients). Glucose 56-63 insulin Homo sapiens 36-43 2258000-5 1990 We have measured the content of the insulin regulatable glucose transporter in a vesicular fraction isolated from muscle biopsies from fasting individuals with Type 2 diabetes and control subjects, and we found that the number of the insulin regulatable glucose transporters expressed in skeletal muscle was unaffected by Type 2 diabetes (0.208 vs 0.205, arbitrary units, p greater than 0.5, control subjects and diabetic patients). Glucose 56-63 insulin Homo sapiens 234-241 2258002-0 1990 The first phase insulin response to intravenous glucose is highly reproducible. Glucose 48-55 insulin Homo sapiens 16-23 2258002-1 1990 To determine the reproducibility of the first phase insulin response to intravenous glucose, ten normal subjects underwent two intravenous glucose tolerance tests separated by at least two weeks. Glucose 84-91 insulin Homo sapiens 52-59 2261849-3 1990 The higher glucose concentration in amniotic fluid in early pregnancy could be explained by a lower fetal metabolic rate in the early stage of development and a low insulin activity of the fetus. Glucose 11-18 insulin Homo sapiens 165-172 2261851-4 1990 In the periurban children there was a marked increase in plasma insulin concentration with increasing plasma glucose concentration, possibly suggesting the development of insulin resistance, or an antecedent state, and incipient glucose intolerance. Glucose 109-116 insulin Homo sapiens 64-71 2261851-4 1990 In the periurban children there was a marked increase in plasma insulin concentration with increasing plasma glucose concentration, possibly suggesting the development of insulin resistance, or an antecedent state, and incipient glucose intolerance. Glucose 109-116 insulin Homo sapiens 171-178 2261851-4 1990 In the periurban children there was a marked increase in plasma insulin concentration with increasing plasma glucose concentration, possibly suggesting the development of insulin resistance, or an antecedent state, and incipient glucose intolerance. Glucose 229-236 insulin Homo sapiens 64-71 2229049-2 1990 Moreover, it appears that glucose modulates insulin receptor affinity through de novo protein synthesis rather than through covalent modification of receptors, since cycloheximide selectively inhibited the glucose-induced increase in insulin binding capacity (ED50 of 360 ng/ml) and restored receptor affinity to control values. Glucose 26-33 insulin Homo sapiens 44-51 2229049-2 1990 Moreover, it appears that glucose modulates insulin receptor affinity through de novo protein synthesis rather than through covalent modification of receptors, since cycloheximide selectively inhibited the glucose-induced increase in insulin binding capacity (ED50 of 360 ng/ml) and restored receptor affinity to control values. Glucose 206-213 insulin Homo sapiens 44-51 2229049-3 1990 Importantly, insulin sensitivity of the glucose transport system was increased by glucose treatment (63%) to an extent comparable with the enhancement in receptor affinity, thus indicating a functional coupling between insulin binding and insulin action. Glucose 40-47 insulin Homo sapiens 13-20 2229049-3 1990 Importantly, insulin sensitivity of the glucose transport system was increased by glucose treatment (63%) to an extent comparable with the enhancement in receptor affinity, thus indicating a functional coupling between insulin binding and insulin action. Glucose 40-47 insulin Homo sapiens 219-226 2229049-3 1990 Importantly, insulin sensitivity of the glucose transport system was increased by glucose treatment (63%) to an extent comparable with the enhancement in receptor affinity, thus indicating a functional coupling between insulin binding and insulin action. Glucose 40-47 insulin Homo sapiens 219-226 2229049-3 1990 Importantly, insulin sensitivity of the glucose transport system was increased by glucose treatment (63%) to an extent comparable with the enhancement in receptor affinity, thus indicating a functional coupling between insulin binding and insulin action. Glucose 82-89 insulin Homo sapiens 13-20 2229049-3 1990 Importantly, insulin sensitivity of the glucose transport system was increased by glucose treatment (63%) to an extent comparable with the enhancement in receptor affinity, thus indicating a functional coupling between insulin binding and insulin action. Glucose 82-89 insulin Homo sapiens 219-226 2229049-3 1990 Importantly, insulin sensitivity of the glucose transport system was increased by glucose treatment (63%) to an extent comparable with the enhancement in receptor affinity, thus indicating a functional coupling between insulin binding and insulin action. Glucose 82-89 insulin Homo sapiens 219-226 2229049-5 1990 On the basis of these studies, we conclude that 1) insulin binding is subject to dual regulation (glucose controls insulin action by enhancing receptor affinity, whereas insulin controls the number of cell surface receptors); and 2) glucose appears to modulate insulin receptor affinity through the rapid biosynthesis of an affinity regulatory protein. Glucose 98-105 insulin Homo sapiens 51-58 2229049-5 1990 On the basis of these studies, we conclude that 1) insulin binding is subject to dual regulation (glucose controls insulin action by enhancing receptor affinity, whereas insulin controls the number of cell surface receptors); and 2) glucose appears to modulate insulin receptor affinity through the rapid biosynthesis of an affinity regulatory protein. Glucose 98-105 insulin Homo sapiens 115-122 2229049-5 1990 On the basis of these studies, we conclude that 1) insulin binding is subject to dual regulation (glucose controls insulin action by enhancing receptor affinity, whereas insulin controls the number of cell surface receptors); and 2) glucose appears to modulate insulin receptor affinity through the rapid biosynthesis of an affinity regulatory protein. Glucose 98-105 insulin Homo sapiens 115-122 2229049-5 1990 On the basis of these studies, we conclude that 1) insulin binding is subject to dual regulation (glucose controls insulin action by enhancing receptor affinity, whereas insulin controls the number of cell surface receptors); and 2) glucose appears to modulate insulin receptor affinity through the rapid biosynthesis of an affinity regulatory protein. Glucose 233-240 insulin Homo sapiens 51-58 2252528-4 1990 Stimulated C-peptide secretion (100 g glucose orally, 1 mg glucagon i.v.) Glucose 38-45 insulin Homo sapiens 11-20 2269580-0 1990 Lactate generation following glucose ingestion: relation to obesity, carbohydrate tolerance and insulin sensitivity. Glucose 29-36 insulin Homo sapiens 96-103 2269580-6 1990 When incremental areas during OGTT were examined, glucose area during OGTT was positively associated with BMI and insulin area was positively associated with both BMI and sum of glucose. Glucose 50-57 insulin Homo sapiens 114-121 2252529-2 1990 Dosage with insulin was minimized with target control of blood glucose levels less than or equal to 7.8 mmol/l before meals. Glucose 63-70 insulin Homo sapiens 12-19 2219271-2 1990 When glucose is used as the secretagogue, cyclosporine slightly stimulates insulin release at substimulatory concentrations of the hexose. Glucose 5-12 insulin Homo sapiens 75-82 2292659-5 1990 Insulin induced a similar decrement of blood glucose levels in all subjects, with a nadir at 30 min. Glucose 45-52 insulin Homo sapiens 0-7 2099997-9 1990 The fact that this phenomenon was not recorded in the same subjects following the fructose tolerance test, whose metabolism is insulin-independent, supports the hypothesis that reduced glucose-induced thermogenesis in obese subjects may depend on insulin resistance. Glucose 185-192 insulin Homo sapiens 127-134 2099997-9 1990 The fact that this phenomenon was not recorded in the same subjects following the fructose tolerance test, whose metabolism is insulin-independent, supports the hypothesis that reduced glucose-induced thermogenesis in obese subjects may depend on insulin resistance. Glucose 185-192 insulin Homo sapiens 247-254 2099998-0 1990 [Use of an automatic blood glucose measurement system for the assessment of insulin resistance during the oral glucose tolerance test]. Glucose 27-34 insulin Homo sapiens 76-83 2219271-7 1990 The evidence gathered here suggests that the inhibitory effect of cyclosporine on insulin release is apparent when glucose is used as a fuel stimulant and is reversed following removal of the stimulant. Glucose 115-122 insulin Homo sapiens 82-89 2203914-0 1990 Insulin injections: rotation of anatomic regions and plasma glucose. Glucose 60-67 insulin Homo sapiens 0-7 2274680-1 1990 Pancreastatin (PST) is known as the peptide which inhibits first phase of glucose-stimulated insulin secretion. Glucose 74-81 insulin Homo sapiens 93-100 2200728-2 1990 Human insulin and the low- and high-affinity analogues showed equivalent glucose utilization rates in the steady state (mean +/- SE 14.7 +/- 1.4, 12.7 +/- 1.5, and 12.2 +/- 1.2 mg.kg-1.min-1, respectively; n = 7). Glucose 73-80 insulin Homo sapiens 6-13 2168124-1 1990 To examine extra-alimentary effects of high-carbohydrate, high-fiber (HCF) diets, insulin-mediated glucose disposal employing the euglycemic clamp and hepatic glucose output (HGO) employing [6,6-2H2]glucose were measured in 12 healthy young and old individuals before and after 21-28 d of an HCF diet. Glucose 99-106 insulin Homo sapiens 82-89 2132195-2 1990 Dose-response curves were constructed for insulin-stimulated glucose disposal. Glucose 61-68 insulin Homo sapiens 42-49 2200728-4 1990 There was an inverse relationship between the insulin levels and the in vitro activities measured by binding to human hepatoma cells (HepG2; 100, 20, and 308%) or by incorporation of glucose into lipids in mouse free fat cells (100, 31, and 207%). Glucose 183-190 insulin Homo sapiens 46-53 2147631-1 1990 To evaluate the impact of ACE-inhibitors on insulin-mediated glucose uptake, glucose-induced glucose uptake, and hepatic glucose production, a sequential glucose clamp was performed in eight normotensive Type 1 diabetic patients after 3 weeks of enalapril therapy 20 mg day-1 and during control conditions. Glucose 61-68 insulin Homo sapiens 44-51 2147634-6 1990 This suggests that increases in insulin insensitivity have a predominant effect on slowly deteriorating glucose tolerance from 1 to 10 years after diagnosis in Type 2 diabetes. Glucose 104-111 insulin Homo sapiens 32-39 2226108-4 1990 When diet and tablet therapy are no longer effective in keeping the fasting blood glucose level less than 6 mM, a basal insulin supplement from a long-acting insulin such as ultralente can be added. Glucose 82-89 insulin Homo sapiens 120-127 2132195-7 1990 Glucose disposal rates, however, were decreased in patients at submaximal insulin levels (ED50 73 +/- 10 vs. 54 +/- 4 mU/l in control subjects, p less than 0.01 whereas maximal glucose disposal was similar (61 +/- 3 vs. 65 +/- 3 mumol.kg-1.min-1). Glucose 0-7 insulin Homo sapiens 74-81 2132195-7 1990 Glucose disposal rates, however, were decreased in patients at submaximal insulin levels (ED50 73 +/- 10 vs. 54 +/- 4 mU/l in control subjects, p less than 0.01 whereas maximal glucose disposal was similar (61 +/- 3 vs. 65 +/- 3 mumol.kg-1.min-1). Glucose 177-184 insulin Homo sapiens 74-81 2226108-7 1990 The dose of insulin required can be predicted from the level of the fasting blood glucose and the degree of obesity, which provides an index of the accompanying insulin resistance. Glucose 82-89 insulin Homo sapiens 12-19 2200728-5 1990 The total amount of glucose infused during and after insulin infusion was equal for the three insulins, whereas glucose utilization as a function of time was somewhat different. Glucose 20-27 insulin Homo sapiens 53-60 2226108-7 1990 The dose of insulin required can be predicted from the level of the fasting blood glucose and the degree of obesity, which provides an index of the accompanying insulin resistance. Glucose 82-89 insulin Homo sapiens 161-168 2226108-8 1990 Based on current evidence, insulin therapy is equally appropriate in patients with insulin deficiency and insulin resistance, because the benefit from maintaining near-normal glucose concentrations probably outweighs a putative risk of hyperinsulinemia. Glucose 175-182 insulin Homo sapiens 27-34 2200728-8 1990 In conclusion, the total effect of equimolar amounts of human insulin and the two insulin analogues on glucose utilization is equal regardless of the different receptor affinities of the insulins. Glucose 103-110 insulin Homo sapiens 62-69 2226108-10 1990 Lowering fasting blood glucose to normal with a basal insulin supplement reduces endogenous insulin production, and this may be advantageous if accompanying production of islet amyloid polypeptide and islet amyloid formation are also reduced. Glucose 23-30 insulin Homo sapiens 54-61 2200728-8 1990 In conclusion, the total effect of equimolar amounts of human insulin and the two insulin analogues on glucose utilization is equal regardless of the different receptor affinities of the insulins. Glucose 103-110 insulin Homo sapiens 82-89 2226108-10 1990 Lowering fasting blood glucose to normal with a basal insulin supplement reduces endogenous insulin production, and this may be advantageous if accompanying production of islet amyloid polypeptide and islet amyloid formation are also reduced. Glucose 23-30 insulin Homo sapiens 92-99 2144295-9 1990 Peak insulin levels during the 3-h oral glucose tolerance test were significantly higher (P less than 0.05) after the 28 days of DHEA (1126 +/- 165 vs. 746 +/- 165 pmol/L) and were accompanied by a 50% increase in the integrated insulin response (P less than 0.01) without a significant change in fasting glucose insulin or glucose-6-phosphate dehydrogenase values. Glucose 40-47 insulin Homo sapiens 5-12 2253832-7 1990 The insulin-stimulated peripheral glucose uptake was reduced in the prednisone-treated group, but normal in cyclosporin-treated subjects. Glucose 34-41 insulin Homo sapiens 4-11 2279518-2 1990 (2) A significant correlation was found between the plasma insulin levels at birth and the basal as well as the maximal plasma insulin values after glucose loading (1.75 g/kg b. Glucose 148-155 insulin Homo sapiens 59-66 2279518-2 1990 (2) A significant correlation was found between the plasma insulin levels at birth and the basal as well as the maximal plasma insulin values after glucose loading (1.75 g/kg b. Glucose 148-155 insulin Homo sapiens 127-134 2279530-5 1990 The ratio of the two peptides was normal or increased: insulin binding % of erythrocytes corresponded to that of the control group, which explains in these cases normal or favourable glucose metabolism. Glucose 183-190 insulin Homo sapiens 55-62 2125042-6 1990 Mathematical calculations using the glucose and insulin responses showed improved beta cell function and peripheral action of insulin in rapid responders. Glucose 36-43 insulin Homo sapiens 126-133 2202884-8 1990 After 4 weeks of chronic hyperinsulinemia, maximal insulin-stimulated glucose utilization was decreased 23% +/- 4% (P less than .05) and insulin sensitivity (ED50) was not significantly altered. Glucose 70-77 insulin Homo sapiens 30-37 1975421-0 1990 Interactions of glucagon and free fatty acids with insulin in control of glucose metabolism. Glucose 73-80 insulin Homo sapiens 51-58 2148776-6 1990 In the group of 9 diabetic patients, significant (p less than 0.05) reductions in fasting plasma glucose, hematocrit and the urinary excretion of sodium and glucose were seen with insulin treatment. Glucose 97-104 insulin Homo sapiens 180-187 2148776-6 1990 In the group of 9 diabetic patients, significant (p less than 0.05) reductions in fasting plasma glucose, hematocrit and the urinary excretion of sodium and glucose were seen with insulin treatment. Glucose 157-164 insulin Homo sapiens 180-187 2273977-3 1990 The clinical results demonstrate good compensation for glucose metabolism by the insulin pump Electronica UV1 01 N. Glucose 55-62 insulin Homo sapiens 81-88 1975421-3 1990 Intralipid infusion resulted, whether glucagon was substituted or not, in a near total suppression of the insulin-induced increase of glucose Rd (Rd at the end of the tests: C test, 6.13 +/- 0.85 mg.kg-1.min-1; G test, 7.29 +/- 0.87 mg.kg-1.min-1; IL test, 3.30 +/- 0.65 mg.kg-1.min-1; IL + G test, 3.57 +/- 0.42 mg.kg-1.min-1). Glucose 134-141 insulin Homo sapiens 106-113 2202884-8 1990 After 4 weeks of chronic hyperinsulinemia, maximal insulin-stimulated glucose utilization was decreased 23% +/- 4% (P less than .05) and insulin sensitivity (ED50) was not significantly altered. Glucose 70-77 insulin Homo sapiens 51-58 2102555-2 1990 Insulin sensitivity-RC was expressed in mg of utilised glucose/kg body weight in minute. Glucose 55-62 insulin Homo sapiens 0-7 2236334-5 1990 Intensive insulin therapy has become commonplace to control plasma glucose levels in the majority of patients receiving insulin therapy. Glucose 67-74 insulin Homo sapiens 10-17 2236334-5 1990 Intensive insulin therapy has become commonplace to control plasma glucose levels in the majority of patients receiving insulin therapy. Glucose 67-74 insulin Homo sapiens 120-127 2168179-1 1990 To determine if the failure of purified beta-cells to secrete insulin in response to a glucose stimulus results from the absence of a cytoskeletal response, the effects of cytochalasins D and B on glucose-induced insulin release were investigated. Glucose 197-204 insulin Homo sapiens 213-220 2168179-2 1990 Glucose alone failed to stimulate insulin release whereas glucose in the presence of glucagon, theophylline, cytochalasin D or B markedly potentiated insulin release. Glucose 58-65 insulin Homo sapiens 150-157 2195347-12 1990 The correlation between macrosomia and the concentrations of animal insulin in cord serum indicates that the transferred insulin has biologic activity and suggests that the formation of antibody to insulin in the mother is a determinant of fetal outcome independent of maternal blood glucose levels. Glucose 284-291 insulin Homo sapiens 121-128 2202297-2 1990 Several lines of evidence suggested that IAPP might affect glucose-stimulated insulin secretion and, therefore, might play a role in the development of impaired insulin secretion which is typical of type 2 diabetes. Glucose 59-66 insulin Homo sapiens 78-85 2202297-3 1990 In this study, the effects of human IAPP (amide) on glucose-stimulated insulin secretion was evaluated in the isolated perfused rat pancreas. Glucose 52-59 insulin Homo sapiens 71-78 2224964-2 1990 Its basic thesis that insulin prevents the new formation of glucose and its supply into the blood stream is still valid, although knowledge on the multiple action of insulin expanded substantially. Glucose 60-67 insulin Homo sapiens 22-29 2224964-3 1990 The theory put forward in 1955 by Levine and Goldstein which ascribed all insulin actions to the influence on the cellular membrane permeability for glucose, could, however, not explain all data associated with insulin, the knowledge of which was expanded steadily. Glucose 149-156 insulin Homo sapiens 74-81 2117389-0 1990 Effects of glyburide on in vivo insulin-mediated glucose disposal. Glucose 49-56 insulin Homo sapiens 32-39 2117389-10 1990 In contrast, the insulin-treated NIDDM patients had significant reductions in mean daily insulin requirement (72 +/- 6 versus 58 +/- 9 units per day; p = 0.05), mean 24-hour plasma glucose levels (153 +/- 10 to 131 +/- 5 mg/dL; p less than 0.05), and glycohemoglobin levels (10.3 +/- 0.7 percent to 8.0 +/- 0.4 percent; p less than 0.05) and an improvement in C-peptide secretion (0.24 +/- 0.07 to 0.44 +/- 0.09 pmol/mL; p = 0.08). Glucose 181-188 insulin Homo sapiens 17-24 2195347-12 1990 The correlation between macrosomia and the concentrations of animal insulin in cord serum indicates that the transferred insulin has biologic activity and suggests that the formation of antibody to insulin in the mother is a determinant of fetal outcome independent of maternal blood glucose levels. Glucose 284-291 insulin Homo sapiens 121-128 2167806-2 1990 The purpose of the present study was to maintain physiological plasma non-esterified fatty acid levels and to (i) examine their effect on skeletal muscle insulin-stimulated glucose uptake and metabolite exchange using the forearm technique, and (ii) evaluate their effect on whole-body glucose uptake and fuel oxidation. Glucose 173-180 insulin Homo sapiens 154-161 2202293-1 1990 Phenylarsine oxide (PAO), a trivalent arsenical, has been shown to inhibit insulin-stimulated glucose transport in 3T3-L1 adipocytes, implicating vicinal dithiols in signal transmission [Frost & Lane (1985) J. Biol. Glucose 94-101 insulin Homo sapiens 75-82 2202293-12 1990 These data further support a role for vicinal dithiols in insulin-stimulated glucose transport. Glucose 77-84 insulin Homo sapiens 58-65 2203598-6 1990 Rule-based logic, statistical methods, and a physiologic model of insulin pharmacokinetics and glucose dynamics are used to help detect meaningful patterns and trends in glucose and insulin data and to suggest approaches for optimizing insulin regimens. Glucose 95-102 insulin Homo sapiens 182-189 2200274-1 1990 Insulin secretion in response to glucose stimulation is reduced in endurance-trained humans. Glucose 33-40 insulin Homo sapiens 0-7 2200274-3 1990 Raising the plasma glucose concentration to approximately 450 mg/dl resulted in a plasma insulin response in the trained men that was approximately 64% lower than that of the untrained (peak values: 54 +/- 8 vs. 149 +/- 35 microU/ml; P less than 0.001). Glucose 19-26 insulin Homo sapiens 89-96 2200274-7 1990 The reduced plasma insulin response in trained people to the stimuli investigated suggests that regular exercise produces either several adaptations within the beta-cell or a single alteration of the beta-cell that results in an attenuation of the insulin secretory response to glucose, arginine, and fat ingestion. Glucose 278-285 insulin Homo sapiens 19-26 2200274-7 1990 The reduced plasma insulin response in trained people to the stimuli investigated suggests that regular exercise produces either several adaptations within the beta-cell or a single alteration of the beta-cell that results in an attenuation of the insulin secretory response to glucose, arginine, and fat ingestion. Glucose 278-285 insulin Homo sapiens 248-255 2132187-2 1990 Six months after transfer from porcine to human insulin there was a mean (+/- SE) increase in pre-breakfast blood glucose of 1.1 +/- 0.6 mmol l-1 (vs a reduction of 1.6 +/- 0.7 mmol l-1 in controls) (p less than 0.01), and a mean increase of pre-lunch blood glucose of 0.9 +/- 0.7 mmol l-1 (vs a reduction of 1.14 +/- 0.7 mmol l-1 in controls) (p less than 0.05). Glucose 114-121 insulin Homo sapiens 48-55 1973673-0 1990 Kinetics of insulin-mediated and non-insulin-mediated glucose uptake in humans. Glucose 54-61 insulin Homo sapiens 12-19 1973673-0 1990 Kinetics of insulin-mediated and non-insulin-mediated glucose uptake in humans. Glucose 54-61 insulin Homo sapiens 37-44 1973673-1 1990 The kinetics of insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU) in humans have not been well defined. Glucose 33-40 insulin Homo sapiens 16-23 1973673-1 1990 The kinetics of insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU) in humans have not been well defined. Glucose 80-87 insulin Homo sapiens 63-70 2132187-2 1990 Six months after transfer from porcine to human insulin there was a mean (+/- SE) increase in pre-breakfast blood glucose of 1.1 +/- 0.6 mmol l-1 (vs a reduction of 1.6 +/- 0.7 mmol l-1 in controls) (p less than 0.01), and a mean increase of pre-lunch blood glucose of 0.9 +/- 0.7 mmol l-1 (vs a reduction of 1.14 +/- 0.7 mmol l-1 in controls) (p less than 0.05). Glucose 258-265 insulin Homo sapiens 48-55 2132194-1 1990 Insulin responses to oral glucose, 125I-insulin binding to monocytes and androgen profiles were studied in a 25-year-old non obese woman with polycystic ovarian disease pre pregnancy, during pregnancy and in the post partum period. Glucose 26-33 insulin Homo sapiens 0-7 2245822-2 1990 When compared to a control group of normal weight glucose stimulated insulin release (I) was significantly increased and tissue sensitivity to insulin (M/I) significantly decreased. Glucose 50-57 insulin Homo sapiens 69-76 2197140-0 1990 Kinetics of in vivo muscle insulin-mediated glucose uptake in human obesity. Glucose 44-51 insulin Homo sapiens 27-34 2197140-1 1990 The kinetics of in vivo insulin-mediated glucose uptake in human obesity have not been previously studied. Glucose 41-48 insulin Homo sapiens 24-31 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 61-68 insulin Homo sapiens 44-51 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 61-68 insulin Homo sapiens 177-184 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 194-201 insulin Homo sapiens 44-51 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 194-201 insulin Homo sapiens 177-184 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 194-201 insulin Homo sapiens 44-51 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 194-201 insulin Homo sapiens 177-184 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 194-201 insulin Homo sapiens 44-51 2245822-4 1990 Glucose stimulated insulin release correlated positively with growth hormone (GH) and somatomedin-C levels, whereas no such a correlation could be obtained for M/I. Glucose 0-7 insulin Homo sapiens 19-26 2197140-8 1990 We conclude that 1) the kinetics of in vivo insulin-mediated glucose uptake in skeletal muscle in human obesity are characterized by reduced Vmax but normal Km; 2) the EG50 for insulin-mediated glucose extraction in skeletal muscle was 6 mM in both lean and obese subjects, consistent with a Km characteristic of the glucose-transport system; 3) obese subjects were unable to generate increases in blood flow in response to hyperglycemia under hyperinsulinemic conditions, and this contributed significantly to lower rates of leg and whole-body glucose uptake. Glucose 194-201 insulin Homo sapiens 177-184 2227801-6 1990 In control fetuses the insulin response following the glucose challenge peaked at 3 min while in IUGR no change in insulin concentration was detected. Glucose 54-61 insulin Homo sapiens 23-30 2209316-6 1990 There were wide ranges of insulin responses to glucose, with the upper tertile of 2-h insulin levels being more than seven times higher than the lower tertile (144 +/- 13 vs. 19 +/- 1 mU/L). Glucose 47-54 insulin Homo sapiens 26-33 2209316-6 1990 There were wide ranges of insulin responses to glucose, with the upper tertile of 2-h insulin levels being more than seven times higher than the lower tertile (144 +/- 13 vs. 19 +/- 1 mU/L). Glucose 47-54 insulin Homo sapiens 86-93 2200718-6 1990 It is possible that this effect of glucose on PKC, although not involved in the initiation of secretion, could explain the potentiation of insulin release observed in the presence of the receptor agonists. Glucose 35-42 insulin Homo sapiens 139-146 2209344-11 1990 In such a patient, combined insulin-sulfonylurea therapy predominantly stimulates basal insulin secretion, resulting in more effective suppression of hepatic glucose production and lower fasting plasma glucose. Glucose 158-165 insulin Homo sapiens 28-35 2209344-11 1990 In such a patient, combined insulin-sulfonylurea therapy predominantly stimulates basal insulin secretion, resulting in more effective suppression of hepatic glucose production and lower fasting plasma glucose. Glucose 202-209 insulin Homo sapiens 28-35 2212389-3 1990 We studied whether we could prevent macrosomia by insulin therapy based on four daily self blood glucose levels (SBG). Glucose 97-104 insulin Homo sapiens 50-57 2210122-3 1990 Other differences that were significantly related to coronary heart disease after adjustment for glucose intolerance were lower high density lipoprotein cholesterol levels (p = 0.001), elevated total triglyceride and very low density lipoprotein triglyceride (p less than 0.001), and elevated fasting insulin and C-peptide levels p = 0.001. Glucose 97-104 insulin Homo sapiens 301-308 2210122-6 1990 Thus, insulin resistance may be the underlying risk factor aetiologically linking glucose intolerance with coronary heart disease. Glucose 82-89 insulin Homo sapiens 6-13 2123183-7 1990 The dose of insulin required to maintain normal plasma glucose value was significantly lower (P less than 0.05) in group I. Glucose 55-62 insulin Homo sapiens 12-19 2212389-8 1990 Insulin was initiated when the SBG monitoring indicated that: (1) the FBS was 80 mg/dl whole blood from fingerstick (WBG) or the plasma glucose (PG) greater than 90 mg/dl and/or (2) the lhpc was greater than 140 mg/dl WBG and/or (3) the patient had persistent ketonuria on the prescribed diet which cleared only when the caloric intake was increased to a point which precipitated postprandial hyperglycemia. Glucose 136-143 insulin Homo sapiens 0-7 2258712-9 1990 High insulin levels (70-80 mU/l) stimulate glucose turnover rate by 300-400%, and the glucose infusion rate agrees well with the rate of appearance (Ra) of glucose, determined with [6,6-2H]glucose. Glucose 43-50 insulin Homo sapiens 5-12 2394967-6 1990 In addition, the rate constant for glucose disappearance (k value) for the intravenous insulin-tolerance test, which reflected the peripheral insulin sensitivity, tended to decrease during MaxEPA treatment and increase during administration of the placebo, there being a significant difference (P less than 0.03) between the changes during the two treatments. Glucose 35-42 insulin Homo sapiens 87-94 2394967-6 1990 In addition, the rate constant for glucose disappearance (k value) for the intravenous insulin-tolerance test, which reflected the peripheral insulin sensitivity, tended to decrease during MaxEPA treatment and increase during administration of the placebo, there being a significant difference (P less than 0.03) between the changes during the two treatments. Glucose 35-42 insulin Homo sapiens 142-149 2198433-8 1990 The posthypoglycemic insulin resistance during a moderate hyperinsulinemic (approximately 30 mU/L) clamp was mainly due to a decreased insulin effect on glucose utilization (control, 2.9 +/- 0.2; hypoglycemia, 2.2 +/- 0.2 mg/kg x min; P less than .02), whereas the insulin effect on glucose production was not significantly different after hypoglycemia. Glucose 153-160 insulin Homo sapiens 21-28 2198433-8 1990 The posthypoglycemic insulin resistance during a moderate hyperinsulinemic (approximately 30 mU/L) clamp was mainly due to a decreased insulin effect on glucose utilization (control, 2.9 +/- 0.2; hypoglycemia, 2.2 +/- 0.2 mg/kg x min; P less than .02), whereas the insulin effect on glucose production was not significantly different after hypoglycemia. Glucose 283-290 insulin Homo sapiens 21-28 2142051-4 1990 However, the total integrated plasma insulin response during a 75 g oral glucose tolerance test was significantly higher (p less than 0.05, Student"s t-test) in offspring of parents with IGT (718 +/- 71 pmol l-1 h) than in the subjects whose parents had normal glucose tolerance (524 +/- 47 pmol l-1 h). Glucose 73-80 insulin Homo sapiens 37-44 2197560-1 1990 A major effect of insulin is to increase glucose transport in muscle and fat. Glucose 41-48 insulin Homo sapiens 18-25 2197560-3 1990 One of these, the insulin-regulatable glucose transporter (IRGT), is primarily expressed in muscle and fat, tissues that exhibit insulin-dependent glucose transport. Glucose 38-45 insulin Homo sapiens 18-25 2197560-3 1990 One of these, the insulin-regulatable glucose transporter (IRGT), is primarily expressed in muscle and fat, tissues that exhibit insulin-dependent glucose transport. Glucose 38-45 insulin Homo sapiens 129-136 2197560-4 1990 Insulin promotes glucose transport in these tissues by stimulating movement of the glucose transporter from an intracellular location to the plasma membrane. Glucose 17-24 insulin Homo sapiens 0-7 2197560-5 1990 Recent studies, however, suggest that an additional effect of insulin in these tissues may be the facilitation of glucose transport, presumably across capillary endothelium. Glucose 114-121 insulin Homo sapiens 62-69 2272403-2 1990 During the induction of differentiation of 3T3-L1 fibroblasts to adipocytes, the cells typically undergo two rounds of cell division followed by accumulation of lipid droplets and expression of insulin-stimulated glucose transport as the cells attain the adipocyte phenotype. Glucose 213-220 insulin Homo sapiens 194-201 2164929-7 1990 The results indicate that the insulin responsive glucose transport in primary fibroblasts is functionally linked to the receptor for IGF-1. Glucose 49-56 insulin Homo sapiens 30-37 2075782-6 1990 Perifusion of islets with glucose provides a dynamic profile of glucose-mediated insulin release and of the ability of the cells to down regulate insulin secretion after the glycemic challenge is interrupted. Glucose 26-33 insulin Homo sapiens 81-88 2075782-6 1990 Perifusion of islets with glucose provides a dynamic profile of glucose-mediated insulin release and of the ability of the cells to down regulate insulin secretion after the glycemic challenge is interrupted. Glucose 64-71 insulin Homo sapiens 81-88 2075783-0 1990 Quantitative and qualitative differences in basal and glucose- and arginine-stimulated insulin secretion in healthy subjects and different stages of NIDDM. Glucose 54-61 insulin Homo sapiens 87-94 2202174-3 1990 In control subjects, the fall in plasma glucose was associated with a slight but significant fall in plasma insulin and a rise in plasma free fatty acid concentrations. Glucose 40-47 insulin Homo sapiens 108-115 2115296-2 1990 Insulin resistance in respect to glucose uptake in peripheral tissues seems to play an important role in the development of glucose intolerance, since subjects with coronary heart disease mainly are hyperinsulinemic. Glucose 33-40 insulin Homo sapiens 0-7 2115296-2 1990 Insulin resistance in respect to glucose uptake in peripheral tissues seems to play an important role in the development of glucose intolerance, since subjects with coronary heart disease mainly are hyperinsulinemic. Glucose 124-131 insulin Homo sapiens 0-7 2115296-3 1990 Insulin resistance may induce not only glucose intolerance but also hypertension, obesity, and dyslipoproteinemia (high very low-density lipoprotein and low high-density lipoprotein values), all variables that add to the risk of coronary heart disease. Glucose 39-46 insulin Homo sapiens 0-7 2115296-6 1990 Insulin resistance in noninsulin-dependent diabetic persons and in hypertensive subjects is located in skeletal muscles, where insulin"s ability to promote nonoxidative glucose metabolism is reduced. Glucose 169-176 insulin Homo sapiens 0-7 2196806-5 1990 From recent studies it seems, however, that intake of contraceptive combinations of ethinyl estradiol in combination with these types of gonanes, such as desogestrel and gestodene, may also be accompanied by increased insulin resistance, specifically, a hyperinsulinemic response to a glucose challenge despite unchanged glucose values compared with a baseline test. Glucose 285-292 insulin Homo sapiens 218-225 2196806-5 1990 From recent studies it seems, however, that intake of contraceptive combinations of ethinyl estradiol in combination with these types of gonanes, such as desogestrel and gestodene, may also be accompanied by increased insulin resistance, specifically, a hyperinsulinemic response to a glucose challenge despite unchanged glucose values compared with a baseline test. Glucose 321-328 insulin Homo sapiens 218-225 2196823-4 1990 During a 180-min insulin infusion, arterial glucose (144 +/- 27 mg/dl) and leucine concentrations (130 +/- 15 mumol/l) decreased (P less than 0.05 or less vs. base line) toward normal, whereas KIC did not change (33 +/- 4 mumol/l, NS). Glucose 44-51 insulin Homo sapiens 17-24 2252758-3 1990 The wearable blood glucose monitor is a 410 g forearm-mounted instrument with three miniature pumps for blood sampling, calibration, and insulin infusion, and a flow cell containing an enzyme-electrode sensor capable of determining plasma glucose levels accurately and precisely in undiluted whole blood. Glucose 19-26 insulin Homo sapiens 137-144 2083058-8 1990 Serum levels of uric acid and insulin response to oral glucose were increased in all obese subjects, but abnormalities of lipid metabolism and fasting hyperinsulinemia were found only in obese NIDDM-relatives. Glucose 55-62 insulin Homo sapiens 30-37 2249418-2 1990 The multicompartment model considers all relevant aspects of glucose kinetics and its dependence on insulin. Glucose 61-68 insulin Homo sapiens 100-107 2249427-2 1990 However, it is necessary to design a device which performs as a closed-loop insulin delivery system, more specifically which rapidly responds to a change in the recipient"s blood glucose concentration by an appropriate change in insulin release. Glucose 179-186 insulin Homo sapiens 76-83 2249430-2 1990 Through mathematical modelling of glucose-insulin dynamics this program is able to simulate glucose and insulin profiles of a 24 h period and display them graphically as curves. Glucose 34-41 insulin Homo sapiens 42-49 2249431-8 1990 ", and "What is the hypothetical response of my blood glucose to a particular amount of insulin?". Glucose 54-61 insulin Homo sapiens 88-95 2249432-3 1990 Six self-monitored glucose values at 3 h intervals, insulin doses, and the effects of insulin on plasma glucose are memorised for calculations. Glucose 104-111 insulin Homo sapiens 86-93 2249432-8 1990 Insulin therapy with two or three injections, fitted by the second program and selected according to the quality score, produced plasma glucose profiles as satisfactory as those obtained with six injections. Glucose 136-143 insulin Homo sapiens 0-7 1979950-5 1990 In the last 60 min of the lower insulin infusion rate glucose infusion rate (4.1 +/- 0.3 vs 2.9 +/- 0.4 mg/Kg x min p less than 0.05) and glucose disappearance rate (3.89 +/- 0.12 vs 2.63 +/- 0.11 mg/Kg x min p less than 0.01) were significantly reduced in patients with Turner. Glucose 54-61 insulin Homo sapiens 32-39 1975743-4 1990 By contrast, clenbuterol induced a dose-dependent increase in insulin release from isolated human islets incubated with 20 mM glucose. Glucose 126-133 insulin Homo sapiens 62-69 2230412-8 1990 Glucose transport activities in isolated adipocytes from a typical PCO patient were decreased, but insulin binding activities were not, which indicates that insulin resistance in this patients is due to some post-receptor defects. Glucose 0-7 insulin Homo sapiens 157-164 1696549-1 1990 Inositol-phosphates, glucosamine and glucose-6-phosphate blocked the effects of insulin on target protein phosphorylation in adipocytes, but the unsubstituted or sulphated derivatives of inositol or of glucose, or N-acetyl-glucosamine were without effect. Glucose 37-44 insulin Homo sapiens 80-87 2177367-1 1990 To examine glucose-stimulated insulin secretion and insulin sensitivity in the normal subjects and patients with impaired glucose tolerance, we performed the oral glucose tolerance test (OGTT) and modified insulin suppression test in 34 non-obese subjects. Glucose 11-18 insulin Homo sapiens 30-37 2177367-4 1990 In addition, the insulin-stimulated glucose uptake was estimated in all subjects by measuring the final 30 min steady-state plasma glucose (SSPG) of a continuous infusion of somatostatin, insulin and glucose for 4 hours (modified insulin suppression test). Glucose 36-43 insulin Homo sapiens 17-24 2191884-7 1990 These findings indicate that prolonging the rate of glucose absorption enhances insulin economy and glucose disposal. Glucose 52-59 insulin Homo sapiens 80-87 2226125-7 1990 A very low proportion of patients needed to add extra regular insulin to the pre-dinner intermediate insulin dose to achieve acceptable glucose control. Glucose 136-143 insulin Homo sapiens 62-69 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 71-78 insulin Homo sapiens 0-7 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 71-78 insulin Homo sapiens 223-230 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 71-78 insulin Homo sapiens 387-394 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 0-7 2142051-4 1990 However, the total integrated plasma insulin response during a 75 g oral glucose tolerance test was significantly higher (p less than 0.05, Student"s t-test) in offspring of parents with IGT (718 +/- 71 pmol l-1 h) than in the subjects whose parents had normal glucose tolerance (524 +/- 47 pmol l-1 h). Glucose 261-268 insulin Homo sapiens 37-44 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 223-230 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 387-394 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 0-7 2142051-6 1990 Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that these changes have a genetic component. Glucose 69-76 insulin Homo sapiens 49-56 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 223-230 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 387-394 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 0-7 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 223-230 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 387-394 2223055-5 1990 Addition of the agonist enhanced insulin release and Ca2+ uptake in the presence of 5.6 mM-glucose, but did not increase insulin release or Ca2+ uptake in 16.7 mM-glucose. Glucose 90-98 insulin Homo sapiens 33-40 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 0-7 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 223-230 2226128-7 1990 Insulin augmented the reduction in the number of cells induced by high glucose when supplemented together for 10 days at concentrations of 10(-6)-10(-12)M. The uptake of glucose increased further to 154% by the addition of insulin to high glucose as compared to that of high glucose alone, however, the decreased Na+/K+ pump activity by high glucose was restored to the control level by insulin. Glucose 170-177 insulin Homo sapiens 387-394 2226128-8 1990 The aggravating effect of insulin to the cellular damage induced by high glucose seems to be mediation via the mechanism other than the decreased Na+/K+ pump activity. Glucose 73-80 insulin Homo sapiens 26-33 2265738-6 1990 In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). Glucose 352-359 insulin Homo sapiens 121-128 2265738-6 1990 In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). Glucose 352-359 insulin Homo sapiens 211-218 2265738-6 1990 In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). Glucose 385-392 insulin Homo sapiens 121-128 2265738-6 1990 In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). Glucose 385-392 insulin Homo sapiens 211-218 2265738-6 1990 In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). Glucose 385-392 insulin Homo sapiens 121-128 2265738-6 1990 In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). Glucose 385-392 insulin Homo sapiens 211-218 2223055-5 1990 Addition of the agonist enhanced insulin release and Ca2+ uptake in the presence of 5.6 mM-glucose, but did not increase insulin release or Ca2+ uptake in 16.7 mM-glucose. Glucose 91-98 insulin Homo sapiens 33-40 1977721-9 1990 Insulin action on FFA metabolism isn ot grossly impaired in obese subjects who are clearly insulin resistant as far as glucose metabolism is concerned. Glucose 119-126 insulin Homo sapiens 0-7 2354749-1 1990 Studies of experimental diabetes in rodents induced by the beta-cell toxin streptozocin have shown that the insulin-resistant glucose transport of peripheral tissues (muscle and adipose) in these animals can be ascribed in part to a pretranslational reduction of the major insulin-sensitive glucose transporter (GLUT4) in these tissues. Glucose 126-133 insulin Homo sapiens 108-115 1696304-2 1990 In a static incubation system, the threshold level of glucose required for the stimulation of insulin secretion from freshly isolated porcine islets was found to be between 2.8 and 4.2 mmol glucose/l. Glucose 54-61 insulin Homo sapiens 94-101 2203725-1 1990 Glucose-stimulated insulin secretion is depressed by training. Glucose 0-7 insulin Homo sapiens 19-26 2203725-8 1990 In conclusion, in men training diminishes both arginine- and glucose-stimulated insulin secretion, indicating a profound beta-cell adaptation. Glucose 61-68 insulin Homo sapiens 80-87 2203725-9 1990 Being enhanced, the effects of insulin on both production and disposal of glucose are changed in the opposite direction to beta-cell secretion by training. Glucose 74-81 insulin Homo sapiens 31-38 2203726-2 1990 Using a three-stage euglycemic clamp, the metabolic clearance rate (MCR) of glucose under increasing insulin concentrations was measured. Glucose 76-83 insulin Homo sapiens 101-108 2203726-4 1990 In the base-line test, under all insulin levels, glucose MCR was significantly lower in obese compared with lean individuals (P less than 0.01). Glucose 49-56 insulin Homo sapiens 33-40 2203726-5 1990 Exercise increased glucose MCR at the highest hormonal concentrations applied to 124 and 134% of base line in OD and in ON, respectively (P less than 0.05); the insulin concentration required for one-half of the maximal clearance rate of glucose achieved in this study decreased from 200 to 130 and from 160 to 95 microU/ml in OD and ON, respectively (P less than 0.05). Glucose 238-245 insulin Homo sapiens 161-168 1696304-2 1990 In a static incubation system, the threshold level of glucose required for the stimulation of insulin secretion from freshly isolated porcine islets was found to be between 2.8 and 4.2 mmol glucose/l. Glucose 190-197 insulin Homo sapiens 94-101 1696304-3 1990 Arginine (5 mmol/l) and 3-isobutyl-l-methylxanthine (1 mmol/l) potentiated insulin release induced by 8.3 mmol glucose/l. Glucose 111-118 insulin Homo sapiens 75-82 2229928-0 1990 Plasma C-peptide response to oral glucose load in hyperthyroidism. Glucose 34-41 insulin Homo sapiens 7-16 2164526-2 1990 Thirty minutes after insulin injection plasma glucose levels were markedly decreased; concomitantly, plasma epinephrine levels had increased about 10-fold; plasma norepinephrine levels, however, increased only moderately. Glucose 46-53 insulin Homo sapiens 21-28 2196569-5 1990 Glucose induction of this 65-kDa protein is in practically all aspects comparable to glucose induction of insulin and glucokinase in pancreatic beta cells. Glucose 85-92 insulin Homo sapiens 106-113 1979604-1 1990 Perioperative management of insulinoma may be facilitated by the use of a glucose-controlled insulin infusion system (GCIIS; Biostator System, Miles Laboratories Inc., Elkhart, Ind.). Glucose 74-81 insulin Homo sapiens 28-35 1979604-8 1990 When the infusion system is programmed appropriately, the glucose infusion rate, as compared to the blood glucose level, reacts more quickly and sensitively to sudden changes in insulin levels. Glucose 58-65 insulin Homo sapiens 178-185 1979604-8 1990 When the infusion system is programmed appropriately, the glucose infusion rate, as compared to the blood glucose level, reacts more quickly and sensitively to sudden changes in insulin levels. Glucose 106-113 insulin Homo sapiens 178-185 2232461-5 1990 In CHD patients, the enhanced glucose uptake after insulin was followed by abnormalities both in aerobic and anaerobic glucose oxidation. Glucose 30-37 insulin Homo sapiens 51-58 2232461-5 1990 In CHD patients, the enhanced glucose uptake after insulin was followed by abnormalities both in aerobic and anaerobic glucose oxidation. Glucose 119-126 insulin Homo sapiens 51-58 2284484-2 1990 The results obtained show a dose-response curve of insulin serum levels to dextrose infusion rate, shifted significantly to the right and bottom which indicates a diminished insulin sensitivity; similarly a moderate decrease in receptor is obtained with no decrease in their affinity and absence of abnormalities in contraregulatory hormones. Glucose 75-83 insulin Homo sapiens 51-58 2096435-5 1990 Insulin resistance and the hyperinsulinism it creates seem to facilitate atherogenesis, even when glucose tolerance is still normal, so that the oral glucose tolerance test is not only poorly reproducible but loses a great deal of its value in the early detection of vascular risk. Glucose 150-157 insulin Homo sapiens 0-7 2284484-2 1990 The results obtained show a dose-response curve of insulin serum levels to dextrose infusion rate, shifted significantly to the right and bottom which indicates a diminished insulin sensitivity; similarly a moderate decrease in receptor is obtained with no decrease in their affinity and absence of abnormalities in contraregulatory hormones. Glucose 75-83 insulin Homo sapiens 174-181 2204104-6 1990 The early and late phases of the insulin and C-peptide responses to glucose were severely reduced. Glucose 68-75 insulin Homo sapiens 33-40 2131527-4 1990 The Turner index [(serum insulin x 100)/(blood sugar--30]) was lower than normal at all points of the GTT, suggesting a decreased insulin secretion in relation to serum glucose level. Glucose 169-176 insulin Homo sapiens 25-32 2204104-6 1990 The early and late phases of the insulin and C-peptide responses to glucose were severely reduced. Glucose 68-75 insulin Homo sapiens 45-54 2187391-5 1990 INTERVENTIONS: The insulin clamp technique was used to produce a stepwise decline in plasma glucose from 5.0 to 2.2 mmol/L over 3 hours. Glucose 92-99 insulin Homo sapiens 19-26 2163202-6 1990 Among nondiabetics, the kinase sensitivity to insulin, calculated as the ratio of the kinase activity at 1 nM insulin in vitro to the kinase activity at 100 nM insulin, was positively correlated with plasma insulin concentrations 2 h after an oral glucose load (r = 0.69, P less than 0.01). Glucose 248-255 insulin Homo sapiens 110-117 2113769-0 1990 Effects of insulin on skeletal muscle glucose storage, oxidation, and glycolysis in humans. Glucose 38-45 insulin Homo sapiens 11-18 2113769-4 1990 Under conditions of insulin stimulation, 49 +/- 5% of leg glucose uptake was stored, 37 +/- 4% was oxidized, and 14 +/- 2% was released as lactate and alanine. Glucose 58-65 insulin Homo sapiens 20-27 2113769-5 1990 We conclude that during physiological hyperinsulinemia and euglycemia 1) skeletal muscle lipid oxidation is nearly entirely suppressed and glucose becomes the primary oxidative substrate of muscle, 2) glucose storage and oxidation are the major pathways of skeletal muscle glucose metabolism and are quantitatively similar at physiological insulin levels, and 3) the majority of insulin-stimulated glycolysis is oxidized, with only a small portion released as lactate or alanine. Glucose 139-146 insulin Homo sapiens 43-50 2113769-5 1990 We conclude that during physiological hyperinsulinemia and euglycemia 1) skeletal muscle lipid oxidation is nearly entirely suppressed and glucose becomes the primary oxidative substrate of muscle, 2) glucose storage and oxidation are the major pathways of skeletal muscle glucose metabolism and are quantitatively similar at physiological insulin levels, and 3) the majority of insulin-stimulated glycolysis is oxidized, with only a small portion released as lactate or alanine. Glucose 201-208 insulin Homo sapiens 43-50 2163202-6 1990 Among nondiabetics, the kinase sensitivity to insulin, calculated as the ratio of the kinase activity at 1 nM insulin in vitro to the kinase activity at 100 nM insulin, was positively correlated with plasma insulin concentrations 2 h after an oral glucose load (r = 0.69, P less than 0.01). Glucose 248-255 insulin Homo sapiens 110-117 2113769-5 1990 We conclude that during physiological hyperinsulinemia and euglycemia 1) skeletal muscle lipid oxidation is nearly entirely suppressed and glucose becomes the primary oxidative substrate of muscle, 2) glucose storage and oxidation are the major pathways of skeletal muscle glucose metabolism and are quantitatively similar at physiological insulin levels, and 3) the majority of insulin-stimulated glycolysis is oxidized, with only a small portion released as lactate or alanine. Glucose 201-208 insulin Homo sapiens 340-347 2163202-6 1990 Among nondiabetics, the kinase sensitivity to insulin, calculated as the ratio of the kinase activity at 1 nM insulin in vitro to the kinase activity at 100 nM insulin, was positively correlated with plasma insulin concentrations 2 h after an oral glucose load (r = 0.69, P less than 0.01). Glucose 248-255 insulin Homo sapiens 46-53 2163202-6 1990 Among nondiabetics, the kinase sensitivity to insulin, calculated as the ratio of the kinase activity at 1 nM insulin in vitro to the kinase activity at 100 nM insulin, was positively correlated with plasma insulin concentrations 2 h after an oral glucose load (r = 0.69, P less than 0.01). Glucose 248-255 insulin Homo sapiens 110-117 2393546-7 1990 Studies in man have shown that insulin and exercise at low intensity have a synergistic effect on glucose uptake, possibly due to an increased insulin inflow to the muscle. Glucose 98-105 insulin Homo sapiens 31-38 2193534-4 1990 B-cell function was evaluated by measuring the acute insulin response (AIR) to glucose injection at fasting glucose (AIRGlc) and the AIR to arginine at multiple clamped glucose levels. Glucose 79-86 insulin Homo sapiens 53-60 2193534-4 1990 B-cell function was evaluated by measuring the acute insulin response (AIR) to glucose injection at fasting glucose (AIRGlc) and the AIR to arginine at multiple clamped glucose levels. Glucose 108-115 insulin Homo sapiens 53-60 2193534-4 1990 B-cell function was evaluated by measuring the acute insulin response (AIR) to glucose injection at fasting glucose (AIRGlc) and the AIR to arginine at multiple clamped glucose levels. Glucose 108-115 insulin Homo sapiens 53-60 2203383-1 1990 Local hormones such as adenosine or prostaglandins can dramatically change the sensitivity of glucose transport in muscle to insulin. Glucose 94-101 insulin Homo sapiens 125-132 2203384-2 1990 Relatives of type 2 diabetic patients, who have normal glucose tolerance, are characterized by hyperinsulinemia and insulin resistance compared to relatives with no family history of diabetes. Glucose 55-62 insulin Homo sapiens 100-107 2203384-3 1990 In individuals with impaired glucose tolerance, insulin resistance is more severe than in those with normal glucose tolerance. Glucose 29-36 insulin Homo sapiens 48-55 2203384-4 1990 The acute insulin response is lower in subjects with impaired glucose tolerance than in those with normal glucose tolerance but the decrease in the acute insulin response is similarly related to increases in plasma glucose as in normal subjects. Glucose 62-69 insulin Homo sapiens 10-17 2203384-5 1990 A high postprandial insulin concentration, as well as the degree of insulin resistance, predicts the transition of glucose tolerance from impaired to diabetic. Glucose 115-122 insulin Homo sapiens 20-27 2203384-5 1990 A high postprandial insulin concentration, as well as the degree of insulin resistance, predicts the transition of glucose tolerance from impaired to diabetic. Glucose 115-122 insulin Homo sapiens 68-75 2393546-7 1990 Studies in man have shown that insulin and exercise at low intensity have a synergistic effect on glucose uptake, possibly due to an increased insulin inflow to the muscle. Glucose 98-105 insulin Homo sapiens 143-150 2163613-5 1990 Fructose 2,6-bisphosphate (Fru-2,6-P2) levels, glucose consumption and lactate production are increased in a dose-dependent manner in HT29 cells treated with PMA or insulin. Glucose 47-54 insulin Homo sapiens 165-172 2393552-3 1990 Blood glucose was regulated by a Biostator controlled glucose infusion during a constant insulin infusion. Glucose 6-13 insulin Homo sapiens 89-96 2393555-4 1990 Insulin resistance is mainly due to a reduction in glucose uptake by muscle tissue. Glucose 51-58 insulin Homo sapiens 0-7 2393555-6 1990 When glucose disposal is determined under similar plasma glucose and insulin concentrations, glucose oxidation, the activity of pyruvate dehydrogenase and glycogen synthase are all reduced. Glucose 5-12 insulin Homo sapiens 69-76 2163613-9 1990 Furthermore, the effects of insulin and PMA on glucose consumption, lactate production, Fru-2,6-P2 levels and PFK2 activity are additive, and the effect of insulin on Fru-2,6-P2 production is not altered by pre-treatment of the cells with the phorbol ester. Glucose 47-54 insulin Homo sapiens 28-35 2189768-7 1990 Use of this assay indicated that, in lean nondiabetic subjects, glucose ingestion resulted in an increase (P less than 0.001) in the plasma concentration of amylin (from 2.03 +/- 0.22 to 3.78 +/- 0.39 pM) and insulin (from 48.3 +/- 3.1 to 265 +/- 44 pM). Glucose 64-71 insulin Homo sapiens 209-216 2378589-6 1990 Free insulin levels did not correlate with total insulin nor antibody levels, but correlated with plasma glucose levels in the infants. Glucose 105-112 insulin Homo sapiens 5-12 2134213-4 1990 Linear regression revealed no relationship of fasting or achieved proinsulin with sex or obesity and a non-significant trend towards increasing fasting and achieved proinsulin with age and fasting plasma glucose. Glucose 204-211 insulin Homo sapiens 165-175 2134213-6 1990 Analysis of partial correlation coefficients, controlling for age and obesity, showed that the Achieved Proinsulin/Achieved C-peptide ratio was related to both fasting (r = 0.27, p = 0.004) and achieved plasma glucose (r = 0.25, p = 0.008). Glucose 210-217 insulin Homo sapiens 104-114 2142039-9 1990 Insulin secretion was assessed following an intravenous bolus of glucose (0.5 g kg-1) at euglycaemia before and after treatment. Glucose 65-72 insulin Homo sapiens 0-7 2192846-5 1990 Individuals with these mutations have a syndrome of mild diabetes or glucose intolerance, which is inherited in an autosomal-dominant mode and is associated with hyperinsulinemia and altered insulin-C-peptide ratios. Glucose 69-76 insulin Homo sapiens 167-174 2192847-2 1990 In type II (non-insulin-dependent) diabetes in humans, a considerable body of evidence has accumulated indicating that a chronic physiological increment in the plasma glucose concentration leads to progressive impairment in insulin secretion and may contribute to insulin resistance as well. Glucose 167-174 insulin Homo sapiens 16-23 2199281-4 1990 Half-maximal glucose infusion rate was reached significantly earlier after injection of modified insulins (mean +/- SD 38 +/- 7 and 43 +/- 5 min) as compared to regular insulin (56 +/- 14 min, p less than 0.01). Glucose 13-20 insulin Homo sapiens 97-104 2192847-2 1990 In type II (non-insulin-dependent) diabetes in humans, a considerable body of evidence has accumulated indicating that a chronic physiological increment in the plasma glucose concentration leads to progressive impairment in insulin secretion and may contribute to insulin resistance as well. Glucose 167-174 insulin Homo sapiens 224-231 2192847-4 1990 In animal models of diabetes, development of insulin resistance is related to downregulation of the glucose-transport system, and a similar phenomenon is also likely to occur in humans. Glucose 100-107 insulin Homo sapiens 45-52 2192848-2 1990 Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Glucose 71-78 insulin Homo sapiens 46-53 2192848-5 1990 In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Glucose 108-115 insulin Homo sapiens 34-41 2192848-6 1990 Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Glucose 61-68 insulin Homo sapiens 40-47 2192849-2 1990 Under physiological circumstances, the small postprandial changes in plasma glucose concentrations (approximately 4.4-6.6 mM) primarily serve as a conditioned modifier of insulin secretion and dramatically alter the responsiveness of islets to a combination of neurohormonal agonists. Glucose 76-83 insulin Homo sapiens 171-178 2192849-5 1990 These two functional classes of neurohumoral agonists act synergistically to enhance insulin secretion when plasma glucose is greater than 6.0 mM but not when it is less than or equal to 4 mM. Glucose 115-122 insulin Homo sapiens 85-92 2192849-6 1990 On the other hand, an increase in plasma glucose concentration to 8-10 mM induces an increase in insulin secretory rate in the absence of any of the neurohormonal agonists. Glucose 41-48 insulin Homo sapiens 97-104 2199281-5 1990 Forty-five min after injection of both insulin analogues glucose infusion rate had increased by 7.4 +/- 1.8 or 6.1 +/- 1.8 mg.kg-1.min-1, reflecting 83 +/- 27 or 67 +/- 15% of maximal regular insulin action. Glucose 57-64 insulin Homo sapiens 39-46 2189885-6 1990 The insulin secretory response before weight loss showed a markedly reduced ability to respond appropriately to an increase in the ambient serum glucose. Glucose 145-152 insulin Homo sapiens 4-11 2114991-6 1990 Even though the mean serum insulin and glucose levels did not differ in the three groups of subjects, the per cent decrease in lipoprotein lipase after oral glucose in smokers was negatively correlated with insulin release into serum in the same subject, i.e., the greater the insulin release, the less the decrease in lipoprotein lipase activity. Glucose 157-164 insulin Homo sapiens 207-214 2114991-6 1990 Even though the mean serum insulin and glucose levels did not differ in the three groups of subjects, the per cent decrease in lipoprotein lipase after oral glucose in smokers was negatively correlated with insulin release into serum in the same subject, i.e., the greater the insulin release, the less the decrease in lipoprotein lipase activity. Glucose 157-164 insulin Homo sapiens 207-214 2189885-11 1990 At an increment of 6 mmol/L glucose above prevailing fasting glucose levels, the average rate of insulin secretion increased 53% (120 +/- 21 to 183 +/- 39 pmol/min.m2, P less than 0.05). Glucose 28-35 insulin Homo sapiens 97-104 2189885-11 1990 At an increment of 6 mmol/L glucose above prevailing fasting glucose levels, the average rate of insulin secretion increased 53% (120 +/- 21 to 183 +/- 39 pmol/min.m2, P less than 0.05). Glucose 61-68 insulin Homo sapiens 97-104 2189887-1 1990 The modified minimal model (MMM), a recently introduced method that assesses insulin sensitivity (SI) by a computed mathematical analysis of the relation between the change in insulin and glucose clearance after a bolus of iv glucose, followed 20 min later by a bolus of tolbutamide, has been standardized in adults, but this method has not been validated in children. Glucose 188-195 insulin Homo sapiens 77-84 2189887-1 1990 The modified minimal model (MMM), a recently introduced method that assesses insulin sensitivity (SI) by a computed mathematical analysis of the relation between the change in insulin and glucose clearance after a bolus of iv glucose, followed 20 min later by a bolus of tolbutamide, has been standardized in adults, but this method has not been validated in children. Glucose 226-233 insulin Homo sapiens 77-84 2189888-1 1990 One of the most prominent actions of insulin is stimulation of the glucose carrier in different cell types, especially adipose cells. Glucose 67-74 insulin Homo sapiens 37-44 2189888-2 1990 However, the exact mechanism of the mode of action of insulin, between receptor binding and stimulation of glucose transport, is not understood in detail. Glucose 107-114 insulin Homo sapiens 54-61 2189888-3 1990 We have shown earlier, that GH plays an important role in the control of the insulin-sensitive glucose carrier system in rat fat cells. Glucose 95-102 insulin Homo sapiens 77-84 2189888-6 1990 In normal fat cells, basal glucose transport was slow (t/2 = 2.5 min) and stimulated by insulin (t/2 = 0.8 min), as expected. Glucose 27-34 insulin Homo sapiens 88-95 2189888-8 1990 After GH administration during several months to GHD patients, glucose transport was again slow in the basal state (t/2 = 3.2 min) and could be stimulated by insulin (t/2 = 0.7 min). Glucose 63-70 insulin Homo sapiens 158-165 2189888-9 1990 These results confirm our earlier findings in rat adipocytes for human adipocytes: GH in vivo is responsible for a glucose transport-limiting factor in the plasma membrane that restricts basal glucose transport and is acutely inhibited by insulin resulting in enhanced glucose transport. Glucose 115-122 insulin Homo sapiens 239-246 2189893-2 1990 Obesity is characterized by decreased rates of skeletal muscle insulin-mediated glucose uptake (IMGU). Glucose 80-87 insulin Homo sapiens 63-70 2189893-10 1990 Therefore, decreased insulin sensitivity in human obesity is not only due to lower glucose extraction in insulin-sensitive tissues but also to lower blood flow to these tissues. Glucose 83-90 insulin Homo sapiens 21-28 2189893-10 1990 Therefore, decreased insulin sensitivity in human obesity is not only due to lower glucose extraction in insulin-sensitive tissues but also to lower blood flow to these tissues. Glucose 83-90 insulin Homo sapiens 105-112 2165083-2 1990 The quantity of insulin and the response to insulin are paramount complementary factors in the regulation of glucose metabolism, and may, at least under certain pathophysiological conditions, also affect cardiovascular function. Glucose 109-116 insulin Homo sapiens 16-23 2165083-2 1990 The quantity of insulin and the response to insulin are paramount complementary factors in the regulation of glucose metabolism, and may, at least under certain pathophysiological conditions, also affect cardiovascular function. Glucose 109-116 insulin Homo sapiens 44-51 2193199-10 1990 A substantial uptake of glucose was achieved and a more positive myocardial balance was obtained for alanine, lactate, and pyruvate with insulin. Glucose 24-31 insulin Homo sapiens 137-144 2203895-5 1990 In an in vivo test using diabetic animals, the double-layered implants provided a sustained release of insulin for 19 d, as judged by the changes in blood glucose levels and serum insulin levels after the subcutaneous implantation. Glucose 155-162 insulin Homo sapiens 103-110 2189884-0 1990 A modified protocol for estimation of insulin sensitivity with the minimal model of glucose kinetics in patients with insulin-dependent diabetes. Glucose 84-91 insulin Homo sapiens 38-45 2189884-1 1990 An exogenous insulin administration-modified, frequently sampled iv glucose tolerance test (FSIGT) for application in insulin-dependent diabetic patients (IDDM) to allow for estimation of insulin sensitivity (SI) and glucose effectiveness (SG) with Bergman"s minimal model of glucose kinetics was investigated. Glucose 68-75 insulin Homo sapiens 13-20 2191186-2 1990 Fasting plasma free fatty acid (FFA) levels, as well as plasma glucose and insulin levels in the fasting state and during an oral glucose tolerance test, displayed significant positive correlations with plasma triglyceride (TG) and VLDL-TG levels (P less than .005). Glucose 130-137 insulin Homo sapiens 75-82 2189884-1 1990 An exogenous insulin administration-modified, frequently sampled iv glucose tolerance test (FSIGT) for application in insulin-dependent diabetic patients (IDDM) to allow for estimation of insulin sensitivity (SI) and glucose effectiveness (SG) with Bergman"s minimal model of glucose kinetics was investigated. Glucose 68-75 insulin Homo sapiens 118-125 2189884-1 1990 An exogenous insulin administration-modified, frequently sampled iv glucose tolerance test (FSIGT) for application in insulin-dependent diabetic patients (IDDM) to allow for estimation of insulin sensitivity (SI) and glucose effectiveness (SG) with Bergman"s minimal model of glucose kinetics was investigated. Glucose 217-224 insulin Homo sapiens 13-20 2191457-10 1990 The integrated insulin response to glucose was not affected by PP. Glucose 35-42 insulin Homo sapiens 15-22 2225658-13 1990 Other endocrinological studies showed no abnormality except for hyporesponsiveness in the secretion of insulin on glucose tolerance test. Glucose 114-121 insulin Homo sapiens 103-110 2186702-1 1990 Glyceraldehyde phosphate, a glycolytic intermediate, and succinic acid (as its methyl ester to make it permeable to the cell), a citric acid cycle intermediate, were the only glucose metabolites of many recently tested that stimulated insulin release. Glucose 175-182 insulin Homo sapiens 235-242 2141134-4 1990 In the years to come, treatment will use other routes of administrations, insulin distribution will be linked to glucose levels and native insulin will be replaced by synthetic insulin analogues the properties of which will vary with chemical substitutions. Glucose 113-120 insulin Homo sapiens 74-81 2125014-6 1990 When patients received insulin alone, daily blood glucose profile and HbA1C worsened, and serum free-insulin levels and C peptide release decreased, while Beta-OH butyrate levels remained low. Glucose 50-57 insulin Homo sapiens 23-30 2185925-4 1990 The early phase of insulin response in the intravenous glucose tolerance test was below the 1st percentile of normal controls in two of the ICA-positive children. Glucose 55-62 insulin Homo sapiens 19-26 2335513-0 1990 Divergent molecular mechanisms for insulin-resistant glucose transport in muscle and adipose cells in vivo. Glucose 53-60 insulin Homo sapiens 35-42 2335513-1 1990 Glucose homeostasis depends on regulated changes in glucose transport in insulin-responsive tissues (e.g. muscle and adipose cells). Glucose 52-59 insulin Homo sapiens 73-80 2335513-7 1990 Although expression of the adipose-muscle glucose transporter predicts the physiological response at the tissue level, factors in the hormonal/metabolic milieu appear to override its increased expression in muscle resulting in insulin-resistant glucose uptake in this tissue in vivo. Glucose 42-49 insulin Homo sapiens 227-234 2186702-7 1990 The effects of glyceraldehyde suggest that glucose signals the first phase of insulin release by an agonist-like mechanism that originates in the cytosol and requires minimal energy. Glucose 43-50 insulin Homo sapiens 78-85 2186702-8 1990 The effects of monomethyl succinate suggest that the signal for the second phase of glucose-induced insulin release originates in the mitochondrion and requires a large amount of energy. Glucose 84-91 insulin Homo sapiens 100-107 2185925-7 1990 In another CF-ICA-positive schoolchild insulin response to the glucose tolerance test fell below the 1st percentile after 6 months. Glucose 63-70 insulin Homo sapiens 39-46 2192194-6 1990 Of the nine diabetics, eight were aware of hypoglycemia at a higher blood glucose level under porcine insulin. Glucose 74-81 insulin Homo sapiens 102-109 2255659-0 1990 [Effect of beta-adrenergic blockade on glucose homeostasis in insulin-induced hypoglycemia during physiological processes in diabetes mellitus]. Glucose 39-46 insulin Homo sapiens 62-69 2110856-4 1990 The insulin secretion of isolated Langerhans islets, perifused with solutions containing 5, 10, or 20 microM fluoride, was found to be significantly inhibited as a function of fluoride levels, both with basal and stimulatory concentrations of glucose. Glucose 243-250 insulin Homo sapiens 4-11 2185663-3 1990 Blood glucose was regulated by a Biostator-controlled glucose infusion during a constant insulin infusion. Glucose 6-13 insulin Homo sapiens 89-96 2189601-3 1990 Plasma GH and insulin responses to stimulation with oral glucose were measured in 7 healthy normal weight individuals and both before and after energy restriction in 7 obese individuals. Glucose 57-64 insulin Homo sapiens 14-21 2140086-4 1990 Plasma insulin responses were measured during an oral glucose tolerance test. Glucose 54-61 insulin Homo sapiens 7-14 2140087-6 1990 The coefficient of variation of blood glucose concentration during the study (3 days each route) was lower with IM than with SC injection of unmodified insulin (33 +/- 4 vs 43 +/- 3%, p less than 0.01). Glucose 38-45 insulin Homo sapiens 152-159 2184947-5 1990 The enhancing effects of insulin on the STA2-induced contractions were affected by extracellular glucose or magnesium ion concentrations. Glucose 97-104 insulin Homo sapiens 25-32 2184947-6 1990 The enhancing effects of insulin were observed only at the glucose concentrations of 100-300 mg/dl and magnesium concentrations of 0.5-1.5 mM. Glucose 59-66 insulin Homo sapiens 25-32 2184947-7 1990 Therefore, insulin was suspected of enhancing TXA2-induced contraction through a process that depends on extracellular glucose and Mg2+. Glucose 119-126 insulin Homo sapiens 11-18 2210019-6 1990 We conclude that: 1) after ingesting 75 g glucose, normal women showed greater glucose uptake per unit muscle mass than normal men, 2) for 3 hours after the ingestion of 75 g glucose, the predominant tendency toward utilizing glucose by a nonoxidative pathway is more marked in normal women than in normal men, and 3) the higher glucose uptake per unit muscle mass in the female group in the presence of an insulin response not significantly different from that of the male group suggests that muscle insulin sensitivity is greater in normal women. Glucose 42-49 insulin Homo sapiens 407-414 2210020-9 1990 Thus, the in vivo insulin resistance of lipoatrophic diabetes concerns not only glucose disposal but also hepatic glucose output and insulin secretion; in addition, the alterations of glucose metabolism were not the same in all subjects. Glucose 80-87 insulin Homo sapiens 18-25 2210020-9 1990 Thus, the in vivo insulin resistance of lipoatrophic diabetes concerns not only glucose disposal but also hepatic glucose output and insulin secretion; in addition, the alterations of glucose metabolism were not the same in all subjects. Glucose 114-121 insulin Homo sapiens 18-25 2401134-4 1990 The simple example of a diabetic patient receiving a continuous insulin infusion, for whom only the current serum glucose and infusion status is known, is suggested as a test problem. Glucose 114-121 insulin Homo sapiens 64-71 1970540-7 1990 Pretreatment with SMS 201-995 completely abolished IAPP and insulin secretion to intravenous glucose injection. Glucose 93-100 insulin Homo sapiens 60-67 1970540-8 1990 A significant correlation was found between plasma IAPP and insulin levels in oral and intravenous glucose administration and between plasma IAPP and C-peptide levels during insulin-induced hypoglycemia. Glucose 99-106 insulin Homo sapiens 60-67 1970540-9 1990 These results suggest that IAPP is cosecreted with insulin in response to a glucose load and secretion of IAPP is inhibited by hypoglycemia and somatostatin. Glucose 76-83 insulin Homo sapiens 51-58 2184020-9 1990 The mitogenic actions of insulin were glucose-dependent and were maximal in the presence of 2.7 mM glucose. Glucose 38-45 insulin Homo sapiens 25-32 2184020-9 1990 The mitogenic actions of insulin were glucose-dependent and were maximal in the presence of 2.7 mM glucose. Glucose 99-106 insulin Homo sapiens 25-32 2185105-1 1990 To evaluate the metabolic consequences of pancreas transplantation with systemic venous drainage on beta-cell function, we examined insulin and C-peptide responses to glucose and arginine in type I (insulin-dependent) diabetic pancreas recipients (n = 30), nondiabetic kidney recipients (n = 8), and nondiabetic control subjects (n = 28). Glucose 167-174 insulin Homo sapiens 132-139 2185105-3 1990 Acute insulin responses to glucose were 416 +/- 44 pM in control subjects, 763 +/- 91 pM in pancreas recipients (P less than 0.01 vs. control), and 589 +/- 113 pM in kidney recipients (NS vs. control). Glucose 27-34 insulin Homo sapiens 6-13 2185105-6 1990 Similar insulin and C-peptide results were obtained with arginine stimulation, and both basal and glucose-stimulated insulin-C-peptide ratios in pancreas recipients were significantly greater than in control subjects. Glucose 98-105 insulin Homo sapiens 117-124 2185105-6 1990 Similar insulin and C-peptide results were obtained with arginine stimulation, and both basal and glucose-stimulated insulin-C-peptide ratios in pancreas recipients were significantly greater than in control subjects. Glucose 98-105 insulin Homo sapiens 125-134 2190773-9 1990 The results demonstrate that intramuscular compared with subcutaneous thigh injection of insulin followed by bicycle exercise induces a marked increase in insulin absorption and a substantial fall in plasma glucose. Glucose 207-214 insulin Homo sapiens 89-96 2112109-2 1990 Because the tissue sites and nature of this insulin antagonism are not well-defined, we studied the effects of two parenterally administered progestins, levonorgestrel (NG) and norethindrone (NE), on insulin-regulated glucose uptake and phenylalanine release by the perfused rat hindquarter. Glucose 218-225 insulin Homo sapiens 200-207 2112109-9 1990 Insulin (100 microU/ml) increased glucose uptake by hindquarters of control and progestin-treated rats as compared to animals in the same treatment group perfused without exogenous insulin (P less than 0.01). Glucose 34-41 insulin Homo sapiens 0-7 2112109-10 1990 High dose NE impaired insulin-stimulated glucose uptake 24% below values of the control group (P less than 0.01). Glucose 41-48 insulin Homo sapiens 22-29 2189819-8 1990 Moreover, compared to NSO, LSO women had significantly higher glucose-stimulated insulin and C-peptide levels. Glucose 62-69 insulin Homo sapiens 81-88 2193907-9 1990 By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. Glucose 84-91 insulin Homo sapiens 14-21 2193907-9 1990 By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. Glucose 84-91 insulin Homo sapiens 64-71 2193907-9 1990 By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. Glucose 120-127 insulin Homo sapiens 14-21 2193907-9 1990 By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. Glucose 120-127 insulin Homo sapiens 64-71 2361884-3 1990 The response of 10 of these men to inactivity was similar to that of young athletes, with an unchanged plasma glucose response and a significantly greater insulin response to an oral glucose tolerance test (OGTT) after 10 days of inactivity. Glucose 183-190 insulin Homo sapiens 155-162 2189901-4 1990 In the present study the insulin response to oral glucose were studied in six healthy subjects before and on the last day of 2 weeks treatment with pinacidil. Glucose 50-57 insulin Homo sapiens 25-32 2163424-1 1990 To investigate the hypothesis that insulin affects the regulation of blood pressure, blood pressure and fasting insulin and glucose levels were measured in seven patients with insulinoma both before and after resection of the insulinoma. Glucose 124-131 insulin Homo sapiens 35-42 2191106-7 1990 Older children tended to have a slightly more prolonged elevation of blood glucose and prolonged elevation of the insulin:glucose ratio postoperatively. Glucose 122-129 insulin Homo sapiens 114-121 2232113-1 1990 The relationship of plasma lipid and apolipoprotein (apo) concentrations and plasma insulin response to oral glucose load to angiographically determined coronary artery disease (CAD) was investigated in 65 normolipidemic (plasma cholesterol less than 230 mg/dl and plasma triglyceride less than 150 mg/dl) males. Glucose 109-116 insulin Homo sapiens 84-91 2232113-8 1990 HDL-cholesterol concentration, the sum of plasma insulin levels and the magnitude of the early insulin response during oral glucose challenge were accurate predictors of the presence of but not the severity of CAD. Glucose 124-131 insulin Homo sapiens 95-102 2186255-1 1990 Insulin-mediated glucose metabolism (euglycemic insulin clamp at plasma insulin concentration of 100 microU/mL) and glucose-stimulated insulin secretion (hyperglycemic clamp) were examined in 42 obese subjects (ideal body weight [IBW], 158 +/- 4%) with normal glucose tolerance and in 36 normal weight (IBW, 102% +/- 1%) age-matched controls. Glucose 17-24 insulin Homo sapiens 0-7 2186255-3 1990 Throughout the physiologic range of plasma insulin concentrations, both the increase in total body glucose uptake and the suppression of hepatic glucose production (HGP) were significantly impaired in the obese group (P less than .001 to .01). Glucose 99-106 insulin Homo sapiens 43-50 2186255-3 1990 Throughout the physiologic range of plasma insulin concentrations, both the increase in total body glucose uptake and the suppression of hepatic glucose production (HGP) were significantly impaired in the obese group (P less than .001 to .01). Glucose 145-152 insulin Homo sapiens 43-50 2186255-4 1990 At the two highest plasma insulin concentrations, inhibition of HGP and the stimulation of glucose disposal were similar in both the obese and control groups. Glucose 91-98 insulin Homo sapiens 26-33 2186255-5 1990 Insulin secretion during the hyperglycemic (+/- 125 mg/dL) clamp was twofold greater in obese subjects than in controls (P less than .01) and was inversely related to the rate of glucose uptake during the insulin clamp (r = -.438, P less than .05), but was still unable to normalize glucose disposal (P less than .05). Glucose 179-186 insulin Homo sapiens 0-7 2186255-5 1990 Insulin secretion during the hyperglycemic (+/- 125 mg/dL) clamp was twofold greater in obese subjects than in controls (P less than .01) and was inversely related to the rate of glucose uptake during the insulin clamp (r = -.438, P less than .05), but was still unable to normalize glucose disposal (P less than .05). Glucose 179-186 insulin Homo sapiens 205-212 2186255-5 1990 Insulin secretion during the hyperglycemic (+/- 125 mg/dL) clamp was twofold greater in obese subjects than in controls (P less than .01) and was inversely related to the rate of glucose uptake during the insulin clamp (r = -.438, P less than .05), but was still unable to normalize glucose disposal (P less than .05). Glucose 283-290 insulin Homo sapiens 0-7 2186256-0 1990 The effect of starvation on insulin-induced glucose disposal and thermogenesis in humans. Glucose 44-51 insulin Homo sapiens 28-35 2179591-2 1990 To determine to what extent day-to-day variation in blood glucose levels can be reduced if insulin is injected in the same anatomic region rather than in different regions using a rotational scheme, as is commonly recommended, 12 type I diabetic subjects were studied. Glucose 58-65 insulin Homo sapiens 91-98 2179591-9 1990 We conclude that the common clinical practice of rotating the anatomic regions used for insulin injections increases day-to-day variation in blood glucose concentration. Glucose 147-154 insulin Homo sapiens 88-95 2188725-6 1990 The insulin sensitivity represents the sensitivity of the glucose metabolism to deviations from the basal requirement. Glucose 58-65 insulin Homo sapiens 4-11 2140921-0 1990 Insulin sensitivity and glucose-induced insulin response changes during adolescence. Glucose 24-31 insulin Homo sapiens 40-47 2140921-1 1990 Recently we reported that insulin resistance and glucose induced insulin release are inversely correlated to age in young healthy siblings of diabetic patients. Glucose 49-56 insulin Homo sapiens 65-72 2108071-4 1990 Islets were proven viable by in vitro insulin response to glucose challenge. Glucose 58-65 insulin Homo sapiens 38-45 2183610-3 1990 This marked insulin resistance was compensated by reciprocal enhancement of the first and second-phase insulin responses to intravenous glucose, which were increased threefold as compared with the nonpregnant women. Glucose 136-143 insulin Homo sapiens 103-110 2108071-8 1990 Off insulin, the average 24-h blood glucose level remained less than 150 mg/dl, with the fasting glucose level at 115 +/- 6 mg/dl and the 2-h postprandial level at 141 +/- 8 mg/dl for 22 days posttransplantation (the time of this study). Glucose 36-43 insulin Homo sapiens 4-11 2108071-8 1990 Off insulin, the average 24-h blood glucose level remained less than 150 mg/dl, with the fasting glucose level at 115 +/- 6 mg/dl and the 2-h postprandial level at 141 +/- 8 mg/dl for 22 days posttransplantation (the time of this study). Glucose 97-104 insulin Homo sapiens 4-11 2180660-0 1990 Blood or urine glucose-based insulin therapy and control of glycemia. Glucose 15-22 insulin Homo sapiens 29-36 2180660-6 1990 Insulin-adjustment algorithms that were tested calculated daily insulin dosages for these computer-simulated patients based on either blood or urine glucose concentrations self-measured 4 times/day before breakfast, lunch, dinner, and bedtime snack. Glucose 149-156 insulin Homo sapiens 0-7 2112100-4 1990 Plasma C-peptide during oral glucose tolerance test was significantly lower than that in Type 2 diabetic patients and normal control subjects (p less than 0.01 to 0.001) and was also consistently but not significantly higher than in Type 1 diabetic patients. Glucose 29-36 insulin Homo sapiens 7-16 2180660-6 1990 Insulin-adjustment algorithms that were tested calculated daily insulin dosages for these computer-simulated patients based on either blood or urine glucose concentrations self-measured 4 times/day before breakfast, lunch, dinner, and bedtime snack. Glucose 149-156 insulin Homo sapiens 64-71 2180660-11 1990 Total daily insulin doses evolved by blood glucose-based algorithms were significantly (P less than 0.05) higher than the doses used by urine glucose-based algorithms (53 vs. 47 U). Glucose 43-50 insulin Homo sapiens 12-19 2180680-3 1990 Glucose-stimulated insulin secretion from islet monolayers was determined after culture in serum-free supplemented medium by either 2- to 3-h static incubations or in a superfusion system with either low (2.8-8.3 mM) or stimulatory (16.7-19.4 mM) glucose concentrations. Glucose 0-7 insulin Homo sapiens 19-26 2180661-3 1990 The Diabetes Control and Complications Trial (DCCT) is a prospective randomized multicenter clinical trial to compare the effects of intensive insulin therapy aimed at near normalization of blood glucose levels with the effects of conventional therapy on the early microvascular complications of insulin-dependent diabetes mellitus. Glucose 196-203 insulin Homo sapiens 143-150 2189770-0 1990 Insulin regulation of glucose and lipid metabolism in massive obesity. Glucose 22-29 insulin Homo sapiens 0-7 2180680-11 1990 After 3 weeks of culture islet monolayers were superfused, and the biphasic glucose-induced insulin secretion of cells maintained in defined medium was indistinguishable from the insulin secretion of cells maintained in medium with 5% fetal bovine serum. Glucose 76-83 insulin Homo sapiens 92-99 2189770-3 1990 Insulin inhibition of hepatic glucose production was impaired in obese subjects. Glucose 30-37 insulin Homo sapiens 0-7 2180680-12 1990 These studies indicate that adult rat beta-cells retain biphasic glucose-induced insulin secretion after extended culture in defined serum-free medium. Glucose 65-72 insulin Homo sapiens 81-88 2180975-0 1990 Impact of obesity on insulin action in volunteers with normal glucose tolerance: demonstration of a threshold for the adverse effect of obesity. Glucose 62-69 insulin Homo sapiens 21-28 2194826-8 1990 The insulin response in oral glucose tolerance tests of children was discussed, who had a constitutional tall stature or Turner"s syndrome, respectively. Glucose 29-36 insulin Homo sapiens 4-11 2191000-2 1990 We studied the effect of increased circulating insulin in response to an oral glucose tolerance test (OGTT) on plasma levels of androgens and oestradiol in PCO patients and in healthy control subjects. Glucose 78-85 insulin Homo sapiens 47-54 1690745-4 1990 Addition of insulin to HepG2 cultures induced a rapid dose-dependent decrease in IGFBP-1 synthesis and secretion independent of the glucose concentration in the medium. Glucose 132-139 insulin Homo sapiens 12-19 2180975-3 1990 Insulin sensitivity was assessed by estimation of the plasma insulin concentration that produced half-maximal glucose disposal (EC50). Glucose 110-117 insulin Homo sapiens 0-7 2180975-3 1990 Insulin sensitivity was assessed by estimation of the plasma insulin concentration that produced half-maximal glucose disposal (EC50). Glucose 110-117 insulin Homo sapiens 61-68 2180975-4 1990 Glucose disposal during the highest insulin infusion was used as an index of maximal insulin responsiveness. Glucose 0-7 insulin Homo sapiens 36-43 2180975-8 1990 We conclude that insulin sensitivity for glucose disposal is impaired in human subjects with normal glucose tolerance who exceed a critical threshold of obesity, which corresponds to an ideal body weight of 120%. Glucose 41-48 insulin Homo sapiens 17-24 2180975-8 1990 We conclude that insulin sensitivity for glucose disposal is impaired in human subjects with normal glucose tolerance who exceed a critical threshold of obesity, which corresponds to an ideal body weight of 120%. Glucose 100-107 insulin Homo sapiens 17-24 2362342-4 1990 Plasma insulin activity and IRI/BS ratio increased in Glucose (+) and a significant difference was found between the two groups. Glucose 54-61 insulin Homo sapiens 7-14 2362342-9 1990 These results suggest that continuous glucose loading may facilitate insulin release from the pancreas and suppress the hyperketonemia and hyperlipidemia during partial gastrectomy. Glucose 38-45 insulin Homo sapiens 69-76 2179721-4 1990 The fasting serum insulin level was significantly lower one year after hemipancreatectomy (33.0 +/- 21.6 vs. 38.4 +/- 21.6 pmol per liter; P less than 0.05), as was the area under the insulin curves during the oral glucose-tolerance test (52,554 +/- 22,320 vs. 76,230 +/- 33,354 pmol per liter per minute; P less than 0.04). Glucose 215-222 insulin Homo sapiens 18-25 2406597-1 1990 Because glucose-stimulated insulin secretion is selectively impaired during the development of insulin-dependent diabetes mellitus (IDDM), we tested the possibility that the glucose transporter of pancreatic islet beta cells is a target of the autoimmune process in patients with IDDM. Glucose 8-15 insulin Homo sapiens 27-34 2180090-2 1990 In comparison with placebo, 50 mg miglitol was able to lower the incremental glucose response significantly at 30 minutes and 60 minutes when insulin was injected: (i) 30 minutes before the meal (2,3 +/- 0,5 mmol/l v. 0,37 +/- 0,2 mmol/l; P less than 0,001; and 5,0 +/- 0,7 mmol/l v. 1,1 +/- 0,8 mmol/l; P less than 0,001); and (ii) immediately before the meal (2,3 +/- 0,5 mmol/l v. 2,2 +/- 0,9 mmol/l; P less than 0,001) respectively. Glucose 77-84 insulin Homo sapiens 142-149 2180090-3 1990 The incremental glucose area under the curve when insulin was injected 30 minutes before breakfast was also significantly reduced on miglitol in comparison with placebo (0,67 +/- 0,15 mmol/l v. 0,16 +/- 0,14 mmol/l; P less than 0,01). Glucose 16-23 insulin Homo sapiens 50-57 2180090-6 1990 It is concluded that: (i) miglitol safely reduces the early post-meal glucose increments in insulin-dependent diabetics; and (ii) its effect enhances the hypoglycaemic response of an appropriately timed injection of insulin. Glucose 70-77 insulin Homo sapiens 92-99 2406597-1 1990 Because glucose-stimulated insulin secretion is selectively impaired during the development of insulin-dependent diabetes mellitus (IDDM), we tested the possibility that the glucose transporter of pancreatic islet beta cells is a target of the autoimmune process in patients with IDDM. Glucose 174-181 insulin Homo sapiens 27-34 2406597-7 1990 The results are consistent with the presence of an antibody against a protein involved in glucose transport by beta cells that would thereby impair glucose-stimulated insulin secretion. Glucose 90-97 insulin Homo sapiens 167-174 2406597-7 1990 The results are consistent with the presence of an antibody against a protein involved in glucose transport by beta cells that would thereby impair glucose-stimulated insulin secretion. Glucose 148-155 insulin Homo sapiens 167-174 2091878-8 1990 It is concluded that (a) long term metabolic diabetes control may affect hypoglycemic counterregulatory mechanisms and (b) intensive insulin therapy may make diabetic patients more vulnerable to hypoglycemia by lowering the effective blood glucose concentration associated with hypoglycemic counterregulation. Glucose 240-247 insulin Homo sapiens 133-140 2185604-2 1990 The effect of the intravenous glucose on plasma levels of glucagon and insulin were evaluated in thirty-five LBW preterm infants who were appropriate for gestational age. Glucose 30-37 insulin Homo sapiens 71-78 2185604-7 1990 In another 12 infants a significant fall in plasma glucagon and a variable but significant plasma insulin release also occurred throughout the 24 h study on continuous intravenous glucose (rate 2.4-2.7 mg/kg/min). Glucose 180-187 insulin Homo sapiens 98-105 2190520-3 1990 The hyperinsulinemic-euglycemic clamp is the reference method for quantifying insulin resistance and can differentiate decreased insulin sensitivity and decreased maximal capacity for glucose uptake. Glucose 184-191 insulin Homo sapiens 9-16 2190520-4 1990 Glucose flux measurements, using glucose labelled with stable isotopes, distinguish hepatic and peripheral factors involved in insulin resistance. Glucose 33-40 insulin Homo sapiens 127-134 2180396-0 1990 Insulin resistance is associated with lipid and lipoprotein abnormalities in subjects with varying degrees of glucose tolerance. Glucose 110-117 insulin Homo sapiens 0-7 1689632-4 1990 Of particular relevance is the finding that this channel is directly regulated by a metabolite of glucose, which is the primary insulin secretagogue. Glucose 98-105 insulin Homo sapiens 128-135 2180971-8 1990 Insulin/glucagon infusion increased plasma glucose concentration (8.7 +/- 1.5 mmol/L), total turnover (18.1 +/- 1.7 mumol/kg.min), and percent recycling (20.4 +/- 6.6%) to values similar to those in type 1 diabetic subjects. Glucose 43-50 insulin Homo sapiens 0-7 2180971-9 1990 The change in glucose metabolism was associated with a significant drop in blood concentrations of alanine (179 +/- 24 mumol/L), lactate (611 +/- 25 mumol/L), and pyruvate (30 +/- 3 mumol/L; all P less than 0.05-0.01 vs. insulin infusion alone). Glucose 14-21 insulin Homo sapiens 221-228 2156647-16 1990 At this high nitrogen intake, the effects of added glucose appear to be mediated by both insulin and glucagon. Glucose 51-58 insulin Homo sapiens 89-96 2196191-2 1990 Insulin secretory capacity was assessed using two glucose-independent parameters of beta cell function. Glucose 50-57 insulin Homo sapiens 0-7 2196191-5 1990 In the diabetic group, fasting was associated with an increase in insulin (+34 +/- 10%; P less than 0.005) and C-peptide (+34 +/- 8%; P less than 0.001) responses to OGTT despite a reduction in basal glycemia from 174 +/- 11 to 86 +/- 4 mg/dl (P less than 0.001) and in glucose response (-20 +/- 3%; P less than 0.001), indicating an improvement of insulin secretory capacity. Glucose 270-277 insulin Homo sapiens 66-73 2307295-1 1990 It has been suggested that the insulin resistance of non-insulin-dependent diabetes mellitus (NIDDM) may be caused by substrate competition between glucose and free fatty acids (FFAs) (Randle"s cycle). Glucose 148-155 insulin Homo sapiens 31-38 2111239-5 1990 Insulin treatment produced the following significant changes: decreases in blood glucose (at 7.00, 10.00, 16.00), mean daily blood glucose, HbA1, urinary glucose and low density lipoprotein (LDL) cholesterol and increased postglucose immunoreactive insulin (IRI) levels. Glucose 81-88 insulin Homo sapiens 0-7 2111239-5 1990 Insulin treatment produced the following significant changes: decreases in blood glucose (at 7.00, 10.00, 16.00), mean daily blood glucose, HbA1, urinary glucose and low density lipoprotein (LDL) cholesterol and increased postglucose immunoreactive insulin (IRI) levels. Glucose 131-138 insulin Homo sapiens 0-7 2111239-5 1990 Insulin treatment produced the following significant changes: decreases in blood glucose (at 7.00, 10.00, 16.00), mean daily blood glucose, HbA1, urinary glucose and low density lipoprotein (LDL) cholesterol and increased postglucose immunoreactive insulin (IRI) levels. Glucose 131-138 insulin Homo sapiens 0-7 2407478-6 1990 In rat skeletal muscle, acute treatment with insulin in vivo increases glucose-transport activity and the number of specific cytochalasin B-binding sites at the plasma membrane. Glucose 71-78 insulin Homo sapiens 45-52 2407476-1 1990 Molecular cloning of cDNA encoding the human erythrocyte facilitated-diffusion glucose transporter (GT) has elucidated its structure and has permitted a careful study of its tissue distribution and of its involvement in processes such as insulin-stimulated glucose uptake by adipose cells or transformation-induced increase in glucose metabolism. Glucose 79-86 insulin Homo sapiens 238-245 2407477-4 1990 Certain cells express unique transporter isoforms, the quantitatively most important of which is the muscle-adipocyte glucose-transporter isoform that functions in response to insulin to clear most of the blood glucose after a meal. Glucose 118-125 insulin Homo sapiens 176-183 2407477-6 1990 This insulin response is dramatically different from that seen in various fibroblastic cells, quantitatively and qualitatively, and suggests the expression in adipose tissue and muscle of a multigene program that defines the insulin-stimulated glucose transport of relevance to organismal glucose homeostasis. Glucose 244-251 insulin Homo sapiens 5-12 2407477-6 1990 This insulin response is dramatically different from that seen in various fibroblastic cells, quantitatively and qualitatively, and suggests the expression in adipose tissue and muscle of a multigene program that defines the insulin-stimulated glucose transport of relevance to organismal glucose homeostasis. Glucose 244-251 insulin Homo sapiens 225-232 2407478-1 1990 Skeletal muscle is the primary tissue responsible for insulin-dependent glucose uptake in vivo; therefore, glucose uptake by this tissue plays an important role in determining glycemia. Glucose 72-79 insulin Homo sapiens 54-61 2407478-1 1990 Skeletal muscle is the primary tissue responsible for insulin-dependent glucose uptake in vivo; therefore, glucose uptake by this tissue plays an important role in determining glycemia. Glucose 107-114 insulin Homo sapiens 54-61 2407478-10 1990 In L6 muscle cells in culture, acute treatment (1 h) with insulin causes recruitment of glucose transporters to the plasma membrane, and prolonged exposure to insulin or to glucose-deprived medium causes increased expression of GLUT-1 mRNA and GLUT-1 protein. Glucose 88-95 insulin Homo sapiens 58-65 1689652-0 1990 Inhibitors of glucose uptake stimulate the production of insulin-like growth factor-binding protein (IGFBP-1) by human fetal liver. Glucose 14-21 insulin Homo sapiens 57-64 2407582-1 1990 The relationship between plasma clearance rate of insulin (PCR) and insulin-stimulated glucose disposal was investigated in 15 healthy subjects and 30 insulin-dependent diabetes mellitus (IDDM) patients with the sequential euglycemic (5 mM) clamp technique (insulin infusion rates of 0.5, 1, 2, and 5 mU.kg-1.min-1 in 2-h steps). Glucose 87-94 insulin Homo sapiens 50-57 2407582-1 1990 The relationship between plasma clearance rate of insulin (PCR) and insulin-stimulated glucose disposal was investigated in 15 healthy subjects and 30 insulin-dependent diabetes mellitus (IDDM) patients with the sequential euglycemic (5 mM) clamp technique (insulin infusion rates of 0.5, 1, 2, and 5 mU.kg-1.min-1 in 2-h steps). Glucose 87-94 insulin Homo sapiens 68-75 2407582-1 1990 The relationship between plasma clearance rate of insulin (PCR) and insulin-stimulated glucose disposal was investigated in 15 healthy subjects and 30 insulin-dependent diabetes mellitus (IDDM) patients with the sequential euglycemic (5 mM) clamp technique (insulin infusion rates of 0.5, 1, 2, and 5 mU.kg-1.min-1 in 2-h steps). Glucose 87-94 insulin Homo sapiens 68-75 2407582-2 1990 In IDDM patients, insulin-stimulated glucose disposal was decreased at low insulinemia (steps 1-3), whereas at maximal insulinemia (step 4), insulin action was normal. Glucose 37-44 insulin Homo sapiens 18-25 2407582-2 1990 In IDDM patients, insulin-stimulated glucose disposal was decreased at low insulinemia (steps 1-3), whereas at maximal insulinemia (step 4), insulin action was normal. Glucose 37-44 insulin Homo sapiens 75-82 2407585-1 1990 A defective glucagon response impairs glucose recovery from insulin-induced hypoglycemia in some insulin-dependent (type I) diabetic patients. Glucose 38-45 insulin Homo sapiens 60-67 2110712-17 1990 The relationship between fasting and glucose-stimulated insulin levels with LH nadir concentrations, pulse amplitude and response to buserelin suggests an etiological role of insulin in the pathogenesis of PCOS. Glucose 37-44 insulin Homo sapiens 56-63 2110712-17 1990 The relationship between fasting and glucose-stimulated insulin levels with LH nadir concentrations, pulse amplitude and response to buserelin suggests an etiological role of insulin in the pathogenesis of PCOS. Glucose 37-44 insulin Homo sapiens 175-182 2106527-6 1990 The sample size was adequate to detect a clinically significant change in insulin-stimulated glucose disposal (i.e. approximately 3.3 mumol/kg.min; P less than or equal to 0.05). Glucose 93-100 insulin Homo sapiens 74-81 2407752-9 1990 These data demonstrate that moderate reduction of serum glucose maintained for a prolonged period results in marked suppression of plasma C-peptide, permitting improved discrimination between normal subjects and patients with insulinomas. Glucose 56-63 insulin Homo sapiens 138-147 2195099-6 1990 These data indicate that: i) patients with insulinoma require large amounts of glucose to remain isoglycemic during a prolonged fast; ii) insulin resistance is a common feature of insulinoma and can be shown even under near physiologic conditions such as a 24-h fasting. Glucose 79-86 insulin Homo sapiens 43-50 2195099-0 1990 The glucose clamp technique for the study of patients with hypoglycemia: insulin resistance as a feature of insulinoma. Glucose 4-11 insulin Homo sapiens 73-80 2407926-0 1990 Effects of dexamethasone on glucose-induced insulin and proinsulin release in low and high insulin responders. Glucose 28-35 insulin Homo sapiens 44-51 2345391-4 1990 The secretory capability of insulin against glucose load was relatively preserved. Glucose 44-51 insulin Homo sapiens 28-35 2407926-0 1990 Effects of dexamethasone on glucose-induced insulin and proinsulin release in low and high insulin responders. Glucose 28-35 insulin Homo sapiens 59-66 2407927-7 1990 There was a significant decrease in insulin-mediated glucose uptake as indicated by tissue accumulation of [3H]-2-deoxyglucose phosphorylation in diaphragm and hindlimb muscles. Glucose 53-60 insulin Homo sapiens 36-43 2204978-1 1990 Non insulin-dependent diabetes mellitus results from the combination in varying proportions of low plasma insulin levels (insulinopenia), peripheral resistance to insulin and increased hepatic glucose production. Glucose 193-200 insulin Homo sapiens 4-11 2182358-0 1990 Effect of insulin on D-glucose transport by human placental brush border membranes. Glucose 21-30 insulin Homo sapiens 10-17 1967767-6 1990 The more physiological plasma insulin levels achieved with the analogue were accompanied by a substantial reduction in postprandial plasma glucose excursions; the integrated area under the incremental plasma glucose curve was 45% lower after the analogue than after actrapid. Glucose 139-146 insulin Homo sapiens 30-37 1967767-6 1990 The more physiological plasma insulin levels achieved with the analogue were accompanied by a substantial reduction in postprandial plasma glucose excursions; the integrated area under the incremental plasma glucose curve was 45% lower after the analogue than after actrapid. Glucose 208-215 insulin Homo sapiens 30-37 2182358-1 1990 We studied the effect of insulin on the uptake of D-glucose by human placental brush border membranes (BBM) in vitro. Glucose 50-59 insulin Homo sapiens 25-32 2182358-5 1990 Preincubation of the placental tissue with insulin for 45 min at 22 degrees C significantly enhanced the D-glucose influx into the membrane vesicles, without influencing the slope of the Hill plot. Glucose 105-114 insulin Homo sapiens 43-50 2182358-6 1990 A dose-response curve of the effect of insulin revealed that although the effect was already significant at 10(-9) M, the maximal activity was reached at 10(-8) M. The influence of insulin on D-glucose uptake was present only when preincubation of the placental tissue with the hormone was performed in the presence of Mn2+. Glucose 192-201 insulin Homo sapiens 39-46 2182358-6 1990 A dose-response curve of the effect of insulin revealed that although the effect was already significant at 10(-9) M, the maximal activity was reached at 10(-8) M. The influence of insulin on D-glucose uptake was present only when preincubation of the placental tissue with the hormone was performed in the presence of Mn2+. Glucose 192-201 insulin Homo sapiens 181-188 2182358-9 1990 We conclude that insulin, at physiological concentrations, enhances glucose uptake by the BBM, and that such a regulation might contribute to the glucose homeostasis in the fetal circulation, independent of the maternal variations in glycemia. Glucose 68-75 insulin Homo sapiens 17-24 2105152-5 1990 During glucose clamp, mean plasma insulin was 172 +/- (1 SEM) 10 as compared to 6 +/- 1 microU/ml during vehicle infusions. Glucose 7-14 insulin Homo sapiens 34-41 2405644-10 1990 Insulin:glucose ratios decreased during SMS therapy. Glucose 8-15 insulin Homo sapiens 0-7 2185069-0 1990 The fuel concept for insulin release: regulation of glucose phosphorylation in pancreatic islets. Glucose 52-59 insulin Homo sapiens 21-28 2121571-0 1990 Localization of rate-limiting defect for glucose disposal in skeletal muscle of insulin-resistant type I diabetic patients. Glucose 41-48 insulin Homo sapiens 80-87 2137755-10 1990 Combination of insulin with the sulphonylurea glipizide in secondary failure Type 2 diabetic patients leads to increased insulin-mediated peripheral glucose disposal. Glucose 149-156 insulin Homo sapiens 15-22 2137755-0 1990 Combination of insulin with glipizide increases peripheral glucose disposal in secondary failure type 2 diabetic patients. Glucose 59-66 insulin Homo sapiens 15-22 2137755-10 1990 Combination of insulin with the sulphonylurea glipizide in secondary failure Type 2 diabetic patients leads to increased insulin-mediated peripheral glucose disposal. Glucose 149-156 insulin Homo sapiens 121-128 2137758-2 1990 Adjustments to insulin infusion rate are determined by trends in blood glucose as well as by absolute concentration, in order to approach normoglycaemia. Glucose 71-78 insulin Homo sapiens 15-22 2137755-2 1990 Endogenous insulin reserve was measured by glucagon stimulation, and insulin-mediated peripheral glucose disposal by a hyperglycaemic (11 mmol l-1) clamp, measurements being repeated after 8 weeks of glipizide or placebo therapy in addition to the patients" usual insulin. Glucose 97-104 insulin Homo sapiens 69-76 2137755-2 1990 Endogenous insulin reserve was measured by glucagon stimulation, and insulin-mediated peripheral glucose disposal by a hyperglycaemic (11 mmol l-1) clamp, measurements being repeated after 8 weeks of glipizide or placebo therapy in addition to the patients" usual insulin. Glucose 97-104 insulin Homo sapiens 69-76 2137755-5 1990 Insulin-mediated glucose disposal rose from 2.5 (1.5-8.0) (median (range] to 4.2 (2.3-8.4) mg kg-1 min-1 in the glipizide group (n = 9, p less than 0.01), but did not change in the placebo group. Glucose 17-24 insulin Homo sapiens 0-7 2227129-1 1990 The reduced postabsorptive rates of systemic glucose clearance in non-insulin-dependent diabetes mellitus (NIDDM) are thought to be the consequence of insulin resistance in peripheral tissues. Glucose 45-52 insulin Homo sapiens 70-77 2184062-7 1990 Activation of D-glucose transport was half-maximal at 49.6 +/- 5.4 pmol/l (diarginylinsulin), 44.8 +/- 5.8 pmol/l (insulin) and at 476.7 +/- 134.3 pmol/l (proinsulin). Glucose 14-23 insulin Homo sapiens 84-91 2184062-7 1990 Activation of D-glucose transport was half-maximal at 49.6 +/- 5.4 pmol/l (diarginylinsulin), 44.8 +/- 5.8 pmol/l (insulin) and at 476.7 +/- 134.3 pmol/l (proinsulin). Glucose 14-23 insulin Homo sapiens 155-165 2227129-2 1990 Although the peripheral tissues involved have not been identified, it is generally assumed to be primarily muscle, the major site of insulin-mediated glucose disposal. Glucose 150-157 insulin Homo sapiens 133-140 2227122-5 1990 When glucose uptake was increased further to 11.11 +/- 0.36 mg.kg-1 FFM.min-1 with less insulin (625 +/- 70 pM) and hyperglycemia, glucose oxidation (3.85 +/- 0.26 mg.kg-1 FFM.min-1) and nonoxidative glucose metabolism (7.26 +/- 0.51 mg.kg-1 FFM.min-1) rose significantly (both P less than 0.05 from matched studies at lower rates of glucose uptake). Glucose 5-12 insulin Homo sapiens 88-95 2227134-7 1990 In addition, dose-response analysis of insulin-stimulated glucose transport, receptor autophosphorylation, and pp185 phosphorylation resulted in ED50 values of 0.3, 12, and 12 ng/ml, respectively. Glucose 58-65 insulin Homo sapiens 39-46 2227135-4 1990 When synthetic human amylin was infused during clamp studies, it inhibited the ability of insulin to stimulate glucose disposal by 56% (96.9 +/- 9.4 vs. 42.4 +/- 5.0 mumol.kg-1.min-1, P less than 0.05) and to suppress hepatic glucose output by 64%. Glucose 111-118 insulin Homo sapiens 90-97 2404746-8 1990 In short-term experiments after 48-h culture with IL-6, there was a dose-dependent inhibition of the glucose-stimulated insulin release. Glucose 101-108 insulin Homo sapiens 120-127 2404746-11 1990 Islets cultured with human recombinant IL-1 beta (25 units/ml) showed a strong inhibition of the insulin accumulation in the culture medium and of glucose-stimulated insulin release and a marked decrease in the islet DNA and insulin content. Glucose 147-154 insulin Homo sapiens 166-173 1969348-8 1990 When, in analogy to insulin/glucose ratios, a diagnostic index was derived by multiplying the steady state glucose infusion rate by the steady state IR-insulin concentration, the diagnostic accuracy was greatly increased (sensitivity and specificity 0.94, respectively), but still lower than that of "amended" insulin/glucose ratios in fasting plasma or at the time of discontinuation of prolonged fasts (1.00). Glucose 107-114 insulin Homo sapiens 20-27 2404746-11 1990 Islets cultured with human recombinant IL-1 beta (25 units/ml) showed a strong inhibition of the insulin accumulation in the culture medium and of glucose-stimulated insulin release and a marked decrease in the islet DNA and insulin content. Glucose 147-154 insulin Homo sapiens 166-173 1969348-8 1990 When, in analogy to insulin/glucose ratios, a diagnostic index was derived by multiplying the steady state glucose infusion rate by the steady state IR-insulin concentration, the diagnostic accuracy was greatly increased (sensitivity and specificity 0.94, respectively), but still lower than that of "amended" insulin/glucose ratios in fasting plasma or at the time of discontinuation of prolonged fasts (1.00). Glucose 107-114 insulin Homo sapiens 20-27 2153707-1 1990 Insulin-stimulated glycogen synthase activity in human skeletal muscle correlates with insulin-mediated glucose disposal rate (M) and is reduced in insulin-resistant subjects. Glucose 104-111 insulin Homo sapiens 0-7 1967614-5 1990 However, similar elevations of the plasma G concentration did lead to higher values of Ra and plasma glucose, although the basal concentration of plasma insulin decreased the increases in Ra and plasma glucose caused by G. The ability of a similar amount of insulin to lower plasma FFA concentrations was greater in magnitude than the decrease in Ra. Glucose 202-209 insulin Homo sapiens 153-160 2153707-1 1990 Insulin-stimulated glycogen synthase activity in human skeletal muscle correlates with insulin-mediated glucose disposal rate (M) and is reduced in insulin-resistant subjects. Glucose 104-111 insulin Homo sapiens 87-94 2406330-7 1990 A decreased postprandial insulin release by calcitonin (mean +/- SEM area under the insulin curve 2,124.6 +/- 382.0 min mU L-1 after placebo versus 640.9 +/- 124.0 min mU L-1 after calcitonin; p less than 0.002) was accompanied by a different pattern of serum glucose concentrations during the infusion of the hormone when compared to the situation with a placebo. Glucose 260-267 insulin Homo sapiens 25-32 2406514-9 1990 Glucose transport was stimulated by insulin independently of cell cycle. Glucose 0-7 insulin Homo sapiens 36-43 2179752-1 1990 Insulin absorption and plasma concentrations of glucose and free insulin. Glucose 48-55 insulin Homo sapiens 0-7 2179752-2 1990 In 6 type 1 diabetic patients treated with a basal-prandial injection regimen with a pen, plasma concentrations of free insulin and glucose were measured over a period of 24 h. We obtained an insulin peak 1 h after injection of regular insulin and lower levels at night. Glucose 132-139 insulin Homo sapiens 192-199 2179752-2 1990 In 6 type 1 diabetic patients treated with a basal-prandial injection regimen with a pen, plasma concentrations of free insulin and glucose were measured over a period of 24 h. We obtained an insulin peak 1 h after injection of regular insulin and lower levels at night. Glucose 132-139 insulin Homo sapiens 192-199 2181421-3 1990 Until the time that a perfect and permanent indwelling glucose sensor can be developed and connected to an insulin infusing device, or much less toxic immunosuppressive drugs enable pancreatic or beta-cell transplantation on a wide basis, we should endeavor to provide the best possible care for our patients with this most difficult disease. Glucose 55-62 insulin Homo sapiens 107-114 2405235-2 1990 Insulin-mediated glucose disposal assessed with the euglycemic insulin clamp technique was significantly decreased in both non-obese (7.2 +/- 2.1 mg/kg/min; P less than .05) and obese hypertensives (5.1 +/- 2.1 mg/kg/min; P less than .01) compared with the controls (8.4 +/- 1.8 mg/kg/min). Glucose 17-24 insulin Homo sapiens 0-7 2405235-2 1990 Insulin-mediated glucose disposal assessed with the euglycemic insulin clamp technique was significantly decreased in both non-obese (7.2 +/- 2.1 mg/kg/min; P less than .05) and obese hypertensives (5.1 +/- 2.1 mg/kg/min; P less than .01) compared with the controls (8.4 +/- 1.8 mg/kg/min). Glucose 17-24 insulin Homo sapiens 63-70 2407006-9 1990 Static glucose stimulation showed excellent function (2-3-fold increase of insulin release over basal levels) with no statistical difference in insulin secretion between MIMS and HP islets. Glucose 7-14 insulin Homo sapiens 75-82 1966976-1 1990 The release of insulin evoked by D-glucose and other nutrient secretagogues in the pancreatic B-cell is causally linked to an increase in ATP generation rate. Glucose 33-42 insulin Homo sapiens 15-22 2180142-5 1990 If metabolic control improves insufficiently (fasting blood glucose depending on age greater than 8 to 11 mmol/l) insulin is indicated. Glucose 60-67 insulin Homo sapiens 114-121 2180142-7 1990 Monitoring fasting blood glucose, or HbA1c in the case of insulin therapy is necessary every 2 or 3 months. Glucose 25-32 insulin Homo sapiens 58-65 2405855-2 1990 In the present study we have investigated whether the compound is able to mimic insulin action on glucose metabolism in human fibroblasts. Glucose 98-105 insulin Homo sapiens 80-87 2405855-6 1990 Therefore the phospho-oligosaccharide appears to be able to strictly reproduce insulin action on glucose metabolism in human fibroblasts. Glucose 97-104 insulin Homo sapiens 79-86 2105656-0 1990 Dissociation of the effects of epinephrine and insulin on glucose and protein metabolism. Glucose 58-65 insulin Homo sapiens 47-54 2169826-6 1990 Insulin resistance appears to be familial and in at least some individuals antedates glucose intolerance. Glucose 85-92 insulin Homo sapiens 0-7 2405701-5 1990 Glucose infusion after 84 h of fasting restored glucose and insulin concentrations and lipolytic rates toward 12-h fasting values. Glucose 0-7 insulin Homo sapiens 60-67 2076025-2 1990 Serum levels of 3-hydroxybutyrate (3-OHBA), acetoacetate (AcAc) and 3-OHBA/AcAc ratio before breakfast were significantly increased in insulin-treated NIDDM patients with well-controlled fasting plasma glucose levels and IDDM patients compared to those in normal subjects. Glucose 202-209 insulin Homo sapiens 135-142 2404452-4 1990 The effects of insulin and ATP on pyruvate dehydrogenase were glucose-dependent whereas the effect of adenosine was glucose-independent. Glucose 62-69 insulin Homo sapiens 15-22 2190616-9 1990 Another biological property that is modulated in a predictable manner by agents which affect the bilayer-hexagonal phase equilibrium is insulin-promoted glucose uptake in adipocytes. Glucose 153-160 insulin Homo sapiens 136-143 2240459-11 1990 The kinetics of insulin and glucagon in DMD may help to maintain the glucose metabolism. Glucose 69-76 insulin Homo sapiens 16-23 2208752-1 1990 Patients with hypertension have been shown to be resistant to insulin-stimulated glucose uptake and hyperinsulinemic when compared to matched control groups with normal blood pressure. Glucose 81-88 insulin Homo sapiens 62-69 2279254-4 1990 The insulin-mediated glucose uptake during the clamp studies showed no variation after placebo or ibopamine therapy. Glucose 21-28 insulin Homo sapiens 4-11 2208753-6 1990 Insulin-mediated glucose metabolism within critical central neurons links dietary intake and central sympathetic outflow. Glucose 17-24 insulin Homo sapiens 0-7 2193770-1 1990 To examine the effect of excess growth hormones on carbohydrate metabolism, we studied glucose-stimulated insulin secretion and glucose utilization in 6 patients with acromegaly and 6 age-, sex- and weight-matched normal subjects. Glucose 87-94 insulin Homo sapiens 106-113 2407389-7 1990 Mean glucose levels were significantly elevated during insulin suppression. Glucose 5-12 insulin Homo sapiens 55-62 2103901-0 1990 Recovery from insulin-induced hypoglycemia after saccharose or glucose administration. Glucose 63-70 insulin Homo sapiens 14-21 2103901-10 1990 It is concluded that glucose acts faster than saccharose in insulin-induced hypoglycemia. Glucose 21-28 insulin Homo sapiens 60-67 2114252-1 1990 A novel spiral wound membrane sandwich (SWMS) design for an implantable bioartificial pancreas is presented and is numerically evaluated using a comprehensive model of the glucose-insulin kinetics within the device. Glucose 172-179 insulin Homo sapiens 180-187 2193770-5 1990 After glucose loading for 3 h, the acromegalic patients also had a higher incremental area under the curve of plasma glucose (p less than 0.05) and serum insulin (p less than 0.05). Glucose 6-13 insulin Homo sapiens 154-161 2193771-8 1990 Insulin increased glucose conversion to cell lipid by 3-fold. Glucose 18-25 insulin Homo sapiens 0-7 1967567-1 1990 Measurements were made of the plasma glucose and insulin responses to a 75 g oral glucose challenge in 50 Chinese born in Taiwan, divided into two groups on the basis of family history of Type 2 diabetes. Glucose 82-89 insulin Homo sapiens 49-56 1967567-3 1990 In addition, in vivo insulin action was estimated by determining the steady-state plasma glucose concentration during a 3-h continuous infusion of glucose, insulin, and somatostatin. Glucose 89-96 insulin Homo sapiens 21-28 2104796-7 1990 It is concluded that in healthy individuals rioprostil influences the basal and glucose-induced levels of glucagon, insulin, and somatostatin. Glucose 80-87 insulin Homo sapiens 116-123 1967567-3 1990 In addition, in vivo insulin action was estimated by determining the steady-state plasma glucose concentration during a 3-h continuous infusion of glucose, insulin, and somatostatin. Glucose 147-154 insulin Homo sapiens 21-28 1967567-4 1990 Steady-state plasma glucose concentration was used as a measure of insulin-induced glucose disposal. Glucose 20-27 insulin Homo sapiens 67-74 1967567-4 1990 Steady-state plasma glucose concentration was used as a measure of insulin-induced glucose disposal. Glucose 83-90 insulin Homo sapiens 67-74 1967567-6 1990 Plasma glucose and insulin concentrations in response to oral glucose were similar in the two groups. Glucose 62-69 insulin Homo sapiens 19-26 2137062-5 1990 After oral glucose there was an exaggerated rise in glucose, insulin, lactate, and pyruvate in patients with Impaired Glucose Tolerance. Glucose 11-18 insulin Homo sapiens 61-68 1967567-9 1990 The results support the view that resistance to insulin-stimulated glucose uptake is present in offspring of diabetic parents. Glucose 67-74 insulin Homo sapiens 48-55 2137065-3 1990 Insulin sensitivity was assessed by the glucose clamp technique with insulin doses of 40 (low dose) and 100 (high dose) mU m-2 min-1. Glucose 40-47 insulin Homo sapiens 0-7 2210052-6 1990 The elevated fasting C-peptide level persisted after adjustment for fasting serum glucose. Glucose 82-89 insulin Homo sapiens 21-30 2137065-4 1990 Glucose disposal rates were 2.5 +/- 0.3 (mean +/- SE) mg kg-1 min-1 during the follicular phase and 3.2 +/- 0.3 mg kg-1 min-1 in the luteal phase with low dose insulin, and 5.9 +/- 0.4 and 6.4 +/- 0.6 mg kg-1 min-1, respectively, with high dose insulin. Glucose 0-7 insulin Homo sapiens 160-167 2137065-4 1990 Glucose disposal rates were 2.5 +/- 0.3 (mean +/- SE) mg kg-1 min-1 during the follicular phase and 3.2 +/- 0.3 mg kg-1 min-1 in the luteal phase with low dose insulin, and 5.9 +/- 0.4 and 6.4 +/- 0.6 mg kg-1 min-1, respectively, with high dose insulin. Glucose 0-7 insulin Homo sapiens 245-252 2210057-5 1990 Matching glucose uptake at the higher rates (10 mg.kg-1 FFM.min-1) required greater than 300 pM of insulin (309 and 632 pM) in both studies and resulted in maximal suppression of FFA (49 vs. 46%, NS) and Fox (both greater than 90%, NS) and similar incremental Gox (2.89 vs. 2.73 mg.kg-1 FFM.min-1, NS) whether at hyperglycemia (15.7 mM) or euglycemia (5.2 mM). Glucose 9-16 insulin Homo sapiens 99-106 2210057-6 1990 Therefore, both hyperinsulinemia and hyperglycemia stimulate glucose uptake and increase intracellular glucose availability, but insulin also regulates Gox by suppression of FFA and Fox. Glucose 61-68 insulin Homo sapiens 21-28 2210057-6 1990 Therefore, both hyperinsulinemia and hyperglycemia stimulate glucose uptake and increase intracellular glucose availability, but insulin also regulates Gox by suppression of FFA and Fox. Glucose 103-110 insulin Homo sapiens 21-28 2210059-4 1990 Insulin-mediated total-body glucose uptake in poorly controlled diabetic subjects (3.6 +/- 0.5 mg.kg-1.min-1) was significantly reduced compared with control subjects (7.5 +/- 0.2 mg.kg-1.min-1; P less than .001) and improved slightly after insulin therapy (4.8 +/- 0.3 mg.kg-1.min-1; P less than .05), although it still remained significantly lower than in control subjects (P less than .01). Glucose 28-35 insulin Homo sapiens 0-7 2210059-4 1990 Insulin-mediated total-body glucose uptake in poorly controlled diabetic subjects (3.6 +/- 0.5 mg.kg-1.min-1) was significantly reduced compared with control subjects (7.5 +/- 0.2 mg.kg-1.min-1; P less than .001) and improved slightly after insulin therapy (4.8 +/- 0.3 mg.kg-1.min-1; P less than .05), although it still remained significantly lower than in control subjects (P less than .01). Glucose 28-35 insulin Homo sapiens 241-248 2210059-9 1990 In conclusion, insulin-mediated glucose metabolism is severely impaired in subjects with both poorly controlled and well-controlled IDDM, whereas the effect of acute insulin infusion on leucine turnover is normal, and combined hyperaminoacidemia/hyperinsulinemia stimulated NOLD to a similar extent in both IDDM and control subjects. Glucose 32-39 insulin Homo sapiens 15-22 2210061-8 1990 The adipocyte/muscle transporter is expressed exclusively in tissues that are insulin sensitive with respect to glucose uptake. Glucose 112-119 insulin Homo sapiens 78-85 2404722-5 1990 Patients had lower total-body insulin-mediated glucose metabolism compared with control subjects (33.9 +/- 14.3 vs. 63.8 +/- 17.2 mumol.kg-1.min-1, P = 0.0002). Glucose 47-54 insulin Homo sapiens 30-37 2404714-7 1990 In addition, insulin-stimulated glucose uptake measured during hyperinsulinemic clamp studies was similar before and after metformin treatment. Glucose 32-39 insulin Homo sapiens 13-20 2139397-1 1990 A simple, unbiased insulin-varying glucose clamp program is described. Glucose 35-42 insulin Homo sapiens 19-26 2139397-4 1990 We present a method which uses an iterative computer program to predict changes in insulin infusion rate required for glucose clamping. Glucose 118-125 insulin Homo sapiens 83-90 2139397-10 1990 Cross-correlation showed that insulin had its maximal effect on the rate of decline of glucose after 15 min, and the nadir of glucose occurred 45 min after a change in insulin infusion rate. Glucose 87-94 insulin Homo sapiens 30-37 2139397-10 1990 Cross-correlation showed that insulin had its maximal effect on the rate of decline of glucose after 15 min, and the nadir of glucose occurred 45 min after a change in insulin infusion rate. Glucose 126-133 insulin Homo sapiens 168-175 2194890-8 1990 Insulin responsiveness, defined as the "glucose consumption: plasma insulin concentration" ratio was reduced in cirrhotics at 7.78 mmol/l (p less than 0.01), but was the same in both groups at 13.80 mmol/l because of a more important enhancement in cirrhotics, reflecting an improvement of insulin action probably at the post-receptor level and of non-insulin-mediated glucose transport. Glucose 40-47 insulin Homo sapiens 0-7 2194890-8 1990 Insulin responsiveness, defined as the "glucose consumption: plasma insulin concentration" ratio was reduced in cirrhotics at 7.78 mmol/l (p less than 0.01), but was the same in both groups at 13.80 mmol/l because of a more important enhancement in cirrhotics, reflecting an improvement of insulin action probably at the post-receptor level and of non-insulin-mediated glucose transport. Glucose 369-376 insulin Homo sapiens 0-7 2227238-5 1990 These results can be related to insulin resistance as attested by a larger increase of glucose and insulin levels in cirrhotics than in controls (p less than 0.001 and p less than 0.001, respectively). Glucose 87-94 insulin Homo sapiens 32-39 2074089-2 1990 With respect to weight-matched controls, patients with CF exhibited a significantly lower glucose tolerance and a globally preserved, although delayed, insulin response to oral glucose tolerance test, while first-phase insulin secretion after i.v. Glucose 177-184 insulin Homo sapiens 152-159 2074090-2 1990 Adipocytes isolated from overnight-fasted obese and NIDDM patients revealed high levels of [Ca2+]i (p less than 0.05 vs. control) in association with a decreased insulin-stimulated glucose uptake (p less than 0.05 vs. controls). Glucose 181-188 insulin Homo sapiens 162-169 2088976-1 1990 Although the human fetal pancreas early in the second trimester of pregnancy contains functional beta cells, its ability to release insulin in response to glucose is either poor or lacking. Glucose 155-162 insulin Homo sapiens 132-139 2095356-1 1990 Fasting insulin concentration and the insulin response to an oral glucose tolerance test were measured in 15 women with polycystic ovary syndrome (PCOS) and 6 weight-matched normal women. Glucose 66-73 insulin Homo sapiens 38-45 2095356-3 1990 Insulin response to an oral glucose test was significantly decreased (p less than 0.05) in PCOS at 30 min, although 63% of these women had mild impairment of glucose tolerance. Glucose 28-35 insulin Homo sapiens 0-7 2202631-1 1990 Early antihypertensive intervention in diabetes often means intervention in a cluster of cardiovascular risk factors including glucose intolerance per se, hyperlipidemia, obesity and hypertension, which are not just coexistent but may be causally linked together by the resistance of peripheral tissues to the action of insulin. Glucose 127-134 insulin Homo sapiens 320-327 2210626-1 1990 It is now widely accepted that insulin stimulates glucose metabolism in its target tissues via recruitment of transporters from a large intracellular pool to the plasma membrane. Glucose 50-57 insulin Homo sapiens 31-38 2272613-4 1990 This strategy comprises the following components: (1) a validated model of the physiological glucose-insulin regulatory system; (2) a procedure for identifying the metabolic situation of a given patient in terms of the model parameters; (3) methods of estimating the pharmacokinetics of insulin and its effect on glycemia, the absorption profiles of ingested glucose equivalents, and the effect of exercise as expressed in equivalents of insulin action; (4) computer procedures of prospective simulation of glycemic profiles around the day under the influence of selected or proposed therapeutic regimes. Glucose 93-100 insulin Homo sapiens 101-108 2272619-4 1990 It facilitates self-care by calculating insulin dosages each day at each meal based on glucose measurements made by the patients themselves. Glucose 87-94 insulin Homo sapiens 40-47 2272627-5 1990 We conclude that this modification of the minimal model may improve the number of intravenous glucose tolerance tests capable of systematic analysis in NIDDM subjects, giving a measure of insulin sensitivity that correlates with more established measures of this parameter. Glucose 94-101 insulin Homo sapiens 188-195 2272628-1 1990 In vivo measurement of insulin sensitivity can be made using the glucose clamp technique or the intravenous glucose tolerance test (IVGTT) with minimal model analysis. Glucose 65-72 insulin Homo sapiens 23-30 2272628-1 1990 In vivo measurement of insulin sensitivity can be made using the glucose clamp technique or the intravenous glucose tolerance test (IVGTT) with minimal model analysis. Glucose 108-115 insulin Homo sapiens 23-30 2272628-2 1990 The glucose clamp provides a direct, readily understandable measure of insulin action but is more demanding for investigators and subjects. Glucose 4-11 insulin Homo sapiens 71-78 2272629-3 1990 By comparing a patient"s basal plasma glucose and insulin (or C-peptide) concentrations with the predictions of a basal homeostatic model, the degree of impairment of beta-cell function and insulin sensitivity can be assessed. Glucose 38-45 insulin Homo sapiens 190-197 2272632-6 1990 In order to maintain normal blood glucose levels he will have to reduce the regular insulin bolus 3) in the morning by -3,3 IU or 4) by -1.7 IU in the evening or he should 5) take +12 g of oral glucose (quickly absorbable carbohydrates). Glucose 34-41 insulin Homo sapiens 84-91 2272633-0 1990 Impact of activated glucose counterregulation on insulin requirements in insulin-dependent diabetes mellitus. Glucose 20-27 insulin Homo sapiens 49-56 2272633-1 1990 The glucose counterregulatory system is one of the most important homeostatic systems in physiology, since it normally prevents hypoglycaemia or, should it occur for any reason such as insulin administration, limits the severity of hypoglycaemia and ultimately may restore normoglycaemia. Glucose 4-11 insulin Homo sapiens 185-192 2272634-7 1990 By viewing blood glucose from this innovative perspective it may be possible to reexamine the relationship between insulin dose and glucose level and thereby improve clinical decision-making. Glucose 17-24 insulin Homo sapiens 115-122 2179148-5 1990 Exercise training induced a significant reduction in fasting levels and in the responses of insulin to a 4.2 MJ meal or an oral glucose load. Glucose 128-135 insulin Homo sapiens 92-99 2230357-6 1990 Impaired insulin release was detected in 21% of the 28 patients examined following ingestion of oral glucose. Glucose 101-108 insulin Homo sapiens 9-16 2230357-8 1990 The serum-insulin, serum-C-peptide and insulin/glucose pattern following an oral glucose load reflected the degree of severity of pancreatitis changes at ERP. Glucose 81-88 insulin Homo sapiens 39-46 1369702-7 1990 Baseline insulin output in vitro was 86 +/- 22 ng/min at 8.0 mM glucose and 2.5 mM calcium. Glucose 64-71 insulin Homo sapiens 9-16 1967178-4 1990 Diabetic subjects were studied during continuous iv insulin infusion, which normalized glucose kinetics before experimental perturbations. Glucose 87-94 insulin Homo sapiens 52-59 1967178-8 1990 However, insulin infusion at doses that normalized the portal insulin concentration (approximately 208 pmol/L) together with glucagon replacement inhibited the rise in glucose production in both normal and IDDM subjects. Glucose 168-175 insulin Homo sapiens 9-16 2199567-6 1990 Fasting capillary plasma glucose value was higher in women with macrosomic newborns (5.3 mmol/l +/- 0.4 vs 4.8 mmol/l +/- 0.4; p less than 0.01) as well as fasting capillary plasma insulin concentration (28.7 mU/L +/- 9.3 vs 17.7 mU/L +/- 6.4; p less than 0.01). Glucose 25-32 insulin Homo sapiens 181-188 2175823-1 1990 Insulin secretion from beta cells of the islets of Langerhans in the endocrine pancreas is regulated by glucose, glucose metabolites, metabolic intermediates such as ATP, acetyl CoA and reduced pyridine nucleotides, and classical second messengers. Glucose 104-111 insulin Homo sapiens 0-7 2175823-1 1990 Insulin secretion from beta cells of the islets of Langerhans in the endocrine pancreas is regulated by glucose, glucose metabolites, metabolic intermediates such as ATP, acetyl CoA and reduced pyridine nucleotides, and classical second messengers. Glucose 113-120 insulin Homo sapiens 0-7 2403623-1 1990 The secretory behavior of insulin- and glucagon-producing cells was found to be perturbed in isolated perfused pancreases removed from rats infused with hypertonic solutions of glucose for 48 hours. Glucose 177-184 insulin Homo sapiens 26-33 2403623-3 1990 Likewise, in isolated islets prepared from the glucose-infused rats, L-arginine or theophylline stimulated insulin release at a low ambient concentration of D-glucose, at variance with the situation found in islets removed from normal rats. Glucose 47-54 insulin Homo sapiens 107-114 2403623-3 1990 Likewise, in isolated islets prepared from the glucose-infused rats, L-arginine or theophylline stimulated insulin release at a low ambient concentration of D-glucose, at variance with the situation found in islets removed from normal rats. Glucose 157-166 insulin Homo sapiens 107-114 2098841-5 1990 The abolished postprandial insulin release by calcitonin was accompanied by a different pattern of serum glucose concentration, when compared to the situation with placebo. Glucose 105-112 insulin Homo sapiens 27-34 2136545-5 1990 Irrespective of the overweight magnitude and the degree of glucose tolerance impairment a more pronounced insulin reaction to glucose was observed. Glucose 59-66 insulin Homo sapiens 106-113 1971732-0 1990 Late effect of tobanum and tobanum + furosemide therapy on the glucose tolerance of patients and on the insulin response to oral glucose doses. Glucose 129-136 insulin Homo sapiens 104-111 2205072-3 1990 The treatment with insulin was necessary to be applied on 70 of the patients (69.3%) in order to achieve normal glucose levels (between 3.3 and 6.6 mmol/l). Glucose 112-119 insulin Homo sapiens 19-26 2404717-3 1990 In MODY patients with low insulin responses, there are delayed and decreased insulin and C-peptide secretory responses to glucose from childhood or adolescence even before glucose intolerance appears, which may represent the basic genetic defect. Glucose 122-129 insulin Homo sapiens 89-98 2404717-6 1990 In a few patients, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they resemble those of early insulin-dependent diabetes mellitus. Glucose 94-101 insulin Homo sapiens 59-66 2404717-6 1990 In a few patients, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they resemble those of early insulin-dependent diabetes mellitus. Glucose 94-101 insulin Homo sapiens 71-80 2404717-8 1990 In contrast are patients from families who have very high insulin responses to glucose, despite glucose intolerance and fasting hyperglycemia similar to that seen in patients with low insulin responses. Glucose 79-86 insulin Homo sapiens 58-65 2404717-12 1990 In a few MODY pedigrees with high insulin responses to glucose and lack of evidence of insulin resistance, a structurally abnormal mutant insulin molecule that is biologically ineffective is secreted. Glucose 55-62 insulin Homo sapiens 34-41 2404722-1 1990 The relationship of in vivo insulin-mediated glucose utilization to the state of physical fitness and the degree of glycemic control was examined in 27 adolescents with insulin-dependent diabetes mellitus (IDDM) compared with 10 nondiabetic adolescent control subjects. Glucose 45-52 insulin Homo sapiens 28-35 2404722-2 1990 In vivo total-body insulin-mediated glucose metabolism was evaluated by the hyperinsulinemic-euglycemic clamp. Glucose 36-43 insulin Homo sapiens 19-26 2651385-3 1989 In T and UT-ex compared with UT, sensitivity for insulin-mediated whole-body glucose uptake was higher [insulin concentrations eliciting half-maximal glucose uptake being 44 +/- 2 (T) and 43 +/- 4 (UT-ex) vs. 52 +/- 3 microU/ml (UT), P less than 0.05] and responsiveness was higher [13.4 +/- 1.2 (T) and 10.9 +/- 0.7 (UT-ex) vs. 9.5 +/- 0.7 mg.min-1.kg-1 (UT), P less than 0.05]. Glucose 77-84 insulin Homo sapiens 49-56 2651385-3 1989 In T and UT-ex compared with UT, sensitivity for insulin-mediated whole-body glucose uptake was higher [insulin concentrations eliciting half-maximal glucose uptake being 44 +/- 2 (T) and 43 +/- 4 (UT-ex) vs. 52 +/- 3 microU/ml (UT), P less than 0.05] and responsiveness was higher [13.4 +/- 1.2 (T) and 10.9 +/- 0.7 (UT-ex) vs. 9.5 +/- 0.7 mg.min-1.kg-1 (UT), P less than 0.05]. Glucose 77-84 insulin Homo sapiens 104-111 2651385-3 1989 In T and UT-ex compared with UT, sensitivity for insulin-mediated whole-body glucose uptake was higher [insulin concentrations eliciting half-maximal glucose uptake being 44 +/- 2 (T) and 43 +/- 4 (UT-ex) vs. 52 +/- 3 microU/ml (UT), P less than 0.05] and responsiveness was higher [13.4 +/- 1.2 (T) and 10.9 +/- 0.7 (UT-ex) vs. 9.5 +/- 0.7 mg.min-1.kg-1 (UT), P less than 0.05]. Glucose 150-157 insulin Homo sapiens 49-56 2651385-3 1989 In T and UT-ex compared with UT, sensitivity for insulin-mediated whole-body glucose uptake was higher [insulin concentrations eliciting half-maximal glucose uptake being 44 +/- 2 (T) and 43 +/- 4 (UT-ex) vs. 52 +/- 3 microU/ml (UT), P less than 0.05] and responsiveness was higher [13.4 +/- 1.2 (T) and 10.9 +/- 0.7 (UT-ex) vs. 9.5 +/- 0.7 mg.min-1.kg-1 (UT), P less than 0.05]. Glucose 150-157 insulin Homo sapiens 104-111 2651385-5 1989 Insulin-stimulated O2 uptake and maximal glucose oxidation rate were higher in T than in UT and UT-ex. Glucose 41-48 insulin Homo sapiens 0-7 2651385-6 1989 Insulin-stimulated conversion or glucose to glycogen and muscle glycogen synthase was higher in T than in UT and UT-ex. Glucose 33-40 insulin Homo sapiens 0-7 2651385-9 1989 It is concluded that physical training induces an adaptive increase in insulin responsiveness of whole-body glucose uptake, which does not reflect increased glycogen deposition in muscle. Glucose 108-115 insulin Homo sapiens 71-78 2404722-6 1990 Among the patients, females had lower total-body insulin-mediated glucose metabolism compared with males (24.2 +/- 2.8 vs. 40.7 +/- 3.4 mumol.kg-1.min-1, P less than 0.001); however, this difference disappeared after correcting for sex differences in fitness levels. Glucose 66-73 insulin Homo sapiens 49-56 3311855-7 1987 Glucose uptake at the lower insulin infusion rate also showed familial aggregation (P less than .01), with family membership independently accounting for approximately 15% of the variance of this measurement. Glucose 0-7 insulin Homo sapiens 28-35 3529778-1 1986 In 9 healthy subjects we evaluated the effect of a constant ranitidine infusion (100 mg) on glucose (mg/dl), insulin (microU/ml) and C-peptide (ng/ml) serum levels promoted by oral glucose tolerance test (75 g). Glucose 181-188 insulin Homo sapiens 109-116 3529778-1 1986 In 9 healthy subjects we evaluated the effect of a constant ranitidine infusion (100 mg) on glucose (mg/dl), insulin (microU/ml) and C-peptide (ng/ml) serum levels promoted by oral glucose tolerance test (75 g). Glucose 181-188 insulin Homo sapiens 133-142 7011721-0 1981 Biosynthetic human insulin: effect in healthy men on plasma glucose and non-esterified fatty acids in comparison with highly purified pork insulin. Glucose 60-67 insulin Homo sapiens 19-26 33765181-3 2021 We previously found that fetuin-A, a hepatokine increasingly secreted by the fatty liver and a determinant of type 2 diabetes, inhibits glucose-stimulated insulin secretion (GSIS) of human islets. Glucose 136-143 insulin Homo sapiens 155-162 33766485-3 2021 Under physiological conditions insulin regulates glucose homeostasis by enhancing glucose disposal in insulin sensitive tissues while also regulating delivery of nutrients through its vasodilation actions on small feed arteries. Glucose 49-56 insulin Homo sapiens 31-38 33766485-3 2021 Under physiological conditions insulin regulates glucose homeostasis by enhancing glucose disposal in insulin sensitive tissues while also regulating delivery of nutrients through its vasodilation actions on small feed arteries. Glucose 49-56 insulin Homo sapiens 102-109 33766485-4 2021 Specifically, insulin-mediated production of nitric oxide from the vascular endothelium leads to increased blood flow enhancing disposal of glucose. Glucose 140-147 insulin Homo sapiens 14-21 33766485-5 2021 Typically, insulin resistance is considered as a decrease in sensitivity or responsiveness to the metabolic actions of insulin including insulin-mediated glucose disposal. Glucose 154-161 insulin Homo sapiens 11-18 33766485-5 2021 Typically, insulin resistance is considered as a decrease in sensitivity or responsiveness to the metabolic actions of insulin including insulin-mediated glucose disposal. Glucose 154-161 insulin Homo sapiens 119-126 33766485-5 2021 Typically, insulin resistance is considered as a decrease in sensitivity or responsiveness to the metabolic actions of insulin including insulin-mediated glucose disposal. Glucose 154-161 insulin Homo sapiens 119-126 2404722-7 1990 Insulin-mediated glucose metabolism correlated with VO2 max in patients and control subjects (r = 0.83, r = 0.81, P less than 0.05). Glucose 17-24 insulin Homo sapiens 0-7 2404722-8 1990 The regression of total-body insulin-mediated glucose metabolism on VO2 max for patients was -2.84 +/- 0.255 VO2 max and for control subjects was 7.12 +/- 0.143 VO2 max, indicating that for similar degrees of physical fitness patients have lower total body insulin-mediated glucose metabolism levels than control subjects. Glucose 46-53 insulin Homo sapiens 29-36 2404722-8 1990 The regression of total-body insulin-mediated glucose metabolism on VO2 max for patients was -2.84 +/- 0.255 VO2 max and for control subjects was 7.12 +/- 0.143 VO2 max, indicating that for similar degrees of physical fitness patients have lower total body insulin-mediated glucose metabolism levels than control subjects. Glucose 46-53 insulin Homo sapiens 257-264 2404722-8 1990 The regression of total-body insulin-mediated glucose metabolism on VO2 max for patients was -2.84 +/- 0.255 VO2 max and for control subjects was 7.12 +/- 0.143 VO2 max, indicating that for similar degrees of physical fitness patients have lower total body insulin-mediated glucose metabolism levels than control subjects. Glucose 274-281 insulin Homo sapiens 29-36 2404722-9 1990 In patients, total-body insulin-mediated glucose metabolism correlated with the degree of glycemic control as assessed by the level of glycosylated hemoglobin (r = -0.63, P less than 0.001). Glucose 41-48 insulin Homo sapiens 24-31 2406181-5 1990 Insulin sensitivity decreased at dawn as compared to the early night hours (approximately 30% increase in the rate of hepatic glucose production, approximately 25% decrease in the rate of peripheral glucose utilisation). Glucose 126-133 insulin Homo sapiens 0-7 2406181-5 1990 Insulin sensitivity decreased at dawn as compared to the early night hours (approximately 30% increase in the rate of hepatic glucose production, approximately 25% decrease in the rate of peripheral glucose utilisation). Glucose 199-206 insulin Homo sapiens 0-7 2407482-7 1990 The nadir in plasma glucose occurred at 45 min following porcine insulin and at 90 min following human insulin injection. Glucose 20-27 insulin Homo sapiens 65-72 2407482-7 1990 The nadir in plasma glucose occurred at 45 min following porcine insulin and at 90 min following human insulin injection. Glucose 20-27 insulin Homo sapiens 103-110 33813879-2 2021 This physiologic distribution is lost when insulin is injected subcutaneously, causing impaired regulation of hepatic glucose production and whole body glucose uptake, as well as arterial hyperinsulinemia. Glucose 118-125 insulin Homo sapiens 43-50 33779055-0 2021 Natural triterpenoids isolated from Akebia trifoliata Stem Explants exerts hypoglycemic effect via inhibits alpha-glucosidase and stimulates glucose uptake in insulin-resistance HepG2 cells. Glucose 141-148 insulin Homo sapiens 159-166 33941550-3 2021 Factors associated with intensive glycemic management and using glucose-lowering medications associated with a high risk of hypoglycemia (high-risk medications (insulin, sulfonylureas, and meglitinides)) were also assessed. Glucose 64-71 insulin Homo sapiens 161-168 33811688-6 2021 Deficient TRAPbeta/SSR2 or TRAPdelta/SSR4 is not associated with any apparent defect of exocytotic mechanism but rather by a decreased abundance of the proinsulin and insulin that accompanies glucose-stimulated secretion. Glucose 192-199 insulin Homo sapiens 152-162 33811688-6 2021 Deficient TRAPbeta/SSR2 or TRAPdelta/SSR4 is not associated with any apparent defect of exocytotic mechanism but rather by a decreased abundance of the proinsulin and insulin that accompanies glucose-stimulated secretion. Glucose 192-199 insulin Homo sapiens 155-162 33764170-4 2021 A 75 g oral glucose tolerance test was performed at baseline (PreBR), after bed rest (PostBR) and rehabilitation (PostRehab) and used to calculate an indicator of insulin sensitivity, metabolic clearance rate. Glucose 12-19 insulin Homo sapiens 163-170 33784187-2 2021 In the AHCL MiniMed 780G system, different algorithm glucose targets for insulin infusion are available and autocorrection boluses are delivered. Glucose 53-60 insulin Homo sapiens 73-80 33769519-7 2021 Glucose consumption assays showed that the bioactivity of entrapped insulin was maintained post-incubation in the enzymatic medium. Glucose 0-7 insulin Homo sapiens 68-75 33765416-5 2021 We further provide our views regarding the timing, dominance, and physiological relevance of these effects and discuss novel concepts regarding insulin regulation of adipose tissue fatty acid metabolism and central nervous system (CNS) signaling to the liver, as regulators of insulin"s extrahepatic effects on glucose production. Glucose 311-318 insulin Homo sapiens 144-151 33821970-1 2021 Loss of the insulin-stimulated glucose uptake in muscle is a crucial event participating in the defect of whole-body metabolism in type 2 diabetes. Glucose 31-38 insulin Homo sapiens 12-19 33765416-5 2021 We further provide our views regarding the timing, dominance, and physiological relevance of these effects and discuss novel concepts regarding insulin regulation of adipose tissue fatty acid metabolism and central nervous system (CNS) signaling to the liver, as regulators of insulin"s extrahepatic effects on glucose production. Glucose 311-318 insulin Homo sapiens 277-284 33812901-1 2021 AIMS: The triglyceride glucose (TyG) index is a marker of insulin resistance. Glucose 23-30 insulin Homo sapiens 58-65 33769945-2 2021 Diabetes and technologies supporting diabetes care as devices monitoring glucose, software analyzing glucose data, and systems delivering insulin are examples of how it is possible to develop remote and structured disease management. Glucose 73-80 insulin Homo sapiens 138-145 33769945-2 2021 Diabetes and technologies supporting diabetes care as devices monitoring glucose, software analyzing glucose data, and systems delivering insulin are examples of how it is possible to develop remote and structured disease management. Glucose 101-108 insulin Homo sapiens 138-145 33786869-1 2021 AIMS: The aim of this study was to determine whether the metabolic glucose profile, based on glycaemic control and insulin requirements, was different in women with gestational diabetes mellitus (GDM) and intrahepatic cholestasis of pregnancy (ICP) compared to women with only GDM. Glucose 67-74 insulin Homo sapiens 115-122 33800541-0 2021 Prediction of Insulin Resistance by Modified Triglyceride Glucose Indices in Youth. Glucose 58-65 insulin Homo sapiens 14-21 33808310-4 2021 Thus, in beta cells, mitochondria play a pivotal role in regulating glucose stimulated insulin secretion (GSIS). Glucose 68-75 insulin Homo sapiens 87-94 33779307-0 2021 In vitro chronic glycation induces AGEs accumulation reducing insulin stimulated glucose uptake and increasing GLP1R in adipocytes. Glucose 81-88 insulin Homo sapiens 62-69 33779307-6 2021 These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake. Glucose 123-130 insulin Homo sapiens 105-112 33779307-6 2021 These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake. Glucose 241-248 insulin Homo sapiens 105-112 33779714-4 2021 KEY FINDINGS: Insulin treatment significantly enhanced the protein expressions of RhoA and Rho kinase (ROCK1 and ROCK2), but decreased glucose consumption. Glucose 135-142 insulin Homo sapiens 14-21 33774848-5 2021 Insulin sensitivity will be determined by the 2-step hyperinsulinaemic-euglycaemic clamp method with deuterated glucose to document liver, muscle and adipose insulin sensitivity. Glucose 112-119 insulin Homo sapiens 0-7 33774848-7 2021 The primary outcome is change in hepatic insulin sensitivity, assessed by change in basal rate of appearance (Ra) of glucose and suppression of endogenous glucose production (EGP) during the low-dose stage of the clamp. Glucose 117-124 insulin Homo sapiens 41-48 33774848-7 2021 The primary outcome is change in hepatic insulin sensitivity, assessed by change in basal rate of appearance (Ra) of glucose and suppression of endogenous glucose production (EGP) during the low-dose stage of the clamp. Glucose 155-162 insulin Homo sapiens 41-48 33801784-9 2021 ANCOVA (r2 = 0.68, p = 0.01) identified dextrose and pH as significant factors influencing insulin stability. Glucose 40-48 insulin Homo sapiens 91-98 33801784-11 2021 The influence of dextrose content suggests that insulin glycation may influence stability. Glucose 17-25 insulin Homo sapiens 48-55 33770092-1 2021 The artificial pancreas is a closed-loop insulin delivery system that automatically regulates glucose levels in individuals with type 1 diabetes. Glucose 94-101 insulin Homo sapiens 41-48 33778936-3 2021 Glucose and sodium levels were normalized following treatment with intravenous fluids, mainly Ringer"s lactate solution and insulin infusion with an initial rate of 0,5 IU/kg/h. Glucose 0-7 insulin Homo sapiens 124-131 33806797-4 2021 Here, we have centered our focus on insulin signaling in skeletal muscle, which is the main site of postprandial glucose disposal in humans. Glucose 113-120 insulin Homo sapiens 36-43 33806715-8 2021 Brain glucose uptake during insulin clamp was not different by gene allele, and it correlated with the M value, in both the rs17782313-C allele carriers and non-carriers. Glucose 6-13 insulin Homo sapiens 28-35 33813244-0 2021 Lower versus standard sucrose dose for treating hypoglycemia in patients with type 1 diabetes mellitus in therapy with predictive low glucose suspend (PLGS) augmented insulin pumps: A randomized crossover trial in Santiago, Chile. Glucose 134-141 insulin Homo sapiens 167-174 33776458-0 2021 A Difference Between Bedtime and Pre-Breakfast Plasma Glucose Levels Indicates the Need for Prandial Insulin in Basal Insulin-Treated Type 2 Diabetic Patients with Normal Fasting Glucose. Glucose 54-61 insulin Homo sapiens 101-108 33776458-0 2021 A Difference Between Bedtime and Pre-Breakfast Plasma Glucose Levels Indicates the Need for Prandial Insulin in Basal Insulin-Treated Type 2 Diabetic Patients with Normal Fasting Glucose. Glucose 54-61 insulin Homo sapiens 118-125 33807619-11 2021 The experimental data provide proof-of-concept for liver-targeted insulin as a way of enhancing glucose therapy for AIP. Glucose 96-103 insulin Homo sapiens 66-73 33815283-1 2021 Glucose and free fatty acids (FFA) are essential nutrients that are both partly regulated by insulin. Glucose 0-7 insulin Homo sapiens 93-100 33767671-9 2021 On the contrary, pre-pregnancy BMI <25 and normal fasting plasma glucose values at OGTT were found to be significantly associated to the use of rapid insulin analogue only. Glucose 65-72 insulin Homo sapiens 150-157 33769715-8 2021 HDL as well as S1P treatment enhanced glucose-stimulated insulin secretion (GSIS). Glucose 38-45 insulin Homo sapiens 57-64 33806355-0 2021 Toxicity Induced by Cytokines, Glucose, and Lipids Increase Apoptosis and Hamper Insulin Secretion in the 1.1E7 Beta Cell-Line. Glucose 31-38 insulin Homo sapiens 81-88 33806355-1 2021 Basic research on types 1 and 2 diabetes mellitus require early stage studies using beta cells or cell lines, ideally of human origin and with preserved insulin secretion in response to glucose. Glucose 186-193 insulin Homo sapiens 153-160 33806355-2 2021 The 1.1E7 cells are a hybrid cell line resulting from the electrofusion of dispersed human islets and PANC-1 cells, capable of secreting insulin in response to glucose, but their survival and function under toxic conditions remains untested. Glucose 160-167 insulin Homo sapiens 137-144 33802289-2 2021 beta-cell mitochondria sense and shape calcium signals, linking the metabolism of glucose and other secretagogues to the generation of signals that promote insulin secretion during nutrient stimulation. Glucose 82-89 insulin Homo sapiens 156-163 33813236-0 2021 Efficacy and safety of sensor augmented insulin pump therapy with low-glucose suspend feature in older adults: A retrospective study in Bogota, Colombia. Glucose 70-77 insulin Homo sapiens 40-47 33776619-0 2021 A comparison of meal tolerance test and oral glucose tolerance test for predicting insulin therapy in patients with gestational diabetes. Glucose 45-52 insulin Homo sapiens 83-90 33776619-1 2021 Aims: To identify factors predicting a need for insulin therapy in gestational diabetes mellitus (GDM) by comparing plasma glucose (PG) levels in a 75-g oral glucose tolerance test (75-g OGTT) with those in a 500-kcal meal tolerance test (MTT) containing 75 g of carbohydrate. Glucose 123-130 insulin Homo sapiens 48-55 33813236-3 2021 METHODS: A retrospective cohort study was conducted in patients >=60 years-old with DM1 and DM2, who started Sensor Augmented Insulin Pump therapy with low-glucose suspend feature (SAP + LGS) at Hospital Universitario San Ignacio diabetes center in Bogota, Colombia. Glucose 156-163 insulin Homo sapiens 126-133 33590375-7 2021 Compared to no OSA, participants with OSA presented higher levels while fasting and after 2 h glucose load of insulin, HOMA-IR, cholesterol, triglycerides, and C-reactive protein (all p < 0.001). Glucose 94-101 insulin Homo sapiens 110-117 33814450-4 2021 OBJECTIVE: Explore potential associations between levels of plasma insulin and glucose with previously acquired plasma apoE, cerebral metabolic rate of glucose (CMRgl), gray matter volume, and neuropsychological test scores. Glucose 79-86 insulin Homo sapiens 67-74 33033064-1 2021 The aim of the present study was to evaluate the effect of sustained physiologic increase ~50 mg/dl in plasma glucose concentration on insulin secretion in normal glucose tolerant (NGT) subjects. Glucose 110-117 insulin Homo sapiens 135-142 33033064-6 2021 Insulin secretion/insulin resistance (disposition) index declined by 60% (2nd clamp step) and by 62% following arginine (both p<0.005) following 72 hour glucose infusion. Glucose 153-160 insulin Homo sapiens 0-7 33033064-6 2021 Insulin secretion/insulin resistance (disposition) index declined by 60% (2nd clamp step) and by 62% following arginine (both p<0.005) following 72 hour glucose infusion. Glucose 153-160 insulin Homo sapiens 18-25 33033064-7 2021 The effect of 72 hour glucose infusion on insulin secretion and insulin sensitivity was similar in subjects with and without FH of T2DM. Glucose 22-29 insulin Homo sapiens 42-49 33814450-4 2021 OBJECTIVE: Explore potential associations between levels of plasma insulin and glucose with previously acquired plasma apoE, cerebral metabolic rate of glucose (CMRgl), gray matter volume, and neuropsychological test scores. Glucose 152-159 insulin Homo sapiens 67-74 33814450-10 2021 CONCLUSION: Plasma apoE3 but not apoE4 may be involved in insulin-independent processes governing plasma glucose levels. Glucose 105-112 insulin Homo sapiens 58-65 33232934-1 2020 Healthy pancreatic beta-cells adapt to systemic insulin resistance to maintain normal blood glucose levels, and a failure of this adaptation leads to type 2 diabetes in humans. Glucose 92-99 insulin Homo sapiens 48-55 33235302-9 2020 In functional assays, ALA treatment abrogated significantly the tunicamycin-mediated transcriptional activation of ATF6 while it enhanced the insulin-stimulated glucose uptake and Glut4 translocation. Glucose 161-168 insulin Homo sapiens 142-149 33234146-1 2020 BACKGROUND: The triglyceride glucose (TyG) index is an inexpensive clinical surrogate marker for insulin resistance. Glucose 29-36 insulin Homo sapiens 97-104 33235302-11 2020 Furthermore, the effect of ALA on insulin-stimulated glucose uptake is significantly reduced in C2C12 and HepG2 cells transfected with DNAJB3 siRNA. Glucose 53-60 insulin Homo sapiens 34-41 32883101-1 2020 BACKGROUND: Estimated glucose disposal rate (eGDR) is a practical measure of Insulin Resistance (IR) which can be easily incorporated into clinical practice. Glucose 22-29 insulin Homo sapiens 77-84 32947641-0 2022 Considering Insulin Secretory Capacity as Measured by a Fasting C-Peptide/Glucose Ratio in Selecting Glucose-Lowering Medications. Glucose 74-81 insulin Homo sapiens 12-19 32947641-0 2022 Considering Insulin Secretory Capacity as Measured by a Fasting C-Peptide/Glucose Ratio in Selecting Glucose-Lowering Medications. Glucose 101-108 insulin Homo sapiens 12-19 32947641-0 2022 Considering Insulin Secretory Capacity as Measured by a Fasting C-Peptide/Glucose Ratio in Selecting Glucose-Lowering Medications. Glucose 101-108 insulin Homo sapiens 64-73 31622905-11 2019 Amongst glucose-related factors, long-term PM2.5 exposure was associated with higher levels of insulin area under the curve (p = 0.03). Glucose 8-15 insulin Homo sapiens 95-102 31950001-0 2020 Higher circulating orosomucoid and lower early-phase insulin secretion in midlife Japanese with slower glucose disposal during oral glucose tolerance tests. Glucose 103-110 insulin Homo sapiens 53-60 33800541-1 2021 The triglyceride glucose (TyG) index, derived from a combination of fasting glucose and triglycerides, has been suggested as a useful marker for insulin resistance (IR), in addition to modified TyG indices that combine obesity parameters. Glucose 17-24 insulin Homo sapiens 145-152 29083510-6 2018 This increase occurs in order to maintain glucose metabolism during the physiological increases in insulin production that are required to balance the 20-fold increase in body weight during childhood and increased insulin resistance during puberty. Glucose 42-49 insulin Homo sapiens 99-106 29083510-6 2018 This increase occurs in order to maintain glucose metabolism during the physiological increases in insulin production that are required to balance the 20-fold increase in body weight during childhood and increased insulin resistance during puberty. Glucose 42-49 insulin Homo sapiens 214-221 26822092-4 2016 We sought to determine whether the diabetes-associated variant in this locus (the T allele of rs7903146) increases fasting endogenous glucose production (EGP), and impairs insulin-induced suppression of EGP and insulin-stimulated glucose disappearance. Glucose 230-237 insulin Homo sapiens 172-179 29428063-3 2018 Here we present an integrated whole-body model of glucose and insulin kinetics which extends the well-known two-compartment glucose minimal model. Glucose 124-131 insulin Homo sapiens 62-69 29428063-13 2018 CONCLUSIONS: We report a new and improved whole-body model of glucose and insulin kinetics which performs robustly under differing conditions and adds useful interpretations in relation to glucose intolerance. Glucose 189-196 insulin Homo sapiens 74-81 26822092-4 2016 We sought to determine whether the diabetes-associated variant in this locus (the T allele of rs7903146) increases fasting endogenous glucose production (EGP), and impairs insulin-induced suppression of EGP and insulin-stimulated glucose disappearance. Glucose 230-237 insulin Homo sapiens 211-218 25897187-0 2015 Adding GLP-1 Receptor Agonist Therapy to Basal Insulin for Postprandial Glucose Control. Glucose 72-79 insulin Homo sapiens 47-54 25963408-2 2015 Insulin signals in hepatocytes to activate Akt, which inhibits Foxo1 suppressing hepatic glucose production (HGP) and allowing the transition to the postprandial state. Glucose 89-96 insulin Homo sapiens 0-7 25963408-4 2015 Liver-specific ablation of the IR (L-Insulin Receptor KO) induces glucose intolerance, insulin resistance and prevents the appropriate transcriptional response to feeding. Glucose 66-73 insulin Homo sapiens 37-44 25963408-6 2015 These data indicate that in the absence of Foxo1, insulin signals via an intermediary extrahepatic tissue to regulate liver glucose production. Glucose 124-131 insulin Homo sapiens 50-57 25676261-3 2015 In the case of insulin secretion from pancreatic beta cells, this pathway involves the uptake of glucose, cell depolarization, calcium entry, and the triggering of the fusion of insulin-containing granules with the cell membrane. Glucose 97-104 insulin Homo sapiens 15-22 24038669-5 2013 To study how energy is allocated between brain and body, we measured plasma insulin, since insulin fulfils the functions of a glucose allocating hormone, i.e., peripheral glucose uptake depends on insulin, central uptake does not. Glucose 126-133 insulin Homo sapiens 76-83 23994650-10 2013 The abrupt increase of serum sCD26/DPP4 after a glucose load may be a marker of insulin resistance that could come from liver or muscle. Glucose 48-55 insulin Homo sapiens 80-87 24038669-5 2013 To study how energy is allocated between brain and body, we measured plasma insulin, since insulin fulfils the functions of a glucose allocating hormone, i.e., peripheral glucose uptake depends on insulin, central uptake does not. Glucose 171-178 insulin Homo sapiens 76-83 22499826-7 2012 An oral glucose tolerance test was performed on 113 men to calculate the insulin sensitivity index. Glucose 8-15 insulin Homo sapiens 73-80 15925010-6 2005 As the blood glucose level rises even a small amount above normal, then acquired defects in the glucose homeostasis system occur--initially to impair the beta cell"s glucose responsiveness to meals by impairing the first phase insulin response--and cause the blood glucose level to rise into the range of impaired glucose tolerance (IGT). Glucose 13-20 insulin Homo sapiens 227-234 19220533-6 2009 For patients using lifestyle alone, one or two oral glucose-lowering agents or insulin there was a progressive decline in the proportion achieving an HbA(1c) <7.0%, that is, 81, 55, 31 and 24%, respectively. Glucose 52-59 insulin Homo sapiens 79-86 16920293-9 2006 Marked decreases in blood glucose levels reflecting the increases in the plasma concentration of insulin were also observed after EP/IP treatment. Glucose 26-33 insulin Homo sapiens 97-104 15925010-6 2005 As the blood glucose level rises even a small amount above normal, then acquired defects in the glucose homeostasis system occur--initially to impair the beta cell"s glucose responsiveness to meals by impairing the first phase insulin response--and cause the blood glucose level to rise into the range of impaired glucose tolerance (IGT). Glucose 96-103 insulin Homo sapiens 227-234 12732668-0 2003 Insulin stimulates liver glucose uptake in humans: an 18F-FDG PET Study. Glucose 25-32 insulin Homo sapiens 0-7 12732668-4 2003 RESULTS: Whole-body insulin-mediated glucose uptake was 35 +/- 7 micro mol/min/kg for normal-IS subjects, 65 +/- 8 micro mol/min/kg for high-IS subjects (P < 0.05 vs. normal IS), and 24 +/- 3 micro mol/min/kg for low-IS subjects (P < 0.05 vs. normal IS and high IS). Glucose 37-44 insulin Homo sapiens 20-27 15925010-6 2005 As the blood glucose level rises even a small amount above normal, then acquired defects in the glucose homeostasis system occur--initially to impair the beta cell"s glucose responsiveness to meals by impairing the first phase insulin response--and cause the blood glucose level to rise into the range of impaired glucose tolerance (IGT). Glucose 96-103 insulin Homo sapiens 227-234 15925010-7 2005 This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, cause additional deterioration in beta-cell function along with further insulin resistance, and the blood glucose levels rise to full-blown diabetes. Glucose 19-26 insulin Homo sapiens 121-128 15925010-7 2005 This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, cause additional deterioration in beta-cell function along with further insulin resistance, and the blood glucose levels rise to full-blown diabetes. Glucose 19-26 insulin Homo sapiens 213-220 8812726-1 1996 Formycin A augments insulin release evoked by glucose (5.6 mm or more), this effect not being rapidly reversible. Glucose 46-53 insulin Homo sapiens 20-27 15322693-5 2004 Oral administration of losartan improved insulin sensitivity, which was determined by an oral glucose tolerance test (OGTT). Glucose 94-101 insulin Homo sapiens 41-48 10334964-5 1999 The plasma cortisol and insulin levels were both significantly positively correlated with the glucose concentration on admission. Glucose 94-101 insulin Homo sapiens 24-31 10334964-7 1999 The glucose and insulin concentrations on admission in 141 MI and UA patients were related to insulin resistance, as judged from subsequent insulin and glucose concentrations measured while fasting and during a glucose tolerance test. Glucose 4-11 insulin Homo sapiens 94-101 10334964-7 1999 The glucose and insulin concentrations on admission in 141 MI and UA patients were related to insulin resistance, as judged from subsequent insulin and glucose concentrations measured while fasting and during a glucose tolerance test. Glucose 4-11 insulin Homo sapiens 94-101 10334964-7 1999 The glucose and insulin concentrations on admission in 141 MI and UA patients were related to insulin resistance, as judged from subsequent insulin and glucose concentrations measured while fasting and during a glucose tolerance test. Glucose 152-159 insulin Homo sapiens 16-23 10334964-7 1999 The glucose and insulin concentrations on admission in 141 MI and UA patients were related to insulin resistance, as judged from subsequent insulin and glucose concentrations measured while fasting and during a glucose tolerance test. Glucose 152-159 insulin Homo sapiens 16-23 9404424-7 1997 Plasma insulin at fasting and 2 hours after glucose were significantly higher in hypertensive patients (44.4 +/- 5.1 pmol/L vs 21.6 +/- 3.2 pmol/L; p < 0.05 and 271.1 +/- 21.6 pmol/L vs 139.1 +/- 15.2 pmol/L; p < 0.001). Glucose 44-51 insulin Homo sapiens 7-14 7884509-3 1995 RESULTS: During oral glucose loading, myocardium-to-background (MB) ratio remarkably deteriorated in NIDDM patients compared with normals because of high plasma glucose and low serum insulin. Glucose 21-28 insulin Homo sapiens 183-190 7806019-4 1994 Insulin resistance was presumed to develop in normal glucose tolerance subjects with hyperinsulinaemia. Glucose 53-60 insulin Homo sapiens 0-7 7806019-6 1994 It was shown that glucose intolerance in the general population was associated with the factors related to insulin resistance. Glucose 18-25 insulin Homo sapiens 107-114 7806019-7 1994 These cross-sectional data, therefore, support the hypothesis that insulin resistance is the primary defect in the development of glucose intolerance in the Japanese general population. Glucose 130-137 insulin Homo sapiens 67-74 7821725-0 1994 Glucose induces oscillatory Ca2+ signalling and insulin release in human pancreatic beta cells. Glucose 0-7 insulin Homo sapiens 48-55 7821725-9 1994 In intact pancreatic islets the glucose induction of well-synchronized [Ca2+]i oscillations had its counterpart in 2-5 min pulses of insulin. Glucose 32-39 insulin Homo sapiens 133-140 7821725-11 1994 It is concluded that glucose stimulation of insulin release in man is determined by the number of beta cells entering into a state with Ca(2+)-induced secretory pulses. Glucose 21-28 insulin Homo sapiens 44-51 7821731-6 1994 It seems likely that longer term effects of fatty acids on this and other aspects of glucose metabolism could be important in the development of insulin resistance in diabetes mellitus in man. Glucose 85-92 insulin Homo sapiens 145-152 7821732-4 1994 The amount of this partially processed precursor of insulin in the circulation indicates the degree of glucose stimulus applied to the beta cell combined with the inherent capacity of the insulin secretory system to respond. Glucose 103-110 insulin Homo sapiens 52-59 7821732-6 1994 Deterioration of the early insulin response to oral glucose is a major feature of the loss of glucose tolerance associated with the transition from normal to impaired glucose tolerance and to NIDDM. Glucose 52-59 insulin Homo sapiens 27-34 7821736-0 1994 Transcription of the insulin gene: towards defining the glucose-sensitive cis-element and trans-acting factors. Glucose 56-63 insulin Homo sapiens 21-28 7821736-1 1994 Previous work has shown that the sequence -196 to -247 of the rat insulin I gene mediates the stimulatory effect of glucose in fetal islets. Glucose 116-123 insulin Homo sapiens 66-73 7821736-5 1994 Incubation of islets with varying glucose levels resulted in a dose-dependent increase in the intensity of the C1 band, while the other nuclear complexes formed with the insulin sequence, or the AP1 and SP1 binding activities used as control, were glucose insensitive. Glucose 248-255 insulin Homo sapiens 170-177 7821736-6 1994 This is thus the first demonstration of a physiologic glucose-sensitive trans-acting factor for the insulin gene, whose further study may markedly enhance our understanding of the regulation of insulin biosynthesis in normal and diabetic beta cells. Glucose 54-61 insulin Homo sapiens 100-107 7821736-6 1994 This is thus the first demonstration of a physiologic glucose-sensitive trans-acting factor for the insulin gene, whose further study may markedly enhance our understanding of the regulation of insulin biosynthesis in normal and diabetic beta cells. Glucose 54-61 insulin Homo sapiens 194-201 8422793-8 1993 Total and VLDL TG concentrations were found to be inversely related to rates of insulin-mediated glucose disposal, and HDL cholesterol concentrations were positively related to glucose disposal. Glucose 97-104 insulin Homo sapiens 80-87 34969446-5 2022 PFOS administration also led to lower serum insulin level both in fasting state and after glucose infusion among male mice. Glucose 90-97 insulin Homo sapiens 44-51 34969446-7 2022 By measuring insulin content in supernatant, 48-hr pretreatment of PFOS (100 mumol/L) decreased the insulin release capacity of beta-TC-6 cells after glucose stimulation. Glucose 150-157 insulin Homo sapiens 13-20 34969446-7 2022 By measuring insulin content in supernatant, 48-hr pretreatment of PFOS (100 mumol/L) decreased the insulin release capacity of beta-TC-6 cells after glucose stimulation. Glucose 150-157 insulin Homo sapiens 100-107 34821358-4 2022 beta-cells lacking TMEM24 exhibit markedly suppressed glucose-induced Ca2+ oscillations and insulin secretion but the underlying mechanism is not known. Glucose 54-61 insulin Homo sapiens 92-99 34419453-4 2022 OBJECTIVE: We defined gestational glucose intolerance physiologic subtypes based on the presence of insulin resistance, insulin deficiency, or mixed pathophysiology, and aimed to determine if these subtypes are at differential risk for adverse outcomes. Glucose 34-41 insulin Homo sapiens 100-107 34419453-5 2022 We hypothesized that women with the insulin resistant subtype of gestational glucose intolerance would have the greatest risk of adverse pregnancy outcomes. Glucose 77-84 insulin Homo sapiens 36-43 34419453-7 2022 We applied homeostasis model assessment to fasting glucose and insulin levels at 16-20 weeks" gestation to assess insulin resistance and deficiency and used these measures to classify women with gestational glucose intolerance into subtypes. Glucose 51-58 insulin Homo sapiens 114-121 34419453-7 2022 We applied homeostasis model assessment to fasting glucose and insulin levels at 16-20 weeks" gestation to assess insulin resistance and deficiency and used these measures to classify women with gestational glucose intolerance into subtypes. Glucose 207-214 insulin Homo sapiens 63-70 34419453-16 2022 CONCLUSION: Insulin resistant gestational glucose intolerance is a high-risk subtype for adverse pregnancy outcomes. Glucose 42-49 insulin Homo sapiens 12-19 34756122-9 2022 The role of the pancreas can be mimicked through closed-loop control of glucose concentrations by automatic injection of insulin or glucagon. Glucose 72-79 insulin Homo sapiens 121-128 34599527-9 2022 Disparate management strategies were observed, although insulin was the commonest glucose-lowering therapy for all patients with diabetes. Glucose 82-89 insulin Homo sapiens 56-63 34904389-1 2022 AIMS: The relationship between insulin resistance (IR) and glucose intolerance with pulmonary hypertension (PH) has been suggested in recent investigations. Glucose 59-66 insulin Homo sapiens 31-38 34704121-9 2022 During clamp, SAF and PAL both decreased insulin-stimulated Rd (p < 0.05 vs VCL), but non-oxidative glucose disposal was lower after PAL compared with SAF (p < 0.05). Glucose 100-107 insulin Homo sapiens 41-48 34932134-8 2022 After proinflammatory cytokine culture, islet function was measured by glucose-stimulated insulin secretion, and HLA-I and HLA-II expression was subsequently evaluated with immunostaining or RNA sequencing. Glucose 71-78 insulin Homo sapiens 90-97 34789923-1 2022 Insulin, which is released by pancreatic islet beta-cells in response to elevated levels of glucose in the blood, is a critical regulator of metabolism. Glucose 92-99 insulin Homo sapiens 0-7 34728775-8 2022 RESULTS: Subjects with higher obesity risk had globally increased insulin-stimulated brain glucose uptake (19 high-risk subjects versus 19 low-risk subjects), and familial obesity risk factors were associated with increased brain glucose uptake (38 subjects) but decreased availability of MORs (41 subjects) and CB1Rs (36 subjects). Glucose 91-98 insulin Homo sapiens 66-73 34789923-2 2022 Insulin triggers the uptake of glucose and fatty acids into the liver, adipose tissue and muscle, and promotes the storage of these nutrients in the form of glycogen and lipids. Glucose 31-38 insulin Homo sapiens 0-7 34728253-2 2022 In the perfused pancreas and isolated islets, GHS-R antagonism, ghrelin immunoneutralization and ghrelin-knockout (Ghr-KO) all increase glucose-induced insulin release. Glucose 136-143 insulin Homo sapiens 152-159 34890648-2 2022 The more recent advent of glucose-responsive automated insulin delivery has started to revolutionise the management of type 1 diabetes in children and adults. Glucose 26-33 insulin Homo sapiens 55-62 34728253-3 2022 Thus, pharmacological, immunological and genetic blockades of ghrelin in the pancreatic islets all markedly augment glucose-induced insulin release, showing that islet-derived ghrelin physiologically restricts insulin release in rodents. Glucose 116-123 insulin Homo sapiens 132-139 34815130-6 2022 Early cellular studies show that hit 1 decreases glucose-stimulating insulin secretion. Glucose 49-56 insulin Homo sapiens 69-76 34906902-8 2022 In human subjects, HME patients presented elevated fasting blood glucose-one of the criteria that define insulin resistance. Glucose 65-72 insulin Homo sapiens 105-112 34530162-0 2022 Far-red light-activated human islet-like designer cells enable sustained fine-tuned secretion of insulin for glucose control in T1D mice. Glucose 109-116 insulin Homo sapiens 97-104 34530162-1 2022 Diabetes affects almost half a billion people, and all individuals with type 1 diabetes and a large portion of individuals with type 2 diabetes rely on self-administration of the peptide hormone insulin to achieve glucose control. Glucose 214-221 insulin Homo sapiens 195-202 34758497-4 2022 RESULTS: In univariable analysis, maternal age, race and ethnicity, insurance, chronic hypertension, gestational age at GDM diagnosis, glucose level after 50-g glucose loading test, and provider type were associated with insulin prescription. Glucose 136-143 insulin Homo sapiens 222-229 34487217-2 2022 We examined the phenotypic features, insulin secretory response to glucose, and response to treatment in subjects with HNF1beta-MODY (MODY 5). Glucose 67-74 insulin Homo sapiens 37-44 34758497-4 2022 RESULTS: In univariable analysis, maternal age, race and ethnicity, insurance, chronic hypertension, gestational age at GDM diagnosis, glucose level after 50-g glucose loading test, and provider type were associated with insulin prescription. Glucose 161-168 insulin Homo sapiens 222-229 34773280-6 2022 Insulin secretion (IS) was measured using the graded glucose infusion test. Glucose 53-60 insulin Homo sapiens 0-7 34491825-1 2022 Background: Expert opinion guidelines and limited data from clinical trials recommend adjustment to bolus insulin doses based on continuous glucose monitor (CGM) trend data, yet minimal evidence exists to support this approach. Glucose 140-147 insulin Homo sapiens 106-113 34536302-9 2022 CONCLUSIONS: Weight management after gestational diabetes diagnosis does not appear to be too late to confer additional benefits to glucose lowering treatment, resulting in lower mean insulin doses, and lower rates of large for gestational age infants without increasing the risk of small for gestational age infants. Glucose 132-139 insulin Homo sapiens 184-191 34664212-6 2022 In healthier older adults, insulin treatment regimens (multiple daily insulin injections or insulin pump therapy) that approximate the normal physiology of insulin secretion should be used to achieve lower glycemic goals, while reducing the risk of hypoglycemia with frequent glucose monitoring (preferably using continuous glucose monitoring systems). Glucose 276-283 insulin Homo sapiens 27-34 34664212-6 2022 In healthier older adults, insulin treatment regimens (multiple daily insulin injections or insulin pump therapy) that approximate the normal physiology of insulin secretion should be used to achieve lower glycemic goals, while reducing the risk of hypoglycemia with frequent glucose monitoring (preferably using continuous glucose monitoring systems). Glucose 324-331 insulin Homo sapiens 27-34 34664212-6 2022 In healthier older adults, insulin treatment regimens (multiple daily insulin injections or insulin pump therapy) that approximate the normal physiology of insulin secretion should be used to achieve lower glycemic goals, while reducing the risk of hypoglycemia with frequent glucose monitoring (preferably using continuous glucose monitoring systems). Glucose 324-331 insulin Homo sapiens 156-163 34676911-0 2022 A systematic review and meta-analysis of interventions to preserve insulin-secreting beta cell function in people newly diagnosed with type 1 diabetes: results from intervention studies aimed at improving glucose control. Glucose 205-212 insulin Homo sapiens 67-74 34848368-7 2022 HUA treatment significantly increased mitochondrial reactive oxygen species (MtROS) levels and decreased insulin-stimulated glucose uptake. Glucose 124-131 insulin Homo sapiens 105-112 34343731-3 2022 One major challenge of diabetes management is the simple and timely administration of insulin to facilitate consistent blood glucose regulation and reduce the incidence of hypoglycemia. Glucose 125-132 insulin Homo sapiens 86-93 34291584-0 2022 A Low Fasting Glucose/Estimated Average Glucose Ratio was Associated with Superior Response to Insulin Degludec/Aspart Compared to Basal Insulin in Patients with Type 2 Diabetes. Glucose 40-47 insulin Homo sapiens 95-102 34904367-1 2022 The triglyceride glucose (TyG) index was regarded as a simple surrogate marker of insulin resistance (IR). Glucose 17-24 insulin Homo sapiens 82-89 34490793-3 2022 METHODS: A long-short-term-memory (LSTM) neural network was designed to predict glucose up to 60 minutes in the future using continuous glucose measurements and insulin data collected from 175 people with T1D (41,318 days) and evaluated on 75 people (11,333 days) from the Tidepool Big Data Donation Dataset. Glucose 80-87 insulin Homo sapiens 161-168 34861777-7 2022 The effectiveness of the proposed adaptive MPC based on rPLS is investigated with in silico subjects of the multivariable glucose-insulin-physiological variables simulator (mGIPsim). Glucose 122-129 insulin Homo sapiens 130-137 34762931-4 2022 Rapid-acting insulin analogs were developed to accelerate the slow subcutaneous (sc) absorption of RHI, thus lowering the 2-h post-prandial plasma glucose (PP-PG) and risk for late hypoglycemia as comparing with RHI. Glucose 147-154 insulin Homo sapiens 13-20 34823065-9 2022 The short-term role of beta-cell ABCB10 activity on glucose-stimulated insulin secretion (GSIS) was determined in isolated islets. Glucose 52-59 insulin Homo sapiens 71-78 34352294-3 2022 Insulin resistance (IR) was quantified by measuring steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Glucose 72-79 insulin Homo sapiens 0-7 34807465-3 2022 Combining insulin with a glucagon-like peptide-1 receptor agonist (GLP-1-RA) may provide additional blood glucose control while limiting undesirable effects including weight gain. Glucose 106-113 insulin Homo sapiens 10-17 34859690-3 2022 We aimed to identify whether alcohol modulates circulating miR associations with measures of glucose/insulin dynamics in PLWH. Glucose 93-100 insulin Homo sapiens 101-108 34266759-3 2022 Insulin treatment is initiated with control levels above the recommendations set by the Clinical Practice Guidelines (CPG) and patients are exposed to very high blood glucose levels during long periods of time. Glucose 167-174 insulin Homo sapiens 0-7 34677817-3 2022 These hormones regulate glucose levels, by stimulating insulin secretion and decreasing glucagon production. Glucose 24-31 insulin Homo sapiens 55-62 34761526-5 2022 Through concomitant optimization of an iADIPO-MPS, it is abled to obtain WAT with more unilocular and significantly larger ( 40%) lipid droplets compared to iADIPO in 2D culture, increased insulin responsiveness of glucose uptake ( 2-3 fold), fatty acid uptake ( 3-6 fold), and 40% suppressing of stimulated lipolysis giving a dynamic range that is competent to current in vivo and ex vivo models, allowing to identify both insulin sensitizers and desensitizers. Glucose 215-222 insulin Homo sapiens 189-196 34761526-5 2022 Through concomitant optimization of an iADIPO-MPS, it is abled to obtain WAT with more unilocular and significantly larger ( 40%) lipid droplets compared to iADIPO in 2D culture, increased insulin responsiveness of glucose uptake ( 2-3 fold), fatty acid uptake ( 3-6 fold), and 40% suppressing of stimulated lipolysis giving a dynamic range that is competent to current in vivo and ex vivo models, allowing to identify both insulin sensitizers and desensitizers. Glucose 215-222 insulin Homo sapiens 425-432 34102861-7 2022 An increase in basal glucose uptake was seen in both levels of adipogenic induction, and a diminished insulin-stimulated glucose uptake was associated with the higher level of adipogenic differentiation, and the greater number of adipocytes. Glucose 121-128 insulin Homo sapiens 102-109 34343731-4 2022 With this research, we construct an insulin delivery system, the delivery system is comprised of phenylboronic acid based fluorescent probes, which is used as glucose responsive linkers, mesoporous silica nanoparticles providing an insulin reservoir, and zinc oxide nanoparticles used as gate keepers. Glucose 159-166 insulin Homo sapiens 36-43 34343731-5 2022 The system with glucose sensitive responsive linker exhibits controlled release of insulin under high glucose concentrations, providing prolonged blood glucose regulation and no risks of hypoglycemia. Glucose 16-23 insulin Homo sapiens 83-90 34343731-5 2022 The system with glucose sensitive responsive linker exhibits controlled release of insulin under high glucose concentrations, providing prolonged blood glucose regulation and no risks of hypoglycemia. Glucose 102-109 insulin Homo sapiens 83-90 34343731-5 2022 The system with glucose sensitive responsive linker exhibits controlled release of insulin under high glucose concentrations, providing prolonged blood glucose regulation and no risks of hypoglycemia. Glucose 152-159 insulin Homo sapiens 83-90 34967298-7 2021 These pollutants disturb glucose homeostasis either by up-regulating or down-regulating the expression of diabetic marker genes like insulin (INS), glucokinase (GCK). Glucose 25-32 insulin Homo sapiens 133-140 34979329-2 2022 Elevated glucose causes beta-cell membrane depolarization and action potential generation, and oscillations in free-Ca2+ activity ((Ca2+)), triggering insulin release. Glucose 9-16 insulin Homo sapiens 151-158 34962151-1 2022 OBJECTVE: To determine if type 2 diabetes patients using basal insulin without prandial insulin with worse glycemic control at baseline would have the greatest benefit from using real-time continuous glucose monitoring (CGM). Glucose 200-207 insulin Homo sapiens 63-70 34962151-1 2022 OBJECTVE: To determine if type 2 diabetes patients using basal insulin without prandial insulin with worse glycemic control at baseline would have the greatest benefit from using real-time continuous glucose monitoring (CGM). Glucose 200-207 insulin Homo sapiens 88-95 34968495-1 2022 Rho subfamily of G proteins (e.g., Rac1) have been implicated in glucose-stimulated insulin secretion from the pancreatic beta-cell. Glucose 65-72 insulin Homo sapiens 84-91 34987576-7 2021 Moreover, two or more diagnostic OGTT glucose levels doubled the risk of insulin therapy (OR = 2.03, IC 95% 1.145-3.612, p=0.016). Glucose 38-45 insulin Homo sapiens 73-80 34951339-2 2022 The aim of this study was to reveal the relationship between triglyceride glucose (TyG) index, a novel parameter for insulin resistance (IR), with LV diastolic function and structure in hypertensive patients. Glucose 74-81 insulin Homo sapiens 117-124 34951149-7 2022 Notably, the co-culture system facilitates sensitive glucose-stimulated insulin secretion from islet organoids and increased glucose utilization in liver organoids by glucose tolerance tests. Glucose 53-60 insulin Homo sapiens 72-79 34954144-1 2022 G6PC2 encodes a glucose-6-phosphatase (G6Pase) catalytic subunit that modulates the sensitivity of insulin secretion to glucose and thereby regulates fasting blood glucose (FBG). Glucose 120-127 insulin Homo sapiens 99-106 34954230-0 2022 The actions of C-peptide in HEK293 cells are dependent upon insulin and extracellular glucose concentrations. Glucose 86-93 insulin Homo sapiens 15-24 34954230-6 2022 The effects of C-peptide appear to be dependent upon the presence of insulin and the absolute, extracellular concentration of glucose. Glucose 126-133 insulin Homo sapiens 15-24 34954230-9 2022 Likewise, the actions of C-peptide on cFos and GPR146 mRNA expressions were affected by changes in extracellular glucose concentration. Glucose 113-120 insulin Homo sapiens 25-34 34954230-10 2022 In particular, C-peptide induced significant elevations in cFos expression in the setting of high (25 mmol) extracellular glucose concentration. Glucose 122-129 insulin Homo sapiens 15-24 34936128-9 2022 The change in interstitial glucose proportion on target in the week following vaccination was most pronounced for people taking metformin/dapagliflozin + basal bolus insulin (change -7.6%) and for people with HbA1c below the median (change -5.7%). Glucose 27-34 insulin Homo sapiens 166-173 34936531-7 2022 Insulin sensitivity improved only in LMP group with 3.1(95%CI 1.5-6.6) times more patients with normal glucose regulation after intervention. Glucose 103-110 insulin Homo sapiens 0-7 34939824-0 2022 Effectiveness of Continuous Glucose Monitoring in Older Adults with Type 2 Diabetes Treated with Basal Insulin. Glucose 28-35 insulin Homo sapiens 103-110 34976418-9 2021 It is especially important to be vigilant of adrenal insufficiency in such patients as the hyperkalemia is resistant to standard therapy of insulin dextrose and can precipitate fatal arrhythmia if treatment is delayed. Glucose 148-156 insulin Homo sapiens 140-147 34942192-7 2022 Insulin sensitivity (M/I ratio) was ~15% lower, acute insulin response (AIR) to intravenous glucose and beta-cell responsivity to oral glucose were ~35% lower, but total insulin secretion rate in the fasting state and after glucose ingestion was ~10% greater in prediabetic than in normoglycemic participants. Glucose 92-99 insulin Homo sapiens 54-61 34942192-7 2022 Insulin sensitivity (M/I ratio) was ~15% lower, acute insulin response (AIR) to intravenous glucose and beta-cell responsivity to oral glucose were ~35% lower, but total insulin secretion rate in the fasting state and after glucose ingestion was ~10% greater in prediabetic than in normoglycemic participants. Glucose 224-231 insulin Homo sapiens 170-177 34931302-7 2022 Tissue size, cell viability, cellular arrangement and polarity, and insulin-mediated glucose uptake by LPMTs were analyzed. Glucose 85-92 insulin Homo sapiens 68-75 34922397-0 2022 Corrigendum to: Association Between Smoking Behavior and Insulin Resistance Using Triglyceride-Glucose Index Among South Korean Adults. Glucose 95-102 insulin Homo sapiens 57-64 34825823-1 2021 The overexpression of PED/PEA15, the phosphoprotein enriched in diabetes/phosphoprotein enriched in the astrocytes 15 protein (here referred simply to as PED), observed in some forms of type II diabetes, reduces the transport of insulin-stimulated glucose by binding to the phospholipase D1 (PLD1). Glucose 248-255 insulin Homo sapiens 229-236 31950001-9 2020 Conclusions: Lower early-phase insulin secretion and low-grade inflammation were associated with slower glucose disposal during an oral glucose tolerance test in midlife Japanese. Glucose 104-111 insulin Homo sapiens 31-38 31950001-9 2020 Conclusions: Lower early-phase insulin secretion and low-grade inflammation were associated with slower glucose disposal during an oral glucose tolerance test in midlife Japanese. Glucose 136-143 insulin Homo sapiens 31-38 34801562-0 2021 Corrigendum to "Insulin exacerbated high glucose-induced epithelial-mesenchymal transition in prostatic epithelial cells BPH-1 and prostate cancer cells PC-3 via MEK/ERK signaling pathway" (Exp. Glucose 41-48 insulin Homo sapiens 16-23 34956580-6 2021 Results: The time needed to control blood glucose <13.8 mmol/L, the amount of insulin needed to control blood glucose <13.8 mmol/L, the time needed to correct DKA, and the amount of insulin needed to correct DKA in the observation group were significantly less than those in the control group (P < 0.05). Glucose 110-117 insulin Homo sapiens 78-85 34956580-10 2021 Conclusion: Continuous subcutaneous injection of insulin analogues is effective in the treatment of diabetic patients with ketoacidosis, which can effectively improve blood glucose, carbon dioxide binding capacity, and glycosylated hemoglobin and accelerate the negative conversion of urinary ketone body. Glucose 173-180 insulin Homo sapiens 49-56 34879878-1 2021 AIMS: Low C-peptide levels, indicating beta-cell dysfunction, are associated with increased within-day glucose variation and hypoglycemia. Glucose 103-110 insulin Homo sapiens 10-19 34889083-2 2022 These effects are driven in part by augmenting glucose-stimulated insulin release (incretin effect), reducing caloric intake and delayed gastric emptying. Glucose 47-54 insulin Homo sapiens 66-73 34879878-6 2021 C-peptide levels were inversely associated with the risk of severe hypoglycemia (OR 0.68 (0.60-0.77)) and visit-to-visit glucose variation (CV, standardized beta-estimate - 0.12 (SE 0.01); ARV, - 0.10 (0.01)) (p < 0.0001 all). Glucose 121-128 insulin Homo sapiens 0-9 34879878-10 2021 C-peptide levels may predict future glucose control patterns and CVD risk, and identify phenotypes influencing clinical decision making in advanced type 2 diabetes. Glucose 36-43 insulin Homo sapiens 0-9 34959394-1 2021 Insulin is a peptide hormone that is key to regulating physiological glucose levels. Glucose 69-76 insulin Homo sapiens 0-7 34944680-3 2021 The aim of the present study was to investigate the effects of a pharmacological NOX4 inhibitor (GLX7013114) on human islet and EndoC-betaH1 cell mitochondrial function, and to correlate such effects with survival in islets of different size, activity, and glucose-stimulated insulin release responsiveness. Glucose 257-264 insulin Homo sapiens 276-283 34944680-6 2021 Moreover, the insulin release from EndoC-betaH1 cells at a high glucose concentration increased with NOX4 inhibition. Glucose 64-71 insulin Homo sapiens 14-21 34871147-7 2021 Women that continued subcutaneous insulin were more likely to be older (30.5 vs. 28.1, p = .04), multiparous (74% vs. 50%, p = .042), and have a continuous glucose monitor (CGM) (93% vs. 43%, p < .001). Glucose 156-163 insulin Homo sapiens 34-41 34944668-5 2021 There is evidence, that physical exercise has impact on a variety of molecular pathways, such as AMP-activated protein kinase and insulin signaling as well as glucose transporter 4 translocation, modulating insulin action, cellular substrate flow and in particular ectopic lipid and glycogen storage in a positive manner. Glucose 159-166 insulin Homo sapiens 207-214 34959930-5 2021 The results showed that TF3 could effectively rise glucose absorption capacity in insulin-resistant HepG2 cells and regulate glucose level in diabetic zebrafish. Glucose 51-58 insulin Homo sapiens 82-89 34883185-0 2022 The use of flash glucose monitoring significantly improves glycemic control in type 2 diabetes managed with basal bolus insulin therapy compared to self-monitoring of blood glucose: A prospective observational cohort study. Glucose 17-24 insulin Homo sapiens 120-127 34855192-1 2022 AIMS: Both pregnancy and polycystic ovary syndrome (PCOS) constitute insulin-resistant states that are associated with an increased prevalence of glucose intolerance. Glucose 146-153 insulin Homo sapiens 69-76 34862200-5 2022 In corroboration, the variant peptide (PST-297S) displays gain-of-potency in several cellular events relevant for cardiometabolic disorders (e.g, increased expression of gluconeogenic genes, increased catecholamine secretion, greater inhibition of insulin-stimulated glucose-uptake) than the wild-type peptide (PST-WT). Glucose 267-274 insulin Homo sapiens 248-255 34861146-0 2021 Implanted pluripotent stem-cell-derived pancreatic endoderm cells secrete glucose-responsive C-peptide in patients with type 1 diabetes. Glucose 74-81 insulin Homo sapiens 93-102 34857543-4 2022 Crucially, acute exposure to high glucose leads to a rapid upregulation of both TRAPgamma/SSR3 and proinsulin protein without change in the respective mRNA levels - observed in cultured rodent beta-cell lines and confirmed in human islets. Glucose 34-41 insulin Homo sapiens 99-109 34857543-5 2022 Strikingly, pancreatic beta-cells with suppressed TRAPgamma/SSR3 expression are blocked in glucose-dependent upregulation of proinsulin (or insulin) biosynthesis. Glucose 91-98 insulin Homo sapiens 125-135 34857543-5 2022 Strikingly, pancreatic beta-cells with suppressed TRAPgamma/SSR3 expression are blocked in glucose-dependent upregulation of proinsulin (or insulin) biosynthesis. Glucose 91-98 insulin Homo sapiens 140-147 34861146-4 2021 After implantation, patients had increased fasting C-peptide levels and increased glucose-responsive C-peptide levels and developed mixed meal-stimulated C-peptide secretion. Glucose 82-89 insulin Homo sapiens 101-110 34855111-7 2022 In vitro the function of pancreatic beta like cells was assessed by measuring glucose-stimulated insulin secretion. Glucose 78-85 insulin Homo sapiens 97-104 34699323-0 2021 Astragalus polysaccharide improve the proliferation and insulin secretion of mouse pancreatic beta cells induced by high glucose and palmitic acid partially through promoting miR-136-5p and miR-149-5p expression. Glucose 121-128 insulin Homo sapiens 56-63 34813241-0 2021 (Insulin/glucose therapy for the treatment of severe calcium channel blocker poisoning in pediatrics. Glucose 9-16 insulin Homo sapiens 1-8 34813241-5 2021 The insulin/glucose therapy is an effective complement to the initial treatment, which is widely studied and used in different pathologies with hemodynamic compromise. Glucose 12-19 insulin Homo sapiens 4-11 34969688-13 2021 CONCLUSIONS: Estradiol-induced IR cleavage causes cellular insulin resistance, and its molecular mechanisms are shared with those by high glucose levels. Glucose 138-145 insulin Homo sapiens 59-66 34251695-1 2021 There has been 100 years of research detailing the role of insulin in glucose, protein and free fatty acid metabolism. Glucose 70-77 insulin Homo sapiens 59-66 34270347-0 2021 Longitudinal Observation of Insulin use and glucose Sensor metrics in Pregnant women with type 1 diabetes using continuous glucose monitors and insulin pumps: The LOIS-P Study. Glucose 44-51 insulin Homo sapiens 144-151 34270347-2 2021 Prospective analysis of continuous glucose monitor (CGM) metrics, insulin pump settings, and insulin delivery can better characterize the changes in glycemic levels and insulin use throughout pregnancy with T1D. Glucose 35-42 insulin Homo sapiens 169-176 34694585-3 2021 Novel hybrid closed-loop (HCL) systems represent the latest treatment modality for T1D, combining modern glucose sensors and insulin pumps with a linked control algorithm to offer automated insulin delivery in response to blood glucose levels and trends. Glucose 228-235 insulin Homo sapiens 190-197 34850295-3 2021 In this study we have generated islet organoids with the ability to respond to glucose stimulation by insulin release. Glucose 79-86 insulin Homo sapiens 102-109 34850295-5 2021 These cells were assembled in matrigel or cross-linked collagen scaffold and compared for their efficacy to release insulin upon stimulation with glucose. Glucose 146-153 insulin Homo sapiens 116-123 34850295-8 2021 The islet organoids in both the cases showed release of insulin upon stimulation with glucose. Glucose 86-93 insulin Homo sapiens 56-63 34402157-0 2021 Glucose control using fast-acting insulin aspart in a real-world setting: a 1-year two-center study in people with type 1 diabetes using continuous glucose monitoring. Glucose 0-7 insulin Homo sapiens 34-41 34588210-0 2021 The Effect of Discontinuing Continuous Glucose Monitoring in Adults With Type 2 Diabetes Treated With Basal Insulin. Glucose 39-46 insulin Homo sapiens 108-115 34610922-9 2021 Insulin sensitivity decreased with age in all participants, and those with glucose intolerance had consistently lower compensatory insulin secretion from childhood. Glucose 75-82 insulin Homo sapiens 131-138 34610922-11 2021 CONCLUSION: Inadequate compensatory insulin secretory response to decreasing insulin sensitivity in early life is the major pathophysiology underlying glucose intolerance in thin rural Indians. Glucose 151-158 insulin Homo sapiens 36-43 34610922-11 2021 CONCLUSION: Inadequate compensatory insulin secretory response to decreasing insulin sensitivity in early life is the major pathophysiology underlying glucose intolerance in thin rural Indians. Glucose 151-158 insulin Homo sapiens 77-84 34417843-7 2021 infusion of a glucose bolus, participants with an A allele had higher early (p < 0.05 at 2 and 4 min) plasma insulin and C-peptide concentrations for a similar elevation in blood glucose as those homozygous for the major (G) allele. Glucose 14-21 insulin Homo sapiens 109-116 34417843-9 2021 CONCLUSIONS/INTERPRETATION: rs373863828-A allele associates with increased glucose-stimulated insulin release without affecting insulin sensitivity, suggesting that CREBRF p.Arg457Gln may increase insulin release to reduce the risk of type 2 diabetes. Glucose 75-82 insulin Homo sapiens 94-101 34417843-9 2021 CONCLUSIONS/INTERPRETATION: rs373863828-A allele associates with increased glucose-stimulated insulin release without affecting insulin sensitivity, suggesting that CREBRF p.Arg457Gln may increase insulin release to reduce the risk of type 2 diabetes. Glucose 75-82 insulin Homo sapiens 197-204 34355342-1 2021 BACKGROUND: The triglyceride-glucose index (TyG), and TyG-driven parameters incorporating TyG and obesity indices have been proposed as reliable indicators of insulin resistance and its related comorbidities. Glucose 29-36 insulin Homo sapiens 159-166 34551207-7 2021 The intervention arm showed improvements in insulin resistance (glucose infusion rate (GIR)), GLS, e", atrial strain, and muscle perfusion in fasting conditions, as well as improved responses of GLS and muscle perfusion to insulin during clamp. Glucose 64-71 insulin Homo sapiens 44-51 34223944-1 2021 PURPOSE: Patients with type 1 diabetes mellitus (T1DM) receiving insulin therapy commonly suffer from insulin-mediated hypoglycemia and require glucagon for glycemic control to achieve normal plasma glucose (PG) levels. Glucose 199-206 insulin Homo sapiens 65-72 34403503-9 2021 IL-20 promoted insulin resistance by inhibiting glucose uptake in mature adipocytes through the SOCS-3 pathway. Glucose 48-55 insulin Homo sapiens 15-22 34791627-3 2021 In this study, we explored the potential role of TWIST1 on glucose transport into the 293T cells in an insulin-dependent and insulin-independent manner. Glucose 59-66 insulin Homo sapiens 103-110 34791627-3 2021 In this study, we explored the potential role of TWIST1 on glucose transport into the 293T cells in an insulin-dependent and insulin-independent manner. Glucose 59-66 insulin Homo sapiens 125-132 34791627-8 2021 However, TWIST1 did not alter the mRNA and protein expressions of the InsR, its substrates (IRS-1 and -2), and GLUT-4 genes in 293T cells which are main factors for insulin-stimulated glucose uptake pathway. Glucose 184-191 insulin Homo sapiens 165-172 34907741-13 2021 Conclusions: Fasting levels of cholesterol, plasma glucose, and atherogenic index were strongly associated with fasting C-peptide levels in healthy individuals. Glucose 51-58 insulin Homo sapiens 120-129 34321614-1 2021 Insulin resistance of glucose utilization is fully restored following BMI normalization after bariatric surgery. Glucose 22-29 insulin Homo sapiens 0-7 34907741-2 2021 Therefore this cross-sectional study investigated fasting cholesterol and glucose levels along with the determination of atherogenic index in a cohort of healthy individuals from the Czech Republic in relation to their fasting C-peptide levels. Glucose 74-81 insulin Homo sapiens 227-236 34128214-10 2021 CONCLUSION: Our findings confirmed the role of GCK and G6PC2 in regulating the pulsatility in insulin secretion thereby influencing insulin-signaling and leading to a gradual modulation in glucose levels in Italian patients with newly diagnosed T2D. Glucose 189-196 insulin Homo sapiens 94-101 34331233-5 2021 In addition, 160Q cells were more prone to apoptosis and exhibited deficient glucose-stimulated insulin expression and secretion. Glucose 77-84 insulin Homo sapiens 96-103 34514867-1 2021 Diabetes is a pandemic manifested through glucose dysregulation mediated via inadequate insulin secretion by beta cells. Glucose 42-49 insulin Homo sapiens 88-95 34563556-6 2021 Moreover, some older antihyperglycemic drugs (metformin, thiazolidinediones), but also novel therapeutic concepts (new peroxisome proliferator-activated receptor agonists, incretin mimetics, sodium glucose cotransporter inhibitors, modulators of energy metabolism) can directly or indirectly reduce insulin resistance. Glucose 198-205 insulin Homo sapiens 299-306 34510301-8 2021 Our results indicate that, in the presence of insulin, deuterium depletion markedly reduced serum levels of glucose, -fructose amine, and -HbA1c, in a dose-dependent manner. Glucose 108-115 insulin Homo sapiens 46-53 34510301-11 2021 These data suggest that deuterium depletion dose-dependently enhances the effect of insulin on GLUT4 translocation and potentiates glucose uptake in diabetic rats, which explains the lower serum glucose, -fructose amine, and -HbA1c concentrations. Glucose 195-202 insulin Homo sapiens 84-91 34634522-5 2021 RESULTS: We identified strong correlations between plasma triacylglycerols (TAGs) and islet gene modules that comprise key regulators of glucose- and lipid-regulated insulin secretion and of the insulin signaling pathway, the two top hits were Gck and Abhd6 for positive and negative correlations, respectively. Glucose 137-144 insulin Homo sapiens 166-173 34634522-9 2021 This cross-species comparative analysis further led to the identification PITPNC1 as a candidate regulator of glucose-stimulated insulin secretion. Glucose 110-117 insulin Homo sapiens 129-136 34651658-4 2021 Insulin exerts a variety of effects, many of which are mediated by Akt, including increasing glucose uptake, promoting glycogen synthesis and inhibiting glycogen degradation, increasing free fatty acid uptake, increasing protein synthesis, promoting muscle hypertrophy and inhibiting protein degradation. Glucose 93-100 insulin Homo sapiens 0-7 34180151-7 2021 Insulin sensitivity was determined from the frequently sampled intravenous glucose tolerance test and minimal modelling. Glucose 75-82 insulin Homo sapiens 0-7 34514867-8 2021 Insulin secretion was observed with glucose stimulation and abrogated following palmitate exposure; a common free fatty acid implicated in human beta cell dysfunction. Glucose 36-43 insulin Homo sapiens 0-7 34809493-1 2022 100 years ago, insulin was first used to successfully lower blood glucose levels in young people living with what was then called juvenile diabetes. Glucose 66-73 insulin Homo sapiens 15-22 34656024-9 2021 The generated IPCs released significant amounts of insulin in response to increasing glucose concentration both in vitro & in vivo. Glucose 85-92 insulin Homo sapiens 51-58 34908336-0 2021 402.2: High Glucose Concentration Increases KATP Channel Activity but Suppresses Mitochondrial Respiration Ability in Insulin-producing Cells Regenerated From Stem Cells. Glucose 12-19 insulin Homo sapiens 118-125 34847289-2 2021 In Type 2 Diabetes (T2D), the lack of beta-cell compensatory mechanisms overcoming peripherally developed insulin resistance is a paramount factor leading to disturbed blood glucose levels and lipid metabolism. Glucose 174-181 insulin Homo sapiens 106-113 34844283-4 2021 OBJECTIVES: To establish the impact of insulin therapy guided by continuous glucose monitoring compared to insulin therapy guided by other forms of glucose data collection on the lives of people with CFRD. Glucose 76-83 insulin Homo sapiens 39-46 34917033-2 2021 Background: The difference in the relationship between beta-cell function and insulin resistance among Africans, Caucasians and East Asians with normal glucose tolerance (NGT) was not well investigated. Glucose 152-159 insulin Homo sapiens 78-85 34108310-8 2021 Using multiple logistic regression analysis, pre-pregnancy body mass index (BMI) >=25 kg/m2, a family history of diabetes, and higher fasting plasma glucose (FPG), 1 h-plasma glucose (PG), and 2 h-PG values increased insulin therapy risk during pregnancy in the E-GDM group. Glucose 149-156 insulin Homo sapiens 217-224 34108310-8 2021 Using multiple logistic regression analysis, pre-pregnancy body mass index (BMI) >=25 kg/m2, a family history of diabetes, and higher fasting plasma glucose (FPG), 1 h-plasma glucose (PG), and 2 h-PG values increased insulin therapy risk during pregnancy in the E-GDM group. Glucose 175-182 insulin Homo sapiens 217-224 34844283-4 2021 OBJECTIVES: To establish the impact of insulin therapy guided by continuous glucose monitoring compared to insulin therapy guided by other forms of glucose data collection on the lives of people with CFRD. Glucose 148-155 insulin Homo sapiens 107-114 34884651-1 2021 Type 2 diabetes (T2D) is a worldwide prevalent metabolic disorder defined by high blood glucose levels due to insulin resistance (IR) and impaired insulin secretion. Glucose 88-95 insulin Homo sapiens 110-117 34884624-1 2021 beta-cells convert glucose (input) resulting in the controlled release of insulin (output), which in turn has the role to maintain glucose homeostasis. Glucose 19-26 insulin Homo sapiens 74-81 34943836-5 2021 One main source of oxidative stress in pancreatic beta-cells appears to be the reactive oxygen species producer NADPH oxidase (NOX) enzyme, which has a role in the glucose-stimulated insulin secretion and in the beta-cell demise during both T1 and T2D. Glucose 164-171 insulin Homo sapiens 183-190 34836963-1 2021 Obesity and type 2 diabetes are associated with disturbances in insulin-regulated glucose and lipid fluxes and severe comorbidities including cardiovascular disease and steatohepatitis. Glucose 82-89 insulin Homo sapiens 64-71 34884501-3 2021 Cellular glucose consumption was significantly elevated in insulin-resistant HepG2 cells after LPMP treatment. Glucose 9-16 insulin Homo sapiens 59-66 34884524-3 2021 Therefore, during pregnancy, maternal insulin resistance arises, which elevates maternal blood glucose levels, and consequently ensures an adequate glucose supply for the developing fetus. Glucose 95-102 insulin Homo sapiens 38-45 34884524-3 2021 Therefore, during pregnancy, maternal insulin resistance arises, which elevates maternal blood glucose levels, and consequently ensures an adequate glucose supply for the developing fetus. Glucose 148-155 insulin Homo sapiens 38-45 34343296-7 2021 Patients with ratio <1.78 were more likely to require insulin for glucose control, while patients with ratio >2.65 were more likely to achieve glucose control with metformin monotherapy. Glucose 66-73 insulin Homo sapiens 54-61 34946023-7 2021 Our results showed that insulin-mediated reduction of UPEC infection in a high-glucose environment was not only due to the downregulation of JAK1/2 and phosphorylated STAT-1/3, but also because of the decreased expression of TLR-4 proteins and pro-inflammatory IL-6. Glucose 79-86 insulin Homo sapiens 24-31 34946023-8 2021 Here, we demonstrated that insulin reduced not only UPEC infection in bladder epithelial cells, but also inhibited the JAK/STAT transduction pathway during infection in a high-glucose environment. Glucose 176-183 insulin Homo sapiens 27-34 34812516-1 2022 Exercise improves the insulin sensitivity of glucose uptake in skeletal muscle. Glucose 45-52 insulin Homo sapiens 22-29 34969592-12 2022 The use of glucose-lowering medications, including insulin, was reduced from baseline in both groups, and patients in the bariatric surgery group required significantly fewer of these medications than those in the medical therapy group. Glucose 11-18 insulin Homo sapiens 51-58 34850005-5 2022 Beyond such PK/PD metrics, next-generation insulin analogs seek to exploit therapeutic mechanisms: glucose-responsive ("smart") analogs, pathway-specific ("biased") analogs, and organ-targeted analogs. Glucose 99-106 insulin Homo sapiens 43-50 34746944-1 2021 Insulin is a principal hormone that is involved in the regulation of glucose levels in the blood. Glucose 69-76 insulin Homo sapiens 0-7 34799672-0 2022 Insulin resistance rewires the metabolic gene program and glucose utilization in human white adipocytes. Glucose 58-65 insulin Homo sapiens 0-7 34799672-8 2022 CONCLUSIONS: Collectively, our data highlight the importance of obesity-derived insulin resistance in impacting the expression of key metabolic genes and impairing the metabolic processes of glucose utilization, and reveal a role for metabolic adaptation in adipose dysfunction in humans. Glucose 191-198 insulin Homo sapiens 80-87 34789613-1 2022 BACKGROUND: Although acute hyperglycemia and insulin resistance (IR) are risk factors for atherosclerosis development through oxidative stress and sympathetic activation in diabetes mellitus, the association of these factors with coronary microvascular function in the early diabetic stage remains controversial.Methods and Results:Using transthoracic echocardiography, coronary flow velocity (CFV) and its reserve (CFVR) as parameters of coronary microvascular function were measured before and 1 h after an oral glucose tolerance test (OGTT) in 40 patients (aged 59+-12 years) without diagnosed diabetes mellitus or coronary artery disease. Glucose 514-521 insulin Homo sapiens 45-52 34551282-7 2021 In adipocytes, KARATE controls insulin-dependent translocation of the glucose transporter GLUT4 to the plasma membrane for glucose uptake. Glucose 70-77 insulin Homo sapiens 31-38 34551282-7 2021 In adipocytes, KARATE controls insulin-dependent translocation of the glucose transporter GLUT4 to the plasma membrane for glucose uptake. Glucose 123-130 insulin Homo sapiens 31-38 34751556-0 2021 Insulin Granule-Loaded MicroPlates for Modulating Blood Glucose Levels in Type-1 Diabetes. Glucose 56-63 insulin Homo sapiens 0-7 34751556-7 2021 Furthermore, following the glucose challenge, diabetic mice implanted with 10H INS-muPL successfully regained glycemic control with a significant reduction in AUC0-120min (799.9 +- 134.83 vs 2234.60 +- 82.72 mg/dL) and increased insulin levels at 7 days post-implantation (1.14 +- 0.11 vs 0.38 +- 0.02 ng/mL), as compared to untreated diabetic mice. Glucose 27-34 insulin Homo sapiens 229-236 34867781-2 2021 Decreased acute insulin response to intravenous glucose tolerance test (IVGTT) during first-phase insulin secretion (FPIS) is a characteristic of diabetes. Glucose 48-55 insulin Homo sapiens 98-105 34867781-3 2021 However, knowledge of the insulin secretion characteristics identified by different time to glucose peak in subjects with different metabolic state is sparse. Glucose 92-99 insulin Homo sapiens 26-33 34867781-9 2021 Glucose peak of most participants in G1 converged at 5 min, and the curves shape of insulin and C-peptide in G2 were the sharpest among three groups. Glucose 0-7 insulin Homo sapiens 84-91 34780283-1 2022 BACKGROUND: Loop is an open-source automated insulin dosing system that allows users unrivaled control over system settings that effect future glucose prediction. Glucose 143-150 insulin Homo sapiens 45-52 34956518-8 2021 CONCLUSION: Insulin glargine combined with repaglinide is an effective and safe regimen in clinical practice, which can effectively control the blood glucose level, lower insulin dosage, and reduce adverse effects of T2D. Glucose 150-157 insulin Homo sapiens 12-19 34426189-8 2021 These results suggest that exposure to certain nitro-PAHs affects glucose homeostasis, partly resulting from the depletion of insulin-stimulating amino acids (Asp, Glu, and Orn). Glucose 66-73 insulin Homo sapiens 126-133 34830194-3 2021 Incretins are peptide hormones derived from the gastrointestinal tract, that besides causing enhancement of insulin secretion after oral glucose intake, participate in many other metabolic processes. Glucose 137-144 insulin Homo sapiens 108-115 34779282-1 2022 Research conducted over the last 50 years has provided insight into the mechanisms by which insulin stimulates glucose transport across the skeletal muscle cell membrane. Glucose 111-118 insulin Homo sapiens 92-99 34836340-7 2021 Dapagliflozin treatment improved insulin resistance by decreasing glucose and insulin levels, increased serum magnesium levels, and reduced urinary magnesium excretion. Glucose 66-73 insulin Homo sapiens 33-40 34751700-2 2021 While insulin is secreted after food intake and is the primary hormone increasing glucose storage as glycogen and fatty acid storage as triglycerides, exercise is a condition where fuel stores need to be mobilized and oxidized. Glucose 82-89 insulin Homo sapiens 6-13 34751700-6 2021 This process is facilitated by an increase in insulin sensitivity of the muscles previously engaged in physical activity which directs glucose to glycogen resynthesis. Glucose 135-142 insulin Homo sapiens 46-53 34265066-9 2021 Despite a decrease in GIP levels, the in-vivo glucose-stimulated insulin secretion was unaffected by melatonin (p=0.78). Glucose 46-53 insulin Homo sapiens 65-72 34774061-1 2021 BACKGROUND: Triglyceride glucose-body mass index (TyG-BMI) has been recommended as an alternative indicator of insulin resistance. Glucose 25-32 insulin Homo sapiens 111-118 34779282-6 2022 Major advances have been made in defining the regulation of the insulin-stimulated glucose transporter, GLUT4, in skeletalmuscle. Glucose 83-90 insulin Homo sapiens 64-71 34636745-4 2021 Insulin resistance was quantified by the estimated glucose disposal rate (eGDR) with higher eGDR levels indicating higher insulin sensitivity (i.e. lower eGDR levels indicating higher insulin resistance). Glucose 51-58 insulin Homo sapiens 0-7 34636745-4 2021 Insulin resistance was quantified by the estimated glucose disposal rate (eGDR) with higher eGDR levels indicating higher insulin sensitivity (i.e. lower eGDR levels indicating higher insulin resistance). Glucose 51-58 insulin Homo sapiens 122-129 34732569-4 2021 In this study, we investigated the hypothesis that genes in the lipid/lipoprotein pathway and those in the glucose metabolic pathway are governed by different transcriptional regulatory logics that affect their response to physiologic (fasting/refeeding) as well as pathophysiologic cues (insulin resistance and hyperglycemia). Glucose 107-114 insulin Homo sapiens 289-296 34763121-0 2022 The association of immediate postpartum glucose values with persistent insulin resistance in patients with gestational diabetes. Glucose 40-47 insulin Homo sapiens 71-78 34744160-2 2021 The anti-insulin effect of hPL raises maternal blood glucose levels, allowing the fetus to use glucose as a nutrient. Glucose 95-102 insulin Homo sapiens 9-16 34750459-2 2021 Here, a glucose-responsive continuous insulin delivery system is developed, where novel polyhedral oligosilsesquioxane (POSS) modified with 3-aminophenylboronic acid (APBA) were used to encapsulate insulin (insulin entrapment efficiency: 73.2%) to prepare a fast response, high stability, good distribution, and excellent biocompatible system. Glucose 8-15 insulin Homo sapiens 38-45 34750459-2 2021 Here, a glucose-responsive continuous insulin delivery system is developed, where novel polyhedral oligosilsesquioxane (POSS) modified with 3-aminophenylboronic acid (APBA) were used to encapsulate insulin (insulin entrapment efficiency: 73.2%) to prepare a fast response, high stability, good distribution, and excellent biocompatible system. Glucose 8-15 insulin Homo sapiens 198-205 34750459-5 2021 The interaction of the PBA and diol containing insulin via boronate ester bond and its interchange with glucose was investigated by FT-IR, 1H NMR and XPS. Glucose 104-111 insulin Homo sapiens 47-54 34750459-6 2021 Furthermore, the successful glucose-triggered release of insulin from the POSS-APBA micelles was investigated at neutral pH. Glucose 28-35 insulin Homo sapiens 57-64 34750459-7 2021 A linear graph was plotted with the measured released insulin vs glucose concentrations, with a linear correlation coefficient (R2) value close to 1. Glucose 65-72 insulin Homo sapiens 54-61 34481876-2 2021 The liver is the organ where insulin is secreted from the pancreas, and it regulates the storage and release of glucose according to the body"s demand. Glucose 112-119 insulin Homo sapiens 29-36 34743379-12 2022 CONCLUSIONS: The administration of greater AGE load in nutritional formula potentially increases the amount of insulin required to maintain blood glucose within a normal range during critical illness. Glucose 146-153 insulin Homo sapiens 111-118 34741238-7 2022 Insulin resistance (IR) was calculated using estimated glucose disposal rate (eGDR) and MS was diagnosed using the international diabetes federation (IDF) consensus definition 2017. Glucose 55-62 insulin Homo sapiens 0-7 34738701-9 2022 The 2-hour glucose value in the oral glucose tolerance test was 0.6 mmol/L lower in boys from the metformin group than in those from the insulin group (p = 0.015). Glucose 11-18 insulin Homo sapiens 137-144 34749616-3 2021 On the other hand, diabetes mellitus is associated with alteration of insulin signaling, which could cause the reduction of glu-cose uptake, metabolic prohibition of energy consuming cells, as well as suppression of glucose to fat conversion in the liver. Glucose 124-132 insulin Homo sapiens 70-77 34749616-3 2021 On the other hand, diabetes mellitus is associated with alteration of insulin signaling, which could cause the reduction of glu-cose uptake, metabolic prohibition of energy consuming cells, as well as suppression of glucose to fat conversion in the liver. Glucose 216-223 insulin Homo sapiens 70-77 34803706-3 2021 It is known that the mCPP, a kind of 5-HT2CR agonist, decreases plasma insulin concentration in mice and previous research in our laboratory found that mCPP inhibited glucose-stimulated insulin secretion (GSIS) by activating 5-HT2CR on the beta cells. Glucose 167-174 insulin Homo sapiens 186-193 34900474-2 2021 The phosphatidylinositol 3-kinase (PI3K) pathway is responsible for activating protein kinase-B (AKT), and activated AKT promotes translation of glucose transporter 4 and glycogen synthesis in insulin-responsive tissues. Glucose 145-152 insulin Homo sapiens 193-200 34834285-3 2021 In this context, the aim of this work was to test the efficiency of exosome-mediated human insulin delivery using exosomes extracted from three different cell lines: hepatocellular carcinoma (HepG2); primary dermal fibroblasts (HDFa) and pancreatic beta cells (RIN-m); all are related to the production and/or the ability to sense insulin and to consequently regulate glucose levels in the extracellular medium. Glucose 368-375 insulin Homo sapiens 91-98 34834285-3 2021 In this context, the aim of this work was to test the efficiency of exosome-mediated human insulin delivery using exosomes extracted from three different cell lines: hepatocellular carcinoma (HepG2); primary dermal fibroblasts (HDFa) and pancreatic beta cells (RIN-m); all are related to the production and/or the ability to sense insulin and to consequently regulate glucose levels in the extracellular medium. Glucose 368-375 insulin Homo sapiens 331-338 34834285-6 2021 Glucose quantification assays revealed that exosome-mediated incorporation of insulin presented significant differences in HDFa and HepG2 cells, enhancing the transport in HDFa, in comparison with free human insulin effects in the regulation of extracellular glucose levels. Glucose 0-7 insulin Homo sapiens 78-85 34834285-6 2021 Glucose quantification assays revealed that exosome-mediated incorporation of insulin presented significant differences in HDFa and HepG2 cells, enhancing the transport in HDFa, in comparison with free human insulin effects in the regulation of extracellular glucose levels. Glucose 0-7 insulin Homo sapiens 208-215 34834285-6 2021 Glucose quantification assays revealed that exosome-mediated incorporation of insulin presented significant differences in HDFa and HepG2 cells, enhancing the transport in HDFa, in comparison with free human insulin effects in the regulation of extracellular glucose levels. Glucose 259-266 insulin Homo sapiens 78-85 34834285-6 2021 Glucose quantification assays revealed that exosome-mediated incorporation of insulin presented significant differences in HDFa and HepG2 cells, enhancing the transport in HDFa, in comparison with free human insulin effects in the regulation of extracellular glucose levels. Glucose 259-266 insulin Homo sapiens 208-215 34735502-1 2021 BACKGROUND: The triglyceride-glucose (TyG) index is a reliable indicator of insulin resistance. Glucose 29-36 insulin Homo sapiens 76-83 34803905-1 2021 Pancreatic beta-cells within the islets of Langerhans respond to rising blood glucose levels by secreting insulin that stimulates glucose uptake by peripheral tissues to maintain whole body energy homeostasis. Glucose 78-85 insulin Homo sapiens 106-113 34803905-1 2021 Pancreatic beta-cells within the islets of Langerhans respond to rising blood glucose levels by secreting insulin that stimulates glucose uptake by peripheral tissues to maintain whole body energy homeostasis. Glucose 130-137 insulin Homo sapiens 106-113 34499434-0 2021 Ultra-Fast Insulin-Pramlintide Co-Formulation for Improved Glucose Management in Diabetic Rats. Glucose 59-66 insulin Homo sapiens 11-18 34732497-13 2021 The characteristics of metformin-treated mothers differed from those of insulin-treated mothers as they were more likely to be obese but had lower glucose concentrations at diagnosis. Glucose 147-154 insulin Homo sapiens 72-79 34727021-2 2022 In the last 20 years this has led to a rise in the prevalence of prediabetes, diabetes and fatty liver in youngsters, due to the high degree of insulin resistance experienced by these patients and the consequent high availability of glucose. Glucose 233-240 insulin Homo sapiens 144-151 34727021-6 2022 METHODS: The model is based on the oral glucose minimal model and assumes that LPR is a fraction (fr) of glucose disposal rate, proportional to glucose concentration and controlled by insulin action. Glucose 105-112 insulin Homo sapiens 184-191 34725723-9 2022 Telehealth monitoring after outpatient initiation provides tools for improvement in glucose control with an insulin pump. Glucose 84-91 insulin Homo sapiens 108-115 34499434-1 2021 Dual-hormone replacement therapy with insulin and amylin in patients with type 1 diabetes has the potential to improve glucose management. Glucose 119-126 insulin Homo sapiens 38-45 34892175-3 2021 A model-based method was recently proposed to assess both contributions from 3-hour insulin-modified intravenous glucose tolerance test (IM-IVGTT); the aim of this study was to assess the reliability of short (1 hour) IM-IVGTT in the application of such model-based method and to evaluate the role of the two contributions in determining insulin clearance in pGDM. Glucose 113-120 insulin Homo sapiens 338-345 34658253-8 2021 Decreased prandial insulin resulted in greater % increase in peak glucose but not in integrated glucose concentrations attributable to non-suppressed glucagon. Glucose 66-73 insulin Homo sapiens 19-26 34524906-2 2021 Our studies in simian immunodeficiency virus (SIV)-infected male macaques demonstrated that chronic binge alcohol (CBA) reduced acute insulin response to glucose (AIRG), and at-risk alcohol use decreased HOMA-beta in PLWH. Glucose 154-161 insulin Homo sapiens 134-141 34892339-5 2021 In this work, we propose a new algorithm to optimize insulin dosing parameters in individuals with T1D who use a continuous glucose monitor and an insulin pump. Glucose 124-131 insulin Homo sapiens 53-60 34891383-10 2021 We test the controller in silico by simulating glucose-insulin dynamics in PBH and healthy nonsurgical individuals. Glucose 47-54 insulin Homo sapiens 55-62 34891642-3 2021 According to well-established clinical guidelines, insulin dosing at mealtime is calculated through an empirical formula which, however, does not take advantage of the knowledge of BG trend provided in real-time by continuous glucose monitoring (CGM) sensors. Glucose 226-233 insulin Homo sapiens 51-58 34433298-4 2021 The co-primary outcomes were changes at 10 weeks versus baseline in insulin resistance as assessed by steady-state plasma glucose during the insulin suppression test and insulin secretion as assessed by insulin secretion rate area under the curve (ISRAUC) during the graded-glucose infusion test. Glucose 122-129 insulin Homo sapiens 68-75 34433298-4 2021 The co-primary outcomes were changes at 10 weeks versus baseline in insulin resistance as assessed by steady-state plasma glucose during the insulin suppression test and insulin secretion as assessed by insulin secretion rate area under the curve (ISRAUC) during the graded-glucose infusion test. Glucose 274-281 insulin Homo sapiens 170-177 34939754-6 2021 Insulin secretion in response to various glucose concentrations was measured. Glucose 41-48 insulin Homo sapiens 0-7 34939754-10 2021 Expression of INSULIN and GLUT-2 genes (P<0.01 and P<0.05, respectively), insulin secretion in response to glucose (P<0.01), and percentage of NG-positive cells (P<0.05) in the 3MA-exposed cells were considerably lower than the cells treated with CDM. Glucose 107-114 insulin Homo sapiens 74-81 34310065-2 2021 Insulin, a hormone secreted from pancreatic beta-cells, decreases blood glucose levels, and glucagon, a hormone secreted from pancreatic alpha-cells, increases blood glucose levels by counterregulation of insulin through stimulation of hepatic glucose production. Glucose 72-79 insulin Homo sapiens 0-7 34310065-2 2021 Insulin, a hormone secreted from pancreatic beta-cells, decreases blood glucose levels, and glucagon, a hormone secreted from pancreatic alpha-cells, increases blood glucose levels by counterregulation of insulin through stimulation of hepatic glucose production. Glucose 166-173 insulin Homo sapiens 205-212 34456247-3 2021 We will try to outline how insulin resistance drives these pathways and inhibits glucose oxidation in the stressed organism. Glucose 81-88 insulin Homo sapiens 27-34 34456247-8 2021 Insulin resistance and decreased Glc oxidation indicate that requirements of Glc for anabolic pathways are high. Glucose 77-80 insulin Homo sapiens 0-7 34456247-10 2021 Insulin resistance prevents irreversible Glc oxidation and stimulates Glc production during stress or growth. Glucose 41-44 insulin Homo sapiens 0-7 34456247-10 2021 Insulin resistance prevents irreversible Glc oxidation and stimulates Glc production during stress or growth. Glucose 70-73 insulin Homo sapiens 0-7 34433630-5 2021 Glucose stimulated insulin secretion was blunted in PLIN2KD cells and improved in PLIN2OE cells. Glucose 0-7 insulin Homo sapiens 19-26 34547451-9 2021 Such contrasting observations raise the question as to whether the prolonged wear of CGM devices is or not the major causative factor for improvement in glucose variability among intensively insulin-treated persons with type 1 diabetes. Glucose 153-160 insulin Homo sapiens 191-198 34608609-1 2021 Insulin represents a mainstay of glucose-lowering therapy for many adults with type 2 diabetes mellitus (T2DM). Glucose 33-40 insulin Homo sapiens 0-7 34608609-3 2021 When choosing an insulin regimen for a frail older person with T2DM, predictability of glucose lowering effect, risk of hypoglycaemia, ease of administration, and simplicity and flexibility of dosing are major determining factors. Glucose 87-94 insulin Homo sapiens 17-24 34866875-1 2021 Background: ACHIEVE Control, a prospective, open-label, randomized, pragmatic, real-life study in insulin-naive people with type 2 diabetes (A1C 8.0-11.0%), demonstrated superiority of insulin glargine 300 units/mL (Gla-300) versus first-generation standard-of-care basal insulin (SOC-BI; glargine 100 units/mL or insulin detemir) in achieving individualized A1C targets without documented symptomatic (glucose <=3.9 mmol/L (<=70 mg/dL) or <3.0 mmol/L (<54 mg/dL)) or severe hypoglycemia (American Diabetes Association level 3) at 6 months. Glucose 403-410 insulin Homo sapiens 98-105 34347253-1 2021 PURPOSE: This study aimed to assess the cross-sectional and longitudinal associations of the triglyceride glucose (TyG) index, a simple surrogate marker of insulin resistance, with intra-cranial and extra-cranial artery stenosis (ICAS and ECAS) in Chinese adults. Glucose 106-113 insulin Homo sapiens 156-163 34467826-4 2021 AREAS COVERED: This paper reviews the design of - and data from - randomized controlled trials (RCTs) to assess glucose lowering efficacy and safety of long-acting insulin analogs for the treatment of type 1 diabetes. Glucose 112-119 insulin Homo sapiens 164-171 34892175-3 2021 A model-based method was recently proposed to assess both contributions from 3-hour insulin-modified intravenous glucose tolerance test (IM-IVGTT); the aim of this study was to assess the reliability of short (1 hour) IM-IVGTT in the application of such model-based method and to evaluate the role of the two contributions in determining insulin clearance in pGDM. Glucose 113-120 insulin Homo sapiens 84-91 34790115-7 2021 The parameters and investigations used in the studies to determine insulin sensitivity were glucose disposal rates, hyperglycemia, and mean glucose uptake. Glucose 92-99 insulin Homo sapiens 67-74 34790115-7 2021 The parameters and investigations used in the studies to determine insulin sensitivity were glucose disposal rates, hyperglycemia, and mean glucose uptake. Glucose 140-147 insulin Homo sapiens 67-74 34790115-10 2021 The analysis showed reduced glucose disposal rates and hence reduced insulin sensitivity with lopinavir (heterogeneity chi-squared = 0.68, I-squared (variation in SMD attributable to heterogeneity) = 0.0%, p = 0.031). Glucose 28-35 insulin Homo sapiens 69-76 34518649-1 2021 Associations of arterial stiffness with glucose, insulin, and proinsulin dynamics during the oral glucose tolerance test (OGTT) remain under debate. Glucose 98-105 insulin Homo sapiens 62-72 34518649-7 2021 All IRI and Pro levels before and after glucose loading and the area under the curve (AUC) values for IRI and Pro increased with higher PWV. Glucose 40-47 insulin Homo sapiens 12-15 34416394-3 2021 Given the potential of newly created insulin-producing cells as a treatment or even cure of type 1 diabetes (T1D) and possibly in severe cases of type 2 diabetes (T2D), multiple academic and commercial laboratories are attempting to derive surrogate glucose-responsive, insulin-producing cells. Glucose 250-257 insulin Homo sapiens 270-277 34590315-2 2021 Glucose uptake of insulin resistant HepG2 cells was measured by glucose oxidase method. Glucose 0-7 insulin Homo sapiens 18-25 34590315-2 2021 Glucose uptake of insulin resistant HepG2 cells was measured by glucose oxidase method. Glucose 64-71 insulin Homo sapiens 18-25 34590315-5 2021 The results showed that glucose uptake was enhanced and the expression of G-6-Pase was inhibited by PHL in insulin resistant HepG2 cells. Glucose 24-31 insulin Homo sapiens 107-114 34480921-5 2021 In the very earliest stages of diabetes development, there is a dramatic loss of glucose-induced first-phase insulin release (FPIR) with only trivial elevations of blood glucose levels. Glucose 81-88 insulin Homo sapiens 109-116 34480921-7 2021 The existence of a sophisticated feedback mechanism between insulin secretion and insulin action on peripheral tissues driven by glucose has been postulated, but it has been difficult to measure increases in blood glucose levels that might have been expected. Glucose 129-136 insulin Homo sapiens 60-67 34480921-7 2021 The existence of a sophisticated feedback mechanism between insulin secretion and insulin action on peripheral tissues driven by glucose has been postulated, but it has been difficult to measure increases in blood glucose levels that might have been expected. Glucose 129-136 insulin Homo sapiens 82-89 34480921-7 2021 The existence of a sophisticated feedback mechanism between insulin secretion and insulin action on peripheral tissues driven by glucose has been postulated, but it has been difficult to measure increases in blood glucose levels that might have been expected. Glucose 214-221 insulin Homo sapiens 82-89 34724122-1 2021 BACKGROUND: The triglyceride-glucose (TyG) index has been considered as insulin resistance (IR) assessment index. Glucose 29-36 insulin Homo sapiens 72-79 34098144-11 2021 Receptor redundancy may have been advantageous in animal evolution, given the role of the ABA/LANCL system in insulin-independent stimulation of cell glucose uptake and energy metabolism. Glucose 150-157 insulin Homo sapiens 110-117 34224918-8 2021 Mechanistically, hypoxia exposure increased insulin-independent glucose uptake compared to standard laboratory conditions (~50%, p < 0.001) and physiological normoxia (~25%, p = 0.019) through AMP-activated protein kinase in primary human myotubes, but not in primary human adipocytes. Glucose 64-71 insulin Homo sapiens 44-51 34720091-4 2021 In this system devoid of in vivo influences, the researchers annotated changes between the sexes and between the most and least insulin-sensitive quintiles of a healthy population (defined by steady-state blood glucose levels). Glucose 211-218 insulin Homo sapiens 128-135 34129291-9 2021 It was also found that when the rising trend in plasma glucose is started, preventive strategies to lessen insulin resistance might not be efficient. Glucose 55-62 insulin Homo sapiens 107-114 34382222-7 2021 Glycolytic metabolism and insulin-mediated glucose uptake were measured via extracellular acidification rate. Glucose 43-50 insulin Homo sapiens 26-33 34536491-7 2021 Development of small-molecule approaches (insulin-mimetic tablets) appears to have stalled, while concepts for glucose-responsive insulin as yet fail to deliver the necessary insulin-to-glucose gradient. Glucose 186-193 insulin Homo sapiens 175-182 34098144-2 2021 In mammals, ABA regulates blood glucose levels by stimulating insulin-independent glucose uptake and metabolism in adipocytes and myocytes, through its receptor LANCL2. Glucose 32-39 insulin Homo sapiens 62-69 34098144-2 2021 In mammals, ABA regulates blood glucose levels by stimulating insulin-independent glucose uptake and metabolism in adipocytes and myocytes, through its receptor LANCL2. Glucose 82-89 insulin Homo sapiens 62-69 34610553-7 2021 Oxidative stress was evaluated measuring F2-isoprostanes by GC-MS. Glucose metabolism and insulin sensitivity were verified by glucose and insulin tolerance tests, ex vivo and in vivo glucose uptake, and Western blotting for insulin signaling. Glucose 127-134 insulin Homo sapiens 90-97 34912428-6 2021 Fasting plasma glucose (FPG) was found to be an independent predictor of whether intensive insulin therapy could be discontinued after three months in a model that included FPG, HbA1c, and body mass index measured at baseline. Glucose 15-22 insulin Homo sapiens 91-98 34809740-5 2021 The insulin concentration was tested by ELISA to evaluate the insulin secretion of islet cells stimulated by high glucose. Glucose 114-121 insulin Homo sapiens 62-69 34809740-12 2021 When high glucose was given, the overexpression of miR-494 further promoted insulin secretion. Glucose 10-17 insulin Homo sapiens 76-83 34728340-0 2022 The switch from rapid-acting to concentrated regular insulin improves glucose control in type 2 diabetes patients on pump therapy: a cohort survey. Glucose 70-77 insulin Homo sapiens 53-60 34728340-11 2022 CONCLUSIONS: U-100 to U-500 insulin switch improves glucose control in CSII T2DM patients, especially with high baseline HbA1c. Glucose 52-59 insulin Homo sapiens 28-35 34718610-8 2022 Stable expression of human wild type MDH2 in MIN6-K8 cell lines enhanced glucose- and GLP-1-stimulated insulin secretion. Glucose 73-80 insulin Homo sapiens 103-110 34836102-11 2021 "Metabolically healthy" patients, but with insulin resistance, had higher blood pressure, glucose, uric acid and triglyceride levels than those without insulin resistance (all p < 0.05). Glucose 90-97 insulin Homo sapiens 43-50 34718610-10 2022 Nematodes carrying equivalent changes at the orthologous positions of the mdh-2 gene showed impaired glucose-stimulated insulin secretion. Glucose 101-108 insulin Homo sapiens 120-127 34829598-3 2021 High concentration of plasma glucose breaks the redox balance, inducing an oxidative stress that promotes chronic inflammation, insulin resistance, and impaired insulin secretion. Glucose 29-36 insulin Homo sapiens 128-135 34770502-2 2021 (1) Background: Intensive insulin therapy using continuous subcutaneous insulin infusion (CSII) with continuous real-time glucose monitoring (rt CGM) is the best option for patients with T1D. Glucose 122-129 insulin Homo sapiens 26-33 34733107-3 2021 GLP-1 increases the glucose level, dependent on insulin secretion from pancreatic beta-cells; it also decreases the abnormally increased level of glucagon, eventually decreasing the blood glucose level in patients with type 2 diabetes. Glucose 20-27 insulin Homo sapiens 48-55 34511291-1 2021 BACKGROUND AND AIMS: Triglyceride-glucose (TyG) index has been reported as a novel surrogate marker of insulin resistance and a risk factor in patients with coronary artery disease. Glucose 34-41 insulin Homo sapiens 103-110 34625361-1 2021 BACKGROUND AND AIMS: Triglyceride-Glucose (TyG) index is an accurate biomarker of insulin resistance, which is potentially associated with adverse cardiovascular events. Glucose 34-41 insulin Homo sapiens 82-89 34778653-6 2021 The results showed that FYGL-3 and FYGL-3-P significantly enhanced the insulin-provoked glucose uptake in insulin-resistant HepG2 cells, detected by the glucose oxidase method. Glucose 88-95 insulin Homo sapiens 71-78 34704817-1 2022 Real-time continuous glucose monitoring (RT-CGM) is superior to blood glucose monitoring (BGM) for adults with insulin-treated type 2 diabetes (T2D); however, the utility of C-peptide levels for predicting the magnitude of the glycemic benefits is controversial. Glucose 21-28 insulin Homo sapiens 111-118 34778653-6 2021 The results showed that FYGL-3 and FYGL-3-P significantly enhanced the insulin-provoked glucose uptake in insulin-resistant HepG2 cells, detected by the glucose oxidase method. Glucose 88-95 insulin Homo sapiens 106-113 34778653-6 2021 The results showed that FYGL-3 and FYGL-3-P significantly enhanced the insulin-provoked glucose uptake in insulin-resistant HepG2 cells, detected by the glucose oxidase method. Glucose 153-160 insulin Homo sapiens 71-78 34778653-6 2021 The results showed that FYGL-3 and FYGL-3-P significantly enhanced the insulin-provoked glucose uptake in insulin-resistant HepG2 cells, detected by the glucose oxidase method. Glucose 153-160 insulin Homo sapiens 106-113 34686554-12 2021 CONCLUSIONS: Our observational data suggest reduced efficacy of insulin-glucose treatment for hyperkalaemia in patients with cirrhosis. Glucose 72-79 insulin Homo sapiens 64-71 34702218-1 2021 AIM: Insulin resistance was reported to increase the risk of ischemic stroke, which can be assessed by the triglyceride glucose (TyG) index. Glucose 120-127 insulin Homo sapiens 5-12 34696774-11 2021 RESULTS: In critically ill children and adults receiving early parenteral nutrition, tight glucose control, as compared with liberal glucose control, lowered mean morning blood glucose on days 1-3 (P < 0.0001) via infusing insulin at a higher dose (P < 0.0001). Glucose 91-98 insulin Homo sapiens 223-230 34696774-11 2021 RESULTS: In critically ill children and adults receiving early parenteral nutrition, tight glucose control, as compared with liberal glucose control, lowered mean morning blood glucose on days 1-3 (P < 0.0001) via infusing insulin at a higher dose (P < 0.0001). Glucose 177-184 insulin Homo sapiens 223-230 34607828-8 2021 In the DKD cohort, higher risks of ESRD were seen with reduced renal function at baseline, high material deprivation, cancer and non-insulin glucose-lowering drugs, and a lower risk was seen with overweight (>=25 kg/m2). Glucose 141-148 insulin Homo sapiens 133-140 34686554-1 2021 OBJECTIVES: To determine if liver cirrhosis is associated with reduced efficacy of insulin-glucose treatment in moderate to severe hyperkalaemia. Glucose 91-98 insulin Homo sapiens 83-90 34686554-4 2021 PARTICIPANTS: This study included 463 adults with a mean age of 68.7+-15.8 years, comprising 79 patients with cirrhosis and 384 without cirrhosis as controls, who received standard insulin-glucose treatment for a serum potassium >=6.0 mmol/L from October 2016 to March 2020. Glucose 189-196 insulin Homo sapiens 181-188 34686554-9 2021 After insulin-glucose treatment, mean potassium lowering was 0.84+-0.58 mmol/L in patients with cirrhosis compared with 1.33+-0.75 mmol/L for controls (p<0.001). Glucose 14-21 insulin Homo sapiens 6-13 34686554-11 2021 By multivariable regression, on average, liver cirrhosis was associated with a reduced potassium lowering effect of 0.42 mmol/L (95% CI 0.22 to 0.63 mmol/L, p<0.001) from insulin-glucose treatment, after adjusting for age, serum creatinine, cancer, pretreatment potassium level, beta-blocker use and cotreatments (sodium polystyrene sulfonate, salbutamol, sodium bicarbonate). Glucose 179-186 insulin Homo sapiens 171-178 34651137-10 2021 Enteral dextrose increased circulating glucose-dependent insulinotropic peptide (76% increase; 95% CI (35-119); p < 0.01) and insulin (53% (17-88); p < 0.01) compared with placebo consistent with preclinical studies, but also increased blood glucose during the 24-hour infusion period (153 mg/dL (119-223) vs 116 mg/dL (91-140); p < 0.01). Glucose 8-16 insulin Homo sapiens 126-133 34651137-12 2021 CONCLUSIONS: Early infusion of low-level enteral dextrose in critically ill septic patients increased circulating levels of insulin and the incretin hormone glucose-dependent insulinotropic peptide without decreasing systemic inflammation. Glucose 49-57 insulin Homo sapiens 124-131 34622517-1 2021 BACKGROUND: Administration of insulin may be associated with substantial cutaneous adverse effects, such as lipoatrophy and lipohypertrophy (LH), which can cause glycemic excursions above and below the target levels for blood glucose. Glucose 226-233 insulin Homo sapiens 30-37 34615525-2 2021 The aim of this study was to investigate the potential association between insulin resistance measured by estimated glucose disposal rate (eGDR) and risk of stroke and mortality thereof in people with T2D. Glucose 116-123 insulin Homo sapiens 75-82 34676131-1 2021 Objective: Receptor activator of NF-kappabeta ligand (RANKL) is crucial for the development of hepatic insulin resistance and poor glucose uptake; therefore, inhibiting RANKL with Denosumab could improve fasting plasma glucose (FPG) and insulin (FPI). Glucose 131-138 insulin Homo sapiens 237-244 34626851-1 2022 BACKGROUND: Glucagon-like peptide-1 receptor agonists (GLP1RA) augment glucose-dependent insulin release and reduce glucagon secretion and gastric emptying, enabling their successful development for the treatment of type 2 diabetes (T2D). Glucose 71-78 insulin Homo sapiens 89-96 34608882-1 2021 INTRODUCTION: Insulin resistance (IR)/glucose intolerance is a critical biologic mechanism for the development of colorectal cancer (CRC) in postmenopausal women. Glucose 38-45 insulin Homo sapiens 14-21 34754656-6 2021 The patient was started on insulin therapy, and she showed clinical improvement with improving blood glucose levels. Glucose 101-108 insulin Homo sapiens 27-34 34639123-3 2021 As the liver is both a major target of insulin signalling and critically involved in glucose metabolism, the aim of this study was to examine the role of GPR21 in the regulation of glucose uptake and production in human hepatocytes. Glucose 181-188 insulin Homo sapiens 39-46 34609455-0 2021 Continuous Glucose Monitoring and Glycemic Control in Patients With Type 2 Diabetes Treated With Basal Insulin-Reply. Glucose 11-18 insulin Homo sapiens 103-110 34609457-0 2021 Continuous Glucose Monitoring and Glycemic Control in Patients With Type 2 Diabetes Treated With Basal Insulin. Glucose 11-18 insulin Homo sapiens 103-110 34609458-0 2021 Continuous Glucose Monitoring and Glycemic Control in Patients With Type 2 Diabetes Treated With Basal Insulin. Glucose 11-18 insulin Homo sapiens 103-110 34390299-5 2021 As a proof-of-concept, the polymersomes encapsulating enzymes could serve as nanoreactors and carries for glucose-stimulated insulin secretion in vivo inspired by human glucokinase, resulting in safe and effective treatment of type 1 diabetes mellitus in mouse models. Glucose 106-113 insulin Homo sapiens 125-132 34601490-8 2021 Baseline blood glucose greater than 98 mg/dl and preconceptional maternal Body Mass Index (BMI) between 26 and 31 kg/height2 increased substantially the probability of insulin therapy (odds ratio (OR) 4.04, 95% confidence interval (CI) CI 2.65-6.17 and 2.21, 95%CI 1.42-3.43, respectively). Glucose 15-22 insulin Homo sapiens 168-175 34601490-11 2021 Overweight women with an abnormal baseline blood glucose at OGTT are at high likelihood for insulin treatment. Glucose 49-56 insulin Homo sapiens 92-99 34601490-13 2021 Overweight women with baseline blood glucose greater than 98 mg/dl at OGTT are at increased risk for insulin treatment and close monitoring and increased physical exercise are required. Glucose 37-44 insulin Homo sapiens 101-108 34450327-5 2021 Moreover, the islets function was evaluated through glucose-induced insulin and C-peptide secretion assay. Glucose 52-59 insulin Homo sapiens 68-75 34175474-6 2021 RESULTS: In humans during the siOGTT, there is a long period (>3hr) of glucose absorption and accordingly a large and sustained insulin response as well as robust suppression of lipolysis and endogenous glucose production (EGP), even in the presence of glucose intolerance. Glucose 71-78 insulin Homo sapiens 128-135 34679116-1 2021 AIMS: Insulin sensitivity and insulin secretion can be estimated by multiple indices from fasting blood samples or blood samples obtained during oral glucose tolerance tests. Glucose 150-157 insulin Homo sapiens 6-13 34679116-1 2021 AIMS: Insulin sensitivity and insulin secretion can be estimated by multiple indices from fasting blood samples or blood samples obtained during oral glucose tolerance tests. Glucose 150-157 insulin Homo sapiens 30-37 34679116-8 2021 As for insulin sensitivity indices that are based on OGTT, the oral glucose insulin sensitivity index had the smallest coefficient of variation (6.5 +- 5.1%). Glucose 68-75 insulin Homo sapiens 7-14 34679116-8 2021 As for insulin sensitivity indices that are based on OGTT, the oral glucose insulin sensitivity index had the smallest coefficient of variation (6.5 +- 5.1%). Glucose 68-75 insulin Homo sapiens 76-83 34679116-10 2021 For the assessment of insulin secretion from fasting variables, the lowest mean coefficient of variation was found for C-peptide based homeostasis model assessment 2 beta with 10.8 +- 8% and the highest discriminant ratio for the C-peptide / Glucose-Ratio (2.18 (1.84-2.63)). Glucose 242-249 insulin Homo sapiens 22-29 34679116-11 2021 Among indices assessing insulin secretion from an OGTT, the lowest coefficient of variation was found for the ratio of the areas under the C-peptide and glucose curves from 0 to 120 minutes with 11.3 +- 9.7%. Glucose 153-160 insulin Homo sapiens 24-31 34160623-0 2021 Association between Smoking Behavior and Insulin Resistance Using Triglyceride-Glucose Index among South Korean adults. Glucose 79-86 insulin Homo sapiens 41-48 34160623-9 2021 Insulin resistance was determined based on the triglyceride-glucose index. Glucose 60-67 insulin Homo sapiens 0-7 34670012-6 2022 We assessed an organ-specific insulin sensitivity in the liver (HGP and %HGP), skeletal muscle (Rd), and adipose tissue (FFA and %FFA) using a hyperinsulinemic-euglycemic clamp study with stable isotope-labeled glucose infusion. Glucose 211-218 insulin Homo sapiens 30-37 34669746-10 2021 After adjustment for serum insulin and leptin, the correlation between serum cortisol and fasting glucose remained significant. Glucose 98-105 insulin Homo sapiens 27-34 34667273-6 2021 Silencing of Cpne3 in INS-1 cells impaired glucose-stimulated insulin secretion (GSIS), insulin content and glucose uptake efficiency without affecting cell viability or inducing apoptosis. Glucose 43-50 insulin Homo sapiens 62-69 34667273-7 2021 Moreover, mRNA and protein expression of the key regulators in glucose sensing and insulin secretion (Insulin, GLUT2, NeuroD1, and INSR) were downregulated in Cpne3-silenced cells. Glucose 63-70 insulin Homo sapiens 102-109 34670070-7 2022 After hydration and insulin treatment, the patient"s mental status and serum glucose and sodium levels improved, and no neurological complications were observed. Glucose 77-84 insulin Homo sapiens 20-27 34736121-7 2021 In conclusion, the impact of metformin on macrophages by suppressing a HIF1alpha-dependent proinflammatory program is likely responsible for a secondary beneficial effect on insulin-mediated glucose uptake and beta-adrenergic responses in brown adipocytes. Glucose 191-198 insulin Homo sapiens 174-181 34690504-1 2021 A relatively recent addition to the arsenal of antidiabetic drugs used for the treatment of type 2 diabetes mellitus (T2DM) has been the "incretin mimetics," a group of drugs that work on the glucagon-like peptide-1 (GLP-1) receptor and enhance insulin secretion from the pancreatic beta-cells in a glucose-dependent manner, more potently in hyperglycemic conditions, while suppressing glucagon secretion at the same time. Glucose 299-306 insulin Homo sapiens 245-252 34371008-2 2021 Accumulating evidence indicates that exposure to nutrient overload induces insulin resistance in these cells, manifested by abolition of the stimulatory effect of insulin on glucose uptake. Glucose 174-181 insulin Homo sapiens 75-82 34371008-2 2021 Accumulating evidence indicates that exposure to nutrient overload induces insulin resistance in these cells, manifested by abolition of the stimulatory effect of insulin on glucose uptake. Glucose 174-181 insulin Homo sapiens 163-170 34651567-2 2021 Evidence to date suggests that the endogenous glucose-insulin system could be involved at some level. Glucose 46-53 insulin Homo sapiens 54-61 34684619-1 2021 BACKGROUND: Insulin resistance (IR) is a condition in which the physiological amount of insulin is insufficient to evoke a proper response of the cell, that is, glucose utilization. Glucose 161-168 insulin Homo sapiens 12-19 34684619-1 2021 BACKGROUND: Insulin resistance (IR) is a condition in which the physiological amount of insulin is insufficient to evoke a proper response of the cell, that is, glucose utilization. Glucose 161-168 insulin Homo sapiens 88-95 34684619-7 2021 To assess insulin sensitivity, we measured the insulin-stimulated glucose uptake, using a glucose uptake test. Glucose 66-73 insulin Homo sapiens 10-17 34684619-7 2021 To assess insulin sensitivity, we measured the insulin-stimulated glucose uptake, using a glucose uptake test. Glucose 66-73 insulin Homo sapiens 47-54 34684619-7 2021 To assess insulin sensitivity, we measured the insulin-stimulated glucose uptake, using a glucose uptake test. Glucose 90-97 insulin Homo sapiens 47-54 34648113-0 2022 Insulin-related lipohypertrophy: ultrasound characteristics, risk factors, and impact of glucose fluctuations. Glucose 89-96 insulin Homo sapiens 0-7 34645432-2 2021 The triglyceride glucose (TyG) index, which was defined by incorporating serum glucose and insulin concentrations, was developed as a surrogate marker of insulin resistance. Glucose 17-24 insulin Homo sapiens 91-98 34645432-2 2021 The triglyceride glucose (TyG) index, which was defined by incorporating serum glucose and insulin concentrations, was developed as a surrogate marker of insulin resistance. Glucose 17-24 insulin Homo sapiens 154-161 34645432-2 2021 The triglyceride glucose (TyG) index, which was defined by incorporating serum glucose and insulin concentrations, was developed as a surrogate marker of insulin resistance. Glucose 79-86 insulin Homo sapiens 154-161 34745906-4 2021 Reactive hypoglycemia is thought to be due to impaired first phase insulin release in response to a glucose load, followed by a delayed and extended second phase insulin secretion; ineffective counterregulatory response to dropping glucose levels may also play a role. Glucose 100-107 insulin Homo sapiens 67-74 34745906-4 2021 Reactive hypoglycemia is thought to be due to impaired first phase insulin release in response to a glucose load, followed by a delayed and extended second phase insulin secretion; ineffective counterregulatory response to dropping glucose levels may also play a role. Glucose 232-239 insulin Homo sapiens 67-74 34745906-4 2021 Reactive hypoglycemia is thought to be due to impaired first phase insulin release in response to a glucose load, followed by a delayed and extended second phase insulin secretion; ineffective counterregulatory response to dropping glucose levels may also play a role. Glucose 232-239 insulin Homo sapiens 162-169 34684734-6 2021 Our results showed that orientin effectively improved metabolic activity, mainly by maintaining substrate utilization which was marked by enhanced glucose and palmitate uptake by liver cells subjected to insulin resistance. Glucose 147-154 insulin Homo sapiens 204-211 34707572-0 2021 The Association Between Triglyceride-Glucose Index as a Marker of Insulin Resistance and the Risk of Breast Cancer. Glucose 37-44 insulin Homo sapiens 66-73 34671683-1 2021 Background: Triglyceride-glucose (TyG) index is a convenient indicator of insulin resistance. Glucose 25-32 insulin Homo sapiens 74-81 34298056-9 2021 Insulin delivery in rats was enhanced by shuffle and penetramax and accompanied by a 10-20-fold decrease in blood glucose with immediate effect on the intestinal mucosa. Glucose 114-121 insulin Homo sapiens 0-7 34144091-1 2021 During diabetes development insulin production and glucose-stimulated insulin secretion (GSIS) are defective due to inflammation-related, yet not fully understood mechanisms. Glucose 51-58 insulin Homo sapiens 70-77 34324868-9 2021 It is common for diabetic patients to undergo insulin therapy to restore normal blood glucose levels. Glucose 86-93 insulin Homo sapiens 46-53 34520887-9 2021 Considering the limited organ supply and risks of immunosuppression, advances in biology (stem cell derived beta cells) or technology (automated insulin delivery systems) will be required to provide a scalable solution to deliver optimal glucose control and reduce CV risk for people with type 1 diabetes. Glucose 238-245 insulin Homo sapiens 145-152 34474209-1 2021 Growing evidencehas described a correlation between aldosterone, obesity, and insulin resistance, suggesting that adipocyte-related factors and mineralocorticoid receptor (MR) overactivation may alter aldosterone secretion, potentially leading to obesity and glucose intolerance. Glucose 259-266 insulin Homo sapiens 78-85 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 311-318 insulin Homo sapiens 357-364 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 311-318 insulin Homo sapiens 433-440 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 311-318 insulin Homo sapiens 498-505 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 311-318 insulin Homo sapiens 560-567 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 311-318 insulin Homo sapiens 603-610 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 387-394 insulin Homo sapiens 357-364 34266892-2 2021 We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Glucose 44-51 insulin Homo sapiens 14-21 34266892-2 2021 We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Glucose 44-51 insulin Homo sapiens 62-69 34266892-2 2021 We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Glucose 44-51 insulin Homo sapiens 173-180 34266892-2 2021 We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Glucose 199-206 insulin Homo sapiens 14-21 34266892-2 2021 We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Glucose 199-206 insulin Homo sapiens 62-69 34266892-2 2021 We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Glucose 199-206 insulin Homo sapiens 173-180 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Glucose 39-46 insulin Homo sapiens 13-20 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Glucose 39-46 insulin Homo sapiens 354-361 34272965-9 2021 Higher baseline fasting insulin corresponded with higher BMIZ (0.41 (95% CI 0.26, 0.55)), SAT (13.9 (95% CI 2.4, 25.4) mm2), VAT (2.0 (95% CI 0.1, 3.8) mm2), HOMA-IR (0.87 (95% CI 0.68, 1.07)) and fasting glucose (0.23 (95% CI 0.09, 0.38) SD). Glucose 205-212 insulin Homo sapiens 24-31 34311283-7 2021 Furthermore, the numerically higher clearance rate (CR) of glucose and more negative glucose AUC following intravenous administration of insulin in Zinc-supplemented groups suggested that the ewes had greater insulin response than control group. Glucose 59-66 insulin Homo sapiens 137-144 34311283-7 2021 Furthermore, the numerically higher clearance rate (CR) of glucose and more negative glucose AUC following intravenous administration of insulin in Zinc-supplemented groups suggested that the ewes had greater insulin response than control group. Glucose 59-66 insulin Homo sapiens 209-216 34362815-1 2021 OBJECTIVE: To assess the progression of type 1 diabetes using time to peak glucose or C-peptide during oral glucose tolerance tests (OGTTs) in autoantibody-positive relatives of people with type 1 diabetes. Glucose 108-115 insulin Homo sapiens 86-95 34593535-4 2021 In this article we will present a testable hypothetical mechanism to explain the role of lipids and ROS in basal hyperinsulinemia and how they differ from glucose-stimulated insulin secretion (GSIS). Glucose 155-162 insulin Homo sapiens 174-181 34505411-2 2021 The aim of this study was to examine the performance of insulin resistance, evaluated using the estimated glucose disposal rate (eGDR) for the identification of metabolic syndrome (MS) and diabetic chronic complications. Glucose 106-113 insulin Homo sapiens 56-63 34872638-2 2021 This protein has been shown to contribute to the glucose-dependent regulation of insulin secretion in pancreatic islets. Glucose 49-56 insulin Homo sapiens 81-88 34556536-4 2021 METHODS: This pre- and postintervention cohort study measured wait times between point-of-care glucose testing and insulin administration. Glucose 95-102 insulin Homo sapiens 115-122 34556536-11 2021 Post-IDC implementation, the average wait time between point-of-care glucose testing and insulin administration decreased from 37 to 25 minutes (P < .05). Glucose 69-76 insulin Homo sapiens 89-96 34229177-6 2021 In this dose range, licochalcone E substantially increased the uptake and consumption of glucose in the insulin resistance model and dose-dependently reduced the concentration of total cholesterol. Glucose 89-96 insulin Homo sapiens 104-111 34348505-2 2021 The objective of this work was to create an algorithm for controlling the function of insulin pumps in closed-loop systems to improve blood glucose management in type 1 diabetic patients by mimicking the pulsatile behaviour of the pancreas. Glucose 140-147 insulin Homo sapiens 86-93 34140628-0 2021 omega-3PUFA supplementation ameliorates adipose tissue inflammation and insulin-stimulated glucose disposal in subjects with obesity: a potential role for apolipoprotein E. Glucose 91-98 insulin Homo sapiens 72-79 34480874-5 2021 Approaches to these problems could be modification of the peptide by adducts, or the use of nanoparticles or insulin patches, which deliver insulin according to glucose concentration. Glucose 161-168 insulin Homo sapiens 109-116 34480874-5 2021 Approaches to these problems could be modification of the peptide by adducts, or the use of nanoparticles or insulin patches, which deliver insulin according to glucose concentration. Glucose 161-168 insulin Homo sapiens 140-147 34375645-0 2021 Rheb1 Promotes Glucose-stimulated Insulin Secretion in Human and Mouse beta-cells by Upregulating GLUT Expression. Glucose 15-22 insulin Homo sapiens 34-41 34375645-3 2021 Here, we demonstrate that the small GTPase Rheb1 is a critical regulator of glucose-stimulated insulin secretion (GSIS) in beta-cells. Glucose 76-83 insulin Homo sapiens 95-102 34315812-2 2021 Recent reports have highlighted how biased agonism at the GLP-1R affects sustained glucose-stimulated insulin secretion through avoidance of desensitisation and downregulation. Glucose 83-90 insulin Homo sapiens 102-109 34464025-2 2021 Insulin-mediated glucose uptake in skeletal muscle and primary myotubes is decreased by obesity, whereas differences in basal glucose metabolism are inconsistent among studies. Glucose 17-24 insulin Homo sapiens 0-7 34154931-1 2021 BACKGROUND: Subcutaneous insulin therapy is associated with important injection site complications, which can influence insulin pharmacokinetics resulting in glycemic fluctuations above and below target levels for blood glucose. Glucose 220-227 insulin Homo sapiens 25-32 34154931-1 2021 BACKGROUND: Subcutaneous insulin therapy is associated with important injection site complications, which can influence insulin pharmacokinetics resulting in glycemic fluctuations above and below target levels for blood glucose. Glucose 220-227 insulin Homo sapiens 120-127 34428602-9 2021 The analysis focused on insulin pumps and technologies for continuous glucose monitoring (CGM). Glucose 70-77 insulin Homo sapiens 24-31 34462181-1 2021 Microtubules (MT) have a role in the intracellular response to insulin stimulation and subsequent glucose transport by glucose transporter 4 (GLUT4), which resides in specialized storage vesicles that travel through the cell. Glucose 98-105 insulin Homo sapiens 63-70 34252390-3 2021 SIRT1 protein levels and activity and AMPK phosphorylation decrease under hyperglycemic conditions, with concomitant inhibition of the effect of insulin on glucose uptake into these cells. Glucose 156-163 insulin Homo sapiens 145-152 34252390-7 2021 We also examined the ability of the NOS/NO pathway to protect podocytes against high glucose-induced alterations of SIRT1/AMPK signaling and insulin-dependent glucose uptake. Glucose 159-166 insulin Homo sapiens 141-148 34252390-8 2021 Inhibition of the NOS/NO pathway reduced SIRT1 protein levels and activity, leading to a decrease in AMPK phosphorylation and blockade of the effect of insulin on glucose uptake. Glucose 163-170 insulin Homo sapiens 152-159 34252390-10 2021 These findings suggest that inhibition of the NOS/NO pathway may result in alterations of the effects of insulin on glucose uptake in podocytes. Glucose 116-123 insulin Homo sapiens 105-112 34521773-4 2021 Oral glucose administration stimulates increased insulin secretion in comparison with isoglycemic intravenous glucose administration, a phenomenon known as the incretin effect. Glucose 5-12 insulin Homo sapiens 49-56 34323098-2 2021 Its role in insulin resistance appears to be of great importance, as it is involved in oxidative stress, the endocrine regulation of insulin, and the regulation of glucose uptake. Glucose 164-171 insulin Homo sapiens 12-19 34616176-1 2021 Background: Triglyceride-glucose (TyG) index has been considered as the reliable marker of insulin resistance (IR), which is one risk factor of kidney stone. Glucose 25-32 insulin Homo sapiens 91-98 34587231-6 2022 We determined insulin concentration 30 min after a 75-g oral glucose load (insulin-30) as a measure of insulin secretion and HOMA-IR as a measure of insulin resistance at baseline. Glucose 61-68 insulin Homo sapiens 14-21 34587231-6 2022 We determined insulin concentration 30 min after a 75-g oral glucose load (insulin-30) as a measure of insulin secretion and HOMA-IR as a measure of insulin resistance at baseline. Glucose 61-68 insulin Homo sapiens 103-110 34463643-7 2021 Glucose-stimulated insulin secretion and production of inflammatory cytokines (TNFa, IL1b and IFNg) were measured by ELISA. Glucose 0-7 insulin Homo sapiens 19-26 34580120-1 2021 The pancreatic beta-cells are essential for regulating glucose homeostasis through the coordinated release of the insulin hormone. Glucose 55-62 insulin Homo sapiens 114-121 34086911-10 2021 At 104 weeks, basal and insulin-stimulated adipocyte glucose uptake increased by 3-fold vs baseline and expression of genes involved in glucose transport, fatty acid oxidation and adipogenesis was upregulated (p<0.01). Glucose 53-60 insulin Homo sapiens 24-31 34086911-10 2021 At 104 weeks, basal and insulin-stimulated adipocyte glucose uptake increased by 3-fold vs baseline and expression of genes involved in glucose transport, fatty acid oxidation and adipogenesis was upregulated (p<0.01). Glucose 136-143 insulin Homo sapiens 24-31 34100545-0 2021 Use of Continuous Glucose Monitor in Critically Ill COVID-19 Patients Requiring Insulin Infusion: An Observational Study. Glucose 18-25 insulin Homo sapiens 80-87 34638768-5 2021 Beta cell function was assessed by glucose-stimulated insulin secretion (GSIS), gene expression by qPCR and RNA-sequencing, and proliferation by incorporation of EdU into newly synthesized DNA. Glucose 35-42 insulin Homo sapiens 54-61 34630911-2 2021 Skeletal muscle is arguably the most important contributor to glucose disposal making it a clear target in insulin resistance and T2D research. Glucose 62-69 insulin Homo sapiens 107-114 34630911-4 2021 Emerging evidence in skeletal muscle implicates influential cross talk between a key anabolic regulatory protein, the mammalian target of rapamycin (mTOR) and its associated complexes (mTORC1 and mTORC2), and the well-described canonical signaling for insulin-stimulated glucose uptake. Glucose 271-278 insulin Homo sapiens 252-259 34630911-6 2021 Here, we briefly review the most recent understanding of insulin signaling in skeletal muscle, and how anabolic responses favoring anabolism directly impact cellular glucose disposal. Glucose 166-173 insulin Homo sapiens 57-64 34568974-7 2021 The evaluated indicators of insulin resistance included fasting glucose, fasting insulin, and homeostasis model assessment-estimated insulin resistance (HOMA-IR) collected pre- and post-intervention. Glucose 64-71 insulin Homo sapiens 28-35 34559683-5 2022 To reach glycated hemoglobin (HbA1c) values of 48 mmol/mol, lifetime rigorous monitoring and management of blood glucose levels via insulin replacement treatment is needed in T1D. Glucose 113-120 insulin Homo sapiens 132-139 34561756-1 2022 AIMS: The two predominant pathophysiological defects resulting in glucose intolerance are beta-cell dysfunction and insulin insensitivity. Glucose 66-73 insulin Homo sapiens 116-123 34561756-2 2022 This study aimed to re-examine beta-cell function and insulin sensitivity across a continuum from normal glucose tolerance (NGT) to early type 2 diabetes (T2DM) employing highly specific insulin, C-peptide and intact proinsulin assays. Glucose 105-112 insulin Homo sapiens 54-61 34561756-4 2022 Following an overnight fast, all underwent a 4-h standardised mixed meal tolerance test (MTT), and on a second day, a sub-group underwent a frequently sampled insulin-modified intravenous glucose tolerance test (FSIVGTT) over a 3-h period. Glucose 188-195 insulin Homo sapiens 159-166 34561756-8 2022 FSIVGTT demonstrated a major reduction in the early insulin response to IV glucose in persons with IGT accompanied by a dramatic fall in insulin sensitivity. Glucose 75-82 insulin Homo sapiens 52-59 34684365-0 2021 Comparing the Fasting and Random-Fed Metabolome Response to an Oral Glucose Tolerance Test in Children and Adolescents: Implications of Sex, Obesity, and Insulin Resistance. Glucose 68-75 insulin Homo sapiens 154-161 34558100-2 2021 The two hormones act in different ways: in fact insulin triggers glucose uptake in muscle and liver cells, removing glucose from the bloodstream and making it available for energy use and storage, while amylin regulates glucose homeostasis. Glucose 65-72 insulin Homo sapiens 48-55 34558100-2 2021 The two hormones act in different ways: in fact insulin triggers glucose uptake in muscle and liver cells, removing glucose from the bloodstream and making it available for energy use and storage, while amylin regulates glucose homeostasis. Glucose 116-123 insulin Homo sapiens 48-55 34565075-6 2021 The ACE2/Ang-(1-7)/Mas axis can enhance glucose tolerance and improve insulin sensitivity by protecting pancreatic beta cells, increasing insulin secretion, improving glucose metabolism in adipose tissue, enhancing glucose uptake by skeletal muscle, and inhibiting hepatic gluconeogenesis. Glucose 215-222 insulin Homo sapiens 70-77 34556670-12 2021 In this study, we identify BBR as a glucose-dependent insulin secretagogue for treating diabetes without causing hypoglycemia that targets KCNH6 channels. Glucose 36-43 insulin Homo sapiens 54-61 34551206-1 2022 AIMS/INTRODUCTION: The union of dipeptidyl peptidase-4 (DPP-4) inhibitors and insulin in patients with type 2 diabetes (T2D) and chronic kidney disease (CKD) provides satisfactory glucose management without increasing adverse events (AEs). Glucose 180-187 insulin Homo sapiens 78-85 34542800-1 2022 PURPOSE: Previous studies suggest that triglyceride-glucose index (TyG) index, as a marker of insulin resistance, may have associations with the risk of cardiovascular diseases (CVD) in elderly population. Glucose 52-59 insulin Homo sapiens 94-101 34616762-9 2021 For EDIH, the percent change in biomarker concentration in the insulin-related biomarkers ranged from +1.3% (glucose) to +8% (homeostatic model assessment for insulin resistance) and -9.7% for IGF-binding protein-1. Glucose 109-116 insulin Homo sapiens 63-70 34279615-2 2021 MATERIALS AND METHODS: Using electronic health records from a tertiary academic center between 2008 and 2020 of 16 848 inpatients receiving subcutaneous insulin who achieved target blood glucose control of 100-180 mg/dL on a calendar day, we trained an ensemble machine learning algorithm consisting of regularized regression, random forest, and gradient boosted tree models for 2-stage TDD prediction. Glucose 187-194 insulin Homo sapiens 153-160 34564455-8 2021 Thus, IDegAsp was more effective than conventional premixed insulin and basal insulin at reducing blood glucose with fewer nocturnal hypoglycemia events. Glucose 104-111 insulin Homo sapiens 78-85 34603025-8 2021 In vitro, gastrodin alleviated insulin resistance by increasing glucose consumption, glucose uptake, and glycogen content in dexamethasone-induced HepG2 cells. Glucose 64-71 insulin Homo sapiens 31-38 34603025-8 2021 In vitro, gastrodin alleviated insulin resistance by increasing glucose consumption, glucose uptake, and glycogen content in dexamethasone-induced HepG2 cells. Glucose 85-92 insulin Homo sapiens 31-38 34428715-2 2021 T2DM is a metabolic disorder, which is characterized by deficiency in insulin or resistance to insulin and thus increases the glucose levels in the blood. Glucose 126-133 insulin Homo sapiens 95-102 34469130-1 2021 This work aims to construct biocompatible, biodegradable core-cross-linked and insulin-loaded nanoparticles which are sensitive to glucose and release insulin via cleavage of the nanoparticles in a high-concentration blood glucose environment. Glucose 131-138 insulin Homo sapiens 79-86 34469130-1 2021 This work aims to construct biocompatible, biodegradable core-cross-linked and insulin-loaded nanoparticles which are sensitive to glucose and release insulin via cleavage of the nanoparticles in a high-concentration blood glucose environment. Glucose 131-138 insulin Homo sapiens 151-158 34469130-1 2021 This work aims to construct biocompatible, biodegradable core-cross-linked and insulin-loaded nanoparticles which are sensitive to glucose and release insulin via cleavage of the nanoparticles in a high-concentration blood glucose environment. Glucose 223-230 insulin Homo sapiens 79-86 34469130-1 2021 This work aims to construct biocompatible, biodegradable core-cross-linked and insulin-loaded nanoparticles which are sensitive to glucose and release insulin via cleavage of the nanoparticles in a high-concentration blood glucose environment. Glucose 223-230 insulin Homo sapiens 151-158 34469130-6 2021 The ability of NPs to load fluorescein isothiocyanate-labeled insulin (FITC-insulin) and their glucose-triggered release behavior were detected by a fluorescence spectrophotometer. Glucose 95-102 insulin Homo sapiens 62-69 34469130-9 2021 This research provides a new method for constructing biodegradable and glucose-sensitive core-cross-linked nanomedicine carriers for controlled insulin release. Glucose 71-78 insulin Homo sapiens 144-151 34521309-2 2022 Glucose requirements post-HDI reflect supraphysiological insulin plasma concentration. Glucose 0-7 insulin Homo sapiens 57-64 34521490-9 2021 These included improvements in fasting blood glucose and reductions in glucose and increase in insulin levels following a glucose tolerance test. Glucose 122-129 insulin Homo sapiens 95-102 34526121-5 2021 MAIN TEXT: Therapy with glucagon-like peptide 1 receptor agonist (GLP-1 RA) promotes strategic changes in the pathophysiological pathway of T2D and improves the secretion of glucagon and insulin, which results in a reduction in blood glucose levels and the promotion of weight loss. Glucose 234-241 insulin Homo sapiens 187-194 34777770-1 2021 Fatty acid amides (FAAs) are a family of second-messenger lipids that target cannabinoid receptors, and are known mediators of glucose-stimulated insulin secretion from pancreatic beta-cells. Glucose 127-134 insulin Homo sapiens 146-153 34777770-5 2021 We designed a probe to release palmitoylethanolamide (PEA), a GPR55 agonist known to stimulate glucose-stimulated insulin secretion (GSIS). Glucose 95-102 insulin Homo sapiens 114-121 34594226-5 2021 Independent of AT1 receptor and peroxisome proliferator-activated receptor gamma (PPARgamma), telmisartan exerted effects on ion channels including voltage-dependent potassium (Kv) channels and L-type voltage-gated calcium channels (VGCCs) to promote extracellular Ca2+ influx, thereby potentiating insulin secretion in a glucose-dependent manner. Glucose 322-329 insulin Homo sapiens 299-306 34423981-0 2021 Glucose and pH Dual-Responsive Polymersomes with Multilevel Self-Regulation of Blood Glucose for Insulin Delivery. Glucose 0-7 insulin Homo sapiens 97-104 34423981-0 2021 Glucose and pH Dual-Responsive Polymersomes with Multilevel Self-Regulation of Blood Glucose for Insulin Delivery. Glucose 85-92 insulin Homo sapiens 97-104 34423981-1 2021 Smart insulin delivery systems now play essential roles in diabetes treatment, whereas most existing systems suffer from insufficient regulation against blood glucose. Glucose 159-166 insulin Homo sapiens 6-13 34423981-2 2021 Here, a glucose and pH dual-responsive insulin delivery system with multilevel self-regulation of blood glucose was constructed. Glucose 8-15 insulin Homo sapiens 39-46 34423981-2 2021 Here, a glucose and pH dual-responsive insulin delivery system with multilevel self-regulation of blood glucose was constructed. Glucose 104-111 insulin Homo sapiens 39-46 34423981-6 2021 This multilevel tunability was reflected directly in in vitro insulin release tests and was proven by the self-regulation of blood glucose in vivo. Glucose 131-138 insulin Homo sapiens 62-69 34760269-1 2021 Insulin resistance (IR) is a state characterized by the inability of tissues to utilize blood glucose particularly liver, muscle, and adipose tissues resulting in hyperglycemia and hyperinsulinemia. Glucose 94-101 insulin Homo sapiens 0-7 34589530-2 2021 The triglyceride glucose (TyG) index has been a convenient and reliable surrogate marker of insulin resistance (IR). Glucose 17-24 insulin Homo sapiens 92-99 34575946-4 2021 By limiting the peripheral use of glucose with consequent hyperglycemia, insulin resistance determines compensatory increased levels of insulin in plasma. Glucose 34-41 insulin Homo sapiens 73-80 34575946-4 2021 By limiting the peripheral use of glucose with consequent hyperglycemia, insulin resistance determines compensatory increased levels of insulin in plasma. Glucose 34-41 insulin Homo sapiens 136-143 34575946-6 2021 In the end, via pathological insulin signaling associated with increased liver gluconeogenesis, elevated levels of glucose are detected in the blood. Glucose 115-122 insulin Homo sapiens 29-36 34515521-1 2022 Background: Use of continuous glucose monitoring (CGM) systems is being rapidly adopted as standard of care for insulin-requiring patients with diabetes. Glucose 30-37 insulin Homo sapiens 112-119 34503961-12 2022 glucose loading when compared to oral glucose loading (51+-15 vs. 132+-29 min; p<0.0001), paralleled by higher insulin doses (6.3 +- 2.2 vs. 2.0 +- 1.69 U; p<0.001). Glucose 0-7 insulin Homo sapiens 111-118 34646376-1 2021 As a first-line treatment for diabetes, the insulin-sensitizing biguanide, metformin, regulates glucose levels and positively affects cardiovascular function in patients with diabetes and cardiovascular complications. Glucose 96-103 insulin Homo sapiens 44-51 34568592-4 2021 We hypothesized that LFV promotes non-insulin-mediated glucose uptake, which is also referred to as AMPK-mediated glucose uptake, in adipocytes at wound sites, thereby alleviating hyperglycemia, which, in turn, accelerates wound healing. Glucose 55-62 insulin Homo sapiens 38-45 34568592-4 2021 We hypothesized that LFV promotes non-insulin-mediated glucose uptake, which is also referred to as AMPK-mediated glucose uptake, in adipocytes at wound sites, thereby alleviating hyperglycemia, which, in turn, accelerates wound healing. Glucose 114-121 insulin Homo sapiens 38-45 34483209-3 2022 The total amount of glucose administration was 4,464 g. It took over three weeks for exogenous insulin to be almost undetectable. Glucose 20-27 insulin Homo sapiens 95-102 34266892-1 2021 We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after (18F)fluorodeoxyglucose and (15O)water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. Glucose 31-38 insulin Homo sapiens 357-364 34486426-0 2021 Methods for Insulin Bolus Adjustment Based on the Continuous Glucose Monitoring Trend Arrows in Type 1 Diabetes: Performance and Safety Assessment in an In Silico Clinical Trial. Glucose 61-68 insulin Homo sapiens 12-19 34487089-9 2021 An inverse correlation was found between 1-hour plasma glucose value during OGTT and insulin secretion-sensitivity index-2 (ISSI-2) (r: -0.3298; p: 0.025), between ISSI-2 and ALT (r: -0.3262; p: 0.027), and between 1-hour plasma glucose value and ISSI-2 (r: -0.537; p: 0.005) in the whole group of beta-TDT patients enrolled in our study. Glucose 55-62 insulin Homo sapiens 85-92 34527069-1 2021 Background: Diabetes mellitus (DM) is a metabolic disorder characterized by a persistent rise in the blood glucose level resulting from defects in cellular insulin function, secretion, or both, which affects millions of people every year. Glucose 107-114 insulin Homo sapiens 156-163 34564415-2 2021 Despite recent advances in insulin formulations, the SC route still suffers from delays and large inter/intra-subject variability that limiting optimal glucose control. Glucose 152-159 insulin Homo sapiens 27-34 34090857-7 2021 However, the efficacy of adipogenic differentiation, stimulation of FABP4 and PPARg protein expressions, and glucose uptake stimulation by insulin were reduced for ASC52Telo-derived adipocytes in comparison with ADSC-derived adipocytes. Glucose 109-116 insulin Homo sapiens 139-146 34575477-8 2021 These observations were correlated with standard glucose-stimulated insulin secretion (GSIS), which resulted in being reduced in cells exposed to Palm but preserved in cells concomitantly exposed to 10 nM Ex-4. Glucose 49-56 insulin Homo sapiens 68-75 34102108-1 2021 Insulin resistance results when peripheral tissues, including adipose, skeletal muscle and liver, do not respond appropriately to insulin causing the ineffective uptake of glucose. Glucose 172-179 insulin Homo sapiens 0-7 34102108-1 2021 Insulin resistance results when peripheral tissues, including adipose, skeletal muscle and liver, do not respond appropriately to insulin causing the ineffective uptake of glucose. Glucose 172-179 insulin Homo sapiens 130-137 34531243-3 2021 The M value is the rate of whole-body glucose metabolism at the hyperinsulinemic plateau (a measure of insulin sensitivity) and is calculated between 60 and 120 min after the start of the insulin infusion in the HEC procedure. Glucose 38-45 insulin Homo sapiens 103-110 34531243-3 2021 The M value is the rate of whole-body glucose metabolism at the hyperinsulinemic plateau (a measure of insulin sensitivity) and is calculated between 60 and 120 min after the start of the insulin infusion in the HEC procedure. Glucose 38-45 insulin Homo sapiens 188-195 34561081-5 2021 As a result, compounds 9-12 were found to increase the glucose uptake of insulin-resistant HepG2 cells by 18.1%, 62.7%, 33.7% and 21.4% at the dose of 50 mumol L-1, respectively. Glucose 55-62 insulin Homo sapiens 73-80 34309808-7 2021 These agents act in a glucose-dependent manner to promote insulin secretion and inhibit glucagon secretion, as well as enhancing satiety and reducing hunger. Glucose 22-29 insulin Homo sapiens 58-65 34342864-0 2021 Shift of Glucose Peak Time During Oral Glucose Tolerance Test is Associated with Changes in Insulin Secretion and Insulin Sensitivity After Therapy with Antidiabetic Drugs in Patients with Type 2 Diabetes. Glucose 9-16 insulin Homo sapiens 92-99 34342864-0 2021 Shift of Glucose Peak Time During Oral Glucose Tolerance Test is Associated with Changes in Insulin Secretion and Insulin Sensitivity After Therapy with Antidiabetic Drugs in Patients with Type 2 Diabetes. Glucose 9-16 insulin Homo sapiens 114-121 34362813-9 2021 With oral glucose ingestion, an ISR-independent ~10% EIC reduction is necessary to explain the observed insulin concentration profiles. Glucose 10-17 insulin Homo sapiens 104-111 34362813-12 2021 Finally, oral glucose ingestion per se reduces insulin clearance. Glucose 14-21 insulin Homo sapiens 47-54 34546079-0 2021 Budget Impact of the Flash Continuous Glucose Monitoring System in Medicaid Diabetes Beneficiaries Treated with Intensive Insulin Therapy. Glucose 38-45 insulin Homo sapiens 122-129 34546079-1 2021 Objective: We assessed the economic impact of using the newest flash continuous glucose monitoring (CGM) among Medicaid beneficiaries with diabetes treated with intensive insulin therapy (IIT). Glucose 80-87 insulin Homo sapiens 171-178 34546082-1 2021 Numerous studies have demonstrated the clinical benefits of continuous glucose monitoring (CGM) use in individuals with type 1 diabetes and type 2 diabetes (T2D) who are treated with intensive insulin therapy. Glucose 71-78 insulin Homo sapiens 193-200 34546086-1 2021 Numerous studies have demonstrated that use of continuous glucose monitoring (CGM) improves glycemic control and reduces diabetes-related hospitalizations and emergency room service utilization in individuals with diabetes who are treated with intensive insulin regimens. Glucose 58-65 insulin Homo sapiens 254-261 34488057-0 2021 Effectiveness of the freestyle libre 2 flash glucose monitoring system on diabetes-self-management practices and glycemic parameters among patients with type 1 diabetes using insulin pump. Glucose 45-52 insulin Homo sapiens 175-182 34310013-3 2021 This is exemplified by the incretin effect (greater insulin secretory response to oral as compared to "isoglycaemic" intravenous glucose administration due to the secretion and action of incretin hormones). Glucose 129-136 insulin Homo sapiens 52-59 34298566-1 2021 The triglyceride-glucose (TyG) index, a recently proposed indicator for insulin resistance, has been related with cardiovascular risks. Glucose 17-24 insulin Homo sapiens 72-79 34378802-3 2021 The present study aims to isolate the constituents of the plant and investigate their effects on the glucose consumption in insulin-resistant HepG2 cells, furthermore, lipid metabolism in oleic acid (OA)-treated HepG2 cells was also studied. Glucose 101-108 insulin Homo sapiens 124-131 34120352-5 2021 RESULTS: Women affected by elevated fasting and post-load glucose concentrations (GDM-CH) showed adverse metabolic profiles already at beginning of pregnancy including a higher degree of insulin resistance as compared to women with normal glucose tolerance and those with isolated defects (especially GDM-IPH). Glucose 58-65 insulin Homo sapiens 187-194 34378802-5 2021 The results revealed that compounds 7, 9, and 10 could enhance glucose consumption significantly in hyperglycemia induced HepG2 cells and insulin-resistant HepG2 cells. Glucose 63-70 insulin Homo sapiens 138-145 34378802-9 2021 To study the chemical constituents and their effects on glucose and lipid metabolism in vitro, we detected glucose consumption in insulin-resistant HepG2 cells, triglyceride content and reactive oxygen species level in OA-treated HepG2 cells. Glucose 107-114 insulin Homo sapiens 130-137 34925590-0 2021 Association of Triglyceride-Glucose Index (TyG index) with HbA1c and Insulin Resistance in Type 2 Diabetes Mellitus. Glucose 28-35 insulin Homo sapiens 69-76 34925590-1 2021 Background: The aim of this study was to assess the association of triglyceride-glucose (TyG) index with glycated haemoglobin (HbA1c) and insulin resistance in type 2 diabetes mellitus (T2DM). Glucose 80-87 insulin Homo sapiens 138-145 34174327-0 2021 Non-glucose modulators of insulin secretion in healthy humans: (dis)similarities between islet and in vivo studies. Glucose 4-11 insulin Homo sapiens 26-33 34349281-1 2021 We detail a six-stage planar differentiation methodology for generating human pluripotent stem cell-derived pancreatic beta cells (SC-beta cells) that secrete high amounts of insulin in response to glucose stimulation. Glucose 198-205 insulin Homo sapiens 175-182 34174327-3 2021 This review is based on the analysis of clinical investigations characterizing the effects of non-glucose modulators of insulin secretion in healthy subjects, and of experimental studies testing the same modulators in islets isolated from normal human donors. Glucose 98-105 insulin Homo sapiens 120-127 34502359-2 2021 Metformin, which is widely prescribed for type 2 diabetes mellitus (T2DM) patients, regulates blood sugar by inhibiting hepatic gluconeogenesis and promoting insulin sensitivity to facilitate glucose uptake by cells. Glucose 192-199 insulin Homo sapiens 158-165 34091125-0 2021 The relationship of glucose-stimulated insulin secretion to cerebral glucose metabolism and cognition in healthy middle-aged and older adults. Glucose 20-27 insulin Homo sapiens 39-46 34604014-9 2021 RESULTS: Significantly higher concentrations of leptin, insulin, homeostatic model assessment for insulin resistance (HOMA-IR) index, and the immunoreactive insulin (IRI)/glucose index were found in the PCOS group than in the control group. Glucose 171-178 insulin Homo sapiens 157-164 34453000-5 2021 To illustrate Bayesian metamodeling, we provide a proof-of-principle metamodel of glucose-stimulated insulin secretion by human pancreatic beta-cells. Glucose 82-89 insulin Homo sapiens 101-108 34453000-6 2021 The input models include a coarse-grained spatiotemporal simulation of insulin vesicle trafficking, docking, and exocytosis; a molecular network model of glucose-stimulated insulin secretion signaling; a network model of insulin metabolism; a structural model of glucagon-like peptide-1 receptor activation; a linear model of a pancreatic cell population; and ordinary differential equations for systemic postprandial insulin response. Glucose 154-161 insulin Homo sapiens 173-180 34604014-15 2021 CONCLUSIONS: (1) Increased leptin concentration observed in women diagnosed de novo with PCOS as well as positive correlations between leptin and HOMA-IR, and IRI/glucose and BMI may indicate a potential role of leptin in the reduction of tissue sensitivity to insulin. Glucose 163-170 insulin Homo sapiens 261-268 34604014-11 2021 In patients with PCOS, a positive correlation was found between the concentrations of insulin and leptin and concentrations of leptin and IRI/glucose. Glucose 142-149 insulin Homo sapiens 86-93 34475786-13 2021 Results: PCOS group showed significant disruptions in sex hormones and a double fold increase in glucose and insulin levels, exhibiting insulin resistance. Glucose 97-104 insulin Homo sapiens 136-143 34502235-3 2021 Moreover, skeletal muscle is particularly important in maintaining body homeostasis, since it is responsible for more than 75% of all insulin-mediated glucose disposal. Glucose 151-158 insulin Homo sapiens 134-141 34578888-5 2021 The need for insulin infusion therapy was associated with higher energy (p = 0.001) and glucose delivered through artificial nutrition (p = 0.040). Glucose 88-95 insulin Homo sapiens 13-20 34446090-3 2021 Insulin-requiring GDM was defined as no insurance claims for diabetes mellitus and a fasting blood glucose level of < 126 mg/dL before pregnancy, and initiation of insulin treatment during pregnancy. Glucose 99-106 insulin Homo sapiens 0-7 34512541-1 2021 Objectives: To evaluate the evolution of subcutaneous glucose during two sessions of monitored aerobic exercise in children or adolescents with type 1 diabetes after adaptation of insulin doses and carbohydrate intake according to a combined algorithm. Glucose 54-61 insulin Homo sapiens 180-187 34180254-9 2022 Identifying the targets of cell signaling into mitochondria and of mitochondrial retrograde metabolic and redox signals to the cell will uncover further molecular mechanisms for insulin secretion stimulated by glucose, branched-chain keto acids, and fatty acids, and the amplification of secretion by GLP-1 and metabotropic receptors. Glucose 210-217 insulin Homo sapiens 178-185 34180254-1 2022 SIGNIFICANCE: Mitochondria determine glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells by elevating ATP synthesis. Glucose 37-44 insulin Homo sapiens 56-63 34452877-1 2021 The Flash Guide (FG) for insulin dosing (A. Chico, C. Gonzalez) was the first document intended for FreeStyle Libre (FSL) user patients to help with decision-making depending on glucose level and trend. Glucose 179-186 insulin Homo sapiens 25-32 34452877-6 2021 The percentage of subjects who used glucose trend in decision-making after receiving the FG increased: for adjusting insulin (51 vs. 83; P=.016), action without insulin (51 vs. 90%; P=.001), and in special circumstances. Glucose 36-43 insulin Homo sapiens 117-124 34452877-6 2021 The percentage of subjects who used glucose trend in decision-making after receiving the FG increased: for adjusting insulin (51 vs. 83; P=.016), action without insulin (51 vs. 90%; P=.001), and in special circumstances. Glucose 36-43 insulin Homo sapiens 161-168 34423393-8 2021 This was accompanied by increased isoproterenol-induced lipolysis and beta-oxidation and reduced lipogenesis, whereas insulin-stimulated glucose uptake was unaltered in transduced myocytes. Glucose 137-144 insulin Homo sapiens 118-125 34429169-2 2021 It is characterized by hyperglycemia, a condition with high glucose level in the blood plasma resulting from defects in insulin secretion or its action and in some cases both the impairment in secretion and also action of insulin coexist. Glucose 60-67 insulin Homo sapiens 222-229 34426942-6 2021 The in vitro insulin release of PECs demonstrated an obvious glucose response profile in different glucose concentrations (0 mg/mL, 2 mg/mL, 5 mg/mL) and presented a switch "on" and "off" release regulation at hyperglycemic or normal state. Glucose 61-68 insulin Homo sapiens 13-20 34426942-6 2021 The in vitro insulin release of PECs demonstrated an obvious glucose response profile in different glucose concentrations (0 mg/mL, 2 mg/mL, 5 mg/mL) and presented a switch "on" and "off" release regulation at hyperglycemic or normal state. Glucose 99-106 insulin Homo sapiens 13-20 34426942-9 2021 Overall, the PECs directly triggered by postprandial glucose in the intestine have a good potential to be applied in intelligent insulin delivery by the oral route. Glucose 53-60 insulin Homo sapiens 129-136 34512170-3 2021 The pancreatic beta cells were treated with isolated exosomes from PaC cell lines, SW1990 and BxPC-3, before measuring the glucose-stimulated insulin secretion (GSIS), validating that SW1990 and BxPC-3 might disrupt GSIS of both beta cell line MIN6 and primary mouse pancreatic islets. Glucose 123-130 insulin Homo sapiens 142-149 34426590-5 2021 Fasting glucose was associated with metabolites of intracellular insulin action and beta-cell dysfunction, namely cysteine-s-sulphate and n-acetylgarginine, whereas fasting insulin was predicted by myristoleoylcarnitine, propionylcarnitine and other metabolites of beta-oxidation of fatty acids. Glucose 8-15 insulin Homo sapiens 65-72 34440929-3 2021 Insulin as an anabolic hormonal was discovered exactly 100 years ago due to its activity in controlling blood glucose level. Glucose 110-117 insulin Homo sapiens 0-7 34485407-8 2021 Insulin sensitivity index (ISI0,120) was calculated from values of fasting and 2-h insulin and glucose concentration of OGTT. Glucose 95-102 insulin Homo sapiens 0-7 34416903-13 2021 Interestingly, overexpression of miRNA-92a-3p in primary skeletal muscle cells increase insulin-stimulated glucose uptake. Glucose 107-114 insulin Homo sapiens 88-95 34407376-1 2022 Significance: Type 1 diabetes (T1D) is characterized by the autoimmune destruction of the insulin secreting beta-cells, with consequent aberrant blood glucose levels. Glucose 151-158 insulin Homo sapiens 90-97 34404339-7 2021 RESULTS: We found: (i) xylitol, but not erythritol, increased rCBF in the hypothalamus, whereas glucose had the opposite effect; (ii) graph analysis of resting functional connectivity revealed a complex pattern of similarities and differences in brain network properties following xylitol, erythritol, and glucose; (iii) erythritol and xylitol induced a rise in CCK and PYY, (iv) erythritol had no and xylitol only minimal effects on glucose and insulin. Glucose 96-103 insulin Homo sapiens 446-453 34404339-7 2021 RESULTS: We found: (i) xylitol, but not erythritol, increased rCBF in the hypothalamus, whereas glucose had the opposite effect; (ii) graph analysis of resting functional connectivity revealed a complex pattern of similarities and differences in brain network properties following xylitol, erythritol, and glucose; (iii) erythritol and xylitol induced a rise in CCK and PYY, (iv) erythritol had no and xylitol only minimal effects on glucose and insulin. Glucose 306-313 insulin Homo sapiens 446-453 34414343-2 2021 We hypothesized that sliding-scale insulin for severe postoperative hyperglycemia (glucose >=180 mg/dL) could lower mean postoperative glucose levels and minimize short-term complications in patients without diabetes undergoing major joint replacement. Glucose 83-90 insulin Homo sapiens 35-42 34414343-2 2021 We hypothesized that sliding-scale insulin for severe postoperative hyperglycemia (glucose >=180 mg/dL) could lower mean postoperative glucose levels and minimize short-term complications in patients without diabetes undergoing major joint replacement. Glucose 135-142 insulin Homo sapiens 35-42 34107273-11 2021 In Exp3, insulin secretion in response to high glucose and 10 mM arginine was 42.43 +-6.34 muU/ml. Glucose 47-54 insulin Homo sapiens 9-16 34400479-6 2021 RESULTS: Presurgery beta-cell glucose sensitivity, a surrogate of beta-cell function, was negatively correlated with known diabetes duration, HbA1c, insulin use, and the diabetes remission scores DiaRem and advanced (Ad)-DiaRem (all P < 0.001). Glucose 30-37 insulin Homo sapiens 149-156 34422424-8 2021 Blood glucose control was initially difficult to achieve due to difficulties in preparing such small doses of insulin and the significant variations in blood glucose concentrations, without ketosis. Glucose 6-13 insulin Homo sapiens 110-117 34512891-11 2021 Although capillary and arterial whole blood glucose do not meet standard guidelines for glucose testing, they can still be used to guide insulin dosing in the operating room. Glucose 44-51 insulin Homo sapiens 137-144 34512891-11 2021 Although capillary and arterial whole blood glucose do not meet standard guidelines for glucose testing, they can still be used to guide insulin dosing in the operating room. Glucose 88-95 insulin Homo sapiens 137-144 34413690-6 2021 Insulin resistance (HOMA-IR) was derived from fasting levels of plasma glucose and plasma insulin, and fat-free and fat mass index (kg/m2) from DXA. Glucose 71-78 insulin Homo sapiens 0-7 34380182-2 2021 The homeostatic model assessment of insulin resistance (HOMA-IR) provides an estimate for IR from fasting glucose and insulin serum concentrations. Glucose 106-113 insulin Homo sapiens 36-43 34422424-8 2021 Blood glucose control was initially difficult to achieve due to difficulties in preparing such small doses of insulin and the significant variations in blood glucose concentrations, without ketosis. Glucose 158-165 insulin Homo sapiens 110-117 34445300-1 2021 Type 2 diabetes mellitus is a widespread medical condition, characterized by high blood glucose and inadequate insulin action, which leads to insulin resistance. Glucose 88-95 insulin Homo sapiens 142-149 34408401-1 2021 Purpose: Long-acting insulin analogues are known to be a major player in the management of glucose levels in type I diabetic patients. Glucose 91-98 insulin Homo sapiens 21-28 34408401-3 2021 To further optimize the properties for steadily controlling glucose level, a novel long-acting insulin INS061 was designed and its efficacy, pharmacokinetics, biodistribution and excretion profiles were investigated in rats. Glucose 60-67 insulin Homo sapiens 95-102 34408401-9 2021 Conclusion: The present structural modifications of human insulin possessed a long-acting profile and glucose-lowering function along with favorable in vivo properties in rats, which establish a foundation for further preclinical and clinical evaluation. Glucose 102-109 insulin Homo sapiens 58-65 34362816-1 2021 OBJECTIVE: To evaluate glucose control using fast-acting insulin aspart (faster aspart) compared with insulin aspart (IAsp) delivered by the MiniMed Advanced Hybrid Closed-Loop (AHCL) system in adults with type 1 diabetes. Glucose 23-30 insulin Homo sapiens 57-64 34444866-6 2021 Insulin-sensitivity was assessed with the gold standard method: the hyperinsulinemic-euglycemic clamp using the isotope (6,6-2H2) glucose and expressed as glucose rate of disposal (Rd) for peripheral insulin sensitivity and suppression of endogenous glucose production (EGP) for hepatic insulin sensitivity. Glucose 130-137 insulin Homo sapiens 0-7 34440773-3 2021 The beta-cells, the major cellular component of the pancreatic islets, secrete insulin, the only hormone capable of lowering the plasma glucose concentration. Glucose 136-143 insulin Homo sapiens 79-86 34444866-6 2021 Insulin-sensitivity was assessed with the gold standard method: the hyperinsulinemic-euglycemic clamp using the isotope (6,6-2H2) glucose and expressed as glucose rate of disposal (Rd) for peripheral insulin sensitivity and suppression of endogenous glucose production (EGP) for hepatic insulin sensitivity. Glucose 155-162 insulin Homo sapiens 0-7 34444866-6 2021 Insulin-sensitivity was assessed with the gold standard method: the hyperinsulinemic-euglycemic clamp using the isotope (6,6-2H2) glucose and expressed as glucose rate of disposal (Rd) for peripheral insulin sensitivity and suppression of endogenous glucose production (EGP) for hepatic insulin sensitivity. Glucose 250-257 insulin Homo sapiens 0-7 34436456-1 2021 The pancreatic beta-cell is purpose-built for the production and secretion of insulin, the only hormone that can remove glucose from the bloodstream. Glucose 120-127 insulin Homo sapiens 78-85 34436456-8 2021 Factors that drive the formation and maturation of SGs and thus the production of insulin are therefore critical for systemic glucose control. Glucose 126-133 insulin Homo sapiens 82-89 34414907-0 2021 Impact of oral anticholinergic on insulin response to oral glucose load in patients with impaired glucose tolerance. Glucose 59-66 insulin Homo sapiens 34-41 34259305-1 2021 Microneedles with insulin-loaded glucose-responsive particles are promising to control the blood glucose levels of diabetic patients. Glucose 33-40 insulin Homo sapiens 18-25 34259305-1 2021 Microneedles with insulin-loaded glucose-responsive particles are promising to control the blood glucose levels of diabetic patients. Glucose 97-104 insulin Homo sapiens 18-25 34165135-6 2021 However, clinical trials and systematic reviews show statistical differences on glucose, insulin, and glycated hemoglobin levels of patients with T2DM, associated with activation mechanisms of transcription factors related to genes of the glucide metabolism and the insulin receptor, and the regulation of intracellular Ca2+ insulin concentrations. Glucose 80-87 insulin Homo sapiens 325-332 34081875-3 2021 Adverse health consequences also manifest years prior to the development of T2D due to underlying insulin resistance and exaggerated postprandial concentrations of the glucose-lowering hormone insulin. Glucose 168-175 insulin Homo sapiens 193-200 34175829-2 2021 RESEARCH DESIGN AND METHODS: C-peptide was measured on maternal serum samples from 127 participants (12, 24, and 34 weeks) and cord blood during the Continuous Glucose Monitoring in Women With Type 1 Diabetes in Pregnancy Trial (CONCEPTT). Glucose 160-167 insulin Homo sapiens 29-38 34405550-2 2021 Under normal conditions cardiac tissue utilizes roughly 70% fatty acids (FA), and 30% glucose for the production of ATP; however, during impaired metabolic conditions like insulin resistance and diabetes glucose metabolism is dysregulated and FA account for 99% of energy production. Glucose 86-93 insulin Homo sapiens 172-179 34405550-5 2021 None-classical TH signaling in the heart has shown to phosphorylate protein kinase B (Akt) and increase activity of phosphoinositide-3-kinase (PI3K), which are critical mediators in the insulin-stimulated glucose uptake pathway. Glucose 205-212 insulin Homo sapiens 186-193 34405550-6 2021 Studies on peripheral tissues such as skeletal muscle and adipocytes have demonstrated TH treatment improved glucose intolerance in a diabetic model and increased insulin-regulated glucose transporter (GLUT4) mRNA levels. Glucose 181-188 insulin Homo sapiens 163-170 34083134-5 2021 Basal and insulin-mediated glucose fluxes were determined during a 2-step hyperinsulinemic-euglycemic clamp with stable isotope-labeled tracers. Glucose 27-34 insulin Homo sapiens 10-17 34373421-1 2021 In insulin-resistant states such as obesity, pancreatic beta-cells proliferate to prevent blood glucose elevations. Glucose 96-103 insulin Homo sapiens 3-10 34154916-2 2021 In various types of diabetes, the pancreatic beta cells fail to secrete sufficient insulin, at some point, to regulate blood glucose levels. Glucose 125-132 insulin Homo sapiens 83-90 34154916-3 2021 Therefore, the replacement of dysfunctional pancreas, islets of Langerhans, or even the insulin-secreting beta cells facilitates physiological regulation of blood glucose levels. Glucose 163-170 insulin Homo sapiens 88-95 34321005-1 2021 BACKGROUND: Triglyceride glucose-body mass index (TyG-BMI) is a recently developed alternative indicator to identify insulin resistance. Glucose 25-32 insulin Homo sapiens 117-124 34360682-1 2021 Fundamental pancreatic beta-cell function is to produce and secrete insulin in response to blood glucose levels. Glucose 97-104 insulin Homo sapiens 68-75 34398053-5 2021 Glycosylated hemoglobin A1c and fasting blood glucose were significantly decreased in patients with lipohypertrophy or subclinical lipohypertrophy (lipohypertrophy without visual and palpation changes) after receiving insulin injection technique education based on ultrasound examination and Chinese guideline than baseline at 3 months (P < .001). Glucose 46-53 insulin Homo sapiens 218-225 34439408-4 2021 Importantly, we found that a combined treatment with the cell permeant iron chelator deferiprone and the glutathione precursor N-acetyl cysteine promoted the structural repair of mitochondria and ER, decreased mitochondrial labile iron and ROS levels, and restored glucose-stimulated insulin secretion. Glucose 265-272 insulin Homo sapiens 284-291 34349617-5 2021 Over 80% of patients with AD have type II diabetes (T2DM) or abnormal serum glucose, suggesting that the pathogenic mechanisms of insulin resistance and AD likely overlap. Glucose 76-83 insulin Homo sapiens 130-137 34271940-1 2021 BACKGROUND: Triglyceride-glucose (TyG) index, a simple surrogate marker of insulin resistance, has been reported to be associated with arterial stiffness. Glucose 25-32 insulin Homo sapiens 75-82 34335462-1 2021 The authors" perspective is described regarding modifications made in their clinic to glucose challenge protocols and mathematical models in order to estimate insulin secretion, insulin sensitivity and glucose effectiveness in patients living with Insulin-Requiring Diabetes and patients who received Pancreatic Islet Transplants to treat Type I diabetes (T1D) with Impaired Awareness of Hypoglycemia. Glucose 86-93 insulin Homo sapiens 159-166 34326816-7 2021 In the present review, we summarize evidence that supports the view that G3PP plays an important role in the regulation of gluconeogenesis and fat storage in hepatocytes, glucose stimulated insulin secretion and nutri-stress in beta-cells, and lipogenesis in adipocytes. Glucose 171-178 insulin Homo sapiens 190-197 34252142-6 2021 In 2D culture, the majority of cells were immature beta-cells with low glucose-stimulated insulin secretion. Glucose 71-78 insulin Homo sapiens 90-97 34252142-7 2021 Transferring to 3D culture immediately after endocrine progenitor cell differentiation, however, improved glucose-stimulated insulin secretion. Glucose 106-113 insulin Homo sapiens 125-132 34238294-1 2021 BACKGROUND: The triglyceride-glucose (TyG) index is an alternative marker of insulin resistance (IR) and is closely associated with the prevalence and prognosis of atherosclerotic cardiovascular disease (ASCVD). Glucose 29-36 insulin Homo sapiens 77-84 34357331-2 2021 The homeostasis model assessment of insulin resistance index (HOMA) is the most used index of IR (Insulin Resistance), validated in overweight and obese patients but not in normal-weight PCOS subjects, who can still present with increased insulin secretion by an oral glucose tolerance test (OGTT). Glucose 268-275 insulin Homo sapiens 36-43 34357331-2 2021 The homeostasis model assessment of insulin resistance index (HOMA) is the most used index of IR (Insulin Resistance), validated in overweight and obese patients but not in normal-weight PCOS subjects, who can still present with increased insulin secretion by an oral glucose tolerance test (OGTT). Glucose 268-275 insulin Homo sapiens 239-246 34359828-1 2021 Pancreatic beta cells secrete insulin in response to stimulation with glucose and other nutrients, and impaired insulin secretion plays a central role in development of diabetes mellitus. Glucose 70-77 insulin Homo sapiens 30-37 34359828-3 2021 The incretin hormones, glucagon-like peptide-1 and gastric inhibitory polypeptide, potentiate glucose-stimulated insulin secretion by binding to G protein-coupled receptors, resulting in stimulation of adenylate cyclase and production of the secondary messenger cAMP, which exerts its intracellular effects through activation of protein kinase A or the guanine nucleotide exchange protein 2A. Glucose 94-101 insulin Homo sapiens 113-120 34275385-0 2021 The impact of flash glucose monitoring on glycated hemoglobin in type 2 diabetes managed with basal insulin in Canada: A retrospective real-world chart review study. Glucose 20-27 insulin Homo sapiens 100-107 34100220-1 2021 BACKGROUND AND OBJECTIVE: Artificial pancreases administering low-dose glucagon in addition to insulin have the scope to improve glucose control in patients with diabetes mellitus type 1. Glucose 129-136 insulin Homo sapiens 95-102 34450712-0 2021 Using Absorption Models for Insulin and Carbohydrates and Deep Leaning to Improve Glucose Level Predictions. Glucose 82-89 insulin Homo sapiens 28-35 34532431-5 2021 Results: At baseline, the maximum creatine kinase-MB (CK-MB), plasma glucose, hemoglobin A1c, high-sensitivity C-reactive protein (CRP), and creatinine levels were higher, while the left ventricular ejection fraction (LVEF) was lower, in the insulin therapy group than in the OHA group. Glucose 69-76 insulin Homo sapiens 242-249 34413118-9 2021 The clinical pharmacology trial in people with type 2 diabetes showed that insulin icodec was well tolerated and has pharmacokinetic/pharmacodynamic properties that are suited for once-weekly dosing, with a mean half-life of 196 hours and close to even distribution of glucose-lowering effect over the entire dosing interval of 1 week. Glucose 269-276 insulin Homo sapiens 75-82 34111687-5 2021 The hypoglycemic effect of PFC-3 in vitro was evaluated by glucose uptake and consumption assays, and the results showed that PFC-3 concentration-dependently enhanced glucose uptake and significantly improved glucose consumption in insulin-resistant HepG2 cells. Glucose 209-216 insulin Homo sapiens 232-239 34232483-1 2021 INTRODUCTION: The objective of this analysis was to estimate the costs associated with using flash glucose monitoring with optional alarms as a replacement for either traditional continuous glucose monitoring (CGM) or routine self-monitoring of blood glucose (SMBG) in adults with diabetes and impaired awareness of hypoglycaemia (IAH) who use intensified insulin therapy, from a Swedish payer perspective, applying assumptions to simulate hypothetical scenarios. Glucose 99-106 insulin Homo sapiens 356-363 34175459-1 2021 Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, that is, glucose uptake. Glucose 127-134 insulin Homo sapiens 0-7 34175459-1 2021 Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, that is, glucose uptake. Glucose 127-134 insulin Homo sapiens 68-75 34181914-3 2021 We discuss not only novel developments of insulin therapy (eg, so-called smart insulin preparation with a glucose-dependent mode of action), but also a group of drug classes for which extensive research efforts have not been rewarded with obvious clinical impact. Glucose 106-113 insulin Homo sapiens 42-49 34181914-3 2021 We discuss not only novel developments of insulin therapy (eg, so-called smart insulin preparation with a glucose-dependent mode of action), but also a group of drug classes for which extensive research efforts have not been rewarded with obvious clinical impact. Glucose 106-113 insulin Homo sapiens 79-86 34393754-6 2021 Results: Mice genetically ablated for alpha-syn became glucose intolerant and insulin resistant with hyperinsulinemia and reduced glucose-stimulated insulin secretion (GSIS). Glucose 130-137 insulin Homo sapiens 78-85 34393754-6 2021 Results: Mice genetically ablated for alpha-syn became glucose intolerant and insulin resistant with hyperinsulinemia and reduced glucose-stimulated insulin secretion (GSIS). Glucose 130-137 insulin Homo sapiens 149-156 34323110-1 2021 BACKGROUND: My Dose Coach (MDC) is a mobile application combined with a web portal that can suggest optimized basal insulin (BI) injection doses using Self-Measured Plasma Glucose (SMPG) and hypoglycemia data. Glucose 172-179 insulin Homo sapiens 116-123 34394128-6 2021 The homeostasis model assessment of insulin resistance (HOMA-IR) was used for insulin resistance estimation and calculated as fasting insulin (muU/ml) x fasting glucose (mmol/L)/22.5. Glucose 161-168 insulin Homo sapiens 36-43 34394128-6 2021 The homeostasis model assessment of insulin resistance (HOMA-IR) was used for insulin resistance estimation and calculated as fasting insulin (muU/ml) x fasting glucose (mmol/L)/22.5. Glucose 161-168 insulin Homo sapiens 78-85 34290145-12 2021 In particular, replacement of the present fructose sensor by an analogous glucose sensor may enable translational development of a "smart" insulin analog to mitigate hypoglycemic risk in diabetes therapy. Glucose 74-81 insulin Homo sapiens 139-146 34376311-3 2022 The PI3K/Akt/mTOR signaling pathway plays a critical role in regulating cellular processes such as growth and proliferation, but also regulates the metabolic effects of insulin such as glucose uptake and glycogen synthesis. Glucose 185-192 insulin Homo sapiens 169-176 34368252-1 2021 The triglyceride-glucose index is a valuable marker of insulin resistance. Glucose 17-24 insulin Homo sapiens 55-62 34301732-0 2021 Glucose Regulation Beyond HbA1c in Type 2 Diabetes Treated With Insulin: Real-World Evidence From the DIALECT-2 Cohort. Glucose 0-7 insulin Homo sapiens 64-71 34301732-1 2021 OBJECTIVE: To investigate glucose variations associated with glycated hemoglobin (HbA1c) in insulin-treated patients with type 2 diabetes. Glucose 26-33 insulin Homo sapiens 92-99 34292976-4 2021 Intriguingly, young insulin SGs are more likely secreted during glucose-stimulated insulin secretion (GSIS) for unknown reasons, while older SGs tend to lose releasability and be degraded. Glucose 64-71 insulin Homo sapiens 83-90 34342959-7 2021 Results: Islet equivalents, (IEQ), viability (FDA/PI), morphology and dynamic glucose stimulated insulin secretion (dGSIS) were evaluated. Glucose 78-85 insulin Homo sapiens 97-104 34085953-4 2021 Insulin-treated patients with type 2 diabetes (n=21, (mean+-SD) age 62.8+-6.5 years, BMI 29.0+-4.2 kg/m2, HbA1c 6.8+-0.5% (51.0+-5.4 mmol/mol)) and matched controls (n=21, age 62.2+-8.3 years, BMI 29.2+-3.5 kg/m2, HbA1c 5.3+-0.3% (34.3+-3.3 mmol/mol)) underwent a sequential hyperglycemic and hypoglycemic clamp with three steady-states of plasma glucose: 1) fasting plasma glucose, 2) hyperglycemia (fasting plasma glucose+10 mmol/L) and 3) hyperinsulinemic hypoglycemia (plasma glucose<3.0 mmol/L). Glucose 347-354 insulin Homo sapiens 0-7 34085953-4 2021 Insulin-treated patients with type 2 diabetes (n=21, (mean+-SD) age 62.8+-6.5 years, BMI 29.0+-4.2 kg/m2, HbA1c 6.8+-0.5% (51.0+-5.4 mmol/mol)) and matched controls (n=21, age 62.2+-8.3 years, BMI 29.2+-3.5 kg/m2, HbA1c 5.3+-0.3% (34.3+-3.3 mmol/mol)) underwent a sequential hyperglycemic and hypoglycemic clamp with three steady-states of plasma glucose: 1) fasting plasma glucose, 2) hyperglycemia (fasting plasma glucose+10 mmol/L) and 3) hyperinsulinemic hypoglycemia (plasma glucose<3.0 mmol/L). Glucose 374-381 insulin Homo sapiens 0-7 34085953-4 2021 Insulin-treated patients with type 2 diabetes (n=21, (mean+-SD) age 62.8+-6.5 years, BMI 29.0+-4.2 kg/m2, HbA1c 6.8+-0.5% (51.0+-5.4 mmol/mol)) and matched controls (n=21, age 62.2+-8.3 years, BMI 29.2+-3.5 kg/m2, HbA1c 5.3+-0.3% (34.3+-3.3 mmol/mol)) underwent a sequential hyperglycemic and hypoglycemic clamp with three steady-states of plasma glucose: 1) fasting plasma glucose, 2) hyperglycemia (fasting plasma glucose+10 mmol/L) and 3) hyperinsulinemic hypoglycemia (plasma glucose<3.0 mmol/L). Glucose 416-423 insulin Homo sapiens 0-7 34085953-4 2021 Insulin-treated patients with type 2 diabetes (n=21, (mean+-SD) age 62.8+-6.5 years, BMI 29.0+-4.2 kg/m2, HbA1c 6.8+-0.5% (51.0+-5.4 mmol/mol)) and matched controls (n=21, age 62.2+-8.3 years, BMI 29.2+-3.5 kg/m2, HbA1c 5.3+-0.3% (34.3+-3.3 mmol/mol)) underwent a sequential hyperglycemic and hypoglycemic clamp with three steady-states of plasma glucose: 1) fasting plasma glucose, 2) hyperglycemia (fasting plasma glucose+10 mmol/L) and 3) hyperinsulinemic hypoglycemia (plasma glucose<3.0 mmol/L). Glucose 480-487 insulin Homo sapiens 0-7 34300672-0 2021 Learning Carbohydrate Digestion and Insulin Absorption Curves Using Blood Glucose Level Prediction and Deep Learning Models. Glucose 74-81 insulin Homo sapiens 36-43 34300672-2 2021 Patients suffering type 1 diabetes depend on the appropriate estimation of the units of insulin they have to use in order to keep blood glucose levels in range (considering the calories taken and the physical exercise carried out). Glucose 136-143 insulin Homo sapiens 88-95 34300672-4 2021 These models tend to receive the insulin units used and the carbohydrate taken as inputs and generate optimal estimations for future blood glucose levels over a prediction horizon. Glucose 139-146 insulin Homo sapiens 33-40 34300672-5 2021 The body glucose kinetics is a complex user-dependent process, and learning patient-specific blood glucose patterns from insulin units and carbohydrate content is a difficult task even for deep learning-based models. Glucose 9-16 insulin Homo sapiens 121-128 34300672-5 2021 The body glucose kinetics is a complex user-dependent process, and learning patient-specific blood glucose patterns from insulin units and carbohydrate content is a difficult task even for deep learning-based models. Glucose 99-106 insulin Homo sapiens 121-128 34300672-6 2021 This paper proposes a novel mechanism to increase the accuracy of blood glucose predictions from deep learning models based on the estimation of carbohydrate digestion and insulin absorption curves for a particular patient. Glucose 72-79 insulin Homo sapiens 172-179 34299331-3 2021 The aim of this work was to evaluate the impact of chronic and intermittent high glucose on the expression of biomolecules of insulin signaling pathway during the differentiation and maturation of human visceral preadipocytes. Glucose 81-88 insulin Homo sapiens 126-133 34299620-0 2021 Identification of Insulin-Mimetic Plant Extracts: From an In Vitro High-Content Screen to Blood Glucose Reduction in Live Animals. Glucose 96-103 insulin Homo sapiens 18-25 34305401-2 2021 The Triglyceride-Glucose (TyG) Index is a proxy of insulin resistance, but the association between the TyG Index and DKD is less certain. Glucose 17-24 insulin Homo sapiens 51-58 34335470-0 2021 Interaction Between Non-Insulin Glucose-Lowering Medication and Exercise in Type 2 Diabetes Mellitus - New Findings on SGLT2 Inhibitors. Glucose 32-39 insulin Homo sapiens 24-31 34285531-7 2021 Compared with an intensive dose of metformin alone, the combination of insulin and metformin was associated with improved glycemic control (change of fasting blood glucose: 2.49 mmol/l vs 1.30 mmol/l, p=0.0016). Glucose 164-171 insulin Homo sapiens 71-78 34337072-0 2021 Fasting Glucose of 6.1 mmol/L as a Possible Optimal Target for Type 2 Diabetic Patients with Insulin Glargine: A Randomized Clinical Trial. Glucose 8-15 insulin Homo sapiens 93-100 34361925-4 2021 The homeostatic model assessment for insulin resistance (HOMA-IR) was determined using fasting glucose and insulin. Glucose 95-102 insulin Homo sapiens 37-44 34377364-1 2021 Activation of human free fatty acid receptor 1 (FFAR1, also called hGPR40) enhances insulin secretion in a glucose-dependent manner. Glucose 107-114 insulin Homo sapiens 84-91 34356863-9 2021 We propose insulin"s primary role is regulating beta-hydroxybutyrate synthesis, while the role of bone regulates glucose uptake sensitivity via osteocalcin. Glucose 113-120 insulin Homo sapiens 11-18 34133152-1 2021 Basal glucose control is commonly maintained by a single, once-daily administration of insulin through subcutaneous injection or a continuous pump-infusion. Glucose 6-13 insulin Homo sapiens 87-94 34218716-12 2021 These findings suggest that insulin prescribing continues to change in response to the development of new therapeutics, advances in insulin delivery technology, and glucose monitoring systems. Glucose 165-172 insulin Homo sapiens 28-35 34353101-5 2021 A 75-g oral glucose tolerance test (OGTT) was performed to diagnose T2DM in each individual, and an insulin releasing test (IRT) was used to calculate selected parameters for glucose, insulin, and C-peptide. Glucose 175-182 insulin Homo sapiens 100-107 34224987-0 2021 The effect of glucose control in liver surgery on glucose kinetics and insulin resistance. Glucose 14-21 insulin Homo sapiens 71-78 34224987-2 2021 The magnitude of insulin resistance can be modulated by glucose control, preoperative nutrition, adequate pain management and minimal invasive surgery. Glucose 56-63 insulin Homo sapiens 17-24 34224987-5 2021 In the treatment group (n = 9), insulin was administered intravenously to keep arterial blood glucose between 6 and 8 mmol/l during surgery. Glucose 94-101 insulin Homo sapiens 32-39 34224987-9 2021 RESULTS: Mean intraoperative glucose was 7.0 mM (SD 0.7) vs 9.1 mM (SD 1.9) in the insulin and control group respectively (p < 0.001; ANOVA). Glucose 29-36 insulin Homo sapiens 83-90 34224987-13 2021 CONCLUSION: Glucose control reduces postoperative insulin resistance in liver surgery. Glucose 12-19 insulin Homo sapiens 50-57 34099518-12 2021 CONCLUSIONS: This tubeless automated insulin delivery system was safe and allowed participants to significantly improve HbA1c levels and time in target glucose range with a very low occurrence of hypoglycemia. Glucose 152-159 insulin Homo sapiens 37-44 34197700-7 2021 Drug treatment impaired peptide chain initiation in myofibrillar protein fractions and insulin-stimulated glucose uptake (p = 0.06) but increased the expression of autophagy markers beclin-1 and microtubule-associated proteins 1A/1B light chain 3B (p < 0.05), and of apoptotic marker, cleaved caspase 3 (p < 0.05). Glucose 106-113 insulin Homo sapiens 87-94 34278114-7 2021 Among them, ginsenoside F2, protocatechuic acid, and salvianolic acid B were selected and validated to promote glucose consumption through activating AMPK phosphorylation and upregulating GLUT4 in insulin-resistant cell model (HepG2/IR) cells. Glucose 111-118 insulin Homo sapiens 197-204 34190340-5 2021 In dispersed islet cells, the glucose response of insulin secretion is attenuated from that seen from whole islets, coordinated oscillations in membrane potential and intracellular Ca2+ activity, as well as the two-phase insulin secretion profile, are missing, and glucagon secretion displays higher basal secretion profile and a reverse glucose-dependent response from that of intact islets. Glucose 30-37 insulin Homo sapiens 50-57 34190340-5 2021 In dispersed islet cells, the glucose response of insulin secretion is attenuated from that seen from whole islets, coordinated oscillations in membrane potential and intracellular Ca2+ activity, as well as the two-phase insulin secretion profile, are missing, and glucagon secretion displays higher basal secretion profile and a reverse glucose-dependent response from that of intact islets. Glucose 338-345 insulin Homo sapiens 50-57 34191199-1 2022 It is difficult to manage postoperative blood glucose levels without hyperglycemia and hypoglycemia in cardiac surgery patients even if continuous intravenous insulin infusion is used. Glucose 46-53 insulin Homo sapiens 159-166 34258291-2 2021 DPP-4 inhibitors are the other type of novel antidiabetic medications which act by preventing GLP-1 inactivation and thereby increasing the activity levels of GLP-1, leading to more glucose-induced insulin release from islet beta-cells and suppression of glucagon release. Glucose 182-189 insulin Homo sapiens 198-205 34059560-1 2021 Background: The oral glucose tolerance test (OGTT)-glucose response curves (GRCs; incessant increase, monophasic, and biphasic) reflect insulin sensitivity and beta-cell function, being worse in the former and superior in the latter. Glucose 21-28 insulin Homo sapiens 136-143 34059560-1 2021 Background: The oral glucose tolerance test (OGTT)-glucose response curves (GRCs; incessant increase, monophasic, and biphasic) reflect insulin sensitivity and beta-cell function, being worse in the former and superior in the latter. Glucose 51-58 insulin Homo sapiens 136-143 34209125-0 2021 Improved Methods for Mid-Term Blood Glucose Level Prediction Using Dietary and Insulin Logs. Glucose 36-43 insulin Homo sapiens 79-86 34193609-5 2021 Through loss- and gain-of-function approaches, we uncovered a mechanism by which PAX6 modulates glucose-stimulated insulin secretion (GSIS) through a cAMP response element-binding protein (CREB)/Munc18-1/2 pathway. Glucose 96-103 insulin Homo sapiens 115-122 34193893-7 2021 Furthermore, we showed that the Ang2 stimulated islets were able to regulate insulin exocytosis through actin-filament polymerization and depolymerization upon glucose challenge, presumably through the CDC42-RAC1-gelsolin mediated insulin secretion signaling pathway. Glucose 160-167 insulin Homo sapiens 77-84 34193893-7 2021 Furthermore, we showed that the Ang2 stimulated islets were able to regulate insulin exocytosis through actin-filament polymerization and depolymerization upon glucose challenge, presumably through the CDC42-RAC1-gelsolin mediated insulin secretion signaling pathway. Glucose 160-167 insulin Homo sapiens 231-238 34203120-2 2021 LRP1 is a scaffold protein for insulin receptor involved in the insulin-induced glucose transporter type 4 (GLUT4) translocation to plasma membrane and glucose uptake in different types of cells. Glucose 152-159 insulin Homo sapiens 64-71 34203120-7 2021 Moreover, alpha2M* enhanced the insulin response increasing insulin-induced glucose uptake rate in the myocardium under normal conditions. Glucose 76-83 insulin Homo sapiens 32-39 34203120-7 2021 Moreover, alpha2M* enhanced the insulin response increasing insulin-induced glucose uptake rate in the myocardium under normal conditions. Glucose 76-83 insulin Homo sapiens 60-67 34077390-12 2021 Oxytocin enhanced glucose-stimulated insulin secretion, activated the mitogen-activated protein kinase pathway, and promoted cell proliferation in INS-1 cells. Glucose 18-25 insulin Homo sapiens 37-44 34248487-9 2021 As for the mechanism, the theory predicts that the energy-deprived brain suppresses insulin secretion via the sympathoadrenal system, thereby preventing insulin-mediated glucose uptake into muscle and fat and, as a result, enhancing insulin-independent glucose uptake via the blood-brain barrier. Glucose 170-177 insulin Homo sapiens 84-91 34248487-9 2021 As for the mechanism, the theory predicts that the energy-deprived brain suppresses insulin secretion via the sympathoadrenal system, thereby preventing insulin-mediated glucose uptake into muscle and fat and, as a result, enhancing insulin-independent glucose uptake via the blood-brain barrier. Glucose 170-177 insulin Homo sapiens 153-160 34248487-9 2021 As for the mechanism, the theory predicts that the energy-deprived brain suppresses insulin secretion via the sympathoadrenal system, thereby preventing insulin-mediated glucose uptake into muscle and fat and, as a result, enhancing insulin-independent glucose uptake via the blood-brain barrier. Glucose 253-260 insulin Homo sapiens 84-91 34248487-9 2021 As for the mechanism, the theory predicts that the energy-deprived brain suppresses insulin secretion via the sympathoadrenal system, thereby preventing insulin-mediated glucose uptake into muscle and fat and, as a result, enhancing insulin-independent glucose uptake via the blood-brain barrier. Glucose 253-260 insulin Homo sapiens 233-240 34166426-1 2021 BACKGROUND: Closed-loop insulin delivery systems, which integrate continuous glucose monitoring (CGM) and algorithms that continuously guide insulin dosing, have been shown to improve glycaemic control. Glucose 77-84 insulin Homo sapiens 24-31 34201708-8 2021 Caffeine inhibited basal and insulin-stimulated glucose transport as well as lipogenesis in rodent adipose cells. Glucose 48-55 insulin Homo sapiens 29-36 34206296-1 2021 Pancreatic beta-cells are responsible for the synthesis and exocytosis of insulin in response to an increase in circulating glucose. Glucose 124-131 insulin Homo sapiens 74-81 34157054-3 2021 Maintaining proper blood glucose levels using insulin and/or other oral antidiabetic drugs (such as Metformin) reduced the detrimental effects of COVID-19. Glucose 25-32 insulin Homo sapiens 46-53 34167889-3 2022 OBJECTIVES: The primary outcome was hypoglycaemia (blood glucose <70 mg/dL) after insulin administration. Glucose 57-64 insulin Homo sapiens 82-89 34188506-3 2021 The triglyceride-glucose (TyG) index is a simple and convenient marker of insulin resistance for use in medical practice. Glucose 17-24 insulin Homo sapiens 74-81 34205659-2 2021 GLP-1 receptor agonists and GLP-1 enhancers have been clinically employed to treat diabetes owing to their glucose-dependent insulin-releasing activity. Glucose 107-114 insulin Homo sapiens 125-132 34205264-2 2021 Glucose absorption is accelerated by incretin hormones, which induce insulin secretion from the pancreas. Glucose 0-7 insulin Homo sapiens 69-76 34205432-0 2021 The Capacity to Secrete Insulin Is Dose-Dependent to Extremely High Glucose Concentrations: A Key Role for Adenylyl Cyclase. Glucose 68-75 insulin Homo sapiens 24-31 34205432-1 2021 Insulin secretion is widely thought to be maximally stimulated in glucose concentrations of 16.7-to-30 mM (300-to-540 mg/dL). Glucose 66-73 insulin Homo sapiens 0-7 34205432-4 2021 Insulin secretion from human islets at 12 mM glucose intervals dose-dependently increased until at least 72 mM glucose. Glucose 45-52 insulin Homo sapiens 0-7 34205432-4 2021 Insulin secretion from human islets at 12 mM glucose intervals dose-dependently increased until at least 72 mM glucose. Glucose 111-118 insulin Homo sapiens 0-7 34205432-6 2021 Intracellular calcium was maximally stimulated in 24 mM glucose despite a further doubling of insulin secretion in higher glucose, implying that insulin secretion above 24 mM occurs through amplifying pathway(s). Glucose 56-63 insulin Homo sapiens 145-152 34205432-6 2021 Intracellular calcium was maximally stimulated in 24 mM glucose despite a further doubling of insulin secretion in higher glucose, implying that insulin secretion above 24 mM occurs through amplifying pathway(s). Glucose 122-129 insulin Homo sapiens 94-101 34205432-6 2021 Intracellular calcium was maximally stimulated in 24 mM glucose despite a further doubling of insulin secretion in higher glucose, implying that insulin secretion above 24 mM occurs through amplifying pathway(s). Glucose 122-129 insulin Homo sapiens 145-152 34205432-8 2021 Murine islets in 24 mM glucose treated with a glucokinase activator secreted as much insulin as islets in 84 mM glucose, indicating that glycolytic capacity exists above 24 mM. Glucose 23-30 insulin Homo sapiens 85-92 34205432-9 2021 Using an incretin mimetic and an adenylyl cyclase activator in 24 mM glucose enhanced insulin secretion above that observed in 84 mM glucose while adenylyl cyclase inhibitor reduced stimulatory effects. Glucose 69-76 insulin Homo sapiens 86-93 34205432-9 2021 Using an incretin mimetic and an adenylyl cyclase activator in 24 mM glucose enhanced insulin secretion above that observed in 84 mM glucose while adenylyl cyclase inhibitor reduced stimulatory effects. Glucose 133-140 insulin Homo sapiens 86-93 34900769-7 2021 Results: The results revealed a significant increase (P < 0.01) in the fasting blood glucose and lipid profile in non-treatment diabetic patients compared to diabetic patients with treatment, and also in diabetic patients with insulin therapy, compared to diabetic patients with Doanil or both therapies. Glucose 85-92 insulin Homo sapiens 227-234 34222388-1 2021 Background: The triglyceride-glucose (TyG) index had been proposed as a reliable surrogate marker of insulin resistance. Glucose 29-36 insulin Homo sapiens 101-108 34077499-0 2021 Effect of Continuous Glucose Monitoring on Glycemic Control in Patients With Type 2 Diabetes Treated With Basal Insulin: A Randomized Clinical Trial. Glucose 21-28 insulin Homo sapiens 112-119 33782700-1 2021 The incretin effect - the amplification of insulin secretion after oral versus intravenous administration of glucose as a mean to improve glucose tolerance - was suspected even before insulin was discovered, and today we know that the effect is due to the secretion of two insulinotropic peptides, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Glucose 109-116 insulin Homo sapiens 43-50 33782700-1 2021 The incretin effect - the amplification of insulin secretion after oral versus intravenous administration of glucose as a mean to improve glucose tolerance - was suspected even before insulin was discovered, and today we know that the effect is due to the secretion of two insulinotropic peptides, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Glucose 138-145 insulin Homo sapiens 43-50 33782700-5 2021 The availability of antagonists for GLP-1 and most recently also for GIP has made it possible to directly estimate the individual contributions to postprandial insulin secretion of a) glucose itself: 26%; b) GIP: 45%; and c) GLP-1: 29%. Glucose 184-191 insulin Homo sapiens 160-167 34235360-3 2021 Objective: This work aimed to evaluate the association of different insulin strategies with glucose control and hospital outcomes after adjustment for patient and physician factors that influence choice of therapy. Glucose 92-99 insulin Homo sapiens 68-75 34203728-1 2021 Several small guanosine triphosphatases (GTPases) from the Ras protein superfamily regulate glucose-stimulated insulin secretion in the pancreatic islet beta-cell. Glucose 92-99 insulin Homo sapiens 111-118 34203728-8 2021 The purpose of this review is to systematically denote the identities and molecular mechanistic steps in the glucose-stimulated insulin secretion pathway that leads to the normal release of insulin. Glucose 109-116 insulin Homo sapiens 128-135 34203728-8 2021 The purpose of this review is to systematically denote the identities and molecular mechanistic steps in the glucose-stimulated insulin secretion pathway that leads to the normal release of insulin. Glucose 109-116 insulin Homo sapiens 190-197 34203830-2 2021 The hormone potentially coordinates with glucagon to modulate blood glucose levels; insulin acts via an anabolic pathway, while glucagon performs catabolic functions. Glucose 68-75 insulin Homo sapiens 84-91 34203830-3 2021 Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain. Glucose 18-25 insulin Homo sapiens 0-7 34203830-3 2021 Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain. Glucose 64-71 insulin Homo sapiens 0-7 34163195-2 2021 Meanwhile, insulin resistance and beta-cell dysfunction are critical factors that mediate the progression from normal glucose tolerance to impaired fasting glucose (IFG) and type 2 diabetes. Glucose 118-125 insulin Homo sapiens 11-18 34177802-12 2021 RIN-m(-/- Adcy7 ) cells showed a significant increase in insulin secretion reaching 54% at low, and 49% at high glucose concentrations, compared to wild-type. Glucose 112-119 insulin Homo sapiens 57-64 34177802-13 2021 In genetic expression analysis Adcy7 loss of function led to a 34.1-fold to 362.8-fold increase in mRNA levels of the insulin regulator genes Ins1 and Ins2 (p <= 0.0002), as well as increased glucose uptake and sensing indicated by higher mRNA levels of Scl2a2 and Gck via upregulation of Pdx1, and Foxa2 leading to the activation of the glucose stimulated-insulin secretion (GSIS) pathway. Glucose 338-345 insulin Homo sapiens 357-364 34147370-1 2022 BACKGROUND: Variable rate intravenous insulin infusions (VRIIIs) are widely used to treat elevated blood glucose (BG) in adult inpatients who are severely ill and/or will miss more than one meal. Glucose 105-112 insulin Homo sapiens 38-45 34140790-5 2021 Results: Age and gestational weeks at GDM diagnosis, pregestational BMI, family history of diabetes mellitus (DM), plasma glucose levels assessed by 75-g OGTT at both the 1-hour and 2-hour time points (PG-1h and PG-2h) and HbA1c level were all significantly different between the patients that received insulin therapy and those did not. Glucose 122-129 insulin Homo sapiens 303-310 34112814-4 2021 We developed a mouse model with a LoF Kcnq1 mutation using CRISPR-Cas9 and hypothesized that this mouse model would display QT prolongation, increased glucose-stimulated insulin secretion and allow for interrogation of Kv7.1 function in islets. Glucose 151-158 insulin Homo sapiens 170-177 34112814-6 2021 Ex vivo, islet glucose-induced insulin release was measured, and beta-cell area quantified by immunohistochemistry. Glucose 15-22 insulin Homo sapiens 31-38 34112814-8 2021 Ex vivo, glucose-stimulated insulin release was increased in islets from homozygous mice at 12-14 weeks, while beta-cell area was reduced. Glucose 9-16 insulin Homo sapiens 28-35 34112814-10 2021 In follow-up studies 8-10 weeks later, beta-cell area was similar in all groups, while glucose-stimulated insulin secretion was now reduced in islets from hetero- and homozygous mice. Glucose 87-94 insulin Homo sapiens 106-113 34207541-1 2021 Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Glucose 99-106 insulin Homo sapiens 0-7 34207541-1 2021 Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Glucose 134-141 insulin Homo sapiens 0-7 34207541-2 2021 Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, i.e., glucose uptake. Glucose 124-131 insulin Homo sapiens 0-7 34207541-2 2021 Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, i.e., glucose uptake. Glucose 124-131 insulin Homo sapiens 68-75 34106350-1 2021 BACKGROUND: Insulin is the key regulator of glucose metabolism, but it is difficult to dissect direct insulin from glucose-induced effects. Glucose 115-122 insulin Homo sapiens 12-19 34077499-1 2021 Importance: Continuous glucose monitoring (CGM) has been shown to be beneficial for adults with type 2 diabetes using intensive insulin therapy, but its use in type 2 diabetes treated with basal insulin without prandial insulin has not been well studied. Glucose 23-30 insulin Homo sapiens 128-135 34077499-11 2021 Conclusions and Relevance: Among adults with poorly controlled type 2 diabetes treated with basal insulin without prandial insulin, continuous glucose monitoring, as compared with blood glucose meter monitoring, resulted in significantly lower HbA1c levels at 8 months. Glucose 143-150 insulin Homo sapiens 98-105 34077502-0 2021 Association of Real-time Continuous Glucose Monitoring With Glycemic Control and Acute Metabolic Events Among Patients With Insulin-Treated Diabetes. Glucose 36-43 insulin Homo sapiens 124-131 34077502-13 2021 Conclusions and Relevance: In this retrospective cohort study, insulin-treated patients with diabetes selected by physicians for real-time continuous glucose monitoring compared with noninitiators had significant improvements in hemoglobin A1c and reductions in emergency department visits and hospitalizations for hypoglycemia, but no significant change in emergency department visits or hospitalizations for hyperglycemia or for any reason. Glucose 150-157 insulin Homo sapiens 63-70 34078114-0 2021 Estimating Enhanced Endogenous Glucose Production in Intensive Care Unit Patients with Severe Insulin Resistance. Glucose 31-38 insulin Homo sapiens 94-101 34103676-5 2022 Glucose and insulin levels were used to estimate insulin resistance with the homeostasis model assessment (HOMA-IR). Glucose 0-7 insulin Homo sapiens 49-56 34123348-11 2021 Insulin resistance reduces glucose tolerance, and can cause greater incidence of insulin saturation and resultant hyperglycaemia. Glucose 27-34 insulin Homo sapiens 0-7 33740034-2 2021 OBJECTIVE: The aim was to investigate the association of prior undernutrition (low BMI, in kg/m2), acquired in adulthood and insulin during an oral glucose tolerance test (OGTT). Glucose 148-155 insulin Homo sapiens 125-132 34078009-4 2021 The predictive accuracy of fasting glucose and insulin levels and other fasting-state indices for assessing insulin sensitivity derived from glucose and insulin levels for abnormal glucose tolerance was evaluated using receiver operating characteristic (ROC) curve analysis. Glucose 141-148 insulin Homo sapiens 108-115 34184638-1 2021 Summary: Activating mutation of glucokinase gene (GCK) causes resetting of insulin inhibition at a lower glucose threshold causing hyperinsulinaemic hypoglycaemia (GCK-HH). Glucose 105-112 insulin Homo sapiens 75-82 34140893-9 2021 The new model also incorporates the central impact of blood flow on insulin-stimulated glucose uptake. Glucose 87-94 insulin Homo sapiens 68-75 33269760-8 2021 Islet amyloid polypeptide (IAPP) is a hormone co-produced and secreted with insulin in pancreatic beta-cells, with a key role in diabetes, as it helps regulate glucose levels and control adiposity and satiation. Glucose 160-167 insulin Homo sapiens 76-83 34136539-1 2021 Background: Triglyceride-glucose (TyG) index is a recently proposed surrogate indicator of insulin resistance. Glucose 25-32 insulin Homo sapiens 91-98 34136580-0 2021 Association of Body Fat Percentage with Time in Range Generated by Continuous Glucose Monitoring during Continuous Subcutaneous Insulin Infusion Therapy in Type 2 Diabetes. Glucose 78-85 insulin Homo sapiens 128-135 34199454-2 2021 While this process is extensively modified by hormones and neurotransmitters, it is the availability of nutrients, above all glucose, which sets the process of insulin synthesis and secretion in motion. Glucose 125-132 insulin Homo sapiens 160-167 34078009-4 2021 The predictive accuracy of fasting glucose and insulin levels and other fasting-state indices for assessing insulin sensitivity derived from glucose and insulin levels for abnormal glucose tolerance was evaluated using receiver operating characteristic (ROC) curve analysis. Glucose 35-42 insulin Homo sapiens 108-115 34103956-6 2021 Results: Maternal age, family history of type 2 diabetes mellitus in a first-degree relative, a prior GDM history, fasting plasma glucose, hemoglobin A1c, gestational age, and body mass index values at the time of GDM diagnosis were the risk factors for insulin treatment. Glucose 130-137 insulin Homo sapiens 254-261 34184638-13 2021 Depending on the glucose level when the blood was taken, and the threshold of glucose-stimulated insulin release (GSIR), the serum insulin and C-peptide levels may be raised (hyperinsulinaemic) or low (hypoinsulinaemic) in patients with activating mutation of GCK. Glucose 17-24 insulin Homo sapiens 131-138 34184638-13 2021 Depending on the glucose level when the blood was taken, and the threshold of glucose-stimulated insulin release (GSIR), the serum insulin and C-peptide levels may be raised (hyperinsulinaemic) or low (hypoinsulinaemic) in patients with activating mutation of GCK. Glucose 78-85 insulin Homo sapiens 131-138 34075130-4 2021 Insulin-mediated whole-body glucose disposal rates (M-value) and insulin-induced changes in muscle microvascular blood volume (DeltaMBV) were determined. Glucose 28-35 insulin Homo sapiens 0-7 34466729-4 2022 As such, patients" BMI and insulin sensitivity displayed a strong inverse correlation: the healthy adipocytes were associated with the highest insulin-induced glucose uptake, while insulin resistance was confirmed in the underweight and severely obese adipocytes. Glucose 159-166 insulin Homo sapiens 27-34 34466729-4 2022 As such, patients" BMI and insulin sensitivity displayed a strong inverse correlation: the healthy adipocytes were associated with the highest insulin-induced glucose uptake, while insulin resistance was confirmed in the underweight and severely obese adipocytes. Glucose 159-166 insulin Homo sapiens 143-150 34071638-8 2021 High glucose-induced insulin-resistant HepG2 cells were used to study the effect of NNP-2 on glucose consumption, and the molecular mechanism of the insulin transduction pathway was studied using RT-qPCR. Glucose 5-12 insulin Homo sapiens 21-28 34071638-8 2021 High glucose-induced insulin-resistant HepG2 cells were used to study the effect of NNP-2 on glucose consumption, and the molecular mechanism of the insulin transduction pathway was studied using RT-qPCR. Glucose 5-12 insulin Homo sapiens 149-156 34123348-11 2021 Insulin resistance reduces glucose tolerance, and can cause greater incidence of insulin saturation and resultant hyperglycaemia. Glucose 27-34 insulin Homo sapiens 81-88 34198457-3 2021 We identify two insulin scores related to glucose concentration in both blood and the gastrointestinal tract. Glucose 42-49 insulin Homo sapiens 16-23 34122330-8 2021 Serological measurements of C-peptide and insulin indicate that Gd-CP027, a high affinity zinc(II) contrast agent, potentiates their secretion only as a function of glucose stimulation. Glucose 165-172 insulin Homo sapiens 28-37 34070638-0 2021 The Quality of Life and Satisfaction with Continuous Glucose Monitoring Therapy in Children under 7 Years of Age with T1D Using the rtCGM System Integrated with Insulin Pump-A Caregivers Point of View. Glucose 53-60 insulin Homo sapiens 161-168 34079310-11 2021 Conclusion: Study subjects with no education, DM history of family members, prolonged DM, insulin medication, and inadequate exercise had higher rate of poor plasma glucose maintenance. Glucose 165-172 insulin Homo sapiens 90-97 34108935-6 2021 The male MatOb offspring developed the highest extent of glucose intolerance and lowest glucose-induced insulin secretion. Glucose 88-95 insulin Homo sapiens 104-111 34108935-10 2021 Overall, our study suggests that maternal obesity induces sex-specific changes to pancreatic HSG in offspring and a lasting effect on offspring insulin secretion, leading to the sex-differences in glucose intolerance. Glucose 197-204 insulin Homo sapiens 144-151 34073781-5 2021 Furthermore, prolonged exposure of L6-GLUT4myc myotubes to BSD raised the glucose uptake under basal conditions without affecting the insulin-stimulated glucose uptake, the effect associated with enhanced translocation of GLUT4 to the cell periphery. Glucose 153-160 insulin Homo sapiens 134-141 34064129-3 2021 We reviewed clinical care practice and hypothesized that early in-hospital transition from intravenous insulin to insulin pump therapy, managed by an endocrine unit trained on post-surgical care, would improve glucose control and impact the length of hospital stay. Glucose 210-217 insulin Homo sapiens 103-110 34064129-3 2021 We reviewed clinical care practice and hypothesized that early in-hospital transition from intravenous insulin to insulin pump therapy, managed by an endocrine unit trained on post-surgical care, would improve glucose control and impact the length of hospital stay. Glucose 210-217 insulin Homo sapiens 114-121 34064129-8 2021 Early pump users also had lower variability in glucose values over 10 days post-intravenous insulin (p = 0.001), and the post-transition median length of stay was shorter by 5 days (median: 11.5 vs. 16.5 days, p = 0.005). Glucose 47-54 insulin Homo sapiens 92-99 34065194-2 2021 Insufficient insulin production causes an increase in blood glucose level that results in DM. Glucose 60-67 insulin Homo sapiens 13-20 34069950-2 2021 Exercise is a first-line therapy for combating chronic disease by improving insulin action through, in part, reducing hepatic glucose production and lipolysis as well as increasing skeletal muscle glucose uptake and vasodilation. Glucose 197-204 insulin Homo sapiens 76-83 34150163-0 2021 Metformin combined with insulin aspart for ameliorating blood glucose levels and maternal and neonatal outcomes in women with gestational diabetes mellitus and chronic hypertension. Glucose 62-69 insulin Homo sapiens 24-31 34150163-1 2021 OBJECTIVE: To investigate the effect of metformin combined with insulin aspart on blood glucose levels and maternal and neonatal outcomes in women with gestational diabetes mellitus (GDM) accompanied by chronic hypertension (CH). Glucose 88-95 insulin Homo sapiens 64-71 34150163-9 2021 CONCLUSION: Metformin combined with insulin aspart for treating GDM and CH can effectively control blood glucose and blood pressure levels and reduce the risk of adverse perinatal and neonatal outcomes, which exerts positive effect in clinical treatment. Glucose 105-112 insulin Homo sapiens 36-43 34122330-8 2021 Serological measurements of C-peptide and insulin indicate that Gd-CP027, a high affinity zinc(II) contrast agent, potentiates their secretion only as a function of glucose stimulation. Glucose 165-172 insulin Homo sapiens 42-49 34068808-3 2021 Since the 1960s, models have been developed to forecast blood glucose levels based on the history of BGLs, insulin dosages, carbohydrate intake, and other physiological and lifestyle factors. Glucose 62-69 insulin Homo sapiens 107-114 34068221-8 2021 T2DM is a metabolic disorder characterized by high blood glucose levels resulting from altered insulin secretion or action. Glucose 57-64 insulin Homo sapiens 95-102 34068827-3 2021 Pancreatic beta-cells are endocrine cells that produce and secrete insulin, an essential endocrine hormone that regulates blood glucose levels. Glucose 128-135 insulin Homo sapiens 67-74 34068808-5 2021 In past work, we have introduced an LSTM-based approach to blood glucose level prediction aimed at "what-if" scenarios, in which people could enter foods they might eat or insulin amounts they might take and then see the effect on future BGLs. Glucose 65-72 insulin Homo sapiens 172-179 34149259-0 2021 Use of Flash Continuous Glucose Monitoring Is Associated With A1C Reduction in People With Type 2 Diabetes Treated With Basal Insulin or Noninsulin Therapy. Glucose 24-31 insulin Homo sapiens 126-133 34064415-1 2021 For many diabetics, daily, lifelong insulin injections are required to effectively manage blood glucose levels and the complications associated with the disease. Glucose 96-103 insulin Homo sapiens 36-43 34064415-12 2021 It was found that 50 IU/kg of entrapped insulin reduced plasma glucose levels by 55% in 60 min, similar to that induced by subcutaneously (s.c.)-administered insulin (1 IU/kg). Glucose 63-70 insulin Homo sapiens 40-47 34556259-0 2021 The triglyceride/glucose index as an insulin resistance marker in the pediatric population and its relation to eating habits and physical activity. Glucose 17-24 insulin Homo sapiens 37-44 34149259-2 2021 Although use of flash continuous glucose monitoring (CGM) has demonstrated A1C reductions in patients with type 2 diabetes treated with a multiple daily injection or insulin pump therapy regimen, the glycemic benefit of this technology in patients with type 2 diabetes using nonintensive treatment regimens has not been well studied. Glucose 33-40 insulin Homo sapiens 166-173 34556259-1 2021 INTRODUCTION: To examine the triglyceride/glucose index (TyG) as an insulin resistance marker in obese children and adolescents and its relation to clinical and biochemical parameters, body composition and lifestyle. Glucose 42-49 insulin Homo sapiens 68-75 35534645-2 2022 Insulin stimulates glucose transport to cells and regulates other intracellular processes that are linked to cellular bioenergetics, such as autophagy, gluconeogenesis, fatty acid metabolism, and mitochondrial homeostasis. Glucose 19-26 insulin Homo sapiens 0-7 34104393-0 2021 Multiple daily insulin injections ameliorate QT interval by lowering blood glucose levels in patients with type 2 diabetes. Glucose 75-82 insulin Homo sapiens 15-22 34104393-9 2021 DeltaQTc was positively correlated with the changes in fasting plasma glucose (DeltaFPG, r = 0.55, p = 0.0008) and glycated albumin (r = 0.38, p = 0.026) following insulin therapy, but not with the final dose of insulin (r = -0.20, p = 0.26). Glucose 70-77 insulin Homo sapiens 164-171 34104393-11 2021 Conclusions: Multiple daily insulin injections can ameliorate QT interval by lowering the blood glucose levels in T2D, suggesting that glycemic control is important for preventing patients with T2D from sudden cardiac death. Glucose 96-103 insulin Homo sapiens 28-35 34316228-0 2021 Serum Irisin Levels and its Association with Blood Glucose and Insulin Indices in Diagnosing Insulin Resistance in Adolescents with Polycystic Ovarian Syndrome. Glucose 51-58 insulin Homo sapiens 93-100 34136157-6 2021 Furthermore, the NBT subfraction reversed the disorders in glucose and lipid metabolism in insulin-resistant HepG2 cells and significantly increased the mRNA expression of phosphoinositide 3-kinases (PI3K) and AKT in insulin-resistant HepG2 cells in a dose-dependent manner. Glucose 59-66 insulin Homo sapiens 91-98 34150440-0 2021 Type 1 diabetes woman with repeated miscarriages successfully gave birth after introducing an insulin pump with a predictive low glucose suspend feature. Glucose 129-136 insulin Homo sapiens 94-101 34150440-1 2021 Sensor-augmented insulin pump therapy with a predictive low glucose suspend (SAP-PLGS) feature is a remarkably progressed modality for the glycemic management of patients with type 1 diabetes. Glucose 60-67 insulin Homo sapiens 17-24 34211933-3 2021 Given the importance of the issue and the limited studies on glucose control using insulin glargine during surgery, we aimed to investigate the effects of glargine on glucose control in patients with diabetes mellitus during vitrectomy surgery. Glucose 61-68 insulin Homo sapiens 83-90 34211933-3 2021 Given the importance of the issue and the limited studies on glucose control using insulin glargine during surgery, we aimed to investigate the effects of glargine on glucose control in patients with diabetes mellitus during vitrectomy surgery. Glucose 167-174 insulin Homo sapiens 83-90 34211933-12 2021 Results: Use of insulin glargine was associated with significantly lower blood glucose levels compared to regular insulin at 90-minutes (p=0.004), 135 minutes (p=0.001), and 6 hours after the operation (p=0.005). Glucose 79-86 insulin Homo sapiens 16-23 35349798-1 2022 BACKGROUND AND OBJECTIVE: Diabetes mellitus manifests as prolonged elevated blood glucose levels resulting from impaired insulin production. Glucose 82-89 insulin Homo sapiens 121-128 35238140-2 2022 MATERIALS AND METHODS: In a nonrandomized interventional study, insulin-treated patients with T2D (N = 21, mean +- SD age 62.8 +- 6.5 years, body mass index (BMI) 29.0 +- 4.2 kg/m2 , glycated haemoglobin (HbA1c) 51.0 +- 5.4 mmol/mol (6.8 +- 0.5%)) and matched controls (N = 21, mean +- SD age 62.2 +- 8.3 years, BMI 29.2 +- 3.5 kg/m2 , HbA1c 34.3 +- 3.3 mmol/L (5.3 +- 0.3%)) underwent one experimental day with plasma glucose (PG) clamped at three different 30-minute steady-state levels: (1) fasting plasma glucose (FPG); (2) hyperglycaemia (FPG + 10 mmol/L); and (3) hyperinsulinaemic hypoglycaemia (PG <3.0 mmol/L). Glucose 419-426 insulin Homo sapiens 64-71 35238140-2 2022 MATERIALS AND METHODS: In a nonrandomized interventional study, insulin-treated patients with T2D (N = 21, mean +- SD age 62.8 +- 6.5 years, body mass index (BMI) 29.0 +- 4.2 kg/m2 , glycated haemoglobin (HbA1c) 51.0 +- 5.4 mmol/mol (6.8 +- 0.5%)) and matched controls (N = 21, mean +- SD age 62.2 +- 8.3 years, BMI 29.2 +- 3.5 kg/m2 , HbA1c 34.3 +- 3.3 mmol/L (5.3 +- 0.3%)) underwent one experimental day with plasma glucose (PG) clamped at three different 30-minute steady-state levels: (1) fasting plasma glucose (FPG); (2) hyperglycaemia (FPG + 10 mmol/L); and (3) hyperinsulinaemic hypoglycaemia (PG <3.0 mmol/L). Glucose 509-516 insulin Homo sapiens 64-71 35244743-1 2022 The ability to maintain normoglycaemia, through glucose-sensitive insulin release, is a key aspect of postnatal beta cell function. Glucose 48-55 insulin Homo sapiens 66-73 35460043-8 2022 CONCLUSION: The marked slowing of GE of glucose induced by lixisenatide is associated with attenuation in the rise of postprandial glucose in both healthy subjects and diabetes and early insulin secretory response in healthy subjects. Glucose 40-47 insulin Homo sapiens 187-194 34136157-3 2021 An insulin-resistant HepG2 cell model induced by glucose, fructose, oleic acid, and palmitic acid was adopted to investigate the effects of maca extracts on regulating glucose and lipid metabolism in this study. Glucose 49-56 insulin Homo sapiens 3-10 34603702-1 2021 Background: Insulin-glucose therapy in hyperkalaemia treatment has a narrow therapeutic index for a safe and efficient use. Glucose 20-27 insulin Homo sapiens 12-19 34603702-12 2021 In the future, clinical studies on hyperkalaemia treatment by insulin-glucose therapy should detail the procedure precisely. Glucose 70-77 insulin Homo sapiens 62-69 34136772-2 2021 This study aimed to evaluate the trends in insulin resistance and beta-cell dysfunction from 2001 to 2016 among US adults with undiagnosed diabetes, prediabetes, and normal glucose regulation and to provide sex-specific information using data from National Health and Nutrition Examination Surveys (NHANES) 2001-2016. Glucose 173-180 insulin Homo sapiens 43-50 34495541-6 2021 N-glycans have also been suggested to have a major role in preventing the impairment of glucose-stimulated insulin secretion by modulating cell surface expression of glucose transporters. Glucose 88-95 insulin Homo sapiens 107-114 34495541-6 2021 N-glycans have also been suggested to have a major role in preventing the impairment of glucose-stimulated insulin secretion by modulating cell surface expression of glucose transporters. Glucose 166-173 insulin Homo sapiens 107-114 34570574-1 2021 BACKGROUND: The Homeostatic Measurement Assessment-Insulin Resistance (HOMA-IR) is a recognized and validated method which uses the levels of fasting glucose in blood and insulin of patients to evaluate the insulin resistance. Glucose 150-157 insulin Homo sapiens 51-58 34570574-1 2021 BACKGROUND: The Homeostatic Measurement Assessment-Insulin Resistance (HOMA-IR) is a recognized and validated method which uses the levels of fasting glucose in blood and insulin of patients to evaluate the insulin resistance. Glucose 150-157 insulin Homo sapiens 207-214 34229319-1 2021 INTRODUCTION: The triglyceride glucose index (TyG index) is a simple and reliable surrogate marker of insulin resistance (IR) that can predict functional outcomes and mortality after acute ischemic stroke (AIS). Glucose 31-38 insulin Homo sapiens 102-109 34587885-7 2021 RESULTS: We found that Ex-4 promoted the expression of insulin synthesis-related genes and in- duced an obvious increase of insulin-positive HT-22 neuronal cells in a high glucose environment. Glucose 172-179 insulin Homo sapiens 124-131 34758716-2 2021 The triglyceride-glucose in-dex(TyG index) is considered as a novel marker of insulin resistance and can represent peripheral tissue insulin sensitivity. Glucose 17-24 insulin Homo sapiens 78-85 34758716-2 2021 The triglyceride-glucose in-dex(TyG index) is considered as a novel marker of insulin resistance and can represent peripheral tissue insulin sensitivity. Glucose 17-24 insulin Homo sapiens 133-140 34139987-3 2021 SGLT2 inhibitors reduce blood glucose levels by causing glucosuria via an insulin-independent pathway. Glucose 30-37 insulin Homo sapiens 74-81 34541956-1 2021 This study aimed to investigate factors affecting blood glucose control among middle-aged and older diabetic patients taking medications or receiving insulin therapy. Glucose 56-63 insulin Homo sapiens 150-157 34541956-7 2021 Adequate nutrition intake and physical activity of patients undergoing diabetes therapy are required for effective blood glucose management for both diabetic drug and insulin therapies. Glucose 121-128 insulin Homo sapiens 167-174 34392929-3 2021 Mitochondria of the pancreatic beta cell play a central role in the secretion of insulin in response to glucose through their ability to produce ATP. Glucose 104-111 insulin Homo sapiens 81-88 34418413-3 2021 Some FAHFAs, including palmitic acid hydroxy stearic acids (PAHSAs), have been shown to improve insulin sensitivity and glucose tolerance in mice by enhancing glucose-stimulated insulin secretion (GSIS), insulin-stimulated glucose transport, insulin action to suppress hepatic glucose production and reducing adipose tissue inflammation. Glucose 159-166 insulin Homo sapiens 96-103 34418413-3 2021 Some FAHFAs, including palmitic acid hydroxy stearic acids (PAHSAs), have been shown to improve insulin sensitivity and glucose tolerance in mice by enhancing glucose-stimulated insulin secretion (GSIS), insulin-stimulated glucose transport, insulin action to suppress hepatic glucose production and reducing adipose tissue inflammation. Glucose 159-166 insulin Homo sapiens 178-185 34418413-3 2021 Some FAHFAs, including palmitic acid hydroxy stearic acids (PAHSAs), have been shown to improve insulin sensitivity and glucose tolerance in mice by enhancing glucose-stimulated insulin secretion (GSIS), insulin-stimulated glucose transport, insulin action to suppress hepatic glucose production and reducing adipose tissue inflammation. Glucose 223-230 insulin Homo sapiens 204-211 34418413-5 2021 Here, we investigated whether PAHSAs, oleic, pamitoleic, and stearic acid hydroxy stearic acids (OAHSAs, POHSAs, and SAHSAs) potentiate GSIS in beta-cells and human islets, insulin-stimulated glucose uptake in adipocytes, and anti-inflammatory effects in immune cells. Glucose 192-199 insulin Homo sapiens 173-180 34418413-8 2021 However, fewer FAHFAs augment insulin-stimulated glucose uptake in adipocytes. Glucose 49-56 insulin Homo sapiens 30-37 34098834-1 2021 AIMS: The MiniMed 670G insulin pump system is the first commercially available hybrid closed-loop (HCL) insulin delivery system and clinical studies have shown that this device is associated with incremental benefits in glycemic control relative to continuous subcutaneous insulin infusion (CSII) with or without continuous glucose monitoring (CGM). Glucose 325-332 insulin Homo sapiens 24-31 34506628-1 2021 BACKGROUND: The triglyceride-glucose index (TyG index) is a novel metabolic marker initially used as an indicator of insulin resistance. Glucose 29-36 insulin Homo sapiens 117-124 34099169-4 2021 In pancreatic beta-cells, channels comprising SUR1 and Kir6.2 mediate glucose-stimulated insulin secretion and are the targets of antidiabetic sulfonylureas. Glucose 70-77 insulin Homo sapiens 89-96 34875861-4 2021 As a biguanide metformin improves glycemic control by inhibiting gluconeogenesis and increasing insulin-mediated glucose utilization in peripheral tissues. Glucose 113-120 insulin Homo sapiens 96-103 34150441-0 2021 Comparative effects of insulin glulisine and lispro on postprandial plasma glucose and lipid profile in Japanese patients with type 2 diabetes mellitus. Glucose 75-82 insulin Homo sapiens 23-30 34859814-1 2022 Adipocytes are key to metabolic regulation, exhibiting insulin-stimulated glucose transport which is underpinned by the insulin-stimulated delivery of glucose transporter-4 (GLUT4)- containing vesicles to the plasma membrane where they dock and fuse increasing cell surface GLUT4 levels. Glucose 74-81 insulin Homo sapiens 55-62 34859814-4 2022 Syntaxin-4 knockout reduced insulin-stimulated glucose transport and adiponectin secretion by ~50% and reduced GLUT4 levels. Glucose 47-54 insulin Homo sapiens 28-35 34859814-8 2022 In sum, we show that Syntaxin-4 knockout results in reduced insulin-stimulated glucose transport, depletion of cellular GLUT4 levels and inhibition of adiponectin secretion but has only modest effects on the translocation capacity of the cells. Glucose 79-86 insulin Homo sapiens 60-67 35405503-2 2022 Prediabetes is a condition in which the blood glucose levels are not high enough to be diagnosed as diabetes, but insulin resistance and beta-cell dysfunction are simultaneously present. Glucose 46-53 insulin Homo sapiens 114-121 35568115-7 2022 HepG2 insulin-resistance (IR) cells model induced by high glucose was used to verify the potential mechanisms of FFSLD against T2DM which were predicted by the network pharmacology. Glucose 58-65 insulin Homo sapiens 6-13 35597530-7 2022 Despite these cases, the secretion of insulin and C-peptide in response to different concentrations of glucose in the 3D group was significantly higher than in the 2D culture. Glucose 103-110 insulin Homo sapiens 38-45 35421551-7 2022 Triphenyl phosphate (TPhP), tricresyl phosphate (TCP), TDCPP, TBP and TBEP enhanced glucose uptake at both basal and insulin-stimulated status. Glucose 84-91 insulin Homo sapiens 117-124 35550884-6 2022 Regression analysis showed an inverse correlation between islet Cd level and plasma insulin following a glucose challenge in males but not in females. Glucose 104-111 insulin Homo sapiens 84-91 35609678-1 2022 INTRODUCTION: Glucagon and insulin are the two most important hormones for glucose metabolism and have been incorporated in the dual-hormonal artificial pancreas, a device for automated glucose regulation for people with diabetes type 1. Glucose 186-193 insulin Homo sapiens 27-34 35609678-3 2022 The delay in glucose-lowering effect after subcutaneous injection of insulin is substantial, in contrast to the elevation of blood glucose values after subcutaneously injected glucagon which is occurs shortly after injection. Glucose 13-20 insulin Homo sapiens 69-76 35470695-5 2022 Accordingly, we further hypothesized that, in T2D individuals, seven days of passive heat treatment via hot water immersion to waist-level would improve leg blood flow responses to an oral glucose load (i.e., endogenous insulin stimulation) via induction of endothelial HSP72. Glucose 189-196 insulin Homo sapiens 220-227 35470695-6 2022 In contrast, we found that: 1) endothelial insulin resistance in T2D mice and humans was not associated with reduced HSP72 in aortas and venous endothelial cells, respectively; 2) after passive heat treatment, improved leg blood flow responses to an oral glucose load did not parallel with increased endothelial HSP72; 3) downregulation of HSP72 (via small-interfering RNA) or upregulation of HSP72 (via heating) in cultured endothelial cells did not impair or enhance insulin signaling, respectively, nor was JNK activity altered. Glucose 255-262 insulin Homo sapiens 43-50 35617802-1 2022 Diabetes mellitus (DM) is a collection of metabolic and pathophysiological disorders manifested with high glucose levels in the blood due to the inability of beta-pancreatic cells to secrete an adequate amount of insulin or insensitivity of insulin towards receptor to oxidize blood glucose. Glucose 106-113 insulin Homo sapiens 213-220 35617802-1 2022 Diabetes mellitus (DM) is a collection of metabolic and pathophysiological disorders manifested with high glucose levels in the blood due to the inability of beta-pancreatic cells to secrete an adequate amount of insulin or insensitivity of insulin towards receptor to oxidize blood glucose. Glucose 106-113 insulin Homo sapiens 241-248 35488481-1 2022 Hybrid closed-loop (HCL) systems are characterised by integrating continuous glucose monitoring (CGM) with insulin pumps which automate insulin delivery via specific algorithms and user-initiated insulin delivery. Glucose 77-84 insulin Homo sapiens 136-143 35577173-0 2022 Hydrogen sulfide disrupts insulin-induced glucose uptake in L6 skeletal muscle cells. Glucose 42-49 insulin Homo sapiens 26-33 35577173-8 2022 Exogenous H2S reduced insulin-induced glucose uptake at 0.5 up to 24 h, an effect dissociated from the level of Akt phosphorylation. Glucose 38-45 insulin Homo sapiens 22-29 35577173-10 2022 In addition, H2S disrupts insulin-induced glucose uptake independent of the Akt pathway. Glucose 42-49 insulin Homo sapiens 26-33 35577173-11 2022 These results suggest that H2S antagonism over insulin-induced glucose uptake could help maintain the plasmatic glucose levels in conditions that provoke hypoglycemia, which could serve as an H2S-regulated mechanism for maintaining glucose plasmatic levels through the inhibition of the skeletal muscle insulin-depended glucose uptake. Glucose 63-70 insulin Homo sapiens 47-54 35577173-11 2022 These results suggest that H2S antagonism over insulin-induced glucose uptake could help maintain the plasmatic glucose levels in conditions that provoke hypoglycemia, which could serve as an H2S-regulated mechanism for maintaining glucose plasmatic levels through the inhibition of the skeletal muscle insulin-depended glucose uptake. Glucose 63-70 insulin Homo sapiens 303-310 35577173-11 2022 These results suggest that H2S antagonism over insulin-induced glucose uptake could help maintain the plasmatic glucose levels in conditions that provoke hypoglycemia, which could serve as an H2S-regulated mechanism for maintaining glucose plasmatic levels through the inhibition of the skeletal muscle insulin-depended glucose uptake. Glucose 112-119 insulin Homo sapiens 47-54 35577173-11 2022 These results suggest that H2S antagonism over insulin-induced glucose uptake could help maintain the plasmatic glucose levels in conditions that provoke hypoglycemia, which could serve as an H2S-regulated mechanism for maintaining glucose plasmatic levels through the inhibition of the skeletal muscle insulin-depended glucose uptake. Glucose 112-119 insulin Homo sapiens 303-310 35577173-11 2022 These results suggest that H2S antagonism over insulin-induced glucose uptake could help maintain the plasmatic glucose levels in conditions that provoke hypoglycemia, which could serve as an H2S-regulated mechanism for maintaining glucose plasmatic levels through the inhibition of the skeletal muscle insulin-depended glucose uptake. Glucose 232-239 insulin Homo sapiens 47-54 35577173-11 2022 These results suggest that H2S antagonism over insulin-induced glucose uptake could help maintain the plasmatic glucose levels in conditions that provoke hypoglycemia, which could serve as an H2S-regulated mechanism for maintaining glucose plasmatic levels through the inhibition of the skeletal muscle insulin-depended glucose uptake. Glucose 320-327 insulin Homo sapiens 47-54 35509133-13 2022 In addition, OBB effectively improved the consumption of glucose in insulin-resistant HepG2 cells. Glucose 57-64 insulin Homo sapiens 68-75 35190812-6 2022 Both in the presence as well as in the absence of obesity, weight loss decreases visceral adipose tissue and liver fat, increases insulin sensitivity in skeletal muscle (insulin-mediated whole-body glucose disposal rate) and in adipose tissue (meal-induced or insulin-induced suppression of plasma free fatty acid concentration), and augments insulin clearance rate, without affecting pancreatic insulin secretion. Glucose 198-205 insulin Homo sapiens 130-137 35190812-6 2022 Both in the presence as well as in the absence of obesity, weight loss decreases visceral adipose tissue and liver fat, increases insulin sensitivity in skeletal muscle (insulin-mediated whole-body glucose disposal rate) and in adipose tissue (meal-induced or insulin-induced suppression of plasma free fatty acid concentration), and augments insulin clearance rate, without affecting pancreatic insulin secretion. Glucose 198-205 insulin Homo sapiens 170-177 35475907-1 2022 OBJECTIVE: To compare the efficacy of low-dose subcutaneous dasiglucagon with oral glucose for prevention of insulin-induced hypoglycemia in people with type 1 diabetes. Glucose 83-90 insulin Homo sapiens 109-116 35143900-5 2022 Glutathionylated Gal-3 prevents Gal-3(WT)-Insulin Receptor interaction and facilitates insulin-induced murine adipocyte p-IRS1(tyr895) and p-AKT(ser473) signaling and glucose uptake in a Gal-3 Cys187 glutathionylation dependent manner in murine adipocytes, as assessed by Western blotting and 2-NBDG uptake assay respectively. Glucose 167-174 insulin Homo sapiens 87-94 35099277-1 2022 BACKGROUND: Continuous Glucose Monitoring (CGM) has been increasingly shown to be beneficial in patients with both type 1 and type 2 diabetes using insulin. Glucose 23-30 insulin Homo sapiens 148-155 35294000-5 2022 As expected, both KATP-GOF and KATP-GOF/GCK+/- mice showed lack of glucose-stimulated insulin secretion. Glucose 67-74 insulin Homo sapiens 86-93 35377441-1 2022 Double C2 Domain Beta (DOC2b) protein is required for glucose-stimulated insulin secretion (GSIS) in beta-cells, the underlying mechanism of which remains unresolved. Glucose 54-61 insulin Homo sapiens 73-80 35512857-7 2022 Glucose-stimulated insulin secretion was observed not only in INS-1E cells but also in rat pancreatic preparations. Glucose 0-7 insulin Homo sapiens 19-26 35534645-4 2022 Previous studies showed that prolonged hyperglycemia is associated with the development of insulin resistance in podocytes, and high glucose-treated podocytes exhibit an increase in mitochondrial fission and decrease in markers of mitophagy. Glucose 133-140 insulin Homo sapiens 91-98 35395220-6 2022 Compared to saline, ileal glucose resulted in minimal increases in blood glucose and plasma insulin and C-peptide, but substantial increases in plasma GLP-1, without affecting ghrelin, GIP or glucagon. Glucose 26-33 insulin Homo sapiens 92-99 35395220-6 2022 Compared to saline, ileal glucose resulted in minimal increases in blood glucose and plasma insulin and C-peptide, but substantial increases in plasma GLP-1, without affecting ghrelin, GIP or glucagon. Glucose 26-33 insulin Homo sapiens 104-113 35534645-6 2022 We suggest that PINK1 inhibition impairs the insulin signaling pathway, in which lower levels of phosphorylated Akt and membrane fractions of the insulin receptor and glucose transporter-4 were observed. Glucose 167-174 insulin Homo sapiens 45-52 35189258-3 2022 Iatrogenic (insulin-induced) hypoglycaemia evokes a homeostatic response commonly referred to as the glucose counter-regulatory response. Glucose 101-108 insulin Homo sapiens 12-19 35292359-8 2022 This enhanced insulin-dependent glucose uptake through increased peroxisome proliferator activated receptor gamma (PPARgamma)-driven expression of GLUT4. Glucose 32-39 insulin Homo sapiens 14-21 35459606-9 2022 DASH and DASH-P scores were inversely associated with fasting plasma glucose (DASH:beta = -0.036 +- 0.012,P = 0.005; DASH-P: beta = -0.04 +- 0.017,P = 0.002), and positively associated with insulin sensitivity (DASH:beta = 0.022 +- 0.012,P = 0.042; DASH-P: = 0.036 +- 0.015,P = 0.014). Glucose 69-76 insulin Homo sapiens 190-197 35490289-7 2022 Insulin protocols should be effective at maintaining glucose concentrations within the specified target range with minimal hypoglycemic events. Glucose 53-60 insulin Homo sapiens 0-7 35490289-8 2022 Monitoring glucose concentrations while on either an intravenous or subcutaneous insulin protocol is essential. Glucose 11-18 insulin Homo sapiens 81-88 35633646-7 2022 Results: HbA1c, lipid profile, testosterone, leptin, adiponectin, TNF-alpha, HOMA-IR, glucose/insulin ratio, AI, fasting glucose-insulin levels were similar. Glucose 121-128 insulin Homo sapiens 129-136 35490958-12 2022 Mediation analysis showed that, insulin resistance, as assessed by triglyceride-glucose index, may underline the relationship between high LFR and increased odds of diabetes. Glucose 80-87 insulin Homo sapiens 32-39 35604110-6 2022 Loss of the CLEC16A C-terminal IDPR in vivo impairs mitophagy, mitochondrial function, and glucose-stimulated insulin secretion, ultimately causing glucose intolerance. Glucose 91-98 insulin Homo sapiens 110-117 35608823-0 2022 Relationships of glucose, GLP-1 and insulin secretion with gastric emptying after a 75g glucose load in type 2 diabetes. Glucose 88-95 insulin Homo sapiens 36-43 35635329-3 2022 Initiation of hyperinsulinemia is triggered by a loss of first phase glucose-stimulated insulin secretion with altered membrane ion channel distribution. Glucose 69-76 insulin Homo sapiens 88-95 35442623-6 2022 The inner layer of the microneedles was integrated with a flexible electroosmotic pump to deliver insulin, and the delivery rate was electrically controlled by the glucose level from the biosensing device. Glucose 164-171 insulin Homo sapiens 98-105 35584802-4 2022 During the past five years, an increasing number of individuals with type 1 diabetes (T1D) and insulin-treated type 2 diabetes (T2D) have adopted use of continuous glucose monitoring (CGM) for daily measurement of glucose levels. Glucose 164-171 insulin Homo sapiens 95-102 35584802-4 2022 During the past five years, an increasing number of individuals with type 1 diabetes (T1D) and insulin-treated type 2 diabetes (T2D) have adopted use of continuous glucose monitoring (CGM) for daily measurement of glucose levels. Glucose 214-221 insulin Homo sapiens 95-102 35616388-8 2022 These results demonstrated the insulin secreted by Min6 upstream simulated and increased the uptake of glucose by the downstream HepG2 cells. Glucose 103-110 insulin Homo sapiens 31-38 35616696-8 2022 Finally, we identified the gene PCDH7 from the beta cell clusters that had the highest number of Ca2+-regulated genes, and showed that cells expressing cell surface PCDH7 protein have enhanced glucose-stimulated insulin secretory function. Glucose 193-200 insulin Homo sapiens 212-219 35619221-3 2022 We investigated metabolic effects of long-term melatonin treatment in patients with type 2 diabetes including determinations of insulin sensitivity and glucose-stimulated insulin secretion. Glucose 152-159 insulin Homo sapiens 171-178 35611506-3 2022 METHOD: Patients with diabetes expected to stay for more than 24hs were enrolled, HbA1c was converted to A1C-derived average glucose (ADAG) by the equation: ADAG = ( (HbA1c * 28.7) - 46.7 ) * 18-1, blood glucose were measured four times a day during the first 7 days after admission, the mean glucose level(MGL) and SOFA (within 3, 5, and 7days) were calculated for each person, GAPadm and GAPmean was calculated as admission blood glucose and MGL minus ADAG, the incidence of moderate hypoglycemia(MH), severe hypoglycemia (SH), total dosage of glucocorticoids and average daily dosage of insulin, duration of renal replacement therapy(RRT), ventilator-free hours, and non-ICU days were also collected. Glucose 125-132 insulin Homo sapiens 592-599 35608484-4 2022 In the intervention group intravenous insulin was commenced at a blood glucose >252 mg/dL and titrated to a target range of 180 to 252 mg/dL. Glucose 71-78 insulin Homo sapiens 38-45 35608823-2 2022 OBJECTIVE: We have evaluated the relationship of plasma glucose, GLP-1 and insulin secretion with GE of a 75g oral glucose load in T2D. Glucose 115-122 insulin Homo sapiens 75-82 35608823-13 2022 CONCLUSION: In T2D, while insulin secretion is the dominant determinant of the 120min plasma glucose, GE also correlates. Glucose 93-100 insulin Homo sapiens 26-33 35604616-1 2022 Triglyceride-glucose index (TyG index) has been used in healthy individuals as a marker of insulin resistance. Glucose 13-20 insulin Homo sapiens 91-98 35597962-6 2022 The homeostatic model assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin levels. Glucose 93-100 insulin Homo sapiens 36-43 35606820-2 2022 Despite recent advances in glucose sensors and insulin pump technology, only a minority of patients meet their glucose targets and face the risk of both acute and long-term complications, some of which are life-threatening. Glucose 111-118 insulin Homo sapiens 47-54 35598217-2 2022 Indeed, the biggest risk for CVD seems to shift to glucose intolerance in humans with insulin resistance. Glucose 51-58 insulin Homo sapiens 86-93 35605918-0 2022 A diarylheptanoid compound from Alpinia officinarum Hance ameliorates high glucose-induced insulin resistance by regulating PI3K/AKT-Nrf2-GSK3beta signaling pathways in HepG2 cells. Glucose 75-82 insulin Homo sapiens 91-98 35605918-5 2022 Glucose uptake and reactive oxygen species (ROS) levels in high glucose-induced insulin-resistant HepG2 cells were assessed using flow cytometry. Glucose 0-7 insulin Homo sapiens 80-87 35605918-5 2022 Glucose uptake and reactive oxygen species (ROS) levels in high glucose-induced insulin-resistant HepG2 cells were assessed using flow cytometry. Glucose 64-71 insulin Homo sapiens 80-87 35594334-6 2022 The relative percentage differences on insulin secretion between three dosages were compared in low and high glucose, respectively. Glucose 109-116 insulin Homo sapiens 39-46 35594334-7 2022 Results: Insulin secretion was higher in samples exposed to 15.6 J/cm2 PBMT in low glucose (p < 0.05), but not in high glucose. Glucose 83-90 insulin Homo sapiens 9-16 35594334-8 2022 When evaluating sex differences, male islets had higher insulin secretion by 15.6 J/cm2 PBMT in low glucose compared with females (p < 0.05). Glucose 100-107 insulin Homo sapiens 56-63 35594334-10 2022 When compared within the control groups (0.0 J/cm2 PBMT), the relative changes on insulin secretion in high glucose was significantly higher on male islets (p < 0.05), but not on female islets. Glucose 108-115 insulin Homo sapiens 82-89 35587736-0 2022 Repurposing pinacol esters of boronic acids for tuning viscoelastic properties of glucose-responsive polymer hydrogels: effects on insulin release kinetics. Glucose 82-89 insulin Homo sapiens 131-138 35590248-1 2022 BACKGROUND: Glucagon serves as an important regulatory hormone for regulating blood glucose concentration with tight feedback control exerted by insulin and glucose. Glucose 84-91 insulin Homo sapiens 145-152 35587736-10 2022 We believe that glucose-responsive hydrogels with tunable viscoelastic properties will pave the way for developing a variety of hydrogels with programmable insulin release properties. Glucose 16-23 insulin Homo sapiens 156-163 35416806-1 2022 Long and automatic control of blood glucose levels in diabetic patients could solve the problems caused by frequent insulin injections. Glucose 36-43 insulin Homo sapiens 116-123 35416806-5 2022 A high glucose level triggers quick insulin release from the SHIDS to reduce the glucose level, which then slows the insulin release. Glucose 7-14 insulin Homo sapiens 36-43 35416806-5 2022 A high glucose level triggers quick insulin release from the SHIDS to reduce the glucose level, which then slows the insulin release. Glucose 7-14 insulin Homo sapiens 117-124 35416806-5 2022 A high glucose level triggers quick insulin release from the SHIDS to reduce the glucose level, which then slows the insulin release. Glucose 81-88 insulin Homo sapiens 36-43 35416806-5 2022 A high glucose level triggers quick insulin release from the SHIDS to reduce the glucose level, which then slows the insulin release. Glucose 81-88 insulin Homo sapiens 117-124 35628392-9 2022 Moreover, GRbeta activates the Akt pathway, increases glucose transports mRNA, increasing glucose uptake and glycogen storage as an insulin-mimetic. Glucose 90-97 insulin Homo sapiens 132-139 35578361-7 2022 The usage of infusion of glucose-insulin-potassium in rice tablet poisoning has been suggested, after its positive beneficial cardiac inotropic effects in patients with beta-blocker and calcium channel blocker poisoning. Glucose 25-32 insulin Homo sapiens 33-40 35213713-8 2022 The inverse relationship between glucagon and glucose was attenuated in individuals with high BMI SDS and high fasting insulin. Glucose 46-53 insulin Homo sapiens 119-126 35578361-8 2022 CASE PRESENTATION: We report the case of a 30-year-old Iranian woman with critical aluminum phosphide poisoning, presented with hypotension and other signs of shock and severe metabolic acidosis, successfully treated with high-dose regular insulin and hypertonic dextrose and discharged from hospital in good condition. Glucose 263-271 insulin Homo sapiens 240-247 35578361-9 2022 In contrast to our previous experiences, in which nearly all patients with critical aluminum phosphide poisoning died, this patient was saved with glucose-insulin-potassium. Glucose 147-154 insulin Homo sapiens 155-162 35628384-1 2022 Insulin signaling is a conserved pathway that orchestrates glucose and lipid metabolism, energy balance, and inflammation, and its dysregulation compromises the homeostasis of multiple systems. Glucose 59-66 insulin Homo sapiens 0-7 35592612-1 2022 Skeletal muscle takes up glucose in an insulin-sensitive manner and is thus important for the maintenance of blood glucose homeostasis. Glucose 25-32 insulin Homo sapiens 39-46 35575196-4 2022 MAIN OUTCOME MEASURES: Confounder-adjusted linear regression analysis was applied to study the associations of day of the week of examination with glucose and insulin responses to an oral glucose tolerance test (OGTT) and fasting triglyceride concentrations. Glucose 188-195 insulin Homo sapiens 159-166 35575196-5 2022 RESULTS: In fully confounder-adjusted models, mean (95% CI) concentrations of fasting glucose, insulin, and triglycerides were slightly higher on Mondays compared with the other weekdays (glucose: 1% (0;2); insulin: 9% (1;18); triglycerides: 5% (2;8)). Glucose 188-195 insulin Homo sapiens 95-102 35575196-6 2022 Interaction analyses revealed that the association of weekday with insulin was only pronounced in men (18% (3;35), but not in women (1% (-8;10)), whereas the associations with glucose and triglycerides were only apparent for individuals with known type 2 diabetes (glucose: 4% (0;7); triglycerides: 14% (6;23) compared to the background population (glucose: 0% (0;1); triglycerides: 3% (0;6)). Glucose 265-272 insulin Homo sapiens 67-74 35575196-6 2022 Interaction analyses revealed that the association of weekday with insulin was only pronounced in men (18% (3;35), but not in women (1% (-8;10)), whereas the associations with glucose and triglycerides were only apparent for individuals with known type 2 diabetes (glucose: 4% (0;7); triglycerides: 14% (6;23) compared to the background population (glucose: 0% (0;1); triglycerides: 3% (0;6)). Glucose 349-356 insulin Homo sapiens 67-74 35577602-1 2022 PURPOSE: Ultra rapid lispro (URLi) is a novel insulin lispro formulation developed to more closely match physiological insulin secretion and improve postprandial glucose control. Glucose 162-169 insulin Homo sapiens 46-53 35552423-1 2022 CONTEXT: Sustained increases in plasma glucose promote skeletal muscle insulin resistance independent from obesity and dyslipidemia (i.e. glucotoxicity). Glucose 39-46 insulin Homo sapiens 71-78 35552423-8 2022 RESULTS: Despite impairing insulin-mediated glucose disposal and suppressing fasting lipid oxidation, hyperglycemia did not alter either the content or composition of skeletal muscle triglycerides, diacylglycerides, or phospholipids. Glucose 44-51 insulin Homo sapiens 27-34 35552423-10 2022 CONCLUSIONS: Our results demonstrate that the major lipid pools in skeletal muscle are unperturbed by sustained increases in glucose availability and suggest that glucotoxicity and lipotoxicity drive insulin resistance through distinct mechanistic pathways. Glucose 125-132 insulin Homo sapiens 200-207 35592612-7 2022 Notably, insulin-sensitive glucose uptake is increased synergistically by nitrite. Glucose 27-34 insulin Homo sapiens 9-16 35592615-7 2022 In addition, insulin and C-peptide were measured through glucose-stimulated insulin secretion (GSIS) assays and ELISA. Glucose 57-64 insulin Homo sapiens 13-20 35592615-7 2022 In addition, insulin and C-peptide were measured through glucose-stimulated insulin secretion (GSIS) assays and ELISA. Glucose 57-64 insulin Homo sapiens 76-83 35546275-7 2022 Most importantly, the type of glucose-lowering medication prescribed at previous visit had the strongest impact on weight change over time independent of participant factors, with use of an SGLT2i or GLP-1 RA associated with 1.0% weight loss versus a 0.6% weight gain with sulfonylureas, thiazolidinediones, meglitinides, or insulin. Glucose 30-37 insulin Homo sapiens 325-332 35626654-6 2022 The tight relationship between mitochondrial dysfunction, reduced glucose-stimulated insulin secretion (GSIS), and diabetes development in human patients is acknowledged. Glucose 66-73 insulin Homo sapiens 85-92 35634501-7 2022 We found that the patient proband and his father exhibited high insulin and C-peptide release after glucose stimulation by insulin and C-peptide release tests. Glucose 100-107 insulin Homo sapiens 64-71 35634501-7 2022 We found that the patient proband and his father exhibited high insulin and C-peptide release after glucose stimulation by insulin and C-peptide release tests. Glucose 100-107 insulin Homo sapiens 123-130 35591905-0 2022 Real-World Analysis of Rapid-Acting Insulin Analog Use and Its Blood Glucose Lowering Effect in Patients with Type 2 Diabetes Mellitus: Results from PASSION Disease Registry in Korea. Glucose 69-76 insulin Homo sapiens 36-43 35538807-7 2022 Molecular studies revealed that these plant-derived molecules induced glucose uptake via increasing GLUT-4 expression and/or translocation through insulin signaling pathway, AMPK pathway, PTP1B activity inhibition or acting as partial PPARgamma agonists. Glucose 70-77 insulin Homo sapiens 147-154 35416225-3 2022 In this work, we developed a glucose-responsive insulin-releasing hydrogel for microneedle dressing fabrication and then investigated its effects on diabetic wound healing. Glucose 29-36 insulin Homo sapiens 48-55 35416225-5 2022 The resultant hydrogel microneedle dressing exhibited adequate mechanical properties, high biocompatibility, glucose-responsive insulin release behavior upon exposure to different glucose solutions, and potent adhesion to the skin compared to hydrogels without microstructures. Glucose 109-116 insulin Homo sapiens 128-135 35416225-7 2022 Therefore, the glucose-responsive insulin-releasing hydrogel microneedle dressing is effective in diabetic wound management and has potential for treatment of other chronic skin injuries. Glucose 15-22 insulin Homo sapiens 34-41 35358060-7 2022 RESULTS: In alternative models, we found a positive association with either basal insulin secretion (mean 0.22, 95% CI 0.01, 0.44 z-scores) or prepuberal beta cell glucose sensitivity (mean 0.23, 95% CI 0.00, 0.46 z-scores) and adult height, while total insulin secretion was negatively related to adult height (mean -0.36, 95% CI -0.57, -0.15 z-scores or mean -0.42, 95% CI -0.69, -0.16 z-scores, respectively). Glucose 164-171 insulin Homo sapiens 254-261 35358060-8 2022 The high total insulin secretion of low adult height patients was mainly due to late (>60 minutes) secretion, and associated with a worse glucose response during OGTT. Glucose 138-145 insulin Homo sapiens 15-22 35524749-1 2022 CONTEXT: Decreased first-phase insulin response (FPIR) during intravenous glucose tolerance testing (IVGTT) is an early indicator of beta-cell dysfunction and predictor of type 1 diabetes (T1D). Glucose 74-81 insulin Homo sapiens 31-38 35522655-6 2022 High glucose increased Fet-A and phosphorylated (Ser312) fetuin-A (pFet-A) expression, which are known to impair insulin signaling. Glucose 5-12 insulin Homo sapiens 113-120 35571731-10 2022 Conclusion: Glimepiride combined with recombinant human insulin injection can improve insulin sensitivity, reduce insulin resistance, significantly reduce glucose and lipids in patients, reduce the occurrence of oxidative stress, promote the secretion of oxidative resistance enzymes, lower the vascular endothelial growth factor (VEGF), reduced the formation of new blood vessels, and inhibit the growth and metastasis of cancer cells. Glucose 155-162 insulin Homo sapiens 56-63 35624603-8 2022 In this report we showed that under microfluidic conditions PAHSA, especially 5-PAHSA, has a positive effect on pseudoislet proliferation, increase in cell number and mass, and glucose-stimulated insulin secretion, which may qualify it as a compound with potential therapeutic properties. Glucose 177-184 insulin Homo sapiens 196-203 35512706-3 2022 Insulin resistance was estimated by Homeostatic model assessment-Insulin resistance 2 (HOMA-IR2) using fasting plasma insulin and glucose. Glucose 130-137 insulin Homo sapiens 0-7 35505313-1 2022 BACKGROUND: A single measurement of the triglyceride-glucose (TyG) index, a simple and reliable surrogate marker of insulin resistance, is associated with ischemic stroke. Glucose 53-60 insulin Homo sapiens 116-123 35509032-4 2022 RESULTS: Carrying a male fetus was associated with lower fasting glucose (difference in mean concentrations 0.1 mmol/L; beta" = 0.063; p = 0.02) and insulin ( 1.1 pmol/L; beta" = 0.075; p = 0.01) concentrations but not with post-load glucose or insulin concentrations. Glucose 237-244 insulin Homo sapiens 151-158 35509124-6 2022 This review focuses on the influence of extracellular vesicles on insulin resistance by regulating inflammation and glucose transporters 4 expression. Glucose 116-123 insulin Homo sapiens 66-73 35600606-2 2022 Glucose lowering drugs reduce blood glucose by modulating insulin secretion and its actions as well as redistributing energy disposal. Glucose 0-7 insulin Homo sapiens 58-65 35563490-3 2022 Insulin injection partially compensates for the role of endogenous insulin which promotes glucose uptake, lipid synthesis and organ growth. Glucose 90-97 insulin Homo sapiens 0-7 35563490-3 2022 Insulin injection partially compensates for the role of endogenous insulin which promotes glucose uptake, lipid synthesis and organ growth. Glucose 90-97 insulin Homo sapiens 67-74 35563490-4 2022 However, lacking the continuous, rapid, and accurate glucose regulation by endogenous functional beta cells, the current insulin injection therapy is unable to treat the root causes of the disease. Glucose 53-60 insulin Homo sapiens 121-128 35586828-1 2022 Objective: To determine if the triglycerides and glucose index (TyG) can be used as a marker for insulin resistance (IR) in Argentinean schoolchildren according to age and sex. Glucose 49-56 insulin Homo sapiens 97-104 35504932-5 2022 Islets embedded in this hydrogel show increased glucose- and KCl-stimulated insulin secretion, and improved mitochondrial function compared to islets cultured without pancreatic matrix. Glucose 48-55 insulin Homo sapiens 76-83 35500603-12 2022 In addition, in a subgroup analysis, no connection could be established between the size of the insulinoma and the amount of insulin that was released after oral glucose exposure. Glucose 162-169 insulin Homo sapiens 125-132 35099302-1 2022 Combining technologies including rapid insulin analogs, insulin pumps, continuous glucose monitors (CGMs), and control algorithms has allowed for the creation of automated insulin delivery (AID) systems. Glucose 82-89 insulin Homo sapiens 172-179 35500938-5 2022 Indirect associations were mediated through the triglyceride-glucose (TyG) index (as an indicator of insulin resistance), mean arterial pressure (MAP), uric acid (UA), and total cholesterol (TC). Glucose 61-68 insulin Homo sapiens 101-108 35565875-0 2022 Large-Scale Data Analysis for Glucose Variability Outcomes with Open-Source Automated Insulin Delivery Systems. Glucose 30-37 insulin Homo sapiens 86-93 35565875-1 2022 Open-source automated insulin delivery (AID) technologies use the latest continuous glucose monitors (CGM), insulin pumps, and algorithms to automate insulin delivery for effective diabetes management. Glucose 84-91 insulin Homo sapiens 22-29 35565875-1 2022 Open-source automated insulin delivery (AID) technologies use the latest continuous glucose monitors (CGM), insulin pumps, and algorithms to automate insulin delivery for effective diabetes management. Glucose 84-91 insulin Homo sapiens 150-157 35373587-2 2022 Although the mechanisms governing glucose-coupled insulin secretion have received the most attention, there is emerging evidence for a multitude of physiological signalling pathways and paracrine networks that collectively regulate insulin, glucagon, and somatostatin release. Glucose 34-41 insulin Homo sapiens 50-57 35373587-2 2022 Although the mechanisms governing glucose-coupled insulin secretion have received the most attention, there is emerging evidence for a multitude of physiological signalling pathways and paracrine networks that collectively regulate insulin, glucagon, and somatostatin release. Glucose 34-41 insulin Homo sapiens 232-239 35114469-1 2022 Insulin is an essential and versatile hormone taking part in the control of blood glucose levels and protein anabolism. Glucose 82-89 insulin Homo sapiens 0-7 35192682-11 2022 Altogether, we provide a repository of TBC1D4 interactors in human and mouse skeletal muscle, which serve as potential regulators of TBC1D4 function and, thus, insulin-stimulated glucose uptake in human skeletal muscle. Glucose 179-186 insulin Homo sapiens 160-167 35100352-4 2022 Whole-body or tissue-specific insulin sensitivity was not altered by JQ-1; however, JQ-1 treatment reduced insulin secretion during both in vivo glucose tolerance testing and ex vivo incubation of isolated islets. Glucose 145-152 insulin Homo sapiens 107-114 35189271-4 2022 Whole pancreas and pancreatic islet transplantation restore endogenous insulin secretion in response to blood glucose levels. Glucose 110-117 insulin Homo sapiens 71-78 35303528-14 2022 At an experimental level, treatment with p,p"-DDE or PCB-153, at concentrations ranging from 1 x 10-15 M to 5 x 10-6 M, impaired the ability of pancreatic beta-cells to produce and secrete insulin in response to glucose. Glucose 212-219 insulin Homo sapiens 189-196 35577748-1 2022 The Flash Guide (FG) for insulin dosing (A. Chico, C. Gonzalez) was the first document intended for FreeStyle Libre (FSL) user patients to help with decision-making depending on glucose level and trend. Glucose 179-186 insulin Homo sapiens 25-32 35577748-6 2022 The percentage of subjects who used glucose trend in decision-making after receiving the FG increased: for adjusting insulin (51 vs. 83; p = 0.016), action without insulin (51 vs. 90%; p = 0.001), and in special circumstances. Glucose 36-43 insulin Homo sapiens 117-124 35577748-6 2022 The percentage of subjects who used glucose trend in decision-making after receiving the FG increased: for adjusting insulin (51 vs. 83; p = 0.016), action without insulin (51 vs. 90%; p = 0.001), and in special circumstances. Glucose 36-43 insulin Homo sapiens 164-171 35218559-0 2022 Muscle hypertrophic effect of inhaled beta2 -agonist is associated with augmented insulin-stimulated whole-body glucose disposal in young men. Glucose 112-119 insulin Homo sapiens 82-89 35339075-3 2022 The aim of this study is to identify predictors of insulin therapy in women diagnosed with GDM once an oral glucose tolerance test (OGTT) is performed during pregnancy. Glucose 108-115 insulin Homo sapiens 51-58 35563431-2 2022 Here we used the human EndoC-betaH1 beta-cell line, the rat beta-cell line INS-1E and dispersed mouse islet cells to assess the effects of endocrine disruptors on cell viability and glucose-stimulated insulin secretion (GSIS). Glucose 182-189 insulin Homo sapiens 201-208 35246864-0 2022 Glucose and oleic acid mediate cellular alterations in GLP-1-induced insulin-positive differentiating UCBMSCs. Glucose 0-7 insulin Homo sapiens 69-76 35246864-1 2022 Coordinated effects of glucose and oleic acid on glucagon-like peptide-1 (GLP-1) mediated differentiation of insulin-positive differentiating umbilical cord mesenchymal stromal cells (dUCBMSCs) was studied using a co-culture of NCI-H716 (GLP-1+) and UCBMSCs (insulin+). Glucose 23-30 insulin Homo sapiens 259-266 35246864-2 2022 The addition of 2.5 mM glucose increased the proliferation of NCI-H716 cells by 30% and induced transformation of UCBMSCs into insulin-secreting cells in 18 days as compared to 22 days in control cells. Glucose 23-30 insulin Homo sapiens 127-134 35218559-3 2022 Thus, we investigated the physiological effects of prolonged beta2 -agonist treatment at inhaled doses resembling those used in respiratory diseases on insulin-stimulated whole-body glucose disposal and putative mechanisms in skeletal muscle and adipose tissue of healthy men. Glucose 182-189 insulin Homo sapiens 152-159 35218559-5 2022 Before and after treatments, we assessed subjects" whole-body insulin-stimulated glucose disposal and body composition, and collected vastus lateralis muscle and abdominal adipose tissue biopsies. Glucose 81-88 insulin Homo sapiens 62-69 35218559-9 2022 Beta2 -agonist treatment in close-to-therapeutic doses may augment whole-body insulin-stimulated glucose disposal in healthy young men and part of the change is likely to be explained by muscle hypertrophy. Glucose 97-104 insulin Homo sapiens 78-85 35218559-12 2022 Herein we show that a 4-week treatment period with daily therapeutic inhalation of beta2 -agonist increases insulin-stimulated whole-body glucose disposal in young healthy lean men. Glucose 138-145 insulin Homo sapiens 108-115 35218559-14 2022 These findings suggest that the enhanced insulin-stimulated whole-body glucose disposal induced by a period of beta2 -agonist treatment in humans, at least in part, is attributed to muscle hypertrophy. Glucose 71-78 insulin Homo sapiens 41-48 35092562-6 2022 The glucose uptake test was performed to select the optimal insulin concentration. Glucose 4-11 insulin Homo sapiens 60-67 35107740-4 2022 Expression of five genes in differentiated beta cells was evaluated by Real-time PCR and western blotting and the potency of insulin release in response to glucose stimulation was evaluated by insulin and C-peptide ELISA kit. Glucose 156-163 insulin Homo sapiens 125-132 35107740-8 2022 Glucose and insulin secretion assay showed that insulin levels and C-peptide secretion were significantly increased in response to 10 mM glucose. Glucose 137-144 insulin Homo sapiens 48-55 35487893-2 2022 Here, we report that Mfn1 and 2 are critical for glucose-stimulated insulin secretion (GSIS) primarily through control of mitochondrial DNA (mtDNA) content. Glucose 49-56 insulin Homo sapiens 68-75 35483674-1 2022 Background: Insulin-treated patients with long duration of type 2 diabetes mellitus (T2DM) are at increased risk of ketoacidosis related to sodium-glucose co-transporter 2 inhibitor (SGLT2i). Glucose 147-154 insulin Homo sapiens 12-19 35571883-8 2022 Results: The results showed that 7-day quercetin supplementation significantly attenuated the post-exercise glucose-induced insulin response, increased total antioxidant capacity (TAC) and superoxidase dismutase (SOD) activities, and mitigated malondialdehyde (MDA) levels during the recovery period (p < 0.05). Glucose 108-115 insulin Homo sapiens 124-131 35571883-11 2022 Conclusion: Our findings concluded that 7-day oral quercetin supplementation enhances high-intensity cycling time to exhaustion, which may be due in part to the increase in whole-body insulin-stimulated glucose uptake and attenuation of exercise-induced oxygen stress and pro-inflammation. Glucose 203-210 insulin Homo sapiens 184-191 35477646-17 2022 CONCLUSIONS: This insulin protocol gradually brought the blood glucose level within target levels in severe COVID-19 patients treated with high-dose steroid. Glucose 63-70 insulin Homo sapiens 18-25 35563231-2 2022 Pancreatic beta-cells are crucial for controlling glucose homeostasis by properly producing and secreting the glucose-lowering hormone insulin, and the dysfunction of beta-cells determines the outcomes for both type 1 and type 2 diabetes. Glucose 110-117 insulin Homo sapiens 135-142 35466722-1 2022 BACKGROUND: Continuous glucose monitoring (CGM) systems are increasingly being adopted as an alternative or adjunct to self-monitoring of blood glucose (SMBG) by patients receiving insulin therapy. Glucose 23-30 insulin Homo sapiens 181-188 35528003-1 2022 In diabetes mellitus (DM) treatment, Continuous Glucose Monitoring (CGM) linked with insulin delivery becomes the main strategy to improve therapeutic outcomes and quality of patients" lives. Glucose 48-55 insulin Homo sapiens 85-92 35528003-6 2022 The UVA/Padova T1DM Simulator is the core element here, which is a computer model of the human metabolic system based on glucose-insulin dynamics in T1D patients. Glucose 121-128 insulin Homo sapiens 129-136 35528003-8 2022 To overcome the limitation of standard glucose sensors, the concept of an islet-based biosensor, which could integrate multiple physiological signals through electrical activity measurement, is assessed here in a closed-loop insulin therapy. Glucose 39-46 insulin Homo sapiens 225-232 35627115-1 2022 Migraine and glucose-related (glycaemic) traits (fasting glucose, fasting insulin, and type 2 diabetes) are common and complex comorbid disorders that cause major economic and social burdens on patients and their families. Glucose 13-20 insulin Homo sapiens 74-81 35627115-5 2022 Multiple publications have suggested that the comorbidity of migraine and glucose-related traits may have a similar complex pathogenic mechanism, including impaired glucose homeostasis, insulin resistance, reduced cerebrovascular reactivity, abnormal brain metabolism, shared genetic factors, neurotransmitters, and sex hormones. Glucose 74-81 insulin Homo sapiens 186-193 35440614-5 2022 We show their efficacy to outline cell identity changes and unravel some of their underlying genetic mechanisms, whether during embryonic pancreas development or in experimental setups aiming at developing glucose-responsive insulin-secreting cells, such as pluripotent stem-cell differentiation or in adult islet cell reprogramming protocols. Glucose 206-213 insulin Homo sapiens 225-232 35166127-1 2022 AIMS: The skeletal muscle maintains glucose disposal via insulin signaling and glucose transport. Glucose 36-43 insulin Homo sapiens 57-64 35234661-1 2022 SGLT2 inhibition induces an insulin-independent reduction in plasma glucose causing increased lipolysis and subsequent lipid oxidation by energy-consuming tissues. Glucose 68-75 insulin Homo sapiens 28-35 35428219-1 2022 BACKGROUND: The triglyceride glucose index combined with body mass index is a new index that reflects the degree of insulin resistance. Glucose 29-36 insulin Homo sapiens 116-123 35437186-11 2022 CONCLUSION: Overall, nurse led insulin protocols can effectively control blood glucose level among critically ill patients. Glucose 79-86 insulin Homo sapiens 31-38 35429128-7 2022 RESULTS: Glucose tolerance was better at 8 a.m., which was explained by the heigher one-hour insulin secretion on OGTT and increased skeletal muscle insulin sensitivity on HE clamp. Glucose 9-16 insulin Homo sapiens 93-100 35429128-7 2022 RESULTS: Glucose tolerance was better at 8 a.m., which was explained by the heigher one-hour insulin secretion on OGTT and increased skeletal muscle insulin sensitivity on HE clamp. Glucose 9-16 insulin Homo sapiens 149-156 35521787-12 2022 Runx1 loss-of-function at the stage of myoblast inhibited myoblast proliferation and differentiation, reduced insulin-stimulated Akt phosphorylation and insulin-stimulated glucose uptake. Glucose 172-179 insulin Homo sapiens 153-160 35551294-2 2022 Dorzagliatin is a dual-acting, orally bioavailable glucokinase activator that enhances glucokinase activity in a glucose-dependent manner, improves glucose-stimulated insulin secretion and demonstrates effects on glycemic control in patients with T2D. Glucose 148-155 insulin Homo sapiens 167-174 35065098-4 2022 UCN3 signaling is a hallmark of functional beta cell maturation, increasing the beta cell glucose threshold for insulin secretion. Glucose 90-97 insulin Homo sapiens 112-119 35571202-4 2022 It is evidenced that glucose/insulin promotes cholesterol biosynthesis and uptake, which have been targeted by several drugs for lipid-lowering, e.g., bempedoic acid, statins, ezetimibe, and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Glucose 21-28 insulin Homo sapiens 29-36 35571202-6 2022 This review would briefly summarize the mechanisms of glucose/insulin-stimulated cholesterol biosynthesis and uptake, and discuss the effect and mechanisms of lipid-lowering drugs and genetic mutations on glucose homeostasis, aiming to help better understand the intricate relationship between glucose and cholesterol metabolism. Glucose 54-61 insulin Homo sapiens 62-69 35571202-6 2022 This review would briefly summarize the mechanisms of glucose/insulin-stimulated cholesterol biosynthesis and uptake, and discuss the effect and mechanisms of lipid-lowering drugs and genetic mutations on glucose homeostasis, aiming to help better understand the intricate relationship between glucose and cholesterol metabolism. Glucose 205-212 insulin Homo sapiens 62-69 35571202-6 2022 This review would briefly summarize the mechanisms of glucose/insulin-stimulated cholesterol biosynthesis and uptake, and discuss the effect and mechanisms of lipid-lowering drugs and genetic mutations on glucose homeostasis, aiming to help better understand the intricate relationship between glucose and cholesterol metabolism. Glucose 294-301 insulin Homo sapiens 62-69 35482056-1 2022 Islet dysfunction is central in type 2 diabetes and full-blown type 2 diabetes develops first when the beta cells lose their ability to secrete adequate amounts of insulin in response to raised plasma glucose. Glucose 201-208 insulin Homo sapiens 164-171 35565811-6 2022 The homeostatic model assessment (HOMA), based on fasting glucose and fasting insulin levels, was employed to index insulin resistance. Glucose 58-65 insulin Homo sapiens 116-123 35487321-6 2022 In parallel, use of glucose lowering drugs (especially metformin and insulin) as well as statins increased from 1999 to 2010, with significant improvement of the lipid control. Glucose 20-27 insulin Homo sapiens 69-76 35574003-0 2022 Basal Insulin Reduces Glucose Variability and Hypoglycaemia Compared to Premixed Insulin in Type 2 Diabetes Patients: A Study Based on Continuous Glucose Monitoring Systems. Glucose 22-29 insulin Homo sapiens 6-13 35574003-0 2022 Basal Insulin Reduces Glucose Variability and Hypoglycaemia Compared to Premixed Insulin in Type 2 Diabetes Patients: A Study Based on Continuous Glucose Monitoring Systems. Glucose 146-153 insulin Homo sapiens 6-13 35476320-1 2022 PURPOSE: To evaluate if a web-based telemedicine system (the Glucoonline system) is effective to improve glucose control in insulin-treated patients with type 1 and type 2 diabetes, as compared to standard of care. Glucose 106-113 insulin Homo sapiens 125-132 35462498-2 2022 It is a long-term challenge for patients to effectively deliver exogenous insulin to maintain glucose levels within the individual"s target range as safely as possible for preventing the development and progression of diabetes complications. Glucose 94-101 insulin Homo sapiens 74-81 35625712-4 2022 We found that insulin-induced uptake of glucose was blunted in cultures of 3T3-L1 grown on media containing o- or m-Tyr. Glucose 40-47 insulin Homo sapiens 14-21 35563026-2 2022 Skeletal muscle is vital for metabolism and physiology and plays a crucial role in insulin-mediated glucose disposal. Glucose 100-107 insulin Homo sapiens 83-90 35563026-5 2022 Myokines have been shown to increase insulin sensitivity, thereby improving glucose disposal and regulating glucose and lipid metabolism. Glucose 76-83 insulin Homo sapiens 37-44 35563026-5 2022 Myokines have been shown to increase insulin sensitivity, thereby improving glucose disposal and regulating glucose and lipid metabolism. Glucose 108-115 insulin Homo sapiens 37-44 35298439-4 2022 Although no effects on beta-cell mass were detected, potentiated glucose-stimulated insulin secretion (GSIS), mitochondrial function, and ATP synthesis were observed. Glucose 65-72 insulin Homo sapiens 84-91 35494421-6 2022 An increased level of plasma insulin over time in the absence of exercising causes accumulation of lipid droplets in hepatocytes and striated muscles thus preventing the movement of glucose transporters shown to result in an increase in insulin resistance due to obesity and further culminates into depression. Glucose 182-189 insulin Homo sapiens 29-36 35494421-6 2022 An increased level of plasma insulin over time in the absence of exercising causes accumulation of lipid droplets in hepatocytes and striated muscles thus preventing the movement of glucose transporters shown to result in an increase in insulin resistance due to obesity and further culminates into depression. Glucose 182-189 insulin Homo sapiens 237-244 35462988-6 2022 Co-culture with endothelial cells created a natural cellular niche with enhanced insulin secretion after glucose stimulation. Glucose 105-112 insulin Homo sapiens 81-88 35090176-1 2022 BACKGROUND: Oral glucose tolerance test (OGTT)-based measures of insulin secretory response have not been validated in pregnancy. Glucose 17-24 insulin Homo sapiens 65-72 35496980-4 2022 Insulin degludec was prescribed to improve HbA1c and fasting plasma glucose (FPG). Glucose 68-75 insulin Homo sapiens 0-7 35582667-11 2022 Minimal model analysis of frequently sampled intravenous glucose tolerance test and oral glucose tolerance test provide an indirect estimate of metabolic insulin sensitivity/resistance. Glucose 57-64 insulin Homo sapiens 154-161 35582667-11 2022 Minimal model analysis of frequently sampled intravenous glucose tolerance test and oral glucose tolerance test provide an indirect estimate of metabolic insulin sensitivity/resistance. Glucose 89-96 insulin Homo sapiens 154-161 35457152-5 2022 Glucagon-like peptide-1 receptor agonists (GLP1-RAs) not only act by reducing body weight but also can affect the mechanisms involved in insulin resistance, like an increasing expression of glucose transporters in insulin-dependent tissues, decreasing inflammation, reducing oxidative stress, and modulating lipid metabolism. Glucose 190-197 insulin Homo sapiens 137-144 35457152-5 2022 Glucagon-like peptide-1 receptor agonists (GLP1-RAs) not only act by reducing body weight but also can affect the mechanisms involved in insulin resistance, like an increasing expression of glucose transporters in insulin-dependent tissues, decreasing inflammation, reducing oxidative stress, and modulating lipid metabolism. Glucose 190-197 insulin Homo sapiens 214-221 35416379-0 2022 Insulin secretion and action affects glucose variability in the early stages of glucose intolerance. Glucose 37-44 insulin Homo sapiens 0-7 35416379-5 2022 RESULTS: Overall insulin secretion and action as well as GV progressively worsened across glucose tolerance categories. Glucose 90-97 insulin Homo sapiens 17-24 35130338-4 2022 In a cross-sectional study of 43 non-diabetic subjects (20 patients with treated hematological malignancies and 23 controls without malignancy) we measured insulin-stimulated whole-body glucose utilization (M) using hyperinsulinemic euglycemic clamps. Glucose 186-193 insulin Homo sapiens 156-163 35092562-9 2022 Furthermore, based on MTT assay and glucose uptake test 10-5 mol/L insulin was chosen as the model group to induce insulin-resistance in HepG2 cells for gene expression analysis. Glucose 36-43 insulin Homo sapiens 67-74 35092562-9 2022 Furthermore, based on MTT assay and glucose uptake test 10-5 mol/L insulin was chosen as the model group to induce insulin-resistance in HepG2 cells for gene expression analysis. Glucose 36-43 insulin Homo sapiens 115-122 35415885-1 2022 INTRODUCTION: There is evidence that fibroblast growth factor (FGF) levels may be implicated in hypoglycemia, with FGF-19 being a potential contributor to insulin-independent pathways driving postprandial hypoglycemia following bariatric surgery and basicFGF (FGF2) being elevated following the mild hypoglycemia occurring post-glucose tolerance test. Glucose 328-335 insulin Homo sapiens 155-162 35245441-5 2022 A scalable magnetic sorting method was developed to enrich for human pluripotent stem cell (hPSC)-derived islet cells using these three antibodies, leading to the formation of islet-like clusters with improved glucose-stimulated insulin secretion and reduced growth upon transplantation. Glucose 210-217 insulin Homo sapiens 229-236 35403348-4 2022 Ultra-rapid-acting insulin analogues can be administered shortly before meals and give better coverage of mealtime-induced glucose excursions than conventional insulin preparations. Glucose 123-130 insulin Homo sapiens 19-26 35410613-2 2022 beta cells maintains glucose homeostasis by identifying blood glucose and accordingly releasing insulin in order to maintain normal physiologic glucose levels. Glucose 21-28 insulin Homo sapiens 96-103 35410613-2 2022 beta cells maintains glucose homeostasis by identifying blood glucose and accordingly releasing insulin in order to maintain normal physiologic glucose levels. Glucose 144-151 insulin Homo sapiens 96-103 35405014-7 2022 First phase insulin release (area under the insulin curve during 10 min after glucose infusion) was increased by almost 4-fold in group II vs I (P=0.01). Glucose 78-85 insulin Homo sapiens 12-19 35405014-10 2022 CONCLUSIONS: Assessment of muscle contractile function in young healthy subjects may prove useful in identifying individuals with insulin resistance and enhanced glucose stimulated insulin secretion prior to onset of clinical manifestations. Glucose 162-169 insulin Homo sapiens 181-188 35457000-8 2022 The screening revealed that most of the tested chemicals have detectable, deleterious effects on glucose-stimulated insulin release, insulin content, electrical activity, gene expression, and/or viability. Glucose 97-104 insulin Homo sapiens 116-123 35397169-10 2022 IE from insulin was larger than IE from C-peptide (weighted mean difference 11.2%, CI (9.2-13.2)%; p<0.0001; I 2=28.1%); the IE difference was inversely associated with glucose tolerance and fasting glucose. Glucose 199-206 insulin Homo sapiens 8-15 35397560-3 2022 However, many protocols developed to differentiate hPSCs into insulin-expressing beta-cells in vitro have generated hPSC-derived beta-cells with either immature phenotype such as impaired glucose-stimulated insulin secretion (GSIS) or a weaker response to GSIS than cadaveric islets. Glucose 188-195 insulin Homo sapiens 62-69 35397560-3 2022 However, many protocols developed to differentiate hPSCs into insulin-expressing beta-cells in vitro have generated hPSC-derived beta-cells with either immature phenotype such as impaired glucose-stimulated insulin secretion (GSIS) or a weaker response to GSIS than cadaveric islets. Glucose 188-195 insulin Homo sapiens 207-214 35394448-2 2022 For most persons living with T1D, the determination of insulin delivery is based on a single measured parameter-glucose. Glucose 112-119 insulin Homo sapiens 55-62 35388464-1 2022 The integrated glucose-insulin model is a semi-mechanistic model describing glucose and insulin after a glucose challenge. Glucose 15-22 insulin Homo sapiens 23-30 35388464-1 2022 The integrated glucose-insulin model is a semi-mechanistic model describing glucose and insulin after a glucose challenge. Glucose 15-22 insulin Homo sapiens 88-95 35388464-1 2022 The integrated glucose-insulin model is a semi-mechanistic model describing glucose and insulin after a glucose challenge. Glucose 76-83 insulin Homo sapiens 23-30 35388464-1 2022 The integrated glucose-insulin model is a semi-mechanistic model describing glucose and insulin after a glucose challenge. Glucose 104-111 insulin Homo sapiens 23-30 35388464-1 2022 The integrated glucose-insulin model is a semi-mechanistic model describing glucose and insulin after a glucose challenge. Glucose 104-111 insulin Homo sapiens 88-95 35388005-4 2022 Glucokinase is expressed in hepatocytes to regulate glycogen synthesis, and in pancreatic beta cells as a glucose sensor to initiate glycolysis and insulin signaling. Glucose 106-113 insulin Homo sapiens 148-155 35388005-6 2022 Finally, citrullination alters glucokinase biologic activity and suppresses glucose-stimulated insulin secretion. Glucose 76-83 insulin Homo sapiens 95-102 35382796-2 2022 Despite using diabetes technologies including continuous glucose monitoring (CGM), insulin pumps and contemporary insulin analogues, most women struggle to achieve and maintain the recommended pregnancy glucose targets. Glucose 203-210 insulin Homo sapiens 83-90 35382796-2 2022 Despite using diabetes technologies including continuous glucose monitoring (CGM), insulin pumps and contemporary insulin analogues, most women struggle to achieve and maintain the recommended pregnancy glucose targets. Glucose 203-210 insulin Homo sapiens 114-121 35382796-3 2022 This study aims to evaluate whether the use of automated closed-loop insulin delivery improves antenatal glucose levels in pregnant women with type 1 diabetes. Glucose 105-112 insulin Homo sapiens 69-76 35384402-10 2022 Hence, blood glucose should be controlled below the baseline to ensure the inhibition of endogenous insulin. Glucose 13-20 insulin Homo sapiens 100-107 34997846-0 2022 Correction to: Flash glucose monitoring and glycemic control in type 1 diabetes with subcutaneous insulin infusion. Glucose 21-28 insulin Homo sapiens 98-105 35192961-3 2022 Risk factors for osteoporosis and AD, such as obesity, type 2 diabetes, aging, chemotherapy, vitamin deficiency, alcohol abuse, and apolipoprotein Eepsilon4 and/or Il-6 gene variants, reduce cellular glucose uptake, and protective factors, such as estrogen, insulin, exercise, mammalian target of rapamycin inhibitors, hydrogen sulfide, and most phytochemicals, increase uptake. Glucose 200-207 insulin Homo sapiens 258-265 35074395-0 2022 Pattern of C-peptide response to oral glucose tolerance test: interest and cut-off values. Glucose 38-45 insulin Homo sapiens 11-20 35365557-2 2022 Initial clinical trials of intensive insulin therapy targeting blood glucose levels of 80 to 110 mg/dL showed improved outcomes, but subsequent trials found no benefits and even increased harm with this approach. Glucose 69-76 insulin Homo sapiens 37-44 35061031-1 2022 G-protein coupled receptor 40 (GPR40) is a promising target to support glucose-induced insulin release in patients with diabetes type 2. Glucose 71-78 insulin Homo sapiens 87-94 35073578-3 2022 Glucose-stimulated insulin secretion (GSIS) was evaluated in response to progesterone sulfates in mouse islets and human islets. Glucose 0-7 insulin Homo sapiens 19-26 35113139-5 2022 Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamps with D-(6,6-2H2)glucose. Glucose 87-94 insulin Homo sapiens 0-7 35306264-6 2022 Insulin resistance was calculated using estimated glucose disposal rate (eGDR) in patients and using HOMA-IR in their parents. Glucose 50-57 insulin Homo sapiens 0-7 35144876-0 2022 Intravenous insulin-dextrose repetition for hyperkalemia: How can we avoid subsequent hypoglycemia? Glucose 20-28 insulin Homo sapiens 12-19 35432202-3 2022 Methods: By creating a GDM mouse model, we tested glucose and insulin tolerance of offspring by intraperitoneal glucose tolerance test (IPGTT), insulin tolerance test (ITT), and pyruvate tolerance test (PTT). Glucose 50-57 insulin Homo sapiens 144-151 35101478-6 2022 Therefore, significant research interest has been focused on designing and developing new insulin delivery technologies to control blood glucose levels and time, which can enhance the patient compliance simultaneously through alternative routes as non-invasive insulin delivery. Glucose 137-144 insulin Homo sapiens 90-97 35101478-6 2022 Therefore, significant research interest has been focused on designing and developing new insulin delivery technologies to control blood glucose levels and time, which can enhance the patient compliance simultaneously through alternative routes as non-invasive insulin delivery. Glucose 137-144 insulin Homo sapiens 261-268 35101478-8 2022 In addition, this review highlights different smart stimuli-responsive insulin delivery systems including glucose, pH, enzymes, near-infrared, ultrasound, magnetic and electric fields, and the application of various polymers as insulin carriers. Glucose 106-113 insulin Homo sapiens 71-78 35433515-2 2022 The only way to treat type 1 diabetes is monitoring insulin, and in this type of diabetes, insulin should be injected into the body in order to reduce the patient"s blood glucose as prescribed by the physician at certain times. Glucose 171-178 insulin Homo sapiens 91-98 35582667-1 2022 Insulin resistance (IR) is insulin failure in normal plasma levels to adequately stimulate glucose uptake by the peripheral tissues. Glucose 91-98 insulin Homo sapiens 0-7 35092621-2 2022 As a result, in the perioperative and postoperative setting, the use of insulin is recommended to maintain glucose levels below 180 mg/dl (10.0 mmol/L). Glucose 107-114 insulin Homo sapiens 72-79 35443376-14 2022 CONCLUSION: In this study, we found that patients with a higher glucagon to insulin ratio in both fasting and postprandial state exhibit worse blood glucose levels i.e, higher HbA1c levels. Glucose 149-156 insulin Homo sapiens 76-83 35576278-1 2022 BACKGROUND: Adiponectin plays an important role in glucose metabolism and released in response to insulin. Glucose 51-58 insulin Homo sapiens 98-105 35507105-1 2022 Insulin has been commonly adopted as a peptide drug to treat diabetes as it facilitates the uptake of glucose from the blood. Glucose 102-109 insulin Homo sapiens 0-7 35104242-5 2022 The insulin-repressible FoxO transcription factors play a key role in mediating the effects of hepatic insulin action on glucose and lipoprotein metabolism. Glucose 121-128 insulin Homo sapiens 4-11 35066003-1 2022 Insulin is the master regulator of glucose, lipid, and protein metabolism. Glucose 35-42 insulin Homo sapiens 0-7 35066003-2 2022 Following ingestion of an oral glucose load or mixed meal, the plasma glucose concentration rises, insulin secretion by the beta cells is stimulated and the hyperinsulinemia, working in concert with hyperglycemia, causes: (i) suppression of endogenous (primarily reflects hepatic) glucose production, (ii) stimulation of glucose uptake by muscle, liver, and adipocytes, (iii) inhibition of lipolysis leading to a decline in plasma FFA concentration which contributes to the suppression of hepatic glucose production and augmentation of muscle glucose uptake, and (iv) vasodilation in muscle, which contributes to enhanced muscle glucose disposal. Glucose 31-38 insulin Homo sapiens 99-106 35066003-3 2022 Herein, the integrated physiologic impact of insulin to maintain normal glucose homeostasis is reviewed and the molecular basis of insulin"s diverse actions in muscle, liver, adipocytes, and vasculature are discussed. Glucose 72-79 insulin Homo sapiens 45-52 35453568-2 2022 However, when beta-cells are continuously exposed to a high glucose concentration for a long period of time, the expression levels of several insulin gene transcription factors are substantially suppressed, which finally leads to pancreatic beta-cell failure found in type 2 diabetes mellitus. Glucose 60-67 insulin Homo sapiens 142-149 35353324-1 2022 Diabetes is characterized by an absolutely inadequate insulin secretion (type 1 diabetes mellitus) or a relative deficit in insulin secretion due to insulin resistance (type 2 diabetes mellitus), both of which result in elevated blood glucose. Glucose 235-242 insulin Homo sapiens 124-131 35353324-1 2022 Diabetes is characterized by an absolutely inadequate insulin secretion (type 1 diabetes mellitus) or a relative deficit in insulin secretion due to insulin resistance (type 2 diabetes mellitus), both of which result in elevated blood glucose. Glucose 235-242 insulin Homo sapiens 149-156 35412022-9 2022 Second is insulin resistance that reduces the amount of glucose metabolized by cells that are not obligate glucose utilizers and increases the release of fatty acids and glycerol from adipose stores that are alternative fuels for tissues and cells. Glucose 56-63 insulin Homo sapiens 10-17 35412022-9 2022 Second is insulin resistance that reduces the amount of glucose metabolized by cells that are not obligate glucose utilizers and increases the release of fatty acids and glycerol from adipose stores that are alternative fuels for tissues and cells. Glucose 107-114 insulin Homo sapiens 10-17 35221224-5 2022 Insulin sensitivity was expressed by glucose infusion rate (M value). Glucose 37-44 insulin Homo sapiens 0-7 35134563-2 2022 In mechanisms of insulin resistance, the roles of glucose, fatty acids and amino acids have been extensively documented in literature. Glucose 50-57 insulin Homo sapiens 17-24 35462880-0 2022 Complete nutrition drink with retrograded starch is low glycemic, and the individual glucose response to the low glycemic complete nutrition drink depends on fasting insulin levels and HOMA-IR in a randomized cross-over control trial. Glucose 85-92 insulin Homo sapiens 166-173 35045191-8 2022 However, we have shown that eliciting insulin secretion via oral glucose loading in healthy people impairs muscle MBF, whilst others have demonstrated intravenous glucose infusion stimulates MBF. Glucose 65-72 insulin Homo sapiens 38-45 35486400-10 2022 Prior to the policy, only 0.3% of all Latina emergency Medicaid recipients with gestational diabetes (2 of 617) received any medication (oral agents or insulin) to manage their blood glucose level. Glucose 183-190 insulin Homo sapiens 152-159 35272971-1 2022 BACKGROUND: Closed-loop insulin delivery systems have the potential to address suboptimal glucose control in children and adolescents with type 1 diabetes. Glucose 90-97 insulin Homo sapiens 24-31 35067907-6 2022 The exact action mechanism behind the glucose-lowering effect of metformin is not clear, but, presumably, metformin utilizes a broad spectrum of molecular mechanisms to control blood glucose including decreasing intestinal glucose absorption, inhibition of the hepatic gluconeogenesis, decreasing insulin resistance, etc. Glucose 183-190 insulin Homo sapiens 297-304 35189549-7 2022 Sleep restriction reduced insulin sensitivity assessed by oral or intravenous glucose tolerance test and homeostatic model assessment of insulin resistance. Glucose 78-85 insulin Homo sapiens 26-33 35505658-5 2022 The intervention resulted in changes in glucose assessment after two hours in oral glucose tolerance test and in insulin assessment after two hours in oral glucose tolerance test. Glucose 156-163 insulin Homo sapiens 113-120 35433783-0 2022 The Effect of Coronavirus Disease-19 Pandemic Lockdown and the Overlapping Ramadan Fasting Period on Glucose Control in Insulin-Treated Patients With Diabetes: A Flash Glucose Monitoring Study. Glucose 101-108 insulin Homo sapiens 120-127 35433783-0 2022 The Effect of Coronavirus Disease-19 Pandemic Lockdown and the Overlapping Ramadan Fasting Period on Glucose Control in Insulin-Treated Patients With Diabetes: A Flash Glucose Monitoring Study. Glucose 168-175 insulin Homo sapiens 120-127 35425793-3 2022 Our results showed that amniotic fluid had a decrease (P < 0.05) in the concentrations of glucose, insulin and hepatocyte growth factor as pregnancy progressed, while maternal serum exhibited the highest concentrations of glucose and insulin at 75 days of gestation (P < 0.05), and a significant positive correlation (P < 0.05) between insulin and citric acid. Glucose 222-229 insulin Homo sapiens 336-343 35409011-1 2022 Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. Glucose 57-64 insulin Homo sapiens 111-118 35150847-10 2022 Intranasal delivery of 3.6 IU/kg insulin-loaded SEN decreased the plasma glucose level remarkably, achieving a maximum reduction of 70%, and the glucose reduction activity lasted for the whole experimental period of 4 h. Histological examination of the nasal mucosa showed no apparent signs of toxicity at the site of administration after single dose of the insulin-loaded SEN. Glucose 73-80 insulin Homo sapiens 33-40 35150847-10 2022 Intranasal delivery of 3.6 IU/kg insulin-loaded SEN decreased the plasma glucose level remarkably, achieving a maximum reduction of 70%, and the glucose reduction activity lasted for the whole experimental period of 4 h. Histological examination of the nasal mucosa showed no apparent signs of toxicity at the site of administration after single dose of the insulin-loaded SEN. Glucose 145-152 insulin Homo sapiens 33-40 35454311-3 2022 Insulin is a highly anabolic peptide hormone that regulates blood glucose levels by hastening cellular glucose uptake as well as controlling carbohydrate, protein, and lipid metabolism. Glucose 66-73 insulin Homo sapiens 0-7 35454311-3 2022 Insulin is a highly anabolic peptide hormone that regulates blood glucose levels by hastening cellular glucose uptake as well as controlling carbohydrate, protein, and lipid metabolism. Glucose 103-110 insulin Homo sapiens 0-7 35371258-1 2022 Background: The triglyceride glucose (TyG) index is a novel surrogate marker of insulin resistance and increases cardiovascular disease risk. Glucose 29-36 insulin Homo sapiens 80-87 35399673-4 2022 However, pathophysiological conditions (insulin resistance) are characterized by a sustained DNL in the liver and aimed at preventing the excess accumulation of glucose, which result in increased tissue content of PA and disrupted homeostatic control of its tissue concentration. Glucose 161-168 insulin Homo sapiens 40-47 35290109-3 2022 In the present study, we demonstrate that plasma Abeta is produced from glucose- and insulin-susceptible peripheral tissues, such as the pancreas, adipose tissues, skeletal muscles, and liver, to inhibit insulin secretion from islet beta-cells. Glucose 72-79 insulin Homo sapiens 204-211 35170319-12 2022 Furthermore, the current statuses of working prototype glucose-responsive "closed-loop" insulin delivery systems are discussed. Glucose 55-62 insulin Homo sapiens 88-95 35372263-0 2022 Synthesis and Characterization of Phenylboronic Acid-Modified Insulin With Glucose-Dependent Solubility. Glucose 75-82 insulin Homo sapiens 62-69 35372263-2 2022 We previously showed that attaching two fluorophenylboronic acid (FPBA) residues to the C-terminal B chain of insulin glargine led to glucose-dependent solubility. Glucose 134-141 insulin Homo sapiens 110-117 35084834-1 2022 Diabetic patients with type 1 or advanced type 2 stages need timely and precise insulin injection to regulate the daily blood glucose levels (BGLs). Glucose 126-133 insulin Homo sapiens 80-87 35084834-3 2022 To achieve prolonged glucose regulation and low hypoglycemia risks, a novel on-demand glucose-responsive glycopolymer system was constructed for insulin delivery, which was self-assembled into nanoparticles by dynamic covalent bonds between two polymers: fluorophenylboronic acid-grafted polymer (poly-F) and polyol polymer (poly-G). Glucose 21-28 insulin Homo sapiens 145-152 35084834-3 2022 To achieve prolonged glucose regulation and low hypoglycemia risks, a novel on-demand glucose-responsive glycopolymer system was constructed for insulin delivery, which was self-assembled into nanoparticles by dynamic covalent bonds between two polymers: fluorophenylboronic acid-grafted polymer (poly-F) and polyol polymer (poly-G). Glucose 86-93 insulin Homo sapiens 145-152 35084834-5 2022 The nanoparticles showed excellent glucose responsiveness in vitro, with controlled insulin release at different glucose concentrations. Glucose 113-120 insulin Homo sapiens 84-91 35334843-6 2022 The primary endpoint was to describe the mean glucose tolerance as indicated by Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) scores at baseline, end-of-fast (EOF), and end-of-refeed (EOR) visits. Glucose 46-53 insulin Homo sapiens 112-119 35268815-3 2022 Diabetes is a metabolic and endocrine illness set apart by hyperglycemia and glucose narrow-mindedness because of insulin opposition. Glucose 77-84 insulin Homo sapiens 114-121 35241770-5 2022 Insulin resistance was calculated using the triglyceride-glucose index from blood samples and was defined as either high or low. Glucose 57-64 insulin Homo sapiens 0-7 35434002-4 2022 Case Description: A 22 years old, male patient had been misdiagnosed with T1DM for 4 years and had experienced poor glucose control with multiple daily insulin injections. Glucose 116-123 insulin Homo sapiens 152-159 35425793-3 2022 Our results showed that amniotic fluid had a decrease (P < 0.05) in the concentrations of glucose, insulin and hepatocyte growth factor as pregnancy progressed, while maternal serum exhibited the highest concentrations of glucose and insulin at 75 days of gestation (P < 0.05), and a significant positive correlation (P < 0.05) between insulin and citric acid. Glucose 90-97 insulin Homo sapiens 336-343 35343255-5 2022 METHODS: Insulin, C-peptide, and glucose assay data from a frequently sampled insulin-modified oral glucose tolerance test trial with 2U SC insulin delivery, paired with a well-validated metabolic model, predict metabolic outcomes for N = 7 healthy adults. Glucose 33-40 insulin Homo sapiens 78-85 35343255-5 2022 METHODS: Insulin, C-peptide, and glucose assay data from a frequently sampled insulin-modified oral glucose tolerance test trial with 2U SC insulin delivery, paired with a well-validated metabolic model, predict metabolic outcomes for N = 7 healthy adults. Glucose 33-40 insulin Homo sapiens 140-147 35343255-5 2022 METHODS: Insulin, C-peptide, and glucose assay data from a frequently sampled insulin-modified oral glucose tolerance test trial with 2U SC insulin delivery, paired with a well-validated metabolic model, predict metabolic outcomes for N = 7 healthy adults. Glucose 100-107 insulin Homo sapiens 78-85 35343255-5 2022 METHODS: Insulin, C-peptide, and glucose assay data from a frequently sampled insulin-modified oral glucose tolerance test trial with 2U SC insulin delivery, paired with a well-validated metabolic model, predict metabolic outcomes for N = 7 healthy adults. Glucose 100-107 insulin Homo sapiens 140-147 35399944-3 2022 These changes include an increase in beta-cell proliferation and beta-cell mass, upregulation of insulin synthesis and insulin content, enhanced cell-to-cell communication, and a lowering of the glucose threshold for insulin secretion, all of which resulting in an increase in glucose-stimulated insulin secretion. Glucose 195-202 insulin Homo sapiens 217-224 35399944-3 2022 These changes include an increase in beta-cell proliferation and beta-cell mass, upregulation of insulin synthesis and insulin content, enhanced cell-to-cell communication, and a lowering of the glucose threshold for insulin secretion, all of which resulting in an increase in glucose-stimulated insulin secretion. Glucose 277-284 insulin Homo sapiens 217-224 35399944-3 2022 These changes include an increase in beta-cell proliferation and beta-cell mass, upregulation of insulin synthesis and insulin content, enhanced cell-to-cell communication, and a lowering of the glucose threshold for insulin secretion, all of which resulting in an increase in glucose-stimulated insulin secretion. Glucose 277-284 insulin Homo sapiens 296-303 35399944-5 2022 Influx of calcium into beta-cells is crucial in the regulation of glucose-stimulated insulin secretion. Glucose 66-73 insulin Homo sapiens 85-92 35408874-5 2022 It is important to recognize that GDM is still commonly diagnosed during the second trimester of pregnancy using the oral glucose tolerance test (OGGT), at a time when both a fetal and maternal pathophysiology is already present, demonstrating the increased blood glucose levels associated with exacerbated insulin resistance. Glucose 122-129 insulin Homo sapiens 307-314 35341134-5 2022 High glucose or insulin significantly inhibited glucose uptake and promoted release of reactive oxygen species in GEnCs. Glucose 48-55 insulin Homo sapiens 16-23 35370948-8 2022 Glucose stimulated insulin secretion revealed increased insulin secretion in response to glucose. Glucose 0-7 insulin Homo sapiens 19-26 35370948-8 2022 Glucose stimulated insulin secretion revealed increased insulin secretion in response to glucose. Glucose 0-7 insulin Homo sapiens 56-63 35370948-8 2022 Glucose stimulated insulin secretion revealed increased insulin secretion in response to glucose. Glucose 89-96 insulin Homo sapiens 19-26 35370948-8 2022 Glucose stimulated insulin secretion revealed increased insulin secretion in response to glucose. Glucose 89-96 insulin Homo sapiens 56-63 35432753-1 2022 Xu et al used the HOMA2 model to estimate the beta-cell function and insulin resistance levels in an individual from simultaneously measured fasting plasma glucose and fasting plasma insulin levels. Glucose 156-163 insulin Homo sapiens 69-76 35345486-2 2022 The triglyceride-glucose (TyG) index, as a credible and convenient marker of insulin resistance, has been shown to be predictive of outcomes for STEMI patients following revascularization. Glucose 17-24 insulin Homo sapiens 77-84 35370744-1 2022 Objective: Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) lower plasma glucose through effects on insulin and glucagon secretion and by decelerating gastric emptying. Glucose 78-85 insulin Homo sapiens 105-112 35273901-2 2022 This lowers glucose levels by increasing insulin secretion and decreasing glucagon secretion. Glucose 12-19 insulin Homo sapiens 41-48 35241836-4 2022 Biphasic glucose-stimulated insulin secretion developed during in vitro maturation, associated with cytoarchitectural reorganization and the increasing presence of alpha cells. Glucose 9-16 insulin Homo sapiens 28-35 35107108-6 2022 In the presence of glucose, GOD converts glucose into H+ and H2O2, driving gradual dissolution of the calcium layer of insulin particles, resulting in long-acting release of insulin. Glucose 19-26 insulin Homo sapiens 119-126 35107108-6 2022 In the presence of glucose, GOD converts glucose into H+ and H2O2, driving gradual dissolution of the calcium layer of insulin particles, resulting in long-acting release of insulin. Glucose 19-26 insulin Homo sapiens 174-181 35107108-6 2022 In the presence of glucose, GOD converts glucose into H+ and H2O2, driving gradual dissolution of the calcium layer of insulin particles, resulting in long-acting release of insulin. Glucose 41-48 insulin Homo sapiens 119-126 35107108-6 2022 In the presence of glucose, GOD converts glucose into H+ and H2O2, driving gradual dissolution of the calcium layer of insulin particles, resulting in long-acting release of insulin. Glucose 41-48 insulin Homo sapiens 174-181 35077932-2 2022 In the context of diabetes technology, current maximal models of glucose homeostasis lack a proper dynamical description of main glucose-related fluxes acting over and from the liver, providing a rather simplistic estimation of key quantities as endogenous glucose production and insulin and glucagon clearance. Glucose 129-136 insulin Homo sapiens 280-287 35365489-9 2022 In vitro, TMZ reduced the oxidative stress reaction, increased the ratios of p-AKT/AKT and p-IRS1/IRS1, and attenuated the insulin stimulation of PA-induced glucose uptake. Glucose 157-164 insulin Homo sapiens 123-130 35043162-5 2022 RESULTS: Increasing fasting glucose (hazard ratio (HR) 1.09 (95% CI 1.04-1.14); P = 0.0003), stimulated glucose (HR 1.50 (1.42-1.59); P < 0.0001), fasting insulin (HR 0.89 (0.83-0.95); P = 0.0009), and glucose-to-insulin ratio (HR 1.29 (1.16-1.43); P < 0.0001) were associated with risk of progression to type 1 diabetes. Glucose 104-111 insulin Homo sapiens 155-162 35183648-1 2022 AIMS: Automated insulin delivery improves glucose control. Glucose 42-49 insulin Homo sapiens 16-23 35043162-5 2022 RESULTS: Increasing fasting glucose (hazard ratio (HR) 1.09 (95% CI 1.04-1.14); P = 0.0003), stimulated glucose (HR 1.50 (1.42-1.59); P < 0.0001), fasting insulin (HR 0.89 (0.83-0.95); P = 0.0009), and glucose-to-insulin ratio (HR 1.29 (1.16-1.43); P < 0.0001) were associated with risk of progression to type 1 diabetes. Glucose 104-111 insulin Homo sapiens 213-220 35052026-15 2022 Conclusion: These findings suggested that DA-1241 augmented glucose-dependent insulin release via stimulation of GLP-1 secretion, and reduced hepatic gluconeogenesis, which might be associated with autophagic blockage, leading to improved glycaemic control. Glucose 60-67 insulin Homo sapiens 78-85 35196393-1 2022 Secretion of insulin from pancreatic beta-cells is complex, but physiological glucose-dependent secretion is dominated by electrical activity, in turn controlled by ATP-sensitive potassium (KATP) channel activity. Glucose 78-85 insulin Homo sapiens 13-20 35014695-1 2022 Pancreatic beta cells secrete insulin in response to glucose, a process that is regulated at multiple levels, including a network of input signals from other organ systems. Glucose 53-60 insulin Homo sapiens 30-37 34998917-3 2022 The dosing of short-acting insulin often involves several steps for the user including blood glucose measurement and integration of potential carbohydrate loads to inform safe and appropriate dosing. Glucose 93-100 insulin Homo sapiens 27-34 35386489-12 2022 Conclusion: Glucose levels significantly influenced the insulin starting infusion rate, with no identified differences in adverse effects or clinical outcomes. Glucose 12-19 insulin Homo sapiens 56-63 34998917-5 2022 Through the application of computer vision, we have developed a smartphone-based system that is able to detect the carbohydrate load of food by simply taking a single image of the food and converting that information into a required insulin dose by incorporating a blood glucose measurement. Glucose 271-278 insulin Homo sapiens 233-240 35212862-7 2022 Glucose and insulin levels increased significantly after a single ECT session (GS: glucose: F (2,25.66) = 39.04, p < 0.001; insulin: PS: F (2,83) = 25.8, p < 0.001; GS: F (2,25.87) = 3.97, p < 0.05) but no chronic effect was detectable. Glucose 0-7 insulin Homo sapiens 124-131 35170854-0 2022 Impact of visit-to-visit fasting plasma glucose variability on the development of diabetes: The mediation by insulin resistance. Glucose 40-47 insulin Homo sapiens 109-116 35212862-7 2022 Glucose and insulin levels increased significantly after a single ECT session (GS: glucose: F (2,25.66) = 39.04, p < 0.001; insulin: PS: F (2,83) = 25.8, p < 0.001; GS: F (2,25.87) = 3.97, p < 0.05) but no chronic effect was detectable. Glucose 83-90 insulin Homo sapiens 12-19 35083870-1 2022 OBJECTIVE: Studies that used an intravenous glucose tolerance test (IVGTT) have suggested that race is an important modulator of insulin sensitivity, beta-cell function, and insulin clearance. Glucose 44-51 insulin Homo sapiens 129-136 35216750-7 2022 The assessed closed-loop device, the Diabeloop for Kids DBL4K hybrid closed-loop system, is an automated blood glucose regulation system composed of a handset, insulin pump, and continuous glucose monitor. Glucose 111-118 insulin Homo sapiens 160-167 34999111-1 2022 AIMS: Insulin potentiates glucose-stimulated insulin secretion. Glucose 26-33 insulin Homo sapiens 6-13 34999111-1 2022 AIMS: Insulin potentiates glucose-stimulated insulin secretion. Glucose 26-33 insulin Homo sapiens 45-52 35083870-1 2022 OBJECTIVE: Studies that used an intravenous glucose tolerance test (IVGTT) have suggested that race is an important modulator of insulin sensitivity, beta-cell function, and insulin clearance. Glucose 44-51 insulin Homo sapiens 174-181 35083870-6 2022 The acute insulin response to the large glucose bolus administered during the IVGTT was double in AA participants compared with NHW participants because of increased insulin secretion and reduced insulin clearance. Glucose 40-47 insulin Homo sapiens 10-17 35083870-6 2022 The acute insulin response to the large glucose bolus administered during the IVGTT was double in AA participants compared with NHW participants because of increased insulin secretion and reduced insulin clearance. Glucose 40-47 insulin Homo sapiens 166-173 35083870-6 2022 The acute insulin response to the large glucose bolus administered during the IVGTT was double in AA participants compared with NHW participants because of increased insulin secretion and reduced insulin clearance. Glucose 40-47 insulin Homo sapiens 196-203 35083870-8 2022 However, AA individuals have greater insulin secretory capacity and reduced insulin clearance capacity than NHW individuals and might be susceptible to hyperinsulinemia after consuming very large amounts of glucose. Glucose 207-214 insulin Homo sapiens 76-83 35295985-9 2022 Upon HHS and sepsis resolution, a basal-bolus insulin therapy was implemented that was followed by significant improvement of daily glucose profiles and progressive reduction of insulin requirement until complete discontinuation. Glucose 132-139 insulin Homo sapiens 46-53 35386772-10 2022 When TG levels spiked again, the patient was put on an insulin infusion with heparin, glucose, and potassium to rapidly reduce TG level. Glucose 86-93 insulin Homo sapiens 55-62 35212158-1 2022 Isthmin-1 is an adipokine that has a potent glucose-lowering effect by stimulating a common intracellular signaling pathway with insulin through a distinct receptor and has an inhibitory effect on lipogenesis in the liver, whereas insulin has the opposite effect. Glucose 44-51 insulin Homo sapiens 129-136 35212158-1 2022 Isthmin-1 is an adipokine that has a potent glucose-lowering effect by stimulating a common intracellular signaling pathway with insulin through a distinct receptor and has an inhibitory effect on lipogenesis in the liver, whereas insulin has the opposite effect. Glucose 44-51 insulin Homo sapiens 231-238 35118996-4 2022 RESULTS: OSA was associated with marked insulin resistance of adipose tissue triglyceride lipolysis and glucose uptake into both skeletal muscles and adipose tissue whereas insulin action on endogenous glucose production, basal insulin secretion and glucose-stimulated insulin secretion during both intravenous and oral glucose tolerance tests were not different between the OSA and Control groups. Glucose 202-209 insulin Homo sapiens 173-180 35118996-4 2022 RESULTS: OSA was associated with marked insulin resistance of adipose tissue triglyceride lipolysis and glucose uptake into both skeletal muscles and adipose tissue whereas insulin action on endogenous glucose production, basal insulin secretion and glucose-stimulated insulin secretion during both intravenous and oral glucose tolerance tests were not different between the OSA and Control groups. Glucose 250-257 insulin Homo sapiens 173-180 35118996-4 2022 RESULTS: OSA was associated with marked insulin resistance of adipose tissue triglyceride lipolysis and glucose uptake into both skeletal muscles and adipose tissue whereas insulin action on endogenous glucose production, basal insulin secretion and glucose-stimulated insulin secretion during both intravenous and oral glucose tolerance tests were not different between the OSA and Control groups. Glucose 320-327 insulin Homo sapiens 173-180 35273567-1 2022 Background: Triglyceride-glucose (TyG) index is a reliable and specific biomarker for insulin resistance and is associated with renal dysfunction. Glucose 25-32 insulin Homo sapiens 86-93 35295991-2 2022 The triglyceride-glucose (TyG) index is frequently used as an indicator of insulin resistance. Glucose 17-24 insulin Homo sapiens 75-82 35267895-6 2022 The homeostatic model assessment (HOMA), based on fasting glucose and fasting insulin levels, was used to index insulin resistance. Glucose 58-65 insulin Homo sapiens 112-119 35216514-3 2022 Skeletal muscle is considered the main site for insulin-stimulated glucose uptake and therefore, a primary target for insulin resistance in the human body. Glucose 67-74 insulin Homo sapiens 48-55 35216514-3 2022 Skeletal muscle is considered the main site for insulin-stimulated glucose uptake and therefore, a primary target for insulin resistance in the human body. Glucose 67-74 insulin Homo sapiens 118-125 35215537-6 2022 Total insulin secretion, adjusted for glucose and insulin sensitivity, increased on the LGI diet (p = 0.002), and trended lower on the HGI diet (p = 0.10; LGI vs. HGI p = 0.001). Glucose 38-45 insulin Homo sapiens 6-13 35252207-6 2022 Currently, taking glucose sensitizing agents, including metformin, SGLT-2 inhibitor, and GLP-1 agonist, is an effective way of lowering insulin levels and controlling PDA development at the same time. Glucose 18-25 insulin Homo sapiens 136-143 35113534-1 2022 In the current study, we report the microfluidic synthesis of a metal-organic framework (MOF) for insulin delivery based on the stimulus response of glucose. Glucose 149-156 insulin Homo sapiens 98-105 35113534-6 2022 Thus, the presence of glucose molecules provided a stimulus for insulin release. Glucose 22-29 insulin Homo sapiens 64-71 35113534-10 2022 Drug release studies confirmed the response of the MOFs to glucose, which triggered insulin release. Glucose 59-66 insulin Homo sapiens 84-91 35216280-1 2022 The recent discovery of the glucose-induced stabilization of hexokinase-2 (HK2) to proteolysis in cell dysfunction in model hyperglycemia has revealed a likely key initiating factor contributing to the development of insulin resistance and vascular complications in diabetes. Glucose 28-35 insulin Homo sapiens 217-224 35051813-5 2022 Furthermore, the optimal compound exhibited greater glucose-lowering effects than lead compound, which might attribute to its synergistic effects by simultaneously modulating insulin secretion and resistance. Glucose 52-59 insulin Homo sapiens 175-182 35168404-0 2022 Safety and Efficacy of an Intensive Care Insulin Infusion Protocol Targeting a Blood Glucose of 140 to 180 mg/dL. Glucose 85-92 insulin Homo sapiens 41-48 35237639-15 2022 Insulin in TNA can improve the blood glucose control of patients. Glucose 37-44 insulin Homo sapiens 0-7 35250801-1 2022 Background: The triglyceride-glucose (TyG) index has recently been proposed as a reliable marker of insulin resistance. Glucose 29-36 insulin Homo sapiens 100-107 35204022-3 2022 The skeletal muscle is the primary tissue responsible for insulin-stimulated glucose uptake. Glucose 77-84 insulin Homo sapiens 58-65 35147898-11 2022 A meta-analysis of seven acute, 1-day randomised crossover trials that sampled mixed-sex adults (aged > 18 years) who were predominately overweight or participants with obesity found that standing as an interruption to prolonged sitting significantly reduced postprandial glucose ( = - 0.31, 95% CI - 0.60, - 0.03; z = - 2.15, p < 0.04) but had no significant effect on insulin or SBP. Glucose 272-279 insulin Homo sapiens 371-378 35177913-1 2022 Purpose: Evidence demonstrates that glucose-sensing technologies have enabled effective glycemic control for adults and children with type 1 diabetes (T1DM) or adults with type 2 diabetes (T2DM) on insulin therapy or non-insulin therapy. Glucose 36-43 insulin Homo sapiens 198-205 35177913-1 2022 Purpose: Evidence demonstrates that glucose-sensing technologies have enabled effective glycemic control for adults and children with type 1 diabetes (T1DM) or adults with type 2 diabetes (T2DM) on insulin therapy or non-insulin therapy. Glucose 36-43 insulin Homo sapiens 221-228 35105572-1 2022 INTRODUCTION: Hypoglycaemia is a frequent adverse event and major barrier for achieving optimal blood glucose levels in people with type 1 or type 2 diabetes using insulin. Glucose 102-109 insulin Homo sapiens 164-171 35216614-1 2022 BACKGROUND: The triglyceride-glucose index (TyG index) has emerged as a reliable surrogate marker of insulin resistance associated with arterial stiffness. Glucose 29-36 insulin Homo sapiens 101-108 35208217-2 2022 Summary answer: almost one in two primary infertile men presented with a triglycerides/glucose index (tyg) suggestive of insulin resistance (ir). Glucose 87-94 insulin Homo sapiens 121-128 35222287-1 2022 Background and Aims: To compare the effects of real-time and retrospective flash glucose monitoring (FGM) on daily glycemic control and lifestyle in patients with type 2 diabetes on premix insulin therapy. Glucose 81-88 insulin Homo sapiens 189-196 35222280-2 2022 It is generally treated with exogenous insulin, maintaining physiological blood glucose levels but also leading to long-term therapeutic complications. Glucose 80-87 insulin Homo sapiens 39-46 35178244-1 2022 Type 2 Diabetes (T2D) is a chronic disease characterized by abnormally high blood glucose levels due to insulin resistance and reduced pancreatic insulin production. Glucose 82-89 insulin Homo sapiens 104-111 35163825-2 2022 Although the mechanisms remain unclear, the adipocyte size appears to be inversely correlated with insulin sensitivity and glucose tolerance, wherein smaller adipocytes are insulin-sensitive and larger adipocytes develop insulin resistance and exhibit an impaired glucose uptake. Glucose 123-130 insulin Homo sapiens 173-180 35163825-6 2022 Furthermore, we demonstrate that inhibitor-treated adipocytes exhibit an enhanced insulin-stimulated glucose uptake as compared with untreated adipocytes, and that this outcome is dependent on the cyclin-dependent kinase 1 (CDK1) activity. Glucose 101-108 insulin Homo sapiens 82-89 35131852-3 2022 Restoring blood glucose physiology required total IgG injections and insulin-specific IgG antibodies detected in total IgG preparations and in the serum of healthy individuals. Glucose 16-23 insulin Homo sapiens 69-76 35131852-6 2022 Interestingly, the low-affinity IgM fraction (anti-insulin IgMlow) neutralizes insulin and leads to increased blood glucose, whereas the high-affinity IgM fraction (anti-insulin IgMhigh) protects insulin from neutralization by anti-insulin IgG, thereby preventing blood glucose dysregulation. Glucose 116-123 insulin Homo sapiens 51-58 35131852-6 2022 Interestingly, the low-affinity IgM fraction (anti-insulin IgMlow) neutralizes insulin and leads to increased blood glucose, whereas the high-affinity IgM fraction (anti-insulin IgMhigh) protects insulin from neutralization by anti-insulin IgG, thereby preventing blood glucose dysregulation. Glucose 116-123 insulin Homo sapiens 79-86 35131852-9 2022 These results suggest that autoreactive antibodies recognizing insulin are key regulators of blood glucose and metabolism, as they control the concentration of insulin in the blood. Glucose 99-106 insulin Homo sapiens 63-70 35131852-9 2022 These results suggest that autoreactive antibodies recognizing insulin are key regulators of blood glucose and metabolism, as they control the concentration of insulin in the blood. Glucose 99-106 insulin Homo sapiens 160-167 35198578-1 2022 Background: We aim to evaluate the four surrogate markers of insulin resistance (IR), including triglyceride-glucose index (TyG), lipid accumulation product index (LAP), visceral adiposity index (VAI), triglycerides to high-density lipoprotein cholesterol ratio (TG/HDL), on prevalence of chronic kidney disease (CKD) and to examine any possible effect modifiers in Chinese hypertensive patients. Glucose 109-116 insulin Homo sapiens 61-68 35123462-1 2022 BACKGROUND: The gut incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide) are secreted by enteroendocrine cells following food intake leading to insulin secretion and glucose lowering. Glucose 214-221 insulin Homo sapiens 192-199 35185759-1 2022 The triglyceride glucose (TyG) index is considered a simple surrogate marker for insulin resistance and has been associated with cerebrovascular diseases. Glucose 17-24 insulin Homo sapiens 81-88 35118893-2 2022 Currently, insulin pumps calculate active insulin using mathematical decay curves, while quantitative measurements of insulin would explicitly provide person-specific PK insulin dynamics to assess remaining active insulin more accurately, permitting more effective glucose control. Glucose 265-272 insulin Homo sapiens 118-125 35118893-2 2022 Currently, insulin pumps calculate active insulin using mathematical decay curves, while quantitative measurements of insulin would explicitly provide person-specific PK insulin dynamics to assess remaining active insulin more accurately, permitting more effective glucose control. Glucose 265-272 insulin Homo sapiens 214-221 35119252-1 2022 Beside its mechanical roles in controlling posture and locomotion, skeletal muscle system, the largest insulin and steroid hormones target tissue, plays a key role in influencing thermoregulation, secondary sexual characteristics, hormones metabolism, and glucose uptake and storage, as well as energetic metabolism. Glucose 256-263 insulin Homo sapiens 103-110 35115614-2 2022 Some reports have shown that SGLT2i treatment improves insulin resistance; however, few studies have evaluated insulin resistance by the glucose clamp method. Glucose 137-144 insulin Homo sapiens 111-118 35115614-12 2022 Insulin resistance with the glucose clamp was not changed, but the HOMA-IR and insulin sensitivity indices were significantly improved. Glucose 28-35 insulin Homo sapiens 0-7 35236998-7 2022 Obesity had a greater effect on insulin resistance: fasting plasma glucose F(1, 53)=6.134, p<0.05; fasting insulin F(1, 53)=31.606, p<0.01; HOMA-IR F(1, 53)=31.670, p<0.01; QUICKI F(1, 53)=16.156, p<0.01. Glucose 67-74 insulin Homo sapiens 32-39 35119572-8 2022 Besides, the recent progress in molecular approaches that focuses on identifying new targets for T2DM (i.e.) consisting of gene therapy, stem cell therapy, and the modulation of insulin signaling pathways for the regulation of glucose storage and uptake also discussed. Glucose 227-234 insulin Homo sapiens 178-185 35190401-1 2022 INTRODUCTION: Insulin is a glucose-lowering hormone that affects carbohydrate, lipid, and protein metabolism. Glucose 27-34 insulin Homo sapiens 14-21 35123262-1 2022 Insulin is the main hypoglycemic hormone, promoting the absorption and storage of glucose and inhibiting its production. Glucose 82-89 insulin Homo sapiens 0-7 35184403-1 2022 BACKGROUND: Persistent hyperglycemia decreases the sensitivity of insulin-sensitive organs to insulin, owing to which cells fail to take up and utilize glucose, which exacerbates the progression of type 2 diabetes mellitus (T2DM). Glucose 152-159 insulin Homo sapiens 66-73 35184403-1 2022 BACKGROUND: Persistent hyperglycemia decreases the sensitivity of insulin-sensitive organs to insulin, owing to which cells fail to take up and utilize glucose, which exacerbates the progression of type 2 diabetes mellitus (T2DM). Glucose 152-159 insulin Homo sapiens 94-101 34524022-9 2022 Insulin formulations with an offset in action greater than FiAsp are needed to provide a meaningful improvement in CL glucose control with exercise. Glucose 118-125 insulin Homo sapiens 0-7 34753799-3 2022 Here we report increased expression of miR-200c in islets from T2D as compared with non-diabetic (ND) donors and display results showing reduced glucose-stimulated insulin secretion in EndoC-betaH1 cells overexpressing miR-200c. Glucose 145-152 insulin Homo sapiens 164-171 34753799-8 2022 Finally, LNA knockdown of miR-200c (LNA200c) increased glucose-stimulated insulin secretion in islets from T2D donors ~3-fold. Glucose 55-62 insulin Homo sapiens 74-81 34848489-7 2022 Moreover, positive linear associations were present in the MBH but not control regions between T2 relaxation time and glucose area under the curve during an OGTT, fasting glucose concentrations, hemoglobin A1c, and visceral adipose tissue mass, whereas negative linear relationships were present in the MBH for markers of insulin sensitivity and beta-cell function. Glucose 118-125 insulin Homo sapiens 322-329 34857533-2 2022 We assessed the temporal change in insulin secretory capacity after RYGB, using oral and intravenous (IV) glucose, in individuals with type 2 diabetes. Glucose 106-113 insulin Homo sapiens 35-42 34880066-2 2022 RESEARCH DESIGN AND METHODS: In cohort 1, insulin secretion, sensitivity, and endogenous insulin clearance were evaluated with an oral glucose tolerance test in 460 recruited participants. Glucose 135-142 insulin Homo sapiens 42-49 34880066-2 2022 RESEARCH DESIGN AND METHODS: In cohort 1, insulin secretion, sensitivity, and endogenous insulin clearance were evaluated with an oral glucose tolerance test in 460 recruited participants. Glucose 135-142 insulin Homo sapiens 89-96 34908124-0 2022 Capillary Endothelial Insulin Transport: The Rate Limiting Step for Insulin-stimulated Glucose Uptake. Glucose 87-94 insulin Homo sapiens 22-29 34908124-0 2022 Capillary Endothelial Insulin Transport: The Rate Limiting Step for Insulin-stimulated Glucose Uptake. Glucose 87-94 insulin Homo sapiens 68-75 35255598-3 2022 To achieve normoglycemia, specific populations of neurons and glia in the hypothalamus sense changes in the blood concentrations of glucose and of glucoregulatory hormones such as insulin, leptin, glucagon-like peptide 1, and glucagon. Glucose 132-139 insulin Homo sapiens 180-187 35393913-2 2022 The triglycerides and glucose (TyG) index, is a reliable and inexpensive surrogate test for detecting insulin resistance. Glucose 22-29 insulin Homo sapiens 102-109 34347589-4 2022 The aim of the present work is to assess linear black-box methods, including a novel non-parametric methodology, for learning individualized models of glucose response to insulin and meal, suitable for model-based prediction and control. Glucose 151-158 insulin Homo sapiens 171-178 34905513-3 2022 RESULTS: Glucose-stimulated insulin secretion (GSIS), an assessment of beta-cell function, was greater in the Ob-NFG-NGT and Ob-NFG-IGT groups than in the lean group, even when insulin sensitivity was matched in the obese and lean groups. Glucose 9-16 insulin Homo sapiens 28-35 35148196-3 2022 Furthermore, the phosphorylation of IRS Tyr632, phosphoinositide 3-kinase (PI3K), and AKT that is involved in the insulin action mechanism was decreased by TNF-alpha, whereas Deglusterol increased their phosphorylations, leading to an increase of glucose uptake rate by 190% through glucose transporter type 4 (GLUT4) compared with TNF-alpha-treated group in C2C12 cells. Glucose 247-254 insulin Homo sapiens 114-121 35148196-6 2022 Deglusterol suppressed insulin resistance and restored insulin sensitivity, which contributed to lowering blood glucose concentrations in the insulin-resistant models, suggesting its potential as a blood glucose-lowering agent for people at high risk of type 2 diabetes or prediabetes. Glucose 112-119 insulin Homo sapiens 142-149 35102369-10 2022 Overweight insulin sensitive subjects may benefit more from a high than a low nutrient quality ER diet with respect to weight loss, due to potential attenuation of glucose-induced lipid synthesis in adipose tissue. Glucose 164-171 insulin Homo sapiens 11-18 35173625-2 2021 In addition to these benefits of regular physical activity, evidence suggests even a single bout of dynamic exercise promotes increased insulin-mediated glucose uptake and insulin sensitivity during the acute recovery period. Glucose 153-160 insulin Homo sapiens 136-143 35173682-6 2021 NAD+-increasing interventions improved capacity to exercise, decreased blood pressure, increased the anti-inflammatory profile and insulin-stimulated glucose disposal, and reduced the fat-free mass. Glucose 150-157 insulin Homo sapiens 131-138 35178031-8 2022 Flash glucose monitoring (FGM) information has been helpful in understanding the pharmacodynamic aspects of alpelisib and insulin titration. Glucose 6-13 insulin Homo sapiens 122-129 35187381-5 2022 In a 75-g oral glucose tolerance test, the serum insulin level reached the highest value of 1124 muU/mL at 180 minutes. Glucose 15-22 insulin Homo sapiens 49-56 35079935-7 2022 Disturbance in bistability is linked with dysregulation of plasma macronutrient levels (glucose, fatty acids and amino acids) in abnormal conditions like insulin and glucagon resistance, which is associated with obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease. Glucose 88-95 insulin Homo sapiens 154-161 35087167-5 2022 Of note, bronchial epithelial cells expanded and differentiated in normal resting glucose medium showed insulin-stimulated glucose uptake which was inhibited by high glucose concentrations. Glucose 82-89 insulin Homo sapiens 104-111 35087167-5 2022 Of note, bronchial epithelial cells expanded and differentiated in normal resting glucose medium showed insulin-stimulated glucose uptake which was inhibited by high glucose concentrations. Glucose 123-130 insulin Homo sapiens 104-111 35087167-5 2022 Of note, bronchial epithelial cells expanded and differentiated in normal resting glucose medium showed insulin-stimulated glucose uptake which was inhibited by high glucose concentrations. Glucose 166-173 insulin Homo sapiens 104-111 35163187-0 2022 Metformin and Insulin Resistance: A Review of the Underlying Mechanisms behind Changes in GLUT4-Mediated Glucose Transport. Glucose 105-112 insulin Homo sapiens 14-21 35066863-11 2022 In all, the oxidation of high doses of tyramine, already reported to inhibit lipolysis in human fat cells, also partially mimic another effect of insulin in these cells, the glucose uptake activation. Glucose 174-181 insulin Homo sapiens 146-153 35048323-1 2022 Glucose uptake is stimulated by insulin via stimulation of glucose transporter 4 (GLUT4) translocation to the plasma membrane from intracellular compartments in adipose tissue and muscles. Glucose 0-7 insulin Homo sapiens 32-39 35064598-1 2022 Glucagon-like peptide-1 (GLP-1) is a potential therapeutic agent for treating type 2 diabetes, owing to its glucose-dependent capability to stimulate insulin secretion. Glucose 108-115 insulin Homo sapiens 150-157 35237425-5 2022 In our in vivo observations, we found that Pb2+ exposure strongly reduced glucose-stimulated insulin secretion and diminished functional pancreatic beta-cell mass. Glucose 74-81 insulin Homo sapiens 93-100 35044537-1 2022 Pancreatic islets are the body"s central rheostat that regulates glucose homeostasis through the production of different hormones, including beta cell-derived insulin. Glucose 65-72 insulin Homo sapiens 159-166 34986826-8 2022 Adjusted RRR for percentages of glucose readings in range were 0.98 (95% Cl 0.97-0.99) for basal-bolus insulin, 0.99 (95% Cl 0.98-1.00) for premixed insulin, and 1.01 (95% Cl 1.00-1.01) for bolus-only insulin, respectively. Glucose 32-39 insulin Homo sapiens 149-156 35386439-5 2022 To solve these issues, a glucose and MMP-9 dual-response temperature-sensitive shape self-adaptive hydrogel (CBP/GMs@Cel&INS) was designed and constructed with polyvinyl alcohol (PVA) and chitosan grafted with phenylboric acid (CS-BA) by encapsulating insulin (INS) and gelatin microspheres containing celecoxib (GMs@Cel). Glucose 25-32 insulin Homo sapiens 252-259 35386439-6 2022 Temperature-sensitive self-adaptive CBP/GMs@Cel&INS provides a new way to balance the fluid-like mobility (self-adapt to deep wounds quickly, approximately 37 C) and solid-like elasticity (protect wounds against external forces, approximately 25 C) of self-adaptive hydrogels, while simultaneously releasing insulin and celecoxib on-demand in the environment of high-level glucose and MMP-9. Glucose 375-382 insulin Homo sapiens 310-317 35068939-1 2022 Purpose: The triglyceride-glucose (TyG) index, a widely accessible measure, has been a surrogate indicator of peripheral insulin resistance, and its clinical importance continues to grow in East Asia. Glucose 26-33 insulin Homo sapiens 121-128 35017617-10 2022 The combination of linagliptin and insulin in hospitalized patients with SARS-CoV-2 infection and hyperglycemia reduced the relative risk of assisted mechanical ventilation by 74% and improved better pre and postprandial glucose levels with lower insulin requirements, and no higher risk of hypoglycemia.This study is registered at clinicaltrials.gov, number NCT04542213 on 09/03/2020. Glucose 221-228 insulin Homo sapiens 35-42 35082757-3 2021 In this work, a novel titration algorithm for long-acting insulin leveraging continuous glucose monitoring (CGM) and smart insulin pens (SIP) data is proposed. Glucose 88-95 insulin Homo sapiens 58-65 34990204-3 2022 Based on evidence supporting its role both in adaptive coupling of insulin secretion to changes in insulin sensitivity and in the regulation of insulin-independent glucose disposal, the central nervous system (CNS) has emerged as a fundamental player in glucose homeostasis. Glucose 164-171 insulin Homo sapiens 144-151 35102177-2 2022 The triglyceride-glucose (TyG) index is a novel marker of insulin resistance, but association with outcomes among AIS patients who have received tPA has not been well elucidated. Glucose 17-24 insulin Homo sapiens 58-65 35126125-10 2021 Conclusion: The use of insulin in the management of gestational hypertriglyceridemia is safe and efficient, and insulin may become a mainstream in the near future to mitigate serum TG and TC levels in the pregnancy period besides regulating the blood glucose level. Glucose 251-258 insulin Homo sapiens 112-119 35053407-7 2022 In addition, the use of siRNA and/or specific inhibitors against selected m6A enzymes demonstrate that these enzymes modulate the expression of genes involved in pancreatic beta-cell identity and glucose-stimulated insulin secretion. Glucose 196-203 insulin Homo sapiens 215-222 35057547-5 2022 Higher BMI, amount of body fat, and selected markers of hyperglycemia and insulin resistance from the meal tolerance test were associated with higher mean glucose levels during the seven days. Glucose 155-162 insulin Homo sapiens 74-81 35070058-11 2022 CONCLUSION: High doses of catecholamines exert insulin-like actions on glucose transport in human adipocytes. Glucose 71-78 insulin Homo sapiens 47-54 35057540-6 2022 There was no statistically significant difference in the rate of insulin therapy between the two groups (p > 0.05), the initial gestational week of the CRD group combined with insulin treatment was significantly higher than that of the control group (p < 0.05), and the risk of insulin therapy was positively correlated with fasting plasma glucose (FPG) in early pregnancy (p < 0.05). Glucose 340-347 insulin Homo sapiens 176-183 35068934-1 2022 Background: The purpose of this study was to investigate the association of the triglyceride glucose (TyG) index, a surrogate marker of insulin resistance (IR) with a high sensitivity of 96.5% and a specificity of 85.0% for the diagnosis of IR, with computed tomography (CT) features in patients with tuberculosis and diabetes mellitus. Glucose 93-100 insulin Homo sapiens 136-143 34825893-7 2022 RESULTS: In RINm5F cells, angiotensin(1-7) induced intracellular cAMP increase, CREB activation, enhanced CFTR expression and potentiated glucose-stimulated insulin secretion, which were abolished by a selective CFTR inhibitor, RNAi-knockdown of CFTR, or inhibition of MAS-1. Glucose 138-145 insulin Homo sapiens 157-164 34996380-1 2022 BACKGROUND: Blood glucose levels during pregnancy may reflect the severity of insulin secretory defects and/or insulin resistance during gestational diabetes mellitus (GDM) pregnancy. Glucose 18-25 insulin Homo sapiens 78-85 34996380-1 2022 BACKGROUND: Blood glucose levels during pregnancy may reflect the severity of insulin secretory defects and/or insulin resistance during gestational diabetes mellitus (GDM) pregnancy. Glucose 18-25 insulin Homo sapiens 111-118 35350119-6 2022 These findings indicate that phenotypic resistance of Candida and Cryptococcus can vary depending on the presence of insulin with glucose and plasma. Glucose 130-137 insulin Homo sapiens 117-124 34996986-1 2022 Diabetes is a serious metabolic disorder with high rate of prevalence worldwide; the disease has the characteristics of improper secretion of insulin in pancreas that results in high glucose level in blood. Glucose 183-190 insulin Homo sapiens 142-149 34986826-8 2022 Adjusted RRR for percentages of glucose readings in range were 0.98 (95% Cl 0.97-0.99) for basal-bolus insulin, 0.99 (95% Cl 0.98-1.00) for premixed insulin, and 1.01 (95% Cl 1.00-1.01) for bolus-only insulin, respectively. Glucose 32-39 insulin Homo sapiens 201-208 34986353-3 2022 Acute genetic ablation of Gpr17 in intestinal epithelium improves glucose tolerance and glucose-stimulated insulin secretion (GSIS). Glucose 88-95 insulin Homo sapiens 107-114 35069449-2 2021 GCK-MODY is characterized by a mild hyperglycemia, mainly due to a higher blood glucose threshold for insulin secretion, and an up-regulated glucose counterregulation. Glucose 80-87 insulin Homo sapiens 102-109 34897341-4 2022 After CWP treatment, the glucose uptake and lipid accumulation were examined in insulin-resistant HepG2 cells. Glucose 25-32 insulin Homo sapiens 80-87 35052782-4 2022 To identify novel genes regulating insulin secretion we developed a robust arrayed siRNA screen measuring basal, glucose-stimulated, and augmented insulin secretion by EndoC-betaH1 cells, a human beta-cell line, in a 384-well plate format. Glucose 113-120 insulin Homo sapiens 35-42 35059413-1 2021 Background: Triglyceride-glucose (TyG) index has been proposed as a reliable indicator for insulin resistance and proved to be closely associated with the severity and mortality risk of infectious diseases. Glucose 25-32 insulin Homo sapiens 91-98 35534112-3 2022 The abnormal regulation of this enzyme influences glucose-stimulated insulin secretion (GSIS), which controls the insulin levels corresponding to the system"s glucose level. Glucose 50-57 insulin Homo sapiens 69-76 34980155-9 2022 SAA1 treatment significantly attenuated insulin-stimulated membrane translocation of glucose transporter 4 and glucose uptake in granulosa cells through induction of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) expression with subsequent inhibition of Akt phosphorylation. Glucose 85-92 insulin Homo sapiens 40-47 34980155-9 2022 SAA1 treatment significantly attenuated insulin-stimulated membrane translocation of glucose transporter 4 and glucose uptake in granulosa cells through induction of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) expression with subsequent inhibition of Akt phosphorylation. Glucose 111-118 insulin Homo sapiens 40-47 35534112-3 2022 The abnormal regulation of this enzyme influences glucose-stimulated insulin secretion (GSIS), which controls the insulin levels corresponding to the system"s glucose level. Glucose 50-57 insulin Homo sapiens 114-121 35534112-3 2022 The abnormal regulation of this enzyme influences glucose-stimulated insulin secretion (GSIS), which controls the insulin levels corresponding to the system"s glucose level. Glucose 159-166 insulin Homo sapiens 69-76 35058312-0 2022 Flash glucose monitoring in type 2 diabetes managed with basal insulin in the USA: a retrospective real-world chart review study and meta-analysis. Glucose 6-13 insulin Homo sapiens 63-70 35058312-2 2022 This real-world study aimed to assess the impact on glycated hemoglobin (HbA1c) of flash glucose monitoring use in adults with type 2 diabetes managed with basal insulin. Glucose 89-96 insulin Homo sapiens 162-169 35016041-0 2022 Glucose variability in subjects with normal glucose tolerance: Relations with body composition, insulin secretion and sensitivity. Glucose 0-7 insulin Homo sapiens 96-103 35534112-3 2022 The abnormal regulation of this enzyme influences glucose-stimulated insulin secretion (GSIS), which controls the insulin levels corresponding to the system"s glucose level. Glucose 159-166 insulin Homo sapiens 114-121 34303334-0 2022 Association between insulin resistance and cardinal rheological parameters in young healthy Japanese individuals during 75 g oral glucose tolerance test. Glucose 130-137 insulin Homo sapiens 20-27 34303334-3 2022 OBJECTIVE: This study intended to reveal the association between indices of insulin resistance and hemorheological parameters during a 75 g oral glucose tolerance test (75-g OGTT). Glucose 145-152 insulin Homo sapiens 76-83 34986498-0 2022 The Triglycerides and Glucose Index is Negatively Associated with Insulin Secretion in Young Adults with Normal Weight. Glucose 22-29 insulin Homo sapiens 66-73 34314367-1 2022 Blood glucose prediction algorithms are key tools in the development of decision support systems and closed-loop insulin delivery systems for blood glucose control in diabetes. Glucose 6-13 insulin Homo sapiens 113-120 34991602-2 2022 Triglyceride-glucose (TyG) index is a reliable indicator of insulin resistance (IR) and is closely related to traditional risk factors of cardiovascular disease (CVD). Glucose 13-20 insulin Homo sapiens 60-67 35223630-11 2022 Conclusion: Metformin hydrochloride combined with insulin pump for GDM can significantly reduce blood glucose level, regulate serum protein factor levels, and improve adverse outcomes for mother and child, which deserves clinical promotion. Glucose 102-109 insulin Homo sapiens 50-57 34952664-0 2022 New tubeless, automated insulin pump improves HgA1c and time in pre-defined glucose range. Glucose 76-83 insulin Homo sapiens 24-31 35099465-0 2022 Classification of Non-Insulin Glucose Lowering Drugs. Glucose 30-37 insulin Homo sapiens 22-29 35099465-1 2022 The ever-changing scenario of diabetes care, especially pharmacotherapy, calls for a framework to help classify non-insulin glucose drugs. Glucose 124-131 insulin Homo sapiens 116-123 2688437-9 1989 When both insulin and glucagon were delivered in a pulsatile manner, the effect of pulsatile glucagon was predominant, maintaining a high endogenous glucose production. Glucose 149-156 insulin Homo sapiens 10-17 35345912-1 2022 PURPOSE: Triglyceride-glucose (TyG) index is a reliable and inexpensive alternative indicator of insulin resistance. Glucose 22-29 insulin Homo sapiens 97-104 35286685-5 2022 We show how translocation reporters can be used to study sub-plasma membrane cAMP signals, including oscillations, in insulin-secreting beta-cells stimulated with glucose and G-protein-coupled receptor agonists. Glucose 163-170 insulin Homo sapiens 118-125 35228448-1 2022 GLP-1 (glucagon-like peptide-1) is one of the incretin hormone secreted from L cells in the small intestine and it is known to promote insulin secretion in a glucose concentration-dependent manner and have a hypoglycemic effect. Glucose 158-165 insulin Homo sapiens 135-142 35228448-3 2022 Semaglutide is a GLP-1 analog that has 94% homology with human GLP-1 and it binds to the GLP-1 receptor in pancreatic beta-cells to induce the insulin secretion in a glucose concentration-dependent manner. Glucose 166-173 insulin Homo sapiens 143-150 34983210-4 2022 As a biguanide metformin improves glycemic control by inhibiting gluconeogenesis and increasing insulin-mediated glucose utilization in peripheral tissues. Glucose 113-120 insulin Homo sapiens 96-103 35180937-1 2022 The glucagon-like peptide-1 (GLP-1) is a pleiotropic hormone very well known for its incretin effect in the glucose-dependent stimulation of insulin secretion. Glucose 108-115 insulin Homo sapiens 141-148 35140569-0 2022 Frequency of serum blood glucose monitoring after hyperkalaemia treatment using insulin and dextrose. Glucose 25-32 insulin Homo sapiens 80-87 35140569-11 2022 Conclusions: The frequency of serum blood glucose monitoring following insulin therapy was low and inconsistent. Glucose 42-49 insulin Homo sapiens 71-78 35059256-7 2022 In subjects with diabetes, along with an increase in AUC glucose, fasting insulin remained constant in the T/T homozygotes and appeared to decrease in the C-allele carriers. Glucose 57-64 insulin Homo sapiens 74-81 35059256-9 2022 In subjects with diabetes stratified into cases with higher AUC glucose than the median, fasting insulin and HOMA-IR were lower in the C-allele carriers than in the T/T homozygotes. Glucose 64-71 insulin Homo sapiens 97-104 35059256-11 2022 Conclusions: The possibility that the association between IAPP genotype and basal insulin level is modified by variation in plasma glucose, resulting in a decreased basal insulin in type 2 diabetes, cannot be excluded. Glucose 131-138 insulin Homo sapiens 82-89 35528476-0 2022 A novel phenolic formulation for treating hepatic and peripheral insulin resistance by regulating GLUT4-mediated glucose uptake. Glucose 113-120 insulin Homo sapiens 65-72 35528476-4 2022 Particularly, it regulated the subcellular location of GLUT4 through endosomes to increase glucose uptake under insulin-resistant condition. Glucose 91-98 insulin Homo sapiens 112-119 35528476-5 2022 Meanwhile, this phytochemicals combination increased glycogen synthesis and decreased glucose production in the insulin-resistant liver cells. Glucose 86-93 insulin Homo sapiens 112-119 2689441-0 1989 A role for malonyl-CoA in glucose-stimulated insulin secretion from clonal pancreatic beta-cells. Glucose 26-33 insulin Homo sapiens 45-52 2689441-1 1989 To gain insight into the relationship between acyl coenzyme A (CoA) esters and glucose-induced insulin release, acyl-CoA profiles were determined in clonal pancreatic beta-cells (HIT). Glucose 79-86 insulin Homo sapiens 95-102 2689441-4 1989 The rise in malonyl-CoA, which preceded insulin secretion, was evident 2 min after exposure to glucose and was sustained for at least 30 min. Glucose 95-102 insulin Homo sapiens 40-47 2687266-10 1989 From these studies we conclude: 1) desensitization of the GTS requires three components--glucose, insulin, and selective amino acids; 2) insulin resistance of the GTS can be induced through several mechanisms, but only glucose-induced desensitization requires amino acids; 3) glucose-induced desensitization is mediated primarily by metabolic events independent of de novo protein synthesis; and 4) glutamine is the primary amino acid modulating glucose-induced loss of MIR. Glucose 219-226 insulin Homo sapiens 137-144 2687266-10 1989 From these studies we conclude: 1) desensitization of the GTS requires three components--glucose, insulin, and selective amino acids; 2) insulin resistance of the GTS can be induced through several mechanisms, but only glucose-induced desensitization requires amino acids; 3) glucose-induced desensitization is mediated primarily by metabolic events independent of de novo protein synthesis; and 4) glutamine is the primary amino acid modulating glucose-induced loss of MIR. Glucose 219-226 insulin Homo sapiens 137-144 2687266-10 1989 From these studies we conclude: 1) desensitization of the GTS requires three components--glucose, insulin, and selective amino acids; 2) insulin resistance of the GTS can be induced through several mechanisms, but only glucose-induced desensitization requires amino acids; 3) glucose-induced desensitization is mediated primarily by metabolic events independent of de novo protein synthesis; and 4) glutamine is the primary amino acid modulating glucose-induced loss of MIR. Glucose 219-226 insulin Homo sapiens 137-144 2687266-11 1989 Overall, these studies reveal that amino acids play an important role in modulating insulin action at the cellular level and provide new insights into the metabolic mechanisms mediating insulin resistance of the glucose transport system. Glucose 212-219 insulin Homo sapiens 84-91 2687266-11 1989 Overall, these studies reveal that amino acids play an important role in modulating insulin action at the cellular level and provide new insights into the metabolic mechanisms mediating insulin resistance of the glucose transport system. Glucose 212-219 insulin Homo sapiens 186-193 2514599-1 1989 We have previously shown that palmitate potentiates, in isolated islets, glucose-induced stimulation of insulin release, "de novo" lipid synthesis, and 45Ca2+ turnover in a correlative manner. Glucose 73-80 insulin Homo sapiens 104-111 2515050-0 1989 Hepatic glucose production in insulin-resistant states. Glucose 8-15 insulin Homo sapiens 30-37 2533043-2 1989 The incremental areas under the insulin and C-peptide responses to oral glucose were significantly greater than the responses to intravenous glucose (insulin: patients 7983 +/- 1937 (+/- SE) vs 3513 +/- 2188 mU l-1 min, p less than 0.002, control subjects 5505 +/- 1035 vs 1066 +/- 484 mU l-1 min, p less than 0.004; C peptide: patients 440 +/- 80 vs 144 +/- 61 nmol l-1 min, p less than 0.01, control subjects 200 +/- 38 vs 63 +/- 16 nmol l-1 min, P less than 0.01). Glucose 72-79 insulin Homo sapiens 32-39 2533043-2 1989 The incremental areas under the insulin and C-peptide responses to oral glucose were significantly greater than the responses to intravenous glucose (insulin: patients 7983 +/- 1937 (+/- SE) vs 3513 +/- 2188 mU l-1 min, p less than 0.002, control subjects 5505 +/- 1035 vs 1066 +/- 484 mU l-1 min, p less than 0.004; C peptide: patients 440 +/- 80 vs 144 +/- 61 nmol l-1 min, p less than 0.01, control subjects 200 +/- 38 vs 63 +/- 16 nmol l-1 min, P less than 0.01). Glucose 72-79 insulin Homo sapiens 44-53 2533043-2 1989 The incremental areas under the insulin and C-peptide responses to oral glucose were significantly greater than the responses to intravenous glucose (insulin: patients 7983 +/- 1937 (+/- SE) vs 3513 +/- 2188 mU l-1 min, p less than 0.002, control subjects 5505 +/- 1035 vs 1066 +/- 484 mU l-1 min, p less than 0.004; C peptide: patients 440 +/- 80 vs 144 +/- 61 nmol l-1 min, p less than 0.01, control subjects 200 +/- 38 vs 63 +/- 16 nmol l-1 min, P less than 0.01). Glucose 141-148 insulin Homo sapiens 150-157 2691176-10 1989 During insulin infusion, adipose tissue glucose uptake increased and could account for more than 100% of oxygen uptake, implying storage of glucose. Glucose 40-47 insulin Homo sapiens 7-14 2691176-10 1989 During insulin infusion, adipose tissue glucose uptake increased and could account for more than 100% of oxygen uptake, implying storage of glucose. Glucose 140-147 insulin Homo sapiens 7-14 2693165-6 1989 After glucagon injection, the relative glucose potentiation of the insulin response was significantly higher than the relative glucose potentiation of the C-peptide response at each level of hyperglycaemia (p less than 0.01). Glucose 39-46 insulin Homo sapiens 67-74 2687296-4 1989 These results can be compared with the inhibitory effect of phenylarsine oxide on insulin-stimulated glucose transport. Glucose 101-108 insulin Homo sapiens 82-89 2687296-6 1989 Further, when cells were prestimulated with insulin causing maximal stimulation of the glucose transport rate, phenylarsine oxide induced a time-dependent reduction to the basal rate (t 1/2 of 10 min), despite the fact that endocytosis was blocked immediately. Glucose 87-94 insulin Homo sapiens 44-51 2489226-3 1989 In addition, the plasma glucose and insulin responses to an oral glucose load were significantly lower in physically active individuals. Glucose 65-72 insulin Homo sapiens 36-43 2614827-2 1989 The maternal and perinatal results of a pregnancy management protocol for insulin-requiring diabetic gravidas which emphasizes rigorous glucose control via ambulatory patient utilization of reflectance meter determinations of fasting and two-hour postprandial blood glucose is summarized in this report. Glucose 136-143 insulin Homo sapiens 74-81 2575711-1 1989 As shown previously clonidine reduces glucose-stimulated insulin release and this effect is mediated by inhibitory postsynaptic alpha 2-adrenoceptors. Glucose 38-45 insulin Homo sapiens 57-64 2575711-4 1989 In the presence of benextramine, clonidine no longer reduced, but on the contrary enhanced, the release of insulin in response to glucose. Glucose 130-137 insulin Homo sapiens 107-114 2575711-6 1989 These results show that the imidazoline derivative clonidine shares the property of other imidazoline compounds to enhance the insulin response to glucose. Glucose 147-154 insulin Homo sapiens 127-134 2687637-9 1989 Insulin sensitivity in vivo is usually expressed as absolute rates of glucose uptake during euglycemic hyperinsulinemia, and if plasma fatty acid elevation were to be studied in vivo an erroneous conclusion may be reached of resistance to hormone action per se. Glucose 70-77 insulin Homo sapiens 0-7 2519375-5 1989 The absorption of glucose from the dialysate fluid in the presence of insulin was greater in diabetics than in non-diabetic patients (p less than 0.01). Glucose 18-25 insulin Homo sapiens 70-77 2695982-6 1989 The time course of plasma insulin concentration paralleled gastric emptying of the aqueous phase, containing most of the meal"s glucose (r = 0.952, P less than 0.001). Glucose 128-135 insulin Homo sapiens 26-33 2690823-8 1989 In addition, staurosporine partially (approximately 60%) inhibited glucose-induced insulin secretion at concentrations (IC50 approximately 10 nM) similar to those required to inhibit TPA-induced insulin secretion, suggesting that staurosporine may act at a step common to both mechanisms, possibly the activation of protein kinase C. However, stimulatory concentrations of glucose did not induce down-regulation of translocation of protein kinase C, and the inhibition of glucose-induced insulin release by staurosporine was incomplete. Glucose 67-74 insulin Homo sapiens 83-90 2686330-2 1989 The cytokine stimulated insulin release both at low and high glucose concentrations during one hour incubations. Glucose 61-68 insulin Homo sapiens 24-31 35296423-4 2022 This condition has been proven to downregulate insulin receptors, both in astrocytes and neurons, triggering a reduction in glucose uptake and glycogen synthesis, mainly during high metabolic demand. Glucose 124-131 insulin Homo sapiens 47-54 2600081-2 1989 It has been hypothesized on the basis of studies on BC3H-1 myocytes that diacylglycerol generation with activation of protein kinase C (PKC) is involved in the stimulation of glucose transport in muscle by insulin (Standaert, M. L., Farese, R. V., Cooper, R. D., and Pollet, R. J. Glucose 175-182 insulin Homo sapiens 206-213 2600081-6 1989 In the present study, we used the rat epitrochlearis muscle to evaluate the possibility that PKC activity mediates the stimulation of glucose transport by insulin in mammalian skeletal muscle. Glucose 134-141 insulin Homo sapiens 155-162 2600081-10 1989 These findings argue against a role of diacylglycerol-mediated PKC activation in the stimulation of skeletal muscle glucose transport by insulin. Glucose 116-123 insulin Homo sapiens 137-144 2689883-0 1989 Expression of an insulin-regulatable glucose carrier in muscle and fat endothelial cells. Glucose 37-44 insulin Homo sapiens 17-24 2689883-1 1989 Insulin rapidly stimulates glucose use in the major target tissues, muscle and fat, by modulating a tissue-specific glucose transporter isoform. Glucose 27-34 insulin Homo sapiens 0-7 2689883-9 1989 It is therefore likely that endothelial cells play an important role in the regulation of glucose use by the major insulin target tissues in normal and diseased states. Glucose 90-97 insulin Homo sapiens 115-122 2692459-2 1989 We have employed the perfused forearm and euglycemic insulin-clamp techniques in combination with a dual-tracer injection to measure basal and insulin-mediated glucose transport in six normal subjects. Glucose 160-167 insulin Homo sapiens 143-150 16837310-2 1989 11.48 +/- 0.9 ml/kg/min) and the sensitivity index, it decreases glucose utilisation at an insulin level of about 550 uU/ml (MCR(glu)max) (17.8 +/- 1.3 v.s. Glucose 65-72 insulin Homo sapiens 91-98 2684709-1 1989 A universal finding in hyperglycemic patients with type II (non-insulin-dependent) diabetes mellitus is that all share a common defect in glucose recognition resulting in abnormal insulin secretion by pancreatic islet beta-cells. Glucose 138-145 insulin Homo sapiens 64-71 2684709-2 1989 This defect is 1) specific for glucose signals rather than global, 2) related to chronic hyperglycemia, and 3) partially reversible after brief treatment with insulin to induce normoglycemia and through use of other pharmacological agents without normalizing glucose levels. Glucose 31-38 insulin Homo sapiens 159-166 2684709-2 1989 This defect is 1) specific for glucose signals rather than global, 2) related to chronic hyperglycemia, and 3) partially reversible after brief treatment with insulin to induce normoglycemia and through use of other pharmacological agents without normalizing glucose levels. Glucose 259-266 insulin Homo sapiens 159-166 2684710-3 1989 Glucose tolerance depends on a complex interaction among insulin secretion from the beta-cells, clearance of the hormone, and the actions of insulin to accelerate glucose disappearance and inhibit endogenous glucose production. Glucose 163-170 insulin Homo sapiens 141-148 2684710-3 1989 Glucose tolerance depends on a complex interaction among insulin secretion from the beta-cells, clearance of the hormone, and the actions of insulin to accelerate glucose disappearance and inhibit endogenous glucose production. Glucose 208-215 insulin Homo sapiens 141-148 2684710-6 1989 With the glucose minimal model, insulin sensitivity (SI) and glucose effectiveness (SG) are measured by computer analysis of the frequently sampled intravenous glucose tolerance test. Glucose 9-16 insulin Homo sapiens 32-39 2684710-10 1989 One assumption of the minimal model is that the time delay in insulin action on glucose utilization in vivo is due to sluggish insulin transport across the capillary endothelium. Glucose 80-87 insulin Homo sapiens 62-69 2684710-10 1989 One assumption of the minimal model is that the time delay in insulin action on glucose utilization in vivo is due to sluggish insulin transport across the capillary endothelium. Glucose 80-87 insulin Homo sapiens 127-134 2695550-6 1989 Fasting glycemia, insulin, and the insulin area under the curve during an oral glucose load are significantly (p less than 0.005) increased in those with the greatest WHR, which is similar to that in NIDD and central obesity. Glucose 79-86 insulin Homo sapiens 35-42 2481706-0 1989 Insulin and variation in glucose levels modify the secretion rates of the growth hormone-independent insulin-like growth factor binding protein-1 in the human hepatoblastoma cell line Hep G2. Glucose 25-32 insulin Homo sapiens 101-108 2481706-4 1989 Insulin suppressed IGFBP-1 secretion maximally at 100 mU/l (-32%) within 6 h. The secretion of IGFBP-1 was stimulated by a decrease in the glucose concentration in the medium, maximally (+25%) with a decrease from 24 to 6 mmol/l. Glucose 139-146 insulin Homo sapiens 0-7 2481706-5 1989 Stimulation by varying glucose levels and suppression by insulin of IGFBP-1 secretion persisted on return to control conditions after the removal of physiological concentrations of glucose (4-12 mmol/l) and insulin (50-500 mU/l). Glucose 181-188 insulin Homo sapiens 57-64 2531831-2 1989 A primed-continuous (1.0 mU/kg x min) infusion of biosynthetic human insulin was administered to acutely raise and maintain plasma insulin concentrations at approximately 75 to 100 microU/mL during four hours while plasma glucose concentrations were maintained constant at the fasting level by a variable infusion of glucose. Glucose 317-324 insulin Homo sapiens 69-76 2688437-11 1989 This study demonstrates that pulsatile delivery of insulin or glucagon in humans has greater effects in modulating endogenous glucose production than continuous infusion. Glucose 126-133 insulin Homo sapiens 51-58 2688437-12 1989 Furthermore, when both insulin and glucagon are delivered intermittently and out of phase, the stimulatory effect of glucagon on endogenous glucose production prevails over the inhibitory effect of insulin. Glucose 140-147 insulin Homo sapiens 23-30 2690608-9 1989 Diabetic patients may have an improvement in glucose concentrations when their therapy is switched from animal-source insulin to human insulin. Glucose 45-52 insulin Homo sapiens 118-125 2690608-9 1989 Diabetic patients may have an improvement in glucose concentrations when their therapy is switched from animal-source insulin to human insulin. Glucose 45-52 insulin Homo sapiens 135-142 2482818-3 1989 Perifusion with PGE2 decreased both the first and second phases of glucose-induced insulin release to 47 +/- 4% of controls. Glucose 67-74 insulin Homo sapiens 83-90 2515048-3 1989 Continuous subcutaneous insulin infusion with a premeal bolus (n = 8) suppressed both fasting and meal-related rises in C-peptide and improved C-peptide response during the posttreatment oral glucose challenge. Glucose 192-199 insulin Homo sapiens 24-31 2515048-3 1989 Continuous subcutaneous insulin infusion with a premeal bolus (n = 8) suppressed both fasting and meal-related rises in C-peptide and improved C-peptide response during the posttreatment oral glucose challenge. Glucose 192-199 insulin Homo sapiens 143-152 2515048-6 1989 Diabetic subjects whose fasting and prandial hyperglycemia were less than 140 and less than 200 mg/dl, respectively, showed a significantly higher C-peptide response during oral glucose challenge after treatment than those whose insulin treatment only normalized (less than 200 mg/dl) prandial but not basal hyperglycemia (greater than 140 mg/dl). Glucose 178-185 insulin Homo sapiens 147-156 2559864-4 1989 During euglycemic insulin clamps, insulin-inhibited endogenous glucose production was improved after gliclazide therapy. Glucose 63-70 insulin Homo sapiens 18-25 2559864-4 1989 During euglycemic insulin clamps, insulin-inhibited endogenous glucose production was improved after gliclazide therapy. Glucose 63-70 insulin Homo sapiens 34-41 2559864-5 1989 Moreover, mean (+/- SE) glucose disposal rate increased from 3.2 +/- 0.7 to 4.8 +/- 0.8 and from 7.9 +/- 0.9 to 10.4 +/- 0.9 mg.kg-1.min-1 at in vivo plasma insulin levels of approximately 75 and approximately 320 mU/L, respectively. Glucose 24-31 insulin Homo sapiens 157-164 2576005-4 1989 Hypoglycemia induced marked insulin resistance shown by lower glucose infusion rates compared with the control study 3.1 +/- 0.3 vs. 6.0 +/- 0.7 mg.kg-1.min-1, P less than .001). Glucose 62-69 insulin Homo sapiens 28-35 2576005-5 1989 This late posthypoglycemic insulin resistance was mainly due to a decreased insulin effect on glucose utilization. Glucose 94-101 insulin Homo sapiens 27-34 2576005-5 1989 This late posthypoglycemic insulin resistance was mainly due to a decreased insulin effect on glucose utilization. Glucose 94-101 insulin Homo sapiens 76-83 2591648-0 1989 The prevalence of impaired glucose counter-regulation during an insulin-infusion test in insulin-treated diabetic patients prone to severe hypoglycaemia. Glucose 27-34 insulin Homo sapiens 64-71 2591648-0 1989 The prevalence of impaired glucose counter-regulation during an insulin-infusion test in insulin-treated diabetic patients prone to severe hypoglycaemia. Glucose 27-34 insulin Homo sapiens 89-96 2591648-8 1989 In such patients, a combined deficiency of adrenaline and glucagon responses to hypoglycaemia is the predominant finding and the disappearance rate of insulin becomes critical for recovery of blood glucose after hypoglycaemia. Glucose 198-205 insulin Homo sapiens 151-158 2684484-4 1989 Thus, when hypertensive subjects, whether obese or of normal body weight, are compared to age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. Glucose 179-186 insulin Homo sapiens 157-164 2684484-6 1989 With the use of the glucose clamp technique coupled with tracer glucose infusion and indirect calorimetry, it can be shown that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal, and is directly correlated with the severity of hypertension. Glucose 20-27 insulin Homo sapiens 132-139 2684484-6 1989 With the use of the glucose clamp technique coupled with tracer glucose infusion and indirect calorimetry, it can be shown that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal, and is directly correlated with the severity of hypertension. Glucose 64-71 insulin Homo sapiens 132-139 2684484-6 1989 With the use of the glucose clamp technique coupled with tracer glucose infusion and indirect calorimetry, it can be shown that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal, and is directly correlated with the severity of hypertension. Glucose 64-71 insulin Homo sapiens 132-139 2689121-3 1989 In MODY patients with low insulin responses, there is a delayed and decreased insulin and C-peptide secretory response to glucose from childhood or adolescence, even before glucose intolerance appears; it may represent the basic genetic defect. Glucose 122-129 insulin Homo sapiens 90-99 2689121-6 1989 In a few, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they may resemble those of early Type I diabetes. Glucose 85-92 insulin Homo sapiens 50-57 2689121-6 1989 In a few, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they may resemble those of early Type I diabetes. Glucose 85-92 insulin Homo sapiens 62-71 2689121-12 1989 In a few MODY pedigrees with high insulin responses to glucose and lack of evidence of insulin resistance, an insulin is secreted which is a structurally abnormal, mutant insulin molecule that is biologically ineffective. Glucose 55-62 insulin Homo sapiens 34-41 2692964-4 1989 But serum glucose levels were increased at 1, 2 and 3 hours in association with high insulin responses during OGTT in all periods of OC therapy, indicating mild to moderate insulin resistance. Glucose 10-17 insulin Homo sapiens 85-92 2693012-0 1989 Computer simulation of plasma insulin and glucose dynamics after subcutaneous insulin injection. Glucose 42-49 insulin Homo sapiens 78-85 2693012-1 1989 We developed a computer program for the simulation of plasma insulin and glucose dynamics after subcutaneous injection of insulin. Glucose 73-80 insulin Homo sapiens 122-129 2693012-3 1989 With the use of a pharmacodynamic model describing the dependence of glucose dynamics on plasma insulin and glucose levels, the program can predict the expected time course of plasma glucose in response to a change in carbohydrate intake, insulin dose, timing, or regimen. Glucose 69-76 insulin Homo sapiens 96-103 2693012-3 1989 With the use of a pharmacodynamic model describing the dependence of glucose dynamics on plasma insulin and glucose levels, the program can predict the expected time course of plasma glucose in response to a change in carbohydrate intake, insulin dose, timing, or regimen. Glucose 69-76 insulin Homo sapiens 239-246 2693012-3 1989 With the use of a pharmacodynamic model describing the dependence of glucose dynamics on plasma insulin and glucose levels, the program can predict the expected time course of plasma glucose in response to a change in carbohydrate intake, insulin dose, timing, or regimen. Glucose 108-115 insulin Homo sapiens 239-246 2693012-3 1989 With the use of a pharmacodynamic model describing the dependence of glucose dynamics on plasma insulin and glucose levels, the program can predict the expected time course of plasma glucose in response to a change in carbohydrate intake, insulin dose, timing, or regimen. Glucose 108-115 insulin Homo sapiens 239-246 2693012-5 1989 The results of several computer simulations are presented showing the effect on a 24-h insulin and glucose profile of systematically changing insulin regimen, dose, timing of meals, or timing of preprandial insulin administration. Glucose 99-106 insulin Homo sapiens 142-149 2693012-5 1989 The results of several computer simulations are presented showing the effect on a 24-h insulin and glucose profile of systematically changing insulin regimen, dose, timing of meals, or timing of preprandial insulin administration. Glucose 99-106 insulin Homo sapiens 142-149 2695375-2 1989 To estimate maximal insulin-stimulated glucose uptake rates (MaxMs), hyperinsulinemic-euglycemic clamps were performed on 245 nondiabetic Pima Indians (126 men, 119 women). Glucose 39-46 insulin Homo sapiens 20-27 2697605-0 1989 Glucose regulation of insulin gene expression. Glucose 0-7 insulin Homo sapiens 22-29 2681510-6 1989 However, glucose tolerance deteriorated significantly (maximal glucose concentration 120 min after glucose load was 10.0 mmol l-1 before and 13.9 mmol l-1 after insulin pulsing, P less than 0.01). Glucose 9-16 insulin Homo sapiens 161-168 2693569-5 1989 These responses are entirely opposite to those of insulin, which rises sharply but transiently after an oral glucose load but is unchanged after an oral fat load. Glucose 109-116 insulin Homo sapiens 50-57 2699996-3 1989 About half of uremic patients can augment their insulin secretion in response to glucose loads to overcome the insulin resistance and maintain glucose tolerance. Glucose 81-88 insulin Homo sapiens 48-55 2699996-3 1989 About half of uremic patients can augment their insulin secretion in response to glucose loads to overcome the insulin resistance and maintain glucose tolerance. Glucose 143-150 insulin Homo sapiens 48-55 2699996-7 1989 Insulin hypersecretion in response to glucose loads occurred only in uremic patients with normal PTH concentrations. Glucose 38-45 insulin Homo sapiens 0-7 2682134-0 1989 Effects of free fatty acids and ketone bodies on in vivo non-insulin-mediated glucose utilization and production in humans. Glucose 78-85 insulin Homo sapiens 61-68 2682134-1 1989 The current study was undertaken to examine the effect of an acute elevation of serum levels of free fatty acids (FFA) and ketone bodies (KB) on non-insulin-mediated glucose uptake (NIMGU) in humans. Glucose 166-173 insulin Homo sapiens 149-156 2682447-0 1989 [Insulin metabolism in obese children tested by oral and intravenous glucose loading]. Glucose 69-76 insulin Homo sapiens 1-8 2682447-7 1989 glucose load produces different degrees in detected by C-peptide insulin secretion in normal as well as in obese children and the secretion rate is practically permanent till the end of the test in both groups. Glucose 0-7 insulin Homo sapiens 65-72 2682447-9 1989 glucose tolerance test in obese children indicates insulin resistance and explains decreased glucose tolerance. Glucose 0-7 insulin Homo sapiens 51-58 2682447-11 1989 glucose load is resulted not only by the insulin reservoir capacity of beta-cells, but also by the insulin excretion capacity of the liver and the receptor activity of target cells. Glucose 0-7 insulin Homo sapiens 41-48 2808335-2 1989 The levels of S14 mRNA in primary hepatocytes increase when glucose in the media is elevated from 5.5 to 27.7 mM in the presence of insulin. Glucose 60-67 insulin Homo sapiens 132-139 2571864-2 1989 Insulin potencies, in terms of the amount of glucose infused to maintain euglycaemia, were almost identical. Glucose 45-52 insulin Homo sapiens 0-7 2515732-5 1989 Metabolism of the glucose load occurred at both normal and high insulin levels in some children. Glucose 18-25 insulin Homo sapiens 64-71 2559242-1 1989 The postprandial insulin requirements after three mixed meals of equal carbohydrate and energy content were assessed in 10 type-1 and 12 type-2 diabetics by a glucose-controlled insulin infusion system. Glucose 159-166 insulin Homo sapiens 178-185 2684032-2 1989 The insulin:glucose ratio (serum insulin concentration pmol/l) divided by the blood glucose concentration (mmol/l) ranged from 12 to 636, mean (SD) 177 (201). Glucose 12-19 insulin Homo sapiens 4-11 2680234-5 1989 The glucose infusion rate required to maintain euglycaemia was insignificantly higher in normal subjects compared with undialysed uraemic subjects at each insulin infusion rate. Glucose 4-11 insulin Homo sapiens 155-162 2680234-10 1989 After treatment with continuous ambulatory peritoneal dialysis, the glucose infusion rate and the total glucose turnover during the clamp rose significantly at all three insulin concentrations (P less than 0.05), but remained insignificantly different from normal control values. Glucose 68-75 insulin Homo sapiens 170-177 2676431-2 1989 However, numerous patients still produce antibody levels that may alter insulin pharmacokinetics, leading to higher postprandial blood glucose levels and to an increased risk for delayed hypoglycemia. Glucose 135-142 insulin Homo sapiens 72-79 2687060-9 1989 Oral glucose tolerance tests on the heterozygous individuals indicate an increased requirement for insulin of the target tissues as concluded from the tendency towards hyperinsulinaemia with no observed hyperglycaemia. Glucose 5-12 insulin Homo sapiens 99-106 2699443-8 1989 The acute normoglycaemia demonstrated that plasma branched chain amino acid levels are more sensitive than plasma glucose to insulin action. Glucose 114-121 insulin Homo sapiens 125-132 2511023-1 1989 Due to a longer plasma half-life and half-time of action on glucose metabolism biosynthetic human proinsulin was thought to be an alternative to long-acting insulin preparations. Glucose 60-67 insulin Homo sapiens 98-108 2511023-1 1989 Due to a longer plasma half-life and half-time of action on glucose metabolism biosynthetic human proinsulin was thought to be an alternative to long-acting insulin preparations. Glucose 60-67 insulin Homo sapiens 101-108 2511023-5 1989 The insulin-mediated glucose disposal (RD) was not changed after either treatment (group A: 176 +/- 18 vs. 192 +/- 19 mg m-2 min-1; group B: 175 +/- 15 vs. 174 +/- 12 mg m-2 min-1 for times 1 and 2, respectively, NS). Glucose 21-28 insulin Homo sapiens 4-11 2674187-10 1989 This study shows that the combined model of insulin and C-peptide is capable of estimating prehepatic insulin secretion from the iv glucose tolerance test and may provide a useful tool to measure secretion in vivo under various pathological conditions. Glucose 132-139 insulin Homo sapiens 44-51 2674187-10 1989 This study shows that the combined model of insulin and C-peptide is capable of estimating prehepatic insulin secretion from the iv glucose tolerance test and may provide a useful tool to measure secretion in vivo under various pathological conditions. Glucose 132-139 insulin Homo sapiens 56-65 2674187-10 1989 This study shows that the combined model of insulin and C-peptide is capable of estimating prehepatic insulin secretion from the iv glucose tolerance test and may provide a useful tool to measure secretion in vivo under various pathological conditions. Glucose 132-139 insulin Homo sapiens 102-109 2677048-9 1989 It is concluded that in contrast to the effect on adipose tissue, physiological concentrations of insulin decrease m-LPLA in proportion to the effect of insulin on muscle glucose uptake, while muscle contractions cause a local, delayed, and transient increase in m-LPLA. Glucose 171-178 insulin Homo sapiens 98-105 2677048-9 1989 It is concluded that in contrast to the effect on adipose tissue, physiological concentrations of insulin decrease m-LPLA in proportion to the effect of insulin on muscle glucose uptake, while muscle contractions cause a local, delayed, and transient increase in m-LPLA. Glucose 171-178 insulin Homo sapiens 153-160 2681552-8 1989 A nadir in CEEG power (8.0 +/- 1.6 microV2) occurred 40 to 55 minutes after insulin injection as glucose levels were rising. Glucose 97-104 insulin Homo sapiens 76-83 2553978-0 1989 Role of kinases in insulin stimulation of glucose transport. Glucose 42-49 insulin Homo sapiens 19-26 2674559-4 1989 In contrast, low levels of IL-1 potentiate the secretion of insulin and thyroid hormones, and intermediate levels of IL-6 double glucose-induced insulin production by beta-cells. Glucose 129-136 insulin Homo sapiens 145-152 2677612-4 1989 Nonseptic burn patients also had a 91% increase in potassium clearance (P less than .05), but their maximal insulin-stimulated glucose uptake was not different from that of bedrested controls. Glucose 127-134 insulin Homo sapiens 108-115 2677612-6 1989 Insulin infusion completely suppressed hepatic glucose production in both septic patients and in nonseptic burn patients. Glucose 47-54 insulin Homo sapiens 0-7 2677612-8 1989 It is concluded that septic and postburn insulin resistance differ in that peripheral glucose uptake in sepsis, but not nonseptic burn injury, is refractory to pharmacologic insulin stimulation, whereas in both states insulin effectively stimulates potassium uptake. Glucose 86-93 insulin Homo sapiens 41-48 2559356-3 1989 Though insulin and IGF-I both stimulate glucose uptake into these cells, the increased binding following glyburide treatment was not associated with any change in glucose uptake. Glucose 40-47 insulin Homo sapiens 7-14 2682625-3 1989 In the present study, the expression of the IRGT was shown to increase in parallel with the acquisition of acutely insulin-stimulated glucose uptake during differentiation of these cells, whereas the level of the HepG2-GT decreased during the course of differentiation in parallel with a decline in basal glucose uptake. Glucose 134-141 insulin Homo sapiens 115-122 2682625-8 1989 We conclude that chronic treatment of 3T3-L1 adipocytes with insulin or tolbutamide increases glucose uptake primarily by means of a selective increase in the expression of the HepG2-GT. Glucose 94-101 insulin Homo sapiens 61-68 2678633-2 1989 Glucose utilization was measured during euglycemic insulin clamp in combination with indirect calorimetry and infusion of [3H-3]-glucose, while beta-cell function was measured during a hyperglycemic clamp. Glucose 0-7 insulin Homo sapiens 51-58 2678633-3 1989 The kidney-transplanted patients were resistant to the glucoregulatory effect of insulin, as demonstrated by a 25% reduction in total glucose disposal compared to control subjects. Glucose 134-141 insulin Homo sapiens 81-88 2678633-5 1989 The reduction in nonoxidative glucose disposal was associated with reduced lean body mass and incapacity to release energy as heat after infusion of insulin, i.e. thermogenic defect. Glucose 30-37 insulin Homo sapiens 149-156 2671740-3 1989 Captopril increased the insulin-mediated disposal of glucose, as compared with placebo, from 5.7 +/- 2.4 to 6.3 +/- 2.5 mg per kilogram of body weight per minute (P less than 0.05), whereas hydrochlorothiazide caused a decrease from 6.4 +/- 2.0 to 5.7 +/- 1.9 (P less than 0.01). Glucose 53-60 insulin Homo sapiens 24-31 2671740-4 1989 Captopril had no effect on the basal insulin concentration, but it decreased the late (30- to 90-minute) insulin response to glucose and increased the early (2- to 6-minute) insulin peak. Glucose 125-132 insulin Homo sapiens 105-112 2671740-4 1989 Captopril had no effect on the basal insulin concentration, but it decreased the late (30- to 90-minute) insulin response to glucose and increased the early (2- to 6-minute) insulin peak. Glucose 125-132 insulin Homo sapiens 105-112 2671740-5 1989 Hydrochlorothiazide increased the basal insulin concentration and the late insulin response to glucose. Glucose 95-102 insulin Homo sapiens 75-82 2504287-2 1989 L-Arginine and L-ornithine stimulate insulin release from pancreatic islets exposed to D-glucose. Glucose 87-96 insulin Homo sapiens 37-44 2550826-7 1989 We now describe a mechanism whereby GABA, co-secreted with insulin from beta cells, may mediate part of the inhibitory action of glucose on glucagon secretion by activating GABAA-receptor Cl- channels in alpha 2 cells. Glucose 129-136 insulin Homo sapiens 59-66 2691217-8 1989 Theophylline stimulated insulin secretion from both glucose-sensitive and non-sensitive islets, while trifluoperazine inhibited glucose-stimulated insulin secretion in previously sensitive islets and increased insulin secretion in previously non-sensitive islets. Glucose 52-59 insulin Homo sapiens 24-31 2691217-8 1989 Theophylline stimulated insulin secretion from both glucose-sensitive and non-sensitive islets, while trifluoperazine inhibited glucose-stimulated insulin secretion in previously sensitive islets and increased insulin secretion in previously non-sensitive islets. Glucose 128-135 insulin Homo sapiens 147-154 2691217-8 1989 Theophylline stimulated insulin secretion from both glucose-sensitive and non-sensitive islets, while trifluoperazine inhibited glucose-stimulated insulin secretion in previously sensitive islets and increased insulin secretion in previously non-sensitive islets. Glucose 128-135 insulin Homo sapiens 147-154 2572124-4 1989 Biostator-regulated insulin infusion normalized fasting levels of blood glucose and reduced the hyperglycemia following glucose ingestion, i.e. blood glucose now rose from 4.6 +/- 0.1 to a maximum of 7.3 +/- 0.8 mmol/l. Glucose 72-79 insulin Homo sapiens 20-27 2572124-4 1989 Biostator-regulated insulin infusion normalized fasting levels of blood glucose and reduced the hyperglycemia following glucose ingestion, i.e. blood glucose now rose from 4.6 +/- 0.1 to a maximum of 7.3 +/- 0.8 mmol/l. Glucose 120-127 insulin Homo sapiens 20-27 2551176-1 1989 The present studies were undertaken to characterize further the influence of synthetic human beta-endorphin (0.5 mg/h) on insulin and glucagon responses to intravenous glucose in humans. Glucose 168-175 insulin Homo sapiens 122-129 2551176-2 1989 Infusion of beta-endorphin in 10 normal volunteers caused a clear-cut inhibition of the overall insulin responses to a glucose pulse (0.33 g/kg iv) with values of glucose disappearance rates in the diabetic range [0.89 +/- 0.09 (P less than 0.01) vs. saline 1.82 +/- 0.15%/min]. Glucose 119-126 insulin Homo sapiens 96-103 2551176-4 1989 The infusion of theophylline (150 mg + 350 mg/h) to increase the intracellular cAMP activity by inhibiting phosphodiesterase completely reversed the inhibitory effect of beta-endorphin on glucose-induced insulin secretion. Glucose 188-195 insulin Homo sapiens 204-211 2551176-8 1989 These data confirm that beta-endorphin stimulates glucagon and inhibits basal and glucose-stimulated insulin secretion and suggest that the opioid influences the intraislet adenylate cyclase activity. Glucose 82-89 insulin Homo sapiens 101-108 2683970-2 1989 The exaggerated plasma insulin and C-peptide responses to oral glucose in obese subjects which is greater for insulin than C-peptide suggests that the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and decreased fractional hepatic extraction of insulin. Glucose 63-70 insulin Homo sapiens 23-30 2683970-2 1989 The exaggerated plasma insulin and C-peptide responses to oral glucose in obese subjects which is greater for insulin than C-peptide suggests that the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and decreased fractional hepatic extraction of insulin. Glucose 63-70 insulin Homo sapiens 35-44 2683970-2 1989 The exaggerated plasma insulin and C-peptide responses to oral glucose in obese subjects which is greater for insulin than C-peptide suggests that the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and decreased fractional hepatic extraction of insulin. Glucose 63-70 insulin Homo sapiens 110-117 2683970-2 1989 The exaggerated plasma insulin and C-peptide responses to oral glucose in obese subjects which is greater for insulin than C-peptide suggests that the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and decreased fractional hepatic extraction of insulin. Glucose 63-70 insulin Homo sapiens 123-132 2683970-2 1989 The exaggerated plasma insulin and C-peptide responses to oral glucose in obese subjects which is greater for insulin than C-peptide suggests that the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and decreased fractional hepatic extraction of insulin. Glucose 63-70 insulin Homo sapiens 110-117 2774262-7 1989 Glucose 5% solution infusion resulted in significantly greater blood lactate accumulation and significantly greater blood glucose and insulin levels, whereas there were no changes in the patients receiving Ringer"s solution. Glucose 0-7 insulin Homo sapiens 134-141 2673162-7 1989 Patient 1, with the mildest degree of glucose intolerance, had decreased fasting insulin and blood glucose levels, improved glucose tolerance, and insulin-mediated glucose disposal, associated with an increase in monocyte insulin receptors. Glucose 38-45 insulin Homo sapiens 81-88 2673162-7 1989 Patient 1, with the mildest degree of glucose intolerance, had decreased fasting insulin and blood glucose levels, improved glucose tolerance, and insulin-mediated glucose disposal, associated with an increase in monocyte insulin receptors. Glucose 38-45 insulin Homo sapiens 147-154 2673162-7 1989 Patient 1, with the mildest degree of glucose intolerance, had decreased fasting insulin and blood glucose levels, improved glucose tolerance, and insulin-mediated glucose disposal, associated with an increase in monocyte insulin receptors. Glucose 38-45 insulin Homo sapiens 147-154 2675810-5 1989 Multiple linear-regression analyses showed that fasting insulin (but not 2-hour insulin) was significantly associated with low HDL cholesterol and high total triglycerides independently from other variables (age, body mass index, waist/hip ratio, alcohol intake, smoking, exercise, and 2-hour glucose). Glucose 293-300 insulin Homo sapiens 56-63 2505990-4 1989 In these patients, the addition of NPH insulin (0.2 +/- 0.01 IU/kg body wt) greatly decreased fasting and postprandial plasma glucose (P less than .001) and glycosylated hemoglobin (P less than .005). Glucose 126-133 insulin Homo sapiens 39-46 2687637-6 1989 Insulin-stimulated rates of glycogen synthesis were 8.6 +/- 1.2, 6.0 +/- 1.8, and 5.8 +/- 0.8 nmol glucose/25 mg/h. Glucose 99-106 insulin Homo sapiens 0-7 2673694-6 1989 The net glucose-area and insulin-area responses to ingested glucose dose (with the decreasing baseline) were then best described by third-order equations. Glucose 60-67 insulin Homo sapiens 25-32 2630378-0 1989 Is glucose self-monitoring beneficial in non-insulin-treated diabetic patients? Glucose 3-10 insulin Homo sapiens 45-52 2670645-3 1989 Thus, we determined in vivo insulin action on peripheral glucose utilization (M) and hepatic glucose production (HGP) with the euglycemic glucose-clamp technique in obese (n = 19) and nonobese (n = 10) PCO women and age- and body-composition-matched normal ovulatory women (n = 11 obese and n = 8 nonobese women). Glucose 57-64 insulin Homo sapiens 28-35 2670645-3 1989 Thus, we determined in vivo insulin action on peripheral glucose utilization (M) and hepatic glucose production (HGP) with the euglycemic glucose-clamp technique in obese (n = 19) and nonobese (n = 10) PCO women and age- and body-composition-matched normal ovulatory women (n = 11 obese and n = 8 nonobese women). Glucose 93-100 insulin Homo sapiens 28-35 2670645-9 1989 Insulin-stimulated glucose utilization was significantly decreased in both PCO groups whether expressed per kilogram total weight (P less than .001) or per kilogram fat free mass (P less than .001) or when divided by the steady-state plasma insulin (l) level (M/l, P less than .001). Glucose 19-26 insulin Homo sapiens 0-7 2688061-9 1989 insulin and glucose administration the relative variations in subcutaneous glucose closely resembled those in blood glucose. Glucose 75-82 insulin Homo sapiens 0-7 2688061-9 1989 insulin and glucose administration the relative variations in subcutaneous glucose closely resembled those in blood glucose. Glucose 75-82 insulin Homo sapiens 0-7 2697526-2 1989 In the present study, serum insulin releasing level after glucose loading was determined in 16 patients with duodenal ulcer (DU) using radioimmunoassay, and was compared with that of normal controls. Glucose 58-65 insulin Homo sapiens 28-35 2697985-6 1989 (3) Insulin-mediated glucose metabolism in the hypothalamus provides a link between dietary intake and sympathetic nervous system activity. Glucose 21-28 insulin Homo sapiens 4-11 2668711-3 1989 Although an absence of diabetes was demonstrated once again in the highlanders, these periurban subjects showed an unexpectedly high insulin response which may be a precursor of glucose intolerance. Glucose 178-185 insulin Homo sapiens 133-140 2753889-1 1989 Recently, we have described a COOH-terminal deletion mutation of the human insulin receptor (HIR delta CT) that exhibits normal insulin-mediated kinase activity and endocytosis, but is inefficient in stimulating glucose transport and glycogen synthase (McClain, D. A., Maegawa, H., Levy, J., Huecksteadt, T., Dull, T. J., Lee, J., Ullrich, A., and Olefsky, J.M. Glucose 212-219 insulin Homo sapiens 75-82 2753889-11 1989 By contrast, only the cells with normal receptors and none of the HIR delta CT clones exhibit increased sensitivity for a metabolic action of insulin, the stimulation of glucose uptake. Glucose 170-177 insulin Homo sapiens 142-149 2672688-4 1989 Similarly, late-phase insulin secretion defined as the insulin increment between 90 and 120 min after initiation of the glucose challenge was enhanced in uremic patients at the two highest glycemic steps (44 +/- 10 vs 16 +/- 2 and 123 +/- 29 vs 44 +/- 5 mU/l, both p less than 0.01). Glucose 120-127 insulin Homo sapiens 22-29 2672688-4 1989 Similarly, late-phase insulin secretion defined as the insulin increment between 90 and 120 min after initiation of the glucose challenge was enhanced in uremic patients at the two highest glycemic steps (44 +/- 10 vs 16 +/- 2 and 123 +/- 29 vs 44 +/- 5 mU/l, both p less than 0.01). Glucose 120-127 insulin Homo sapiens 55-62 2672688-5 1989 The raised late-phase insulin response allowed comparable glucose disposal in the two groups (uremic patients: 9.2 +/- 1.0 and 15.5 +/- 1.6 mg.kg-1.min-1. Glucose 58-65 insulin Homo sapiens 22-29 2672688-7 1989 The slopes of potentiation, i.e. the slopes of the regression lines expressing the relationship between changes in insulin increments and changes in glucose, were markedly steeper in uremic patients (0.45 +/- 0.09 and 0.66 +/- 0.20, early and late-phase respectively) than in controls (0.20 +/- 0.06 and 0.25 +/- 0.03). Glucose 149-156 insulin Homo sapiens 115-122 2764690-8 1989 There was, however, a significant correlation (r = -0.59, p = 0.001) between the decrease in blood glucose level and the amount of regular insulin used in the routine morning dose. Glucose 99-106 insulin Homo sapiens 139-146 2568955-1 1989 Glucose uptake by heart, skeletal muscle, and adipose tissue is acutely regulated by insulin, which stimulates facilitative glucose transport, at least in part, by promoting the translocation of transporters from an intracellular pool to the plasma membrane. Glucose 0-7 insulin Homo sapiens 85-92 2568955-1 1989 Glucose uptake by heart, skeletal muscle, and adipose tissue is acutely regulated by insulin, which stimulates facilitative glucose transport, at least in part, by promoting the translocation of transporters from an intracellular pool to the plasma membrane. Glucose 124-131 insulin Homo sapiens 85-92 2673656-1 1989 Using the glucose and insulin values from a 5-hr oral glucose tolerance test, nine quantitative measures have been developed to separate normal, "flat-curve," and non-insulin-dependent diabetic (NIDD) patients. Glucose 54-61 insulin Homo sapiens 22-29 2753235-1 1989 The minimal model approach to estimating insulin sensitivity (Sl) and glucose effectiveness in promoting its own disposition at basal insulin (SG) is a powerful tool that has been underutilized given its potential applications. Glucose 70-77 insulin Homo sapiens 134-141 2753235-7 1989 In addition, because of the different metabolic fates of the two deuterated tracers, there were minor differences in basal insulin-derived measures of glucose effectiveness, but these differences were negligible for parameters describing insulin-stimulated processes. Glucose 151-158 insulin Homo sapiens 123-130 2506091-0 1989 Different effects of insulin and oral antidiabetic agents on glucose and energy metabolism in type 2 (non-insulin-dependent) diabetes mellitus. Glucose 61-68 insulin Homo sapiens 21-28 2506091-4 1989 Insulin improved glycaemic control primarily by reducing basal hepatic glucose production (p less than 0.05), but had no significant effect on peripheral glucose metabolism. Glucose 71-78 insulin Homo sapiens 0-7 2506091-9 1989 We conclude that insulin and glibenclamide/metformin have different long-term effects on glucose and energy metabolism in Type 2 diabetes. Glucose 89-96 insulin Homo sapiens 17-24 2683715-4 1989 Hyperinsulinemic men showed a tendency toward decreased insulin sensitivity after consuming fructose on the basis of an increased insulin-to-glucose ratio and decreased insulin binding to erythrocytes. Glucose 141-148 insulin Homo sapiens 5-12 2683715-4 1989 Hyperinsulinemic men showed a tendency toward decreased insulin sensitivity after consuming fructose on the basis of an increased insulin-to-glucose ratio and decreased insulin binding to erythrocytes. Glucose 141-148 insulin Homo sapiens 56-63 2683715-4 1989 Hyperinsulinemic men showed a tendency toward decreased insulin sensitivity after consuming fructose on the basis of an increased insulin-to-glucose ratio and decreased insulin binding to erythrocytes. Glucose 141-148 insulin Homo sapiens 56-63 2698363-0 1989 [Recent data on the regulation of glucose transport and glucose transporters in insulin-sensitive tissues]. Glucose 34-41 insulin Homo sapiens 80-87 2698366-4 1989 The maximum glucose need was followed by a slow fall in insulin levels with a duration of action of 17 hours. Glucose 12-19 insulin Homo sapiens 56-63 2698367-5 1989 The beta cells secreted large amounts of insulin throughout this period, and secretion was stimulated by raising the glucose concentration in the medium from 5.6 to 16.8 mM. Glucose 117-124 insulin Homo sapiens 41-48 2680438-13 1989 Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Glucose 77-85 insulin Homo sapiens 144-151 2689190-4 1989 The basal insulin values remained unchanged but the insulin response was slightly insignificantly increased after 10 and 20 minutes following glucose application depending on the duration of therapy. Glucose 142-149 insulin Homo sapiens 52-59 2684835-3 1989 In addition the patients with polycystic ovaries showed higher mean basal IRI and C-peptide levels, higher mean glucose stimulated IRI and C-peptide levels and higher mean incremental IRI and C-peptide values. Glucose 112-119 insulin Homo sapiens 139-148 2684835-3 1989 In addition the patients with polycystic ovaries showed higher mean basal IRI and C-peptide levels, higher mean glucose stimulated IRI and C-peptide levels and higher mean incremental IRI and C-peptide values. Glucose 112-119 insulin Homo sapiens 139-148 2684835-4 1989 The molar ratios of C-peptide/IRI were significantly lower in the PCOD group at all time intervals after glucose stimulation when compared to the normal women. Glucose 105-112 insulin Homo sapiens 20-29 2668321-9 1989 These ultradian oscillations of glucose and insulin levels were temporally correlated, with a tendency for glucose pulses to lead insulin pulses by 15-30 min. Glucose 32-39 insulin Homo sapiens 130-137 2668321-9 1989 These ultradian oscillations of glucose and insulin levels were temporally correlated, with a tendency for glucose pulses to lead insulin pulses by 15-30 min. Glucose 107-114 insulin Homo sapiens 44-51 2668321-9 1989 These ultradian oscillations of glucose and insulin levels were temporally correlated, with a tendency for glucose pulses to lead insulin pulses by 15-30 min. Glucose 107-114 insulin Homo sapiens 130-137 2668321-10 1989 These results demonstrate in normal subjects the existence of a diurnal variation in glucose tolerance distinct from the dawn phenomenon observed in diabetic subjects and indicate that spontaneous 100- to 150-min oscillations in peripheral glucose and insulin levels characterize stimulated pancreatic function, with the amplitude of the oscillations being dependent on the size of the stimulus. Glucose 85-92 insulin Homo sapiens 252-259 2668322-7 1989 These results indicate the coexistence of marked insulin resistance and constant ability to decrease plasma glucose level. Glucose 108-115 insulin Homo sapiens 49-56 2681497-0 1989 Impaired glucose tolerance in Thai adults: serum insulin profiles after a 75 gram oral glucose load. Glucose 9-16 insulin Homo sapiens 49-56 2681497-0 1989 Impaired glucose tolerance in Thai adults: serum insulin profiles after a 75 gram oral glucose load. Glucose 87-94 insulin Homo sapiens 49-56 2667643-2 1989 After primary culture for 5 days in the presence of glucose, the lipogenic response to insulin increased, the glucagon response decreased and noradrenaline produced the same degree of inhibition at 3 h. At 24 h, insulin produced an even higher increase on lipogenesis parallel to an increase in fatty acid synthase activity. Glucose 52-59 insulin Homo sapiens 87-94 2667643-2 1989 After primary culture for 5 days in the presence of glucose, the lipogenic response to insulin increased, the glucagon response decreased and noradrenaline produced the same degree of inhibition at 3 h. At 24 h, insulin produced an even higher increase on lipogenesis parallel to an increase in fatty acid synthase activity. Glucose 52-59 insulin Homo sapiens 212-219 2757059-7 1989 In addition, total insulin-stimulated glucose metabolism was reduced (5.07 +/- 0.22 versus 7.09 +/- 0.56 mg/kg.LBM.minute; p less than 0.001), and this was mainly accounted for by a reduction in non-oxidative glucose metabolism (glycogen synthesis and anaerobic glycolysis) (1.78 +/- 0.22 versus 3.54 +/- 0.49 mg/kg.LBM.minute; p less than 0.001). Glucose 38-45 insulin Homo sapiens 19-26 2757059-7 1989 In addition, total insulin-stimulated glucose metabolism was reduced (5.07 +/- 0.22 versus 7.09 +/- 0.56 mg/kg.LBM.minute; p less than 0.001), and this was mainly accounted for by a reduction in non-oxidative glucose metabolism (glycogen synthesis and anaerobic glycolysis) (1.78 +/- 0.22 versus 3.54 +/- 0.49 mg/kg.LBM.minute; p less than 0.001). Glucose 209-216 insulin Homo sapiens 19-26 2757059-8 1989 The severity of hepatic and peripheral insulin resistance correlated with the plasma glucose concentration but was unrelated to insulin secretion. Glucose 85-92 insulin Homo sapiens 39-46 2803236-2 1989 The insulin effect on glucose uptake is not sufficiently explained by a simple glucose-carrier translocation model. Glucose 22-29 insulin Homo sapiens 4-11 2803236-2 1989 The insulin effect on glucose uptake is not sufficiently explained by a simple glucose-carrier translocation model. Glucose 79-86 insulin Homo sapiens 4-11 2803236-5 1989 We found that inositol phosphate (IP)-oligosaccharides isolated from the drug Actovegin, as well as the alkaloid vinblastine, show a partial insulin-like effect on glucose-transport activity of fat-cells (3-O-methylglucose uptake, expressed as % of equilibrium value per 4 s: basal 5.8%, insulin 59%, IP-oligosaccharides 30%, vinblastine 29%) without inducing carrier translocation. Glucose 164-171 insulin Homo sapiens 141-148 2527130-9 1989 We conclude that ultralente insulin can give an improved fasting blood glucose concentration but that in those patients with more marked fasting hyperglycaemia or with a nocturnal hypoglycaemia problem it offers no clinical advantage over human lente insulin in a twice-daily injection regimen. Glucose 71-78 insulin Homo sapiens 28-35 2666204-0 1989 Decreased activation rate of insulin-stimulated glucose transport in adipocytes from obese subjects. Glucose 48-55 insulin Homo sapiens 29-36 2666204-1 1989 Recent studies from our laboratory have shown that the rate at which insulin activates glucose disposal in vivo is much slower in obese subjects compared with lean controls. Glucose 87-94 insulin Homo sapiens 69-76 2666204-2 1989 To determine if this was caused by an abnormality in activation of insulin-stimulated glucose transport at the cellular level, we measured the rate at which insulin stimulated glucose transport in human adipocytes from obese volunteers. Glucose 86-93 insulin Homo sapiens 67-74 2666204-2 1989 To determine if this was caused by an abnormality in activation of insulin-stimulated glucose transport at the cellular level, we measured the rate at which insulin stimulated glucose transport in human adipocytes from obese volunteers. Glucose 176-183 insulin Homo sapiens 157-164 2666204-4 1989 Maximal insulin-stimulated (4300 pM insulin) glucose transport rates were significantly decreased in obesity (2.81 +/- 0.81 vs. 1.15 +/- 0.20 pmol.10(-5) cells.10 s-1, P less than .005). Glucose 45-52 insulin Homo sapiens 8-15 2666204-4 1989 Maximal insulin-stimulated (4300 pM insulin) glucose transport rates were significantly decreased in obesity (2.81 +/- 0.81 vs. 1.15 +/- 0.20 pmol.10(-5) cells.10 s-1, P less than .005). Glucose 45-52 insulin Homo sapiens 36-43 2666204-5 1989 It took longer for adipocytes from obese subjects to achieve half-maximal activation of insulin-stimulated glucose transport than those from lean subjects (15 +/- 2 vs. 9.4 +/- 1.2 min, P less than .05). Glucose 107-114 insulin Homo sapiens 88-95 2666204-6 1989 The slower overall rates of activation of maximal insulin-stimulated glucose transport observed in adipocytes from obese subjects mirror the slower rates of stimulation of glucose disposal in vivo, which suggests that the in vivo findings are caused by a cellular abnormality in insulin action at a step beyond the binding of insulin to its receptor. Glucose 69-76 insulin Homo sapiens 50-57 2666204-6 1989 The slower overall rates of activation of maximal insulin-stimulated glucose transport observed in adipocytes from obese subjects mirror the slower rates of stimulation of glucose disposal in vivo, which suggests that the in vivo findings are caused by a cellular abnormality in insulin action at a step beyond the binding of insulin to its receptor. Glucose 69-76 insulin Homo sapiens 279-286 2666204-6 1989 The slower overall rates of activation of maximal insulin-stimulated glucose transport observed in adipocytes from obese subjects mirror the slower rates of stimulation of glucose disposal in vivo, which suggests that the in vivo findings are caused by a cellular abnormality in insulin action at a step beyond the binding of insulin to its receptor. Glucose 69-76 insulin Homo sapiens 279-286 2666204-6 1989 The slower overall rates of activation of maximal insulin-stimulated glucose transport observed in adipocytes from obese subjects mirror the slower rates of stimulation of glucose disposal in vivo, which suggests that the in vivo findings are caused by a cellular abnormality in insulin action at a step beyond the binding of insulin to its receptor. Glucose 172-179 insulin Homo sapiens 50-57 2666106-8 1989 The rIL-1 beta-treated islets showed a marked reduction of glucose-stimulated insulin release. Glucose 59-66 insulin Homo sapiens 78-85 2546962-4 1989 In comparison to normal fibroblasts, [125I]insulin binding, insulin-stimulated [14C]glucose, and [3H]thymidine uptake, and insulin-stimulated autophosphorylation were each reduced by approximately 50-60% of the absolute values in controls. Glucose 84-91 insulin Homo sapiens 60-67 2546962-4 1989 In comparison to normal fibroblasts, [125I]insulin binding, insulin-stimulated [14C]glucose, and [3H]thymidine uptake, and insulin-stimulated autophosphorylation were each reduced by approximately 50-60% of the absolute values in controls. Glucose 84-91 insulin Homo sapiens 60-67 2666106-15 1989 These combined observations suggest that exposure to IL-1 induces a preferential decrease in glucose-mediated insulin release and mitochondrial glucose metabolism. Glucose 93-100 insulin Homo sapiens 110-117 2666174-4 1989 The basal (6 +/- 1 versus 7 +/- 1 microU/ml) and glucose-stimulated (42 +/- 5 versus 43 +/- 6 microU/ml) insulin responses were similar in the follicular and luteal studies. Glucose 49-56 insulin Homo sapiens 105-112 2666174-5 1989 However, glucose uptake was significantly higher during the follicular versus the luteal phase (10.99 +/- 0.97 versus 6.93 +/- 0.37 mg/kg-min; P less than 0.01), as was the ratio of glucose uptake to insulin concentration (30.0 +/- 5.5 versus 19.7 +/- 3.7, P less than 0.01). Glucose 9-16 insulin Homo sapiens 200-207 2673694-9 1989 At this dose of glucose, the increase in insulin was only 15 microU/ml. Glucose 16-23 insulin Homo sapiens 41-48 2676668-0 1989 The glucose dependent insulinotropic polypeptide response to oral glucose and mixed meals is increased in patients with type 2 (non-insulin-dependent) diabetes mellitus. Glucose 4-11 insulin Homo sapiens 22-29 2680087-3 1989 A rapid decrease in the mean serum glucose concentration was seen in both the lean and obese groups following the initiation of insulin therapy. Glucose 35-42 insulin Homo sapiens 128-135 2680087-4 1989 The glucose concentration of the lean patients plateaued after the second day of insulin treatment, whereas the obese patients" levels continued to fall after the third and fourth days. Glucose 4-11 insulin Homo sapiens 81-88 2698305-0 1989 Defective insulin-mediated splanchnic glucose regulation and glucose clearance: early glucose homeostatic defects in nondiabetic, young offspring of patients with noninsulin-dependent diabetes mellitus. Glucose 38-45 insulin Homo sapiens 10-17 2668332-11 1989 These results suggest that (a) altered expression of the adipose cell/muscle GT forms the molecular basis for the dysregulated glucose transport response to insulin characteristic of diabetes, (b) the expression of two types of GTs in rat adipose cells is regulated independently, and (c) alterations in mRNA levels are only part of the mechanism for in vivo regulation of the expression of either GT species. Glucose 127-134 insulin Homo sapiens 157-164 2661589-5 1989 Glucose disposal was reduced in the NIDD patients at the three highest plasma insulin concentrations, and this was accounted for by defects in both glucose oxidation and nonoxidative glucose metabolism. Glucose 0-7 insulin Homo sapiens 78-85 2666485-1 1989 Plasma glucose and insulin responses and basal and insulin-stimulated glucose uptake were determined in 24 non-obese, healthy, physically active individuals, divided into two groups on the basis of age. Glucose 70-77 insulin Homo sapiens 51-58 2666485-4 1989 Furthermore, there was a significant correlation between age and total plasma glucose (r = 0.63, P less than .001) and insulin (r = 0.44, P less than .01) during the glucose tolerance test. Glucose 166-173 insulin Homo sapiens 119-126 2666485-7 1989 Glucose uptake during euglycemic clamp studies was also reduced in the older group, and this was true if the clamps were performed at plasma insulin concentration of approximately 10 microU/mL (P less than .05) or 60 microU/mL (P less than .10). Glucose 0-7 insulin Homo sapiens 141-148 2666485-9 1989 The fact that the increase in glucose uptake when plasma insulin was raised six-fold was similar in both groups suggests that insulin sensitivity does not decline with age. Glucose 30-37 insulin Homo sapiens 57-64 2673889-0 1989 A further comparison of insulin- and phorbol ester-stimulated glucose transport in adipocytes. Glucose 62-69 insulin Homo sapiens 24-31 2673889-1 1989 Insulin and 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) stimulatory effects on adipocyte glucose transport were compared for their sensitivity to: (1) sphingosine and staurosporine, two potent protein kinase C (PKC) inhibitors; and (2) phenylarsine oxide (PhAsO), a dithiol reagent blocking insulin-stimulated glucose transport. Glucose 101-108 insulin Homo sapiens 0-7 2673889-4 1989 Insulin and PMA both altered PKC along with glucose transport, either by increasing its activity in the cytosol or by promoting its translocation to membrane. Glucose 44-51 insulin Homo sapiens 0-7 2673889-8 1989 The results suggest that insulin activates adipocyte glucose transport through: (1) a PKC-dependent mechanism requiring cellular dithiols, responsible for a part of the hormone-induced increase in transport Vmax; and (2) a PKC-independent mechanism responsible for both a further increase in transport Vmax and a decrease in transport Km. Glucose 53-60 insulin Homo sapiens 25-32 2674586-5 1989 In addition, diabetes mellitus is associated with peripheral insulin resistance, which may result in a deterioration of the overall glucose homeostasis and consequently make the treatment more difficult to manage. Glucose 132-139 insulin Homo sapiens 61-68 2546561-5 1989 Similarly, insulin receptor tyrosine kinase as assessed by receptor autophosphorylation and phosphorylation of the substrate poly-(Glu/Tyr) was not fully activated by treatment of cells with the insulin dimer (31 and 42% of the effect of insulin, respectively) in concentrations which maximally activate glucose transport and give rise to full insulin receptor occupancy (5 X 10(-7) M). Glucose 304-311 insulin Homo sapiens 11-18 2546561-8 1989 It is concluded that a partial phosphorylation of insulin receptors and a submaximal tyrosine kinase activation are sufficient for full stimulation of glucose transport in the adipocyte. Glucose 151-158 insulin Homo sapiens 50-57 2618527-5 1989 insulin infusion, plasma glucose fell to almost normal levels within roughly 3h; RCS levels showed a gradual reduction becoming significant at 180 min. Glucose 25-32 insulin Homo sapiens 0-7 2665517-0 1989 Effect of 7 days of bed rest on dose-response relation between plasma glucose and insulin secretion. Glucose 70-77 insulin Homo sapiens 82-89 2665517-1 1989 Physical training decreases glucose-stimulated insulin secretion. Glucose 28-35 insulin Homo sapiens 47-54 2665517-3 1989 At 11 and 20 mM glucose, insulin concentrations in plasma were higher after (87 +/- 11 and 303 +/- 63 microU/ml) than before (63 +/- 5 and 251 +/- 50 microU/ml, P less than 0.05) bed rest. Glucose 16-23 insulin Homo sapiens 25-32 2665517-7 1989 It is concluded that bed rest for 7 days increases the glucose-stimulated insulin response, at least partly due to a beta-cell adaptation increasing glucose-stimulated insulin secretion. Glucose 55-62 insulin Homo sapiens 74-81 2665517-7 1989 It is concluded that bed rest for 7 days increases the glucose-stimulated insulin response, at least partly due to a beta-cell adaptation increasing glucose-stimulated insulin secretion. Glucose 55-62 insulin Homo sapiens 168-175 2665517-7 1989 It is concluded that bed rest for 7 days increases the glucose-stimulated insulin response, at least partly due to a beta-cell adaptation increasing glucose-stimulated insulin secretion. Glucose 149-156 insulin Homo sapiens 74-81 2665517-7 1989 It is concluded that bed rest for 7 days increases the glucose-stimulated insulin response, at least partly due to a beta-cell adaptation increasing glucose-stimulated insulin secretion. Glucose 149-156 insulin Homo sapiens 168-175 2665518-2 1989 When Intralipid infusion was begun at the start of the insulin clamp, the increase in insulin-mediated glucose oxidation was completely inhibited, and the rise in nonoxidative glucose disposal was diminished by 22%. Glucose 103-110 insulin Homo sapiens 86-93 2505753-2 1989 In glucose-deprived cells, insulin decreased glycogen breakdown, but did not affect polysaccharide levels when glucose was present. Glucose 3-10 insulin Homo sapiens 27-34 2667925-4 1989 In control experiments (infusion of insulin alone), plasma glucose increased from 5.6 +/- 0.6 mM at 2400 to 11.1 +/- 1.3 mM at 0900 (P = .0024). Glucose 59-66 insulin Homo sapiens 36-43 2668254-6 1989 Insulin action on glucose uptake and tyrosine release of the thighs at mean plasma insulin concentrations of 67 (clamp step I) and 447 microU/ml (clamp step II) was decreased by immobilization, whereas immobilization did not affect insulin action on thigh exchange of free fatty acids, glycerol, O2, or potassium. Glucose 18-25 insulin Homo sapiens 0-7 2668254-6 1989 Insulin action on glucose uptake and tyrosine release of the thighs at mean plasma insulin concentrations of 67 (clamp step I) and 447 microU/ml (clamp step II) was decreased by immobilization, whereas immobilization did not affect insulin action on thigh exchange of free fatty acids, glycerol, O2, or potassium. Glucose 18-25 insulin Homo sapiens 83-90 2668254-8 1989 Seven days of one-legged immobilization causes local decreased insulin action on thigh glucose uptake and net protein degradation. Glucose 87-94 insulin Homo sapiens 63-70 2677109-3 1989 Glucose at the concentration of 25 mM produced a bidirectional effect; it increased high-affinity insulin binding but decreased low-affinity binding. Glucose 0-7 insulin Homo sapiens 98-105 2666426-5 1989 Using the euglycemic clamp technique, the dose-response curves describing the effects of insulin on glucose disposal were comparable before and after GH treatment. Glucose 100-107 insulin Homo sapiens 89-96 2666426-6 1989 There was a consistent 1.5- to 2-fold increase in plasma insulin and C-peptide concentrations during GH treatment, in both the basal and postprandial states, and after oral glucose or iv glucagon stimulation. Glucose 173-180 insulin Homo sapiens 57-64 2666426-6 1989 There was a consistent 1.5- to 2-fold increase in plasma insulin and C-peptide concentrations during GH treatment, in both the basal and postprandial states, and after oral glucose or iv glucagon stimulation. Glucose 173-180 insulin Homo sapiens 69-78 2666428-12 1989 We conclude that acute infections induce severe and long-lasting insulin resistance, which is localized to glucose-utilizing pathways. Glucose 107-114 insulin Homo sapiens 65-72 2666429-4 1989 The results demonstrated that the ability of insulin to stimulate disposal of a glucose load was significantly reduced in the subjects with a positive family history of noninsulin-dependent diabetes. Glucose 80-87 insulin Homo sapiens 45-52 2677535-13 1989 The training protocol had little effect on the glucose response, but did significantly lower (P less than 0.05) the plasma insulin response to a glucose load. Glucose 145-152 insulin Homo sapiens 123-130 2677535-14 1989 In response to a 100 g oral glucose load insulin declined regardless of age, with the insulin sum of the young and elderly being, 31.8% and 32.6% lower, respectively, after training. Glucose 28-35 insulin Homo sapiens 41-48 2677535-14 1989 In response to a 100 g oral glucose load insulin declined regardless of age, with the insulin sum of the young and elderly being, 31.8% and 32.6% lower, respectively, after training. Glucose 28-35 insulin Homo sapiens 86-93 2701029-3 1989 Insulin radioimmunoassay (IRI) is measured to know the amount of hormone incretion and to verify its efficacy in the glucose utilization. Glucose 117-124 insulin Homo sapiens 0-7 2672490-2 1989 To promote improved understanding of the basis for treatment with multiple insulin injections, regulation of glucose metabolism in normal individuals is reviewed. Glucose 109-116 insulin Homo sapiens 75-82 2662695-10 1989 Net increase in acute insulin response after iv glucose and after iv arginine was significantly correlated to the net increase in erythrocyte magnesium content after dietary magnesium supplementation. Glucose 48-55 insulin Homo sapiens 22-29 2675533-5 1989 In response to the glucose load, insulin in plasma was significantly less in VSD infants. Glucose 19-26 insulin Homo sapiens 33-40 2675533-7 1989 We conclude that compared to healthy infants, those with symptomatic VSD have normal glucose tolerance, increased secretion rate of insulin, but decreased levels of circulating insulin in response to an intravenous glucose load. Glucose 215-222 insulin Homo sapiens 177-184 2667859-13 1989 In the patients and normal subjects plasma insulin rose after glucose. Glucose 62-69 insulin Homo sapiens 43-50 2668407-3 1989 Insulin-mediated glucose uptake, measured with the euglycaemic insulin clamp technique, decreased during atenolol treatment, from 7.1 to 5.6 mg/kg per min (P = 0.05). Glucose 17-24 insulin Homo sapiens 0-7 2668407-3 1989 Insulin-mediated glucose uptake, measured with the euglycaemic insulin clamp technique, decreased during atenolol treatment, from 7.1 to 5.6 mg/kg per min (P = 0.05). Glucose 17-24 insulin Homo sapiens 63-70 2661589-9 1989 In conclusion, our findings demonstrate that insulin resistance is a general characteristic of glucose and FFA metabolism in NIDDM, and involves both oxidative and nonoxidative pathways. Glucose 95-102 insulin Homo sapiens 45-52 2677109-1 1989 The effect of Con A and glucose on insulin binding and receptor-mediated degradation by intact erythrocytes was studied. Glucose 24-31 insulin Homo sapiens 35-42 2544784-0 1989 Increased glucose transport by human fibroblasts with a heritable defect in insulin binding. Glucose 10-17 insulin Homo sapiens 76-83 2677680-2 1989 In primary cultured adipocytes, chronic exposure to glucose plus insulin (24 h), but neither agent alone, markedly decreased (less than 50%) glucose transport activity; however, neither glucose nor insulin regulated the number of glucose transporters or levels of transporter mRNA whether normalized per total RNA, RNA per cell, or as a fraction of CHO-B mRNA. Glucose 141-148 insulin Homo sapiens 65-72 2677680-9 1989 3) Insulin heterologously inhibits regulation of the glucose transport system by dexamethasone. Glucose 53-60 insulin Homo sapiens 3-10 2550060-0 1989 Design of a selective insulin receptor tyrosine kinase inhibitor and its effect on glucose uptake and metabolism in intact cells. Glucose 83-90 insulin Homo sapiens 22-29 2550060-8 1989 Inhibition of insulin-stimulated glucose oxidation in isolated rat adipocytes and 2-deoxyglucose uptake into CHO cells was observed with these prodrugs. Glucose 33-40 insulin Homo sapiens 14-21 2550060-9 1989 Our data provide additional evidence for the involvement of the insulin receptor tyrosine kinase in the regulation of glucose uptake and metabolism. Glucose 118-125 insulin Homo sapiens 64-71 2567374-1 1989 Changes in serum insulin concentrations during deterioration of glucose tolerance were studied in 81 Pima Indians who worsened from normal to impaired glucose tolerance (IGT); 44 who changed from IGT to non-insulin-dependent diabetes mellitus (NIDDM); 27 who were seen at diagnosis of NIDDM and 1.4-8.5 years later; and 11 subjects who were seen at each of these stages. Glucose 64-71 insulin Homo sapiens 17-24 2567374-5 1989 These longitudinal data show that, as glucose tolerance worsens, insulin and glucose concentrations in individuals follow the inverted-U-shaped relation previously reported in cross-sectional population studies. Glucose 38-45 insulin Homo sapiens 65-72 2666069-9 1989 Thus, the improvement in glucose tolerance by some of the diabetics seems to have arisen from improvements in their insulin resistance and insulin response to a glucose load. Glucose 25-32 insulin Homo sapiens 116-123 2666069-9 1989 Thus, the improvement in glucose tolerance by some of the diabetics seems to have arisen from improvements in their insulin resistance and insulin response to a glucose load. Glucose 25-32 insulin Homo sapiens 139-146 2666069-9 1989 Thus, the improvement in glucose tolerance by some of the diabetics seems to have arisen from improvements in their insulin resistance and insulin response to a glucose load. Glucose 161-168 insulin Homo sapiens 139-146 2766337-4 1989 Body mass index and concentrations of serum total cholesterol decreased significantly, insulin levels fell in the first and fourth hour of a glucose tolerance test. Glucose 141-148 insulin Homo sapiens 87-94 2735914-3 1989 Phenylarsine oxide, an inhibitor of insulin-stimulated glucose transport, blocked not only insulin-stimulated protein synthesis but constitutive protein synthesis as well (Ki, 3 microM). Glucose 55-62 insulin Homo sapiens 36-43 2735914-3 1989 Phenylarsine oxide, an inhibitor of insulin-stimulated glucose transport, blocked not only insulin-stimulated protein synthesis but constitutive protein synthesis as well (Ki, 3 microM). Glucose 55-62 insulin Homo sapiens 91-98 2671856-1 1989 Insulin therapy, based on urine glucose concentration, controlled by a dosage-measuring computer]. Glucose 32-39 insulin Homo sapiens 0-7 2499151-9 1989 This observation contrasts the well known insulin insensitivity, suggesting separate mechanisms for glucose uptake elicited by insulin and thyroid hormones. Glucose 100-107 insulin Homo sapiens 127-134 2667570-4 1989 Under these conditions endogenous insulin secretion was suppressed, and differences in SSPG concentration allowed comparisons of the ability of exogenous insulin to stimulate disposal of an identical glucose load in different individuals. Glucose 200-207 insulin Homo sapiens 154-161 2658536-0 1989 Xylitol vs glucose: effect on the rate of gastric emptying and motilin, insulin, and gastric inhibitory polypeptide release. Glucose 11-18 insulin Homo sapiens 72-123 2667570-3 1989 In separate studies, insulin-stimulated glucose uptake was estimated by measuring the steady-state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 30 minutes of a 180-minute continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 40-47 insulin Homo sapiens 21-28 2667570-3 1989 In separate studies, insulin-stimulated glucose uptake was estimated by measuring the steady-state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 30 minutes of a 180-minute continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 40-47 insulin Homo sapiens 125-132 2667570-3 1989 In separate studies, insulin-stimulated glucose uptake was estimated by measuring the steady-state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 30 minutes of a 180-minute continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 40-47 insulin Homo sapiens 125-132 2667570-3 1989 In separate studies, insulin-stimulated glucose uptake was estimated by measuring the steady-state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 30 minutes of a 180-minute continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 40-47 insulin Homo sapiens 125-132 2667570-3 1989 In separate studies, insulin-stimulated glucose uptake was estimated by measuring the steady-state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 30 minutes of a 180-minute continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 106-113 insulin Homo sapiens 21-28 2667570-3 1989 In separate studies, insulin-stimulated glucose uptake was estimated by measuring the steady-state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 30 minutes of a 180-minute continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 106-113 insulin Homo sapiens 21-28 2567576-2 1989 Insulin (15 mU.M-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 2 microU/ml), and plasma glucose decreased from 88 +/- 2 to 53 +/- 1 mg/dl for 12 h. In study 1, plasma glucose, glucose fluxes (D-[3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored. Glucose 101-108 insulin Homo sapiens 0-7 2567576-2 1989 Insulin (15 mU.M-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 2 microU/ml), and plasma glucose decreased from 88 +/- 2 to 53 +/- 1 mg/dl for 12 h. In study 1, plasma glucose, glucose fluxes (D-[3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored. Glucose 180-187 insulin Homo sapiens 0-7 2567576-2 1989 Insulin (15 mU.M-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 2 microU/ml), and plasma glucose decreased from 88 +/- 2 to 53 +/- 1 mg/dl for 12 h. In study 1, plasma glucose, glucose fluxes (D-[3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored. Glucose 180-187 insulin Homo sapiens 0-7 2660587-0 1989 Insulin inhibition of overnight glucose production and gluconeogenesis from lactate in NIDDM. Glucose 32-39 insulin Homo sapiens 0-7 2660587-5 1989 During insulin therapy, fasting plasma glucose decreased from 188 +/- 13 to 99 +/- 7 mg/dl (P less than 0.001) due to inhibition of glucose Ra from 3.0 +/- 0.1 to 2.2 +/- 0.1 mumol.kg-1.min-1 (P less than 0.005). Glucose 39-46 insulin Homo sapiens 7-14 2660587-5 1989 During insulin therapy, fasting plasma glucose decreased from 188 +/- 13 to 99 +/- 7 mg/dl (P less than 0.001) due to inhibition of glucose Ra from 3.0 +/- 0.1 to 2.2 +/- 0.1 mumol.kg-1.min-1 (P less than 0.005). Glucose 132-139 insulin Homo sapiens 7-14 2686866-5 1989 When an intravenous glucose tolerance test was performed during the last hour of hyperthermia signs of impaired first phase and enhanced second phase insulin responses were recorded. Glucose 20-27 insulin Homo sapiens 150-157 2731364-0 1989 Correlation of HbA1C, glycated serum proteins and albumin, and fructosamine with the 24-h glucose profile of insulin-dependent pregnant diabetics. Glucose 90-97 insulin Homo sapiens 109-116 16837278-4 1989 The venous plasma insulin level rose during infusion of 5% dextrose (p<0.001). Glucose 59-67 insulin Homo sapiens 18-25 2499444-2 1989 Preliminary trials indicate that surgical implantation of a hybrid device containing living insulin-secreting tissue may function as a combined glucose sensor and insulin-infusion pump. Glucose 144-151 insulin Homo sapiens 92-99 2499444-5 1989 For the minority of diabetic patients who have insulin-dependent diabetes, the benefit afforded by a bionic device establishing internal insulin release regulated by silently sensed blood glucose level is more than enough payoff for the discomfort and surgery involved in its implantation. Glucose 188-195 insulin Homo sapiens 47-54 2542108-10 1989 Insulin stimulated [14C]glucose incorporation into cellular lipid in a dose-dependent manner, with 50% effective concentration (EC50) of 0.3 nM. Glucose 24-31 insulin Homo sapiens 0-7 2548853-4 1989 These PTK blockers inhibit the insulin induced [14C]glucose assimilation into lipids (lipogenesis), but fail to inhibit the anti-lipolytic effect of the hormone. Glucose 52-59 insulin Homo sapiens 31-38 2656336-5 1989 The impaired secretion is localized to the final release process in that neither glucose-stimulated proinsulin synthesis nor its conversion to insulin is affected. Glucose 81-88 insulin Homo sapiens 100-110 2656347-7 1989 Basal hepatic glucose production measured with D-[3-3H]glucose was lower in the insulin-resistant group (1.53 +/- 0.11 mg.kg-1.min-1) than in the insulin-sensitive group (1.88 +/- 0.06 mg.kg-1.min-1) or normal control subjects (1.93 +/- 0.05 mg.kg-1.min-1). Glucose 14-21 insulin Homo sapiens 80-87 2684618-4 1989 Insulin resistance was demonstrated by fasting hyperinsulinemia, insulin tolerance test and euglycemic glucose clamp test, and large doses of insulin with CSII were not effective in controlling blood glucose. Glucose 103-110 insulin Homo sapiens 0-7 2731461-3 1989 There was a high and linear correlation between total amount of insulin delivered to restore blood glucose values and amount of CHO consumed: 12.1 +/- 1.3 to 31.2 +/- 5.2 U insulin were needed for 116 +/- 16 to 198 +/- 24 min. Glucose 99-106 insulin Homo sapiens 64-71 2498378-2 1989 Fasting serum insulin levels decreased from 177 +/- 45 (+/- SE) to 123 +/- 43 pmol/L (P less than 0.01) and insulin release in response to 100 g oral glucose administration decreased from 223.0 +/- 29.2 to 55.6 +/- 7.9 nmol.min/L (P less than 0.002) after diazoxide administration. Glucose 150-157 insulin Homo sapiens 108-115 2656733-8 1989 Plasma insulin rose by 36 +/- 7 (+/- SE) pmol/L (5 +/- 1 microU/mL) in the lean and 129 +/- 22 pmol/L (18 +/- 3 microU/mL) in the obese subjects, whereas plasma glucagon, PP, and glucose levels were similar in both groups. Glucose 179-186 insulin Homo sapiens 7-14 2524556-7 1989 We conclude that glucose-stimulated insulin secretion is normally increased during puberty, a response that may compensate for puberty-induced defects in insulin sensitivity. Glucose 17-24 insulin Homo sapiens 36-43 2695816-5 1989 Our data show that in this population of young non-insulin-dependent diabetics, the low peripheral insulin response to an oral glucose challenge is a possible consequence of diminished beta-cell secretion, as hepatic insulin extraction is at near normal value. Glucose 127-134 insulin Homo sapiens 51-58 2695816-5 1989 Our data show that in this population of young non-insulin-dependent diabetics, the low peripheral insulin response to an oral glucose challenge is a possible consequence of diminished beta-cell secretion, as hepatic insulin extraction is at near normal value. Glucose 127-134 insulin Homo sapiens 99-106 2565912-13 1989 The 24-h serum insulin values decreased and those of glucose increased during treatment; after oral glucose, serum insulin was lower and glucose was higher. Glucose 100-107 insulin Homo sapiens 115-122 2565912-13 1989 The 24-h serum insulin values decreased and those of glucose increased during treatment; after oral glucose, serum insulin was lower and glucose was higher. Glucose 100-107 insulin Homo sapiens 115-122 2565912-14 1989 However, after 12 months of treatment, the 8-h serum insulin profile and peak serum insulin after oral glucose administration had returned to pretreatment values, while serum glucose remained abnormal. Glucose 103-110 insulin Homo sapiens 84-91 2657326-0 1989 Differential effects of insulin and hyperglycemia on intracellular glucose disposition in humans. Glucose 67-74 insulin Homo sapiens 24-31 2657326-1 1989 Insulin stimulates both glucose oxidation and nonoxidative glucose disposal (glycogen and lipid synthesis, anaerobic glycolysis) in vivo. Glucose 24-31 insulin Homo sapiens 0-7 2657326-1 1989 Insulin stimulates both glucose oxidation and nonoxidative glucose disposal (glycogen and lipid synthesis, anaerobic glycolysis) in vivo. Glucose 59-66 insulin Homo sapiens 0-7 2497435-8 1989 The responses of plasma insulin and the insulin/glucose ratio were significantly greater in infants receiving enterally than parenterally infused glucose. Glucose 146-153 insulin Homo sapiens 24-31 2497435-8 1989 The responses of plasma insulin and the insulin/glucose ratio were significantly greater in infants receiving enterally than parenterally infused glucose. Glucose 146-153 insulin Homo sapiens 40-47 2497435-10 1989 The infants of diabetic mothers and the large-for-gestational-age infants had more rapid insulin response to orogastrically administered glucose, but their GIP responses were similar to that of normal infants. Glucose 137-144 insulin Homo sapiens 89-96 2497435-11 1989 These findings suggest that, at term gestation, the newborn infants have a "functional" enteroinsular axis in response to glucose, i.e. the rising plasma GIP contributed in part to the enhanced insulin response to enterally infused glucose. Glucose 232-239 insulin Homo sapiens 194-201 2500169-8 1989 END POINT: Evaluation of effects of treatment with metoprolol and atenolol on glucose, insulin, and lipid metabolism and glucose disposal mediated by insulin. Glucose 78-85 insulin Homo sapiens 150-157 2500169-8 1989 END POINT: Evaluation of effects of treatment with metoprolol and atenolol on glucose, insulin, and lipid metabolism and glucose disposal mediated by insulin. Glucose 121-128 insulin Homo sapiens 150-157 2500169-13 1989 Despite decreased sensitivity to insulin the increase in insulin concentration in response to an intravenous glucose tolerance test was small, suggesting inhibition of release of insulin. Glucose 109-116 insulin Homo sapiens 33-40 2500169-13 1989 Despite decreased sensitivity to insulin the increase in insulin concentration in response to an intravenous glucose tolerance test was small, suggesting inhibition of release of insulin. Glucose 109-116 insulin Homo sapiens 57-64 2500169-13 1989 Despite decreased sensitivity to insulin the increase in insulin concentration in response to an intravenous glucose tolerance test was small, suggesting inhibition of release of insulin. Glucose 109-116 insulin Homo sapiens 57-64 2675519-2 1989 Pregnant women had higher mean fasting and post-glucose plasma immunoreactive insulin (IRI) compared to non-pregnant controls (p less than 0.001). Glucose 48-55 insulin Homo sapiens 78-85 2648801-4 1989 Levels of production of immunoreactive insulin by islet cells that had been infected by rubella virus were lower than those observed in control cultures, under conditions of high glucose concentration (11.1 mmol/L) in the medium. Glucose 179-186 insulin Homo sapiens 39-46 2598472-8 1989 However, proinsulin was reduced after oral glucose (4.7 +/- 0.7 vs. 7.9 +/- 2.0 pmol/l, P less than 0.05) as was C-peptide (0.9 +/- 0.2 vs 2.6 +/- 0.3 nmol/l, P less than 0.05). Glucose 43-50 insulin Homo sapiens 9-19 2564365-8 1989 Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. Glucose 34-41 insulin Homo sapiens 0-7 2564365-8 1989 Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. Glucose 34-41 insulin Homo sapiens 17-24 2564365-8 1989 Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. Glucose 34-41 insulin Homo sapiens 112-119 2564365-8 1989 Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. Glucose 172-179 insulin Homo sapiens 0-7 2564365-8 1989 Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. Glucose 172-179 insulin Homo sapiens 17-24 2692943-0 1989 Effect of human proinsulin on blood glucose control and metabolic instability in type 1 diabetes mellitus. Glucose 36-43 insulin Homo sapiens 16-26 2692943-1 1989 UNLABELLED: The effect of human biosynthetic proinsulin (PRO) on blood glucose (BG) control and glucose excursions was studied in a nonrandomized design in eight patients with unstable type 1 diabetes mellitus and compared with that of human NPH insulin. Glucose 71-78 insulin Homo sapiens 45-55 2692943-1 1989 UNLABELLED: The effect of human biosynthetic proinsulin (PRO) on blood glucose (BG) control and glucose excursions was studied in a nonrandomized design in eight patients with unstable type 1 diabetes mellitus and compared with that of human NPH insulin. Glucose 71-78 insulin Homo sapiens 57-60 2692944-8 1989 Fasting insulin was not different, but at 90 and 120 min, insulin was higher in the high WHR subgroup who had also higher fasting, 90 and 120 min glucose. Glucose 146-153 insulin Homo sapiens 58-65 2707117-7 1989 The same may be expected in well-controlled IDDM patients in conventional therapy because a correlation exists between insulin requirement for conventional therapy and insulin delivered during glucose-controlled insulin infusion. Glucose 193-200 insulin Homo sapiens 119-126 2707117-7 1989 The same may be expected in well-controlled IDDM patients in conventional therapy because a correlation exists between insulin requirement for conventional therapy and insulin delivered during glucose-controlled insulin infusion. Glucose 193-200 insulin Homo sapiens 168-175 2707117-7 1989 The same may be expected in well-controlled IDDM patients in conventional therapy because a correlation exists between insulin requirement for conventional therapy and insulin delivered during glucose-controlled insulin infusion. Glucose 193-200 insulin Homo sapiens 168-175 2653971-8 1989 Parallel to the suppression of insulin release was a steady increase in the serum glucose during calcitonin infusion, with the highest glucose concentration of 5.8 (0.53) mmol/l at the end of infusion of the hormone. Glucose 82-89 insulin Homo sapiens 31-38 2653971-8 1989 Parallel to the suppression of insulin release was a steady increase in the serum glucose during calcitonin infusion, with the highest glucose concentration of 5.8 (0.53) mmol/l at the end of infusion of the hormone. Glucose 135-142 insulin Homo sapiens 31-38 2651503-1 1989 The relationship between maternal glucose levels and the concentration of glucose and insulin levels in human milk from diabetic women has not been elucidated. Glucose 34-41 insulin Homo sapiens 86-93 2651503-6 1989 The plasma glucose was then lowered back to baseline with intravenous insulin over 20 minutes. Glucose 11-18 insulin Homo sapiens 70-77 2666706-4 1989 The combination of the insulin test and exercise in coronary patients with normal glucose tolerance values helps to detect disturbances of regulatory mechanisms at the erythrocyte level and can be used as an adjuvant method for the assessment of latent carbohydrate metabolic disorders. Glucose 82-89 insulin Homo sapiens 23-30 2659622-3 1989 In the OGTT and SGT test, the insulin responses (SIRI/SPG ratios) for normal, borderline and DM1 (fasting plasma glucose less than 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) groups of the elderly (60 and above) were not significantly different from those for normal group of young and middle-aged (below 60) and were significantly higher for elderly group than for the young and middle-aged group in each glucose tolerance group. Glucose 113-120 insulin Homo sapiens 30-37 2659622-3 1989 In the OGTT and SGT test, the insulin responses (SIRI/SPG ratios) for normal, borderline and DM1 (fasting plasma glucose less than 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) groups of the elderly (60 and above) were not significantly different from those for normal group of young and middle-aged (below 60) and were significantly higher for elderly group than for the young and middle-aged group in each glucose tolerance group. Glucose 419-426 insulin Homo sapiens 30-37 2649887-0 1989 Activation of glucose uptake by insulin and insulin-like growth factor I in Xenopus oocytes. Glucose 14-21 insulin Homo sapiens 44-51 2649887-1 1989 Xenopus laevis oocytes possess a glucose transport system that is activated 3- to 5-fold by insulin-like growth factor I (Ka = 3 nM) and insulin (Ka = 200-250 nM), properties suggesting activation mediated by an insulin-like growth factor I receptor. Glucose 33-40 insulin Homo sapiens 92-99 2649887-6 1989 Taken together the results implicate the tyrosine-specific protein kinase activity of a cell-surface insulin-like growth factor I receptor in the activation of glucose transport in the Xenopus oocyte. Glucose 160-167 insulin Homo sapiens 101-108 2484909-6 1989 Further thyroid hormones and insulin exerted an additive effect on glucose uptake. Glucose 67-74 insulin Homo sapiens 29-36 2647150-6 1989 The measurement of blood glucose lowering in the rabbit by kangaroo insulin is consistent with this conclusion. Glucose 25-32 insulin Homo sapiens 68-75 2649103-2 1989 Both these pancreastatins inhibited glucose-stimulated insulin secretion at a concentration of 100 nM. Glucose 36-43 insulin Homo sapiens 55-62 2648723-6 1989 The clamp study revealed that metformin treatment was associated with an enhanced insulin-mediated glucose utilization (370 +/- 38 vs 313 +/- 33 mg.m-2.min-1, P less than 0.01), whereas insulin-mediated suppression of hepatic glucose production was unchanged. Glucose 99-106 insulin Homo sapiens 82-89 2648723-6 1989 The clamp study revealed that metformin treatment was associated with an enhanced insulin-mediated glucose utilization (370 +/- 38 vs 313 +/- 33 mg.m-2.min-1, P less than 0.01), whereas insulin-mediated suppression of hepatic glucose production was unchanged. Glucose 226-233 insulin Homo sapiens 186-193 2645916-5 1989 Peak serum insulin levels after glucose correlated inversely with the decline in sodium excretion (r = .67, P less than .10). Glucose 32-39 insulin Homo sapiens 11-18 2923142-4 1989 A delayed insulin response to glucose was observed in both mother and sister, and diabetes developed during his mother"s gestation. Glucose 30-37 insulin Homo sapiens 10-17 2492963-11 1989 Two weeks of basal insulin supplementation lowered fasting glucose concentrations (from 219 +/- 22 to 144 +/- 21 mg/dl; P less than .01) and integrated postprandial glycemic response (from 814 +/- 68 to 621 +/- 72 min.mg.ml-1) but not to normal. Glucose 59-66 insulin Homo sapiens 19-26 2492963-13 1989 Basal insulin supplementation decreased (P less than .05) both splanchnic uptake of ingested glucose and hepatic glucose release. Glucose 93-100 insulin Homo sapiens 6-13 2492963-13 1989 Basal insulin supplementation decreased (P less than .05) both splanchnic uptake of ingested glucose and hepatic glucose release. Glucose 113-120 insulin Homo sapiens 6-13 2494016-2 1989 Antecubital venous plasma glucose and insulin concentrations after ingestion of 75 g of glucose were higher in six normal subjects when studied at an ambient temperature of 33 degrees C at an ambient temperature of 23 degrees C; the mean area under the glucose-time curve increased from 833 at 23 degrees C to 990 mmol min-1 at 33 degrees C, that for insulin from 5300 to 7900 m-units min 1-1. Glucose 88-95 insulin Homo sapiens 38-45 2494016-2 1989 Antecubital venous plasma glucose and insulin concentrations after ingestion of 75 g of glucose were higher in six normal subjects when studied at an ambient temperature of 33 degrees C at an ambient temperature of 23 degrees C; the mean area under the glucose-time curve increased from 833 at 23 degrees C to 990 mmol min-1 at 33 degrees C, that for insulin from 5300 to 7900 m-units min 1-1. Glucose 88-95 insulin Homo sapiens 351-358 2494016-2 1989 Antecubital venous plasma glucose and insulin concentrations after ingestion of 75 g of glucose were higher in six normal subjects when studied at an ambient temperature of 33 degrees C at an ambient temperature of 23 degrees C; the mean area under the glucose-time curve increased from 833 at 23 degrees C to 990 mmol min-1 at 33 degrees C, that for insulin from 5300 to 7900 m-units min 1-1. Glucose 88-95 insulin Homo sapiens 38-45 2494016-2 1989 Antecubital venous plasma glucose and insulin concentrations after ingestion of 75 g of glucose were higher in six normal subjects when studied at an ambient temperature of 33 degrees C at an ambient temperature of 23 degrees C; the mean area under the glucose-time curve increased from 833 at 23 degrees C to 990 mmol min-1 at 33 degrees C, that for insulin from 5300 to 7900 m-units min 1-1. Glucose 88-95 insulin Homo sapiens 351-358 2645190-3 1989 Insulin release in response to GLP-I-(7-37) is highly dependent on the ambient glucose concentration; no response is detectable at a glucose concentration of 2.8 mM, and at 6.6 and 16.7 mM, insulin release is augmented by 4.7 and 22.8 ng/ml, respectively. Glucose 79-86 insulin Homo sapiens 0-7 2645190-3 1989 Insulin release in response to GLP-I-(7-37) is highly dependent on the ambient glucose concentration; no response is detectable at a glucose concentration of 2.8 mM, and at 6.6 and 16.7 mM, insulin release is augmented by 4.7 and 22.8 ng/ml, respectively. Glucose 133-140 insulin Homo sapiens 0-7 2645121-1 1989 Postabsorptive and postprandial glucose concentrations are regulated by the interaction of insulin and the counterinsulin hormones. Glucose 32-39 insulin Homo sapiens 91-98 2651603-5 1989 Insulin may have the greatest effect upon blood glucose, but may also be associated with the greatest likelihood of nuisance for the patient. Glucose 48-55 insulin Homo sapiens 0-7 2671746-9 1989 6) The molar ratio of insulin levels (during glucose loading)/glucagon levels (during L-alanine loading) was a good indicator of systemic glucose homeostasis from the hormonal aspect. Glucose 45-52 insulin Homo sapiens 22-29 2671746-9 1989 6) The molar ratio of insulin levels (during glucose loading)/glucagon levels (during L-alanine loading) was a good indicator of systemic glucose homeostasis from the hormonal aspect. Glucose 138-145 insulin Homo sapiens 22-29 2918840-6 1989 Patients in the second group who had abnormal glucose tolerance had a delay in insulin secretion in response to glucose, indicating a deterioration of insulin reserve in the beta cells. Glucose 46-53 insulin Homo sapiens 79-86 2664924-3 1989 In condition A, blood glucose levels correlated significantly to both insulin and glucagon; NEFA, glycerol and 3OH-B correlated only to insulin. Glucose 22-29 insulin Homo sapiens 70-77 2496531-6 1989 Older age, normal weight in connection with higher blood glucose and lower insulin concentrations as an expression of the insulin deficit of higher degree render in most cases possible a treatment with SH-preparations. Glucose 57-64 insulin Homo sapiens 122-129 2644893-1 1989 The insulinotropic action of glucose, the most potent physiologic insulin secretagogue, involves its metabolism. Glucose 29-36 insulin Homo sapiens 4-11 2644893-3 1989 We tested the abilities of a number of glucose metabolites to stimulate insulin release from pancreatic islets. Glucose 39-46 insulin Homo sapiens 72-79 2644893-5 1989 In numerous experiments over 3 years, insulin release by 4 mM glyceraldehyde phosphate ranged from 50 to 200% of that initiated by 16.7 mM glucose--a near-maximal insulin stimulus. Glucose 139-146 insulin Homo sapiens 38-45 2644893-5 1989 In numerous experiments over 3 years, insulin release by 4 mM glyceraldehyde phosphate ranged from 50 to 200% of that initiated by 16.7 mM glucose--a near-maximal insulin stimulus. Glucose 139-146 insulin Homo sapiens 163-170 2647447-1 1989 It is well known that in diabetes mellitus the early phase insulin release response to glucose becomes blunted. Glucose 87-94 insulin Homo sapiens 59-66 2647447-4 1989 Therefore, in the present study the autonomic function was investigated in different degrees of the early phase insulin release response to glucose loading in borderline diabetes mellitus (B-DM) as well as the early stage of diabetes mellitus (E-DM). Glucose 140-147 insulin Homo sapiens 112-119 2644250-7 1989 Desensitization of the glucose transport system has previously been shown to occur after adipocytes are exposed to high glucose and insulin. Glucose 23-30 insulin Homo sapiens 132-139 2644250-9 1989 After treatment, the glucose transport was markedly insulin-resistant (60% loss in maximal insulin responsiveness and a marked loss in insulin sensitivity), whereas the protein synthesis system exhibited neither diminished insulin responsiveness nor loss of insulin sensitivity. Glucose 21-28 insulin Homo sapiens 52-59 2644250-9 1989 After treatment, the glucose transport was markedly insulin-resistant (60% loss in maximal insulin responsiveness and a marked loss in insulin sensitivity), whereas the protein synthesis system exhibited neither diminished insulin responsiveness nor loss of insulin sensitivity. Glucose 21-28 insulin Homo sapiens 91-98 2644250-11 1989 From these studies we conclude that desensitization of the glucose transport system by glucose and insulin treatment appears to be specific for this particular effector system and does not reflect a state of generalized cellular insulin resistance. Glucose 59-66 insulin Homo sapiens 99-106 2697484-0 1989 Glucose tolerance and insulin response to glucose load before and after enzyme inducing therapy in subjects with glucose intolerance and patients with NIDDM having hyperinsulinemia or relative insulin deficiency. Glucose 42-49 insulin Homo sapiens 22-29 2697484-2 1989 Plasma glucose (BG) and insulin (IRI) response to glucose loading (OGTT) was investigated before and after placebo and phenobarbitone (PB) therapy in patients with glucose intolerance and NIDDM treated with diet only, sulphonylureas (SU) plus metformin (M) or insulin. Glucose 50-57 insulin Homo sapiens 0-37 2697485-4 1989 On treatment there was a transient increase of both the peak and the late insulin response to intravenous glucose while neither intravenous nor oral glucose tolerance were consistently altered. Glucose 106-113 insulin Homo sapiens 74-81 2671575-0 1989 The impact of low carbohydrate consumption on glucose tolerance, insulin concentration and insulin response to glucose challenge in Dogrib Indians. Glucose 111-118 insulin Homo sapiens 65-98 2671575-5 1989 The impact of low carbohydrate consumption on oral glucose tolerance, insulin concentration (IC), and insulin response (IR) to oral glucose challenge can thus be examined in this population. Glucose 132-139 insulin Homo sapiens 102-109 2657747-5 1989 Injections of hGH1-43 dramatically enhanced the effect of insulin on glucose clearance of obese yellow Avy/A and ob/ob mice and increased the insulin-stimulated glucose oxidation in adipose tissue of yellow mice, but had no direct effect on blood glucose or insulin levels of either genotype. Glucose 69-76 insulin Homo sapiens 58-65 2657747-5 1989 Injections of hGH1-43 dramatically enhanced the effect of insulin on glucose clearance of obese yellow Avy/A and ob/ob mice and increased the insulin-stimulated glucose oxidation in adipose tissue of yellow mice, but had no direct effect on blood glucose or insulin levels of either genotype. Glucose 161-168 insulin Homo sapiens 142-149 2657747-5 1989 Injections of hGH1-43 dramatically enhanced the effect of insulin on glucose clearance of obese yellow Avy/A and ob/ob mice and increased the insulin-stimulated glucose oxidation in adipose tissue of yellow mice, but had no direct effect on blood glucose or insulin levels of either genotype. Glucose 161-168 insulin Homo sapiens 142-149 2657747-5 1989 Injections of hGH1-43 dramatically enhanced the effect of insulin on glucose clearance of obese yellow Avy/A and ob/ob mice and increased the insulin-stimulated glucose oxidation in adipose tissue of yellow mice, but had no direct effect on blood glucose or insulin levels of either genotype. Glucose 161-168 insulin Homo sapiens 142-149 2657747-5 1989 Injections of hGH1-43 dramatically enhanced the effect of insulin on glucose clearance of obese yellow Avy/A and ob/ob mice and increased the insulin-stimulated glucose oxidation in adipose tissue of yellow mice, but had no direct effect on blood glucose or insulin levels of either genotype. Glucose 161-168 insulin Homo sapiens 142-149 2657747-7 1989 Tissues from lean agouti and obese yellow mice treated with HP in vitro showed decreased basal and insulin-stimulated glucose oxidation as well as decreased 14C incorporation into lipids. Glucose 118-125 insulin Homo sapiens 99-106 2503865-9 1989 It is concluded that enteral infusion of glucose preserves insulin action and glucose tolerance after colorectal resection, whereas intravenous infusion of glucose does not. Glucose 41-48 insulin Homo sapiens 59-66 2669963-4 1989 18F-Labeled insulin retains the essential biological properties of native insulin, as measured in vitro by binding to insulin receptors on human cells and stimulation of glucose metabolism in rat adipocytes. Glucose 170-177 insulin Homo sapiens 12-19 2669963-4 1989 18F-Labeled insulin retains the essential biological properties of native insulin, as measured in vitro by binding to insulin receptors on human cells and stimulation of glucose metabolism in rat adipocytes. Glucose 170-177 insulin Homo sapiens 74-81 2669963-4 1989 18F-Labeled insulin retains the essential biological properties of native insulin, as measured in vitro by binding to insulin receptors on human cells and stimulation of glucose metabolism in rat adipocytes. Glucose 170-177 insulin Homo sapiens 74-81 2673564-9 1989 The results also showed that correlation between insulin secretion level and blood glucose value was significantly negative. Glucose 83-90 insulin Homo sapiens 49-56 2656686-8 1989 When 3T3/HIR cells were preincubated with MA10, subsequent insulin- or IGF-I-stimulated deoxy[14C]glucose uptake was markedly inhibited. Glucose 98-105 insulin Homo sapiens 59-66 2504278-9 1989 The endogenous diacylglycerol which accumulates in secretagogue-stimulated islets may participate in insulin secretion because exogenous diacylglycerol induces insulin secretion from islets, and an inhibitor of diacylglycerol metabolism to phosphatidic acid augments glucose-induced insulin secretion. Glucose 267-274 insulin Homo sapiens 101-108 2543399-3 1989 Insulin receptor mRNA levels and insulin binding activity were reduced in HepG2 cultured at lower glucose concentrations. Glucose 98-105 insulin Homo sapiens 33-40 2656669-5 1989 The in vitro-synthesized protein reacted with a monoclonal antibody, 1F8, which recognizes the insulin-regulatable glucose transporter expressed in rat skeletal muscle, heart, and adipocytes. Glucose 115-122 insulin Homo sapiens 95-102 2656669-7 1989 The high levels in adult skeletal muscle and subcutaneous fat of mRNA encoding the adult skeletal muscle glucose transporter and its specific reactivity with monoclonal antibody 1F8 suggest that this protein is the major insulin-regulatable glucose transporter expressed in skeletal muscle and other insulin-responsive tissues. Glucose 105-112 insulin Homo sapiens 221-228 2656669-7 1989 The high levels in adult skeletal muscle and subcutaneous fat of mRNA encoding the adult skeletal muscle glucose transporter and its specific reactivity with monoclonal antibody 1F8 suggest that this protein is the major insulin-regulatable glucose transporter expressed in skeletal muscle and other insulin-responsive tissues. Glucose 105-112 insulin Homo sapiens 300-307 2656669-7 1989 The high levels in adult skeletal muscle and subcutaneous fat of mRNA encoding the adult skeletal muscle glucose transporter and its specific reactivity with monoclonal antibody 1F8 suggest that this protein is the major insulin-regulatable glucose transporter expressed in skeletal muscle and other insulin-responsive tissues. Glucose 241-248 insulin Homo sapiens 221-228 2656669-7 1989 The high levels in adult skeletal muscle and subcutaneous fat of mRNA encoding the adult skeletal muscle glucose transporter and its specific reactivity with monoclonal antibody 1F8 suggest that this protein is the major insulin-regulatable glucose transporter expressed in skeletal muscle and other insulin-responsive tissues. Glucose 241-248 insulin Homo sapiens 300-307 2656674-7 1989 Glucose alone, however, was effective in preventing recovery of insulin sensitivity but not recovery of MIR. Glucose 0-7 insulin Homo sapiens 64-71 2656674-8 1989 In the presence of 20 mM glucose, low doses of insulin (treatment EC50 = 0.22-0.46 ng/ml) effectively prevented recovery of both MIR and insulin sensitivity. Glucose 25-32 insulin Homo sapiens 47-54 2656674-8 1989 In the presence of 20 mM glucose, low doses of insulin (treatment EC50 = 0.22-0.46 ng/ml) effectively prevented recovery of both MIR and insulin sensitivity. Glucose 25-32 insulin Homo sapiens 137-144 2666058-4 1989 Since impairment of target cell sensitivity to insulin action and hyperglycemia may be caused by the stress hormones, cortisol, epinephrine and growth hormone included, with in part intrinsic rhythmicity, as well as by dehydration and by prolonged insulin withdrawal, a secondary feed-back signal on insulin release may easily be induced by rising blood glucose levels. Glucose 354-361 insulin Homo sapiens 47-54 2565999-9 1989 The transfer of IDDM subjects from porcine to human insulin seems to alter warning symptoms of low blood glucose concentration, with consequent impairment of its early recognition. Glucose 105-112 insulin Homo sapiens 52-59 2658451-5 1989 However, after treatment, both glucagon secretory activity and plasma glucose recovery following insulin-induced hypoglycemia were restored to normal. Glucose 70-77 insulin Homo sapiens 97-104 2658451-8 1989 These results suggest that the impaired recovery of plasma glucose levels from insulin-induced hypoglycemia in patients with anorexia nervosa is primarily attributable to impaired pancreatic alpha-secretory capability. Glucose 59-66 insulin Homo sapiens 79-86 2655469-4 1989 Glucose-stimulated insulin, proinsulin, and C-peptide levels were lower in T than in UT. Glucose 0-7 insulin Homo sapiens 19-26 2655469-11 1989 The training-induced decrease in glucose-stimulated insulin secretion is accurately matched to increased insulin action, keeping glucose disposal constant at any given plasma glucose concentration. Glucose 33-40 insulin Homo sapiens 52-59 2655469-11 1989 The training-induced decrease in glucose-stimulated insulin secretion is accurately matched to increased insulin action, keeping glucose disposal constant at any given plasma glucose concentration. Glucose 129-136 insulin Homo sapiens 52-59 2655469-11 1989 The training-induced decrease in glucose-stimulated insulin secretion is accurately matched to increased insulin action, keeping glucose disposal constant at any given plasma glucose concentration. Glucose 129-136 insulin Homo sapiens 52-59 2655471-3 1989 After the overnight and 3-day fasts, insulin restoration (0.2 mU.kg-1.min-1) alone resulted in transient decrements in glucose production and only 15 and 19% decrements in plasma glucose, respectively. Glucose 119-126 insulin Homo sapiens 37-44 2655471-3 1989 After the overnight and 3-day fasts, insulin restoration (0.2 mU.kg-1.min-1) alone resulted in transient decrements in glucose production and only 15 and 19% decrements in plasma glucose, respectively. Glucose 179-186 insulin Homo sapiens 37-44 2655471-4 1989 Selective glucagon deficiency (somatostatin infusion with insulin and growth hormone replacement) resulted in transient decrements in glucose production and additional 24 and 29% decrements in plasma glucose, respectively. Glucose 134-141 insulin Homo sapiens 58-65 2655471-4 1989 Selective glucagon deficiency (somatostatin infusion with insulin and growth hormone replacement) resulted in transient decrements in glucose production and additional 24 and 29% decrements in plasma glucose, respectively. Glucose 200-207 insulin Homo sapiens 58-65 2655543-6 1989 During oral glucose tolerance testing a significant increase in the plasma glucose and insulin peaks was recorded after betamethasone and, to a lesser extent, after prednisone and deflazacort. Glucose 12-19 insulin Homo sapiens 87-94 2524334-3 1989 The improvement in blood glucose control was accompanied by an increase in postprandial plasma insulin concentration measured hourly from 0800 to 1600 h (p less than 0.001). Glucose 25-32 insulin Homo sapiens 95-102 2524334-5 1989 Mean (+/- SE) insulin-mediated glucose metabolic clearance rate was evaluated during glucose clamp studies, and was significantly higher (p less than 0.001) after glibenclamide therapy at steady-state insulin levels of approximately 10 mU l-1 (53 +/- 3 vs 38 +/- 2 ml-2 min-1) and approximately 70 mU l-1 (78 +/- 9 vs 55 +/- 6 ml m-2 min-1). Glucose 31-38 insulin Homo sapiens 14-21 2524334-5 1989 Mean (+/- SE) insulin-mediated glucose metabolic clearance rate was evaluated during glucose clamp studies, and was significantly higher (p less than 0.001) after glibenclamide therapy at steady-state insulin levels of approximately 10 mU l-1 (53 +/- 3 vs 38 +/- 2 ml-2 min-1) and approximately 70 mU l-1 (78 +/- 9 vs 55 +/- 6 ml m-2 min-1). Glucose 31-38 insulin Homo sapiens 201-208 2524334-5 1989 Mean (+/- SE) insulin-mediated glucose metabolic clearance rate was evaluated during glucose clamp studies, and was significantly higher (p less than 0.001) after glibenclamide therapy at steady-state insulin levels of approximately 10 mU l-1 (53 +/- 3 vs 38 +/- 2 ml-2 min-1) and approximately 70 mU l-1 (78 +/- 9 vs 55 +/- 6 ml m-2 min-1). Glucose 85-92 insulin Homo sapiens 14-21 2524334-6 1989 Hepatic glucose production was also lower following glibenclamide treatment at both the lower (56 +/- 5 vs 68 +/- 5 mg m-2 min-1) and higher 22 +/- 4 vs 32 +/- 6 mg m-2 min-1) insulin levels. Glucose 8-15 insulin Homo sapiens 176-183 2653928-4 1989 Insulin resistance was demonstrated and quantified by a marked drop in the insulin sensitivity index (Sl) from 6.72 +/- 0.77 to 2.47 +/- 0.36 x 10(-5) min-1/pM (P less than .0001) and resulted in a doubling of basal immunoreactive insulin levels (from 75 +/- 7 to 157 +/- 21 pM, P less than .001) with no change in fasting glucose (5.5 +/- 0.1 vs. 5.7 +/- 0.1 mM). Glucose 323-330 insulin Homo sapiens 0-7 2653928-4 1989 Insulin resistance was demonstrated and quantified by a marked drop in the insulin sensitivity index (Sl) from 6.72 +/- 0.77 to 2.47 +/- 0.36 x 10(-5) min-1/pM (P less than .0001) and resulted in a doubling of basal immunoreactive insulin levels (from 75 +/- 7 to 157 +/- 21 pM, P less than .001) with no change in fasting glucose (5.5 +/- 0.1 vs. 5.7 +/- 0.1 mM). Glucose 323-330 insulin Homo sapiens 75-82 2653929-0 1989 Bedtime insulin for suppression of overnight free-fatty acid, blood glucose, and glucose production in NIDDM. Glucose 68-75 insulin Homo sapiens 8-15 2653929-1 1989 We studied the clinical effectiveness and mechanism underlying the glucose-lowering effect of evening insulin therapy. Glucose 67-74 insulin Homo sapiens 102-109 2653929-6 1989 The decrements in overnight glucose and FFA levels after 2 wk of bedtime insulin therapy were closely correlated (r = .86, (P less than .001). Glucose 28-35 insulin Homo sapiens 73-80 2653935-7 1989 Insulin-stimulated glucose disposal was reduced by 22% (P less than .005), and insulin clearance increased by 18% (P less than .02) after IFN administration. Glucose 19-26 insulin Homo sapiens 0-7 2653935-8 1989 When the insulin-clamp study was repeated in patients with steady-state hyperinsulinemia that was 12% higher (P less than .005) after IFN, the glucose disposal rate was still reduced by 15% (P less than .01). Glucose 143-150 insulin Homo sapiens 9-16 2656140-5 1989 Insulin responsiveness was markedly elevated; the steady-state glucose infusion rate (SSGIR) of step 4 was 104 vs. 64 mumol.kg-1.min-1 (range 50-79) in controls and 61 mumol.kg-1.min-1 (range 47-69) in IDDM subjects. Glucose 63-70 insulin Homo sapiens 0-7 2668051-5 1989 During exercise, plasma glucose and insulin levels were significantly lower (p less than 0.05 and p less than 0.01) after fructose than after glucose. Glucose 142-149 insulin Homo sapiens 36-43 2695278-7 1989 These studies reveal that the artificial beta-cell insulin therapy is capable of restoring to normal not only the abnormal glucose metabolism of conventionally treated diabetics, but also other substrate metabolism related to the lipid and protein homeostasis of the organism. Glucose 123-130 insulin Homo sapiens 51-58 2539976-11 1989 5) Labeling in the presence of 7 mM glucose plus 5.0 nM IL-1 resulted in a significant reduction in the subsequent PI and insulin responses. Glucose 36-43 insulin Homo sapiens 122-129 2550272-0 1989 Reversal of glucose-induced inhibition of insulin release by dibutyryl cyclic AMP. Glucose 12-19 insulin Homo sapiens 42-49 2550272-1 1989 Insulin release in response to glucose was measured after culture of islets from ob/obmice in a medium deficient in Ca2+. Glucose 31-38 insulin Homo sapiens 0-7 2550272-2 1989 When present at a concentration of 6 mmol/l, glucose inhibited, insulin release. Glucose 45-52 insulin Homo sapiens 64-71 2550272-4 1989 The inhibitory action of glucose on insulin release disappeared in the presence of 1 mmol/l dibutyryl cyclic AMP. Glucose 25-32 insulin Homo sapiens 36-43 2550272-7 1989 It is concluded that cyclic AMP plays a major role in controlling the balance between the stimulatory and inhibitory components in the glucose action on insulin release. Glucose 135-142 insulin Homo sapiens 153-160 2651092-0 1989 Dexamethasone regulates the glucose transport system in primary cultured adipocytes: different mechanisms of insulin resistance after acute and chronic exposure. Glucose 28-35 insulin Homo sapiens 109-116 2651092-2 1989 Acutely, 20 nM dexamethasone led to a 65% decrease in basal and a 31% decrement in maximally insulin-stimulated glucose transport (ED50 = 3-4 nM; t1/2 = 50 min). Glucose 112-119 insulin Homo sapiens 93-100 2651092-11 1989 2) Glucose modulates desensitization of the glucose transport system by insulin, but not by dexamethasone, and thus, there are both glucose-dependent and -independent mechanisms of insulin resistance. Glucose 3-10 insulin Homo sapiens 72-79 2651092-11 1989 2) Glucose modulates desensitization of the glucose transport system by insulin, but not by dexamethasone, and thus, there are both glucose-dependent and -independent mechanisms of insulin resistance. Glucose 3-10 insulin Homo sapiens 181-188 2651092-11 1989 2) Glucose modulates desensitization of the glucose transport system by insulin, but not by dexamethasone, and thus, there are both glucose-dependent and -independent mechanisms of insulin resistance. Glucose 44-51 insulin Homo sapiens 72-79 2651092-11 1989 2) Glucose modulates desensitization of the glucose transport system by insulin, but not by dexamethasone, and thus, there are both glucose-dependent and -independent mechanisms of insulin resistance. Glucose 44-51 insulin Homo sapiens 181-188 2651092-11 1989 2) Glucose modulates desensitization of the glucose transport system by insulin, but not by dexamethasone, and thus, there are both glucose-dependent and -independent mechanisms of insulin resistance. Glucose 132-139 insulin Homo sapiens 181-188 2651092-12 1989 3) Insulin can heterologously inhibit dexamethasone"s effects on glucose transport at both early and late phases of desensitization. Glucose 65-72 insulin Homo sapiens 3-10 2663744-9 1989 Glucose and maltodextrin induced the same insulin response. Glucose 0-7 insulin Homo sapiens 42-49 2673961-1 1989 To examine the effect of hyperthyroidism on carbohydrate metabolism, we studied glucose-stimulated insulin secretion and glucose utilization in 8 subjects with Graves" disease before and after treatment for hyperthyroidism and 8 age-, sex- and weight-matched normal subjects. Glucose 80-87 insulin Homo sapiens 99-106 2673961-6 1989 After glucose loading, the plasma glucose (P less than 0.05), serum insulin (P less than 0.05) and C-peptide (P less than 0.05) responses were significantly higher in hyperthyroid patients at all times up to 180 minutes. Glucose 6-13 insulin Homo sapiens 68-75 2523898-4 1989 The basal plasma IGF-I and insulin concentrations and incremental 0-60 min insulin areas in response to glucose rose significantly throughout puberty (P less than 0.001 for all parameters) and declined to prepubertal levels by the third decade of life. Glucose 104-111 insulin Homo sapiens 75-82 2654170-5 1989 With the same glucose clamp protocol, physiological hyperinsulinemia for 150 min (676 +/- 40 pmol/L), obtained by the infusion of 2 mU/kg.min insulin, caused suppression of the plasma C-peptide level from 536 +/- 119 to 273 +/- 65 pmol/L during hyperglycemia and from 268 +/- 41 to 151 +/- 23 pmol/L during euglycemia (n = 9; P less than 0.005 in each clamp). Glucose 14-21 insulin Homo sapiens 57-64 2657326-5 1989 Under euglycemic conditions (protocols A and D), the presence of higher plasma insulin levels (80 +/- 6 v 39 +/- 5 microU/mL) caused the expected stimulation of both glucose oxidation (4.08 +/- 0.29 v 3.27 +/- 0.36 mg/min/kg) and nonoxidative glucose uptake (4.84 +/- 0.67 v 2.96 +/- 0.77 mg min/kg). Glucose 166-173 insulin Homo sapiens 79-86 2657326-5 1989 Under euglycemic conditions (protocols A and D), the presence of higher plasma insulin levels (80 +/- 6 v 39 +/- 5 microU/mL) caused the expected stimulation of both glucose oxidation (4.08 +/- 0.29 v 3.27 +/- 0.36 mg/min/kg) and nonoxidative glucose uptake (4.84 +/- 0.67 v 2.96 +/- 0.77 mg min/kg). Glucose 243-250 insulin Homo sapiens 79-86 2494092-4 1989 After rapid thaw (37 degrees C) and overnight culture, insulin release in response to high glucose and theophylline challenge determined in vitro functional viability. Glucose 91-98 insulin Homo sapiens 55-62 2499441-9 1989 The concomitant elevation of serum insulin and glucose suggests that an insulin-resistant state was induced which, if evident at the ovarian level, may be a factor mediating the adverse effects of exogenous GH on ovarian function. Glucose 47-54 insulin Homo sapiens 72-79 2656169-0 1989 Suppression by insulin treatment of glucose-induced inhibition of insulin release in non-insulin-dependent diabetics. Glucose 36-43 insulin Homo sapiens 15-22 2656169-0 1989 Suppression by insulin treatment of glucose-induced inhibition of insulin release in non-insulin-dependent diabetics. Glucose 36-43 insulin Homo sapiens 66-73 2656169-0 1989 Suppression by insulin treatment of glucose-induced inhibition of insulin release in non-insulin-dependent diabetics. Glucose 36-43 insulin Homo sapiens 66-73 2714828-0 1989 Optimal insulin infusion resulting from a mathematical model of blood glucose dynamics. Glucose 70-77 insulin Homo sapiens 8-15 2714828-3 1989 First, the insulin infusion program which results in an initially high blood glucose level being reduced to acceptable levels. Glucose 77-84 insulin Homo sapiens 11-18 2646314-3 1989 After oral glucose administration, the hyperandrogenic women had higher serum insulin concentrations than the normal women (P = 0.05). Glucose 11-18 insulin Homo sapiens 78-85 2646314-6 1989 Basal and insulin-mediated suppressions of hepatic glucose production determined from [3-3H]glucose specific activity were similar in the two groups. Glucose 51-58 insulin Homo sapiens 10-17 2654305-0 1989 Systemic delivery of insulin through eyes to lower the glucose concentration. Glucose 55-62 insulin Homo sapiens 21-28 2657320-4 1989 Based on the initial infusions, the insulin-dependent fractional glucose disappearance rate (X) during pulsatile insulin delivery (3.0 +/- 0.4 min-1 X 10(2), n = 6) was 73% of that of the continuous infusions (4.1 +/- 0.3 min-1 X 10(2), n = 12). Glucose 65-72 insulin Homo sapiens 36-43 2668713-2 1989 The study was conducted on 5 young women with PCOS, all of normal weight and glucose tolerance in whom the glucose-insulin clamp test had revealed reduced peripheral glucose uptake that was not influenced by other conditions typically associated with insulin-resistance. Glucose 107-114 insulin Homo sapiens 115-122 2657964-6 1989 In diabetic children, an adequate insulin therapy is required to allow the full benefit of muscular activity on glucose assimilation and to reach the same level of physical performance as the non-diabetic. Glucose 112-119 insulin Homo sapiens 34-41 2673493-1 1989 The plasma glucose and insulin response to oral glucose or carbohydrate meal tolerance tests were determined in 78 normal controls, 71 persons with IGT and 110 patients with NIDDM. Glucose 48-55 insulin Homo sapiens 23-30 2673493-2 1989 The results showed that: (1) The fasting serum insulin levels and insulin/glucose ratio were all higher in persons with IGT than those in the normal controls, and they were normal in diabetics with fasting plasma glucose less than 7.8 mmol/L. Glucose 74-81 insulin Homo sapiens 47-73 2673493-3 1989 In diabetics with fasting plasma glucose at 7.8-20.3 mmol/L, fasting insulin levels were within normal limit, but the values of insulin/glucose ratio were significantly decreased. Glucose 33-40 insulin Homo sapiens 69-76 2673493-3 1989 In diabetics with fasting plasma glucose at 7.8-20.3 mmol/L, fasting insulin levels were within normal limit, but the values of insulin/glucose ratio were significantly decreased. Glucose 33-40 insulin Homo sapiens 128-135 2673493-4 1989 (2) After glucose challenge, the values of serum insulin/glucose ratio were all increased in IGT, but were progressively decreased in diabetics as fasting plasma glucose gradually became higher. Glucose 10-17 insulin Homo sapiens 49-56 2673493-4 1989 (2) After glucose challenge, the values of serum insulin/glucose ratio were all increased in IGT, but were progressively decreased in diabetics as fasting plasma glucose gradually became higher. Glucose 57-64 insulin Homo sapiens 49-56 2673493-4 1989 (2) After glucose challenge, the values of serum insulin/glucose ratio were all increased in IGT, but were progressively decreased in diabetics as fasting plasma glucose gradually became higher. Glucose 57-64 insulin Homo sapiens 49-56 2673493-7 1989 When fasting plasma glucose was greater than 11.1 mmol/L, insulin/glucose ratio was decreased significantly. Glucose 20-27 insulin Homo sapiens 58-65 2673493-7 1989 When fasting plasma glucose was greater than 11.1 mmol/L, insulin/glucose ratio was decreased significantly. Glucose 66-73 insulin Homo sapiens 58-65 2647147-19 1989 These results suggest that the major actions of phenylarsine oxide observed in adipocytes are not direct effects on the transporter, but rather effects on the pathways by which insulin regulates glucose transport activity (Frost, S.C. and Lane, M.D. Glucose 195-202 insulin Homo sapiens 177-184 2538055-1 1989 In a 49-year-old woman with empty sella syndrome, corticotropin (ACTH) deficiency and various abnormalities, including increased thyrotropin (TSH) secretion, growth hormone (GH) deficiency, and inappropriately high insulin with early phase hypoglycemia, during an oral glucose tolerance test were found. Glucose 269-276 insulin Homo sapiens 215-222 2646944-5 1989 There was a positive correlation before training between maximum O2 uptake (Vo2 max) and total body glucose disposal rate (M) at the 40 mU.m-2.min-1 insulin infusion (r = 0.69, P less than 0.02). Glucose 100-107 insulin Homo sapiens 149-156 2645827-7 1989 Since mitochondrial metabolism is probably essential for glucose-induced insulin release and the metabolism of succinate and leucine (without or with glutamine) involves mitochondrial respiration exclusively, these results might indicate that mitochondrial metabolism generates conditions or factors that are transmitted to the cytosol to increase inositol trisphosphate formation and thus calcium mobilization and insulin release. Glucose 57-64 insulin Homo sapiens 73-80 2663195-6 1989 After oral glucose administration plasma insulin was assessed by radiooimmuncassay (IRI). Glucose 11-18 insulin Homo sapiens 41-48 2546845-2 1989 His serum exerted potent insulin-like activity: (a) it stimulated insulin receptor autophosphorylation and kinase activity in cell-free systems, this effect being additive to insulin; (b) it increased glucose transport in isolated soleus muscle. Glucose 201-208 insulin Homo sapiens 25-32 2654455-10 1989 A delayed and exceeded C-peptide and insulin response to the oral glucose load was determined with deteriorating glucose tolerance. Glucose 66-73 insulin Homo sapiens 37-44 2654455-10 1989 A delayed and exceeded C-peptide and insulin response to the oral glucose load was determined with deteriorating glucose tolerance. Glucose 113-120 insulin Homo sapiens 37-44 2654759-4 1989 The present study assesses the efficiency of the insulin/insulin feedback in acanthosis nigricans patients, measuring the inhibition of the production of C-peptide (the indicator of beta cell secretion) induced by the administration of exogenous insulin during glucose clamping. Glucose 261-268 insulin Homo sapiens 49-56 2654759-6 1989 The study using the glucose-insulin clamp technique was conducted on 4 Acanthosis Nigricans patients with normal glucose tolerance and 4 healthy controls, the drop in C-peptide levels after the administration of exogenous insulin being assessed in the course of both steady states. Glucose 20-27 insulin Homo sapiens 28-35 2697868-5 1989 A slight increase in the insulin-sensitivity was seen in the early morning in 3 patients in whom the glucose consumption during the constant insulin infusion was 4 mg/min/kg b.w. Glucose 101-108 insulin Homo sapiens 25-32 2697868-5 1989 A slight increase in the insulin-sensitivity was seen in the early morning in 3 patients in whom the glucose consumption during the constant insulin infusion was 4 mg/min/kg b.w. Glucose 101-108 insulin Homo sapiens 141-148 2665998-10 1989 The serum immunoreactive insulin (IRI) was elevated from the basal level to 289 microU/l, showing the prominent peak response at 30 min after the load, and both the serum potassium and the grasping power decreased significantly, although the blood glucose fluctuated within the normal level. Glucose 248-255 insulin Homo sapiens 25-32 2563455-1 1989 A highly specific two-site immunoradiometric assay for insulin was used to measure the plasma insulin response to 75 g glucose administered orally to 49 patients with non-insulin-dependent diabetes (NIDDM). Glucose 119-126 insulin Homo sapiens 55-62 2563455-1 1989 A highly specific two-site immunoradiometric assay for insulin was used to measure the plasma insulin response to 75 g glucose administered orally to 49 patients with non-insulin-dependent diabetes (NIDDM). Glucose 119-126 insulin Homo sapiens 94-101 2563455-2 1989 The plasma insulin concentration 30 min after glucose ingestion was lower in the diabetic patients than in matched controls for both non-obese (11-83 pmol/l vs 136-297 pmol/l, p less than 0.01) and obese subjects (23-119 pmol/l vs 137-378 pmol/l, p less than 0.01). Glucose 46-53 insulin Homo sapiens 11-18 2536700-1 1989 Insulin stimulates glucose transport into adipocytes, at least in part, via the translocation of intracellular transporters to the plasma membrane. Glucose 19-26 insulin Homo sapiens 0-7 2669756-5 1989 Evidence suggests that the small peptide fragment of insulin may be internalized and acts at the post-binding site(s) of the glucose metabolic pathway in target tissues. Glucose 125-132 insulin Homo sapiens 53-60 2492913-6 1989 Further, glucose management was being coordinated by three teams: intensive care, nutrition support, and the renal service, with physicians from each service prescribing insulin therapy. Glucose 9-16 insulin Homo sapiens 170-177 2524556-7 1989 We conclude that glucose-stimulated insulin secretion is normally increased during puberty, a response that may compensate for puberty-induced defects in insulin sensitivity. Glucose 17-24 insulin Homo sapiens 154-161 2644136-4 1989 Insulin therapy that normalizes blood glucose levels markedly decreases intestinal cholesterol synthesis in diabetic animals to a level similar to that observed in control animals. Glucose 38-45 insulin Homo sapiens 0-7 2649327-1 1989 Glucose clamping has become a widely used test for assessing insulin sensitivity and beta-cell function. Glucose 0-7 insulin Homo sapiens 61-68 2644145-1 1989 Serum proinsulin is disproportionately elevated both in the basal state and after an oral glucose load in non-insulin-dependent diabetes mellitus (NIDDM). Glucose 90-97 insulin Homo sapiens 6-16 2644145-3 1989 We investigated the effect of glycemic control by dietary treatment on serum proinsulin level in the basal state and in response to an oral glucose load. Glucose 140-147 insulin Homo sapiens 77-87 2644145-9 1989 Insulin response to oral glucose increased after dietary treatment, whereas proinsulin response did not change, resulting in a significant decrease in the molar ratio of the area under the curve of proinsulin to insulin after glucose load (from 0.28 +/- 0.12 to 0.13 +/- 0.07, P less than .001). Glucose 25-32 insulin Homo sapiens 0-7 2644145-9 1989 Insulin response to oral glucose increased after dietary treatment, whereas proinsulin response did not change, resulting in a significant decrease in the molar ratio of the area under the curve of proinsulin to insulin after glucose load (from 0.28 +/- 0.12 to 0.13 +/- 0.07, P less than .001). Glucose 226-233 insulin Homo sapiens 0-7 2644145-9 1989 Insulin response to oral glucose increased after dietary treatment, whereas proinsulin response did not change, resulting in a significant decrease in the molar ratio of the area under the curve of proinsulin to insulin after glucose load (from 0.28 +/- 0.12 to 0.13 +/- 0.07, P less than .001). Glucose 226-233 insulin Homo sapiens 76-86 2644145-9 1989 Insulin response to oral glucose increased after dietary treatment, whereas proinsulin response did not change, resulting in a significant decrease in the molar ratio of the area under the curve of proinsulin to insulin after glucose load (from 0.28 +/- 0.12 to 0.13 +/- 0.07, P less than .001). Glucose 226-233 insulin Homo sapiens 198-208 2644145-9 1989 Insulin response to oral glucose increased after dietary treatment, whereas proinsulin response did not change, resulting in a significant decrease in the molar ratio of the area under the curve of proinsulin to insulin after glucose load (from 0.28 +/- 0.12 to 0.13 +/- 0.07, P less than .001). Glucose 226-233 insulin Homo sapiens 79-86 2496077-2 1989 Sensitivity for insulin-mediated whole-body glucose uptake was not affected by acute exercise [insulin concentrations eliciting 50% of maximal insulin-mediated glucose uptake being 44 +/- 2 (C) vs. 46 +/- 3 (E) microU/ml] but was decreased after detraining (54 +/- 2 microU/ml, P less than 0.05) to levels comparable to those found in untrained subjects [Am. Glucose 44-51 insulin Homo sapiens 16-23 2659308-4 1989 In addition to an anti-insulin antibody with a high binding capacity, hyperglucagonemia (260 pg/ml with a plasma glucose level of 61 mg/dl) was observed, which returned to normal in parallel with the decrease in the insulin binding capacity of the plasma one month after beginning the treatment with propylthiouracil. Glucose 113-120 insulin Homo sapiens 23-30 2649445-0 1989 Glucose tolerance and insulin response to glucose load in body builders. Glucose 42-49 insulin Homo sapiens 22-29 2496077-7 1989 Near-maximal insulin-mediated glucose uptake (responsiveness) was higher than in untrained subjects and not influenced by acute exercise or detraining [13.4 +/- 1.2 (C), 12.2 +/- 0.9 (E), and 12.2 +/- 0.3 (DT) mg.min-1.kg-1]. Glucose 30-37 insulin Homo sapiens 13-20 2496078-3 1989 Increased insulin action on glucose uptake was found in the exercised compared with the rested thigh at mean plasma insulin concentrations of 23, 40, and 410 microU/ml. Glucose 28-35 insulin Homo sapiens 10-17 2496078-3 1989 Increased insulin action on glucose uptake was found in the exercised compared with the rested thigh at mean plasma insulin concentrations of 23, 40, and 410 microU/ml. Glucose 28-35 insulin Homo sapiens 116-123 2492598-12 1989 We conclude that insulin infusion improves glucose tolerance in extremely low birth weight infants and allows hyperglycemic infants to achieve adequate energy intake similar to that of infants who do not become hyperglycemic. Glucose 43-50 insulin Homo sapiens 17-24 2645306-1 1989 As muscle wasting and resistance to insulin-mediated glucose utilization are features of Cushing"s syndrome (CS), we examined glucose and amino acid metabolism in six patients with CS and six normal subjects before and during euglycemic hyperinsulinemic clamp studies (plasma insulin concentrations, approximately 0.36, approximately 0.65, and approximately 10.05 mmol/L). Glucose 53-60 insulin Homo sapiens 36-43 2645306-5 1989 In contrast, insulin-mediated glucose utilization was impaired in the CS patients at each clamp step (P less than 0.05). Glucose 30-37 insulin Homo sapiens 13-20 2645308-4 1989 The plasma glucose disappearance rate during the 3- to 15-min period following the insulin injection was taken as a measure of insulin action. Glucose 11-18 insulin Homo sapiens 127-134 2645308-7 1989 These results suggest that the 15-min ITT is suitable as a simple and rapid estimation of in vivo insulin action when glucose clamp studies are not feasible, as in large series of subjects or serial studies. Glucose 118-125 insulin Homo sapiens 98-105 2921598-8 1989 The muscle electrolyte changes can be explained by a decrease in the insulin mediated Na/k-pump activity across the cell membrane or a smaller number of insulin receptors on the skeletal muscle cell in patients with glucose intolerance. Glucose 216-223 insulin Homo sapiens 69-76 2921598-8 1989 The muscle electrolyte changes can be explained by a decrease in the insulin mediated Na/k-pump activity across the cell membrane or a smaller number of insulin receptors on the skeletal muscle cell in patients with glucose intolerance. Glucose 216-223 insulin Homo sapiens 153-160 2493157-3 1989 During infusions with glucose substitutes in severely ill patients with glucose intolerance it is sometimes possible to avoid insulin therapy since the first steps in the metabolism of these carbohydrates are insulin-independent. Glucose 22-29 insulin Homo sapiens 126-133 2645397-2 1989 administration of a proteolysis-resistant insulin analog lowers serum glucose levels, suggesting uptake and/or diffusion of intact insulin across the epithelium of the large intestine; however, no rigorous studies of insulin degradation and/or transepithelial flux in vitro have been reported with isolated colonic epithelium. Glucose 70-77 insulin Homo sapiens 42-49 2493157-3 1989 During infusions with glucose substitutes in severely ill patients with glucose intolerance it is sometimes possible to avoid insulin therapy since the first steps in the metabolism of these carbohydrates are insulin-independent. Glucose 22-29 insulin Homo sapiens 209-216 2567660-4 1989 It is suggested that use of insulin in addition to intravenous glucose infusion may be beneficial to glucose utilization in EHF. Glucose 101-108 insulin Homo sapiens 28-35 2493157-3 1989 During infusions with glucose substitutes in severely ill patients with glucose intolerance it is sometimes possible to avoid insulin therapy since the first steps in the metabolism of these carbohydrates are insulin-independent. Glucose 72-79 insulin Homo sapiens 126-133 2562908-5 1989 We also find that okadaic acid mimics the effect of insulin on glucose transport in adipocytes, which suggests that this process is stimulated by a serine/threonine phosphorylation event. Glucose 63-70 insulin Homo sapiens 52-59 2650737-2 1989 We have recently found that this type of mutation, which abolishes the effects of insulin on glucose metabolism, was without any effect on the mitogenic effect of the hormone [Debant, A. Glucose 93-100 insulin Homo sapiens 82-89 2645741-7 1989 In selected patients the serum insulin response to oral glucose was markedly reduced. Glucose 56-63 insulin Homo sapiens 31-38 2662797-4 1989 It was established that hypoglycemia, induced by insulin, the mean values of SP1 in the maternal serum on 24th hour were considerably higher, but in the induced hyperglycemia the values of SP1 were higher on the 24th h than on 60 respectively 120 min after the beginning of glucose infusion. Glucose 274-281 insulin Homo sapiens 49-56 2644251-11 1989 These studies, together with those in the companion paper, demonstrate that the pleiotropic actions of insulin on enhancing glucose uptake and protein synthesis are mediated through divergent pathways that can be independently regulated. Glucose 124-131 insulin Homo sapiens 103-110 2508399-3 1989 The mean C-peptide concentration after glucose infusion was significantly (p less than 0.05) lower for the SCA patients as compared to the controls. Glucose 39-46 insulin Homo sapiens 9-18 2648913-4 1989 The problem group rises higher rates of insulin after a glucose tolerance test than after the study of fisiologic secretion of insulin in 24 hours, but the other group shows similar answer in both tests. Glucose 56-63 insulin Homo sapiens 40-47 2491037-6 1989 The maximum insulin level was produced at the same time as maximum serum glucose level, taking place 60 minutes later. Glucose 73-80 insulin Homo sapiens 12-19 2675887-0 1989 [Cardiac resuscitation using glucose-insulin--a case report]. Glucose 29-36 insulin Homo sapiens 37-44 2669881-5 1989 Insulin-dependent tissues stop using glucose; the liver converts fatty acids to ketone bodies, which increase about 100-fold in the fasting human; and the brain substitutes ketone bodies for more than one half of what would otherwise be an obligatory consumption of 100 to 150 g glucose per day in humans. Glucose 37-44 insulin Homo sapiens 0-7 2683982-4 1989 At the basal condition, group CTO had fasting and glucose-stimulated insulin levels significantly higher than group PTO; fasting (but not stimulated) C peptide levels were also higher in CTO compared with PTO. Glucose 50-57 insulin Homo sapiens 69-76 2683982-7 1989 In both groups weight loss led to a significant drop in fasting and glucose-stimulated insulin and C peptide levels. Glucose 68-75 insulin Homo sapiens 87-94 2669881-5 1989 Insulin-dependent tissues stop using glucose; the liver converts fatty acids to ketone bodies, which increase about 100-fold in the fasting human; and the brain substitutes ketone bodies for more than one half of what would otherwise be an obligatory consumption of 100 to 150 g glucose per day in humans. Glucose 279-286 insulin Homo sapiens 0-7 2669881-15 1989 The high concentrations of counterregulatory hormones, cortisol, epinephrine, and glucagon will minimize glucose utilization by insulin-sensitive tissues, despite high concentrations of both glucose and insulin, but these hormones are not able to prevent suppression of ketone body synthesis in the liver. Glucose 105-112 insulin Homo sapiens 128-135 2655619-1 1989 Glucose is the single most important signal for stimulating insulin secretion from the B-cells in the pancreatic islets. Glucose 0-7 insulin Homo sapiens 60-67 2673126-5 1989 After insulin loading, the mean hormone concentration in plasma samples increased to 447.11 pmol/l +/- 277.01 (n = 83) (P less than 0.001), and the glucose concentration dropped to 2.55 mmol/l +/- 1.08 (n = 83) (P less than 0.001). Glucose 148-155 insulin Homo sapiens 6-13 2916920-6 1989 The use of an "open loop" insulin pump averts these problems and may provide better glucose control for selected spinal cord injury patients with Type I diabetes. Glucose 84-91 insulin Homo sapiens 26-33 2659049-13 1989 Increasing amounts of glucose are required to maintain the blood sugar at increasing doses of intraperitoneal regular insulin up to 5 U. Glucose 22-29 insulin Homo sapiens 118-125 2488710-5 1989 Practically none of the subjects had abnormal glycemic values after the glucose load, however the insulin levels were highly elevated in 80% of the patients, resulting in a great insulin/glucose ratios. Glucose 187-194 insulin Homo sapiens 98-105 2700067-4 1989 In order to further improve the control of glycemia, the following steps of an evolving system of electrochemical glucose sensing and monitoring should be envisaged: (1) fast-acting extracorporeal glucometers for incidental analyses, (2) intracorporeal sensors for short-term but easily repeated use to follow any kind of open-loop insulin therapy and to provide appropriate hypoglycemia-warning signals, (3) intracorporeal sensors as an essential part of automated feedback-controlled systems for insulin delivery. Glucose 114-121 insulin Homo sapiens 332-339 2695195-0 1989 Peripheral muscle glucose and potassium transport in a family with acanthosis nigricans and insulin resistance. Glucose 18-25 insulin Homo sapiens 92-99 2695195-1 1989 This study was designed to determine the forearm exchange of glucose and potassium in four members of a family exhibiting acanthosis nigricans and insulin resistance. Glucose 61-68 insulin Homo sapiens 147-154 2695195-4 1989 In the latter patient, the dissociation observed between glucose and potassium transport suggests several manners of differential impairment of insulin action and/or steps distal to the insulin receptor as being responsible for insulin resistance. Glucose 57-64 insulin Homo sapiens 144-151 2463195-5 1989 Drug-cultured HFP also retained the ability to release insulin in response to a glucose/theophylline challenge. Glucose 80-87 insulin Homo sapiens 55-62 2642438-11 1989 When corrected for the presence of the contaminant, glucose turnover determined with [6-3H]glucose during insulin infusion (9.5 +/- 0.6 mg.kg-1.min-1) no longer differed from either the glucose infusion rate or that determined with [6-14C]glucose. Glucose 52-59 insulin Homo sapiens 106-113 2642438-12 1989 Therefore, the underestimation of glucose turnover during insulin infusion and negative glucose production rates observed with traditional methods to analyze plasma radioactivity and commercially available tracers is the result of an artifactual increase in [6-3H]glucose specific activity. Glucose 34-41 insulin Homo sapiens 58-65 2651188-3 1989 The plasma insulin response was significantly greater (p less than 0.001) than normal in those with either impaired glucose tolerance or Type 2 diabetes and a fasting plasma glucose concentration less than 8 mmol/l. Glucose 116-123 insulin Homo sapiens 11-18 2653752-1 1989 The effect of sex on longitudinal changes in serum C-peptide immunoreactivity (CPR) response to the oral glucose tolerance test (OGTT) was examined up to 48 mo in 30 islet cell antibody-positive (ICA+), non-insulin-dependent diabetes mellitus (NIDDM) subjects (15 men, 15 women) who were matched for age, duration of diabetes, and mode of treatment. Glucose 105-112 insulin Homo sapiens 51-60 2656328-5 1989 The results show that all the non-insulin dependent patients at diagnosis had large post-prandial glucose excursions, and that the post-prandial rise in insulin was delayed. Glucose 98-105 insulin Homo sapiens 34-41 2680363-0 1989 Diabetic state-induced regulation of glucose uptake to skeletal muscle by insulin: a possible mechanism of its enhancement and autoinhibition. Glucose 37-44 insulin Homo sapiens 74-81 2721810-6 1989 Glucose profiles were similar but associated with basal and stimulated hyperinsulinaemia in the obese subjects indicating insulin resistance. Glucose 0-7 insulin Homo sapiens 76-83 2566470-6 1989 Serum glucose levels decreased by 46% and were significantly correlated with serum insulin levels (r = -0.66; p = 0.003). Glucose 6-13 insulin Homo sapiens 83-90 2462489-3 1989 In addition, the cells were stimulated by insulin in various acute and long term metabolic processes, including glucose transport, glycogen formation, amino acid uptake, and thymidine uptake and incorporation into DNA. Glucose 112-119 insulin Homo sapiens 42-49 2547602-2 1989 Data presented in this manuscript demonstrate an insulin-like effect of PMA, a tumor promoting agent that mimics the action of diacylglycerol, in isolated adipocytes on; (a) glucose oxidation using uniformly labelled, C-1-labelled and C-6-labelled glucose, (b) epinephrine-induced lipolysis and (c) low Km cAMP phosphodiesterase activity. Glucose 174-181 insulin Homo sapiens 49-56 2547602-2 1989 Data presented in this manuscript demonstrate an insulin-like effect of PMA, a tumor promoting agent that mimics the action of diacylglycerol, in isolated adipocytes on; (a) glucose oxidation using uniformly labelled, C-1-labelled and C-6-labelled glucose, (b) epinephrine-induced lipolysis and (c) low Km cAMP phosphodiesterase activity. Glucose 248-255 insulin Homo sapiens 49-56 2542036-2 1989 There was significantly reduced mean tissue sensitivity to insulin, expressed as the ratio of glucose disposal rate to serum insulin concentration (M/I), in untreated patients compared to the control group. Glucose 94-101 insulin Homo sapiens 59-66 2550245-6 1989 In the insulin + hANP experiment the nadir of blood glucose was decreased to 1.3 from the 2.0 mmol.1-1 found in the insulin-only experiment. Glucose 52-59 insulin Homo sapiens 7-14 2659341-0 1989 Gastric emptying and serum insulin levels after intake of glucose-polymer solutions. Glucose 58-65 insulin Homo sapiens 27-34 2680555-12 1989 Several observations of differences based on sex have emerged from recent studies of insulin-dependent diabetes: 1) the HLA-DR4 antigen is more frequent among female diabetic patients; 2) male HLA-identical siblings of diabetics have a lowered insulin response to glucose administered intravenously; 3) in areas of low insulin-dependent diabetes incidence, the patterns of onset by age differ markedly between the sexes. Glucose 264-271 insulin Homo sapiens 85-92 2689169-2 1989 Post-exercise muscle uptake and the intracellular fate of glucose was studied after oral or intravenous glucose administrations which caused similar plasma glucose concentrations, but high and moderate plasma insulin concentrations, respectively. Glucose 104-111 insulin Homo sapiens 209-216 2689169-2 1989 Post-exercise muscle uptake and the intracellular fate of glucose was studied after oral or intravenous glucose administrations which caused similar plasma glucose concentrations, but high and moderate plasma insulin concentrations, respectively. Glucose 104-111 insulin Homo sapiens 209-216 2698352-0 1989 The insulin response to oral glucose, concentrations of total cholesterol, triglycerides and uric acid in women with idiopathic hirsutism. Glucose 29-36 insulin Homo sapiens 4-11 2698352-5 1989 The insulin response to oral glucose was significantly higher in the IH and OB-IH groups compared with the control group (p less than 0.01). Glucose 29-36 insulin Homo sapiens 4-11 2698354-0 1989 Decreased plasma C-peptide to insulin molar ratio after oral glucose in elderly subjects. Glucose 61-68 insulin Homo sapiens 17-26 2698354-0 1989 Decreased plasma C-peptide to insulin molar ratio after oral glucose in elderly subjects. Glucose 61-68 insulin Homo sapiens 30-37 2698354-4 1989 Blood glucose level was significantly higher in elderly subjects than in young at 30 and 60 min, and insulin level was also significantly higher in elderly subjects than in young subjects at 60 min after glucose ingestion. Glucose 204-211 insulin Homo sapiens 101-108 2698354-5 1989 C-peptide response after glucose ingestion was similar in both groups. Glucose 25-32 insulin Homo sapiens 0-9 2698354-6 1989 The molar ratio of C-peptide to insulin after glucose ingestion in elderly subjects was slightly lower than that in young subjects, and the difference between the incremental areas of C-peptide and insulin divided by the incremental area of C-peptide were significantly lower in elderly subjects. Glucose 46-53 insulin Homo sapiens 19-28 2698354-6 1989 The molar ratio of C-peptide to insulin after glucose ingestion in elderly subjects was slightly lower than that in young subjects, and the difference between the incremental areas of C-peptide and insulin divided by the incremental area of C-peptide were significantly lower in elderly subjects. Glucose 46-53 insulin Homo sapiens 32-39 2693383-3 1989 Both insulin secretion and insulin resistance were ameliorated by perfect glucose control with VLCD. Glucose 74-81 insulin Homo sapiens 5-34 2695481-9 1989 The results suggest that BRL 35135 improves glucose tolerance by an increase in insulin sensitivity that is independent of body weight. Glucose 44-51 insulin Homo sapiens 80-87 2645262-4 1989 However, plasma insulin levels were similar with glucose and glucose polymer ingestions and significantly higher than with water or fructose ingestion. Glucose 49-56 insulin Homo sapiens 16-23 2645262-4 1989 However, plasma insulin levels were similar with glucose and glucose polymer ingestions and significantly higher than with water or fructose ingestion. Glucose 61-68 insulin Homo sapiens 16-23 2643339-5 1989 Forearm glucose uptake (FGU) was increased 5 times by insulin in the resting state, due largely to increased fractional extraction (P less than 0.05). Glucose 8-15 insulin Homo sapiens 54-61 2643339-10 1989 In summary, basal and insulin-stimulated glucose utilization is not augmented by prior high-intensity exercise, partly because nonexercised muscle is insulin resistant. Glucose 41-48 insulin Homo sapiens 22-29 2643341-5 1989 A sixfold cellular enlargement was associated with increase in both basal and insulin-stimulated glucose transport activity in the intact cell, and a 300-600% increase in insulin stimulating effect per se. Glucose 97-104 insulin Homo sapiens 78-85 2663241-5 1989 The insulin response to the glucose load was significantly enhanced in all the three groups of hypertensive patients compared with those of matched normotensive controls. Glucose 28-35 insulin Homo sapiens 4-11 2504564-6 1989 Mean insulin levels were likewise increased, and were highest in the group of children with impaired glucose tolerance. Glucose 101-108 insulin Homo sapiens 5-12 2535989-5 1989 Perifusion with glucose elicited a biphasic release of insulin, with the response rising sixfold from basal secretion. Glucose 16-23 insulin Homo sapiens 55-62 2566520-6 1989 A significant decrease was obtained for an insulin level of 11.9 +/- 0.4 mU.l-1, a value intermediate between those decreasing glycerol (10.1 +/- 0.7 mU.l-1) and stimulating total body glucose uptake (18.5 +/- 0.8 mU.l-1). Glucose 185-192 insulin Homo sapiens 43-50 2642847-3 1989 High glucose content (28.0 mM) stimulated the formation of abundant ICCs that contained decreased amounts of insulin. Glucose 5-12 insulin Homo sapiens 109-116 2642847-4 1989 In contrast, culture at a low (5.6-mM) glucose concentration increased the ICC insulin content but decreased the number of ICCs formed. Glucose 39-46 insulin Homo sapiens 79-86 2642865-3 1989 However, basal insulin levels and acute insulin responses to glucose were threefold greater in the recipients. Glucose 61-68 insulin Homo sapiens 40-47 2651186-0 1989 Determination and kinetic analysis of non-insulin mediated glucose uptake in type 1 (insulin-dependent) diabetes mellitus. Glucose 59-66 insulin Homo sapiens 42-49 2651186-1 1989 In man, total glucose uptake is the sum of insulin mediated glucose uptake and non-insulin mediated glucose uptake. Glucose 14-21 insulin Homo sapiens 43-50 2651186-1 1989 In man, total glucose uptake is the sum of insulin mediated glucose uptake and non-insulin mediated glucose uptake. Glucose 14-21 insulin Homo sapiens 83-90 2651186-1 1989 In man, total glucose uptake is the sum of insulin mediated glucose uptake and non-insulin mediated glucose uptake. Glucose 60-67 insulin Homo sapiens 43-50 2651186-1 1989 In man, total glucose uptake is the sum of insulin mediated glucose uptake and non-insulin mediated glucose uptake. Glucose 60-67 insulin Homo sapiens 43-50 2651186-3 1989 In order to assess non-insulin mediated glucose uptake in Type 1 diabetes, we measured steady-state rates of glucose uptake during glucose clamps at 5.27, 9.71 and 12.5 mmol/l using low (0.25 mU.kg-1.min-1), intermediate (0.75 mU.kg-1.min-1) and high (1.50 mU.kg-1.min-1) insulin infusion rates in 10 subjects with Type 1 diabetes. Glucose 40-47 insulin Homo sapiens 23-30 2651186-4 1989 For insulin infusion rates of 0.25, 0.75 and 1.50 mU.kg-1.min-1 as plasma glucose rose from 5.27 to 9.71 mmol/l, total glucose uptake increased by 35, 43 and 52 percent respectively (p less than 0.05 for each insulin infusion rate). Glucose 119-126 insulin Homo sapiens 4-11 2651186-6 1989 At each glycaemic level, glucose uptake correlated significantly with plasma free insulin (r = 0.81, p less than 0.01 at 5.71 mmol/l; r = 0.84, p less than 0.01 at 9.71 mmol/l; r = 0.73, p less than 0.02 at 12.5 mmol/l). Glucose 25-32 insulin Homo sapiens 82-89 2651186-7 1989 Linear regression analysis to a point corresponding to plasma free insulin equalling zero, yielded values for non-insulin mediated glucose uptake (mmol.kg-1.min-1) of 0.11, 0.14, 0.18 at plasma glucose of 5.27, 9.7 and 12.5 mmol/l respectively. Glucose 131-138 insulin Homo sapiens 67-74 2651186-7 1989 Linear regression analysis to a point corresponding to plasma free insulin equalling zero, yielded values for non-insulin mediated glucose uptake (mmol.kg-1.min-1) of 0.11, 0.14, 0.18 at plasma glucose of 5.27, 9.7 and 12.5 mmol/l respectively. Glucose 131-138 insulin Homo sapiens 114-121 2651186-7 1989 Linear regression analysis to a point corresponding to plasma free insulin equalling zero, yielded values for non-insulin mediated glucose uptake (mmol.kg-1.min-1) of 0.11, 0.14, 0.18 at plasma glucose of 5.27, 9.7 and 12.5 mmol/l respectively. Glucose 194-201 insulin Homo sapiens 67-74 2651186-7 1989 Linear regression analysis to a point corresponding to plasma free insulin equalling zero, yielded values for non-insulin mediated glucose uptake (mmol.kg-1.min-1) of 0.11, 0.14, 0.18 at plasma glucose of 5.27, 9.7 and 12.5 mmol/l respectively. Glucose 194-201 insulin Homo sapiens 114-121 2651186-8 1989 Thus, increasing plasma glucose concentrations were associated with increasing rates of non-insulin mediated glucose uptake. Glucose 24-31 insulin Homo sapiens 92-99 2651186-8 1989 Thus, increasing plasma glucose concentrations were associated with increasing rates of non-insulin mediated glucose uptake. Glucose 109-116 insulin Homo sapiens 92-99 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 58-65 insulin Homo sapiens 9-16 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 58-65 insulin Homo sapiens 94-101 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 58-65 insulin Homo sapiens 94-101 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 111-118 insulin Homo sapiens 9-16 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 111-118 insulin Homo sapiens 94-101 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 111-118 insulin Homo sapiens 94-101 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 111-118 insulin Homo sapiens 9-16 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 111-118 insulin Homo sapiens 94-101 2651186-9 1989 For each insulin infusion rate used, the percent of total glucose uptake accounted for by non-insulin mediated glucose uptake remained independent of plasma glucose concentration, but decreased as insulin infusion rate increased. Glucose 111-118 insulin Homo sapiens 94-101 2606730-2 1989 Reports have described an insulin suppressive effect of SMS 201-995 that results in elevations of blood glucose. Glucose 104-111 insulin Homo sapiens 26-33 2684699-4 1989 Insulin increased glucose 1,6-P2 from a basal value of 70 +/- 6 to 135 +/- 12 mumol/kg dry wt (P less than 0.001). Glucose 18-25 insulin Homo sapiens 0-7 2462571-7 1989 After oral glucose administration, the insulin concentration (423 +/- 72 pmol/L) was maximal 30 min after glucose treatment, and significant suppression of the IGF-BP concentration occurred at 90 min. Glucose 11-18 insulin Homo sapiens 39-46 2642485-7 1989 A significant positive correlation was found between the decreases in plasma testosterone levels and the decreases in glucose-stimulated insulin levels. Glucose 118-125 insulin Homo sapiens 137-144 2462571-7 1989 After oral glucose administration, the insulin concentration (423 +/- 72 pmol/L) was maximal 30 min after glucose treatment, and significant suppression of the IGF-BP concentration occurred at 90 min. Glucose 106-113 insulin Homo sapiens 39-46 2642485-8 1989 Moreover, the decreases in the waist to hip ratio correlated positively with the decreases in glucose-stimulated insulin levels and inversely with the decreases in plasma 17 beta-estradiol. Glucose 94-101 insulin Homo sapiens 113-120 2642489-3 1989 The plasma glucose targets were achieved by exogenous insulin and variable glucose infusions. Glucose 11-18 insulin Homo sapiens 54-61 2647909-2 1989 Confirming our previous studies and those of others, the present results show that the glucose infusion rate (DR), an estimate of in vivo insulin sensitivity, was significantly diminished in MyD. Glucose 87-94 insulin Homo sapiens 138-145 2646365-3 1989 The defect in insulin-mediated glucose disposal involves peripheral tissues, primarily muscle, and most likely reflects a disturbance in glycogen synthesis. Glucose 31-38 insulin Homo sapiens 14-21 2650692-4 1989 The glucose/insulin ratio is increased in fasting as well as after meals. Glucose 4-11 insulin Homo sapiens 12-19 2488384-5 1989 The technique was modified in order to inject intraperitoneally, 4 times per day, insulin to control blood glucose level in CAPD patients. Glucose 107-114 insulin Homo sapiens 82-89 2810441-2 1989 Despite resumption of oral intake on day 3, she required iv glucose for 6 days, during which time serum free insulin levels remained elevated. Glucose 60-67 insulin Homo sapiens 109-116 2810441-3 1989 Glucose requirements closely matched those calculated from published euglycemic clamp data on maximal glucose disposal rates during insulin infusion. Glucose 0-7 insulin Homo sapiens 132-139 2682604-5 1989 During the combination of Aminoplasmal + glucose, there was a small and only transient increase of plasma insulin levels that did not occur during Aminosteril + glucose. Glucose 41-48 insulin Homo sapiens 106-113 2658195-0 1989 [Elimination of the instability of blood glucose level as a measure of increasing the effectiveness of insulin therapy in insulin-dependent diabetes mellitus]. Glucose 41-48 insulin Homo sapiens 103-110 2677968-12 1989 In some individuals abnormal insulin response to glucose--loss of first phase insulin release during intravenous glucose tolerance test--precedes insulin deficiency. Glucose 49-56 insulin Homo sapiens 29-36 2677968-12 1989 In some individuals abnormal insulin response to glucose--loss of first phase insulin release during intravenous glucose tolerance test--precedes insulin deficiency. Glucose 49-56 insulin Homo sapiens 78-85 2677968-12 1989 In some individuals abnormal insulin response to glucose--loss of first phase insulin release during intravenous glucose tolerance test--precedes insulin deficiency. Glucose 113-120 insulin Homo sapiens 29-36 2677968-12 1989 In some individuals abnormal insulin response to glucose--loss of first phase insulin release during intravenous glucose tolerance test--precedes insulin deficiency. Glucose 113-120 insulin Homo sapiens 78-85 2643195-1 1989 The effects of insulin on glucose utilization were investigated in seven nonobese patients before and 24 hours after elective cholecystectomy. Glucose 26-33 insulin Homo sapiens 15-22 2643195-4 1989 In isolated fat cells after surgery there was a significant overall reduction of 35% to 50% of the effects of insulin on 3-0-methylglucose transport and lipogenesis at 1 mumol/L of glucose (where hexose transport is rate-limiting for insulin action). Glucose 131-138 insulin Homo sapiens 110-117 2643195-8 1989 It was concluded that an elective moderate surgical trauma induces a rapid and marked insulin resistance that is not the result of postoperative nutritional restriction and involves a postreceptor binding alteration of glucose transport. Glucose 219-226 insulin Homo sapiens 86-93 2750332-7 1989 The thermic effect of glucose or to meal ingestion is blunted in obese subjects with insulin resistance. Glucose 22-29 insulin Homo sapiens 85-92 2697952-3 1989 Euphylline (applied as an inhibitor of nucleotide phosphodiesterase), calcium gluconate and the adrenomimetic drug isadrin consistently increased insulinemia and the blood level of C-peptide in patients with chronic pancreatitis both with moderate and appreciable derangements of glucose tolerance. Glucose 280-287 insulin Homo sapiens 181-190 2692339-3 1989 Three types of insulin response to glucose load, similar to those in diabetes mellitus, have been revealed in the patients with psoriasis. Glucose 35-42 insulin Homo sapiens 15-22 2503912-3 1989 Serum insulin responses were low but appropriate to blood glucose in grade II and grade III PEM and were lower (p less than 0.001) in Grade IV PEM subjects. Glucose 58-65 insulin Homo sapiens 6-13 3059740-1 1988 A radioimmunoassay, using an antiserum that is specific for human proinsulin, has been used to study the response of serum proinsulin to low (25 g) and high (75 g) oral glucose loads in non-obese patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 169-176 insulin Homo sapiens 123-133 3059740-4 1988 Following 25 g and 75 g glucose loads, the rises in serum immunoreactive insulin and C-peptide concentrations in both groups of diabetic patients were impaired and delayed relative to those in the control subjects. Glucose 24-31 insulin Homo sapiens 73-80 3059816-0 1988 Rates and tissue sites of non-insulin- and insulin-mediated glucose uptake in humans. Glucose 60-67 insulin Homo sapiens 30-37 3059816-1 1988 In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Glucose 78-85 insulin Homo sapiens 61-68 3059816-1 1988 In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Glucose 78-85 insulin Homo sapiens 61-68 3059823-0 1988 Interaction of carnitine with insulin-stimulated glucose metabolism in humans. Glucose 49-56 insulin Homo sapiens 30-37 2849310-0 1988 Independent stimulation of glucose metabolism and Na+-K+ exchange by insulin in the human forearm. Glucose 27-34 insulin Homo sapiens 69-76 2849310-2 1988 To test whether insulin-induced glucose and potassium uptake are linked processes in vivo, we used the perfused forearm technique in healthy volunteers. Glucose 32-39 insulin Homo sapiens 16-23 2849310-4 1988 When an intra-arterial ouabain infusion (0.72 microgram.min-1.100 ml-1, producing local levels of approximately 0.5 mM) was superimposed on the insulin infusion, potassium uptake was blocked (0.026 +/- 0.190 ml.min-1.100 ml-1, P less than 0.02), and glucose uptake was decreased (to 3.31 +/- 0.34 mumol.min-1.100 ml-1, P less than 0.03). Glucose 250-257 insulin Homo sapiens 144-151 3057897-7 1988 A major component of cellular insulin resistance in NIDDM involves the glucose transport system. Glucose 71-78 insulin Homo sapiens 30-37 3057897-8 1988 Exposure of cells to insulin normally results in enhanced glucose transport mediated by translocation of glucose transporters from a low-density microsomal intracellular pool to the plasma membrane. Glucose 58-65 insulin Homo sapiens 21-28 2463830-0 1988 Inhibition by forskolin of insulin-stimulated glucose transport in L6 muscle cells. Glucose 46-53 insulin Homo sapiens 27-34 2972576-5 1988 The dose-response curves of insulin stimulation assessed by glucose incorporation and alpha-aminoisobutyric acid uptake showed normal responsiveness, and ED50 was significantly shifted to the right in fibroblasts from both patients. Glucose 60-67 insulin Homo sapiens 28-35 2972576-8 1988 These results indicate that 1) the defect is specific to the insulin-receptor binding in these patients, 2) insulin and IGF-I activate glucose incorporation and alpha-aminoisobutyric acid uptake mainly through their own specific receptors, but 3) the IGF-I receptor appears to have a more important role in stimulating thymidine incorporation than the insulin receptor in physiological condition or, alternatively, an unknown postreceptor process with cascade signal transmission may overcome the decreased insulin-receptor binding to produce a normal dose-response curve. Glucose 135-142 insulin Homo sapiens 61-68 2975568-0 1988 A mixed meal potentiates the insulin sensitivity of glucose transport and metabolism in adipocytes from patients with type 2 diabetes mellitus. Glucose 52-59 insulin Homo sapiens 29-36 2975568-1 1988 Post-glucose enhancement of insulin action may represent a physiological mechanism for the acute regulation of insulin sensitivity of target tissues. Glucose 5-12 insulin Homo sapiens 28-35 2975568-1 1988 Post-glucose enhancement of insulin action may represent a physiological mechanism for the acute regulation of insulin sensitivity of target tissues. Glucose 5-12 insulin Homo sapiens 111-118 2975568-4 1988 In the fasting state 6 patients had a significant response of glucose transport and lipogenesis to insulin whereas two exhibited non-responsiveness. Glucose 62-69 insulin Homo sapiens 99-106 2975568-5 1988 In the 6 responders insulin sensitivity, as estimated by the insulin concentration at which half-maximal effect was achieved, increased for glucose transport (before, 260 +/- 46 pmoll-1; after, 105 +/- 21 pmol l-1; p less than 0.05) and for lipogenesis (before, 36 +/- 9 pmol l-1; after, 9 +/- 2 pmol l-1; p less than 0.05). Glucose 140-147 insulin Homo sapiens 20-27 2975568-5 1988 In the 6 responders insulin sensitivity, as estimated by the insulin concentration at which half-maximal effect was achieved, increased for glucose transport (before, 260 +/- 46 pmoll-1; after, 105 +/- 21 pmol l-1; p less than 0.05) and for lipogenesis (before, 36 +/- 9 pmol l-1; after, 9 +/- 2 pmol l-1; p less than 0.05). Glucose 140-147 insulin Homo sapiens 61-68 2975568-7 1988 In the two primary non-responders intake of the meal was associated with average increase in maximal insulin responsiveness of 52% for glucose transport and 28% for lipogenesis. Glucose 135-142 insulin Homo sapiens 101-108 3142811-5 1988 The cirrhotic patients required less glucose to maintain the clamp in response to 0.1 unit per kg per hr insulin (6.7 +/- 0.5 vs. control 8.3 +/- 0.4 mg per kg per min, p less than 0.05) and deposited less glycogen in muscle during the clamp (8.6 +/- 0.5 vs. 12.0 +/- 1.4 mg per gm protein, p less than 0.05). Glucose 37-44 insulin Homo sapiens 105-112 3053747-8 1988 The mean plasma glucose concentrations were similar before both studies and rose to 9.5 and 8.6 mmol/L in the first 65 min during continuous and pulsatile insulin administration, respectively. Glucose 16-23 insulin Homo sapiens 155-162 3053747-11 1988 In the last 65 min the glucose infusion rate was significantly higher during pulsatile than during continuous insulin delivery. Glucose 23-30 insulin Homo sapiens 110-117 3053748-1 1988 The changes in peripheral serum insulin and plasma C-peptide levels and in the insulin secretory rate in response to iv glucose (0.5 g/kg BW) administration were studied in seven normal subjects. Glucose 120-127 insulin Homo sapiens 79-86 3053748-8 1988 In conclusion, after bolus iv glucose administration: 1) the insulin secretory rate is more closely represented by changes in peripheral serum insulin than in plasma C-peptide levels; and 2) no change in endogenous insulin clearance occurs. Glucose 30-37 insulin Homo sapiens 61-68 3053748-8 1988 In conclusion, after bolus iv glucose administration: 1) the insulin secretory rate is more closely represented by changes in peripheral serum insulin than in plasma C-peptide levels; and 2) no change in endogenous insulin clearance occurs. Glucose 30-37 insulin Homo sapiens 143-150 3053748-8 1988 In conclusion, after bolus iv glucose administration: 1) the insulin secretory rate is more closely represented by changes in peripheral serum insulin than in plasma C-peptide levels; and 2) no change in endogenous insulin clearance occurs. Glucose 30-37 insulin Homo sapiens 143-150 3053749-11 1988 We conclude that 1) insulin-mediated glucose uptake by forearm skeletal muscle is markedly impaired in type II diabetes and improves only marginally after 2 weeks of intensive insulin therapy; 2) in contrast, no appreciable abnormality in forearm FFA metabolism is demonstrable in insulin-treated type II diabetic patients; and 3) FFA do not contribute to the insulin-treated skeletal muscle insulin resistance that occurs in patients with type II diabetes mellitus. Glucose 37-44 insulin Homo sapiens 20-27 3054431-8 1988 With insulin, glucose tissue uptake was not influenced, but glucose oxidation expressed as percentage of glucose tissue uptake was normalized. Glucose 14-21 insulin Homo sapiens 5-12 3054432-1 1988 We previously have shown that ingested beef protein is just as potent as glucose in stimulating a rise in insulin concentration in type II diabetic patients. Glucose 73-80 insulin Homo sapiens 106-113 3054432-3 1988 Therefore, we considered it important to determine if other common dietary proteins also strongly stimulate an increase in insulin concentration when given with glucose. Glucose 161-168 insulin Homo sapiens 123-130 3054432-6 1988 Following ingestion of the meals containing protein, the plasma insulin concentration was increased further and remained elevated longer compared with the meal containing glucose alone. Glucose 171-178 insulin Homo sapiens 64-71 3054432-7 1988 The relative area under the insulin response curve was greatest following ingestion of the meal containing cottage cheese (360%) and was least with egg white (190%) compared with that following glucose alone (100%). Glucose 194-201 insulin Homo sapiens 28-35 3053082-5 1988 Thus intensified insulin treatment was shown to improve glucose metabolism, lower HDL-cholesterol and in this way improve the risk profile for macroangiopathy. Glucose 56-63 insulin Homo sapiens 17-24 2744929-6 1989 Insulin action was estimated by measurement of fasting blood glucose, insulin and free fatty acids (FFA) concentrations. Glucose 61-68 insulin Homo sapiens 0-7 3064631-7 1988 The plasma insulin and C-peptide responses to glucose were delayed in diabetic patients compared to controls but were not affected by ethanol. Glucose 46-53 insulin Homo sapiens 11-18 3064631-7 1988 The plasma insulin and C-peptide responses to glucose were delayed in diabetic patients compared to controls but were not affected by ethanol. Glucose 46-53 insulin Homo sapiens 23-32 3057941-0 1988 Hyperkalemic cardiac arrest after cardiac surgery following high-dose glucose-insulin-potassium infusion for inotropic support. Glucose 70-77 insulin Homo sapiens 78-85 3066348-3 1988 We found that AlCl3 has a partial insulin-like effect on glucose transport activity (3-O-methylglucose uptake, expressed as % of equilibrium value per 4 s: basal 9.6 +/- 2, AlCl3 29.6 +/- 4, insulin 74.0 +/- 3). Glucose 57-64 insulin Homo sapiens 34-41 3066348-10 1988 IN CONCLUSION: (1) the data show that AlCl3, probably through activation of a pertussis-toxin-inhibitable G protein, and PLC are able to modulate the intrinsic glucose carrier activity; (2) as pertussis toxin did not modify the effect of insulin, it seems unlikely that the insulin signal on glucose transport involves activation of this specific G protein. Glucose 160-167 insulin Homo sapiens 238-245 3066348-10 1988 IN CONCLUSION: (1) the data show that AlCl3, probably through activation of a pertussis-toxin-inhibitable G protein, and PLC are able to modulate the intrinsic glucose carrier activity; (2) as pertussis toxin did not modify the effect of insulin, it seems unlikely that the insulin signal on glucose transport involves activation of this specific G protein. Glucose 160-167 insulin Homo sapiens 274-281 3149465-0 1988 Insulin infusions in infants of birthweight less than 1250 g and with glucose intolerance. Glucose 70-77 insulin Homo sapiens 0-7 3149465-2 1988 During the insulin infusions there was a significant increase in both the mean energy intake (60.8 +/- 25.1 cal/kg per day to 79.9 +/- 24.5 cal/kg per day; P less than 0.001) and the mean amount of intravenous dextrose tolerated (7.0 +/- 2.7 mg/kg per min to 9.2 +/- 2.6 mg/kg per min; P less than 0.01). Glucose 210-218 insulin Homo sapiens 11-18 3149465-5 1988 We conclude that continuous insulin infusion is a safe and effective way of managing glucose intolerance in very low birthweight infants, provided adequate means for continuous monitoring of blood glucose are available. Glucose 85-92 insulin Homo sapiens 28-35 3056758-2 1988 Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. Glucose 33-40 insulin Homo sapiens 14-21 3056758-2 1988 Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. Glucose 101-108 insulin Homo sapiens 14-21 3056758-5 1988 The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Glucose 71-78 insulin Homo sapiens 25-32 3056758-5 1988 The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Glucose 71-78 insulin Homo sapiens 52-59 3056758-9 1988 Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Glucose 93-100 insulin Homo sapiens 74-81 3056761-5 1988 ICCs cultured for 7 days in the presence of GH secreted more insulin when incubated for 120 min in 20 mM than in 2 mM glucose (2.1-fold response, P less than .05), whereas ICCs maintained in basal medium did not respond to glucose. Glucose 118-125 insulin Homo sapiens 61-68 3067923-1 1988 We have assessed insulin action in five hyperthyroid patients, pre- and post-radioactive iodine therapy using oral glucose tolerance tests, monocyte insulin binding and dose response curves generated with the euglycemic clamp technique. Glucose 115-122 insulin Homo sapiens 17-24 3067923-8 1988 At maximum insulin concentrations the glucose disposal rate was enhanced in the thyrotoxic patients, 686 +/- 19 vs 567 +/- 26 mg/M2/min (p less than 0.01). Glucose 38-45 insulin Homo sapiens 11-18 3071486-0 1988 Impaired insulin-induced erythrocyte magnesium accumulation is correlated to impaired insulin-mediated glucose disposal in type 2 (non-insulin-dependent) diabetic patients. Glucose 103-110 insulin Homo sapiens 9-16 3071486-0 1988 Impaired insulin-induced erythrocyte magnesium accumulation is correlated to impaired insulin-mediated glucose disposal in type 2 (non-insulin-dependent) diabetic patients. Glucose 103-110 insulin Homo sapiens 86-93 3073092-2 1988 Numerous studies have shown that cyclo-oxygenase derivatives, mainly PGE2, reduce the insulin response to glucose whereas lipo-oxygenase derivatives, mainly 15-HPETE, stimulate insulin secretion. Glucose 106-113 insulin Homo sapiens 86-93 3073092-5 1988 Play in favor of this hypothesis the fact that the administration of PGE inhibits the insulin response to arginine in type-2 diabetics but not in normal subject and the fact that the administration of salicylates could improve the insulin response to glucose in some of these patients. Glucose 251-258 insulin Homo sapiens 231-238 3073905-0 1988 Repetitive stimulation of insulin secretion with arginine and glucose. Glucose 62-69 insulin Homo sapiens 26-33 3073905-1 1988 Glucose and arginine are both known to be potent insulin secretagogues and to potentiate each others insulin secretion. Glucose 0-7 insulin Homo sapiens 49-56 3073905-1 1988 Glucose and arginine are both known to be potent insulin secretagogues and to potentiate each others insulin secretion. Glucose 0-7 insulin Homo sapiens 101-108 3073905-2 1988 We investigated if repetitive infusion of arginine leads to comparable insulin secretion during fasting and if the additional infusion of glucose leads to a change in the pattern of the insulin secretion during repeated infusion of arginine. Glucose 138-145 insulin Homo sapiens 186-193 3056752-2 1988 Analysis of glucose disposal when compared with insulin concentration suggested insulin resistance as a factor in the causation of impaired glucose disposal. Glucose 12-19 insulin Homo sapiens 80-87 3147185-7 1988 The tissue sensitivity to insulin was similar in the two groups but glucose-stimulated insulin secretion was markedly impaired in homozygotes for the class 3 allele. Glucose 68-75 insulin Homo sapiens 87-94 3147185-9 1988 Similarly impaired in class 3/3 persons was the glucose + arginine-stimulated insulin secretion (P less than 0.05). Glucose 48-55 insulin Homo sapiens 78-85 3147186-5 1988 Glucose utilization and suppression of lipolysis were normally stimulated by insulin. Glucose 0-7 insulin Homo sapiens 77-84 3147186-7 1988 We conclude that insulin resistance involves mainly glucose rather than lipid and is selective at the hepatic level. Glucose 52-59 insulin Homo sapiens 17-24 3063707-0 1988 Plasma glucose and insulin responses to oral and intravenous glucose in cold-exposed humans. Glucose 61-68 insulin Homo sapiens 19-26 3068222-14 1988 These results support the hypothesis that the hyperglycemia observed during hyperammonemia may result from an under-utilization of glucose by insulin-sensitive tissues. Glucose 131-138 insulin Homo sapiens 142-149 3066814-1 1988 Insulin resistance in hyperthyroidism seems to depend on increased glucose production rather than on decreased glucose utilization. Glucose 67-74 insulin Homo sapiens 0-7 3066814-1 1988 Insulin resistance in hyperthyroidism seems to depend on increased glucose production rather than on decreased glucose utilization. Glucose 111-118 insulin Homo sapiens 0-7 3143744-6 1988 In vitro insulin-stimulated 2-deoxyglucose uptake was reduced by insulin and glucose infusion (25% stimulation before infusion, 5.4% at 3 h, and 0.85% at 6 h of infusion). Glucose 35-42 insulin Homo sapiens 9-16 3143744-6 1988 In vitro insulin-stimulated 2-deoxyglucose uptake was reduced by insulin and glucose infusion (25% stimulation before infusion, 5.4% at 3 h, and 0.85% at 6 h of infusion). Glucose 35-42 insulin Homo sapiens 65-72 3143744-10 1988 Rat adipocytes were preincubated with 1-10 mM glucose and 10 ng/ml insulin for 24 h. Measurements of 2-deoxyglucose uptake demonstrated insulin resistance in these cells. Glucose 46-53 insulin Homo sapiens 136-143 3071597-2 1988 The increase in insulin and other gut hormones induced by the glucose loading can be blocked by a synthetic long-acting somatostatin analogue. Glucose 62-69 insulin Homo sapiens 16-23 3060827-3 1988 Results from euglycemic glucose clamp study showed decreases in both insulin sensitivity and responsiveness. Glucose 24-31 insulin Homo sapiens 69-76 3060827-9 1988 The decrease in insulin responsiveness demonstrated in the glucose clamp study may result from a defect at the rate-limiting step in the postbinding process of insulin action, presumably a defect in the glucose transport system in muscle tissues. Glucose 59-66 insulin Homo sapiens 16-23 3060827-9 1988 The decrease in insulin responsiveness demonstrated in the glucose clamp study may result from a defect at the rate-limiting step in the postbinding process of insulin action, presumably a defect in the glucose transport system in muscle tissues. Glucose 203-210 insulin Homo sapiens 16-23 3068827-7 1988 Insulin and glucose infusion was followed by an increased leg uptake of glucose (from 0.15 +/- 0.14 to 1.06 +/- 0.16 mmol/min/100 ml, p less than 0.05), and by a changed splanchnic glucose balance (from -8.2 +/- 2.8 to +4.0 +/- 1.2 mmol/kg/min, p less than 0.01). Glucose 72-79 insulin Homo sapiens 0-7 3057892-1 1988 Patients with mild or early non-insulin-dependent diabetes mellitus often display a delay in insulin response followed by late hyperinsulinemia during oral glucose tolerance testing. Glucose 156-163 insulin Homo sapiens 32-39 3057893-4 1988 All three phospholipid effects of insulin also generate diacylglycerol, which activates protein kinase C, and this may contribute to insulin effects on glucose transport, ion and amino acid transport, protein synthesis, and gene expression (messenger RNA synthesis). Glucose 152-159 insulin Homo sapiens 34-41 3057893-4 1988 All three phospholipid effects of insulin also generate diacylglycerol, which activates protein kinase C, and this may contribute to insulin effects on glucose transport, ion and amino acid transport, protein synthesis, and gene expression (messenger RNA synthesis). Glucose 152-159 insulin Homo sapiens 133-140 3057894-7 1988 The efficiency of glucose uptake by the peripheral tissues is also impaired due to a combination of decreased insulin secretion and defective cellular insulin action. Glucose 18-25 insulin Homo sapiens 110-117 3054549-7 1988 The differences in insulin sums according to family history remained statistically significant in analyses of covariance, which controlled for variations in body-mass index, body-fat distribution, and level of blood glucose. Glucose 216-223 insulin Homo sapiens 19-26 3146971-7 1988 In addition to that of [2-3H]glycerol, insulin increased [U-14C]glucose and [1,2,3-3H]glycerol incorporation into DAG and other glycerolipids. Glucose 64-71 insulin Homo sapiens 39-46 3145064-11 1988 The hypoglycaemic response to insulin analogue was a plasma glucose nadir at 60 minutes with both doses compared with 90 and 120 minutes with soluble insulin at 0.5 and 0.1 U/kg respectively. Glucose 60-67 insulin Homo sapiens 30-37 3060188-8 1988 Diabetes was three times more common in Bangladeshis than in Europeans and serum insulin concentrations measured after a glucose load were twice as high in Bangladeshis. Glucose 121-128 insulin Homo sapiens 81-88 3069398-3 1988 The observations of simultaneously low fasting blood glucose and plasma-insulin levels in anorectic patients could suggest increased insulin sensitivity in AN. Glucose 53-60 insulin Homo sapiens 133-140 3069398-5 1988 During an oral glucose-tolerance test, an impaired glucose-tolerance occurring despite sustained insulin response to glucose is usually found in anorectic patients before treatment; these abnormalities are, at least partially, reversed after successful refeeding. Glucose 15-22 insulin Homo sapiens 97-104 3069398-9 1988 This seemed to occur despite a relative increase in insulin response to glucose, which again may be related to insulin resistance in these undernourished subjects. Glucose 72-79 insulin Homo sapiens 52-59 3069398-9 1988 This seemed to occur despite a relative increase in insulin response to glucose, which again may be related to insulin resistance in these undernourished subjects. Glucose 72-79 insulin Homo sapiens 111-118 3069398-12 1988 Only the recently developed minimal model method allows us to discriminate between changes in insulin secretion and action after intravenous glucose injection and thus to infer accurately the sensitivity of the tissues to insulin. Glucose 141-148 insulin Homo sapiens 94-101 3069528-5 1988 With refrigerated insulin, the plasma free insulin peak was greater (53 +/- 5 versus 45 +/- 6 mU/l) and occurred earlier (2.5 +/- 0.2 versus 6 +/- 0.3 h), and the glucose infusion rate showed a greater (16.5 +/- 1.2 versus 14.5 +/- 0.9 mumol.kg-1.min-1) and earlier peak (3.2 +/- 0.2 versus 6 +/- 0.4 h) as compared to that occurring with the non-refrigerated insulin (p less than 0.05). Glucose 163-170 insulin Homo sapiens 18-25 3069528-5 1988 With refrigerated insulin, the plasma free insulin peak was greater (53 +/- 5 versus 45 +/- 6 mU/l) and occurred earlier (2.5 +/- 0.2 versus 6 +/- 0.3 h), and the glucose infusion rate showed a greater (16.5 +/- 1.2 versus 14.5 +/- 0.9 mumol.kg-1.min-1) and earlier peak (3.2 +/- 0.2 versus 6 +/- 0.4 h) as compared to that occurring with the non-refrigerated insulin (p less than 0.05). Glucose 163-170 insulin Homo sapiens 43-50 3141236-0 1988 Metabolic effects of low-dose insulin therapy on glucose metabolism in diabetic ketoacidosis. Glucose 49-56 insulin Homo sapiens 30-37 3141236-1 1988 The effect of low-dose insulin treatment (5-10 U/h) on hepatic glucose production (HGP) and peripheral glucose disposal was determined in 5 insulin-dependent diabetes mellitus (IDDM) subjects who were admitted with diabetic ketoacidosis (DKA; plasma glucose 598 +/- 50 mg/dl, blood pH 7.20 +/- 0.06, plasma bicarbonate 12 +/- 2 meq/L). Glucose 63-70 insulin Homo sapiens 23-30 3141236-3 1988 After the institution of insulin therapy (1 mU.kg-1.min-1), the plasma glucose concentration fell at the rate of 60 +/- 5 mg.dl-1.h-1 to reach a value of 220 +/- 10 mg/dl, which was maintained constant for 2 h (insulin-clamp technique). Glucose 71-78 insulin Homo sapiens 25-32 3141236-3 1988 After the institution of insulin therapy (1 mU.kg-1.min-1), the plasma glucose concentration fell at the rate of 60 +/- 5 mg.dl-1.h-1 to reach a value of 220 +/- 10 mg/dl, which was maintained constant for 2 h (insulin-clamp technique). Glucose 71-78 insulin Homo sapiens 211-218 3141236-5 1988 The decline in plasma glucose concentration during insulin therapy primarily resulted from a suppression of HGP (from 4.3 +/- 0.5 to 1.7 +/- 0.2 mg.kg-1.min-1, P less than .01) and to a lesser extent from the stimulation of tissue glucose disposal (1.7 +/- 0.2 to 2.6 +/- 0.3 mg.kg-1.min-1, P less than .01). Glucose 22-29 insulin Homo sapiens 51-58 3141236-5 1988 The decline in plasma glucose concentration during insulin therapy primarily resulted from a suppression of HGP (from 4.3 +/- 0.5 to 1.7 +/- 0.2 mg.kg-1.min-1, P less than .01) and to a lesser extent from the stimulation of tissue glucose disposal (1.7 +/- 0.2 to 2.6 +/- 0.3 mg.kg-1.min-1, P less than .01). Glucose 231-238 insulin Homo sapiens 51-58 2846655-7 1988 These data suggest that the decreased insulin-stimulated glucose disposal and reduced glycogen synthase activation observed in insulin resistance could be secondary to a low fasting glycogen synthase phosphatase activity. Glucose 57-64 insulin Homo sapiens 38-45 3059816-0 1988 Rates and tissue sites of non-insulin- and insulin-mediated glucose uptake in humans. Glucose 60-67 insulin Homo sapiens 43-50 3059816-1 1988 In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Glucose 8-15 insulin Homo sapiens 61-68 3059816-1 1988 In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Glucose 8-15 insulin Homo sapiens 108-115 3050530-2 1988 In type 2 (non-insulin-dependent) diabetes mellitus, it is insulin-resistance in skeletal muscle, the chief site of insulin-mediated glucose disposal in humans, that predominantly accounts for the low rates of glucose clearance from the blood, and hence for impaired glucose tolerance. Glucose 133-140 insulin Homo sapiens 59-66 3050530-2 1988 In type 2 (non-insulin-dependent) diabetes mellitus, it is insulin-resistance in skeletal muscle, the chief site of insulin-mediated glucose disposal in humans, that predominantly accounts for the low rates of glucose clearance from the blood, and hence for impaired glucose tolerance. Glucose 133-140 insulin Homo sapiens 59-66 3050530-2 1988 In type 2 (non-insulin-dependent) diabetes mellitus, it is insulin-resistance in skeletal muscle, the chief site of insulin-mediated glucose disposal in humans, that predominantly accounts for the low rates of glucose clearance from the blood, and hence for impaired glucose tolerance. Glucose 210-217 insulin Homo sapiens 59-66 3050530-2 1988 In type 2 (non-insulin-dependent) diabetes mellitus, it is insulin-resistance in skeletal muscle, the chief site of insulin-mediated glucose disposal in humans, that predominantly accounts for the low rates of glucose clearance from the blood, and hence for impaired glucose tolerance. Glucose 210-217 insulin Homo sapiens 59-66 2902721-1 1988 The effect of hyperglycemia on insulin-induced glucose metabolism (M) was investigated in healthy subjects using sequential clamp protocols at constant insulin + somatostatin infusions and varying plasma glucose. Glucose 47-54 insulin Homo sapiens 31-38 2902721-3 1988 At increasing glucose (6.7 mmol/l), M further increased (9.7 to 19.2 mg.kg-1.min-1) with the plasma insulin level (0.41 to 2.99 nmol/l). Glucose 14-21 insulin Homo sapiens 100-107 2902721-4 1988 At a plasma glucose level of 9.8 mmol/l insulin (0.42 to 3.17 nmol/l) was still effective to increase M (13.7 to 25.2 mg.kg-1.min-1). Glucose 12-19 insulin Homo sapiens 40-47 2907708-4 1988 Supplementation with 3 U insulin for only one week reduced both gamma GT and glucose levels. Glucose 77-84 insulin Homo sapiens 25-32 3176815-0 1988 Characterization of the insulin resistance of glucose utilization in adipocytes from patients with hyper- and hypothyroidism. Glucose 46-53 insulin Homo sapiens 24-31 3176815-1 1988 UNLABELLED: Insulin action on glucose utilization was characterized in adipocytes from 10 thyrotoxic patients, 6 hypothyroid patients and 10 age- and sex-matched control subjects. Glucose 30-37 insulin Homo sapiens 12-19 3176815-2 1988 In thyrotoxic patients insulin binding at low insulin concentrations was reduced (P less than 0.05) and accompanied by impaired insulin sensitivity of glucose transport (P less than 0.02), glucose oxidation (P less than 0.05) and lipogenesis (P less than 0.05). Glucose 151-158 insulin Homo sapiens 23-30 3176815-6 1988 IN CONCLUSION: In man, both hyper- and hypothyroidism are characterized by insulin resistance of adipocyte glucose utilization localized to insulin binding as well as to insulin-stimulated glucose transport and metabolism. Glucose 107-114 insulin Homo sapiens 75-82 3176815-6 1988 IN CONCLUSION: In man, both hyper- and hypothyroidism are characterized by insulin resistance of adipocyte glucose utilization localized to insulin binding as well as to insulin-stimulated glucose transport and metabolism. Glucose 107-114 insulin Homo sapiens 140-147 3176815-6 1988 IN CONCLUSION: In man, both hyper- and hypothyroidism are characterized by insulin resistance of adipocyte glucose utilization localized to insulin binding as well as to insulin-stimulated glucose transport and metabolism. Glucose 107-114 insulin Homo sapiens 140-147 3052050-8 1988 On the other hand, insulin in glucose, 5 mU/kg/minute intravenously, effectively lowered plasma potassium levels from 5.62 to 4.70 mmol/liter, and hemodialysis induced the most rapid decline from 5.63 to 4.29 mmol/liter. Glucose 30-37 insulin Homo sapiens 19-26 3052050-11 1988 CONCLUSION: We conclude that in patients with terminal renal failure undergoing maintenance hemodialysis, intravenous bicarbonate is ineffective in lowering plasma potassium rapidly, and epinephrine is effective in only half the patients, whereas insulin in glucose is a fast and reliable form of therapy for hyperkalemic emergencies. Glucose 258-265 insulin Homo sapiens 247-254 2975551-3 1988 Insulin action was measured as the amount of glucose infused. Glucose 45-52 insulin Homo sapiens 0-7 2975551-9 1988 We conclude that when glucose concentrations are maintained by euglycaemic clamps the peak of unmodified insulin action is later and the duration longer than traditionally recognized, insulin AUC does not predict insulin action, and the higher variability of insulin action compared with the indices of absorption suggests that day-to-day changes in tissue insulin sensitivity contribute more to the variability in insulin action than changes in absorption. Glucose 22-29 insulin Homo sapiens 105-112 3046967-3 1988 Insulin secretion rates were calculated during a 1-h baseline period and during 3 h of glucose clamping from a two-compartmental analysis of peripheral C-peptide concentrations with individual kinetic parameters derived after intravenous bolus injections of biosynthetic human C-peptide. Glucose 87-94 insulin Homo sapiens 0-7 3046967-8 1988 In conclusion, a reduction in endogenous insulin clearance occurs during greater stimulation of insulin secretion at higher glucose-clamp levels. Glucose 124-131 insulin Homo sapiens 41-48 3047161-4 1988 At 13-15 weeks, glucose and arginine enhanced insulin release in some experiments, whereas glucagon and theophylline were always potent stimuli (mean response, 4-fold regardless of the glucose concentration). Glucose 16-23 insulin Homo sapiens 46-53 3047161-5 1988 At 17-22 weeks, both glucose alone (20 mmol/L) and arginine (10 mmol/L, with 2 mmol/L glucose) induced a small (1.4- to 1.5-fold) increase in insulin release. Glucose 21-28 insulin Homo sapiens 142-149 3047161-5 1988 At 17-22 weeks, both glucose alone (20 mmol/L) and arginine (10 mmol/L, with 2 mmol/L glucose) induced a small (1.4- to 1.5-fold) increase in insulin release. Glucose 86-93 insulin Homo sapiens 142-149 3047162-1 1988 The dose-response relationships between portal venous insulin concentrations and hepatic glucose production and between peripheral insulin concentrations and peripheral glucose utilization were determined in 8 nonobese and 17 obese premenopausal women with either upper or lower body fat localization. Glucose 89-96 insulin Homo sapiens 54-61 3047162-6 1988 The insulin concentrations that had half-maximal effects on glucose production and utilization were similar in each group. Glucose 60-67 insulin Homo sapiens 4-11 3047162-10 1988 The marked peripheral insulin resistance in the former group may account for the increased prevalence of glucose intolerance. Glucose 105-112 insulin Homo sapiens 22-29 3170749-4 1988 Peripheral insulin action was also assessed in vivo by glucose disposal rates (GDR) measured during a hyperinsulinemic (300 mU/M2 per min) euglycemic clamp. Glucose 55-62 insulin Homo sapiens 11-18 3050370-8 1988 No relationship was observed between insulin-mediated glucose uptake and total cholesterol, low density lipoprotein (LDL)-cholesterol, and HDL-cholesterol values. Glucose 54-61 insulin Homo sapiens 37-44 3052595-0 1988 Insulin regulation of glucose metabolism in HT29 colonic adenocarcinoma cells: activation of glycolysis without augmentation of glucose transport. Glucose 22-29 insulin Homo sapiens 0-7 3052595-1 1988 The effects of insulin on glucose transport and metabolism were examined in cultured HT29 human colonic adenocarcinoma cells. Glucose 26-33 insulin Homo sapiens 15-22 3052595-6 1988 Glucose consumption increased from 0.33 +/- 0.03 mumol/mg protein per h to 0.49 +/- 0.05 mumol/mg protein per h and lactate production was augmented from 0.67 +/- 0.04 mumol/mg protein per h to 0.87 +/- 0.06 mumol/mg protein per h in response to 10(-7) to 10(-5) M insulin. Glucose 0-7 insulin Homo sapiens 265-272 3051005-6 1988 In skeletal muscle exposed to 120 nM amylin for 1 hr, there was a marked decrease in both basal and submaximally insulin-stimulated rates of glycogen synthesis, which resulted in significant reduction in the rates of insulin-stimulated glucose uptake. Glucose 236-243 insulin Homo sapiens 217-224 2458350-13 1988 Our results support the hypothesis that turnover of the phosphoryl group of pp15, a product of insulin receptor tyrosine kinase action, is coupled to signal transmission to the glucose transport system. Glucose 177-184 insulin Homo sapiens 95-102 2852514-11 1988 With once daily insulin mean concentrations of fasting plasma glucose fell from 12.6 to 7.6 mmol/l (p less than 0.001) and haemoglobin A1 from 14.6% to 11.2% (p less than 0.001). Glucose 62-69 insulin Homo sapiens 16-23 3048098-0 1988 Gestational diabetes reverses the circadian variation of plasma insulin response to intravenous glucose. Glucose 96-103 insulin Homo sapiens 64-71 3065016-1 1988 Evaluation of free insulin levels and insulin action on glucose metabolism after combined and separate subcutaneous administration. Glucose 56-63 insulin Homo sapiens 38-45 3065017-5 1988 Insulin was delivered at an average rate of 2.1 +/- 5.2 U/h and controlled the serum glucose levels within a range of 132 +/- 32 mg/dl. Glucose 85-92 insulin Homo sapiens 0-7 3064959-0 1988 Meticulous glucose control in diabetic persons using insulin. Glucose 11-18 insulin Homo sapiens 53-60 3064959-1 1988 The one advantage a physician has in designing a regimen to control glucose values in a patient with IDDM is that the physiologic mechanism underlying IDDM is homogeneous: All patients are deficient in insulin and tend to be responsive to physiologic amounts of exogenous insulin. Glucose 68-75 insulin Homo sapiens 202-209 2457529-11 1988 These results suggest that insulin resistance in this patient was due to a circulating factor of low molecular weight that uncoupled insulin stimulation of glucose transport from receptor binding and phosphorylation. Glucose 156-163 insulin Homo sapiens 27-34 2457529-11 1988 These results suggest that insulin resistance in this patient was due to a circulating factor of low molecular weight that uncoupled insulin stimulation of glucose transport from receptor binding and phosphorylation. Glucose 156-163 insulin Homo sapiens 133-140 3064959-9 1988 For most diabetic persons who administer insulin, split, mixed doses given several times throughout the day allow the patient to use a lower total dose and minimize risk of hypoglycemia while improving the potential for glucose control. Glucose 220-227 insulin Homo sapiens 41-48 2457530-6 1988 When challenged for 30 min with 16.7 mM glucose, 1 mM 3-isobutyl-1-methylxanthine, 4 mM tolbutamide, or 10(-6) M glucagon, insulinoma cells responded by a 1.5-, 1.5-, 2-, or 3-fold increase, respectively, in insulin release above baseline levels. Glucose 40-47 insulin Homo sapiens 123-130 2970411-0 1988 Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. Glucose 91-98 insulin Homo sapiens 53-60 2970411-4 1988 Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). Glucose 73-80 insulin Homo sapiens 6-13 2970411-4 1988 Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). Glucose 73-80 insulin Homo sapiens 18-27 2970411-5 1988 This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. Glucose 63-70 insulin Homo sapiens 126-133 3044887-0 1988 Inhibition of insulin-stimulated glucose transport by factor extracted from serum of insulin-resistant patient. Glucose 33-40 insulin Homo sapiens 14-21 3044887-0 1988 Inhibition of insulin-stimulated glucose transport by factor extracted from serum of insulin-resistant patient. Glucose 33-40 insulin Homo sapiens 85-92 3044887-6 1988 The factor also inhibited stimulation of glucose transport in adipocytes by the insulin mimickers hydrogen peroxide and sodium vanadate. Glucose 41-48 insulin Homo sapiens 80-87 3044887-7 1988 In vitro incubation of rat soleus muscles in the presence of the factor resulted in inhibition of insulin-stimulated glucose transport. Glucose 117-124 insulin Homo sapiens 98-105 3044892-2 1988 Insulin action was measured in 10 nondiabetic and 8 diabetic patients with hypertriglyceridemia (fasting plasma triglyceride 800 +/- 154 and 1105 +/- 445 mg/dl, respectively, P NS; fasting plasma glucose 99 +/- 3 and 161 +/- 12 mg/dl, respectively, P less than .001) and in 8 weight-matched normolipemic nondiabetic individuals (fasting plasma triglyceride and glucose 110 +/- 21 and 91 +/- 3 mg/dl). Glucose 196-203 insulin Homo sapiens 0-7 3044892-2 1988 Insulin action was measured in 10 nondiabetic and 8 diabetic patients with hypertriglyceridemia (fasting plasma triglyceride 800 +/- 154 and 1105 +/- 445 mg/dl, respectively, P NS; fasting plasma glucose 99 +/- 3 and 161 +/- 12 mg/dl, respectively, P less than .001) and in 8 weight-matched normolipemic nondiabetic individuals (fasting plasma triglyceride and glucose 110 +/- 21 and 91 +/- 3 mg/dl). Glucose 361-368 insulin Homo sapiens 0-7 3044892-4 1988 Insulin stimulation of glucose uptake in vivo during intravenous hyperinsulinemic clamp and in vitro in adipocytes were measures of insulin"s glucoregulatory action. Glucose 23-30 insulin Homo sapiens 0-7 3044892-4 1988 Insulin stimulation of glucose uptake in vivo during intravenous hyperinsulinemic clamp and in vitro in adipocytes were measures of insulin"s glucoregulatory action. Glucose 23-30 insulin Homo sapiens 70-77 3065002-6 1988 Glucose recovery from the nadir was impaired in diabetic subjects compared with control subjects and correlated inversely with free-insulin levels. Glucose 0-7 insulin Homo sapiens 132-139 3071442-2 1988 After starting insulin treatment, fasting blood glucose decreased from 12.9 +/- 0.5 mmol/l (mean +/- SEM) to 9.8 +/- 1.2 mmol/l (p = 0.03), but the decrease of glycosylated haemoglobin Alc was not significant (9.0 +/- 0.4% vs. 8.3 +/- 0.6%). Glucose 48-55 insulin Homo sapiens 15-22 3143656-5 1988 When insulin resistance was overcome, plasma glucose continued to fall despite witholding insulin and late hypoglycaemia occurred in three episodes. Glucose 45-52 insulin Homo sapiens 5-12 2842361-7 1988 The insulinoma patients had increased plasma insulin and C-peptide responses to glucagon despite having low blood glucose levels. Glucose 114-121 insulin Homo sapiens 4-11 3045145-5 1988 From 30 min before to 60 min after the glucose nadir the [125I]insulin absorption rate was depressed compared to that during normoglycemia. Glucose 39-46 insulin Homo sapiens 63-70 3047522-0 1988 First-phase insulin response to glucose in nonobese or obese subjects with glucose intolerance: analysis by C-peptide secretion rate. Glucose 32-39 insulin Homo sapiens 12-19 3047522-0 1988 First-phase insulin response to glucose in nonobese or obese subjects with glucose intolerance: analysis by C-peptide secretion rate. Glucose 75-82 insulin Homo sapiens 12-19 3047522-1 1988 This study was proposed to clarify the impairment of first-phase insulin response to glucose in subjects with glucose intolerance by analysis of C-peptide secretion rate after glucose or glucagon injection. Glucose 85-92 insulin Homo sapiens 65-72 3047522-1 1988 This study was proposed to clarify the impairment of first-phase insulin response to glucose in subjects with glucose intolerance by analysis of C-peptide secretion rate after glucose or glucagon injection. Glucose 110-117 insulin Homo sapiens 65-72 3047522-1 1988 This study was proposed to clarify the impairment of first-phase insulin response to glucose in subjects with glucose intolerance by analysis of C-peptide secretion rate after glucose or glucagon injection. Glucose 110-117 insulin Homo sapiens 65-72 3047522-11 1988 This study provides the precise time course of first- and second-phase insulin response to glucose injection in nonobese and obese subjects with IGT or NIDDM as well as convincing evidence of the progressive reduction of first-phase insulin response with increasing severity of glucose intolerance. Glucose 91-98 insulin Homo sapiens 71-78 3047522-11 1988 This study provides the precise time course of first- and second-phase insulin response to glucose injection in nonobese and obese subjects with IGT or NIDDM as well as convincing evidence of the progressive reduction of first-phase insulin response with increasing severity of glucose intolerance. Glucose 278-285 insulin Homo sapiens 233-240 3047522-12 1988 First-phase insulin response to glucose might be slightly delayed in some obese subjects with NIDDM. Glucose 32-39 insulin Homo sapiens 12-19 3047523-7 1988 Minimal model analysis revealed a corresponding 35% decrease in insulin sensitivity (SI 4.85 +/- 1.51 v 7.28 +/- 1.16 min-1 microU-1 mL-1 x 10(4), P less than .05) but no significant differences between glucose-mediated glucose disposal or pancreatic B-cell responsiveness. Glucose 203-210 insulin Homo sapiens 64-71 3047523-7 1988 Minimal model analysis revealed a corresponding 35% decrease in insulin sensitivity (SI 4.85 +/- 1.51 v 7.28 +/- 1.16 min-1 microU-1 mL-1 x 10(4), P less than .05) but no significant differences between glucose-mediated glucose disposal or pancreatic B-cell responsiveness. Glucose 220-227 insulin Homo sapiens 64-71 3047523-8 1988 The glucose disposition index (si* phi2), a direct measure of an individual"s overall insulin- mediated glucose disposal, was reduced by 70% in the NE-infussed subjects (si* phi2 69 +/-22 v 223 +/- 76 mg-1 ml-1 min-3 x 10(2), p< .05). Glucose 4-11 insulin Homo sapiens 86-93 3047523-8 1988 The glucose disposition index (si* phi2), a direct measure of an individual"s overall insulin- mediated glucose disposal, was reduced by 70% in the NE-infussed subjects (si* phi2 69 +/-22 v 223 +/- 76 mg-1 ml-1 min-3 x 10(2), p< .05). Glucose 104-111 insulin Homo sapiens 86-93 3047525-5 1988 The in vitro stimulatory effect of insulin on [14C]glucose oxidation by parametrial adipose tissue was unchanged at three hours but suppressed six hours following administration of RCM-hGH. Glucose 51-58 insulin Homo sapiens 35-42 3047525-6 1988 When the plasma insulin level of ob/ob mice was increased threefold by the administration of neutral protamine Hagedorn (NPH) insulin, the in vitro stimulatory effect of insulin on [14C]glucose oxidation by adipose tissue isolated from these animals was not altered, suggesting that insulin-induced receptor or postreceptor changes do not account for the increased insulin resistance produced by RCM-hGH. Glucose 186-193 insulin Homo sapiens 16-23 3419322-1 1988 In order to verify whether intersite differences exist in glucose metabolism of subcutaneous human adipose tissue, basal and insulin-stimulated 14C-1-glucose incorporation into triglycerides and the activities of some enzymes of glucose disposal were tested in abdominal and gluteal adipose tissue of 31 nondiabetic obese otherwise healthy women during isocaloric diet and after 2 weeks of very-low-calorie-protein-sparing modified diet. Glucose 150-157 insulin Homo sapiens 125-132 3419426-12 1988 Because glucokinase can couple changes in the blood glucose concentration to changes in the glycolytic flux rate and corresponding changes in the rate of insulin secretion, it may function as a glucose signal recognition enzyme in the pancreatic B cell. Glucose 194-201 insulin Homo sapiens 154-161 3067075-9 1988 Because of increased insulin requirement and decreased endogenous insulin production, the administration of large amount of glucose immediately after operation should be undertaken carefully. Glucose 124-131 insulin Homo sapiens 21-28 3067075-9 1988 Because of increased insulin requirement and decreased endogenous insulin production, the administration of large amount of glucose immediately after operation should be undertaken carefully. Glucose 124-131 insulin Homo sapiens 66-73 3050268-4 1988 After glucose ingestion, the incremental areas under the two hour plasma glucose and insulin curves were significantly smaller during ingestion of the high NaCl diet (glucose p less than 0.005 and insulin p less than 0.025). Glucose 6-13 insulin Homo sapiens 85-92 2970226-1 1988 Insulin and insulin-like growth factor I (IGF-I) stimulate glucose transport in skeletal muscle through separate receptors. Glucose 59-66 insulin Homo sapiens 0-7 2970227-3 1988 Insulin secretion is greater from the alpha- than from the beta-anomer when the D-glucose level is below 22 mM. Glucose 80-89 insulin Homo sapiens 0-7 3044137-5 1988 We conclude that T4 treatment promotes glucose disposal and oxidation, T3 decreases noninsulin-mediated glucose storage but does not antagonize insulin action. Glucose 104-111 insulin Homo sapiens 87-94 2906021-2 1988 The blood glucose level during a somatostatin (100 micrograms/h)-insulin (0.4 mU.kg-1.min-1)-glucose (4.5 mg.kg-1.min-1)-infusion-test performed between 10.30 and 14.30 hours served as an indicator of the total body insulin resistance. Glucose 10-17 insulin Homo sapiens 65-72 3050363-4 1988 Plasma C-peptide responses were lower in the athletes, both fasting (geometric mean 0.28 v 0.62 nmol/L, P less than .05), and at the end of all clamps (at 7.5, 10, and 15 mmol/L plasma glucose, respectively, 0.65 v 1.43, 1.25 v 2.85, and 2.40 v 4.46 nmol/L each, P less than .05). Glucose 185-192 insulin Homo sapiens 7-16 3050363-8 1988 The attenuation of beta-cell responsiveness over a wide glucose range may be an adaptation to the enhanced peripheral insulin sensitivity seen in athletes. Glucose 56-63 insulin Homo sapiens 118-125 3061759-10 1988 The role of glycogen synthase is most notable at supraphysiological plasma insulin concentrations; and since glucose uptake at these insulin concentrations is highly familial independent of the degree of obesity, we suggest that there may be a specific genetic defect expressed in skeletal muscle that reduces insulin responsiveness in some subjects. Glucose 109-116 insulin Homo sapiens 133-140 3061759-10 1988 The role of glycogen synthase is most notable at supraphysiological plasma insulin concentrations; and since glucose uptake at these insulin concentrations is highly familial independent of the degree of obesity, we suggest that there may be a specific genetic defect expressed in skeletal muscle that reduces insulin responsiveness in some subjects. Glucose 109-116 insulin Homo sapiens 133-140 3065112-8 1988 In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Glucose 116-123 insulin Homo sapiens 88-95 3065113-3 1988 The low acute insulin response to intravenous glucose has been proposed as a marker of both pre-Type 1 and pre-Type 2 (non-insulin-dependent) diabetes. Glucose 46-53 insulin Homo sapiens 14-21 3065113-3 1988 The low acute insulin response to intravenous glucose has been proposed as a marker of both pre-Type 1 and pre-Type 2 (non-insulin-dependent) diabetes. Glucose 46-53 insulin Homo sapiens 123-130 3065113-5 1988 The low acute insulin response was defined by a peak insulin value (sum of plasma insulin at 2 and 5 min after glucose load, 0.3 g/kg body weight) below 50 microU/ml. Glucose 111-118 insulin Homo sapiens 14-21 3065113-10 1988 In conclusion, low acute insulin response to glucose is a sensitive but non-specific marker of early stages of Type 1 diabetes as this anomaly is shared by both Type 2 and Type 1 diabetes. Glucose 45-52 insulin Homo sapiens 25-32 3075183-0 1988 Plasma glucose response after intravenous injection of tolbutamide in insulin-treated type I and type II diabetic patients. Glucose 7-14 insulin Homo sapiens 70-77 3075183-5 1988 Both serum C-peptide and plasma glucose after tolbutamide load responded differently between Type I and Type II diabetics on insulin therapy, and it was thought that tolbutamide load-glucose response test may be a useful method to estimate the residual beta-cell function in the diabetics. Glucose 32-39 insulin Homo sapiens 125-132 3075183-5 1988 Both serum C-peptide and plasma glucose after tolbutamide load responded differently between Type I and Type II diabetics on insulin therapy, and it was thought that tolbutamide load-glucose response test may be a useful method to estimate the residual beta-cell function in the diabetics. Glucose 183-190 insulin Homo sapiens 11-20 3075183-5 1988 Both serum C-peptide and plasma glucose after tolbutamide load responded differently between Type I and Type II diabetics on insulin therapy, and it was thought that tolbutamide load-glucose response test may be a useful method to estimate the residual beta-cell function in the diabetics. Glucose 183-190 insulin Homo sapiens 125-132 3135175-2 1988 The current study assessed whether a peptide representing this deleted region could enhance insulin-stimulated glucose uptake in the intact rat and if this effect was localized in liver and/or muscle. Glucose 111-118 insulin Homo sapiens 92-99 3135175-5 1988 Glucose was infused alone and with two rates of infusion of insulin. Glucose 0-7 insulin Homo sapiens 60-67 3135175-8 1988 Basal glucose release from the liver was suppressed by both hGH-(32-46) and insulin alone, and this decrease was not enhanced by combining insulin with hGH-(32-46). Glucose 6-13 insulin Homo sapiens 76-83 3135175-12 1988 These findings suggest that GH peptides independently suppress glucose outflow from the liver and potentiate insulin action by facilitating glucose uptake by peripheral tissues. Glucose 140-147 insulin Homo sapiens 109-116 3293980-0 1988 Effects of human growth hormone on insulin-stimulated glucose metabolism in 3T3-F442A adipocytes. Glucose 54-61 insulin Homo sapiens 35-42 3293980-2 1988 The means by which GH produces insulin resistance may be through direct suppression of glucose metabolism in target cells (insulin-independent) or by interfering with the ability of insulin to stimulate glucose metabolism (insulin-dependent). Glucose 87-94 insulin Homo sapiens 31-38 3293980-2 1988 The means by which GH produces insulin resistance may be through direct suppression of glucose metabolism in target cells (insulin-independent) or by interfering with the ability of insulin to stimulate glucose metabolism (insulin-dependent). Glucose 203-210 insulin Homo sapiens 31-38 3293980-14 1988 Insulin stimulated the conversion of glucose to lipid when tested alone or in the presence of GH. Glucose 37-44 insulin Homo sapiens 0-7 3294042-9 1988 The magnitude of the rise in circulating androgens is proportional to the magnitude of the insulin response to the glucose load. Glucose 115-122 insulin Homo sapiens 91-98 2899090-0 1988 Somatostatin enhances insulin-mediated glucose disposal in elderly subjects. Glucose 39-46 insulin Homo sapiens 22-29 2899090-3 1988 To examine the effect of SRIH on insulin-mediated glucose disposal in the elderly, we studied 12 (7 men and 5 women) healthy nonobese subjects, aged 65-80 yr. Paired 3-h euglycemic insulin clamp studies were performed in random order employing insulin alone (22 mU/m2.min) or insulin with SRIH (250 micrograms/h) and glucagon (0.4 ng/kg.min) to maintain normal basal plasma glucagon levels. Glucose 50-57 insulin Homo sapiens 33-40 2899090-8 1988 We conclude that SRIH augments insulin-mediated glucose disposal in healthy older subjects at physiological levels of insulin. Glucose 48-55 insulin Homo sapiens 31-38 3049515-0 1988 Glucose transport into rat skeletal muscle: interaction between exercise and insulin. Glucose 0-7 insulin Homo sapiens 77-84 3049515-4 1988 After 180 min, when approximately 66% of the exercise-induced increase in sugar transport had worn off, both the responsiveness and sensitivity of the glucose transport process to insulin were increased. Glucose 151-158 insulin Homo sapiens 180-187 3292558-6 1988 Although glucose was infused at a constant rate, significant pulses were found in glucose, insulin, and C-peptide levels and ISR; the pulse durations of these parameters were 182 +/- 30 (+/- SE), 89 +/- 5, 100 +/- 8, and 85 +/- 5 min, respectively, and their periodicities were 208 +/- 33, 106 +/- 7, 114 +/- 10, and 106 +/- 7 min. Glucose 9-16 insulin Homo sapiens 91-98 3292563-2 1988 While ethanol increased fasting plasma glucose and serum insulin concentrations, after insulin administration plasma glucose concentrations fell to similar nadirs in the ethanol [2.5 +/- 0.2 (+/- SE) mmol/L] and control studies (2.3 +/- 0.1 mmol/L). Glucose 117-124 insulin Homo sapiens 87-94 3403714-1 1988 Decreased insulin stimulation of glucose transport in muscle from morbidly obese and diabetic subjects. Glucose 33-40 insulin Homo sapiens 10-17 3403714-6 1988 Morbidly obese patients, with or without NIDDM, have a severe state of insulin resistance in glucose transport. Glucose 93-100 insulin Homo sapiens 71-78 3043146-2 1988 We sought to quantitate the impact of absolute bed rest alone on insulin regulation of glucose metabolism in six healthy subjects. Glucose 87-94 insulin Homo sapiens 65-72 3043146-4 1988 Euglycemic insulin clamp studies demonstrated the development of resistance to insulin"s stimulation of whole-body glucose utilization. Glucose 115-122 insulin Homo sapiens 11-18 3043146-4 1988 Euglycemic insulin clamp studies demonstrated the development of resistance to insulin"s stimulation of whole-body glucose utilization. Glucose 115-122 insulin Homo sapiens 79-86 3043146-5 1988 This change was characterized by a rightward shift of the insulin dose-response curve (insulin concentration at which 50% of maximal stimulation occurred was 45 +/- 3 (SE) microU/mL in the base line period and 78 +/- 8 microU/mL after seven days of bed rest, P less than .01) with little alteration in the maximal response in the rate of glucose uptake (baseline 15.4 +/- 1.4 mg/kg.min and bed rest 14.0 +/- 1.3 mg/kg.min). Glucose 338-345 insulin Homo sapiens 58-65 3043146-5 1988 This change was characterized by a rightward shift of the insulin dose-response curve (insulin concentration at which 50% of maximal stimulation occurred was 45 +/- 3 (SE) microU/mL in the base line period and 78 +/- 8 microU/mL after seven days of bed rest, P less than .01) with little alteration in the maximal response in the rate of glucose uptake (baseline 15.4 +/- 1.4 mg/kg.min and bed rest 14.0 +/- 1.3 mg/kg.min). Glucose 338-345 insulin Homo sapiens 87-94 3043146-6 1988 In contrast to the shift of sensitivity of whole-body glucose utilization to insulin, suppression of hepatic glucose output by insulin was unchanged by seven days of bed rest. Glucose 54-61 insulin Homo sapiens 77-84 3043146-8 1988 These studies demonstrate that the limited physical activity dictated by bed rest for as little as seven days is associated with substantial resistance to insulin"s effects on glucose metabolism. Glucose 176-183 insulin Homo sapiens 155-162 3294522-1 1988 A greater plasma concentration of insulin after isoglycemic enteral than after parenteral administration of glucose is called the incretin effect. Glucose 108-115 insulin Homo sapiens 34-41 2847108-4 1988 Serum glucose levels were elevated 2-fold and serum insulin levels were elevated 3-fold in the glucose-infused fetuses. Glucose 95-102 insulin Homo sapiens 52-59 3293339-7 1988 Maximum incremental C-peptide response improved both to glucagon (214 +/- 32 after vs 134 +/- 48 pmol/l before, P = 0.05) and to glucose iv bolus injection (284 +/- 53 vs 113 +/- 32 pmol/l, P less than 0.05). Glucose 129-136 insulin Homo sapiens 20-29 3293339-8 1988 Peak insulin response, measured after iv glucose infusion, also tended to be higher in the post-CSII test (42 +/- 18 vs 22 +/- 5.6 mU/l). Glucose 41-48 insulin Homo sapiens 5-12 3293455-6 1988 Glucose tolerance and insulin response, measured as areas under the curve after a 75 gm oral glucose load, were improved in both exercise groups compared with controls, with more marked improvement in the treadmill group. Glucose 93-100 insulin Homo sapiens 22-29 3293455-7 1988 The only difference achieving statistical significance was the insulin levels 30 minutes or less after glucose ingestion, representing the first phase of insulin release. Glucose 103-110 insulin Homo sapiens 63-70 3293455-7 1988 The only difference achieving statistical significance was the insulin levels 30 minutes or less after glucose ingestion, representing the first phase of insulin release. Glucose 103-110 insulin Homo sapiens 154-161 3046411-2 1988 In a prospective randomised study in 20 insulin-dependent diabetics who had minor surgery under general anaesthesia we compared the metabolic responses to intravenous glucose-insulin-potassium infusion with those who had conventional subcutaneous insulin administration. Glucose 167-174 insulin Homo sapiens 175-182 3395276-4 1988 The plasma insulin response to an oral glucose challenge was markedly reduced after training (p less than 0.001). Glucose 39-46 insulin Homo sapiens 11-18 2906299-2 1988 In our studies, infusion of lysine acetylsalicylate (72 mg/min) increased basal insulin levels and amplified insulin responses to glucose (5 g i.v. Glucose 130-137 insulin Homo sapiens 109-116 2906299-6 1988 Calcitonin and somatostatin, two agents that inhibit basal and glucose-stimulated insulin secretion, inhibited the insulin response to glucose in presence of LAS infusion. Glucose 63-70 insulin Homo sapiens 82-89 2906299-6 1988 Calcitonin and somatostatin, two agents that inhibit basal and glucose-stimulated insulin secretion, inhibited the insulin response to glucose in presence of LAS infusion. Glucose 135-142 insulin Homo sapiens 82-89 2970918-9 1988 Furthermore, in the group with residual insulin secretion we found a correlation (p less than 0.01) of low HbA1c with high frequency of self-monitoring of blood glucose and high perceived vulnerability. Glucose 161-168 insulin Homo sapiens 40-47 3065105-0 1988 The pattern of basal and stimulated insulin responses to intravenous glucose in first degree relatives of type 1 (insulin-dependent) diabetic children and unrelated adults aged 5 to 50 years. Glucose 69-76 insulin Homo sapiens 36-43 3065109-0 1988 Variability of the first phase insulin response to intravenous glucose. Glucose 63-70 insulin Homo sapiens 31-38 3066652-3 1988 However, the interaction between diabetes and obesity has been poorly characterized and the metabolic disturbances contributing to the defect in insulin-mediated glucose uptake have not been defined. Glucose 162-169 insulin Homo sapiens 145-152 3133262-3 1988 Pharmacologic inhibition of arachidonate metabolism by both lipoxygenase and cyclooxygenase pathways with BW 755C strongly suppressed glucose-induced insulin secretion from perifused human islets, and the selective cyclooxygenase inhibitor indomethacin enhanced insulin secretion. Glucose 134-141 insulin Homo sapiens 150-157 3133262-4 1988 These findings are similar to those reported for islets isolated from rats and suggest that arachidonate metabolites may modulate glucose-induced insulin secretion in humans. Glucose 130-137 insulin Homo sapiens 146-153 3203573-4 1988 Several patients reporting flocculated insulin, including one hospitalized with ketoacidosis, experienced unusual and unexplained elevation in blood glucose concentration for several days before flocculation was observed. Glucose 149-156 insulin Homo sapiens 39-46 3290007-1 1988 To evaluate the effect of strict glycemic control of insulin-dependent diabetes mellitus (IDDM) on the plasma glucose threshold initiating counterregulatory hormone responses to hypoglycemia, we used the glucose clamp technique to produce a standardized gradual glucose decline from 90 to 40 mg/dl in seven young IDDM patients before and after 2-6 mo of intensified insulin therapy. Glucose 110-117 insulin Homo sapiens 53-60 3290009-5 1988 On day 0, IL-1 was found to totally inhibit glucose-stimulated insulin release, partially inhibit glucose oxidation, and induce a decrease in islet DNA content. Glucose 44-51 insulin Homo sapiens 63-70 3290009-6 1988 However, these islets were able to release insulin after stimulation with glucose plus theophylline, although the absolute rate of insulin secretion was lower than that of the control group. Glucose 74-81 insulin Homo sapiens 43-50 3290009-7 1988 After 6 days in culture, the insulin-secretory response to glucose and the glucose oxidation rates of the IL-1-pretreated islets were completely restored, but there remained a reduced islet DNA content. Glucose 59-66 insulin Homo sapiens 29-36 2897973-3 1988 The pancreatic exocrine response to secretin was decreased, whereas the insulin and/or glucagon responses to glucose and arginine were normal. Glucose 109-116 insulin Homo sapiens 72-79 3288650-5 1988 The cancer patients had significantly higher insulin responses after glucose administration than normal women (sum of 1, 2, and 3 h postglucose values, 5545 +/- 1526 vs. 1444 +/- 156 pmol/L; P less than 0.02), even though their glucose responses were similar. Glucose 69-76 insulin Homo sapiens 45-52 3292584-0 1988 Relationship between plasma glucose and insulin concentration, glucose production, and glucose disposal in normal subjects and patients with non-insulin-dependent diabetes. Glucose 28-35 insulin Homo sapiens 40-47 3292681-3 1988 The amplitude of stimulation of glucose utilization was decreased (p less than 0.05) in the type I patients compared with the subjects without diabetes during both a constant and a variable insulin infusion, whether measured as the peak (2.24 +/- 0.11 mg/kg/min vs 3.18; +/- 0.18 mg/kg/min constant and 2.80 +/- 0.30 mg/kg/min vs 3.54 +/- 0.23 mg/kg/min variable) or integrated response above basal (54 +/- 2 mg/kg vs 115 +/- 26 mg/kg constant and 60 +/- 26 mg/kg vs 147 +/- 21 mg/kg, variable). Glucose 32-39 insulin Homo sapiens 190-197 3292681-4 1988 In addition, the rate of activation of glucose utilization (slope 0 to 90 minutes) was decreased (p less than 0.02) in the type I patients compared with subjects without diabetes during both the constant (0.003 +/- 0.001 mg/kg/min 2 vs 0.008 +/- 0.002 mg/kg/min 2) and variable (0.006 +/- 0.002 mg/kg/min 2 vs 0.015 +/- 0.002 mg/kg/min 2) insulin infusions. Glucose 39-46 insulin Homo sapiens 339-346 3292682-0 1988 Diabetes mellitus and insulin effect on glucose metabolism. Glucose 40-47 insulin Homo sapiens 22-29 3290622-6 1988 Thus, normalization of the A-cell sensitivity to glucose in insulin-dependent diabetic subjects requires further amelioration of the intermediary metabolism than can be achieved with insulin pump treatment. Glucose 49-56 insulin Homo sapiens 60-67 3290623-7 1988 While fasting glucose responsivity to endogenous insulin is impaired in healthy older men, the FFA response appears to be preserved. Glucose 14-21 insulin Homo sapiens 49-56 3288620-2 1988 This led us to the original proposal that diacylglycerol may contribute to the mediation of insulin action, especially stimulation of glucose transport. Glucose 134-141 insulin Homo sapiens 92-99 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 232-239 insulin Homo sapiens 32-39 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 232-239 insulin Homo sapiens 110-117 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 232-239 insulin Homo sapiens 110-117 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 232-239 insulin Homo sapiens 110-117 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 376-383 insulin Homo sapiens 32-39 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 376-383 insulin Homo sapiens 110-117 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 376-383 insulin Homo sapiens 110-117 3288620-9 1988 Furthermore, we have shown that insulin-generated diacylglycerol satisfies several criteria for a mediator of insulin action, including the demonstration that insulin-stimulated endogenous diacylglycerol generation is antecedent to glucose transport and has an identical insulin dose-response curve and moreover that the magnitude and time course of subsequent stimulation of glucose transport is reproduced by the addition of the simple exogenous diacylglyerol, dioctanoylglycerol, in the complete absence of the hormone. Glucose 376-383 insulin Homo sapiens 110-117 3288620-10 1988 These results establish a central role for insulin-induced glycerolipid metabolism in mediating insulin-stimulated glucose transport in BC3H-1 myocytes. Glucose 115-122 insulin Homo sapiens 43-50 3288620-10 1988 These results establish a central role for insulin-induced glycerolipid metabolism in mediating insulin-stimulated glucose transport in BC3H-1 myocytes. Glucose 115-122 insulin Homo sapiens 96-103 2838998-2 1988 Acute insulin response (mean change 3-10 min) to iv glucose (0.33 g/kg) was decreased by 40% during the infusion of prostaglandin E2 (10 micrograms/min) and glucose disappearance rates were reduced (P less than 0.05). Glucose 52-59 insulin Homo sapiens 6-13 2838998-2 1988 Acute insulin response (mean change 3-10 min) to iv glucose (0.33 g/kg) was decreased by 40% during the infusion of prostaglandin E2 (10 micrograms/min) and glucose disappearance rates were reduced (P less than 0.05). Glucose 157-164 insulin Homo sapiens 6-13 3287913-2 1988 During a 20 mU/m2/minute euglycemic clamp (insulin level, 88 microU/ml) procedure, while the patient with hypokalemic periodic paralysis demonstrated severe resistance to insulin-mediated glucose uptake (glucose uptake 50 percent of that of normal control subjects, n = 17), his plasma potassium declined to a degree similar to that seen in normal subjects. Glucose 188-195 insulin Homo sapiens 171-178 3287913-2 1988 During a 20 mU/m2/minute euglycemic clamp (insulin level, 88 microU/ml) procedure, while the patient with hypokalemic periodic paralysis demonstrated severe resistance to insulin-mediated glucose uptake (glucose uptake 50 percent of that of normal control subjects, n = 17), his plasma potassium declined to a degree similar to that seen in normal subjects. Glucose 204-211 insulin Homo sapiens 171-178 3287913-5 1988 Glucose disposal rates during this high-dose insulin infusion were one-half that seen in lean control subjects (n = 19) and similar to those in obese control subjects. Glucose 0-7 insulin Homo sapiens 45-52 3287913-7 1988 The ability of insulin to induce hypokalemia is enhanced in this syndrome even in the presence of marked coexistent obesity-related resistance to the action of insulin to promote glucose utilization. Glucose 179-186 insulin Homo sapiens 15-22 3287913-7 1988 The ability of insulin to induce hypokalemia is enhanced in this syndrome even in the presence of marked coexistent obesity-related resistance to the action of insulin to promote glucose utilization. Glucose 179-186 insulin Homo sapiens 160-167 3287951-0 1988 Preservation of insulin effects on glucose production and proteolysis during fasting. Glucose 35-42 insulin Homo sapiens 16-23 3287951-6 1988 In conclusion, insulin suppresses proteolysis equally well before and after brief fasting, and endogenous glucose production is more completely suppressed by insulin after brief fasting than after an overnight fast. Glucose 106-113 insulin Homo sapiens 158-165 3288006-6 1988 Although glucose intolerance was marked during surgery (K10-60 min = 0.892 +/- 0.286% min-1), the glucose-induced insulin response remained similar to that observed in patients in group II, while growth hormone, cortisol, epinephrine, and norepinephrine concentrations increased significantly. Glucose 98-105 insulin Homo sapiens 114-121 3288006-7 1988 These known stress factors thus seemed to enhance glucose intolerance through a diminished response to insulin action and/or an enhanced hepatic glucose output, rather than by further impairing pancreatic insulin secretion. Glucose 50-57 insulin Homo sapiens 103-110 3293693-8 1988 These results indicate that insulin resistance after elective abdominal surgery is due to a postreceptor deficit in glucose utilization, as indicated by the downward shift of the dose-response curves. Glucose 116-123 insulin Homo sapiens 28-35 3289993-7 1988 We found that fasting plasma insulin and C-peptide values were slightly increased in the twins, whereas the responses of insulin and C-peptide to oral glucose tolerance tests (OGTT) and meals were similar in the twins and within normal range. Glucose 151-158 insulin Homo sapiens 121-128 3289993-11 1988 Furthermore, the maximal insulin-mediated glucose uptake in peripheral tissues was reduced by 40% in the diabetic twin. Glucose 42-49 insulin Homo sapiens 25-32 3289994-4 1988 Augmentation of the early insulin response caused a 33 +/- 4% reduction in the glycemic response to a mixed meal (P less than .005); the peak blood glucose increment above baseline was reduced by 1.4 mM (P less than .005) to an increment identical to nondiabetic subjects (3.3 +/- 0.3 vs. 3.2 +/- 0.2 mM), and blood glucose levels were still 0.9 mM lower after 180 min (P less than .05). Glucose 148-155 insulin Homo sapiens 26-33 3289999-2 1988 Insulin-mediated glucose disposal was approximately 30% lower (P less than .03) with GI (9.2 +/- 1.2 mg.kg-1.min-1, mean +/- SE) than with the nonglycosylated hormone (12.6 +/- 0.7 mg.kg-1.min-1) at comparable plasma insulin concentrations (approximately 90 microU/ml). Glucose 17-24 insulin Homo sapiens 0-7 3289999-2 1988 Insulin-mediated glucose disposal was approximately 30% lower (P less than .03) with GI (9.2 +/- 1.2 mg.kg-1.min-1, mean +/- SE) than with the nonglycosylated hormone (12.6 +/- 0.7 mg.kg-1.min-1) at comparable plasma insulin concentrations (approximately 90 microU/ml). Glucose 17-24 insulin Homo sapiens 217-224 3289999-4 1988 We conclude that in vitro extensive glycosylation of insulin reduces its biological activity in vivo, as reflected by insulin-mediated glucose disposal, probably at a postreceptor level. Glucose 135-142 insulin Homo sapiens 53-60 3289999-4 1988 We conclude that in vitro extensive glycosylation of insulin reduces its biological activity in vivo, as reflected by insulin-mediated glucose disposal, probably at a postreceptor level. Glucose 135-142 insulin Homo sapiens 118-125 2969796-1 1988 States of hyperinsulinemia with resistance to insulin action on glucose disposal are frequently associated with proliferative tissue abnormalities of the skin (acanthosis nigricans), ovary, and heart. Glucose 64-71 insulin Homo sapiens 15-22 2969796-6 1988 Thus, insulin action mediated through the IGF-I receptor may initiate growth-promoting tissue effects in the face of limited insulin effect on glucose metabolism. Glucose 143-150 insulin Homo sapiens 6-13 3042316-2 1988 In 8 nondiabetic subjects, salivary insulin levels increased after an oral glucose load but with a delay in peak concentrations of approximately 45 min in comparison with serum insulin levels. Glucose 75-82 insulin Homo sapiens 36-43 3044777-7 1988 It is possible that such an alteration could lead to a shift of the biological response curve of insulin to the left in some target tissues thereby causing hyperlipaemia by diverting glucose into triglyceride. Glucose 183-190 insulin Homo sapiens 97-104 3046976-0 1988 Serum proinsulin levels at fasting and after oral glucose load in patients with type 2 (non-insulin-dependent) diabetes mellitus. Glucose 50-57 insulin Homo sapiens 6-16 3046976-0 1988 Serum proinsulin levels at fasting and after oral glucose load in patients with type 2 (non-insulin-dependent) diabetes mellitus. Glucose 50-57 insulin Homo sapiens 9-16 3046976-3 1988 With this assay system, we studied the serum proinsulin concentration at fasting and after an oral 100 g glucose load in 25 healthy subjects, 21 subjects with impaired glucose tolerance and 40 patients with Type 2 (non-insulin-dependent) diabetes mellitus. Glucose 105-112 insulin Homo sapiens 45-55 3046976-6 1988 After a 100 g oral glucose load, serum proinsulin increased more slowly than insulin. Glucose 19-26 insulin Homo sapiens 39-49 3046976-6 1988 After a 100 g oral glucose load, serum proinsulin increased more slowly than insulin. Glucose 19-26 insulin Homo sapiens 42-49 3046976-7 1988 The proinsulin response after an oral glucose load was augmented in subjects with impaired glucose tolerance and diabetes, while the insulin response decreased with the elevation of fasting plasma glucose. Glucose 38-45 insulin Homo sapiens 4-14 3046976-7 1988 The proinsulin response after an oral glucose load was augmented in subjects with impaired glucose tolerance and diabetes, while the insulin response decreased with the elevation of fasting plasma glucose. Glucose 38-45 insulin Homo sapiens 7-14 3046976-7 1988 The proinsulin response after an oral glucose load was augmented in subjects with impaired glucose tolerance and diabetes, while the insulin response decreased with the elevation of fasting plasma glucose. Glucose 91-98 insulin Homo sapiens 4-14 3046976-7 1988 The proinsulin response after an oral glucose load was augmented in subjects with impaired glucose tolerance and diabetes, while the insulin response decreased with the elevation of fasting plasma glucose. Glucose 91-98 insulin Homo sapiens 7-14 3046976-8 1988 Diabetic patients with high fasting plasma glucose had a very poor insulin response, but the proinsulin response was similar to control subjects. Glucose 43-50 insulin Homo sapiens 67-74 3131129-2 1988 Insulin-stimulated glucose oxidation, as determined by measurement of 14CO2 production, was enhanced 106% after administration of hGH-(1-43) at a dosage of 1 microgram/day for 3 days. Glucose 19-26 insulin Homo sapiens 0-7 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 107-114 insulin Homo sapiens 264-271 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 107-114 insulin Homo sapiens 440-447 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 264-271 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 440-447 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 264-271 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 440-447 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 264-271 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 440-447 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 264-271 3286157-3 1988 As compared to normal subjects, patients with chronic pancreatitis showed: (1) significantly higher plasma glucose levels after oral glucose load (area under the plasma glucose curve 1708 +/- 142 vs 1208 +/- 47 mmol/liter X 240 min, P less than 0.005); (2) plasma insulin levels significantly higher at fasting (0.11 +/- 0.008 vs 0.08 +/- 0.005 nmol/liter, P less than 0.01) but not after oral glucose administration (area under the plasma insulin curve 79 +/- 12 vs 88 +/- 16 nmol/liter X 240 min); (3) significantly lower plasma C-peptide concentrations both in the fasting state (0.15 +/- 0.01 vs 0.54 +/- 0.05 nmol/liter, P less than 0.001) and after oral glucose load (area under the plasma C-peptide curve 211 +/- 30 vs 325 +/- 37 nmol/liter X 240 min, P less than 0.05). Glucose 133-140 insulin Homo sapiens 440-447 2967305-1 1988 We evaluated the insulin response to a standard oral glucose tolerance test (OGTT) and in vitro insulin binding to erythrocytes (RBC) in 26 women from 3 groups: Group NW, normal women (n = 11); Group DS, women (n = 9) with elevated serum DHEAS concentrations, greater than 400 micrograms/dl (greater than 10.84 mumol/L); and Group IR, women (n = 6) with elevated basal plasma insulin concentrations (IRI). Glucose 53-60 insulin Homo sapiens 17-24 3266252-3 1988 In a multiple linear (step-wise) regression analysis, body mass index, age, immunoreactive insulin two hours after glucose load and serum total cholesterol contributed directly to the BP value but the weekly ethanol intake did not. Glucose 115-122 insulin Homo sapiens 91-98 3290250-11 1988 To demonstrate that endogenous CCK could modify the plasma glucose and insulin responses to oral glucose, oral glucose was given with 50 g of lipid containing long-chain triglycerides. Glucose 97-104 insulin Homo sapiens 71-78 3290250-11 1988 To demonstrate that endogenous CCK could modify the plasma glucose and insulin responses to oral glucose, oral glucose was given with 50 g of lipid containing long-chain triglycerides. Glucose 97-104 insulin Homo sapiens 71-78 3290257-11 1988 Peripheral insulin resistance relates to decreased metabolic glucose clearance (MCR) and inadequate increase of uptake during glucose infusion. Glucose 61-68 insulin Homo sapiens 11-18 3290257-11 1988 Peripheral insulin resistance relates to decreased metabolic glucose clearance (MCR) and inadequate increase of uptake during glucose infusion. Glucose 126-133 insulin Homo sapiens 11-18 3131630-10 1988 The ratio between glucose infusion rate and the average plasma insulin level was calculated as an index of insulin-mediated glucose metabolism; G/I X 100 was markedly reduced during combined TPN (4.5 +/- 0.8 v 20.7 +/- 3.7; P less than .05). Glucose 124-131 insulin Homo sapiens 107-114 3131630-12 1988 In conclusion, during combined TPN a state of insulin resistance is induced and more insulin is required to achieve a normal glucose utilization. Glucose 125-132 insulin Homo sapiens 85-92 3287091-0 1988 The beta cell glucose stimulus-response curve in normal humans assessed by insulin and C-peptide secretion rates. Glucose 14-21 insulin Homo sapiens 75-82 3287091-0 1988 The beta cell glucose stimulus-response curve in normal humans assessed by insulin and C-peptide secretion rates. Glucose 14-21 insulin Homo sapiens 87-96 3287091-6 1988 In response to glucose, C-peptide concentrations rose less quickly than did insulin concentrations, but the estimated first- and second-phase secretion rates were similar when assessed from either the C-peptide or insulin concentrations. Glucose 15-22 insulin Homo sapiens 24-33 3287091-7 1988 First-phase secretion peaks were larger than inspection of the plasma concentration data might suggest, with median values of 1.3, 2.0, and 2.9 nmol/min for C-peptide in response to 7.5, 10, and 15 mmol/L glucose clamp levels, respectively. Glucose 205-212 insulin Homo sapiens 157-166 3287091-9 1988 The slopes of the curves of steady-state insulin and C-peptide secretion rates v the four glucose levels (basal plus the three clamp levels) were maximally steep between 7.5 and 10 mmol/L in the majority of subjects, consistent with in vitro sigmoidal responses. Glucose 90-97 insulin Homo sapiens 41-48 3287379-0 1988 Glucose stimulates proinsulin biosynthesis by a dose-dependent recruitment of pancreatic beta cells. Glucose 0-7 insulin Homo sapiens 19-29 3287379-1 1988 Glucose is a well-known stimulus of proinsulin biosynthesis. Glucose 0-7 insulin Homo sapiens 36-46 3287379-5 1988 The sigmoidal dose-response curve for glucose-induced proinsulin biosynthesis thus reflects a heterogeneous responsiveness of pancreatic beta cells rather than a progressively increasing activity of functionally homogeneous cells. Glucose 38-45 insulin Homo sapiens 54-64 2906021-2 1988 The blood glucose level during a somatostatin (100 micrograms/h)-insulin (0.4 mU.kg-1.min-1)-glucose (4.5 mg.kg-1.min-1)-infusion-test performed between 10.30 and 14.30 hours served as an indicator of the total body insulin resistance. Glucose 93-100 insulin Homo sapiens 65-72 2906021-6 1988 In comparison with the control study the infusion of adrenaline decreased the need for intravenous glucose significantly over the initial 2 h. Furthermore, during the somatostatin-insulin-glucose infusion test the blood glucose rose significantly (p less than 0.05) over the initial 2 h; thereafter no significant differences between the two studies were seen. Glucose 99-106 insulin Homo sapiens 180-187 2906021-6 1988 In comparison with the control study the infusion of adrenaline decreased the need for intravenous glucose significantly over the initial 2 h. Furthermore, during the somatostatin-insulin-glucose infusion test the blood glucose rose significantly (p less than 0.05) over the initial 2 h; thereafter no significant differences between the two studies were seen. Glucose 188-195 insulin Homo sapiens 180-187 3057545-3 1988 The results obtained show that PGE1 does not modify insulin release induced by glucose 1.63 mM (non stimulant concentration) but that this PG significantly diminishes the insulin release induced by glucose 16.3 mM (stimulant concentration) after 15 and 30 min of incubation. Glucose 198-205 insulin Homo sapiens 171-178 2901133-6 1988 In the same group glucose-induced insulin and somatostatin release were greater than in the fed state. Glucose 18-25 insulin Homo sapiens 34-41 3057545-0 1988 Inhibitory effects of PGE1 on glucose induced insulin release in isolated islets of Langerhans. Glucose 30-37 insulin Homo sapiens 46-53 3283552-5 1988 Mean plasma insulin concentrations increased during an oral glucose-tolerance test, from 1200 to 1770 pmol per liter (from 167 to 247 microU per milliliter). Glucose 60-67 insulin Homo sapiens 12-19 3283552-6 1988 In 151 subjects with normal glucose tolerance, the insulin concentration measured during an oral glucose-tolerance test correlated with the plasma glucose concentration (r = 0.48, P less than or equal to 0.0001). Glucose 28-35 insulin Homo sapiens 51-58 3283552-6 1988 In 151 subjects with normal glucose tolerance, the insulin concentration measured during an oral glucose-tolerance test correlated with the plasma glucose concentration (r = 0.48, P less than or equal to 0.0001). Glucose 97-104 insulin Homo sapiens 51-58 3283552-6 1988 In 151 subjects with normal glucose tolerance, the insulin concentration measured during an oral glucose-tolerance test correlated with the plasma glucose concentration (r = 0.48, P less than or equal to 0.0001). Glucose 97-104 insulin Homo sapiens 51-58 3283552-8 1988 In contrast, plasma insulin concentrations in the diabetics decreased as glucose concentrations increased (r = -0.75, P less than or equal to 0.0001), suggesting deficient secretion of insulin. Glucose 73-80 insulin Homo sapiens 20-27 3283553-7 1988 First-phase (0 to 10 minutes) insulin secretory responses to glucose administered intravenously were not significantly impaired in the relatives (geometric mean, 188 pmol per liter [26.2 mU per liter]; range of SD, +103 to -67 pmol per liter [+14.4 to -9.3 mU per liter]), as compared with the controls (geometric mean, 231 pmol per liter [32.2 mU per liter]; range of SD, +131 to -83 pmol per liter [+18.2 to -11.6 mU per liter]). Glucose 61-68 insulin Homo sapiens 30-37 3285221-4 1988 A fourth possible glucose transport system is the insulin-dependent carrier that may be specific to muscle and adipose tissue. Glucose 18-25 insulin Homo sapiens 50-57 3285221-7 1988 Here we present data supporting the latter concept based upon a monoclonal antibody against the fat cell glucose transporter that identifies a unique, insulin-regulatable glucose transport protein in muscle and adipose tissue. Glucose 105-112 insulin Homo sapiens 151-158 2898853-5 1988 At all steps, insulin infusion was accompanied by significantly lower glucose disposal rates [( 3(-3)H]glucose) in uraemic patients compared with controls (P less than 0.05 or less). Glucose 70-77 insulin Homo sapiens 14-21 2898853-5 1988 At all steps, insulin infusion was accompanied by significantly lower glucose disposal rates [( 3(-3)H]glucose) in uraemic patients compared with controls (P less than 0.05 or less). Glucose 103-110 insulin Homo sapiens 14-21 2898853-6 1988 Moreover, the restraining potency of insulin on endogenous glucose production was much more prominent in healthy than in uraemic subjects at the lowest three infusion rates (0.6 +/- 1.0 versus 1.4 +/- 0.3 (mean +/- 1 SD), -0.3 +/- 0.7 versus 0.7 +/- 0.3, and -1.1 +/- 0.7 versus 0.2 +/- 0.6 mg.kg-1.min-1; P less than 0.05, P less than 0.01 and P less than 0.01, respectively), implying a shift to the right of the dose-response curve in uraemia. Glucose 59-66 insulin Homo sapiens 37-44 3291532-6 1988 The hysterotomy-derived ICC responded to 10 mmol/l theophylline plus 20 mmol/l glucose by a 12.2 +/- 3.1 (SEM, N = 7) fold increase in insulin release, as compared with a 5.4 +/- 0.9 fold response of the prostaglandin ICC (N = 16; P less than 0.02). Glucose 79-86 insulin Homo sapiens 135-142 3291532-7 1988 Despite the low proportion of B-cells, (pro)insulin biosynthesis accounted for 10% of the total protein biosynthesis in low (2 mmol/l) glucose. Glucose 135-142 insulin Homo sapiens 44-51 3284381-9 1988 These findings indicate that the decreased insulin secretory response to a glucose stimulus in people who exercise regularly is a relatively short-term effect of exercise. Glucose 75-82 insulin Homo sapiens 43-50 3284382-5 1988 The decrease in glucose uptake was not compensated for by increased uptake of free fatty acids but was accompanied by decreases in plasma insulin and increases in plasma epinephrine and norepinephrine. Glucose 16-23 insulin Homo sapiens 138-145 3285821-6 1988 When VLDL was disturbed jointly with LDL and HDL, the mean insulin response adjusted for age, gender, glucose response, BMI, blood pressure, and smoking was high compared to the reference group (166.0 vs. 122.5, p less than 0.001). Glucose 102-109 insulin Homo sapiens 59-66 3042031-0 1988 Insulin, somatomedin-C, human chorionic gonadotropin, and forskolin enhance glucose oxidation by granulosa cells. Glucose 76-83 insulin Homo sapiens 0-7 3046601-0 1988 The response of adipocyte glucose metabolism and fatty acid release to adenosine deaminase, insulin and perifusion. Glucose 26-33 insulin Homo sapiens 92-99 3075903-5 1988 Primary insulin treatment is advisable in patients with hyperglycaemic symptoms and fasting blood glucose levels above 15 mmol/l, as in these patients the major defect will be insulin deficiency rather than insulin resistance. Glucose 98-105 insulin Homo sapiens 8-15 3293660-10 1988 Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P less than 0.01) but neither were affected by the HFD. Glucose 85-92 insulin Homo sapiens 5-12 3293660-14 1988 Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance. Glucose 38-45 insulin Homo sapiens 0-7 3289828-3 1988 On the basis of the maximum daily dose variation allowed, seven twice-daily glucose determinations and the previous insulin dose, the program generated "cautious" and "normal" insulin dose adjustment for 66 patients which correlated well with the judgements made by four expert diabetologists. Glucose 76-83 insulin Homo sapiens 176-183 2968880-3 1988 Insulin sensitivity was measured as the glucose disappearance rate (k) during an intravenous insulin tolerance test. Glucose 40-47 insulin Homo sapiens 0-7 3044865-2 1988 This article describes a euglucaemic hyperinsulinaemic clamp study of alterations in glucose and/or insulin metabolism in four members of a single family with familial multiple lipomatosis. Glucose 85-92 insulin Homo sapiens 42-49 3066562-4 1988 The present results confirmed our previous studies and in vitro data, showing that the first phase insulin release is not inhibited by a calcium antagonist and strongly indicated that glucose stimulated insulin secretion has two phases of release: (1) the first phase of release, which is independent from extracellular calcium; (2) the second phase of release, which was inhibited by calcium antagonists, is dependent from calcium uptake from an extracellular source. Glucose 184-191 insulin Homo sapiens 99-106 3066562-4 1988 The present results confirmed our previous studies and in vitro data, showing that the first phase insulin release is not inhibited by a calcium antagonist and strongly indicated that glucose stimulated insulin secretion has two phases of release: (1) the first phase of release, which is independent from extracellular calcium; (2) the second phase of release, which was inhibited by calcium antagonists, is dependent from calcium uptake from an extracellular source. Glucose 184-191 insulin Homo sapiens 203-210 2970411-9 1988 Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) Glucose 42-49 insulin Homo sapiens 20-27 3044887-2 1988 An acid-alcohol extract of the patient"s serum contained a factor that inhibited insulin-stimulated glucose transport in rat adipocytes. Glucose 100-107 insulin Homo sapiens 81-88 2974783-4 1988 If diet and maximal oral therapy fail to keep fasting blood glucose levels below 6 mmol l-1 then the addition of a basal insulin supplement, e.g. from a once daily injection of ultralente insulin, can restore near-normal fasting blood glucose levels without the need for full insulin replacement therapy. Glucose 60-67 insulin Homo sapiens 121-128 2974783-4 1988 If diet and maximal oral therapy fail to keep fasting blood glucose levels below 6 mmol l-1 then the addition of a basal insulin supplement, e.g. from a once daily injection of ultralente insulin, can restore near-normal fasting blood glucose levels without the need for full insulin replacement therapy. Glucose 235-242 insulin Homo sapiens 121-128 3042372-5 1988 Basal and insulin-stimulated [U-14C]glucose oxidation to 14CO2 in adipose tissue were measured in vitro after in vivo treatments; insulin release by isolated pancreatic islets was determined in vitro. Glucose 36-43 insulin Homo sapiens 10-17 3042372-6 1988 Acute injections of hGH-(1-43) with insulin dramatically increased glucose clearance in diabetic (P less than 0.05) and hypophysectomized (P less than 0.01) rats. Glucose 67-74 insulin Homo sapiens 36-43 3042372-10 1988 Therefore, these experiments show hGH-(1-43) to be an insulin potentiator that increases insulin-stimulated glucose clearance and glucose oxidation without an increase in insulin secretion, and they suggest that the peptide may have a physiological role in regulating carbohydrate metabolism. Glucose 108-115 insulin Homo sapiens 54-61 3042372-10 1988 Therefore, these experiments show hGH-(1-43) to be an insulin potentiator that increases insulin-stimulated glucose clearance and glucose oxidation without an increase in insulin secretion, and they suggest that the peptide may have a physiological role in regulating carbohydrate metabolism. Glucose 108-115 insulin Homo sapiens 89-96 3042372-10 1988 Therefore, these experiments show hGH-(1-43) to be an insulin potentiator that increases insulin-stimulated glucose clearance and glucose oxidation without an increase in insulin secretion, and they suggest that the peptide may have a physiological role in regulating carbohydrate metabolism. Glucose 130-137 insulin Homo sapiens 54-61 3292505-5 1988 When the plasma insulin concentration was maintained at approximately 2,000 microU.ml-1 (a maximally effective concentration), the rate of glucose disposal was not significantly different before (15.3 +/- 0.5 mg.kg-1.min-1) compared with after (14.5 +/- 0.4 mg.kg-1.min-1) 10 days without exercise. Glucose 139-146 insulin Homo sapiens 16-23 3294066-11 1988 It is concluded that the augmentation of the glucose-induced insulin release by intraduodenal administration of phenylalanine cannot be related to cholecystokinin release, but rather is explained by the combined effects of elevated glucose and phenylalanine concentrations. Glucose 45-52 insulin Homo sapiens 61-68 3294066-11 1988 It is concluded that the augmentation of the glucose-induced insulin release by intraduodenal administration of phenylalanine cannot be related to cholecystokinin release, but rather is explained by the combined effects of elevated glucose and phenylalanine concentrations. Glucose 232-239 insulin Homo sapiens 61-68 3294068-3 1988 In the control euglycaemic clamp studies with insulin infusion at 0.2 and 1.0 mU.kg-1.min-1, endogenous glucose production was suppressed from the basal rate of 2.0 +/- 0.3 mg.kg-1min-1 to 1.1 +/- 0.7 mg.kg-1.min-1 and -0.4 +/- 0.7 mg.kg-1min-1 respectively. Glucose 104-111 insulin Homo sapiens 46-53 3294068-5 1988 When the euglycaemic clamp studies were coupled with lipid-heparin infusion at comparable low and high rates of insulin infusion, endogenous glucose production increased (1.8 +/- 0.7 mg.kg-1.min-1, p less than 0.001, and 0.3 +/- 0.6 mg.kg-1.min-1, p less than 0.05, respectively), and glucose utilization decreased (2.1 +/- 0.3 mg.kg-1.min-1, not significant, and 3.2 +/- 0.7 mg.kg-1.min-1, p less than 0.001 respectively). Glucose 141-148 insulin Homo sapiens 112-119 3042578-0 1988 Insulin modulates early-phase noradrenaline response to glucose ingestion in humans. Glucose 56-63 insulin Homo sapiens 0-7 3292505-4 1988 When the plasma insulin concentration was maintained at approximately 78 microU.ml-1 (a submaximal level), glucose disposal rate averaged 8.7 +/- 0.5 mg.kg-1.min-1 before and 6.7 +/- 0.6 mg.kg-1.min-1 after 10 days of activity (P less than 0.001). Glucose 107-114 insulin Homo sapiens 16-23 2846676-5 1988 The increased insulin responses to glucose, despite a normal C-peptide response, further supports the importance of impaired degradation in the pathogenesis of hyperinsulinemia after challenge. Glucose 35-42 insulin Homo sapiens 14-21 2834414-0 1988 Alterations in insulin receptor autophosphorylation in insulin resistance: correlation with altered sensitivity to glucose transport and antilipolysis to insulin. Glucose 115-122 insulin Homo sapiens 15-22 2834414-0 1988 Alterations in insulin receptor autophosphorylation in insulin resistance: correlation with altered sensitivity to glucose transport and antilipolysis to insulin. Glucose 115-122 insulin Homo sapiens 55-62 2834414-5 1988 These data indicate a significant correlation between changes in sensitivity of glucose transport and antilipolysis to insulin and receptor kinase activity in those patients and suggest that defective coupling of insulin binding to insulin action at the level of phosphorylation of the insulin receptor may cause the insulin resistance in this group of patients. Glucose 80-87 insulin Homo sapiens 119-126 2834414-5 1988 These data indicate a significant correlation between changes in sensitivity of glucose transport and antilipolysis to insulin and receptor kinase activity in those patients and suggest that defective coupling of insulin binding to insulin action at the level of phosphorylation of the insulin receptor may cause the insulin resistance in this group of patients. Glucose 80-87 insulin Homo sapiens 213-220 2834414-5 1988 These data indicate a significant correlation between changes in sensitivity of glucose transport and antilipolysis to insulin and receptor kinase activity in those patients and suggest that defective coupling of insulin binding to insulin action at the level of phosphorylation of the insulin receptor may cause the insulin resistance in this group of patients. Glucose 80-87 insulin Homo sapiens 213-220 2834414-5 1988 These data indicate a significant correlation between changes in sensitivity of glucose transport and antilipolysis to insulin and receptor kinase activity in those patients and suggest that defective coupling of insulin binding to insulin action at the level of phosphorylation of the insulin receptor may cause the insulin resistance in this group of patients. Glucose 80-87 insulin Homo sapiens 213-220 3284915-8 1988 The results indicate that glucagon stimulates glucose cycling, and this stimulatory effect is augmented when the insulin response to glucagon infusion is blocked. Glucose 46-53 insulin Homo sapiens 113-120 2846676-9 1988 The C-peptide responses to glucose and glucagon challenges were suppressed despite pharmacologic stimulation. Glucose 27-34 insulin Homo sapiens 4-13 2901737-9 1988 A greater decrease in the plasma glucose level was observed in the group treated with insulin and the analog than in the group injected only with insulin. Glucose 33-40 insulin Homo sapiens 86-93 3285129-3 1988 Significant negative linear correlations were found between serum insulin and blood glucose, plasma nonesterified fatty acids, blood glycerol and blood total ketone bodies concentrations. Glucose 84-91 insulin Homo sapiens 66-73 3285129-4 1988 The insulin-glucose dose-response curve showed a significant left shift at 3 months with a further significant improvement at 12 months. Glucose 12-19 insulin Homo sapiens 4-11 3285133-4 1988 During the euglycemic (91.2 +/- 3.0 mg glucose/dL plasma) clamps, plasma insulin levels were increased by 700% (0.76 +/- 0.12 to 5.3 +/- 0.29 ng/mL, P less than .001) and plasma glucagon levels decreased by 19%, compared with baseline. Glucose 39-46 insulin Homo sapiens 73-80 3285134-2 1988 Insulin action was determined with a sequential euglycemic (5.0 mmol/L) glucose clamp technique using insulin infusion rates of 0.5, 1.0, 2.0, and 5.0 mU.kg-1.min-1 in four periods of two hours each. Glucose 72-79 insulin Homo sapiens 0-7 2901737-9 1988 A greater decrease in the plasma glucose level was observed in the group treated with insulin and the analog than in the group injected only with insulin. Glucose 33-40 insulin Homo sapiens 146-153 2835843-8 1988 Perifusion with glucose elicited a biphasic release of insulin with the mean response (microU/islet/min) rising to a first peak of 0.5 and constant second phase secretion of 0.25, followed by a return to baseline. Glucose 16-23 insulin Homo sapiens 55-62 3286165-6 1988 Women who successfully used insulin pumps were typically from the private sector and in better glucose control at study entry. Glucose 95-102 insulin Homo sapiens 28-35 2897274-7 1988 Insulin action was estimated by determination of the steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations during the last 60 min of a continuous 180-min intravenous infusion of somatostatin, crystalline insulin, and glucose. Glucose 92-99 insulin Homo sapiens 0-7 2897274-7 1988 Insulin action was estimated by determination of the steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations during the last 60 min of a continuous 180-min intravenous infusion of somatostatin, crystalline insulin, and glucose. Glucose 232-239 insulin Homo sapiens 0-7 2897274-8 1988 Under these conditions endogenous insulin secretion is suppressed, SSPI concentrations are similar in all individuals, and SSPG concentrations provide a quantitative estimate of insulin-stimulated glucose disposal. Glucose 197-204 insulin Homo sapiens 178-185 3293866-2 1988 Concurrent with low serum glucose levels, the concentrations of C-peptide and insulin were markedly elevated. Glucose 26-33 insulin Homo sapiens 78-85 3291523-5 1988 Insulin-stimulated initial rates of glucose uptake by adipocytes were higher after CSII (1.78 +/- 0.16 vs 2.35 +/- 0.27 pmol per cm2 cell membrane per 20 sec, P less than 0.005). Glucose 36-43 insulin Homo sapiens 0-7 3056636-1 1988 In 40 tall and short children we have demonstrated using oral glucose tolerance tests that there is an increase in serum insulin concentration during puberty with no change in blood glucose concentration. Glucose 62-69 insulin Homo sapiens 121-128 3042255-0 1988 Proinsulin, insulin, and C-peptide in cystic fibrosis after an oral glucose tolerance test. Glucose 68-75 insulin Homo sapiens 0-10 2837418-2 1988 Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by fasting and postprandial hyperglycemia in conjunction with reduced rates of insulin-stimulated glucose disposal and storage in peripheral tissues, including muscle. Glucose 163-170 insulin Homo sapiens 4-11 3042255-1 1988 The beta-cell response to an oral glucose load was studied in 22 patients with cystic fibrosis (CF) by means of insulin, C-peptide and proinsulin, and the results compared with those from 20 healthy sex and age matched controls. Glucose 34-41 insulin Homo sapiens 112-119 3042255-1 1988 The beta-cell response to an oral glucose load was studied in 22 patients with cystic fibrosis (CF) by means of insulin, C-peptide and proinsulin, and the results compared with those from 20 healthy sex and age matched controls. Glucose 34-41 insulin Homo sapiens 121-130 3042255-5 1988 By contrast, the area under the proinsulin curve was significantly higher in the CF patients with impaired glucose tolerance compared with both controls (p less than 0.05) and with the CF normal glucose tolerance group (p less than 0.02). Glucose 107-114 insulin Homo sapiens 32-42 3042255-6 1988 In the CF patients with impaired glucose tolerance the proinsulin level was significantly elevated at 120 minutes (median 50 pmol/l) and at 180 minutes (29 pmol/l) as compared with the controls (24 and 19 pmol/l p less than 0.01) and with the CF patients with normal glucose tolerance (21 and 16 pmol/l p less than 0.01). Glucose 33-40 insulin Homo sapiens 55-65 3288531-5 1988 Conversely, studies concerning the effect of insulin on glucose transport (estimated by facilitated diffusion of 2-deoxyglucose) or glycogen synthesis (estimated by incorporation of glucose into cellular glycogen) revealed the presence of heterogeneous alterations among the different patient cell lines. Glucose 56-63 insulin Homo sapiens 45-52 3288531-5 1988 Conversely, studies concerning the effect of insulin on glucose transport (estimated by facilitated diffusion of 2-deoxyglucose) or glycogen synthesis (estimated by incorporation of glucose into cellular glycogen) revealed the presence of heterogeneous alterations among the different patient cell lines. Glucose 120-127 insulin Homo sapiens 45-52 3288531-7 1988 These data suggest the presence of primary postbinding defects in glucose cellular pathways that give rise to insulin resistance in cells from lipoatrophic diabetic patients. Glucose 66-73 insulin Homo sapiens 110-117 3279064-5 1988 Peripheral glucose utilization rates were expressed as M (milligrams per kg/min) or the ratio of M over the prevailing plasma insulin concentration (M/I). Glucose 11-18 insulin Homo sapiens 126-133 3285118-4 1988 Glucose-stimulated plasma insulin concentrations during oral glucose tolerance testing were significantly lower, and supine diastolic blood pressure was reduced (P less than 0.05) as a result of the training program. Glucose 0-7 insulin Homo sapiens 26-33 3041865-0 1988 Plasma insulin response to oral glucose load in Meniere"s disease. Glucose 32-39 insulin Homo sapiens 7-14 3279811-9 1988 In conclusion diminished insulin clearance may be seen after marked stimulation of insulin secretion with larger doses of oral and iv glucose. Glucose 134-141 insulin Homo sapiens 25-32 3133266-4 1988 During insulin treatment the fasting plasma glucose fell from 14.5 +/- 0.8 to 8.8 +/- 0.4 mmol/l and the HbA1 concentration from 12.6 +/- 0.4 to 9.2 +/- 0.2%. Glucose 44-51 insulin Homo sapiens 7-14 3133266-7 1988 Addition of glibenclamide to insulin resulted in a further reduction of the fasting plasma glucose (7.9 +/- 0.5 mmol/l) and HbA1 (8.3 +/- 0.2%) concentration whereas the basal (0.21 +/- 0.03 nmol/l) and glucagon-stimulated C-peptide concentrations (0.34 +/- 0.06 nmol/l) increased again. Glucose 91-98 insulin Homo sapiens 29-36 3282149-1 1988 Insulin is a major regulator of glucose and body protein homeostasis, both of which demonstrate age-related changes. Glucose 32-39 insulin Homo sapiens 0-7 3282149-2 1988 To clarify insulin"s role in these age-related changes and to compare age-related glucose and protein homeostatic responses, insulin-mediated aspects of glucose and amino acid metabolism were simultaneously examined in healthy postabsorptive young (n = 5, mean age, 25 years) and elderly (n = 5, mean age, 76 years) men. Glucose 153-160 insulin Homo sapiens 125-132 3281000-3 1988 Although insulin-stimulated glucose metabolism in the prepubertal children with thalassemia was similar to that in controls (normal prepubertal children) (319 +/- 23 vs. 314 +/- 41 mg per square meter of body-surface area per minute, P not significant), the response to insulin was markedly impaired in the pubertal children with thalassemia (155 +/- 18 vs. 224 +/- 15 mg per square meter per minute in normal pubertal controls, P less than 0.01). Glucose 28-35 insulin Homo sapiens 9-16 3281000-4 1988 Plasma insulin levels rose excessively after oral glucose administration in the pubertal subjects with thalassemia, but not in the prepubertal patients (P less than 0.001). Glucose 50-57 insulin Homo sapiens 7-14 3128361-3 1988 During a gradual fall in blood glucose concentration induced by a bolus injection of insulin followed by an intravenous infusion of insulin, during 60 minutes of biochemical hypoglycaemia, and after restoration of normoglycaemia with intravenous glucose electroencephalograms were evaluated continuously by period-amplitude analysis; blood samples were taken every 10 minutes throughout. Glucose 31-38 insulin Homo sapiens 85-92 3124685-8 1988 MEASUREMENTS AND MAIN RESULTS: Insulin and glyburide produced similar improvement in fasting blood glucose levels and hemoglobin A1c concentrations, similar frequencies of mild symptomatic hypoglycemia, and similar weight gain despite dietary reinforcement. Glucose 99-106 insulin Homo sapiens 31-38 2894176-0 1988 Insulin resistance after oral glucose tolerance testing in patients with major depression. Glucose 30-37 insulin Homo sapiens 0-7 3422801-10 1988 The basal insulin concentration and the insulin response to glucose infusion in the patients were similar to that of the volunteers, but the plasma cortisol level was similar in volunteers and in the patients (p less than 0.05). Glucose 60-67 insulin Homo sapiens 40-47 3042489-0 1988 Insulin and C-peptide responses to oral glucose load in hypothyroid patients. Glucose 40-47 insulin Homo sapiens 0-7 3042489-0 1988 Insulin and C-peptide responses to oral glucose load in hypothyroid patients. Glucose 40-47 insulin Homo sapiens 12-21 3046854-6 1988 Analysis of area under the curve showed that mean insulin levels were statistically significantly higher after aspartame than after saccharin or unsweetened beverage in normal subjects only, but the magnitude of the difference was small and unlikely to be of physiological importance in the absence of differences in glucose levels. Glucose 317-324 insulin Homo sapiens 50-57 3286329-0 1988 Maturation of insulin response to glucose during human fetal and neonatal development. Glucose 34-41 insulin Homo sapiens 14-21 3286329-2 1988 The insulin release in response to glucose was studied in perifused isletlike cell clusters (ICCs) obtained from human fetal or neonatal pancreases at various stages of development: 12-15 gestational wk (n = 7), 17-20 wk (n = 13), 22.5 wk (n = 2, 1 diabetic pregnancy), and 26-44 wk (n = 6, postnatal samples). Glucose 35-42 insulin Homo sapiens 4-11 3286330-1 1988 Six men with a low rate of insulin-stimulated, non-oxidative carbohydrate disposal (storage) and six with a high storage rate were recruited for study of the fate of insulin-stimulated glucose uptake. Glucose 185-192 insulin Homo sapiens 166-173 3286329-4 1988 Insulin release increased to a detectable level (greater than 0.1 pg.ICC-1.min-1) during glucose stimulation in four of seven of the youngest fetuses. Glucose 89-96 insulin Homo sapiens 0-7 3286329-8 1988 The mean rates of insulin release after 5-12 min of glucose stimulation were 4.8 pg.ICC-1.min-1 in newborn infants and 2.1 pg.ICC-1.min-1 in 17- to 20-wk fetuses. Glucose 52-59 insulin Homo sapiens 18-25 3286330-0 1988 Muscle glycogen synthesis and disposition of infused glucose in humans with reduced rates of insulin-mediated carbohydrate storage. Glucose 53-60 insulin Homo sapiens 93-100 3286330-3 1988 From the disposition of label, the rate of insulin-mediated glucose incorporation into glycogen in the low-storage subjects was one-fourth that of the high-storage subjects (P less than .02). Glucose 60-67 insulin Homo sapiens 43-50 3280588-10 1988 Glucose production was significantly increased in the hyperthyroid patients during the basal state (17.6 +/- 0.9 vs. 11.5 +/- 0.5 mumol/kg.min; P less than 0.001) and remained elevated during the final 0.5 h of the low (12.1 +/- 1.1 vs. 5.9 +/- 1.7; P less than 0.01) and high (3.2 +/- 1.2 vs. 0.5 +/- 0.3; P less than 0.05) insulin infusion rates. Glucose 0-7 insulin Homo sapiens 325-332 3075554-7 1988 Evaluation of insulin action was determined by euglycemic clamp technique, provided by the BIOSTATOR, whose function was transformed into a glucose-controlled dextrose infusion system. Glucose 140-147 insulin Homo sapiens 14-21 3075554-7 1988 Evaluation of insulin action was determined by euglycemic clamp technique, provided by the BIOSTATOR, whose function was transformed into a glucose-controlled dextrose infusion system. Glucose 159-167 insulin Homo sapiens 14-21 3075554-8 1988 The amount of glucose delivered by the system in order to keep the blood glucose steady state concentrations at the fasting level was utilized as the measure of biological activity of the injected insulin on glucose metabolism. Glucose 14-21 insulin Homo sapiens 197-204 3075554-8 1988 The amount of glucose delivered by the system in order to keep the blood glucose steady state concentrations at the fasting level was utilized as the measure of biological activity of the injected insulin on glucose metabolism. Glucose 73-80 insulin Homo sapiens 197-204 3075554-8 1988 The amount of glucose delivered by the system in order to keep the blood glucose steady state concentrations at the fasting level was utilized as the measure of biological activity of the injected insulin on glucose metabolism. Glucose 73-80 insulin Homo sapiens 197-204 3075555-5 1988 Since subcutaneously (SC) administered insulin gave rise to short-term hyperphagia in 24 day-old rat pups we assessed the effects of SC versus IP insulin on the blood glucose level. Glucose 167-174 insulin Homo sapiens 39-46 3280483-1 1988 Plasma glucose and insulin responses to both a 75-g oral glucose challenge and to conventional meals were determined in eight patients with hypertension and compared with values of a control population. Glucose 57-64 insulin Homo sapiens 19-26 3290076-2 1988 The concentration-response curve of insulin secretion to glucose was shifted leftwards with AD-4610 (0.1 mM) without altering either the threshold concentration of glucose to induce insulin secretion or the maximal insulin response to glucose, indicating increased sensitivity of the pancreatic B-cells to glucose. Glucose 57-64 insulin Homo sapiens 36-43 3127418-5 1988 Urinary glucose excretion decreased from 48 +/- 19 g/day before treatment to 20 +/- 9 g/day at the end of glyburide treatment and 2 +/- 1 g/day at the end of insulin treatment. Glucose 8-15 insulin Homo sapiens 158-165 3284873-4 1988 Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. Glucose 222-229 insulin Homo sapiens 150-157 3350907-0 1988 Resistance to insulin-stimulated-glucose uptake in patients with hypertension. Glucose 33-40 insulin Homo sapiens 14-21 3350907-1 1988 Plasma glucose and insulin responses to a glucose challenge and insulin-stimulated glucose uptake were measured in 24 age-, weight-, and sex-matched Chinese men (8 with normal blood pressure, 8 with untreated hypertension, and 8 patients with hypertension treated with thiazide and beta-adrenergic antagonist drugs). Glucose 42-49 insulin Homo sapiens 19-26 3350907-1 1988 Plasma glucose and insulin responses to a glucose challenge and insulin-stimulated glucose uptake were measured in 24 age-, weight-, and sex-matched Chinese men (8 with normal blood pressure, 8 with untreated hypertension, and 8 patients with hypertension treated with thiazide and beta-adrenergic antagonist drugs). Glucose 42-49 insulin Homo sapiens 19-26 3350907-2 1988 Plasma glucose and insulin responses were determined by measuring plasma glucose and insulin concentrations before and at 30-min intervals for 2 h after a 75-g oral glucose dose. Glucose 73-80 insulin Homo sapiens 19-26 3350907-2 1988 Plasma glucose and insulin responses were determined by measuring plasma glucose and insulin concentrations before and at 30-min intervals for 2 h after a 75-g oral glucose dose. Glucose 73-80 insulin Homo sapiens 19-26 3350907-3 1988 Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 19-26 insulin Homo sapiens 0-7 3350907-3 1988 Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 19-26 insulin Homo sapiens 104-111 3350907-3 1988 Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 19-26 insulin Homo sapiens 216-223 3350907-3 1988 Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 19-26 insulin Homo sapiens 216-223 3350907-3 1988 Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 85-92 insulin Homo sapiens 0-7 3350907-3 1988 Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Glucose 85-92 insulin Homo sapiens 0-7 3350907-5 1988 The results indicated that the men with hypertension, whether treated or untreated, had significantly elevated plasma glucose (P less than 0.001) and insulin (P less than 0.001) responses to the oral glucose dose compared to the normal men. Glucose 200-207 insulin Homo sapiens 150-157 3350907-7 1988 Since the mean SSPI concentrations were similar in the 3 groups [approximately 70 microU/mL (502 pmol/L)], insulin was less effective in promoting glucose disposal in both groups with hypertension. Glucose 147-154 insulin Homo sapiens 107-114 3278193-4 1988 Serum glucose and insulin levels after an oral glucose load were significantly higher in the hirsute women. Glucose 47-54 insulin Homo sapiens 18-25 2839760-3 1988 The diagnosis of insulinoma was easily available from serum IRI (immunoreactive insulin)/plasma glucose ratio in all of the ten cases. Glucose 96-103 insulin Homo sapiens 17-24 2839760-11 1988 Furthermore, simultaneous monitoring of plasma glucose and serum IRI by quick radioimmunoassay seemed to be a good guide to the completeness of resection of insulin producing tumors. Glucose 47-54 insulin Homo sapiens 157-164 3293029-3 1988 A considerable increase in the levels of insulin and C-peptide after glucose intake and a considerable decrease in the sensitivity to insulin were observed in the 2nd group. Glucose 69-76 insulin Homo sapiens 41-48 3293029-3 1988 A considerable increase in the levels of insulin and C-peptide after glucose intake and a considerable decrease in the sensitivity to insulin were observed in the 2nd group. Glucose 69-76 insulin Homo sapiens 53-62 3277018-10 1988 However, their fasting insulin and triglyceride levels were inappropriately high for their very low body mass index and fasting glucose levels. Glucose 128-135 insulin Homo sapiens 23-30 3044067-3 1988 During insulin therapy, blood glucose levels (228 +/- 13 versus 123 +/- 18 mg/dl, p less than 0.001) and the basal glucose production rate (p less than 0.001) decreased, and the insulin secretory response to glucagon at a standardized glucose level, insulin action in vivo, and insulin binding and action in vitro in fat cells improved significantly. Glucose 30-37 insulin Homo sapiens 7-14 3044067-3 1988 During insulin therapy, blood glucose levels (228 +/- 13 versus 123 +/- 18 mg/dl, p less than 0.001) and the basal glucose production rate (p less than 0.001) decreased, and the insulin secretory response to glucagon at a standardized glucose level, insulin action in vivo, and insulin binding and action in vitro in fat cells improved significantly. Glucose 115-122 insulin Homo sapiens 7-14 3044067-5 1988 The mean daily glucose concentration after post-insulin oral therapy correlated with the initial pre-insulin therapy glucose concentration (r = 0.83, p less than 0.001). Glucose 15-22 insulin Homo sapiens 48-55 3044067-5 1988 The mean daily glucose concentration after post-insulin oral therapy correlated with the initial pre-insulin therapy glucose concentration (r = 0.83, p less than 0.001). Glucose 15-22 insulin Homo sapiens 101-108 3044067-5 1988 The mean daily glucose concentration after post-insulin oral therapy correlated with the initial pre-insulin therapy glucose concentration (r = 0.83, p less than 0.001). Glucose 117-124 insulin Homo sapiens 101-108 3044067-10 1988 The mechanism behind the change of glycemic control after cessation of insulin therapy seems to be an increase in the basal glucose production rate rather than deterioration of extrahepatic insulin action or the insulin secretory response. Glucose 124-131 insulin Homo sapiens 71-78 3282953-7 1988 The variability of insulin responses to intravenous glucose severely limits their value as early predictors of B-cell failure. Glucose 52-59 insulin Homo sapiens 19-26 3292314-3 1988 However, insulin clearance, whether calculated as the molar ratio of integrated C-peptide to integrated insulin responses (6.9 +/- 0.7 vs. 14.2 +/- 3.8, P = .005) or from the formula insulin clearance equals insulin secretion divided by integrated insulin responses (1.1 +/- 0.2 vs. 2.5 +/- 0.7 L.min-1.m-2, respectively, P = .002), was less for oral than for intravenous glucose. Glucose 372-379 insulin Homo sapiens 9-16 3292317-5 1988 The C-peptide model also provides a direct prehepatic measure of beta-cell sensitivity to glucose, expressed by two parameters related to first (phi IC)- and second (phi IIC)-phase insulin secretion. Glucose 90-97 insulin Homo sapiens 4-13 3293879-1 1988 It has been previously demonstrated that Indians have an exaggerated insulin response to oral glucose when compared to Africans. Glucose 94-101 insulin Homo sapiens 69-76 3126668-3 1988 Insulin-mediated glucose uptake was higher on E and ER days compared with R days. Glucose 17-24 insulin Homo sapiens 0-7 3126668-10 1988 The conclusions drawn are that prolonged moderate exercise increases insulin action on glucose uptake in humans by reducing apparent Km and increasing Vmax. Glucose 87-94 insulin Homo sapiens 69-76 3279746-7 1988 The sustained plasma glucose levels after the amylose meal with reduced insulin requirement suggest amylose starch may be of potential benefit to carbohydrate-sensitive or diabetic individuals. Glucose 21-28 insulin Homo sapiens 72-79 3279811-2 1988 Insulin secretion rates were calculated during a 1-h base line and for 5 h after glucose administration from a two-compartmental analysis of peripheral C-peptide concentrations using individual kinetic parameters derived after iv bolus injections of biosynthetic human C-peptide. Glucose 81-88 insulin Homo sapiens 0-7 3279811-7 1988 The poststimulatory MCR decreased with increasing doses of both oral and iv glucose concomitant with the greater insulin secretory response (P = 0.0014). Glucose 76-83 insulin Homo sapiens 113-120 3283431-0 1988 [Relation between body fat distribution, insulin levels and glucose tolerance in obese females]. Glucose 60-67 insulin Homo sapiens 41-48 3283431-5 1988 In the women with upper body fat localization (WHR greater than 0.90) significantly higher basal and glucose-stimulated insulin concentrations were established than in the women with a lower body type of obesity (WHR less than 0.78) (basal insulin 27.4 +/- 11.5 vs. 15.4 +/- 8.8 mU/l, p less than 0.05, insulin area 779 +/- 320 vs. 468 +/- 237 U, p less than 0.05). Glucose 101-108 insulin Homo sapiens 120-127 3283431-5 1988 In the women with upper body fat localization (WHR greater than 0.90) significantly higher basal and glucose-stimulated insulin concentrations were established than in the women with a lower body type of obesity (WHR less than 0.78) (basal insulin 27.4 +/- 11.5 vs. 15.4 +/- 8.8 mU/l, p less than 0.05, insulin area 779 +/- 320 vs. 468 +/- 237 U, p less than 0.05). Glucose 101-108 insulin Homo sapiens 240-247 3279571-8 1988 ICC maintained in either FCS or HS displayed significant rates of (pro)insulin biosynthesis in vitro and an increased insulin release when exposed to 16.7 mM glucose plus 5 mM theophylline. Glucose 158-165 insulin Homo sapiens 118-125 3279571-11 1988 When the perfusion fluid was changed from one containing 2.8 mM glucose to one containing 16.7 mM glucose +/- 5 mM theophylline, the secretion of insulin increased within a few min. Glucose 64-71 insulin Homo sapiens 146-153 3279571-11 1988 When the perfusion fluid was changed from one containing 2.8 mM glucose to one containing 16.7 mM glucose +/- 5 mM theophylline, the secretion of insulin increased within a few min. Glucose 98-105 insulin Homo sapiens 146-153 3277829-4 1988 The data support the view that, in type II diabetics, ACE inhibition raises the insulin-stimulated glucose uptake of the whole organism, predominantly due to an increased glucose uptake by the skeletal musculature. Glucose 99-106 insulin Homo sapiens 80-87 3277829-4 1988 The data support the view that, in type II diabetics, ACE inhibition raises the insulin-stimulated glucose uptake of the whole organism, predominantly due to an increased glucose uptake by the skeletal musculature. Glucose 171-178 insulin Homo sapiens 80-87 3279804-1 1988 We measured total body insulin-mediated glucose uptake, carbohydrate oxidation, storage (nonoxidative disposal), muscle glycogen synthase activity, and muscle glucose 6-phosphate (G-6-P) content in response to five levels of insulinemia (means 16, 52, 152, 573, and 5,550 microU/ml) in 16 male glucose-tolerant volunteers. Glucose 40-47 insulin Homo sapiens 23-30 3279804-2 1988 Insulin dissociation constants (KDs) for disposal, storage, and synthase activity (but not for oxidation) are coincident, suggesting that storage via glycogen synthesis could be a major determinant of glucose disposal. Glucose 201-208 insulin Homo sapiens 0-7 3279804-5 1988 The coincidence of insulin sensitivities for disposal, storage, and synthase activity suggest that storage via glycogen synthesis could be a major determinant of glucose disposal. Glucose 162-169 insulin Homo sapiens 19-26 3282953-0 1988 Between and within subject variation of the first phase insulin response to intravenous glucose. Glucose 88-95 insulin Homo sapiens 56-63 2962851-1 1988 Addition of mammalian insulin to a nutritionally rich, chemically defined culture medium affects Neurospora crassa "slime" (wall-less) cells, as indicated by enhancement of growth, extension of viability at the stationary phase of growth, alteration of morphology, and stimulation of glucose oxidation. Glucose 284-291 insulin Homo sapiens 22-29 3276717-12 1988 In contrast to the responses to EGF, insulin- and IGF1-activation of S6 kinase was enhanced when glucose was present and depended on the presence of bicarbonate in the medium. Glucose 97-104 insulin Homo sapiens 37-44 3276722-5 1988 After the fat meal, peak insulin and C-peptide levels in response to iv glucose were 60% greater than those after carbohydrate alone despite similar peak blood glucose levels. Glucose 72-79 insulin Homo sapiens 25-32 3276722-7 1988 We conclude that glucose-stimulated insulin secretion is increased early after fat ingestion, possibly due to a rise in GIP or other incretins. Glucose 17-24 insulin Homo sapiens 36-43 3276729-2 1988 Insulin secretion rates were substantially higher than normal in the obese subjects after an overnight fast (86.7 +/- 7.1 vs. 50.9 +/- 4.8 pmol/m2 per min, P less than 0.001, mean +/- SEM), over a 24-h period on a mixed diet (279.6 +/- 24.2 vs. 145.8 +/- 8.8 nmol/m2 per 24 h, P less than 0.001), and during a hyperglycemic intravenous glucose infusion (102.2 +/- 10.8 vs. 57.2 +/- 2.8 nmol/m2 per 180 min, P less than 0.001). Glucose 336-343 insulin Homo sapiens 0-7 3276730-14 1988 In both groups of subjects, greater than 80% of insulin pulses were concomitant with a pulse in glucose concentration in the postmeal period. Glucose 96-103 insulin Homo sapiens 48-55 3284873-4 1988 Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. Glucose 270-277 insulin Homo sapiens 150-157 3284873-4 1988 Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. Glucose 270-277 insulin Homo sapiens 150-157 3284873-4 1988 Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. Glucose 270-277 insulin Homo sapiens 150-157 3284873-4 1988 Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. Glucose 270-277 insulin Homo sapiens 150-157 3284873-4 1988 Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. Glucose 270-277 insulin Homo sapiens 150-157 3077893-0 1988 [Insulin response to the oral glucose tolerance test in obese patients and in subjects with a family history of diabetes mellitus]. Glucose 30-37 insulin Homo sapiens 1-8 3283208-6 1988 Basal oxytocin levels and glucose response to insulin did not change after weight reduction. Glucose 26-33 insulin Homo sapiens 46-53 2893241-3 1988 The insulin sensitivity, measured as the glucose utilization rate during steady state of euglycemia (M) was significantly decreased (P less than .01) among the patients compared to the controls (5.5 +/- 1.9 mg/kg BW/min [mean +/- SD] and 7.2 +/- 1.2, respectively). Glucose 41-48 insulin Homo sapiens 4-11 2455081-0 1988 [Inhibitory action of galanin on insulin secretion--effects on basal and glucose-stimulated secretion of insulin]. Glucose 73-80 insulin Homo sapiens 105-112 3275462-6 1988 Comparative studies of initial glucose uptake after 10 s and tracer D-glucose conversion to total lipids after 90 min showed high coefficients of correlation between basal rates (r = 0.87), maximal response above basal level to insulin (r = 0.92) and insulin sensitivity (r = 0.78). Glucose 68-77 insulin Homo sapiens 228-235 3275462-12 1988 Both basal, half-maximal and maximal insulin-stimulated rates of adipocyte glucose utilization were dependent on the glucose concentration. Glucose 75-82 insulin Homo sapiens 37-44 3275462-12 1988 Both basal, half-maximal and maximal insulin-stimulated rates of adipocyte glucose utilization were dependent on the glucose concentration. Glucose 117-124 insulin Homo sapiens 37-44 3275462-13 1988 Thus, comparing lipogenesis at tracer and at 0.5 mmol/l medium glucose concentration, it was shown that the higher medium glucose concentration was associated with a 60% lowering of the basal rate, a 35% reduction in the percentage response above baseline to maximal insulin stimulation and a 4-fold increase in the insulin sensitivity. Glucose 122-129 insulin Homo sapiens 267-274 3275462-13 1988 Thus, comparing lipogenesis at tracer and at 0.5 mmol/l medium glucose concentration, it was shown that the higher medium glucose concentration was associated with a 60% lowering of the basal rate, a 35% reduction in the percentage response above baseline to maximal insulin stimulation and a 4-fold increase in the insulin sensitivity. Glucose 122-129 insulin Homo sapiens 316-323 3043988-2 1988 The microprocessor recommends modification of the insulin doses so as to reach a pre-prandial blood glucose value of 110 mg/dl or a urine glucose concentration of 0.1 g/dl. Glucose 100-107 insulin Homo sapiens 50-57 3043988-2 1988 The microprocessor recommends modification of the insulin doses so as to reach a pre-prandial blood glucose value of 110 mg/dl or a urine glucose concentration of 0.1 g/dl. Glucose 138-145 insulin Homo sapiens 50-57 2903616-5 1988 Insulin resistance was determined by a constant rate intravenous infusion of somatostatin, insulin and glucose. Glucose 103-110 insulin Homo sapiens 0-7 2894750-2 1988 Blood glucose levels during a somatostatin (100 micrograms X h-1)-insulin (0.4 mU X kg-1 X min-1)-glucose (4.5 mg X kg-1)-infusion test (SIGIT) performed between 11 a.m. and 3 p.m. served as an indicator of total body insulin resistance. Glucose 6-13 insulin Homo sapiens 66-73 2894750-7 1988 We conclude that hypoglycemia evokes a state of insulin resistance for several hours, as demonstrated by elevated blood glucose levels during a somatostatin-insulin-glucose-infusion test. Glucose 120-127 insulin Homo sapiens 48-55 2894750-7 1988 We conclude that hypoglycemia evokes a state of insulin resistance for several hours, as demonstrated by elevated blood glucose levels during a somatostatin-insulin-glucose-infusion test. Glucose 120-127 insulin Homo sapiens 157-164 3144155-1 1988 Insulin-induced antilipolysis was investigated in fat cells obtained after an overnight fast and 60 min after glucose ingestion in seven non-obese patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 110-117 insulin Homo sapiens 0-7 3126626-1 1988 The effect of combined insulin-glibenclamide therapy on glucose control was evaluated in a double-blind placebo controlled study of 20 patients with non-insulin-dependent diabetes mellitus (NIDDM) and second failure to oral antidiabetic therapy with glibenclamide or glipizide. Glucose 56-63 insulin Homo sapiens 23-30 3144155-3 1988 After treatment, the antilipolytic potency of insulin in fat cells was threefold enhanced (p less than 0.05) in the fasting state and remained unaltered after glucose ingestion. Glucose 159-166 insulin Homo sapiens 46-53 3144155-4 1988 In untreated NIDDM oral glucose induced a significant (p less than 0.01) increase in insulin sensitivity. Glucose 24-31 insulin Homo sapiens 85-92 3134799-8 1988 Reduced glucose storage in muscle, regulated by glycogen synthase, is important in determining insulin resistance especially at high plasma insulin concentrations and it is possible that a specific genetic defect may be the cause of this. Glucose 8-15 insulin Homo sapiens 95-102 3134799-8 1988 Reduced glucose storage in muscle, regulated by glycogen synthase, is important in determining insulin resistance especially at high plasma insulin concentrations and it is possible that a specific genetic defect may be the cause of this. Glucose 8-15 insulin Homo sapiens 140-147 3144155-5 1988 In consequence, in the glucose-fed state insulin sensitivity was similar before and after therapy. Glucose 23-30 insulin Homo sapiens 41-48 3144155-9 1988 At the same time, fasting and glucose-stimulated circulating insulin were significantly (p less than 0.01) increased. Glucose 30-37 insulin Homo sapiens 61-68 3218908-4 1988 Sulphonylureas also potentiate the action of insulin in peripheral glucose uptake and metabolism, even when no measurable effects on insulin receptors can be demonstrated. Glucose 67-74 insulin Homo sapiens 45-52 3285636-3 1988 We compared insulin concentrations during oral glucose tolerance test and insulin receptor binding to both monocytes and erythrocytes from 9 patients with CF, with results from 10 healthy controls of similar body weight. Glucose 47-54 insulin Homo sapiens 12-19 3285636-4 1988 The insulin: glucose ratio was increased in the fasting state (p less than 0.05) in patients with CF compared to controls, indicating an increased insulin resistance in CF-patients. Glucose 13-20 insulin Homo sapiens 4-11 3285636-4 1988 The insulin: glucose ratio was increased in the fasting state (p less than 0.05) in patients with CF compared to controls, indicating an increased insulin resistance in CF-patients. Glucose 13-20 insulin Homo sapiens 147-154 3285636-5 1988 The total insulin secretion during oral glucose tolerance test as judged by the area beneath the insulin curve was similar in the two groups, but insulin secretion was significantly delayed in patients with CF. Glucose 40-47 insulin Homo sapiens 10-17 3276163-3 1988 An insulin sensitivity index was calculated as the reciprocal of the insulin and glucose product multiplied by 10,000. Glucose 81-88 insulin Homo sapiens 3-10 2908423-0 1988 Insulin affects glucose uptake by muscle and mammary tissues of lactating ewes. Glucose 16-23 insulin Homo sapiens 0-7 3281577-0 1988 Effects of ingesting glucose and some of its polymers on serum glucose and insulin levels in men and women. Glucose 21-28 insulin Homo sapiens 75-82 3281577-6 1988 At any glucose dose level the serum insulin response was approximately 40% greater in men compared to women. Glucose 7-14 insulin Homo sapiens 36-43 2908423-6 1988 These observations confirm the role of insulin in regulating glucose uptake by skeletal muscle and raise the possibility that insulin also regulates glucose uptake by the mammary gland. Glucose 61-68 insulin Homo sapiens 39-46 2908423-6 1988 These observations confirm the role of insulin in regulating glucose uptake by skeletal muscle and raise the possibility that insulin also regulates glucose uptake by the mammary gland. Glucose 149-156 insulin Homo sapiens 126-133 3277616-0 1988 Qualitative and quantitative comparison of glucose transport activity and glucose transporter concentration in plasma membranes from basal and insulin-stimulated rat adipose cells. Glucose 43-50 insulin Homo sapiens 143-150 3071387-10 1988 The changes in the concentrations of glucose, lactate, pyruvate, alanine and insulin in the blood were also related to the amount of the glucose load. Glucose 137-144 insulin Homo sapiens 77-84 3277616-2 1988 In these membranes, the magnitude of glucose-transport stimulation in response to insulin was compared with the concentration of transporters as measured with the cytochalasin-B-binding assay or by immunoblotting with an antiserum against the human erythrocyte glucose transporter. Glucose 37-44 insulin Homo sapiens 82-89 3277616-4 1988 Under carefully controlled homogenization conditions, insulin-treated adipose cells yielded plasma membranes with a glucose transport activity 10-15-fold higher than that in membranes from basal cells. Glucose 116-123 insulin Homo sapiens 54-61 3071387-12 1988 It is suggested that the modulation of this oxidative response to glucose ingestion occurs in the insulin-dependent tissues. Glucose 66-73 insulin Homo sapiens 98-105 3154682-7 1988 Serum insulin levels during oral glucose tolerance test at 120 min were decreased after pindolol therapy, but no significant changes were found in C-peptide levels during treatment periods. Glucose 33-40 insulin Homo sapiens 6-13 2978011-1 1988 The effects of endogenous opiates on insulin response to oral glucose load were studied in obese subjects and in lean healthy volunteers. Glucose 62-69 insulin Homo sapiens 37-44 2978011-7 1988 These data suggest that increased endogenous opiates may affect insulin response to glucose in obese with impaired or normal oral glucose tolerance test. Glucose 84-91 insulin Homo sapiens 64-71 2978011-7 1988 These data suggest that increased endogenous opiates may affect insulin response to glucose in obese with impaired or normal oral glucose tolerance test. Glucose 130-137 insulin Homo sapiens 64-71 3064931-7 1988 Therefore, the role played by insulin in the control of blood glucose levels seems to be programmed on a circadian basis rather than by a time independent feedback phenomenon as postulated by the conventional homeostatic hypothesis. Glucose 62-69 insulin Homo sapiens 30-37 2452047-0 1988 Relationship between ionic surroundings and insulin actions on glucose transport and Na,K-pump in muscles. Glucose 63-70 insulin Homo sapiens 44-51 2452047-2 1988 It is well known that insulin has various effects on glucose transport and the Na,K-pump in muscles. Glucose 53-60 insulin Homo sapiens 22-29 2452047-6 1988 In this review article, the actions of ionic surroundings and insulin on glucose transport in muscles are discussed; in particular, the effects of changes in extracellular and/or intracellular concentrations of Na, K, Ca and H ions will be mentioned. Glucose 73-80 insulin Homo sapiens 62-69 2452047-13 1988 The relationship between the insulin-induced change in membrane potential and glucose transport will be also mentioned. Glucose 78-85 insulin Homo sapiens 29-36 3275557-6 1988 Infusion of insulin at a rate of 0.15 U.kg-1.h-1 for 60 min caused a continuous decrease in the plasma glucose level, resulting in neuroglycopenia in 7 of the 10 CPR nonresponders but only 2 of the CPR responders. Glucose 103-110 insulin Homo sapiens 12-19 3284711-4 1988 In addition the insulin:glucose ratios were also significantly increased (34.3 (8.5) v 24.6 (6.7), p less than 0.01), consistent with decreased insulin sensitivity. Glucose 24-31 insulin Homo sapiens 16-23 2964328-5 1988 Postoperatively, the rise in insulin in the glucose primed NIDDM patients contrasted with the slower rise in the non-glucose primed NIDDM patients who were also hyperglycaemic by this stage. Glucose 44-51 insulin Homo sapiens 29-36 3276474-5 1988 Fasting insulin levels and insulin responses to oral glucose (elevation above basal) were elevated. Glucose 53-60 insulin Homo sapiens 8-34 3276480-3 1988 The greater increase in insulin could be explained largely, but not entirely, by the protein and fructose in the mixed meal (85%) which, in addition to glucose, are known insulin secretagogues. Glucose 152-159 insulin Homo sapiens 24-31 3280370-2 1988 However, to achieve glucose homeostasis in human diabetic patients, insulin release by microencapsulated islets must increase in response to a glucose load. Glucose 20-27 insulin Homo sapiens 68-75 3076563-0 1988 Blood levels of insulin, glucagon and gastrin following intravenous and oral glucose administration in children with simple obesity. Glucose 77-84 insulin Homo sapiens 16-23 3292304-1 1988 We determined in 5 control subjects and in one patient with total congenital lipoatrophy (LA) the effect of insulin infusion on glucose flux and some aspects of lipid metabolism. Glucose 128-135 insulin Homo sapiens 108-115 3292304-3 1988 Raising peripheral insulin levels to 28 +/- 3 mU.l-1 suppressed endogenous glucose production in the control subjects whereas in LA significant (2.01 mg.kg-1.min-1) production persisted even when peripheral insulinemia was raised to 58 mU.l-1. Glucose 75-82 insulin Homo sapiens 19-26 3292304-4 1988 Insulin infusion in control subjects increased progressively glucose utilization to a final value of 15.7 +/- 0.7 mg.kg-1.min-1 (corresponding plasma insulin: 482 +/- 44 mU.l-1). Glucose 61-68 insulin Homo sapiens 0-7 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 41-48 insulin Homo sapiens 0-7 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 91-98 insulin Homo sapiens 118-125 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 91-98 insulin Homo sapiens 169-176 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 91-98 insulin Homo sapiens 169-176 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 91-98 insulin Homo sapiens 118-125 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 91-98 insulin Homo sapiens 169-176 3292304-5 1988 Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). Glucose 91-98 insulin Homo sapiens 169-176 3292305-3 1988 After intra-nasal insulin administration, plasma insulin levels rose from 5 +/- 1 to 38 +/- 10 mU/l (2p less than 0.01) at min 15, blood glucose concentrations decreased from 4.4 +/- 0.2 to 3.2 +/- 0.3 mmol/l (2p less than 0.01) at min 45, plasma C-peptide levels diminished from 327 +/- 31 to 174 +/- 28 mumol/l (2p less than 0.01) at min 60 and plasma free fatty acids concentrations fell from 336 +/- 109 to 130 +/- 31 mumol/l (2p less than 0.05) at min 30. Glucose 137-144 insulin Homo sapiens 18-25 3292305-5 1988 There was a close relationship between the individual maximal decreases in blood glucose levels and the individual maximal increases in plasma insulin (r = 0.81), glucagon (r = 0.88), cortisol (r = 0.87) and growth hormone (r = 0.76) concentrations. Glucose 81-88 insulin Homo sapiens 143-150 2900205-3 1988 The effect of SMS 201-995 (50 micrograms s.c.) on glucose control by exogenous insulin has been documented in a series of type I diabetics after stabilization of blood sugar by an artificial pancreas. Glucose 50-57 insulin Homo sapiens 79-86 3056808-9 1988 Subcutaneous injection of equipotent amounts of biosynthetic human proinsulin and biosynthetic human insulin have similar effects on blood glucose levels. Glucose 139-146 insulin Homo sapiens 67-77 3056808-9 1988 Subcutaneous injection of equipotent amounts of biosynthetic human proinsulin and biosynthetic human insulin have similar effects on blood glucose levels. Glucose 139-146 insulin Homo sapiens 70-77 3056809-0 1988 Effect of a two hour proinsulin infusion on the glucose lowering potency of a following insulin injection. Glucose 48-55 insulin Homo sapiens 21-31 3056809-0 1988 Effect of a two hour proinsulin infusion on the glucose lowering potency of a following insulin injection. Glucose 48-55 insulin Homo sapiens 24-31 3056809-7 1988 Insulin injection directly after proinsulin infusion decreased blood glucose from 3.81 to 2.52 mmol/l. Glucose 69-76 insulin Homo sapiens 0-7 3056813-4 1988 The intensity and frequency of the glucose infusions given by the BIOSTATOR equipment enable us to draw conclusions regarding the hypoglycaemic efficacy of human proinsulin. Glucose 35-42 insulin Homo sapiens 162-172 3248787-1 1988 The long-term function of glucose sensors under in-vivo conditions is the first prerequisite in the development of glucose-controlled insulin infusion systems. Glucose 26-33 insulin Homo sapiens 134-141 3248787-1 1988 The long-term function of glucose sensors under in-vivo conditions is the first prerequisite in the development of glucose-controlled insulin infusion systems. Glucose 115-122 insulin Homo sapiens 134-141 3286444-4 1988 The clinical syndrome associated with the secretion of an abnormal insulin or proinsulin molecule presents with apparent endogenous insulin resistance with inappropriate high levels of insulin for the prevailing blood glucose concentration and a high insulin/C-peptide ratio due to the reduced catabolism of the abnormal insulin molecule. Glucose 218-225 insulin Homo sapiens 78-88 3286444-4 1988 The clinical syndrome associated with the secretion of an abnormal insulin or proinsulin molecule presents with apparent endogenous insulin resistance with inappropriate high levels of insulin for the prevailing blood glucose concentration and a high insulin/C-peptide ratio due to the reduced catabolism of the abnormal insulin molecule. Glucose 218-225 insulin Homo sapiens 67-74 3286444-4 1988 The clinical syndrome associated with the secretion of an abnormal insulin or proinsulin molecule presents with apparent endogenous insulin resistance with inappropriate high levels of insulin for the prevailing blood glucose concentration and a high insulin/C-peptide ratio due to the reduced catabolism of the abnormal insulin molecule. Glucose 218-225 insulin Homo sapiens 81-88 3286444-4 1988 The clinical syndrome associated with the secretion of an abnormal insulin or proinsulin molecule presents with apparent endogenous insulin resistance with inappropriate high levels of insulin for the prevailing blood glucose concentration and a high insulin/C-peptide ratio due to the reduced catabolism of the abnormal insulin molecule. Glucose 218-225 insulin Homo sapiens 81-88 3280704-6 1988 It is concluded that the dynamics of insulin release by the tumoral cells, when compared to that of normal islet cells, are characterized by several anomalies, including a high basal ratio between secretion and content, a low threshold (less than or equal to 1.4 mmol/l) in the secretory response to D-glucose, and a lesser responsiveness to nutrient than nonnutrient secretagogues. Glucose 300-309 insulin Homo sapiens 37-44 2961783-2 1988 Further, since women with PCO have significantly higher basal and/or glucose-stimulated plasma insulin levels, we also examined the effects of chronic hyperinsulinemia on gonadotropin and gonadal steroid secretion. Glucose 69-76 insulin Homo sapiens 95-102 2961783-5 1988 The obese PCO women had significantly increased basal and glucose-stimulated plasma insulin levels compared to the other groups, the nonobese PCO and the obese normal women had similar insulin levels, and the nonobese normal women had the lowest insulin levels. Glucose 58-65 insulin Homo sapiens 84-91 3056816-6 1988 During the test period with basal proinsulin infusion, plasma glucose control (MBG, MAGE, M-value) was significantly better (P less than 0.05) when compared to periods with basal insulin infusion. Glucose 62-69 insulin Homo sapiens 34-44 3056816-6 1988 During the test period with basal proinsulin infusion, plasma glucose control (MBG, MAGE, M-value) was significantly better (P less than 0.05) when compared to periods with basal insulin infusion. Glucose 62-69 insulin Homo sapiens 37-44 3056816-8 1988 It is concluded that subcutaneous basal proinsulin infusion, supplemented by subcutaneous premeal insulin administration, can be used for glucose control of patients with type I diabetes. Glucose 138-145 insulin Homo sapiens 40-50 3056816-8 1988 It is concluded that subcutaneous basal proinsulin infusion, supplemented by subcutaneous premeal insulin administration, can be used for glucose control of patients with type I diabetes. Glucose 138-145 insulin Homo sapiens 43-50 3056817-1 1988 The investigation on hand leads to the conclusion that HPRO can additively increase the blood glucose lowering effect of endogenous and exogenously administered insulin. Glucose 94-101 insulin Homo sapiens 161-168 3065208-4 1988 On the contrary at higher insulin infusion rate (0.6 mU/kg.min) plasma glucose levels and GIR remained unaffected throughout the study. Glucose 71-78 insulin Homo sapiens 26-33 3069695-0 1988 Effects of insulin on glucose transport and lipolysis. Glucose 22-29 insulin Homo sapiens 11-18 3074037-1 1988 An electrocatalytic glucose sensor is a very useful component of an artificial beta cell in controlling the insulin dosage in the diabetes therapy. Glucose 20-27 insulin Homo sapiens 108-115 3397043-3 1988 The subjects with polycystic ovaries presented a significantly greater mean glucose response area for the same or greater mean insulin response area than the obese or nonobese normal subjects. Glucose 76-83 insulin Homo sapiens 127-134 3058617-5 1988 There was an inverse correlation between fasting plasma glucose and summated means of glucose and insulin levels after an oral glucose tolerance test and HDL cholesterol in the two groups; on the contrary a positive relationship between the same parameters and HDL triglyceride occurred. Glucose 56-63 insulin Homo sapiens 98-105 3069763-6 1988 This diminished responsiveness of TG to an insulin, glucose infusion in normotriglyceridemic obese subjects is another manifestation of the insulin resistance of obesity. Glucose 52-59 insulin Homo sapiens 43-50 3069763-6 1988 This diminished responsiveness of TG to an insulin, glucose infusion in normotriglyceridemic obese subjects is another manifestation of the insulin resistance of obesity. Glucose 52-59 insulin Homo sapiens 140-147 3069764-6 1988 Both IGT and diabetes, on the other hand, were associated with increased plasma insulin and free fatty acid (FFA) levels, both in the fasting state and following glucose ingestion (P = 0.05-P less than 0.002). Glucose 162-169 insulin Homo sapiens 80-87 3069764-8 1988 Duration of obesity had significant metabolic consequences in its own right: a fall in the insulin response to glucose (P = 0.05) and in the rate of total glucose oxidation (P = 0.03), and a rise in post-OGTT glucose levels (P = 0.04). Glucose 111-118 insulin Homo sapiens 91-98 3069766-4 1988 The major change in adipocyte metabolism was a decrease in basal and insulin-stimulated glucose utilization in NIDDM, relative to the enhanced responses observed in cells from the obese-hyperinsulinemic monkeys. Glucose 88-95 insulin Homo sapiens 69-76 3069766-6 1988 Basal and insulin-stimulated glucose utilization dropped markedly as hyperinsulinemia progressed into diabetes. Glucose 29-36 insulin Homo sapiens 10-17 3275693-10 1988 When chased at 16.7 mM glucose, there was a significant decrease in the secretion of newly made insulin in the old islets compared with the young islets. Glucose 23-30 insulin Homo sapiens 96-103 3275693-13 1988 The differential effects of aging on these steps in the insulin synthesis-secretion pathway may be due to varying impairments in signals transducing the glucose stimulus into the wide range of B cell responses to glucose. Glucose 153-160 insulin Homo sapiens 56-63 3275693-13 1988 The differential effects of aging on these steps in the insulin synthesis-secretion pathway may be due to varying impairments in signals transducing the glucose stimulus into the wide range of B cell responses to glucose. Glucose 213-220 insulin Homo sapiens 56-63 3275857-0 1988 Quantification of the relative impairment in actions of insulin on hepatic glucose production and peripheral glucose uptake in non-insulin-dependent diabetes mellitus. Glucose 75-82 insulin Homo sapiens 56-63 3063989-5 1988 The technique was modified in order to inject insulin intraperitoneally, four times per day, to control blood glucose level. Glucose 110-117 insulin Homo sapiens 46-53 3050976-2 1988 The serum insulin concentration increased proportionally (p less than 0.01) to the serum glucose concentration. Glucose 89-96 insulin Homo sapiens 10-17 3065776-9 1988 However, when the concentration of glucose was increased to 20 or 30 mM, stimulation of insulin secretion returned to levels achieved with TPA alone. Glucose 35-42 insulin Homo sapiens 88-95 3126291-4 1988 The overall relationship between the C-peptide (Cc), glyburide (Cd), and glucose (Cg) serum concentrations is successfully described by operator equations of the form, Cc(t) = t-infinity psi p(t-u)phi t(Cd(u), Cg(u)) du or Cc(t) = t-infinity psi p(t-u)phi t(Cd(u), Cg(u),u) du. Glucose 73-80 insulin Homo sapiens 37-46 3275857-0 1988 Quantification of the relative impairment in actions of insulin on hepatic glucose production and peripheral glucose uptake in non-insulin-dependent diabetes mellitus. Glucose 109-116 insulin Homo sapiens 56-63 3275857-2 1988 We, therefore, determined the dose-response characteristics for insulin-mediated suppression of hepatic glucose production (GP) and stimulation of peripheral glucose uptake (GU) in 14 NIDDM subjects and 14 age- and weight-matched nondiabetic volunteers (NV) using the glucose clamp sequential insulin infusion technique along with isotopic estimation of glucose flux. Glucose 104-111 insulin Homo sapiens 64-71 3055103-8 1988 During the suckling period, the concentration of lipid-derived substrates is high as well as the muscle capacity for their oxidation; moreover, insulin concentration is low and insulin sensitivity of muscle glucose utilization is also reduced. Glucose 207-214 insulin Homo sapiens 177-184 3076251-0 1988 [Controlled release systems of insulin using glucose-responsive polymers]. Glucose 45-52 insulin Homo sapiens 31-38 3061180-2 1988 A flat blood sugar and insulin curve by oral glucose tolerance test was found without manifested hyperglycemia and hyperinsulinemia. Glucose 45-52 insulin Homo sapiens 23-30 2826429-4 1987 Insulin (200 nM) stimulated glucose transport in basal fibroblasts by only 9%. Glucose 28-35 insulin Homo sapiens 0-7 2826429-5 1987 However, addition of insulin for 30 min to cells that had been treated for 4 h with dexamethasone completely reversed the dexamethasone-induced decrease in glucose transport and also reversed the dexamethasone-induced changes in glucose transporter polypeptide content of the plasma membrane and P2 fractions. Glucose 156-163 insulin Homo sapiens 21-28 2826429-5 1987 However, addition of insulin for 30 min to cells that had been treated for 4 h with dexamethasone completely reversed the dexamethasone-induced decrease in glucose transport and also reversed the dexamethasone-induced changes in glucose transporter polypeptide content of the plasma membrane and P2 fractions. Glucose 229-236 insulin Homo sapiens 21-28 2827061-5 1987 Insulin sensitivity, measured by the "steady state plasma glucose", obtained after a 150 min glucose-insulin-somatostatin infusion, improved in all patients but two. Glucose 58-65 insulin Homo sapiens 0-7 3320203-5 1987 A half-maximal inhibition of glucose-stimulated insulin release after 7 days of culture was obtained with 100 pg/ml of rIL-1 beta, whereas 1000 pg/ml of rIL-1 alpha were necessary to obtain an equivalent effect. Glucose 29-36 insulin Homo sapiens 48-55 2890903-4 1987 During an intravenous glucose load, it greatly enhanced insulin release and significantly reduced peak plasma glucose concentrations, compared with a control saline infusion, even inducing postinfusion reactive hypoglycaemia. Glucose 22-29 insulin Homo sapiens 56-63 3318380-3 1987 The Asian Indians had significantly higher insulin levels than the Americans at every sampling time during the glucose tolerance test except for the 3-h sample. Glucose 111-118 insulin Homo sapiens 43-50 2892412-1 1987 Restriction fragment length polymorphisms in the insulin gene hypervariable region are compared among 93 women with gestational onset diabetes mellitus and 146 women with normal glucose tolerance during pregnancy. Glucose 178-185 insulin Homo sapiens 49-56 2892414-1 1987 We attempted to improve the precision of the estimation of insulin sensitivity (S1) from the minimal model technique by modifying insulin dynamics during a frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 187-194 insulin Homo sapiens 59-66 2892414-1 1987 We attempted to improve the precision of the estimation of insulin sensitivity (S1) from the minimal model technique by modifying insulin dynamics during a frequently sampled intravenous glucose tolerance test (FSIGT). Glucose 187-194 insulin Homo sapiens 130-137 3322017-11 1987 Similarly, maximal increases in immunoreactive insulin levels after glucose ingestion were significantly greater (p less than 0.01) in obese anovulatory women compared with other groups. Glucose 68-75 insulin Homo sapiens 47-54 3315785-2 1987 Insulin secretion and clearance in response to the administration of oral and intravenous glucose was investigated in nine normal men. Glucose 90-97 insulin Homo sapiens 0-7 3315786-3 1987 Both fasting plasma insulin concentration and glucose-stimulated (hyperglycemic clamp) insulin secretion were significantly (P less than .001) increased in the obese subjects. Glucose 46-53 insulin Homo sapiens 87-94 3315786-9 1987 After the 6-wk training program, insulin-mediated total-body glucose metabolism increased due to significant improvements in peripheral glucose uptake (P less than .01) and more effective suppression of hepatic glucose production (P less than .05). Glucose 61-68 insulin Homo sapiens 33-40 3315786-9 1987 After the 6-wk training program, insulin-mediated total-body glucose metabolism increased due to significant improvements in peripheral glucose uptake (P less than .01) and more effective suppression of hepatic glucose production (P less than .05). Glucose 136-143 insulin Homo sapiens 33-40 3315790-7 1987 We postulate that the decreased rate of tissue glucose uptake and storage associated with insulin resistance is the major cause of the lower thermic effect of ingested glucose in NIDDM. Glucose 47-54 insulin Homo sapiens 90-97 3315790-7 1987 We postulate that the decreased rate of tissue glucose uptake and storage associated with insulin resistance is the major cause of the lower thermic effect of ingested glucose in NIDDM. Glucose 168-175 insulin Homo sapiens 90-97 3447811-2 1987 Insulin was infused for 2 consecutive 100 minute periods at 40 and 400 mU.m-2.min-1, plasma glucose being maintained by 20% dextrose infusion via a Biostator. Glucose 92-99 insulin Homo sapiens 0-7 3330036-6 1987 The amount of glucose delivered by the BIOSTATOR in order to maintain blood glucose steady state concentrations at the "basal" level was taken as a measure of biological activity of the injected insulin. Glucose 14-21 insulin Homo sapiens 195-202 3316262-0 1987 Sex differences in insulin action on glucose transport and transporters in human omental adipocytes. Glucose 37-44 insulin Homo sapiens 19-26 3316264-8 1987 GH also caused increased insulin release when the ICCs were stimulated with 16.7 mM glucose plus 5 mM theophylline. Glucose 84-91 insulin Homo sapiens 25-32 3325486-3 1987 During the 40-mU.m-2.min-1 insulin infusion, the glucose disposal rate was 10.2 +/- 0.5 mg.kg fat-free mass (FFM)-1.min-1 in the trained group compared with 8.0 +/- 0.6 mg.kg FFM-1.min-1 in the untrained group (P less than 0.01). Glucose 49-56 insulin Homo sapiens 27-34 3325486-6 1987 These data demonstrate that 1) the improved insulin action in healthy trained subjects is due to increased sensitivity to insulin, with no change in responsiveness to insulin, and 2) trained subjects have a smaller plasma insulin response to an identical glucose stimulus than untrained individuals. Glucose 255-262 insulin Homo sapiens 44-51 2894388-5 1987 Insulin secretion from nontumorous pancreatic cells surrounding an insulinoma was dose-dependently stimulated by glucose. Glucose 113-120 insulin Homo sapiens 0-7 2894388-11 1987 In conclusion, it was shown that insulin release by the cultured B cells obtained from several pathological conditions differed with regard to the autonomy of hormone release (glucose sensitivity) and the sensitivity to somatostatin and its analog. Glucose 176-183 insulin Homo sapiens 33-40 2891015-2 1987 Designation of HIR and LIR was done on the basis of mathematical modeling of the insulin response to a glucose infusion test. Glucose 103-110 insulin Homo sapiens 81-88 2891015-4 1987 Hyperglycemic clamping (60 min, 11 mmol/L of glucose) induced diphasic insulin and C-peptide responses in all groups. Glucose 45-52 insulin Homo sapiens 83-92 2891015-9 1987 Conversely, the glucose utilization (mg/kg/min) to insulin (mU/L) = M/L ratio was markedly increased in LIR with high insulin sensitivity but not in other groups. Glucose 16-23 insulin Homo sapiens 51-58 2891015-9 1987 Conversely, the glucose utilization (mg/kg/min) to insulin (mU/L) = M/L ratio was markedly increased in LIR with high insulin sensitivity but not in other groups. Glucose 16-23 insulin Homo sapiens 118-125 3317264-6 1987 Hormonal analyses indicated (1) inappropriate early release of glucagon (300 pg/mL at 15 minutes) in patient 1, (2) exuberant early release of insulin (maximum 190 +/- 15 microU/mL) resulting in rapid decrease in glucose concentration in all patients, (3) development and/or persistence of hypoglycemia after the decline in circulating insulin to undetectable levels, and (4) inadequate glucagon response to hypoglycemia resulting in sustained hypoglycemia. Glucose 213-220 insulin Homo sapiens 143-150 3441927-10 1987 Insulin responses to oral glucose were exaggerated and delayed in 21 of 26 patients. Glucose 26-33 insulin Homo sapiens 0-7 2822236-0 1987 Influence of D-glucose upon the respiratory and secretory response of insulin-producing tumor cells to 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid. Glucose 13-22 insulin Homo sapiens 70-77 2822236-2 1987 The metabolic and secretory effects of 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid are opposed to those of D-glucose, which increases respiration, ATP content, and insulin release, while lowering NH4+ production and 14CO2 output from the prelabeled cells. Glucose 110-119 insulin Homo sapiens 167-174 3318831-0 1987 Analysis of proinsulin conversion activated by prior glucose: evidence that glucose stimulates synthesis of the conversion enzyme. Glucose 53-60 insulin Homo sapiens 12-22 3318831-0 1987 Analysis of proinsulin conversion activated by prior glucose: evidence that glucose stimulates synthesis of the conversion enzyme. Glucose 76-83 insulin Homo sapiens 12-22 3318831-1 1987 We examined the mechanism by which prior glucose exposure accelerates conversion of proinsulin to insulin in pancreatic islets. Glucose 41-48 insulin Homo sapiens 84-94 3318831-1 1987 We examined the mechanism by which prior glucose exposure accelerates conversion of proinsulin to insulin in pancreatic islets. Glucose 41-48 insulin Homo sapiens 87-94 3318831-2 1987 Using actinomycin A, introduced at different times after a 3H-leucine pulse to block the intracellular transport of proinsulin, transport was found to be slightly accelerated after prolonged glucose. Glucose 191-198 insulin Homo sapiens 116-126 3331233-0 1987 Plasma insulin and C-peptide responses to oral glucose load after physical exercise in men with normal and impaired glucose tolerance. Glucose 47-54 insulin Homo sapiens 7-14 3331233-0 1987 Plasma insulin and C-peptide responses to oral glucose load after physical exercise in men with normal and impaired glucose tolerance. Glucose 47-54 insulin Homo sapiens 19-28 3331233-5 1987 The data indicate that the reduced insulin response to OGTT during postexercise recovery in healthy subjects is due to diminished insulin secretion without any substantial changes in the hormone removal from blood, whereas in the glucose intolerant men the latter process may be enhanced. Glucose 230-237 insulin Homo sapiens 35-42 3314457-0 1987 Blood pressure reduction after oral glucose loading and its relation to age, blood pressure and insulin. Glucose 36-43 insulin Homo sapiens 96-103 3318492-4 1987 Mean (+/- SE) insulin-stimulated glucose uptake, quantified in vivo by the euglycemic hyperinsulinemic clamp technique, was significantly greater in physically trained individuals at steady-state plasma insulin concentrations of approximately 10 microU/ml (3.41 +/- 0.14 vs. 2.73 +/- 0.22 mg.kg fat free mass-1.min-1, P less than 0.05) and 50 microU/ml (13.58 +/- 0.75 vs. 9.82 +/- 0.53 mg.kg fat free mass-1.min-1, P less than 0.001). Glucose 33-40 insulin Homo sapiens 14-21 3318492-4 1987 Mean (+/- SE) insulin-stimulated glucose uptake, quantified in vivo by the euglycemic hyperinsulinemic clamp technique, was significantly greater in physically trained individuals at steady-state plasma insulin concentrations of approximately 10 microU/ml (3.41 +/- 0.14 vs. 2.73 +/- 0.22 mg.kg fat free mass-1.min-1, P less than 0.05) and 50 microU/ml (13.58 +/- 0.75 vs. 9.82 +/- 0.53 mg.kg fat free mass-1.min-1, P less than 0.001). Glucose 33-40 insulin Homo sapiens 91-98 3318492-5 1987 In addition, mean (+/- SE) hepatic glucose production rate was lower in physically trained subjects at insulin levels of 10 microU/ml (0.63 +/- 0.19 vs. 1.19 +/- 0.22 mg.kg body wt-1.min-1, P less than 0.05) and 50 microU/min (0.18 +/- 0.14 vs. 0.60 +/- 0.17 mg.kg body wt-1.min-1, P less than 0.05). Glucose 35-42 insulin Homo sapiens 103-110 3326443-5 1987 Diabetic children with basal C-peptide levels higher than 0.6 ng/ml had lower blood glucose levels (187 +/- 43 vs 315 +/- 20 mg/dl, p less than 0.02), but no difference in blood glucose or any other parameter was observed as a function of the increase in CPR after breakfast. Glucose 84-91 insulin Homo sapiens 29-38 3330434-2 1987 Precise quantification of insulin sensitivity in vivo is essential for elucidation of the pathogenesis of observed glucose intolerance. Glucose 115-122 insulin Homo sapiens 26-33 3330434-3 1987 The euglycaemic glucose clamp of Andres and colleagues assesses insulin action by disrupting the negative feedback relationship of glucose and insulin. Glucose 16-23 insulin Homo sapiens 64-71 3330434-8 1987 The dose-response relationship between insulin and Rd also provides a measure of sensitivity from the glucose clamp: the ED50 (and Rdmax), analogous to the Km and Vmax of Michaelis-Menten analysis. Glucose 102-109 insulin Homo sapiens 39-46 3330434-10 1987 Glucose clearance (Rd/G) has also been used to assess insulin sensitivity in subjects of differing glycaemia, but because it fails to rise in proportion to glucose it is an inappropriate measure. Glucose 0-7 insulin Homo sapiens 54-61 3330434-11 1987 Hence, we have introduced the insulin sensitivity index SIP(clamp), defined as the action of insulin to increase glucose clearance (delta Rd/(G delta I], which is independent of prevailing glycaemia and insulinaemia. Glucose 113-120 insulin Homo sapiens 30-37 3330434-11 1987 Hence, we have introduced the insulin sensitivity index SIP(clamp), defined as the action of insulin to increase glucose clearance (delta Rd/(G delta I], which is independent of prevailing glycaemia and insulinaemia. Glucose 113-120 insulin Homo sapiens 93-100 3330434-12 1987 Lastly, we proposed the minimal model method, which determines insulin sensitivity (SI) from analysis of the simple intravenous glucose tolerance test (IVGTT). Glucose 128-135 insulin Homo sapiens 63-70 3330434-14 1987 Furthermore, minimal model analysis will also yield SG, the parameter of insulin-independent glucose disappearance. Glucose 93-100 insulin Homo sapiens 73-80 3330434-15 1987 We conclude that assessment of insulin sensitivity, whilst important, must be considered in the context of its relation to pancreatic function and insulin-dependent glucose disappearance. Glucose 165-172 insulin Homo sapiens 31-38 3330434-15 1987 We conclude that assessment of insulin sensitivity, whilst important, must be considered in the context of its relation to pancreatic function and insulin-dependent glucose disappearance. Glucose 165-172 insulin Homo sapiens 147-154 3330435-6 1987 By using the euglycaemic insulin clamp technique or by giving oral glucose loads, it has been shown that the main effect of insulin on carbohydrate metabolism is to stimulate glucose storage. Glucose 67-74 insulin Homo sapiens 124-131 3330435-6 1987 By using the euglycaemic insulin clamp technique or by giving oral glucose loads, it has been shown that the main effect of insulin on carbohydrate metabolism is to stimulate glucose storage. Glucose 175-182 insulin Homo sapiens 124-131 3330435-7 1987 By raising plasma free fatty acid levels with a neutral fat infusion in lean subjects, both glucose oxidation and glucose storage were imparied during euglycaemic insulin clamps. Glucose 92-99 insulin Homo sapiens 163-170 3330435-9 1987 In obese diabetic patients, the impairment in glucose storage was more pronounced than in non-diabetic obese; this defect was particularly marked during euglycaemic insulin clamps, but it was also present after an oral glucose load. Glucose 46-53 insulin Homo sapiens 165-172 3330036-7 1987 The glucose infusion rate increased after insulin administration, reaching statistical significance after 3 hr. Glucose 4-11 insulin Homo sapiens 42-49 3330037-6 1987 In islet B cells cultured in a medium with 16.7 mM glucose, insulin biosynthesis induced by 16.7 mM glucose was enhanced by 158% when cultured in basal medium without glucose. Glucose 51-58 insulin Homo sapiens 60-67 3330037-6 1987 In islet B cells cultured in a medium with 16.7 mM glucose, insulin biosynthesis induced by 16.7 mM glucose was enhanced by 158% when cultured in basal medium without glucose. Glucose 100-107 insulin Homo sapiens 60-67 3330037-6 1987 In islet B cells cultured in a medium with 16.7 mM glucose, insulin biosynthesis induced by 16.7 mM glucose was enhanced by 158% when cultured in basal medium without glucose. Glucose 100-107 insulin Homo sapiens 60-67 3330037-8 1987 However, the addition of 16.7 mM 2-deoxyglucose to the basal medium resulted in a 293% increase in glucose-induced insulin biosynthesis despite a 16% drop in the proinsulin mRNA activity, and primed a dose-dependent increase of insulin biosynthesis over the concentration range of 0 to 16.7 mM glucose. Glucose 40-47 insulin Homo sapiens 115-122 3311856-8 1987 In contrast, nonoxidative glucose disposal was markedly inhibited in nondiabetic and diabetic obese patients during the euglycemic insulin clamp but not during the OGTT. Glucose 26-33 insulin Homo sapiens 131-138 3311856-13 1987 We conclude that 1) reduced glucose oxidation and reduced nonoxidative glucose disposal partake of the insulin resistance of nondiabetic obese and diabetic obese individuals; 2) hyperglycemia provides a compensatory mechanism for the defect in nonoxidative glucose disposal in nondiabetic obese subjects; however, this compensation is characteristically lost when overt diabetes ensues; and 3) increased lipid oxidation may contribute, in part, to the defects in glucose oxidation and nonoxidative glucose uptake in obesity. Glucose 71-78 insulin Homo sapiens 103-110 3311856-13 1987 We conclude that 1) reduced glucose oxidation and reduced nonoxidative glucose disposal partake of the insulin resistance of nondiabetic obese and diabetic obese individuals; 2) hyperglycemia provides a compensatory mechanism for the defect in nonoxidative glucose disposal in nondiabetic obese subjects; however, this compensation is characteristically lost when overt diabetes ensues; and 3) increased lipid oxidation may contribute, in part, to the defects in glucose oxidation and nonoxidative glucose uptake in obesity. Glucose 71-78 insulin Homo sapiens 103-110 3315397-10 1987 There was an increase in serum insulin levels during both cycles; this was significantly greater with the 1% amino acid solution than the 1.36% glucose. Glucose 144-151 insulin Homo sapiens 31-38 3329123-5 1987 The insulin response was significantly higher after the lactose and glucose meals than after the milk and fructose meals. Glucose 68-75 insulin Homo sapiens 4-11 3329124-5 1987 Insulin binding was similar in those women who remained glucose intolerant and those who returned to normal glucose tolerance postpartum. Glucose 56-63 insulin Homo sapiens 0-7 3666316-2 1987 Human adipose tissue lipoprotein lipase (LPL) is stimulated in vivo by an insulin-glucose infusion. Glucose 82-89 insulin Homo sapiens 74-81 3666316-11 1987 Response of cellular LPL to the hormonal regulator insulin-like growth factor I (IGF-I) was modulated by medium glucose. Glucose 112-119 insulin Homo sapiens 51-58 3311718-0 1987 Chelation of intracellular calcium prevents stimulation of glucose transport by insulin and insulinomimetic agents in the adipocyte. Glucose 59-66 insulin Homo sapiens 80-87 3311718-8 1987 The concentrations for half-maximal inhibition (IC50) of stimulated glucose transport by quin2-AM were 26, 35, 25, 14, and 34 microM for insulin, vanadate, Con A, H2O2, and TPA, respectively. Glucose 68-75 insulin Homo sapiens 137-144 3311718-9 1987 Quin2-AM maximally inhibited stimulated glucose uptake by greater than 85% for all of the insulin mimetic agents. Glucose 40-47 insulin Homo sapiens 90-97 3311718-10 1987 In contrast the maximal inhibition of insulin-stimulated glucose transport by quin2-AM was 55 +/- 4%. Glucose 57-64 insulin Homo sapiens 38-45 3311718-11 1987 Therefore, stimulation of glucose transport by insulin and other diverse compounds appears to involve at least one common calcium-dependent intermediate step. Glucose 26-33 insulin Homo sapiens 47-54 3319468-3 1987 Administration of insulin significantly lowered plasma glucose, accompanied by a significant increase in FPA from 0.9 +/- 0.1 ng/ml to 4.3 +/- 1.6 ng/ml (P less than 0.05) as well as a significant increase in circulating levels of epinephrine and growth hormone. Glucose 55-62 insulin Homo sapiens 18-25 3322729-1 1987 An algorithm was developed to determine whether an individualized insulin infusion could maintain plasma glucose in a desirable steady state after surgery. Glucose 105-112 insulin Homo sapiens 66-73 3322729-2 1987 In 24 patients, insulin was provided according to a "glucose-feedback" formula to maintain plasma glucose between 120 and 180 mg/dl (6.7-10.0 mM). Glucose 53-60 insulin Homo sapiens 16-23 3322729-2 1987 In 24 patients, insulin was provided according to a "glucose-feedback" formula to maintain plasma glucose between 120 and 180 mg/dl (6.7-10.0 mM). Glucose 98-105 insulin Homo sapiens 16-23 3328718-2 1987 Prior to the study diabetic patients were maintained normoglycaemic overnight by a glucose controlled insulin infusion. Glucose 83-90 insulin Homo sapiens 102-109 3328720-3 1987 The plasma immunoreactive insulin and C-peptide levels increased to higher levels after an oral glucose load than after an intravenous infusion of glucose. Glucose 96-103 insulin Homo sapiens 26-33 3328720-3 1987 The plasma immunoreactive insulin and C-peptide levels increased to higher levels after an oral glucose load than after an intravenous infusion of glucose. Glucose 96-103 insulin Homo sapiens 38-47 3328720-3 1987 The plasma immunoreactive insulin and C-peptide levels increased to higher levels after an oral glucose load than after an intravenous infusion of glucose. Glucose 147-154 insulin Homo sapiens 26-33 3328720-3 1987 The plasma immunoreactive insulin and C-peptide levels increased to higher levels after an oral glucose load than after an intravenous infusion of glucose. Glucose 147-154 insulin Homo sapiens 38-47 3328720-4 1987 The incremental areas under the immunoreactive insulin and C-peptide curves during arginine infusion were significantly greater (p less than 0.01) after oral than after intravenous glucose administration. Glucose 181-188 insulin Homo sapiens 47-54 3328720-4 1987 The incremental areas under the immunoreactive insulin and C-peptide curves during arginine infusion were significantly greater (p less than 0.01) after oral than after intravenous glucose administration. Glucose 181-188 insulin Homo sapiens 59-68 3328721-3 1987 Insulin secretion as manifested by C-peptide levels remained suppressed for 3-4 h after insulin hypoglycaemia despite return of blood glucose to baseline by 90 min. Glucose 134-141 insulin Homo sapiens 0-7 3328721-4 1987 Glucose kinetic data (3-3H-glucose) performed in six of the subjects indicated that the prolonged insulin resistance was due to significantly increased hepatic glucose production and to suppressed glucose utilisation, persisting for at least 4 h after counterregulatory hormone levels had returned to normal. Glucose 27-34 insulin Homo sapiens 98-105 3328721-4 1987 Glucose kinetic data (3-3H-glucose) performed in six of the subjects indicated that the prolonged insulin resistance was due to significantly increased hepatic glucose production and to suppressed glucose utilisation, persisting for at least 4 h after counterregulatory hormone levels had returned to normal. Glucose 160-167 insulin Homo sapiens 98-105 3327903-0 1987 Impaired glucose counterregulation after insulin-induced hypoglycemia in thalassemic patients. Glucose 9-16 insulin Homo sapiens 41-48 3312937-4 1987 By the fourth month, glucose tolerance had improved with significantly lower T0, T30, and T60 insulin levels. Glucose 21-28 insulin Homo sapiens 94-101 3312938-2 1987 Glucose utilization during 0.4, 1.0, and 10.0 mU/kg x min insulin infusions (producing insulin concentrations ranging from approximately 50 to 2,000 microU/mL) was lower (p less than .02 to .001) in lean and obese diabetic patients compared to weight-matched nondiabetic subjects indicating insulin resistance. Glucose 0-7 insulin Homo sapiens 58-65 3312938-2 1987 Glucose utilization during 0.4, 1.0, and 10.0 mU/kg x min insulin infusions (producing insulin concentrations ranging from approximately 50 to 2,000 microU/mL) was lower (p less than .02 to .001) in lean and obese diabetic patients compared to weight-matched nondiabetic subjects indicating insulin resistance. Glucose 0-7 insulin Homo sapiens 87-94 3312938-2 1987 Glucose utilization during 0.4, 1.0, and 10.0 mU/kg x min insulin infusions (producing insulin concentrations ranging from approximately 50 to 2,000 microU/mL) was lower (p less than .02 to .001) in lean and obese diabetic patients compared to weight-matched nondiabetic subjects indicating insulin resistance. Glucose 0-7 insulin Homo sapiens 87-94 3312938-4 1987 Suppression of glucose production was impaired (P less than .03 and .001) in both the lean and obese diabetic subjects at physiologic but not supraphysiologic insulin concentrations. Glucose 15-22 insulin Homo sapiens 159-166 3312939-6 1987 Insulin resistance in the elderly similarly affects glucose and branched-chain amino acid metabolism, with possible relevant effects on whole-body protein turnover. Glucose 52-59 insulin Homo sapiens 0-7 3118326-5 1987 There was no difference in blood glucose or serum insulin levels between the two groups 24 hours after beginning the infusion; however, at 48 hours there was a significantly (P less than .01) higher insulin level in infants receiving amino acid and glucose infusion compared with those receiving only glucose. Glucose 249-256 insulin Homo sapiens 199-206 3321544-4 1987 After treatment there was a 36% increase in fasting serum insulin concentration (7.6 (0.7) versus 5.6 (0.5) mU/l) and a 32% increase in the area under the serum insulin concentration curve after glucose challenge. Glucose 195-202 insulin Homo sapiens 161-168 3311808-0 1987 Regulation and specificity of glucose-stimulated insulin gene expression in human islets of Langerhans. Glucose 30-37 insulin Homo sapiens 49-56 3311808-2 1987 We report a dosage dependent stimulation of both mRNA levels and insulin secretion by extracellular glucose, and present evidence that islet responsiveness can be divided into two temporal phases: an early response, apparently under post-transcriptional control, and a late phase in which insulin messenger accumulates. Glucose 100-107 insulin Homo sapiens 65-72 3311808-2 1987 We report a dosage dependent stimulation of both mRNA levels and insulin secretion by extracellular glucose, and present evidence that islet responsiveness can be divided into two temporal phases: an early response, apparently under post-transcriptional control, and a late phase in which insulin messenger accumulates. Glucose 100-107 insulin Homo sapiens 289-296 2894103-8 1987 However, after two days of culture accumulative insulin secretory response was reduced and at the end of seven days was less than the insulin produced in low glucose medium. Glucose 158-165 insulin Homo sapiens 134-141 3310655-7 1987 We conclude that 1) prolonged persistence of the increased permeability of mammalian muscle to glucose after exercise requires a low concentration of insulin, and 2) reversal of the increase in permeability does not require glucose transport, glycogen synthesis, or protein synthesis. Glucose 95-102 insulin Homo sapiens 150-164 3310656-2 1987 In small fat cells from 2-mo-old rats, donor"s food restriction led to decreased basal and insulin-stimulated glucose oxidation and fatty acid synthesis but led to increased lactate production, which increased from 4% of total glucose metabolized by cells from fed rats to 62% by cells from fasted rats. Glucose 110-117 insulin Homo sapiens 91-98 3310658-5 1987 At physiological matched rates of glucose disposal, insulin stimulated carbohydrate oxidation 2.4-fold more than glucose. Glucose 34-41 insulin Homo sapiens 52-59 3310658-10 1987 Although FFA availability is almost solely determined by insulin, both glucose and insulin can increase carbohydrate oxidation by increasing glucose availability. Glucose 141-148 insulin Homo sapiens 83-90 3674058-7 1987 All patients had elevated fasting insulin levels; most of them also had an exaggerated insulin response to a glucose load. Glucose 109-116 insulin Homo sapiens 87-94 3307584-0 1987 Biosynthetic human insulin improves postprandial glucose excursions in type I diabetics. Glucose 49-56 insulin Homo sapiens 19-26 3314886-6 1987 Insulin therapy resulted in similar decreases in fasting plasma glucose and increases in fasting free insulin concentrations in all 4 groups. Glucose 64-71 insulin Homo sapiens 0-7 2888695-0 1987 Loss of early phase of insulin release in humans impairs glucose tolerance and blunts thermic effect of glucose. Glucose 57-64 insulin Homo sapiens 23-30 2888695-9 1987 Surprisingly, we found that glucose-induced thermogenesis was reduced in association with loss of the early phase of insulin release (control 102 +/- 21.3 vs. SRIF 72 +/- 27.8 J/5 h, P less than .001). Glucose 28-35 insulin Homo sapiens 117-124 3121350-8 1987 We conclude that these results demonstrate the stimulatory effect of captopril on insulin-induced glucose disposal of the whole body, which appears to be a result of increased glucose utilization by peripheral tissues. Glucose 98-105 insulin Homo sapiens 82-89 3121350-8 1987 We conclude that these results demonstrate the stimulatory effect of captopril on insulin-induced glucose disposal of the whole body, which appears to be a result of increased glucose utilization by peripheral tissues. Glucose 176-183 insulin Homo sapiens 82-89 3308376-2 1987 Glucose levels, 120 min after the load, were inversely and significantly related to insulin sensitivity, measured by means of the euglycemic "glucose clamp" technique (r = -0.746). Glucose 0-7 insulin Homo sapiens 84-91 3308376-2 1987 Glucose levels, 120 min after the load, were inversely and significantly related to insulin sensitivity, measured by means of the euglycemic "glucose clamp" technique (r = -0.746). Glucose 142-149 insulin Homo sapiens 84-91 3325280-3 1987 On the average, in both normal and diabetic subjects, the increases in plasma glucose (PG) and insulin (IRI) were the largest with the oral glucose load and the smallest with the high protein meal. Glucose 140-147 insulin Homo sapiens 95-102 3428864-4 1987 It is concluded that the in vitro promotion of glucose oxidation by hGH requires insulin. Glucose 47-54 insulin Homo sapiens 81-88 3320007-6 1987 The rate of basal glucose transport clearance fell from 28.1 +/- 5.7 fl.cell-1.s-1 to 22.9 +/- 5.6 fl.cell-1.s-1 (P less than 0.005), and the insulin-stimulated increase in glucose transport rate rose from 196 +/- 26 to 279 +/- 33% (P less than 0.025) during the exercise. Glucose 18-25 insulin Homo sapiens 142-149 3320007-7 1987 Thus, in the adipocytes during exercise, the basal glucose transport rate and the responsiveness of glucose transport to insulin changed in the absence of alterations in insulin binding. Glucose 100-107 insulin Homo sapiens 121-128 3308941-1 1987 Central nervous system function during insulin-induced reductions in plasma glucose was studied by measuring plasma epinephrine concentrations and testing cognitive function. Glucose 76-83 insulin Homo sapiens 39-46 3308941-2 1987 Mild glucose reduction [mean plasma glucose, 62 +/- 3 (+/- SEM) mg/dL (3.4 +/- 0.2 mmol/L)] was induced with an iv insulin infusion at the rate of 40 mU/kg.h for 180 min in 7 normal subjects. Glucose 5-12 insulin Homo sapiens 115-122 3308941-4 1987 In contrast, when hypoglycemia was induced (plasma glucose, less than 42 mg/dL; 2.3 mmol/L) by bolus injection of insulin in 4 normal subjects, cognitive function was impaired in every subject, as demonstrated by a delay in completion of the trail-making test. Glucose 51-58 insulin Homo sapiens 114-121 3308958-0 1987 Long-term effect of insulin on glucose transport and insulin binding in cultured adipocytes from normal and obese humans with and without non-insulin-dependent diabetes. Glucose 31-38 insulin Homo sapiens 20-27 3308958-5 1987 The 24-h insulin exposure of adipocytes from control subjects decreased basal and insulin-stimulated glucose transport. Glucose 101-108 insulin Homo sapiens 9-16 3308958-5 1987 The 24-h insulin exposure of adipocytes from control subjects decreased basal and insulin-stimulated glucose transport. Glucose 101-108 insulin Homo sapiens 82-89 3308958-8 1987 The insulin-induced reduction in insulin sensitivity and responsiveness for glucose transport in three groups were due to alterations at insulin binding and postbinding levels. Glucose 76-83 insulin Homo sapiens 4-11 3308958-8 1987 The insulin-induced reduction in insulin sensitivity and responsiveness for glucose transport in three groups were due to alterations at insulin binding and postbinding levels. Glucose 76-83 insulin Homo sapiens 33-40 3308958-8 1987 The insulin-induced reduction in insulin sensitivity and responsiveness for glucose transport in three groups were due to alterations at insulin binding and postbinding levels. Glucose 76-83 insulin Homo sapiens 33-40 2958673-7 1987 A ten-day treatment with naloxone (1.2 mg twice a day) did not change the metabolic and hormonal responses to an oral glucose load (75 g) in lean but significantly inhibited the insulin and C-peptide responses to glucose in obese people. Glucose 213-220 insulin Homo sapiens 190-199 3309545-3 1987 The basal serum insulin concentration and the maximum insulin response to glucose loading were significantly higher (P less than .001 and P less than .01, respectively) in the patient group. Glucose 74-81 insulin Homo sapiens 54-61 3328849-1 1987 We describe two insulin-dependent diabetic females who presented with severe hypoglycaemia associated with atrial fibrillation which reverted to sinus rhythm after intravenous dextrose. Glucose 176-184 insulin Homo sapiens 16-23 3117315-5 1987 Insulin: glucose ratios were raised between half an hour and two hours after the start of the infusion. Glucose 9-16 insulin Homo sapiens 0-7 3117315-8 1987 At the time of the hypoglycaemia plasma insulin concentrations were inappropriately high as shown by a consistent and often considerable increase in the insulin:glucose ratio. Glucose 161-168 insulin Homo sapiens 40-47 3117315-8 1987 At the time of the hypoglycaemia plasma insulin concentrations were inappropriately high as shown by a consistent and often considerable increase in the insulin:glucose ratio. Glucose 161-168 insulin Homo sapiens 153-160 3307402-9 1987 As this study showed, many patients with NIDDM currently receiving treatment with low-dose insulin can have maintained and some even improved glucose and lipid parameters when therapy is converted to glipizide. Glucose 142-149 insulin Homo sapiens 91-98 3307403-6 1987 In the group receiving insulin/glipizide, mean fasting plasma glucose levels decreased from 241.1 mg/dl at baseline to 217.0 mg/dl; two-hour postprandial glucose levels increased from 267.2 to 279.0 mg/dl; glycosylated hemoglobin decreased from 9.1 to 7.5 percent; and post-Sustacal C-peptide levels increased from 0.6 to 1.0 pmol/ml. Glucose 62-69 insulin Homo sapiens 23-30 3307403-6 1987 In the group receiving insulin/glipizide, mean fasting plasma glucose levels decreased from 241.1 mg/dl at baseline to 217.0 mg/dl; two-hour postprandial glucose levels increased from 267.2 to 279.0 mg/dl; glycosylated hemoglobin decreased from 9.1 to 7.5 percent; and post-Sustacal C-peptide levels increased from 0.6 to 1.0 pmol/ml. Glucose 154-161 insulin Homo sapiens 23-30 3307403-7 1987 At the end of 10 weeks, insulin administration was associated with a more rapid decrease in the levels of fasting plasma glucose, two-hour postprandial glucose, and glycosylated hemoglobin, but there was no significant difference between the two therapies by the end of the study. Glucose 121-128 insulin Homo sapiens 24-31 3307403-7 1987 At the end of 10 weeks, insulin administration was associated with a more rapid decrease in the levels of fasting plasma glucose, two-hour postprandial glucose, and glycosylated hemoglobin, but there was no significant difference between the two therapies by the end of the study. Glucose 152-159 insulin Homo sapiens 24-31 3312788-6 1987 Following the glucose load, plasma insulin levels were significantly enhanced in precirrhotic patients at 90 and 120 min and increased at all times in cirrhotic patients. Glucose 14-21 insulin Homo sapiens 35-42 3275860-5 1988 Basally, glucose production was slightly higher in diabetics than in controls (2.51 +/- 0.24 v 2.28 +/- 0.11 mg/kg.min, NS) even though the former had higher plasma glucose (189 +/- 19 v 93 +/- 2 mg/dL, P less than .001) and insulin (23 +/- 4 v 12 +/- 1 microU/mL, P less than .05) concentrations. Glucose 9-16 insulin Homo sapiens 225-232 3307372-5 1987 These findings indicate that, even in early life, a central body fat pattern relates positively to insulin response to glucose load. Glucose 119-126 insulin Homo sapiens 99-106 3307425-3 1987 A significant (p less than 0.01) increase in total insulin dose was found during the initial treatment period (7 +/- 2 days) until the target glucose range was achieved. Glucose 142-149 insulin Homo sapiens 51-58 2828139-12 1987 The posthypoglycaemic insulin resistance was due to a less pronounced insulin effect on both glucose production (clamp I 0.29 +/- 0.21, clamp II 0.86 +/- 0.19 mg . Glucose 93-100 insulin Homo sapiens 22-29 3314727-1 1987 The relation between hepatic glucose production rate (HGPR) and plasma concentrations of insulin and glucagon was investigated in four term neonates who had severe hypoglycaemia. Glucose 29-36 insulin Homo sapiens 89-96 3314727-6 1987 In view of the normal plasma insulin concentrations at a time when the hepatic glucose production rate was reduced, we feel that the absolute concentration of insulin may be less important than the insulin/glucagon molar ratio in the control of glucose homeostasis in this group of infants. Glucose 79-86 insulin Homo sapiens 159-166 3314727-6 1987 In view of the normal plasma insulin concentrations at a time when the hepatic glucose production rate was reduced, we feel that the absolute concentration of insulin may be less important than the insulin/glucagon molar ratio in the control of glucose homeostasis in this group of infants. Glucose 79-86 insulin Homo sapiens 159-166 3314727-6 1987 In view of the normal plasma insulin concentrations at a time when the hepatic glucose production rate was reduced, we feel that the absolute concentration of insulin may be less important than the insulin/glucagon molar ratio in the control of glucose homeostasis in this group of infants. Glucose 245-252 insulin Homo sapiens 159-166 3314727-6 1987 In view of the normal plasma insulin concentrations at a time when the hepatic glucose production rate was reduced, we feel that the absolute concentration of insulin may be less important than the insulin/glucagon molar ratio in the control of glucose homeostasis in this group of infants. Glucose 245-252 insulin Homo sapiens 159-166 2448070-9 1987 The change in this ERC with oral glucose correlated with the incremental insulin response over 2 h (rs = -0.53, P less than 0.006) and to the insulin resistance (rs = -0.56, P less than 0.003). Glucose 33-40 insulin Homo sapiens 73-80 2448070-9 1987 The change in this ERC with oral glucose correlated with the incremental insulin response over 2 h (rs = -0.53, P less than 0.006) and to the insulin resistance (rs = -0.56, P less than 0.003). Glucose 33-40 insulin Homo sapiens 142-149 2828139-12 1987 The posthypoglycaemic insulin resistance was due to a less pronounced insulin effect on both glucose production (clamp I 0.29 +/- 0.21, clamp II 0.86 +/- 0.19 mg . Glucose 93-100 insulin Homo sapiens 70-77 2828139-17 1987 The insulin resistance on both glucose production and utilisation was prevented by propranolol. Glucose 31-38 insulin Homo sapiens 4-11 2828139-18 1987 Thus, the present study demonstrates that hypoglycaemia elicits a prolonged insulin resistance which is due to a less pronounced effect of insulin to both inhibit splanchnic glucose production and to stimulate peripheral glucose utilisation. Glucose 174-181 insulin Homo sapiens 76-83 2828139-18 1987 Thus, the present study demonstrates that hypoglycaemia elicits a prolonged insulin resistance which is due to a less pronounced effect of insulin to both inhibit splanchnic glucose production and to stimulate peripheral glucose utilisation. Glucose 174-181 insulin Homo sapiens 139-146 3123287-0 1987 Effect of insulin immunization on glucose tolerance in normal rats. Glucose 34-41 insulin Homo sapiens 10-17 3322911-0 1987 The effects of glucose-dependent insulinotropic polypeptide infused at physiological concentrations in normal subjects and type 2 (non-insulin-dependent) diabetic patients on glucose tolerance and B-cell secretion. Glucose 15-22 insulin Homo sapiens 33-40 3315513-3 1987 The insulin bolus at 2300 h induced a significant rise in plasma free-insulin levels at 2400 h (+6.9 +/- 1.8 mU/L, P less than .01), resulting in an early and marked fall in blood glucose concentrations between 2300 and 0100 h (-2.7 +/- 0.5 mM, P less than .001), with hypoglycemic values in five patients. Glucose 180-187 insulin Homo sapiens 4-11 3315513-3 1987 The insulin bolus at 2300 h induced a significant rise in plasma free-insulin levels at 2400 h (+6.9 +/- 1.8 mU/L, P less than .01), resulting in an early and marked fall in blood glucose concentrations between 2300 and 0100 h (-2.7 +/- 0.5 mM, P less than .001), with hypoglycemic values in five patients. Glucose 180-187 insulin Homo sapiens 70-77 3322913-6 1987 These results demonstrate that the plasma insulin response to glucose is independently correlated with blood pressure. Glucose 62-69 insulin Homo sapiens 42-49 3322915-3 1987 glucose infusion test even when the insulin sensitivity as estimated by the somatostatin-insulin-glucose infusion test was taken into account. Glucose 0-7 insulin Homo sapiens 36-43 3322915-3 1987 glucose infusion test even when the insulin sensitivity as estimated by the somatostatin-insulin-glucose infusion test was taken into account. Glucose 0-7 insulin Homo sapiens 89-96 3322917-0 1987 Derivation of a quantitative measure of insulin sensitivity from the intravenous tolbutamide test using the minimal model of glucose dynamics. Glucose 125-132 insulin Homo sapiens 40-47 3319860-3 1987 Statistically significantly higher blood glucose values (P less than 0.05) were recorded 6 and 9 h after insulin administration by means of a jet injector, as well as statistically significant higher MBG values (P less than 0.05), thus indicating a faster and shorter effect achieved in comparison to that produced by the syringe injected insulin. Glucose 41-48 insulin Homo sapiens 105-112 3319861-3 1987 During an intravenous glucose tolerance test, the incremental area under the curve for C-peptide and glucose was unchanged, but decreased for insulin, after felodipine. Glucose 22-29 insulin Homo sapiens 87-96 3319861-3 1987 During an intravenous glucose tolerance test, the incremental area under the curve for C-peptide and glucose was unchanged, but decreased for insulin, after felodipine. Glucose 22-29 insulin Homo sapiens 142-149 3319861-7 1987 The increased insulin clearance could be expected to be coupled to a change in glucose tolerance, but this was unaltered during long-term calcium antagonism. Glucose 79-86 insulin Homo sapiens 14-21 3319862-1 1987 Plasma glucose and insulin responses to both oral and intravenous glucose stimulation were evaluated in heroin and methadone addicts, compared to healthy control subjects. Glucose 66-73 insulin Homo sapiens 19-26 2957389-2 1987 To determine whether activation by insulin of glycogen synthase (GS), phosphofructokinase (PFK), or pyruvate dehydrogenase (PDH) in skeletal muscle regulates intracellular glucose metabolism, subjects were studied basally and during euglycemic insulin infusions of 12, 30, and 240 mU/m2 X min. Glucose 172-179 insulin Homo sapiens 35-42 3306278-6 1987 However, we found somewhat lower glucose levels and higher insulin levels in the response to oral glucose challenges after catheterization, but these differences were statistically not significant. Glucose 98-105 insulin Homo sapiens 59-66 3305551-1 1987 This study examined the prevalence of both basal and glucose-stimulated hyperinsulinemia and acanthosis nigricans (AN) as well as the relationship between insulin and androgen levels in hyperandrogenic women. Glucose 53-60 insulin Homo sapiens 77-84 3309352-3 1987 In addition, basal and peak glucose and insulin levels in response to a standard (0.5 gm/kg) intravenous glucose stimulus were measured immediately thereafter to determine if insulin levels reflected insulin production. Glucose 105-112 insulin Homo sapiens 40-47 3309352-5 1987 Peak insulin response to glucose infusion declined from Groups 1 to 3 (51 +/- 14, 42.4 +/- 31, 20.4 +/- 6.8 microU/ml, respectively) with Group 3 exhibiting a significantly decreased mean peak level compared to the other groups. Glucose 25-32 insulin Homo sapiens 5-12 3306278-7 1987 Glucose loads of 50 mg/kg (0.75 g) administered directly to the pancreas via the celiac artery produced peak insulin levels similar to peripheral glucose loads some tenfold larger. Glucose 0-7 insulin Homo sapiens 109-116 2887735-2 1987 There is resistance to insulin-stimulated glucose uptake in patients with hypertension, which is associated with glucose intolerance and hyperinsulinaemia. Glucose 42-49 insulin Homo sapiens 23-30 3626867-2 1987 These effects are presumably due to the role of Cr in glucose tolerance factor (GTF), a complex of Cr and nicotinic acid believed to facilitate insulin binding. Glucose 54-61 insulin Homo sapiens 144-151 3670133-2 1987 It is postulated that in the resting state insulin-dependent tissue uptake of glucose is limited by the rate of blood flow, capillary permeability, and the number of perfused capillaries in the skeletal muscles. Glucose 78-85 insulin Homo sapiens 43-50 3303897-8 1987 Rises in plasma glucose tended to be higher in P than NP women, suggesting that insulin"s effects on glucose and BCAA uptake may be mediated separately. Glucose 16-23 insulin Homo sapiens 80-87 3299096-5 1987 However, total insulin-induced glucose uptake was markedly impaired (3.80 +/- 0.32 vs. 6.31 +/- 0.42 mg per minute per kilogram of body weight in 11 age- and weight-matched controls, P less than 0.001). Glucose 31-38 insulin Homo sapiens 15-22 3299096-9 1987 We conclude that this insulin resistance involves glucose but not lipid or potassium metabolism, is located in peripheral tissues but not the liver, is limited to nonoxidative pathways of intracellular glucose disposal, and is directly correlated with the severity of hypertension. Glucose 50-57 insulin Homo sapiens 22-29 3299096-9 1987 We conclude that this insulin resistance involves glucose but not lipid or potassium metabolism, is located in peripheral tissues but not the liver, is limited to nonoxidative pathways of intracellular glucose disposal, and is directly correlated with the severity of hypertension. Glucose 202-209 insulin Homo sapiens 22-29 3303897-8 1987 Rises in plasma glucose tended to be higher in P than NP women, suggesting that insulin"s effects on glucose and BCAA uptake may be mediated separately. Glucose 101-108 insulin Homo sapiens 80-87 2885238-3 1987 Glucose-potentiated insulin secretion was calculated as the slope of the curve relating increasing ambient glucose levels to the acute insulin response to an intravenous pulse of 5 g of L-arginine. Glucose 107-114 insulin Homo sapiens 20-27 3303967-6 1987 At 1 mumol/l of glucose, where hexose transport is rate limiting, sensitivity and responsiveness of insulin-induced lipogenesis were inhibited by fasting. Glucose 16-23 insulin Homo sapiens 100-107 3303967-8 1987 At 1-10 mmol/l of glucose, where hexose metabolism is rate limiting, insulin stimulated lipogenesis before fasting but was totally ineffective after fasting. Glucose 18-25 insulin Homo sapiens 69-76 3303967-11 1987 Fasting inhibits the lipogenic effect of insulin due to postreceptor changes involving both transport and metabolism of glucose, making lipogenesis unresponsive to insulin at physiological glucose concentrations. Glucose 120-127 insulin Homo sapiens 41-48 3303967-11 1987 Fasting inhibits the lipogenic effect of insulin due to postreceptor changes involving both transport and metabolism of glucose, making lipogenesis unresponsive to insulin at physiological glucose concentrations. Glucose 189-196 insulin Homo sapiens 41-48 3311483-3 1987 The decrease in blood glucose concentrations after insulin injection (0.15 U/kg i.v. Glucose 22-29 insulin Homo sapiens 51-58 3297892-0 1987 Insulin treatment improves glucose-induced insulin release in rats with NIDDM induced by streptozocin. Glucose 27-34 insulin Homo sapiens 0-7 3297892-0 1987 Insulin treatment improves glucose-induced insulin release in rats with NIDDM induced by streptozocin. Glucose 27-34 insulin Homo sapiens 43-50 3311559-3 1987 A computer simulation study using this model showed that the following insulin infusion algorithm is feasible for closed-loop glycemic control by selecting appropriate parameters (Kp/Kd/Kc = 0.0056/0.92/-0.11), IIR(t) = Kp G(t)+Kd d G(t)/dt+Kc, where IIR(t) is the subcutaneous insulin infusion rate at time t (min), G(t) is the blood glucose concentration and Kp, Kd, Kc are the constants. Glucose 335-342 insulin Homo sapiens 71-78 3297892-6 1987 Fed basal plasma glucose levels decreased in diabetic rats from 183 +/- 8 to 136 +/- 10 mg/dl after the 1-day insulin treatment and to 135 +/- 5 mg/dl after the 5-day insulin treatment (vs. 116 +/- 3 mg/dl in control rats). Glucose 17-24 insulin Homo sapiens 110-117 3297892-6 1987 Fed basal plasma glucose levels decreased in diabetic rats from 183 +/- 8 to 136 +/- 10 mg/dl after the 1-day insulin treatment and to 135 +/- 5 mg/dl after the 5-day insulin treatment (vs. 116 +/- 3 mg/dl in control rats). Glucose 17-24 insulin Homo sapiens 167-174 3297892-8 1987 Although the 1-day insulin treatment did not modify the lack of glucose response in the diabetic rats, the 5-day insulin treatment improved their glucose-induced insulin secretion. Glucose 146-153 insulin Homo sapiens 113-120 3297892-9 1987 Moreover, insulin therapy improved the priming effect of glucose on a second stimulation with glucose. Glucose 57-64 insulin Homo sapiens 10-17 3297892-9 1987 Moreover, insulin therapy improved the priming effect of glucose on a second stimulation with glucose. Glucose 94-101 insulin Homo sapiens 10-17 3297892-10 1987 The return of this glucose effect was hardly detectable after the 1-day insulin therapy but was clearly present after the 5-day treatment. Glucose 19-26 insulin Homo sapiens 72-79 2889657-0 1987 Pre-exposure to glucagon impairs glucose recovery after insulin-induced hypoglycemia in man. Glucose 33-40 insulin Homo sapiens 56-63 3311782-1 1987 Circulating levels of insulin and C-peptide in response to oral glucose administration (75 g) were measured in 25 PCOS patients (13 were obese and 12 non-obese) without acanthosis nigricans and in 12 non-obese normal cycling women of similar age. Glucose 64-71 insulin Homo sapiens 22-29 3311782-1 1987 Circulating levels of insulin and C-peptide in response to oral glucose administration (75 g) were measured in 25 PCOS patients (13 were obese and 12 non-obese) without acanthosis nigricans and in 12 non-obese normal cycling women of similar age. Glucose 64-71 insulin Homo sapiens 34-43 3311782-5 1987 Hyperprolactinaemic PCO patients had neither basal level nor sums of insulin and C-peptide levels in response to glucose greater than normoprolactinaemic PCO patients. Glucose 113-120 insulin Homo sapiens 81-90 3311782-7 1987 Total serum testosterone levels correlated significantly with fasting levels and the sum of C-peptide levels in response to glucose. Glucose 124-131 insulin Homo sapiens 92-101 3311782-8 1987 The correlations of total serum testosterone levels with fasting and the sum of insulin levels in response to glucose were also positive but not significant. Glucose 110-117 insulin Homo sapiens 80-87 2885337-1 1987 We examined the effect of somatostatin (SRIH) infusion on insulin-mediated glucose disposal (Rd) in normal young subjects (n = 8) to determine the influence of SRIH on insulin action. Glucose 75-82 insulin Homo sapiens 58-65 2886515-5 1987 Hypoglycemia induced an insulin resistance with a lower steady state glucose infusion rate following the hypoglycemia during placebo as compared to the control study (2.5 +/- 0.5 and 4.8 +/- 1.0 mg/kg min, respectively, P less than 0.05). Glucose 69-76 insulin Homo sapiens 24-31 3600284-2 1987 The glucose infusion was accompanied by a rise over basal values in both glucose (99 +/- 10 mg/dL) and insulin (36 +/- 7 microU/mL) plasma levels, with a further rise of both curves during the Intralipid infusion (140 +/- 7 mg/dL and 53 +/- 12 microU/mL). Glucose 4-11 insulin Homo sapiens 73-130 3300786-7 1987 Thus, it is unlikely that the stimulation of glucose transport by insulin, PDGF and EGF involve transporter phosphorylation. Glucose 45-52 insulin Homo sapiens 66-73 3298939-3 1987 The studies were followed by a hyperglycemic clamp to determine whether cephalic responses would alter overall glucose disposal or glucose-stimulated insulin secretion. Glucose 131-138 insulin Homo sapiens 150-157 3310832-9 1987 After hyperglycaemic clamps at 7.5, 10 and 15 mmol/L glucose, type II diabetics both on and off sulphonylurea, were found to have lower proinsulin concentrations compared with normal subjects, commensurate with the diabetics" lower insulin responses. Glucose 53-60 insulin Homo sapiens 136-146 3300653-0 1987 Insulin stimulation of adipocyte membrane glucose transport. Glucose 42-49 insulin Homo sapiens 0-7 3300653-2 1987 Aspects of the mechanism by which insulin stimulates the membrane glucose transport system were examined by assessing the influence of the bilayer lipid structure on transport stimulation characteristics, and considering the form of the insulin dose-response curve. Glucose 66-73 insulin Homo sapiens 34-41 3300653-7 1987 Curve-fitting experimental insulin dose-response data for stimulation of 2-deoxy-D-glucose and D-glucose uptake provided an estimate of an insulin "association constant" for transport regulation that may be compared with recent insulin receptor binding data. Glucose 81-90 insulin Homo sapiens 27-34 3300653-7 1987 Curve-fitting experimental insulin dose-response data for stimulation of 2-deoxy-D-glucose and D-glucose uptake provided an estimate of an insulin "association constant" for transport regulation that may be compared with recent insulin receptor binding data. Glucose 81-90 insulin Homo sapiens 139-146 3298262-1 1987 We have reported previously that phenylarsine oxide (PAO) blocks insulin-stimulated glucose transport in 3T3-L1 adipocytes (Frost, S. C., and Lane, M. D. (1985) J. Biol. Glucose 84-91 insulin Homo sapiens 65-72 3318257-3 1987 In the basal state, the heroin addicts had markedly reduced insulin responses to intravenous glucose and low glucose disappearance rates (p less than 0.01 vs controls). Glucose 93-100 insulin Homo sapiens 60-67 3318257-4 1987 The infusion of sodium salicylate caused a striking increase of the acute insulin response to intravenous glucose (from 14.5 +/- 4 microU/ml to 88 +/- 11 microU/ml, p less than 0.001) and restored to normal the reduced glucose tolerance (KG from 1.10 +/- 0.1% min-1 to 2.04 +/- 0.19% min-1). Glucose 106-113 insulin Homo sapiens 74-81 3314601-0 1987 [Use of insulin-glucose therapy for the correction of carbohydrate metabolism during open-heart surgery]. Glucose 16-23 insulin Homo sapiens 8-15 3297000-2 1987 To evaluate the effect of the glucose-induced insulin release on peripheral substrate metabolism, we studied muscle metabolism in seven patients after elective surgery and in four healthy volunteers combining the forearm and the euglycemic glucose clamp technique (insulin infusion, 0.2 mU/kg per minute). Glucose 30-37 insulin Homo sapiens 46-53 3297000-4 1987 After 90 minutes of insulin infusion, the whole-body glucose infusion rate was significantly lower in patients who had elective surgery, although plasma insulin concentrations were comparable. Glucose 53-60 insulin Homo sapiens 20-27 2884157-11 1987 We conclude that in IDDM and in totally pancreatectomized patients, administration of insulin with subsequent normalization of blood glucose is accompanied by a decline in plasma levels of SLI in the fasted state, whereas the apparent response to a meal is enhanced. Glucose 133-140 insulin Homo sapiens 86-93 3689144-7 1987 Ration specific reactions could only be proved for the parameters glucose and urea out of the metabolites (insulin, glucose, cholesterol, urea tri-iodine thyronine and thyroxine). Glucose 66-73 insulin Homo sapiens 107-114 3304745-0 1987 Studies on glucose intolerance in chronic renal failure: estimation of insulin sensitivity before and after initiation of hemodialysis. Glucose 11-18 insulin Homo sapiens 71-78 3304745-1 1987 Using the euglycemic insulin clamp technique, we quantified insulin resistance in the genesis of the glucose intolerance observed in patients with CRF. Glucose 101-108 insulin Homo sapiens 60-67 2958378-4 1987 There was a statistically significant correlation between the 2 hour blood glucose value and the fasting plasma insulin level (R = 0.55, p less than 0.05). Glucose 75-82 insulin Homo sapiens 112-119 2956040-5 1987 Fasting blood glucose level was 8.3 mmol/l during treatment with human insulin and 8.7 mmol/l during treatment with porcine insulin (p less than 0.1). Glucose 14-21 insulin Homo sapiens 71-78 2956040-5 1987 Fasting blood glucose level was 8.3 mmol/l during treatment with human insulin and 8.7 mmol/l during treatment with porcine insulin (p less than 0.1). Glucose 14-21 insulin Homo sapiens 124-131 2956042-1 1987 In order to define the relationship between treatment-induced changes in diabetic control and improvement in in vivo insulin-stimulated glucose utilization (insulin clamp technique) 30 patients with non-insulin-dependent diabetes mellitus (NIDDM) were treated with either insulin, glipizide or diet alone, depending on their initial weight. Glucose 136-143 insulin Homo sapiens 117-124 3304897-5 1987 It is concluded that the addition of phenoxybenzamine to subcutaneously injected insulin increases the bioavailability of insulin for at least 3 h, which leads to a greater fall in plasma glucose concentrations. Glucose 188-195 insulin Homo sapiens 81-88 2956042-3 1987 These changes in fasting plasma glucose concentration were associated with an improvement in insulin-stimulated glucose uptake, which increased by 69% after insulin, 45% after glipizide, and 72% after weight reduction. Glucose 32-39 insulin Homo sapiens 93-100 2956042-3 1987 These changes in fasting plasma glucose concentration were associated with an improvement in insulin-stimulated glucose uptake, which increased by 69% after insulin, 45% after glipizide, and 72% after weight reduction. Glucose 32-39 insulin Homo sapiens 157-164 2956042-3 1987 These changes in fasting plasma glucose concentration were associated with an improvement in insulin-stimulated glucose uptake, which increased by 69% after insulin, 45% after glipizide, and 72% after weight reduction. Glucose 112-119 insulin Homo sapiens 93-100 2956042-3 1987 These changes in fasting plasma glucose concentration were associated with an improvement in insulin-stimulated glucose uptake, which increased by 69% after insulin, 45% after glipizide, and 72% after weight reduction. Glucose 112-119 insulin Homo sapiens 157-164 2956042-5 1987 These results appear to suggest that the ability of any specific treatment to improve diabetic control can vary independently of its effect on in vivo insulin-stimulated glucose utilization. Glucose 170-177 insulin Homo sapiens 151-158 3304897-5 1987 It is concluded that the addition of phenoxybenzamine to subcutaneously injected insulin increases the bioavailability of insulin for at least 3 h, which leads to a greater fall in plasma glucose concentrations. Glucose 188-195 insulin Homo sapiens 122-129 3304906-3 1987 Elevated insulin levels and their hypoglycaemic effect persisted for less than 2 h whereas with subcutaneous insulin (8 units) elevated insulin levels and evidence of hypoglycaemic action were still present at 4 h. By contrast, in the meal studies both forms of insulin had similar effects on serum insulin levels and blood glucose. Glucose 324-331 insulin Homo sapiens 109-116 3315765-1 1987 Intranasal insulin is effective in raising serum insulin (IRI) levels and lowering blood glucose levels in normal subjects and in diabetics, but its bioavailability is low. Glucose 89-96 insulin Homo sapiens 11-18 3304906-3 1987 Elevated insulin levels and their hypoglycaemic effect persisted for less than 2 h whereas with subcutaneous insulin (8 units) elevated insulin levels and evidence of hypoglycaemic action were still present at 4 h. By contrast, in the meal studies both forms of insulin had similar effects on serum insulin levels and blood glucose. Glucose 324-331 insulin Homo sapiens 109-116 3304906-3 1987 Elevated insulin levels and their hypoglycaemic effect persisted for less than 2 h whereas with subcutaneous insulin (8 units) elevated insulin levels and evidence of hypoglycaemic action were still present at 4 h. By contrast, in the meal studies both forms of insulin had similar effects on serum insulin levels and blood glucose. Glucose 324-331 insulin Homo sapiens 109-116 3315766-0 1987 Insulin-mediated glucose disposal in type 1 (insulin-dependent) diabetic subjects treated by continuous subcutaneous or intraperitoneal insulin fusion. Glucose 17-24 insulin Homo sapiens 0-7 3304906-3 1987 Elevated insulin levels and their hypoglycaemic effect persisted for less than 2 h whereas with subcutaneous insulin (8 units) elevated insulin levels and evidence of hypoglycaemic action were still present at 4 h. By contrast, in the meal studies both forms of insulin had similar effects on serum insulin levels and blood glucose. Glucose 324-331 insulin Homo sapiens 109-116 3315766-0 1987 Insulin-mediated glucose disposal in type 1 (insulin-dependent) diabetic subjects treated by continuous subcutaneous or intraperitoneal insulin fusion. Glucose 17-24 insulin Homo sapiens 45-52 3308566-0 1987 Is insulin the key factor to explain the associations between body mass, blood pressure and glucose? Glucose 92-99 insulin Homo sapiens 3-10 3315766-1 1987 In order to determine if intraperitoneal insulin infusion could improve the insulin resistance of type 1 diabetic patients we have used the englycaemic insulin clamp technique in order to study the effects of insulin on glucose disposal in four C peptide negative type 1 diabetic patients treated by continuous subcutaneous or intraperitoneal insulin infusion and in five control subjects. Glucose 220-227 insulin Homo sapiens 41-48 3315766-2 1987 Compared to control subjects, the diabetic patients treated by subcutaneous insulin infusion had a decreased maximal capacity of glucose utilization (diabetics: 12.6 +/- 0.3 mg.kg-1.min-1; controls: 15.7 +/- 0.7 mg/kg-1.min-1, p less than 0.01) and a trend towards higher half-maximally effective insulin concentrations (diabetics: 70 +/- 11 mU/l-1, controls: 48 +/- 4 mU/l-1). Glucose 129-136 insulin Homo sapiens 76-83 3556284-3 1987 HIT cells were loaded with 32P and stimulated with either 40 mM K+ or 19.4 mM glucose, both of which trigger the immediate release of insulin. Glucose 78-85 insulin Homo sapiens 134-141 3556281-3 1987 Insulin sensitivity, derived from an intravenous glucose tolerance test with a minimal-modeling technique, was lower in the siblings (P less than .01). Glucose 49-56 insulin Homo sapiens 0-7 3556284-1 1987 We have previously shown in a glucose-responsive insulin-secreting beta-cell line (HIT cells) that a cell membrane-depolarizing concentration of K+ causes an influx of extracellular Ca2+ that elevates the free cytosolic Ca2+ concentration ([Ca2+]i) and activates insulin secretion. Glucose 30-37 insulin Homo sapiens 49-56 3556284-10 1987 However, glucose activates the immediate release of insulin by another, as yet undefined, mechanism. Glucose 9-16 insulin Homo sapiens 52-59 3297813-0 1987 Androgen and insulin response to an oral glucose challenge in hyperandrogenic women. Glucose 41-48 insulin Homo sapiens 13-20 3622196-8 1987 The approach by which the insulinemia was kept constant by the artificial pancreas seems to be a valuable tool for studying glycemic responses to different meals in IDDM patients who otherwise show great variations in circulating insulin and glucose levels when treated by subcutaneously administered insulin. Glucose 242-249 insulin Homo sapiens 26-33 2886485-1 1987 Because this laboratory has been able to demonstrate only a small and somewhat inconsistent stimulation of glucose metabolism by insulin in porcine adipose tissue in vitro, the tissue was preincubated with insulin to attempt to enhance the hormone effect. Glucose 107-114 insulin Homo sapiens 129-136 3305276-0 1987 The effect of high-glucose condition on insulin binding to IM-9 lymphocytes. Glucose 19-26 insulin Homo sapiens 40-47 3305276-1 1987 The long-term effect of high-glucose condition on insulin binding to IM-9 cells was studied by incubating the cells in RPMI-1640 medium containing 450 mg/dl of glucose. Glucose 29-36 insulin Homo sapiens 50-57 3305276-1 1987 The long-term effect of high-glucose condition on insulin binding to IM-9 cells was studied by incubating the cells in RPMI-1640 medium containing 450 mg/dl of glucose. Glucose 160-167 insulin Homo sapiens 50-57 3305276-2 1987 Insulin binding began to decrease after incubation for 6 days in high-glucose-treated cells, and significantly decreased after 14 days due to the reduction of receptor affinity. Glucose 70-77 insulin Homo sapiens 0-7 3034949-5 1987 Incubation experiments revealed that a low glucose concentration (15 mg/dL) was sufficient to produce maximal insulin release. Glucose 43-50 insulin Homo sapiens 110-117 3323058-1 1987 Insulin and acetylcholine (ACh) are both known to promote glucose uptake by liver of birds. Glucose 58-65 insulin Homo sapiens 0-7 3323058-4 1987 In the present study the action of these three inhibitors of AChE alone as well as in combination with insulin and acetylcholine on in vitro glucose uptake by pigeon liver slices was investigated. Glucose 141-148 insulin Homo sapiens 103-110 3323094-0 1987 C-peptide kinetics following an intravenous glucose load in children undergoing regular hemodialysis. Glucose 44-51 insulin Homo sapiens 0-9 3323094-1 1987 Following an intravenous glucose tolerance test (iv-GTT) we investigated the relationship between glucose kinetics and c-peptide release in 15 children and adolescents requiring regular hemodialysis. Glucose 98-105 insulin Homo sapiens 119-128 3034950-6 1987 There was a significant positive correlation between basal plasma vasopressin and nadir glucose concentrations and a significant negative correlation between basal plasma vasopressin and the integrated fall in glucose after insulin administration (P less than 0.01 and P less than 0.025, respectively). Glucose 210-217 insulin Homo sapiens 224-231 3110217-2 1987 We also determined whether increasing the rate of glucose disposal by hyperglycemia at a fixed insulin concentration activates glycogen synthase. Glucose 50-57 insulin Homo sapiens 95-102 3110217-4 1987 The ED50: s for insulin stimulation of whole body and forearm glucose disposal were similar and unaffected by glycemia. Glucose 62-69 insulin Homo sapiens 16-23 3110217-5 1987 Glycogen synthase activation was exponentially related to the insulin-mediated component of whole body and forearm glucose disposal at each glucose concentration. Glucose 115-122 insulin Homo sapiens 62-69 3110217-5 1987 Glycogen synthase activation was exponentially related to the insulin-mediated component of whole body and forearm glucose disposal at each glucose concentration. Glucose 140-147 insulin Homo sapiens 62-69 3309453-10 1987 Insulin resistance exists because glucose tolerance is simultaneously impaired. Glucose 34-41 insulin Homo sapiens 0-7 3116347-1 1987 A nonlinear mathematical model which incorporates both beta-cell kinetics and a glucose-insulin feedback system is proposed for describing the time variations of plasma glucose and insulin levels. Glucose 80-87 insulin Homo sapiens 88-95 3296980-2 1987 The results demonstrated a significant increase in both the plasma glucose and insulin response to a 75-g oral glucose challenge (two-way analysis of variance). Glucose 111-118 insulin Homo sapiens 79-86 3296980-4 1987 Finally, the greater the plasma glucose insulin response to oral glucose and both systolic and diastolic and insulin responses to oral glucose, the lower the plasma high-density lipoprotein concentrations, and the higher the ratio of plasma low-density lipoprotein cholesterol to high-density lipoprotein cholesterol. Glucose 32-39 insulin Homo sapiens 40-47 3296980-4 1987 Finally, the greater the plasma glucose insulin response to oral glucose and both systolic and diastolic and insulin responses to oral glucose, the lower the plasma high-density lipoprotein concentrations, and the higher the ratio of plasma low-density lipoprotein cholesterol to high-density lipoprotein cholesterol. Glucose 65-72 insulin Homo sapiens 40-47 3296982-6 1987 Elevated stimulated glucose levels predicted the need for insulin therapy. Glucose 20-27 insulin Homo sapiens 58-65 3301441-13 1987 Insulin and glucagon allow an increase in glucose availability for the active metabolic processes which occur during arousal. Glucose 42-49 insulin Homo sapiens 0-7 3301443-2 1987 The MODY patients metabolised less glucose (4.8 +/- 0.3 mg/Kg/min) than the classical NIDDM patients (7.0 +/- 0.5 mg/Kg/min) at an insulin infusion rate of 1.0 mU/Kg/min (p less than 0.05). Glucose 35-42 insulin Homo sapiens 131-138 3315795-5 1987 Insulin mediated glucose uptake did not change, indicating that the degree of exercise training failed to improve in vivo insulin sensitivity. Glucose 17-24 insulin Homo sapiens 0-7 3315795-6 1987 Significant associations were found between the following parameters measured: fasting concentrations of triglycerides and insulin, very low density lipoprotein-triglycerides and glucose, and measures of in vivo insulin resistance and fasting insulin levels, suggesting that insulin resistance in these glucose intolerant subjects may play a role in their hypertriglyceridaemia. Glucose 303-310 insulin Homo sapiens 212-219 3315795-6 1987 Significant associations were found between the following parameters measured: fasting concentrations of triglycerides and insulin, very low density lipoprotein-triglycerides and glucose, and measures of in vivo insulin resistance and fasting insulin levels, suggesting that insulin resistance in these glucose intolerant subjects may play a role in their hypertriglyceridaemia. Glucose 303-310 insulin Homo sapiens 212-219 3315795-6 1987 Significant associations were found between the following parameters measured: fasting concentrations of triglycerides and insulin, very low density lipoprotein-triglycerides and glucose, and measures of in vivo insulin resistance and fasting insulin levels, suggesting that insulin resistance in these glucose intolerant subjects may play a role in their hypertriglyceridaemia. Glucose 303-310 insulin Homo sapiens 212-219 2887501-5 1987 For the glucose infusion rate (M value), it was significantly greater in our normal subjects in response to insulin + SRIF as compared to insulin alone (12.0 + 0.9 vs 8.8 +/- 1.4; P less than 0.01). Glucose 8-15 insulin Homo sapiens 108-115 2887501-5 1987 For the glucose infusion rate (M value), it was significantly greater in our normal subjects in response to insulin + SRIF as compared to insulin alone (12.0 + 0.9 vs 8.8 +/- 1.4; P less than 0.01). Glucose 8-15 insulin Homo sapiens 138-145 3623414-1 1987 Erythrocyte (RBC) insulin receptors and the insulin response to glucose load (oGTT) were evaluated in ten male, non-obese, non-insulin dependent diabetic patients (NIDDM) before and after 14 and 90 days of 250 mg/day of chlorpropamide administration. Glucose 64-71 insulin Homo sapiens 44-51 2952663-7 1987 There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. Glucose 88-95 insulin Homo sapiens 122-129 3553221-0 1987 Variations in insulin-stimulated glucose uptake in healthy individuals with normal glucose tolerance. Glucose 33-40 insulin Homo sapiens 14-21 3553221-0 1987 Variations in insulin-stimulated glucose uptake in healthy individuals with normal glucose tolerance. Glucose 83-90 insulin Homo sapiens 14-21 3553221-3 1987 The plasma insulin response to oral glucose inversely correlated with the M value (r = -0.60; P less than 0.001), being highest in those with the lowest M (quartile 1) and lowest in those with the highest M (quartile 4). Glucose 36-43 insulin Homo sapiens 11-18 3553221-5 1987 These results document that insulin-stimulated glucose uptake varies widely in subjects with normal glucose tolerance, and that these differences are independent of any change in the plasma glucose response to oral glucose. Glucose 47-54 insulin Homo sapiens 28-35 3553221-5 1987 These results document that insulin-stimulated glucose uptake varies widely in subjects with normal glucose tolerance, and that these differences are independent of any change in the plasma glucose response to oral glucose. Glucose 100-107 insulin Homo sapiens 28-35 3553221-5 1987 These results document that insulin-stimulated glucose uptake varies widely in subjects with normal glucose tolerance, and that these differences are independent of any change in the plasma glucose response to oral glucose. Glucose 100-107 insulin Homo sapiens 28-35 3553221-5 1987 These results document that insulin-stimulated glucose uptake varies widely in subjects with normal glucose tolerance, and that these differences are independent of any change in the plasma glucose response to oral glucose. Glucose 100-107 insulin Homo sapiens 28-35 3295474-1 1987 Pima Indian adults with normal glucose tolerance have higher plasma glucose and insulin concentrations than Caucasian adults. Glucose 31-38 insulin Homo sapiens 80-87 2439077-0 1987 Glucose stimulates insulin release without altering cyclic AMP production or inositolphospholipid turnover in freshly obtained human insulinoma cells. Glucose 0-7 insulin Homo sapiens 19-26 2439077-1 1987 Glucose, forskolin, IBMX and carbachol all stimulated insulin release from freshly obtained human insulinoma cells. Glucose 0-7 insulin Homo sapiens 54-61 3553949-3 1987 During the insulin infusion, the plasma glucose level stabilized at 60 to 70 mg per deciliter (3.3 to 3.9 mmol per liter) in the subjects without diabetes and the patients with poorly controlled diabetes, because of a rebound increase in hepatic glucose production. Glucose 40-47 insulin Homo sapiens 11-18 3553949-5 1987 The hypoglycemia in the patients with well-controlled diabetes was associated with a lowering of the plasma threshold of glucose that triggered a release of epinephrine (less than 45 mg of glucose per deciliter, or 2.5 mmol per liter, vs. greater than 55 mg per deciliter, or 3.1 mmol per liter, in the other groups, P less than 0.01) as well as an enhanced sensitivity to the suppressive effects of insulin on hepatic glucose production. Glucose 121-128 insulin Homo sapiens 400-407 3553949-7 1987 We conclude that strict control of diabetes induces physiologic alterations (delayed release of epinephrine and persistent suppression of glucose production) that impair glucose counterregulation to doses of insulin in the therapeutic range. Glucose 138-145 insulin Homo sapiens 208-215 3553949-7 1987 We conclude that strict control of diabetes induces physiologic alterations (delayed release of epinephrine and persistent suppression of glucose production) that impair glucose counterregulation to doses of insulin in the therapeutic range. Glucose 170-177 insulin Homo sapiens 208-215 3106656-4 1987 Treatment with glyburide, 20 mg/d (plus insulin), compared with placebo (plus insulin) resulted in a significant reduction in mean basal glucose (232 +/- 12 vs 262 +/- 11 mg/dL [12.8 vs 14.4 mmol/L]) and hemoglobin A1C (10.2% +/- 0.5% vs 10.9% +/- 03%) concentrations. Glucose 137-144 insulin Homo sapiens 40-47 3106656-4 1987 Treatment with glyburide, 20 mg/d (plus insulin), compared with placebo (plus insulin) resulted in a significant reduction in mean basal glucose (232 +/- 12 vs 262 +/- 11 mg/dL [12.8 vs 14.4 mmol/L]) and hemoglobin A1C (10.2% +/- 0.5% vs 10.9% +/- 03%) concentrations. Glucose 137-144 insulin Homo sapiens 78-85 3296597-6 1987 The result showed that insulin, 200 mU/l, induced a shift in composition of neutral sugars by decreasing the amount of galactose relative to glucose and mannose. Glucose 141-148 insulin Homo sapiens 23-30 2883055-1 1987 The aim of this study was to investigate the role of plasma glucagon levels on the blood glucose response to intravenous insulin administered continuously or in a pulsatile manner. Glucose 89-96 insulin Homo sapiens 121-128 2883055-6 1987 For plasma glucagon levels approximately equal to 130 pg/ml, plasma glucose remained steady throughout the experiments, but during the last 40 min, plasma glucose levels were significantly lower when insulin was administered intermittently. Glucose 155-162 insulin Homo sapiens 200-207 2883058-6 1987 Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). Glucose 7-14 insulin Homo sapiens 52-59 2883058-9 1987 When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. Glucose 60-67 insulin Homo sapiens 44-51 3297590-7 1987 Both glucose-stimulated insulin and arginine-stimulated glucagon release were suppressed by xenogeneic antiserum not only in the presence but also in the absence of complement. Glucose 5-12 insulin Homo sapiens 24-31 3297592-5 1987 In Group I, the glucose disappearance rate was normal and a brisk acute insulin response (AIR) to glucose was noted. Glucose 98-105 insulin Homo sapiens 72-79 3297592-8 1987 On the other hand, the glucose intolerance in Group II patients could be due to inadequate insulin secretion to overcome insulin resistance of CLD. Glucose 23-30 insulin Homo sapiens 91-98 3297592-8 1987 On the other hand, the glucose intolerance in Group II patients could be due to inadequate insulin secretion to overcome insulin resistance of CLD. Glucose 23-30 insulin Homo sapiens 121-128 3301482-0 1987 Derivation of a quantitative measure of insulin sensitivity from the intravenous tolbutamide test using the minimal model of glucose dynamics. Glucose 125-132 insulin Homo sapiens 40-47 3301482-1 1987 Using the decay phase of the glucose response during an intravenous tolbutamide test, a minimal model of glucose dynamics was used to calculate a value for an "index of insulin sensitivity". Glucose 29-36 insulin Homo sapiens 169-176 3301482-1 1987 Using the decay phase of the glucose response during an intravenous tolbutamide test, a minimal model of glucose dynamics was used to calculate a value for an "index of insulin sensitivity". Glucose 105-112 insulin Homo sapiens 169-176 3301482-2 1987 This index describes the efficiency of insulin in accelerating the instantaneous rate of glucose disposal, and provides a measure of insulin resistance. Glucose 89-96 insulin Homo sapiens 39-46 3301482-7 1987 Estimates of the index of insulin sensitivity from intravenous glucose tolerance or intravenous tolbutamide procedures both on and off treatment were significantly correlated (off treatment: rs = 0.71, n = 9, p less than 0.05; on treatment: rs = 0.69, n = 9, p less than 0.05); (C) A group of patient undergoing investigations for suspected disturbances in carbohydrate metabolism was studied, each patient having had both an intravenous tolbutamide and intravenous glucose tolerance test. Glucose 63-70 insulin Homo sapiens 26-33 3301482-7 1987 Estimates of the index of insulin sensitivity from intravenous glucose tolerance or intravenous tolbutamide procedures both on and off treatment were significantly correlated (off treatment: rs = 0.71, n = 9, p less than 0.05; on treatment: rs = 0.69, n = 9, p less than 0.05); (C) A group of patient undergoing investigations for suspected disturbances in carbohydrate metabolism was studied, each patient having had both an intravenous tolbutamide and intravenous glucose tolerance test. Glucose 466-473 insulin Homo sapiens 26-33 3304785-6 1987 Glucose concentrations fell after intraperitoneal injection of insulin, but not after subcutaneous injection. Glucose 0-7 insulin Homo sapiens 63-70 3311480-4 1987 The amount of glucose required to maintain normoglycaemia during the insulin infusions was significantly less in the cortisone study than in the control study, while the parameter estimates for the kinetics of insulin disappearance from plasma were unaffected by cortisone. Glucose 14-21 insulin Homo sapiens 69-76 3621802-2 1987 To assess the effects of intravenously administered ethanol on insulin mediated glucose disposal, euglycaemic clamps at 3 different plasma insulin levels and insulin receptor binding studies on circulating monocytes after alcohol infusion were performed. Glucose 80-87 insulin Homo sapiens 63-70 3621802-5 1987 These results demonstrate that alcohol can adversely influence the insulin mediated glucose disposal. Glucose 84-91 insulin Homo sapiens 67-74 3552633-1 1987 Insulin stimulation of 2-deoxyglucose transport and lipogenesis from glucose was examined in fat cells in which protein kinase C had been down-modulated by a 3 h pretreatment with 5 X 10(-7) M 4 beta-phorbol 12 beta-myristate, 13 alpha-acetate (PMA). Glucose 30-37 insulin Homo sapiens 0-7 3556373-2 1987 The effect on weight, hyperglycaemia and insulin response to oral glucose was measured in all subjects, and in 7, peripheral insulin resistance was estimated using a hyperinsulinaemic glucose clamp at two insulin infusion rates (40 and 400 mU m-2 X min-1). Glucose 66-73 insulin Homo sapiens 41-48 3556373-4 1987 The plasma insulin response to oral glucose was unchanged after diet therapy. Glucose 36-43 insulin Homo sapiens 11-18 3549759-3 1987 Stimulation of isotopically determined glucose utilization above the basal value was lower in the obese than in the lean subjects during the variable [2.4 +/- 0.5 (+/- SEM) vs. 5.4 +/- 0.7 g/m2; P = 0.004] and the constant (2.9 +/- 0.7 vs 4.2 +/- 0.9 g/m2; P = 0.32) insulin infusions; however, the differences were only significant with the variable insulin infusion. Glucose 39-46 insulin Homo sapiens 267-274 3549759-3 1987 Stimulation of isotopically determined glucose utilization above the basal value was lower in the obese than in the lean subjects during the variable [2.4 +/- 0.5 (+/- SEM) vs. 5.4 +/- 0.7 g/m2; P = 0.004] and the constant (2.9 +/- 0.7 vs 4.2 +/- 0.9 g/m2; P = 0.32) insulin infusions; however, the differences were only significant with the variable insulin infusion. Glucose 39-46 insulin Homo sapiens 351-358 3549759-4 1987 The variable insulin infusion also was associated with lower rates of activation of glucose utilization (slope, 0-90 min, 0.27 +/- 0.05 vs. 0.55 +/- 0.09 mg/m2 X min 2; P = 0.01) in obese compared to lean subjects. Glucose 84-91 insulin Homo sapiens 13-20 3549759-6 1987 Despite identical amounts of insulin, stimulation of glucose utilization was greater (P less than 0.03) during the variable than during the constant insulin infusion in the lean subjects. Glucose 53-60 insulin Homo sapiens 149-156 3549761-5 1987 These results indicate that powerlifters who ingest anabolic steroids have diminished glucose tolerance, which is likely to be secondary to insulin resistance. Glucose 86-93 insulin Homo sapiens 140-147 3295105-1 1987 We have investigated the ability of glucose, human GH and human placental lactogen (hPL) to alter the content and release of somatomedin C/insulin-like growth factor I (SM-C/IGF-I), and the biosynthesis, content and release of insulin from cultured human fetal pancreas. Glucose 36-43 insulin Homo sapiens 139-146 3295105-1 1987 We have investigated the ability of glucose, human GH and human placental lactogen (hPL) to alter the content and release of somatomedin C/insulin-like growth factor I (SM-C/IGF-I), and the biosynthesis, content and release of insulin from cultured human fetal pancreas. Glucose 36-43 insulin Homo sapiens 227-234 3295105-6 1987 Incubation in the presence of 16.7 mmol glucose/l caused an increase of insulin release from explants, but had no consistent action on insulin content, compared with medium containing 2.7 mmol glucose/l. Glucose 40-47 insulin Homo sapiens 72-79 3553851-4 1987 In the remaining 5 of the 9 diabetic patients, uninterrupted insulin treatment prior to the study and a seven-hour intravenous insulin treatment during the study period decreased not only the concentrations of plasma glucose and leucine and leucine flux, but also leucine oxidation (P less than .01). Glucose 217-224 insulin Homo sapiens 61-68 3553851-4 1987 In the remaining 5 of the 9 diabetic patients, uninterrupted insulin treatment prior to the study and a seven-hour intravenous insulin treatment during the study period decreased not only the concentrations of plasma glucose and leucine and leucine flux, but also leucine oxidation (P less than .01). Glucose 217-224 insulin Homo sapiens 127-134 3553852-1 1987 Raised levels of free fatty acids (FFA) compete with glucose for utilization by insulin-sensitive tissues, and, therefore, they may induce insulin resistance in the normal subject. Glucose 53-60 insulin Homo sapiens 80-87 3553852-4 1987 Upon raising plasma insulin levels to approximately 60 microU/mL while maintaining euglycemia, whole body glucose utilization (3H-3-glucose) rose similarly without (from 66 +/- 7 to 113 +/- 11 mg/min m2, P less than .02) or with (from 70 +/- 7 to 137 +/- 19 mg/min m2, P less than .02) concomitant lipid infusion. Glucose 106-113 insulin Homo sapiens 20-27 2885899-5 1987 The effect of GRP-(1-27) on insulin secretion was enhanced with increasing perfusate glucose levels, whereas the effects upon somatostatin and pancreatic polypeptide secretion were independent of perfusate glucose levels. Glucose 85-92 insulin Homo sapiens 28-35 3296457-3 1987 Treatment with parenteral insulin alone resulted in a decrease of the serum glucose value from 41 +/- 14 (standard deviation) to 11 +/- 5 mmol per liter (P <.001) and of serum potassium level from 5.2 +/- 1.2 to 4.0 +/- 0.6 mmol per liter (P <.001). Glucose 76-83 insulin Homo sapiens 26-33 3551573-0 1987 Glucose tolerance and insulin response to glucose in nondiabetic young male survivors of myocardial infarction. Glucose 42-49 insulin Homo sapiens 22-29 3551573-1 1987 Intravenous and oral glucose tolerance, as well as insulin response to glucose ingestion and a glucose infusion test, were investigated in 104 male nondiabetic survivors of myocardial infarction under the age of 45 years and in 100 matched control subjects randomly selected from the general population. Glucose 71-78 insulin Homo sapiens 51-58 3551573-4 1987 The magnitude of the early insulin response during the glucose infusion test, along with the high density lipoprotein cholesterol concentration, correlated inversely and independently with degree and extent of coronary atheromatosis, whereas the low density lipoprotein cholesterol level showed a positive correlation with severity of coronary atheromatosis. Glucose 55-62 insulin Homo sapiens 27-34 3551628-3 1987 When intravenous insulin infusion was stopped, plasma vasopressin, osmolality, and glucose increased over the ensuing 5 h, whereas plasma sodium decreased, and blood volume and pressure did not change. Glucose 83-90 insulin Homo sapiens 17-24 3551628-5 1987 However, when plasma osmolality and glucose were raised by infusion of hypertonic dextrose, plasma vasopressin increased significantly in diabetic patients under insulin-deplete but not under insulin-replete conditions and actually decreased in healthy controls. Glucose 82-90 insulin Homo sapiens 162-169 3551628-7 1987 This change in osmoreceptor specificity may be explained by postulating that glucose transport by osmoreceptor neurons as insulin dependent. Glucose 77-84 insulin Homo sapiens 122-129 3552109-1 1987 A study of glucose, insulin, lipids and lipoproteins in myotonic dystrophy (MyD) has shown elevation of fasting plasma insulin, triglycerides and very low density lipoproteins (VLDL) but no significant difference from normal in the fasting plasma glucose, total cholesterol or low and high density lipoproteins. Glucose 11-18 insulin Homo sapiens 119-126 3102297-8 1987 The MCR of glucose during both insulin infusions was reduced in NIDDM compared with lean subjects but was very similar to that in obese nondiabetics. Glucose 11-18 insulin Homo sapiens 31-38 3304783-11 1987 Our study shows that short term insulin therapy in patients with NIDDM who had failed on diet alone has advantages over sulphonylurea therapy in that it achieves better diabetic control and an improved B-cell response to glucose stimulation. Glucose 221-228 insulin Homo sapiens 32-39 3549254-0 1987 Direct effects of glucose on proinsulin synthesis and processing during desensitization. Glucose 18-25 insulin Homo sapiens 29-39 3549254-2 1987 In this study, both glucose-regulated proinsulin biosynthesis and its processing during glucose-induced desensitization were examined at critical periods during 24 h. Although insulin secretion declined at 24 h to one third the 3 h maximum rate, the total rate of proinsulin biosynthesis, assessed by [3H]leucine incorporation, was unchanged at 0, 3, and 24 h of glucose (11 mM) exposure. Glucose 20-27 insulin Homo sapiens 38-48 3549254-6 1987 In contrast, the conversion rate of proinsulin to insulin progressively increased with prolonged prior glucose exposure, the major increase occurring by 3 h of glucose preincubation. Glucose 103-110 insulin Homo sapiens 36-46 3549254-6 1987 In contrast, the conversion rate of proinsulin to insulin progressively increased with prolonged prior glucose exposure, the major increase occurring by 3 h of glucose preincubation. Glucose 103-110 insulin Homo sapiens 39-46 3549254-6 1987 In contrast, the conversion rate of proinsulin to insulin progressively increased with prolonged prior glucose exposure, the major increase occurring by 3 h of glucose preincubation. Glucose 160-167 insulin Homo sapiens 36-46 3549254-6 1987 In contrast, the conversion rate of proinsulin to insulin progressively increased with prolonged prior glucose exposure, the major increase occurring by 3 h of glucose preincubation. Glucose 160-167 insulin Homo sapiens 39-46 3549254-9 1987 These results indicate that the conversion rate of proinsulin to insulin is a glucose-regulated process requiring synthesis of a pool of either converting enzyme(s) or other regulating protein before initiation of proinsulin synthesis. Glucose 78-85 insulin Homo sapiens 51-61 3549254-9 1987 These results indicate that the conversion rate of proinsulin to insulin is a glucose-regulated process requiring synthesis of a pool of either converting enzyme(s) or other regulating protein before initiation of proinsulin synthesis. Glucose 78-85 insulin Homo sapiens 54-61 3549254-9 1987 These results indicate that the conversion rate of proinsulin to insulin is a glucose-regulated process requiring synthesis of a pool of either converting enzyme(s) or other regulating protein before initiation of proinsulin synthesis. Glucose 78-85 insulin Homo sapiens 214-224 2884179-3 1987 somatostatin (100 micrograms/h) - insulin (0.4 mU/kg/min) glucose (3 mg/kg/min) - infusion test (SIGIT). Glucose 58-65 insulin Homo sapiens 34-41 3108067-6 1987 Teleost insulin did not alter the pattern of hepatic glycogen depletion, while it did increase glucose levels and serine flux to glucose, glycogen, and lipids, and alanine flux to CO2 and glucose. Glucose 95-102 insulin Homo sapiens 8-15 3108067-6 1987 Teleost insulin did not alter the pattern of hepatic glycogen depletion, while it did increase glucose levels and serine flux to glucose, glycogen, and lipids, and alanine flux to CO2 and glucose. Glucose 129-136 insulin Homo sapiens 8-15 3108067-6 1987 Teleost insulin did not alter the pattern of hepatic glycogen depletion, while it did increase glucose levels and serine flux to glucose, glycogen, and lipids, and alanine flux to CO2 and glucose. Glucose 129-136 insulin Homo sapiens 8-15 3108067-9 1987 Teleost insulin had an additive effect on the glucagon-induced increases in total glucose production and gluconeogenesis from serine, while glucagon offset the insulin stimulation of serine flux to glycogen and CO2. Glucose 82-89 insulin Homo sapiens 8-15 3550798-8 1987 The temporal kinetic relationship of insulin-activated receptor beta-subunit phosphorylation, followed by the phosphorylation of p15 and then increased hexose uptake rate, is consistent with an intermediary signaling role for pp15 in insulin-stimulated glucose uptake. Glucose 253-260 insulin Homo sapiens 37-44 3550798-8 1987 The temporal kinetic relationship of insulin-activated receptor beta-subunit phosphorylation, followed by the phosphorylation of p15 and then increased hexose uptake rate, is consistent with an intermediary signaling role for pp15 in insulin-stimulated glucose uptake. Glucose 253-260 insulin Homo sapiens 234-241 3548311-1 1987 This study proposed to determine whether the stimulation of insulin secretion observed in humans infused with fructose when glucose levels were elevated could be observed when fructose was consumed during postprandial hyperglycemia. Glucose 124-131 insulin Homo sapiens 60-67 3548311-3 1987 Fructose consumption following glucose or starch drinks produced significantly higher levels of plasma insulin, but not plasma glucose, as compared to corresponding drinks consumed without fructose. Glucose 31-38 insulin Homo sapiens 103-110 3555746-0 1987 Basal, oxytocin-, and insulin-stimulated glucose oxidation in human endometrium. Glucose 41-48 insulin Homo sapiens 22-29 3555746-6 1987 In samples of late luteal phase, glucose oxidation was stimulated by both oxytocin and insulin. Glucose 33-40 insulin Homo sapiens 87-94 3038454-4 1987 The in vivo insulin stimulated glucose uptake was estimated by determining the metabolic clearance rate (MCR) of glucose in the steady state of a simultaneous infusion during 150 min of glucose (33 mumol/kg/min) and insulin (50 mU/kg/hr). Glucose 31-38 insulin Homo sapiens 12-19 3038454-4 1987 The in vivo insulin stimulated glucose uptake was estimated by determining the metabolic clearance rate (MCR) of glucose in the steady state of a simultaneous infusion during 150 min of glucose (33 mumol/kg/min) and insulin (50 mU/kg/hr). Glucose 31-38 insulin Homo sapiens 216-223 3038454-4 1987 The in vivo insulin stimulated glucose uptake was estimated by determining the metabolic clearance rate (MCR) of glucose in the steady state of a simultaneous infusion during 150 min of glucose (33 mumol/kg/min) and insulin (50 mU/kg/hr). Glucose 113-120 insulin Homo sapiens 12-19 3038454-4 1987 The in vivo insulin stimulated glucose uptake was estimated by determining the metabolic clearance rate (MCR) of glucose in the steady state of a simultaneous infusion during 150 min of glucose (33 mumol/kg/min) and insulin (50 mU/kg/hr). Glucose 113-120 insulin Homo sapiens 12-19 3556103-3 1987 Fasting plasma total insulin (1.22 nM = 183 microU/ml) and proinsulin (0.48 nM) were elevated and greatly increased after oral glucose. Glucose 127-134 insulin Homo sapiens 21-28 3556103-3 1987 Fasting plasma total insulin (1.22 nM = 183 microU/ml) and proinsulin (0.48 nM) were elevated and greatly increased after oral glucose. Glucose 127-134 insulin Homo sapiens 59-69 3556103-4 1987 Glucose-clamp studies revealed delayed insulin clearance. Glucose 0-7 insulin Homo sapiens 39-46 3319027-1 1987 The euglycaemic glucose clamp technique has been used to assess insulin resistance in patients with colorectal adenocarcinoma. Glucose 16-23 insulin Homo sapiens 64-71 3319027-4 1987 Glucose disposal was significantly decreased in the cancer group at all insulin infusion rates, whilst attained insulin levels and metabolic clearance rates of insulin were comparable in the control and cancer groups. Glucose 0-7 insulin Homo sapiens 72-79 3319027-5 1987 Analysis of dose-response data allowed assessment of sensitivity (insulin concentration of half maximal glucose disposal) and responsiveness (maximal glucose disposal). Glucose 104-111 insulin Homo sapiens 66-73 3294879-12 1987 These findings suggest that immunoreactive CRH is present in peripheral plasma; the increase in plasma immunoreactive CRH after insulin-induced hypoglycemia may reflect stimulation of hypothalamic CRH release; the increase in plasma immunoreactive CRH after glucose administration may reflect extrahypothalamic CRH release; and the lack of diurnal variation in plasma immunoreactive CRH together with the lack of suppression of CRH by dexamethasone suggest that basal plasma CRH is of extrahypothalamic origin. Glucose 258-265 insulin Homo sapiens 128-135 3294880-1 1987 To analyze B-cell mechanisms in obesity, we measured the relationship (slope of potentiation) between glucose levels and acute insulin responses (AIR) to isoproterenol or arginine in nondiabetic subjects ranging from lean to markedly obese. Glucose 102-109 insulin Homo sapiens 127-134 3309114-6 1987 A within-subject study comparing five different insulin doses ranging from 0.004 to 0.3 units/kg showed dose-related effects on blood glucose with nadir concentrations of 4.1 +/- 0.6 mmol/l (after the smallest dose of insulin) and 0.8 +/- 0.1 mmol/l (after the largest dose of insulin). Glucose 134-141 insulin Homo sapiens 48-55 3306298-5 1987 This delay in the absorption of soluble insulin caused a greater rise in plasma glucose levels such that the incremental glucose area over eight hours was 25.5 +/- 4.4 mmol.L-1.h for premixed insulin compared with 10.4 +/- 6.2 mmol.L-1.h for separate injections (P less than 0.05). Glucose 80-87 insulin Homo sapiens 40-47 3306298-5 1987 This delay in the absorption of soluble insulin caused a greater rise in plasma glucose levels such that the incremental glucose area over eight hours was 25.5 +/- 4.4 mmol.L-1.h for premixed insulin compared with 10.4 +/- 6.2 mmol.L-1.h for separate injections (P less than 0.05). Glucose 121-128 insulin Homo sapiens 40-47 3306298-5 1987 This delay in the absorption of soluble insulin caused a greater rise in plasma glucose levels such that the incremental glucose area over eight hours was 25.5 +/- 4.4 mmol.L-1.h for premixed insulin compared with 10.4 +/- 6.2 mmol.L-1.h for separate injections (P less than 0.05). Glucose 121-128 insulin Homo sapiens 192-199 3296781-5 1987 Intraportal insulin infusion in perfusion studies suppressed glucagon-stimulated increases in glucose output from control livers but failed to suppress glucose production by cirrhotic livers, suggesting the presence of hepatic insulin resistance in cirrhosis. Glucose 94-101 insulin Homo sapiens 12-19 3113971-4 1987 The mean dose-response curve describing glucose-induced insulin release showed increased maximal capacity to secrete insulin in obese controls, while the responses of lean as well as obese Type 2 DM were reduced by more than 80%. Glucose 40-47 insulin Homo sapiens 56-63 3552801-1 1987 Oral glucose administration to normal humans stimulates insulin release and simultaneously enhances the action of insulin by producing a rapid increase in tissue insulin sensitivity by a mechanism separate from the amount of hormone released. Glucose 5-12 insulin Homo sapiens 56-63 3552801-1 1987 Oral glucose administration to normal humans stimulates insulin release and simultaneously enhances the action of insulin by producing a rapid increase in tissue insulin sensitivity by a mechanism separate from the amount of hormone released. Glucose 5-12 insulin Homo sapiens 114-121 3552801-1 1987 Oral glucose administration to normal humans stimulates insulin release and simultaneously enhances the action of insulin by producing a rapid increase in tissue insulin sensitivity by a mechanism separate from the amount of hormone released. Glucose 5-12 insulin Homo sapiens 114-121 3552801-2 1987 We determined whether insulin-resistant patients with myotonic dystrophy lose the ability to produce the normal rapid increase in tissue insulin action after oral glucose. Glucose 163-170 insulin Homo sapiens 22-29 3552801-2 1987 We determined whether insulin-resistant patients with myotonic dystrophy lose the ability to produce the normal rapid increase in tissue insulin action after oral glucose. Glucose 163-170 insulin Homo sapiens 137-144 3552801-5 1987 Glucose infusion rates at 20-120 min (GIR20-120) during euglycemic insulin infusions without prior glucose were 2.87 +/- 0.6 mg X kg-1 X min-1 in patients with myotonic dystrophy compared to 4.70 +/- 0.3 mg X kg-1 X min-1 in normal subjects. Glucose 0-7 insulin Homo sapiens 67-74 3552801-6 1987 Euglycemic insulin infusions after glucose ingestion were begun after arterialized blood glucose values had returned to baseline. Glucose 89-96 insulin Homo sapiens 11-18 3552801-9 1987 These results confirmed the existence of a decrease in whole-body insulin sensitivity in myotonic dystrophy and indicated that the patients lack the normal mechanism that enhances insulin action after oral glucose. Glucose 206-213 insulin Homo sapiens 180-187 3552803-7 1987 In individual subjects the relationship of blood glucose, plasma NEFA, and blood total ketones (log scale) with the simultaneously occurring plasma insulin level (log scale) was linear for each metabolite. Glucose 49-56 insulin Homo sapiens 148-155 3112004-2 1987 The rate of glucose utilization is mainly restricted by the degree of insulin resistance which may be localized at the receptor (down regulation, tyrosine kinase?) Glucose 12-19 insulin Homo sapiens 70-77 3112004-6 1987 The glucose infusion rate is usually adapted by monitoring the glucose and insulin levels in the patients; furthermore, insulin-resistant states may be detected by these parameters. Glucose 4-11 insulin Homo sapiens 75-82 3112004-6 1987 The glucose infusion rate is usually adapted by monitoring the glucose and insulin levels in the patients; furthermore, insulin-resistant states may be detected by these parameters. Glucose 4-11 insulin Homo sapiens 120-127 3112007-6 1987 It was shown repeatedly during the last few decades that glucose formed in the liver during metabolism of glucose substitutes and delivered to the circulation is obviously metabolized without an increase in blood glucose concentration and without additional requirement of insulin. Glucose 57-64 insulin Homo sapiens 273-280 3112007-6 1987 It was shown repeatedly during the last few decades that glucose formed in the liver during metabolism of glucose substitutes and delivered to the circulation is obviously metabolized without an increase in blood glucose concentration and without additional requirement of insulin. Glucose 106-113 insulin Homo sapiens 273-280 3112007-6 1987 It was shown repeatedly during the last few decades that glucose formed in the liver during metabolism of glucose substitutes and delivered to the circulation is obviously metabolized without an increase in blood glucose concentration and without additional requirement of insulin. Glucose 106-113 insulin Homo sapiens 273-280 3294899-3 1987 At the lowest insulin level, the Michaelis constants (Ks:s) for glucose disposal in whole body (8.7 +/- 1.1 mM) and across forearm (7.4 +/- 1.4) mM) were compatible with a Ks determined in vitro for the transport system. Glucose 64-71 insulin Homo sapiens 14-21 3294899-5 1987 We interpret the apparent increase of Ks by insulin to reflect a shift in the rate-limiting step from glucose transport to some step beyond transport. Glucose 102-109 insulin Homo sapiens 44-51 2436949-1 1987 Glucose-stimulated insulin release from rodent pancreatic B-cells is thought to be initiated by the closing of ATP-sensitive K+ channels in the plasma membrane as a consequence of glucose metabolism. Glucose 0-7 insulin Homo sapiens 19-26 2884792-4 1987 Insulin was irresponsive to the glucose load we used, suggesting that glucose-induced glucagon suppression was also insulin independent. Glucose 70-77 insulin Homo sapiens 0-7 2884792-4 1987 Insulin was irresponsive to the glucose load we used, suggesting that glucose-induced glucagon suppression was also insulin independent. Glucose 70-77 insulin Homo sapiens 116-123 3032715-2 1987 The insulin sensitivity and responsiveness of glucose transport in freshly isolated adipocytes were significantly reduced in NIDDM subjects compared with nondiabetics. Glucose 46-53 insulin Homo sapiens 4-11 3109862-4 1987 human proinsulin on separate occasions, plasma glucose decreased more rapidly after insulin, and the nadir was slightly lower, but integrated hypoglycemic responses were similar. Glucose 47-54 insulin Homo sapiens 6-16 3109862-4 1987 human proinsulin on separate occasions, plasma glucose decreased more rapidly after insulin, and the nadir was slightly lower, but integrated hypoglycemic responses were similar. Glucose 47-54 insulin Homo sapiens 9-16 3297577-1 1987 The dynamic relationship of glucose concentrations and insulin secretion during the postabsorptive state is complex and has been associated with a variety of cyclic rhythms. Glucose 28-35 insulin Homo sapiens 55-62 3297578-8 1987 With CSII, however, good glucose control was associated with normalization of 125I-insulin binding to monocytes (4.7 +/- 0.27%). Glucose 25-32 insulin Homo sapiens 83-90 3552792-2 1987 Herein, we measured urinary insulin clearance during oral glucose tolerance tests in proband with abnormal insulinemia (44-yr-old female), three affected family members, two unaffected family members, two other hyperinsulinemic patients with obesity, five non-insulin-dependent diabetic patients, and five normal control subjects. Glucose 58-65 insulin Homo sapiens 28-35 3552793-1 1987 The effects of small increases in plasma insulin on hepatic glucose production are incompletely understood. Glucose 60-67 insulin Homo sapiens 41-48 3595396-0 1987 Adipocyte insulin binding and action in moderately obese NIDDM patients after dietary control of plasma glucose: reversal of postbinding abnormalities. Glucose 104-111 insulin Homo sapiens 10-17 3595396-6 1987 The basal (non-insulin-stimulated) glucose transport (tracer glucose concentration 5 microM) increased from 25 +/- 12 to 44 +/- 14 pmol X 90 min-1 X 10 cm-2 surface area (P less than .02). Glucose 35-42 insulin Homo sapiens 15-22 3595396-6 1987 The basal (non-insulin-stimulated) glucose transport (tracer glucose concentration 5 microM) increased from 25 +/- 12 to 44 +/- 14 pmol X 90 min-1 X 10 cm-2 surface area (P less than .02). Glucose 61-68 insulin Homo sapiens 15-22 3595396-7 1987 The maximally insulin-stimulated glucose transport rate increased from 35 +/- 20 to 78 +/- 26 pmol/90 min (P less than .01). Glucose 33-40 insulin Homo sapiens 14-21 3595396-10 1987 Glucose conversion rates to total lipids increased 34 +/- 62 and 65 +/- 80% in basal cells and maximally insulin-stimulated cells, respectively (.2 greater than P greater than .1, .1 greater than P greater than .05). Glucose 0-7 insulin Homo sapiens 105-112 3595431-3 1987 After glucose loading, blood glucose and total insulin levels increased abnormally. Glucose 6-13 insulin Homo sapiens 47-54 3034755-8 1987 In this regard it is to stress that glucose ingestion induces in obese patients, differently from normal subjects, insulin hypersecretion and the B-Ep secretion, possibly from gastro-enteric tract and/or pancreatic isles. Glucose 36-43 insulin Homo sapiens 115-122 2881942-0 1987 In vivo regulation of non-insulin-mediated and insulin-mediated glucose uptake by epinephrine. Glucose 64-71 insulin Homo sapiens 47-54 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 8-15 insulin Homo sapiens 58-65 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 8-15 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 8-15 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 8-15 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 58-65 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 58-65 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 114-121 2881942-1 1987 In vivo glucose uptake (Rd) occurs via two mechanisms: 1) insulin-mediated glucose uptake (IMGU), which occurs in insulin-sensitive tissues, and 2) noninsulin-mediated glucose uptake (NIMGU), which occurs in both insulin-sensitive and insulin-insensitive tissues. Glucose 75-82 insulin Homo sapiens 114-121 2951394-0 1987 Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus. Glucose 60-67 insulin Homo sapiens 39-46 2951394-3 1987 beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. Glucose 95-102 insulin Homo sapiens 75-82 3033648-0 1987 Monoclonal antibodies to the human insulin receptor that activate glucose transport but not insulin receptor kinase activity. Glucose 66-73 insulin Homo sapiens 35-42 3033648-5 1987 However, like insulin, two of the three antibodies stimulated glucose transport in isolated human adipocytes. Glucose 62-69 insulin Homo sapiens 14-21 3033648-8 1987 They also raise the possibility that certain actions of insulin such as stimulation of glucose transport may not require the activation of receptor kinase activity. Glucose 87-94 insulin Homo sapiens 56-63 3296088-4 1987 The effectiveness of glucose solutions in correcting these problems is limited for 2 main reasons: concentrations greater than 2.5% slow the rate of gastric emptying and thus fluid absorption, while provoking a secretion of insulin with a resultant hypoglycaemia. Glucose 21-28 insulin Homo sapiens 224-231 3104713-0 1987 Effect of phorbol and glucose on insulin secretion from the human fetal pancreas. Glucose 22-29 insulin Homo sapiens 33-40 3548333-4 1987 The correlation between fasting plasma insulin and HDL cholesterol remained statistically significant in non-insulin-dependent diabetic subjects and in female non-diabetic control subjects after adjustment for body mass index, alcohol intake, physical activity, smoking, and fasting plasma glucose. Glucose 290-297 insulin Homo sapiens 39-46 3829396-3 1987 These new sensors for use with whole blood should be able to clarify the fate of the intermediary metabolites of glucose in diabetic patients receiving infusions of drugs or insulin. Glucose 113-120 insulin Homo sapiens 174-181 3297831-0 1987 Relationships between insulin secretion, insulin metabolism and insulin resistance in mild glucose intolerance. Glucose 91-98 insulin Homo sapiens 22-71 3297831-1 1987 The aim of this study was to evaluate whether the correlation between insulin resistance and peripheral hyperinsulinaemia existing in mild glucose intolerance corresponds to a relationship between insulin resistance and insulin overproduction by the pancreas. Glucose 139-146 insulin Homo sapiens 70-77 3297831-1 1987 The aim of this study was to evaluate whether the correlation between insulin resistance and peripheral hyperinsulinaemia existing in mild glucose intolerance corresponds to a relationship between insulin resistance and insulin overproduction by the pancreas. Glucose 139-146 insulin Homo sapiens 109-116 3297831-1 1987 The aim of this study was to evaluate whether the correlation between insulin resistance and peripheral hyperinsulinaemia existing in mild glucose intolerance corresponds to a relationship between insulin resistance and insulin overproduction by the pancreas. Glucose 139-146 insulin Homo sapiens 109-116 3297831-5 1987 Insulin resistance was estimated by the rate of glucose disappearance from plasma after i.v. Glucose 48-55 insulin Homo sapiens 0-7 3297831-10 1987 Glucose disappearance rate from plasma correlated positively with the C-peptide: insulin molar ratio (r = 0.626, p less than 0.001). Glucose 0-7 insulin Homo sapiens 81-88 3297835-10 1987 In the liver, both insulin sensitivity and glucokinase activity are reduced, so that glucose is spared and the muscular glycogen store can be restored. Glucose 85-92 insulin Homo sapiens 19-26 3297836-4 1987 The finding of a reduced C-peptide to insulin ratio during the intravenous glucose tolerance test suggests that hepatic extraction of insulin could also be altered in Werner"s syndrome, as found in several hyperinsulinism conditions, therefore contributing to peripheral hyperinsulinism. Glucose 75-82 insulin Homo sapiens 134-141 3304782-5 1987 When measured by an index of the dextrose infusion rate required to maintain euglycaemia the two insulin preparations gave similar values for the first 16 hours, maximum values being obtained during the fourth hour after administration. Glucose 33-41 insulin Homo sapiens 97-104 3108067-11 1987 It is suggested that insulin functions in sea raven hepatocytes to increase glycogen stores through increased amino acid utilization and/or to increase glucose production for transport to, and storage in, glucose-utilizing tissues (e.g., muscle). Glucose 152-159 insulin Homo sapiens 21-28 3108067-11 1987 It is suggested that insulin functions in sea raven hepatocytes to increase glycogen stores through increased amino acid utilization and/or to increase glucose production for transport to, and storage in, glucose-utilizing tissues (e.g., muscle). Glucose 205-212 insulin Homo sapiens 21-28 3549468-2 1987 A reduction in the biologic action of insulin, at a point beyond the insulin receptor (postbinding site), is primarily responsible for the reduced rate of glucose utilization. Glucose 155-162 insulin Homo sapiens 38-45 3546350-3 1987 Insulin dynamics were studied during the hyperglycemic clamp (change in glucose, 7 mmol L-1 for 2 h) by measuring the area under the insulin and C-peptide response curves, representing, respectively, systemic insulin response and insulin production. Glucose 72-79 insulin Homo sapiens 0-7 3546350-7 1987 Thus, the liver serves a gate-keeping role in regulating the systemic insulin response to a glucose challenge. Glucose 92-99 insulin Homo sapiens 70-77 3546350-11 1987 Similarly, insulin sensitivity, as measured by the ratio of glucose metabolised per U endogenous insulin, normalized with weight loss and weight maintenance. Glucose 60-67 insulin Homo sapiens 11-18 3546354-1 1987 In this study we have attempted to quantify the plasma insulin response to glucose and insulin action in 22 nonobese subjects: 11 with normal glucose tolerance and 11 with mild [mean fasting plasma glucose concentration, 128 +/- (+/- SEM) 5 mg/dL] noninsulin-dependent diabetes mellitus (NIDDM). Glucose 75-82 insulin Homo sapiens 55-62 3546354-3 1987 Insulin action was assessed by measuring glucose uptake during insulin clamp studies performed at steady state plasma insulin levels of approximately 10 and 60 microU/mL, with the difference between the 2 values defined as insulin-stimulated glucose uptake. Glucose 41-48 insulin Homo sapiens 0-7 3546354-3 1987 Insulin action was assessed by measuring glucose uptake during insulin clamp studies performed at steady state plasma insulin levels of approximately 10 and 60 microU/mL, with the difference between the 2 values defined as insulin-stimulated glucose uptake. Glucose 242-249 insulin Homo sapiens 0-7 3546354-5 1987 However, mean (+/- SEM) insulin-stimulated glucose uptake was markedly reduced (P less than 0.001) in patients with type 2 diabetes mellitus (112 +/- 72 vs. 336 +/- 44 mg/m2 min-1). Glucose 43-50 insulin Homo sapiens 24-31 3546354-7 1987 These data indicate that a defect in insulin-stimulated glucose uptake can occur in NIDDM in the absence of significant hyperglycemia and/or hypoinsulinemia. Glucose 56-63 insulin Homo sapiens 37-44 3550376-2 1987 Insulin secretion to oral glucose showed significant improvement, while C-peptide release by glucagon showed no significant difference before and after diet treatment. Glucose 26-33 insulin Homo sapiens 0-7 3296134-0 1987 Impaired early insulin response to intravenous glucose in alcoholic liver cirrhosis. Glucose 47-54 insulin Homo sapiens 15-22 3030131-7 1987 Insulin-stimulated lactate production and glucose transport without affecting the other parameters. Glucose 42-49 insulin Homo sapiens 0-7 3555432-8 1987 The results also confirm that plasma insulin is positively related to triglycerides and negatively related to high density lipoprotein cholesterol independently of plasma glucose and body mass index. Glucose 171-178 insulin Homo sapiens 37-44 3301158-1 1987 Glucose-stimulated insulin secretion was assessed in relation to the DNA polymorphism flanking the insulin gene in 16 women who had had gestational diabetes. Glucose 0-7 insulin Homo sapiens 19-26 3301158-1 1987 Glucose-stimulated insulin secretion was assessed in relation to the DNA polymorphism flanking the insulin gene in 16 women who had had gestational diabetes. Glucose 0-7 insulin Homo sapiens 99-106 3542653-0 1987 Adverse effects of insulin antibodies on postprandial plasma glucose and insulin profiles in diabetic patients without immune insulin resistance. Glucose 61-68 insulin Homo sapiens 19-26 3542653-5 1987 The effects of insulin antibodies on postprandial plasma free-insulin and glucose levels could be accounted for substantially by the association constant of the high-affinity insulin-antibody binding sites (K1); patients in the highest quartile for K1 had significantly slower initial increments in plasma free insulin (0.31 +/- 0.04 vs. 0.46 +/- 0.06 microU/min, P less than .05) and greater postprandial hyperglycemia (peak value 237 +/- 10 vs. 166 +/- 12 mg/dl, P less than .001) than patients in the lowest quartile. Glucose 74-81 insulin Homo sapiens 15-22 3542653-6 1987 We conclude that moderate insulin-antibody titers commonly found in insulin-treated patients can slow the early increase in plasma free insulin after subcutaneous injection and that this impairs postprandial glucose tolerance; such an effect may limit the effectiveness of intensive insulin therapy. Glucose 208-215 insulin Homo sapiens 26-33 3542653-6 1987 We conclude that moderate insulin-antibody titers commonly found in insulin-treated patients can slow the early increase in plasma free insulin after subcutaneous injection and that this impairs postprandial glucose tolerance; such an effect may limit the effectiveness of intensive insulin therapy. Glucose 208-215 insulin Homo sapiens 68-75 3542653-6 1987 We conclude that moderate insulin-antibody titers commonly found in insulin-treated patients can slow the early increase in plasma free insulin after subcutaneous injection and that this impairs postprandial glucose tolerance; such an effect may limit the effectiveness of intensive insulin therapy. Glucose 208-215 insulin Homo sapiens 68-75 3542653-6 1987 We conclude that moderate insulin-antibody titers commonly found in insulin-treated patients can slow the early increase in plasma free insulin after subcutaneous injection and that this impairs postprandial glucose tolerance; such an effect may limit the effectiveness of intensive insulin therapy. Glucose 208-215 insulin Homo sapiens 68-75 3542654-2 1987 However, we recently demonstrated kinetic defects in insulin action in insulin-resistant nondiabetic obese subjects: activation of insulin-stimulated glucose disposal was slower and deactivation was faster in obese than in normal subjects. Glucose 150-157 insulin Homo sapiens 53-60 3542654-2 1987 However, we recently demonstrated kinetic defects in insulin action in insulin-resistant nondiabetic obese subjects: activation of insulin-stimulated glucose disposal was slower and deactivation was faster in obese than in normal subjects. Glucose 150-157 insulin Homo sapiens 71-78 3552918-1 1987 To investigate whether correction of fasting hyperglycemia per se improves the insulin secretion in type 2 diabetic subjects, plasma insulin response to 75 g oral glucose load has been studied after acute and chronic normalization of fasting plasma glucose levels in 7 overt type 2 diabetic subjects. Glucose 163-170 insulin Homo sapiens 133-140 3552918-4 1987 After 1-3 month control of hyperglycemia, the insulin response to glucose in the subjects was significantly improved compared to those without treatments. Glucose 66-73 insulin Homo sapiens 46-53 3552918-5 1987 Results indicate that chronic metabolic control is essential for the improvement of insulin response to glucose in type 2 diabetic subjects, and also suggest that the impaired insulin secretion in type 2 diabetes is not due to hyperglycemia per se, but due to the metabolic derangements which lead to chronic hyperglycemia. Glucose 104-111 insulin Homo sapiens 84-91 3546468-5 1987 These data suggest that the ability of insulin to maintain normal plasma glucose levels deteriorates with age, whereas regulation of FFA levels does not. Glucose 73-80 insulin Homo sapiens 39-46 3553124-8 1987 Only decap adipose tissue demonstrated an insulin stimulation of glucose oxidation and lipogenesis. Glucose 65-72 insulin Homo sapiens 42-49 15237309-6 1987 These results suggest that epidural anesthesia with 5 g/hr glucose loading may facilitate insulin release from the islet and peripheral blood uptake particularly during the early period of surgery while many other factors such as GH, cortisol and vagal stimulation seemed to be involved in the later period of surgery. Glucose 59-66 insulin Homo sapiens 90-97 3102539-3 1987 In vivo peripheral insulin action was measured during insulin infusion of 40 mU/m2 X min with plasma glucose clamped at fasting levels. Glucose 101-108 insulin Homo sapiens 19-26 2950219-3 1987 Irrespective of glucose dose, glucose tolerance testing elicited a threefold greater insulin response, but equivalent euglycemia, in pubertal versus prepubertal children (P less than 0.05). Glucose 30-37 insulin Homo sapiens 85-92 3543679-1 1987 We compared the glucose-lowering effect of proinsulin, the precursor molecule of insulin, with that of insulin itself. Glucose 16-23 insulin Homo sapiens 43-53 3543679-1 1987 We compared the glucose-lowering effect of proinsulin, the precursor molecule of insulin, with that of insulin itself. Glucose 16-23 insulin Homo sapiens 46-53 3543679-4 1987 Glucose clearance was stimulated less by proinsulin, reflecting its preferential action in suppressing glucose output. Glucose 0-7 insulin Homo sapiens 41-51 3543679-4 1987 Glucose clearance was stimulated less by proinsulin, reflecting its preferential action in suppressing glucose output. Glucose 103-110 insulin Homo sapiens 41-51 3543679-8 1987 Proinsulin reduced plasma glucose more effectively than an equal unit dosage of NPH insulin, but since higher doses of NPH insulin were not used, no conclusions could be drawn about the relative desirability of these preparations for clinical use. Glucose 26-33 insulin Homo sapiens 0-10 3543679-9 1987 We conclude that subcutaneously injected proinsulin has prolonged pharmacokinetics in plasma and can normalize plasma glucose in NIDDM characterized by severe hyperglycemia; as compared with the hypoglycemic effects of regular insulin, those of proinsulin are mostly due to suppression of hepatic glucose output, with little stimulation of glucose disposal and less hypoglycemia; and proinsulin may have a role in the treatment of NIDDM. Glucose 118-125 insulin Homo sapiens 41-51 3543679-9 1987 We conclude that subcutaneously injected proinsulin has prolonged pharmacokinetics in plasma and can normalize plasma glucose in NIDDM characterized by severe hyperglycemia; as compared with the hypoglycemic effects of regular insulin, those of proinsulin are mostly due to suppression of hepatic glucose output, with little stimulation of glucose disposal and less hypoglycemia; and proinsulin may have a role in the treatment of NIDDM. Glucose 118-125 insulin Homo sapiens 44-51 3543679-9 1987 We conclude that subcutaneously injected proinsulin has prolonged pharmacokinetics in plasma and can normalize plasma glucose in NIDDM characterized by severe hyperglycemia; as compared with the hypoglycemic effects of regular insulin, those of proinsulin are mostly due to suppression of hepatic glucose output, with little stimulation of glucose disposal and less hypoglycemia; and proinsulin may have a role in the treatment of NIDDM. Glucose 297-304 insulin Homo sapiens 41-51 3543679-9 1987 We conclude that subcutaneously injected proinsulin has prolonged pharmacokinetics in plasma and can normalize plasma glucose in NIDDM characterized by severe hyperglycemia; as compared with the hypoglycemic effects of regular insulin, those of proinsulin are mostly due to suppression of hepatic glucose output, with little stimulation of glucose disposal and less hypoglycemia; and proinsulin may have a role in the treatment of NIDDM. Glucose 297-304 insulin Homo sapiens 44-51 2439067-2 1987 Two antibodies which reacted with receptor alpha-subunit and completely inhibited 125I-insulin binding mimicked the actions of insulin to stimulate lipogenesis from [14C]glucose and to inhibit catecholamine-induced lipolysis. Glucose 170-177 insulin Homo sapiens 87-94 2439067-2 1987 Two antibodies which reacted with receptor alpha-subunit and completely inhibited 125I-insulin binding mimicked the actions of insulin to stimulate lipogenesis from [14C]glucose and to inhibit catecholamine-induced lipolysis. Glucose 170-177 insulin Homo sapiens 127-134 3297042-1 1987 The L6 skeletal muscle cell line has been identified as a suitable model to study the action of insulin on glucose uptake in muscle [Klip, Li & Logan (1984) Am. Glucose 107-114 insulin Homo sapiens 96-103 3551060-3 1987 The results demonstrated the fasting C-peptide concentrations and, independently of this, the simultaneously measured glucose level had a significant predictive power, e.g. only patients with fasting glycemia of greater than 12 mmol/l and C-peptide concentrations exceeding 700 pmol/l did not require insulin during follow-up. Glucose 118-125 insulin Homo sapiens 301-308 2881485-8 1987 Thus at low infusion rates proinsulin exerts its effect predominantly by suppressing hepatic glucose production without measurable stimulation of peripheral glucose disposal. Glucose 93-100 insulin Homo sapiens 27-37 2884060-9 1987 Plasma proinsulin formed a higher percentage of the immunoreactive insulin in fasting plasma samples of both A (36%) and B (43%) than in less hyperglycaemic MODs on diet alone (26%) or sulphonylurea therapy (17%) and the glucose stimulated proinsulin content was even higher (A, 50%; B, 53%; MODs, diet, 19%; sulphonylureas, 16%). Glucose 221-228 insulin Homo sapiens 7-17 2884060-9 1987 Plasma proinsulin formed a higher percentage of the immunoreactive insulin in fasting plasma samples of both A (36%) and B (43%) than in less hyperglycaemic MODs on diet alone (26%) or sulphonylurea therapy (17%) and the glucose stimulated proinsulin content was even higher (A, 50%; B, 53%; MODs, diet, 19%; sulphonylureas, 16%). Glucose 221-228 insulin Homo sapiens 10-17 3032719-2 1987 Both substances reduced the maximal responsiveness of the glucose transport system to insulin by approximately 50%. Glucose 58-65 insulin Homo sapiens 86-93 3100365-8 1987 In contrast to the IDDM patients, the insulin-treated NIDDM subjects exhibited significant reductions in daily insulin requirement (72 +/- 6 vs. 58 +/- 9 U/day), mean 24-h plasma glucose concentration (153 +/- 10 vs. 131 +/- 5 mg/dl), glucosuria (14 +/- 5 vs. 4 +/- 1 g/day), and glycosylated hemoglobin (10.3 +/- 0.7 vs. 8.0 +/- 0.4%) after glyburide treatment (all P less than or equal to .05). Glucose 179-186 insulin Homo sapiens 38-45 3542641-0 1987 Effect of stress hormones on splanchnic substrate and insulin disposal after glucose ingestion in healthy humans. Glucose 77-84 insulin Homo sapiens 54-61 3542643-9 1987 When isolated adipocytes were incubated with heparin, there was a dose-dependent inhibition of insulin-stimulated glucose oxidation and, to a lesser extent, of basal glucose oxidation. Glucose 114-121 insulin Homo sapiens 95-102 3542644-5 1987 After age, a high 2-h plasma insulin response to a glucose load was the factor most predictive of progression from normal tolerance to both diabetes (P less than .001) and IGT (P less than .01). Glucose 51-58 insulin Homo sapiens 29-36 3542647-4 1987 Sensitivity of glucose disposal to insulin in the physiologic range (measured as change in glucose disposal rate per unit change in insulin concentration between clamps at approximately 10 and approximately 100 microU/ml) was very low in these diabetic subjects and did not change after weight loss. Glucose 15-22 insulin Homo sapiens 35-42 3542647-4 1987 Sensitivity of glucose disposal to insulin in the physiologic range (measured as change in glucose disposal rate per unit change in insulin concentration between clamps at approximately 10 and approximately 100 microU/ml) was very low in these diabetic subjects and did not change after weight loss. Glucose 15-22 insulin Homo sapiens 132-139 3542647-4 1987 Sensitivity of glucose disposal to insulin in the physiologic range (measured as change in glucose disposal rate per unit change in insulin concentration between clamps at approximately 10 and approximately 100 microU/ml) was very low in these diabetic subjects and did not change after weight loss. Glucose 91-98 insulin Homo sapiens 35-42 3542647-5 1987 Adipocyte cell size, basal and maximal insulin-stimulated glucose transport, and half-maximal rate for transport did not change after weight loss. Glucose 58-65 insulin Homo sapiens 39-46 3552827-6 1987 Insulin response to oral glucose and mean body mass index were both related to non-Aboriginal genetic admixture with higher values in Aboriginal subjects than in their non-Aboriginal neighbours, and highest values were found in those with no detectable non-Aboriginal HLA haplotypes. Glucose 25-32 insulin Homo sapiens 0-7 3817165-3 1987 Insulin response to hyperglycaemia is normal, but analysis of glucose disposal with time suggests insulin resistance as a factor in the causation of impaired glucose disposal. Glucose 62-69 insulin Homo sapiens 98-105 3543054-4 1987 Suppression of HGP and stimulation of total glucose disposal were impaired at each insulin step after glucagon (P less than 0.05-0.01). Glucose 44-51 insulin Homo sapiens 83-90 3543054-5 1987 The reduction in insulin-mediated glucose uptake was entirely due to diminished non-oxidative glucose utilization. Glucose 34-41 insulin Homo sapiens 17-24 3543054-5 1987 The reduction in insulin-mediated glucose uptake was entirely due to diminished non-oxidative glucose utilization. Glucose 94-101 insulin Homo sapiens 17-24 3298388-1 1987 The present study was designed to compare insulin extraction by the liver following oral glucose administrations of different size, in order to evaluate insulin removal by the liver in relation to the insulin exposure, and to the amount of ingested glucose. Glucose 89-96 insulin Homo sapiens 42-49 3298388-5 1987 Similarly, insulin concentrations were significantly higher following 150 g than after 50 g glucose ingestion: insulin incremental areas of 0.52 +/- 0.09 vs. 0.20 +/- 0.04 nmol/l X min (p less than 0.001). Glucose 92-99 insulin Homo sapiens 11-18 3298388-5 1987 Similarly, insulin concentrations were significantly higher following 150 g than after 50 g glucose ingestion: insulin incremental areas of 0.52 +/- 0.09 vs. 0.20 +/- 0.04 nmol/l X min (p less than 0.001). Glucose 92-99 insulin Homo sapiens 111-118 3553682-0 1987 Computerized glucose clamp method for the determination of insulin sensitivity in diabetic subjects. Glucose 13-20 insulin Homo sapiens 59-66 3553682-1 1987 A new, simplified computerized glucose clamp method was performed for estimation of glucose utilization at the insulin level of postprandial level. Glucose 31-38 insulin Homo sapiens 111-118 3553682-1 1987 A new, simplified computerized glucose clamp method was performed for estimation of glucose utilization at the insulin level of postprandial level. Glucose 84-91 insulin Homo sapiens 111-118 3553682-6 1987 Average glucose infusion rate was 7.59 +/- 0.85 (mg/kg/min) in normal, and this was significantly lowered in NIDDM (42.3 +/- 3.4) at steady state, indicating a decreased insulin sensitivity for glucose utilization in NIDDM. Glucose 194-201 insulin Homo sapiens 170-177 3573413-4 1987 Following 75 g oral glucose intake, his blood sugar and insulin levels were 150 mg/dl and 15 mu Iu/ml at 0 min, 373 mg/dl and 757 mu Iu/ml at 60 min and 34 mg/dl and greater than 1,000 mu Iu/ml at 120 min, respectively. Glucose 20-27 insulin Homo sapiens 56-63 3543820-6 1987 Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Glucose 60-67 insulin Homo sapiens 0-7 3103120-3 1987 Quin-2 loading inhibited insulin-stimulated glucose transport (IC50, 26 microM quin-2 AM) without affecting basal activity. Glucose 44-51 insulin Homo sapiens 25-32 3103120-4 1987 The ability of insulin to stimulate glucose uptake in quin-2-loaded cells could be partially restored by preincubating cells with buffer supplemented with 1.2 mM CaCl2 and the Ca2+ ionophore A23187. Glucose 36-43 insulin Homo sapiens 15-22 3103120-5 1987 These conditions had no effect on basal activity and omission of CaCl2 from the buffer prevented the restoration of insulin-stimulated glucose uptake by A23187. Glucose 135-142 insulin Homo sapiens 116-123 3103120-6 1987 Quin-2 loading also inhibited insulin-stimulated glucose oxidation (IC50, 11 microM quin-2 AM) and the ability of insulin to inhibit cAMP-stimulated lipolysis (IC50, 78 microM quin-2 AM), without affecting their basal activities. Glucose 49-56 insulin Homo sapiens 30-37 3103120-10 1987 One involves insulin stimulation of glucose transport and oxidation, whereas the other involves the antilipolytic action of insulin. Glucose 36-43 insulin Homo sapiens 13-20 3554614-2 1987 In this case, despite a quite low fasting plasma glucose value (29 mg/100 ml), a 75 g oral glucose tolerance test (OGTT) showed a diabetic curve and extremely high immunoreactive insulin (IRI) levels were observed. Glucose 91-98 insulin Homo sapiens 179-186 3327334-5 1987 The maximal rate of glucose disposal after injury was half that found in controls and the pattern of response was consistent with the insulin resistance being a post-receptor defect. Glucose 20-27 insulin Homo sapiens 134-141 3539932-0 1987 Dissociation of insulin-stimulated glucose transport from the translocation of glucose carriers in rat adipose cells. Glucose 35-42 insulin Homo sapiens 16-23 3539932-1 1987 Cycloheximide, a potent inhibitor of protein synthesis, has been used to examine the relationship between recruitment of hexose carriers and the activation of glucose transport by insulin in rat adipocytes. Glucose 159-166 insulin Homo sapiens 180-187 3539932-6 1987 However, the number of glucose carriers in plasma membranes prepared from cells incubated with cycloheximide and insulin was markedly reduced compared to that from cells incubated with insulin alone (14 and 34 pmol/mg protein, respectively). Glucose 23-30 insulin Homo sapiens 113-120 3539932-10 1987 Despite this reduction, insulin is still able to maximally stimulate glucose uptake. Glucose 69-76 insulin Homo sapiens 24-31 3539932-11 1987 Thus, these data suggest an apparent dissociation between insulin stimulation of glucose transport activity and the recruitment of glucose carriers by the hormone. Glucose 81-88 insulin Homo sapiens 58-65 2892337-11 1987 However, after Sandostatin administration this relation was lost in the period between 22.00 and 07.00 h, indicating a different effect of insulin on glucose levels during the nights Sandostatin was given. Glucose 150-157 insulin Homo sapiens 139-146 2892337-12 1987 Early morning glucose rises were associated with free insulin levels below 20 mU/l. Glucose 14-21 insulin Homo sapiens 54-61 2892339-6 1987 The postprandial rise of insulin levels was reversed by SMS, leading to a more pronounced postprandial rise of glucose, whereas the postprandial secretion of glucagon was also reversed by SMS. Glucose 111-118 insulin Homo sapiens 25-32 2956817-3 1987 Insulin releasing action of PMS was dose-, time- and temperature-related, occurred in the absence of glucose, and was inhibited by epinephrine, but not by mannoheptulose. Glucose 101-108 insulin Homo sapiens 0-7 3604753-5 1987 Fasting and post-glucagon plasma C-peptide levels in diabetics showed an inverse association to plasma glucose levels and a positive association to degree of obesity, but no association with the known duration of diabetes. Glucose 103-110 insulin Homo sapiens 33-42 3630779-2 1987 At blood glucose concentration less than 7 mmol/l both the C-peptide responses and the maximal (6 min) C-peptide concentrations during the glucagon tests were significantly lower than the corresponding values found during the meal tests. Glucose 9-16 insulin Homo sapiens 59-68 3630779-2 1987 At blood glucose concentration less than 7 mmol/l both the C-peptide responses and the maximal (6 min) C-peptide concentrations during the glucagon tests were significantly lower than the corresponding values found during the meal tests. Glucose 9-16 insulin Homo sapiens 103-112 3544866-2 1987 In this study, the response of glucose uptake, glycogen synthesis, and glucose utilization via glycolysis (glycolytic utilization) to stimulation by insulin and/or acute exercise were determined in isolated muscles from rats with moderate renal insufficiency that were exercise trained or remained sedentary. Glucose 31-38 insulin Homo sapiens 149-156 3544866-2 1987 In this study, the response of glucose uptake, glycogen synthesis, and glucose utilization via glycolysis (glycolytic utilization) to stimulation by insulin and/or acute exercise were determined in isolated muscles from rats with moderate renal insufficiency that were exercise trained or remained sedentary. Glucose 71-78 insulin Homo sapiens 149-156 3544866-4 1987 The enhanced insulin responsiveness of both glycogen synthesis and glucose uptake following acute exercise, noted in control animals, was less in rats with moderate renal insufficiency, but the enhanced basal rate and insulin sensitivity after exercise were unaffected by moderate renal insufficiency. Glucose 67-74 insulin Homo sapiens 13-20 3544866-5 1987 Exercise training increased the insulin sensitivity and responsiveness of muscle glucose uptake and glycolytic utilization in rats with moderate renal insufficiency and in controls. Glucose 81-88 insulin Homo sapiens 32-39 3544866-7 1987 These findings are compatible with the concept that moderate renal insufficiency is associated with a postreceptor defect in insulin"s action in muscle, detectable only following maximal stimulation of glucose transport by insulin and exercise, and partially correctable by exercise training. Glucose 202-209 insulin Homo sapiens 125-132 3315012-5 1987 Differences in mean serum glucose and insulin levels were found when glucose or glucose polymers were used as the test carbohydrate. Glucose 69-76 insulin Homo sapiens 38-45 3315012-5 1987 Differences in mean serum glucose and insulin levels were found when glucose or glucose polymers were used as the test carbohydrate. Glucose 69-76 insulin Homo sapiens 38-45 3315012-7 1987 This suggests that glucose polymers were hydrolyzed and absorbed and evoked a sufficient glucose and insulin response. Glucose 19-26 insulin Homo sapiens 101-108 3552059-5 1987 Concomitantly, an insulin-resistant state develops in the mother to help sparing glucose for the pregnant uterus. Glucose 81-88 insulin Homo sapiens 18-25 3330460-9 1987 Long-term HCD improved the tolerance to oral glucose, i.e., it decreased serum glucose and insulin responses to an oral glucose load. Glucose 45-52 insulin Homo sapiens 91-98 2966652-2 1987 Expression is demonstrated by the presence in the serum of human insulin (determined by a radioimmunoassay for the human C-peptide), the level of which increases upon glucose stimulus, and by the presence of human insulin mRNA in pancreas, but not in the other tissues tested. Glucose 167-174 insulin Homo sapiens 65-72 2966652-2 1987 Expression is demonstrated by the presence in the serum of human insulin (determined by a radioimmunoassay for the human C-peptide), the level of which increases upon glucose stimulus, and by the presence of human insulin mRNA in pancreas, but not in the other tissues tested. Glucose 167-174 insulin Homo sapiens 121-130 2966652-2 1987 Expression is demonstrated by the presence in the serum of human insulin (determined by a radioimmunoassay for the human C-peptide), the level of which increases upon glucose stimulus, and by the presence of human insulin mRNA in pancreas, but not in the other tissues tested. Glucose 167-174 insulin Homo sapiens 214-221 2878848-3 1987 To assess whether doses of SRIF commonly used in human investigation have any effect on insulin-stimulated glucose disposal rates, we measured the rate in 6 normal subjects (mean fasting serum glucose level, 93 +/- 2 mg/dl) during euglycemic (approximately equal to 85 mg/dl) hyperinsulinemic (40 mU X m-2 X min-1) clamp studies both with and without the concomitant infusion of SRIF (600 micrograms/hr). Glucose 107-114 insulin Homo sapiens 88-95 3105985-7 1987 Deliberate cessation of either conventional or subcutaneous insulin infusion therapy for 7 h under close in-hospital control resulted in similar metabolic changes: a slight nonconstant increase of blood glucose, and an abrupt rise of blood 3-hydroxybutyrate to 3 mM, with massive ketonuria. Glucose 203-210 insulin Homo sapiens 60-67 3114028-0 1987 Effect of bombesin on glucose-induced insulin release in humans. Glucose 22-29 insulin Homo sapiens 38-45 3114028-1 1987 The effect of bombesin on basal and glucose-stimulated insulin release was studied in male healthy volunteers. Glucose 36-43 insulin Homo sapiens 55-62 3114028-5 1987 On the contrary, the insulin response to intravenous glucose (20 g) was significantly increased by bombesin without changes in plasma glucose levels. Glucose 53-60 insulin Homo sapiens 21-28 3114028-6 1987 Finally, when glucose was infused into the duodenum, thus bypassing the stomach, the insulin response was significantly increased by the peptide. Glucose 14-21 insulin Homo sapiens 85-92 3114028-8 1987 These data clearly demonstrate that the direct effect of bombesin on insulin release is stimulatory and suggest that the inhibitory effect observed after oral glucose is connected with the action of the peptide on gastric emptying, the delay of which slows the entry of glucose into the small bowel. Glucose 270-277 insulin Homo sapiens 69-76 3552514-3 1987 Changes in glucose uptake at an insulin infusion rate of 1.0 mU X kg-1 X min-1 varied greatly from diagnosis to 6 mo. Glucose 11-18 insulin Homo sapiens 32-39 3552514-5 1987 At an insulin infusion rate of 10 mU X kg-1 X min-1 there was improvement in glucose uptake from diagnosis to 6 mo that did not reach statistical significance. Glucose 77-84 insulin Homo sapiens 6-13 3552515-4 1987 With the same insulin infusion rates, glucose disposal was 4.94 +/- 0.55 (P less than .01) and 8.99 +/- 0.66 (P less than .01), respectively, after metformin treatment. Glucose 38-45 insulin Homo sapiens 14-21 3552515-8 1987 Hepatic glucose production was higher in the diabetic patients at basal insulin levels, but not at higher insulin concentrations, and was not significantly changed by drug treatment. Glucose 8-15 insulin Homo sapiens 72-79 3129276-3 1987 Insulin secretion was stimulated with 100 g glucose (orally) and 1.0 mg glucagon i.v. Glucose 44-51 insulin Homo sapiens 0-7 3315537-5 1987 Both hypoglycaemia and high fasting plasma glucose were avoided by reducing the amount of short-acting insulin and increasing that of intermediate-acting insulin, so that the short-acting/intermediate-acting insulin ratio was significantly lower during BHI therapy, although the total daily insulin dose remained unchanged. Glucose 43-50 insulin Homo sapiens 103-110 3315537-5 1987 Both hypoglycaemia and high fasting plasma glucose were avoided by reducing the amount of short-acting insulin and increasing that of intermediate-acting insulin, so that the short-acting/intermediate-acting insulin ratio was significantly lower during BHI therapy, although the total daily insulin dose remained unchanged. Glucose 43-50 insulin Homo sapiens 154-161 3315537-5 1987 Both hypoglycaemia and high fasting plasma glucose were avoided by reducing the amount of short-acting insulin and increasing that of intermediate-acting insulin, so that the short-acting/intermediate-acting insulin ratio was significantly lower during BHI therapy, although the total daily insulin dose remained unchanged. Glucose 43-50 insulin Homo sapiens 154-161 3315537-5 1987 Both hypoglycaemia and high fasting plasma glucose were avoided by reducing the amount of short-acting insulin and increasing that of intermediate-acting insulin, so that the short-acting/intermediate-acting insulin ratio was significantly lower during BHI therapy, although the total daily insulin dose remained unchanged. Glucose 43-50 insulin Homo sapiens 154-161 3780558-4 1987 In this cell type, both insulin and hydrogen peroxide produced a marked increase in glucose transport after a 30-min incubation. Glucose 84-91 insulin Homo sapiens 24-31 3549287-3 1987 The increase in blood glucose levels was accompanied by a similar increase in insulin concentrations in all three groups despite lower resting insulin levels in conditions D1 and D2. Glucose 22-29 insulin Homo sapiens 78-85 3549287-3 1987 The increase in blood glucose levels was accompanied by a similar increase in insulin concentrations in all three groups despite lower resting insulin levels in conditions D1 and D2. Glucose 22-29 insulin Homo sapiens 143-150 3297726-5 1987 Unlike insulin-stimulated glucose transport, in which permeability is reversed rapidly upon removal of the insulin, the increase in membrane permeability following contractile activity can persist for many hours. Glucose 26-33 insulin Homo sapiens 7-14 3297726-6 1987 It has also been reported that the stimulatory effects of insulin and contraction are additive, and that prostaglandin E2 augments the effect of insulin on glucose transport but has no effect on contraction-facilitated glucose transport. Glucose 156-163 insulin Homo sapiens 145-152 3297726-7 1987 Collectively, these findings suggest that insulin and contractile activity increase membrane permeability to glucose by independent mechanisms. Glucose 109-116 insulin Homo sapiens 42-49 3327757-3 1987 The metabolic clearance rate (MCR) of glucose, which reflects peripheral tissue insulin sensitivity, is derived from the resulting steady-state blood glucose. Glucose 38-45 insulin Homo sapiens 80-87 3327757-3 1987 The metabolic clearance rate (MCR) of glucose, which reflects peripheral tissue insulin sensitivity, is derived from the resulting steady-state blood glucose. Glucose 150-157 insulin Homo sapiens 80-87 2447002-1 1987 This review article is an attempt to schematize the major alterations in ionic fluxes and B cell membrane potential that underlie the changes in insulin release brought about by glucose and by other stimulators or inhibitors. Glucose 178-185 insulin Homo sapiens 145-152 3782431-0 1987 Resistance to insulin suppression of plasma free fatty acid concentrations and insulin stimulation of glucose uptake in noninsulin-dependent diabetes mellitus. Glucose 102-109 insulin Homo sapiens 79-86 3782431-1 1987 The ability of insulin to stimulate tissue glucose uptake and lower plasma FFA concentrations was quantified in 12 individuals with normal glucose tolerance and 12 patients with noninsulin-dependent diabetes mellitus (NIDDM), further subdivided into obese and nonobese subjects. Glucose 43-50 insulin Homo sapiens 15-22 3782431-4 1987 The ability of insulin to either suppress plasma FFA concentrations or stimulate glucose uptake was significantly reduced (P less than 0.001) in patients with NIDDM, and this was true of both the obese and nonobese groups. Glucose 81-88 insulin Homo sapiens 15-22 3782431-6 1987 Finally, a significant correlation (r = -0.67; P less than 0.001) between insulin-stimulated glucose uptake and plasma FFA concentration was found in the entire group. Glucose 93-100 insulin Homo sapiens 74-81 3656048-4 1987 Glucose control was achieved by continuous subcutaneous insulin infusion pumps (CSIIP) in 18 patients, and 34 women received intensive insulin therapy (IIT). Glucose 0-7 insulin Homo sapiens 56-63 3479615-2 1987 The fall in plasma glucose elicited by the highest dose of insulin (1.0 i.u./kg) given to the neonates was slower in onset and less severe in effect than 0.5 i.u./kg in the older foals. Glucose 19-26 insulin Homo sapiens 59-66 3102788-8 1987 We conclude that separate insulin infusion is a reasonable and cost-effective alternative when treating glucose intolerance in patients receiving TPN. Glucose 104-111 insulin Homo sapiens 26-33 3313140-8 1987 Stone formers with an exaggerated urinary risk factor response to sucrose were found to have abnormally high and sustained blood levels of insulin following a standard glucose test meal. Glucose 168-175 insulin Homo sapiens 139-146 3552918-0 1987 Study of insulin response to oral glucose load after acute and chronic glycemic control in type 2 diabetic subjects. Glucose 34-41 insulin Homo sapiens 9-16 3313411-0 1987 Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man. Glucose 47-54 insulin Homo sapiens 30-37 3540958-2 1987 The ability of insulin, IGF-I, and IGF-II to stimulate glucose uptake in TA1 mouse adipocytes was also inhibited. Glucose 55-62 insulin Homo sapiens 15-22 3296383-4 1987 Insulin stimulated adipose tissue glucose oxidation in a dose-dependent way in the control subjects. Glucose 34-41 insulin Homo sapiens 0-7 3541319-8 1987 In vitro insulin response to glucose challenge demonstrated that grafted HFP was capable of insulin secretion in the presence of high glucose while fresh fetal tissue was not. Glucose 29-36 insulin Homo sapiens 9-16 3442106-0 1987 [Glucose-controlled insulin infusion systems (GCIIS, artificial pancreas) in therapy of diabetes mellitus and organic hyperinsulinism]. Glucose 1-8 insulin Homo sapiens 20-27 3590719-4 1987 The 30-day treatment at the hospital covering a special diet, infusions of glucose with insulin, alvesin, cerucal and ampicillin during the first 10 days and alcid V throughout the treatment, rapidly eliminated the alterations, normalization of ESR and discharge of the patient as healthy on 38th day after the intoxication. Glucose 75-82 insulin Homo sapiens 88-95 2954064-4 1986 The steady state regulation of plasma glucose offers a wide range of possible investigations: clinical, such as measuring insulin activity in states of insulin resistance, urinary excretion of glucose and renal threshold; therapeutic, like evaluating the hypoglycemic activity of commercial insulins, or alternative routes of insulin administration, such as the peritoneum; physiopathological, for better evaluation of metabolic alterations in diabetes by measuring the turnover of various substrates. Glucose 38-45 insulin Homo sapiens 122-129 2954064-4 1986 The steady state regulation of plasma glucose offers a wide range of possible investigations: clinical, such as measuring insulin activity in states of insulin resistance, urinary excretion of glucose and renal threshold; therapeutic, like evaluating the hypoglycemic activity of commercial insulins, or alternative routes of insulin administration, such as the peritoneum; physiopathological, for better evaluation of metabolic alterations in diabetes by measuring the turnover of various substrates. Glucose 38-45 insulin Homo sapiens 152-159 2954064-4 1986 The steady state regulation of plasma glucose offers a wide range of possible investigations: clinical, such as measuring insulin activity in states of insulin resistance, urinary excretion of glucose and renal threshold; therapeutic, like evaluating the hypoglycemic activity of commercial insulins, or alternative routes of insulin administration, such as the peritoneum; physiopathological, for better evaluation of metabolic alterations in diabetes by measuring the turnover of various substrates. Glucose 38-45 insulin Homo sapiens 152-159 2878619-2 1986 The results demonstrated that glucose uptake at insulin levels of approximately 100 microU/ml was significantly greater (P less than 0.001) in normal individuals in response to insulin plus SRIF as compared with insulin alone. Glucose 30-37 insulin Homo sapiens 177-184 3024495-5 1986 At variance with the situation found in normal insulin-producing cells, the transport of D-glucose into the tumoral cells may thus play a regulatory role in its metabolism. Glucose 89-98 insulin Homo sapiens 47-54 3673037-5 1987 The glucose tolerance test showed lowered tolerance in 8 patients (12.7%) and 5 of them reacted with increased insulin response. Glucose 4-11 insulin Homo sapiens 111-118 3023346-3 1986 The metabolism of glucose is required for insulin secretion although the link between glucose metabolism and the cellular events resulting in insulin release is unknown. Glucose 18-25 insulin Homo sapiens 42-49 3535899-1 1986 Our recent findings indicate that glucose-induced insulin secretion from isolated pancreatic islets is temporally associated with accumulation of substantial amounts of free arachidonic acid and that arachidonate may serve as a second messenger for intracellular calcium mobilization in islets. Glucose 34-41 insulin Homo sapiens 50-57 3535899-9 1986 These findings indicate that the insulin secretagogue D-glucose induces phospholipid hydrolysis in islets and suggest that PC may be the major source of free arachidonate which accumulates in glucose-stimulated islets. Glucose 54-63 insulin Homo sapiens 33-40 3535899-9 1986 These findings indicate that the insulin secretagogue D-glucose induces phospholipid hydrolysis in islets and suggest that PC may be the major source of free arachidonate which accumulates in glucose-stimulated islets. Glucose 56-63 insulin Homo sapiens 33-40 3537810-6 1986 The 49-residue peptide strongly inhibits glucose-induced insulin release from the isolated perfused pancreas and was therefore named pancreastatin. Glucose 41-48 insulin Homo sapiens 57-64 3538842-5 1986 Overfeeding elevated basal insulin concentrations in all subjects and increased the insulin response to intravenous glucose in four of five subjects. Glucose 116-123 insulin Homo sapiens 84-91 3538877-5 1986 When compared with lean patients, obese patients with previous gestational diabetes had significantly greater insulin response to the intravenous glucose tolerance test and insulin resistance. Glucose 146-153 insulin Homo sapiens 110-117 3538897-6 1986 The intracarotid infusion of D-glucose, however, caused a rapid increase in both the serum insulin concentration and IBF. Glucose 29-38 insulin Homo sapiens 91-98 2878619-0 1986 Somatostatin potentiation of insulin-induced glucose uptake in normal individuals. Glucose 45-52 insulin Homo sapiens 29-36 2878619-1 1986 The ability of somatostatin (SRIF) to enhance insulin-stimulated glucose uptake was evaluated during clamp studies in normal individuals and patients with non-insulin-dependent diabetes mellitus (NIDDM). Glucose 65-72 insulin Homo sapiens 46-53 2878619-2 1986 The results demonstrated that glucose uptake at insulin levels of approximately 100 microU/ml was significantly greater (P less than 0.001) in normal individuals in response to insulin plus SRIF as compared with insulin alone. Glucose 30-37 insulin Homo sapiens 48-55 3026411-5 1986 Soy fiber supplementation also significantly reduced insulin responses to oral glucose challenge by 20% in Type II-A hypercholesterolemic and by 16.5% in Type IV hypertriglyceridemic patients. Glucose 79-86 insulin Homo sapiens 53-60 3533681-0 1986 Insulin dose-response characteristics for suppression of glycerol release and conversion to glucose in humans. Glucose 92-99 insulin Homo sapiens 0-7 3533681-1 1986 To compare the dose-response characteristics for suppression of lipolysis and suppression of glucose production by insulin, 13 normal nonobese individuals were infused with insulin at rates of 0.1, 0.2, 0.4, 0.8, and 1.6 mU X kg-1 X min-1 while normoglycemia was maintained with the glucose clamp technique. Glucose 93-100 insulin Homo sapiens 115-122 3533681-7 1986 Nevertheless, the insulin concentration that produced half-maximal suppression of glucose appearance was twice as great as that required for half-maximal suppression of glycerol appearance (26 +/- 2 vs. 13 +/- 2 microU/ml, P less than .001). Glucose 82-89 insulin Homo sapiens 18-25 3533681-8 1986 Insulin decreased both the absolute rate of glycerol conversion to plasma glucose and the percent of glycerol disposal appearing in plasma glucose (both P less than .001). Glucose 74-81 insulin Homo sapiens 0-7 3533681-8 1986 Insulin decreased both the absolute rate of glycerol conversion to plasma glucose and the percent of glycerol disposal appearing in plasma glucose (both P less than .001). Glucose 139-146 insulin Homo sapiens 0-7 3533684-5 1986 Hepatic glucose production (Ra) was suppressed by greater than 95% during each euglycemic clamp and during the 20-h insulin infusion. Glucose 8-15 insulin Homo sapiens 116-123 3533684-6 1986 After the insulin infusion, Ra and glucose utilization rate returned to the initial basal level within 1 h, as did insulin levels. Glucose 35-42 insulin Homo sapiens 10-17 3539464-1 1986 This study has evaluated insulin resistance under steady-state conditions using the glucose clamp technique. Glucose 84-91 insulin Homo sapiens 25-32 3539464-8 1986 At insulin levels of 200-250 mUl-1, approximately 80% of the whole body glucose uptake could be accounted for by the peripheral tissues. Glucose 72-79 insulin Homo sapiens 3-10 3545930-0 1986 Cultured fibroblasts as a suitable model for studying insulin action on glucose uptake. Glucose 72-79 insulin Homo sapiens 54-61 3545930-1 1986 The action of insulin on glucose uptake in human or animal cultured fibroblasts has been subject of several studies. Glucose 25-32 insulin Homo sapiens 14-21 3545930-5 1986 In addition, as the response to insulin depends greatly on culture conditions (confluency, serum or glucose starvation ...) this cellular model must be used carefully in studies concerning insulin action on glucose uptake. Glucose 100-107 insulin Homo sapiens 32-39 3545930-5 1986 In addition, as the response to insulin depends greatly on culture conditions (confluency, serum or glucose starvation ...) this cellular model must be used carefully in studies concerning insulin action on glucose uptake. Glucose 207-214 insulin Homo sapiens 32-39 3545930-5 1986 In addition, as the response to insulin depends greatly on culture conditions (confluency, serum or glucose starvation ...) this cellular model must be used carefully in studies concerning insulin action on glucose uptake. Glucose 207-214 insulin Homo sapiens 189-196 3536516-10 1986 Like H-ISP, apo A-II isolated from human plasma also had no insulin-like activity by itself, but stimulated the effect of insulin on CO2 production from labeled glucose in isolated rat adipocytes. Glucose 161-168 insulin Homo sapiens 122-129 3546049-0 1986 Insulin stimulates glucose transport in isolated human adipose cells through a translocation of intracellular glucose transporters to the plasma membrane: a preliminary report. Glucose 19-26 insulin Homo sapiens 0-7 3546049-1 1986 Insulin"s effect on glucose transport activity and the subcellular distribution of glucose transporters have been examined in isolated human abdominal adipose cells, by measuring 3-O-methylglucose transport and specific D-glucose-inhibitable cytochalasin B binding to plasma membranes and low-density microsomes, respectively. Glucose 20-27 insulin Homo sapiens 0-7 3546049-1 1986 Insulin"s effect on glucose transport activity and the subcellular distribution of glucose transporters have been examined in isolated human abdominal adipose cells, by measuring 3-O-methylglucose transport and specific D-glucose-inhibitable cytochalasin B binding to plasma membranes and low-density microsomes, respectively. Glucose 220-229 insulin Homo sapiens 0-7 3546049-2 1986 Insulin appears to stimulate glucose transport in isolated human adipose cell through the translocation of glucose transporters from a large intracellular pool to the plasma membrane as initially postulated for rat adipose and muscle cells. Glucose 29-36 insulin Homo sapiens 0-7 3542852-1 1986 To estimate physical training effects quantitatively, the relationship between tissue sensitivity to exogenous insulin (glucose metabolism determined by euglycemic insulin-clamp technique) and maximal oxygen uptake (VO2 max) was defined in 9 well-trained athletes and 14 untrained subjects with normal glucose tolerance. Glucose 120-127 insulin Homo sapiens 111-118 3546167-0 1986 A comparison of regular insulin and vesicle encapsulated insulin on glucose metabolism in diabetic subjects. Glucose 68-75 insulin Homo sapiens 57-64 3546167-4 1986 Dose-response analysis indicated that VEI insulin was one-third as potent as UI, both on stimulation of glucose utilization and suppression of hepatic glucose production. Glucose 104-111 insulin Homo sapiens 42-49 3546167-4 1986 Dose-response analysis indicated that VEI insulin was one-third as potent as UI, both on stimulation of glucose utilization and suppression of hepatic glucose production. Glucose 151-158 insulin Homo sapiens 42-49 3537009-0 1986 Assessment of insulin action in insulin-dependent diabetes mellitus using [6(14)C]glucose, [3(3)H]glucose, and [2(3)H]glucose. Glucose 82-89 insulin Homo sapiens 14-21 3537009-0 1986 Assessment of insulin action in insulin-dependent diabetes mellitus using [6(14)C]glucose, [3(3)H]glucose, and [2(3)H]glucose. Glucose 98-105 insulin Homo sapiens 14-21 3537009-0 1986 Assessment of insulin action in insulin-dependent diabetes mellitus using [6(14)C]glucose, [3(3)H]glucose, and [2(3)H]glucose. Glucose 98-105 insulin Homo sapiens 14-21 3537009-3 1986 In the nondiabetic subjects, glucose turnover rates determined with [6(14)C]glucose during insulin infusion were lower (P less than 0.02) than those determined with [2(3)H]glucose and higher (P less than 0.01) than those determined with [3(3)H]glucose. Glucose 29-36 insulin Homo sapiens 91-98 3537009-3 1986 In the nondiabetic subjects, glucose turnover rates determined with [6(14)C]glucose during insulin infusion were lower (P less than 0.02) than those determined with [2(3)H]glucose and higher (P less than 0.01) than those determined with [3(3)H]glucose. Glucose 76-83 insulin Homo sapiens 91-98 3537009-3 1986 In the nondiabetic subjects, glucose turnover rates determined with [6(14)C]glucose during insulin infusion were lower (P less than 0.02) than those determined with [2(3)H]glucose and higher (P less than 0.01) than those determined with [3(3)H]glucose. Glucose 76-83 insulin Homo sapiens 91-98 3537009-3 1986 In the nondiabetic subjects, glucose turnover rates determined with [6(14)C]glucose during insulin infusion were lower (P less than 0.02) than those determined with [2(3)H]glucose and higher (P less than 0.01) than those determined with [3(3)H]glucose. Glucose 76-83 insulin Homo sapiens 91-98 3537009-4 1986 In IDDM, glucose turnover rates measured with [6(14)C]glucose during insulin infusion were lower (P less than 0.05) than those determined with [2(3)H]glucose, but were not different from those determined with [3(3)H]glucose. Glucose 9-16 insulin Homo sapiens 69-76 3537009-4 1986 In IDDM, glucose turnover rates measured with [6(14)C]glucose during insulin infusion were lower (P less than 0.05) than those determined with [2(3)H]glucose, but were not different from those determined with [3(3)H]glucose. Glucose 54-61 insulin Homo sapiens 69-76 3537009-4 1986 In IDDM, glucose turnover rates measured with [6(14)C]glucose during insulin infusion were lower (P less than 0.05) than those determined with [2(3)H]glucose, but were not different from those determined with [3(3)H]glucose. Glucose 54-61 insulin Homo sapiens 69-76 3537009-4 1986 In IDDM, glucose turnover rates measured with [6(14)C]glucose during insulin infusion were lower (P less than 0.05) than those determined with [2(3)H]glucose, but were not different from those determined with [3(3)H]glucose. Glucose 54-61 insulin Homo sapiens 69-76 3537009-7 1986 [6(14)C] and [3(3)H]glucose but not [2(3)H]glucose indicated impairment in insulin-induced suppression of glucose production. Glucose 20-27 insulin Homo sapiens 75-82 3537010-3 1986 When compared with the nonobese women, obese women had significantly greater prehepatic production and portal vein levels of insulin both basally and following glucose stimulation. Glucose 160-167 insulin Homo sapiens 125-132 3537011-9 1986 The biological activities of the normal component, the abnormal component and her pancreatic insulin to stimulate glucose oxidation in rat adipocytes were found to be 100, 8, and 60% of standard human insulin, respectively. Glucose 114-121 insulin Homo sapiens 93-100 3543229-0 1986 An abnormal response of the adrenal cortex to insulin: glucose in essential hypertension. Glucose 55-62 insulin Homo sapiens 46-53 3571854-1 1986 Insulin autoimmune syndrome is characterized by spontaneous hypoglycemia, glucose intolerance, hyperinsulinemia and insulin-binding antibodies in serum without previous immunization. Glucose 74-81 insulin Homo sapiens 0-7 3543261-8 1986 Insulin seemed to be the major mechanism of regulation of glucose, FFA and ketone body metabolism since pancreatic production and arterial concentrations of insulin decreased with progressive fasting. Glucose 58-65 insulin Homo sapiens 0-7 3543261-8 1986 Insulin seemed to be the major mechanism of regulation of glucose, FFA and ketone body metabolism since pancreatic production and arterial concentrations of insulin decreased with progressive fasting. Glucose 58-65 insulin Homo sapiens 157-164 3103341-5 1986 After the peak values have been reached, the decrease of glucose from the blood is delayed up to the second postoperative day, although during the whole testing period the insulin secretion--calculated according to the insulinogenic index - corresponds to the glucose stimulation. Glucose 260-267 insulin Homo sapiens 172-179 3024340-7 1986 In conjunction with preoperative localization, we have used intraoperative monitoring of glucose levels as a guide to the completeness of resection of insulin producing tumors. Glucose 89-96 insulin Homo sapiens 151-158 3535799-6 1986 The ability of insulin (100 mU/ml) to stimulate hexose transport was returned by glucose refeeding and this was not affected by tunicamycin. Glucose 81-88 insulin Homo sapiens 15-22 2878704-4 1986 The patient with impaired glucose tolerance due to insulin deficiency developed diabetes mellitus after four months" treatment; concomitant treatment with glibenclamide resulted in a decreased glucose concentration and increased insulin concentration. Glucose 26-33 insulin Homo sapiens 51-58 3538447-1 1986 The insulin response to a 75 g oral glucose load was studied in 26 indian patients with impaired glucose tolerance (IGT) and 26 controls matched for age, sex and weight. Glucose 36-43 insulin Homo sapiens 4-11 2430570-0 1986 Galanin inhibits glucose-stimulated insulin release by a mechanism involving hyperpolarization and lowering of cytoplasmic free Ca2+ concentration. Glucose 17-24 insulin Homo sapiens 36-43 2430570-3 1986 Glucose-stimulated insulin secretion was inhibited by galanin under these conditions, indicating a direct effect of the peptide on the beta-cells. Glucose 0-7 insulin Homo sapiens 19-26 2430570-7 1986 The results indicate that galanin inhibition of glucose-stimulated insulin release involves hyperpolarization with a subsequent decrease in cytoplasmic free Ca2+. Glucose 48-55 insulin Homo sapiens 67-74 3535799-8 1986 Specific 125I-insulin binding was increased by glucose refeeding of glucose-starved cells and this change in binding was inhibited by tunicamycin and cycloheximide. Glucose 47-54 insulin Homo sapiens 14-21 3535799-8 1986 Specific 125I-insulin binding was increased by glucose refeeding of glucose-starved cells and this change in binding was inhibited by tunicamycin and cycloheximide. Glucose 68-75 insulin Homo sapiens 14-21 3535532-5 1986 Feeding of the HiFAT diet resulted in a greater than 50% reduction in net whole-body glucose utilization at midphysiological insulin levels (90-100 mU/l) due to both reduced glucose disposal and, to a lesser extent, failure to suppress liver glucose output. Glucose 85-92 insulin Homo sapiens 125-132 3538738-2 1986 In the 28 diabetics who had been followed for more than 6 months, the relation between the amount of insulin or CPR in the pancreas and the stability of fasting serum glucose during diabetic life before death was analyzed together with the relation between the serum CPR response to the breakfast tolerance test before death and insulin content at autopsy. Glucose 167-174 insulin Homo sapiens 101-108 3535532-9 1986 HiFAT feeding also resulted in major decreases in basal and insulin-stimulated conversion of glucose to lipid in liver (26-60%) and brown adipose tissue (88-90%) with relatively less effect in white adipose (0-43%). Glucose 93-100 insulin Homo sapiens 60-67 2946276-6 1986 Similarly, in vivo experiments demonstrated that a diabetic host with a high blood glucose level and a low insulin level exhibited development of growth of a receptor-negative tumor with accelerated growth rate in contrast to growth of a receptor-positive tumor with slower growth rate in a normal host with normal serum insulin and blood glucose levels. Glucose 339-346 insulin Homo sapiens 107-114 3539293-2 1986 Since polymorphisms in the region 5" to the insulin gene have been associated with blood glucose levels, we have studied this polymorphism in AD patients. Glucose 89-96 insulin Homo sapiens 44-51 3314982-16 1986 The cold stress induced by shearing may also inhibit insulin secretion resulting in increased plasma glucose concentrations. Glucose 101-108 insulin Homo sapiens 53-60 3530853-6 1986 After a week of intensive insulin therapy in which the same diabetic subjects received 94 +/- 36 U/day of insulin, postabsorptive plasma glucose declined to 117 +/- 26 mg/dl. Glucose 137-144 insulin Homo sapiens 26-33 3530853-6 1986 After a week of intensive insulin therapy in which the same diabetic subjects received 94 +/- 36 U/day of insulin, postabsorptive plasma glucose declined to 117 +/- 26 mg/dl. Glucose 137-144 insulin Homo sapiens 106-113 3530853-9 1986 Additional intensive insulin therapy in these diabetic subjects improved plasma glucose but did not alter leucine kinetics. Glucose 80-87 insulin Homo sapiens 21-28 3545955-7 1986 The insulin response was greater than could be explained by the glucose response for all meals except apples. Glucose 64-71 insulin Homo sapiens 4-11 3549121-0 1986 Sequential infusions of glucose and insulin at prefixed rates: a simple method for assessing insulin sensitivity and insulin responsiveness. Glucose 24-31 insulin Homo sapiens 93-100 3549121-1 1986 In a previous study a close correlation was demonstrated between metabolic clearance rates of glucose (MCR) at an insulin infusion rate of 50 mU X kg-1 hr-1 when assessed with the isoglycaemic clamp technique and the simple, concomitant infusion of insulin and glucose at a fixed rate. Glucose 94-101 insulin Homo sapiens 114-121 3549121-1 1986 In a previous study a close correlation was demonstrated between metabolic clearance rates of glucose (MCR) at an insulin infusion rate of 50 mU X kg-1 hr-1 when assessed with the isoglycaemic clamp technique and the simple, concomitant infusion of insulin and glucose at a fixed rate. Glucose 94-101 insulin Homo sapiens 249-256 3549121-4 1986 Insulin mediated glucose disposal, expressed as MCR, was assessed during the steady states of sequential, concomitant infusions of insulin at 50, 150 and 500 mU X kg-1 hr-1 and glucose at 33, 44 and 55 mumol X kg-1 min-1 for 150, 120 and 120 min, respectively. Glucose 17-24 insulin Homo sapiens 0-7 3545858-5 1986 There was, however, a relationship between advancing age and early (IRI area 0-30 min), late (IRI area 30-120 min) and total (IRI area 0-120 min) insulin response to glucose. Glucose 166-173 insulin Homo sapiens 146-153 2878866-3 1986 Conversely, addition of SMS 201-995 to insulin treatment led to normalization of blood glucose. Glucose 87-94 insulin Homo sapiens 39-46 3534516-7 1986 The improvement in glucose tolerance and beta-cell function induced by insulin treatment seems to be of more limited duration than the improvements in basal hepatic glucose production and in insulin action. Glucose 19-26 insulin Homo sapiens 71-78 3534514-3 1986 Glucose and insulin responses were elevated from one to three hours after oral glucose in FA. Glucose 79-86 insulin Homo sapiens 12-19 3534516-2 1986 When compared to the pretreatment period, 48 hours after discontinuing insulin treatment fasting plasma glucose had fallen (P = 0.005), fasting serum insulin had risen (P = 0.005), and fasting hepatic glucose production measured by 3H-3-glucose turnover had fallen (P = 0.008). Glucose 104-111 insulin Homo sapiens 71-78 3534516-3 1986 The metabolic clearance rate of glucose measured with the glucose clamp rose significantly after treatment at insulin infusion rates of 40 mU m-2 min-1 (P = 0.015) and 400 mU m-2 min-1 (P = 0.012). Glucose 32-39 insulin Homo sapiens 110-117 3534516-3 1986 The metabolic clearance rate of glucose measured with the glucose clamp rose significantly after treatment at insulin infusion rates of 40 mU m-2 min-1 (P = 0.015) and 400 mU m-2 min-1 (P = 0.012). Glucose 58-65 insulin Homo sapiens 110-117 3534516-4 1986 The serum insulin and C-peptide responses to oral glucose improved after the treatment in association with the improvement in glucose tolerance, but the plasma glucose response was unchanged. Glucose 50-57 insulin Homo sapiens 10-17 3534516-4 1986 The serum insulin and C-peptide responses to oral glucose improved after the treatment in association with the improvement in glucose tolerance, but the plasma glucose response was unchanged. Glucose 50-57 insulin Homo sapiens 22-31 3534516-4 1986 The serum insulin and C-peptide responses to oral glucose improved after the treatment in association with the improvement in glucose tolerance, but the plasma glucose response was unchanged. Glucose 126-133 insulin Homo sapiens 10-17 3534516-4 1986 The serum insulin and C-peptide responses to oral glucose improved after the treatment in association with the improvement in glucose tolerance, but the plasma glucose response was unchanged. Glucose 126-133 insulin Homo sapiens 22-31 3534516-4 1986 The serum insulin and C-peptide responses to oral glucose improved after the treatment in association with the improvement in glucose tolerance, but the plasma glucose response was unchanged. Glucose 126-133 insulin Homo sapiens 10-17 3534516-4 1986 The serum insulin and C-peptide responses to oral glucose improved after the treatment in association with the improvement in glucose tolerance, but the plasma glucose response was unchanged. Glucose 126-133 insulin Homo sapiens 22-31 3534516-6 1986 Six weeks after discontinuing insulin, the patients" fasting hepatic glucose production was still reduced compared to pretreatment (P = 0.028) and insulin action was still improved at both the lower (P = 0.028) and the higher (P = 0.028) insulin infusion rates, but the fasting plasma glucose and insulin and C-peptide responses to oral glucose had returned to pretreatment values. Glucose 69-76 insulin Homo sapiens 30-37 3534516-6 1986 Six weeks after discontinuing insulin, the patients" fasting hepatic glucose production was still reduced compared to pretreatment (P = 0.028) and insulin action was still improved at both the lower (P = 0.028) and the higher (P = 0.028) insulin infusion rates, but the fasting plasma glucose and insulin and C-peptide responses to oral glucose had returned to pretreatment values. Glucose 285-292 insulin Homo sapiens 30-37 3534516-6 1986 Six weeks after discontinuing insulin, the patients" fasting hepatic glucose production was still reduced compared to pretreatment (P = 0.028) and insulin action was still improved at both the lower (P = 0.028) and the higher (P = 0.028) insulin infusion rates, but the fasting plasma glucose and insulin and C-peptide responses to oral glucose had returned to pretreatment values. Glucose 285-292 insulin Homo sapiens 30-37 3543715-1 1986 The behavioral effects of carbon tetrachloride-produced impairment of liver function, insulin-produced reduction of plasma glucose levels, and the reduction of food and water intake have been evaluated. Glucose 123-130 insulin Homo sapiens 86-93 3533913-7 1986 These data contradict the hypothesis that insulin secretion is triggered by a more reduced cytosolic redox state and instead indicate that insulin secretion is initiated by other metabolic coupling factor(s) generated in beta cells stimulated by high glucose. Glucose 251-258 insulin Homo sapiens 139-146 2430419-3 1986 In the absence of aminoacids in the perfusion medium, A cell blindness to glucose was corrected by physiological levels of insulin (2 ng/ml); insulinodependency of A cells, and unresponsiveness of D cells to glucose, probably not ruled by insulin, were observed. Glucose 74-81 insulin Homo sapiens 123-130 3766633-4 1986 Glucose tolerance and the insulin response to oral glucose remained unchanged in both groups during the treatment period. Glucose 51-58 insulin Homo sapiens 26-33 3789961-2 1986 The SRID system consists of an encapsulated glycosylated insulin bound to concanavalin A (conA) that exchanges insulin with glucose through a reversible chemical reaction between glucose and conA-insulin (C-I). Glucose 124-131 insulin Homo sapiens 57-64 3789961-2 1986 The SRID system consists of an encapsulated glycosylated insulin bound to concanavalin A (conA) that exchanges insulin with glucose through a reversible chemical reaction between glucose and conA-insulin (C-I). Glucose 179-186 insulin Homo sapiens 57-64 3789961-4 1986 Using these calculated reaction rate constants, the insulin release rate was predicted from a SRID cylindrical pouch in response to a change in glucose concentration. Glucose 144-151 insulin Homo sapiens 52-59 3789961-5 1986 The insulin release rate was found to be strongly affected by the diffusivity coefficients of insulin and glucose within the pouch, the radius of the pouch, membrane permeability, C-I concentration, and the kinetic rate constants. Glucose 106-113 insulin Homo sapiens 4-11 3304724-5 1986 After 75 g glucose, the rise in serum proinsulin to a maximum concentration of 0.082 +/- 0.012 nmol/l in patients of Group A and to 0.070 +/- 0.019 nmol/l in Group B was not significantly different at any time point up to 180 min from the rise in healthy subjects (to 0.063 +/- 0.005 nmol/l). Glucose 11-18 insulin Homo sapiens 38-48 3304724-6 1986 After 25 g glucose, the response of serum proinsulin in Group B patients (maximum concentration 0.035 +/- 0.003 nmol/l) was not significantly different from that in healthy subjects (maximum concentration 0.032 +/- 0.003 nmol/l) but a slightly enhanced release was observed in the Group A patients (maximum concentration 0.049 +/- 0.003 nmol/l) that was significantly greater (P less than 0.05) at 60 min post-glucose. Glucose 11-18 insulin Homo sapiens 42-52 3304724-7 1986 In contrast, the concentrations of serum immunoreactive insulin and immunoreactive C-peptide in all patients with cirrhosis were significantly elevated compared with healthy subjects both in the fasted state and at several time points following high and low oral glucose. Glucose 263-270 insulin Homo sapiens 56-63 3542161-2 1986 When C6-labelled glucose was used, insulin induced a slightly greater increase in glucose oxidation in dystrophic adipose tissue at both ages. Glucose 17-24 insulin Homo sapiens 35-42 3542161-3 1986 When C1-labelled glucose was used, insulin enhanced glucose oxidation in dystrophic tissue more than twice normal in tissues from young animals and five times normal in tissues from the old ones. Glucose 17-24 insulin Homo sapiens 35-42 2875910-3 1986 Glucose disposal rate between the 2nd and 4th h of a euglycemic insulin clamp, developed through a constant infusion of insulin (0.77 mU X kg-1 X min-1) together with somatostatin (80 ng X kg-1 X min-1), was 2.5-fold higher in a DG-5128-treated group (P less than .01) than in a control group. Glucose 0-7 insulin Homo sapiens 64-71 3100372-4 1986 The increase in clamp glucose requirements (insulin 0.1 U X kg-1 X h-1) between injection therapy and continuous subcutaneous insulin infusion was significant (6.2 +/- 0.9 (SE) to 7.0 +/- 0.9 mg X kg-1 X min-1, p less than 0.05), but small compared to differences between subjects. Glucose 22-29 insulin Homo sapiens 44-51 3100372-4 1986 The increase in clamp glucose requirements (insulin 0.1 U X kg-1 X h-1) between injection therapy and continuous subcutaneous insulin infusion was significant (6.2 +/- 0.9 (SE) to 7.0 +/- 0.9 mg X kg-1 X min-1, p less than 0.05), but small compared to differences between subjects. Glucose 22-29 insulin Homo sapiens 126-133 3530612-7 1986 Creatinine adjusted rates of whole body glucose disposal were 30-40% lower in the myotonic dystrophy group at all three doses of insulin compared with the normals. Glucose 40-47 insulin Homo sapiens 129-136 3530841-6 1986 The correlation between abdominal adipocyte size and fasting insulin concentration (r = .91 and .18, t = 2.8, P = .01) was stronger in children from glucose-intolerant than from glucose-tolerant pregnancies, respectively. Glucose 149-156 insulin Homo sapiens 61-68 3542618-3 1986 The mean diurnal blood glucose concentration during the initial ten days of insulin treatment was 11.7 +/- 0.5 mmol/l (mean +/- SEM) in group A and 6.4 +/- 0.3 mmol/l in group B (P less than 0.01) and 6.0 +/- 0.3 mmol/l in group B during the 7 days with intensified treatment 15 months later. Glucose 23-30 insulin Homo sapiens 76-83 3542670-0 1986 Salivary insulin concentrations in type 2 (non-insulin-dependent) diabetic patients and obese non-diabetic subjects: relationship to changes in plasma insulin levels after an oral glucose load. Glucose 180-187 insulin Homo sapiens 9-16 3542670-1 1986 The presence of immunoreactive insulin in saliva and its relationship to plasma immunoreactive insulin was investigated in healthy subjects, newly diagnosed non-obese Type 2 (non-insulin-dependent) diabetic patients and obese non-diabetic subjects, basally and after an oral glucose tolerance test. Glucose 275-282 insulin Homo sapiens 31-38 3542670-7 1986 We conclude that salivary immunoreactive insulin can be found in Type 2 diabetic patients and in obese non-diabetic subjects, as well as normal volunteers, that plasma and salivary insulin are related after a glucose load, and that differences exist in salivary insulin secretion patterns among the three groups of subjects. Glucose 209-216 insulin Homo sapiens 41-48 3640682-1 1986 Insulin sensitivity and pancreatic responsivity are the two main factors controlling glucose tolerance. Glucose 85-92 insulin Homo sapiens 0-7 3640682-7 1986 From the model parameters, it is possible to extract four indices: SG, the ability of glucose per se to enhance its own disappearance at basal insulin, SI, the tissue insulin sensitivity index, phi 1, first phase pancreatic responsivity, and phi 2, second phase pancreatic responsivity. Glucose 86-93 insulin Homo sapiens 143-150 3536704-6 1986 Even during the glucose-induced insulin secretion, in the presence of sparteine infusion, plasma glucose levels were significantly lower while plasma insulin levels were significantly higher when compared to those observed after glucose alone. Glucose 16-23 insulin Homo sapiens 32-39 3536704-7 1986 The acute insulin response (AIR) was 42 +/- 10 microU/ml after glucose alone vs 67 +/- 9 microU/ml after glucose plus sparteine (P less than 0.05). Glucose 63-70 insulin Homo sapiens 10-17 3528209-3 1986 Mean fasting plasma insulin was significantly higher in cirrhotic patients [26.1 +/- 2.3 vs. 12.4 +/- 0.6 (+/- SE) microU/ml; P less than 0.001], while fasting plasma glucose levels were similar in the 2 groups. Glucose 167-174 insulin Homo sapiens 20-27 3528210-11 1986 These data suggest that the increased tissue utilization of glucose in this hypoglycemic patient was caused by proliferation of insulin receptors in liver and muscle induced by his nonislet cell tumor through an unknown humoral mechanism(s). Glucose 60-67 insulin Homo sapiens 128-135 3745404-12 1986 We conclude that 1) Met has an acute insulin-like effect in vitro independent of its ability to increase insulin binding; 2) Met acts in vivo predominantly at a postreceptor site to lower plasma glucose; 3) the glucose-lowering effect is independent of pretreatment insulin binding status; and 4) the increase in insulin binding after Met treatment in patients with NIDDM and low insulin binding occurs without changes in insulin concentrations. Glucose 211-218 insulin Homo sapiens 37-44 3531236-2 1986 We examined insulin"s effects on glucose transport and on subcellular transporter distribution in isolated human omental adipocytes of various sizes. Glucose 33-40 insulin Homo sapiens 12-19 3540079-0 1986 Impaired insulin response to glucose but not to arginine in heroin addicts. Glucose 29-36 insulin Homo sapiens 9-16 3540079-2 1986 The heroin users had an exaggerated rise in plasma glucose concentrations following oral sugar, which persisted until the end of the study (102 +/- 5 mg/dl in addicts vs 72 +/- 3 mg/dl in controls at 240 min, p less than 0.01) and significantly lower insulin responses (insulin peak 28 +/- 4 microU/ml in addicts vs 67 +/- 8 microU/ml in controls, p less than 0.01). Glucose 51-58 insulin Homo sapiens 251-258 3540079-2 1986 The heroin users had an exaggerated rise in plasma glucose concentrations following oral sugar, which persisted until the end of the study (102 +/- 5 mg/dl in addicts vs 72 +/- 3 mg/dl in controls at 240 min, p less than 0.01) and significantly lower insulin responses (insulin peak 28 +/- 4 microU/ml in addicts vs 67 +/- 8 microU/ml in controls, p less than 0.01). Glucose 51-58 insulin Homo sapiens 270-277 3540080-0 1986 Further evidence that insulin metabolism is a major determinant of peripheral insulin response to oral glucose in subjects with mild glucose intolerance. Glucose 103-110 insulin Homo sapiens 22-29 3540080-0 1986 Further evidence that insulin metabolism is a major determinant of peripheral insulin response to oral glucose in subjects with mild glucose intolerance. Glucose 133-140 insulin Homo sapiens 22-29 3540080-1 1986 In mild glucose intolerance plasma concentration of C-peptide seems to give an estimate of pancreatic B cell secretion more reliable than plasma insulin itself. Glucose 8-15 insulin Homo sapiens 52-61 3540080-2 1986 In the present study we measured the plasma levels of insulin and C-peptide after oral glucose load in 100 mildly glucose intolerant subjects, focusing our attention on high and low insulin responders. Glucose 87-94 insulin Homo sapiens 54-61 3540080-2 1986 In the present study we measured the plasma levels of insulin and C-peptide after oral glucose load in 100 mildly glucose intolerant subjects, focusing our attention on high and low insulin responders. Glucose 87-94 insulin Homo sapiens 66-75 3540080-8 1986 These results give further support to the concept that in mild glucose intolerance insulin metabolism is a major determinant of peripheral insulin response to oral glucose load. Glucose 63-70 insulin Homo sapiens 83-90 3540081-0 1986 Effect of domperidone on the release of insulin after intravenous glucose load in man. Glucose 66-73 insulin Homo sapiens 40-47 3540081-1 1986 To determine whether the blockade of the dopaminergic system is capable of modifying glucose-induced insulin release in man, the responses of insulin to an iv glucose load were measured at various domperidone infusion rates. Glucose 85-92 insulin Homo sapiens 101-108 3540081-2 1986 The infusion of 5 micrograms/kg/min of domperidone increased significantly plasma insulin levels during the acute phase of glucose-induced insulin release and lowered plasma glucose values at 50 and 60 min; the k of glucose disappearance improved significantly. Glucose 123-130 insulin Homo sapiens 82-89 3540081-2 1986 The infusion of 5 micrograms/kg/min of domperidone increased significantly plasma insulin levels during the acute phase of glucose-induced insulin release and lowered plasma glucose values at 50 and 60 min; the k of glucose disappearance improved significantly. Glucose 123-130 insulin Homo sapiens 139-146 3540081-3 1986 At lower domperidone infusion rates the acute increment of insulin after glucose load was indistinguishable from the response observed at 5 micrograms/kg/min until 0.5 microgram/kg/min, while similar responses in control and experimental tests were observed at 0.25 microgram/kg/min. Glucose 73-80 insulin Homo sapiens 59-66 3540081-4 1986 A group of subjects was submitted to an arginine load in order to establish whether the effect observed with domperidone was specific for the glucose-induced insulin release; but, this time, we did not observe any significant effect during the domperidone-induced dopaminergic blockade. Glucose 142-149 insulin Homo sapiens 158-165 3540081-7 1986 Since domperidone is a specific antagonist of dopamine D2-receptors, we propose that dopamine might exert a specific inhibiting effect on glucose-induced insulin release through this class of dopamine receptors. Glucose 138-145 insulin Homo sapiens 154-161 3537496-2 1986 High insulin levels in the range of 350 microU/ml (normal range less than 20 microU/ml) were detected which rose to peak levels of 2,460 microU/ml (normal range less than 300 microU/ml) after oral glucose. Glucose 197-204 insulin Homo sapiens 5-12 3537496-8 1986 Quantitation of free insulin during a hypoglycemic attack (3.5 h after oral glucose, with a blood sugar of 20 mg/dl) showed an increased insulin level of 50 microU/ml. Glucose 76-83 insulin Homo sapiens 21-28 3537496-10 1986 We believe that the insulin antibodies present in this patient"s serum (who supposedly never received insulin) led to the formation of a large circulating insulin pool, binding the insulin released after glucose stimulation, and causing hypoglycemias by delayed postprandial liberation of bound insulin. Glucose 204-211 insulin Homo sapiens 20-27 3020345-5 1986 The cultured fibroblasts from the patient showed decreased glucose incorporation at the low insulin concentration with normal maximal stimulation, and the insulin dose response curve was shifted to the right. Glucose 59-66 insulin Homo sapiens 92-99 3095717-5 1986 Treatments which decrease cellular glucose utilization directly (2-DG) or indirectly (insulin) increase food intake while exogenous glucagon (which produces hyperglycemia) decreases it. Glucose 35-42 insulin Homo sapiens 86-93 3531761-8 1986 However, the normal stimulation of glucose uptake by insulin was abolished by growth hormone. Glucose 35-42 insulin Homo sapiens 53-60 3537424-0 1986 Effects of glucose injection and cold exposure on secretory responses of insulin, glucagon and 11-hydroxycorticosteroids in piglets. Glucose 11-18 insulin Homo sapiens 73-80 3763272-6 1986 One unexpected observation was the apparent normalization of blood glucose homeostasis on higher dextrose doses among some infants after only one three- to six-hour treatment with insulin. Glucose 97-105 insulin Homo sapiens 180-187 3095909-8 1986 We conclude that nutrients sensitize insulin-releasing cells to subsequent stimulation by glibenclamide, thereby aggravate a blood-glucose-lowering effect of the drug. Glucose 131-138 insulin Homo sapiens 37-44 3532392-2 1986 After oral glucose, significant increases in serum glucose, insulin, and GIP levels occurred both before and after gastric bypass. Glucose 11-18 insulin Homo sapiens 60-67 3528154-0 1986 Insulin-dependent phosphorylation of the insulin receptor-protein kinase and activation of glucose transport in 3T3-L1 adipocytes. Glucose 91-98 insulin Homo sapiens 0-7 3528154-0 1986 Insulin-dependent phosphorylation of the insulin receptor-protein kinase and activation of glucose transport in 3T3-L1 adipocytes. Glucose 91-98 insulin Homo sapiens 41-48 3528154-13 1986 These kinetic experiments in situ and protein kinase activity measurements in vitro support the hypothesis that beta-subunit phosphorylation is an intermediate step linking insulin binding to the increased glucose transport rate. Glucose 206-213 insulin Homo sapiens 173-180 3541915-0 1986 The insulin-like effect of sodium vanadate on adipocyte glucose transport is mediated at a post-insulin-receptor level. Glucose 56-63 insulin Homo sapiens 4-11 3541915-0 1986 The insulin-like effect of sodium vanadate on adipocyte glucose transport is mediated at a post-insulin-receptor level. Glucose 56-63 insulin Homo sapiens 96-103 3541915-7 1986 A 2 h treatment caused 60% loss of receptors, and a shift to the right in the dose-response curve for insulin stimulation of glucose transport (EC50 0.3 ng of insulin/ml in controls, 1.2 ng/ml in treated cells). Glucose 125-132 insulin Homo sapiens 102-109 3541915-7 1986 A 2 h treatment caused 60% loss of receptors, and a shift to the right in the dose-response curve for insulin stimulation of glucose transport (EC50 0.3 ng of insulin/ml in controls, 1.2 ng/ml in treated cells). Glucose 125-132 insulin Homo sapiens 159-166 3532658-5 1986 In fat cells, both basal and insulin stimulated rates of glucose transport were 35% lower (P less than 0.05) in the middle-aged than in the young subjects. Glucose 57-64 insulin Homo sapiens 29-36 3532658-6 1986 Basal and insulin stimulated rates of glucose oxidation and lipogenesis were both markedly lower (P less than 0.01) in the middle-aged than in the young group. Glucose 38-45 insulin Homo sapiens 10-17 3529983-0 1986 Insulin sensitivity in adipocytes from subjects with varying degrees of glucose tolerance. Glucose 72-79 insulin Homo sapiens 0-7 3529983-2 1986 This study analyzed the relationship between insulin sensitivity of glucose transport and glycemia in a large group of nondiabetic-nonglucose-intolerant subjects with a wide range of glycemic response to oral glucose. Glucose 68-75 insulin Homo sapiens 45-52 3529983-4 1986 Isolated adipocytes were prepared in vitro after an abdominal fat biopsy, ED50 of insulin for glucose transport was correlated with 2-h postload glucoses, but not between insulin binding per cell or per cell surface area or in ED50 of insulin for antilipolysis and 2-h postglucose load glucoses. Glucose 94-101 insulin Homo sapiens 82-89 3529983-4 1986 Isolated adipocytes were prepared in vitro after an abdominal fat biopsy, ED50 of insulin for glucose transport was correlated with 2-h postload glucoses, but not between insulin binding per cell or per cell surface area or in ED50 of insulin for antilipolysis and 2-h postglucose load glucoses. Glucose 145-153 insulin Homo sapiens 82-89 3529983-4 1986 Isolated adipocytes were prepared in vitro after an abdominal fat biopsy, ED50 of insulin for glucose transport was correlated with 2-h postload glucoses, but not between insulin binding per cell or per cell surface area or in ED50 of insulin for antilipolysis and 2-h postglucose load glucoses. Glucose 286-294 insulin Homo sapiens 82-89 3529983-5 1986 Although only 17% of the variation in glucose tolerance could be explained by a change in the sensitivity of glucose transport to insulin, the data suggests that a postinsulin-binding defect in the coupling of insulin binding to glucose transport may be an early step in the development of insulin resistance in human adipocytes. Glucose 38-45 insulin Homo sapiens 130-137 3529983-5 1986 Although only 17% of the variation in glucose tolerance could be explained by a change in the sensitivity of glucose transport to insulin, the data suggests that a postinsulin-binding defect in the coupling of insulin binding to glucose transport may be an early step in the development of insulin resistance in human adipocytes. Glucose 109-116 insulin Homo sapiens 130-137 3529983-5 1986 Although only 17% of the variation in glucose tolerance could be explained by a change in the sensitivity of glucose transport to insulin, the data suggests that a postinsulin-binding defect in the coupling of insulin binding to glucose transport may be an early step in the development of insulin resistance in human adipocytes. Glucose 109-116 insulin Homo sapiens 168-175 3529984-2 1986 Insulin concentrations were sequentially raised from 8 +/- 1 to 43 +/- 6 and 101 +/- 14 and to 1,487 +/- 190 microU/ml, while maintaining euglycemia with adequate glucose infusions. Glucose 163-170 insulin Homo sapiens 0-7 3527825-8 1986 Glucose-stimulated insulin release from perifused islets was markedly depressed in CyA-treated islets. Glucose 0-7 insulin Homo sapiens 19-26 2876895-4 1986 The AMI patients were continuously hyperglycaemic, but their relative insulin response i.e. plasma glucose/insulin ratio was identical to that of non-AMI patients. Glucose 99-106 insulin Homo sapiens 70-77 3527748-0 1986 Insulin stimulation of glucose uptake and the transmembrane potential of muscle cells in culture. Glucose 23-30 insulin Homo sapiens 0-7 2946637-4 1986 Hepatic glucose production decreased in diabetic subjects during hyperinsulinemia (insulin infusion of 20 mU/m2 X min; plasma free insulin levels of 40 +/- 4 mU/l) from 2.9 +/- 0.6 mg/kg min to 0.2 +/- 0.1 mg/kg X min after 120 min, and plasma free fatty acid (FFA) concentrations decreased from 1.33 +/- 0.29 to 0.38 +/- 0.08 mmol/l. Glucose 8-15 insulin Homo sapiens 70-77 2946637-4 1986 Hepatic glucose production decreased in diabetic subjects during hyperinsulinemia (insulin infusion of 20 mU/m2 X min; plasma free insulin levels of 40 +/- 4 mU/l) from 2.9 +/- 0.6 mg/kg min to 0.2 +/- 0.1 mg/kg X min after 120 min, and plasma free fatty acid (FFA) concentrations decreased from 1.33 +/- 0.29 to 0.38 +/- 0.08 mmol/l. Glucose 8-15 insulin Homo sapiens 83-90 2946637-6 1986 Compared to 8 non-diabetic subjects, type 1-diabetics demonstrated a diminished effect of hyperinsulinemia on peripheral glucose clearance (2.4 +/- 0.04 vs 4.2 +/- 0.5 ml/kg X min, P less than 0.01), whereas hepatic glucose production and plasma FFA levels were similarly suppressed by insulin. Glucose 121-128 insulin Homo sapiens 95-102 2946637-7 1986 The data indicate that sulfonylurea treatment did not improve the diminished insulin sensitivity of peripheral glucose clearance in type 1-diabetic subjects; insulin action on hepatic glucose production and lipolysis was unimpaired in diabetics and remained uninfluenced by glibornuride. Glucose 184-191 insulin Homo sapiens 158-165 3527961-2 1986 To evaluate possible risk factors, we compared blood pressures and plasma glucose and insulin responses to orally administered glucose in 19 above-knee amputees from the Vietnam War (mean age, 36 +/- 1 years) with those of 12 age-matched unilateral below-elbow amputees. Glucose 127-134 insulin Homo sapiens 86-93 2874153-6 1986 The glucose infusion rate required to maintain the glucose clamp with basal insulin levels was 1.08 +/- 0.20 and 2.67 +/- 0.39 mg/kg X min at glucose concentrations of 146 +/- 1 and 202 +/- 1 mg/dl, respectively. Glucose 4-11 insulin Homo sapiens 76-83 2874153-6 1986 The glucose infusion rate required to maintain the glucose clamp with basal insulin levels was 1.08 +/- 0.20 and 2.67 +/- 0.39 mg/kg X min at glucose concentrations of 146 +/- 1 and 202 +/- 1 mg/dl, respectively. Glucose 51-58 insulin Homo sapiens 76-83 2874153-6 1986 The glucose infusion rate required to maintain the glucose clamp with basal insulin levels was 1.08 +/- 0.20 and 2.67 +/- 0.39 mg/kg X min at glucose concentrations of 146 +/- 1 and 202 +/- 1 mg/dl, respectively. Glucose 51-58 insulin Homo sapiens 76-83 2875083-0 1986 Role of insulin and glucagon in the response of glucose and alanine kinetics in burn-injured patients. Glucose 48-55 insulin Homo sapiens 8-15 2875083-1 1986 We investigated the roles of insulin and glucagon as mediators of changes in glucose and alanine kinetics during the hypermetabolic response to injury in 10 burn patients by infusing somatostatin with and without insulin replacement. Glucose 77-84 insulin Homo sapiens 29-36 2875083-8 1986 In severely burned patients hyperglucagonemia stimulates increased glucose production, basal insulin suppression glucose production, stimulates basal glucose clearance, and is important for regulation of plasma amino acid concentrations, and the selective lowering of glucagon while maintaining basal insulin constant normalized glucose kinetics. Glucose 113-120 insulin Homo sapiens 93-100 2875083-8 1986 In severely burned patients hyperglucagonemia stimulates increased glucose production, basal insulin suppression glucose production, stimulates basal glucose clearance, and is important for regulation of plasma amino acid concentrations, and the selective lowering of glucagon while maintaining basal insulin constant normalized glucose kinetics. Glucose 113-120 insulin Homo sapiens 93-100 3525600-2 1986 The results suggested that the ambient level of plasma glucose might be an important factor in determining the pharmacokinetics of regular insulin. Glucose 55-62 insulin Homo sapiens 139-146 3525600-5 1986 The onset of insulin action occurred at similar times at both glucose concentrations (0.6 +/- 0.1 h at 276 mg/dl vs. 0.5 +/- 0.1 h at 130 mg/dl; P greater than 0.05). Glucose 62-69 insulin Homo sapiens 13-20 3525600-6 1986 Peak insulin action (determined from the time of the maximal glucose infusion rate) was delayed in the studies done at 276 mg/dl (4.7 +/- 0.2 h) compared to that in studies done at mean glucose concentrations of 130 mg/dl (4.3 +/- 0.2 h; P less than 0.05). Glucose 61-68 insulin Homo sapiens 5-12 3525600-6 1986 Peak insulin action (determined from the time of the maximal glucose infusion rate) was delayed in the studies done at 276 mg/dl (4.7 +/- 0.2 h) compared to that in studies done at mean glucose concentrations of 130 mg/dl (4.3 +/- 0.2 h; P less than 0.05). Glucose 186-193 insulin Homo sapiens 5-12 3525600-7 1986 The duration of insulin action was also significantly prolonged in the studies done at the higher glucose concentrations (9.1 +/- 0.3 h at 276 mg/dl vs. 7.7 +/- 0.2 h at 130 mg/dl; P less than 0.01). Glucose 98-105 insulin Homo sapiens 16-23 3537183-1 1986 Basal and insulin-stimulated neutral glyceride syntheses from glucose were studied in fat cells of different size (fat cell volume, 0.07-0.20, 0.20-0.60, 0.60-1.00, 1.00-1.50 micron3 X 10(6)) obtained from subcutaneous adipose tissues in 20 subjects aged 3 months to 67 years. Glucose 62-69 insulin Homo sapiens 10-17 3537183-4 1986 The stimulating effect of insulin on conversion of glucose to neutral glyceride was not significantly different from the basal rate in fat cells of each size taken from the mature subjects, whereas in fat cells from growing subjects, it was significantly different from the basal rate in each fat cell size category. Glucose 51-58 insulin Homo sapiens 26-33 3528745-1 1986 Smoking increases counterregulatory hormone secretion and reduces capillary flow, both of which could reduce insulin mediated glucose disposal. Glucose 126-133 insulin Homo sapiens 109-116 3528745-2 1986 To evaluate whether smoking has any effect on body sensitivity to insulin, we measured insulin-mediated glucose disposal (1 mU euglycemic insulin clamp) during acute smoking in seven male type I diabetic patients. Glucose 104-111 insulin Homo sapiens 87-94 3528745-2 1986 To evaluate whether smoking has any effect on body sensitivity to insulin, we measured insulin-mediated glucose disposal (1 mU euglycemic insulin clamp) during acute smoking in seven male type I diabetic patients. Glucose 104-111 insulin Homo sapiens 87-94 3528745-7 1986 During acute smoking the rate of insulin-mediated glucose uptake (7.3 +/- 1.0 mg/kg/min) was not significantly different from that without cigarettes (6.8 +/- 0.7 mg/kg/min). Glucose 50-57 insulin Homo sapiens 33-40 3537754-0 1986 Plasma insulin response to oral glucose in alcoholics with and without exocrine pancreatic hypersecretion. Glucose 32-39 insulin Homo sapiens 7-14 3737060-1 1986 Insulin-dependent diabetic women without adequate glucose control have a higher spontaneous abortion rate when compared with the general population. Glucose 50-57 insulin Homo sapiens 0-7 3534980-1 1986 The intravenous insulin tolerance test (ITT) allows general assessment of insulin sensitivity by determining the fall in plasma glucose after injection of 0.1 unit/kg regular insulin. Glucose 128-135 insulin Homo sapiens 16-23 3534980-1 1986 The intravenous insulin tolerance test (ITT) allows general assessment of insulin sensitivity by determining the fall in plasma glucose after injection of 0.1 unit/kg regular insulin. Glucose 128-135 insulin Homo sapiens 74-81 3534980-1 1986 The intravenous insulin tolerance test (ITT) allows general assessment of insulin sensitivity by determining the fall in plasma glucose after injection of 0.1 unit/kg regular insulin. Glucose 128-135 insulin Homo sapiens 74-81 3541473-2 1986 Hyperinsulinemia revealed during intravenous glucose tolerance test and reduced glucose tolerance are evidence of relative insular insufficiency and substantiate pathogenetically the inclusion of insulin in the complex of intensive therapy applied in the early postoperative treatment of patients with tumors located in the sellar-diencephalic area. Glucose 45-52 insulin Homo sapiens 5-12 3026341-0 1986 Antagonistic regulation of the glucose/glucose 6-phosphate cycle by insulin and glucagon in cultured hepatocytes. Glucose 31-38 insulin Homo sapiens 68-75 3026341-4 1986 At constant 5 mM-glucose and 2 mM-lactate concentrations insulin increased glucokinase flux by 35%; it decreased glucose-6-phosphatase flux from glycogen by 50%, from lactate by 15% and reverse flux from external glucose by 65%, i.e. overall by 40%. Glucose 17-24 insulin Homo sapiens 57-64 3026341-4 1986 At constant 5 mM-glucose and 2 mM-lactate concentrations insulin increased glucokinase flux by 35%; it decreased glucose-6-phosphatase flux from glycogen by 50%, from lactate by 15% and reverse flux from external glucose by 65%, i.e. overall by 40%. Glucose 113-120 insulin Homo sapiens 57-64 3026341-7 1986 In conclusion, under basic conditions without added hormones the glucose/glucose 6-phosphate cycle showed only a minor net glucose uptake, of 0.03 mumol/min per g of hepatocytes; this flux was increased by insulin to a net glucose uptake of 0.21 mumol/min per g and reversed by glucagon to a net glucose release of 0.22 mumol/min per g. Since the glucose 6-phosphate concentrations after hormone treatment did not correlate with the glucose-6-phosphatase flux, it is suggested that the hormones influenced the enzyme activity directly. Glucose 65-72 insulin Homo sapiens 206-213 3026341-7 1986 In conclusion, under basic conditions without added hormones the glucose/glucose 6-phosphate cycle showed only a minor net glucose uptake, of 0.03 mumol/min per g of hepatocytes; this flux was increased by insulin to a net glucose uptake of 0.21 mumol/min per g and reversed by glucagon to a net glucose release of 0.22 mumol/min per g. Since the glucose 6-phosphate concentrations after hormone treatment did not correlate with the glucose-6-phosphatase flux, it is suggested that the hormones influenced the enzyme activity directly. Glucose 73-80 insulin Homo sapiens 206-213 3026341-7 1986 In conclusion, under basic conditions without added hormones the glucose/glucose 6-phosphate cycle showed only a minor net glucose uptake, of 0.03 mumol/min per g of hepatocytes; this flux was increased by insulin to a net glucose uptake of 0.21 mumol/min per g and reversed by glucagon to a net glucose release of 0.22 mumol/min per g. Since the glucose 6-phosphate concentrations after hormone treatment did not correlate with the glucose-6-phosphatase flux, it is suggested that the hormones influenced the enzyme activity directly. Glucose 73-80 insulin Homo sapiens 206-213 3026341-7 1986 In conclusion, under basic conditions without added hormones the glucose/glucose 6-phosphate cycle showed only a minor net glucose uptake, of 0.03 mumol/min per g of hepatocytes; this flux was increased by insulin to a net glucose uptake of 0.21 mumol/min per g and reversed by glucagon to a net glucose release of 0.22 mumol/min per g. Since the glucose 6-phosphate concentrations after hormone treatment did not correlate with the glucose-6-phosphatase flux, it is suggested that the hormones influenced the enzyme activity directly. Glucose 73-80 insulin Homo sapiens 206-213 3526918-10 1986 Furthermore, it appears that splanchnic glucose output responds earlier to proinsulin exposure than suppression of C-peptide release or stimulation of peripheral glucose utilization. Glucose 40-47 insulin Homo sapiens 75-85 3089579-1 1986 The effect of insulin on glucose metabolism through different pathways and the glucose transporters in Harding-Passey melanoma cells have been studied. Glucose 25-32 insulin Homo sapiens 14-21 3089579-6 1986 The number of high affinity cytochalasin B binding sites was 175,000 receptors/cell (about 0.6 pmol/mg protein) and Kd = 1 X 10(-7) M. Insulin increased glucose utilization and lactate production by about 70% and caused a 56% increase in transport without alterations in the Kd of the site. Glucose 153-160 insulin Homo sapiens 135-142 3533220-1 1986 Insulin release was examined in human subjects after lingual applications of D-glucose and its anomers. Glucose 77-86 insulin Homo sapiens 0-7 3533220-2 1986 A dose-dependent increase in the insulin release was noted following the application of equilibrated D-glucose consisting of 36% alpha- and 64% beta-anomer. Glucose 101-110 insulin Homo sapiens 33-40 3525287-7 1986 After intravenous glucose stimulation, insulinopenia was present in 70% of ICA and insulin-autoantibody-positive individuals in contrast to only 23% of ICA-positive, insulin-autoantibody-negative persons. Glucose 18-25 insulin Homo sapiens 39-46 3525287-7 1986 After intravenous glucose stimulation, insulinopenia was present in 70% of ICA and insulin-autoantibody-positive individuals in contrast to only 23% of ICA-positive, insulin-autoantibody-negative persons. Glucose 18-25 insulin Homo sapiens 83-90 3525288-0 1986 Efficacy of pulsatile versus continuous insulin administration on hepatic glucose production and glucose utilization in type I diabetic humans. Glucose 74-81 insulin Homo sapiens 40-47 3525288-0 1986 Efficacy of pulsatile versus continuous insulin administration on hepatic glucose production and glucose utilization in type I diabetic humans. Glucose 97-104 insulin Homo sapiens 40-47 3525288-6 1986 Insulin-stimulated glucose utilization was not significantly altered in either study (2.55 +/- 0.27 vs. 2.92 +/- 0.23 mg X kg-1 X min-1). Glucose 19-26 insulin Homo sapiens 0-7 3525288-7 1986 When in further studies the total insulin dose given during the pulsatile study was infused continuously (0.6 mU X kg-1 X min-1), HGP in the basal state and residual HGP during the insulin-clamp study were 25-30% higher than in the pulsatile experiments, whereas glucose utilization was not significantly different. Glucose 263-270 insulin Homo sapiens 34-41 3533668-3 1986 The aim of the present study was to investigate the effect of surgical portosystemic shunt on plasma glucose and insulin responses to glucose administration in a group of cirrhotic patients. Glucose 134-141 insulin Homo sapiens 113-120 16831764-7 1986 The hypoglycemic action of insulin, expressed as % decrement from the pre-test blood glucose level, was unchanged during epidural anaesthesia but reduced during general anaesthesia (22.4 +/- 1.8% pre-operatively vs 7.5 +/- 1.3% intra-operatively, p < 0.01). Glucose 85-92 insulin Homo sapiens 27-34 3093436-7 1986 Glucose infusion elevated plasma concentrations of glucose (P less than .05) and insulin (P less than .07) and reduced (P less than .05) fat and protein mobilization, even though it depressed feed intake (P less than .001), compared with saline infusion. Glucose 0-7 insulin Homo sapiens 81-88 3522617-1 1986 To determine whether the dawn phenomenon occurs in normal elderly subjects and thus contributes to the progressive mild fasting hyperglycemia of aging, we examined the effect of physiological insulin levels on glucose disposal and hepatic glucose production (HGO) between 0530 and 0800 h, and 0930 and 1200 h. Paired euglycemic insulin clamp studies (8 mU/m2 X min) were performed on healthy old subjects (n = 5), employing [3H]glucose methodology to measure glucose production and disposal rates. Glucose 210-217 insulin Homo sapiens 192-199 3522621-0 1986 Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses. Glucose 31-38 insulin Homo sapiens 87-96 3522621-3 1986 Both insulin and C-peptide concentrations as well as calculated integrated insulin secretion rates increased with increasing oral glucose loads. Glucose 130-137 insulin Homo sapiens 5-12 3522621-3 1986 Both insulin and C-peptide concentrations as well as calculated integrated insulin secretion rates increased with increasing oral glucose loads. Glucose 130-137 insulin Homo sapiens 17-26 3522621-3 1986 Both insulin and C-peptide concentrations as well as calculated integrated insulin secretion rates increased with increasing oral glucose loads. Glucose 130-137 insulin Homo sapiens 75-82 3522621-5 1986 The percent contribution of incretin factors to total immunoreactive insulin responses after 25, 50, and 100 g glucose (85.6%, 74.9%, and 93.0%; response to oral load, 100%) was significantly higher than their contribution to integrated C-peptide responses (27.6-62.9%) or calculated integrated insulin secretion rates (19.2-61.0%). Glucose 111-118 insulin Homo sapiens 69-76 3522621-6 1986 These findings indicate that the degree of incretin stimulation of insulin secretion depends on the amount of glucose ingested. Glucose 110-117 insulin Homo sapiens 67-74 3522623-9 1986 Thus, continuous and pulsatile insulin iv infusion, resulting in physiological peripheral plasma insulin levels, altered the glucose turnover parameters equally, in particular inhibiting EGP, which was stimulated by glucagon during the first part of the study, and stimulating peripheral glucose uptake at the end of the study period. Glucose 125-132 insulin Homo sapiens 31-38 3522623-9 1986 Thus, continuous and pulsatile insulin iv infusion, resulting in physiological peripheral plasma insulin levels, altered the glucose turnover parameters equally, in particular inhibiting EGP, which was stimulated by glucagon during the first part of the study, and stimulating peripheral glucose uptake at the end of the study period. Glucose 288-295 insulin Homo sapiens 31-38 3525609-0 1986 In vivo kinetics of insulin action on peripheral glucose disposal and hepatic glucose output in normal and obese subjects. Glucose 49-56 insulin Homo sapiens 20-27 3525609-4 1986 Deactivation of the insulin effect to stimulate glucose disposal rate (Rd) was faster in the obese group compared with normal individuals after all comparable insulin infusions. Glucose 48-55 insulin Homo sapiens 20-27 3531300-1 1986 The effects of insulin in the maternal circulation on the placental clearance of 3-O-methyl glucose were investigated in 7 animals in the presence of a constant maternal glucose concentration. Glucose 92-99 insulin Homo sapiens 15-22 3526084-0 1986 Gastric inhibitory polypeptide and insulin response to increasing doses of oral glucose: dependency on glucose amount and volume of the test drink. Glucose 80-87 insulin Homo sapiens 35-42 3526086-5 1986 Maximal responsiveness to insulin was a glucose utilization rate of 450 +/- 20 mg/min/m2 in normals, unchanged in obese, 42% increased in hyperthyroid, and 34% decreased in Cushing"s syndrome patients. Glucose 40-47 insulin Homo sapiens 26-33 3736412-1 1986 To compare in vivo insulin action in patients with diabetes secondary to pancreatic diseases (n = 9) to that in type I diabetic patients (n = 13) and in normal subjects (n = 8), we measured insulin-mediated glucose disposal by the euglycemic insulin clamp technique. Glucose 207-214 insulin Homo sapiens 190-197 3736412-1 1986 To compare in vivo insulin action in patients with diabetes secondary to pancreatic diseases (n = 9) to that in type I diabetic patients (n = 13) and in normal subjects (n = 8), we measured insulin-mediated glucose disposal by the euglycemic insulin clamp technique. Glucose 207-214 insulin Homo sapiens 190-197 3736412-6 1986 During hyperinsulinemia induced by the clamp, glucose production (measured using 3-3H-glucose infusion) was completely suppressed in both the pancreatogenic diabetic patients and the normal subjects indicating that the impairment of in vivo insulin action was localized to the peripheral tissues. Glucose 46-53 insulin Homo sapiens 12-19 3529363-0 1986 Insulin-mediated glucose metabolism is related to liver structure and microsomal function. Glucose 17-24 insulin Homo sapiens 0-7 3532594-7 1986 The results on liver cirrhosis in connection with studies on glucose metabolism show that under basal conditions insulin insensitivity is due to peripheral resistance (primarily muscle) according to a postreceptor defect. Glucose 61-68 insulin Homo sapiens 113-120 3523245-3 1986 To determine whether puberty is associated with decreased insulin-stimulated glucose metabolism, we compared the results of euglycemic insulin-clamp studies in adults and prepubertal and pubertal children with and without insulin-dependent diabetes. Glucose 77-84 insulin Homo sapiens 58-65 3523245-4 1986 In nondiabetic pubertal children, insulin-stimulated glucose metabolism (201 +/- 12 mg per square meter of body surface area per minute) was sharply reduced, as compared with that of prepubertal children and adults (316 +/- 34 and 290 +/- 21 mg per square meter, respectively; P less than 0.01), despite comparable hyperinsulinemia (insulin levels of 80 to 90 microU per milliliter). Glucose 53-60 insulin Homo sapiens 34-41 3523245-6 1986 At each stage of development, the stimulating effect of insulin on glucose metabolism was decreased by 33 to 42 percent in the children with diabetes (P less than 0.01). Glucose 67-74 insulin Homo sapiens 56-63 3523246-4 1986 Changes in serum insulin concentrations in response to the glucose challenge were quantified by the area under the serum insulin curve. Glucose 59-66 insulin Homo sapiens 17-24 3523246-4 1986 Changes in serum insulin concentrations in response to the glucose challenge were quantified by the area under the serum insulin curve. Glucose 59-66 insulin Homo sapiens 121-128 3523247-2 1986 Two weeks after diagnosis, the rate of glucose uptake during hyperinsulinemia, a measure of insulin action, was 32 percent lower in the patients with diabetes than in 30 matched normal subjects (P less than 0.01), but it rose to normal during the subsequent three months. Glucose 39-46 insulin Homo sapiens 66-73 3529781-3 1986 The response to oral glucose in the diabetic patients was measured during maintenance of similar peripheral plasma free insulin levels as in the normal subjects during the oral glucose tolerance test (OGTT). Glucose 21-28 insulin Homo sapiens 120-127 3530002-0 1986 Plasma insulin response to oral glucose load in Meniere"s disease. Glucose 32-39 insulin Homo sapiens 7-14 3728554-4 1986 All the patients had elevated insulin levels in the fasting state and in response to an oral glucose load. Glucose 93-100 insulin Homo sapiens 30-37 3728554-5 1986 The mechanism for the resistance to insulin was a post-receptor binding defect or a structural abnormality in circulating insulin, since glucose tolerance and plasma cortisol, somatomedin, growth hormone, and insulin receptor concentrations in peripheral monocytes were all normal. Glucose 137-144 insulin Homo sapiens 122-129 3527260-2 1986 Thus, we employed such compounds as potential inhibitors of the insulin-dependent activation of glucose transport in fat cells. Glucose 96-103 insulin Homo sapiens 64-71 3527260-4 1986 We find that synthetic dipeptides which are metalloendoprotease substrates rapidly and reversibly inhibit insulin-activated glucose oxidation in a dose-dependent manner but exhibit essentially no effect on basal levels. Glucose 124-131 insulin Homo sapiens 106-113 3527260-6 1986 That is, the dipeptide substrates inhibit insulin-activated glucose uptake to a greater extent than basal transport, and they do so even when vesicle translocation and fusion have already taken place as in ATP-depleted cells and isolated vesicles. Glucose 60-67 insulin Homo sapiens 42-49 3017797-7 1986 Glucose production was completely inhibited by the low insulin level during placebo infusion. Glucose 0-7 insulin Homo sapiens 55-62 3017797-10 1986 Glucose utilization increased from 2.53 +/- 0.17 to 7.28 +/- 0.88 mg X kg-1 X min-1 during placebo when the insulin levels were increased from 4 +/- 0.3 to 51 +/- 3 mU/l. Glucose 0-7 insulin Homo sapiens 108-115 3017797-11 1986 Increasing the insulin levels 150-fold to approximately 7500 mU/l only doubled the glucose utilization (14.68 +/- 1.14 mg X kg-1 X min-1). Glucose 83-90 insulin Homo sapiens 15-22 3017797-12 1986 Adrenaline induced a pronounced inhibition of glucose utilization at both insulin levels (78% and 37% inhibition respectively). Glucose 46-53 insulin Homo sapiens 74-81 3017797-15 1986 The inhibitory effect on glucose uptake is maintained even at high insulin levels when hepatic glucose production is completely abolished. Glucose 25-32 insulin Homo sapiens 67-74 3017797-15 1986 The inhibitory effect on glucose uptake is maintained even at high insulin levels when hepatic glucose production is completely abolished. Glucose 95-102 insulin Homo sapiens 67-74 3093130-1 1986 Previous observations indicate that substantial amounts of insulin are degraded intracellularly in isolated pancreatic islets exposed to low or physiological glucose concentrations. Glucose 158-165 insulin Homo sapiens 59-66 3093130-3 1986 The aim of the present investigation was to elucidate the role of glucose both in the intracellular insulin degradation and in the lysosomal changes associated with crinophagy in the pancreatic islets. Glucose 66-73 insulin Homo sapiens 100-107 3093130-11 1986 Furthermore, it is suggested that glucose does not interfere directly with crinophagy but rather affects intracellular degradation of insulin in the pancreatic B cells by changing retention of secretory material. Glucose 34-41 insulin Homo sapiens 134-141 3522315-4 1986 During infusion of insulin with the Biostator, plasma free insulin decreased 40% (from 14 +/- 1 to 9 +/- 1 microU/ml, P less than .01), insulin clearance increased 54% (from 11 +/- 1 to 17 +/- 2 ml/min, P less than .05), and plasma glucose increased from 101 +/- 4 to 217 +/- 27 mg/dl, P less than .01. Glucose 232-239 insulin Homo sapiens 19-26 3522315-6 1986 The increases in plasma glucose during infusion of insulin with the Biostator and the Harvard pump were not significantly different (t = 1.44, P = .19). Glucose 24-31 insulin Homo sapiens 51-58 3530592-11 1986 On the contrary, the terbutaline-induced increment in blood glucose concentration was inhibited by glipizide and the glucose elimination rate after glucose injection was slightly enhanced by glipizide; effects explained by the higher plasma insulin levels. Glucose 117-124 insulin Homo sapiens 241-248 3530592-11 1986 On the contrary, the terbutaline-induced increment in blood glucose concentration was inhibited by glipizide and the glucose elimination rate after glucose injection was slightly enhanced by glipizide; effects explained by the higher plasma insulin levels. Glucose 117-124 insulin Homo sapiens 241-248 3530594-1 1986 The blood glucose response to a brief infusion of insulin (0.012 U/kg body wt) was studied in the initial phase of Type 1 diabetes in 21 children and in 20 healthy controls. Glucose 10-17 insulin Homo sapiens 50-57 3530594-5 1986 Further evidence for a relationship between the insulin sensitivity and the severity of the diabetic state was found in the correlation between the percentual blood glucose decrement and the fasting blood glucose (r = -0.79, p less than 0.01), the glucose assimilation rate (r = 0.71, p less than 0.01), as well as the blood glucose level at 120 min during the OGTT (r = -0.76, p less than 0.01). Glucose 165-172 insulin Homo sapiens 48-55 3530594-5 1986 Further evidence for a relationship between the insulin sensitivity and the severity of the diabetic state was found in the correlation between the percentual blood glucose decrement and the fasting blood glucose (r = -0.79, p less than 0.01), the glucose assimilation rate (r = 0.71, p less than 0.01), as well as the blood glucose level at 120 min during the OGTT (r = -0.76, p less than 0.01). Glucose 205-212 insulin Homo sapiens 48-55 3530594-5 1986 Further evidence for a relationship between the insulin sensitivity and the severity of the diabetic state was found in the correlation between the percentual blood glucose decrement and the fasting blood glucose (r = -0.79, p less than 0.01), the glucose assimilation rate (r = 0.71, p less than 0.01), as well as the blood glucose level at 120 min during the OGTT (r = -0.76, p less than 0.01). Glucose 205-212 insulin Homo sapiens 48-55 3530594-5 1986 Further evidence for a relationship between the insulin sensitivity and the severity of the diabetic state was found in the correlation between the percentual blood glucose decrement and the fasting blood glucose (r = -0.79, p less than 0.01), the glucose assimilation rate (r = 0.71, p less than 0.01), as well as the blood glucose level at 120 min during the OGTT (r = -0.76, p less than 0.01). Glucose 205-212 insulin Homo sapiens 48-55 3527928-0 1986 Fasting and feeding variations of insulin requirements and insulin binding to erythrocytes at different times of the day in insulin dependent diabetics--assessed under the condition of glucose-controlled insulin infusion. Glucose 185-192 insulin Homo sapiens 59-66 3527928-0 1986 Fasting and feeding variations of insulin requirements and insulin binding to erythrocytes at different times of the day in insulin dependent diabetics--assessed under the condition of glucose-controlled insulin infusion. Glucose 185-192 insulin Homo sapiens 59-66 3527928-0 1986 Fasting and feeding variations of insulin requirements and insulin binding to erythrocytes at different times of the day in insulin dependent diabetics--assessed under the condition of glucose-controlled insulin infusion. Glucose 185-192 insulin Homo sapiens 59-66 3527928-4 1986 Following an equilibrating phase of 14 hours after the connection to the glucose-controlled insulin infusion system the blood samples were taken at 0800, 1200 and 1800. Glucose 73-80 insulin Homo sapiens 92-99 3525429-2 1986 Administration of glucose significantly increased circulating blood glucose and serum insulin concentrations before the salbutamol injection. Glucose 18-25 insulin Homo sapiens 86-93 3519649-4 1986 However, glucose disposal rates correlated inversely with disease severity in the ALS patients, at both the low (r = -0.76; P less than 0.01) and high (r = -0.83; P less than 0.001) insulin infusion rates. Glucose 9-16 insulin Homo sapiens 182-189 3519650-0 1986 Glucoregulatory function of thyroid hormones: interaction with insulin depends on the prevailing glucose concentration. Glucose 97-104 insulin Homo sapiens 63-70 3519651-0 1986 Effects of ketone bodies on basal and insulin-stimulated glucose utilization in man. Glucose 57-64 insulin Homo sapiens 38-45 3519651-1 1986 Using the euglycemic clamp technique, we investigated the effects of high ketone body levels on basal and insulin-stimulated glucose utilization in normal subjects. Glucose 125-132 insulin Homo sapiens 106-113 3519651-8 1986 During control euglycemic hyperinsulinemic clamps (1 and 10 mU kg-1 min-1 insulin infusion), endogenous glucose production was suppressed at the lowest insulin infusion rate; glucose utilization increased first to 7.32 +/- 0.96 mg kg-1 min-1 and then to 16.5 +/- 1.27 mg kg-1 min-1. Glucose 104-111 insulin Homo sapiens 74-81 3531757-4 1986 With the needle, more effective insulin action to compensate glucose content is achieved as compared to the conventional design. Glucose 61-68 insulin Homo sapiens 32-39 3542449-9 1986 There was a significant inverse correlation between blood glucose and serum free-insulin levels in the early morning (r = - .60, P less than .01). Glucose 58-65 insulin Homo sapiens 81-88 3542456-9 1986 Although the diet consumed by each subject on the 2nd study day was identical to that of the 1st day, the mean glucose increase was greater after needle-injected insulin than after jet-spray injection. Glucose 111-118 insulin Homo sapiens 162-169 3542456-10 1986 This indicates that the greater amount of free insulin observed after jet-injected insulin had a direct effect in lowering the plasma glucose. Glucose 134-141 insulin Homo sapiens 47-54 3542456-10 1986 This indicates that the greater amount of free insulin observed after jet-injected insulin had a direct effect in lowering the plasma glucose. Glucose 134-141 insulin Homo sapiens 83-90 3545725-3 1986 The purpose of our study was to investigate the effect of premixing lente and soluble insulin of U100 strength on plasma insulin levels and glucose requirements during glucose clamping for 8 h in eight healthy volunteers. Glucose 140-147 insulin Homo sapiens 86-93 3091936-2 1986 The ability of transplanted islets to restore normoglycemia in recipients was not affected by tissue contamination, but the insulin response to glucose challenge 12 weeks after transplantation was negatively correlated with the amylase content of this additional tissue transplant. Glucose 144-151 insulin Homo sapiens 124-131 3544159-4 1986 Insulin-dependent glucose disposal was impaired at different levels of alcoholemia, probably through an impairment of the glycolytic pathway. Glucose 18-25 insulin Homo sapiens 0-7 3521312-1 1986 Stepwise glucose clamps were used to study beta-cell insulin response to glucose in normal and noninsulin-dependent diabetic subjects and to study changes in response after hyperglycemia. Glucose 73-80 insulin Homo sapiens 53-60 3526785-2 1986 Already in week 10, fasting plasma glucose was decreased and the glucose-induced insulin secretion increased as compared with post partum. Glucose 65-72 insulin Homo sapiens 81-88 3526785-4 1986 In week 32, glucose tolerance had deteriorated, although the levels of both fasting and glucose-induced insulin were higher than those found in early pregnancy and post partum. Glucose 88-95 insulin Homo sapiens 104-111 3526785-7 1986 Pregnancy has, however, at this very early stage already affected glucose homeostasis as seen by the decrease in fasting plasma glucose and the increase in the insulin response to glucose. Glucose 66-73 insulin Homo sapiens 160-167 3521312-2 1986 In normal subjects, insulin increment, delta I, correlated with glucose increment above basal, delta G, during the first 6 min of hyperglycemia, r = 0.748, P less than 0.0001. Glucose 64-71 insulin Homo sapiens 20-27 3087153-6 1986 In this study, we found a positive correlation between TEI and insulin-stimulated rates of glucose disposal (r = 0.91, p less than 0.001). Glucose 91-98 insulin Homo sapiens 63-70 3521319-3 1986 During the 4 h after glucose ingestion the plasma insulin concentration increased by 33 +/- 4 microU/ml and this was associated with a significant increase in carbohydrate oxidation and decrement in lipid oxidation. Glucose 21-28 insulin Homo sapiens 50-57 3089815-4 1986 The whole body glucose metabolic rate was decreased to about half control values (21 mumol min-1 kg-1, range 6-28) and the insulin sensitivity of the glucose metabolism was decreased to about 15% (9.4 m3 min-1 kg-1, range 3.6-14.4). Glucose 150-157 insulin Homo sapiens 123-130 3730047-1 1986 We determined the insulin response to an oral glucose ingestion and levels of serum lipoproteins in 25 untreated patients with type 2 diabetes mellitus, in 26 subjects with impaired glucose tolerance (IGT), and in 35 non-diabetic control subjects. Glucose 46-53 insulin Homo sapiens 18-25 3517032-4 1986 The mean insulin response to glucose was twice as high in the hypertensive patients (25.8 +/- 0.2 mU/ml X 2 h) as in the normotensive subjects (11.3 +/- 0.2; P less than 0.001), yet the glucose incremental area was 3-fold higher in the former (10.9 +/- 1.0 g/dl X 2 h) than in the latter (3.5 +/- 0.7; P less than 0.001), thus indicating more severe insulin resistance. Glucose 29-36 insulin Homo sapiens 9-16 3522195-3 1986 The insulin response was assessed as the ratio of the increase in plasma insulin concentration to the increase in blood glucose concentration at 30 min. Glucose 120-127 insulin Homo sapiens 4-11 3522195-4 1986 There was a small insulin response to glucose on day 1 in the premature infants and this increased slowly over the remainder of the study period regardless of the route of administration of glucose or of the mode of nutrition. Glucose 38-45 insulin Homo sapiens 18-25 3522195-4 1986 There was a small insulin response to glucose on day 1 in the premature infants and this increased slowly over the remainder of the study period regardless of the route of administration of glucose or of the mode of nutrition. Glucose 190-197 insulin Homo sapiens 18-25 3525269-0 1986 Insulin and C-peptide responses to 75 g oral glucose load in the healthy man. Glucose 45-52 insulin Homo sapiens 0-7 3525269-0 1986 Insulin and C-peptide responses to 75 g oral glucose load in the healthy man. Glucose 45-52 insulin Homo sapiens 12-21 3525269-6 1986 After glucose ingestion, both insulin and C-peptide plasma levels correlated significantly with the corresponding glucose levels. Glucose 6-13 insulin Homo sapiens 30-37 3525269-6 1986 After glucose ingestion, both insulin and C-peptide plasma levels correlated significantly with the corresponding glucose levels. Glucose 6-13 insulin Homo sapiens 42-51 3525269-6 1986 After glucose ingestion, both insulin and C-peptide plasma levels correlated significantly with the corresponding glucose levels. Glucose 114-121 insulin Homo sapiens 30-37 3525269-6 1986 After glucose ingestion, both insulin and C-peptide plasma levels correlated significantly with the corresponding glucose levels. Glucose 114-121 insulin Homo sapiens 42-51 3525269-7 1986 During fasting, C-peptide but no insulin level correlated to glucose level. Glucose 61-68 insulin Homo sapiens 16-25 3517028-0 1986 Effect of differences in glucose tolerance on insulin"s ability to regulate carbohydrate and free fatty acid metabolism in obese individuals. Glucose 25-32 insulin Homo sapiens 46-53 3517028-1 1986 The effect of variations in glucose tolerance on insulin"s ability to regulate glucose uptake and plasma glucose and FFA concentrations was assessed in 22 obese individuals [8 with normal glucose tolerance, 7 with impaired glucose tolerance (IGT), and 7 with noninsulin-dependent diabetes mellitus (NIDDM)]. Glucose 28-35 insulin Homo sapiens 49-56 3517028-1 1986 The effect of variations in glucose tolerance on insulin"s ability to regulate glucose uptake and plasma glucose and FFA concentrations was assessed in 22 obese individuals [8 with normal glucose tolerance, 7 with impaired glucose tolerance (IGT), and 7 with noninsulin-dependent diabetes mellitus (NIDDM)]. Glucose 79-86 insulin Homo sapiens 49-56 3517028-1 1986 The effect of variations in glucose tolerance on insulin"s ability to regulate glucose uptake and plasma glucose and FFA concentrations was assessed in 22 obese individuals [8 with normal glucose tolerance, 7 with impaired glucose tolerance (IGT), and 7 with noninsulin-dependent diabetes mellitus (NIDDM)]. Glucose 79-86 insulin Homo sapiens 49-56 3517028-1 1986 The effect of variations in glucose tolerance on insulin"s ability to regulate glucose uptake and plasma glucose and FFA concentrations was assessed in 22 obese individuals [8 with normal glucose tolerance, 7 with impaired glucose tolerance (IGT), and 7 with noninsulin-dependent diabetes mellitus (NIDDM)]. Glucose 79-86 insulin Homo sapiens 49-56 3517028-2 1986 Patients with IGT had ambient insulin levels that were higher than normal, associated with elevated postprandial glucose levels and a marked reduction in insulin-stimulated glucose uptake. Glucose 173-180 insulin Homo sapiens 30-37 3517028-2 1986 Patients with IGT had ambient insulin levels that were higher than normal, associated with elevated postprandial glucose levels and a marked reduction in insulin-stimulated glucose uptake. Glucose 173-180 insulin Homo sapiens 154-161 3517028-5 1986 Hyperinsulinemia in patients with NIDDM was associated with a significant decline in insulin-stimulated glucose uptake as well as with significant increases in both ambient plasma glucose and FFA concentrations. Glucose 104-111 insulin Homo sapiens 5-12 3517028-5 1986 Hyperinsulinemia in patients with NIDDM was associated with a significant decline in insulin-stimulated glucose uptake as well as with significant increases in both ambient plasma glucose and FFA concentrations. Glucose 180-187 insulin Homo sapiens 5-12 3517028-7 1986 These data indicate that insulin resistance in obese individuals varies as a function of degree of glucose tolerance, and insulin resistance in patients with NIDDM involves defects in the regulation of both plasma glucose and FFA metabolism. Glucose 99-106 insulin Homo sapiens 25-32 3517028-7 1986 These data indicate that insulin resistance in obese individuals varies as a function of degree of glucose tolerance, and insulin resistance in patients with NIDDM involves defects in the regulation of both plasma glucose and FFA metabolism. Glucose 214-221 insulin Homo sapiens 122-129 3527520-0 1986 The importance of diabetes heredity in lean subjects on insulin secretion, blood lipids and oxygen uptake in the pathogenesis of glucose intolerance. Glucose 129-136 insulin Homo sapiens 56-63 3527520-4 1986 IGT individuals showed an impaired insulin response to glucose with significantly lower absolute values of insulin and C-peptide during the early phase of the oral glucose tolerance test (OGTT) than in non-hereditary normoglycemic subjects, but not significantly lower than in the hereditary group. Glucose 55-62 insulin Homo sapiens 35-42 3527520-4 1986 IGT individuals showed an impaired insulin response to glucose with significantly lower absolute values of insulin and C-peptide during the early phase of the oral glucose tolerance test (OGTT) than in non-hereditary normoglycemic subjects, but not significantly lower than in the hereditary group. Glucose 55-62 insulin Homo sapiens 119-128 3527520-4 1986 IGT individuals showed an impaired insulin response to glucose with significantly lower absolute values of insulin and C-peptide during the early phase of the oral glucose tolerance test (OGTT) than in non-hereditary normoglycemic subjects, but not significantly lower than in the hereditary group. Glucose 164-171 insulin Homo sapiens 35-42 3527520-5 1986 Similarly, at most time points of the OGTT the ratios of insulin and C-peptide to glucose were significantly lower in the IGT group than in the non-hereditary group, while these differences were less pronounced in comparison with the hereditary group. Glucose 82-89 insulin Homo sapiens 69-78 3527522-3 1986 Fasting plasma glucose levels were controlled by simply adjusting the rate of exogenous insulin delivery when the observed level was outside the range of 100-120 mg/dl. Glucose 15-22 insulin Homo sapiens 88-95 3527523-5 1986 Patients with poor overnight metabolic control and raised fasting blood glucose concentrations may benefit from human ultralente insulin, used as part of their twice-daily insulin regimen. Glucose 72-79 insulin Homo sapiens 129-136 3525363-4 1986 These results suggest that decrease of glucose tolerance is secondary to peripheral insulin resistance. Glucose 39-46 insulin Homo sapiens 84-91 3525363-7 1986 The results of the euglycaemic glucose clamp confirmed the insulin resistance especially for the highest insulin infusion rates. Glucose 31-38 insulin Homo sapiens 59-66 3525363-7 1986 The results of the euglycaemic glucose clamp confirmed the insulin resistance especially for the highest insulin infusion rates. Glucose 31-38 insulin Homo sapiens 105-112 2872232-11 1986 It is concluded that a large proportion of the thermic response to glucose/insulin infusions is due to glucose metabolism alone. Glucose 67-74 insulin Homo sapiens 75-82 2872232-11 1986 It is concluded that a large proportion of the thermic response to glucose/insulin infusions is due to glucose metabolism alone. Glucose 103-110 insulin Homo sapiens 75-82 3517029-0 1986 Type I diabetes is characterized by insulin resistance not only with regard to glucose, but also to lipid and amino acid metabolism. Glucose 79-86 insulin Homo sapiens 36-43 3517032-4 1986 The mean insulin response to glucose was twice as high in the hypertensive patients (25.8 +/- 0.2 mU/ml X 2 h) as in the normotensive subjects (11.3 +/- 0.2; P less than 0.001), yet the glucose incremental area was 3-fold higher in the former (10.9 +/- 1.0 g/dl X 2 h) than in the latter (3.5 +/- 0.7; P less than 0.001), thus indicating more severe insulin resistance. Glucose 29-36 insulin Homo sapiens 350-357 3517032-4 1986 The mean insulin response to glucose was twice as high in the hypertensive patients (25.8 +/- 0.2 mU/ml X 2 h) as in the normotensive subjects (11.3 +/- 0.2; P less than 0.001), yet the glucose incremental area was 3-fold higher in the former (10.9 +/- 1.0 g/dl X 2 h) than in the latter (3.5 +/- 0.7; P less than 0.001), thus indicating more severe insulin resistance. Glucose 186-193 insulin Homo sapiens 9-16 3526480-3 1986 Significant lipogenic or lipolytic hormonal effects upon lactate metabolism were observed only in the presence of glucose, as insulin primarily increased lactate conversion to fatty acids while epinephrine promoted lactate oxidation. Glucose 114-121 insulin Homo sapiens 126-133 3519679-1 1986 Evidence for insulin resistance involving glucose and amino acid metabolism. Glucose 42-49 insulin Homo sapiens 13-20 3519679-7 1986 Glucose disposal was reduced at all insulin levels in the patients. Glucose 0-7 insulin Homo sapiens 36-43 3519679-10 1986 We conclude that in type 1 diabetes a resistance to the metabolic effects of insulin on both glucose and amino acid metabolism is present. Glucose 93-100 insulin Homo sapiens 77-84 3519685-4 1986 The insulin resistance of aging is therefore due to a reduction in the capacity of the glucose uptake system, while the affinity of glucose utilization (EC50 and Km) is unchanged. Glucose 87-94 insulin Homo sapiens 4-11 3520212-8 1986 We conclude that the beta adrenergic nervous system and, specifically, the beta-1 receptor mediates the thermogenic response to glucose/insulin infusion. Glucose 128-135 insulin Homo sapiens 136-143 3529502-8 1986 Cellobiose and lactose, which have a beta(1-4) linkage to glucose molecule at the reducing end, inhibited insulin release stimulated by D-glucose. Glucose 136-145 insulin Homo sapiens 106-113 3529502-2 1986 Insulin release from the isolated islets was 26.2 microU/5 islets/hr in carbohydrate-free medium and increased by the addition of D-glucose or D-mannose. Glucose 130-139 insulin Homo sapiens 0-7 3529502-3 1986 L-Glucose was ineffective by itself but potentiated the insulin release stimulated by D-glucose. Glucose 0-9 insulin Homo sapiens 56-63 3529502-3 1986 L-Glucose was ineffective by itself but potentiated the insulin release stimulated by D-glucose. Glucose 86-95 insulin Homo sapiens 56-63 3726444-5 1986 The results indicate that when determining the level of plasma C-peptide after stimulation with glucagon, in order to distinguish between insulin-dependent and non-insulin-dependent diabetic patients, it is critical to take into account the consequence of low blood glucose values and to standardize the test conditions in regard to pre-test meals. Glucose 266-273 insulin Homo sapiens 63-72 3529664-1 1986 The aim of the optimization of insulin supply in insulin-dependent diabetes mellitus is by means of restoration of blood glucose regulation resembling the physiological control to contribute to the secondary prevention of the late diabetes-specific complications. Glucose 121-128 insulin Homo sapiens 31-38 3529502-7 1986 However, they potentiated the insulin release when D-glucose was also present. Glucose 51-60 insulin Homo sapiens 30-37 3529502-8 1986 Cellobiose and lactose, which have a beta(1-4) linkage to glucose molecule at the reducing end, inhibited insulin release stimulated by D-glucose. Glucose 58-65 insulin Homo sapiens 106-113 3525245-3 1986 Plasma insulin was measured in 12 patients and the mean values of these patients reached above normal levels after oral glucose load. Glucose 120-127 insulin Homo sapiens 7-14 3525245-11 1986 From these observations, it is likely that glucose intolerance in Cushing"s syndrome is primarily due to the effects of chronic glucocorticoid excess on tissue metabolism of glucose as characterized by the presence of insulin resistance, which is not due to a defect in insulin-receptor binding but rather caused by the alteration in post-receptor mechanism, and increased secretion of insulin can be considered as a compensatory mechanism. Glucose 43-50 insulin Homo sapiens 218-225 3520336-2 1986 It is synthesized by the beta-cells of pancreatic islets, and circulating insulin levels are regulated by several small molecules, notably glucose, amino acids, fatty acids and certain pharmacological agents. Glucose 139-146 insulin Homo sapiens 74-81 3520336-6 1986 We report here that the human insulin gene is expressed in a tissue-specific manner in the islets of these transgenic mice, and that serum human insulin levels are properly regulated by glucose, amino acids and tolbutamide, an oral hypoglycaemic agent. Glucose 186-193 insulin Homo sapiens 30-37 3520336-6 1986 We report here that the human insulin gene is expressed in a tissue-specific manner in the islets of these transgenic mice, and that serum human insulin levels are properly regulated by glucose, amino acids and tolbutamide, an oral hypoglycaemic agent. Glucose 186-193 insulin Homo sapiens 145-152 3539151-0 1986 [Can the glucose load test predict insulin requirement in gestational diabetes with normal fasting blood glucose (Type B)? Glucose 9-16 insulin Homo sapiens 35-42 3525245-12 1986 In some patients, however, a decrease in insulin secreting capacity, the cause of which is not clear but at least related to the patient"s age, is found and seems to lead to severe glucose intolerance. Glucose 181-188 insulin Homo sapiens 41-48 3517644-3 1986 Therapy with either tolazamide or exogenous insulin resulted in a similar lowering (P less than 0.05) of postabsorptive glucose-production rates (from 2.3 +/- 0.1 to 2.0 +/- 0.2 and 1.8 +/- 0.1 mg per kilogram of body weight per minute, respectively) but not to normal (1.5 +/- 0.1 mg per kilogram per minute). Glucose 120-127 insulin Homo sapiens 44-51 3517644-4 1986 Both tolazamide and exogenous insulin increased (P less than 0.05) glucose utilization at supraphysiologic insulin concentrations (from 6.2 +/- 0.7 to 7.7 +/- 0.6 mg per kilogram per minute with tolazamide and to 7.8 +/- 0.6 mg per kilogram per minute with exogenous insulin) to nondiabetic rates (7.9 +/- 0.5 mg per kilogram per minute). Glucose 67-74 insulin Homo sapiens 30-37 3517644-4 1986 Both tolazamide and exogenous insulin increased (P less than 0.05) glucose utilization at supraphysiologic insulin concentrations (from 6.2 +/- 0.7 to 7.7 +/- 0.6 mg per kilogram per minute with tolazamide and to 7.8 +/- 0.6 mg per kilogram per minute with exogenous insulin) to nondiabetic rates (7.9 +/- 0.5 mg per kilogram per minute). Glucose 67-74 insulin Homo sapiens 107-114 3517644-4 1986 Both tolazamide and exogenous insulin increased (P less than 0.05) glucose utilization at supraphysiologic insulin concentrations (from 6.2 +/- 0.7 to 7.7 +/- 0.6 mg per kilogram per minute with tolazamide and to 7.8 +/- 0.6 mg per kilogram per minute with exogenous insulin) to nondiabetic rates (7.9 +/- 0.5 mg per kilogram per minute). Glucose 67-74 insulin Homo sapiens 107-114 3010729-0 1986 Insulin-induced cytoplasmic alkalinization and glucose transport in muscle cells. Glucose 47-54 insulin Homo sapiens 0-7 3010729-1 1986 Insulin stimulates glucose uptake into muscle within minutes, preceding stimulation of glycolysis. Glucose 19-26 insulin Homo sapiens 0-7 3522327-8 1986 The maximal insulin-stimulated glucose transport rates averaged 143 +/- 15 and 143 +/- 15 fl/cell X s, and the ED50:s 218 +/- 124 and 160 +/- 28 pmol/l (NS) in fat cells prepared from needle biopsy and surgically removed adipose tissue respectively. Glucose 31-38 insulin Homo sapiens 12-19 3525054-1 1986 It has been postulated that glucose regulation is secondary to maintenance of normal basal insulin secretion. Glucose 28-35 insulin Homo sapiens 91-98 3514331-1 1986 To evaluate the role of glucagon in insulin-mediated glucose metabolism, we studied four men and four women, ranging in age from 30-73 yr (mean +/- SEM, 54 +/- 5) who had undergone complete pancreatic resection for cancer or chronic pancreatitis 16-58 mo previously. Glucose 53-60 insulin Homo sapiens 36-43 3514335-6 1986 Arteriovenous plasma glucose differences were higher after oral glucose administration and were positively correlated with plasma insulin concentrations. Glucose 21-28 insulin Homo sapiens 130-137 3514649-0 1986 Effect of insulin on glucose uptake and metabolism in the human placenta. Glucose 21-28 insulin Homo sapiens 10-17 3514335-6 1986 Arteriovenous plasma glucose differences were higher after oral glucose administration and were positively correlated with plasma insulin concentrations. Glucose 64-71 insulin Homo sapiens 130-137 2938985-3 1986 We did not find any argument in favor of the development of a state of insulin resistance in women using these compounds, because erythrocyte receptor binding was not modified and plasma insulin responses to glucose were decreased. Glucose 208-215 insulin Homo sapiens 187-194 3514652-0 1986 Glucose storage is a major determinant of in vivo "insulin resistance" in subjects with normal glucose tolerance. Glucose 95-102 insulin Homo sapiens 51-58 3956886-5 1986 The glucose transport system in fat cells from both groups of pregnant women was characterized by impaired maximal (P less than 0.05) and half-maximal (P less than 0.05) response to insulin. Glucose 4-11 insulin Homo sapiens 182-189 3956886-8 1986 In conclusion, both in late normal and diabetic pregnancy, insulin binding to adipocytes is significantly reduced and accompanied by decreased insulin sensitivity and reduced maximal insulin responsiveness of glucose transport and by impaired basal and maximally insulin-stimulated glucose metabolism. Glucose 209-216 insulin Homo sapiens 59-66 3087853-6 1986 The insulin-like growth factor, MSA, which is 1% as potent as insulin in stimulating glucose oxidation in rat fat cells and in inhibiting 125I-insulin binding to human fibroblasts, is 25% as potent as insulin in stimulating glycogen synthase. Glucose 85-92 insulin Homo sapiens 4-11 3089865-3 1986 Insulin secretion was evaluated in both groups by insulin and C-peptide response to an intravenous glucose tolerance test and by 24 h urinary excretion of C-peptide. Glucose 99-106 insulin Homo sapiens 0-7 3514652-1 1986 In vivo "resistance" to the action of insulin on glucose uptake is commonly found in obesity and is characteristic of noninsulin-dependent diabetes mellitus in obese subjects. Glucose 49-56 insulin Homo sapiens 38-45 3514649-1 1986 The effect of insulin on glucose uptake, transfer, and metabolism was investigated in the human placenta perfused in vitro. Glucose 25-32 insulin Homo sapiens 14-21 3514652-7 1986 At the high insulin infusion rate, over 70% of the difference in glucose uptake between subjects with a low or high capacity for glucose disposal was due to glucose storage. Glucose 65-72 insulin Homo sapiens 12-19 3514652-7 1986 At the high insulin infusion rate, over 70% of the difference in glucose uptake between subjects with a low or high capacity for glucose disposal was due to glucose storage. Glucose 129-136 insulin Homo sapiens 12-19 3082700-10 1986 The insulin-induced suppression of GH was also observed when cells were grown in glucose-free medium. Glucose 81-88 insulin Homo sapiens 4-11 3514652-7 1986 At the high insulin infusion rate, over 70% of the difference in glucose uptake between subjects with a low or high capacity for glucose disposal was due to glucose storage. Glucose 129-136 insulin Homo sapiens 12-19 3514652-8 1986 These studies demonstrated that in normal subjects at both physiological and maximally stimulating plasma insulin concentrations, glucose storage is a major factor in distinguishing between those with low or high rates of insulin-mediated glucose disposal. Glucose 130-137 insulin Homo sapiens 106-113 3514652-8 1986 These studies demonstrated that in normal subjects at both physiological and maximally stimulating plasma insulin concentrations, glucose storage is a major factor in distinguishing between those with low or high rates of insulin-mediated glucose disposal. Glucose 130-137 insulin Homo sapiens 222-229 3514652-8 1986 These studies demonstrated that in normal subjects at both physiological and maximally stimulating plasma insulin concentrations, glucose storage is a major factor in distinguishing between those with low or high rates of insulin-mediated glucose disposal. Glucose 239-246 insulin Homo sapiens 106-113 3514652-8 1986 These studies demonstrated that in normal subjects at both physiological and maximally stimulating plasma insulin concentrations, glucose storage is a major factor in distinguishing between those with low or high rates of insulin-mediated glucose disposal. Glucose 239-246 insulin Homo sapiens 222-229 3514652-9 1986 Since glucose storage may be a specifically activated process, we hypothesize that failure to activate glucose storage is a major defect causing in vivo insulin resistance in subjects with normal glucose tolerance. Glucose 6-13 insulin Homo sapiens 153-160 3514652-9 1986 Since glucose storage may be a specifically activated process, we hypothesize that failure to activate glucose storage is a major defect causing in vivo insulin resistance in subjects with normal glucose tolerance. Glucose 103-110 insulin Homo sapiens 153-160 3514652-9 1986 Since glucose storage may be a specifically activated process, we hypothesize that failure to activate glucose storage is a major defect causing in vivo insulin resistance in subjects with normal glucose tolerance. Glucose 103-110 insulin Homo sapiens 153-160 3517068-2 1986 In comparison to the controls, diabetic subjects had a 65% reduction in plasma insulin levels in response to an oral glucose load. Glucose 117-124 insulin Homo sapiens 79-86 3088434-7 1986 CONCLUSION: Impaired glucose utilisation in severely stressed premature infants with parenteral nutrition might be due to stress induced peripheral insulin resistance. Glucose 21-28 insulin Homo sapiens 148-155 3010619-3 1986 To do so, we studied the decline in blood glucose concentration, as induced by iv insulin infusion, from a given hyperglycaemic level. Glucose 42-49 insulin Homo sapiens 82-89 3010619-4 1986 With high levels of GH (GH = 120 micrograms/l), the slope of the straight line representing the decrease in blood glucose after insulin infusion was -0.71, the time required to achieve normoglycaemic levels, 270 min, and the corrected area under the curve representing blood glucose 26 070 units2. Glucose 114-121 insulin Homo sapiens 128-135 3010619-4 1986 With high levels of GH (GH = 120 micrograms/l), the slope of the straight line representing the decrease in blood glucose after insulin infusion was -0.71, the time required to achieve normoglycaemic levels, 270 min, and the corrected area under the curve representing blood glucose 26 070 units2. Glucose 275-282 insulin Homo sapiens 128-135 3519338-0 1986 Serum immunoreactive insulin responses to a glucose load in Asian Indian and European type 2 (non-insulin-dependent) diabetic patients and control subjects. Glucose 44-51 insulin Homo sapiens 21-28 3519338-1 1986 The serum immunoreactive insulin response to an oral glucose load was estimated in 15 Asian Indian and 29 European non-diabetic subjects, and in 45 Asian Indian and 72 European Type 2 (non-insulin-dependent) diabetic patients. Glucose 53-60 insulin Homo sapiens 25-32 3519338-2 1986 In the non-diabetic group, basal insulin values were higher in the Asian Indians than the Europeans (16.7 +/- 3.0 vs. 6.9 +/- 0.7 mU/l, p less than 0.001), and remained higher throughout the glucose tolerance test. Glucose 191-198 insulin Homo sapiens 33-40 3519338-8 1986 The insulin response to a glucose load is also greater in the Asian Indians. Glucose 26-33 insulin Homo sapiens 4-11 3517554-6 1986 The glucose infusion rates required to maintain euglycemia were 35% lower (P less than 0.01) after hydrocortisone due to decreased insulin effects on metabolic clearance rate of glucose and diminished suppression of hepatic glucose production (0.4 +/- 0.1 v -0.1 +/- 0.1 mg/kg X minute, p less than 0.05, 3-3H-glucose infusion method). Glucose 4-11 insulin Homo sapiens 131-138 3517554-6 1986 The glucose infusion rates required to maintain euglycemia were 35% lower (P less than 0.01) after hydrocortisone due to decreased insulin effects on metabolic clearance rate of glucose and diminished suppression of hepatic glucose production (0.4 +/- 0.1 v -0.1 +/- 0.1 mg/kg X minute, p less than 0.05, 3-3H-glucose infusion method). Glucose 178-185 insulin Homo sapiens 131-138 3517554-6 1986 The glucose infusion rates required to maintain euglycemia were 35% lower (P less than 0.01) after hydrocortisone due to decreased insulin effects on metabolic clearance rate of glucose and diminished suppression of hepatic glucose production (0.4 +/- 0.1 v -0.1 +/- 0.1 mg/kg X minute, p less than 0.05, 3-3H-glucose infusion method). Glucose 178-185 insulin Homo sapiens 131-138 3517560-5 1986 Mean plasma glucose, fructose, and insulin were reduced by both drugs during the first two hours following the sucrose load and led to a decrease of the suprabasal glucose oxidation (oxidation above baseline) during the first two hours of the test. Glucose 164-171 insulin Homo sapiens 35-42 3518639-4 1986 Insulin concentrations after oral glucose challenge showed inadequate insulin secretion with respect to the degree of hyperglycaemia in these children. Glucose 34-41 insulin Homo sapiens 0-7 3720497-4 1986 The premeal insulin dosages, as delivered by the patients, varied significantly in relation to the time of the day, and to the premeal plasma glucose concentration. Glucose 142-149 insulin Homo sapiens 12-19 3514677-6 1986 Since it has recently been observed that glucose feeding may rapidly modify insulin action in human adipocytes, fat cells were also obtained 60 min after an 100-g oral glucose load. Glucose 41-48 insulin Homo sapiens 76-83 3956771-1 1986 To determine whether there exists an altered sensitivity to insulin in hyperprolactinemia, we studied, in 15 women with microprolactinomas, the insulin effects on glucose, PRL, GH, and cortisol before and after successful adenoma removal. Glucose 163-170 insulin Homo sapiens 144-151 3519411-3 1986 The results documented relationships between incremental plasma insulin response to glucose and degree of fasting hyperglycemia (r = -.045, P less than 0.05) and insulin-stimulated glucose utilization (r = 0.25, P = NS). Glucose 84-91 insulin Homo sapiens 64-71 3519411-3 1986 The results documented relationships between incremental plasma insulin response to glucose and degree of fasting hyperglycemia (r = -.045, P less than 0.05) and insulin-stimulated glucose utilization (r = 0.25, P = NS). Glucose 181-188 insulin Homo sapiens 162-169 3519411-4 1986 These data indicate that differences in insulin secretory response accounted for only approximately 20% of the variance in fasting plasma glucose level and 6% of the variance in insulin resistance in NIDDM. Glucose 138-145 insulin Homo sapiens 40-47 3082935-0 1986 Enhancement of insulin action after oral glucose ingestion. Glucose 41-48 insulin Homo sapiens 15-22 3082935-1 1986 Previous investigations in normal humans and rats have shown an increase in insulin sensitivity and binding affinity of adipocytes isolated 1-3 h after glucose ingestion. Glucose 152-159 insulin Homo sapiens 76-83 3525178-8 1986 We have attempted to explore the time relationship between the overnight drop in free insulin levels and the rises in blood glucose by a distribution-free statistical analysis, correlating successive changes in time between the two profiles. Glucose 124-131 insulin Homo sapiens 86-93 3512671-2 1986 Glucose tolerance, as evaluated by the plasma glucose response to 75 g of oral glucose deteriorated with age, associated with an increase in plasma insulin levels. Glucose 46-53 insulin Homo sapiens 148-155 3512590-5 1986 The onset of action of sc insulin, as indicated by a 10% fall in serum glucose, was similar in both patient groups [1.9 +/- 0.1 (+/- SEM) hour in Ab-negative and 1.8 +/- 0.1 h in Ab-positive patients]. Glucose 71-78 insulin Homo sapiens 26-33 3512590-6 1986 The peak effect of insulin action, as determined by the nadir of serum glucose, was 4.6 +/- 0.2 h in the previously untreated patients, not significantly different from the value in the diabetic patients with insulin Abs (5.2 +/- 0.4 h). Glucose 71-78 insulin Homo sapiens 19-26 3512590-9 1986 However, the peak effect and total duration of insulin action were significantly correlated with the baseline serum glucose levels. Glucose 116-123 insulin Homo sapiens 47-54 3082935-4 1986 After 15- and 25-g oral glucose loads during the 20-120-min interval of insulin infusion, glucose infusion rates increased by 44 +/- 6% (P less than 0.0001) and 47 +/- 9% (P less than 0.0002), respectively. Glucose 90-97 insulin Homo sapiens 72-79 3082935-8 1986 Studies were carried out to mimic the insulin curve seen after 15- and 25-g oral glucose loads. Glucose 81-88 insulin Homo sapiens 38-45 3512591-4 1986 The maximum plasma insulin response to glucose ranged between 475-1630 microU/ml. Glucose 39-46 insulin Homo sapiens 19-26 3514677-8 1986 It is concluded that, in the fasting state, the action of insulin on glucose utilization but not on lipolysis is impaired in adipose tissue of acromegalic patients because of a postreceptor defect. Glucose 69-76 insulin Homo sapiens 58-65 3512591-5 1986 When studied in November 1982, insulin (0.1 U/kg) caused a fall in blood glucose concentration of only 25% (normal, greater than 50%), and maximal glucose utilization during the euglycemic hyperinsulinemic clamp was 7.5 mg/kg . Glucose 73-80 insulin Homo sapiens 31-38 3512591-5 1986 When studied in November 1982, insulin (0.1 U/kg) caused a fall in blood glucose concentration of only 25% (normal, greater than 50%), and maximal glucose utilization during the euglycemic hyperinsulinemic clamp was 7.5 mg/kg . Glucose 147-154 insulin Homo sapiens 31-38 3082935-10 1986 These results demonstrate a rapid enhancement of insulin action after oral glucose challenge in normal humans. Glucose 75-82 insulin Homo sapiens 49-56 3515118-0 1986 Basal and glucose- and arginine-stimulated serum concentrations of insulin, C-peptide, and glucagon in hyperthyroid patients. Glucose 10-17 insulin Homo sapiens 67-74 3517494-1 1986 Resistance to insulin-mediated glucose disposal occurs in uninjured skeletal muscle of trauma patients but the effect of insulin on the accelerated proteolysis of trauma is unknown. Glucose 31-38 insulin Homo sapiens 14-21 3515118-3 1986 The insulin response was similar in the hyperthyroid and normal subjects after glucose administration and significantly lower during arginine infusion in the hyperthyroid patients. Glucose 79-86 insulin Homo sapiens 4-11 3515118-0 1986 Basal and glucose- and arginine-stimulated serum concentrations of insulin, C-peptide, and glucagon in hyperthyroid patients. Glucose 10-17 insulin Homo sapiens 76-85 3515118-4 1986 The serum C-peptide response to both glucose and arginine administration was markedly blunted in the hyperthyroid patients, and the plasma glucagon response to arginine infusion was decreased. Glucose 37-44 insulin Homo sapiens 10-19 2869694-0 1986 Response to glucose infusion in humans: role of changes in insulin concentration. Glucose 12-19 insulin Homo sapiens 59-66 3515118-6 1986 The apparent discrepancy between C-peptide and insulin secretion in the hyperthyroid patients following glucose administration might be due to diminished hepatic extraction of insulin or enhanced metabolism of C-peptide. Glucose 104-111 insulin Homo sapiens 33-42 3515118-6 1986 The apparent discrepancy between C-peptide and insulin secretion in the hyperthyroid patients following glucose administration might be due to diminished hepatic extraction of insulin or enhanced metabolism of C-peptide. Glucose 104-111 insulin Homo sapiens 47-54 3515118-6 1986 The apparent discrepancy between C-peptide and insulin secretion in the hyperthyroid patients following glucose administration might be due to diminished hepatic extraction of insulin or enhanced metabolism of C-peptide. Glucose 104-111 insulin Homo sapiens 210-219 3515119-0 1986 Potentiation of glucose-stimulated insulin release by tolazamide and paradoxical absence of glucose facilitation (Staub effect) in non-insulin-dependent diabetes. Glucose 16-23 insulin Homo sapiens 35-42 3515119-5 1986 The characteristic loss of early phase insulin release after the first intravenous glucose injection was recovered with the third injection. Glucose 83-90 insulin Homo sapiens 39-46 3515119-7 1986 Despite dramatic potentiation of glucose-stimulated insulin release and further improvement of early phase insulin release, K values again failed to progressively rise. Glucose 33-40 insulin Homo sapiens 52-59 3515119-9 1986 The applicability of the glucose facilitatory effect to the treatment of NIDDM might be limited to subjects in whom adjunctive measures have reestablished effective tissue responsiveness to endogenous insulin. Glucose 25-32 insulin Homo sapiens 201-208 3513584-6 1986 Significantly more patients in the home glucose monitoring group were receiving insulin therapy (50% versus 21%). Glucose 40-47 insulin Homo sapiens 80-87 3513584-7 1986 We believe that intensive home glucose monitoring will allow for the early identification of those gestational diabetic patients needing insulin and thus reduce the incidence of macrosomia and large for gestational age infants. Glucose 31-38 insulin Homo sapiens 137-144 3513613-2 1986 To determine whether similar defects occur after chronic growth hormone excess, insulin dose-response curves for stimulation of glucose utilization and suppression of glucose production and monocyte and erythrocyte insulin binding were determined in five acromegalic patients and six healthy volunteers of comparable age, sex, and obesity. Glucose 128-135 insulin Homo sapiens 80-87 2869694-5 1986 The plasma concentration of glucose also increased to the same extent during the 4 mg X kg-1 X min-1 infusion in both protocols, which indicated that the spontaneous insulin response to the glucose infusion (an increase from 11 +/- 2 to 24 +/- 3 microU/ml) did not stimulate the peripheral clearance of glucose. Glucose 28-35 insulin Homo sapiens 166-173 3513613-3 1986 During infusion of insulin, glucose infusion rates required to maintain euglycemia were significantly lower (P less than 0.02 all) in the acromegalic patients than in the control subjects. Glucose 28-35 insulin Homo sapiens 19-26 3513613-4 1986 Suppression of glucose production was impaired in the acromegalic subjects at insulin concentrations in the physiological range but not at insulin concentrations in the supraphysiological range. Glucose 15-22 insulin Homo sapiens 78-85 2869694-5 1986 The plasma concentration of glucose also increased to the same extent during the 4 mg X kg-1 X min-1 infusion in both protocols, which indicated that the spontaneous insulin response to the glucose infusion (an increase from 11 +/- 2 to 24 +/- 3 microU/ml) did not stimulate the peripheral clearance of glucose. Glucose 190-197 insulin Homo sapiens 166-173 3513613-5 1986 In contrast stimulation of glucose utilization was decreased in the acromegalic subjects at both physiological and supraphysiological insulin concentrations. Glucose 27-34 insulin Homo sapiens 134-141 3513613-8 1986 The decrease in glucose utilization at supraphysiological insulin concentrations in the acromegalic subjects and the normal monocyte and erythrocyte insulin binding suggest a postbinding alteration in insulin action. Glucose 16-23 insulin Homo sapiens 58-65 2869694-5 1986 The plasma concentration of glucose also increased to the same extent during the 4 mg X kg-1 X min-1 infusion in both protocols, which indicated that the spontaneous insulin response to the glucose infusion (an increase from 11 +/- 2 to 24 +/- 3 microU/ml) did not stimulate the peripheral clearance of glucose. Glucose 190-197 insulin Homo sapiens 166-173 3512342-8 1986 Deactivation of stimulated glucose transport was determined by incubating equivalent concentrations of insulin (0.166 and 1.66 nM) and HPro (4.44 and 22.2 nM) until full stimulation was achieved, washing cells free of unbound hormone, and initiating dissociation and deactivation by resuspension in hormone-free buffer. Glucose 27-34 insulin Homo sapiens 103-110 3513629-0 1986 Regulation of hepatic glucose output during exercise by circulating glucose and insulin in humans. Glucose 22-29 insulin Homo sapiens 80-87 3513629-1 1986 We have tested the hypothesis that hepatic glucose output (Ra) during exercise in humans is subject to feedback control by circulating glucose within a control range that is determined by the circulating insulin concentration. Glucose 43-50 insulin Homo sapiens 204-211 3513629-6 1986 During the fixed-rate glucose and insulin infusion, plasma glucose fell from the commencement of exercise but stabilized at a lower level. Glucose 59-66 insulin Homo sapiens 34-41 3513629-8 1986 Insulin affects Ra and regulates the steady-state glucose level by altering the sensitivity of this control system. Glucose 50-57 insulin Homo sapiens 0-7 3512339-6 1986 In groups 1-3, insulin stimulated adipose tissue glucose oxidation in a dose-dependent way, and the sensitivity and responsiveness to insulin were comparable. Glucose 49-56 insulin Homo sapiens 15-22 3512341-0 1986 In vivo deactivation of proinsulin action on glucose disposal and hepatic glucose production in normal man. Glucose 45-52 insulin Homo sapiens 24-34 3512341-0 1986 In vivo deactivation of proinsulin action on glucose disposal and hepatic glucose production in normal man. Glucose 74-81 insulin Homo sapiens 24-34 3512341-1 1986 We have studied the deactivation of the in vivo actions of insulin and biosynthetic human proinsulin (recombinant DNA) to stimulate the glucose disposal rate (GDR) and to inhibit hepatic glucose output (HGO) in man. Glucose 136-143 insulin Homo sapiens 59-66 3512341-1 1986 We have studied the deactivation of the in vivo actions of insulin and biosynthetic human proinsulin (recombinant DNA) to stimulate the glucose disposal rate (GDR) and to inhibit hepatic glucose output (HGO) in man. Glucose 136-143 insulin Homo sapiens 90-100 3518739-1 1986 The effect of bradykinin on insulin-stimulated glucose metabolism was studied in 5 operated patients using the euglycemic insulin clamp technique and the forearm catheter technique. Glucose 47-54 insulin Homo sapiens 28-35 3516606-9 1986 Because of this difference in plasma glucose rise, twice as much insulin was administered i.p. Glucose 37-44 insulin Homo sapiens 65-72 3516771-3 1986 Pancreatic B-cell function was assessed by the insulin response to an oral glucose tolerance test. Glucose 75-82 insulin Homo sapiens 47-54 3519045-7 1986 Thus it can be concluded that hyperglycaemia enhances the insulin secretory response to non-glucose stimuli and that following correction of the hyperglycaemia patients with NIDDY have an attenuated insulinaemic response. Glucose 92-99 insulin Homo sapiens 58-65 3512343-4 1986 During intraduodenal infusion of glucose, insulin concentrations in plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. Glucose 33-40 insulin Homo sapiens 42-49 3512343-4 1986 During intraduodenal infusion of glucose, insulin concentrations in plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. Glucose 198-205 insulin Homo sapiens 42-49 3512346-2 1986 Although the minimal-model-based insulin sensitivity index (S1) can be estimated from the results of a simple 180-min intravenous glucose tolerance test (IVGTT), its relationship to widely accepted but technically more difficult clamp-based techniques has not been resolved in humans. Glucose 130-137 insulin Homo sapiens 33-40 2869053-7 1986 When changes in insulin and glucagon were prevented, plasma glucose concentration fell, particularly in the high-insulin group. Glucose 60-67 insulin Homo sapiens 16-23 2422103-1 1986 Twenty-four hour glucose levels were measured in nineteen insulin treated type I diabetics both during insulin plus aprotinin treatments and insulin by itself. Glucose 17-24 insulin Homo sapiens 58-65 3516960-5 1986 Insulin response to glucose infusion was greater in obese than in lean heifers, whether determined as actual concentration (P less than .01) or as insulin response areas (P less than .05) above base-line concentrations. Glucose 20-27 insulin Homo sapiens 0-7 3516960-5 1986 Insulin response to glucose infusion was greater in obese than in lean heifers, whether determined as actual concentration (P less than .01) or as insulin response areas (P less than .05) above base-line concentrations. Glucose 20-27 insulin Homo sapiens 147-154 2869053-7 1986 When changes in insulin and glucagon were prevented, plasma glucose concentration fell, particularly in the high-insulin group. Glucose 60-67 insulin Homo sapiens 113-120 3514831-0 1986 Gastrointestinal enhanced insulin release in response to glucose in newborn infants. Glucose 57-64 insulin Homo sapiens 26-33 3005370-4 1986 The functions of the insulin receptor were examined by measuring specific 125I-insulin binding (receptor concentration, affinity, specificity, pH-, time-, and temperature dependence), insulin-induced down-regulation of the receptor, insulin-stimulated autophosphorylation of the beta-subunit, and phosphorylation of exogenous substrates as well as insulin-stimulated glucose uptake in glioblastoma cells. Glucose 367-374 insulin Homo sapiens 21-28 3514831-6 1986 Plasma insulin responses were greater in infants receiving glucose via the GI route. Glucose 59-66 insulin Homo sapiens 7-14 3514831-8 1986 The present data suggest that in the term newborn infant, GI enhanced insulin release occurs only when a threshold of plasma glucose concentration has been exceeded. Glucose 125-132 insulin Homo sapiens 70-77 3512954-8 1986 In vivo glucose utilization insulin dose response curves were determined in 3 acanthotic subjects using the euglycemic clamp technique. Glucose 8-15 insulin Homo sapiens 28-35 2419732-5 1986 Plasma insulin levels after the glucose load were significantly lower at ten and 30 minutes in the group without damage, in early or late abstinence. Glucose 32-39 insulin Homo sapiens 7-14 3512920-5 1986 It also inhibited insulin secretion in response to an exogenous dextrose load (e.g., the priming fluid of the cardiopulmonary bypass circuit) or a glucagon injection, but this inhibition was lifted by rewarming. Glucose 64-72 insulin Homo sapiens 18-25 3512920-9 1986 Glucose-clamp studies indicated that insulin resistance was initiated by anesthesia and surgical trauma, and further accentuated by cardiopulmonary bypass, in association with elevated levels of hormones indicative of surgical stress. Glucose 0-7 insulin Homo sapiens 37-44 3512920-10 1986 Regardless of body temperature changes, the assimilation of glucose by nondiabetic subjects during and immediately after bypass called for the infusion of large doses of insulin. Glucose 60-67 insulin Homo sapiens 170-177 3515701-0 1986 Insulin secretion during intravenous glucose tolerance tests in non-insulin-dependent diabetes in the young. Glucose 37-44 insulin Homo sapiens 0-7 3515701-1 1986 The phasic response of insulin to intravenous glucose was studied in 9 patients with non-insulin-dependent diabetes in the young (NIDDY), with 3-generation transmission of the disease; and 9 age-, weight- and sex-matched reference subjects. Glucose 46-53 insulin Homo sapiens 23-30 3511647-3 1986 Multiple doses of insulin are usually necessary for tight control of blood glucose in patients with insulin-dependent diabetes. Glucose 75-82 insulin Homo sapiens 18-25 3511690-6 1986 However, prazosin was associated with an increase in the fasting blood glucose level and a decrease in the peak insulin value after glucose injection, both of which were dose-related effects. Glucose 132-139 insulin Homo sapiens 112-119 3511690-7 1986 The data indicate that the glucose turnover was at least as good after a switch from diuretic to prazosin treatment as before at lower insulin values. Glucose 27-34 insulin Homo sapiens 135-142 3511712-1 1986 Fasting insulin concentrations and the insulin response to an oral glucose tolerance test were measured in six virilized women with ovarian hyperthecosis and six weight-matched normal women. Glucose 67-74 insulin Homo sapiens 39-46 3511712-5 1986 Insulin response to an oral glucose tolerance test was greatly increased (p less than 0.01) in comparison to normal women and women with polycystic ovarian disease. Glucose 28-35 insulin Homo sapiens 0-7 3010944-0 1986 Glucose-stimulated sequestration of Ca2+ in clonal insulin-releasing cells. Glucose 0-7 insulin Homo sapiens 51-58 3516748-4 1986 The insulin response to glucose was expressed as the ratio of the incremental area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG), during the first 30 minutes and the latter part of the test. Glucose 24-31 insulin Homo sapiens 4-11 3516161-0 1986 3,5,3"-Triiodothyronine regulates insulin level in the circulation following glucose ingestion in humans. Glucose 77-84 insulin Homo sapiens 34-41 3516161-1 1986 To clarify the relationship between the 3,5,3"-triiodothyronine (T3) response and the insulin response after glucose ingestion in humans, serum T3, immunoreactive insulin (IRI), C-peptide immunoreactivity (CPR), nonesterified fatty acid (NEFA) and plasma glucose levels were measured in 11 nonobese inpatients with normal glucose tolerance after oral 75 g glucose tolerance test. Glucose 109-116 insulin Homo sapiens 86-93 3510921-2 1986 To determine the functional characteristics of the remaining receptors on these cells, insulin-stimulated glucose uptake, insulin internalization, and insulin-induced receptor loss were evaluated in monolayer fibroblasts obtained from this subject. Glucose 106-113 insulin Homo sapiens 87-94 3516748-4 1986 The insulin response to glucose was expressed as the ratio of the incremental area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG), during the first 30 minutes and the latter part of the test. Glucose 24-31 insulin Homo sapiens 93-100 3510924-2 1986 Insulin sensitivity was measured in a group of seven thyrotoxic patients and in a group of seven normal subjects by means of the glucose clamp technique. Glucose 129-136 insulin Homo sapiens 0-7 3510924-10 1986 The major route of insulin-stimulated glucose disposal in the hyperthyroid patients appears to be glucose oxidation. Glucose 38-45 insulin Homo sapiens 19-26 3516748-4 1986 The insulin response to glucose was expressed as the ratio of the incremental area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG), during the first 30 minutes and the latter part of the test. Glucose 122-129 insulin Homo sapiens 4-11 3510924-10 1986 The major route of insulin-stimulated glucose disposal in the hyperthyroid patients appears to be glucose oxidation. Glucose 98-105 insulin Homo sapiens 19-26 3511099-5 1986 The patient"s insulin was purified from serum and shown to possess both reduced binding and ability to stimulate glucose uptake and oxidation in vitro. Glucose 113-120 insulin Homo sapiens 14-21 3512245-5 1986 The common and important indications for routine glucose analysis include evaluation of symptomatically ill patients with known diabetes or patients with altered mental status or coma of unknown etiology; patients on insulin or sulfonylureas; sick neonates; patients with a variety of drug intoxications; and patients suffering from significant systemic illness or injury likely to manifest with physiologic stress expressed as glucose intolerance. Glucose 49-56 insulin Homo sapiens 217-224 3514489-7 1986 It was concluded that the interplay of various factors, CAP, upright posture and impaired renal functions resulting in suppression of aldosterone and insulin played a role in the paradoxical glucose-induced serum potassium elevation. Glucose 191-198 insulin Homo sapiens 150-157 3516823-6 1986 Glucose production was inhibited with the lowest insulin infusion rate and a marked increase in glucose metabolic clearance rate occurred with the highest insulin infusion. Glucose 0-7 insulin Homo sapiens 49-56 3516823-6 1986 Glucose production was inhibited with the lowest insulin infusion rate and a marked increase in glucose metabolic clearance rate occurred with the highest insulin infusion. Glucose 0-7 insulin Homo sapiens 155-162 3516823-6 1986 Glucose production was inhibited with the lowest insulin infusion rate and a marked increase in glucose metabolic clearance rate occurred with the highest insulin infusion. Glucose 96-103 insulin Homo sapiens 155-162 3517121-0 1986 Muscarinic cholinergic modulation of insulin response to an intravenous glucose tolerance test in normal man. Glucose 72-79 insulin Homo sapiens 37-44 3941163-5 1986 In accordance with the binding data, the dose-response curve for insulin"s stimulatory effect on glucose incorporation into triglycerides was shifted to the right. Glucose 97-104 insulin Homo sapiens 65-72 3517121-1 1986 The effect of pirenzepine, a specific muscarinic cholinergic receptor antagonist, on insulin and glucagon responses to an intravenous injection of glucose was investigated in eight normal adult subjects. Glucose 147-154 insulin Homo sapiens 85-92 3517121-5 1986 In contrast, pirenzepine significantly decreased insulin release induced by glucose administration. Glucose 76-83 insulin Homo sapiens 49-56 3511350-5 1986 There was a slight delay in the insulin rise following oral glucose on the C-peptide infusion day, but differences between mean values for individual sampling times were not statistically significantly different. Glucose 60-67 insulin Homo sapiens 75-84 3080654-0 1986 Overnutrition induced decrease in insulin action for glucose storage: in vivo and in vitro in man. Glucose 53-60 insulin Homo sapiens 34-41 2868380-1 1986 This is a case presentation of a 32-year-old man with a one year history of symptomatic hypoglycemia and documented elevations of his fasting plasma insulin to glucose ratio, caused by islet cell hyperplasia. Glucose 160-167 insulin Homo sapiens 149-156 3511351-12 1986 It is suggested that the persistent normal glucose uptake, following glycemic control that has been sufficient to normalize plasma metabolites, will limit glycemic excursions caused by acute reductions in plasma-free insulin concentration. Glucose 43-50 insulin Homo sapiens 217-224 3080654-1 1986 The effect of short-term overnutrition on insulin action for glucose disposal was assessed in 15 Southwest American Indians (mean wt = 74 +/- 6 kg). Glucose 61-68 insulin Homo sapiens 42-49 3525915-0 1986 [Studies on glucose intolerance in chronic renal failure--estimation of insulin sensitivity before and after introduction of hemodialysis]. Glucose 12-19 insulin Homo sapiens 72-79 3080654-2 1986 After two weeks of weight maintenance and again after two weeks of 62% greater caloric intake (constant ratio of fat:carbohydrate:protein), insulin action for glucose disposal was measured using the euglycemic clamp technique with plasma insulin concentrations of about 110 and 1800 uU/mL. Glucose 159-166 insulin Homo sapiens 140-147 3080654-7 1986 The mean total insulin mediated glucose disposal rate decreased from 11.6 +/- 0.5 to 10.3 +/- 0.7, P less than 0.01, at the high insulin concentration. Glucose 32-39 insulin Homo sapiens 15-22 3080654-7 1986 The mean total insulin mediated glucose disposal rate decreased from 11.6 +/- 0.5 to 10.3 +/- 0.7, P less than 0.01, at the high insulin concentration. Glucose 32-39 insulin Homo sapiens 129-136 3080654-10 1986 The results indicate that short-term overnutrition results in reduced insulin action for glucose storage and disposal which is correlated with increased fasting insulin concentrations. Glucose 89-96 insulin Homo sapiens 70-77 3080654-10 1986 The results indicate that short-term overnutrition results in reduced insulin action for glucose storage and disposal which is correlated with increased fasting insulin concentrations. Glucose 89-96 insulin Homo sapiens 161-168 3080654-11 1986 Reduced glycogen synthase activity may contribute to the effect of overnutrition on in vivo insulin-mediated glucose storage. Glucose 109-116 insulin Homo sapiens 92-99 3945188-3 1986 The results indicated that adipocytes from the two groups were comparable in average cell size, basal and maximum insulin-stimulated glucose transport, glucose metabolism at 5.5 mmol/L glucose, ED50 of insulin for glucose transport and the inhibition of lipolysis, basal lipolysis rates, and insulin binding. Glucose 133-140 insulin Homo sapiens 114-121 3959858-4 1986 Additional benefits derived from exercise training include improved insulin-mediated glucose utilization, lower serum lipid concentrations, and improved psychological distress scores and anxiety levels. Glucose 85-92 insulin Homo sapiens 68-75 3080101-3 1986 Mean (SEM) plasma glucose concentration and glycosylated haemoglobin (HbA1) value improved significantly in the insulin infusion group (glucose 10.1 (1.0) v 5.3 (0.3) mmol/l (182 (18) v 95 (5) mg/100 ml); HbA1 9.6 (0.8) v 7.6 (0.5)%; p less than 0.001 and p less than 0.005, run in v experimental periods) but not in the control group. Glucose 18-25 insulin Homo sapiens 112-119 3510463-0 1986 The insulin and glucose response to an oral glucose load in non-insulin-dependent diabetes in the young. Glucose 44-51 insulin Homo sapiens 4-11 3511525-2 1986 Recently, new strategies of insulin therapy have been developed to normalize blood glucose control, with a view to preventing late complications of diabetes and increasing patients" well-being. Glucose 83-90 insulin Homo sapiens 28-35 3080101-3 1986 Mean (SEM) plasma glucose concentration and glycosylated haemoglobin (HbA1) value improved significantly in the insulin infusion group (glucose 10.1 (1.0) v 5.3 (0.3) mmol/l (182 (18) v 95 (5) mg/100 ml); HbA1 9.6 (0.8) v 7.6 (0.5)%; p less than 0.001 and p less than 0.005, run in v experimental periods) but not in the control group. Glucose 136-143 insulin Homo sapiens 112-119 2871688-8 1986 Insulin secretion following glucose load was enhanced disproportionately. Glucose 28-35 insulin Homo sapiens 0-7 2876589-4 1986 Insulin decreased blood glucose by 1.5 mmol/l and simultaneous suppression of glucagon resulted in a more pronounced hypoglycemia enhancing the adrenaline and cortisol responses. Glucose 24-31 insulin Homo sapiens 0-7 3096047-3 1986 The dosage of insulin was adjusted to produce a nadir in blood glucose of reversible 1 mmol/L. Glucose 63-70 insulin Homo sapiens 14-21 3464150-7 1986 Significant positive correlations were found between the increase of plasma cortisol levels during normal pregnancy and the concomitant decrease in glucose tolerance indicating that the increased cortisol levels might be involved in the development of the insulin resistance found in normal pregnancy. Glucose 148-155 insulin Homo sapiens 256-263 3532664-5 1986 The IDM"s are able to respond to both physiologic and metabolic stress with an increased catecholamine secretion during the first hours of life, and the catecholamines seem to counteract the inhibitory effect of insulin on lipolysis and, at least partly, to oppose the blood glucose lowering effect of insulin. Glucose 275-282 insulin Homo sapiens 212-219 3532665-3 1986 Even though the insulin responses to oral glucose and mixed meals are equally large in gestational diabetics and normal pregnant women, the insulin responses of the gestational diabetics differ in two pertinent ways from those of the normals. Glucose 42-49 insulin Homo sapiens 16-23 3513553-2 1986 Using a radiotracer method, binding of insulin to dialysate containers was determined at various times up to 48 hours after addition of 10, 20, 40, and 80 units of insulin each to 2 L of either 1.5% or 4.25% dextrose dialysate solution. Glucose 208-216 insulin Homo sapiens 39-46 3535397-4 1986 The responses of plasma insulin and C-peptide to oral glucose increased significantly during the exercise period. Glucose 54-61 insulin Homo sapiens 24-31 3535397-4 1986 The responses of plasma insulin and C-peptide to oral glucose increased significantly during the exercise period. Glucose 54-61 insulin Homo sapiens 36-45 3544691-1 1986 The effects of continuous ambulatory peritoneal dialysis (CAPD) on glucose tolerance and serum immunoreactive insulin and glucagon responses to oral glucose over the first year of therapy were studied in 13 uremic patients. Glucose 149-156 insulin Homo sapiens 110-117 3530110-0 1986 Insulin metabolism is a major factor responsible for high or low peripheral insulin levels in response to oral glucose loading in the healthy man. Glucose 111-118 insulin Homo sapiens 0-7 3555256-0 1986 Cell biology of insulin"s stimulatory action on glucose transport and its perturbation in altered metabolic states. Glucose 48-55 insulin Homo sapiens 16-23 3530110-0 1986 Insulin metabolism is a major factor responsible for high or low peripheral insulin levels in response to oral glucose loading in the healthy man. Glucose 111-118 insulin Homo sapiens 76-83 3530110-4 1986 Their insulin incremental area after glucose averaged 0.25 +/- 0.01 nmol X 1-1 X min and 0.078 +/- 0.005 nmol X 1-1 X min, respectively (p less than 0.001). Glucose 37-44 insulin Homo sapiens 6-13 3530110-6 1986 The glycemic profile after oral glucose load was higher in low insulin responders than in high insulin responders. Glucose 32-39 insulin Homo sapiens 63-70 3530110-6 1986 The glycemic profile after oral glucose load was higher in low insulin responders than in high insulin responders. Glucose 32-39 insulin Homo sapiens 95-102 2875745-4 1986 Postprandial blood glucose response was exaggerated in one insulin-dependent diabetic while in the other, glucose tolerance was improved. Glucose 19-26 insulin Homo sapiens 59-66 2869870-7 1986 This suggests that insulin contributes minimally, but significantly, to regulation of plasma glucose levels during stressful experiences or the fasting state. Glucose 93-100 insulin Homo sapiens 19-26 3754160-0 1986 Simplified evaluation and documentation of data from glucose-controlled insulin infusion systems. Glucose 53-60 insulin Homo sapiens 72-79 3315255-1 1986 The aim of the study was to document during one to two years individual rhythmic patterns in blood glucose and injected insulin in self-controlled insulin dependent (C-peptide negative) diabetics with home blood glucose monitoring. Glucose 99-106 insulin Homo sapiens 147-154 3511933-8 1986 The results indicate that the insulin mediated glucose disposal rate can be altered by drugs influencing hepatic microsomal enzyme activity. Glucose 47-54 insulin Homo sapiens 30-37 3514018-5 1986 Thus, fenfluramine apparently has the capacity to lower glucose in patients receiving insulin therapy. Glucose 56-63 insulin Homo sapiens 86-93 2951129-4 1986 Insulin-mediated glucose disposal was reduced (p less than 0.01 and less than 0.01) at insulin infusion rates 1 and 6 mU/kg/min in untreated patients (18.5 +/- 1.9 and 33.8 +/- 4.5 mumol/kg/min) when compared with controls (35.8 +/- 3.4 and 62.0 +/- 4.7 mumol/kg/min) and was improved (p less than 0.01 and less than 0.01) following insulin treatment (36.1 +/- 4.6 and 64.8 +/- 4.2 mumol/kg/min). Glucose 17-24 insulin Homo sapiens 0-7 2866996-3 1986 The responses to GRF-40 were modified by the prevailing glucose level: higher insulin and somatostatin and lower glucagon responses were obtained at high rather than low glucose. Glucose 56-63 insulin Homo sapiens 78-85 3539668-3 1986 From the quantal Mouse Convulsion Method using around 600 mice per sample to the quantitative Mouse Blood Glucose method using an average of 120 mice per sample in which the fall in the blood glucose levels is used to estimate the potency of insulin by its hypoglycaemic effect. Glucose 106-113 insulin Homo sapiens 242-249 3539668-3 1986 From the quantal Mouse Convulsion Method using around 600 mice per sample to the quantitative Mouse Blood Glucose method using an average of 120 mice per sample in which the fall in the blood glucose levels is used to estimate the potency of insulin by its hypoglycaemic effect. Glucose 192-199 insulin Homo sapiens 242-249 3754230-5 1986 In vitamin D-deficient epileptic and geriatric patients, the 2- and 3-h insulin levels after glucose ingestion were increased when compared with control values, and glucagon secretion was not suppressed by glucose. Glucose 93-100 insulin Homo sapiens 72-79 3536495-5 1986 The ingestion of glucose (lg X kg-1 body weight) 45 min before exercise produced a 50% rise in blood glucose and a 3-fold rise in plasma insulin at zero min of exercise. Glucose 17-24 insulin Homo sapiens 137-144 3005153-2 1986 After glucose administration, abnormal insulin release accompanied by glucose intolerance were observed, whereas the high glucagon circulating levels were only partially blocked after glucose or somatostatin infusion. Glucose 6-13 insulin Homo sapiens 39-46 3522450-7 1986 In conclusion, this study shows that the low glucose-induced thermogenesis in obese diabetics during glucose insulin infusion is mainly related to a reduced rate of glucose uptake; in addition, inhibition of gluconeogenesis by the glucose/insulin infusion may also contribute to decrease the thermogenic response. Glucose 45-52 insulin Homo sapiens 109-116 3522450-7 1986 In conclusion, this study shows that the low glucose-induced thermogenesis in obese diabetics during glucose insulin infusion is mainly related to a reduced rate of glucose uptake; in addition, inhibition of gluconeogenesis by the glucose/insulin infusion may also contribute to decrease the thermogenic response. Glucose 101-108 insulin Homo sapiens 109-116 3522450-7 1986 In conclusion, this study shows that the low glucose-induced thermogenesis in obese diabetics during glucose insulin infusion is mainly related to a reduced rate of glucose uptake; in addition, inhibition of gluconeogenesis by the glucose/insulin infusion may also contribute to decrease the thermogenic response. Glucose 101-108 insulin Homo sapiens 109-116 3525443-2 1986 With the glucose clamp technique, when infusing glucose and insulin simultaneously, one can study glucose metabolism under steady states glucose and insulin plasma levels. Glucose 9-16 insulin Homo sapiens 60-67 3525443-2 1986 With the glucose clamp technique, when infusing glucose and insulin simultaneously, one can study glucose metabolism under steady states glucose and insulin plasma levels. Glucose 9-16 insulin Homo sapiens 149-156 3525443-2 1986 With the glucose clamp technique, when infusing glucose and insulin simultaneously, one can study glucose metabolism under steady states glucose and insulin plasma levels. Glucose 48-55 insulin Homo sapiens 149-156 3525443-2 1986 With the glucose clamp technique, when infusing glucose and insulin simultaneously, one can study glucose metabolism under steady states glucose and insulin plasma levels. Glucose 48-55 insulin Homo sapiens 149-156 3525443-2 1986 With the glucose clamp technique, when infusing glucose and insulin simultaneously, one can study glucose metabolism under steady states glucose and insulin plasma levels. Glucose 48-55 insulin Homo sapiens 149-156 3510000-12 1986 During iv infusion of glucose, plasma insulin levels increased more in the hyperthyroid group (66% vs. 37%, P less than 0.05). Glucose 22-29 insulin Homo sapiens 38-45 3510000-19 1986 The data also demonstrate a diminished inhibitory effect of endogenous insulin on splanchnic glucose production, suggesting the presence of hepatic resistance to insulin in hyperthyroidism. Glucose 93-100 insulin Homo sapiens 71-78 2881028-14 1986 However it must be underlined that the insulin secretory effect of most nutrients requires the presence of glucose which is consequently a permissive factor. Glucose 107-114 insulin Homo sapiens 39-46 2881028-17 1986 Of the gastrointestinal hormones, GIP (gastric inhibitory polypeptide) appears to play the most important physiological role in potentiating the insulin secretory effect of glucose. Glucose 173-180 insulin Homo sapiens 145-152 3510013-3 1986 In late pregnancy the gestational diabetics revealed significantly elevated fasting glucose levels compared with the normal pregnant women and after the glucose challenge their insulin responses were significantly diminished and the suppression of glucagon less pronounced. Glucose 153-160 insulin Homo sapiens 177-184 3520622-4 1986 Diurnal variation of insulin sensitivity as judged by dividing glucose infusion rate by the ambient serum free insulin level (M/FI ration), was only noted in the low dose insulin infusion clamp study (AM:14.6 +/- 2.4, PM:10.5 +/- 1.1, p less than 0.05). Glucose 63-70 insulin Homo sapiens 21-28 3010407-10 1986 However, it has been shown that hepatic gluconeogenesis decreases during euglycaemic hyperinsulin clamp, mainly due to a decrease in the hepatic supply of glucose precursors following insulin action in extrahepatic tissues. Glucose 155-162 insulin Homo sapiens 90-97 2876502-6 1986 The insulin requirements during conventional subcutaneous insulin therapy were reduced by 28% (p less than 0.01) in seven patients without deterioration of metabolic control (mean blood glucose levels, 153.8) versus 154.7 mg/dl). Glucose 186-193 insulin Homo sapiens 4-11 3544165-5 1986 In addition, glucose given by stomach tube prior to ethionine did not prevent the action of ethionine, though it did maintain plasma glucose levels and prevented the decrease in plasma insulin and increase in plasma glucagon. Glucose 13-20 insulin Homo sapiens 185-192 3935405-6 1985 The blood glucose level during insulin-glibenclamide therapy was 35-45 mg/dl below that during insulin-placebo treatment at all time points investigated. Glucose 10-17 insulin Homo sapiens 31-38 3911958-0 1985 Inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose as a glucokinase inhibitor. Glucose 14-21 insulin Homo sapiens 33-40 3911958-1 1985 Pseudo-alpha- and pseudo-beta-DL-glucose, the isomers of 5-hydroxymethyl-1,2,3,4-cyclohexanetetrol with alpha-gluco and beta-gluco configurations, were used as synthetic analogs of glucose anomers to study the mechanism of glucose-stimulated insulin release by pancreatic islets. Glucose 33-40 insulin Homo sapiens 242-249 3911958-4 1985 The alpha-isomer, but not the beta-isomer, inhibited both glucose-stimulated insulin release (44% inhibition at 20 mM) and islet glucokinase activity (36% inhibition at 20 mM) in a concentration-dependent manner and to a comparable degree. Glucose 58-65 insulin Homo sapiens 77-84 3905459-1 1985 We have previously described, in insulin-dependent diabetic subjects (IDDM), a small, but significant, increase in the insulin clearance rate (ICR) during 0600-0800 h as compared with 0100-0300 h. To determine whether this increase was also seen at more physiologic levels of insulin replacement, we calculated ICR during euglycemic clamp studies in 13 patients with IDDM with a constant infusion of insulin at 20 mU/min/m2 and during insulin replacement from the Biostator GCIIS without exogenous glucose. Glucose 498-505 insulin Homo sapiens 119-126 3905459-1 1985 We have previously described, in insulin-dependent diabetic subjects (IDDM), a small, but significant, increase in the insulin clearance rate (ICR) during 0600-0800 h as compared with 0100-0300 h. To determine whether this increase was also seen at more physiologic levels of insulin replacement, we calculated ICR during euglycemic clamp studies in 13 patients with IDDM with a constant infusion of insulin at 20 mU/min/m2 and during insulin replacement from the Biostator GCIIS without exogenous glucose. Glucose 498-505 insulin Homo sapiens 119-126 3905459-1 1985 We have previously described, in insulin-dependent diabetic subjects (IDDM), a small, but significant, increase in the insulin clearance rate (ICR) during 0600-0800 h as compared with 0100-0300 h. To determine whether this increase was also seen at more physiologic levels of insulin replacement, we calculated ICR during euglycemic clamp studies in 13 patients with IDDM with a constant infusion of insulin at 20 mU/min/m2 and during insulin replacement from the Biostator GCIIS without exogenous glucose. Glucose 498-505 insulin Homo sapiens 119-126 3910489-0 1985 Insulin and C-peptide responses to glucose load in cystic fibrosis. Glucose 35-42 insulin Homo sapiens 0-7 3910489-0 1985 Insulin and C-peptide responses to glucose load in cystic fibrosis. Glucose 35-42 insulin Homo sapiens 12-21 3910489-1 1985 Immunoreactive Insulin and C-peptide responses to glucose load were estimated in patients with cystic fibrosis and in controls. Glucose 50-57 insulin Homo sapiens 27-36 3910489-2 1985 Both insulin and C-peptide responses were low in cystic fibrosis patients and the changes were more marked in those with glucose intolerance. Glucose 121-128 insulin Homo sapiens 5-12 3910489-2 1985 Both insulin and C-peptide responses were low in cystic fibrosis patients and the changes were more marked in those with glucose intolerance. Glucose 121-128 insulin Homo sapiens 17-26 3912243-8 1985 An improvement was seen at both submaximal and maximal insulin levels in both groups, correlating with improvement in glucose tolerance in the diabetic subjects. Glucose 118-125 insulin Homo sapiens 55-62 3912243-15 1985 This mechanism, as well as the improved peripheral insulin responsiveness seen in the whole body and also seen at the cellular level, probably both contribute to an improvement in glucose tolerance. Glucose 180-187 insulin Homo sapiens 51-58 3936737-1 1985 Interactions between naloxone, phentolamine and lysine acetylsalicylate upon glucose induced insulin release. Glucose 77-84 insulin Homo sapiens 93-100 3936737-2 1985 Non insulin-dependent diabetes mellitus (Type II) is characterized by the loss of the acute insulin response to glucose. Glucose 112-119 insulin Homo sapiens 4-11 3936737-3 1985 Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. Glucose 121-128 insulin Homo sapiens 101-108 3936737-5 1985 In diabetics, acute insulin responses to glucose were significantly increased by all the agents tested (naloxone, phentolamine and lysine acetylsalicylate), but only the cyclooxygenase inhibitor significantly augmented second phase insulin secretion and glucose disappearance rates. Glucose 41-48 insulin Homo sapiens 20-27 3936737-5 1985 In diabetics, acute insulin responses to glucose were significantly increased by all the agents tested (naloxone, phentolamine and lysine acetylsalicylate), but only the cyclooxygenase inhibitor significantly augmented second phase insulin secretion and glucose disappearance rates. Glucose 254-261 insulin Homo sapiens 20-27 3936737-6 1985 The combined infusion of the three agents caused a striking increase of the acute insulin response to glucose (response before: 3 +/- 2 uU/ml; after: 22 +/- 6 uU/ml, p less than 0.01). Glucose 102-109 insulin Homo sapiens 82-89 3936737-8 1985 In normals, insulin responses to glucose were also significantly increased by the combined infusions of the drugs, but to a significantly lesser extent than that of diabetics. Glucose 33-40 insulin Homo sapiens 12-19 3936737-9 1985 This different degree of insulin potentiation between normals and diabetics under the infusion of the three agents persisted even when the prestimulus glucose level of normals was matched to that of diabetics by a glucose infusion. Glucose 151-158 insulin Homo sapiens 25-32 3936737-9 1985 This different degree of insulin potentiation between normals and diabetics under the infusion of the three agents persisted even when the prestimulus glucose level of normals was matched to that of diabetics by a glucose infusion. Glucose 214-221 insulin Homo sapiens 25-32 3910408-2 1985 The lowered insulin response (P less than 0.001) to glucose challenge during heating and the subsequent prolonged hyperglycemia (P less than 0.001) after heating were observed, when compared to OGTT under thermoneutral conditions (23 degrees C). Glucose 52-59 insulin Homo sapiens 12-19 3912201-7 1985 However, adults with circulating ICA were characterized by a significantly lower insulin response to glucose. Glucose 101-108 insulin Homo sapiens 81-88 3914416-5 1985 The changes in the plasma insulin level almost paralleled those in the plasma glucose level. Glucose 78-85 insulin Homo sapiens 26-33 3910533-0 1985 C-peptide to insulin molar ratios at fasting and after oral glucose in 247 healthy subjects. Glucose 60-67 insulin Homo sapiens 13-20 3908420-0 1985 Let myth of amended insulin/glucose ratio die. Glucose 28-35 insulin Homo sapiens 20-27 2999163-0 1985 Insulin stimulation of glucose transport and metabolism in a human Wilms" tumor-derived myoblast-like cell line: modulation of hormone effects by glucose deprivation. Glucose 23-30 insulin Homo sapiens 0-7 2999163-5 1985 Insulin stimulated net glucose uptake and incorporation into glycogen in a dose-dependent manner in glucose-fed and starved cells. Glucose 23-30 insulin Homo sapiens 0-7 2999163-5 1985 Insulin stimulated net glucose uptake and incorporation into glycogen in a dose-dependent manner in glucose-fed and starved cells. Glucose 100-107 insulin Homo sapiens 0-7 2999163-6 1985 These insulin responses were markedly enhanced in glucose-starved cells. Glucose 50-57 insulin Homo sapiens 6-13 2999163-7 1985 Insulin accelerated 2-deoxyglucose transport in glucose-fed cells but did not further stimulate basal glucose transport in glucose-deprived cells. Glucose 27-34 insulin Homo sapiens 0-7 2999163-7 1985 Insulin accelerated 2-deoxyglucose transport in glucose-fed cells but did not further stimulate basal glucose transport in glucose-deprived cells. Glucose 48-55 insulin Homo sapiens 0-7 2999163-7 1985 Insulin accelerated 2-deoxyglucose transport in glucose-fed cells but did not further stimulate basal glucose transport in glucose-deprived cells. Glucose 48-55 insulin Homo sapiens 0-7 2999163-8 1985 Insulin increased the incorporation of [3H]leucine into protein in glucose-fed or -starved MBL cells equally. Glucose 67-74 insulin Homo sapiens 0-7 2999163-11 1985 We conclude that MBL cells resemble fibroblasts in their insulin-independent stimulation of glucose transport in response to glucose-deprivation; when provided with glucose, they respond to insulin like fibroblasts. Glucose 92-99 insulin Homo sapiens 57-64 2999163-11 1985 We conclude that MBL cells resemble fibroblasts in their insulin-independent stimulation of glucose transport in response to glucose-deprivation; when provided with glucose, they respond to insulin like fibroblasts. Glucose 125-132 insulin Homo sapiens 57-64 2999163-12 1985 However, after brief glucose-starvation, the stimulated glucose transport system is no longer insulin-responsive in MBL cells, while pathways leading to the synthesis of macromolecules demonstrate preserved or enhanced stimulation by insulin, suggesting that these cells may serve as models to study the regulation of receptor-response coupling by the metabolic milieu. Glucose 56-63 insulin Homo sapiens 94-101 3840492-4 1985 Total glucose oxidation corresponded, in hyperthyroid patients, to the highest rate obtained with progressively increasing insulin and glucose administration in normal man. Glucose 6-13 insulin Homo sapiens 123-130 3902865-3 1985 The first phase (0-10 min) insulin secretory response to iv glucose was significantly lower in both lean and obese former GDM compared to that in normal women (3,480 +/- 548% vs. 8,234 +/- 1,337% basal . Glucose 60-67 insulin Homo sapiens 27-34 3902865-5 1985 The second phase (10-60 min) insulin response to glucose was also significantly lower in lean former GDM women and tended to be lower in obese former GDM women compared to that in their respective controls. Glucose 49-56 insulin Homo sapiens 29-36 3902868-4 1985 The decrement in blood glucose levels after injection of mutant insulin was 22.6% that after injection of normal insulin. Glucose 23-30 insulin Homo sapiens 64-71 3902868-4 1985 The decrement in blood glucose levels after injection of mutant insulin was 22.6% that after injection of normal insulin. Glucose 23-30 insulin Homo sapiens 113-120 3902868-5 1985 The blood glucose-lowering effect of the mutant insulin, evaluated by the time required to reach the nadir, was slightly prolonged (30 vs. 45 min). Glucose 10-17 insulin Homo sapiens 48-55 2856762-8 1985 The ability of glucose, but not xylose, to induce a similar degree of hypotension suggests that insulin may play an important role in postcibal hypotension. Glucose 15-22 insulin Homo sapiens 96-103 2933497-7 1985 Mean glucose disappearance rate during an insulin tolerance test was 6.7%/min in lean controls, 5.19%/min in obese controls, and 2.35%/min in study patients (P less than 0.02). Glucose 5-12 insulin Homo sapiens 42-49 3001273-4 1985 Systemic glucose concentration decreased only during the highest dose insulin infusion. Glucose 9-16 insulin Homo sapiens 70-77 3001273-5 1985 In eight subjects who received insulin during euglycemic glucose clamping, FVR also decreased. Glucose 57-64 insulin Homo sapiens 31-38 3906353-3 1985 Similar changes in blood glucose occurred during insulin infusion but insulin concentrations were higher in women. Glucose 25-32 insulin Homo sapiens 49-56 3906353-5 1985 Significant differences were found between normal men and women for the effect of insulin upon blood glucose concentration. Glucose 101-108 insulin Homo sapiens 82-89 3906363-2 1985 In general, atherosclerosis of the coronary, cerebral, and peripheral arteries is associated with abnormally high insulin responses to oral glucose. Glucose 140-147 insulin Homo sapiens 114-121 3906363-4 1985 Populations who are at high risk for cardiovascular disease have higher insulin responses to oral glucose than those at lower risk. Glucose 98-105 insulin Homo sapiens 72-79 3906363-5 1985 Prospective studies carried out in Australia, Finland, and France have shown that elevated insulin levels, either fasting or in response to oral glucose, have a predictive role in the development of cardiovascular disease. Glucose 145-152 insulin Homo sapiens 91-98 3909371-0 1985 Fasting plasma C-peptide levels in health and impaired glucose tolerance: relations to blood glucose and relative body weight. Glucose 55-62 insulin Homo sapiens 15-24 3909371-2 1985 Fasting C-peptide levels were correlated with relative body weight (r = 0.48) and fasting blood glucose concentrations (r = 0.43), yielding a multiple correlation coefficient of 0.56, and the multiple regression equation: FCP (nmol/l) = -0.89 + 0.61 X RBW + 0.16 X FBG (mmol/l). Glucose 96-103 insulin Homo sapiens 8-17 3909371-4 1985 In 26 subjects with impaired glucose tolerance, fasting plasma C-peptide levels were even more strongly correlated with relative body weight (r = 0.63) and fasting blood glucose concentrations (r = 0.47). Glucose 29-36 insulin Homo sapiens 63-72 3909372-3 1985 The insulin response to glucose was expressed as the ratio of the area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG). Glucose 24-31 insulin Homo sapiens 4-11 3911614-5 1985 Short term effects of insulin on the exocrine pancreas in vitro, using isolated pancreatic acini, like stimulation of glucose- and aminoacid uptake, stimulation of proteinsynthesis, phosphorylation of certain proteins and stimulation of CCK induced amylase release are discussed. Glucose 118-125 insulin Homo sapiens 22-29 3512209-0 1986 Acute insulin response to glucagon, tolbutamide, and glucose in non-insulin-dependent diabetes of the young. Glucose 53-60 insulin Homo sapiens 6-13 3512209-1 1986 Acute insulin release in response to maximal intravenous doses of glucose (0.5 g/kg), tolbutamide (1 g), and glucagon (1 mg) was studied in 10 subjects with non-insulin-dependent diabetes of the young (NIDDY) and 10 age-, sex-, and weight-matched controls. Glucose 66-73 insulin Homo sapiens 6-13 3514067-2 1986 We reported previously on impaired basal and insulin-stimulated glucose utilization in adipocytes from Type 1 diabetic subjects. Glucose 64-71 insulin Homo sapiens 45-52 3514067-7 1986 We conclude that continuous subcutaneous insulin infusion of Type 1 diabetic patients for 6 months aggravates the defects in basal (non-insulin-stimulated) and maximally insulin-stimulated glucose utilization of isolated adipocytes despite an optimization of glycaemic control and a near-normalization of plasma metabolites. Glucose 189-196 insulin Homo sapiens 41-48 3514342-1 1986 In this report, we present an analysis of glucose and insulin responses during oral glucose tolerance tests in 369 siblings of Type 1 diabetic patients. Glucose 84-91 insulin Homo sapiens 54-61 3514343-3 1986 Despite higher glucose increases, immunoreactive insulin and connecting peptide responses after oral glucose were delayed in diabetic patients. Glucose 101-108 insulin Homo sapiens 49-56 3514344-1 1986 Addition of highly purified human Interleukin-1 to the culture medium of isolated rat islets of Langerhans for 6 days led to 88% inhibition of glucose-induced insulin-release, reduction of islet contents of insulin and glucagon to 31% and 8% respectively, and disintegration of the islets. Glucose 143-150 insulin Homo sapiens 159-166 3957707-4 1986 This confirms the concept of the third trimester as a catabolic phase within the maternal system, and provides support for the view that the insulin resistance of pregnancy may be a compensatory response to overcome the inhibitive effects of metabolites such as fatty acids on peripheral uptake of glucose. Glucose 298-305 insulin Homo sapiens 141-148 3517111-9 1986 The sucrose diet generally gave lower insulin levels in response to the glucose load. Glucose 72-79 insulin Homo sapiens 38-45 2866196-2 1986 In one series of experiments, normalization of blood glucose was achieved by Biostator-controlled feedback infusion of insulin. Glucose 53-60 insulin Homo sapiens 119-126 3944257-6 1986 These findings suggest the possibility that, under conditions of high ambient glucose, excess glucose entry in cells that are insulin independent for glucose transport may, directly or indirectly, perturb DNA function. Glucose 78-85 insulin Homo sapiens 126-133 3944257-6 1986 These findings suggest the possibility that, under conditions of high ambient glucose, excess glucose entry in cells that are insulin independent for glucose transport may, directly or indirectly, perturb DNA function. Glucose 94-101 insulin Homo sapiens 126-133 3944257-6 1986 These findings suggest the possibility that, under conditions of high ambient glucose, excess glucose entry in cells that are insulin independent for glucose transport may, directly or indirectly, perturb DNA function. Glucose 94-101 insulin Homo sapiens 126-133 3542627-2 1986 When the response of insulin secretion to glucose administration during clonidine therapy was compared with that after 12 days of wash-out for clonidine in this patient (who was then receiving phentolamine mesylate), there was a marked suppression of insulin secretion to stimulation by intravenous glucose during oral clonidine therapy. Glucose 42-49 insulin Homo sapiens 21-28 3542627-2 1986 When the response of insulin secretion to glucose administration during clonidine therapy was compared with that after 12 days of wash-out for clonidine in this patient (who was then receiving phentolamine mesylate), there was a marked suppression of insulin secretion to stimulation by intravenous glucose during oral clonidine therapy. Glucose 42-49 insulin Homo sapiens 251-258 3542627-2 1986 When the response of insulin secretion to glucose administration during clonidine therapy was compared with that after 12 days of wash-out for clonidine in this patient (who was then receiving phentolamine mesylate), there was a marked suppression of insulin secretion to stimulation by intravenous glucose during oral clonidine therapy. Glucose 299-306 insulin Homo sapiens 251-258 3554221-0 1986 Insulin response in obese and nonobese offspring of conjugal Indian diabetic parents with increasing glucose intolerance. Glucose 101-108 insulin Homo sapiens 0-7 3304396-0 1986 [Insulin secretion and utilization of insulin in piglets after insulin, arginine and glucose loads]. Glucose 85-92 insulin Homo sapiens 1-8 3081885-3 1986 A peak rise of insulin after glucose administration was absent in patients managed with SLD, whereas an insulin level during the arginine test reached 302 +/- 12.7 pmol/l. Glucose 29-36 insulin Homo sapiens 15-22 3321096-2 1986 Both hepoxilins are active in stimulating the release of insulin from these cells in the presence of 10 mM glucose. Glucose 107-114 insulin Homo sapiens 57-64 3532556-0 1986 [Glucose clamping--a modern method for research on insulin secretion and resistance]. Glucose 1-8 insulin Homo sapiens 51-58 3002352-0 1985 Regulation of the glucose enhanced insulin pool. Glucose 18-25 insulin Homo sapiens 35-42 3002352-1 1985 Exposure of islets to high levels of glucose at a critical time leads to enhanced insulin release when later stimulated by glucose. Glucose 37-44 insulin Homo sapiens 82-89 3002352-1 1985 Exposure of islets to high levels of glucose at a critical time leads to enhanced insulin release when later stimulated by glucose. Glucose 123-130 insulin Homo sapiens 82-89 3911958-5 1985 These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release. Glucose 54-61 insulin Homo sapiens 73-80 3911958-5 1985 These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release. Glucose 54-61 insulin Homo sapiens 281-288 3911958-5 1985 These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 73-80 3911958-5 1985 These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 281-288 3911958-5 1985 These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 73-80 3911958-5 1985 These results strongly suggest that the inhibition of glucose-stimulated insulin release by pseudo-alpha-DL-glucose is due to the inhibition of islet glucokinase by the glucose analog, providing additional evidence for the essential role of islet glucokinase in glucose-stimulated insulin release. Glucose 108-115 insulin Homo sapiens 281-288 3909372-3 1985 The insulin response to glucose was expressed as the ratio of the area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG). Glucose 24-31 insulin Homo sapiens 81-88 3909372-3 1985 The insulin response to glucose was expressed as the ratio of the area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG). Glucose 110-117 insulin Homo sapiens 4-11 3909372-6 1985 With application of these indices in the non-obese groups, there was an increased mean total insulin release (AUCI, delta AUCI) while the mean insulin response to glucose (delta AUCI/delta AUCG) was decreased in GI-subjects compared with normoglycaemic subjects. Glucose 163-170 insulin Homo sapiens 143-150 3002669-7 1985 Therefore the effect of adrenaline on insulin release is mediated by way of inhibitory alpha 2 adrenoceptors in the pancreas, while the release of insulin in response to glucose in a resting subject is independent of the alpha-adrenergic system. Glucose 170-177 insulin Homo sapiens 147-154 2864239-9 1985 Single islet cell first and second phase insulin responses to 5.5 mM glucose were enhanced 2.2-fold (P less than 0.01) and 2.8-fold (P less than 0.05), respectively, in the presence of exogenous glucagon, resulting in secretory profiles characteristic of intact islets. Glucose 69-76 insulin Homo sapiens 41-48 2864239-10 1985 Reaggregation of single islet cells was associated with markedly increased first and second phase insulin responses to both glucose and arginine stimulation. Glucose 124-131 insulin Homo sapiens 98-105 2951120-0 1985 Defective non-insulin-mediated and insulin-mediated glucose transport and metabolism in adipocytes from obese and lean patients with untreated type 2 diabetes mellitus. Glucose 52-59 insulin Homo sapiens 35-42 2951120-3 1985 In lean diabetic patients both non-insulin-mediated (basal) and maximally insulin-stimulated glucose transport and metabolism were significantly reduced (all p less than 0.01). Glucose 93-100 insulin Homo sapiens 35-42 2951120-3 1985 In lean diabetic patients both non-insulin-mediated (basal) and maximally insulin-stimulated glucose transport and metabolism were significantly reduced (all p less than 0.01). Glucose 93-100 insulin Homo sapiens 74-81 2951120-6 1985 Insulin-stimulated glucose transport and metabolism were significantly reduced (p less than 0.01, p less than 0.05). Glucose 19-26 insulin Homo sapiens 0-7 3899812-0 1985 Insulin-mediated glucose uptake in nondialyzed and dialyzed uremic insulin-dependent diabetic subjects. Glucose 17-24 insulin Homo sapiens 0-7 3899812-5 1985 Step 3 glucose infusion rate (GIR), the last 30 min of the infusion period, was extremely suppressed in nondialyzed uremic IDD subjects, amounting to 53% of that in healthy subjects (7.7 +/- 0.7 versus 14.4 +/- 0.9 mg X kg-1 X min-1, P less than 0.001) indicating severe insulin resistance in peripheral tissues. Glucose 7-14 insulin Homo sapiens 271-278 3899815-9 1985 It is concluded that fasting and glucose refeeding are associated with marked alterations in the antilipolytic effect of insulin on human fat cells of obese subjects. Glucose 33-40 insulin Homo sapiens 121-128 3910497-1 1985 To determine whether hyperaminoacidaemia may modify insulin-mediated glucose disposal, normal subjects were studied with the euglycaemic glucose-clamp technique, with or without an amino acid infusion, at a rate sufficient to duplicate the plasma concentration of most amino acids. Glucose 69-76 insulin Homo sapiens 52-59 3936738-1 1985 The effect of sulphonylurea therapy for 3 weeks on glucose-stimulated insulin secretion and insulin resistance was studied in Type 2 diabetic patients. Glucose 51-58 insulin Homo sapiens 70-77 2867040-3 1985 Indirect evidence suggests that changes in the serum potassium are at least contributory, although the principal mechanism of thiazide-induced hyperglycemia is probably a reduction in the insulin response to glucose. Glucose 208-215 insulin Homo sapiens 188-195 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 18-25 insulin Homo sapiens 42-49 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 18-25 insulin Homo sapiens 143-150 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 18-25 insulin Homo sapiens 143-150 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 159-166 insulin Homo sapiens 143-150 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 159-166 insulin Homo sapiens 143-150 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 159-166 insulin Homo sapiens 143-150 3908398-4 1985 administration of glucose with increasing insulin doses under somatostatin coverage was used to establish the dose-response characteristics of insulin-induced glucose clearance [insulin vs. Kg (glucose disappearance rate, %/min). Glucose 159-166 insulin Homo sapiens 143-150 3908398-7 1985 In both lean and obese subjects, BHI and pork insulin had comparable effects on glucose clearance. Glucose 80-87 insulin Homo sapiens 46-53 3908398-8 1985 Similarly, the effect of s.c. insulin on the serum glucose values during OGTT was the same when BHI or pork insulin were used. Glucose 51-58 insulin Homo sapiens 30-37 3900120-5 1985 More specifically, hyperinsulinemic patients with mild diabetes (fasting plasma glucose, less than 140 mg/dl) maintained normal ambient FFA levels, while FFA concentrations were significantly elevated in patients with severe NIDDM (fasting plasma glucose, greater than 250 mg/dl), with insulin concentrations comparable to those in normal subjects. Glucose 80-87 insulin Homo sapiens 24-31 3900120-5 1985 More specifically, hyperinsulinemic patients with mild diabetes (fasting plasma glucose, less than 140 mg/dl) maintained normal ambient FFA levels, while FFA concentrations were significantly elevated in patients with severe NIDDM (fasting plasma glucose, greater than 250 mg/dl), with insulin concentrations comparable to those in normal subjects. Glucose 247-254 insulin Homo sapiens 24-31 2865274-1 1985 Although insulin is extremely potent in regulating glucose transport in insulin-sensitive tissues, all tissues are capable of taking up glucose by facilitated diffusion by means of a noninsulin-mediated glucose uptake (NIMGU) system. Glucose 51-58 insulin Homo sapiens 9-16 3003299-5 1985 In control studies there was a profound fall in serum glucose and plasma potassium after insulin, associated with increments in plasma renin activity, which correlated with those of aldosterone but not with those of ACTH and cortisol. Glucose 54-61 insulin Homo sapiens 89-96 3003299-7 1985 During converting enzyme inhibition the insulin-induced decrements in glucose and potassium, as well as the increments in ACTH, cortisol and aldosterone, were similar to those observed in control studies, whereas the increments in plasma renin activity were much greater. Glucose 70-77 insulin Homo sapiens 40-47 3905456-1 1985 The effect of insulin in physiological concentrations on hormone secretion by human term trophoblast cell culture was studied in relation to insulin control of glucose transport and utilization. Glucose 160-167 insulin Homo sapiens 141-148 3905456-4 1985 Phloridzin, an inhibitor of glucose transport, interfered with the stimulatory effect of insulin on hPL secretion, but stimulated insulin inhibition of estradiol secretion when added by itself. Glucose 28-35 insulin Homo sapiens 89-96 3905456-5 1985 The results indicate that hPL response to insulin is dependent on glucose transport, but is independent of glycolysis. Glucose 66-73 insulin Homo sapiens 42-49 3908590-9 1985 In addition, insulin binding correlated significantly with Insulin Sum, Glucose Sum at 75g OGTT, TG and FFA in serum. Glucose 72-79 insulin Homo sapiens 13-20 3904751-7 1985 This study suggests that de novo synthesis of phosphatidic acid provides a link between glucose metabolism and the release of insulin. Glucose 88-95 insulin Homo sapiens 126-133 4050917-1 1985 Insulin-dependent diabetic women without adequate glucose control have a higher rate of spontaneous abortions than does the general population of pregnant women. Glucose 50-57 insulin Homo sapiens 0-7 3901765-7 1985 We conclude that in third trimester, pregnant nondiabetic and insulin-dependent diabetic subjects have parallel hepatic and peripheral responsiveness to glucose and insulin compared to their nonpregnant counterparts. Glucose 153-160 insulin Homo sapiens 62-69 3902039-1 1985 Care of the diabetic pregnant woman requires a proper understanding of anticipated changes in insulin therapy as a guide for establishing and maintaining strict glucose control. Glucose 161-168 insulin Homo sapiens 94-101 2994586-2 1985 Two patients with insulinomas had unusual glucose and insulin-secretory dynamics in response to prolonged fasting. Glucose 42-49 insulin Homo sapiens 18-25 2994586-6 1985 The diagnosis of an insulinoma can usually be made by obtaining simultaneous glucose and insulin values during a prolonged supervised fast. Glucose 77-84 insulin Homo sapiens 20-27 3908178-3 1985 The infusion of the three agents at doses known to affect insulin secretion (10 micrograms/min, 15 ng/kg/min, 0.5 mg im, respectively) produced the expected inhibitory effects upon insulin responses to an intravenous glucose challenge. Glucose 217-224 insulin Homo sapiens 58-65 3908178-5 1985 In particular, the acute insulin response to glucose decreased from a control value of 50 +/- 9 microU/ml to a value of 21 +/- 6 microU/ml (p less than 0.02). Glucose 45-52 insulin Homo sapiens 25-32 3908178-6 1985 The inhibitory effect of epinephrine (15 ng/kg/min) upon glucose-induced insulin secretion was partially reversed by sodium salicylate, an inhibitor of endogenous prostaglandin synthesis, which increased but not normalized, either the acute insulin response and the glucose disappearance rates. Glucose 57-64 insulin Homo sapiens 73-80 3908179-7 1985 In all women the fasting plasma insulin levels and the glucose--or protein--induced insulin response is increased in pregnancy. Glucose 55-62 insulin Homo sapiens 84-91 3930321-1 1985 The effects of prior high-intensity cycle exercise (85% VO2 max) to muscular exhaustion on basal and insulin-stimulated glucose metabolism were studied in obese, insulin-resistant, and normal subjects. Glucose 120-127 insulin Homo sapiens 101-108 3930321-6 1985 In the obese subjects, insulin-stimulated glucose disposal was increased significantly, but not totally corrected to normal. Glucose 42-49 insulin Homo sapiens 23-30 3930321-8 1985 Thus, the major effect of prior exercise was to increase insulin-stimulated glucose disposal in the obese subjects and to alter the pathways of glucose metabolism to favor NOGD and decrease glucose oxidation. Glucose 76-83 insulin Homo sapiens 57-64 3934020-3 1985 An increase in insulin release was observed when microencapsulated islets were stimulated by glucose+theophylline, and when microencapsulated RINm5F cells were stimulated by arginine+theophylline. Glucose 93-100 insulin Homo sapiens 15-22 4043555-4 1985 The insulin sensitivity index (SI) was determined after an intravenous glucose tolerance test (IVGTT) using the minimal model of insulin kinetics. Glucose 71-78 insulin Homo sapiens 4-11 2866155-3 1985 Although values after lunch and the evening snack were not significantly different, overall mean 24 hr plasma glucose concentrations were significantly less with WY-41,747 plus insulin than with insulin alone (136 +/- 9 vs. 176 +/- 13, P less than 0.05). Glucose 110-117 insulin Homo sapiens 177-184 3905555-7 1985 There was a significant decrease in mean fasting plasma glucose (P less than 0.001) and a rise in insulin (P less than 0.05) levels after insulin treatment. Glucose 56-63 insulin Homo sapiens 138-145 3905556-4 1985 Glucose disposal at maximal insulin levels was 11.9 +/- 0.4 mg/kg/min in normals, with a 29% decrease in obese and a 42% decrease in Cushing"s syndrome patients. Glucose 0-7 insulin Homo sapiens 28-35 2863282-4 1985 Glucose, alpha-ketoisocaproic acid, theophylline, glucagon, and tolbutamide each stimulated insulin release 2- to 3-fold and somatostatin release 1.5- to 2-fold. Glucose 0-7 insulin Homo sapiens 92-99 2863282-5 1985 Epinephrine and somatostatin both inhibited glucose-stimulated insulin release. Glucose 44-51 insulin Homo sapiens 63-70 2863282-7 1985 Subcultured islet cells released insulin into the medium during a subsequent 8-day period and when challenged with glucose responded with a 1.6-fold increase in insulin output. Glucose 115-122 insulin Homo sapiens 33-40 3897260-7 1985 Evaluation of the insulin-glycerol mixture used in the pump revealed that moderate degradation of insulin occurred in the pump during the 21-day flow cycle, resulting in 6-12% increases in fasting blood glucose levels; in addition, higher mol wt species of immunoreactive insulin were present in the patients" serum. Glucose 203-210 insulin Homo sapiens 18-25 3897260-7 1985 Evaluation of the insulin-glycerol mixture used in the pump revealed that moderate degradation of insulin occurred in the pump during the 21-day flow cycle, resulting in 6-12% increases in fasting blood glucose levels; in addition, higher mol wt species of immunoreactive insulin were present in the patients" serum. Glucose 203-210 insulin Homo sapiens 98-105 3897260-7 1985 Evaluation of the insulin-glycerol mixture used in the pump revealed that moderate degradation of insulin occurred in the pump during the 21-day flow cycle, resulting in 6-12% increases in fasting blood glucose levels; in addition, higher mol wt species of immunoreactive insulin were present in the patients" serum. Glucose 203-210 insulin Homo sapiens 98-105 2934464-1 1985 In order to verify the relationship between insulin resistance and hyperandrogenism in Polycystic ovary disease (PCOD), circulating levels of insulin in response to oral glucose tolerance test (OGTT) were assessed in 23 PCOD patients and 10 matched control subjects without obesity, acanthosis nigricans and impaired glucose tolerance. Glucose 170-177 insulin Homo sapiens 142-149 3900631-2 1985 Insulin sensitivity is determined from the amount of glucose metabolized under steady state conditions. Glucose 53-60 insulin Homo sapiens 0-7 3900631-5 1985 Insulin sensitivity as measured by M (glucose metabolized), MCRg (metabolic clearance of glucose), and M/I ratio (glucose metabolized per unit insulin) were all significantly decreased in the diabetic subjects (P less than 0.005). Glucose 38-45 insulin Homo sapiens 0-7 3900631-5 1985 Insulin sensitivity as measured by M (glucose metabolized), MCRg (metabolic clearance of glucose), and M/I ratio (glucose metabolized per unit insulin) were all significantly decreased in the diabetic subjects (P less than 0.005). Glucose 89-96 insulin Homo sapiens 0-7 3900631-5 1985 Insulin sensitivity as measured by M (glucose metabolized), MCRg (metabolic clearance of glucose), and M/I ratio (glucose metabolized per unit insulin) were all significantly decreased in the diabetic subjects (P less than 0.005). Glucose 89-96 insulin Homo sapiens 0-7 3908907-4 1985 In human adipocytes, half-maximal stimulation of initial rates of glucose uptake was observed at 11.6 +/- 5.1 vs 2.9 +/- 1.3 pmol/l for sulphated and neutral insulin respectively, and half-maximal inhibition of lipolysis at 31.0 +/- 13.5 vs 7.3 +/- 2.5 pmol/l respectively. Glucose 66-73 insulin Homo sapiens 158-165 3908907-6 1985 However, in rat adipocytes the biological potency of sulphated insulin was found to be much lower than anticipated from the binding data, half-maximal stimulation of initial rates of glucose uptake being observed at 757 +/- 299 vs 35 +/- 13 pmol/l respectively and half-maximal inhibition of lipolysis at 35.9 +/- 12.1 vs 1.5 +/- 0.5 pmol/l respectively. Glucose 183-190 insulin Homo sapiens 63-70 2995870-5 1985 The results revealed anomalies in insulinaemia and glycaemia behaviour such as have already, in part, been described in organic hyperinsulinism, e.g. the discrepancy between insulin and glucose levels after prolonged fasting. Glucose 186-193 insulin Homo sapiens 34-41 2995870-11 1985 The mechanism behind the lipid mobilisation anomalies of insulinomas is also discussed in the light of its apparent connection with the glucose/insulin interaction characteristic of the condition. Glucose 136-143 insulin Homo sapiens 57-64 3931463-2 1985 In adipocytes from patients with type II non-insulin-dependent diabetes, there is increasing evidence indicating that sulfonylureas ameliorate a post-receptor defect in insulin action by potentiating the insulin-stimulated glucose transport normally seen in these cells. Glucose 223-230 insulin Homo sapiens 169-176 3931463-4 1985 With the use of cytochalasin B, a potent competitive inhibitor of glucose transport, glucose-sensitive cytochalasin B binding was studied in basal and insulin-stimulated adipocytes from control and sulfonylurea-treated tissue. Glucose 85-92 insulin Homo sapiens 151-158 3931463-6 1985 It did, however, increase the insulin-induced recruitment of the glucose carrier from the microsome to the plasma membrane by 27 to 31 percent. Glucose 65-72 insulin Homo sapiens 30-37 3931463-7 1985 This suggests that the molecular mechanism of sulfonylurea-enhanced insulin-stimulated glucose transport is the recruitment of glucose transporters from an intracellular microsomal storage pool to the plasma membrane. Glucose 87-94 insulin Homo sapiens 68-75 3898692-4 1985 By infusing insulin during the euglycaemic clamp similar levels were reached during both glucose clamps. Glucose 89-96 insulin Homo sapiens 12-19 3898803-6 1985 Insulin levels correlated with N-bal only in the presence of dietary glucose (r = 0.72, p less than .01). Glucose 69-76 insulin Homo sapiens 0-7 3899013-1 1985 Homogenates of insulin-producing tumoral cells catalyzed the phosphorylation of glucose, mannose, and fructose. Glucose 80-87 insulin Homo sapiens 15-22 3899013-7 1985 Although glucose caused a modest increase in insulin output from the tumoral cells, this effect was saturated at a low glucose concentration (2.8 mM) and less marked than that of other secretagogues (e.g., L-leucine, L-ornithine, or forskolin). Glucose 9-16 insulin Homo sapiens 45-52 3899013-9 1985 These findings point to regulatory mechanisms distal to glucose phosphorylation in the control of glucose metabolism in insulin-producing cells. Glucose 56-63 insulin Homo sapiens 120-127 3899013-9 1985 These findings point to regulatory mechanisms distal to glucose phosphorylation in the control of glucose metabolism in insulin-producing cells. Glucose 98-105 insulin Homo sapiens 120-127 2935094-2 1985 We studied the effects of several regimens of insulin therapy on serum glucose (SG) in 24 noninsulin dependent diabetic patients (NIDDs). Glucose 71-78 insulin Homo sapiens 46-53 4041955-8 1985 The profiles of blood glucose, insulin and glucose infusion rates provided by the artificial endocrine pancreas suggested that the insulin resistance began to be reversed shortly after removal of the phaeochromocytoma. Glucose 22-29 insulin Homo sapiens 131-138 4041955-8 1985 The profiles of blood glucose, insulin and glucose infusion rates provided by the artificial endocrine pancreas suggested that the insulin resistance began to be reversed shortly after removal of the phaeochromocytoma. Glucose 43-50 insulin Homo sapiens 131-138 3902302-2 1985 The rate of glucose utilization and its rate of oxidation are largely determined by the maternal glucose concentration and are mediated in part by insulin. Glucose 12-19 insulin Homo sapiens 147-154 3902302-3 1985 Thus, glucose and insulin act together to substitute glucose oxidation for the oxidation of other energy substrates and to direct glucose carbon into glycogen, fat, and protein accretion. Glucose 53-60 insulin Homo sapiens 18-25 2863188-0 1985 Quantitation of insulin-stimulated glucose disposal in patients with non-insulin-dependent diabetes mellitus. Glucose 35-42 insulin Homo sapiens 16-23 2863188-2 1985 To quantify the amount of glucose taken up in response to a known increase in insulin concentration, two consecutive studies were performed on 10 patients with mild to moderate NIDDM (mean fasting glucose = 146 mg/dl) and 10 normal subjects. Glucose 26-33 insulin Homo sapiens 78-85 2863188-3 1985 Endogenous insulin secretion was inhibited by somatostatin and plasma glucose level maintained at 180 mg/dl for 5. Glucose 70-77 insulin Homo sapiens 11-18 2863188-7 1985 Thus, insulin-stimulated glucose uptake in patients with NIDDM was only one-fifth of that in normals, and accounted for only 31% (38 divided by 121) of total glucose disposal during the clamp study. Glucose 25-32 insulin Homo sapiens 6-13 2863188-7 1985 Thus, insulin-stimulated glucose uptake in patients with NIDDM was only one-fifth of that in normals, and accounted for only 31% (38 divided by 121) of total glucose disposal during the clamp study. Glucose 158-165 insulin Homo sapiens 6-13 2863188-8 1985 These data indicate that the majority of previous insulin clamp studies of in vivo insulin action in patients with NIDDM, in which total glucose disposal and insulin-stimulated glucose disposal have been equated, have underestimated the magnitude of insulin resistance present in NIDDM. Glucose 137-144 insulin Homo sapiens 50-57 2863188-8 1985 These data indicate that the majority of previous insulin clamp studies of in vivo insulin action in patients with NIDDM, in which total glucose disposal and insulin-stimulated glucose disposal have been equated, have underestimated the magnitude of insulin resistance present in NIDDM. Glucose 177-184 insulin Homo sapiens 50-57 2993084-1 1985 Defective glucose counterregulation occurs in some insulin-dependent diabetic subjects (IDDMs) as a result of a combined deficiency of glucagon (IRG) and epinephrine (EPI) secretion in response to insulin-induced hypoglycemia. Glucose 10-17 insulin Homo sapiens 51-58 3896896-1 1985 NIDDM is characterized by decreased insulin secretory responses to glucose and to nonglucose stimuli, hyperglucagonemia, and decreased tissue sensitivity to insulin. Glucose 67-74 insulin Homo sapiens 36-43 3896896-6 1985 During an intravenous glucose tolerance test (IVGTT), relative first- and second-phase insulin responses to glucose were decreased in subjects with former GDM (2316 +/- 560 versus 7798 +/- 1036% of basal X min, P = 0.004; and 8340 +/- 946 versus 14,509 +/- 2556, P = 0.04). Glucose 22-29 insulin Homo sapiens 87-94 3896896-6 1985 During an intravenous glucose tolerance test (IVGTT), relative first- and second-phase insulin responses to glucose were decreased in subjects with former GDM (2316 +/- 560 versus 7798 +/- 1036% of basal X min, P = 0.004; and 8340 +/- 946 versus 14,509 +/- 2556, P = 0.04). Glucose 108-115 insulin Homo sapiens 87-94 3896896-10 1985 The response at 600 mg/dl is termed the AIRmax and is used as an index of glucose-regulated insulin secretory capacity. Glucose 74-81 insulin Homo sapiens 92-99 3896898-0 1985 Effects of intravenous and oral glucose administration on insulin action in human fat cells. Glucose 32-39 insulin Homo sapiens 58-65 3896898-1 1985 The effects of various forms of glucose administration on insulin action were investigated in isolated human fat cells. Glucose 32-39 insulin Homo sapiens 58-65 3896898-8 1985 glucose administration, adipocyte insulin binding was significantly reduced by 20% owing to a decrease in the high-affinity binding, whereas the concentrations of insulin producing the half-maximum inhibitions of basal and isoprenaline-induced rates of glycerol release were unaltered. Glucose 0-7 insulin Homo sapiens 34-41 3896898-9 1985 Sixty minutes after oral glucose ingestion, insulin sensitivity increased 7-30-fold (P less than 0.05-0.01) and high-affinity insulin binding increased by 25% (P less than 0.05). Glucose 25-32 insulin Homo sapiens 44-51 3896898-9 1985 Sixty minutes after oral glucose ingestion, insulin sensitivity increased 7-30-fold (P less than 0.05-0.01) and high-affinity insulin binding increased by 25% (P less than 0.05). Glucose 25-32 insulin Homo sapiens 126-133 3896900-1 1985 The reduction in blood glucose in non-insulin-dependent diabetes mellitus (NIDDM) brought about by the use of phenobarbital (PB), a hepatic microsomal enzyme inducer, suggests an improvement in insulin sensitivity. Glucose 23-30 insulin Homo sapiens 38-45 3902422-3 1985 This regimen decreased the insulin dose while continuing to maintain adequate metabolic control, as reflected by fasting plasma glucose (FPG) less than 150 mg/dl and HbA1 levels less than 9%, and reduced number of hypoglycemic episodes to almost nil in a group of subjects with adequate metabolic control before institution of combination therapy. Glucose 128-135 insulin Homo sapiens 27-34 3905476-4 1985 In addition, age and hypertension had a borderline association to coronary heart disease in men, whereas smoking and high 2-h post-glucose serum insulin level showed a significant association in women. Glucose 131-138 insulin Homo sapiens 145-152 3905478-0 1985 Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man. Glucose 47-54 insulin Homo sapiens 30-37 3905478-2 1985 When in healthy subjects arterial plasma glucose was acutely raised and maintained at +7 mmol/l above fasting level, the plasma insulin response was enhanced by ASA (70 +/- 7 vs. 52 +/- 7 mU/l), whereas the plasma C-peptide response was identical. Glucose 41-48 insulin Homo sapiens 128-135 3905480-4 1985 Glucagon-like peptide-1 stimulates insulin release at 10 and 16.7 mmol/l glucose in a dose-dependent manner. Glucose 73-80 insulin Homo sapiens 35-42 3926463-11 1985 Nanomolar concentrations of 5-HETE elicited a rapid and transient increase in insulin release, which was additive to the release response to a submaximal stimulatory concentration of glucose, whereas micromolar 5-HETE did not affect insulin release. Glucose 183-190 insulin Homo sapiens 78-85 3928421-5 1985 Insulin-induced increases in glucose transport and oxidation were demonstrable in receptor-positive cells but not in receptor-negative cells. Glucose 29-36 insulin Homo sapiens 0-7 4053932-4 1985 Insulin sensitivity, assessed via the euglycemic clamp technique at insulin infusion rates of 100 mU/M2/min, showed an increase of insulin-mediated glucose disposal from 274 +/- 33 to 338 +/- 28 mg/M2/min, representing an increase in insulin sensitivity of 23 +/- 5% (P less than 0.01). Glucose 148-155 insulin Homo sapiens 0-7 4053932-4 1985 Insulin sensitivity, assessed via the euglycemic clamp technique at insulin infusion rates of 100 mU/M2/min, showed an increase of insulin-mediated glucose disposal from 274 +/- 33 to 338 +/- 28 mg/M2/min, representing an increase in insulin sensitivity of 23 +/- 5% (P less than 0.01). Glucose 148-155 insulin Homo sapiens 68-75 4053932-4 1985 Insulin sensitivity, assessed via the euglycemic clamp technique at insulin infusion rates of 100 mU/M2/min, showed an increase of insulin-mediated glucose disposal from 274 +/- 33 to 338 +/- 28 mg/M2/min, representing an increase in insulin sensitivity of 23 +/- 5% (P less than 0.01). Glucose 148-155 insulin Homo sapiens 131-138 4053932-4 1985 Insulin sensitivity, assessed via the euglycemic clamp technique at insulin infusion rates of 100 mU/M2/min, showed an increase of insulin-mediated glucose disposal from 274 +/- 33 to 338 +/- 28 mg/M2/min, representing an increase in insulin sensitivity of 23 +/- 5% (P less than 0.01). Glucose 148-155 insulin Homo sapiens 131-138 2862020-4 1985 Glucose inhibits amino acid-induced glucagon release through a direct insulin-independent action upon pancreatic A cells. Glucose 0-7 insulin Homo sapiens 70-77 2862021-5 1985 These results strongly support the concept that the potent in vivo insulin-releasing action of glucose and leucine is not only dependent on their fuel capacity in pancreatic B cells but also on the concurrent cAMP levels in these cells. Glucose 95-102 insulin Homo sapiens 67-74 3897043-8 1985 Both systolic and diastolic blood pressure were found to be significantly related to fasting serum insulin level (r = 0.47, p = 0.005 and r = 0.68, p less than 0.001) even when age, weight, and serum glucose level were controlled (r = 0.41, p = 0.025 and r = 0.62, p less than 0.001 respectively). Glucose 200-207 insulin Homo sapiens 99-106 4043927-2 1985 The present studies were undertaken to see if intravenous (IV) glucose challenge provokes a similar increase in monocyte insulin binding affinity. Glucose 63-70 insulin Homo sapiens 121-128 3902718-4 1985 Therefore, insulin resistance in TTX does not reside at the postreceptor peripheral tissue level, but may be the consequence of increased hepatic glucose production. Glucose 146-153 insulin Homo sapiens 11-18 3905736-0 1985 Insulin response to glucose in estrous and diestrous obese and lean heifers. Glucose 20-27 insulin Homo sapiens 0-7 3900136-0 1985 Evidence that insulin resistance is responsible for the decreased thermic effect of glucose in human obesity. Glucose 84-91 insulin Homo sapiens 14-21 3900136-9 1985 These results suggest that the defect in the thermic effect of glucose observed in obese subjects is due to their insulin resistance, which is responsible for a lower rate of glucose uptake and hence decreased rate of glucose storage, which is an energy-requiring process. Glucose 63-70 insulin Homo sapiens 114-121 3900136-9 1985 These results suggest that the defect in the thermic effect of glucose observed in obese subjects is due to their insulin resistance, which is responsible for a lower rate of glucose uptake and hence decreased rate of glucose storage, which is an energy-requiring process. Glucose 175-182 insulin Homo sapiens 114-121 3900136-9 1985 These results suggest that the defect in the thermic effect of glucose observed in obese subjects is due to their insulin resistance, which is responsible for a lower rate of glucose uptake and hence decreased rate of glucose storage, which is an energy-requiring process. Glucose 175-182 insulin Homo sapiens 114-121 3932800-6 1985 Frequent serum controls of electrolytes and glucose are necessary to control electrolyte and insulin therapy. Glucose 44-51 insulin Homo sapiens 93-100 3897770-7 1985 Fasting blood levels were not appreciably different in the various groups, but after the glucose load an unusually high insulin secretory response occurred in black children, especially black girls. Glucose 89-96 insulin Homo sapiens 120-127 3897770-11 1985 Black children also tended to have higher insulin/free fatty acid ratios during the glucose tolerance test. Glucose 84-91 insulin Homo sapiens 42-49 3894969-5 1985 In addition, 6 of 12 nondiabetic relatives with islet-cell antibodies had abnormally low insulin responses--below the third percentile in 6 and below the first percentile in 4--on their initial intravenous glucose challenge. Glucose 206-213 insulin Homo sapiens 89-96 3898828-3 1985 In addition, it has recently been recognized that correction of glucose intolerance leads to an improvement in insulin secretion and a reduction in insulin resistance. Glucose 64-71 insulin Homo sapiens 111-118 3898829-1 1985 Patients with non-insulin-dependent diabetes mellitus have enlarged islets of Langerhans, an increased number of insulin-secreting beta cells, and a "horseshoe-shaped" relationship between plasma insulin and glucose levels. Glucose 208-215 insulin Homo sapiens 18-25 3894356-3 1985 Subsequent treatment of diabetic animals with insulin for 5 days produced non-ketotic animals with normal blood glucose, and the affinity of carnitine palmitoyltransferase for malonyl-CoA was increased to the control level. Glucose 112-119 insulin Homo sapiens 46-53 3901813-3 1985 Glucose stimulated insulin-release, and contents of insulin and glucagon in islets incubated with cytokine-rich supernatants were markedly reduced. Glucose 0-7 insulin Homo sapiens 19-26 3893253-6 1985 Intensive insulin treatment of patients with type I diabetes causes a generalized reduction in counterregulatory hormone release after a moderate fall in blood glucose levels. Glucose 160-167 insulin Homo sapiens 10-17 3936451-3 1985 A ten times increase in urinary C-peptide (m: 47.2 +/- 33.3 nmol/m2-1) as compared with controls shows an hypersecretion of insulin induced by the high infusion delivery of glucose. Glucose 173-180 insulin Homo sapiens 124-131 3894118-1 1985 To determine whether glucose-mediated as well as insulin-mediated regulation of glucose utilization and glucose production is impaired in patients with insulin-dependent diabetes mellitus (IDDM), six nonobese, diabetic patients and seven age-, sex-, and weight-matched nondiabetic subjects were studied. Glucose 80-87 insulin Homo sapiens 49-56 3894118-1 1985 To determine whether glucose-mediated as well as insulin-mediated regulation of glucose utilization and glucose production is impaired in patients with insulin-dependent diabetes mellitus (IDDM), six nonobese, diabetic patients and seven age-, sex-, and weight-matched nondiabetic subjects were studied. Glucose 80-87 insulin Homo sapiens 49-56 3894118-4 1985 Thus, although stimulation of glucose utilization by insulin is impaired in patients with IDDM, the ability of an increase in glucose concentration to increase glucose utilization does not appear to differ from that present in nondiabetic subjects, at insulin concentrations in the low physiologic range. Glucose 30-37 insulin Homo sapiens 53-60 3894119-2 1985 We studied the effect of aerobic training and detraining on insulin-stimulated glucose disposal and on erythrocyte insulin receptor binding. Glucose 79-86 insulin Homo sapiens 60-67 3894130-3 1985 Insulin-mediated glucose metabolism in the diabetic patients pre-CSII (3.92 +/- 0.36 mg/kg X min) was reduced by 44% compared with controls (7.03 +/- 0.22 mg/kg X min; P less than 0.001). Glucose 17-24 insulin Homo sapiens 0-7 3894130-5 1985 However, insulin-mediated glucose utilization still remained significantly below control values (P less than 0.01). Glucose 26-33 insulin Homo sapiens 9-16 3902540-0 1985 Beta-cell cytoplasmic Ca2+ balance as a determinant for glucose-stimulated insulin release. Glucose 56-63 insulin Homo sapiens 75-82 3902540-1 1985 The introduction of new techniques and the access to clonal lines of insulin-secreting cells have enabled re-evaluation of glucose effects on Ca2+ movements in pancreatic beta cells. Glucose 123-130 insulin Homo sapiens 69-76 3902540-4 1985 With the demonstration that glucose can not only increase but also lower cytoplasmic Ca2+, it follows that exposure to the sugar under certain conditions results in a paradoxical inhibition of insulin release. Glucose 28-35 insulin Homo sapiens 193-200 3902540-5 1985 In diabetic patients this may be manifest as prompt reduction of circulating concentrations of insulin and C-peptide after an intravenous injection of glucose. Glucose 151-158 insulin Homo sapiens 95-102 3902545-11 1985 The incretin effect of oral glucose is smaller if plasma levels of C-peptide rather than insulin are measured. Glucose 28-35 insulin Homo sapiens 89-96 3902545-12 1985 However, decreased hepatic extraction of insulin after glucose ingestion only accounts partially for the incretin effect. Glucose 55-62 insulin Homo sapiens 41-48 3915258-0 1985 Serum free C-peptide response to oral glucose loading as a parameter for the monitoring of pancreatic B-cell function in diabetic patients. Glucose 38-45 insulin Homo sapiens 11-20 3939115-3 1985 Insulin-dependent diabetics (IDDM) with history of ketosis or ketoacidosis and/or unstable plasma glucose, and patients refractory to sulfonylureas had lower UCPR values (8.5 +/- 6.6 and 22.3 +/- 14.6 micrograms/day) than the other insulin-treated patients (45.4 +/- 30.7 micrograms/day). Glucose 98-105 insulin Homo sapiens 0-7 4043489-4 1985 This might result in an inappropriate adaptation of the insulin dose, when the estimated blood glucose is used in connection with a classic algorithm. Glucose 95-102 insulin Homo sapiens 56-63 2410233-3 1985 Glucose (25 mM) alone caused a prompt release of both 65Zn and insulin. Glucose 0-7 insulin Homo sapiens 63-70 2410233-6 1985 However, the ratio of 65Zn to insulin fractional secretion was only 0.16, indicating that glucose not only causes cosecretion of zinc associated with stored insulin, but also independently decreases 65Zn efflux from extragranular sources. Glucose 90-97 insulin Homo sapiens 157-164 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 180-187 insulin Homo sapiens 4-11 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 99-106 insulin Homo sapiens 4-11 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 99-106 insulin Homo sapiens 78-85 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 99-106 insulin Homo sapiens 78-85 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 99-106 insulin Homo sapiens 78-85 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 180-187 insulin Homo sapiens 78-85 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 180-187 insulin Homo sapiens 78-85 3902605-1 1985 The insulin clamp technique, which is often assumed to measure the ability of insulin to stimulate glucose uptake, actually measures both insulin-independent and insulin-dependent glucose uptake. Glucose 180-187 insulin Homo sapiens 78-85 3902605-2 1985 In contrast, the minimal model technique, recently introduced by Bergman, Philips and Cobelli (1981), attempts to directly estimate insulin sensitivity (insulin-dependent glucose uptake = S1) by measurement of plasma glucose and insulin values during a 3 hour intravenous glucose tolerance test (IVGTT). Glucose 171-178 insulin Homo sapiens 132-139 3902605-2 1985 In contrast, the minimal model technique, recently introduced by Bergman, Philips and Cobelli (1981), attempts to directly estimate insulin sensitivity (insulin-dependent glucose uptake = S1) by measurement of plasma glucose and insulin values during a 3 hour intravenous glucose tolerance test (IVGTT). Glucose 171-178 insulin Homo sapiens 153-160 3902605-2 1985 In contrast, the minimal model technique, recently introduced by Bergman, Philips and Cobelli (1981), attempts to directly estimate insulin sensitivity (insulin-dependent glucose uptake = S1) by measurement of plasma glucose and insulin values during a 3 hour intravenous glucose tolerance test (IVGTT). Glucose 171-178 insulin Homo sapiens 153-160 3902605-8 1985 One explanation for this observation is that the insulin-independent component of total glucose disposal both varies widely among patients and contributes significantly to glucose uptake as assessed by the insulin clamp technique. Glucose 88-95 insulin Homo sapiens 49-56 3902605-8 1985 One explanation for this observation is that the insulin-independent component of total glucose disposal both varies widely among patients and contributes significantly to glucose uptake as assessed by the insulin clamp technique. Glucose 88-95 insulin Homo sapiens 206-213 3902605-8 1985 One explanation for this observation is that the insulin-independent component of total glucose disposal both varies widely among patients and contributes significantly to glucose uptake as assessed by the insulin clamp technique. Glucose 172-179 insulin Homo sapiens 49-56 3902605-8 1985 One explanation for this observation is that the insulin-independent component of total glucose disposal both varies widely among patients and contributes significantly to glucose uptake as assessed by the insulin clamp technique. Glucose 172-179 insulin Homo sapiens 206-213 4044105-6 1985 However, the insulin sensitivity index, defined as the rate of plasma glucose decline divided by the increment rise in insulin, was clearly higher in the joggers (0.098 +/- 0.009 vs 0.057 +/- 0.005, P less than 0.05). Glucose 70-77 insulin Homo sapiens 13-20 3924948-1 1985 The effect of glibenclamide treatment on insulin-mediated glucose disposal was studied in eight C-peptide-negative type I diabetic patients. Glucose 58-65 insulin Homo sapiens 41-48 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glucose 21-28 insulin Homo sapiens 4-11 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glucose 21-28 insulin Homo sapiens 91-98 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glucose 21-28 insulin Homo sapiens 91-98 4066641-2 1985 Purification of this insulin-stimulating peptide (ISP) was monitored by an adipose-explant assay in which stimulation of fatty acid synthesis from glucose by insulin was measured. Glucose 147-154 insulin Homo sapiens 21-28 2864633-2 1985 Somatostatin administration in a relatively high dosage (initially 145 micrograms/m2 body surface as bolus followed by a continuous infusion of the same dose per hour) resulted in a suppression of the circulating insulin concentration leading to a less abrupt fall of the postprandial plasma glucose level. Glucose 292-299 insulin Homo sapiens 213-220 2951129-4 1986 Insulin-mediated glucose disposal was reduced (p less than 0.01 and less than 0.01) at insulin infusion rates 1 and 6 mU/kg/min in untreated patients (18.5 +/- 1.9 and 33.8 +/- 4.5 mumol/kg/min) when compared with controls (35.8 +/- 3.4 and 62.0 +/- 4.7 mumol/kg/min) and was improved (p less than 0.01 and less than 0.01) following insulin treatment (36.1 +/- 4.6 and 64.8 +/- 4.2 mumol/kg/min). Glucose 17-24 insulin Homo sapiens 333-340 2951136-0 1986 A comparison of biosynthetic human insulin with porcine insulin in the blood glucose control of diabetic pregnancy. Glucose 77-84 insulin Homo sapiens 35-42 2951136-0 1986 A comparison of biosynthetic human insulin with porcine insulin in the blood glucose control of diabetic pregnancy. Glucose 77-84 insulin Homo sapiens 56-63 2951136-4 1986 In the group treated with human insulin, fasting blood glucose could only be controlled by significantly greater doses of human isophane insulin injected before the evening meal. Glucose 55-62 insulin Homo sapiens 32-39 2951136-4 1986 In the group treated with human insulin, fasting blood glucose could only be controlled by significantly greater doses of human isophane insulin injected before the evening meal. Glucose 55-62 insulin Homo sapiens 137-144 3901250-5 1985 Disturbances of the entero-insular axis are best evaluated by estimating the incretin effect (i.e. comparing the insulin response to oral glucose with the insulin response to an isoglycaemic i.v. Glucose 138-145 insulin Homo sapiens 113-120 2410271-8 1985 Glucose uptake, glycogen synthase, uridine incorporation into RNA and acetate incorporation into lipid are all stimulated to varying degrees by physiological concentrations of insulin. Glucose 0-7 insulin Homo sapiens 176-183 2861817-1 1985 N-p-tosylglycine, which inhibits transglutaminase activity in islet homogenates, was found to cause a rapid and sustained facilitation of insulin release evoked by D-glucose, L-leucine or the association of Ba2+ and theophylline in intact islets. Glucose 164-173 insulin Homo sapiens 138-145 2861817-4 1985 N-p-tosylglycine (5.0 mM) slightly enhanced insulin release evoked by a high concentration of glucose (16.7 mM) and failed to affect significantly the secretory response to the association of L-leucine and L-glutamine or that of D-glucose and gliclazide. Glucose 94-101 insulin Homo sapiens 44-51 3907235-0 1985 Glycemic control with an artificial pancreas improves insulin responses to both oral and glucose in nonobese noninsulin-dependent diabetic subjects. Glucose 89-96 insulin Homo sapiens 54-61 3907235-1 1985 Insulin secretory responses to both oral and intravenous glucose were investigated in 12 nonobese noninsulin-dependent diabetic subjects before and after strict metabolic control of blood glucose levels without weight loss. Glucose 57-64 insulin Homo sapiens 0-7 3907235-3 1985 Initially, the insulin response to oral glucose was weak and delayed, but increased significantly after treatment (p less than 0.01), although none of the diabetic subjects achieved completely normal glucose tolerance. Glucose 40-47 insulin Homo sapiens 15-22 3907235-8 1985 In absolute terms, the insulin responses of the post-treatment tests were not significantly different from those of sex-, age- and weight-matched control subjects, but were significantly lower if related to the corresponding plasma glucose responses (insulinogenic index lower than that of controls). Glucose 232-239 insulin Homo sapiens 23-30 3907236-10 1985 We concluded that type I diabetic patients showing severe metabolic instability produced more glucose, ketone bodies and glycerol after insulin withdrawal than control "stable" patients. Glucose 94-101 insulin Homo sapiens 136-143 4014301-4 1985 Current trends toward intensive insulin therapy for rapid near-normalization of blood glucose levels will increase the recognition of this entity. Glucose 86-93 insulin Homo sapiens 32-39 2992534-6 1985 The decline of free fatty acids (FFA) and insulin at the end of the mackerel period reached the level of significance 60 min and 120 min, respectively, after glucose load. Glucose 158-165 insulin Homo sapiens 42-49 21274022-2 1985 Better understanding of insulin"s physiology, its interaction with glucose and other aspects of metabolism, and knowledge of hyperglycemia"s detrimental effects, have contributed to a drive to keep blood glucose levels as close to non-diabetic norms as possible. Glucose 67-74 insulin Homo sapiens 24-31 2417774-2 1985 A combination of insulin (800 u) and aprotinin (10,000 u) given twice daily also produced adequate glucose homeostasis for a period of 12 months. Glucose 99-106 insulin Homo sapiens 17-24 2995184-7 1985 These data suggest that the chronic hyperinsulinaemia causes suppression of hepatic glucose production, and a state of insulin insensitivity which appears to be due to a post-receptor defect. Glucose 84-91 insulin Homo sapiens 41-48 3002703-3 1985 A mathematical model for the interaction between Ca and cyclic AMP in the process of glucose-stimulated insulin release from the pancreatic B-cell is presented. Glucose 85-92 insulin Homo sapiens 104-111 3002703-6 1985 Such a dissociated time course allows for a fair simulation of both 45Ca efflux and insulin release from islets perifused in the absence or presence of Ca and exposed to a sudden increase in extracellular glucose concentration. Glucose 205-212 insulin Homo sapiens 84-91 3030616-1 1985 A 30-year-old Caucasian who developed gestational diabetes in her first pregnancy requiring 58 U insulin daily and who subsequently adopted a high fibre, low fat diet and who was able to maintain normal glucose tolerance throughout a second pregnancy is reported. Glucose 203-210 insulin Homo sapiens 97-104 3891475-5 1985 insulin administration to both groups of subjects resulted in similar reductions in glucose concentrations, which were maintained below 50 mg/dl for at least 30 min. Glucose 84-91 insulin Homo sapiens 0-7 3896591-0 1985 Genetic regulation of the kinetics of glucose-induced insulin release in man. Glucose 38-45 insulin Homo sapiens 54-61 3896591-2 1985 Insulin release and sensitivity were estimated from glucose and insulin curves obtained at a glucose infusion test performed on altogether 601 subjects belonging to 155 nuclear families. Glucose 52-59 insulin Homo sapiens 0-7 3896591-4 1985 Three variables obtained by a computer model were analysed, i.e. the glucose regulation of insulin release by a direct stimulatory event (KI) and time-dependent modulatory events (KP) as well as insulin sensitivity (KG). Glucose 69-76 insulin Homo sapiens 91-98 3899824-0 1985 Continuous infusion of glucose with model assessment: measurement of insulin resistance and beta-cell function in man. Glucose 23-30 insulin Homo sapiens 69-76 3899824-1 1985 Continuous infusion of glucose with model assessment (CIGMA) is a new method of assessing glucose tolerance, insulin resistance and beta-cell function. Glucose 23-30 insulin Homo sapiens 109-116 3899824-3 1985 These are similar to postprandial levels, change slowly, and depend on the dynamic interaction between the insulin produced and its effect on glucose turnover. Glucose 142-149 insulin Homo sapiens 107-114 3899825-0 1985 Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Glucose 92-99 insulin Homo sapiens 30-37 4042806-5 1985 Insulin response to an intravenous glucose tolerance test was abnormally low. Glucose 35-42 insulin Homo sapiens 0-7 3901231-2 1985 Insulin in saliva during the oral glucose tolerance test in female patients. Glucose 34-41 insulin Homo sapiens 0-7 3901231-3 1985 The radioimmunoassay (RIA) of insulin was performed in the serum and saliva of 27 female patients during the oral glucose tolerance test (OGTT). Glucose 114-121 insulin Homo sapiens 30-37 3901231-6 1985 The results show that immunoreactive insulin (IRI) is present in saliva and its concentration increases during the glucose stimulation test from 6.48 +/- 1.13 microU/ml (means +/- SEM) in basal conditions at peak values of 45.46 +/- 10.14 microU/ml at 2 hrs after glucose intake. Glucose 115-122 insulin Homo sapiens 37-44 3901231-6 1985 The results show that immunoreactive insulin (IRI) is present in saliva and its concentration increases during the glucose stimulation test from 6.48 +/- 1.13 microU/ml (means +/- SEM) in basal conditions at peak values of 45.46 +/- 10.14 microU/ml at 2 hrs after glucose intake. Glucose 264-271 insulin Homo sapiens 37-44 3889037-2 1985 Insulin was infused until the whole blood glucose level fell to or below 60 mg/dl. Glucose 42-49 insulin Homo sapiens 0-7 3889039-1 1985 The study was carried out to quantify the ability of physiological increases in the plasma insulin concentration to stimulate glucose disposal above basal levels in 25 normal subjects and 25 patients with noninsulin-dependent diabetes mellitus (NIDDM). Glucose 126-133 insulin Homo sapiens 91-98 3889039-4 1985 Glucose disposal rates increased in both normal subjects and NIDDM patients when plasma insulin concentrations were increased to about 90 microU/ml; however, the increment was much greater in normal subjects. Glucose 0-7 insulin Homo sapiens 88-95 3889039-5 1985 Thus, glucose disposal only rose to a mean (+/- SEM) value of 145 +/- 7 mg/m2 X min in patients with NIDDM, representing an approximate 30% increase due to insulin. Glucose 6-13 insulin Homo sapiens 156-163 3889039-6 1985 In contrast, a similar elevation of plasma insulin in normal subjects resulted in an increase in glucose disposal of approximately 300%, reaching a mean (+/- SEM) value of 310 +/- 24 mg/m2 X min. Glucose 97-104 insulin Homo sapiens 43-50 3889039-7 1985 These results indicate that the defect in insulin-stimulated glucose uptake is significantly greater in patients with NIDDM than has previously been found. Glucose 61-68 insulin Homo sapiens 42-49 3889041-9 1985 Insulin-stimulated glucose transport in these fibroblasts also was normal, but there was a mild (20%) reduction in the concentration of cytochalasin B-binding sites in erythrocyte ghosts. Glucose 19-26 insulin Homo sapiens 0-7 3894421-0 1985 Effect of insulin on the distribution and disposition of glucose in man. Glucose 57-64 insulin Homo sapiens 10-17 3894421-2 1985 Little is known, however, about insulin"s effect on the distribution and exchange of glucose in body pools. Glucose 85-92 insulin Homo sapiens 32-39 3894421-12 1985 Insulin-independent glucose uptake was estimated (from published data) at 75% of basal glucose uptake, and was constrained not to change with euglycemic hyperinsulinemia. Glucose 20-27 insulin Homo sapiens 0-7 3894421-12 1985 Insulin-independent glucose uptake was estimated (from published data) at 75% of basal glucose uptake, and was constrained not to change with euglycemic hyperinsulinemia. Glucose 87-94 insulin Homo sapiens 0-7 3894421-15 1985 Furthermore, a significant direct correlation was found to exist between the change in size of the slow pool and the insulin-stimulated rate of total glucose turnover (r=0.92, P<0.01). Glucose 150-157 insulin Homo sapiens 117-124 3894421-16 1985 We conclude that hyperinsulinemia, independent of hyperglycemia, markedly increases the exchangeable mass of glucose in the body, presumably reflecting the accumulation of free, intracellular glucose in insulin-dependent tissues. Glucose 109-116 insulin Homo sapiens 22-29 3894421-16 1985 We conclude that hyperinsulinemia, independent of hyperglycemia, markedly increases the exchangeable mass of glucose in the body, presumably reflecting the accumulation of free, intracellular glucose in insulin-dependent tissues. Glucose 192-199 insulin Homo sapiens 22-29 3894423-0 1985 Influence of a 60-hour fast on insulin-mediated splanchnic and peripheral glucose metabolism in humans. Glucose 74-81 insulin Homo sapiens 31-38 3894423-2 1985 In this situation insulin resistance contributes to the glucose intolerance, but it is not known which tissue or tissues are responsible for the decreased insulin sensitivity. Glucose 56-63 insulin Homo sapiens 18-25 3923028-0 1985 Effects of salicylate, tolbutamide, and prostaglandin E2 on insulin responses to glucose in noninsulin-dependent diabetes mellitus. Glucose 81-88 insulin Homo sapiens 60-67 3923028-6 1985 Resetting the prestimulus glucose level to control values by infusing glucose caused a further increase in the second, but not the first, phase of glucose-induced insulin secretion, indicating that the prestimulus glucose level had a role in regulating subsequent insulin release. Glucose 26-33 insulin Homo sapiens 163-170 3923028-6 1985 Resetting the prestimulus glucose level to control values by infusing glucose caused a further increase in the second, but not the first, phase of glucose-induced insulin secretion, indicating that the prestimulus glucose level had a role in regulating subsequent insulin release. Glucose 70-77 insulin Homo sapiens 163-170 3923028-6 1985 Resetting the prestimulus glucose level to control values by infusing glucose caused a further increase in the second, but not the first, phase of glucose-induced insulin secretion, indicating that the prestimulus glucose level had a role in regulating subsequent insulin release. Glucose 70-77 insulin Homo sapiens 163-170 4030559-1 1985 The effects of an exercise-induced muscle glycogen reduction and an elevated muscle glycogen concentration on glucose tolerance and the insulin response to an oral glucose tolerance test (GTT) were examined. Glucose 164-171 insulin Homo sapiens 136-143 2995635-3 1985 Dietary glucose causes a slightly greater insulin rise than cooked starch containing an equal amount of carbohydrate, and high fiber starchy foods cause a much lesser insulin response than does glucose in solution. Glucose 8-15 insulin Homo sapiens 42-49 3913861-0 1985 [The effect of age on the response of insulin and C-peptide to oral glucose in non-insulin-dependent diabetes]. Glucose 68-75 insulin Homo sapiens 38-45 3913861-0 1985 [The effect of age on the response of insulin and C-peptide to oral glucose in non-insulin-dependent diabetes]. Glucose 68-75 insulin Homo sapiens 50-59 3897693-5 1985 At low insulin concentrations dextrose requirements were diminished in all diabetic subjects. Glucose 30-38 insulin Homo sapiens 7-14 2859524-4 1985 In control experiments (infusion of insulin alone), plasma glucose increased from 98 +/- 5 mg per deciliter at midnight to 225 +/- 36 at 8:00 a.m. (P less than 0.001), glucose production increased by 65 per cent (P less than 0.001), and glucose clearance decreased by 50 per cent (P less than 0.001). Glucose 59-66 insulin Homo sapiens 36-43 2864239-3 1985 Perifusion studies measured nonstimulated and glucose- and arginine-stimulated insulin release from the three islet tissues. Glucose 46-53 insulin Homo sapiens 79-86 2864239-8 1985 Glucose (5.5-30 mM) and L-arginine (5-20 mM) elicited first phase insulin responses from single islet cells that were not significantly different from those observed with intact islets; in contrast, second phase responses of single islets to glucose were approximately 50% those seen with intact islets, and their second phase responses to arginine were absent. Glucose 0-7 insulin Homo sapiens 66-73 3924104-6 1985 All three compounds suppress glucose-induced insulin secretion and 12-hydroxyeicosatetraenoic acid (12-HETE) synthesis by isolated pancreatic islets with similar concentration dependence. Glucose 29-36 insulin Homo sapiens 45-52 3924216-3 1985 The diabetics showed appreciable insulin resistance, manifested by a 40% reduction in the rate of insulin mediated glucose disposal, which was unrelated to the presence of insulin antibodies. Glucose 115-122 insulin Homo sapiens 33-40 3924216-3 1985 The diabetics showed appreciable insulin resistance, manifested by a 40% reduction in the rate of insulin mediated glucose disposal, which was unrelated to the presence of insulin antibodies. Glucose 115-122 insulin Homo sapiens 98-105 3924216-3 1985 The diabetics showed appreciable insulin resistance, manifested by a 40% reduction in the rate of insulin mediated glucose disposal, which was unrelated to the presence of insulin antibodies. Glucose 115-122 insulin Homo sapiens 98-105 3923961-6 1985 The glyburide-induced fall in plasma glucose concentration was associated with improvements in both insulin secretion and insulin action, but only the enhanced insulin action correlated with the reduction in fasting and postprandial glucose levels. Glucose 37-44 insulin Homo sapiens 100-107 3893447-5 1985 The results, examined separately in men and women documented a significant negative relationship between plasma insulin and HDL cholesterol level, as well as pointing out that both HDL cholesterol and insulin are significantly correlated to degree of hypertriglyceridemia, degree of obesity and level of glucose tolerance. Glucose 304-311 insulin Homo sapiens 201-208 3893447-6 1985 The partial correlation coefficients between HDL cholesterol and plasma insulin levels at fasting in men and post-glucose load in women, demonstrated an independent relationship between increased plasma insulin and decreased plasma HDL concentration. Glucose 114-121 insulin Homo sapiens 72-79 3893447-6 1985 The partial correlation coefficients between HDL cholesterol and plasma insulin levels at fasting in men and post-glucose load in women, demonstrated an independent relationship between increased plasma insulin and decreased plasma HDL concentration. Glucose 114-121 insulin Homo sapiens 203-210 3888743-7 1985 This may reflect an increased magnitude of glucose intolerance in the insulin-treated group. Glucose 43-50 insulin Homo sapiens 70-77 2990849-6 1985 The increased level of insulin was related to the level of glucose during the infusion, while no changes were found during saline infusion. Glucose 59-66 insulin Homo sapiens 23-30 3888744-5 1985 The insulin responses to oral glucose and mixed meals are equally large in these two groups, but the insulin response per unit of glycemic stimulus is significantly lower in the gestational diabetic subjects than in the controls. Glucose 30-37 insulin Homo sapiens 4-11 3888747-5 1985 Insulin therapy was associated with a reduction in mean glucose concentrations so that the profile was similar to the controls, while in the diet-alone group the reduction was less. Glucose 56-63 insulin Homo sapiens 0-7 3158511-0 1985 Phorbol ester provokes insulin-like effects on glucose transport, amino acid uptake, and pyruvate dehydrogenase activity in BC3H-1 cultured myocytes. Glucose 47-54 insulin Homo sapiens 23-30 3891467-2 1985 Plasma C-peptide responses to glucose and to arginine in the diabetic subjects were both significantly reduced at all glucose concentrations studied (P less than 0.01-0.005). Glucose 30-37 insulin Homo sapiens 7-16 3888749-8 1985 Until the relative importance of all of these variables is adequately assessed, criteria for selection of women with pregnancy-onset diabetes for insulin therapy are most likely to be based on fasting and postprandial plasma glucose concentrations. Glucose 225-232 insulin Homo sapiens 146-153 3891467-2 1985 Plasma C-peptide responses to glucose and to arginine in the diabetic subjects were both significantly reduced at all glucose concentrations studied (P less than 0.01-0.005). Glucose 118-125 insulin Homo sapiens 7-16 3891467-3 1985 The modulating effect of glucose on both islet A- and B-cell responses (slope of relation between plasma C-peptide or glucagon response versus plasma glucose concentration) was reduced greater than 80% in the diabetic subjects (P less than 0.01). Glucose 25-32 insulin Homo sapiens 105-114 3897356-1 1985 The authors have studied insulin receptors on peripheral blood monocytes and insulin sensitivity, evaluated by simultaneous infusion of glucose, insulin and somatostatin in 10 control subjects and in 20 obese patients with normal glucose tolerance. Glucose 136-143 insulin Homo sapiens 25-32 3889028-9 1985 Thus, deterioration of metabolic control in noninsulin-dependent diabetic patients by hyperthyroidism is due primarily to enhancement of basal HGP and its reduced suppressibility by insulin and glucose. Glucose 194-201 insulin Homo sapiens 47-54 3889032-2 1985 In these patients, glucose was ingested on two occasions, once alone and once during insulin infusion using an artificial endocrine pancreas to maintain blood glucose at levels similar to those in normal subjects. Glucose 19-26 insulin Homo sapiens 85-92 3889540-6 1985 This heightened insulin release occurred in the presence of glucose-stimulated insulin secretion. Glucose 60-67 insulin Homo sapiens 16-23 3889540-6 1985 This heightened insulin release occurred in the presence of glucose-stimulated insulin secretion. Glucose 60-67 insulin Homo sapiens 79-86 2582429-9 1985 This in turn may stimulate the expression of insulin-related sequences, which may result in higher utilization of glucose, thus bringing about the macrosomia and high incidence of malformation and still-births known to result from pregnancies in diabetics. Glucose 114-121 insulin Homo sapiens 45-52 2989759-4 1985 As expected, continuous subcutaneous insulin infusion lowered mean 24-h plasma glucose (from 203 +/- 21 to 112 +/- 7 mg/dl, p less than 0.01) and GH (from 17.7 +/- 2.1 to 9.2 +/- 1.2 ng/ml, p less than 0.01) to values observed in normal controls. Glucose 79-86 insulin Homo sapiens 37-44 3160017-8 1985 Its responsibility for inducing insulin-resistance may account for the fact that corticosteroids, which are rapidly effective against giant cell arteritis, normalise oral glucose tolerance tests. Glucose 171-178 insulin Homo sapiens 32-39 3890856-6 1985 Since the activator of PDH is modulated by physiological perturbation such as oral glucose ingestion, known to cause changes in circulating insulin levels, it may possibly be related to insulin mediator. Glucose 83-90 insulin Homo sapiens 140-147 3895577-6 1985 All of 7 patients with myotonic dystrophy also were shown to have an excessive response of endogenous insulin to a glucose challenge. Glucose 115-122 insulin Homo sapiens 102-109 3890856-6 1985 Since the activator of PDH is modulated by physiological perturbation such as oral glucose ingestion, known to cause changes in circulating insulin levels, it may possibly be related to insulin mediator. Glucose 83-90 insulin Homo sapiens 186-193 3890851-0 1985 Insulin-like stimulation of glucose transport in isolated adipocytes by fatty acids. Glucose 28-35 insulin Homo sapiens 0-7 3887598-2 1985 Thirty minutes after oral glucose administration both insulin and C-peptide levels were significantly higher in the white group. Glucose 26-33 insulin Homo sapiens 54-61 3890455-1 1985 The pattern of insulin secretion following an oral glucose load and the insulin receptor status and insulin sensitivity of adipocytes have been studied in patients with thyrotoxicosis and in matched controls. Glucose 51-58 insulin Homo sapiens 15-22 3887944-1 1985 To determine the effect of thyroid hormone excess on insulin secretion, metabolism and action in humans, we examined intravenous glucose tolerance, glucose-induced insulin secretion, insulin clearance, monocyte insulin receptor binding, and the dose-response characteristics for the effects of insulin on glucose production, uptake, oxidation, and nonoxidative disposal in 10 normal volunteers for 14 days before and after oral administration of triiodothyronine (T3) in doses that increased plasma T3 to levels observed in spontaneous thyrotoxicosis (P less than 0.001). Glucose 148-155 insulin Homo sapiens 164-171 2866056-4 1985 When glucose disposal was expressed as metabolic clearance rate significant strong correlations were found between the euglycaemic clamp technique and the insulin sensitivity test with (r = 0.90) and without (r = 0.83) somatostatin. Glucose 5-12 insulin Homo sapiens 155-162 3887944-1 1985 To determine the effect of thyroid hormone excess on insulin secretion, metabolism and action in humans, we examined intravenous glucose tolerance, glucose-induced insulin secretion, insulin clearance, monocyte insulin receptor binding, and the dose-response characteristics for the effects of insulin on glucose production, uptake, oxidation, and nonoxidative disposal in 10 normal volunteers for 14 days before and after oral administration of triiodothyronine (T3) in doses that increased plasma T3 to levels observed in spontaneous thyrotoxicosis (P less than 0.001). Glucose 148-155 insulin Homo sapiens 164-171 3887944-1 1985 To determine the effect of thyroid hormone excess on insulin secretion, metabolism and action in humans, we examined intravenous glucose tolerance, glucose-induced insulin secretion, insulin clearance, monocyte insulin receptor binding, and the dose-response characteristics for the effects of insulin on glucose production, uptake, oxidation, and nonoxidative disposal in 10 normal volunteers for 14 days before and after oral administration of triiodothyronine (T3) in doses that increased plasma T3 to levels observed in spontaneous thyrotoxicosis (P less than 0.001). Glucose 148-155 insulin Homo sapiens 164-171 3887944-1 1985 To determine the effect of thyroid hormone excess on insulin secretion, metabolism and action in humans, we examined intravenous glucose tolerance, glucose-induced insulin secretion, insulin clearance, monocyte insulin receptor binding, and the dose-response characteristics for the effects of insulin on glucose production, uptake, oxidation, and nonoxidative disposal in 10 normal volunteers for 14 days before and after oral administration of triiodothyronine (T3) in doses that increased plasma T3 to levels observed in spontaneous thyrotoxicosis (P less than 0.001). Glucose 148-155 insulin Homo sapiens 164-171 3887944-4 1985 Insulin-induced suppression of glucose production was impaired (Km 22 +/- 3 vs. 37 +/- 7 microU/ml, P less than 0.02); maximal insulin-induced glucose uptake (10.7 +/- 0.6 vs. 13.0 +/- 0.9 mg X kg-1 X min-1, P less than 0.001) and oxidation (3.41 +/- 0.30 vs. 5.34 +/- 0.59 mg X kg-1 X min-1, P less than 0.001) were increased without a significant change in Km. Glucose 31-38 insulin Homo sapiens 0-7 3887944-4 1985 Insulin-induced suppression of glucose production was impaired (Km 22 +/- 3 vs. 37 +/- 7 microU/ml, P less than 0.02); maximal insulin-induced glucose uptake (10.7 +/- 0.6 vs. 13.0 +/- 0.9 mg X kg-1 X min-1, P less than 0.001) and oxidation (3.41 +/- 0.30 vs. 5.34 +/- 0.59 mg X kg-1 X min-1, P less than 0.001) were increased without a significant change in Km. Glucose 143-150 insulin Homo sapiens 0-7 3887944-4 1985 Insulin-induced suppression of glucose production was impaired (Km 22 +/- 3 vs. 37 +/- 7 microU/ml, P less than 0.02); maximal insulin-induced glucose uptake (10.7 +/- 0.6 vs. 13.0 +/- 0.9 mg X kg-1 X min-1, P less than 0.001) and oxidation (3.41 +/- 0.30 vs. 5.34 +/- 0.59 mg X kg-1 X min-1, P less than 0.001) were increased without a significant change in Km. Glucose 143-150 insulin Homo sapiens 127-134 2952415-1 1985 In 10 healthy men, we have compared the respective effects of an intravenous injection of glucagon (1 mg) and an oral glucose load (75 G) in eliciting the release of C-peptide and insulin from the pancreas. Glucose 118-125 insulin Homo sapiens 166-175 2952415-1 1985 In 10 healthy men, we have compared the respective effects of an intravenous injection of glucagon (1 mg) and an oral glucose load (75 G) in eliciting the release of C-peptide and insulin from the pancreas. Glucose 118-125 insulin Homo sapiens 180-187 2952415-2 1985 Serum C-peptide and insulin concentrations increased respectively to median values of 190% and 500% at 6 minutes after glucagon injection, and 344% and 794% at 30 minutes and 268% and 278% at 60 minutes following glucose ingestion. Glucose 213-220 insulin Homo sapiens 6-15 2952415-2 1985 Serum C-peptide and insulin concentrations increased respectively to median values of 190% and 500% at 6 minutes after glucagon injection, and 344% and 794% at 30 minutes and 268% and 278% at 60 minutes following glucose ingestion. Glucose 213-220 insulin Homo sapiens 20-27 2952415-4 1985 We conclude that oral glucose loading is probably the test of choice to elicit C-peptide release when screening populations of normal subjects for adequacy of beta cell function. Glucose 22-29 insulin Homo sapiens 79-88 3888836-4 1985 Sufficient intravenous insulin (0.2-0.6 units/kg) was administered to decrease plasma glucose 68% from the basal level or to less than 60 mg/dl within 90 minutes. Glucose 86-93 insulin Homo sapiens 23-30 3884239-2 1985 With fresh islets, both insulin release and biosynthesis were increased by raising glucose concentrations, although the response was a variable one. Glucose 83-90 insulin Homo sapiens 24-31 3884239-4 1985 Insulin release at 20 mmol of glucose/l was inhibited by adrenaline (0.1 mmol/l), and potentiated by theophylline (10 mmol/l) in the presence of 5 mmol of glucose/l, in islets cultured for 4 days. Glucose 30-37 insulin Homo sapiens 0-7 3884239-4 1985 Insulin release at 20 mmol of glucose/l was inhibited by adrenaline (0.1 mmol/l), and potentiated by theophylline (10 mmol/l) in the presence of 5 mmol of glucose/l, in islets cultured for 4 days. Glucose 155-162 insulin Homo sapiens 0-7 3884239-5 1985 After culture for 8 days, islets still showed an increase in insulin release and biosynthesis in response to glucose. Glucose 109-116 insulin Homo sapiens 61-68 3884239-6 1985 Pancreas slices derived from fresh human tissue also responded to increasing concentrations of glucose with a sigmoidal curve for insulin release. Glucose 95-102 insulin Homo sapiens 130-137 3926729-2 1985 Insulin added to the parenteral feed significantly raised the plasma insulin concentration and lowered the blood glucose. Glucose 113-120 insulin Homo sapiens 0-7 2581996-8 1985 In the islets perifused with high glucose concentration, IBMX lysed a greater number of vesicles and caused enhanced release of insulin. Glucose 34-41 insulin Homo sapiens 128-135 2581996-12 1985 SRIF inhibited insulin release by 20 microU/100 islets initially perifused with low glucose (30 mg/dl) and by 875 microU/100 islets perifused with high glucose (300 mg/dl). Glucose 84-91 insulin Homo sapiens 15-22 3885035-3 1985 The intranasal insulin (1 U per kilogram of body weight in 1 per cent laureth-9) was rapidly absorbed (in 15 minutes); it lowered the plasma glucose level by 50 per cent in 45 minutes in fasting normal controls and by 50 per cent in 120 minutes in fasting diabetics. Glucose 141-148 insulin Homo sapiens 15-22 2984220-4 1985 We now show that insulin, even in the presence of high extracellular glucose concentrations, will induce 95K and 82K GRP synthesis while suppressing 85K and 69K HSP synthesis. Glucose 69-76 insulin Homo sapiens 17-24 3884649-9 1985 In conclusion, there appear to be marked regional variations in fasting-mediated changes in insulin action on glucose metabolism in human adipose tissue. Glucose 110-117 insulin Homo sapiens 92-99 3889056-5 1985 Glucose use (milligrams per kilogram per minute) was significantly lower in cirrhotics at all three steady state plasma insulin levels: 3.04 +/- 0.34 vs. 7.72 +/- 0.61 (P less than 0.001) at approximately 100; 6.05 +/- 1.07 vs. 11.45 +/- 1.24 (P less than 0.001) at approximately 1,000; and 11.69 +/- 0.69 vs. 14.13 +/- 0.74 (P less than 0.05) at approximately 10,000 microU/ml. Glucose 0-7 insulin Homo sapiens 120-127 3889056-10 1985 Glucose transport values on isolated adipocytes were significantly lower in cirrhotics both basally (P less than 0.001) and at maximal insulin concentration (P less than 0.05). Glucose 0-7 insulin Homo sapiens 135-142 3889056-11 1985 These results suggest that insulin resistance in human cirrhosis is more dependent on depressed peripheral glucose use than on increased endogenous glucose production, and that a combined receptor and postreceptor defect in insulin action on target cells seems to be present. Glucose 107-114 insulin Homo sapiens 27-34 3889056-11 1985 These results suggest that insulin resistance in human cirrhosis is more dependent on depressed peripheral glucose use than on increased endogenous glucose production, and that a combined receptor and postreceptor defect in insulin action on target cells seems to be present. Glucose 148-155 insulin Homo sapiens 27-34 3887036-5 1985 In this altered environment, insulin failed to suppress endogenous glucose production and resulted in reduced glucose disposal. Glucose 110-117 insulin Homo sapiens 29-36 3894762-1 1985 It is now well established that longstanding human uremia is associated with impaired in vivo insulin action on glucose utilization of peripheral target tissues. Glucose 112-119 insulin Homo sapiens 94-101 3894762-4 1985 In contrast (14C)-D-glucose transport exhibited decreased sensitivity to insulin. Glucose 18-27 insulin Homo sapiens 73-80 3894762-9 1985 Taken together these results suggest that the insulin resistance of adipocytes from patients with chronic uremia may be accounted for primarily by postbinding defects localized to glucose transport and metabolism. Glucose 180-187 insulin Homo sapiens 46-53 3885035-4 1985 The glucose-lowering potency depended on the insulin dose and surfactant concentration. Glucose 4-11 insulin Homo sapiens 45-52 3885035-6 1985 After intranasal insulin used before meals (1 U per kilogram in 1 per cent laureth-9), the two-hour postprandial glucose level increased above before-meal levels by 38 mg per deciliter, as compared with 191 mg per deciliter after intranasal placebo in patients with Type I diabetes (P less than 0.05). Glucose 113-120 insulin Homo sapiens 17-24 3920907-5 1985 Glycosylated hemoglobin (HbA1c), serum glucose, and C-peptide responses to oral glucose were evaluated. Glucose 80-87 insulin Homo sapiens 52-61 3885430-1 1985 The insulin response to a 100 g oral glucose load was studied in 20 non-obese, healthy Indian females and 20 matched Indian males. Glucose 37-44 insulin Homo sapiens 4-11 3000117-9 1985 Our data, as a whole, confirm that growth hormone response to insulin-induced glucose fall is not critical in acute glucose counterregulation in insulin-dependent diabetics. Glucose 78-85 insulin Homo sapiens 62-69 3885889-5 1985 Neither fasting nor postprandial insulin levels changed significantly with weight loss, but estimates of insulin-stimulated glucose disposal demonstrated a 15% (group 1) and 42% (group 2) improvement. Glucose 124-131 insulin Homo sapiens 105-112 2984994-5 1985 Whereas previous studies have suggested that D-glucose and/or cAMP may inhibit ATPase activities in islets, these results indicate that the agents, i.e., D-glucose and cAMP, which stimulate and/or potentiate insulin secretion from the islet cell, do not modify Ca2+ fluxes by directly regulating the islet-cell plasma membrane (Ca2+ + Mg2+)-ATPase. Glucose 45-54 insulin Homo sapiens 208-215 2984994-5 1985 Whereas previous studies have suggested that D-glucose and/or cAMP may inhibit ATPase activities in islets, these results indicate that the agents, i.e., D-glucose and cAMP, which stimulate and/or potentiate insulin secretion from the islet cell, do not modify Ca2+ fluxes by directly regulating the islet-cell plasma membrane (Ca2+ + Mg2+)-ATPase. Glucose 154-163 insulin Homo sapiens 208-215 3838425-6 1985 From the recognized glucose profiles that occur after consumption of different carbohydrates, snacks as well as exercise and insulin can now be programmed for intensively treated, insulin-dependent diabetics. Glucose 20-27 insulin Homo sapiens 125-132 3882502-6 1985 In vivo peripheral insulin action was measured using the euglycemic glucose clamp technique during an insulin infusion of 40 mU/m2 X min, with blood glucose clamped at a concentration of 75 mg/dl using a variable glucose infusion. Glucose 68-75 insulin Homo sapiens 19-26 2982683-2 1985 The glucose potentiation slope was measured in normal and non-insulin-dependent diabetic subjects (NIDDM). Glucose 4-11 insulin Homo sapiens 62-69 3894135-0 1985 Correction of diabetic pattern of insulin release from islets of the spiny mouse (Acomys cahirinus) by glucose priming in vitro. Glucose 103-110 insulin Homo sapiens 34-41 3894135-2 1985 In both groups, insulin response to glucose (16.7 mmol/l) was delayed in comparison with that of rat islets, the release kinetics being analogous to that of human Type 2 (non-insulin-dependent) diabetes. Glucose 36-43 insulin Homo sapiens 16-23 3882738-0 1985 Presentation of a new method for specific measurement of in vivo insulin-stimulated glucose disposal in humans: comparison of this approach with the insulin clamp and minimal model techniques. Glucose 84-91 insulin Homo sapiens 65-72 3894135-3 1985 Thirty min priming of the isolated Acomys islets with glucose (16.7 mmol/l) resulted in potentiation of the insulin release to a second stimulation. Glucose 54-61 insulin Homo sapiens 108-115 3886476-8 1985 Insulin infusions resulted in severe, prolonged depressions of plasma glucose and alanine levels. Glucose 70-77 insulin Homo sapiens 0-7 3886766-0 1985 Effect of habitual physical activity on regulation of insulin-stimulated glucose disposal in older males. Glucose 73-80 insulin Homo sapiens 54-61 3886766-3 1985 Measurements were made of body mass index (BMI), percentage body fat by underwater weighing, maximal O2 consumption by bicycle ergometry (VO2max), and insulin-stimulated glucose disposal by the insulin clamp technique. Glucose 170-177 insulin Homo sapiens 151-158 3886766-4 1985 The results demonstrated that insulin-stimulated glucose disposal was significantly increased (P less than 0.001) in the normal older subjects who exercised regularly. Glucose 49-56 insulin Homo sapiens 30-37 3886766-6 1985 These data are consistent with the view that the extensive variation previously noted in in vivo insulin-stimulated glucose disposal of older subjects is related to differences in habitual physical activity. Glucose 116-123 insulin Homo sapiens 97-104 3886702-1 1985 To assess the possible effects of lipid metabolism on insulin-mediated glucose disposal, 18 nondiabetic Pima Indian women (age 18-35 yr) were studied using 1-14C-palmitate infusion to measure free fatty acid turnover rate followed by a euglycemic clamp (clamp) to measure in vivo insulin-mediated glucose disposal (M). Glucose 71-78 insulin Homo sapiens 54-61 3882738-1 1985 This study was initiated to compare the abilities of two alternative approaches to the measurement of insulin-dependent glucose disposal in normal humans. Glucose 120-127 insulin Homo sapiens 102-109 3886702-5 1985 The fall in lipid oxidation was highly correlated with the increase in glucose oxidation during the insulin infusion (r = 0.96, P less than or equal to 0.0001). Glucose 71-78 insulin Homo sapiens 100-107 3882738-2 1985 The ability of insulin to stimulate glucose disposal was measured in 12 normal subjects by determining glucose disposal rates during insulin clamp studies carried out at both basal insulin concentrations (approximately 6 microU/ml) and during a period of sustained hyperinsulinemia (approximately 60 microU/ml). Glucose 36-43 insulin Homo sapiens 15-22 3886704-2 1985 The hyperinsulinemic-euglycemic clamp technique has been used to measure one component of the thermic effect of food, insulin and insulin-mediated glucose disposal. Glucose 147-154 insulin Homo sapiens 9-16 3882738-2 1985 The ability of insulin to stimulate glucose disposal was measured in 12 normal subjects by determining glucose disposal rates during insulin clamp studies carried out at both basal insulin concentrations (approximately 6 microU/ml) and during a period of sustained hyperinsulinemia (approximately 60 microU/ml). Glucose 103-110 insulin Homo sapiens 15-22 3886704-8 1985 The results showed that the thermic response to insulin and glucose infusions was similar in the two racial groups during high-dose insulin infusions but was markedly reduced in the Indians compared with the Caucasians during low-dose insulin infusions. Glucose 60-67 insulin Homo sapiens 132-139 3886704-8 1985 The results showed that the thermic response to insulin and glucose infusions was similar in the two racial groups during high-dose insulin infusions but was markedly reduced in the Indians compared with the Caucasians during low-dose insulin infusions. Glucose 60-67 insulin Homo sapiens 132-139 3882738-3 1985 The increment in glucose disposal was defined as insulin-dependent disposal and compared to estimates of insulin action generated by both the conventional insulin clamp approach and the minimal model technique. Glucose 17-24 insulin Homo sapiens 49-56 3882738-4 1985 The results documented an extremely close correlation (r = 0.99; P less than 0.001) between the direct determination of insulin-dependent glucose disposal and insulin-stimulated glucose disposal as estimated by the insulin clamp technique. Glucose 138-145 insulin Homo sapiens 120-127 3882738-4 1985 The results documented an extremely close correlation (r = 0.99; P less than 0.001) between the direct determination of insulin-dependent glucose disposal and insulin-stimulated glucose disposal as estimated by the insulin clamp technique. Glucose 178-185 insulin Homo sapiens 159-166 3882738-4 1985 The results documented an extremely close correlation (r = 0.99; P less than 0.001) between the direct determination of insulin-dependent glucose disposal and insulin-stimulated glucose disposal as estimated by the insulin clamp technique. Glucose 178-185 insulin Homo sapiens 159-166 3882738-5 1985 In contrast, there was a poor correlation (r = 0.44; P = NS) between insulin sensitivity as estimated by the minimal model technique and insulin-dependent glucose disposal. Glucose 155-162 insulin Homo sapiens 137-144 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 41-48 insulin Homo sapiens 76-83 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 41-48 insulin Homo sapiens 120-127 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 41-48 insulin Homo sapiens 120-127 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 41-48 insulin Homo sapiens 120-127 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 162-169 insulin Homo sapiens 76-83 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 162-169 insulin Homo sapiens 76-83 3882738-6 1985 These results indicate that the value of glucose disposal determined by the insulin clamp approach, which includes both insulin-independent and insulin-dependent glucose disposal, provides an excellent estimate of insulin-dependent glucose disposal in subjects with normal glucose tolerance. Glucose 162-169 insulin Homo sapiens 76-83 3886702-0 1985 Relationship between insulin-mediated glucose disposal and lipid metabolism in man. Glucose 38-45 insulin Homo sapiens 21-28 3884963-3 1985 However, circulating total and free insulin levels were not increased, and during testing by the euglycemic clamp method, the glucose response to increasing free insulin concentrations was within the range found in eight subjects with insulin-dependent diabetes. Glucose 126-133 insulin Homo sapiens 162-169 3884965-4 1985 Basal and maximum (8 nmol/L) insulin-stimulated glucose transport rates by isolated adipocytes increased by 83% (P less than 0.02) and 110% (P less than 0.01), respectively, after overfeeding, associated with an increase of 118% (P less than 0.01) in the incremental response to maximal insulin stimulation. Glucose 48-55 insulin Homo sapiens 29-36 3884965-4 1985 Basal and maximum (8 nmol/L) insulin-stimulated glucose transport rates by isolated adipocytes increased by 83% (P less than 0.02) and 110% (P less than 0.01), respectively, after overfeeding, associated with an increase of 118% (P less than 0.01) in the incremental response to maximal insulin stimulation. Glucose 48-55 insulin Homo sapiens 287-294 3884965-6 1985 Maximum insulin-stimulated total glucose utilization rates by isolated adipocytes incubated at 5.5 mmol/L glucose were 63% greater after overfeeding, due to increases in lactate formation, triglyceride synthesis, and CO2 production. Glucose 33-40 insulin Homo sapiens 8-15 3884965-6 1985 Maximum insulin-stimulated total glucose utilization rates by isolated adipocytes incubated at 5.5 mmol/L glucose were 63% greater after overfeeding, due to increases in lactate formation, triglyceride synthesis, and CO2 production. Glucose 106-113 insulin Homo sapiens 8-15 3884966-2 1985 Serum free CPR responses during 100 g oral glucose tolerance test (OGTT) were significantly lower in patients with insulin treatment for five years or more than in those with insulin treatment for less than five years although their previous immunoreactive insulin (IRI) responses during OGTT before insulin treatment showed no significant difference. Glucose 43-50 insulin Homo sapiens 115-122 3890129-5 1985 Although the serum insulin concentrations did not differ between diabetic and non-diabetic subjects, the insulin to glucose ratio was lower in the diabetics than in the non-diabetic subjects (p less than 0.05) indicating some degree of relative insulin deficiency in the diabetic patients. Glucose 116-123 insulin Homo sapiens 105-112 3890140-2 1985 Mean serum insulin levels increased significantly and similarly on both occasions, indicating that both the glucose- and GIP-induced insulin release is unaffected by atropine. Glucose 108-115 insulin Homo sapiens 133-140 3896263-5 1985 It is concluded that a small sovrabasal insulin dose would be probably required by diabetic patients after a protein meal: this is however so small that a carbohydrates related insulin dose given before a normal mixed meal would be able to normalize aminoacids as well as glucose metabolism. Glucose 272-279 insulin Homo sapiens 177-184 3883799-11 1985 Surprisingly, individual differences in obesity and maximal aerobic capacity accounted for only half the variability observed in insulin action in these glucose tolerant subjects. Glucose 153-160 insulin Homo sapiens 129-136 3838930-6 1985 Computer-assisted insulin delivery resulted in lower mean blood glucose (162 versus 130 mg/dl) and hemoglobin A1c (7.2% versus 5.8%) values when compared with precomputer values. Glucose 64-71 insulin Homo sapiens 18-25 3888754-2 1985 Hyperglycaemia, even when mild, can attenuate the secretory response of pancreatic beta and alpha cells to increments in glucose and can impair insulin-mediated glucose transport, thus impeding its own correction and initiating a cycle of progressive self-exacerbation and metabolic deterioration. Glucose 161-168 insulin Homo sapiens 144-151 3882486-5 1985 As seen with anti-R from a previous patient, desensitization consisted of both a dramatic decrease in the maximal responsiveness of the cells to insulin and a shift in the dose-response curve for insulin-stimulated glucose oxidation. Glucose 215-222 insulin Homo sapiens 196-203 3882489-4 1985 Adipocyte insulin binding and in vivo insulin dose-response curves for glucose disposal using the euglycemic clamp technique were measured before and after therapy to assess the effect on receptor and postreceptor insulin action. Glucose 71-78 insulin Homo sapiens 38-45 3882489-4 1985 Adipocyte insulin binding and in vivo insulin dose-response curves for glucose disposal using the euglycemic clamp technique were measured before and after therapy to assess the effect on receptor and postreceptor insulin action. Glucose 71-78 insulin Homo sapiens 38-45 3882489-6 1985 The insulin dose-response curve for overall glucose disposal remained right-shifted compared with age-matched controls, but the mean maximal glucose disposal rate increased by 74% from 160 +/- 14 to 278 +/- 18 mg/m2/min (P less than 0.0005). Glucose 44-51 insulin Homo sapiens 4-11 3899461-5 1985 The correlation of initial pressure with plasma insulin remained significant even when allowing for age, surface area, BMI, and plasma concentrations of glucose, urea, creatinine, sodium and urate. Glucose 153-160 insulin Homo sapiens 48-55 3884577-3 1985 After glucose ingestion, the rises in plasma glucose (P less than 0.01) and insulin (P less than 0.001) were 2.4- and 5.8-fold greater than when fructose was consumed. Glucose 6-13 insulin Homo sapiens 76-83 4042532-4 1985 The clamping was performed during 150 min using a glucose controlled insulin infusion system (Biostator). Glucose 50-57 insulin Homo sapiens 69-76 4042532-6 1985 Tissue sensitivity to insulin was expressed as glucose uptake (M) at steady state (90-150 min) over steady state serum insulin concentration (I). Glucose 47-54 insulin Homo sapiens 22-29 3884577-4 1985 After 30 min of exercise following glucose ingestion, the plasma glucose concentration had declined to a nadir of 3.9 +/- 0.3 mmol/l, and plasma insulin had returned to basal levels. Glucose 35-42 insulin Homo sapiens 145-152 3884577-5 1985 The fall in plasma glucose was closely related to the preexercise glucose (r = 0.98, P less than 0.001) and insulin (r = 0.66, P less than 0.05) levels. Glucose 19-26 insulin Homo sapiens 108-115 3882735-3 1985 During a hyperglycemic clamp (plasma glucose raised 125 mg/dl above basal level) maintained for 90 min, plasma insulin increased 4- to 5-fold (early) and then to values 8- to 10-fold above baseline (late). Glucose 37-44 insulin Homo sapiens 111-118 2857727-1 1985 The effect of insulin treatment on the rate of decline of plasma glucose concentration was determined in nine patients with hyperosmolar hyperglycemic nonketosis [HHNK; mean plasma glucose, 999 +/- 59 (+/- SEM) mg/dl] and in six normal subjects rendered hyperglycemic by a combined infusion of somatostatin and glucose (mean plasma glucose, 653 +/- 28 mg/dl). Glucose 65-72 insulin Homo sapiens 14-21 2857727-2 1985 Both the fractional glucose turnover and the half-time of the fall in plasma glucose during low dose (5-10 U/h) insulin treatment were reduced 10-fold (P less than 0.001) in the diabetic patients compared with the hyperglycemic normal subjects. Glucose 20-27 insulin Homo sapiens 112-119 2857727-3 1985 In the hyperosmolar patients, the mean glucose clearance during insulin treatment was only 7% that in the normal subjects (P less than 0.001). Glucose 39-46 insulin Homo sapiens 64-71 2857727-4 1985 The rate of plasma glucose decline in our hyperosmolar patients after hydration and insulin administration was 80 +/- 7 mg/dl X h. This decline is comparable to the results reported in other series, although in striking contrast to the 508 +/- 32 mg/dl X h decline in normal subjects (P less than 0.001). Glucose 19-26 insulin Homo sapiens 84-91 3882736-1 1985 We studied the dose-response characteristics of insulin"s ability to modulate its own secretion in normal and type II diabetic (NIDDM) subjects by measuring suppression of serum C-peptide levels during insulin infusions with the plasma glucose level held constant. Glucose 236-243 insulin Homo sapiens 48-55 3882736-9 1985 However, if plasma glucose was allowed to fall during the insulin infusions, there was a rapid decrease in serum C-peptide to 30% of basal levels, analogous to that in normal subjects. Glucose 19-26 insulin Homo sapiens 58-65 3883095-3 1985 Glucose concentrations, both fasting and during oral glucose tolerance testing, remained stable but both fasting insulin concentrations and insulin responses to oral glucose decreased (P less than 0.1 and less than 0.01, respectively). Glucose 166-173 insulin Homo sapiens 140-147 3921731-3 1985 A peak systemic glucose uptake of 7.0 +/- 0.4 mg/kg body weight/min was found at a plasma insulin concentration of 3192 +/- 150 mU/liter and a blood glucose concentration of 10.2 +/- 0.1 mmol/liter. Glucose 16-23 insulin Homo sapiens 90-97 2860737-2 1985 Insulin sensitivity for glucose utilization was measured by using cyclic somatostatin. Glucose 24-31 insulin Homo sapiens 0-7 3883950-5 1985 In addition, septic patients exhibited a decreased pancreatic insulin secretory response to an intravenous glucose tolerance test as evidenced by a significantly depressed peak insulin value (17 microU/cc) relative to injured patients (77 microU/cc). Glucose 107-114 insulin Homo sapiens 62-69 3883967-7 1985 Insulin-treated diabetics had about five times the rate of those with normal glucose tolerance. Glucose 77-84 insulin Homo sapiens 0-7 2858423-5 1985 This failure of a decrement in plasma glucose to suppress insulin secretion and to stimulate glucagon secretion was not observed when comparable hypoglycaemia was induced by exogenous insulin after a prolonged euglycaemic clamp. Glucose 38-45 insulin Homo sapiens 58-65 3888200-0 1985 Insulin and C-peptide secretion from B cells in human subjects stimulated with glucose. Glucose 79-86 insulin Homo sapiens 0-7 3888200-0 1985 Insulin and C-peptide secretion from B cells in human subjects stimulated with glucose. Glucose 79-86 insulin Homo sapiens 12-21 3884405-11 1985 CAPD offers excellent control of blood glucose levels using the intraperitoneal route to administer insulin. Glucose 39-46 insulin Homo sapiens 100-107 3881207-5 1985 However, the patients showed a threefold increase of plasma insulin after glucose. Glucose 74-81 insulin Homo sapiens 60-67 3881304-0 1985 Effect of insulin antibodies on insulin pharmacokinetics and glucose utilization in insulin-dependent diabetic patients. Glucose 61-68 insulin Homo sapiens 10-17 3884420-3 1985 Increasing glucose over a range 0-20 mmol/l resulted in a sigmoidal stimulation of insulin release (28.8 +/- 5.2 to 118.4 +/- 25.8 microU . Glucose 11-18 insulin Homo sapiens 83-90 3884420-6 1985 There was a marked correlation between the insulin secretory response of the islets to glucose and their rate of glucose oxidation (5.9 +/- 0.3 at glucose 2 mmol/l up to 25.8 +/- 1.8 pmol . Glucose 87-94 insulin Homo sapiens 43-50 3884420-6 1985 There was a marked correlation between the insulin secretory response of the islets to glucose and their rate of glucose oxidation (5.9 +/- 0.3 at glucose 2 mmol/l up to 25.8 +/- 1.8 pmol . Glucose 113-120 insulin Homo sapiens 43-50 3884420-10 1985 Stimulation of insulin secretion by glucose was dependent upon the presence of extracellular Ca2+. Glucose 36-43 insulin Homo sapiens 15-22 3884420-13 1985 This report demonstrates for the first time the sigmoidal nature of glucose-stimulated insulin release from isolated human islets, and its correlation with enhanced glucose oxidation. Glucose 68-75 insulin Homo sapiens 87-94 3967778-4 1985 When consumed in the last hour before exercise, the insulin stimulated-uptake of glucose from blood often results in hypoglycemia, greater dependence on muscle glycogen, and an earlier onset of exhaustion than when no CHO is fed. Glucose 81-88 insulin Homo sapiens 52-59 3967778-6 1985 The form of CHO (i.e., glucose, fructose, sucrose) ingested may produce different blood glucose and insulin responses, but the rate of muscle glycogen resynthesis is about the same regardless of the structure. Glucose 23-30 insulin Homo sapiens 100-107 3882760-2 1985 In this study insulin-stimulated glucose metabolism by normal rat adipocytes was used as a bioassay to identify the resistance activity, assess the effect of chemical modification on it, and the clinical states associated with its production. Glucose 33-40 insulin Homo sapiens 14-21 3880768-0 1985 Insulin-stimulated glucose disposal is not increased in anorexia nervosa. Glucose 19-26 insulin Homo sapiens 0-7 3892914-1 1985 The insulin response to glucose taken orally is increased in patients with impaired glucose tolerance (IGT) but decreased in those with type II diabetes mellitus. Glucose 24-31 insulin Homo sapiens 4-11 3880768-1 1985 Insulin-stimulated glucose disposal was investigated using the euglycemic hyperinsulinemic glucose clamp technique in six women with anorexia nervosa (27.3 +/- 4.9 yr old; weight, 38.8 +/- 6.6 kg) and compared to results obtained in six normal women (22.6 +/- 1.2 yr old; weight, 58 +/- 2.5 kg) and seven obese women (26.8 +/- 7.7 yr old; weight, 92.5 +/- 13.8 kg). Glucose 19-26 insulin Homo sapiens 0-7 3880768-6 1985 The indices of insulin sensitivity measured were the MCR of glucose and the ratio of glucose infused to insulin infused (G/I). Glucose 60-67 insulin Homo sapiens 15-22 3880768-10 1985 Thus, insulin-stimulated glucose disposal is normal in patients with anorexia nervosa, a finding that contrasts with the previously reported increase in erythrocyte insulin receptors in this disease. Glucose 25-32 insulin Homo sapiens 6-13 3881648-4 1985 Measurements of glucose utilization during constant infusions of insulin, showed significant changes with changing energy state, falling with overeating and rising with undereating. Glucose 16-23 insulin Homo sapiens 65-72 3881650-2 1985 h) on basal and glucose-stimulated insulin secretion in healthy and obese hyperinsulinemic subjects, the plasma C-peptide response was measured during maintenance of euglycemia and hyperglycemia by means of the glucose clamp technique. Glucose 16-23 insulin Homo sapiens 35-42 3884996-1 1985 Insulin responses to oral glucose loads were studied in patients with obstructive jaundice and compared with those of other liver diseases (fatty liver, chronic hepatitis and liver cirrhosis), pancreatic diseases, and definite diabetes mellitus. Glucose 26-33 insulin Homo sapiens 0-7 3884996-2 1985 Compared with their corresponding glucose intolerance, high insulin responses were characteristic in fatty liver, chronic hepatitis and liver cirrhosis, and insulin responses and insulinogenic index decreased in chronic hepatitis and liver cirrhosis as glucose intolerance progressed. Glucose 253-260 insulin Homo sapiens 157-164 3884996-4 1985 However, in obstructive jaundice with the pancreatic ducts intact, high insulin responses were observed in almost half of the cases with insulinogenic index above 0.5, and insulin response and insulinogenic index decreased as glucose intolerance progressed. Glucose 226-233 insulin Homo sapiens 72-79 3892914-3 1985 The acute insulin response to intravenously administered glucose is absent in cases of both IGT and type II diabetes when the fasting plasma glucose level exceeds 115 mg per dl. Glucose 57-64 insulin Homo sapiens 10-17 2857269-2 1985 It is suggested that, for some patients, treatment based on intermediate-acting insulin taken at bedtime will have more success than conventional regimens in lowering fasting, and thereby mean, plasma glucose concentrations, without causing hypoglycaemia. Glucose 201-208 insulin Homo sapiens 80-87 3892914-3 1985 The acute insulin response to intravenously administered glucose is absent in cases of both IGT and type II diabetes when the fasting plasma glucose level exceeds 115 mg per dl. Glucose 141-148 insulin Homo sapiens 10-17 3892914-5 1985 The absent acute insulin response to intravenously administered glucose can be restored by alpha-adrenergic blockade, prostaglandin synthesis inhibition, dopaminergic blockade and euglycemia. Glucose 64-71 insulin Homo sapiens 17-24 3882089-1 1985 Added TAME (N alpha-p-tosyl-1-anginine methyl ester) or BAME (benzoyl-anginine methyl ester) inhibited insulin induced activation of glucose oxidation and fat cell PDH activation without affecting spermine action on PDH activation and glucose oxidation in fat cells. Glucose 133-140 insulin Homo sapiens 103-110 3976026-0 1985 [Plasma concentrations of C-peptide and glucose during glucose tolerance tests. Glucose 55-62 insulin Homo sapiens 26-35 3882089-1 1985 Added TAME (N alpha-p-tosyl-1-anginine methyl ester) or BAME (benzoyl-anginine methyl ester) inhibited insulin induced activation of glucose oxidation and fat cell PDH activation without affecting spermine action on PDH activation and glucose oxidation in fat cells. Glucose 235-242 insulin Homo sapiens 103-110 3882089-4 1985 These results suggest that certain actions of insulin (glucose oxidation, generation of PDH regulators) are mediated by proteolytic events, while insulin-induced down regulation and negative cooperativity of insulin receptors are not mediated by activation of endogenous proteases. Glucose 55-62 insulin Homo sapiens 46-53 3890450-5 1985 On the contrary, 0.2 mg/kg (i.e. 12-14 mg per subject as total amount) given to 3 women and 6 men led to a glucose-induced insulin release significantly lower than that recorded in basal conditions, with corresponding greater plasma glucose elevation. Glucose 107-114 insulin Homo sapiens 123-130 3907294-2 1985 Plasma insulin levels showed positive correlations, besides to blood glucose levels, to body mass index, plasma triglyceride level and blood pressure and inverse correlations to leisure time physical activity and objectively measured physical fitness. Glucose 69-76 insulin Homo sapiens 7-14 3918396-6 1985 Furthermore, 2 h pre-incubation with insulin (100 mIU/ml) increased glucose incorporation by cultured porcine granulosa cells as determined by pulsing with D-[14C](U)-glucose. Glucose 68-75 insulin Homo sapiens 37-44 3918396-6 1985 Furthermore, 2 h pre-incubation with insulin (100 mIU/ml) increased glucose incorporation by cultured porcine granulosa cells as determined by pulsing with D-[14C](U)-glucose. Glucose 167-174 insulin Homo sapiens 37-44 3918396-8 1985 These results suggest that porcine granulosa cells possess insulin receptors and that insulin, mediated by its specific receptors, enhances glucose metabolism by stimulating glycogen synthase. Glucose 140-147 insulin Homo sapiens 86-93 3918399-5 1985 In contrast, the maximum insulin-induced glucose oxidation was markedly decreased before treatment, whereas it was totally normalized after treatment. Glucose 41-48 insulin Homo sapiens 25-32 3898761-0 1985 Insulin-stimulated glucose disposal in patients with type I (IDDM) and type II (NIDDM) diabetes mellitus. Glucose 19-26 insulin Homo sapiens 0-7 3898761-1 1985 In conclusion, there is considerable data documenting the presence of resistance to insulin-stimulated glucose uptake in patients with either IDDM or NIDDM. Glucose 103-110 insulin Homo sapiens 84-91 3898761-4 1985 As a corollary, it seems reasonable to suggest that resistance to insulin-stimulated glucose uptake is not a primary defect in the pathogenesis of IDDM. Glucose 85-92 insulin Homo sapiens 66-73 3898761-6 1985 In contrast, resistance to insulin-stimulated glucose uptake does not seem to be a simple function of severity of hyperglycemia in patients with NIDDM, and significant insulin resistance can exist in these patients in association with only mild carbohydrate intolerance. Glucose 46-53 insulin Homo sapiens 27-34 3898761-7 1985 Furthermore, although the decline in insulin-stimulated glucose disposal present in patients with significant fasting hyperglycemia can be increased by instituting excellent metabolic control with exogenous insulin, it cannot be restored to normal. Glucose 56-63 insulin Homo sapiens 37-44 3898761-7 1985 Furthermore, although the decline in insulin-stimulated glucose disposal present in patients with significant fasting hyperglycemia can be increased by instituting excellent metabolic control with exogenous insulin, it cannot be restored to normal. Glucose 56-63 insulin Homo sapiens 207-214 3898762-1 1985 In normal man, glucose serves to regulate basal insulin secretion by its participation with insulin in a feedback loop. Glucose 15-22 insulin Homo sapiens 48-55 3898762-2 1985 In addition, glucose stimulates insulin secretion directly and potentiates insulin responses to nonglucose stimuli such as amino acids, beta-adrenergic stimuli, and gut hormones. Glucose 13-20 insulin Homo sapiens 32-39 3898762-3 1985 Maximal glycemic potentiation of the acute insulin response to IV arginine occurs at a glucose level of approx. Glucose 87-94 insulin Homo sapiens 43-50 3898762-6 1985 In addition, the first phase (0-10 min) insulin response to IV glucose is absent in virtually all patients with overt NIDDM. Glucose 63-70 insulin Homo sapiens 40-47 3898762-9 1985 However, insulin responses to arginine are lower than those of nondiabetic controls when compared at multiple matched glucose levels. Glucose 118-125 insulin Homo sapiens 9-16 3898762-10 1985 Indeed, maximal potentiation by glucose of the insulin response to arginine is markedly subnormal in NIDDM, suggesting a loss of functional B cell secretory capacity. Glucose 32-39 insulin Homo sapiens 47-54 3898763-8 1985 Consistent with this, the post-receptor defect is partially reversible by insulin therapy, which leads to a 50-70% reversal of the reduced rates of in vivo glucose disposal and in vitro glucose transport. Glucose 156-163 insulin Homo sapiens 74-81 3898763-8 1985 Consistent with this, the post-receptor defect is partially reversible by insulin therapy, which leads to a 50-70% reversal of the reduced rates of in vivo glucose disposal and in vitro glucose transport. Glucose 186-193 insulin Homo sapiens 74-81 3898763-15 1985 One of insulin"s major biologic effects is the promotion of overall glucose metabolism, and abnormalities of this aspect of insulin action can lead to a number of important clinical and pathophysiologic states including Type II diabetes, also known as non-insulin-dependent diabetes mellitus (NIDDM). Glucose 68-75 insulin Homo sapiens 7-14 3898767-5 1985 Within NIDDM and within MODY there are differences in the magnitude of insulin responses to glucose, differences in target tissue responsiveness to insulin in vivo, and differences in receptor and post-receptor effects of insulin. Glucose 92-99 insulin Homo sapiens 71-78 3898767-9 1985 The natural history of carbohydrate metabolism and of insulin secretory responses to glucose in early Type I diabetes and in MODY with low insulin secretory responses are illustrated and similarities and dissimilarities compared and contrasted. Glucose 85-92 insulin Homo sapiens 54-61 3898767-9 1985 The natural history of carbohydrate metabolism and of insulin secretory responses to glucose in early Type I diabetes and in MODY with low insulin secretory responses are illustrated and similarities and dissimilarities compared and contrasted. Glucose 85-92 insulin Homo sapiens 139-146 3909766-10 1985 Plasma insulin response to glucose was more exaggerated in those with the Werner syndrome than in normal aged subjects. Glucose 27-34 insulin Homo sapiens 7-14 3909766-11 1985 The euglycemic glucose clamp method revealed lower glucose disposal rates and insulin sensitivity indices in the Werner syndrome than in normal subjects of similar age. Glucose 15-22 insulin Homo sapiens 78-85 3883764-2 1985 In response to oral glucose, the proband exhibited marked hyperinsulinism (maximum plasma insulin = 4,120 microU/ml), the father had mild hyperinsulinism (maximum plasma insulin = 240 microU/ml), and the mother was normal. Glucose 20-27 insulin Homo sapiens 63-70 3931537-4 1985 The fasting plasma glucose concentrations were lower during the insulin plus glibenclamide period than during the insulin plus placebo period and the difference tended to increase at the end of each study period (p less than 0.01 and 0.001). Glucose 19-26 insulin Homo sapiens 64-71 3931537-4 1985 The fasting plasma glucose concentrations were lower during the insulin plus glibenclamide period than during the insulin plus placebo period and the difference tended to increase at the end of each study period (p less than 0.01 and 0.001). Glucose 19-26 insulin Homo sapiens 114-121 3931537-6 1985 The 24-hour urinary glucose excretion was reduced during the insulin + glibenclamide period compared with insulin + placebo (p less than 0.05). Glucose 20-27 insulin Homo sapiens 61-68 2986528-3 1985 Activation of this kinase is believed to generate a signal that eventually results in insulin"s action on glucose, lipid, and protein metabolism. Glucose 106-113 insulin Homo sapiens 86-93 3888064-3 1985 Prior to clinical diabetes, islet-cell antibodies and activated T lymphocytes are found in conjunction with a slowly progressive loss of intravenous glucose-stimulated insulin secretion. Glucose 149-156 insulin Homo sapiens 168-175 3911737-0 1985 Insulin infusion normalizes cardiovascular responses and plasma noradrenaline after oral glucose in type 1 (insulin-dependent) diabetes. Glucose 89-96 insulin Homo sapiens 0-7 3911737-1 1985 We examined whether the abnormal regulation of the cardiovascular system and plasma noradrenaline observed after oral glucose in insulin-dependent diabetic patients could be normalized by intravenous infusion of insulin. Glucose 118-125 insulin Homo sapiens 129-136 3911737-6 1985 The present study indicates that physiologic increments in plasma insulin concentration are of importance in the regulation of the cardiovascular system and plasma NA following an oral glucose load. Glucose 185-192 insulin Homo sapiens 66-73 2408593-2 1985 Gentamicin significantly reduced the insulin release in the absence as well as in the presence of increasing concentrations of glucose. Glucose 127-134 insulin Homo sapiens 37-44 3909997-0 1985 Relationship between insulin response to intravenous glucose and plasma lipoproteins in healthy men. Glucose 53-60 insulin Homo sapiens 21-28 2408593-7 1985 We suggest that gentamicin reduces glucose-induced insulin release by blocking the entry of Ca2+ into the B-cells. Glucose 35-42 insulin Homo sapiens 51-58 3909997-3 1985 The Insulin Response to a bolus of intravenous glucose (0.50 g/kg) was significantly correlated with VLDL-Triglyceride (p less than 0.01), VLDL-Cholesterol (p less than 0.01) and with the "Atherogenic Index" (Formula: see text) (p less than 0.01). Glucose 47-54 insulin Homo sapiens 4-11 2998492-2 1985 In the fetus at term, insulin and glucagon secretion can be modified by long-term changes in glucose concentration but the responsiveness of A and B cells to glucose is lower than in the adult. Glucose 93-100 insulin Homo sapiens 22-29 3933479-0 1985 Glucose uptake in isolated heart cells: studies on the role of insulin. Glucose 0-7 insulin Homo sapiens 63-70 3933479-3 1985 Insulin action on the glucose carrier is exclusively due to an increase in Vmax with no changes in Km. Glucose 22-29 insulin Homo sapiens 0-7 3884055-5 1985 The insulin response to glucose was similar. Glucose 24-31 insulin Homo sapiens 4-11 3888211-1 1985 Demonstration of an inhibitory effect of glucose on insulin release in the mouse and man. Glucose 41-48 insulin Homo sapiens 52-59 3888211-5 1985 The dual effect of glucose on cytosolic Ca2+ had its counterpart in the release of insulin. Glucose 19-26 insulin Homo sapiens 83-90 3888211-6 1985 Whereas 20 mmol/l of glucose stimulated the release of insulin from mouse islets previously stored in a Ca2+-deficient medium, the sugar was clearly inhibitory when present at a concentration of 6 mmol/l. Glucose 21-28 insulin Homo sapiens 55-62 3888211-7 1985 Intravenous glucose tolerance tests revealed a temporary glucose depression of the serum concentrations of insulin and C-peptide in several patients with diabetes. Glucose 12-19 insulin Homo sapiens 107-114 3922718-0 1985 Different patterns of blood sugar and serum insulin levels after different glucose preparations. Glucose 75-82 insulin Homo sapiens 44-51 3888211-7 1985 Intravenous glucose tolerance tests revealed a temporary glucose depression of the serum concentrations of insulin and C-peptide in several patients with diabetes. Glucose 12-19 insulin Homo sapiens 119-128 3888211-8 1985 In a mentally retarded girl with hyperinsulinemia associated with acanthosis nigricans the glucose suppression of circulating insulin was prolonged and sufficiently pronounced to suggest an almost complete inhibition of the secretory activity of the pancreatic B-cells. Glucose 91-98 insulin Homo sapiens 38-45 3896283-2 1985 In the first study, the effect of acute dosing (via an intravenous infusion of 5 mg h-1 for 3 h) on the glucose, insulin, hormonal, and intermediary metabolite responses to an intravenous glucose tolerance test was determined in six healthy male volunteers. Glucose 188-195 insulin Homo sapiens 113-120 3914387-0 1985 Intravenous insulin normalizes cardiovascular function and sympathetic activity after oral glucose in insulin-dependent diabetic patients. Glucose 91-98 insulin Homo sapiens 12-19 3912064-5 1985 Closed-loop systems are infusion systems located outside the body which deliver insulin according to glucose values that are measured continuously. Glucose 101-108 insulin Homo sapiens 80-87 3922718-6 1985 Our findings of different effects of the same amount of glucose administered in various forms on pattern of blood sugar and insulin cannot been explained from our material. Glucose 56-63 insulin Homo sapiens 124-131 3915254-1 1985 In this article we have described the hypothesis that insulin stimulates glucose transport through glucose transporter translocation from an intracellular pool to the plasma membrane. Glucose 73-80 insulin Homo sapiens 54-61 3882369-5 1985 Central to our diagnostic algorithm was the glucose response to 0.1 U/kg insulin administered subcutaneously and intravenously. Glucose 44-51 insulin Homo sapiens 73-80 3882369-8 1985 However, if an "abnormal" glucose response to the insulin challenge tests was observed, the location of the insulin resistance was identified as being subcutaneous, intravascular, or at the peripheral tissue. Glucose 26-33 insulin Homo sapiens 50-57 3882369-8 1985 However, if an "abnormal" glucose response to the insulin challenge tests was observed, the location of the insulin resistance was identified as being subcutaneous, intravascular, or at the peripheral tissue. Glucose 26-33 insulin Homo sapiens 108-115 3882370-0 1985 C-Peptide responses to glucose load in maturity-onset diabetes of the young (MODY). Glucose 23-30 insulin Homo sapiens 0-9 3884415-1 1985 The release of insulin from the human pancreas in response to glucose is known to be either poor or absent in the fetus, whereas in the infant and adult, the response is much greater. Glucose 62-69 insulin Homo sapiens 15-22 3888495-8 1985 We conclude that insulin pump treatment for 6 months results in a near normalization of glucose and FFA metabolism, resulting in an improved quality of life. Glucose 88-95 insulin Homo sapiens 17-24 3971844-7 1985 In 12 subjects a 15% reduction in basal insulin infusion rate increased the mean +/- SEM dawn glycemic increase from 0.58 +/- 0.25 mmol/L to 2.7 +/- 0.76 mmol/L (P less than 0.025) as well as significantly increasing the nocturnal nadir and 0800 h plasma glucose concentrations. Glucose 255-262 insulin Homo sapiens 40-47 3887544-9 1985 By this procedure, the maximal binding of 125I-Insulin was 10.55 +/- 0.78% (mean +/- SD) in five normal volunteers and 6.79 +/- 1.77 (mean +/- SD) in five obese nondiabetic patients, having an enhanced insulin response in the oral glucose tolerance test. Glucose 231-238 insulin Homo sapiens 47-54 3905391-0 1985 Contribution of the exercise-induced increment in glucose storage to the increased insulin sensitivity of endurance athletes. Glucose 50-57 insulin Homo sapiens 83-90 3905391-1 1985 The present study was designed to evaluate the contribution of the exercise-induced increment in glucose storage to the increased insulin sensitivity characterizing endurance athletes. Glucose 97-104 insulin Homo sapiens 130-137 3905391-5 1985 As expected, preexercise values of non-trained subjects revealed a much higher insulin response to glucose, and a lower glucose storage and lipid oxidation compared to results obtained in endurance trained individuals. Glucose 99-106 insulin Homo sapiens 79-86 3905391-11 1985 On day 3 after exercise, glucose and insulin responses to glucose were similar to preexercise values. Glucose 58-65 insulin Homo sapiens 37-44 3905391-12 1985 These results indicate that the increase in glucose storage by acute exercise is not systematically associated with an improved glucose homeostasis, suggesting that other adaptive mechanisms also contribute to the improvement of insulin sensitivity in endurance athletes. Glucose 44-51 insulin Homo sapiens 229-236 3913598-0 1985 The relation between growth hormone, cortisol and insulin and plasma levels of free fatty acids and glucose in healthy mothers at delivery and their newborn children. Glucose 100-107 insulin Homo sapiens 50-57 2995196-4 1985 Glucose feeding and the resultant rise in insulin are, therefore, associated with a considerable reduction in urine acidity and Na, K, Cl, and phosphorus excretion. Glucose 0-7 insulin Homo sapiens 42-49 3915254-2 1985 In addition, we have shown that changes in the numbers and subcellular distributions of glucose transporters correlate with alterations in insulin-stimulated glucose transport activity in several experimental models of insulin resistance and hyperresponsiveness. Glucose 88-95 insulin Homo sapiens 139-146 3915254-2 1985 In addition, we have shown that changes in the numbers and subcellular distributions of glucose transporters correlate with alterations in insulin-stimulated glucose transport activity in several experimental models of insulin resistance and hyperresponsiveness. Glucose 88-95 insulin Homo sapiens 219-226 3915254-4 1985 Thus, evidence has been presented for changes in glucose transporter intrinsic activity that both inhibit and augment insulin-stimulated glucose transport rates. Glucose 49-56 insulin Homo sapiens 118-125 3908274-5 1985 After intravenous insulin, plasma glucose fell significantly less in patients than in controls (p less than 0.01). Glucose 34-41 insulin Homo sapiens 18-25 3928473-10 1985 The insulin/glucose ratio was significantly decreased at the end of surgery in term and preterm neonates. Glucose 12-19 insulin Homo sapiens 4-11 3908274-9 1985 These results indicate that glucose intolerance occurs frequently in gonadal dysgenesis and is associated with normal or increased insulin secretory responses. Glucose 28-35 insulin Homo sapiens 131-138 3902687-15 1985 Furthermore, the insulin response to the glucose load, whether elevated or decreased before weight loss, tended towards normalization after weight reduction. Glucose 41-48 insulin Homo sapiens 17-24 2578425-1 1985 The stimulation of glucose uptake and RNA synthesis by insulin was studied in cultured fibroblasts from patients with an inherited affinity defect of the insulin receptor. Glucose 19-26 insulin Homo sapiens 55-62 3905643-5 1985 These results are consistent with the hypothesis that insulin regulates glucose transport activity in adipocytes by causing translocation of the glucose transport apparatus in a reversible manner, and that the translocation, or recycling, of the glucose transport apparatus is brought about by exo- and endocytosis. Glucose 72-79 insulin Homo sapiens 54-61 3905643-5 1985 These results are consistent with the hypothesis that insulin regulates glucose transport activity in adipocytes by causing translocation of the glucose transport apparatus in a reversible manner, and that the translocation, or recycling, of the glucose transport apparatus is brought about by exo- and endocytosis. Glucose 145-152 insulin Homo sapiens 54-61 3905643-5 1985 These results are consistent with the hypothesis that insulin regulates glucose transport activity in adipocytes by causing translocation of the glucose transport apparatus in a reversible manner, and that the translocation, or recycling, of the glucose transport apparatus is brought about by exo- and endocytosis. Glucose 145-152 insulin Homo sapiens 54-61 3905645-0 1985 Relationship between obesity and maximal insulin-stimulated glucose uptake in vivo and in vitro in man. Glucose 60-67 insulin Homo sapiens 41-48 3905646-0 1985 Sensitivity of glucose uptake to insulin in vitro and in vivo in obese Pima Indians. Glucose 15-22 insulin Homo sapiens 33-40 3905652-8 1985 When there is inappropriate hypothalamic suppression of growth hormone, the anti-insulin activity of growth hormone acts to raise plasma glucose levels even higher. Glucose 137-144 insulin Homo sapiens 81-88 3908351-3 1985 For these purposes, we measured and correlated: (1) insulin sensitivity, estimated by glucose disappearance rate from plasma after intravenous insulin injection; (2) insulin secretion by the pancreas, estimated by fasting C-peptide levels in peripheral blood; (3) insulin metabolism, estimated by means of C-peptide: insulin molar ratio in peripheral blood. Glucose 86-93 insulin Homo sapiens 52-59 3934092-0 1985 Insulin-mediated glucose metabolism in the relationship between dietary intake and sympathetic nervous system activity. Glucose 17-24 insulin Homo sapiens 0-7 3934092-1 1985 The data reviewed here demonstrate a role for insulin-mediated glucose metabolism in the relationship between fasting, carbohydrate intake, and sympathetic activity. Glucose 63-70 insulin Homo sapiens 46-53 3934092-2 1985 A model relating insulin-mediated glucose metabolism to sympathetic nervous system activity during fasting and carbohydrate feeding is presented. Glucose 34-41 insulin Homo sapiens 17-24 3900179-5 1985 Stimulated glucose and insulin levels during an insulin tolerance test, intravenous glucose tolerance test, and standard meal demonstrated a similar pattern, although the changes due to either diet or weight loss were minimal. Glucose 11-18 insulin Homo sapiens 48-55 2981087-3 1985 Oral glucose loading resulted in normal glucose curves, subnormal peak insulin responses of 12-20 microU/ml in three hypocalcemic patients, and normal peak serum insulin values of 30-40 microU/ml in two normocalcemic patients. Glucose 5-12 insulin Homo sapiens 71-78 3880558-3 1985 While two of the obese patients had normal glucose tolerance, all had fasting hyperinsulinemia (P less than 0.02 vs. normal subjects) and exaggerated insulin responses after oral glucose challenge, as defined by area under the 3-h insulin response curve (P less than 0.01 vs. normal subjects). Glucose 179-186 insulin Homo sapiens 150-157 3880558-4 1985 That this hyperinsulinemia represented in vivo insulin resistance was supported by the glucose and insulin responses in four individuals to an iv glucose bolus analyzed by the minimal modeling technique. Glucose 87-94 insulin Homo sapiens 15-22 3880558-4 1985 That this hyperinsulinemia represented in vivo insulin resistance was supported by the glucose and insulin responses in four individuals to an iv glucose bolus analyzed by the minimal modeling technique. Glucose 87-94 insulin Homo sapiens 47-54 3880560-0 1985 Pathogenesis of age-related glucose intolerance in man: insulin resistance and decreased beta-cell function. Glucose 28-35 insulin Homo sapiens 56-63 3880848-3 1985 With a glucose-free prime, cardiopulmonary bypass induced a slight hyperglycemia but no endogenous insulin response, suggesting a partial inhibition of insulin secretion. Glucose 7-14 insulin Homo sapiens 152-159 3870620-0 1985 Simplified evaluation and documentation of data from glucose controlled insulin infusion systems--artefact handling. Glucose 53-60 insulin Homo sapiens 72-79 3883047-2 1985 Considering this fact glucagon and insulin responses to oral glucose and intravenous arginine were studied in 22 CF children and adolescents. Glucose 61-68 insulin Homo sapiens 35-42 3883047-6 1985 On the other hand the data reveal that there is only a defect in the beta cell function consisting in a delayed insulin release selective to glucose whereas responsiveness to other stimuli for example tolbutamide and arginine is undisturbed. Glucose 141-148 insulin Homo sapiens 112-119 3883047-8 1985 Yet in patients with normal oral glucose tolerance endogenous insulin secretion is significantly reduced. Glucose 33-40 insulin Homo sapiens 62-69 3870620-1 1985 A computerized method for artefact handling, which occurs during recording and evaluation of data from glucose controlled insulin infusion systems (GCIIS) is demonstrated: Recording phase: "Interrupt"-Mode: Restoring of the original linear data-time relation is achieved by using an additional time channel. Glucose 103-110 insulin Homo sapiens 122-129 3883072-3 1985 Exercise during insulin excess results in inhibition of hepatic glucose production and accelerated muscle glucose utilization and results in hypoglycemia. Glucose 64-71 insulin Homo sapiens 16-23 3883072-3 1985 Exercise during insulin excess results in inhibition of hepatic glucose production and accelerated muscle glucose utilization and results in hypoglycemia. Glucose 106-113 insulin Homo sapiens 16-23 3916635-4 1985 Viability of the islets both before and after the freeze-thaw sequence was established by secretion of insulin in response to stimulation with both theophylline and high glucose in a dynamic perifusion system. Glucose 170-177 insulin Homo sapiens 103-110 3906417-6 1985 After an intravenous glucose load, the insulin-to-glucose ratio decreased in parallel with the increase in binding after dialysis. Glucose 21-28 insulin Homo sapiens 39-46 3939680-3 1985 The diffusion patterns of insulin and glucose were shown to be better than those described for the best artificial membranes, the 50% diffusion being reached at min 42 for 125 I-Insulin and at min 11 for D-glucose. Glucose 38-45 insulin Homo sapiens 178-185 3939680-3 1985 The diffusion patterns of insulin and glucose were shown to be better than those described for the best artificial membranes, the 50% diffusion being reached at min 42 for 125 I-Insulin and at min 11 for D-glucose. Glucose 204-213 insulin Homo sapiens 26-33 3906417-6 1985 After an intravenous glucose load, the insulin-to-glucose ratio decreased in parallel with the increase in binding after dialysis. Glucose 50-57 insulin Homo sapiens 39-46 3917568-6 1985 This physician should follow a definite protocol of subcutaneous insulin administration guided by appropriate monitoring of blood glucose response. Glucose 130-137 insulin Homo sapiens 65-72 3883127-1 1985 In 20 cases with carcinoma of pancreas, 15 cases with chronic pancreatitis and 17 control cases, the levels of insulin in portal and peripheral blood after glucose infusions and the microscopical changes of pancreatic islet cells were examined. Glucose 156-163 insulin Homo sapiens 111-118 3883127-4 1985 In the cases with carcinoma of pancreas, the rate of disappearance of glucose (K-index) to 60" sigma 0" IRI in portal blood was low value and the glucose tolerance per insulin unit was decreased. Glucose 146-153 insulin Homo sapiens 168-175 6439036-13 1984 In summary, combination therapy consisting of glyburide and insulin moderately improved glucose control in type II diabetes mellitus at the end of four weeks. Glucose 88-95 insulin Homo sapiens 60-67 3991568-3 1985 In contrast (14C)-D-glucose transport exhibited decreased sensitivity to insulin. Glucose 18-27 insulin Homo sapiens 73-80 3991568-5 1985 The non-insulin and the maximally insulin stimulated glucose transport of adipocytes from uraemic patients was normal. Glucose 53-60 insulin Homo sapiens 34-41 3991568-7 1985 Taken together these results suggest that the insulin resistance of adipocytes from patients with chronic uraemia may be primarily accounted for by post-binding defects localised to glucose transport and metabolism. Glucose 182-189 insulin Homo sapiens 46-53 6152172-1 1984 The day-time variations of blood sugar and associated changes in plasma insulin and somatostatin levels in response to glucose-glucagon load were investigated in eight healthy volunteers. Glucose 119-126 insulin Homo sapiens 72-79 6391139-7 1984 Summed insulin levels after the oral glucose tolerance were significantly different by age and season. Glucose 37-44 insulin Homo sapiens 7-14 6393677-8 1984 In conclusion, semisynthetic human insulin is equally effective as porcine insulin in regulating glucose kinetics in the basal state and during exercise. Glucose 97-104 insulin Homo sapiens 35-42 6393677-8 1984 In conclusion, semisynthetic human insulin is equally effective as porcine insulin in regulating glucose kinetics in the basal state and during exercise. Glucose 97-104 insulin Homo sapiens 75-82 6239714-4 1984 There was deterioration of glucose tolerance with increased plasma insulin concentrations and these effects were progressive with time. Glucose 27-34 insulin Homo sapiens 67-74 6391408-1 1984 In a patient with severe hypertension in association with insulin-induced hypoglycemia and prior therapy with propranolol hydrochloride, intravenous 50% dextrose significantly reduced arterial pressure on two occasions. Glucose 153-161 insulin Homo sapiens 58-65 6094291-1 1984 The acute administration of a beta receptor-stimulating agent profoundly affects insulin-mediated glucose metabolism; however, little is known about the impact of chronic beta receptor stimulation on glucose metabolism and insulin sensitivity. Glucose 98-105 insulin Homo sapiens 81-88 6094291-4 1984 However, insulin-stimulated total glucose metabolism increased by 29% (7.0 +/- 0.47 versus 9.05 +/- 0.67 mg/min X kg; P less than 0.02). Glucose 34-41 insulin Homo sapiens 9-16 6094291-5 1984 Insulin-stimulated, nonoxidative glucose disposal increased by 45% (3.62 +/- 0.42 versus 5.26 +/- 0.48 mg/min X kg; P less than 0.01), while insulin-stimulated glucose oxidation did not change significantly (3.38 +/- 0.15 versus 3.79 +/- 0.22 mg/min X kg). Glucose 33-40 insulin Homo sapiens 0-7 6094291-5 1984 Insulin-stimulated, nonoxidative glucose disposal increased by 45% (3.62 +/- 0.42 versus 5.26 +/- 0.48 mg/min X kg; P less than 0.01), while insulin-stimulated glucose oxidation did not change significantly (3.38 +/- 0.15 versus 3.79 +/- 0.22 mg/min X kg). Glucose 160-167 insulin Homo sapiens 141-148 6094291-8 1984 We conclude that chronic beta receptor stimulation with TS improves insulin-stimulated glucose disposal in man, mostly by improving nonoxidative glucose disposal, i.e., "glucose storage. Glucose 87-94 insulin Homo sapiens 68-75 6389235-5 1984 Glycemic control was established in diabetic patients by intravenously infusing insulin in response to measured glucose concentrations on a moment-to-moment basis for a period of several days. Glucose 112-119 insulin Homo sapiens 80-87 6391746-4 1984 In the second study, fasting and oral glucose stimulated C-peptide/insulin ratios were compared in 16 cirrhotic and 18 weight matched control subjects. Glucose 38-45 insulin Homo sapiens 67-74 6397366-3 1984 When insulin was present, however, metformin stimulated glucose conversion into both triglycerides and CO2. Glucose 56-63 insulin Homo sapiens 5-12 6397366-6 1984 In conclusion, metformin seems to exert its effect on glucose metabolism by potentiating the action of insulin at a post-receptor level, possibly on the rate of glucose transport. Glucose 54-61 insulin Homo sapiens 103-110 6391746-9 1984 Following the glucose load in 13 of the control and seven of the cirrhotic group, the C-peptide/insulin ratio fell in both groups but was significantly lower in the cirrhotic compared to control subjects at 30, 60 and 120 min, consistent with possible impairment of hepatic insulin extraction. Glucose 14-21 insulin Homo sapiens 96-103 6397366-6 1984 In conclusion, metformin seems to exert its effect on glucose metabolism by potentiating the action of insulin at a post-receptor level, possibly on the rate of glucose transport. Glucose 161-168 insulin Homo sapiens 103-110 6397368-0 1984 Altered glucose transport conferring post-receptor insulin resistance to a patient with lipoatrophic diabetes. Glucose 8-15 insulin Homo sapiens 51-58 6396100-5 1984 With treatment, plasma insulin increased 2-fold at fasting and 7-fold at 2 hours after oral glucose. Glucose 92-99 insulin Homo sapiens 23-30 6397387-4 1984 In interferon-treated islets glucose-stimulated insulin secretion was unaltered from that of control islets; however, glucose-stimulated proinsulin biosynthesis was specifically inhibited by interferon (48%, p less than 0.025). Glucose 29-36 insulin Homo sapiens 48-55 6397387-4 1984 In interferon-treated islets glucose-stimulated insulin secretion was unaltered from that of control islets; however, glucose-stimulated proinsulin biosynthesis was specifically inhibited by interferon (48%, p less than 0.025). Glucose 118-125 insulin Homo sapiens 137-147 16829459-6 1984 In patients with glucose load the number of receptors decreased and receptor affinity to insulin at physiological concentration decreased. Glucose 17-24 insulin Homo sapiens 89-96 16829459-7 1984 The results suggest that in patients receiving a glucose load the receptor changes indicate the perioperative development of insulin resistance at receptor level. Glucose 49-56 insulin Homo sapiens 125-132 6099816-4 1984 This finding may help explain blood glucose levels and the inappropriate plasma insulin response to oral glucose often observed in these patients. Glucose 105-112 insulin Homo sapiens 80-87 6398261-2 1984 When the insulin dose delivered is adjusted to achieve a near match of the peripheral plasma glucose profile, the 24 h profiles of free fatty acids, glycerol, lactate and beta-hydroxybutyrate and the hormones, insulin, glucagon, cortisol and catecholamines were identical. Glucose 93-100 insulin Homo sapiens 9-16 6398253-2 1984 Serum C-peptide and insulin responses to oral glucose load were measured in 69 offspring of conjugal diabetic parents (OCDP). Glucose 46-53 insulin Homo sapiens 20-27 6398258-5 1984 Employing the glucose clamp technique with the aid of an artificial pancreas (Biostator), glucose disposal during insulin infusion (0.1 U/kg in 60 min) was calculated by the amount of glucose required to keep the blood glucose at preinfusion levels. Glucose 90-97 insulin Homo sapiens 114-121 6386838-6 1984 The comparison of the corresponding plasma levels and areas of C-peptide and insulin after glucose showed that for the same C-peptide value, the insulin value was higher in the obese group. Glucose 91-98 insulin Homo sapiens 145-152 6398258-5 1984 Employing the glucose clamp technique with the aid of an artificial pancreas (Biostator), glucose disposal during insulin infusion (0.1 U/kg in 60 min) was calculated by the amount of glucose required to keep the blood glucose at preinfusion levels. Glucose 90-97 insulin Homo sapiens 114-121 6398258-5 1984 Employing the glucose clamp technique with the aid of an artificial pancreas (Biostator), glucose disposal during insulin infusion (0.1 U/kg in 60 min) was calculated by the amount of glucose required to keep the blood glucose at preinfusion levels. Glucose 90-97 insulin Homo sapiens 114-121 6386838-6 1984 The comparison of the corresponding plasma levels and areas of C-peptide and insulin after glucose showed that for the same C-peptide value, the insulin value was higher in the obese group. Glucose 91-98 insulin Homo sapiens 77-84 6386838-7 1984 Last, in obese subjects the parameter used as an estimate of hepatic removal of insulin after oral glucose inversely correlated with the fasting insulin concentration and the insulin incremental area after glucose. Glucose 99-106 insulin Homo sapiens 80-87 6386838-7 1984 Last, in obese subjects the parameter used as an estimate of hepatic removal of insulin after oral glucose inversely correlated with the fasting insulin concentration and the insulin incremental area after glucose. Glucose 206-213 insulin Homo sapiens 80-87 6386838-8 1984 These results suggest that in obesity peripheral hyperinsulinemia depends on pancreatic hypersecretion of insulin in the fasting state and impaired hepatic insulin metabolism after oral glucose loading. Glucose 186-193 insulin Homo sapiens 54-61 6389533-2 1984 It was found that insulin decreased the infinite-cis Km for both D-glucose and D-galactose influx by 44 and 56%, respectively, while the Vmax was unchanged. Glucose 65-74 insulin Homo sapiens 18-25 6490795-0 1984 Site of insulin resistance in type 1 diabetes: insulin-mediated glucose disposal in vivo in relation to insulin binding and action in adipocytes in vitro. Glucose 64-71 insulin Homo sapiens 8-15 6490795-0 1984 Site of insulin resistance in type 1 diabetes: insulin-mediated glucose disposal in vivo in relation to insulin binding and action in adipocytes in vitro. Glucose 64-71 insulin Homo sapiens 47-54 6490795-0 1984 Site of insulin resistance in type 1 diabetes: insulin-mediated glucose disposal in vivo in relation to insulin binding and action in adipocytes in vitro. Glucose 64-71 insulin Homo sapiens 47-54 6490795-3 1984 In each subject, insulin-mediated glucose disposal in vivo was measured by the euglycemic clamp technique. Glucose 34-41 insulin Homo sapiens 17-24 6490795-9 1984 Basal and insulin-stimulated rates of glucose transport were not significantly different in diabetic and normal subjects. Glucose 38-45 insulin Homo sapiens 10-17 6490795-14 1984 In conclusion, insulin-mediated glucose disposal in vivo is reduced in conventionally treated type 1 diabetic patients. Glucose 32-39 insulin Homo sapiens 15-22 6390088-2 1984 The metabolism of glucose in the B cell is controlled by two different enzymes, hexokinase and glucokinase, whose activities are lowered during fasting; this coincides with lowered levels of blood glucose and blood insulin and with a blocking of the insulin-secretory response toward glucose. Glucose 18-25 insulin Homo sapiens 215-222 6392812-1 1984 The effect of muscle strength training on glucose tolerance and the insulin response after glucose feeding was investigated in eight healthy male subjects. Glucose 91-98 insulin Homo sapiens 68-75 6389533-3 1984 The Km for D-glucose efflux in the presence of insulin decreased by 47% when compared to controls, and the change in Vmax was statistically insignificant. Glucose 11-20 insulin Homo sapiens 47-54 6388353-0 1984 Dexamethasone-induced insulin resistance enhances B cell responsiveness to glucose level in normal men. Glucose 75-82 insulin Homo sapiens 22-29 6387483-2 1984 In control experiments, in which both glucose counterregulation and insulin waning were allowed to occur, plasma glucose levels decreased from 94 +/- 3 to 47 +/- 7 mg per deciliter and then increased to 289 +/- 20 mg per deciliter at 12 hours because of a marked increase in glucose production. Glucose 113-120 insulin Homo sapiens 68-75 6387483-2 1984 In control experiments, in which both glucose counterregulation and insulin waning were allowed to occur, plasma glucose levels decreased from 94 +/- 3 to 47 +/- 7 mg per deciliter and then increased to 289 +/- 20 mg per deciliter at 12 hours because of a marked increase in glucose production. Glucose 113-120 insulin Homo sapiens 68-75 6387483-3 1984 When the waning of insulin action was prevented by insulin infusion, glucose production increased less (P less than 0.01), but marked rebound hyperglycemia still occurred (188 +/- 26 mg per deciliter at 12 hours). Glucose 69-76 insulin Homo sapiens 19-26 6387483-3 1984 When the waning of insulin action was prevented by insulin infusion, glucose production increased less (P less than 0.01), but marked rebound hyperglycemia still occurred (188 +/- 26 mg per deciliter at 12 hours). Glucose 69-76 insulin Homo sapiens 51-58 6387483-4 1984 When both insulin waning and glucose counterregulation were prevented by infusion of both glucose and insulin, glucose production did not increase, and rebound hyperglycemia did not occur. Glucose 90-97 insulin Homo sapiens 10-17 6388357-1 1984 By use of the glucose clamp sequential insulin infusion technique, we compared the dose-response characteristics of insulin-mediated glucose disposal in 17 patients with noninsulin-dependent diabetes mellitus (NIDDM) and 13 age- and weight-matched nondiabetic volunteers. Glucose 133-140 insulin Homo sapiens 116-123 6388357-4 1984 The presence of defective coupling in itself could explain the abnormal insulin dose-response characteristics for glucose disposal in NIDDM and differentiates the insulin resistance of this condition from that of obesity in which coupling is normal. Glucose 114-121 insulin Homo sapiens 72-79 6388357-4 1984 The presence of defective coupling in itself could explain the abnormal insulin dose-response characteristics for glucose disposal in NIDDM and differentiates the insulin resistance of this condition from that of obesity in which coupling is normal. Glucose 114-121 insulin Homo sapiens 163-170 6388353-6 1984 Similarly, matched increments in glucose level produced greater increments in prestimulus insulin level during Dex (P less than 0.03). Glucose 33-40 insulin Homo sapiens 90-97 6388355-8 1984 The effect of insulin on glucose utilization in erythroblast and reticulocyte preparations was negligible, as assessed by CO2 and lactate production. Glucose 25-32 insulin Homo sapiens 14-21 6388356-1 1984 To examine the effect of experimental hyperthyroidism induced by triiodothyronine (T3) administration on glucose utilization and glucose-stimulated insulin secretion, euglycemic insulin clamp studies (A), hyperglycemic clamp studies (B), and estimation of splanchnic glucose metabolism after an oral glucose load by means of the hepatic venous catheter technique (C) were performed in healthy volunteers whose serum T3 concentration had been increased from 1.1 +/- 0.02 (SE) to 3.5 +/- 0.2 ng/ml. Glucose 129-136 insulin Homo sapiens 148-155 6388356-1 1984 To examine the effect of experimental hyperthyroidism induced by triiodothyronine (T3) administration on glucose utilization and glucose-stimulated insulin secretion, euglycemic insulin clamp studies (A), hyperglycemic clamp studies (B), and estimation of splanchnic glucose metabolism after an oral glucose load by means of the hepatic venous catheter technique (C) were performed in healthy volunteers whose serum T3 concentration had been increased from 1.1 +/- 0.02 (SE) to 3.5 +/- 0.2 ng/ml. Glucose 129-136 insulin Homo sapiens 148-155 6395946-2 1984 Insulin stimulates the rate of glucose transport in muscle and fat tissue by incorporation of transporters from internal membranes into the plasma membrane. Glucose 31-38 insulin Homo sapiens 0-7 6388503-1 1984 Studies were carried out on cultures of human skin fibroblasts to explore the effects of culture medium glucose levels on insulin binding and action. Glucose 104-111 insulin Homo sapiens 122-129 6388503-2 1984 Cell cultures in 5.55 mM glucose-containing medium depleted their medium glucose within 3 days, and at that time exhibited elevated deoxy-D-glucose (2-DG) transport (84% greater than control cultures fed 22.2 mM glucose) and failure of insulin to stimulate 2-DG transport (an insulin:control transport ratio of 1.02). Glucose 25-32 insulin Homo sapiens 236-243 6388503-2 1984 Cell cultures in 5.55 mM glucose-containing medium depleted their medium glucose within 3 days, and at that time exhibited elevated deoxy-D-glucose (2-DG) transport (84% greater than control cultures fed 22.2 mM glucose) and failure of insulin to stimulate 2-DG transport (an insulin:control transport ratio of 1.02). Glucose 25-32 insulin Homo sapiens 276-283 6388503-5 1984 Exposure to increasing concentrations of glucose for 18 h led to a glucose concentration-dependent increase in specific insulin binding. Glucose 41-48 insulin Homo sapiens 120-127 6388503-5 1984 Exposure to increasing concentrations of glucose for 18 h led to a glucose concentration-dependent increase in specific insulin binding. Glucose 67-74 insulin Homo sapiens 120-127 6388503-7 1984 The results indicate that basal sugar transport, and insulin binding and action can be regulated by the amount of glucose in the medium. Glucose 114-121 insulin Homo sapiens 53-60 6391388-5 1984 The group on insulin infusion treatment achieved a mean plasma glucose of 9.8 mmol/l (176.4 mg/100 ml), a median M value of 50 mmol/l (900 mg/100 ml) and a mean glycosylated haemoglobin of 9.1% during the year. Glucose 63-70 insulin Homo sapiens 13-20 6395946-11 1984 With this technique it was shown that insulin does not change [Ca2+]i while stimulating glucose transport in L6 muscle cells. Glucose 88-95 insulin Homo sapiens 38-45 6389223-0 1984 beta-Hydroxybutyrate increases the insulin sensitivity of adipocyte glucose transport at a postreceptor level. Glucose 68-75 insulin Homo sapiens 35-42 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 61-68 insulin Homo sapiens 6-13 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 61-68 insulin Homo sapiens 44-51 6389223-1 1984 The effect of insulin on glucose transport (2-deoxyglucose uptake) in adipocytes was measured in the absence and in the presence of 10 mM sodium-DL-beta-hydroxybutyrate. Glucose 25-32 insulin Homo sapiens 14-21 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 61-68 insulin Homo sapiens 44-51 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 61-68 insulin Homo sapiens 44-51 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 264-271 insulin Homo sapiens 44-51 6389223-7 1984 beta-Hydroxybutyrate increased the sensitivity of glucose transport to stimulation by the anti-receptor antibody, demonstrating that insulin itself does not have to be present. Glucose 50-57 insulin Homo sapiens 133-140 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 264-271 insulin Homo sapiens 44-51 6242816-2 1984 At an insulin infusion rate of 1 mU/kg/min, insulin mediated glucose disposal was significantly greater (p less than 0.02) following delivery (1.194 +/- 0.138 mmol/m2/min) than in pregnancy (0.761 +/- 0.072 mmol/m2/min) and the rate of decline in insulin mediated glucose disposal, at the end of the insulin infusion, was significantly greater (p less than 0.02) following delivery (24.78 +/- 4.22 mumol/m2/min2) than in pregnancy (15.17 +/- 2.00 mumol/m2/min2). Glucose 264-271 insulin Homo sapiens 44-51 6389228-2 1984 Glucose and counterregulatory hormone responses to a high-dose (1.7 mU/kg/min) insulin infusion were studied in 6 patients who had undergone total pancreatectomy, and the results were compared with those of normal controls and patients with other clinical forms of diabetes. Glucose 0-7 insulin Homo sapiens 79-86 6389225-6 1984 A similar 100-fold difference was also observed in competitive binding experiments conducted at 37 degrees C. The biologic potency of human proinsulin was evaluated by its ability to stimulate glucose incorporation into total fat cell lipid and also by its antilipolytic activity. Glucose 193-200 insulin Homo sapiens 140-150 6391994-8 1984 The pre-treatment metabolic clearance rate of glucose in all diabetic studies with insulin levels greater than 30 mU/l was 2.6 +/- 0.4 and rose to 3.9 +/- 0.5 ml X kg-1 X min-1 following insulin therapy. Glucose 46-53 insulin Homo sapiens 83-90 6389225-7 1984 Glucose incorporation into lipid was half-maximal at a proinsulin concentration of 1.5 +/- 0.4 X 10(-8) M, whereas the same response was observed at an insulin concentration of 5.2 +/- 1 X 10(-11) M. Proinsulin also demonstrated an antilipolytic potency that was less than 1% that of insulin. Glucose 0-7 insulin Homo sapiens 55-65 6391994-8 1984 The pre-treatment metabolic clearance rate of glucose in all diabetic studies with insulin levels greater than 30 mU/l was 2.6 +/- 0.4 and rose to 3.9 +/- 0.5 ml X kg-1 X min-1 following insulin therapy. Glucose 46-53 insulin Homo sapiens 187-194 6389225-7 1984 Glucose incorporation into lipid was half-maximal at a proinsulin concentration of 1.5 +/- 0.4 X 10(-8) M, whereas the same response was observed at an insulin concentration of 5.2 +/- 1 X 10(-11) M. Proinsulin also demonstrated an antilipolytic potency that was less than 1% that of insulin. Glucose 0-7 insulin Homo sapiens 58-65 6397293-0 1984 The response of blood intermediary metabolite levels to 24 hours treatment with a blood glucose-controlled insulin infusion system in type 1 diabetes. Glucose 88-95 insulin Homo sapiens 107-114 6397293-8 1984 Abnormalities of intermediary metabolite levels persist during feedback normalization of blood glucose levels, with evidence of influences from both prior diabetic control, and current insulin delivery. Glucose 95-102 insulin Homo sapiens 185-192 6389225-7 1984 Glucose incorporation into lipid was half-maximal at a proinsulin concentration of 1.5 +/- 0.4 X 10(-8) M, whereas the same response was observed at an insulin concentration of 5.2 +/- 1 X 10(-11) M. Proinsulin also demonstrated an antilipolytic potency that was less than 1% that of insulin. Glucose 0-7 insulin Homo sapiens 200-210 6389225-8 1984 The time course over which insulin and proinsulin stimulated glucose incorporation into lipid was the same, as was the time course over which the stimulation dissipated after removal of the hormones. Glucose 61-68 insulin Homo sapiens 27-34 6389225-8 1984 The time course over which insulin and proinsulin stimulated glucose incorporation into lipid was the same, as was the time course over which the stimulation dissipated after removal of the hormones. Glucose 61-68 insulin Homo sapiens 39-49 6383936-0 1984 Kinetics of glucose metabolism in relation to insulin concentrations in patients with alcoholic cirrhosis and in healthy persons. Glucose 12-19 insulin Homo sapiens 46-53 6383936-1 1984 To characterize the insulin resistance in alcoholic cirrhosis we determined in vivo insulin-glucose disposal dose-response relationships in 6 patients with alcoholic cirrhosis of varying severity and in 6 control subjects, using the glucose-insulin clamp technique. Glucose 92-99 insulin Homo sapiens 84-91 6383936-6 1984 The calculated affinity constant (i.e., the concentration of insulin leading to half-maximum glucose metabolism) of patients with cirrhosis was higher than that of normal controls (104 +/- 30 vs. 32 +/- 3 mU/L, mean +/- SD). Glucose 93-100 insulin Homo sapiens 61-68 6386947-9 1984 Thus, age-related differences in muscle mass and sensitivity of peripheral tissues to insulin-mediated glucose uptake and metabolism are not paralleled by alterations in whole body leucine kinetics in the postabsorptive state. Glucose 103-110 insulin Homo sapiens 86-93 6394779-3 1984 Rate of glucose turnover (mg/kg/min) was defined as metabolic clearance of glucose and corresponding plasma immunoreactive insulin values were determined. Glucose 8-15 insulin Homo sapiens 123-130 6389598-4 1984 Similarly, glucose oxidation increased from 0.100 +/- 0.015 to 0.266 +/- 0.022 g/min (P less than 0.001) at approximately microU/ml insulin and from 0.082 +/- 0.013 to 0.295 +/- 0.018 g/min (P less than 0.001) at approximately 620 microU/ml insulin. Glucose 11-18 insulin Homo sapiens 132-139 6389598-4 1984 Similarly, glucose oxidation increased from 0.100 +/- 0.015 to 0.266 +/- 0.022 g/min (P less than 0.001) at approximately microU/ml insulin and from 0.082 +/- 0.013 to 0.295 +/- 0.018 g/min (P less than 0.001) at approximately 620 microU/ml insulin. Glucose 11-18 insulin Homo sapiens 241-248 6394779-4 1984 The ratio of metabolic clearance of glucose to plasma insulin is a reflection of endogenous insulin sensitivity. Glucose 36-43 insulin Homo sapiens 92-99 6394779-14 1984 The ratio of metabolic glucose clearance to plasma insulin followed a similar pattern the primarily to the substantial decrease in insulin levels. Glucose 23-30 insulin Homo sapiens 131-138 6388352-3 1984 In the first group, the glucose-insulin infusion (0.03 U insulin X kg-1 X h-1 and 0.25 g glucose X kg-1 X h-1) was begun 30 min before the start of the test meal and ended 15 min after subjects had voluntarily stopped eating. Glucose 24-31 insulin Homo sapiens 32-39 6387364-2 1984 In each subject, body composition (% fat and % muscle), maximal aerobic power (VO2 max) and whole body insulin-mediated glucose metabolism were measured. Glucose 120-127 insulin Homo sapiens 103-110 6387364-8 1984 CONCLUSIONS: (1) Insulin-mediated glucose disposal is inversely related to adiposity in normal weight healthy males and females. Glucose 34-41 insulin Homo sapiens 17-24 6387366-0 1984 Insulin resistance in the aged: a quantitative evaluation of in vivo insulin sensitivity and in vitro glucose transport. Glucose 102-109 insulin Homo sapiens 0-7 6387366-2 1984 This phenomenon has been further investigated with the aid of sophisticated techniques, such as the euglycemic clamp, which, when coupled with the measurement of hepatic glucose production, showed that "impaired tissue sensitivity to insulin is the primary factor responsible for the decrease of glucose tolerance in advancing age." Glucose 170-177 insulin Homo sapiens 234-241 6083538-2 1984 Glucose responses segregated patients into two groups: Group I with normal carbohydrate tolerance associated with normal to slightly increased insulin responses, and Group II with impaired carbohydrate tolerance associated with insulinopenia. Glucose 0-7 insulin Homo sapiens 143-150 6387959-0 1984 Insulin response to oral glucose in young, non-obese Indian males with myocardial infarction. Glucose 25-32 insulin Homo sapiens 0-7 6397028-5 1984 Conversely, a positive relationship occurred between C-peptide levels and the parameter we used for estimating insulin sensitivity, i.e. glucose disappearance rate after i.v. Glucose 137-144 insulin Homo sapiens 111-118 6385899-4 1984 This review discusses the methodology of capillary blood glucose monitoring and its application to insulin adjustments. Glucose 57-64 insulin Homo sapiens 99-106 6388352-5 1984 In the second group, the glucose-insulin mixture (insulin bolus of 12 mU/kg plus 0.03 U insulin X kg-1 X h-1 and 0.125 g glucose X kg-1 X h-1) was delivered 12 min after an appetizer was served and just as the test meal began. Glucose 25-32 insulin Homo sapiens 33-40 6388352-5 1984 In the second group, the glucose-insulin mixture (insulin bolus of 12 mU/kg plus 0.03 U insulin X kg-1 X h-1 and 0.125 g glucose X kg-1 X h-1) was delivered 12 min after an appetizer was served and just as the test meal began. Glucose 25-32 insulin Homo sapiens 50-57 6388352-8 1984 The changes induced in these studies by the glucose-insulin infusions mimicked normal insulin and glucose levels seen shortly before satiation is complete in a meal. Glucose 44-51 insulin Homo sapiens 52-59 6391976-2 1984 For this purpose, we examined the insulin and C-peptide responses to a 75 g oral glucose tolerance test in a group of 55 healthy subjects each having one parent with type 2 diabetes mellitus, and in a group of 55 individuals without a family history of diabetes. Glucose 81-88 insulin Homo sapiens 46-55 6388651-3 1984 The inhibitory effect of glucose upon 45Ca efflux from prelabeled pancreatic islets was simulated in a mathematical model for Ca2+-cyclic AMP interaction in the process of glucose-induced insulin release. Glucose 25-32 insulin Homo sapiens 188-195 6388651-3 1984 The inhibitory effect of glucose upon 45Ca efflux from prelabeled pancreatic islets was simulated in a mathematical model for Ca2+-cyclic AMP interaction in the process of glucose-induced insulin release. Glucose 172-179 insulin Homo sapiens 188-195 6397178-5 1984 Glucose concentrations after a 1.6 MJ test meal were reduced by Acarbose from peak values of 17.3 +/- 1.0 to 15.0 +/- 1.1 mmol/l and were associated with lower post-prandial C-peptide (CPR) and insulin responses. Glucose 0-7 insulin Homo sapiens 194-201 6383904-0 1984 The enteric enhancement of glucose-stimulated insulin release. Glucose 27-34 insulin Homo sapiens 46-53 6391976-8 1984 In conclusion, the healthy offspring of only one non-insulin-dependent diabetic parent show a normal beta-cell response to glucose, and normal removal of insulin by the liver. Glucose 123-130 insulin Homo sapiens 53-60 6391986-2 1984 Immunoreactive insulin occurs in human saliva and concentrations increase after oral glucose ingestion. Glucose 85-92 insulin Homo sapiens 15-22 6391986-4 1984 The mean +/- SEM concentration of extracted salivary immunoreactive insulin in five normal volunteers increased during an oral glucose tolerance test from basal values of 36 +/- 3.0 to 291 +/- 40 pmol/l; however, the peak occurred 45-90 min later than in serum. Glucose 127-134 insulin Homo sapiens 68-75 6148358-0 1984 Relationship between skeletal muscle insulin resistance, insulin-mediated glucose disposal, and insulin binding. Glucose 74-81 insulin Homo sapiens 57-64 6392097-0 1984 [Postoperative insulin resistance of lipolysis and ketogenesis using the glucose clamp technic]. Glucose 73-80 insulin Homo sapiens 15-22 6090502-7 1984 When glycogen metabolism was studied, insulin stimulated [3H]glucose incorporation into glycogen in a biphasic manner; one phase that was 20-30% of the maximal response occurred over 1-100 pM, and the other phase occurred over 100 pM-100 nM. Glucose 61-68 insulin Homo sapiens 38-45 6148358-0 1984 Relationship between skeletal muscle insulin resistance, insulin-mediated glucose disposal, and insulin binding. Glucose 74-81 insulin Homo sapiens 57-64 6148358-5 1984 The increase in percentage of synthase I in response to submaximal steady state plasma insulin (SSPI) of approximately 100 microU/ml achieved by the infusion of somatostatin, insulin, and glucose, however, was significantly lower in obese than in nonobese subjects, and was inversely correlated with WHR. Glucose 188-195 insulin Homo sapiens 87-94 6148358-11 1984 Our results suggest that in premenopausal women, impaired skeletal muscle insulin sensitivity that results in decreased glucose storage capacity may contribute to the diminished efficiency of glucose disposal and insulin resistance that are associated with upper body obesity. Glucose 120-127 insulin Homo sapiens 74-81 6148358-11 1984 Our results suggest that in premenopausal women, impaired skeletal muscle insulin sensitivity that results in decreased glucose storage capacity may contribute to the diminished efficiency of glucose disposal and insulin resistance that are associated with upper body obesity. Glucose 192-199 insulin Homo sapiens 74-81 6384267-0 1984 Relationships between insulin secretion, insulin action, and fasting plasma glucose concentration in nondiabetic and noninsulin-dependent diabetic subjects. Glucose 76-83 insulin Homo sapiens 22-29 6480801-6 1984 The hypoglycemic action of the drug is consistent with the existence of an insulin-independent effect of fatty acid oxidation on glucose metabolism in man. Glucose 129-136 insulin Homo sapiens 75-82 6384267-8 1984 Insulin action was measured as total insulin-mediated glucose disposal, glucose oxidation, and storage rates, using the euglycemic clamp with simultaneous indirect calorimetry at plasma insulin concentrations of 135 +/- 5 and 1738 +/- 59 microU/ml. Glucose 54-61 insulin Homo sapiens 0-7 6384267-8 1984 Insulin action was measured as total insulin-mediated glucose disposal, glucose oxidation, and storage rates, using the euglycemic clamp with simultaneous indirect calorimetry at plasma insulin concentrations of 135 +/- 5 and 1738 +/- 59 microU/ml. Glucose 54-61 insulin Homo sapiens 37-44 6384267-8 1984 Insulin action was measured as total insulin-mediated glucose disposal, glucose oxidation, and storage rates, using the euglycemic clamp with simultaneous indirect calorimetry at plasma insulin concentrations of 135 +/- 5 and 1738 +/- 59 microU/ml. Glucose 72-79 insulin Homo sapiens 0-7 6384267-11 1984 Decreased peripheral insulin availability leads to increased FFA concentrations and lipid oxidation rates (and probably also increased concentrations of gluconeogenic precursors) that together stimulate gluconeogenesis, hepatic glucose production, and progressive hyperglycemia. Glucose 228-235 insulin Homo sapiens 21-28 6384269-5 1984 Insulin responses to arginine were lower in diabetics than in controls at all matched glucose levels (P less than 0.001 at all levels). Glucose 86-93 insulin Homo sapiens 0-7 6384269-7 1984 In contrast, PG50 was similar in diabetics and controls (234 +/- 28 vs. 197 +/- 20 mg/dl, P equals NS) and insulin responses in both groups approached or attained maxima at a glucose level of approximately 460 mg/dl. Glucose 175-182 insulin Homo sapiens 107-114 6390972-0 1984 Duration of type I diabetes affects glucagon and glucose responses to insulin-induced hypoglycemia. Glucose 49-56 insulin Homo sapiens 70-77 6384269-11 1984 In summary, patients with NIDDM possess markedly decreased maximal insulin responsiveness to the potentiating effects of glucose. Glucose 121-128 insulin Homo sapiens 67-74 6384270-4 1984 In these studies, the glucose clamp technique was employed to isolate perturbations in plasma glucose and plasma insulin as potential mediators of the regulation of the mitogen-induced T lymphocyte insulin receptor. Glucose 22-29 insulin Homo sapiens 113-120 6384270-16 1984 Acute changes in plasma insulin by the glucose clamp technique are perceived by the T lymphocyte and displayed in tissue culture by an alteration in lectin-induced insulin receptors. Glucose 39-46 insulin Homo sapiens 24-31 6384270-16 1984 Acute changes in plasma insulin by the glucose clamp technique are perceived by the T lymphocyte and displayed in tissue culture by an alteration in lectin-induced insulin receptors. Glucose 39-46 insulin Homo sapiens 164-171 6390972-2 1984 To identify predictive factors for this abnormality and for the capability of glycemic counterregulation, we investigated the relationship between the duration of diabetes and glucagon and glucose responses to insulin-induced hypoglycemia. Glucose 189-196 insulin Homo sapiens 210-217 6395872-2 1984 This phenomenon, if present, could lead to errors in adapting the basal insulin infusion in CSII treated diabetic patients, because a normal glucose level in the morning could be associated with asymptomatic hypoglycemic values in the night. Glucose 141-148 insulin Homo sapiens 72-79 6393448-2 1984 Insulin levels at fasting state and after glucose loading were 149 +/- 63 microU/ml (mean +/- S.D.) Glucose 42-49 insulin Homo sapiens 0-7 6383069-1 1984 The L6 muscle cell line is proposed as an excellent cell culture system for studying glucose transport and its regulation by serum and insulin throughout myogenesis. Glucose 85-92 insulin Homo sapiens 135-142 6382002-4 1984 The propositus, a 12-year-old girl, had borderline glucose intolerance and markedly elevated immunoreactive-insulin levels on oral glucose-tolerance testing. Glucose 131-138 insulin Homo sapiens 108-115 6382002-6 1984 Two of four siblings, the father, and the paternal grandfather also had elevated fasting insulin immunoreactivity in the presence of normal plasma glucose concentrations and elevated levels of proinsulin-like material. Glucose 147-154 insulin Homo sapiens 89-96 6433719-1 1984 It has been proposed that Ca2+ ions mediate the stimulation by insulin of glucose uptake in muscle (Clausen, T., Cell Calcium 1:311-325, 1980). Glucose 74-81 insulin Homo sapiens 63-70 6391571-1 1984 Monensin, a specific sodium ionophore, has been shown to reduce glucose-induced proinsulin biosynthesis by 30% and to completely inhibit the intracellular conversion of proinsulin to insulin. Glucose 64-71 insulin Homo sapiens 80-90 3902687-10 1985 When exaggerated the insulin response to the glucose load fell to normal values whereas the insulin response increased in the diabetic patients in whom it was initially blunted. Glucose 45-52 insulin Homo sapiens 21-28 6391571-1 1984 Monensin, a specific sodium ionophore, has been shown to reduce glucose-induced proinsulin biosynthesis by 30% and to completely inhibit the intracellular conversion of proinsulin to insulin. Glucose 64-71 insulin Homo sapiens 83-90 6389057-3 1984 Individual improvement in control of plasma glucose was directly proportional to degree of hyperglycemia before training and correlated well with an observed improvement in the early (30-min) plasma insulin response to oral glucose (all six subjects). Glucose 44-51 insulin Homo sapiens 199-206 6386558-1 1984 By means of the euglycaemic insulin clamp technique the rate of insulin-mediated peripheral glucose disposal (GDR) was compared in response to intravenous infusions of highly purified beef insulin (BI) and biosynthetic human insulin (BHI), infused at 1 and 6 mU/kg/min, in healthy volunteers. Glucose 92-99 insulin Homo sapiens 64-71 6386558-1 1984 By means of the euglycaemic insulin clamp technique the rate of insulin-mediated peripheral glucose disposal (GDR) was compared in response to intravenous infusions of highly purified beef insulin (BI) and biosynthetic human insulin (BHI), infused at 1 and 6 mU/kg/min, in healthy volunteers. Glucose 92-99 insulin Homo sapiens 64-71 6381179-4 1984 We found that conventionally treated diabetic subjects were extremely insulin resistant with regard to peripheral glucose uptake. Glucose 114-121 insulin Homo sapiens 70-77 6381179-10 1984 We conclude that conventionally treated IDDMs are insulin resistant with regard to peripheral glucose uptake. Glucose 94-101 insulin Homo sapiens 50-57 6386558-1 1984 By means of the euglycaemic insulin clamp technique the rate of insulin-mediated peripheral glucose disposal (GDR) was compared in response to intravenous infusions of highly purified beef insulin (BI) and biosynthetic human insulin (BHI), infused at 1 and 6 mU/kg/min, in healthy volunteers. Glucose 92-99 insulin Homo sapiens 64-71 6389057-3 1984 Individual improvement in control of plasma glucose was directly proportional to degree of hyperglycemia before training and correlated well with an observed improvement in the early (30-min) plasma insulin response to oral glucose (all six subjects). Glucose 224-231 insulin Homo sapiens 199-206 6389240-5 1984 Insulin delivered to the latter sites stimulates several important processes, including reabsorption of sodium, phosphate, and glucose. Glucose 127-134 insulin Homo sapiens 0-7 6389059-4 1984 Improvement in control occurred during "increased" insulin dosage with reduction of glycosylated hemoglobin levels (P less than 0.001), self-monitored blood glucose levels (P less than 0.001), and 24-h urine glucose excretion (P less than 0.01). Glucose 157-164 insulin Homo sapiens 51-58 6389241-5 1984 At all insulin concentrations and in the absence of insulin, rates of glucose conversion to lipids were decreased more than 50% (p less than 0.05), whereas rates of glucose oxidation were unaffected. Glucose 70-77 insulin Homo sapiens 7-14 6389060-2 1984 The plasma glucose and insulin response was determined over the subsequent 5 h. The plasma glucose area above the baseline following a glucose meal was reduced 34% when protein was given with the glucose. Glucose 91-98 insulin Homo sapiens 23-30 6389060-2 1984 The plasma glucose and insulin response was determined over the subsequent 5 h. The plasma glucose area above the baseline following a glucose meal was reduced 34% when protein was given with the glucose. Glucose 91-98 insulin Homo sapiens 23-30 6397290-4 1984 They also had higher fasting (p less than 0.01) and post-glucose (p less than 0.04) plasma insulin concentrations per body mass index than those with normal ECGs. Glucose 57-64 insulin Homo sapiens 91-98 6432610-8 1984 Insulin-mediated glucose metabolism (insulin clamp technique) was reduced by 55% in NIDDM (2.91 versus 6.39 mg/kg X min, P less than 0.001). Glucose 17-24 insulin Homo sapiens 0-7 6397290-10 1984 Insulin levels post-glucose were greater at 5 yr in those with cardiac abnormality but, as with the higher diastolic blood pressure and fasting glucose concentration then (both p less than 0.05), this difference was not significant initially. Glucose 20-27 insulin Homo sapiens 0-7 6389060-2 1984 The plasma glucose and insulin response was determined over the subsequent 5 h. The plasma glucose area above the baseline following a glucose meal was reduced 34% when protein was given with the glucose. Glucose 91-98 insulin Homo sapiens 23-30 6432610-8 1984 Insulin-mediated glucose metabolism (insulin clamp technique) was reduced by 55% in NIDDM (2.91 versus 6.39 mg/kg X min, P less than 0.001). Glucose 17-24 insulin Homo sapiens 37-44 6432610-9 1984 After glyburide, insulin-mediated glucose metabolism increased by 26% to 3.67 mg/kg X min (P less than 0.01). Glucose 34-41 insulin Homo sapiens 17-24 6389060-4 1984 The insulin area following glucose was only modestly greater than with a protein meal (97 +/- 35, 83 +/- 19 microU X h/ml, respectively). Glucose 27-34 insulin Homo sapiens 4-11 6499638-2 1984 An artificial insulin infusion system was used to set and maintain glucose concentrations during testing at each of three levels: hypoglycemia (55 mg/dl), euglycemia (110 mg/dl), and hyperglycemia (300 mg/dl). Glucose 67-74 insulin Homo sapiens 14-21 6389060-5 1984 When glucose was given with protein, the mean insulin area was considerably greater than when glucose or protein was given alone (247 +/- 33 microU X h/ml). Glucose 5-12 insulin Homo sapiens 46-53 6389060-5 1984 When glucose was given with protein, the mean insulin area was considerably greater than when glucose or protein was given alone (247 +/- 33 microU X h/ml). Glucose 94-101 insulin Homo sapiens 46-53 6389060-6 1984 When various amounts of protein were given with 50 g glucose, the insulin area response was essentially first order. Glucose 53-60 insulin Homo sapiens 66-73 6389060-8 1984 The insulin areas were not significantly different for each meal but were higher when protein + glucose was given. Glucose 96-103 insulin Homo sapiens 4-11 6381305-5 1984 Concentrations of insulin in plasma were high for the prevailing concentrations of glucose, and peak urinary excretion of nitrogen coincided with maximum levels of insulin. Glucose 83-90 insulin Homo sapiens 18-25 6389061-0 1984 Decreased serum C-peptide/insulin molar ratios after oral glucose ingestion in hyperthyroid patients. Glucose 58-65 insulin Homo sapiens 26-33 6386699-1 1984 A simple computer model is described for the simulation of insulin binding to cell surface receptors on adipocytes and the subsequent stimulation of glucose uptake. Glucose 149-156 insulin Homo sapiens 59-66 6430945-12 1984 Basal hepatic glucose production in the diabetic patients during the first study (2.78 +/- 0.14 mg/kg X min) was 56% higher than in the normal subjects (1.78 +/- 0.04 mg/kg X min, P less than 0.001), and remained unchanged during insulin therapy. Glucose 14-21 insulin Homo sapiens 230-237 6381541-6 1984 The elevated basal and peak postprandial plasma glucose concentrations (252 +/- 33 and 452 +/- 31 mg/dl) of diabetic subjects when insulin deficient were decreased by intensive insulin therapy to values (82 +/- 6 and 193 +/- 10 mg/dl, P less than 0.01) that approximated those of nondiabetic subjects (93 +/- 3 and 140 +/- 15 mg/dl, respectively). Glucose 48-55 insulin Homo sapiens 131-138 6381541-8 1984 Intensive insulin therapy decreased (P less than 0.01) both total (1,581 +/- 98 mg/kg per 8 h) and endogenous (478 +/- 67 mg/kg per 8 h) glucose appearance to rates that approximated those observed in the nondiabetic subjects, but did not alter meal-related glucose appearance. Glucose 137-144 insulin Homo sapiens 10-17 6091078-13 1984 The diagnosis can be confirmed by demonstrating an inappropriately high circulating insulin level, for the ambient blood glucose concentration. Glucose 121-128 insulin Homo sapiens 84-91 6381541-8 1984 Intensive insulin therapy decreased (P less than 0.01) both total (1,581 +/- 98 mg/kg per 8 h) and endogenous (478 +/- 67 mg/kg per 8 h) glucose appearance to rates that approximated those observed in the nondiabetic subjects, but did not alter meal-related glucose appearance. Glucose 258-265 insulin Homo sapiens 10-17 6381541-10 1984 Intensive insulin therapy restored postprandial suppression of endogenous glucose production to rates observed in nondiabetic subjects. Glucose 74-81 insulin Homo sapiens 10-17 6392794-10 1984 The "effectiveness" of rectal insulin preparations is suggested to be evaluated by four criteria: the pharmacological availability via the area under the % glucose reduction-time profile, the maximum glucose concentration reduction, Cmax, the time to reach the maximum reduction, tmax, and the mean residence time for glucose reduction, MRT. Glucose 156-163 insulin Homo sapiens 30-37 6381963-3 1984 Then, practically identical metabolic states were achieved by connecting the patients to a glucose-controlled insulin infusion system (Biostator) 12 hours before the study. Glucose 91-98 insulin Homo sapiens 110-117 6381963-8 1984 In the second study, 24 hours of near-normoglycemia was attained by the glucose-controlled insulin infusion system, the patients being supine and having identical meals at identical intervals. Glucose 72-79 insulin Homo sapiens 91-98 6204710-2 1984 Two insulin dependent diabetics showed persistent discrepancies between their capillary blood glucose values and their glycosylated haemoglobin values measured by agar gel electrophoresis: the blood values were normal but the glycosylated haemoglobin values were raised. Glucose 94-101 insulin Homo sapiens 4-11 6390995-10 1984 This peripheral insulin resistance is shown by the simultaneous large increases in concentrations of serum insulin, blood glucose and concentration of free fatty acids. Glucose 122-129 insulin Homo sapiens 16-23 6540601-1 1984 The glucose transport activity solubilized from the basal and plus insulin forms of the Golgi-rich fraction of adipocytes was partially characterized, and the results were compared with those of the activity obtained from the plus insulin form of the plasma membrane-rich fraction. Glucose 4-11 insulin Homo sapiens 67-74 6382897-5 1984 Insulin sensitivity, measured as the glucose disappearance rate, KITT, in response to iv-insulin, was not significantly influenced by age or age at onset, but decreased consistently with the duration of the disease (P less than 0.001). Glucose 37-44 insulin Homo sapiens 0-7 6382897-5 1984 Insulin sensitivity, measured as the glucose disappearance rate, KITT, in response to iv-insulin, was not significantly influenced by age or age at onset, but decreased consistently with the duration of the disease (P less than 0.001). Glucose 37-44 insulin Homo sapiens 89-96 6378698-1 1984 The safety, reproducibility, and reliability of an insulin infusion test for assessment of adequate glucose counterregulation were evaluated in 18 patients with type I (insulin-dependent) diabetes mellitus. Glucose 100-107 insulin Homo sapiens 51-58 6380304-2 1984 This effect is mediated by a transient increase in hepatic glucose production and an inhibition of glucose disposal by insulin-dependent tissues. Glucose 99-106 insulin Homo sapiens 119-126 6380308-1 1984 Defective recovery from insulin-induced hypoglycemia, due to combined deficiencies of glucagon and epinephrine secretory responses to plasma glucose decrements, occurs in some patients with insulin-dependent diabetes mellitus (IDDM). Glucose 141-148 insulin Homo sapiens 24-31 6380308-2 1984 Patients with IDDM determined to have inadequate glucose counterregulation during an insulin infusion test (40 mU X kg-1 X h-1) with bedside plasma glucose monitoring and clinical observation have been found to have a 25-fold greater risk of severe hypoglycemia during subsequent intensive therapy than patients with adequate glucose counterregulation. Glucose 49-56 insulin Homo sapiens 85-92 6380308-2 1984 Patients with IDDM determined to have inadequate glucose counterregulation during an insulin infusion test (40 mU X kg-1 X h-1) with bedside plasma glucose monitoring and clinical observation have been found to have a 25-fold greater risk of severe hypoglycemia during subsequent intensive therapy than patients with adequate glucose counterregulation. Glucose 148-155 insulin Homo sapiens 85-92 6380308-2 1984 Patients with IDDM determined to have inadequate glucose counterregulation during an insulin infusion test (40 mU X kg-1 X h-1) with bedside plasma glucose monitoring and clinical observation have been found to have a 25-fold greater risk of severe hypoglycemia during subsequent intensive therapy than patients with adequate glucose counterregulation. Glucose 148-155 insulin Homo sapiens 85-92 6378696-7 1984 glucose (rate of decline, 20-40 microU/ml insulin release/yr; correlation coefficient, 0.9). Glucose 0-7 insulin Homo sapiens 42-49 6381274-0 1984 Intravenous glucose tolerance, insulin response to glucose, peripheral sensitivity to insulin, and serum lipoproteins in post-myocardial infarct patients with normal fasting blood glucose. Glucose 51-58 insulin Homo sapiens 31-38 6381274-0 1984 Intravenous glucose tolerance, insulin response to glucose, peripheral sensitivity to insulin, and serum lipoproteins in post-myocardial infarct patients with normal fasting blood glucose. Glucose 51-58 insulin Homo sapiens 31-38 6378698-3 1984 No patient experienced symptoms requiring discontinuation of the test and plasma glucose concentrations increased spontaneously after stopping the insulin infusion. Glucose 81-88 insulin Homo sapiens 147-154 6378699-9 1984 Dose-response analysis demonstrated that proinsulin-mediated glucose disposal was approximately 8% that of insulin. Glucose 61-68 insulin Homo sapiens 41-51 6378699-9 1984 Dose-response analysis demonstrated that proinsulin-mediated glucose disposal was approximately 8% that of insulin. Glucose 61-68 insulin Homo sapiens 44-51 6434319-2 1984 Exogenous insulin was infused by means of an automated glucose controlled insulin infusion system. Glucose 55-62 insulin Homo sapiens 10-17 6434418-2 1984 This nutrient-induced thermogenesis represents 6 to 8% of the energy infused when glucose is infused with insulin (glucose clamp technique) to healthy subjects. Glucose 82-89 insulin Homo sapiens 106-113 6434418-2 1984 This nutrient-induced thermogenesis represents 6 to 8% of the energy infused when glucose is infused with insulin (glucose clamp technique) to healthy subjects. Glucose 115-122 insulin Homo sapiens 106-113 6434418-3 1984 At physiological plasma insulin levels (i.e. below 200 microU/ml), glucose induced thermogenesis (GIT) was 6%, whereas at supraphysiological levels (i.e. greater than 400 microU/ml) GIT was 8% of the energy content of glucose infused. Glucose 67-74 insulin Homo sapiens 24-31 6434319-3 1984 The data demonstrate that (i) insulin requirement almost doubled in patients as compared to controls to obtain similar blood glucose responses to i.v. Glucose 125-132 insulin Homo sapiens 30-37 6492695-2 1984 The earlier increase of insulin infusion rates in the latter case resulted in lower postprandial glucose concentrations during the first 90 min after meal intake. Glucose 97-104 insulin Homo sapiens 24-31 6492695-3 1984 Incremental areas under the blood glucose curves during this time were significantly lower when insulin infusion rates rose earlier (4.5 X 10(3) +/- 0.5 X 10(3) vs 2.1 X 10(3) +/- 0.6 X 10(3) mg/dl X min; p less than 0.02). Glucose 34-41 insulin Homo sapiens 96-103 6387248-3 1984 Patients with CHD displayed decreased basal levels of triiodothyronine, total and free thyroxin and increased concentrations of immunoreactive insulin in the blood which was attended with decreased tolerance to glucose. Glucose 211-218 insulin Homo sapiens 143-150 6492695-7 1984 It is concluded that increases of postprandial insulin infusion rates occurring earlier than increases of blood glucose levels are important for optimizing glucose profiles and possibly reflect physiologic conditions. Glucose 156-163 insulin Homo sapiens 47-54 6379375-2 1984 Both a half-maximum concentration of insulin for the stimulation of glucose transport (ED50 [transport]) and a half-maximum concentration of insulin for the suppression of 25 nmol/L isoproterenol-stimulated lipolysis (ED50 [antilipolysis]) were significantly (P less than 0.05) greater in the moderately obese subjects than in the lean subjects as well as greater in the severely obese group than in the moderately obese group. Glucose 68-75 insulin Homo sapiens 37-44 6377919-11 1984 During an oral glucose load insulin-dependent diabetics show abnormalities in the regulation of cardiovascular function and sympathetic nervous activity that may be related to the lack of rise in endogenous insulin in these patients. Glucose 15-22 insulin Homo sapiens 28-35 6382139-2 1984 In 29 of 36 patients, serum insulin levels both in fasting and in response to oral glucose load were measured. Glucose 83-90 insulin Homo sapiens 28-35 6331036-0 1984 Insulin hypoglycaemia test guided by a glucose controlled insulin infusion system. Glucose 39-46 insulin Homo sapiens 58-65 6331036-2 1984 This study describes that a glucose controlled insulin infusion system (GCIIS) permits to perform the IHT with standardized hypoglycaemia. Glucose 28-35 insulin Homo sapiens 47-54 6375349-1 1984 An 18-year-old man had cystic fibrosis (CF) and insulin-resistant carbohydrate intolerance characterized by (1) obesity, basal hyperinsulinemia, and hyperglucagonemia; (2) impaired oral glucose tolerance; (3) hyperinsulinemia in response to oral and intravenous (IV) administration of glucose and to IV administration of tolbutamide; (4) exaggerated gastric inhibitory polypeptide secretion following orally administered glucose; and (5) diminished sensitivity to insulin administered IV compared with other patients with CF. Glucose 186-193 insulin Homo sapiens 48-55 6375349-1 1984 An 18-year-old man had cystic fibrosis (CF) and insulin-resistant carbohydrate intolerance characterized by (1) obesity, basal hyperinsulinemia, and hyperglucagonemia; (2) impaired oral glucose tolerance; (3) hyperinsulinemia in response to oral and intravenous (IV) administration of glucose and to IV administration of tolbutamide; (4) exaggerated gastric inhibitory polypeptide secretion following orally administered glucose; and (5) diminished sensitivity to insulin administered IV compared with other patients with CF. Glucose 285-292 insulin Homo sapiens 48-55 6387756-3 1984 The glucose response showed a low, flat curve with a delayed peak, and increased secretion of insulin and growth hormone occurred. Glucose 4-11 insulin Homo sapiens 94-101 6331454-5 1984 The effects of glucose and isoprenaline on insulin binding were not related to the lipolytic activities these two agents. Glucose 15-22 insulin Homo sapiens 43-50 6393673-2 1984 Insulin sensitivity, assessed by glucose disappearance rate after intravenous bolus injection of insulin, was reduced but not significantly different from controls in subjects with chronic persistent hepatitis, while it was significantly reduced in individuals suffering from chronic active hepatitis or liver cirrhosis. Glucose 33-40 insulin Homo sapiens 0-7 6393673-2 1984 Insulin sensitivity, assessed by glucose disappearance rate after intravenous bolus injection of insulin, was reduced but not significantly different from controls in subjects with chronic persistent hepatitis, while it was significantly reduced in individuals suffering from chronic active hepatitis or liver cirrhosis. Glucose 33-40 insulin Homo sapiens 97-104 6380335-1 1984 An assessment of continuous glucose-insulin-potassium infusion, and traditional treatment. Glucose 28-35 insulin Homo sapiens 36-43 6380335-3 1984 Twelve diabetics received continuous glucose-insulin-potassium (GIK) infusion for at least 4 hours after surgery terminated. Glucose 37-44 insulin Homo sapiens 45-52 6380335-4 1984 Six diabetic patients having morning surgery received a proportion of their morning insulin dose with intravenous glucose (25 g) before surgery and the remaining five operated on in the afternoon received their morning insulin with breakfast. Glucose 114-121 insulin Homo sapiens 84-91 6377986-5 1984 We also found a significant relation (P less than .01) between the amount of insulin taken as a single overdose and either the total amount of IV glucose administered or the total time of IV glucose treatment until the hypoglycemic effects of excess insulin had resolved (glucose [g] = 52 + (.699) (dose U), R = .929 and time [h] = 10.5 + (.028) (dose U), R = .817). Glucose 146-153 insulin Homo sapiens 77-84 6377986-5 1984 We also found a significant relation (P less than .01) between the amount of insulin taken as a single overdose and either the total amount of IV glucose administered or the total time of IV glucose treatment until the hypoglycemic effects of excess insulin had resolved (glucose [g] = 52 + (.699) (dose U), R = .929 and time [h] = 10.5 + (.028) (dose U), R = .817). Glucose 191-198 insulin Homo sapiens 77-84 6377920-3 1984 The key additional role of catecholamines in the development of stress hyperglycemia is interference with the normal feedback control of insulin and glucagon secretion by circulating glucose levels. Glucose 183-190 insulin Homo sapiens 137-144 6377986-5 1984 We also found a significant relation (P less than .01) between the amount of insulin taken as a single overdose and either the total amount of IV glucose administered or the total time of IV glucose treatment until the hypoglycemic effects of excess insulin had resolved (glucose [g] = 52 + (.699) (dose U), R = .929 and time [h] = 10.5 + (.028) (dose U), R = .817). Glucose 191-198 insulin Homo sapiens 77-84 6377920-6 1984 Diabetic patients who have impaired islet responses to glucose will be particularly prone to the development of marked hyperglycemia during stress states because they may be unable to respond to the influence of hyperglycemia in counteracting adrenergic inhibition of insulin secretion and stimulation of glucagon secretion. Glucose 55-62 insulin Homo sapiens 268-275 6242784-2 1984 The plasma insulin response to oral glucose was assessed at the time of diagnosis. Glucose 36-43 insulin Homo sapiens 11-18 6385956-5 1984 The islet cell antibodies block glucose stimulated insulin secretion in vitro without complement, while Type I diabetic sera with complement are beta cell cytotoxic irrespective of their ICA concentration. Glucose 32-39 insulin Homo sapiens 51-58 6242785-5 1984 Plasma glucose concentrations fell consistently more rapidly with insulin/PGE1 than with insulin alone although the differences were small (mean fall +/- S.E.M. Glucose 7-14 insulin Homo sapiens 66-73 6086002-2 1984 Transfer from pork to human insulin was associated with a 1.2 +/- 0.5 mmol/l deterioration (p less than 0.05) in the fasting blood glucose level, while the opposite change caused a 1.1 +/- 0.5 mmol/l improvement (p less than 0.05). Glucose 131-138 insulin Homo sapiens 28-35 6088218-7 1984 Increasing rates of insulin infusion disclosed significant relationships between resulting plasma glucose and cortisol concentrations. Glucose 98-105 insulin Homo sapiens 20-27 6376218-0 1984 A comparison of the relative effects of obesity and non-insulin-dependent diabetes mellitus on in vivo insulin-stimulated glucose utilization. Glucose 122-129 insulin Homo sapiens 56-63 6147291-3 1984 The insulin infusion rate required to maintain blood glucose at 6.7 mmol/l at a set low glucose infusion rate provides an index of insulin action in vivo. Glucose 53-60 insulin Homo sapiens 4-11 6147291-3 1984 The insulin infusion rate required to maintain blood glucose at 6.7 mmol/l at a set low glucose infusion rate provides an index of insulin action in vivo. Glucose 53-60 insulin Homo sapiens 131-138 6147291-3 1984 The insulin infusion rate required to maintain blood glucose at 6.7 mmol/l at a set low glucose infusion rate provides an index of insulin action in vivo. Glucose 88-95 insulin Homo sapiens 4-11 6147291-3 1984 The insulin infusion rate required to maintain blood glucose at 6.7 mmol/l at a set low glucose infusion rate provides an index of insulin action in vivo. Glucose 88-95 insulin Homo sapiens 131-138 6147291-5 1984 The insulin infusion rate needed to maintain the set blood glucose level did not differ significantly between the three experimental conditions (1.2 +/- 0.2 versus 1.3 +/- 0.3 versus 1.2 +/- 0.3 U/h). Glucose 59-66 insulin Homo sapiens 4-11 6381036-5 1984 Natural estrogens can improve glucose tolerance through a beta-cytotropic effect and enhanced insulin sensitivity. Glucose 30-37 insulin Homo sapiens 94-101 6381195-4 1984 A low dose infusion of insulin or an equipotent dose of one of the dimers significantly prolonged the effects of an insulin bolus on plasma glucose but not on non-esterified fatty acids. Glucose 140-147 insulin Homo sapiens 23-30 6381195-4 1984 A low dose infusion of insulin or an equipotent dose of one of the dimers significantly prolonged the effects of an insulin bolus on plasma glucose but not on non-esterified fatty acids. Glucose 140-147 insulin Homo sapiens 116-123 6383922-3 1984 Islets cultured in the presence of the higher cyclosporin A concentration had impaired islet proinsulin biosynthesis and insulin release when challenged with high glucose concentration. Glucose 163-170 insulin Homo sapiens 96-103 6503348-5 1984 The combination of individually programmed profiles and preprandial insulin bolus significantly reduced the postprandial blood glucose level and increase (P less than 0.001). Glucose 127-134 insulin Homo sapiens 68-75 6503348-6 1984 Our investigations suggest that individually programmed insulin infusion profiles are able to smooth blood glucose fluctuations. Glucose 107-114 insulin Homo sapiens 56-63 6234574-3 1984 The in vivo study used a Biostator artificial pancreas: rapid decrease of plasma glucose concentrations was observed under insulin infusion at a constant rate of 200 mU/min with either porcine or semi-synthetic human insulin despite maximum glucose infusion rate (400 mg/min), but not with bovine insulin and a low glucose infusion rate (150 mg/min). Glucose 81-88 insulin Homo sapiens 123-130 6732235-7 1984 These results indicate that the subcellular distribution of internalized insulin and of intracellular glucose transport activity are different, suggesting that the pathways of intracellular processing of the insulin receptor and the glucose transport mechanism are different. Glucose 233-240 insulin Homo sapiens 73-80 6373458-13 1984 This alteration in beta-cell responsiveness probably underlies our prior observation of slowly progressive loss of i.v.-glucose-induced insulin release in islet cell antibody-positive siblings to type I diabetic subjects. Glucose 120-127 insulin Homo sapiens 136-143 6373464-8 1984 Fasting plasma insulin concentration fell (23 +/- 2 mU/L before, 12 +/- 1 mU/L after) and the insulin response to glucose improved (incremental area under the insulin curve: 61 +/- 18 mU/L/h before, 104 +/- 21 mU/L/h after). Glucose 114-121 insulin Homo sapiens 94-101 6373464-8 1984 Fasting plasma insulin concentration fell (23 +/- 2 mU/L before, 12 +/- 1 mU/L after) and the insulin response to glucose improved (incremental area under the insulin curve: 61 +/- 18 mU/L/h before, 104 +/- 21 mU/L/h after). Glucose 114-121 insulin Homo sapiens 94-101 6381187-9 1984 Adaptive growth responses to an increased insulin demand occur in a number of hereditary diabetic syndromes in animals, but in some of these there is an inherited restriction on the capacity for B-cell proliferation leading to further deterioration of the glucose tolerance. Glucose 256-263 insulin Homo sapiens 42-49 6327239-2 1984 To analyze the role of cell coupling in glucose-induced insulin release, single B-cells were reaggregated in vitro and then tested for their secretory capability. Glucose 40-47 insulin Homo sapiens 56-63 6327396-1 1984 Glucose, the major physiological stimulus for insulin secretion, induces a periodic bursting pattern of Ca2+ action potentials that are thought to mediate the uptake of Ca2+ into the intracellular pool of free Ca2+, which controls the rate of insulin release. Glucose 0-7 insulin Homo sapiens 46-53 6389293-0 1984 Comparison of the effect of semisynthetic human insulin and porcine insulin on glucose kinetics, plasma free fatty acid and amino acid levels in man. Glucose 79-86 insulin Homo sapiens 48-55 6389293-5 1984 The metabolic clearance rate of glucose increased during infusion of human insulin by 120%, C-peptide levels decreased by 41% and plasma FFA concentrations fell by 74%. Glucose 32-39 insulin Homo sapiens 75-82 6389293-8 1984 Thus, the results demonstrate that semisynthetic human and porcine insulin are aequipotent with respect to suppression of hepatic glucose output, stimulation of glucose clearance, inhibition of insulin secretion, lipolysis and proteolysis. Glucose 130-137 insulin Homo sapiens 67-74 6389294-1 1984 We have examined insulin binding to the erythrocyte insulin receptor in normal males following a short fast and a test meal or glucose load. Glucose 127-134 insulin Homo sapiens 17-24 6389295-1 1984 The amount of insulin required to maintain similar blood glucose concentrations during an eight hour infusion of either saline or growth hormone (2 micrograms/kg/hr) was determined in five fed, insulin-dependent diabetic subjects during closed-loop insulin delivery. Glucose 57-64 insulin Homo sapiens 14-21 6373809-0 1984 Biosynthetic human insulin and proinsulin have additive but not synergistic effects on total body glucose disposal. Glucose 98-105 insulin Homo sapiens 19-26 6373809-0 1984 Biosynthetic human insulin and proinsulin have additive but not synergistic effects on total body glucose disposal. Glucose 98-105 insulin Homo sapiens 31-41 6373809-3 1984 As an initial study, multiple euglycemic clamp studies were performed in six normal subjects to construct dose-response curves for insulin- and proinsulin-mediated glucose disposal. Glucose 164-171 insulin Homo sapiens 131-154 6373809-5 1984 Analysis of these dose-response curves indicated that proinsulin-mediated glucose disposal was approximately 7% that of insulin. Glucose 74-81 insulin Homo sapiens 54-64 6373809-5 1984 Analysis of these dose-response curves indicated that proinsulin-mediated glucose disposal was approximately 7% that of insulin. Glucose 74-81 insulin Homo sapiens 57-64 6373809-8 1984 Analysis of the dose-response curves for insulin and proinsulin was also useful in predicting the glucose disposal rate during the combination study (290 +/- 19 mg/M2 X min). Glucose 98-105 insulin Homo sapiens 41-48 6373809-8 1984 Analysis of the dose-response curves for insulin and proinsulin was also useful in predicting the glucose disposal rate during the combination study (290 +/- 19 mg/M2 X min). Glucose 98-105 insulin Homo sapiens 53-63 6373809-9 1984 Thus, using either approach to predict the glucose disposal rates, insulin and proinsulin appeared to have additive effects on total body glucose disposal. Glucose 138-145 insulin Homo sapiens 67-74 6373809-9 1984 Thus, using either approach to predict the glucose disposal rates, insulin and proinsulin appeared to have additive effects on total body glucose disposal. Glucose 138-145 insulin Homo sapiens 79-89 6373813-7 1984 During the insulin infusion, hepatic glucose production was totally suppressed before T4 and T3 treatment, but was 0.96 +/- 0.39 mg kg-1 min-1 during T4 and T3 treatment. Glucose 37-44 insulin Homo sapiens 11-18 6373813-9 1984 In conclusion, glucose metabolism in experimental hyperthyroidism is characterized by 1) increases in basal glucose production and utilization; 2) antagonism between the effect of insulin and hyperthyroidism at the hepatic level; and 3) lack of peripheral insulin resistance in spite of marked alteration in erythrocyte insulin binding affinity. Glucose 15-22 insulin Homo sapiens 180-187 6373813-9 1984 In conclusion, glucose metabolism in experimental hyperthyroidism is characterized by 1) increases in basal glucose production and utilization; 2) antagonism between the effect of insulin and hyperthyroidism at the hepatic level; and 3) lack of peripheral insulin resistance in spite of marked alteration in erythrocyte insulin binding affinity. Glucose 15-22 insulin Homo sapiens 256-263 6373814-4 1984 This finding indicates that proinsulin is approximately 7.3% as biologically active as insulin on a molar basis in maintaining glucose control. Glucose 127-134 insulin Homo sapiens 28-38 6373814-4 1984 This finding indicates that proinsulin is approximately 7.3% as biologically active as insulin on a molar basis in maintaining glucose control. Glucose 127-134 insulin Homo sapiens 31-38 6373814-6 1984 After maintaining euglycemia overnight with an infusion of insulin or proinsulin and then acutely stopping these infusions, the rise in plasma glucose after proinsulin was delayed significantly compared to insulin, consistent with proinsulin"s slower clearance. Glucose 143-150 insulin Homo sapiens 70-80 6373814-6 1984 After maintaining euglycemia overnight with an infusion of insulin or proinsulin and then acutely stopping these infusions, the rise in plasma glucose after proinsulin was delayed significantly compared to insulin, consistent with proinsulin"s slower clearance. Glucose 143-150 insulin Homo sapiens 157-167 6373814-6 1984 After maintaining euglycemia overnight with an infusion of insulin or proinsulin and then acutely stopping these infusions, the rise in plasma glucose after proinsulin was delayed significantly compared to insulin, consistent with proinsulin"s slower clearance. Glucose 143-150 insulin Homo sapiens 157-167 6373827-0 1984 Defective glucose counterregulation after subcutaneous insulin in noninsulin-dependent diabetes mellitus. Glucose 10-17 insulin Homo sapiens 55-62 6373827-4 1984 This abnormality in glucose production was nearly completely compensated for by a paradoxical decrease in glucose utilization after injection of insulin (basal 2.11 +/- 0.03----1.86 +/- 0.06 mg/kg per min at 21/2 h in diabetics vs. basal 2.08 +/- 0.04----2.39 +/- 0.11 mg/kg per min at 21/2 h nondiabetics, P less than 0.01), which could not be accounted for by differences in plasma glucose concentrations; the net result was a modest prolongation of hypoglycemia. Glucose 20-27 insulin Homo sapiens 145-152 6373827-4 1984 This abnormality in glucose production was nearly completely compensated for by a paradoxical decrease in glucose utilization after injection of insulin (basal 2.11 +/- 0.03----1.86 +/- 0.06 mg/kg per min at 21/2 h in diabetics vs. basal 2.08 +/- 0.04----2.39 +/- 0.11 mg/kg per min at 21/2 h nondiabetics, P less than 0.01), which could not be accounted for by differences in plasma glucose concentrations; the net result was a modest prolongation of hypoglycemia. Glucose 106-113 insulin Homo sapiens 145-152 6373827-4 1984 This abnormality in glucose production was nearly completely compensated for by a paradoxical decrease in glucose utilization after injection of insulin (basal 2.11 +/- 0.03----1.86 +/- 0.06 mg/kg per min at 21/2 h in diabetics vs. basal 2.08 +/- 0.04----2.39 +/- 0.11 mg/kg per min at 21/2 h nondiabetics, P less than 0.01), which could not be accounted for by differences in plasma glucose concentrations; the net result was a modest prolongation of hypoglycemia. Glucose 106-113 insulin Homo sapiens 145-152 6371274-3 1984 A small dose (3 to 5 units) of rapid-acting insulin given 30 minutes before ingestion of ice cream reduced the modest plasma glucose excursion. Glucose 125-132 insulin Homo sapiens 44-51 6427534-5 1984 The peak glucose and insulin levels and their decline after the glucose loading were delayed in the diabetic patients. Glucose 64-71 insulin Homo sapiens 21-28 6379576-0 1984 [Effect of a 36-hour fast on blood glucose and insulin responses to the glucose stimulus in the normal subject]. Glucose 72-79 insulin Homo sapiens 47-54 6202683-2 1984 Stimulation of glucose release by 8-bromo-cAMP, which is not appreciably hydrolyzed by phosphodiesterase, was also inhibited by insulin in the presence of d-4-(3-butoxy-4-methoxybenzyl)-2- imidizolidione . Glucose 15-22 insulin Homo sapiens 128-135 6371526-4 1984 However, her endogenous immunoreactive insulin showed reduced biologic activity during a glucose-clamp study with hyperglycemia and a reduced ability to bind to the insulin receptor and stimulate glucose transport in vitro. Glucose 89-96 insulin Homo sapiens 39-46 6371526-4 1984 However, her endogenous immunoreactive insulin showed reduced biologic activity during a glucose-clamp study with hyperglycemia and a reduced ability to bind to the insulin receptor and stimulate glucose transport in vitro. Glucose 196-203 insulin Homo sapiens 39-46 6370728-0 1984 Translocation hypothesis of insulin action on glucose transport. Glucose 46-53 insulin Homo sapiens 28-35 6370728-1 1984 This article reviews the experimental data that support the translocation hypothesis of insulin action on glucose transport in adipocytes. Glucose 106-113 insulin Homo sapiens 88-95 6370728-2 1984 According to this hypothesis, 1) most of the glucose transport mechanism in the basal (no insulin) form of fat cells is associated with an unidentified subcellular structure (the storage site), which is separated into the Golgi-rich fraction by centrifugation, and 2) the function of insulin is to induce translocation of the glucose transport mechanism from the above storage site to the plasma membrane. Glucose 45-52 insulin Homo sapiens 284-291 6372519-2 1984 One possible explanation for these findings is that mild hyperglycemia per se can cause an adaptive increase in islet sensitivity to glucose, leading to increased insulin output at a given glucose level. Glucose 133-140 insulin Homo sapiens 163-170 6428120-3 1984 The combination of insulin and glibenclamide was more effective in lowering the fasting blood glucose (P = 0.026) and 24 h urine glucose (P = 0.042) than the combination of insulin and placebo. Glucose 94-101 insulin Homo sapiens 19-26 6376219-3 1984 Mean integrated plasma insulin response to glucose increased 2.5-fold after insulin therapy, but this improvement varied considerably from patient to patient. Glucose 43-50 insulin Homo sapiens 23-30 6376219-3 1984 Mean integrated plasma insulin response to glucose increased 2.5-fold after insulin therapy, but this improvement varied considerably from patient to patient. Glucose 43-50 insulin Homo sapiens 76-83 6376219-4 1984 Insulin action also increased with insulin treatment and the resulting values were no longer significantly different from a weight- and age-matched group of subjects with normal glucose tolerance. Glucose 178-185 insulin Homo sapiens 0-7 6376219-6 1984 The insulin-induced improvements in glucose tolerance persisted for at least 2 wk after insulin withdrawal, and were associated with continued increased insulin secretion and insulin action. Glucose 36-43 insulin Homo sapiens 4-11 6376219-6 1984 The insulin-induced improvements in glucose tolerance persisted for at least 2 wk after insulin withdrawal, and were associated with continued increased insulin secretion and insulin action. Glucose 36-43 insulin Homo sapiens 88-95 6376220-0 1984 Insulin-stimulated glucose disposal increases with time in patients with non-insulin-dependent diabetes mellitus. Glucose 19-26 insulin Homo sapiens 0-7 6376220-1 1984 The relative effects of time versus ambient glucose concentration on insulin-stimulated glucose uptake was estimated by performing 5-h insulin clamp studies in patients with NIDDM. Glucose 44-51 insulin Homo sapiens 69-76 6376220-1 1984 The relative effects of time versus ambient glucose concentration on insulin-stimulated glucose uptake was estimated by performing 5-h insulin clamp studies in patients with NIDDM. Glucose 88-95 insulin Homo sapiens 69-76 6376220-5 1984 The time-dependent increase in glucose MCR was associated with an approximate 30% increase in steady-state plasma insulin concentrations when comparing the second and fifth hours. Glucose 31-38 insulin Homo sapiens 114-121 6381006-4 1984 This improved glucose control with either CSII or MI was associated with an increase in sural nerve conductivity from 42.9 to 45 m/s and a decrease in proteinuria from 1.9 to 0.5 g/24 h. The 24-h insulin dose consisted of 45 U before the study, 44 U during CSII, and 56 U during MI. Glucose 14-21 insulin Homo sapiens 196-203 6442226-5 1984 With this constant rate insulin infusion pump, and no supplementation of insulin dose by other means, the plasma glucose control is excellent and serum lipid and glycosylated haemoglobin (HbA1) levels have returned to normal. Glucose 113-120 insulin Homo sapiens 24-31 6468796-3 1984 In non-diabetic subjects, as has been shown previously for Caucasiod subjects, both obesity and fasting plasma glucose levels were determinants of fasting serum C-peptide. Glucose 111-118 insulin Homo sapiens 161-170 6468796-5 1984 Taken overall, mean fasting serum C-peptide increased then possibly fell in subjects grouped by increasing 2-h post-glucose plasma glucose levels. Glucose 116-123 insulin Homo sapiens 34-43 6468796-5 1984 Taken overall, mean fasting serum C-peptide increased then possibly fell in subjects grouped by increasing 2-h post-glucose plasma glucose levels. Glucose 131-138 insulin Homo sapiens 34-43 6468801-4 1984 The subgroup of diabetic patients who required insulin for the control of their blood glucose did not have a higher frequency of thyroid microsomal antibodies when compared with non-insulin-requiring diabetic patients. Glucose 86-93 insulin Homo sapiens 47-54 6386641-0 1984 The role of insulin, glucagon and growth hormone in the regulation of plasma glucose and free fatty acid levels in anorexia nervosa. Glucose 77-84 insulin Homo sapiens 12-19 6747013-0 1984 Defective phagocytosis in insulin controlled diabetics: evidence for a reaction between glucose and opsonising proteins. Glucose 88-95 insulin Homo sapiens 26-33 6377008-1 1984 We have examined the effect of human growth hormone (HGH) on both basal and insulin stimulated glucose uptake in human fibroblasts. Glucose 95-102 insulin Homo sapiens 76-83 6377008-2 1984 High concentrations of HGH (100 micrograms/mL) depressed both basal and insulin-stimulated glucose uptake by 25%. Glucose 91-98 insulin Homo sapiens 72-79 6428619-6 1984 C peptide concentrations, however, did help predict the response to insulin, the fasting C peptide to glucose ratio being considerably lower in those patients whose control was better on insulin. Glucose 102-109 insulin Homo sapiens 68-75 6428619-6 1984 C peptide concentrations, however, did help predict the response to insulin, the fasting C peptide to glucose ratio being considerably lower in those patients whose control was better on insulin. Glucose 102-109 insulin Homo sapiens 187-194 6374455-1 1984 We assessed glucose counterregulation during intensive insulin therapy in 20 patients with insulin-dependent diabetes mellitus (IDDM) by injecting therapeutic doses of regular insulin subcutaneously after overnight maintenance of euglycemia. Glucose 12-19 insulin Homo sapiens 55-62 6374455-1 1984 We assessed glucose counterregulation during intensive insulin therapy in 20 patients with insulin-dependent diabetes mellitus (IDDM) by injecting therapeutic doses of regular insulin subcutaneously after overnight maintenance of euglycemia. Glucose 12-19 insulin Homo sapiens 91-98 6374455-6 1984 Rates of plasma glucose recovery from hypoglycemia were inversely correlated with plasma free insulin concentrations (r = -0.84, P less than 0.01); the latter in turn were directly correlated with insulin-antibody binding (r = 0.94, P less than 0.01). Glucose 16-23 insulin Homo sapiens 94-101 6374455-6 1984 Rates of plasma glucose recovery from hypoglycemia were inversely correlated with plasma free insulin concentrations (r = -0.84, P less than 0.01); the latter in turn were directly correlated with insulin-antibody binding (r = 0.94, P less than 0.01). Glucose 16-23 insulin Homo sapiens 197-204 6375230-8 1984 Thus a small but significant greater decline in potassium levels with similar glucose requirements was found during iv administration of porcine insulin compared with human insulin. Glucose 78-85 insulin Homo sapiens 145-152 6146261-3 1984 The release of insulin and somatostatin was measured at various concentrations of glucose in the perfusate, and the corresponding dose-response curves were derived. Glucose 82-89 insulin Homo sapiens 15-22 6744100-2 1984 This has led to speculation that retinal microangiopathy might be prevented or its progression halted by controlling the blood glucose concentration to lower levels than has been possible in the past with conventional insulin therapy and conventional monitoring. Glucose 127-134 insulin Homo sapiens 218-225 6381189-2 1984 The amount of glucose infused is a measure of insulin sensitivity. Glucose 14-21 insulin Homo sapiens 46-53 6381191-5 1984 Insulin concentrations increased to significantly higher levels in patients with idiopathic haemochromatosis than in the control subjects from 30 to 180 min after the glucose load (p less than or equal to 0.01), while fasting insulin concentrations were not significantly different (p greater than 0.05). Glucose 167-174 insulin Homo sapiens 0-7 6378863-4 1984 Arterial blood concentration of glucose decreased from 3.23 mM (control) to 1.51 mM (insulin), then increased to 4.29 mM (glucose). Glucose 32-39 insulin Homo sapiens 85-92 6378863-7 1984 Uptake (two steers) of glucose from blood (mmol/h) increased from 38 (control) to 76 (insulin) and 99 (glucose). Glucose 23-30 insulin Homo sapiens 86-93 6428120-3 1984 The combination of insulin and glibenclamide was more effective in lowering the fasting blood glucose (P = 0.026) and 24 h urine glucose (P = 0.042) than the combination of insulin and placebo. Glucose 129-136 insulin Homo sapiens 19-26 6372519-2 1984 One possible explanation for these findings is that mild hyperglycemia per se can cause an adaptive increase in islet sensitivity to glucose, leading to increased insulin output at a given glucose level. Glucose 189-196 insulin Homo sapiens 163-170 6375445-1 1984 Use of continuous intravenous insulin-glucose-potassium infusions. Glucose 38-45 insulin Homo sapiens 30-37 6370165-1 1984 The temporal relationship between the level of blood glucose and the frequency of ventricular premature contractions (VPCs) during 24 hours was examined in a 45-year-old man with diabetes mellitus who was treated with a regular insulin injection. Glucose 53-60 insulin Homo sapiens 228-235 6370165-4 1984 The insulin tolerance test produced frequent VPCs during hypoglycemia, which was suppressed by glucose administration. Glucose 95-102 insulin Homo sapiens 4-11 6376218-4 1984 In addition, insulin-stimulated glucose utilization, as assessed by determination of glucose metabolic clearance rate (MCR), was not different as a function of obesity. Glucose 32-39 insulin Homo sapiens 13-20 6376218-4 1984 In addition, insulin-stimulated glucose utilization, as assessed by determination of glucose metabolic clearance rate (MCR), was not different as a function of obesity. Glucose 85-92 insulin Homo sapiens 13-20 6376025-2 1984 The loss of the acute plasma insulin response to intravenous glucose is seen in patients with relatively mild degrees of fasting hyperglycemia, but patients with severe fasting hyperglycemia also demonstrate absolute hypoinsulinemia in response to an oral glucose challenge. Glucose 61-68 insulin Homo sapiens 29-36 6432288-5 1984 The glucose lowering effect of intravenous insulin was significantly diminished in primary hyperparathyroidism compared with controls (P less than 0.01). Glucose 4-11 insulin Homo sapiens 43-50 6373455-0 1984 Relationship between the plasma insulin response to oral glucose and insulin-stimulated glucose utilization in normal subjects. Glucose 57-64 insulin Homo sapiens 32-39 6373455-0 1984 Relationship between the plasma insulin response to oral glucose and insulin-stimulated glucose utilization in normal subjects. Glucose 57-64 insulin Homo sapiens 69-76 6373455-0 1984 Relationship between the plasma insulin response to oral glucose and insulin-stimulated glucose utilization in normal subjects. Glucose 88-95 insulin Homo sapiens 32-39 6373455-0 1984 Relationship between the plasma insulin response to oral glucose and insulin-stimulated glucose utilization in normal subjects. Glucose 88-95 insulin Homo sapiens 69-76 6373455-1 1984 The relationship between in vivo insulin-stimulated glucose utilization (euglycemic clamp technique) and various estimates of the plasma insulin response to oral glucose was defined in 62 subjects with normal glucose tolerance. Glucose 52-59 insulin Homo sapiens 33-40 6376025-2 1984 The loss of the acute plasma insulin response to intravenous glucose is seen in patients with relatively mild degrees of fasting hyperglycemia, but patients with severe fasting hyperglycemia also demonstrate absolute hypoinsulinemia in response to an oral glucose challenge. Glucose 256-263 insulin Homo sapiens 29-36 6373455-1 1984 The relationship between in vivo insulin-stimulated glucose utilization (euglycemic clamp technique) and various estimates of the plasma insulin response to oral glucose was defined in 62 subjects with normal glucose tolerance. Glucose 162-169 insulin Homo sapiens 137-144 6373455-1 1984 The relationship between in vivo insulin-stimulated glucose utilization (euglycemic clamp technique) and various estimates of the plasma insulin response to oral glucose was defined in 62 subjects with normal glucose tolerance. Glucose 162-169 insulin Homo sapiens 137-144 6373455-2 1984 Both the incremental insulin increase above fasting (r = 0.61) and the total integrated insulin response (r = 0.65) were highly correlated (P less than 0.001) with in vivo insulin action, and the relationship between total insulin response and insulin action remained significant (r = 0.61, P less than 0.001) when corrected for variations in total glucose response, age, and obesity. Glucose 349-356 insulin Homo sapiens 21-28 6373455-2 1984 Both the incremental insulin increase above fasting (r = 0.61) and the total integrated insulin response (r = 0.65) were highly correlated (P less than 0.001) with in vivo insulin action, and the relationship between total insulin response and insulin action remained significant (r = 0.61, P less than 0.001) when corrected for variations in total glucose response, age, and obesity. Glucose 349-356 insulin Homo sapiens 88-95 6373455-2 1984 Both the incremental insulin increase above fasting (r = 0.61) and the total integrated insulin response (r = 0.65) were highly correlated (P less than 0.001) with in vivo insulin action, and the relationship between total insulin response and insulin action remained significant (r = 0.61, P less than 0.001) when corrected for variations in total glucose response, age, and obesity. Glucose 349-356 insulin Homo sapiens 88-95 6373455-2 1984 Both the incremental insulin increase above fasting (r = 0.61) and the total integrated insulin response (r = 0.65) were highly correlated (P less than 0.001) with in vivo insulin action, and the relationship between total insulin response and insulin action remained significant (r = 0.61, P less than 0.001) when corrected for variations in total glucose response, age, and obesity. Glucose 349-356 insulin Homo sapiens 88-95 6373455-4 1984 A significant correlation also existed between insulin action and response in these subjects (r = 0.67, P less than 0.001), which remained significant (r = 0.65) when differences in total glucose response, obesity, age, and maximal oxygen consumption were taken into account. Glucose 188-195 insulin Homo sapiens 47-54 6373455-5 1984 These data demonstrate that there is a significant correlation between insulin response and insulin action in normal individuals that can account for approximately one-third of the total variance in insulin action seen in subjects with normal glucose tolerance. Glucose 243-250 insulin Homo sapiens 71-78 6373455-5 1984 These data demonstrate that there is a significant correlation between insulin response and insulin action in normal individuals that can account for approximately one-third of the total variance in insulin action seen in subjects with normal glucose tolerance. Glucose 243-250 insulin Homo sapiens 92-99 6373455-5 1984 These data demonstrate that there is a significant correlation between insulin response and insulin action in normal individuals that can account for approximately one-third of the total variance in insulin action seen in subjects with normal glucose tolerance. Glucose 243-250 insulin Homo sapiens 92-99 6373455-6 1984 Thus, determination of plasma insulin levels after an oral glucose challenge can only provide a qualitative estimate of insulin-stimulated glucose utilization. Glucose 59-66 insulin Homo sapiens 30-37 6373455-6 1984 Thus, determination of plasma insulin levels after an oral glucose challenge can only provide a qualitative estimate of insulin-stimulated glucose utilization. Glucose 139-146 insulin Homo sapiens 30-37 6373455-6 1984 Thus, determination of plasma insulin levels after an oral glucose challenge can only provide a qualitative estimate of insulin-stimulated glucose utilization. Glucose 139-146 insulin Homo sapiens 120-127 6376017-0 1984 Oral propranolol and metoprolol both impair glucose recovery from insulin-induced hypoglycemia in insulin-dependent diabetes mellitus. Glucose 44-51 insulin Homo sapiens 66-73 6376018-11 1984 However, with the basal insulin infusion rate necessary to achieve near-normal fasting blood glucose levels, moderate exercise in the postabsorptive state may result in hypoglycemia with CSII. Glucose 93-100 insulin Homo sapiens 24-31 6376025-5 1984 This metabolic defect is independent of obesity, and the severity of the resistance to insulin-stimulated glucose uptake increases with magnitude of hyperglycemia. Glucose 106-113 insulin Homo sapiens 87-94 6376034-3 1984 The insulin-resistant patients had fasting hyperinsulinemia (19 +/- 4 vs 11 +/- 1 microU/ml in nondiabetic subjects, P less than 0.05), decreased erythrocyte insulin receptor binding (4.8 +/- 0.4 vs 5.8 +/- 0.3%/1.6 X 10(9) cells in nondiabetic subjects, P less than 0.05), and impairment in both insulin-induced suppression of glucose production (Km 97 +/- 31 vs 21 +/- 7 microU/ml in nondiabetic subjects, P less than 0.05), and insulin-induced stimulation of glucose utilization (Km and Vmax 176 +/- 29 microU/ml and 5.8 +/- 0.7 mg/kg/min vs 50 +/- 2 microU/ml and 9.1 +/- 0.6 mg/kg/min in nondiabetic subjects, both P less than 0.05). Glucose 328-335 insulin Homo sapiens 4-11 6376026-2 1984 In normal people, glucose directly stimulates insulin release and also plays a key role as a potentiator of nonglucose stimulants of the B-cells. Glucose 18-25 insulin Homo sapiens 46-53 6376034-3 1984 The insulin-resistant patients had fasting hyperinsulinemia (19 +/- 4 vs 11 +/- 1 microU/ml in nondiabetic subjects, P less than 0.05), decreased erythrocyte insulin receptor binding (4.8 +/- 0.4 vs 5.8 +/- 0.3%/1.6 X 10(9) cells in nondiabetic subjects, P less than 0.05), and impairment in both insulin-induced suppression of glucose production (Km 97 +/- 31 vs 21 +/- 7 microU/ml in nondiabetic subjects, P less than 0.05), and insulin-induced stimulation of glucose utilization (Km and Vmax 176 +/- 29 microU/ml and 5.8 +/- 0.7 mg/kg/min vs 50 +/- 2 microU/ml and 9.1 +/- 0.6 mg/kg/min in nondiabetic subjects, both P less than 0.05). Glucose 462-469 insulin Homo sapiens 4-11 6376242-1 1984 Glucose counter-regulation during insulin-induced hypoglycaemia was studied in Type 1 diabetic patients without evidence of autonomic neuropathy and compared with that of a non-diabetic control group. Glucose 0-7 insulin Homo sapiens 34-41 6376026-7 1984 However, as the glucose level falls during therapy the insulin level may tend to return toward pretreatment values, thereby masking the improvement of B-cell function. Glucose 16-23 insulin Homo sapiens 55-62 6376030-7 1984 On active treatment, insulin levels rose coincident with a fall in fasting blood glucose and an improvement in glucose tolerance and near-normalization of plasma lactate, pyruvate, free fatty acids, glycerol, and ketone bodies, all of which relapsed to initial values after placebo. Glucose 81-88 insulin Homo sapiens 21-28 6376030-7 1984 On active treatment, insulin levels rose coincident with a fall in fasting blood glucose and an improvement in glucose tolerance and near-normalization of plasma lactate, pyruvate, free fatty acids, glycerol, and ketone bodies, all of which relapsed to initial values after placebo. Glucose 111-118 insulin Homo sapiens 21-28 6428842-4 1984 In our studies we have found that sulfonylureas possess a selective regulatory in vivo effect on the cellular insulin binding to monocytes, independent of the diet and changes in plasma glucose and insulin concentrations. Glucose 186-193 insulin Homo sapiens 110-117 6376033-5 1984 In addition to resistance to insulin"s effects to promote glucose disposal, type II diabetic patients also exhibit a marked increase in the rate of entry of glucose into the circulation from the liver, as manifested by accelerated rates of hepatic glucose production. Glucose 58-65 insulin Homo sapiens 29-36 6381072-4 1984 The glucose-stimulated insulin response of the early secretion phase (0--5 min) decreased during the follow-up study in relatives of type-II diabetics with normal CHT (in tendency) and with glucose intolerance (p less than 0.05) but not in relatives of type-I diabetics. Glucose 4-11 insulin Homo sapiens 23-30 6381072-4 1984 The glucose-stimulated insulin response of the early secretion phase (0--5 min) decreased during the follow-up study in relatives of type-II diabetics with normal CHT (in tendency) and with glucose intolerance (p less than 0.05) but not in relatives of type-I diabetics. Glucose 190-197 insulin Homo sapiens 23-30 6381073-0 1984 Metabolic and hormonal responses during a glucose controlled insulin infusion (Biostator) in subjects with impaired glucose tolerance. Glucose 42-49 insulin Homo sapiens 61-68 6381073-1 1984 The short-term effect of the glucose-controlled insulin infusion system (GCIIS) Biostator on metabolic and hormonal responses was studied in 10 non-obese subjects with glucose intolerance and insulin low response to glucose. Glucose 29-36 insulin Homo sapiens 48-55 6381073-5 1984 Glucose-induced endogenous insulin secretion (C-peptide) was significantly reduced during the GCIIS study possibly due to inhibition of insulin secretion by exogenous insulin and/or by lower blood glucose concentration after normalization of glucose tolerance. Glucose 0-7 insulin Homo sapiens 27-34 6381073-5 1984 Glucose-induced endogenous insulin secretion (C-peptide) was significantly reduced during the GCIIS study possibly due to inhibition of insulin secretion by exogenous insulin and/or by lower blood glucose concentration after normalization of glucose tolerance. Glucose 242-249 insulin Homo sapiens 27-34 6371116-3 1984 The total glucose and insulin responses following the oral glucose load were increased by 24% and 127% respectively in the elderly compared with the young (24,524 +/- 1,080 vs. 19,734 +/- 702 mg/dl X min and 24,289 +/- 3,401 vs. 10,700 +/- 1,209 microU/ml X min). Glucose 59-66 insulin Homo sapiens 22-29 6371057-12 1984 Analysis of the serum insulin from two nondiabetic siblings revealed that normal insulin increased from approximately 2 to 15% of total serum insulin after the ingestion of glucose and that the proportion of the normal hormone plateaued or fell while the level of total insulin continued to rise. Glucose 173-180 insulin Homo sapiens 81-88 6371057-12 1984 Analysis of the serum insulin from two nondiabetic siblings revealed that normal insulin increased from approximately 2 to 15% of total serum insulin after the ingestion of glucose and that the proportion of the normal hormone plateaued or fell while the level of total insulin continued to rise. Glucose 173-180 insulin Homo sapiens 81-88 6371057-12 1984 Analysis of the serum insulin from two nondiabetic siblings revealed that normal insulin increased from approximately 2 to 15% of total serum insulin after the ingestion of glucose and that the proportion of the normal hormone plateaued or fell while the level of total insulin continued to rise. Glucose 173-180 insulin Homo sapiens 81-88 6371165-8 1984 Response of insulin secretion to 3 mg/ml glucose appeared 6 hours after thawing, and the response to both 3 mg/ml glucose and 10 mmol/L theophylline was recovery to the same level as nonfrozen islet cells after 12 hours. Glucose 41-48 insulin Homo sapiens 12-19 6374287-0 1984 The effect of free fatty acids on insulin-mediated glucose uptake. Glucose 51-58 insulin Homo sapiens 34-41 6374287-1 1984 Free fatty acids (FFA) have been shown in vitro to inhibit insulin-mediated glucose uptake by muscle and have been proposed as in vivo mediators of peripheral insulin resistance. Glucose 76-83 insulin Homo sapiens 59-66 6371625-3 1984 Mean maternal and fetal serum glucose and insulin and sodium concentrations at delivery differed among all groups in direct relationship to the rate of glucose infusion. Glucose 152-159 insulin Homo sapiens 42-49 6371443-6 1984 Glucose-stimulated insulin concentrations were unchanged by propranolol and combined blockade, whereas there was a trend (P = 0.07) toward an increased response to glucose during phentolamine administration. Glucose 0-7 insulin Homo sapiens 19-26 6371444-5 1984 Increases of insulin clearance rates were most marked (greater than 15%) in patients whose blood glucose rose during continuous insulin administration. Glucose 97-104 insulin Homo sapiens 13-20 6371444-5 1984 Increases of insulin clearance rates were most marked (greater than 15%) in patients whose blood glucose rose during continuous insulin administration. Glucose 97-104 insulin Homo sapiens 128-135 6722256-0 1984 Simplified evaluation and documentation of data from glucose controlled insulin infusion system (GCIIS). Glucose 53-60 insulin Homo sapiens 72-79 6377421-0 1984 Phenobarbital treatment enhances insulin mediated glucose metabolism in man. Glucose 50-57 insulin Homo sapiens 33-40 6377421-3 1984 We hence investigated insulin mediated glucose metabolism before and after a ten day course of PB therapy in healthy, nondiabetic subjects using the euglycemic glucose clamp technique. Glucose 39-46 insulin Homo sapiens 22-29 6377415-0 1984 [Comparison of insulin and growth hormone levels in oral and intravenous glucose overload in normal and obese women]. Glucose 73-80 insulin Homo sapiens 15-22 6423182-5 1984 This direct relation of plasma magnesium concentration with glucose disposal was unexplained by its influence on insulin secretion but was related to insulin sensitivity; hence magnesium may be an important determinant of insulin sensitivity in maturity onset diabetes. Glucose 60-67 insulin Homo sapiens 150-157 6423182-5 1984 This direct relation of plasma magnesium concentration with glucose disposal was unexplained by its influence on insulin secretion but was related to insulin sensitivity; hence magnesium may be an important determinant of insulin sensitivity in maturity onset diabetes. Glucose 60-67 insulin Homo sapiens 150-157 6382893-3 1984 The glucose and insulin responses in the OGTT in both the smoking and non-smoking operated cases showed higher early peak values and a subsequent rapid drop of the levels with lower 120-min values of both glucose and insulin compared to the average screening cohort. Glucose 4-11 insulin Homo sapiens 217-224 6382893-3 1984 The glucose and insulin responses in the OGTT in both the smoking and non-smoking operated cases showed higher early peak values and a subsequent rapid drop of the levels with lower 120-min values of both glucose and insulin compared to the average screening cohort. Glucose 205-212 insulin Homo sapiens 16-23 6376661-0 1984 The response of C-peptides and insulin to intravenous glucose load in bilharzial hepatic fibrosis. Glucose 54-61 insulin Homo sapiens 31-38 6375004-5 1984 Four out of 9 RPMI 1640-cultured and 8 out of 11 TC 199-cultured explants responded with an increased insulin release when challenged with high glucose-plus-theophylline after one week of culture. Glucose 144-151 insulin Homo sapiens 102-109 6232527-1 1984 Prolonged blood glucose normalization by continuous infusion of insulin]. Glucose 16-23 insulin Homo sapiens 64-71 6329863-9 1984 The reduction of blood glucose concentrations together with unchanged serum insulin concentrations is compatible with improved peripheral insulin sensitivity. Glucose 23-30 insulin Homo sapiens 138-145 6370388-4 1984 During the period of early fluid therapy large amounts of glucose without additional insulin were given, resulting in elevated blood glucose and high plasma insulin levels. Glucose 58-65 insulin Homo sapiens 157-164 6235108-9 1984 These findings suggest that glucose uptake is a rate-limiting step in glycolysis in quiescent 3T3 fibroblasts and that the stimulatory effect of insulin on glycolysis is mediated by enhanced glucose entry. Glucose 28-35 insulin Homo sapiens 145-152 6235108-9 1984 These findings suggest that glucose uptake is a rate-limiting step in glycolysis in quiescent 3T3 fibroblasts and that the stimulatory effect of insulin on glycolysis is mediated by enhanced glucose entry. Glucose 191-198 insulin Homo sapiens 145-152 6376232-4 1984 Insulin-mediated glucose disposal was lower in the diabetic than in the non-diabetic subjects at the two lower insulin infusion rates (mean +/- SEM = 2.03 +/- 0.27 versus 4.8 +/- 0.64 mg X kg-1 X min-1 at the first insulin infusion rate, p less than 0.01, and 5.59 +/- 0.59 versus 8.36 +/- 0.61 mg X kg-1 X min-1 at the second insulin infusion rate, p less than 0.01). Glucose 17-24 insulin Homo sapiens 0-7 6376232-4 1984 Insulin-mediated glucose disposal was lower in the diabetic than in the non-diabetic subjects at the two lower insulin infusion rates (mean +/- SEM = 2.03 +/- 0.27 versus 4.8 +/- 0.64 mg X kg-1 X min-1 at the first insulin infusion rate, p less than 0.01, and 5.59 +/- 0.59 versus 8.36 +/- 0.61 mg X kg-1 X min-1 at the second insulin infusion rate, p less than 0.01). Glucose 17-24 insulin Homo sapiens 111-118 6376232-4 1984 Insulin-mediated glucose disposal was lower in the diabetic than in the non-diabetic subjects at the two lower insulin infusion rates (mean +/- SEM = 2.03 +/- 0.27 versus 4.8 +/- 0.64 mg X kg-1 X min-1 at the first insulin infusion rate, p less than 0.01, and 5.59 +/- 0.59 versus 8.36 +/- 0.61 mg X kg-1 X min-1 at the second insulin infusion rate, p less than 0.01). Glucose 17-24 insulin Homo sapiens 215-222 6376232-4 1984 Insulin-mediated glucose disposal was lower in the diabetic than in the non-diabetic subjects at the two lower insulin infusion rates (mean +/- SEM = 2.03 +/- 0.27 versus 4.8 +/- 0.64 mg X kg-1 X min-1 at the first insulin infusion rate, p less than 0.01, and 5.59 +/- 0.59 versus 8.36 +/- 0.61 mg X kg-1 X min-1 at the second insulin infusion rate, p less than 0.01). Glucose 17-24 insulin Homo sapiens 215-222 6376232-5 1984 However, insulin-induced glucose uptake did not differ significantly between the two groups at the third and fourth rates of insulin infusion. Glucose 25-32 insulin Homo sapiens 9-16 6376233-4 1984 However, over the remainder of the 11 h post-injection period, the plasma glucose level was lower after semi-synthetic human insulin. Glucose 74-81 insulin Homo sapiens 125-132 6373492-3 1984 Their periods of hypothermia were short and irregular and the active periods sometimes lasted several days; their body weight increased during the winter months; in spring, the sensitivity of B cells to glucose was low, decreasing insulin secretion in vivo and in vitro, and the adipocytes were insulin resistant. Glucose 203-210 insulin Homo sapiens 231-238 6373492-3 1984 Their periods of hypothermia were short and irregular and the active periods sometimes lasted several days; their body weight increased during the winter months; in spring, the sensitivity of B cells to glucose was low, decreasing insulin secretion in vivo and in vitro, and the adipocytes were insulin resistant. Glucose 203-210 insulin Homo sapiens 295-302 6373492-5 1984 Their phases of lethargy were long and regular (about 15 days), separated by active periods (6-8 hr); their body weight decreased during the winter months; in spring the B-cell secretion was increased and the sensitivity of the tissues to insulin ensured a high peripheral glucose utilization. Glucose 273-280 insulin Homo sapiens 239-246 6423429-5 1984 Endogenous insulin secretion increased in all subjects, but the increase was most marked in those subjects who continued to exhibit fasting hyperglycemia (fasting serum glucose greater than 175 mg/dl) after 3 mo of therapy. Glucose 169-176 insulin Homo sapiens 11-18 6373542-3 1984 With medium glucose at 5.6 mmol/l, cells from diabetic subjects displayed an increase in collagen and protein radio-activities in the extracellular medium in the presence of insulin at 10(2) or 10(3) mU/l. Glucose 12-19 insulin Homo sapiens 174-181 6368294-2 1984 Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. Glucose 144-151 insulin Homo sapiens 18-25 6368294-13 1984 The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. Glucose 29-36 insulin Homo sapiens 89-96 6365945-10 1984 Basal hepatic glucose production was directly related to the fasting plasma glucose level (r = 0.67, P less than 0.001) and inversely proportional to fasting insulin concentration (r = -0.48, P less than 0.05) in the diabetic patients. Glucose 14-21 insulin Homo sapiens 158-165 6368295-6 1984 Intensive therapy (three daily injections of insulin) instituted in 7 out of 13 IDDM patients for up to 9 mo improved MBG (124 +/- 6 mg/dl, P less than 0.01) and ketoamine-HbA1 (7.9 +/- 0.02%, P less than 0.01) but not rates of plasma glucose recovery (0.31 +/- 0.01 mg/dl X min) and plasma glucagon (AUC 0.69 +/- 0.07 ng/ml X 150 min) and epinephrine (AUC 14.9 +/- 0.17 ng/ml X 150 min) responses. Glucose 235-242 insulin Homo sapiens 45-52 6373323-1 1984 Many cases of type II diabetes present an anomaly of insulin secretion which is characterized by a missing, reduced, or delayed glucose-stimulated insulin output from the beta cell. Glucose 128-135 insulin Homo sapiens 53-60 6699133-0 1984 The role of the glucose transport system in the postreceptor defect in insulin action associated with human aging. Glucose 16-23 insulin Homo sapiens 71-78 6423666-1 1984 We have studied the relationship between in vivo insulin-mediated glucose disposal rates, muscle glycogen content, and muscle glycogen synthase activity in 25 southwest American Indians with normal glucose tolerance and with varying degrees of glucose intolerance. Glucose 66-73 insulin Homo sapiens 49-56 6423666-2 1984 Insulin-mediated glucose disposal (M) was measured by using the hyperinsulinemic euglycemic clamp technique at plasma insulin concentrations of 134 +/- 7 and 1709 +/- 72 microU/ml, with simultaneous indirect calorimetry to assess glucose oxidation and storage rates. Glucose 17-24 insulin Homo sapiens 0-7 6423666-2 1984 Insulin-mediated glucose disposal (M) was measured by using the hyperinsulinemic euglycemic clamp technique at plasma insulin concentrations of 134 +/- 7 and 1709 +/- 72 microU/ml, with simultaneous indirect calorimetry to assess glucose oxidation and storage rates. Glucose 230-237 insulin Homo sapiens 0-7 6423666-4 1984 The results showed that muscle glycogen synthase activity at the end of the euglycemic clamp was well correlated with insulin-mediated glucose storage rates at both low (r = 0.50, P less than 0.02) and high (r = 0.78, P less than 0.0001) insulin concentrations; and also correlated with M (r = 0.66, P less than 0.001 and r = 0.76, P less than 0.0001). Glucose 135-142 insulin Homo sapiens 118-125 6423666-6 1984 The change in muscle glycogen content did not correlate with glucose storage rates or M. The data suggest the possible importance of glycogen synthesis in muscle in determining in vivo insulin-mediated glucose disposal rates in man. Glucose 202-209 insulin Homo sapiens 185-192 6372249-5 1984 Insulin may play a role in the myocardial adjustment to an ischemic insult by enhancing glucose intake and suppressing lipolysis and ketogenesis. Glucose 88-95 insulin Homo sapiens 0-7 6366551-1 1984 The dawn phenomenon is a condition recently described in patients with insulin-dependent diabetes mellitus (IDDM) that is characterized by abrupt increases in fasting levels of plasma glucose or insulin requirements or both between 5 and 9 a.m., in the absence of antecedent hypoglycemia. Glucose 184-191 insulin Homo sapiens 71-78 6382065-0 1984 [Behavior of blood sugar and insulin during oral glucose stimulation after gastric surgery performed using different reconstructive technics]. Glucose 49-56 insulin Homo sapiens 29-36 6390121-0 1984 [Prospective evaluation of the insulin infusion test to establish the adequacy of glucose counterregulation during hypoglycemia in type 1 diabetics undergoing intensive insulin therapy]. Glucose 82-89 insulin Homo sapiens 31-38 6421424-2 1984 In a double blind crossover study in 18 diabetics human ultralente insulin was as effective as beef ultralente insulin in controlling basal plasma glucose concentrations (median 5.7 mmol/l (103 mg/100 ml) with human and 6.3 mmol/l (114 mg/100 ml) with beef ultralente insulin respectively). Glucose 147-154 insulin Homo sapiens 67-74 6367331-4 1984 At near normal blood glucose level the daily insulin requirements decreased from 44.8 +/- 2.9 U pre-dialysis to 35.0 +/- 2.3 U post-dialysis (P less than 0.001). Glucose 21-28 insulin Homo sapiens 45-52 6367483-0 1984 Sex difference in insulin-stimulated glucose transport in rat and human adipocytes. Glucose 37-44 insulin Homo sapiens 18-25 6367483-1 1984 In an effort to determine whether differences in basal and maximum insulin-stimulated glucose transport by isolated adipocytes are a function of donor sex, we measured glucose transport rates in the absence and presence of 8 nM insulin in adipocytes isolated from the abdominal subcutaneous fat tissue of nine male and ten female subjects with varying degrees of obesity and in adipocytes isolated from the abdominal subcutaneous and retroperitoneal fat tissue of (180-220 g) male and female rats. Glucose 86-93 insulin Homo sapiens 67-74 6367483-2 1984 Because maximal insulin-stimulated glucose transport rate per cell of adipocytes isolated from subcutaneous abdominal tissue of male and female subjects was constant in each sex, the data have been normalized on the basis of transport per cell. Glucose 35-42 insulin Homo sapiens 16-23 6367483-3 1984 The results demonstrated that basal and maximal insulin-stimulated glucose transport per cell was 53-75% higher per cell in the females versus males in adipocytes from human subcutaneous abdominal adipose tissue (P less than 0.01). Glucose 67-74 insulin Homo sapiens 48-55 6367483-6 1984 These results indicate that basal and maximum insulin-stimulated glucose transport is higher by adipocytes isolated from females and that this difference is independent of adipose cell size and species. Glucose 65-72 insulin Homo sapiens 46-53 6367676-5 1984 Changes in plasma levels of insulin early after glucose ingestion in these patients, however, were significantly less both before and after surgery than in normal controls, and were not concomitant with the initial increase in plasma GIP. Glucose 48-55 insulin Homo sapiens 28-35 6367676-6 1984 On the other hand, plasma levels of insulin greatly increased immediately after glucose ingestion in accordance with a rapid elevation of plasma GIP in 11 gastrectomized patients in whom the duodenum and the pancreas were preserved intact and who served as the control group. Glucose 80-87 insulin Homo sapiens 36-43 6697742-1 1984 The urine glucose concentration is commonly used to monitor indirectly the degree of hyperglycemia in critically ill patients and to adjust insulin dosage. Glucose 10-17 insulin Homo sapiens 140-147 6370767-4 1984 When insulin was infused together with adrenaline and propranolol in normal subjects in doses exceeding those given to the diabetics (plasma insulin rose threefold), the rise in glucose production was still threefold greater than in the diabetic patients (p less than 0.02). Glucose 178-185 insulin Homo sapiens 5-12 6370770-3 1984 Raising plasma glucose to 6.7 mmol/l during the same insulin infusion returned mean C-peptide (2688 +/- 581 pg/ml) and the acute glucagon response to arginine (447 +/- 146 pg X ml-1 X 10 min-1) close to basal levels. Glucose 15-22 insulin Homo sapiens 53-60 6373313-2 1984 There was a stimulatory effect on the insulin secretion in FNDW even if glucose alone was used, which became more pronounced if IBMX was added to the incubation medium. Glucose 72-79 insulin Homo sapiens 38-45 6376009-1 1984 The glucose clamp technique has been used to evaluate the metabolic activity of NPH biosynthetic insulin in diabetic subjects free from anti-insulin antibodies. Glucose 4-11 insulin Homo sapiens 97-104 6090253-0 1984 [Hydrogen peroxide, the 2d messenger for insulin action on the metabolism of glucose and fat bodies in adipose tissue. Glucose 77-84 insulin Homo sapiens 41-48 6143716-3 1984 Starvation for 48 h blocked both the glucose-induced stimulation and inhibition of insulin and somatostatin and the glucagon secretion. Glucose 37-44 insulin Homo sapiens 83-90 6370817-1 1984 Exaggerated insulin response to oral glucose was demonstrated in peripheral blood of patients with chronic hepatic diseases. Glucose 37-44 insulin Homo sapiens 12-19 6370817-6 1984 Insulin response to oral glucose was significantly greater in CAH patients than in controls, whereas C-Peptide levels and areas were quite similar in the two groups. Glucose 25-32 insulin Homo sapiens 0-7 6384143-0 1984 Inhibition by calcium antagonist of coupling of insulin binding and insulin action on glucose transport in isolated fat cells. Glucose 86-93 insulin Homo sapiens 48-75 6363441-4 1984 In contrast, insulin-mediated glucose disposal at all insulin increments was much lower in the obese group (0.33 +/- 0.03, 0.56 +/- 0.04, and 1.39 +/- 0.04 mg/kg X min) than in the lean group (0.78 +/- 0.06, 1.67 +/- 0.12, and 4.96 +/- 0.26; P less than 0.001). Glucose 30-37 insulin Homo sapiens 13-20 6363441-4 1984 In contrast, insulin-mediated glucose disposal at all insulin increments was much lower in the obese group (0.33 +/- 0.03, 0.56 +/- 0.04, and 1.39 +/- 0.04 mg/kg X min) than in the lean group (0.78 +/- 0.06, 1.67 +/- 0.12, and 4.96 +/- 0.26; P less than 0.001). Glucose 30-37 insulin Homo sapiens 54-61 6368584-1 1984 After intravenous glucose/insulin infusion there is an increase in oxygen consumption and energy expenditure that has been referred to as thermogenesis. Glucose 18-25 insulin Homo sapiens 26-33 6699133-1 1984 In an attempt to elucidate the cellular mechanisms of the insulin resistance associated with aging, insulin-mediated glucose transport was studied in isolated adipocytes obtained from 14 elderly subjects (mean age +/- SE, 69 +/- 2 yr) and 11 nonelderly (40 +/- 4 yr) subjects using the nonmetabolized glucose analogue 3-O-methylglucose. Glucose 117-124 insulin Homo sapiens 100-107 6699133-2 1984 In elderly subjects with normal oral glucose tolerance tests, maximal insulin-stimulated glucose transport was reduced compared to nonelderly control levels [1.26 +/- 0.17 (+/- SE) vs. 1.96 +/- 0.26 pmol/2 X 10(5) cells X 15 sec; P less than 0.025). Glucose 37-44 insulin Homo sapiens 70-77 6699133-2 1984 In elderly subjects with normal oral glucose tolerance tests, maximal insulin-stimulated glucose transport was reduced compared to nonelderly control levels [1.26 +/- 0.17 (+/- SE) vs. 1.96 +/- 0.26 pmol/2 X 10(5) cells X 15 sec; P less than 0.025). Glucose 89-96 insulin Homo sapiens 70-77 6699133-4 1984 The elderly group with the greatest decrease in in vitro glucose transport also had the greatest decrease in in vivo insulin-stimulated glucose disposal, whereas the elderly subjects with the mildest in vitro defect also had the smallest reduction in in vivo glucose disposal. Glucose 57-64 insulin Homo sapiens 117-124 6699133-4 1984 The elderly group with the greatest decrease in in vitro glucose transport also had the greatest decrease in in vivo insulin-stimulated glucose disposal, whereas the elderly subjects with the mildest in vitro defect also had the smallest reduction in in vivo glucose disposal. Glucose 136-143 insulin Homo sapiens 117-124 6374040-5 1984 The results showed that the glucose infusion rate, an estimate of in vivo insulin sensitivity, ws significantly diminished in ALS patients compared to both normal and disease controls. Glucose 28-35 insulin Homo sapiens 74-81 6699133-4 1984 The elderly group with the greatest decrease in in vitro glucose transport also had the greatest decrease in in vivo insulin-stimulated glucose disposal, whereas the elderly subjects with the mildest in vitro defect also had the smallest reduction in in vivo glucose disposal. Glucose 136-143 insulin Homo sapiens 117-124 6374040-6 1984 These results demonstrate that the insulin resistance in this disorder cannot be explained by a decrease in glucose-receptor space and suggest a primary carbohydrate aberration in the disease process itself. Glucose 108-115 insulin Homo sapiens 35-42 6371371-5 1984 Under basal conditions the acute increase in plasma glucose and insulin after glucose loading was accompanied by a significant decrease (P less than 0.01) in plasma cortisol and aldosterone and by a significant increase in plasma renin activity (P less than 0.01); plasma potassium was decreased slightly but not significantly. Glucose 78-85 insulin Homo sapiens 64-71 6374968-0 1984 A study of serum free C-peptide responses to oral glucose load in diabetic patients: with special reference to types of diabetes and methods of treatment. Glucose 50-57 insulin Homo sapiens 22-31 6372074-2 1984 After a glucose load patients without duodenal passage had significantly higher glucose and significantly smaller insulin levels than patients with duodenal passage. Glucose 8-15 insulin Homo sapiens 114-121 6369531-5 1984 However, fasting plasma glucose concentration fell and mean (+/- SEM) incremental insulin response to oral glucose increased significantly (p less than 0.05) with drug therapy (51.1 +/- 14.6 microU/ml vs 17.1 +/- 1.5 microU/ml). Glucose 107-114 insulin Homo sapiens 82-89 6365504-0 1984 [Insulin and C-peptide in chronic liver diseases during oral glucose tolerance testing]. Glucose 61-68 insulin Homo sapiens 1-8 6698968-3 1984 Following the cessation of cell division and subsequent spontaneous differentiation, the resulting myocytes develop a 5-fold increase in specific 125I-insulin binding and demonstrate physiologic insulin-stimulated glucose and amino acid uptake (100% increase above baseline) with half-maximum stimulation at 1-3 nM in agreement with the known in vivo and in vitro insulin sensitivity of muscle tissue. Glucose 214-221 insulin Homo sapiens 195-202 6698968-3 1984 Following the cessation of cell division and subsequent spontaneous differentiation, the resulting myocytes develop a 5-fold increase in specific 125I-insulin binding and demonstrate physiologic insulin-stimulated glucose and amino acid uptake (100% increase above baseline) with half-maximum stimulation at 1-3 nM in agreement with the known in vivo and in vitro insulin sensitivity of muscle tissue. Glucose 214-221 insulin Homo sapiens 195-202 6698968-4 1984 Insulin stimulation of 2-deoxyglucose uptake is detectable within 3 min, becomes maximal within 15 min, and is mediated by a rapid increase of plasma membrane transport units, as determined by D-glucose-inhibitable cytochalasin B binding, resulting in a 2-fold increase in the Vmax for 2-deoxyglucose transport with no change in Km. Glucose 193-202 insulin Homo sapiens 0-7 6365504-4 1984 The C-peptide/insulin ratio, a measure of hepatic insulin degradation, was significantly decreased after glucose uptake. Glucose 105-112 insulin Homo sapiens 4-13 6365504-4 1984 The C-peptide/insulin ratio, a measure of hepatic insulin degradation, was significantly decreased after glucose uptake. Glucose 105-112 insulin Homo sapiens 14-21 6363863-1 1984 Glucose in concentrations of 20 mg% (or greater) significantly inhibited 14C-labelled ascorbic acid (1.25 mg%) uptake in endothelial cells in the presence of insulin (1600 microU/ml). Glucose 0-7 insulin Homo sapiens 158-165 6368388-8 1984 The amount of glucose infused to maintain hyperglycaemia too serves as a measure of tissue sensitivity to endogenous insulin. Glucose 14-21 insulin Homo sapiens 117-124 6422547-3 1984 Larger doses of insulin lead to only slightly better control of mean blood glucose level and to a clearly less marked increase in triglycerides (TG) in a series of patients otherwise treated identically. Glucose 75-82 insulin Homo sapiens 16-23 6422547-6 1984 Peripheral insulin resistance is presumed to be the pathogenetic factor in this hypertriglyceridaemia, mia, which can be avoided by higher doses of insulin or decreased glucose load. Glucose 169-176 insulin Homo sapiens 11-18 6695271-0 1984 C-peptide response to a glucose load in young blacks and Indians with insulin-dependent diabetes mellitus. Glucose 24-31 insulin Homo sapiens 0-9 6364842-1 1984 We examined the ability of physiological hyperinsulinemia to enhance potassium and glucose uptake by splanchnic and peripheral tissues in 12 chronically uremic subjects by using the euglycemic insulin clamp technique in combination with hepatic and femoral venous catheterization. Glucose 83-90 insulin Homo sapiens 46-53 6364842-7 1984 In contrast, insulin-mediated glucose uptake is markedly impaired. Glucose 30-37 insulin Homo sapiens 13-20 6367619-4 1984 A highly significant decrease in the whole body glucose disposal rate was seen during the 120-minute insulin infusion in the patients with myotonic dystrophy compared with normal subjects at all three insulin dosages (20 mU/m2/min: 2.18 +/- 0.29 [standard error] versus 5.49 +/- 1.72 mg/kg/min, p less than 0.0001; 80 mU/m2/min: 4.16 +/- 0.34 versus 8.49 +/- 0.45 mg/kg/min, p less than 0.0001; 200 mU/m2/min: 5.22 +/- 0.53 versus 10.06 +/- 0.50 mg/kg/min, p less than 0.0001). Glucose 48-55 insulin Homo sapiens 101-108 6367619-4 1984 A highly significant decrease in the whole body glucose disposal rate was seen during the 120-minute insulin infusion in the patients with myotonic dystrophy compared with normal subjects at all three insulin dosages (20 mU/m2/min: 2.18 +/- 0.29 [standard error] versus 5.49 +/- 1.72 mg/kg/min, p less than 0.0001; 80 mU/m2/min: 4.16 +/- 0.34 versus 8.49 +/- 0.45 mg/kg/min, p less than 0.0001; 200 mU/m2/min: 5.22 +/- 0.53 versus 10.06 +/- 0.50 mg/kg/min, p less than 0.0001). Glucose 48-55 insulin Homo sapiens 201-208 6367619-6 1984 This adjusted glucose disposal rate was 15 to 25% lower (p less than 0.02) in the patients with myotonic dystrophy at insulin infusion rates of 20 and 80 mU. Glucose 14-21 insulin Homo sapiens 118-125 6367619-7 1984 During the 200 mU insulin infusions, the adjusted glucose disposal rate remained lower than that in normal subjects but was of borderline statistical significance. Glucose 50-57 insulin Homo sapiens 18-25 6363165-7 1984 Biologic potency, assessed by measuring glucose transport in rat adipocytes, showed that biosynthetic human proinsulin had 10% of the biologic activity of insulin, suggesting close coupling between binding to receptors and membrane generated cellular response. Glucose 40-47 insulin Homo sapiens 108-118 6363165-7 1984 Biologic potency, assessed by measuring glucose transport in rat adipocytes, showed that biosynthetic human proinsulin had 10% of the biologic activity of insulin, suggesting close coupling between binding to receptors and membrane generated cellular response. Glucose 40-47 insulin Homo sapiens 111-118 6363170-1 1984 The pretreatment of isolated islets of Langerhans with concanavalin A (Con A) completely blocks alloxan from suppressing the insulin release response to glucose. Glucose 153-160 insulin Homo sapiens 125-132 6363170-6 1984 The insulin biosynthetic effect of glucose appears to be mediated through a separate mechanism. Glucose 35-42 insulin Homo sapiens 4-11 6363173-0 1984 Use of glucose uptake and glucose clearance for the evaluation of insulin action in vivo. Glucose 7-14 insulin Homo sapiens 66-73 6363173-0 1984 Use of glucose uptake and glucose clearance for the evaluation of insulin action in vivo. Glucose 26-33 insulin Homo sapiens 66-73 6142057-3 1984 During somatostatin with insulin alone mean glucose production fell from 1.5 +/- 0.05 to 0.7 +/- 0.2 mg/kg per min and mean plasma glucose declined from 93 +/- 3 to 67 +/- 4 mg/dl over 1 h; glucose production then increased to base-line rates and plasma glucose plateaued at 64-67 mg/dl over 2 h. This plateau was associated with, and is best attributed to, an eightfold increase in mean plasma epinephrine. Glucose 44-51 insulin Homo sapiens 25-32 6142057-5 1984 These data provide further support for the concept that maintenance of the postabsorptive plasma glucose concentration is a function of insulin and glucagon, not of insulin alone, and that adrenergic mechanisms do not normally play a critical role. Glucose 97-104 insulin Homo sapiens 136-143 6363437-7 1984 The dose-response curve for insulin stimulation of glucose disposal in well controlled diabetic subjects was comparable to that in normal subjects, with half-maximally effective insulin levels of 84 microU/ml in the diabetic patients compared to 70 microU/ml in normal subjects and virtually identical maximal rates of glucose disposal (433 +/- 11 vs. 411 +/- 17 mg/M2 X min in controls). Glucose 51-58 insulin Homo sapiens 28-35 6363874-6 1984 At each increment of insulin infused, steady-state glucose infusion rates for porcine insulin were 1.12 +/- 0.22, 1.90 +/- 0.59, 4.28 +/- 0.61, and 9.37 +/- 0.66 mg/kg/min compared with 1.27 +/- 0.42, 2.38 +/- 0.20, 4.25 +/- 0.43, and 8.87 +/- 0.67 mg/kg/min for semisynthetic human insulin. Glucose 51-58 insulin Homo sapiens 86-93 6363437-7 1984 The dose-response curve for insulin stimulation of glucose disposal in well controlled diabetic subjects was comparable to that in normal subjects, with half-maximally effective insulin levels of 84 microU/ml in the diabetic patients compared to 70 microU/ml in normal subjects and virtually identical maximal rates of glucose disposal (433 +/- 11 vs. 411 +/- 17 mg/M2 X min in controls). Glucose 51-58 insulin Homo sapiens 178-185 6363437-7 1984 The dose-response curve for insulin stimulation of glucose disposal in well controlled diabetic subjects was comparable to that in normal subjects, with half-maximally effective insulin levels of 84 microU/ml in the diabetic patients compared to 70 microU/ml in normal subjects and virtually identical maximal rates of glucose disposal (433 +/- 11 vs. 411 +/- 17 mg/M2 X min in controls). Glucose 319-326 insulin Homo sapiens 28-35 6363438-0 1984 Influence of changes in insulin receptor binding during insulin infusions on the shape of the insulin dose-response curve for glucose disposal in man. Glucose 126-133 insulin Homo sapiens 24-31 6363438-0 1984 Influence of changes in insulin receptor binding during insulin infusions on the shape of the insulin dose-response curve for glucose disposal in man. Glucose 126-133 insulin Homo sapiens 56-63 6363438-0 1984 Influence of changes in insulin receptor binding during insulin infusions on the shape of the insulin dose-response curve for glucose disposal in man. Glucose 126-133 insulin Homo sapiens 56-63 6374254-9 1984 However, the concentration of insulin (22 microunits/ml) required for half-maximal stimulation of glucose metabolism was not altered by pretreatment with uremic serum. Glucose 98-105 insulin Homo sapiens 30-37 6363874-6 1984 At each increment of insulin infused, steady-state glucose infusion rates for porcine insulin were 1.12 +/- 0.22, 1.90 +/- 0.59, 4.28 +/- 0.61, and 9.37 +/- 0.66 mg/kg/min compared with 1.27 +/- 0.42, 2.38 +/- 0.20, 4.25 +/- 0.43, and 8.87 +/- 0.67 mg/kg/min for semisynthetic human insulin. Glucose 51-58 insulin Homo sapiens 86-93 6366723-9 1984 Indeed, plasma insulin levels after oral glucose in patients on CSIGH exceeded those observed in normal controls, suggesting that CSIGH had induced a degree of insulin resistance. Glucose 41-48 insulin Homo sapiens 15-22 6363874-10 1984 These data suggest that semisynthetic human insulin has equivalent biologic effects on overall glucose metabolism compared with porcine insulin in insulin-dependent diabetes. Glucose 95-102 insulin Homo sapiens 44-51 6363875-5 1984 The amount of glucose infused to maintain euglycemia and its ratio to steady-state insulin levels was significantly lower in the obese subjects, suggesting an impaired insulin action on glucose metabolism. Glucose 14-21 insulin Homo sapiens 83-90 6363875-8 1984 Our data suggest that insulin resistance in obesity reduces hormonal effects on glucose as well as on BCAA metabolism. Glucose 80-87 insulin Homo sapiens 22-29 6144197-5 1984 Plasma insulin concentrations in response to oral glucose tolerance test and arginine infusion were markedly low. Glucose 50-57 insulin Homo sapiens 7-14 6364435-11 1984 Insulin resistance assessed in four patients by measurement of glucose clearance during insulin and glucose infusion improved from a mean of 77 ml/min before operation to 228 ml/min after operation. Glucose 63-70 insulin Homo sapiens 0-7 6364435-11 1984 Insulin resistance assessed in four patients by measurement of glucose clearance during insulin and glucose infusion improved from a mean of 77 ml/min before operation to 228 ml/min after operation. Glucose 63-70 insulin Homo sapiens 88-95 6364435-11 1984 Insulin resistance assessed in four patients by measurement of glucose clearance during insulin and glucose infusion improved from a mean of 77 ml/min before operation to 228 ml/min after operation. Glucose 100-107 insulin Homo sapiens 0-7 6323814-0 1984 [Diagnosis and surgery of an insulinoma using a glucose-controlled insulin infusion system]. Glucose 48-55 insulin Homo sapiens 29-36 6141162-1 1984 Glucose exerts opposite effects upon glucagon and insulin release from the endocrine pancreas. Glucose 0-7 insulin Homo sapiens 50-57 6141162-7 1984 Glucose releases 30-fold more insulin from islets than from single B-cells, but this marked difference is not associated with differences in glucose handling. Glucose 0-7 insulin Homo sapiens 30-37 6141162-9 1984 It is concluded that the dependency of glucose-induced insulin release upon the functional coordination between islet cells is not mediated through changes in glucose metabolism. Glucose 39-46 insulin Homo sapiens 55-62 6323814-2 1984 Preoperatively, using the glucose controlled insulin infusion system (GCIIS) for glucose clamping at various blood glucose levels, autonomous insulin production was demonstrated and intravenous glucose needs for maintenance of normoglycaemia were evaluated. Glucose 26-33 insulin Homo sapiens 45-52 6323814-2 1984 Preoperatively, using the glucose controlled insulin infusion system (GCIIS) for glucose clamping at various blood glucose levels, autonomous insulin production was demonstrated and intravenous glucose needs for maintenance of normoglycaemia were evaluated. Glucose 26-33 insulin Homo sapiens 142-149 6397030-3 1984 The fasting and 2 hr postprandial (PP) glucose showed higher pairwise correlations in MZ (r = 0.78 and 0.56) than DZ (r = 0.08 and -0.05) pairs whereas fasting and PP insulin levels and the areas under the PP glucose and insulin curves were weakly and similarly correlated in MZ and DZ twins. Glucose 39-46 insulin Homo sapiens 167-174 6372345-0 1984 Effect of surgical trauma on plasma insulin and somatostatin in response to glucose. Glucose 76-83 insulin Homo sapiens 36-43 6372345-2 1984 In accordance with previous findings the increase of insulin in response to glucose was significantly (p less than 0.001) reduced 2 hours after laparotomy as compared to control subjects. Glucose 76-83 insulin Homo sapiens 53-60 6375226-4 1984 The insulin-treated group had lower, but not normal, plasma glucose and higher levels of glycerol than the women treated with diet only. Glucose 60-67 insulin Homo sapiens 4-11 6385632-4 1984 The high insulin group, compared with the low insulin group, had overall higher glucose, insulin and C-peptide levels, significantly higher increment 0-40 min of insulin but not C-peptide, and significantly lower maximal oxygen uptake. Glucose 80-87 insulin Homo sapiens 9-16 6382920-5 1984 On this basis, it was found that 67.7% of our patients showed some abnormality in the relationship between the blood levels of glucose and insulin. Glucose 127-134 insulin Homo sapiens 139-146 6388588-3 1984 When 14 men (9 normal weight and 5 obese) aged between 20 and 50 years consumed a 50 g glucose load together with 50 g ethanol over an hour, their early plasma insulin response was significantly higher and their later fall in plasma glucose significantly lower than after drinking the same amount of a starch solution (maize meal) and alcohol. Glucose 87-94 insulin Homo sapiens 160-167 6395671-6 1984 Sufficient circulating insulin is probably chronically available to the cells in this moderately impaired state, so that an acute decrease in delta IRI in response to glucose in an iv-administered GTT does not cause significant impairment in glucose clearance. Glucose 167-174 insulin Homo sapiens 23-30 6696066-5 1984 Similarly, plasma glucose and insulin determinations have shown that the secretion of insulin is increased during food ingestion but only with the MF situation. Glucose 18-25 insulin Homo sapiens 86-93 6380393-2 1984 The pharmacokinetic difference between continuous subcutaneous insulin infusion and conventional injection therapy is discussed and can explain the difference between the obtained levels of blood glucose control. Glucose 196-203 insulin Homo sapiens 63-70 6399195-5 1984 What are the causes (receptor or post receptor defect) and the tissues producing or utilizing glucose involved in insulin resistance? Glucose 94-101 insulin Homo sapiens 114-121 6383363-3 1984 The model considers physiologically relevant unit processes like endogenous glucose production, insulin-independent glucose uptake from its apparent distribution space, insulin-dependent glucose utilization, glucose-dependent insulin supply, and insulin catabolism. Glucose 116-123 insulin Homo sapiens 96-103 6383363-3 1984 The model considers physiologically relevant unit processes like endogenous glucose production, insulin-independent glucose uptake from its apparent distribution space, insulin-dependent glucose utilization, glucose-dependent insulin supply, and insulin catabolism. Glucose 116-123 insulin Homo sapiens 96-103 6383363-3 1984 The model considers physiologically relevant unit processes like endogenous glucose production, insulin-independent glucose uptake from its apparent distribution space, insulin-dependent glucose utilization, glucose-dependent insulin supply, and insulin catabolism. Glucose 116-123 insulin Homo sapiens 96-103 6395913-2 1984 Large dose (100 U) as well as low dose (1 U) of CT inhibits glucose-induced insulin responses, reduces the suppressive effect of glucose on glucagon secretion and impairs glucose tolerance. Glucose 60-67 insulin Homo sapiens 76-83 6360768-5 1984 Insulin clearance was (mean +/- SEM) 277 +/- 41 ml/min/m2 between 0700 and 0800 h compared with 256 +/- 41 ml/min/m2 between 0200 and 0300 h (P less than 0.05), while glucose infusion rates were the same [3.86 +/- 0.52 mg/kg/min from 0730 to 0800 h versus 3.99 +/- 0.51 mg/kg/min from 0230 to 0300 h (P = NS)]. Glucose 167-174 insulin Homo sapiens 0-7 6526265-5 1984 All patients demonstrated an increase in sensitivity to insulin as indicated by a decrease in the fasting blood glucose concentration and a decrease in insulin requirement during the glucose challenge (P less than 0.02). Glucose 112-119 insulin Homo sapiens 56-63 6526265-5 1984 All patients demonstrated an increase in sensitivity to insulin as indicated by a decrease in the fasting blood glucose concentration and a decrease in insulin requirement during the glucose challenge (P less than 0.02). Glucose 183-190 insulin Homo sapiens 56-63 6526265-5 1984 All patients demonstrated an increase in sensitivity to insulin as indicated by a decrease in the fasting blood glucose concentration and a decrease in insulin requirement during the glucose challenge (P less than 0.02). Glucose 183-190 insulin Homo sapiens 152-159 6141989-0 1984 Insulin sensitivity in pancreatitis, liver diseases, steroid treatment and hyperthyroidism assessed by glucose, insulin and somatostatin infusion. Glucose 103-110 insulin Homo sapiens 0-7 6141989-1 1984 In order to assess insulin sensitivity for glucose utilization in the other type of diabetes, insulin sensitivity tests were performed in subjects with pancreatitis, liver disease, steroid treatment and hyperthyroidism. Glucose 43-50 insulin Homo sapiens 19-26 6368584-4 1984 After propranolol infusion, insulin-mediated glucose uptake was significantly reduced, 6.89 +/- 0.41 (P less than 0.02). Glucose 45-52 insulin Homo sapiens 28-35 6368584-7 1984 The increments in energy expenditure (0.10 +/- 0.01 vs. 0.03 +/- 0.01 kcal/min) and glucose/insulin-induced thermogenesis (4.9 +/- 0.5 vs. 1.5 +/- 0.5%) were reduced by 70% during the propranolol/insulin clamp study. Glucose 84-91 insulin Homo sapiens 92-99 6368584-9 1984 These results indicate that activation of the beta adrenergic receptor plays an important role in the insulin/glucose-mediated increase in energy expenditure and thermogenesis. Glucose 110-117 insulin Homo sapiens 102-109 6368585-3 1984 The results of these euglycemic studies indicated that insulin-stimulated peripheral glucose disposal was decreased in the Type II diabetics due to a combined receptor (rightward shift in the dose-response curve) and postreceptor defect in insulin action (decreased maximal response), whereas the decrease in insulin-mediated suppression of hepatic glucose output (HGO) was consistent with a defect in insulin binding (rightward shift in dose-response curve). Glucose 85-92 insulin Homo sapiens 55-62 6368585-3 1984 The results of these euglycemic studies indicated that insulin-stimulated peripheral glucose disposal was decreased in the Type II diabetics due to a combined receptor (rightward shift in the dose-response curve) and postreceptor defect in insulin action (decreased maximal response), whereas the decrease in insulin-mediated suppression of hepatic glucose output (HGO) was consistent with a defect in insulin binding (rightward shift in dose-response curve). Glucose 85-92 insulin Homo sapiens 240-247 6368585-3 1984 The results of these euglycemic studies indicated that insulin-stimulated peripheral glucose disposal was decreased in the Type II diabetics due to a combined receptor (rightward shift in the dose-response curve) and postreceptor defect in insulin action (decreased maximal response), whereas the decrease in insulin-mediated suppression of hepatic glucose output (HGO) was consistent with a defect in insulin binding (rightward shift in dose-response curve). Glucose 85-92 insulin Homo sapiens 240-247 6368585-3 1984 The results of these euglycemic studies indicated that insulin-stimulated peripheral glucose disposal was decreased in the Type II diabetics due to a combined receptor (rightward shift in the dose-response curve) and postreceptor defect in insulin action (decreased maximal response), whereas the decrease in insulin-mediated suppression of hepatic glucose output (HGO) was consistent with a defect in insulin binding (rightward shift in dose-response curve). Glucose 85-92 insulin Homo sapiens 240-247 6368585-5 1984 In the presence of their basal level of hyperglycemia, the noninsulin-dependent diabetes mellitus (NIDDM) subjects exhibited rates of overall glucose disposal that were similar to those observed in control subjects studied at euglycemia at similar steady state insulin concentrations. Glucose 142-149 insulin Homo sapiens 62-69 6368585-6 1984 This suggests that in Type II diabetics, the mass action effect of glucose partially compensates for the marked decrease in insulin-stimulated glucose uptake observed under euglycemic conditions. Glucose 67-74 insulin Homo sapiens 124-131 6368585-6 1984 This suggests that in Type II diabetics, the mass action effect of glucose partially compensates for the marked decrease in insulin-stimulated glucose uptake observed under euglycemic conditions. Glucose 143-150 insulin Homo sapiens 124-131 6368585-7 1984 However, even in the presence of hyperglycemia, insulin levels below 100 microU/ml had little effect and maximally effective insulin levels increased peripheral glucose disposal only 2.8-fold (142 +/- 7-413 +/- 47 mg/M2 per min) above basal in the Type II diabetics, compared with a sixfold increase (75 +/- 4-419 +/- 34 mg/M2 per min) in the control subjects studied at euglycemia. Glucose 161-168 insulin Homo sapiens 125-132 6368586-13 1984 Furthermore, in adipocytes of subjects of normal weight, oral glucose rapidly stimulates the sensitivity of the antilipolytic effect of insulin, apparently because of changes at postreceptor sites. Glucose 62-69 insulin Homo sapiens 136-143 6368586-14 1984 This short-term regulation of insulin action following the ingestion of glucose does not seem to be present in obesity. Glucose 72-79 insulin Homo sapiens 30-37 6368588-0 1984 Relationship between obesity and maximal insulin-stimulated glucose uptake in vivo and in vitro in Pima Indians. Glucose 60-67 insulin Homo sapiens 41-48 6368588-2 1984 We have studied the relationship between the degree of obesity (as estimated by underwater weighing) and the maximal insulin-stimulated glucose disposal rate (M) in vivo in 52 glucose-tolerant Pima Indian males. Glucose 136-143 insulin Homo sapiens 117-124 6368588-4 1984 The maximal insulin-stimulated glucose transport rate (MTR) was also measured in isolated abdominal adipocytes from the same subjects to determine whether differences in M could be explained by differences in glucose transport. Glucose 31-38 insulin Homo sapiens 12-19 6368588-11 1984 We concluded that differences in M in these glucose-tolerant subjects must be explained by factor(s) other than maximal oxygen uptake, age, maximal insulin-stimulated glucose transport in vitro, or degree of adiposity per se. Glucose 167-174 insulin Homo sapiens 148-155 6477542-5 1984 Perfect glycaemic control was established by infusing insulin either intravenously or subcutaneously in response to measured glucose concentrations on a moment-to-moment basis in diabetics for a period of several days. Glucose 125-132 insulin Homo sapiens 54-61 6362704-9 1984 These results suggest that improved glucose tolerance by clofibrate might be derived from the enhanced tissue sensitivity to insulin, probably through an enhanced affinity of insulin receptors. Glucose 36-43 insulin Homo sapiens 125-132 6362704-9 1984 These results suggest that improved glucose tolerance by clofibrate might be derived from the enhanced tissue sensitivity to insulin, probably through an enhanced affinity of insulin receptors. Glucose 36-43 insulin Homo sapiens 175-182 6395991-0 1984 Plasma insulin and glucose levels in diabetic patients undergoing continuous ambulatory peritoneal dialysis using insulin only in the dialysate. Glucose 19-26 insulin Homo sapiens 114-121 6439409-8 1984 While glyburide produces an insulin release response to glucose that parallels a normal physiological response, it appears to also decrease resistance to insulin and sensitize the receptors while utilizing the patient"s available endogenous insulin. Glucose 56-63 insulin Homo sapiens 28-35 6373160-3 1984 After 3 months of gliclazide therapy (240 mg/day) in addition to a low carbohydrate diet, the intravenous glucose tolerance test showed a significant reduction in blood sugar levels and in the partial and total areas under the blood sugar curve, as well as an improvement in early insulin secretion, characterized by a significant increase in plasma C-peptide at 4, 10 and 20 minutes. Glucose 106-113 insulin Homo sapiens 281-288 6373160-3 1984 After 3 months of gliclazide therapy (240 mg/day) in addition to a low carbohydrate diet, the intravenous glucose tolerance test showed a significant reduction in blood sugar levels and in the partial and total areas under the blood sugar curve, as well as an improvement in early insulin secretion, characterized by a significant increase in plasma C-peptide at 4, 10 and 20 minutes. Glucose 106-113 insulin Homo sapiens 350-359 6368151-1 1984 The dawn phenomenon, a tendency for glucose to rise between 0500 and 0800 h in subjects with diabetes, is also reflected as an increase in insulin required to maintain normoglycemia during closed-loop insulin infusion. Glucose 36-43 insulin Homo sapiens 139-146 6368151-1 1984 The dawn phenomenon, a tendency for glucose to rise between 0500 and 0800 h in subjects with diabetes, is also reflected as an increase in insulin required to maintain normoglycemia during closed-loop insulin infusion. Glucose 36-43 insulin Homo sapiens 201-208 6368151-7 1984 The mechanism underlying this increased insulin need may be similar in diabetes and nondiabetes, with the ensuing rise in glucose being dependent on the availability of compensatory insulin. Glucose 122-129 insulin Homo sapiens 40-47 6368151-7 1984 The mechanism underlying this increased insulin need may be similar in diabetes and nondiabetes, with the ensuing rise in glucose being dependent on the availability of compensatory insulin. Glucose 122-129 insulin Homo sapiens 182-189 6368154-1 1984 The insulin response to a 100-g oral glucose load was studied in 40 obese (percent desirable weight greater than or equal to 120%) and 40 nonobese (less than 120%) age- and sex-matched Indian patients with non-insulin-dependent diabetes in the young. Glucose 37-44 insulin Homo sapiens 4-11 6368299-1 1984 In a 5-12 year follow-up study of 288 subjects with impaired glucose tolerance after a 100-g glucose load, 48 worsened to overt Type 2 (non-insulin-dependent) diabetes with the elevation of fasting blood glucose. Glucose 93-100 insulin Homo sapiens 140-147 6368299-3 1984 In addition, subjects with a lower insulin response to glucose showed a higher incidence of worsening to the disease, irrespective of blood glucose levels. Glucose 55-62 insulin Homo sapiens 35-42 6378609-0 1984 [Changes in blood insulin levels in obese children during fasting and after oral administration of glucose]. Glucose 99-106 insulin Homo sapiens 18-25 6383778-4 1984 Similar results of insulin secretion were to be seen as well in a group of diabetics, selected at random, when glucose-, tolbutamide- and glucagon stimulation of insulin secretion were evaluated as in patients first examined after longer diabetes duration (about 6,5 years, n = 51). Glucose 111-118 insulin Homo sapiens 162-169 6141989-2 1984 Insulin sensitivity for glucose utilization decreased in subjects with liver disease, steroid treatment and hyperthyroidism irrespective of the presence or absence of glucose intolerance. Glucose 24-31 insulin Homo sapiens 0-7 6386646-0 1984 Effect of pharmacological doses of oxytocin on insulin response to glucose in normal man. Glucose 67-74 insulin Homo sapiens 47-54 6378816-4 1984 Relative body weight, body fat, fasting and glucose-stimulated insulin levels, triglycerides, total cholesterol, but not high-density lipoprotein cholesterol, significantly decreased after caloric restriction. Glucose 44-51 insulin Homo sapiens 63-70 6392122-8 1984 Basal and maximum insulin-stimulated glucose transport were similar after a four-day fast. Glucose 37-44 insulin Homo sapiens 18-25 6365941-3 1984 Insulin usage was more frequent in patients with a longer duration of diabetes, younger age at diagnosis and poor recent glucose control. Glucose 121-128 insulin Homo sapiens 0-7 6374252-1 1984 The insulin and C-peptide response to glucose (50 g), given intraperitoneally or enterally, and the elimination rate of these compounds has been studied in five nondiabetic patients on continuous ambulatory peritoneal dialysis (CAPD). Glucose 38-45 insulin Homo sapiens 4-11 6374252-1 1984 The insulin and C-peptide response to glucose (50 g), given intraperitoneally or enterally, and the elimination rate of these compounds has been studied in five nondiabetic patients on continuous ambulatory peritoneal dialysis (CAPD). Glucose 38-45 insulin Homo sapiens 16-25 6382374-2 1984 For the first 30 min following insulin administration, the rate of change in glucose levels was significantly less among the patients with major depressive disorder than among either the patients with dysthymic disorder or the normal control subjects. Glucose 77-84 insulin Homo sapiens 31-38 6382374-4 1984 Therefore, the insulin resistance in terms of glucose levels that is observed in patients with major depressive disorder is not generalized to other substances affected by insulin. Glucose 46-53 insulin Homo sapiens 15-22 6397777-1 1984 The effects of lithium, dexamethasone, nortriptyline and their combinations on insulin sensitivity, expressed as a drop of plasma glucose in response to insulin challenge, were investigated in healthy volunteers. Glucose 130-137 insulin Homo sapiens 79-86 6397777-1 1984 The effects of lithium, dexamethasone, nortriptyline and their combinations on insulin sensitivity, expressed as a drop of plasma glucose in response to insulin challenge, were investigated in healthy volunteers. Glucose 130-137 insulin Homo sapiens 153-160 6424179-0 1984 Is phospholipase A2 a "glucose sensor" responsible for the phasic pattern of insulin release? Glucose 23-30 insulin Homo sapiens 77-84 6424179-1 1984 The mechanisms involved in the characteristic, normal biphasic pattern of glucose-induced insulin release (which is grossly altered in type II diabetics) have not been definitely elucidated. Glucose 74-81 insulin Homo sapiens 90-97 6424179-4 1984 Pancreatic islets contain a glucose-sensitive phospholipase A2, and glucose has been shown to increase the accumulation of islet lipoxygenase-derived products which appear to be "third messengers" mediating insulin release. Glucose 28-35 insulin Homo sapiens 207-214 6424179-4 1984 Pancreatic islets contain a glucose-sensitive phospholipase A2, and glucose has been shown to increase the accumulation of islet lipoxygenase-derived products which appear to be "third messengers" mediating insulin release. Glucose 68-75 insulin Homo sapiens 207-214 6424179-5 1984 Blockade either of islet phospholipase(s) or of islet lipoxygenase totally abrogates glucose-induced insulin release. Glucose 85-92 insulin Homo sapiens 101-108 6424179-7 1984 Labile oxygenated metabolites (lipid peroxides and epoxides) transduce the glucose signal into insulin release. Glucose 75-82 insulin Homo sapiens 95-102 6424179-8 1984 The available data (albeit incomplete) are compatible with the formulation that the biphasic pattern of glucose-induced insulin release could be explained by dynamic changes in the availability of arachidonic acid and its consequent oxygenation. Glucose 104-111 insulin Homo sapiens 120-127 6358757-6 1983 Oral glucose loading increased the relative insulin-releasing activity in the HPLC subfractions from obese children. Glucose 5-12 insulin Homo sapiens 44-51 6416540-1 1983 Insulin responsiveness was studied with the euglycaemic glucose clamp technique in seven patients with type I diabetes and in six control subjects matched for age and weight. Glucose 56-63 insulin Homo sapiens 0-7 6416540-2 1983 The glucose disposal rate was significantly reduced in the diabetic subjects when they were receiving conventional insulin treatment compared with the control group, showing insulin resistance in the diabetics. Glucose 4-11 insulin Homo sapiens 115-122 6416540-2 1983 The glucose disposal rate was significantly reduced in the diabetic subjects when they were receiving conventional insulin treatment compared with the control group, showing insulin resistance in the diabetics. Glucose 4-11 insulin Homo sapiens 174-181 6416540-6 1983 Dose response studies showed an increased glucose disposal rate at all plasma insulin concentrations, including the maximum insulin concentration, indicating a predominant effect of the continuous infusion regimen at the postreceptor level. Glucose 42-49 insulin Homo sapiens 78-85 6419621-3 1983 Infusion of lysine acetylsalicylate to block the synthesis of endogenous PGE increased by twofold total insulin response to glucose and also converted insulin release to a multiphasic pattern. Glucose 124-131 insulin Homo sapiens 104-111 6419621-6 1983 On the basis of these results, it is hypothesized that endogenous PGE released in response to glucose stimulation exert an inhibiting effect on insulin release that becomes biphasic in appearance. Glucose 94-101 insulin Homo sapiens 144-151 6364983-3 1983 [14C]Glucose incorporation into glycogen was maximally stimulated approximately 80% by insulin, whereas maximum stimulation by insulin-ricin B hybrid was greater than 100%. Glucose 5-12 insulin Homo sapiens 87-94 6363176-4 1983 Even at 150 min after glucose ingestion, splanchnic output and arterial concentrations of glucose, lactate, insulin and C-peptide were still above their respective basal values while those of non-esterified fatty acids and glucagon were reduced. Glucose 22-29 insulin Homo sapiens 108-115 6363176-4 1983 Even at 150 min after glucose ingestion, splanchnic output and arterial concentrations of glucose, lactate, insulin and C-peptide were still above their respective basal values while those of non-esterified fatty acids and glucagon were reduced. Glucose 22-29 insulin Homo sapiens 120-129 6368305-5 1983 It was suggested that administration of BCAA with glucose caused hypoglycemia in cirrhotics with encephalopathy, possibly by synergistic action of BCAA and glucose on serum insulin level. Glucose 50-57 insulin Homo sapiens 173-180 6368305-5 1983 It was suggested that administration of BCAA with glucose caused hypoglycemia in cirrhotics with encephalopathy, possibly by synergistic action of BCAA and glucose on serum insulin level. Glucose 156-163 insulin Homo sapiens 173-180 6363239-2 1983 Dissociation between C-peptide and insulin response to glucose was observed in several diabetics. Glucose 55-62 insulin Homo sapiens 35-42 6363239-5 1983 The chlorpropamide-responsive patients presented higher insulin levels after the glucose challenge and a lower hepatic insulin extraction than the non-responsive ones. Glucose 81-88 insulin Homo sapiens 56-63 6355137-2 1983 When the plasma glucose concentration was acutely raised and maintained at 125 mg/dl above the basal level after treatment with aspirin (3 g daily for 3 days), acute (0-10 min) and sustained (20-120 min) insulin release were 70% and 45% greater than before treatment. Glucose 16-23 insulin Homo sapiens 204-211 6355137-4 1983 Consequently, the ratio of the glucose infusion rate to the plasma insulin level, an index of tissue sensitivity to endogenous insulin, decreased by 30%, indicative of impaired insulin action. Glucose 31-38 insulin Homo sapiens 127-134 6355139-2 1983 Fasting and glucose-stimulated plasma C-peptide values in diet-controlled diabetics were similar to those in normal subjects. Glucose 12-19 insulin Homo sapiens 38-47 6355139-8 1983 However, their C-peptide responses to glucose were significantly blunted. Glucose 38-45 insulin Homo sapiens 15-24 6355141-4 1983 Insulin release induced by 20 mmol/liter D-glucose during 30 min of stimulation decreased from 900 ng insulin (median; range, 814-1138) from pancreata of mice injected with control Ig to 511 ng (range, 130-786) from pancreata of mice injected with diabetic Ig (P less than 0.003). Glucose 41-50 insulin Homo sapiens 0-7 6355141-4 1983 Insulin release induced by 20 mmol/liter D-glucose during 30 min of stimulation decreased from 900 ng insulin (median; range, 814-1138) from pancreata of mice injected with control Ig to 511 ng (range, 130-786) from pancreata of mice injected with diabetic Ig (P less than 0.003). Glucose 41-50 insulin Homo sapiens 102-109 6355141-5 1983 Both the initial peak and the sustained second phase of glucose-stimulated insulin release were depressed in 4 of the 5 pancreata from mice injected with diabetic Ig. Glucose 56-63 insulin Homo sapiens 75-82 6358258-2 1983 It has been previously reported that maximum insulin-stimulated glucose transport and utilization were both decreased, while basal lipolysis was increased in adipocytes from obese subjects with noninsulin-dependent diabetes mellitus (NIDDM). Glucose 64-71 insulin Homo sapiens 45-52 6358258-4 1983 The results demonstrate that maximum insulin-stimulated glucose transport (P less than 0.02) and glucose incorporation into triglyceride (P less than 0.01) and CO2 (P less than 0.05) (at 5.5 mM glucose) increased and basal lipolysis decreased (P less than 0.05) after 4 wk of insulin treatment. Glucose 56-63 insulin Homo sapiens 37-44 6358258-4 1983 The results demonstrate that maximum insulin-stimulated glucose transport (P less than 0.02) and glucose incorporation into triglyceride (P less than 0.01) and CO2 (P less than 0.05) (at 5.5 mM glucose) increased and basal lipolysis decreased (P less than 0.05) after 4 wk of insulin treatment. Glucose 97-104 insulin Homo sapiens 37-44 6358258-4 1983 The results demonstrate that maximum insulin-stimulated glucose transport (P less than 0.02) and glucose incorporation into triglyceride (P less than 0.01) and CO2 (P less than 0.05) (at 5.5 mM glucose) increased and basal lipolysis decreased (P less than 0.05) after 4 wk of insulin treatment. Glucose 97-104 insulin Homo sapiens 276-283 6358258-4 1983 The results demonstrate that maximum insulin-stimulated glucose transport (P less than 0.02) and glucose incorporation into triglyceride (P less than 0.01) and CO2 (P less than 0.05) (at 5.5 mM glucose) increased and basal lipolysis decreased (P less than 0.05) after 4 wk of insulin treatment. Glucose 97-104 insulin Homo sapiens 37-44 6358258-4 1983 The results demonstrate that maximum insulin-stimulated glucose transport (P less than 0.02) and glucose incorporation into triglyceride (P less than 0.01) and CO2 (P less than 0.05) (at 5.5 mM glucose) increased and basal lipolysis decreased (P less than 0.05) after 4 wk of insulin treatment. Glucose 97-104 insulin Homo sapiens 276-283 6358258-7 1983 Finally, the improvement in maximal insulin-stimulated glucose transport correlated with the fall in fasting hyperglycemia (r = 0.77, P less than 0.01). Glucose 55-62 insulin Homo sapiens 36-43 6358781-3 1983 Although the fasting concentrations of insulin, glucagon, and GH were significantly higher in the heroin addicts, they had markedly reduced plasma insulin responses to intravenous glucose (acute insulin response, calculated as the mean change in insulin levels over 3 to 10 minutes: 10 +/- 5 microU/mL in the addicts v 44 +/- 9 microU/mL in the controls, P less than 0.001) and glucose utilization rates in the diabetic range (KG: 0.96 +/- 0.09%/min in the addicts v 1.65 +/- 0.10%/min in the controls, P less than 0.01). Glucose 180-187 insulin Homo sapiens 39-46 6358781-3 1983 Although the fasting concentrations of insulin, glucagon, and GH were significantly higher in the heroin addicts, they had markedly reduced plasma insulin responses to intravenous glucose (acute insulin response, calculated as the mean change in insulin levels over 3 to 10 minutes: 10 +/- 5 microU/mL in the addicts v 44 +/- 9 microU/mL in the controls, P less than 0.001) and glucose utilization rates in the diabetic range (KG: 0.96 +/- 0.09%/min in the addicts v 1.65 +/- 0.10%/min in the controls, P less than 0.01). Glucose 180-187 insulin Homo sapiens 147-154 6358781-3 1983 Although the fasting concentrations of insulin, glucagon, and GH were significantly higher in the heroin addicts, they had markedly reduced plasma insulin responses to intravenous glucose (acute insulin response, calculated as the mean change in insulin levels over 3 to 10 minutes: 10 +/- 5 microU/mL in the addicts v 44 +/- 9 microU/mL in the controls, P less than 0.001) and glucose utilization rates in the diabetic range (KG: 0.96 +/- 0.09%/min in the addicts v 1.65 +/- 0.10%/min in the controls, P less than 0.01). Glucose 180-187 insulin Homo sapiens 147-154 6358781-3 1983 Although the fasting concentrations of insulin, glucagon, and GH were significantly higher in the heroin addicts, they had markedly reduced plasma insulin responses to intravenous glucose (acute insulin response, calculated as the mean change in insulin levels over 3 to 10 minutes: 10 +/- 5 microU/mL in the addicts v 44 +/- 9 microU/mL in the controls, P less than 0.001) and glucose utilization rates in the diabetic range (KG: 0.96 +/- 0.09%/min in the addicts v 1.65 +/- 0.10%/min in the controls, P less than 0.01). Glucose 180-187 insulin Homo sapiens 147-154 6588267-7 1983 An increase in the affinity of insulin for receptors on mononuclear cells was associated with a 20% decrease in fasting plasma insulin levels (24 +/- 7 to 19 +/- 2 microU/ml, N = 8; P less than 0.05) and a 42% improvement in glucose disappearance rates (1.9 +/- 1.0 to 2.6 +/- 1.2% per min, N = 6) in E. There were no changes in the body weights or diets of the patients. Glucose 225-232 insulin Homo sapiens 31-38 6424111-5 1983 Additional studies showed that [SerB24]insulin and [SerB25]insulin have about 16% and 0.5% of the activity of normal insulin, respectively, in stimulating glucose oxidation by isolated rat adipocytes. Glucose 155-162 insulin Homo sapiens 39-46 6424111-5 1983 Additional studies showed that [SerB24]insulin and [SerB25]insulin have about 16% and 0.5% of the activity of normal insulin, respectively, in stimulating glucose oxidation by isolated rat adipocytes. Glucose 155-162 insulin Homo sapiens 59-66 6424111-5 1983 Additional studies showed that [SerB24]insulin and [SerB25]insulin have about 16% and 0.5% of the activity of normal insulin, respectively, in stimulating glucose oxidation by isolated rat adipocytes. Glucose 155-162 insulin Homo sapiens 59-66 6320319-2 1983 In the presence of glucose (2.8 mM), both procedures resulted in an immediate and sustained stimulation of 45Ca and insulin release from prelabelled islets. Glucose 19-26 insulin Homo sapiens 116-123 6367143-0 1983 Pancreatic polypeptide and insulin contents in diabetic and nondiabetic human pancreas and their relationship to the stability of the fasting serum glucose. Glucose 148-155 insulin Homo sapiens 27-34 6367143-6 1983 In those diabetics where there was less than 0.5 U/g of insulin in the tail pancreas, the stability of the fasting serum glucose was very poor, indicating an unstable type of diabetes. Glucose 121-128 insulin Homo sapiens 56-63 6393431-3 1983 BWI) and a diminished insulin response to glucose load were significant independent risk factors for worsening to diabetes. Glucose 42-49 insulin Homo sapiens 22-29 6393436-4 1983 2) Insulin response to glucose in patients with normal glucose tolerance was similar to that in controls, while insulin response in patients with impaired glucose tolerance showed a delayed peak. Glucose 23-30 insulin Homo sapiens 3-10 6393436-4 1983 2) Insulin response to glucose in patients with normal glucose tolerance was similar to that in controls, while insulin response in patients with impaired glucose tolerance showed a delayed peak. Glucose 55-62 insulin Homo sapiens 3-10 6393446-10 1983 These results suggest that the AEP, Biostator, could be useful in the clinical management of unstable diabetics by providing a more precise estimate of patients insulin requirements, especially those of short-acting insulin, leading to a better long-term control of blood glucose. Glucose 272-279 insulin Homo sapiens 161-168 6680478-2 1983 In untreated borderline diabetics, high or normal insulin responders became normal for glucose tolerance 10 years later. Glucose 87-94 insulin Homo sapiens 50-57 6369964-3 1983 At the clinical level in man, the rate-limiting step for insulin-stimulated disposal of oral glucose in vivo is glucose transport into peripheral tissues, chiefly muscle, whereas the contributions of insulin suppression of hepatic glucose output and stimulation of glucose oxidation are quite limited. Glucose 93-100 insulin Homo sapiens 57-64 6369964-3 1983 At the clinical level in man, the rate-limiting step for insulin-stimulated disposal of oral glucose in vivo is glucose transport into peripheral tissues, chiefly muscle, whereas the contributions of insulin suppression of hepatic glucose output and stimulation of glucose oxidation are quite limited. Glucose 112-119 insulin Homo sapiens 57-64 6369969-4 1983 The major effect of the drug appears to be mediated by its alteration of insulin sensitivity, but glipizide also causes a sustained increase in glucose-stimulated insulin secretion in most patients. Glucose 144-151 insulin Homo sapiens 163-170 6369970-6 1983 Finally, glipizide treatment was associated with improvements in both the plasma insulin response to mixed meals and estimates of in vivo insulin-stimulated glucose utilization. Glucose 157-164 insulin Homo sapiens 138-145 6369971-2 1983 The insulin-stimulated glucose metabolic clearance rate, assessed by the insulin clamp technique, was compared in 40 normal subjects and 40 age- and weight-matched patients with noninsulin-dependent diabetes mellitus. Glucose 23-30 insulin Homo sapiens 4-11 6369971-4 1983 This difference was highly statistically significant (p less than 0.001) and documents the extreme resistance to insulin-stimulated glucose utilization seen in noninsulin-dependent diabetes mellitus. Glucose 132-139 insulin Homo sapiens 113-120 6369971-5 1983 Patients with noninsulin-dependent diabetes mellitus were also shown to have a lower than normal plasma insulin response to an oral glucose challenge. Glucose 132-139 insulin Homo sapiens 17-24 6416511-3 1983 Higher fasting blood glucose concentrations occurred during treatment with human insulin than with porcine insulin (mean 12.0 (SD 2.1) v 11.0 (2.4) mmol/1; mean 216 (SD 38) v 198 (43) mg/100 ml; p less than 0.05), but there were no significant differences at other time points during the day. Glucose 21-28 insulin Homo sapiens 81-88 6356926-5 1983 Plasma insulin concentrations were slightly but significantly higher than control values in response to oral and intravenous administration of glucose while subjects were using oral contraceptives. Glucose 143-150 insulin Homo sapiens 7-14 6139809-2 1983 Insulin sensitivity was determined in normal subjects and in subjects with possible insulin-resistance by simultaneous infusion of somatostatin, insulin and glucose. Glucose 157-164 insulin Homo sapiens 0-7 6356745-2 1983 The fasting plasma insulin concentration and the insulin response to glucose are often increased, indicating some insulin resistance in this disease. Glucose 69-76 insulin Homo sapiens 49-56 6356745-2 1983 The fasting plasma insulin concentration and the insulin response to glucose are often increased, indicating some insulin resistance in this disease. Glucose 69-76 insulin Homo sapiens 49-56 6227251-8 1983 After receiving 100 gm of oral glucose, hirsute patients with PCO had significantly higher insulin responses compared to those of control subjects despite similar glucose responses. Glucose 31-38 insulin Homo sapiens 91-98 6356895-3 1983 The administration of insulin by this route provides acceptable plasma glucose control with no need for subcutaneous injections. Glucose 71-78 insulin Homo sapiens 22-29 6315263-3 1983 Concurrent infusion of 10% dextrose at 250 ml/h for 2 h prevented the increase in plasma ir-beta EP levels, suggesting an effect of hypoglycaemia rather than a direct effect of insulin. Glucose 27-35 insulin Homo sapiens 177-184 6352157-2 1983 The basal blood glucose level was elevated by 0.5 mmol/l, associated with a threefold increase in basal serum insulin compared with seven normal controls. Glucose 16-23 insulin Homo sapiens 110-117 6357902-9 1983 In subjects with type I and type II diabetes mellitus, serum insulin levels increased in a manner similar to controls, and resulted in a prompt reduction of blood glucose concentration. Glucose 163-170 insulin Homo sapiens 61-68 6357902-10 1983 However, in contrast to normal subjects, the duration of the glucose response was more prolonged, lasting as long as 5 h. Nasal administration of insulin as an aerosol with bile salts or bile salt analogs should be further evaluated as a possible nonparenteral approach to insulin therapy. Glucose 61-68 insulin Homo sapiens 146-153 6360599-8 1983 These findings are in accord with recent in vivo studies showing that type I diabetic patients are also resistant to the stimulating effect of insulin on glucose disposal. Glucose 154-161 insulin Homo sapiens 143-150 6360777-1 1983 Studies were carried out in 32 obese patients and 30 normal-weight control subjects to ascertain the response of glucose-dependent insulinotropic polypeptide (GIP) and insulin to (1) oral and intravenous glucose (10 obese and 10 control subjects), (2) oral fat and intravenous glucose (eight obese and six control subjects) and (3) mixed test meal (14 obese and 14 control subjects). Glucose 113-120 insulin Homo sapiens 131-138 6360777-1 1983 Studies were carried out in 32 obese patients and 30 normal-weight control subjects to ascertain the response of glucose-dependent insulinotropic polypeptide (GIP) and insulin to (1) oral and intravenous glucose (10 obese and 10 control subjects), (2) oral fat and intravenous glucose (eight obese and six control subjects) and (3) mixed test meal (14 obese and 14 control subjects). Glucose 204-211 insulin Homo sapiens 131-138 6360777-3 1983 The total integrated response of insulin in obese subjects after oral glucose was 54.1 versus 33.3 nmol . Glucose 70-77 insulin Homo sapiens 33-40 6360777-6 1983 After intravenous glucose the integrated insulin response was 8.8 in the obese versus 5.0 nmol . Glucose 18-25 insulin Homo sapiens 41-48 6416909-8 1983 Insulin-mediated glucose utilization (M) was 6.69 +/- 0.51 mg/kg X min in the control study and decreased to 5.84 +/- 0.40 mg/kg X min following the exposure to hyperosmolality (P less than 0.05).2+ +/- 0.60 versus 4.30 +/- 0.43 mg/kg X min per microU/ml X 100). Glucose 17-24 insulin Homo sapiens 0-7 6138367-14 1983 When insulin is deficient, on the other hand, elevated rates of lipolysis may contribute to hyperglycemia not by competition for fuel utilization, but through an enhancement of endogenous glucose output. Glucose 188-195 insulin Homo sapiens 5-12 6352723-2 1983 Fasting hypoglycemia was found to be due both to an insulin-induced decrease in hepatic glucose output to 3.95 +/- 0.30 (SEM) mg/kg X min, a value about two thirds of normal, and to a glucose utilization rate of 4.25 +/- 0.32 mg/kg X min, which exceeded glucose production by about 8%. Glucose 88-95 insulin Homo sapiens 52-59 6352723-2 1983 Fasting hypoglycemia was found to be due both to an insulin-induced decrease in hepatic glucose output to 3.95 +/- 0.30 (SEM) mg/kg X min, a value about two thirds of normal, and to a glucose utilization rate of 4.25 +/- 0.32 mg/kg X min, which exceeded glucose production by about 8%. Glucose 184-191 insulin Homo sapiens 52-59 6352727-0 1983 Insulin-mediated glucose disposal in type I diabetes: evidence for insulin resistance. Glucose 17-24 insulin Homo sapiens 0-7 6352727-0 1983 Insulin-mediated glucose disposal in type I diabetes: evidence for insulin resistance. Glucose 17-24 insulin Homo sapiens 67-74 6352727-15 1983 Multiple glucose clamp studies were also performed at three different insulin infusion rates (21, 73, and 760 mU/m2 X min, respectively) to generate an insulin-dose response curve for glucose disposal in six diabetic patients treated with continuous sc insulin infusion for at least 6 months. Glucose 184-191 insulin Homo sapiens 152-159 6352727-15 1983 Multiple glucose clamp studies were also performed at three different insulin infusion rates (21, 73, and 760 mU/m2 X min, respectively) to generate an insulin-dose response curve for glucose disposal in six diabetic patients treated with continuous sc insulin infusion for at least 6 months. Glucose 184-191 insulin Homo sapiens 152-159 6352727-16 1983 This allowed investigation of the effect of chronic strict insulin therapy leading to normal glucose and intermediary metabolite levels and identification of the cellular mechanism of insulin resistance. Glucose 93-100 insulin Homo sapiens 59-66 6355186-4 1983 The insulin sensitivity index (glucose metabolic clearance rate in ml/kg per min) was significantly lower (P less than 0.001) after prednisone at all three steady state plasma insulin levels: 2.8 +/- 0.3 vs. 7.4 +/- 1.1 at approximately 100 microU/ml; 6.0 +/- 0.5 vs. 12.2 +/- 1.1 at approximately 1,000 microU/ml; 7.4 +/- 0.6 vs. 14.4 +/- 0.5 at approximately 10,000 microU/ml. Glucose 31-38 insulin Homo sapiens 4-11 6355186-6 1983 Suppression of glucose production at steady state plasma insulin level of approximately 100 microU/ml was less after prednisone (1.01 +/- 0.35 vs. 0.14 +/- 0.13, NS), and total at approximately 1,000 and approximately 10,000 microU/ml after both prednisone and placebo. Glucose 15-22 insulin Homo sapiens 57-64 6312251-0 1983 Increased insulin binding to adipocytes and monocytes and increased insulin sensitivity of glucose transport and metabolism in adipocytes from non-insulin-dependent diabetics after a low-fat/high-starch/high-fiber diet. Glucose 91-98 insulin Homo sapiens 10-17 6312251-0 1983 Increased insulin binding to adipocytes and monocytes and increased insulin sensitivity of glucose transport and metabolism in adipocytes from non-insulin-dependent diabetics after a low-fat/high-starch/high-fiber diet. Glucose 91-98 insulin Homo sapiens 68-75 6312251-7 1983 When lipogenesis was studied at a tracer glucose concentration at which glucose transport seems to be rate limiting, insulin sensitivity increased (P less than 0.02). Glucose 41-48 insulin Homo sapiens 117-124 6312251-7 1983 When lipogenesis was studied at a tracer glucose concentration at which glucose transport seems to be rate limiting, insulin sensitivity increased (P less than 0.02). Glucose 72-79 insulin Homo sapiens 117-124 6312251-9 1983 Moreover, when CO2 production and lipogenesis were studied at a higher glucose concentration, where steps beyond transport seem to be rate limiting for glucose metabolism, increased insulin sensitivity was also observed. Glucose 71-78 insulin Homo sapiens 182-189 6312251-9 1983 Moreover, when CO2 production and lipogenesis were studied at a higher glucose concentration, where steps beyond transport seem to be rate limiting for glucose metabolism, increased insulin sensitivity was also observed. Glucose 152-159 insulin Homo sapiens 182-189 6353136-0 1983 The physiologic action of insulin on glucose uptake and its relevance to the interpretation of the metabolic clearance rate of glucose. Glucose 37-44 insulin Homo sapiens 26-33 6353136-0 1983 The physiologic action of insulin on glucose uptake and its relevance to the interpretation of the metabolic clearance rate of glucose. Glucose 127-134 insulin Homo sapiens 26-33 6353136-2 1983 The metabolic clearance rate of glucose (MCRG), has been used as an in vivo measure of insulin action, because it was said to be independent of the prevailing glucose concentration. Glucose 32-39 insulin Homo sapiens 87-94 6353136-4 1983 In this study, the effect of insulin concentration on the rate of glucose uptake (Ru) and on the MCRG was studied during euglycemia (5.1 +/- 0.3 mmol/L) and moderate hyperglycemia (10.4 +/- 0.5 mmol/L) in 17 experiments on nine normal ambulant volunteers. Glucose 66-73 insulin Homo sapiens 29-36 6353136-6 1983 At low insulin concentrations (less than 5 microU/mL) the increase in glucose uptake in response to hyperglycemia was small (5.3 +/- 2.3 mumol/kg/min). Glucose 70-77 insulin Homo sapiens 7-14 6353136-7 1983 In contrast, with insulin levels more than 25 microU/mL, there was a steep rise in glucose uptake with hyperglycemia (55 +/- 3 mumol/kg/min; range: 44-74 mumol/kg/min). Glucose 83-90 insulin Homo sapiens 18-25 6353136-8 1983 The metabolic clearance rate of glucose fell by an average of 32% with hyperglycemia in the studies at the lowest insulin levels (2.2 +/- 0.6 v 1.5 +/- 0.1 mL/kg/min; 0.15 greater than P greater than 0.1). Glucose 32-39 insulin Homo sapiens 114-121 6353136-10 1983 It is concluded that (1) low concentrations of insulin are essential for the increase in glucose disposal during hyperglycemia; and (2) provided insulin levels are more than 25 microU/mL and plasma glucose less than 11 mmol/L, MCRG is independent of the plasma glucose concentration and is therefore a valid measure of insulin-mediated glucose uptake. Glucose 89-96 insulin Homo sapiens 47-54 6353136-10 1983 It is concluded that (1) low concentrations of insulin are essential for the increase in glucose disposal during hyperglycemia; and (2) provided insulin levels are more than 25 microU/mL and plasma glucose less than 11 mmol/L, MCRG is independent of the plasma glucose concentration and is therefore a valid measure of insulin-mediated glucose uptake. Glucose 198-205 insulin Homo sapiens 47-54 6353136-10 1983 It is concluded that (1) low concentrations of insulin are essential for the increase in glucose disposal during hyperglycemia; and (2) provided insulin levels are more than 25 microU/mL and plasma glucose less than 11 mmol/L, MCRG is independent of the plasma glucose concentration and is therefore a valid measure of insulin-mediated glucose uptake. Glucose 198-205 insulin Homo sapiens 47-54 6353136-10 1983 It is concluded that (1) low concentrations of insulin are essential for the increase in glucose disposal during hyperglycemia; and (2) provided insulin levels are more than 25 microU/mL and plasma glucose less than 11 mmol/L, MCRG is independent of the plasma glucose concentration and is therefore a valid measure of insulin-mediated glucose uptake. Glucose 198-205 insulin Homo sapiens 47-54 6353137-5 1983 After oral glucose all groups of patients had elevated plasma levels of glucose, insulin, and C peptide compared with the controls. Glucose 11-18 insulin Homo sapiens 81-88 6361975-1 1983 The amount-of-substance rate of glucose metabolism and its sensitivity to the concentration of insulin was quantified in 10 non-diabetic patients with alcoholic cirrhosis of varying severity, using the "glucose clamp technique". Glucose 32-39 insulin Homo sapiens 95-102 6361975-1 1983 The amount-of-substance rate of glucose metabolism and its sensitivity to the concentration of insulin was quantified in 10 non-diabetic patients with alcoholic cirrhosis of varying severity, using the "glucose clamp technique". Glucose 203-210 insulin Homo sapiens 95-102 6361975-3 1983 During the hyperglycaemic clamp (blood glucose at 12.5 mmol/l) the glucose metabolic rate (divided by body mass) was 27 +/- 4 mumol X min-1 X kg-1 at an insulin concentration of 998 +/- 158 pmol/l. Glucose 67-74 insulin Homo sapiens 153-160 6361975-4 1983 Thus the insulin sensitivity of the tissue glucose metabolism was 22 +/- 7 m3 X min-1 X kg-1. Glucose 43-50 insulin Homo sapiens 9-16 6353916-1 1983 Studies utilizing glucose-controlled insulin infusion systems were undertaken to more accurately define the glucose and insulin requirements during the first stage of labor induced by oxytocin in 12 insulin-dependent diabetic women in whom normoglycemia had been maintained before delivery. Glucose 18-25 insulin Homo sapiens 37-44 6354230-5 1983 In comparison with a control group of patients, the insulin infusion caused a marked decrease in circulating glucose, non-esterified fatty acids and beta-hydroxybutyrate concentrations, and an increase in blood lactate values. Glucose 109-116 insulin Homo sapiens 52-59 6651715-1 1983 Previous studies on men under conditions of total bed rest, and laboratory animals under limited physical activity, have shown resistance to insulin-induced glucose uptake and, conversely, increased sensitivity to insulin with exercise training. Glucose 157-164 insulin Homo sapiens 141-148 6352376-8 1983 Instead, total insulin dose was estimated using a dietary glucose/insulin (G/I) ratio. Glucose 58-65 insulin Homo sapiens 15-22 6352380-6 1983 Under the influence of PEG insulin, diminished incorporation of 14C and/or 3H into adipose tissues was observed in all cases, yet both natural insulin and the derivative lowered the blood glucose to the same extent. Glucose 188-195 insulin Homo sapiens 143-150 6137430-6 1983 First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. Glucose 57-64 insulin Homo sapiens 24-31 6357915-0 1983 Glucose utilization in Type 1 (insulin-dependent) diabetes: Evidence for a defect not reversible by acute elevations of insulin. Glucose 0-7 insulin Homo sapiens 31-38 6357915-1 1983 It has long been assumed that replacement of insulin in insulin-deficient diabetic patients will normalise glucose utilization. Glucose 107-114 insulin Homo sapiens 45-52 6357915-6 1983 In the control subjects, a 1-mmol/l rise in glucose concentration (with insulin remaining constant) resulted in a 12.3 +/- 1.3 mumol.kg-1.min-1 rise in glucose utilization. Glucose 44-51 insulin Homo sapiens 72-79 6357915-6 1983 In the control subjects, a 1-mmol/l rise in glucose concentration (with insulin remaining constant) resulted in a 12.3 +/- 1.3 mumol.kg-1.min-1 rise in glucose utilization. Glucose 152-159 insulin Homo sapiens 72-79 6357915-7 1983 In contrast, in the diabetic patients, a 1-mmol/l rise in blood glucose resulted in a rise in glucose utilization of only 3.8 +/- 0.8 mumol.kg-1.min-1 (p less than 0.001), in the presence of similar concentrations of plasma insulin. Glucose 64-71 insulin Homo sapiens 224-231 6357915-7 1983 In contrast, in the diabetic patients, a 1-mmol/l rise in blood glucose resulted in a rise in glucose utilization of only 3.8 +/- 0.8 mumol.kg-1.min-1 (p less than 0.001), in the presence of similar concentrations of plasma insulin. Glucose 94-101 insulin Homo sapiens 224-231 6357919-4 1983 After 36 h fasting the oral glucose tolerance test stimulated higher blood glucose concentrations at 60, 90 and 120 min (p less than 0.0125) and higher plasma insulin concentrations at similar time points (p less than 0.05), but stimulated plasma GIP concentrations were similar after 12 and 36 h fasts. Glucose 28-35 insulin Homo sapiens 159-166 6416850-3 1983 The insulin response to an intravenous glucose load was enhanced preoperatively [95 mU/1 +/- 41 (SD)] in twenty-six prospectively studied patients compared to postoperative (65 +/- 41 mU/1) investigations (P less than 0.01). Glucose 39-46 insulin Homo sapiens 4-11 6355180-1 1983 To assess possible cellular mechanisms of in vitro resistance in noninsulin-dependent diabetes mellitus (NIDDM), maximum insulin-stimulated glucose transport and utilization and insulin binding were measured in adipocytes isolated from weight-matched normal glycemic subjects and patients with NIDDM. Glucose 140-147 insulin Homo sapiens 121-128 6355180-4 1983 Both maximum insulin-stimulated glucose transport and utilization in adipocytes from diabetic subjects were 40% (P less than 0.01) and 32% (P less than 0.05) lower, respectively, than values obtained for subjects with normal glucose tolerance. Glucose 32-39 insulin Homo sapiens 13-20 6355180-4 1983 Both maximum insulin-stimulated glucose transport and utilization in adipocytes from diabetic subjects were 40% (P less than 0.01) and 32% (P less than 0.05) lower, respectively, than values obtained for subjects with normal glucose tolerance. Glucose 225-232 insulin Homo sapiens 13-20 6355180-6 1983 Furthermore, fasting plasma glucose concentrations of diabetic subjects were negatively correlated with both maximum insulin-stimulated glucose transport (r = -0.56, P less than 0.05) and glucose utilization (r = -0.67, P less than 0.05). Glucose 28-35 insulin Homo sapiens 117-124 6355180-6 1983 Furthermore, fasting plasma glucose concentrations of diabetic subjects were negatively correlated with both maximum insulin-stimulated glucose transport (r = -0.56, P less than 0.05) and glucose utilization (r = -0.67, P less than 0.05). Glucose 136-143 insulin Homo sapiens 117-124 6355180-6 1983 Furthermore, fasting plasma glucose concentrations of diabetic subjects were negatively correlated with both maximum insulin-stimulated glucose transport (r = -0.56, P less than 0.05) and glucose utilization (r = -0.67, P less than 0.05). Glucose 136-143 insulin Homo sapiens 117-124 6355180-9 1983 These results demonstrate that both maximal insulin-stimulated glucose transport and utilization, and the sensitivity of the glucose transport system to insulin, was decreased in adipocytes isolated from subjects with NIDDM. Glucose 63-70 insulin Homo sapiens 44-51 6352838-10 1983 After intravenous insulin administration, there was only a 40% decline in plasma glucose concentration from basal values in the patients with cirrhosis whereas the controls showed a 60% decline, demonstrating that the patients with cirrhosis had significant insulin resistance. Glucose 81-88 insulin Homo sapiens 18-25 6352838-14 1983 In conclusion, patients with hepatic cirrhosis have significant glucose intolerance characterized by hyperinsulinemia, hyperglucagonemia, insulin resistance, and down-regulation of insulin receptors. Glucose 64-71 insulin Homo sapiens 106-113 6352838-14 1983 In conclusion, patients with hepatic cirrhosis have significant glucose intolerance characterized by hyperinsulinemia, hyperglucagonemia, insulin resistance, and down-regulation of insulin receptors. Glucose 64-71 insulin Homo sapiens 138-145 6352839-4 1983 Positive, significant correlations were found between WHR and both systolic and diastolic blood pressure and between WHR and the total integrated plasma glucose and insulin responses during 4 hr oral glucose tolerance tests. Glucose 200-207 insulin Homo sapiens 165-172 6352839-7 1983 Women in the highest quartile had systolic and diastolic blood pressure as well as total plasma glucose and insulin responses during glucose tolerance tests that significantly exceeded mean values of subjects in the lowest quartile. Glucose 133-140 insulin Homo sapiens 108-115 6350810-1 1983 We examined the response of plasma glucose concentration and glucose counterregulatory factors (eg, glucagon, epinephrine, growth hormone, cortisol, and norepinephrine) to insulin-induced hypoglycemia in four patients with Shy-Drager syndrome and in five control subjects to determine if glucose counterregulation occurred in the patients with sympathetic and parasympathetic nervous system defects. Glucose 35-42 insulin Homo sapiens 172-179 6350810-1 1983 We examined the response of plasma glucose concentration and glucose counterregulatory factors (eg, glucagon, epinephrine, growth hormone, cortisol, and norepinephrine) to insulin-induced hypoglycemia in four patients with Shy-Drager syndrome and in five control subjects to determine if glucose counterregulation occurred in the patients with sympathetic and parasympathetic nervous system defects. Glucose 61-68 insulin Homo sapiens 172-179 6350810-1 1983 We examined the response of plasma glucose concentration and glucose counterregulatory factors (eg, glucagon, epinephrine, growth hormone, cortisol, and norepinephrine) to insulin-induced hypoglycemia in four patients with Shy-Drager syndrome and in five control subjects to determine if glucose counterregulation occurred in the patients with sympathetic and parasympathetic nervous system defects. Glucose 61-68 insulin Homo sapiens 172-179 6350810-3 1983 Although the insulin-induced hypoglycemia in the control subjects provoked a rapid release of epinephrine, followed by an increase in the plasma glucagon, growth hormone, and cortisol levels, it did not cause a significant increase in any of the glucose counterregulatory factors in the patients. Glucose 246-253 insulin Homo sapiens 13-20 6137924-8 1983 Moreover, significant correlation coefficients were found between the glucose to insulin ratio and the A (r = -0.59; P less than 0.01) and the DHEA-S (r = -0.50; P less than 0.05) plasma levels. Glucose 70-77 insulin Homo sapiens 81-88 6137926-0 1983 Oral glucose tolerance test and insulin sensitivity in low insulin responders. Glucose 5-12 insulin Homo sapiens 59-66 6137926-7 1983 Borderline and decreased OGTT, in most instances, was accompanied by decreased insulin sensitivity, implying that a subgroup of low insulin responders exhibited signs of both impaired insulin response to glucose and insulin resistance. Glucose 204-211 insulin Homo sapiens 132-139 6137926-7 1983 Borderline and decreased OGTT, in most instances, was accompanied by decreased insulin sensitivity, implying that a subgroup of low insulin responders exhibited signs of both impaired insulin response to glucose and insulin resistance. Glucose 204-211 insulin Homo sapiens 132-139 6353831-3 1983 In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. Glucose 76-83 insulin Homo sapiens 56-63 6353831-3 1983 In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. Glucose 76-83 insulin Homo sapiens 135-142 6353831-3 1983 In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. Glucose 116-123 insulin Homo sapiens 56-63 6353831-3 1983 In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. Glucose 116-123 insulin Homo sapiens 135-142 6353831-3 1983 In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. Glucose 116-123 insulin Homo sapiens 56-63 6353831-3 1983 In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. Glucose 116-123 insulin Homo sapiens 135-142 6353831-4 1983 This effect was not observed when glucose was given iv in another group of 5 subjects in whom the significant blunting of the insulin response was accompanied by a significant decrease in glucose tolerance. Glucose 34-41 insulin Homo sapiens 126-133 6351598-4 1983 Significant positive correlations were seen between insulin (measured as fasting insulin and the 3 hour area under the insulin curve during the oral glucose tolerance test) and the atherogenic lipids, total and low density lipoprotein cholesterol and triglycerides ranging from r = +0.14 (p less than 0.01) to r = + 0.35 (p less than 0.001). Glucose 149-156 insulin Homo sapiens 52-59 6351598-4 1983 Significant positive correlations were seen between insulin (measured as fasting insulin and the 3 hour area under the insulin curve during the oral glucose tolerance test) and the atherogenic lipids, total and low density lipoprotein cholesterol and triglycerides ranging from r = +0.14 (p less than 0.01) to r = + 0.35 (p less than 0.001). Glucose 149-156 insulin Homo sapiens 81-88 6351598-4 1983 Significant positive correlations were seen between insulin (measured as fasting insulin and the 3 hour area under the insulin curve during the oral glucose tolerance test) and the atherogenic lipids, total and low density lipoprotein cholesterol and triglycerides ranging from r = +0.14 (p less than 0.01) to r = + 0.35 (p less than 0.001). Glucose 149-156 insulin Homo sapiens 81-88 6351598-6 1983 A computed score of insulin activity, which the authors call the insulin-glucose sensitivity index, shows equally strong correlations but of reverse sign. Glucose 73-80 insulin Homo sapiens 20-27 6351598-6 1983 A computed score of insulin activity, which the authors call the insulin-glucose sensitivity index, shows equally strong correlations but of reverse sign. Glucose 73-80 insulin Homo sapiens 65-72 6357285-2 1983 In a numerical experiment the model imitated changed levels of sucrose, insulin glucagon and gastrointestinal hormones in the blood in response to the ingested 50 g of glucose. Glucose 168-175 insulin Homo sapiens 72-79 6347499-0 1983 The physiological effects of insulin-induced hypoglycaemia in man: responses at differing levels of blood glucose. Glucose 106-113 insulin Homo sapiens 29-36 6354520-3 1983 Plasma GIP and insulin responses to oral glucose loading were significantly higher than normal in both groups. Glucose 41-48 insulin Homo sapiens 15-22 6354520-4 1983 The degree of exaggerated plasma GIP and insulin secretions was more prominent and earlier in totally gastrectomized patients than in duodenal ulcer patients, and was positively correlated with the blood glucose increase during glucose ingestion. Glucose 204-211 insulin Homo sapiens 41-48 6354520-4 1983 The degree of exaggerated plasma GIP and insulin secretions was more prominent and earlier in totally gastrectomized patients than in duodenal ulcer patients, and was positively correlated with the blood glucose increase during glucose ingestion. Glucose 228-235 insulin Homo sapiens 41-48 6354722-0 1983 The effect of glucose, tolbutamide, and arginine on C-peptide release during remission in type I diabetes mellitus. Glucose 14-21 insulin Homo sapiens 52-61 6354722-16 1983 The C-peptide response to oral glucose was sluggish with no effect on the following arginine infusion. Glucose 31-38 insulin Homo sapiens 4-13 6357912-4 1983 We studied the diurnal patterns of intermediary metabolites, free insulin, and glucagon using the Biostator (glucose-controlled insulin infusion system) and intensive subcutaneous insulin therapy in five patients after total pancreatectomy, five after partial pancreatectomy and seven patients with Type 1 diabetes. Glucose 109-116 insulin Homo sapiens 128-135 6400702-7 1983 Fluctuations in blood glucose were avoided when exercise was performed in the fasting state with basal insulin infusion. Glucose 22-29 insulin Homo sapiens 103-110 6400703-5 1983 The fast glucose intake, compared with the slow ingestion, resulted in an earlier rise in blood glucose levels, accompanied by a faster serum insulin and C-peptide response. Glucose 9-16 insulin Homo sapiens 142-149 6400704-5 1983 Such a correlation was also found in vitro regarding the insulin response to glucose and IBMX. Glucose 77-84 insulin Homo sapiens 57-64 6653856-6 1983 While fasting and post-prandial plasma glucose values were significantly higher in insulin-treated than in type II diabetes (p less than 0.001), no differences in GHb values were observed between the two groups (10.31 +/- 0.23% vs 9.80 +/- 0.36%). Glucose 39-46 insulin Homo sapiens 83-90 6653856-8 1983 A correlation between PIL and plasma glucose values was observed only in the insulin-treated group and was weaker (p less than 0.005). Glucose 37-44 insulin Homo sapiens 77-84 6357983-3 1983 The rate of glucose infusion (mg/min, mean +/- SEM) required to maintain euglycaemia during the last 40 minutes of each insulin infusion for porcine (P) and human (H) insulin was not significantly different. Glucose 12-19 insulin Homo sapiens 120-127 6357983-4 1983 However, when the glucose infusion rate was expressed as a function of the mean serum insulin level (mU/l) over the same period of time the values for P and H at 4.8 and 7.2 U/hr were not significantly different but H was greater than P (13.6 +/- 1.9, v 10.8 +/- 1.9, p less than .05) at 2.4 U/hr. Glucose 18-25 insulin Homo sapiens 86-93 6416979-3 1983 Insulin/glucose ratios fell by 17.3% at 60 minutes and rose by 14.2% at 180 minutes. Glucose 8-15 insulin Homo sapiens 0-7 6136528-4 1983 After 2 h of insulin and glucose infusion in series 1, glucose uptake had increased to 23.5 +/- 2.3 mg/kg per min and insulin concentration to 199 +/- 21 microU/ml. Glucose 25-32 insulin Homo sapiens 118-125 6136528-4 1983 After 2 h of insulin and glucose infusion in series 1, glucose uptake had increased to 23.5 +/- 2.3 mg/kg per min and insulin concentration to 199 +/- 21 microU/ml. Glucose 55-62 insulin Homo sapiens 13-20 6409929-7 1983 Thus, among the potentially important glucose regulatory factors, only transient increments in insulin, transient decrements in glucagon, and late increments in epinephrine are specific for glucose ingestion. Glucose 190-197 insulin Homo sapiens 95-102 6370851-0 1983 Plasma insulin response to oral glucose load in hepatic cirrhosis. Glucose 32-39 insulin Homo sapiens 7-14 6359133-3 1983 The correlation between a high insulin response and the glucose level was absent. Glucose 56-63 insulin Homo sapiens 31-38 6310564-7 1983 The expression of preproinsulin-beta-galactosidase activity was measured in the presence of high glucose, insulin, dexamethasone, or epidermal growth factor but no regulatory changes were observed. Glucose 97-104 insulin Homo sapiens 18-31 6310564-7 1983 The expression of preproinsulin-beta-galactosidase activity was measured in the presence of high glucose, insulin, dexamethasone, or epidermal growth factor but no regulatory changes were observed. Glucose 97-104 insulin Homo sapiens 24-31 6349697-2 1983 Exposure to insulin resulted in increased glucose uptake from the media and in the rate of glucose conversion to CO2. Glucose 42-49 insulin Homo sapiens 12-19 6349697-2 1983 Exposure to insulin resulted in increased glucose uptake from the media and in the rate of glucose conversion to CO2. Glucose 91-98 insulin Homo sapiens 12-19 6349697-5 1983 The presence of low doses of insulin (10-25 microunits/ml) caused a significant increase in the incorporation of glucose into both surfactant and residual phosphatidylcholine. Glucose 113-120 insulin Homo sapiens 29-36 6349697-6 1983 Insulin at levels of 100 microunits/ml or higher resulted in a significant decrease in glucose incorporation into both phosphatidylcholine fractions. Glucose 87-94 insulin Homo sapiens 0-7 6349697-8 1983 The addition of 400 microunits/ml of insulin to media containing 20 mM glucose, however, resulted in a 20% decrease in choline incorporation into surfactant phosphatidylcholine but had no effect on choline incorporation into residual phosphatidylcholine. Glucose 71-78 insulin Homo sapiens 37-44 6356658-5 1983 A main effect of the insulin consists in furthering the transport of glucose transport molecules from the interior of the cells into the membranes, by which means the intake of glucose is temporarily much increased. Glucose 69-76 insulin Homo sapiens 21-28 6356658-5 1983 A main effect of the insulin consists in furthering the transport of glucose transport molecules from the interior of the cells into the membranes, by which means the intake of glucose is temporarily much increased. Glucose 177-184 insulin Homo sapiens 21-28 6225336-13 1983 Insulin had a greater binding tendency in 5% dextrose injection than in 0.9% sodium chloride injection in both experiments regardless of the filter treatment. Glucose 45-53 insulin Homo sapiens 0-7 6351759-6 1983 The insulin pump seems to be an acceptable form of treatment for some children and young adults with diabetes mellitus and gives near physiological control of blood glucose. Glucose 165-172 insulin Homo sapiens 4-11 6347772-6 1983 Patients with the most severe type II diabetes (SU-treated group) demonstrated, in contrast to the less severely diabetic patients, a marked reduction in both basal and insulin-stimulated glucose incorporation into triglycerides showing the presence of a pronounced postreceptor defect. Glucose 188-195 insulin Homo sapiens 169-176 6347772-7 1983 The insulin effect on glucose incorporation correlated negatively with the fasting glucose levels, suggesting that the postreceptor defect seen in the adipocyte reflects perturbations in other organs, like muscle or liver, of greater importance for glucose homeostasis. Glucose 22-29 insulin Homo sapiens 4-11 6345256-9 1983 Similarly, in 8 patients, increased branched-chain amino acid response also correlated with the index of tissue sensitivity to insulin obtained by means of the glucose clamp technique during continuous insulin infusion (r = -0.809). Glucose 160-167 insulin Homo sapiens 127-134 6345256-9 1983 Similarly, in 8 patients, increased branched-chain amino acid response also correlated with the index of tissue sensitivity to insulin obtained by means of the glucose clamp technique during continuous insulin infusion (r = -0.809). Glucose 160-167 insulin Homo sapiens 202-209 6354732-0 1983 A stimulatory effect of tolbutamide on the insulin-mediated glucose uptake in subjects with impaired glucose tolerance (IGT). Glucose 60-67 insulin Homo sapiens 43-50 6354732-2 1983 The present investigation was undertaken in order to elucidate whether or not there is also an acute effect of sulfonylureas on insulin-mediated glucose uptake. Glucose 145-152 insulin Homo sapiens 128-135 6354732-4 1983 In vivo insulin sensitivity was assessed by using the glucose controlled insulin infusion system (Biostator) without or with a contemporary 3-hour tolbutamide infusion. Glucose 54-61 insulin Homo sapiens 8-15 6354732-12 1983 On the other hand, for the disposal of identical quantities of glucose the necessary amount of insulin has been found to be reduced by one third due to tolbutamide treatment indicating a higher insulin sensitivity. Glucose 63-70 insulin Homo sapiens 95-102 6354732-12 1983 On the other hand, for the disposal of identical quantities of glucose the necessary amount of insulin has been found to be reduced by one third due to tolbutamide treatment indicating a higher insulin sensitivity. Glucose 63-70 insulin Homo sapiens 194-201 6223044-1 1983 To determine whether insulin resistance occurs in polycystic ovarian disease (PCO) in the absence of obesity and acanthosis nigricans, circulating levels of insulin in response to oral glucose administration were measured in 10 nonobese PCO patients without acanthosis nigricans and in 10 normal women matched for weight and height. Glucose 185-192 insulin Homo sapiens 157-164 6223044-3 1983 In PCO patients, the mean +/- SE basal insulin level (18.7 +/- 2.9 microU/ml) and the sum of the insulin levels in response to glucose (674 +/- 119 microU/ml) were significantly greater than those in the control group (11.0 +/- 0.8 microU/ml and 248 +/- 29 microU/ml, respectively). Glucose 127-134 insulin Homo sapiens 97-104 6348089-4 1983 Serum glucose (48 +/- 2 mg/dl) and insulin levels (45 +/- 3 microU/ml) were significantly higher in the glucose-treated fetuses than serum glucose (23 +/- 2 mg/dl, P less than 0.001) and insulin (15 +/- 3 microU/ml, P less than 0.001) in the controls. Glucose 104-111 insulin Homo sapiens 35-42 6348089-4 1983 Serum glucose (48 +/- 2 mg/dl) and insulin levels (45 +/- 3 microU/ml) were significantly higher in the glucose-treated fetuses than serum glucose (23 +/- 2 mg/dl, P less than 0.001) and insulin (15 +/- 3 microU/ml, P less than 0.001) in the controls. Glucose 104-111 insulin Homo sapiens 187-194 6348089-4 1983 Serum glucose (48 +/- 2 mg/dl) and insulin levels (45 +/- 3 microU/ml) were significantly higher in the glucose-treated fetuses than serum glucose (23 +/- 2 mg/dl, P less than 0.001) and insulin (15 +/- 3 microU/ml, P less than 0.001) in the controls. Glucose 104-111 insulin Homo sapiens 35-42 6348089-4 1983 Serum glucose (48 +/- 2 mg/dl) and insulin levels (45 +/- 3 microU/ml) were significantly higher in the glucose-treated fetuses than serum glucose (23 +/- 2 mg/dl, P less than 0.001) and insulin (15 +/- 3 microU/ml, P less than 0.001) in the controls. Glucose 104-111 insulin Homo sapiens 187-194 6352578-6 1983 The maximum rise in plasma insulin concentration in response to a 100-g oral glucose load was 100% higher after 10 days without exercise than when the subjects were exercising regularly. Glucose 77-84 insulin Homo sapiens 27-34 6348222-9 1983 We conclude that insulin is an important mediator of arginine- and glucose-induced hypercalciuria in the rat. Glucose 67-74 insulin Homo sapiens 17-24 6346002-3 1983 Plasma glucose levels were significantly higher in patients with NIDDM throughout the glucose tolerance test, and this was associated with a marked reduction in plasma insulin response. Glucose 7-14 insulin Homo sapiens 168-175 6346002-3 1983 Plasma glucose levels were significantly higher in patients with NIDDM throughout the glucose tolerance test, and this was associated with a marked reduction in plasma insulin response. Glucose 86-93 insulin Homo sapiens 168-175 6346005-5 1983 After restoration of normocalcemia and normocalcemia and normophosphatemia we found significantly lower glucose and insulin levels following arginine infusion and a significantly increased hypoglycemic response to parenterally administered insulin, probably indicating partial improvement of glucose tolerance after surgery. Glucose 292-299 insulin Homo sapiens 240-247 6348987-3 1983 In this study we investigated the influence of epinephrine on insulin-mediated glucose uptake by peripheral tissue. Glucose 79-86 insulin Homo sapiens 62-69 6136627-3 1983 Basal levels of growth hormone and of pancreatic and gastric hormones were reduced and the response of growth hormone, insulin and C-peptide to stimuli such as arginine, glucose, glibenclamide and calcium was virtually abolished. Glucose 170-177 insulin Homo sapiens 119-126 6346896-1 1983 Our aim was to develop the glucose clamp (GC) technique in the conscious rat for assessment of in vivo insulin sensitivity. Glucose 27-34 insulin Homo sapiens 103-110 6351658-2 1983 The glycemic and insulin response to an oral glucose load was studied in 17 children with acute lymphoblastic leukemia (ALL) and 13 normal controls. Glucose 45-52 insulin Homo sapiens 17-24 6315250-2 1983 Effects of various tannins and related compounds on adrenocorticotropic hormone-induced lipolysis and insulin-induced lipogenesis from glucose in fat cells. Glucose 135-142 insulin Homo sapiens 102-109 6409465-5 1983 Insulin corrects DKA largely via suppression of lipolysis (and thus ketone body production); insulin suppresses glucose production at lower levels than it does ketone body production. Glucose 112-119 insulin Homo sapiens 93-100 6134649-3 1983 The mean plasma glucose concentrations were lower when pulsed insulin was given [mean for the last hour: 4.66 +/- 0.08 mmol/L (+/- SEM) versus 5.53 +/- 0.06 mmol/L (+/- SEM) for steady infusion], diverging significantly (P less than 0.05 paired t test) 7 h after the start of the study. Glucose 16-23 insulin Homo sapiens 62-69 6345239-2 1983 Insulin secretion was estimated by determining plasma insulin responses to a 75-g oral challenge, and in vivo insulin-stimulated glucose uptake by the euglycemic clamp technique. Glucose 129-136 insulin Homo sapiens 110-117 6345239-4 1983 However, insulin-stimulated glucose utilization by the two groups was equal during the euglycemic clamp studies. Glucose 28-35 insulin Homo sapiens 9-16 6352210-2 1983 Of these three regimens, administration of insulin 60 min before meal ingestion provided plasma glucose and insulin profiles closest to normal and permitted less insulin to be used. Glucose 96-103 insulin Homo sapiens 43-50 6413233-5 1983 Oral glucose tolerance test demonstrated an increased stimulation of insulin in two cases, no other symptoms of diabetes mellitus were found. Glucose 5-12 insulin Homo sapiens 69-76 6363178-2 1983 In the patients with cirrhosis the serum levels of proinsulin and immunoreactive insulin were significantly higher in the fasting state and after glucose loading than in the healthy subjects. Glucose 146-153 insulin Homo sapiens 51-61 6363178-2 1983 In the patients with cirrhosis the serum levels of proinsulin and immunoreactive insulin were significantly higher in the fasting state and after glucose loading than in the healthy subjects. Glucose 146-153 insulin Homo sapiens 54-61 6365642-1 1983 Insulin action was assessed in 5 cytoplasmic islet cell antibody (ICA) positive non-diabetics, 8 ICA positive (type I) non-insulin-treated diabetics, 7 ICA negative insulin-treated diabetics by measurement of steady state plasma glucose (SSPG) levels during a combined intravenous infusion of propranolol, adrenaline, glucose and insulin. Glucose 229-236 insulin Homo sapiens 0-7 6348060-6 1983 The ED50 for insulin stimulation of glucose utilization occurred at a higher level of receptor occupancy in abdominal than in femoral fat. Glucose 36-43 insulin Homo sapiens 13-20 6348060-8 1983 Differences at the postreceptor rather than at the receptor level are probably responsible for the enhanced insulin-induced glucose utilization in femoral fat. Glucose 124-131 insulin Homo sapiens 108-115 6409929-11 1983 At the time glucose returned to base line, insulin levels (49+/-12 muU/ml) remained fourfold higher than base line (P < 0.01); thereafter they declined but never fell below base line. Glucose 12-19 insulin Homo sapiens 43-50 6645999-7 1983 Insulin secretion occurs in response to blood glucose level and could be excessive if the regulatory mechanism is overtaxed by large sugar intake. Glucose 46-53 insulin Homo sapiens 0-7 6350368-7 1983 It is proposed that the recovered thermic effect of infused insulin/glucose is due to the different contributions of gluconeogenesis in the fasting state and during the glucose clamp before and after weight loss. Glucose 68-75 insulin Homo sapiens 60-67 6350368-7 1983 It is proposed that the recovered thermic effect of infused insulin/glucose is due to the different contributions of gluconeogenesis in the fasting state and during the glucose clamp before and after weight loss. Glucose 169-176 insulin Homo sapiens 60-67 6135135-3 1983 The levels of fasting plasma insulin and the integrated insulin response to glucose were significantly greater (P less than 0.01) in obese than in nonobese Pimas. Glucose 76-83 insulin Homo sapiens 56-63 6135135-5 1983 The fractional gastric emptying rates after a glucose load were strongly correlated with the integrated responses of both plasma glucose and insulin in the nonobese Caucasians (r = 0.88, 0.90; P less than 0.01) but not in either Pima group. Glucose 46-53 insulin Homo sapiens 141-148 6224483-5 1983 Islets prelabelled with [32P]Pi and incubated with 28 mM-glucose secreted significantly more insulin and had greater incorporation of radioactivity into the 54 kDa protein than did islets incubated under basal conditions in the presence of 5 mM-glucose. Glucose 56-64 insulin Homo sapiens 93-100 6351149-8 1983 There was a significant inverse correlation between the arterial plasma glucose level and the V-A difference in PGFM concentration across the uterus during feeding, fasting and insulin infusion. Glucose 72-79 insulin Homo sapiens 177-184 6350132-6 1983 Thus, glucose tolerance improved under unchanged absolute insulin concentrations. Glucose 6-13 insulin Homo sapiens 58-65 6344653-0 1983 Estimation and kinetic analysis of insulin-independent glucose uptake in human subjects. Glucose 55-62 insulin Homo sapiens 35-42 6342138-0 1983 Glucose stimulation of the antilipolytic effect of insulin in humans. Glucose 0-7 insulin Homo sapiens 51-58 6342138-2 1983 The addition of glucose to the incubation medium was associated with an increase in insulin sensitivity and an increase in the maximum insulin effect. Glucose 16-23 insulin Homo sapiens 84-91 6342138-2 1983 The addition of glucose to the incubation medium was associated with an increase in insulin sensitivity and an increase in the maximum insulin effect. Glucose 16-23 insulin Homo sapiens 135-142 6342138-3 1983 The results suggest that glucose plays an important role in regulating the antilipolytic action of insulin in humans. Glucose 25-32 insulin Homo sapiens 99-106 6344653-2 1983 Because glucose uptake was found to be a linear function of plasma insulin at each plasma glucose concentration (r greater than 0.92, P less than 0.01), glucose uptake at 0 plasma insulin was estimated by linear regression analysis. Glucose 8-15 insulin Homo sapiens 67-74 6344653-2 1983 Because glucose uptake was found to be a linear function of plasma insulin at each plasma glucose concentration (r greater than 0.92, P less than 0.01), glucose uptake at 0 plasma insulin was estimated by linear regression analysis. Glucose 90-97 insulin Homo sapiens 67-74 6344653-2 1983 Because glucose uptake was found to be a linear function of plasma insulin at each plasma glucose concentration (r greater than 0.92, P less than 0.01), glucose uptake at 0 plasma insulin was estimated by linear regression analysis. Glucose 90-97 insulin Homo sapiens 67-74 6344653-5 1983 min-1 for plasma glucose concentrations of 60, 95, and 160 mg/dl, respectively) produced a linear Eadie-Hofstee plot, suggesting that insulin-independent glucose uptake followed Michaelis-Menten kinetics. Glucose 17-24 insulin Homo sapiens 134-141 6344653-5 1983 min-1 for plasma glucose concentrations of 60, 95, and 160 mg/dl, respectively) produced a linear Eadie-Hofstee plot, suggesting that insulin-independent glucose uptake followed Michaelis-Menten kinetics. Glucose 154-161 insulin Homo sapiens 134-141 6344653-6 1983 The Km for glucose uptake at 0 plasma insulin (congruent to 10 mM) was similar to those observed for glucose uptake at the other plasma insulin concentrations studied (congruent to 9-12 mM), but its Vmax was less (5.2 vs. 6.4, 18.5, and 26.8 mg . Glucose 11-18 insulin Homo sapiens 38-45 6344653-6 1983 The Km for glucose uptake at 0 plasma insulin (congruent to 10 mM) was similar to those observed for glucose uptake at the other plasma insulin concentrations studied (congruent to 9-12 mM), but its Vmax was less (5.2 vs. 6.4, 18.5, and 26.8 mg . Glucose 11-18 insulin Homo sapiens 136-143 6344653-10 1983 The method described herein provides an assessment of insulin-independent glucose uptake in vivo that may prove useful in distinguishing between intrinsic defects of the glucose transport system and those due to defects in insulin action. Glucose 74-81 insulin Homo sapiens 54-61 6344653-10 1983 The method described herein provides an assessment of insulin-independent glucose uptake in vivo that may prove useful in distinguishing between intrinsic defects of the glucose transport system and those due to defects in insulin action. Glucose 74-81 insulin Homo sapiens 223-230 6349736-0 1983 Insulin secretion during the glucose tolerance test in antisocial personality. Glucose 29-36 insulin Homo sapiens 0-7 6349736-1 1983 In 23 young male adults with antisocial personality, mostly guilty of violent crimes, insulin measurements during the glucose tolerance test showed an enhanced insulin secretion only in those with unsocialized aggressive conduct disorder. Glucose 118-125 insulin Homo sapiens 86-93 6354781-0 1983 Immunoglobulin from insulin-dependent diabetic children inhibits glucose-induced insulin release. Glucose 65-72 insulin Homo sapiens 20-27 6354781-0 1983 Immunoglobulin from insulin-dependent diabetic children inhibits glucose-induced insulin release. Glucose 65-72 insulin Homo sapiens 81-88 6354781-2 1983 The dynamics of insulin release in response to glucose and partially purified antibodies were determined in dispersed rat islet cells perifused on small columns of Biogel P-2 beads. Glucose 47-54 insulin Homo sapiens 16-23 6354776-5 1983 The insulin response to glucose was variable in all infants and most of them showed a delayed rise of serum insulin. Glucose 24-31 insulin Homo sapiens 4-11 6354781-3 1983 After perifusion at 5.5 mmol/L D-glucose in the presence of healthy control immunoglobulin, the rate of insulin release increased in a biphasic manner after stimulation with 30 mmol/L D-glucose. Glucose 31-40 insulin Homo sapiens 104-111 6354776-5 1983 The insulin response to glucose was variable in all infants and most of them showed a delayed rise of serum insulin. Glucose 24-31 insulin Homo sapiens 108-115 6354781-3 1983 After perifusion at 5.5 mmol/L D-glucose in the presence of healthy control immunoglobulin, the rate of insulin release increased in a biphasic manner after stimulation with 30 mmol/L D-glucose. Glucose 184-193 insulin Homo sapiens 104-111 6363048-1 1983 We examined the responses of serum free C-peptide immunoreactivity (CPR) during a 100 g oral glucose tolerance test (OGTT) on diabetic patients undergoing different kinds and durations of treatment. Glucose 93-100 insulin Homo sapiens 40-49 6420141-4 1983 Before surgery, his plasma growth hormone level was 3,000 ng/ml, glucose tolerance was almost normal and insulin response to glucose load was enhanced. Glucose 125-132 insulin Homo sapiens 105-112 6347984-6 1983 The high protein diet produced a relative improvement in plasma insulin responses for the blood glucose levels attained following the meal. Glucose 96-103 insulin Homo sapiens 64-71 6341390-4 1983 For these reasons, we speculated that the defect in adipocyte glucose transport might also be corrected with exogenous insulin therapy. Glucose 62-69 insulin Homo sapiens 119-126 6341390-13 1983 These studies demonstrated that the decrease in adipocyte glucose transport activity in type II diabetes is practically reversible by intensive insulin therapy. Glucose 58-65 insulin Homo sapiens 144-151 6345584-4 1983 Similar steady-state serum insulin levels led to a peripheral glucose disposal rate of 151+/-17 mg/m(2) per min in the elderly compared with a value of 247+/-12 mg/m(2) per min in the nonelderly, thus documenting the presence of insulin resistance in the elderly subjects. Glucose 62-69 insulin Homo sapiens 27-34 6343416-6 1983 These studies suggest that endogenous opioids contribute to glucose recovery from insulin-induced hypoglycemia and therefore may be important to glucose homeostasis in normal man. Glucose 60-67 insulin Homo sapiens 82-89 6841466-4 1983 The kinetics of blood-to-brain glucose transport were measured in animals whose blood glucose concentration had been altered by glucose or insulin injections. Glucose 31-38 insulin Homo sapiens 139-146 6136624-2 1983 A persistent hyperinsulinemia was found in patients with disordered carbohydrate metabolism, both in cases of glucose stimulation and insulin inhibition, where glandular function was assessed on the basis of S-peptide concentration as opposed to the control level. Glucose 110-117 insulin Homo sapiens 18-25 6341770-4 1983 In addition, the positive correlation between plasma glucose and plasma insulin levels observed in the physically trained subjects was significantly smaller than that note in the nontrained subjects, indicating reduced insulin requirements in physically-trained persons. Glucose 53-60 insulin Homo sapiens 72-79 6341770-4 1983 In addition, the positive correlation between plasma glucose and plasma insulin levels observed in the physically trained subjects was significantly smaller than that note in the nontrained subjects, indicating reduced insulin requirements in physically-trained persons. Glucose 53-60 insulin Homo sapiens 219-226 6341773-6 1983 After insulin was infused for four hours, serum phosphate had decreased in all subjects (P less than 0.001) and strongly correlated with glucose disposal rates (r = 0.76, P less than 0.005). Glucose 137-144 insulin Homo sapiens 6-13 6341773-9 1983 The biologic effect of insulin on glucose utilization and plasma phosphate shifts is clearly diminished. Glucose 34-41 insulin Homo sapiens 23-30 6341776-0 1983 Influence of ambient glucose and insulin concentrations on adipocyte insulin binding. Glucose 21-28 insulin Homo sapiens 69-76 6341776-9 1983 This up-regulation was seen even in a high glucose concentration (28 mM) but was completely prevented by the presence of insulin in the medium. Glucose 43-50 insulin Homo sapiens 121-128 6341776-10 1983 Furthermore, when rat adipocytes were incubated with insulin in the presence of a high glucose concentration (28 mM) there was a significant further decrease in insulin binding compared with that of parallel incubations performed in 5.6 mM glucose. Glucose 87-94 insulin Homo sapiens 53-60 6341776-10 1983 Furthermore, when rat adipocytes were incubated with insulin in the presence of a high glucose concentration (28 mM) there was a significant further decrease in insulin binding compared with that of parallel incubations performed in 5.6 mM glucose. Glucose 87-94 insulin Homo sapiens 161-168 6341776-10 1983 Furthermore, when rat adipocytes were incubated with insulin in the presence of a high glucose concentration (28 mM) there was a significant further decrease in insulin binding compared with that of parallel incubations performed in 5.6 mM glucose. Glucose 240-247 insulin Homo sapiens 53-60 6341776-10 1983 Furthermore, when rat adipocytes were incubated with insulin in the presence of a high glucose concentration (28 mM) there was a significant further decrease in insulin binding compared with that of parallel incubations performed in 5.6 mM glucose. Glucose 240-247 insulin Homo sapiens 161-168 6341777-4 1983 Intravenous glucose required to maintain basal blood glucose levels (4.2 +/- 0.1 mmole/liter) during insulin infusion was 34.3 +/- 3.0 gm with a mean rate of 273 +/- 29 mg/min in the second hour of insulin infusion. Glucose 12-19 insulin Homo sapiens 101-108 6341777-4 1983 Intravenous glucose required to maintain basal blood glucose levels (4.2 +/- 0.1 mmole/liter) during insulin infusion was 34.3 +/- 3.0 gm with a mean rate of 273 +/- 29 mg/min in the second hour of insulin infusion. Glucose 12-19 insulin Homo sapiens 198-205 6341879-3 1983 Eight had an excessive insulin response to a glucose challenge. Glucose 45-52 insulin Homo sapiens 23-30 6351440-3 1983 The complexity of the regimen necessary for successful control of blood glucose levels depends largely on a patient"s relative deficiency of endogenous insulin. Glucose 72-79 insulin Homo sapiens 152-159 6353497-0 1983 [Plasma insulin following a glucose overload in patients with Klinefelter"s syndrome]. Glucose 28-35 insulin Homo sapiens 8-15 6342388-4 1983 Insulin significantly increased HDL-C and body weight, and decreased glucose, triglycerides and LDL-C. Changes in HDL-C showed a significant inverse association with changes in triglycerides and direct correlation with changes in body weight, but no significant association with changes in fasting serum glucose or LDL-C. Glucose 69-76 insulin Homo sapiens 0-7 6342388-4 1983 Insulin significantly increased HDL-C and body weight, and decreased glucose, triglycerides and LDL-C. Changes in HDL-C showed a significant inverse association with changes in triglycerides and direct correlation with changes in body weight, but no significant association with changes in fasting serum glucose or LDL-C. Glucose 304-311 insulin Homo sapiens 0-7 6307614-3 1983 This decrease in fasting glucose was achieved along with the discontinuation of oral hypoglycemic agents in 24 of 31 patients and of insulin in 13 of 18 patients; one patient was placed on insulin. Glucose 25-32 insulin Homo sapiens 133-140 6307614-3 1983 This decrease in fasting glucose was achieved along with the discontinuation of oral hypoglycemic agents in 24 of 31 patients and of insulin in 13 of 18 patients; one patient was placed on insulin. Glucose 25-32 insulin Homo sapiens 189-196 6339152-0 1983 Insulin-induced glucose utilization influences triglyceride metabolism. Glucose 16-23 insulin Homo sapiens 0-7 6339152-2 1983 We have investigated the possibility that the effect of insulin on triglyceride metabolism is related to the individual"s responsiveness to insulin-mediated glucose utilization. Glucose 157-164 insulin Homo sapiens 56-63 6339152-2 1983 We have investigated the possibility that the effect of insulin on triglyceride metabolism is related to the individual"s responsiveness to insulin-mediated glucose utilization. Glucose 157-164 insulin Homo sapiens 140-147 6339152-11 1983 Resistance to insulin (in terms of glucose utilization) may therefore be one significant, independent factor determining the plasma triglyceride concentration. Glucose 35-42 insulin Homo sapiens 14-21 6341122-5 1983 From 2400-0300 to 0600-0900 h, mean insulin infusion rates required to maintain blood glucose values between 109 and 120 mg/dl increased by 0.21 +/- 0.05 mU/kg/min during the SAL infusion, and 0.16 +/- 0.04 mU/kg/min during the DEX infusion, when plasma cortisols were suppressed to less than or equal to 2 micrograms/dl. Glucose 86-93 insulin Homo sapiens 36-43 6341122-8 1983 We conclude that the nocturnal variability in insulin requirements persists despite suppression of the pituitary-adrenocortical axis, and that increased free insulin clearance or degradation may contribute to the "dawn phenomenon" of rising prebreakfast glucose despite constant insulin infusion. Glucose 254-261 insulin Homo sapiens 158-165 6341122-8 1983 We conclude that the nocturnal variability in insulin requirements persists despite suppression of the pituitary-adrenocortical axis, and that increased free insulin clearance or degradation may contribute to the "dawn phenomenon" of rising prebreakfast glucose despite constant insulin infusion. Glucose 254-261 insulin Homo sapiens 158-165 6341123-0 1983 Demonstration of a relationship between level of physical training and insulin-stimulated glucose utilization in normal humans. Glucose 90-97 insulin Homo sapiens 71-78 6341123-1 1983 The relationship between level of physical training and in vivo insulin-stimulated glucose utilization was investigated in 33 healthy nonobese subjects. Glucose 83-90 insulin Homo sapiens 64-71 6341123-4 1983 This relationship was independent of age and obesity and accounted for over 40% of the variance in insulin-stimulated glucose utilization among these subjects. Glucose 118-125 insulin Homo sapiens 99-106 6341123-5 1983 In addition, significant correlations existed between VO2 max and the plasma glucose (r = -0.35, P less than 0.05) and insulin (r = -0.37, P less than 0.05) responses to an oral glucose load. Glucose 178-185 insulin Homo sapiens 119-126 6341127-0 1983 Discrepancy between plasma C-peptide and insulin response to oral and intravenous glucose. Glucose 82-89 insulin Homo sapiens 27-36 6341127-0 1983 Discrepancy between plasma C-peptide and insulin response to oral and intravenous glucose. Glucose 82-89 insulin Homo sapiens 41-48 6341127-1 1983 Plasma insulin, proinsulin, and C-peptide responses to 25 g glucose orally and intravenously administered were measured in 10 healthy males. Glucose 60-67 insulin Homo sapiens 32-41 6341127-4 1983 The higher plasma insulin response after oral glucose was not due to crossreactivity with proinsulin in the insulin assay. Glucose 46-53 insulin Homo sapiens 18-25 6341127-5 1983 These results suggest that the higher plasma insulin response during an oral glucose load is due at least partially to a lower hepatic extraction of insulin. Glucose 77-84 insulin Homo sapiens 45-52 6341127-5 1983 These results suggest that the higher plasma insulin response during an oral glucose load is due at least partially to a lower hepatic extraction of insulin. Glucose 77-84 insulin Homo sapiens 149-156 6347779-4 1983 Considering the values at 23.00 h as reference, interruption of the insulin infusion resulted in (1) a rapid decrease in plasma free insulin significant after 1 h and reaching a nadir of 6 +/- 2 mU/l after 6 h; (2) a rise in blood glucose which was significant at hour 3 and reached 17.4 +/- 1.9 mmol/l at hour 6; (3) a moderate increase in plasma nonesterified fatty acids which remained in the range of 700-800 mumol/l; (4) an early and linear rise in plasma 3-hydroxybutyrate, significant after 1 h and averaging 1290 +/- 140 mumol/l after 6 h; (5) a late increase (hour 5) in plasma glucagon. Glucose 231-238 insulin Homo sapiens 68-75 6347780-1 1983 One of the reasons for the variability of blood glucose regulation in Type 1 (insulin-dependent) diabetic patients is the huge variation in subcutaneous absorption of intermediate-acting insulin. Glucose 48-55 insulin Homo sapiens 78-85 6347780-9 1983 Compared with the known large variability in the absorption of intermediate-acting insulin, continuous subcutaneous insulin infusion offers a precise and reproducible way of insulin administration resulting in post-prandial serum insulin peaks sufficient to maintain near-normal blood glucose levels. Glucose 285-292 insulin Homo sapiens 116-123 6347780-9 1983 Compared with the known large variability in the absorption of intermediate-acting insulin, continuous subcutaneous insulin infusion offers a precise and reproducible way of insulin administration resulting in post-prandial serum insulin peaks sufficient to maintain near-normal blood glucose levels. Glucose 285-292 insulin Homo sapiens 116-123 6347780-9 1983 Compared with the known large variability in the absorption of intermediate-acting insulin, continuous subcutaneous insulin infusion offers a precise and reproducible way of insulin administration resulting in post-prandial serum insulin peaks sufficient to maintain near-normal blood glucose levels. Glucose 285-292 insulin Homo sapiens 116-123 6347783-3 1983 During insulin withdrawal, the patients who best maintained their circulating free insulin levels showed the smallest increases in blood glucose and 3-hydroxybutyrate concentrations. Glucose 137-144 insulin Homo sapiens 7-14 6352348-4 1983 No changes were observed concerning weight, total body K, skinfold tolerance, which was strictly normal before training, remained unchanged, but the insulin response to the oral glucose load decreased by 24% (2 p less than 0.025). Glucose 178-185 insulin Homo sapiens 149-156 6352348-6 1983 IN CONCLUSION: a 6 week training period, performed on strictly healthy young males, studied at rest, induced an increase in VO2 max, a decrease in plasma triglycerides and a lower insulin response to oral glucose while glucose tolerance and exogenous glucose oxidation remained unchanged. Glucose 205-212 insulin Homo sapiens 180-187 6400673-3 1983 In uncontrolled insulin-dependent diabetics, normalization of plasma glucose by an insulin infusion improves red cell deformability in 2 h. Insulin infusion (0.2 U/kg/h) [the initial hyperglycemia being maintained (hyperglycemic clamp)] also improves red cell deformability. Glucose 69-76 insulin Homo sapiens 140-147 6413265-4 1983 There was a significant decrease in fasting and glucose-stimulated insulin levels after two years of glibenclamide treatment in both the normal and low insulin-responders. Glucose 48-55 insulin Homo sapiens 67-74 6861627-7 1983 However, glucose acts as a further stimulus of insulin release from a sulfonylurea-primed pancreas. Glucose 9-16 insulin Homo sapiens 47-54 6350027-1 1983 We studied the insulin sensitivity in 5 normal subjects and 5 subjects with impaired carbohydrate tolerance using the glucose controlled insulin infusion system (BIOSTATOR). Glucose 118-125 insulin Homo sapiens 15-22 6350027-1 1983 We studied the insulin sensitivity in 5 normal subjects and 5 subjects with impaired carbohydrate tolerance using the glucose controlled insulin infusion system (BIOSTATOR). Glucose 118-125 insulin Homo sapiens 137-144 6350027-4 1983 Calculating the average insulin glucose ratio for 24 hours, the mean values amounted to 3531 and 9319 ng/gm (p less than 0.01) in subjects with normal and impaired carbohydrate tolerance, respectively, indicating that insulin resistance is the main cause of decreased glucose utilization in the latter group. Glucose 32-39 insulin Homo sapiens 24-31 6350027-4 1983 Calculating the average insulin glucose ratio for 24 hours, the mean values amounted to 3531 and 9319 ng/gm (p less than 0.01) in subjects with normal and impaired carbohydrate tolerance, respectively, indicating that insulin resistance is the main cause of decreased glucose utilization in the latter group. Glucose 32-39 insulin Homo sapiens 218-225 6350027-4 1983 Calculating the average insulin glucose ratio for 24 hours, the mean values amounted to 3531 and 9319 ng/gm (p less than 0.01) in subjects with normal and impaired carbohydrate tolerance, respectively, indicating that insulin resistance is the main cause of decreased glucose utilization in the latter group. Glucose 268-275 insulin Homo sapiens 24-31 6350027-4 1983 Calculating the average insulin glucose ratio for 24 hours, the mean values amounted to 3531 and 9319 ng/gm (p less than 0.01) in subjects with normal and impaired carbohydrate tolerance, respectively, indicating that insulin resistance is the main cause of decreased glucose utilization in the latter group. Glucose 268-275 insulin Homo sapiens 218-225 6339540-9 1983 It is concluded that nonselective beta-blockade prolongs the hypoglycemic response to insulin through an increased tissue uptake of glucose which is not counteracted by an increased glucose production. Glucose 132-139 insulin Homo sapiens 86-93 6339540-9 1983 It is concluded that nonselective beta-blockade prolongs the hypoglycemic response to insulin through an increased tissue uptake of glucose which is not counteracted by an increased glucose production. Glucose 182-189 insulin Homo sapiens 86-93 6341382-5 1983 Insulin inhibits degradation of long-lived proteins in the presence or absence of glucose and amino acids in the medium, but is maximally effective only at high concentrations (10(-5) M). Glucose 82-89 insulin Homo sapiens 0-7 6341759-0 1983 Plasma glucose and insulin responses to oral glucose in nonobese subjects and patients with endogenous hypertriglyceridemia. Glucose 45-52 insulin Homo sapiens 19-26 6341759-4 1983 Similar findings were also observed in patients with endogenous hypertriglyceridemia whose index of obesity was between 1.1 and 1.2, ie, there was a 25% increase in the plasma glucose response (P less than 0.001) and a 37% increase in the plasma insulin response (P less than 0.001). Glucose 176-183 insulin Homo sapiens 246-253 6341765-0 1983 Propranolol and hyperthyroidism: serum free fatty acids and glucose-induced insulin release in nondiabetic thyrotoxic patients during treatment to clinical compensation. Glucose 60-67 insulin Homo sapiens 76-83 6341765-8 1983 Both the increased levels of FFA and of T3 could be involved in this pattern of the insulin response of nondiabetic thyrotoxic patients, since the secretion of insulin during the first 10 min after intravenous glucose was directly correlated to fasting serum FFA before propranolol, and serum T3 was directly correlated with total insulin response after clinical compensation. Glucose 210-217 insulin Homo sapiens 84-91 6341765-8 1983 Both the increased levels of FFA and of T3 could be involved in this pattern of the insulin response of nondiabetic thyrotoxic patients, since the secretion of insulin during the first 10 min after intravenous glucose was directly correlated to fasting serum FFA before propranolol, and serum T3 was directly correlated with total insulin response after clinical compensation. Glucose 210-217 insulin Homo sapiens 160-167 6341765-8 1983 Both the increased levels of FFA and of T3 could be involved in this pattern of the insulin response of nondiabetic thyrotoxic patients, since the secretion of insulin during the first 10 min after intravenous glucose was directly correlated to fasting serum FFA before propranolol, and serum T3 was directly correlated with total insulin response after clinical compensation. Glucose 210-217 insulin Homo sapiens 160-167 6341766-4 1983 The amount of insulin needed to maintain normoglycemia in subjects with insulin-dependent diabetes, studied with a glucose controlled insulin infusion system was generally the same with human and pork insulin. Glucose 115-122 insulin Homo sapiens 14-21 6352998-0 1983 [Glucose intolerance associated with aging: tissue sensitivity to insulin assessed by euglycemic glucose clamp]. Glucose 1-8 insulin Homo sapiens 66-73 6352998-0 1983 [Glucose intolerance associated with aging: tissue sensitivity to insulin assessed by euglycemic glucose clamp]. Glucose 97-104 insulin Homo sapiens 66-73 6367014-2 1983 The patients had normal fasting serum levels of insulin and normal insulin response to intravenous glucose loading. Glucose 99-106 insulin Homo sapiens 67-74 6191388-6 1983 Insulin release is enhanced due to an increase in the sensitivity of the B-cell to glucose challenge. Glucose 83-90 insulin Homo sapiens 0-7 6404377-0 1983 Intermediate acting insulin given at bedtime: effect on blood glucose concentrations before and after breakfast. Glucose 62-69 insulin Homo sapiens 20-27 6404377-8 1983 By contrast, when the evening dose of intermediate acting insulin was delayed until bedtime the nocturnal rise in blood glucose concentration started later and was significantly lower both fasting (7 . Glucose 120-127 insulin Homo sapiens 58-65 6342324-0 1983 Relation between plasma insulin and blood glucose in a cross-sectional population study of the oral glucose tolerance test. Glucose 42-49 insulin Homo sapiens 24-31 6349202-10 1983 Insulin response to oral glucose was lower than the one to IVGTT, probably because of diminished secretion of the gastrointestinal hormones which stimulate insulin release. Glucose 25-32 insulin Homo sapiens 0-7 6349202-10 1983 Insulin response to oral glucose was lower than the one to IVGTT, probably because of diminished secretion of the gastrointestinal hormones which stimulate insulin release. Glucose 25-32 insulin Homo sapiens 156-163 6340456-6 1983 Glucose storage during the insulin clamp (ie, glucose uptake minus glucose oxidation) was 0.13, 0.33, and 0.40 g/min for each group and exogenous lipid storage was 0.17, 0.18, and 0.19 g/min, respectively. Glucose 0-7 insulin Homo sapiens 27-34 6346801-12 1983 In surviving rats from dosage groups 20 and 200 U/kg/day of either insulin preparation higher plasma glucose levels than in the control were observed 24 hours after dosing. Glucose 101-108 insulin Homo sapiens 67-74 6340630-8 1983 A glucose tolerance test demonstrated fasting hyperinsulinemia and exaggerated serum insulin response to the glucose load. Glucose 2-9 insulin Homo sapiens 51-58 6347438-0 1983 Insulin sensitivity in hyperthyroidism: measurement by the glucose clamp technique. Glucose 59-66 insulin Homo sapiens 0-7 6347438-9 1983 These findings suggest that insulin-stimulated glucose metabolism and inhibition of ketogenesis are normal in hyperthyroidism. Glucose 47-54 insulin Homo sapiens 28-35 6134651-8 1983 In comparison with control subjects, insulin release was normal in response to arginine and tolbutamide but was reduced in response to oral and intravenous glucose, while glucagon and growth hormone release were similar in both groups. Glucose 156-163 insulin Homo sapiens 37-44 6345247-3 1983 Stimulation of insulin secretion by intravenous glucose, tolbutamide or sodium salicylate increased the amplitude of the insulin oscillations while the frequency remained stable. Glucose 48-55 insulin Homo sapiens 15-22 6345247-4 1983 Patients with a truncal vagotomy or after Whipple"s operation had longer-term oscillations of 33 and 37 min periodicity (autocorrelation: p less than 0.0001), with insulin-associated glucose swings four times larger than those of normal subjects. Glucose 183-190 insulin Homo sapiens 164-171 6345247-5 1983 Type 2 (non-insulin-dependent) diabetic patients had a similarly increased insulin-associated glucose swing of six times that seen in normal subjects. Glucose 94-101 insulin Homo sapiens 12-19 6345247-5 1983 Type 2 (non-insulin-dependent) diabetic patients had a similarly increased insulin-associated glucose swing of six times that seen in normal subjects. Glucose 94-101 insulin Homo sapiens 75-82 6345247-6 1983 The hypothesis is proposed that the 14-min cycle of insulin production is controlled by a "pacemaker" which assists glucose homeostasis. Glucose 116-123 insulin Homo sapiens 52-59 6357771-3 1983 Five months after the onset of diabetes, oral glucose produced a small increase in insulin and a paradoxical rise in both glucagon immunoreactivity (GI) and growth hormone (GH). Glucose 46-53 insulin Homo sapiens 83-90 6339536-1 1983 [125I]Insulin binding to insulin receptors on circulating monocytes was studied in 9 patients with acromegaly associated with fasting hyperglycemia and was compared to previously reported studies of 11 patients with acromegaly who had normal or nearly normal glucose tolerance and 29 normal volunteers. Glucose 259-266 insulin Homo sapiens 25-32 6339560-10 1983 These observations demonstrate that conventional insulin therapy is effective in facilitating glucose entry into muscle. Glucose 94-101 insulin Homo sapiens 49-56 6833952-3 1983 The resistance appears to reflect a post-receptor interference with the insulin-induced biosynthesis of the anabolic enzymes, acetyl Co-A carboxylase and fatty acid synthetase, which are required for the conversion of glucose into storage lipid. Glucose 218-225 insulin Homo sapiens 72-79 6403135-3 1983 The ratio of insulin to C-peptide concentrations doubled 30 minutes after oral glucose was given; no comparable rise was seen with intravenous glucose (p = 0.01). Glucose 79-86 insulin Homo sapiens 13-20 6403135-4 1983 This finding is interpreted as evidence for decreased hepatic extraction of insulin after administration of oral glucose. Glucose 113-120 insulin Homo sapiens 76-83 6338676-0 1983 Further support for heterogeneity of insulin response and insulin sensitivity in non-obese subjects with glucose intolerance. Glucose 105-112 insulin Homo sapiens 37-44 6338676-0 1983 Further support for heterogeneity of insulin response and insulin sensitivity in non-obese subjects with glucose intolerance. Glucose 105-112 insulin Homo sapiens 58-65 6338676-2 1983 Insulin response was studied by means of a 2 h glucose infusion. Glucose 47-54 insulin Homo sapiens 0-7 6338676-5 1983 In patients with glucose intolerance the early (delta IRI area 0-5 min) and late (delta IRI area 30-120 min) insulin responses to iv glucose were significantly reduced in comparison to controls. Glucose 17-24 insulin Homo sapiens 109-116 6338676-5 1983 In patients with glucose intolerance the early (delta IRI area 0-5 min) and late (delta IRI area 30-120 min) insulin responses to iv glucose were significantly reduced in comparison to controls. Glucose 133-140 insulin Homo sapiens 109-116 6338676-6 1983 Controls and subjects with glucose intolerance showed considerable heterogeneity of insulin responses. Glucose 27-34 insulin Homo sapiens 84-91 6338676-9 1983 There was a weak significant inverse correlation between insulin response to glucose and insulin sensitivity for the two groups combined and for controls and subjects with glucose intolerance separately. Glucose 77-84 insulin Homo sapiens 57-64 6338676-9 1983 There was a weak significant inverse correlation between insulin response to glucose and insulin sensitivity for the two groups combined and for controls and subjects with glucose intolerance separately. Glucose 77-84 insulin Homo sapiens 89-96 6338676-9 1983 There was a weak significant inverse correlation between insulin response to glucose and insulin sensitivity for the two groups combined and for controls and subjects with glucose intolerance separately. Glucose 172-179 insulin Homo sapiens 57-64 6338677-2 1983 This induced a deterioration of the glucose tolerance with higher levels of glucose, insulin and C-peptide. Glucose 36-43 insulin Homo sapiens 85-92 6338677-2 1983 This induced a deterioration of the glucose tolerance with higher levels of glucose, insulin and C-peptide. Glucose 36-43 insulin Homo sapiens 97-106 6338736-3 1983 Total body glucose uptake during each of the five insulin clamp studies was 0.41, 0.50, 0.66, 0.74, and 0.77 g/min, respectively. Glucose 11-18 insulin Homo sapiens 50-57 6339093-5 1983 These results suggested that although the blood glucose level was considered to be one of the important factors influencing the retinal circulation, insulin had a direct effect on the platelet function in improving the retinal circulation in addition to lowering the blood glucose level. Glucose 273-280 insulin Homo sapiens 149-156 6133710-4 1983 The plasma glucose, C-peptide, and insulin (immunoreactive) responses to human insulin and porcine insulin were identical in the studies with and without somatostatin. Glucose 11-18 insulin Homo sapiens 79-86 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 79-86 insulin Homo sapiens 248-255 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 79-86 insulin Homo sapiens 338-345 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 165-172 insulin Homo sapiens 248-255 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 165-172 insulin Homo sapiens 338-345 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 165-172 insulin Homo sapiens 248-255 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 165-172 insulin Homo sapiens 338-345 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 165-172 insulin Homo sapiens 248-255 6345584-11 1983 Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. Glucose 165-172 insulin Homo sapiens 338-345 6345584-12 1983 This carbohydrate intolerance appears to be the consequence of peripheral insulin resistance caused by a postreceptor defect in target tissue insulin action, which causes both a decrease in the maximal rate of peripheral glucose disposal and a rightward shift in the insulin action dose-response curve. Glucose 221-228 insulin Homo sapiens 74-81 6345584-12 1983 This carbohydrate intolerance appears to be the consequence of peripheral insulin resistance caused by a postreceptor defect in target tissue insulin action, which causes both a decrease in the maximal rate of peripheral glucose disposal and a rightward shift in the insulin action dose-response curve. Glucose 221-228 insulin Homo sapiens 142-149 6345584-12 1983 This carbohydrate intolerance appears to be the consequence of peripheral insulin resistance caused by a postreceptor defect in target tissue insulin action, which causes both a decrease in the maximal rate of peripheral glucose disposal and a rightward shift in the insulin action dose-response curve. Glucose 221-228 insulin Homo sapiens 142-149 6345585-1 1983 To clarify the nature of the insulin resistance of aging we studied the dose response for insulin-induced glucose disposal and the binding of insulin to circulating monocytes in healthy young and old men. Glucose 106-113 insulin Homo sapiens 90-97 6345585-1 1983 To clarify the nature of the insulin resistance of aging we studied the dose response for insulin-induced glucose disposal and the binding of insulin to circulating monocytes in healthy young and old men. Glucose 106-113 insulin Homo sapiens 90-97 6133710-4 1983 The plasma glucose, C-peptide, and insulin (immunoreactive) responses to human insulin and porcine insulin were identical in the studies with and without somatostatin. Glucose 11-18 insulin Homo sapiens 79-86 6337902-5 1983 The two major sources of confusion have been failure to distinguish glucose-induced acute insulin responses from insulin secretion in general and failure to appreciate that the behavior of indomethacin is not consistent with the effects of other nonsteroidal antiinflammatory drugs (cyclooxygenase inhibitors) on glucose homeostasis and insulin secretion. Glucose 68-75 insulin Homo sapiens 90-97 6341144-7 1983 Our data suggest that growth hormone excess rapidly produces insulin antagonistic effects that may contribute to stress-induced glucose intolerance and lipolysis, even though fasting glucose levels remain unchanged. Glucose 128-135 insulin Homo sapiens 61-68 6341390-14 1983 This closely corresponds to the reversal by insulin therapy of the postreceptor defect expressed in vivo and provides further evidence that a cellular cause of the postreceptor defect in type II diabetes is a decrease in glucose transport system activity in the major insulin target tissues. Glucose 221-228 insulin Homo sapiens 44-51 6343024-0 1983 Normalization of fasting blood glucose levels in insulin-requiring diabetes: the role of ethanol abstention. Glucose 31-38 insulin Homo sapiens 49-56 6343025-0 1983 Comparison of the biologic activity of porcine and semisynthetic human insulins using the glucose-controlled insulin infusion system in insulin-dependent diabetes. Glucose 90-97 insulin Homo sapiens 71-78 6341390-14 1983 This closely corresponds to the reversal by insulin therapy of the postreceptor defect expressed in vivo and provides further evidence that a cellular cause of the postreceptor defect in type II diabetes is a decrease in glucose transport system activity in the major insulin target tissues. Glucose 221-228 insulin Homo sapiens 268-275 6341392-3 1983 Three dosages of oral glucose (10, 25, and 100 g) administered to normal volunteers resulted in 1.8 +/- 0.5, 2.7 +/- 1.1, and 7.2 +/- 1.6 U endogenous insulin secretion, respectively. Glucose 22-29 insulin Homo sapiens 151-158 6341392-5 1983 Decreasing insulin extraction by the liver (67-53-42%) in the presence of increasing insulin exposure (2.6-4.4-13.2 U) was observed during the dose-response to glucose. Glucose 160-167 insulin Homo sapiens 11-18 6341392-5 1983 Decreasing insulin extraction by the liver (67-53-42%) in the presence of increasing insulin exposure (2.6-4.4-13.2 U) was observed during the dose-response to glucose. Glucose 160-167 insulin Homo sapiens 85-92 6345584-2 1983 Serum glucose and insulin levels were significantly elevated in the elderly subjects compared with the nonelderly subjects during a 75-g oral glucose tolerance test, suggesting an insulin resistant state. Glucose 6-13 insulin Homo sapiens 180-187 6345584-2 1983 Serum glucose and insulin levels were significantly elevated in the elderly subjects compared with the nonelderly subjects during a 75-g oral glucose tolerance test, suggesting an insulin resistant state. Glucose 142-149 insulin Homo sapiens 18-25 6345584-2 1983 Serum glucose and insulin levels were significantly elevated in the elderly subjects compared with the nonelderly subjects during a 75-g oral glucose tolerance test, suggesting an insulin resistant state. Glucose 142-149 insulin Homo sapiens 180-187 6338038-4 1983 During glucose infusion (5.6 +/- 0.3 mg X kg-1 min-1), compared with saline controls, the preterms had a rise in plasma glucose and plasma insulin, and the GPR was 1.4 mg X kg-1 min-1 (range, 0-4.4) vs. 3.0 mg X kg-1 min-1 (range, 1.8-4.1) (saline controls). Glucose 7-14 insulin Homo sapiens 139-146 6338038-5 1983 In the term infants, only the plasma insulin concentration was elevated when the glucose infused (5.7 +/- 0.3 mg X kg-1 min-1) infants were compared with the saline controls and GPR was 0.4 X kg-1 min-1 (range, 0-2.6) vs. 3.4 mg X kg-1 min-1 (range, 2.8-5.7) (saline controls). Glucose 81-88 insulin Homo sapiens 37-44 6338038-6 1983 In comparison to saline infused adults, glucose infusion (3.2 +/- 0.1 mg X kg-1 min-1) resulted in a significant rise in plasma glucose and in plasma insulin; and the GPR was reduced to 0.1 mg X kg-1 min-1 (range, 0-0.3) from 2.0 mg X kg-1 min-1 (range, 1.5-2.4). Glucose 40-47 insulin Homo sapiens 150-157 6338042-9 1983 Stepwise regression analysis revealed that both LDL SR and FCR correlated positively and linearly with insulin response to glucose loading, but negatively and curvilinearly with fasting plasma glucose and glucose response. Glucose 123-130 insulin Homo sapiens 103-110 6338045-0 1983 Marked increase in insulin sensitivity of human fat cells 1 hour after glucose ingestion. Glucose 71-78 insulin Homo sapiens 19-26 6338045-1 1983 The effect of glucose ingestion on insulin action was investigated in isolated human fat cells. Glucose 14-21 insulin Homo sapiens 35-42 6338045-4 1983 Insulin binding increased significantly by 20-30% after glucose ingestion. Glucose 56-63 insulin Homo sapiens 0-7 6338045-6 1983 The concentration of insulin producing half-maximum inhibition (ED(50)) of basal lipolysis was 50 muU/ml before and 0.25 muU/ml after glucose ingestion (P < 0.01), which represented a 200-fold difference. Glucose 134-141 insulin Homo sapiens 21-28 6338045-7 1983 As regards isoprenaline-induced lipolysis, the ED(50) for insulin inhibition was 30 muU/ml before and 2.5 muU/ml after oral glucose (P < 0.01), which was a 12-fold difference. Glucose 124-131 insulin Homo sapiens 58-65 6338045-9 1983 It is concluded that glucose ingestion is accompanied by a marked increase in insulin sensitivity of human fat cells and this may be an important modulating factor in the overall scheme of insulin action. Glucose 21-28 insulin Homo sapiens 78-85 6338045-9 1983 It is concluded that glucose ingestion is accompanied by a marked increase in insulin sensitivity of human fat cells and this may be an important modulating factor in the overall scheme of insulin action. Glucose 21-28 insulin Homo sapiens 189-196 6827417-6 1983 In a detailed study of 19 infants who received glucose, the highly significant (P less than 0.001) fall in SI (delta = -3.7%) was accompanied by an equally significant rise in serum values for insulin (delta = +21.6 mcu/ml) and fall in serum free fatty acids (delta = -0.51 mEq/L). Glucose 47-54 insulin Homo sapiens 193-200 6402554-0 1983 Reciprocal changes in plasma glucose and serum calcium levels during glucose and insulin administration. Glucose 29-36 insulin Homo sapiens 81-88 6338491-3 1983 In type I diabetes, blood glucose levels should be controlled as rigidly as possible with multiple insulin injections and self-monitoring of glucose level. Glucose 26-33 insulin Homo sapiens 99-106 6340405-10 1983 Plasma levels of NEFA and 3-HB remained unchanged, whereas glucose and insulin decreased after rehydration with glucose-free solutions, i.e. Ringer, Ringer lactate and Ringerdex. Glucose 112-119 insulin Homo sapiens 71-78 6612073-0 1983 [Hyperinsulinism and insulin resistance diagnosed by oral and intravenous glucose loading and by the tolbutamide test in polycystic ovary syndrome]. Glucose 74-81 insulin Homo sapiens 6-13 6344327-5 1983 This exaggerated GIP response to an oral glucose load in proportion to the glucose intolerance indicates a relative failure of the beta cell response to GIP in diabetics and that the mechanism involved in hypersecretion of GIP would be diminution of the inhibition of GIP release caused by insulin in diabetics. Glucose 41-48 insulin Homo sapiens 290-297 6351380-0 1983 Insulin response to oral glucose in young African and Indian noninsulin-dependent diabetic patients in Natal. Glucose 25-32 insulin Homo sapiens 0-7 6351380-1 1983 The insulin response to an oral glucose load was studied in 24 Indian and 14 African patients with NIDDM and 20 controls. Glucose 32-39 insulin Homo sapiens 4-11 6351380-2 1983 The maximal insulin levels attained during the glucose tolerance test were significantly lower, and the peak insulin response occurred later in the diabetic patients compared to controls. Glucose 47-54 insulin Homo sapiens 12-19 6343025-8 1983 These studies indicate that semisynthetic human insulin is as effective as porcine insulin in maintaining near-normal blood glucose control in short-term intravenous studies using artificial pancreas techniques in insulin-dependent diabetes. Glucose 124-131 insulin Homo sapiens 48-55 6343032-11 1983 The plasma glucose-reducing effect was slightly greater after s.c. injection of 0.05 U/kg of human insulin than after s.c. injection of the same dose of porcine insulin. Glucose 11-18 insulin Homo sapiens 99-106 6343032-11 1983 The plasma glucose-reducing effect was slightly greater after s.c. injection of 0.05 U/kg of human insulin than after s.c. injection of the same dose of porcine insulin. Glucose 11-18 insulin Homo sapiens 161-168 6343033-1 1983 Using the glucose clamp technique, human insulin (Novo) and natural porcine insulin were found to have identical potency in terms of glucose delivery in the second hour of i.v. Glucose 133-140 insulin Homo sapiens 41-48 6343033-1 1983 Using the glucose clamp technique, human insulin (Novo) and natural porcine insulin were found to have identical potency in terms of glucose delivery in the second hour of i.v. Glucose 133-140 insulin Homo sapiens 76-83 6343033-5 1983 Glucose requirement to maintain normoglycemia for the first 5 h after injection was 49.6 +/- 8.2 g for conventional bovine insulin, 50.4 +/- 10.0 g for highly purified bovine, 40.5 +/- 6.9 g for human insulin, and 50.6 +/- 12.4 g for porcine insulin (NS by analysis of variance). Glucose 0-7 insulin Homo sapiens 201-218 6343033-5 1983 Glucose requirement to maintain normoglycemia for the first 5 h after injection was 49.6 +/- 8.2 g for conventional bovine insulin, 50.4 +/- 10.0 g for highly purified bovine, 40.5 +/- 6.9 g for human insulin, and 50.6 +/- 12.4 g for porcine insulin (NS by analysis of variance). Glucose 0-7 insulin Homo sapiens 201-208 6343034-2 1983 Evaluation was carried out through three methods: (1) glucose-controlled insulin infusion system on two separate days during the patients" ingestion of mixed meals; (2) euglycemic clamp method; and (3) evaluation of patients for 3 mo using short- and intermediate-acting insulins. Glucose 54-61 insulin Homo sapiens 73-80 6343034-3 1983 Employing the glucose-controlled insulin infusion system resulted in mean daily insulin requirements of 84 +/- 9 U and 85 +/- 6 U SEM for porcine and human insulin, respectively (P = NS). Glucose 14-21 insulin Homo sapiens 33-40 6343034-3 1983 Employing the glucose-controlled insulin infusion system resulted in mean daily insulin requirements of 84 +/- 9 U and 85 +/- 6 U SEM for porcine and human insulin, respectively (P = NS). Glucose 14-21 insulin Homo sapiens 80-87 6343034-3 1983 Employing the glucose-controlled insulin infusion system resulted in mean daily insulin requirements of 84 +/- 9 U and 85 +/- 6 U SEM for porcine and human insulin, respectively (P = NS). Glucose 14-21 insulin Homo sapiens 80-87 6343034-5 1983 At each insulin infusion rate, the steady-state glucose infusion rates for porcine insulin were 1.12 +/- 0.22, 1.90 +/- 0.58, 4.28 +/- 0.61, and 9.37 +/- 0.66 mg/kg/min compared with 1.27 +/- 0.42, 2.38 +/- 0.20, 4.25 +/- 0.43, and 8.87 +/- 0.67 mg/kg/min for human insulin. Glucose 48-55 insulin Homo sapiens 83-90 6343034-5 1983 At each insulin infusion rate, the steady-state glucose infusion rates for porcine insulin were 1.12 +/- 0.22, 1.90 +/- 0.58, 4.28 +/- 0.61, and 9.37 +/- 0.66 mg/kg/min compared with 1.27 +/- 0.42, 2.38 +/- 0.20, 4.25 +/- 0.43, and 8.87 +/- 0.67 mg/kg/min for human insulin. Glucose 48-55 insulin Homo sapiens 83-90 6343039-2 1983 Although both insulin regimens resulted in similar plasma glucose profiles, values were lower during the night with porcine insulin treatment. Glucose 58-65 insulin Homo sapiens 14-21 6343039-3 1983 These differences in plasma glucose response may represent an increased effectiveness of porcine insulin. Glucose 28-35 insulin Homo sapiens 97-104 6343039-5 1983 Also, the potency of the porcine insulin used was greater than that of the human insulin and may have contributed to the differences in glucose response. Glucose 136-143 insulin Homo sapiens 33-40 6343039-5 1983 Also, the potency of the porcine insulin used was greater than that of the human insulin and may have contributed to the differences in glucose response. Glucose 136-143 insulin Homo sapiens 81-88 6337541-8 1983 When chronic overtreatment is suspected, insulin therapy must be modified to better approximate physiologic needs for glucose disposal. Glucose 118-125 insulin Homo sapiens 41-48 6337579-1 1983 The glucose response to a standard insulin tolerance test (ITT) has been reported to be blunted in the acute phase of heterogeneous depressive disorders and to be normal in the recovered phase. Glucose 4-11 insulin Homo sapiens 35-42 6338893-4 1983 Plasma insulin concentrations increased significantly in the group receiving 5% dextrose showing that the usual suppression of insulin during abdominal surgery can be overcome by a strong glycaemic stimulus. Glucose 80-88 insulin Homo sapiens 7-14 6192799-4 1983 glucose tolerance testing those with complications had significantly lower serum insulin concentration (at 40 and 60 min 15.2 +/- 2.9 and 11.7 +/- 2.5 mU-1 respectively) than those without (26.1 +/- 4.7 and 24.3 +/- 3.6 mU-1, p less than 0.01). Glucose 0-7 insulin Homo sapiens 81-88 6338893-4 1983 Plasma insulin concentrations increased significantly in the group receiving 5% dextrose showing that the usual suppression of insulin during abdominal surgery can be overcome by a strong glycaemic stimulus. Glucose 80-88 insulin Homo sapiens 127-134 6341138-0 1983 Insulin-counteracting hormones: their impact on glucose metabolism. Glucose 48-55 insulin Homo sapiens 0-7 6337896-2 1983 To evaluate the roles of counterregulatory hormones and insulin antibodies in the impairment of plasma glucose recovery from hypoglycemia in diabetes mellitus, and to assess the relationship between the glucagon response and duration of the disease, 21 insulin-dependent diabetic patients and 10 nondiabetic subjects were studied. Glucose 103-110 insulin Homo sapiens 56-63 6337173-4 1983 Intestinal augmentation of insulin release occurred during the high dose intraduodenal glucose infusion (P less than 0.001) but not during the lower doses. Glucose 87-94 insulin Homo sapiens 27-34 6337173-6 1983 At increments of plasma glucose above 17 mg/dl, the augmentation of gut-mediated insulin release was dependent on the degree of hyperglycemia (r = 0.81; P less than 0.01). Glucose 24-31 insulin Homo sapiens 81-88 6342012-2 1983 However, evidence concerning the penetration of peripheral glucose and insulin into the cerebrospinal fluid (CSF) and the relationship between both peripheral and CSF glucose and insulin levels is still missing. Glucose 167-174 insulin Homo sapiens 179-186 6342012-7 1983 However, infusion of a combination of insulin and glucose in the third ventricle leads to a gradual increase in peripheral glucose and elicits a disappearance of the decrease in peripheral glucose after glucose only infusion into the CSF. Glucose 123-130 insulin Homo sapiens 38-45 6342012-7 1983 However, infusion of a combination of insulin and glucose in the third ventricle leads to a gradual increase in peripheral glucose and elicits a disappearance of the decrease in peripheral glucose after glucose only infusion into the CSF. Glucose 123-130 insulin Homo sapiens 38-45 6342012-7 1983 However, infusion of a combination of insulin and glucose in the third ventricle leads to a gradual increase in peripheral glucose and elicits a disappearance of the decrease in peripheral glucose after glucose only infusion into the CSF. Glucose 123-130 insulin Homo sapiens 38-45 6342930-2 1983 The plasma glucose concentration is maintained at steady basal (euglycemic) or elevated (hyperglycemic) levels during various insulin infusions. Glucose 11-18 insulin Homo sapiens 126-133 6835186-0 1983 [Importance of plasma C-peptide evaluation during the oral glucose tolerance test in infantile and juvenile obesity]. Glucose 59-66 insulin Homo sapiens 22-31 6342930-4 1983 From the measured time course of plasma glucose concentration, using the model, the program estimates the insulin-dependent increase in fractional disappearance rate of glucose (X). Glucose 40-47 insulin Homo sapiens 106-113 6342930-4 1983 From the measured time course of plasma glucose concentration, using the model, the program estimates the insulin-dependent increase in fractional disappearance rate of glucose (X). Glucose 169-176 insulin Homo sapiens 106-113 6402060-2 1983 Continuous intraperitoneal administration of insulin through a permanently inserted polyethylene catheter connected to an open-loop peristaltic pump led to an appreciable improvement in mean blood glucose concentration, mean amplitude of glycaemic excursions, and M value and to normalisation of intermediate metabolic products. Glucose 197-204 insulin Homo sapiens 45-52 6337482-1 1983 Patients with noninsulin-dependent diabetes mellitus (NIDDM) are characterized by a loss of the normal ability of insulin to stimulate glucose uptake. Glucose 135-142 insulin Homo sapiens 17-24 6401923-3 1983 In vitro studies using isolated adipocytes suggest that the postreceptor defect in insulin action resides at the level of the glucose transport system. Glucose 126-133 insulin Homo sapiens 83-90 6337482-2 1983 The effects of diet, exercise, sulfonylurea compounds, and exogenous insulin on in vivo insulin-stimulated glucose uptake have been reviewed in this presentation. Glucose 107-114 insulin Homo sapiens 69-76 6337482-2 1983 The effects of diet, exercise, sulfonylurea compounds, and exogenous insulin on in vivo insulin-stimulated glucose uptake have been reviewed in this presentation. Glucose 107-114 insulin Homo sapiens 88-95 6337484-2 1983 Several techniques that have been used to quantify in vivo insulin-stimulated glucose uptake in patients with noninsulin-dependent diabetes mellitus (NIDDM) have been critically reviewed. Glucose 78-85 insulin Homo sapiens 59-66 6337484-4 1983 Although th details of the techniques that have been used vary considerably, the results obtained with all of them are quite consistent, and demonstrate unequivocally that the ability of insulin to stimulate glucose utilization is markedly reduced in patients with NIDDM. Glucose 208-215 insulin Homo sapiens 187-194 6337349-16 1983 As the time goes on more and more patients develop glucose intolerance, quite early became insulin-dependent, are disposed to severe diabetic metabolic decompensation and can show vascular, cardiac or renal complication. Glucose 51-58 insulin Homo sapiens 91-98 6880857-1 1983 Nine of 16 patients with inflammatory connective tissue diseases (rheumatoid arthritis, polymyalgia rheumatica, scleroderma and mixed connective tissue disease) had glucose intolerance defined a a K-rate less than one but a normal early insulin response to intravenous glucose loading. Glucose 165-172 insulin Homo sapiens 237-244 6340422-4 1983 In patients with latent or manifest diabetes, the increase in C-peptide after oral glucose was lower than in healthy subjects, while insulin sensitivity, estimated with euglycemic insulin clamp technique, was within the same range as in healthy subjects. Glucose 83-90 insulin Homo sapiens 62-71 6880857-5 1983 It is suggested that glucose intolerance in chronic inflammation is a consequence of a peripheral insulin antagonism and an inhibition of insulin secretion. Glucose 21-28 insulin Homo sapiens 98-105 6880857-5 1983 It is suggested that glucose intolerance in chronic inflammation is a consequence of a peripheral insulin antagonism and an inhibition of insulin secretion. Glucose 21-28 insulin Homo sapiens 138-145 31986857-1 1983 Among a group of African green monkeys (Cercopithecus aethiops), plasma insulin concentrations were greater following either intravenous (IV) glucose infusion or oral feeding at 0800 compared with IV glucose or oral feeding at 1700. Glucose 142-149 insulin Homo sapiens 72-79 6576623-6 1983 Our results indicate that the stimulation of the beta cells usually reaches a maximum around a blood glucose level of 10-12 mmol/l leading to a curve linear relationship between serum C-peptide and blood glucose. Glucose 101-108 insulin Homo sapiens 184-193 6576623-6 1983 Our results indicate that the stimulation of the beta cells usually reaches a maximum around a blood glucose level of 10-12 mmol/l leading to a curve linear relationship between serum C-peptide and blood glucose. Glucose 204-211 insulin Homo sapiens 184-193 31986857-3 1983 Insulin/glucose ratios were greater following either IV glucose infusion or oral feeding at 0800 compared with 1700. Glucose 8-15 insulin Homo sapiens 0-7 31986857-3 1983 Insulin/glucose ratios were greater following either IV glucose infusion or oral feeding at 0800 compared with 1700. Glucose 56-63 insulin Homo sapiens 0-7 6344749-1 1983 Prostaglandins of the E series are implicated as regulators of glucose homeostasis because of their effects on glucose production and secretion of insulin and glucagon. Glucose 63-70 insulin Homo sapiens 147-154 6360028-3 1983 Insulin sensitivity was assessed by glucose disappearance rate after insulin injection (0.1 IU/kg body weight). Glucose 36-43 insulin Homo sapiens 0-7 6667341-0 1983 Transient glucose intolerance in rats after a single injection of serum from a diabetic patient with an unusual insulin resistance. Glucose 10-17 insulin Homo sapiens 112-119 6336701-0 1983 Regulation of splanchnic and peripheral glucose uptake by insulin and hyperglycemia in man. Glucose 40-47 insulin Homo sapiens 58-65 6403293-0 1983 Intrasplenic islet autografts: insulin response to intravenous glucose challenge. Glucose 63-70 insulin Homo sapiens 31-38 6337838-10 1983 These results show that glucose disposal and insulin response to glucose injection are not adversely modified by the precompetitive "glycogen loading" procedure. Glucose 65-72 insulin Homo sapiens 45-52 6336706-2 1983 The glucose clamp technique was used to measure insulin resistance and insulin response to glucose. Glucose 91-98 insulin Homo sapiens 71-78 6336706-3 1983 During the euglycemic clamp, at comparable steady-state levels of glucose and insulin, the mean glucose infusion rate, which indicates the rate of glucose utilization, was lower in the retinopathy group than in the nonretinopathy group (6.1 +/- 0.5 versus 8.1 +/- 0.7 mg . Glucose 96-103 insulin Homo sapiens 78-85 6336706-3 1983 During the euglycemic clamp, at comparable steady-state levels of glucose and insulin, the mean glucose infusion rate, which indicates the rate of glucose utilization, was lower in the retinopathy group than in the nonretinopathy group (6.1 +/- 0.5 versus 8.1 +/- 0.7 mg . Glucose 96-103 insulin Homo sapiens 78-85 6341014-6 1983 Diabetologists need to reconsider the applicability of urine glucose measurements in evaluation of adequacy of therapy and in adjustment of insulin dosage. Glucose 61-68 insulin Homo sapiens 140-147 6341018-1 1983 Glucagon normally plays a primary role in promoting glucose recovery from insulin-induced hypoglycemia. Glucose 52-59 insulin Homo sapiens 74-81 6341018-8 1983 The efficacy of glucose counterregulation in a given patient may determine the degree to which euglycemia can be achieved with aggressive insulin therapy in that patient. Glucose 16-23 insulin Homo sapiens 138-145 6343099-0 1983 Insulin receptor binding and insulin-mediated glucose uptake in type-II-diabetics. Glucose 46-53 insulin Homo sapiens 29-36 6343099-4 1983 Under these conditions the amount of metabolized glucose (M) has been calculated and served as a measure of insulin-stimulated glucose disposal. Glucose 49-56 insulin Homo sapiens 108-115 6343099-4 1983 Under these conditions the amount of metabolized glucose (M) has been calculated and served as a measure of insulin-stimulated glucose disposal. Glucose 127-134 insulin Homo sapiens 108-115 6343099-10 1983 Assuming that insulin binding to red blood cells mimic that to target cells we conclude that the cause of reduced glucose utilization in type-II-diabetes lies mainly in changes of postreceptor events rather than in receptor binding. Glucose 114-121 insulin Homo sapiens 14-21 6341194-3 1983 10 patients had overt glucose intolerance; of these, 4 were insulin-deficient, 3 had a loss of an acute insulin response to glucose, and 3 had marked hyperglucagonemia with normal to increased insulin levels. Glucose 124-131 insulin Homo sapiens 104-111 6341194-5 1983 Therefore, according to this study, at least three factors are clearly implicated in the production of glucose intolerance after an acute episode of pancreatitis: hypoinsulinemia, delayed insulin secretory response and hyperglucagonemia. Glucose 103-110 insulin Homo sapiens 167-174 6198304-7 1983 Either via a messenger generated by this reaction, or via insulin"s subsequent direct interaction with intracellular organelles, such as the Golgi-endoplasmic reticulum, protein synthesis is initiated and glucose transport is increased. Glucose 205-212 insulin Homo sapiens 58-65 6358071-4 1983 Diazoxide treatment resulted in a significant suppression of glucose-stimulated early (insulin area 0-30 min) (P less than 0.05), late (insulin area 30-120 min) (P less than 0.01) and total insulin response (insulin area 0-120 min) (P less than 0.01) as well as a mild deterioration of glucose tolerance. Glucose 61-68 insulin Homo sapiens 87-94 6358071-4 1983 Diazoxide treatment resulted in a significant suppression of glucose-stimulated early (insulin area 0-30 min) (P less than 0.05), late (insulin area 30-120 min) (P less than 0.01) and total insulin response (insulin area 0-120 min) (P less than 0.01) as well as a mild deterioration of glucose tolerance. Glucose 61-68 insulin Homo sapiens 136-143 6358071-4 1983 Diazoxide treatment resulted in a significant suppression of glucose-stimulated early (insulin area 0-30 min) (P less than 0.05), late (insulin area 30-120 min) (P less than 0.01) and total insulin response (insulin area 0-120 min) (P less than 0.01) as well as a mild deterioration of glucose tolerance. Glucose 61-68 insulin Homo sapiens 136-143 6358071-4 1983 Diazoxide treatment resulted in a significant suppression of glucose-stimulated early (insulin area 0-30 min) (P less than 0.05), late (insulin area 30-120 min) (P less than 0.01) and total insulin response (insulin area 0-120 min) (P less than 0.01) as well as a mild deterioration of glucose tolerance. Glucose 61-68 insulin Homo sapiens 136-143 6361735-1 1983 The insulin and C-peptide kinetics due to glucose (50 g), given intraperitoneally or enterally has been compared in five non-diabetic patients on continuous ambulatory peritoneal dialysis (CAPD). Glucose 42-49 insulin Homo sapiens 16-25 6379315-1 1983 Broadbased clinical research during recent years has shown that programme controlled insulin infusion with externally portable devices is an excellent means for improving glucose control of labile diabetics. Glucose 171-178 insulin Homo sapiens 85-92 6346435-1 1983 The euglycemic insulin clamp technique coupled with isotopic measurement of the glucose utilization rate ([3-3H] glucose), described previously in man, has been adapted to characterize and quantify insulin sensitivity in vivo in the rat. Glucose 80-87 insulin Homo sapiens 198-205 6338503-6 1983 An average insulin dose of 8.0 to 9.0 U/kg/day was required to normalize body weights, plasma glucose, and plasma glucagon of streptozotocin diabetic rats treated with the Alzet osmotic minipump Model 2002. Glucose 94-101 insulin Homo sapiens 11-18 6763264-0 1982 [Insulin secretion induced by glucose or arginine in non-obese volunteers. Glucose 30-37 insulin Homo sapiens 1-8 6356314-10 1983 These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). Glucose 102-109 insulin Homo sapiens 77-84 6356314-10 1983 These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). Glucose 158-165 insulin Homo sapiens 119-126 6372078-12 1983 The most interesting results related to glucose metabolism were found otherwise as follows: The sum of insulin (276.4 +/- 20.1 before and 255.1 +/- 19.0 after p less than 0.05) and glucose levels (but not fasting values) decreased (28.3 +/- 1.6 before and 27.8 +/- 1.4 after p less than 0.01) after training in obesity. Glucose 40-47 insulin Homo sapiens 103-110 6372078-17 1983 Patients with diabetes type II showed initially lower basal and insulin-stimulated glucose incorporation into triglycerides. Glucose 83-90 insulin Homo sapiens 64-71 6353825-0 1983 [Features of insulin tolerance to glucose in primary and secondary forms of progressive muscular dystrophy]. Glucose 34-41 insulin Homo sapiens 13-20 6754331-3 1982 After administration of glucose there was a definite rise in blood-glucose, serum-insulin and C-peptide concentrations. Glucose 24-31 insulin Homo sapiens 82-89 6754331-3 1982 After administration of glucose there was a definite rise in blood-glucose, serum-insulin and C-peptide concentrations. Glucose 24-31 insulin Homo sapiens 94-103 6760674-2 1982 The changes in serum amino acid concentrations, as observed 3 h after ceasing a 3 h infusion of insulin and glucagon in 500 ml glucose solution, were an elevation of serum branched chain amino acid (BACA) levels and of the molar ratio of BCAA/aromatic amino acid (AAA) levels in patients with liver cirrhosis. Glucose 127-134 insulin Homo sapiens 96-103 6754726-0 1982 Effects of temperature on basal and insulin-stimulated glucose transport activities in fat cells. Glucose 55-62 insulin Homo sapiens 36-43 6754726-10 1982 The Arrhenius plot of the basal glucose transport activity determined in the presence of dinitrophenol was apparently linear from 10 to 37 degrees C and parallel to that of the plus insulin activity measured either in the presence or absence of dinitrophenyl. Glucose 32-39 insulin Homo sapiens 182-189 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 37-44 insulin Homo sapiens 0-7 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 37-44 insulin Homo sapiens 155-162 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 37-44 insulin Homo sapiens 283-290 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 193-200 insulin Homo sapiens 0-7 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 193-200 insulin Homo sapiens 155-162 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 193-200 insulin Homo sapiens 283-290 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 193-200 insulin Homo sapiens 0-7 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 193-200 insulin Homo sapiens 155-162 6754726-11 1982 Insulin itself slowly stimulated the glucose transport activity at 10 degrees C. These results are consistent with the view that (a) low temperature, like insulin, induces translocation of the glucose transport activity from an intracellular storage site to the plasma membrane, (b) insulin stimulates glucose transport activity without changing its activation energy, and (c) subcellular membranes do not entirely stop their movement at a low temperature, e.g, at 10 degrees C. Glucose 193-200 insulin Homo sapiens 283-290 6761645-4 1982 In contrast, the amounts of insulin released during the immediate post-operative period were more regular and reproducible (mean: 2.36 U/h for a glucose intake of 200-250 g/24 h). Glucose 145-152 insulin Homo sapiens 28-35 6759275-1 1982 We have investigated plasma glucose and insulin responses to 75 g glucose in 12 young, full-blood Aborigines before and after 2 weeks on a diet derived almost exclusively from seafood. Glucose 66-73 insulin Homo sapiens 40-47 6761184-0 1982 Inorganic phosphate-insulin relationships in normal subjects and in patients with moderate glucose intolerance. Glucose 91-98 insulin Homo sapiens 20-27 6761184-4 1982 In NGT and in IGT1 subjects, oral glucose administration was followed by a fall in serum phosphate level that was well correlated with the total insulin released. Glucose 34-41 insulin Homo sapiens 145-152 6761184-7 1982 The present results support the hypothesis that in IGT1 patients a reduced glucose-induced insulin release and in IGT2 patients, a peripheral resistance to insulin action could be the determinant of impaired glucose tolerance. Glucose 75-82 insulin Homo sapiens 91-98 6818083-1 1982 Insulin secretion was monitored in monkey islets isolated by collagenase digestion and exposed to leucine and arginine with and without glucose. Glucose 136-143 insulin Homo sapiens 0-7 6752171-0 1982 Insulin-stimulated glucose transport in cultured fibroblasts from normal and noninsulin-dependent (type II) diabetic human subjects. Glucose 19-26 insulin Homo sapiens 0-7 6751926-4 1982 However, all patients had elevated insulin levels after oral glucose. Glucose 61-68 insulin Homo sapiens 35-42 6759357-0 1982 An assessment of the new NIH diagnostic criteria for diabetes mellitus according to insulin response in a 75 g oral glucose tolerance test and levels of hemoglobin AIC. Glucose 116-123 insulin Homo sapiens 84-91 6759357-2 1982 We measured insulin levels during 75 g oral glucose tolerance test (75 g OGTT) and hemoglobin AIC levels in patients diagnosed as having impaired glucose tolerance (IGT) or non-insulin dependent diabetes (NIDDM) according to the NIH criteria. Glucose 44-51 insulin Homo sapiens 12-19 6132848-3 1983 After insulin withdrawal during the saline infusion, glucose and potassium levels rose markedly (delta maximum: glucose, 12.0 +/- 1.5 mmol/l; potassium, 0.73 +/- 0.12 mmol/l), while glucagon showed a slight, but significant increment (delta maximum: 10.6 +/- 1.0 pmol/ml, p less than 0.05). Glucose 53-60 insulin Homo sapiens 6-13 6752171-1 1982 We have studied the effects of insulin on glucose transport in cultured fibroblasts obtained from six normal subjects and six patients with type II or noninsulin-dependent diabetes mellitus. Glucose 42-49 insulin Homo sapiens 31-38 6757260-0 1982 Contribution of glucose and gluconeogenic substrates to insulin-stimulated glycogen synthesis in cultured fetal hepatocytes. Glucose 16-23 insulin Homo sapiens 56-63 6757268-0 1982 Insulin increases the maximum velocity for glucose uptake without altering the Michaelis constant in man. Glucose 43-50 insulin Homo sapiens 0-7 6757268-4 1982 With both methods, increases in plasma insulin from 18 microunits/ml to 80 and 150 microunits/ml were found to increase the maximum velocity (Vmax) for glucose uptake nearly three- and fivefold, respectively, (P less than 0.025 and P less than 0.001) without significantly altering the Michaelis constant (Km). Glucose 152-159 insulin Homo sapiens 39-46 6757268-5 1982 Because an increase in the affinity or molecular activity of transport sites or provision of additional transport sites that differed from those present basally should have altered the Km, whereas a mere increase in the number of transport sites would have only increased the Vmax, our results indicate that in man, insulin may increase glucose uptake merely by providing additional transport sites. Glucose 337-344 insulin Homo sapiens 316-323 6762217-1 1982 The problem of hyperinsulinism and insulin resistance, previously observed by us in PCOS using the tolbutamide test, was studied in the present research using intravenous glucose tolerance test (IVGTT). Glucose 171-178 insulin Homo sapiens 20-27 6815417-10 1982 When insulin was given with glucose to maintain normoglycemia, the rate of alanine synthesis was unchanged. Glucose 28-35 insulin Homo sapiens 5-12 6760120-1 1982 Porcine extracted monocomponent insulins and human semi-synthetic insulins obtained by enzymatic conversion of porcine insulin had exactly the same clinical effectiveness on blood glucose balance when compared with an artificial pancreas during two 48-hour studies 2 or 3 days apart. Glucose 180-187 insulin Homo sapiens 32-39 6753588-1 1982 Continuous insulin infusion has been advocated for strict glucose control during labor in insulin-requiring diabetic patients. Glucose 58-65 insulin Homo sapiens 11-18 6818951-2 1982 Exposure of fat-pads to increasing concentrations of K+ in the presence of insulin stimulates the incorporation of labelled glucose into glycogen. Glucose 124-131 insulin Homo sapiens 75-82 6818951-6 1982 Ouabain reinforced the effect of insulin on the conversion of glucose into glycogen in a Na+ medium and in a equimolar Na+-K+ medium, but not in a K+ medium. Glucose 62-69 insulin Homo sapiens 33-40 6757014-0 1982 The effect of graded doses of insulin on total glucose uptake, glucose oxidation, and glucose storage in man. Glucose 47-54 insulin Homo sapiens 30-37 6753617-5 1982 (4) The insulin response to intravenous glucose suggests an impairment in the first phase of insulin secretion in the surgically treated group, demonstrating a role for the vagus in insulin secretion. Glucose 40-47 insulin Homo sapiens 8-15 6129168-5 1982 The B-cell-enriched fraction (90% B cells, 3% A cells, 2% D cells) exhibited significant insulin secretory responses to glucose (16.7 mM), and 3-isobutyl-1-methylxanthine (0.1 mM), during a 24-h culture period, and these responses were slightly greater than those observed in the original mixed islet cell preparation (66% B cells, 14% A cells, and 4% D cells). Glucose 120-127 insulin Homo sapiens 89-96 6299658-0 1982 Insulin secretion and metabolic changes in maturity onset diabetes mellitus and glucose intolerance. Glucose 80-87 insulin Homo sapiens 0-7 6293901-4 1982 It thus appears that impairment of glucose-stimulated insulin release was unlikely to be due to insufficient intracellular cyclic AMP. Glucose 35-42 insulin Homo sapiens 54-61 6765523-6 1982 The early morning glucose sample was also greater on human insulin (9.6 mmol/L [pork] versus 12.1 mmol/L [human insulin], P less than 0.001). Glucose 18-25 insulin Homo sapiens 59-66 6765523-5 1982 In pork insulin-treated patients greater values while on human insulin were found for mean glucose (9.0 mmol/L [pork] versus 9.7 mmol/L [human insulin], P = 0.05), "M" index (65.0 [pork] versus 79.6 [human insulin], P less than 0.025), and total daily insulin dose (50.9 U/day [pork] versus 52.5 U/day [human insulin], P less than 0.001). Glucose 91-98 insulin Homo sapiens 8-15 6765540-7 1982 A more rapid decrease in the blood glucose concentration was observed after injection of both human insulin preparations than after porcine insulin. Glucose 35-42 insulin Homo sapiens 100-107 6765540-7 1982 A more rapid decrease in the blood glucose concentration was observed after injection of both human insulin preparations than after porcine insulin. Glucose 35-42 insulin Homo sapiens 140-147 6765540-11 1982 Although all investigations were performed under identical experimental conditions and equal dosages of each insulin were injected, higher insulin concentrations and a stronger biologic effect, shown by larger amount of dextrose delivered, were observed in both human insulins than in porcine insulin. Glucose 220-228 insulin Homo sapiens 109-116 6765523-5 1982 In pork insulin-treated patients greater values while on human insulin were found for mean glucose (9.0 mmol/L [pork] versus 9.7 mmol/L [human insulin], P = 0.05), "M" index (65.0 [pork] versus 79.6 [human insulin], P less than 0.025), and total daily insulin dose (50.9 U/day [pork] versus 52.5 U/day [human insulin], P less than 0.001). Glucose 91-98 insulin Homo sapiens 63-70 6765545-5 1982 A tendency was noted, however, that NPH human insulin has a faster onset of action and that the serum glucose minimum for NPH human insulin lasts longer. Glucose 102-109 insulin Homo sapiens 132-139 6765523-5 1982 In pork insulin-treated patients greater values while on human insulin were found for mean glucose (9.0 mmol/L [pork] versus 9.7 mmol/L [human insulin], P = 0.05), "M" index (65.0 [pork] versus 79.6 [human insulin], P less than 0.025), and total daily insulin dose (50.9 U/day [pork] versus 52.5 U/day [human insulin], P less than 0.001). Glucose 91-98 insulin Homo sapiens 63-70 6765545-6 1982 The serum glucose curves after the application of regular and NPH human insulin initially lie closer together than after the respective PPI preparations. Glucose 10-17 insulin Homo sapiens 72-79 6821493-5 1982 Within 24 h insulin therapy led to continuous improvement in blood glucose to 187 +/- 90 (ketoacidotic patients) and 172 +/- 28 mg/dl (nonketoacidotic group) and normalization of pH, base excess, and osmolality. Glucose 67-74 insulin Homo sapiens 12-19 6765523-5 1982 In pork insulin-treated patients greater values while on human insulin were found for mean glucose (9.0 mmol/L [pork] versus 9.7 mmol/L [human insulin], P = 0.05), "M" index (65.0 [pork] versus 79.6 [human insulin], P less than 0.025), and total daily insulin dose (50.9 U/day [pork] versus 52.5 U/day [human insulin], P less than 0.001). Glucose 91-98 insulin Homo sapiens 63-70 6765549-2 1982 Intravenous insulin tolerance tests showed identical effects on plasma glucose when a bolus of 0.1 U/kg was injected. Glucose 71-78 insulin Homo sapiens 12-19 6765523-5 1982 In pork insulin-treated patients greater values while on human insulin were found for mean glucose (9.0 mmol/L [pork] versus 9.7 mmol/L [human insulin], P = 0.05), "M" index (65.0 [pork] versus 79.6 [human insulin], P less than 0.025), and total daily insulin dose (50.9 U/day [pork] versus 52.5 U/day [human insulin], P less than 0.001). Glucose 91-98 insulin Homo sapiens 63-70 6765523-5 1982 In pork insulin-treated patients greater values while on human insulin were found for mean glucose (9.0 mmol/L [pork] versus 9.7 mmol/L [human insulin], P = 0.05), "M" index (65.0 [pork] versus 79.6 [human insulin], P less than 0.025), and total daily insulin dose (50.9 U/day [pork] versus 52.5 U/day [human insulin], P less than 0.001). Glucose 91-98 insulin Homo sapiens 63-70 6749880-2 1982 All three glucocorticoids caused significant reduction of glucose tolerance as assessed by glucose and insulin areas under oral glucose tolerance text curves and insulin sensitivity in response to 0.1 U insulin/kg BW, iv. Glucose 58-65 insulin Homo sapiens 103-110 6759350-0 1982 Glucose metabolism in the basal state and during a two-hour glucose infusion in low insulin responders and control subjects. Glucose 60-67 insulin Homo sapiens 84-91 6759224-6 1982 As regards the effect of insulin on glucose oxidation, for the control subjects ED50 was 30 microunits/ml, whereas in NIDDM patients, insulin exerted no stimulatory effect. Glucose 36-43 insulin Homo sapiens 25-32 6757619-4 1982 Two thirds to three quarters of the observed increment in RMR following the insulin and glucose infusion in this study can be accounted for by the metabolic processing of the infused glucose for storage purposes. Glucose 183-190 insulin Homo sapiens 76-83 6757860-7 1982 Human insulin was tolerated and proved effective in controlling both blood glucose levels and skin rashes in response to conventional insulins. Glucose 75-82 insulin Homo sapiens 6-13 6749468-5 1982 In addition, a glucose-lowering effect was seen which led to a definite improvement in the control of diabetes both with glibenclamide and with insulin. Glucose 15-22 insulin Homo sapiens 144-151 6819874-0 1982 [Plasma glucose, insulin and C-peptide responses in normal subjects to 100, 75 and 50 grams of glucose load during glucose tolerance test]. Glucose 95-102 insulin Homo sapiens 29-38 6819874-0 1982 [Plasma glucose, insulin and C-peptide responses in normal subjects to 100, 75 and 50 grams of glucose load during glucose tolerance test]. Glucose 95-102 insulin Homo sapiens 29-38 6819876-0 1982 [Plasma insulin, glucose and C-peptide responses to oral glucose tolerance test in patients with liver disease]. Glucose 57-64 insulin Homo sapiens 8-15 6819876-0 1982 [Plasma insulin, glucose and C-peptide responses to oral glucose tolerance test in patients with liver disease]. Glucose 57-64 insulin Homo sapiens 29-38 6751244-1 1982 To assess the mechanisms of insulin resistance following injury, we examined the relationship between insulin levels and glucose disposal in nine nonseptic, multiple trauma patients (average age 32 years, Injury Severity Score 22) five to 13 days postinjury. Glucose 121-128 insulin Homo sapiens 102-109 6751244-13 1982 In conclusion, this study demonstrated that (1) the maximal rate of glucose disposal is reduced in trauma patients; (2) the metabolic clearance rate of insulin in the injured patients is almost twice normal and; (3) insulin resistance following injury appears to occur in peripheral tissues, probably skeletal muscle, and is consistent with a postreceptor defect. Glucose 68-75 insulin Homo sapiens 216-223 6754515-4 1982 In both groups of diabetic subjects, the rates of hepatic glucose production were inappropriately high for the prevailing plasma glucose and insulin levels, indicating the presence of hepatic resistance to insulin. Glucose 58-65 insulin Homo sapiens 141-148 6754515-13 1982 Insulin-stimulated glucose clearance was reduced to a similar extent in Type 2 (54%) and Type 1 (61%) diabetic subjects, and correlated directly with fasting glucose clearance. Glucose 19-26 insulin Homo sapiens 0-7 6754515-13 1982 Insulin-stimulated glucose clearance was reduced to a similar extent in Type 2 (54%) and Type 1 (61%) diabetic subjects, and correlated directly with fasting glucose clearance. Glucose 158-165 insulin Homo sapiens 0-7 6754516-20 1982 Therefore, following insulin treatment of uncontrolled Type 2 (non-insulin-dependent) diabetes, the initially increased basal hepatic glucose production, and decreased hepatic sensitivity, return towards normal. Glucose 134-141 insulin Homo sapiens 21-28 6759224-7 1982 The results obtained suggest that the effect of insulin on glucose utilization in normoinsulinemic NIDDM may be diminished in spite of normal insulin binding to receptors. Glucose 59-66 insulin Homo sapiens 48-55 6759224-7 1982 The results obtained suggest that the effect of insulin on glucose utilization in normoinsulinemic NIDDM may be diminished in spite of normal insulin binding to receptors. Glucose 59-66 insulin Homo sapiens 87-94 6754516-20 1982 Therefore, following insulin treatment of uncontrolled Type 2 (non-insulin-dependent) diabetes, the initially increased basal hepatic glucose production, and decreased hepatic sensitivity, return towards normal. Glucose 134-141 insulin Homo sapiens 67-74 6759226-3 1982 The mean incremental glucose disposal rates (IGDR) fell more slowly following discontinuation of the 40- and 120-mU/m2/min insulin infusions, so that the time required for the IGDRs to fall to one-half their initial values (D50 IGDR) were were 42 +/- 5 and 78 +/- 1 min, respectively. Glucose 21-28 insulin Homo sapiens 123-130 6754517-2 1982 Intravenous insulin was initially delivered via a closed-loop infusion system programmed to lower mean blood glucose from 11.3 +/- 1.8 to 4.8 +/- 0.4 mmol/l over approximately 3.5 h. Blood glucose was then maintained at this level for 4 h. At this time, the closed-loop infusion was discontinued and replaced by an open-loop system. Glucose 109-116 insulin Homo sapiens 12-19 6758991-0 1982 Evidence for an autosomal recessive gene regulating the persistence of the insulin response to glucose in man. Glucose 95-102 insulin Homo sapiens 75-82 6758991-1 1982 The significance of genetic factors for insulin release after glucose infusion was studied in 155 nuclear families of which 59 were control families and 96 had been ascertained through a parent with onset of diabetes after 30 years of age. Glucose 62-69 insulin Homo sapiens 40-47 6759219-1 1982 With advancing age, glucose-induced insulin release is decreased in vitro, yet circulating insulin levels after glucose challenge are not decreased in the elderly. Glucose 20-27 insulin Homo sapiens 36-43 6759219-1 1982 With advancing age, glucose-induced insulin release is decreased in vitro, yet circulating insulin levels after glucose challenge are not decreased in the elderly. Glucose 112-119 insulin Homo sapiens 91-98 6759219-8 1982 Alterations in C1 contribute to changes in insulin levels with age and may reconcile the discrepancy between in vivo and in vitro studies of glucose-induced insulin release. Glucose 141-148 insulin Homo sapiens 43-50 6759219-8 1982 Alterations in C1 contribute to changes in insulin levels with age and may reconcile the discrepancy between in vivo and in vitro studies of glucose-induced insulin release. Glucose 141-148 insulin Homo sapiens 157-164 6759223-3 1982 After baseline measurements, the patients were treated with enough long-acting insulin to maintain their fasting plasma glucose in the range of 100--125 mg/dl. Glucose 120-127 insulin Homo sapiens 79-86 6293963-5 1982 Cells from fresh insulinoma incubated with increasing concentrations of extracellular glucose released increasing amounts of IRI up to approximately 15 mM glucose, which paralleled changes in plasma insulin obtained during a preoperative glucose tolerance test. Glucose 86-93 insulin Homo sapiens 17-24 6293963-5 1982 Cells from fresh insulinoma incubated with increasing concentrations of extracellular glucose released increasing amounts of IRI up to approximately 15 mM glucose, which paralleled changes in plasma insulin obtained during a preoperative glucose tolerance test. Glucose 155-162 insulin Homo sapiens 17-24 6293963-5 1982 Cells from fresh insulinoma incubated with increasing concentrations of extracellular glucose released increasing amounts of IRI up to approximately 15 mM glucose, which paralleled changes in plasma insulin obtained during a preoperative glucose tolerance test. Glucose 155-162 insulin Homo sapiens 17-24 6757082-0 1982 Discrepant effect of the prostaglandin synthesis inhibitor acetylsalicylic acid on insulin and C-peptide response to glucose in man. Glucose 117-124 insulin Homo sapiens 95-104 6757082-1 1982 The prostaglandin synthesis inhibitor acetylsalicylic acid (ASA) increases acute insulin response to glucose and improves glucose tolerance in man. Glucose 101-108 insulin Homo sapiens 81-88 6757082-9 1982 The improvement of glucose tolerance after ASA application seems to be related to the biologic effect of higher circulating insulin levels but not to alteration of insulin antagonists, such as IRG, HGH and NEFA. Glucose 19-26 insulin Homo sapiens 124-131 6286709-5 1982 Stimulation of [3H]glucose uptake was minimal with low insulin levels (1--10 ng/ml) relative to controls, but was comparable at higher insulin concentrations (1--10 micrograms/ml). Glucose 19-26 insulin Homo sapiens 55-62 6752636-0 1982 Insulin secretory response to oral glucose load, diabetic microangiopathy and diabetic control: a study in non-insulin dependent diabetics. Glucose 35-42 insulin Homo sapiens 0-7 6752636-4 1982 The glucose induced increments of insulin levels (delta IRI) at reassessment correlated inversely with the degree of diabetic control, measured by Haemoglobin A1 (r = -0.466, p less than 0.01), and with the mean fasting blood glucose throughout the follow up period (r = -0.491, p less than 0.01). Glucose 4-11 insulin Homo sapiens 34-41 6752636-4 1982 The glucose induced increments of insulin levels (delta IRI) at reassessment correlated inversely with the degree of diabetic control, measured by Haemoglobin A1 (r = -0.466, p less than 0.01), and with the mean fasting blood glucose throughout the follow up period (r = -0.491, p less than 0.01). Glucose 226-233 insulin Homo sapiens 34-41 6750546-0 1982 The relation between glucose tolerance and insulin binding to circulating monocytes in obese children. Glucose 21-28 insulin Homo sapiens 43-50 6750546-1 1982 The quantitative relation between insulin binding to circulating monocytes in vitro and glucose tolerance in obese children in vivo is reported. Glucose 88-95 insulin Homo sapiens 34-41 6750546-4 1982 The glucose tolerance expressed by sigma BS (milligrams/100 ml), the sum of the plasma glucose (blood sugar [BS]) values at OGTT, was significantly correlated with the degree of overweight (r = .316, P less than .01) and more highly with sigma IRI (microunits per milliliter), the sum of immunoreactive insulin (IRI) values at OGTT (r = .512, P less than .001). Glucose 4-11 insulin Homo sapiens 303-310 6181562-0 1982 Evidence that glucose "marks" beta cells resulting in preferential release of newly synthesized insulin. Glucose 14-21 insulin Homo sapiens 96-103 6181562-1 1982 Studies of isolated islets labeled with radioactive leucine show that glucose at a critical time "marks" islets in such a way as to cause preferential release of newly synthesized insulin. Glucose 70-77 insulin Homo sapiens 180-187 7050125-0 1982 Evidence that translocation of the glucose transport activity is the major mechanism of insulin action on glucose transport in fat cells. Glucose 35-42 insulin Homo sapiens 88-95 7050125-0 1982 Evidence that translocation of the glucose transport activity is the major mechanism of insulin action on glucose transport in fat cells. Glucose 106-113 insulin Homo sapiens 88-95 7050125-3 1982 In this study, the glucose transport activity in the plasma membrane-rich fraction (either in the basal or plus insulin state) was solubilized, reconstituted, and assayed with an overall efficiency of 25-35%. Glucose 19-26 insulin Homo sapiens 112-119 7050125-4 1982 Four agents known to have insulin-like effects on the glucose transport activity in intact fat cells (hydrogen peroxide, sodium vanadate, trypsin, and p-chloromercuriphenyl sulfonate) not only increased the transport activity in the plasma membrane-rich fraction, but also decreased the activity in the Golgi-rich fraction. Glucose 54-61 insulin Homo sapiens 26-33 7050125-6 1982 Upon administration of insulin to fat cells, and subsequent elimination of the hormone, the glucose transport activities associated with the plasma membrane-rich and Golgi-rich fractions were affected almost concomitantly towards opposite directions. Glucose 92-99 insulin Homo sapiens 23-30 7050125-7 1982 It is proposed as a working hypothesis that translocation of the glucose transport system to the plasma membrane from the Golgi-rich fraction is the major, if not the sole, mechanism by which insulin stimulates glucose transport in fat cells. Glucose 65-72 insulin Homo sapiens 192-199 7050125-7 1982 It is proposed as a working hypothesis that translocation of the glucose transport system to the plasma membrane from the Golgi-rich fraction is the major, if not the sole, mechanism by which insulin stimulates glucose transport in fat cells. Glucose 211-218 insulin Homo sapiens 192-199 6758385-2 1982 Despite the differences in the peripheral insulin content during the intravenous glucose tolerance test negative correlations between the KG-value and the sodium concentration of the erythrocytes were found in the groups investigated. Glucose 81-88 insulin Homo sapiens 42-49 6751010-3 1982 Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. Glucose 0-7 insulin Homo sapiens 59-66 6753574-7 1982 In D5W admixtures, as the fill volume at constant insulin I 125 concentration was doubled and quadrupled, the adherence of insulin decreased in all three bottle sizes (200, 250, and 500 ml). Glucose 3-6 insulin Homo sapiens 50-57 6753574-7 1982 In D5W admixtures, as the fill volume at constant insulin I 125 concentration was doubled and quadrupled, the adherence of insulin decreased in all three bottle sizes (200, 250, and 500 ml). Glucose 3-6 insulin Homo sapiens 123-130 6753574-9 1982 Increasing insulin concentrations over the range of 50-300 units/liter in D5W and 0-50 units/liter in NS resulted in decreased adherence. Glucose 74-77 insulin Homo sapiens 11-18 6818069-3 1982 In the ketoacidotic subjects, the mean glucose clearance during insulin treatment was only 8% of that in the controls (P less than 0.001). Glucose 39-46 insulin Homo sapiens 64-71 6818069-4 1982 In the normal subjects, tissue glucose clearance during insulin treatment of the hyperglycemia (5.8 0.7 ml/min . Glucose 31-38 insulin Homo sapiens 56-63 6818069-6 1982 In the ketoacidotic patients, a history of prior insulin therapy, but not the degree of hyperglycemia at the time of admission, was associated with a more rapid rate of decline of plasma glucose in response to insulin treatment. Glucose 187-194 insulin Homo sapiens 49-56 6818069-6 1982 In the ketoacidotic patients, a history of prior insulin therapy, but not the degree of hyperglycemia at the time of admission, was associated with a more rapid rate of decline of plasma glucose in response to insulin treatment. Glucose 187-194 insulin Homo sapiens 210-217 6753574-10 1982 The addition of 1-60 meq/liter of KCl resulted in a significant decrease of insulin adhering from D5W and an insignificant decrease from NS admixtures. Glucose 98-101 insulin Homo sapiens 76-83 7051814-5 1982 Serum lipoprotein levels, obesity, BP, and plasma insulin levels were all correlated after a glucose load, implying causal interrelationships. Glucose 93-100 insulin Homo sapiens 50-57 6759226-6 1982 The times required for insulin action to decrease to one-half the initial values in the periphery (D50 IGDR) and in the liver (R50 HGO) were correlated with the preceding steady-state glucose disposal rates in individual subjects (r = 0.75, P less than 0.001 and r = 0.58, P less than 0.05, respectively). Glucose 184-191 insulin Homo sapiens 23-30 6818069-1 1982 The effect of "low-dose" (6--10 U/h) insulin treatment on the rate of decline of plasma glucose concentration was determined in 15 diabetic subjects admitted in ketoacidosis (plasma glucose = 948 79 mg/dl) and in six normal volunteers rendered hyperglycemic by a combined infusion of somatostatin and glucose (plasma glucose = 653 28 mg/dl). Glucose 88-95 insulin Homo sapiens 37-44 6818069-2 1982 The fractional glucose turnover and the half-time of the fall in plasma glucose during insulin treatment were both 10-fold reduced (P less than 0.001) in the diabetics as compared with the controls. Glucose 15-22 insulin Homo sapiens 87-94 6126124-6 1982 We conclude from these studies that restoration of glucose production during sustained insulin and glucagon deficiency is not attributable to a) onset of insulin deficiency because insulin is equally depressed in both experimental settings, b) glucose autoregulation even though adequate substrate is available, or c) an alpha-adrenergic mechanism because plasma catecholamines were very high and alpha-receptors were not blocked. Glucose 51-58 insulin Homo sapiens 87-94 6818069-2 1982 The fractional glucose turnover and the half-time of the fall in plasma glucose during insulin treatment were both 10-fold reduced (P less than 0.001) in the diabetics as compared with the controls. Glucose 72-79 insulin Homo sapiens 87-94 6751608-2 1982 This technique interrupts the physiological glucose-insulin relationship by placing a patient"s blood glucose concentration under an investigator"s control, for quantification of the pancreatic beta-cell response during hyperglycemic clamps and of sensitivity of body tissue to exogenous insulin during normoglycemic clamps. Glucose 44-51 insulin Homo sapiens 52-59 6751608-3 1982 We report the development of a glucose clamping algorithm for use with the Biostator glucose-controlled insulin-infusion system (Horm. Glucose 85-92 insulin Homo sapiens 104-111 6754494-3 1982 Insulin resistance was determined by measuring the steady state plasma glucose response (SSPG) to a continuous infusion of glucose (6 mg . Glucose 71-78 insulin Homo sapiens 0-7 6751902-11 1982 There was, in addition, a decrease in glucose recycling during both subcutaneous insulin therapy and feedback control in the diabetic subjects. Glucose 38-45 insulin Homo sapiens 81-88 6754494-3 1982 Insulin resistance was determined by measuring the steady state plasma glucose response (SSPG) to a continuous infusion of glucose (6 mg . Glucose 123-130 insulin Homo sapiens 0-7 6751904-2 1982 Overall, there was a 25% improvement in glucose tolerance, a 58% increase in plasma insulin response during the glucose tolerance test, a 13.6% fall in fasting plasma triglyceride levels with no change in fasting cholesterol levels and a 5.1% fall in body weight. Glucose 112-119 insulin Homo sapiens 84-91 6751904-4 1982 These were mainly men of average age 63 years, who were 20% above their ideal body weight, and had milder glucose intolerance and higher residual insulin response to glucose before treatment than the 16% of patients who remained poorly controlled. Glucose 166-173 insulin Homo sapiens 146-153 6754494-15 1982 In comparison to controls the mean SSPG was significantly higher in subjects with IGT (during low and high glucose infusion) suggesting the existence of insulin resistance in these subjects. Glucose 107-114 insulin Homo sapiens 153-160 6751904-5 1982 These latter patients were mainly older women, 9% above their ideal body weight and with more marked glucose intolerance and less insulin response to glucose. Glucose 150-157 insulin Homo sapiens 130-137 6754494-18 1982 In conclusion, our results have confirmed the validity of an infusion technique of glucose, insulin, epinephrine and propranolol for evaluation of insulin sensitivity in vivo. Glucose 83-90 insulin Homo sapiens 147-154 6754492-7 1982 These data show that the response of glucose, insulin and glucagon to an oral glucose tolerance test in various respects is different to that obtained by the more physiological stimulation with a breakfast meal. Glucose 78-85 insulin Homo sapiens 46-53 6754493-2 1982 Glucose tolerance did not deteriorate after treatment, despite a reduction in the early insulin response to glucose, resetting of the C-peptide response at a lower level and a reduction in glucose-mediated glucagon suppression. Glucose 108-115 insulin Homo sapiens 88-95 7128971-0 1982 Glucose control in mobile type 1 (insulin-dependent) diabetic patients by means of a semi-automatic feedback controlled insulin infusion system. Glucose 0-7 insulin Homo sapiens 34-41 6754494-19 1982 In addition, our findings have added further support for insulin resistance in subjects with IGT which is directly proportional to the degree of glucose intolerance. Glucose 145-152 insulin Homo sapiens 57-64 6813260-6 1982 Insulin, itself, affects glucose transport minimally and mainly at supraphysiologic concentrations. Glucose 25-32 insulin Homo sapiens 0-7 6754562-7 1982 In addition, daily insulin treatment prevented a severe increase of fasting plasma glucose and glucagon. Glucose 83-90 insulin Homo sapiens 19-26 7050220-4 1982 There was a marginally significant correlation (r = -0.21) between age and insulin-stimulated glucose utilization, which fell to -0.13 when controlled for RBW. Glucose 94-101 insulin Homo sapiens 75-82 7050220-8 1982 The cause of the glucose intolerance associated with aging seems to be loss of normal in vivo insulin action. Glucose 17-24 insulin Homo sapiens 94-101 6750316-3 1982 Insulin levels were significantly elevated 30 min after consumption of 12.5, 25, or 50 g of glucose, and were higher after the 50 g dose than after 12.5 g. Changes in plasma glucose concentrations were small and did not correlate with glucose dose. Glucose 92-99 insulin Homo sapiens 0-7 6750314-2 1982 Studies of adipocytes from obese before fasting showed a significant reduction of insulin binding when expressed to cell surface area and rightward shifts of the insulin dose response curves (decreased insulin sensitivity) for glucose transport, glucose oxidation, lipogenesis and antilipolysis. Glucose 227-234 insulin Homo sapiens 162-169 6284782-3 1982 Insulin resistance was documented by the presence of fasting hyperglycemia and glucose intolerance together with hyperinsulinemia as well as resistance to exogenous insulin. Glucose 79-86 insulin Homo sapiens 0-7 7050326-2 1982 To examine this question, growth velocity was measured in nine type 1 diabetic patients (age 14 +/- 3 years) before and after six months of intensive insulin treatment either with the insulin pump or with multiple injections, which lowered mean plasma glucose concentration from 270 +/- 96 to 105 +/- 55 mg/dl and total glycosylated hemoglobin from 12.4 +/- 3.0 to 8.4 +/- 1.5% (mean +/- SD). Glucose 252-259 insulin Homo sapiens 150-157 6750314-2 1982 Studies of adipocytes from obese before fasting showed a significant reduction of insulin binding when expressed to cell surface area and rightward shifts of the insulin dose response curves (decreased insulin sensitivity) for glucose transport, glucose oxidation, lipogenesis and antilipolysis. Glucose 227-234 insulin Homo sapiens 162-169 6750316-3 1982 Insulin levels were significantly elevated 30 min after consumption of 12.5, 25, or 50 g of glucose, and were higher after the 50 g dose than after 12.5 g. Changes in plasma glucose concentrations were small and did not correlate with glucose dose. Glucose 174-181 insulin Homo sapiens 0-7 6750314-2 1982 Studies of adipocytes from obese before fasting showed a significant reduction of insulin binding when expressed to cell surface area and rightward shifts of the insulin dose response curves (decreased insulin sensitivity) for glucose transport, glucose oxidation, lipogenesis and antilipolysis. Glucose 246-253 insulin Homo sapiens 82-89 6750314-2 1982 Studies of adipocytes from obese before fasting showed a significant reduction of insulin binding when expressed to cell surface area and rightward shifts of the insulin dose response curves (decreased insulin sensitivity) for glucose transport, glucose oxidation, lipogenesis and antilipolysis. Glucose 246-253 insulin Homo sapiens 162-169 6750314-2 1982 Studies of adipocytes from obese before fasting showed a significant reduction of insulin binding when expressed to cell surface area and rightward shifts of the insulin dose response curves (decreased insulin sensitivity) for glucose transport, glucose oxidation, lipogenesis and antilipolysis. Glucose 246-253 insulin Homo sapiens 162-169 6750314-4 1982 Moreover, decreased maximal glucose transport capacities were present in rat cells from obese both in the basal and maximally insulin stimulated states. Glucose 28-35 insulin Homo sapiens 126-133 6750314-5 1982 Similarly, the percentage response above basal level to maximal insulin stimulation of glucose oxidation and lipogenesis was impaired to these cells. Glucose 87-94 insulin Homo sapiens 64-71 6750316-3 1982 Insulin levels were significantly elevated 30 min after consumption of 12.5, 25, or 50 g of glucose, and were higher after the 50 g dose than after 12.5 g. Changes in plasma glucose concentrations were small and did not correlate with glucose dose. Glucose 174-181 insulin Homo sapiens 0-7 6755441-1 1982 It was detected that the blood immunoreactive insulin (IRI) level in thyrotoxic patients is changed on an empty stomach and after glucose load and the pancreatic beta-cell response to hyperglycemia is raised. Glucose 130-137 insulin Homo sapiens 46-53 6750314-9 1982 However, due to marked post receptor alterations, the insulin stimulated glucose utilization was severely blunted. Glucose 73-80 insulin Homo sapiens 54-61 6750314-10 1982 Thus, the glucose transport system of adipocytes from all fasted subjects was totally unresponsive to insulin, while some of the fasted patients had a slight response of glucose oxidation and lipogenesis in the presence of insulin in maximally effective concentrations. Glucose 10-17 insulin Homo sapiens 223-230 6750314-10 1982 Thus, the glucose transport system of adipocytes from all fasted subjects was totally unresponsive to insulin, while some of the fasted patients had a slight response of glucose oxidation and lipogenesis in the presence of insulin in maximally effective concentrations. Glucose 170-177 insulin Homo sapiens 223-230 6214733-5 1982 Fasting and peak serum insulin responses to glucose were abnormally high in most patients with polycystic ovary syndrome. Glucose 44-51 insulin Homo sapiens 23-30 7051847-5 1982 The insulin concentrations causing half-maximal responses (a measure of the sensitivity to insulin) of glucose transport, glucose metabolism and lipolysis were similar in fat cells from the two sexes, which is consistent with the comparable values of insulin receptor binding when adjusted to cell surface. Glucose 103-110 insulin Homo sapiens 4-11 6290753-5 1982 Elevated serum proinsulin and, in most patients, an increased insulin secretion rate are usually found after administration of agents such as glucose or leucine. Glucose 142-149 insulin Homo sapiens 15-25 6290753-5 1982 Elevated serum proinsulin and, in most patients, an increased insulin secretion rate are usually found after administration of agents such as glucose or leucine. Glucose 142-149 insulin Homo sapiens 18-25 7051847-5 1982 The insulin concentrations causing half-maximal responses (a measure of the sensitivity to insulin) of glucose transport, glucose metabolism and lipolysis were similar in fat cells from the two sexes, which is consistent with the comparable values of insulin receptor binding when adjusted to cell surface. Glucose 122-129 insulin Homo sapiens 4-11 7051847-5 1982 The insulin concentrations causing half-maximal responses (a measure of the sensitivity to insulin) of glucose transport, glucose metabolism and lipolysis were similar in fat cells from the two sexes, which is consistent with the comparable values of insulin receptor binding when adjusted to cell surface. Glucose 103-110 insulin Homo sapiens 91-98 7051847-7 1982 Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization. Glucose 27-34 insulin Homo sapiens 92-99 7051887-1 1982 Use of continuous intravenous infusion of insulin-glucose-potassium solution. Glucose 50-57 insulin Homo sapiens 42-49 7051847-7 1982 Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization. Glucose 43-50 insulin Homo sapiens 92-99 7051847-7 1982 Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization. Glucose 43-50 insulin Homo sapiens 92-99 7103278-2 1982 We evaluated a practical closed-loop system of insulin delivery consisting of hourly blood glucose determinations using glucose oxidase reagent strips and an intravenous infusion of insulin controlled by a commonly available controller. Glucose 91-98 insulin Homo sapiens 47-54 7051847-7 1982 Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization. Glucose 43-50 insulin Homo sapiens 92-99 7051847-7 1982 Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization. Glucose 43-50 insulin Homo sapiens 92-99 7051847-7 1982 Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization. Glucose 43-50 insulin Homo sapiens 92-99 6813263-7 1982 In contrast to mixed solutions, infusion of glucose alone caused a pronounced increase of the insulin levels and hyperglycemia in some patients suffering from liver cirrhosis. Glucose 44-51 insulin Homo sapiens 94-101 6761205-3 1982 The insulin dose-response characteristics for suppression of glucose production and stimulation of glucose utilization and their relationship to monocyte insulin binding were determined in six normal volunteers after 12-h infusion of growth hormone and 12-h infusion of saline. Glucose 61-68 insulin Homo sapiens 4-11 6761205-3 1982 The insulin dose-response characteristics for suppression of glucose production and stimulation of glucose utilization and their relationship to monocyte insulin binding were determined in six normal volunteers after 12-h infusion of growth hormone and 12-h infusion of saline. Glucose 99-106 insulin Homo sapiens 4-11 6761205-8 1982 Insulin dose-response curves for both suppression of glucose production (half-maximal response at 37 +/- 3 versus 20 +/- 3 microunits/ml, P less than 0.01) and stimulation of glucose utilization (half-maximal response at 98 +/- 8 versus 52 +/- 8 microunits/ml, P less than 0.01) were shifted to the right with preservation of normal maximal responses to insulin. Glucose 53-60 insulin Homo sapiens 0-7 6761205-8 1982 Insulin dose-response curves for both suppression of glucose production (half-maximal response at 37 +/- 3 versus 20 +/- 3 microunits/ml, P less than 0.01) and stimulation of glucose utilization (half-maximal response at 98 +/- 8 versus 52 +/- 8 microunits/ml, P less than 0.01) were shifted to the right with preservation of normal maximal responses to insulin. Glucose 175-182 insulin Homo sapiens 0-7 6761205-10 1982 Thus, except at near maximal insulin receptor occupancy, the action of insulin on glucose production and utilization per number of monocyte insulin receptors occupied was decreased. Glucose 82-89 insulin Homo sapiens 71-78 6761208-0 1982 Influence of plasma glucose and insulin concentration on plasma glucose clearance in man. Glucose 64-71 insulin Homo sapiens 32-39 7045154-7 1982 When obese and nonobese patients were compared, the obese subjects with normal glucose tolerance released a greater amount of IRGIP and insulin than the normal weight controls, whereas no significant difference between obese and nonobese could be found within the IGT and DM groups. Glucose 79-86 insulin Homo sapiens 136-143 6751896-0 1982 Insulin delivery rate in response to glucose and arginine infusion in hyperthyroidism. Glucose 37-44 insulin Homo sapiens 0-7 6751896-1 1982 Insulin delivery rates were estimated from the peripheral serum insulin response to a single bolus injection of glucose or arginine in eight normal subjects and eight patients with hyperthyroidism. Glucose 112-119 insulin Homo sapiens 0-7 6751896-1 1982 Insulin delivery rates were estimated from the peripheral serum insulin response to a single bolus injection of glucose or arginine in eight normal subjects and eight patients with hyperthyroidism. Glucose 112-119 insulin Homo sapiens 64-71 6751896-4 1982 The delivered insulin in response to glucose infusion was similar in the two groups. Glucose 37-44 insulin Homo sapiens 14-21 6751896-11 1982 In hyperthyroidism, therefore, glucose intolerance appears to be primarily related to an antagonism of the hepatic effect of insulin by thyroxine rather than an inhibitory effect of thyroxine on insulin secretion. Glucose 31-38 insulin Homo sapiens 125-132 7046438-9 1982 The resulting abatement of the patient"s hyperinsulinism (fasting plasma insulin = 37 microunits/ml) was accompanied by the appearance of menses, normalization of glucose tolerance, and amelioration of the acanthosis. Glucose 163-170 insulin Homo sapiens 46-53 6807390-2 1982 Insulin absorption correlated with plasma insulin (r = 0.97, p less than 0.001) and blood glucose (r = -0.87, p less than 0.01) concentrations. Glucose 90-97 insulin Homo sapiens 0-7 6749586-4 1982 After ingestion of 25 g glucose, the cumulative insulin production rate exceeded normal values (p less than 0.05), but was below normal with 100 g glucose (p less than 0.01). Glucose 24-31 insulin Homo sapiens 48-55 6756004-3 1982 For glucagon, the increase was present at all times tested, for insulin this rise was significant only during the first 60 min of the arginine test and during the rapid secretory phase following glucose injection. Glucose 195-202 insulin Homo sapiens 64-71 6759080-5 1982 Improvement in glucose tolerance was associated with an increase in fasting and postglucose serum insulin and C-peptide concentration. Glucose 15-22 insulin Homo sapiens 98-105 6759080-5 1982 Improvement in glucose tolerance was associated with an increase in fasting and postglucose serum insulin and C-peptide concentration. Glucose 15-22 insulin Homo sapiens 110-119 6283873-4 1982 Fasting triglycerides and high-density lipoprotein cholesterol were inversely related at base-line; insulin response to oral glucose was inversely related to high-density lipoprotein cholesterol levels at the end of the study. Glucose 125-132 insulin Homo sapiens 100-107 6298039-0 1982 Important role of adrenergic mechanisms in acute glucose counterregulation following insulin-induced hypoglycemia in type I diabetes. Glucose 49-56 insulin Homo sapiens 85-92 6761199-2 1982 Under these conditions (minimal plasma glucose 27.4 +/- 1 mg/dl) the decrease of serum potassium concentration (0.9 mVal/L) is mediated by two mechanisms: insulin-induced (0.48 mVal/L) and epinephrine-induced (0.42 mVal/L) cellular uptake of potassium. Glucose 39-46 insulin Homo sapiens 155-162 6749586-10 1982 These data suggest that obese hyperinsulinaemic Type 2 diabetic patients may represent a subgroup of diabetic patients with predominantly peripheral, but compensated hepatic, insulin resistance being associated with an increased basal insulin production rate which only exhausts after ingestion of a large glucose load. Glucose 306-313 insulin Homo sapiens 35-42 6759077-9 1982 The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. Glucose 83-90 insulin Homo sapiens 20-27 6759079-0 1982 Insulin responses to glucose in non-insulin-dependent diabetic subjects with and without the chlorpropamide-alcohol flush: effect of salicylate and naloxone. Glucose 21-28 insulin Homo sapiens 0-7 7044833-4 1982 Therefore, it might be expected that insulin would have a less important role in regulating glucose and carbohydrate metabolism in the ruminant animal. Glucose 92-99 insulin Homo sapiens 37-44 6751813-3 1982 The nadir of blood glucose (19.0 +/- 2.7 ng/100 ml) is detected 30 min following insulin application, paralleled by suppressed levels of FFA and beta-hydroxybutyrate. Glucose 19-26 insulin Homo sapiens 81-88 7044833-8 1982 Insulin appears to indirectly alter hepatic glucose production by decreasing the release of gluconeogenic precursors from peripheral tissues. Glucose 44-51 insulin Homo sapiens 0-7 7044833-6 1982 Insulin may promote lipid deposition by increasing adipocyte membrane permeability to glucose with subsequent metabolism to alpha-glycerolphosphoric acid and thereby stimulating fatty acid esterification. Glucose 86-93 insulin Homo sapiens 0-7 7042734-3 1982 Both the patient"s in vivo dose-response curve for insulin-stimulated glucose transport in isolated adipocytes were shifted to the right and showed marked decreases in the maximal insulin response. Glucose 70-77 insulin Homo sapiens 51-58 6123524-0 1982 Differential effects of insulin on splanchnic and peripheral glucose disposal after an intravenous glucose load in man. Glucose 61-68 insulin Homo sapiens 24-31 6123524-1 1982 The present study was designed to investigate the mechanisms by which insulin regulates the disposal of an intravenous glucose load in man. Glucose 119-126 insulin Homo sapiens 70-77 6123524-21 1982 IT IS CONCLUDED THAT: (a) the suppressive effect of hyperglycemia on hepatic glucose output is strictly dependent on the degree of hepatic insulinization; (b) insulin plays an essential role in promoting splanchnic glucose uptake after an intravenous glucose load whereas hyperglycemia per se is totally unable to activate this process; (c) peripheral glucose uptake is markedly stimulated by hyperglycemia even in the face of insulin deficiency. Glucose 77-84 insulin Homo sapiens 139-146 6123524-21 1982 IT IS CONCLUDED THAT: (a) the suppressive effect of hyperglycemia on hepatic glucose output is strictly dependent on the degree of hepatic insulinization; (b) insulin plays an essential role in promoting splanchnic glucose uptake after an intravenous glucose load whereas hyperglycemia per se is totally unable to activate this process; (c) peripheral glucose uptake is markedly stimulated by hyperglycemia even in the face of insulin deficiency. Glucose 77-84 insulin Homo sapiens 159-166 6123524-21 1982 IT IS CONCLUDED THAT: (a) the suppressive effect of hyperglycemia on hepatic glucose output is strictly dependent on the degree of hepatic insulinization; (b) insulin plays an essential role in promoting splanchnic glucose uptake after an intravenous glucose load whereas hyperglycemia per se is totally unable to activate this process; (c) peripheral glucose uptake is markedly stimulated by hyperglycemia even in the face of insulin deficiency. Glucose 215-222 insulin Homo sapiens 159-166 6123524-21 1982 IT IS CONCLUDED THAT: (a) the suppressive effect of hyperglycemia on hepatic glucose output is strictly dependent on the degree of hepatic insulinization; (b) insulin plays an essential role in promoting splanchnic glucose uptake after an intravenous glucose load whereas hyperglycemia per se is totally unable to activate this process; (c) peripheral glucose uptake is markedly stimulated by hyperglycemia even in the face of insulin deficiency. Glucose 215-222 insulin Homo sapiens 159-166 6123524-21 1982 IT IS CONCLUDED THAT: (a) the suppressive effect of hyperglycemia on hepatic glucose output is strictly dependent on the degree of hepatic insulinization; (b) insulin plays an essential role in promoting splanchnic glucose uptake after an intravenous glucose load whereas hyperglycemia per se is totally unable to activate this process; (c) peripheral glucose uptake is markedly stimulated by hyperglycemia even in the face of insulin deficiency. Glucose 215-222 insulin Homo sapiens 159-166 6123524-23 1982 Our data, thus, indicate that insulin rather than hyperglycemia regulates splanchnic glucose disposal in man. Glucose 85-92 insulin Homo sapiens 30-37 7042734-3 1982 Both the patient"s in vivo dose-response curve for insulin-stimulated glucose transport in isolated adipocytes were shifted to the right and showed marked decreases in the maximal insulin response. Glucose 70-77 insulin Homo sapiens 180-187 7045192-7 1982 Fasting glucose was significantly correlated to insulin (r = .30 , p less than .001). Glucose 8-15 insulin Homo sapiens 48-55 6750603-10 1982 This was further substantiated by the fact that, at the same insulin levels, glucose utilization did not increase more in the diabetics than in the controls, although the glycemia reached was considerably higher in the diabetics. Glucose 77-84 insulin Homo sapiens 61-68 6750603-0 1982 Insulin resistance and decreased insulin response to glucose in lean type 2 diabetics. Glucose 53-60 insulin Homo sapiens 33-40 7088631-0 1982 Use of a glucose-controlled insulin infusion system in children and adolescents with insulin-dependent diabetes. Glucose 9-16 insulin Homo sapiens 28-35 7088631-1 1982 Seven children and adolescents (aged 8 to 23 years, mean 16 years) with poorly controlled insulin-dependent diabetes mellitus were evaluated with a glucose-controlled insulin infusion system (GCIIS) to determine whether its use could help define appropriate long-term insulin treatment regimens and increase patient understanding and compliance with such regimens. Glucose 148-155 insulin Homo sapiens 167-174 7088631-5 1982 The continuous documentation of blood glucose levels provided by the GCIIS was valuable in educating patients about the interrelationship between insulin, exercise, and diet. Glucose 38-45 insulin Homo sapiens 146-153 6750603-9 1982 With the lower glucose load, metabolic clearance rate decreased more markedly in diabetics, again suggesting insulin resistance. Glucose 15-22 insulin Homo sapiens 109-116 6750603-16 1982 The insulin resistance could mainly be ascribed to inadequate glucose uptake, but a defect in glucose-induced suppression of glucose production may also have contributed. Glucose 62-69 insulin Homo sapiens 4-11 6749565-2 1982 Insulin levels at fasting state and after glucose loading were 149 +/- 63 microunits/ml (mean +/- SD) and over 1000 microunits/ml, respectively, while fasting levels of blood glucose were 77.7 +/- 8.9 mg/dl (mean +/- SD). Glucose 42-49 insulin Homo sapiens 0-7 7052089-0 1982 Direct effect of glucose on the preproinsulin mRNA level in isolated pancreatic islets. Glucose 17-24 insulin Homo sapiens 32-45 6750967-5 1982 It is suggested that factors other than the response of plasma radioimmunoassayable insulin contribute to the production of glucose intolerance in cases of extensive pediatric pancreatectomy. Glucose 124-131 insulin Homo sapiens 84-91 7046669-2 1982 After reduction of body weight to ideal values, patients whose peak serum insulin levels were initially 64 microunits/mL or greater had reductions of blood glucose values from 227 +/- 24 to 122 +/- 10 mg/dL (fasting) and from 400 +/- 49 to 160 +/- 11 mg/dL (two hours postprandial); at C-peptide peaks of 6.0 ng/mL or greater, these blood glucose values fell from 244 +/- 30 to 118 +/- 12 mg/mL and from 400 +/- 51 to 160 +/- 16 mg/dL, respectively. Glucose 156-163 insulin Homo sapiens 74-81 7046428-5 1982 Plasma insulin response to glucose was also reduced significantly. Glucose 27-34 insulin Homo sapiens 7-14 7046669-5 1982 These results suggest that levels of insulin or C peptide induced during glucose tolerance testing distinguish between two types of hyperglycemic obesity-insulin-dependent diabetes mellitus and insulin-resistant obesity. Glucose 73-80 insulin Homo sapiens 37-44 6759265-0 1982 Glucose modulation of insulin and glucagon secretion in nondiabetic and diabetic man. Glucose 0-7 insulin Homo sapiens 22-29 7042732-5 1982 The highest dose of baclofen significantly increased insulin responses to glucose and raised basal glucagon levels (P less than 0.01). Glucose 74-81 insulin Homo sapiens 53-60 7049777-1 1982 In six patients with chemical diabetes, insulin resistance was assessed by the steady-state plasma glucose (SSPG) level during a constant infusion of epinephrine, propranolol, glucose and insulin. Glucose 99-106 insulin Homo sapiens 40-47 7049783-2 1982 During inhibition of endogenous insulin secretion by epinephrine + propranolol, glucose infusion produced an increase in carbohydrate oxidation when plasma glucose levels reached approximately 200 mg/100 ml. Glucose 80-87 insulin Homo sapiens 32-39 7049783-3 1982 Addition of exogenous insulin to the glucose infusion was accompanied by a further rise in carbohydrate oxidation and a decrease in plasma glucose level. Glucose 37-44 insulin Homo sapiens 22-29 7049783-3 1982 Addition of exogenous insulin to the glucose infusion was accompanied by a further rise in carbohydrate oxidation and a decrease in plasma glucose level. Glucose 139-146 insulin Homo sapiens 22-29 7049783-4 1982 It was concluded that hyperglycemia without insulin response represents a compensatory mechanism which favours peripheral glucose utilization. Glucose 122-129 insulin Homo sapiens 44-51 6750938-3 1982 Glucose-stimulated insulin response is enhanced in hypertensives, even if glucose tolerance is normal. Glucose 0-7 insulin Homo sapiens 19-26 6750703-2 1982 We elucidated that, in five patients with hyperparathyroidism, GIP and insulin responded remarkably to glucose ingestion, and that hypercalcaemia appeared to have a stimulatory effect on glucose-induced GIP release as well as on insulin release. Glucose 103-110 insulin Homo sapiens 71-78 6750703-2 1982 We elucidated that, in five patients with hyperparathyroidism, GIP and insulin responded remarkably to glucose ingestion, and that hypercalcaemia appeared to have a stimulatory effect on glucose-induced GIP release as well as on insulin release. Glucose 187-194 insulin Homo sapiens 229-236 6750703-7 1982 The potentiated response of insulin to glucose may be caused, in part, by GIP. Glucose 39-46 insulin Homo sapiens 28-35 6753107-0 1982 Release of gastric inhibitory polypeptide and insulin in response to intrajejunal glucose in duodenal ulcer patients before and after truncal vagotomy. Glucose 82-89 insulin Homo sapiens 46-53 6753108-4 1982 It is concluded that the increased GIP and insulin response to glucose among duodenal ulcer patients may be explained by increased gastric emptying, known to occur in these patients. Glucose 63-70 insulin Homo sapiens 43-50 7044093-9 1982 In response to a glucose load, insulin and glucose decreased significantly by wk 31 of treatment. Glucose 17-24 insulin Homo sapiens 31-38 7048770-5 1982 At comparable peripheral steady state insulin levels the relative decrease of the plasma glucose and free fatty acid concentration is a measure of the insulin sensitivity in vivo. Glucose 89-96 insulin Homo sapiens 38-45 7048770-5 1982 At comparable peripheral steady state insulin levels the relative decrease of the plasma glucose and free fatty acid concentration is a measure of the insulin sensitivity in vivo. Glucose 89-96 insulin Homo sapiens 151-158 6753477-0 1982 Inhibition of the insulin response to glucose after treatment with cyproheptadine. Glucose 38-45 insulin Homo sapiens 18-25 6753099-11 1982 The lack of enhancement of peripherally measured insulin secretion seemed, if anything, to overestimate B-cell secretory rates since the ratio of insulin to C-peptide was increased (from 37 to 89) after priming with glucose, suggesting that the hepatic clearance of insulin was decreased during the second glucose challenge. Glucose 216-223 insulin Homo sapiens 146-153 6753099-11 1982 The lack of enhancement of peripherally measured insulin secretion seemed, if anything, to overestimate B-cell secretory rates since the ratio of insulin to C-peptide was increased (from 37 to 89) after priming with glucose, suggesting that the hepatic clearance of insulin was decreased during the second glucose challenge. Glucose 216-223 insulin Homo sapiens 146-153 6753099-12 1982 It is concluded that (1) facilitation of glucose disposal by previous glucose administration can be induced by amounts of glucose equivalent to those associated with meal intake, (2) enhancement of insulin release is not an obligatory component of the facilitated glucose disposal, (3) decreased hepatic clearance of insulin may accompany the Staub-Traugott effect. Glucose 70-77 insulin Homo sapiens 317-324 6753099-12 1982 It is concluded that (1) facilitation of glucose disposal by previous glucose administration can be induced by amounts of glucose equivalent to those associated with meal intake, (2) enhancement of insulin release is not an obligatory component of the facilitated glucose disposal, (3) decreased hepatic clearance of insulin may accompany the Staub-Traugott effect. Glucose 70-77 insulin Homo sapiens 317-324 6753099-12 1982 It is concluded that (1) facilitation of glucose disposal by previous glucose administration can be induced by amounts of glucose equivalent to those associated with meal intake, (2) enhancement of insulin release is not an obligatory component of the facilitated glucose disposal, (3) decreased hepatic clearance of insulin may accompany the Staub-Traugott effect. Glucose 70-77 insulin Homo sapiens 317-324 6282137-1 1982 The weak base acridine orange (AO) has been shown to be accumulated by the insulin-containing secretory granules of cultured beta-cells in response to high glucose. Glucose 156-163 insulin Homo sapiens 75-82 7042109-5 1982 The findings suggest that insulin resistance develops during drug therapy and disturbs both glucose and lipid metabolism. Glucose 92-99 insulin Homo sapiens 26-33 7042050-7 1982 Plasma insulin was elevated less after maltose than after glucose infusion. Glucose 58-65 insulin Homo sapiens 7-14 7172978-1 1982 It is generally acknowledged that the ideal automatic insulin infusion system would be a closed loop that metered insulin delivery in response to a feedback sensor such as an implantable glucose detector. Glucose 187-194 insulin Homo sapiens 54-61 6765120-1 1982 It is now possible to virtually normalize ambient blood glucose levels in insulin-dependent diabetic women during pregnancy. Glucose 56-63 insulin Homo sapiens 74-81 6765122-5 1982 The insulin dose should be modified periodically according to bedside glucose monitoring. Glucose 70-77 insulin Homo sapiens 4-11 6756834-7 1982 Model simulations reaffirm expectations concerning the poor blood glucose control attainable by intramuscular insulin injection. Glucose 66-73 insulin Homo sapiens 110-117 6756834-8 1982 Simulations of blood glucose regulation by an artificial pancreas using closed-loop feedback control for controlling insulin delivery rate reveal hyperinsulinemia that results in a net shift in the deposition of a glucose load from liver to peripheral tissues. Glucose 21-28 insulin Homo sapiens 117-124 6756834-9 1982 Simulations of this system in which the time delay for glucose measurement is varied from 1.5 to 30 min show that increases in sensor delay result in progressive loss in glucose regulation, exacerbation of hyperinsulinemia, and increased insulin requirements. Glucose 55-62 insulin Homo sapiens 211-218 6756836-0 1982 Insulin delivery systems: do they need a glucose sensor? Glucose 41-48 insulin Homo sapiens 0-7 6756838-10 1982 Effects of insulin upon glucose waned first, followed by effects upon potassium and then lipolysis. Glucose 24-31 insulin Homo sapiens 11-18 6759255-6 1982 These data indicate that the glucose metabolic clearance rate (MCR), but not glucose utilization rate (M), can be used to compare in vivo insulin action when insulin clamp studies are performed in subjects with different basal plasma glucose concentrations. Glucose 29-36 insulin Homo sapiens 138-145 6759255-6 1982 These data indicate that the glucose metabolic clearance rate (MCR), but not glucose utilization rate (M), can be used to compare in vivo insulin action when insulin clamp studies are performed in subjects with different basal plasma glucose concentrations. Glucose 29-36 insulin Homo sapiens 158-165 7188047-1 1982 Restoration of near-normal glucose metabolism with the insulin pump reduces retinal fluorescein leakage and microalbuminuria in diabetes. Glucose 27-34 insulin Homo sapiens 55-62 7037819-7 1982 The integrated plasma insulin levels during the oral glucose tolerance test tripled after both hGH preparations. Glucose 53-60 insulin Homo sapiens 22-29 7037822-8 1982 Since the insulin response was enhanced only when both the glucose and GIP responses were magnified, we conclude that endogenous GIP is a glucose-dependent insulinotropic factor. Glucose 59-66 insulin Homo sapiens 10-17 7037822-8 1982 Since the insulin response was enhanced only when both the glucose and GIP responses were magnified, we conclude that endogenous GIP is a glucose-dependent insulinotropic factor. Glucose 138-145 insulin Homo sapiens 10-17 7102013-5 1982 On the other hand from the prompt decrease of free fatty acids and glycerin under glucose-induced hyperinsulinaemia was concluded to an unrestricted efficacy of the insulin in the fatty tissue in the sense of the furthering of lipogenesis and inhibition of the lipolysis. Glucose 82-89 insulin Homo sapiens 103-110 7041606-2 1982 The relative chromium response at insulin peak was inversely correlated with the total insulin (r = -0.451, p less than 0.05) as well as with the ratio of the total insulin to the total glucose (r = -0.554, p less than 0.02). Glucose 186-193 insulin Homo sapiens 34-41 7043177-0 1982 Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects. Glucose 21-28 insulin Homo sapiens 88-95 7043177-7 1982 It is also suggested that the enhanced E and GH secretion found in trained subjects injected with insulin, is possibly related to the greater fall in plasma glucose in the trained subjects compared to the non-trained subjects. Glucose 157-164 insulin Homo sapiens 98-105 7043180-0 1982 Insulin stimulation of glucose oxidation in cultured human skin fibroblasts. Glucose 23-30 insulin Homo sapiens 0-7 7051589-5 1982 The increase of the reduced reserves of glycogen in liver and muscle after the offer of glucose refers to preserved regulation mechanisms in supply of substrates despite peripheral insulin resistance. Glucose 88-95 insulin Homo sapiens 181-188 6812531-3 1982 Compared to the conventional regimen, low-dose insulin infusion showed several advantages: 1) better control of blood glucose level, 2) no risk of hypoglycemia and hypokaliemia, 3) rapid decrease of urinary ketone bodies and 4) gradual acidosis correction. Glucose 118-125 insulin Homo sapiens 47-54 6803696-8 1982 It is postulated that cells normally impermeable to glucose, when serum insulin levels are low, become permeable in some severely starved patients, for reasons unknown. Glucose 52-59 insulin Homo sapiens 72-79 6759249-8 1982 When a low-dose insulin infusion was given to approximate the increases of portal venous insulin during therapy, similar falls of glucose production occurred. Glucose 130-137 insulin Homo sapiens 16-23 7041844-4 1982 Patients had mild glucose intolerance that did not change after hemofiltration, although the exaggerated insulin responses to glucose administration did significantly decrease in period 2. Glucose 126-133 insulin Homo sapiens 105-112 6759249-10 1982 The small fall in glucose production in those patients whose insulin level did not rise during therapy suggests an additional contribution by some other mechanism. Glucose 18-25 insulin Homo sapiens 61-68 7047270-4 1982 In contrast, glucose uptake in diabetics was independent of glucose concentration but dependent on insulin uptake over an insulin concentration range up to 140 mU/l; glucose uptake reached the same levels as in control subjects but only at higher concentration and higher uptake of insulin. Glucose 13-20 insulin Homo sapiens 99-106 7047270-4 1982 In contrast, glucose uptake in diabetics was independent of glucose concentration but dependent on insulin uptake over an insulin concentration range up to 140 mU/l; glucose uptake reached the same levels as in control subjects but only at higher concentration and higher uptake of insulin. Glucose 13-20 insulin Homo sapiens 122-129 7047270-4 1982 In contrast, glucose uptake in diabetics was independent of glucose concentration but dependent on insulin uptake over an insulin concentration range up to 140 mU/l; glucose uptake reached the same levels as in control subjects but only at higher concentration and higher uptake of insulin. Glucose 13-20 insulin Homo sapiens 122-129 7047270-7 1982 It is concluded that in Type 2 diabetes: (1) the superficial forearm tissues show decreased responsiveness to the stimulatory effect of both hyperglycaemia and hyperinsulinaemia on glucose utilization but the NEFA-lowering effect of insulin is undiminished, and (2) tissue uptake of insulin is normal, despite the decrease in receptor capacity that has been demonstrated by others. Glucose 181-188 insulin Homo sapiens 165-172 7050344-16 1982 The rising ketone body levels in starvation and after exercise were accompanied by simultaneous increases in the plasma insulin/glucagon ratios; in both, glucose ingestion increased the ratio further, while alanine decreased it. Glucose 154-161 insulin Homo sapiens 120-127 7043173-3 1982 Insulin action at steady state was expressed as metabolic clearance rate of glucose (MCRG) rather than overall rate of glucose disappearance (M or Rd). Glucose 76-83 insulin Homo sapiens 0-7 7043173-3 1982 Insulin action at steady state was expressed as metabolic clearance rate of glucose (MCRG) rather than overall rate of glucose disappearance (M or Rd). Glucose 119-126 insulin Homo sapiens 0-7 7043174-10 1982 Glucose integrated concentration showed no correlation with free insulin integrated concentration, however, it did correlate inversely with the percentage of total insulin in the free insulin fraction. Glucose 0-7 insulin Homo sapiens 164-171 7043174-10 1982 Glucose integrated concentration showed no correlation with free insulin integrated concentration, however, it did correlate inversely with the percentage of total insulin in the free insulin fraction. Glucose 0-7 insulin Homo sapiens 164-171 6278610-9 1982 Thus, continuous infusion of insulin added to the rehydration solution, including isotonic bicarbonate, isotonic saline, glucose and electrolytes is as effective as discontinuous insulin infusion, but with a lower incidence of complications. Glucose 121-128 insulin Homo sapiens 29-36 6295856-3 1982 In search of possible factors which impair insulin release, we have investigated the effect of naloxone, a specific opiate receptor blocker, on insulin responses to glucose in subjects with non-insulin-dependent diabetes, as well as in normal subjects. Glucose 165-172 insulin Homo sapiens 144-151 6295856-5 1982 Acute insulin response to glucose (mean change 3-10 min insulin), second phase insulin secretion (change 10-60 min), as well as glucose disappearance rates (%/min) were significantly increased in the diabetics receiving the two higher doses of naloxone (2 and 4 mg, respectively). Glucose 26-33 insulin Homo sapiens 6-13 6801979-3 1982 Eventually, insulin levels were lower than would have been expected from the prevailing glucose values. Glucose 88-95 insulin Homo sapiens 12-19 6759249-7 1982 Patients with a rise in fasting insulin during therapy had a greater fall in glucose production than those whose insulin did not rise (25.4 +/- 8.1 vs. 7.8 +/- 2.4 mg/m2/min; P less than 0.005). Glucose 77-84 insulin Homo sapiens 32-39 7039319-3 1982 Paradoxically, it antagonizes the effects of insulin on glucose metabolism in adipose tissue and skeletal muscle. Glucose 56-63 insulin Homo sapiens 45-52 6121186-5 1982 Conversely, raised insulin resistance in the absence of decreased beta-cell function induces only a small rise in basal plasma glucose concentrations, which stimulates a compensatory increase in basal plasma insulin concentrations from a normal beta-cell capacity. Glucose 127-134 insulin Homo sapiens 19-26 6121186-5 1982 Conversely, raised insulin resistance in the absence of decreased beta-cell function induces only a small rise in basal plasma glucose concentrations, which stimulates a compensatory increase in basal plasma insulin concentrations from a normal beta-cell capacity. Glucose 127-134 insulin Homo sapiens 208-215 6121186-6 1982 However, if the beta-cell dysfunction is sufficient to induce a basal plasma glucose concentration of 5-6 mmol/l, a slight rise in insulin resistance causes pronounced basal hyperglycaemia. Glucose 77-84 insulin Homo sapiens 131-138 7038916-0 1982 The insulin and glucose response to an oral glucose load in non-insulin-dependent diabetes in the young. Glucose 44-51 insulin Homo sapiens 4-11 7038916-5 1982 The insulin and glucose response during a 3-hour period revealed fasting hyperinsulinism with a delayed and attenuated insulin response, a much lower insulin area and higher glucose ares, a lower insulin-glucose ratio and a lower modified Seltzer insulinogenic index when compared with 50 non-diabetic reference subjects. Glucose 16-23 insulin Homo sapiens 78-85 7038916-5 1982 The insulin and glucose response during a 3-hour period revealed fasting hyperinsulinism with a delayed and attenuated insulin response, a much lower insulin area and higher glucose ares, a lower insulin-glucose ratio and a lower modified Seltzer insulinogenic index when compared with 50 non-diabetic reference subjects. Glucose 174-181 insulin Homo sapiens 4-11 7038916-5 1982 The insulin and glucose response during a 3-hour period revealed fasting hyperinsulinism with a delayed and attenuated insulin response, a much lower insulin area and higher glucose ares, a lower insulin-glucose ratio and a lower modified Seltzer insulinogenic index when compared with 50 non-diabetic reference subjects. Glucose 174-181 insulin Homo sapiens 78-85 7040887-2 1982 It utilizes closed-loop insulin delivery device (GCIIS, Biostator) capable of infusing glucose and insulin according to preselected algorithms. Glucose 87-94 insulin Homo sapiens 24-31 7040887-3 1982 In euglycemic patients, insulin was infused by GCIIS to maintain euglycemia in the face of challenges with gradually increasing doses on intravenously administered glucose. Glucose 164-171 insulin Homo sapiens 24-31 7041498-9 1982 Continuous intravenous infusion of 10% glucose solution (500 ml every 6 hours) with potassium and insulin seems to be very safe if continuous monitoring of the blood and urine glucose and ketones is observed. Glucose 39-46 insulin Homo sapiens 98-105 7039348-2 1982 In our studies, even the infusion of the 1-U dose of calcitonin was found to inhibit by 45% the acute insulin response to a glucose (20 g) pulse. Glucose 124-131 insulin Homo sapiens 102-109 7039348-5 1982 The inhibition of the acute insulin response to glucose was 65% and up to 90% with the infusion of the 4- and 8-U doses, respectively. Glucose 48-55 insulin Homo sapiens 28-35 7039348-9 1982 These results demonstrate that a) calcitonin inhibits glucose-induced insulin responses and deteriorates glucose tolerance in normal humans in a dose-dependent manner; b) calcitonin reduces the suppressive effect of glucose on glucagon secretion in a dose-related fashion; and c) both theophylline and calcium reverse the inhibitory effect of calcitonin on insulin secretion. Glucose 54-61 insulin Homo sapiens 357-364 7039348-7 1982 The inhibitory effect of calcitonin on insulin responses to glucose (5 g) and glucose tolerance was reversed by both theophylline and calcium. Glucose 60-67 insulin Homo sapiens 39-46 7039348-9 1982 These results demonstrate that a) calcitonin inhibits glucose-induced insulin responses and deteriorates glucose tolerance in normal humans in a dose-dependent manner; b) calcitonin reduces the suppressive effect of glucose on glucagon secretion in a dose-related fashion; and c) both theophylline and calcium reverse the inhibitory effect of calcitonin on insulin secretion. Glucose 54-61 insulin Homo sapiens 70-77 7041639-5 1982 The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Glucose 10-17 insulin Homo sapiens 77-84 7041639-5 1982 The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Glucose 10-17 insulin Homo sapiens 182-189 6279190-7 1982 The augmenting effect of insulin was equally effective upon culturing in a glucose-free medium and was not associated with significant alterations in testicular cell number or cellular DNA or protein content. Glucose 75-82 insulin Homo sapiens 25-32 7042430-7 1982 Since the diabetic subjects were found to have an intact insulin response to the glucose load, it is suggested that resistance to insulin-stimulated potassium uptake into cells might be involved in the pathogenesis of the paradoxical hyperkalaemia induced by acute hyperglycaemia. Glucose 81-88 insulin Homo sapiens 57-64 6759240-4 1982 Seven of the twelve fetuses showed a marked insulin response to an acute glucose-theophylline challenge. Glucose 73-80 insulin Homo sapiens 44-51 7042430-7 1982 Since the diabetic subjects were found to have an intact insulin response to the glucose load, it is suggested that resistance to insulin-stimulated potassium uptake into cells might be involved in the pathogenesis of the paradoxical hyperkalaemia induced by acute hyperglycaemia. Glucose 81-88 insulin Homo sapiens 130-137 7042432-1 1982 Insulin effect was investigated in 20 chronic alcoholics by use of an insulin and glucose infusion which suppressed endogenous insulin secretion. Glucose 82-89 insulin Homo sapiens 0-7 7042432-1 1982 Insulin effect was investigated in 20 chronic alcoholics by use of an insulin and glucose infusion which suppressed endogenous insulin secretion. Glucose 82-89 insulin Homo sapiens 127-134 7047252-4 1982 The injection of insulin or tolbutamide was followed by a marked elevation of circulating hPP which was abolished by preventing the hypoglycemic effect of these substances by intravenous glucose infusion. Glucose 187-194 insulin Homo sapiens 17-24 7075914-1 1982 We have investigated plasma glucose and immunoreactive insulin responses to 75-g oral glucose in lean, young, full-blood Aboriginal men from urban and rural communities and made comparisons with age- and weight-matched Caucasoids. Glucose 86-93 insulin Homo sapiens 55-62 7037914-1 1982 Plasma glucose and insulin responses to an oral dextrose tolerance test and to a mixed-meal test were determined in fully ambulatory residents of a retirement community. Glucose 48-56 insulin Homo sapiens 19-26 7037914-7 1982 The ability to document increases in the plasma glucose and insulin responses to a mixed meal suggests that aging, at least in women, is associated with day-long elevations of both plasma glucose and insulin concentrations. Glucose 48-55 insulin Homo sapiens 200-207 7037914-7 1982 The ability to document increases in the plasma glucose and insulin responses to a mixed meal suggests that aging, at least in women, is associated with day-long elevations of both plasma glucose and insulin concentrations. Glucose 188-195 insulin Homo sapiens 60-67 6804901-4 1982 Before treatment the non-insulin-dependent diabetic patients demonstrated significantly increased glucose values and decreased insulin values as compared with the values of the control subjects. Glucose 98-105 insulin Homo sapiens 25-32 7045141-0 1982 Comparison of the effects of insulin and H2O2 on adipocyte glucose transport. Glucose 59-66 insulin Homo sapiens 29-36 7047633-2 1982 The role of calcium in glucose-stimulated early phase insulin release in vivo. Glucose 23-30 insulin Homo sapiens 54-61 7047633-3 1982 Extensive in vitro studies have demonstrated that an increase in the concentration of Ca2+ in the cytosol of the beta-cell of islets of Langherhans is essential for the glucose-stimulated insulin release. Glucose 169-176 insulin Homo sapiens 188-195 7047633-4 1982 However, there are controversies as to whether both phases of insulin release are equally dependent upon glucose-stimulated uptake of extracellular calcium. Glucose 105-112 insulin Homo sapiens 62-69 7047633-5 1982 Previous studies performed in vivo, have demonstrated an inhibitory effect of verapamil, an organic antagonist of calcium transport into cells, on the release of insulin induced by an oral glucose load. Glucose 189-196 insulin Homo sapiens 162-169 7047633-6 1982 The present study was designed to investigate whether calcium antagonists are capable of inhibiting the rapid release of insulin that follows the iv infusion of glucose. Glucose 161-168 insulin Homo sapiens 121-128 7043172-0 1982 Similarities between insulin, hydrogen peroxide, concanavalin A, and anti-insulin receptor antibody stimulated glucose transport: increase in the number of transport sites. Glucose 111-118 insulin Homo sapiens 21-28 7043172-0 1982 Similarities between insulin, hydrogen peroxide, concanavalin A, and anti-insulin receptor antibody stimulated glucose transport: increase in the number of transport sites. Glucose 111-118 insulin Homo sapiens 74-81 7043172-1 1982 Plasma membranes from insulin or insulin mimicker (hydrogen peroxide, anti-insulin receptor antibody, and concanavalin A) treated adipocytes showed an increase in glucose transport compared to control cells due to an increase in Vmax and not due to alteration in Km. Glucose 163-170 insulin Homo sapiens 22-120 7046731-8 1982 Chloroquine, and also bacitracin, at concentrations that inhibited insulin degradation, decreased the insulin-stimulated incorporation of [14C]glucose into glycogen over 2 h. This effect of chloroquine was specific, since it did not modify the basal glycogenesis, or the glycogenic effect of a glucose load in the absence of insulin. Glucose 294-301 insulin Homo sapiens 102-109 6127792-5 1982 After oral glucose, further increases of GIP to 111 (68.8-171) pM and of insulin to 103 (33-131) mU/l were observed. Glucose 11-18 insulin Homo sapiens 73-80 7038942-4 1982 In fatally injured patients with measurable alcohol concentrations, insulin and glucose levels were markedly different from those for the corresponding surviving patients, p less than 0.001 and less than 0.01, respectively, with particularly large differences in the insulin-glucose ratio, p less than 0.001. Glucose 275-282 insulin Homo sapiens 267-274 7044844-4 1982 Significantly higher responses of plasma GIP and insulin were observed after the glucose ingestion in the patients with hyperparathyroidism as compared with the values in the normal subjects, and integrated GIP and insulin responses to the glucose ingestion for 120 min in the patients with hyperparathyroidism were significantly greater than the values in the normal subjects. Glucose 81-88 insulin Homo sapiens 49-56 7044357-6 1982 These results are consistent with the view that residual beta cell function contributes to improved glucose control in the yearly years of insulin dependency but alpha cell function and insulin antibodies do not. Glucose 100-107 insulin Homo sapiens 139-146 7044844-4 1982 Significantly higher responses of plasma GIP and insulin were observed after the glucose ingestion in the patients with hyperparathyroidism as compared with the values in the normal subjects, and integrated GIP and insulin responses to the glucose ingestion for 120 min in the patients with hyperparathyroidism were significantly greater than the values in the normal subjects. Glucose 240-247 insulin Homo sapiens 215-222 7044844-8 1982 Significantly higher responses of plasma GIP and insulin to the glucose ingestion were observed during calcium infusion as compared with the values during saline infusion. Glucose 64-71 insulin Homo sapiens 49-56 7046731-8 1982 Chloroquine, and also bacitracin, at concentrations that inhibited insulin degradation, decreased the insulin-stimulated incorporation of [14C]glucose into glycogen over 2 h. This effect of chloroquine was specific, since it did not modify the basal glycogenesis, or the glycogenic effect of a glucose load in the absence of insulin. Glucose 143-150 insulin Homo sapiens 67-74 7046731-8 1982 Chloroquine, and also bacitracin, at concentrations that inhibited insulin degradation, decreased the insulin-stimulated incorporation of [14C]glucose into glycogen over 2 h. This effect of chloroquine was specific, since it did not modify the basal glycogenesis, or the glycogenic effect of a glucose load in the absence of insulin. Glucose 143-150 insulin Homo sapiens 102-109 7039338-8 1982 With insulin alone, glucose production (GP) fell to zero. Glucose 20-27 insulin Homo sapiens 5-12 7039338-14 1982 To determine whether this effect was mediated by hyperglycemia per se or glucose-induced hyperinsulinemia, between 180 and 240 min we increased either a) the insulin infusion (by 0.25 mU . Glucose 73-80 insulin Homo sapiens 94-101 6759231-3 1982 Insulin secretion in response to intravenous arginine and glucose was evaluated in S2H, S0H, and matched controls. Glucose 58-65 insulin Homo sapiens 0-7 6759231-4 1982 Intravenous arginine and glucose elicited an exaggerated acute phase of insulin secretion in S2H compared with controls when analyzed as incremental insulin area 0-10", peak level attained, and mean insulin levels postinjection. Glucose 25-32 insulin Homo sapiens 72-79 6759231-4 1982 Intravenous arginine and glucose elicited an exaggerated acute phase of insulin secretion in S2H compared with controls when analyzed as incremental insulin area 0-10", peak level attained, and mean insulin levels postinjection. Glucose 25-32 insulin Homo sapiens 149-156 6804384-8 1982 In group II the low-dosed supply of carbohydrates produced a correspondingly lower insulin secretion which on the one hand enabled increased lipolysis and on the other hand resulted in the utilization of carbohydrates in insulin-independent organs essential for glucose utilization. Glucose 262-269 insulin Homo sapiens 83-90 6802653-3 1982 Fasting insulin levels were significantly lower in the elderly but post-glucose insulin responses in the first hour were similar in young and elderly subjects. Glucose 72-79 insulin Homo sapiens 80-87 7040191-6 1982 Basal levels of plasma insulin and its response to glucose load did not change after bromocriptine treatment. Glucose 51-58 insulin Homo sapiens 23-30 6120181-1 1982 Initially euglycemic (overnight insulin-infused) patients with insulin-dependent diabetes mellitus (IDDM), compared with nondiabetic controls, exhibit similar, but somewhat delayed plasma glucose nadirs, delayed glucose recovery from hypoglycemia, and posthypoglycemic hyperglycemia after the rapid intravenous injection of 0.075 U/kg of regular insulin. Glucose 188-195 insulin Homo sapiens 32-39 6120181-1 1982 Initially euglycemic (overnight insulin-infused) patients with insulin-dependent diabetes mellitus (IDDM), compared with nondiabetic controls, exhibit similar, but somewhat delayed plasma glucose nadirs, delayed glucose recovery from hypoglycemia, and posthypoglycemic hyperglycemia after the rapid intravenous injection of 0.075 U/kg of regular insulin. Glucose 188-195 insulin Homo sapiens 63-70 6120181-1 1982 Initially euglycemic (overnight insulin-infused) patients with insulin-dependent diabetes mellitus (IDDM), compared with nondiabetic controls, exhibit similar, but somewhat delayed plasma glucose nadirs, delayed glucose recovery from hypoglycemia, and posthypoglycemic hyperglycemia after the rapid intravenous injection of 0.075 U/kg of regular insulin. Glucose 212-219 insulin Homo sapiens 32-39 6120181-1 1982 Initially euglycemic (overnight insulin-infused) patients with insulin-dependent diabetes mellitus (IDDM), compared with nondiabetic controls, exhibit similar, but somewhat delayed plasma glucose nadirs, delayed glucose recovery from hypoglycemia, and posthypoglycemic hyperglycemia after the rapid intravenous injection of 0.075 U/kg of regular insulin. Glucose 212-219 insulin Homo sapiens 63-70 7033272-0 1982 Improvement of insulin secretion but not insulin resistance after short term control of plasma glucose in obese type II diabetics. Glucose 95-102 insulin Homo sapiens 15-22 7033272-3 1982 After 10 days of therapy, plasma insulin and C-peptide responses to oral glucose were significantly improved. Glucose 73-80 insulin Homo sapiens 33-40 7033272-3 1982 After 10 days of therapy, plasma insulin and C-peptide responses to oral glucose were significantly improved. Glucose 73-80 insulin Homo sapiens 45-54 7033272-4 1982 Insulin-induced glucose rates, estimated by the glucose clamp technique, averaged 1.08 +/- 0.30 mg/kg. Glucose 16-23 insulin Homo sapiens 0-7 7033272-4 1982 Insulin-induced glucose rates, estimated by the glucose clamp technique, averaged 1.08 +/- 0.30 mg/kg. Glucose 48-55 insulin Homo sapiens 0-7 7033272-6 1982 These indicate that short term control of plasma glucose improved insulin secretion but not insulin sensitivity. Glucose 49-56 insulin Homo sapiens 66-73 7033275-2 1982 Plasma glucose and insulin levels during oral glucose loading were significantly higher in women with predominantly upper body segment obesity than in women with lower body segment obesity. Glucose 46-53 insulin Homo sapiens 19-26 7035494-3 1982 During infusion of glucose alone, blood glucose rose twofold, insulin levels and net posthepatic insulin release increased three- to fourfold, and net splanchnic glucose output switched from a net output (1.65+/-0.12 mg/kg(-1) per min(-1)) to a net uptake (1.56+/-0.18). Glucose 19-26 insulin Homo sapiens 62-69 7035494-3 1982 During infusion of glucose alone, blood glucose rose twofold, insulin levels and net posthepatic insulin release increased three- to fourfold, and net splanchnic glucose output switched from a net output (1.65+/-0.12 mg/kg(-1) per min(-1)) to a net uptake (1.56+/-0.18). Glucose 19-26 insulin Homo sapiens 97-104 7040499-2 1982 Serum glucose concentrations rose immediately after the infusion of phenytoin followed by a significant increase in serum insulin values (P less than 0.05). Glucose 6-13 insulin Homo sapiens 122-129 7043166-3 1982 of normal body weight, the acute insulin response to glucose is defective while that to pharmacologic agents such as tolbutamide is less impaired. Glucose 53-60 insulin Homo sapiens 33-40 7043169-3 1982 When the insulin dose of the diabetic subject was reduced by 15% or 25%, the concentrations of blood and urinary glucose were significantly increased by the rate of urinary 3-methylhistidine excretion was not increased further. Glucose 113-120 insulin Homo sapiens 9-16 7043169-5 1982 It appears that blood and urine glucose levels are more sensitive to changes in insulin availability than protein catabolism. Glucose 32-39 insulin Homo sapiens 80-87 6801160-4 1982 The addition of insulin to placental villi in vitro showed increased glucose uptake, glycogen content and glycogen synthetase I form activity both in early and term placental villi. Glucose 69-76 insulin Homo sapiens 16-23 6801160-6 1982 Collectively, the data suggest the presence of insulin receptor in placental villi varying its concentration with gestational age, where insulin plays a role in adjusting glucose uptake and glycogenesis. Glucose 171-178 insulin Homo sapiens 47-54 6813942-6 1982 During the glucose regimen plasma insulin increased by 270% and plasma testosterone by 60%. Glucose 11-18 insulin Homo sapiens 34-41 6813942-10 1982 The glucose and amino acid regimens augmented the response of insulin to glucagon by 180 and 50%, respectively, but decreased that of growth hormone by 59 and 80%, respectively. Glucose 4-11 insulin Homo sapiens 62-69 7041329-4 1982 In the glucose tolerance test, insulin response was reduced in the patients with moderate or severe diabetes. Glucose 7-14 insulin Homo sapiens 31-38 7041329-8 1982 Glucagon with or without tolbutamide produced a far greater maximal response of plasma insulin in all the diabetic groups than in the normal subjects, while glucose produced a not significantly different increment of plasma insulin between the normal subjects and the mild diabetics. Glucose 157-164 insulin Homo sapiens 224-231 7034539-8 1982 Furthermore, these observations raise the possibility that decreased binding of insulin by placental insulin receptors, which is reported to occur in placentas from diabetic women, may be accompanied by a relatively decreased umbilical uptake of glucose for a given maternal concentration of glucose, but not of lactate. Glucose 246-253 insulin Homo sapiens 80-87 7034539-8 1982 Furthermore, these observations raise the possibility that decreased binding of insulin by placental insulin receptors, which is reported to occur in placentas from diabetic women, may be accompanied by a relatively decreased umbilical uptake of glucose for a given maternal concentration of glucose, but not of lactate. Glucose 292-299 insulin Homo sapiens 80-87 7044377-2 1982 During the affinity change the half-maximal sensitivity of glucose transport to insulin stimulation was unaltered. Glucose 59-66 insulin Homo sapiens 80-87 7044377-4 1982 There was not a simple relationship between receptor affinity and insulin stimulation of glucose transport in the adipocyte. Glucose 89-96 insulin Homo sapiens 66-73 6765158-0 1982 Expression of the insulin gene: regulation by glucose, hydrocortisone and growth hormone in mouse pancreatic islets in organ culture. Glucose 46-53 insulin Homo sapiens 18-25 6765158-2 1982 In islets cultured at 20 mM glucose for up to 7 days, the level of preproinsulin mRNA remained constant, but in islets kept at 3.3 mM glucose the preproinsulin mRNA level decreased within 24 h to one tenth of the level in islets maintained at 20 mM glucose. Glucose 28-35 insulin Homo sapiens 67-80 6765158-2 1982 In islets cultured at 20 mM glucose for up to 7 days, the level of preproinsulin mRNA remained constant, but in islets kept at 3.3 mM glucose the preproinsulin mRNA level decreased within 24 h to one tenth of the level in islets maintained at 20 mM glucose. Glucose 134-141 insulin Homo sapiens 146-159 6765158-2 1982 In islets cultured at 20 mM glucose for up to 7 days, the level of preproinsulin mRNA remained constant, but in islets kept at 3.3 mM glucose the preproinsulin mRNA level decreased within 24 h to one tenth of the level in islets maintained at 20 mM glucose. Glucose 134-141 insulin Homo sapiens 146-159 6765158-3 1982 The level of preproinsulin mRNA could, however, be completely restored by subsequent incubation at 20 mM glucose for 3 days. Glucose 105-112 insulin Homo sapiens 13-26 6765158-4 1982 These results suggest that glucose has a direct effect on the level of preproinsulin mRNA in pancreatic islets. Glucose 27-34 insulin Homo sapiens 71-84 6122339-6 1982 The increase in insulin binding could contribute to blood glucose control during metoprolol treatment. Glucose 58-65 insulin Homo sapiens 16-23 6126999-6 1982 Thus, the interaction of insulin and somatostatin on glucose metabolism is complex and time-dependent. Glucose 53-60 insulin Homo sapiens 25-32 7170951-2 1982 During the test the serum triglyceride level did not change notably, FFA values decreased significantly under the glucose load, most likely due to insulin mobilisation. Glucose 114-121 insulin Homo sapiens 147-154 7036749-0 1982 Insulin stimulation of Na+ transport and glucose metabolism in cultured kidney cells. Glucose 41-48 insulin Homo sapiens 0-7 7036749-7 1982 Insulin was also found to increase the incorporation of radiolabeled glucose into glycogen. Glucose 69-76 insulin Homo sapiens 0-7 7036751-1 1982 In a glucose-free bicarbonate Ringer (5% CO2 in N2), insulin increased intracellular pH (pHi), as determined by [14C]dimethadione, by 0.12 +/- 0.02 and stimulated glycolysis, as monitored by anaerobic lactate production, by 42.9 +/- 3.5% in paired frog sartorius muscles. Glucose 5-12 insulin Homo sapiens 53-60 6762118-6 1982 h-1 of glucose with 20 mu insulin; G. V: 16,66 g . Glucose 7-14 insulin Homo sapiens 26-33 6762118-7 1982 h-1 of glucose with 40 mu insulin. Glucose 7-14 insulin Homo sapiens 26-33 7032366-7 1982 Umbilical venous glucose and insulin levels correlated significantly (p less than 0.001) with the rate of glucose infusion to the mother and her blood glucose level. Glucose 106-113 insulin Homo sapiens 29-36 7032366-7 1982 Umbilical venous glucose and insulin levels correlated significantly (p less than 0.001) with the rate of glucose infusion to the mother and her blood glucose level. Glucose 106-113 insulin Homo sapiens 29-36 6125193-2 1982 2 Serum insulin and serum C-peptide secretion in response to a glucose load were inhibited (2P less than 0.01) by metoprolol and propranolol but not by pindolol. Glucose 63-70 insulin Homo sapiens 8-15 6756618-4 1982 Both produced a slight stimulation of basal glucose transport and metabolism, a marked inhibition of insulin-stimulated glucose transport and metabolism, and a marked decrease in insulin binding. Glucose 120-127 insulin Homo sapiens 101-108 6760964-0 1982 The question of early insulin response to glucose in patients with ischemic heart disease: a retrospective study in twins. Glucose 42-49 insulin Homo sapiens 22-29 6129073-5 1982 Glucose clearance was consistently depressed, and the magnitude of change in glucose clearance was directly correlated to the magnitude of the reduction in insulin concentration induced by the somatostatin infusion (P less than 0.01). Glucose 77-84 insulin Homo sapiens 156-163 6129073-8 1982 These results suggested that in burn patients hyperglucagonemia stimulates glucose production and that insulin is effective in enhancing glucose clearance. Glucose 137-144 insulin Homo sapiens 103-110 6749365-4 1982 Nevertheless, empirical studies with non-glucose-controlled portable programmed infusion systems delivering insulin by intravenous, subcutaneous, or intraperitoneal routes have suggested that these techniques can produce near-normoglycemia under everyday conditions in a high proportion of insulin-dependent diabetic subjects. Glucose 41-48 insulin Homo sapiens 108-115 6754145-0 1982 Effect of oral glucose loading on plasma insulin, potassium, renin and aldosterone in normal subjects and patients with primary hyperaldosteronism. Glucose 15-22 insulin Homo sapiens 41-48 6754145-3 1982 Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups; plasma renin activity was significantly increased only in normal subjects. Glucose 0-7 insulin Homo sapiens 59-66 6125307-2 1982 The dynamics of insulin and glucagon secretion by the isolated perfused cat pancreas was studied in response to glucose and amino acid stimuli. Glucose 112-119 insulin Homo sapiens 16-23 6125307-4 1982 Insulin secretion is biphasic in response to either glucose or amino acid stimuli. Glucose 52-59 insulin Homo sapiens 0-7 7039946-5 1982 During surgery, monitoring of blood glucose concentration determines the adequacy of insulin dosage, which can be adjusted to maintain glucose concentrations within the desired range. Glucose 36-43 insulin Homo sapiens 85-92 7039946-5 1982 During surgery, monitoring of blood glucose concentration determines the adequacy of insulin dosage, which can be adjusted to maintain glucose concentrations within the desired range. Glucose 135-142 insulin Homo sapiens 85-92 7039948-1 1982 The current understanding of diabetes points to a bihormonal abnormality in which the level of glucagon is inappropriately high relative to the level (or activity) of insulin, causing a rate of hepatic glucose production that is high relative to glucose utilization. Glucose 202-209 insulin Homo sapiens 167-174 6127273-2 1982 Somatostatin (1.1 microgram/kg/h) infused 30 min before and continued 60 min after the ingestion of glucose did not affect fasting levels of any of the above parameters while it significantly suppressed the GIP and insulin response to glucose. Glucose 235-242 insulin Homo sapiens 215-222 6127273-3 1982 The same somatostatin dose infused 30 min after the ingestion of glucose decreased significantly the raised levels of GIP and insulin and further increased blood glucose levels. Glucose 65-72 insulin Homo sapiens 126-133 6754298-1 1982 The present study was designed to improve the conventional subcutaneous insulin treatment of labile insulin-dependent diabetic patients by means of the artificial B-cell (Biostator) during a combination of conventional treatment and a glucose-controlled insulin infusion. Glucose 235-242 insulin Homo sapiens 72-79 6754298-6 1982 Using a preselected blood glucose level of 80 mg/dl (4.44 mmol/L), the additional insulin requirement amounted to 45.5 +/- 11.1 U/24 h (N = 6). Glucose 26-33 insulin Homo sapiens 82-89 6754299-1 1982 This study examines the feasibility of deriving the 24-h insulin requirement of insulin-dependent diabetic patients who were devoid of any endogenous insulin release (IDD) from the insulin-production rate (IPR) of healthy man (basal, 17 mU/min; stimulated 1.35 U/12.5 g glucose). Glucose 270-277 insulin Homo sapiens 57-64 6759209-7 1982 The synchronous pulsatile secretion of glucagon and insulin may be a mechanism by which insulin"s hepatic effects are limited, thereby maintaining hepatic glucose production but allowing sufficient peripheral insulin concentrations to inhibit excessive catabolism. Glucose 155-162 insulin Homo sapiens 52-59 6759209-7 1982 The synchronous pulsatile secretion of glucagon and insulin may be a mechanism by which insulin"s hepatic effects are limited, thereby maintaining hepatic glucose production but allowing sufficient peripheral insulin concentrations to inhibit excessive catabolism. Glucose 155-162 insulin Homo sapiens 88-95 7037506-5 1982 The insulin response to oral glucose was, however, far higher (431.3 +/- 58.2 pmol/l) than that obtained after GIP and glucose infusion (191.6 +/- 30.9 pmol/l, p less than 0.001). Glucose 29-36 insulin Homo sapiens 4-11 7037507-3 1982 The glucose delivery required to maintain euglycaemia in the second hour of insulin infusion was 13.9 +/- 2.1 g (mean +/- SEM) and 14.7 +/- 1.5 g (NS) at the lower dose for porcine and human insulins respectively, and 27.1 +/- 2.5 and 28.0 +/- 2.9 g (NS) at the higher dose. Glucose 4-11 insulin Homo sapiens 76-83 6761105-1 1982 RBC insulin binding was examined in Reye"s survivors and families of affected patients to determine whether their previously reported hyperinsulinemic responses to oral glucose are accompanied by alterations in insulin binding and could contribute to the hypercatabolism seen in this disorder. Glucose 169-176 insulin Homo sapiens 139-146 6762299-1 1982 In 32 nonobese and 8 obese patients with acute pancreatitis [AP] and 12 control subjects the insulin response to oral and intravenous glucose load was studied. Glucose 134-141 insulin Homo sapiens 93-100 6762299-2 1982 It has been shown, that secretion of insulin after oral glucose was significantly impaired and delayed in nonobese patients in comparison to control. Glucose 56-63 insulin Homo sapiens 37-44 6183173-4 1982 A marked correlation between plasma PF4 values and plasma glucose levels was shown in insulin-dependent diabetics only whereas a significant positive correlation with plasma triglycerides and plasma triglyceride VLDL and a negative correlation with cholesterol-HDL was shown in insulin-independent diabetics. Glucose 58-65 insulin Homo sapiens 86-93 7037586-3 1982 Fasting serum insulin concentration was raised in the patient group (0.12 +/- 0.02 vs 0.07 +/- 0.01 nmol/l, p less than 0.05 and hyperinsulinaemia persisted after oral glucose. Glucose 168-175 insulin Homo sapiens 14-21 7042656-0 1982 Relation of habitual diet to fasting plasma insulin concentration and the insulin response to oral glucose. Glucose 99-106 insulin Homo sapiens 74-81 6121763-3 1982 During SRIF infusion IRI and C-peptide response to oral glucose was significantly reduced in both groups as compared with the response under saline infusion. Glucose 56-63 insulin Homo sapiens 29-38 6749716-3 1982 This insulin resistance may be the basis for the hyperinsulinemia response to a glucose challenge. Glucose 80-87 insulin Homo sapiens 5-12 6749718-5 1982 In these last case, the presence of a normal rate of glucose oxidation demonstrates that their apparent insulin resistance was not resulting from deficiency of peripheral glucose oxidation, but from a major alteration in glucose storage. Glucose 53-60 insulin Homo sapiens 104-111 6749718-5 1982 In these last case, the presence of a normal rate of glucose oxidation demonstrates that their apparent insulin resistance was not resulting from deficiency of peripheral glucose oxidation, but from a major alteration in glucose storage. Glucose 171-178 insulin Homo sapiens 104-111 6749718-7 1982 Whatever the nature of the underlying biochemical mechanisms, this study shows that insulin resistance can occur not only from lack of peripheral glucose oxidation, but also from impairment of the capacity of the storing tissues to store glucose in the first hours following immediately oral glucose intake. Glucose 146-153 insulin Homo sapiens 84-91 6749718-7 1982 Whatever the nature of the underlying biochemical mechanisms, this study shows that insulin resistance can occur not only from lack of peripheral glucose oxidation, but also from impairment of the capacity of the storing tissues to store glucose in the first hours following immediately oral glucose intake. Glucose 238-245 insulin Homo sapiens 84-91 6749718-7 1982 Whatever the nature of the underlying biochemical mechanisms, this study shows that insulin resistance can occur not only from lack of peripheral glucose oxidation, but also from impairment of the capacity of the storing tissues to store glucose in the first hours following immediately oral glucose intake. Glucose 238-245 insulin Homo sapiens 84-91 6749719-5 1982 After glucose administration the C-peptide/insulin ratio was significantly reduced in hepatic steatosis compared to controls. Glucose 6-13 insulin Homo sapiens 33-42 6749719-5 1982 After glucose administration the C-peptide/insulin ratio was significantly reduced in hepatic steatosis compared to controls. Glucose 6-13 insulin Homo sapiens 43-50 6752238-4 1982 Failure of insulin and growth hormone production have been associated with glucose intolerance, excessive urinary nitrogen loss and a fatal outcome. Glucose 75-82 insulin Homo sapiens 11-18 7033265-0 1982 Cortisol-induced insulin resistance in man: impaired suppression of glucose production and stimulation of glucose utilization due to a postreceptor detect of insulin action. Glucose 68-75 insulin Homo sapiens 17-24 7033265-2 1982 The insulin dose-response characteristics for suppression of glucose production and stimulation of glucose utilization and their relationship to monocyte and erythrocyte insulin receptor binding were determined in six normal volunteers after 24-h infusion of cortisol and 24-h infusion of saline. Glucose 61-68 insulin Homo sapiens 4-11 7033265-2 1982 The insulin dose-response characteristics for suppression of glucose production and stimulation of glucose utilization and their relationship to monocyte and erythrocyte insulin receptor binding were determined in six normal volunteers after 24-h infusion of cortisol and 24-h infusion of saline. Glucose 99-106 insulin Homo sapiens 4-11 7033265-5 1982 Insulin dose-response curves for both suppression of glucose production (half-maximal response at 81 +/- 19 vs. 31 +/ 5 microU/ml; P less than 0.05) and stimulation of glucose utilization (half-maximal response at 104 +/- 9 vs. 64 +/- 7 microU/ml; P less than 0.01) were shifted to the right, with preservation of normal maximal responses to insulin. Glucose 53-60 insulin Homo sapiens 0-7 7033265-5 1982 Insulin dose-response curves for both suppression of glucose production (half-maximal response at 81 +/- 19 vs. 31 +/ 5 microU/ml; P less than 0.05) and stimulation of glucose utilization (half-maximal response at 104 +/- 9 vs. 64 +/- 7 microU/ml; P less than 0.01) were shifted to the right, with preservation of normal maximal responses to insulin. Glucose 168-175 insulin Homo sapiens 0-7 7033265-7 1982 However, except at near-maximal insulin receptor occupancy, the action of insulin on glucose production and utilization per number of monocyte and erythrocyte insulin receptors occupied was decreased. Glucose 85-92 insulin Homo sapiens 74-81 7033268-0 1982 Glucose enhancement of insulin action: elevated glucose levels increase insulin stimulation of 2-deoxyglucose uptake in cultured human fibroblasts. Glucose 48-55 insulin Homo sapiens 23-30 7033268-1 1982 Insulin stimulation of 2-deoxyglucose uptake in cultured human skin fibroblasts has been examined in the presence of varying concentrations of extracellular glucose. Glucose 30-37 insulin Homo sapiens 0-7 7033268-2 1982 When cell monolayers were preincubated in glucose-free medium, insulin stimulation of hexose transport was small. Glucose 42-49 insulin Homo sapiens 63-70 7033268-3 1982 Increasing glucose levels from 2.7 to 16.7 mM in the preincubation medium enhanced insulin-stimulation 2-deoxyglucose uptake (18-65% of basal uptake). Glucose 11-18 insulin Homo sapiens 83-90 7033268-4 1982 Insulin stimulation of hexose transport in the presence of glucose was the result of an increase in the Vmax without a significant change in the Km of transport. Glucose 59-66 insulin Homo sapiens 0-7 7033268-5 1982 Maximum enhancement of insulin action was achieved 18-24 h after glucose exposure. Glucose 65-72 insulin Homo sapiens 23-30 7033268-9 1982 These data demonstrate that extracellular glucose levels influence insulin action in cultured fibroblasts. Glucose 42-49 insulin Homo sapiens 67-74 7033268-10 1982 This implies that insulin responsiveness in vivo may be regulated in some systems by ambient glucose levels. Glucose 93-100 insulin Homo sapiens 18-25 6764506-3 1982 Over the first 72 h of insulin administration the mean amount of glucose tolerated rose from 0.35 +/- 0.06 to 0.67 +/- 0.06 g/kg/h and caloric intake derived from intravenous glucose increased from 29 to 56 kcal/kg/day. Glucose 65-72 insulin Homo sapiens 23-30 6764506-3 1982 Over the first 72 h of insulin administration the mean amount of glucose tolerated rose from 0.35 +/- 0.06 to 0.67 +/- 0.06 g/kg/h and caloric intake derived from intravenous glucose increased from 29 to 56 kcal/kg/day. Glucose 175-182 insulin Homo sapiens 23-30 7041066-0 1982 Defective insulin response to intravenous glucose in congenital lactic acidosis. Glucose 42-49 insulin Homo sapiens 10-17 6190296-4 1982 Substitution of the impermeant salt sodium isethionate for NaCl led to a 90% decrease in glucose-stimulated insulin release with no inhibition of somatostatin receptor recruitment. Glucose 89-96 insulin Homo sapiens 108-115 7048736-2 1982 Glucose loading was followed by an increase in ILA and radioimmune insulin (RII) levels both in patients with breast fibroadenomatosis and healthy controls. Glucose 0-7 insulin Homo sapiens 67-74 7032273-6 1981 The largest increase in high-density lipoprotein cholesterol and decreases in insulin and glucose were found in those subjects having normal glucose levels together with elevated insulin levels at base-line. Glucose 90-97 insulin Homo sapiens 179-186 7032273-6 1981 The largest increase in high-density lipoprotein cholesterol and decreases in insulin and glucose were found in those subjects having normal glucose levels together with elevated insulin levels at base-line. Glucose 141-148 insulin Homo sapiens 78-85 7030826-0 1981 The effect of insulin on the disposal of intravenous glucose. Glucose 53-60 insulin Homo sapiens 14-21 7037487-2 1981 The present study was aimed at investigating the effect of metergoline, a powerful and long-lasting antiserotoninergic agent, on insulin responses to glucose and arginine in adult-onset diabetic subjects. Glucose 150-157 insulin Homo sapiens 129-136 7040144-8 1981 Higher mean post-glucose plasma insulin was associated with lower high density lipoprotein cholesterol levels (1.18 +/- 0.32 mmol/l, p less than 0.05) and increased high density lipoprotein triglyceride levels (0.14 +/- 0.07) mmol/l, p less than 0.01) when compared with the men with low post-glucose plasma insulin (1.40 +/- 0.36 mmol/l and 0.09 +/- 0.03 mmol/l respectively). Glucose 17-24 insulin Homo sapiens 32-39 7040144-8 1981 Higher mean post-glucose plasma insulin was associated with lower high density lipoprotein cholesterol levels (1.18 +/- 0.32 mmol/l, p less than 0.05) and increased high density lipoprotein triglyceride levels (0.14 +/- 0.07) mmol/l, p less than 0.01) when compared with the men with low post-glucose plasma insulin (1.40 +/- 0.36 mmol/l and 0.09 +/- 0.03 mmol/l respectively). Glucose 17-24 insulin Homo sapiens 308-315 7040144-8 1981 Higher mean post-glucose plasma insulin was associated with lower high density lipoprotein cholesterol levels (1.18 +/- 0.32 mmol/l, p less than 0.05) and increased high density lipoprotein triglyceride levels (0.14 +/- 0.07) mmol/l, p less than 0.01) when compared with the men with low post-glucose plasma insulin (1.40 +/- 0.36 mmol/l and 0.09 +/- 0.03 mmol/l respectively). Glucose 293-300 insulin Homo sapiens 32-39 7028773-9 1981 Finally, the enhanced neonatal glucose tolerance of these babies may be related not only to the hyperinsulinemia but also to increased insulin sensitivity mediated, in part, by the increased insulin receptor binding. Glucose 31-38 insulin Homo sapiens 101-108 7028776-1 1981 Immunoreactive insulin responses to a 20-g iv glucose challenge during a 7.5 mg/m2/min tolbutamide infusion were studied in 21 untreated noninsulin-dependent male diabetics. Glucose 46-53 insulin Homo sapiens 15-22 7028776-9 1981 However, changes in the glucose level significantly modulate the sulfonylurea influence on the second phase insulin response to glucose. Glucose 24-31 insulin Homo sapiens 108-115 7028776-9 1981 However, changes in the glucose level significantly modulate the sulfonylurea influence on the second phase insulin response to glucose. Glucose 128-135 insulin Homo sapiens 108-115 7037798-5 1981 Glucose starvation and the administration of insulin under appropriate conditions are known to increase the Vmax for glucose uptake in certain cells, and high cell density in vitro is known to decrease the Vmax. Glucose 117-124 insulin Homo sapiens 45-52 7031209-1 1981 In patients with insulin-dependent diabetes, the therapeutic effect of prescribed insulin is routinely judged by the response of the blood glucose concentration. Glucose 139-146 insulin Homo sapiens 17-24 7031209-4 1981 Free insulin rather than total insulin values determine the plasma glucose concentration and the degree of long-term glycemic control as reflected by levels of hemoglobin A1C. Glucose 67-74 insulin Homo sapiens 5-12 6796801-3 1981 The plasma insulin response was significantly correlated with the load of glucose (r = 0.86; p less than 0.001) whereas such correlation was not observed with the blood glucose response. Glucose 74-81 insulin Homo sapiens 11-18 7027716-1 1981 Early insulin and C-peptide response to intravenous glucose, blood lipids and HLA-types. Glucose 52-59 insulin Homo sapiens 18-27 7027716-6 1981 Measures of the early insulin and C-peptide response to glucose were equally well correlated to maternal kt values (r = 0.40, P less than 0.001). Glucose 56-63 insulin Homo sapiens 34-43 7030247-3 1981 Insulin secretory capacity was measured by C-peptide response during a standard 100-g oral glucose tolerance test in 24 patients who achieved normalization of plasma glucose level as a result of dietary therapy alone. Glucose 91-98 insulin Homo sapiens 0-7 7030247-3 1981 Insulin secretory capacity was measured by C-peptide response during a standard 100-g oral glucose tolerance test in 24 patients who achieved normalization of plasma glucose level as a result of dietary therapy alone. Glucose 166-173 insulin Homo sapiens 0-7 7028543-10 1981 We conclude that the insulin infusion pump, managed at home, is a highly efficient way to achieve normal or near-normal glucose levels in the pregnant diabetic. Glucose 120-127 insulin Homo sapiens 21-28 7028556-1 1981 The circulatory, renal, and hormonal responses to physiological elevation of plasma insulin induced with oral glucose have been studied in seven healthy subjects. Glucose 110-117 insulin Homo sapiens 84-91 7032981-0 1981 [Effect of glucose and lactic acid on the insulin-depositing function of erythrocytes]. Glucose 11-18 insulin Homo sapiens 42-49 7029002-2 1981 Alterations in the growth hormone regulatory mechanism occurred among septic patients who manifested severe glucose intolerance which was associated with suppression of insulin production. Glucose 108-115 insulin Homo sapiens 169-176 7035664-1 1981 The insulin response after a glucose challenge was studied in 11 male patients with diffuse idiopathic skeletal hyperostosis (DISH) and in 8 age, sex and weight matched controls. Glucose 29-36 insulin Homo sapiens 4-11 7041239-9 1981 Repeated OGTTs revealed a set of constants for the algorithms, which enabled normal glucose tolerance to be achieved with smaller amounts of insulin. Glucose 84-91 insulin Homo sapiens 141-148 6120606-0 1981 Two-hour glucose and insulin responses after a standardized oral glucose load in relation to serum gamma-glutamyl transferase and alcohol consumption. Glucose 65-72 insulin Homo sapiens 21-28 7041509-2 1981 After a fast intravenous glucose loading given just before the administration of epidural bupivacaine, similar but more variable serum immunoreactive insulin levels were found as compared with those determined after a slower intravenous glucose infusion in patients under general anaesthesia. Glucose 25-32 insulin Homo sapiens 150-157 6269448-2 1981 The artificial pancreas is a glucose-controlled insulin and dextrose infusion system uniquely suited for the control of blood glucose concentrations during surgery. Glucose 29-36 insulin Homo sapiens 48-55 7340695-2 1981 In physiology, insulin binding decreases with age; it is lower in women during the luteal phase of the menstrual cycle or during administration of oestrogen-progestogen oral contraceptives; it exhibits diurnal variation; it increases after physical training; it depends on the diet, being inversely correlated with its carbohydrate content; finally, rapid variations in binding affinity are observed after glucose ingestion or after breakfast. Glucose 406-413 insulin Homo sapiens 15-22 7032518-0 1981 Effect of calcium on the net insulin secretion and the immunoreactive insulin response per unit of glucose. Glucose 99-106 insulin Homo sapiens 70-77 7037227-2 1981 Insulin biosynthesis by pancreatic islet cells is predominantly regulated by change in plasma glucose concentration. Glucose 94-101 insulin Homo sapiens 0-7 6115785-4 1981 When glucose concentration was increased to more than twice basal fasting levels, the glucose disposal rate increased significantly at all three insulin levels. Glucose 5-12 insulin Homo sapiens 145-152 6115785-4 1981 When glucose concentration was increased to more than twice basal fasting levels, the glucose disposal rate increased significantly at all three insulin levels. Glucose 86-93 insulin Homo sapiens 145-152 6115785-6 1981 These results are explained by an alternative model of glucose transport in which insulin-independent tissues such as brain have a relatively fixed glucose uptake, while other tissues have glucose transport systems which take up glucose at a rate proportional to its plasma concentration. Glucose 55-62 insulin Homo sapiens 82-89 6115785-6 1981 These results are explained by an alternative model of glucose transport in which insulin-independent tissues such as brain have a relatively fixed glucose uptake, while other tissues have glucose transport systems which take up glucose at a rate proportional to its plasma concentration. Glucose 148-155 insulin Homo sapiens 82-89 6115785-6 1981 These results are explained by an alternative model of glucose transport in which insulin-independent tissues such as brain have a relatively fixed glucose uptake, while other tissues have glucose transport systems which take up glucose at a rate proportional to its plasma concentration. Glucose 148-155 insulin Homo sapiens 82-89 6115785-6 1981 These results are explained by an alternative model of glucose transport in which insulin-independent tissues such as brain have a relatively fixed glucose uptake, while other tissues have glucose transport systems which take up glucose at a rate proportional to its plasma concentration. Glucose 148-155 insulin Homo sapiens 82-89 6797784-6 1981 The early insulin response to glucose increased by 50 percent in the contraceptive ring roup after one year of treatment, but not in the oral contraceptive group. Glucose 30-37 insulin Homo sapiens 10-17 7026334-6 1981 The morning insulin injection should probably be taken immediately on rising, to prevent the pre-breakfast plasma glucose rise. Glucose 114-121 insulin Homo sapiens 12-19 7032897-0 1981 Changes of early insulin responses to glucose in obese subjects with normal and impaired carbohydrate tolerance. Glucose 38-45 insulin Homo sapiens 17-24 7032897-1 1981 We have studied changes in the sensitivity of the early insulin response to glucose by means of an intravenous pulse-stimulation of 1.0 g, 2.5 g and 5.0 glucose at intervals of 30 min in 24 non-obese healthy controls without a family history of diabetes and in obese subjects with normal (n = 7) and pathological carbohydrate tolerance (n = 23). Glucose 76-83 insulin Homo sapiens 56-63 7032897-7 1981 There was a significant correlation between early insulin response during GIT and maximal insulin response revealed by staircase glucose stimulation in obese subjects with pathological CHT. Glucose 129-136 insulin Homo sapiens 50-57 7032897-7 1981 There was a significant correlation between early insulin response during GIT and maximal insulin response revealed by staircase glucose stimulation in obese subjects with pathological CHT. Glucose 129-136 insulin Homo sapiens 90-97 7032897-10 1981 In contrast to this, a reduced sensitivity of the early insulin response to glucose is suggested in obesity with pathological CHT. Glucose 76-83 insulin Homo sapiens 56-63 7032897-11 1981 A staircase glucose stimulation seems to be a useful tool in studying the early insulin response to glucose. Glucose 12-19 insulin Homo sapiens 80-87 7032897-11 1981 A staircase glucose stimulation seems to be a useful tool in studying the early insulin response to glucose. Glucose 100-107 insulin Homo sapiens 80-87 7047154-2 1981 The capacity of insulin receptors was significantly decreased in well controlled (33.7 +/- 2.2) and poorly controlled (32.4 +/- 2.3) groups compared with normal subjects (43.1 +/- 2.3 sites/cell), while fasting insulin levels of diabetics were comparable to normal subjects but their insulin response to a glucose challenge was considerably decreased. Glucose 306-313 insulin Homo sapiens 16-23 7286498-2 1981 The amount of insulin required for the assimilation of a 50 g glucose load during the various hormone infusions was determined by means of an automated glucose-controlled insulin infusion system and used as an index of insulin effectiveness. Glucose 62-69 insulin Homo sapiens 14-21 7286498-2 1981 The amount of insulin required for the assimilation of a 50 g glucose load during the various hormone infusions was determined by means of an automated glucose-controlled insulin infusion system and used as an index of insulin effectiveness. Glucose 152-159 insulin Homo sapiens 14-21 7286498-2 1981 The amount of insulin required for the assimilation of a 50 g glucose load during the various hormone infusions was determined by means of an automated glucose-controlled insulin infusion system and used as an index of insulin effectiveness. Glucose 152-159 insulin Homo sapiens 171-178 7286498-5 1981 The effectiveness of metabolic control by insulin was assessed by a marked decrease in plasma nonesterified free fatty acids and ketone bodies upon its administration after glucose ingestion in all groups studied. Glucose 173-180 insulin Homo sapiens 42-49 7286498-7 1981 Whereas it may well be that over-insulinization of the patients by the glucose controlled insulin infusion system has overcome and disguised the smaller diabetogenic effects of cortisol and glucagon. Glucose 71-78 insulin Homo sapiens 33-40 7026616-5 1981 This corresponded to in vivo glucose clamp results showing only a rightward shift in the insulin dose-response curve for overall glucose disposal in these three subjects (1980. Glucose 129-136 insulin Homo sapiens 89-96 7026616-9 1981 In the remaining eight obese patients, the in vitro glucose transport studies showed not only a rightward shift in the dose-response curves but also a marked decrease in basal and maximally insulin-stimulated rates of transport, indicating a postreceptor defect in insulin action. Glucose 52-59 insulin Homo sapiens 190-197 7026616-9 1981 In the remaining eight obese patients, the in vitro glucose transport studies showed not only a rightward shift in the dose-response curves but also a marked decrease in basal and maximally insulin-stimulated rates of transport, indicating a postreceptor defect in insulin action. Glucose 52-59 insulin Homo sapiens 265-272 7026616-11 1981 In conclusion, these results indicate that the mechanism of the postreceptor defect in insulin action, which exists in many obese patients, is related to a decrease in the activity of the glucose transport effector system. Glucose 188-195 insulin Homo sapiens 87-94 7028704-4 1981 After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. Glucose 6-13 insulin Homo sapiens 93-100 7028704-4 1981 After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. Glucose 44-51 insulin Homo sapiens 93-100 7028704-6 1981 The fall in plasma glucose was closely related to the preexercise levels of plasma insulin (r = 0.82, P less than 0.001) and glucose (r = 0.81, P less than 0.001). Glucose 19-26 insulin Homo sapiens 83-90 7028704-8 1981 This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise. Glucose 25-32 insulin Homo sapiens 184-191 7028704-8 1981 This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise. Glucose 137-144 insulin Homo sapiens 184-191 7287908-1 1981 We have assessed the mechanisms involved in the pathogenesis of the insulin resistance associated with impaired glucose tolerance and Type II diabetes mellitus by exploring, by means of the euglycemic glucose-clamp technique, the in vivo dose-response relationship between serum insulin and the overall rate of glucose disposal in 14 control subjects; 8 subjects with impaired glucose tolerance, and 23 subjects with Type II diabetes. Glucose 112-119 insulin Homo sapiens 68-75 7287908-1 1981 We have assessed the mechanisms involved in the pathogenesis of the insulin resistance associated with impaired glucose tolerance and Type II diabetes mellitus by exploring, by means of the euglycemic glucose-clamp technique, the in vivo dose-response relationship between serum insulin and the overall rate of glucose disposal in 14 control subjects; 8 subjects with impaired glucose tolerance, and 23 subjects with Type II diabetes. Glucose 201-208 insulin Homo sapiens 68-75 7287908-3 1981 In the subjects with impaired glucose tolerance, the dose-response curve was shifted to the right (half-maximally effective insulin level 240 vs. 135 microunits/ml for controls), but the maximal rate of glucose disposal remained normal. Glucose 30-37 insulin Homo sapiens 124-131 7287908-11 1981 (b) In patients with fasting hyperglycemia, insulin resistance is due to both decreased insulin receptors and postreceptor defect in the glucose mechanisms. Glucose 137-144 insulin Homo sapiens 44-51 7028922-1 1981 The effect of insulin on the transport of 2-deoxyglucose and the oxidation of glucose in chopped adipose tissue was investigated in 14 myotonic dystrophy (MyD) patients and 28 age and size-matched control subjects. Glucose 49-56 insulin Homo sapiens 14-21 7028922-5 1981 Both the basal and insulin-stimulated glucose oxidation were significantly less in the MyD group. Glucose 38-45 insulin Homo sapiens 19-26 6270511-3 1981 Possible components of a eumetabolic therapy include: aspirin, as a potentiator of glucose-stimulated insulin secretion; GTF, to directly enhance the efficacy of insulin; weight loss, exercise, and fasting, to help reduce tissue resistance to insulin; mitochondrial "metavitamins", to optimize the oxidative disposal of excess substrate; a high-fiber, low-fat diet, which appears superior to traditional diabetic diets as a promoter of glucose tolerance. Glucose 83-90 insulin Homo sapiens 102-109 7295860-3 1981 Paradoxical glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Glucose 12-19 insulin Homo sapiens 69-76 7295860-4 1981 PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Glucose 38-45 insulin Homo sapiens 220-227 7295860-4 1981 PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Glucose 163-170 insulin Homo sapiens 220-227 7295860-5 1981 PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Glucose 38-45 insulin Homo sapiens 220-227 7295860-5 1981 PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Glucose 163-170 insulin Homo sapiens 220-227 6122102-0 1982 DNA insertion sequences near the insulin gene affect glucose regulation. Glucose 53-60 insulin Homo sapiens 33-40 7031287-2 1982 Twelve ambulatory patients (six women and six men; mean age, 29 years) with type I diabetes were treated with a continuous subcutaneous open-loop insulin pump in an attempt to effect better glucose control. Glucose 190-197 insulin Homo sapiens 146-153 6760387-1 1982 The dose-response relationship between plasma insulin and systemic glucose uptake was studied before, one hour after and 6 months after valvular surgery in 11 patients with valvular aortic stenosis. Glucose 67-74 insulin Homo sapiens 46-53 6760387-2 1982 The immediate effect of valvular surgery was a dramatic rightward shift of the dose-response curve and a decrease in glucose uptake at peak insulin activity. Glucose 117-124 insulin Homo sapiens 140-147 6760388-4 1982 Insulin and C-peptide response to the glucose challenge was smaller preoperatively whereas the glucose response was the same pre- and postoperatively. Glucose 38-45 insulin Homo sapiens 0-7 6796445-2 1981 Acute insulin response to glucose (0.33 g/kg) was significantly decreased by colchicine (3 mg i.v.). Glucose 26-33 insulin Homo sapiens 6-13 7338293-9 1981 Similar results were obtained in six newly diagnosed insulin dependent diabetic patients both before and after the first 30 days of insulin treatment, even though a marked decrease in young cell HbAlc would be expected with the improved glucose control observed. Glucose 237-244 insulin Homo sapiens 53-60 7033284-3 1981 One, the insulin kinetics model, yields parameters of first-phase (phi 1) and second-phase (phi 2) responsivity of the beta-cells to glucose. Glucose 133-140 insulin Homo sapiens 9-16 7033284-4 1981 The other glucose kinetics model yields the insulin sensitivity parameters, SI. Glucose 10-17 insulin Homo sapiens 44-51 7033285-0 1981 Synergistic interaction between exercise and insulin on peripheral glucose uptake. Glucose 67-74 insulin Homo sapiens 45-52 7033285-9 1981 When hyperinsulinemia and exercise were combined (study 3), glucose uptake averaged 15.06 +/- 0.98 mg/kg per min (P less than 0.01) and this was significantly (P less than 0.001) greater than the sum of glucose uptake when exercise and the insulin clamp were performed separately. Glucose 60-67 insulin Homo sapiens 10-17 7033285-12 1981 These results demonstrate that (a) insulin and exercise act synergistically to enhance glucose disposal in man, and (b) muscle is the primary tissue responsible for the increase in glucose metabolism following hyperinsulinemia and exercise. Glucose 87-94 insulin Homo sapiens 35-42 7031419-1 1981 The facilitation of glucose disposal (Staub-Traugott effect) and potentiation of serum insulin (IRI) concentration normally occurring after closely spaced intravenous glucose loads, are known to disappear after prolonged starvation. Glucose 167-174 insulin Homo sapiens 87-94 7031419-4 1981 However, the Staub-Traugott effect and insulin secretory dynamics after stimulation by repetitive intravenous glucose loading were preserved by this glucose modified fast, while baseline serum glucagon levels (IRG) were significantly lower, and the basal IRI/IRG ratios were thus unchanged from the fed state. Glucose 110-117 insulin Homo sapiens 39-46 7031419-4 1981 However, the Staub-Traugott effect and insulin secretory dynamics after stimulation by repetitive intravenous glucose loading were preserved by this glucose modified fast, while baseline serum glucagon levels (IRG) were significantly lower, and the basal IRI/IRG ratios were thus unchanged from the fed state. Glucose 149-156 insulin Homo sapiens 39-46 7031419-7 1981 It is suggested that minimal amounts of carbohydrate during fasting preserve the insulin potentiating action of glucose, preferentially sparing a delayed releasable pool of insulin, while protecting the glucose utilization mechanisms, including increased glycolysis, responsible for the Staub-Traugott effect. Glucose 112-119 insulin Homo sapiens 81-88 6798594-1 1981 Recent evidence suggests that glucose stimulation of insulin release may trigger a classic negative feedback loop involving local release of an inhibitor of beta cell function. Glucose 30-37 insulin Homo sapiens 53-60 6798594-4 1981 At lease one arachidonate derivative (prostaglandin E) inhibits insulin secretion, and several inhibitors of prostaglandin synthesis augment glucose-induced insulin release in normal subjects and type II diabetics. Glucose 141-148 insulin Homo sapiens 157-164 7039639-0 1981 [Relations between the blood insulin response and kalemia during the glucose tolerance test]. Glucose 69-76 insulin Homo sapiens 29-36 6795545-4 1981 With the use of glucose-1-phosphate the quantity of insulin administered could be significantly reduced (P less than 0.01) thereby an increased utilization of glucose, induced by the phosphorylated saccharide, was confirmed. Glucose 16-23 insulin Homo sapiens 52-59 7027714-0 1981 Forearm insulin uptake in healthy subjects after oral glucose and intravenous glipizide. Glucose 54-61 insulin Homo sapiens 8-15 7027714-5 1981 When the fractional insulin uptake values for these four 60 min periods were compared it was found that the uptake of insulin was significantly higher for the 60 min period that was obtained in response to glucose without glipizide pre-treatment, than it was for any of the other 60 min periods. Glucose 206-213 insulin Homo sapiens 118-125 7026970-1 1981 Noninsulin dependent diabetics have insulin responses to nonglucose secretagogues that are subnormal for their plasma glucose levels. Glucose 60-67 insulin Homo sapiens 3-10 7026970-2 1981 Since endogenous prostaglandins have been implicated in the abnormal insulin responses to glucose in diabetics, the present study was performed to explore whether prostaglandins might also play a role in the defective insulin responses to nonglucose stimuli. Glucose 90-97 insulin Homo sapiens 69-76 7026972-1 1981 The reduced insulin response of trained subjects in the presence of normal glucose tolerance has been confirmed. Glucose 75-82 insulin Homo sapiens 12-19 7026972-4 1981 However, when the subjects were on a restricted diet (2076 cal/day) the reduced insulin response to a glucose load was retained. Glucose 102-109 insulin Homo sapiens 80-87 7026972-7 1981 For all these studies a correlation (p less than 0.01) was found between the secretion of insulin in response to glucose challenge and both basal plasma glucose and insulin. Glucose 113-120 insulin Homo sapiens 90-97 7026972-7 1981 For all these studies a correlation (p less than 0.01) was found between the secretion of insulin in response to glucose challenge and both basal plasma glucose and insulin. Glucose 113-120 insulin Homo sapiens 165-172 7026972-7 1981 For all these studies a correlation (p less than 0.01) was found between the secretion of insulin in response to glucose challenge and both basal plasma glucose and insulin. Glucose 153-160 insulin Homo sapiens 90-97 7027498-4 1981 Patients with pancreatitis also had a diminished insulin response to glucose. Glucose 69-76 insulin Homo sapiens 49-56 6798379-6 1981 The surgeon can also anticipate a more predictable control of blood glucose level during major surgery when a continuous insulin infusion regimen is used. Glucose 68-75 insulin Homo sapiens 121-128 7035234-4 1981 Total insulin response to oral glucose, calculated as insulin area, was significantly exaggerated (p less than 0.01 vs control value). Glucose 31-38 insulin Homo sapiens 6-13 7035234-4 1981 Total insulin response to oral glucose, calculated as insulin area, was significantly exaggerated (p less than 0.01 vs control value). Glucose 31-38 insulin Homo sapiens 54-61 7041509-1 1981 Glucose loading caused a significant increase in insulin response (IRI) in patients undergoing caesarean section both under general anaesthesia and under epidural analgesia. Glucose 0-7 insulin Homo sapiens 49-56 6117492-5 1981 Since similar steady-state levels of exogenous insulin were achieved, the resulting steady-state plasma glucose level provided a direct estimate of the ability of insulin to dispose of the infused glucose. Glucose 104-111 insulin Homo sapiens 163-170 6117492-5 1981 Since similar steady-state levels of exogenous insulin were achieved, the resulting steady-state plasma glucose level provided a direct estimate of the ability of insulin to dispose of the infused glucose. Glucose 197-204 insulin Homo sapiens 163-170 6117492-6 1981 The glucose levels were higher in subjects with impaired glucose tolerance with values of 14.6 +/- 1.8 mmol/l compared with 5.1 +/- 1.2 mmol/l in control subjects (p less than 0.01), thus indicating insulin resistance. Glucose 4-11 insulin Homo sapiens 199-206 6117492-7 1981 There was a direct correlation between the steady-state plasma glucose level and glucose tolerance suggesting that the degree of glucose intolerance is proportional to the degree of insulin resistance. Glucose 63-70 insulin Homo sapiens 182-189 6117492-7 1981 There was a direct correlation between the steady-state plasma glucose level and glucose tolerance suggesting that the degree of glucose intolerance is proportional to the degree of insulin resistance. Glucose 81-88 insulin Homo sapiens 182-189 6117492-7 1981 There was a direct correlation between the steady-state plasma glucose level and glucose tolerance suggesting that the degree of glucose intolerance is proportional to the degree of insulin resistance. Glucose 81-88 insulin Homo sapiens 182-189 6796326-8 1981 Intravenous or intramuscular regular insulin after urine tests for glucose and ketones alone should not be given. Glucose 67-74 insulin Homo sapiens 37-44 7028551-1 1981 The relationship between the pre-stimulus glucose level and immunoreactive insulin responses to a glucose challenge (20-g IV) was studied in normal subjects. Glucose 42-49 insulin Homo sapiens 75-82 7028551-1 1981 The relationship between the pre-stimulus glucose level and immunoreactive insulin responses to a glucose challenge (20-g IV) was studied in normal subjects. Glucose 98-105 insulin Homo sapiens 75-82 7028551-3 1981 In contrast, the second phase response (10-60 min insulin area after glucose pulse) to intravenous glucose fell during insulin infusion and increased during the glucose infusion. Glucose 69-76 insulin Homo sapiens 50-57 7028551-3 1981 In contrast, the second phase response (10-60 min insulin area after glucose pulse) to intravenous glucose fell during insulin infusion and increased during the glucose infusion. Glucose 99-106 insulin Homo sapiens 50-57 7028551-3 1981 In contrast, the second phase response (10-60 min insulin area after glucose pulse) to intravenous glucose fell during insulin infusion and increased during the glucose infusion. Glucose 99-106 insulin Homo sapiens 119-126 7028551-3 1981 In contrast, the second phase response (10-60 min insulin area after glucose pulse) to intravenous glucose fell during insulin infusion and increased during the glucose infusion. Glucose 99-106 insulin Homo sapiens 50-57 7028551-3 1981 In contrast, the second phase response (10-60 min insulin area after glucose pulse) to intravenous glucose fell during insulin infusion and increased during the glucose infusion. Glucose 99-106 insulin Homo sapiens 119-126 7028551-4 1981 Overall, a linear relationship was found between the change of pre-stimulus glucose or level from the control to that during the insulin or glucose infusion and the change in second phase response (r = 0.65, n = 14, p less than 0.02). Glucose 76-83 insulin Homo sapiens 129-136 7028551-8 1981 These findings suggest that changes in basal or pre-stimulus plasma glucose during therapy with sulphonylurea drugs may be expected to influence the second phase insulin responses to glucose challenge. Glucose 68-75 insulin Homo sapiens 162-169 7028551-8 1981 These findings suggest that changes in basal or pre-stimulus plasma glucose during therapy with sulphonylurea drugs may be expected to influence the second phase insulin responses to glucose challenge. Glucose 183-190 insulin Homo sapiens 162-169 7028554-2 1981 All patients and control subjects had normal glucose tolerance, but the patients had increased fasting and integrated insulin response to oral glucose. Glucose 143-150 insulin Homo sapiens 118-125 7035020-0 1981 [Action of insulin on the glucose transport system--on the "translocation hypothesis" (author"s transl)]. Glucose 26-33 insulin Homo sapiens 11-18 7035023-0 1981 [The effect of insulin microinjection into hypothalamus on plasma glucose (author"s transl)]. Glucose 66-73 insulin Homo sapiens 15-22 7035027-0 1981 [Mechanism of insulin action on glucose and lipid metabolism in hepatocytes (author"s transl)]. Glucose 32-39 insulin Homo sapiens 14-21 6114964-9 1981 These insulin-like effects of hGH were no longer evident after 2 h. Subsequently, when glucose was infused, plasma glucose increased to 133 +/- 4 mg/dl compared to the 104 +/- 6 mg/dl observed in control studies (P less than 0.01). Glucose 87-94 insulin Homo sapiens 6-13 6114964-9 1981 These insulin-like effects of hGH were no longer evident after 2 h. Subsequently, when glucose was infused, plasma glucose increased to 133 +/- 4 mg/dl compared to the 104 +/- 6 mg/dl observed in control studies (P less than 0.01). Glucose 115-122 insulin Homo sapiens 6-13 6790562-2 1981 Insulin binding was significantly decreased in Klinefelter subjects (P less than 0.01 at insulin concentrations of 0.051 and 0.136 mmol/liter); however, their fasting glucose concentration was normal (87 +/- 17), and the glucose disappearance rate was slightly increased (2.3 +/- 0.9; P less than 0.2). Glucose 167-174 insulin Homo sapiens 0-7 6790562-2 1981 Insulin binding was significantly decreased in Klinefelter subjects (P less than 0.01 at insulin concentrations of 0.051 and 0.136 mmol/liter); however, their fasting glucose concentration was normal (87 +/- 17), and the glucose disappearance rate was slightly increased (2.3 +/- 0.9; P less than 0.2). Glucose 221-228 insulin Homo sapiens 0-7 7021580-1 1981 The effect of weight loss and caloric restriction on plasma glucose concentrations and insulin and glucagon secretion in response to oral and iv glucose and arginine infusions was examined in 8 subjects with type II diabetes mellitus of greater than 5 yr duration (long term diabetes). Glucose 145-152 insulin Homo sapiens 87-94 6796715-4 1981 This effect may result from either a change in the insulin/glucagon ratio, induced by glucose, or from the anticatabolic influence of branched chain amino acids on muscle protein turnover. Glucose 86-93 insulin Homo sapiens 51-58 6796715-8 1981 Conversely, the insulin, glucagon, and free fatty acid levels with glucose alone were not altered with the addition of branched chain amino acids. Glucose 67-74 insulin Homo sapiens 16-23 6790904-5 1981 Insulin stimulation of total glucose incorporation was reduced in cells from the patient. Glucose 29-36 insulin Homo sapiens 0-7 6790904-8 1981 The data indicate alterations in both cell glucose metabolism and insulin response which may be related to the observed insulin resistance of this disorder. Glucose 43-50 insulin Homo sapiens 120-127 7031791-0 1981 [Insulin and its cellular receptors in changes in glucose metabolism]. Glucose 50-57 insulin Homo sapiens 1-8 7023164-10 1981 The production of glucose by the liver also seems to be increased either due to insulin resistance or portal venous shunting of insulin. Glucose 18-25 insulin Homo sapiens 80-87 7023164-10 1981 The production of glucose by the liver also seems to be increased either due to insulin resistance or portal venous shunting of insulin. Glucose 18-25 insulin Homo sapiens 128-135 7020488-3 1981 Insulin-taking diabetics given no insulin or a fraction of their usual dose preoperatively developed rising plasma glucose concentrations beginning with the start of operation. Glucose 115-122 insulin Homo sapiens 0-7 6114891-0 1981 Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system. Glucose 46-53 insulin Homo sapiens 65-72 6763894-2 1981 Insulin responses during 100 g glucose tolerance tests (GTT) were compared between three groups of patients with varying degrees of glucose intolerance. Glucose 31-38 insulin Homo sapiens 0-7 6763894-6 1981 Patients in Group A were found to have consistently subnormal insulin responses whether glucose tolerance was normal (i.e. previous abnormality of glucose tolerance), borderline, or diabetic. Glucose 88-95 insulin Homo sapiens 62-69 6763894-7 1981 In contrast, patients in Group C without fasting hyperglycemia had enhanced rather than decreased insulin responses when glucose tolerance was the more impaired. Glucose 121-128 insulin Homo sapiens 98-105 6763894-15 1981 Thus, patients with glucose intolerance due to extra-pancreatic causes may secrete insulin at a higher rate than normal so long as the FBG level remains below 120 mg/100 ml, but a further deterioration in glucose metabolism may lead to a failure of insulin secretory mechanisms. Glucose 20-27 insulin Homo sapiens 83-90 6763894-15 1981 Thus, patients with glucose intolerance due to extra-pancreatic causes may secrete insulin at a higher rate than normal so long as the FBG level remains below 120 mg/100 ml, but a further deterioration in glucose metabolism may lead to a failure of insulin secretory mechanisms. Glucose 20-27 insulin Homo sapiens 249-256 7018974-8 1981 These results indicate that in metabolically distinct types of skeletal muscles glucose uptake can differ markedly, and this is related to differences in the insulin binding capacities of these muscles. Glucose 80-87 insulin Homo sapiens 158-165 7021283-4 1981 A twofold rise of plasma proinsulin concentration was also found in thyrotoxic patients during a prolonged fast, and during intravenous and oral glucose tolerance tests. Glucose 145-152 insulin Homo sapiens 25-35 7019230-8 1981 Plasma insulin and C-peptide responses to glucose were significantly reduced (P less than 0.01) by calcitonin at all times after the start of the test in both normal and IGT groups. Glucose 42-49 insulin Homo sapiens 7-14 7019230-8 1981 Plasma insulin and C-peptide responses to glucose were significantly reduced (P less than 0.01) by calcitonin at all times after the start of the test in both normal and IGT groups. Glucose 42-49 insulin Homo sapiens 19-28 6166697-7 1981 Insulin release stimulated by 500 mg/dl glucose, 10 mM theophylline, and 200 micrograms/ml tolbutamide was increased 1.5- to 3.7-fold in comparison with that stimulated by 100 mg/dl glucose. Glucose 40-47 insulin Homo sapiens 0-7 6166697-7 1981 Insulin release stimulated by 500 mg/dl glucose, 10 mM theophylline, and 200 micrograms/ml tolbutamide was increased 1.5- to 3.7-fold in comparison with that stimulated by 100 mg/dl glucose. Glucose 182-189 insulin Homo sapiens 0-7 6113483-8 1981 The plasma glucose responses to s.c. injection of this insulin into the anterior abdominal wall and to i.m. Glucose 11-18 insulin Homo sapiens 55-62 7025859-2 1981 A sharp rise of insulin sensitivity (expressed as glucose required/insulin evoked ratio) was obtained in the morning, confirming our previous data observed by insulin tolerance test, but in a more physiological condition. Glucose 50-57 insulin Homo sapiens 16-23 7020317-5 1981 During elevation of insulin by glucose infusion, it varied predominantly with the rate of insulin secretion. Glucose 31-38 insulin Homo sapiens 20-27 7020317-5 1981 During elevation of insulin by glucose infusion, it varied predominantly with the rate of insulin secretion. Glucose 31-38 insulin Homo sapiens 90-97 7020317-17 1981 The clearance of endogenous insulin was lower than that of exogenous insulin at normoglycaemia, but of similar size during glucose infusion. Glucose 123-130 insulin Homo sapiens 28-35 7304075-2 1981 Fasting plasma insulin levels were consistently low and a subnormal insulin response to provocative stimuli (oral glucose and i.v. Glucose 114-121 insulin Homo sapiens 15-22 6116449-4 1981 Concomitant examination of plasma insulin, however, differentiates between the intravenous and the oral glucose tolerance test. Glucose 104-111 insulin Homo sapiens 34-41 6116449-5 1981 While the high insulin levels after oral glucose administration are rather increasing with age, the minor insulin reaction after the intravenous glucose route is decreasing with advancing age. Glucose 41-48 insulin Homo sapiens 15-22 6788631-3 1981 The response of total cell glucose metabolism to insulin was assessed by measurement of 14C-glucose uptake. Glucose 27-34 insulin Homo sapiens 49-56 6788631-4 1981 Insulin stimulated cell glucose incorporation in nondiabetic cells up to twofold with half-maximal stimulation at approximately 3 X 10(-9) M insulin. Glucose 24-31 insulin Homo sapiens 0-7 6788631-4 1981 Insulin stimulated cell glucose incorporation in nondiabetic cells up to twofold with half-maximal stimulation at approximately 3 X 10(-9) M insulin. Glucose 24-31 insulin Homo sapiens 141-148 7018811-8 1981 During glucose-containing infusions, insulin levels were 40% higher than those during glucose-free infusions. Glucose 7-14 insulin Homo sapiens 37-44 7018961-5 1981 Both PGE synthesis inhibitors shifted the glucose dose-insulin response curves to the left at low glucose concentrations and augmented maximal insulin release at high glucose concentrations. Glucose 42-49 insulin Homo sapiens 55-62 7024026-5 1981 Sucrose, in contrast, induced a greater post-prandial rise in blood glucose levels despite counter-regulation by the glucose-controlled insulin infusion system. Glucose 117-124 insulin Homo sapiens 136-143 7024027-1 1981 The insulin response of isolated islet cells to glucose and theophylline in vitro was studied after incubation with lymphocytes. Glucose 48-55 insulin Homo sapiens 4-11 7024027-3 1981 A significant inhibition of insulin response to glucose and theophylline as compared to insulin release in a "basal" medium was found after incubation with blood lymphocytes from 21 out of 23 insulin-dependent diabetics (mean secretion index 18 +/- 18 versus 118 + 8 (SEM) % in control subjects). Glucose 48-55 insulin Homo sapiens 28-35 7049629-2 1981 A 100-U insulin suppository (mean 1.8 U/kg) given to the diabetic subjects caused four times as great a fall in plasma glucose compared with the normal subjects given the same dose (mean 1.6 U/kg). Glucose 119-126 insulin Homo sapiens 8-15 7049629-3 1981 The insulin response after suppository administration demonstrated a significantly positive correlation (r = 0.83, P less than 0.01) with the plasma glucose level before administration. Glucose 149-156 insulin Homo sapiens 4-11 7049629-4 1981 Diabetic subjects given a 100-U insulin suppository (mean 1.7 U/kg) 15 min after meals three times daily showed a significant (P less than 0.05) improvement in postprandial hyperglycemia accompanied by a restoration of the normal circadian profile of plasma IRI and a reduction of urinary glucose from 26 +/- 5.9 to 2.0 +/- 1.0 g/day. Glucose 289-296 insulin Homo sapiens 32-39 7049632-4 1981 The plasma insulin response to glucose shows little change with age. Glucose 31-38 insulin Homo sapiens 11-18 7307296-0 1981 [Normalization of glucose metabolism by continuous subcutaneous insulin infusion therapy and management of pregnancy and delivery in an unstable diabetic woman (author"s transl)]. Glucose 18-25 insulin Homo sapiens 64-71 7017343-10 1981 The results indicate that even mild hyperinsulinism interferes with normal metabolic responses to exercise, and suggest that fall in insulin concentration seen with exercise is an important regulatory process, not merely a secondary consequences of a declining plasma glucose level. Glucose 268-275 insulin Homo sapiens 41-48 7033585-0 1981 [Intravenous glucose tolerance test during anesthesia-insulin response and glucose clearance (author"s transl)]. Glucose 13-20 insulin Homo sapiens 54-61 6268962-6 1981 Likewise, the increase in glycolytic flux, which is associated with the process of glucose-stimulated insulin release, is attributable not solely to a mass action phenomenon but also to the activation of phosphofructokinase by fructose 2.6-bisphosphate. Glucose 83-90 insulin Homo sapiens 102-109 6268962-8 1981 The fact that certain nutrient secretagogues (e.g. D-glucose and L-leucine) act in the B-cell both as substrates and enzyme activators permits reconciliation of the substrate site and regulatory site hypotheses for insulin release. Glucose 51-60 insulin Homo sapiens 215-222 7022305-3 1981 Multiple injections of regular and long-acting insulin coordinate physiologically with the serum glucose, minimize hyperglycemia and lessen diabetic retinopathy. Glucose 97-104 insulin Homo sapiens 47-54 7022793-2 1981 When placed into organ culture, nonfrozen control and freeze-recovered pancreas tissue secreted radioimmoassayable insulin in response to glucose plus theophylline, but not to glucose alone. Glucose 138-145 insulin Homo sapiens 115-122 7018254-0 1981 Dose-response characteristics for effects of insulin on production and utilization of glucose in man. Glucose 86-93 insulin Homo sapiens 45-52 7018254-1 1981 To determine the dose-response characteristics for the effects of insulin on glucose production, glucose utilization, and overall glucose metabolism in normal man, 15 healthy subjects were infused with insulin for 8 h at sequential rates ranging from 0.2 to 5.0 mU.kg-1.min-1; each rate was used for 2 h. Glucose production and utilization were measured isotopically ([3-3H]glucose). Glucose 77-84 insulin Homo sapiens 66-73 7018254-3 1981 Glucose production was completely suppressed at plasma insulin concentrations of approximately 60 microunits/ml. Glucose 0-7 insulin Homo sapiens 55-62 7018254-4 1981 Maximal glucose utilization (10-11 mg.kg-1.min-1) occurred at insulin concentrations of 200-700 microunits/ml. Glucose 8-15 insulin Homo sapiens 62-69 7018254-5 1981 The concentration of insulin causing half-maximal glucose utilization (55 + 7 microunits/ml) was significantly greater than that required for half-maximal suppression of glucose production (29 +/- 2 microunits/ml, P less than 0.01). Glucose 50-57 insulin Homo sapiens 21-28 7018254-5 1981 The concentration of insulin causing half-maximal glucose utilization (55 + 7 microunits/ml) was significantly greater than that required for half-maximal suppression of glucose production (29 +/- 2 microunits/ml, P less than 0.01). Glucose 170-177 insulin Homo sapiens 21-28 7018254-6 1981 Maximal effects of insulin on glucose production and utilization occurred at plasma insulin concentrations causing 11 and 49% insulin receptor occupancy, respectively. Glucose 30-37 insulin Homo sapiens 19-26 7018254-6 1981 Maximal effects of insulin on glucose production and utilization occurred at plasma insulin concentrations causing 11 and 49% insulin receptor occupancy, respectively. Glucose 30-37 insulin Homo sapiens 84-91 7018254-7 1981 The above dose-response relationships indicate that in man 1) glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; 2) both hepatic and peripheral tissues may contain "spare" insulin receptors; and 3) relatively minor changes in plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism. Glucose 62-69 insulin Homo sapiens 120-127 7018254-7 1981 The above dose-response relationships indicate that in man 1) glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; 2) both hepatic and peripheral tissues may contain "spare" insulin receptors; and 3) relatively minor changes in plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism. Glucose 62-69 insulin Homo sapiens 230-237 7018254-7 1981 The above dose-response relationships indicate that in man 1) glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; 2) both hepatic and peripheral tissues may contain "spare" insulin receptors; and 3) relatively minor changes in plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism. Glucose 62-69 insulin Homo sapiens 230-237 7018254-7 1981 The above dose-response relationships indicate that in man 1) glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; 2) both hepatic and peripheral tissues may contain "spare" insulin receptors; and 3) relatively minor changes in plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism. Glucose 62-69 insulin Homo sapiens 230-237 7018946-4 1981 The islets isolated from fetuses of insulin-dependent mothers are glucose-sensitive with respect to hormone release and biosynthesis. Glucose 66-73 insulin Homo sapiens 36-43 7014314-5 1981 The insulin response to glucose was increased in pregnancy in all three groups. Glucose 24-31 insulin Homo sapiens 4-11 7027987-0 1981 [Plasma insulin, C-peptide and glucose concentrations in type I diabetic children after a morning injection of insulin (author"s transl)]. Glucose 31-38 insulin Homo sapiens 111-118 7021276-0 1981 The effects of a low-dose intravenous insulin infusion upon plasma glucose and non-esterified fatty acid levels in very obese and non-obese human subjects. Glucose 67-74 insulin Homo sapiens 38-45 7014316-0 1981 Effects of insulin and insulin-like agents on the glucose transport system of cultured human fibroblasts. Glucose 50-57 insulin Homo sapiens 11-35 7018946-3 1981 Prolongation of the glucose exposure or the addition of theophylline resulted in a significantly enhanced insulin release. Glucose 20-27 insulin Homo sapiens 106-113 7021276-2 1981 The dose of insulin was chosen so as to have its sole or predominant hypoglycaemic effect upon hepatic glucose release. Glucose 103-110 insulin Homo sapiens 12-19 7021276-4 1981 In the controls the fall in plasma glucose and non-esterified fatty acids was significantly and inversely correlated with the basal plasma insulin level. Glucose 35-42 insulin Homo sapiens 139-146 7021278-11 1981 Insulin levels, similar to those found after a meal, rapidly reversed the effects of glucagon on non-esterified fatty acid, glucose and potassium. Glucose 124-131 insulin Homo sapiens 0-7 6114914-4 1981 Thus the integrated amounts of insulin required for glucose hormone were temporarily suppressed by somatostatin. Glucose 52-59 insulin Homo sapiens 31-38 6114915-2 1981 Treatment with insulin only in 20 patients caused normalization of blood glucose levels within 6 hours and resolution of ketoacidosis within 5 hours. Glucose 73-80 insulin Homo sapiens 15-22 7021279-6 1981 The initial uptake of tracer methylglucose in insulin-stimulated cells was inhibited by unlabelled methylglucose and by D-glucose with inhibition constants of about 3.8 and 7.7 mmol/l respectively. Glucose 120-129 insulin Homo sapiens 46-53 7021279-7 1981 Uptake of tracer 2-deoxyglucose (50 mumol/l) in insulin-stimulated adipocytes was linear from 10 s to 5 min whereas the rate of uptake in the presence of 3 mmol/l of D-glucose was markedly decreased suggesting that deoxyglucose uptake after a few minutes is mainly limited by hexokinase in the presence of glucose. Glucose 24-31 insulin Homo sapiens 48-55 6263106-0 1981 Coupling of insulin binding and insulin action on glucose transport in fat cells. Glucose 50-57 insulin Homo sapiens 12-39 7015073-1 1981 Insulin has major effects on both glucose and branched chain amino acid metabolism. Glucose 34-41 insulin Homo sapiens 0-7 7015073-4 1981 The obese group had a slower glucose disappearance rate after glucose challenge (0.84 plus or minus 0.06 vs. 1.11 plus or minus 0.07 hr(-1); p less than 0.01) despite having a greater serum insulin response to the glucose load (26 plus or minus 4 vs 11 plus or minus 1 insulin area units; p less than 0.01), confirming insulin resistance. Glucose 62-69 insulin Homo sapiens 269-276 7015073-4 1981 The obese group had a slower glucose disappearance rate after glucose challenge (0.84 plus or minus 0.06 vs. 1.11 plus or minus 0.07 hr(-1); p less than 0.01) despite having a greater serum insulin response to the glucose load (26 plus or minus 4 vs 11 plus or minus 1 insulin area units; p less than 0.01), confirming insulin resistance. Glucose 62-69 insulin Homo sapiens 269-276 7015073-4 1981 The obese group had a slower glucose disappearance rate after glucose challenge (0.84 plus or minus 0.06 vs. 1.11 plus or minus 0.07 hr(-1); p less than 0.01) despite having a greater serum insulin response to the glucose load (26 plus or minus 4 vs 11 plus or minus 1 insulin area units; p less than 0.01), confirming insulin resistance. Glucose 62-69 insulin Homo sapiens 269-276 7015073-4 1981 The obese group had a slower glucose disappearance rate after glucose challenge (0.84 plus or minus 0.06 vs. 1.11 plus or minus 0.07 hr(-1); p less than 0.01) despite having a greater serum insulin response to the glucose load (26 plus or minus 4 vs 11 plus or minus 1 insulin area units; p less than 0.01), confirming insulin resistance. Glucose 62-69 insulin Homo sapiens 269-276 7014596-7 1981 Furthermore, normalization of plasma free insulin profiles can be achieved, with sharp peaks of insulin coincident with the rise in glucose at each meal. Glucose 132-139 insulin Homo sapiens 42-49 7014596-7 1981 Furthermore, normalization of plasma free insulin profiles can be achieved, with sharp peaks of insulin coincident with the rise in glucose at each meal. Glucose 132-139 insulin Homo sapiens 96-103 7024593-0 1981 [Insulin responses and its hepatic extraction with intravenous glucose and glucagon stimulation in obstructive jaundice (author"s transl)]. Glucose 63-70 insulin Homo sapiens 1-8 7017987-4 1981 During the glucose infusion, insulin levels rose to 177.0 +/- 56.0 microU/ml in the controls and to 127.0 +/- 27.0 microU/ml in the trauma group. Glucose 11-18 insulin Homo sapiens 29-36 6263106-1 1981 The initial lag phase of insulin action on glucose transport in adipocytes reflects an unknown process that couples receptor binding and glucose transport activity. Glucose 43-50 insulin Homo sapiens 25-32 6263106-1 1981 The initial lag phase of insulin action on glucose transport in adipocytes reflects an unknown process that couples receptor binding and glucose transport activity. Glucose 137-144 insulin Homo sapiens 25-32 6262168-2 1981 Initially, insulinoma patients had a greater plasma insulin (42 +/- 9 versus 15 +/- 1 microunits/ml) and glucagon levels (214 +/- 31 versus 158 +/- 21 pg/ml) than normal subjects, P less than 0.05, but their plasma glucose levels (81 +/- 4 mg/dl) and rates of glucose production and utilization (1.71 +/- 0.08 and 1.74 +/- 0.08 mg/kg . Glucose 215-222 insulin Homo sapiens 11-18 7014307-6 1981 Glucose is also infused at a rate sufficient to prevent an insulin-induced fall in glucose concentration, and the amount of glucose required to maintain the basal plasma glucose level provides the estimates of insulin resistance. Glucose 83-90 insulin Homo sapiens 59-66 6262168-2 1981 Initially, insulinoma patients had a greater plasma insulin (42 +/- 9 versus 15 +/- 1 microunits/ml) and glucagon levels (214 +/- 31 versus 158 +/- 21 pg/ml) than normal subjects, P less than 0.05, but their plasma glucose levels (81 +/- 4 mg/dl) and rates of glucose production and utilization (1.71 +/- 0.08 and 1.74 +/- 0.08 mg/kg . Glucose 260-267 insulin Homo sapiens 11-18 7014307-6 1981 Glucose is also infused at a rate sufficient to prevent an insulin-induced fall in glucose concentration, and the amount of glucose required to maintain the basal plasma glucose level provides the estimates of insulin resistance. Glucose 124-131 insulin Homo sapiens 210-217 7014307-6 1981 Glucose is also infused at a rate sufficient to prevent an insulin-induced fall in glucose concentration, and the amount of glucose required to maintain the basal plasma glucose level provides the estimates of insulin resistance. Glucose 124-131 insulin Homo sapiens 210-217 7014307-2 1981 One method, the insulin suppression test, is performed by continuously infusing epinephrine, propranolol, insulin, and glucose. Glucose 119-126 insulin Homo sapiens 16-23 7014307-8 1981 Furthermore, both methods of assessing insulin resistance indicated that the greater the degree of glucose intolerance, the more severe the insulin resistance. Glucose 99-106 insulin Homo sapiens 39-46 7014307-8 1981 Furthermore, both methods of assessing insulin resistance indicated that the greater the degree of glucose intolerance, the more severe the insulin resistance. Glucose 99-106 insulin Homo sapiens 140-147 7014308-2 1981 When the pH of the incubation medium was decreased from 7.6 to 6.8, insulin stimulation of glycogen synthase and total glucose uptake was decreased. Glucose 119-126 insulin Homo sapiens 68-75 7014307-4 1981 Because the steady-state insulin level is the same in all subjects, the height of the steady-state plasma glucose level provides a direct estimate of insulin resistance. Glucose 106-113 insulin Homo sapiens 150-157 7014308-6 1981 In the presence of 3-hydroxybutyrate, insulin binding increased, but insulin action on glycogen synthase and total glucose uptake was unaffected. Glucose 115-122 insulin Homo sapiens 69-76 7014311-4 1981 In contrast, the longer plasma insulin cycles (greater than 10 min) of normal subjects were associated with a plasma glucose oscillation that rose before the end of the cycle. Glucose 117-124 insulin Homo sapiens 31-38 7021384-1 1981 UNLABELLED: Intravenous insulin infusion with a glucose controlled insulin infusion system (GCIIS) is known to restore glucose homeostasis. Glucose 48-55 insulin Homo sapiens 24-31 7021384-1 1981 UNLABELLED: Intravenous insulin infusion with a glucose controlled insulin infusion system (GCIIS) is known to restore glucose homeostasis. Glucose 48-55 insulin Homo sapiens 67-74 7014311-6 1981 The associated glucose changes may reflect the entrainment, by the insulin cycles, of glucose production or utilization. Glucose 15-22 insulin Homo sapiens 67-74 7014307-6 1981 Glucose is also infused at a rate sufficient to prevent an insulin-induced fall in glucose concentration, and the amount of glucose required to maintain the basal plasma glucose level provides the estimates of insulin resistance. Glucose 0-7 insulin Homo sapiens 59-66 7014311-6 1981 The associated glucose changes may reflect the entrainment, by the insulin cycles, of glucose production or utilization. Glucose 86-93 insulin Homo sapiens 67-74 6112234-0 1981 Clinical significance of altered insulin sensitivity in diabetes mellitus assessed by glucose, insulin, and somatostatin infusion. Glucose 86-93 insulin Homo sapiens 33-40 7047114-4 1981 Significant differences in the response of blood glucose and 3-hydroxybutyrate levels reflected the differences in plasma free insulin levels. Glucose 49-56 insulin Homo sapiens 127-134 6112234-1 1981 Insulin sensitivity has been determined in primary nonobese diabetics and subjects with borderline glucose intolerance by a newly devised technique using glucose, insulin, and somatostatin infusion. Glucose 99-106 insulin Homo sapiens 0-7 6112234-1 1981 Insulin sensitivity has been determined in primary nonobese diabetics and subjects with borderline glucose intolerance by a newly devised technique using glucose, insulin, and somatostatin infusion. Glucose 154-161 insulin Homo sapiens 0-7 6112234-2 1981 Insulin sensitivity for glucose utilization was decreased in both adult- and juvenile-onset diabetics. Glucose 24-31 insulin Homo sapiens 0-7 6112234-4 1981 In lean subjects with borderline glucose intolerance, insulin sensitivity was decreased, although an overlap with normal was noted. Glucose 33-40 insulin Homo sapiens 54-61 6112234-5 1981 All obese subjects with borderline glucose intolerance had reduced insulin sensitivity. Glucose 35-42 insulin Homo sapiens 67-74 6112655-8 1981 When glucose was infused with somatostatin, insulin, and glucagon, plasma insulin was maintained at levels 50% above baseline while glucagon remained at preinfusion levels. Glucose 5-12 insulin Homo sapiens 44-51 6112234-6 1981 An inverse relationship was observed between insulin sensitivity and fasting plasma glucose (FPG), and a significant correlation was observed between FPG and steady state plasma glucose levels (SSPG; r = 0.57; P less than 0.001). Glucose 84-91 insulin Homo sapiens 45-52 6112655-8 1981 When glucose was infused with somatostatin, insulin, and glucagon, plasma insulin was maintained at levels 50% above baseline while glucagon remained at preinfusion levels. Glucose 5-12 insulin Homo sapiens 74-81 6112655-15 1981 However, the extra-insulin evoked by hyperglycemia is necessary for the glucoregulatory system to respond to the glucose load with maximal effectiveness. Glucose 113-120 insulin Homo sapiens 19-26 6455503-4 1981 The fasting blood glucose level and blood glucose response to insulin were similar for the two groups. Glucose 42-49 insulin Homo sapiens 62-69 6112234-8 1981 These results indicate that decreased sensitivity of insulin for peripheral glucose utilization may play an important role in the pathogenesis of diabetes. Glucose 76-83 insulin Homo sapiens 53-60 7211820-4 1981 As a parameter of cellular glucose kinetics, a "peripheral insulin resistance" was defined as one-hour glucose (mg/dl) X one-hour insulin (microU/ml). Glucose 27-34 insulin Homo sapiens 59-66 6112718-3 1981 In the high diabetic risk subjects: 1) the OGTT was normal; 2) the insulin response to carbohydrate ingestion was significantly higher than in normals and, of course, in diabetics; 3) the fasting glucagon levels showed no significant differences from the normals; 4) significant suppression of fasting glucagon concentration was observed in normals after oral glucose, but not in high diabetic risk subjects and in diabetic patients. Glucose 360-367 insulin Homo sapiens 67-74 7017376-0 1981 [Behavior of C-peptide during the oral glucose tolerance test in obese children]. Glucose 39-46 insulin Homo sapiens 13-22 7018150-0 1981 Previous exposure to glucose enhances insulin and suppresses glucagon responses to arginine in man. Glucose 21-28 insulin Homo sapiens 38-45 7018150-5 1981 glucose during 0-60 min, followed by a "rest period" of 60-120 min, the insulin release induced by the amino acid was further enhanced, glucagon and GH release were unaffected and blood glucose depressed below control levels. Glucose 0-7 insulin Homo sapiens 72-79 7018150-6 1981 When arginine was preceded by a small oral glucose load (0.5 g/kg) the initial insulin response to arginine was augmented, the initial glucagon response was slightly but significantly depressed and blood glucose lowered while the growth hormone response was unaffected. Glucose 43-50 insulin Homo sapiens 79-86 7018150-7 1981 CONCLUSIONS: (1) a near-physiological intake of glucose increases insulin and depresses glucagon secretion evoked by amino acids resulting in increased glucose disposal; (2) the modifications of the insulin and glucagon responses constitute separate components in the feed-back regulation of glucose homeostasis. Glucose 48-55 insulin Homo sapiens 66-73 6113725-0 1981 The influence of GGT, COHb% and body weight on the 2-h glucose and insulin response after a standardized oral glucose load. Glucose 110-117 insulin Homo sapiens 67-74 6264722-3 1981 The plasma insulin levels during this first glucose-clamp were comprised between 18 and 50 microunits/ml. Glucose 44-51 insulin Homo sapiens 11-18 6264722-7 1981 Both in the basal state and during diazoxide treatment a circadian pattern of glucose requirement was noted, with lower glucose need and plasma insulin levels during the night. Glucose 78-85 insulin Homo sapiens 144-151 7211820-4 1981 As a parameter of cellular glucose kinetics, a "peripheral insulin resistance" was defined as one-hour glucose (mg/dl) X one-hour insulin (microU/ml). Glucose 103-110 insulin Homo sapiens 59-66 7211820-7 1981 After controlling for body weight, only white children in the high blood pressure strata with high insulin resistance had a positive association between fasting plasma glucose and systolic blood pressure. Glucose 168-175 insulin Homo sapiens 99-106 6785095-7 1981 Basal and glucose stimulated insulin secretion were suppressed 60 min after the start of the GH infusion, while insulin response to i.v. Glucose 10-17 insulin Homo sapiens 29-36 7030721-4 1981 Insulin secretion was significantly increased in IAP treated pancreatic islets by the glucose and the arginine stimuli. Glucose 86-93 insulin Homo sapiens 0-7 7014136-9 1981 There is a negative correlation between plasma catecholamine levels and reduced insulin secretion following the administration of glucose in the postoperative phase. Glucose 130-137 insulin Homo sapiens 80-87 7009630-3 1981 The total insulin response to oral glucose, calculated as the insulin area, was significantly exaggerated (P less than 0.01 vs. the control value). Glucose 35-42 insulin Homo sapiens 10-17 7262044-8 1981 In patients with atherosclerotic peripheral vascular disease the results suggest an altered metabolism of glucose, which is shunted into insulin-insensitive glucuronate pathway in conditions of endogenous hypercortisolism. Glucose 106-113 insulin Homo sapiens 137-144 7262046-6 1981 Under comparable steady-state insulin levels the decrease in plasma glucose and free fatty acids (FFA) was considered as estimate of insulin sensitivity in vivo. Glucose 68-75 insulin Homo sapiens 133-140 7262046-12 1981 Physical fitness increased by delta PWC170 of 31.1 +/- 11.6 W. In addition, the combined training and diet programme for 4 weeks resulted in a significant improvement of insulin sensitivity in vivo as indicated by an augmented insulin-induced decrease in plasma glucose and FFA (17.60 +/- 3.91%, vs 36.40 +/- 5.54%; p less than 0.05 and 35.90 +/- 6.95% vs 56.50 +/- 3.63%; p less than 0.05; respectively). Glucose 262-269 insulin Homo sapiens 227-234 7030723-1 1981 Insulin binding to circulating erythrocytes was studied in 32 maturity onset-type diabetic patients with varying degrees of insulin response to oral glucose. Glucose 149-156 insulin Homo sapiens 0-7 7021500-5 1981 Although insulin concentrations decreased rapidly to basal levels within 10 min after the onset of exercise in the preexercise glucose group (P less than 0.05), blood glucose continued to decrease throughout exercise. Glucose 127-134 insulin Homo sapiens 9-16 7021500-8 1981 Differences in the preexercise insulin environment appear to exert a persistent effect on glucose uptake throughout exercise. Glucose 90-97 insulin Homo sapiens 31-38 7009630-3 1981 The total insulin response to oral glucose, calculated as the insulin area, was significantly exaggerated (P less than 0.01 vs. the control value). Glucose 35-42 insulin Homo sapiens 62-69 7017734-3 1981 In the patient"s fibroblasts, maximal insulin-stimulated glucose incorporation was less than 25% of that in control fibroblasts, whereas stimulation by hydrogen peroxide, an insulinomimetic agent that acts distal to the insulin receptor, was normal. Glucose 57-64 insulin Homo sapiens 38-45 7010077-2 1981 Despite the small dose of insulin used, plasma glucose levels tended to be 1 to 2 mmole/liter lower at 35 degrees C than at 20 degrees C. These findings indicate that a rise in ambient temperature augments insulin absorption, in insulin-treated diabetic patients. Glucose 47-54 insulin Homo sapiens 206-213 7024392-2 1981 There are no reports about this effect in uremic patients in which frequently calcitonin, gastrin, growth hormone, and insulin response to glucose administration is increased. Glucose 139-146 insulin Homo sapiens 119-126 7017734-0 1981 Stimulation of glucose incorporation and amino acid transport by insulin and an insulin-like growth factor in fibroblasts with defective insulin receptors cultured from a patient with leprechaunism. Glucose 15-22 insulin Homo sapiens 65-72 7017735-0 1981 Abnormal regulation of monocyte insulin-binding affinity after glucose ingestion in patients with myotonic dystrophy. Glucose 63-70 insulin Homo sapiens 32-39 7017734-0 1981 Stimulation of glucose incorporation and amino acid transport by insulin and an insulin-like growth factor in fibroblasts with defective insulin receptors cultured from a patient with leprechaunism. Glucose 15-22 insulin Homo sapiens 80-87 7017734-0 1981 Stimulation of glucose incorporation and amino acid transport by insulin and an insulin-like growth factor in fibroblasts with defective insulin receptors cultured from a patient with leprechaunism. Glucose 15-22 insulin Homo sapiens 80-87 7017735-3 1981 Monocytes from 10 normal volunteers developed a significantly increased insulin-binding affinity by 2 hr after glucose ingestion (mean +/- SEM, 11.7 +/- 2.7 ng/ml compared to basal 50% insulin displacement value of 23.3 +/- 2.2 ng/ml, P less than 0.005). Glucose 111-118 insulin Homo sapiens 72-79 7017734-2 1981 We now examine the effect of this defect on two acute metabolic actions of insulin thought to be mediated by the insulin receptor, glucose incorporation and N-methyl-alpha-aminoisobutyric acid (Me-AiBu) uptake. Glucose 131-138 insulin Homo sapiens 75-82 7017735-3 1981 Monocytes from 10 normal volunteers developed a significantly increased insulin-binding affinity by 2 hr after glucose ingestion (mean +/- SEM, 11.7 +/- 2.7 ng/ml compared to basal 50% insulin displacement value of 23.3 +/- 2.2 ng/ml, P less than 0.005). Glucose 111-118 insulin Homo sapiens 185-192 16435484-0 1981 GIP and insulin responses to oral glucose in coeliac patients before and after treatment. Glucose 34-41 insulin Homo sapiens 8-15 7011013-2 1981 The dual role of glucose to directly stimulate insulin release and to potentiate insulin secretion to other islet regulators is emphasized. Glucose 17-24 insulin Homo sapiens 47-54 7011013-2 1981 The dual role of glucose to directly stimulate insulin release and to potentiate insulin secretion to other islet regulators is emphasized. Glucose 17-24 insulin Homo sapiens 81-88 7011013-7 1981 The model shows why this increase in plasma glucose occurs and the importance of this hyperglycemia to the restoration of insulin responses to nonglucose secretagogues, second-phase insulin secretion to glucose and basal insulin. Glucose 44-51 insulin Homo sapiens 122-129 6164591-0 1981 Insulin-stimulated glucose uptake, leucine incorporation into protein, and uridine incorporation into RNA in skin fibroblast cultures from patients with diabetes mellitus. Glucose 19-26 insulin Homo sapiens 0-7 6263727-0 1981 Glucose controlled insulin infusion system (Biostator) application during surgery for a presumed pancreatic microinsulinoma. Glucose 0-7 insulin Homo sapiens 19-26 6263727-1 1981 A glucose controlled insulin infusion system has been used during and after surgery for organic hyperinsulinism in a 37 year old woman. Glucose 2-9 insulin Homo sapiens 21-28 7008893-2 1981 The patients were all treated with a glucose/insulin/potassium infusions regimen, but the cardiac group needed much greater amounts of insulin (1.0 unit/g of glucose) than the non-cardiac group (0.3 units/g) to achieve a similar level of control. Glucose 158-165 insulin Homo sapiens 135-142 7011736-2 1981 The results demonstrated that this insulin preparation binds to receptors with full binding potency and also exerts normal biologic activity to stimulate adipocyte glucose oxidation and glucose transport. Glucose 164-171 insulin Homo sapiens 35-42 7011736-2 1981 The results demonstrated that this insulin preparation binds to receptors with full binding potency and also exerts normal biologic activity to stimulate adipocyte glucose oxidation and glucose transport. Glucose 186-193 insulin Homo sapiens 35-42 7011741-1 1981 Biosynthetic human insulin (BHI) was compared to pancreatic human insulin and sperm whale insulin in terms of ability to stimulate incorporation of glucose into isolated rat adipocytes and thymidine into DNA in chick embryo fibroblasts. Glucose 148-155 insulin Homo sapiens 19-26 7011741-3 1981 Sperm whale insulin was more potent than the human insulins in stimulating glucose incorporation into rat adipocytes. Glucose 75-82 insulin Homo sapiens 12-19 7009645-0 1981 Insulin increases glucose transfer across the blood-brain barrier in man. Glucose 18-25 insulin Homo sapiens 0-7 7011749-0 1981 Algorithms for adjustment of insulin dosage by patients who monitor blood glucose. Glucose 74-81 insulin Homo sapiens 29-36 7016619-8 1981 The within subject reproducibility of the plasma glucose and insulin response to the serial glucose loads was excellent. Glucose 92-99 insulin Homo sapiens 61-68 7009645-1 1981 The influence of insulin on unidirectional flux of glucose across the blood-brain barrier and on net uptake of glucose by the brain was investigated in seven fasting patients. Glucose 51-58 insulin Homo sapiens 17-24 7011719-1 1981 In the last 2 years we have developed a new method for determining insulin biologic activity with the help of the glucose-controlled insulin infusion system (GCIIS). Glucose 114-121 insulin Homo sapiens 67-74 7011719-1 1981 In the last 2 years we have developed a new method for determining insulin biologic activity with the help of the glucose-controlled insulin infusion system (GCIIS). Glucose 114-121 insulin Homo sapiens 133-140 7011719-5 1981 After subcutaneous injection of the insulin to be tested in healthy persons (not in insulin-dependent diabetic subjects), the blood glucose level falls, and this is checked by the counterregulatory glucose delivery from the apparatus. Glucose 132-139 insulin Homo sapiens 36-43 7011719-5 1981 After subcutaneous injection of the insulin to be tested in healthy persons (not in insulin-dependent diabetic subjects), the blood glucose level falls, and this is checked by the counterregulatory glucose delivery from the apparatus. Glucose 198-205 insulin Homo sapiens 36-43 7011719-6 1981 The time and intensity of glucose delivery from the GCIIS reflect the insulin effect, so that each insulin manifests its own particular biologic activity. Glucose 26-33 insulin Homo sapiens 70-77 7011719-6 1981 The time and intensity of glucose delivery from the GCIIS reflect the insulin effect, so that each insulin manifests its own particular biologic activity. Glucose 26-33 insulin Homo sapiens 99-106 6260823-9 1981 The presence of an insulin-insensitive, facilitated transport system for glucose in vascular endothelium has relevance for glucose metabolism in this tissue, and potentially for the association of certain vascular diseases (e.g., diabetic microangiopathy, atherosclerosis) with altered glucose homeostasis. Glucose 73-80 insulin Homo sapiens 19-26 6260823-9 1981 The presence of an insulin-insensitive, facilitated transport system for glucose in vascular endothelium has relevance for glucose metabolism in this tissue, and potentially for the association of certain vascular diseases (e.g., diabetic microangiopathy, atherosclerosis) with altered glucose homeostasis. Glucose 123-130 insulin Homo sapiens 19-26 7009645-7 1981 The main finding was an increased extraction of glucose from 14 to 21% and a highly significant increase in unidirectional flux (CBF X unidirectional extraction X arterial glucose concentration) from 0.46 to 0.66 mumol/g X min during insulin infusion (plasma insulin approximately 1,500 microU/ml). Glucose 172-179 insulin Homo sapiens 234-241 7009645-9 1981 It follows that the backflux of glucose from the brain was increased during insulin application. Glucose 32-39 insulin Homo sapiens 76-83 7009645-10 1981 The effect of insulin might be a speeding up of the glucose carrier in analogy to heart muscle. Glucose 52-59 insulin Homo sapiens 14-21 7008850-2 1981 On the other hand, the half-time of deactivation of hexose transport in insulin-pretreated cells was of the same magnitude as that of dissociation of receptor-bound insulin both in the absence and presence of glucose (about 8 min). Glucose 209-216 insulin Homo sapiens 72-79 7018100-4 1981 It was investigated to what extent the insulin values correlated with the fasting blood glucose level. Glucose 88-95 insulin Homo sapiens 39-46 7018100-8 1981 In 24% of the patients an increase of the insulin levels in the blood after administration of glucose was missing altogether. Glucose 94-101 insulin Homo sapiens 42-49 7018102-1 1981 On the basis of the estimation of the plasma glucose and the insulin concentrations in 10-minute intervals during 24 hours by the mathematical analysis (multiple regression) over relations between the behaviour of plasma glucose and insulin concentration insulin secretion rates independent of plasma glucose can be calculated. Glucose 221-228 insulin Homo sapiens 61-68 7018102-1 1981 On the basis of the estimation of the plasma glucose and the insulin concentrations in 10-minute intervals during 24 hours by the mathematical analysis (multiple regression) over relations between the behaviour of plasma glucose and insulin concentration insulin secretion rates independent of plasma glucose can be calculated. Glucose 221-228 insulin Homo sapiens 61-68 6257679-6 1981 The addition to the medium of glucose, fructose, pyruvate, or lactate enhanced the insulin-induced increase in glucokinase, but only fructose, pyruvate, and lactate increased the activity of the enzyme in the absence of insulin. Glucose 30-37 insulin Homo sapiens 83-90 6257679-6 1981 The addition to the medium of glucose, fructose, pyruvate, or lactate enhanced the insulin-induced increase in glucokinase, but only fructose, pyruvate, and lactate increased the activity of the enzyme in the absence of insulin. Glucose 30-37 insulin Homo sapiens 220-227 6781424-5 1981 The preoperative insulin response during a glucose tolerance test was blunted or delayed in the three patients tested. Glucose 43-50 insulin Homo sapiens 17-24 7010984-3 1981 The hormone and substrate response to dietary protein plus glucose was a substantial rise in insulin (p less than 0.005), glucose (p less than 0.005), and fall in free fatty acid and ketone levels (p less than 0.005). Glucose 59-66 insulin Homo sapiens 93-100 6261607-3 1981 In case of need (blood glucose level) additional insulin up to 200 U/h, maximum 800 U/10 h, was supplied. Glucose 23-30 insulin Homo sapiens 49-56 7020069-4 1981 Following addition of insulin a dose-related rise in ADCC, lactate release, and glucose uptake was observed. Glucose 80-87 insulin Homo sapiens 22-29 7009290-2 1981 Glucose levels were maintained using a glucose controlled insulin infusion system. Glucose 0-7 insulin Homo sapiens 58-65 7009290-2 1981 Glucose levels were maintained using a glucose controlled insulin infusion system. Glucose 39-46 insulin Homo sapiens 58-65 7021006-2 1981 After withdrawal of the evening insulin injection the fasting blood glucose and serum IR-GIP levels were elevated and decreased significantly following intravenous insulin towards normal values. Glucose 68-75 insulin Homo sapiens 32-39 7021006-3 1981 There was a significant positive correlation between levels of blood glucose and serum IR-GIP before and during insulin application. Glucose 69-76 insulin Homo sapiens 112-119 7261414-6 1981 The mean insulin levels basally and after glucose loading were lower than those of the normal controls. Glucose 42-49 insulin Homo sapiens 9-16 7007804-1 1981 We have previously postulated that resistance to insulin-mediated glucose uptake was the basic metabolic abnormality in patients with endogenous hypertriglyceridemia. Glucose 66-73 insulin Homo sapiens 49-56 7007804-2 1981 In this situation, glucose tolerance would tend to deteriorate, and could only be maintained by the increased secretion of insulin. Glucose 19-26 insulin Homo sapiens 123-130 7014485-3 1981 In stimulating glucose oxidation and lipogenesis the analogue exhibited potencies of 0.19% and 0.14%, respectively, as compared to insulin. Glucose 15-22 insulin Homo sapiens 131-138 7007440-4 1981 In uremic subjects insulin-mediated glucose metabolism was reduced by 47% compared with controls (3.71 +/- 0.20 vs. 7.38 +/- 0.26 mg/kg . Glucose 36-43 insulin Homo sapiens 19-26 7007440-17 1981 These results indicate that: (a) suppression of hepatic glucose production by physiologic hyperinsulinemia is not impaired by uremia, (b) insulin-mediated glucose uptake by the liver is normal in uremic subjects, and (c) tissue insensitivity to insulin is the primary cause of insulin resistance in uremia. Glucose 56-63 insulin Homo sapiens 95-102 7020069-6 1981 Most of the stimulation was seen within the physiological concentration range of insulin, and the insulin concentration resulting in 50% of the maximal effect was nearly the same for ADCC, lactate release, and glucose uptake (about 100 pM). Glucose 210-217 insulin Homo sapiens 98-105 7020069-7 1981 The insulin stimulation of ADCC correlated with the stimulation of lactate release and glucose uptake. Glucose 87-94 insulin Homo sapiens 4-11 6266182-6 1981 The glucose concentration in the medium influenced the insulin release in a dose dependent manner. Glucose 4-11 insulin Homo sapiens 55-62 6266182-8 1981 Both in the acute and the chronic experiments maximal insulin release was found at 10 mM glucose. Glucose 89-96 insulin Homo sapiens 54-61 7036659-0 1981 Does verapamil influence glucose-induced insulin release in man? Glucose 25-32 insulin Homo sapiens 41-48 7010856-3 1981 At comparable insulin doses, continuous subcutaneous insulin infusion provided a significantly lower mean daily blood glucose. Glucose 118-125 insulin Homo sapiens 53-60 7036659-7 1981 It was found that the blood glucose and serum insulin responses to oral glucose were unaffected by verapamil both in the portal and in the peripheral venous blood. Glucose 72-79 insulin Homo sapiens 46-53 7039239-0 1981 Immunoreactive insulin and C-peptide responses to various insulin secretory stimuli in subjects with type 2 diabetes and in control subjects during continuous glucose monitoring. Glucose 159-166 insulin Homo sapiens 15-22 6791607-5 1981 The dose of insulin was estimated at a ratio of 1 IU per 1 gm of excess glucose over 2.0 gm/l. Glucose 72-79 insulin Homo sapiens 12-19 7006388-5 1981 Mechanisms of insulin resistance can be evaluated by constructing in vivo dose-response curves using the euglycemic glucose clamp technique. Glucose 116-123 insulin Homo sapiens 14-21 7006388-10 1981 In these patients, the in vivo dose-response curve between plasma insulin levels and glucose disposal demonstrates a rightward shift with no change in maximal insulin responsiveness. Glucose 85-92 insulin Homo sapiens 66-73 7006391-5 1981 Under development are implantable continuous infusion devices and implantable glucose sensors that could in the future lead to a miniaturized implantable glucose-controlled insulin administration system. Glucose 78-85 insulin Homo sapiens 173-180 7006391-5 1981 Under development are implantable continuous infusion devices and implantable glucose sensors that could in the future lead to a miniaturized implantable glucose-controlled insulin administration system. Glucose 154-161 insulin Homo sapiens 173-180 7006392-2 1981 Whereas in normal man plasma glucose varies little during exercise, the insulin-dependent diabetic subject may experience an increase in plasma glucose, a modest decrease or a marked decrease which can result in symptomatic hypoglycemia. Glucose 144-151 insulin Homo sapiens 72-79 6456793-2 1981 1) In the so-called closed-loop systems, insulin delivery is regulated by the concomitant plasma glucose level. Glucose 97-104 insulin Homo sapiens 41-48 7021126-6 1981 The serum-insulin-analysis gave 28 x lower figures during the acute phase compared to the healing-phase, whereas the determination of the C-peptide showed higher figures matching the enhanced glucose concentrations, which proves a normal regulation of insulin-secretion during the acute phase of disease in hepatitis. Glucose 192-199 insulin Homo sapiens 138-147 6809327-2 1981 The insulin production in response to a glucose challenge is decreased. Glucose 40-47 insulin Homo sapiens 4-11 6809327-4 1981 The correlation between the insulin response to a glucose challenge and the activities of glycolytic and oxidative rate-limiting enzymes in muscle tissue suggests a common denominator for these metabolic alterations. Glucose 50-57 insulin Homo sapiens 28-35 7009119-0 1981 Quantitative and qualitative changes in the early insulin response to glucose in subjects with impaired carbohydrate tolerance. Glucose 70-77 insulin Homo sapiens 50-57 7009528-11 1981 The blunted response of insulin after glucose administration in athletes is due to an enhanced plasma clearance. Glucose 38-45 insulin Homo sapiens 24-31 7014300-1 1981 A total of 32 pairs of obese fathers or mothers and their obese offsprings, aged 20 yr or younger, from 25 families with established hyperinsulinemic obesity aged 11-20 yr equally showed an insulin hyperresponse to glucose, the offspring 10 yr or younger revealed a rather normal insulin response, despite the presence of obesity, and this contrasted with their fathers or mothers. Glucose 215-222 insulin Homo sapiens 190-197 7014300-4 1981 The results suggest that the insulin hypersecretion is not the primary trait in this form of familial obesity and that the insulin response to glucose becomes augmented during the maturation years of 11-20, thus resulting in the accumulation of hyperinsulinemic and hyperlipidemic adults in the family. Glucose 143-150 insulin Homo sapiens 123-130 7024157-8 1981 Insulin production after oral glucose load did not change in either of the two groups. Glucose 30-37 insulin Homo sapiens 0-7 7016966-4 1981 The C-peptide/IRI ratio, which was lower than normal both during fasting and after glucose load, presented the lowest values in patients with normal OGTT. Glucose 83-90 insulin Homo sapiens 4-13 6787107-5 1981 There was a significant inverse correlation between the mean insulin and glucose levels in individual subjects. Glucose 73-80 insulin Homo sapiens 61-68 7029319-4 1981 The clinical significance of the disorders and methods for evaluation of insulin response to oral glucose are discussed. Glucose 98-105 insulin Homo sapiens 73-80 6784135-5 1981 Acute insulin response to glucose (20 g) was significantly increased by LAS (response before LAS=26 +/- 10%; during LAS=77+15%, mean+/-SEM, mean change 3-10 min insulin, % basal, n=8, p 0.01), as well as second phase insulin secretion (before LAS=1437+/-316%; during LAS=3960+/-550%, change 10-60 min, uU/ml-min, % basal, p less than 0.01). Glucose 26-33 insulin Homo sapiens 6-13 7017570-3 1981 There was a markedly blunted insulin secretory response to glucagon, tolbutamide, glucose, and arginine. Glucose 82-89 insulin Homo sapiens 29-36 7033953-3 1981 It was determined that a decrease in insulin sensitivity and insulin resistance prevailed in patients with disturbed glucose tolerance (the doubtful type of glycemic curve, latent diabetes). Glucose 117-124 insulin Homo sapiens 37-44 7033953-3 1981 It was determined that a decrease in insulin sensitivity and insulin resistance prevailed in patients with disturbed glucose tolerance (the doubtful type of glycemic curve, latent diabetes). Glucose 117-124 insulin Homo sapiens 61-68 6784135-5 1981 Acute insulin response to glucose (20 g) was significantly increased by LAS (response before LAS=26 +/- 10%; during LAS=77+15%, mean+/-SEM, mean change 3-10 min insulin, % basal, n=8, p 0.01), as well as second phase insulin secretion (before LAS=1437+/-316%; during LAS=3960+/-550%, change 10-60 min, uU/ml-min, % basal, p less than 0.01). Glucose 26-33 insulin Homo sapiens 161-168 7013292-3 1981 This paper gives a review of the development, principle of function and clinical application of the glucose controlled insulin infusion system (closed loop system) and of the so-called open loop system without feedback to the glucose values. Glucose 100-107 insulin Homo sapiens 119-126 7034150-5 1981 Incubation of erythrocytes in medium containing glucose showed that deformability was significantly improved in the presence of insulin. Glucose 48-55 insulin Homo sapiens 128-135 7034154-5 1981 The effect of duodenal acidification on the glucose-stimulated GIP and insulin release was investigated in man by intraduodenal infusion of glucose with a pH of 6.5 of 1.5 (no. Glucose 44-51 insulin Homo sapiens 71-78 7013292-4 1981 Results of our own investigations with GCIIS "Biostator", the development of an algorithm of our for the correlation between glucose and insulin behaviour and the first results with the insulin therapy with micropumps (open loop system) were demonstrated and discussed critically. Glucose 125-132 insulin Homo sapiens 137-144 7222867-3 1981 In patients with chronic active hepatitis the C-peptide/insulin-ratio, a measure for hepatic insulin degradation, was significantly lowered after glucose uptake. Glucose 146-153 insulin Homo sapiens 56-63 6783495-5 1980 Patients receiving a mixed sugar solution of glucose, fructose and xylitol at a ratio of 1:2:1 require less exogenous insulin and yet maintain a lower blood glucose concentration. Glucose 45-52 insulin Homo sapiens 118-125 7007871-1 1980 The acute effects of insulin on 3H incorporation into lipid from glucose was measured in 3T3-L1 fatty fibroblasts cultured with and without insulin at 10 microgram/ml for 7 days. Glucose 65-72 insulin Homo sapiens 21-28 7008861-1 1980 The reactivity of the pancreas in normal and in decapitated in utero fetuses from mothers with experimental diabetes was evaluated from the increased insulin secretion in vitro in response to glucose and theophylline. Glucose 192-199 insulin Homo sapiens 150-157 6255805-0 1980 Prostaglandin synthesis inhibitors reverse alpha-adrenergic inhibition of acute insulin response to glucose. Glucose 100-107 insulin Homo sapiens 80-87 6255805-4 1980 The lower dose of epinephrine diminished the acute insulin response (AIR) after a 20-g intravenous glucose pulse (control, 463 +/- 149; epinephrine, 97 +/- 38% of basal insulin, mean +/- SE, n = 6, P < 0.02); SS markedly augmented the AIR during epinephrine towards control values (339 +/- 137%; P < 0.02). Glucose 99-106 insulin Homo sapiens 51-58 7002673-10 1980 Estimating these characteristic parameters of insulin kinetics from IVGTT data has potential for quantitating the individual factors contributing to glucose-stimulated insulin secretion in intact animal models, and it may be applicable to man. Glucose 149-156 insulin Homo sapiens 46-53 7002673-10 1980 Estimating these characteristic parameters of insulin kinetics from IVGTT data has potential for quantitating the individual factors contributing to glucose-stimulated insulin secretion in intact animal models, and it may be applicable to man. Glucose 149-156 insulin Homo sapiens 168-175 7002671-10 1980 Granule movement also decreased when insulin release was inhibited by lowering glucose from 16.5 mM to 2.7 mM. Glucose 79-86 insulin Homo sapiens 37-44 7014042-7 1980 Mean peripheral insulin concentrations were significantly increased after 50 or 75 g of glucose as compared with the 25 g dose (P less than 0.02). Glucose 88-95 insulin Homo sapiens 16-23 7009246-0 1980 Relation between hemoglobin AI and determinations of glucose in diabetics treated with and without insulin. Glucose 53-60 insulin Homo sapiens 99-106 7014042-9 1980 Total integrated areas under the response curves for glucose, insulin and GIP showed a graded increase in circulating insulin and GIP (P less than 0.01) as the amount of ingested glucose was increased from 25 to 75 g. These findings show that increasing doses of glucose stimulated greater levels of GIP and insulin and further support the insulinotropic properties of endogenous GIP in man. Glucose 53-60 insulin Homo sapiens 118-125 7014042-9 1980 Total integrated areas under the response curves for glucose, insulin and GIP showed a graded increase in circulating insulin and GIP (P less than 0.01) as the amount of ingested glucose was increased from 25 to 75 g. These findings show that increasing doses of glucose stimulated greater levels of GIP and insulin and further support the insulinotropic properties of endogenous GIP in man. Glucose 179-186 insulin Homo sapiens 62-69 7014042-9 1980 Total integrated areas under the response curves for glucose, insulin and GIP showed a graded increase in circulating insulin and GIP (P less than 0.01) as the amount of ingested glucose was increased from 25 to 75 g. These findings show that increasing doses of glucose stimulated greater levels of GIP and insulin and further support the insulinotropic properties of endogenous GIP in man. Glucose 179-186 insulin Homo sapiens 118-125 7014042-9 1980 Total integrated areas under the response curves for glucose, insulin and GIP showed a graded increase in circulating insulin and GIP (P less than 0.01) as the amount of ingested glucose was increased from 25 to 75 g. These findings show that increasing doses of glucose stimulated greater levels of GIP and insulin and further support the insulinotropic properties of endogenous GIP in man. Glucose 179-186 insulin Homo sapiens 62-69 7014042-9 1980 Total integrated areas under the response curves for glucose, insulin and GIP showed a graded increase in circulating insulin and GIP (P less than 0.01) as the amount of ingested glucose was increased from 25 to 75 g. These findings show that increasing doses of glucose stimulated greater levels of GIP and insulin and further support the insulinotropic properties of endogenous GIP in man. Glucose 179-186 insulin Homo sapiens 118-125 6108331-8 1980 Under normocalcemic conditions, the insulin response to glucose and glucose tolerance were significantly greater than values measured during hypocalcemia. Glucose 56-63 insulin Homo sapiens 36-43 7009363-6 1980 The plasma insulin levels of bilharzial patients in the fasting state and 60 minutes after glucose infusion were higher than in healthy children. Glucose 91-98 insulin Homo sapiens 11-18 7009363-7 1980 The calculated insulin/glucose ratio after glucose infusion was similar in bilharzial and healthy children. Glucose 43-50 insulin Homo sapiens 15-22 7009366-0 1980 Plasma insulin response to glucose infusion in obese non-diabetic and diabetic subjects. Glucose 27-34 insulin Homo sapiens 7-14 7009366-5 1980 In 20 obese subjects with normal OGTT, both the initial and the later plasma insulin responses to glucose infusion were higher than in controls. Glucose 98-105 insulin Homo sapiens 77-84 6108331-9 1980 However, somatostatin blunted the insulin response to glucose and significantly decreased glucose utilization. Glucose 54-61 insulin Homo sapiens 34-41 7002949-8 1980 The peak insulin and GIP responses with the glucose and glucose/acid combinations were similar with both the oral and intraduodenal routes. Glucose 44-51 insulin Homo sapiens 9-16 7002949-8 1980 The peak insulin and GIP responses with the glucose and glucose/acid combinations were similar with both the oral and intraduodenal routes. Glucose 56-63 insulin Homo sapiens 9-16 7002949-9 1980 There was, however, a potentiation of both the GIP and insulin responses when intraduodenal acid was given with glucose. Glucose 112-119 insulin Homo sapiens 55-62 7002954-9 1980 The observed decrease in insulin binding to the RBCs of obese children and adolescents correlated with fasting hyperinsulinemia and, therefore, may contribute to the etiology of the insulin resistance or glucose intolerance observed in these patients. Glucose 204-211 insulin Homo sapiens 25-32 7002954-9 1980 The observed decrease in insulin binding to the RBCs of obese children and adolescents correlated with fasting hyperinsulinemia and, therefore, may contribute to the etiology of the insulin resistance or glucose intolerance observed in these patients. Glucose 204-211 insulin Homo sapiens 116-123 7256722-2 1980 The blood glucose levels in thyrotoxicosis rose after the administration of glycerol deposit elevation of the plasma levels of insulin. Glucose 10-17 insulin Homo sapiens 127-134 7012840-1 1980 Groups of subjects with different degrees of glucose intolerance were examined in order to determine, first, the capacity of the beta cells to release insulin upon glucose stimulation and, second, sensitivity to insulin. Glucose 164-171 insulin Homo sapiens 151-158 7012840-4 1980 Computer analysis of the glucose and insulin curves during a standardized glucose infusion test made possible the measurement of the initiatory (parameters KI and IP) and potentiatory (parameter KP) effects of glucose on insulin release and of the sensitivity to endogenous insulin (parameter KG). Glucose 74-81 insulin Homo sapiens 37-44 7012840-4 1980 Computer analysis of the glucose and insulin curves during a standardized glucose infusion test made possible the measurement of the initiatory (parameters KI and IP) and potentiatory (parameter KP) effects of glucose on insulin release and of the sensitivity to endogenous insulin (parameter KG). Glucose 74-81 insulin Homo sapiens 37-44 7012840-8 1980 These data suggest that all stages of glucose intolerance are accompanied by a decreased ability of glucose to initiate insulin release and by decreased sensitivity to insulin. Glucose 38-45 insulin Homo sapiens 120-127 7012840-8 1980 These data suggest that all stages of glucose intolerance are accompanied by a decreased ability of glucose to initiate insulin release and by decreased sensitivity to insulin. Glucose 38-45 insulin Homo sapiens 168-175 7012840-8 1980 These data suggest that all stages of glucose intolerance are accompanied by a decreased ability of glucose to initiate insulin release and by decreased sensitivity to insulin. Glucose 100-107 insulin Homo sapiens 120-127 7012840-9 1980 These derangements seem to be partially compensated for by enhancement of the capacity of glucose to potentiate insulin release in subjects with decreased oral but normal intravenous glucose tolerance tests. Glucose 90-97 insulin Homo sapiens 112-119 6999353-3 1980 When glucose was infused to maintain a constant hyperglycemic level (125 mg per deciliter [6.9 mmol per liter] above basal levels), the glucose infusion rate was 36 per cent less in the hypophosphatemic group than in controls (4.90 +/- 0.34 mg per kilogram of body weight per minute vs. 7.64 +/- 0.37, P < 0.001), although responses to endogenous insulin were similar. Glucose 5-12 insulin Homo sapiens 350-357 7006076-8 1980 During long-term ambulatory treatment with the insulin pump improved metabolic control was achieved, as shown by lower mean blood glucose values, decreased urinary glucose excretion and by lowering of hemoglobin AIc. Glucose 130-137 insulin Homo sapiens 47-54 7429029-3 1980 The subjects with glucose intolerance had significantly higher insulin levels than either the glucose-tolerant or normal control subjects. Glucose 18-25 insulin Homo sapiens 63-70 7226566-4 1980 This exaggerated PP response to oral glucose loading was partially but significantly improved after the treatment, with an augmented response of plasma insulin. Glucose 37-44 insulin Homo sapiens 152-159 7000584-9 1980 Vinblastine and chloroquine both significantly inhibited insulin-stimulated glucose incorporation into glycogen without affecting basal levels. Glucose 76-83 insulin Homo sapiens 57-64 7000587-3 1980 The rates of glucose production, disappearance, and fractional disappearance were related to the range of glucagon and insulin levels in each individual. Glucose 13-20 insulin Homo sapiens 119-126 7000587-8 1980 In the normals the fractional disappearance rate of glucose was positively related to serum levels of insulin, whereas in the hypertriglyceridemics it was lower than normal and did not change in relation to insulin concentration. Glucose 52-59 insulin Homo sapiens 102-109 7002569-3 1980 10 subjects had normal glucose tolerance; in them nifedipine administration reduced the insulin response to oral glucose in the first 60 min, but improved glucose tolerance. Glucose 113-120 insulin Homo sapiens 88-95 7002569-3 1980 10 subjects had normal glucose tolerance; in them nifedipine administration reduced the insulin response to oral glucose in the first 60 min, but improved glucose tolerance. Glucose 113-120 insulin Homo sapiens 88-95 6999007-3 1980 In 8 patients studied during halothane inhalation anesthesia before operation, the acute insulin response (AIR) to glucose (5 g, IV) fell to 51 +/- 3% of the preanesthesia AIR (mean +/- SEM; P < 0.001). Glucose 115-122 insulin Homo sapiens 89-96 6999010-0 1980 Glucose kinetics in leprechaunism: accelerated fasting due to insulin resistance. Glucose 0-7 insulin Homo sapiens 62-69 7002978-4 1980 Following intravenous injection of insulin, the recovery of the blood glucose concentrations was significantly reduced in asthmatic patients. Glucose 70-77 insulin Homo sapiens 35-42 7001183-6 1980 Meanwhile, glucose clearance is decreased because of elevated circulating levels of catecholamines and low insulin concentrations. Glucose 11-18 insulin Homo sapiens 107-114 7001179-3 1980 Inhalation anesthesia alone was found to suppress basal insulin levels and the insulin response to intravenous glucose with no significant increase in plasma norepinephrine and a decrease in plasma epinephrine. Glucose 111-118 insulin Homo sapiens 79-86 6997131-10 1980 The rise induced by adrenergic beta-receptor stimulation with epinephrine plus phentolamine was equivalent to the rise from 40 +/- 11 to 280 +/- 48 pM caused by an insulin-induced fall in serum glucose of about 50% and that induced by isoproterenol infusion, which caused a fourfold rise from 69 +/- 3 to 271 +/- 84 pM. Glucose 194-201 insulin Homo sapiens 164-171 6256217-0 1980 [Insulin response to glucose and arginine in patients with isolated ACTH deficiency (author"s transl)]. Glucose 21-28 insulin Homo sapiens 1-8 7001974-7 1980 Our data suggest marked sensitivity to the insulin antagonistic effects of epinephrine and may provide a mechanism for stress-induced glucose intolerance. Glucose 134-141 insulin Homo sapiens 43-50 6777169-8 1980 Correlations between total cholesterol and lipoprotein cholesterol values in serum and blood glucose and plasma insulin at fast and during OGTT and changes in these parameters demonstrate interrelationships between lipid and carbohydrate metabolism. Glucose 93-100 insulin Homo sapiens 112-119 6778693-1 1980 The efficiency of insulin (decrease of the blood glucose per unit of insulin administered) was assessed in 610 cases of diabetic ketoacidosis (316 females, 274 males, aged 3 to 72 years) in terms of the degree of plasma acidemia. Glucose 49-56 insulin Homo sapiens 18-25 6778693-5 1980 The somewhat lower efficiency of insulin in the advanced and severe cases of ketoacidosis appears to be due to vascular collapse encountered in 38 cases (6 advanced ketoacidosis and 32 severe ketoacidosis), since in these patients the fall in blood glucose per unit insulin was only 15.8 mg/l. Glucose 249-256 insulin Homo sapiens 33-40 6106647-7 1980 In obese Southwestern American Indians with glucose intolerance, abnormalities beyond the site of insulin binding to its receptor may explain the observed increase in in vivo insulin resistance. Glucose 44-51 insulin Homo sapiens 175-182 6106647-1 1980 Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. Glucose 49-56 insulin Homo sapiens 32-39 6106647-1 1980 Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. Glucose 114-121 insulin Homo sapiens 32-39 6106647-1 1980 Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. Glucose 114-121 insulin Homo sapiens 32-39 6998996-5 1980 Fasting plasma insulin was higher (P < 0.001) in the pregnant group, and plasma insulin responses to the oral glucose tolerance test were higher (P < 0.05) in the pregnant, OC-35, and OC-50 groups compared to that in the control group. Glucose 113-120 insulin Homo sapiens 83-90 6106647-2 1980 To determine whether the insulin resistance of glucose-intolerant obese subjects can be accounted for by obesity alone, insulin-mediated glucose disposal was measured in 14 glucose-intolerant and 21 nondiabetic. Glucose 47-54 insulin Homo sapiens 25-32 6777226-7 1980 Incubation the cells in fresh media without serum and glucose for up to 24 h before assay enhances the cellular response to insulin. Glucose 54-61 insulin Homo sapiens 124-131 6999003-5 1980 Both alpha- and alpha- plus beta-blockade restored the insulin response to glucose but failed to correct the glucose intolerance. Glucose 75-82 insulin Homo sapiens 55-62 6795073-1 1981 Disease of coronary, cerebral, and peripheral arteries is associated with exaggerated insulin responses to oral glucose. Glucose 112-119 insulin Homo sapiens 86-93 6795073-2 1981 In three populations, high fasting or post-glucose insulin levels have a predictive value in the incidence of ischemic heart disease and in cardiac mortality. Glucose 43-50 insulin Homo sapiens 51-58 6795073-4 1981 Insulin, in small concentrations, has effects on arterial tissue including stimulation of smooth muscle cell proliferation and of glucose incorporation into lipid. Glucose 130-137 insulin Homo sapiens 0-7 7000417-4 1980 In confirmation of previous studies, patients with cirrhosis had high post-glucose serum insulin levels and were glucose intolerant (mean incremental glucose area 954 +/- 186 compared with 482 +/- 35 mmol 3 h-1 l-1 in controls; P < 0.05). Glucose 75-82 insulin Homo sapiens 89-96 7002688-1 1980 Insulin responses to intravenous fructose and glucose were measured in 15 patients with maturity-onset diabetes mellitus. Glucose 46-53 insulin Homo sapiens 0-7 7002688-2 1980 In eight patients given fructose first the insulin responses to fructose and glucose were similar. Glucose 77-84 insulin Homo sapiens 43-50 7002688-3 1980 In seven patients given glucose first the insulin response to subsequently infused fructose was significantly greater than to glucose. Glucose 24-31 insulin Homo sapiens 42-49 7002688-3 1980 In seven patients given glucose first the insulin response to subsequently infused fructose was significantly greater than to glucose. Glucose 126-133 insulin Homo sapiens 42-49 7002688-4 1980 Multiple regression analysis showed that the ratio of the fructose to glucose insulin response, assessed by area under the insulin serum concentration-time curve (F/G ratio) in individual patients, correlated most closely with prefructose infusion plasma glucose. Glucose 70-77 insulin Homo sapiens 78-85 7002688-5 1980 Similar analysis, applied to results in 27 normal subjects, showed that the most important determinant of the insulin response to fructose in this group also was the immediate prefructose infusion plasma glucose. Glucose 204-211 insulin Homo sapiens 110-117 7002689-4 1980 In a group of eight nonobese type II, non-insulin-dependent diabetics, glucose oxidation both in the basal rate and in response to the load was slightly decreased (13 and 14 g, respectively) and glucose storage decreased to 40 g. These results suggest that, in type I diabetics, complete insulin deficiency seriously impairs two major mechanisms regulating glucose homeostasis, i.e., glucose storage and oxidation, while, in type II diabetics, the remaining insulin secretion attentuates these disturbances. Glucose 71-78 insulin Homo sapiens 288-295 6776017-3 1980 These subjects also showed a subnormal rise in plasma insulin after oral glucose. Glucose 73-80 insulin Homo sapiens 54-61 7000652-4 1980 Blood glucose fell transiently in the controls, but not in the patients, during the Himsworth test (100 g glucose orally plus 0.05 U insulin per kg body weight intravenously). Glucose 6-13 insulin Homo sapiens 133-140 6772676-7 1980 These findings may explain the well known extrapancreatic effect of sulfonylurea agents to improve insulin-mediated tissue glucose metabolism. Glucose 123-130 insulin Homo sapiens 99-106 6997329-6 1980 Maximum prehepatic insulin production induced by a 100-g oral glucose tolerance test was 91 +/- 1.2 mU/70 kg.min, with a cumulative hormone secretion of 11.4 +/- 2.0 U over the 5 h of observation. Glucose 62-69 insulin Homo sapiens 19-26 6997331-2 1980 Those acromegalic subjects who were not diabetic exhibited excessive insulin responses to glucose and arginine stimulation. Glucose 90-97 insulin Homo sapiens 69-76 6997331-4 1980 Acromegalic patients who also had insulin-independent diabetes had a markedly reduced insulin response to glucose stimulation, while arginine-induced insulin secretion was relatively well preserved. Glucose 106-113 insulin Homo sapiens 34-41 6106149-2 1980 Neither of the beta-blocking agents accelerated the plasma glucose lowering effect of insulin. Glucose 59-66 insulin Homo sapiens 86-93 6997676-3 1980 During insulin infusion, euglycemia was maintained by variable glucose infusion. Glucose 63-70 insulin Homo sapiens 7-14 6997676-4 1980 When insulin was infused at 1 mU/kg/min the net splanchnic production of 14C-glucose was suppressed by 80% but glucagon infused at the end of the study resulted in substantial release of 14C-glucose from the liver suggesting marked accumulation of labeled glucose in glycogen. Glucose 77-84 insulin Homo sapiens 5-12 6997676-5 1980 When insulin was infused at 5 mU/kg/min the splanchnic release of 14C-glucose was also markedly suppressed but in contrast to the lower insulin dose very little labeled glucose accumulated in glycogen. Glucose 70-77 insulin Homo sapiens 5-12 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 110-117 insulin Homo sapiens 74-81 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 170-177 insulin Homo sapiens 74-81 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 170-177 insulin Homo sapiens 223-230 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 170-177 insulin Homo sapiens 223-230 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 170-177 insulin Homo sapiens 74-81 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 170-177 insulin Homo sapiens 223-230 6997676-7 1980 These data demonstrate that in 48-hr fasted man, (1) a small increment in insulin concentration will suppress glucose production but mostly by diverting the newly formed glucose into glycogen; (2) at higher concentrations, insulin will inhibit glucose production mainly by suppressing glucoeogenesis; and (3) this insulin-induced suppression of gluconeogenesis is due to an intrahepatic effect rather than an effect on the splanchnic extraction of alanine. Glucose 170-177 insulin Homo sapiens 223-230 6253986-0 1980 [Present-day concepts of the mechanism of the glucose induction of insulin secretion]. Glucose 46-53 insulin Homo sapiens 67-74 6105520-4 1980 Plasma glucose decrement with the two insulins was similar but human insulin was perhaps slightly more potent than porcine insulin at the low dose, and slightly less so at the high. Glucose 7-14 insulin Homo sapiens 38-45 7003563-0 1980 [Blood serum levels of C-peptide and insulin in diabetics and healthy persons after intravenous administration of glucagon and glucose]. Glucose 127-134 insulin Homo sapiens 23-32 7003563-0 1980 [Blood serum levels of C-peptide and insulin in diabetics and healthy persons after intravenous administration of glucagon and glucose]. Glucose 127-134 insulin Homo sapiens 37-44 7001830-2 1980 The insulin response to glucose and the peripheral sensitivity to insulin were evaluated by using the individual blood glucose and plasma insulin curves for parameter identification in a mathematical model. Glucose 24-31 insulin Homo sapiens 4-11 6251375-1 1980 Regulation of blood glucose levels by the liver is primarily achieved by the action of two peptide hormones, insulin and glucagon, which bind to specific receptors associated with the hepatocyte plasma membrane. Glucose 20-27 insulin Homo sapiens 109-116 6105438-6 1980 Early changes in blood-glucose after untreated hypoglycaemia seem to be primarily due to changes in free insulin rather than a response to antagonist hormones. Glucose 23-30 insulin Homo sapiens 105-112 6997078-0 1980 Actin filament formation in pancreatic beta-cells during glucose stimulation of insulin secretion. Glucose 57-64 insulin Homo sapiens 80-87 7001830-2 1980 The insulin response to glucose and the peripheral sensitivity to insulin were evaluated by using the individual blood glucose and plasma insulin curves for parameter identification in a mathematical model. Glucose 119-126 insulin Homo sapiens 4-11 6157364-0 1980 Reversal of insulin effects in fat cells may require energy for deactivation of glucose transport, but not deactivation of phosphodiesterase. Glucose 80-87 insulin Homo sapiens 12-19 7001830-2 1980 The insulin response to glucose and the peripheral sensitivity to insulin were evaluated by using the individual blood glucose and plasma insulin curves for parameter identification in a mathematical model. Glucose 119-126 insulin Homo sapiens 66-73 7001830-2 1980 The insulin response to glucose and the peripheral sensitivity to insulin were evaluated by using the individual blood glucose and plasma insulin curves for parameter identification in a mathematical model. Glucose 119-126 insulin Homo sapiens 66-73 7001830-3 1980 The mean glucose tolerance was significantly decreased in the patients, most likely due to decreased peripheral insulin sensitivity. Glucose 9-16 insulin Homo sapiens 112-119 6997162-4 1980 In a case of 9 months-old fetus, in which a small but significant increase of insulin release was observed with glucose (300 mg/ml). Glucose 112-119 insulin Homo sapiens 78-85 6998814-3 1980 After the first culture period, the basal insulin secretion rate of 5.2 microunits/islet/h seen with 2 mmol/l glucose was increased approx. Glucose 110-117 insulin Homo sapiens 42-49 6998814-5 1980 The islets retained the insulin-secretory response to 20 mmol/l glucose throughout the period of study. Glucose 64-71 insulin Homo sapiens 24-31 6998814-7 1980 Fructose however increased insulin release in the presence of 4 mmol/l glucose. Glucose 71-78 insulin Homo sapiens 27-34 6998814-8 1980 Caffeine elicited insulin release in the absence of glucose and enhanced insulin release in response to 10 mmol/l glucose. Glucose 114-121 insulin Homo sapiens 73-80 6998814-9 1980 Glucose-stimulated insulin release was inhibited by trifluoperazine (25 mumol/l). Glucose 0-7 insulin Homo sapiens 19-26 6995791-2 1980 Blood glucose concentration was well controlled throughout breakfast, lunch, and supper during the intraperitoneal insulin infusion as assessed by both the mean glucose concentration and the integrated "glucose exposure.# Plasma free insulin concentration demonstrated a meal-related rise and fall similar to that observed in normal, nondiabetic persons. Glucose 6-13 insulin Homo sapiens 115-122 6997162-6 1980 Caffeine (5 and 10 mM), a phosphodiesterase inhibitor, potentiated insulin release by itself and also induced the glucose-stimulated insulin release from the fetal pancreata in the dose related manner. Glucose 114-121 insulin Homo sapiens 133-140 6997162-10 1980 By contrast, glucose (100 and 300 mg/100 ml), tolbutamide (100 microgram/ml), L-arginine (10 mM) and caffeine (5 mM) caused a significant increase of insulin release from adult pancreata. Glucose 13-20 insulin Homo sapiens 150-157 6995791-2 1980 Blood glucose concentration was well controlled throughout breakfast, lunch, and supper during the intraperitoneal insulin infusion as assessed by both the mean glucose concentration and the integrated "glucose exposure.# Plasma free insulin concentration demonstrated a meal-related rise and fall similar to that observed in normal, nondiabetic persons. Glucose 6-13 insulin Homo sapiens 234-241 6995791-2 1980 Blood glucose concentration was well controlled throughout breakfast, lunch, and supper during the intraperitoneal insulin infusion as assessed by both the mean glucose concentration and the integrated "glucose exposure.# Plasma free insulin concentration demonstrated a meal-related rise and fall similar to that observed in normal, nondiabetic persons. Glucose 161-168 insulin Homo sapiens 115-122 6995792-1 1980 In the present study, a colchicine binding assay was used to measure changes in islet polymerized and depolymerized tubulin at intervals characterizing the biphasic pattern of glucose-induced insulin release i.e., 2.5, 5.5, 10.5, and 30.5 min. Glucose 176-183 insulin Homo sapiens 192-199 6994486-3 1980 During the oral glucose tolerance test, baseline C-peptide in five normal subjects was 1.5 +/- 0.8 ng/ml, and at 60 min was 5.6 +/- 1.6 ng/ml. Glucose 16-23 insulin Homo sapiens 49-58 6993262-0 1980 The insulin response to glucose infusion in gestational diabetes. Glucose 24-31 insulin Homo sapiens 4-11 6257458-6 1980 In contrast, patients in group A showed a marked reduction in their insulin response when bran was mixed with the glucose. Glucose 114-121 insulin Homo sapiens 68-75 6993263-0 1980 The insulin response to glucose infusion in normal human pregnancy. Glucose 24-31 insulin Homo sapiens 4-11 6993263-1 1980 To study insulin response and insulin sensitivity a glucose infusion test was devised. Glucose 52-59 insulin Homo sapiens 30-37 6993263-4 1980 Intravenous glucose tolerance in the non-pregnant women was observed to correlate with the insulin sensitivity index (r = 0.61, p less than 0.05) but in the pregnant women it correlated with the insulin response (r = 0.66, p less than 0.01). Glucose 12-19 insulin Homo sapiens 91-98 6993263-4 1980 Intravenous glucose tolerance in the non-pregnant women was observed to correlate with the insulin sensitivity index (r = 0.61, p less than 0.05) but in the pregnant women it correlated with the insulin response (r = 0.66, p less than 0.01). Glucose 12-19 insulin Homo sapiens 195-202 6993263-5 1980 These findings support the hypothesis that in the non-pregnant state intravenous glucose tolerance may be primarily related to insulin sensitivity while during pregnancy it may be related to the degree of compensatory hyperinsulinism. Glucose 81-88 insulin Homo sapiens 127-134 7471642-12 1980 Plasma concentrations of insulin ranged from very low to very high and appeared to depend on the concentrations of both glucose and alanine. Glucose 120-127 insulin Homo sapiens 25-32 6993264-3 1980 After the transplantation there was an increase in the fasting plasma C-peptide level, and B-cell stimulation with glucose or glucagon evoked a C-peptide response. Glucose 115-122 insulin Homo sapiens 144-153 7002536-8 1980 There ws an inverse relationship between the per cent decrease of plasma glucose concentration and the insulin secretion pattern revealed by the glucose infusion test. Glucose 73-80 insulin Homo sapiens 103-110 6108875-3 1980 Acute insulin response (mean change 3"-10") to glucose was almost completely suppressed by somatostatin (500 microgram/h) and glucose utilization was decreased. Glucose 47-54 insulin Homo sapiens 6-13 7002536-8 1980 There ws an inverse relationship between the per cent decrease of plasma glucose concentration and the insulin secretion pattern revealed by the glucose infusion test. Glucose 145-152 insulin Homo sapiens 103-110 6108875-5 1980 This last drug, when infused alone, increased both the acute insulin response to glucose and glucose tolerance. Glucose 81-88 insulin Homo sapiens 61-68 7006943-6 1980 The relationship between endogenous insulin secretion and glucose control was examined in those patients with diabetes for longer than 5 yr. Glucose 58-65 insulin Homo sapiens 36-43 6995249-0 1980 The stimulus-secretion coupling of glucose-induced insulin release. Glucose 35-42 insulin Homo sapiens 51-58 6993538-4 1980 The rate of glucose utilization by the whole body as well as by forearm muscle was dependent upon the insulin concentration. Glucose 12-19 insulin Homo sapiens 102-109 6995249-3 1980 Changes in extracellular pH affected insulin output from pancreatic islets stimulated with either glucose or alpha-ketoisocaproate. Glucose 98-105 insulin Homo sapiens 37-44 6995253-0 1980 A possible role for insulin in the prevention of glucose-induced paradoxical hyperkalemia during sodium depletion. Glucose 49-56 insulin Homo sapiens 20-27 6995478-2 1980 Both insulin and MSA produce acute metabolic responses (stimulation of glucose oxidation in isolated fat cells) as well as growth effects (stimulation of [(3)H]thymidine incorporation into DNA in cultured fibroblasts). Glucose 71-78 insulin Homo sapiens 5-12 6995478-7 1980 Blockade of insulin receptors with Fab fragments produced a 30-fold rightward shift in the dose response for stimulation of glucose oxidation by both insulin and MSA. Glucose 124-131 insulin Homo sapiens 12-19 6995478-7 1980 Blockade of insulin receptors with Fab fragments produced a 30-fold rightward shift in the dose response for stimulation of glucose oxidation by both insulin and MSA. Glucose 124-131 insulin Homo sapiens 150-157 6247604-3 1980 Intravenous infusion of verapamil, an organic antagonist of calcium transport into cells, produced a marked and significant inhibition of glucose-, glucagon- and sulfonylurea-induced increases in serum insulin in normal subjects. Glucose 138-145 insulin Homo sapiens 202-209 6779295-5 1980 Authors results suggest the presence of insulin in human erythrocytes and it release from erythrocytes during the first phase after glucose loading. Glucose 132-139 insulin Homo sapiens 40-47 6993499-0 1980 Release of insulin analogues in man, stimulated with glucose. Glucose 53-60 insulin Homo sapiens 11-18 7000239-4 1980 The fall in blood glucose values was proportional to the increased rate of insulin absorption (r = 0.30; p < 0.01). Glucose 18-25 insulin Homo sapiens 75-82 6998245-1 1980 Insulin secretion in response to an oral glucose challenge during acute hypercalcaemia was studied. Glucose 41-48 insulin Homo sapiens 0-7 6998245-7 1980 On the other hand, the total mean insulin concentration, expressed as the area under the 3 h glucose tolerance curve, and the insulin peak at 30 min were significantly increased during hypercalcaemia (P < 0.001). Glucose 93-100 insulin Homo sapiens 34-41 6994939-2 1980 While receiving DPH, insulin response to glucose was less than that in the control group, both in absolute terms and when related to the blood glucose level. Glucose 41-48 insulin Homo sapiens 21-28 6994939-2 1980 While receiving DPH, insulin response to glucose was less than that in the control group, both in absolute terms and when related to the blood glucose level. Glucose 143-150 insulin Homo sapiens 21-28 6994939-5 1980 Thus, the tendency of DPH to impair the insulin response to glucose has been confirmed in this controlled study. Glucose 60-67 insulin Homo sapiens 40-47 6997101-8 1980 No relationship was found between the degree of portosystemic shunting and fasting concentrations of glucagon and insulin, and the insulin response to glucose. Glucose 151-158 insulin Homo sapiens 131-138 6768635-6 1980 glucose, 56% augmentation of insulin release was noted (277 +/- 38 microU/ml, P less than 0.005). Glucose 0-7 insulin Homo sapiens 29-36 6989850-1 1980 The influence of insulin on transport and utilization of amino acids and glucose in purified human peripheral blood monocytes has been studied. Glucose 73-80 insulin Homo sapiens 17-24 6995516-5 1980 Plasma glucose and insulin peaks were both significantly lower after fructose ingestion as compared with glucose and sucrose. Glucose 105-112 insulin Homo sapiens 19-26 6997333-1 1980 UNLABELLED: To assess the mechanisms of the insulin resistance in human obesity, we have determined, using a modification of the euglycemic glucose clamp technique, the shape of the in vivo insulin-glucose disposal dose-response curves in 7 control and 13 obese human subjects. Glucose 140-147 insulin Homo sapiens 190-197 6997333-1 1980 UNLABELLED: To assess the mechanisms of the insulin resistance in human obesity, we have determined, using a modification of the euglycemic glucose clamp technique, the shape of the in vivo insulin-glucose disposal dose-response curves in 7 control and 13 obese human subjects. Glucose 198-205 insulin Homo sapiens 44-51 6997333-1 1980 UNLABELLED: To assess the mechanisms of the insulin resistance in human obesity, we have determined, using a modification of the euglycemic glucose clamp technique, the shape of the in vivo insulin-glucose disposal dose-response curves in 7 control and 13 obese human subjects. Glucose 198-205 insulin Homo sapiens 190-197 6997333-3 1980 The glucose disposal rate was decreased in all obese subjects compared with controls (101 +/- 16 vs. 186 +/- 16 mg/M2/min) during the 40 mU/M2/min insulin infusion. Glucose 4-11 insulin Homo sapiens 147-154 6997333-5 1980 In nine of the obese subjects, the dose-response curves were shifted to the right, and maximal glucose disposal rates (at a maximally effective insulin concentration) were markedly decreased, indicating both a receptor and a postreceptor defect. Glucose 95-102 insulin Homo sapiens 144-151 6997333-10 1980 Insulin binding to isolated adipocytes obtained from the obese subjects was decreased, and a highly significant inverse linear relationship was demonstrated between insulin binding and the serum insulin concentration required for halfmaximal stimulation of glucose disposal. Glucose 257-264 insulin Homo sapiens 165-172 6997333-10 1980 Insulin binding to isolated adipocytes obtained from the obese subjects was decreased, and a highly significant inverse linear relationship was demonstrated between insulin binding and the serum insulin concentration required for halfmaximal stimulation of glucose disposal. Glucose 257-264 insulin Homo sapiens 195-202 7000878-4 1980 The study demonstrated that protein deprivation results in decreased fasting blood glucose levels associated with diminution in fasting, and total insulin output when presented with a glucose load. Glucose 184-191 insulin Homo sapiens 147-154 6993794-6 1980 Evidence is presented which indicates that glucose and tolbutamide act via different mechanism to stimulate insulin release. Glucose 43-50 insulin Homo sapiens 108-115 6104347-5 1980 PGI2 repressed glucose-induced insulin release in some normoglycemic patients but in others it either increased it or did not affect it. Glucose 15-22 insulin Homo sapiens 31-38 6997872-4 1980 The relative potencies of the analogs in stimulating glucose oxidation by rat adipocytes decreased in the order porcine insulin > [LeuB24]insulin > [LeuB25]insulin. Glucose 53-60 insulin Homo sapiens 120-127 7010231-0 1980 Starvation potentiates glucose uptake by insulin-treated muscle. Glucose 23-30 insulin Homo sapiens 41-48 6997872-4 1980 The relative potencies of the analogs in stimulating glucose oxidation by rat adipocytes decreased in the order porcine insulin > [LeuB24]insulin > [LeuB25]insulin. Glucose 53-60 insulin Homo sapiens 141-148 6997872-4 1980 The relative potencies of the analogs in stimulating glucose oxidation by rat adipocytes decreased in the order porcine insulin > [LeuB24]insulin > [LeuB25]insulin. Glucose 53-60 insulin Homo sapiens 141-148 6994726-0 1980 Stimulation of glucose transport and oxidation in adipocytes by fatty acids: evidence for a regulatory role in the cellular response to insulin. Glucose 15-22 insulin Homo sapiens 136-143 6990786-9 1980 alpha-Adrenergic effects on glucose production and clearance may be mediated by inhibition of insulin secretion. Glucose 28-35 insulin Homo sapiens 94-101 6993916-3 1980 At the same time, an attempt was made to evaluate the evidence implicating abnormalities of insulin secretion and/or insulin action in the development of glucose intolerance with age. Glucose 154-161 insulin Homo sapiens 92-99 6993780-0 1980 Effects of standard oral glucose loading on the renin-angiotensin-aldosterone system and its relationship to circulating insulin. Glucose 25-32 insulin Homo sapiens 121-128 6769727-1 1980 Prostaglandin (PG) E2 stimulates glucose-induced insulin release from isolated rat pancreatic islets but inhibits acute insulin release to intravenous (i.v.) Glucose 33-40 insulin Homo sapiens 49-56 6991327-3 1980 When plasma glucose levels were maintained by means of a concomitant variable glucose infusion during tolbutamide, the insulin responses to both isoproterenol and arginine were enhanced (isoproterenol: delta AIR = +55 +/- 15 microU/ml, n = 6, p less than 0.001; arginine: delta AIR = +137 +/- 34 microU/ml, n = 8, p less than 0.001). Glucose 12-19 insulin Homo sapiens 119-126 6991327-3 1980 When plasma glucose levels were maintained by means of a concomitant variable glucose infusion during tolbutamide, the insulin responses to both isoproterenol and arginine were enhanced (isoproterenol: delta AIR = +55 +/- 15 microU/ml, n = 6, p less than 0.001; arginine: delta AIR = +137 +/- 34 microU/ml, n = 8, p less than 0.001). Glucose 78-85 insulin Homo sapiens 119-126 7000592-5 1980 After the glucose load, plasma insulin and glucose levels were positively correlated in rural people. Glucose 10-17 insulin Homo sapiens 31-38 7389568-7 1980 Some centers advocate insulin administration if dietary management does not consistently maintain the fasting plasma glucose below 105 mg/dl and the 2-h postprandial glucose below 120 mg/dl. Glucose 117-124 insulin Homo sapiens 22-29 7389568-7 1980 Some centers advocate insulin administration if dietary management does not consistently maintain the fasting plasma glucose below 105 mg/dl and the 2-h postprandial glucose below 120 mg/dl. Glucose 166-173 insulin Homo sapiens 22-29 7000592-6 1980 In contrast, for the urban group the relation best fitted a quadratic function, with decline in plasma insulin at high levels of glucose. Glucose 129-136 insulin Homo sapiens 103-110 6990184-3 1980 Our studies thus far indicate that a major effect of this drug is a potentiation of insulin action, which leads to an improvement in glucose utilization. Glucose 133-140 insulin Homo sapiens 84-91 6990184-4 1980 However, glipizide, in distinction from those sulfonylureas that have been examined previously, also causes a long-term increase in glucose-stimulated insulin secretion. Glucose 132-139 insulin Homo sapiens 151-158 6771756-0 1980 Evidence that insulin causes translocation of glucose transport activity to the plasma membrane from an intracellular storage site. Glucose 46-53 insulin Homo sapiens 14-21 6992089-1 1980 Maternal and fetal serum insulin response to glucose, leucine and leucine plus glucose was examined by infusions to normal pregnant women at term immediately before cesarean section. Glucose 45-52 insulin Homo sapiens 25-32 6992089-2 1980 The maternal infusion of glucose (50 g) for 30 or 60 minutes was associated with a marked hyperglycemia and with a rise in serum insulin in mother and fetus. Glucose 25-32 insulin Homo sapiens 129-136 6992089-3 1980 The fetal insulin response to the administration of glucose for 60 minutes was higher (p less than 0.01) than when the same dose was given for 30 minutes, while the blood glucose was lower (p less than 0.01). Glucose 52-59 insulin Homo sapiens 10-17 6992089-4 1980 The maternal infusion of a smaller dose of glucose (25 g) or leucine (15 g) for 60 minutes produced an increase in serum insulin only in the mothers. Glucose 43-50 insulin Homo sapiens 121-128 6996339-4 1980 After three days of biguanide treatment, a highly significant (p less than 0.001) increase in insulin sensitivity was noted in the group of biguanide responders, which was significantly (p less than 0.02) correlated with their previous blood glucose response to long-term biguanide therapy. Glucose 242-249 insulin Homo sapiens 94-101 6106613-1 1980 Previous studies have shown that autoantibodies against insulin receptors found in certain patients with severe insulin resistance stimulate glucose transport and metabolism in fat cell and muscle preparations. Glucose 141-148 insulin Homo sapiens 56-63 6106613-1 1980 Previous studies have shown that autoantibodies against insulin receptors found in certain patients with severe insulin resistance stimulate glucose transport and metabolism in fat cell and muscle preparations. Glucose 141-148 insulin Homo sapiens 112-119 6987121-0 1980 Glucose and insulin responses to oral glucose in overt non-insulin-dependent diabetics with and without the islet cell antibody. Glucose 38-45 insulin Homo sapiens 12-19 6998801-3 1980 Endogenous secretion of insulin was suppressed following administration of exogenous insulin and this persisted long after the blood glucose concentration had returned to normal. Glucose 133-140 insulin Homo sapiens 24-31 6998801-3 1980 Endogenous secretion of insulin was suppressed following administration of exogenous insulin and this persisted long after the blood glucose concentration had returned to normal. Glucose 133-140 insulin Homo sapiens 85-92 6990173-0 1980 Insulin secretion improves following dietary control of plasma glucose in severely hyperglycemic obese patients. Glucose 63-70 insulin Homo sapiens 0-7 6990173-3 1980 Insulin secretory responses to oral glucose and intravenous tolbutamide were assessed before and after the diet. Glucose 36-43 insulin Homo sapiens 0-7 6990173-5 1980 The insulin response to oral glucose was completely flat, although modest secretion was evoked by tolbutamide. Glucose 29-36 insulin Homo sapiens 4-11 6990173-7 1980 At restudy, improved oral glucose tolerance was accompanied by significant increases in the insulin secretory responses to both glucose and tolbutamide. Glucose 26-33 insulin Homo sapiens 92-99 6990173-7 1980 At restudy, improved oral glucose tolerance was accompanied by significant increases in the insulin secretory responses to both glucose and tolbutamide. Glucose 128-135 insulin Homo sapiens 92-99 6988747-3 1980 The insulin response to glucose infusion was increased 3.8 times in late pregnancy, whereas the suppression of glucagon was similar in late pregnancy and post partum. Glucose 24-31 insulin Homo sapiens 4-11 7020065-2 1980 Enzyme activities were negatively correlated to 0-40 min plasma insulin increments determined preoperatively by oral glucose tolerance tests. Glucose 117-124 insulin Homo sapiens 64-71 6994381-3 1980 The level of insulin and C-peptide after i. v. glucose-load was found higher in psoriasis-patients (hyperinsulinism). Glucose 47-54 insulin Homo sapiens 13-20 6994381-3 1980 The level of insulin and C-peptide after i. v. glucose-load was found higher in psoriasis-patients (hyperinsulinism). Glucose 47-54 insulin Homo sapiens 25-34 6988823-0 1980 [Early insulin response following intravenous glucose loading in acromegaly]. Glucose 46-53 insulin Homo sapiens 7-14 7004047-0 1980 Insulin response to an intravenous glucose load in potentially diabetic pregnant women. Glucose 35-42 insulin Homo sapiens 0-7 6446443-5 1980 However, a significant and persistent increased insulin level was noted in all subjects, after initiation of the hormone treatment, during the first thirty minutes of intravenous glucose load. Glucose 179-186 insulin Homo sapiens 48-55 6768605-10 1980 In diabetics on insulin this supra-normal level of insulin during physical activity decreases hepatic glucose production and increases peripheral glucose uptake with a resultant tendency to hypoglycemia. Glucose 102-109 insulin Homo sapiens 16-23 6768605-10 1980 In diabetics on insulin this supra-normal level of insulin during physical activity decreases hepatic glucose production and increases peripheral glucose uptake with a resultant tendency to hypoglycemia. Glucose 102-109 insulin Homo sapiens 51-58 6768605-13 1980 Physical activity can disturb the stability of diabetes when insulin levels are either too low or too high leading to high and low blood glucose responses respectively. Glucose 137-144 insulin Homo sapiens 61-68 6989697-2 1980 Cr also inhibited basal secretion of insulin in the presence of 5.5 mmol/l glucose and insulin secretion stimulated by 50 mmol/l K+ or 15 mmol/l L-leucine. Glucose 75-82 insulin Homo sapiens 37-44 6991320-0 1980 Insulin resistance in obesity as analyzed by the response of glucose kinetics to glucagon infusion. Glucose 61-68 insulin Homo sapiens 0-7 6991320-4 1980 By relating the changes in the rates of glucose production, utilization, and fractional disappearance to immunoreactive glucagon and insulin, it is possible to assess the body"s sensitivity to physiologic levels of these two hormones. Glucose 40-47 insulin Homo sapiens 133-140 6991320-7 1980 They also showed that insulin was much less effective in promoting glucose utilization in the obese persons than it was in the normal ones. Glucose 67-74 insulin Homo sapiens 22-29 6991320-10 1980 Thus, it is suggested that, in the presence of insulin resistance, the responsiveness of B-cells will determine whether the glucose tolerance will be nore homeostasis in other conditions associated with glucose intolerance, the metabolic basis of which is undefined. Glucose 124-131 insulin Homo sapiens 47-54 6991326-0 1980 Nonaggregating insulin solutions for long-term glucose control in experimental and human diabetes. Glucose 47-54 insulin Homo sapiens 15-22 6993053-3 1980 On the other hand, a dose-dependent acute suppressive effect of bromocriptine on plasma IRI response to oral glucose was observed, suggesting a direct effect of bromocriptine on the release of insulin from beta cells. Glucose 109-116 insulin Homo sapiens 193-200 6993138-1 1980 Several insulin models are examined as to their responses to various insulin inputs and glucose utilization and production control. Glucose 88-95 insulin Homo sapiens 8-15 6993138-2 1980 It is shown that the action of insulin on glucose utilization correlates best with model compartments having a 30--50-min delay compared with plasma, whereas glucose production control is rapid. Glucose 42-49 insulin Homo sapiens 31-38 6993141-5 1980 the delayed entry of insulin into the circulation in achieving normal glucose levels and patterns. Glucose 70-77 insulin Homo sapiens 21-28 6993142-0 1980 Glucagon responses to hypoglycemia in type I diabetic men after 24-hour glucoregulation by glucose-controlled insulin infusion. Glucose 91-98 insulin Homo sapiens 110-117 6993145-1 1980 A method of insulin therapy that appears to achieve better control of diabetes than present conventional methods is the use of insulin infusion devices--either glucose-controlled feedback (closed-loop) systems or the preprogrammed (open-loop) infusion pump. Glucose 160-167 insulin Homo sapiens 12-19 6993145-1 1980 A method of insulin therapy that appears to achieve better control of diabetes than present conventional methods is the use of insulin infusion devices--either glucose-controlled feedback (closed-loop) systems or the preprogrammed (open-loop) infusion pump. Glucose 160-167 insulin Homo sapiens 127-134 6993145-3 1980 Its use in insulin-dependent diabetic patients to provide either intravenous doses or a continuous subcutaneous insulin infusion resulted in significant reductions in blood glucose levels, glycemic excursions and 24-h glucose excretion. Glucose 173-180 insulin Homo sapiens 11-18 6993145-3 1980 Its use in insulin-dependent diabetic patients to provide either intravenous doses or a continuous subcutaneous insulin infusion resulted in significant reductions in blood glucose levels, glycemic excursions and 24-h glucose excretion. Glucose 173-180 insulin Homo sapiens 112-119 6993153-1 1980 The application of "closed-loop" glucose-controlled insulin infusion in metabolic research and in the management of diabetic patients in acute emergency situations has stimulated the development of portable insulin infusion devices intended for the long-term stabilization of glucose levels. Glucose 33-40 insulin Homo sapiens 52-59 6993153-1 1980 The application of "closed-loop" glucose-controlled insulin infusion in metabolic research and in the management of diabetic patients in acute emergency situations has stimulated the development of portable insulin infusion devices intended for the long-term stabilization of glucose levels. Glucose 33-40 insulin Homo sapiens 207-214 6993153-1 1980 The application of "closed-loop" glucose-controlled insulin infusion in metabolic research and in the management of diabetic patients in acute emergency situations has stimulated the development of portable insulin infusion devices intended for the long-term stabilization of glucose levels. Glucose 276-283 insulin Homo sapiens 52-59 6993153-1 1980 The application of "closed-loop" glucose-controlled insulin infusion in metabolic research and in the management of diabetic patients in acute emergency situations has stimulated the development of portable insulin infusion devices intended for the long-term stabilization of glucose levels. Glucose 276-283 insulin Homo sapiens 207-214 6987257-4 1980 The results show that the glucose response to insulin; hypoglycemic symptoms; and the adrenaline, noradrenaline, and cortisol responses to hypoglycemia were not influenced by ketone infusion at any dose rate. Glucose 26-33 insulin Homo sapiens 46-53 6245691-10 1980 Insulin, at concentrations (10(-6) M) that enhance glucose uptake into intact adipocytes, did not affect the fluidity of ghosts suspended in buffers with or without Ca2+. Glucose 51-58 insulin Homo sapiens 0-7 6243677-6 1980 Under these conditions of euglycemia, the amount of glucose metabolized equals the glucose infusion rate and is a measure of tissue sensitivity to insulin. Glucose 52-59 insulin Homo sapiens 147-154 6243677-8 1980 During insulin administration alone, glucose metabolism averaged 5.49+/-0.58 mg/kg.min. Glucose 37-44 insulin Homo sapiens 7-14 6243677-9 1980 When epinephrine was infused with insulin, glucose metabolism fell by 41% to 3.26 mg/kg.min (P < 0.001). Glucose 43-50 insulin Homo sapiens 34-41 6243677-10 1980 After insulin alone, hepatic glucose production declined by 92% to 0.16+/-0.08 mg/kg.min. Glucose 29-36 insulin Homo sapiens 6-13 6987259-1 1980 To study the effect of physiological increments in plasma secretin concentrations on basal and glucose-stimulated insulin release, bolus iv glucose injections (5 g) were given to normal weight volunteers (less than 108% ideal BW) before, during, and 30 min after a secretin infusion at a rate of 0.125 U/kg.h, raising mean plasma immunoreactive secretin to 35.5 +/- 8.3 pg/ml. Glucose 95-102 insulin Homo sapiens 114-121 6987259-2 1980 Acute insulin responses to glucose were unaffected during or after the secretin infusion. Glucose 27-34 insulin Homo sapiens 6-13 6243728-2 1980 Compared with normal subjects, patients with insulinoma had significantly lower glucose and higher insulin levels during both the fed and the fasted states. Glucose 80-87 insulin Homo sapiens 45-52 7018518-2 1980 Effects of an infusion of calcium on insulin and glucagon secretion induced by intravenous administration of glucose]. Glucose 109-116 insulin Homo sapiens 37-44 6986776-0 1980 Effects of exogenous insulin on excursions and diurnal rhythm of plasma glucose in pregnant diabetic patients with and without residual beta-cell function. Glucose 72-79 insulin Homo sapiens 21-28 6990147-0 1980 Interaction of a newly isolated intestinal polypeptide (PHI) with glucose and arginine to effect the secretion of insulin and glucagon. Glucose 66-73 insulin Homo sapiens 114-121 6103627-6 1980 In the euthyroid state mean serum insulin concentrations after the glucose load were not significantly different from the values found when the patients were hyperthyroid. Glucose 67-74 insulin Homo sapiens 34-41 6987752-7 1980 As serum insulin but not glucose also varied cross-sectionally in Blacks with increasing standards of living, there is further mathematical evidence that serum glucose concentrations are more directly under genetic control than are insulin concentrations. Glucose 160-167 insulin Homo sapiens 9-16 6986766-9 1980 We conclude that normalization or near normalization of blood glucose levels can be achieved with a portable subcutaneous insulin infusion system when continuously used to treat patients with juvenile-onset, insulin-dependent diabetes outside the hospital for three to eight months. Glucose 62-69 insulin Homo sapiens 122-129 6245892-2 1980 A significant positive correlation existed between the maximal increase in plasma cAMP and the maximal decrease in plasma glucose in normals during insulin-induced hypoglycaemia. Glucose 122-129 insulin Homo sapiens 148-155 6986299-3 1980 The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. Glucose 59-66 insulin Homo sapiens 16-23 6989758-6 1980 The insulin concentration in the portal vein blood after a glucose load shows significant variations to the insulin concentration in the cubital vein blood. Glucose 59-66 insulin Homo sapiens 4-11 6986299-4 1980 Intravenous infusion of glucose had a slight but significant inhibitory effect on fat-stimulated increase of IR-GIP, which cannot be related to endogenous insulin release in these insulin-deficient diabetics. Glucose 24-31 insulin Homo sapiens 155-162 6986299-5 1980 It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. Glucose 53-60 insulin Homo sapiens 24-31 6986299-5 1980 It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. Glucose 190-197 insulin Homo sapiens 24-31 7007192-5 1980 During pulsatile perfusion there was a significant increase in insulin which, however, was clearly diminished in relation to glucose levels. Glucose 125-132 insulin Homo sapiens 63-70 7007192-7 1980 The secondary postoperative increase in insulin can be accounted for by intravenous administration of glucose and, particularly, after pulsatile perfusion, indicates an almost completely normal response of pancreatic beta-cells. Glucose 102-109 insulin Homo sapiens 40-47 6989758-6 1980 The insulin concentration in the portal vein blood after a glucose load shows significant variations to the insulin concentration in the cubital vein blood. Glucose 59-66 insulin Homo sapiens 108-115 7189510-2 1980 After glucose monitoring, the maschine steers an insulin infusion pump by means of adequate algorithms to obtain a glucose balance in labile diabetic inpatients. Glucose 115-122 insulin Homo sapiens 49-56 6987601-0 1980 Effects of a sustained insulin infusion upon glucose uptake and oxygenation of the ovine fetus. Glucose 45-52 insulin Homo sapiens 23-30 6247781-3 1980 The nature of IAP-action is characterized by enhancement of insulin secretory response to glucose and other stimulants. Glucose 90-97 insulin Homo sapiens 60-67 6988933-1 1980 The effect of an ordinary lipid-lowering diet on serum insulin response to oral glucose load was investigated in a randomized, primary preventive trial of the Oslo Study of coronary heart disease in healthy high risk middle aged men. Glucose 80-87 insulin Homo sapiens 55-62 6988933-3 1980 Increased levels of serum insulin and elevated insulin response to oral glucose load has been shown in earlier studies to be associated with increased susceptibility for atherosclerotic diseases. Glucose 72-79 insulin Homo sapiens 47-54 6986529-0 1980 Portal and peripheral vein concentrations of insulin after glucose and arginine infusions in morbidly obese subjects. Glucose 59-66 insulin Homo sapiens 45-52 7002168-4 1980 The C-peptide/IRI ratio, which was lower than normal both during fasting and after glucose load, presented the lowest value in patients with ascites. Glucose 83-90 insulin Homo sapiens 4-13 6998243-4 1980 The main point consists in an attempt to maintain a normal blood glucose level by administering increasing doses of insulin. Glucose 65-72 insulin Homo sapiens 116-123 7001839-4 1980 The ratio of (portal insulin area -- hepatic insulin area) /portal insulin area after glucose injection exceeded that after glipizide injection (p < 0.05). Glucose 86-93 insulin Homo sapiens 21-28 7001839-5 1980 This finding indicates a greater fractional hepatic extraction of insulin after glucose than after glipizide. Glucose 80-87 insulin Homo sapiens 66-73 7001839-9 1980 This time less insulin was taken up by the forearm tissues after the glucose load and in one subject insulin in venous blood samples exceeded that in corresponding arterial blood samples. Glucose 69-76 insulin Homo sapiens 15-22 7001839-10 1980 It is concluded that glipizide when given before a glucose load affects the uptake of insulin by peripheral tissues during the glucose load. Glucose 127-134 insulin Homo sapiens 86-93 6999837-0 1980 C-peptide and proinsulin after oral glucose. Glucose 36-43 insulin Homo sapiens 14-24 7001862-8 1980 Lower plasma insulin levels in response to glucose were also found in these patients on alprenolol than on metoprolol. Glucose 43-50 insulin Homo sapiens 13-20 7004095-1 1980 The intravenous glucose tolerance and glucose-stimulated early insulin response (EIR) were studied in late pregnancy and post partum in a reference (R) group of 9 women and in 18 women with latent gestational diabetes (LD), defined as a k-value of < 0.66/h and a normal fasting blood glucose concentration. Glucose 38-45 insulin Homo sapiens 63-70 7004095-1 1980 The intravenous glucose tolerance and glucose-stimulated early insulin response (EIR) were studied in late pregnancy and post partum in a reference (R) group of 9 women and in 18 women with latent gestational diabetes (LD), defined as a k-value of < 0.66/h and a normal fasting blood glucose concentration. Glucose 38-45 insulin Homo sapiens 63-70 7008508-11 1980 insulin infusion with preprogramed pump devices resulted in blood glucose fluctuations comparable with those during Biostator treatment. Glucose 66-73 insulin Homo sapiens 0-7 6938114-2 1980 Thus, in well-controlled insulin-treated patients with mild hyperglycaemia and no or minimal ketonemia the utilization of FFA, blood glucose and glycogen by working muscle is similar to that of healthy subjects, and exercise is accompanied by a fall in blood glucose levels. Glucose 133-140 insulin Homo sapiens 25-32 7010904-9 1980 Insulin mediated glucose uptake (as measured by insulin clamp technique) also rose by 30% after physical training (p less than 0.01). Glucose 17-24 insulin Homo sapiens 0-7 7010904-9 1980 Insulin mediated glucose uptake (as measured by insulin clamp technique) also rose by 30% after physical training (p less than 0.01). Glucose 17-24 insulin Homo sapiens 48-55 7010905-3 1980 Residual endogenous insulin secretion, governed by the blood glucose values, serves as a modulator. Glucose 61-68 insulin Homo sapiens 20-27 7025551-0 1980 The blood-brain barrier: an overview with special reference to insulin effects on glucose transport. Glucose 82-89 insulin Homo sapiens 63-70 6246779-0 1980 A role for prostaglandins as mediators of alpha-adrenergic inhibition of the acute insulin response to glucose. Glucose 103-110 insulin Homo sapiens 83-90 6769309-0 1980 Improvement of defective insulin responses to glucose, arginine, and beta-adrenergic stimulation in diabetics by sodium salicylate. Glucose 46-53 insulin Homo sapiens 25-32 7350796-0 1980 Feasibility of maintaining normal glucose profiles in insulin-dependent pregnant diabetic women. Glucose 34-41 insulin Homo sapiens 54-61 6444267-4 1980 These results indicate that changing the insulin injection site from the leg to the abdomen or arm accelerates the absorption of insulin and diminishes the postprandial rise in plasma glucose. Glucose 184-191 insulin Homo sapiens 41-48 6778449-7 1980 There is a significant correlation between blood glucose and insulin levels (r = 0.62 p < 0.001). Glucose 49-56 insulin Homo sapiens 61-68 6245006-1 1980 The models proposed for the means whereby the B-cell recognises glucose and related compounds as signals for insulin release and biosynthesis are discussed. Glucose 64-71 insulin Homo sapiens 109-116 6766414-2 1980 Release of insulin into the culture medium correlated with lowering of fasting blood glucose in the diabetic recipient. Glucose 85-92 insulin Homo sapiens 11-18 6773725-2 1980 Plasma glucose reached 250 mg/dl in 3.4 +/- 0.4 h with the high-dose insulin group compared with 5.4 +/- 0.5 h with the low-dose insulin group (P < 0.01). Glucose 7-14 insulin Homo sapiens 69-76 6986310-3 1980 Insulin biosynthesis was stimulated by glucose; however, the incorporation of 3H-L-leucine into proinsulin was surprisingly high (52% after 3 h) vs. insulin (48%), which suggests a possible block in the conversion of proinsulin to insulin. Glucose 39-46 insulin Homo sapiens 0-7 6986310-4 1980 Insulin secretion was stimulated during perifusion with 19.3 mM glucose (1.6 X prestimulation level), 1.5 microM glucagon (2.4), 5mM leucine (2.4), 10 mM arginine (2.7), and 10 mM theophylline (10.0). Glucose 64-71 insulin Homo sapiens 0-7 6986310-6 1980 After 12 days there was a 3.4-fold increase in insulin secretion in the presence of 22 mM glucose compared with 5.5 mM glucose, and the explant insulin content rose in the presence of high glucose levels by 89%. Glucose 90-97 insulin Homo sapiens 47-54 6988263-1 1980 The changes in insulin response to a 100 g glucose tolerance test after treatment by diet, sulphonylurea and insulin were compared in non-ketotic diabetic patients who had fasting blood glucose concentrations higher than 160 mg/100 ml. Glucose 43-50 insulin Homo sapiens 15-22 6988263-4 1980 The degree of improvement of insulin response was similar between different treatment groups, when their fasting blood glucose decreased below 140 mg/100 ml and the glucose tolerance curves were improved to a similar extent. Glucose 119-126 insulin Homo sapiens 29-36 6988263-6 1980 The data suggest that the poor insulin response in overt diabetes results not only from an inherent insensitivity of B-cells to glucose but also from the metabolic derangement of diabetes. Glucose 128-135 insulin Homo sapiens 31-38 6988265-7 1980 Early and late insulin release (summed increases over basal for 2--10 min and 10--60 min) during intravenous glucose tolerance testing increased during glipizide, but not during tolbutamide therapy. Glucose 109-116 insulin Homo sapiens 15-22 6988265-8 1980 Post prandial insulin increments over basal during an oral glucose tolerance test also increased during glipizide, but not tolbutamide therapy. Glucose 59-66 insulin Homo sapiens 14-21 6988280-1 1980 Insulin secretion rates after glucose loading were calculated from peripheral venous IRI concentrations considering half life and distribution space of exogenous insulin in normal men and dogs. Glucose 30-37 insulin Homo sapiens 0-7 6988280-2 1980 The coefficients of multiple linear regression analysis between insulin secretion rates and plasma glucose (level and order and rate of change) were used as algorithm parameters in glucose-controlled insulin infusions. Glucose 99-106 insulin Homo sapiens 200-207 6988280-2 1980 The coefficients of multiple linear regression analysis between insulin secretion rates and plasma glucose (level and order and rate of change) were used as algorithm parameters in glucose-controlled insulin infusions. Glucose 181-188 insulin Homo sapiens 64-71 6988280-2 1980 The coefficients of multiple linear regression analysis between insulin secretion rates and plasma glucose (level and order and rate of change) were used as algorithm parameters in glucose-controlled insulin infusions. Glucose 181-188 insulin Homo sapiens 200-207 6991318-2 1980 Mean hourly insulin infusion rates, required to maintain plasma glucose concentrations at approximately 100 mg/dl, were remarkably stable from 2400 h to 0600 h; however, a twofold to threefold increase in insulin requirements was observed in each subject between 0600 h and 0900 h. This increase in amount of basal insulin required was not associated with increases in plasma glucagon or growth hormone concentrations, but occurred simultaneously with normal diurnal increases in plasma cortisol. Glucose 64-71 insulin Homo sapiens 12-19 6996966-8 1980 Although basal insulin levels were similar in the three groups, there were striking intergroup differences in the insulin responses to glucose. Glucose 135-142 insulin Homo sapiens 114-121 6996966-11 1980 The data suggest that these Aborigines have an abnormally high insulin response to glucose, which is ameliorated, but not normalized, by reverting to their traditional life-style. Glucose 83-90 insulin Homo sapiens 63-70 6996973-1 1980 Patients have been shown to be able to monitor their blood glucose and administer insulin to optimize and normalize blood glucose levels. Glucose 122-129 insulin Homo sapiens 82-89 6996973-7 1980 Subsequently, insulin is adjusted so that patients are given an insulin regimen that will coordinate peaks of insulin with peaks of blood glucose associated with a meal pattern. Glucose 138-145 insulin Homo sapiens 14-21 6996973-7 1980 Subsequently, insulin is adjusted so that patients are given an insulin regimen that will coordinate peaks of insulin with peaks of blood glucose associated with a meal pattern. Glucose 138-145 insulin Homo sapiens 64-71 6996973-7 1980 Subsequently, insulin is adjusted so that patients are given an insulin regimen that will coordinate peaks of insulin with peaks of blood glucose associated with a meal pattern. Glucose 138-145 insulin Homo sapiens 64-71 6996974-3 1980 However, self-measurement of blood glucose as a guide to insulin taken before each meal and at bedtime can, in selected patients, increase the frequency of normal glucose levels without undue hypoglycemia. Glucose 35-42 insulin Homo sapiens 57-64 6996974-3 1980 However, self-measurement of blood glucose as a guide to insulin taken before each meal and at bedtime can, in selected patients, increase the frequency of normal glucose levels without undue hypoglycemia. Glucose 163-170 insulin Homo sapiens 57-64 6996975-1 1980 Normalization of plasma glucose concentration with subcutaneous injections of insulin has been difficult. Glucose 24-31 insulin Homo sapiens 78-85 6996975-2 1980 With intravenous insulin delivery, normalization of plasma glucose concentration in adult-onset diabetic patients has been achieved when their plasma insulin concentration was normalized. Glucose 59-66 insulin Homo sapiens 17-24 6996975-2 1980 With intravenous insulin delivery, normalization of plasma glucose concentration in adult-onset diabetic patients has been achieved when their plasma insulin concentration was normalized. Glucose 59-66 insulin Homo sapiens 150-157 6996975-7 1980 When plasma insulin profiles were normalized in insulin-dependent diabetic subjects lacking endogenous insulin secretion, an improvement in meal-related glucose excursions was observed. Glucose 153-160 insulin Homo sapiens 12-19 6996975-7 1980 When plasma insulin profiles were normalized in insulin-dependent diabetic subjects lacking endogenous insulin secretion, an improvement in meal-related glucose excursions was observed. Glucose 153-160 insulin Homo sapiens 48-55 7408607-2 1980 The patients learn through home glucose monitoring how their blood sugar levels vary with changes in diet, exercise, and insulin. Glucose 32-39 insulin Homo sapiens 121-128 6989593-0 1980 Changes in carbohydrate tolerance and early insulin response to glucose in potential diabetics: a follow-up study of 2--4 years. Glucose 64-71 insulin Homo sapiens 44-51 6989594-6 1980 Two 30-minute-periods of insulin infusion (8 and 16 mU/kg, primed by a start injection of 1 and 2 mU/kg, respectively) provoked a decrease of plasma glucose and FFA concentrations by 35 +/- 12.5% and 55 +/- 30.2%, respectively. Glucose 149-156 insulin Homo sapiens 25-32 6998696-1 1980 It was attempted to evaluate the usual parameters of the glucose-infusion-test (GIT) from the biocybernetic point of view by considering the blood sugar and insulin-behaviour as a dynamic characteristic according to suddenly elevated glucose level. Glucose 57-64 insulin Homo sapiens 157-164 6998696-1 1980 It was attempted to evaluate the usual parameters of the glucose-infusion-test (GIT) from the biocybernetic point of view by considering the blood sugar and insulin-behaviour as a dynamic characteristic according to suddenly elevated glucose level. Glucose 234-241 insulin Homo sapiens 157-164 6998696-3 1980 The usual parameters of the glucose-infusion-test for the blood sugar and insulin behaviour contain essential biocybernetically important informations, certain restrictions and additional suggestions are given. Glucose 28-35 insulin Homo sapiens 74-81 7191804-9 1980 The post-exercise insulin increase was reduced during the course corresponding to a reduction in blood glucose levels. Glucose 103-110 insulin Homo sapiens 18-25 7439809-8 1980 There was a positive correlation between plasma insulin values during oral glucose tolerance test and serum and VLDL triglycerides when E2V was administered. Glucose 75-82 insulin Homo sapiens 48-55 6161071-0 1980 Role of cyclic AMP in insulin release evoked by glucose and other secretagogues. Glucose 48-55 insulin Homo sapiens 22-29 6161071-1 1980 A close coupling in time-course and dose-dependency exists between cyclic AMP and insulin responses to glucose as tested in isolated islets of Langerhans from the rate and other species. Glucose 103-110 insulin Homo sapiens 82-89 6161071-4 1980 "Classical" cyclic AMP-raising agents such as the methylxanthines are unable to induce substantial insulin release in the absence of glucose; however, short-term previous exposure to 27.7 mM glucose transforms 3-isobutyl-1-methylxanthine into a potent insulin-releasing agent. Glucose 191-198 insulin Homo sapiens 99-106 6161071-4 1980 "Classical" cyclic AMP-raising agents such as the methylxanthines are unable to induce substantial insulin release in the absence of glucose; however, short-term previous exposure to 27.7 mM glucose transforms 3-isobutyl-1-methylxanthine into a potent insulin-releasing agent. Glucose 191-198 insulin Homo sapiens 252-259 7005057-2 1980 The secretion of insulin in response to glucose (20mM) plus isobutyl-methylxanthine (0.5mM) was associated with a calcium dependent increase in the turnover of the major classes of phospholipids and an increase production of 1:2 diacylglycerol and triacylglycerol. Glucose 40-47 insulin Homo sapiens 17-24 6993387-3 1980 Plasma-insulin concentrations decreased during oral glucose-tolerance test (OGTT), an effect which was more clearly seen after atropine administration. Glucose 52-59 insulin Homo sapiens 7-14 6998881-7 1980 Two hypotheses have been proposed to explain the improvement in CHO utilization during exercise after a glucose load: (1) The fall in FFA is sufficient to suppress the inhibition of CHO uptake and oxidation; (2) The insulin resistance decreases during exercise. Glucose 104-111 insulin Homo sapiens 216-223 6988486-2 1980 A simple method is described for regulating these insulin requirements during infusions of 50% glucose based on beside monitoring of blood glucose. Glucose 95-102 insulin Homo sapiens 50-57 6988486-2 1980 A simple method is described for regulating these insulin requirements during infusions of 50% glucose based on beside monitoring of blood glucose. Glucose 139-146 insulin Homo sapiens 50-57 6255018-2 1980 Isolated hepatocytes also showed a diminution of glucagon stimulated glucose output in response to insulin, while adipocytes responded with increased rates of glucose oxidation, lipid synthesis and decreased glycerol output. Glucose 69-76 insulin Homo sapiens 99-106 7350174-4 1980 The PCOD group had significantly higher levels of glucose at 1, 2, and 3 h, with similar significant increases in plasma insulin levels at 0, 2, and 3 h. A significant correlation was found between plasma insulin response areas and plasma testosterone (P less than 0.001) in the control and PCOD patients. Glucose 50-57 insulin Homo sapiens 205-212 7373008-0 1980 Response of insulin receptors to oral glucose in normal subjects. Glucose 38-45 insulin Homo sapiens 12-19 6765974-2 1980 An iv bolus of insulin administered prior to low-dose insulin infusion accelerated the decline of plasma glucose concentration during the first hour of treatment, but differences in decline of mean plasma glucose concentration were not apparent thereafter. Glucose 105-112 insulin Homo sapiens 15-22 6765974-2 1980 An iv bolus of insulin administered prior to low-dose insulin infusion accelerated the decline of plasma glucose concentration during the first hour of treatment, but differences in decline of mean plasma glucose concentration were not apparent thereafter. Glucose 105-112 insulin Homo sapiens 54-61 6765974-2 1980 An iv bolus of insulin administered prior to low-dose insulin infusion accelerated the decline of plasma glucose concentration during the first hour of treatment, but differences in decline of mean plasma glucose concentration were not apparent thereafter. Glucose 205-212 insulin Homo sapiens 15-22 7005567-6 1980 Therapeutically great differences resulted in reaching and equilibrium of serum glucose in the pancreas resected insulin-dependent patients, because they were dependent on carbohydrates for energy. Glucose 80-87 insulin Homo sapiens 113-120 7351877-8 1980 These results indicate that fructose, sorbitol, and xylitol are oxidized at a higher rate than glucose during suppression of endogenous insulin secretion, without any significant rise in glycemia. Glucose 95-102 insulin Homo sapiens 136-143 6767217-1 1980 Four hyperglycemia very low birthweight (VLBW) infants were given a constant infusion of insulin with parenteral alimentation in order to improve glucose tolerance. Glucose 146-153 insulin Homo sapiens 89-96 6767217-4 1980 It is suggested that insulin "resistance", instead of insulin deficiency, may be responsible for glucose intolerance in some infants. Glucose 97-104 insulin Homo sapiens 21-28 6770336-3 1980 Insulin secretion in response to glucose, potassium and tolbutamide was lower in a Sr2+ than in a Ca2+ medium, even at the optimum concentration of 2.5 mmol/l. Glucose 33-40 insulin Homo sapiens 0-7 6987642-4 1980 The mechanisms of disturbances in the early insulin response to glucose and diagnostic significance of the tests under study are discussed. Glucose 64-71 insulin Homo sapiens 44-51 7050993-0 1980 Intraperitoneal insulin for control of glucose level in insulin dependent diabetic patients treated by CAPD. Glucose 39-46 insulin Homo sapiens 16-23 6988899-0 1980 [The insulin level in the glucose tolerance test in patients with obesity and varying carbohydrate tolerance (author"s transl)]. Glucose 26-33 insulin Homo sapiens 5-12 6990057-0 1980 [Analysis of insulin secretion pattern during glucose tolerance test (author"s transl)]. Glucose 46-53 insulin Homo sapiens 13-20 7020029-0 1980 [Insulin secretion after oral glucose in descendants of coronary patients]. Glucose 30-37 insulin Homo sapiens 1-8 7015475-3 1980 It was found that the correlation between insulin/glucose and plasma GIP concentrations during an OGTT can be expressed by the equation: log y = log a + bx, where y = [insulin]/[glucose], and x is the plasma GIP concentration. Glucose 50-57 insulin Homo sapiens 42-49 7015475-3 1980 It was found that the correlation between insulin/glucose and plasma GIP concentrations during an OGTT can be expressed by the equation: log y = log a + bx, where y = [insulin]/[glucose], and x is the plasma GIP concentration. Glucose 50-57 insulin Homo sapiens 168-175 7015475-3 1980 It was found that the correlation between insulin/glucose and plasma GIP concentrations during an OGTT can be expressed by the equation: log y = log a + bx, where y = [insulin]/[glucose], and x is the plasma GIP concentration. Glucose 178-185 insulin Homo sapiens 42-49 7015475-4 1980 This empirical correlation between [insulin]/[glucose] and [GIP] reduces the plasma parameters measured during OGTT to a simple relationship. Glucose 46-53 insulin Homo sapiens 36-43 7015475-5 1980 It may prove valuable in the analysis of differences in the relationship glucose-insulin-GIP between groups of subjects and in the description of alterations in glucose homeostasis longitudinally in individuals undergoing therapy. Glucose 73-80 insulin Homo sapiens 81-88 6773256-0 1980 Studies on synergism between glucose and amino acids with respect to insulin release in vitro. Glucose 29-36 insulin Homo sapiens 69-76 6773256-1 1980 The mutual enhancement of the effect of insulin release by glucose and amino acids is not clearly understood. Glucose 59-66 insulin Homo sapiens 40-47 6773256-2 1980 Present in vitro studies with isolated rat islets were undertaken to elaborate the role of amino acids on insulin release, particularly their interaction with glucose as well as among each other, which has been reported to lead to synergism in the human subjects. Glucose 159-166 insulin Homo sapiens 106-113 505005-0 1979 A glucose-controlled insulin-delivery system: semisynthetic insulin bound to lectin. Glucose 2-9 insulin Homo sapiens 21-28 505005-3 1979 Glucose regulation of exogenous insulin delivery could have important applications in the therapy of diabetes mellitus. Glucose 0-7 insulin Homo sapiens 32-39 517648-8 1979 It is suggested that glucose is more important than insulin in modulating the fractional hepatic uptake of insulin. Glucose 21-28 insulin Homo sapiens 107-114 393434-5 1979 A significant correlation was found between the fasting triglyceride level and the sum of insulin values determined during the oral glucose tolerance test in healthy Lp(a-) but not in Lp(a+) individuals. Glucose 132-139 insulin Homo sapiens 90-97 394885-1 1979 We have investigated the use of a glucose-controlled insulin infusion system, or artificial beta cell. Glucose 34-41 insulin Homo sapiens 53-60 398297-4 1979 After two days subcutaneous adipose tissue was removed from the abdominal wall by needle biopsy for characterization of insulin-stimulated (1-14C) glucose incorporation into triglycerides. Glucose 147-154 insulin Homo sapiens 120-127 398297-6 1979 In vitro the insulin-stimulated incorporation of labeled glucose into triglycerides of adipose tissue was diminished in asymptomatic diabetics. Glucose 57-64 insulin Homo sapiens 13-20 26922819-3 1979 A continuous glucose monitoring apparatus was used to relate the concentrations of glucose during the day to concomitant levels of free insulin and cortisol. Glucose 13-20 insulin Homo sapiens 136-143 26922819-3 1979 A continuous glucose monitoring apparatus was used to relate the concentrations of glucose during the day to concomitant levels of free insulin and cortisol. Glucose 83-90 insulin Homo sapiens 136-143 119646-5 1979 C-peptide secretion followed the flucturations of the glucose level during 24 h in each individual patient. Glucose 54-61 insulin Homo sapiens 0-9 119646-6 1979 As a group, C-peptide secretors were better controlled than non-secretors with respect to mean blood glucose, M-value and the lability index and showed higher free insulin levels despite a similar daily insulin dosage. Glucose 101-108 insulin Homo sapiens 12-21 117019-5 1979 Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Glucose 38-45 insulin Homo sapiens 0-7 117019-5 1979 Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Glucose 135-142 insulin Homo sapiens 0-7 117019-6 1979 Acute phase insulin release in response to iv glucose gradually increased throughout the study. Glucose 46-53 insulin Homo sapiens 12-19 117019-9 1979 Reduction in tissue resistance to the action of insulin also appeared to be of major importance in the recovery of normal glucose tolerance in this subject. Glucose 122-129 insulin Homo sapiens 48-55 511981-6 1979 Thus, in a normal man capable of secreting appropriate amounts of insulin in response to the ingestion of glucose, glucagon plays no appreciable role in the disposition of this glucose load. Glucose 106-113 insulin Homo sapiens 66-73 231734-6 1979 The observed minor effect of insulin or intravenous glucose on hepatic glucose uptake compared to the effect of oral doses of glucose suggests that an additional factor other than insulin can produce hepatic glucose uptake: this factor could be, and probably is, the hepatic parasympathetic nerves. Glucose 71-78 insulin Homo sapiens 29-36 231734-6 1979 The observed minor effect of insulin or intravenous glucose on hepatic glucose uptake compared to the effect of oral doses of glucose suggests that an additional factor other than insulin can produce hepatic glucose uptake: this factor could be, and probably is, the hepatic parasympathetic nerves. Glucose 71-78 insulin Homo sapiens 29-36 231734-6 1979 The observed minor effect of insulin or intravenous glucose on hepatic glucose uptake compared to the effect of oral doses of glucose suggests that an additional factor other than insulin can produce hepatic glucose uptake: this factor could be, and probably is, the hepatic parasympathetic nerves. Glucose 71-78 insulin Homo sapiens 29-36 514079-0 1979 Insulin secretory dynamics after two consecutive intravenous stimulations with glucose and/or tolbutamide. Glucose 79-86 insulin Homo sapiens 0-7 514079-1 1979 Intravenous glucose and/or tolbutamide administered in two consecutive pulses 30 and 60 min apart to the same subjects using identical doses showed that insulin secretory responses was altered during a subsequent stimulation and that this was modulated by the time factor. Glucose 12-19 insulin Homo sapiens 153-160 514079-2 1979 Insulin response was more sustained after the second glucose pulses and the insulin peak response was delayed and diminished if the second glucose dose was given 30 min after the first, but not if given 60 min later. Glucose 53-60 insulin Homo sapiens 0-7 514079-2 1979 Insulin response was more sustained after the second glucose pulses and the insulin peak response was delayed and diminished if the second glucose dose was given 30 min after the first, but not if given 60 min later. Glucose 139-146 insulin Homo sapiens 0-7 514079-2 1979 Insulin response was more sustained after the second glucose pulses and the insulin peak response was delayed and diminished if the second glucose dose was given 30 min after the first, but not if given 60 min later. Glucose 139-146 insulin Homo sapiens 76-83 514079-7 1979 These studies do not support the two-pool theory, or at least restrict it to glucose-stimulated insulin response. Glucose 77-84 insulin Homo sapiens 96-103 515718-4 1979 Endocrine pancreatic insufficiency may account directly for alterations observed in individuals with decreased or absent insulin response to glucose load, wheras metabolic factors such as adipose mass, hepatic steatosis, and peripheral insulin resistance appear to be responsible for alterations in carbohydrate oxidation and storage in subjects with relative endocrine pancreatic insufficiency, particularly obese diabetics. Glucose 141-148 insulin Homo sapiens 121-128 515719-4 1979 On the insulin regimen a prompt and lasting improvement was observed in the metabolic parameters (blood glucose levels both fasting and after food intake, Hb A1c, serum insulin, glucagon and serum lipid concentrations). Glucose 104-111 insulin Homo sapiens 7-14 386121-4 1979 The average plasma glucose cycle was two minutes in advance of the plasma insulin. Glucose 19-26 insulin Homo sapiens 74-81 386121-5 1979 In the subjects with less regular plasma insulin cycles, a similar plasma glucose rise was demonstrated two minutes before the insulin rise. Glucose 74-81 insulin Homo sapiens 41-48 488547-4 1979 With similar steady state levels of plasma insulin (SSPI) maintained in all subjects, the height of the steady state plasma glucose concentration (SSPG) was considered an index of total body sensitivity to insulin-mediated glucose uptake. Glucose 223-230 insulin Homo sapiens 206-213 226351-3 1979 In this study we treated hypox rats with human GH, ACTH, and T3, alone or in combination, and examined the effects of insulin on glucose incorporation into fat cells and on 3-O-methylglucose transport. Glucose 129-136 insulin Homo sapiens 118-125 226351-8 1979 The basal glucose transport rate returns toward normal and again responds to insulin. Glucose 10-17 insulin Homo sapiens 77-84 226351-10 1979 GH seems to induce a change of the glucose-carrier system; it leads to a restriction of glucose transport, which is acutely modulated by insulin. Glucose 35-42 insulin Homo sapiens 137-144 226351-10 1979 GH seems to induce a change of the glucose-carrier system; it leads to a restriction of glucose transport, which is acutely modulated by insulin. Glucose 88-95 insulin Homo sapiens 137-144 389633-7 1979 After the first feed with glucose the average increase of glycaemia was 13.59 mg%, of insulin 2.46 muU/ml, and of C-peptide 0.59 ng/ml. Glucose 26-33 insulin Homo sapiens 86-93 389633-7 1979 After the first feed with glucose the average increase of glycaemia was 13.59 mg%, of insulin 2.46 muU/ml, and of C-peptide 0.59 ng/ml. Glucose 26-33 insulin Homo sapiens 114-123 488008-0 1979 Glucose infusion potentiates the acute insulin response to nonglucose stimuli during the infusion of somatostatin. Glucose 0-7 insulin Homo sapiens 39-46 488008-1 1979 These studies assessed the ability of glucose infusions to potentiate the acute insulin response (AIR) to iv isoproterenol (12 micrograms), arginine (750 mg), or glucose (5 g) that was previously inhibited by an infusion of somatostatin (SRIF). Glucose 38-45 insulin Homo sapiens 80-87 488008-8 1979 These data suggest that the potentiating effects of glucose and the inhibiting effects of SRIF may be mediated by a common mechanism affecting insulin release. Glucose 52-59 insulin Homo sapiens 143-150 511097-6 1979 In isolated fat cells in vitro, [HisA8]insulin showed a relative potency of 2.46 in stimulating glucose oxidation (human insulin = 1), whereas [D-CysA6,A11]insulin had a potency of only 0.00027. Glucose 96-103 insulin Homo sapiens 39-46 386029-0 1979 Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal plasma insulin and glucose concentrations. Glucose 160-167 insulin Homo sapiens 23-30 386029-3 1979 A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. Glucose 170-177 insulin Homo sapiens 41-48 386029-3 1979 A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. Glucose 193-200 insulin Homo sapiens 41-48 386029-3 1979 A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. Glucose 193-200 insulin Homo sapiens 41-48 386029-4 1979 The degree to which beta cell deficiency increases basal plasma glucose reflects the hyperbolic shape of the normal insulin secretory response to different glucose concentrations. Glucose 64-71 insulin Homo sapiens 116-123 386029-4 1979 The degree to which beta cell deficiency increases basal plasma glucose reflects the hyperbolic shape of the normal insulin secretory response to different glucose concentrations. Glucose 156-163 insulin Homo sapiens 116-123 386029-6 1979 From the basal plasma insulin and glucose concentrations, the model provides an estimate of the degree to which both beta cell deficiency and insulin resistance contribute to diabetes. Glucose 34-41 insulin Homo sapiens 142-149 523439-3 1979 The highest insulin response to glucose load was in persons with "doubtful" glucose tolerance test results. Glucose 76-83 insulin Homo sapiens 12-19 523439-0 1979 [Relationship between the results of glucose tolerance test and plasma content of immunoreactive insulin in the relatives of patients with juvenile form of diabetes mellitus]. Glucose 37-44 insulin Homo sapiens 97-104 523439-3 1979 The highest insulin response to glucose load was in persons with "doubtful" glucose tolerance test results. Glucose 32-39 insulin Homo sapiens 12-19 499682-0 1979 Insulin production rate following glucose ingestion estimated by splanchnic C-peptide output in normal man. Glucose 34-41 insulin Homo sapiens 0-7 499682-4 1979 The results demonstrate a basal insulin production rate of 0.017 +/- 0.002 U/min (mean +/- SEM) or 2.04 U/2 h. Values rose in a dose dependent manner from 2.6 +/- 1.1 U/2 h after ingestion of 12.5 g of glucose to 10.8 +/- 1.1 U/2 h following a glucose load of 100 g. Insulin retention by the liver was estimated at 0.012 +/- 0.001 U/min in the basal state, and ranged from 47-85% (70 +/- 2%) of production following an oral glucose load. Glucose 202-209 insulin Homo sapiens 32-39 499682-4 1979 The results demonstrate a basal insulin production rate of 0.017 +/- 0.002 U/min (mean +/- SEM) or 2.04 U/2 h. Values rose in a dose dependent manner from 2.6 +/- 1.1 U/2 h after ingestion of 12.5 g of glucose to 10.8 +/- 1.1 U/2 h following a glucose load of 100 g. Insulin retention by the liver was estimated at 0.012 +/- 0.001 U/min in the basal state, and ranged from 47-85% (70 +/- 2%) of production following an oral glucose load. Glucose 244-251 insulin Homo sapiens 32-39 499682-4 1979 The results demonstrate a basal insulin production rate of 0.017 +/- 0.002 U/min (mean +/- SEM) or 2.04 U/2 h. Values rose in a dose dependent manner from 2.6 +/- 1.1 U/2 h after ingestion of 12.5 g of glucose to 10.8 +/- 1.1 U/2 h following a glucose load of 100 g. Insulin retention by the liver was estimated at 0.012 +/- 0.001 U/min in the basal state, and ranged from 47-85% (70 +/- 2%) of production following an oral glucose load. Glucose 244-251 insulin Homo sapiens 32-39 396302-0 1979 Insulin stimulation of glucose entry in cultured human fibroblasts. Glucose 23-30 insulin Homo sapiens 0-7 396302-1 1979 The effect of insulin on glucose entry has been studied in monolayer cultures of human diploid fibroblastic cells. Glucose 25-32 insulin Homo sapiens 14-21 396302-2 1979 Influence of insulin on total cell glucose incorporation was evaluated using [14C] glucose. Glucose 35-42 insulin Homo sapiens 13-20 396302-3 1979 Glucose incorporation was increased up to two-fold in the presence of insulin. Glucose 0-7 insulin Homo sapiens 70-77 396302-5 1979 The action of insulin was enhanced by preincubation in glucose-free medium. Glucose 55-62 insulin Homo sapiens 14-21 394200-2 1979 This report compares the effects of four inhibitors of PGE synthesis on the acute insulin response to glucose and subsequent glucose disappearance rates. Glucose 102-109 insulin Homo sapiens 82-89 381941-1 1979 Insulin isolated from the pancreas of a diabetic patient with fasting hyperinsulinaemia showed decreased activity in binding to cell membrane insulin receptors and in stimulating cellular 2-deoxyglucose transport and glucose oxidation. Glucose 195-202 insulin Homo sapiens 0-7 381941-1 1979 Insulin isolated from the pancreas of a diabetic patient with fasting hyperinsulinaemia showed decreased activity in binding to cell membrane insulin receptors and in stimulating cellular 2-deoxyglucose transport and glucose oxidation. Glucose 195-202 insulin Homo sapiens 75-82 468830-6 1979 Insulin, leucine (2 mM) and a mixture of branched chain amino acids at normal plasma levels increased latency of cathepsin D in hearts that were perfused with buffer containing glucose. Glucose 177-184 insulin Homo sapiens 0-7 382871-10 1979 Under these steady-state conditions of euglycemia, the glucose infusion rate equals glucose uptake by all the tissues in the body and is therefore a measure of tissue sensitivity to exogenous insulin. Glucose 55-62 insulin Homo sapiens 192-199 111886-6 1979 Glucose administered at a rate of 3 to 4 g er unit of insulin infused in the low-dose group maintained a serum glucose of 150 to 250 mg/dl. Glucose 0-7 insulin Homo sapiens 54-61 111886-6 1979 Glucose administered at a rate of 3 to 4 g er unit of insulin infused in the low-dose group maintained a serum glucose of 150 to 250 mg/dl. Glucose 111-118 insulin Homo sapiens 54-61 115730-6 1979 The insulin response to oral glucose was enhanced. Glucose 29-36 insulin Homo sapiens 4-11 481974-3 1979 A "reactive" response to the direct infusion of glucose is postulated on the basis of the clinical response and a decrease in serum insulin/blood glucose ratio. Glucose 48-55 insulin Homo sapiens 132-139 525210-3 1979 In persons with normal CHT the insulin-stimulated (62.5 microU/ml) glucose conversion to CO2 by adipocytes as well as fat pads increased significantly up to 156 +/- 14% and 285 +/- 30%, respectively. Glucose 67-74 insulin Homo sapiens 31-38 525210-4 1979 Insulin enhanced the glucose incorporation into triglycerides up to 154 +/- 20% (fat cells) and 258 +/- 30% (fat pads) in adipose tissue from subjects displaying a normal CHT. Glucose 21-28 insulin Homo sapiens 0-7 572289-3 1979 The blood glucose level was well controlled with the insulin preparation. Glucose 10-17 insulin Homo sapiens 53-60 380423-5 1979 Insulin-dependent diabetes was also demonstrated in one patient with a normal preoperative glucose tolerance test. Glucose 91-98 insulin Homo sapiens 0-7 499287-5 1979 Basal and glucose-stimulated insulin secretion were not affected by either drug in any subjects. Glucose 10-17 insulin Homo sapiens 29-36 383881-2 1979 The calculation takes one minute and it takes into account glucose degradation, insulin half life in vivo, and the delay between blood sampling and insulin action on the blood glucose value. Glucose 176-183 insulin Homo sapiens 148-155 383881-4 1979 Operator decision is based on digitally converted tables, which are analogous to the graph of proportional control, and on glucose equivalent tables, which give the insulin effect on glucose as a function of time. Glucose 183-190 insulin Homo sapiens 165-172 36413-9 1979 These results indicate that in man (a) restoration of normoglycemia after insulin-induced hypoglycemia is primarily due to a compensatory increase in glucose production; (b) intact glucagon secretion, but not growth hormone secretion, is necessary for normal glucose counterregulation, and (c) adrenergic mechanisms do not normally play an essential role in this process but become critical to recovery from hypoglycemia when glucagon secretion is impaired. Glucose 150-157 insulin Homo sapiens 74-81 36413-9 1979 These results indicate that in man (a) restoration of normoglycemia after insulin-induced hypoglycemia is primarily due to a compensatory increase in glucose production; (b) intact glucagon secretion, but not growth hormone secretion, is necessary for normal glucose counterregulation, and (c) adrenergic mechanisms do not normally play an essential role in this process but become critical to recovery from hypoglycemia when glucagon secretion is impaired. Glucose 259-266 insulin Homo sapiens 74-81 526090-2 1979 Insulin, gastrin and glucagon responses to oral glucose and intravenous arginine in peptic ulcer patients. Glucose 48-55 insulin Homo sapiens 0-7 398700-6 1979 The shape of the insulin response curve is similar to that of glucose curve. Glucose 62-69 insulin Homo sapiens 17-24 87725-6 1979 In addition to restoring plasma-glucose to normal, treatment of diabetes with a portable insulin-infusion system results in restoration of normal lipid and aminoacid metabolism. Glucose 32-39 insulin Homo sapiens 89-96 733065-3 1978 Blood insulin patterns after oral glucose loading, however, were less easy to interpret. Glucose 34-41 insulin Homo sapiens 6-13 6997120-4 1980 Plasma glucose correlated with C-peptide (r = 0.21, p < 0.001) and insulin (r = 0.32, p < 0.001), indicating greater secretion where fasting glucose was higher. Glucose 7-14 insulin Homo sapiens 70-77 6997121-5 1980 Concurrently, the insulin response was augmented (3.4 vs 6.4 U/l X 180 min), resulting in improved glucose tolerance. Glucose 99-106 insulin Homo sapiens 18-25 519875-4 1979 No correlation between growth hormone and somatomedin B in acromegaly was detected; however, somatomedin B appeared to be related to the insulin response during the oral glucose tolerance test. Glucose 170-177 insulin Homo sapiens 137-144 91538-10 1979 Oral glucose produced an 8 fold increase in proinsulin concentration but a decline in the plasma proinsulin/insulin molar ratio. Glucose 5-12 insulin Homo sapiens 44-54 91538-10 1979 Oral glucose produced an 8 fold increase in proinsulin concentration but a decline in the plasma proinsulin/insulin molar ratio. Glucose 5-12 insulin Homo sapiens 97-107 91538-10 1979 Oral glucose produced an 8 fold increase in proinsulin concentration but a decline in the plasma proinsulin/insulin molar ratio. Glucose 5-12 insulin Homo sapiens 47-54 118030-0 1979 Capillary permeability in healthy males with different insulin response to glucose. Glucose 75-82 insulin Homo sapiens 55-62 118030-2 1979 The main finding was that, in both age groups, CDC was significantly negatively correlated to the early phase of insulin response to an intravenous glucose load. Glucose 148-155 insulin Homo sapiens 113-120 118030-5 1979 These data indicate that subjects with low insulin response to glucose have a higher capillary permeability than high responders, and that muscle capillary permeability increases with age. Glucose 63-70 insulin Homo sapiens 43-50 490204-0 1979 Hepatic-portal glucose and insulin levels: relationship to glucose-induced satiety and hunger. Glucose 59-66 insulin Homo sapiens 27-34 490204-1 1979 The hepatic-portal infusions of both smaller and larger glucose loads, which had no significant effect on food intake in chronic feeding experiments, produced only a brief dose-dependent peak-like elevation in glucose and insulin levels. Glucose 56-63 insulin Homo sapiens 222-229 490204-5 1979 Present results thus demonstrate that various glucose-induced feeding phenomena are associated and apparently dependent for their expression on distinct, prolonged changes in glycemia and insulin levels. Glucose 46-53 insulin Homo sapiens 188-195 231776-3 1979 Reactive hypoglycaemia resulted from an increased rate of glucose assimilation and possibly also from a decreased rate of gluconeogenesis due to the immense insulin secretion provoked by glucose or food. Glucose 187-194 insulin Homo sapiens 157-164 504226-0 1979 Gastric inhibitory polypeptide, insulin, and glucose changes produced by growth hormone, prednisolone, glucagon, insulin, fasting, or diazoxide. Glucose 45-52 insulin Homo sapiens 113-120 494984-4 1979 Only the LD had glucose intolerance, which was associated with a reduced first phase insulin response to all glucose loads with a decreased maximal secretory capacity (low V max). Glucose 109-116 insulin Homo sapiens 85-92 485602-4 1979 In four additional burn patients and seven normal controls, the effects of exogenously infused insulin on the metabolism of infused glucose were evaluated. Glucose 132-139 insulin Homo sapiens 95-102 389723-2 1979 Insulin release and synthesis were stimulated by glucose or mannose but not by allose, altrose, gulose, idose, galactose or talose. Glucose 49-56 insulin Homo sapiens 0-7 467810-1 1979 Prostaglandin E (PGE) infusion in normal man inhibits the acute insulin response to glucose. Glucose 84-91 insulin Homo sapiens 64-71 467810-4 1979 Acute insulin response to glucose (20 g i.v.) Glucose 26-33 insulin Homo sapiens 6-13 467810-8 1979 These findings demonstrate that (1) furosemide inhibits glucose-induced acute insulin responses and (2) LAS completely reverses the inhibitory effect of furosemide and also accelerates glucose disposal. Glucose 56-63 insulin Homo sapiens 78-85 467811-7 1979 We conclude that the liver modifies the distribution and removal of pancreatically released insulin in response to acute increases in insulin or glucose. Glucose 145-152 insulin Homo sapiens 92-99 504775-0 1979 Insulin effects on glucose utilization by human lymphocytes. Glucose 19-26 insulin Homo sapiens 0-7 400065-0 1979 Impaired plasms immunoreactive insulin response to glucose in elderly hypertensive patients with abnormal clucose tolerance. Glucose 51-58 insulin Homo sapiens 31-38 400065-3 1979 Patients with abnormal glucose tolerance showed significantly lower plasms immunoreactive insulin concentrations at 30 min and 60 min after the glucose load compared with patients with normal glucose tolerance. Glucose 23-30 insulin Homo sapiens 90-97 400065-3 1979 Patients with abnormal glucose tolerance showed significantly lower plasms immunoreactive insulin concentrations at 30 min and 60 min after the glucose load compared with patients with normal glucose tolerance. Glucose 144-151 insulin Homo sapiens 90-97 400065-3 1979 Patients with abnormal glucose tolerance showed significantly lower plasms immunoreactive insulin concentrations at 30 min and 60 min after the glucose load compared with patients with normal glucose tolerance. Glucose 144-151 insulin Homo sapiens 90-97 230060-5 1979 Intravenous glucose tolerance was reduced with normal or slightly increased fasting blood glucose and insulin values before and during the test. Glucose 12-19 insulin Homo sapiens 102-109 390082-1 1979 Glucose and other metabolizable sugars which elicit insulin release from the beta-cell of the pancreatic islet induce repetitive oscillations in the beta-cell transmembrane potential. Glucose 0-7 insulin Homo sapiens 52-59 399844-0 1979 [Insulin response and NEFA behavior in volunteers with a flat response to oral glucose tolerance test]. Glucose 79-86 insulin Homo sapiens 1-8 111634-5 1979 Insulin concentrations rose with glucose intake but were low for the level of plasma glucose. Glucose 33-40 insulin Homo sapiens 0-7 446919-0 1979 Ethnic variability in the plasma insulin response to oral glucose in Polynesian and Micronesian subjects. Glucose 58-65 insulin Homo sapiens 33-40 446919-1 1979 The pattern of insulin response to oral glucose over a wide range of glucose tolerance has been studied in two separate ethnic groups--Polynesians and Micronesians. Glucose 40-47 insulin Homo sapiens 15-22 447855-0 1979 Pattern of insulin delivery after intravenous glucose injection in man and its relation to plasma glucose disappearance. Glucose 46-53 insulin Homo sapiens 11-18 447855-0 1979 Pattern of insulin delivery after intravenous glucose injection in man and its relation to plasma glucose disappearance. Glucose 98-105 insulin Homo sapiens 11-18 447855-1 1979 Plasma insulin concentrations after pulse intravenous injection of glucose show an early rise, which declines towards the prestimulation level smoothly. Glucose 67-74 insulin Homo sapiens 7-14 447855-4 1979 The data were analyzed by deconvolution, which made it possible to compute the glucose-induced posthepatic insulin delivery rate minute by minute. Glucose 79-86 insulin Homo sapiens 107-114 447855-12 1979 Both the first and the second spike of insulin delivery, but not the total insulin output during the test, showed a significant, positive correlation with the plasma glucose disappearance rate computed between 10 and 60 min. Glucose 166-173 insulin Homo sapiens 39-46 400001-2 1979 Insulin response to small intravenous loads of glucose and to pindolol infusion]. Glucose 47-54 insulin Homo sapiens 0-7 400448-1 1979 Determination of plasma insulin and C peptide after intravenous administration of glucose]. Glucose 82-89 insulin Homo sapiens 24-31 87724-0 1979 Continuous subcutaneous insulin infusion: improved blood-glucose and intermediary-metabolite control in diabetics. Glucose 57-64 insulin Homo sapiens 24-31 481365-0 1979 Feedback control dynamics for glucose controlled insulin infusion system. Glucose 30-37 insulin Homo sapiens 49-56 481365-1 1979 Miles Laboratories has developed a Glucose Controlled Insulin Infusion System (GCIIS) designated by the Trademark (BIOSTATOR) as a tool to investigate the physiologic control parameters of carbohydrate metabolism and regulatory deficiencies in diabetes. Glucose 35-42 insulin Homo sapiens 54-61 111449-0 1979 Effect of two sulphonylureas on the dose kinetics of glucose-induced insulin release in normal and diabetic subjects. Glucose 53-60 insulin Homo sapiens 69-76 111449-6 1979 The glucose-insulin dose relationships, established by giving glucose alone, demonstrated curves that were flatter, and shifted to the right of the control in diabetics and low insulin responders, the changes being more marked in the former group. Glucose 4-11 insulin Homo sapiens 12-19 111449-8 1979 The dose-response relation for glucose-induced insulin release was completely normalized in low responders when sulphonylureas were added. Glucose 31-38 insulin Homo sapiens 47-54 111449-9 1979 In the group of mild diabetics, insulin response to glucose was enhanced by sulphonylureas only to a modest extent, the dose-response curves remaining grossly abnormal. Glucose 52-59 insulin Homo sapiens 32-39 222222-2 1979 Biochemically, the association of an increased value of immunoreactive insulin with a low glucose value is diagnostic of insulin-mediated hypoglycemia. Glucose 90-97 insulin Homo sapiens 71-78 454160-5 1979 Insulin stimulated glucose uptake to the same extent in muscles from rats in early sepsis, late sepsis, and from control rats. Glucose 19-26 insulin Homo sapiens 0-7 454160-6 1979 Even at an insulin concentration that produced submaximal stimulation of glucose uptake, no difference in glucose uptake between the three groups of muscles was observed. Glucose 73-80 insulin Homo sapiens 11-18 36318-8 1979 From the data, we assume that the observed increase of NADPH may lead via GSH to an increase in the number of such thiol groups in the beta-cell membrane, which are believed to be related to stimulation of insulin release and, thus, to increase the sensitivity of the beta-cell to stimulation by glucose and/or leucine. Glucose 296-303 insulin Homo sapiens 206-213 221136-17 1979 Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic. Glucose 45-52 insulin Homo sapiens 154-161 467846-3 1979 In normal subjects at glycaemic levels above 130 mg/100 ml, glucose uptake was independent of glucose concentration;it was directly related in insulin concentration but not to insulin uptake. Glucose 60-67 insulin Homo sapiens 143-150 467846-4 1979 In non-obese maturity-onset diabetic subjects, glucose uptake was dependent on glucose concentration and insulin uptake, but not on insulin concentration. Glucose 47-54 insulin Homo sapiens 105-112 467846-6 1979 For a given change in insulin concentration the increase in glucose uptake was as great in diabetics as in controls, but the effect of insulin was mediated through a mechanism involving its uptake. Glucose 60-67 insulin Homo sapiens 22-29 477046-2 1979 A blunted serum C-peptide response to intravenous glucose, glucagon and tolbutamide was also found. Glucose 50-57 insulin Homo sapiens 16-25 478080-10 1979 It is concluded that lowered serum glucose levels after long term treatment with chlorpropamide occured while plasma insulin response to glucose was no greater than before treatment. Glucose 137-144 insulin Homo sapiens 117-124 478081-3 1979 Intravenous glucose tolerance test showed a reduced glucose tolerance coupled with very high insulin levels. Glucose 12-19 insulin Homo sapiens 93-100 478083-3 1979 Oral glucose is able to suppress the hyperglucagonemia and further to increase the elevated insulin levels of cirrhotics leading to a rise of IRI/IRG. Glucose 5-12 insulin Homo sapiens 92-99 447800-0 1979 Potentiation of insulin secretory responses by plasma glucose levels in man: evidence that hyperglycemia in diabetes compensates for imparied glucose potentiation. Glucose 54-61 insulin Homo sapiens 16-23 288060-5 1979 In adipocytes anti-insulin IgG in the same concentration range only inhibits the binding of insulin and suppresses insulin-mediated glucose oxidation. Glucose 132-139 insulin Homo sapiens 19-26 505025-0 1979 Insulin response to glucose and insulin sensitivity in hypocalcaemic patients. Glucose 20-27 insulin Homo sapiens 0-7 523983-5 1979 It is concluded that (1) a significant insulin release from muscle tissue or its vascular bed occurs and continues at undiminished rate during prolonged work, (2) a substantial amount must be bound in the tissue, unless local synthesis takes place and (3) despite this loss of insulin from the forearm no major change in glucose and FFA extraction occurs with duration of work. Glucose 321-328 insulin Homo sapiens 39-46 222000-1 1979 A glucose-controlled insulin and glucose infusion system (Biostator system, Miles Laboratories Inc., Elkhart, Ind.) Glucose 2-9 insulin Homo sapiens 21-28 222000-10 1979 The glucose-controlled insulin and glucose infusion system appears to be a useful instrument for intraoperative management of patients with suspected insulinomas. Glucose 4-11 insulin Homo sapiens 23-30 462471-2 1979 The 72-hr sequential glucose uptake by the cells of both species in culture dishes was enhanced only slightly with time by the addition of insulin to culture medium, and this enhancement was statistically not significant. Glucose 21-28 insulin Homo sapiens 139-146 86774-7 1979 containing 75 microgram or more oestrogen, and this was associated with impairment of the early insulin response to glucose. Glucose 116-123 insulin Homo sapiens 96-103 373870-4 1979 Following the onset of cardiopulmonary bypass, serum glucose values rose rapidly to a mean of 972 mg/dl (54.0 mmol/l) and were associated with high circulating concentrations of insulin in the range of 216 microU/ml [1549.8 pmol/l]. Glucose 53-60 insulin Homo sapiens 178-185 376552-2 1979 Insulin sensitivity was determined by the insulin clamp technique in which the plasma insulin is acutely raised and maintained 100 muU/ml above the fasting level and plasma glucose is held constant at fasting levels by a variable glucose infusion. Glucose 173-180 insulin Homo sapiens 0-7 376552-2 1979 Insulin sensitivity was determined by the insulin clamp technique in which the plasma insulin is acutely raised and maintained 100 muU/ml above the fasting level and plasma glucose is held constant at fasting levels by a variable glucose infusion. Glucose 230-237 insulin Homo sapiens 0-7 376552-3 1979 The amount of glucose infused is a measure of overall tissue sensitivity to insulin. Glucose 14-21 insulin Homo sapiens 76-83 376552-9 1979 When they were restudied after prior normalization (with insulin) of the fasting plasma glucose (100+/-1 mg/dl), the glucose infusion rate during the insulin clamp was 30% lower than observed in association with hyperglycemia (P < 0.01). Glucose 88-95 insulin Homo sapiens 57-64 376552-9 1979 When they were restudied after prior normalization (with insulin) of the fasting plasma glucose (100+/-1 mg/dl), the glucose infusion rate during the insulin clamp was 30% lower than observed in association with hyperglycemia (P < 0.01). Glucose 88-95 insulin Homo sapiens 150-157 376552-9 1979 When they were restudied after prior normalization (with insulin) of the fasting plasma glucose (100+/-1 mg/dl), the glucose infusion rate during the insulin clamp was 30% lower than observed in association with hyperglycemia (P < 0.01). Glucose 117-124 insulin Homo sapiens 57-64 376552-9 1979 When they were restudied after prior normalization (with insulin) of the fasting plasma glucose (100+/-1 mg/dl), the glucose infusion rate during the insulin clamp was 30% lower than observed in association with hyperglycemia (P < 0.01). Glucose 117-124 insulin Homo sapiens 150-157 429528-0 1979 Paradoxical inhibition of insulin secretion by glucose in human diabetes mellitus. Glucose 47-54 insulin Homo sapiens 26-33 447832-3 1979 In all three groups of studies, continuous infusion of insulin resulted in an initial decline in plasma glucose followed by stabilization after 60-180 min. Glucose 104-111 insulin Homo sapiens 55-62 447832-8 1979 The rebound increment in glucose output was significant (P < 0.05) by 30 min after initiation of the insulin infusion and preceded, by 30-45 min, a significant rise in circulating counterregulatory hormones. Glucose 25-32 insulin Homo sapiens 104-111 447832-9 1979 With the lower insulin infusion dose, plasma insulin rose two- to threefold, plasma glucose initially fell at a rate of 0.37+/-0.04 mg/min for 75 min and stabilized at 67+/-3 mg/dl after 75 min. Glucose 84-91 insulin Homo sapiens 15-22 447832-13 1979 However, the initial fall in plasma glucose was almost entirely a result of suppression of glucose output, which showed a twofold greater decline (60+/-6%) than in controls (27+/-5%, P <0.01) and remained suppressed throughout the insulin infusion. Glucose 36-43 insulin Homo sapiens 234-241 447832-13 1979 However, the initial fall in plasma glucose was almost entirely a result of suppression of glucose output, which showed a twofold greater decline (60+/-6%) than in controls (27+/-5%, P <0.01) and remained suppressed throughout the insulin infusion. Glucose 91-98 insulin Homo sapiens 234-241 447832-14 1979 In contrast, the late stabilization in plasma glucose was a result of a fall in glucose uptake to values 50% below basal (P < 0.001) and 39% below that observed in controls at termination of the insulin infusion (P < 0.01). Glucose 46-53 insulin Homo sapiens 198-205 449698-8 1979 Thus, whenever insulin levels rise in response to an increase in hyperglycemia, as they do spontaneously in nondiabetics and in adult-type diabetics and as they do when juvenile diabetics are given supplementary insulin together with the glucose bolus, the decline in IRG in response to an i.v. Glucose 238-245 insulin Homo sapiens 15-22 110975-3 1979 The achieved levels of plasma insulin satisfy the transport of glucose and the inhibition of lipolysis. Glucose 63-70 insulin Homo sapiens 30-37 449692-2 1979 Glucose tolerance and plasma lipids were normal, but plasma insulin increased to 340 muU/ml during an oral glucose tolerance test. Glucose 107-114 insulin Homo sapiens 60-67 449698-0 1979 Effects of insulin on the response of immunoreactive glucagon to an intravenous glucose load in human diabetes. Glucose 80-87 insulin Homo sapiens 11-18 449698-5 1979 The magnitude of their glucose-induced IRG decline was not augmented by exogenous insulin, even when insulin levels were acutely raised above 300 micro units/ml. Glucose 23-30 insulin Homo sapiens 101-108 449698-10 1979 The findings are compatible with the view that glucose-induced suppression of IRG may require a concomitant rise in insulin. Glucose 47-54 insulin Homo sapiens 116-123 471590-0 1979 Suppression of gluconeogenesis and endogenous glucose production by exogenous insulin administration in the newborn lamb. Glucose 46-53 insulin Homo sapiens 78-85 484162-6 1979 In obese hypoglycemics the blood glucose nadir was inversely proportional to the time of the insulin peak (i.e. the later the insulin peak the lower the blood glucose nadir) but correlated poorly to maximum insulin values. Glucose 33-40 insulin Homo sapiens 93-100 484162-6 1979 In obese hypoglycemics the blood glucose nadir was inversely proportional to the time of the insulin peak (i.e. the later the insulin peak the lower the blood glucose nadir) but correlated poorly to maximum insulin values. Glucose 33-40 insulin Homo sapiens 126-133 484162-6 1979 In obese hypoglycemics the blood glucose nadir was inversely proportional to the time of the insulin peak (i.e. the later the insulin peak the lower the blood glucose nadir) but correlated poorly to maximum insulin values. Glucose 33-40 insulin Homo sapiens 126-133 484165-1 1979 Analysis of the course of D-glucose binding to insulin has shown that the mechanism of glucose-insulin interaction is a cooperative process. Glucose 26-35 insulin Homo sapiens 47-54 484165-2 1979 Binding of D-glucose molecules to insulin is facilitated by the dissociation of insulin aggregates caused by insulin-glucose interaction. Glucose 11-20 insulin Homo sapiens 34-41 484166-6 1979 Analysis of the glucose and insulin responses to the glucose infusion test indicated that 31.6% of the patients had a delayed and sluggish insulin response to the glucose load, fitting the criteria suggested for the diagnosis of prediabetes, versus 10% of the appropriate controls. Glucose 53-60 insulin Homo sapiens 28-35 484166-6 1979 Analysis of the glucose and insulin responses to the glucose infusion test indicated that 31.6% of the patients had a delayed and sluggish insulin response to the glucose load, fitting the criteria suggested for the diagnosis of prediabetes, versus 10% of the appropriate controls. Glucose 53-60 insulin Homo sapiens 139-146 484166-6 1979 Analysis of the glucose and insulin responses to the glucose infusion test indicated that 31.6% of the patients had a delayed and sluggish insulin response to the glucose load, fitting the criteria suggested for the diagnosis of prediabetes, versus 10% of the appropriate controls. Glucose 53-60 insulin Homo sapiens 28-35 484166-6 1979 Analysis of the glucose and insulin responses to the glucose infusion test indicated that 31.6% of the patients had a delayed and sluggish insulin response to the glucose load, fitting the criteria suggested for the diagnosis of prediabetes, versus 10% of the appropriate controls. Glucose 53-60 insulin Homo sapiens 139-146 484166-7 1979 In particular, simulation of the plasma insulin responses by a square-wave glucose stimulus, confirmed that in a significantly higher number of patients the early insulin peak was below normal limits. Glucose 75-82 insulin Homo sapiens 40-47 484166-7 1979 In particular, simulation of the plasma insulin responses by a square-wave glucose stimulus, confirmed that in a significantly higher number of patients the early insulin peak was below normal limits. Glucose 75-82 insulin Homo sapiens 163-170 374171-3 1979 In one insulin-dependent diabetic with high anti-insulin-binding capacity, the blood glucose response after an oral glucose challenge was not normalized by the artificial beta cell and the glucagon secretion was paradoxically increased. Glucose 85-92 insulin Homo sapiens 7-14 428694-4 1979 The insulin response to galactose was greatly enhanced by IV glucose (mean area under plasma insulin curve with galactose alone 236.5 +/- 66.0, with galactose + IV glucose 451.9 +/- 81.6, p less than 0.025). Glucose 61-68 insulin Homo sapiens 4-11 428694-4 1979 The insulin response to galactose was greatly enhanced by IV glucose (mean area under plasma insulin curve with galactose alone 236.5 +/- 66.0, with galactose + IV glucose 451.9 +/- 81.6, p less than 0.025). Glucose 61-68 insulin Homo sapiens 93-100 428694-4 1979 The insulin response to galactose was greatly enhanced by IV glucose (mean area under plasma insulin curve with galactose alone 236.5 +/- 66.0, with galactose + IV glucose 451.9 +/- 81.6, p less than 0.025). Glucose 164-171 insulin Homo sapiens 4-11 428694-7 1979 The lower plasma GIP and galactose levels observed following oral galactose in the presence of IV glucose may be accounted for either by postulating that insulin inhibits the absorption of oral galactose, or that insulin exerts a negative feed-back control on GIP release and accelerates galactose disposition in the body. Glucose 98-105 insulin Homo sapiens 154-161 428694-7 1979 The lower plasma GIP and galactose levels observed following oral galactose in the presence of IV glucose may be accounted for either by postulating that insulin inhibits the absorption of oral galactose, or that insulin exerts a negative feed-back control on GIP release and accelerates galactose disposition in the body. Glucose 98-105 insulin Homo sapiens 213-220 437366-2 1979 Insulin"s suppression by diazoxide in these 10 subjects resulted in a mild glucose intolerance and an increase in insulin"s receptors in seven of the 10 subjects. Glucose 75-82 insulin Homo sapiens 0-7 111943-10 1979 Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. Glucose 50-57 insulin Homo sapiens 66-73 111943-10 1979 Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. Glucose 129-136 insulin Homo sapiens 66-73 421995-7 1979 All the cirrhotic patients showed a significantly reduced C-peptide/insulin ratio after glucose administration. Glucose 88-95 insulin Homo sapiens 68-75 428580-6 1979 The increased insulin secretion needed to maintain the blood glucose concentration suggests that the released progesterone may have a systemic effect. Glucose 61-68 insulin Homo sapiens 14-21 467374-1 1979 The authors have estimated a correlation between the total insulin areas after glucose loading and total somatotropin areas during insulin-induced hypoglycaemia in 30 patients with obesity, as well as in a selected group of 16 patients with simple (essential) obesity. Glucose 79-86 insulin Homo sapiens 59-66 467377-0 1979 Effect of alpha-adrenergic blockade on insulin response to glucose infusion in protodiabetic subjects. Glucose 59-66 insulin Homo sapiens 39-46 510227-4 1979 Similar characteristics of insulin concentrations measured during an oral glucose tolerance test and adipose-cell hypertrophy of the same degree may suggest a comparable influence on the development of carbohydrate intolerance and hypertriglyceridemia. Glucose 74-81 insulin Homo sapiens 27-34 573770-3 1979 After intravenous glucose load, there was a decrease of the coefficient of glucose utilization and of the insulin response both of which were highly significant (p less than 0.01). Glucose 18-25 insulin Homo sapiens 106-113 36543-1 1979 The immediate and direct regulation of insulin release by circulating nutrients, especially glucose, is thought to be mediated in the pancreatic B-cell by a sequence of metabolic, ionic, and motile events. Glucose 92-99 insulin Homo sapiens 39-46 36543-8 1979 The dose-response curves for these parameters yield a sigmoidal pattern analogous to that which depicts the rate of insulin release at increasing glucose concentrations. Glucose 146-153 insulin Homo sapiens 116-123 399187-3 1979 The C-peptide/IRI ratio decreased after the oral glucose load in both groups studied. Glucose 49-56 insulin Homo sapiens 4-13 763270-0 1979 Reduction to normal of plasma glucose in juvenile diabetes by subcutaneous administration of insulin with a portable infusion pump. Glucose 30-37 insulin Homo sapiens 93-100 763270-7 1979 These results demonstrate that plasma glucose can be lowered to normal in ambulatory patients with brittle juvenile diabetes using a portable, subcutaneous insulin infusion system for two to four days. Glucose 38-45 insulin Homo sapiens 156-163 443288-4 1979 The insulin response to glucose was unaltered during pyridoxine therapy. Glucose 24-31 insulin Homo sapiens 4-11 221281-0 1979 Effect of somatostatin on the potentiating action of glucagon, cyclic adenosine monophosphate and theophylline on glucose-induced insulin release. Glucose 114-121 insulin Homo sapiens 130-137 221281-1 1979 The effect of glucagon on the inhibition of the insulin response to glucose induced by somatostatin was investigated in humans and in the isolated perfused rat pancreas. Glucose 68-75 insulin Homo sapiens 48-55 221281-2 1979 Both in vivo and in vitro somatostatin suppressed glucose-induced insulin release. Glucose 50-57 insulin Homo sapiens 66-73 428685-0 1979 Use of a glucose controlled insulin infusion system (artificial beta cell) to control diabetes during surgery. Glucose 9-16 insulin Homo sapiens 28-35 446905-1 1979 The characteristics of the glucose and insulin responses during the glucose tolerance test (GTT) in obese people as a group have not been established. Glucose 68-75 insulin Homo sapiens 39-46 446907-3 1979 Restoring normal glucose levels in mild diabetes by an insulin infusion further reduces the C-peptide concentration, but both the plasma glucose and the C-peptide return to their "set" level when the insulin is withdrawn. Glucose 17-24 insulin Homo sapiens 55-62 446907-3 1979 Restoring normal glucose levels in mild diabetes by an insulin infusion further reduces the C-peptide concentration, but both the plasma glucose and the C-peptide return to their "set" level when the insulin is withdrawn. Glucose 17-24 insulin Homo sapiens 200-207 446907-3 1979 Restoring normal glucose levels in mild diabetes by an insulin infusion further reduces the C-peptide concentration, but both the plasma glucose and the C-peptide return to their "set" level when the insulin is withdrawn. Glucose 137-144 insulin Homo sapiens 55-62 446907-3 1979 Restoring normal glucose levels in mild diabetes by an insulin infusion further reduces the C-peptide concentration, but both the plasma glucose and the C-peptide return to their "set" level when the insulin is withdrawn. Glucose 137-144 insulin Homo sapiens 200-207 520116-10 1979 Multivariate analyses showed that the value of high 1-h or 2-h postload plasma insulin level for predicting CHD risk was independent of other risk factors, including blood glucose levels during OGTT. Glucose 172-179 insulin Homo sapiens 79-86 761441-0 1979 Effect of d- and dl-propranolol on glucose-stimulated insulin release. Glucose 35-42 insulin Homo sapiens 54-61 761441-2 1979 The increase in serum insulin 45 to 90 min after glucose ingestion was reduced during the infusion of either d- or dl-propranolol. Glucose 49-56 insulin Homo sapiens 22-29 761441-4 1979 The insulin/glucose ratios were reduced by both d- and dl-propranolol during the time of maximum glucose and insulin responses. Glucose 12-19 insulin Homo sapiens 4-11 761441-4 1979 The insulin/glucose ratios were reduced by both d- and dl-propranolol during the time of maximum glucose and insulin responses. Glucose 12-19 insulin Homo sapiens 109-116 761441-4 1979 The insulin/glucose ratios were reduced by both d- and dl-propranolol during the time of maximum glucose and insulin responses. Glucose 97-104 insulin Homo sapiens 4-11 761441-6 1979 Since d-propranolol has no appreciable beta adrenoceptor blocking activity, it appears that the suppression of glucose-stimulated insulin release by propranolol may be due primarily to local anesthetic properties which are exerted equally by both isomers. Glucose 111-118 insulin Homo sapiens 130-137 34554-2 1979 Immunoreactive GIP released by duodenal acidification is biologically active because it augments the glucose-induced release of immunoreactive insulin (IRI). Glucose 101-108 insulin Homo sapiens 143-150 34554-4 1979 From this it is concluded that the initial capacity to augment the glucose-induced insulin release (incretin activity) of hydrochloric acid is due to its ability to release GIP. Glucose 67-74 insulin Homo sapiens 83-90 429498-0 1979 Augmented insulin responses to glucose after secretin priming in diabetic subjects. Glucose 31-38 insulin Homo sapiens 10-17 429501-1 1979 It has been shown that the incretin effect - i.e. the gastrointestinal potentiation of the insulin response to oral glucose - is reduced in late normal pregnancy. Glucose 116-123 insulin Homo sapiens 91-98 470930-1 1979 A new family of insulin secretogogues that resemble glucose in hydrogen bonding possibilities. Glucose 52-59 insulin Homo sapiens 16-23 763155-11 1979 The glucose clearance rate increased only when sufficient insulin was infused with the 4 mg/kg . Glucose 4-11 insulin Homo sapiens 58-65 220725-6 1979 Urinary C-peptide/blood glucose ratio showed a steady improvement of insulin secretion during the remission period. Glucose 24-31 insulin Homo sapiens 69-76 108019-1 1979 In immature human placentas, the activity of the I (glucose-6-phosphate-independent) form of glycogen synthase is significantly increased by insulin, glucose and by both compounds associated. Glucose 52-59 insulin Homo sapiens 141-148 369260-0 1979 Potentiation and inhibition of insulin release in man following priming with glucose and with arginine--effect of somatostatin. Glucose 77-84 insulin Homo sapiens 31-38 369389-0 1979 Stimulus-secretion coupling of glucose-induced insulin release. Glucose 31-38 insulin Homo sapiens 47-54 369391-0 1979 Early insulin and glucagon response to subsequent pulses of arginine, glucose, and tolbutamide in normal man. Glucose 70-77 insulin Homo sapiens 6-13 419916-3 1979 During induction of paralysis by a prolonged oral glucose load, one patient showed 24-h variations in the insulin binding to monocytes not differing from those observed in normals. Glucose 50-57 insulin Homo sapiens 106-113 419916-4 1979 After iv administration of glucose, these patients showed an elevated initial insulin response compared with the normals (P less than 0.1). Glucose 27-34 insulin Homo sapiens 78-85 419917-6 1979 A weighting function of derivative response, reflecting the insulin secretion per unit of rate of change in blood glucose concentration, was calculated from blood glucose concentration (input) and insulin concentration (output) by the deconvolution method. Glucose 114-121 insulin Homo sapiens 60-67 419917-6 1979 A weighting function of derivative response, reflecting the insulin secretion per unit of rate of change in blood glucose concentration, was calculated from blood glucose concentration (input) and insulin concentration (output) by the deconvolution method. Glucose 163-170 insulin Homo sapiens 60-67 311740-0 1979 Evidence for an involvement of kinin liberation in the priming action of insulin on glucose uptake into skeletal muscle. Glucose 84-91 insulin Homo sapiens 73-80 365659-2 1979 So far the human islets have been kept in tissue culture, without attachment, in medium RPMI 1640 supplemented with 10% calf serum for more than 9 months, with preservation of the ability to release insulin in response to glucose stimulation. Glucose 222-229 insulin Homo sapiens 199-206 369927-11 1979 Finally, the changes in the metabolism of insulin are not large, making it unlikely that they are the sole cause of the major alterations in glucose tolerance seen with aging, obesity, or diabetes. Glucose 141-148 insulin Homo sapiens 42-49 399925-1 1979 This study aimed at investigating the effect of exogenous prostaglandin E1 (PGE1) administration on both basal and glucose-stimulated insulin secretion in normal man. Glucose 115-122 insulin Homo sapiens 134-141 399925-6 1979 In other six normal volunteers, PGE1 (0.5 microgram/kg/min) significantly reduced both insulin response to intravenous glucose and glucose tolerance. Glucose 119-126 insulin Homo sapiens 87-94 467357-1 1979 Insulin and adrenaline were both found to stimulate the glucose utilization of Tetrahymena, although somewhat differently. Glucose 56-63 insulin Homo sapiens 0-7 763147-9 1979 Likewise, the area under the glucose-induced plasma insulin curve was significantly greater than normal (1.46 +/- 0.21 mU/ml . Glucose 29-36 insulin Homo sapiens 52-59 432553-4 1979 This abnormality was corrected by insulin when excess glucose was present, but not by insulin alone. Glucose 54-61 insulin Homo sapiens 34-41 432553-5 1979 It is suggested that this patient"s erythrocytes may have been altered by placental lactogen and/or prolactin in such a way as to make them abnormally dependent on insulin for the uptake of glucose. Glucose 190-197 insulin Homo sapiens 164-171 425445-0 1979 [Immunoreactive insulin content in the dynamics of the glucose tolerance test in coronary arteriosclerosis]. Glucose 55-62 insulin Homo sapiens 16-23 425589-8 1979 These results are indicating peripheral insulin resistance regarding the assimilation of glucose and leucine (at least in patients with portocaval shunts). Glucose 89-96 insulin Homo sapiens 40-47 362213-3 1979 We found that in catabolic patients, insulin and glucose produced a strikingly greater inhibition of protein breakdown that glucose alone, and that glucose alone was marginally more protein sparing than a regimen containing mainly fat (intralipid and sorbitol). Glucose 124-131 insulin Homo sapiens 37-44 362213-3 1979 We found that in catabolic patients, insulin and glucose produced a strikingly greater inhibition of protein breakdown that glucose alone, and that glucose alone was marginally more protein sparing than a regimen containing mainly fat (intralipid and sorbitol). Glucose 124-131 insulin Homo sapiens 37-44 231878-0 1979 Insulin response to an oral glucose load in relation to Lp(a)/pre-beta 1-lipoprotein levels in non-diabetic patients with peripheral vascular disease and in controls. Glucose 28-35 insulin Homo sapiens 0-7 285561-1 1979 Glucose tolerance and insulin response to intravenous and oral glucose challenges in 226 normal subjects and 25 subjects with mild or chemical diabetes. Glucose 63-70 insulin Homo sapiens 22-29 371340-0 1979 Insulin in portal, hepatic and peripheral venous blood after glucose, tolbutamide and glipizide stimulation. Glucose 61-68 insulin Homo sapiens 0-7 371342-1 1979 The contribution of decreased hepatic insulin extraction to the relative hyperinsulinemia after oral glucose load as compared to intravenous glucose load was studied in 6 normal weight male volunteers by means of an analysis of the relationship between peripheral venous concentrations of insulin and C-peptide following similar glycemic stimuli after oral and intravenous glucose administration. Glucose 101-108 insulin Homo sapiens 38-45 371342-2 1979 The incremental areas under the insulin and C-peptide curves were higher during oral as compared to intravenous glucose administration, 436 (251--762) per cent and 267 (124-378) per cent respectively (mean and range). Glucose 113-120 insulin Homo sapiens 33-40 371342-3 1979 The ratio between corresponding incremental areas of insulin and C-peptide were 53 (17--103 per cent higher during oral glucose load. Glucose 120-127 insulin Homo sapiens 53-60 371342-4 1979 These findings suggest that the augmented peripheral insulin levels after oral glucose administration are caused by a combination of increased beta cell secretion and decreased hepatic insulin extraction. Glucose 79-86 insulin Homo sapiens 53-60 371342-4 1979 These findings suggest that the augmented peripheral insulin levels after oral glucose administration are caused by a combination of increased beta cell secretion and decreased hepatic insulin extraction. Glucose 79-86 insulin Homo sapiens 185-192 120672-6 1979 Oral glucose load and arginine infusion resulted in a significantly enhanced insulin release. Glucose 5-12 insulin Homo sapiens 77-84 758722-8 1979 These results show that in SGA infants primed with H, the rise of plasma glucose concentration after L-alanine administration is observed with low plasma insulin levels and without stimulation of glucagon secretion. Glucose 73-80 insulin Homo sapiens 154-161 758722-9 1979 They suggest that H induced a reduced peripheral utilization of glucose by lowering the plasma levels of insulin and a production of glucose from alanine through gluconeogenesis. Glucose 64-71 insulin Homo sapiens 105-112 495274-3 1979 3) The decrease in insulin is accompanied by a fall in plasma glucose and in the I/G ratio, suggesting an increase in insulin sensitivity. Glucose 62-69 insulin Homo sapiens 19-26 495279-0 1979 Effect of intravenous glucose,leucine and arginine on concerntration of insulin in maternal and umbilical cord serum. Glucose 22-29 insulin Homo sapiens 72-79 315159-0 1979 Possible involvement of kinins and prostaglandins in the translation of insulin action on glucose uptake into skeletal muscle. Glucose 90-97 insulin Homo sapiens 72-79 398679-3 1979 With a 30 months mean time interval between the two tests, a highly significant negative correlation was found between insulin-secretion capacity of the first test and blood glucose area of the last one. Glucose 174-181 insulin Homo sapiens 119-126 507744-2 1979 In our investigation we found slight changes in the carbohydrate metabolism during and after treatment with Fysioquens but it was chiefly the changes in plasma insulin response during glucose tolerance tests that were significant. Glucose 184-191 insulin Homo sapiens 160-167 582980-5 1979 Possible reasons for this behaviour could be additional insulin-independent effects of tolbutamide on the glucose metabolism. Glucose 106-113 insulin Homo sapiens 56-63 371613-4 1979 On the other hand exercise potentiates the blood glucose lowering effect of subcutaneously injected insulin; therefore precautions have to be taken in order to avoid hypoglycemia in insulin-dependent diabetics especially during and after more strenous exercise. Glucose 49-56 insulin Homo sapiens 100-107 114240-2 1979 During glucose infusion a striking increase of insulin levels took place, which was higher in the infants of diabetic mothers. Glucose 7-14 insulin Homo sapiens 47-54 233077-3 1979 The clinical diagnosis is confirmed by the repeated demonstrated that: 1) Symptomatic episodes produced by fasting are in fact due to hypoglycaemia (plasma glucose level less than 2.5 mmol/litre) 2) Such episodes are relieved by glucose administration 3) Concomitant hyperinsulinaemia is present (serum insulin greater than 8 micro-units/ml in the fasting state). Glucose 229-236 insulin Homo sapiens 272-279 365654-2 1979 Lanthanum inhibits insulin secretion stimulated by glucose and by acetylcholine to basal levels. Glucose 51-58 insulin Homo sapiens 19-26 365654-3 1979 Epinephrine and lanthanum have additive effects in inhibiting insulin secretion to glucose stimulation. Glucose 83-90 insulin Homo sapiens 62-69 365654-4 1979 The effect of epinephrine prestimulation on insulin secretion to subsequent glucose challenge varies markedly, depending on the presence or absence of bicarbonate ion: epinephrine priming is reversed in the absence of bicarbonate, and effect possibly related to reduced calcium uptake. Glucose 76-83 insulin Homo sapiens 44-51 570137-5 1979 In contrast, in response to a glucose tolerance test, both the free insulin and C-peptide responses were normal as was glucose tolerance. Glucose 30-37 insulin Homo sapiens 80-89 761717-0 1979 Role of insulin and glucagon in the regulation of hepatic glucose production during exercise. Glucose 58-65 insulin Homo sapiens 8-15 500381-9 1979 The mean insulin concentration was lower also after intravenous glucose, but the early insulin peak was preserved. Glucose 64-71 insulin Homo sapiens 9-16 119699-1 1979 A glucose-controlled insulin infusion system (Biostator) was used to determine patient insulin requirement for clinical evaluation of a portable pump system (technical development by Siemens AG). Glucose 2-9 insulin Homo sapiens 21-28 119699-1 1979 A glucose-controlled insulin infusion system (Biostator) was used to determine patient insulin requirement for clinical evaluation of a portable pump system (technical development by Siemens AG). Glucose 2-9 insulin Homo sapiens 87-94 387567-3 1979 In patients with chronic pancreatitis the plasma insulin response to oral glucose and intravenous arginine was reduced. Glucose 74-81 insulin Homo sapiens 49-56 395069-0 1979 Insulin treatment and state of control before, during, and after connection to a glucose controlled insulin infusion system (Biostator). Glucose 81-88 insulin Homo sapiens 100-107 395070-0 1979 Use of glucose-controlled insulin infusion system for improvement of subcutaneous insulin regimen. Glucose 7-14 insulin Homo sapiens 26-33 395070-0 1979 Use of glucose-controlled insulin infusion system for improvement of subcutaneous insulin regimen. Glucose 7-14 insulin Homo sapiens 82-89 395072-1 1979 Using a Biostator glucose-controlled insulin infusion system to monitor blood glucose during surgery, we have shown that both nondiabetic and diabetic patients have a tendency towards hyperglycemia during surgery. Glucose 18-25 insulin Homo sapiens 37-44 395072-5 1979 The biostator glucose-controlled insulin infusion system could be used in feedback mode as an apparently safe and effective means of controlling blood glucose during surgery on diabetic patients. Glucose 14-21 insulin Homo sapiens 33-40 395075-4 1979 According to our results, pregnancy complicated by diabetes can be foreseen as one of the main applications of a glucose-controlled insulin infusion system. Glucose 113-120 insulin Homo sapiens 132-139 395082-6 1979 Knowing the daily insulin dosage as calculated from the Biostator, normal blood glucose levels can be achieved with a fixed profile of insulin given by a portable pump. Glucose 80-87 insulin Homo sapiens 18-25 395082-6 1979 Knowing the daily insulin dosage as calculated from the Biostator, normal blood glucose levels can be achieved with a fixed profile of insulin given by a portable pump. Glucose 80-87 insulin Homo sapiens 135-142 395083-0 1979 Comparison of a perfusion syringe (Mill Hill Infusor) and a glucose-controlled insulin infusion system in the regulation of diabetes mellitus. Glucose 60-67 insulin Homo sapiens 79-86 395083-1 1979 In a preliminary study, three unstable, juvenile diabetics were first connected to a glucose-controlled insulin infusion system (Biostator), and subsequently to a portable infusor (Mill Hill Infuser) for continuous subcutaneous insulin application. Glucose 85-92 insulin Homo sapiens 104-111 395087-1 1979 A closed-loop glucose controlled insulin infusion system was developed, consisting of elements for continuous blood glucose analysis, a computer control system, and infusion systems. Glucose 14-21 insulin Homo sapiens 33-40 395087-1 1979 A closed-loop glucose controlled insulin infusion system was developed, consisting of elements for continuous blood glucose analysis, a computer control system, and infusion systems. Glucose 116-123 insulin Homo sapiens 33-40 395094-9 1979 We conclude from these data that early increases in insulin infusion rates followed by a rapid decrease seem to reduce insulin requirements after glucose ingestion. Glucose 146-153 insulin Homo sapiens 52-59 395094-9 1979 We conclude from these data that early increases in insulin infusion rates followed by a rapid decrease seem to reduce insulin requirements after glucose ingestion. Glucose 146-153 insulin Homo sapiens 119-126 395095-7 1979 The Concentration of glycosylated hemoglobin, markedly higher than normally before the connection with AEP, showed a slight but significant decrease during glucose-controlled insulin infusion. Glucose 156-163 insulin Homo sapiens 175-182 395098-7 1979 The inhibition of the glucose-stimulated insulin secretion was examined in group II by clamping BG at a raised level. Glucose 22-29 insulin Homo sapiens 41-48 395098-8 1979 The stimulation of insulin secretion by glucose during insulin infusion was examined in group III by stepwise BG rises from the fasting level. Glucose 40-47 insulin Homo sapiens 19-26 395098-8 1979 The stimulation of insulin secretion by glucose during insulin infusion was examined in group III by stepwise BG rises from the fasting level. Glucose 40-47 insulin Homo sapiens 55-62 395098-15 1979 We conclude that exogenous insulin inhibits beta cell secretion, depending on the BG level, the mode of glucose stimulation, and the time relation between glucose and insulin application. Glucose 104-111 insulin Homo sapiens 27-34 395098-15 1979 We conclude that exogenous insulin inhibits beta cell secretion, depending on the BG level, the mode of glucose stimulation, and the time relation between glucose and insulin application. Glucose 155-162 insulin Homo sapiens 27-34 393648-1 1979 Evidence of deficient glucose-stimulated early insulin release despite hyperinsulinemia. Glucose 22-29 insulin Homo sapiens 47-54 393648-3 1979 SERT measures the fall in fasting blood glucose after a short infusion of insulin, performed so as to simulate the early phase of insulin release to the acute stimulus of an intravenous glucose load (ERex). Glucose 40-47 insulin Homo sapiens 74-81 422700-0 1979 Hyperglycemia per se (insulin and glucagon withdrawn) can inhibit hepatic glucose production in man. Glucose 74-81 insulin Homo sapiens 22-29 422700-6 1979 These data in normal man indicate that hyperglycemia per se with insulin and glucagon acutely withdrawn can suppress splanchnic glucose production but does not induce net splanchnic glucose storage. Glucose 128-135 insulin Homo sapiens 65-72 759995-4 1979 Insulin always rose significantly with increasing scattering of the individual values with higher glucose loads. Glucose 98-105 insulin Homo sapiens 0-7 156932-0 1979 Plasma insulin, carbohydrate, and free fatty acid changes in newly born infants of diabetic and non-diabetic mothers after loading with glucose, fructose, and galactose. Glucose 136-143 insulin Homo sapiens 7-14 156932-5 1979 The highest insulin response with difference between IDM and IHM occurred after loading with glucose. Glucose 93-100 insulin Homo sapiens 12-19 231295-4 1979 Hyperinsulinism was established by determinations of blood glucose and plasma insulin in the fasting state. Glucose 59-66 insulin Homo sapiens 5-12 394311-2 1979 There was a large day-to-day variation in the predialysis blood glucose levels, which it was difficult to control by adjusting the insulin dose. Glucose 64-71 insulin Homo sapiens 131-138 723761-3 1978 Insulin requirement had been previously determined by means of an artifical beta-cell (Glucose Controlled Insulin Infusion System). Glucose 87-94 insulin Homo sapiens 0-7 723761-3 1978 Insulin requirement had been previously determined by means of an artifical beta-cell (Glucose Controlled Insulin Infusion System). Glucose 87-94 insulin Homo sapiens 106-113 367155-4 1978 Insulin and C-peptide measurements during glucose tolerance tests suggest abnormal beta cell function and possibly insulin resistance as causes for this abnormality. Glucose 42-49 insulin Homo sapiens 0-7 367155-4 1978 Insulin and C-peptide measurements during glucose tolerance tests suggest abnormal beta cell function and possibly insulin resistance as causes for this abnormality. Glucose 42-49 insulin Homo sapiens 12-21 367155-4 1978 Insulin and C-peptide measurements during glucose tolerance tests suggest abnormal beta cell function and possibly insulin resistance as causes for this abnormality. Glucose 42-49 insulin Homo sapiens 115-122 747892-0 1978 The effect of serum ionized calcium elevation on somatostatin inhibition of glucose-induced insulin release in humans. Glucose 76-83 insulin Homo sapiens 92-99 747892-1 1978 The effect of somatostatin on the insulin response to an acute intravenous glucose load was studied in five normal subjects before and after induction hypercalcaemia. Glucose 75-82 insulin Homo sapiens 34-41 747892-2 1978 In the normocalcaemic state, the insulin response to glucose was depressed by somatostatin. Glucose 53-60 insulin Homo sapiens 33-40 747892-3 1978 In the hypercalcaemic state, insulin responses to glucose in the presence of somatostatin, were partially restored and appeared to be related to the level of increment of serum ionized calcium. Glucose 50-57 insulin Homo sapiens 29-36 747892-4 1978 It is concluded that, in the human being, hypercalcaemia and somatostatin have opposite actions on glucose-stimulated insulin secretion. Glucose 99-106 insulin Homo sapiens 118-125 105908-2 1978 The glycaemic and insulinaemic response to oral glucose was measured at baseline, after 1 week and at 3 months, and the results related to adipocyte insulin receptors estimated from fat biopsies taken on each occasion and to the weight lost. Glucose 48-55 insulin Homo sapiens 18-25 105908-3 1978 Adipocyte insulin binding was found to be significantly inversely correlated with the insulinaemic response to oral glucose (r = -0.54, P less than 0.05), an inverse relationship maintained even after weight loss had been achieved and displayed within as well as between subjects. Glucose 116-123 insulin Homo sapiens 10-17 729892-2 1978 The acute insulin responses to intravenous glucose and tolbutamide were studied serially in middle aged subjects with a wide spectrum of glucose tolerance. Glucose 43-50 insulin Homo sapiens 10-17 729892-4 1978 In normal weight patients, insulin response to glucose, subnormal in chemical diabetes, was almost absent when fasting blood glucose was elevated. Glucose 47-54 insulin Homo sapiens 27-34 729892-4 1978 In normal weight patients, insulin response to glucose, subnormal in chemical diabetes, was almost absent when fasting blood glucose was elevated. Glucose 125-132 insulin Homo sapiens 27-34 751797-0 1978 Insulin delivery rate in response to glucose infusion in normal and diabetic subjects. Glucose 37-44 insulin Homo sapiens 0-7 751797-1 1978 The insulin delivery rates were estimated in 8 normal and 8 diabetic subjects from the results of peripheral insulin response to a single bolus iv injection of glucose, taking account of fractionally removed insulin. Glucose 160-167 insulin Homo sapiens 4-11 751797-1 1978 The insulin delivery rates were estimated in 8 normal and 8 diabetic subjects from the results of peripheral insulin response to a single bolus iv injection of glucose, taking account of fractionally removed insulin. Glucose 160-167 insulin Homo sapiens 109-116 751797-1 1978 The insulin delivery rates were estimated in 8 normal and 8 diabetic subjects from the results of peripheral insulin response to a single bolus iv injection of glucose, taking account of fractionally removed insulin. Glucose 160-167 insulin Homo sapiens 109-116 751797-2 1978 The delivered insulin response to 0.5 g/Kg body weight of glucose injection was biphasic in normal and diabetic subjects. Glucose 58-65 insulin Homo sapiens 14-21 751797-6 1978 The insulin delivery rates during the first and second phases fitted by the same line to the glucose concentration at each period. Glucose 93-100 insulin Homo sapiens 4-11 751797-7 1978 This suggests that a common glucoreceptor or glucose-mediated signal of the insulin response might exist during both phases. Glucose 45-52 insulin Homo sapiens 76-83 739270-6 1978 Forearm insulin infusion demonstrated normal stimulation of muscle glucose uptake in the patients with centronuclear myopathy and neurogenic atrophy in contrast to the markedly diminished response to insulin seen in the patient with myotonic dystrophy. Glucose 67-74 insulin Homo sapiens 8-15 581509-0 1978 Effects of adrenergic stimulating and blocking agents on glucose-induced insulin responses in human thyrotoxicosis. Glucose 57-64 insulin Homo sapiens 73-80 723636-3 1978 The drop in plasma glucose level that occurred during the fast was associated with a drop in plasma insulin level. Glucose 19-26 insulin Homo sapiens 100-107 723646-2 1978 Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. Glucose 361-368 insulin Homo sapiens 56-63 723646-2 1978 Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. Glucose 361-368 insulin Homo sapiens 138-145 723646-2 1978 Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. Glucose 361-368 insulin Homo sapiens 138-145 723646-2 1978 Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. Glucose 361-368 insulin Homo sapiens 138-145 723646-2 1978 Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. Glucose 361-368 insulin Homo sapiens 138-145 82091-1 1978 It is suggested that hepatic uptake of orally ingested glucose depends not only on insulin secretion but also on the release of a gastrointestinal factor which mediates insulin action on the liver. Glucose 55-62 insulin Homo sapiens 83-90 102400-2 1978 Standard and constant rates of insulin and dextrose infusion resulted in satisfactory control of blood glucose concentrations during labour, after major surgery, and in patients recovering from ketoacidosis (average insulin infusion rates 1, 2, and 3 U/h respectively). Glucose 103-110 insulin Homo sapiens 31-38 111810-3 1978 The present paper describes a new test using normal isolated pancreatic cells as target cells and evaluating the effect of activated or non-activated macrophages on the insulin secretion response to glucose stimulation. Glucose 199-206 insulin Homo sapiens 169-176 360062-4 1978 Insulin-mediated glucose uptake (determined in the adult patient) was 25 per cent greater than mean control levels. Glucose 17-24 insulin Homo sapiens 0-7 360062-6 1978 Insulin-mediated glucose uptake fell to 30 per cent below the mean control rate. Glucose 17-24 insulin Homo sapiens 0-7 719912-3 1978 The insulin response to such meals was correlated positively with the increment in glucose but reduction of protein content below 8 g caused a signficant reduction in the increment in plasma insulin per unit increase in plasma glucose. Glucose 83-90 insulin Homo sapiens 4-11 719912-3 1978 The insulin response to such meals was correlated positively with the increment in glucose but reduction of protein content below 8 g caused a signficant reduction in the increment in plasma insulin per unit increase in plasma glucose. Glucose 227-234 insulin Homo sapiens 4-11 719912-3 1978 The insulin response to such meals was correlated positively with the increment in glucose but reduction of protein content below 8 g caused a signficant reduction in the increment in plasma insulin per unit increase in plasma glucose. Glucose 227-234 insulin Homo sapiens 191-198 744568-0 1978 Effect of alrestatin sodium on glucose-stimulated insulin secretion in the fasted anaesthetized rat. Glucose 31-38 insulin Homo sapiens 50-57 744568-3 1978 However, in response to an intravenous glucose tolerance test, plasma insulin levels were significantly increased above the values observed in the animal during a control test. Glucose 39-46 insulin Homo sapiens 70-77 744568-7 1978 It is suggested that alrestatin may play a useful role in the therapy of diabetes mellitus since it can augment insulin secretion when glucose is administered to a fasted animal in which the acute insulin response has been shown to be like that of the human diabetic, and in addition, can lower arginine-stimulated glucagon secretion in the animal, the latter being a model of an action that is observed in the human diabetic. Glucose 135-142 insulin Homo sapiens 112-119 400737-2 1978 Prior to the infusion of glucose, insulin administration resulted in stable levels of plasma glucose (76 +/- 8 mg/dl) and glucose output (1.9 +/- 0.1 mg kg-1min-1). Glucose 93-100 insulin Homo sapiens 34-41 400737-2 1978 Prior to the infusion of glucose, insulin administration resulted in stable levels of plasma glucose (76 +/- 8 mg/dl) and glucose output (1.9 +/- 0.1 mg kg-1min-1). Glucose 93-100 insulin Homo sapiens 34-41 400737-3 1978 The addition of glucose produced a 2-3 fold rise in plasma glucose and a prompt fall in glucose output to 0.2-0.4 mg kg-1min-1, despite the unchanged rate of insulin infusion and the absence of a reduction in plasma glucagon or catecholamines. Glucose 16-23 insulin Homo sapiens 158-165 400737-5 1978 We conclude that in the presence of basal insulin levels hyperglycemia inhibits glucose output independent of a rise in insulin or a fall in anti-insulin hormones. Glucose 80-87 insulin Homo sapiens 42-49 718857-4 1978 The des(pentapeptide B(1-5))-insulin possesses a potency of 1.2 IU/mg when assayed by the glucose-oxidation method in isolated fat cells and 3.7 IU/mg by the radioimmunoassay technique. Glucose 90-97 insulin Homo sapiens 29-36 365174-0 1978 The stimulus-secretion coupling of glucose-induced insulin release. Glucose 35-42 insulin Homo sapiens 51-58 365174-3 1978 In isolated pancreatic islets, pyruvate causes a shift to the left of the sigmoidal curve relating the rate of insulin release to the ambient glucose concentration. Glucose 142-149 insulin Homo sapiens 111-118 696859-4 1978 In the presence of a glucose concentration of 7.5 mmol/liter, VIP enhanced insulin release without affecting glucagon release. Glucose 21-28 insulin Homo sapiens 75-82 756709-2 1978 As shown in the literature, glucose led to a slight sugar increase at 60", a marked increase in insulin at 60", and a pronounced fall in NEFA at 120". Glucose 28-35 insulin Homo sapiens 96-103 687419-6 1978 They also showed significantly higher growth hormone and lower blood glucose levels on the day of intermediate insulin plus regular insulin than on the day of intermediate insulin. Glucose 69-76 insulin Homo sapiens 111-118 214343-0 1978 Initial lag-phase in the action of insulin on glucose transport and cAMP levels in fat cells. Glucose 46-53 insulin Homo sapiens 35-42 724682-1 1978 Immunoreactive insulin level proved to be elevated in the blood serum on fasting stomach and at various periods after glucose administration in patients with cirrhosis of the liver with normal glucose tolerance. Glucose 118-125 insulin Homo sapiens 15-22 724682-1 1978 Immunoreactive insulin level proved to be elevated in the blood serum on fasting stomach and at various periods after glucose administration in patients with cirrhosis of the liver with normal glucose tolerance. Glucose 193-200 insulin Homo sapiens 15-22 365176-7 1978 At 20mM-pyruvate, release of prelabelled proinsulin and insulin and incorporation of [3H]leucine into proinsulin reached values approximately half of those obtained with 20mM-glucose. Glucose 174-182 insulin Homo sapiens 102-112 707588-5 1978 The insulin requirements needed to achieve optimal glucose control with the Biostator were highly variable (range, 20 to 157 U. per 24 hours) but very similar to those previously calculated to provide optimal control by conventional means. Glucose 51-58 insulin Homo sapiens 4-11 707340-2 1978 In the patients the fractional disappearance rate of glucose was significantly reduced, basal immunoreactive insulin was significantly raised, and while the early immunoreactive insulin response to glucose was similar in patients and controls, the late response was increased. Glucose 198-205 insulin Homo sapiens 178-185 707341-2 1978 Unlike glucose dialysis, glucose-free dialysis caused marked decreases in blood levels of glucose, insulin, lactate, and pyruvate along with profound increases in acetoacetate and beta-hydroxybutyrate. Glucose 25-32 insulin Homo sapiens 99-106 707341-2 1978 Unlike glucose dialysis, glucose-free dialysis caused marked decreases in blood levels of glucose, insulin, lactate, and pyruvate along with profound increases in acetoacetate and beta-hydroxybutyrate. Glucose 25-32 insulin Homo sapiens 99-106 6988933-0 1980 Serum insulin response to oral glucose load during a dietary intervention trial in healthy coronary high risk men: the Oslo study. Glucose 31-38 insulin Homo sapiens 6-13 747986-0 1978 The response of glucose, insulin and FFA to intravenous glucose and glucagon in elderly subjects in the course of morning and afternoon tests. Glucose 56-63 insulin Homo sapiens 25-32 700259-3 1978 Model and clinical testing have focused particularly on the fast phase of insulin response to vascular glucose. Glucose 103-110 insulin Homo sapiens 74-81 700259-6 1978 Variable dosage glucose studies suggest that the amount of insulin released during the fast phase rather than the insulin release rate is regulated by the glucose level. Glucose 16-23 insulin Homo sapiens 59-66 747986-1 1978 The response of glucose, FFA and immunoreactive insulin to intravenous glucose and glucagon was examined in 6 apparently healthy subjects aged 67-77 years at 08(00) and 18(00) with a 3 day interval. Glucose 71-78 insulin Homo sapiens 48-55 357890-3 1978 High concentrations of the drug (0.3 mM or more) fail to affect Ba2+-induced insulin secretion but inhibit glucose-stimulated proinsulin biosynthesis, 45Ca net uptake and insulin release. Glucose 107-114 insulin Homo sapiens 126-136 364009-8 1978 However, under suitable conditions, the glucose-induced secondary rise in 45calcium efflux is not totally suppressed whilst insulin release is totally abolished. Glucose 40-47 insulin Homo sapiens 124-131 700259-6 1978 Variable dosage glucose studies suggest that the amount of insulin released during the fast phase rather than the insulin release rate is regulated by the glucose level. Glucose 155-162 insulin Homo sapiens 59-66 701484-4 1978 The effect of an intrabrachial arterial insulin infusion (100 mu U/kg per min) on glucose uptake was determined in six cases of myotonic dystrophy, six normal subjects, and in seven disease control subjects with myotonia or wasting from other disorders. Glucose 82-89 insulin Homo sapiens 40-47 701484-7 1978 After 25 min of intra-arterial insulin, the mean peak muscle glucose uptake in myotonic dystrophy was 2.54 +/- 0.54 mu mol/min per 100 ml forearm compared to 5.24 +/- 0.86 mu mol/min per 100 ml for disease controls (P is less than 0.05). Glucose 61-68 insulin Homo sapiens 31-38 750568-0 1978 Immuno reactive insulin response to glucose stimulus in prediabetics. Glucose 36-43 insulin Homo sapiens 16-23 356269-1 1978 Perifusion experiments have shown that there is a discharge of inorganic phosphate into the medium when insulin secretion from isolated islets is stimulated by glucose. Glucose 160-167 insulin Homo sapiens 104-111 705237-5 1978 Glucose loading resulted in elevated insulin levels and a minor rise in blood glucose level was seen in the patients compared to the control subjects. Glucose 0-7 insulin Homo sapiens 37-44 705576-0 1978 Glucose kinetics and responsiveness to insulin in the rat injured by burn. Glucose 0-7 insulin Homo sapiens 39-46 283423-2 1978 Euglycemic hyperinsulinemia [induced by a priming plus continuous infusion of insulin resulting in plasma insulin levels of 400-1200 muunits (international)/ml and a variable glucose infusion] caused a 5- to 6-fold increase above basal in total glucose turnover. Glucose 175-182 insulin Homo sapiens 16-23 283423-2 1978 Euglycemic hyperinsulinemia [induced by a priming plus continuous infusion of insulin resulting in plasma insulin levels of 400-1200 muunits (international)/ml and a variable glucose infusion] caused a 5- to 6-fold increase above basal in total glucose turnover. Glucose 175-182 insulin Homo sapiens 78-85 283423-6 1978 After the oral glucose, net splanchnic glucose uptake increased to values 6-fold higher than with intravenous glucose despite unchanged plasma glucose levels and plasma insulin concentrations well below those observed in the studies with euglycemic hyperinsulinemia. Glucose 15-22 insulin Homo sapiens 169-176 283423-9 1978 These findings suggest that orally consumed glucose causes the release of a gastrointestinal factor that enhances insulin-mediated glucose uptake by the liver. Glucose 44-51 insulin Homo sapiens 114-121 283423-9 1978 These findings suggest that orally consumed glucose causes the release of a gastrointestinal factor that enhances insulin-mediated glucose uptake by the liver. Glucose 131-138 insulin Homo sapiens 114-121 361435-0 1978 Glucose stimulation of the proinsulin synthesis in isolated pancreatic islets without increasing amount of proinsulin mRNA. Glucose 0-7 insulin Homo sapiens 27-37 28664-2 1978 In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Glucose 71-78 insulin Homo sapiens 60-67 567493-12 1978 RL-PR-C hepatocytes responded to insulin binding by an increase in glycogen synthesis from glucose. Glucose 91-98 insulin Homo sapiens 33-40 725173-0 1978 [Objective analysis of blood sugar and insulin by the oral glucose tolerance test]. Glucose 59-66 insulin Homo sapiens 39-46 686547-4 1978 Insulin or pharmacologic doses of desoxycorticosterone acetate eliminated the glucose-induced hyperkalemia. Glucose 78-85 insulin Homo sapiens 0-7 28664-2 1978 In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Glucose 71-78 insulin Homo sapiens 162-169 28664-2 1978 In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Glucose 90-97 insulin Homo sapiens 60-67 28664-2 1978 In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Glucose 90-97 insulin Homo sapiens 162-169 709899-2 1978 In each individual, insulin secretion during an intravenous glucose tolerance test was greater when the plasma calcium was higher. Glucose 60-67 insulin Homo sapiens 20-27 81157-2 1978 Plasma glucose decreased from a mean value of 250 mg/100 ml to 117 mg/100 ml during the first 85 min after insulin. Glucose 7-14 insulin Homo sapiens 107-114 99098-2 1978 Insulin resistance, which develops in sepsis, decreases glucose utilization, but plasma insulin levels are sufficiently elevated to prevent lipolysis, resulting in a further energy deficit. Glucose 56-63 insulin Homo sapiens 0-7 700280-0 1978 Characterisation of the effect of intravenous infusion of glucose and tolbutamide on the insulin delivery rate in man. Glucose 58-65 insulin Homo sapiens 89-96 709899-4 1978 These findings could be explained by the suggestion that insulin secretion provoked by orally administered glucose is enhanced by gut hormones which may stimulate insulin secretion by a mechanism independent of extracellular calcium. Glucose 107-114 insulin Homo sapiens 57-64 101402-3 1978 There was no significant difference between serum insulin concentrations on the two doses, however, serum insulin/blood glucose ratio was higher during the larger dose of glibenclamide. Glucose 120-127 insulin Homo sapiens 106-113 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 78-85 insulin Homo sapiens 94-101 709899-4 1978 These findings could be explained by the suggestion that insulin secretion provoked by orally administered glucose is enhanced by gut hormones which may stimulate insulin secretion by a mechanism independent of extracellular calcium. Glucose 107-114 insulin Homo sapiens 163-170 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 78-85 insulin Homo sapiens 144-151 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 169-176 insulin Homo sapiens 94-101 400725-4 1978 Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. Glucose 9-16 insulin Homo sapiens 69-76 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 169-176 insulin Homo sapiens 144-151 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 169-176 insulin Homo sapiens 94-101 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 169-176 insulin Homo sapiens 144-151 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 169-176 insulin Homo sapiens 94-101 700281-1 1978 In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. Glucose 169-176 insulin Homo sapiens 144-151 710679-2 1978 Insulin responses to glucose during PGE1 infusion (0.2 microgram/Kg/min) were significantly lower than in control infusions (p less than 0.001 at 2, 5, 10 and 15 min). Glucose 21-28 insulin Homo sapiens 0-7 309427-0 1978 Inhibition of insulin action on glucose uptake into skeletal muscle by a Kallikrein-trypsin inhibitor. Glucose 32-39 insulin Homo sapiens 14-21 400725-4 1978 Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. Glucose 9-16 insulin Homo sapiens 107-114 400727-1 1978 To investigate the role of gastric inhibitory polypeptide (GIP) in the hypersecretion of glucose-stimulated insulin release in duodenal ulcer disease, serum glucose, insulin, and immunoreactive GIP (IR-GIP) were measured in 18 healthy subjects and 10 duodenal ulcer patients after glucose ingestion. Glucose 89-96 insulin Homo sapiens 108-115 400727-5 1978 The exaggerated insulin release to oral glucose may be due to the synergistic action of higher blood glucose and greater IR-GIP release in this disease. Glucose 40-47 insulin Homo sapiens 16-23 400727-5 1978 The exaggerated insulin release to oral glucose may be due to the synergistic action of higher blood glucose and greater IR-GIP release in this disease. Glucose 101-108 insulin Homo sapiens 16-23 359352-0 1978 Insulin action on glucose uptake into skeletal muscle: inhibition of endogenous biosynthesis of prostaglandins. Glucose 18-25 insulin Homo sapiens 0-7 735397-0 1978 Serum insulin levels following intravenous tolbutamide and subsequent oral glucose loading in Nigerians. Glucose 75-82 insulin Homo sapiens 6-13 279910-1 1978 Exposure of adipocytes to antibodies to the insulin receptor results in a blockade of (125)I-labeled insulin binding, stimulation of glucose oxidation, and many more insulin-like effects. Glucose 133-140 insulin Homo sapiens 44-51 698607-0 1978 A glucose-controlled insulin infusion system for diabetic women during labour. Glucose 2-9 insulin Homo sapiens 21-28 698607-1 1978 A glucose-controlled insulin infusion system was used to control blood glucose concentration during labour or caesarean section in six insulin-dependent diabetics. Glucose 2-9 insulin Homo sapiens 21-28 359390-7 1978 This may be due, in part, to a decrease in glucose-induced insulin release during the first thirty minutes following oral glucose. Glucose 43-50 insulin Homo sapiens 59-66 679460-0 1978 Development and evaluation of a glucose analyzer for a glucose controlled insulin infusion system ((Biostator). Glucose 32-39 insulin Homo sapiens 74-81 679460-0 1978 Development and evaluation of a glucose analyzer for a glucose controlled insulin infusion system ((Biostator). Glucose 55-62 insulin Homo sapiens 74-81 679460-1 1978 The Glucose-Controlled Insulin Infusion System (Biostator) is a modular, computerized, feedback control system for dynamic control of blood glucose concentrations in diabetics. Glucose 4-11 insulin Homo sapiens 23-30 359390-7 1978 This may be due, in part, to a decrease in glucose-induced insulin release during the first thirty minutes following oral glucose. Glucose 122-129 insulin Homo sapiens 59-66 710371-3 1978 Insulin secretion in response to the oral glucose administration was exaggerated in 3 patients, while it was supressed in 2 patients who had severely impaired glucose tolerance. Glucose 42-49 insulin Homo sapiens 0-7 353075-17 1978 The surprising apparent lack of consistency in the change in beta cell response postdialysis is explained by the strong inverse correlation between beta cell sensitivity to glucose and tissue sensitivity to insulin (r = -0.920; P < 0.001). Glucose 173-180 insulin Homo sapiens 207-214 98446-0 1978 [Insulin concentration in polytraumatized patients during infusion of glucose, fructose and sorbitol]. Glucose 70-77 insulin Homo sapiens 1-8 98446-1 1978 Serum insulin concentration was measured during infusion of glucose, fructose or sorbitol for several days in polytraumatized patients. Glucose 60-67 insulin Homo sapiens 6-13 98446-9 1978 However, in many cases glucose can be administered only if insulin is given additionally. Glucose 23-30 insulin Homo sapiens 59-66 680420-0 1978 The relationship of insulin response to a glucose stimulus over a wide range of glucose tolerance. Glucose 42-49 insulin Homo sapiens 20-27 27696-5 1978 The study indicates that insulin administration to diabetics with high blood glucose levels may lead to transient decreases in red cell 2,3-DPG and in oxygen-releasing capacity of the red blood cells. Glucose 77-84 insulin Homo sapiens 25-32 679944-4 1978 Exercise with glucose ingestion blunted almost completely the normal insulin response to glucose. Glucose 14-21 insulin Homo sapiens 69-76 679944-4 1978 Exercise with glucose ingestion blunted almost completely the normal insulin response to glucose. Glucose 89-96 insulin Homo sapiens 69-76 400719-6 1978 The circadian variation in insulin binding was grossly parallel to the well known variations in insulin sensitivity and glucose tolerance during the day. Glucose 120-127 insulin Homo sapiens 27-34 668726-8 1978 A statistically significant correlation between glucose and insulin is only demonstrable in the maternal blood. Glucose 48-55 insulin Homo sapiens 60-67 400133-7 1978 When fed as pure substances to fasted subjects, the nonglucose carbohydrate nutritive sweeteners, fructose, xylitol, and sorbitol, are absorbed relatively slowly and produce less postprandial hyperglycemia and insulin response than sucrose or glucose. Glucose 55-62 insulin Homo sapiens 210-217 699935-4 1978 A diabetic-like insulin response after 50.0 g oral glucose intake was found in 10 out of 26 examined patients. Glucose 51-58 insulin Homo sapiens 16-23 690322-1 1978 Insulin glucose therapy can correct hyponatraemia and renal sodium retention in burns, sepsis and circulatory failure. Glucose 8-15 insulin Homo sapiens 0-7 658622-2 1978 Adult-onset diabetics have markedly diminished or absent acute insulin responses to glucose that can be partially restored by sodium salicylate infusion. Glucose 84-91 insulin Homo sapiens 63-70 355075-3 1978 For similar means of fasting plasma glucose, basal plasma insulin mean was significantly higher during thyrotoxicosis. Glucose 36-43 insulin Homo sapiens 58-65 355075-5 1978 During CGI, early insulin responses to similar plasma glucose increments, were comparable for both hyper and euthyroid subjects. Glucose 54-61 insulin Homo sapiens 18-25 355075-7 1978 These results suggest the presence of an insulin-resistant state in hyperthyroidism which may either disappear during a chronic glucose infusion and/or be accompanied by a deficient late glucose-induced insulin release. Glucose 128-135 insulin Homo sapiens 41-48 659629-18 1978 However, in five of seven subjects given insulin whose blood glucose concentration rose by 20 mg/dl or more after oral glucose, there was an increase in plasma insulin concentration associated with the elevation in IR-GIP. Glucose 61-68 insulin Homo sapiens 41-48 350903-4 1978 The amount of glucose infused is a measure of tissue sensitivity to insulin and averaged 285+/-15 mg/m(2) per min in controls compared to 136+/-13 mg/m(2) per min in obese subjects (P <0.001). Glucose 14-21 insulin Homo sapiens 68-75 400712-4 1978 The increase in insulin binding during exercise correlated with the fall in plasma glucose but not with the decrease in plasma insulin or increase in blood ketones. Glucose 83-90 insulin Homo sapiens 16-23 229148-3 1978 Fasting serum insulin levels were consistently depressed, and in two of the cases remained low even after an oral glucose load. Glucose 114-121 insulin Homo sapiens 14-21 400713-0 1978 Glucose-lowering effect of insulin by different routes in obese and lean nonketotic diabetic patients. Glucose 0-7 insulin Homo sapiens 27-34 659629-18 1978 However, in five of seven subjects given insulin whose blood glucose concentration rose by 20 mg/dl or more after oral glucose, there was an increase in plasma insulin concentration associated with the elevation in IR-GIP. Glucose 61-68 insulin Homo sapiens 160-167 400713-8 1978 After iv insulin, plasma glucose at 30, 40, 50, and 60 min was significantly lower than after im and sc insulin (P less than 0.001), but over the 4-h study period, the glucose-lowering effect and the area under the curves for glucose response to IRI by the three routes were the same in both lean and obese diabetic subjects. Glucose 25-32 insulin Homo sapiens 9-16 659629-18 1978 However, in five of seven subjects given insulin whose blood glucose concentration rose by 20 mg/dl or more after oral glucose, there was an increase in plasma insulin concentration associated with the elevation in IR-GIP. Glucose 119-126 insulin Homo sapiens 41-48 400713-12 1978 These studies demonstrated that although iv injection of insulin produces a more rapid initial decline in plasma glucose, the overall glucose-lowering effect by insulin given iv, im or sc is similar in nonketotic lean or obese diabetic subjects. Glucose 113-120 insulin Homo sapiens 57-64 400713-12 1978 These studies demonstrated that although iv injection of insulin produces a more rapid initial decline in plasma glucose, the overall glucose-lowering effect by insulin given iv, im or sc is similar in nonketotic lean or obese diabetic subjects. Glucose 134-141 insulin Homo sapiens 161-168 659629-18 1978 However, in five of seven subjects given insulin whose blood glucose concentration rose by 20 mg/dl or more after oral glucose, there was an increase in plasma insulin concentration associated with the elevation in IR-GIP. Glucose 119-126 insulin Homo sapiens 160-167 659629-19 1978 Thus, the effect of glucose-released IR-GIP on insulin secretion is dependent upon the presence of some degree of hyper-glycemia and is not inhibited in the presence of marked hyperinsulinemia. Glucose 20-27 insulin Homo sapiens 47-54 659634-12 1978 In nondiabetic azotemic subjects, mean fasting glucose and immunoreactive insulin levels were increased 24.3% (P = 0.005) and 130% (P = 0.046), respectively.These results in patients with chronic renal failure demonstrate (a) increased glucose production and utilization, (b) increased gluconeogenesis from alanine, (c) increased alanine production and utilization, and (d) a relative impairment to glucose disposal. Glucose 236-243 insulin Homo sapiens 74-81 78210-0 1978 Insulin-reaction test for diagnosis of low renal threshold for glucose in African diabetics. Glucose 63-70 insulin Homo sapiens 0-7 572898-3 1978 Effects of insulin on fetal growth may be direct influences on cell proliferation or insulin may indirectly affect growth through stimulation of glucose and amino acid uptake into fetal tissues. Glucose 145-152 insulin Homo sapiens 11-18 661568-2 1978 Somatostatin inhibited glucose-stimulated insulin release and reduced plasma glucagon by 50%--65%. Glucose 23-30 insulin Homo sapiens 42-49 661568-5 1978 The degree of late glucose intolerance was inversely related to postglucose plasma insulin concentrations (p less than 0.01). Glucose 19-26 insulin Homo sapiens 83-90 277948-8 1978 Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient"s insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system. Glucose 17-24 insulin Homo sapiens 140-147 277948-8 1978 Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient"s insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system. Glucose 17-24 insulin Homo sapiens 140-147 277948-8 1978 Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient"s insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system. Glucose 283-290 insulin Homo sapiens 140-147 277948-8 1978 Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient"s insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system. Glucose 283-290 insulin Homo sapiens 140-147 27109-4 1978 In men serum insulin-, GH- and total corticoid levels correlate positive significant with glucose and cholesterol levels, relative body weight and blood pressure, which possibly shows, that these hormones may play a role in the development of degenerative heart and blood vessel diseases. Glucose 90-97 insulin Homo sapiens 13-20 572898-3 1978 Effects of insulin on fetal growth may be direct influences on cell proliferation or insulin may indirectly affect growth through stimulation of glucose and amino acid uptake into fetal tissues. Glucose 145-152 insulin Homo sapiens 85-92 580833-1 1978 In a family with maturity-onset type of diabetes mellitus inherited as a dominant, autosomal trait (MODY), the HLA genotypes were compared with the glucose tolerance and the plasma insulin response to oral glucose. Glucose 206-213 insulin Homo sapiens 181-188 580833-2 1978 In the members with impaired glucose tolerance, the plasma insulin response was of the insulino-tardic type, while those with normal or borderline glucose tolerance had a normal plasma insulin response. Glucose 29-36 insulin Homo sapiens 59-66 580833-2 1978 In the members with impaired glucose tolerance, the plasma insulin response was of the insulino-tardic type, while those with normal or borderline glucose tolerance had a normal plasma insulin response. Glucose 29-36 insulin Homo sapiens 87-94 556385-1 1978 The effect of 1 week clofibrate administration on glucose and insulin responses to oral glucose and to intravenous tolbutamide was evaluated in 21 patients with mild maturity-onset diabetes (fasting plasma glucose 108-152 mg/100 ml). Glucose 88-95 insulin Homo sapiens 62-69 658613-9 1978 This functional abnormality correlates directly with the fasting glucose and is reversed by insulin treatment. Glucose 65-72 insulin Homo sapiens 92-99 556385-2 1978 After treatment, oral glucose tolerance and hypoglycaemic effect of tolbutamide were significantly improved; plasma insulin response was reduced after glucose and unmodified after tolbutamide; fasting plasma glucose was also significantly reduced. Glucose 151-158 insulin Homo sapiens 116-123 350677-2 1978 The release of C-peptide was measured after a (1) normal intravenous glucose tolerance test, (2) a double glucose tolerance test, (3) an arginine infusion, and (4) after an intravenous glucose tolerance test followed by an arginine infusion. Glucose 69-76 insulin Homo sapiens 15-24 350677-2 1978 The release of C-peptide was measured after a (1) normal intravenous glucose tolerance test, (2) a double glucose tolerance test, (3) an arginine infusion, and (4) after an intravenous glucose tolerance test followed by an arginine infusion. Glucose 106-113 insulin Homo sapiens 15-24 658614-0 1978 Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia. Glucose 28-35 insulin Homo sapiens 47-54 350677-2 1978 The release of C-peptide was measured after a (1) normal intravenous glucose tolerance test, (2) a double glucose tolerance test, (3) an arginine infusion, and (4) after an intravenous glucose tolerance test followed by an arginine infusion. Glucose 106-113 insulin Homo sapiens 15-24 669099-0 1978 The effect of acetylsalicylic acid on insulin response to glucose and arginine in normal man. Glucose 58-65 insulin Homo sapiens 38-45 355007-0 1978 Reproducibility of the blood glucose and plasma insulin response to identical oral glucose load performed one year appart. Glucose 83-90 insulin Homo sapiens 48-55 369883-0 1978 Effect of calcitonin on glucose--stimulated insulin secretion in normal, obese and prediabetic subjects. Glucose 24-31 insulin Homo sapiens 44-51 669099-2 1978 Pretreatment with ASA augmented the early insulin response to a standard IV glucose tolerance test (25 g) in 7 normal subjects (p is less than 0.05 at 2 min; p is less than 0.02 at 5 min; p is less than 0.01 at 10 min). Glucose 76-83 insulin Homo sapiens 42-49 669099-6 1978 A possible role of prostaglandins upon the insulin responses to glucose and arginine is discussed. Glucose 64-71 insulin Homo sapiens 43-50 647213-0 1978 Mechanism of action of insulin in diabetic patients: a dose-related effect on glucose production and utilisation. Glucose 78-85 insulin Homo sapiens 23-30 647213-4 1978 The rate of fall of plasma glucose concentration was faster on the high-dose infusion of insulin than on the low, whereas the fall in plasma free fatty acids, glycerol, and keton bodies was the same on both insulin infusions. Glucose 27-34 insulin Homo sapiens 89-96 647213-5 1978 The mechanism whereby the two rates of insulin administration lowered plasma glucose concentration differed: during the low-dose infusion the decrease in the glucose concentration was produced entirely by a fall of hepatic glucose output, whereas during the high-dose insulin infusion the glucose concentration fell because both the rate of glucose production fell and the rate of glucose utilisation rose. Glucose 77-84 insulin Homo sapiens 39-46 647592-4 1978 The results of an oral glucose tolerance test were normal; an appropriate insulin response was demonstrated in one patient, and a slightly elevated basal insulin value with a delayed insulin response to oral administration of glucose was demonstrated in the other. Glucose 226-233 insulin Homo sapiens 154-161 647213-5 1978 The mechanism whereby the two rates of insulin administration lowered plasma glucose concentration differed: during the low-dose infusion the decrease in the glucose concentration was produced entirely by a fall of hepatic glucose output, whereas during the high-dose insulin infusion the glucose concentration fell because both the rate of glucose production fell and the rate of glucose utilisation rose. Glucose 158-165 insulin Homo sapiens 39-46 647592-4 1978 The results of an oral glucose tolerance test were normal; an appropriate insulin response was demonstrated in one patient, and a slightly elevated basal insulin value with a delayed insulin response to oral administration of glucose was demonstrated in the other. Glucose 226-233 insulin Homo sapiens 154-161 647213-5 1978 The mechanism whereby the two rates of insulin administration lowered plasma glucose concentration differed: during the low-dose infusion the decrease in the glucose concentration was produced entirely by a fall of hepatic glucose output, whereas during the high-dose insulin infusion the glucose concentration fell because both the rate of glucose production fell and the rate of glucose utilisation rose. Glucose 158-165 insulin Homo sapiens 39-46 647213-5 1978 The mechanism whereby the two rates of insulin administration lowered plasma glucose concentration differed: during the low-dose infusion the decrease in the glucose concentration was produced entirely by a fall of hepatic glucose output, whereas during the high-dose insulin infusion the glucose concentration fell because both the rate of glucose production fell and the rate of glucose utilisation rose. Glucose 158-165 insulin Homo sapiens 39-46 647213-5 1978 The mechanism whereby the two rates of insulin administration lowered plasma glucose concentration differed: during the low-dose infusion the decrease in the glucose concentration was produced entirely by a fall of hepatic glucose output, whereas during the high-dose insulin infusion the glucose concentration fell because both the rate of glucose production fell and the rate of glucose utilisation rose. Glucose 158-165 insulin Homo sapiens 39-46 647213-6 1978 In all experiments there was a direct relation between a fall in serum potassium concentration and the fall in plasma glucose concentration irrespective of the mechanism that reduced the glucose concentration.These results indicate that in uncontrolled diabetics low-dose insulin infusions lower the blood glucose concentration entirely by reducing glucose production from the liver and that the effect of insulin on potassium transport is independent of its effect on glucose uptake. Glucose 118-125 insulin Homo sapiens 272-279 647213-6 1978 In all experiments there was a direct relation between a fall in serum potassium concentration and the fall in plasma glucose concentration irrespective of the mechanism that reduced the glucose concentration.These results indicate that in uncontrolled diabetics low-dose insulin infusions lower the blood glucose concentration entirely by reducing glucose production from the liver and that the effect of insulin on potassium transport is independent of its effect on glucose uptake. Glucose 187-194 insulin Homo sapiens 272-279 647213-6 1978 In all experiments there was a direct relation between a fall in serum potassium concentration and the fall in plasma glucose concentration irrespective of the mechanism that reduced the glucose concentration.These results indicate that in uncontrolled diabetics low-dose insulin infusions lower the blood glucose concentration entirely by reducing glucose production from the liver and that the effect of insulin on potassium transport is independent of its effect on glucose uptake. Glucose 187-194 insulin Homo sapiens 272-279 360748-6 1978 The insulin/glucagon molar ratio was significantly reduced after glucose infusion in these two groups. Glucose 65-72 insulin Homo sapiens 4-11 647213-6 1978 In all experiments there was a direct relation between a fall in serum potassium concentration and the fall in plasma glucose concentration irrespective of the mechanism that reduced the glucose concentration.These results indicate that in uncontrolled diabetics low-dose insulin infusions lower the blood glucose concentration entirely by reducing glucose production from the liver and that the effect of insulin on potassium transport is independent of its effect on glucose uptake. Glucose 187-194 insulin Homo sapiens 272-279 360749-4 1978 Five of the myotonic patients had glucose intolerance; 7 had exaggerated immunoreactive insulin (IRI) response to glucose. Glucose 114-121 insulin Homo sapiens 88-95 360749-5 1978 One of the 9 relatives demonstrated glucose intolerance and none had exaggerated insulin response to glucose. Glucose 101-108 insulin Homo sapiens 81-88 647213-6 1978 In all experiments there was a direct relation between a fall in serum potassium concentration and the fall in plasma glucose concentration irrespective of the mechanism that reduced the glucose concentration.These results indicate that in uncontrolled diabetics low-dose insulin infusions lower the blood glucose concentration entirely by reducing glucose production from the liver and that the effect of insulin on potassium transport is independent of its effect on glucose uptake. Glucose 187-194 insulin Homo sapiens 272-279 360750-7 1978 A negative correlation was found between blood glucose levels and biological activity of insulin on adipocytes. Glucose 47-54 insulin Homo sapiens 89-96 645900-0 1978 Studies of glucose transport system of fat cells: effects of insulin and insulin mimickers. Glucose 11-18 insulin Homo sapiens 73-80 580541-0 1978 Insulin test: precisions of and correlations between glucose and hormone responses. Glucose 53-60 insulin Homo sapiens 0-7 645900-8 1978 Overall, these findings suggest that the chemical agents may be useful as probes to study certain aspects of insulin-mediated activation of glucose transport. Glucose 140-147 insulin Homo sapiens 109-116 648744-7 1978 Although the severity of hyperthyroidism decreases with age, age-related glucose intolerance was much more apparent in hyperthyroid patients because of the age-related decrease of basal concentration, the peak level attained, and the total magnitude of insulin response. Glucose 73-80 insulin Homo sapiens 253-260 648762-6 1978 It is suggested that the patient"s serum and insulin promote glucose transport and glycolysis through a common pathway, but act differently on glycogen synthesis. Glucose 61-68 insulin Homo sapiens 45-52 209452-3 1978 The insulin derivative retained 1.15% of its potency in stimulating glucose oxidation in fat cells but retained about 8.3% of its binding affinity toward receptors. Glucose 68-75 insulin Homo sapiens 4-11 348543-0 1978 Glucose stimulated proinsulin biosynthesis rates of turn off after cessation of the stimulus. Glucose 0-7 insulin Homo sapiens 19-29 348543-1 1978 Proinsulin biosynthesis was stimulated progressively to a plateau level at 45 min by 5.5 mmol/1 glucose. Glucose 96-103 insulin Homo sapiens 0-10 348543-4 1978 In contrast, exposure to 20 mmol/1 glucose caused a prolonged increase in proinsulin biosynthesis which was still apparent at 75 min. Glucose 35-42 insulin Homo sapiens 74-84 348543-6 1978 When proinsulin biosynthesis was stimulated by 20 mmol/1 glucose in the presence of actinomycin D, there was a rapid switch off of biosynthesis and no persistent effect. Glucose 57-64 insulin Homo sapiens 5-15 348543-7 1978 Thus, two controls for regulation of proinsulin biosynthesis can be characterised: a prompt, rapidly reversible stimulation in response to low or high glucose concentrations and a persistent stimulation in response to high glucose concentrations. Glucose 151-158 insulin Homo sapiens 37-47 348543-7 1978 Thus, two controls for regulation of proinsulin biosynthesis can be characterised: a prompt, rapidly reversible stimulation in response to low or high glucose concentrations and a persistent stimulation in response to high glucose concentrations. Glucose 223-230 insulin Homo sapiens 37-47 684304-0 1978 [Plasma insulin response to an orally administered glucose overload in obese and normal weight subjects (author"s transl)]. Glucose 51-58 insulin Homo sapiens 8-15 97078-1 1978 Maturity onset diabetes (MOD) is characterized by the fact that the response of insulin secretion to glucose loading is either completely missing or is reduced if compared with that of persons whose metabolism is intact. Glucose 101-108 insulin Homo sapiens 80-87 345832-0 1978 Blood insulin responses to blood glucose levels in high output sepsis and spetic shock. Glucose 33-40 insulin Homo sapiens 6-13 205476-1 1978 Plasma insulin response to oral glucose, insulin resistance, and insulin suppression of hepatic glucose production were studied in 11 normal subjects and 11 hypertriglyceridaemic patients. Glucose 32-39 insulin Homo sapiens 7-14 205476-2 1978 Patients with hypertriglyceridaemia had a significantly higher insulin response to oral glucose. Glucose 88-95 insulin Homo sapiens 63-70 205476-3 1978 Insulin resistance was also significantly greater in hypertriglyceridaemic subjects as determined by measuring the steady-state plasma glucose response during a continuous infusion of epinephrine, propranolol, glucose, and exogenous insulin. Glucose 135-142 insulin Homo sapiens 0-7 205476-3 1978 Insulin resistance was also significantly greater in hypertriglyceridaemic subjects as determined by measuring the steady-state plasma glucose response during a continuous infusion of epinephrine, propranolol, glucose, and exogenous insulin. Glucose 210-217 insulin Homo sapiens 0-7 205476-4 1978 Insulin suppression of hepatic glucose production was calculated from the results of two studies in which glucose turnover rate was measured by a continuous infusion of 3H-2-glucose. Glucose 31-38 insulin Homo sapiens 0-7 565310-0 1978 Effect of secretin on basal- and glucose-stimulated insulin secretion in man. Glucose 33-40 insulin Homo sapiens 52-59 565310-5 1978 A concomitant rise in insulin levels was however only observed during infusions of glucose. Glucose 83-90 insulin Homo sapiens 22-29 640244-3 1978 glucose on the plasma level of pancreatic glucagon, plasma immunoreactive insulin (IRI), and plasma growth hormone (GH) was assessed in eight normal and 10 insulin-treated diabetic subjects. Glucose 0-7 insulin Homo sapiens 74-81 668642-1 1978 In 25 patients having a history of acute pancreatitis (AP) in anamnesis one year ago and in 12 control subjects the insulin response to oral glucose was investigated and in some cases the exocrine function of pancreas was evaluated. Glucose 141-148 insulin Homo sapiens 116-123 755038-0 1978 Effect of control of blood glucose on plasma insulin responses to various stimuli in secondary failures to oral hypoglycemic agents and in newly diagnosed, maturity onset, ketosis-resistant diabetics. Glucose 27-34 insulin Homo sapiens 45-52 76227-2 1978 The plasma-potassium rose promptly after a drink of 50 g glucose in 8 insulin-dependent diabetics who had not had insulin for approximately 14-26 hours. Glucose 57-64 insulin Homo sapiens 70-77 674691-3 1978 Methylated PGE2 kept basal serum insulin level unchanged, but significantly reduced insulin response by 15 +/- 6 microunits/ml to intravenous glucose pulse injection /0.1 g/kg/ or by 45 +/- 11 microunits/ml to intraduodenal glucose infusion /0.5 g/kg-hr/. Glucose 142-149 insulin Homo sapiens 84-91 674691-5 1978 These studies demonstrate that methylated PGE2 analogue given orally, intraduodenally or intravenously results in a potent suppression of insulin response to glucose challenge. Glucose 158-165 insulin Homo sapiens 138-145 256548-4 1978 The diurnal glucose variability, expressed as the standard deviation of the mean, was found to be inversely correlated with the residual C-peptide response in insulin-requiring diabetics. Glucose 12-19 insulin Homo sapiens 159-166 354029-1 1978 Plasma insulin responses to a 4-hour glucose tolerance (100 g) were studied in urbanized Black people. Glucose 37-44 insulin Homo sapiens 7-14 631695-1 1978 Serum insulin levels were determined in patients with myotonic dystrophy after intravenous administration of glucose and were found to be higher than in control persons in about 60%. Glucose 109-116 insulin Homo sapiens 6-13 737079-0 1978 [Effect of glucose and amino acids on insulin secretion]. Glucose 11-18 insulin Homo sapiens 38-45 629631-8 1978 In two brittle diabetics, the blood glucose level was stabilized on intravenously administered insulin infusion, and in these patients, meals caused only a moderate hyperglycemia. Glucose 36-43 insulin Homo sapiens 95-102 629634-3 1978 Eleven of 12 patients had decreased insulin requirement: mean decrement in insulin dose, 40%; mean decrement in fasting blood glucose level, 33%; mean decrement in peak blood glucose level, 42%. Glucose 127-134 insulin Homo sapiens 36-43 629634-3 1978 Eleven of 12 patients had decreased insulin requirement: mean decrement in insulin dose, 40%; mean decrement in fasting blood glucose level, 33%; mean decrement in peak blood glucose level, 42%. Glucose 176-183 insulin Homo sapiens 36-43 640235-12 1978 The elevated plasma glucose levels in normals must be due to the suppressive effects of somatostatin on insulin secretion. Glucose 20-27 insulin Homo sapiens 104-111 640239-4 1978 When this amount of glucose was infused during the last 30 minutes of a two-and-a-half-hour infusion of a mixture of essential amino acids, there was a rapid and striking increase in serum insulin. Glucose 20-27 insulin Homo sapiens 189-196 658630-1 1978 The response of Gastric Inhibitory Polypeptide (GIP) and insulin to a 50 g oral glucose tolerance test (OGTT) and an intravenous glucose infusion (IVGI), which copied the changes in plasma glucose concentrations during the OGTT, were measured in 10 patients with duodenal ulcer and in 10 healthy control subjects. Glucose 80-87 insulin Homo sapiens 57-64 658632-2 1978 In 25 young healthy persons we found a significant positive correlation between insulin binding and glucose disappearance rate both after glucose (R = 0.68, p less than 0.001) and insulin (R = 0.49, p less than 0.02) given intravenously. Glucose 100-107 insulin Homo sapiens 80-87 658632-2 1978 In 25 young healthy persons we found a significant positive correlation between insulin binding and glucose disappearance rate both after glucose (R = 0.68, p less than 0.001) and insulin (R = 0.49, p less than 0.02) given intravenously. Glucose 138-145 insulin Homo sapiens 80-87 688978-3 1978 In the presence of insulin (62.5 muU/ml) the production of carbon dioxide from glucose by adipose tissue fragments of nonobese controls as well as diabetics increased up to 286 +/- 62% and 198 +/- 14.7%, respectively. Glucose 79-86 insulin Homo sapiens 19-26 626287-0 1978 Insulin-induced attenuation of glucose-stimulated gastric inhibitory polypeptide secretion. Glucose 31-38 insulin Homo sapiens 0-7 205476-4 1978 Insulin suppression of hepatic glucose production was calculated from the results of two studies in which glucose turnover rate was measured by a continuous infusion of 3H-2-glucose. Glucose 106-113 insulin Homo sapiens 0-7 205476-7 1978 These data demonstrate that hepatic glucose production can be suppressed to an equal degree in normal and hypertriglyceridaemic subjects at comparable circulating insulin levels, at the same time that resistance to insulin-stimulated glucose uptake is observed in the hypertriglyceridaemic individuals. Glucose 36-43 insulin Homo sapiens 163-170 205476-7 1978 These data demonstrate that hepatic glucose production can be suppressed to an equal degree in normal and hypertriglyceridaemic subjects at comparable circulating insulin levels, at the same time that resistance to insulin-stimulated glucose uptake is observed in the hypertriglyceridaemic individuals. Glucose 234-241 insulin Homo sapiens 215-222 681448-0 1978 Protection of the ischaemic myocardium by glucose-insulin-potassium infusion assessed by ventricular function and electron microscopy. Glucose 42-49 insulin Homo sapiens 50-57 343466-0 1978 Importance of insulin secretion based on the rate of change in blood glucose concentration in glucose tolerance, assessed by the artificial beta cell. Glucose 94-101 insulin Homo sapiens 14-21 580135-2 1978 Significant correlation between blood glucose and serum free (but not bound) insulin was found. Glucose 38-45 insulin Homo sapiens 77-84 626287-1 1978 Administration of exogenous insulin before and after intraduodenal glucose results in blunting of the GIP response to glucose. Glucose 67-74 insulin Homo sapiens 28-35 626287-1 1978 Administration of exogenous insulin before and after intraduodenal glucose results in blunting of the GIP response to glucose. Glucose 118-125 insulin Homo sapiens 28-35 620577-3 1978 In four patients the glucose-insulin-potassium solution was instilled directly into the right pulmonary artery from the tip of the Swan-Ganz catheter. Glucose 21-28 insulin Homo sapiens 29-36 639762-1 1978 Epinephrine and insulin increased glucose uptake in Planaria, but epinephrine did so to a much grater extent. Glucose 34-41 insulin Homo sapiens 16-23 340115-2 1978 A theoretical investigation of the intravenous glucose tolerance test has been carried out based on recent findings on the kinetics in man of insulin production, distribution, disposal and action, and of glucose turnover and distribution. Glucose 47-54 insulin Homo sapiens 142-149 639766-0 1978 Derivation and experimental proof of a new algorithm for the artificial B-cell based on the individual analysis of the physiological insulin-glucose relationship. Glucose 141-148 insulin Homo sapiens 133-140 639766-4 1978 The regression coefficients were used as algorithm parameters for continuous plasma glucose dependent intravenous insulin administration in the same animals after induction of an insulin-dependent diabetes. Glucose 84-91 insulin Homo sapiens 114-121 639766-6 1978 The insulin responsiveness, however, varies from day to day; tusing this insulin dosage pattern we observed nearly normal plasma glucose curves and slightly elevated insulin reactions after glucose loading. Glucose 129-136 insulin Homo sapiens 4-11 639766-6 1978 The insulin responsiveness, however, varies from day to day; tusing this insulin dosage pattern we observed nearly normal plasma glucose curves and slightly elevated insulin reactions after glucose loading. Glucose 190-197 insulin Homo sapiens 4-11 340000-5 1978 In five out of 14 studies the subcutaneous insulin infusion significantly lowered the mean blood glucose concentration without producing hypoglycaemic symptoms; in another six patients the mean blood glucose concentration was maintained. Glucose 97-104 insulin Homo sapiens 43-50 340000-8 1978 The results of this preliminary study suggest that a continuous subcutaneous insulin infusion may be a means of maining physiological glucose concentrations in diabetics. Glucose 134-141 insulin Homo sapiens 77-84 340001-2 1978 Among 47 patients with maturity onset diabetes the 29 fast acetylators were older at diagnosis and, at a given glucose concentration, had a higher pretreatment fasting insulin concentration than slow acetylators. Glucose 111-118 insulin Homo sapiens 168-175 340001-3 1978 They also had a larger first-phase insulin secretion in response to intravenous glucose both before and after one month"s dietary treatment. Glucose 80-87 insulin Homo sapiens 35-42 31757-6 1978 However, after initiation of extracorporal circulation only ACTH, cortisol, and, to a lesser degree, the glucose and insulin response to glucose were lowered by morphine anaesthesia. Glucose 137-144 insulin Homo sapiens 117-124 339957-3 1978 Isolated pancreatic islets releasing insulin in response to glucose stimulation have been used as a specific example. Glucose 60-67 insulin Homo sapiens 37-44 716771-6 1978 No significant difference was found when the glucose and insulin responses in the two glucagon tests were compared, in contrast to previous findings that preloading with glucose resulted in a significantly increased response of insulin to glucagon. Glucose 170-177 insulin Homo sapiens 228-235 618684-4 1978 With glucose supplementation plasma insulin rose significantly and the arterial ammonia increase produced by lunch (+42 +/- 3 microgram/100 ml) did not differ from that observed in the control test; but the rise in venous ammonemia was lower (+12 +/- 4 microgram/100 ml; p less than 0.01) with a significant increase in arterio-venous ammonia difference. Glucose 5-12 insulin Homo sapiens 36-43 645445-4 1978 glucose tolerance test, in 189 cases including plasma insulin measurements, was performed as part of an internal medical screening examination. Glucose 0-7 insulin Homo sapiens 54-61 754799-0 1978 [Influence of verapamil on blood sugar and insulin secretion after intravenous administration of glucose and on somatotropin secretion after insulin stimulation]. Glucose 97-104 insulin Homo sapiens 43-50 665365-5 1978 Rodbell and Blecher have already shown an insulin-like action of phospholipases towards the uptake of glucose and amino-acids by adipocytes. Glucose 102-109 insulin Homo sapiens 42-49 665365-7 1978 Results from these studies give new suggestions on insulin action; phospholipase activation changes membrane physiochemical properties inducing an increase of glucose carrier mobility and leading the membrane cyclase enzyme (s) towards GMP cyclic synthesis. Glucose 159-166 insulin Homo sapiens 51-58 571280-5 1978 Emphasis is placed on the fact that alterations in blood glucose concentrations are indirectly responsible, via effects on insulin secretion, for the extrahepatic control of ketogenesis. Glucose 57-64 insulin Homo sapiens 123-130 752578-2 1978 Despite elevation of insulin levels following glucose infusion, no effect on muscular fractional extraction of glucose and no decrease of lactate and alanine production was found, whereas muscular lipolysis was inhibited to a normal extent and ketone utilization was reduced. Glucose 46-53 insulin Homo sapiens 21-28 400127-0 1978 Jet injection of insulin during self-monitoring of blood glucose. Glucose 57-64 insulin Homo sapiens 17-24 620487-10 1978 After an intravenous galactose load in the fed state insulin appears to inhibit hepatic glucose release. Glucose 88-95 insulin Homo sapiens 53-60 343466-0 1978 Importance of insulin secretion based on the rate of change in blood glucose concentration in glucose tolerance, assessed by the artificial beta cell. Glucose 69-76 insulin Homo sapiens 14-21 400128-4 1978 It suggests that optimal diabetic control will be achieved only when newer methods of insulin delivery are available to the clinician that match plasma insulin requirements to the simultaneous plasma glucose concentration. Glucose 200-207 insulin Homo sapiens 86-93 568549-4 1978 Her plasma insulin response to glucose loading was also higher. Glucose 31-38 insulin Homo sapiens 11-18 344115-3 1978 Basal insulin or C-peptide levels become subnormal if normal fasting plasma glucose levels are attained with insulin. Glucose 76-83 insulin Homo sapiens 6-13 344115-6 1978 The reduced insulin response of diabetics to intravenous glucose is slightly increased when basal normoglycemia is established, suggesting that the high plasma glucose levels compromise beta cell function. Glucose 57-64 insulin Homo sapiens 12-19 344115-6 1978 The reduced insulin response of diabetics to intravenous glucose is slightly increased when basal normoglycemia is established, suggesting that the high plasma glucose levels compromise beta cell function. Glucose 160-167 insulin Homo sapiens 12-19 640973-0 1978 Insulin and glucose effects on glucose metabolism in pregnant and nonpregnant ewes. Glucose 31-38 insulin Homo sapiens 0-7 721369-4 1978 Glucose disappearance rates were highly correlated (r = 0.80) with the acute insulin response to glucose. Glucose 0-7 insulin Homo sapiens 77-84 721369-4 1978 Glucose disappearance rates were highly correlated (r = 0.80) with the acute insulin response to glucose. Glucose 97-104 insulin Homo sapiens 77-84 631736-4 1978 It is suggested and clofibrate improves glucose utilization by reducing insulin resistance irrespective of its effects on serum lipids concentration. Glucose 40-47 insulin Homo sapiens 72-79 35671-1 1978 Energy turnover of septic burned patients was favourably influenced by infusion of glucose 40% one unit of Insulin for each 3 grams of glucose along with 0.5% protein preparate and 50-100 grams of aminoacids, administered by way of a cave cathether. Glucose 83-90 insulin Homo sapiens 107-114 290734-2 1978 In both groups, insulin levels were highest after meals, between 11 a.m. and 7 p.m.; in cirrhotic subjects, but not in controls, plasma glucose levels were also higher at these times. Glucose 136-143 insulin Homo sapiens 16-23 723265-6 1978 Cytochalasin B binding activity was also retained by extracted membrane vesicles and D-glucose uptake into extracted vesicles derived from untreated or insulin-treated fat cells was inhibited by cytochalasin B. Glucose 85-94 insulin Homo sapiens 152-159 752025-2 1978 Plasma C-peptide during intravenous glucose tolerance in neonates from normal and insulin-treated diabetic mothers. Glucose 36-43 insulin Homo sapiens 7-16 35671-1 1978 Energy turnover of septic burned patients was favourably influenced by infusion of glucose 40% one unit of Insulin for each 3 grams of glucose along with 0.5% protein preparate and 50-100 grams of aminoacids, administered by way of a cave cathether. Glucose 135-142 insulin Homo sapiens 107-114 619223-2 1978 The peptide prolonged the depression of blood glucose concentration brought about by insulin during intravenous insulin tolerance tests in rats. Glucose 46-53 insulin Homo sapiens 85-92 619223-2 1978 The peptide prolonged the depression of blood glucose concentration brought about by insulin during intravenous insulin tolerance tests in rats. Glucose 46-53 insulin Homo sapiens 112-119 105487-0 1978 [Plasma level of insulin and glucagon during parenteral feeding with glucose and fructose in the early postoperative phase]. Glucose 69-76 insulin Homo sapiens 17-24 635445-5 1978 The degree of the greater hormone response was dependent on the glucose increase after the test meal in the case of insulin and GIP, but not in the case of gastrin. Glucose 64-71 insulin Homo sapiens 116-123 635445-6 1978 It is concluded: firstly, that a faster glucose absorption (possibly due to rapid initial gastric emptying or increased intestinal motility) is responsible for the high and short-lasting glucose peak and the increased GIP and insulin secretion; secondly, that the GIP response could well be causally related to the insulin response; thirdly, that hyposcretion of GIP is ruled out as a possible factor in the pathogenesis of gastric acid hypersecretion of duodenal ulcer patients. Glucose 40-47 insulin Homo sapiens 226-233 589316-1 1977 Administration of a low-dose insulin infusion to normal subjects results in a mild drop in blood glucose concentration (1.1 mmol/1 (20 mg/100 ml)) and the resetting of the basal glucose at the lower concentration. Glucose 97-104 insulin Homo sapiens 29-36 589316-1 1977 Administration of a low-dose insulin infusion to normal subjects results in a mild drop in blood glucose concentration (1.1 mmol/1 (20 mg/100 ml)) and the resetting of the basal glucose at the lower concentration. Glucose 178-185 insulin Homo sapiens 29-36 343587-2 1977 The percentage of proinsulin was increased in 11 patients and correlated with plasma glucose, but not with IRI. Glucose 85-92 insulin Homo sapiens 18-28 343587-4 1977 Sequential studies in one patient showed normalization of the proportion of proinsulin following lowering of the plasma glucose level. Glucose 120-127 insulin Homo sapiens 76-86 414664-6 1977 These findings suggest that insulin secretion is modified by glucose not only in the short term but also by a separate effect acting over many hours. Glucose 61-68 insulin Homo sapiens 28-35 414664-10 1977 This specific role of glucose in the long-term potentiation of insulin secretion make it the carbohydrate of choice for the intravenous feeding in postoperative patients. Glucose 22-29 insulin Homo sapiens 63-70 603273-2 1977 Early changes due to operation in the insulin response to glucose. Glucose 58-65 insulin Homo sapiens 38-45 603273-5 1977 On the morning after operation, both phases of the insulin response to glucose were increased. Glucose 71-78 insulin Homo sapiens 51-58 589939-8 1977 During preoperative glucose infusions there was an increase in the percentage of the total plasma IRI present as high-molecular-weight forms (i.e. proinsulin plus the species of mol. Glucose 20-27 insulin Homo sapiens 147-157 590640-0 1977 Deranged insulin-secretory dynamics in offspring of two diabetic parents after double stimulation with intravenous glucose. Glucose 115-122 insulin Homo sapiens 9-16 590640-6 1977 (4) There was a significant reduction in the insulin response per unit change in glucose after the first glucose pulse that was accentuated after the second pulse. Glucose 81-88 insulin Homo sapiens 45-52 590640-6 1977 (4) There was a significant reduction in the insulin response per unit change in glucose after the first glucose pulse that was accentuated after the second pulse. Glucose 105-112 insulin Homo sapiens 45-52 590650-4 1977 Conversion of [UP14C]glucose to lipids was stimulated half-maximally by about 0.05 nmol/l of insulin (similar to rat adipocytes). Glucose 21-28 insulin Homo sapiens 93-100 617312-9 1977 The only distinguishing factor among the infants was higher insulin production in infants of diabetic mothers during the 60-min intravenous glucose tolerance test which persisted up to 4 h following the infusion. Glucose 140-147 insulin Homo sapiens 60-67 706302-0 1978 [Growth hormone and insulin in the blood in pancreatic cancer during the glucose tolerance test]. Glucose 73-80 insulin Homo sapiens 20-27 412782-3 1977 Insulin admixture per 100 g of glucose is not constant. Glucose 31-38 insulin Homo sapiens 0-7 579580-0 1977 Plasma insulin response following intravenous glucose in gestational diabetics. Glucose 46-53 insulin Homo sapiens 7-14 579580-7 1977 discriminant analysis) were to verify differences in acute insulin release of the beta-cell and the cumulative insulin response following intravenous glucose. Glucose 150-157 insulin Homo sapiens 111-118 579584-0 1977 [The use of the discriminant analysis for judging the glucose tolerance of pregnant women by time-dependent measurements of serum insulin (author"s transl)]. Glucose 54-61 insulin Homo sapiens 130-137 579584-1 1977 This article deals with the problem of judging the carbohydrate metabolism of women in pregnancy and childbed only by time-dependent measurements of serum insulin after an intravenous glucose tolerance test. Glucose 184-191 insulin Homo sapiens 155-162 579584-3 1977 The investigation of 390 serum insulin curves coming from 195 women showed that the application of the mathematical model of the linear discriminant analysis leads to a very good separation between the groups with a pathological and with a normal glucose tolerance. Glucose 247-254 insulin Homo sapiens 31-38 590092-3 1977 Insulin treatment (1-20 IU/h) with a motor infusion pump and infusion of hypertonic solutions decreased serum osmolarity by 2-4 mosmol/l X h. The faster fall of glucose in the extracellular space was compensated by hypertonic saline infusions (up to 365 mosmol/l). Glucose 161-168 insulin Homo sapiens 0-7 198659-3 1977 The simultaneous demonstration of low plasma glucose, high immunoreactive insulin and suppressed C-peptide immunoreactivity represents a triad of results pathognomonic of exogenous insulin administration. Glucose 45-52 insulin Homo sapiens 181-188 607838-0 1977 [Serum insulin concentration, basal and during an standardized oral glucose tolerance test in healthy children (author"s transl)]. Glucose 68-75 insulin Homo sapiens 7-14 201401-0 1977 The mechanism of action of polypeptide hormones with special reference to insulin"s action on glucose transport. Glucose 94-101 insulin Homo sapiens 74-81 201401-6 1977 The purpose of this communication is to describe some aspects of the mechanism of insulin action on transmembrane glucose transport, and to disucss general aspects of polypeptide hormone action in relation to the specific findings with insulin. Glucose 114-121 insulin Homo sapiens 82-89 608602-0 1977 [Changes in the content of immunoreactive insulin and growth hormone during glucose tolerance test in children with chronic lung diseases]. Glucose 76-83 insulin Homo sapiens 42-49 591302-0 1977 Relationship between food intake and insulin response to oral glucose tolerance test in short lean children. Glucose 62-69 insulin Homo sapiens 37-44 591302-5 1977 It is concluded that the insulin response to the oral glucose tolerance test is not related to caloric intake. Glucose 54-61 insulin Homo sapiens 25-32 908753-12 1977 Cells pretreated with this serum in a concentration which inhibited binding by 80% also showed a five-fold shift to the right in the dose response of insulin-stimulated glucose oxidation, whereas spermine-stimulated glucose oxidation was unaffected. Glucose 169-176 insulin Homo sapiens 150-157 925138-2 1977 Steady state plasma glucose level (SSPG) which should be inversely proportional to insulin sensitivity was obtained. Glucose 20-27 insulin Homo sapiens 83-90 925138-4 1977 In 5 insulin-treated diabetics and in 5 subjects with borderline glucose tolerance including 2 obese subjects, insulin sensitivity for glucose utilization was also significantly diminished. Glucose 65-72 insulin Homo sapiens 111-118 925138-4 1977 In 5 insulin-treated diabetics and in 5 subjects with borderline glucose tolerance including 2 obese subjects, insulin sensitivity for glucose utilization was also significantly diminished. Glucose 135-142 insulin Homo sapiens 111-118 909020-0 1977 Lack of gastrointestinal enhancement of the insulin response to glucose in newborn infants. Glucose 64-71 insulin Homo sapiens 44-51 909020-3 1977 The plasma insulin responses to glucose were not enhanced by NG administration. Glucose 32-39 insulin Homo sapiens 11-18 926070-1 1977 The effects of excessive maternal weight gain during pregnancy (five cases) and of glucose infusion in the mother (five cases) on insulin levels are compared with the insulin levels in a control group (19 normal pregnancies) by radioimmunologic determination of insulin levels in the amniotic fluid and in maternal and fetal blood. Glucose 83-90 insulin Homo sapiens 130-137 926070-4 1977 After an infusion of 25 mg of glucose in the mother, the mean maternal insulin values were 53.6 +/- 13.74 muU per ml; fetal, 24.7 +/- 6.67 muU per ml; and amniotic fluid, 14.3 +/- 5.52 muU per ml. Glucose 30-37 insulin Homo sapiens 71-78 926070-5 1977 Insulin concentrations in maternal blood (p less than 0.001), fetal blood (p less than 0.001) and amniotic fluid (p less than 0.001) were higher in pregnancies with excessive weight gain as compared to those in the control group, whereas the glucose infusion in the mother increased the concentration of insulin in the three components studied. Glucose 242-249 insulin Homo sapiens 0-7 333225-0 1977 Endogenous insulin fluctuations during glucose-induced paralysis in patients with familial periodic hypokalemia. Glucose 39-46 insulin Homo sapiens 11-18 599724-0 1977 [The relationship between age and the insulin response to glucose load (author"s transl)]. Glucose 58-65 insulin Homo sapiens 38-45 334502-4 1977 Insulin infusion was regulated either manually with an adjustable infusion pump (7 patients) or automatically with an artificial endocrine pancreas (glucose-controlled insulin infusion system; 11 patients). Glucose 149-156 insulin Homo sapiens 168-175 923108-4 1977 Three rather than two injections of soluble insulin gave improved blood glucose control but two combined injections of short and medium acting insulins gave nearly as good results. Glucose 72-79 insulin Homo sapiens 44-51 923108-5 1977 A long acting insulin was needed to prevent raised plasma glucose levels overnight. Glucose 58-65 insulin Homo sapiens 14-21 590205-5 1977 In the case of the women with simple obesity an insulin increased secretion with one peak of the hormone release was found following the glucose administration. Glucose 137-144 insulin Homo sapiens 48-55 590205-6 1977 In the hypothalamic obesity group two peaks of insulin release were noted, and in the maternal obesity group a bigger maximal output of insulin was noted after the glucose administration together with two release peaks and a positive correlation between the total insulin area and anthropometric indices of excessive body weight. Glucose 164-171 insulin Homo sapiens 136-143 590205-6 1977 In the hypothalamic obesity group two peaks of insulin release were noted, and in the maternal obesity group a bigger maximal output of insulin was noted after the glucose administration together with two release peaks and a positive correlation between the total insulin area and anthropometric indices of excessive body weight. Glucose 164-171 insulin Homo sapiens 136-143 590207-1 1977 The effect of intravenous injection of 0.1 I.U./kg insulin on blood glucose response and on lipolysis, induced by intravenous infusion of 0.2 microgram/kg - min norepinephrine, were studied in 12 normal subjects and 17 obese patients with normal 50 g oral glucose tolerance test and normal thyroid function. Glucose 68-75 insulin Homo sapiens 51-58 908463-0 1977 Insulin responses in equivocal and definite diabetes, with special reference to subjects who had mild glucose intolerance but later developed definite diabetes. Glucose 102-109 insulin Homo sapiens 0-7 561836-4 1977 The potential value of the device as an investigational tool is shown by demonstrating that regulation of the blood glucose concentration with insulin for seven to 24 hours does not alter circulating glucagon concentrations in the juvenile diabetic patients studied. Glucose 116-123 insulin Homo sapiens 143-150 605445-1 1977 Twelve apparently healthy subjects who showed a low insulin response to glucose were selected from two different age groups, 6 from youngers aged 19 to 22 and 6 from olders above 65 years old, and responses of insulin and growth hormone secretion to an intravenous administration of arginine were investigated. Glucose 72-79 insulin Homo sapiens 52-59 908685-3 1977 The ingestion of 75 g of glucose 45 min before exercise produced a 3.3-fold increase in plasma insulin and a 38% rise in plasma glucose at 0 min of exercise. Glucose 25-32 insulin Homo sapiens 95-102 910906-9 1977 These results indicate that insulin-requiring diabetics absorb glucose, Na, and H2O normally. Glucose 63-70 insulin Homo sapiens 28-35 895526-4 1977 Basal and integrated insulin concentrations were greater during intravenous glucose testing in the obese subjects, whereas similar glucagon suppression was observed in both groups. Glucose 76-83 insulin Homo sapiens 21-28 895528-4 1977 This elevation of plasma glucose was accompanied by a clear rise of glucagon levels (peak: 60% at 140 min, p = 0.0007) and by increased concentrations of circulating insulin and growth hormone. Glucose 25-32 insulin Homo sapiens 166-173 895529-4 1977 During fasting, insulin elevation after a glucose load was significantly delayed in lean subjects but not in the obese. Glucose 42-49 insulin Homo sapiens 16-23 895529-6 1977 In normals fasting resulted in a significant decrease of the blood glucose response to insulin injection, whereas in fasting obese subjects glucose response was unchanged. Glucose 67-74 insulin Homo sapiens 87-94 895529-7 1977 The results obtained suggest that the effect of fasting on insulin release and insulin sensitivity was more pronounced in lean than in obese subjects, which resulted in greater deterioration of glucose tolerance in the lean population. Glucose 194-201 insulin Homo sapiens 59-66 895529-7 1977 The results obtained suggest that the effect of fasting on insulin release and insulin sensitivity was more pronounced in lean than in obese subjects, which resulted in greater deterioration of glucose tolerance in the lean population. Glucose 194-201 insulin Homo sapiens 79-86 613688-5 1977 The data obtained suggest that glucose intolerance in uremia is related mainly to peripheral insulin resistance and is not due to hyperglucagonemia. Glucose 31-38 insulin Homo sapiens 93-100 892239-4 1977 One of these had a low and the other an augmented insulin response to glucose challenge. Glucose 70-77 insulin Homo sapiens 50-57 908474-3 1977 Phenformin was found to decrease postprandial hyperglycaemia significantly when compared with control values, and its addition to insulin further decreased the postprandial glucose rise below that found with insulin alone (p less than 0.005). Glucose 173-180 insulin Homo sapiens 130-137 411723-6 1977 The latter suggested that a degree of insulin resistance had been produced secondary to the early profound lowering of the blood glucose following glibenclamide. Glucose 129-136 insulin Homo sapiens 38-45 330566-6 1977 Infusion of sodium salicylate (SS), an inhibitor of endogenous prostaglandin synthesis, augmented acute insulin responses to glucose in normals (response before SS = 313+/-62%; during SS = 660+/-86%; P < 0.001). Glucose 125-132 insulin Homo sapiens 104-111 330566-9 1977 This was accompanied by a fourfold augmentation in second phase insulin secretion (second phase before SS = 1,696+/-430%; during SS = 5,176+/-682%; change 10-60 min insulin, muU/ml.min,% basal, P < 0.001) and by acceleration of glucose disappearance rates (K(G) before SS = 0.56+/-0.06; during SS = 1.02+/-0.17%/min, P < 0.005). Glucose 231-238 insulin Homo sapiens 64-71 330566-10 1977 These findings uniquely demonstrate that (a) PGE(2) inhibits glucose-induced acute insulin responses and decreases glucose disposal in nondiabetic humans and (b) SS restores acute insulin responses, augments second phase insulin secretion, and accelerates glucose disposal in hyperglycemic, adultonset diabetics. Glucose 61-68 insulin Homo sapiens 83-90 903405-1 1977 Insulin action was assessed by measuring insulin-mediated glucose disposal (KI) in 13 non-ketotic diabetic patients both before treatment and after normalization of plasma glucose by diet (5 patients) or sulfonylurea (glipizide) therapy (8 patients). Glucose 58-65 insulin Homo sapiens 0-7 903405-1 1977 Insulin action was assessed by measuring insulin-mediated glucose disposal (KI) in 13 non-ketotic diabetic patients both before treatment and after normalization of plasma glucose by diet (5 patients) or sulfonylurea (glipizide) therapy (8 patients). Glucose 58-65 insulin Homo sapiens 41-48 903405-1 1977 Insulin action was assessed by measuring insulin-mediated glucose disposal (KI) in 13 non-ketotic diabetic patients both before treatment and after normalization of plasma glucose by diet (5 patients) or sulfonylurea (glipizide) therapy (8 patients). Glucose 172-179 insulin Homo sapiens 0-7 894407-7 1977 At five months, the insulin, glucagon, and growth hormone responses to glucose and to somatostatin were normalized. Glucose 71-78 insulin Homo sapiens 20-27 337288-1 1977 The following was examined in 60 adult persons with normal weight and obesity: insulin level during the glucose tolerance test and lymphocyte sensitization to insulin and the pancreas tissue. Glucose 104-111 insulin Homo sapiens 79-86 337288-2 1977 An increased insulin level both on fasting stomach and after glucose tolerance was noted in obese persons. Glucose 61-68 insulin Homo sapiens 13-20 337288-3 1977 A delayed elevation of insulin level, particularly in combination of obesity with deranged glucose tolerance was often seen. Glucose 91-98 insulin Homo sapiens 23-30 337288-5 1977 Lymphocyte sensitization to insulin was characteristic of cases when the glucose was flat, insulin secretion--moderately elevated and insulin/glucose index--increased. Glucose 73-80 insulin Homo sapiens 28-35 337288-5 1977 Lymphocyte sensitization to insulin was characteristic of cases when the glucose was flat, insulin secretion--moderately elevated and insulin/glucose index--increased. Glucose 142-149 insulin Homo sapiens 28-35 928319-2 1977 Adipose tissue sensitivity to insulin was studied by the influence of insulin to the intensity of incorporation of carbohydrate of labeled glucose into the common lipids of the adipose tissue in its incubation with various insulin concentrations. Glucose 139-146 insulin Homo sapiens 30-37 928319-2 1977 Adipose tissue sensitivity to insulin was studied by the influence of insulin to the intensity of incorporation of carbohydrate of labeled glucose into the common lipids of the adipose tissue in its incubation with various insulin concentrations. Glucose 139-146 insulin Homo sapiens 70-77 928319-2 1977 Adipose tissue sensitivity to insulin was studied by the influence of insulin to the intensity of incorporation of carbohydrate of labeled glucose into the common lipids of the adipose tissue in its incubation with various insulin concentrations. Glucose 139-146 insulin Homo sapiens 70-77 892236-2 1977 The pattern of insulin response to oral and/or intravenous glucose has been claimed to be characteristic of diabetes and even prediabetes. Glucose 59-66 insulin Homo sapiens 15-22 874246-3 1977 Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. Glucose 70-77 insulin Homo sapiens 0-7 142518-5 1977 Insulin treatment of normal animals 30 or 15 min prior to perfusion resulted in an approximate doubling of the incorporation of glucose into the phosphatidylcholine and phosphatidylglycerol isolated from the surfactant and residual fractions of the lung. Glucose 128-135 insulin Homo sapiens 0-7 335997-2 1977 Suloctidil (0.5 to 5.0 micrometer) inhibits insulin release evoked by glucose or alpha-ketoisocaproate in pancreatic islets. Glucose 70-77 insulin Homo sapiens 44-51 330243-0 1977 Induction of insulin biosynthesis by anomers of D-glucose. Glucose 48-57 insulin Homo sapiens 13-20 874246-3 1977 Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. Glucose 70-77 insulin Homo sapiens 115-122 197189-2 1977 Both biosynthesis and secretion of insulin were strongly stimulated by incubation of islet tumour cells in the presence of increasing glucose concentrations in the range 2-8 mmol/1. Glucose 134-141 insulin Homo sapiens 35-42 874246-3 1977 Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. Glucose 124-131 insulin Homo sapiens 0-7 875735-0 1977 Amino acid modulation of glucose-induced insulin and glucagon release in diabetic patients. Glucose 25-32 insulin Homo sapiens 41-48 875735-3 1977 However, amino acid infusion over a period of 60 min started immediately before oral glucose loading evoked a sustained rise of plasma insulin associated with a lesser degree of glucagon secretion, thus causing significant improvement of the blood glucose curve. Glucose 85-92 insulin Homo sapiens 135-142 875735-3 1977 However, amino acid infusion over a period of 60 min started immediately before oral glucose loading evoked a sustained rise of plasma insulin associated with a lesser degree of glucagon secretion, thus causing significant improvement of the blood glucose curve. Glucose 248-255 insulin Homo sapiens 135-142 195754-3 1977 The relationship of the fasting plasma triglyceride concentration to the plasma immunoreaction insulin response to 50 g glucose orally was investigated. Glucose 120-127 insulin Homo sapiens 95-102 871822-1 1977 The Ames Dextrostix-Eyetone system was evaluated for monitoring the blood glucose concentration during insulin-induced hypoglycaemia. Glucose 74-81 insulin Homo sapiens 103-110 862563-0 1977 Role of rate of change of glucose concentration as a signal for insulin release. Glucose 26-33 insulin Homo sapiens 64-71 895007-3 1977 Our investigations demonstrated a dose dependent blood glucose decrease with each sulfonylurea corresponding with the insulin levels after intravenous application. Glucose 55-62 insulin Homo sapiens 118-125 872954-0 1977 Comparison of ethinylestradiol and mestranol in sequential-type oral contraceptives in their effects on blood glucose and serum insulin in oral glucose tolerance tests. Glucose 144-151 insulin Homo sapiens 128-135 873073-4 1977 Intravenous insulin delivery rates were determined by control parameters responsive to both glucose concentration and its rate of change. Glucose 92-99 insulin Homo sapiens 12-19 905262-6 1977 The mentioned changes in the glycemia level, of the insulin and growth hormone level after glucose administration were more pronounced in cirrhosis of the liver than in chronic hepatitis, and in late stages of portal cirrhosis than at its early stages. Glucose 91-98 insulin Homo sapiens 52-59 874055-0 1977 The augmentation effects of secretin on the insulin responses to known stimuli: specificity for glucose. Glucose 96-103 insulin Homo sapiens 44-51 874055-6 1977 Secretin only augmented the acute insulin responses to 5 g glucose pulses (pre-secretin glucose; 28 +/- 20 muU/ml, mean +/- SD; post-secretin glucose pulse: 45 +/- 37 muU/ml, P less than 0.5), an increase of 56 +/- 21% (P less than .005). Glucose 59-66 insulin Homo sapiens 34-41 874055-7 1977 A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Glucose 104-111 insulin Homo sapiens 84-91 874055-7 1977 A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Glucose 104-111 insulin Homo sapiens 158-165 874055-7 1977 A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Glucose 190-197 insulin Homo sapiens 84-91 874055-7 1977 A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Glucose 190-197 insulin Homo sapiens 158-165 874055-7 1977 A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Glucose 190-197 insulin Homo sapiens 84-91 874055-7 1977 A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Glucose 190-197 insulin Homo sapiens 158-165 874055-9 1977 The specificity of secretin for augmenting glucose stimulated insulin release suggets a possible role for secretin in carbohydrate metabolism. Glucose 43-50 insulin Homo sapiens 62-69 918960-5 1977 Insulin response to oral glucose was investigated in 74 patients with subclinical diabetes. Glucose 25-32 insulin Homo sapiens 0-7 918960-11 1977 In addition, it is suggested that abnormal response of plasma insulin to glucose, delayed and/or decreased, might be one of the prominent findings in diagnosis of diabetes mellitus. Glucose 73-80 insulin Homo sapiens 62-69 193007-4 1977 Basal serum insulin levels were within normal fasting levels for this age group but inappropriately elevated for the blood glucose levels. Glucose 123-130 insulin Homo sapiens 12-19 406785-8 1977 The vitamins, insulin, heparin and magnesium, in usual therapeutic concentrations, appeared to be compatible in the protein hydrolysate/dextrose solution. Glucose 136-144 insulin Homo sapiens 14-21 407039-5 1977 After institution of insulin treatment (4-8 u/h), glucose and glucagon levels decreased rapidly, and in five of the eight subjects glucagon levels reached undetectable concentrations (less than 3.0 pmol/l) during the initial treatment period. Glucose 50-57 insulin Homo sapiens 21-28 193750-0 1977 Glucose-induced proinsulin biosynthesis. Glucose 0-7 insulin Homo sapiens 16-26 863127-8 1977 It is concluded that insulin replacement, coordinated with meals in a physiologic manner, can virtually normalize plasma glucose even without feedback control of delivery rates. Glucose 121-128 insulin Homo sapiens 21-28 892126-2 1977 No elevation in plasma insulin was observed and similarly no rise in plasma C-peptide immunoreactivity occurred, indicating that somatostatin inhibits glucose-induced C-peptide release as well as insulin release. Glucose 151-158 insulin Homo sapiens 167-176 874043-0 1977 Dose response to insulin in man: differential effects on glucose and ketone body regulation. Glucose 57-64 insulin Homo sapiens 17-24 874052-0 1977 Change in affinity of insulin receptors following oral glucose in normal adults. Glucose 55-62 insulin Homo sapiens 22-29 874052-2 1977 In each study five hours after glucose ingestion, the competition-inhibition curve was shifted to the left and was steeper than that in the basal study; the amount of insulin that caused a 50% decrease in specific binding of 125I-insulin in the basal study was 3-11 fold higher than at 5 hours after glucose. Glucose 31-38 insulin Homo sapiens 167-174 874052-2 1977 In each study five hours after glucose ingestion, the competition-inhibition curve was shifted to the left and was steeper than that in the basal study; the amount of insulin that caused a 50% decrease in specific binding of 125I-insulin in the basal study was 3-11 fold higher than at 5 hours after glucose. Glucose 31-38 insulin Homo sapiens 230-237 874052-2 1977 In each study five hours after glucose ingestion, the competition-inhibition curve was shifted to the left and was steeper than that in the basal study; the amount of insulin that caused a 50% decrease in specific binding of 125I-insulin in the basal study was 3-11 fold higher than at 5 hours after glucose. Glucose 300-307 insulin Homo sapiens 167-174 895011-0 1977 [Relation between the glucose tolerance test, level of lipids, lipoproteins, insulin and growth hormone in the blood of patients with ischemic heart disease]. Glucose 22-29 insulin Homo sapiens 77-84 870793-1 1977 A 20-yr-old female with congenital lipoatrophic diabetes was studied, with the following findings: (1) Serum insulin levels increased after both oral glucose and intravenous arginine administration; there was no growth hormone response to the latter. Glucose 150-157 insulin Homo sapiens 109-116 870793-7 1977 (6) Progressive increases in doses of regular insulin before each meal resulted in up to a total of 9000 units/day being required before normal blood glucose levels were achieved. Glucose 150-157 insulin Homo sapiens 46-53 930174-7 1977 The hypertrophic fat cell needs more insulin for the induction of glucose than the normal lipocyte. Glucose 66-73 insulin Homo sapiens 37-44 328014-0 1977 The stimulus-secretion coupling of glucose-induced insulin release. Glucose 35-42 insulin Homo sapiens 51-58 328014-1 1977 Insulin release due to glycogenolysis in glucose-deprived islets. Glucose 41-48 insulin Homo sapiens 0-7 328014-3 1977 When pancreatic islets are preincubated for 20h in the presence of glucose (83.3mM) and thereafter transferred to a glucose-free medium, theophylline (1.4mM) provokes a dramatic stimulation of insulin release. Glucose 67-74 insulin Homo sapiens 193-200 328014-18 1977 These data suggest that stimulation of glycolysis from endogenous stores of glycogen is sufficient to provoke insulin release even in glucose-deprived islets, as if the binding of extracellular glucose to hypothetical plasma-membrane glucoreceptors is not an essential feature of the stimulus-secretion coupling process. Glucose 194-201 insulin Homo sapiens 110-117 876830-1 1977 With the external artificial pancreas used by the authors, blood glucose is continuously controlled by insulin delivered through an IV infusion and adjusted to two parameters: instantaneous blood glucose levels and increasing or decreasing patterns of blood glucose. Glucose 65-72 insulin Homo sapiens 103-110 327148-2 1977 As the degradation of C-peptide preferably takes place in the kidney we performed an intravenous glucose load in 32 patients with kidney diseases. Glucose 97-104 insulin Homo sapiens 22-31 861562-0 1977 Control of blood glucose during labour in diabetic women with combined glucose and low-dose insulin infusion. Glucose 17-24 insulin Homo sapiens 92-99 871187-2 1977 As a uniform stimulus for secreting insulin, 100 gm of glucose was administered orally to all patients and glucose tolerance tests were carried out. Glucose 55-62 insulin Homo sapiens 36-43 192616-11 1977 This last IVGTT revealed a glucose disappearance rate of 0.98 per cent per minute, and the slope of the regression line of serum-insulin response (IRI) on blood glucose (BG) was markedly decreased to 0.005 micronU./ml. Glucose 161-168 insulin Homo sapiens 129-136 321218-10 1977 The results are discussed in light of the two prevailing hypotheses explaining glucose induced insulin release, i.e., the receptor and the metabolism hypotheses. Glucose 79-86 insulin Homo sapiens 95-102 856648-7 1977 During the period of rapidly falling blood glucose, only plasma insulin showed any change; its response lagged behind the decline in blood glucose. Glucose 43-50 insulin Homo sapiens 64-71 856648-8 1977 By the time the fasting glucose level was attained, the plasma insulin was still almost three times the basal level. Glucose 24-31 insulin Homo sapiens 63-70 856648-9 1977 We concluded that under our experimental conditions the rate of fall in blood glucose and the degree of hypoglycemia achieved is primarily determined by the plasma insulin concentration. Glucose 78-85 insulin Homo sapiens 164-171 856649-0 1977 Serum insulin response to slow-rise glucose infusion in "genetic prediabetics" (offspring of two diabetic parents). Glucose 36-43 insulin Homo sapiens 6-13 856649-1 1977 The insulin response to a programed slow-rise glucose infusion designed to mimic the postprandial rise in glucose was studied in five offspring of two diabetic parents (ODP) and seven normal subjects. Glucose 46-53 insulin Homo sapiens 4-11 856649-5 1977 When the glucose infusion test was preceded by an acute load of glucose, similar findings in the insulin secretory dynamics were found in the ODP group. Glucose 9-16 insulin Homo sapiens 97-104 856649-5 1977 When the glucose infusion test was preceded by an acute load of glucose, similar findings in the insulin secretory dynamics were found in the ODP group. Glucose 64-71 insulin Homo sapiens 97-104 873093-4 1977 The highest insulin secretory capacity was found in subjects with the least unstable blood glucose concentration (r=0.57, p less than 0.03), and these patients required the smallest insulin doses (r=0.54, P less than 0.04). Glucose 91-98 insulin Homo sapiens 12-19 887627-6 1977 An individual model of blood glucose dynamics in the course of 24 hours is set on the computer, and then the optimal scheme of insulin treatment is chosen. Glucose 29-36 insulin Homo sapiens 127-134 356174-5 1977 Rate limiting enzyme activities in muscle tissue, phosphofructokinase and cytochrome c oxidase correlated signficantly with plasma insulin and glucose during glucose challenge. Glucose 158-165 insulin Homo sapiens 131-138 907735-0 1977 [Blood sugar and insulin levels during intravenous administration of glucose and the Rastinon test in patients with hemicrania]. Glucose 69-76 insulin Homo sapiens 17-24 347781-0 1977 [The effect of age on serum insulin level following intravenous administration of glucose, tolbutamide and glucagon]. Glucose 82-89 insulin Homo sapiens 28-35 611854-0 1977 [Serum insulin levels and blood glucose after oral glucose loading in chronic liver patients with normal and with increased body weight]. Glucose 51-58 insulin Homo sapiens 7-14 192066-3 1977 There was observed during this glucose infusion a borderline normal insulin response with a fall in plasma free fatty acids and in plasma leucine. Glucose 31-38 insulin Homo sapiens 68-75 403756-1 1977 After an intravenous glucose load in man, total serum amino acid concentrations are rapidly depressed and remain below baseline values for at least 2 to 3 hr after serum glucose and insulin have returned to preload concentrations. Glucose 21-28 insulin Homo sapiens 182-189 403756-3 1977 Although the infectious process may have some effect on insulin-stimulated hepatic disposal of a glucose load, it does not appear to influence the ability on insulin to decrease the rate of release of certain amino acids from skeletal muscle. Glucose 97-104 insulin Homo sapiens 56-63 403869-3 1977 This equality requires appropriate secretion mixtures of the biologic antagonists, insulin and glucagon, directed by a glucose sensor. Glucose 119-126 insulin Homo sapiens 83-90 862204-4 1977 Diabetics have decreased insulin responses to oral glucose compared with the meal, and the deficient insulin response to glucose probably accounts for both the raised fasting plasma glucose levels and the abnormal oral GTT. Glucose 51-58 insulin Homo sapiens 25-32 862204-5 1977 The initial insulin response to a meal is normal in mild diabetics, and is probably stimulated by secretogogues other than glucose. Glucose 123-130 insulin Homo sapiens 12-19 862206-8 1977 The glucose and glucagon responses of control subjects to insulin administration were in sharp contrast to the diabetics: blood glucose levels fell rapidly to hypoglycaemic levels and were associated with a major rise in glucagon levels (mean rise 116 pmol/1, P less than 0.001). Glucose 4-11 insulin Homo sapiens 58-65 140089-7 1977 It is suggested that, whether in response to glucose or erythrose, an increase in glycolytic flux may represent the key process involved in the identification of the secretagogue, a subsequent remodeling of calcium fluxes being apparently responsible for the activation of the insulin-releasing system. Glucose 45-52 insulin Homo sapiens 277-284 403100-6 1977 As all subjects achieve simolas SSPI while simultaneously receiving similar glucose loads, the SSPG can be used to measure individual insulin sensitivity. Glucose 76-83 insulin Homo sapiens 134-141 856655-1 1977 The plasma insulin response to both a small increase and decrease in the plasma glucose has been studied in normal and diabetic, non-obese subjects. Glucose 80-87 insulin Homo sapiens 11-18 856655-2 1977 In a second investigation the plasma insulin concentrations were measured during a gradual reduction of the raised fasting plasma glucose of diabetes to normal levels. Glucose 130-137 insulin Homo sapiens 37-44 856655-3 1977 In both studies, diabetic patients were found to have a markedly impaired response of the fasting plasma insulin to small changes in plasma glucose. Glucose 140-147 insulin Homo sapiens 105-112 845355-0 1977 A device for expressing the serum insulin glucose relationship in diabetes, hyper- or hypothyroidsm, and chronic hepatitis. Glucose 42-49 insulin Homo sapiens 34-41 845355-1 1977 When the serum insulin valves during a 50-gm oral glucose tolerance test were expressed as the function of glucose concentrations, a good linear relationship was found in normal subjects and in patients with diabetes, hyperthroidism, hypothroidism or chronic hepatitis. Glucose 50-57 insulin Homo sapiens 15-22 845355-1 1977 When the serum insulin valves during a 50-gm oral glucose tolerance test were expressed as the function of glucose concentrations, a good linear relationship was found in normal subjects and in patients with diabetes, hyperthroidism, hypothroidism or chronic hepatitis. Glucose 107-114 insulin Homo sapiens 15-22 845355-3 1977 The insulin index decreased with increasing maximal blood glucose concentration during the glucose tolerance test in diabetic patients. Glucose 58-65 insulin Homo sapiens 4-11 845358-3 1977 Results of 1 50-gm glucose tolerance test indicated a high fasting insulin level with an exaggerated response to glucose. Glucose 19-26 insulin Homo sapiens 67-74 845358-3 1977 Results of 1 50-gm glucose tolerance test indicated a high fasting insulin level with an exaggerated response to glucose. Glucose 113-120 insulin Homo sapiens 67-74 839365-3 1977 Infusion of glucose promptly suppressed glucagon values in the normal as well as in the diabetic children pretreated with half of their usual morning dose of insulin. Glucose 12-19 insulin Homo sapiens 158-165 839365-5 1977 Administration of insulin during an ongoing glucose infusion in the diabetic patients lowered their blood glucose concentration; the concentration of glucagon rose transiently when the glucose concentration fell. Glucose 44-51 insulin Homo sapiens 18-25 839365-5 1977 Administration of insulin during an ongoing glucose infusion in the diabetic patients lowered their blood glucose concentration; the concentration of glucagon rose transiently when the glucose concentration fell. Glucose 106-113 insulin Homo sapiens 18-25 839365-5 1977 Administration of insulin during an ongoing glucose infusion in the diabetic patients lowered their blood glucose concentration; the concentration of glucagon rose transiently when the glucose concentration fell. Glucose 106-113 insulin Homo sapiens 18-25 870748-4 1977 From these data it is evident that besides insulin there is another physiological agent able to enhance glucose entry into the muscle cell. Glucose 104-111 insulin Homo sapiens 43-50 403600-0 1977 [Loss of insulin during the infusion of insulin in glucose and nutrient solutions]. Glucose 51-58 insulin Homo sapiens 9-16 403600-0 1977 [Loss of insulin during the infusion of insulin in glucose and nutrient solutions]. Glucose 51-58 insulin Homo sapiens 40-47 403600-4 1977 As in pure glucose solutions of various concentrations a loss of insulin amounting to about 30% was determined in high-caloric solutions containing aminoacids. Glucose 11-18 insulin Homo sapiens 65-72 849412-0 1977 Insulin stimulation of glucose transport in adipose cells. Glucose 23-30 insulin Homo sapiens 0-7 102234-1 1977 Gestamimetic amounts of progesterone enhance basal and glucose-stimulated insulin production. Glucose 55-62 insulin Homo sapiens 74-81 102234-2 1977 Contraceptive doses of synthetic progestins cause a moderate increase or no change in glucose-stimulated insulin production, depending on route of administration and species tested. Glucose 86-93 insulin Homo sapiens 105-112 320805-4 1977 Oral-glucose-tolerance test: In 20 untreated patients the glucose- and insulin responses were significantly increased. Glucose 5-12 insulin Homo sapiens 71-78 320805-6 1977 Intravenous-glucose-tolerance test: In 28 untreated patients the K-values were significantly decreased and the insulin response increased. Glucose 11-19 insulin Homo sapiens 111-118 320805-11 1977 The glucose tolerance tests point to an increased peripheral insulin resistance. Glucose 4-11 insulin Homo sapiens 61-68 842491-7 1977 The improvement in glucose metabolism on high CHO diets appears to results from increased insulin sensitivity. Glucose 19-26 insulin Homo sapiens 90-97 190074-1 1977 Insulin can modulate glucagon-stimulated hepatic glucose production and is considered to be the major factor acting in vivo to exert a couterregulatory action to glucagon. Glucose 49-56 insulin Homo sapiens 0-7 320076-9 1977 Following intravenous insulin, the mean per cent fall in glucose before and during HTP was significantly less than in controls (p less than 0.01). Glucose 57-64 insulin Homo sapiens 22-29 323089-2 1977 Glucose intolerance, hyperinsulinemia and elevated C-peptide levels were found in cirrhotics after glucose loading and in uremics during the later part of the glucose response. Glucose 99-106 insulin Homo sapiens 51-60 323089-2 1977 Glucose intolerance, hyperinsulinemia and elevated C-peptide levels were found in cirrhotics after glucose loading and in uremics during the later part of the glucose response. Glucose 159-166 insulin Homo sapiens 51-60 838169-0 1977 Relation of fasting plasma glucose concentration to plasma insulin and glucagon concentrations. Glucose 27-34 insulin Homo sapiens 59-66 838169-5 1977 The high fasting plasma glucose probably results from the decreased insulin-secretory response to glucose. Glucose 24-31 insulin Homo sapiens 68-75 838169-5 1977 The high fasting plasma glucose probably results from the decreased insulin-secretory response to glucose. Glucose 98-105 insulin Homo sapiens 68-75 858443-4 1977 A minimal concentration of insulin is apparently indispensable to increase glucose utilisation during muscular effort. Glucose 75-82 insulin Homo sapiens 27-34 324882-2 1977 A significative increase of plasma insulin was observed at basal status and after a glucose load not only in subjects with clinical or subclinical diabetes but also in those patients without carbohydrate abnormalities. Glucose 84-91 insulin Homo sapiens 35-42 324882-3 1977 This increase is apparently not correlated to any clinical characteristic and is associated in fasting and after glucose load with increased proinsulin-like component levels especially in patients with clinical or subclinical diabetes. Glucose 113-120 insulin Homo sapiens 141-151 558952-3 1977 The pattern of plasma FFA and glucose response to exogenous insulin was similar in both groups. Glucose 30-37 insulin Homo sapiens 60-67 558952-5 1977 The significance of the differential effect of endogenous insulin on FFA and glucose metabolism in pregnant insulin-independent Natal Indian diabetics is discussed. Glucose 77-84 insulin Homo sapiens 58-65 558952-5 1977 The significance of the differential effect of endogenous insulin on FFA and glucose metabolism in pregnant insulin-independent Natal Indian diabetics is discussed. Glucose 77-84 insulin Homo sapiens 108-115 838848-0 1977 Insulin-glucagon interaction in controlling splanchnic glucose production in normal man. Glucose 55-62 insulin Homo sapiens 0-7 838848-1 1977 The interaction of glucagon and insulin in controlling hepatic glucose production in man has been inferred from studies of immunoreactive glucagon and insulin. Glucose 63-70 insulin Homo sapiens 32-39 838848-1 1977 The interaction of glucagon and insulin in controlling hepatic glucose production in man has been inferred from studies of immunoreactive glucagon and insulin. Glucose 63-70 insulin Homo sapiens 151-158 838848-2 1977 This study directly examines the interaction of glucagon and insulin in controlling net splanching glucose production (NSGP) in eight normal men. Glucose 99-106 insulin Homo sapiens 61-68 65573-7 1977 The required insulin dose need not be determined empirically, but can be calculated from the basal plasma-glucose level and the degree of obesity. Glucose 106-113 insulin Homo sapiens 13-20 15276-0 1977 The influence of insulin upon the metabolism of glucose by the brain. Glucose 48-55 insulin Homo sapiens 17-24 320878-4 1977 The highest insulin response to VIP (100.3+/-8.1 muU/min) approached the highest insulin response to glucose (119.9 +/- 12.0 muU/min). Glucose 101-108 insulin Homo sapiens 81-88 402088-8 1977 It is concluded that the administration of the investigated combination of glucose, fructose, and xylitol is justified in patients in whom hyperglycemia during infusion of glucose alone is difficult to control with insulin. Glucose 75-82 insulin Homo sapiens 215-222 577165-1 1977 In 10 insulin-independent diabetic patients and 5 healthy volunteers the basal and glucose-stimulated insulin secretion was tested before and during oral treatment with the beta-blocker 1-(4-nitrophenyl)-2-isopropylaminoethanol (nifenalol, Inpea). Glucose 83-90 insulin Homo sapiens 102-109 190047-5 1977 Insulin, however, by exerting a slower influence on the sensitivity of the liver to glucose, is very effective in "optimizing" the amount of glycogen which the liver stores during food intake. Glucose 84-91 insulin Homo sapiens 0-7 402275-6 1977 In the group which was given the glucose load during infusion of only Ringer"s lactate solution, plasma levels of insulin significantly increased soon after the glucose load and the gradually decreased. Glucose 33-40 insulin Homo sapiens 114-121 402275-6 1977 In the group which was given the glucose load during infusion of only Ringer"s lactate solution, plasma levels of insulin significantly increased soon after the glucose load and the gradually decreased. Glucose 161-168 insulin Homo sapiens 114-121 402275-7 1977 In another group which was given the glucose load during infusion of Ringer"s lactate and phentolamine, plasma levels of insulin also increased significantly after the glucose load and remained elevated during surgery. Glucose 37-44 insulin Homo sapiens 121-128 402275-7 1977 In another group which was given the glucose load during infusion of Ringer"s lactate and phentolamine, plasma levels of insulin also increased significantly after the glucose load and remained elevated during surgery. Glucose 168-175 insulin Homo sapiens 121-128 402275-8 1977 The maximum increment of plasma insulin after the glucose load in the latter group was significantly higher than that in the former group. Glucose 50-57 insulin Homo sapiens 32-39 834147-3 1977 Glucose utilization during insulin tolerance tests carried out in 6 diabetics was significantly enhanced after treatment. Glucose 0-7 insulin Homo sapiens 27-34 834147-6 1977 These data suggest that the improvement in glucose metabolism observed during short-term clofibrate administration may be due to increased insulin sensitivity. Glucose 43-50 insulin Homo sapiens 139-146 558399-0 1977 [Pancreatic endocrine dysfunction in chronic pancreatitis, with special reference to plasma pancreatic glucagon and insulin responses to oral glucose load]. Glucose 142-149 insulin Homo sapiens 116-123 847746-0 1977 Plasma C-peptide response to oral glucose in low insulin responders, subdiabetic, and diabetic subjects. Glucose 34-41 insulin Homo sapiens 7-16 847746-0 1977 Plasma C-peptide response to oral glucose in low insulin responders, subdiabetic, and diabetic subjects. Glucose 34-41 insulin Homo sapiens 49-56 847746-1 1977 It is one of the characteristic features in diabetes mellitus that insulin response to glucose is low. Glucose 87-94 insulin Homo sapiens 67-74 847746-8 1977 In the low insulin responders C-peptide response to glucose was observed to be lower like that of insulin than in the normal insulin responders. Glucose 52-59 insulin Homo sapiens 11-18 847746-8 1977 In the low insulin responders C-peptide response to glucose was observed to be lower like that of insulin than in the normal insulin responders. Glucose 52-59 insulin Homo sapiens 30-39 833144-5 1977 The insulin-like effects elicited by polyamines in fat cells (e.g. enhancement of glucose transport and inhibition of cAMP-mediated lipolysis) were dependent on H2O2 production. Glucose 82-89 insulin Homo sapiens 4-11 833144-9 1977 These findings indicate that the polyamines do not themselves mimic the actions of insulin but that the insulin-like effects result from the formation of H2O2 which has been shown to stimulate glucose transport. Glucose 193-200 insulin Homo sapiens 104-111 596101-2 1977 DPH treatment for 3 days with a dose of 300 mg/die (100 mg, 3 times daily) significantly decreased the insulin release after glucose ingestion, but did not alter the basal insulin level. Glucose 125-132 insulin Homo sapiens 103-110 596103-1 1977 The insulin response to oral glucose and to i.v tolbutamide was stuied in a group of hyperuricemic subjects and in a group of weight-matched controls. Glucose 29-36 insulin Homo sapiens 4-11 596103-3 1977 Insulin response to oral glucose was enhanced in hyperuricemic subjects. Glucose 25-32 insulin Homo sapiens 0-7 610292-0 1977 Role of divalent cations in cold and ouabain sensitive glucose uptake of adipose tissue stimulated by insulin. Glucose 55-62 insulin Homo sapiens 102-109 888734-3 1977 Studies of the systemic factors that regulate insulin release in myotonic dystrophy have shown that excessive insulin release occurs on oral glucose tolerance testing with diminished peripheral effectiveness. Glucose 141-148 insulin Homo sapiens 110-117 13654-7 1977 They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. Glucose 92-99 insulin Homo sapiens 42-49 13654-7 1977 They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. Glucose 133-140 insulin Homo sapiens 42-49 13654-7 1977 They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. Glucose 133-140 insulin Homo sapiens 42-49 842974-3 1977 After oral glucose load abnormal responses in insulin secretion were obtained in all of them, and in one patient blood glucose curve was consistent with probable chemical diabetes. Glucose 11-18 insulin Homo sapiens 46-53 192160-1 1977 Fenfluramine in therapeutic concentrations causes a significant and dose related increase in glucose uptake into isolated rat and human skeletal muscle in the presence of insulin. Glucose 93-100 insulin Homo sapiens 171-178 562650-3 1977 The glucose-stimulated plasma insulin levels were significantly reduced during Suisynchron treatment and 21 days after the end of treatment. Glucose 4-11 insulin Homo sapiens 30-37 21113-0 1977 Regulation of the conversion of glucose into fat in white adipose tissue by insulin [proceedings]. Glucose 32-39 insulin Homo sapiens 76-83 143314-0 1977 [Influence of temperature on insulin secretion induced by different concentrations of glucose]. Glucose 86-93 insulin Homo sapiens 29-36 350523-1 1977 Glucose is an effective stimulus for the release of insulin from pancreatic beta-cells but its pre-eminence for the physiological control of insulin secretion is now challenged. Glucose 0-7 insulin Homo sapiens 52-59 350523-2 1977 The insulin response to oral glucose is much greater than the response to intravenous glucose because an intestinal factor, or factors, has a powerful stimulant effect on insulin secretion. Glucose 29-36 insulin Homo sapiens 4-11 320081-1 1977 At concentrations higher than 10 mM, the cationic amino acid, arginine, inhibited the incorporation of neutral amino acids such as alanine, threonine, valine and leucine into insulin in the presence of glucose. Glucose 202-209 insulin Homo sapiens 175-182 830563-1 1977 The responses of glucagon, growth hormone, and insulin secretion to the oral administration of glucose and to the intravenous infusion of saline, arginine, and insulin were measured in seven patients who had stable diabetes, eight who had unstable diabetes, and seven healthy volunteers. Glucose 95-102 insulin Homo sapiens 47-54 830563-3 1977 The oral glucose and arginine infusion tests demonstrated partial preservation of insulin-secretory ability in stable diabetics and its virxual absence in unstable diabetics. Glucose 9-16 insulin Homo sapiens 82-89 838201-3 1977 Early insulin responses were measured after a high dose (50 g/1.73 m2) of rapidly injected glucose in 31 subjects who had repeatedly shown "lag-storage" curves in the OGTT, in 24 controls and in 19 mild maturity-onset diabetics. Glucose 91-98 insulin Homo sapiens 6-13 832653-4 1977 The insulin/glucose ratio after the end of the infusion was significantly higher than during the period of infusion of the drug. Glucose 12-19 insulin Homo sapiens 4-11 832653-5 1977 In latent diabetic patients CPZ infusion significantly diminished the insulin/glucose ratio during an intravenous glucose tolerance test. Glucose 114-121 insulin Homo sapiens 70-77 844788-7 1977 The effect of insulin on glucose incorporation was stimulating to the same extent as in the controls but the metabolis rate was even in the presence of insulin still below that of the controls. Glucose 25-32 insulin Homo sapiens 14-21 908554-6 1977 Two thirds of the short normal patients showed poor insulin responses to either amino acid or glucose stimulation. Glucose 94-101 insulin Homo sapiens 52-59 723265-0 1978 Retention of insulin-stimulated D-glucose transport activity by adipocyte plasma membranes following extraction of extrinsic proteins. Glucose 32-41 insulin Homo sapiens 13-20 723265-1 1978 Plasma membrane vesicles prepared from adipocytes incubated with insulin exhibited accelerated D-glucose transport activity characteristic to insulin action on intact fat cells. Glucose 95-104 insulin Homo sapiens 65-72 723265-1 1978 Plasma membrane vesicles prepared from adipocytes incubated with insulin exhibited accelerated D-glucose transport activity characteristic to insulin action on intact fat cells. Glucose 95-104 insulin Homo sapiens 142-149 723265-2 1978 Both control and insulin-stimulated D-glucose transport activities were inhibited by cytochalasin B and thiol reagents. Glucose 36-45 insulin Homo sapiens 17-24 723265-5 1978 Both control and insulin-activated D-glucose transport activities were retained by plasma membrane vesicles extracted with dimethylmaleic anhydride. Glucose 35-44 insulin Homo sapiens 17-24 617330-2 1977 Insulin levels at the moment of glucose-induced reactive hypoglycemia have been compared with zero-hour insulin levels in 108 subjects in whom the blood glucose had decreased to 50 mg percent or less (50 to 31 mg) at the third, fourth, or fifth hour in the course of an oral glucose tolerance test (1.75 g/kg of body weight). Glucose 32-39 insulin Homo sapiens 0-7 617330-12 1977 In subjects with insulin levels at the time of reactive hypoglycemia equal to or below the starting value, the low blood glucose level cannot be attributed to insulin. Glucose 121-128 insulin Homo sapiens 17-24 617339-3 1977 The closest relation was found between stimulated IRI values and the Broca index (3) the ratio glucose/insulin was lower in the obese women before and after a glucose load. Glucose 159-166 insulin Homo sapiens 103-110 19572-11 1977 The increase of maternal and fetal glucose was associated with an elevation of immuno-reactive insulin (IRI). Glucose 35-42 insulin Homo sapiens 95-102 19572-19 1977 The increase of insulin per glucose rise was correlated to fetal body weight. Glucose 28-35 insulin Homo sapiens 16-23 19572-21 1977 From these observations it may be concluded that in the human fetus insulin secretion following a single glucose load is generally low, however, it increases in cases where the maternal insulin response to glucose load is abnormal. Glucose 105-112 insulin Homo sapiens 68-75 19572-21 1977 From these observations it may be concluded that in the human fetus insulin secretion following a single glucose load is generally low, however, it increases in cases where the maternal insulin response to glucose load is abnormal. Glucose 206-213 insulin Homo sapiens 68-75 63654-3 1977 Plasma C-peptide and insulin response to an oral glucose load have therefore been assessed in 14 cirrhotic and 7 normal subjects. Glucose 49-56 insulin Homo sapiens 21-28 834141-2 1977 In addition, the secretory capacities of the alpha and beta cells were assessed by measurement of the amounts of glucagon and insulin released after intravenous administration of glucose and arginine, respectively. Glucose 179-186 insulin Homo sapiens 126-133 318742-7 1977 Speculation In spite of the complicating role of obesity, adolescence, and the small sample size, it is interesting to note that the correlation coefficients between triglyceride and insulin/glucose area (0.36), and insulin area (0.30), although not significant (P less than 0.1), were considerably higher in hypertriglyceridemic children than in normal subjects in whom comparable correlation coefficients were 0.08 and 0.08. Glucose 191-198 insulin Homo sapiens 183-190 264686-5 1977 Infusion of exogenous insulin so as to restore plasma insulin to preinfusion values or cessation of the somatostatin infusion with restoration of endogenous insulin secretion resulted in a prompt reduction of plasma glucose to baseline values. Glucose 216-223 insulin Homo sapiens 22-29 577018-2 1977 Also we measured using this assay system, human proinsulin C-peptide in blood after oral administration of glucose to normal subject. Glucose 107-114 insulin Homo sapiens 48-58 577018-6 1977 The measured values of human proinsulin-C-peptide in blood, using this assay system, showed insulin secretory reaction after oral administration of glucose. Glucose 148-155 insulin Homo sapiens 29-39 835136-0 1977 Insulin response to glucose or glucagon in subclinical diabetes previously injected with tolbutamide. Glucose 20-27 insulin Homo sapiens 0-7 835136-2 1977 These patients showed a delayed response of plasma insulin during oral glucose loading. Glucose 71-78 insulin Homo sapiens 51-58 835136-3 1977 In the tolbutamide-glucose test, in which glucose loading followed the intravenous tolbutamide injection at a 60-min interval, the insulin level at 90 min was significantly lowered in a group of 20 patients with subclinical diabetes. Glucose 19-26 insulin Homo sapiens 131-138 325916-3 1977 Viability was assessed by light microscopy of sections stained with aldehyde fuchsin and by measuring the insulin output of islets in response to a glucose stimulus in vitro using a perifusion system. Glucose 148-155 insulin Homo sapiens 106-113 794823-0 1976 [A method of studying insulin secretion in humans: the glucose stimulation test, followed by tolbutamide]. Glucose 55-62 insulin Homo sapiens 22-29 794823-1 1976 Various parameters of the insulin secretion in man may be appreciated and calculated by studying the insulin response to an intravenous pulse of glucose followed 120 minutes later by one of tolbutamide. Glucose 145-152 insulin Homo sapiens 26-33 794823-1 1976 Various parameters of the insulin secretion in man may be appreciated and calculated by studying the insulin response to an intravenous pulse of glucose followed 120 minutes later by one of tolbutamide. Glucose 145-152 insulin Homo sapiens 101-108 1005204-0 1976 [Insulin secretion following intravenous glucose tolerance test in chronic pancreatitis]. Glucose 41-48 insulin Homo sapiens 1-8 1005185-0 1976 [Insulin secretion following intravenous glucose load in patients having undergone acute pancreatitis]. Glucose 41-48 insulin Homo sapiens 1-8 1036650-0 1976 The effect of atropine on the insulin release caused by oral and intravenous glucose in human subjects. Glucose 77-84 insulin Homo sapiens 30-37 1036650-2 1976 Insulin release after oral glucose was significantly diminished by atropine, and this effect could not be ascribed to the drug delaying glucose absorption. Glucose 27-34 insulin Homo sapiens 0-7 1036650-3 1976 However, insulin release brought about by intravenous glucose was not altered by atropine. Glucose 54-61 insulin Homo sapiens 9-16 1052820-6 1976 Mammalian-like insulin responses to glucose, glucagon, Mg2+ lack, and tolbutamide suggest similarities between avian and mammalian beta-cell insulin secretory mechanisms. Glucose 36-43 insulin Homo sapiens 15-22 187517-5 1976 This was correlated with the insulin response to an oral glucose load and with the plasma FFA flux measured by a continuous infusion of 14C palmitate. Glucose 57-64 insulin Homo sapiens 29-36 992227-2 1976 In normal man, glucose ingestion is accompanied by a rise in insulin and fall in glucagon and is primarily disposed of in the liver, an organ sensitive to both hormones. Glucose 15-22 insulin Homo sapiens 61-68 992227-4 1976 Furthermore, minor elevations in blood glucose elicit increments in insulin concentration and inhibition of hepatic glucose output in the absence of changes in plasma glucagon. Glucose 39-46 insulin Homo sapiens 68-75 1026624-1 1976 The insulin resistance seen in obesity, which is characterized by elevated basal levels of insulin and an exaggerated insulin response to such stimuli as glucose ingestion, was thought to be related to another common characteristic of obesity--enlargement of the fat cell. Glucose 154-161 insulin Homo sapiens 4-11 187613-3 1976 The patient displayed exaggerated plasma insulin responses following oral glucose (peak response: 447 muU/ml at 30 min) and following 1 gm of iv tolbutamide (peak response: 719 muU/ml at 5 min) with symptomatic profound hypoglyceria during both tests. Glucose 74-81 insulin Homo sapiens 41-48 187613-6 1976 During the infusion of exogenous insulin (0.1 U/kg for 60 min) serum C-peptide reactivity suppressed to less than 1.3 ng/ml when the plasma glucose fell below 40 mg/dl representing normal suppression. Glucose 140-147 insulin Homo sapiens 33-40 1004956-0 1976 [Blood insulin following oral glucose and L-phenylalanine administration in children with phenylketonuria]. Glucose 30-37 insulin Homo sapiens 7-14 824621-2 1976 A bolus of 10 units of insulin followed by an average of 15 units delivered via an infusion pomp induce an immediate and regular decrease of blood glucose levels (1.63 +/- 0.15 g/h). Glucose 147-154 insulin Homo sapiens 23-30 187069-4 1976 The model predicts that, although insulin can inhibit glucose production by lowering phosphorylase and gluconeogenesis, only an insulin-mediated induction of glucokinase can account for insulin"s action to potentiate the effect of glucose alone on glycogen synthesis. Glucose 54-61 insulin Homo sapiens 34-41 187069-4 1976 The model predicts that, although insulin can inhibit glucose production by lowering phosphorylase and gluconeogenesis, only an insulin-mediated induction of glucokinase can account for insulin"s action to potentiate the effect of glucose alone on glycogen synthesis. Glucose 231-238 insulin Homo sapiens 34-41 187069-4 1976 The model predicts that, although insulin can inhibit glucose production by lowering phosphorylase and gluconeogenesis, only an insulin-mediated induction of glucokinase can account for insulin"s action to potentiate the effect of glucose alone on glycogen synthesis. Glucose 231-238 insulin Homo sapiens 128-135 189957-2 1976 Whereas the metabolism of glucose is controlled by hormones such as insulin, fructose uptake and phosphorylation in the liver occurs independently of hormones and its ultimate metabolic fate is unpredictable. Glucose 26-33 insulin Homo sapiens 68-75 825369-0 1976 Effect of insulin on glucose transport in DMBA-induced mammary tumors. Glucose 21-28 insulin Homo sapiens 10-17 12072-12 1976 Glibenclamide and glucose induce secretion of insulin originating in the same compartment. Glucose 18-25 insulin Homo sapiens 46-53 792424-2 1976 It is proposed that insulin release is initiated by glucose interacting with a glucoreceptor on the plasma membrane. Glucose 52-59 insulin Homo sapiens 20-27 792424-4 1976 It is postulated that after initiation of secretion, continued insulin release is under the control of phosphorylated intermediates of glucose metabolism, i.e. glucose-6-phosphate and phosphoenol pyruvate, operating via a membrane-bound protein kinase. Glucose 135-142 insulin Homo sapiens 63-70 10504-7 1976 A comparison was made of the capacity of native beef insulin and its triacetyl derivative to stimulate glucose oxidation by epididymal fat pads. Glucose 103-110 insulin Homo sapiens 53-60 976928-3 1976 Based on clinical experience as well as on the basis of data published by the author dealing with animal experiments and clinical research studies the hypothesis of the "permissive role" of insulin with respect to the stimulatory effect of exercise on muscle glucose metabolism is put foreward and discussed. Glucose 259-266 insulin Homo sapiens 190-197 994952-10 1976 It is suggested that continuation of low-dose insulin infusion, together with 5% dextrose solution, after the plasma glucose level reaches 200 mg/100 ml, may hasten the clearance of ketones, preventing relapse. Glucose 117-124 insulin Homo sapiens 46-53 791435-2 1976 Viablity has been assessed by light microscopy of sections stained with Gomori"s aldehyde fuchsin and by measuring the insulin release from islets in vitro in response to a glucose stimulus. Glucose 173-180 insulin Homo sapiens 119-126 976605-1 1976 Important role of the rise of blood glucose in the second phase of insulin release induced by argiinine. Glucose 36-43 insulin Homo sapiens 67-74 976605-7 1976 Pretreatment with either glucose or xylitol almost completely restored the biphasic insulin response to arginine in patients with hyperthyroidism, whereas pretreatment with aminophylline only partially improved the insulin response. Glucose 25-32 insulin Homo sapiens 84-91 976605-11 1976 The second phase of arginine-induced insulin release seems more dependent on glucose than the first phase. Glucose 77-84 insulin Homo sapiens 37-44 976638-4 1976 CPR responses to glucose were subnormal in diabetics, very low in juvenile-type cases, and often poor in patients on insulin treatment. Glucose 17-24 insulin Homo sapiens 117-124 188635-3 1976 The mechanism of insulin response to glucose has been a controversy as to whether the secretion is transmitted by beta-receptor or independent glucose receptor. Glucose 37-44 insulin Homo sapiens 17-24 967015-6 1976 The nondiabetic group was also distinguished by a significantly greater plasma insulin:blood glucose ratio in the oral glucose tolerance test. Glucose 93-100 insulin Homo sapiens 79-86 826919-4 1976 Glucose supressed the release of 3H-NE, suggesting overall that the noradrenergic feeding system in the hypothalamus of the monkey is modulated by the regional level of glucose as well as the local concentration of insulin. Glucose 0-7 insulin Homo sapiens 215-222 1006147-1 1976 Glucose-stimulated insulin secretion was measured in six normal subjects in the resting supine position, during standing, and during a period of moderate exercise in the supine position. Glucose 0-7 insulin Homo sapiens 19-26 1006147-5 1976 Glucose-stimulated insulin secretion was the same during the first 10 min after the injection of glucose in the three experiments. Glucose 0-7 insulin Homo sapiens 19-26 1006147-5 1976 Glucose-stimulated insulin secretion was the same during the first 10 min after the injection of glucose in the three experiments. Glucose 97-104 insulin Homo sapiens 19-26 185056-2 1976 We studied insulin responses to glucose with and without cholecystokinin-pancreozymin and aminophyllin infusions in normal, chronic pancreatitic and genetic (maturity-onset) diabetic subjects. Glucose 32-39 insulin Homo sapiens 11-18 185056-7 1976 Infusions of aminophyllin enhanced insulin responses (Imax) to glucose injection in normal subjects and to a lesser degree in pancreatitic subjects, but decreased sensitivity to glucose (increase in G50) in both groups. Glucose 63-70 insulin Homo sapiens 35-42 185056-11 1976 Crude cholecystokinin-pancreozymin changed the shape of the glucose/insulin dose response curve in normal, pancreatitic and diabetic subjects. Glucose 60-67 insulin Homo sapiens 68-75 973871-0 1976 [Intravenous and oral glucose: production of insulin and growth hormone in the newborn infant]. Glucose 22-29 insulin Homo sapiens 45-52 973871-1 1976 Insulin production in response to intravenous and high and low oral glucose administration was investigated in 15 healthy fasting newborns. Glucose 68-75 insulin Homo sapiens 0-7 973871-2 1976 Results show that in spite of the fact that the highest blood glucose was obtained by the intravenous load, the highest insulin levels corresponded to the high oral glucose. Glucose 165-172 insulin Homo sapiens 120-127 786513-0 1976 Significance of genetic factors for the plasma insulin response to glucose in healthy subjects. Glucose 67-74 insulin Homo sapiens 47-54 786513-1 1976 The intravenous glucose tolerance and plasma insulin response to glucose infusion were analysed in a twin and family material, comprising 279 healthy subjects. Glucose 65-72 insulin Homo sapiens 45-52 786513-2 1976 The relation between the blood glucose and plasma insulin values was studied by an analysis of the principal eigenvalues. Glucose 31-38 insulin Homo sapiens 50-57 786634-0 1976 Insulin action on glucose transport and calcium fluxes in developing muscle cells in vitro. Glucose 18-25 insulin Homo sapiens 0-7 786634-4 1976 Km-values of about 13 mM basal and 32 mM for insulin stimulation were determined and discussed with respect to the glucose transport mechanism. Glucose 115-122 insulin Homo sapiens 45-52 786634-6 1976 Moreover, the ionophore A 23187 could be shown to mimic the insulin effect on glucose uptake. Glucose 78-85 insulin Homo sapiens 60-67 786634-8 1976 We propose that insulin increases the free cytoplasmic calcium concentration, which may be the intracellular signal for the stimulation of glucose transport. Glucose 139-146 insulin Homo sapiens 16-23 955305-13 1976 Similar results were observed when hyperinsulinemia without hyperglycemia was produced by simultaneous administration of insulin and glucose. Glucose 133-140 insulin Homo sapiens 40-47 789223-3 1976 This dose-response curve is somewhat shifted to the left in comparison with previously published data for glucose-induced insulin release. Glucose 106-113 insulin Homo sapiens 122-129 783201-5 1976 The acute phase responses of insulin to intravenous, maximal stimulating doses of glucose (20 g) and arginine (2.5 g) were measured in five insulin-independent diabetics. Glucose 82-89 insulin Homo sapiens 29-36 956401-5 1976 In the subjects initially receiving the glucose infusion, arterial insulin concentration rose by 5-12 muU/ml, while splanchnic glucose output fell by 85-100%. Glucose 40-47 insulin Homo sapiens 67-74 956689-7 1976 Fasting triglyceride levels showed a significant positive correlation with the serum insulin area of the oral glucose tolerance test in the normals wna prediabetic persons, and also showed a significant positive correlation with the blood glucose area of the prediabetic and chemical diabetic patients. Glucose 110-117 insulin Homo sapiens 85-92 956689-8 1976 It is suggested that a normal relationship between triglyceride concentration and insulin response to glucose is lost in chemical diabetes. Glucose 102-109 insulin Homo sapiens 82-89 956690-0 1976 The effect of age on plasma proinsulin-like material after oral glucose. Glucose 64-71 insulin Homo sapiens 28-38 781574-0 1976 Plasma insulin response following oral and intravenous glucose in pregnant diabetic women. Glucose 55-62 insulin Homo sapiens 7-14 781574-3 1976 The plasma insulin response to intravenous and oral glucose was studied in third trimester pregnant insulin-independent diabetic and normal control patients. Glucose 52-59 insulin Homo sapiens 11-18 948369-2 1976 To assess the effect of diet and injection of short and intermediate acting insulin on glucose, diabetic patients tested their urine daily for glucose and had biweekly serum glucose tests. Glucose 87-94 insulin Homo sapiens 76-83 947442-5 1976 Close monitoring of insulin and glucose concentrations after intravenous insulin in three patients showed that despite the short half life of insulin the effect of the intravenous bolus lasted for about 60 minutes. Glucose 32-39 insulin Homo sapiens 73-80 947442-5 1976 Close monitoring of insulin and glucose concentrations after intravenous insulin in three patients showed that despite the short half life of insulin the effect of the intravenous bolus lasted for about 60 minutes. Glucose 32-39 insulin Homo sapiens 73-80 978863-0 1976 [Clinical studies on insulin response to glucose tolerance test in patients with pulmonary tuberculosis (author"s transl)]. Glucose 41-48 insulin Homo sapiens 21-28 941941-1 1976 The objective of management in the pregnant diabetic patient is to achieve physiologic glucose homeostasis through the use of diet and insulin. Glucose 87-94 insulin Homo sapiens 135-142 942294-1 1976 In peripheral and portal venous blood, the immunoreactive insulin (IRI) and glucose levels in response to orally and intravenously administered glucose were measured in 14 patients with selective gastric vagotomy and pyloroplasty (SGV+P) and in 17 control subjects with other abdominal surgery. Glucose 144-151 insulin Homo sapiens 58-65 955297-8 1976 Mean values for fasting plasma insulin and for peak insulin response to intravenously administered glucose did not change significantly. Glucose 99-106 insulin Homo sapiens 52-59 955298-1 1976 Insulin resistance and the ability of insulin to inhibit hepatic glucose production and to increas efficiency of glucose uptake were determined in 24 nonobese individuals: eight subjects with normal oral glucose tolerance, eight patients with chemical diabetes, and eight nonketotic patients with fasting hyperglycemia (greater than 150 mg. per cent). Glucose 65-72 insulin Homo sapiens 38-45 955298-2 1976 Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. Glucose 70-77 insulin Homo sapiens 0-7 955298-2 1976 Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. Glucose 70-77 insulin Homo sapiens 115-122 955298-2 1976 Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. Glucose 124-131 insulin Homo sapiens 0-7 955298-3 1976 This approach permits us to inhibit levels of exogenous insulin, and use the height of the steady-state plasma glucose response as a direct estimate of insulin resistance. Glucose 111-118 insulin Homo sapiens 152-159 955298-4 1976 The ability of insulin to inhibit hepatic glucose production and to increase efficiency of glucose uptake was calculated from the results of two studies in which a continuous infusion of 3H-2-glucose was used to measure glucose turnover rate. Glucose 42-49 insulin Homo sapiens 15-22 955298-4 1976 The ability of insulin to inhibit hepatic glucose production and to increase efficiency of glucose uptake was calculated from the results of two studies in which a continuous infusion of 3H-2-glucose was used to measure glucose turnover rate. Glucose 91-98 insulin Homo sapiens 15-22 955298-10 1976 Thus, insulin resistance exists in monoketotic diabetes, and the greater the degree of glucose intolerance, the greater the insulin resistance. Glucose 87-94 insulin Homo sapiens 124-131 955298-11 1976 The resistance to the insulin infusion in patients with chemical diabetes seemed to be mainly a function of the inability of insulin to increase efficiency of glucose uptake, since insulin did retain its ability to inhibit glucose production (although not to normal levels). Glucose 159-166 insulin Homo sapiens 125-132 955298-14 1976 Significant differences exist in the responsiveness of various tissues to the two general aspects of insulin"s action on glucose homeostasis, and these differences provide a physiologic basis for the variations in degree of over-all insulin resistance that are present in the three groups of subjects. Glucose 121-128 insulin Homo sapiens 101-108 955298-14 1976 Significant differences exist in the responsiveness of various tissues to the two general aspects of insulin"s action on glucose homeostasis, and these differences provide a physiologic basis for the variations in degree of over-all insulin resistance that are present in the three groups of subjects. Glucose 121-128 insulin Homo sapiens 233-240 964510-5 1976 Short and intermediate acting insulins given once or twice daily to diabetics maintained serum glucose levels within the normal range throughout the 24 h. Despite wide variation in serum total insulin levels, peripheral free insulin concentrations in well-controlled diabetics fell within a relatively narrow range that was higher than in controls. Glucose 95-102 insulin Homo sapiens 30-37 950374-3 1976 The glucose disappearance rate (K value) was calculated for each test between 5 min and 25 min after iv injection of insulin. Glucose 4-11 insulin Homo sapiens 117-124 960101-3 1976 A significant positive correlation was found to be present between the plasma triglyceride (TG) level and the insulin response to glucose load. Glucose 130-137 insulin Homo sapiens 110-117 960101-6 1976 The ratio of sum of plasma insulin values to that of blood glucose values during glucose tolerance test was markedly increased in patients with elevated TG. Glucose 81-88 insulin Homo sapiens 27-34 951048-0 1976 [Plasma insulin and GH during oral glucose load in liver cirrhosis]. Glucose 35-42 insulin Homo sapiens 8-15 136033-4 1976 The reactive insulin- but not HGH-levels were significantly raised, 32 % of the patients with Huntington"s chorea had abnormal glucose-tolerance tests, compared with 3.2 % in a control group. Glucose 127-134 insulin Homo sapiens 13-20 937206-3 1976 The glucose-insulin-potassium solution was composed of 300 g of glucose, 50 units of regular insulin and 80 mEq of potassium ion per liter, and was infused at a rate of 1.5 ml/kg per hour through the right atrial port of an indwelling Swan-Ganz thermodilution catheter. Glucose 4-11 insulin Homo sapiens 12-19 952747-2 1976 The pattern of insulin response to glucose is similar to that seen in typical mild maturity-onset diabetes. Glucose 35-42 insulin Homo sapiens 15-22 959937-1 1976 The plasma insulin response to oral glucose in normal, non-pregnant, premenopausal Indian, Black, andWhite women was investigated. Glucose 36-43 insulin Homo sapiens 11-18 962906-0 1976 Insulin"s effect on glucose oxidation independent of glucose transport. Glucose 20-27 insulin Homo sapiens 0-7 182185-7 1976 The drug reduced the insulin response following a glucose load with some decrease in glucose levels. Glucose 50-57 insulin Homo sapiens 21-28 182185-7 1976 The drug reduced the insulin response following a glucose load with some decrease in glucose levels. Glucose 85-92 insulin Homo sapiens 21-28 976210-4 1976 A statistically significant insulin-high-response without disturbed carbohydrate tolerance was seen in 25% after intravenous glucose infusion and in 28% after oral glucose load. Glucose 125-132 insulin Homo sapiens 28-35 1278604-6 1976 When infusing glucose alone we noted that the duration rather than the degree of hyperglycemia determined the fetal insulin response. Glucose 14-21 insulin Homo sapiens 116-123 1278604-7 1976 In fact, when glucose is given to the mother for 60 minutes the fetal insulin response is higher than when the same dose is infused for 30 minutes. Glucose 14-21 insulin Homo sapiens 70-77 783030-1 1976 The artificial beta cell is a Glucose Controlled Insulin (and dextrose) Infusion System (GCIIS) for maintaining normoglycemia in diabetic conditions and other disturbances of metabolism. Glucose 30-37 insulin Homo sapiens 49-56 783030-2 1976 The insulin and dextrose infusion rates are calculated by a microcomputer according to the static glucose concentration (proportional control) and to its rate of change (dynamic control). Glucose 98-105 insulin Homo sapiens 4-11 955557-9 1976 In our patients the diabetogenic effect of triamcinolone was inversely related to the saturation with thyroid hormones and an increased response of insulin to glucose load was observed only in euthyroidism. Glucose 159-166 insulin Homo sapiens 148-155 1278606-6 1976 By using these two parameters obtained during standard intravenous glucose tolerance testing, we have shown that it is possible to calculate the rate of glucose infusion required to achieve successfully in man a ramp of plasma glucose of any desired steepness and to characterize the consequent insulin secretion. Glucose 153-160 insulin Homo sapiens 295-302 1278606-6 1976 By using these two parameters obtained during standard intravenous glucose tolerance testing, we have shown that it is possible to calculate the rate of glucose infusion required to achieve successfully in man a ramp of plasma glucose of any desired steepness and to characterize the consequent insulin secretion. Glucose 153-160 insulin Homo sapiens 295-302 976210-4 1976 A statistically significant insulin-high-response without disturbed carbohydrate tolerance was seen in 25% after intravenous glucose infusion and in 28% after oral glucose load. Glucose 164-171 insulin Homo sapiens 28-35 1278607-0 1976 Insulin response to oral glucose in patients with a previous myocardial infarction and in patients with peripheral vascular disease. Glucose 25-32 insulin Homo sapiens 0-7 1278607-2 1976 The insulin response to an oral glucose load (100 gm.) Glucose 32-39 insulin Homo sapiens 4-11 1022600-0 1976 [Effects of treatment with clofibrate on insulin response to venous overload with glucose]. Glucose 82-89 insulin Homo sapiens 41-48 6491-2 1976 Insulin decreased the mean (+/-SEM) plasma glucose from 89+/-3 to 39+/-2 mg/dl 25 min after injection, but this decline ceased despite serum insulin levels of 153+/-22 mul/ml. Glucose 43-50 insulin Homo sapiens 0-7 6491-3 1976 Before insulin, glucose inflow and outflow were constant averaging 125.3+/-7.1 mg/kg per h. 15 min after insulin, mean glucose outflow increased threefold, but then decreased at 25 min, reaching a rate 15% less than the preinsulin rate. Glucose 119-126 insulin Homo sapiens 105-112 6491-8 1976 Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Glucose 74-81 insulin Homo sapiens 6-13 959752-6 1976 Insulin at a physiological concentration (300 mU/l) and dexamethasone (0.001 mmol/l) had slight but significant effects on the incorporation rate of alanine into glucose and glycogen, respectively. Glucose 163-170 insulin Homo sapiens 0-7 6491-8 1976 Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Glucose 112-119 insulin Homo sapiens 6-13 800643-0 1976 [Dynamics of the content of immunoreactive insulin and sugar in the blood during tests with glucose, tolbutamide and leucine in patients with Cushing"s syndrome]. Glucose 92-99 insulin Homo sapiens 43-50 73696-2 1976 In diabetes this hepatic "insulin sensor" increases the basal plasma-glucose until the impaired beta cells are sufficiently stimulated to secrete normal basal insulin concentrations. Glucose 69-76 insulin Homo sapiens 26-33 73696-2 1976 In diabetes this hepatic "insulin sensor" increases the basal plasma-glucose until the impaired beta cells are sufficiently stimulated to secrete normal basal insulin concentrations. Glucose 69-76 insulin Homo sapiens 159-166 179751-5 1976 The increase was absent when hypoglycaemia was lessened by infusion of glucose after insulin injection. Glucose 71-78 insulin Homo sapiens 85-92 820228-4 1976 The amount of insulin necessary to lower plasma glucose to 250 mg/dl was 263 +/- 45 U in the high-dose group and 46 +/- 5 U in the low-dose group. Glucose 48-55 insulin Homo sapiens 14-21 995768-4 1976 The dose-effect relationship curve was plotted against the effect of glucose utilization caused by increasing concentrations of insulin in the suspensions of adipocytes of lean and obese subjects. Glucose 69-76 insulin Homo sapiens 128-135 995768-6 1976 It was found that adipocytes of 15 subjects with hyperthrophic obesity showed a significantly decreased effect of insulin regulating glucose utilization and glycerol release. Glucose 133-140 insulin Homo sapiens 114-121 995768-8 1976 The curve of relationship between insulin concentration in the incubation medium and its effect on glucose utilization by the adipocytes was changed. Glucose 99-106 insulin Homo sapiens 34-41 932179-0 1976 The effect of rate and dose of glucose infusion on the acute insulin response in man. Glucose 31-38 insulin Homo sapiens 61-68 1278602-0 1976 Insulin and free fatty acid levels during oral glucose tolerance tests and their relation to age in 70 healthy children. Glucose 47-54 insulin Homo sapiens 0-7 1278602-3 1976 It is demonstrated that (1) glucose levels are significantly lower in young children (younger than five years); (2) there are no significant age-related changes in free fatty acid concentration; (3) insulin levels are increasing constantly and significantly with age, the most strikingly at the age of onset of puberty; the absence of notable changes in glucose tolerance results in a rise of the I/G ratio as well. Glucose 28-35 insulin Homo sapiens 199-206 1278602-3 1976 It is demonstrated that (1) glucose levels are significantly lower in young children (younger than five years); (2) there are no significant age-related changes in free fatty acid concentration; (3) insulin levels are increasing constantly and significantly with age, the most strikingly at the age of onset of puberty; the absence of notable changes in glucose tolerance results in a rise of the I/G ratio as well. Glucose 354-361 insulin Homo sapiens 199-206 932179-1 1976 Two types of studies have been done to determine the importance of the rate of plasma glucose concentration change to the magnitude of the acute insulin response following an intravenous glucose injection in normal men. Glucose 86-93 insulin Homo sapiens 145-152 932179-1 1976 Two types of studies have been done to determine the importance of the rate of plasma glucose concentration change to the magnitude of the acute insulin response following an intravenous glucose injection in normal men. Glucose 187-194 insulin Homo sapiens 145-152 932179-2 1976 When an identical amount of glucose (20 g) was given at varying infusion rates (1.67 g/min to 66.7 g/min), the magnitude of the acute insulin response was found to be proportional to the rate. Glucose 28-35 insulin Homo sapiens 134-141 932179-4 1976 When 5 g of glucose was given in 0.3 and 3 minutes, a sub-maximal acute insulin response resulted which was still rate-dependent (delta peak IRI=35.5 +/- 5 at 5 g/0.3 minutes, 21.8 +/- 3 at 5 g/3 minutes). Glucose 12-19 insulin Homo sapiens 72-79 1020610-4 1976 The circadian variation of the insulin-induced hypoglycemia depends on the time recovery from the glucose fall rather than on lower circulating glucose levels attained following hormone injection. Glucose 98-105 insulin Homo sapiens 31-38 1268654-1 1976 Insulin supplements, predominantly as a constant basal fish insulin infusion, were given to patients with mild diabetes to reduce the overnight fasting glucose level to normal. Glucose 152-159 insulin Homo sapiens 0-7 1268654-2 1976 The basal plasma human insulin levels were reduced to subnormal levels by the infusion, and the insulin response to intravenous glucose was enhanced. Glucose 128-135 insulin Homo sapiens 96-103 969331-0 1976 [Blood insulin content in adolescents as indicated by the standard glucose tolerance test]. Glucose 67-74 insulin Homo sapiens 7-14 969704-0 1976 [The effect of caffeine on the serum insulin level during intravenous glucose tolerance test in patients with chemical diabetes]. Glucose 70-77 insulin Homo sapiens 37-44 969704-5 1976 Insulin levels showed a decrease particularly during the first five minutes after glucose. Glucose 82-89 insulin Homo sapiens 0-7 1020610-4 1976 The circadian variation of the insulin-induced hypoglycemia depends on the time recovery from the glucose fall rather than on lower circulating glucose levels attained following hormone injection. Glucose 144-151 insulin Homo sapiens 31-38 179434-3 1976 In the patients with successful extended right hepatectomy, gradually increasing and long-standing hyperglycemia (linear GTT pattern) in response to an oral glucose load was not observed after hepatectomy and the insulin response was significantly greater than that in controls. Glucose 157-164 insulin Homo sapiens 213-220 780246-6 1976 When insulin release was stimulated, by incubating islets in high glucose concentrations or by increasing the intracellular concentration of cyclic AMP there was a reduction in the content of subunit protein. Glucose 66-73 insulin Homo sapiens 5-12 1269841-14 1976 In addition, mean insulin levels were significantly higher during hyperglycemic than during normoglycemic glucose levels at similar postnatal age. Glucose 106-113 insulin Homo sapiens 18-25 131727-4 1976 The basal rate of glucose incorporation into the lipids was enhanced in the explants cultured with insulin. Glucose 18-25 insulin Homo sapiens 99-106 131727-6 1976 Thus, it seems that prolonged exposure to insulin leads to a diminished acute effect of the hormone on glucose metabolism. Glucose 103-110 insulin Homo sapiens 42-49 131727-13 1976 Most probably, then, this stimulating effect of insulin is exerted on the membrane and the rate of glucose transport. Glucose 99-106 insulin Homo sapiens 48-55 1011418-0 1976 [Development of an automatic system of insulin infusion controlled by blood sugar, its system for the determination of glucose and control algorithms]. Glucose 119-126 insulin Homo sapiens 39-46 817952-2 1976 Both peptides were inactive alone and active only in the presence of insulin to enhance glucose uptake, glycogen synthesis, and glycogen synthase conversion to the active I form in vitro and in vivo. Glucose 88-95 insulin Homo sapiens 69-76 817952-4 1976 No response was obtained with glucose alone, but the presence of glucose did enhance the response of insulin alone or insulin in the presence of peptide. Glucose 65-72 insulin Homo sapiens 101-108 817952-4 1976 No response was obtained with glucose alone, but the presence of glucose did enhance the response of insulin alone or insulin in the presence of peptide. Glucose 65-72 insulin Homo sapiens 118-125 1270578-5 1976 Intravenous insulin injection produced an increase in plasma glucagon and cortisol reaching a 2-fold increase above the fasting level 30 minutes after the glucose nadir. Glucose 155-162 insulin Homo sapiens 12-19 1270578-6 1976 An equivalent amount of intramuscular insulin produced a maximal increase in plasma insulin at 50 minutes (45 +/- 4 muU/ml) and caused a 35% drop in plasma glucose at 60 minutes, which effects were greater than those caused by subcutaneous injection (highest IRI = 36 +/- 3.5 muU/ml and 23% glucose drop at 180 minutes). Glucose 156-163 insulin Homo sapiens 38-45 1270578-6 1976 An equivalent amount of intramuscular insulin produced a maximal increase in plasma insulin at 50 minutes (45 +/- 4 muU/ml) and caused a 35% drop in plasma glucose at 60 minutes, which effects were greater than those caused by subcutaneous injection (highest IRI = 36 +/- 3.5 muU/ml and 23% glucose drop at 180 minutes). Glucose 291-298 insulin Homo sapiens 38-45 1270578-8 1976 Our studies suggest that, in normal lean subjects, insulin injection by the intramuscular route provides a faster absorption of insulin with a concomitant greater drop in plasma glucose than does injection by the subcutaneous route. Glucose 178-185 insulin Homo sapiens 51-58 1273731-1 1976 A study was undertaken to establish the plasma insulin response to an oral glucose load of 100 g in pregnant diabetic Indian women living in Natal. Glucose 75-82 insulin Homo sapiens 47-54 935327-2 1976 When conditioning procedures are employed, the repeated administration of large amounts of insulin, or of glucose, leads to a conditioned decrease of blood glucose whereas the repeated administration of smaller amounts of insulin leads to a conditioned increase of glucose. Glucose 156-163 insulin Homo sapiens 91-98 973964-2 1976 Statistical analysis indicated that the relationships between age and both glucose uptake and the response to insulin were significant, older patients in general having higher uptakes. Glucose 75-82 insulin Homo sapiens 110-117 935327-2 1976 When conditioning procedures are employed, the repeated administration of large amounts of insulin, or of glucose, leads to a conditioned decrease of blood glucose whereas the repeated administration of smaller amounts of insulin leads to a conditioned increase of glucose. Glucose 156-163 insulin Homo sapiens 91-98 946563-0 1976 Diminished sensitivity of the insulin response to glucose following growth hormone influsion in man. Glucose 50-57 insulin Homo sapiens 30-37 946563-1 1976 The acute effect of growth hormone (GH) administration on the dose-kinetics of glucose-stimulated insulin release was investigated in eight healthy, non-obese male subjects. Glucose 79-86 insulin Homo sapiens 98-105 946563-6 1976 Both the initial late phases of insulin response to glucose were impaired following GH treatment. Glucose 52-59 insulin Homo sapiens 32-39 946563-9 1976 The blood glucose-plasma insulin dose-response curves were shifted to the right of the control ones when glucose infusion was preceded by GH. Glucose 10-17 insulin Homo sapiens 25-32 946563-9 1976 The blood glucose-plasma insulin dose-response curves were shifted to the right of the control ones when glucose infusion was preceded by GH. Glucose 105-112 insulin Homo sapiens 25-32 946563-10 1976 These findings suggest that GH diminishes the sensitivity of the islet for the insulin releasing action of glucose. Glucose 107-114 insulin Homo sapiens 79-86 946564-2 1976 Comparison of the effects of somatostatin on insulin release induced by glucose, glucagon and tolbutamide. Glucose 72-79 insulin Homo sapiens 45-52 818514-6 1976 While the clinical application of somatostatin in diabetes mellitus seems problematic at present, the use of a glucose-controlled system of insulin infusion ("artificial pancreas") makes possible a metabolic state approaching the healthy condition. Glucose 111-118 insulin Homo sapiens 140-147 769633-3 1976 The paradoxical hyperkalemic response to glucose in patients with combined hormonal deficiency was blunted by prior administration of desoxycorticosterone acetate and abolished by prior administration of insulin. Glucose 41-48 insulin Homo sapiens 204-211 773721-1 1976 From the dose-response relations between glucose and insulin after oral glucose loading, a reproducible parameter for beta-cell response was deduced. Glucose 41-48 insulin Homo sapiens 53-60 946564-3 1976 Somatostatin in as small a dose as 70 mug given over a period of 90 min to seven healthy subjects inhibited insulin release induced by glucose (500 mg/kg as a bolus + 20 mg/kg/min). Glucose 135-142 insulin Homo sapiens 108-115 946564-5 1976 Somatostatin in nine subjects also inhibited insulin release induced by glucagon and tolbutamide, and this inhibition was of the same order of magnitude as that of glucose induced insulin release. Glucose 164-171 insulin Homo sapiens 180-187 773721-1 1976 From the dose-response relations between glucose and insulin after oral glucose loading, a reproducible parameter for beta-cell response was deduced. Glucose 72-79 insulin Homo sapiens 53-60 1052263-1 1976 The data herein presented describe, identify, and quantitate interrelationships among blood glucose and serum insulin, growth hormone, cortisol, and glucagon levels of hospitalized insulin-treated diabetic patients. Glucose 92-99 insulin Homo sapiens 110-117 773721-2 1976 The main advantage of this parameter -corrected insulin response, defined as CIR = I- 100/G(G-70)- lies in it independence from the initial or reached glucose level. Glucose 151-158 insulin Homo sapiens 48-55 773722-2 1976 Approximation of the peripheral insulin resistance after oral glucose loading. Glucose 62-69 insulin Homo sapiens 32-39 773722-3 1976 A parameter of peripheral insulin activity (A = 10(4)/IpGp) can be obtained after oral glucose loading by simple calcuation using insulin and glucose levels at the glucose peak. Glucose 87-94 insulin Homo sapiens 26-33 773722-3 1976 A parameter of peripheral insulin activity (A = 10(4)/IpGp) can be obtained after oral glucose loading by simple calcuation using insulin and glucose levels at the glucose peak. Glucose 142-149 insulin Homo sapiens 26-33 1052263-1 1976 The data herein presented describe, identify, and quantitate interrelationships among blood glucose and serum insulin, growth hormone, cortisol, and glucagon levels of hospitalized insulin-treated diabetic patients. Glucose 92-99 insulin Homo sapiens 181-188 773722-3 1976 A parameter of peripheral insulin activity (A = 10(4)/IpGp) can be obtained after oral glucose loading by simple calcuation using insulin and glucose levels at the glucose peak. Glucose 142-149 insulin Homo sapiens 26-33 773722-6 1976 The parameters allow one to separate the contributions of beta-cell function and peripheral insulin resistance to the glucose tolerance observed after glucose loading. Glucose 118-125 insulin Homo sapiens 92-99 178856-10 1976 When glucose, ATP and Ca2+ are added together a positive cooperative effect is produced with over 85% of the total insulin, added in the form of beta-granules, being released into the medium in 10 min. Glucose 5-12 insulin Homo sapiens 115-122 773722-6 1976 The parameters allow one to separate the contributions of beta-cell function and peripheral insulin resistance to the glucose tolerance observed after glucose loading. Glucose 151-158 insulin Homo sapiens 92-99 820717-5 1976 When glucagon was infused along with insulin, plasma glucose levels rose from 94 +/- 8 to 126 +/- 12 mg/100 ml over 1 h (P less than 0.01); growth hormone, beta-hydroxy-butyrate, alanine, FFA, and glycerol levels did not change. Glucose 53-60 insulin Homo sapiens 37-44 4730-5 1976 For excluding of a disturbance of the carbohydrate metabolism in addition to blood sugar determinations, glucose tolerance and tolbutamide tests, the determination of insulin activity is indicated. Glucose 105-112 insulin Homo sapiens 167-174 1263839-5 1976 Dialysis does not improve glucose tolerance, but does increase glucose-stimulated insulin release suggesting that insulin antagonism is not ameliorated. Glucose 63-70 insulin Homo sapiens 82-89 820717-6 1976 When insulin was withdrawn, plasma glucose, beta-hydroxybutyrate, FFA, and glycerol all rose to higher levels (P less than 0.01) than those observed under similar conditions when somatostatin alone had been infused to suppress glucagon secretion. Glucose 35-42 insulin Homo sapiens 5-12 1272253-3 1976 Transport of 3-O-methylglucose, a non-metabolizable analogue of glucose, occurred by facilitated diffusion, was inhibited by glucose, phloridzin, cytochalasin B and dipyridamole, and was rapidly stimulated by insulin as well as lectins. Glucose 23-30 insulin Homo sapiens 209-216 178501-4 1976 Insulin release after such an enzymatic attack is characterized by an enhanced basal secretion and a diminished and delayed glucose response. Glucose 124-131 insulin Homo sapiens 0-7 1272253-3 1976 Transport of 3-O-methylglucose, a non-metabolizable analogue of glucose, occurred by facilitated diffusion, was inhibited by glucose, phloridzin, cytochalasin B and dipyridamole, and was rapidly stimulated by insulin as well as lectins. Glucose 64-71 insulin Homo sapiens 209-216 176151-8 1976 Insulin addition (10 nM) stimulated [14C]glucose incorporation into glycogen at all stages of the culture when grown in the presence of cortisol; no glycogenic response to insulin was observed 6 hours after transplantation where cortisol was not previously introduced. Glucose 41-48 insulin Homo sapiens 0-7 1259488-0 1976 Insulin response to glucose in hypermetabolic burn patients. Glucose 20-27 insulin Homo sapiens 0-7 1259488-6 1976 In these burn patients, hypermetabolism and negative nitrogen balance occurred in association with a normal insulin response to glucose. Glucose 128-135 insulin Homo sapiens 108-115 176077-5 1976 It is shown that the concentrations of insulin needed to obtain an antilipolytic effect is far below that needed to stimulate glucose incorporation. Glucose 126-133 insulin Homo sapiens 39-46 179741-3 1976 In this way it has been possible to show that the glucose of ACD blood stimulates insulin and GH secretion and that the stimulation of insulin secretion is less, and that of GH more, if the transfusion is performed via the umbilical artery rather than via the vein. Glucose 50-57 insulin Homo sapiens 82-89 1253528-5 1976 Comparison of the regressions of glucose oxidation rates on mean cell size indicated: (i) that insulin produced a significant increase in activity over the basal value in both groups, and (ii) that basal and insulin-stimulated activity were both significantly lower in diabetic than in non-diabetic adipose tissue. Glucose 33-40 insulin Homo sapiens 95-102 1253528-5 1976 Comparison of the regressions of glucose oxidation rates on mean cell size indicated: (i) that insulin produced a significant increase in activity over the basal value in both groups, and (ii) that basal and insulin-stimulated activity were both significantly lower in diabetic than in non-diabetic adipose tissue. Glucose 33-40 insulin Homo sapiens 208-215 1261074-4 1976 In a previous paper, we reported significant differences between Lp(a+) and Lp(a-) individuals with respect to the relationships between insulin level and blood glucose concentration, and between insulin level and fasting triglyceride concentration. Glucose 161-168 insulin Homo sapiens 137-144 947950-0 1976 Insulin release is glucose anomeric specific in the human. Glucose 19-26 insulin Homo sapiens 0-7 946344-0 1976 Effect of somatostatin on basal and glucose induced insulin release in five patients with hyperinsulinaemia. Glucose 36-43 insulin Homo sapiens 52-59 946344-2 1976 These three subjects also showed a marked insulin response to glucose infusion. Glucose 62-69 insulin Homo sapiens 42-49 946344-4 1976 In the patient with islet hyperplasia and in one of the adenoma patients, who had an exaggerated insulin response to glucose (maximal response 10-30 times the basal insulin value), somatostatin also suppressed glucose induced insulin release. Glucose 117-124 insulin Homo sapiens 97-104 946344-5 1976 Our data suggest a beneficial therapeutic effect of somatostatin in patients with spontaneous hyperinsulinism with a pronounced insulin response to glucose. Glucose 148-155 insulin Homo sapiens 99-106 1107504-6 1976 Peak plasma insulin levels increased in response to glucose administration after HGH suggesting that GH has a direct effect on the pancreatic beta cell which is not mediated by Sm. Glucose 52-59 insulin Homo sapiens 12-19 931713-2 1976 A tendency to higher blood glucose levels and a statistically significant increase in insulin levels were found in the older age group in response to the glucose load. Glucose 154-161 insulin Homo sapiens 86-93 931713-5 1976 Our findings demonstrate the necessity of applying norms for the oral glucose tolerance test according to age, particularly with respect to insulin values. Glucose 70-77 insulin Homo sapiens 140-147 944163-0 1976 Diurnal variation in blood sugar and serum insulin in response to glucose and/or glucagon in healthy subjects. Glucose 66-73 insulin Homo sapiens 43-50 944163-6 1976 However, the insulin/glucose ratio (I/G) was significantly lower at 18.00 at 55-85 men. Glucose 21-28 insulin Homo sapiens 13-20 944163-11 1976 The existence of a diurnal variation in the blood sugar after intravenous glucose load, as well as after glucagon, seems to be correlated to a simultaneous diurnal variation in the insulin response, suggesting decreased pancreatic beta-cell activity in the afternoon. Glucose 74-81 insulin Homo sapiens 181-188 1254373-0 1976 Inhibitory effect of an intravenous glucose load on basal and insulin-stimulated gastric acid secretion in man. Glucose 36-43 insulin Homo sapiens 62-69 1254373-1 1976 The effect of intravenous glucose on basal and insulin-stimulated gastric acid secretion was investigated in a crossover study on four healthy subjects. Glucose 26-33 insulin Homo sapiens 47-54 1250162-0 1976 The influence of oral glucose loading on the insulin response to i.v. Glucose 22-29 insulin Homo sapiens 45-52 1273492-0 1976 The early serum insulin response to intravenous glucose in patients with decreased glucose tolerance and in subjects with a familial history of diabetes mellitus. Glucose 48-55 insulin Homo sapiens 16-23 1256946-2 1976 The response to an intravenous injection of glucose was utilized to measure the insulin response of the infants at 6 months. Glucose 44-51 insulin Homo sapiens 80-87 1273492-2 1976 The possible predictive value for later diabetes mellitus of early serum insulin response after intravenous glucose administration was evaluated by studying subjects with a familial history of diabetes mellitus and patients with different degrees of glucose intolerance. Glucose 250-257 insulin Homo sapiens 73-80 1273492-3 1976 The following conclusions were drawn: The early appearance of glucose-stimulated serum insulin should be studied during the first 6 min after start of the glucose injection. Glucose 62-69 insulin Homo sapiens 87-94 55717-6 1976 Pharmacological agents such as diazoxide, which inhibit glucose-induced insulin release, may have a place in preserving and restoring insulin secretion in diabetes. Glucose 56-63 insulin Homo sapiens 72-79 1273492-3 1976 The following conclusions were drawn: The early appearance of glucose-stimulated serum insulin should be studied during the first 6 min after start of the glucose injection. Glucose 155-162 insulin Homo sapiens 87-94 936702-0 1976 [Carbohydrate tolerance and behavior of insulin in the glucose infusion test in persons with normal weight with prediabetic suspicion]. Glucose 55-62 insulin Homo sapiens 40-47 1273492-5 1976 Serum insulin values in patients with decreased glucose tolerance and subjects with a familial history of diabetes mellitus were best characterized by an insulin concentration index (glucose-stimulated early serum insulin concentration divided by basal serum insulin concentration). Glucose 48-55 insulin Homo sapiens 6-13 1249055-14 1976 The inhibition constant estimated from such experiments was about 5 mM both in the absence and the presence of insulin, and the insulin-induced increase in the rate of glucose incorporation was similar to the increase in the rate of the 3-O-methylglucose exchange process. Glucose 168-175 insulin Homo sapiens 128-135 791729-3 1976 Mg2+ in high concentration (10 to 20 mEq/l) caused a dose-related inhibition of glucose-induced 45calcium net uptake and subsequent insulin release in isolated islets. Glucose 80-87 insulin Homo sapiens 132-139 1032812-7 1976 Both the fasting plasma insulin and insulin response following glucose injection were lower in patients with severe pre-eclampsia than in those with mild pre-eclampsia or a normal pregnancy. Glucose 63-70 insulin Homo sapiens 24-31 1247351-3 1976 Heterogeneity of insulin responses to glucose was foung among nonobese patients with maturity-onset-type diabetes. Glucose 38-45 insulin Homo sapiens 17-24 1032812-7 1976 Both the fasting plasma insulin and insulin response following glucose injection were lower in patients with severe pre-eclampsia than in those with mild pre-eclampsia or a normal pregnancy. Glucose 63-70 insulin Homo sapiens 36-43 1247351-4 1976 Prospective studies in young patients have shown that glucose intolerance may not progress for as long as 22 years and that subnormal insulin responses to glucose have not decreased further, up to 12 years. Glucose 155-162 insulin Homo sapiens 134-141 1247351-7 1976 Thus, insulin response to glucose has prognostic implications. Glucose 26-33 insulin Homo sapiens 6-13 1245144-7 1976 The insulin levels were examined under glucose load by the radioimmunological assay of Hales and Randle. Glucose 39-46 insulin Homo sapiens 4-11 1253525-8 1976 In the diabetic subjects, there was an inverse correlation between the insulin at 60 min after glucose and the 77Br/133Xe clearance ratio. Glucose 95-102 insulin Homo sapiens 71-78 1253525-11 1976 The results demonstrate that a reduced insulin response to oral glucose is associated with increased capillary permability and may play a role in the development of microangiopathy. Glucose 64-71 insulin Homo sapiens 39-46 814025-3 1976 In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. Glucose 33-40 insulin Homo sapiens 52-59 1248452-3 1976 When glucose was given during phentolamine administration, insulin levels rose more in the epinephrine-treated animals than in the hypoxic animals, despite similar blood glucose levels. Glucose 5-12 insulin Homo sapiens 59-66 765121-4 1976 Cytochalasin B also caused a partial inhibition of 45calcium uptake and proinsulin synthesis evoked by glucose in low concentration (5.6 mM), these findings being compatible with a modest impairment of the process of glucose recognition by the beta-cell. Glucose 103-110 insulin Homo sapiens 72-82 1262429-0 1976 Relationships between fasting plasma glucose levels and insulin secretion during intravenous glucose tolerance tests. Glucose 37-44 insulin Homo sapiens 56-63 177444-3 1976 The mean concentration of serum insulin increased from 19 muU/ml during fasting to maximum of 90 muU/ml after 60 min of glucose load and then gradually declined to 38 muU/ml by 180 min. Glucose 120-127 insulin Homo sapiens 32-39 1278122-0 1976 Alterations of insulin-secreting response to glucose in human infants during the early postnatal period. Glucose 45-52 insulin Homo sapiens 15-22 1278122-3 1976 The younger infants tended to have delayed and diminished insulin responses to a glucose load than did older infants. Glucose 81-88 insulin Homo sapiens 58-65 1278122-4 1976 The ratio of the increment of insulin concentration to the increment of glucose concentration at 30 minutes following a glucose load in younger infants, aged one to 20 days, was below 0.4. Glucose 72-79 insulin Homo sapiens 30-37 1278122-4 1976 The ratio of the increment of insulin concentration to the increment of glucose concentration at 30 minutes following a glucose load in younger infants, aged one to 20 days, was below 0.4. Glucose 120-127 insulin Homo sapiens 30-37 1262429-2 1976 The acute insulin response was present in subjects with fasting glucose levels below 115 mg/dl but was absent above this level. Glucose 64-71 insulin Homo sapiens 10-17 1262429-0 1976 Relationships between fasting plasma glucose levels and insulin secretion during intravenous glucose tolerance tests. Glucose 93-100 insulin Homo sapiens 56-63 1262429-3 1976 The glucose disappearance rate related to the relative acute insulin response in subjects with fasting glucose below 115 mg/dl and to total insulin response when fasting glucose levels were above 115 mg/dl. Glucose 4-11 insulin Homo sapiens 61-68 1262429-3 1976 The glucose disappearance rate related to the relative acute insulin response in subjects with fasting glucose below 115 mg/dl and to total insulin response when fasting glucose levels were above 115 mg/dl. Glucose 4-11 insulin Homo sapiens 140-147 814623-4 1976 Insulin therapy is titrated against the change in blood glucose concentration. Glucose 56-63 insulin Homo sapiens 0-7 1262429-3 1976 The glucose disappearance rate related to the relative acute insulin response in subjects with fasting glucose below 115 mg/dl and to total insulin response when fasting glucose levels were above 115 mg/dl. Glucose 103-110 insulin Homo sapiens 61-68 1262429-3 1976 The glucose disappearance rate related to the relative acute insulin response in subjects with fasting glucose below 115 mg/dl and to total insulin response when fasting glucose levels were above 115 mg/dl. Glucose 103-110 insulin Homo sapiens 61-68 826064-8 1976 Furthermore it was found that L-leucine and B-hydroxybutyric acid were able to replace glucose as a long-term stimulus of the insulin biosynthesis, while succinate and HB 419 did not share this property. Glucose 87-94 insulin Homo sapiens 126-133 1258486-6 1976 Basal glucose oxidation was slightly, but significantly increased by insulin. Glucose 6-13 insulin Homo sapiens 69-76 1258487-2 1976 A decrease in blood glucose level was observed in 6 patients during the course of the day, accompanied by an increase in immunoreactive insulin during the first half of the day and an increase in the insulinogenic index. Glucose 20-27 insulin Homo sapiens 136-143 788425-3 1976 Serum-immunoreactive insulin response on glucose load was observed during the operation of 13 patients. Glucose 41-48 insulin Homo sapiens 21-28 788425-8 1976 The probable pathomechanism of the lacking insulin secretion on glucose is discussed. Glucose 64-71 insulin Homo sapiens 43-50 58542-0 1976 Pre-beta1-lipoprotein and Lp(a) antigen in relation to triglyceride levels and insulin release following an oral glucose load in middle-aged males. Glucose 113-120 insulin Homo sapiens 79-86 58542-3 1976 At 60 min during the OGTT, triglyceride and insulin correlated significantly in pre-beta1-/Lp(a-) individuals, but not in pre-beta1 + or Lp (a+) individuals; on the other hand, insulin correlated significantly with blood glucose at this time in the pre-beta1 + and Lp(a+) individuals, but not in the pre-beta1-/Lp(a-). Glucose 221-228 insulin Homo sapiens 177-184 184688-1 1976 The insulin level has been determined simultaneously in portal and hepatic venous blood in four patients with insuloma before and after administration of glucose and tolbutamide. Glucose 154-161 insulin Homo sapiens 4-11 814810-3 1976 The mean plasma insulin response of patients with either borderline abnormalities of glucose tolerance or chemical diabetes was equal to or greater than that of normal subjects at all points during the glucose tolerance test. Glucose 85-92 insulin Homo sapiens 16-23 1030569-3 1976 The activity of glucose metabolism in obese individuals was found to be inversely related to the degree of obesity under basal conditions as well as under the effect of insulin. Glucose 16-23 insulin Homo sapiens 169-176 1031550-3 1976 Insulin secretory response to glucose was reduced in Type V and heterogeneous in Type IV hyperlipoproteinaemia. Glucose 30-37 insulin Homo sapiens 0-7 1030569-0 1976 Basal and insulin-stimulated glucose metabolism of isolated human fat cells. Glucose 29-36 insulin Homo sapiens 10-17 814810-5 1976 On the other hand, the mean insulin response of patients with moderate fasting hyperglycemia (plasma glucose of 110 to 150 mg/100 ml) was somewhat attenuated, and patients with severe fasting hyperglycemia (plasma glucose greater than 150 mg/100 ml) had unequivocal insulin deficiency. Glucose 101-108 insulin Homo sapiens 28-35 943938-1 1976 The response of plasma insulin concentration to an oral glucose tolerance test (OGTT) and to the maximum stimulatory effect obtained with administration of glucose, glucagon and tolbutamide was studied in 24 siblings of diabetic children and in ten obese children. Glucose 56-63 insulin Homo sapiens 23-30 181221-1 1976 The interaction of glucose, the major physiological regulator of insulin secretion, with the beta-cell involves the recognition of glucose as a signal, the transduction of this recognition into an intracellular event and the coupling of the event to the exocytotic discharge of insulin from secretory granules. Glucose 19-26 insulin Homo sapiens 65-72 945078-4 1976 The insulin response to glucose was poor in both SGA and AGA infants, but there was no significant difference between these two groups of infants. Glucose 24-31 insulin Homo sapiens 4-11 181221-1 1976 The interaction of glucose, the major physiological regulator of insulin secretion, with the beta-cell involves the recognition of glucose as a signal, the transduction of this recognition into an intracellular event and the coupling of the event to the exocytotic discharge of insulin from secretory granules. Glucose 131-138 insulin Homo sapiens 65-72 943248-0 1976 [Fetal secretion of insulin in response to glucose loading]. Glucose 43-50 insulin Homo sapiens 20-27 954785-0 1976 Insulin response and portal-peripheral insulin difference during the oral glucose tolerance test in patients after abdominal operations. Glucose 74-81 insulin Homo sapiens 39-46 954785-5 1976 After glucose load the increasing portal insulin as well as the peripheral and portal glucose correlate with the portal-peripheral insulin difference (p less than 0.001). Glucose 6-13 insulin Homo sapiens 41-48 954785-5 1976 After glucose load the increasing portal insulin as well as the peripheral and portal glucose correlate with the portal-peripheral insulin difference (p less than 0.001). Glucose 6-13 insulin Homo sapiens 131-138 954785-5 1976 After glucose load the increasing portal insulin as well as the peripheral and portal glucose correlate with the portal-peripheral insulin difference (p less than 0.001). Glucose 86-93 insulin Homo sapiens 131-138 954785-7 1976 It can be concluded that in the early postoperative period in patients with a diminished oral glucose tolerance (large glucose areas) there is an even greater insulin response in comparison to patients with normal oral glucose tolerance. Glucose 94-101 insulin Homo sapiens 159-166 954785-7 1976 It can be concluded that in the early postoperative period in patients with a diminished oral glucose tolerance (large glucose areas) there is an even greater insulin response in comparison to patients with normal oral glucose tolerance. Glucose 119-126 insulin Homo sapiens 159-166 954785-7 1976 It can be concluded that in the early postoperative period in patients with a diminished oral glucose tolerance (large glucose areas) there is an even greater insulin response in comparison to patients with normal oral glucose tolerance. Glucose 119-126 insulin Homo sapiens 159-166 954785-8 1976 On the other hand, however, in those patients with diminished glucose tolerance, the insulin response is essentially delayed. Glucose 62-69 insulin Homo sapiens 85-92 1245265-7 1976 In late pregnancy the magnitude of the insulin response to oral glucose (i.e., the incremental insulin area above fasting baseline) was equally and significantly enhanced in the normals and the gestational diabetics. Glucose 64-71 insulin Homo sapiens 39-46 1245265-7 1976 In late pregnancy the magnitude of the insulin response to oral glucose (i.e., the incremental insulin area above fasting baseline) was equally and significantly enhanced in the normals and the gestational diabetics. Glucose 64-71 insulin Homo sapiens 95-102 1245265-8 1976 However, when the insulin response during the first 60 minutes of the OGTT was expressed per unit of glucose stimulus (i.e., the delta insulin/delta glucose ratio) a significantly higher mean response was found in the normal pregnants than in the gestational diabetics. Glucose 101-108 insulin Homo sapiens 18-25 1245265-8 1976 However, when the insulin response during the first 60 minutes of the OGTT was expressed per unit of glucose stimulus (i.e., the delta insulin/delta glucose ratio) a significantly higher mean response was found in the normal pregnants than in the gestational diabetics. Glucose 149-156 insulin Homo sapiens 18-25 1245266-1 1976 The effect of chronic changes in serum glucose concentration on refraction was studied by increasing the dose of insulin or chlorpropamide in 10 diabetic patients who initially had relatively high glucose concentrations. Glucose 39-46 insulin Homo sapiens 113-120 179924-5 1976 At least, this was the conclusion drawn from studies carried out by means of a glucose-controlled insulin and glucose infusion system (GCIGIS) -or artificial pancreas-which delivers short-acting insulin and glucose on demand intravenously. Glucose 79-86 insulin Homo sapiens 98-105 179924-5 1976 At least, this was the conclusion drawn from studies carried out by means of a glucose-controlled insulin and glucose infusion system (GCIGIS) -or artificial pancreas-which delivers short-acting insulin and glucose on demand intravenously. Glucose 79-86 insulin Homo sapiens 195-202 179924-5 1976 At least, this was the conclusion drawn from studies carried out by means of a glucose-controlled insulin and glucose infusion system (GCIGIS) -or artificial pancreas-which delivers short-acting insulin and glucose on demand intravenously. Glucose 110-117 insulin Homo sapiens 195-202 179924-5 1976 At least, this was the conclusion drawn from studies carried out by means of a glucose-controlled insulin and glucose infusion system (GCIGIS) -or artificial pancreas-which delivers short-acting insulin and glucose on demand intravenously. Glucose 110-117 insulin Homo sapiens 195-202 179927-1 1976 The insulin response to oral glucose, tolbutamide, arginine, pancreozymin and cerulein was studied in a group of subjects with insuloma and a group of normal control subjects. Glucose 29-36 insulin Homo sapiens 4-11 187365-0 1976 [Changes in serum C-peptide in glucose tolerance test; with special reference to diabetes and insulinoma]. Glucose 31-38 insulin Homo sapiens 18-27 1278843-2 1976 An exaggerated insulin response to oral glucose was associated with reactive hypoglycemia in the post-gastrectomy syndrome, in normal-weight patients with chemical diabetes and 44% of the patients with the isolated syndrome. Glucose 40-47 insulin Homo sapiens 15-22 812887-6 1976 During the glucose system there was a significantly higher level of pyruvate, lactate, alanine, and immunoreactive insulin, consistent with glucose being the principal source of energy. Glucose 11-18 insulin Homo sapiens 115-122 812887-6 1976 During the glucose system there was a significantly higher level of pyruvate, lactate, alanine, and immunoreactive insulin, consistent with glucose being the principal source of energy. Glucose 140-147 insulin Homo sapiens 115-122 1052833-1 1976 The data herein presented describe, identify, and quantitate interrelationships among blood glucose and serum insulin, growth hormone, cortisol, and glucagon levels of hospitalized insulin-treated diabetic patients. Glucose 92-99 insulin Homo sapiens 110-117 993793-4 1976 The administration of glucose after insulin provoked an increase of free and total tryptophan. Glucose 22-29 insulin Homo sapiens 36-43 1052833-1 1976 The data herein presented describe, identify, and quantitate interrelationships among blood glucose and serum insulin, growth hormone, cortisol, and glucagon levels of hospitalized insulin-treated diabetic patients. Glucose 92-99 insulin Homo sapiens 181-188 813175-6 1976 In the presence of 300 mg/100 ml glucose, insulin at 10(-7) M in creased %I to 8 +/- 2, and galactose greater than 75 mg/100 ml increased %I to 8 +/- 1. Glucose 33-40 insulin Homo sapiens 42-49 775483-2 1976 The content of immunoreactive insulin (IRI) in the blood serum was examined with the aid of sets for radioimmunological determination on fasting stomach and in dynamics during the standard glucose-tolerance test. Glucose 189-196 insulin Homo sapiens 30-37 1086478-2 1976 Systematic analysis was made of structural requirements for possible priming action of D-glucose and 40 related compounds in the presence of insulin to enhance subsequent labeled D-glucose uptake at 0 degrees C. It was concluded that a major portion if not all of the H-bonding groups on the D-glucose molecules are involved although their relative importance varies. Glucose 87-96 insulin Homo sapiens 141-148 1086478-2 1976 Systematic analysis was made of structural requirements for possible priming action of D-glucose and 40 related compounds in the presence of insulin to enhance subsequent labeled D-glucose uptake at 0 degrees C. It was concluded that a major portion if not all of the H-bonding groups on the D-glucose molecules are involved although their relative importance varies. Glucose 179-188 insulin Homo sapiens 141-148 1086478-2 1976 Systematic analysis was made of structural requirements for possible priming action of D-glucose and 40 related compounds in the presence of insulin to enhance subsequent labeled D-glucose uptake at 0 degrees C. It was concluded that a major portion if not all of the H-bonding groups on the D-glucose molecules are involved although their relative importance varies. Glucose 179-188 insulin Homo sapiens 141-148 1246534-7 1976 If glucose and lipid levels remain high after six months of such therapy, insulin should be used. Glucose 3-10 insulin Homo sapiens 74-81 1201102-0 1975 Metal ion- and phosphate-mediated transport of glucose by insulin. Glucose 47-54 insulin Homo sapiens 58-65 1064141-4 1976 The effect of various concentrations of glucose (63, 90, 135 and 180 mg per 100 ml) in the perfusion medium on the secretion of insulin and pancreatic glucagon was investigated in order to observe the performance characteristics of this preparation. Glucose 40-47 insulin Homo sapiens 128-135 1064141-5 1976 Increasing concentrations of glucose caused a significantly greater insulin release, whereas the glucagon response was significantly reduced. Glucose 29-36 insulin Homo sapiens 68-75 1064142-1 1976 The insulin response to oral glucose ingestion was measured in six patients with the Zollinger-Ellison (ZE) syndrome, five patients with partial gastrectomy (antrectomy for duodenal ulcer) and six matched normal subjects. Glucose 29-36 insulin Homo sapiens 4-11 1221276-4 1975 There was poor correlation among the six patients between the blood glucose levels and serum insulin levels, and between the injected dose and the serum levels. Glucose 68-75 insulin Homo sapiens 93-100 1273505-5 1976 Insulin secretion was stimulated only during the glucose infusion. Glucose 49-56 insulin Homo sapiens 0-7 1193311-0 1975 Relationship between insulin response to oral glucose load and creatinine clearance. Glucose 46-53 insulin Homo sapiens 21-28 1197090-0 1975 [Insulin secretion oral glucose tolerance test in acute pancreatitis]. Glucose 24-31 insulin Homo sapiens 1-8 2460-8 1975 In contrast to newborn infants of healthy mothers a biphasic/insulin release was found during the intravenous glucose loads in newborn infants of insulin-treated diabetic mothers. Glucose 110-117 insulin Homo sapiens 61-68 1193311-1 1975 In order to investigate the relationship between insulin response to oral glucose load and renal function, a 100-gm. Glucose 74-81 insulin Homo sapiens 49-56 1193311-5 1975 Insulin area during oral glucose load increased in proportion to the decrease in creatinine clearance. Glucose 25-32 insulin Homo sapiens 0-7 1193313-6 1975 Maximum insulin-stimulated glucose oxidation (increase over basal) was significantly enhanced (p less than 0.05) in tissue from obese subjects, whereas insulin-mediated glucose incorporation into glycogen was similar in controls and obese subjects on weight-maintaining diets. Glucose 27-34 insulin Homo sapiens 8-15 1193313-6 1975 Maximum insulin-stimulated glucose oxidation (increase over basal) was significantly enhanced (p less than 0.05) in tissue from obese subjects, whereas insulin-mediated glucose incorporation into glycogen was similar in controls and obese subjects on weight-maintaining diets. Glucose 169-176 insulin Homo sapiens 152-159 1193313-7 1975 Insulin-stimulated glucose oxidation was imparied in tissue from subjects on hypocaloric diets although fat-cell diameter was similar to those of obese subjects on weight-maintaining diets. Glucose 19-26 insulin Homo sapiens 0-7 1193313-8 1975 The effect of insulin on glucose incorporation into glycogen in isolated adipocytes was also studied. Glucose 25-32 insulin Homo sapiens 14-21 1193313-11 1975 These results indicate that in vitro glucose oxidation by adipose tissue, in both the absence and the presence of insulin, is largely determined by dietary factors. Glucose 37-44 insulin Homo sapiens 114-121 1194911-1 1975 Patients with severe depression have been observed previously to have a reduced rate of glucose utilization accompanied by elevated serum insulin levels during the intravenous glucose tolerance test (GTT) and a reduced metabolic responsiveness to exogenous insulin during the insulin tolerance test (ITT). Glucose 176-183 insulin Homo sapiens 138-145 1107346-5 1975 Fractionation disclosed that most of the normal gestational increase in basal and glucose-stimulated TIR can be ascribed to insulin rather than disproportionate increments in proinsulin-like components. Glucose 82-89 insulin Homo sapiens 124-131 1107346-9 1975 Following glucose administration in the severe diabetics, the relative contribution from proinsulin to TIR was altered so that ratios of circulating proinsulin/insulin were increased at all levels of blood sugar. Glucose 10-17 insulin Homo sapiens 89-99 1107346-9 1975 Following glucose administration in the severe diabetics, the relative contribution from proinsulin to TIR was altered so that ratios of circulating proinsulin/insulin were increased at all levels of blood sugar. Glucose 10-17 insulin Homo sapiens 149-159 1107346-9 1975 Following glucose administration in the severe diabetics, the relative contribution from proinsulin to TIR was altered so that ratios of circulating proinsulin/insulin were increased at all levels of blood sugar. Glucose 10-17 insulin Homo sapiens 92-99 1195779-1 1975 Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower. Glucose 156-163 insulin Homo sapiens 69-76 1195779-1 1975 Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower. Glucose 156-163 insulin Homo sapiens 83-90 1195779-1 1975 Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower. Glucose 156-163 insulin Homo sapiens 125-134 1204766-1 1975 Tryptophan (4-10 mM) reduces the stimulating effect of insulin on glucose uptake, CO2 output and lactate production by adipose tissue. Glucose 66-73 insulin Homo sapiens 55-62 1195779-1 1975 Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower. Glucose 156-163 insulin Homo sapiens 83-90 1195779-1 1975 Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower. Glucose 156-163 insulin Homo sapiens 83-90 1196132-5 1975 Basal triglyceride synthesis from labeled glucose was low in relation to plasma insulin. Glucose 42-49 insulin Homo sapiens 80-87 175208-0 1975 [Influence of somatastatin on oral glucose tolerance in autonomous hypersecretion of growth hormone, prolactin or insulin (author"s transl)]. Glucose 35-42 insulin Homo sapiens 114-121 175208-4 1975 Only the peak of the blood sugar curve was shifted from one to two and a half hours after glucose administration; insulin and hGH levels were regularly suppressed after somatostatin whereas hPRL remained unchanged in most instances. Glucose 90-97 insulin Homo sapiens 114-121 175208-6 1975 These findings show that the pathologic glucose tolerance due to insulin antagonism could not be improved by somatostatin in contrast to the deteriorated glucose tolerance in insulinopenic states. Glucose 40-47 insulin Homo sapiens 65-72 813120-4 1975 After oral loading with glucose the total rise in glucose and the rise in insulin in the late phase were diminished. Glucose 24-31 insulin Homo sapiens 74-81 1182202-0 1975 The effect of digitonin of the stimulation by insulin of glucose uptake by isolated fat cells. Glucose 57-64 insulin Homo sapiens 46-53 1184740-8 1975 When insulin was infused in the diabetic groups at a rate of 0.4 U/kg-min together with glucose, raising mean plasma insulin to between 300 and 600 muU/ml, differences from the hyperglycemic nondiabetics were no longer statistically significant. Glucose 88-95 insulin Homo sapiens 117-124 1182202-2 1975 At low concentrations of digitonin, the stimulation of glucose uptake by insulin was inhibited without severe cell damage as estimated by the leakage of lactate dehydrogenase from the cells. Glucose 55-62 insulin Homo sapiens 73-80 1104216-6 1975 Insulin sensitivity was difficult to assess in the diabetic patients because basal plasma glucose concentrations were elevated. Glucose 90-97 insulin Homo sapiens 0-7 1104216-7 1975 At any given insulin concentration, the diabetics metabolized approximately the same amount of glucose as the normal subjects but the fact that this rate of glucose turnover occurred at higher plasma glucose concentrations probably indicated insulin resistance. Glucose 95-102 insulin Homo sapiens 13-20 1104216-7 1975 At any given insulin concentration, the diabetics metabolized approximately the same amount of glucose as the normal subjects but the fact that this rate of glucose turnover occurred at higher plasma glucose concentrations probably indicated insulin resistance. Glucose 157-164 insulin Homo sapiens 13-20 1104216-7 1975 At any given insulin concentration, the diabetics metabolized approximately the same amount of glucose as the normal subjects but the fact that this rate of glucose turnover occurred at higher plasma glucose concentrations probably indicated insulin resistance. Glucose 157-164 insulin Homo sapiens 242-249 1104216-9 1975 Diminishing sensitivity to insulin was reflected in an increasing fasting plasma insulin and insulin/glucose ratio except in patients with diabetes. Glucose 101-108 insulin Homo sapiens 27-34 1104216-10 1975 GH responses to insulin infusion in normal subjects reflected the pattern of fall of plasma glucose. Glucose 92-99 insulin Homo sapiens 16-23 1104216-11 1975 In the diabetic patients GH secretion appeared to be related to the infusion of insulin and occurred before plasma glucose had fallen to hypoglycaemic levels. Glucose 115-122 insulin Homo sapiens 80-87 1183734-8 1975 Older subjects had higher glucose levels and heavier females had higher insulin levels two hours after glucose administration. Glucose 103-110 insulin Homo sapiens 72-79 1192705-4 1975 In patients managed conservatively there was glucose intolerance associated with a diminished early insulin response to glucose, suggesting inadequate nutrition in the period between the overdose and the glucose tolerance test. Glucose 120-127 insulin Homo sapiens 100-107 1192705-4 1975 In patients managed conservatively there was glucose intolerance associated with a diminished early insulin response to glucose, suggesting inadequate nutrition in the period between the overdose and the glucose tolerance test. Glucose 120-127 insulin Homo sapiens 100-107 1200041-2 1975 Severe hyperkalemia associated with spontaneous hyperglycemia as well as with the intravenous infusions of glucose occurred in an insulin-requiring diabetic patient in the absence of potassium administration, the use of diuretics which inhibit urinary potassium excretion or acidemia. Glucose 107-114 insulin Homo sapiens 130-137 1200041-5 1975 In this patient, the serum potassium concentration increases after the intravenous infusions of glucose because there is insufficient aldosterone and insulin to reverse the transfer of potassium to the extracellular fluid which normally occurs after hypertonic infusions of glucose. Glucose 96-103 insulin Homo sapiens 150-157 1200041-6 1975 Although DOCA replacement modifies the distribution of potassium in the extracellular fluid and blunts the hyperkalemic effect of intravenous infusions of glucose, a rise in the insulin level is required for the usual hypokalemic response to intravenously administered glucose. Glucose 269-276 insulin Homo sapiens 178-185 1227847-0 1975 Effect of glucose infusion on venous blood levels of immunoreactive proinsulin activity, insulin activity and fat parameters in healthy and protodiabetic subjects. Glucose 10-17 insulin Homo sapiens 71-78 1185889-6 1975 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. Glucose 35-42 insulin Homo sapiens 7-14 1185889-6 1975 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. Glucose 105-112 insulin Homo sapiens 7-14 1185889-9 1975 After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. Glucose 53-60 insulin Homo sapiens 28-35 1185889-9 1975 After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. Glucose 186-193 insulin Homo sapiens 28-35 1221384-1 1975 A study was made of 16 patients with the initial mild form of diabetes mellitus in whom the immunoreactive insulin (IRI) indices in glucose loading pointed to a good reactivity of the beta-cells of the insular apparatus of the pancreas. Glucose 132-139 insulin Homo sapiens 107-114 171158-0 1975 The influence of insulin on glucose permeability and metabolism of human granulocytes. Glucose 28-35 insulin Homo sapiens 17-24 171158-6 1975 An important fraction of the extra glucose consumed under the influence of insulin was recovered as neither glycogen nor lactate, nor was it oxidized in the Krebs cycle. Glucose 35-42 insulin Homo sapiens 75-82 171158-9 1975 The fate of the extra glucose consumed under the influence of insulin therefore remains questionable. Glucose 22-29 insulin Homo sapiens 62-69 1101599-1 1975 The time and dose dependency of the effects of a 30-min long iv infusion of human growth hormone (GH) on glucose tolerance and glucose-stimulated insulin release was investigated in 19 healthy subjects. Glucose 127-134 insulin Homo sapiens 146-153 1242153-5 1975 The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. Glucose 80-87 insulin Homo sapiens 19-26 1212982-0 1975 Dietary therapy and insulin secretory response to glucose in adult-onset non-obese diabetic subjects. Glucose 50-57 insulin Homo sapiens 20-27 1101599-0 1975 Acute effects of exogenous growth hormone in man: time- and dose-bound modification of glucose tolerance and glucose-induced insulin release. Glucose 109-116 insulin Homo sapiens 125-132 1175861-1 1975 Insulin resistance has been invoked to explain the glucose intolerance observed in hypothyroid patients. Glucose 51-58 insulin Homo sapiens 0-7 1101599-5 1975 Glucose-stimulated insulin release was significantly inhibited 1 h after administration of a relatively high GH dose (40 mug per kg), both if expressed as mean plasma insulin levels, or as insulin release per magnitude of glucose stimulation (insulinogenic index). Glucose 0-7 insulin Homo sapiens 19-26 1101599-5 1975 Glucose-stimulated insulin release was significantly inhibited 1 h after administration of a relatively high GH dose (40 mug per kg), both if expressed as mean plasma insulin levels, or as insulin release per magnitude of glucose stimulation (insulinogenic index). Glucose 0-7 insulin Homo sapiens 167-174 1101599-5 1975 Glucose-stimulated insulin release was significantly inhibited 1 h after administration of a relatively high GH dose (40 mug per kg), both if expressed as mean plasma insulin levels, or as insulin release per magnitude of glucose stimulation (insulinogenic index). Glucose 0-7 insulin Homo sapiens 167-174 1101599-5 1975 Glucose-stimulated insulin release was significantly inhibited 1 h after administration of a relatively high GH dose (40 mug per kg), both if expressed as mean plasma insulin levels, or as insulin release per magnitude of glucose stimulation (insulinogenic index). Glucose 222-229 insulin Homo sapiens 19-26 1100461-1 1975 Ethanol at an average blood concentration of 1 mg. per milliliter enhanced the immediate (first-phase) and prolonged (second-phase) insulin response to an intravenous glucose load in nonfasting normal human subjects. Glucose 167-174 insulin Homo sapiens 132-139 1175861-6 1975 In response to insulin administration, plasma glucose concentrations declined to the nadir of 36 +/- 4, 43 +/- 3, and 38 +/- 4 mg. per 100 ml. Glucose 46-53 insulin Homo sapiens 15-22 1212982-5 1975 Insulin response to oral glucose loading was improved, particularly in the later stage of oral glucose tolerance test. Glucose 25-32 insulin Homo sapiens 0-7 1165235-0 1975 Time course of termination of the glucose transport action of insulin in adipocytes. Glucose 34-41 insulin Homo sapiens 62-69 1165235-4 1975 Termination of the glucose transport action of insulin (which includes insulin-receptor disassociation and all other steps leading to decelerated glucose entry) began within 2 min and was complete within 30 min. Glucose 19-26 insulin Homo sapiens 47-54 1165235-4 1975 Termination of the glucose transport action of insulin (which includes insulin-receptor disassociation and all other steps leading to decelerated glucose entry) began within 2 min and was complete within 30 min. Glucose 146-153 insulin Homo sapiens 47-54 1102318-1 1975 Plasma adrenaline-blood glucose interrelationships in insulin-induced hypoglycaemia in man have been studied using a sensitive double-isotope derivative method for adrenaline estimation. Glucose 24-31 insulin Homo sapiens 54-61 1165235-6 1975 For comparison, the time course of initiation of the glucose transport action of insulin was measured under the same conditions. Glucose 53-60 insulin Homo sapiens 81-88 1081045-1 1975 The influence of various components of plasma hemostatic system on the assimilation of glucose by isolated rat hemidiaphragm in the presence of insulin was investigated. Glucose 87-94 insulin Homo sapiens 144-151 791728-10 1975 Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Glucose 16-23 insulin Homo sapiens 94-101 1165627-3 1975 Though there has been interference with the glucose tolerance, the serum proinsulin in the OGTT showed increased levels too. Glucose 44-51 insulin Homo sapiens 73-83 1165628-8 1975 In patients with a pathologic glucose assimilation it is not the insulin secretion that is delayed but the insulin regression (disappearance rate) in portal venous blood. Glucose 30-37 insulin Homo sapiens 65-72 791728-13 1975 Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Glucose 116-123 insulin Homo sapiens 155-162 1165628-10 1975 In patients with a normal glucose assimilation the insulin concentrations curve in portal venous blood shows an oscillating course during the first 30 min. Glucose 26-33 insulin Homo sapiens 51-58 1158041-5 1975 In all these diabetic groups, the glucose tolerance improved after treatment for diabetes mellitus, while the insulin response to the glucose did not show any remarkable change. Glucose 134-141 insulin Homo sapiens 110-117 1158041-10 1975 The relationship between the response of glucose and plasma insulin and between glucose and glucagon to arginine was investigated, and the importance of the changes in the insulin:glucagon ratio was emphasized. Glucose 41-48 insulin Homo sapiens 60-67 1234578-7 1975 The decrease in blood glucose during insulin administration did not correlate with the increase in carbohydrate oxidation. Glucose 22-29 insulin Homo sapiens 37-44 1234578-13 1975 Addition of insulin markedly decreased the elevated FFA levels and lowered blood glucose. Glucose 81-88 insulin Homo sapiens 12-19 1158042-0 1975 Age-adjusted analysis of insulin responses during normal and abnormal glucose tolerance tests in children and adolescents. Glucose 70-77 insulin Homo sapiens 25-32 1234578-16 1975 In comparison with the insulin test, this double amount seems to correlate well with the higher blood glucose levels measured before insulin administration. Glucose 102-109 insulin Homo sapiens 23-30 1234578-16 1975 In comparison with the insulin test, this double amount seems to correlate well with the higher blood glucose levels measured before insulin administration. Glucose 102-109 insulin Homo sapiens 133-140 1159058-5 1975 The acute insulin response to the glucose pulse when expressed either as the area above basal for the 10 min post stimulation or as the mean encremental increase above basal at 3, 4 and 5 min (delta 3-5 IRI) was the same in both timing and magnitude for the old and young subjects. Glucose 34-41 insulin Homo sapiens 10-17 1234578-17 1975 The results suggest that insulin indirectly stimulates carbohydrate oxidation by facilitating glucose transport into the cells and lowering FFA levels, and that epinephrine favours lipid oxidation through its lipolytic effects and its suppression of insulin release. Glucose 94-101 insulin Homo sapiens 25-32 1183916-5 1975 Hypoglycemia-induced increases in epinephrine and glucagon, secretion may contribute to the restoration of the normal plasma glucose concentration after insulin-induced hypoglycemia. Glucose 125-132 insulin Homo sapiens 153-160 1183919-3 1975 Insulin significantly increased glucose uptake, glycogen content, the membrane transport of alpha-amino-isobutyric acid (AIB), the incorporation of leucine into protein and tended to increase the membrane transport of the nonutilizable model monosaccharide 3-0-methylglucose. Glucose 32-39 insulin Homo sapiens 0-7 1238209-0 1975 [Changes in the C-peptide level in diabetes at glucose loading]. Glucose 47-54 insulin Homo sapiens 16-25 1159064-9 1975 The insulin response to the glucose pulse also was significantly lower during steroid treatment. Glucose 28-35 insulin Homo sapiens 4-11 1159064-10 1975 Thus, prednisone apparently has an early inhibitory effect on the insulin response to glucose. Glucose 86-93 insulin Homo sapiens 66-73 781374-1 1975 Twenty patients with myocardial infarction and 10 normal individuals were subjected to a carbohydrates tolerance test, and their secretion of insulin and somatotrophic hormone in response to intravenous injections of glucose was studied. Glucose 217-224 insulin Homo sapiens 142-149 168278-10 1975 In face of a massively greater insulin response in an insuloma patient (greater than 1,000 muU per milliliter), the decreases in the levels of individual free amino acids following glucose were within the range of values obtained in the normal volunteer subjects. Glucose 181-188 insulin Homo sapiens 31-38 1176974-1 1975 Autistic children subjected to the stress of insulin-induced hypoglycemia showed slower recovery of blood glucose, and faster and intractable cortisol response in the 3 hours following the stress. Glucose 106-113 insulin Homo sapiens 45-52 1165623-1 1975 The present investigation was designed to determine whether the circadian rhythm of glucose utilization is based on a quantitatively different release of insulin and/or on changing secretory dynamics of the hormone. Glucose 84-91 insulin Homo sapiens 154-161 807787-5 1975 Insulin response, both to glucose and to arginine infusion, was clearly reduced. Glucose 26-33 insulin Homo sapiens 0-7 808195-1 1975 We tested the hypothesis that during infusion of amino acids without dextrose, there is less insulin stimulation, which, in turn, permits lipolysis. Glucose 69-77 insulin Homo sapiens 93-100 1155478-4 1975 A familial incidence of diabetes mellitus and delayed insulin response to an oral glucose load support a classification of prediabetes or suspected diabetes mellitus for these patients. Glucose 82-89 insulin Homo sapiens 54-61 808195-2 1975 The results suggest that dextrose infusion stimulates insulin and inhibits lipolysis. Glucose 25-33 insulin Homo sapiens 54-61 1158037-12 1975 The effect of induced hyperglycemia on the acute phase of insulin and glucagon secretion was assessed by administering the arginine during marked elevation of ambient glucose concentration achieved by the intravenous administration of glucose. Glucose 235-242 insulin Homo sapiens 58-65 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 30-37 insulin Homo sapiens 10-17 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 30-37 insulin Homo sapiens 113-120 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 30-37 insulin Homo sapiens 113-120 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 124-131 insulin Homo sapiens 10-17 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 124-131 insulin Homo sapiens 113-120 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 124-131 insulin Homo sapiens 113-120 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 124-131 insulin Homo sapiens 10-17 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 124-131 insulin Homo sapiens 113-120 1173969-7 1975 The serum insulin response to glucose was significantly increased at all stages of gestation and in parallel the insulin-to-glucose index calculated for the total areas below the insulin and glucose concentration curves increased significantly. Glucose 124-131 insulin Homo sapiens 113-120 1173969-8 1975 The fasting insulin-to-glucose index also increased and was found to be significantly correlated to the stage of gestation. Glucose 23-30 insulin Homo sapiens 12-19 1173969-9 1975 The shape of the glucose and insulin curves was modified in the opposite direction by pregnancy: the peak value of glucose was delayed whereas that of insulin was advanced. Glucose 116-123 insulin Homo sapiens 29-36 1189493-1 1975 In altogether 32 test persons with normal weight and obese test persons glucose-insulin-tolerance-tests were carried out. Glucose 72-79 insulin Homo sapiens 80-87 1189493-4 1975 The parameters of lipolysis glycerol and free fatty acids show after a glucose-stimulated insulin excretion and after exogenic insulin application a somewhat retarded decrease in obese persons compared with the control group. Glucose 71-78 insulin Homo sapiens 90-97 1189493-6 1975 The two fundamental physiological effects of insulin in the carbohydrate and fat metabolism -- glucose utilization and inhibition of lipolysis -- seem to be distrubed in the same way in obesity. Glucose 95-102 insulin Homo sapiens 45-52 1175672-5 1975 Scalded rats responded to intravenous glucose injection (1-0 g/kg) with a further rise in plasma insulin concentration, which remained normal for the prevailing blood glucose concentration. Glucose 38-45 insulin Homo sapiens 97-104 1173503-8 1975 The findings suggested that the early, insulin-like effect of GH on blood glucose is distinct from its effect on the pancreas. Glucose 74-81 insulin Homo sapiens 39-46 1175672-7 1975 After intravenous insulin injection (1-0 U/kg) the initial rate coefficient for fall of blood glucose concentration was significantly lower (p less than 0-02) in scalded (mean 3-9 percent min. Glucose 94-101 insulin Homo sapiens 18-25 1175672-9 1975 The minimum in blood glucose concentration after insulin injection was reached at 10 min. Glucose 21-28 insulin Homo sapiens 49-56 1175672-13 1975 It was concluded that the impairment of glucose utilization in scalded rats (Heath and Corney, 1973) is due to decreased sensitivity to insulin rather than to suppression of insulin release. Glucose 40-47 insulin Homo sapiens 136-143 1155514-3 1975 Mean glucose levels calculated from five daily analysis 28 days before delivery were determined in insulin-dependent and gestational diabetic patients (pregnancy glucose level). Glucose 5-12 insulin Homo sapiens 99-106 1155514-7 1975 Insulin-dependent diabetic patients had suppressed lipid mobilization in the afternoon when glucose levels were almost normal. Glucose 92-99 insulin Homo sapiens 0-7 1173506-6 1975 In mildly diabetic subjects, insulin response to glucose infusion was low and sluggish, only a minor initial response being observed. Glucose 49-56 insulin Homo sapiens 29-36 1173506-7 1975 Pretreatment with glucose modified the profile of the insulin response, a clear-cut initial response of greater magnitude being obtained at least in some of the patients. Glucose 18-25 insulin Homo sapiens 54-61 1173503-9 1975 The latter is a suppressive one, consistent with earlier findings on glucose-induced insulin release. Glucose 69-76 insulin Homo sapiens 85-92 1173506-8 1975 The sensitivity of the islet to the potentiating action of glucose was higher in low insulin responders than in controls, the minimal glucose concentration needed to induce potentiations of the forthcoming response being much lower. Glucose 59-66 insulin Homo sapiens 85-92 1173506-8 1975 The sensitivity of the islet to the potentiating action of glucose was higher in low insulin responders than in controls, the minimal glucose concentration needed to induce potentiations of the forthcoming response being much lower. Glucose 134-141 insulin Homo sapiens 85-92 1173504-0 1975 Potentiation of insulin release by glucose in man. Glucose 35-42 insulin Homo sapiens 16-23 1173506-9 1975 The dose-response curve for the relationship between the blood glucose level of the preinfusion period and the percentual enhancement of the insulin response obtained at the second stimulation was, in low insulin response obtained at the second stimulation was, in low insulin responders, higher than and shifted to the left of the curve of the control subjects. Glucose 63-70 insulin Homo sapiens 141-148 1173506-9 1975 The dose-response curve for the relationship between the blood glucose level of the preinfusion period and the percentual enhancement of the insulin response obtained at the second stimulation was, in low insulin response obtained at the second stimulation was, in low insulin responders, higher than and shifted to the left of the curve of the control subjects. Glucose 63-70 insulin Homo sapiens 205-212 1173504-3 1975 When a hyperglycaemic plateau of around 300 mg/100 ml was induced by the first glucose infusion, the insulin response to a second challenge was enhanced over the range of stimulations used. Glucose 79-86 insulin Homo sapiens 101-108 1173506-9 1975 The dose-response curve for the relationship between the blood glucose level of the preinfusion period and the percentual enhancement of the insulin response obtained at the second stimulation was, in low insulin response obtained at the second stimulation was, in low insulin responders, higher than and shifted to the left of the curve of the control subjects. Glucose 63-70 insulin Homo sapiens 205-212 1173504-4 1975 Both the early and late phase insulin responses were amplified, the enhancement being more marked with higher stimulatory levels of glucose. Glucose 132-139 insulin Homo sapiens 30-37 808121-8 1975 The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. Glucose 94-101 insulin Homo sapiens 4-11 814837-5 1975 The duration of reduced glucose utilisation is 5-10 days during which period increased addition of insulin (24-18 U insulin/50 g glucose) is advisable. Glucose 129-136 insulin Homo sapiens 99-106 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 141-148 insulin Homo sapiens 41-48 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 141-148 insulin Homo sapiens 95-102 1173504-6 1975 These findings suggest that the synergism between the glucose pretreatment, and the insulin releasing effect of glucose, is of multiplicative type, resulting in increase of the maximum effect of the glucose. Glucose 54-61 insulin Homo sapiens 84-91 1173504-6 1975 These findings suggest that the synergism between the glucose pretreatment, and the insulin releasing effect of glucose, is of multiplicative type, resulting in increase of the maximum effect of the glucose. Glucose 112-119 insulin Homo sapiens 84-91 1173504-6 1975 These findings suggest that the synergism between the glucose pretreatment, and the insulin releasing effect of glucose, is of multiplicative type, resulting in increase of the maximum effect of the glucose. Glucose 112-119 insulin Homo sapiens 84-91 1173505-0 1975 Potentiation of insulin release by glucose in man. Glucose 35-42 insulin Homo sapiens 16-23 1173505-3 1975 If two consecutive glucose infusions are administered with 40 min of rest between, the insulin response to the second challenge is markedly potentiated. Glucose 19-26 insulin Homo sapiens 87-94 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 141-148 insulin Homo sapiens 95-102 1173505-4 1975 When the insulin response to the first glucose infusion was suppressed by 65% with the aid of adrenaline, potentiation of the insulin response to the second infusion was not modified. Glucose 39-46 insulin Homo sapiens 9-16 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 141-148 insulin Homo sapiens 95-102 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 216-223 insulin Homo sapiens 41-48 1173505-7 1975 Pretreatment of the subjects with a glucose infusion enhanced also the insulin responses to glucagon and to tolbutamide, given intravenously 50 min later. Glucose 36-43 insulin Homo sapiens 71-78 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 216-223 insulin Homo sapiens 95-102 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 216-223 insulin Homo sapiens 95-102 1173506-0 1975 Potentiation of insulin release by glucose in man. Glucose 35-42 insulin Homo sapiens 16-23 814837-6 1975 After this time the action of endogenous insulin was improved to such an extent that the added insulin could be reduced to 12 U insulin/50 g glucose up to the third week and later (up to 49 days) to 8 U insulin/50 g glucose. Glucose 216-223 insulin Homo sapiens 95-102 1173506-1 1975 Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Glucose 0-7 insulin Homo sapiens 48-55 1173506-1 1975 Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Glucose 0-7 insulin Homo sapiens 162-169 1173506-1 1975 Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Glucose 32-39 insulin Homo sapiens 48-55 1173506-1 1975 Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Glucose 32-39 insulin Homo sapiens 162-169 1173506-1 1975 Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Glucose 130-137 insulin Homo sapiens 48-55 125668-12 1975 ), suggesting that the decreased plasma insulin levels following intravenous glucose were due to impaired insulin secretion rather than accelerated insulin destruction. Glucose 77-84 insulin Homo sapiens 40-47 125668-12 1975 ), suggesting that the decreased plasma insulin levels following intravenous glucose were due to impaired insulin secretion rather than accelerated insulin destruction. Glucose 77-84 insulin Homo sapiens 106-113 1206849-2 1975 On the 30th day the carbohydrates tolerance test was conducted, and the content of immunoreactive insulin was determined after a glucose provocation. Glucose 129-136 insulin Homo sapiens 98-105 237331-4 1975 The insulin responses to continuous nasogastric and continuous intravenous glucose were similar, and nitrogen excretion did not differ between those two groups. Glucose 75-82 insulin Homo sapiens 4-11 1223830-2 1975 A significant rise of fasting insulinemia and hypersecretion of insulin after intravenous glucose loading were observed. Glucose 90-97 insulin Homo sapiens 30-37 1226368-0 1975 [Blood sugar level and immunoreactive insulin in the blood plasma in pregnant women with supposed prediabetes in the dynamics of a normal glucose tolerance test]. Glucose 138-145 insulin Homo sapiens 38-45 1103265-6 1975 The early increases in glucose-stimulated serum insulin concentrations in the two tests were significantly correlated (r equals 0.87), and this equation for linear regress was y equals 0.81 x + 10. Glucose 23-30 insulin Homo sapiens 48-55 237331-5 1975 The increased insulin levels seen with intermittent glucose were not accompanied by greater protein sparing. Glucose 52-59 insulin Homo sapiens 14-21 1135074-0 1975 [Insulin secretion following oral glucose tolerance test in chronic pancreatitis]. Glucose 34-41 insulin Homo sapiens 1-8 170711-4 1975 Increased levels in the maximal plasma insulin were observed in 63%, 100% and 56% through the glucose test, the tolbutamide test and the arginine test, respectively. Glucose 94-101 insulin Homo sapiens 39-46 48896-6 1975 plasma-insulin between the first and second tests was predicted by the result of the initial tests, the improvement of glucose tolerance between the two tests, and the degree of weight reduction. Glucose 119-126 insulin Homo sapiens 7-14 1149785-0 1975 The glucose-induced gastrointestinal stimulation of insulin secretion in man: relation to age and to gastrin release. Glucose 4-11 insulin Homo sapiens 52-59 168111-6 1975 Exogenous insulin which has been shown by others to inhibit insulin secretion in vitro, blunted the glucose-induced cAMP rise. Glucose 100-107 insulin Homo sapiens 10-17 165982-5 1975 On the one hand, insulin action (glucose transport) is inhibited by compounds (cholera toxin, ACTH, glucagon and L-norepinephrine) that stimulate adenylate cyclase; conversely, insulin both inhibits the lipolytic action of these compounds, and raises cellular levels of cyclic GMP. Glucose 33-40 insulin Homo sapiens 17-24 789145-0 1975 Feed-back inhibition of insulin secretion in subjects with high and low insulin response to glucose. Glucose 92-99 insulin Homo sapiens 24-31 165982-5 1975 On the one hand, insulin action (glucose transport) is inhibited by compounds (cholera toxin, ACTH, glucagon and L-norepinephrine) that stimulate adenylate cyclase; conversely, insulin both inhibits the lipolytic action of these compounds, and raises cellular levels of cyclic GMP. Glucose 33-40 insulin Homo sapiens 177-184 165982-7 1975 The role of membrane phosphorylation in the action of insulin is discussed in the context of experiments demonstrating a specific inhibition by ATP of insulin-mediated glucose transport, in association with the phosphorylation of two specific membrane proteins. Glucose 168-175 insulin Homo sapiens 54-61 165982-7 1975 The role of membrane phosphorylation in the action of insulin is discussed in the context of experiments demonstrating a specific inhibition by ATP of insulin-mediated glucose transport, in association with the phosphorylation of two specific membrane proteins. Glucose 168-175 insulin Homo sapiens 151-158 165983-3 1975 Stimulation of glucose oxidation by insulin is reduced in large cells. Glucose 15-22 insulin Homo sapiens 36-43 789145-1 1975 The plasma insulin response to two successive stimulations by glucose was measured in 12 healthy subjects, 5 of whom demonstrated subnormal insulin responses to glucose infusion (low insulin responders). Glucose 62-69 insulin Homo sapiens 11-18 789145-1 1975 The plasma insulin response to two successive stimulations by glucose was measured in 12 healthy subjects, 5 of whom demonstrated subnormal insulin responses to glucose infusion (low insulin responders). Glucose 161-168 insulin Homo sapiens 140-147 807496-1 1975 Early insulin release after oral glucose is absent in protein-calorie malnutrition (PCM). Glucose 33-40 insulin Homo sapiens 6-13 789145-1 1975 The plasma insulin response to two successive stimulations by glucose was measured in 12 healthy subjects, 5 of whom demonstrated subnormal insulin responses to glucose infusion (low insulin responders). Glucose 161-168 insulin Homo sapiens 140-147 789145-6 1975 The integrated insulin response and the integrated insulinogenic index during the 20 min following glucose administration were also significantly inhibited at the second glucose challenge in subjects with low insulin responders. Glucose 99-106 insulin Homo sapiens 51-58 789145-6 1975 The integrated insulin response and the integrated insulinogenic index during the 20 min following glucose administration were also significantly inhibited at the second glucose challenge in subjects with low insulin responders. Glucose 170-177 insulin Homo sapiens 15-22 789145-6 1975 The integrated insulin response and the integrated insulinogenic index during the 20 min following glucose administration were also significantly inhibited at the second glucose challenge in subjects with low insulin responders. Glucose 170-177 insulin Homo sapiens 51-58 1095439-4 1975 per kilogram of glucose resulted in much higher levels of insulin and I/G (p smaller than 0.005), lower glucagon levels (p smaller than 0.05), and slightly higher triglycerides (N.S.) Glucose 16-23 insulin Homo sapiens 58-73 789145-8 1975 It is suggested that this inhibition of insulin release on repeating the stimulus, (a) may offer an explanation sustained stimulation by glucose; (b) is probably generated by the phenomenon of insulin secretion, and (c) might thus represent a negative feed-back loop in insulin secretion. Glucose 137-144 insulin Homo sapiens 40-47 168302-0 1975 Proceedings: Structural modifications to the insulin molecule and their effects on glucose metabolism. Glucose 83-90 insulin Homo sapiens 45-52 1149953-4 1975 Although secreted from the pancreas in equimolar concentrations, the molar ratio of C-peptide to insulin in peripheral blood was about 7 in the fasting state, falling to about 5 in the glucose stimulated condition. Glucose 185-192 insulin Homo sapiens 84-93 1149953-4 1975 Although secreted from the pancreas in equimolar concentrations, the molar ratio of C-peptide to insulin in peripheral blood was about 7 in the fasting state, falling to about 5 in the glucose stimulated condition. Glucose 185-192 insulin Homo sapiens 97-104 1149953-9 1975 In normal humans the peripheral C-peptide responses to the oral glucose load showed less relative variation than do the insulin responses. Glucose 64-71 insulin Homo sapiens 32-41 1158071-1 1975 The insulin response to oral and intravenous glucose was measured in ten patients after resection of antrum, duodenum, proximal jejunum, and the head of pancreas (Whipple"s operation). Glucose 45-52 insulin Homo sapiens 4-11 1142379-7 1975 It is concluded that an excessive rise in circulating immunoreactive insulin in response to glucose is a common abnormality in dystrophia myotonica and reflects genetic heterogeneity in this condition. Glucose 92-99 insulin Homo sapiens 69-76 1142379-8 1975 Futhermore, if the index patient in a family demostrates this abnormality, it is suggested that the 30- or 60-min blood insulin level during a glucose tolerance test is a useful methold of intra-family screen-ing for asymptomatic heterozygotes at an early stage before the development of physical defects. Glucose 143-150 insulin Homo sapiens 120-127 1154379-3 1975 In glucose tolerance test, insulin response was reduced in the patients with severe diabetes. Glucose 3-10 insulin Homo sapiens 27-34 1153201-13 1975 In patients whose insulin and proinsulin levels were determined, the insulin response to an oral glucose load was typical of adult onset diabetes, i.e., delayed hyperinsulinemia with concomitant hyperglycemia. Glucose 97-104 insulin Homo sapiens 18-25 1153201-13 1975 In patients whose insulin and proinsulin levels were determined, the insulin response to an oral glucose load was typical of adult onset diabetes, i.e., delayed hyperinsulinemia with concomitant hyperglycemia. Glucose 97-104 insulin Homo sapiens 30-40 1153201-13 1975 In patients whose insulin and proinsulin levels were determined, the insulin response to an oral glucose load was typical of adult onset diabetes, i.e., delayed hyperinsulinemia with concomitant hyperglycemia. Glucose 97-104 insulin Homo sapiens 33-40 49469-0 1975 Plasma-lipids and glucose/insulin relationship in non-insulin-requiring diabetics with and without retinopathy. Glucose 18-25 insulin Homo sapiens 54-61 1154379-8 1975 Tolbutamide or glucagon II caused a significant difference in plasma insulin response in all the diabetic groups compared with the normal subjects, while glucose or glucagon I showed a significant increment of plasma insulin between the normal subjects and the severe diabetics. Glucose 154-161 insulin Homo sapiens 217-224 49469-7 1975 While the blood-sugar concentrations were similiar in the two groups the absolute insulin increment and the relative insulin response to a 50 g. oral glucose load were significantly lower in those with retinopathy than in those without. Glucose 150-157 insulin Homo sapiens 117-124 1199241-1 1975 In a complex examination of clinically healthy persons, with postprandial glucosuria or affected with a hereditary diabetes mellitus differences were found in the dynamics of the insulin secretion in oral and venous glucose tolerance dependent on the character of the glucose tolerance. Glucose 216-223 insulin Homo sapiens 179-186 210730-1 1975 The response of plasma glucose and insulin to infusion of glucose and of epinephrine plus propranolol were examined in normal subjects and in two patients with surgically proven insulin-secreting islet cell tumors. Glucose 58-65 insulin Homo sapiens 35-42 811177-4 1975 Thus, with this small initial dose of insulin the 2-hour plasma insulin values were within the range which in adults has been associated with a maximum fall in blood glucose concentration. Glucose 166-173 insulin Homo sapiens 38-45 1098658-3 1975 Incubation of islets of Langerhans in vitro in the presence of colchicine produced a progressive inhibition of the insulin-secretory response to glucose, which was dependent on the time of incubation. Glucose 145-152 insulin Homo sapiens 115-122 811177-4 1975 Thus, with this small initial dose of insulin the 2-hour plasma insulin values were within the range which in adults has been associated with a maximum fall in blood glucose concentration. Glucose 166-173 insulin Homo sapiens 64-71 811177-7 1975 Over the 2 hours after the initial dose of insulin the mean rate of fall of blood glucose for all 3 patients was 73 mg/100 ml per hour. Glucose 82-89 insulin Homo sapiens 43-50 805337-17 1975 Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal. Glucose 81-88 insulin Homo sapiens 61-68 15959962-0 1975 Insulin control of glucose metabolism in man: a new kinetic analysis. Glucose 19-26 insulin Homo sapiens 0-7 15959962-1 1975 Analyses of the control of glucose metabolism by insulin have been hampered by changes in bloog glucose concentration induced by insulin administration with resultant activation of hypoglycemic counterregulatory mechanisms. Glucose 27-34 insulin Homo sapiens 49-56 15959962-1 1975 Analyses of the control of glucose metabolism by insulin have been hampered by changes in bloog glucose concentration induced by insulin administration with resultant activation of hypoglycemic counterregulatory mechanisms. Glucose 27-34 insulin Homo sapiens 129-136 15959962-1 1975 Analyses of the control of glucose metabolism by insulin have been hampered by changes in bloog glucose concentration induced by insulin administration with resultant activation of hypoglycemic counterregulatory mechanisms. Glucose 96-103 insulin Homo sapiens 49-56 15959962-1 1975 Analyses of the control of glucose metabolism by insulin have been hampered by changes in bloog glucose concentration induced by insulin administration with resultant activation of hypoglycemic counterregulatory mechanisms. Glucose 96-103 insulin Homo sapiens 129-136 15959962-2 1975 To eliminate such mechanisms, we have employed the glucose clamp technique which allows maintenance of fasting blood glucose concentration during and after the administration of insulin. Glucose 51-58 insulin Homo sapiens 178-185 15959962-3 1975 Analyses of six studies performed in young healthy men in the postabsorptive state utilizing the concurrent administration of [14C]glucose and 1 mU/kg per min (40 mU/m2 per min) porcine insulin led to the development of kinetic models for insulin and for glucose. Glucose 131-138 insulin Homo sapiens 239-246 15959962-3 1975 Analyses of six studies performed in young healthy men in the postabsorptive state utilizing the concurrent administration of [14C]glucose and 1 mU/kg per min (40 mU/m2 per min) porcine insulin led to the development of kinetic models for insulin and for glucose. Glucose 255-262 insulin Homo sapiens 186-193 1128232-3 1975 In contrast, ethanol intake had no effect on the glucagon response to glucose ingestion; These data suggest that ethanol enhances glucose-stimulated insulin secretion. Glucose 130-137 insulin Homo sapiens 149-156 15959962-4 1975 These models account quantitatively for the control of insulin on glucose utilization and on endogenous glucose production during nonsteady states. Glucose 66-73 insulin Homo sapiens 55-62 15959962-4 1975 These models account quantitatively for the control of insulin on glucose utilization and on endogenous glucose production during nonsteady states. Glucose 104-111 insulin Homo sapiens 55-62 15959962-11 1975 During the glucose clamp experiments plasma insulin levels reached a plateau of 95 +/-8 microU/ml. Glucose 11-18 insulin Homo sapiens 44-51 15959962-12 1975 Over the entire range of insulin levels studied, glucose losses were best correlated with levels of insulin in a slowly equilibrating insulin compartment of a three-compartment insulin model. Glucose 49-56 insulin Homo sapiens 25-32 15959962-12 1975 Over the entire range of insulin levels studied, glucose losses were best correlated with levels of insulin in a slowly equilibrating insulin compartment of a three-compartment insulin model. Glucose 49-56 insulin Homo sapiens 100-107 1128232-4 1975 The dampened blood glucose rise observed with ethanol may be related to the augmented insulin response or to decreased gastrointestinal absorption of glucose. Glucose 19-26 insulin Homo sapiens 86-93 15959962-12 1975 Over the entire range of insulin levels studied, glucose losses were best correlated with levels of insulin in a slowly equilibrating insulin compartment of a three-compartment insulin model. Glucose 49-56 insulin Homo sapiens 100-107 15959962-12 1975 Over the entire range of insulin levels studied, glucose losses were best correlated with levels of insulin in a slowly equilibrating insulin compartment of a three-compartment insulin model. Glucose 49-56 insulin Homo sapiens 100-107 1144316-2 1975 In difference to the adipose tissue of healthy persons, in the lipoatrophic adipose tissue there occurred under the effect of insulin-novocain mixture a marked increase in the incorporation of C-14-labeled glucose into the total lipids of the adipose tissue. Glucose 206-213 insulin Homo sapiens 126-133 15959962-14 1975 Insulin also rapidly decreased the endogenous glucose production to 33% of its basal level (0.58 mg/kg per min), this suppression being maintained for at least 40 min after exogenous insulin infusion was terminated and after plasma insulin concentrations had returned to basal levels. Glucose 46-53 insulin Homo sapiens 0-7 15959962-15 1975 The change in glucose utilization per unit change in insulin in the slowly equilibrating insulin compartment is proposed as a new measure for insulin sensitivity. Glucose 14-21 insulin Homo sapiens 53-60 15959962-15 1975 The change in glucose utilization per unit change in insulin in the slowly equilibrating insulin compartment is proposed as a new measure for insulin sensitivity. Glucose 14-21 insulin Homo sapiens 89-96 15959962-15 1975 The change in glucose utilization per unit change in insulin in the slowly equilibrating insulin compartment is proposed as a new measure for insulin sensitivity. Glucose 14-21 insulin Homo sapiens 89-96 15959962-16 1975 This defines insulin effects more precisely than previously used measures, such as plasma glucose/plasma insulin concentration ratios. Glucose 90-97 insulin Homo sapiens 13-20 237539-0 1975 Binding of D-glucose to insulin. Glucose 11-20 insulin Homo sapiens 24-31 237539-1 1975 Binding of D-glucose to insulin has been studied by equilibrium dialysis. Glucose 11-20 insulin Homo sapiens 24-31 237539-3 1975 The average amount of glucose molecules bound per insulin molecule is eight, two molecules in the first and six during the second step of binding. Glucose 22-29 insulin Homo sapiens 50-57 237539-4 1975 The intrinsic binding constants for both steps are almost the same (6-10-2 M-minus 1 and 1-10-3 M-minus 1) which can be explained by assuming: (1) that after binding of the first two molecules a conformational change of insulin occurs which facilitates the binding of the next six molecules of D-glucose; or (2) that in the second step of binding the glucose binds to hydrophobic regions which are unmasked by dissociation of the insulin dimer. Glucose 294-303 insulin Homo sapiens 220-227 237539-4 1975 The intrinsic binding constants for both steps are almost the same (6-10-2 M-minus 1 and 1-10-3 M-minus 1) which can be explained by assuming: (1) that after binding of the first two molecules a conformational change of insulin occurs which facilitates the binding of the next six molecules of D-glucose; or (2) that in the second step of binding the glucose binds to hydrophobic regions which are unmasked by dissociation of the insulin dimer. Glucose 296-303 insulin Homo sapiens 220-227 237539-5 1975 Using a three-dimensional model of the insulin molecule areas of the protein molecule where binding of glucose can occur were selected. Glucose 103-110 insulin Homo sapiens 39-46 237539-6 1975 The glucose-binding site very probably involves the area at the insulin surface where most of the invariant and modification-selective residues are present. Glucose 4-11 insulin Homo sapiens 64-71 1125698-7 1975 Truncal vagotomy resulted in a diminished insulin response to oral glucose, which could have been due to vagal denervation of the pancreas or, more probably, impaired release of small-bowel hormones which normally augment the pancreatic insulin response. Glucose 67-74 insulin Homo sapiens 42-49 1125699-4 1975 Oral glucose elicited significantly higher concentrations of plasma insulin in patients who had undergone selective and highly selective vagotomy than in those treated by truncal vagotomy. Glucose 5-12 insulin Homo sapiens 68-75 1125699-6 1975 The insulin secreted in response to intravenous glucose expressed as a percentage of that secreted in response to oral glucose was 112% for truncal vagotomy, 51% for selective vagotomy, and 52% for highly selective vagotomy. Glucose 48-55 insulin Homo sapiens 4-11 1125699-6 1975 The insulin secreted in response to intravenous glucose expressed as a percentage of that secreted in response to oral glucose was 112% for truncal vagotomy, 51% for selective vagotomy, and 52% for highly selective vagotomy. Glucose 119-126 insulin Homo sapiens 4-11 1125699-7 1975 Truncal vagotomy thus led to a diminished insulin response to oral glucose, which was probably due to impaired release of small-bowel hormones. Glucose 67-74 insulin Homo sapiens 42-49 1130520-3 1975 The same relationship between acid secretion and glucose was observed when hypoglycemia was induced by intravenous injection of insulin. Glucose 49-56 insulin Homo sapiens 128-135 1136855-0 1975 Portal and cubital serum insulin during oral, portal and cubital glucose tolerance tests. Glucose 65-72 insulin Homo sapiens 25-32 1136855-2 1975 A significant rise in portal glucose and insulin was found 1/2-2 min after oral glucose intake. Glucose 80-87 insulin Homo sapiens 41-48 1136855-5 1975 In the cubital vein the insulin concentration after oral glucose intake was significantly higher than after i.v. Glucose 57-64 insulin Homo sapiens 24-31 1174086-4 1975 Stimulation with 100 g oral glucose, in analogy to the total insulin, significantly increased proinsulin levels, remaining, however, below the insulin levels. Glucose 28-35 insulin Homo sapiens 61-68 1174086-4 1975 Stimulation with 100 g oral glucose, in analogy to the total insulin, significantly increased proinsulin levels, remaining, however, below the insulin levels. Glucose 28-35 insulin Homo sapiens 94-104 1174086-4 1975 Stimulation with 100 g oral glucose, in analogy to the total insulin, significantly increased proinsulin levels, remaining, however, below the insulin levels. Glucose 28-35 insulin Homo sapiens 97-104 1174086-8 1975 In relation to the weight reduction lower proinsulin and insulin levels were noticed before and after stimulation with glucose. Glucose 119-126 insulin Homo sapiens 42-52 1174086-8 1975 In relation to the weight reduction lower proinsulin and insulin levels were noticed before and after stimulation with glucose. Glucose 119-126 insulin Homo sapiens 45-52 168060-5 1975 After removal of adenoma, insulin response to glucose, glucagon and leucine was improved. Glucose 46-53 insulin Homo sapiens 26-33 1132602-5 1975 Two-hour insulin levels were highest in the group with two-hour plasma glucose levels between 140-169 mg,/100 ml. Glucose 71-78 insulin Homo sapiens 9-16 1132602-11 1975 Glucose level was the major determinant of post-load insulin responses, but these were also significantly influenced by obesity. Glucose 0-7 insulin Homo sapiens 53-60 1171040-3 1975 However there were diurnal and seasonal variations in the blood glucose/plasma insulin relationship. Glucose 64-71 insulin Homo sapiens 79-86 1092707-1 1975 In normal men, the administration of somatostatin almost completely abolished the glucose stimulated insulin-release seen during control studies (without somatostatin), and caused a further reduction in glucagon secretion beyond that induced by hyperglycemia. Glucose 82-89 insulin Homo sapiens 101-108 1092707-6 1975 These data establish that the administration of somatostatin can effectively block the release of insulin stimulated by arginine and glucose, can attenuate the release of glucagon induced by arginine and can enhance the glucose-mediated glucagon suppression. Glucose 133-140 insulin Homo sapiens 98-105 1127073-0 1975 The insulin response to intravenous fructose in relation to blood glucose levels. Glucose 66-73 insulin Homo sapiens 4-11 1127073-3 1975 In contrast, the insulin response was strikingly augmented when preinfusion blood glucose and plasma insulin levels were moderately elevated. Glucose 82-89 insulin Homo sapiens 17-24 1124147-0 1975 [Insulin secretion in obese and diabetic children evaluated with venous perfusion of glucose and stimulation with glucagon. Glucose 85-92 insulin Homo sapiens 1-8 1091119-3 1975 The present studies have demonstrated that the growth hormone releaseinhibiting factor of the hypothalamus, somatostatin, exerts a prominent inhibiting action on glucose induced insulin release in man. Glucose 162-169 insulin Homo sapiens 178-185 1091119-5 1975 Our findings therefore suggest that the inhibiting effect of somatostatin on glucose induced insulin release is not mediated by the alpha-adrenergic receptors. Glucose 77-84 insulin Homo sapiens 93-100 1130181-4 1975 When insulin was infused at a rate which simulated a normal early insulin response to intravenous glucose, blood glucose decreased to the same extent as it did in healthy subjects. Glucose 98-105 insulin Homo sapiens 5-12 1130181-4 1975 When insulin was infused at a rate which simulated a normal early insulin response to intravenous glucose, blood glucose decreased to the same extent as it did in healthy subjects. Glucose 98-105 insulin Homo sapiens 66-73 1130181-5 1975 When a normal early insulin response was simulated during the intravenous glucose tolerance test, the glucose assimilation rate was normalized. Glucose 74-81 insulin Homo sapiens 20-27 1130181-5 1975 When a normal early insulin response was simulated during the intravenous glucose tolerance test, the glucose assimilation rate was normalized. Glucose 102-109 insulin Homo sapiens 20-27 1147652-1 1975 Early insulin response to rapid intravenous injection of glucose was studied in 7 cases of cystic fibrosis aged 8 months to 9 1/2 years. Glucose 57-64 insulin Homo sapiens 6-13 1225247-0 1975 [Blood insulin levels during oral glucose tolerance tests in the obese child. Glucose 34-41 insulin Homo sapiens 7-14 1225247-2 1975 A significant increase in basic and post-stimulation insulin secretion was observed in 173 obese children undergoing oral glucose tolerance tests. Glucose 122-129 insulin Homo sapiens 53-60 1090474-2 1975 Since glucose regulation of glucagon (IRG) secretion may be insulin dependent, we have evaluated IRG secretion in this setting of hypoglycemia and insulin deficiency. Glucose 6-13 insulin Homo sapiens 60-67 1116652-0 1975 Effect of glucose priming on insulin response in the premature infant. Glucose 10-17 insulin Homo sapiens 29-36 1116652-4 1975 When this administration of glucose was preceded by a two-hour infusion of glucose, there was a striking increase in serum insulin. Glucose 28-35 insulin Homo sapiens 123-130 1116652-4 1975 When this administration of glucose was preceded by a two-hour infusion of glucose, there was a striking increase in serum insulin. Glucose 75-82 insulin Homo sapiens 123-130 1131869-0 1975 [Effect of tolbutamide and butylbiguanide on the blood sugar level and level of immunoreductive serum insulin after a glucose infusion in healthy subjects (author"s transl)]. Glucose 118-125 insulin Homo sapiens 102-109 1112448-3 1975 The lowest blood glucose concentration was obtained 30 min after the injection of insulin. Glucose 17-24 insulin Homo sapiens 82-89 1117064-3 1975 Since similar steady-state levels of plasma insulin are achieved in all subjects, the plasma glucose concentration observed during the steady-state period is a measure of an individual"s insulin resistance. Glucose 93-100 insulin Homo sapiens 187-194 1116447-4 1975 After stimulation with glucose, proinsulin levels were significantly raised, analogous to total insulin, but les marked than the latter. Glucose 23-30 insulin Homo sapiens 32-42 1116447-4 1975 After stimulation with glucose, proinsulin levels were significantly raised, analogous to total insulin, but les marked than the latter. Glucose 23-30 insulin Homo sapiens 35-42 1116447-6 1975 The greater the overweight the later maximal insulin levels were reached after oral glucose administration: proinsulin peaks occurred later than insulin peaks. Glucose 84-91 insulin Homo sapiens 45-52 1116447-6 1975 The greater the overweight the later maximal insulin levels were reached after oral glucose administration: proinsulin peaks occurred later than insulin peaks. Glucose 84-91 insulin Homo sapiens 108-118 1116447-6 1975 The greater the overweight the later maximal insulin levels were reached after oral glucose administration: proinsulin peaks occurred later than insulin peaks. Glucose 84-91 insulin Homo sapiens 111-118 1155295-1 1975 Forty-seven elderly men engaged in regular and vigorous exercise had significantly lower plasma insulin levels during oral glucose tolerance tests than their controls. Glucose 123-130 insulin Homo sapiens 96-103 1125145-2 1975 The results indicate that blood sugar and serum insulin levels in response to oral glucose loading do not alter significantly in the menstrual cycle. Glucose 83-90 insulin Homo sapiens 48-55 166897-0 1975 Mechanisms of glucose stimulated insulin secretion in health and in diabetes: some re-evaluations and proposals. Glucose 14-21 insulin Homo sapiens 33-40 1122924-0 1975 Changes in insulin immunoreactivity across the coronary circulation in man during infusions of glucose and a fat emulsion. Glucose 95-102 insulin Homo sapiens 11-18 1170119-0 1975 Diurnal variation in the effects of insulin on blood glucose, plasma non-esterified fatty acids and growth hormone. Glucose 53-60 insulin Homo sapiens 36-43 1227824-0 1975 [Correlations between human portal and peripheral venous insulin and proinsulin concentrations under glucose infusion]. Glucose 101-108 insulin Homo sapiens 69-79 166406-0 1975 Insulin secretion: mechanism of the stimulation by glucose. Glucose 51-58 insulin Homo sapiens 0-7 46055-4 1975 Glucose, without effect on these enzymes, did induce insulin secretion from insulin granules and plasma membranes in vitro. Glucose 0-7 insulin Homo sapiens 53-60 46055-4 1975 Glucose, without effect on these enzymes, did induce insulin secretion from insulin granules and plasma membranes in vitro. Glucose 0-7 insulin Homo sapiens 76-83 46055-5 1975 The model proposes a mechanism whereby glucose may trigger first-phase insulin secretion; reinforcing mechanisms, such as raised levels of cyclic adenosine monophosphate, could augment subsequent secretion. Glucose 40-47 insulin Homo sapiens 72-79 1089309-0 1975 Vesicular binesis: glucose effect on insulin secretory vesicles. Glucose 19-26 insulin Homo sapiens 37-44 1121656-1 1975 The use of continuous indirect calorimetry in the course of a 100 g OGTT in 10 normal subjects has shown that carbohydrate oxidation rises with the secondary fall in blood glucose, suggesting that it could result from glucose stored under the influence of insulin. Glucose 172-179 insulin Homo sapiens 256-263 1121656-4 1975 On the other hand, in 7 obese diabetics with high plasma insulin levels carbohydrate oxidation was found to be low, suggesting that carbohydrate intolerance could result from the non-oxidation of glucose. Glucose 196-203 insulin Homo sapiens 57-64 1172893-0 1975 Glucose tolerance in newborn infants of healthy mothers: its relationship to the mothers" insulin response to glucose infusion. Glucose 110-117 insulin Homo sapiens 90-97 1172893-1 1975 It has earlier been postulated that a low insulin response to a glucose infusion is characteristic for the prediabetic individual (Cerasi & Luft 1967c). Glucose 64-71 insulin Homo sapiens 42-49 1229805-4 1975 These findings suggest that changes in plasma pyruvate, lactate and inorganic phosphates induced by insulin, and regarded as espressions of its peripheral metabolism, are greatly dependent on the beta-adrenergic effect of the endogenous catecholamines released during the time when blood glucose values are low. Glucose 288-295 insulin Homo sapiens 100-107 1199704-1 1975 Effects of a low and a high insulin response to glucose in the mothers. Glucose 48-55 insulin Homo sapiens 28-35 1117893-6 1975 The calculated insulin area during an oral glucose load was significantly correlated with serum calcium (5.1 to 12.2 mg per deciliter), and a linear relation was obtained (y = 1.59x - 3.3, r = 0.81, p less than 0.001), although a relation with the glucose area was not found. Glucose 43-50 insulin Homo sapiens 15-22 1117893-6 1975 The calculated insulin area during an oral glucose load was significantly correlated with serum calcium (5.1 to 12.2 mg per deciliter), and a linear relation was obtained (y = 1.59x - 3.3, r = 0.81, p less than 0.001), although a relation with the glucose area was not found. Glucose 248-255 insulin Homo sapiens 15-22 1199704-2 1975 Twenty-eight healthy women, 17 with high and 11 with low insulin response to glucose but with normal glucose tolerance, were followed throughout pregnancy. Glucose 77-84 insulin Homo sapiens 57-64 1207275-1 1975 During abdominal surgery the basal and glucose stimulated insulin secretion rate is reduced. Glucose 39-46 insulin Homo sapiens 58-65 1241502-0 1975 Serum insulin values during oral glucose tolerance test in various age groups. Glucose 33-40 insulin Homo sapiens 6-13 1130434-8 1975 These findings suggest that, compared to the action of peripherally administered insulin, intraportally injected exogenous insulin or tolbutamide-induced endogenous insulin has a greater hepatic and a lesser peripheral effect on glucose metabolism. Glucose 229-236 insulin Homo sapiens 123-130 1130434-8 1975 These findings suggest that, compared to the action of peripherally administered insulin, intraportally injected exogenous insulin or tolbutamide-induced endogenous insulin has a greater hepatic and a lesser peripheral effect on glucose metabolism. Glucose 229-236 insulin Homo sapiens 123-130 182367-1 1975 Insulin accelerates the entry of glucose and amino acids into muscle cells by acting upon the "carrier-facilitated" transport mechanism. Glucose 33-40 insulin Homo sapiens 0-7 182367-12 1975 Since the ischemic heart is dependent upon glucose as the major fuel, insulin lack may deprive the heart of adequate substrate. Glucose 43-50 insulin Homo sapiens 70-77 1120542-5 1975 It was also found that obese mild diabetics had significantly greater absolute insulin responses to both the five-minute and two-minute glucose injections than did their nonobese counterparts. Glucose 136-143 insulin Homo sapiens 79-86 1195081-0 1975 Infants of mothers with a high and of mothers with a low insulin response to glucose infusion. Glucose 77-84 insulin Homo sapiens 57-64 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 46-53 insulin Homo sapiens 27-34 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 46-53 insulin Homo sapiens 141-148 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 46-53 insulin Homo sapiens 141-148 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 161-168 insulin Homo sapiens 27-34 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 161-168 insulin Homo sapiens 141-148 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 161-168 insulin Homo sapiens 141-148 1207275-2 1975 An arginine-infusion of 0,5 g/kg over 30 minutes is able to stimulate the basal as well as the glucose stimulated insulin secretion under stress condition. Glucose 95-102 insulin Homo sapiens 114-121 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 161-168 insulin Homo sapiens 27-34 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 161-168 insulin Homo sapiens 141-148 1207275-3 1975 A synergism between the effect of arginine and blood glucose concentration concerning the influence on insulin secretion can be proven. Glucose 53-60 insulin Homo sapiens 103-110 1195081-5 1975 A prospective study of the insulin reponse to glucose during pregnancy [9] has been previously published, which included 11 women with a low insulin response to glucose infusion (GIT) - a prediabetic type of insulin response according to the definition of Cerasi and Luft [5] - and a control group of 14 women with a high insulin response to glucose infusion. Glucose 161-168 insulin Homo sapiens 141-148 1214932-0 1975 [The effect of insulin on the intensity of glucose and glycogen biosynthesis from acetate in the cerebral hemispheres]. Glucose 43-50 insulin Homo sapiens 15-22 1110865-2 1975 Compared with the normal group, the patients with cystic fibrosis had significantly impaired glucose tolerance and significantly lower serum immunoreactive insulin levels during oral and intravenous glucose tolerance tests; serum insulin levels were also significantly lower after intravenous administration of tolbutamide in the patients with cystic fibrosis, but the reduction in blood glucose concentration in each group was not significantly different. Glucose 199-206 insulin Homo sapiens 156-163 1196660-0 1975 [Effect of insulin and glucagon on the anomeric composition of D-glucose in blood (author"s transl)]. Glucose 63-72 insulin Homo sapiens 11-18 1196660-1 1975 The effect of insulin and glucagon on the anomeric composition of D-glucose in blood of children in the timecourse of tolerance tests has been investigated. Glucose 66-75 insulin Homo sapiens 14-21 1196660-2 1975 Employing an improved enzymatic micromethod, specific for the anomers of D-glucose, insulin could be shown to raise the percentage of the alpha-anomer of the total serum glucose, whereas glucagon has no direct effect on the anomeric composition. Glucose 73-82 insulin Homo sapiens 84-91 1196660-2 1975 Employing an improved enzymatic micromethod, specific for the anomers of D-glucose, insulin could be shown to raise the percentage of the alpha-anomer of the total serum glucose, whereas glucagon has no direct effect on the anomeric composition. Glucose 75-82 insulin Homo sapiens 84-91 1196660-3 1975 However, an insulin-like effect could be observed in the second part of the glucagon tolerance test, e.g. alpha-D-glucose increased relatively to total glucose in serum and erythrocytes. Glucose 114-121 insulin Homo sapiens 12-19 1110865-3 1975 During an intravenous insulin test, the decrease in blood glucose concentration was the same for both groups, in spite of significantly lower serum insulin levels in the patients with cystic fibrosis .The percentage fall in plasma free fatty acids was at least as great in the patients with cystic fibrosis as in normals during the test procedures; while a significant decrease in plasma alpha-amino nitrogen after intravenously administered insulin was seen only in the patients with cystic fibrosis. Glucose 58-65 insulin Homo sapiens 22-29 1110865-4 1975 These studies suggest that the carbohydrate intolerance of cystic fibrosis is consequent upon an impaired insulin response to glucose, but that this insulin deficiency is partly compensated for by increased peripheral tissue sensitivity to insulin. Glucose 126-133 insulin Homo sapiens 106-113 1054501-1 1975 The biological activity of Sepharose-insulin in different assays in vitro, e.g., stimulation of glucose oxidation, lipogenesis, and antilipolysis and activation of pyruvate dehydrogenase (EC 1.2.4.1) activity, has been investigated. Glucose 96-103 insulin Homo sapiens 37-44 1135175-0 1975 [Blood sugar and plasma immunoreactive insulin levels in healthy pregnant women undergoing the glucose tolerance test]. Glucose 95-102 insulin Homo sapiens 39-46 1234784-8 1975 In view of these results we can affirm that analysis if the inter-relation between glucose and insulin is a good exponet for evaluation of the grade of analgesic protection, offered by a drug, against nociceptive stimuli triggered by surgery. Glucose 83-90 insulin Homo sapiens 95-102 1188312-0 1975 Effect of vagotomy on insulin release after oral and intravenous glucose administration. Glucose 65-72 insulin Homo sapiens 22-29 1188312-2 1975 The potentiating effect on insulin release of orally administered glucose was not abolished by total vagotomy, meaning that vagal mechanisms are not likely to play a major role in this potentiation in man. Glucose 66-73 insulin Homo sapiens 27-34 173015-10 1975 Serum insulin 30 and 60 minutes after an oral glucose loading decreased in the patients on combined treatment, whereas the insulin response remained normal in patients taking Secholex alone. Glucose 46-53 insulin Homo sapiens 6-13 1227006-0 1975 [Diagnostic relevance of 3-hour blood glucose value and serum insulin concentration in the oral glucose tolerance test]. Glucose 96-103 insulin Homo sapiens 62-69 1119116-3 1975 Reaction of the insulin activity of blood, after loading with glucose, secretine and pancreosimine, was also decreased. Glucose 62-69 insulin Homo sapiens 16-23 1224616-4 1975 For a better idea about the insulin response volume, provoked by glucose loading, they compare the sums of the insulinemic values and "insulinogenic index", among the control subjects and the patients examined. Glucose 65-72 insulin Homo sapiens 28-35 1224616-8 1975 The highest insulinogenic index is in NGT patients and is with about 50% higher than that of the control subjects while in patients with PGT it is quite the reverse, i. e.--glucose tolerance deteriorated parallelly with the reducing of insulin response to glucose stimulus or, in other words--normal glucose tolerance in patients maintained by the increased insulin production. Glucose 173-180 insulin Homo sapiens 12-19 1224616-8 1975 The highest insulinogenic index is in NGT patients and is with about 50% higher than that of the control subjects while in patients with PGT it is quite the reverse, i. e.--glucose tolerance deteriorated parallelly with the reducing of insulin response to glucose stimulus or, in other words--normal glucose tolerance in patients maintained by the increased insulin production. Glucose 256-263 insulin Homo sapiens 12-19 1224616-8 1975 The highest insulinogenic index is in NGT patients and is with about 50% higher than that of the control subjects while in patients with PGT it is quite the reverse, i. e.--glucose tolerance deteriorated parallelly with the reducing of insulin response to glucose stimulus or, in other words--normal glucose tolerance in patients maintained by the increased insulin production. Glucose 256-263 insulin Homo sapiens 236-243 1224616-8 1975 The highest insulinogenic index is in NGT patients and is with about 50% higher than that of the control subjects while in patients with PGT it is quite the reverse, i. e.--glucose tolerance deteriorated parallelly with the reducing of insulin response to glucose stimulus or, in other words--normal glucose tolerance in patients maintained by the increased insulin production. Glucose 256-263 insulin Homo sapiens 12-19 1224616-8 1975 The highest insulinogenic index is in NGT patients and is with about 50% higher than that of the control subjects while in patients with PGT it is quite the reverse, i. e.--glucose tolerance deteriorated parallelly with the reducing of insulin response to glucose stimulus or, in other words--normal glucose tolerance in patients maintained by the increased insulin production. Glucose 256-263 insulin Homo sapiens 236-243 1199572-0 1975 [Dynamics of immunoreactive insulin during glucose tolerance test of patients with thyrotoxicosis]. Glucose 43-50 insulin Homo sapiens 28-35 4442669-0 1974 Insulin secretory response of diabetics during the period of improvement of glucose tolerance to normal range. Glucose 76-83 insulin Homo sapiens 0-7 4452392-0 1974 [Clinical and experimental investigations regarding the response of insulin under continuous infusion of glucose: contribution to the diagnosis of diabetes premellitus(author"s transl)]. Glucose 105-112 insulin Homo sapiens 68-75 4457437-0 1974 [Insulin secretion after glucose loading. Glucose 25-32 insulin Homo sapiens 1-8 4457437-1 1974 Studies on insulin secretion in healthy and diabetic subjects after administration of glucose]. Glucose 86-93 insulin Homo sapiens 11-18 4620122-2 1974 Influence of food deprivation and glucose refeeding in vitro on insulin secretion. Glucose 34-41 insulin Homo sapiens 64-71 4440699-0 1974 Serum glucagon and insulin levels and their relationship to blood glucose values in patients with acute myocardial infarction and acute coronary insufficiency. Glucose 66-73 insulin Homo sapiens 19-26 4430416-0 1974 Insulin response to glucose and tolbutamide in "essential" versus "pancreatic" mild glucose intolerance. Glucose 20-27 insulin Homo sapiens 0-7 1153688-2 1975 The nephrotic syndrome was associated with a smaller secretion of insulin in response to intravenous glucose and tolbutamide than occurred in normals. Glucose 101-108 insulin Homo sapiens 66-73 4466653-1 1974 Behavior of plasma lipids, glucose tolerance, and plasma insulin after glucose load during treatment with clofibrate]. Glucose 71-78 insulin Homo sapiens 57-64 4430416-0 1974 Insulin response to glucose and tolbutamide in "essential" versus "pancreatic" mild glucose intolerance. Glucose 84-91 insulin Homo sapiens 0-7 4608369-0 1974 The influence of glucose on gastrin and insulin release in the enteroinsular axis. Glucose 17-24 insulin Homo sapiens 40-47 4423206-0 1974 Glucose- and tolbutamide-mediated insulin response after preinfusion with ethanol. Glucose 0-7 insulin Homo sapiens 34-41 4141548-0 1974 [Long-term effects of the estrogen-gestagen combination preparation Ovosiston on glucose level in the insulin tolerance test]. Glucose 81-88 insulin Homo sapiens 102-109 4461527-0 1974 Proceedings: Studies on the role of superficial fat cell SH-groups in basal and insulin-stimulated glucose uptake. Glucose 99-106 insulin Homo sapiens 80-87 4470082-0 1974 [Various insulin-secretion patterns in the early phase following oral administration of glucose and cellulose]. Glucose 88-95 insulin Homo sapiens 9-16 4439409-0 1974 Insulin response to tolbutamide-glucose load in normal and diabetic subjects. Glucose 32-39 insulin Homo sapiens 0-7 4421859-0 1974 Oscillation in insulin response to glucose stimulation. Glucose 35-42 insulin Homo sapiens 15-22 4607598-0 1974 The artificial beta cell--a continuous control of blood sugar by external regulation of insulin infusion (glucose controlled insulin infusion system). Glucose 106-113 insulin Homo sapiens 88-95 4607598-0 1974 The artificial beta cell--a continuous control of blood sugar by external regulation of insulin infusion (glucose controlled insulin infusion system). Glucose 106-113 insulin Homo sapiens 125-132 4413915-1 1974 An increased glucose-induced insulin response has been observed in patients susceptible to malignant hyperpyrexia. Glucose 13-20 insulin Homo sapiens 29-36 4412890-0 1974 Early response of plasma insulin to small doses of intravenous glucose: effect of obesity. Glucose 63-70 insulin Homo sapiens 25-32 4424575-0 1974 A mathematical model for the glucose induced insulin release in man. Glucose 29-36 insulin Homo sapiens 45-52 4847245-9 1974 The decline in free fatty acids after intravenous injection of glucose showed a negative correlation with plasma noradrenaline and a positive correlation with the initial rise in insulin. Glucose 63-70 insulin Homo sapiens 179-186 4421829-0 1974 Insulin response to intravenous glucose during long-term treatment with propranolol. Glucose 32-39 insulin Homo sapiens 0-7 4843759-0 1974 The relation between a large baby at birth and diminished maternal first phase insulin response to glucose. Glucose 99-106 insulin Homo sapiens 79-86 4449797-0 1974 [Content of immunoreactive insulin in the blood plasma of persons of different ages (without carbohydrate metabolic disorders) and the effect on this index of a glucose load]. Glucose 161-168 insulin Homo sapiens 27-34 4855253-3 1974 The mean fall in plasma glucose was 58% four hours after the start of insulin. Glucose 24-31 insulin Homo sapiens 70-77 4828443-0 1974 Effect of intravenous glucose infusion on plasma insulin removal rate. Glucose 22-29 insulin Homo sapiens 49-56 4603502-0 1974 [Effect of norepinephrine on glucose-stimulated insulin secretion in man]. Glucose 29-36 insulin Homo sapiens 48-55 4830181-0 1974 Relationship between insulin response during the intravenous glucose tolerance test, rate of fractional glucose removal and the degree of insulin resistance in normal adults. Glucose 61-68 insulin Homo sapiens 21-28 4830181-0 1974 Relationship between insulin response during the intravenous glucose tolerance test, rate of fractional glucose removal and the degree of insulin resistance in normal adults. Glucose 104-111 insulin Homo sapiens 21-28 4830181-0 1974 Relationship between insulin response during the intravenous glucose tolerance test, rate of fractional glucose removal and the degree of insulin resistance in normal adults. Glucose 104-111 insulin Homo sapiens 138-145 4856884-11 1974 Insulin in compartment 3 was found to correlate remarkably with the time-course of the servo-controlled glucose infusion. Glucose 104-111 insulin Homo sapiens 0-7 1218530-0 1975 [Serum insulin concentration following oral glucose loading in thyrotoxicosis and myxedema]. Glucose 44-51 insulin Homo sapiens 7-14 1225517-8 1975 In 13 persons the proinsulin fraction of the total insulin after stimulation with glucose and tolbutamid has been registered. Glucose 82-89 insulin Homo sapiens 18-28 1225517-8 1975 In 13 persons the proinsulin fraction of the total insulin after stimulation with glucose and tolbutamid has been registered. Glucose 82-89 insulin Homo sapiens 21-28 1225517-9 1975 The proinsulin shows in the oral glucose tolerance test compared to insulin a lower and delayed increase. Glucose 33-40 insulin Homo sapiens 4-14 1225517-9 1975 The proinsulin shows in the oral glucose tolerance test compared to insulin a lower and delayed increase. Glucose 33-40 insulin Homo sapiens 7-14 4856884-13 1974 We conclude that compartment 3 insulin (rather than plasma insulin) is a more direct determinant of glucose utilization. Glucose 100-107 insulin Homo sapiens 31-38 4827582-2 1974 Effects of insulin on glucose concentrations in inner ear fluids and cochlear microphonics. Glucose 22-29 insulin Homo sapiens 11-18 4205794-0 1974 Insulin response in patients receiving concentrated infusions of glucose and casein hydrolysate for complete parenteral nutrition. Glucose 65-72 insulin Homo sapiens 0-7 4816971-0 1974 Letter: Insulin response to intravenous glucose during beta-adrenergic blockade. Glucose 40-47 insulin Homo sapiens 8-15 4817159-0 1974 Diurnal variation in glucose tolerance: associated changes in plasma insulin, growth hormone, and non-esterified fatty acids. Glucose 21-28 insulin Homo sapiens 69-76 4409874-0 1974 [Insulin concentrations in portal venous blood in man after glucose infusion (author"s transl)]. Glucose 60-67 insulin Homo sapiens 1-8 4817159-5 1974 The plasma insulin response was less at the 30 minute time point in the afternoon, but significantly exceeded the morning values at 120 and 150 minutes after the glucose load. Glucose 162-169 insulin Homo sapiens 11-18 4817159-7 1974 Fasting non-esterified fatty acid levels were significantly higher before the afternoon test.The relatively impaired glucose tolerance in the afternoon is associated with a delayed insulin response to the glucose load. Glucose 117-124 insulin Homo sapiens 181-188 4812442-4 1974 Intravenous infusion of glucose in CRF patients resulted in significant elevations and prolonged disappearance of plasma glucose and insulin when compared to control subjects (P < 0.01). Glucose 24-31 insulin Homo sapiens 133-140 4816888-0 1974 Quantitative study on the potentiating effect of arginine on glucose-induced insulin response in healthy, prediabetic, and diabetic subjects. Glucose 61-68 insulin Homo sapiens 77-84 4848680-0 1974 [Evaluation of blood sugar and blood insulin levels in the oral glucose tolerance test]. Glucose 64-71 insulin Homo sapiens 37-44 4812443-4 1974 Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol. Glucose 45-52 insulin Homo sapiens 0-7 4426303-0 1974 The effect of secretin on glucose-stimulated insulin secretion in man. Glucose 26-33 insulin Homo sapiens 45-52 4476353-0 1974 [Proceedings: Blood sugar and insulin responses by continuous glucose administration. Glucose 62-69 insulin Homo sapiens 30-37 4476353-2 1974 The insulin response and growth hormone reaction to continuous administration of glucose and maltose]. Glucose 81-88 insulin Homo sapiens 4-11 4476364-0 1974 [Proceedings: Effect of secretion on insulin secretory stimulation capacity of glucose]. Glucose 79-86 insulin Homo sapiens 37-44 4847245-6 1974 Intravenous glucose tolerance was reduced in patients with AMI, especially in patients with high plasma noradrenaline and a low initial rise in insulin. Glucose 12-19 insulin Homo sapiens 144-151 4847245-8 1974 The statistical effects of serum insulin and plasma noradrenaline on the glucose tolerance could not be separated from each other. Glucose 73-80 insulin Homo sapiens 33-40 4811508-0 1974 Circadian variation of the blood glucose, plasma insulin and human growth hormone levels in response to an oral glucose load in normal subjects. Glucose 112-119 insulin Homo sapiens 49-56 4441222-0 1974 [Measurement of plasma insulin and growth hormone after oral glucose tolerance test in patients with alcoholic cirrhosis]. Glucose 61-68 insulin Homo sapiens 23-30 4136648-0 1974 Early insulin response to glucose injected intravenously in patients with localized granuloma annulare. Glucose 26-33 insulin Homo sapiens 6-13 4212407-0 1974 The effect of insulin on the permeability of phosphatidyl choline bimolecular membranes to glucose. Glucose 91-98 insulin Homo sapiens 14-21 4836738-0 1974 Insulin levels in cerebrospinal fluid following glucose load in humans. Glucose 48-55 insulin Homo sapiens 0-7 4774078-0 1973 Effect of cortisol on the insulin response to intravenous glucose. Glucose 58-65 insulin Homo sapiens 26-33 4357617-8 1974 We have also noted significant decreases after weight reduction in the insulin and glucose responses during the oral glucose tolerance test (37% decrease and 12% decrease, respectively). Glucose 117-124 insulin Homo sapiens 71-78 4808635-9 1974 It is concluded (a) that glucagon at high concentration is capable of stimulating lipolysis and ketogenesis in insulin-deficient diabetic man; (b) that insulin, mole for mole, has more antilipolytic activity in man than glucagon has lipolytic activity; and (c) that glucagon, on a molar basis, has greater stimulatory activity than insulin has inhibitory activity on hepatic glucose release. Glucose 375-382 insulin Homo sapiens 152-159 4805339-0 1973 Plasma insulin concentration in response to glucose given by different routes. Glucose 44-51 insulin Homo sapiens 7-14 4750452-8 1973 Glucose utilization was increased and lactate output decreased during the ethanol periods, presumably a consequence of the changing arterial concentrations and increased insulin level. Glucose 0-7 insulin Homo sapiens 170-177 4206393-0 1973 Effect of diphenylhydantoin on insulin response in the oral glucose tolerance test in children and adolescents. Glucose 60-67 insulin Homo sapiens 31-38 4148542-0 1973 Effect of blockade of the alpha-adrenergic receptors on insulin response to glucose infusion in prediabetic subjects. Glucose 76-83 insulin Homo sapiens 56-63 4585589-0 1973 Computer assisted analysis of insulin response to glucose stimulus. Glucose 50-57 insulin Homo sapiens 30-37 4784786-0 1973 Evidence for two types of juvenile obesity on the basis of body composition and insulin release following small doses of glucose. Glucose 121-128 insulin Homo sapiens 80-87 4749399-0 1973 Insulin patterns in equivocal glucose tolerance tests (chemical diabetes). Glucose 30-37 insulin Homo sapiens 0-7 4767005-0 1973 The different responses of blood amino acids and blood glucose to the administration of insulin to patients with acromegaly. Glucose 55-62 insulin Homo sapiens 88-95 4126646-0 1973 Letter: Plasma-insulin levels during oral glucose loads in prediabetics. Glucose 42-49 insulin Homo sapiens 15-22 4801016-0 1973 [Blood level of sugar, free fatty acids and immunoreactive insulin in patients with diffuse toxic goiter during a course of glucose tolerance test]. Glucose 124-131 insulin Homo sapiens 59-66 4746913-0 1973 Differences in insulin release in response to glucose and tolbutamide stimulation. Glucose 46-53 insulin Homo sapiens 15-22 4774119-0 1973 Paradoxical effects of theophylline and its interaction with insulin on glucose metabolism in adipose tissue. Glucose 72-79 insulin Homo sapiens 61-68 4729005-0 1973 Effects of an oral glucose load on serum immunoreactive insulin, free fatty acid, growth hormone and blood sugar levels in young and elderly subjects. Glucose 19-26 insulin Homo sapiens 56-63 4785429-0 1973 Effect of transient elevation of plasma insulin within physiologic levels (simulated early insulin response) on blood glucose. Glucose 118-125 insulin Homo sapiens 40-47 4785429-0 1973 Effect of transient elevation of plasma insulin within physiologic levels (simulated early insulin response) on blood glucose. Glucose 118-125 insulin Homo sapiens 91-98 4800353-0 1973 Early insulin response to glucose stimulation in siblings of juvenile diabetics. Glucose 26-33 insulin Homo sapiens 6-13 4765989-2 1973 Effects on plasma insulin in glucose-intolerant subjects without marked hyperinsulinemia. Glucose 29-36 insulin Homo sapiens 18-25 4767365-0 1973 Plasma insulin and free fatty acids in young people with postprandial glycosuria: plasma insulin response in the cases with borderline glucose tolerance test. Glucose 135-142 insulin Homo sapiens 89-96 4727242-0 1973 Insulin concentration in portal and peripheral venous blood after oral glucose in human pancreatitis. Glucose 71-78 insulin Homo sapiens 0-7 4197819-0 1973 An absolute requirement for insulin in the control of hepatic glycogenesis by glucose. Glucose 78-85 insulin Homo sapiens 28-35 4717996-0 1973 Estimation of the early insulin response to intravenous glucose injection. Glucose 56-63 insulin Homo sapiens 24-31 4719190-0 1973 Relationship between fasting plasma insulin level and resistance to insulin-mediated glucose uptake in normal and diabetic subjects. Glucose 85-92 insulin Homo sapiens 36-43 4719190-0 1973 Relationship between fasting plasma insulin level and resistance to insulin-mediated glucose uptake in normal and diabetic subjects. Glucose 85-92 insulin Homo sapiens 68-75 4351776-0 1973 Effect of hydrocortisone and corticotropin on glucose-induced insulin and proinsulin secretion in man. Glucose 46-53 insulin Homo sapiens 62-69 4703228-0 1973 The effect of gastrin on basal- and glucose-stimulated insulin secretion in man. Glucose 36-43 insulin Homo sapiens 55-62 4733090-1 1973 In genetic prediabetic subjects (the glucose tolerant offspring of two diabetic parents or the identical twin of a known diabetic) serum insulin concentrations after glucose administration are subnormal. Glucose 37-44 insulin Homo sapiens 137-144 4733090-1 1973 In genetic prediabetic subjects (the glucose tolerant offspring of two diabetic parents or the identical twin of a known diabetic) serum insulin concentrations after glucose administration are subnormal. Glucose 166-173 insulin Homo sapiens 137-144 4733090-2 1973 Maintenance of glucose tolerance in this setting is apparently paradoxical, suggesting increased tissue insulin sensitivity. Glucose 15-22 insulin Homo sapiens 104-111 4733090-6 1973 Conversely, the sum of increments in serum insulin was subnormal for the first 2 h. The insulin index (the sum of increments in insulin divided by the sum of increments in glucose) was significantly lower in prediabetics throughout the test. Glucose 172-179 insulin Homo sapiens 88-95 4733090-6 1973 Conversely, the sum of increments in serum insulin was subnormal for the first 2 h. The insulin index (the sum of increments in insulin divided by the sum of increments in glucose) was significantly lower in prediabetics throughout the test. Glucose 172-179 insulin Homo sapiens 88-95 4542575-2 1973 Insulin increased the rate of net Na extrusion from Na-loaded frog skeletal muscle into glucose-free Na-Ringer. Glucose 88-95 insulin Homo sapiens 0-7 4714111-2 1973 During the phase of subclinical diabetes her plasma immunoreactive insulin response to oral glucose was markedly increased, but when she became symptomatic gross insulin deficiency had supervened. Glucose 92-99 insulin Homo sapiens 67-74 4710447-0 1973 Plasma glucose and insulin responses to oral glucose with chronic diphenylhydantoin therapy. Glucose 45-52 insulin Homo sapiens 19-26 4703228-1 1973 The effect of gastrin on basal- and glucose-stimulated insulin secretion was studied in 32 normal, young subjects. Glucose 36-43 insulin Homo sapiens 55-62 4703228-8 1973 When 15.6 ng (7.1 pmol) gastrin per kg body weight and 25 g glucose were injected simultaneously, the glucose-induced insulin response was potentiated (from 2.32+/-0.33 to 4.33+/-0.98 nmol per liter per 20 min, P < 0.02), even though gastrin concentrations only increased to 71.2+/-6.6 pmol per liter. Glucose 60-67 insulin Homo sapiens 118-125 4703228-8 1973 When 15.6 ng (7.1 pmol) gastrin per kg body weight and 25 g glucose were injected simultaneously, the glucose-induced insulin response was potentiated (from 2.32+/-0.33 to 4.33+/-0.98 nmol per liter per 20 min, P < 0.02), even though gastrin concentrations only increased to 71.2+/-6.6 pmol per liter. Glucose 102-109 insulin Homo sapiens 118-125 4406484-0 1974 Insulin response to glucose infusion during pregnancy. Glucose 20-27 insulin Homo sapiens 0-7 4703228-14 1973 In physiologic concentrations gastrin potentiates the glucose-stimulated insulin secretion and is without effect on basal insulin secretion. Glucose 54-61 insulin Homo sapiens 73-80 4632779-0 1973 Plasma insulin in intravenous glucose and amino acid infusion. Glucose 30-37 insulin Homo sapiens 7-14 4219867-7 1974 Plasma free fatty acids and amino acids decreased, plasma insulin and growth hormone increased markedly in response to 16% glucose. Glucose 123-130 insulin Homo sapiens 58-65 4724686-0 1973 The regulation of splanchnic glucose production in subjects with low insulin response--a compensatory mechanism in prediabetes? Glucose 29-36 insulin Homo sapiens 69-76 4573352-5 1973 In addition, cytochalasin B lowered the threshold concentration for the stimulant action of glucose upon insulin release. Glucose 92-99 insulin Homo sapiens 105-112 4350576-0 1973 Inhibitors of proteolysis and glucose uptake by diaphragm muscle in vitro under insulin action. Glucose 30-37 insulin Homo sapiens 80-87 4693648-12 1973 Glucose utilization appears to be impaired by HC, but is restored by additional glucose and insulin. Glucose 0-7 insulin Homo sapiens 92-99 4693651-2 1973 Acute serum insulin responses in 10 normal subjects after rapid intravenous injection of glucose (5 g) or isoproterenol (2 mug) were of similar magnitude and timing (glucose: 431+/-349%; mean Delta3-5" insulin (IRI)+/-SD, per cent basal and isoproterenol: 359+/-216%; mean Delta2-4" IRI+/-SD, per cent basal). Glucose 89-96 insulin Homo sapiens 12-19 4693651-2 1973 Acute serum insulin responses in 10 normal subjects after rapid intravenous injection of glucose (5 g) or isoproterenol (2 mug) were of similar magnitude and timing (glucose: 431+/-349%; mean Delta3-5" insulin (IRI)+/-SD, per cent basal and isoproterenol: 359+/-216%; mean Delta2-4" IRI+/-SD, per cent basal). Glucose 166-173 insulin Homo sapiens 12-19 4693651-4 1973 (a) To determine whether glucose-induced insulin secretion is dependent upon beta adrenergic activity, the effect of beta adrenergic blockade with intravenous propranolol (0.08 mg/min) upon acute insulin responses to isoproterenol and glucose were compared in normal subjects. Glucose 25-32 insulin Homo sapiens 41-48 4685092-2 1973 The present investigation was undertaken to observe the effect on 24-h triglyceride, free fatty acid, blood sugar, and plasma insulin profiles of inhibition of nocturnal lipolysis by glucose or nicotinic acid in normal subjects and in patients with type IV hyperlipoproteinemia. Glucose 183-190 insulin Homo sapiens 126-133 4574907-0 1973 Insulin concentrations in portal venous and peripheral venous blood in man following administration of glucose, galactose, xylitol and tobutamide. Glucose 103-110 insulin Homo sapiens 0-7 4542062-0 1973 Insulin secretion in human neonates during longterm infusion of glucose. Glucose 64-71 insulin Homo sapiens 0-7 4542069-0 1973 The effect of diabetes mellitus and insulin on the absorption of glucose, water and electrolytes by the small intestine in man. Glucose 65-72 insulin Homo sapiens 36-43 4713540-0 1973 [Studies of the behavior of plasma insulin and somatotropin after oral glucose overload in patients with viral hepatitis]. Glucose 71-78 insulin Homo sapiens 35-42 4693651-8 1973 These data suggest that insulin responses to glucose in normal subjects are mediated by specific pancreatic glucose receptors which are independent from beta adrenergic receptors and that abnormal glucose-induced insulin secretion in diabetics is due to defects within glucose receptors and not beta adrenergic receptors as has been previously hypothesized. Glucose 45-52 insulin Homo sapiens 24-31 4693651-8 1973 These data suggest that insulin responses to glucose in normal subjects are mediated by specific pancreatic glucose receptors which are independent from beta adrenergic receptors and that abnormal glucose-induced insulin secretion in diabetics is due to defects within glucose receptors and not beta adrenergic receptors as has been previously hypothesized. Glucose 108-115 insulin Homo sapiens 24-31 4694989-0 1973 Insulin response to oral glucose in patients with preeclampsia. Glucose 25-32 insulin Homo sapiens 0-7 4203504-0 1973 Effects of insulin on glucose metabolism in vascular and intestinal smooth muscle. Glucose 22-29 insulin Homo sapiens 11-18 4771108-0 1973 Serum insulin after intravenous administration of glucose before and after total vagotomy. Glucose 50-57 insulin Homo sapiens 6-13 4691251-0 1973 Plasma insulin and K values during intravenous glucose tolerance test in newborn infants with erythroblastosis foetalis. Glucose 47-54 insulin Homo sapiens 7-14 4790130-0 1973 [Influence of glucagon and insulin on glucose resorption in man]. Glucose 38-45 insulin Homo sapiens 27-34 4345761-1 1973 Effects of sodium valerate on secretion and of adrenocorticotrophin-induced premature parturition on the insulin secretory response to glucose. Glucose 135-142 insulin Homo sapiens 105-112 4208215-0 1973 [Insulin secretion following combined administration of glucose and different sulfonylurea compounds in equipotential doses in metabolically healthy persons]. Glucose 56-63 insulin Homo sapiens 1-8 5071337-0 1972 Effect of weight changes on serum insulin response in subjects with normal oral glucose tolerance. Glucose 80-87 insulin Homo sapiens 34-41 4637151-2 1972 A significantly greater rise in blood glucose concentration was observed in the duodenal ulcer group, and this was associated with a significantly greater output of insulin. Glucose 38-45 insulin Homo sapiens 165-172 4653874-2 1972 Fifteen infants of diabetic mothers treated with insulin had a much greater fall in blood glucose of 77.5 mg/100 ml and a smaller rise of glucagon of 20.9 pg/ml. Glucose 90-97 insulin Homo sapiens 49-56 4655973-0 1972 Insulin responses to glucose and secretin in uraemic and normal subjects. Glucose 21-28 insulin Homo sapiens 0-7 4636407-0 1972 [Measurement of early insulin response in glucose loading]. Glucose 42-49 insulin Homo sapiens 22-29 4678007-2 1972 Plasma insulin during intravenous glucose tolerance test. Glucose 34-41 insulin Homo sapiens 7-14 5079926-0 1972 Insulin response to glucose, tolbutamide, secretin, and isoprenaline in maturity-onset diabetes mellitus. Glucose 20-27 insulin Homo sapiens 0-7 4673031-0 1972 [Changes in serum immunoreactive insulin in diabetes during the glucose tolerance and tolbutamide tests and its clinical significance]. Glucose 64-71 insulin Homo sapiens 33-40 4630099-0 1972 Antagonism of insulin action on glucose metabolism in white fat cells by dexamethasone. Glucose 32-39 insulin Homo sapiens 14-21 4636701-0 1972 Insulin fixation and glucose uptake by forearm tissues in response to infusions of physiological amounts of insulin in non-diabetic subjects. Glucose 21-28 insulin Homo sapiens 108-115 4636705-1 1972 Differences in the insulin and glucagon responses to glucose between normal infants and infants from diabetic mothers. Glucose 53-60 insulin Homo sapiens 19-26 4559946-3 1972 Except at low concentrations, prolonged single steps of glucose elicited early spikes of insulin and a slowly rising second phase. Glucose 56-63 insulin Homo sapiens 89-96 4559946-4 1972 Total insulin in the initial spikes increased with higher glucose concentrations. Glucose 58-65 insulin Homo sapiens 6-13 4559946-6 1972 Total insulin released in this early phase approximated a sigmoidal function of glucose concentration; mathematical differentiation of this function gave a skewed bell-shaped distribution curve. Glucose 80-87 insulin Homo sapiens 6-13 4559946-7 1972 Staircase stimulations caused insulin to be released as a series of transient spikes which did not correlate with the increment of glucose but rather to the available insulin for a given glucose concentration minus that released in previous steps. Glucose 131-138 insulin Homo sapiens 30-37 4343430-0 1972 Glucose-dependent, pH-sensitive insulin effect on the motor nerve terminal. Glucose 0-7 insulin Homo sapiens 32-39 4555783-0 1972 Acute and steady-state insulin responses to glucose in nonobese diabetic subjects. Glucose 44-51 insulin Homo sapiens 23-30 4555783-4 1972 DIABETICS HAD BASAL INSULIN LEVELS INDISTINGUISHABLE FROM NORMALS (DIABETICS: 10.7+/-4; normals: 10.7+/-5, mean +/-SD, muU/ml), but had significantly elevated basal glucose levels (diabetics: 161+/-27; normals: 88+/-7, mg/100 ml, P < 0.05). Glucose 165-172 insulin Homo sapiens 20-27 4555783-5 1972 The mean early insulin response (3-5 min Delta IRI) after a 5 g glucose pulse (P1) was significantly diminished in diabetics (diabetics 6.4+/-9; normals: 32.5+/-14, muU/ml, P < 0.01) consistent with a defective storage pool output. Glucose 64-71 insulin Homo sapiens 15-22 4555783-6 1972 The glucose disappearance rate, K(G), decreased in parallel with the early insulin response and the slope of the regression line between these two variables was virtually identical with that calculated from 16 normal subjects. Glucose 4-11 insulin Homo sapiens 75-82 4555783-7 1972 Similar to normal subjects, during the short glucose infusion, the acute insulin response to P2 was diminished in diabetics (P < 0.02). Glucose 45-52 insulin Homo sapiens 73-80 4555783-10 1972 In contrast to the diminished acute insulin responses to glucose pulses, diabetics have steady-state insulin levels after 20 hr of glucose infusion similar to those of normal subjects (diabetics: 25.7+/-13; normals: 32.5+/-14, muU/ml). Glucose 57-64 insulin Homo sapiens 36-43 4555783-10 1972 In contrast to the diminished acute insulin responses to glucose pulses, diabetics have steady-state insulin levels after 20 hr of glucose infusion similar to those of normal subjects (diabetics: 25.7+/-13; normals: 32.5+/-14, muU/ml). Glucose 131-138 insulin Homo sapiens 101-108 5078362-0 1972 [Effect of prednisone on variations in the immunoreactive insulin blood level after intravenous injection of glucose in children]. Glucose 109-116 insulin Homo sapiens 58-65 5078376-0 1972 [Blood insulin study in the course of oral glucose tolerance test in children with growth hormone deficiency]. Glucose 43-50 insulin Homo sapiens 7-14 4623275-0 1972 Patterns of insulin response to glucose in protein-calorie malnutrition. Glucose 32-39 insulin Homo sapiens 12-19 5016054-0 1972 Carbohydrate and lipid oxidation in normal human subjects: its influence on glucose tolerance and insulin response to glucose. Glucose 118-125 insulin Homo sapiens 98-105 4557375-0 1972 Inductive effects of glucose on the insulin secretory and synthetic apparatus of the pancreatic -cell. Glucose 21-28 insulin Homo sapiens 36-43 4553012-0 1972 Insulin release from human foetal pancreas in response to glucose, leucine and arginine. Glucose 58-65 insulin Homo sapiens 0-7 4501590-3 1972 Insulins and insulin derivatives that varied in their potency to stimulate glucose oxidation in the fat cell and to inhibit binding of [(125)I]insulin to purified plasma membranes, varied in an analogous fashion in their ability to inhibit the binding of labeled insulin to human lymphocytes. Glucose 75-82 insulin Homo sapiens 13-20 5012416-0 1972 [Release of insulin from the pancreas after glucose and tolbutamide administration]. Glucose 44-51 insulin Homo sapiens 12-19 5009122-10 1972 In two offspring from different pygmy mothers and Bantu fathers, insulin responses to glucose were initially normal and increased in a normal manner after HGH treatment. Glucose 86-93 insulin Homo sapiens 65-72 5075226-4 1972 The hormonal activity of each of these iodinated insulin preparations was measured from their effect on the production of (14)CO(2) from [1-(14)C]glucose by isolated adipose cells. Glucose 146-153 insulin Homo sapiens 49-56 5029115-0 1972 Different clinical types of Indian diabetics: characterization based on response of immuno-reactive plasma insulin to glucose and tolbutamide load. Glucose 118-125 insulin Homo sapiens 107-114 4665512-0 1972 [Influence of insulin on glucose absorption in man]. Glucose 25-32 insulin Homo sapiens 14-21 5004177-0 1971 Immunohistological demonstration of insulin in islets of langerhans after stimulation of insulin secretion by glucose, sulphonylureas and insulin antibodies. Glucose 110-117 insulin Homo sapiens 36-43 5004177-0 1971 Immunohistological demonstration of insulin in islets of langerhans after stimulation of insulin secretion by glucose, sulphonylureas and insulin antibodies. Glucose 110-117 insulin Homo sapiens 89-96 5004177-0 1971 Immunohistological demonstration of insulin in islets of langerhans after stimulation of insulin secretion by glucose, sulphonylureas and insulin antibodies. Glucose 110-117 insulin Homo sapiens 89-96 4342202-0 1971 The role of insulin in the regulation of glucose metabolism. Glucose 41-48 insulin Homo sapiens 12-19 5158903-11 1971 Insulin decreased the [(14)C]glucose solubilized by phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid, but not by sphingomyelin. Glucose 29-36 insulin Homo sapiens 0-7 5150192-2 1971 When 75% of the dietary carbohydrate was derived from food containing polysaccharides, the mean plasma insulin response to oral glucose was decreased relative to that seen following complementary diets providing carbohydrate mainly as simple sugars. Glucose 128-135 insulin Homo sapiens 103-110 4938132-5 1971 Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Glucose 49-56 insulin Homo sapiens 19-26 4938132-5 1971 Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Glucose 49-56 insulin Homo sapiens 121-128 4938132-5 1971 Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Glucose 49-56 insulin Homo sapiens 121-128 4938132-5 1971 Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Glucose 109-116 insulin Homo sapiens 19-26 4938132-5 1971 Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Glucose 109-116 insulin Homo sapiens 19-26 4938132-5 1971 Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Glucose 109-116 insulin Homo sapiens 19-26 4938132-6 1971 Thus epinephrine appears to inhibit selectively the rapid insulin response to glucose but not to influence insulin output stimulated by prolonged hyperglycemia. Glucose 78-85 insulin Homo sapiens 58-65 4938132-7 1971 These observations provide further evidence for a model of insulin secretion which includes a small storage pool available for immediate release to a glucose challenge and a more slowly responding pool regulating insulin secretion in the basal and steady state. Glucose 150-157 insulin Homo sapiens 59-66 5094588-7 1971 There was a delayed plasma insulin response to an oral glucose test in two of fourteen controls (14 percent). Glucose 55-62 insulin Homo sapiens 27-34 5571120-0 1971 Investigation of some theoretical models relating the concentrations of glucose and insulin in plasma. Glucose 72-79 insulin Homo sapiens 84-91 5099366-0 1971 Role of insulin in the regulation of hepatic glucose production. Glucose 45-52 insulin Homo sapiens 8-15 5116162-2 1971 Plasma insulin and growth hormone during intravenous glucose tolerance test. Glucose 53-60 insulin Homo sapiens 7-14 28603925-0 1971 The Pattern of Plasma Insulin Response to Glucose in Patients with a Previous Myocardial Infarction-The Respective Effects of Age and Disease. Glucose 42-49 insulin Homo sapiens 22-29 28603925-3 1971 The respective influences of age and cardio-vascular disease on the pattern of the plasma insulin and blood sugar responses to the glucose load were dissociated on the basis of analysis of variance.-Advancing age was associated with a rise in the mean blood sugar level during OGTT and a lowering of the glucose assimilation coefficient during IVGTT, but it was not accompanied by a significant change in the plasma insulin levels during either of the two tests.-Cardiovascular disease was associated with an augmentation of the mean blood sugar level during OGTT, but also with a prolonged and excessive response in plasma insulin. Glucose 131-138 insulin Homo sapiens 90-97 5134213-0 1971 [Behavior of plasmatic levels of insulin and somatotropin during intravenous glucose administration in macrosomic newborn infants and children of diabetic mothers]. Glucose 77-84 insulin Homo sapiens 33-40 5293632-1 1971 I. Serum-insulin response to glucose in normal Chinese. Glucose 29-36 insulin Homo sapiens 9-16 5568060-0 1971 [Serum insulin during oral glucose tolerance]. Glucose 27-34 insulin Homo sapiens 7-14 4933890-0 1971 Serum immunoreactive insulin levels during glucose tolerance and intensive islet stimulation. Glucose 43-50 insulin Homo sapiens 21-28 4933891-0 1971 Serum immunoreactive insulin levels during glucose tolerance and intensive islet stimulation. Glucose 43-50 insulin Homo sapiens 21-28 5556899-0 1971 Differential plasma insulin response to glucose and glucagon stimulation following ethanol priming. Glucose 40-47 insulin Homo sapiens 20-27 5560917-2 1971 Insulin responses to secretin and pancreozymin, and to oral and intravenous glucose, in patients suffering from chronic insufficiency of the exocrine pancreas. Glucose 76-83 insulin Homo sapiens 0-7 5552414-6 1971 Initially, there was a fourfold increase in serum insulin concentration after glucose and a threefold increase after maltose infusion. Glucose 78-85 insulin Homo sapiens 50-57 4325738-1 1971 Estimation of plasma glucose and immunoreactive insulin concentrations in normal subjects after an overnight fast showed that subjects with high basal plasma glucose levels tended to have high plasma insulin concentrations. Glucose 21-28 insulin Homo sapiens 200-207 4325738-1 1971 Estimation of plasma glucose and immunoreactive insulin concentrations in normal subjects after an overnight fast showed that subjects with high basal plasma glucose levels tended to have high plasma insulin concentrations. Glucose 158-165 insulin Homo sapiens 48-55 4325738-1 1971 Estimation of plasma glucose and immunoreactive insulin concentrations in normal subjects after an overnight fast showed that subjects with high basal plasma glucose levels tended to have high plasma insulin concentrations. Glucose 158-165 insulin Homo sapiens 200-207 4325738-2 1971 A similar correlation between glucose and insulin levels was seen in patients with obesity and various endocrine disorders. Glucose 30-37 insulin Homo sapiens 42-49 4325738-3 1971 The suppression of plasma insulin levels associated with hypoglycaemia was used to derive an "amended insulin-glucose ratio," which appeared to be a good discriminant for the diagnosis of insulinomas. Glucose 110-117 insulin Homo sapiens 26-33 4325738-3 1971 The suppression of plasma insulin levels associated with hypoglycaemia was used to derive an "amended insulin-glucose ratio," which appeared to be a good discriminant for the diagnosis of insulinomas. Glucose 110-117 insulin Homo sapiens 102-109 4323910-5 1971 Five of the eight had evidence of subnormal insulin production in response to oral glucose. Glucose 83-90 insulin Homo sapiens 44-51 5581123-0 1971 Effect of vagal denervation on insulin release after oral and intravenous glucose. Glucose 74-81 insulin Homo sapiens 31-38 5101781-6 1971 When glucose concentrations were plotted against paired insulin values, the correlation in both dwarfs and normals was significant. Glucose 5-12 insulin Homo sapiens 56-63 5100818-0 1971 Plasma insulin response to an oral glucose load in noncoronary heart disease. Glucose 35-42 insulin Homo sapiens 7-14 4263111-0 1971 [Effect of insulin on cellular permeability to glucose]. Glucose 47-54 insulin Homo sapiens 11-18 5128324-0 1971 Glucose tolerance and insulin response to glucose in two large families with diabetic mothers in the first generation. Glucose 42-49 insulin Homo sapiens 22-29 5005530-0 1971 [Behavior of serum insulin in the double intravenous glucose tolerance test in diabetics before and during glibenclamide therapy]. Glucose 53-60 insulin Homo sapiens 19-26 5155911-0 1971 [Behavior of lipids and metabolites of lipid resp. glucose metabolism in the plasma of diabetics during treatment with diet, oral antidiabetic drugs and insulin]. Glucose 51-58 insulin Homo sapiens 153-160 5480853-7 1970 These observations indicate that secretin in contrast to glucose stimulates insulin release which is uniphasic. Glucose 57-64 insulin Homo sapiens 76-83 5480737-0 1970 Plasma insulin and glucose responses of healthy subjects to varying glucose loads during three-hour oral glucose tolerance tests. Glucose 68-75 insulin Homo sapiens 7-14 5480737-0 1970 Plasma insulin and glucose responses of healthy subjects to varying glucose loads during three-hour oral glucose tolerance tests. Glucose 68-75 insulin Homo sapiens 7-14 5492253-1 1970 Plasma insulin levels were determined following oral glucose in 12 patients with adult coeliac disease, after oral lactose in four patients with alactasia, and in age-matched control subjects. Glucose 53-60 insulin Homo sapiens 7-14 5492253-3 1970 The separation of the plasma insulin curve from the blood sugar curve after glucose is in keeping with the concept that a factor responsible for stimulating insulin secretion is released from the gut during or after absorption of glucose. Glucose 76-83 insulin Homo sapiens 157-164 5492253-3 1970 The separation of the plasma insulin curve from the blood sugar curve after glucose is in keeping with the concept that a factor responsible for stimulating insulin secretion is released from the gut during or after absorption of glucose. Glucose 230-237 insulin Homo sapiens 29-36 5492253-3 1970 The separation of the plasma insulin curve from the blood sugar curve after glucose is in keeping with the concept that a factor responsible for stimulating insulin secretion is released from the gut during or after absorption of glucose. Glucose 230-237 insulin Homo sapiens 157-164 5485833-2 1970 The peak acid output after insulin (measured as the two consecutive 15-minute samples giving the highest acid output) was significantly correlated with the lowest concentration of blood glucose, the fall in blood glucose, the rate of fall of blood glucose, and the maximum fall of blood glucose in any 15 minutes. Glucose 186-193 insulin Homo sapiens 27-34 5485833-2 1970 The peak acid output after insulin (measured as the two consecutive 15-minute samples giving the highest acid output) was significantly correlated with the lowest concentration of blood glucose, the fall in blood glucose, the rate of fall of blood glucose, and the maximum fall of blood glucose in any 15 minutes. Glucose 213-220 insulin Homo sapiens 27-34 5485833-2 1970 The peak acid output after insulin (measured as the two consecutive 15-minute samples giving the highest acid output) was significantly correlated with the lowest concentration of blood glucose, the fall in blood glucose, the rate of fall of blood glucose, and the maximum fall of blood glucose in any 15 minutes. Glucose 213-220 insulin Homo sapiens 27-34 5485833-2 1970 The peak acid output after insulin (measured as the two consecutive 15-minute samples giving the highest acid output) was significantly correlated with the lowest concentration of blood glucose, the fall in blood glucose, the rate of fall of blood glucose, and the maximum fall of blood glucose in any 15 minutes. Glucose 213-220 insulin Homo sapiens 27-34 5485833-6 1970 Extreme hypoglycaemia, below about 15 mg/100 ml of blood glucose, inhibits insulin-stimulated acid secretion. Glucose 57-64 insulin Homo sapiens 75-82 5449149-0 1970 Study of the relationship between plasma insulin concentration and efficiency of glucose uptake in normal and mildly diabetic subjects. Glucose 81-88 insulin Homo sapiens 41-48 5456764-1 1970 Insulin response to oral glucose, intravenous tolbutamide and rapid intravenous glucose infusion in genetic prediabetics. Glucose 25-32 insulin Homo sapiens 0-7 5456764-1 1970 Insulin response to oral glucose, intravenous tolbutamide and rapid intravenous glucose infusion in genetic prediabetics. Glucose 80-87 insulin Homo sapiens 0-7 5472235-0 1970 [Changes in blood insulin level induced by intravenous or oral glucose in various types of diabetes mellitus]. Glucose 63-70 insulin Homo sapiens 18-25 5420996-3 1970 This rise was preceded by a sharp decline in the concentration of circulating insulin.In 72% of the patients (IHD sub-group) the blood glucose values after oral glucose satisfied the criteria for the diagnosis of diabetes mellitus. Glucose 135-142 insulin Homo sapiens 78-85 5420996-6 1970 After oral sodium tolbutamide the IHD sub-group patients showed a greater insulin response and a greater rebound increase in circulating NEFA than did the AD.These differences in response to oral glucose and to sodium tolbutamide suggest that the pathogenesis of the impaired glucose tolerance in IHD may be different from that responsible for abnormal carbohydrate tolerance in asymptomatic diabetics without evident atherosclerosis. Glucose 196-203 insulin Homo sapiens 74-81 5470184-0 1970 [Oral load glucose test in gastroresected patients: changes in blood sugar and immuno-reactive insulin]. Glucose 11-18 insulin Homo sapiens 95-102 4910526-0 1970 Effects of repetitive glucose loads on plasma concentrations of glucose, insulin and free fatty acids: paradoxical insulin responses in subjects with mild glucose intolerance. Glucose 22-29 insulin Homo sapiens 115-122 4910526-0 1970 Effects of repetitive glucose loads on plasma concentrations of glucose, insulin and free fatty acids: paradoxical insulin responses in subjects with mild glucose intolerance. Glucose 64-71 insulin Homo sapiens 115-122 4910526-0 1970 Effects of repetitive glucose loads on plasma concentrations of glucose, insulin and free fatty acids: paradoxical insulin responses in subjects with mild glucose intolerance. Glucose 64-71 insulin Homo sapiens 115-122 4907844-0 1970 Insulin response during prolonged glucose infusion. Glucose 34-41 insulin Homo sapiens 0-7 5415678-16 1970 The potentiating effect is of such magnitude to suggest that secretin is the dominant factor in the enteric component of insulin release after an oral glucose load. Glucose 151-158 insulin Homo sapiens 121-128 5461203-10 1970 After oral administration of 100 g of glucose, the proinsulin levels tended to rise similarly to insulin. Glucose 38-45 insulin Homo sapiens 51-61 5461203-10 1970 After oral administration of 100 g of glucose, the proinsulin levels tended to rise similarly to insulin. Glucose 38-45 insulin Homo sapiens 54-61 5461203-14 1970 When the values for serum proinsulin were expressed as percentage of the insulin levels, there was a decrease in the per cent proinsulin in the first hour of the glucose tolerance test. Glucose 162-169 insulin Homo sapiens 26-36 5461203-14 1970 When the values for serum proinsulin were expressed as percentage of the insulin levels, there was a decrease in the per cent proinsulin in the first hour of the glucose tolerance test. Glucose 162-169 insulin Homo sapiens 29-36 5461203-14 1970 When the values for serum proinsulin were expressed as percentage of the insulin levels, there was a decrease in the per cent proinsulin in the first hour of the glucose tolerance test. Glucose 162-169 insulin Homo sapiens 126-136 4190847-0 1970 Insulin levels in thyrotoxicosis and primary myxoedema: response to intravenous glucose and glucagon. Glucose 80-87 insulin Homo sapiens 0-7 4932461-2 1970 Insulin secretory rate in relation to the survival time and the glucose concentration of the medium]. Glucose 64-71 insulin Homo sapiens 0-7 4321815-1 1970 V. Inhibition of glucose-induced insulin secretion by endogenous insulin in vitro]. Glucose 17-24 insulin Homo sapiens 33-40 5505269-0 1970 [Blood sugar and serum insulin (IRI) after oral glucose loading in myocadrdial infarction]. Glucose 48-55 insulin Homo sapiens 23-30 5795407-0 1969 Plasma insulin response during oral glucose tolerance tests in newborns of normal and gestational diabetic mothers. Glucose 36-43 insulin Homo sapiens 7-14 5795851-0 1969 Steady state plasma insulin response to continuous glucose infusion in normal and diabetic subjects. Glucose 51-58 insulin Homo sapiens 20-27 4947792-0 1969 Isotope dilution studies of the effect of insulin and diabetes on glucose transfer rates. Glucose 66-73 insulin Homo sapiens 42-49 5407077-0 1969 The effect of moderate and high doses of human growth hormone on the insulin response to glucose infusion in prediabetic subjects. Glucose 89-96 insulin Homo sapiens 69-76 5767965-0 1969 [The effect of treatment of hyperthyroidism and myxedema on glucose assimilation and the response of free fatty acids and insulin following intravenous glucose administration]. Glucose 152-159 insulin Homo sapiens 122-129 5774317-3 1969 However, it improved sufficiently to cause the discontinuance of insulin therapy for at least four months.The insulin output in response to double glucose tolerance tests was increased during remission. Glucose 147-154 insulin Homo sapiens 65-72 5774317-4 1969 The degree of remission seemed to be related to the magnitude of the insulin response to glucose. Glucose 89-96 insulin Homo sapiens 69-76 5776745-0 1969 Early insulin response to intravenous glucose in steroid-stress diabetes. Glucose 38-45 insulin Homo sapiens 6-13 4674990-2 1972 There was a significantly greater release of insulin one hour after oral glucose in the gastrectomy patients (p < 0.05). Glucose 73-80 insulin Homo sapiens 45-52 4341465-7 1972 Not only may these two hormones, insulin and glucagon, regulate the metabolism of more than glucose alone but they are, in turn, regulated by more than glucose. Glucose 92-99 insulin Homo sapiens 33-40 4341465-7 1972 Not only may these two hormones, insulin and glucagon, regulate the metabolism of more than glucose alone but they are, in turn, regulated by more than glucose. Glucose 152-159 insulin Homo sapiens 33-40 5075509-4 1972 Under the incubation conditions used with glucose in the medium, the antilipolytic effect of insulin on the basal as well as on the adrenaline- and isopropylnoradrenaline-stimulated lipolysis was not consistent at any cell size studied. Glucose 42-49 insulin Homo sapiens 93-100 4559946-7 1972 Staircase stimulations caused insulin to be released as a series of transient spikes which did not correlate with the increment of glucose but rather to the available insulin for a given glucose concentration minus that released in previous steps. Glucose 187-194 insulin Homo sapiens 30-37 4559946-7 1972 Staircase stimulations caused insulin to be released as a series of transient spikes which did not correlate with the increment of glucose but rather to the available insulin for a given glucose concentration minus that released in previous steps. Glucose 187-194 insulin Homo sapiens 167-174 4559946-8 1972 The sum of total insulin released as spikes in a staircase series leading to a given glucose concentration was the same as when that concentration was used as a single step. Glucose 85-92 insulin Homo sapiens 17-24 4559946-9 1972 Interrupted prolonged glucose infusions indicated the second phase of insulin release could prime the pancreas and that the first and second phases were interrelated. Glucose 22-29 insulin Homo sapiens 70-77 4559947-1 1972 Recent studies have suggested that secretin, like glucose, stimulates a rapid insulin response from a small storage pool. Glucose 50-57 insulin Homo sapiens 78-85 4559947-3 1972 Contrary to previous studies demonstrating that the acute insulin response to a small (5 g) pulse of glucose given 45 min after the start of the glucose infusion was significantly diminished compared to the response to the preinfusion pulse, the acute insulin response (2-5 min Deltaimmuno-reactive insulin muU/ml) to 15-U secretin pulses exhibited a greater than twofold increase (before: 31.1+/-15.4; during: 71.2+/-40.4, muU/ml, mean +/-SD, P < 0.02). Glucose 101-108 insulin Homo sapiens 58-65 4559947-3 1972 Contrary to previous studies demonstrating that the acute insulin response to a small (5 g) pulse of glucose given 45 min after the start of the glucose infusion was significantly diminished compared to the response to the preinfusion pulse, the acute insulin response (2-5 min Deltaimmuno-reactive insulin muU/ml) to 15-U secretin pulses exhibited a greater than twofold increase (before: 31.1+/-15.4; during: 71.2+/-40.4, muU/ml, mean +/-SD, P < 0.02). Glucose 101-108 insulin Homo sapiens 252-259 4559947-3 1972 Contrary to previous studies demonstrating that the acute insulin response to a small (5 g) pulse of glucose given 45 min after the start of the glucose infusion was significantly diminished compared to the response to the preinfusion pulse, the acute insulin response (2-5 min Deltaimmuno-reactive insulin muU/ml) to 15-U secretin pulses exhibited a greater than twofold increase (before: 31.1+/-15.4; during: 71.2+/-40.4, muU/ml, mean +/-SD, P < 0.02). Glucose 101-108 insulin Homo sapiens 252-259 4559947-3 1972 Contrary to previous studies demonstrating that the acute insulin response to a small (5 g) pulse of glucose given 45 min after the start of the glucose infusion was significantly diminished compared to the response to the preinfusion pulse, the acute insulin response (2-5 min Deltaimmuno-reactive insulin muU/ml) to 15-U secretin pulses exhibited a greater than twofold increase (before: 31.1+/-15.4; during: 71.2+/-40.4, muU/ml, mean +/-SD, P < 0.02). Glucose 145-152 insulin Homo sapiens 58-65 4559947-7 1972 Similar to the observation that the magnitude of the insulin response to secretin was glucose dependent, the glucose-stimulated output appeared to be secretin dependent. Glucose 86-93 insulin Homo sapiens 53-60 4559947-8 1972 Thus the acute insulin response to 5 g glucose was increased after secretin pretreatment (presecretin: 34.9+/-14.8; postsecretin: 50.5+/-22.5 muU/ml. Glucose 39-46 insulin Homo sapiens 15-22 4559947-10 1972 The effect of epinephrine and propranolol on acute insulin responses to secretin and glucose was also different. Glucose 85-92 insulin Homo sapiens 51-58 4559947-12 1972 The results of these studies indicate that although both glucose and secretin stimulate a rapid insulin response, these responses are easily differentiated. Glucose 57-64 insulin Homo sapiens 96-103 4559947-13 1972 The data suggest that glucose and secretin stimulate functionally separate storage pools of insulin, but that the acute response to either stimulus is partly determined by exposure to the other. Glucose 22-29 insulin Homo sapiens 92-99 4625833-0 1972 Glucose-stimulated insulin secretion during "remission" of juvenile diabetes. Glucose 0-7 insulin Homo sapiens 19-26 4554506-0 1972 Effect of various concentrations of glucose on insulin biosynthesis. Glucose 36-43 insulin Homo sapiens 47-54 4668877-0 1972 [Effect of insulin on glucose uptake by adipose tissue in the suslik Citellus suslicus during winter hibernation and arousal]. Glucose 22-29 insulin Homo sapiens 11-18 5051802-0 1972 Serum immunoreactive insulin response to oral glucose and intravenous sodium tolbutamide administration in relation to obesity. Glucose 46-53 insulin Homo sapiens 21-28 5051803-0 1972 Immunoreactive insulin and free fatty acid responses to oral glucose tolerance test, blood lipid changes and electron microscopic findings in muscle capillaries of obese subjects. Glucose 61-68 insulin Homo sapiens 15-22 24683634-5 1972 per kilogram per hour of glucose to prevent hypoglycemia.Insulin levels of more than 1,200 muU. Glucose 25-32 insulin Homo sapiens 57-64 5044225-0 1972 Stimulatory effect of insulin on glucose metabolism of thymus lymphocytes. Glucose 33-40 insulin Homo sapiens 22-29 5027110-0 1972 Glucose-independent stimulation of lipogenesis by insulin. Glucose 0-7 insulin Homo sapiens 50-57 5063343-0 1972 Effect of glucose on plasma glucagon, growth hormone, and insulin in exchange transfusion. Glucose 10-17 insulin Homo sapiens 58-65 5054760-1 1972 Study of the insulin response to glucose stimulation in several clinical forms of diabetes]. Glucose 33-40 insulin Homo sapiens 13-20 5038808-0 1972 Peripheral glucose uptake in relation to physiological levels of plasma and lymph insulin. Glucose 11-18 insulin Homo sapiens 82-89 5066843-0 1972 Effect of adrenergic blocking agents on insulin response to glucose infusion in man. Glucose 60-67 insulin Homo sapiens 40-47 5082900-0 1972 [The behaviour of blood sugar and serum insulin (IRI) after oral administration of glucose in different stages of myocardial infarction]. Glucose 83-90 insulin Homo sapiens 40-47 5060671-1 1972 In patients with portal hypertension, plasma insulin levels were raised both fasting and after oral glucose or intravenous tolbutamide. Glucose 100-107 insulin Homo sapiens 45-52 5060671-5 1972 The insulin response after operation was only higher after intensive pancreatic beta cell stimulation by a combination of glucose, tolbutamide, and glucagon. Glucose 122-129 insulin Homo sapiens 4-11 5071515-0 1972 Behavior of glycemia and serum insulin level (IRI) in myocardial infarction after oral glucose load. Glucose 87-94 insulin Homo sapiens 31-38 4143592-1 1971 The insulin response to a glucose load has been investigated in twenty-five patients with small-vessel disease (ischaemic lesions of toes or feet in the presence of foot pulses). Glucose 26-33 insulin Homo sapiens 4-11 4143593-0 1971 Insulin response to glucose in patients with peripheral vascular disease, arteritis, and Raynaud"s phenomenon. Glucose 20-27 insulin Homo sapiens 0-7 4143593-1 1971 Twenty-three patients with peripheral vascular disease due to atheromatous blocks in large vessels, four patients with arteritis, and twenty patients with Raynaud"s phenomenon were tested for insulin response to glucose. Glucose 212-219 insulin Homo sapiens 192-199 4143593-3 1971 Insulin output after glucose in patients with atheromatous blocks in large peripheral arteries fell into three categories: (1) normal glucose tolerance and insulin output, the insulin rise (peak/basal ratio) comparing well with the rise in controls; (2) carbohydrate intolerance with a prediabetic pattern of glucose-tolerance test, and raised circulating insulin levels both fasting insulin and after glucose, so that the insulin rise was lower than normal; or (3) the flat insulin responses after glucose that had been noted in small-vessel disease with normal glucose tolerance. Glucose 21-28 insulin Homo sapiens 0-7 4143593-5 1971 High but not delayed insulin peaks were seen after a glucose stimulus in some patients with arteritis and with Raynaud"s phenomenon. Glucose 53-60 insulin Homo sapiens 21-28 5129311-2 1971 Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Glucose 91-98 insulin Homo sapiens 57-64 5129311-4 1971 The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Glucose 4-11 insulin Homo sapiens 43-50 5129311-5 1971 Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. Glucose 176-183 insulin Homo sapiens 150-157 5129311-8 1971 When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected. Glucose 94-101 insulin Homo sapiens 113-120 5129311-9 1971 These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. Glucose 187-194 insulin Homo sapiens 103-110 5129311-9 1971 These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. Glucose 187-194 insulin Homo sapiens 150-157 5129319-9 1971 IT IS CONCLUDED THAT: (a) blood glucose becomes an increasingly important substrate for muscle oxidation during prolonged exercise of this type: (b) peripheral glucose utilization increases in exercise despite a reduction in circulating insulin levels: (c) increased hepatic output of glucose, primarily by means of augmented glycogenolysis, contributes to blood glucose homeostasis in exercise and provides an important source of substrate for exercising muscle. Glucose 32-39 insulin Homo sapiens 237-244 4337656-0 1971 Antagonism between glucose and epinephrine regarding insulin secretion. Glucose 19-26 insulin Homo sapiens 53-60 5115587-0 1971 Evidence that glucose load is an important determinant of plasma insulin response in normal subjects. Glucose 14-21 insulin Homo sapiens 65-72 4938132-0 1971 Epinephrine: selective inhibition of the acute insulin response to glucose. Glucose 67-74 insulin Homo sapiens 47-54 4938132-1 1971 An epinephrine infusion of 6 mug/min decreased the rapid insulin response to a 5 g glucose pulse by 96% (P < 0.001) compared with the preinfusion control. Glucose 83-90 insulin Homo sapiens 57-64 4938132-2 1971 In contrast when an identical epinephrine infusion was superimposed on a prolonged glucose infusion, elevated steady-state insulin levels did not decrease, but increased from 26.9 +/-6 (mean +/-SD, muU/ml) to 56.8 +/-15 muU/ml (P < 0.05) in parallel with the epinephrine-induced hyperglycemia. Glucose 83-90 insulin Homo sapiens 123-130 4330005-3 1971 By 2 hr after oral glucose, the concentration of the proinsulin-like component increased and the insulin component concentration decreased so that the percentage of the proinsulin-like component was essentially the same as in the basal state. Glucose 19-26 insulin Homo sapiens 53-63 4330005-6 1971 Acute stimulation with glucose, tolbutamide, leucine, and streptozotocin mainly released the insulin component resulting in a fall in the per cent proinsulin-like component with a subsequent increase in percentage of this component as the total insulin concentration returns towards basal levels. Glucose 23-30 insulin Homo sapiens 93-100 4330005-6 1971 Acute stimulation with glucose, tolbutamide, leucine, and streptozotocin mainly released the insulin component resulting in a fall in the per cent proinsulin-like component with a subsequent increase in percentage of this component as the total insulin concentration returns towards basal levels. Glucose 23-30 insulin Homo sapiens 147-157 4330005-6 1971 Acute stimulation with glucose, tolbutamide, leucine, and streptozotocin mainly released the insulin component resulting in a fall in the per cent proinsulin-like component with a subsequent increase in percentage of this component as the total insulin concentration returns towards basal levels. Glucose 23-30 insulin Homo sapiens 150-157 4327576-7 1971 Proinsulin responses were studied in four normal subjects and one patient with an insulinoma after a glucose load. Glucose 101-108 insulin Homo sapiens 0-10 4936881-0 1971 Relationship between intravenous glucose loads, insulin responses and glucose disappearance rate. Glucose 70-77 insulin Homo sapiens 48-55 5098919-0 1971 The insulin response to glucose in patients with non-diabetic glycosuria. Glucose 24-31 insulin Homo sapiens 4-11 5148303-0 1971 [The effect of insulin preparations bound to polymers on blood sugar levels and glucose absorption by isolated diaphragm tissue (preliminary report)]. Glucose 80-87 insulin Homo sapiens 15-22 5097575-4 1971 Infusion of glucose at 25 mg/kg per min for 20 min resulted in a fivefold increase in arterial insulin levels and in reversal of splanchnic glucose balance to a net uptake. Glucose 12-19 insulin Homo sapiens 95-102 4327980-0 1971 Effect of theophylline on glucagon and glucose-mediated plasma insulin responses in subhuman primate fetus and neonate. Glucose 39-46 insulin Homo sapiens 63-70 4331561-2 1971 20% of the [(125)I]insulin binding was inhibited by unlabeled insulin at 10(-9) M (6 ng/ml), equivalent to insulin concentrations in hepatic portal blood; inhibition of [(125)I]insulin binding was 80% at 10(-7) M and 90% at 10(-5) M. Eight insulins and derivatives with biological potencies that differed over a 100-fold range inhibited the binding of [(125)I]insulin to liver membranes in direct proportion to their ability to stimulate glucose oxidation in isolated fat cells. Glucose 438-445 insulin Homo sapiens 19-26 5090130-0 1971 Determinants of insulin response to glucose absorption from human small bowel. Glucose 36-43 insulin Homo sapiens 16-23 5284366-0 1971 Effect of adrenaline and glucose on release of glucagon and insulin in vitro. Glucose 25-32 insulin Homo sapiens 60-67 5560137-0 1971 The pattern of early insulin response to oral glucose. Glucose 46-53 insulin Homo sapiens 21-28 5138402-0 1971 [Dynamics of serum immunoreactive insulin levels following the ingestion of various quantities of glucose]. Glucose 98-105 insulin Homo sapiens 34-41 5550639-0 1971 [Immunoreactive insulin and blood glucose levels following oral glucose load in patientss with dumping-syndrome]. Glucose 65-72 insulin Homo sapiens 17-24 5554966-0 1971 [Functional kinetics of insulin, lipids and cortisol after intravenous glucose loading in the early stages of essential hypertension]. Glucose 71-78 insulin Homo sapiens 24-31 5135325-0 1971 [Changes in blood insulin of the umbilical cord after serum glucose perfusion in the mother during labor]. Glucose 60-67 insulin Homo sapiens 18-25 5540877-0 1971 Is there a common beta cell insulin compartment stimulated by glucose and tolbutamide? Glucose 62-69 insulin Homo sapiens 28-35 5539004-5 1971 The lower glucose levels were associated with higher plasma insulin levels. Glucose 10-17 insulin Homo sapiens 60-67 5578370-0 1971 [Behavior of glucose assimilation index in liver cirrhosis after glucose, tolbutamide and insulin loading]. Glucose 13-20 insulin Homo sapiens 90-97 5155964-0 1971 [Serum insulin in non-diabetic obese subjects following repeated glucose infusions]. Glucose 65-72 insulin Homo sapiens 7-14 5540818-0 1971 [Serum insulin and growth hormone during glucose loading in liver cirrhosis]. Glucose 41-48 insulin Homo sapiens 7-14 4921648-0 1970 Effects of insulin and growth hormone on the flux rates of plasma glucose and plasma free fatty acids in man. Glucose 66-73 insulin Homo sapiens 11-18 5480843-0 1970 Comparison of impedance to insulin-mediated glucose uptake in normal subjects and in subjects with latent diabetes. Glucose 44-51 insulin Homo sapiens 27-34 5480843-2 1970 This factor is termed impedance and represents the tissues" insensitivity or resistance to insulin-mediated glucose uptake. Glucose 108-115 insulin Homo sapiens 91-98 5477100-0 1970 Effect of exercise on glucose and insulin response to glucose infusion. Glucose 54-61 insulin Homo sapiens 34-41 11945385-0 1970 RNA synthesis and the stimulation of insulin biosynthesis by glucose. Glucose 61-68 insulin Homo sapiens 37-44 4918328-6 1970 60 mM potassium ion, on the other hand, not only restores the insulin secretory response to glucose (200 mg/100 ml) but results in an added stimulation of insulin secretion in the presence of DPH. Glucose 92-99 insulin Homo sapiens 62-69 5524678-0 1970 Simultaneous determination of insulin in brachial and portal veins during glucose infusion in normal and prediabetic subjects. Glucose 74-81 insulin Homo sapiens 30-37 5496674-0 1970 [Correction of hyperkalemia by administering glucose with insulin]. Glucose 45-52 insulin Homo sapiens 58-65 4988208-3 1970 Fetal plasma glucose concentrations were minimally altered by direct fetal insulin injections, whereas neonatal glucose levels declined with similar injections. Glucose 13-20 insulin Homo sapiens 75-82 4988208-5 1970 When the amount of insulin given the fetus was increased, fetal plasma glucose concentrations did decline. Glucose 71-78 insulin Homo sapiens 19-26 4988208-8 1970 Obtunded fetal plasma glucose responses to direct fetal insulin administration may be a function of placental transfer of glucose from the maternal pool. Glucose 22-29 insulin Homo sapiens 56-63 4988208-8 1970 Obtunded fetal plasma glucose responses to direct fetal insulin administration may be a function of placental transfer of glucose from the maternal pool. Glucose 122-129 insulin Homo sapiens 56-63 5426392-0 1970 Effects of decaffeinated and nondecaffeinated coffee ingestion on blood glucose and plasma radioimmunoreactive insulin responses to rapid intravenous infusion of glucose in normal man. Glucose 162-169 insulin Homo sapiens 111-118 5422431-5 1970 In addition, following glucose ingestion there appeared to be a more normal plasma insulin and growth hormone response and improved glucose tolerance. Glucose 23-30 insulin Homo sapiens 83-90 5444245-0 1970 Early insulin responses to glucose and to tolbutamide in maturity-onset diabetes. Glucose 27-34 insulin Homo sapiens 6-13 5515384-0 1970 [The behaviour of the serum insulin level in non obese adult diabetics after intravenous glucose, tolbutamide and glucagon]. Glucose 89-96 insulin Homo sapiens 28-35 4912301-0 1970 The occurrence of low insulin response to glucose infusion in children. Glucose 42-49 insulin Homo sapiens 22-29 5415678-3 1970 The insulin release after an oral glucose load is both earlier and greater than would be expected from the glycemic stimulus. Glucose 34-41 insulin Homo sapiens 4-11 5415678-9 1970 A highly significant (P<0.01) potentiation of the insulin response to the post-secretin glucose infusion was observed. Glucose 91-98 insulin Homo sapiens 53-60 5419876-0 1970 Insulin and glucose levels in umbilical cord blood after infusions of glucose and glucose with insulin to women in labour. Glucose 12-19 insulin Homo sapiens 95-102 5419876-0 1970 Insulin and glucose levels in umbilical cord blood after infusions of glucose and glucose with insulin to women in labour. Glucose 70-77 insulin Homo sapiens 0-7 5419876-0 1970 Insulin and glucose levels in umbilical cord blood after infusions of glucose and glucose with insulin to women in labour. Glucose 70-77 insulin Homo sapiens 95-102 5419876-0 1970 Insulin and glucose levels in umbilical cord blood after infusions of glucose and glucose with insulin to women in labour. Glucose 70-77 insulin Homo sapiens 0-7 5419876-0 1970 Insulin and glucose levels in umbilical cord blood after infusions of glucose and glucose with insulin to women in labour. Glucose 70-77 insulin Homo sapiens 95-102 4315767-0 1970 Mechanisms in the control of insulin release by glucose and other substances. Glucose 48-55 insulin Homo sapiens 29-36 5410388-0 1970 The effect of insulin on glucose metabolism of the incubated human placenta. Glucose 25-32 insulin Homo sapiens 14-21 5495570-0 1970 [Changes of blood glucose level and the acidity of gastric juice in patients with duodenal ulcers after 2-deoxy-D-glucose and insulin administration]. Glucose 18-25 insulin Homo sapiens 126-133 5485574-0 1970 Serum insulin response to oral glucose in pernicious anemia. Glucose 31-38 insulin Homo sapiens 6-13 5409266-2 1969 Changes in immuno-reactive insulin after oral administration of glucose in normal subjects and subjects with pancreatic diabetes]. Glucose 64-71 insulin Homo sapiens 27-34 4311236-0 1969 Plasma insulin: fluctuations in the "big" insulin component in man after glucose and other stimuli. Glucose 73-80 insulin Homo sapiens 7-14 4311236-5 1969 In young thin subjects with idiopathic glucose intolerance associated with normal concentrations of plasma insulin, an identical pattern of big insulin was observed. Glucose 39-46 insulin Homo sapiens 144-151 4311236-6 1969 In thin subjects in whom elevations of per cent big at 90-120 min during the standard test were only modest, starvation for 48 hr before the glucose administration resulted in a more pronounced rise in the per cent big insulin. Glucose 141-148 insulin Homo sapiens 219-226 4899852-0 1969 Offspring of two diabetic parents: differential serum insulin responses to intravenous glucose and tolbutamide. Glucose 87-94 insulin Homo sapiens 54-61 5355340-8 1969 Elevation of forearm insulin in eight subjects from postabsorptive (12 muU/ml) to high physiologic levels (157 muU/ml) in addition to stimulating muscle glucose uptake blocked muscle alpha amino nitrogen release by 74%. Glucose 153-160 insulin Homo sapiens 21-28 5355340-11 1969 Doubling forearm insulin levels (from 10 to 20 muU/ml) in eight subjects increased muscle glucose uptake in three and blocked alpha amino nitrogen output in two although both effects were seen concurrently in only one subject. Glucose 90-97 insulin Homo sapiens 17-24 5355340-16 1969 Doubling basal insulin approaches the threshold both for blockade of muscle amino acid output and stimulation of glucose uptake, effects which appear to occur independently. Glucose 113-120 insulin Homo sapiens 15-22 5355342-0 1969 Insulin responses to glucose: evidence for a two pool system in man. Glucose 21-28 insulin Homo sapiens 0-7 5355342-2 1969 After the first glucose pulse, insulin responses measured immunologically reached a peak between 3 and 5 min and rapidly returned to base line. Glucose 16-23 insulin Homo sapiens 31-38 5355342-3 1969 A short glucose infusion of 300 mg/min decreased the rapid insulin response to a second glucose pulse (- 58%), but after a longer infusion (20 hr) the acute insulin response to a third pulse was restored to normal. Glucose 8-15 insulin Homo sapiens 59-66 5355342-3 1969 A short glucose infusion of 300 mg/min decreased the rapid insulin response to a second glucose pulse (- 58%), but after a longer infusion (20 hr) the acute insulin response to a third pulse was restored to normal. Glucose 88-95 insulin Homo sapiens 59-66 5355342-5 1969 Other observations during these studies showed that a short glucose infusion of either 100 mg/min or 300 mg/min produced a parallel rise in glucose and insulin, but continuation of the infusion for 20 hr was associated with a "paradoxical" fall in glucose and continued rise in insulin. Glucose 60-67 insulin Homo sapiens 152-159 5355342-6 1969 These observations are considered incompatible with a simple linear model often used to describe the relation between plasma glucose and serum insulin. Glucose 125-132 insulin Homo sapiens 143-150 5402386-0 1969 [Behavior of plasmatic values of FFA and insulin in the premature newborn infant exposed to double intravenous overloading of glucose]. Glucose 126-133 insulin Homo sapiens 41-48 5345934-1 1969 The blood glucose and plasma insulin response to oral glucose and slow intravenous infusion of glucose was determined in seven patients who had undergone partial gastrectomy or gastroenterostomy. Glucose 54-61 insulin Homo sapiens 29-36 5345934-1 1969 The blood glucose and plasma insulin response to oral glucose and slow intravenous infusion of glucose was determined in seven patients who had undergone partial gastrectomy or gastroenterostomy. Glucose 54-61 insulin Homo sapiens 29-36 5345934-2 1969 Similar studies were conducted in normal subjects; in these experiments oral glucose administration was replaced by infusion of glucose direct into the jejunum in order to simulate the rapid gastric emptying which occurs after gastric surgery.Peak insulin levels were much higher after oral or intrajejunal glucose, though peak blood glucose levels were higher after intravenous glucose. Glucose 128-135 insulin Homo sapiens 248-255 5345934-2 1969 Similar studies were conducted in normal subjects; in these experiments oral glucose administration was replaced by infusion of glucose direct into the jejunum in order to simulate the rapid gastric emptying which occurs after gastric surgery.Peak insulin levels were much higher after oral or intrajejunal glucose, though peak blood glucose levels were higher after intravenous glucose. Glucose 128-135 insulin Homo sapiens 248-255 5345934-2 1969 Similar studies were conducted in normal subjects; in these experiments oral glucose administration was replaced by infusion of glucose direct into the jejunum in order to simulate the rapid gastric emptying which occurs after gastric surgery.Peak insulin levels were much higher after oral or intrajejunal glucose, though peak blood glucose levels were higher after intravenous glucose. Glucose 128-135 insulin Homo sapiens 248-255 5345934-2 1969 Similar studies were conducted in normal subjects; in these experiments oral glucose administration was replaced by infusion of glucose direct into the jejunum in order to simulate the rapid gastric emptying which occurs after gastric surgery.Peak insulin levels were much higher after oral or intrajejunal glucose, though peak blood glucose levels were higher after intravenous glucose. Glucose 128-135 insulin Homo sapiens 248-255 4911916-0 1969 Human fetal insulin response after acute maternal glucose administration during labor. Glucose 50-57 insulin Homo sapiens 12-19 5359315-0 1969 The insulin response to glucose in patients with pancreatic disease. Glucose 24-31 insulin Homo sapiens 4-11 5396254-0 1969 [Blood insulin levels in fasting normal subjects and after oral glucose load]. Glucose 64-71 insulin Homo sapiens 7-14 5822079-1 1969 The effects of a maternal intravenous glucose load on the fetal plasma levels of glucose and insulin have been studied in 11 patients before the onset of labour. Glucose 38-45 insulin Homo sapiens 93-100 5822079-3 1969 Following this, the rate of fall in fetal plasma glucose closely reflected that in the mother.Serial fetal insulin estimations carried out in 8 of the 11 subjects following maternal glucose showed an early rise in fetal insulin in four and a delayed rise in one; in the remaining three there was no definite change.It is concluded that the blood glucose level of the fetus is controlled by that of the mother, but that the fetal pancreas at term may respond to hyperglycaemia by the secretion of insulin. Glucose 182-189 insulin Homo sapiens 107-114 5822079-3 1969 Following this, the rate of fall in fetal plasma glucose closely reflected that in the mother.Serial fetal insulin estimations carried out in 8 of the 11 subjects following maternal glucose showed an early rise in fetal insulin in four and a delayed rise in one; in the remaining three there was no definite change.It is concluded that the blood glucose level of the fetus is controlled by that of the mother, but that the fetal pancreas at term may respond to hyperglycaemia by the secretion of insulin. Glucose 182-189 insulin Homo sapiens 220-227 5822079-3 1969 Following this, the rate of fall in fetal plasma glucose closely reflected that in the mother.Serial fetal insulin estimations carried out in 8 of the 11 subjects following maternal glucose showed an early rise in fetal insulin in four and a delayed rise in one; in the remaining three there was no definite change.It is concluded that the blood glucose level of the fetus is controlled by that of the mother, but that the fetal pancreas at term may respond to hyperglycaemia by the secretion of insulin. Glucose 182-189 insulin Homo sapiens 107-114 5822079-3 1969 Following this, the rate of fall in fetal plasma glucose closely reflected that in the mother.Serial fetal insulin estimations carried out in 8 of the 11 subjects following maternal glucose showed an early rise in fetal insulin in four and a delayed rise in one; in the remaining three there was no definite change.It is concluded that the blood glucose level of the fetus is controlled by that of the mother, but that the fetal pancreas at term may respond to hyperglycaemia by the secretion of insulin. Glucose 182-189 insulin Homo sapiens 220-227 5360814-0 1969 The significance of the blood glucose level for plasma insulin response to intravenously administered tolbutamide in healthy subjects. Glucose 30-37 insulin Homo sapiens 55-62 5350107-3 1969 In gastrectomy patients a significant correlation was found between the height of the peak blood glucose and insulin levels for the same individual. Glucose 97-104 insulin Homo sapiens 109-116 5350107-6 1969 In two cases, hypoglycaemia followed an abnormally large insulin response to oral glucose. Glucose 82-89 insulin Homo sapiens 57-64 5822593-2 1969 However, in these subjects, insulin rose and fell in proportion to the magnitude of change in plasma glucose induced by small intravenous infusions of glucose. Glucose 101-108 insulin Homo sapiens 28-35 5822593-2 1969 However, in these subjects, insulin rose and fell in proportion to the magnitude of change in plasma glucose induced by small intravenous infusions of glucose. Glucose 151-158 insulin Homo sapiens 28-35 5822593-3 1969 The minimal dose of glucose to cause a significant rise in insulin above the fasting level was similar in normal subjects, obese nondiabetic subjects, and in obese, hyperglycemic adult diabetics. Glucose 20-27 insulin Homo sapiens 59-66 5822593-5 1969 These results suggested that the secretion of insulin was under regulation by changes in blood glucose but was not stimulated in proportion to the stable raised blood glucose concentration of the hyperglycemic diabetic. Glucose 95-102 insulin Homo sapiens 46-53 5822593-8 1969 The concentration of plasma insulin paralleled that of plasma glucose. Glucose 62-69 insulin Homo sapiens 28-35 5808104-0 1969 Effect of insulin on the incorporation of 14C of radioactive glucose into glycogen and carbon dioxide in cerebral cortical slices. Glucose 61-68 insulin Homo sapiens 10-17 5343865-0 1969 Growth hormone and insulin levels in newly discovered glucose intolerance. Glucose 54-61 insulin Homo sapiens 19-26 5800368-0 1969 Insulin and corticoid response to intravenous fructose in relation to glucose tolerance. Glucose 70-77 insulin Homo sapiens 0-7 5803650-0 1969 Relation between insulin levels and glucose disappearance in normal and diabetic patients. Glucose 36-43 insulin Homo sapiens 17-24 4897290-0 1969 Potentiation of the plasma insulin response to glucose by prior administration of alcohol. Glucose 47-54 insulin Homo sapiens 27-34 5802626-1 1969 Plasma insulin and growth hormone level after a glucose load. Glucose 48-55 insulin Homo sapiens 7-14 5366870-0 1969 [Blood insulin levels during oral glucose administration in 43 obese children]. Glucose 34-41 insulin Homo sapiens 7-14 5794064-1 1969 Blood sugar and plasma insulin responses to oral glucose in normal weight, overweight, and gouty patients. Glucose 49-56 insulin Homo sapiens 23-30 5785000-3 1969 Conversion of glucose to glyceride fatty acids was readily demonstrable with concentrated cell suspensions and was stimulated 3- to 8-fold by insulin. Glucose 14-21 insulin Homo sapiens 142-149 5774112-1 1969 Intravenous administration of porcine secretin or pancreozymin or synthetic human gastrin II resulted in raised increments in serum immunoreactive insulin during intravenous infusion of glucose in normal man. Glucose 186-193 insulin Homo sapiens 147-154 5774112-2 1969 Enhancement of serum immunoreactive insulin by each hormone was associated with accelerated disposal of glucose. Glucose 104-111 insulin Homo sapiens 36-43 5774112-5 1969 Enteric infusion of hydrochloric acid, or stimulation of gastric acid secretion by betazole, presumed to cause release of endogenous secretin, led to enhancement of insulin secretion during intravenous infusion of glucose. Glucose 214-221 insulin Homo sapiens 165-172 5774112-6 1969 Enteric infusion of arginine, presumed to cause release of endogenous pancreozymin, led to a rise in serum immunoreactive insulin not attributable to effects of circulating glucose and amino acids. Glucose 173-180 insulin Homo sapiens 122-129 4886257-0 1969 Insulin-glucose dispersion and interaction system. Glucose 8-15 insulin Homo sapiens 0-7 5773066-0 1969 Growth hormone and glucose interrelationships in diabetes: studies with insulin infusion during continuous blood glucose analysis. Glucose 19-26 insulin Homo sapiens 72-79 5763835-1 1969 Changes in glucose utilization and secretion of insulin and growth hormone. Glucose 11-18 insulin Homo sapiens 48-55 5764310-0 1969 Regulatory effects of insulin and liver on brain glucose metabolism. Glucose 49-56 insulin Homo sapiens 22-29 4974624-10 1969 In contrast to the fetal experiments, glucose injection in the neonate elicited a delayed rise in the concentration of plasma insulin. Glucose 38-45 insulin Homo sapiens 126-133 5790049-0 1969 Obesity--its role in the regulation of the insulin response to glucose. Glucose 63-70 insulin Homo sapiens 43-50 5702244-0 1968 Plasma insulin response to oral glucose in the parents and sibs of children with diabetes mellitus. Glucose 32-39 insulin Homo sapiens 7-14 5729726-0 1968 Serum insulin and glucagon during the glucose tolerance test. Glucose 38-45 insulin Homo sapiens 6-13 4175553-0 1968 Serum-insulin response to glucose and aminoacids in the premature infant. Glucose 26-33 insulin Homo sapiens 6-13 5701068-0 1968 [Triglyceride level and insulin concentration in plasma following oral glucose administration in patients with primary carbohydrate-induced hypertriglyceridemia]. Glucose 71-78 insulin Homo sapiens 24-31 5675421-10 1968 A wide range of insulin delivery rates was found among patients with similar plasma glucose concentrations, suggesting that there exists considerable variability in responsiveness to endogenous insulin among these patients. Glucose 84-91 insulin Homo sapiens 16-23 5764009-3 1969 In one of the patients, insulin sensitivity with respect to glucose and the hypoglycemia-induced growth hormone rise seemed greater during estrogen therapy. Glucose 60-67 insulin Homo sapiens 24-31 5362851-0 1969 Effect of hypophysectomy on post-glucose injection rise of plasmatic insulin. Glucose 33-40 insulin Homo sapiens 69-76 4177392-0 1968 Effects of insulin on intestinal glucose absorption. Glucose 33-40 insulin Homo sapiens 11-18 4175086-0 1968 Influence of gastric emptying-rate and of insulin response on oral glucose tolerance in thyroid disease. Glucose 67-74 insulin Homo sapiens 42-49 5675316-0 1968 Study of the relationship between glucose and insulin responses to an oral glucose load in man. Glucose 34-41 insulin Homo sapiens 46-53 5675316-0 1968 Study of the relationship between glucose and insulin responses to an oral glucose load in man. Glucose 75-82 insulin Homo sapiens 46-53 5706046-0 1968 Serum-insulin levels in children during glucose tolerance tests. Glucose 40-47 insulin Homo sapiens 6-13 5678679-0 1968 [Free fatty acids and glucose in the blood of insulin resistant diabetics]. Glucose 22-29 insulin Homo sapiens 46-53 4971521-0 1968 [Synergetic action between glucose and hypotlycemic sulfamides on insulin secretion]. Glucose 27-34 insulin Homo sapiens 66-73 19873627-7 1968 Transport in muscle is the most important rate-controlling step for glucose utilization and is strongly accelerated by hypoxia, work, and insulin. Glucose 68-75 insulin Homo sapiens 138-145 19873627-9 1968 Insulin also stimulates glucose transport in adipose tissue. Glucose 24-31 insulin Homo sapiens 0-7 5698912-0 1968 Effect of hypothermia on the secretion of immunoreactive insulin in response to glucose. Glucose 80-87 insulin Homo sapiens 57-64 19873627-16 1968 The glucose transport and adenyl cyclase systems are not grossly affected by trypsin, indicating that the insulin effector system is a separate entity. Glucose 4-11 insulin Homo sapiens 106-113 4301688-3 1968 In these 14 patients the plasma insulin response was also determined after oral and intravenous glucose, after oral leucine, and after intravenous tolbutamide, and the value of these tests in the recognition and differential diagnosis of insulinoma was compared with that of the intravenous glucagon test. Glucose 96-103 insulin Homo sapiens 32-39 5653208-0 1968 The relationship between endogenous serum insulin concentration and glucose uptake in the forearm muscles of nondiabetics. Glucose 68-75 insulin Homo sapiens 42-49 5653208-1 1968 IN A SERIES OF EXPERIMENTS ON THE HUMAN FOREARM, PREPARATION DESIGNED TO EXAMINE THE EFFECTS OF VARIATIONS IN IMMUNOLOGICALLY DETERMINED ENDOGENOUS SERUM INSULIN LEVELS AND OF BLOOD GLUCOSE CONCENTRATIONS ON MUSCULAR GLUCOSE UPTAKE, THE FOLLOWING RESULTS WERE OBTAINED: (a) A highly significant correlation between muscular glucose uptake and simultaneous arterial serum insulin concentration. Glucose 182-189 insulin Homo sapiens 154-161 5653208-1 1968 IN A SERIES OF EXPERIMENTS ON THE HUMAN FOREARM, PREPARATION DESIGNED TO EXAMINE THE EFFECTS OF VARIATIONS IN IMMUNOLOGICALLY DETERMINED ENDOGENOUS SERUM INSULIN LEVELS AND OF BLOOD GLUCOSE CONCENTRATIONS ON MUSCULAR GLUCOSE UPTAKE, THE FOLLOWING RESULTS WERE OBTAINED: (a) A highly significant correlation between muscular glucose uptake and simultaneous arterial serum insulin concentration. Glucose 182-189 insulin Homo sapiens 371-378 5653208-1 1968 IN A SERIES OF EXPERIMENTS ON THE HUMAN FOREARM, PREPARATION DESIGNED TO EXAMINE THE EFFECTS OF VARIATIONS IN IMMUNOLOGICALLY DETERMINED ENDOGENOUS SERUM INSULIN LEVELS AND OF BLOOD GLUCOSE CONCENTRATIONS ON MUSCULAR GLUCOSE UPTAKE, THE FOLLOWING RESULTS WERE OBTAINED: (a) A highly significant correlation between muscular glucose uptake and simultaneous arterial serum insulin concentration. Glucose 217-224 insulin Homo sapiens 154-161 5653208-1 1968 IN A SERIES OF EXPERIMENTS ON THE HUMAN FOREARM, PREPARATION DESIGNED TO EXAMINE THE EFFECTS OF VARIATIONS IN IMMUNOLOGICALLY DETERMINED ENDOGENOUS SERUM INSULIN LEVELS AND OF BLOOD GLUCOSE CONCENTRATIONS ON MUSCULAR GLUCOSE UPTAKE, THE FOLLOWING RESULTS WERE OBTAINED: (a) A highly significant correlation between muscular glucose uptake and simultaneous arterial serum insulin concentration. Glucose 217-224 insulin Homo sapiens 371-378 5653208-1 1968 IN A SERIES OF EXPERIMENTS ON THE HUMAN FOREARM, PREPARATION DESIGNED TO EXAMINE THE EFFECTS OF VARIATIONS IN IMMUNOLOGICALLY DETERMINED ENDOGENOUS SERUM INSULIN LEVELS AND OF BLOOD GLUCOSE CONCENTRATIONS ON MUSCULAR GLUCOSE UPTAKE, THE FOLLOWING RESULTS WERE OBTAINED: (a) A highly significant correlation between muscular glucose uptake and simultaneous arterial serum insulin concentration. Glucose 324-331 insulin Homo sapiens 154-161 5653208-1 1968 IN A SERIES OF EXPERIMENTS ON THE HUMAN FOREARM, PREPARATION DESIGNED TO EXAMINE THE EFFECTS OF VARIATIONS IN IMMUNOLOGICALLY DETERMINED ENDOGENOUS SERUM INSULIN LEVELS AND OF BLOOD GLUCOSE CONCENTRATIONS ON MUSCULAR GLUCOSE UPTAKE, THE FOLLOWING RESULTS WERE OBTAINED: (a) A highly significant correlation between muscular glucose uptake and simultaneous arterial serum insulin concentration. Glucose 324-331 insulin Homo sapiens 371-378 5653208-3 1968 (c) A maximal insulin effect on muscular glucose uptake at arterial serum insulin concentrations at about 200 muU/ml. Glucose 41-48 insulin Homo sapiens 14-21 5653208-3 1968 (c) A maximal insulin effect on muscular glucose uptake at arterial serum insulin concentrations at about 200 muU/ml. Glucose 41-48 insulin Homo sapiens 74-81 5698067-0 1968 [Glucide metabolism in premature infant: insulin response to slow glucose influsion]. Glucose 66-73 insulin Homo sapiens 41-48 5241475-0 1968 Insulin response to glucose in the presence of oral hypoglycemics. Glucose 20-27 insulin Homo sapiens 0-7 5648445-0 1968 Effects of intrahypothalamic glucose injection on eating and drinking elicited by insulin. Glucose 29-36 insulin Homo sapiens 82-89 5716242-0 1968 [On glucose-insulin treatment in progressive muscular dystrophies]. Glucose 4-11 insulin Homo sapiens 12-19 5641614-0 1968 Elevated serum human growth hormone and decreased serum insulin in prediabetic males after intravenous tolbutamide and glucose. Glucose 119-126 insulin Homo sapiens 56-63 16695937-8 1968 When adipose tissue of obese individuals showed impaired responsiveness to insulin, their plasma insulin levels, after oral glucose, were elevated. Glucose 124-131 insulin Homo sapiens 75-82 5714494-0 1968 [Action of fasting and insulin on the synthesis of fatty acids beginning with glucose specifically marked with carbon and hydrogen]. Glucose 78-85 insulin Homo sapiens 23-30 4952858-0 1968 Diminished serum insulin response to glucose in genetic prediabetic males with normal glucose tolerance. Glucose 37-44 insulin Homo sapiens 17-24 5689961-0 1968 Plasma insulin responses to glucose in normal and subclinical diabetic women treated with oral contraceptive agents. Glucose 28-35 insulin Homo sapiens 7-14 4863616-0 1967 Effect of insulin on the rate of glucose distribution. Glucose 33-40 insulin Homo sapiens 10-17 6074000-0 1967 Plasma insulin responses to oral and intravenous glucose: studies in normal and diabetic sujbjects. Glucose 49-56 insulin Homo sapiens 7-14 6074000-1 1967 The plasma insulin responses of normal weight and obese, diabetic, and nondiabetic subjects to intravenous glucose was only 30-40% of that seen after oral glucose, indicating that alimentary mechanism(s) in addition to the arterial blood sugar concentration regulate insulin secretion. Glucose 107-114 insulin Homo sapiens 11-18 6074000-8 1967 Therefore, in the noninsulin-requiring maturity-onset diabetic, the glycemic insulinogenic stimulus for a given oral glucose load is significantly greater than in normal subjects and accounts for the excessive plasma insulin responses observed late in the course of an oral glucose tolerance test. Glucose 117-124 insulin Homo sapiens 21-28 5582727-0 1967 Influence of a rapid intravenous injection of glucose or tolbutamide on plasma-insulin concentration in normal and diabetic subjects. Glucose 46-53 insulin Homo sapiens 79-86 6057488-0 1967 Effects of insulin on glucose metabolism in isolated human fat cells. Glucose 22-29 insulin Homo sapiens 11-18 5620801-0 1967 [Immunologically measurable insulin(IMI) in normal, obese and obese, diabetic subjects after intravenous administration of glucose, tolbutamide and glucagon]. Glucose 123-130 insulin Homo sapiens 28-35 6057488-1 1967 Isolated fat cells were used for the study of in vitro effects of insulin on glucose metabolism in human and rat adipose tissue. Glucose 77-84 insulin Homo sapiens 66-73 6057488-2 1967 In human subcutaneous fat cells, effects of insulin could be detected at concentrations of glucose in the medium from 1 to 10 micro moles/ml. Glucose 91-98 insulin Homo sapiens 44-51 6064605-0 1967 Inhibition by phlorizin of insulin- and protease-stimulated glucose utilization in isolated adipose cells. Glucose 60-67 insulin Homo sapiens 27-34 6042615-1 1967 Studies on plasma insulin and blood glucose levels during an intravenous glucose tolerance test. Glucose 73-80 insulin Homo sapiens 18-25 5620805-0 1967 The normal insulin response to glucose. Glucose 31-38 insulin Homo sapiens 11-18 6061732-0 1967 The significance of basal insulin levels in the evaluation of the insulin response to glucose in diabetic and nondiabetic subjects. Glucose 86-93 insulin Homo sapiens 26-33 6033188-0 1967 Factors affecting the inhibitory action of insulin on lipolysis in a glucose-free medium. Glucose 69-76 insulin Homo sapiens 43-50 16695927-6 1967 In 17 subjects, glucose oxidation and lipid synthesis by adipose tissue segments and isolated fat cells were measured and showed a definite response to physiological doses of crystalline pork insulin. Glucose 16-23 insulin Homo sapiens 192-199 6061732-0 1967 The significance of basal insulin levels in the evaluation of the insulin response to glucose in diabetic and nondiabetic subjects. Glucose 86-93 insulin Homo sapiens 66-73 6061732-1 1967 The level of insulin after an overnight fast (basal) in 37 obese and nonobese male subjects with normal and abnormal carbohydrate tolerance was directly related to the increase in insulin concentration during a 3 hr 100 g oral glucose tolerance test. Glucose 227-234 insulin Homo sapiens 13-20 4860797-0 1967 The insulin response to glucose: a comparison between oral and intravenous tolerance tests. Glucose 24-31 insulin Homo sapiens 4-11 6061732-1 1967 The level of insulin after an overnight fast (basal) in 37 obese and nonobese male subjects with normal and abnormal carbohydrate tolerance was directly related to the increase in insulin concentration during a 3 hr 100 g oral glucose tolerance test. Glucose 227-234 insulin Homo sapiens 180-187 6061732-3 1967 Thus obesity predicted with the magnitude of the insulin response to glucose ingestion. Glucose 69-76 insulin Homo sapiens 49-56 6061732-5 1967 The insulin levels of all subjects with normal carbohydrate tolerance promptly rose 5-7-fold, and reached peak values 1 hr after oral glucose. Glucose 134-141 insulin Homo sapiens 4-11 6061732-7 1967 In all subjects the insulin response (quantitated by calculation of the area circumscribed by a plot of the per cent change in insulin with time) showed a significant inverse correlation with the glucose response. Glucose 196-203 insulin Homo sapiens 20-27 6061732-7 1967 In all subjects the insulin response (quantitated by calculation of the area circumscribed by a plot of the per cent change in insulin with time) showed a significant inverse correlation with the glucose response. Glucose 196-203 insulin Homo sapiens 127-134 6034762-7 1967 Insulin stimulated glucose flux without increasing the value of V(max). Glucose 19-26 insulin Homo sapiens 0-7 6028754-0 1967 Influence of anti-insulin serum on glucose metabolism. Glucose 35-42 insulin Homo sapiens 18-25 6061732-9 1967 Elevated levels of insulin, in both the basal state and in response to glucose, were related to obesity. Glucose 71-78 insulin Homo sapiens 19-26 6022061-0 1967 Epinephrine antagonism of insulin-dependent glucose uptake in the toad bladder. Glucose 44-51 insulin Homo sapiens 26-33 4292884-0 1967 Effects of insulin and phospholipase A on glucose transport across the plasma membrane of free adipose cells. Glucose 42-49 insulin Homo sapiens 11-18 5338206-0 1967 The plasma insulin response to glucose infusion in healthy subjects and in diabetes mellitus. Glucose 31-38 insulin Homo sapiens 11-18 5338207-0 1967 Further studies on healthy subjects with low and high insulin response to glucose infusion. Glucose 74-81 insulin Homo sapiens 54-61 5338208-0 1967 Insulin response to glucose infusion in diabetic and non-diabetic monozygotic twin pairs. Glucose 20-27 insulin Homo sapiens 0-7 6025075-0 1967 Insulin response in glucose-tolerance tests. Glucose 20-27 insulin Homo sapiens 0-7 4164072-0 1967 Failure of insulin response to glucose load during operation and after myocardial infarction. Glucose 31-38 insulin Homo sapiens 11-18 6071595-0 1967 An analogue computer model for the insulin response to glucose infusion. Glucose 55-62 insulin Homo sapiens 35-42 16742511-7 1967 There is some release of labelled insulin when such slices are further incubated in media of low glucose content. Glucose 97-104 insulin Homo sapiens 34-41 6020731-0 1967 Effect of pulse administration of glucose or glucagon on insulin secretion in vitro. Glucose 34-41 insulin Homo sapiens 57-64 16742511-8 1967 When the glucose content of the medium is raised, little additional radioactive insulin is released in the first hour after labelling. Glucose 9-16 insulin Homo sapiens 80-87 16742511-9 1967 However, there is a marked increase in specific radioactivity of insulin released from slices in response to a high concentration of glucose in the second and third hours. Glucose 133-140 insulin Homo sapiens 65-72 5339718-0 1966 Effects of glucose concentration on incorporation of [3H]leucine into insulin using isolated mammalian islets of Langerhans. Glucose 11-18 insulin Homo sapiens 70-77 5335649-0 1967 Insulin secretion by isolated islets in presence of glucose, insulin and anti-insulin serum. Glucose 52-59 insulin Homo sapiens 0-7 5335535-0 1967 Serum immunoreactive insulin response during prolonged glucose infusions in nondiabetic and diabetic humans. Glucose 55-62 insulin Homo sapiens 21-28 5620790-0 1967 [Investigations concerning the insulin effect on intestinal resorption of glucose and fructose]. Glucose 74-81 insulin Homo sapiens 31-38 6023769-1 1967 Insulin secretory responses to paired intravenous and oral glucose loads were determined in 38 nonobese individuals classified as normal (nondiabetic) subjects, "mild" diabetics (fasting blood glucose below 105 mg per 100 ml), or "moderate" diabetics (fasting glucose below 192 mg per 100 ml). Glucose 59-66 insulin Homo sapiens 0-7 6023769-4 1967 In the nonobese group, normal subjects responded to massive hyperglycemia after rapid injection of glucose with immediate and maximal outpouring of insulin, in contrast to a desultory insulinogenic response in patients with mild diabetes, and no initial response at all in moderate diabetics. Glucose 99-106 insulin Homo sapiens 148-155 6023775-5 1967 Both insulin and cyanide increased lactate production in the presence of glucose. Glucose 73-80 insulin Homo sapiens 5-12 5973133-0 1966 [Estimation of insulin efficacy in obesity by the response of blood insulin and glucose to intravenous tolbutamide]. Glucose 80-87 insulin Homo sapiens 15-22 5920806-0 1966 Stimulation of glucose metabolism in brown adipose tissue by addition of insulin in vitro. Glucose 15-22 insulin Homo sapiens 73-80 4902707-2 1966 Inhibition of glucose induced insulin release by diazoxide]. Glucose 14-21 insulin Homo sapiens 30-37 5957477-0 1966 Plasma insulin responses to glucose and tolbutamide of normal weight and obese diabetic and nondiabetic subjects. Glucose 28-35 insulin Homo sapiens 7-14 5946185-0 1966 [Considerations on the variations of the 6th electrocardiographic wave under potassium and dextrose-insulin load in a case of a hypopotassemic syndrome in a cirrhotic patient]. Glucose 91-99 insulin Homo sapiens 100-107 5919281-0 1966 The effect of insulin and diabetes on glucose metabolism in human skin. Glucose 38-45 insulin Homo sapiens 14-21 4293997-0 1966 [Determination of antibody inhibited and noninhibited serum insulin activity in obesity and the reaction following intravenous glucose administration]. Glucose 127-134 insulin Homo sapiens 60-67 5325046-0 1966 Effects of insulin and diabetes on flux rates of plasma glucose and free fatty acids. Glucose 56-63 insulin Homo sapiens 11-18 5928896-0 1966 On the mechanism of action of phospholipase A and insulin on glucose entry into free adipose cells. Glucose 61-68 insulin Homo sapiens 50-57 5932061-2 1966 Basal and insulin-stimulated glucose metabolism. Glucose 29-36 insulin Homo sapiens 10-17 24173299-6 1966 The difference in changes in concentration of non-esterified fatty acids and glyoerol in response to a variety of test situations may well be the result of both the glucose-dependent lipogenetic and the glucose-independent antilipolytic effect of insulin. Glucose 165-172 insulin Homo sapiens 247-254 24173299-6 1966 The difference in changes in concentration of non-esterified fatty acids and glyoerol in response to a variety of test situations may well be the result of both the glucose-dependent lipogenetic and the glucose-independent antilipolytic effect of insulin. Glucose 203-210 insulin Homo sapiens 247-254 4158892-0 1966 Normal insulin response to glucose. Glucose 27-34 insulin Homo sapiens 7-14 5330862-0 1966 The influences of insulin on the hepatic metabolism of glucose. Glucose 55-62 insulin Homo sapiens 18-25 5907155-0 1966 Effect of insulin infusion of pancreas on blood glucose. Glucose 48-55 insulin Homo sapiens 10-17 4287739-0 1966 Some observations on the influence of insulin, prednisolone and free amino acids on the glucose metabolism in cultivated liver tissue. Glucose 88-95 insulin Homo sapiens 38-45 14014605-0 1963 Uptake of glucose dependent on insulin in the isolated bladder of the toad. Glucose 10-17 insulin Homo sapiens 31-38 5986266-0 1966 [Comparison of the effect produced by glucagon-free insulin administered by splenoportal route and by peripheral venous route on the degree and course of hypoglycemia and on the peripheral consumption of glucose in normal subjects]. Glucose 204-211 insulin Homo sapiens 52-59 5870516-0 1965 Intestinal transport of glucose and sodium: changes in alloxan diabetes and effects of insulin. Glucose 24-31 insulin Homo sapiens 87-94 5871670-0 1965 Effect of hypophysectomy on post-glucose injection rise of plasmatic insulin. Glucose 33-40 insulin Homo sapiens 69-76 14197562-3 1964 Small amounts of insulin were secreted in response to these glucose infusions, but in insulin-dependent diabetics incapable of altering plasma insulin to any great extent, the effect of glucose upon free fatty acids could be obtained provided the subjects were primed with long-acting insulin before the infusions were begun. Glucose 60-67 insulin Homo sapiens 17-24 14197562-3 1964 Small amounts of insulin were secreted in response to these glucose infusions, but in insulin-dependent diabetics incapable of altering plasma insulin to any great extent, the effect of glucose upon free fatty acids could be obtained provided the subjects were primed with long-acting insulin before the infusions were begun. Glucose 186-193 insulin Homo sapiens 17-24 14080678-0 1963 GLUCOSE UPTAKE BY HELA CELLS AS INFLUENCED BY INSULIN. Glucose 0-7 insulin Homo sapiens 46-53 5900413-0 1966 The effects of caffeine, deoxyribose nucleic acid and insulin on the metabolism of glucose by adipose tissue in vitro. Glucose 83-90 insulin Homo sapiens 54-61 4230149-0 1966 [Effect of 6-aminonicotinic acid amide on insulin dependant glucose uptake in epididymal fat tissue]. Glucose 60-67 insulin Homo sapiens 42-49 5866839-0 1965 Phospholipase C and mechanisms of action of insulin and cortisol on glucose entry into free adipose cells. Glucose 68-75 insulin Homo sapiens 44-51 14198303-0 1964 INSULIN-LIKE ACTIVITY IN PANCREATIC VEIN BLOOD AFTER GLUCOSE LOADING AND EPINEPHRINE HYPERGLYCEMIA. Glucose 53-60 insulin Homo sapiens 0-7 5839963-0 1964 [Action of tolbutamide and insulin on the disappearance curve of hyperglycemia provoked by intravenous administration of glucose]. Glucose 121-128 insulin Homo sapiens 27-34 13950627-0 1963 Reduction by phenformin of excessive insulin levels after glucose loading in obese and diabetic subjects. Glucose 58-65 insulin Homo sapiens 37-44 14025572-0 1963 [Determination of insulin activity in human serum after glucose-loading as a test of the functional capacity of the pancreas]. Glucose 56-63 insulin Homo sapiens 18-25 13999622-0 1963 Effects of insulin on hepatic glucose production and utilization. Glucose 30-37 insulin Homo sapiens 11-18 13943114-0 1962 The normal and diabetic patterns of insulin response to glucose. Glucose 56-63 insulin Homo sapiens 36-43 13756162-0 1961 Transport of glucose across blood-aqueous barriers as affected by insulin. Glucose 13-20 insulin Homo sapiens 66-73 14493218-0 1962 Correlation of the effects of insulin and of muscular contraction in vitro on uptake of glucose by the frog. Glucose 88-95 insulin Homo sapiens 30-37 13910496-0 1962 Quantitative effects of glucose, sulfonylureas, salicylate, and indole-3-acetic acid on the secretion of insulin activity into pancreatic venous blood. Glucose 24-31 insulin Homo sapiens 105-112 13863498-0 1962 Gastric emptying and change of blood glucose level, as affected by glucagon and insulin. Glucose 37-44 insulin Homo sapiens 80-87 13683765-0 1961 Studies on the state of insulin in blood: the role of glucose in the in vivo dissociation of insulin complexes. Glucose 54-61 insulin Homo sapiens 93-100 13687493-0 1961 Studies on binding of glucose by insulin. Glucose 22-29 insulin Homo sapiens 33-40 13742500-0 1961 [Changes in the insulin activity of the blood of normal and diabetic subjects after oral glucose overloading]. Glucose 89-96 insulin Homo sapiens 16-23 13783941-0 1961 [On the effect of insulin and glucagon on glucose metabolism of the epididymal fat appendix of rats in vitro. Glucose 42-49 insulin Homo sapiens 18-25 13734210-0 1961 [Action of glucagon or insulin on the release or uptake of glucose by the isolated liver of the toad]. Glucose 59-66 insulin Homo sapiens 23-30 13766269-0 1961 Effect of insulin, phlorizin and some metabolic inhibitors on the glucose absorption from the intestine. Glucose 66-73 insulin Homo sapiens 10-17 13740422-0 1960 Effects of insulin on blood glucose entry and removal rates in man. Glucose 28-35 insulin Homo sapiens 11-18 13715508-0 1961 [Effect of glucose on the dynamics of blood pentoses and hexoses under the influence of insulin in animals]. Glucose 11-18 insulin Homo sapiens 88-95 13760946-0 1961 Regulation of blood glucose concentration: hepatic action of insulin. Glucose 20-27 insulin Homo sapiens 61-68 13787085-0 1960 Comparison of plasma insulin levels following administration of tolbutamide and glucose. Glucose 80-87 insulin Homo sapiens 21-28 13725036-0 1960 An effect of insulin on production of glucose during hepatic glycogenolysis. Glucose 38-45 insulin Homo sapiens 13-20 13727773-2 1960 The effect of insulin on glucose penetration and phosphorylation in frog muscle. Glucose 25-32 insulin Homo sapiens 14-21 14444360-0 1960 Influence of insulin and tolbutamide on glucose oxidation in man. Glucose 40-47 insulin Homo sapiens 13-20 13822857-0 1960 Effect of an insulin infusion on hepatic output of glucose. Glucose 51-58 insulin Homo sapiens 13-20 14413768-0 1960 Significance of changes in blood glucose specific activity following insulin administration. Glucose 33-40 insulin Homo sapiens 69-76 14408981-0 1960 Action of digoxin and insulin on transport of glucose through myocardial cell membrane. Glucose 46-53 insulin Homo sapiens 22-29 14419685-2 1960 Evidence for a direct immediate effect of insulin on the balance of glucose across the liver. Glucose 68-75 insulin Homo sapiens 42-49 14399740-0 1959 Direct measurement of the effect of insulin on the uptake of glucose by peripheral muscles in normal subjects, diabetics and acromegalics. Glucose 61-68 insulin Homo sapiens 36-43 14426976-0 1959 [The renal threshold for glucose in recent diabetes mellitus of children in insulin treatment]. Glucose 25-32 insulin Homo sapiens 76-83 13814676-0 1959 Effects of exogenous and endogenous insulin on glucose utilization and production. Glucose 47-54 insulin Homo sapiens 36-43 13833386-0 1959 Role of insulin in two pathways of glucose metabolism: in vivo glucosamine and glycogen synthesis. Glucose 35-42 insulin Homo sapiens 8-15 14437036-0 1959 Effects of insulin and tolbutamide on blood glucose entry and removal rates. Glucose 44-51 insulin Homo sapiens 11-18 13847456-0 1959 Hyperpolarization of muscle by insulin in a glucose-free environment. Glucose 44-51 insulin Homo sapiens 31-38 13649694-0 1959 The action of insulin on the transport of glucose through the cell membrane. Glucose 42-49 insulin Homo sapiens 14-21 13561858-0 1958 Direct effects of tolbutamide and insulin on peripheral glucose uptake; a comparative study in man. Glucose 56-63 insulin Homo sapiens 34-41 14403977-0 1959 [The influence of insulin and oral antidiabetics on the glucose uptake and gas exchange of isolated fatty tissue]. Glucose 56-63 insulin Homo sapiens 18-25 13654261-2 1959 The effect of insulin on glucose utilization as measured by the manometric determination of carbon dioxide output. Glucose 25-32 insulin Homo sapiens 14-21 13637592-0 1959 A comparison of the influence of tolbutamide and small doses of insulin on the splanchnic output and peripheral uptake of glucose in man. Glucose 122-129 insulin Homo sapiens 64-71 13637594-0 1959 Changes induced by insulin and tolbutamide in the glucose output of the liver. Glucose 50-57 insulin Homo sapiens 19-26 13574022-0 1958 Action of insulin and tolbutamide on blood glucose entry and removal. Glucose 43-50 insulin Homo sapiens 10-17 13593348-0 1958 [Studies on the effect of insulin and blood sugar-lowering sulfonylurea combinations on glucose content of the aqueous humor]. Glucose 88-95 insulin Homo sapiens 26-33 14444771-0 1959 Plasma insulin activity after glucose: an index of insulogenic reserve in normal and diabetic man. Glucose 30-37 insulin Homo sapiens 7-14 13597738-0 1958 Effects of insulin, tolbutamide and phenethyldiguanidine on peripheral glucose uptake in man. Glucose 71-78 insulin Homo sapiens 11-18 13500212-2 1958 In diabetic persons taking large doses of insulin, or who needed insulin for control, hyperglycemia, ketosis, and increased excretion of glucose in the urine developed when tolbutamide was substituted for insulin or was used before insulin therapy was begun. Glucose 137-144 insulin Homo sapiens 42-49 13563697-2 1958 The preference for glucose solutions and its modification by injections of insulin. Glucose 19-26 insulin Homo sapiens 75-82 13619222-0 1958 [Effect of prolonged intra-arterial administration of small quantities of insulin on peripheral glucose consumption]. Glucose 96-103 insulin Homo sapiens 74-81 13584041-0 1958 [Modification of the effective insulin level in the blood after a glucose meal in normal subjects and in diabetics]. Glucose 66-73 insulin Homo sapiens 31-38 13603520-0 1958 The effect of insulin and orinase on plasma glucose turnover and oxidation in humans. Glucose 44-51 insulin Homo sapiens 14-33 13424687-0 1957 Effect of insulin on utilization and production of circulating glucose. Glucose 63-70 insulin Homo sapiens 10-17 13332058-0 1956 The interaction of glucagon and insulin on blood glucose. Glucose 49-56 insulin Homo sapiens 32-39 13341167-0 1956 [Stimulating effect of insulin on glucose consumption by the diaphragm and cellular integrity]. Glucose 34-41 insulin Homo sapiens 23-30 13295301-0 1956 The effect of insulin on the pathways of conversion of glucose to fatty acids in the liver. Glucose 55-62 insulin Homo sapiens 14-21 13298710-0 1956 Enhancement of oxidative phosphorylation of glucose by insulin. Glucose 44-51 insulin Homo sapiens 55-62 13263911-0 1955 Regulation of glucose utilization in tumors by a stress-modified insulin: anti-insulin system. Glucose 14-21 insulin Homo sapiens 65-72 13263911-0 1955 Regulation of glucose utilization in tumors by a stress-modified insulin: anti-insulin system. Glucose 14-21 insulin Homo sapiens 80-87 13298021-0 1955 [Effects of insulin on tubular reabsorption of glucose in normal subjects]. Glucose 47-54 insulin Homo sapiens 12-19 14354668-0 1955 Insulin-like effect of anterior pituitary extract in accelerating the transfer of glucose across the blood-aqueous barrier. Glucose 82-89 insulin Homo sapiens 0-7 13310951-0 1955 [Blood insulin activity following glucose tolerance test]. Glucose 34-41 insulin Homo sapiens 7-14 13203366-0 1954 [Metabolism of glucose in dystrophic infants studied by means of glucose tolerance tests and adrenalin and insulin tests]. Glucose 15-22 insulin Homo sapiens 107-114 13241979-0 1955 [Effect of temperature, cortisone and insulin on erythrocyte permeability to fructose and glucose. Glucose 90-97 insulin Homo sapiens 38-45 13114413-0 1953 Insulin and the relation between phosphate transport and glucose metabolism. Glucose 57-64 insulin Homo sapiens 0-7 13175204-0 1954 The effect of insulin on the excretion of glucose and phosphate by the kidney of the cat. Glucose 42-49 insulin Homo sapiens 14-21 13174552-0 1954 The influence of insulin on glucose utilization in adipose and hepatic tissues in vitro. Glucose 28-35 insulin Homo sapiens 17-24 13092270-0 1953 Influence of glucose concentration on the action of insulin. Glucose 13-20 insulin Homo sapiens 52-59 12995993-0 1952 Factors determining effect of insulin on metabolism of glucose in ascorbic acid deficiency and scurvy in the monkey. Glucose 55-62 insulin Homo sapiens 30-37 13067231-0 1953 [Mode of action of insulin on the intestinal absorption of glucose]. Glucose 59-66 insulin Homo sapiens 19-26 13117928-0 1953 Insulin-reversible inhibition of glucose utilization by serum lipoprotein fractions. Glucose 33-40 insulin Homo sapiens 0-7 13121029-0 1953 Effect of insulin on maximal rate of renal tubular uptake of glucose in non-diabetic humans. Glucose 61-68 insulin Homo sapiens 10-17 13106021-2 1953 Variations in the endogenous blood alcohol, pyruvic acid and glucose in the superficial venous circulation after insulin load and after glucose load in muscle diseases]. Glucose 61-68 insulin Homo sapiens 113-120 13105890-0 1953 [Behavior of some free glycogen-forming amino acids after administration of glucose and of glucose with insulin]. Glucose 91-98 insulin Homo sapiens 104-111 14946711-0 1952 The influence of insulin on the permeability of the blood-aqueous barrier to glucose. Glucose 77-84 insulin Homo sapiens 17-24 14938447-0 1952 Effect on femoral A-V glucose difference of insulin injected into an antecubital vein and into a femoral artery. Glucose 22-29 insulin Homo sapiens 44-51 13126598-0 1952 The effect of insulin on hepatic utilization of glucose. Glucose 48-55 insulin Homo sapiens 14-21 14944459-0 1952 [Influence of alloxan pancreas extract on the action of insulin on glucose consumption in the isolated diaphragm]. Glucose 67-74 insulin Homo sapiens 56-63 18100177-0 1948 Effect of insulin on tubular reabsorption of glucose in diabetic patients. Glucose 45-52 insulin Homo sapiens 10-17 14865140-0 1951 [Effect of insulin on the intestinal absorption of glucose]. Glucose 51-58 insulin Homo sapiens 11-18 14814204-0 1951 Effect of diabetes and insulin of the maximum capacity of the renal tubules to reabsorb glucose. Glucose 88-95 insulin Homo sapiens 23-30 14903806-0 1951 The effect of insulin and pituitary hormones on glucose uptake in muscle. Glucose 48-55 insulin Homo sapiens 14-21 14808299-0 1950 Influence of fasting on the effect of insulin on glucose oxidation. Glucose 49-56 insulin Homo sapiens 38-45 20342749-0 1947 The comparative action of insulin on the disposal of intravenous fructose and glucose. Glucose 78-85 insulin Homo sapiens 26-33 20340930-0 1947 The effect of diabetes and insulin on glucose Tm. Glucose 38-45 insulin Homo sapiens 27-34 18938813-0 1948 A paradoxical effect of insulin on glucose assimilation. Glucose 35-42 insulin Homo sapiens 24-31 19986582-5 1928 (4) Increase of deficient intracellular oxygenation by insulin hypodermically (5 units at beginning and end of glucose injection). Glucose 111-118 insulin Homo sapiens 55-62 20993177-0 1946 Effect of insulin, insulin-dextrose, and water diuresis on metabolism of isopropyl alcohol. Glucose 27-35 insulin Homo sapiens 19-26 33950348-8 2021 CONCLUSIONS: The lockdown due to COVID-19 pandemic had a negative impact on body weight and glucose control in T2DM patients, in particular in those on insulin treatment. Glucose 92-99 insulin Homo sapiens 152-159 32896081-2 2021 Notwithstanding CSII"s benefits, insulin dependent diabetic patients rarely achieve optimal glucose control. Glucose 92-99 insulin Homo sapiens 33-40 31240952-7 2021 However, the insulin-secretory response to glucose and glibenclamide was unchanged by amrinone. Glucose 43-50 insulin Homo sapiens 13-20 32473788-14 2021 They are abundantly expressed in white and brown adipose tissue, and increase fat oxidation, energy expenditure and insulin-mediated glucose uptake. Glucose 133-140 insulin Homo sapiens 116-123 33626236-2 2021 Since local blood flow influences the rate of insulin absorption from the subcutaneous tissue, we hypothesised that an increase in blood glucose levels-occurring as the result of glucose infusion or food intake-could modulate the pharmacokinetic properties of subcutaneously administered insulin. Glucose 137-144 insulin Homo sapiens 46-53 33626236-2 2021 Since local blood flow influences the rate of insulin absorption from the subcutaneous tissue, we hypothesised that an increase in blood glucose levels-occurring as the result of glucose infusion or food intake-could modulate the pharmacokinetic properties of subcutaneously administered insulin. Glucose 137-144 insulin Homo sapiens 288-295 33626236-2 2021 Since local blood flow influences the rate of insulin absorption from the subcutaneous tissue, we hypothesised that an increase in blood glucose levels-occurring as the result of glucose infusion or food intake-could modulate the pharmacokinetic properties of subcutaneously administered insulin. Glucose 179-186 insulin Homo sapiens 46-53 33626236-2 2021 Since local blood flow influences the rate of insulin absorption from the subcutaneous tissue, we hypothesised that an increase in blood glucose levels-occurring as the result of glucose infusion or food intake-could modulate the pharmacokinetic properties of subcutaneously administered insulin. Glucose 179-186 insulin Homo sapiens 288-295 33882365-1 2021 Insulin, a peptide hormone and a key regulator of blood glucose level, is routinely administered to type-I diabetic patients to achieve the required glycemic control. Glucose 56-63 insulin Homo sapiens 0-7 33631318-1 2021 Insulin is the main anabolic hormone secreted by beta-cells of the pancreas stimulating the assimilation and storage of glucose in muscle and fat cells. Glucose 120-127 insulin Homo sapiens 0-7 32994312-5 2021 RESULTS: Whole-body insulin sensitivity (SI 104: 0.54+-0.12 before vs 0.82+-0.11 after BPD, p=0.024 and 0.41+-0.09 before vs 0.65+-0.09/pM/min after RYGB, p=not significant) and Glucose Disposition Index increased only after BPD. Glucose 178-185 insulin Homo sapiens 20-27 33753887-0 2021 omega-3PUFA supplementation ameliorates adipose tissue inflammation and insulin-stimulated glucose disposal in subjects with obesity: a potential role for apolipoprotein E. Glucose 91-98 insulin Homo sapiens 72-79 32994312-8 2021 Bypassing the jejunum is beneficial in terms of insulin-mediated glucose disposal in obesity. Glucose 65-72 insulin Homo sapiens 48-55 33753887-11 2021 These changes were associated with a 25% increase in insulin-stimulated glucose disposal (4.7 +- 0.6 mg/kg ffm min vs. 5.9 +- 0.9 mg/kg ffm min) despite no change in body weight. Glucose 72-79 insulin Homo sapiens 53-60 33753887-14 2021 These findings are associated with significant improvement of insulin-stimulated glucose disposal. Glucose 81-88 insulin Homo sapiens 62-69 33737253-8 2021 There is a fairly good, though not complete, qualitative and quantitative coherence between insulin secretion rates measured in vivo and in vitro during stimulation with physiological glucose concentrations, but the concordance fades out under extreme conditions. Glucose 184-191 insulin Homo sapiens 92-99 33621891-9 2021 CONCLUSIONS: ICU patients with extremely high dose insulin infusions had more hypoglycemia and took longer to achieve glucose targets compared to those with lower requirements. Glucose 118-125 insulin Homo sapiens 51-58 33650017-5 2021 METHODS: We selected 35 SNPs strongly associated with fasting glucose (p < 5 x 10-8) in a non-diabetic European-descent population from the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) (n = 133,010). Glucose 62-69 insulin Homo sapiens 169-176 34050775-5 2021 The IR binding assay was used to determine unknown amounts of insulin secreted by MIN6 beta cell line after stimulation with glucose, arginine, ornithine, dopamine, and serotonin. Glucose 125-132 insulin Homo sapiens 62-69 34052801-29 2021 The score of the Hungarian test - in accordance with the literature - correlates negatively with age, positively with the year of insulin-usage and with the number of daily insulin intake and of blood glucose measurement. Glucose 201-208 insulin Homo sapiens 130-137 34050757-3 2021 The aim of the study was to evaluate insulin action on glucose (Gox) and lipid (Lox) oxidation, non-oxidative glucose metabolism (Gnonox), and serum free fatty acid (FFA) in different PCOS phenotypes. Glucose 55-62 insulin Homo sapiens 37-44 34050775-0 2021 A radioligand receptor binding assay for measuring of insulin secreted by MIN6 cells after stimulation with glucose, arginine, ornithine, dopamine, and serotonin. Glucose 108-115 insulin Homo sapiens 54-61 34047962-1 2021 INTRODUCTION: While continuous glucose monitoring (CGM) has been shown to decrease both hyper- and hypoglycemia in insulin-treated diabetes, its value in non-insulin-treated type 2 diabetes (T2D) and prediabetes is unclear. Glucose 31-38 insulin Homo sapiens 115-122 34045668-2 2021 Whilst exercise stimulated activation of AMP-activated protein kinase (AMPK), an important energy sensor, has been highlighted for its potential to promote insulin-stimulated glucose uptake, the underlying mechanisms for this remain largely unknown. Glucose 175-182 insulin Homo sapiens 156-163 34044667-1 2022 OBJECTIVES: Triglyceride-glucose index (TyG index), which is defined as the simple and novel marker of insulin resistance, is becoming increasingly important as a promising predictive marker for atherosclerotic diseases. Glucose 25-32 insulin Homo sapiens 103-110 34051232-0 2021 Glucose treatment of human pancreatic beta-cells enhances translation of mRNAs involved in energetics and insulin secretion. Glucose 0-7 insulin Homo sapiens 106-113 34051232-6 2021 Among the list of glucose-induced proteins, we identified the proconvertase PCSK1, an enzyme involved in the proteolytic conversion of proinsulin to insulin, whose translation was induced within minutes following glucose treatment. Glucose 18-25 insulin Homo sapiens 135-145 34051232-6 2021 Among the list of glucose-induced proteins, we identified the proconvertase PCSK1, an enzyme involved in the proteolytic conversion of proinsulin to insulin, whose translation was induced within minutes following glucose treatment. Glucose 18-25 insulin Homo sapiens 138-145 34051232-6 2021 Among the list of glucose-induced proteins, we identified the proconvertase PCSK1, an enzyme involved in the proteolytic conversion of proinsulin to insulin, whose translation was induced within minutes following glucose treatment. Glucose 213-220 insulin Homo sapiens 135-145 34051232-6 2021 Among the list of glucose-induced proteins, we identified the proconvertase PCSK1, an enzyme involved in the proteolytic conversion of proinsulin to insulin, whose translation was induced within minutes following glucose treatment. Glucose 213-220 insulin Homo sapiens 138-145 34034759-1 2021 BACKGROUND: Chronic superphysiological glucose and insulin concentrations are known to trigger several tissue and organ failures, including insulin resistance, oxidative stress and chronic low-grade inflammation. Glucose 39-46 insulin Homo sapiens 140-147 34021189-3 2021 The consensus model, as well as a class of currently prescribed anti-diabetic drugs, are based around the observation that glucose-evoked ATP production in beta-cells leads to closure of cell membrane ATP-gated potassium (KATP) channels, plasma membrane depolarisation, Ca2+ influx, and finally the exocytosis of insulin granules. Glucose 123-130 insulin Homo sapiens 313-320 34016966-6 2021 Upon direct and high affinity binding of sFNDC4 to GPR116, sFNDC4 promoted insulin signaling and insulin-mediated glucose uptake in white adipocytes. Glucose 114-121 insulin Homo sapiens 97-104 34018016-7 2021 To further define the role of LMO3 in insulin-stimulated glucose uptake, insulin signaling, adipocyte bioenergetics, as well as endocrine function, experiments were conducted in 3T3-L1 adipocytes and newly differentiated human primary mature adipocytes, engineered for transient gain or loss of LMO3 expression, respectively. Glucose 57-64 insulin Homo sapiens 38-45 34018016-14 2021 Together with increased PPARgamma activity and Ncoa1 expression, these gene expression changes promote insulin-induced GLUT4 translocation, glucose uptake in addition to increased mitochondrial oxidative capacity, limiting HFD-induced adipose dysfunction. Glucose 140-147 insulin Homo sapiens 103-110 34050775-7 2021 We observed the stimulation of glucose-induced insulin secretion from MIN6 cells by arginine, weaker stimulation by ornithine, but inhibitory effects of dopamine. Glucose 31-38 insulin Homo sapiens 47-54 33998292-0 2021 Exercise Effect on Insulin-Dependent and Insulin-Independent Glucose Utilization in Healthy and Type 1 Diabetes Individuals. Glucose 61-68 insulin Homo sapiens 41-48 34003539-2 2021 The aim of this real-life study was to investigate the patient profiles in which IGlarU300 and IDegAsp were preferred and the insulin combinations after which each of them were mostly used, and also to analyze the effect of these two insulin analogs on blood glucose regulation and hypoglycemia. Glucose 259-266 insulin Homo sapiens 234-241 34003799-7 2021 During hypoglycemia, glucagon secretion in CPEP was two times higher than SAL, which increased net hepatic glucose output and reduced the amount of exogenous glucose required to maintain glycemia. Glucose 107-114 insulin Homo sapiens 43-47 34004183-12 2021 Negative association was found between potential overtreatment and use of insulin/combined insulin and oral glucose-lowering medication. Glucose 108-115 insulin Homo sapiens 74-81 34004183-12 2021 Negative association was found between potential overtreatment and use of insulin/combined insulin and oral glucose-lowering medication. Glucose 108-115 insulin Homo sapiens 91-98 33995841-10 2021 The dextrose-containing fluids should accompany intravenous insulin to correct metabolic acidosis, ketonemia and to avoid hypoglycemia. Glucose 4-12 insulin Homo sapiens 60-67 33995848-1 2021 Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing beta-cells of the pancreatic islets by autoreactive T cells, leading to high blood glucose levels and severe long-term complications. Glucose 184-191 insulin Homo sapiens 83-90 33995848-2 2021 The typical treatment indicated in T1D is exogenous insulin administration, which controls glucose levels; however, it does not stop the autoimmune process. Glucose 91-98 insulin Homo sapiens 52-59 33995849-2 2021 Among the several metabolic and growth-promoting effects of insulin, insulin resistance is defined as an attenuated effect of insulin on glucose metabolism, primarily the limited export of blood glucose into skeletal muscle and adipose tissue. Glucose 137-144 insulin Homo sapiens 69-76 34055806-2 2021 In this study, we improved a previous strategy to produce beta cells using extracellular vesicles (EVs) derived from mature beta cells and differentiated beta cells from iPSCs (i-Beta cells), which secreted insulin under glucose stimulation in vitro and ameliorated hyperglycemia in vivo. Glucose 221-228 insulin Homo sapiens 207-214 33977536-5 2022 Some, but not all, in vitro work demonstrate positive effects on glucose-stimulated insulin secretion, which is more marked at higher kisspeptin concentrations. Glucose 65-72 insulin Homo sapiens 84-91 33977536-6 2022 Acute and chronic in vivo rodent, non-human primate and human studies reveal enhancement of glucose-stimulated insulin secretion in response to pharmacological doses of kisspeptin. Glucose 92-99 insulin Homo sapiens 111-118 33977536-8 2022 Kisspeptin influences metabolism by modulating energy expenditure (including brown adipose tissue thermogenesis and locomotor activity), reducing food intake in the first few hours following central or peripheral administration, regulating fat mass and increasing glucose-stimulated insulin secretion in rodents and/or humans. Glucose 264-271 insulin Homo sapiens 283-290 33896337-3 2021 Activation of GPR119 stimulates the secretion of glucagon-like peptide-1 (GLP-1) in the intestinal tract and glucose-dependent release of insulin in pancreatic beta-cells. Glucose 109-116 insulin Homo sapiens 138-145 33965768-8 2021 RESULTS: As a mixture, higher urinary phthalate biomarker concentrations during pregnancy were associated with post-delivery concentrations of plasma glucose (interquartile range [IQR] difference: 0.13 SD, 95%CrI: 0.05, 0.20), plasma insulin (IQR difference: 0.06 SD, 95%CrI: -0.02, 0.14), HOMA-IR (IQR difference: 0.08 SD, 95% CrI: 0.01, 0.16), and HbA1c% (IQR difference: 0.15 SD, 95%CrI: 0.05, 0.24). Glucose 150-157 insulin Homo sapiens 234-241 33957017-0 2021 Faster lipid beta-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1alpha in human podocytes. Glucose 88-95 insulin Homo sapiens 104-111 33949213-1 2021 Hypoxia-induced insulin resistance appears to suppress exogenous glucose oxidation during metabolically-matched aerobic exercise during acute (<8-h) high-altitude (HA) exposure. Glucose 65-72 insulin Homo sapiens 16-23 33949213-12 2021 Coupling global metabolomics and glucose kinetic data suggest that the underlying cause for diminished exogenous glucose oxidative capacity during aerobic exercise is acute hypoxia-mediated peripheral insulin resistance. Glucose 33-40 insulin Homo sapiens 201-208 33949213-12 2021 Coupling global metabolomics and glucose kinetic data suggest that the underlying cause for diminished exogenous glucose oxidative capacity during aerobic exercise is acute hypoxia-mediated peripheral insulin resistance. Glucose 113-120 insulin Homo sapiens 201-208 33951176-2 2021 The biological activity of FGF21 was first shown to induce insulin independent glucose uptake in adipocytes through the GLUT1 transporter. Glucose 79-86 insulin Homo sapiens 59-66 33951176-5 2021 In this paper, we revisited the original finding and found that insulin independent glucose uptake in adipocytes is preserved in the presence of an insulin receptor antagonist. Glucose 84-91 insulin Homo sapiens 64-71 33951176-5 2021 In this paper, we revisited the original finding and found that insulin independent glucose uptake in adipocytes is preserved in the presence of an insulin receptor antagonist. Glucose 84-91 insulin Homo sapiens 148-155 33965231-6 2021 Cellular limitations to plasticity include the balance between beta-cell proliferation and apoptosis, the appearance of beta-cell oxidative stress, impaired glucose-stimulated insulin secretion, and sensitivity to circulating cytokines and responsiveness to programmed death receptor-1. Glucose 157-164 insulin Homo sapiens 176-183 33949379-2 2021 Measuring glucose concentration enables patient-specific insulin therapy, and is essential to reduce the severity of the disease, potential complications, and related mortalities. Glucose 10-17 insulin Homo sapiens 57-64 33948909-3 2021 METHODS: On the basis of data collected from a literature review, the cost of glucose monitoring was modelled for patients with T2DM on a basal-bolus insulin regimen. Glucose 78-85 insulin Homo sapiens 150-157 34017831-2 2021 The global gene expression differences between paired immature and mature beta cells have been studied, but the dynamics of transcriptional events, correlating with temporal development of glucose-stimulated insulin secretion (GSIS), remain to be fully defined. Glucose 189-196 insulin Homo sapiens 208-215 34017831-8 2021 In particular, beta cells developed robust insulin secretion at high glucose several days after birth, coincident with the establishment of glucose-induced calcium influx. Glucose 69-76 insulin Homo sapiens 43-50 34017831-8 2021 In particular, beta cells developed robust insulin secretion at high glucose several days after birth, coincident with the establishment of glucose-induced calcium influx. Glucose 140-147 insulin Homo sapiens 43-50 33444083-1 2021 Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder, characterized by persistent elevation of blood glucose either due to insulin resistance or insulin insufficiency. Glucose 104-111 insulin Homo sapiens 126-133 33903257-4 2021 We show that acute blockade of the MFGE8/beta5 pathway enhances while acute augmentation dampens insulin-stimulated glucose uptake. Glucose 116-123 insulin Homo sapiens 97-104 33676026-2 2021 IR is characterized by a marked reduction in the magnitude and/or delayed onset of insulin to stimulate glucose disposal. Glucose 104-111 insulin Homo sapiens 83-90 33676026-3 2021 This condition is due to defects in one or several intracellular intermediates of the insulin signaling cascade, ranging from insulin receptor substrate (IRS) inactivation to reduced glucose phosphorylation and oxidation. Glucose 183-190 insulin Homo sapiens 86-93 33580322-1 2021 Recurring insulin-induced hypoglycemia (RIIH) in males correlates with maladaptive glucose counter-regulatory collapse and acclimated expression of ventromedial hypothalamic nucleus (VMN) nitric oxide (NO) and gamma-aminobutyric acid (GABA) metabolic transmitter biomarkers, e.g., neuronal nitric oxide synthase (nNOS) and glutamate decarboxylase65/67 (GAD). Glucose 83-90 insulin Homo sapiens 10-17 32497708-1 2021 BACKGROUND: - This study aimed to assess the efficacy of insulin pumps with automated predictive low-glucose insulin suspension in a real-world setting compared with stand-alone flash glucose monitoring (FGM). Glucose 101-108 insulin Homo sapiens 57-64 32529519-0 2021 Using the Secretion Ratios of Insulin and C-peptide During the 2-h Oral Glucose Tolerance Test to Diagnose Insulinoma. Glucose 72-79 insulin Homo sapiens 30-37 33454830-1 2021 Present-day treatments for people that are insulin dependent require multiple insulin injections, sometimes with an insulin pump, coupled with regular blood glucose monitoring. Glucose 157-164 insulin Homo sapiens 43-50 33502032-1 2021 AIMS: To understand the relationship between insulin resistance (IR), assessed as estimated Glucose Disposal Rate (eGDR) and microvascular/macrovascular complications in people with type 1 diabetes (T1D). Glucose 92-99 insulin Homo sapiens 45-52 33511440-0 2021 Heterogeneity in insulin-stimulated glucose uptake among different muscle groups in healthy lean people and people with obesity. Glucose 36-43 insulin Homo sapiens 17-24 33511440-2 2021 The goal of the study was to evaluate the relationships among muscle fibre type composition, perfusion and insulin-stimulated glucose uptake rates in healthy, lean people and people with obesity. Glucose 126-133 insulin Homo sapiens 107-114 33511440-3 2021 METHODS: We measured insulin-stimulated whole-body glucose disposal and glucose uptake and perfusion rates in five major muscle groups (erector spinae, obliques, rectus abdominis, hamstrings, quadriceps) in 15 healthy lean people and 37 people with obesity by using the hyperinsulinaemic-euglycaemic clamp procedure in conjunction with [2H]glucose tracer infusion (to assess whole-body glucose disposal) and positron emission tomography after injections of [15O]H2O (to assess muscle perfusion) and [18F]fluorodeoxyglucose (to assess muscle glucose uptake). Glucose 51-58 insulin Homo sapiens 21-28 33511440-7 2021 In addition, insulin-stimulated whole-body glucose disposal relative to fat-free mass provides a reliable index of muscle glucose uptake rate. Glucose 43-50 insulin Homo sapiens 13-20 33550441-3 2021 The nascent understanding of the link between non-physiologically regulated glucose levels and these complications led to the development of new treatment tools in the 1970s and 1980s that facilitated the delivery of insulin to achieve glucose levels closer to non-diabetic levels. Glucose 76-83 insulin Homo sapiens 217-224 33550441-3 2021 The nascent understanding of the link between non-physiologically regulated glucose levels and these complications led to the development of new treatment tools in the 1970s and 1980s that facilitated the delivery of insulin to achieve glucose levels closer to non-diabetic levels. Glucose 236-243 insulin Homo sapiens 217-224 33550443-1 2021 Hypoglycaemia (blood glucose concentration below the normal range) has been recognised as a complication of insulin treatment from the very first days of the discovery of insulin, and remains a major concern for people with diabetes, their families and healthcare professionals today. Glucose 21-28 insulin Homo sapiens 108-115 33550443-1 2021 Hypoglycaemia (blood glucose concentration below the normal range) has been recognised as a complication of insulin treatment from the very first days of the discovery of insulin, and remains a major concern for people with diabetes, their families and healthcare professionals today. Glucose 21-28 insulin Homo sapiens 171-178 33589845-7 2021 HPTP1B is a key regulator at an early stage in the signalling cascade of the insulin hormone for glucose uptake into cells. Glucose 97-104 insulin Homo sapiens 77-84 32081036-2 2021 There are limited data to guide the optimal insulin profile to rapidly achieve target glucose and minimize healthcare professional input. Glucose 86-93 insulin Homo sapiens 44-51 33752962-9 2021 Fasting and 2-h glucose were associated with early insulin and C-peptide responses (range: r - 0.37 to -0.40) as well as late insulin and total insulin and C-peptide responses (range: r - 0.50 to -0.60). Glucose 16-23 insulin Homo sapiens 51-58 33336396-7 2021 The insulin mediated glucose uptake is also stimulated by Wnt3a at both basal and insulin resistant states. Glucose 21-28 insulin Homo sapiens 4-11 33336396-7 2021 The insulin mediated glucose uptake is also stimulated by Wnt3a at both basal and insulin resistant states. Glucose 21-28 insulin Homo sapiens 82-89 30045350-8 2021 When blood glucose falls, 53% gave glucose and 47% reduced insulin. Glucose 11-18 insulin Homo sapiens 59-66 33544449-7 2021 Islets exposed to acute hypoxia (1-2% O2 ) or to inflammatory cytokines (including IFN-gamma, TNF-alpha, IL-B) in vitro undergo apoptosis and a rapid decline in glucose-stimulated insulin secretion. Glucose 161-168 insulin Homo sapiens 180-187 33930258-5 2021 These wearable glucose sensors can be integrated with implantable drug delivery systems, including an insulin pump, glucose responsive insulin release implant, and islets transplantation, to form self-regulating closed-loop systems. Glucose 15-22 insulin Homo sapiens 102-109 33995278-1 2021 Diabetes mellitus (DM) is a metabolic disease, now prevalent worldwide, which is characterized by a relative or absolute lack of insulin secretion leading to chronically increased blood glucose levels. Glucose 186-193 insulin Homo sapiens 129-136 33914316-6 2021 Patients treated with insulin pumps with CGM and additional functions of automatic insulin delivery suspension on low glucose level (SLG) or predictive low glucose suspend (PLGS) during the third trimester and after pregnancy achieved a significantly lower HbA1c than the other CSII patients. Glucose 118-125 insulin Homo sapiens 22-29 33914316-6 2021 Patients treated with insulin pumps with CGM and additional functions of automatic insulin delivery suspension on low glucose level (SLG) or predictive low glucose suspend (PLGS) during the third trimester and after pregnancy achieved a significantly lower HbA1c than the other CSII patients. Glucose 118-125 insulin Homo sapiens 83-90 33914316-6 2021 Patients treated with insulin pumps with CGM and additional functions of automatic insulin delivery suspension on low glucose level (SLG) or predictive low glucose suspend (PLGS) during the third trimester and after pregnancy achieved a significantly lower HbA1c than the other CSII patients. Glucose 156-163 insulin Homo sapiens 22-29 33915598-9 2021 The delivery of hospital-to-home transitional self-monitoring blood glucose behaviour was more likely for individuals with higher pre-discharge self-efficacy, higher post-discharge self-efficacy, more attention to pre-hospitalization glycaemic status and post-discharge insulin usage and those without an insensitive foot. Glucose 68-75 insulin Homo sapiens 270-277 33933677-2 2021 However, peripheral dopamine directly modulates glucose uptake in insulin-sensitive tissues and lipid metabolism in adipose tissue (AT). Glucose 48-55 insulin Homo sapiens 66-73 33390422-5 2021 Following a standardized meal test, ETD for change from baseline in postprandial glucose (PPG) increment at 1 hour was -16.91 mg/dL (-32.15;-1.68) for mealtime fast-acting insulin aspart and 40.16 mg/dL (25.46;54.87) for post-meal fast-acting insulin aspart, both versus insulin aspart. Glucose 81-88 insulin Homo sapiens 172-179 33996873-6 2021 Overall, the isoenergetic substitution of fructose for glucose resulted in a statistically significant but clinically irrelevant reduction in fasting blood glucose, insulin, and triglyceride concentrations. Glucose 55-62 insulin Homo sapiens 165-172 33907279-0 2021 Log-linear relationship between endogenous insulin secretion and glycemic variability in patients with type 2 diabetes on continuous glucose monitoring. Glucose 133-140 insulin Homo sapiens 43-50 33905087-12 2021 Sub-group meta-analyses identified that metabolic state modified glucose and insulin responses, in which aerobic exercise significantly decreased glucose (mean difference: - 0.27 mmol/L; 95% CI, - 0.55 to - 0.00 mmol/L; P = 0.049; I2: 89.72%, large heterogeneity) and insulin (mean difference: - 42.63 pmol/L; 95% CI, - 66.18 to - 19.09 pmol/L; P < 0.001; I2: 81.29%, large heterogeneity) concentrations in the postprandial but not fasted state. Glucose 146-153 insulin Homo sapiens 77-84 33895917-4 2022 Glucose increase is the principal determinant of GLP-1 increase with the consequent stimulation of insulin secretion, the latter balanced by a paradoxical glucagon increase that stimulates EGP to prevent hypoglycaemia. Glucose 0-7 insulin Homo sapiens 99-106 33887969-0 2021 The Triglyceride-Glucose Index, a Predictor of Insulin Resistance, Is Associated With Subclinical Atherosclerosis. Glucose 17-24 insulin Homo sapiens 47-54 33967958-11 2021 Under simulated conditions of the IGT stage (8.3 mmol/L glucose + 50 ng/mL insulin), the inhibitory effect of high insulin concentration on miR-21 expression in the cells attenuated the activation by high glucose concentration, resulting in the downregulation of miR-21, upregulation of ET-1 and downregulation of NO secretion. Glucose 205-212 insulin Homo sapiens 75-82 33967958-11 2021 Under simulated conditions of the IGT stage (8.3 mmol/L glucose + 50 ng/mL insulin), the inhibitory effect of high insulin concentration on miR-21 expression in the cells attenuated the activation by high glucose concentration, resulting in the downregulation of miR-21, upregulation of ET-1 and downregulation of NO secretion. Glucose 205-212 insulin Homo sapiens 115-122 33967961-2 2021 In particular, beta cells produce and secrete insulin, an essential hormone regulating glucose uptake and metabolism. Glucose 87-94 insulin Homo sapiens 46-53 33830730-10 2021 Insulin loaded into MSN-NH2@COOH/CPP5 reduced the diabetic rats" blood glucose level by nearly 50%. Glucose 71-78 insulin Homo sapiens 0-7 33894345-1 2021 OBJECTIVE: Frequent, usually hourly, finger-prick capillary blood glucose measurement is standard care, used to drive insulin infusion rates for inpatients being resuscitated from diabetic ketoacidosis (DKA). Glucose 66-73 insulin Homo sapiens 118-125 33894345-10 2021 Minor differences in predicted insulin infusion rates were noted in 2/10 patients at higher glucose concentrations and may relate to the lag in change in glucose in the interstitial space, but it is likely that standard frequent insulin infusion rate adjustments would prevent any alteration in clinical outcomes. Glucose 92-99 insulin Homo sapiens 31-38 33894345-10 2021 Minor differences in predicted insulin infusion rates were noted in 2/10 patients at higher glucose concentrations and may relate to the lag in change in glucose in the interstitial space, but it is likely that standard frequent insulin infusion rate adjustments would prevent any alteration in clinical outcomes. Glucose 154-161 insulin Homo sapiens 31-38 33884531-6 2021 Homeostatic model assessment of insulin resistance was determined from fasting insulin and glucose. Glucose 91-98 insulin Homo sapiens 32-39 34027219-1 2021 Introduction: We aimed to see whether insulin glargine U300 can provide better blood glucose control while reducing hypoglycaemia in a more homogeneous population compared to previous studies. Glucose 85-92 insulin Homo sapiens 38-45 33866404-10 2021 What is Known: Insulin preparation in NICUs is a risky task because it is a two-step preparation Diluted in dextrose, insulin aspart is unstable, with formation of potentially toxic glycated derivatives What is New: This work proposes a new insulin therapy protocol validated by HPLC-UV for NICU allowing suppression of the formation of glycated insulin, to significantly reduce deviations from theoretical concentrations and to limit adsorption phenomena This protocol is validated in case of co-infusion of parenteral nutrition. Glucose 112-120 insulin Homo sapiens 17-24 33866404-10 2021 What is Known: Insulin preparation in NICUs is a risky task because it is a two-step preparation Diluted in dextrose, insulin aspart is unstable, with formation of potentially toxic glycated derivatives What is New: This work proposes a new insulin therapy protocol validated by HPLC-UV for NICU allowing suppression of the formation of glycated insulin, to significantly reduce deviations from theoretical concentrations and to limit adsorption phenomena This protocol is validated in case of co-infusion of parenteral nutrition. Glucose 112-120 insulin Homo sapiens 247-254 33866404-10 2021 What is Known: Insulin preparation in NICUs is a risky task because it is a two-step preparation Diluted in dextrose, insulin aspart is unstable, with formation of potentially toxic glycated derivatives What is New: This work proposes a new insulin therapy protocol validated by HPLC-UV for NICU allowing suppression of the formation of glycated insulin, to significantly reduce deviations from theoretical concentrations and to limit adsorption phenomena This protocol is validated in case of co-infusion of parenteral nutrition. Glucose 112-120 insulin Homo sapiens 247-254 33865915-7 2021 A first clinical study and numerous pre-clinical data show the potential, but also the challenges of designing an insulin that quickly reacts to blood glucose changes and prevents hypoglycaemia and pronounced hyperglycaemia. Glucose 151-158 insulin Homo sapiens 114-121 33865916-3 2021 Insulin is required for both types of diabetes when other means of controlling glucose are insufficient. Glucose 79-86 insulin Homo sapiens 0-7 33937238-3 2021 The characteristics of metabolic syndrome (MetS), including obesity, glucose intolerance, dyslipidemia and hypertension, may activate multiple mechanisms, such as insulin resistance, oxidative stress and inflammatory pathways, thereby contributing to increased risks of developing atherosclerosis and T2DM. Glucose 69-76 insulin Homo sapiens 163-170 33845179-5 2021 MAJOR CONCLUSIONS: While brain insulin signaling plays only a small role in central nervous system glucose regulation, it has a significant impact on the metabolic health of the brain. Glucose 99-106 insulin Homo sapiens 31-38 33855427-1 2021 Diabetes mellitus is a chronic disease characterized by high glucose levels (hyperglycemia) due to metabolic disorders that prevent patients from producing sufficient amounts of insulin. Glucose 61-68 insulin Homo sapiens 178-185 33855800-1 2021 Women with polycystic ovary syndrome (PCOS) exhibit reduced muscle insulin-mediated glucose uptake, potentially attributed to altered muscle mass; however, this is inconclusive. Glucose 84-91 insulin Homo sapiens 67-74 33844157-5 2021 The primary nutrient that stimulates insulin secretion is glucose, but also, there are multiple dietary and hormonal factors influencing that response. Glucose 58-65 insulin Homo sapiens 37-44 33844157-6 2021 Many studies of the physiology of beta-cells have highlighted the importance of glucose, fructose, amino acids, and free fatty acids on insulin secretion. Glucose 80-87 insulin Homo sapiens 136-143 33837820-2 2021 There is a growing number of GDM patients requiring only a single dose of basal insulin at night to achieve glucose control. Glucose 109-116 insulin Homo sapiens 81-88 33837820-5 2021 The aim of this study was to investigate the impact of such lifestyle factors on insulin requirement in GDM patients, in particular on long-acting insulin to control fasting glucose levels. Glucose 174-181 insulin Homo sapiens 81-88 33837820-5 2021 The aim of this study was to investigate the impact of such lifestyle factors on insulin requirement in GDM patients, in particular on long-acting insulin to control fasting glucose levels. Glucose 174-181 insulin Homo sapiens 147-154 33600878-9 2021 Another important and original aspect of the reported work is that revelation that the pH, lactate and glucose levels increased under the stress conditions and the changes tended to be more pronounced in diabetic rats (both untreated and long-acting insulin-treated) compared to normal rats. Glucose 103-110 insulin Homo sapiens 250-257 33600878-10 2021 Long-acting insulin treatment was shown to shorten the duration of the pH and glucose changes in response to stress when compared to the untreated diabetic rats. Glucose 78-85 insulin Homo sapiens 12-19 33839290-3 2021 Glucagon-like peptide-1 receptor (GLP-1R) is the receptor of GLP-1, an incretin hormone that causes insulin secretion in a glucose-dependent manner. Glucose 123-130 insulin Homo sapiens 100-107 33918552-10 2021 CONCLUSION: The results of this study seem to point to a possible difference in the peripheral use of glucose between patients with bulbar onset ALS and spinal onset ALS, who appear to have possible insulin resistance. Glucose 102-109 insulin Homo sapiens 199-206 33839084-2 2021 The triglyceride-glucose index (TyG), a measure of metabolic dysfunction, is associated with metabolic syndrome and insulin resistance, but its relationship to lung health is unknown. Glucose 17-24 insulin Homo sapiens 116-123 33369112-14 2021 CONCLUSION: Agonist-independent and glucagon-stimulated GLP1R signalling in beta-cells contributes to basal and glucose-induced cAMP production and insulin secretion. Glucose 112-119 insulin Homo sapiens 148-155 34012367-5 2021 Five had hyperglycemia (1 with grade 3) with fasting glucose levels of up to 450 mg/dL that required hospitalization and insulin therapy. Glucose 53-60 insulin Homo sapiens 121-128 33413911-11 2021 Excess fructose intake can impair insulin-induced suppression of glucose production, stimulate de novo lipogenesis, and increase intrahepatic and blood triglyceride concentrations. Glucose 65-72 insulin Homo sapiens 34-41 33745582-1 2021 BACKGROUND & AIMS: It is believed that diets high in glycemic index (GI), glycemic load (GL), Insulin index (II), and Insulin load (IL) are associated with the increased risks of certain cancers through increasing serum glucose or insulin levels. Glucose 220-227 insulin Homo sapiens 118-125 33185480-1 2021 BACKGROUND: The Medtronic MiniMed 670G system adjusts basal insulin delivery in response to continuous glucose monitoring levels and is already in use in clinical practice. Glucose 104-111 insulin Homo sapiens 61-68 33336888-4 2021 Using hyperinsulinaemic clamp technique, plasma glucose (PG) levels were reduced with either a rapid or slow decline rate while maintaining fixed insulin levels. Glucose 48-55 insulin Homo sapiens 11-18 33563655-0 2021 Remote Continuous Glucose Monitoring With a Computerized Insulin Infusion Protocol for Critically Ill Patients in a COVID-19 Medical ICU: Proof of Concept. Glucose 18-25 insulin Homo sapiens 57-64 33741353-0 2021 A standardized glucose-insulin-potassium infusion protocol in surgical patients: use of real clinical data from a clinical data warehouse. Glucose 15-22 insulin Homo sapiens 23-30 33741353-1 2021 AIMS: We evaluated the clinical usefulness of a new unified glucose-insulin-potassium (GIK) regimen in a general surgical department. Glucose 60-67 insulin Homo sapiens 68-75 33660172-2 2021 Due to the alarming number of patients, there is great need to therapies targeting functions which can help in maintaining the homeostasis of glucose levels and improving insulin sensitivity. Glucose 142-149 insulin Homo sapiens 171-178 32706490-9 2021 Decreased number of days hospitalized and the use of intensive glucose control with regular insulin were associated with decreased odds of developing hyperglycemia. Glucose 63-70 insulin Homo sapiens 92-99 34034759-10 2021 CONCLUSION: Overall, the present investigation demonstrates that calystegines from Hyoscyamus albus provide cytoprotection to the HepG2 cells against insulin/glucose induced insulin resistance and apoptosis due to the regulation of SIRT1/Foxo1/G6PC/mTOR and NF-kappaB/JNK/TLR4 signaling pathways. Glucose 158-165 insulin Homo sapiens 174-181 34017668-9 2021 Significant reduction in first-phase insulin secretion, as measured as insulinogenic (0-30) index, was only observed among two-hour glucose categories, not among the fasting glucose categories. Glucose 132-139 insulin Homo sapiens 37-44 34017668-9 2021 Significant reduction in first-phase insulin secretion, as measured as insulinogenic (0-30) index, was only observed among two-hour glucose categories, not among the fasting glucose categories. Glucose 174-181 insulin Homo sapiens 37-44 33991342-6 2021 Homeostatic model assessment of insulin resistance was determined from fasting glucose/insulin. Glucose 79-86 insulin Homo sapiens 32-39 33992101-4 2021 Both patients received aggressive insulin infusion and subcutaneous insulin therapy to obtain adequate glucose management. Glucose 103-110 insulin Homo sapiens 68-75 33988040-1 2021 Type II diabetes mellitus (T2DM) is a metabolic disorder that is characterized by chronically elevated glucose caused by insulin resistance. Glucose 103-110 insulin Homo sapiens 121-128 33693827-7 2021 Though, LDL cholesterol levels were positively associated with insulin clearance assessed from C-peptide and insulin concentrations, both in the fasting state and post glucose load (p<0.0001, ss=0.09 and p<0.0001, ss=0.06, respectively). Glucose 168-175 insulin Homo sapiens 63-70 34055765-0 2021 A Microfluidic Hanging-Drop-Based Islet Perifusion System for Studying Glucose-Stimulated Insulin Secretion From Multiple Individual Pancreatic Islets. Glucose 71-78 insulin Homo sapiens 90-97 34055765-1 2021 Islet perifusion systems can be used to monitor the highly dynamic insulin release of pancreatic islets in glucose-stimulated insulin secretion (GSIS) assays. Glucose 107-114 insulin Homo sapiens 67-74 34055765-1 2021 Islet perifusion systems can be used to monitor the highly dynamic insulin release of pancreatic islets in glucose-stimulated insulin secretion (GSIS) assays. Glucose 107-114 insulin Homo sapiens 126-133 34055765-5 2021 Upon glucose stimulation, reproducible biphasic insulin release was simultaneously observed from all islets in the system. Glucose 5-12 insulin Homo sapiens 48-55 34023734-6 2021 Clozapine dose-dependently decreased the glucose infusion rate, reflecting pronounced insulin resistance. Glucose 41-48 insulin Homo sapiens 86-93 34044354-0 2021 The in vivo Tetrahymena thermophila extracellular glucose drop assay for characterization of mammalian insulin activity. Glucose 50-57 insulin Homo sapiens 103-110 34015585-4 2021 Nonetheless, new evidences are emerging to support insulin-mediated aggressive glucose-lowering treatment as a possible trigger of high mortality rate in diabetic COVID-19 patients, putting the clinician in a confounding and difficult dilemma for the treatment of COVID-19 patients with metabolic comorbidities. Glucose 79-86 insulin Homo sapiens 51-58 34015585-7 2021 Especially, we provide a balanced overview on the clinical application of glucose-lowering drugs (insulin and metformin), angiotensin-converting-enzyme inhibitors, and angiotensin receptor blockers. Glucose 74-81 insulin Homo sapiens 98-105 33955251-3 2021 To avoid lowering glucose levels toward too low levels, the algorithms used to calculate the insulin dose have to take a number of other factors into account. Glucose 18-25 insulin Homo sapiens 93-100 33965365-2 2021 This protein has been shown to contribute to the glucose-dependent regulation of insulin secretion in pancreatic islets. Glucose 49-56 insulin Homo sapiens 81-88 33965365-10 2021 Non-G allele carriers showed a significant improvement in fasting glucose levels (AA vs. AG + GG) (-6.1 +- 1.4 md/dL vs. -1.2 +- 0.7 mg/dl; p = 0.01), fasting insulin levels (-3.6 +- 0.2 mU/L vs. -1.3 +- 0.6 mU/L; p = 0.02) and HOMA-IR (-1.2 +- 0.2 units vs. -0.3 +- 0.2 units; p = 0.01). Glucose 66-73 insulin Homo sapiens 159-166 33953224-7 2021 Furthermore, knockdown of CD82 expression by siRNA or inhibition of CD82 by monoclonal antibodies in NGN3+ cells suppressed the function of beta cells with glucose-stimulated insulin secretion, suggesting that CD82 plays a role in maturation of EP cells to beta cells. Glucose 156-163 insulin Homo sapiens 175-182 33065743-6 2021 Women in the severe insulin resistance group demonstrated evidence of suboptimal glycemic control as evidenced by higher mean hemoglobin A1c (HbA1c) values (7.2 [ +- 1.1] vs. 6.6 [ +- 1.3%], p = 0.003), higher mean fasting (104.0 [ +- 17.4] vs. 95.2 [ +- 11.7 mg/dL], p < 0.001) and postprandial glucose values (132.4 [ +- 17.2] vs. 121.9 [ +- 16.9 mg/dL]), p < 0.001), and a higher percentage of total glucose values that were elevated above targets (37.7 [95% confidence interval (CI): 26.8-50] vs. 25.6 [95% CI: 13.3-41.3%], p < 0.001). Glucose 300-307 insulin Homo sapiens 20-27 33065743-6 2021 Women in the severe insulin resistance group demonstrated evidence of suboptimal glycemic control as evidenced by higher mean hemoglobin A1c (HbA1c) values (7.2 [ +- 1.1] vs. 6.6 [ +- 1.3%], p = 0.003), higher mean fasting (104.0 [ +- 17.4] vs. 95.2 [ +- 11.7 mg/dL], p < 0.001) and postprandial glucose values (132.4 [ +- 17.2] vs. 121.9 [ +- 16.9 mg/dL]), p < 0.001), and a higher percentage of total glucose values that were elevated above targets (37.7 [95% confidence interval (CI): 26.8-50] vs. 25.6 [95% CI: 13.3-41.3%], p < 0.001). Glucose 408-415 insulin Homo sapiens 20-27 33719586-2 2021 In the last 100 years, significant pharmacological advances took place in the field of insulin therapy, bringing closer the goal of optimal glucose control along with decreased diabetes-related complications. Glucose 140-147 insulin Homo sapiens 87-94 32056196-2 2021 By tightly coupling nutrient sensing and granule exocytosis beta-cells adjust the secretion of insulin to the circulating blood glucose levels. Glucose 128-135 insulin Homo sapiens 95-102 32056196-4 2021 Mitochondria play a crucial role in beta-cell during nutrient stimulation, linking the metabolism of glucose and other secretagogues to the generation of signals that promote insulin secretion. Glucose 101-108 insulin Homo sapiens 175-182 33107758-1 2021 The Ambulatory Glucose Profile (AGP) and the frequency distribution for glucose by ranges are well established as standard methods for display, analysis and interpretation of glucose data arising from self-monitoring, continuous glucose monitoring and automated insulin delivery systems. Glucose 72-79 insulin Homo sapiens 262-269 33107758-1 2021 The Ambulatory Glucose Profile (AGP) and the frequency distribution for glucose by ranges are well established as standard methods for display, analysis and interpretation of glucose data arising from self-monitoring, continuous glucose monitoring and automated insulin delivery systems. Glucose 175-182 insulin Homo sapiens 262-269 33107758-1 2021 The Ambulatory Glucose Profile (AGP) and the frequency distribution for glucose by ranges are well established as standard methods for display, analysis and interpretation of glucose data arising from self-monitoring, continuous glucose monitoring and automated insulin delivery systems. Glucose 175-182 insulin Homo sapiens 262-269 33710398-1 2021 Insulin replacement therapy for diabetes mellitus seeks to minimise excursions in blood glucose concentration above or below the therapeutic range (hyper- or hypoglycaemia). Glucose 88-95 insulin Homo sapiens 0-7 33710398-3 2021 Such "smart" systems or insulin analogues seek to provide hormonal activity proportional to blood glucose levels without external monitoring. Glucose 98-105 insulin Homo sapiens 24-31 33725276-1 2021 INTRODUCTION: In persons with type 1 diabetes (T1D) insulin dosing can be adjusted based on trend arrows derived from continuous glucose monitoring (CGM). Glucose 129-136 insulin Homo sapiens 52-59 33730337-1 2021 INTRODUCTION: Basal-bolus (BB) and premixed insulin regimens may lower fasting plasma glucose (FPG) and postprandial plasma glucose (PPG), but are complex to use and associated with weight gain and hypoglycaemia. Glucose 86-93 insulin Homo sapiens 44-51 33730337-1 2021 INTRODUCTION: Basal-bolus (BB) and premixed insulin regimens may lower fasting plasma glucose (FPG) and postprandial plasma glucose (PPG), but are complex to use and associated with weight gain and hypoglycaemia. Glucose 124-131 insulin Homo sapiens 44-51 33579639-0 2021 The triglyceride / glucose index as an insulin resistance marker in the pediatric population and its relation to eating habits and physical activity. Glucose 19-26 insulin Homo sapiens 39-46 33579639-1 2021 INTRODUCTION: To examine the triglyceride/glucose index (TyG) as an insulin resistance marker in obese children and adolescents and its relation to clinical and biochemical parameters, body composition and lifestyle. Glucose 42-49 insulin Homo sapiens 68-75 33719017-1 2021 BACKGROUND: Intranasal insulin is a potential treatment for neurodegenerative disease shown to increase cerebral glucose uptake, reduce amyloid plaques, and improve verbal memory in cognitively impaired as well as healthy adults. Glucose 113-120 insulin Homo sapiens 23-30 33693956-1 2021 Insulin resistance (IR) is defined as impaired insulin function, reduced glucose uptake and increased glucose production, which can result in type II diabetes, metabolic syndrome and even bone metabolic disorders. Glucose 73-80 insulin Homo sapiens 0-7 33693956-1 2021 Insulin resistance (IR) is defined as impaired insulin function, reduced glucose uptake and increased glucose production, which can result in type II diabetes, metabolic syndrome and even bone metabolic disorders. Glucose 102-109 insulin Homo sapiens 0-7 33892108-1 2021 Under type-2 diabetes, insulin resistance develops in skeletal muscles as a key defect and to study the disorder, its manifestation, and possible solution, measurement of glucose uptake is a fundamental necessity. Glucose 171-178 insulin Homo sapiens 23-30 33631146-0 2021 The MafA-target gene PPP1R1A regulates GLP1R-mediated amplification of glucose-stimulated insulin secretion in beta-cells. Glucose 71-78 insulin Homo sapiens 90-97 33631146-1 2021 The amplification of glucose-stimulated insulin secretion (GSIS) through incretin signaling is critical for maintaining physiological glucose levels. Glucose 21-28 insulin Homo sapiens 40-47 33631146-1 2021 The amplification of glucose-stimulated insulin secretion (GSIS) through incretin signaling is critical for maintaining physiological glucose levels. Glucose 134-141 insulin Homo sapiens 40-47 33737242-2 2021 Therefore, preserving beta-cell mass and stimulating insulin secretion only in response to glucose for avoiding the hypoglycemia risks, are the most state-of-the-art option for the treatment of T2D. Glucose 91-98 insulin Homo sapiens 53-60 33737242-3 2021 In this study we tested two correlated hypothesis that 1/ the endogenous peptide released from sortilin, known as PE, that stimulates insulin secretion only in response to glucose, protects beta-cells against death induced by cytokines, and 2/ Spadin and Mini-Spadin, two synthetic peptides derived from PE, that mimic the effects of PE in insulin secretion, also provide beneficial effect on beta-cells survival. Glucose 172-179 insulin Homo sapiens 134-141 34042297-9 2021 In addition, we found a positive association between insulin sensitivity and the expression of glucose transporter type 4 as well as PDH. Glucose 95-102 insulin Homo sapiens 53-60 32878567-6 2021 The maturity (compaction and creatine kinase activity), mechanical integrity (Young"s Modulus), organization (myotube orientation), and metabolic capacity (insulin-stimulated glucose-uptake) were all reduced by diabetes. Glucose 175-182 insulin Homo sapiens 156-163 32878567-7 2021 Treating constructs with adipogenic induction media increased the quantity of lipid within the diabetic TE-SkM constructs, and caused changes in construct compaction, cell orientation, and insulin-stimulated glucose uptake in both lean and diabetic samples. Glucose 208-215 insulin Homo sapiens 189-196 33947164-2 2021 Triglyceride-glucose index (TyG) is a simple marker of insulin resistance; however, it has been investigated only by two studies in OSA. Glucose 13-20 insulin Homo sapiens 55-62 33996680-3 2021 The most advanced Food and Drug Administration- and European Medicines Agency-approved devices are hybrid closed-loop (HCL) systems, which deliver insulin subcutaneously in response to glucose levels according to an automated algorithm. Glucose 185-192 insulin Homo sapiens 147-154 33967958-1 2021 Background: Impaired glucose tolerance (IGT) is an important prediabetic stage characterized by elevated concentrations of glucose and insulin in the blood. Glucose 21-28 insulin Homo sapiens 135-142 33967958-9 2021 MiR-21 was observed to play a key role by directly controlling the activation of the insulin signaling pathways when the cells were cotreated with different concentrations of insulin and glucose. Glucose 187-194 insulin Homo sapiens 85-92 33967958-11 2021 Under simulated conditions of the IGT stage (8.3 mmol/L glucose + 50 ng/mL insulin), the inhibitory effect of high insulin concentration on miR-21 expression in the cells attenuated the activation by high glucose concentration, resulting in the downregulation of miR-21, upregulation of ET-1 and downregulation of NO secretion. Glucose 56-63 insulin Homo sapiens 115-122 33417713-8 2021 MODY8-iPSC-derived beta cells were able to secrete insulin upon glucose dynamic perifusion. Glucose 64-71 insulin Homo sapiens 51-58 33879720-9 2021 Serum beta-hydroxybutyrate levels or urinalysis could be used as screening tools for euDKA in patients scheduled for emergency surgery, in order to preoperatively administer rapid fluid resuscitation and insulin infusion with dextrose solution, which should continue postoperatively along with serum beta-hydroxybutyrate monitoring. Glucose 226-234 insulin Homo sapiens 204-211 33888131-1 2021 BACKGROUND: The triglyceride-glucose index (TyG index) has been proposed as a simple and reliable alternative insulin resistance (IR) marker, while the homeostasis model assessment for IR (HOMA-IR) is the most frequently used index. Glucose 29-36 insulin Homo sapiens 110-117 33967936-2 2021 The triglyceride glucose (TYG) index has been proposed as a marker of insulin resistance. Glucose 17-24 insulin Homo sapiens 70-77 33888596-4 2021 Insulin-stimulated glucose disposal, assessed by using the hyperinsulinemic-euglycemic clamp, and skeletal muscle insulin signaling (phosphorylation of AKT and mTOR) increased after NMN supplementation, but did not change after placebo treatment. Glucose 19-26 insulin Homo sapiens 0-7 33958903-2 2021 Surreptitious hypoglycemic syndrome is the deliberate use of insulin preparations or oral hypoglycemic drugs aimed to reduce blood glucose level. Glucose 131-138 insulin Homo sapiens 61-68 33878763-0 2022 The Effect of Prandial Insulin Applied for Fat Protein Units on Postprandial Glucose Excursions in Type 1 Diabetes Patients with Insulin Pump Therapy: Results of a Randomized, Controlled, Cross-Over Study. Glucose 77-84 insulin Homo sapiens 23-30 33878763-0 2022 The Effect of Prandial Insulin Applied for Fat Protein Units on Postprandial Glucose Excursions in Type 1 Diabetes Patients with Insulin Pump Therapy: Results of a Randomized, Controlled, Cross-Over Study. Glucose 77-84 insulin Homo sapiens 129-136 33959097-1 2021 Insulin and muscle contractions mediate glucose transporter 4 (GLUT4) translocation and insertion into the plasma membrane (PM) for glucose uptake in skeletal muscles. Glucose 40-47 insulin Homo sapiens 0-7 33875484-4 2021 Insulin-naive adults (n = 205) with type 2 diabetes and HbA1c 7-10% while treated with oral glucose-lowering medications initiated once-weekly icodec titrations A (prebreakfast self-measured blood glucose target 80-130 mg/dL; adjustment +-21 units/week; n = 51), B (80-130 mg/dL; +-28 units/week; n = 51), or C (70-108 mg/dL; +-28 units/week; n = 52), or once-daily insulin glargine U100 (IGlar U100) (80-130 mg/dL; +-4 units/day; n = 51), all titrated weekly. Glucose 92-99 insulin Homo sapiens 0-7 33875484-4 2021 Insulin-naive adults (n = 205) with type 2 diabetes and HbA1c 7-10% while treated with oral glucose-lowering medications initiated once-weekly icodec titrations A (prebreakfast self-measured blood glucose target 80-130 mg/dL; adjustment +-21 units/week; n = 51), B (80-130 mg/dL; +-28 units/week; n = 51), or C (70-108 mg/dL; +-28 units/week; n = 52), or once-daily insulin glargine U100 (IGlar U100) (80-130 mg/dL; +-4 units/day; n = 51), all titrated weekly. Glucose 197-204 insulin Homo sapiens 0-7 34053833-1 2021 BACKGROUND AND AIMS: The triglyceride-glucose (TyG) index is a reliable marker of insulin resistance, which is a substantial risk factor for cardiovascular diseases. Glucose 38-45 insulin Homo sapiens 82-89 33923452-3 2021 This review summates the current knowledge, focusing in particular on the roles of Rho GEFs in the processes of glucose-stimulated insulin secretion by pancreatic beta cells and insulin-stimulated glucose uptake into skeletal muscle and adipose tissues. Glucose 112-119 insulin Homo sapiens 131-138 33923452-3 2021 This review summates the current knowledge, focusing in particular on the roles of Rho GEFs in the processes of glucose-stimulated insulin secretion by pancreatic beta cells and insulin-stimulated glucose uptake into skeletal muscle and adipose tissues. Glucose 197-204 insulin Homo sapiens 178-185 33923452-5 2021 Among the mammalian Rho GEFs, P-Rex1, Vav2, Vav3, Tiam1, Kalirin and Plekhg4 were shown to mediate the insulin-stimulated translocation of the glucose transporter GLUT4 to the plasma membrane and/or insulin-stimulated glucose uptake in skeletal muscle or adipose tissue. Glucose 143-150 insulin Homo sapiens 103-110 33923452-5 2021 Among the mammalian Rho GEFs, P-Rex1, Vav2, Vav3, Tiam1, Kalirin and Plekhg4 were shown to mediate the insulin-stimulated translocation of the glucose transporter GLUT4 to the plasma membrane and/or insulin-stimulated glucose uptake in skeletal muscle or adipose tissue. Glucose 143-150 insulin Homo sapiens 199-206 33923452-5 2021 Among the mammalian Rho GEFs, P-Rex1, Vav2, Vav3, Tiam1, Kalirin and Plekhg4 were shown to mediate the insulin-stimulated translocation of the glucose transporter GLUT4 to the plasma membrane and/or insulin-stimulated glucose uptake in skeletal muscle or adipose tissue. Glucose 218-225 insulin Homo sapiens 103-110 33923452-5 2021 Among the mammalian Rho GEFs, P-Rex1, Vav2, Vav3, Tiam1, Kalirin and Plekhg4 were shown to mediate the insulin-stimulated translocation of the glucose transporter GLUT4 to the plasma membrane and/or insulin-stimulated glucose uptake in skeletal muscle or adipose tissue. Glucose 218-225 insulin Homo sapiens 199-206 33923452-6 2021 The Rho GEFs P-Rex1, Vav2, Tiam1 and beta-PIX were found to control the glucose-stimulated release of insulin by pancreatic beta cells. Glucose 72-79 insulin Homo sapiens 102-109 33855888-0 2021 Patients with Type 2 Diabetes and Residual Insulin Secretory Capacity Realize Glycemic Benefits from Real-Time Continuous Glucose Monitoring. Glucose 122-129 insulin Homo sapiens 43-50 33853374-1 2021 BACKGROUND: While we expect that patients who adjust their insulin delivery algorithms between clinic visits to have better glucose control compared to those who do not, this effect has not been quantified. Glucose 124-131 insulin Homo sapiens 59-66 33842983-14 2021 This is the first study to report CpGs near G6PC2, an important gene for regulating insulin secretion, mediating the effects of GWAS-significant SNPs on fasting glucose. Glucose 161-168 insulin Homo sapiens 84-91 33921274-1 2021 Despite the great progress made in insulin preparation and titration, many patients with diabetes are still experiencing dangerous fluctuations in their blood glucose levels. Glucose 159-166 insulin Homo sapiens 35-42 33839794-4 2021 MAIN MEASURES: Insulin sensitivity was estimated from an oral glucose tolerance test (OGTT) at baseline and year 3, and by euglycemic-hyperinsulinemic clamp at baseline only. Glucose 62-69 insulin Homo sapiens 15-22 33839794-10 2021 CONCLUSION: Both HDL containing apoC-III and apoC-III in HDL adversely affect the beneficial properties of HDL on insulin response to glucose. Glucose 134-141 insulin Homo sapiens 114-121 33840267-2 2021 METHODS: This article describes a unique EC/UC discharge insulin starter kit protocol with clinician instructions via an Electronic Medical Record (EMR) order set that includes: starting doses for insulin, a prescription for glucose monitoring supplies, and an emergent referral to diabetes education at International Diabetes Center. Glucose 225-232 insulin Homo sapiens 57-64 33836819-1 2021 BACKGROUND: Continuous glucose monitoring systems are increasingly being adopted as an alternative to self-monitoring of blood glucose (SMBG) by persons with diabetes mellitus receiving insulin therapy. Glucose 23-30 insulin Homo sapiens 186-193 33965350-4 2021 That error is probably caused by a dysmetabolic signal from the foregut, stimulated by food, that limits entry of 2-carbon fragments into the tricarboxylic acid cycle, the accumulation of lactate and, in turn, increases in glucose and insulin. Glucose 223-230 insulin Homo sapiens 235-242 33997648-4 2021 We describe a case of hypertriglyceridemia-induced acute pancreatitis in a 34-year-old nondiabetic woman treated with a reduced-dose insulin infusion that was complicated by hypoglycemic episodes requiring dextrose infusion titrations. Glucose 206-214 insulin Homo sapiens 133-140 33997648-5 2021 Empirical initiation of a higher dextrose concentration infusion with glucose level titrations should be considered to avoid hypoglycemia for nondiabetic patients treated with an insulin infusion to lower triglyceride levels. Glucose 33-41 insulin Homo sapiens 179-186 33827670-16 2021 Insulin antibodies change glucose dynamics and could increase the incidence of hypoglycemic episodes. Glucose 26-33 insulin Homo sapiens 0-7 33826918-1 2021 As the principal tissue for insulin-stimulated glucose disposal, skeletal muscle is a primary driver of whole-body glycemic control. Glucose 47-54 insulin Homo sapiens 28-35 33826918-4 2021 We discuss the discoveries that have led to our current understanding of how insulin promotes glucose uptake in muscle. Glucose 94-101 insulin Homo sapiens 77-84 33827994-0 2021 Bihormonal dysregulation of insulin and glucagon contributes to glucose intolerance development at one year post-delivery in women with gestational diabetes: a prospective cohort study using an early postpartum 75-g glucose tolerance test. Glucose 64-71 insulin Homo sapiens 28-35 33586491-1 2021 Pancreatic beta-cells perform glucose-stimulated insulin secretion, a process at the center of type 2 diabetes etiology. Glucose 30-37 insulin Homo sapiens 49-56 33129755-9 2021 CONCLUSIONS: The balance between glucagon and insulin secretion is significantly associated with abdominal obesity and important for maintaining glucose homeostasis. Glucose 145-152 insulin Homo sapiens 46-53 33743285-7 2021 Insulin sensitivity (IS) was assessed using an oral glucose tolerance test (OGTT), the Homeostasis Model Assessment (HOMA-IR), HOMA-Adiponectin Model Assessment (HOMA-AD), the Quantitative Insulin Sensitivity Check Index (QUICKI), the Triglyceride and Glucose Index (TyG) and the Leptin-to-Adiponectin Ratio (LAR). Glucose 52-59 insulin Homo sapiens 0-7 33743285-10 2021 OGTT peak at 30 min correlated best with reduction in endogenous glucose release (EGR) during low insulin HEC (r = -0.6, p = 0.01), whereas HOMA-IR correlated best with whole-body glucose disposal (WGD) (r = -0.6, p = 0.01) and glucose infusion rate (r = -0.6, p = 0.01) during high insulin HEC. Glucose 65-72 insulin Homo sapiens 98-105 33931977-1 2021 Understanding how automated insulin delivery (AID) algorithm features impact glucose control under full closed loop delivery represents a critical step toward reducing patient burden by eliminating the need for carbohydrate entries at mealtimes. Glucose 77-84 insulin Homo sapiens 28-35 33368935-0 2021 A model-based approach to investigate the relationship between glucose-insulin dynamics and dapagliflozin treatment effect in patients with T2DM. Glucose 63-70 insulin Homo sapiens 71-78 33368935-1 2021 AIMS: We developed a quantitative systems pharmacology model to describe the effect of dapagliflozin (a sodium-glucose cotransporter 2 [SGLT2] inhibitor) on glucose-insulin dynamics in type 2 diabetes mellitus (T2DM) patients and identified key determinants of treatment-mediated glycated hemoglobin (HbA1c) reduction. Glucose 111-118 insulin Homo sapiens 165-172 33368935-5 2021 RESULTS: The integrated glucose-insulin-dapagliflozin (IGID) model successfully described plasma glucose and insulin levels, as well as UGE in response to oral glucose tolerance tests and meal intake. Glucose 24-31 insulin Homo sapiens 32-39 33368935-5 2021 RESULTS: The integrated glucose-insulin-dapagliflozin (IGID) model successfully described plasma glucose and insulin levels, as well as UGE in response to oral glucose tolerance tests and meal intake. Glucose 97-104 insulin Homo sapiens 32-39 33368935-5 2021 RESULTS: The integrated glucose-insulin-dapagliflozin (IGID) model successfully described plasma glucose and insulin levels, as well as UGE in response to oral glucose tolerance tests and meal intake. Glucose 97-104 insulin Homo sapiens 32-39 33368935-8 2021 CONCLUSIONS: The developed model framework is the first to integrate SGLT2 inhibitor mechanism of action with both short-term glucose-insulin dynamics and long-term glucose control (HbA1c). Glucose 126-133 insulin Homo sapiens 134-141 33515756-1 2021 AIMS: We (a) describe our implementation of a continuous glucose monitoring (CGM) guideline to support intravenous (IV) insulin administration and reduce point of care (POC) glucose monitoring frequency in the COVID-19 medical intensive care unit (MICU) and (b) evaluate nurses experience with implementation of CGM and hybrid POC + CGM protocol using the PARIHS framework for implementation. Glucose 57-64 insulin Homo sapiens 120-127 32394816-5 2021 Inactivity also affects glucose homeostasis as just few days of step reduction or bed rest, reduce insulin sensitivity, principally in muscle. Glucose 24-31 insulin Homo sapiens 99-106 32648022-8 2021 Continuous glucose monitoring enabled an effect of NZBC extract to be observed under free-living conditions and highlights the potential of anthocyanin-rich supplements as a viable strategy to reduce insulin resistance. Glucose 11-18 insulin Homo sapiens 200-207 32755873-1 2021 People with Type 1 diabetes (T1D) require regular exogenous infusion of insulin to maintain their blood glucose concentration in a therapeutically adequate target range. Glucose 104-111 insulin Homo sapiens 72-79 32915722-1 2021 OBJECTIVE: Multiple daily injections (MDI) therapy is the most common treatment for type 1 diabetes (T1D) including basal insulin doses to keep glucose levels constant during fasting conditions and bolus insulin doses with meals. Glucose 144-151 insulin Homo sapiens 122-129 32915722-3 2021 Here, we present a novel model-based iterative algorithm that optimizes insulin doses using previous-day glucose, insulin, and meal data. Glucose 105-112 insulin Homo sapiens 72-79 33504931-9 2021 In addition, a network of 89 metabolites, primarily phosphatidylcholines, plasmalogens, sphingomyelins, and ceramides showed consistent negative correlations with insulin at visit 1 and post-challenge glucose at visit 2, while positive correlation with adiponectin at visit 2. Glucose 201-208 insulin Homo sapiens 163-170 33998292-2 2021 Exercise effects (EE) on whole body glucose rate of disappearance (Rd) occur through insulin- independent (IIRd) and insulin-dependent (IDRd) mechanisms. Glucose 36-43 insulin Homo sapiens 85-92 33998292-2 2021 Exercise effects (EE) on whole body glucose rate of disappearance (Rd) occur through insulin- independent (IIRd) and insulin-dependent (IDRd) mechanisms. Glucose 36-43 insulin Homo sapiens 117-124 33468396-4 2021 Further analyses suggest the HbA1c association may be modified by diabetes therapy regimen: rs12970134 AA genotype was associated with higher HbA1c under non-intensive therapy conditions (<3 insulin injections/day or monitoring blood glucose<3 times/day [p = 0.004]), but not under intensive therapy (>=3 injections/day or insulin pump and monitoring glucose>=3 times/day [p = 0.71]). Glucose 234-241 insulin Homo sapiens 323-330 32006145-1 2021 Intensive care unit (ICU) patients develop stress induced insulin resistance causing hyperglycemia, large glucose variability and hypoglycemia. Glucose 106-113 insulin Homo sapiens 58-65 33319507-1 2021 AIMS/INTRODUCTION: The triglyceride-glucose (TyG) index has been proposed as a reliable and simple marker of insulin resistance. Glucose 36-43 insulin Homo sapiens 109-116 33468396-4 2021 Further analyses suggest the HbA1c association may be modified by diabetes therapy regimen: rs12970134 AA genotype was associated with higher HbA1c under non-intensive therapy conditions (<3 insulin injections/day or monitoring blood glucose<3 times/day [p = 0.004]), but not under intensive therapy (>=3 injections/day or insulin pump and monitoring glucose>=3 times/day [p = 0.71]). Glucose 351-358 insulin Homo sapiens 191-198 33468396-4 2021 Further analyses suggest the HbA1c association may be modified by diabetes therapy regimen: rs12970134 AA genotype was associated with higher HbA1c under non-intensive therapy conditions (<3 insulin injections/day or monitoring blood glucose<3 times/day [p = 0.004]), but not under intensive therapy (>=3 injections/day or insulin pump and monitoring glucose>=3 times/day [p = 0.71]). Glucose 351-358 insulin Homo sapiens 323-330 33599044-2 2021 The available evidence indicates that insulin directly acts on the CNS, in particular the hypothalamus, to regulate hepatic glucose production, thereby controlling whole-body glucose metabolism. Glucose 124-131 insulin Homo sapiens 38-45 33794675-1 2021 BACKGROUND: Physical activity can cause glucose fluctuations both during and after it is performed, leading to hurdles in optimal insulin dosing in people with type 1 diabetes (T1D). Glucose 40-47 insulin Homo sapiens 130-137 33794675-9 2021 Physical activity-informed insulin dosing of meals eaten soon after a walking bout has a potential of mitigating physical activity related glucose reduction in the early postprandial phase. Glucose 139-146 insulin Homo sapiens 27-34 33605461-0 2021 Limonoids isolated from fruits of Swietenia macrophylla king enhance glucose consumption in insulin-resistant HepG2 cells via activating PPARgamma. Glucose 69-76 insulin Homo sapiens 92-99 33605461-9 2021 In this study, limonoids were isolated from the fruit of S. macrophylla and their effects on the glucose consumption of insulin-resistant HepG2 cells were studied. Glucose 97-104 insulin Homo sapiens 120-127 33507001-3 2021 This review focuses on the effects of insulin and diabetes on the activity and glucose sensitivity of hypothalamic glucose-sensing neurones. Glucose 79-86 insulin Homo sapiens 38-45 33507001-4 2021 We highlight the role of electrophysiological data in understanding how insulin regulates glucose-sensing neurones. Glucose 90-97 insulin Homo sapiens 72-79 33710714-7 2021 Moreover, we explore the hypothesis that pregnancy is associated with site-specific central insulin resistance that is adaptive, allowing for the increases in peripheral insulin secretion without the consequences of increased central and peripheral insulin functions, such as to stimulate glucose uptake into maternal tissues or to inhibit food intake. Glucose 289-296 insulin Homo sapiens 92-99 33507001-6 2021 The mechanisms by which hypothalamic neurones sense glucose are discussed with an emphasis on those glucose-sensing neurones already shown to be modulated by insulin. Glucose 52-59 insulin Homo sapiens 158-165 33507001-6 2021 The mechanisms by which hypothalamic neurones sense glucose are discussed with an emphasis on those glucose-sensing neurones already shown to be modulated by insulin. Glucose 100-107 insulin Homo sapiens 158-165 33507001-7 2021 Next, the literature pertaining to how insulin alters the activity and glucose sensitivity of these hypothalamic glucose-sensing neurones is described. Glucose 71-78 insulin Homo sapiens 39-46 33507001-10 2021 To conclude, electrophysiological data from the hippocampus are evaluated aiming to provide clues regarding how insulin might influence neuronal plasticity in glucose-sensing neurones. Glucose 159-166 insulin Homo sapiens 112-119 33724579-3 2021 Specifically, insulin action in astrocytes has received special emphasis given its newly discovered regulatory role in brain glucose uptake, which until recently was assumed to be an insulin independent process. Glucose 125-132 insulin Homo sapiens 14-21 33724579-3 2021 Specifically, insulin action in astrocytes has received special emphasis given its newly discovered regulatory role in brain glucose uptake, which until recently was assumed to be an insulin independent process. Glucose 125-132 insulin Homo sapiens 183-190 33724579-4 2021 We now know that insulin signalling in astrocytes regulates metabolic processes and behavioural responses through coupling brain glucose uptake with nutrient availability to maintain energy balance and systemic glucose homeostasis. Glucose 129-136 insulin Homo sapiens 17-24 33788828-1 2021 Plasma glucose and insulin responses following an oral glucose challenge are representative of glucose tolerance and insulin resistance, key indicators of type 2 diabetes mellitus pathophysiology. Glucose 7-14 insulin Homo sapiens 117-124 33137487-2 2021 The idea of protecting against hypoglycaemia by engineering an insulin preparation that can auto-adjust its biological activity to fluctuating blood glucose levels has been pursued since the 1970"s, but despite thousands of publications, no system that works well enough for practical use has reached clinical practice. Glucose 149-156 insulin Homo sapiens 63-70 33137487-3 2021 SCOPE OF REVIEW: This review will summarize and scrutinize known approaches for making glucose-sensitive insulin therapies. Glucose 87-94 insulin Homo sapiens 105-112 33137487-5 2021 MAJOR CONCLUSIONS: The vast majority of published systems are not suitable for product development, but a few glucose-sensitive insulin concepts have recently reached clinical trials, and there is hope that glucose-sensitive insulin will become available to people with diabetes within the coming years. Glucose 110-117 insulin Homo sapiens 128-135 33137487-5 2021 MAJOR CONCLUSIONS: The vast majority of published systems are not suitable for product development, but a few glucose-sensitive insulin concepts have recently reached clinical trials, and there is hope that glucose-sensitive insulin will become available to people with diabetes within the coming years. Glucose 207-214 insulin Homo sapiens 225-232 33128591-6 2021 Lixisenatide increased the 16.7 mM glucose-stimulated insulin secretion, but not by 5.6 mM glucose, in the islets of healthy rats, without changing the insulin intracellular content. Glucose 35-42 insulin Homo sapiens 54-61 33660027-0 2021 Lithium enhances exercise-induced glycogen breakdown and insulin-induced AKT activation to facilitate glucose uptake in rodent skeletal muscle. Glucose 102-109 insulin Homo sapiens 57-64 33660027-4 2021 In streptozotocin-induced T1DM mice, Li/low-dose insulin facilitates glucose uptake through increase the level of exocyst complex component 7 (Exoc7) and Ser473-AKT. Glucose 69-76 insulin Homo sapiens 49-56 33694300-0 2021 Rat prostaglandin EP3 receptor is highly promiscuous and is the sole prostanoid receptor family member that regulates INS-1 (832/3) cell glucose-stimulated insulin secretion. Glucose 137-144 insulin Homo sapiens 156-163 33694300-4 2021 Here, we define EP3 as the sole prostanoid receptor family member expressed in a rat beta-cell-derived line that regulates glucose-stimulated insulin secretion. Glucose 123-130 insulin Homo sapiens 142-149 33694300-5 2021 Several other agonists classically understood as selective for other prostanoid receptor family members also reduce glucose-stimulated insulin secretion, but these effects are only observed at relatively high concentrations, and, using a well-characterized EP3-specific antagonist, are mediated solely by cross-reactivity with rat EP3. Glucose 116-123 insulin Homo sapiens 135-142 33132064-2 2021 The aim of this paper is to measure the change in HbA1c, and the Coefficient of Variation in glucose levels, when using CGM, once the effect of other relevant variables, such as gender, actual age, the years the patient has had diabetes, use of an insulin pump, the presence of autoimmune disease, other associated pathologies, and weekly hours of exercise, are controlled for. Glucose 93-100 insulin Homo sapiens 248-255 33788828-1 2021 Plasma glucose and insulin responses following an oral glucose challenge are representative of glucose tolerance and insulin resistance, key indicators of type 2 diabetes mellitus pathophysiology. Glucose 55-62 insulin Homo sapiens 19-26 33788828-1 2021 Plasma glucose and insulin responses following an oral glucose challenge are representative of glucose tolerance and insulin resistance, key indicators of type 2 diabetes mellitus pathophysiology. Glucose 55-62 insulin Homo sapiens 117-124 33854483-2 2021 We conducted a minimal modeling analysis of glucose effectiveness at zero insulin (GEZI) using intravenous glucose tolerance test data from subjects with type 2 diabetes (T2D, n=154) and non-diabetic (ND) subjects (n=343). Glucose 44-51 insulin Homo sapiens 74-81 33038776-3 2021 In vitro assays demonstrated that Up-3 and Up-4 had strong alpha-glucosidase inhibitory activity, and Up-3, Up-4, and Up-5 could improve the glucose uptake in insulin-resistant HepG2 cells without affecting their viability. Glucose 141-148 insulin Homo sapiens 159-166 33785482-9 2021 This study lays the foundations for investigating novel therapeutic approaches to target the glucose/insulin axis in combination with PI3K/AKT/mTORC1 inhibitors in HR+/HER2 aBC patients. Glucose 93-100 insulin Homo sapiens 101-108 33854483-5 2021 The resulting model was also employed to calculate the proportion of the non-insulin-dependent net glucose uptake in each subject receiving an intravenous glucose load. Glucose 99-106 insulin Homo sapiens 77-84 33854483-5 2021 The resulting model was also employed to calculate the proportion of the non-insulin-dependent net glucose uptake in each subject receiving an intravenous glucose load. Glucose 155-162 insulin Homo sapiens 77-84 33834073-1 2021 Objective: Type 2 diabetes mellitus is a chronic metabolic disease caused by insulin resistance or insulin deficiency resulting in elevated blood glucose levels. Glucose 146-153 insulin Homo sapiens 77-84 33928207-5 2021 The resultant elevated plasma glucose levels at 1-hour and 2-hours mimicked the loss of first-phase insulin release seen in early type 1 and type 2 diabetes. Glucose 30-37 insulin Homo sapiens 100-107 33208570-9 2021 Our results using isCGM in an actual clinical setting showed that 7-day use of SGLT2-I with intensive insulin therapy improved plasma glucose fluctuations and mean plasma glucose levels without inducing hypoglycemia in patients with T1DM. Glucose 134-141 insulin Homo sapiens 102-109 33208570-9 2021 Our results using isCGM in an actual clinical setting showed that 7-day use of SGLT2-I with intensive insulin therapy improved plasma glucose fluctuations and mean plasma glucose levels without inducing hypoglycemia in patients with T1DM. Glucose 171-178 insulin Homo sapiens 102-109 33382888-1 2021 PURPOSE: Skeletal muscle is the primary site for insulin-stimulated glucose disposal and muscle insulin resistance is central to abnormal glucose metabolism in obesity. Glucose 68-75 insulin Homo sapiens 49-56 33382888-4 2021 RESULTS: Insulin-stimulated glucose disposal (Si) was reduced by > 60% (P < 0.0001) in the obese group in Protocol 2; however, the phosphorylation of Akt and its downstream effector AS160 were not different between non-obese and obese groups. Glucose 28-35 insulin Homo sapiens 9-16 33749808-2 2021 The triglyceride-glucose (TyG) index is a novel surrogate marker of insulin resistance and is associated with cardiovascular diseases. Glucose 17-24 insulin Homo sapiens 68-75 33683280-2 2021 The transplanted islets release insulin in response to changes in blood glucose levels. Glucose 72-79 insulin Homo sapiens 32-39 33743067-6 2021 Calcium influx was enhanced during glucose and tolbutamide treatments, suggesting that DMSO"s mechanism of action is upstream of calcium-dependent insulin granule exocytosis. Glucose 35-42 insulin Homo sapiens 147-154 33740836-3 2022 The basal insulin requirement was adjusted to keep the blood glucose level from bedtime to before breakfast within a 30-mg/dL difference. Glucose 61-68 insulin Homo sapiens 10-17 33740836-4 2022 The bolus insulin dose before meal was adjusted to keep the blood glucose level below 140 and 200 mg/dL before and 2 h after each meal, respectively. Glucose 66-73 insulin Homo sapiens 10-17 33715620-4 2021 Insulin sensitivity was assessed as estimated glucose disposal rate (eGDR), which was validated against the euglycaemic-hyperinsulinemic clamp technique. Glucose 46-53 insulin Homo sapiens 0-7 33450256-3 2021 Glucagon-like peptide-1 (GLP-1) release and glucose-stimulated insulin secretion (GSIS) were evaluated in human colonic epithelial cell line NCI-H716 and mouse insulinoma cell line MIN6 by enzyme-linked immunosorbent assay (ELISA), respectively. Glucose 44-51 insulin Homo sapiens 63-70 33791724-5 2021 A screen of protein hormones that regulate glucose homeostasis reveals that the insulin sensitizing adipokine adiponectin is reduced in hyperglycemic COVID-19 patients. Glucose 43-50 insulin Homo sapiens 80-87 33828527-0 2021 Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test. Glucose 114-121 insulin Homo sapiens 62-69 33726723-1 2021 BACKGROUND: Blood glucose (BG) management is crucial for type-1 diabetes patients resulting in the necessity of reliable artificial pancreas or insulin infusion systems. Glucose 18-25 insulin Homo sapiens 144-151 33721199-7 2021 The primary outcome was the change in glucose concentration 30 min after intranasal insulin administration. Glucose 38-45 insulin Homo sapiens 84-91 33721199-9 2021 In non-T2DM patients, 40 IU intranasal insulin did not affect glucose concentration, while 80 IU intranasal insulin led to a statistically significant but not clinically important decrease in blood glucose levels (mean difference, 0.4 mMol L-1; 95% confidence interval, 0.1 to 0.7). Glucose 198-205 insulin Homo sapiens 108-115 33725905-11 2021 We will perform a 75-g oral glucose tolerance test before and at 24 weeks after the start of this 5-ALA/SFC treatment to evaluate glucose-dependent insulin responses. Glucose 130-137 insulin Homo sapiens 148-155 33382888-3 2021 METHODS: We defined a linear range of insulin-stimulated systemic and leg glucose uptake in 14 obese and 14 non-obese volunteers using a 2-step insulin clamp (Protocol 1) and then examined the obesity-related defects in muscle insulin action in 16 non-obese and 25 obese male and femal volunteers matched for fitness using a one-step, hyperinsulinemic, euglycemic clamp coupled with muscle biopsies (Protocol 2). Glucose 74-81 insulin Homo sapiens 38-45 33709538-1 2021 Despite the potential deleterious effect of COVID-19 lockdown on individuals with type 1 diabetes mellitus (T1DM), a stable or even improved glycaemic control has been reported in paediatric subjects treated with continuous subcutaneous insulin infusion (CSII) using continuous or flash glucose monitoring (CGM/FGM). Glucose 287-294 insulin Homo sapiens 237-244 33704799-2 2022 This is facilitated by reductions in maternal peripheral insulin sensitivity, which enable glucose to be available in the maternal circulation for transfer to the fetus for growth. Glucose 91-98 insulin Homo sapiens 57-64 33693742-9 2021 Combined supplementation with HNG and insulin significantly improved glucose consumption in normal and humanin-siRNA-transfected COV434 cells. Glucose 69-76 insulin Homo sapiens 38-45 33704799-3 2022 To balance this process and avoid excessive hyperglycemia and glucose intolerance in the mother during pregnancy, maternal pancreatic beta-cells undergo remarkable changes in their function including increasing their proliferation and glucose stimulated insulin secretion. Glucose 235-242 insulin Homo sapiens 254-261 33705613-9 2021 RESULTS: Oral administration of the lyophilized aqueous extract of date seeds and insulin injection for 30 days significantly decreased blood glucose levels in STZ-diabetic rats and protected them against undesirable changes in lipid parameters, including cholesterol, triglycerides, LDL cholesterol, VLDL cholesterol and atherosclerosis index. Glucose 142-149 insulin Homo sapiens 82-89 33688832-6 2021 METHODS: We collected data from 3029 patients to design a machine learning model that can identify when a woman with GDM needs to switch to medications (insulin or metformin) by analyzing the data related to blood glucose and other risk factors. Glucose 214-221 insulin Homo sapiens 153-160 33719596-4 2021 In HCL systems, more rapid modulation of glucose via automated insulin delivery may result in greater rhythmic coordination and euglycemia. Glucose 41-48 insulin Homo sapiens 63-70 33566368-0 2021 Insulin-dependent glucose consumption dynamics in 3D primary human liver cultures measured by a sensitive and specific glucose sensor with nanoliter input volume. Glucose 18-25 insulin Homo sapiens 0-7 33692359-3 2021 Also, the present study details the data curation process used to extract and match glucose values to insulin therapy. Glucose 84-91 insulin Homo sapiens 102-109 33687790-0 2021 Fasting and Postprandial Plasma Glucose Contribution to HbA1c and Time in Range in People with Type 2 Diabetes on Basal and Bolus Insulin Therapy: Results from a Pooled Analysis of Insulin Lispro Clinical Trials. Glucose 32-39 insulin Homo sapiens 130-137 33300990-8 2021 RESULTS: Sucrose vs glucose ingestion provoked a less robust rise in glucose (p<0.0001), insulin (p<0.0001), GLP-1 (p<0.0001), and PYY (p=0.02), whereas acyl-ghrelin suppression was similar between the sugars. Glucose 20-27 insulin Homo sapiens 89-96 33300990-10 2021 There were interactions between insulin sensitivity and sugar for glucose (p=0.003) and insulin (p=0.04), and a sex by sugar interaction for GLP-1 (p=0.01); males demonstrated smaller increases in GLP-1 in response to oral sucrose vs glucose. Glucose 66-73 insulin Homo sapiens 32-39 33500122-6 2021 However, there is variability in insulin sensitivity, and this creates variability in glucose levels and insulin requirements and increases the frequency of hypo- and hyperglycemia. Glucose 86-93 insulin Homo sapiens 33-40 33687921-7 2021 Similar associations were observed for cord plasma OxLDL to LDL ratio in relation to cord plasma glucose to insulin ratio and proinsulin to insulin ratio. Glucose 97-104 insulin Homo sapiens 108-115 33146746-1 2021 Insulin is produced by pancreatic beta-cells, and once released to the blood, the hormone stimulates glucose uptake and suppresses glucose production. Glucose 101-108 insulin Homo sapiens 0-7 33146746-1 2021 Insulin is produced by pancreatic beta-cells, and once released to the blood, the hormone stimulates glucose uptake and suppresses glucose production. Glucose 131-138 insulin Homo sapiens 0-7 33146746-2 2021 Defects in both the availability and action of insulin lead to elevated plasma glucose levels and are major hallmarks of type-2 diabetes. Glucose 79-86 insulin Homo sapiens 47-54 33485076-2 2021 The model yields estimates of insulin sensitivity and the meal-related appearance of glucose from insulin and glucose data after an oral glucose challenge. Glucose 85-92 insulin Homo sapiens 98-105 33485076-6 2021 The proposed modelling procedure is applied to glucose and insulin data from subjects with normal glucose tolerance consuming three consecutive meals in intervals of four hours. Glucose 98-105 insulin Homo sapiens 59-66 32940537-1 2021 BACKGROUND: Automated insulin delivery (AID) systems have demonstrated improvements in time-in-range (TIR, blood glucose 70-180 mg/dL) without increasing hypoglycemia. Glucose 113-120 insulin Homo sapiens 22-29 33050728-1 2021 OBJECTIVE: Several studies have shown that closed-loop automated insulin delivery (the artificial pancreas) improves glucose control compared to sensor-augmented pump therapy. Glucose 117-124 insulin Homo sapiens 65-72 33050728-11 2021 CONCLUSIONS: Our study confirms findings that automated insulin delivery improves glucose control compared to sensor-augmented pump therapy (Funded by National Institute of Health; ClinicalTrials.gov number, NCT02846831). Glucose 82-89 insulin Homo sapiens 56-63 33119135-7 2021 RESULTS: Compared with carbohydrate counting, the food insulin index algorithm significantly decreased peak glucose excursion (-57%, p = 0.02), incremental area under the curve (-65%, p = 0.02) and coefficient variation of blood glucose (-37%, p = 0.03) in the high-GI meal, though there was no difference between two algorithms in the low-GI meal. Glucose 108-115 insulin Homo sapiens 55-62 33241460-2 2021 The aim of this study was to characterise the neuroendocrine response to various glucose concentrations in overweight and insulin-resistant individuals compared with lean individuals. Glucose 81-88 insulin Homo sapiens 122-129 33480828-1 2021 BACKGROUND: Recent development and availability of several connected insulin pens with digital memory is likely to expand the availability of glucose and insulin metrics that previously had been available only for the much smaller number of people using insulin pumps. Glucose 142-149 insulin Homo sapiens 69-76 33480828-5 2021 RESULTS: We propose the following metrics to be included in the one page report: A) Glucose Metrics: simplified glucose distribution in the form of a stacked bar chart showing percentages of time below-, above- or within-target ranges overall and (optionally) by date, by time of day, or day of the week,; B) Insulin Metrics: types and doses, and timing of basal and bolus insulin; C) An enhanced Ambulatory Glucose Profile or "AGP+" showing glucose data points and/or distributions (10th through 90th-percentiles), dosages and timing of basal and bolus insulins and (optionally) graphical display of risk of hypoglycemia and hyperglycemia; and D) User experience regarding technology usage, frequency of alerts for hypo- and hyperglycemia, and information regarding lifestyle, meals, exercise and sleep, if available; E) Clinical insights and interpretation. Glucose 112-119 insulin Homo sapiens 309-316 33341896-1 2021 Insulin secretion from pancreatic beta cells is tightly regulated by glucose and paracrine signals within the microenvironment of islets of Langerhans. Glucose 69-76 insulin Homo sapiens 0-7 33711016-5 2021 We conducted two-sample uni- and multivariable mendelian randomization (MR) analysis to test whether (i) 10 cardiometabolic traits (fasting insulin, high-density lipoprotein and triglycerides representing an insulin resistance phenotype, and 7 related cardiometabolic traits: low-density lipoprotein, fasting plasma glucose, glycated haemoglobin, leptin, body mass index, glucose tolerance, and type 2 diabetes) could be causally associated with schizophrenia; and (ii) inflammation could be a shared mechanism for these phenotypes. Glucose 316-323 insulin Homo sapiens 208-215 33842134-3 2021 The hyperkalemia, presumed to be secondary to considerable tumor manipulation, was successfully controlled with calcium, bicarbonate, and insulin with dextrose. Glucose 151-159 insulin Homo sapiens 138-145 33693776-5 2021 Beta-cell function modelling was undertaken to describe the relationship between insulin secretion and glucose concentration. Glucose 103-110 insulin Homo sapiens 81-88 33651228-6 2021 The combination of SGLT2i and insulin improved hemoglobin A1c (HbA1c), fasting plasma glucose (FPG), daily insulin dose, body weight, and blood pressure, which varied greatly by different follow-ups. Glucose 86-93 insulin Homo sapiens 30-37 33356994-0 2021 Separating Insulin-Mediated and Non-Insulin-Mediated Glucose Uptake during Aerobic Exercise in People with Type 1 Diabetes. Glucose 53-60 insulin Homo sapiens 36-43 33356994-6 2021 A novel application of linear regression of Rd across the three insulin studies allowed separation of insulin-mediated from non-insulin-mediated glucose uptake before, during and after exercise. Glucose 145-152 insulin Homo sapiens 64-71 33356994-10 2021 Insulin-mediated glucose uptake rose during exercise and persisted hours afterward, while non-insulin mediated effect was limited to the exercise period. Glucose 17-24 insulin Homo sapiens 0-7 33561625-1 2021 Interactions between the pancreatic extracellular matrix (ECM) and islet cells are known to regulate multiple aspects of islet physiology, including survival, proliferation, and glucose-stimulated insulin secretion. Glucose 178-185 insulin Homo sapiens 197-204 33039327-7 2021 Both residents and clerks prescribed more insulin when the reported blood glucose was higher, or the patient had positive ketones and prescribed less insulin when the patient had hypoglycemic unawareness. Glucose 74-81 insulin Homo sapiens 42-49 32897887-3 2021 Type 2 DM occurs when the pancreas is unable to produce adequate insulin to regulate glucose levels and when there is a decrease in sensitivity to insulin in the body. Glucose 85-92 insulin Homo sapiens 65-72 33241460-11 2021 CONCLUSIONS/INTERPRETATION: This study supports the hypothesis that altered responses of insulin-antagonistic hormones and the ANS to glucose fluctuations occur in overweight and insulin-resistant individuals, and that these responses are probably partly mediated by the CNS. Glucose 134-141 insulin Homo sapiens 89-96 33241460-11 2021 CONCLUSIONS/INTERPRETATION: This study supports the hypothesis that altered responses of insulin-antagonistic hormones and the ANS to glucose fluctuations occur in overweight and insulin-resistant individuals, and that these responses are probably partly mediated by the CNS. Glucose 134-141 insulin Homo sapiens 179-186 33269551-2 2021 Used correctly, these insulin delivery systems offer better glucose control and reduced risk of hypoglycemia and represent the most advanced form of insulin delivery available for people with type 1 diabetes. Glucose 60-67 insulin Homo sapiens 22-29 33269554-3 2021 Imeglimin"s mechanism of action involves dual effects: 1) amplification of glucose-stimulated insulin secretion (GSIS) and preservation of beta-cell mass; 2) enhanced insulin action including the potential for inhibition of hepatic glucose output and improvement in insulin signaling in both liver and skeletal muscle. Glucose 75-82 insulin Homo sapiens 94-101 33446523-1 2021 OBJECTIVE: Whereas insulin resistance is expressed as reduced glucose uptake in peripheral tissues, the relationship between insulin resistance and brain glucose metabolism remains controversial. Glucose 62-69 insulin Homo sapiens 19-26 33446523-2 2021 Our aim was to examine the association of insulin resistance and brain glucose uptake (BGU) during a euglycemic hyperinsulinemic clamp in a large sample of study participants across a wide range of age and insulin sensitivity. Glucose 71-78 insulin Homo sapiens 42-49 33662836-2 2021 We aimed to examine glycemic control metrics using flash glucose monitoring during insulin treatment and the clinical outcome in hospitalized patients with COVID-19. Glucose 57-64 insulin Homo sapiens 83-90 33566368-0 2021 Insulin-dependent glucose consumption dynamics in 3D primary human liver cultures measured by a sensitive and specific glucose sensor with nanoliter input volume. Glucose 119-126 insulin Homo sapiens 0-7 33566368-7 2021 By comparing isogenic insulin-resistant and insulin-sensitive liver cultures we furthermore show that insulin and extracellular glucose levels account for 55% and 45% of hepatic glucose consumption, respectively. Glucose 128-135 insulin Homo sapiens 22-29 33566368-7 2021 By comparing isogenic insulin-resistant and insulin-sensitive liver cultures we furthermore show that insulin and extracellular glucose levels account for 55% and 45% of hepatic glucose consumption, respectively. Glucose 128-135 insulin Homo sapiens 44-51 33566368-7 2021 By comparing isogenic insulin-resistant and insulin-sensitive liver cultures we furthermore show that insulin and extracellular glucose levels account for 55% and 45% of hepatic glucose consumption, respectively. Glucose 128-135 insulin Homo sapiens 44-51 33434932-9 2021 While certain bile acids upregulated CAMP expression in vitro, high glucose/insulin as well as GLP-1 had an inhibitory effect. Glucose 68-75 insulin Homo sapiens 76-83 31810389-0 2021 The Differential and Combined Action of Insulin Glargine and Lixisenatide on the Fasting and Postprandial Components of Glucose Control. Glucose 120-127 insulin Homo sapiens 40-47 33415834-6 2021 Besides, the triglyceride-glucose index (TyG) first published by South American authors showed a good correlation with the insulin clamp technique and HOMA-IR index. Glucose 26-33 insulin Homo sapiens 123-130 31941361-2 2021 This study investigated feasibility of a new approach to basal insulin initiation, where the dose needed to reach a glycemic target is estimated from two weeks of insulin and continuous glucose monitoring (CGM) data. Glucose 186-193 insulin Homo sapiens 63-70 33434144-8 2021 Similarly, nNOS overexpression increased triglyceride production, decreased glucose utilization, and downregulated insulin-induced expression of p-IRbeta, p-Akt, and p-GSK3beta in the HepG2 cells. Glucose 76-83 insulin Homo sapiens 115-122 33115283-6 2021 In vivo assay, high fat and glucose diet and streptozotocin (STZ) induced insulin resistance in mice by increasing the body weight, fasting blood glucose (FBG) level, oral glucose tolerance, fasting insulin level and insulin resistance index. Glucose 28-35 insulin Homo sapiens 74-81 33115283-6 2021 In vivo assay, high fat and glucose diet and streptozotocin (STZ) induced insulin resistance in mice by increasing the body weight, fasting blood glucose (FBG) level, oral glucose tolerance, fasting insulin level and insulin resistance index. Glucose 28-35 insulin Homo sapiens 199-206 33115283-6 2021 In vivo assay, high fat and glucose diet and streptozotocin (STZ) induced insulin resistance in mice by increasing the body weight, fasting blood glucose (FBG) level, oral glucose tolerance, fasting insulin level and insulin resistance index. Glucose 28-35 insulin Homo sapiens 199-206 33118415-1 2021 BACKGROUND: Computerized insulin infusion protocols have demonstrated higher staff satisfaction, better compliance with protocols, and increased time with glucose in range compared to paper protocols. Glucose 155-162 insulin Homo sapiens 25-32 33347614-0 2021 TSPAN-7 as a key regulator of glucose-stimulated Ca2+ influx and insulin secretion. Glucose 30-37 insulin Homo sapiens 65-72 33246193-1 2021 The synthetic glucose receptors help to develop glucose sensors and alternative insulin therapies. Glucose 14-21 insulin Homo sapiens 80-87 33220095-5 2021 Insulin sensitivity and insulin secretion were assessed by an intravenous-glucose-tolerance-test (IVGTT) and a hyperinsulinemic euglycemic clamp (HEC). Glucose 74-81 insulin Homo sapiens 0-7 33220095-9 2021 Glucose during the IVGTT was unaffected, but there was a tendency towards lower insulin and C-peptide levels in the first minutes after glucose administration in G-allele carriers. Glucose 136-143 insulin Homo sapiens 80-87 33747402-4 2021 Results: The first-phase insulin response (FPIR), expressed as the sum of 1 and 3 minutes insulin, to intravenous glucose tolerance test (IVGTT), was between the 1st and 3rd percentile in two patients and between the 3rd and 10th percentile in five. Glucose 114-121 insulin Homo sapiens 25-32 33747402-7 2021 Interestingly, the patients who developed DM had, at baseline, the lowest value of the insulinogenic index (IGI: 0.08 and 0.25), defined as the ratio of the increment of plasma insulin to plasma glucose during the first 30 minutes after OGTT. Glucose 195-202 insulin Homo sapiens 87-94 32929844-6 2021 In obesity, PKD signalling is linked to reduced insulin signalling and dysfunction in adipose tissue, liver and heart, whilst in the pancreas, PKD is essential for the compensatory increase in glucose-stimulated insulin secretion from beta-cells during obesity. Glucose 193-200 insulin Homo sapiens 48-55 33401003-2 2021 The purpose of this study was to investigate the impact of kappa-CGN on glucose intolerance and insulin resistance from the perspective that kappa-CGN may interfere with insulin receptor function and affect insulin sensitivity and signaling, thereby leading to body weight loss. Glucose 72-79 insulin Homo sapiens 170-177 33145960-2 2021 Current protocols drive stem cells through stages of directed differentiation and maturation and produce cells that secrete insulin in response to glucose. Glucose 147-154 insulin Homo sapiens 124-131 33679137-6 2021 Increasing the dose to 10 microg/mL or more resulted in detrimental effects with respect to viability and glucose-stimulated insulin release. Glucose 106-113 insulin Homo sapiens 125-132 33718798-5 2021 Empirical initiation of a higher dextrose concentration infusion with glucose level titrations should be considered to avoid hypoglycemia for nondiabetic patients treated with an insulin infusion to lower triglyceride levels. Glucose 33-41 insulin Homo sapiens 179-186 33718425-4 2021 Despite a ~50% lower insulin sensitivity index (Si) in insulin-resistant than in insulin-sensitive subjects, which was accompanied by significantly greater acute insulin response to glucose (AIRg) and fasting insulin concentration but not different fasting glucose concentration, there were no significant differences between groups in the blood lipid profile (p >= 0.44) or the lipoprotein subclass concentrations (p >= 0.30) and particle sizes (p >= 0.43). Glucose 182-189 insulin Homo sapiens 55-62 33718425-4 2021 Despite a ~50% lower insulin sensitivity index (Si) in insulin-resistant than in insulin-sensitive subjects, which was accompanied by significantly greater acute insulin response to glucose (AIRg) and fasting insulin concentration but not different fasting glucose concentration, there were no significant differences between groups in the blood lipid profile (p >= 0.44) or the lipoprotein subclass concentrations (p >= 0.30) and particle sizes (p >= 0.43). Glucose 182-189 insulin Homo sapiens 55-62 33718425-4 2021 Despite a ~50% lower insulin sensitivity index (Si) in insulin-resistant than in insulin-sensitive subjects, which was accompanied by significantly greater acute insulin response to glucose (AIRg) and fasting insulin concentration but not different fasting glucose concentration, there were no significant differences between groups in the blood lipid profile (p >= 0.44) or the lipoprotein subclass concentrations (p >= 0.30) and particle sizes (p >= 0.43). Glucose 182-189 insulin Homo sapiens 55-62 33718425-4 2021 Despite a ~50% lower insulin sensitivity index (Si) in insulin-resistant than in insulin-sensitive subjects, which was accompanied by significantly greater acute insulin response to glucose (AIRg) and fasting insulin concentration but not different fasting glucose concentration, there were no significant differences between groups in the blood lipid profile (p >= 0.44) or the lipoprotein subclass concentrations (p >= 0.30) and particle sizes (p >= 0.43). Glucose 182-189 insulin Homo sapiens 55-62 33606677-0 2021 Imeglimin amplifies glucose-stimulated insulin release from diabetic islets via a distinct mechanism of action. Glucose 20-27 insulin Homo sapiens 39-46 33663065-1 2021 BACKGROUND: Diabetes is a chronic metabolic disease characterized by elevated blood glucose levels due to insulin resistance and beta-cell dysfunction. Glucose 84-91 insulin Homo sapiens 106-113 33566311-7 2021 ALMS1 regulate glucose transport through the actin cytoskeleton, which plays an important role in insulin-stimulated GLUT4 transport. Glucose 15-22 insulin Homo sapiens 98-105 33682835-0 2021 Optimal Blood Glucose Monitoring Interval for Insulin Infusion in Critically Ill Non-Cardiothoracic Patients: A Pilot Study. Glucose 14-21 insulin Homo sapiens 46-53 33682835-1 2021 OBJECTIVE: The American Diabetes Association and the Society of Critical Care Medicine recommend monitoring blood glucose (BG) every 1-2 hours in patients receiving insulin infusion to guide titration of insulin infusion to maintain serum glucose in the target range; however, this is based on weak evidence. Glucose 114-121 insulin Homo sapiens 165-172 33682835-1 2021 OBJECTIVE: The American Diabetes Association and the Society of Critical Care Medicine recommend monitoring blood glucose (BG) every 1-2 hours in patients receiving insulin infusion to guide titration of insulin infusion to maintain serum glucose in the target range; however, this is based on weak evidence. Glucose 114-121 insulin Homo sapiens 204-211 33634518-1 2021 Insulin has long been known as a metabolic hormone critical in the treatment of diabetes for its peripheral effects on blood glucose. Glucose 125-132 insulin Homo sapiens 0-7 33317342-0 2021 Needle-free jet injection of insulin glargine improves glycaemic control in patients with type 2 diabetes mellitus: a study based on the flash glucose monitoring system. Glucose 143-150 insulin Homo sapiens 29-36 33317342-2 2021 The aim of this study was to investigate the effects of insulin glargine injection given with a QS-P jet injector on the glucose profile using a professional mode flash glucose monitoring (FGM) system in patients with type 2 diabetes mellitus (T2DM). Glucose 121-128 insulin Homo sapiens 56-63 33317342-2 2021 The aim of this study was to investigate the effects of insulin glargine injection given with a QS-P jet injector on the glucose profile using a professional mode flash glucose monitoring (FGM) system in patients with type 2 diabetes mellitus (T2DM). Glucose 169-176 insulin Homo sapiens 56-63 33679602-10 2020 Conclusions: The sensitive insulin assay performed excellent in diagnosing CHI with optimal p-insulin cut-offs at 12.3 pmol/L (2.0 mU/L), and 10.6 pmol/L (1.8 mU/L), at p-glucose <3.2 mmol/L, and <3.0 mmol/L, respectively. Glucose 171-178 insulin Homo sapiens 27-34 33679687-2 2020 Insulin is well known as the critical hormone in the maintenance of glucose in physiologic response. Glucose 68-75 insulin Homo sapiens 0-7 33606677-1 2021 Pancreatic islet beta-cell dysfunction is characterized by defective glucose-stimulated insulin secretion (GSIS) and is a predominant component of the pathophysiology of diabetes. Glucose 69-76 insulin Homo sapiens 88-95 33602208-1 2021 BACKGROUND: Triglyceride-glucose (TyG) index was recently suggested to be a reliable surrogate marker of insulin resistance. Glucose 25-32 insulin Homo sapiens 105-112 33679974-0 2021 Study Design and Data Analysis of Artificial Pancreas Device Systems with Closed-Loop Glucose-Sensing Insulin Delivery. Glucose 86-93 insulin Homo sapiens 102-109 33597626-7 2021 Fasting serum C-peptide levels negatively correlated with glucose CV (P < 0.01). Glucose 58-65 insulin Homo sapiens 14-23 33665204-7 2020 IRAP is associated with and translocated in a stoechiometric fashion to the plasma membrane together with GLUT4 in response to insulin in skeletal muscle and adipose tissue which are the two major glucose storage sites. Glucose 197-204 insulin Homo sapiens 127-134 33593356-4 2021 Available literature indicates that UA can decrease glucose-stimulated insulin secretion and cause beta-cell death. Glucose 52-59 insulin Homo sapiens 71-78 33382998-1 2021 Hyperglycaemia causes pancreatic beta-cells to release insulin that then attaches to a specific expression of receptor isoform and reverses high glucose concentrations. Glucose 145-152 insulin Homo sapiens 55-62 33382998-5 2021 While insulin-activated IRS/PI3K/PKB pathway cascades are primarily known to reduce glucose production, it was recently discovered to increase the Hh signaling pathway"s stability, thereby activating the PI3K/PKB/mammalian target of rapamycin complex 2 (mTORC2) signaling pathway. Glucose 84-91 insulin Homo sapiens 6-13 33325917-10 2021 A survey of the state of the art of closed-loop insulin delivery strategies in response to blood glucose level fluctuation is provided together with insights into the emerging key technologies for diagnosis and drug development. Glucose 97-104 insulin Homo sapiens 48-55 33573649-1 2021 BACKGROUND: Triglyceride glucose (TyG) index is considered a reliable alternative marker of insulin resistance and an independent predictor of cardiovascular (CV) outcomes. Glucose 25-32 insulin Homo sapiens 92-99 33493298-4 2021 For this purpose, primary rat or human adipocytes, and cultured 3T3-L1 adipocytes, were treated with either of the allosteric activators, or AICAR, and basal and insulin-stimulated glucose uptake was assessed. Glucose 181-188 insulin Homo sapiens 162-169 33493298-7 2021 Our results show that insulin-stimulated adipocyte glucose uptake was significantly reduced by A-769662 but not 991, yet neither activator had any clear effects on basal or insulin-stimulated Akt/AS160 signaling. Glucose 51-58 insulin Homo sapiens 22-29 33659254-5 2021 Besides the consequence of pancreatic endocrine dysfunction, we focus on insulin-responsive tissues and glucose transportation to explain glucose homeostasis alteration in CFRD. Glucose 138-145 insulin Homo sapiens 73-80 33659254-7 2021 Furthermore, we demonstrated insulin-induced glucose transporter 4 (GLUT4) translocation to the cell membrane was abnormal in the CFTR knockout mice muscle fibers, suggesting that defective intracellular GLUT4 transportation may be the cause of impaired insulin responses and glucose homeostasis. Glucose 45-52 insulin Homo sapiens 29-36 33554958-1 2021 Glucagon-like peptide-1 (GLP-1) is an incretin hormone that potentiates glucose-stimulated insulin secretion. Glucose 72-79 insulin Homo sapiens 91-98 33565712-8 2021 In vitro insulin secretion after a glucose challenge was similar between DCD and DBD islets. Glucose 35-42 insulin Homo sapiens 9-16 33169429-6 2021 The glucose responsive cleavable linker in these GRIs allow changes in glucose levels to drive the release of active insulin from a circulating depot. Glucose 4-11 insulin Homo sapiens 117-124 33169429-6 2021 The glucose responsive cleavable linker in these GRIs allow changes in glucose levels to drive the release of active insulin from a circulating depot. Glucose 71-78 insulin Homo sapiens 117-124 33572228-5 2021 In addition, exercise induces numerous metabolic benefits, including increases in insulin-independent muscle glucose uptake and insulin sensitivity. Glucose 109-116 insulin Homo sapiens 82-89 33550589-3 2021 Reduction in pancreatic islet beta cell reserve eventually manifests as impaired first-phase insulin response to glucose and abnormal glucose tolerance, which progresses until the functional capacity for beta cell secretion can no longer meet the demand for insulin to control glycemia. Glucose 113-120 insulin Homo sapiens 93-100 33561956-10 2021 Moreover, the problem areas for patients with T2DM mostly included multi-step calculations according to food label interpretations, and adequate insulin dosage based on current blood glucose levels and carbohydrate intake. Glucose 183-190 insulin Homo sapiens 145-152 33541316-1 2021 BACKGROUND: Diabetes mellitus is a chronic non-infectious medical condition which is evident by raised levels of glucose in the blood, because the body cannot produce any or enough of the hormone insulin or use insulin effectively. Glucose 113-120 insulin Homo sapiens 196-203 33665291-5 2021 Insulin resistance was assessed using the homeostasis model assessment (HOMA-IR) formula derived from fasting insulin and glucose levels. Glucose 122-129 insulin Homo sapiens 0-7 33549815-8 2021 Among 1501 intensive care unit patients with sepsis who were started on insulin infusions, 37.0% (95% CI 34.6-39.5%) were initiated at a blood glucose level below 180 mg/dL, the guideline recommended starting threshold. Glucose 143-150 insulin Homo sapiens 72-79 33285243-2 2021 Zinc finger protein 407 (ZFP407) positively regulates PPARgamma target gene expression and insulin-stimulated glucose uptake in cultured adipocytes. Glucose 110-117 insulin Homo sapiens 91-98 33541316-1 2021 BACKGROUND: Diabetes mellitus is a chronic non-infectious medical condition which is evident by raised levels of glucose in the blood, because the body cannot produce any or enough of the hormone insulin or use insulin effectively. Glucose 113-120 insulin Homo sapiens 211-218 33546200-1 2021 Diabetes is a chronic metabolic disorder characterized by inappropriately elevated glucose levels as a result of impaired pancreatic beta cell function and insulin resistance. Glucose 83-90 insulin Homo sapiens 156-163 33491547-5 2021 She was admitted to internal medicine department and discharged one week later: insulin was administered with normalization of blood glucose levels and the involuntary movements gradually disappeared. Glucose 133-140 insulin Homo sapiens 80-87 32791009-6 2021 Human SH-SY5Y neuroblastoma cells exposed to varied concentrations of RE showed a dose-dependent increase in glucose uptake, with a significant increase observed following treatment with 5microg/mL RE for 2h (159+-20.81% of control) that was comparable to maximum insulin stimulation (135.6+-3.2% of control). Glucose 109-116 insulin Homo sapiens 264-271 33546278-4 2021 To this aim, INS-1E cells were exposed to 10 muM of the main EVOO PCs for up to 24 h. Under these conditions, survival, insulin biosynthesis, glucose-stimulated insulin secretion (GSIS), and intracellular signaling activation (protein kinase B (AKT) and cAMP response element-binding protein (CREB)) were evaluated. Glucose 142-149 insulin Homo sapiens 161-168 33535042-4 2021 CRISPR-Cas9-mediated deletion of the variant region, or of the associated enhancer, from human pancreas-derived EndoC-betaH1 cells impairs glucose-stimulated insulin secretion. Glucose 139-146 insulin Homo sapiens 158-165 33401104-4 2021 beta-cells or native islets are accompanied by helper cells, also referred to as accessory cells, to generate a cell cluster that is not only able to accurately secrete insulin in response to glucose, but also superior in terms of other key features (e.g. maintaining a vasculature, longer durability in vivo and not necessitating immunosuppression after transplantation). Glucose 192-199 insulin Homo sapiens 169-176 32363521-8 2021 The blood glucose level was (p < 0.01) lower in group G3 compared to group G1 suggesting the insulin-like activity of Zn. Glucose 10-17 insulin Homo sapiens 93-100 33035729-7 2021 Insulin sensitivity was estimated by the oral glucose sensitivity index (OGIS) and the M-value relative to insulin levels. Glucose 46-53 insulin Homo sapiens 0-7 33288281-4 2021 After 1, 6 and 24 h exposure of isolated islets to different concentrations (1-50 nM) of TCDD we assayed: i) cell survival; ii) ultrastructure; iii) glucose-stimulated insulin secretion (GSIS); iv) expression of selected genes. Glucose 149-156 insulin Homo sapiens 168-175 33051888-8 2021 In cultured HepG2 hepatocellular cells, we found that depletion of Pqlc2 by siRNA-mediated knockdownimpaired the insulin-induced glucose uptake,inhibited GLUT2 mRNA level and suppressed the insulin-induced Aktphosphorylation.By contrary, knockdownof Pqlc2 did not affect thecAMP/dexamethasone-induced gluconeogenesis.In conclusion, our study provides important information onprotein profile change during prolonged fasting with iTRAQ-and LC-MS/MS-based quantitative proteomics, and identifies Pqlc2 as a potential regulator of hepatic glucose metabolism and insulin signaling pathwayin this process. Glucose 129-136 insulin Homo sapiens 113-120 33315628-3 2021 RECENT FINDINGS: Second-generation rapid-acting insulin analogues (i.e. faster insulin aspart and ultrarapid-acting lispro) have shown to be safe, efficient and superior in controlling postprandial plasma glucose levels without an increase in hypoglycaemia. Glucose 205-212 insulin Homo sapiens 48-55 33315628-3 2021 RECENT FINDINGS: Second-generation rapid-acting insulin analogues (i.e. faster insulin aspart and ultrarapid-acting lispro) have shown to be safe, efficient and superior in controlling postprandial plasma glucose levels without an increase in hypoglycaemia. Glucose 205-212 insulin Homo sapiens 79-86 33315628-6 2021 Due to a faster absorption, it is possible to inject the prandial insulin analogues more closely or even after meals without compromising postprandial glucose control. Glucose 151-158 insulin Homo sapiens 66-73 33582911-6 2021 Insulin-stimulated glucose uptake was measured by glucose oxidase/peroxidase assay. Glucose 19-26 insulin Homo sapiens 0-7 33582911-6 2021 Insulin-stimulated glucose uptake was measured by glucose oxidase/peroxidase assay. Glucose 50-57 insulin Homo sapiens 0-7 33582911-10 2021 After induction of mature adipocytes by adipogenesis of hAMSC, the model of insulin-resistant adipocytes was successfully established by TNF-alpha and high glucose intervention. Glucose 156-163 insulin Homo sapiens 76-83 33582911-11 2021 After exosome treatment, the insulin-stimulated glucose uptake was significantly increased. Glucose 48-55 insulin Homo sapiens 29-36 33369575-4 2021 Additional research would be helpful to further assess the ability of newer automated insulin systems to aid in tight glucose management goals during pregnancy and show value in receiving FDA approval. Glucose 118-125 insulin Homo sapiens 86-93 33123769-4 2021 Insulin sensitivity was measured as the glucose infusion rate (GIR) from a hyperinsulinaemic-euglycaemic clamp. Glucose 40-47 insulin Homo sapiens 0-7 33077684-1 2021 With the development of insulin resistance (IR), there is a compensatory increase in the plasma insulin response to offset the defect in insulin action in order to maintain normal glucose tolerance. Glucose 180-187 insulin Homo sapiens 24-31 33077684-1 2021 With the development of insulin resistance (IR), there is a compensatory increase in the plasma insulin response to offset the defect in insulin action in order to maintain normal glucose tolerance. Glucose 180-187 insulin Homo sapiens 96-103 33077684-1 2021 With the development of insulin resistance (IR), there is a compensatory increase in the plasma insulin response to offset the defect in insulin action in order to maintain normal glucose tolerance. Glucose 180-187 insulin Homo sapiens 96-103 33200487-0 2021 Majority of people with type 1 diabetes and multiple daily insulin injection benefit by using Continuous Glucose Monitoring: An analysis based on the GOLD randomised trial (GOLD-5). Glucose 105-112 insulin Homo sapiens 59-66 33200487-1 2021 AIMS: The aim of this study was to identify responders to continuous glucose monitoring (CGM) in relation to reductions in HbA1c and percentage of time in hypoglycaemia after initiation of CGM for persons with Type 1 Diabetes treated with multiple daily insulin injections. Glucose 69-76 insulin Homo sapiens 254-261 33217117-7 2021 Urinary glucose excretion was increased threefold using dapagliflozin (149+-42 vs. 49+-23 g/24h) with a total insulin reduction of 22% (39.7+-12.7 U vs. 30.6+-10.4 U, p=0.004). Glucose 8-15 insulin Homo sapiens 110-117 33310126-0 2021 Ramadan Fasting in Insulin-treated Patients is Associated with Potentially Unfavourable Changes in Glucose Metrics: a Flash Glucose Monitoring (FGM) Study. Glucose 99-106 insulin Homo sapiens 19-26 33891835-2 2021 Insulin is a hormone produced by the beta cells of the pancreas in response to elevated blood glucose. Glucose 94-101 insulin Homo sapiens 0-7 33427875-1 2021 Pancreatic beta cells secrete insulin in response to increased glucose concentrations. Glucose 63-70 insulin Homo sapiens 30-37 33427875-6 2021 https://doi.org/10.1083/jcb.202010039) use 3D FIB-SEM to study the architecture of these cells and to elucidate how glucose stimulation remodels microtubules to control insulin secretory granule exocytosis. Glucose 116-123 insulin Homo sapiens 169-176 33604390-6 2021 Real-time PCR, western blotting, and glucose-stimulated insulin secretion (GSIS) analysis were used to analyze the KLF11 variant that regulates insulin expression and insulin secretion activity in beta cell lines. Glucose 37-44 insulin Homo sapiens 56-63 33206345-2 2021 The present study aimed to characterize the ability of MaR1 to prevent the alterations induced by TNF-alpha on insulin actions in glucose uptake and Akt phosphorylation in cultured human adipocytes from overweight/obese subjects, as well as to investigate the effects of MaR1 acute and chronic administration on Akt phosphorylation in absence/presence of insulin in white adipose tissue (WAT) and skeletal muscle from lean and diet-induced obese (DIO) mice. Glucose 130-137 insulin Homo sapiens 111-118 32720783-0 2021 A 4-week diet with exercise intervention had a better effect on blood glucose levels compared to diet only intervention in obese individuals with insulin resistance. Glucose 70-77 insulin Homo sapiens 146-153 32776775-8 2021 For example, relative to time spent in other behaviors, 30 min/day more MVPA and LPA were both associated with lower 2-hour post glucose load insulin level (-11.8% and -2.7%, respectively). Glucose 129-136 insulin Homo sapiens 142-149 33179277-0 2021 Association of British Clinical Diabetologists (ABCD) and Diabetes UK joint position statement and recommendations on the use of sodium-glucose cotransporter inhibitors with insulin for treatment of type 1 diabetes (Updated October 2020). Glucose 136-143 insulin Homo sapiens 174-181 33271386-10 2021 Insulin sensitivity was examined by western blot and glucose uptake assay. Glucose 53-60 insulin Homo sapiens 0-7 33293347-5 2021 RESULTS: Compared with subjects without NAFLD, those with NAFLD demonstrated impaired insulin-mediated suppression of glucose production and attenuated-not increased-glucose-stimulated/high-insulin lipogenesis. Glucose 118-125 insulin Homo sapiens 86-93 33293347-7 2021 Hepatocellular insulin signaling, assessed for the first time in humans, exhibited a proximal block in insulin-resistant subjects: Signaling was attenuated from the level of the insulin receptor through both glucose and lipogenesis pathways. Glucose 208-215 insulin Homo sapiens 15-22 33293347-7 2021 Hepatocellular insulin signaling, assessed for the first time in humans, exhibited a proximal block in insulin-resistant subjects: Signaling was attenuated from the level of the insulin receptor through both glucose and lipogenesis pathways. Glucose 208-215 insulin Homo sapiens 103-110 33358969-0 2021 Technological innovation of Continuous Glucose Monitoring (CGM) as a tool for commercial aviation pilots with insulin-treated diabetes and stakeholders/regulators: a new chance to improve the directives? Glucose 39-46 insulin Homo sapiens 110-117 33358969-5 2021 CGM clearly showed to prevent hypoglycemic events in insulin-treated diabetic patients by allowing strict monitoring and trend prediction of glucose levels. Glucose 141-148 insulin Homo sapiens 53-60 33369793-17 2021 The findings of our study suggest that milk casein hydrolysate enhances glucose uptake by activating insulin-independent AMP-activated protein kinase signaling in skeletal muscle cells, which might be mediated by a milk casein hydrolysate-derived peptide, namely, isoleucine-proline-proline. Glucose 72-79 insulin Homo sapiens 101-108 33446570-2 2021 Human pancreatic beta cells produce and secrete insulin in response to physiological cues like glucose, and these hallmark functions improve in the years after birth. Glucose 95-102 insulin Homo sapiens 48-55 32750935-1 2021 OBJECTIVE: The automation of insulin treatment is the most challenge aspect of glucose management for type 1 diabetes owing to unexpected exogenous events (e.g., meal intake). Glucose 79-86 insulin Homo sapiens 29-36 32750935-7 2021 In the in silico trial with a variation of insulin sensitivity and dawn phenomenon, the policy achieved a mean glucose of 124.72 mg/dL and percentage time in the normal range of 89.56%. Glucose 111-118 insulin Homo sapiens 43-50 33458829-9 2021 Docking studies showed the complex had better interactions with insulin signaling targets (GLUT-4 and PKB) than p-hydrobenzoic acid, which may influence its glucose uptake effects. Glucose 157-164 insulin Homo sapiens 64-71 33181191-8 2021 At the cellular level, human PAK1-deficient beta-cells showed blunted glucose-stimulated insulin secretion and reduced mitochondrial function. Glucose 70-77 insulin Homo sapiens 89-96 33220491-12 2021 In vivo infusion experiments revealed that while insulin (0.015 nmol/kg/min) and GIV dcVILP (0.75nmol/kg/min) stimulated a comparable glucose uptake in heart, skeletal muscle and brown adipose tissue, GIV dcVILP stimulated ~2 fold higher glucose uptake in white adipose tissue (WAT) compared to insulin. Glucose 134-141 insulin Homo sapiens 49-56 33273729-5 2021 Kisspeptin modulates glucose-stimulated insulin secretion, food intake and/or energy expenditure in animal models and humans. Glucose 21-28 insulin Homo sapiens 40-47 33536639-5 2021 Infection is associated with morphological, transcriptional and functional changes, including reduced numbers of insulin-secretory granules in beta-cells and impaired glucose-stimulated insulin secretion. Glucose 167-174 insulin Homo sapiens 186-193 33146450-7 2021 ConclusionsCPAP treatment significantly improved glycemic control and insulin resistance which is indicated by the decreased levels of HbA1c, fasting glucose, and HOMA-IR in patients with type 2 diabetes and contemporary OSA. Glucose 150-157 insulin Homo sapiens 70-77 33141425-8 2021 Insulin is involved in maintaining the vitality of organs and regulate the metabolism of glucose, protein and lipids. Glucose 89-96 insulin Homo sapiens 0-7 33434724-7 2021 We report that olanzapine inhibits the effects of central KATP channel activation resulting in perturbation of whole body insulin sensitivity, specifically via inhibition of glucose utilization, while leaving central KATP channel-mediated suppression of glucose production intact. Glucose 174-181 insulin Homo sapiens 122-129 33141425-9 2021 Insulin insensitivity decreases the uptake of glucose in the organs and results in loss of skeletal muscles and adipose tissues. Glucose 46-53 insulin Homo sapiens 0-7 33373089-5 2021 Within the dynamic pH-stable skeleton of the protein hydrogels, polymersomes with loaded PEGylated insulin biomacromolecules demonstrate a pH-responsive reversible swelling-deswelling and a desirable, on-demand cargo release which is induced by the enzymatic oxidation of glucose to gluconic acid. Glucose 272-279 insulin Homo sapiens 99-106 33503433-5 2021 In parallel with reduced beta cell recruitment, CDK2 restricts oxidative glucose metabolism while promoting glucose-dependent amplification of insulin secretion. Glucose 108-115 insulin Homo sapiens 143-150 33486704-4 2021 RESULTS: Incubation of MIN-6 cells with low glucose and total HDL increased insulin release two-fold. Glucose 44-51 insulin Homo sapiens 76-83 33486704-5 2021 Meanwhile, when high glucose and HDL were used, insulin release increased more than five times. Glucose 21-28 insulin Homo sapiens 48-55 33486704-7 2021 The insulin content of the MIN-6 cells incubated with low glucose and any of the five HDL subclasses had a modest reduction compared with their controls. Glucose 58-65 insulin Homo sapiens 4-11 33486704-9 2021 CONCLUSIONS: HDL can trigger insulin secretion under low, normal, and high glucose conditions. Glucose 75-82 insulin Homo sapiens 29-36 33551987-1 2020 Background and Objectives: Triglyceride-glucose (TyG) is an emerging vital indicator of insulin resistance and is associated with increased risk of T2DM and cardiovascular events. Glucose 40-47 insulin Homo sapiens 88-95 33484736-1 2021 Diabetes Mellitus is a group of diseases characterized by high blood glucose levels due to patients" inability to produce sufficient insulin. Glucose 69-76 insulin Homo sapiens 133-140 33479282-9 2021 Knockdown of ADH1B expression decreased insulin-stimulated glucose uptake. Glucose 59-66 insulin Homo sapiens 40-47 33463547-1 2021 Both basal and glucose-stimulated insulin release occur primarily by insulin secretory granule exocytosis from pancreatic beta cells, and both are needed to maintain normoglycemia. Glucose 15-22 insulin Homo sapiens 34-41 33463547-1 2021 Both basal and glucose-stimulated insulin release occur primarily by insulin secretory granule exocytosis from pancreatic beta cells, and both are needed to maintain normoglycemia. Glucose 15-22 insulin Homo sapiens 69-76 33462097-1 2021 INTRODUCTION: The successful treatment of type 1 diabetes (T1D) requires those affected to employ insulin therapy to maintain their blood glucose levels as close to normal to avoid complications in the long-term. Glucose 138-145 insulin Homo sapiens 98-105 33398164-4 2021 Glucose stimulates insulin secretion from beta-cells in a bi-modal fashion, and new insights about the underlying mechanisms, particularly relating to the second or amplifying phase of this secretory response, have been recently gained. Glucose 0-7 insulin Homo sapiens 19-26 33572903-1 2021 Pancreatic beta-cell insulin secretion, which responds to various secretagogues and hormonal regulations, is reviewed here, emphasizing the fundamental redox signaling by NADPH oxidase 4- (NOX4-) mediated H2O2 production for glucose-stimulated insulin secretion (GSIS). Glucose 225-232 insulin Homo sapiens 21-28 33659881-1 2021 Insulin"s activation of PI3K/Akt signaling, stimulates glucose uptake by enhancing delivery of GLUT4 to the cell surface. Glucose 55-62 insulin Homo sapiens 0-7 33525758-4 2021 Moreover, the cell assay revealed that the addition of MeOH-E (12.5 microg/mL) increased about 37% of glucose uptake in insulin resistant (IR) HepG2 as compared to untreated IR HepG2 cells. Glucose 102-109 insulin Homo sapiens 120-127 33532655-5 2021 Moreover, insulin regulates the bioavailability of the sodium-glucose co-transporters-SGLT2 inhibitor, and inhibits renal gluconeogenesis. Glucose 62-69 insulin Homo sapiens 10-17 33613155-0 2021 Pentadecanoic acid promotes basal and insulin-stimulated glucose uptake in C2C12 myotubes. Glucose 57-64 insulin Homo sapiens 38-45 33613155-6 2021 Objective: The present study aimed to investigate the effect and potential mechanism of action of PA on basal and insulin stimulated glucose uptake in C2C12 myotubes. Glucose 133-140 insulin Homo sapiens 114-121 33613155-13 2021 Moreover, PA significantly promoted insulin-stimulated glucose uptake in myotubes. Glucose 55-62 insulin Homo sapiens 36-43 33325779-0 2021 First outpatient evaluation of a tubeless automated insulin delivery system with customizable glucose targets in children and adults with type 1 diabetes. Glucose 94-101 insulin Homo sapiens 52-59 32745838-0 2021 Polyphenol-rich extract of Zhenjiang aromatic vinegar ameliorates high glucose-induced insulin resistance by regulating JNK-IRS-1 and PI3K/Akt signaling pathways. Glucose 71-78 insulin Homo sapiens 87-94 33452188-0 2021 Real-time continuous glucose monitoring versus self-monitoring of blood glucose in adults with insulin-treated type 2 diabetes: a protocol for a randomised controlled single-centre trial. Glucose 21-28 insulin Homo sapiens 95-102 33249079-1 2021 Glucose production and the consumption of high levels of carbohydrate increase the chance of insulin resistance, especially in cases of obesity. Glucose 0-7 insulin Homo sapiens 93-100 33435964-1 2021 BACKGROUND: The triglyceride-glucose (TyG) index, which is a simple surrogate marker of insulin resistance, has been suggested as a contributor of cardiovascular disease. Glucose 29-36 insulin Homo sapiens 88-95 33521071-0 2020 The Triglyceride-Glucose Index, an Insulin Resistance Marker, Was Non-linear Associated With All-Cause and Cardiovascular Mortality in the General Population. Glucose 17-24 insulin Homo sapiens 35-42 33519707-0 2020 Observations on Glucose Excursions With the Use of a Simple Protocol for Insulin, Following Antenatal Betamethasone Administration. Glucose 16-23 insulin Homo sapiens 73-80 33445702-6 2021 Moreover, glucose uptake in insulin-resistant HepG2 cell line was analyzed. Glucose 10-17 insulin Homo sapiens 28-35 33445702-10 2021 We also found that H. tuberosus showed a less toxicity in mouse fibroblast cells and enhance the glucose uptake in insulin-resistant HepG2 cells. Glucose 97-104 insulin Homo sapiens 115-122 33469328-15 2021 Conclusion: Overall, insulin glargine biosimilar EZL and originator insulin glargine LAN have shown a similar immunogenicity profile, as well as efficacy in providing glucose control and safety findings in T2D populations. Glucose 167-174 insulin Homo sapiens 68-75 33469328-15 2021 Conclusion: Overall, insulin glargine biosimilar EZL and originator insulin glargine LAN have shown a similar immunogenicity profile, as well as efficacy in providing glucose control and safety findings in T2D populations. Glucose 167-174 insulin Homo sapiens 21-28 33438288-4 2021 The recovery, viability, insulin content, endocrine cellular composition, GLUT2 expression in beta cells, differentiation and proliferation potential, and glucose-stimulated insulin secretion of PPIs were assessed on days 3, 7, and 14 of tissue culture (n = 5 on each day). Glucose 155-162 insulin Homo sapiens 174-181 33438288-5 2021 RESULTS: Compared with day 7 of tissue culture, islets on day 14 had a lower recovery, GLUT2 expression in beta cells, proliferation capacity of endocrine cells, and glucose-induced insulin stimulation index. Glucose 166-173 insulin Homo sapiens 182-189 33488074-1 2021 The glucose-sensitive self-adjusting drug delivery system simulates the physiological model of the human pancreas-secreting insulin and then precisely regulates the release of hypoglycemic drugs and controls the blood sugar. Glucose 4-11 insulin Homo sapiens 124-131 33488074-4 2021 Among these, the glucose-sensitive polymer carrier based on PBA has the advantages of better stability, long-term storage, and reversible glucose response, and the loading of insulin in it can achieve the controlled release of drugs in the human environment. Glucose 17-24 insulin Homo sapiens 175-182 33428210-7 2022 Exercise training induced adaptation in the energy sensing AMP-activated protein kinase (AMPK) and the insulin-sensitive glucose transporter GLUT4 protein levels are sensitive to pre-exercise feeding status in both healthy individuals and in individuals classified as overweight or obese. Glucose 121-128 insulin Homo sapiens 103-110 33417747-6 2021 RESULTS: Glutamine dose-dependently amplified insulin secretion in the presence of high glucose in both MIN6-K8 cells and Glud1KObetaCL. Glucose 88-95 insulin Homo sapiens 46-53 33432036-1 2021 The triglyceride-glucose (TyG) index is a simple surrogate marker of insulin resistance. Glucose 17-24 insulin Homo sapiens 69-76 33417277-6 2021 Homeostasis model assessment of insulin resistance (HOMA-IR) values was calculated as: fasting glucose (mmol/L)xfasting insulin (mIU/L)/22.5. Glucose 95-102 insulin Homo sapiens 32-39 33417747-14 2021 Our data also suggest that glutamine exerts a permissive effect on glucose-induced insulin secretion. Glucose 67-74 insulin Homo sapiens 83-90 33402193-0 2021 The insulin resistance by triglyceride glucose index and risk for dementia: population-based study. Glucose 39-46 insulin Homo sapiens 4-11 33511337-0 2021 Oral minimal model-based estimates of insulin sensitivity in obese youth depend on oral glucose tolerance test protocol duration. Glucose 88-95 insulin Homo sapiens 38-45 33511337-1 2021 Introduction: The Oral Minimal Model (OMM), a differential-equations based mathematical model of glucose-insulin dynamics, utilizes data from a frequently sampled oral glucose tolerance test (OGTT) to quantify insulin sensitivity ( S I ). Glucose 97-104 insulin Homo sapiens 105-112 33405297-7 2021 With increasing insulin dose, a step-wise reduction in mean glucose excursion was observed from 1-6 hr (p=0.008). Glucose 60-67 insulin Homo sapiens 16-23 33419065-2 2021 Insulin regulates glucose homeostasis via its effects on glucose production from the liver and kidneys and glucose disposal in peripheral tissues (mainly skeletal muscle). Glucose 18-25 insulin Homo sapiens 0-7 33419065-2 2021 Insulin regulates glucose homeostasis via its effects on glucose production from the liver and kidneys and glucose disposal in peripheral tissues (mainly skeletal muscle). Glucose 57-64 insulin Homo sapiens 0-7 33419065-3 2021 Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. Glucose 16-23 insulin Homo sapiens 56-63 33419065-3 2021 Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. Glucose 82-89 insulin Homo sapiens 56-63 33419065-3 2021 Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. Glucose 82-89 insulin Homo sapiens 56-63 33419065-4 2021 During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. Glucose 132-139 insulin Homo sapiens 50-57 33419065-4 2021 During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. Glucose 210-217 insulin Homo sapiens 50-57 33400373-2 2021 Protein tyrosine phosphatase 1B (PTP1B), a negative regulator for insulin and leptin signaling, potentially modulates glucose and energy homeostasis. Glucose 118-125 insulin Homo sapiens 66-73 33419065-4 2021 During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. Glucose 210-217 insulin Homo sapiens 50-57 33399259-0 2021 Effective Use of Computerized Insulin Dose Adjustment Algorithms on Continuous Glucose Monitoring Results by a Clinical Pharmacist - Proof-of-Concept. Glucose 79-86 insulin Homo sapiens 30-37 32478975-4 2021 In this review we summarize proposed pathophysiological mechanisms underlying the association between low muscle mass and poor clinical outcomes in older cancer patients including 1) systemic inflammation; 2) insulin-dependent glucose handling; 3) mitochondrial function; 4) protein status, and; 5) pharmacokinetics of anticancer drugs. Glucose 227-234 insulin Homo sapiens 209-216 33861444-2 2021 The transition from normal glucose tolerance to type 2 diabetes (T2D) is preceded by increased Insulin resistance (IR), an independent predictor of the development of T2D in high risk (e.g. obese populations, pre-diabetes) individuals. Glucose 27-34 insulin Homo sapiens 95-102 33515428-4 2021 Intranasally administered insulin is assumed to trigger improvements in synaptic plasticity and regional glucose uptake as well as alleviations of Alzheimer"s disease neuropathology; additional contributions of changes in hypothalamus-pituitary-adrenocortical axis activity and sleep-related mechanisms are discussed. Glucose 105-112 insulin Homo sapiens 26-33 31916517-8 2021 RESULTS: The exposure of long-term air pollution such as haze reduced insulin-dependent glucose uptake, leading to insulin resistance; damage beta cell function, leading to decreased insulin secretion, and promote subcutaneous fat accumulation. Glucose 88-95 insulin Homo sapiens 115-122 31916517-8 2021 RESULTS: The exposure of long-term air pollution such as haze reduced insulin-dependent glucose uptake, leading to insulin resistance; damage beta cell function, leading to decreased insulin secretion, and promote subcutaneous fat accumulation. Glucose 88-95 insulin Homo sapiens 115-122 32310854-10 2021 CONCLUSIONS: In T2DM patients, the addition of DPP-4 inhibitors to routine subcutaneous insulin therapy may significantly reduce hypoglycemic events while maintaining acceptable recommended ranges of glucose. Glucose 200-207 insulin Homo sapiens 88-95 32504504-9 2021 BeWo cells cultured with high glucose and insulin showed decreased SDF2 expression, while high glucose increased CHOP and sXBP1 expression, which was then significantly reverted with insulin treatment. Glucose 30-37 insulin Homo sapiens 183-190 32504504-9 2021 BeWo cells cultured with high glucose and insulin showed decreased SDF2 expression, while high glucose increased CHOP and sXBP1 expression, which was then significantly reverted with insulin treatment. Glucose 95-102 insulin Homo sapiens 183-190 33115825-6 2021 We uncovered deficits in insulin secretion, partly due to reduced mitochondrial oxygen consumption rate, glucose-stimulated Ca2+ flux, and reduced insulin content associated with loss of eIF4E, the mRNA 5"-cap binding protein of the initiation complex and binding partner of eIF4G1. Glucose 105-112 insulin Homo sapiens 25-32 33115828-7 2021 In contrast, despite insulin exerting a glucose lowering effect, it failed to improve myocardial function and fibrosis. Glucose 40-47 insulin Homo sapiens 21-28 33122393-6 2021 In LCSFA-HFD, whole body insulin sensitivity and peripheral insulin-stimulated glucose disposal were reduced. Glucose 79-86 insulin Homo sapiens 60-67 32453474-9 2021 Finally, minor allele T of rs846906 associated with higher prevalence of arterial hypertension, higher body mass index and waist circumference, thus conferring risk to a lower estimated glucose disposal rate, a surrogate marker of insulin sensitivity (OR=1.23; CI95% = 1.06-1.42; p=0.004). Glucose 186-193 insulin Homo sapiens 231-238 32758007-1 2021 Continuous glucose monitoring (CGM) is safe and effective in improving glycemic control in insulin-treated patients with diabetes. Glucose 11-18 insulin Homo sapiens 91-98 32902125-4 2021 10 h exposure of insulin aspart was higher with FA vs. IAsp (p = 0.037) in line with the 10% higher insulin requirements to achieve similar glucose control. Glucose 140-147 insulin Homo sapiens 17-24 33157117-2 2021 Triglyceride-glucose (TyG) index is a marker of insulin resistance. Glucose 13-20 insulin Homo sapiens 48-55 33581594-6 2021 Oral glucose lowering drugs can be considered in patients with mild COVID illness who have mild hyperglycemia [pre-meal blood glucose of <180 mg/dl (10 mmol/L) and post-meal blood glucose of <250 mg/dl (13.9 mmol/L)] and no contraindication to the use of these agents.. All patients with moderate-severe disease and/or hyperglycemia of greater severity should be initiated on insulin therapy. Glucose 5-12 insulin Homo sapiens 376-383 32628602-1 2021 INTRODUCTION: New evidences suggest that combining basal insulin with glucagone-like peptide 1 receptor agonists (GLP-1RA) in patients with type 2 diabetes could promptly ameliorate the glucose control and prevent both hypoglycaemia and weight gain compared with more intensive insulin regimens. Glucose 186-193 insulin Homo sapiens 57-64 32628602-4 2021 RESULTS: FRCs provide a significative improvement in glucose control in both insulin-naive (-1.4% to -2% HbA1c from aseline) and insulin-experienced (-1.5% to -2% HbA1c from baseline) type 2 diabetic patients with moderate glucose impairment. Glucose 53-60 insulin Homo sapiens 77-84 32628602-4 2021 RESULTS: FRCs provide a significative improvement in glucose control in both insulin-naive (-1.4% to -2% HbA1c from aseline) and insulin-experienced (-1.5% to -2% HbA1c from baseline) type 2 diabetic patients with moderate glucose impairment. Glucose 53-60 insulin Homo sapiens 129-136 32660410-1 2021 OBJECTIVE: Glucose metabolism increases ATP/ADP ratio within the beta-cells and causes ATP-sensitive K+ (KATP) channel closure and consequently insulin secretion. Glucose 11-18 insulin Homo sapiens 144-151 33456363-1 2021 Background: The triglyceride-glucose (TyG) index has been reported to be a simple and reliable surrogate marker of insulin resistance. Glucose 29-36 insulin Homo sapiens 115-122 33180640-9 2021 The 3 hr insulin:glucose iAUC was reduced following lunch in both SQUAT (30%) and WALK (23%) compared to SIT (p<0.05). Glucose 17-24 insulin Homo sapiens 9-16 33428210-16 2022 Exercise before versus after nutrient intake can also result in an increase in skeletal muscle GLUT4 and CHC22 levels, which are involved in insulin-stimulated glucose transport. Glucose 160-167 insulin Homo sapiens 141-148 33390180-0 2021 Using trend arrows in continuous glucose monitoring systems for insulin adjustment in clinical practice: Brazilian Diabetes Society Position Statement. Glucose 33-40 insulin Homo sapiens 64-71 33390180-1 2021 This manuscript reports the Brazilian Diabetes Society Position Statement for insulin adjustments based on trend arrows observed in continuous glucose monitoring systems. Glucose 143-150 insulin Homo sapiens 78-85 32548833-6 2021 Pharmacological treatment is initiated if conservative strategies fail to provide expected glucose levels during follow-ups.Insulin has been the first choice for the treatment of diabetes during pregnancy. Glucose 91-98 insulin Homo sapiens 124-131 32548833-8 2021 However, a high percentage of women, which may be up to 46% may require additional insulin to maintain expected blood glucose levels. Glucose 118-125 insulin Homo sapiens 83-90 32524720-6 2021 There was a larger increase of glucose during tests in which exogenous insulin was used (+7.9 vs. +5.3 mmol/L, p<0.001) and exogenous insulin use was associated with a slightly lower estimated peak C-peptide (relative change: -15%, p=0.02). Glucose 31-38 insulin Homo sapiens 71-78 32755490-5 2021 However, it has been hypothesised that mammalian target of rapamycin complex 1 (mTORC1) hyperactivation in the presence of amino acid overload contributes to reduced insulin-stimulated glucose uptake due to insulin receptor substrate (IRS) degradation and reduced Akt-AS160 activity. Glucose 185-192 insulin Homo sapiens 166-173 32755490-8 2021 Novelty bullet: Excess amino acids may over-activate mTOR, resulting in desensitisation of IRS-1 and reduced insulin-mediated glucose uptake. Glucose 127-134 insulin Homo sapiens 110-117 32640211-4 2021 We hypothesized that augmented insulin secretion may explain how liraglutide indirectly mediates cardioprotection, which thereby increases myocardial glucose oxidation. Glucose 150-157 insulin Homo sapiens 31-38 31916517-8 2021 RESULTS: The exposure of long-term air pollution such as haze reduced insulin-dependent glucose uptake, leading to insulin resistance; damage beta cell function, leading to decreased insulin secretion, and promote subcutaneous fat accumulation. Glucose 88-95 insulin Homo sapiens 70-77 33092512-5 2021 A medical savour who works on diabetic problem had been known that the level of glucose in plasma changes independently as regard to eating habits and use of insulin and medicines. Glucose 80-87 insulin Homo sapiens 158-165 33098852-6 2021 Primary outcome measure was change in the whole-body insulin sensitivity index (Matsuda index) derived from the oral glucose tolerance test (OGTT) over the treatment period. Glucose 117-124 insulin Homo sapiens 53-60 32564762-5 2021 However, these protocols produce beta-like cells that show low glucose stimulated insulin secretion [GSIS] function and mirror GSIS profile of functionally immature neonatal beta-cells. Glucose 63-70 insulin Homo sapiens 82-89 33292149-8 2021 Besides enhancing glucose-evoked insulin release from pancreatic beta-cells, these therapeutic agents also play a vital role to facilitate neurite outgrowth and nerve conduction velocity in dorsal root ganglion. Glucose 18-25 insulin Homo sapiens 33-40 33067312-0 2021 Glucose-Sensing Mediated by Portal GLP-1 Receptor is Markedly Impaired in Insulin-Resistant Obese Animals. Glucose 0-7 insulin Homo sapiens 74-81 33067312-7 2021 We propose that insulin-resistance, through a reduction in GLP-1r density, leads to functional portal desensitization with a consequent suppression of vagal sensitivity to portal glucose. Glucose 179-186 insulin Homo sapiens 16-23 33651867-3 2021 Amyloid deposition at insulin injection sites can interfere with absorption, leading to poor glucose control. Glucose 93-100 insulin Homo sapiens 22-29 32885596-9 2021 We suggest that reducing carbohydrate at the expense of fat or protein, could further improve glucose control during fully closed-loop insulin therapy in hospital. Glucose 94-101 insulin Homo sapiens 135-142 32886401-1 2021 The glucose-dependent insulinotropic polypeptide (GIP) fragment GIP(3-30)NH2 is a selective, competitive GIP receptor antagonist, and doses of 800-1200 pmol/kg/min inhibit GIP-induced potentiation of glucose-stimulated insulin secretion by >80% in humans. Glucose 4-11 insulin Homo sapiens 22-29 32886401-5 2021 GIP-induced potentiation of glucose-stimulated insulin secretion was reduced by 44 +- 10% and 84 +- 10% during D and E, respectively. Glucose 28-35 insulin Homo sapiens 47-54 33314006-1 2021 INTRODUCTION: The aim of this study was to evaluate change in laboratory-measured HbA1c in patients with either type 1 diabetes (T1D) or type 2 diabetes (T2D) on insulin therapy following initiation of the FreeStyle Libre flash glucose monitoring system. Glucose 229-236 insulin Homo sapiens 162-169 32455427-4 2021 Specifically, we provide evidence that the key diabetogenic cytokine IL-1beta disrupts functionality of the beta cell circadian clock and impairs circadian regulation of glucose-stimulated insulin secretion. Glucose 170-177 insulin Homo sapiens 189-196 33017586-2 2021 Apart from its effects on glucose level, insulin has an important role in the reproductive system directly by binding on insulin and IGF receptors in the brain and testis. Glucose 26-33 insulin Homo sapiens 41-48 32746033-1 2021 OBJECTIVE: The aim of this work is to propose a new machine-learning based model to improve the calculation of mealtime insulin boluses (MIB) in type 1 diabetes (T1D) therapy using continuous glucose monitoring (CGM) data. Glucose 192-199 insulin Homo sapiens 120-127 33159943-0 2021 Monitoring the formation of insulin oligomers using a NIR emitting glucose-conjugated BODIPY dye. Glucose 67-74 insulin Homo sapiens 28-35 33832651-3 2021 Pancreatic beta-cells secrete insulin at high glucose concentration, thereby finely regulating glycaemia by the hypoglycaemic effects of this hormone. Glucose 46-53 insulin Homo sapiens 30-37 33832653-1 2021 Type 2 diabetes (T2D), a heterogeneous disorder derived from metabolic dysfunctions, leads to a glucose overflow in the circulation due to both defective insulin secretion and peripheral insulin resistance. Glucose 96-103 insulin Homo sapiens 154-161 33832653-4 2021 Here, we review the physiological FFA roles onto glucose-stimulated insulin secretion (GSIS) and the pathological ones affecting many steps of the mechanisms and modulation of GSIS. Glucose 49-56 insulin Homo sapiens 68-75 32977263-6 2021 Insulin resistance was assessed by triglycerides and glucose (TyG) index. Glucose 53-60 insulin Homo sapiens 0-7 32205007-1 2021 INTRODUCTION: Skeletal muscle is the primary site of glucose uptake and its reduction would increase insulin resistance, which is a determinant factor for diseases such as type 2 diabetes mellitus, hypertension, and metabolic syndrome. Glucose 53-60 insulin Homo sapiens 101-108 33400644-3 2021 Glucose concentration values are affected by various physiological and metabolic variations, such as physical activity (PA) and acute psychological stress (APS), in addition to meals and insulin. Glucose 0-7 insulin Homo sapiens 187-194 33191527-1 2021 KEY POINTS: Exercise, insulin-infusion and low-glucose mixed-nutrient meal ingestion increases muscle microvascular blood flow which in part facilitates glucose delivery and disposal. Glucose 153-160 insulin Homo sapiens 22-29 33097945-0 2021 Effect of exercise intensity on exogenous glucose requirements to maintain stable glycemia at high insulin levels in type 1 diabetes. Glucose 42-49 insulin Homo sapiens 99-106 33097945-1 2021 CONTEXT: Under basal insulin levels, there is an inverted U relationship between exercise intensity and exogenous glucose requirements to maintain stable blood glucose levels in type 1 diabetes (T1D), with no glucose required for intense exercise (80% VO2 peak), implying that high intensity exercise is not conducive to hypoglycemia. Glucose 114-121 insulin Homo sapiens 21-28 33097945-1 2021 CONTEXT: Under basal insulin levels, there is an inverted U relationship between exercise intensity and exogenous glucose requirements to maintain stable blood glucose levels in type 1 diabetes (T1D), with no glucose required for intense exercise (80% VO2 peak), implying that high intensity exercise is not conducive to hypoglycemia. Glucose 160-167 insulin Homo sapiens 21-28 33097945-1 2021 CONTEXT: Under basal insulin levels, there is an inverted U relationship between exercise intensity and exogenous glucose requirements to maintain stable blood glucose levels in type 1 diabetes (T1D), with no glucose required for intense exercise (80% VO2 peak), implying that high intensity exercise is not conducive to hypoglycemia. Glucose 160-167 insulin Homo sapiens 21-28 31640408-1 2021 INTRODUCTION: It is important to have accurate information regarding when individuals with type 1 diabetes have eaten and taken insulin to reconcile those events with their blood glucose levels throughout the day. Glucose 179-186 insulin Homo sapiens 128-135 31833388-1 2021 BACKGROUND: Although real-time continuous glucose monitoring (rtCGM) has been shown to improve glycemic control in patients with type 1 diabetes mellitus and type 2 diabetes mellitus treated with insulin, rates of adoption have been low. Glucose 42-49 insulin Homo sapiens 196-203 33091596-6 2021 Meanwhile, during the differentiation of pPSCs into insulin-secreting cells, we found that the maturation marker genes Insulin, NKX6.1, MafA, and NeuroD1 was upregulated in insulin-secreting cell masses differentiationed from pPSCs after FA treatment, and the functional molecules Insulin and C-peptide were increased, the ability to secrete insulin in response to high glucose was also increased. Glucose 370-377 insulin Homo sapiens 52-59 33091596-6 2021 Meanwhile, during the differentiation of pPSCs into insulin-secreting cells, we found that the maturation marker genes Insulin, NKX6.1, MafA, and NeuroD1 was upregulated in insulin-secreting cell masses differentiationed from pPSCs after FA treatment, and the functional molecules Insulin and C-peptide were increased, the ability to secrete insulin in response to high glucose was also increased. Glucose 370-377 insulin Homo sapiens 119-126 33091596-6 2021 Meanwhile, during the differentiation of pPSCs into insulin-secreting cells, we found that the maturation marker genes Insulin, NKX6.1, MafA, and NeuroD1 was upregulated in insulin-secreting cell masses differentiationed from pPSCs after FA treatment, and the functional molecules Insulin and C-peptide were increased, the ability to secrete insulin in response to high glucose was also increased. Glucose 370-377 insulin Homo sapiens 173-180 33091596-6 2021 Meanwhile, during the differentiation of pPSCs into insulin-secreting cells, we found that the maturation marker genes Insulin, NKX6.1, MafA, and NeuroD1 was upregulated in insulin-secreting cell masses differentiationed from pPSCs after FA treatment, and the functional molecules Insulin and C-peptide were increased, the ability to secrete insulin in response to high glucose was also increased. Glucose 370-377 insulin Homo sapiens 173-180 32729150-1 2021 The integrated minimal model allows assessment of clinical diagnosis indices, for example, insulin sensitivity (SI ) and glucose effectiveness (SG ), from data of the insulin-modified intravenous glucose tolerance test (IVGTT), which is laborious with an intense sampling schedule, up to 32 samples. Glucose 196-203 insulin Homo sapiens 167-174 33191527-5 2021 High-glucose ingestion 3 h post-exercise leads to greater postprandial blood glucose, non-esterified fatty acids, and fat oxidation, and a delay in the insulin response to the meal compared to control. Glucose 5-12 insulin Homo sapiens 152-159 33689522-5 2021 Glucose profile was assessed by using fasting glycemia, insulin, and glycated hemoglobin. Glucose 0-7 insulin Homo sapiens 56-63 33129839-6 2021 In vivo functional parameters of insulin secretion, assessed by hyperglycemic clamp, negatively correlated with the increase in fibers [beta-cell Glucose Sensitivity (r = -0.84; p = 0.01), incremental second-phase insulin secretion (r = -0.84, p = 0.03) and arginine-stimulated insulin secretion (r = -0.76, p = 0.04)]. Glucose 146-153 insulin Homo sapiens 33-40 33100202-3 2021 FFAR1/GPR40 have high level of expression in beta-cells of pancreas and requirement of glucose for stimulating insulin release results in immense stimulation to utilise these targets in the medication of T2DM. Glucose 87-94 insulin Homo sapiens 111-118 33175605-1 2021 Insulin controls glucose uptake into muscle and fat cells by inducing a net redistribution of GLUT4 from intracellular storage to the plasma membrane (PM). Glucose 17-24 insulin Homo sapiens 0-7 33349659-5 2021 We used the assay for continuous quantification of glucose and insulin concentrations in the blood of live diabetic rats to resolve inter-animal differences in the pharmacokinetic response to insulin as well as discriminate pharmacokinetic profiles from different insulin formulations. Glucose 51-58 insulin Homo sapiens 192-199 33349659-5 2021 We used the assay for continuous quantification of glucose and insulin concentrations in the blood of live diabetic rats to resolve inter-animal differences in the pharmacokinetic response to insulin as well as discriminate pharmacokinetic profiles from different insulin formulations. Glucose 51-58 insulin Homo sapiens 192-199 33886863-8 2021 CONCLUSION: The phased implementation of a formal education program, fostering the use of electronic insulin therapy protocols and dynamic manuals, received good adherence and has shown to be safe and effective for blood glucose control in critically ill patients, with a concomitant decrease in hypoglycemia. Glucose 221-228 insulin Homo sapiens 101-108 33400857-3 2021 We previously demonstrated that the leucine metabolite, alpha-ketoisocaproate (KIC), inhibited insulin-stimulated glucose transport in myotubes. Glucose 114-121 insulin Homo sapiens 95-102 33400857-6 2021 Although KIC suppressed insulin-stimulated glucose transport, addition of the inflammatory factors did not worsen this effect. Glucose 43-50 insulin Homo sapiens 24-31 33400857-10 2021 Depletion of E1alpha subunit of branched-chain alpha-keto acid dehydrogenase, the enzyme that catalyzes the oxidative decarboxylation of KIC, suppressed insulin-stimulated glucose transport, especially in cells incubated in KIC. Glucose 172-179 insulin Homo sapiens 153-160 33400857-11 2021 Thus, defects in BCAA catabolism are contributory to insulin resistance of glucose transport in myotubes, especially in the presence of KIC. Glucose 75-82 insulin Homo sapiens 53-60 33433056-2 2021 In obesity, skeletal muscle, the main tissue responsible for insulin-mediated glucose uptake, exhibits dysregulation of insulin signaling, glucose uptake, lipid metabolism, and mitochondrial function, thus, promoting type 2 diabetes. Glucose 78-85 insulin Homo sapiens 61-68 33433056-2 2021 In obesity, skeletal muscle, the main tissue responsible for insulin-mediated glucose uptake, exhibits dysregulation of insulin signaling, glucose uptake, lipid metabolism, and mitochondrial function, thus, promoting type 2 diabetes. Glucose 139-146 insulin Homo sapiens 61-68 33278756-11 2021 Only in Con ewes, serum glucose levels showed significant fluctuations throughout the entire observation period (P 0.05) and were correlated negatively with those of beta-hydroxybutyrate (r2: 0.70; P < 0.01, r2: 0.76; P < 0.01) and positively with insulin (r2: 0.46; P < 0.05, r2: 0.59; P < 0.05) on d 30 and 14 a.p., respectively. Glucose 24-31 insulin Homo sapiens 250-257 33463901-7 2021 Paradigms are now being challenged by growing evidence of a phenomenon called glucotoxicity, providing an explanation for the benefits of lowering glucose levels with insulin therapy in these patients. Glucose 147-154 insulin Homo sapiens 167-174 33109424-0 2021 Corrigendum to "Acacetin enhances glucose uptake through insulin-independent GLUT4 translocation in L6 myotubes" [Phytomedicine 68 (2020)/153178]. Glucose 34-41 insulin Homo sapiens 57-64 33243626-1 2021 Prolonged hyperglycemia is toxic to pancreatic beta cells, generating excessive reactive oxygen species, defective glucose-stimulated insulin secretion, decreased insulin production, and eventually beta cell death and diabetes. Glucose 115-122 insulin Homo sapiens 134-141 33250274-1 2021 Individuals with type 1 and advanced type 2 diabetes require daily insulin therapy to maintain blood glucose levels in normoglycemic ranges to prevent associated morbidity and mortality. Glucose 101-108 insulin Homo sapiens 67-74 33250274-2 2021 Optimal insulin delivery should offer both precise dosing in response to real-time blood glucose levels as well as a feasible and low-burden administration route to promote long-term adherence. Glucose 89-96 insulin Homo sapiens 8-15 32761185-2 2020 GLUT12 was initially isolated as a novel GLUT4-like transporter involved in insulin-dependent glucose transport. Glucose 94-101 insulin Homo sapiens 76-83 33490853-2 2021 Objective: The purpose of this study was to determine the relationship between the longitudinal changes in weight/body composition and insulin sensitivity and response in women with normal glucose tolerance (NGT) and those who developed GDM. Glucose 189-196 insulin Homo sapiens 135-142 33383953-1 2020 The triglyceride glucose (TyG) index, a product of triglyceride and fasting glucose, is a reliable marker for insulin resistance. Glucose 17-24 insulin Homo sapiens 110-117 33383953-1 2020 The triglyceride glucose (TyG) index, a product of triglyceride and fasting glucose, is a reliable marker for insulin resistance. Glucose 76-83 insulin Homo sapiens 110-117 33396420-7 2020 Islets from 12 week Cd-treated animals had significantly less glucose-stimulated insulin release compared to islets from saline-treated control animals. Glucose 62-69 insulin Homo sapiens 81-88 25905318-9 2000 It is also well established that improvement in glucose control with goal-directed insulin regimens reduces hospital complications and mortality in critically ill, as well as in general medicine and surgery patients ((6-11)). Glucose 48-55 insulin Homo sapiens 83-90 32761185-11 2020 These tissue distributions suggest a unique function of GLUT12, besides that of an insulin-dependent glucose transport. Glucose 101-108 insulin Homo sapiens 83-90 33375551-3 2020 The anti-diabetic regimen is currently based on insulin injection, but the patient is planning to start the use of an insulin pump to have better control of glucose levels. Glucose 157-164 insulin Homo sapiens 118-125 33369175-1 2021 AIMS/INTRODUCTION: Controlling postprandial glucose levels in patients with type 1 diabetes (T1D) is challenging even under the adequate treatment of insulin injection. Glucose 44-51 insulin Homo sapiens 150-157 33100269-9 2020 In a beta-cell selective manner, these findings indicate that nitric oxide targets the same metabolic pathways necessary for glucose stimulated insulin secretion for protection from viral lysis. Glucose 125-132 insulin Homo sapiens 144-151 33332410-5 2020 The prediction is usually made for about 30 minutes and insulin delivery is restarted at the previous level if a rise in blood glucose is predicted within the next 30 minutes (hybrid closed loop system, HCL this is known as a predictive low glucose suspend system (PLGS)). Glucose 127-134 insulin Homo sapiens 56-63 33355055-7 2021 It has been observed to attain tight blood glucose control we need to increase insulin dose in group A from 45.5 +- 16.5 IU/Day to 51.5 +- 14.5 at week 12 (P<0.01) and which further increased to 53.8 +- 12.8 IU/Day at week 24 (P<0.01). Glucose 43-50 insulin Homo sapiens 79-86 33325020-7 2020 Insulin sensitivity was assessed from the glucose infusion rate (GIR) during the last 30 minutes in the hyperbaric chamber (SS1) and the first 30 minutes after exit (SS2). Glucose 42-49 insulin Homo sapiens 0-7 33720614-2 2020 The mechanism of their action is based on insulin-independent reduction of glucose reabsorption in the proximal renal tubules, which leads to stimulation of its excretion in the urine and, accordingly, to a decrease in the concentration of glucose in the blood plasma. Glucose 75-82 insulin Homo sapiens 42-49 33720614-2 2020 The mechanism of their action is based on insulin-independent reduction of glucose reabsorption in the proximal renal tubules, which leads to stimulation of its excretion in the urine and, accordingly, to a decrease in the concentration of glucose in the blood plasma. Glucose 240-247 insulin Homo sapiens 42-49 33376380-9 2020 Significant interactions were observed for glucose at ICU admission, admission type, and insulin use (Interaction P <0.05). Glucose 43-50 insulin Homo sapiens 89-96 32822700-1 2020 Akt/PKB regulates numerous processes in the mammalian cell, including cell survival and proliferation, and glucose uptake in response to insulin. Glucose 107-114 insulin Homo sapiens 137-144 32987063-0 2020 Synthetic enzyme-based nanoparticles act as smart catalyst for glucose responsive release of insulin. Glucose 63-70 insulin Homo sapiens 93-100 32987063-1 2020 BACKGROUND: Earlier studies have attempted to create electronic free insulin delivery systems using different glucose sensing mechanism, no successful clinical translation as hitherto been made. Glucose 110-117 insulin Homo sapiens 69-76 32987063-2 2020 This study aimed to assess the faster responsiveness of the insulin release from this enzyme based nanoparticles which is a self-regulated insulin delivery system constructed by loading with insulin, enzyme glucose oxidase into hyaluronic acid and 2-nitroimidazole forming enzyme-based nanoparticles which works in accordance to the blood glucose level. Glucose 207-214 insulin Homo sapiens 60-67 32987063-2 2020 This study aimed to assess the faster responsiveness of the insulin release from this enzyme based nanoparticles which is a self-regulated insulin delivery system constructed by loading with insulin, enzyme glucose oxidase into hyaluronic acid and 2-nitroimidazole forming enzyme-based nanoparticles which works in accordance to the blood glucose level. Glucose 207-214 insulin Homo sapiens 139-146 32987063-2 2020 This study aimed to assess the faster responsiveness of the insulin release from this enzyme based nanoparticles which is a self-regulated insulin delivery system constructed by loading with insulin, enzyme glucose oxidase into hyaluronic acid and 2-nitroimidazole forming enzyme-based nanoparticles which works in accordance to the blood glucose level. Glucose 207-214 insulin Homo sapiens 139-146 32987063-2 2020 This study aimed to assess the faster responsiveness of the insulin release from this enzyme based nanoparticles which is a self-regulated insulin delivery system constructed by loading with insulin, enzyme glucose oxidase into hyaluronic acid and 2-nitroimidazole forming enzyme-based nanoparticles which works in accordance to the blood glucose level. Glucose 339-346 insulin Homo sapiens 60-67 32987063-2 2020 This study aimed to assess the faster responsiveness of the insulin release from this enzyme based nanoparticles which is a self-regulated insulin delivery system constructed by loading with insulin, enzyme glucose oxidase into hyaluronic acid and 2-nitroimidazole forming enzyme-based nanoparticles which works in accordance to the blood glucose level. Glucose 339-346 insulin Homo sapiens 139-146 32987063-2 2020 This study aimed to assess the faster responsiveness of the insulin release from this enzyme based nanoparticles which is a self-regulated insulin delivery system constructed by loading with insulin, enzyme glucose oxidase into hyaluronic acid and 2-nitroimidazole forming enzyme-based nanoparticles which works in accordance to the blood glucose level. Glucose 339-346 insulin Homo sapiens 139-146 32987063-6 2020 RESULTS: This enzyme- based nanoparticles were having average diameter of around 193 nm and stability studies showed that nanoparticles were stable upto 30 days at 4 C. In-vitro studies showed the release of insulin from nanoparticle conjugates which was effectively correlated with the external glucose concentration created where different concentrations of glucose taken thus facilitating the stabilization of blood glucose levels in the hyperglycemia state which was achieved within 10 min. Glucose 297-304 insulin Homo sapiens 209-216 32987063-6 2020 RESULTS: This enzyme- based nanoparticles were having average diameter of around 193 nm and stability studies showed that nanoparticles were stable upto 30 days at 4 C. In-vitro studies showed the release of insulin from nanoparticle conjugates which was effectively correlated with the external glucose concentration created where different concentrations of glucose taken thus facilitating the stabilization of blood glucose levels in the hyperglycemia state which was achieved within 10 min. Glucose 361-368 insulin Homo sapiens 209-216 32987063-6 2020 RESULTS: This enzyme- based nanoparticles were having average diameter of around 193 nm and stability studies showed that nanoparticles were stable upto 30 days at 4 C. In-vitro studies showed the release of insulin from nanoparticle conjugates which was effectively correlated with the external glucose concentration created where different concentrations of glucose taken thus facilitating the stabilization of blood glucose levels in the hyperglycemia state which was achieved within 10 min. Glucose 361-368 insulin Homo sapiens 209-216 33319790-8 2020 After an oral glucose load insulin concentration increased intravenously, but not in the intracutaneous or subcutaneous compartments, while glucose, lactate and pyruvate concentrations increased in all compartments. Glucose 14-21 insulin Homo sapiens 27-34 33325645-0 2021 Impact of endogenous insulin secretion on the improvement of glucose variability in Japanese patients type 2 diabetes treated with canagliflozin plus teneligliptin. Glucose 61-68 insulin Homo sapiens 21-28 33328554-0 2020 The Association of Insulin-dextrose Treatment with Hypoglycemia in Patients with Hyperkalemia. Glucose 27-35 insulin Homo sapiens 19-26 33328554-3 2020 In a retrospective cohort study in a tertiary hospital network, we included 421 adult patients with a serum potassium >= 6.0 mmol/L who received insulin-dextrose treatment. Glucose 153-161 insulin Homo sapiens 145-152 33320449-7 2021 Chronically elevated FFAs seem to decrease insulin biosynthesis, glucose-stimulated insulin secretion and beta-cell glucose sensitivity. Glucose 65-72 insulin Homo sapiens 84-91 33333850-3 2020 For many years, glucagon has been thought of as the counterregulatory hormone to insulin with a primary function of increasing blood glucose concentrations and protecting against hypoglycemia. Glucose 133-140 insulin Homo sapiens 81-88 33364490-8 2020 Further analysis indicated that Fm-RpL10a could stimulate glucose utilisation by insulin-resistant cells (IRCs) and healthy cells. Glucose 58-65 insulin Homo sapiens 81-88 33327428-7 2020 In beta cells, the impaired mitochondrial energy metabolism is accompanied by reduced insulin secretion at all glucose levels, but the differences, compared to a normal beta cell, are the most pronounced in hyperglycemia. Glucose 111-118 insulin Homo sapiens 86-93 33363418-11 2020 DD was found to be significantly higher in type 1 DM (p=0.04), insulin only in treatment regime (p=0.04), physical inactivities (p=0.02), times of mild hypoglycemia (time/month) (p=0.01), and fasting plasma glucose (mmol/l) (p=0.04). Glucose 207-214 insulin Homo sapiens 63-70 33720570-9 2020 Against the background of elevated glucose levels, an increase in basal insulin levels was observed (p=0.001). Glucose 35-42 insulin Homo sapiens 72-79 33720595-6 2020 The longer duration of action, reduced glucose variability and a lower risk of hypoglycemia seen with the latest generation of basal insulin analogs compared to the previous generation simplify titration and may increase patient compliance. Glucose 39-46 insulin Homo sapiens 133-140 33302273-5 2021 At the same blood glucose level, the dosage of exogenous insulin needed by patients in the PD group was larger than that in the HD group (p < 0.05). Glucose 18-25 insulin Homo sapiens 57-64 33322512-1 2020 Under healthy conditions, pancreatic beta-cells produce and secrete the insulin hormone in response to blood glucose levels. Glucose 109-116 insulin Homo sapiens 72-79 33322512-2 2020 Under diabetic conditions, however, beta-cells are compelled to continuously secrete larger amounts of insulin to reduce blood glucose levels, and thereby, the beta-cell function is debilitated in the long run. Glucose 127-134 insulin Homo sapiens 103-110 33365205-8 2020 Methods: We illustrate this by critically re-examining a specific case of the causal role of insulin in glucose homeostasis using five different approaches (1) Systematic review of tissue specific insulin receptor knock-outs, (2) Systematic review of insulin suppression and insulin enhancement experiments, (3) Differentiating steady state and post-meal state glucose levels in streptozotocin treated rats in primary experiments, (4) Mathematical and theoretical considerations and (5) Glucose-insulin relationship in human epidemiological data. Glucose 104-111 insulin Homo sapiens 93-100 33365205-9 2020 Results: All the approaches converge on the inference that although insulin action hastens the return to a steady state after a glucose load, there is no evidence that insulin action determines the steady state level of glucose. Glucose 128-135 insulin Homo sapiens 68-75 33322719-2 2020 Insulin resistance is a state of a weakened response of tissues such as skeletal muscle, adipose tissue, and liver to insulin, which causes an increase in blood glucose levels. Glucose 161-168 insulin Homo sapiens 0-7 33322719-2 2020 Insulin resistance is a state of a weakened response of tissues such as skeletal muscle, adipose tissue, and liver to insulin, which causes an increase in blood glucose levels. Glucose 161-168 insulin Homo sapiens 118-125 33322719-4 2020 Skeletal muscle is an important insulin-sensitive tissue that accounts for about 80% of insulin-dependent glucose uptake. Glucose 106-113 insulin Homo sapiens 32-39 33322719-4 2020 Skeletal muscle is an important insulin-sensitive tissue that accounts for about 80% of insulin-dependent glucose uptake. Glucose 106-113 insulin Homo sapiens 88-95 33291227-4 2020 Their IMCL levels were measured by proton-magnetic resonance spectroscopy, and their insulin sensitivity was evaluated by glucose infusion rate (GIR) during a euglycemic-hyperinsulinemic clamp. Glucose 122-129 insulin Homo sapiens 85-92 33298443-2 2020 Here, we report a unique application of soft x-ray tomography to generate three-dimensional reconstructions of whole pancreatic beta cells at different time points following glucose-stimulated insulin secretion. Glucose 174-181 insulin Homo sapiens 193-200 33298443-4 2020 Our results show that glucose stimulation caused rapid changes in biochemical composition and/or density of insulin packing, increased mitochondrial volume, and closer proximity of insulin vesicles to mitochondria. Glucose 22-29 insulin Homo sapiens 108-115 33298443-4 2020 Our results show that glucose stimulation caused rapid changes in biochemical composition and/or density of insulin packing, increased mitochondrial volume, and closer proximity of insulin vesicles to mitochondria. Glucose 22-29 insulin Homo sapiens 181-188 33284818-8 2020 Moreover, culturing islets in 200 muM Nec-1 supplemented media not only failed to improve the insulin release but resulted in a lower glucose-induced insulin stimulation index compared to islets cultured in media added with 100 muM Nec-1. Glucose 134-141 insulin Homo sapiens 150-157 33278477-8 2021 This case series demonstrates that critically ill patients are at risk of developing euglycemic ketosis during CKRT, which can be mitigated by providing adequate caloric intake and using glucose-containing CKRT solutions with appropriate insulin therapy. Glucose 187-194 insulin Homo sapiens 238-245 33329885-2 2020 Under normal physiological conditions, glucose metabolism is coupled to beta-cell insulin secretion so that blood glucose levels are maintained within the physiological range of 3.5-5.5 mmol/L. Glucose 39-46 insulin Homo sapiens 82-89 33427385-7 2020 We will also look at the peripheral interaction of the NPY system with insulin release, thereby closing the loop between these two energy and glucose homeostasis controlling systems and highlighting the critical interaction points that may be dysregulated in conditions of obesity and diabetes. Glucose 142-149 insulin Homo sapiens 71-78 33329885-8 2020 SST plays a potent role in the regulation of both insulin and glucagon secretion in response to changes in glucose levels by negative feedback mechanism. Glucose 107-114 insulin Homo sapiens 50-57 32966127-5 2020 Myotubes derived from severely obese individuals with type 2 diabetes exhibited impaired insulin-mediated glucose partitioning with reduced rates of glycogen synthesis and glucose oxidation and increased rates of nonoxidized glycolytic products, when compared with myotubes derived from the nondiabetic individuals (P < 0.05). Glucose 106-113 insulin Homo sapiens 89-96 32272872-3 2020 AT dysfunction was evaluated through associations of the ALR with F/P insulin-glucose axis, lipid-lipoprotein metabolism, and inflammatory markers. Glucose 78-85 insulin Homo sapiens 70-77 32718202-3 2020 Chronic insulin treatment significantly decreased lipid droplet size, insulin signalling and insulin-stimulated glucose uptake. Glucose 112-119 insulin Homo sapiens 8-15 32718202-4 2020 3T3-L1 displayed an increased basal glucose internalization following chronic insulin treatment, which was associated with increased GLUT1 expression. Glucose 36-43 insulin Homo sapiens 78-85 32966127-5 2020 Myotubes derived from severely obese individuals with type 2 diabetes exhibited impaired insulin-mediated glucose partitioning with reduced rates of glycogen synthesis and glucose oxidation and increased rates of nonoxidized glycolytic products, when compared with myotubes derived from the nondiabetic individuals (P < 0.05). Glucose 172-179 insulin Homo sapiens 89-96 32966127-8 2020 These data suggest that intramyocellular insulin-mediated glucose partitioning is intrinsically altered in the skeletal muscle of severely obese women with type 2 diabetes in a manner that favors the production of glycolytic end products. Glucose 58-65 insulin Homo sapiens 41-48 32324062-1 2020 BACKGROUND: Considering current insulin action profiles and the nature of glycemic responses to insulin, there is an acute need for longer-term, accurate, blood glucose predictions to inform insulin dosing schedules and enable effective decision support for the treatment of type 1 diabetes (T1D). Glucose 161-168 insulin Homo sapiens 32-39 33401880-4 2020 Insulin resistance (IR), i.e., whole-body decreased glucose uptake in response to physiological insulin levels, determines impaired glucose homeostasis and it is recognized as cardinal trigger of T2D and cardiovascular disease in both adults and children. Glucose 52-59 insulin Homo sapiens 0-7 33401880-4 2020 Insulin resistance (IR), i.e., whole-body decreased glucose uptake in response to physiological insulin levels, determines impaired glucose homeostasis and it is recognized as cardinal trigger of T2D and cardiovascular disease in both adults and children. Glucose 52-59 insulin Homo sapiens 96-103 32966883-11 2020 Moreover, JUP silencing reduced the expression of PKB and the downstream substrate AS160, and consequently attenuated activity in the insulin signalling pathway, including insulin-induced glucose uptake. Glucose 188-195 insulin Homo sapiens 134-141 32966883-11 2020 Moreover, JUP silencing reduced the expression of PKB and the downstream substrate AS160, and consequently attenuated activity in the insulin signalling pathway, including insulin-induced glucose uptake. Glucose 188-195 insulin Homo sapiens 172-179 33227625-3 2020 The absorption of glucose in the small intestine is not only a determinant of the appearance of exogenous glucose in the peripheral circulation, but is also coupled to the release of gastrointestinal hormones that in turn influence postprandial glucose metabolism through modulating gastrointestinal motor function, insulin and glucagon secretion, and subsequent energy intake. Glucose 18-25 insulin Homo sapiens 316-323 32945898-8 2020 CONCLUSIONS/INTERPRETATION: GH-induced insulin resistance in skeletal muscle is: (1) causally linked to lipolysis; (2) not associated with either accumulation of DAGs and ceramides or impaired insulin signalling; (3) likely to involve substrate competition between glucose and lipid intermediates. Glucose 265-272 insulin Homo sapiens 39-46 30633571-5 2020 Past and recent findings on the existence of insulin-like and mimetic materials, such as the glucose tolerance factor, in lower eukaryotes, in particular Neurospora crassa and yeast, will be presented. Glucose 93-100 insulin Homo sapiens 45-52 33384471-1 2020 Several new technologies use computer algorithms to analyze a person"s blood glucose response to insulin treatment, calculate the person"s next recommended insulin dose, advise the person regarding when to check blood glucose next, and provide alerts regarding glucose control for the individual patient or across a hospital system. Glucose 77-84 insulin Homo sapiens 97-104 32885684-7 2020 After treatment, 10 patients developed impaired fasting glucose and 13 developed insulin resistance.Conclusion: The increase in blood glucose levels may be associated with the paradoxically increase of histamine levels in the blood by omalizumab. Glucose 134-141 insulin Homo sapiens 81-88 32324062-11 2020 CONCLUSIONS: A shallow neural network, using features extracted from past CGM data and insulin logs is able to achieve multi-hour glucose predictions with satisfactory accuracy. Glucose 130-137 insulin Homo sapiens 87-94 32324062-1 2020 BACKGROUND: Considering current insulin action profiles and the nature of glycemic responses to insulin, there is an acute need for longer-term, accurate, blood glucose predictions to inform insulin dosing schedules and enable effective decision support for the treatment of type 1 diabetes (T1D). Glucose 161-168 insulin Homo sapiens 96-103 32994278-4 2020 Both melanophilin-mutated leaden mouse and melanophilin-downregulated human pancreatic beta cells exhibit impaired glucose-stimulated insulin secretion, with a specific reduction in fusion events that bypass stable docking to the plasma membrane. Glucose 115-122 insulin Homo sapiens 134-141 32324062-1 2020 BACKGROUND: Considering current insulin action profiles and the nature of glycemic responses to insulin, there is an acute need for longer-term, accurate, blood glucose predictions to inform insulin dosing schedules and enable effective decision support for the treatment of type 1 diabetes (T1D). Glucose 161-168 insulin Homo sapiens 96-103 32978791-1 2020 Insulin stimulates glucose uptake via the translocation of the glucose transporter GLUT4 to the plasma membrane in adipocytes. Glucose 19-26 insulin Homo sapiens 0-7 33067260-0 2020 Sustained Impact of Real-Time Continuous Glucose Monitoring in Adults With Type 1 Diabetes on Insulin Pump Therapy: Results After the 24-Month RESCUE Study. Glucose 41-48 insulin Homo sapiens 94-101 32656694-8 2020 Genetic alterations can affect insulin production, thus compromising the regulation of glucose utilization by tissues. Glucose 87-94 insulin Homo sapiens 31-38 32842794-2 2020 Insulin pump technologies have advanced dramatically in the last several years to integrate with continuous glucose monitors (CGM) and incorporate control algorithms. Glucose 108-115 insulin Homo sapiens 0-7 32842794-3 2020 These control algorithms automate some insulin delivery in response to the glucose information received from the CGM to reduce the occurrence of hypoglycemia and hyperglycemia and improve overall glycemic control. Glucose 75-82 insulin Homo sapiens 39-46 33055139-0 2020 Six Months of Hybrid Closed-Loop Versus Manual Insulin Delivery With Fingerprick Blood Glucose Monitoring in Adults With Type 1 Diabetes: A Randomized, Controlled Trial. Glucose 87-94 insulin Homo sapiens 47-54 33462955-0 2020 The dual glucose-dependent insulinotropic peptide and glucagon-like peptide-1 receptor agonist, tirzepatide, improves lipoprotein biomarkers associated with insulin resistance and cardiovascular risk in patients with type 2 diabetes. Glucose 9-16 insulin Homo sapiens 27-34 32978791-1 2020 Insulin stimulates glucose uptake via the translocation of the glucose transporter GLUT4 to the plasma membrane in adipocytes. Glucose 63-70 insulin Homo sapiens 0-7 33199991-2 2020 Mitochondria uses pyruvate to produce ATP as an intermediate link between glucose intake and insulin secretion in beta-cells, in a process known as glucose-stimulated insulin secretion (GSIS). Glucose 74-81 insulin Homo sapiens 167-174 33199991-2 2020 Mitochondria uses pyruvate to produce ATP as an intermediate link between glucose intake and insulin secretion in beta-cells, in a process known as glucose-stimulated insulin secretion (GSIS). Glucose 148-155 insulin Homo sapiens 93-100 32978791-2 2020 Several lines of evidence suggest that the small GTPase Rac1 plays an important role in insulin-stimulated glucose uptake in skeletal muscle and adipocytes. Glucose 107-114 insulin Homo sapiens 88-95 33199991-2 2020 Mitochondria uses pyruvate to produce ATP as an intermediate link between glucose intake and insulin secretion in beta-cells, in a process known as glucose-stimulated insulin secretion (GSIS). Glucose 148-155 insulin Homo sapiens 167-174 32978791-6 2020 Collectively, these results suggest the involvement of FLJ00068 downstream of Akt2 in insulin-stimulated glucose uptake signaling in adipocytes. Glucose 105-112 insulin Homo sapiens 86-93 32785654-8 2020 MAIN OUTCOME MEASURES: We measured femoral, lumbar, and thoracic BM insulin-stimulated glucose uptake (GU) and fasting free fatty acid uptake (FFAU) using positron-emission tomography and bone turnover markers from plasma. Glucose 87-94 insulin Homo sapiens 68-75 32398753-13 2020 Both surrogate measures give similar information about insulin resistance of glucose and lipid metabolism in fat cells. Glucose 77-84 insulin Homo sapiens 55-62 31742469-6 2020 In the insulin-resistant human hepatoma HepG2 cells, compound 25 with the moderate PTP1B inhibition and preferable pharmaceutical properties can significantly increase insulin-stimulated glucose uptake and showed the insulin resistance ameliorating effect. Glucose 187-194 insulin Homo sapiens 7-14 31742469-6 2020 In the insulin-resistant human hepatoma HepG2 cells, compound 25 with the moderate PTP1B inhibition and preferable pharmaceutical properties can significantly increase insulin-stimulated glucose uptake and showed the insulin resistance ameliorating effect. Glucose 187-194 insulin Homo sapiens 168-175 31742469-6 2020 In the insulin-resistant human hepatoma HepG2 cells, compound 25 with the moderate PTP1B inhibition and preferable pharmaceutical properties can significantly increase insulin-stimulated glucose uptake and showed the insulin resistance ameliorating effect. Glucose 187-194 insulin Homo sapiens 168-175 32916040-14 2020 Thus, insulin-induced regulation of key proteins important for transport and intracellular flux of glucose towards glycogen storage in the recovery from exercise, does not differ between fibre types. Glucose 99-106 insulin Homo sapiens 6-13 33012601-1 2020 AIMS: We compared 20 previously reported indices of insulin sensitivity derived from samples during an oral glucose tolerance test (OGTT) to determine which was best in predicting incident type 2 diabetes. Glucose 108-115 insulin Homo sapiens 52-59 33247665-3 2020 The traditional approach of sliding scale insulin (SSI) therapy for the temporary management of blood glucose levels in hospitalized patients, has now given way to basal-bolus insulin (BBI) therapy. Glucose 102-109 insulin Homo sapiens 42-49 32902875-5 2020 Insulin sensitivity was quantified as the glucose infusion rate/insulin (M/I) from a hyperglycemic clamp. Glucose 42-49 insulin Homo sapiens 0-7 32926928-6 2020 The disrupted insulin signaling has pathological outcome in form of disturbed glucose homeostasis, altered bioenergetic state which increases build-up of senile plaques (Abeta), neurofibrillary tangles (tau), decline in transportation of glucose and activation of inflammatory pathways. Glucose 78-85 insulin Homo sapiens 14-21 33058852-8 2020 In isolated human and mouse islets exogenous CCL25 inhibited glucose-induced insulin secretion in a concentration-dependent manner, enhanced cytokine-induced apoptosis and significantly reduced forskolin-induced elevation in cAMP levels. Glucose 61-68 insulin Homo sapiens 77-84 33259010-8 2020 Insulin-resistant macrophages showed lower glucose uptake, GLUT-1 and GLUT-3 expression, and increased hallmarks of mitochondrial dysfunction. Glucose 43-50 insulin Homo sapiens 0-7 32985060-1 2020 OBJECTIVE: Despite increased diabetes device use, few adolescents with type 1 diabetes (T1D) meet glycemic targets.We examine associations between utilization of insulin pumps and continuous glucose monitoring (CGM) and glycemic control. Glucose 191-198 insulin Homo sapiens 162-169 32939893-3 2020 Covariance pattern mixture models (CPMM) identified response phenotypes defined by changes in insulin sensitivity as measured using a 2-hour oral glucose tolerance test. Glucose 146-153 insulin Homo sapiens 94-101 32200516-7 2020 Treatment with the histone deacetylase inhibitor 4-phenylbutyrate (4-PBA) increased the magnitude of insulin response from a 1.2-fold increase in glucose uptake in the untreated state to a 1.4-fold increase after 4-PBA treatment. Glucose 146-153 insulin Homo sapiens 101-108 32844324-4 2020 Subsequently, T1DM patients rely on the administration of exogenous insulin sources to maintain their blood glucose levels. Glucose 108-115 insulin Homo sapiens 68-75 32200516-9 2020 CONCLUSION: Although tissue-engineered human myobundles exhibit a modest increase in glucose uptake in response to insulin, they recapitulate key features of in vivo insulin sensitivity and exhibit relevant drug-mediated perturbations in contractile function and glucose metabolism. Glucose 85-92 insulin Homo sapiens 115-122 32917496-1 2020 BACKGROUND AND AIMS: Triglyceride glucose (TyG) index is considered a new surrogate marker of insulin resistance that associated with the development of vascular disease. Glucose 34-41 insulin Homo sapiens 94-101 33330672-1 2020 The triglyceride glucose (TyG) index has been proposed to be a surrogate of insulin resistance. Glucose 17-24 insulin Homo sapiens 76-83 32976960-8 2020 Adipose tissue treated with environmentally-relevant concentrations of BPA for 24 hours had reduced insulin-stimulated glucose uptake, without altered gene and protein levels of key insulin signalling pathway markers. Glucose 119-126 insulin Homo sapiens 100-107 32976960-9 2020 CONCLUSIONS: We found that human adipose tissue treated with environmentally-relevant concentrations of BPA for 24 hours, but not BPS, reduced expression of proinflammatory genes and adipokines Furthermore, BPA reduced glucose uptake in adipocytes independently of insulin signalling. Glucose 219-226 insulin Homo sapiens 265-272 33243251-9 2020 Therapeutic inhibition of inflammation and stimulation of glucose availability in cones by insulin signaling might prevent RD-associated cone death until the RD can be surgically repaired and improve visual outcome after RD. Glucose 58-65 insulin Homo sapiens 91-98 33274014-3 2020 Insulin promotes glucose utilization in part through promoting glucose entry into the skeletal and adipose tissues. Glucose 17-24 insulin Homo sapiens 0-7 33274014-3 2020 Insulin promotes glucose utilization in part through promoting glucose entry into the skeletal and adipose tissues. Glucose 63-70 insulin Homo sapiens 0-7 33274014-4 2020 This has been thought to be achieved through insulin-induced GLUT4 translocation from intracellular compartments to the cell membrane, which increases the overall rate of glucose flux into a cell. Glucose 171-178 insulin Homo sapiens 45-52 32960514-12 2020 CONCLUSIONS: Once-weekly treatment with insulin icodec had glucose-lowering efficacy and a safety profile similar to those of once-daily insulin glargine U100 in patients with type 2 diabetes. Glucose 59-66 insulin Homo sapiens 40-47 32431137-5 2020 Insulin resistance was evaluated using HOMA-IR, QUICK-I, fasting glucose /insulin ratio, Matsuda index, and total insulin levels during OGTT. Glucose 65-72 insulin Homo sapiens 0-7 33222694-3 2020 The triglyceride glucose (TyG) index, a novel surrogate marker of insulin resistance and systemic inflammation, has not yet been shown to be associated with sarcopenia. Glucose 17-24 insulin Homo sapiens 66-73 33581015-0 2020 Effects of metformin and insulin therapy regimens on postpartum oral glucose tolerance test results in pregnant women with gestational diabetes mellitus: a comparative study. Glucose 69-76 insulin Homo sapiens 25-32 33581015-1 2020 OBJECTIVES: The main purpose of this study was to compare the effects of two regimens of metformin and insulin therapy on postpartum oral glucose tolerance test (OGTT) results in pregnant women with gestational diabetes mellitus (GDM). Glucose 138-145 insulin Homo sapiens 103-110 33239385-1 2020 Pregnancy is a physiological state of continuous adaptation to changing maternal and fetal nutritional needs, including a reduction of maternal insulin sensitivity allowing for appropriately enhanced glucose availability to the fetus. Glucose 200-207 insulin Homo sapiens 144-151 33240683-4 2020 SG1, SG3 and SG4 could significantly enhance glucose uptake of insulin-resistant HepG2 cells at non-cytotoxic concentration. Glucose 45-52 insulin Homo sapiens 63-70 33218355-1 2020 BACKGROUND: Solute carrier family 2 member 1 (SLC2A1; previously known as glucose transporter 1), is the most abundant glucose transporter in human endometrium and is up-regulated during decidualization, whereas high insulin may have a negative impact on this process. Glucose 74-81 insulin Homo sapiens 217-224 33218355-1 2020 BACKGROUND: Solute carrier family 2 member 1 (SLC2A1; previously known as glucose transporter 1), is the most abundant glucose transporter in human endometrium and is up-regulated during decidualization, whereas high insulin may have a negative impact on this process. Glucose 119-126 insulin Homo sapiens 217-224 33218355-2 2020 The present study aimed to investigate the effect of insulin on the expression of SLC2A1 and glucose uptake in decidualizing human endometrial stromal cells. Glucose 93-100 insulin Homo sapiens 53-60 33218355-10 2020 Glucose uptake increased upon decidualization, whereas insulin treatment resulted in a slight inhibition of the glucose uptake, although not significant for all insulin concentrations. Glucose 112-119 insulin Homo sapiens 55-62 33218280-6 2021 The University of Virginia (UVa)/Padova T1DM simulator is used to generate experimental scenarios and test the ability of the methodology to accurately reproduce changes in glucose concentration to alteration in meal and insulin inputs. Glucose 173-180 insulin Homo sapiens 221-228 33282306-5 2020 Optimal glucose control in intensive care is limited by manual sampling of glucose and intravenous insulin adjustment, as well as increased nursing workload and the need of protective equipment. Glucose 8-15 insulin Homo sapiens 99-106 33365210-6 2020 Hyperinsulinemic hypoglycemia (HH), caused by dysregulation of insulin secretion from pancreatic beta-cells, leads to insulin driven glucose entry into the tissues and inhibits glycolysis, gluconeogenesis, fatty acid release, and ketone body synthesis. Glucose 133-140 insulin Homo sapiens 5-12 33365210-6 2020 Hyperinsulinemic hypoglycemia (HH), caused by dysregulation of insulin secretion from pancreatic beta-cells, leads to insulin driven glucose entry into the tissues and inhibits glycolysis, gluconeogenesis, fatty acid release, and ketone body synthesis. Glucose 133-140 insulin Homo sapiens 63-70 32946868-7 2020 In vitro, ECT (15 and 30 muM) alleviated insulin resistance by increasing glucose consumption, glucose uptake and glycogen content in high glucose-induced HepG2 cells. Glucose 74-81 insulin Homo sapiens 41-48 33217903-6 2020 Leveraging the approval of real-time continuous glucose monitors and sophisticated algorithms that partially automate insulin infusion pumps has improved glycemic control, decreasing the burden of diabetes management. Glucose 48-55 insulin Homo sapiens 118-125 33274235-1 2020 Diabetes mellitus (DM) is a chronic metabolic disorder commonly characterized by high blood glucose levels, resulting from defects in insulin production or insulin resistance, or both. Glucose 92-99 insulin Homo sapiens 134-141 33191314-1 2021 AIM: The triglyceride-glucose index (TyG index) is proposed as a surrogate parameter for insulin resistance (IR) and, when elevated, is related to increased cardiovascular risks. Glucose 22-29 insulin Homo sapiens 89-96 33274235-1 2020 Diabetes mellitus (DM) is a chronic metabolic disorder commonly characterized by high blood glucose levels, resulting from defects in insulin production or insulin resistance, or both. Glucose 92-99 insulin Homo sapiens 156-163 33176650-4 2021 Here we discuss that environmental contaminants with estrogenic capacity such as bisphenol A (BPA) could develop pharmacological effects similar to those of E2, which could affect ss-pancreatic cell function by increasing the biosynthesis of glucose-induced insulin after extranuclear ER binding. Glucose 242-249 insulin Homo sapiens 258-265 33282827-1 2020 The current standard treatment for Type 1 diabetes is the administration of exogenous insulin to manage blood glucose levels. Glucose 110-117 insulin Homo sapiens 86-93 33142057-5 2020 Although less proadipogenic than rosiglitazone, 7j significantly increases adipocyte insulin-stimulated glucose uptake and efficiently promotes white-to-brown adipocyte conversion. Glucose 104-111 insulin Homo sapiens 85-92 33224195-0 2020 Utilizing Technology-Enabled Intervention to Improve Blood Glucose Self-Management Outcome in Type 2 Diabetic Patients Initiated on Insulin Therapy: A Retrospective Real-World Study. Glucose 59-66 insulin Homo sapiens 132-139 32735879-7 2020 The CAGE/insulin patches placed in the rat buccal pouch in vivo lowered blood glucose levels in a dose-dependent manner (up to 50% drop recorded) with no obvious tissue damage at the application site. Glucose 78-85 insulin Homo sapiens 9-16 33855202-2 2021 Imeglimin is a first-in-class novel drug candidate that improves glycaemia and glucose-stimulated insulin secretion in preclinical models and patients. Glucose 79-86 insulin Homo sapiens 98-105 33182622-7 2020 In pre-diabetes and compromised metabolic states such as obesity, insulin resistance, and glucose intolerance, beta cells biosynthesize and secrete more insulin, i.e., hyperfunction. Glucose 90-97 insulin Homo sapiens 153-160 33855202-6 2021 Results: Imeglimin treatment significantly improved glucose-stimulated insulin secretion (augmentation of the insulinogenic index) and improved glycaemia. Glucose 52-59 insulin Homo sapiens 71-78 33154349-3 2020 Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression of key components of the secretory machinery of beta-cells, resulting in impaired glucose- or KCl-induced insulin release and calcium signaling. Glucose 181-188 insulin Homo sapiens 205-212 33855205-6 2021 Insulin responses to the glucose challenge on OGTT ranged between 13.0 and 143 mIU/L after 120 minutes with C-peptide values between 0.74 and 4.60 nmol/L. Glucose 25-32 insulin Homo sapiens 0-7 32855238-5 2020 Dose-dependent activation of P2Y14 by UDP-G suppressed glucose-stimulated insulin secretion (GSIS) and knockdown of P2Y14 abolished the UDP-G effect. Glucose 55-62 insulin Homo sapiens 74-81 33151639-3 2021 Incretin preparations that regulate both insulin and glucagon secretion in a blood glucose-dependent manner have a low risk of hypoglycemia and weight gain. Glucose 83-90 insulin Homo sapiens 41-48 32888406-4 2020 We find that T2D iMyos in culture exhibit multiple defects mirroring human disease, including an altered insulin signaling, decreased insulin-stimulated glucose uptake, and reduced mitochondrial oxidation. Glucose 153-160 insulin Homo sapiens 134-141 33139788-1 2020 The relationship between the plasma insulin (INS) concentration-time course and plasma glucose concentration-time course during and after pulsatile INS administration to rats was characterized using a pharmacokinetic-pharmacodynamic (PK-PD) model. Glucose 87-94 insulin Homo sapiens 36-43 33145848-3 2021 Insulin is considered a fundamental component of DKA treatment as it promotes the peripheral tissues" utilization of glucose in peripheral tissues by reducing hepatic gluconeogenesis and suppressing ketogenesis.1. Glucose 117-124 insulin Homo sapiens 0-7 33147479-1 2020 The consensus model of glucose-stimulated insulin secretion (GSIS) holds that ATP generation by oxidative phosphorylation directly regulates KATP channel activity and thus insulin granule release, a concept inconsistent with bioenergetic principles. Glucose 23-30 insulin Homo sapiens 42-49 33147479-1 2020 The consensus model of glucose-stimulated insulin secretion (GSIS) holds that ATP generation by oxidative phosphorylation directly regulates KATP channel activity and thus insulin granule release, a concept inconsistent with bioenergetic principles. Glucose 23-30 insulin Homo sapiens 172-179 33204261-6 2020 Several models based on artificial intelligence techniques were developed to analyze glycemic patterns based on continuous glucose monitoring and clinical variables in order to estimate the basal insulin dose. Glucose 123-130 insulin Homo sapiens 196-203 33153010-2 2020 Individuals with T1D control their blood glucose through exogenous insulin replacement therapy, often using multiple daily injections or pumps. Glucose 41-48 insulin Homo sapiens 67-74 33153226-7 2020 The challenge in developing a therapeutic solution based on GSIS (glucose-stimulated insulin secretion) enhancers targeted at PDEs is the selective inhibition of their activity only within beta cells. Glucose 66-73 insulin Homo sapiens 85-92 33147803-2 2020 The development of T2D increases the risk of AD disease, while AD patients can show glucose imbalance due to an increased insulin resistance. Glucose 84-91 insulin Homo sapiens 122-129 32877776-1 2020 Here we describe the development of a dual electrochemical immunosensor microchip for simultaneous detection of insulin (I) and cortisol (C) biomarkers that can enhance the ability to improve glucose regulation using automated insulin delivery. Glucose 192-199 insulin Homo sapiens 112-119 33313226-14 2020 Faecium was also revealed, suggesting that the crosstalke between miRNA and gut microbiota may regulate the insulin secretion and signal transduction by controling key genes of glucose metabolism during the development of T2DM. Glucose 177-184 insulin Homo sapiens 108-115 32738275-7 2020 RESULTS: In STZ-treated mice, blood glucose and serum TNF-alpha and IGF-1 were reduced by insulin alone, and normalized when MA-[D-Leu-4]-OB3 was given in combination with insulin. Glucose 36-43 insulin Homo sapiens 90-97 32877776-1 2020 Here we describe the development of a dual electrochemical immunosensor microchip for simultaneous detection of insulin (I) and cortisol (C) biomarkers that can enhance the ability to improve glucose regulation using automated insulin delivery. Glucose 192-199 insulin Homo sapiens 227-234 32725362-6 2020 As adjuvants to insulin for patients with type 1 diabetes, sodium-glucose cotransporter inhibitors improve blood glucose control and reduce total daily insulin dose and body weight. Glucose 66-73 insulin Homo sapiens 16-23 32961506-2 2020 In this review, we discuss firstly the regulation and roles of mitochondrial Ca2+ transport in glucose-regulated insulin secretion, and the molecular machinery involved. Glucose 95-102 insulin Homo sapiens 113-120 32725362-6 2020 As adjuvants to insulin for patients with type 1 diabetes, sodium-glucose cotransporter inhibitors improve blood glucose control and reduce total daily insulin dose and body weight. Glucose 66-73 insulin Homo sapiens 152-159 33183669-6 2020 The meta-analysis suggested a significant effect of DASH diet on fasting plasma levels of glucose (WMD = -6.239 mg/dl; 95% CI: -11.915, -0.563, p = 0.031), but not for the homeostasis model assessment of insulin resistance (WMD = -1.038; 95% CI: -2.704, 0.627, p = 0.22). Glucose 90-97 insulin Homo sapiens 204-211 32855171-9 2020 Notably, in cultured male and female islets, T enhanced glucose-stimulated insulin secretion (GSIS). Glucose 56-63 insulin Homo sapiens 75-82 32873588-8 2020 Insulin was positively associated with adult T2DM after adjustment for BMI and glucose and added to T2DM discrimination. Glucose 79-86 insulin Homo sapiens 0-7 32873590-4 2020 In CON, the training intervention increased whole-body insulin action by 26% and insulin-stimulated leg glucose uptake by 53% together with increased insulin-stimulated leg blood flow and a more oxidative muscle fiber type distribution. Glucose 104-111 insulin Homo sapiens 81-88 32873590-4 2020 In CON, the training intervention increased whole-body insulin action by 26% and insulin-stimulated leg glucose uptake by 53% together with increased insulin-stimulated leg blood flow and a more oxidative muscle fiber type distribution. Glucose 104-111 insulin Homo sapiens 81-88 32873590-6 2020 These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Glucose 159-166 insulin Homo sapiens 60-67 32873590-6 2020 These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Glucose 159-166 insulin Homo sapiens 189-196 32873590-6 2020 These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Glucose 159-166 insulin Homo sapiens 189-196 32873590-6 2020 These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Glucose 208-215 insulin Homo sapiens 60-67 32873590-6 2020 These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Glucose 208-215 insulin Homo sapiens 189-196 32873590-6 2020 These data suggest that the impaired increase in whole-body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated leg blood flow. Glucose 208-215 insulin Homo sapiens 189-196 32909193-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 117-124 insulin Homo sapiens 29-36 32909193-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 207-214 insulin Homo sapiens 29-36 32909193-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 207-214 insulin Homo sapiens 140-147 32909193-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 207-214 insulin Homo sapiens 140-147 32909193-2 2020 Do-It-Yourself Artificial Pancreas Systems (DIY APS) are a form of hybrid closed-loop system that use open-source algorithms, which govern the delivery of insulin in response to interstitial glucose and other variables that are personalized to an individual. Glucose 191-198 insulin Homo sapiens 155-162 32621047-3 2020 METHODS: In a randomized, double-blind, prospective study, 358 recently diagnosed type 2 diabetes (T2D) patients, who on a combined therapy with metformin and insulin glargine had a fasting plasma glucose (FGP) of <7.2 mmol/L but a 2-h postprandial plasma glucose (2hPPG) >10 mmol/L, were assigned to three groups of additional treatment with either repaglinide, acarbose, or repaglinide-plus-acarbose for 4 months. Glucose 197-204 insulin Homo sapiens 159-166 32964214-2 2020 The historical narrative positions these hormones in opposition, with insulin primarily responsible for glucose-lowering and glucagon-driving elevations in glucose. Glucose 104-111 insulin Homo sapiens 70-77 32964214-2 2020 The historical narrative positions these hormones in opposition, with insulin primarily responsible for glucose-lowering and glucagon-driving elevations in glucose. Glucose 156-163 insulin Homo sapiens 70-77 32738350-4 2020 Further biological activity studies revealed that compounds 7a, 17b and 17f could effectively enhance insulin-stimulated glucose uptake with no significant cytotoxicity. Glucose 121-128 insulin Homo sapiens 102-109 32671413-15 2020 The association was more prominent in those with a younger age at diabetes onset and receiving treatment with both oral glucose-lowering medication and insulin. Glucose 120-127 insulin Homo sapiens 152-159 32676816-19 2020 Upon infection, there was an increased viral titre in the cell culture supernatant and a marked reduction in glucose-stimulated insulin secretion (112.9 +- 24.4 vs 209.8 +- 24.4 ng [mg protein]-1 h-1; p = 0.006), compared with uninfected controls, but cellular viability remained unaffected. Glucose 109-116 insulin Homo sapiens 128-135 32687239-4 2020 Baseline measurements include assessment of the stool microbiome and administration of an oral glucose tolerance test, which will yield indexes of insulin sensitivity, insulin secretion, and insulin clearance. Glucose 95-102 insulin Homo sapiens 147-154 32687239-4 2020 Baseline measurements include assessment of the stool microbiome and administration of an oral glucose tolerance test, which will yield indexes of insulin sensitivity, insulin secretion, and insulin clearance. Glucose 95-102 insulin Homo sapiens 168-175 32687239-4 2020 Baseline measurements include assessment of the stool microbiome and administration of an oral glucose tolerance test, which will yield indexes of insulin sensitivity, insulin secretion, and insulin clearance. Glucose 95-102 insulin Homo sapiens 168-175 32618405-5 2020 Insulin doses should be titrated once weekly in 2-unit steps, guided by individualized fasting plasma glucose targets and based on patient goals, preferences and hypoglycaemia risk. Glucose 102-109 insulin Homo sapiens 0-7 33020802-16 2020 Glucose handling (GTT AUC) was poorer and basal insulin levels were higher in IVF-ET-2Cell males than in IVF-ET-BL (P < 0.05) with the glucose:insulin ratio more negatively correlated with body weight in IVF-ET-2Cell males than in other groups. Glucose 135-142 insulin Homo sapiens 48-55 33020802-16 2020 Glucose handling (GTT AUC) was poorer and basal insulin levels were higher in IVF-ET-2Cell males than in IVF-ET-BL (P < 0.05) with the glucose:insulin ratio more negatively correlated with body weight in IVF-ET-2Cell males than in other groups. Glucose 135-142 insulin Homo sapiens 143-150 32374513-0 2020 Effect of Real-life insulin pump with predictive low-glucose management use for 3 months: Analysis of the patients treated in a Japanese center. Glucose 53-60 insulin Homo sapiens 20-27 32851580-1 2020 The free fatty acid receptor 1 (FFAR1, formerly GPR40), is a potential G protein-coupled receptor (GPCR) target for the treatment of type 2 diabetes mellitus (T2DM), as it enhances glucose-dependent insulin secretion upon activation by endogenous long-chain free fatty acids. Glucose 181-188 insulin Homo sapiens 199-206 32374513-1 2020 AIMS/INTRODUCTION: In Japan, an insulin pump with predictive low-glucose management (PLGM) was launched in 2018. Glucose 65-72 insulin Homo sapiens 32-39 32374513-2 2020 It automatically suspends insulin delivery when the sensor detects or predicts low glucose values. Glucose 83-90 insulin Homo sapiens 26-33 32592269-2 2020 The Oral Minimal Model (OMM) has been developed in order to measure insulin sensitivity using an easy oral glucose load such as an oral glucose tolerance test (OGTT), instead of an hyperinsulinemic-euglycemic clamp (HE-Clamp), a more invasive and time-consuming procedure. Glucose 107-114 insulin Homo sapiens 68-75 32790176-4 2020 We find that TSPAN-7 reduces beta-cell glucose-stimulated Ca2+ entry, slows Ca2+ oscillation frequency, and decreases glucose-stimulated insulin secretion. Glucose 118-125 insulin Homo sapiens 137-144 32790176-8 2020 ABSTRACT: Glucose-stimulated insulin secretion (GSIS) is regulated by calcium (Ca2+ ) entry into pancreatic beta-cells through voltage-dependent Ca2+ (CaV ) channels. Glucose 10-17 insulin Homo sapiens 29-36 32790176-17 2020 Finally, TSPAN-7 KD in human beta-cells increased basal (5.6 mM glucose) and stimulated (45 mM KCl + 14 mM glucose) insulin secretion. Glucose 107-114 insulin Homo sapiens 116-123 32813449-3 2020 Among PLWT1D, the islet cells in the pancreas produce insufficient amounts of the glucose-regulating hormone, insulin, resulting in the need for chronic insulin replacement therapy. Glucose 82-89 insulin Homo sapiens 110-117 33879436-1 2020 Dipeptidyl peptidase IV (DPP-4) and Glucagon like peptide 1 (GLP-1) has profound effect on insulin and glucagon secretion; ultimately decreasing glucose levels. Glucose 145-152 insulin Homo sapiens 91-98 32830408-7 2020 CONCLUSION: Sex hormone-binding globulin regulates GLUT1 expression via the cAMP/PKA/CREB1 pathway and affects glucose transport in the placenta, which can induce insulin resistance and gestational diabetes. Glucose 111-118 insulin Homo sapiens 163-170 32639626-2 2020 Forkhead box O6 (FoxO6) is a transcription factor mediating insulin signaling to glucose and lipid metabolism, therefore, dysregulated FoxO6 is involved in hepatic insulin resistance. Glucose 81-88 insulin Homo sapiens 60-67 32815257-6 2020 Due to the enhanced cell-matrix interaction, islets encapsulated within the AEC microcapsules ( 640 microm) display sevenfold increase in cell growth over 1 week of culture and characteristic glucose-stimulated insulin response in vitro. Glucose 192-199 insulin Homo sapiens 211-218 33022588-8 2020 Glucose levels at all different time points during OGTT, baseline insulin, Homeostasis model assessment of insulin resistance (HOMA-IR), total cholesterol and LDL were statistically significantly (p<0.05) associated with MS, in univariable logistic regression analysis. Glucose 0-7 insulin Homo sapiens 107-114 32592269-2 2020 The Oral Minimal Model (OMM) has been developed in order to measure insulin sensitivity using an easy oral glucose load such as an oral glucose tolerance test (OGTT), instead of an hyperinsulinemic-euglycemic clamp (HE-Clamp), a more invasive and time-consuming procedure. Glucose 136-143 insulin Homo sapiens 68-75 32738022-0 2020 The Efficacy and Safety of Insulin Pump Therapy with Predictive Low Glucose Suspend Feature in Decreasing Hypoglycemia in Children with Type 1 Diabetes Mellitus: a systematic review and meta-analysis. Glucose 68-75 insulin Homo sapiens 27-34 32738022-1 2020 BACKGROUND: Automated insulin delivery (AID) with predictive low glucose suspend feature (PLGS) has the potential to reduce risk of hypoglycemia in patients with T1DM. Glucose 65-72 insulin Homo sapiens 22-29 32741045-5 2020 RESULTS: We identified 13 focus areas that categorized youth goalintentions.Each session where youthgoal setting concurrently incorporatedblood glucose monitoring (BG), CGM, and insulin dosing was associated with a 0.4% (95% CI: -0.77, -0.01; P = 0.03) lower HbA1c at the end of intervention participation. Glucose 144-151 insulin Homo sapiens 178-185 33143284-2 2020 Research suggests that taste stimulation can induce the cephalic phase insulin response before food has reached the digestion, priming the body for an incoming glucose load. Glucose 160-167 insulin Homo sapiens 71-78 32815454-1 2020 Glucagon-like peptide-1 (GLP-1) is a hormone of the incretin system responsible for a variety of glucoregulatory effects, including glucose-dependent secretion of insulin and inhibition of glucagon release, the effects of which are impaired in people with type 2 diabetes (T2D). Glucose 132-139 insulin Homo sapiens 163-170 33109604-6 2020 We uncovered deficits in insulin secretion, partly due to reduced mitochondrial oxygen consumption rate, glucose-stimulated Ca2+ flux, and reduced insulin content associated with loss of eIF4E, the mRNA 5"-cap binding protein of the initiation complex and binding partner of eIF4G1. Glucose 105-112 insulin Homo sapiens 25-32 33195355-1 2020 Objective: The triglyceride-glucose (TyG) index is a reliable surrogate of insulin resistance and a marker for ischemic stroke (IS) incident. Glucose 28-35 insulin Homo sapiens 75-82 33109219-1 2020 BACKGROUND: Both triglyceride glucose-body mass index (TyG-BMI) and non-alcoholic fatty liver disease (NAFLD) are linked to insulin resistance (IR). Glucose 30-37 insulin Homo sapiens 124-131 32969458-1 2020 Insulin administration at mealtimes for the control of postprandial glucose is a major part of basal-bolus insulin therapy; however, painful subcutaneous (SC) injections lead to poor patient compliance. Glucose 68-75 insulin Homo sapiens 0-7 33553034-9 2020 Insulin resistance (HOMA-IR) was calculated from serum insulin and plasma glucose values. Glucose 74-81 insulin Homo sapiens 0-7 33120872-8 2020 SMA-insulin efficiently stimulated glucose uptake in HepG-2 hepatic cells and was transported across the Caco-2 epithelial cells in vitro by 46% and ex vivo across intestinal epithelium by 22%. Glucose 35-42 insulin Homo sapiens 4-11 33105763-2 2020 By inhibiting sodium and glucose reabsorption from the proximal tubules, the improvement in insulin resistance and natriuresis improved the cardiovascular mortality in diabetes mellitus (DM) patients. Glucose 25-32 insulin Homo sapiens 92-99 32769216-9 2020 Similarly, both (D-Ala2)GIP and xenin-25-Gln stimulated insulin-induced glucose uptake in 3T3-L1 adipocytes, but this effect was annulled by dual treatment. Glucose 72-79 insulin Homo sapiens 56-63 33096658-6 2020 Specific AAs (i.e., leucine and isoleucine) co-ingested with glucose exerted a synergistic effect on the postprandial insulin response and attenuated the glucose response compared to glucose intake alone in healthy participants. Glucose 61-68 insulin Homo sapiens 118-125 33096618-3 2020 Serum iron and glucose levels are subjected to hormonal regulation by hepcidin and insulin, respectively. Glucose 15-22 insulin Homo sapiens 83-90 33096618-5 2020 Insulin is a protein hormone secreted from pancreatic beta-cells that stimulates glucose uptake and metabolism via insulin receptor signaling. Glucose 81-88 insulin Homo sapiens 0-7 33060722-1 2020 People with type 1 diabetes (T1D) require exogenous administration of insulin, which stimulates the translocation of the GLUT4 glucose transporter to cell membranes. Glucose 127-134 insulin Homo sapiens 70-77 33087848-2 2020 A key regulator of insulin- and exercise-stimulated glucose uptake and GLUT4 trafficking is TBC1D1. Glucose 52-59 insulin Homo sapiens 19-26 32781053-6 2020 AMPK participates in insulin signaling, therefore controls glucose uptake and podocytes insulin sensitivity. Glucose 59-66 insulin Homo sapiens 21-28 33045957-4 2021 OBJECTIVE: The activity of endogenous GLP-1 and GIP prolong and extend with DPP IV inhibitors which are responsible for stimulation of insulin secretion and regulate blood glucose level. Glucose 172-179 insulin Homo sapiens 135-142 33066504-1 2020 Insulin resistance (IR) is apparent when tissues responsible for clearing glucose from the blood, such as adipose and muscle, do not respond properly to appropriate signals. Glucose 74-81 insulin Homo sapiens 0-7 33066504-3 2020 Certain (poly)phenols, as supplements or in foods, can improve insulin resistance by several mechanisms including lowering postprandial glucose, modulating glucose transport, affecting insulin signalling pathways, and by protecting against damage to insulin-secreting pancreatic beta-cells. Glucose 136-143 insulin Homo sapiens 63-70 32878940-1 2020 Besides regulating glucose levels, insulin has been reported to participate actively in many other functions such as modulating inflammatory reaction. Glucose 19-26 insulin Homo sapiens 35-42 33036033-6 2022 Overexpression of let7b-5p increased insulin content and decreased glucose-stimulated insulin secretion, whereas silencing of let7b-5p reduced insulin content and secretion. Glucose 67-74 insulin Homo sapiens 86-93 33041312-5 2021 The homeostasis model assessment index for insulin resistance was based on fasting and 2-hr postload glucose and insulin concentrations. Glucose 101-108 insulin Homo sapiens 43-50 33036033-6 2022 Overexpression of let7b-5p increased insulin content and decreased glucose-stimulated insulin secretion, whereas silencing of let7b-5p reduced insulin content and secretion. Glucose 67-74 insulin Homo sapiens 86-93 33020504-2 2020 This study aims to examine the efficacy of synthetic FFA2- and FFA3-ligands to modulate glucose-stimulated insulin secretion (GSIS) in human pseudoislets which display intact glucose responsiveness. Glucose 88-95 insulin Homo sapiens 107-114 33039672-1 2021 AIM: Current guideline recommends insulin as fourth-line glucose-lowering medications. Glucose 57-64 insulin Homo sapiens 34-41 33154737-8 2020 ISHOMA insulin sensitivity index was calculated from glucose and C-peptide (ELISA) serum concentrations. Glucose 53-60 insulin Homo sapiens 7-14 33116951-4 2020 Insulin regulates the influx of glucose into the cell by upregulating the glucose transporter type 4 (GLUT4) expression on the plasma membrane. Glucose 32-39 insulin Homo sapiens 0-7 33116951-4 2020 Insulin regulates the influx of glucose into the cell by upregulating the glucose transporter type 4 (GLUT4) expression on the plasma membrane. Glucose 74-81 insulin Homo sapiens 0-7 33028568-2 2020 Aggressive rehydration and continuous intravenous insulin resulted in improved blood glucose levels; however, metabolic acidosis persisted. Glucose 85-92 insulin Homo sapiens 50-57 32422353-1 2020 ETHNOPHARMACOLOGICAL RELEVANCE: Costus pictus D. Don, commonly known as insulin plant, is a traditional Indian antidiabetic herbal medicine with glucose-lowering and insulin secretory effects having been reported in animal models and humans with Type 2 diabetes. Glucose 145-152 insulin Homo sapiens 72-79 33007789-4 2022 INS-1 cell proliferation was analyzed using a cell counting kit-8 (CCK-8)assay, and the glucose-stimulated insulin secretion was measured using an ELISA kit. Glucose 88-95 insulin Homo sapiens 107-114 33006553-1 2021 OBJECTIVE: Characteristics of the glucose response during oral glucose tolerance test (OGTT) may reflect differences in insulin secretion and action. Glucose 34-41 insulin Homo sapiens 120-127 33007789-7 2022 The glucose-stimulated insulin secretion and the proliferation of INS-1 cells were enhanced by LINC-P21 knockdown, but the overexpression of LINC-P21 led to opposite effects. Glucose 4-11 insulin Homo sapiens 23-30 33006553-1 2021 OBJECTIVE: Characteristics of the glucose response during oral glucose tolerance test (OGTT) may reflect differences in insulin secretion and action. Glucose 63-70 insulin Homo sapiens 120-127 32822725-0 2020 Elaidate, a trans fatty acid, suppresses insulin signaling for glucose uptake in a manner distinct from that of stearate. Glucose 63-70 insulin Homo sapiens 41-48 33019410-0 2020 The ratio of estimated average glucose to fasting plasma glucose level as an indicator of insulin resistance in young adult diabetes: An observational study. Glucose 31-38 insulin Homo sapiens 90-97 33019410-0 2020 The ratio of estimated average glucose to fasting plasma glucose level as an indicator of insulin resistance in young adult diabetes: An observational study. Glucose 57-64 insulin Homo sapiens 90-97 33019410-6 2020 The ratio of estimated average glucose to fasting plasma glucose level correlates with insulin resistance in young adult diabetes. Glucose 31-38 insulin Homo sapiens 87-94 33019410-6 2020 The ratio of estimated average glucose to fasting plasma glucose level correlates with insulin resistance in young adult diabetes. Glucose 57-64 insulin Homo sapiens 87-94 32294394-8 2020 The 1.8-fold-increase in postprandial insulin after dairy compared to non-dairy treatment may explain the reduction in blood glucose without an increase in subsequent energy intake. Glucose 125-132 insulin Homo sapiens 38-45 33002153-5 2020 :: To predict the effect of patient hematocrit on the performance of a glucose meter and its corresponding impact on insulin-dosing error. Glucose 71-78 insulin Homo sapiens 117-124 33002153-9 2020 A hospital inpatient insulin dose algorithm was used to determine the frequency of insulin dose error between reference glucose and meter glucose results. Glucose 120-127 insulin Homo sapiens 83-90 33002153-9 2020 A hospital inpatient insulin dose algorithm was used to determine the frequency of insulin dose error between reference glucose and meter glucose results. Glucose 138-145 insulin Homo sapiens 83-90 32822725-2 2020 Since elaidate is a C18 unsaturated fatty acid with a steric structure similar to that of a C18 saturated fatty acid (stearate), we previously revealed that insulin-dependent glucose uptake was impaired in adipocytes exposed to elaidate prior to and during differentiation similar to stearate. Glucose 175-182 insulin Homo sapiens 157-164 32729464-0 2020 Measuring glucose at the site of insulin delivery with a redox-mediated sensor. Glucose 10-17 insulin Homo sapiens 33-40 32609902-9 2020 MAIN OUTCOME MEASURES: glucose and insulin during oral glucose tolerance test. Glucose 55-62 insulin Homo sapiens 35-42 32729464-1 2020 Automated insulin delivery systems for people with type 1 diabetes rely on an accurate subcutaneous glucose sensor and an infusion cannula that delivers insulin in response to measured glucose. Glucose 100-107 insulin Homo sapiens 10-17 32729464-9 2020 Despite a small artifact, which is likely due to dilution by fluid delivery, it is possible to continuously measure glucose in a cannula that simultaneously delivers insulin. Glucose 116-123 insulin Homo sapiens 166-173 33060070-1 2020 OBJECTIVE: Glucose disposal by insulin-responsive tissues maintains the body glucose homeostasis and insulin resistance leads to a risk of developing type 2 diabetes (T2DM). Glucose 11-18 insulin Homo sapiens 31-38 33060070-2 2020 Insulin stimulates the translocation of glucose transporter isoform 4 (GLUT4) vesicles from intracellular compartments to the plasma membrane to facilitate glucose uptake. Glucose 40-47 insulin Homo sapiens 0-7 33060070-8 2020 Insulin-stimulated GLUT4 vesicle translocation and glucose uptake were detected using immunofluorescence techniques and quantified in primary adipocytes from Hap1 -/- mice. Glucose 51-58 insulin Homo sapiens 0-7 33060070-14 2020 Furthermore, the insulin-stimulated GLUT4 vesicle translocation and glucose uptake were defective in Hap1 -/- adipocytes. Glucose 68-75 insulin Homo sapiens 17-24 32737138-6 2020 RESULTS: National spending on glucose-lowering medications increased by $40.6 billion (240%), of which insulin and noninsulin medications contributed $28.6 billion (169%) and $12.0 billion (71%), respectively. Glucose 30-37 insulin Homo sapiens 103-110 31335989-9 2020 Diabetes distress was higher among those prescribed non-insulin glucose-lowering drugs (vs. no glucose-lowering drugs), but was not associated with other clinical or socio-demographic characteristics. Glucose 64-71 insulin Homo sapiens 56-63 32737138-11 2020 CONCLUSIONS: The increase in national spending on glucose-lowering medications during the past decade was mostly associated with the increased costs for insulin, analogs in particular, and newer noninsulin medicines; and cost-per-user had a larger effect than the number of users. Glucose 50-57 insulin Homo sapiens 153-160 32617755-6 2020 The peak blood glucose level was significantly higher in the PH group [PH: median 472 mg/dL, NPH: median 275 mg/dL, p < 0.001], and a higher proportion of subjects in the PH group required insulin therapy [PH: 100% (7/7) vs. NPH: 22% (4/22)]. Glucose 15-22 insulin Homo sapiens 189-196 32876863-10 2020 CONCLUSIONS: The addition of DPP4i to insulin is associated with a statistically significant reduction in glycemic control as measured by HbA1c, fasting plasma glucose, and 2-h postprandial glucose, without increasing the risk of hypoglycemia and weight gain. Glucose 160-167 insulin Homo sapiens 38-45 32876863-10 2020 CONCLUSIONS: The addition of DPP4i to insulin is associated with a statistically significant reduction in glycemic control as measured by HbA1c, fasting plasma glucose, and 2-h postprandial glucose, without increasing the risk of hypoglycemia and weight gain. Glucose 190-197 insulin Homo sapiens 38-45 32894309-2 2020 Deeper understanding of the coupling mechanisms that link glucose metabolism in these cells to the control of insulin secretion is therefore likely to be essential to develop new therapies. Glucose 58-65 insulin Homo sapiens 110-117 32894309-4 2020 Genetic evidence flowing from both monogenic forms of diabetes and genome-wide association studies for the more common type 2 diabetes, supports the importance for normal glucose-stimulated insulin secretion of metabolic signalling via altered ATP generation, while also highlighting unsuspected roles for Zn2+ storage, intracellular lipid transfer and other processes. Glucose 171-178 insulin Homo sapiens 190-197 32894309-9 2020 Thus, we argue that defective oxidative glucose metabolism is central to beta cell failure in diabetes, acting both at the level of single beta cells and potentially across the whole islet to impair insulin secretion. Glucose 40-47 insulin Homo sapiens 199-206 32957125-6 2020 The other study assessed insulin sensitivity by a frequently sampled intravenous glucose tolerance test (FSIGT) at three time points: baseline, during the third HBOT and 24-hours post-HBOT (n = 9). Glucose 81-88 insulin Homo sapiens 25-32 32894317-5 2020 While the release products of the beta cell inhibit alpha cell function, the alpha cell releases factors that are stimulatory for beta cell function and increase glucose-stimulated insulin secretion. Glucose 162-169 insulin Homo sapiens 181-188 32152511-5 2020 Insulin resistance was assessed by triglycerides and glucose (TyG) index. Glucose 53-60 insulin Homo sapiens 0-7 31546272-6 2020 RESULTS: During oral-glucose-tolerance-test, women harboring the T allele displayed significantly higher glucose values at 60 min (p=0.034) and were more likely to require insulin therapy even after adjusting for confounders, such as BMI and age. Glucose 21-28 insulin Homo sapiens 172-179 32745202-4 2020 Insulin secretion during the OGTT, measured with ( C-Pep/ G)0-120, increased in the three groups (from 0.30+-0.06 to 0.48+-0.10; 0.29+-0.05 to 0.98+-0.23; and 0.24+-0.06 to 1.09+-0.12 in subjects receiving CANA, LIRA and CANA/LIRA respectively, p=0.02 for CANA Vs LIRA, p<0.0001, CANA/LIRA Vs CANA), and the increase in insulin secretion was associated with an increase in beta cell glucose sensitivity (29+-5 to 55+-11; 33+-6 to 101+-16; and 28+-6 to 112+-12, respectively, p=0.01 for CANA Vs LIRA, p<0.0001, CANA/LIRA Vs CANA). Glucose 383-390 insulin Homo sapiens 0-7 32690941-4 2020 The compound enhances insulin secretion in a glucose-, ligand- and GLP-1R-dependent manner. Glucose 45-52 insulin Homo sapiens 22-29 32814902-2 2020 Here we generate human islet-like organoids (HILOs) from induced pluripotent stem cells and show that non-canonical WNT4 signalling drives the metabolic maturation necessary for robust ex vivo glucose-stimulated insulin secretion. Glucose 193-200 insulin Homo sapiens 212-219 32882526-6 2020 In addition, IPCs derived from T1D- and T2D-specific iPSCs showed comparable glucose-stimulated insulin secretion as IPCs derived from ND-specific iPSCs. Glucose 77-84 insulin Homo sapiens 96-103 32435825-7 2020 The intervention was an insulin infusion to titrate blood glucose between 135 and 180 mg/Dl (7.5 and 10 mmol/l). Glucose 58-65 insulin Homo sapiens 24-31 32957125-10 2020 CONCLUSIONS: The hyperinsulinaemic, euglycaemic glucose clamp demonstrated a significant increase in peripheral insulin sensitivity during a single, 2-hour HBOT session in a group of men who were obese or overweight but without diabetes. Glucose 48-55 insulin Homo sapiens 22-29 33209776-0 2020 Idiopathic post prandial glucose lowering, a whistle blower for subclinical hypothyroidism and insulin resistance. Glucose 25-32 insulin Homo sapiens 95-102 33209776-6 2020 The objective for this study was to look for subclinical hypothyroidism (SCH) and insulin resistance (IR) in Idiopathic Post prandial glucose lowering and the correlation between thyroid stimulating hormone (TSH) with IR in them. Glucose 134-141 insulin Homo sapiens 82-89 33209776-13 2020 Conclusions: The study highlights the importance of evaluating glycoregulatory hormones like thyroid hormones and insulin in cases with idiopathic post prandial glucose lowering for early diagnosis and prevention of overt clinical diseases like Hypothyroidism and Diabetes Mellitus. Glucose 161-168 insulin Homo sapiens 114-121 32990538-8 2021 Insulin mimetic property was evaluated as glucose uptake in L6 myotubes, while the complex was docked against GLUT-4 and PKB. Glucose 42-49 insulin Homo sapiens 0-7 32993618-12 2020 RESULTS: Blood glucose was lowered by insulin therapy in the Short-term insulin (DM) and Long-term insulin (DM) groups before the operation. Glucose 15-22 insulin Homo sapiens 38-45 32993618-12 2020 RESULTS: Blood glucose was lowered by insulin therapy in the Short-term insulin (DM) and Long-term insulin (DM) groups before the operation. Glucose 15-22 insulin Homo sapiens 72-79 32993618-12 2020 RESULTS: Blood glucose was lowered by insulin therapy in the Short-term insulin (DM) and Long-term insulin (DM) groups before the operation. Glucose 15-22 insulin Homo sapiens 72-79 32990863-5 2020 Nebivolol improves insulin resistance-related variables (fasting glucose, fasting insulin, and HOMA-IR; P < 0.001, 0.01, and 0.01 respectively). Glucose 65-72 insulin Homo sapiens 19-26 33133845-16 2020 Poor insulin injection technique is an important modifiable risk factor for uncontrolled blood glucose levels. Glucose 95-102 insulin Homo sapiens 5-12 32998286-9 2020 Glucose uptake assays using a fluorescent dye, 2-NBDG (2-N-(Nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose), revealed that AST increased glucose uptake in 3T3-L1 adipocytes and L6 myotubes under insulin resistance conditions. Glucose 0-7 insulin Homo sapiens 202-209 32968829-2 2020 Stimuli-responsive, "closed-loop" systems are particularly attractive due to their ability to mimic dynamic ss cell function by releasing insulin in response to fluctuating glucose levels in real-time and with minimal patient discomfort. Glucose 173-180 insulin Homo sapiens 138-145 32993148-5 2020 Next, we will focus on summarizing the evidence for their interactions in basic cellular activities, including the cell cycle, cell polarity and migration, neuronal pattering, glucose-mediated insulin secretion, biliary regulation, and bone formation. Glucose 176-183 insulin Homo sapiens 193-200 33201616-7 2020 Our patient achieved reasonable glucose control without weight gain using a combination of basal insulin and a GLP-1 receptor agonist. Glucose 32-39 insulin Homo sapiens 97-104 32962281-5 2020 Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Glucose 238-245 insulin Homo sapiens 77-84 32857071-1 2020 protect hepatic HepG2 cells from high glucose-induced insulin resistance and oxidative stress. Glucose 38-45 insulin Homo sapiens 54-61 32815965-3 2020 Furthermore, occurrence of NAFLD may lead to a cocktail of disease consequences caused by the altered metabolism of glucose, lipids, and lipoproteins, for instance, insulin resistance, type II diabetes, nonalcoholic steatohepatitis (NASH), liver fibrosis, and even hepatocarcinogenesis. Glucose 116-123 insulin Homo sapiens 165-172 32977552-4 2020 Insulin resistance is associated with impaired glucose uptake, resulting from defective post-receptor insulin responses, decreased glucose transport, impaired glucose phosphorylation, oxidation and glycogen synthesis in the muscle. Glucose 47-54 insulin Homo sapiens 0-7 32977552-4 2020 Insulin resistance is associated with impaired glucose uptake, resulting from defective post-receptor insulin responses, decreased glucose transport, impaired glucose phosphorylation, oxidation and glycogen synthesis in the muscle. Glucose 47-54 insulin Homo sapiens 102-109 32957570-3 2020 The aim of our study was to evaluate the association between baseline plasma C-peptide level and the development of type 2 diabetes independent of glucose and insulin levels and to examine potential effect-modification by variables related to kidney function. Glucose 147-154 insulin Homo sapiens 77-86 32962087-9 2020 All of the examined fatty acids attenuated the insulin-signaling pathway and radically reduced glucose uptake following insulin stimulation. Glucose 95-102 insulin Homo sapiens 120-127 32945187-0 2022 Use of Personal Continuous Glucose Monitoring Device Is Associated With Reduced Risk of Hypoglycemia in a 16-Week Clinical Trial of People With Type 1 Diabetes Using Continuous Subcutaneous Insulin Infusion. Glucose 27-34 insulin Homo sapiens 190-197 32957570-9 2020 In multivariable-adjusted Cox regression models, we observed a significant positive association of C-peptide with the risk of type 2 diabetes independent of glucose and insulin levels (hazard ratio (HR): 2.35; 95% confidence interval (CI): 1.49-3.70). Glucose 157-164 insulin Homo sapiens 99-108 32957570-11 2020 In this population-based cohort, elevated C-peptide levels are associated with an increased risk of type 2 diabetes independent of glucose, insulin levels, and clinical risk factors. Glucose 131-138 insulin Homo sapiens 42-51 32840371-7 2020 In addition, compounds 18, 22, and 28 were found to stimulat glucose uptake in the insulin-resistant HepG2 cells in the dose from 6.25 to 100 muM. Glucose 61-68 insulin Homo sapiens 83-90 33544469-8 2021 MYR supplementation also reversed the loss of functionality in hIAPP exposed pancreatic islets via restoration of glucose-stimulated insulin secretion. Glucose 114-121 insulin Homo sapiens 133-140 32937117-1 2020 Glucose homeostasis is maintained through organ crosstalk that regulates secretion of insulin to keep blood glucose levels within a physiological range. Glucose 108-115 insulin Homo sapiens 86-93 32464315-0 2020 Curcumin metabolites contribute to the effect of curcumin on ameliorating insulin sensitivity in high-glucose-induced insulin-resistant HepG2 cells. Glucose 102-109 insulin Homo sapiens 74-81 33101365-8 2020 That impaired ability of glucose uptake is rescued by insulin is also consistent with previously reported lower proliferation rates of VSMCs derived from CADASIL subjects. Glucose 25-32 insulin Homo sapiens 54-61 32464315-0 2020 Curcumin metabolites contribute to the effect of curcumin on ameliorating insulin sensitivity in high-glucose-induced insulin-resistant HepG2 cells. Glucose 102-109 insulin Homo sapiens 118-125 32464315-7 2020 The effect of the metabolic products of CUR on insulin sensitivity was evaluated in high glucose (HG)-induced insulin-resistant HepG2 cells. Glucose 89-96 insulin Homo sapiens 47-54 32464315-7 2020 The effect of the metabolic products of CUR on insulin sensitivity was evaluated in high glucose (HG)-induced insulin-resistant HepG2 cells. Glucose 89-96 insulin Homo sapiens 110-117 32911464-8 2020 In conclusion, LNK plays a pivotal role in adipose glucose transport by regulating insulin-mediated IRS1/PI3K/Akt/AS160 signaling. Glucose 51-58 insulin Homo sapiens 83-90 32918486-7 2021 Applying NBI to the motivating diabetes trial, we found that baseline fasting insulin is an important biomarker that leads to an improvement over an existing ITR based only on patient"s baseline fasting plasma glucose (FPG), age and body mass index (BMI) to reduce FPG over a period of 52 weeks" treatment. Glucose 210-217 insulin Homo sapiens 78-85 32933059-0 2020 PPARGC1A Gene Promoter Methylation as a Biomarker of Insulin Secretion and Sensitivity in Response to Glucose Challenges. Glucose 102-109 insulin Homo sapiens 53-60 32933059-7 2020 The CpG hypomethylation in the promoter position -783 of the PPARGC1A gene in leukocytes may represent a biomarker of reduced insulin sensitivity after the ingestion of glucose. Glucose 169-176 insulin Homo sapiens 126-133 32932777-8 2020 Therefore, the beneficial actions of vitamin D include diminished insulin resistance which is observed as an improvement of glucose and lipid metabolism in insulin-sensitive tissues. Glucose 124-131 insulin Homo sapiens 66-73 32932777-8 2020 Therefore, the beneficial actions of vitamin D include diminished insulin resistance which is observed as an improvement of glucose and lipid metabolism in insulin-sensitive tissues. Glucose 124-131 insulin Homo sapiens 156-163 33013705-5 2020 Composite Z-scores were calculated for changes in insulin sensitivity (C_IS: rate of glucose disposal/insulin at steady state during hyperinsulinemic euglycemic clamp, HOMA-IR, and HbA1C) and cardiometabolic risk (C_CMR: waist circumference, triglycerides, and fasting glucose). Glucose 85-92 insulin Homo sapiens 50-57 33463010-7 2021 Sections of pancreas and isolated islets from normal donors and donors with prediabetes were tested for markers of inflammation and glucose-stimulated insulin secretion (GSIS). Glucose 132-139 insulin Homo sapiens 151-158 32696329-1 2020 The artificial pancreas system or an automated insulin dosing system has been the "holy grail" for patients with type 1 diabetes and their caregivers who have over the years wanted to "close the loop" between monitoring of glucose and delivery of insulin. Glucose 223-230 insulin Homo sapiens 47-54 32922559-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 207-214 insulin Homo sapiens 29-36 32922559-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 207-214 insulin Homo sapiens 140-147 32922559-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 207-214 insulin Homo sapiens 140-147 32922559-2 2020 Do-It-Yourself Artificial Pancreas Systems (DIY APS) are a form of hybrid closed-loop system that use open-source algorithms, which govern the delivery of insulin in response to interstitial glucose and other variables that are personalized to an individual. Glucose 191-198 insulin Homo sapiens 155-162 32907593-7 2020 Homeostatic model assessment, IR = insulin resistance (HOMA-IR) was calculated by using the obtained insulin and fasting blood glucose values before neoadjuvant chemotherapy (fasting insulin x fasting glucose/405). Glucose 127-134 insulin Homo sapiens 35-42 32899870-4 2020 Whereas p38 MAPK increases insulin-independent glucose uptake and oxidative metabolism in muscles during exercise, it contrastingly mediates insulin resistance and glucose intolerance during metabolic syndrome development. Glucose 47-54 insulin Homo sapiens 27-34 32955501-8 2020 The ECM obtained was tested for cytotoxicity and encapsulated with human pancreatic islets which showed a positive cellular behavior with insulin secretion when stimulated with glucose challenge. Glucose 177-184 insulin Homo sapiens 138-145 33088464-6 2020 Adiponectin appears to increase insulin sensitivity by improving glucose and lipid metabolisms. Glucose 65-72 insulin Homo sapiens 32-39 32876527-2 2020 It has been shown that mitochondrial metabolites, transported by the citrate carrier (CIC), dicarboxylate carrier (DIC), oxoglutarate carrier (OGC), and mitochondrial pyruvate carrier (MPC) play a vital role in the regulation of glucose-stimulated insulin secretion (GSIS). Glucose 229-236 insulin Homo sapiens 248-255 32922559-1 2020 Hybrid closed-loop automated insulin delivery systems have helped type 1 diabetes (T1D) users close the loop between glucose monitoring and insulin delivery, a very important step in efforts to simulate the glucose-responsive insulin secretory function of a healthy pancreas. Glucose 117-124 insulin Homo sapiens 29-36 32899979-2 2020 However, due to the various variability, uncertainty and complex glucose dynamics, optimizing the doses of insulin delivery to minimize the risk of hyperglycemia and hypoglycemia is still an open problem. Glucose 65-72 insulin Homo sapiens 107-114 32899979-3 2020 (2) Methods: In this work, we propose a novel insulin bolus advisor which uses deep reinforcement learning (DRL) and continuous glucose monitoring to optimize insulin dosing at mealtime. Glucose 128-135 insulin Homo sapiens 46-53 32982980-14 2020 To our knowledge, this is the first report of SPS described shortly after the initiation of insulin therapy that required basal insulin to achieve tolerable muscle symptoms and better glucose control, without the development of diabetic ketoacidosis. Glucose 184-191 insulin Homo sapiens 128-135